Heart failure Flashcards

1
Q

Heart failure

A

A state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body

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2
Q

Impact of heart failure in the UK

A

In-hospital mortality- 9.4%
30 day mortality in those surviving to discharge- 6.1%
Overall 30 day mortality- 14.9%

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3
Q

Cardiac output

A

= heart rate x stoke volume

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4
Q

Contractility

A

The intrinsic ability of the myocardium to contract

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5
Q

Preload

A

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

Affected by venous blood pressure

Increases with increasing blood volume and vasoconstriction

Decreases with blood volume loss and vasodilation

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6
Q

Afterload

A

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

The pressure in the aorta/ pulmonary artery that the left/ right ventricular muscle must overcome to eject blood

Increases with hypertension and vasoconstriction

Decreases with vasodilation

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7
Q

Frank- Starling Laq

A

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

Only true up to certain point, at some stage the fibres become over-stretched and the force of contraction is reduced

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8
Q

Low output heart failure

A

Systolic heart failure

Diastolic heart failure

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9
Q

High output heart failure

A

Occurs in context of other medical conditions which increase demands on cardiac output

Heart itself functions normally but cannot keep up unusually high demand for blood to one or more organs

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10
Q

Causes of high output heart failure

A
Thyrotoxicosis
Profound anaemia
Pregnancy
Pagets disease
Acromegaly
Sepsis
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11
Q

Systolic heart failure

A

Progressive deterioration myocardial contractile function

  • ischeamic injury
  • volume overload
  • pressure overload
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12
Q

Diastolic heart failure

A

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

  • significant left ventricular hypertrophy
  • infiltrative disorders
  • constrictive pericarditis
  • restrictive cardiomyopathy
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13
Q

Causes of heart failure

A

Coronary heart disease

Hypertensive heart disease

Valvular heart disease

Myocardial disease/ cardiomyopathies

Congenital heart disease

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14
Q

Cardiomyopathies

A

Diffuse disease of the heart muscle leading to functional impairment

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15
Q

Dilated cardiomyopathy

A

Various causes, 50% familial

ETOH, pregnancy, systemic disease, muscular dystrophies

Drig toxicity (chemotherapy- anthracyclines, herceptin)

Myocarditis- aetiology includes viral

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16
Q

Hypertrophic cardiomyopathy

A

Hereditary

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17
Q

Restrictive cardiomyopathy

A

Rare

Amyloid the main cause in the UK

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18
Q

Activation of neurohormonal system in heart failure

A

Release of noradrenaline

  • increases HR and myocardial contractility
  • causes vasoconstriction

Release of ANP/ BNP

Activation of renin angiotensin aldosterone system

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19
Q

Vasoconstriction compensation

A

Increases resistance against which heart has to pump

May therefore decrease cardiac output

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20
Q

Na and water retention compensation

A

Increases fluid volume

Increases preload

If too much stretch, decreases contractile strength and CO

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21
Q

Excessive tachycardia compensation

A

Decreases diastolic filling time

Decreases ventricular filling

Decreases SV and CO

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22
Q

Clinical types of heart failure

A

Left sided, right sided and biventricular failure

Acute and chronic heart failure

Compensated and decompensated heart failure

23
Q

Left side heart failure

A

Blood blocks up progressively from left atrium to pulmonary circulation

Causes

  • ischaemic heart disease
  • hypertension
  • valvular heart disease
  • myocardial disease
24
Q

