Cardiac Flashcards
How to evaluate nature of cardiac disease?
H&P and ordering appropriate labs
- History: -known diagnosis, past evaluations/hospitalizations, tests, meds/compliance
- cardiac sx (past and current): exercise tolerance, CP, SOB, syncope, orrthopnea, palpitations SAD POE - PE: signs for HF -Rhythm, murmurs, S3 gallop, crackles, edema, JVD
3: Labs: CXR EKG, echo
How do you know when pt is optimized
signs and sx controlled to minimize surgical complications
when should one order a cardiac consult
After assessment, unable to determine nature of disease or I believe pt is not optimized for scheduled (not emergent) surgery
What is one met? 4 mets?
1 met= resting state 3.5.ml/kg/min >4 mets walking up flight stairs or hill
METS<4: eat, dress, use toilet, walk around, walk a block or 2 on level ground slowly
METS=4: light housework, climb a flight of stairs
METS>4: walk@4 mph, run short distances, heavy housework, moderate recreational activities
METS>10: participate in strenuous sports
How do you evaluate a patient periop cardiac risk
identify any active cardiac conditions
identify surgical risk
idenify fxn status
- no risk factors, proceed to OR.
- 1-2, proceed to OR with HR control, or consider non-invasive testing if it will change management. -3 or more and undergoing intermediate risk surgery proceed to OR with HR control, or consider non-invasive testing if it will change management.
- If the patient has 3 or more and undergoing vascular surgery, consider testing if it will change management.
When to obtain preop EKG
Pre-operative EKG, with a level of evidence B:
There is no Class I recommendation for acquiring an EKG.
In a patient with known coronary heart disease, going for moderate or high risk surgery, (Class 2a recommendation)
In patients without known heart disease, going for moderate to high-risk surgery, ( Class 2b recommendation)
There appears to be no benefit for asymptomatic patients going for low risk surgery
When is it reasonable to evaluate LV fxn preoperatively
There is no Class 1 recommendation, all 2a
reasonable to evaluate LV function in
- patients with dyspnea of unknown origin
- patients with known heart disease with worsening dyspnea or change in clinicsl status
- clinically stable pt with prior LV dysfunction with no eval in >12 months
RCRI and MACE %
what qualifies as CAD
Revised Cardiac Index
Risk factors are: history of ischemia or heart disease, CHF, CVA, Cr > 2.0, IDDM, high risk surgery
CAD: unstable angina, MI, use nitrate, , active + stress test, path q wave
0-0.4% risk of cardiac complications
1-0.9% risk of cardiac complications
2-7% risk of cardiac complications
3-11% risk of cardiac complications
Active cardiac conditions
- Unstable coronary syndroms:
unstable angina (ACS)
recent MI (30 days)
- Decompensated heart failure
- Significant arrythmia:
High grade AV block, Mobitz II AV block, 3rd degree block
Symptomatic ventricular arrythmia or sx brady
SVR with HR>100 at rest
Newly recognized ventricular tachycardia
4: Severe valvular disease:
1. Severe AS (Mean gradient >40 mmHg, aortic valve area <1 cm2, or symptomatic)
2. Symptomatic MS (DOE, exertional presyncope, or heart failure)
Low risk/intermediate/ high risk surgery
ABCEs
Low risk <1%: ambulatory, breast, cataracts, endoscopic, superficial
Intermediate risk: 1-5%
- carotid endarterectomy, head/neck,
- Intraperitoneal/Intrathoracic,
orthopedic, prostate
High risk: aortic/other major vascular procedures, peripheral vascular surgery >5%
ST elevation vs depression
depression indicate ischemia:
New horizontal or downsloping ST-depression ≥0.5 mm in two contiguous leads and/or T inversion >1 mm in two contiguous leads with prominent R wave or R/S ratio >1.
elevation: epicardial ischemia-vasospasm, infaraction (rare during non cardiac surgery)
New ST-segment elevation at the J-point in two contiguous leads with the cut-points:
-≥1 mm in all leads except V2-V3.
V2-V3: ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, or ≥1.5 mm in women regardless of age.
