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Cardiology Flashcards

1
Q

Cardiogenic shock definition

A

Acute circulatory failure causing inadequate oxygen utilisation by cells, caused by cardiac dysfunction
hypo perfusion with or without hypotension
phenotypes - commonest cold and wet
usually characterised by SBP < 90, HR > 60, oliguria, congestion

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2
Q

Ventricular assist devices

A

Type of mechanical circulatory support, which can be short or longterm which provides flow in order to maintain cardiac output
LVAD
RVAD
BiVAD
Total artificial heart
Minimally invasive - impella

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3
Q

Indications for VAD

A

Bridge to recovery - CS
Bridge to candidacy - improve organ perfusion and assess for transplant
Bridge to transplant
Destination therapy (international)

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4
Q

VAD components

A
  • inflow cannula (to pump)
  • outflow cannula
  • pump
  • electrical controller
  • cable connecting device to controller
  • power supply
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5
Q

VAD mechanisms

A

Pneumatic, hydraulic, mechanical pusher plate - pulsatile
continuous non-pulsatile - rotor, centrifugal

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6
Q

Contraindications to VAD insertion

A

General - age > 65 with biventricular failure
Resp - severe dysfunction fixed pulmonary HTN
CVS - severe valve lesions
CNS - severe stroke, inadequate psychosocial support
Renal - longterm RRT
Liver - cirrhosis, high BMI
Haem- contraindication to anticoagulant

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7
Q

VAD complications

A

Early:
Bleeding
Tamponade
RV failure
Haempdynamic instability
Late
LVAD failure
arrhythmias
pump thrombosis
embolic stroke
anticoagulation related e.g. ICH

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8
Q

Collapsed patient with LVAD

A
  • signs of life and breathing (pulse may be absent)
  • if no signs of life, auscultate for humming sound. if absent, LVAD failure
  • ventilate and try to restart
  • ensure power source working
    if device not failed likely pathologies
  • ventricular rrhythmias - defib
  • hypovolaemia

CPR controversial - likely to dislodge cannula, disrupt anastomosis. maybe if all other failed

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9
Q

Causes of bradycardia

A

Intrinsic
- idiopathic (degenerative)
- ischaemia
- cardiomyopathy
- infiltrative - sarcoid
- infective - paravalvular abscess, myocarditis
- psot cardiac surgery
extrinsic
- training
- drugs
- hyothermia
- metabolic abnormalities
- electrolyte abnormalities
- high icp

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10
Q

Types of pacing

A

percussion
transcutaneous
epicardial
endocardial (temp / perm)

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11
Q

How does pacing work?

A

delivery of electrical stimulus to the myocardium resulting in wave of depolarisation and contraction of the cardiac chambers.
relies on intact myocardial and or conducting tissue.

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12
Q

Generic PM classification

A

I - chamber paced O, A, V, D
II - chamber sense O, A, V, D
III - Response to sensing O, I, T, D
IV - Rate modulation O, R
V - multisite pacing O, A, V, D

Inhibition means that if there is spontaneous cardiac activity, the pacemaker is inhibited

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13
Q

Examples of atrial pacemaker modes

A

AOO - asynchronous atrial pacing (no sensing, no modulation). usually response to AAI with magnet. If SA node intact, will compete. If fast enough then SA node signal will fall on refractory period.
AAI - atrial demand pacing. senses atrial activity. if above threshold then pacemaker doesn’t;t do anything. if atrial firing too slow, pacemaker takes over. relies on intact AVN

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14
Q

Examples of ventricular pacemaker modes

A

If AVN doesn’t work or fibrillating atria
downside is poor a-v synchrony and poor rv-lv synchrony (RV ejection reduced, LV and atria contracting simultaneously)
limited to people in outpatient setting who are fairly stationary or in icu when atria and AVN have failed
VOO - magnet applied to VVI. Spread from right –> left –> LBBB. risk of r on t.
VVI - ventricle sensed, if QRS complex generated pacemaker does nothing. will fire if no ventricular activity

