Summary

This document discusses various heart diseases, including heart failure, which is the common endpoint of many cardiac conditions. It details the causes, symptoms, and treatment options for different types of heart diseases, such as ischemic heart disease, congenital heart diseases, and valvular diseases. The document also covers underlying mechanisms and clinical features of these diseases.

Full Transcript

Heart Diseases Heart Failure Heart failure, often referred to as congestive heart failure (CHF), is the common end point for many forms of cardiac disease and is typically a progressive condition with a poor prognosis. CHF occurs when the heart cannot generate sufficient output to meet...

Heart Diseases Heart Failure Heart failure, often referred to as congestive heart failure (CHF), is the common end point for many forms of cardiac disease and is typically a progressive condition with a poor prognosis. CHF occurs when the heart cannot generate sufficient output to meet the metabolic demands of the tissues or can only do so at higher than normal filling pressures. Heart Failure The inability to eject blood (systolic failure) results from inadequate myocardial contractile function, usually as a consequence of ischemic heart disease or hypertension. Diastolic failure refers to an inability of the heart to adequately relax and fill. Increased filling volumes dilate the heart, and enhance contractility and stroke volume. As long as the dilated ventricle can maintain cardiac output by this means, the patient is said to be in compensated heart failure. With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the body, and the patient develops decompensated heart failure. Heart Failure Activation of neurohumoral systems (Release of the neurotransmitter norepinephrine, RAAS, ANA - atrial natriuretic peptide). Myocardial structural changes, including increased muscle mass. Cardiac myocytes adapt to the increased workload by assembling new sarcomeres, a change that is accompanied by myocyte enlargement (hypertrophy). Left-Sided Heart Failure The most common causes of left sided cardiac failure are ischemic heart disease, systemic hypertension, mitral or aortic valve disease, and primary diseases of the myocardium. The morphologic and clinical effects of left-sided CHF stem from diminished systemic perfusion and elevated back pressures within the pulmonary circulation. Morphology Clinical Features Dyspnea (shortness of breath) on exertion is usually the earliest and most significant symptom of left-sided heart failure; cough is also common as a consequence of fluid transudation into air spaces. As failure progresses, patients experience dyspnea when recumbent (orthopnea) because the supine position increases venous return from the lower extremities. Clinical Features Other manifestations of left ventricular failure include an enlarged heart (cardiomegaly) and tachycardia. Atrial fibrillation causes stasis of the blood frequently leading to the formation of thrombi that can shed emboli, causing infarction in other organs (e.g stroke). Treatment Treatment for CHF is focused on correcting the underlying cause. Salt restriction and pharmacologic agents that reduce volume overload (diuretics). Increase myocardial contractility (positive inotropes). Reduce afterload (adrenergic blockade or inhibitors of angiotensin- converting enzymes). Right-Sided Heart Failure Right-sided heart failure is usually the consequence of left- sided heart failure since any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart. The causes of right-sided heart failure include all those that induce left-sided heart failure. Cor pulmonale is an enlarged right ventricle that happens because of a lung condition. Pushing against high pressure in the pulmonary artery. Clinical Features. The clinical manifestations are related to systemic and portal venous congestion and include hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. As CHF progresses, patients may become cyanotic and acidotic, as a consequence of decreased tissue perfusion resulting from both diminished cardiac output and increasing congestion. Congenital Heart Diseases Congenital heart diseases are abnormalities of the heart or great vessels that are present at birth. They account for 20% to 30% of all birth defects. Pathogenesis. Congenital heart disease most commonly arises from faulty embryogenesis during gestational weeks 3 through 8, when major cardiovascular structures develop. The cause is unknown in almost 90% of cases. Clinical Features The various structural anomalies in congenital heart disease can be assigned to three major groups based on their hemodynamic and clinical consequences: 1. Malformations causing a left-to-right shunt. 2. Malformations causing a right-to left shunt (cyanotic congenital heart diseases). 3. Malformation causing obstruction. Malformations Associated With Left-to-Right Shunts Morphology Congenital Heart Diseases Malformations associated with left-to-right shunts are the most common and include ASDs, VSDs, and PDA. Shunting results in right-sided volume overload that eventually causes pulmonary hypertension and, with reversal of flow and right-to-left shunting, cyanosis. Malformations associated with right-to-left shunts include tetralogy of Fallot and transposition of the great arteries. Obstructive lesions include forms of aortic coarctation; the clinical severity of these lesions depends on the degree of stenosis and the patency of the ductus arteriosus. Ischemic Heart Disease Abroad term encompassing several closely related syndromes caused by an imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional demands. In more than 90% of cases, IHD is a consequence of reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease. Ischemic Heart Disease Cardiac ischemia may be the result of increased demand (e.g., with increased