How would you treat myocardial ischemia
- Look at vitals
- 100% O2
- tachy and HTN: deepen anesthetic BB
hypotensive and tachy: phenypehrine, fluids
arythmias: cardiovert/defib, anti-dysarythmic,
consider nitro in absence of hypotension
Induction in patient with severe CAD
Goal: optimize myocardial supply and demand: avoid tachycardia, hypotension, hypertension, hypoxia, excessive contractility. suffiently blunt sympathetic stim during laryngoscopy
- aline, pressors like phenyephrine available, esmolol available (fast onset, short duration B1 selective)
- induce with etomidate (min CV side effects), lido (blunt laryngoscopy), fent
Difficult airway: awake fiberoptic with adequate topicalization sedation, to avoid tachycardia and HTN
When is risk for periop MI the greatest
First 3 days post op
myocardial supply and demand factors
supply: HR, CPP=AdP-LVEDP, hypotension, O2 content, coronary artery diameter
Demand: tachycardia, wall tension (preload and afterload), contractility
HTN consideration head to toe
perioperative risks,
preop assessment
potential causes
Head to toe
neuro: shift in cerebral autoregulation, stroke, retinopathy
cards: LVH, CAD/MI, arrythmia, CHF (diastolic dys)
renal: overactivity of renin angiotensin-aldosterone system, CKD
concerns : BP instability, arrythmias, MI, stroke, CHF, hypoperfusion/end organ ischemia w reduction
Preop:
History:
- cause (essential, coartation aorta, OSA/obesity renal, endocrine-pheo, hyperaldosterone, cushing, thyroid/parathyroid),
- degree of control, baseline, meds
- end organ effects
PE: signs CHF
Labs: BUN/Cr-renal involement, NA K diruetic effects
EKG for LVH (S in V1 + R in V5 or V6 ≥ 35 mm), arrythmia, ischemia, strain (ST depression and T-wave inversion)
CXR: cardiomegaly, pulm edema
Goal: keep BP within 20% of baseline
Indication for central cathter or PAC, TEE, a line
CVC
- monitor CVP/fluid status
- venous access in pt w poor access, drug/hyperailmetation infusion
- pacing
- aspiration of air during venous emboli
PAC
monitor filling pressures, PAP, PCWP, CO, MV02, SVR, PVR
TEE
- eval global fxn
- RWA (Most sensitive indicator of ischemia)
- fluid status
- estimate preload (filling pressures
- judge accuracy of cardiac procedures
- assess unexplained hemodynamic disturbances
a line
- monitor BP on a continuous beat to beat basis,
- ABG freq sampling
- CPB (non pulsatile flow)
How much does perfusion pressure decrease for every cm above heart
0.7–> 10cm is 7mmHg
RF for PA rupture with PAC
elderly
AC or coagulopathy
PHTN
hypothermia
overinflation of balloon
What conditions confound ischemia detection?
LVH/strain: LV strain pattern: ST depression and T wave inversion in the lateral leads
LBBB; Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-V6))
digoxin: Downsloping ST depression with a characteristic “Salvador Dali sagging” appearance Flattened, inverted, or biphasic T waves.
pacing: ride side looks like RBBB
Causes increased MV02
- most common- wedged PAC
- sepsis (increased CO, decreased Vo2)
- cirrhosis (increased CO)
- hypothermia (decreased VO2)
- cyanide toxicity (increased CO, decreased V02)
causes that impair ability of proximal pressure CVP PCWP of relecting downstream pressures?
Aneursym types acccording to Crawford
most difficult to repair. highest risk of paraplegia/renal failure
Type 2,3
Type 2
Aortic dissection types
5 types of endoleak
- proximalor distal graft attachment leak sites
- retrograde slow into sac from side branches intercostal artery
- defect/tear in graft or overlap issue
- graft wall porosity
- increaseed aneursym diameter without idenificable cause
I and 3 may require urgent intervention 2,4 usually not
How does SNP infusion lead to toxicity
signs
tx
SNP enters RBC and release NO and formation of CN.
CN can bind to methemoglobin (cyanometheoglobin), thiosulfate (thiocyante) or bind to cytochrome oxidase impairing oxygen utilization.
