Cardiac

Question 1

What do AS patients rely on?

Answer 1

Preload, diastolic pressure & systolic function

Question 2

How do you transcutaneously pace?

Answer 2

-sedate pt
-Place pads in AP position (black on anterior chest, red on posterior chest)
-connect to ecg leads
-set pacemaker to demand
-turn pacing rate to >30bpm above pts intrinsic rhythm
-set mA to 70
start pacing & increase mA until pacing rate captured on monitor. Once pacing captured, set the current @ 5-10mA above threshold
If pacing rate not captured @ current of 130mA, resite electrodes & repeat

(epicardial 10mA, rate 80)

Question 3

What pharmacologic chronotropes don’t rely on AV node conduction but work directly on the myocardium?

Answer 3

Isoprenaline, adrenaline, dobutamine (act directly on the cardiomyocytes to increase cAMP & increase chronotropy)

Question 4

What is R on T & what’s it’s significance?

Answer 4

The superimposition of an ectopic beat on the T wave of a preceding beat, which may precipitate ventricular tachyarrhythmias. This is very rare especially if pacing the pt above their intrinsic rate.

Question 5

When would you consider asynchronously pacing a patient?

Answer 5

1. if they are pacemaker-depending & EMI is going to impact their pacemaker function intra-operatively
2. If they are very unwell & asynchronous pacing increasing their HR supports their cardiac output to take them out of a shocked state in the setting of…
3. Pharmacologic chronotropy not being available or carrying a higher risk than asynchronous pacing

Question 6

How does atropine work?

Answer 6

A tertiary amine, competitive antagonist of ACh @ muscurinic receptors, onset 60 seconds & duration 30-60mins

Question 7

How does glycol work?

Answer 7

Quaternary amine so doesn’t cross the BBB (is charged), onset 2-3mins (so better matched w neostigmine) & DOA 30-60mins

Question 8

What’s MINS? Main findings of the VISION trial (a prospective cohort study that recruited adults >45yo undergoing noncardiac surgery, receiving a general or regional anesthetic, and requiring hospital admission)

Answer 8

MAY be due to cumulative period hypotension & myocardial infarcts.
TnT >0.03ng/mL but only 16% have ischaemic symptoms, 87% present within 2 days, 96% within 3 days,
VISION trial showed 8% incidence of MINS & 10% with MINS died within 30 days

Question 9

What are the elements of the predictive scoring for MINS?

Answer 9

Age >75 (1 point), anterior ischaemic changes (1 point), STEMI or L) BBB (2 points). mortality for 1 point 10%, 2 pts 20%, 3 points 30%, 4 points 50%

Question 10

What are signs of RV strain on ECG?

Answer 10

ST depression & T wave inversion in leads corresponding to the RV (V1-3 +/- V4, inferior leads (most pronounced in III as it’s the most rightward facing), large R wave in V1 & S wave in V5,6, R) axis deviation, poor R wave progression

Question 11

What are major cardiac adverse events?

Answer 11

Myocardial ischaemia, infarction, angina, CCF, AV block, arrhythmias, cardiac arrest

Question 12

What are the components of Lee’s RCI & % risk of MACE? How useful is this risk stratification?

Answer 12

Procedure: suprainguinal vascular, intraTx or intraabdomimal
Pt: IHD, IDDM, Cerevrobasc disease, Cr >2g/dL, CCF
0 point= 0.4%
1= 0.9
2= 6.6
3=11

There’s a linear relationship Btwn higher score & higher risk but it’s unclear if this is of benefit

(*30 day death, MI, cardiac arrest 0-3.9, 1=6, 2=10.1, 3+=15%)

Question 13

What are the classifications of blood pressure?

Answer 13

Normal SBP <120 & DBP <80, elevated 120-129 & DBP <80, Class 1 HTN is 130-139 OR 80-89 & Class 2 HTN is >=140 OR >=90, if BP is in 2 categories, assign to the highest

Question 14

At what BP level should planned elective major surgery deferral be considered? What should be done & why?

Answer 14

SBP >=180mmHg or DBP >=110mmHg- surgery deferred, BP-lowering Rx should be discussed & commenced as pts have increased risk of complications including MI & renal failure (esp if DBP >=110mmHg)

Question 15

What should happen to B blockers in pts w HTN undergoing major surgery who’ve chronically been on B blockers? How about commencement of B blockers?

Answer 15

Continue them if used chronically. Abrupt cessation of B blockers (since up-regulate B-adrenergic receptors w chronic use & may get SVT w abrupt cessation) or clonidine (withdrawal–> rebound sympathetic outflow- tachycardia, HTN, anxiety, sweat, headaches) may be harmful (if it’s taken for angina more concerning, risk ischaemia & acute withdrawal can = substantial M & M). Should not start B-blocker naive pts on these drugs on the day of surgery as they incr risk of stroke & mortality (thought to be related to intra-op hypoT).

Question 16

What is masked HTN?

Answer 16

Normal BP in clinic but elevated out. May occur in 10% of ppl.

Question 17

What are some end-organ effects of chronic HTN?

Answer 17

LV hypertrophy, diastolic dysfunction, atherosclerotic coronary artery disease, heart failure, glomerular injury, renal tubular ischema & ESRF

Question 18

What did the POISE trial meta-analysis say about B blockers?

Answer 18

commencing <=24hrs prep reduces risk of nonfatal MI but incr risk of stroke, hypoT, Brady & death- the trial was criticised as the B blockers weren’t titrated (there’s sig pharmacogenetics variability in response so they should be titrated to HR weeks before surgery)

Question 19

According to the ACC/AHA 2014 guidelines, when might it be appropriate to consider commencement of B blockers (preferably >1 day before surgery & always with long enough to assess tolerability & safety)?

Answer 19

If intermediate or high-risk periop tests, if >3 RCRI factors. As per ESC/ESA 2014 guidelines, don’t start them for low-risk surgery.

Question 20

What’s the controversy with ACEII inhibitors & ARBs preoperatively?

Answer 20

Their continuation may be associated w intra-op hypoT & clinically sig intra-op hypoT is independently ass’d w increased risk of MI, stroke & death so some recommend withholding them at least 24hrs before major surgery but the evidence is conflicting- if continue, be aware of the risk of intra-op hypoT with these drugs & be prepared to manage it. Witholding them may risk postoperative hypertension. It’s reasonable to continue ACE-Is or ARBs under supervision (particularly if poorly controlled HTN or heart failure) & if they’re discontinued, to re-initiate asap post.

Question 21

Should CCBs be continued? what about commencing them for cardioprotection?

Answer 21

Continue them, limited evidence for commencing them in meta-analysis, most benefits are from diltiazem.

Question 22

Should alpha-2 agonists be used for cardioprotection?

Answer 22

No- they reduce central SNS activity & peripheral NAdr release so may attenuate surgical stress response AND their reduction in HR can reduce myocardial O2 balance- they may reduce MI & mortality after vascular surgery but should prob not be used for “cardioprotection” in non-cardiac surgery.

Question 23

How do dexmed & clonidine vary wrt their alpha 2 selectivity?

Answer 23

dexmed 1600:1 alpha 2 & it’s a selective full agonist, clonidine 400:1 alpha 2 partial agonist

Question 24

Where do nitrates work?

Answer 24

venous capacitance vessels & large coronaries mainly- cause peripheral pooling of blood & decreased cardiac ventricular wall tension

Question 25

Determinants of ventricular wall tension?

Answer 25

σ = ΔP.r/2ω

Question 26

Are there guidelines regarding periop use of nitrates?

Answer 26

No, but a sensible approach is for the pt to continue their usual doses esp if used for symptom control of angina.

Question 27

What’s the ejection fraction?

Answer 27

SV/EDV

Question 28

How is heart failure classified?

Answer 28

Signs (most commonly, dyspnoea, fatigue, exercie intolerance, unintentional WL, refractory vol overload, hypotension, signs inadequate perfusion) +/- symptoms is criteria 1 but signs mightn’t be present esp in early stages of HFpEF & in pts on diuretics.

2nd criteria is the EF
HFrEF (<=40%), HFmrEF (41-49%), HFpEF (>50%)

3rd criteria is, for mrEF & pEF, elevated BNP (normal doesn’t rule out; eg. NT-proBNP >125pg/mL, BNP >=35pg/mL) at least one additional criterion: relevant structural heart disease (LVA &/or LAA), diastolic dysfunction (evidence of spont or provokable incr LV filling pressures eg. elevated natriuretic peptide, noninvasive/invasive haemodynamic measurement (eg. E/e’ is ratio of maximum velocity of E-wave of mitral valve inflow by maximal velocity of E (early LV passive inflow), diastolic dysfunction suggested by >=15, E/e’ <8 considered normal, normal E/A is 0.8-2, in severe diastolic dysfunction E»A (impaired relaxation A>E)

Normal LA size <=20cm2 (severe enlargement >40cm2)
Normal LV EDV 120mL

Question 29

What do you consider when approaching heart failure?

Answer 29

Detailed Hx & examination to determine CAUSE:
-ischaemic, MI
-HTN
-valvular heart disease
-cardiomyopathies (esp familial)
-autoimmune/rheumatologic/connective tissue disease
-infiltrative (sarcoidosis, amyloid, haemochromatosis)
-endocrine/metabolic (acromegaly, thyroid, pheochromocytoma, diabetes, obesity)
-rhythm-related (eg. tachy-induced cardiomyopathy, RV pacing)
-myocarditis (infectious, toxin or medication, hypersensitivity/ immunological)
-peripartum
-takotsubo cardiomyopathy
-substance abuse (ETOH, cocaine, methamphetamine)
-high-output HF from AV fistula)

&

quantify SEVERITY (NYHA, 1= no symptoms or limitation ordinary activity, II= mild symptoms & sl limitation ordinary, III= moderate symptoms, marked function limit, IV severe & uncomfy @ rest, current or prev HF known to be ass’d with periop complications so HF is considered an independent prognostic variable for all cardiac risk scores
potential contributors= anaemia, thyroid disease, sleep-disordered breathing.

CLINICAL CONGESTION is an important adverse risk factor in HF.

Symptoms congestion:
orthopnoea, bendopnoea

Signs:
jugular venous distension, square-wave response to valsalva, LL oedema

Investigations:
12-lead ecg
CXR if S&S instability (reveals cardiomegaly, pulmonary venous congestion, interstitial or alv oedema (transudate gravity-dependent), may reveal alt causes for the pts symptoms).
Stage 1: cephalisation (upper lobe vascular redistribution (most useful in erect CXR) where LA pressure elevated 10-15mmHg (normal is 5-10mmHg)) or PCWP 13-18mmHg, cardiomegaly, broad vascular pedicle (>85mm pathologic in most cases), incr artery:bronchus ratio esp hilum & upper lobes (arteries usually larger in lower lobes).
Stage 2 w PCWP approx 18-25mmHg: kerley lines (fluid leaks into peripheral interlobular septa), peribronchial cuffing, hazy vessel contour, thickened interlobar fissure
Stage 3: alveolar oedema: PCWP >25mmHg: consolidation, air bronchograms, cottonwool appearance, pleural effusion (need 175mL pleural fluid effusion for costophrenic meniscus PA, 75mL lateral)

interstitial oedema & alv oedema modestly specific for HF but relatively insensitive, cardiomegaly may be absent.

echo if progressive symptoms/nil within ?1 yr?, additional imaging (eg. cMRI (useful info re: cardiac volumes, mass, EF of L) & R) ventricles, provides info re: inschaemia, infiltrative or infiltrative cardiomyopathies), CT) if echo inadequate, to Ax LVEF). if suspect myocardial ischaemia, CT or invasive angiography. Stress testing.
echo: cardiac structure & function, myocardium/pericardium or valve abnormalities, chamber dimensions & motion.
Re-evaluation of EF (>40 days after MI, >90 days afer revasc, >90 days after GDMT) useful to detrmine candidacy for ICD or CRT.
labs: CBC, urinalysis, electrolytes, BUN, Cr, glucose, fasting lipids, LFTs, Fe studies, TSH
BNP, NT-proBNP: useful for pts presenting with dyspnoea (support Dx or exclusion of HF), in chronic HF helps w risk stratification, prognosis, lower in obesity, cardiac causes incl HF, ACS, LVH, valvular heart disease, pericardial disease, AF, myocarditis, cardiac surgery, CV, cancer chemo. non-cardiac: age. anaemia, renal failure, OSA, severe pneumonia, PE, PAH, critical illness, bacterial sepsis, severe burns.

Functional status:
NYHA: no limitation to physical activity from HF. II= comfy @ rest, slight symptoms from HF w ordinary activity. III: comfy @ rest but Sx of HF w < ordinary activity.
CPET for advanced treatments (LVAD, heart transplant) or to evaluate causes of dyspnoea. Peak VO2 <=14mL/kg/min= cutoff to distinguish pts who may derive survival benefit from heart transplant, for those who tolerate B blockers, <=12mL/kg/min VO2 peak cutoff for trancardiac transplant listing..
6MWT: distance walked roughly correlates with prognosis in HF. <300m roughly correlates to NYHA III-IV symptoms, ass’d w worse survival free of transplant. 6MWT useful correlate of functional capacity if the pt doesn’t walk >490m.

Question 30

:) Who requires a 12-lead ecg?

Answer 30

Those with active cardiovascular signs or symptoms or those with risk factors from RCRI. To look for signs of myocardial ischaemia & arrhythmia.

Question 31

:) Is there evidence for routine ordering of prep CXR for pts w chronic stable HF? how about resting echo? how should NHYA4 pts be managed periop?

Answer 31

No. Echo also not routinely recommended if chronic stable unless S&S of worsening heart failure as this may guide periop-Mx, NYHA class IV (acutely decompensated HF) should ideally have surgery postponed & cardiology opinion sought for HF medication titration.

Question 32

:) How is NT-proBNP relevant?

Answer 32

BNP is a myofibrillar protein. The N-terminal fragment of proBNP is released by the heart in response to ischaema or stress- elevated NT-proBNP values are independently & incrementally associated with increased risk of vascular death & myocardial injury or infarction within 30 days of surgery. Adding NT-proBNP to RCRI improves cardiac risk prediction cf RCRI alone. Should not routinely be used until it’s validated in larger studies & its use is associated with improved clinical outcomes. May be useful if considering possible stress testing or other Ix where a low value helps downgrade estimated risk.

Question 33

What’s the evidence for supervised aerobic exercise for HF patients?

Answer 33

HF-ACTION trial: multi-centre, RCT >2000 pts. After adjusting for prognostic confounders, supervised aerobic exercise significantly reduces all-cause mortality & all-cause hospitalisation. Also evidence to show improved functional status, QoL & peak O2 uptake, cardiac structure & function (improved LVEF, LVEDV & LVESF) after exercise training. Most evidence is in pts with HFrEF.

Question 34

What’s the evidence for pre-habilitation in pts with heart failure?

Answer 34

may shorten hospital stay & reduce risk of postoperative complications, it’s effective in improving physical performance in pts planned for intra-ado & intra-Tx surgery. It’s unclear what type of exercise & duration is beneficial but it’s recommended to commence it during the waiting period for elective surgery as pts may be doing little physical activity while waiting.

Question 35

What is frailty?

Answer 35

Represents a state of vulnerability to stressors (eg. hospitalisation & surgery), increases the risk of adverse outcomes (eg. falls, delirium, disability)

Question 36

Have pre-op echos been shown to be associated with improved survival or shorter hospital stay in intermediate to high risk non cardiac surgery?

Answer 36

No, nor has pre-op medical consultation.

Question 37

What are some sources of EMI in the OT?

Answer 37

electrocautery, RFA, evoked potential monitoring, extracorporeal shock wave lithotripsy, ECT, nerve stimulators. Mechanical interference also a concern (eg. inserting a CVC guide

Question 38

What are the timeframes for pacemaker/other device checks? What other things should I know?

Answer 38

pacemakers should be checked within 12 months, ICDs within 6/12 & CRT devices within 3-6 months prior to surgery. Hx/exam should identify any signs of device malfunction (dizziness, syncope, deteriorating functional status). Indication for the device, whether the pt is device-dependent, recommendations from the cardiologist after any device check, type & site of the procedure, pt position & anticipated EMI or mechanical interference should be established. Establish what needs to happen (eg. asynchronous mode if pacemaker-dependent & high chance EMI, reprogram device so anti-tachycardia function & delivery of shock are suspended. Turn off advanced functions (eg. rate response, sleep/rest mode).

Question 39

Is device reprogramming required for surgery below the umbilicus?

Answer 39

Generally not, but need intra-op pacemaker monitoring & ICD deactivation/reactivation.

Question 40

:) What are the NYHA classes of HF?

Answer 40

Class I: no limitation of physical activity, ordinary physical activity doesn’t cause undue fatigue, palpitation or dyspnoea.
II: slight limitation of physical activity- comfortable at rest but ordinary activity causes fatigue, palpitation or dyspnoea.
III: marked limitation of physical activity; comfortable @ rest, < ordinary physical activity–> fatigue, palpitations or dyspnoea.
IV: unable to undertake physical activity without discomfort. Symptoms @ rest. If any physical activity undertaken, discomfort increased.

Question 41

What are considered high, intermediate & low risk procedures & what does this mean?

Answer 41

Risk relates to combined 30-day incidence of cardiac death & non-fatal MI- surgical type without considering pts comorbidities.

High surgical risk (>5%): aortic & major vascular surgery, open LL vascular surgery, pneuomonectomy, pulmonary or liver transplant.

Intermediate risk (1-5%): intra-peritoneal & intra-thoracic, CEA/CAS, endovascular AAA, head & neck, cholecystectomy, orthopaedic major (hip & spine), prostate major.

Low (<1%) risk: endoscopy, superficial procedures, cataract, breast surgery, ambulatory surgery, thyroid.

Question 42

How does coronary artery disease impact periop risk?
Implications for anaestheic management?
In patients with known coronary artery disease or risk factors for CAD undergoing non-emergent surgery, when should pharmacologic stress testing be done?

Answer 42

pre-op Dx of CAD only marginally incr risk periop death; risk major periop complications 0.8% if no known Hx CAD, 4% known CAD, 6.7% if high risk (due to surgical stress O2 supply:demand mismatch, risk periop ischaemia/infarction. risk plaque rupture. hypercoaguable state

pre-op:
consider functional capacity (DASI, NYHA)
NYHAI= no symptoms (fatigue, palpitations, chest pain, dyspnoea, syncope) & normal functional status
NYHAII= mild symptoms w normal activity, comfortable w rest, mild limitation functional status
NYHAIII= moderate symptoms w less than normal activity, comfortable only @ rest, marked limitation functional status
NYHAIV= severe symptoms w features of heart failure w minimal physical activity, even @ rest. severe limitation of functional status

60 days should have elapsed within MI (without coronary intervention) & noncardiac surgery. MI within 6/12 of noncardiac surgery incr risk of CVA, which is ass’d w 8-fold incr periop mortality rate. Risk of CV death & nonfatal MI persists for 6/12 following MI, so best to wait until after 6/12 at least for elective surgeyr.

Ax & Mx as per ACC/AHA.
Pts w good functional capacity (>4METs) have excellent prognosis even if stable CAD or risk factors.
Lee’s RCRI 0=3.9% (30-day death, MI, cardiac arrest)
1=6%
2=10.1%
3+=15%
According to ACC/AHA, elevated risk MACE is >1%.
If they have elevated risk of MACE AND <4METS or their METS are unknown. HOWEVER, very high risk pts (eg. recent MI (within 90 days), unstable angina, decomp HF, high-grade arrhythmias, haemodynamically important valvular disease (esp AF)) should be optimally treated by Cardiologist pre-op.

All pts optimise anaemia, medical Mx
continue longstanding B blockers (not start on day of OT, continue CCB, statins, dig, nitrates; withold ARB & ACEI & diuretics on am of OT if risk fuid shifts/blood loss (continue for minor OT)
(consider antiplatelets; balance risk haemorrhage w thrombosis/steonsis; balance on pt risk & surgical risk (eg. noncompressible site spinal/intracranial/posterior chamber eye/prostate), ideally BMS at least 1/12 DAPT, DES 6/12 (for SIHD) & for ACS DAPT 12/12; if high bleeding risk, BMS may stop DAPT after 1/12, DES may stop aspirin after 1/12 & P2Y12 3/12 if high risk bleeding for SIHD, ACS could stop aspirin 1-3/12 or stop P2Y12 after 6/12 if high bleeding risk.
aspirin no evidence bleeding risk wrt reduce cardiac or neuro morbidity vs bleed risk eg. GI, in primary prevention

5-lead ecg, art line
limit O2 demand (DOA, analgesia), optimise DO2 (maintain MAP within 20%, euvolaemia)

Postop: ischaemia most often 24-48hrs postop

Question 43

By how much does the physiological response to major surgery increase O2 demand?

Answer 43

up to 40%

Question 44

What is one MET?

Answer 44

the resting O2 consumption of a 40yo 70kg male, 3.5mLO2/kg/min

Question 45

What are the implications of not being able to sustain 4 METS?

Answer 45

adverse outcomes following high-risk surgery

Question 46

Examples of 1-4METS

Answer 46

eating, dressing, dishwashing, walking around the house

Question 47

4-10METS

Answer 47

climbing a flight of stairs (4METs), walking on flat @ >6km/hr, briefly running, playing golf, heavy housework

Question 48

> 10METS

Answer 48

strenuous sport, singles tennis, football, swimming

Question 49

Whats the DASI?

Answer 49

Duke activity status index, 12 measures of functional capacity, provides prognostic info re: surg risk

Question 50

What does DASI >=34 indicate?

Answer 50

Has been shown in prospective cohort study of >1500pts to be ass’d w reduced odds of 30-day death but <34 incr odds 30-day death

Question 51

What’s the 6MWT?

Answer 51

A simple measure of aerobic exercise capacity, developed ty the American thoracic society. Just need a stopwatch & 30m unimpeded walkway

Question 52

What does a 6MWT of >563m indicate?

Answer 52

anaerobic threshold of 11mL/kg/min

Question 53

What’s the CPET?

Answer 53

Dynamic, non-invasive assessment of cardiopulmonary system @ rest & during exercise
An objective test of O2 uptake

Deficiencies in CPET-derived anaerobic threshold, peak O2 consumption & ventilatory efficiency for CO2 (VE/VCO2 aka minute ventilation / CO2 production) are ass’d w poor postop outcomes (mortality, morbidity, ICU admission, LoS in hospital) after intra-abdo surgery.

BTPS= minute ventilation @ body temp, ambient pressure saturated w water vapour

Aids risk assessment (pts with insufficient cardiopulmonary capacity to increase O2 delivery to match incr periop O2 consumption are more likely to experience organ dysfunction), identification of comorbidities to be optimised, periop planning (eg. ICU).

Data represented graphically on nine-panel plot

CV system panels 2,3,5
Ventilation panels 1,4,7
V/! panels 6,8,9

Important considerations:

1. is the test maximal effort (why was it stopped?). Maximal effort= achieving >80% predicted work or 80% HR max (220-age), OR achieving a RER (VCO2/VO2) of >1.15 (panel 8)
2. What is the VO2peak? VO2peak <15mLO2/kg/min= greater risk of periop complications (VO2 max often can’t be achieved by elderly deconditioned individuals so VO2 peak (highest VO2 measured) is recorded.
3. Is the VO2:work relationship normal? (VO2 should increase as workload (black line) increases, usually 10mLO2/min/W)
4. Can the AT be determined? (panel 5, the point where the O2 demand of the muscles exceeds ability of cardiopulmonary system to supply O2; anaerobic metabolism which produces lactic acid (buffered by bicarb, generating CO2), see VCO2 incr disproportionately cf VO2, VCO2 line steeper gradient; from the anaerobic threshold, VE incr disproportionately to VO2 but prop to VCO2.
5. If so, what is the VO2 @ AT? VO2 <10.2mLO2/kg/min @ AT greater risk periop complications.
6. Does HR incr linearly w exercise intensity then rapidly decrease immediately after cessation of exercise?
7. Does O2 pulse increase w exercise? (VO2/HR, surrogate for SV, panel 2)
8. Is there ventilatory limitation? Normal response is the VE incr linearly w exercise up to AT then higher incr in VE (driven by incr CO2 production). May be limted by obst or rest lung disease; FEV1 & FVC are measured using static spirometry before start of CPET.
   MVV= maximum volume of air that can be inhaled & exhaled within 1 min. Can multiply FEV1 x 40. Normal pts VE shouldn’t exceed 80% of the MVV (panel 7). SpO2 should stay >95%.
9. Where there ecg changes?

Question 54

If the CPET has an AT of <11mL/kg/min & ischemia changes on test ecg, what’s the periop mortality?

Answer 54

43%

Question 55

and if no ecg changes?

Answer 55

5.5%

Question 56

What are some uses of CPET?

Answer 56

1. risk stratification- predicting periop mortality 2. informed decision making re: periop management including risk reduction
2. Planning re: disposition incl HDU
3. Dx of resp & cardiac diseases (incl. occult)

Question 57

For which procedure is CPET routinely recommended?

Answer 57

All AAA repairs

Question 58

What do you need for CPET (5 things)?

Answer 58

1. treadmill or static bike 2. computer-controlled ramped incr in workload 3. calibrated pneumotachograph to measure gas flow & composition (rapid gas analyser) 4. continuous 12-lead ecg recording & pulse ox, NIBP 5. trained operator

10 mins for test

Question 59

What’s the inability to climb 2 flights of stairs, in pts at elevated cardiac risk undergoing non-cardiac surgery, associated with?

Answer 59

Cardiac death & cardiac events @ 30 days & at 12 months

Question 60

What particular features of a CHD history confer high periop morbidity & mortality risk?
Moderate risk?

Answer 60

CCCPPOV
Particularly high risk if cyanotic defect with PAH (eg. Eisenmenger syndrome)
Cyanotic heart defects
Complex heart disease with significant comorbidities (eg. CHF, valve dysfunction, anticoagulation)
Complex ventricular arrhythmias
Severe pulmonary artery HTN
Prior Fontan procedure
Severe L)-sided heart obstruction
Severe systemic ventricular dysfunction (EF <37%)

Moderate risk:
prosthetic valve or conduit
intracardiac shunt
moderate systemic ventricular dysfunction
moderate L)-heart obstruction

Question 61

What are Anaesthetic considerations with Blalock-Taussig shunt?

Answer 61

surgical connection between subclavian artery and pulmonary artery. Absent pulse or lower BP on ipsilateral side- use the CL side for measurement, or lower limb if bilateral.

Question 62

Anaesthetic considerations with coarctation repair?

Answer 62

may be residual narrowing of the aorta so may have decreased LE BP +/- UE HTN- use the UL for BP but if major discrepancy, for major surgery, useful to monitor both UL & LL invasively or non invasively as the LL BP reflects perfusion of mesenteric, renal, hepatic & spinal beds.
If L) subclavian flap repair of coarctation, must use R) UL for BP.

Question 63

Anaesthetic considerations if the pt has had previous ECMO?

Answer 63

require routine screening for patency of vascular access prior to cardiac or major non cardiac surgery, esp if emergency peripheral cannulation may become necessary

Question 64

What are some non cardiac sequelae of CHD which should be considered by Anaesthetists prior to noncardiac surgery?

Answer 64

-Associated syndromes (eg. Down or Williams syndrome)

Airway:
may have upper airway abnormalities related to previous prolonged post intubation or cardiac surgery (eg. RLN damage causing hoarseness after repair of aortic arch coarctation)

Congenital syndromes (eg. DiGeorge, Cornelia de Lange, Trisomy 21) ass’d w abnormalities of upper airway (eg, large tongue, retrognathia, difficult intubation)

Tracheomalacia w partial tracheal collapse during expiration may cause chronic stridor, worsening after extubation, pts w large LA or pulmonary artery compressing the trachea (eg. absent PV or ToF) or if repair of congenital ring, may have tracheomalacia, may require reintubation.

Breathing:

May have restrictive ventilatory defect from previous thoracotomies, phrenic nerve damage from prev surgery eg, aortic arch repairs, generalised muscle weakness- may require more prolonged post I&V

D:
May be cognitive issues if associated syndromes
May be periop anxiety from many medical encounters
May have opioid tolerance if multiple previous surgeries

Haematological:

-Erythrocytosis from chronic hypoxaemia, high Hb & Hct, limit fasting time & initiate IVT preoperative if concerned about hyper viscosity symptoms. Limit phlebotomy which may lead to Fe deficiency & inadequate Hb to maintain tissue oxygenation EXCEPT if Hct >65% prep, ACC/AHA recommend isovolemic phlebotomy to dilute to Hct of 45%.

-Conventional transfusion thresholds don’t apply to cyanotic patients, who rely on high Hb to maintain tissue oxygenation- individually define transfusion thresholds. (typically 120-150g/L in cyanotic pts)

-may develop acquired von willebrand syndrome & decision should be made re: using desmopressin or vWF concentrates for prophylaxis against bleeding

Question 65

What may happen to INR in pts with Hct >55 to 60%?

Answer 65

falsely elevated if measured w standard citrate tubes so use corrected citrate tubes for these pts

Question 66

what’s the key haemodynamic goal in pts with R) to L) shunt? Why?

Answer 66

Maintain or increase SVR, avoid systemic vasodilation, avoid increases in PVR (eg. hypoxaemia, hypercarbia)

reduced SVR reduces LVEDP & LAP which will increase R) to L) shunt, hypoxaemia & cyanosis. Increased PVR will increase R)-sided pressures & also increase R) to L) shunt.

Question 67

Which medication is best for maintaining or increasing SVR in R) to L) shunt?

Answer 67

Vasopressin, since increases SVR without increasing PVR.

Question 68

What are the key haemodynamic goals in pts w L) to R) shunt? why?

Answer 68

maintain or lower SVR, avoid decreases in PVR (ie. avoid hyperopia, hypocarbia)
Because increased SVR increases LVEDP & LAP which increase L) to R) shunt. reduced PA pressure also increases L) to R) shunt. Use phenylephrine.

Question 69

What drug best to increase SVR in L) to R) shunt?

Answer 69

phenylephrine, as tends to increase systemic and pulmonary vascular resistance

Question 70

What’s the effect of GA on L) to R) shunt?

Answer 70

Unpredictable, since it reduces SVR but the the IPPV may also decrease PVR. want to lower FiO2 & limit hyperventilation which all reduce PVR.

Question 71

What are the haemodynamic goals for Fontan physiology (cavopulmonary palliation)? ie. what do we need to avoid?

Answer 71

Decrease PVR, maintain preload, maintain myocardial contractility (ie. avoid increases in pulmonary vascular resistance (hypoxia, hypercarbia), avoid hypovolemia (rely on adequate RAP, maintain adequate preload w fluid replacement), avoid myocardial depressants (initiate inotropes as indicated, since reduced LV performance & increased LAP may markedly reduce the transpulmonary pressure gradient, increase RA pressures & cause R) heart failure))

Question 72

What proportion of strokes are attributed to AF?

Answer 72

20%

Question 73

What’s pAF, persistent AF & persistent longstanding AF?

Answer 73

paroxysmal= AF that ceases spontaneously within 72hrs of onset, AF that ceases within 1 week of Rx.
Persistent= AF that continues >= 7 days.
Long-standing persistent AF= lasts >=12/12

Question 74

What are some complications of AF?

Answer 74

reduces LV filling & CO
Thromboembolic events (20% of strokes attributed to AF)
causes cognitive impairment
vascular dementia
(despite anticoagulation)

Question 75

What are some risk factors for AF?

Answer 75

genetics (esp early-onset AF)
ETOH dependence
Congenital heart disease
HTN
(–> atrial remodelling, electrical dissociation between muscle bundles & conduction pathways–> re-entry pathways & arrhythmias)

Question 76

What’s the main site of thrombus formation with the stasis of blood flow with atrial dilation in AF?

Answer 76

L) atrial appendage

Question 77

What are the 5 domains of Rx for AF & examples/implications?

