Heart failure Flashcards

1
Q

What events lead to heart failure?

A

Cardiac growth and remodelling due to reflex mechanisms that aim to maintain CO, e.g. increased SNS
Increase HR and contractility
Atrial and venous constriction
Increased catecholamines
Increased renin release, as renal perfusion decreases.

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2
Q

Compare cardiac remodelling is systolic and diastolic hypertension.

A

Systolic- dilated

Diastolic - hypertrophy

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3
Q

How is heart failure treated?

A

Lifestyle changes
Drugs reducing cardiac workload
Drugs increasing cardiac contractility

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4
Q

What are examples of K+ sparing diuretics?

A

Aldosterone agonists - spironolactone, eplerenone
Na+ channel blockers - amiloride

Act as distal tubule/collecting duct

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5
Q

What is the mechanism of action aldosterone agonists, e.g. spironolactone, eplerenone?

A

Act at the distal tubule/collecting duct as diuretics, oppose cardiac remodelling.

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6
Q

How can hypokalaemia be prevented in use of K+ sparing diuretics?

A

Use K+ sparing diuretics with thiazide or loop diuretics

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7
Q

What is the benefit of non-selective over selective beta blockers?

A

Alpha receptor antagonist reduces afterload

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8
Q

When are beta-blockers used in heart failure?

A

Adjunct to conventional therapy when the patient is stable, starting with low doses and slowly increasing

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9
Q

What are the side effects and clinical considerations of beta blockers?

A

Cold extremities with antagonised beta2 receptors, provocation of asthma, heart failure if unstable, mask glycaemic episodes in diabetes as stop tremors

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10
Q

List the positive ionotropic agents that are used in HF.

A

Cardiac glycosides - digoxin

Beta1 adrenoceptor agonists

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11
Q

What is the mechanism of action of digoxin?

A

Inhibits Na/K ATPase, increasing inracellular NA, activating Na+/Ca2+ exchanger, increasing myocardial intracellular Ca2+

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12
Q

What is the therapeutic effect of digoxin?

A

Increased myocardial contractility and reduced O2 use, increases CO

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13
Q

When is digoxin most effective?

A

Cardiomyopathies, some dysrhythmias

Less effective in CHF secondary to hypertension.

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14
Q

What is the major concern in use of digoxin?

A

Narrow safety margin, 75% absorption, long 1/2-life of 30-40 hours (mainly excreted by kidneys)

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15
Q

How long does it take to reach the steady state for digoxin?

A

A week

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16
Q

List the ADRs of digoxin.

A

CVS: dysrrhythmia
GIT: anorexia, nausea, vomiting, diarrhoea
Nervous system: stimulates vagal and vomiting centres, visual disturbance, disorientation, agitation, hallucination

17
Q

Why is the use of beta1 adrenoceptor agonists, such as dobutamine, limited?

A

Desensitisation while there is already down-regulation of beta1 adrenoceptors in CHF
Can trigger dysrhythmias

18
Q

What are the peripheral vasodilators used in HF?

A

Nitrovasodilators
Hydralazine
Milrinone

19
Q

What is the mechanism of action of nitrovasodilators?

A

Organic nitrates that donates NO to smooth muscle, e.g. isosorbide dinirate, GTN, sodium nitroprusside

20
Q

What are side effects of hydralazine?

A

Hypotension, flushing, head ache, tachycardia

21
Q

What is the mechanism of action of milrinone?

A

Ionotropic and vasodilator activity

Phosphodiesterase inhibition increases cAMP in cardiac and vascular smooth muscle.