Principles of Cardiac dysfunction Failure of the pump : Damaged muscle contracts or relaxes weakly or inadequately. An obstruction to flow : This overworks the chamber behind obstruction. Regurgitation flow: Some of the output from each contraction is refluxed back—volume workload to ventricles. Disorders of cardiac conduction. Disruption of the continuity of the circulatory system.

Pathophysiology of heart failure

Notes to heart physiology Essential functions of the heart To cover metabolic needs of body tissue (oxygen, substrates) by adequate blood supply. To receive all blood coming back from the tissue to the heart. Essential conditions for fulfilling these functions Normal structure and functions of the heart. Adequate filling of the heart by blood.

Cardiac Output CO = Stroke volume X heart rate =70 ml X 60 beats/min =4,200 ml/min. Volume of blood ejected per minute Each ventricle ejects approximately 70mL of blood/ beat Averages between 4-8L/min

Cardiac (heart) Failure: A state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body.

Cardiac (heart) Failure: Characterized by: Diminished cardiac output (forward failure) Damming back of blood in the venous system (backward failure), or Both

Pathophysiology Adaptive mechanisms by which the CVS maintains arterial pressure & perfusion of vital organs : The Frank-Starling mechanism : >preload of dilation helps to sustain cardiac performance by enhancing contractility. Myocardial structural change : Augmented muscle mass (hypertrophy) with or without cardiac chamber dilatation. Activation of neurohumoral system : Release of norepinephrine – >heart rate—augments myocardial contractility. Activation of renin – angiotensin – aldoterone system. Release of atrial natriuretic peptide.

Failure of adaptive mechanisms Pathophysiology Failure of adaptive mechanisms Heart failure

Pathophysiology Systolic dysfunction: Progressive detoriation of myocardial contractile function. Occurs in cases of Ischemic injury, pressure or volume overload and DCM. E.g. IHD and HTN.

Diastolic dysfunction: Inability of the heart chamber to relax, expand, and fill sufficiently during diastole to accommodate an adequate ventricular blood volume. E.g. Massive LVH, myocardial fibrosis, deposition of amyloid, or constrictive pericarditis.

Pathophysiology The onset of HF is preceded by Cardiac hypertrophy : compensatory response of the myocardium to > mechanical work. The stimuli > the rate of protein synthesis, the amount of protein in each cell, size of myocytes, numbers of sacromeres & mitochondria : the mass & size of heart. Also accompanied by selective up regulation of several immediate early response gene & embryonic forms of contractile & other proteins.

Sequence of events in CH and its progression to HF. VALVULAR DISEASE MYOCARDIAL INFARCTION HYPERTENSION Regional dysfunction Pressure overload Pressure and/or Volume overload Sequence of events in CH and its progression to HF. ↑Cardiac Work ↑Wall stress Cell stretch Hypertrophy and/or dilatation Cardiac dysfunction Characterized by ↑Heart size & mass ↑Protein synthesis Induction of Immediate-early genes Induction of fetal gene programme. Abnormal proteins Fibrosis Inadequate vasculature Characterized by Heart failure (systolic/diastolic) Arrhythmias Neurohumoral stimulation

Effects of heart failure Hypoxia. Venous congestions.

Types of heart failure Left sided, right sided & biventricular heart failure. Acute & chronic heart failure. Compensated & decompensated HF. Forward & backward heart failure. Systolic & diastolic dysfunction.

Left sided heart failure Progressive damming of the blood within the pulmonary circulation and the consequences of diminished peripheral BP and flow. Causes : IHD Systemic HTN, MI, valvular disease, Non – ischemic myocardial disease.

Left sided heart failure: Morphology Depends on the cause of the disease process. Left ventricle is usually hypertrophied and often dilated. Secondary enlargement of the left atrium.

Left sided heart failure: Morphology Lungs: Pressure in the pulmonary veins are transmitted retrograde to the capillaries and arteries. Pulmonary congestion and oedema. Heavy wet lungs. Pulmonary changes: A perivascular and interstitial transudate, particularly in the interlobular septa. Progressive oedematous widening of alveolar spaces. Accumulation of oedema fluid in the alveolar spaces. Siderophages or heart failure cells.

Clinical manifestation: Dyspnoea (breathlessness): Exaggeration of the normal breathlessness that follows exertion. Orthopnea: Dyspnoea on lying down that is relieved by sitting or standing. Paroxysmal noctural dyspnea: An extension of orthopnea with attacks of extreme dyspnoea bordering on suffocation, usually occurring at night. Cough

Left sided heart failure: KIDNEYS: Decrease cardiac output Reduction in renal perfusion Activation of renin – angiotensin – aldostrerone system Retention of salt and water with consequent expansion of the interstitial fluid and blood volumes. Pulmonary oedema in lungs.

Left sided heart failure: BRAIN: Hypoxic encephalopathy Clinical features: Irritability Loss of attention Restlessness Stupor and coma

Right sided heart failure. Usually as a consequences of left sided heart failure. Cor pulmonale: chronic severe PHT due to increased resistance within the pulmonary circulation. Other causes : multiple pulmonary emboli, valvular diseases.

Right sided heart failure. Hypertrophy and dilation are generally confined to right ventricle and atrium. LIVER AND PORTAL SYSTEM: Passive Congestive hepatomegaly (Nutmeg liver ) Centrilobular necrosis along with the sinusoidal congestion in case of severe central congestion. Cardiac sclerosis or cardiac cirrhosis. Congestive splenomegaly (300 – 500gm). Ascites: accumulation of transudate in the peritoneal cavity.

Heart failure LHF RHF Pulmonary congestion and oedema. Cough Dyspnoea Orthopnea PND Absence of respiratory symptoms/insignificant. Systemic (and portal) venous congestive syndrome. Hepatosplenomegaly Peripheral oedema Pleural effusion Ascites.