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15
Q

Dual chamber pacing benefits

A
  • add atrial systolic volume to ventricular ejection
  • prevents retrograde atrial contraction
  • Better QOL
  • lower risk of AF
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16
Q

Dual chamber modes

A

VAT - broken AVN. atria sensed, then paces ventricle. AVN becomes large pacemaker loop. Ventricular pacing broad
DDD
- if normal A and V contraction PM does nothing
- if one chamber doesn’t;t contract PM takes over
- if both don’t contract atrial then ventricle zapped, pre-determined interval

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17
Q

CRT-D / CRT-P

A

cardiac resynchronisation therapy - improve cardiac function, symptoms, morbidity in chronic HF
If ICD indicated then CRT-D

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18
Q

Pacemaker check in patient with temporary wires

A

every day
1. underlying rhythm - reduce PM rate to see native rhythm
2. sensitivity - minimum current the PM can sense, lower number = greater sensitivity. leave sensitivity at half the pacing threshold (sensitivity at which sense indicator flashes during each endogenous depolarisation)
3. Capture threshold - minimum output required to stimulate action potential - confirmed with QRS complex after each spike. reduce energy output until QRS no longer follows each spike. leave output at twice the capture threshold
4. rate - optimum 80-90. may wean to backup e.g. 40.

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19
Q

pacemaker problems

A

output failure - failure to produce a pacing spike
failure to capture - spikes don’t lead to qrs
over sensing - inappropriate inhibition of pacing in response to non-cardiac signal
undersensing - continues to pace, ignoring intrinsic cardiac activity
cross talk - DDD, ventricular wire senses atrial contraction and interprets as ventricular activity, therefore not pacing ventricle . if no AV conduction then no ventricular output
endless loop tachycardia - atrial wire internets ventricular contraction as atrial, leading to another ventricular contraction and so on.

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20
Q

overdrive pacing

A

Slow VT
pace above rate to take over myocardial activity and convert to sinus rhythm

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21
Q

OOHCA epidemiology

A

55 per 100,000
most at home
98% adults
50% witnessed
80% cardiac in origin
25% shockable initially
70% bystander cpr
< 10% survive to hospital discharge

In hospital
- PEA 52% asystole 20% shockable 17%
53% ROSC 23.6% survival to discharge

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22
Q

Key concepts in cardiac arrest management

A
  • early recognition
  • early cpr to buy time
  • early defibrillation to restart heart
  • post-resucitation care to restore qol

priorities
- competence at practical skills - CPR, defibrillation, simple airway management
- recognise shockable / non-shockable
- Hs and Ts

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23
Q

Drugs in cardiac arrest

A
  • adrenaline - non-shockable 3-5 mins. shockable after 3rd shock
  • amiodarone - refractory VT/VF after 3rd shock
  • calcium chloride - hyperkalaemia or calcium channel blocker OD
  • alteplase - PE
  • sodium bicarb. hyperkalaemia, TCA OD
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24
Q

