Heart Failure Flashcards

1
Q

What is heart failure?

A

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

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2
Q

What are the types of heart failure? How are they categorised?

A

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)

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3
Q

What is preload? What is afterload?

A

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

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4
Q

What are the causes of heart failure?

A

coronary artery disease
hypertension
valvular heart disease
infections
dysrhythmias
chronic alcohol consumption
myocardial infarction
diabetes

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5
Q

What are the symptoms of heart failure?

A

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

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6
Q

What are lifestyle interventions for heart failure?

A

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

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7
Q

What are pharmacological treatments for heart failure?

A

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

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8
Q

How do thiazides work? How do loop diuretics work? How do potassium sparing diuretics work?

What are the side effects?

A

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)

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9
Q

How do mineralocorticoid receptor antagonists work? What are the side effects and interactions?

A

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

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10
Q

How do ACE inhibitors work? What are the side effects?

A

prevent angiotensin converting enzyme from producing angiotensin II (vasoconstrictor)

side effects
- first dose hypotension, cough, angio oedema, deterioration of renal function

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11
Q

How do angiotensin receptor blockers work? What are the side effects?

A

blocking receptors that the angiotensin acts on, specifically AT1 receptors

side effects
- deterioration of renal function, hypotension

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12
Q

What are contraindications for beta blockers? What are drug interactions?

A

asthma
uncontrolled heart failure
peripheral vascular disease
severe bradycardia
hypotension or shock
clinically significant heart block or heart rate

interactions
- verapamil, diltiazem, digoxin

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13
Q

Why is digoxin toxicity enhanced by hypokalaemia?

A

hypokalaemia means digoxin can more readily binds to potassium place in the Na/K ATPase pump
- enables greater effect/function

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14
Q

How do angiotensin receptor/neprilysin inhibitors work?

A

inhibition of neprilysin blocks the breakdown of natriuretic peptide
- vasodilator and increase diuresis

sacubitril/valsartan

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15
Q

How does ivabradine work?

A

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

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