Page 297 - Concise Pathology for Exam Preparation ( PDFDrive )
P. 297
282 SECTION II Diseases of Organ Systems
• After load, which refers to the pressure against which the left ventricle contracts. The
main determinants of after load are total peripheral resistance and left ventricle size
• Myocardial contractility mainly depends on the levels of circulating catecholamines
• Heart failure is characterized by a decrease in cardiac output (except in high output
failure) increased preload, as well as after load and decreased myocardial contractility.
• Compensated heart failure: Compensated heart failure implies that the compensatory
changes have prevented the development of overt heart failure; a minor added insult
like an infection may precipitate severe heart failure.
• Compensatory mechanisms are mediated through renin–angiotensin system and au-
tonomic nervous system and include
• Increased myocardial contractility
• Myocardial hypertrophy
• Neurohormonal mechanisms:
(i) Sympathetic stimulation
(ii) Activation of renin–angiotensin system
(iii) Release of atrial natriuretic peptide
Types of heart failure
• Systolic and diastolic heart failure
• Systolic heart failure is characterized by an abnormality of myocardial contraction.
• Diastolic heart failure is characterized by an abnormality of ventricular relaxation,
which causes poor ventricular filling and high filling pressure.
• Acute and chronic heart failure
• Acute heart failure develops suddenly. The sudden reduction in cardiac output
results in systemic hypotension without peripheral oedema, eg, acute myocardial
infarction and rupture of a cardiac valve.
• Chronic heart failure develops gradually. Here, systemic arterial pressure is well-
maintained, but oedema develops, eg, dilated cardiomyopathy and multivalvular
disease.
• Left-sided, right-sided and biventricular heart failure
• Left-sided (left ventricular) heart failure
• ‘Left side’ is a term for the functional unit of left atrium, left ventricle, mitral valve
and aortic valve.
• There is reduction in left ventricular output, increase in left atrial pressure and
increase in pulmonary venous pressure.
• Acute increase in left atrial pressure causes pulmonary congestion and pulmonary
oedema, eg, in myocardial infarction.
• Gradual increase in left atrial pressure causes reflex pulmonary hypertension, but
no pulmonary oedema, eg, aortic stenosis.
• Right-sided (right ventricular) heart failure
• ‘Right side’ is a term for the functional unit of right atrium, right ventricle, tricuspid
valve and pulmonary valve.
• There is reduction in right ventricular output, which results in systemic venous
congestion leading to accumulation of fluid in the body, resulting in swelling and
oedema.
• Seen in corpulmonale, pulmonary valvular stenosis and multiple pulmonary
emboli.
• Biventricular heart failure: There is failure of both left and right ventricles, eg, disease
processes affecting both ventricles like dilated cardiomyopathy and ischaemic heart
disease or disease of left heart leading to chronic elevation of left atrial pressure, pul-
monary hypertension and subsequent right ventricular failure.
• Forward and backward heart failure
• Forward heart failure: decreased cardiac output
• Backward heart failure: normal cardiac output, but marked salt and water retention
and pulmonary and systemic venous congestion
• High output and low output heart failure
• High output heart failure is associated with an increased cardiac output, eg, cardiac
failure associated with hyperthyroidism, anaemia, pregnancy, arteriovenous fistulae,
beriberi and Paget disease.
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