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103: Theme 3 > Heart failure > Flashcards

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
Q

LV failure on the kidneys

A

Decreased cardiac output

Reduction in renal perfusion

Activation of RAAS

Retention of salt and water with expansion of interstitial fluid and blood volumes

26
Q

LV failure on the brain

A

Hypoxic encephalopathy

Irritability

Loss of attention

Restlessness

Stupor and coma

27
Q

Right side heart failure

A

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
Q

RH failure on liver and portal system

A

Congestive hepatomegaly

Centrilobular necrosis when severe

Cardiac cirrhosis

29
Q

RH failure on spleen

A

Congestive splenomegaly

30
Q

RH failure on abdomen

A

Ascites- accumulation of transudate in peritoneal cavity

31
Q

RH failure on subcutaneous tissue

A

Peripheral oedema of dependent portions of body especially ankles

Sacral oedema if bedridden

32
Q

RH failure of pleural and pericardial space

A

Effusions

33
Q

Biventricular failure

A

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
Q

Clinical presentation of heart failure

A

Due to excess fluid accumulation

  • dyspnoea
  • orthopnoea, PND
  • oedema
  • hepatic congestion
  • ascites

Due to reduction in CO

  • fatigue
  • weakness
35
Q

Class I heart failure

A

No limitation of physical activity

36
Q

Class II heart failure

A

Slight limitation of ordinary activity

37
Q

Class III heart failure

A

Marked limitation, even during less than ordinary activity

38
Q

Class IV heart failure

A

Severe limitation with symptoms at rest

39
Q

Clinical signs of cardiac failure

A

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
Q

Acute pulmonary oedema

A

MEDICAL EMERGENCY

  • acute breathlessness
  • pallor
  • cyanosis
  • sweating
  • rapid pulse
  • hypoxia
  • crackles in lungs
41
Q

Clinical tests in heart failure

A 
CXR
ECG
Blood investigations
Echocardiogram/ MRI/ CT
CTCA
42
Q

Current drug treatment

A

ACEi/ ARBs

ARNI

Aldosterone antagonists

Beta blockers

SA node blockade

Diuretics

43
Q

ACEi/ ARBs

A

Block angiotensin

  • enalapril, ramipril, perindopril
  • losartan, candesartan, irebesartan
44
Q

ARNI

A

Angiotensin receptor inhibitor
- sacubitril, valsartan

Acts in activated RAAS
Blocks production of angiotensin
Promotes natriuresis

Side effects

  • hypotension
  • renal impairment
45
Q

Aldosterone antagonists

A

Spironolactone

Eplerenone

46
Q

Beta blockers

A

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
Q

SA node blockade

A

Ivabradine

Blocks If channel with SA node
Slows HR, no BP effect
Orally with dose titration

Side effects

  • visual aura
  • bradycardia
48
Q

Diuretics

A

Loops- furosemide, bumetanide

Thiazides- bendrofluamethiazise, indapamide

Quinazolines- metolazone

49
Q

Loop diuretics

A

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
Q

Mineralocorticoid receptor antagonists

A

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
Q

ACE inhibitors

- pril

A

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
Q

Digoxin

A

Action

  • increases myocardial contractility
  • slows conduction at AV node
  • excreted by kidney

Given

  • acute HF especially in AF
  • chronic HF in selected cases
53
Q

Immediate treatment of acute pulmonary oedema

A

High flow oxygen

IV morphine

IV nitrates

IV furesimide

54
Q

Definitive treatment of acute pulmonary oedema

A

Identity cause

Oral diuretics

Medical therapy

Revascularisation if appropriate

103: Theme 3 (17 decks)

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