Post-cardiac arrest syndrome

A
  • brain injury
  • myocardial dysfunction
  • systemic ischaemia-reperfusion injury
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25
management priorities in cardiac cause
PPCI within 120 mins - prolonged door to balloon time in STEMI associated with increased mortality secure airway and IV access NG and antiplatelets cardio and neuroprotective maintaining MAP, temperature delays - scan, cvc, art line
26
CT pre angio
if signs of cerebral or PE pre arrest - headache - seizures - focal neurological deficit - SOB / hypoxaemia
27
TOMAHAWK trial
delayed / selective PCI vs immediate PCI in OHCA NSTEMI - if haemodynamically and electrically stable appears no benefit to immediate PCI. 2021 ERC guideline - consider emergent angiography if high suspicion of occlusion e.g. shockable
28
Post-resuscitation care
RESP - LPV PO2 10-13 sats 94-98 PCO2 4.5-6 CVS - MAP > 65 RENAL ; UO > 0.5ml/kg/hr GLUCOSE 6-10 TEMP < 37.8 AVOID SEIZURES
29
Neuroprognostication
M < 3 at 72 hrs without confounders Two + of following = likely poor outcome - CT / MRI showing hypoxic injury - SSEPs absent - Absent pupillary response - NSE > 60 at 48 or 72 hr - malignant EEG > 24hr - status myoclonus < 72hr
30
e-CPR
VA ECMO - bridge to specific intervention inclusion may be - known reversible cause - prolonged resuscitation anticipated - signs of life during cpr - short no flow and low flow times ARREST trial - benefit
31
Cardiac arrest in CICU
Hypovolaemia - bleeding - medical (coaguloapthy, platelets)/ surgical (drain output e.g. 400ml 1st hr, 200ml in consecutive hours) - vasodialtroy shock / capillary leak - vasoplegia rewarming, sepsis, anaphylaxis Low CO - myocardial stunning, metabolic dysfunction, reperfusion injury, ischaemia Hypoxia - pulmonary oedema - misplaced ETT Electrolytes - hypo / hyperkalaemia - hypomagnesaemia hypothermia - failure to warm from bypass tension - kinked drain tamponade toxin - e.g. protamine reaction thrombosis - coronary artery occlsion / PE dysrthyhmias - AF, VT
32
Cardiac advance life support
management of cardiac arrest in post-op cardiac patient cardiac arrest may present unconventionally - absence of pulsatile arterial trace, reduction in ETCO2 questionable benefit to CPR / Adrenaline - surgical complications high, may be worsened by mechanical injury
33
CALS protocolr
VF / VT - 3 x shocks / BLS / amiodarone Asystole / bradycardia - pace if wires / BLS / external pacing PEA - BLS / turn off pacing to exclude VF Resternortomy shock every 2 mins FiO2 1.0, o PEEP Exclude PTX / HTX Adrenaline only by senior
34
restternotomy
full scrub sacrificed in interest of time decontamination, sterile drape and gloves scalpel to reopen assistant hold wires while operator cuts assistant pulls wires out internal cardiac massage / drainage of tamponade
35
cardiac tamponade
condition whereby compression of the heart leads to increased intrapericardial pressure, impaired right ventricular filling, ultimately leading to obstructive shock and cardiac arrest Causes - neoplastic - primary cardiac, lung, lymphoma - infective - EBV, CMB, HIV, TB, pneumococcal - iatrogenic - PCI, TAVI, ICD - Trauma - vascular - type a dissection - renal failure causes of effusion unlikely to progress to tamponase - autoimmune - thyroid - dressers syndrome
36
diagnosis of cardiac tamponade
clinical - becks triad muffled heart sounds, hypotension, raised JVP - pulsus paradoxical - pressure drop 10mmhg on inspiration others - electrical alternans, low voltage qrs - cxr - large cardia shadow - echo - effusion / ra / rv diastolic collapse - diastolic rv collapse - 90% sensitivity - systolic ra collapse - earliest sign - plethoric ivc (> 20mm and < 50% reduction) tamponade depends on compliance of pericardium and time rather than size
37
constrictive pericarditis vs cardiac tamponade