metabolic acidosis, increased MV02, arrythmias, tachyphylaxis
minimal risk if infusion kept below 0.5 mg/kg/h
tx: 100% O2, sodium thiosulfate, amyl nitrate or sodium nitrate –>oxidize hemoglobin to met hemoglobin, B12
Difference between pre and post ductal coartation
- Coartation
- Post ductal: upper extremity HTN later in life
- Preductal: LE cyanosis as PDA closes
Concerns with a enlarging thoracic aneursym
- Compression
- structures: trachea, bronchus: difficult intubation (DLT L bronchus may be compressed) hemoptsis
- nerves: SLN, RLN (hoarseness)
- vasculature: SVC syndrome
- Thrombosis/emboli
- Rupture/massive bleeding
- Dilation aortic root (AI)
concerns with an expanding throacic dissection
- AI
- ischemia (extension into coronaries)
- stroke (extension to innominate or carotid),
- pericardial tamponade,
- hemothorax (rupture into pleura)
- CXR: widened mediastinum suggests mediastinal bleeding
Concerns for a aneursym repair
- Anesthesia
- Difficult airway-compression (airway compression, SVC syndrome edma), DLT
- Cross clamp
- neuro
- Paraplegia-
- Loss motor with intact vibration and proprioception, sensory (ASA syndrome)
- epidural hematoma if neuraxial performed
- Stroke: emboli, hypotension
- Paraplegia-
- CV
- Aneurysm: rupture, thrombosis, compression (SVC, AI
- MI, CHF
- Pulm
- Post op pulmonary dysfxn from manipulation of diaphragm and lungs
- Damage to phrenic or RLN
- GI: mesenteric ischemia
- Heme
- Coagulopathy: activation of coagulation (aneurysm thrombogenic), DIC
- dilution effects of massive transfusion,
- Renal
- Post op AKI
RF for paraplegia for aneursym repair
- rupture/emergency
2. prolonged cross clamp
3. location and extent of aneurysm
- detachment of radicular arteries
- advanced age
- vascular insufficiency
Induction goal for aneursym
- Avoid HTNaneurysm rupture while avoiding precipitous drops in BP myocardial ischemia
Monitoring for aneursym
- Aline
- Potential for hypertension above clamp and inadequate perfusion below–> place proximal and distal.
- During cross clamp upper a line would provide info about cerebral and cardiac perfusion while lower a line would allow monitoring of distal perfusion pressure to kidney, spinal cord, mesentery.
- A line on L for ascending repair, and a line on R for descending repair ( clamp often placed proximal to L subclavian in surgery involving proximal descending aorta)
- PAC helpful?
- In pt with poor functioning myocardium or suprarenal clamp
- Increase PCWP after clamp may indicate myocardial ischemia
- Lumbar drain
- Spinal cord perfusion: distal aortic pressure-ICP or CVP
- Passive drainage of CSF to a pressure of 8-10mmHg during procedure and 48 hrs post op
- Zero to mid axillary line or external auditory meatus when supine
- Clamp induced increases CSF pressure: hyperemia above clamp increased ICP–>redistribution CSF into intrathecal space increased
- Neuromonitoring
- SSEP to monitor for cord fxn: monitors posterior column but predicts anterior function as well
How is spinal cord perfused?
- 2 posterior spinal cords supply posterior 1/3 of spinal cord
- Single anterior spinal artery (from basilar and vertebral ) supplies anterior 2/3 of cord motor) with contribution from radicular arteries most important being Adamkiewicz (major supply of lower 2/3 of spinal cord T9-T12 60% time)
Physio effects of cross clamp placement and removal
- Supraceliac: preload increases (redistribution from splanchnic circ), infraceliac may decrease (blood pools in splanchnic circ)
- preserved LV fxn: increase preload increase afterload, increase CO and contractility (2/2 increase preload and afterload), poor fxn- decreased contractility may occur with reductions in CO
- PCWP may increase due to increase preload, increase afterload, ischemia (LVEDP increases without increase AdP
- Spinal cord perfusion decreases
- Distal aortic pressure decreases, CSF pressure increases (hyperemia from upper HTN)
- Metabolic: increased catecholamine release, decreased MV02, decreased total body oxygen consumption, metabolic acidosis
- Release: hypotension 2/2 distal pooling blood, ischemia mediated vasodilation, release of vasoactive mediators and myocardial depressants
What determines the effect of aortic cross clamp on BP
- Level of clamp: supraceliac more HTN
- Severity of cardiac dz-poor myocardial diseases predisposes to hypotension and ischemia
- Presence of occlusive disease-associated with dev of collaterals and less HTN with clamp
- Sympathetic tone and volume status: hypovolemia and low sympathetic tone reduce preload lessening HTN
How to reduce harmful effects of aortic cross clamp
- Appropriate monitors: prox and distal aline, PAC
- Vasodilator for clamp placement
- Long clamp times expected consider shunt
- Aortic arch involved consider DHCA
- End organ protection for kidney and cord
How to prepare for cross clamp release?
- admin vasodilator to facilitate volume loading
- d/c vasodilator just prior to release (guide w TEE or PCWP), and lower depth anesthesia
- correct any electrolyte abnormalities, acid base or coagulopathy
- inotropes and vasopressors available to tx sustained reductions SVR
- ask for slow release of clamp-lessen the suddenness of hypotension allow time for physiologic compensation or medical intervention
What do you do if there is ischemia when clamp placed?