Answer 77

1. Rate control (reduces symptoms, may assist preserving cardiac function- eg. B blockers, CCB, doesn’t reduce M&M)
2. Rhythm control- electrical or chemical cardioversion
3. Thromboprophylaxis- oral or L) AA closure devices
4. Control associated symptoms (heart failure, IHD)
5. Identify & Rx precipitating factors (thyrotoxicosis, sepsis)

Question 78

What are the components of CHA2DS2Vasc score?

Answer 78

CHF- symptoms or impaired LV function (2 points)
HTN >=140/90 on 2+ occasions or taking antihypertensives (1 point)
Age >=75 (2 points)
DM- fasting BGL >7 or on OHGA/insulin
Stroke/TIA/thromboembolic event (2 points)
Vascular disease (prev MI, peripheral artery disease or aortic plaque) (1 point)
Age 65-74 (1 point)
Female (1 point)

Question 79

Which CHA2DS2Vasc scores warrant OAC?

Answer 79

> =2 in males & >=3 in females

Question 80

How does warfarin impact stroke & mortality risk in AF?

Answer 80

Reduces stroke risk 66% & mortality by 25% cf aspirin or not therapy
OACS have similar efficacy to warfarin but less risk intracerebral haemorrhage

Question 81

Which pts may benefit from the LAA closure device, which is passed percutaneously transvenously to plug the LAA (once TOE has confirmed it’s free of atrial thrombus, TOE also used post-procedure to confirm position, 50%= incomplete occlusion)?

Answer 81

HASBLED score >3
Relative contraindication to anticoagulation (eg. ICH, renal failure, coagulation disorders)
Medication non-compliance

Question 82

How does LAA closure device efficacy & complications compare to warfarin in non-valvular AF?

Answer 82

comparable efficacy, low side effects (which include cardiac tamponade, ischaemic stroke from air emboli, arrhythmias)

Question 83

What’s the most effective way to restore sinus rhythm within 48hrs of onset of acute AF?

Answer 83

synchronised DC
In unstable AF, it’s the Rx of choice

Question 84

What needs to happen if AF has persisted for >48hrs, prior to electrical cardioversion?

Answer 84

DOACs must be taken for at least 3/52 & continued for 4/52 after the cardio version

Question 85

What can be done prior to electrical cardioversion if the pt is not taking anticoagulation?

Answer 85

A TOE to exclude atrial thrombus

Question 86

In what proportion of pts with acute AF will pharmacologic cardioversion restore sinus?

Answer 86

50%

Question 87

How does AF catheter ablation compare to anti-arrhythmic medications for restoring sinus?

Answer 87

More effective with similar complication rates

Question 88

Which pts get catheter ablation for AF?

Answer 88

2nd line therapy for those intolerant to anti-arryhthmics or those with symptomatic paroxysmal AF or persistent or longstanding persistent AF

Question 89

What class anti arrhythmic is flecainide? mechanism? adverse effects?

Answer 89

1c, Na+ channel blocker, hypotension & QT prolongation, avoid in structural heart disease & IHD

Question 90

What class of anti-arrhythmic is ibutilide? mechanism? adverse effects, cautions?

Answer 90

III, blocker delayed rectifier K+ channels, QT prolong & tornadoes, avoid if hypoK, QT prop, severe LVH & low LVEF

Question 91

What class anti arrhythmic is amiodarone?

Answer 91

I (blocks Na+ channels in inactive state), III (K+ channel block), IV (CCB) & B blocker (non-competitive alpha & B blockade)

Question 92

Is amiodarone suitable for patients with heart failure or IHD?

Answer 92

yes

Question 93

What are some adverse effects of amiodarone?

Answer 93

Optic: neuropathy/neuritis, corneal microdeposits
metallic taste
Peripheral neuropathy (w prol use), prox muscle wasting, tremors
Cutaneous: photosensitivity, slate-grey appearance
Respiratory: alveolar pneumonitis or interstitial fibrosis (5-15%, fatal in 10%), risk acute pulm toxicity if high FiO2
Liver: increase in transaminases, may have fatty infiltration/cirrhosis
cardiac: prol AP & RP so risk prol QTc or torsades (correct electrolytes before commence). Bradycardia refractory to atropine, sinus arrest, may be prone to hypoT from alpha & beta block & may be refractory to sympathomimetics (also if given IV rapidly, the polysorbate may cause hypotension)
Haem: inhibit vit K dep CFs so potentate warfarin effects (also inhibit CYP3A4 & is highly PB so may also potentiate warfarin through those mechanisms)
thyroid: due to structural similarity to thyroxine, inhibit peripheral conversion T4-T3. Hypo or hyper, early or delayed, may resolve or require thyroidectomy
Other drug: risk dig tox (CYP3A4, PB), risk bradyarrhythmias worse if on CCBs
CYP3A4 inhibition incr plasma [] digoxin, procainamide, quinidine, warfarin

Question 94

What are some drugs which may –> QT prolongation?

Answer 94

sotalol>amiodarone, TCA, thiazides, thiopentone, oxytocin & carbetocin, droperidol (black box warning), halothane & isoflurane, neostigmine, methadone

Question 95

What are the 2 common ablation techniques?

Answer 95

Radiofrequency energy (burning), cryothermy (freezing)

Question 96

What are the targets for AF catheter ablation?

Answer 96

pulmonary vein isolation (pulmonary vein Ostia) used for paroxysmal AF, also target the LA “substrate” with persistent AF

Question 97

Is a TOE required before an ablation procedure? why?

Answer 97

Yes, to exclude LAA thrombus

Question 98

Where is the ablation catheter passed for catheter ablation for AF?

Answer 98

femoral vein, passed up into the RA. Intra-atrial septum is punctured with fluoroscopy & TOE guidance, catheters are passed into the LA

Question 99

What are some complications of all ablation devices?

Answer 99

vascular or cardiac injury (eg. posterior atrial wall perforation, aortic perforation)
pseudoaneurysms
haematomas
AV fistulae
oesophageal damage
pericardial effusions
tamponade
phrenic nerve injury which is usually transient, recovering within 8/52
PV stenosis (commoner with smaller balloons as they pass more distally into the PV)
Strokes & TIAs are rare as pts continue anticoagulation perioperatively

Question 100

What are some complications of catheter ablation for AF?

Answer 100

posterior atrial wall perforation, aortic perforation

Question 101

In what situation may cryoablation be chosen over radio-frequency ablation?

Answer 101

if heart block is a concern (eg. if the aberrant pathways close to the AV node), since cryoablation is transiently reversible

Question 102

How does radio frequency ablation work?

Answer 102

High energy current concentrated at the tip of the catheter, heats the tissue causing cellular necrosis

Question 103

How does cryoablation work?

Answer 103

-Cryogenic energy (-50- minus 70 degrees) causes tissue freezing hence cellular necrosis
-Cryoballoon filled with liquid nitrogen, guide wire inserted into the pulmonary vein under fluoroscopic guidance, balloon inflated & occlusion tested with contrast injection, tissue is cooled with the liquid nitrogen-inflated balloon for 180-300s.
-for the R)-sided PV ablation, the phrenic nerve conduction is monitored to minimise risk phrenic nerve damage, it’s paced & diaphragmatic contraction monitored

Question 104

What proportion of R)-sided pulmonary vein ablation is associated with phrenic nerve damage? what is an anaesthetic consideration during phrenic nerve monitoring (with phrenic nerve pacing & monitoring of the diaphragm contraction)

Answer 104

1-2%
Pt must not be paralysed during phrenic n monitoring

Question 105

Aside from the radiofrequency & cryoablation, what are other means of catheter ablation?

Answer 105

endoscopic laser balloon ablation & radio frequency hot balloon ablation (heated to 70-75degc)

Question 106

What’s a benefit of the radio frequency ablation vs the balloon devices?

Answer 106

radio frequency doesn’t rely on fluoroscopy so there’s less exposure to that but but it relies on the mapping; the balloon ablation techniques do require fluoroscopy but the mapping systems (eg, CT or MRI or magnetic navigation system)

Question 107

What’s a benefit of the radio frequency ablation vs the balloon devices?

Answer 107

radio frequency doesn’t rely on fluoroscopy so there’s less exposure to that but but it relies on the mapping; the balloon ablation techniques do require fluoroscopy but the mapping systems (eg, CT or MRI or magnetic navigation system)

Question 108

What’s a benefit of the radio frequency ablation vs the balloon devices?

Answer 108

radio frequency doesn’t rely on fluoroscopy so there’s less exposure to that but but it relies on the mapping; the balloon ablation techniques do require fluoroscopy but the mapping systems (eg, CT or MRI or magnetic navigation system)

Question 109

During which ablation procedures is heparin given & what’s the target ACT?

Answer 109

L)-sided, 250-300s, antagonised with protamine

Question 110

What’s the NBG code?

Answer 110

System for classifying pacemakers:
I: Chamber paced (O=none, V=ventricle, A=atrium, D=dual)
II: Chamber sensed (O, V, A, D)
Response to sensing (O=none, I=inhibit, T=triggered, D=triggered & inhibited)
Rate modulation, where HR altered to meet physiological needs eg, respond to incr RR/vibration (O=none, R= rate modulation)
multisite pacing (O, A, V or D)
(prev antitachyarrhythmia function (S (shock), P (pace), D (dual- shock & pace)))

AAI= most common atrial single-chamber pacing mode. atrial demand pacing. pacemaker only steps in when the atrial rate drops below preset.
AOO= response when magnet placed over atrial single-chamber PM (eg. an AAI); pm paces at a preset rate.
VVI= ventricular demand pacing. if qrs rate below preset, it’ll fire. magnet over VVI becomes VOO (asynch vent pacing). risk r on t.
Dual chamber most commonly DDD; dormant if normal activity. it’ll deliver stimulus to either chamber if depolarisation fails below present rate in any chamber. if neither A nor vent, delivers pacing A&V w pre-programmed gap (normal PR interval delay) so globally synchronous. magnet over DDD–> DOO.

AICD:
these devices only pace when HR drops <40bpm
Shocked (O, A, V, D)
Antitachy pacing (O, A, V, D)- w defib if needed
Detection (E (ecg signal processing), H (ecg & haemodynamic variables))
Antibrady pacing chamber (O, A, V, D)

subcut ICDs in axilla don’t have pacing

Question 111

Where are leadless pacemakers placed? Who are they particularly good for?

Answer 111

Via a femoral sheath into the RV, guided by a catheter. they fix into the myocardium of the RV septum. The thin RV free wall is avoided to prevent perforation.
useful for pts with damaged upper central venous systems or renal failure pts to spare their veins for dialysis.
they pace the heart when it drops below a set threshold.

Question 112

What are some indications for ICDs? PPM?

Answer 112

Primary prevention in pts who are at high risk of SCD due to life-threatening VT/VF despite optimal medical management:
-prior MI @ least 40 days ago & LVEF <=30%
-cardiomyopathy, NYHA lass II-III & LVEF <=35%
-channelopathies eg. Brugada
-cLQTS
& as secondary prevention in pts who have survived a life-threatening arrhythmia (eg. previous or inducible VT/VF)

SA node disease, eg. sick sinus (based on correlation w brady & symptoms; generally HR <40bpm or pauses >4secs produce symptoms but there’s no threshold number for defining need for PPM) or high-grade or syptommatic AV block.
PPMs for bradycardia (often only start pacing when HR falls below present level eg. <60bpm)

isoprenaline: 3mg (15mL) in 35mL 5% dextrose, makes a total volume 50mL. start at 0.5-2mcg/min (0.5-2mL/hr)via CVC

Question 113

Which way does the IV septum usually depolarise? and with a pacemaker? how does CRT assist this?

Answer 113

L) to R), with a pacemaker it’s R) to L) so RV filling occurs earlier than LV which may decrease SV & CO.
CRT paces both the R) & L) ventricles simultaneously so it’ll replicate L)- to R) septal depolarisation, mimicking normal physiology, more coordinated contraction.

Question 114

How can you tell a pt has CRT on CXR? what are the benefits & indication?

Answer 114

3 leads; one in RA, one in RV & one in coronary sinus to pace the LV, generator box subcut or sub-pectorally. resynchronises the walls of the LV via the pacing leads in the RV & coronary sinus. Improves haemodynamics & symptoms & prognosis- indicated for heart failure + wide QRS (L)BBB)

Question 115

What’s the indication for CRT? Is it of benefit? what’s the rate of non-response?

Answer 115

NYHA II or III HF with reduced LVEF <35%, QRS >130ms, L) BBB.
Reduces M&M but up to 30% non-responders

Question 116

What are the most common complications of CRT device insertion?

Answer 116

coronary sinus dissection, PTx, bleeding

Question 117

Are ablation procedures usually day surg or overnight?

Answer 117

R)-sided day surgery, L)-sided involving transeptal puncture stay overnight in case of pericardial effusion +/- cardiac tamponade

Question 118

What are some considerations for planning anaesthetic for EP laboratory procedures?

Answer 118

Pt: anything from young pts with cardiomyopathies or channellopathies to elderly with multiple comorbidities, to those w corrected CHD who may have complex anatomy & may be prone to sudden decompensation. Sedation or GA (eg. pt or surg preference, if TOE/protracted/transseptal puncture, device deployment)
multiple monitoring (eg. for mapping, ecg) best placed awake when the pt can move easily

Surg:
may require art line for high-risk L)-sided procedures or for pt factors eg. severe LV dysfunction
understanding of TOE views to aid w safe transeptal puncture helpful esp as more procedures done w uninterrupted OAC or heparin upon venous access vs after LA access
immobile & prevention of coughing essential for accurate mapping of arrhythmia pathways
-smooth emergence & limit coughing to avoid groin haematoma
-minimal pain (LA at puncture site, simple analgesia)

Remote anaesthesia:
-unfamiliar environment (wrt standard & emergency procedures, room ergonomics) & equipment (standard & emergency, bed movement capabilities (ensure a radiographer familiar w bed operation present during induction))
-personnel in the cardiac team may be unfamiliar with GA & anaesthesia requirements however must have skilled assistant & appropriate recovery area with trained staff & monitoring
-hazards (radiation, C-arm, fluoroscopy, need lead gowns)
-limited pt access (airway plan, pressure points padded/protected, narrow table)
-need to ensure organised for plans a/b/c with all equipment available, temp probe & warming, consider IDC if long procedure
-lights may be dimmed for procedurals

Question 119

How’s flutter ablation done?

Answer 119

generally day case under sedation or GA w LMA; atrial flutter arises from the RA & ablation simply involves a single line burn btwn IVC & tricuspid isthmus (CTI ablation). generally no transeptal puncture, TOE. Low risk tamponade.

Question 120

How’s AF cryoablation done?

Answer 120

GA as it involves transseptal puncture & TOE, phrenic nerve monitored during cryoablation R) upper PV so no NMBD after initial induction/intubation

Question 121

What’s a particular intra-op consideration for radio frequency AF ablation?

Answer 121

saline irrigation of the radiofrequency catheter tip adds an additional 1.5L saline so limit IV fluid & consider IDC to limit pt fidget & groin haematoma

Question 122

What medication may the surgeon prescribe after an ablation procedure with TOE?

Answer 122

PPI for 4/52 due to risk oesophageal damage after heparinisation

Question 123

What sort of GA should be used for AVNRT/atrial tachycardia ablation

Answer 123

TIVA, since volatiles may theoretically suppress arrhythmias & for some procedures it’s essential to stimulate the arrhythmia to define it’s origin (there IS limited evidence that VA suppresses arrhythmia or impacts the outcome of ablation procedures)

Question 124

What are some particular considerations for VT ablation?

Answer 124

Epicardial as well as endocardial ablation may be required so sub-xiphisternal puncture may occur, risks liver, stomach, internal thoracic artery damage, risk tamponade with the irrigation fluid or epicardial bleeding, L) phrenic nerve damage also a risk so pacing of the nerve may be performed to map it’s path along the lateral ventricular wall

Question 125

How is anaesthesia usually administered for ICD insertion?

Answer 125

GA generally avoided unless it’s a young pt for primary prevention or if device testing is required (rare); subcut ICD insertion particularly painful so GA + LMA may be chosen

Question 126

What are the cutoffs for aortic mean gradient mild/mod/severe/critical?

Answer 126

<20mmHg, 20-39mmHg, >40mmHg, >80mmHg

Question 127

What are the cutoffs for aortic valve area for mild/mod/severe/critical AS?

Answer 127

> 1.5cm2, 1-1.5cm2, <1cm2 (or <0.5cm2/m2 BSA), <0.5cm2

Question 128

What’s the dimensionless performance index in AS?

Answer 128

a dimensionless measure of AS severity
ratio of (LVOT velocity/aortic valve velocity)
independent of flow
Useful in pts who have a failing LV as the mean gradient may underestimate the severity of AS
DPI <0.25 implies AVA <0.75cm2 (severe AS)

Question 129

What’s TAADs?

Answer 129

familial thoracic aortic aneurysm & dissection

Question 130

What’s a modified Bentall’s operation?

Answer 130

Aortic root and ascending aorta replacement by synthetic graft

Question 131

What are acquired causes of thoracic aortic aneurysm & dissection?

Answer 131

HTN & atherosclerosis

Question 132

What are congenital causes of thoracic aortic aneurysm & dissection?

Answer 132

Bicuspid aortic valve
Connective tissue diseases: Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome
PCKD

Question 133

What’s a true aortic aneurysm?

Answer 133

Permanent dilatation of the aorta at least 50% greater than it’s original size, involving all wall layers

Question 134

What’s a pseudo aneurysm?

Answer 134

rupture through the layers of the aorta, held together by blood & surrounding tissues

Question 135

What’s an aortic dissection?

Answer 135

disruption of the intimal layer of the aorta, with bleeding within the wall

Question 136

What’s the annual rate of rupture, dissection or death for a thoracoabdominal aorta exceeding 6cm in diameter?

Answer 136

14.1%

Question 137

What’s the 5-year survival of pts with descending or thoracoabdominal aortic aneurysms managed conservatively?

Answer 137

10-20%

Question 138

what are some indications for an aortic aneurysm to be treated?

Answer 138

increasing diameter >1cm/year, absolute size >6.5cm or >6cm if the pt has connective tissue disease
symptomatic enlargement- pain or compression on adjacent structures
rupture or acute dissection

Question 139

What’s the Crawford classification for thoracoabdominal aortic aneurysms?

Answer 139

Extent I: from the left subclavian artery to below the diaphragm
(ii) Extent II: from the left subclavian artery to the aortic bifurcation
(iii) Extent III: from the lower half of the descending thoracic aorta extending to the aortic bifurcation
(iv) Extent IV: disease confined to the abdominal aorta

Question 140

Which segments of the aorta are particularly prone to dissection?

Answer 140

the relatively fixed ascending or isthmus segments

Question 141

Where is a Stanford type A aortic aneurysm located?
and type B?

Answer 141

It involves the ascending aorta, is more harmful
Stanford type B is distal to L) subclavian- often medically managed unless impaired organ perfusion, aortic rupture etc

Question 142

what’s the 2-day mortality of a pt with untreated Stanford type A aortic dissection? 6 month? why?

Answer 142

50%
90%
usually due to rupture of the false lumen & fatal haemorrhage

Question 143

What’s the surgical mortality for a type A aortic dissection repair?

Answer 143

30%

Question 144

What’s the DeBakey classification of aortic dissections?

Answer 144

type 1: intimal tear in ascending aorta, aneurysm involves whole aorta
type 2: intimal tear in ascending aorta, aneurysm involves section just up to inominate
type 3: intimal tear in descending segment, starting distal to L) subclavian, generally involves desc thoracic aorta only but may extend proximally into the arch

Question 145

What are some essential elements of the pre-op evaluation of a patient with thoracic/thoracoabdominal aortic aneurysms?

Answer 145

-Functional capacity (for risk stratification & prediction of postop complications)
-Hx of cardiac, resp, renal, hepatic, neurological disease
-Any evidence of involvement of adjacent structures, eg. dyspnoea/stridor suggests tracheal or L) main bronchus compression, dysphagia tracheal compression, voice hoarseness= stretching of RLN
-baseline neuro exam
-PFTs useful (w transfer factor if OLV anticipated)
-Ax for CAD

Question 146

What are aneurysms of the aortic root & proximal ascending aorta often associated with?

Answer 146

bicuspid aortic valve, a cause of aortic stenosis

Question 147

How may TOE be useful in thoracic/thoracoabdominal aortic surgery?

Answer 147

helps guide surgical approach & anticipate potential problems with weaning from CPB, eg:
measure of the aortic root dimensions (help decide re: replacing the valve)
Identification of pericardial collection or tamponade (which may be associated with type A dissection)
assistance with placement of coronary sinus cannula for delivery of cardioplegia & to confirm adequate positioning of the venous line of a bypass circuit when sited via femoral fein
supports de-airing at end of surgery
allows assessment of ventricular function & residual AR if native valve remains in situ

Question 148

What are the implications of aortic arch repair?

Answer 148

interruption to cerebral blood supply so use CPB with deep hypothermic circulatory arrest (DHCA)

Question 149

How may cerebral perfusion be maintained during DHCA?

Answer 149

antegrade by cannulation of the arteries as they branch from the aortic arch or via the art line into the R) axillary, subclavian or innominate artery or retrograde via cannulation of the IJV

Question 150

What’s the purpose of hypothermia during DHCA?

Answer 150

effective technique to protect the CNS & other viscera in the presence of reduced or absent blood flow, through reducing metabolic activity & attenuating the inflammatory response to reperfusion

Question 151

How is hypothermia achieved during DHCA?

Answer 151

Core temp allowed to decrease spontaneously
additional cooling provided by the heater/cooler on the CPB circuit
some centres apply topical cooling to the head- evidence for this is extrapolated from animal studies, if used care needs to be taken to protect pts eyes

Question 152

How much safe circulatory arrest time can occur with deep hypothermia (14.1-20deg) vs moderate hypothermia (20.1-28deg)?

Answer 152

20-30mins vs 10-20mins

Question 153

risks & benefits of deep hypothermia?

Answer 153

risks= coaguloapthy & increased inflammatory response
benefits= reduced incidence of renal & hepatic failure, stroke paraplegia & death.

Question 154

Which temperature measurement site most accurately reflects cerebral temperature?

Answer 154

nasopharynx

Question 155

What surrogate markers of cerebral metabolism may be used?

Answer 155

jugular bulb venous SpO2, EEG

Question 156

Which drugs may be variably used for pharmacological protection of the brain & spinal cord during hypothermia (there’s little evidence)?

Answer 156

thiopental, magnesium, lignocaine, methylprednisolone

Question 157

At what levels should intracerebral oxygen saturations be maintained with near-infrared spectroscopy?

Answer 157

within 25% of baseline

Question 158

What’s near-infrared spectroscopy?

Answer 158

continuous, real-time monitoring of anterior cerebral oxygenation- looks at the proportion of light absorbed attributable to oxygenated & deoxygenated Hb within the cerebral cortex, using adhesive diodes on the forehead

Question 159

What steps could be taken if inadequate cerebral perfusion was found on near-infrared spectroscopy?

Answer 159

check cannulation sites
increase flow rate within the CPB circuit
optimise [] Hb
increase hypothermia & PCO2 to promote vasodilation

Question 160

If surgery of the descending aorta involves a clamp distal to the L) subclavian artery, what type of bypass is preferred?

Answer 160

partial left heart bypass (PLHB)

Question 161

What are some benefits of PLHB?

Answer 161

allows perfusion of organs distal to the aortic XC & reduces some of the L) heart after load (which may be ass’d with increased contractility & O2 demand outstripping supply–> ischemia)

Question 162

What level of heparinisation is required for the limited extracorporeal circulation without oxygenator which occurs with PLHB?

Answer 162

partial heparinisation, ACT 200-300s

Question 163

what level of cooling is required for PLHB?

Answer 163

passive cooling to around 34deg c, this is all that’s required due to the maintenance of cerebral perfusion

Question 164

during PLHB what is proximal MAP maintained at? and distal aortic pressure? how to maintain these pressures?

Answer 164

80-90mmHg, 60-70mmHg
may maintain proximal & distal pressures by augmenting flow from the bypass circuit, may alleviate proximal HTN by increasing bypass flow or pharmacological means (eg. GA agent, GTN), but need to maintain adequate proximal MAP for coronary flow

Question 165

during PLHB what is proximal MAP maintained at? and distal aortic pressure? how to maintain these pressures?

Answer 165

80-90mmHg, 60-70mmHg
may maintain proximal & distal pressures by augmenting flow from the bypass circuit, may alleviate proximal HTN by increasing bypass flow or pharmacological means (eg. GA agent, GTN), but need to maintain adequate proximal MAP for coronary flow

Question 166

discuss physiology of aortic cross clamp

Answer 166

sudden increase in LV afterload & proximal arterial pressure, which may cause incr myocardial contractility & supply:demand mismatch
organs distal to the clamp risk lack perfusion (warmers off)
when aorta opened, risk significant blood loss; have cell salvage & rapid infusers
can advance XC sequentially to limit visceral ischemia, or could directly cannulate vessels eg. SMA or renal arteries
Unclamping aorta in later stages of operation ass’d w reduced MAP due to decr afterload, VD via release vasoactive mediators (which also promote myocardial depression)- anticipate this with vasopressors & ensuring adequate intravascular volume. Attenuate this response with gradual controlled XC release

Question 167

What are some anaesthetic considerations for surgery of the descending aorta?

Answer 167

clear communication with surgeon about extent of the aneurysm, where clamp will be placed, what bypass technique used
Consideration of X-clamp physiology & use of bypass
positioning for thoracolaparotomy
short-acting NDNMBD to facilitate neurophysiological monitoring
consideration of CSF drain, plans for action if reduction in MEP amplitude >50%
OLV allows exposure of thoracic aorta via deflation of L) lung
Either a L)-sided DLT provided the aneurysm isn’t compressing the L) main too much, otherwise a R)-sided DLT or single-lumen tube with a BB. usually exchange the DLT for a single @ end of case
place a R) radial & L) femoral artery catheter
Large IV into femoral vein
CVC & sheath in L) IJV (if in the R), there may be issues with kinking once the pt positioned)
temp probes in the nasopharynx & bladder (hypothermia used)
High bleeding risk: cell saver, X-match, TxA, protamine on separation of CPB, other products based on PoCT

postop:
sedation holds for neuro monitoring
multimodal analgesia- consider Tx epidural (significant incision) but issues with aiming to have sensory but not motor block. if an intrathecal catheter, can administer diamorphine or morphine.

Question 168

What proportion of extent II aneurysms may end up with paraplegia? how about overall with thoracic aortic surgery?

Answer 168

up to 50%
4-16% overall

Question 169

What proportion of extent II aneurysms may end up with paraplegia? how about overall with thoracic aortic surgery?

Answer 169

up to 50%
4-16% overall

Question 170

What’s the physiology behind the risk of paraplegia with thoracic aortic surgery?

Answer 170

cross clamp reduces arterial blood pressure & increases CVP, compromising spinal cord perfusion & replacement of sections of aorta requires interruption of arterial collaterals, risking spinal cord ischemia & reperfusion injury

Question 171

What are some risk factors for paraplegia with thoracic aortic surgery?

Answer 171

Patient facortrs:
advanced age
previous surgery to distal aorta
DM
severe peripheral vascular or atherosclerotic disease

surgical factors:
more extensive aneurysm
longer duration of aortic XC
emergency surgery

anaesthetic:
perioperative hypotension

Question 172

What measures may reduce the risk of spinal cord ischaemia during thoracic aortic surgery?

Answer 172

drainage of CSF to maintain ScPP, via a CSF drainage catheter; this may reduce incidence of postop neurological deficits by 80%
use of neurophysiological monitoring- MEPs monitor activity of the descending motor pathways in the anterior SC (stimulation of motor cortex via subnormal electrodes, monitor muscle contractions peripherally), the LL MEPs are significantly dampened cf UL MEPs when spinal cord ischaemia occurs. SSEPs used less frequently- allow monitoring of posterior ascending sensory columns.
sequential clamping of aorta
minimal XC time
preimplantation of intercostal & lumbar segmental vessels
minimising periop hypotension

Question 173

What’s the equation for spinal cord perfusion pressure (ScPP)?

Answer 173

ScPP=MAP-CSFP

Question 174

What is the goal CSF pressure with CSF drainage during thoracic aneurysm surgery? how maintain & how long monitor?

Answer 174

10-15mmHg, drain CSF to maintain this (at rates of up to 20mL/hr), continue monitoring of CSF pressure & drainage for up to 72hrs postop, monitor ICP, continue neurophysiological monitoring (MEPs while sedated, regular re-Ax of LL power while awake)

Question 175

What’s the target SCPP, CSFP & MAP used for safe spinal cord perfusion during thoracic aneurysm surgery? how achieve this? What to do if evidence of SC ischemia?

Answer 175

70mmHg
CSFP maintained <15mmHg
minimum MAP 80mmHg

may need to drive up MAP w vasopressor such as NADr, if can’t keep CSFP <15mmHg via the CSF drain, may need to augment the MAP further

if evidence of spinal cord ischemia, increase the SCPP & MAP target in 5mmHg increments

Question 176

What’s a spinal drain? where place? risks?

Answer 176

transduced intrathecal catheter at L3-4 or L4-5. Risks spinal headache, neural haemorrhage or haematoma, meningitis, intracranial hypotension, catheter fracture.

Question 177

How long does it take for cell death if no perfusion & normal metabolism?

Answer 177

3-5 mins

Question 178

which anaesthetic agents/drugs affect which neurophysiological monitoring?

Answer 178

NMBDs & volatiles affect MEPs but not SSEPs

Question 179

What to do if LL MEPs reduce in amplitude >50%?

Answer 179

reimplant the intercostal arteries into the graft
measures to improve SC perfusion (reduce CSF pressure by draining it up to 20mL/hr, increase MAP- aim MAP >80mmHg & distal aortic pressure >60mmHg, maintain Hb >100g/L, if physiological variables don’t improve in 3-5mins, surgically intervene)

Question 180

What to do if a pt has neurological impairment developing postop?

Answer 180

delayed paraplegia has better prognosis than immediate, can be reversed if recognised promptly

COPS:

CSF drain status- if catheter patent, lie the pt flat & maintain CSFP <5mmHg. Insert a drain if not patent or present.
Optimise O2 delivery- supplemental or tracheal intubation & IPPV- SpO2 >95%, Hb [] >120g/L, cardiac index >2.5L/min/m2
Patient status: MAP, SCPP, cognitive status- keep SCPP >80mmHg & MAP >90mmHg

Question 181

What’s the overall operative mortality & rate of severe adverse outcomes after TAAA repair? what are some significant complictiations?

Answer 181

10%, 15%
hypothermia, delirium, coagulopathy, cardiovascular instability, metabolic disturbance, respiratory failure, renal failure, CVA

Question 182

How long can a spinal drain remain in if concern re: spinal cord perfusion?

Answer 182

up to 1 week

Question 183

*what is R) heart failure?

Answer 183

a clinical syndrome [that arises] due to an alteration of structure and/or function of the right heart circulatory system [and] leads to suboptimal delivery of blood flow (high or low) to the pulmonary circulation, and/or elevated venous pressures – at rest or with exercise

Question 184

*what’s the most anterior chamber of the heart?

Answer 184

RV

Question 185

*How does the RV differ cf LV? how is this useful to it’s function?

Answer 185

thin-walled, low-pressure chamber
to maintain pulmonary perfusion pressure & deliver mixed venous blood to the pulmonary vasculature for gas exchange, maintains low systemic venous pressure which helps prevent systemic organ congestion

Question 186

*how does the RV appear in longitudinal and transverse cross-section?

Answer 186

triangular, crescent-shaped

Question 187

*What facilitates venous return to the RA?

