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
what are the two ways in which preload and after load are reduced to decrease cardiac workload to treat heart failure?
relaxing vascular smooth muscle and reducing blood volume
26
what is the main mechanism for decreasing blood volume in heart failure treatment?
inhibiting the RAAS system and mobilise the oedematous fluid
27
what is the first step in treating chronic heart failure?
DAB (diuretic, ACE inhibitor/ARB, Beta blocker)
28
which loop diuretic is used in the first step of heart failure treatment?
furosemide
29
at which point in the kidney tubule does furosemide work (accounts for 20-30% fluid reabsorption)
the thick ascending loop
30
what are two ACE inhibitors used in treatment of chronic heart failure?
ramipril and lisinopril
31
what are three angiotensin receptor antagonists used in treatment of chronic heart failure?
candesartan, valsartan and (losartan)
32
which class of NYHA heart failure is it recommended to use beta blockers in?
class 2-4
33
what are the two beta blockers most commonly used for treatment of heart failure?
carevedilol and bisoprolol
34
what drugs have a contraindication for use with beta blockers?
rate-limiting calcium channel blockers (verapamil and diltiazem) digoxin amiodarone
35
what is the second step of treatment in chronic heart failure?
aldosterone antagonists
36
what is the main aldosterone antagonist used?
spironolactone
37
what class of NYHA heart failure is it recommended to use aldosterone antagonists in?
class 2-4
38
with which type of drug is there a risk of angiodema (rare side effect)?
ACE inhibitors
39
which drug can cause gynaecomastia?
spironolactone
40
which class of drugs can cause HYPOkalaemia?
loop diuretics (eg furosemdie)
41
what is the 3rd/4t step in treatment of chronic heart failure?
sacubitril-valsartan nomination or ivabradine (if HR is over 75bpm)
42
what is the name of an additional thiazide like diuretic that can be used in the treatment of heart failure if symptoms persist?
metolazone
43
what drug can be used to treat atrial fibrillation?
digoxin
44
how does digoxin reduce conduction velocity in the AV node?
by reducing SAN firing rate
45
how does digoxin increase contractility?
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
what are some characteristic digoxin side effects?
blurred or yellow vision
47
what are the aims for treating acute heart failure?
normalise ventricular filling pressures | restore adequate tissue perfusion
48
what is the definition of acute heart failure?
sudden worsening of signs and symptoms of heart failure as a result of severe congestion of multiple organs
49
what is the first line in treating acute heart failure?
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
what is the aim of increasing contractility in acute heart failure?
increase stroke volume and increase cardiac output to clear pooled blood from ventricles
51
what happens when the baroreceptors detect an increase in blood pressure caused by an increase in CO?
they decrease sympathetic nerve supply and decrease HR and TPR
52
what type of inotropes are used to increase myocardial contractility?
beta-agonists
53
which beta agonist works on beta 1 and 2 receptors and works in cariogenic shock?
dobutamine
54
which beta agonist works to increase renal perfusion at low doses and increase Bp at high does?
dopamine
55
what beta agonist is used to increase myocardial contractility in bradycardia and heart block emergencies?
isoprenaline
56
which vasopressor is used to treat severe septic shock to raise Bp and cause vasoconstriction?
noradrenaline