Ch - 19 Disorders of Cardiac Function Flashcards
What is coronary artery disease CAD? What are the coronary arteries?
CAD describes heart disease caused by impaired coronary blood flow. They can cause a spectrum of ischemic disorders ranging from angina to myocardial infarction as well as conduction defects, heart failure, and sudden cardiac death
The are left main coronary artery and left anterior descending artery.
Pathogenesis - Most common cause is atherosclerosis, the lesions can be anywhere but they are usually in the first several cm of the left anterior descending and left circumflex artery or along the entire length of the right coronary artery. Normally divided into two broad disorders; acute coronary syndromes and chronic ischemic heart disease. Two lesions; fixed or stable plaque and unstable plaque. Fixed is usually associated with stable angina. Unstable with unstable angina and MI. It is usually a plaque disruption followed by thrombosis.
What is Acute coronary syndrome?
ACS spectrum of acute ischemic heart diseases ranging from unstable ischemia and acute MI based on the presence or absence of an ST segment elevation or depression on the ECG. Whether the pt should be considered for acute reperfusion therapy. Troponin I is used to determine if an MI occurred.
ECG changes are ST segment elevation, T wave inversion, and development of abnormal Q wave. These changes may not present immediately depending on the duration of the ischemic event, its extent, and its location. T wave and ST segment represent ventricular repolarization phase of the cardiac action potential and the first to be involved in MI and injury.
Serum biomarkers
Cardiac specific troponin I and troponin T, creatine kinase MB and myoglobin. Troponin begins to arise after event with 3 hours and may remain elevated for 7-10 days.
Unstable angina/Non ST elevation Myocardial Infarction - unstable angina has no bio markers, whereas Nstemi has bio markers but no ST segment elevation can be depression is a less urgent case. Still means ischemia occurred.
Acute ST elevation myocardial infarction - is necrosis of myocardial tissue, the specific area is determined by the affected coronary artery.
What is pathologic changes in ACS? Diagnosis and Treatment? Myocardial postinfarction recovery period?
The size and pattern of the infarct depends on the location and extent of occlusion, amount of heart tissue supplied by the vessel, duration of the occlusion, metabolic needs of the affected tissue, extent of collateral circulation, and other factors such as heart rate, BP and cardiac rhythm.
The onset of STEMI involves abrupt and significant chest pain. Can radiate to the left arm, neck or jaw is common is more prolonged and not relieved by nitroglycerin Maybe GI complaints. Sudden death occurs from acute MI within 1 hour of onset.
Diagnosis - Prompt medical care, at first both NSTEMI and STEMI is treated the same till bio markers can be done and ECG data.
Treatment - ECG and continuous monitoring, oxygen, aspirin, nitrates, morphine, antiplatelet and anticoagulant therapy, B adrenergic blocking agents and ACE inhibitor. Immediate reperfusion therapy fibrinolytic therapy, percutaneous coronary intervention. or coronary artery bypass grafting.
Percutaneous coronary intervention PCI with stent. or CABG coronary artery bypass grafting.
After MI - necrotic zone, surrounding zone which will recover, outer zone which cells are ischemic and can be salvaged if blood flow reestablished. If blood flow can be reestablished within 20-40 minutes. The cells that undergo necrosis are replaced with scar tissue about 2-3 days after. Can develop pericarditis from 2 days to week to months after MI is thought to be autoimmune issue.
What is chronic ischemic heart disease?
MI is defined as the inability of the coronary arteries to supply blood to meet the metabolic demands of the heart. CAD is divided into 3 classifications
Chronic stable angina - angina pectoris is symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia. Is usually precipitated by situation that inc the work demands of the heart, physical exertion, exposure to cold and emotional stress. Usually associated with pain can be relieved by rest or nitroglycerin
Silent myocardial ischemia - occurs in the absence of anginal pain. Maybe caused from diabetic neuropathy
Variant (vasospastic) angina - is caused by coronary artery spasm. Not understood but could be a combo of pathologic processes endothelial dysfunction, hyperactive sympathetic nervous system responses, defective handling of calcium by vascular smooth muscle, or altered nitric oxide production
Diagnosis and Treatment - is based on detailed pain history, the presence of risk, invasive and noninvasive studies and laboratory studies. To prevent MI, symptom control and lifestyle changes. Smoking cessation. Drugs -nitrates, beta blockers and calcium channel blockers CABG indicated in pt with double or triple vessel disease.
