Cardiovascular System and Diseases PDF

Heart Four valves: To maintain unidirectional blood flow through the heart- incomplete valve function can cause hypoxia Heart Myocardium: The cardiac muscle composed primarily of a collection of specialized muscle cells called cardiac myocytes Ventricular myocytes are arranged circumferentially in a...

Heart Four valves: To maintain unidirectional blood flow through the heart- incomplete valve function can cause hypoxia Heart Myocardium: The cardiac muscle composed primarily of a collection of specialized muscle cells called cardiac myocytes Ventricular myocytes are arranged circumferentially in a spiral orientation and contract during systole and relax during diastole Heart blood supply To meet energy need, cardiac muscles rely almost exclusively on constant supply of oxygenated blood via the coronary arteries Three major epicardial coronary arteries 1.Left anterior descending (LAD) artery, most commonly effect by plaque 2.Left circumflex (LCX) artery 3.Right Coronary artery Most coronary arterial blood flow to the myocardium occurs during ventricular diastole, when the microcirculation is not compressed by cardiac contraction Cardiac conduction system Regulates the heart rate and rhythm Excitable tissue: can for action potentials with electrical signal cardiac muscle, nervous system Sensory system Skeletal muscle ◼ ◼ ◼ ◼ Why is the SA node tissue a pacemaker and not other tissues? The node can go very fast, cardio myocytes can beat 40 times a minute so SA node is the control The sinoatrial (SA) pacemaker of the heart, the SA node, located near the junction of the right atrial appendage and the superior vena cava The AV node, located in the right atrium along the atrial septum; The bundle of His, which courses from the right atrium to the summit of the ventricular septum; and its major divisions The right and left bundle branches, which further arborize in the respective ventricles through the anteriorsuperior and posterior-inferior divisions of the left bundle and the Purkinje network Disorders of cardiac conduction Conduction defects (arrhythmias) due to uncoordinated generation of impulses lead to non- uniform and inefficient contraction of the heart Ventricular fibrillation- the heart cannot contract properly and pump Blood out, will probably have a cardiac arrest (stop beating) Compensatory mechanisms The Frank-Starling mechanism: Increased filling volumes dilate the heart and thereby increase functional cross-bridge formation within the sarcomeres → contractility Myocardial adaptations, including hypertrophy (athletes coping with high demand)with or without cardiac chamber dilation Activation of neurohumoral systems: 1) Release of noradrenaline by adrenergic cardiac nerves of the autonomic nervous system (↑heart rate, myocardial contractility, vascular resistance) 2) Activation of the renin-angiotensin-aldosterone system, final product will constrict muscle and will retain sodium and water in increase heart output 3) Release of atrial natriuretic peptide, does opposite to 2, reduces water and sodium to counteract the system above The latter two factors act to adjust filling volumes and pressures Blood pressure Blood pressure is a function of cardiac output and peripheral vascular resistance ▪ Systemic and local tissue blood pressures must be maintained within a narrow range ▪ Hypotension (low pressures) results in inadequate organ perfusion and can lead to dysfunction or tissue death ▪ Hypertension (high pressures) can cause vessel and end-organ damage Hypertension Clinically significant hypertension: According to the National Heart, Lung, and Blood Institute of the U.S.A. ◼ ◼ ◼ a sustained diastolic pressure greater than 89 mm Hg or a sustained systolic pressure in excess of 139 mm Hg associated with a measurably increased risk of atherosclerosis Hypertension classification ◼ ◼ Essential (idiopathic) hypertension: do not know the full reason, not genetic ~90-95% cases A complex, multi-factorial disorder Genetic factors play an important role Secondary hypertension, from a disease, for example diabetes Blood pressure regulation Blood volume Na Mineralocorticoids Atriopeptin Humoral factors Constrictors Angiotensin II Catecholamines Endothelin Dilators Prostaglandins Kinins NO Cardiac Peripheral BP = X output resistance Cardiac factors Heart rate Contractility Local factors pH hypoxia Neural factors Constrictors α-adrenergic Dilators β-adrenergic Symptoms of hypertension Persistent headache Blurred or double vision Nosebleeds Shortness of breath Hypertensive heart diseases Compensated stage may be asymptomatic, and can be diagnosed by electrocardiogram or echocardiography Progress to heart failure or ischemic heart disease Pathological feature - Atherosclerotic plaques ◼ Characterized by intimal lesions - atheromas (atheromatous or atherosclerotic plaques) ◼ The plaques protrude into vessel lumens ◼ The plaque consists of a raised lesion with a soft, yellow, grumous core of lipid (mainly cholesterol and cholesterol esters) covered by a