Heart Failure Flashcards
What is heart failure?
HF is a clinical syndrome characterized by typical symptoms
- caused by a structural and/or functional cardiac abnormality
= resulting in a reduced cardiac output and/ or elevated intracardiac pressures at rest or during stress
What are the types of heart failure? How are they categorised?
Based on the LVEF (left ventricular ejection fraction)
LVEF ≥ 50%: Preserved ejection fraction (HFpEF )
LVEF 40-49%: Mid-range ejection fraction (HFmEF)
LVEF < 40%: Reduced ejection fraction (HFrEF)
What is preload? What is afterload?
preload
- the amount of blood the heart must pump with each beat
- depends on venous return to heart and accompanying stretch of muscle fibres
afterload
- pressure that must be overcome for the heart to pump blood into the arterial system
- depends on systemic vascular resistance
What are the causes of heart failure?
coronary artery disease
hypertension
valvular heart disease
infections
dysrhythmias
chronic alcohol consumption
myocardial infarction
diabetes
What are the symptoms of heart failure?
orthopnoea (SOB when lying flat, require pillows to sleep)
paroxysmal nocturnal dyspnoea (SOB that wakes you at night)
oedema
diaphoresis (excessive sweating/night sweats)
pulmonary congestion
fatigue
dyspnoea
chest pain
reduced exercise tolerance
dizziness
syncope
confusion, agitation
What are lifestyle interventions for heart failure?
smoking cessation
weight management
exercise
cardiac rehabilitation
diet/salt intake
vaccinations
- annual flu, pneumococcal
fluid restriction
- 1.5-2 L/day
drugs to avoid
- NSAIDs
What are pharmacological treatments for heart failure?
diuretics
- thiazides, loop diuretics, potassium sparing diuretics
ACE inhibitors
angiotensin receptor blockers (ARB)
aldosterone/mineralocorticoid receptor antagonists (MRA)
angiotensin receptor/neprilysin inhibitor (ARNI)
beta blockers
digoxin
hydrazine/isosorbide mononitrate
ivabradine
sodium glucose cotransporter 2 inhibitor
How do thiazides work? How do loop diuretics work? How do potassium sparing diuretics work?
What are the side effects?
bendroflumethazide
- block Na/Cl transporter in the distal convoluted tubule
furosemide
- block the Na/K/2Cl transporter in the loop of henle
amiloride
- block Na reabsorption by binding to Na channels or aldosterone receptors
side effects
- hypokalaemia, hyperglycaemia, hyperuricaemia, social disruption (incontinence)
How do mineralocorticoid receptor antagonists work? What are the side effects and interactions?
competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention
side effects
- gynaecomastia, menstrual irregularities, hyperkalaemia, testicular atrophy
interactions
- potassium supplements and sparing diuretics
How do ACE inhibitors work? What are the side effects?
prevent angiotensin converting enzyme from producing angiotensin II (vasoconstrictor)
side effects
- first dose hypotension, cough, angio oedema, deterioration of renal function
How do angiotensin receptor blockers work? What are the side effects?
blocking receptors that the angiotensin acts on, specifically AT1 receptors
side effects
- deterioration of renal function, hypotension
What are contraindications for beta blockers? What are drug interactions?
asthma
uncontrolled heart failure
peripheral vascular disease
severe bradycardia
hypotension or shock
clinically significant heart block or heart rate
interactions
- verapamil, diltiazem, digoxin
Why is digoxin toxicity enhanced by hypokalaemia?
hypokalaemia means digoxin can more readily binds to potassium place in the Na/K ATPase pump
- enables greater effect/function
How do angiotensin receptor/neprilysin inhibitors work?
inhibition of neprilysin blocks the breakdown of natriuretic peptide
- vasodilator and increase diuresis
sacubitril/valsartan
How does ivabradine work?
selectively blocks the If channel by binding to a site in the channel pore
- this reduces the f-current and thereby reduces the slope of the slow diastolic depolarisation phase of the action potential in the sinoatrial node cells
- this results in an increase in the time required to reach the voltage threshold for action potential initiation