What are endocardial and valvular disorders? Infectious endocarditis? ca
IE is a serious and potentially life threatening infection of the inner surface of the heart including cardiac valves. Infection leads to vegetations and destruction of underlying cardiac tissues. Can be caused by fungi or other microorganism but is usually bacteria. Usually classified into acute or subacute-chronic depending on onset, etiology, severity of disease. Usually rapid and occurs in pt with previously normal cardiac valves history of IV drug abuse whereas chronic pt usually have underlying heart valve abnormalities.
Etiology - two factors contribute; a portal of entry - could be infection, a dental or surgical procedure, IV injection of a contaminated surface, oral cavity, gut or sc injury. Can be infections associated with cardiovascular prostheses and devices pacemakers. Staphylococcal are the leading cause. Caused friable, bulky and potentially destructive vegetative lesion form on the heart valves.
Mani - signs can include fever, signs of systemic infection, development of heart murmur, evidence of embolic distribution of vegetative lesions. Anorexia, malaise, lethargy. Small petechial hemorrhages result when emboli lodge in small vessels of the skin, nail beds, cough dyspnea, arthralgia or arthritis.
Diagnosis and treatment - Blood culture remains the most definitive procedure. Can have negative blood culture delaying treatment. Transthoracic and transesophageal echocardiography are primary tech for detection. Treatment Antibiotics and surgery . prevention for pt with predisposing congenital or valvular disorders undergoing dental or surgery.
What is Rheumatic Heart Disease RF?
It is an immune-mediated, multisystem inflammatory disease that occurs a few weeks after a group A streptococcal pharyngitis in children and young adults. Acute RHD is the cardiac manifestation of RF and is associated with inflammation of all three layers of the heart. Chronic deformity and impairment of one or more of the heart valves is the most important consequence of RHD.
Pathogenesis - RF doesn’t involve direct bacterial infection of the heart. Its an immunologic response. Antibodies directed against the M protein of certain strains of Streptococci cross react with glycoprotein antigens in the heart, joints, and other tissues to produce an autoimmune response through a phenomenon molecular mimicry
Clinic features - can be acute, recurrent, chronic disorder. Acute stage of rheumatic fever includes a history of an initiating steptococcal infection and subsequent development of discrete inflammatory lesion seen on histopathologic exam . These heart lesion are called Aschoff bodies. Recurrent phase involves extension of the cardiac effects of the disease. Chronic is by permanent deformity of the heart valves which usually doesn’t appear for at least 10 years after. Usually have sore throat, fever, headache, abd pain, nausea, vomiting, swollen glands. The course of the disease is characterized by a constellation of findings that includes carditis, migratory polyarthritis of the large joints, erythema marginatum, sc nodules, and Sydenham chorea. May cause pericarditis which is all three layers of mitral insufficiency and even heart failure. Can show as pericardial friction rubs, arrhythmias, new heart murmur.
Diagnosis - made with lab tests for evidence of GAS infection and cardinal symptoms. lab tests for elevated WBC,ESR, and CRP.
Treatment and prevention - Is a throat culture, takes 24-48 hours to produce. Antibiotics, anti-inflammatory drugs and selective restriction of activities. Penicillin , salicylates and corticosteroids for inflammatory. Surgery for valve repair maybe needed. Can use penicillin for prophylaxis.
What is valvular heart disease? Hemodynamic derangements? Mitral Valve Stenosis?
The function of the heart valves is to promote unidirectional flow of blood through the chambers of the heart. Dysfunction of the valves can be from congenital defects, trauma, ischemia, degenerative changes, and inflammation. Most common are the mitral and aortic valves. Two types of mechanical disruption; narrowing of the valvular opening, and distortion of the valve, doesn’t close properly. Regurgitant valve doesn’t close properly, permitting the backward flow of blood to occur when the valve should be closed.