similariites - diastolic dysfunction nad prserverd EF - increased ventricular interdependence - increased respiratory variation of vent inflow / outflow timing - constrictive - filling impaired by reaching elastic limit of pericardium. early diastole not affected - tamponade - impaired filling throughout pressure - constrictive pericarditis prevents transmission of -ve intrathoracic pressures in inspiration chambers - RA pressure remains constant - ra pressure decrease during inspiration in tamponade
38
pericardial drainage
if stabile - 12-24hr - if shock - immediate indications for surgical drainage - trauma - ventricular rupture - type a dissection - purulent effusion in septic patient contraindication to immediate - uncrectte coagulaopathy - pet < 50 - incr > 1.5
39
supportive measures in tamponade
- avoid surges in catecholamines - pain etc - fluid bluses - tertiary centre if possible
40
Hypertensive emergency
severe hypertension in association with acute hypertension mediated organ dysfunction - malignant hypertension - HTN + fundoycopic changes, microangiopathy, DIC (fibrinoid necrosis) - sudden severe phaeochromocytoma - severe PET - acute hypertension with other conditions - dissection, acute MI, acute HF - hypertensive encephalopathy - SAH, ICH
41
symptoms of hypertensive emergency
hypertensive encephalopathy - headache, visual disturbance, lethargy, seizure, LOC others - chest pain, duponoea, dizziness PRES - clinics-radiological diagnosis - hypertensive encephalopathy with white matter vasogenic oedema in occipital lobe
42
IX HTN emergency
All - fundiscotm ECG, bloods, ACR, pregnancy test in women Specifics - echo, CT/MRI brain, CT aorta, CXR, US renal
43
BP targets
malignancy / encephalopathy - 25% reduction MAP ACS / Pulm oedema - sBP < 140 Dissection - sBP < 120 Stroke < 185/110 if thrombolysis otherwise none
44
Infective endocarditis
infection of the endocardium - valves, walls haematogenous spread of organisms may gain access to blood stream due to IVDU / dental / immunosuppression seed onto cardiac structure - non-native sterile thrombotic vegetation - mass in heart, organisms adhere during bacteraemia - facilitated by platelets and fibrin
45
clinical features of IE
insidious presentations - fever - weight loss, anorexia - murmur - thromboembolic / immune phenomonen acute / complications - heart failure - cariogenic shock - septic shock - myocarditis - abscess - pervalvular extension - conduction disorders - septic emboli
46
diagnosis of IE
clinical suspicion Dukes criteria - 2 major / 1 major 3 minor / 5 minor major - intracardiac mass on echo - +ve micro - 2 separate isolates of typical organism minor - fever - patient risk - ivdi or prosthetic - vascular phenomena - arterial emboli, septic pulmonary infarcts, ICH, conjunctival haemorrhage, Janewy lesion - immune phenomena - osler node, Roth spot, GN - micro not meeting major
47
organisms in IE
- strep viridans / bovis and staph aureus - HACEK - haemophilus, actinobacillus, cardiobacterium, eikenalla, kingella
48
Indications for surgical management in IE
Hear failure - severe regurgitation obstruction, refractory pulmonary oedema, cariogenic shock uncontrolled infection - abscess, MDR organism, fungi prevention of emboli - very large vegetation
49
ACS
STEMI NSTEMI UA (no biomarker change) In addition - cardiac arrest - electrical or haemodynamic instability with CS
50
MI diagnosis
- raised biomarker - at least 1 of - symptom of ischaemia - new ST/T/LBBB - new loss of viable myocardium / rwma - intracoronary thrombus on angiography
51
STEMI ECG changes
2mm STE in V2-3 1mm STE in 2 contiguous other leads New LBBB Old LBBB and sgarbossa
52
MI classification
Type 1 - acute thrombus / plaque rupture Type 2 - O2 supply / demand mismatch, normal coronaries Type 3 - death Type 4 - related to PCI Type 5 - related to CABG
53
definitive management of STEMI
- STEMI presenting within 12 hrs of onset of symptoms and within 120 mins of time thrombolysis could be given - fibrinolysis if PPCI cannot be delivered within 120mins. repeat ECG / rescue PCI
54
Antithrombotic managaement STEMI
DAPT aspirin / prasugrel. ticagrelor if not for PPCI PPCI - GP IIb/IIIa inhibitor anticoguatlion - UFH, enoxparin
55
Mx NSTEMI