- Remove clamp, 100% oxygen
- If improve with release: lower systolic pressure with vasodilator (SNP, NO, nicardipine),
- Goal: reduce afterload to avoid cardiac ischemia but maintain adequate perfusion to coronaries and tissues distal to clamp
- Ask to shunt
How to minimize cord ischemia during cross clamp of aorta?
- Avoid hypotension MAP>80, maintain normal Hct and PaO2, (monitorand maintain adeuwate MAP above and below cord)
- Avoid hyperglycemia
- Lower ICP w spinal drain (15cc / 15 min max 60cc) ICP 8-10
- Monitor cord with SSEP MEP
- Careful with vasodilators or high conc on inhalational agents (vasodilation increase ICP which transmitted to cord and lower distal perfusion)
- Min clamp time, use shunt, reattach segmental arteries
- Passive Hypothermia to 34 for prolonged clamp time (decrease CMRO2 5% for each 1C)
- Intrathecal papervine for spinal cord vasodilation
Measures to reduce renal damage during aortic cross clamp?
- Maintain normovolemic state and renal perfusion pressure
- hyothermia 34
- Surgical: short cross clamp time,consider shunt
- Drugs
- Contrast used ask for nonionic, iso-osmolar, low in viscosity
- Avoid nephrotoxins: ASA, ACE, aminoglycosides, NSAIDs
- Renal protective drugs: no evidence for improved outcomes
- Mannitol
- Dopamine-theoretical ability to improve renal blood flow and UOP, esp if concomitant hypotension
- Fenoldopam- dopamine agonist that dilates renal vasculature (splanchnic as well), use when HTN
- N acetyl cysteine (replenish glutathione)
Theortical advantage of mannitol for admin prior to cross clamp (6)
- scavenges oxygen free radicals
- lower blood viscosity
- improve renal cortical blood flow
- increase renal prostaglandins
- reduce renal renin release
- diuresis may maintain renal tubular patency (reducing likelihood of oliguria and problems w fluid management
Risk factors for renal ischemia after cross clamp
cardiac dz,
renal insufficiency
advanced age
prolonged clamp time >30 min
Causes of renal impairement during aneursym repair 6
- hypotension
- contrast
- embolization air/debris despite clamp below
- clamp: suprarenal clamp reduces flow 80-90, infra 40% 2/2 alterations in RAAS & vasoconstriction, resdistribution blood flow to the cortex
- aneurysmal/surgical/stent disruption renals
post op complications associated with aneusrym or dissection repair
- Surgery: endoleak, migration, post implantation stent syndrome (fever, leukocytosis, elevated inflammatory mediators-NSAIDS)
- CNS: paraplegia, stroke
- CV: myocardial ischemia and CHF most common
- Pulm: resp failure
- gut ischemia
- renal impairment: ATN most common, contrast induced nephropathy
Benefit and risks of epidural for aortic repair
- pro
- neuro: improved pain relief,
- CV: improved graft patency, dilation coronary arteries (thoracic), attenuated stress response
- Pulm: improved resp fxn
- GI: improved GI motility
- Heme: decreased periop hypercoagubility, decreased rate DVTs
- Cons: bleeding (hematoma), infection (abscess), nerve injury, headache, backache. Symathetomy, high spinal
How to treat aortic dissection?
- Distal: medically
- Proximal: surgically
- Lower BP to 90-120mmHg first using esmolol (titratable and short half life), then using nitro or SNP, (titratable and short half life). Vasodilators first may increase shear forces and extend dissection (increase dP/dT)
How to obtain hemodynamic stillness for graft depolyment
- Hemodynamically still: adenosine (AV block), pace 150-180 (decrease preload, CO), atrial flow occlusion
- Newer grafts: temp reduction CO MAP 60-70 HR 50-60
- Hemodynamically still: adenosine (AV block), pace 150-180 (decrease preload, CO), atrial flow occlusion
indications for endocarditis ppx
- Prothestic cardiac valve
- Prior IE
- Cardiac transplant with cardiac valulopathy
- Unrepaired cyanotic CHD, repaired cyanotic CHD lesion within 6 months using prothetic material, repaired CHD with residual defects at site adjacent to prothetic device/patch
protamine rxns?