The mitral valve AV controls the directional flow of blood between the left atrium and the left ventricle. The edges or cusps of both AV valves are anchored to the papillary muscles by the chordae tendineae. Is under high pressure as the ventricles push the blood into the systemic circulation.
Stenosis represents the incomplete opening of the mitral valve during diastole, with left atrial distension and impaired filling of the left ventricle. Is the result of rheumatic fever. less frequently the defect is congenital and manifests during infancy or early childhood or calcification in elderly pt. Is characterized by fibrous replacement of valvular tissue, along with stiffness and fusion of the valve apparatus. Mani- are pulmonary congestion dyspnea with exertion, dec cardiac output owing to impaired left ventricular filling, and left atrial enlargement with the development of atrial arrhythmias and mural thrombi. Severe stenosis palpitations, chest pain, weakness and fatigue are common.
Mitral valve regurgitation? mitral valve prolapse?
Regurgitation is characterized by incomplete closure of the mitral valve, with the left ventricular stroke volume being divided between the forward stroke volume that moves blood into the aorta and the regurgitant stroke volume that moves it back into the left atrium during systole. Caused by IE or RHD, can rupture the chordae tendineae or papillary muscles, due to an MI, papillary muscle dysfunction, or stretching of the valve structures due to dilation of the left ventricle or valve orifice. Feature of mitral valve is enlarged or hypertrophied left ventricle, a hyperdynamic left ventricular impulse, and a pansystolic heart murmur. Eventually leads to pulmonary congestion.
Mitral valve prolapse referred as floppy mitral valve syndrome, happens to 1 -2.5% of population. Is seen in thin women and may be familial. A mucinous degeneration of the mitral valve leaflets that causes them to become enlarged and floppy so that they prolapse or balloon back into the left atrium during systole. Are asymptomatic and is discovered in routine physical exam. Minority of pt have chest pain, dyspnea, fatigue, anxiety, palpitations, and light headedness. Not associated with exercise. Treatment focuses on the relief of symptoms and the prevention of complications with beta blockers and cessation of stimulants like coffee. Antibiotic prophylaxis’s before dental or surgery. Daily aspirin therapy as inc transient ischemic attacks more frequently. Might need valve surgery.
Aortic valve disorders? Aortic Valve stenosis?
The aortic valve located between the left ventricle and aorta, has three cuplike cusps and sometimes is referred to as the aortic semilunar valve because its leaflets are crescent or moon shaped. Has no chordae tendineae. Valve opens up so when pressure the blood flows out and then close when the pressure stops and falls back closed.
Aortic valve stenosis - is the narrowing of the valve orifice with increased resistance to ejection of blood from the left ventricle into the aorta. Causes are congenital valve malformations and acquired calcification of a normal aortic valve. It usually become evident around the sixth and seventh decades in persons with bicuspid aortic valves, and not until the eighth and ninth decades. Range from mild to severe and obstructed. Usually develops gradually and the left ventricle becomes thicker to adapt.
Is first diagnosed with auscultation of a loud systolic ejection murmur or a single or paradoxically split second heart sound. Symptoms angina, syncope and heart failure develop. Angina is common with advanced stenosis and is similar to CAD
Aortic valve regurgitation? Diagnosis and Treatment?
Regurgitation of aortic is the result of an incompetent aortic valve that allows blood to flow back to the left ventricle during diastole. As a result the left ventricle increases its stroke volume to accommodate blood entering from the pulmonary veins in addition to the volume of blood leaking back through. May cause scarring on the valve leaflets or from enlargement of the valve orifice to the extent that the valve leaflets no longer meet. Causes are RH, idiopathic dilation of the aorta, congenital abnormalities, infective endocarditis, and Marfan syndrome. Hypertension, trauma, and failure of a prosthetic valve. Acute if by large regurgitation without time to adapt from infective endocarditis, trauma, aortic dissection. Frank Starling mech to cope by inc heart rate, but leads to pulmonary edema. Chronic the left ventricle starts to enlarge. Leads to widening of the arterial pulse pressure
Diagnosis and Treatment - through cardiac auscultation. Echocardiography, pulsed doppler US or invasive cardiac catheterization. Medical management or valvular replacement or balloon catherization.