- aspirin loading - fondaparinux - DAPT - GRACE score for risk immediate invasive management if unstable shock, arrhythmias - invasive < 24h if high risk established NSTEMI, dynamic hcnages
56
secondary prevention
ACEi, beta blocker, stain DAPT 12mo
57
Causes of AF in critical illness
- pre-existing AF - sepsis / infection - greater catecholamines - hypovolaemia - PE - Electrolyte abnormalities - vasoactive substances - atrial stretch - volume overload chronic structural / electrical remodelling - age. daiebets, HF arrhythmogenic atrial subtrate and trigger
58
Mx new AF
adverse features (shock, syncope, chest pain, pulmonary oedema) - DCCV correct reversible - electrolytes - ischaemia - oxygenation - volume status - infection manage instability - rate related -b eta blockers - rhythm related magnesium ,amiodarone anticoagulation
59
DDX broad complex tachycardia
Regualar - VT - SVT with BBB Irregular - AF with BBB - Pre-excited AF
60
Long QT
Start of QRS to end of T wave affected by HR QTc = Qt / square root of RR 430ms men 450ms women Long QT syndrome - long QT is absence of secondary cause - inherited Long QT in critical care - Drugs - Antipsychotics - haloperidol - antiarrhtyhmics - amidoarone, sotalol - TCA, - others - maclroides, fluconazole electrolytes - K, Mg, ca Hypthermia Raised ICP
61
Torsades de Pointe
polymorphic VT multiple ventricular foci resulting in variable QRS amplitude, axis, duration associated with prolonged QT. leads to VF address precipitating cause 2G MgSo4 overdrive pacing DCCV if unstable defibrillation if arrest
62
Cardiomyopathy
structurally and functionally abnormal heart muscle in absence of coronary artery disease, hypertension, valvular, congenital heart disease
63
Types of cardiomyopathy
Primary - Dilated - enlargement leads to deficient actin/myosin cross linking. systolic failure, embolic. familial = various. non-familial = prgancny, Kawasaki, myocarditis, alocohol - Hypertrophic - myocardial hypertrophy in absence of haemodynamic stress. Familial = glycogen storage disease. non familial = athletic training - Restrictive - stiff ventricles, impaired diastolic filling and dysfunction. hazardous anaesthesia (-ve inotropy, IPPV, vasodilation all problematic). familial = haemochromatosis non-familial = amyloid, scleroderma, radiation - ARVC - myocardial cells replaced by adipose or fibrous tissue. Each phenotype - familial and non-familial forms Secondary - Toxins : alcohol - Ischaemia - Inflammatory : viral myocarditis - Metabolic : amyloidosis - Peripartum
64
Takutsubo cardiomyopathy
potentially reversible cause of acute HF transient regional LV apical or mid-apical dysfunction without obstructive coronary disease may mimic ACS - T wave, cardiac enzymes, chest pain elevated NA concentrations - emotional or physical stress. apical ballooning stress induced cardiomyopathy may also occur in neurogenic myocardial stunning complications - acute HF LVOTO, MR, LV thrombus Mx - acute HF - vasoactive, MCS, ECMO - LVOTO - fluid, beta blocker - palm oedema - diuretics - thromboembolism - dyshythmias
65
peripartum cardiomyopathy
rare idiopathic CM systolic dysfunction LVEF < 45% 3rd trimester or month postpartum
66
heart failure definition
clinical syndrome structural / functional abnormality of the heart leading to elevated intracardiac pressures and or inadequate cardiac output at rest and / or during exercise acute / chronic / acute on chronic preserved EF / mild / mod / severe
67
Mx chronic heart failure
- beta blockers - spironolactone - ACEi - SGLT-2 others - loop diuretics - ARB Non-pharm - smoking cessation, weight loss, cardiac rehab - underlying disease - cardiac reynchornisation - MCS/transplantA
68
Advanced heart failure
persistence of HF symptoms despite maximal therapy - NYHA III / IV - Severe cardiac dysfunction (EF < 30% / isolated RV / non-operable severe valve / persistently high BNP) - decompensation - episodes of pulmonary or systemic congestion, or low output, or malignant arrhythmias - severe exervice impairment
69
causes of acute Heart failure
