Heart failure Flashcards
Heart failure
A state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body
Impact of heart failure in the UK
In-hospital mortality- 9.4%
30 day mortality in those surviving to discharge- 6.1%
Overall 30 day mortality- 14.9%
Cardiac output
= heart rate x stoke volume
Contractility
The intrinsic ability of the myocardium to contract
Preload
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
Afterload
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
Frank- Starling Laq
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
Low output heart failure
Systolic heart failure
Diastolic heart failure
High output heart failure
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
Causes of high output heart failure
Thyrotoxicosis Profound anaemia Pregnancy Pagets disease Acromegaly Sepsis
Systolic heart failure
Progressive deterioration myocardial contractile function
- ischeamic injury
- volume overload
- pressure overload
Diastolic heart failure
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
Causes of heart failure
Coronary heart disease
Hypertensive heart disease
Valvular heart disease
Myocardial disease/ cardiomyopathies
Congenital heart disease
Cardiomyopathies
Diffuse disease of the heart muscle leading to functional impairment
Dilated cardiomyopathy
Various causes, 50% familial
ETOH, pregnancy, systemic disease, muscular dystrophies
Drig toxicity (chemotherapy- anthracyclines, herceptin)
Myocarditis- aetiology includes viral
Hypertrophic cardiomyopathy
Hereditary
Restrictive cardiomyopathy
Rare
Amyloid the main cause in the UK
Activation of neurohormonal system in heart failure
Release of noradrenaline
- increases HR and myocardial contractility
- causes vasoconstriction
Release of ANP/ BNP
Activation of renin angiotensin aldosterone system
Vasoconstriction compensation
Increases resistance against which heart has to pump
May therefore decrease cardiac output
Na and water retention compensation
Increases fluid volume
Increases preload
If too much stretch, decreases contractile strength and CO
Excessive tachycardia compensation
Decreases diastolic filling time
Decreases ventricular filling
Decreases SV and CO
Clinical types of heart failure
Left sided, right sided and biventricular failure
Acute and chronic heart failure
Compensated and decompensated heart failure
Left side heart failure
Blood blocks up progressively from left atrium to pulmonary circulation
Causes
- ischaemic heart disease
- hypertension
- valvular heart disease
- myocardial disease
LV failure on the lungs
Pressure in pulmonary veins transmitted to capillaries and arteries
Pulmonary congestion and oedema
Heavy wet lungs
- breathless
- orthopnoea
- paroxysmal nocturnal dyspnoea
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
LV failure on the brain
Hypoxic encephalopathy
Irritability
Loss of attention
Restlessness
Stupor and coma
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
RH failure on liver and portal system
Congestive hepatomegaly
Centrilobular necrosis when severe
Cardiac cirrhosis
RH failure on spleen
Congestive splenomegaly
RH failure on abdomen
Ascites- accumulation of transudate in peritoneal cavity
RH failure on subcutaneous tissue
Peripheral oedema of dependent portions of body especially ankles
Sacral oedema if bedridden
RH failure of pleural and pericardial space
Effusions
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
Clinical presentation of heart failure
Due to excess fluid accumulation
- dyspnoea
- orthopnoea, PND
- oedema
- hepatic congestion
- ascites
Due to reduction in CO
- fatigue
- weakness
Class I heart failure
No limitation of physical activity
Class II heart failure
Slight limitation of ordinary activity
Class III heart failure
Marked limitation, even during less than ordinary activity
Class IV heart failure
Severe limitation with symptoms at rest
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
Acute pulmonary oedema
MEDICAL EMERGENCY
- acute breathlessness
- pallor
- cyanosis
- sweating
- rapid pulse
- hypoxia
- crackles in lungs
Clinical tests in heart failure
CXR ECG Blood investigations Echocardiogram/ MRI/ CT CTCA
Current drug treatment
ACEi/ ARBs
ARNI
Aldosterone antagonists
Beta blockers
SA node blockade
Diuretics
ACEi/ ARBs
Block angiotensin
- enalapril, ramipril, perindopril
- losartan, candesartan, irebesartan
ARNI
Angiotensin receptor inhibitor
- sacubitril, valsartan
Acts in activated RAAS
Blocks production of angiotensin
Promotes natriuresis
Side effects
- hypotension
- renal impairment
Aldosterone antagonists
Spironolactone
Eplerenone
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
SA node blockade
Ivabradine
Blocks If channel with SA node
Slows HR, no BP effect
Orally with dose titration
Side effects
- visual aura
- bradycardia
Diuretics
Loops- furosemide, bumetanide
Thiazides- bendrofluamethiazise, indapamide
Quinazolines- metolazone
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
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
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
Digoxin
Action
- increases myocardial contractility
- slows conduction at AV node
- excreted by kidney
Given
- acute HF especially in AF
- chronic HF in selected cases
Immediate treatment of acute pulmonary oedema
High flow oxygen
IV morphine
IV nitrates
IV furesimide
Definitive treatment of acute pulmonary oedema
Identity cause
Oral diuretics
Medical therapy
Revascularisation if appropriate