heart rate or hypertension); diminished blood volume (e.g., with hypotension or shock); diminished blood oxygenation (e.g., due to pneumonia or CHF); or diminished blood oxygen-carrying capacity (e.g., due to anemia or carbon monoxide poisoning). The term acute coronary syndrome is applied to any of the three catastrophic manifestations of IHD: unstable angina, MI, and SCD. Pathogenesis of Ischemic Heart Disease IHD is a consequence of inadequate coronary perfusion relative to myocardial demand. In the majority of cases this is due to either or both of the following: Preexisting (“fixed”) atherosclerotic occlusion of the coronary arteries. Acute plaque change with superimposed thrombosis and/or vasospasm. Angina Pectoris Angina pectoris is intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia that is insufficient to cause myocyte necrosis. Types of angina Myocardial Infarction (MI) Commonly referred to as a “heart attack” is necrosis of the heart muscle resulting from ischemia. Pathogenesis: the majority of MIs are caused by acute thrombosis within coronary arteries. An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intra plaque hemorrhage, or mechanical forces, exposing sub endothelial collagen and necrotic plaque contents to the blood. Platelets adhere, aggregate, and are activated, releasing thromboxane A2, adenosine diphosphate (ADP), and serotonin, all of which cause further platelet aggregation and vasospasm. Clinical Features The classic MI is characterized by severe, crushing substernal chest pain (or pressure) that radiates to the neck, jaw, epigastrium, or left arm. In contrast to angina pectoris, the associated pain typically lasts several minutes to hours and is not relieved by nitroglycerin or rest. Silent MI MIs are entirely asymptomatic. Such “silent” infarcts are particularly common in patients with underlying diabetes (in whom autonomic neuropathy may prevent perception of pain) and in older adults. Electrocardiographic abnormalities are important for the diagnosis of MI; these include Q waves, ST segment changes, and T wave inversions. ACS STEMI is invariably due to complete occlusion of a coronary artery and indicates the presence of a transmural infarct. Typically, patients need urgent coronary artery thrombolysis or stent placement. NSTEMI is not associated with complete coronary artery occlusion or full-thickness infarction and can often be managed conservatively. ACS The laboratory evaluation of MI is based on measuring blood levels of normally intracellular proteins that leak out of injured myocardial cells through damaged cell membranes. These molecules include myoglobin, cardiac troponins , creatine kinase (CK; specifically, the myocardial isoform, CK-MB). Arrhythmias Aberrant rhythms can be initiated anywhere in the conduction system, from the sinoatrial (SA) node down to the level of an individual myocyte; they are typically designated as originating from the atrium (supraventricular) or within the ventricular myocardium. The cardiac conduction system SA Node (60-100) AV Node (40-60) Purkinje Fibers (20- 40) Arrhythmias Abnormalities in myocardial conduction can be sustained or paroxysmal. They can manifest as tachycardia (fast heart rate); bradycardia (slow heart rate); an irregular rhythm with normal ventricular contraction. Sudden Cardiac Death (SCD) Defined as unexpected death due to cessation of normal cardiac electrical activity with hemodynamic collapse. SCD results most commonly from lethal arrhythmias such as ventricular tachycardia, ventricular fibrillation, and asystole. SCD The prognosis of many patients at risk for SCD, including those with chronic IHD, is markedly improved by implantation of a pacemaker or an automatic cardioverter defibrillator, which senses and electrically counteracts episodes of ventricular fibrillation. Hypertensive Heart Disease Hypertensive heart disease can affect either the left ventricle or the right ventricle. In the latter case, the disorder is due to primary pulmonary disease and is called cor pulmonale. Elevated pressures induce myocyte hypertrophy and interstitial fibrosis that increase wall thickness and stiffness. The chronic pressure overload of systemic hypertension causes left ventricular concentric hypertrophy, often associated with left atrial dilation due to impaired diastolic filling of the ventricle. Persistently elevated pressure overload can cause ventricular failure with dilation. Cor Pulmonale Cor pulmonale results from pulmonary hypertension due to primary lung parenchymal (e.g., COPD) or vascular disorders (pulmonary hypertension). Hypertrophy of both the right ventricle and the right atrium is characteristic. Valvular Heart Disease Valve pathology can lead to occlusion (stenosis) and/or regurgitation(insufficiency); acquired aortic or mitral valve stenosis. Stenosis typically results from valve calcification, as in aortic stenosis; abnormal matrix synthesis and turnover leads to myxomatous degeneration and insufficiency. Inflammatory valve diseases cause post-inflammatory scarring. Rheumatic heart disease results from antistreptococcal antibodies that cross-react with cardiac tissues. Acute infective endocarditis is a life-threatening inflammation of the inner lining of the heart's chambers and valves caused most often by S. aureus Cardiomyopathies and Myocarditis Cardiomyopathy refers to intrinsic cardiac muscle disease; there may be specific causes, or it may be idiopathic. The three general pathophysiologic categories of cardiomyopathy are dilated (DCM) (accounting for 90% of the cases), hypertrophic (HCM), and restrictive (least common). Myocarditis Myocarditis is inflammation of the heart muscle or myocardium. This inflammation weakens the heart muscle, making it harder for your heart to pump. This can be caused by viral infections or inflammatory conditions.

Use Quizgecko on...
Browser
Browser