acute heart failure
CC4 Cardiology MRCEM syllabus , see also chronic heart failure
joblist: evidence from mike's presentation re GTN. LR for each. reformat to easier to read format, currently more like DP format. link to NICE guidelines.
clinical presentation
airway/breathing
circulation
- ↓ cardiac output
- pulm cap wedge pressure ↑ as patient gets more unwell
disability
- anything that comes with brain hypoperfusion
exposure
- hypoperfusion →
- peripheral vasoconstriction
- ↑ lactate
etiology: why now?
Think about causes of an acute detioeration in cardiac function
Feel free to sort this into whatever surgical sieve you prefer.
- cardiomyopathy: ischaemia (big ticket), other cardiomyopathies e.g. takotsubo, myocarditis, alcoholic; autoimmune or congenital; trauma (contusion)
- volume overload: iatrogenic, renal failure
- hypovolaemia: dehydration, overdiuresis
- arrhythmia
- valve dysfunction including LVOTO
- drug-related
- non-adherence to therapies
- iatrogenic
- negative inotropy - e.g. beta blockade
- volume overload
- cardiotoxic effects of pchemotherapy agents
- alcohol, cocaine
- SEPSIZZZZ... endocarditis, myocarditis
management/interventions
- CPAP/BIPAP
- invasive ventilation might be needed for haemodynamic instability, or if required for procedures
- therapeutic drainage? → to buy time to correct the heart failure
afterload reduction
- GTN
- inodilators - milrinone or dobutamine
- milrinone works slowly
- inopressors - norad, low dose adrenaline (to make use of the +ve inotropic effects)
managing fluid status
- tricky to say the least......
- 50% are euvolaemic (source needed)
- Depends on Right heart failure
treating underlying cause
- tachyarrhythmia - if AF etc., maybe useful. but sinus tachy might be part of compensation!
- MI → revascularisation
pitfalls
- don't start beta blockers in this context - this is for stable chronic heart failure
- don't rely just on furosemide - plus evidence points to benefit from vasodilation rather than diuresis