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18. heart part 1   basic & congestive heart failure

18. heart part 1 basic & congestive heart failure






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    18. heart part 1   basic & congestive heart failure 18. heart part 1 basic & congestive heart failure Presentation Transcript

    • HEART September 19, 2011
    • NORMAL 250 to 300 gms. in females 300 to 350 gms. in males right ventricular thickness 0.3 to 0.5 cm. left ventricular thickness 1.3 to 1.5 cm. Hypertrophy vs. dilatation. cardiomegaly
    • MYOCARDIUM Composed of branching and anastomosing striated muscle cells (cardiac myocytes) Cardiac myocytes have 5 major components:  Cell membrane  Sarcoplasmic reticulum  Contractile elements  Mitochondrion  nucleus
    • Myocardium SARCOMERE – functional intracellular contractile unit of the cardiac muscle. Shorter sarcomere have considerable overlap of actin and myosin with consequent reduction in contractile forces (Frank-Starling mechanism) Cardiac myocytes account for 90% of the volume of the heart but only 25% of the total cells (other cells – endothelial cells and connective tissue cells)
    • Myocardium  Atrial myocytes are generally smaller in diameter and less structured than ventricular myocytes.  Some atrial cells have distinctive electron dense granules – specific atrial granules.  Storage site of atrial natriuretic peptides, that can induce vasodilatation, natriuresis, suppression of renin-angiotensin-aldosterone axis and fall in arterial pressure.
    • Myocardium Specialized excitatory and conduction myocytes regulate the heart’s rate/rhythm  SA Node - Sinoatrial pacemaker  AV Node  Bundle of His  Right and left bundle branches
    • Blood Supply Heart generates energy exclusively by the oxidation of substrates so it relies heavily on adequate flow of oxygenated blood. Epicardial coronary arteries are 5-10 cm. long, 2-4 mm in diameter that run along the external surface of the heart Intramural arteries – penetrate the myocardium
    • Blood supply Three major epicardial arteries:  Left anterior descending (LAD)  Left circumflex (LCX)  Right coronary artery (RCA)
    • Blood Supply Blood flows during diastole when the microcirculation is not compressed by the contraction. Anterior descending branch of the left coronary artery - apex, anterior surface of the left ventricle and anterior 2/3 of the interventricular septum Right coronary artery - right ventricular free wall, adjacent half of the posterior wall of the left ventricle & posterior third of interventricular septum.
    • Blood supply Functionally the right and left coronary arteries behave as end arteries Collateral circulation – usually with little blood coursing through them
    • Valves Maintain unidirectional blood flow Normally are thin and translucent Free margins of AV valves are attached to chordae tendinae which are attached to papillary muscles Lined by endothelium and composed of a dense collagenous core (fibrosa) and loose connective tissue (spongiosa)
    • Effects of Aging  Brown atrophy - lipofuscin deposits  Basophilic degeneration - gray blue deposits (?glucan)  fewer myocytes, increased collagen and variable deposits of amyloid.  Reduced left ventricular cavity  calcification of mitral annulus
    • Cardiovascular Dysfunction Loss of blood Disorders of cardiac conduction Obstructed flow Regurgitant flow Pump failure  Contractile dysfunction (systolic failure)  Inadequate filling.
    • Congestive Heart Failure Heart unable to maintain an output sufficient for the metabolic requirements of the body. Occurs either because of a decreased myocardial capacity to contract or because or an inability to fill the cardiac chambers with blood. Most due to systolic dysfunction.
    • Congestive heart failure Factors that affect cardiac response to hemodynamic burden:  Frank-Starling Mechanism  Myocardial hypertrophy with or without cardiac chamber dilation  Activation of neurohumoral systems  Release of norepinephrine by adrenergic cardiac nerves  Activation of renin-angiotensin-aldosterone system  Release of atrial natriuretic peptide
    • Congestive heart failure Most instances are the result of progressive deterioration of myocardial contractile function (systolic dysfunction). The most frequent causes are hypertension and IHD Diastolic dysfunction – when heart cannot fill properly (e.g. massive left ventricular hypertrophy, fibrosis etc.)
    • Cardiac Hypertrophy  Normal myocytes = 15 µm in diameter.  Hyperplasia cannot occur in an adult heart.  Pattern of hypertrophy reflects the stimulus:  concentric hypertrophy in pressure over-loaded ventricles ex. HPN or aortic stenosis.  Eccentric hypertrophy in volume over-loaded ventricles ex. mitral regurgitation.
    • Cardiac Hypertrophy In many cases heart failure is preceded by cardiac hypertrophy There is an increase in the rate of protein synthesis, the amount of protein in each cell, the size of the myocyte, the number of sarcomeres and mitochondria – consequently the total mass and size of the heart.
    • Cardiac Hypertrophy The pattern of hypertrophy reflects the nature of the stimulus:  Pressureoverloaded ventricles develop concentric hypertrophy (reduced cavity diameter)  Volume overloaded ventricles develop hypertrophy accompanied by dilation (increased ventricular diameter).
    • Cardiac hypertrophy constitute atenuous balance between adaptivecharacteristics and potentiallydeleterious structural and
    • Physiologic hypertrophy inducedby regular strenuous exercise seems tobe an extension of normal growth andhave minimal or no deleterious effect.
    • Congestive heart failure ischaracterized by diminished cardiacoutput (forward failure) or dammingback of blood in the venous system(backward failure)
    • Congestive heart failure Morphologic changes of CHF are distant from the heart and are produced by the hypoxic and congestive effects of the failing circulation.
    • Congestive heart failure Left-sided and right-sided failurecan occur independently but failure ofone side cannot exist for long withouteventually straining the other –producing global heart failure.
    • Left Sided Heart Failure Most often caused by: 1. Ischemic heart disease 2. Hypertension 3. Aortic and mitral valvular diseases 4. Non-ischemic Myocardial diseases.
    • Left Sided Heart Failure Left ventricle is usually hypertrophied & often dilated. Secondary enlargement of the atrium is frequently present.
    • Lungs - Left sided heart failure. Pulmonary congestion and edema Lung changes include: 1. Perivascular and interstitial transudate 2. Progressive edematous widening of alveolar septa. 3. Accumulation of edema fluid in alveolar spaces. “heart-failure cells”
    • Kidney - Left sided heart failure. Reduction in renal perfusion which activate renin- angiotensin-aldosterone system inducing retention of salt and water with consequent expansion of the interstitial fluid and blood volume. Acute tubular necrosis. Pre-renal azotemia.
    • Brain - Left sided heart failure. Hypoxic encephalopathy withirritability, loss of attention span andrestlessness which may evenprogress to stupor and coma.
    • Right sided Heart failure.  Usually a consequence of left sided heart failure.  Pure right sided heart failure occurs in Cor pulmonale i.e.. Right ventricular pressure overload induced by intrinsic diseases of the lung or pulmonary vasculature.
    • Right sided Heart failure. LUNGS – minimal congestion LIVER  slightly increased in size and weight  “nutmeg” appearance
    • Right sided Heart failure. KIDNEY – congestion BRAIN- hypoxic encephalopathy Subcutaneous edema on dependent portions of the body
    • In many cases of frank cardiacdecompensation, the patientpresents with biventricularcongestive heart failure.