CHAMPIT C - coronary ACS H - Hypertensive emegrency A - Arrhythmia M - mechanical - rupture, trauma, valve P - PE I - Infection - myocarditis, sepsis T - tamponade (+ drugs)
70
presentation of acute HF
congestion - SOB, cough, orthopnoea, PND, raised JVP, gut congestion, hepatomegaly, ascites hypoperfusion - cold, sweaty, oliguria, altered consciousness - lactate, acidosis, creatinine
71
cariogenic shock
syndrome of life threatening tissue hypo perfusion due to inadequate cardiac output from primary cardiac dysfunction - SBP < 90 - despite adequate filling - signs of ypoperfusion A - at risk - no signs or symptoms B - Beginning - relationship time hypotension C - classic CS - hypo perfusion beyond volume resuscitation D - deteriorating - failing to respond despite vasoactive, MCS E - extremis - cardiac arrest ongoing CPR / ECMO INTERMACS - 1-4 micht be suitable for short term MCS. 5-7 stable ambulatory
72
MX acute left HF
myocardial hypperfusion - increae O2 delivery - high flow O2, cpap, IPPV, increase perfusion - inopressor, IABP, inodialtor reduce myocardial O2 demand - beta blocker, reduce afterload (vasodilator improve myocardial function - inotrope, revascularisation, alternative pump - VAD< ECMO specialis input, transfer, relief of symptoms - opiates
73
HFpEF
HF symptoms / signs with EF > 50% diastolic HF passive and active filling of ventricle
74
cardiorenal syndromes
1. acute decompensated HF --> AKI 2. Chronic HF --> CKD 3. AKI --> acute HF 4. CKD --> chronic HF 5. codevelopment of HF and CKD
75
Pulmonary hypertension
mPAP > 20 on right heart cath 1 - PAH - idiopathic. PAWP < 15 and PVR > 3 wood units 'pre-capillary' 2 - due to LVF 3 - due to CLD 4 - due to chronic thromboembolic 5 - due to systemic disease
76
pathophysiology of pulmonary HTN
1 - vascular smooth muscle hyper troy 2 - diastolic dysfunction, ball up of pressure, MR 3 - HPVC 4 - obstruction of pulmonary vascular bed
77
Chronic pulmonary HTN Mx
- General - rehab, infection prevention - ca channel blockers - endothelia receptor blockers - bosentan - PDE5 ihinitors - supplemental O2 - lung transplant
78
Pulmonary HTN implications for critical care
admission - RHF and supportive care prognosis - under 50 PAH 80% 5yr survival - pulm HTN needing ICU - 40% mortality (esienmengers may be better as chronic RV remodelling - intubation - haemodynamic collapse worse outcomes - low systemic BP - low sodium - high creatinine morbidity and mortality with surgery
79
right heart failure
clinical signs and symptoms - dyspnoea, reduced exercise, fatigue, dizziness - decompensation - JVP, hepatomegaly, a ascites, peripheral oedema echo - TAPSE > 17, P/V overload - RV:LV EDD > 1 rising lactate, low SCVO2 and anuria PAC
80
right heart failure mx
general -underlying cause - O2 - avoid hypoxia, hypercarbia, acidosis - avoid pain, hypothermia - advanced monitoring - IBP, CVP, CO, PAC - fluid assessment, may benefit from fluid or diuretics specific treatments - increase forward flow - milrinone - reduce PAP - milrinone, epoprostonel, - sildenafil - maintain systemic BP (vasopressin less effect on PVR than NA) - liaise with tertiary centre / ecmo
81
aortic dissection
creation of false lumen between layers of the aortic wall after creation of defect high pressure blood flow extends the tear intimal tear implicated occurring at regions of high stress and pressure predisposing factors are high BP and integrity of vessel wall risk factors - BP related - HTN, stimulant drugs, pregnancy - wall related - connective tissue disease, dyslipidaemia / plaques, aneurysm, iatrogenic
82
classification of aortic dissection
acute < 2 w chronic > 2 week stanford A - proximal - ascending aorta B - distal - distal to left SCA DeBakey I - ascending tear, dissection involves all of thoracic aorta II - ascending tear, dissection in ascending only III descending, usually descrninfin only a extends to diaphrgam b beyond diaphragm
83
presentation dissection