Answer 187

Gradient between MSFP (normal 7-10mmHg) of the peripheral vasculature (normally 7-10mmHg) & RAP & CVP (normally 0mmHg)
venous return= MSFP - (RAP/RVR)

Question 188

*What facilitates venous return to the RA?

Answer 188

Gradient between MSFP (normal 7-10mmHg) of the peripheral vasculature (normally 7-10mmHg) & RAP & CVP (normally 0mmHg)
venous return= MSFP - (RAP/RVR)

Question 189

What % increase in plasma volume triggers high vs low-pressure baroreceptors?

Answer 189

> 10% for high-pressure baroreceptors (VD, reduced HR/contractility), 5-10% for low-pressure (ANP secretion)

Question 190

What’s cardiac resynchronisation therapy?

Answer 190

atrial, biventricular pacing +/- ICD (CRT-P or CRT-D)

Question 191

What are different types of cardiac implanted electrical devices & briefly what do they entail?

Answer 191

pacemaker (paces RA, RV +/- LV, senses the underlying cardiac rhythm & if it senses a P wave it’ll inhibit atrial pacing, if senses intrinsic R wave will inhibit ventricular pacing, has algorithms for sensing (eg. AF) & making sure pt doesn’t go into a very fast rhythm. It protects from bradycardia, varies rate according to pt activity)

implanted cardioverter defibrillator (ICD)- does everything a pacemaker can + overdrive pace VT, deliver a small, synchronised cardioverting shock for VT (10J), deliver a large defibrillating shock for VF (30J), has atrial & ventricular pacing & shocking leads

cardiac resynchronisation therapy- atrial, biventricular pacemaker +/- ICD (CRT-P or CRT-D)

implanted cardiac monitor= implanted loop recorder

Question 192

Disadvantages of unipolar pacemaker circuits?

Answer 192

much bigger electrical current pathway, greater potential for interference

Question 193

What do the 3 letters on pacemaker classifications stand for?

Answer 193

chamber paced, chamber sensed & what happens (eg. inhibited, triggered)

Question 194

What does VVI mean?

Answer 194

ventricular beat, ventricle sensed, inhibits

Question 195

What does VVT mean?

Answer 195

gives a ventricular pacing beat if senses in ventricle

Question 196

What does DDD stand for?

Answer 196

Paces dual AV, senses dual AV, dual functions of both inhibiting & triggering beats ie. senses in atria, waits for AV delay then triggers a beat in the ventricle

Question 197

What are the VOO, AOO & DOO pacemakers?

Answer 197

asynchronous

Question 198

What are the VVIR, AAIR & DDDR pacemakers?

Answer 198

rate responsive

Question 199

What does a magnet do for a pacemaker?

Answer 199

it stops it from sensing interference or intrinsic rhythm, so turns the pacing ON to “asynchronous” mode; care in pts w native rhythm, risk precipitating malignant arrhythmia

Question 200

What does a magnet do for an ICD?

Answer 200

it stops the ATP & defib functions; stops sensing VF so it turns the shocking function OFF- usually doesn’t turn pacing ON or alter pacing

Question 201

What are the general indications for using a magnet over an implanted cardiac electrical device in OT?

Answer 201

either to stop the pacemaker from sensing interference & for stopping the shocking function of an ICD.
NOT appropriate for pts who have an ICD + are PM dependent (these devices require a tech to actually reprogram & recheck it postop)
Not appropriate prone (hard to get it on the pt)
Indicated for procedures where electrocautery/diathermy is to be used ABOVE the navel (pts having bipolar pacing leads tends to protect from issues w interference when procedure below navel).

Question 202

Questions to consider with pre-op Ax when deciding if reprogramming necessary?

Answer 202

What’s the surgical site- is interference likely? (supra-umbilical)
Is the pt pacemaker dependent or ICD?- in this case, may need to switch to asynchronous mode or reprogram
Sometimes may turn off rate response modes (rarely)

Question 203

Aside from considering re: reprogramming +/- magnet, what are other considerations with pacemaker pts during surgery?

Answer 203

monitor their actual pulse, not ecg (which is distorted)
need access to the device- defibrillator pads on (10-15cm from device).

Question 204

What does the ICD PM PM mnemonic mean for pre-op Ax of pts with pacemaker?

Answer 204

Identify the PM/ICD (easiest way is if the pt has a pacemaker card)
Consult the local expert- much nuance btwn devices
Bipolar diathermy safer. If monopolar, pathway from diathermy to plate directed away from device/leads Diathemy plate away from the pacemaker

Pulse oximeter/palpate or art line to be used when ECG unreadable
monitor ECG (using the “diagnostic” or “pacemaker” bandpass filter preferred for showing higher-frequency incl pacing spikes) esp when ICD function “off” & UNTIL the device is turned on again (along with continuous pulse ox & an external defibrillator with pacing capability immediately available & defibrillator pads left in place)- ie. continual ecg monitoring from the time pacemaker tech turns it off to when they turn it on again & measures ready for possible urgent cardioversion, defibrillator or transcutaneous pacing (should place defibrillator pads before anti-taccharrhythmia functions of an ICD have been disabled +/- asynchronous pacing enabled to allow Rx of malignant arrhythmias (do NOT place the pads over the ICD- place A-P if standard L)-sided CIED used), an external defibrillator with pacing capability should be immediately available.

Program & reprogram post-op if surgery > umbilicus, proximate (<=15cm) to the PM or Prone or PM dependent or advanced functions (eg. RR triggered by MV)
Magnet if inappropriate inhibition or shocks

Question 205

If you put a magnet on a pacemaker for ECT, do you need to recheck the PM?

Answer 205

no as it’s such a brief pulse HOWEVER should interrogate a pacemaker within 1 month of Rx & any ICD needs to be deactivated or magnet applied.

Question 206

What surgical factors increase the risk of EMI for a pacemaker?

Answer 206

unipolar vs bipolar diathermy
high voltage (coagulation) mode vs low voltage (cutting) mode
nearer the pulse generator or leads of an ICD or PM (supra-umbilical)

Question 207

Would antitacchycardia functions be suspended in an ICD pt or asynchronous mode initiated for pacing-dependent pts for CVC insertion?

Answer 207

some clinicians may do so (guide wire movement may lead to inhibition of pacing function or delivery of an inappropriate shock

Question 208

What are the steps if a patient with a magnet applied to an ICD has an intra-op cardiac emergency (eg. VF)?

Answer 208

alert clinicians, stop all EMI, remove magnet to permit reactivation of the ICD’s anti-taccharrhythmia function, external defibrillator to cardiovert or defibrillate with the pads that were placed on the pt prior to procedure, should printout ecg for later analysis

Question 209

When do we assume a pt is pacing dependent?

Answer 209

if all beats are paced

Question 210

What are some situations where postop CIED evaluation should occur?

Answer 210

if reprogramming occurred
if the pt underwent emergency surgery sans appropriate preop CIED evaluation
if suspicion the anti-tachyarrhythmia therapy may have been permanently disabled vs suspended, if pts are haemodynamically unstable intra-op, if the CIED is exposed to significant EMI (eg. monopolar superior to umbilicus), surgery-specific (eg, thoracotomy)

Question 211

In which situations may device reprogramming (vs magnet) be needed? when may magnet be appropriate?

Answer 211

if ICD & pacing dependent with electrosurgery unit use superior to umbilicus
if unable to access magnet (eg. prone) or unable to keep it in place after pt positioning
if EMI within 15cm of the device
if movement or shock may create a hazard (eg. intraocular surgery)
for patients where reprogramming is necessary as the cardiac function would be compromised in asynchronous mode eg. the paced HR may need to be increased (to augment periop cardiac output & DO2 in pts with sinus node incompetence)
if a magnet would interfere with the sterility of the surgical field
to disable a minute ventilation sensor to prevent inappropriately high rate around monopolar radio frequency instruments
to disable a mechanical rate sensor if the OT likely to produce mechanical stimulation near the pulse generator (eg. breast surgery)

If the response to magnet is known & the effect is desirable, pt is supine & access to magnet is adequate (it can be observed & easily removed), magnet may suffice

Question 212

According to Livhits 2011, what’s the 30-day risk of MI if perform OT within 30, 60, 90 & 180 days of a MI? 30 day mortality rate if performed within 30-60, 90 & 180 days of a MI?

Answer 212

32%, 19%, 8%, 6%
14%, 11.5%, 10.5%, 9.9%

Question 213

What perioperative adverse event, which is associated with an 8-fold increase in mortality, is independently associated with a Hx of MI within 6/12 of surgery?

Answer 213

periop CVA

Question 214

According to the 2014 ACC/AHA guidelines, how many days should elapse between MI (without coronary intervention) & non-cardiac surgery?

Answer 214

at least 60

Question 215

Is active heart failure or coronary artery disease associated with higher 30-day postop mortality? does the stability of heart failure matter?

Answer 215

HF
yes- pts with stable HF have same morality as those sans HF

Question 216

What confers higher perioperative risk? signs & symptoms of active heart failure or LVEF?

Answer 216

S&S, however LVEF <30% is associated with poor periop outcomes & long-term mortality in elevated-risk non-cardiac surgery

Question 217

Does HFpEF confer higher perioperative risk?

Answer 217

Yes- in a meta-analysis pts with HFpEF had lower all-cause mortality than those pts with reduced EF (although mortality did not substantially reduce until LVEF fell <40%) but the absolute mortality rate was higher in pts with HFpEF than those sans HF, also diastolic dysfunction is associated with higher rates of MACE, prolonged hospital LoS & higher rates of postop HF

Question 218

If a pt has a malignant arrhythmia & requires defib, how long does it take for the device to charge?

Answer 218

30 seconds

Question 219

What’s a great way to help limit risk of my patient getting MINS?

Answer 219

set alarms for within 10-20% of the pt’s MAP

Question 220

What is DCCV & how perform?

Answer 220

DC shock to convert arrhythmia back to sinus, 5-10mins, position supine
IV & standard monitoring, propofol +/- LMA, ?RSI & ETT if pt/aspiration factors, if obese or difficult airway can defib in lateral position
Often remote site w pts who are CV unstable
Check K+, needs to be normal as myocardium can become unstable
IF in AF >24hr & not anticoagulated, should check LA for clot w TOE before cardioversion (can be done under propofol sedation- if clot present, anticoag for 4/52 required, then check again- if clear, proceed)
Connect ecg leads through the defibrillator & synchronise to the R wave
ALS defib safety & remove O2 during shock
For AF, start 150J biphasic defib, 200J standard
For atrial flutter, 50J & incr by increments of 50J
Recovery position w supplemental O2 postop
Digoxin incr risk arrhythmias- omit on the day. Amiodarone improves the success of cardioversion to sinus. Important hasn’t missed any doses of anticoag if on.

Question 221

What’s 4 METs?

Answer 221

VO2 max

Question 222

How does DSE & MPS compare?

Answer 222

equivalent- institution experience plays a role

Question 223

Which pts did benefit from preop coronary revascularisation prophylaxis in the Coronary artery revascularisation prophylaxis trial?

Answer 223

Those with unprotected L) main disease:
90% L) main disease or 90% circumflex + 90% LAD

Question 224

Should ACE-I or ARBs be stopped prior to surgery?

Answer 224

Yes- VISION study

Question 225

What’s the timeframe for increased risk of stent thrombosis for DES & BMS?

Answer 225

6/12 for both; but can stop antiplatelets sooner for BMS

Question 226

Latest guidelines re: stents

Question 227

What DBP helps maintain coronary perfusion?

Answer 227

> =60mmHg

Question 228

Problem with COX-2 inhibitors in a pt with IHD?

Answer 228

Incr risk of thrombosis

Question 229

assessing cardiac axis

Question 230

what condition u waves associated with?

Answer 230

?? hypokalaemia??

Question 231

ST elevations in leads V5-6 corresponds to which myocardial area?

Answer 231

APEX!

Question 232

ST depression in leads V1-V3 corresponds to transmural ischaemia to which area?

Answer 232

posterior

Question 233

What degree of elevation in the R) leads is considered significant?

Answer 233

0.5mm

Question 234

ST depression >5mm (or 0.5) in 2 or more contiguous leads? (?)

Question 235

Wellen’s

Answer 235

TWI lead I & aVF, 75% LAD stenosis?

Question 236

over how many leads do pathological q waves need to be?

Answer 236

2 or more

Question 237

What are some clinical uses of PACs?

Answer 237

DIAGNOSTIC:
-Interpretation of haemodynamic values & pressure tracings to:
Differentiate shock (cardiogenic, distributive (eg. sepsis), hypovolaemic, obstructive (eg. massive PE)))
Differentiate mechanisms of pulmonary oedema (cardiogenic, non cardiogenic)
Evaluate pulmonary HTN
Dx pericardial tamponade, L)-R) intracardiac shunt, unexplained dysponea, lymphangitic spread of tumour or flat embolism (from contents aspirated)

THERAPEUTIC:
Guide pharmacologic therapy (vasopressors, inotropes, vasodilators eg. if ulm HTN)
Guide nonpharmacologic therapy (fluid Mx, burns, sepsis, heart failure)
Ax response to pulm HTN-specific terapy

Question 238

What are the physiologic measures that can be obtained from accurately placed PACs?

Answer 238

Direct:
CVP
RAP
RVP
PAP
PCWP
CO
SvO2 (mixed venous oxyhaemoglobin saturation)

Indirect:
Systemic vascular resistance (SVR = 80 x [mean artery pressure – CVP]/CO)
Pulmonary vascular resistance (PVR = 80 x [mean PAp – PAOP]/CO)
Cardiac index (CI = CO/body surface area)
Stroke volume index (SVI = CI/heart rate)
Left ventricular stroke work index (LVSWI = [mean systemic artery pressure – PAOP] x SVI x 0.136)
Right ventricular stroke work index (RVSWI = [mean PAp – CVP] x SVI x 0.136)
Oxygen delivery (DO2 = CI x 13.4 x hemoglobin concentration x arterial oxygen saturation)
Oxygen uptake (VO2 = CI x 13.4 x hemoglobin concentration x [arterial oxygen saturation – venous oxygen saturation])

Question 239

What’s normal RA pressure?

Answer 239

0-7mmHg

Question 240

What are some causes of elevated RA pressure?

Answer 240

Hypervolaemia
Tricuspid valvular disease (regurgitation, stenosis)
RV disease (infarction, hypertrophy, cardiomyopathy)
pulmonic stenosis
pulmonary HTN or pulm embolism
L) to R) shunts
LV systolic heart failure
Constrictive (cardiac tamponade, constrictive pericardial disease)

Question 241

How to interpret an elevated RA pressure in PAH vs pulm stenosis or RV infarction?

Answer 241

with PAH the elevated RAP is associated with PAP >=25mmHg but the PAP is normal in PS or RV dysfunction (see table 1 useful tables)

Question 242

How are the RAP, RVEFP & PCWP in constrictive disorders (restrictive CM, cardiac tamponade, restrictive pericardial diseases)?

Answer 242

equal

Question 243

what’s typically higher on RAP trace? A or v wave? situation where not?

Answer 243

a, slightly

if TCR, tall v waves which may even obliterate the C wave if severe tricuspid regurgitation

Question 244

Which pathology is associated with a RV “square-root sign” pressure form?

Answer 244

constrictive pathologies (pericarditis, tamopnade, restrictive cardiomyopathy)- figure 2

Question 245

What are the characteristics of RA pressure tracings in tricuspid regurg? and stenosis?

Answer 245

tall V waves which may obliterate the C wave if the TCR is severe
cannon a waves

Question 246

What causes a cannon a wave? associated conditions?

Answer 246

simultaneous contraction of atrium & ventricle while TCV closed, occurs with A-V dissociation
ventricular tachycardia or ventricular pacing
CHB
AVNT
tricuspid stenosis

Question 247

What causes a cannon a wave? associated conditions?

Answer 247

simultaneous contraction of atrium & ventricle while TCV closed, occurs with A-V dissociation
ventricular tachycardia or ventricular pacing
CHB
AVNT
tricuspid stenosis

Question 248

what’s the RAP trace like in TC stenosis? Other conditions ass’d w diminishing of the y descent?

Answer 248

incr amplitude of a wave with slow descent of y wave

tamponade (normally CVP 0-8mmHg, 8-12mmHg in tamponade)

Question 249

what are some conditions associated with exaggerated y descent?

Answer 249

those that lead to rapid RV filling, constrictive pericarditis, restrictive cardiomyopathy, severe TCR

Question 250

Normal RV systolic pressure?

Answer 250

15-25mmHg

Question 251

Normal RVEDP?

Answer 251

3-12mmHg

Question 252

What can be the aetiology of elevated RV pressure?

Answer 252

elevated PAP (eg. pulm HTN, pulm embolism; if RV pressure >40mmHg (rare), it’s usually due to chronically elevated PAP)
pulmonic valve disorders (pulm stenosis is characterised by pressure gradient btwn RV & PA)
diseases primarily affecting the RV (tend to get elevated RVEDP with cardiomyopathy, RV ischaemia, RV infarction, cardiac constriction, cardiac tamponade or RV failure due to pulm HTN. Increase in RVESP occurs but generally it’s not as severe as with pulm vascular or pulmonic valve disorders.

Question 253

at what point is RVEDP measured?

Answer 253

after the a wave, just prior to systolic upstroke on the RV pressure tracing

Question 254

normal PA systolic pressures? diastolic? normal mPAP?

Answer 254

15-25mmHg, 8-15mmHg, normal mean 16mmHg (10-22mmHg)

Question 255

what’s elevated mPAP?

Answer 255

> 22mmHg

Question 256

what are the causes of pulm HTN?

Answer 256

pulmonary arterial HTN (idiopathic, connective tissue disease, congenital heart disease: group 1)
pulm HTN due to L) heart disease (group 2)
pulm HTN due to chronic pulmonary disease/hypoxaemia (group 3)
pulm HTN due to chronic pulmonary thromboembolism (group 4)
pulm HTN due to multifactorial (eg. sickle cell, group 5)

Question 257

If we see a very elevated PA systolic pressure (eg. >40-50mmHg), what condition is it likely to be?

Answer 257

chronic eg. PH, while acute conditions (eg. PE) rarely so high

Question 258

when may we see fluctuations in the PA pressure?

Answer 258

irregular heart rhythms (eg. AF), due to variability in diastolic filling

Question 259

What does the dicrotic notch on the PA pressure tracing represent?

Answer 259

closure of pulmonic valve

Question 260

What’s west zone 3?

Answer 260

area where Ppa > Ppc > Palv

Question 261

What are the best conditions for measuring the PAOP?

Answer 261

pt supine, end-exp, west zone 3, get 3 measurements & use the mean

Question 262

normal PCWP?

Answer 262

mean of 9, range of 6-15mmHg

Question 263

what’s an important consideration in interpretation of PCWP values?

Answer 263

it only is useful to estimate LVEDP (ie. ventricular preload) if there’s no obstruction to flow btwn LA & LV & the compliance of the LV is normal, so it may be inaccurate in cases of large MI or cardiac tamponade.

Question 264

what are important considerations for the interpretation of RA pressure waveform?

Answer 264

it’s ability to reflect venous return & RVEDP depend on competent tricuspid valve

Question 265

what conditions may raise the PAOP?

Answer 265

Any condition raising the LVEDP, eg:
LV systolic dysfunction (infarction, cardiomyopathy), LV diastolic dysfunction
mitral or aortic valve dysfunction (stenosis or regurgitation)
hypertrophic cardiomyopathy
hypervolaemia
large R) to L) shunts
cardiac tamponade, constrictive & restrictive cardiomyopathies

Question 266

which conditions may lower the PAOP?

Answer 266

hypovolaemia
pulmonary venoocclusive disease (normal or low)
obstructive shock due to large PE

Question 267

what are some differences btwn the PCWP & RA pressure traces?

Answer 267

the pressure is slightly higher (6-15mmHg vs 0-8mmHg), the C wave (reflects MV closure) is often not seen

Question 268

what are some differences btwn the PCWP & RA pressure traces?

Answer 268

the pressure is slightly higher (6-15mmHg vs 0-8mmHg), the C wave (reflects MV closure) is often not seen

Question 269

are there delays btwn ecg recording & pulm art catheter tracing?

Answer 269

yes, 80-100ms delay for RA pressure measurements due to length of tubing
120ms delay in PCWP readings due to transmission of activity from LA pressure through pulmonary vasculature to catheter tip

Question 270

what conditions may cause large a waves on the PCWP tracing?

Answer 270

any condition with increased resistance to LV filling, eg:
mitral stenosis
LV systolic or diastolic dysfunction
LV volume overload
myocardial ischaemia, infarction w decr LV compliance

Question 271

what may v waves on the PCWP tracing represent? is a large V wave specific for MR?

Answer 271

MR
any acute incr LA volume (eg. acute VSD)

large V wave is NOT specific for Dx of MR but if the v wave normal, this is specific for ABSENCE of mod-severe MR

Question 272

:) what are the mean gradients for mild/mod/severe AS?

Answer 272

normal <5
<20
20-40
>40mmHg

Question 273

:) How does peak jet velocity relate to AS severity?

Answer 273

higher peak flow velocity= more narrow orifice/higher gradient (Bernoulli)

Normal <1.5m/s
mild <3m/s
moderate 3-4m/s
Severe >4m/s

Question 274

:) What are the dimensions of AVA correlating with degrees of AS severity?

Answer 274

normal 3-4cm2
mild >1.5cm2
mod 1-1.5cm2
severe <1cm2
critical <0.5cm2

Question 275

:) haemodynamic goals in AS? likely culprits if deteriorates?

Answer 275

rhythm: NORMAL
rate: sinus, 60-80 (avoid tachycardia to preserve diastolic perfusion & optimise LV filling, avoid Brady since extra filling won’t augment SV (stiff ventricle), they poorly tolerate AF as this reduces diastolic filling/perfusion/O2 supply AND they rely on the ATRIAL KICK- will become unstable if lose this. Augmenting contractility won’t improve SV. Brady will reduce CO)- consider glycol if Brady on induction
preload: “full”- eu or hypervolaemic (ie. preload with alb)
afterload: HIGH-NORMAL is VITAL in AS, for diastolic perfusion pressure. metaraminol is the 2nd drug give after O2
contractility: isn’t a problem UNLESS in LV failure (in which case ephedrine)- will limit -ve inotropy but unlikely to require an inotrope (which may be detrimental if risk LVOTO)
coronary perfusion pressure (ADP-LVEDP): defend a higher diastolic (>=60mmHg) w metaraminol

chambers:
LV abnormal- first hypertrophied but functional, then eccentric hypertrophy, dilation & poor function
Aorta: is it aneurysmal?
pulmonary vasculature is relatively normal unless LV burnt out, RV is generally normal

If AS deteriorates:
1. volume (eg. 4% alb)
2. squeeze/incr afterload (eg. metaraminol)
3. if Brady ++, glycol (atropine likely too tachycardic)
unlikely a contractility problem

Question 276

:) what to give a pt with AS if Brady on induction? 2nd drug to give an AS PT on induction?

Answer 276

200mcg glycol
metaraminol (after O2, defend a higher diastolic pressure min 60mmHg for coronary perfusion)

Question 277

:) haemodynamic goals for aortic regurg? what to do if AR deteriorates?

Answer 277

rhythm: sinus- we are avoiding VF!
rate: 80+, rapid rate favours forward flow, limits diastolic filling which risks LV dilatation & VF. may give pre-ind glycol to keep rate >80 & to tolerate fent. They are often in AF & usually tolerate this since the ventricle usually gigantic & they don’t lose much without atrial kick
preload: euvolaemia. need to maintain adequate preload due to incr LV size & compliance. If overloaded, DON’T aggressively diurese (need to be “full”)
afterload: low/normal, which augments CO & reduces regurgitant volume. don’t need to defend afterload as aorta full. ensure not overloaded with limited “squeeze” (NAdr or Metaraminol to maintain DBP, reserve metaraminol for if DBP extremely low, as it incr afterload & may lead to brady)
contractility: manage with +ve inotropes/chronotropes, limit -ve inotropy
Cor pp= ADP-LVEDP: defend a DBP of @ least 60 (they have high LV EDP so risk ischaemia)

chambers:
LV is dilated, volume overloaded, usually dysfunctional
aorta: big or N
pulm vasculature: more likely to have pulm HTN
RV: commonly dysfunctional

If induce & goes badly, likely a rate issue- give ephedrine or Ca++ to get their HR up

Question 278

+ haemodynamic goals for mitral stenosis? what if their haemodynamics go off?

Answer 278

rhythm: sinus (POORLY tolerate AF)
rate: sinus 60-80 (they may tolerate 50bpm) +ve chronotropy is a problem
preload: Euvolaemia. Hypervolaemia is poorly tolerated. OK to be slightly on the hypovolaemic side (unlikely in aortic stenosis).
Afterload: ensure diastolic doesn’t drop below 60mmHg
Contractility: generally LV contractility isn’t a problem but impaired RV contractility is a concern; if abnormal R) heart, give “R) heart anaesthetic”
CorPP: ensure diastolic up (>=60mmHg)

chambers:
LA: dilated
LV tends to be normal, it’s protected from pressure & volume overload. generally if they’re unstable it’s not to do with LV output, the problem is usually atria, rhythm or pulm vasculature
pulmonary vasculature: usually always have pulm HTN, the degree of which depends on how medically optimised they are (diuresis important). ALWAYS optimise pulm HTN in mitral stenosis.

if pt unstable:
cardiovert any rapid AF back to slow sinus
if sinus tachycardia, give B blocker to slow rate since L) heart likely normal
* these pts likely have pulm HTN; address all factors to limit rise in PVR, R) heart anaesthetic

Question 279

:) particular concern for pts with mitral stenosis on preop assessment?

Answer 279

-these pts very likely have pulmonary HTN
-establish functional status, tolerance of lying flat, degree of RV dilation & RV function on echo (periop concern depends a lot on their RV dilation)
-severity of pulm HTN depends on their medical Mx

Question 280

:) haemodynamic goals pulm HTN? if come unstuck?

Answer 280

2 broad goals are:
1. keep PVR as low as possible
2. protect the R) heart

1.
limiting SNS stimulation (anxiolytics, analgesia)- lungs full of alpha 1 adrenoceptors
avoid acidosis, hypoxia, hypercapnia, hypothermia
avoid hyper-inflated or low lung volumes or valsalva (“I will ventilate my pt with 6-7mL/kg TVs & a PEEP of 5, titrate rate to an ETCO2 30-35 which I’ll verify on an ABG at 35-40”)
avoid nitrous; overall ketamine OK since it’s got a lack of -ve inotropy
avoid alpha 1 agonism
good drugs= vasopressin (incr SVR but no change on PVR)
ephedrine OK

2. R) heart anaesthetic
   rhythm sinus
   rate 80-100
   euvolaemic
   low RV afterload (achieve by avoiding spikes in PVR)
   avoid -ve inotropes (start +ve inotropes or an inodilator)
   ensure diastolic doesn’t drop below 60mmHg; coronary perfusion pressure is vital- if inadequate, vicious spiral into R) heart failure & inadequate output

Question 281

:) haemodynamic goals in MR? if come unstuck?

Answer 281

rhythm: these pts are often in AF so they can tolerate sans atrial kick but if in fast AF & unstable, there’s an argument to cardiovert
rate: 80, avoid bradycardia & excessive diastolic filling
preload: keep them full (their heart is large & compliant so maintain preload)
afterload: reduce (reduces regurgitant volumes, improves forward flow & CO)
contractility: can give inotropes; limit -ve inotropy (propofol OK as it reduces SVR)
cor pp: DBP >60mmHg

In MR the LA tends to be dilated & they may have AF
the LV is dilated
if the pt has severe MR & their EF is not supra-normal (eg. >75), their LV IS NOT NORMAL. they often have systolic dysfunction & are volume overloaded. LVEDP is higher & they’re vulnerable to coronary ischaemia.
almost always have pulm HTN, degree of which depends on their medical Mx
R) heart may also be dysfunctional

MR is the only valve lesion that tends to improve with anaesthesia; ensure adequate rate & afterload not excessive

Question 282

:) What are differentials for a pt in shock (hypotensive/low CO state)?

Answer 282

-hypovolaemic (eg. haemorrhage)
-cardiogenic (eg. acute ventricular failure)
-obstructive (eg. tamponade, PTx)
-distributive (anaphylaxis, profound vasodilation from anaes drugs, neurogenic, severe sepsis/SIRs)

Question 283

:) how is echo useful in assessing the haemodynamically unstable patient?

Answer 283

may help narrow the differential for causes of shock for a pt with hypotensive/low CO state (hypovol, cariogenic, obstructive, distributive)

the TRANSGASTRIC, MID-PAPILLARY SHORT-AXIS VIEW GIVES 90% OF THE INFORMATION. can flip to the RV view by turning probe to Ax RV function

ask:

a) Full or empty?
Assess qualitatively (if pap muscles kissing, empty) or quantitatively (diastole is more sensitive time for volume measurement; LVEDA in diastole <8 is empty, >14 is full, some resources say 10-20)

b) Are the walls moving into the centre & out again- normal or abnormal appearance of wall motion?

c) is there a pericardial collection (thin ring of fluid around heart)?

d) look @ systole & compare with diastole- if the ventricle is in a low afterload state, it’ll be empty @ end-systole (LVESA=0)

Question 284

:) goals for CABG?

Answer 284

a “hot” CABG= unstable symptoms, “cold”= stable

main aims= improve myocardial O2 provision & reduce myocardial O2 demand (HR, contractility, wall tension)

HR: normal sinus 60-90bpm
preserve contractility by limiting -ve inotropy
preserve wall tension by limiting chamber distension (euvolaemia) & minimising afterload
defend diastolic perfusion by avoiding hypotension (CorPP= ADP-LVEDP), keep LVEDP >=60mmHg

Anaesthetic:
induction thorough pre-O2, avoid -ve inotropy & hypotension
avoid propofol
5mg midaz & 500microg fent or 0.5mg/kg ketamine & 250microg fentanyl
paralyse, tube, run gas in backgrond
infuse either NAdr (CVC) or if peripheral, metaraminol, keeping DBP >=60mmHg

Question 285

:) what’s the surrogate for pulm artery pressure?

Answer 285

MEAN PAP is approx 0.6 x RVSP + 2
provided pulmonary valve is normal, peak RV systolic pressure should be the same as pulm artery pressure

Question 286

:) How is RVSP calculated from echo?

Answer 286

take the tricuspid regurg jet velocity (velocity through tricuspid valve)

delta P = 4v2 (ie. pressure gradient btwn RV & RA is 4x velocity of the jet of blood btwn the chambers, squared)

RVSP then is 4v2 + RA pressure (assume it’s 5-10, may give CVP which is a surrogate for RA pressure)

Question 287

:) How is RVSP calculated from echo?

Answer 287

take the tricuspid regurg jet velocity (velocity through tricuspid valve)

delta P = 4v2 (ie. pressure gradient btwn RV & RA is 4x velocity of the jet of blood btwn the chambers, squared)

RVSP then is 4v2 + RA pressure (assume it’s 5-10, may give CVP which is a surrogate for RA pressure)

Question 288

+ what’s the R) heart anaesthetic?

Answer 288

sinus
rate 80-100bpm
euvolaemia
LOW RV afterload (avoid spikes in PVR)
AVOID -ve inotropes (start +ve inotropes or inodilator)
maintain DBP 60mmHg for cor perfusion

Question 289

:) what’s my induction plan for SEVERE pulmonary HTN (even if the pt is functionally well):

Answer 289

Consider their function, symptoms, treatment & echo.