- histamine release from mast cell degregration and hypotension
- anaphlaxitc and anaphylactoid; NPH, fish w vertebra allergy, prior protamine exposure
- Catastrophic pHTN with R heart failure: protamine heparin complexes induce release of thromboxane A: tx milrinone, nitric oxide, epi, 70U/kg heparin to break up complexes, CBP
common induction for cardiac surgery
narcotic based technique: chest wall rigidity
- least myocardial depression
- minimal reduction SVR
- high dose reduce stress response (release of hormones and vasoactive substances in response to hypothermia, hemodilution, surgery (catecholamines, cortisol, ADH, glucose, acute phase reactants)
midaz to limit recall
etomidate: lack of significant CV effects
inhalational agent
Ketamine: HTN tacycardia, myocardial depression in catecholamine depleted pts
Why must pt be Anticoagulated before bypass ?
cannula and bypass circuit is thrombogenic and at risk of thrombosis with occulsion
reservoir blood sits
How does heparin work?
what to do if ACT does not rise after heparin?
accerelates the action of AT3 to inhibit thrombin (9,10,11,12,13)
ensure it was given in properly (central line) and proper dose. repeat ACT (need 450>
give more heparin
give AT 3 (via FFP or AT concentrate)
Why does BP need to be lowered before aortic cannulation
aortic cannulation can cause aortic dissection
Hypotension after initiation of CBP
- hemodilution: decreases SVR (depends on vascular tone and viscosity) from pump priming solution (usually transient as hypotension induced vasoconstricton and endogenous catecholamine increase BP
- arterial or venous malfunction or malposition: aortic cannula inserted into aortic wall–>dissection, inserted into inmoninate or carotid (cerebal edema/hemorrhage), venous cannula kinked or malpositioned,
- switch of venous and aortic cannula
*** aortic cannula in inmoniate would see HTN w R sided a line and hypotension w L sided a line
venous reservoir is not filling well and CVP elevated, causes?
- obstruction to venous flow: air lock, mechanical (kinking, clamping,
- incorrect cannula size
- low table position (drain by gravity)
- look for signs to confirm obstruction to venous flow-facial engorgement, conjunctival chemosis
Should case be canceled if pt develops facial blanching, mydriasis, chemosis?
yes, cerebral edema/injury may have occured. measure to provide cerebral protection (hyperventilation, mannitol, higher cerebral perfusion pressure may be needed
Steps of CBP
E H CCC
R R D W
- expsoure heart and vessels
- heparize, check act, aortic and venous cannula
Cool
- CBP initiated
- once Vfib starts ~28C aorta cross clamped
- cardioplegia admin to cease electrical activity
- surgery
- rewarming
- remove aortic cross clamp
- Defib when heart at least 30C
- wean off CPB
At what CO does CPB begin?
Why is it important to know if on partial or complete bypass?
full flows at 2.5L/min/m^2. After that higher flows risk HTN dissection, trauma to blood elements
-as long as there some pulm blood flow, there is potential for shunt unless ventilaton is provided
When is retrograde cardiopelgia given?
What does cardoplegia do?
high grade cardiac coronary artery lesions. AS
Given cardioplegia via coronary sinus
induce asytole, electromehachical silecne (decrease demand). hyperkalemic solution that lowers resting memebrane potential inducing VF
- 8ml/100g/min at rest for normal contracting heart (10% total body O2 consumption)
- 2ml/100g/min fibrillating heart @ 22C
- <0.3ml/100g.min electromechanical quiescent heart
What to do if protamine admin during CBP?
cease CBP
manual cardiac massage if not hypothermic
readmin heparin,
replace oxygenator and CBP circuit
Goal for BP during CBP
MAP 50 as long as pt didnt have altered autoreg from HTN. consider MAP 70 for pt w cerebrovascular dz. AVoid MAP>100 due to concern of aortic dissection, bleeding, cerebral edema,
Causes of hypokalemia and hyperkalemia on CBP
why is it important to monitor glucose
hyperkalemia: abs of cardioplegia, hemolysis, acidosis, admin of K
hypokalemia: DILUTION w non K solutions, alkalosis
- hyperglycemia exacerbates neurologic injury if cerebal ischemia occurs (also can cause osmotic diuresis, impair wound healing,)
How to reduce chances of coagulopathy while on CBP?
limit hemodilution
limit cartotomy suction
normothermic CBP, assure adequate rewarming
use appropriate heparin and protamine dose
admin antifibrinolytic
alpha and ph stat?
strategies to manage acid base balance during hypothermia on CBP
alpha stat:
- keep alpha constant (ionidation of major intracellular buffer histidine),
- allow alkalosis to happen.
