heart failure - treatment and management Flashcards
Classification of heart failure
NYHA functional classification (class 1-4)
Class 1 heart failure
No symptomatic limitation of physical activity
Class 2 heart failure
Slight limitation to physical activity
- Ordinary physical activity gives symptoms
- No symptoms at rest
Class 3 heart failure
Limitation to physical activity
- less than ordinary activity = symptoms
- no symptoms at rest
Class 4 heart failure
Inability to carry out any physical activity without symptoms
- may have symptoms at rest
- discomfort increases with any degree of physical activity
Investigations heart failure
Do they have heart failure (history, examination, investigations)
What sort of heart failure do they have? (HFrEF, HFpEF, valvular, RV heart failure, high output heart failure)
What is causing heart failure? (ischaemic heart disease, hypertension, viral ETOH (ethanol alcohol))
What is HFrEF? usually
Left ventricular systolic dysfunction
What is HFpEF? usually
Stiff left ventricular (diastolic - not called this anymore)
Symptomatic treatment heart failure
Furosemide (reduce fluid levels)
Which heart failure is prognosis treatment effective for?
HFrEF
Prognosis treatments (drugs)
ACE inhibitors Angiotensin receptor blockers Beta blocker Mineralocorticoid receptor antagonist (eg spironolactone) SGLT2 inhibitors (diabetes)
New prognosis drugs treatment
Sacubitril valsartan
Other prognosis treatment (no drugs)
Implantable cardioverter defibrillator (control arrhythmias)
Biventricular pacemaker - make rhythm better speed if heart too slow
Immediate treatment heart failure presentation
Furosemide
O2 (if hypoxic)
Respiratory support - if needed eg CPAP
IV nitrates, morphine
Problem with beta blockers
Slow heart rate in already low cardiac output situation
If heart rate is keeping alive (ie stroke volume is very small) = BAD
What drugs may be needed in atrial fibrillation?
Anti-coagulants (high risk of thrombus forming in atria)
What can CXR show in heart failure?
Cardiomegaly Upper lobe diversion (pulmonary veins dilated) Fluid in fissure (boundaries of lung) Pleural effusions Kerley B lines (horizontal white lines)
Furosemide
Immediate effects 30 mins peaking 60-90 mins
Higher doses needed in renal failure
Monitoring furosemide
HR, BP, O2 CXR
Fluid balance (in vs out)
Hourly urine output
Daily weights (1kg weight loss per day)
Left ventricular aneurysm ECG and Xray
Broad QRS lines (V shape)
Boot shaped heart x-ray
Blood tests heart failure gold standard
NTpro-BNP
natriuretic peptide released in response to atrial/ventricular stretch from fluid overload
range varies with age/gender (atrial fibrillation can increase)
Other blood tests heart failure
FBC (anaemic?)
U&E’s (renal function deteriorates in HF, Na+ K+ levels needed for medications)
LFT’s (hepatic congestion? = elevated)
Clotting (need anticoagulants?)
Thyroid, Vit D, CRP (is it heart failure from heart)
Why do we get heart failure?
2 sides:
Dark side, makes things worse - RAAS system and baroreceptor sympathetic stimulation
Light side - Increase ANP and BNP (doesnt activate until TOO LATE)
What does increase ANP and BNP cause?
Increase natriuresis - sodium excretion
Increase diuresis
Vasodilation
Decrease RAAS activity
Sacubitril valsartan how does it work
Slows breakdown of natriuretic peptides - helps
Key history questions heart failure
Recent viral illness Anabolic steroids ETOH (alcohol) Smoking Family history
Investigations heart failure
Echocardiogram
Stress Cardiac MRI/coronary angiogram (ischaemia?)
What does RAAS do in heart failure?
Angiotensin 2 =
vasoconstriction
enhanced sympathetic activity
salt and water retention
Drugs targeting RAAS
ACE inhibitors (no angiotensin 2 produced) ARB - blocks angiotensin acting on receptors
What does RAAS and sympathetic activation overall result in?
Increased myocardial oxygen demand
Myocardial hypertrophy
Decreased contractility
Myocyte damage (direct cardiotoxicity of long term SNS activation)
What does short term activation of SNS do?
Tachycardia
Increase cardiac contractility
Vasoconstriction
What does long term activation of SNS do?
B adrenergic receptors are down regulated/uncoupled (no longer sensitive)
Noradrenaline then induces hypertrophy/myocyte apoptosis via a-receptors
Upregulates RAAS
What do B blockers do?
Reduce HR
Reduce BP (and CO)
= reduced myocardial oxygen demand
Resensitise receptors (stop unwanted catacholamine effects) Reduce mobilisation of glycogen
Problem with Beta blockers?
Failing myocardium may be dependent on HR for cardiac output
If lowered could be detrimental
start low dose
What is spironolactone (aldosterone receptor antagonist) used for?
When using ACE inhibitor and ARB therapy, aldosterone can ‘escape’ and return to normal concentrations
Blocks effects on receptor
Biventricular pacemaker location
Lead in coronary sinus vein
Right atrium ventricle
Biventricular defibrillator X-ray
Bright white coil/worm base of heart
What is needed when treating HFrEF?
Cardiac rehab Multidisciplinary team Patient education Pallative care/transplant evidence based treatments
Summary all investigations
Bloods (NTpro-BNP, FBC)
ECG
CXR
Transthoracic echocardiogram
Cardiac MRI (ischaemia/myopathy)
Coronary angiography (x-ray vessels)
Cardiomyopathy blood test screen (eg haemachromatosis)
Genetics
HFpEF treatments
Control BP
Limited evidence spironolactone ?
Valvular/structural treatments
Surgery to repair valve/replace
When does RV failure occur?
Usually secondary to LV failure
If isolated could be chronic lung condition - refer to specialist
