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module 103 - theme 3 > heart failure > Flashcards

heart failure Flashcards

1
Q

what is the definition of heart failure?

A
  • a state that developed when the heart fails to maintain an adequate cardiac output to meet the demands of the body
  • results from any structural or functional abnormality that impairs the ability of the ventricle to eject blood or fill with blood
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2
Q

at rest what is the normal value of cardiac output?

A

70mls/kg/min

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3
Q

what is the equation for cardiac output?

A

heart rate x stroke volume

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4
Q

what does an increased heart rate generally lead to?

A

increased cardiac output

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5
Q

what generally happens to the heart during systole and diastole?

A
  • heart contracts in systole
  • heart relaxes in diastole
  • ventricles fill in diastole
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6
Q

what does an excessively high heart rate result in?

A

a decrease in the amount of time allowed for the ventricles to fill in diastole which causes SV and therefore CO to fall

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7
Q

what is contractility?

A

the intrinsic ability of the myocardium to contract

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8
Q

what is preload?

A

the volume of blood stretching of cardiomyocytes at the end of diastole prior to the next contraction

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9
Q

what is afterload?

A

the resistance/end load against which the ventricle contracts to eject blood

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10
Q

what affects preload?

A

the venous blood pressure and the rate of venous return to the heart which in turn is affected by venous tone and volume of circulating blood

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11
Q

what increases and decreases preload?

A
  • increases with increasing blood volume and vasoconstriction
  • decreases with blood volume loss and vasodilation
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12
Q

what does the Frank-Starling law do?

A

describes the relationship between preload and cardiac output

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13
Q

what does the Frank-Starling law state?

A

an increase in volume of blood filling the heart stretches and the heart muscle fibres causing greater contractile forces, which, in turn increases stroke volume

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14
Q

what is an issue with the Frank-Starling law?

A

it is only true up to a certain point as at some stage the fibres become overstretched and the force of contraction is reduced

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15
Q

what increases and decreases afterload?

A
  • increases with hypertension and vasoconstriction

- decreases with vasodilation

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16
Q

what happens after afterload increases?

A

cardiac output decreases

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17
Q

what are the 2 types of low output heart failure?

A
  • systolic heart failure

- diastolic heart failure

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18
Q

what is high output heart failure?

A
  • occurs in the context of other medical conditions which increase demand on cardiac output, causing a clinical picture of Hf
  • the heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one of more organs in the body
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19
Q

what are the causes of high output heart failure?

A
  • thyrotoxicosis
  • profound anaemia
  • pregnancy
  • paget’s disease
  • acromegaly
  • sepsin
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20
Q

what is systolic heart failure?

A

progressive deterioration myocardial contractile function

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21
Q

what causes systolic heart failure?

A
  • ischaemic injury
  • volume overload
  • pressure overload
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22
Q

what is diastolic heart failure?

A

inability of the heart chamber to relax, expand and fill sufficiently during diastole to accommodate an adequate blood volume

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23
Q

what causes diastolic heart failure?

A
  • significant left ventricular hypertrophy
  • infiltrative disorders
  • constrictive pericarditis
  • restrictive cardiomyopathy
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24
Q

what are the general causes of heart failure?

A
  • coronary heart disease
  • hypertensive heart disease
  • valvular heart disease
  • myocardial disease/cardiomyopathies
  • congenital heart disease
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25
Q

what are cardiomyopathies?

A

diffuse disease of the heart muscle leading to functional impairment

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26
Q

what are the 3 different types of cardiomyopathies?

A
  • dilated cardiomyopathy
  • hypertrophic cardiomyopathy (hereditary)
  • restrictive cardiomyopathy (rare)
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27
Q

what causes dilated cardiomyopathy?

A
  • ETOH
  • pregnancy
  • systemic disease
  • muscular dystrophies
  • drug toxicity
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28
Q

what are the 3 compensatory mechanisms that kick in to maintain arterial pressure and perfusion of vital organs?

