Congestive Cardiac failure Flashcards
What is heart failure?
Heart failure is the inability of the heart to function as a pump, resulting in inadequate cardiac output to meet the physiological demands.
What is the prevalence of heart failure?
1-3% in general population ; 10% in elderly pop.
What are the main causes of heart failure?
- Ischaemic heart disease (40%)
- Dilated Cardiomyopathy (35%)
- Hypertension (20%)
Other causes:
- Undilated cardiomyopathy i.e. hypertrophic, restrictive (sarcoidosis/amyloidosis)
- Valvular heart disease
- Congenital heart disease
- Right heart failure inc. right ventricular infarct, pulmonary hypertension, pulmonary embolism, COPD
- Alcohol & drugs
- Arrhythmias i.e. AF, bradycardia
- Pericardial disease
There are physiological compensatory changes in the initial stages of heart failure to maintain cardiac output but overtime these become overwhelmed and pathological, leading to decompensated heart failure (HF).
What are the 9 factors which eventually result in decompensated heart failure?
- Increase preload
- Increased after load
- Increased contractility
- Salt & water retention
- Myocardial remodelling i.e. left ventricular hypertrophy
- Abnormal calcium homeostasis
- Increase in ANP and BNP
- Endothelium dysfunction
- ADH increase (severe chronic HF - sinister prognosis)
What effects does venous return (preload) have on HF?
Explain changes in early HF.
Explain changes in severe HF.
Explain changes in very severe HF.
Heart failure leads to reduction in volumed ejected with each heart beat => increased diastolic volume => stretches the myocardial fibres => momentarily restoring contractility (Starling’s law)
Early HF: cardiac output is maintained by increase in venous pressure, therefore diastolic volume and an increase in heart rate to compensate for low stroke volume.
Severe HF: Increased venous pressure = dyspnoea due to accumulation of interstitial and alveolar fluid, ascites with hepatomegaly and oedema from increased systemic venous pressure.
=> Cardiac output at rest not reduced but is compromised in exercise
Very severe HF: cardiac output at rest is reduced despite high venous pressure => redistributed to perfuse vital organs i.e. brain, heart, kidneys
What constituents contribute to afterload (outflow resistance)?
What effects does afterload (outflow resistance) have on HF?
- Pulmonary and systemic resistance
- Physical characteristics of vessel wall
- Volume of blood ejected
Increase in after load decreases cardiac output => further increase in end-diastolic volume => dilation of ventricles => further increasing afterload.
What effects does myocardial contractility have on HF?
Sympathetic nervous system activated in HF via baroreceptors (early compensatory mechanism) => increased cardiac work => myocyte damage => decreased cardiac output => HF
What is the underlying mechanism of salt and water retention in HF?
Increase venous pressure occurs when ventricles fail => leading to retention of salt & water in the interstitium.
Low renal perfusion due to reduced cardiac output => RAAS activation => further salt & water retention => further increases venous pressure.
*ANP acts to reduce excess Na+ (compensatory)
Describe the changes left ventricle undergoes in HF.
Left ventricular remodelling : leading to hypertrophy, loss of myocytes and increased interstitial fibrosis.
Cardiomyopathy: progressive ventricular dilation or hypertrophy without ischaemic myocardial injury or infarction.
When are Atrial Natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) released and what are their roles?
- ANP - released from atrial myocytes in response to stretch. ANP levels used for prognosis and haemodynamic state.
i. Induces diuresis
ii. Natriuresis (excretion of Na in urine)
iii. Vasodilation
iv. Suppression of RAAS
ANP increased in congestive heart failure
- BNP - secreted by the ventricles due to increased myocardial wall stress. BNP levels correlate with ventricular wall stress and severity of heart failure.
What changes are seen in endothelial function in HF?
Endothelium dependent vasodilation in peripheral blood vessels is impaired due to reduction in nitric oxide (vasodilator) activity and increase in endothelin (vasoconstrictor).
Endothelin also results in sympathetic stimulation, RAAS activation and LVH.
All leading to => haemodynamic disturbance
What are the effects of andtidiuretic hormone (ADH) in HF?
ADH is raised in severe chronic HF => hyponatraemia => sinister prognosis.
Key Classification of HF based on left ventricular ejection fraction.
Describe systolic heart failure aka heart failure with reduced ejection fraction (HFREF).
What is the ejection fraction?
What causes this?
Inability of the ventricles to contract normally => reduced cardiac output.
Ejection fraction <40%
Causes: ischaemic heart disease, MI, cardiomyopathy, hypertension
Key Classification of HF based on left ventricular ejection fraction.
Describe diastolic heart failure aka heart failure with preserved ejection fraction (HFPEF).
What is the ejection fraction?
What causes this?
Inability of the ventricles to relax (due to increased ventricular wall stiffness and decreased left ventricular compliance) and fill normally => increased filling pressures => reduced cardiac output
Ejection fraction >50%
Causes: ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity
*more common in elderly, hypertensive patients
What are the symptoms of left ventricle failure?
Dyspnoea Poor exercise tolerance Fatigue Orthopnoea Paroxysmal nocturnal dyspnoea Nocturnal cough ± pink frothy sputum Wheeze Nocturia Cold peripheries Weight loss