The perioperative concern for these pts is all dependent on how their RV is performing (ie. how it’s withstood the pressure load).
either it’s normal size & function, heterometric (dilated but performing well) or severely dilated with severe TR/dysfunction

Tertiary centre with adult HDU, consult cardiac anaesthetist & have them aware of case/someone available with TOE if come unstuck

Large PIVC
art line awake
CVC awake (for the inotropes/NAdr to defend their baseline)
low threshold for pads on

GOAL=KEEP THE PATIENT HAEMODYNAMICALLY WHERE THEY ARE. “R) heart isn’t going to know it’s having an anaesthetic”

-dobutamine 2.5microg/kg/min (the B2 provides pulm VD & the B1 provides contractility)- it’s a +ve chronotrope with some inotropy. 2.5 is the rate if elective, 5 if the RV isn’t coping, if >=7.5, likely to get incr rate without much more inotropy.
-Noradrenaline (2microg/)- balance the B1

option A:
-pre-oxygenate WELL
-midaz 3mg, fent 250microg. NO PROPOFOL. turn gas on. give LARGE DOSE rocuronium once lost verbal response.
(*if they are mild/mod pulm HTN, give fent/midaz & if still awake can “earn” some propofol)
-put in a guedel & GENTLY commence PPV, with MINIMAL peak pressures, just to oxygenate & remove CO2
-tube, cuff up & GENTLE APL (eg. 12cmH2O)
-on ventilator, 6-7mL/kg TVs with 5mmHg of PEEP

option B:
-spont vent induction in pulmonary HTN, beauty being we separate the induction from PPV by a long time, useful to separate these potential times of haemodynamic risk by time & to do them very gently

thereafter, attention to detail:
-Immediate ABG to see A-a gradient. Titrate RR to EtCO2 to 30-35mmHg, confirm on gas as 35-40mmHg. Optimal rate challenge if pt is obese/has obstructive lung disease.
-CLEAR communication with surgeon re: challenges eg. gas on, head down.
-multimodal analgesia (to limit opioids/hypercarbia which may–> deterioration of PVR)

if a problem encountered, revisit haemodynamic goals:
-euvolaemic?
-RV afterload?
-rate & rhythm?

Extubation:
competing interests- want the pt awake & breathing spont so avoid hypoxia & hypercarbia but want to avoid cough (incr PVR, de-recruits, removes FRC)
once adequate TVs & awake, extubate & take straight onto high-flow to blow off CO2
remifentanil is a risk

Question 290

:) induction plan for a pt with pulm HTN who’s also an aspiration risk?

Answer 290

2 important competing interests, of which aspiration= the biggest risk to the pt

big drip, art line & CVC awake. dobutamine & NAdr running

excellent pre-O2
RSI with cricoid
ketamine 1mg/kg (add fentanyl)
rocuronium
tube

Question 291

:) haemodynamic goals for pericardial tamponade?

Answer 291

it’s a filling problem; the ventricles +/- atria are collapsed
we need to maintain ventricular pressure by maximal vasoconstriction

NAdr running

RSI with ketamine, roc

Question 292

:) SS_CS 1.1 Discuss the physiology of hypothermia and deep hypothermic
cardiac arrest:
-what’s mild/mod/deep hypothermia?
-why is it used?
-what temp generally selected for CABG?
-what temp generally selected for valve repair/replacement
-what’s the physiological rationale of deep hypothermia for procedures needing DHCA?
-for how long is DHCA considered safe?
-for which procedures is deep hypothermia generally selected? why?
-what’s selective antegrade cerebral perfusion? and retrograde cerebral perfusion?
-what are some anaesthetic considerations & what to have prepared for deep hypothermia?
-what are the physiological effects of deep hypothermia?
-what are the sites of temperature monitoring during cooling & hypothermia?
-how long does rewarming take?
-what’s the target temp for separation from CPB?

Answer 292

-mild hypothermia is 32-35degC, moderate is 28-32, deep is <28deg C
-a strategy protecting the brain & vital organs from ischaemia during CPB for many cardiac surgical procedures; CMRO2 reduces 7% per degC reduction temp
-34degC (mild hypothermia)
-moderate hypothermia (due to length/complexity of the procedure)
-given that CMRO2 decreases ++ with hypothermia (by a factor of 2.3 for every 10degC decr body temp), brain is less likely to suffer ischaemia, given the brain’s tolerance to ischema is correlated with metabolic rate.
-DHCA considered safe for 30-45mins
-procedures requiring temporary elective circulatory arrest of cerebral & systemic flow (eg. repair of portions of asc aorta or aortic arch), to achieve EEG isoelectricity (generally @ nasopharyngeal temp of 18deg) & protect the brain & other vital organs (spinal cord, kidneys, liver, GIT) from ischaemia during circulatory arrest. Systemic cooling is achieved using the heat exchanger in the CPB circuit. The DHCA permits permits reconstruction of aorta without cross clamping a diseased aorta or possibly instrumenting & injuring aortic arch branch vessels.
-cerebral protection strategies such as SACP & RCP may be used. SACP is when the brain is selectively perfused using CPB circuit via direct cannulation of axillary artery or aortic arch branch vessels RCP provides partial perfusion to the brain using cardiopulmonary bypass circuit during interruption of antegrade cerebral perfusion. If SACP or RCP are used, warmer temp (eg. 28deg) often used.
-PHYSIOLOGIC CHANGES OF DEEP HYPOTHERMIA MAY PERSIST DURING POST-BYPASS & POSTOP AFTER REWARMING. NEED ADEQUATE VENOUS ACCESS & BLOOD PRODUCTS (typically 4-6 units rbc & FFP) along with vasoactive infusions to Rx the VC that usually occurs with cooling/hypothermia & VD that occurs with rewarming/reperfusion. Insulin infusion to control hyperglycaemia (nearly every pt has hyperglycaemia after DHCA, SHOULD BE MAINTAINED <10mmol/L, conscious of avoiding hypoG & that insulin may exac hypoK post-bypass. Require 12-lead ecg, SpO2 probe, ETCO2, arterial line (if distal aortic arch, R) art line may be more accurate since the L) subclavian may be temp occluded/interrupted, in some cases multiple art lines useful & if SACP is used, bilateral IACs required), CVC, ?PAC via a sheath, TOE, consider defib/pacing pads, IDC, temp probes nasopharyngeal/bladder. Can’t deliver any drugs during DHCA so give all prior. Brain monitoring with EEG (aiming for electrocortical silence for DHCA to ensure maximal suppression of cerebral metabolic activity prior to CPB pump flow discontinued- since volatile & other GA agents interfere, cease them during deliberate hypothermia to avoid interference with detection of hypothermia-induced electrocortical silence & for depth of anaesthesia- recommence agents as soon as EEG activity reappeared during rewarming) & cerebral oximetry (near-infrared spectroscopy (NIRS) is used to continuously monitor cerebral regional O2 saturation in frontal cortex. It ISN’T affected by anaesthetic agents & doesn’t require pulsatile perfusion. Use it to monitor any unilateral decrease in rSO2, should be communicated immediately to surgeon.

-HAEMATOLOGICAL: bleeding diathesis due to decreased platelet count, slowing of enzymes in coagulation cascade, enhanced fibrinolysis. May get coagulopathy from ischemia-reperfusion injury & DIC may occur. during hypothermia there’s delayed metabolism/excretion of heparin but this reverses during rewarming (recheck ACT every 30mins during DHCA). Hb target insufficient evidence but suggest Hb >75 & hct >22%.
-CARDIOVASCULAR: prol PR & QRS. brady. decr CO. vasoconstriction during hypothermia, vasodilation during rewarming.
-HYPERGLYCEMIA: stress response, glucocorticoid/catecholamine admin
-METABOLIC: decreased MR & O2 consumption during cooling/hypothermia then incr MR during rewarming (esp if shiver)
-DECR METABOLISM OF DRUGS, ANAES REQUIREMENT
-L)-shift OHDC, incr binding affinity of Hb to O2. most institutions use alpha-stat for ABGs.
metabolic acidosis is common during repercussion after DHCA, may get hyperK, incr lactate ++. May give sodium bicarb 8.4% (50mEq/50mL) if pH <7.2 or BD <-7mEq/L but care re: hypernatraemia.
-venous inflow & arterial outlet; the temp gradient btwn them is maintained @ <10degC. may measure arterial inflow (temp decrease first during active cooling), then nasopharyngeal temp. bladder temp (“core temp” estimate) usually slowest to change. The venous outflow temp is “systemic”, the bladder estimates “core”. No temp should ever exceed 37 deg C during rewarming, esp art outflow.
-may be 60-90mins in a mod or deeply hypothermic pt, since the rate is <=0.5degC/minute & gradient btwn venous inflow & arterial outlet is maintained <=4degC once temp >30 deg.
-nasopharyngeal temp 37degC

Question 293

:) what are the haemodynamic goals for an acute aortic dissection?

Answer 293

• precise BP control to avoid hypertension that may extend the dissection, rupture an aneurysm or cause heart failure in a pt with AR (SBP goal <120mmHg)
• if cardiac tamponade, ensure intravascular volume & after load are maintained, avoid vasodilation & myocardial depression
  -avoid B-blockers or small incremental doses only if cardiac tamponade or acute AR due to aortic dissection as they can worsen HF or precipitate cariogenic shock in these conditions
  -treat any immediately reversible causes of cardiogenic shock or malperfusion of the extremities due to aortic dissection (eg. cardiac tamponade, hypovolaemia, low SVR, severe ventricular dysfunction, severe valvular dysfunction)- may be diagnosed with TOE.

Question 294

:) fundamental difference btwn alpha-stat & pH stat?

Answer 294

alpha-stat = temp-uncorrected gas measurements. at any given pt temp, it results in lower PaCO2 values & higher pH values cf pH-stat. advocates of pH-stat corrected to actual temp suggest that the higher CO2 concentrations & vasodilation are advantageous to decreasing duration of cooling & rewarming.

Question 295

:) SS_CS 1.2 evaluate means of estimating cardiac output
-what are the indications/uses of cardiac output monitoring?
-what are the characteristics of an ideal device for measuring CO?
-what’s considered the gold standard for CO monitoring & why is it’s use diminishing?
-what are 3 “invasive” methods of CO measurement?
-what does “minimally invasive CO monitoring” mean?

Answer 295

-considered a surrogate for tissue O2 delivery- used to identify pts @ high risk of M&M, guide fluid management, inotropes, vasoactive agents.

-Ideal device would be noninvasive, accurate, universally applicable (easy to use) & completely reliable. Such a device doesn’t currently exist.

INVASIVE METHODS OF CO MEASUREMENT:

-Thermodilution using PA catheter considered gold standard against which all new methods of CO monitoring are measured, however there’s a lack of evidence showing it improves clinical outcomes, along with risks (PA rupture, arrhythmia on insertion, infection, thrombosis or embolism) & fact that accurate placement requires skill (despite being relatively easy to use once positioned)- use diminishing.

-1. THERMODILUTION method is either the PAC method or transpulmonary gradient (for calibration of the pulse-contour analysis system).
For initial calibration. cold saline injected into central vein. Analyse variations in blood temperature taken by temp sensor in thermistor of PAC or, for transpulmonary, in a major artery (femoral/brachial/axillary).
Cardiac output is proportional to the AUC (change in temp vs time) x HR, for transpulmonary the rate of rise of temp time curve is later & slower.
the CO is calculated using the stuart hamilton equation, which assumes: complete mixing of indicator & blood, constant flow & no indicator lost in system. Errors are mainly related to violation of these assumption.
Benefits: accurate
Limitations: not continuous, transpulmonary less accurate if pulm congestion & shunting (given that the PAC method measures R) heart CO, transpulmonary measures L) & if there’s significant shunt there’ll be variation from “gold standard”). The pulse contour analysis does have beat-to-beat measurement but displays data in a 30sec window.

2. INDICATOR-BASED DILUTION:
   lithium injected into central or peripheral vein, OR indocyanine green (non-toxic, short half-life) injected via PAC.
   Concentration of the indicator is measured peripherally & the wash-out curve over time plotted, similar to thermodilution curve. it’s replotted semi-logarithmically to correct for dye re-circulation. CO is calculated based on injected dose, AUC & it’s duration (short duration= higher CO).
   Based on the initial calibration, the root mean square method is applied to the arterial pressure signal for subsequent measurements & no additional lithium required.
   Pros: Correlation btwn lithium dilution & thermodilution is acceptable.
   Cons: not continuous. Recalibration needs to be performed after significant haemodynamic changes or other interventions altering vascular impedance. inaccurate if intercurrent lithium, contraindication to lithium or if pt <40kg or 1st trimester pregnancy. concern re: taking multiple volumes in critically unwell pt.
3. FICK PRINCIPLE:
   based on the indirect Fick equation, the principle that Q = M / (V-A) where Q= the flow of blood through organ/min, M= number of moles of the substance added to the blood by an organ per min, V= venous and A= arterial concentrations of a substance.
   given that 250mL/min O2 is delivered to the pulmonary vasculature & the venous O2 content is 200mL/L & arterial is 50mL/L, cardiac output can be calculated as 5L/min
   pros= very accurate, surrogate methods (thermodilution, indicator dilution) less accurate.
   cons= not clinically practical; requires intubation & gas sampling via tube & the measurement of oxygen may fluctuate with addition of O2 to the circuit & also requires pulm artery catheter (invasive) to obtain pulmonary mixed venous O2 content. Inaccurate if thoracic trauma, pulmonary congestion or significant shunt, low MV & high CO. Relies on constant tidal volumes, inaccurate in sport breathing.
4. Pulse contour analysis:
   utilises principle that CO is proportional to arterial pulse pressure, based on Windkessel model.
   An algorithm is used to determine CO.
   Benefits: In general, show good agreement with CO measures with PAC.
   Limitations: require invasive method (thermodilution or lithium) for recalibration.
   while beat-to-beat monitoring occurs, displays data of CO every 20-30seconds.
   requires optimal arterial signal (inaccurate if under or over-damped)
   less accurate with AR, arrhythmia or IABP or changes in SVR.

MINIMALLY INVASIVE= can be used to calculate CO without insertion of PAC.

Aortic doppler:
measure blood flow through aorta by US waves reflected from rbcs, using doppler equation
the doppler beam must be aligned with blood flow in the descending aorta.
the VTI (integral of instantaneous blood flow velocities during one cardiac cycle) for the LVOT is calculated from the area under velocity-time curve & multiplied by CSA or aorta (determined by M-mode ultrasound or from a nomogram using height/wt/age) x HR to get CO. A correction factor is used as only 70% of CO passes through desc Tx aorta.
either oesophageal or transcutaneous (suprasternal probe)

Benefits of oes: has good clinical agreement with PAC thermodilution for changes in CO but variable agreement for absolute values & for high & low CO states. Has been used to successfully guide fluid Mx. can be continuous.

Benefits of transcut: noninvasive. can be continuous.

Cons of oes: require a skilled operator, HIGHLY operator-dependent, tiny variation in position greatly influences measurements of CSA & flow (poor alignment underestimates CO), equipment expensive, relatively invasive, requires sedation & ventilation, risk perf, CI in some pts. To get continuous values, requires constant presence of expert user.
equations assume LAMINAR & constant flow. turbulent flow in the aorta reduces measurement accuracy.
use of a nomogram introduces measurement error (esp as CSA changes with vascular tone & volume status).
relies on assumption that fixed proportion (70%) of blood flow is through desc aorta- therefore inaccurate if AR, aortic XC.
interfered with by surgical cautery.

cons of transcut: varying results wrt accuracy. uses nomogram for valve area estimation & proprietary algorithm using doppler to determine VTI measurements- this has limitations of age, weight etc & may not correlate with the biometric variables of the individual patient. Transcutaneous is inaccurate with significant valve stenosis.

Bedside echo:
determine CSA of LVOT through parasternal short-axis view.
obtain pulsed wave doppler signal of LVOT (usually in the apical 5-chamber view) to determine LVOT VTI

given CO= HR x SV,
CO= HR x VTI x CSA

pros: convenient as many devices have software to automatically calculate.
in experienced hands, fairly reliable method for determining CO & serial measurements associated with volume responsiveness.
Can also use this method at carotid artery, feasible even in cardiac arrest.
Limitation= highly operator-dependent, reliability of serial measurements depend on accuracy of positioning.

Arterial pulse waveform analysis: calculate CO based on arterial pulse waveform of an art line. integrate the area under the systolic arterial pressure time trace.
Benefits: minimally invasive, correlates well with echo yet doesn’t correlate well with PAC methods, despite tracking CO reliably over time. More useful for TRENDS vs absolute values.
Limitations: less accurate for absolute measurement than calibrated devices. less accurate if art line trace over or under-damped, if sig AR, arrhythmia or IABP. While gets beat-to-beat, the display is intermittent.
Arterial waveform-based devices that calculate cardiac index using arterial pressure curve & vascular resistance data inconsistently predict CO, fluid responsiveness & SV in haemodynamically compromised pts who are getting fluid boluses or vasoactive agents.

Thoracic electric bioimpedance:
Uses low-voltage electrodes placed on chest. Measures electrical resistance to high freq, low-magnitude current. The higher the fluid content within the chest cavity, the lower the electrical impedance (opposition of flow to an electrical current), since fluid conducts electricity.
As the heart cycles through systole & diastole, volume of blood in Tx changes, this can be measured & extrapolated to determine CO.
Pros: One of the least invasive CO measurement methods. Early studies showed poor correlation with invasive measures, more recently improved accuracy even in states of volume overload although accuracy in haemodynamic instability & critically ill pts isn’t well-tested. thought to be useful for estimating changes but not absolute measurements for CO.
Limitations:
low signal to noise ratio
electrode position often impractical, internal bioimpedance measurements on a tracheal tube= a way around this. limited usefulness in awake pts since very sensitive to movement.
arrhythmias may lead to inaccuracy (uses the R-R interval)
diathermy interferes.

Thoracic bioreactance: modification of bioimpedance, designed to increase the “signal-to-noise” ratio (poor signal:noise ratio is a limitation of thoracic electrical bioimpedance). detects “phase shift” in alternating current voltage across thorax- the phase shift depends on pulsatile flow which is mainly from the aorta, so the bioreactance signal correlates with aortic flow.
Pros: higher signal: noise ratio. Evidence mixed: observational data suggests use of a tioreactance device ass’d with lower fluid balance, mech vent days & ICU stay/vasopressor/haemodialysis use, other studies report poor correlation btwn bioreactance & thermodilution.
Cons: Electrocautery & external pacemakers interfere with bioreactance signal. Severe aortic insufficiency & other Tx aortic pathology may impact accuracy.

Question 296

:) what’s the lower limit of BP auto regulation below which vasodilatory capacity is exhausted, for kidney & brain & coronary circulation?

Answer 296

kidney 70-80mmHg
brain 60-65mmHg
coronary 50-55mmHg

varies widely across population/physical or disease states

Question 297

:) what’s the equation for venous return? what impacts all 3 parameters?

Answer 297

VR = (mean systemic filling pressure - RAP) / venous resistance

respiration, autonomic tone, IAP & body position,

Question 298

:) what’s the normal distribution of CO to various organs?

Answer 298

heart 5%
brain 14%
muscle 20%
kidneys 22%
liver 25%

Question 299

:) SS_CS 1.3: describe pharmacological and non-pharmacological strategies to relieve anxiety in pts presenting for cardiac surgery

Answer 299

Benefits= improves pt satisfaction, may reduce myocardial O2 demand (SNS stimulation)

NON-PHARM:
-Pre-anaes assessment in advance of procedure, introducing self, discussing expected preoperative course of events, risks/benefits/alternatives for anaesthetic management, give patient opportunity to have questions answered & any concerns addressed. Patient can have support person with them if desired, provide verbal & written information.
-Offer music, minimal people/noise on induction.
-Ensure pre-warm patient, minimise fasting time (eg. pt first in the morning).

PHARMACOLOGICAL:
-some will benefit from premedication with small incremental doses of short-acting IV benzodiazepine for anxiolysis (midaz 0.5-2mg) +/- opioid (fent 10-50microg) particularly for invasive lines.
Take care wrt timing for consent discussions, risk of disinhibition/movement with line placement & that pt will require observation & supplemental O2 once sedation commenced. Gentle/lower-dose titration if critical AS or pulm HTN or severe vent dysfunction & extremes of age.
ERAS protocols emphasise minimal anxiolysis.

Question 300

:)SS_CS 1.3: Describe the anatomy of the heart and great vessels, particularly in relationship to the use of ultrasound imaging
-benefits of TTE
-limitations of TTE
-which TTE view is best for interrogating an ASD, RV dimensions/wall thickness or anterior pericardial effusions?

Answer 300

-noninvasive, wide availability, lack of radiation exposure
-thoracic skeleton & lungs or body habitus limit usefulness of images in some pts
-subcostal 4-chamber, supine full inspn knees bent to relax abs. probe immediately below or to R) of xiphoid. interatrial septum is nearly perpendicular to the US beam @ this point.

Haemodynamic assessment:
TTE: parasternal long axis view the most information
parasternal short axis
apical 4 chamber (pt roll 30 deg L)
Subxiphoid

cardiogenic: hypokinetic, RWMAs, dilated, IVC dilated
obstructive: PE: large RV. tamponade: fluid pericardium (<1cm post=small effusion), diastolic collapse of RV, later see LV collapse. IVC dilates due to incr venous pressure.
hypovol: small hyperdynamic LV. Sniff test: >50% collapse IVC suggests low CVP. <50% collapse suggests CVP >10mmHg. no collapse= significantly elevated CVP.
distributive: LV hyperdynamic but good size (collapse on systole)

Can look @ haemoperitoneum (RUQ), aorta in haem unstable.

Question 301

:) SS_CS 1.4: discuss the perioperative assessment of myocardial ischaemia
-what features on history?
-what features of examination?
-what investigations could be considered preoperatively for a pt if concern re: IHD?
-what are some ecg changes suggestive of ischaemia?
-what’s the difference between 3 & 5-lead ecg?
-indications for art line monitoring?
-indications/utility for TOE in detecting myocardial ischaemia?
-what’s more sensitive in detecting myocardial ischaemia? TOE/ecg/PAC?
-what’s an acute coronary syndrome?
-what are causes of troponin elevation aside from acute thrombotic MI or supply:demand mismatch?
-what troponin should be used for diagnosis of acute MI?
-what is required for the diagnosis of ACUTE MI?
-what’s are useful tests pre-op for pts at high risk periop myocardial injury?
-how soon after onset of acute MI do cardiac trops begin to rise?
-what’s a type 2 MI?
-how does MINS vary from acute MI? significance of MINS?
-what’s the utility of measuring troponin screening for MINS?
-clinical significance & utility of BNP?

Answer 301

monitoring for imbalances in myocardial O2 supply vs demand & for development of ischaemia

History:
*approx 65% of pts with perioperative MI do not experience ischaemic symptoms (POISE), potentially due to anaesthetic/analgesic/amnestic agents.
ischaemic chest pain (usually worse with activities incr cardiac O2 demand), more discomfort/squeezing vs pain.
More likely if PHx ACS or other vascular disease ass’d with risk cardiac ischaemia. Risk factors= older, male, DM, HTN, dyslipidaemia, cigarette smoking, recent use of cocaine/sympathomimetics.
ass’d symptoms= breathlessness, nausea, diaphoresis, presyncope, clamminess, fatigue.
atypical symptoms more common in elderly or DM.

Examination:
rapid ABC assessment.
Evidence of systemic hypo perfusion: hypotension, tachycardia, impaired cognition/collapse, cool/pale/clammy, respiratory distress (tachypnoea, desaturation)
evidence of heart failure: jugular venous distension, peripheral oedema, pulsatile liver, new or worsening pulmonary crackles, new S3 gallop (best heard @ apex L) lateral, due to incr atrial pressure increasing flow rates as in with new MR- it may be common in young ppl or pregnancy if high volume & compliant ventricle), new or worsening MR murmur (early systolic murmur)
rapid assessment for neurological focal lesions or cognitive deficits that may preclude use of thrombolysis

Investigations:
-ecg (5-lead), art line, TOE, serial troponin, basic electrolytes, renal function, CBC with platelets

-continuous ECG monitoring for myocardial ischaemia or arrhythmia- ecg is a relatively insensitive method for developing myocardial ischaemia but can be detected, leads II & V5 or V4 in particular. intraoperative & post ST changes are associated sith cardiac M&M in pts @ high-risk for myocardial ischaemia.
-early ecg may be normal. hyper acute T waves (particularly in anterior chest) are often the first sign. ST changes evident within hours- ST depressions tend to be horizontal with ischaemia. ST elevation in 2 or more anatomically contiguous leads= the most common finding with myocardial infarction. pathological Q waves suggest necrosis & may take 1-24hrs to develop. there may be new L) BBB. there may be arrhythmia.

-3-lead ecg just has RA, LA & LL & monitor displays the bipolar leads I, II & III
-5-lead has RA, LA, RL & LL & a single unipolar chest lead (brown, depends on the position, V1-6). Monitor can display I, III, III, aVR, aVL, aVF & a single precordial lead- can set the display for whichever leads but usually II & V5.

-patient: severe CAD, cardiomyopathy, haemodynamic instability, or if stable IHD but major surgery likely to cause rapid blood loss or large fluid shifts. If arrhythmias art line more accurate than NIBP.
surg: prolonged procedure, if significant haemodynamic shifts or blood loss are anticipated & rapid detection is vital. if pt access limited.

-intraop TOE may be useful for detection of new RWMA’s in pts @ high risk, if major surgery. can also use it to determine cause of unexplained persistent or life-threatening circulatory instability (eg. hypovol, cardiac tamponade, PE, ventricular dysfunction, valvular stenosis or regurgitation, LVOTO).

-TOE monitoring has higher sensitivity for detecting myocardial ischaemia than ECG or PAC BUT there’s no data that TOE use reduces the instance of adverse perioperative cardiac events.

-ACS= pts with suspicion or confirmation of acute myocardial ischaemia or infarction. the 3 types are NSTEMI, STEMI or UA. UA= ecg findings without elevated trop (rare now with high-sensitivity trop). NSTEMI= elevated biomarkers without STEMI pattern on ECG.

-Non-cardiac causes: end-stage renal disease, sepsis, stroke
-Cardiac causes:
Type 1 MI (athero-thrombosis)
type 2 MI: supply:demand mismatch (hypoT, anaemia)
tachyarrhythmias
acute heart failure
acute myocarditis (esp women, who present like MI but have normal coronaries- cardiac MRI useful), takotsubo syndrome (more modest elevations)
PE with acute R) heart overload
trauma (eg. during CPR or electrical cardio version)

-high-sensitivity cardiac troponin I & T.

-acute myocardial infarction (clinical event due to the death of cardiomyocytes, caused by ischaemia), requires both evident of acute myocardial injury (defined as a troponin above the 99th percentile of the ULN with a rise/fall of troponin observed) & clinical evidence of ischaemia (symptoms or abnormal ecg (new significant ST/T changes, new L) BBB, pathological Q waves), evidence RWMAs). Trops elevate 3-6hrs, peak 12-24hrs & may remain elevated for 2wks, depending on renal function.
Other causes elev trop aside from myocardial necrosis= CCF, dysrhythmia, myocarditis, pulm embolus, acute SAH, severe sepsis, burns, rhabdo, renal failure.

-Useful to have a pre-op troponin & 12-lead ecg for high-risk pts (eg. in-hospital surgery with RCRI factors, may also include if >=65yo- the canadian guidelines suggest post-op troponin for pts with baseline risk >5% of cardiovascular death or non-fatal MI 30 days after surgery, ie. get pre-op BNP if age >=65, RCRI >=1 or if 45-64 with significant CV disease. If the NT-proBNP was +ve (>=300mg/L or BNP >=92mg/L or if BNP couldn’t be obtained but they have the risk factors, measure post-op trop daily 48-72hrs & obtain ecg in PACU. as per UTD, could get preop trop & high-sensitivity trop at 6-12hrs, days 1, 2 & 3 after surgery.

-2-3hrs after onset of acute myocardial infarction.

-MI consequent to incr myocardial O2 demand or decreased supply (eg. tachyarrhythmias, HTN or hypoT, anaemia, respects failure)

-MINS: myocardial injury is elevated troponin (with at least 1 value >99th percentile ULN), considered acute if a rise/fall of cTn. MINS= myocardial cell injury during the first 30 days after non cardiac surgery due to ischaemic etiology (ie. no evidence sepsis, rAF, PE etc). MINS is independently associated with mortality, cadiac arrest, CHF. MINS includes MI (symptomatic & non-symptomatic) & pts with elevated trop but no symptoms, ECG abnorms or other criteria meeting universal definition of MI AND no evidence of nonischaemic ethology for their troponin elevation.

-identification of elevated trop may prompt initiation of secondary prevention (eg. aspirin, statins, cardiology involvement, lifestyle measures) or more frequent ecg that may detect MI, however the ACC/AHA guidelines state that the usefulness of post-op screening of high-risk pts using trop & ECG is uncertain.

-pre- & post-op elevations of BNP are associated with increased 30-day risk of adverse cardiovascular events, including MI & also elevated 6-month mortality but it’s role in care of pts undergoing non cardiac surgery hasn’t been established.

Question 302

:) SS_CS 1.4: discuss the periop Ax of cardiac rhythm
-define tacchy & brady arrhythmia
-what underlying pathology may an intraop arrhythmia suggest?
-first consideration with an arrhythmia?
-what are pre-op risk factors for arrhythmia?
-how to monitor for arrhythmias intra-op?
-what are some causes of intraop sinus bradycardia?
-management of sinus brady with haemodynamic instability (hypoT, altered mental status, ischaemic chest pain, acute heart failure, signs of shock)?
-Mx of sinus brady (severe <40bpm) with haematological stability?
-do glycopyrrolate or atropine work for bradycardia due to conduction delays originating below AV node?
-where put the pads for transcut pacing?
-what’s a contraindication for transvenous pacing?
-where is a transvenous pacing lead placed & how locate correctly?
-intraop management of sinus node dysfunction?
-what should be in place prior to inserting a PAC for a pt with L) BBB?
-causes of intraop BBB?
-causes of new-onset periop AV block?
-how describe type mobitz II 2nd degree AV block?
-does 2nd degree AV block in periop period require pacing?
-does 3rd degree AV block in periop period require pacing?
-causes of sinus tachy?
-in which pts is it particularly important to lower HR
-in which pts avoid B blocker?
-markers of haemodynamic instability with tachycardia?
-how to manage an unstable tachycardia?
-how to manage a tachycardia with a pulse if the pt is stable (after addressing cause eg. oxygen, analgesia/anaesthesia)?
-adenosine dosing regimen?
-how is cardioversion different from defibrillation?
-what is the preferred position of pad placement for electrical cardioversion of atrial tachyarrhythmias? why?
-benefit of biphasic vs monophonic defibrillators?
-what’s the initial energy selection for cardio version of AF? A flutter? supra ventricular tachycardias? VT with pulse, VF or pulseless VT?
-for how long is therapeutic anticoagulation recommended prior to & after cardioversion (to reduce risk of thromboembolism?)
-any special considerations for cardio version in pregnancy?
-precautions for defibrillation with a pacemaker?
-why is there a relative contraindication to cardio version in the setting of digitalis toxicity?
-complications of cardio version?
-how are 3 ways that internal cardioversion can be performed?
-shocks of up to how many joules, on internal pacing, don’t affect the function of permanent pacemakers?
-what are some perioperative causes of AF?
-management approach for pts with AF & RVR with haemodynamic stability?
-in which pts avoid B blockers & CCBs?
-with what is multifocal atrial tachycardia usually associated? how distinguish it on ecg? how treat it?
-what are potential aetiologies of wide QRS atrial tachyarrhythmias?
-how does SVT with aberrant conduction appear (eg. SVT with BB)?
-how may vagal manoeuvers or adenosine be useful for STABLE patients with a wide complex atrial tachyarrhythmia? what is required during these treatments?
-how manage a haemodynamically unstable wide complex tacchyarrhythmia?
-what is it critical to determine with a pt with WPW? why does that matter?
-do pts with antidromic have narrow or wide QRS?
-characteristics & possible causes of ventricular arrhythmias?
-how does ventricular flutter appear?
-how many successive beats need to be seen for a label of VT? is there atrial activity?
-how to manage VT with diminished pulse vs no pulse?
-how manage haemodynamically unstable vs stable TdP?
-what’s non sustained VT? how to manage?
-what’s postop management of a pt who has an intraop arrhythmia?

