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Theme 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Heart failure definition

A

Failure to maintain an adequate cardiac output to meet the demands of the body

Structural or functional abnormality - impairs ability of ventricles to eject blood or fill

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2
Q

CO

A

HR x SV

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3
Q

Preload

A

Is affected by venous blood pressure and the rate of venous return to the heart

This, in turn, is affected by venous tone and volume of circulating blood

Preload increases with increasing blood volume and vasoconstriction

Preload decreases with blood volume loss and vasodilatation

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4
Q

Frank-Starling Law

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

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5
Q

Afterload

A

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

The greater the aortic/pulmonary pressure, the greater the afterload on the left/right ventricle respectively

Afterload increase with hypertension and vasoconstriction

Afterload decreases with vasodilatation

As the afterload increases, cardiac output decreases

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6
Q

LOHF

A

Systolic heart failure

Diastolic heart failure

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7
Q

HOHF

A

The heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one or more organs in the body

Causes: thyrotoxicosis, profound anaemia, pregnancy, pagets disease, acromegaly, sepsis

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8
Q

Systolic heart failure

A

Progressive deterioration myocardial contractile function

Ischaemic injury
Volume overload
Pressure overload

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9
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 (LVH) e.g HCM
Infiltrative disorders
Constrictive pericarditis
Restrictive cardiomyopathy

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10
Q

HF causes

A 
Coronary Heart Disease
Hypertensive Heart Disease
Valvular Heart Disease
Myocardial Disease/ Cardiomyopathies
Congenital Heart Disease
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11
Q

Activation of neurohormonal system

A

Release of Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
Release of ANP/BNP
Activation of renin-angiotensin – aldosterone system

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12
Q

Compensatory mechanisms

A

Vasoconstriction
Na and water retention
Excessive Tachycardia

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13
Q

Pressure Overload

A

Concentric left ventricular hypertrophy
E.g. Hypertension or aortic stenosis
Augmented muscle may reduce the cavity diameter
Cross sectional areas of the myocytes are increased

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14
Q

Volume overload

A

Chamber dilatation with increased ventricular pressure
E.g. mitral or aortic regurgitation
Deposition of new sarcomeres
Increased cell length and width
Muscle mass and wall thickness are increased in proportion to chamber diameter

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15
Q

Left side HF

A

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

Causes:
Ischaemic heart disease
Hypertension
Valvular heart disease
Myocardial disease
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16
Q

Left side HF - lungs

A

Breathlessness
Orthopnoea
Paroxysmal nocturnal dyspnoea

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17
Q

Left side HF - kidneys

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

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18
Q

Left side HF - brain

A 
Hypoxic encephalopathy
Irritability
Loss of attention
Restlessness
Stupor and coma
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19
Q

Right side HF

A

Usually as a consequence of left sided heart failure (congestive cardiac failure

Cor-pulmonale:
Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli

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20
Q

Right side HF- Cor Pulmonale

A

Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli

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21
Q

Right side HF - other causes

A

Valvular heart disease

Congenital heart disease

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22
Q

RHF - liver and portal system

A

Congestive hepatomegaly
Centrilobular necrosis when severe
Cardiac cirrhosis

23
Q

RHF - spleen

A

Congestive splenomegaly

24
Q

RHF - abdomen

A

Ascites - accumulation of transudate in peritoneal cavity

25
Q

RHF - subcutaneous tissue

A

Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema
Sacral oedema if bedridden

26
Q

RHF - Pleural and pericardial space

A

Effusions

27
Q

RHF systemic effects

A 
Liver and portal system
Spleen
Abdomen 
Subcutaneous tissue 
Pleural and pericardial space
28
Q

Biventricular failure

A

Either due to the same pathological process on each side of the heart
OR
Consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure

29
Q

HF clinical presentation

A 
Due to excess fluid accumulation
Dyspnoea
Orthopnoea, paroxysmal nocturnal dyspnoea
Oedema
Hepatic congestion
Ascites

Due to reduction in cardiac output
Fatigue
Weakness

30
Q

HF clinical presentation - due to excess fluid accumulation

A 
Dyspnoea
Orthopnoea, paroxysmal nocturnal dyspnoea
Oedema
Hepatic congestion
Ascites
31
Q