- pH reported at 37: goal is to have temp uncorrect ABG read 7.4
mainatins intracellular OH/H ratio (and theoretically enzymatic fxn)-priortize intracellular environmemt
-preserves autoreg, decreases cerebral blood flow, and embolic load potentially improving neuro outcomes in adults (1 mech of brain injury is embolic events
pH stat: keep
- pH constant at 7.4 and PaC02 at 40
- treat resp alkalosis by adding Co2 (priortize extracellular environment)
- blood gas reported at hypothermic temp
- primary mechanism of brain injury in peds pt is ischemia , enhanced cerbral blood flow may benefit this popuation
Steps by surgeon t wean from bypass
steps by anesthesia to wean from CPB
- air evaucated from heart and grafts
- venous return to pump is slowed by gradually occluding venous cannula, increases RA and RV filling causing heart to begin ejecting
- aortic pump flow reduced in 0.5-1 L/min increments.
- CBP terminated when SBP around 90-100 and pump flows are 1L/min or less
venous and aortic cannula removed
anesthesia
AB (airway breathing)-ventilate pt,recruit to open up atelectasis, confirm normal ABG
C (CV)-rezero monitors, turn on capnograph and pulse ox, confirm HR 70-100, rythm sinus (temp >30 cardiovert if still fibrillating), connect pacemaker wires, inspect heart on TEE
D (drugs: add midaz, paralyze, start vasoactivemeds and inotopes as needed, resusuitation drugs ready
Electrolytes fluid: confirm normal K and glucose at min. fluids given as 100cc aliquotes by perfusionist to achieve adequate filling pressures by CVP PA and direct inspection
H (Heme); hbg at least 7 (higher for others), autologous blood, cell salavge, homologous blood admin
T (temp)core temp at least 36 and shell tem at least 33 before weaning. nitroprusside may allow faster shell warming. overly rapid warming–>air bubble formation and increase CMR02
Why might one have trouble cardioverting to SR from VF in weaning period?
- cold heart. needs to be 30C
- ischemic heart
- elevated K
Causes of coaulopathy after bypass
- abnormal plt fxn-activation on nonendothealil surfaces-oxygenator, filter, cartiotomy suction, hypothermia, nitro protamine
preserve function: autologous blood collection, less use of cartiotomy suction, no bubble oxygenator
- thrombocytopenia
- hemodilution of coag factors
- residual heparin:inadequate neutralizaton, heparin rebound (4-6 hrs after neutralization from dissociation of heparin), residual heparin from scavanged blood
- fibrinolysis- increase plasmin 2/2 to release of TPA (tissue plasminogen activator) from endothelium during CPB, decrease levels plasminogen activator inhibitor
- DIC
- hypothermia
etiology failure to wean
LV failure: vent problems,
-preload (excess inadequate)
ischemia (graft malfunction-kink/clot/air), supply demand mismatch
valve failure inadequate myocardial protection, reperfusion injury, arrythmia,
myocardial depressants: meds, acidosis electrolytes (hyperK hypo ca),
RV failure: pulm HTN
Low SVR (meds (volatile, vasodilator, protamine), hemodilution, hyperthermia, sepsis, anaphalaxsis
Why is neuro deficit more common w valve surgery ?
How to deair heart?
How to treat massive air embolism?
- air more likely to enter heart during open heart procedures
- allow heart to fill more completey (occlude veous cannuala), aspirate air from aortic vent, LV vent, or needle in apex. vigoruous ventilation flushes air out of pulm veins and heart
- stop bypass; place pt in steep Tburg; hypothermic retrograde SVC perfusion with intermittent carotid occulusion; hyperbaric O2
- blood pumped retrograde into jugular system–>blood and air in brain pushed retrograde down vertebral and carotid arteries where air can be vented. Intermittient carotid compression may facilitate expulsion of air through vertebrals.
complications after CPB
neuro: recall, neuro deficits
cards: weaning
resp: pulm edema (cardiogenic, post transfusion), PTX, hemothorax, PA rupture
aki
temp: delayed postop hypothermia
RF for neuro deficits after CPB
Pt: Cerebrovascular dz, DM, aortic atherscolosis
procedure; open chamber, CPB>90 min, hemodynamic instability, multiple aortic instrumentation
equiptment: bubble oxygenator, lack inflow arterial filters, N20
When do induce theraputic hypothermia post cardiac arrest
How?