Answer 302

-tacchyarrhythmia is HR >100bpm, brady <60bpm
-myocardial ischaemia, electrolyte abnormalities, a procedure- or medication-specific ethology
-is it causing haemodynamic instability?
-PATIENT PRE-EXISTING ECG ABNORMALITIES (eg. AF, QTc prolongation, BBB, WPW pattern), MEDICATION EFFECTS (eg. -ve chronotropic agents such as B blockers, CCBs, dig, amiodarone) may cause drug-induced sinus brady, anti cholinesterase agents may also cause sinus brady particularly if the anticholinergic is underdosed, sugammadex may cause severe sinus brady or asystole (care ++ if give to a pt already on an agent slowing HR), opioids, vasoconstrictors. Medications prolonging QT: antiemetics: droperidol, ondans. analgesics: methadone (some anaesthetic drugs (eg. opioids, dexmedetomidine, midaz, ketamine, volatiles) may mildly prolong QT but are unlikely to cause TdP). antiarrhythmics (amiodarone, ibutilide, sotalol), antimicrobials (quinidine, fluconazole, azithromycin, metronidazole), antineoplastic drugs, bronchodilators (terbutaline), neurologic (donepezil), oxytocin’s (carbetocin, oxytocin), antipsychotics (haloperidol, chlorpromazine), TCAs, SSRIs (escitalopram)
ELECTROLYTE ABNORMALITIES- hypokalemia (if K+ <2.5 may lead to QT prol (other ecg findings of hypoK incl ST depression, decr T wave amplitude, U wave), replete if <3.5, 20mEq over 2 hrs if peripheral (risk phlebitis). Hyperkalemia (multiple conduction abnormalities such as BBBs or AV block or VF/VT). hypomagnesemia (widens QRS & risks torsades/AF while hyperMg++ risks conduction defects, brady, hypoT (if pt has renal insufficiency may Rx hypermag w isotonic fluids & a loop diuretic, occ they need postop dialysis). hypoCa++ may prol QTc but less likely trigger TdP than hypoKal or hypoMg. HyperCa++ shortens AP (shortens QT)- Rx w saline hydration. METABOLIC & RESP ABNORMALITIES (eg. hypoxaemia, hypo/hypercarbia, acid/base disturbances). ANAEMIA or DEHYDRATION. MYOCARDIAL ISCHAEMIA or FAILURE. SURGICAL- intrathoracic, interventional eg. cardiac catheterisation), ECT. ANAESTHETIC- intravascular access (eg. PAC or CVC placement), LAST.
-pts @ risk of myocardial ischaemia should have leads II & V5 displayed, if an unidentifiable arrhythmia develops, display all available leads & obtain a 12-lead ecg asap. if concerned re: artefact, set in “monitor” or “filter” mode- can also use “pacing mode” to assist detection of paced rhythms. distinguish artefact from true arrhythmia by comparing with art line/pulse ox.
-vagal reflexes (eg. oculocardiac (traction of EOMs —> PSNS response via ophthalmic branch of trigeminal nerve) peritoneal stretch with laparoscopy, carotid endarterectomy (removal of plaque may–> carotid sinus nerve stimulation reflex brady & hypoT (pre-Rx w glycolic or local lignocaine infiltration may help). neuraxial (high T1-4)- best treated with beta-adrenergic agonist eg. ephedrene, meds (eg. B-blockers as above).
-atropine 0.5mg, may repeat 3-5 minutely up to total 3mg. Rarely, may require temporary pacing. Rarely, transcutaneous pacing +/- epinephrine infusion 2-10microg/minute.
-consider glycolic 0.2mg first (increments up to 1mg) to avoid undesirable tachy, could use atropine 0.2mg at a time. ephedrine if ass’d w hypoT. If transplanted, anticholinergics typically not effective so isoprenaline (or epinephrine) chosen.
-no- pacing.
-R) infraclav, LV apex
-mechanical prosthetic TCV
-RV, fluoroscopy
-address cause (eg. drug toxicity from B-blockers, myocardial ischaemia). if haemodynamically unstable, atropine, consider chronotrope (eg. isoprenaline), if acutely unstable, temporary pacing.
-pacing pads, since the PAC may cause R) BBB when entering RV which may –> CHB
-central vascular interventions (eg. placing PAC), hyperkalemia, myocardial ischaemia or intrinsic cardiac disease.
-intrinsic cardiac disease, periop ischaemia, electrolyte abnormalities, excessive vagal tone, prior surgical or trans catheter AVR.
-ratio of P waves:QRS complexes
-yes, if severe bradycardia or haemodynamic compromise
-yes, since the intrinsic ventricular rhythm is usually very slow
-SNS stimulation (eg. deepen anaes/analgesia), hypovolaemia, anaemia, fever, MH, hypoxaemia, hypercarbia, sepsis.
-IHD, aortic or mitral stenosis (diastolic perfusion, LV filling)
-hypovolaemic, bleeding, decompensated HF, bronchospasm, marked conduction system impairment (eg. sinus node dysfunction)
-hypotension, altered mental state, signs of myocardial ischaemia or acute heart failure, signs of shock
-synchronised cardioversion (sedation, if regular narrow-complex, consider adenosine)
-consider if wide or narrow; if narrow & regular, vagal manoeuvres or adenosine (this will generally work if AV nodal dependent), B-blocker or CCB. If wide, adenosine ONLY if wide monomorphic, otherwise anti arrhythmic infusion (eg. amiodarone first does 150mg over 10 mins then maintenance infusion 1mg/min for 6hrs). alternative= sotalol 1.5mg/kg over 5 mins (not if prolonged QT).
-adenosine 6mg rapid bolus, after 1-2mins can give 12mg, if not effective within 1-2mins can give another 12mg.
-cardioversion the shock is synchronised with QRS. defibrillation the shock is asynchronous, delivered randomly during the cardiac cycle.
-A-P, higher success rate & lower energy requirements, more favourable shock vector through atria, reduced thoracic impedance
-biphasic terminate shock @ lower energy
-AF 120-200J, A flutter 50-100J, supraventricular tachycardia 50-100J, VT with pulse 100J (but only useful if distinct QRS & T waves are identified- if the VT is polymorphic there’s a risk of R on T which is why asynchronous with 200J biphasic is done for these circumstances, VF or pulseless VT 200-360J; higher energy for obese or pts known to be difficult to cardiovert. VF much more likely to be successfully converted if prompt defibrillation.
-3-4wks. if not, TOE prior to cardioversion but still need therapeutic anticoagulation after the cardio version.
-standard process with monitoring of foetus
-pads @ least 12cm from pulse generator, AP position, if elective cardio version use the lowest energy possible to limit damage to device & electrode-myocardial interface. Interrogate & evaluate pacemaker afterwards. if an ICD, can do internal cardio version by an electrophysiologist.
-digitalis sensitises the myocardium so cardio version may trigger additional arrhythmias. if required urgently & no time to correct clinical toxicity & hypokalaemia (which is ideally corrected prior to cardio version), select lowest possible energy level. for atrial flutter could do rapid atrial pacing. for VF, could give prophylactic lignocaine 1mg/kg.
-benign: skin irritation, self-limiting (hypotension from anaesthesia, ecg changes such as transient ST elevation) or serious (postcardioversion arrhythmias, thromboembolism, myocardial necrosis esp with high energies, myocardial dysfunction (global LV dysfunction due to myocardial stunning), pulmonary oedema)
-using a preexisting ICD to deliver a clinician-directed shock, epicardial wires placed during surgery or internal paddles applied directly to the epicardium during sternotomy, 2 defibrillation electrodes placed in the right atrium & coronary sinus or RA & PA, then intracardiac shocks delivered by an external defibrillator
-up to 20J
-hypovolaemia/hypotension, hypoxaemia, infection, anaemia, trauma, pain (SNS stimulation/catecholamine release/arrhythmogenicity)
-rate control with B blocker or CCB (better than CV as they may have a LAA thrombus), if it’s <120bpm may still treat with rate control if consider that @ risk ischaemia or haemodynamic instability (eg. esmolol 10-25mg or metoprolol 1-5mg) to decrease HR to <=80bpm, provided BP adequate
-AVOID CCBs & B-blockers if LV systolic dysfunction.
-often ass’d with underlying disorder (eg. severe pulmonary disease, CAD, valvular heart disease, hypoMg++, theophylline, elderly). usually @ least 3 distinct P wave morphologies (isoelectric baseline btwn the P waves, atrial rate is irregular, PR interval varies) & rapid irregular ventricular rate- can be difficult to distinguish from AF. often doesn’t cause significant haemodynamic compromise. definitive Rx= address underlying cause, if unstable may need antiarrhythmic for rate control. may progress to AF.
-aberrent conduction or pre-excitation, AF with BBB, drugs (eg. amiodarone), electrolyte abnormalities (eg. hyperkalemia)
-monomorphic with very regular RR interval
-there is time- a 12-lead ecg should be obtained, may be useful to rule out VT (presence of AV dissociation &/or QRS >=0.16s). Vagal manoeuvres or adenosine may be diagnostic & may be therapeutic- use a continuous rhythm strip with any maenouvre intended to slow or terminate an SVT & refer for cardiology consult asap.
-cardioversion
-whether the conduction is orthodromic (antegrade through AVN, retro through accessory) or antidromic (antegrade through accessory & retro through AVN). impacts the management for acute termination of AVRT; if orthodromic, treat the same as other SVT where the aim is to lengthen AVN refractoriness (vagal, adenosine). however if antidromic & unsure of the diagnosis, AVOID AVN-specific blocking drugs & Rx with procainamide (if certain about the Dx can Rx as per orthodromic).
-antidromic it’s always wide (while with orthodromic it’ll be either wide or narrow)- this is why standard AVN-blocking drugs shouldn’t be administered, since this may speed conduction through accessory pathways, incr vent rate, compound haemodynamic instability & may degenerate rhythm into unstable VT or VF.
-QRS >120ms. Hypoxia, Hypovolaemia, Hypo/hyperkalemia, hypo/per thermia, Hydrogen ion (acidosis), Toxins, Tamponade, Tension PTx, Thrombus.
-rapid VT with rates usually >240bpm, predominantly monomorphic QRS & no atrial activity
-3 or more. P waves aren’t distinct but can be seen with no relationship to QRS complexes.
-synchronised cardioversion (100J) vs defibrillation (200J)
-immediate defibrillation vs 2g IV MgSO4 slow bolus, if no response, can do temporary transvenous overdrive pacing @ approx 100bpm for TdP w long QT not responding to MgIV, as always cards consult.
-3 or more consecutive ventricular beats @ rate >120bpm but last <30secs. If the rate is >100 but no compromise to cardiac function, can use a B blocker or CCB or even amiodarone or class 1B (lignocaine)- similar to pts with PVCs (which are generally clinically insignificant but if they are frequent may be ass’d w myocardial ischaemia or electrolyte abnormalities), myocardial ischaemia or electrolyte abnormalities should be suspected & treated.
-ongoing continuous ecg monitoring in PACU, cardiology consult if clinically significant arrhythmia or evidence myocardial ischaemia.

Question 303

:) SS_CS 1.4: Discuss the periop Ax of LV systolic & diastolic function
-what are potential mechanisms behind the clinical syndrome of heart failure?
-define heart failure?
-how do the ACCF/AHA stages of HF compare with the NYHA classification?
-what features look for on history?
-risk factors for HF?
-what features on examination?
-what is classed as elevated JVP?
-what are some physical signs of pulmonary HTN?
-what investigations?
-do most patients with HFrEF have a normal ecg? how about HFpEF?
-what look for on ecg in pt suspecting HF?
-when echo warranted? what is the echo definition of HFrEF, HFmid-rangeEF and HFpEF & causes of each? how is echo useful for HF?
-what is the utility of BNP in pts with S&S of HF? what are some conditions where BNP may be elevated? are BNP levels typically lower or higher in obesity?
-utility of troponin?
-why would I check CBC? EUC? LFTs? fasting BGL?
-what are some findings of HF on CXR?
-what are tests to Ax the LVEF aside from echo?
-what’s the clinical gold standard for diagnosis of HF?

Answer 303

-LV dysfunction, valvular heart disease, RV dysfunction, pericardial disease, obstructive lesion in heart or great vessel, high-output HF

-a complex clinical syndrome characterised by present or prior symptoms (eg. dyspnoea or fatigue) and evidence of cardiac dysfunction as a cause. Haemodynamically, means that the heart is either unable to pump blood to the body at a rate commensurate with its needs or can only do so @ high filling pressures. There may or may not be physical signs. It can result from any structural or functional cardiac disorder impairing the ability of the ventricle to fill with or eject blood.
It’s a clinical diagnosis based on Hx, physical exam, lab & imaging data.
-Stage A= at high risk of HF but no structural heart disease or HF symptoms (none)
Stage B= structural heart disease but no symptoms of HF
Stage C= structural heart disease with prior or current HF symptoms (NYHA I-III)
stage D- refractory HF, requires specialised interventions (NYHAIV)

-History:
Functional status: NYHA classification (independently predicts mortality)
Symptoms related to fluid accumulation (dyspnoea, orthopnoea/PND, dependent pitting oedema, pain from hepatic congestion) or inadequate cardiac output (fatigue/weakness, ischaemic chest discomfort/dyspnoea/pre-syncope, particularly on exertion), arrhythmia (palpitations/lightheadedness)
if acute, more likely dyspnoea/PND (RHF R) UQ pain). chronic may have anorexia (splanchnic hypo perfusion, hepatic congestion, bowel oedema)
-risk factors (older age, HTN, Hx IHD, Hx AF, obesity, loop diuretic)

-Examination:
-general appearance (eg. tolerance of exertion of walking into clinic), diaphoresis, colour & warmth of peripheries (cool peripheries= compensate for low CO state by incr SNS outflow & shunting CO to vital organs)
-vitals, esp BP (narrow pulse pressure often seen if greater cardiac dysfunction- suspect decreases CO if pulse pressure <25mmHg or pulse pressure/SBP is <20-25%), rate & rhythm of pulse (resting tachycardia suggests more significant cardiac dysfunction, pulses alternans (varying of pulse amplitude with alternate beats) is virtually pathognomonic of severe LV systolic dysfunction.
-cap refill (degree of peripheral vasoconstriction)
-displaced apex beat (lateral to MCL) in LV enlargement, less useful in HFpEF
-may get parasternal lift if RV hypertrophy/enlargement
-gallop rhythm (S3, end of rapid diastolic ventricular filling, if elevated LA pressure and LVEDP (can be normal in chn & athletes)). S4= atrium pushing blood into stiff or hypertrophic LV.
-lung crepitations (more prominent in acute or subacute disease)
-elevated JVP (a sign RHF, often concomitant with L))
-hepatomegaly, splenomegaly
-peripheral oedema (LLs, scrotum, ascites)

-oscillation of IJV >3-4cm above sternal angle, with head of bed elevated to 30 degrees. or >7-8cm total distance above RA.

-pulm HTN may have incr intensity of P2, murmur of pulm or tricuspid insufficiency (pulm regurg= diastolic decresc murmur L) upper SE, tricuspid murmur= high pitched holosystolic, L) lower sternal border radiates to R), parasternal lift, may have elevated CVP due to RVF–> pulsatile hepatomegaly & ascites.

Ix:
-ECG, echo, bloods: bnp, troponin, CBC

-No! if a pt has a normal ECG, LV systolic dysfunction is very unlikely (98% NPV). In contrast, pts with HFpEF often have normal 12-lead ecg although they may have AF or a paced rhythm.

-ECG to look for signs of ischaemia (eg. pathologic q waves), acute or prior MI, arrhythmia, LA enlargement, LV hypertrophy & as a perioperative baseline

-Echo warranted periop if S&S worsening HF. HFrEF is EF<=40%, ischaemic & dilated CM. HFmrEF is EF 41-49%, ischaemic & dilated. HFpEF is LVEF>=50%, may be restrictive/hypertrophic/non-compaction. no single echo parameter is diagnostic of HF. some pts can have reduced EF without clinical syndrome of HF, some have HFpEF- it’s useful for identifying findings consistent with HF & to identify potential causes (eg. LV systolic or diastolic dysfunction, valve dysfunction, LV hypertrophy, valve stenosis, valve regurgitation, LA enlargement, elevated est PA systolic pressure, regional wall abnormalities, pericardial diseases)

-NT-proBNP or BNP provides evidence re: whether HF is present- a normal BNP (<100pg/mL) has high NPV in a pt with resting dyspnoea. Most dyspnoeic pts with HF have values >400pg/mL, between 100-400pg/mL, low S&S for HF. consider PE, LV dysfunction sans exac, cor pulmonale. It’s more likely high in pts with HFrEF & may be normal in HFpEF. Elevations may occur with elevated R) heart pressures (eg. if PE), AF even without HF, increases with age & is higher in women than men, renal dysfunction, sepsis, sacubitril-valsartan (since sacubitril inhibits BNP degradation) but NT-proBNP not impacted by neprilysin inhibitor (NRNi= angiotensin receptor-neprilysin inhibitor. sacubitril-valsartan. lowers RAS activity & inhibit breakdown of several vasoactive peptides. it reduces the risk of clinical deterioration & hospitalisation in pts w symp HF & prolongs survival in pts w reduced LVEF. Adverse effects incl hypotension, cough, hyperkalaemia, hypersensitivity, renal impariment. BNP lower in obesity.

BNP may be useful if considering additional periop testing (eg. Troponin postop) however it’s use is yet to be correlated with clinical outcomes- may be useful if considering periop stress testing or other Ix where a low value helps downgrade estimated risk.

-trop useful if acute decompensated HF or suspected ACS, useful to have a baseline in case perioperative testing eg. MINS

-anaemia or infection may exac HF. EUC assesses for associated conditions, hyponatremia may occur with severe HF, renal impairment may be caused by or contribute to HF exac. LFTs may be impacted by hepatic congestion. fasting glucose assists if underlying DM.

-cardiomegaly (C:T width ratio >50%), cephalisation of pulmonary vessels, kerley B-lines, peribronchial cuffing, pleural effusions.

-radionucleide ventriculography or myocardial perfusion imaging, cardiac MRI, cardiac CT.

-haemodynamic exercise test using R) heart cath- PCWP >=15mmHg at rest or >=25mmHg during exercise.

Question 304

:) commonest cause of mitral stenosis?

Answer 304

rheumatic fever
mitral annular calcification (elderly)
occasionally congenital or after radiation

Question 305

:) how to grade severity of mitral stenosis?

Answer 305

A-D, based on:
-valve anatomy
-valve haemodynamics
-haemodynamic consequences
-symptoms

A= “at risk” of MS, mild MV doming during diastole. normal transmitral flow velocity. no haemodynamic consequences or symptoms
B= progressive MS, valve area >1.5cm2 but some commissurual fusion, diastolic doming. diastolic pressure half-time <150ms, increased transmitral flow velocities. mild-moderate LA enlargement but normal pulmonary pressure at rest, no symptoms.
C= asymptomatic, severe MS. commissural fusion, diastolic doming as above but MVA <=1.5cm2 (would be <-1cm2 with asymptomatic very sever). diastolic pressure half time >=150ms (>=220ms with very severe MS). Severe LA enlargement & PASP >30mmHg (50mmHg from AHA)
D= symptomatic, severe MS. valve anatomy as above with area as above, same valve haemodynamics & haemodynamic consequences but the pt has decreased exercise tolerance & exertion dyspnoea.
severity can be difficult to determine wrt transmitral gradient since it’s influenced by HR & SV.

Question 306

What’s the Jervell and Lange-Nielsen syndrome?

Answer 306

autosomal recessive phenotype of congenital long QTs, associated with profound sensorineural hearing loss & higher risk for sudden death cf autosomal dominant LQTs.
12-lead ecg should be performed to screen for LQTs in all children with congenital sensorineural deafness.

Question 307

What’s the Romano-Ward syndrome?

Answer 307

autosomal dominant form of congenital long QT syndrome, more common than autosomal recessive, purely cardiac phenotype

Question 308

What’s Takotsubo cardiomyopathy?

Answer 308

transient, reversible stress-induced cardiomyopathy w LV hypokinesis & apical ballooning w ST elevations & incr cardiac enzymes. more common older women.

Question 309

what’s pacing dependency?

Answer 309

no intrinsic rhythm >40bpm or haemodynamic instability w the intrinsic rhythm

Question 310

What’s infective endocarditis & anaes implications?

Answer 310

a predominantly bacterial infection of a native or prosthetic heart valve or the cardiac endothelial surface
high mortality (20% in hospital), leading causes of death: heart failure (an indication for surgery), cerebrovascular embolism (ischaemic stroke= more common than haemorrhage, also meningitis or brain abscess are risks. for CVA, some may get endovascular Rx), arrhythmia, sepsis.
other complications= renal failure, pulmonary complications (esp R)-sided endocarditis, eg. septic embolisation into pulmonary vasculature).
IE requires prompt early Dx, management, multi-D; 50% of pts meet criteria for surgery (heart failure, uncontrolled infection (eg. abscess), preventing systemic embolic events); generally trend towards earlier surgery. Timing controversial if endocarditis complicated by cerebrovascular events; if major ischaemic stroke & severe neurologic damage or large ICH, delay valve surgery for at least 4 wks. timing of surgery= area of controversy & lack of data.
in developing world, rheumatic valve disease= most common risk factor
developed world: congenital or degenerative valvular disease, prosthetic valves or CIEDs main risk factors
noncardiac risks= IVDU, indwelling intravascular devices (eg. haemodialysis, compromised immunity, Ca

mainly involves heart valves, sometimes in the mural endocardium
phases:
bacteremia
adhesion (attach to inflamed/damaged cardiac endothelial surfaces)
proliferation (vegetation of plt/fibrin, subsequently biofilm
infection may cause structural damage to cardiac tissue, the vegetation can lead to septic embolisation (eg brain, kidneys, skin (dissemination)

Presentation:
fever, malaise (non-specific)
Evaluate as per modified Duke criteria (high S&S)
blood culture
echo (TTE= first test if clinical suspicion. TOE should be undergone in all pts w high index of suspicion, has much higher sens & spec for detecting vegetations on native or prosthetic valve). suggested by oscillating intracardiac mass (irregularly shaped, heterogenous), abscess, new partial dehiscence of prosthetic vale, new valve regurg/thickening/perforation.
sometimes cardiac CTA, nuclear imaging

once confirm, empiric bactericidal ABx asap & consult ID

Most cases GP cocci (staph, strep, enterococci) but regional & pt-related variation. immunocompromised may have fungal or yeast infection.

Long-term high-dose ABx indicated due to biofilm, difficult to eradicate biofilm on prothetic material so often complete hardware removal recommended.
generally remove all indwelling lines before surgery.
Intr-op, CPB & ultrafiltration may impact antibiotic serum levels, may drop below MIC, seek ID advice.

Periop risk factors:
pt: age, female, diabetes, immunosuppression & frailty
IE-related:
s-aureus, fungal, prosthetic valve, nosocomial IE or multivalve involvement, vegetation >10mm (on L)-side, >20m on R) side)
complication-related:
cardiogenic or septic shock, CVA, renal failure, ongoing bacteremia
surg-related:
urgent surgery, prev cardiac surg, XC time, CPB time, re-sternotomy due to bleeding

pts w IE often have normocytic-normochronic anaemia.
incr risk periop bleeding but also hypercoaguable state.
should manage bleeding using POCT but it’s unknown if normal values for non-IE on algorithms equally useful in IE.

intra-op:
Ax pt for septic shock
consider NIRS, document any pre-op neuro deficits & early postop Ax.
all pts w IE requiring surgery should have intraop echo.
risks coagulopathy; IE has interplay btwn inflammation & coagulation.
pts w IE may have relative heparin resistance. ATIII level lower & fibrinogen higher.
Can Mx heparin resistance w escalating doses of heparin, antithrombin or FFP. Bivalirudin an alternative.
Steroids not routinely recommended for cardiac surgery but if septic shock & ongoing vasopressor requirement, 2021 Surviving Sepsis Campaign Guidelines have weak recommendation for corticosteroids. no specific evidence to guide periop steroids for card surg due to IE. Hemoadsorption (blood purification w cytokine adsorber in CPB sicruit)= relatively new approach, awaiting RCTs eg. REMOVE trial.
If IE suspected & pt having GA, opportunistic TOE so don’t need extra GA.

Postop almost all need ICU, management organ dysfunction (eg. persistent septic shock, refractory HF, coagulpathy, ARF, stroke, conduction abnormalities). Ongoing, these pts are at risk of reinfection, need to have ABx prophylaxis for future procedures accompanied by bacteremia.

Question 311

clinical manifestations & Dx of myocarditis

Answer 311

suspect in pts with or without cardiac S&S (excessive fatigue or exercise intolerance, chest pain, unexplained sinus tachy, S3/4 or summation gallop, new cardiomegaly on CXR, new-onset/worsening HF, acute pericarditis, cardiogenic shock)who present w rise in cardiac biomarkers, change in ECG suggestive of acute myocardial injury, arrhythmia or abnormalities of ventricular systolic dysfunction, esp if new or unexplained.
initial tests= ecg, trops & CXR. could consider ESR or CRP or BNP if Dx of HF is uncertain.
echo for all pts
only endomyocardial biopsy if it’ll significantly impact management.

causes may include infection (incl COVID-19 or HIV), hypersensitivity (eg. to Covid 19 vaccine, ABx, diuretics), cardiotoxins (eg. cocaine, catecholamines, radiation), systemic disorders (eg. IBD, sarcoid, thyrotoxicosis).

Rx & prognosis depends on the cause.
General measures incl HF therapy, Rx arrhythmias. if refractory HF despite optimum medical therapy, VAD or cardiac transplant. some pts w immune-mediated cause may need immunosuppressive therapy.

avoid NSAIDs, heavy ETOH, exercise.

pts should have serial echo.

Question 312

SS_CS 1.4: Discuss the perioperative assessment of right ventricular function and pulmonary artery
pressure

Answer 312

Clinical:
History:
Aetiologies of pulm HTN (eg. Idiopathic, LV failure, pulmonary disease, chronic thromboembolism, misc (HIV, sarcoidosis)
Symptoms of low CO state (NYHA, DASI, fatigue/dyspnoea on exertion)

Examination:
Signs of low CO state (hypotension, visible dyspnoea on exertion, cool peripheries, oliguria)
S3 heart sound
Holosystolic murmur (LSE radiates to RSE) of TCR
Elevated JVP
Hepatojugular reflux
Pulsatile liver
Peripheral oedema

Investigations:
Incr lactate, deranged biochem (eg. elevated LFTs if hepatic congestion, renal impairment if organ hypoperfusion from inadequate CO)
ECG: normal or may show RAD, R) BBB, RVH (where QRS <120ms, dominant R wave in V1, >=7mm, ST depression/TWI in leads V1-V4, deep S waves in V5, V6, I, aVL), S1Q3T3 triad of RV strain

Echo:
RV thin-walled, low-pressure so better tolerates increases in preload vs sudden incr afterload
In response to chronic afterload: progressively hypertrophies & incr contractility to maintain output. Decompensation:
-RV dilation (heterometric= dilated but performing well)
-impaired contractility & impaired CO
-septal bowing if RVEDP>LVEDP
-tricuspid annular dilatation & regurgitation reduce forward flow
-Tricuspid regurg jet permits estimation of RVSP:
-RVSP= 4v2 + RAP (or CVP), is equivalent to PASP in absence of pulm stenosis
-more susceptible to arrhythmias (dilated) & ischaemia (CorPP = ADP - RVEDP, particularly if systemic hypotension)
-TAPSE normal >16mm, <14mm suggests RV dysfunction
-Fractional area change <35% indicates RV systolic dysfunction
-Mitral stenosis may be ass’d with palm HTN

Cardiac MRI= most accurate noninvasive technique to assess RV (mass, volume, EF, perfusion)

PA catheter reserved or situations where additional info outweighs risks involved (PA rupture, arrhythmia’s); no evidence for its use
Must be zeroed & referenced (usually w pt lying supine)

Question 313

measured & derived values from PAC

Answer 313

direct measure:
CVP
RA & RV pressure
PAp
PAOP
PAWP
PCWP
CO
SmvO2

indirect:
SVR = 80 x (MAP - CVP) / CO
PVR = 80 x (mean PAp - PAOP) / CO
CI (= CO / BSA)
Stroke vol index = CI / HR
DO2 = CI x 1.34 x Hb x SaO2
VO2 = CI x 1.34 x Hb x (SaO2 - SmvO2)

Question 314

Course of floating a PAC & confirmation of placement

Answer 314

Indications:
Only for critically unwell pts if there’s a clinical question regarding haemodynamic status or diagnosis that can’t be answered otherwise & whouch could change management.
monitoring PA & PAOP, RA & RV pressure, CO & CI, SVR, PVR & SvO2.
useful for unexplained shock (differentiation among causes of shock, differentiation between mechanisms of pulm oedema), evaluation of pulm HTN.
To guide fluid resus, titrate vasopressors, assess Haemodynamic effects of changes in ventilator settings & response to meds (eg. specific to pulm HTN).
occasionally preop for high-risk cardiopulmonary surgery.
Risks= arrhythmias (esp sustained vent or BBBs), misplacement, knotting, vessel, myocardial or valve rupture.
infection, thromboembolic events, ulm infarction.
PA perforation.
VAE

data misinterpreation (improperly calibrated or leveled, non-zone-3 transduction. over/ or under inflation of balloon, due to under or over interpretation of PCWP.
Contraindications (absolute): infection @ the site, lack of consent, during cardiopulm bypass, if RVAD.
Relative: significant coagulopathy or thrombocytopemia, electrolyte or acid-base disturbances.
High risk if Eisenmenger’s (risk PA rupture), those with a BBB (risk CHB), those with a defib or pacemaker, prosthetic or stenotic pulm valve.

Sites include IJ, subclavian, femoral, antecubital.
R) IJV preferred or L) subclavian (either IJ for cardiac surgery), could use femoral or antecubigal if no option.
Trained personnel
Equipment for catheter insertion, pressure monitoring, sedation
US w sterile sheath.
resus equipment.
telemetry monitoring throughout placement.
potentially fluoroscopic staff & equip (eg. if femoral approach or high risk pt eg. L) BBB)

Pt trendelenburg (jugular, subclavian).
sterile wide field.
anxiolysis
LIA
WIDE-BORE (8.5Fr), short, CVC placed.
confirm in the target vein before PAC placed: lack of pulsatile flow, transduction of pressure waveform, blood gas analysis. pressure transduction preferred method. CXR to help exclude PTx.
PA catheter ports flushed, check balloon integrity & ability to transduce pressure.
advance transducer through introducer (supine position).

CVP 8-12mmHg (normal person 1-6mmHg)
Balloon inflated once transducer indicates the tip of the catheter is in SVC or RA, @ about 20cm. Only inflate it when advance, deflate it when withdraw.
RA mean pressure 0-7mmHg
RV diastolic pressure 3-12, peak systolic pressure 15-25mmHg, @ 30-35cm
If no RV waveform seen after 40cm, it must be coiled in the RA. Deflate balloon, draw back 20cm, then advance w balloon inflated.
Rarely it may enter LA; LA waveforms same curves but slightly higher amplitude. Precedes PCWP. Also higher SaO2 in LA.
Risk of arrhythmia greatest when the catheter tip is in RV, so pass swiftly across pulmonic valve.
PASP 15-25mmHg/4-15mmHg, @ 40-45cm, there’s a dicrotic notch.
Peak systolic pressure in the PA occurs just prior to T wave, peak V wave of PCOP tracing occurs after the T wave. wedge position approx 50cm.
Normal mean PCOP (reflects LA pressure) is 4-12mmHg, see a & v waves, may not see c wave
Once in place, fix catheter & deflate balloon.

