Heart Failure Flashcards
Define heart failure
A condition in which the heart fails to discharge its contents properly
A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure
Define chronic heart failure
A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of renal, neural and hormonal responses
List heart failure causes
Most common cause is ischaemic heart disease (IHD)
Hypertension
Dilated cardiomyopathy - enlarged and cannot pump blood effectively
Pathogen, alcohol/drugs/poisoning, pregnancy, idiopathic (spontaneous), radiation
Valve and myocardium structural defects
Restrictive cardiomyopathy - restrictive filling of ventricles
Eg. Amyloidosis
Hypertrophic cardiomyopathy - heart muscle becomes abnormally thick
Pericardial disease
High output heart failure - heart cannot keep up with cardiac output needed
Arrhythmia
State the ejection fraction of heart
50-60%
State left ventricular end systolic and diastolic volume
LV end systolic volume - 75mL
LV end diastolic volume - 150mL
Outline the pathophysiology of LV systolic dysfunction
Increased left ventricular capacity and reduced LV cardiac output
Thinning of myocardium wall - fibrosis and necrosis of myocardium, activity of matrix proteinases
Mitral valve incompetence as diameter of wall increases but valves do not change size
Weakened heart more susceptible to adrenaline surge and cardiac arrhythmia
Left ventricular hypertrophy and thickening of LV wall
Over time cannot be sustained, leading to global thinning of myocardium wall
Due to increased pressure due to hypertension
Non ischaemic cardiac myopathy
Outline the pathophysiology of heart failure with preserved ejection fraction (HFpEF)
○ Often seen in elderly, female and history of hypertension/diabetes/obesity
Heart does not relax properly in diastole
Thicker and shorter cardiomyocytes
Increased deposition of collagen
Impaired diastolic LV filling - with increased LA and pulmonary artery pressures
LV filling becomes dependent on high LA pressure
RV dysfunction can result form high LA and PA pressure
Triggers neuro-hormonal activation
Reduces cardiac output
What type of cardiac failure is it when both sides of heart are affected
Biventricular/congestive cardiac failure
Describe how oedema can form from heart failure
Net filtration pressure = hydrostatic pressure - osmotic pressure
Hydrostatic pressure increases with increasing circulation volume - more oedema Kidney perfusion decreases as it reacts as if bleeding is occurring
Increase sodium and water retention
Some of the sodium and water escapes from vessels and into tissues
Osmotic pressure decrease may be due to lack of dietary protein
What are clinical characteristics of heart failure
Pitting oedema
Skeletal muscle changes - reduced skeletal muscle blood flow
Reduction in skeletal muscle mass
Abnormalities of structure and function
Contribute to fatigue and exercise intolerance
Renal effects
Increase Na/H2O retention due to neuro-hormonal activation
In severe heart failure, renal blood flow falls leading to reduced GFR and subsequent rise in serum urea and creatinine
Chronic ischaemia leads to thinning of kidney and shrinking, loss of nephrons and function
Anaemia - kidney source of erythropoietin, decrease leads to anaemia
What are symptoms of left heart failure
Fatigue, exertional dyspnoea (difficulty breathing)
Orthopnoea and paroxysmal nocturnal dyspnoea (PND) - breathlessness when lying down
Fluid heard as crackles in the chest - pulmonary oedema
Tachycardia Cardiomegaly - displaced apex beat
3rd or 4th heart sound
Functional murmur of mitral regurgitation
Peripheral oedema
What are symptoms of right sided heart failure
Liver enlargement due to increase fluid accumulation in areas drained by systemic vein
Fatigue, dyspnoea, anorexia, nausea
Increase in jugular vein pressure
Dependent pitting oedema
Ascites - abnormal accumulation of fluid in abdominal cavity
Pleural effusion - accumulation of fluid around lung
Outline the role of sympathetic system in heart failure
Baroreceptor-mediated response
Attempt to compensate for low cardiac output in heart failure
Cardiac contractility increase, arterial and venous vasoconstriction, tachycardia
Long-term deleterious effects
ß-adrenergic receptors become downregulated over time
Noradrenaline induces cardiac hypertrophy
Induce up-regulation of RAAS
Reduction in heart rate variability (reduced parasympathetic and increase sympathetic)
Describe the deleterious long term effects of AT1R
Potent vasoconstrictor - decreases cardiac output, increase afterloads
Promotes left ventricle hypertrophy and myocyte dysfunction
Promotes aldosterone release
Promotes Na/H2O retention through aldosterone
Enhances sympathetic activity
Identify drugs to manipulate cardiac output
Beta blockers - reduce force of contraction and heart rate
ACE inhibitors - prevents production of angiotensin II and thus prevents vasoconstriction, water retention
MRA - mineralocorticoid receptor antagonist
Sacubitril/valsartan is recommended to replace ACE inhibitors
Simultaneously inhibits neprilysin and blocks AT1 receptors
Blocking AT1 receptor prevents effects of angiotensin II
Blocking neprilysin enhances ANP, BNP, CNP
Leads to vasorelaxation, decrease in blood pressure, decrease in sympathetic tone, decrease in aldesterone
