Heart Failure Flashcards
Cardiac Output and Stroke Volume
CO = Heart rate x SV
typically 70mls/kg/min
Stroke volume affected by contractility, preload and afterload
(preload: increases with increasing blood volume and vasoconstriction)
(afterload: the resistance against which the ventricle contracts to eject blood; increases with hypertension and vasoconstriction; as afterload increases, CO decreases)
Frank-Starling Law
An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which increases SV
Only true up to a certain point, then CO decreases
High vs Low Output Heart Failure
Low output heart failure: systolic or diastolic heart failure
High output heart failure: occurs in context of other medical conditions which increases CO; the heart cannot keep up with the unusually high demand for blood; causes: thyrotoxicosis, profound anaemia, pregnancy, Pagets disease, acromegaly, sepsis
Systolic vs Diastolic HF
Systolic HF: progressive deterioration myocardial contractile function - ischaemic injury, volume/pressure overload
Diastolic HF: 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
Cardiomyopathies
Dilated: 50% familial, ETOH, pregnancy, systemic disease, drug toxicity, muscular dystrophies, myocarditis
Hypertrophic: hereditary
Restrictive (rare): amyloid is the main cause in the UK
Pathophysiology of HF
Pump failure leads to reduced SV and CO - compensatory mechanisms kick in to maintain arterial pressure and perfusion of vital organs
Frank starling mechanism: vasoconstriction, increased venous return/preload, heart muscle fibres stretch, enhanced contractility
Myocardial structural change - augmented muscle mass
Activation of neurohormonal system: release of noradrenaline (vasoconstriction), release of ANP/BNP, activation of RAAS
Compensatory mechanisms worsen HF - vasoconstriction, Na and water retention, excessive tachycardia –> decreased SV and CO
Left sided heart failure
Blood backs up progressively from LA to pulmonary circulation
Causes: IHD, hypertension, valvular HD, myocardial disease
Lungs: pulmonary congestion and oedema - breathlessness, orthopnoea, dyspnoea
Kidneys: decreased CO, reduced renal perfusion, activation of RAAS
brain: hypoxic encephalopathy, irritability, loss of attention, restlessness, stupor and coma
Right sided heart failure
Consequence of left sided heart failure
Cor pulmonale - due to increased resistance within the pulmonary circulation - result of resp disease (COPD or PE), valvular heart disease, congenital disease
Systemic effects:
Liver and portal system (congestive hepatomegaly, centrilobular necrosis, cardiac cirrhosis)
Spleen - congestive splenomegaly
Abdomen - ascites
Subcutaneous tissue - PE (ankles and pretibial oedema) and sacral oedema if bedridden
Pleural and pericardial space - effusions
Clinical signs of cardiac failure
Cool, pale, cyanotic extremities Tachycardia Elevated JVP 3rd heart sound - gallop rhythm Displaced apex - LV enlargement Crackles or decreased breath sounds at bases PE, ascites Hepatomegaly Tests: CXR, ECG, Blood investigations, echo, cardiac MRI, CT, coronary angiography
Loop diruetics
Frusemide, bumetanide
IV/orally
Inhibit Na+ reabsorption from proximal tubule
K+ loss from distal tubule
Potend (can lead to electrolyte abnormalities, hypovolaemia and diminished renal perfusion)
Mineralcortocoid Receptor Antagonists
Eplerenone, spironolactone
Acts on distal tubule
Promotes Na+ excretion and K+ reabsorption
Reduces hypertrophy and fibrosis
Principle side effects: gynaecomastia, electrolyte and renal function abnormalities
ACE inhibitors
Ramipril, perindopril…
Orally in small doses with slow titration
Act on activated RAAS
Block production of angiotensin - vasodilation, BP lowering, reduce cardiac work
Side effects: cough, hypotension, renal impairment
Beta blockers
Bisoprolol, carvedilol, metoprolol
Given orally in small doses with slow titration
Slow HR, reduce BP
Treats arrhythmias
Principle side effects: bronchospasm, claudication
Ivabradine
Given orally
Blocks If channel within the SA node
Slow HR, no effect on BP
Side effects: visual aura, bradycardia
Digoxin
Increases myocardial contractility
Slows conduction at AV node
Excreted by kidney - toxicity important
Given with acute HF esp in AF and chronic HF in selected cases
