18. heart part 1 basic & congestive heart failurePresentation 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.