Why?
any pt comatose following ROSC after being resusitated for out of hx VF, or initial rythm VF, or in hx cardiac arrest
cooling blanket ice pack, infusion cold fluids to reduce temp to 32-34C for 12-24 hrs while monitoring core temp
protection for brain and other organs in those who remain comatose after cardiac arrest
Post cardiac arrest care
EKG changes in pregnancy
Q wave inferior leads
ST-segment depression and T-wave inversion in the inferior and lateral leads
LAD
heart is displaced cephalad and laterally, a
what can overestimate or underestimate severity of AS
How to grade AS
hyperdynamic circulation over estimate transvalvular gradient, LV failure underestimate. Look at AVA
critical >50, <0.7
Severe: >40 <1.0
Moderate 25-40 1-1.5
Mild <25 1.5-2
normal: <5 2.5-4
MS <5 >5-10, >10
What is myocardial preconditioning
- exposure to certain drugs serves to protect the myocardium against subsequent myocardial ischemia and reperfusion injury. volatile agents as low as 0.25MAC may serve this purpose. involves myocardial K ATP channels/
- may limit infarct size, prevent dysarrythmias, and preserve myocardial fxn
What to do if pt has ST depressions
ddx (4)
optimize myocardial oxygen supply and demand
-supply:
100% oxygen (correct hypoxia)
slow HR
correct anemia
optimize CPP=AdP-LVEDP
-demand
avoid tachycardia
maintain sinus
decrease afterload: nitro
decrease wall tension
- NSTEMI: with elevated troponin
- unstable angina (non infraction subendocardial ischemia
- digoxin (with short QT and prominant U waves)
- hypokalemia: (long QT, prominant U wave, inverted/flattened T wave
-SE of SNP
increase CBF and ICP
hypotension, reflex tachy
attenuated HPV
CN toxicity (tachyplaxsis, met acidosis, increased SmO2 w prolonged infusions
filling pressures
Hypotension
- Filling pressures high:
1. CO high: low SVR, hypervolemia
2. CO low: LV dysfxn - filling pressures low:
1. CO high: low SVR, hypovolemia
2. CO low: hypovolemia, RV failure
What would you like to know about ischemic cardiomyopathy
location of damage, and additional myocardium at risk
current fxn
which vessels comprised and any intervention
past and current symptomology
going on to bypass check
HAD2SUE Remember this mnemonic.
- *Heparin**: Always give prior to bypass.
- *ACT**: Always check before going on bypass (450 seconds)
- *Drugs**: Do you need anything (Non depolarizing neuromuscular blocker).
- *Drips**: Turn off the inotropes etc.
- *Swan**: Pull the PA catheter back 5 cm to avoid pulmonary arterial occlusion/rupture.
- *Urine**: Account for bypass urine
- *Emboli**: Check the Arterial cannula for bubbles.
coming off bypass
WARMVP:
warm,, admin midaz
Anemia/electrolytes/acidbase
Rhythmn: rate ok? need to be paced? defib at 30C
Monitors/alarms/rezero lines
Ventilation: deair, check compliance/recruit
Perfusion: pump flow, cardiac fxn on TEE, admin vasopressors and inotropes
Cardiac enzyme
myoglobin 1-3, 12, 24
CKMB 1-6, 12-24, 3 days (marker of reinfarction)
tropnin 1-6, 12-24, 7-10 days
digoxin mech
signs toxicity (normal 0.5-2ng/mL)
factors that exacerbate toxicity
- Inhibit sodium potassium ATPase increase intracellular sodium decrease activity of sodium calcium exchangerincrease intracellular calciumincreased contraction, lengthen phase 4 and 0 of cardiac AP (decreased rate)
- Toxicity
- Neuro: confusion, visual disturbances
- Cardiac: EKG changes (ST depressions), arrhythmias.
- GI: hypersalvation, N/V
- Potentiate toxicity: hypokalemia, hypomagnesium, hypercalemia
Reasons for lack if Pacemaker capture
what do you do?