white fibrous cap Structure of atherosclerotic plaques ◼ A superficial fibrous cap – SM cells, relatively dense collagen ◼ Beneath and to the side of the cap ("shoulder") - a more cellular area containing macrophages, T cells, SM cells ◼ Necrotic core (deep to the fibrous cap, containing lipid, debris from dead cells, foam cells (lipid inside), fibrin, variably organized thrombus, and other plasma proteins) ◼ The cholesterol, frequently present as crystalline aggregates or "clefts” ◼ Neovascularization (due to chronic inflammation) at the periphery of the lesions 3 principal components: 1. Cells: SMCs, macrophages, and other leukocytes 2. Extracellular matrices: collagen, elastin, proteoglycans 3. Intracellular and extracellular lipid Key pathogenic events ◼ Endothelial injury: increases vascular permeability, leukocyte adhesion (adhesion proteins will be expressed), and thrombosis ◼ Accumulation of lipoproteins: (mainly LDL) in the vessel wall ◼ Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells ◼ Platelet adhesion- start of clotting, they attract clotting factors --> thrombosis ◼ Factor release from activated platelets, macrophages, and vascular wall cells --> SMC recruitment and further accumulation of macrophages ◼ SMC proliferation and ECM production- makes blood vessels narrow ◼ Lipid accumulation: both extracellularly and within cells (macrophages and SMCs) Consequences of atherosclerotic plaques ◼ Rupture, ulceration, or erosion of the intimal surface → highly thrombogenic substances → thrombosis ◼ Haemorrhage into a plaque. Rupture of the fibrous cap → intra-plaque haemorrhage → plaque rupture ◼ Atheroembolism. Plaque rupture → atherosclerotic debris into bloodstream → microemboli ◼ Aneurysm formation. Atherosclerosis-induced pressure, ischemic atrophy, loss of elastic tissue → weakness → aneurysmal dilation and potential rupture Stages of atherosclerotic pathogenesis and complications Rupture gets bigger and bigger= lumen gets smaller and smaller Clinical outcomes of atherosclerotic diseases The principal outcomes depend on    Size of the involved vessels, coronary artery= effect the heart, brain artery= stroke Relative stability of the plaque itself, want to increase stability of plaque Degree of degeneration (underlying arterial wall ) Major consequences: ◼ Myocardial infarction (heart attack) ◼ Cerebral infarction (stroke) ◼ Aortic aneurysms ◼ Peripheral vascular disease (gangrene of the legs), can stay in patient for a long time Ischemic heart disease Ischemic heart disease (IHD) is the leading cause of death worldwide for both men and women In more than 90% of cases, the cause of myocardial ischemia is reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries (blockage) Clinical manifestations: ◼ Angina pectoris, chest pain ◼ Myocardial infarction, the most important form of IHD ◼ Heart failure ◼ Sudden cardiac death Causes of coronary arterial occlusion ◼ Coronary atherosclerosis (90%) ◼ Vasospasm with or without coronary atherosclerosis ◼ Emboli from the left atrium in association with atrial fibrillation ◼ Others Clinical Features ◼ The most frequent symptom of acute myocardial infarction is severe chest pain ◼ This often develops suddenly but may build up gradually, and generally lasts for several hours ◼ Pain is usually accompanied by profuse sweating, nausea and vomiting ◼ Many patients give a previous history of angina or non-specific chest pain in the weeks before the acute event ◼ In at least 10% of patients, myocardial infarction is painless or 'silent'; this is particularly true in the elderly Heart failure Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation. It is often called congestive heart failure (CHF), is a common, usually progressive condition with a poor prognosis. CHF occurs when the heart 1. Is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or 2. Can do so only at an elevated filling pressure Left-sided heart failure Most common causes: due to failed left ventricular chamber, so pulmonary blood cannot be pumped back, all the tissue in the left- hand side on the hear tis compromised ▪ Ischemic heart disease ▪ Hypertension ▪ Aortic and mitral valvular diseases ▪ Myocardial disease The morphological and clinical effects of left-sided CHF primarily result from 1) congestion of the pulmonary circulation 2) stasis of blood in the left-sided chambers 3) hypoperfusion of tissues leading to organ dysfunction Right-sided heart failure Most commonly a secondary consequence of left-sided heart failure due to increase in pressure in the pulmonary circulation Morphology: ◼ Heart: Hypertrophy and dilation of the right atrium and ventricle ◼ Liver: Congestive hepatomegaly, because blood from here and the spleen needs to be taken back to the vena cava ◼ Spleen: Congestive splenomegaly ◼ Lung: Pulmonary oedema ◼ Accumulation of fluid in pleural, pericardial, or peritoneal spaces (effusions) ◼ Oedema of the peripheral: Ankle (pedal) and pretibial oedema is a hallmark of right-sided heart failure, clinically, you can differentiate between the two