severe pain, loss of pulse volume sudden chest pain - ripping, tearing, stabbing back pain (more in type b) associated with tachycardia hyper/hypotension, sweating, breathlessness, stroke, syncope, differential pulses
84
air leak syndrome
movement of air from air containing cavity to one which doesn't usual contain air - tracheobronchail tree - sinuses - GI tract - can compromise function and compress important striations - PTX, pnuemomediastinum, pneumoperitoneum, pneumocephalus, pneumopericardium, subcutaenous emphysema
85
pneumothorax classificatio
spontaneous - primary - no underlying lung disease - secondary - underlying lung disease traumatic iatrogenic (ventilator, CVC, bronchoscopy, pleurocentesis, tacheostomy
86
bronchopleural fistual
connection between pleural space and major bronchus air leak - persisten = more than 4 days post ip
87
mx PTX
unstable = drain Primary spontaensou - < 2cm conservative - breathless or > 2cm needle aspration. - if remain breathless or > 2cm - drain secondary spontaensou - breathless or > 2cm - drain traumatic and iatrogenic generally need drain PPV - drain
88
suction on chest drain
not routine persistent air leak / incomplete re-expansion high volume low pressure
89
management of large air leak
airway - check position ventilation - luv, spont, differential / single lung / ecmo monitoringserial definitive - conservative, surgical or bronchoscpic repairs
90
urgical review in sponaenous
- persistent air leak 5 days seconda ipsilateral ptx 1st contraleteral
91
Cardiac output monitoring
clinical - vital signs / GCS / UO / CRT non-invasive - tran-thoracic bioimpendence - TTE minimally invasive - PICCO - LIDCO - ODM Invasive - PAC
92
PAC
8Fr 110cm - distal lumen - measure PCWP / SVO2 - Proximal lumen - 30cm RA - inject ate +/- 2nd for infusions (blue) - Balloon port - red - 1.5ml - thermistor 3.7cm from end - monitoring connection
93
PAC waveforms
- CVP - 3-8mmhg - RV - systolic 25 diastolic 0-10 - PA - Systolic 25 diastolic rise 10-20 + dicrotic notcg - PCWP - 4-12 Landmarks - RA 20cm RV 30cm PA 40cm
94
PA measurements
Measured - CVP - RAP - RVP - PAP - PCWP - SVO2 - core temperature - CO Derived - mean - mPAP / mRVP - CI - SV / SVI - SVR / PVR / SVR / PVRI SVRI (MAP – CVP)/CI x 79.92 1900-2400 dyn/sec/cm5/m2 PVRI (mPAP - PCWP) / CI x 79.92
95
SVO2 vs SCVO2
SCVO2 = central O2 sat (SVC) SVO2 = mixed (PA) In health - SVO2 > SVCO2 (SVC from brain -greter O2 extraction) Conditions when SVCO2 > SVO2 - Anaesthesia (reduced cerebral O2 extraction) - Shock - blood returning via IVC lower O2
96
PACman
- PAC no improvement in mortality, LOS - 10% complication rate - alternatives available
97
Oesophageal doppler
Doppler effect - when a sound wave is reflected off a moving object, the frequency shift is proportional to the velocity of the object ultrasound frequency, reflects of RBCs in descending aorta velocity-time curve of blood flow stroke disstance - distance travelled by blood in one heart beat multiple by aortic CSA = SV 90cm, trace at 40cm assumptions - angle of prove to direction of blood flow constant - aortic CSA constant - laminar flow - 70% CO via descending aorta
98
ODM interpretation
- Low SV - fluid - Low FTc - fluid (330-360) - Low PV - inotrope - low PV and low FTc - reduce afterload
99
PICCO
thermistor tipped femoral a line + cvc transpulmonary thermodilution pulse contour analysis (AUC systolic arterial pressure waveform is proportional to SV) - SVV / CO / SVR GEDV / EVLW / CI / ITBV
100
PICCO inaccurate
Significant shunt Significant PE Significant AS IABP Pneumonectomy
101
PICCO interpretation
CI < 3 - Low preload (low GEDV / ITBV) - low EVLW - give fluid - high EVLW - give fluid cautiously - high preload - low EVLW - catecholamine - high EVLOW - catecholamine and fluid removal CI > 3 - low preload GEDV/ITBV - fluid - high preload - high preload, low EVLW - good
102
Lidco
standard arterial line, CVC not needed interference if on lithium, shunts, NMBD transpulmnonary lithium dilution - measures lithium on arterial side via change in voltage - generates blood flow

FFICM (14 decks)

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