Once placed, PAC XR should confirm position; should be in zone 3 (Pa > Pc > PA; if not zone 3, alveolar pressure swings interfere w accurate assessment of PCWP). Best time to measure PAOP is end-expiration w pt supine tip of catheter in zone 3 of lung. Measure 3x & calculate mean.
It should cross the midline by no more than 3-5cm.

5 ports:
distal (pressure monitoring) port
proximal (drug infusion) port, also for CVP monitoring.
Balloon inflation port.
There may also be a RV infusion port that can also be used for pacing.
Thermistor connector.

If see large V wave on CVP trace, suggests TCR.

Question 315

PA catheter complications

Answer 315

During insertion:
-atrial/ventricular arrhythmias, usually self-limiting, mitigate by correcting electrolyte & acid:base disturbances prior to insertion
-RBBB occurs in approx 5%, so shouldn’t float a PAC in pts with L) BBB without ability to institute immediate cardiac pacing
-perforation cardiac chamber
-rupture of a cardiac valve
-*pulmonary artery rupture
*limit by ensuring balloon fully inflated (so tip doesn’t protrude beyond balloon) during insertion. Suspect with sudden resp distress & shock.

-misplacement (can usually be corrected with manoeuvres)
-knotting: if suspected, do NOT withdraw. Imaging, consider cold sterile saline. May need guide wire in Cath lab under fluoroscopic guidance or surgical extraction.

Question 316

Tricuspid regurg:

Answer 316

Often asymptomatic/without clinical findings; detected on echo.

Abnormal degrees of TR most often SECONDARY (eg. Due to annular dilation/leaflet tethering if RV pressure or volume overload; the leaflets & chords apparently anatomically normal but functional regurg due to dilatation of the tricuspid annulus).
Pulmonary HTN & secondary RV dilatation may be due to:
LV failure
Mitral regurgitation
Mitral stenosis
Primary pulmonary disease
L)—>R) shunt (ASD, VSD, anomalous pulmonary venous return)
Eisenmenger syndrome
Stenosis of pulmonic valve or pulmonary artery
Hyperthyroidism

RV diseases that may cause secondary TR incl:
Cardiomyopathies
IHD (RV myocardial & tricuspid papillary muscles)

PRIMARY disorders of the valve causing TR:
Rarer
Pacemaker leads impinging on valve leaflets or problems with the pacing
Endomyocardial biopsy
Deceleration/chest wall injury
IE
Ebstein anomaly (most common form of congenital disease affecting TCV; the septal leaflet of the TCV is displaced apically, the anterior leaflet becomes long (sail-like), the tricuspid valve apparatus becomes dilated & there’s a large atrialised portion of the RV.

Clinical presentation varies greatly, depending on degree of anatomic abnormality. Antenatal lithium exposure may predispose.
May have ass’d CV defects, eg. PFO, ASD, VSD, pulmonary atresia, PDA, accessory conduction pathways, predisposing to arrhythmias, left heart lesions are occasionally identified, it may be small due to severe TCR.

May have severe TCR & R)-sided heart failure, significant cyanosis due to R)—> L) interatrial shunting.
May have prominent “a” wave in distended jugular veins, hepatomegaly.
May have widely split S1 & S2 due to R) BBB. May have S3. Holosystolic murmur from TR, incr intensity w inspiration.
May present late in life with paradoxical systemic embolism or arrhythmias.)

Rheumatic valve disease
Carcinoid
IHD affecting RV w pap muscle dysfunction or rupture
Myxomatous degeneration ass’d w TCV prolapse
Connective tissue disorder

TCR generally clinically silent unless severe, since the RA so compliant.
S&S are of RHF; chronic RV pressure/volume overload—> RV systolic dysfunction & low forward CO.

Symptoms:
Sensation of pulsation in the neck
Exertion dyspnoea/pre-syncope
Painful hepatosplenomegaly, ascites, peripheral oedema.
Symptoms due to pulmonary HTN (symptoms of low CO: fatigue, weakness, dyspnoea, exercise intolerance).

Signs: elevated JVP, with distinct “c-v” (regurgitant) wave (tall V wave which may obliterate C wave) due to systolic regurg into RA, enlarged/pulsatile & tender liver, ascites, peripheral oedema, regurgitant murmur (holosystolic, louder with leg raise or inspiration), RV heave, cachectic
Elevated CVP may contribute to impaired renal function since incr intra-ado venous pressure—> reduced GFR.
ascites, liver failure.
Signs of L)-sided failure may dominate if the TR is due to LHF: impaired output, hypotension.

Stages of TCR:
B= progressive (mild-mod), central jet <50% RA, VCW <0.7, ERO <0.4cm2, regurgitant vol <45mL, no haemodynamic consequences or physical signs
C= asymptomatic severe; central jet >=50% RA, vena contracta width >=0.7cm, effective regurgitant orifice >=0.4cm, regurg vol >=45mL, hepatic vein systolic flow reversal. The RA will have c-V wave. The pt will have elevated venous pressures but no symptoms.
D= symptomatic severe, same valve haemodynamics as cat B but dyspnoea on exertion, fatigue, ascites, oedema.
Pulmonary HTN: RVH, RAD & tall R waves in V1-2, prominent S waves V5-6, inverted T waves & ST depression V1-3, incomplete R) BBB. P pulmonale= peaked p waves in lead II.

Question 317

Causes of over & under-damping on PAC trace

Answer 317

underdamped= stopcocks, excessive tubing lengths, pt factors (tachycardia, high output states)
overdamped= air bubbles, overly compliant tubing, kinked catheters, blood clot in the tubing, no fluid or low flush bag pressure (eliminate these issues by changing the equipment)

Question 318

SS_CS 1.4: discuss the perioperative assessment of shunts

Answer 318

ASD= the most common congenital cardiac disease in adults, 10% of CHD overall. Insignificant if <1cm. Haemodynamically significant if Qp:Qs >1.5:1 & significant RV dilatation.
Ass’d w L)-R) shunting causing volume overload R) heart.
Transient R)-L) shunting may occur, esp if brady or decreased Pit (may explain paradoxical embolism). Significant R)-L) shunt may develop if severe pulm HTN or TCR develops or if sig ASD & pulm stenosis.
LA enlargement seen esp in later life–> AF, diastolic dysfunction.
Physical findings of isolated ASD depend on size & location of defect, size of shunt @ atrial level & pulm artery pressures.
A few will develop central cyanosis.
paradoxical embolisation can occur (particularly if PFO)

Exam:
RV heave LSE
systolic murmur @ LSE (if there’s enough flow) with wide fixed splitting of 2nd heart sounds (the typical finding in pts w large ASD & L)-R) shunt w normal PaP)
if pulm HTN, accentuated pulmonic component of S2

IF also pulm HTN:
S4
holostystolic murmur of TR if RV & RA enlargement

clinical signs of RV volume overload (elev JVP, hepatic congestion, pedal oedema)

atrial arrhythmias: esp A fib, which may cause palpitations, dyspnoea & risk cardioembolic events

pulm HTN (due to capacitance of pulmonary vasculature, pulm pressures don’t sig rise unless volume of Qp exceeds 2.5x baseline.

If eisenmenger, cyanosis & clubbing

may also see cyanosis if significant ASD & pulmonary stenosis.

may get platypnoea-orthodeoxia if the 2 necessary components are present (to produce arterial desaturation & dyspnoea when moving to upright)
1. an interatrial shunt (eg. PFO, ASD, hepatopulmonary syndrome, pulm AVMs)
2. a functional component, promoting abnormal shunting when moving to upright, eg. deformity in atrial septum or RA increasing streaming through the defect.

Ix:
-echo: can do with agitated saline maneuvers, assess for RV volume or pressure overload & evaluation of PA pressure
-Cardiac MRI: can estimate the Qp:Qs (pulmonary to systemic blood flow) to determine if ASD closure is indicated. Can do this indirectly (either velocity-encoded phase contrast MRI looking at Qs & Qp (inaccurate if significant regurgitation or low shunt) OR volumetric analysis (difference between LV & RV stroke volumes; inaccurate if regurgitation or VSD). OR directly (en face phase contrast MRI of the septal defect).
Rarely cardiac cath (invasive); eg. if inconclusive Ax of severity & if haemodynamicaly significant (which is causing RA/RV enlargement with Qp:Qs >= 1.5:1), determine Qs & Qp from fick equation, (shunt fraction= (SaO2-SmvO2)/(PvO2-PAO2))

The systemic & pulmonary blood flows are calculated from the Fick equation.
Determine systemic blood flow from SaO2, SmvO2 & measured pulmonary venous O2 saturation (assumed to equal SpO2 if no R)-L) shunt) & PaO2 (measured pulmonary artery saturation)

Question 319

SS_CS 1.5:
Steps & considerations for CABG

Answer 319

CABG typically done by midline sternotomy & CPB

Off-pump either with full sternotomy or small ant L) thoracotomy; benefits of avoiding potential morbidity ass’d with aortic cannulation & XC (eg. embolism of aortic plaque, stroke) & CPB (SIRS, plt activation, fibrinolysis, bleeding, vasodilatory shock). HOWEVER outcomes (death, CV events, need for revascularisation) no better with OPCAB cf on-pump BUT it may be chosen for pts @ very high risk for stroke (eg. extensive atheromatous involvement of asc aorta).

Differences for off-pump:
-less systemic anticoagulation (100-200 units/kg heparin), ACT 250-300s.
-NO TxA.
-Fluid LOAD (15-20mL/kg to maintain haemodynamic stability during coronary artery grafting & manipulation, cf fluid restriction pre-bypass for on-pump).
-Trendelenberg often used to improve preload during OPCAB
-Haemodynamic instability during manipulation of heart common; vasopressors or even atrial pacing often required.
-Postop ischaemia risk after revascularisation since the heart wasn’t protected from ischaemia w CPB & pleg; continual ECG & TOE monitoring.
-Maintain intra-op NORMOTHERMIA.
-consider converting to on-pump if significant haem instability, malignant arrhythmias, global ventricular ischaemia or technical difficulty mobilising coronary vessels.

Steps:
pre-bypass (optimise myocardial O2 supply/demand)
positioning meticulous
incision (blunt nociception), sternotomy, retraction, harvesting peripheral vein(s)/artery, dissect IMA from chest, exposure heart & great vessels, are the fundamental surgical steps prior to aortic & venous cannulation.

PRE-OP:
History/exam/Ix & consent

PREBYPASS:
-if placing pads, L) scapula & R) lateral thorax
-IVC, sedation, art line, CVC. Generally NO PAC (lack of evidence for mortality benefit, risks).
-BIS
-NIRS to keep rSO2 within 20% of baseline IF pt has significant cerebrovascular disease, concomitant asc aorta or arch procedure.
-Induction: goals- maintain optimal myocardial O2 supply (reduce HR (still allowing perfusion), optimise O2 content (Hb, SaO2), optimise coronary blood flow (DBP, LVEDP, cor vasc resistance)) & minimise demand (HR optimisation (low normal 50-80bpm), minimise wall stress (reduced LVEDV, reduce LV wall thickness, reduced SBP (keep within 20% baseline) aka LV afterload), reduce contractility): PREVENT, DETECT & TREAT MYOCARDIAL ISCHAEMIA (ecg, TOE for RWMAs; hypo or akinesis, elevations in LV or RF filling pressures (eg. CVP); Mx tachy & hypoT w pure alpha agonist, tachy w HTN by incr depth or analgesia OR beta blocker).
-ABx prophylaxis
-positioning- meticulous to avoid injuries eg. brachial plexus injury with compression of upper arm by steel posts on operating table. watch head position during sternal retractor (may lift head).
-pl catheter w temp probe (bladder= “core” temp), nasopharyngeal temp probe (the oxygenator arterial outlet temp= the most reliable surrogate for cerebral temp during cooling & rewarming.
-restrict fluid (CPB= haemodilution)
-prebypass TTE: regional LV wall abnormalities, global LV & RV function, structure & function of valves, Tx aorta, inter-atrial septum, LA w LAA, detect ischaemia, hypovolaemia, hypervolaemia or low SVR

INCISION & STERNOTOMY:
-anticipate nociception, Rx with opioid & DOA to limit HTN & tacchy
-temporarily interrupt ventilation during sternotomy to avoid lung injury
-while harvesting the internal mammary, reduce TVs. harvesting of peripheral vein(s)/artery.

HEPARINISATION:
-administer, ensure adequate anticoagulation with ACT

ANTIFIBRINOLYTIC:
-to minimise microvascular bleeding

Cardiopulmonary bypass:
-venous cannula drain blood from RA or SVC/IVC- generally passive drainage (but can add suction) into
-venous reservoir (drugs & sampling here)
-pump (generally roller) draws blood from reservoir, propels through heat exchanger, oxygen or gas exchanger & arterial line filter, blood returned to pt via arterial cannula in asc aorta or other major artery.
-additional circuit pumps & components employed as needed to suction blood from surgical field, deliver cardioplegia, decompress heart chambers via a vent, remove fluid (ultrafiltration).

CPB initiation:
-perfusionist completes CPB setup, primes, tests alarms & circuit
-Prior to cannulation, asc aorta evaluated by palpation & with TOE to avoid areas of atheromatous disease or calcification (reduces risk of cerebral embolism & post-op stroke & AKI). If severe asc aortic calcification, alternative sites may be chosen. During aortic cannulation, reduce SBP to <100mmHg to reduce risk aortic dissection
-during venous cannulation, treat hypotension or initiate CPB for malignant arrhythmias
-CPB is initiated gradually (with retrograde autologous priming to reduce haemodilution from crystalloid prime)
-perfusionist assumes control of O2 delivery, CO2 removal & pump flow; DISCONTINUE CONTROLLED VENTILATION (once full CPB flow achieved (2.4L/min/m2 for normothermic pts to approximate a normal cardiac index; reduce if hypothermia. MAP >=65mmHg but higher if older or cerebrovascular disease, no >100mmHg, ABG to ensure SvO2 >=75% throughout CPB; check ABG, BE, lactate + ACT every 30mins, note by lack of pulsations on art line) & VOLATILE via anaes circuit
-DISCONTINUE CARDIOVASCULAR SUPPORT (eg. inotropes)
-discontinue and IABP counterpulsation
-MAINTAIN ANESTHESIA: TIVA or anaes vaporiser to CPB circuit
-BIS
-NMBAs to prevent movement or shivering
-Just prior to aortic X-clamp, perfusionist reduces pump flow rate to reduce MAP. Aortic XC is placed, antegrade cardioplegia delivered (via a cannula in prox asc aorta), need to ensure complete myocardial arrest (no ECG electrical activity)
-TOE monitoring for aortic insufficiency & LV distension during antegrade cardioplegia delivery. TOE assessment of coronary sinus catheter placement for retrograde cardioplegia delivery if that’s also done (for complete cardiac arrest & myocardial preservation), assess correct LV vent placement & effective LV decompression.
-I ensure adequate propofol for depth, vasopressors for perfusionist, alarms silenced on anaes machine (CPB mode)

CPB maintenance:
-cooling: temp gradient btwn venous inflow & arterial outlet <10deg
-MAP >=65mmHg (or >=75mmHg if cerebrovascular disease or severe aortic atherosclerosis)
-Hb >=75 & Hct >=22%
-maintain SvO2 >=75% (increase pump flow if <75%)
-rewarming: slow (<-0.5degC/minute, keep temp gradient btwn venous inflow & art outlet <=4degC. Avoid hypothermia; target temp is 37degC @ nasopharyngeal, 35.5degc @ bladder
AXC is removed; consider lignocaine immediately prior to AXC removal (decr risk of VF), pacing wires, defibrillate w 10-20J if VF immediately after XC removal (but identify & treat underlying causes eg. hypothermia, hypokalemia, hypomagnesemia, air embolism, LV distension), give antiarrhythmic agents if necessary (eg. amiodarone 300mg (dilute to 20mL w glucose 5%, give IV over 1-2mins)

CPB weaning:
checklist to identify & correct abnormalities prior to weaning:
WAAARRRRRMM
Warm: nasopharyngeal temp 37 (not higher- risks cerebral injury), bladder 35.5
Anaesthesia: TIVA
Adjuvant drugs: antiarrhythmics, inotropes, vasoactives immediately available
Air: de-airing to reduce cerebral, coronary & systemic air embolisation. Aided by TOE. may place pt trendelenberg.
Rhythm: needs adequate perfusing heart rhythm before weaning. if can’t achieve sinus or if bradycardia, epicardial pacing. if AV conduction normal, atrial pacing. otherwise AV pacing (for AV synchrony & optimal ventricular preloading).
Rate: HR 80-90bpm to maximise CO without compromising coronary diastolic perfusion time.
Resistance: vasopressors if low SVR.
Respiration: resume PPV & correct any resp problems prior to weaning.
Metabolism/labs: Hb (pt-specific target; 70-80g/L, correct K+ & Ca++ & pH abnormalities; Ca++ 1.09-1.3mmol/L, K+ 4-5.5mmol/L.
Monitors: ensure all functioning, zeroed, visible/audible.

POSTBYPASS:
-venous decannulation; TOE assessment for adequate ventricular filling
-anticoagulation reversal: dose heparin 0.7-1mg per 100units heparin, administer protamine slowly (administer slowly to limit vasodilation; initial 10mg test dose, then no more than 5mg/min) watch for adverse effects; anaphylactoid/hypotension (if given too rapidly; vasopressors), anaphylaxis (eg. if ABx from protamine-containing insulin or allergy. Have Adr & resus equipment available. may need to re-heparinise & go onto CPB), pulm HTN (acute pulm VC & RV failure; rare & severe reaction, may get bronchospasm & noncardiogenic pulm oedema. Mx similar to anaphylactic along w inhaled pulm VD, may need return to CPB or V-V ECMO), bradycardia. Give protamine after weaning from CPB but before aortic decannulation. suction of blood from surgi al field discontinued after protamine admin begins. Monitor ACT, since plasma [] residual heparin can insidiously increase after initial protamine (as heparinised blood from CPB pump is reinfused & plasma tissues–> blood or as released from tissues–> blood esp if lg doses were given; consider protamine infusion 25mg/hr for 4-6hrs post-op).
If heparin was readministered to re-establish CPB due to severe heparin reaction, Rx for presumed anaphylaxis & give systemic steroid, antihistamine H1 & H2 antagonist. Epinephrine infusion +/- Nepi or vaso. if refractory shock, methylene blue 1-2mg/kg before attempt to wean.
No guidelines re: heparin reversal here; could give FFP, plt, fibrinogen, rbcs (risks massive transfusion). ECMO if severe noncardiogenic pulm oedema or resp distress syndrome.
Bivalirudin half life 45mins, anticoag resolve within approx 2hrs.
-pump suckers turned off & intravascular vents removed
-aortic decannulation: SBP <100mmHg to reduce risk aortic dissection
-insertion of temporary/backup epicardial pacing wires pacemaker setting optimised
-reinfusion of pump blood
Postbypass TOE:
-regional LV wall abnormalities, global LV & RV function, LV & RV chamber sizes to Ax intravascular volume status, asc aorta to rule out dissection
-HAEMOSTASIS: POCT to ensure heparin reversed, assess other coagulation parameters if bleeding persists (manage anaemia/thrombocytopenia/coagulopathy)
-Haemodynamic stability: manage with volume, vasopressors, inotropes, pulmonary vasodilators
-CHEST CLOSURE: observe RV compression & dysfunction, coronary graft compromise, pacing wire displacement, lung compression

TRANSPORT TO ICU & HANDOVER:
-optimal pt condition, airway equip & emergency drugs & defib immediately available, continuous ECG, SpO2, iABP monitoring during transport.

Problems related to CPB:

-blood contact with nonendothelial surfaces of CPB circuit induces intense inflammatory response–> plt activation, coagulation & decreases levels of circulating coagulation factors.
-Endothelial cells & leukocytes are activated & mediators that may contribute to capillary leakage & tissue oedema are released.
-This inflammatory sequence may be behind many of the challenges w CPB weaning (MI, vasodilation, bleeding).

-Priming solution (1-2L balanced crystalloid)==> haemodilution (anaemia/coagulopathy)

Intra-operative problems after CPB:

-CV instability (inadequate preload, compromised contractility (global or focal LV or RV dysfunction), decr afterload (reduced SVR & vasoplegia), HR too low or high, rhythm disturbance w loss of AV synchrony)
-hypotension; may be the central to peripheral arterial pressure gradient which resolves w time, consider whether need volume, vasopressor, pulm VD, inotrope- assess based on CVP, CO (normal 5-6L/min, normal cardiac INDEX is 2.5-4.2 L/min/m2), BP, LV & RV function
-LV dysfunction; address reversible surgical factors, HR, pacing mode, vasoactive drugs (usually inotrope & vasodilator to optimise CI). if diastolic dysfunction, ensure euvolaemia & AV synchrony.
-RV dysfunction: may be pre-existing, new pulm HTN, RV ischaemia/infarct, intra-coronary or pulmonary air embolism or TCR; intracardiac air may preferentially enter RCA–> RV dysfunction. Manifests as incr CVP w systemic hypotension (reduced functional RV preload). RV may be pressure overloaded (L)-shift of septum during systole) or volume overloaded (L-shift of septum during diastole). Manage by ensuring BP & CorPP are adequate, preventing incr PVR, avoiding excessive fluid, inotropic support with IV agents that also produce pulm arterial VD (milrinone, dobutamine), often combined w vasopressin or Norep to maintain systemic perfusion pressure. Refractory RV failure–> aerosolised vasodilator for pulm HTN & to reduce RV afterload. Nitric oxide 5-20ppm (care met Hb if high prolonged doses, abrupt discontinuation may–> rebound pulm HTN). epoprostenol nebuliser: 30ng/kg/min. milrinone inhaled.
-vasoplegia: NAdr, haemodynamic-guided fluid therapy, add vasopressin if refractory. Refractory vasoplegia= methylene blue (1.5mg/kg over 1 hr)
-arrhythmias: AF= the most common arrhythmia after cardiac surgery, usually develops 2-5 days postop. sync CV in immediate postbypass period. or amiodarone 150mg over 10 mins then infusion 1mg/min. esmolol, metop or diltiazem for rate control. vent arrhythmias: open chest internal defib 10-20J, amiodarone if recurs, correct triggers (hypothermia, hypoK, hypoMg).
-bradycardia, heart block, asystole: epicardial pacing.
-Arterial air embolisation, esp RCA; ischaemia to inf LV wall & RV, arrhythmias (esp heart block). neuro dysfunction or seizures. Prevention w aggressive de-airing during weaning process (TOE monitoring) & venting LV or aortic root, may use inotropes or vasopressors to incr BP & cor perfusion until residual air cleared from heart & coronaries. ABC approach, supportive therapies (O2, vent, vol resus, vasopressors), position L) lateral decubitus if venous, supine arterial. HBOT= definitive Rx if haemodynamically unstable or cardiopulm/end-organ compromise, ideally 4-6 hrs but benefit up to 30hrs. supportive therapy= high FiO2 (incr rate resorption embolised air), Rx any seizures.
-surgical/technical issues
-LVOTO may occur after MV or AV procedures or other procedures in pts w severe underlying LVH. Mx by incr LV volume, incr SVR, decr inotropy or HR (epicardial pacing may help if bradycardia results).
-Cardiogenic shock: temporary mechanical circulatory support (eg. IABP, VAD, ECMO)

PULMONARY PROBLEMS:
-airway obstruction, bronchospasm (eg. protamine reaction, transfusion reaction, hypothermia, inadequate depth, pre-existing asthma or COPD). deepen, B2 agonist (IV salbutamol 250microg over 5min, infn 5mcg/min after 200microg load over 1 min), IV epi 5-10microg boluses (up to 100mcg/bolus) or 2-10mcg/min infusion if needed.
-pulmonary oedema: cardiogenic (pre-existing or new-onset heart failure w extra fluid during CPB, may be due to protamine, TRALI (rapid development (usually within 1-2hrs, may be up to 6hrs) of lung injury & non-cardiogenic pulm oedema due to activation immune cells in lungs, following blood product transfusion. Fever, chills, hypox resp failure, pulm infiltrates on CXR w normal cardiac silhouette, pink frothy sputum; may be life-threatening), sequestration of neutrophils in pulm capillaries, localised inflammatory response (incr capillary permeability)). Give diuretic. If very high PAP, inhaled NO or epoprostenol. ECMO if severe.

BLEEDING & COAGULOPATHY; may be contirbuted by:
-inadequate surgical haemostasis: meticulous, systematic check at appropriate perfusion pressures.
-loss of plts & coagulation factors, hemodilution (eg. due to high vol cell saver use)
-hypothermia: active rewarming coming off bypass, maintain normothermia postbypass & postop.
-residual heparin
Heparin half-life 60-90mins, so anticoagulant effect may persist 4-6hrs
Protamine: may require additional infusion 25mg/hr extending over 2-4hrs postop to help avoid “heparin rebound”, which is more likely if active cooling during CPB or pts w “heparin resistance” if large dose given. POC heparin-protamine titration assay can document residual heparin effect.
-CPB effects: haemodilution, hypothermic coagulopathy, plt activation & consumption, hyperfibrinolysis from the CPB circuit.
-ROTEM-guided transfusion (rapid) along w standard lab tests to guide transfusion strategies. Aim Hb >70 & Hcg >21%, higher target if severe haemorrhage/organ ischaemia. Cell saver before allogenic rbcs.
-fibrinogen <1.5 (or fibtem A5 <=10); fib conc pref as doesn’t need thawing but more expensive & it’ll only raise fibrinogen (doesn’t have vWF, VIII, XIII & fibronectin)
-prothrombin complex concentrates incl 4-factor (inactive II, VII, IX, X AND heparin). 3 factor inactivated II, IX & X, no heparin, little/no VI. activated PCC has 4 factors with VII mostly in activated form (factor 8 inhibitor bypassing activity), no heparin; activated higher prothrombotic risk, rarely used). Only give if other causes of intractable microvascular bleeding (eg. surgical sources, plt, fibrinogen) ruled out & avoid if DIC or HIT risk factors.
-rFVIIa rarely given for intractable life-threatening coagulopathic bleeding after CPB, off-label, high thromboembolism rates & mortality. only use if other causes ruled out. 20mcg/kg every 15 mins.
-may reinstitute some TxA.
-DDAVP 0.3mcg/kg ONLY for rare cases of pts w acquired plt defects (uremia or acquired vW syndrome eg. chronic AS or LVAD) if persistent bleeding. slowly over 30mins to avoid vasodilation. tachyphylaxis occurs. Adverse= HTN, hypoT, flushing, fluid overload, hyponatremia (risks seizures if don’t free-H2O restrict), rare thrombotic events.

Postop ongoing monitoring for bleeding, timely preop cessation anticoags & antiplt. carefully define pts transfusion target.

METABOLIC:
hypocalcemia: CaCl
hypoK; potassium 10-20mmol over 30mins (CVC, haem monitoring)
hyperkalemia (from pleg or cellular shifts w resp or metabolic acidosis. more often a prob if renal impairment): hypervent, Ca, glucose & insulin, B-agonist, frusemide (diuresis)
hypoMg: IV 1-2g.
hyperglycaemia: Rx to keep <10, not too low (incr risk stroke if tight control).

OLIGURIA: aim >=0.5mL/kg/hr. check IDC, check TOE to exclude dissection, ensure euvolaemia, maintain adequate CI >2L/min/m2.

HYPOTHERMIA: “afterdrop” of core temp after rewarming. incr room temp, warm products, FAWD. Continue rewarming after arrive in ICU. it exac myocardial dysfunction, bleeding (plt dysfunction, coag factors), decr metabolism of IV administered drugs.

Neurol complications of cardiac surgery:
-stroke (eg. atheromatous, gas emboli, hypoerfusion)
-neurophyschiatric abnorms (disturbances in memory, executive function; may be related to microemboli) or encephalopathy
-peripheral neuropathies
: allied health, surveillance, optimise physiologic parameters & nutrition, functional recovery, limit sedative/hypnotics

Question 320

Preop evaluation for cardiac surgery:

Answer 320

-Hx/exam/Ix to assess & minimise risks for anaesthetic & operation.
-explain plan to pt, informed consent.
-alleviate anxiety.
ONLY delay surgery to optimise modifiable conditions IF: surgery elective, can significantly improve the medical condition & risk of postponing surgery < benefit of optimising condition. Eg. prehabilitation.

Cardiovascular risks:

-MYOCARDIAL ISCHAEMIA; low risk= angina sans preop MI scheduled electively. intermediate= acute MI but haemodynamically stable (if presents within 6hrs of symptom onset, urgent revascularisation to maximise myocardial salvage, otherwise myocardial necrosis has reached its peak (after 6hrs), delay surgery for 3-4 days may improve operative M&M, may delay 5-7 days if P2Y12 receptor blocker. High risk= haemodynamically unstable
-CCF: etiology & degree of RV or LV dysfunction +/- concomitant pulm HTN
-CEREBROVASCULAR OR PROX AORTIC ATHEROSCLEROSIS= a risk factor for periop stroke, eg. significant CAS >80%. Manage either by ensuring aspirin, B-blockers, statins continued, consider multi-D discussion re: timing of CEA.
If significant proximal aortic atherosclerosis, may consider off-pump CABG.

Noncardiac risks:

Unmodifiable:
-FEMALE GENDER
-OLDER AGE
Modifiable
-RENAL INSUFFICIENCY
-ANAEMIA (incr risk rbc transfusion & adverse outcomes eg. LoS if females have preop Hb >130g/L, males preop Hb >140g/L; may be appropriate to delay elective cardiac surgery to diagnose cause & correct such preop anaemia eg. replete Fe/B12/folate; Ferritin <100g/L with OR WITHOUT anaemia ass/d w incr mortality, periop transfusions, MACE; 6-8wks is required for full correction of anaemia preop. oral Fe if 4-6wks preop, if less time, IV Fe; after IV Fe, 1-2 wks required to improve Hb 10g/L), current tobacco
-DM: normoglycaemia (maintain BGL <10 on CPB)
-HTN: continue chronic antihypertensives (EXCEPT withold ACE-I & ARBs am of surgery UNLESS for poorly controlled HTN or for HF, also withold diuretics the morning of surgery UNLESS the pt has HF with difficult fluid balance).
-COPD: optimise lung function (smoking cessation, intensification of bronchodilators, in some cases a course of systemic glucocorticoids, ABx (eg. if copiois sputum), education re: insp muscle training (eg. incentive spirometry)).
-THYROID DYSFUNCTION
-Screen for ABSOLUTE contraindications to TOE: oesophagectomy or planned oesophagectomy, operations involving pharynx, oesophagus or stomach, perf viscous, oes stricture/tumour/perforation/laceration/diverticulum. Active UGI bleed. RELATIVE contraindications: neck/mediastinal radiotherapy, Hx GI surgery, recent UGI bleed, barret’s, known or suspected C-spine injury, severe restriction in neck mobility, symtomatic hiatus hernia, oes varices, coagulopathy, thrombocytopemia, active peptic ulcer, Zenkers/hypopharyngeal diverticulum.

Examination:
-assess ease of IV access, peripheral pulses re: best site for IABP monitoring.
-dental exam (esp if prosthetic material implantation planned)
-skin infections/ulcers
-predictors of difficult airway
-obesity
-cardioresp exam

Ix: ecg, cath, echo.
other: Hb, plt, coags, glucose, renal function.

X-match @ least 2U pact rbcs; check G&H antibodies & expiry.

Re-sternotomy chest CT to assess risk of vascular injury (relation of aorta, RV free wall).