A
  • The Frank-Starling mechanism
  • myocardial structural change
  • activation of neurohormonal system
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29
Q

what happens with the Frank-Starling compensatory mechanism?

A
  • vasoconstriction
  • increased venous return to the heart
  • increased preload
  • heart muscle fibres stretch
  • enhanced contractility
30
Q

what happens with the myocardial structural change compensatory mechanism?

A

augmented muscle mass with or without cardiac chamber dilatation

31
Q

what happens with the activation of neurohormal system compensatory mechanism?

A
  • release of noradrenaline: increases heart rate and myocardial contractility, causes vasoconstriction
  • release ANP/BNP
  • activation of renin-angiotensin: aldosterone system
32
Q

what 3 side effects can the compensatory mechanisms cause on the body?

A
  • vasoconstriction: increases resistance against which heart has to pump and therefore may decrease CO
  • Na and water retention: increased fluid volume which increases preload, if too much stretch it leads to decrease contractile strength and CO
  • excessive tachycardia: this leads to decreased diastolic filling time leading to decreased ventricular filling leading to decreased SV and CO
33
Q

what are the clinical types of heart failure?

A
  • left sided, right sided and biventricular
  • acute and chronic
  • compensated and decompensated
34
Q

what happens with left sided heart failure?

A

blood backs up progressively from the left atrium to the pulmonary circulation

35
Q

what are the causes of left sided heart failure?

A
  • ischaemic heart disease
  • hypertension
  • valvular heart disease
  • myocardial disease
36
Q

what causes pulmonary congestion and oedema and left sided heart failure?

A

the pressure in the pulmonary veins is transmitted retrogradely to the capillaries and arteries

37
Q

what effects to heavy wet lungs have on the body with left sided heart failure?

A
  • breathlessness (dyspnoea) exaggerated of the normal breathlessness that follows exertion
  • orthopnoea: breathlessness lying flat that is relieved by sitting or standing
  • paroxysmal nocturnal dyspnoea: an extension of orthopnoea with attacks of extreme dyspnoea bordering on suffocation usually occurring at night
38
Q

what happens to the kidneys with left ventricular failure?

A
  • decreased cardiac output
  • reduction in renal perfusion
  • activation of renin: angiotensin: aldosterone system
  • retention of salt and water with consequent expansion of interstitial fluid and blood volumes
39
Q

what happens to the brain with left ventricular failure?

A
  • hypoxic encephalopathy
  • irritability
  • loss of attention
  • restlessness
  • stupor and coma
40
Q

what is normally a big cause of right sided heart failure?

A

usually as a consequence of left sided heart failure (congestive cardiac failure)

41
Q

what is cor-pulmonale?

A
  • right sided heart failure due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
  • usually as a result of respiratory disease
42
Q

what are the other causes of right sided heart failure?

A
  • valvular heart disease

- congenital heart disease

43
Q

what are the systemic effects on the liver and portal system of right heart failure?

A
  • congestive hepatomegaly
  • centrilobar necrosis when severe
  • cardiac cirrhosis
44
Q

what are the systemic effects on the spleen of right heart failure?

A

congestive splenomegaly

45
Q

what are the systemic effects on the abdomen of right heart failure?

A

ascites: accumulation of transudate in peritoneal cavity

46
Q

what are the systemic effects on the subcutaneous tissue of right heart failure?

A
  • peripheral oedema of dependent portions of the body (especially ankle and pretibial oedema)
  • sacral oedema
47
Q

what are the systemic effects on the pleural and pericardial space of right heart failure?

A

effusions

48
Q

what causes biventricular failure?

A
  • due to the same pathological process on each side of the heart
    OR
  • a consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular riskier
49
Q

what is the clinical presentation of biventricular failure due to excess fluid accumulation?

A
  • dyspnoea
  • orthopnoea, paroxysmal nocturnal dyspnoea
  • oedema
  • hepatic congestion
  • ascites
50
Q

what is the clinical presentation of biventricular failure due to reaction in cardiac output?