Delivery of insufficient energy for depolarization
- MI (increased energy required for depolrization
- acid base distrubances,
electrolyte abnormalites (mag K ca-raise the depolarization threshold)
lead dislodgement
-PPM malfunction
steps
100% oxygen confirm oxygenation vent
atropine, transcutaneous pacing
check electrolytes
Roller pumps vs centrifugal bypass pump
disadvantage of roller
- Roller pumps:
- forward flow produced by compression of tubing by 2 roller heads
- pulsatile flow
- no sensitive to preload, afterload (kicking, occlusion, increased SVR, clamp placement), reliability produces certain amount of flow based on pump speed (flow is constant, no pressure dependent)
- disadvantages:
- increased damage to RBC
- potential to deliver large quantities of air if air entrained
- risk of overpressurization leading to tubing separation or rupture (no sensitivity to changes in afterload)
- risks of spallation from wear
- risk of preload occlusion negative pressure induced cavitation (dev of microbublles)
- centrifugal pump
- rotational force responsible for forward flow
- flow is pressure dependent: sensitive to changes in preload and afterload (output not directly related to rpm),
- less damaging to RBC
- stop functioning if large amount air entrained
- disadvantage: non-pulsatile flow, only partially able to compensate for decreased forward flow with increase in speed from increased distal pressure
PCWP tracing
acute MR
a v dissociation
a fib
large V wave, no x decent, steep y decent
cannon a waves
no a waves
How IABP works
-how to synchronize
increase perfusion during diastole and decrease afterload during systole
- positioned below L subclavian (prevent cerebral emboli)
- synchonized w cardiac cycle w arterial line (aortic valve closure-dicrhotic notch) or EKG (R wave)
set to ratio of 1:2 to allow for comparison of nature beat to augmented beats
ICD and PPM abbreviations
Eval AICD preop
- Type and model of device, Indication for placement, when placed (<3 months more likely to be dislodged during central line placement, cardiac surgery, or manipulation of intracardiac catheters)
- underlying rhythm and rate, Pacer dependent, pacing threshold, recoded arrhythmic events
- programmed mode, response to magnet (usually disables tachydysrythmia detection therapy), reprogramming needed,
- Last checked (6 months ICD, 12 months PPM), functioning properly, battery life (should be at least 3 months),alert status on lead or generator( lead could be oversensing),
issues w electrocautery and AICD
How to reduce risk
- Inhibition of pacing function: interference from electrosurgical unit may be interpreted as intrinsic heart activityinhibit pacing
- Triggering of tachydysthymia therapy, shock
- Internal damage to the device (>6inchs fromAICD)
- Electrocautery
- Use bipolar electrocautery (two blades act as active and return electrodereduces EMI
- Limit use of electrocautery if possible
- use short intermittent irregular bursts at lowest energy when required
- Return plate:
- Ensure proper complete contact
- Place return plate as close to operative site and as far away from CIED to avoid passage of current though generator or leads (try to keep the path 6 inches away from CIED)
- AICD
- Disable tachydysrhythmia sensing and treatment (higher risk above umbilicus)-magnet (Assuming can be secured in place magnet allows advantage of quickly resuming tachycardia sensing and treatment by removal of magnet during intraop VT/VF)
- If pacer dependent reprogram to asynchronous mode (if AICD)
- Disable rate responsive sensors-can lead to faster than expected pacing rates
- Have temporary pacing and defibrillation equipment
When do admin bicarb during code
ph <7.2
severe acidois causes myocardial depression, increased risk of arrythmias, and resistance to inotropes and vasoconstrictors
severe hyperkalemia
refractory to resus despite 5-10 min resusitation
complications of a fib ablation
CVA, air embolism
atrial perforation,
tamponade, pericardial effusion
AV block, arrytmias
valve trauma
Causes of Afib
Goals of care
valve disease, HTN, LVH, cardiomyopathy
PE, hyperthroid,
excessive ETOH/caffeine
slow the rate, restore and mainatin SR, prevent stroke w a/c
causes of syncope
neuro: seizure, stroke
cards; AS, HCOM, arrythmia, MI, vasovagal
endocrine: hypoglycemia
How does increased LAP lead to TR
increase LAP–>transmitted to pulm system–>elevatedpulm pressures over time result in pulm vascular changes anddevelopment of pHTN–>RV pressure overload–>RVH–> RV dilation –>TR
Criteria for severe AS MS
mild >1.5
moderate 1-1.5
severe <1
Gradient AS
Mild 5-25, mod 25-40 severe >40
Gradient MS
mild <5
mod 5-10
severe >10
pHTN goals
avoid hypoxia hypercarbia acidosis
avoid nitrous
avoid tachycardia-(impaired LV filling and increased LAP–>increased RV afterload
avoid excessive airway pressures (PEEP, mean airway pressure)
ddx increased CVP
R heart failure
ischemia, PE, tamponade
No peep in VAE
- potential for impaired venous return
- less effective than jugular venous compression in increasing cerebal venous pressure in sitting position
- may result in paradoxical embolism
heart transplant considerations
HTN: may be 2/2 cynclosporin. tx ACE or CCB. nefidipinecauses vasodilation, BB avoided since cardiac responsiveness during exercise dependent on circulating catecholamines
denervated heart-preload dependent (denervated heart increases CO by increasing SV
allograft dysfxn: fever, maliase, arrythmias, SOB, myocardial dysfxn
accelerated CAD
immunosupressive agents may have effects on NMDB, kidney fxn, and infection risk (cyclosporin, azthioprine, prendisone)
use direct agents: epi, isopetereono
no response to indirect agents: ephredrine
it cannot respond to peripheral stimuli that might induce hemodynamic changes: carotid massage, laryngoscopy, or Valsalva, OCR
absence of vagal influence–>resting tachycardia