Medication management:
antihypertensives as above.
Cease non-statin cholesterol meds (niacin & fibric acid derivatives risk rhabodo, myopathy); lipid-lowering agents that are bile sequestrants interfere w bowel absorption of multiple meds.
continue aspirin, withold P2Y12 antagonists 5-7 days
Stop warfain, NOACS (dabigatran 48hrs (4 doses) if CrCl >50, skip 8 doses in the 4 days before procedure) if CrCl <50; rivaroxaban skip doses the 2 days before procedure; apixaban skip 2 days before procedure), heparins; warfarin 5 days)
Coagulation tests:
-Direct Xa inhibitors: incr anti-Xa but the lab needs to know which anticoagulant to calibrate. Rivaroxaban & apix MAY incr aPTT. Normal PT suggests clin significant riva not present, while apix little effect on PT.
Dabigatran DOES incr aPTT, possibly PT, NOT anti-Xa. Thrombin time sensitive to Dabigatran; normal TT suggests absence of significant dabi effect.
UFH incr APTT, LMWH may. UFH only incr PT @ high [] (>1unit/mL). Heparins all incr the anti-Xa.

ICDs usually reprogrammed, PPMs reprogrammed to asynchronous mode if pacemaker dependent, the threshold of the pacemaker is usually incr by ischaemia/reperfusion injury/myocardial trauma & this may result in failure of capture so temporary epicardial wires are routine during cardiac surgery.

Emergency surgery:
focussed Hx (allergies, medications (esp antiplt/anticoag), prev anaesthetics, fasting status, most recent labs.
IV & art line (CVC often post-induction)
Blood products (eg. MHP; ensure valid G&H)
if recent antiplt, give PLATELETS.
If warfarin, 4-factor PCC 1500-2000U IV over 10 mins (recheck INR after 15mins), along with vit K 10mg over 10-20mins (since PCC limited DOA; incr 4-6 to 48hrs)
dabigatran: idarucizumab OR (if unavail: activated PCC with factor 8 inhibitor bypassing activity), consider TxA, discontinue anticoagulant (half life normal renal function 12-17hrs), activated charcoal (if dose within 2hrs), haemodialysis.
apixaban/rivaroxaban: adnexanet alfa OR 4-factor unactivated PCC, TxA, discontinue (apixa half live 8-15hrs, riva 5-9hrs), only charcoal if very recent.
If the pt had fibrinolysis, may be necessary to incr fibrinogen w cryo, plasma, fib conc, along with antifibrinolytic.

There may be IABP in place or IABP placed.
all monitoring before anaes induction incl art line & CVC.
external defib pads pre-induction, pacemaker/defib ready @ the bedside.
In some cases, prep/drape ready prior to induction w team ready to urgently establish CPB.
inotropic & vasopressor infusions connected ready to infuse.
Minimal haemodynamic disturbance on induction, eg. fent 5-10microg/kg, midaz 0.05-0.1mg/kg, volatile.
May need pacing, vasoactive infusions for adequate CO pre-bypass.
CPB asap.

Question 321

TAVI

Answer 321

Indications:
Severe symptomatic AS w high peri-op risk for AVR or other CI to surgery

CI:
life expectancy <12/12, endocarditis, severe MR, CAD requiring intervention, no suitable access route.

Complications:
stroke
other vascular complications
haemorrhage (incl retroperitoneal)
paravalvular leak
AR
pacemaker requirement

98% procedural success, 30d mort <5%

Anaesthetic considerations:
Remote location
high radiation
Transfemoral TAVI generally under LA/sedation
Remi useful in keeping pt still & slow RR but able to obey commands
risk sedation= pt immobility not assured, unable to use TOE, harder to manage major complications. Need to be prepared for conversion to GA.

Haemodynamic goals for AS:
slow rate (60-80)
avoid arrhythmias (preload-dep ventricle relies on “atrial kick”)
Adequate afterload for diastolic perfusion
euvolaemia
avoid -ve inotropy

art line, 5-lead ecg, CVP, SpO2, EtCO2
external defib pads on
large-bore IVC
insert CVC with sheath (in case post-procedure pacing required)
infusions ready; GTN, NAdr, Adr

rapid ventricular transvenous pacing to minimise LV output during device deployment; ensure adequate pre-pacing MAP but don’t over-treat as risk of overshoot BP when rapid pacing off

Complications:
Hypovolaemia (& blood loss from puncture sites may be concealed)
Hypotension, ischaemia, arrhythmias (eg. w manipulation of wires)
Tamponade risk
Arterial injury (eg. aortic dissection)
Delirium, seizure, stroke (atheroma, calcific or air embolus)
Paravalvular regurg; >50% have minor, 15% have moderate

Balloon valvuloplasty evidence contentious
still <1cm2 after procedure
re-stenosis common @ 6/12
risk stroke, AR, AMI, death (15%!)

PARTNER trial:
NEJM 2010: TAVI superior to standard medical therapy (despite incr 30-day mort insignificant, significant reduction in 1 yr & 2 yr mortality w NNT of 4). TAVI DID have sig incr risk of storke cf SMP, also incr vascular compliations & major bleeding. no diff in AKI, new arrhythmias.

Question 322

Heparin resistance

Answer 322

Failure to reach ACT >400sec w 400u/kg heparin

Various etiologies eg:
-ATIII deficiency (hereditary or acquired)
-incr heparin-binding levels
-incr heparin Cl (eg. splenomegaly)
-high factor VIII or fibrinogen
-liver insufficiency
-error (eg. ACT measurement, drug error w heparin dosing)

Risk factors:
-ATIII <60%
-prior heparin therapy
-platelets >300
-age >65

Stepwise Mx:
-give more heparin up to a max total 600u/kg
-ATIII concentrate OR FFP (AT [] preferred; less volume, less risk of infection/other transfusion complications) in pts suspected to have AT deficiency (not reliable to measure after received heparin; can only diagnose ATIII deficiency if was measured preop). Effect of AT supplementation on clinically meaningful outcomes is unclear.
-Can measure heparin concentrations; if >=4u/mL, reasonable to initiate CPB since this is the critical [] heparin to prevent thrombosis during CPB
-if the heparin resistance is due to thrombocytosis, elevated fibrinogen, elevated FVIII, initiation of CPB & the haemodilution with that likely to mitigate these factors.
-If large amounts of heparin given, it will accumulate in tissues & later “heparin rebound”, pre-emptively treat w additional protamine as an infusion for 6hrs after CPB terminated.

Question 323

Heparin-induced thrombocytopenia

Answer 323

HIT1= mild, transient drop in plt count, typically within first 2 days of heparin exposure & plts typically return to normal even w continued heparin administration
appears to be direct heparin effect on platelets, non-immune plt aggregation
typical plt count nadir approx 100. Not clinically significant, NOT ass’d w thrombosis.

HIT2= Clinically significant, antibodies to heparin-platelet factor 4 complex (these are IgG & are rapidly formed), induces plt activation, thrombocytopenia & incr ++ risk for venous & arterial thrombosis (HITT; heparin-induced thrombocytopenia & thrombosis). Risk of thrombosis incl life-threatening limb gangrene, persists until both heparin is eliminated AND a non-heparin anticoagulant is initiated.
Typically 5-10 days after heparin initiation.

HIT more common w UFH but can occur with any

4T’s score for pretest probability of HIT, helps to guide decision re HIT antibody testing & if presumptive Dx is to be made.
-thrombocytopenia (degree)
-timing of plt fall
-thrombosis or other sequelae
-other causes of thrombosis present?

If pt for CPB & suspect Hx HIT:

If NO heparin antibodies, can use heparin intra-op for cardiac surgery if needed but avoid pre-op heparin (eg. flushes) or post-op (eg. VTE proph)

If heparin antibodies present, delay surgery if possible

If urgent surgery & Abs present or unknown, either:
-bivalirudin (IV direct thrombin inhibitor) can be used (with or without CPB)
-plasmapheresis prior to surgery
-high-dose IVIG prior to heparinisation
-co-administer epoprostenol (inhibits plt aggregation) w the heparin intra-op

(& avoid pre- or post-op heparin exposure)

Monitor pts postop; serial plts (esp D5-10) high index of suspicion, Ax 4T’s & antibody testing.

Education re: avoiding heparin in the future (in record) medic alert, non-heparin anticoagulant for VTE prophylaxis

If strong clinical suspicion of HITs, initiate Rx even before labs available.
Discontinue all heparin, stop any warfarin (reverse w vit K if thrombosis. Warfarin shouldn’t be used until anticoag w a non-heparin agent is established or before plt count >150 due to risk of skin necrosis w rapid depletion of protein C)., initiate a non-heparin anticoagulant in therapeutic doses given the thrombosis risk (provided pt doesn’t have clinically significant bleeding).
-want to halt plt activation asap.

Question 324

Valve surgery:

Answer 324

Intraop TOE to confirm & characterise valve pathology, refine surgical plan, monitor air removal after cardiotomy & to assess adequacy of repaired valves (repeatedly after termination of bypass, since paravalvular leaks can develop w time & increases in systemic pressure).
It’s particularly important to identify >mild AR, which limits delivery of adequate antegrade cardioplegia into the coronary artery ostia after XC asc aorta (much of it would regurg back & risk failure of pleg or distension of LV); strategies= retrograde pleg or LV vent for LV decompression. ALSO, AR relative CI to IABP.

Aortic stenosis OT:
-pre-op, severity of AS, ass’d AR or other valve/cardiac disease, RV & LV dysfunction, CAD. If AS & high pulm-systemic ratio (ratio mPAP:MAP) higher risk.

-intra-op, small incremental midaz to reduce stress response but caution if critical AS, severe vent dysfunction, elderly
-Prebypass, haemodynamic goals of AS:
rate sinus 60-80; design anaes to maintain slow HR, opioid-based & adeeequate depth, blunt SNS, vasoconstrictor & fluids if tachy related to hypoT, slow HR w B blocker if necessary
preload euvolaemia (avoid hypo)
maintain contractility
adequate afterload for cor perfusion

-midline sternotomy
-aortic cannulation & initiate CPB. cardioplegia.
-open aorta, AV excised & all calcific debris removed from surgical field (this risks cerebral infarction)
-the aortic annulus is measured, prosthetic (bioprosthetic or mechanical) valve placed.
-aorta closed, air fastidiously removed from asc aorta & L) heart.
-XC removed, heart reperfused, wean from CPB.

-most pts have epicardial pacing wires attached to RA & RV to maintain stable postbypass rhythm (risk postop AV block)
-don’t generally need inotropes during weaning from CPB after AVR (since LV contractility typically well-preserved in most pts w severe AS.

Often need to manage hypertension from the hypertrophied hyperdynamic LV that’s no longer ejecting across a stenotic valve.
HTN incr risk arterial bleeding & potential for aortic dissection @ cannulation site; Mx with incr depth anaesthesia (VA, GTN, esmolol).
Usually need epicardial pacing as AV conduction abnormalities common after AVR.

Aortic regurg:
causes LV volume overload, dilatation, eccentric hypertrophy.
biventricular function usually intact with mod-severe AR BUT DCM can occur in advanced stages, w LV failure, reduced EF & CO, incr LA & pulm artery pressures.
Pts w chronic AR often have low diastolic pressures & wide pulse pressure which is usually well-tolerated unless concomitant CAD too.

Pre-op:

Determine severity:

Acute: eg. due to acute aortic dissection, traumatic rupture valve leaflets or endocarditis. Rapid volume overload of relatively noncompliant LV, LA pressures incr, decr CorPP, sudden onset severe HF & cardiogenic shock. Requires urgent intensive medical Mx & emergency cardiac surgical repair; IV vasodilators +/- dobutamine while awaiting surgery.

Varying degrees of chronic:
A= “at risk”, bicuspid, AV sclerosis, IE or Hx RHD. valve consequences, haemodynamic consequences or symptoms
B= “progressive”, mild-moderate calcification, dilated sinuses, rheumatic valve changes. Valve haemodynamics show mild AR (jet width <25% LVOT) or moderate (25-64%. no symptoms, haemodynamic consequences normal LV systolic function & volume normal or slightly dilated
C= asymptomatic severe: calcific disease, bicuspid valve, dilated aortic sinuses, jet width >=65% of LVOT, evidence LV dilatation
There may be some LV systolic dysfunction & depressed LVEF but pt remains asymtpomatic
D= symptomatic severe; pt may have normal systolic dysfunction or varying severity of systolic dysfunction, mod-severe LV dilation, exertional dyspnoea or angina & more severe HF symptoms

Pre-op for chronic, along w AR severity, Ax if ass’d aortic root dilation, coexisting AS, function of other valves, presence/severity of HF.
Pts must be medically optimised (intensive Mx for HFrEF: first line= a diuretic, angiotensin system agent (ACE-Is, ARB, ARNI). 2nd line add on mineralocorticoid receptor antagonist, SGLT2 (-))
Rx for HTN (SBP >140mmHg) is indicated; ACE-I, ARBs or DHP CCBs favoured (vs B-blockers which risk elevating SBP due to reduced HR & incr SV & incr diastolic filling time may exac regurgitant volume)

Intra-op:
haemodynamic goals pre-bypass:
-rate 80-100, consider glyco
-sinus
-normal to low afterload (but ensure DBP >=60mmHg); prevent HTN with adequate DoQ & effective analgesia. gently titrate agents to manage hypoT.
-normal to low afterload, avoid fluid overload; pre-op diuresis & slight hypovolaemia OK; use restrictive fluid management & use IV GTN infusion for volume overload (provides preload reduction)
-avoid -ve inotropy & bradycardia; if require inotropic support, milrinone, dob or low-dose epinephrine preferred

Pre-bypass TOE, looking at severity (largest jet width in LVOT, as a % of the LVOT; mild is <405, SEVERE >=65% OF LVOT. Also measure narrowest neck of regurgitant jet (vena contracta), valve features to determine repair vs replacement.

Midline sternotomy, establish CPB, AXC, cardioplegia usually delivered retrograde via coronary sinus or the aortic root is opened & cardioplegia delivered directly into coronary ostia.
Native valve leaflets excised (if for replacement), annulus measured, prosthetic valve implanted).
De-air.

Postbypass TOE to ensure valve functioning.

Contractility is typically preserved in pts presenting for SAVR but if LV dilatation/dysfunction, may require inotropic support; pref for milrinone or dob (B agonist w inodilator properties). counter vasodilation with alpha-adrenergic agent (phenylephrine, norepinephrine).
consideration for epicardial pacing.

MR:
primary or secondary, acute or chronic
chronic MR–> volume overload of LV, LA, LV & LA enlargement, incr LA pressures & atrial dysrhythmias (esp AF), PVR & elevated PaP.
Primary MR= disease of leaflets/supporting structures (eg. annular dilatation, leaflet prolapse) due to degen/rheumatic disease.
IF LVEF IS REDUCED IN PT W CHRONIC PRIMARY MR, LIKELY SIGNIFICANT LV SYSTOLIC DYSFUNCTION, PT @ HIGH RISK LT POOR OUTCOMES.
Secondary chronic/functional MR results from underlying LV dysfunction (ischaemic or non-ischaemic in origin).

Pre-op Ax severity:
Acute eg. ruptured chordae (degenerative MV disease, IE), papillary m rupture (eg. MI). These pts may get FLASH pulmonary oedema, acute RHF, cardiogenic shock. intensive medical stabilisation, urgent surgical repair w high periop risk (if the acute MR is due to ischaemia, PCI may correct). For pts awaiting definitive Rx, IABP may beneficially reduce LV afterload & incr diastolic coronary perfusion.

Chronic:
Determine severity of MR:
A= At risk; central jet area <20% LA
B= progressive; central jet MR 20-40% LA, mild LA enlargement only (not LV or elev PAP)
C= asymptomatic severe: MR jet >40% LA, vena contracta >=0.7cm, regurgitant fraction >=50%, mod-severe LA enlargement, LV enlargement, pulm HTN, C1= preserved LVEF, C2= LVEF <=60%
D= symptomatic severe: pts have decr ET/exertional dyspnoea, LA enlargement, LV enlargement, pulm HTN.
Ax presence/severity of HF, ass’d MS, other cardiac valve pathology, LV dysfunction indicating ischaemia/cardiomyopathy.
CXR may show signs of pulm oedema & RH enlargement.
Pts having elective MVR for chronic MR must be medically optimised.
Many have coexisting AF & are on anticoagulation; ensure appropriate periop instructions.

Dynamic MR may occur w hypertrophic cardiomyopathy; such pts may have ventricular septal myectomy to relieve LVOTO & MV/papillary muscle abnormalities addressed @ the time.

Intra-op:
Haemodynamic goals:
rate 80-100
avoid bradycardia (augments diastolic filling & regurgitant volume)
avoid arrhythmias (AF poorly tolerated)
normal-low afterload, avoid HTN but maintain diastolic perfusion (gentle titrated Rx for hypoT)
normal-low preload (avoid hypervol); restrictive fluid Mx & IV GTN infusion if vol overload)
avoid elev PaP
avoid -ve inotropy, if need inotrope, milrinone or dob
If secondary to IHD, ensure:
adequate myocardial O2 supply (DBP adequate & LVEDP limited, limit incr corVR, goal Hb, SaO2) & limit demand (avoid excessive afterload or volume load, blunt SNS responses & tachycardia, adequate anaesthesia & analgesia)

Pre-CPB echo: may see pulm vein flow reversal w severe MR. look @ width of venal contracta. Consider aiming to recreate normal haemodynamic conditions to correctly Ax valve (eg. MR may be underestimated after induciton due to decr SNS tone & afterload).
determine whether anatomy best suited to repair or replacement.
Examine for other valve or ventricular abnormalities. examine RV for dysfunction due tchronic pulm HTN.
Acute MR: TOE essential to determine mechanism, haemodynamics, ventricular function
Severity: mild jet <20% LA, mod 20-40% LA, severe >40%
jet brief in mild, holosystolic in severe
vena contracta <2cm mild, 3-6 mod, >=7 severe
however acute MR may have low jet velocity which may underestimate degree of regurg.

Midline sternotomy, CPB, open LA (directly or via septum. bicaval venous cannulation.
close LA, de-air, remove AXC.
There’s a minimally invasive MVR via small R) thoracotomy with or without CPB. external defib pads esp if robot. short-acting anaes agents, normothermia, aim for extubation soon after surgery (1-2 hrs), multimodal anaesthesia eg. PB, SAP, PECS blocks.

Postbypass TOE; ensure gradient across valve not too high, return haemodynamic parameters to baseline prior to completing assessment of valve function (reduces risk for underestimating residual MR).

If preop LV impairment, often require inotropic support in the immediate postbypass period. In some cases, LV failure occurs w attempts to terminate CPB. Milrinone, esp if elev PVR, often also need Norepi to avoid excessive vasodilation. may need IABP to assist afterload reduction.
acute refractory RHF with high PVR may occur in some pts during attempted weaning from CPB.
Arrhythmias esp AF are common; may need synchronised cardioversion (esp if sinus was present before CPB), consider amiodarone esp if cardioversion unsuccessful, as well as correction of K+ & Mg++ to high-normal.
bleeding is a common complication.

Mitral stenosis:
impaired LV filling due to obstruction to LA outflow. LA pressure & PVR increase. Afib is common. often chronic pulm HTN & RV failure. LV is underloaded but may get fibrosis.
Rheumatic heart disease= most common cause. Other aetiology= severe mitral annular calcification.

Pre-op:
determine severity:
A= “at risk”; valve anatomy shows “doming” during diastole
B= “progressive”; rheumatic changes, commissural fusion, diastolic doming MV leaflets, MVA >1.5cm2, the haemodynamics show incr transmitral flow velocities, diastolic pressure half-time <150ms. some LA enlargement but PaP normal.
C= asymptomatic severe: rheumatic changes or commissural fusion/diastolic doming. MVA <=1.5cm2. diastolic pressure half-time >=150ms. LA enlargement severe, PASP >30mmHg but still no Sx.
D= symptomatic severe. decr ET, exertional dyspnoea.

Determine other lesions eg. MR, LAA thrombosis, RV dysfunction (CXR may show pulm oedema & R) heart enlargement).
Optimise medical therapy prior to elective surgery but don’t delay symptomatic pts.
particularly, pharmacological control tachycardia & arrhythmias (up to & including day of OT)
many pts are on anticoagulation; instructions.

Intra-op:
BZD titrated may be useful to Mx tacchycardia-related anxiety.

Haemodynamic goals:
rate 50-70 but avoid severe brady
avoid AF/SVT (cardiovery if no LA thrombus)
avoid pain-induced tachycardia. relatively slow HR (eg. opioid-based), slow anaes induction. Slow HR w B block if needed.
avoid fluid overload (euvolaemia); if pt acute w flash pulm oedema, 100% O2, PEEP, consider intubation & controlled ventilation
protect R) heart (avoid incr PVR, maintain DBP >60mmHg for right heart; maintain afterload)
avoid excessive inotropy (LV contractility gen not the issue); want to maintain RV contractility; milrinone or dobutamine & maintain SVR & systemic BP (eg. epinephrine)

Prebypass toe:
severity severe <=1.5cm MVA, very severe <1cm, progressive >1.5cm
diastolic pressure half time mild (progressive) <150ms; severe >=150, v severe >=220ms
mean gradient <5mmHg for progressive & severe, >10 very severe
pulm artery systolic pressure <30 progressive, >30 severe, >50 v severe

Postbypass: the LV is at risk of acute failure following CPB since it’s been chronically “underloaded”; inodilators may be needed (esp if concomitant PVR & RV dysfunction), may also need Norep to avoid excessive systmic VD.
acute RV dysfunciton also a risk.
Arrhythmias, esp AF.
bleeding.

TCR: 80-100 rate, low afterload (ie. low PVR), adequate diastolic perfusion RV (normal SVR).
TCS: 60-80bpm HR, low normal PVR, adequate preload (normal SVR)
pulm regurg: HR 80-100bpm, limit PVR, SVR normal.
pulm stenosis: slow 60-80bpm HR, avoid tachycardia to optimise RV SV & CO, tachy may incr dynamic RVOTO & reduce time in diastole (coronary perfusion). normal-low PVR & normal SVR.

When combined lesions, eg:
-AS with AR; typically the AR will be mild. general goal is to maintain pre-anaes baseline HR & cardiac loading to maintain CO & limit myocardial O2 consumption. typically 70-80bpm, maintain normal preload, afterload, SVR & contractility.
-MS with MR is common. 70-80bpm, normal-low normal SVR, normal contractility.
-valve & coronary disease: risk myocardial ischaemia. targets= pts baseline haemodynamic profile. optimise DO2 & limit demand.
-TR & MR or stenosis: prebypass haemodynamics emphasises the predominant lesion. the pt will often be on therapy for chronic RHF/pulm HTN (if severe TR); avoid hypox/hypercarbia, chronically administered pulm VD agents continued perioperatively.

Question 325

Initial pharmacologic therapy for HFrEF:

Answer 325

Combo therapy for all pts:
First-line regimen
-a diuretic
-Angiotensin system blocker (ARNI, ACE-I or single agent ARB)
AND
-a B-blocker

Secondary pharmacologic:
-mineralocorticoid receptor antagonist
-SGLT2 inhibitor

Question 326

Surgical steps/considerations Type A aortic dissection

Answer 326

Surgical emergency
Goals= prevent rupture, treat complications (eg. acute aortic insufficiency, cardiac tamponade, antegrade propagation of dissection into aortic arch (–> stroke) or retrograde to aortic root (–> MI or distal malperfusion syndromes). Particularly urgent to repair if malperfusion syndrome (regional ischaemia; different approaches could be taken eg. “malperfusion first” for any visceral ischaemia with TEVAR, then definitive arch repair, IF no evidence tamponade etc).

Clear coordination vital.

art line, temp IDC, CVC, intraop TOE. Sometimes 2nd art line. Cerebral oximetry, depth of anaesthesia monitoring/cerebral EEG.

Routinely uses hypothermic circulatory arrest & establishment of CPB & systemic hypothermia are immediate priorities. Can tolerate up to 45mins deep hypothermia (<20 deg) w circulatory arrest; antegrade or retrograde cerebral perfusion techniques may prolong safe duration. MANY pts w acute type A aortic dissection present w neurologic injury/stroke. cerebral perfusion extends “safe” duration of circulatory arrest & allows uniform & continued cooling of the brain + provides nutritive blood flow.
Antegrade cerebral perfusion is easily accomplished when axillary artery cannulation is use.
Need to monitor bilateral cerebral O2 sats during circulatory arrest (since clamping both innominate & L) common carotid is often necessary for adequate antegrade flow). If incomplete CoW, may also need to perfuse L) common carotid. If using femoral or aortic, balloon-tipped catheters straight into inominate (unilat) & L) CCA (bilat). direct cerebral vessel cannulation effective ACP but clutters surgical field& risk direct vessel injury.

Retrograde cerebral perfusion: from SVC. A school of thought that it may be suitable for shorter arrest times (concern over lack nutritive flow) but evidence unclear; theoretically may flush embolic debris from cerebral circulation.

-Exposure (median sternotomy +/- additional cannula sites)
-Surgeon cannulates a true lumen: usually asc aorta. Alt= R) axillary or femoral; risk rupture if direct aortic cannulation.
-adjuncts (ACP or RCP) established.
-Once CPB & systemic hypothermia achieved, LV vent.
-either clamp aorta or if can’t safely XC, circulatory arrest, pump off & aorta resected/reconstructed.
-Cardioplegia.
-gradually cool, circulatory arrest.
-repair/replace distal extent.
-de-air & prepare for recommencement CPB.
-systemically rewarm, complete proximal extent of repair.
-main concerns following CPB weaning= haemorrhage (often PCC, factor VII), operative integrity.

Postop: focus on supporting end-organs, haemodynamic monitoring (CONTROL HTN IS CRUCIAL TO PREVENT HAEMORRHAGE!), continued Ax for haemorrhage, early neurologic exam, spinal cord injury monitoring (if TEVAR occurred with significant coverage).
Annual surveillance.

Question 327

Type B dissections

Answer 327

Distal to the L) subclavian.

Chronic if present >90 days.

Uncomplicated generally managed medically (ANTI-IMPULSE therapy; control BP & HR, reducing shear stress & preventing progression, malperfusion, aneurysmal degeneration or rupture) w periodic imaging surveillance.
TARGETS (anti-impulse therapy management is the same for acute & chronic type B dissection):
HR <60bpm
SBP 100-120mmHg.
adequate pain management.
First line B-blockers (reduce HR, contractility, BP, wall stress), may add CCB.
If need additonal BP control, vasodilators.
Regimen:
esmolol load 500mcg/kg IV over 1 min, then infusion 50mcg/kg/min. titrate up to max 300mcg/kg/min.
Labetalol 20mg bolus then 20-80mg every 10 mins (max 300mg) OR infusion 1mcg/kg/min after 20mg bolus to max 10mcg/kg/min.
metoprolol 5mg every 5 mins for 3 doses. can repeat additional doses every 4hrs. B1 selective.
verapamil 5-10mg IV. or diltiazem (both non-DHPs). 0.2mg/kg then infusion 5mg/hr.
Avoid all of these if decomp HF. All may cause 1st degree HB.
esmolol vesicant, very short half-life reduced w anaemia. nausea/flush/bronchospasm (but is B1 sel).
labetalol nausea/paraesthesias/bronchospasm (caution ++ in reactive airway disease (nonsel B1 & B2 as well as alpha 1)).
CCBs: dizziness, nausea, brady.

vasodilators 1st line nitroprusside. risks elevated ICP & decr cerebral & coronary flow.
cyanide & thiocyanate toxicity. m spasm. nausea/flush/sweat.
GTN 2nd line: 50mg in 90mL 5% glucose, initial rate 3mL/hr (25microg/min). risk tacchy (reflex), flush, headache, vomit, metHb, tolerance w prolonged use. useful if coronary ischaemia or APO. very rapidly titratable.

All pts w aneurysm should avoid strenuous physical activity that would spike BP (eg. isometric, dynamic resistance); unproven in trials.

Acute aortic dissection presentation:
-sharp knife-like pain ant chest, radn neck/back/abdo. May have syncope or stroke if more likely asc aorta (or Horners, UL weakness, absent carotid or subvclavian pulses). if desc, more likely back/abdo pain along w chest, altered femoral pulses, LL pain/paraesthesia/motor deficit/acute paraplegia.
-the pt may have a Hx of risk factors for TAAD, eg. AAA, known bicuspid AV or coarctation, known syndrome ass’d with TAA/D (marfan, EDS, LD, turners).
-palpate for differences btwn pulses each side, difference in BP each arm.
-signs of aortic regurg or tamponade.
-signs ischaemic stroke, SC ischaemia.
Obtain ecg (signs of ACS eg. Type A may extend to coronary ostia, RCA most commonly affected). D-dimer, CBC, electrolytes, LDH, cardiac markers, coags, type & X-match (if D-dimer <500ng/dL, less likely aortic dissection).
CXR: widened mediastinum/unexplained pleural effusion consistent w dissection, esp if unilateral.
If haemodynamically stable & don’t suspect asc aorta involved, CTA or MRA. If n/a or contraindication, TOE.
Key diagnosis= evidence of intimal dissection flap.
Unstable or strong suspicion of asc aorta involved, get TOE (portable, yields Dx within mins, can do in the ED, 98% sensitivity & up to 96% specificity). if not immediately avail, CTA (has sens up to 95%, spec up to 100% BUT has lower sensitivity for the asc aorta) . TTE may help identify complications of asc aortic dissection (AV regurg, hemopericardium, inf ischaemia) but not sensitive for dissection. TTE has less sens & spec cf CTA, MRA or TEE.

2x large-bore IVs, art line for continuous HR & BP monitoring.
CONTROL Hr & BP:
HR <60bpm.
SBP 100-120mmHg.
Use B-blocker first (eg. esmolol or labetalol), if not tolerated, verapamil or diltiazem. Once HR <60, if SBP >120mmHg, add vasodilator.
IV opioid analgesia.
IDC to assess UO & renal perfusion.
Asc aortic dissection= surgical emergency, straight to OT (call ahead, skilled assistants preparing OT with CVC, warm line warm OT drugs drawn ready) with intra-op TOE.
If involves desc aorta w evidence malperfusion, urgent stent-grafting or surgery.
if only desc Tx aorta or abdo WITHOUT ischaemia, ICU for medical Mx of haemodynamics & serial imaging.
Pt must be @ a centre with cardiac surgical/vascular surgical services, equipment & support for CPB & endovascular stent-graft capability.

complications (eg. aneurysmal degeneration, malperfusion, rupture (emergency if malperfusion or rupture)) or other high risk features (eg. recurrent pain, persistent uncontrolled HTN) considered from intervention intervention.
Aneurysmal degeneration >4cm= most common indication for intervention (if connective tissue disorder, consider @ smaller diameters), recurrent pain 2nd most common indication for repair.

TEVAR= first-line if anatomically faesible & no connective tissue disorders. Otherwise open (incr periop M&M).
In-hospital mortality higher for pts w type B dissection having intervention cf medical mangement, not surprising since those requiring intervention typically have compliacted disease. If uncomplicated, mort similar with or without intervention.
mortality is incr if open vs endovascular repair (oppen higher risk of mort, AKI, resp failure, bleeding) but stroke, MI, paraplegia, mesenteric ischaemia, SCI, reintervention, sepsis similar.
long-term outcomes similar if medically vs intervention management.

Question 328

List indications for application of external defibrillation/pacing ME FEx pads prior to surgery

Answer 328

External pacing pads indicated for any situation where anticipate the need for re-establishing haemodynamics that are acutely compromised by a slow or fast HR with an acute reversible cause unlikely to require permanent pacing.
Put the monitor on “diagnostic” bandpass filter mode (allows clear display of higher-freq signals like pacing spikes).