A
  • fatigue

- weakness

51
Q

what are the New York heart association classifications of heart failure?

A
  • class I: no limitation of physical activity
  • class II: slight limitation or ordinary activity
  • class III: marked limitation, even during less-than-ordinary activity
  • class IV: severe limitation with symptoms at rest
52
Q

what are the clinical signs of cardiac failure?

A
  • cool, pale, cyanotic extremities
  • tachycardia
  • elevated JVP
  • third heart sound (S3) - gallop rhythm
  • displaced apex (LV enlargement)
  • crackles or decreased breath sounds at bases on chest auscultation
  • peripheral oedema
  • ascites
  • hepatomegaly
53
Q

what are the clinical tests in heart failure?

A
  • CXR
  • ECG
  • blood investigations
  • echocardiogram/cardiac MRI or CT/CT-PET
  • CTCA/coronary angiography
54
Q

give the 2 examples of loop diuretics

A
  • frusemide

- bumetanide

55
Q

what do loop diuretics do?

A
  • inhibit Na+ reabsorption from proximal tubule
  • K+ loss from distal tubule
  • can be given IV or orally
  • potent can lead to: electrolyte abnormalities, hypovolaemia and diminished renal perfusions
56
Q

give the 2 examples of minteralocorticoid receptor antagonists

A
  • epelerenone

- spironolactone

57
Q

how do mineralocorticoid receptor antagonists work?

A
  • acts on distal tubule
  • promotes Na+ extortion and K+ reabsorption
  • reduces hypertrophy and fibrosis
  • principle side effects: gynaecomastia, electrolyte and renal function abnormalities
58
Q

give the 5 examples of ACE inhibitors

A
  • ramipril
  • perindopril
  • enalapril
  • captopril
  • lisinopril
59
Q

how do ACE inhibitors work?

A
  • act on activated renin: angiotensin system
  • given orally in small episodes with slow titration
  • block production of angiotensin: vasodilation, BP lowering, reduce cardiac work
  • principle side effects: cough, hypotension, renal impairment
60
Q

give the 3 examples of beta blockers

A
  • bisoprolol
  • carvedilol
  • metoprolol
61
Q

how do beta blockers work?

A
  • block the action of adrenaline and noradrenaline on adrenergic beta receptors
  • slow HR, reduce BP
  • given orally in small doses with slow titration
  • (treat arrhythmias)
  • principle side effects: bronchospasm, claudication
62
Q

give the example of a SA node blockade

A

ivabradine

63
Q

how do SA node blockades work?

A
  • blocks the If channel with the SA node
  • slow HR, no effect on BP
  • given orally with dose titration
  • principle side effects: visual aura, bradycardia
64
Q

what is the action of digoxin?

A
  • increased myocardial contractility
  • slows condiction at the AV node (use in AF)
  • excreted by the kidney: toxicity important
65
Q

when is digoxin given?

A
  • acute Hf especially in AF

- chronic HF in selected cases

66
Q

give the example of ARNI

A

sacubitril valsartan

67
Q

how does ARNI work?

A
  • acts of activated renin: angiotensin system
  • also blocks breakdown of ANP/BNP
  • blocks production of angiotensin: vasodilation, BP lowering, reduce cardiac work
  • promotes natriuresis: sodium excretion, vasodilation, reduce hypertrophy and fibrosis
  • principle side effects: hypotension, renal impairment
68
Q

what are the other therapies used to treat heart failure?

A
  • cardiac resynchronisation therapy
  • implantable cardioverter defibrillator
  • dialysis and ultrafiltration
  • ventricular assist decide
  • intra-aortic balloon pump
  • cardiac translation
  • (stem cell therapy)
69
Q

how many wires do pacemakers have?

A

2 wires but biventricular pacemakers have an additional 3rd lead designed to conduct signals directly into the left ventricle

70
Q

how does biventricular pacing work?

A
  • conduct pacing signals to specific regions of the heart
  • combination of all 3 leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole

module 103 - theme 3 (17 decks)

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