Lecture 10.1 - Pathophysiology of Heart Failure PDF
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Aston University
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This lecture provides a detailed overview of the pathophysiology of heart failure, exploring different types, causes, and clinical implications. It discusses concepts like ejection fraction, systolic and diastolic heart failure, and the interplay of various factors contributing to the disease.
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Frank-Starling law in the failing myocardium: ◦Increased venous return to the heart -> increases stroke volume via an increase in contractile strength of the left ventricle ◦The ability of the heart to change stroke volume in response to venous return is called Frank-Starling...
Frank-Starling law in the failing myocardium: ◦Increased venous return to the heart -> increases stroke volume via an increase in contractile strength of the left ventricle ◦The ability of the heart to change stroke volume in response to venous return is called Frank-Starling mechanism ◦In a failing myocardium - this does not happen. There is a physical limit to the relationship between cardiac stretch and contractility ◦Beyond this limit - further increases in preload have a negative effect on stroke volume Heart failure (HF): ◦Complex clinical syndrome resulting from any structural and/or functional impairment of ventricular filling or ejection Acute vs chronic: ◦Acute heart failure: ‣ Characterised by a rapid onset of symptoms and/or signs of heart failure ‣ Requires urgent evaluation and treatment ‣ Most common causes: acute myocardial dysfunction (ischaemic, inflammatory), acute valvulopathy, arrhythmias (Vfib), pulmonary embolism, drugs (e.g. beta blockers) ‣ May present suddenly with cardiogenic shock or subacutely with decompensation of chronic heart failure ◦Chronic heart failure: ‣ Progressive cardiac dysfunction from structural and/or functional cardiac abnormalities ‣ Usually precipitated by conditions that affect the muscle (e.g. cardiomyopathy), vessels (e.g. ischaemic heart disease), valves (e.g. aortic stenosis), or conduction (e.g. atrial fibrillation) ‣ Characterised by progressive symptoms with episodes of acute deterioration ‣ Classified into systolic (HFrEF) or diastolic (HFpEF) Ejection fraction: ◦Stroke volume = volume of blood pumped per beat ~70ml ◦Volume of blood that is present in ventricles at the end of diastole (beginning of systole) (EDV) ~110ml ◦Ejection fraction - fraction of blood that gets pumped compared to the volume of blood that is in the ventricles at the beginning of contraction ‣ EDF = stroke volume/EDV = 70/110 = 64% ‣ Normal ejection fraction ~ 55-70% Systolic HF/HF with reduced ejection fraction (HFrEF): ◦Heart cannot pump enough blood ◦Systolic dysfunction ◦Stroke volume reduced due to reduced contractility ‣ E.g. MI, dilated cardiomyopathy ◦Reduced ejection fraction ◦Progressive ventricular dilatation or eccentric hypertrophy Diastolic HF/HF with preserved ejection fraction (HFpEF): ◦Reduced filling of the heart ◦Diastolic dysfunction ◦Preserved ejection fraction ◦Associated with concentric hypertrophy ◦Increased stiffness of ventricular walls: ‣ Increased afterload ‣ Reduced preload: MI, constrictive pericarditis, cardiac tamponade Ventricular remodelling in systolic and diastolic heart failure: Right sided heart failure: ◦Reduced contractility - MI ◦Increased afterload ◦Increased preload - pulmonary valve/tricuspid valve regurgitation ◦More commonly develop from left sided heart failure High output vs low output: ◦High output HF: ‣ There is high CO >8L/min ‣ But heart unable to meet increased demand despite normal cardiac function E.g. hyperthyroidism, severe anaemia ‣ Increased demand due to shunting of blood from arterial to venous side AV fistula (usually found in the leg), thiamine deficiency (in chronic alcoholics) Pathophysiology of heart failure: ◦In heart failure, the decreased CO causes a decreased BP (BP = CO x TPR) ◦Reduced BP causes: ‣ Baroreceptors to detect the low BP and stimulate an increase sympathetic drive that leads to: Increased heart rate, increased peripheral resistance - causes decompensated heart failure ◦Activation of the renin-angiotensin-aldosterone system that causes: ‣ Increased sodium retention leading to increased water retention (water follows sodium) and this increases the circulating volume ‣ Anti-diuretic hormone release ‣ Vasoconstriction ◦This is all an attempt to increase the BP but really culminates in an increased afterload and preload which puts even more strain on the failing heart Signs and symptoms - left sided heart failure: ◦Blood will accumulate in the left atrium and pulmonary veins and pulmonary venous circulation ◦Pulmonary venous pressure increases -> leads to pulmonary congestion as blood backs up from left side to lungs ◦Fluid leaks out into interstitial fluid of pulmonary tissues -> pulmonary oedema ◦Decreased ventilation across alveoli -> hypoxia ◦Severe reduction in CO -> reduced BP -> to compensate this TPR increases (cold/pale extremities) ◦Organ malperfusion can affect brain (encephalopathy), heart (infarction), kidney (acute kidney injury), intestine (acute mesenteric ischaemia) ◦Ischaemia can lead to increased lactic acid -> pH drops triggering acidosis ◦Symptoms: ‣ Dyspnoea ‣ Cough (often dry) ‣ Orthopnoea (difficulty lying flat, so can become breathless) ‣ Paroxysmal nocturnal dyspnoea (waking up breathless at night) ◦Signs: ‣ Crackles/rales on auscultation (bi-basal) ‣ Tachycardia ‣ Cardiomegaly ‣ 3rd and 4th heart sounds Signs and symptoms - right sided heart failure: ◦Increased pressure in pulmonary veins causes difficulty of RV to pump through the pulmonary circulation ◦Either caused by left ventricular failure or respiratory disease ◦If caused by respiratory disease - it is termed 'cor pulmonale' ◦Blood accumulate in the systemic venous circulation -> increased central venous pressure (CVP) as blood backs up into the JVP ◦Symptoms: ‣ Dyspnoea ‣ Chest discomfort ‣ Swelling ◦Signs: ‣ Jugular venous distension ‣ Hepatic congestion ‣ Peripheral oedema ‣ Ascites Signs and symptoms - congestive heart failure: ◦Both the right and left ventricles affected - combination of signs and symptoms ‣ Systemic and pulmonary congestion ◦Symptoms: ‣ Dyspnoea ‣ Cough (often dry) ‣ Orthopnoea (difficulty lying flat) ‣ Paroxysmal nocturnal dyspnoea (waking up breathless at night) ‣ Chest discomfort ‣ Swelling ◦Signs: ‣ Crackles/rales on auscultation (bi-basal) ‣ Tachycardia ‣ Cardiomegaly ‣ 3rd and 4th heart sounds ‣ Jugular venous distension ‣ Hepatic congestion ‣ Peripheral oedema ‣ Ascites