PT factors:
-If a pt has had pacemaker reprogrammed or anti-tachyarrhythmia functions of an ICD electively disabled +/- asynchronous mode enabled prior to surgery
-Pt who has known significant AV or SA node disease
-if has a CIED & concern about device malfunction (place pads @ least 10-15cm away from edge
-Pt presenting to OT medically compromised 7 at risk of severe bradycardia (eg. significant risk for hyperkalemia, cardiac trauma, bacterial endocarditis w aortic valve involvement
-significant pathology with risk of arrest eg. cardiac tamponade

Procedure factors:
-Surgery where significant blood loss anticipated
-interventional cardiology procedures where there’s risk of damage to bundle branches, eg. risk catheter trauma during TAVI or ablation procedures
-emergency cardiac surgery where there is risk of need for pacing/defibrillation support before onto bypass

Question 329

Transvenous pacing:

Answer 329

The preferred mode for MOST pts
More confortable cf transcutaenous
more durable than both transcut & epicardial pacing if anticipate need for days to wks
Pts are restricted to bed or chair.
Avoid or use caution if:
-intermittent, mild symptoms who tolerate the bradycardia well (eg. symptomatic CHB with adequate escape rhythm or symptomatic sinus node dysfunction with rare pauses.
-prosthetic TCV
-MI who’s had thrombolysis & receiving aggressive anticoagulation or antiplatelets

SITE SELECTION:
-commonly L) subclavian (more freedom of pt motion, better if a long-term temp pacemaker
-IJ: ease of advancing to heart
-brachial not recommended (unstable site, risk cardiac puncture)
-femoral: VTE risk, infection, RV perf; pt needs to stay continuously supine w leg straight.

PLACEMENT: Aiming for RV apex.
-guided by lead markings, continuous ecg (PVCs or non-sustained VT common if the lead tip encounters RV myocardium), or fluoroscopy or continuous echo. If the pt is pacemaker dependent, fluoroscopy should be used.
Occasionally, temp biventricular pacing by putting a lead in coronary vein via coronary sinus.
rarely an atrial lead is placed transvenously.
Placement can be done via specialised pulmonary artery catheters w pacing capability but leads less stable than dedicated transvenous pacing wires.
SETTINGS:
Connect pacing wires to box (black -ve, red +ve), check batteries OK
set to demand
turn rate to 30bpm>intrinsic rate. set output to 4mA.
Once the catheter in place & pacing captured, deflate balloon & decr mA to find threshold. then double it.
generally a rate of 60-70 adequate, paeds or postop faster.
Set pacemaker output at least 2-3x pacing threshold (minimum output for pacemaker capture). Ideally the pacing threshold should be <=1mA, esp if pacemaker-dependent.

COMPLICATIONS:
Venous access-related:
-bleeding
-myocardial perforation (may–> tamponade)
-pulmonary embolism
-air embolism
-arrhythmias
-PTx

once inserted:
-dislodgement/disconnection (may–> asystole)
-infection

CXR & 12-lead ecg immed after placement
continuous ecg during duration of temporary pacing

Question 330

Transcutaneous pacing:

Answer 330

Initiated rapidly when urgent temporary pacing needed.
pads in anterior (R) chest) & L) lateral or A(R) chest)P(L) scapula) positions, IN ADDITION to adhesive electrodes for telemetry.

Main limitations:
-high capture thresholds due to impedance of chest wall structures, pt movement or poor adhesion.
-pt discomfort since high energy levels are needed to overcome impedence of chest wall, so can only use temporarily in unconscious or sedated pt.

Question 331

Epicardial pacing

Answer 331

following cardiac surgeries, for temporary pacing if brady or overdrive if postop tachyarrhythmia.
Atrium (if AV conduction intact), ventricle or both, wires tunnelled & externalised.

Issues:
-generally only use for a few days since if >1 wk, pacing threshold rises & may not get reliable capture.
-having minimal output energy extends longevity of pacing wires
-consider steroids (reduce inflammatory reaction to wire)
-NOT MRI compatible (ferrous material in pacing box)

Application:
surgeon passes wires
rate 80/min (above native rate)
set output 10mA, turn down to see capture threshold (where QRS no longer follows a pacing spike). turn output to 2x capture threshold.

Risks:
infection
myocardial damage
perforation
tamponade
disruption coronary anastomoses
microshock induced arrhythmia

pacemaker issues:
under/oversensing
failure to capture
output failure
unstable lead position
pacemaker-mediated tachycardia

Question 332

internal defib

Answer 332

pt should have patent airway (I&V), supine, sterile conditions (chest already open), all metal objects removed from pts skin, excess fluid suctioned from mediastinum, internal paddles, place one over RA or RV, other apex. Use lowest energy possible to convert (minimise myocardial damage); generally BIPHASIC 5-20J for pulseless rhythms. 10-40J monophasic. State “all clear” to ensure all off pt/bed/equipment. defibrillate. Ax pt response.

If internal cardiac massage, flat fingers & avoid lifting apex of heart. 100/min.

Question 333

specific issues w “re-do” card surg

Answer 333

Incr m&m
Re-entry injury: adherence of mediastinal structures to undersurface of sternum (CT may identify pts @ risk) risks cardiac injury on re-sternotomy. CPB set up ready to go.
Increasingly complex access to the heart (scarring, fibrosis), challenging dissection & suture placement, incr OT times.
May be higher risk due to the underlying condition that precipitated the redo.
Higher bleeding risk.
Incr risk of needing postop IABP, postop stroke, wound infection.

Question 334

ECMO

Answer 334

Indications:
For acute severe cardiac or pulmonary failure potentially reversible & unresponsive to conventional management.

Hypoxic resp failure with P/F <100mmHg despite optimisation of ventilator settings.
Severe ARDS with P/F <70
Hypercapnic resp failure w pH <7.2
Ventilatory support as a bridge to lung or heart transplant or placement of a VAD
Massive PE
cardiogenic shock or cardiac arrest, failure to wean from CPB following cardiac surgery.

Only contraindication:
conditions incompatible with recovery (severe neurology, end-stage malignancy). Relative CIs= uncontrollable bleeeding, very poor prognosis from primary condition.

Results in resp failure are better if ECMO within 7 days of intubation.

Blood is drained from vascular system.
Circulated by a mechanical pump,
Passed through heat exchanger.
Passes through oxygenator, where Hb fully saturated w O2, CO2 is removed.
Reinfused into circulation.

VA ECMO provides respiratory & haemodynamic support; blood extracted from RA, returned to arterial system, bypassing heart & lungs. Provides resp & haemodynamic support.
VV ECMO provides respiratory support; blood extracted from VC, returned to the RA (cannula out of IVC through fem vein, into RA via SVC).

Anticoagulated with hepairn.
cannulation via seldinger technique.
VV: usually fem vein & R) IJ, aim the outflow cannula @ junction IVC & RA, inflow junction SVC & RA.
VA: femoral vein to access IVC or RA for drainage, arterial cannula in R) femoral artery.

Following cannulation, blood flow increased until resp & haemodynamic parameters are satisfactory.
Aim SaO2 >90% for VA, >75% for VV.
SvO2 20-25% less than arterial.
adequate tissue perfusion (BP, venous SO2, lactate).
Once resp & haemodynamic goals achieved, maintain blood flow @ that rate. Frequent assess & adjust based on venous HbO2 sats. Adjustments include: increasing blood flow, increasing intravascular volume, increasing [Hb]. reducing temp to decrease systemic O2 uptake may help.

Anticoagulation sustained with continuous UFH infusion or direct thrombin inhibitor, titrated to an ACT of 180-210 seconds. Decrease the ACT target if bleeding.
POCT with ROTEM may help.
If AT3 deficiency suspected, measure; if <50% normal, replace AT3.
Platelets are constantly consumed; maintain >50 (may require plt transfusion).
Maintain Hb >120g/L.
Ventilator settings are reduced to avoid barotrauma & volutrauma & O2 toxicity; maintain Pplat <20cmH2O, FiO2 <0.5.
Early tracheostomy generally performed to reduce dead space & improve pt comfort.

Near-maximal blood flow rates are desired for VV ECMO (to optimise DO2). Flow rate for VA ECMO must be high enough for perfusion pressure & O2 sats but low enough for sufficient preload & LV output.

Diuresis is often warranted once the pt stable on ECMO (since most are fluid overloaded when ECMO initiated).

Constantly monitor LV output; pulsatility on art line waveform, frequent echo; consider inotropes or IABP.

Weaning:
-if resp failure, improvements in radiographic appearance, pulmonary compliance & O2 sats indicate the pt ready to be weaned from ECMO. Turn off the countercurrent sweep gas through the oxygenator but keep the extracorporeal blood flow constant; if manages well on ventilatory, can wean.
-with cardiac failure, enhanced aortic pulsatility correlates with LV output & indicates the pt may be ready to be liberated from ECMO. Temporarily clamp the drainage & infusion lines (keep them circulating with heparinised saline); VA ECMO trials are shorter due to higher risk thrombus formation.
Cannulae removed, haemostasis by compressing site (VA, @ least 30mins compression @ arterial site).

Complications:

-Mainly bleeding & thromboembolism;

-Bleeding= due to continuous anticoagulation & plt dysfunction. meticulous surgical technique, maintaining plt >50,000, maintaining target ACT all reduce bleeding.

-Thromboembolism= due to thrombus formation in the circuit. Higher impact with VA ECMO due to infusion into systemic circulation. Ensure anticoagulation @ target, vigilant observation of circuit for signs of clot formation, sudden change in pressure gradient across oxygenator suggests thrombus development. If clots, immediate circuit/component exchange (have primed circuits @ the bedside).

-femoral site for VA cannulation preferred (relatively easy), risks ischaemia ipsilateral LL. If use common carotid, risk watershed cerebral infarction. Subclavian another option.

-vessel perforation/haemorrhage, arterial dissection, distal ischaemia, incorrect cannulation.

-cardiac failure (in pts having ECMO for CPR) is 50%

-neurologic injury for resp failure pts 10%

-HITTs: change anticoagulant eg. argatroban which has short half-life & similar ACT target range.

renal failure

infection

VA ECMO-specific:

-PULMONARY HAEMORRHAGE is a complication specific to VA-ECMO; impaired LV ejection may lead to incr LV & LA pressure; pulm oedema occurs when LA pressure >25mmHg- may indicate need for immediate decompression to avoid (eg. insertion drainage cannula LA or LV vent).

-Cardiac thrombosis can occur if stasis of blood (if LV output not maintained).

-Differential hypoxia is a risk specific to VA ECMO; fully saturated blood infused into the femoral artery preferentially perfuses LLs & abdo viscera, blood ejected from heart selectively perfuses heart, brain, ULs. The blood perfusing lower part may have higher O2 sats. MONITOR SpO2 in R) UPPER EXTREMITY to avoid unrecognised cardiac & cerebral hypoxia. May correct poor upper extremity hypoxia by infusing oxygenated blood into RA.

ECMO vs CPB:
ECMO long-term (eg. up to 30 days) heart & lung support to allow intrinsic recovery of heart & lungs.
CPB typically via transthoracic cannulation under GA while ECMO may be done under LA
CPB operated by perfusionists.
CPB allows bloodless surgical field & supports various types of surgical procedures.

CPB may be used for non-cardiac surgery if:
-mediastinal mass or tracheal cases
-lung transplant
-liver transplantation
-large aneurysms (eg. aortic, cerebral)
-pulmonary thromboendarterectomy or thrombectomy

Question 335

Postop cardiac surg:

Answer 335

Common for haemodynamic instability 6-12hrs following cardiac surg w CPB, depending on severity of underlying cardiac disease (ventricular function) & key intraop events (haemodilution, blood products, duration CPB & AXC, myocardial protection).
-H2O & Na overload: despite intravascular vol relatively low, diuresis may be needed.
-SIRS: inflammation, coagulopathy, organ dysfunction. 12-24hrs of worsening organ dysfunction & coagulopathy generally proportional to duration of CPB.
-Myocardial dysfunction: ischaemia (attenuated by cardiooplegia & hypothermia) but then ischaemia-reperfusion w release of AXC; may worsen myocardial dysfunction 12-24hrs.

Goals:
Adequate DO2: Hb >=75 unless other pt/procedure-specific target, Hc 21-24%, SpO2 >90% (avoid hyperoxia), CI >2L/min/m2 (without PAC, use clinical surrogates eg. peripheral perfusion, lactate, ScVO2, UO, haemodynamic parameters. Can use TOE if pts with inadequate DO2 unresponsive to fluids inotropes.

Haemostasis: Blood in chest tubes <400mL/hr in first postop hr, <200mL/hr first 2hrs.

Sedation: short-acting (prop +/- fent), aim for EXTUBATION WITHIN 6HRS OF ICU ARRIVAL IF ROUTINE CARD SURG, ESP ERACS. Avoid BZD (delirium, incr mech vent & ICU stay)

Analgesia:
ERACS multimodal, opioid-sparing, age-adjusted; local & regional
Frequent pain assessment vital: behavioural pain scale if pt can’t communicate (facial expression, UL movements, compliance w mech vent): important to manage pain appropriately to limit risk pulm complications, CV complications (catecholamines), delirium.
Paracetamol, opioids (oral once PO intake established), limit duration & dose (adverse effects sedation, ileus, delirium), PONV Rx.
Avoid NSIADs due to risks renal dysfunction (if pre-existing dysfunction or sig bleeding). controversial w concern re: thrombotic complications, also NSAIDs incr CVR (sl higher RR for Coxibs).

Question 336

Postop cardiac surg:

Answer 336

Common for haemodynamic instability 6-12hrs following cardiac surg w CPB, depending on severity of underlying cardiac disease (ventricular function) & key intraop events (haemodilution, blood products, duration CPB & AXC, myocardial protection).
-H2O & Na overload: despite intravascular vol relatively low, diuresis may be needed.
-SIRS: inflammation, coagulopathy, organ dysfunction. 12-24hrs of worsening organ dysfunction & coagulopathy generally proportional to duration of CPB.
-Myocardial dysfunction: ischaemia (attenuated by cardiooplegia & hypothermia) but then ischaemia-reperfusion w release of AXC; may worsen myocardial dysfunction 12-24hrs.
-inotropes/vasopressors weaned as pathophys of CPB resolves.

Goals:
Adequate DO2: Hb >=75 unless other pt/procedure-specific target, Hc 21-24%, SpO2 >90% (avoid hyperoxia), CI >2L/min/m2 (without PAC, use clinical surrogates eg. peripheral perfusion, lactate, ScVO2, UO, haemodynamic parameters. Can use TOE if pts with inadequate DO2 unresponsive to fluids inotropes.

Haemostasis: Blood in chest tubes <400mL/hr in first postop hr, <200mL/hr first 2hrs.

Sedation: short-acting (prop +/- fent), aim for EXTUBATION WITHIN 6HRS OF ICU ARRIVAL IF ROUTINE CARD SURG, ESP ERACS. Avoid BZD (delirium, incr mech vent & ICU stay). Prolonged intubation incr morbidity, mortality, cost.
To optimise chances timely extubation, ongoing judicious fluid, temp control, lung prot vent, limit BZD, opioid-sparing, reverse NMBAs (only reverse when pt warmed to >36deg c to avoid shiver). wonce reversed, wean sedation, once pt awake & follows commands, PSV & spont breathing trial.
Following extubation, nasal O2 (NHF or NIV if preop hypoxaemia or COPD). CPAP for those w severe OSA.

Lung protective ventilation reduces postop pulm complications:
6-8mL/kg IBW
RR 10-14 (adj based on PaCO2)
PEEP 5-8cmH2O (may need higher if pulm oedema)
Pplan <20cmH2O
low driving pressure (PP-PEEP) at <15cmH2O

Analgesia:
ERACS multimodal, opioid-sparing, age-adjusted; local & regional
Frequent pain assessment vital: behavioural pain scale if pt can’t communicate (facial expression, UL movements, compliance w mech vent): important to manage pain appropriately to limit risk pulm complications, CV complications (catecholamines), delirium.
Paracetamol, opioids (oral once PO intake established), limit duration & dose (adverse effects sedation, ileus, delirium), PONV Rx.
Avoid NSIADs due to risks renal dysfunction (if pre-existing dysfunction or sig bleeding). controversial w concern re: thrombotic complications.
thoracic nerve blocks could be considered.

Arrhythmias: AF the most common post card surg, days 2-5, metoprolol 12.5-25mg BD or TDS as soon as haemodynamics allow. alternatives amiodarone or sotalol, atrial pacing.nantioxidant vitamins (C, E)

Cardiac arrest:
most in the first 5 postop hrs.
most common causes: ischaemia (eg. air in coronary circ, graft inadequacy), sig bleeding, cardiac tamponade, PTx, arrhythmias, loss of pacemaker capture).
MANAGEMENT:
-don’t immediately initiate cardiac compressions- risk disruption surgical repair.
-don’t give full 1mg epinephrine (may incr BP ++, could disrupt arterial suture lines). 50mcg incrementally.
-avoid atropine for asystole or severe brady, use pacing instead.

Steps:
1. identify rhythm
-if VF or pulseless VT, 3 successive defib shocks 150J, 300mg IV amiodarone.
-if bradycardia or asystole: DDD pacing 80-100bpm w maximal current settings (atrial 20mA, vent 25mA).
-if PEA, halt pacemaker to ensure not VF. If PEA confirmed, external cardiac compressions while opening the chest.

Also open the chest if VF, VT, asystole or severe brady are unresponsive to initial measures after 1 min.
-CPR while open chest through fresh sternotomy wound (within 5 mins)
-internal cardiac massage 100-120/min
-discontinue mech vent & sedation, manually vent w ambu bag w FiO2 @ 1.0 & rate 2 breaths: 30 compressions
-switch IABP triggering mode to arterial tracing
-internal defib 20J/s for VF
-continue resus w internal cardiac massage, epinephrine, internal defib or pacing as indicated.

Delirium:
non-pharmacologic:
-sensory input (glasses, hearing aid)
-normal sleep patterns
-cognitive stimulation
-encourage MOBILITY
-hydration & nutrition
-analgesia
-investigate treatable causes (med-induced, substance withdrawal, other medical conditions)

Asymptomatic stroke common on MRI, not nec ass’d w worse neurocog outcome.
MRI to Dx, manage BP & ensure adequate perfusion (Rx >220/>120 or lower target as d/w surgeons, supplemental O2 for SpO2 >92%, hyperglycaemia treated but not too low, avoid fever. consider mechanical thrombectomy (thrombolysis & anticoag avoided!), antiplts (aspirin or clopidogrel) unless absolute contraindications. Statin usually recommended anyway. consider HBOT if surgical air embolus.

BGL 7.7-10. poor glucose control incr M&M.

Oral diet asap.

mobility: chest physio within hours, chair postop day 1, mobilise w assistance 3x/day after physio evaluation.
Early mobility reduces infections, delirium, VTE & other complications (eg. muscle mass loss, sleep disturbance, insulin resistance)

-VTE prophylaxis: mobility, mech prophylaxis, pharmacologic on night of surgery once haemostasis attained; heparin 5000IU subcut BD.

First 24hrs focus on:
early PO intake, PONV prevention, multimodal analgesia, delirium screening, early ambulation.
POD1 remove invasive monitors & IDC.
remove drains once output <100mL per 8 hrs for 2x 8hrs.

ERACS: standardised multi D multimodal interventions spanning pre/intra/op aiming to minimise stress response to surg & anaes, achieve early extubation, shortened ICU & hospital stay, reduce complications & improve outcomes.

Pre-op:
-pre anaes consult incl education re: meds, planned use of multimodal, expectation of early extubation & postop recovery in ERACS programs.
-pt blood management principles (identify diagnose optimise anaemia)
-some pts benefit from prehab (eg. if frailty, malnutrition, cognitive dysfunction, smoking cessation needed).

Day of surgery:
-multimodal opioid sparing analgesia (short-acting opioid only).
-panadol pre-incision, neuraxial for selected.
-minimise BZD.
-follow fasting guidelines, ensure not excessive fast (clear fluids up to 2hrs)
-limit meds which impair neurocog (bzd, anticholinergics, opioids), BIS & avoid excessive depth anaesthesia; literature conflicting but avoid deep, NIRS.
-lung-protective vent w low driving pressure & PEEP
-overall restrictive fluids given CPB= haemodilution. zero-balance pre & post bypass. TOE-guided fluid resus (small LV @ end-diastole, small IVC). PAC, oes doppler, SVV.
-POCG-guided coagulation tests & transfusion.
-haemodynamic management: adequate CPB pump flow for MAP 50-80mmHg (higher if elderly, cerebrovasc disease)
-thermoregulation; aim nasopharyngeal temp 37 for esparation from CPB, core temp at least 35.5. actively warm to normothermia & maintain postbypass & postop.
-BGL 7.7-10.
-PONV prophylaxis.

Postop:
early extubation, mobility, enteral intake, VTE prophylaxis, normal sleep/wake cycles, multimodal analgesia opioid sparing, anti-emetics.

Question 337

Doses for P2Y12 inhibitors after acute STEMI

Answer 337

prasugrel 60mg load then 10mg/day
ticagrelor 180mg load then 90BD
clopidogrel 600mg load then 75mg/day

Pts undergoing invasive approach, delay P2Y12 until diagnostic angiography.

Ticagrelor superior efficacy cf clopi
clopi lower bleeding risk cf prasu

Withold prasugrel 7 days preop
ticagrelor & clop 5 days

Question 338

Cutoff ventilatory efficiency for predicting 90-day mortality

Answer 338

39 (minute ventilation: CO2 excretion)

Question 339

Benefits of NSQIP:

Answer 339

mortality & morbidity, looks at many types of complicationseg. VTE, renal failure, discharge to a health facility

SORT= 30 day mortality
LRCRI: 30 day death, cardiac arrest, non-fatlal MI
euroscore risk in-hospital mortality after cardiac surgery

Question 340

CCS angina grades

Answer 340

I-IV
I: ordinary physical activity (eg. walk, climb stairs) NO angina, angina with strenuous.
II: slight limitation ordinary activity: angina if fast walk or up stair/hill or after meals/cold/wind/emotional stress.
III: marked liitation ordinary activity. 1-2 blocks level, one flight stairs normal pace= angina.
IV: unable to do any physical activity without discomfort. may have rest angina.

Question 341

How to manage risk MINS:

Answer 341

Pre: no known methods, consider B blockers, statins, witholding RAAS inhibitors
Intra: BP control: MAP <=65mmHg or rel decr 30% from baseline is ass/d w MINS
degree & duration impacted cardiac mortality & injury
systolic, map & diastolic all important
Postop: monitoring
MANAGE study LANCET 2018: dabigatran after MINS lowers risk major vascular ocomplications sans incr bleeding risk

Question 342

How to manage risk MINS:

Answer 342

Pre: no known methods, consider B blockers, statins, witholding RAAS inhibitors
Intra: BP control: MAP <=65mmHg or rel decr 30% from baseline is ass/d w MINS
degree & duration impacted cardiac mortality & injury
systolic, map & diastolic all important
Postop: monitoring
MANAGE study LANCET 2018: dabigatran after MINS lowers risk major vascular ocomplications sans incr bleeding risk

Question 343

How to manage risk MINS:

Answer 343

Pre: no known methods, consider B blockers, statins, witholding RAAS inhibitors
Intra: BP control: MAP <=65mmHg or rel decr 30% from baseline is ass/d w MINS
degree & duration impacted cardiac mortality & injury
systolic, map & diastolic all important
Postop: monitoring
MANAGE study LANCET 2018: dabigatran after MINS lowers risk major vascular ocomplications sans incr bleeding risk

Question 344

What does ESC 2022 recommend wrt valves?

Answer 344

symp or asympt severe AR, valve surgery recommended before elective intermediate or high-risk NCS
asympt severe AS elective high-risk NCS, consider SAVR or TAVI in liaison w Heart Team. if time-sensitive NCS, could consider BAV.

for MR, severe (symp or asympt severe w LV dysfunction) shoud have valve intervention before intermed or high-risk NCS if time allows. Consider valve intervention for severe secondary MR pts who are symptomatic despite GDMT if acceptable procedural risk.

Question 345

ESC 2022 guidelines re: dyspnoea & HF?

Answer 345

get BNPs for pts w dyspnoea/peripheral oedema (along with ecg) unless known non-cardiac. Get TTE if BNP elevated prior to NCS in pts w dyspnoea/peripheral oedema. regularly assess volume status & signs organ perfusion intra-op for pts w HF undergoing NCS.

Question 346

ESC arrhythmia guidelines:

Answer 346

AF & instability: emergency electrical CV
syptomatic monomorphic sustained VT despite optimal medical therapy (if myocardial scar), ablate before elective NCS
defer until PPM if indications for pacing exist
consider ablation for pts w symptomatic, rucurrent or persistent SVT despiite other Rx, prior to high-risk non-urgent NCS

Question 347

where do the leads go for PPMs?

Answer 347

RV single lead, RA & RV dual chamber
Biventricular: RV & LV (via coronary sinus)

Question 348

What’s antitachycardia pacing?

Answer 348

ICDs have it (& pacemaker function)
A burst of overdrive pacing is used attempting to terminate VT (it’s less painful & uses less battery than shock). if still VT, shock delivered.

Question 348

What’s antitachycardia pacing?

Answer 348

ICDs have it (& pacemaker function)
A burst of overdrive pacing is used attempting to terminate VT (it’s less painful & uses less battery than shock). if still VT, shock delivered.

Question 349

consider device reprogramming if:

Answer 349

sig dependence, advanced CEID functions (eg. rate responsiveness triggered by MV, sleep/rest mode), positioning not possible for magnet (OT close to device, prone)

Question 350

Pacemaker dependency definition

Answer 350

Pacemaker dependency was defined as the presence of a complete atrioventricular dissociation in patients in sinus rhythm or the presence of an escape rhythm <50 beats per minute in atrial fibrillation patients, combined with a percentage of ventricular pacing since implantation >90%.

Question 351

ESC HTN categories:

Answer 351

normal <120 & <80
elevated 120-129 & <80
stage 1 HTN 130-139 or 80-90
stage 2 >=140 or >=90
hypertensive crisis >180 or >120

Question 352

ESC 2022: which pts having elective PAD or AAA surgery should have cardiac workup & optimisation

Answer 352

Poor functional capacity or significant risk factors or symptoms (eg. Mod-severe angina, decomposition HF)

Question 353

what’s peripartum cardiomyopathy?

Answer 353

Heart failure in last onth preg. or 5/12 postpartum in absence of prior heart disease, no determinable cause, strict echo indication of LV dysfunction (EF <45% or fractional shorterning <30% or end-diastolic dimension >2.7cm per m2 BSA, 1:1500-4000)

echo usually shows dilation (not always)

Ass’d. wincr mortality rate (particularly vent arrhythmias, HF, sudden death, TE events)

Partial or complete LV recovery is common, more common than other types of DCM
There is risk recurrence in subsequent pregnancies & adverse outcomes (particularly if LVEF was <=25% @ Dx or. ifit didn’t improve to >50% btwn pregs; such pts should be counselled to avoid future pregnancies).

Mx:
1. STABILISE
2. oxygen, assist vent as needed
3. -optimise preload
-fluid balance & diuretics
-treat coexisting conditions
-consider dig (class C) for atrial arrhythmias
-anticoag
-B blockers
-inotropic support
-vasodilators (hydralazine C, nitrates, amlodipine (C) antepartum. postnatal: ACE-I or ARBs). Avoid ARNIs D, ACE-Is, ARBs, mineralocorticoid receptor antagonists in pregnancy (CI).
evidence re: immune therapy inconclusive.
2. Delivery: obs indications multi-D
3. mechanical circulatory support & device therapy (ICD, IABP, LVAD)
4. heart transplant

Question 354

Management for HF:

Answer 354

Stage A (at risk):
Mx BP as per GDMT
if T2DM & established CVD or high CV risk, SGLT2i to prevent hospitalisations for HF

Question 354

Management for HF:

Answer 354

Stage A (at risk):
-Mx BP as per GDMT (aim <130/80 if CVD risk is >=10%)
-if T2DM & established CVD or high CV risk, SGLT2i to prevent hospitalisations for HF & to improve survival
-lifestyle: exercise, wt, diet, smoking (for all)
-at risk pts screening with BNP then GDMT & team-based care can help with prevention

Stage B:
if LVEF <=40%, ACE-i, ARB if intolerant of ACE-i, B blocker
pts with LVEF <=30%, >1yr survival, >40d post MI who have NYHA 1 symptoms while receiving GDMT: ICD (primary prevention sudden cardiac death, reduce total mortality)

mort benefit: ACEi (impede maladaptive remodelling), ARB, B blockers reduce mort (for pts w recent or remote MI or ACS & LVEF<=40%, cardio-specific B blockers reduce mort). If prev MI or ACS, statins for prevention of symptomatic HF & adverse CV events.
B blockers improve symptoms of HF in pts w LVEF <=40%, impede adverse remodeling
ACEi impede maladaptive remodeling after acute MI, reduce mort, HF hospitalisations, progression to severe HF cf placebo.
AVOID thiazolinediones if LVEF <50% (incr risk HF incl hospitalisations), if LVEF <50%, non-dhp CCBs w -ve inotropic effects may be harmful.

HFrEF <=40% (stage C)
ARNI in NYHA II-III (reduces M&M further to ACEi or ARB (don’t give ARNi + ACEi or within 36hrs of last dose); ARNi improve health status, reduce NT-proBNP & improve LV remodeling cf ACEi/ARB, reduce HF hospitalisation. more hypotension w arni cf acei.
ACEi or ARB in II-IV (reduces M&M, useful when ARNI not fesible) no arni. or acei if angoiedema (arb ok)
B blocker (carvedilol, SR metoprolol or bisoprolol) reduce mort & hospitalisations
MRA reduce M&M, if eGFR >30 & K <5. monitor K & renal function carefully.
SGLT2i reduce mort & hospitalisations, irrespective of T2DM
diuretics prn for decongestion, improve symptoms, prevent worsening HF. start with loop, then add thiazide. aim. wdiuretics= lowest dose for euvolaemia, aim to eliminate clinical evidence of fluid retention. MRA have mortality benefit, others no known mort effect so always combine diuretics w other GDMT.

could consider hydralazine/ISDN if african amergican w optimal therapy, or if can’t tolerate other agents

could consider ivabradine if NYHA II to III, HFrEF (<=35%) w GDMT @ max tolerated dose, sinus w HR >=70bpm @ rest. Ivabradine may reduce HF hospitalisations & CV death.
Consider Vericiguat (oral soluble guanylate cyclase stimulator, targets cGMP pathway, smooth muscle relaxation & reduced hypertrophy, inflammation, fibrosis) if II-IV, LVEF <45%, recent HFH, elevated NP levels
digoxin: if HFrEF symptomatic despite GDPT, it may reduce hospitalisations in HF.

consider ICD if NHYA II-III, LVEF <=35%, >1yr survival: for primary prevention SCD
if the above but NYHA I, consider ICD if LVEF <=30%

Consider CRT in pts w cardiomyopathy or HFrEF &:

consider CRT-D if NYHA II-III, ambulatory IV, LVEF <=35%, NSR & QRS >=150ms w LBBB

Pts w HF on GDMT >3mo & >40d after MI, >1yr expected survival, LVEF <=35%,
If NYHA II-Amb class IV, consider if LBBB >=150ms (class 1 recommendation; lower grades if non LBBB or shorter QRS)

If NYHA 1 consider if LVEF <=30%, ischaemic CM, LBB >=150ms
consider if AF or sinus w RV pacing frequent or anticipated
consider if LVEF 36-50% if high degree or complete HB
refractory consider transplant

low sodium diet to reduce congestive symptoms, exercise, cardiac rehab, omega-3 polyunsaturated fatty acid, avoid NSAIDs

Avoid:
NSAIDs (PG inhibition incr Na & water retention, SVR, blunt response to diuretics)
Thiazolinediones (may CCB)
Flecainide= -ve inotrope w proarrhythmic effects
Sotalol has proarrhythmic properties & B blockade
CCCBNs non-DHP: -ve inotropy
thiazolinediones (incr insulin sensitivity) incr fluid retention & HF events
DPP-4 inhibitors enhance glucose-dependent insulin secretion, slows gastric emptying, reduces postprandial glucagon.