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second year > pathophysiology of heart failure > Flashcards

pathophysiology of heart failure Flashcards

1
Q

in systolic or diastolic dysfunction, is the ejection fraction reduced to less than 40% (the usual is 50-65%)?

A

systolic dysfunction

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2
Q

what are some conditions that cause a direct decrease in contractility in systolic dysfunction?

A

ischaemic heart disease
coronary artery disease
dilated cardiomyopathies

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3
Q

what are some valve dysfunctions that cause systolic dysfunction?

A

mitral and aortic regurgitation and aortic stenosis

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4
Q

what does systolic dysfunction ultimately result in?

A

increased end diastolic volume and pressure (increased preload)
ventricular dilation
decrease in cardiac output

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5
Q

what is the main problem in diastolic dysfunction?

A

impaired relaxation (decreased filling capacity)

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6
Q

what is a condition that reduces ventricular expansion?

A

restrictive pericarditis

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7
Q

what is a condition that causes increased heart wall thickness?

A

ventricular hypertrophy

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8
Q

pericardial tamponade can also cause diastolic dysfunction, what is pericardial tamponade?

A

build up of fluid in the pericardium restricting ventricular filling

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9
Q

in which side of heart failure does a ‘back up’ of blood cause oedema and ascites?

A

right sided heart failure

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10
Q

in which side of heart failure is there congestion of the GI tract causing weight loss and anorexia?

A

right side

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11
Q

which valve dysfunction causes prolonged right ventricular isovolaemic contraction in right sided heart failure? (2)

A

tricuspid regurgitation

pulmonary valve stenosis

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12
Q

which ventricular remodelling resulting from right sided heart failure canc cause left ventricular heart failure?

A

shift of intraventricular septum

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13
Q

in which side of heart failure is there decreased tissue perfusion and therefore signs of hypoxia and cyanosis?

A

left side

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14
Q

which sided heart failure is a cough with frothy sputum a sign of?

A

left sided heart failure (resulting from pulmonary congestion)

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15
Q

which side of heart failure is paroxysmal nocturnal dyspnea a sign of?

A

left side (pulmonary congestion and redistribution of fluid)

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16
Q

which valve stenosis can cause left sided heart failure?

A

mitral and aortic valve stenosis

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17
Q

what are the three compensatory mechanisms which try to compensate for heart failure but ultimately result in a worsening of the heart failure?

A
  • frank starling mechanism
  • sympathetic nerve activity
  • renin-angiotensin-aldosterone system
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18
Q

how does the frank starling mechanism attempt to increase cardiac output?

A

by increasing preload and venous return and causing an increased dilation of the ventricles (ultimately this can result in dilated cardiomyopathies)

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19
Q

what problems does the frank starling mechanism cause in heart failure?

A
  • decrease in actin/myosin overlap so decrease in tension generation
  • increase in oxygen demand to generate this tension
  • pulmonary congestion
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20
Q

what changes does increased sympathetic nerve activity result in?

A

increase in contractility and heart rate

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21
Q

why is increased vasoconstriction as a result of increased sympathetic nerve activity bad in heart failure?

A

decreases tissue perfusion (blood flow only to essential organs)

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22
Q

which compensatory mechanism does decreased tissue perfusion stimulate?

A

release of renin from the kidneys

this causes release of angiotensin

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23
Q

what does angiotensin 11 cause?

A

directly causes vasoconstriction

causes release of aldosterone which causes fluid and salt retention

24
Q

what myocardial remodelling are angiotensin 11 and aldosterone involved in?

A

inflammatory responses leading to deposition of collagen and fibroblasts in the ventricles which leads to stiffness and a decrease in contractility

25
Q

what are the two ways in which preload and after load are reduced to decrease cardiac workload to treat heart failure?

A

relaxing vascular smooth muscle and reducing blood volume

26
Q

what is the main mechanism for decreasing blood volume in heart failure treatment?

A

inhibiting the RAAS system and mobilise the oedematous fluid

27
Q

what is the first step in treating chronic heart failure?

A

DAB (diuretic, ACE inhibitor/ARB, Beta blocker)

28
Q

which loop diuretic is used in the first step of heart failure treatment?

A

furosemide

29
Q

at which point in the kidney tubule does furosemide work (accounts for 20-30% fluid reabsorption)

A

the thick ascending loop

30
Q

what are two ACE inhibitors used in treatment of chronic heart failure?

A

ramipril and lisinopril

31
Q

what are three angiotensin receptor antagonists used in treatment of chronic heart failure?

A

candesartan, valsartan and (losartan)

32
Q

which class of NYHA heart failure is it recommended to use beta blockers in?

A

class 2-4

33
Q

what are the two beta blockers most commonly used for treatment of heart failure?

A

carevedilol and bisoprolol

34
Q

what drugs have a contraindication for use with beta blockers?

A

rate-limiting calcium channel blockers (verapamil and diltiazem)
digoxin
amiodarone

35
Q

what is the second step of treatment in chronic heart failure?

A

aldosterone antagonists

36
Q

what is the main aldosterone antagonist used?

A

spironolactone

37
Q

what class of NYHA heart failure is it recommended to use aldosterone antagonists in?

A

class 2-4

38
Q

with which type of drug is there a risk of angiodema (rare side effect)?

A

ACE inhibitors

39
Q

which drug can cause gynaecomastia?

A

spironolactone

40
Q

which class of drugs can cause HYPOkalaemia?

A

loop diuretics (eg furosemdie)

41
Q

what is the 3rd/4t step in treatment of chronic heart failure?

A

sacubitril-valsartan nomination or ivabradine (if HR is over 75bpm)

42
Q

what is the name of an additional thiazide like diuretic that can be used in the treatment of heart failure if symptoms persist?

A

metolazone

43
Q

what drug can be used to treat atrial fibrillation?

A

digoxin

44
Q

how does digoxin reduce conduction velocity in the AV node?

A

by reducing SAN firing rate

45
Q

how does digoxin increase contractility?

A

by indirectly increasing SR levels of calcium by inhibiting the sodium/potassium ATPase and preventing calcium being pumped out by the sodium calcium exchanger

46
Q

what are some characteristic digoxin side effects?

A

blurred or yellow vision

47
Q

what are the aims for treating acute heart failure?

A

normalise ventricular filling pressures

restore adequate tissue perfusion

48
Q

what is the definition of acute heart failure?

A

sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs

49
Q

what is the first line in treating acute heart failure?

A

LMNOP
(L = loop diuretic (furosemide))
M = Morphine (IV opiates to reduce anxiety and cause vasodilation and reduce preload)
N = nitrates (sublingual GTN to cause vasodilation and reduce preload and after load)
O = oxygen to maintain O2 saturation levels
P = positioning (keep patient upright)

50
Q

what is the aim of increasing contractility in acute heart failure?

A

increase stroke volume and increase cardiac output to clear pooled blood from ventricles

51
Q

what happens when the baroreceptors detect an increase in blood pressure caused by an increase in CO?

A

they decrease sympathetic nerve supply and decrease HR and TPR

52
Q

what type of inotropes are used to increase myocardial contractility?

A

beta-agonists

53
Q

which beta agonist works on beta 1 and 2 receptors and works in cariogenic shock?

A

dobutamine

54
Q

which beta agonist works to increase renal perfusion at low doses and increase Bp at high does?

A

dopamine

55
Q

what beta agonist is used to increase myocardial contractility in bradycardia and heart block emergencies?

A

isoprenaline

56
Q

which vasopressor is used to treat severe septic shock to raise Bp and cause vasoconstriction?

A

noradrenaline

second year (24 decks)

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