Cardiology Flashcards
Cardiogenic shock definition
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
Ventricular assist devices
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
Indications for VAD
Bridge to recovery - CS
Bridge to candidacy - improve organ perfusion and assess for transplant
Bridge to transplant
Destination therapy (international)
VAD components
- inflow cannula (to pump)
- outflow cannula
- pump
- electrical controller
- cable connecting device to controller
- power supply
VAD mechanisms
Pneumatic, hydraulic, mechanical pusher plate - pulsatile
continuous non-pulsatile - rotor, centrifugal
Contraindications to VAD insertion
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
VAD complications
Early:
Bleeding
Tamponade
RV failure
Haempdynamic instability
Late
LVAD failure
arrhythmias
pump thrombosis
embolic stroke
anticoagulation related e.g. ICH
Collapsed patient with LVAD
- 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
Causes of bradycardia
Intrinsic
- idiopathic (degenerative)
- ischaemia
- cardiomyopathy
- infiltrative - sarcoid
- infective - paravalvular abscess, myocarditis
- psot cardiac surgery
extrinsic
- training
- drugs
- hyothermia
- metabolic abnormalities
- electrolyte abnormalities
- high icp
Types of pacing
percussion
transcutaneous
epicardial
endocardial (temp / perm)
How does pacing work?
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.
Generic PM classification
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
Examples of atrial pacemaker modes
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
Examples of ventricular pacemaker modes
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
Dual chamber pacing benefits
- add atrial systolic volume to ventricular ejection
- prevents retrograde atrial contraction
- Better QOL
- lower risk of AF
Dual chamber modes
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
CRT-D / CRT-P
cardiac resynchronisation therapy - improve cardiac function, symptoms, morbidity in chronic HF
If ICD indicated then CRT-D
Pacemaker check in patient with temporary wires
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.
pacemaker problems
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.
overdrive pacing
Slow VT
pace above rate to take over myocardial activity and convert to sinus rhythm
OOHCA epidemiology
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
Key concepts in cardiac arrest management
- 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
Drugs in cardiac arrest
- 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
Post-cardiac arrest syndrome
- brain injury
- myocardial dysfunction
- systemic ischaemia-reperfusion injury
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
CT pre angio
if signs of cerebral or PE pre arrest
- headache
- seizures
- focal neurological deficit
- SOB / hypoxaemia
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
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
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
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
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
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
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
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
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
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
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
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
supportive measures in tamponade
- avoid surges in catecholamines - pain etc
- fluid bluses
- tertiary centre if possible
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