LV failure on the lungs

A

Pressure in pulmonary veins transmitted to capillaries and arteries

Pulmonary congestion and oedema

Heavy wet lungs

  • breathless
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
25
LV failure on the kidneys
Decreased cardiac output Reduction in renal perfusion Activation of RAAS Retention of salt and water with expansion of interstitial fluid and blood volumes
26
LV failure on the brain
Hypoxic encephalopathy Irritability Loss of attention Restlessness Stupor and coma
27
Right side heart failure
Usually as consequent of left side failure Cor pulmonale - right failure as pulmonary hypertension from increased resistance in pulmonary circulation - usually result of respiratory disease Other causes - valvular heart disease - congenital heart disease
28
RH failure on liver and portal system
Congestive hepatomegaly Centrilobular necrosis when severe Cardiac cirrhosis
29
RH failure on spleen
Congestive splenomegaly
30
RH failure on abdomen
Ascites- accumulation of transudate in peritoneal cavity
31
RH failure on subcutaneous tissue
Peripheral oedema of dependent portions of body especially ankles Sacral oedema if bedridden
32
RH failure of pleural and pericardial space
Effusions
33
Biventricular failure
Either due to same pathological process on each side OR Consequence of left heart failure leading to volume overload of pulmonary circulation and eventually RV causing RV failure
34
Clinical presentation of heart failure
Due to excess fluid accumulation - dyspnoea - orthopnoea, PND - oedema - hepatic congestion - ascites Due to reduction in CO - fatigue - weakness
35
Class I heart failure
No limitation of physical activity
36
Class II heart failure
Slight limitation of ordinary activity
37
Class III heart failure
Marked limitation, even during less than ordinary activity
38
Class IV heart failure
Severe limitation with symptoms at rest
39
Clinical signs of cardiac failure
Cool, pale, cyanotic extremities Tachycardia Elevated JVP Third heart sound- gallop rhythm Displaced apex Crackles/ decreases breath sounds at bases Peripheral oedema Ascites Hepatomegaly
40
Acute pulmonary oedema
MEDICAL EMERGENCY - acute breathlessness - pallor - cyanosis - sweating - rapid pulse - hypoxia - crackles in lungs
41
Clinical tests in heart failure
``` CXR ECG Blood investigations Echocardiogram/ MRI/ CT CTCA ```
42
Current drug treatment
ACEi/ ARBs ARNI Aldosterone antagonists Beta blockers SA node blockade Diuretics
43
ACEi/ ARBs
Block angiotensin - enalapril, ramipril, perindopril - losartan, candesartan, irebesartan
44
ARNI
Angiotensin receptor inhibitor - sacubitril, valsartan Acts in activated RAAS Blocks production of angiotensin Promotes natriuresis Side effects - hypotension - renal impairment
45
Aldosterone antagonists
Spironolactone Eplerenone
46
Beta blockers
Counteract active sympathetic system - carvedilol - bisoprolol - metoprolol Block noradrenaline/ adrenaline on adrenergic beta receptors Slow HR, reduce BP Orally, small doses, slow titration Side effects - bronchospasms - claudication
47
SA node blockade
Ivabradine Blocks If channel with SA node Slows HR, no BP effect Orally with dose titration Side effects - visual aura - bradycardia
48
Diuretics
Loops- furosemide, bumetanide Thiazides- bendrofluamethiazise, indapamide Quinazolines- metolazone
49
Loop diuretics
Inhibit Na+ re-absorption from the proximal tubule K+ loss from distal tube Can be IV or oral Can lead to - electrolyte abnormalities - hypovolaemia and diminished renal perfusion
50
Mineralocorticoid receptor antagonists
Eplerenone, spironolactone Acts on distal dube Promotes Na+ excretion and K+ re-absorption Reduces hypertrophy and fibrosis Side effects - gynaecomastia - electrolyte and renal function abnormalities
51
ACE inhibitors | - pril
Act on activated renin angiotensin system Given orally, small doses, slow titration Block production of angiotensin - vasodilation - BP lowering - reduce cardiac work Side effects - cough - hypotension - renal impairment
52
Digoxin
Action - increases myocardial contractility - slows conduction at AV node - excreted by kidney Given - acute HF especially in AF - chronic HF in selected cases
53
Immediate treatment of acute pulmonary oedema
High flow oxygen IV morphine IV nitrates IV furesimide
54
Definitive treatment of acute pulmonary oedema
Identity cause Oral diuretics Medical therapy Revascularisation if appropriate