HF clinical presentation - Ddue to reduction in cardiac output

A

Fatigue

Weakness

32
Q

Classification of HF

A

I: No limitation
II: Slight limitation
III: Marked limitation
IV: Severe limitation

33
Q

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
34
Q

Acute Pulmonary Oedema

A 
Acute Breathlessness
Pallor
Cyanosis
Sweating
Rapid Pulse
Hypoxia
Crackles in Lungs
35
Q

Clinical tests in HF

A 
CXR
ECG
Blood investigations 
Echocardiogram / Cardiac MRI or CT / CT-PET
CTCA / Coronary angiography
36
Q

Current drug treatment

A 
Aldosterone antagonists
ARNI 
ACEi/ARBs
Beta-blockers
SA Node Blockade
37
Q

Current drug treatment - ACEi / ARBs

A

Enalapril, Ramipril, Perindopril

Losartan, Candesartan, Irbesartan

38
Q

Current drug treatment - ARNI

A

Sacubitril Valsartan

39
Q

Current drug treatment - Aldosterone antagonists

A

Spironolactone, Eplerenone

40
Q

Current drug treatment - Beta-blockers

A

Carvedilol, Bisoprolol, Metoprolol

41
Q

Current drug treatment -SA Node Blockade

A

Ivabradine

42
Q

Current drug treatment - Diuretics

A

Loops – Furosemide, Bumetanide
Thiazides – Bendrofluamethiazide, Indapamide
Quinazolines - Metolazone

43
Q

Loop diuretics

A

FRUSEMIDE, BUMETANIDE
Inhibit Na+ re-absorption from the proximal tubule
K+ loss from distal tubule
Can be given iv or orally

Potent – can lead to:
electrolyte abnormalities
hypovolaemia and diminished renal perfusion

44
Q

Mineralocorticoid Receptor Antagonists

A

EPLERENONE, SPIRONOLACTONE
Acts on distal tubule
Promotes Na+ excretion and K+ re-absorption
Reduces hypertrophy and fibrosis

Principle Side-Effects
Gynaecomastia (esp. Spironolactone)
Electrolyte (K+ high) and renal function abnormalities

45
Q

ACE Inhibitors

A

RAMIPRIL, PERINDOPRIL, ENALAPRIL, CAPTOPRIL, LISINOPRIL
Act on activated renin - angiotensin system
Given orally in small doses with slow titration
Block production of angiotensin:
Vasodilatation
BP lowering
Reduce cardiac work

Principle Side-Effects: cough, hypotension, renal impairment

46
Q

ARNI

A

SACUBITRIL VALSARTAN
Acts on activated renin - angiotensin system
Also blocks breakdown of ANP/BNP
Block production of angiotensin:
Vasodilatation, BP lowering, reduce cardiac work
Promote natriuresis
Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis

Principle Side-Effects: hypotension, renal impairment

47
Q

Beta blockers

A

BISOPROLOL, CARVEDILOL, METOPROLOL
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

48
Q

SAN blockade

A

IVABRADINE
Blocks the If channel within the SA node
Slow HR, no effect on BP
Given orally with dose titration

Principle Side-Effects
Visual aura
Bradycardia

49
Q

Digoxin

A

Action:
Increases myocardial contractility
Slows conduction at the AV node (use in AF)
Excreted by kidney - Toxicity important

Given:
Acute HF especially in AF
Chronic HF in selected cases

50
Q

Treatment of Acute Pulmonary Oedema - Immediate

A

High flow oxygen
IV Morphine
IV Nitrates
IV Frusemide

+/- Assisted Ventilation

51
Q

Treatment of Acute Pulmonary Oedema - Definitive

A

Identify Cause
Oral diuretics
Medical Therapy
Revascularisation if appropriate

52
Q

Other therapies

A 
Cardiac Resynchronisation Therapy (CRT)
Implantable Cardioverter Defibrillator (ICD)
Dialysis & Ultrafiltration
Ventricular Assist Device (LVAD/RVAD)
Intra-aortic balloon pump
Cardiac transplantation
(Stem cell therapy)
53
Q

CRT (Biventricular pacing)

A

Standard pacemakers equipped with two wires (or “leads”) conduct pacing signals to specific regions of heart. Biventricular pacemakers have an additional third lead designed to conduct signals directly into the left ventricle. Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.

Theme 3 (16 decks)

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