What are disorders of the pericardium? Acute pericarditis?
Pericardium is the double layered fibroserous sac that encircles the heart. Has two layers thin inner layer visceral pericardium which adheres to the epicardium and an outer fibrous layer the parietal pericardium attached to the great vessels that enter and leave the heart. IT can allow for moderate changes but can’t stretch to accommodate rapid dilation of the heart or accumulation of pericardial fluid without inc pericardial and intracardiac pressures.
Acute pericarditis -, signs resulting from pericardial inflammation of less then 2 weeks duration, may result from an infection or noninfectious disease. Viral infections are the most common. Include bacterial, mycobacterial infections, connective tissue diseases , uremia, postcardiac surgery, neoplastic invasion of the pericardium, radiation, trauma, drug toxicity and contiguous inflammatory processes. Causing exudate which leads to fibrin and heals by resolution or becomes scar tissue and adhesions Mani - triad of chest pain, auscultatory pericardial friction rub and ECG changes. nearly all have chest pain and fever. treatment depends on the cause, antibiotics for infection
What is pericardial effusion? and cardiac tamponade?
Is the accumulation of fluid in the pericardial cavity, usually the result of inflammatory or infectious process that includes pericarditis. May develop with neoplasms, cardiac surgery, trauma. It exerts its effects through compression of the heart chambers. Echocardiogram is a rapid accurate noninvasive of diagnosis. Treatment depends on the extent of effusion. Small diuretics are given and NSAIDs, colchicine or corticosteriods. Pericardiocentesis to remove the fluid is the initial treatment with larger effusions.
Pericardial effusion can lead to cardiac tamponade in which there is compression of the heart due to accumulation of fluid or blood in the pericardial sac. Caused by bleeding into the pericardial sac after blunt penetrating injury, rupture of the heart from MI, complications from percutaneous cardiac procedures or device placement or retrograde bleeding from aortic dissection. Result in inc intracardiac pressure, progressive limitation of ventricular diastolic filling and reduction in stroke volume and cardiac output. Results in elevated central venous pressure, jugular vein distention, a fall in systolic BP, narrowed pulse pressure, and signs of circulatory shock. Treatment closed pericardiocentesis in which fluid is removed from the pericardial sac through a needle inserted through the chest wall.
What is constrictive pericarditis?
Fibrous scar tissue develops between the visceral and parietal layers of the serous pericardium. The scar tissue in time contracts and interferes with diastolic filling of the heart at which point cardiac output and reserve become fixed. Caused usually by inflammation from infections, mediastinal radiation, or cardiac surgical trauma. Characterized by high venous pressure, low cardiac output, narrow pulse pressure, and fluid retention. Ascites is a prominent early finding. Exercise intolerance, muscle wasting and weight loss develop in end stage. Surgical removal or resection of the pericardium
What are cardiomyopathies? Primary? hypertrophic cardiomyopathy?
They are disorders of the heart muscle. Usually associated with disorders of myocardial performance, which may be mechanical or electrical. Two major groups:
Primary cardiomyopathies - are classified as genetic, mixed, or acquired, based on their etiology.
Hypertrophic cardiomyopathy - is characterized by unexplained left ventricular hypertrophy with, disproportionate thickening of the ventricular septum, abnormal diastolic filling, cardiac arrhythmias and in some cases, intermittent left ventricular outflow obstruction. Is the most common cause of sudden cardiac death in young athletes
mani - are highly variable and may progress to end stage heart failure with left ventricular remodeling and systolic dysfunction. Symptoms are dyspnea and chest pain. syncope and typically post exertional. Atrial fib is a longterm consequence. Ventricular arrhythmias are also common and sudden death may occur.
Diagnosis and treatment - 2d echocardiography, ECG, and continuous ambulatory monitoring. MRI, DNA testing.
Medical management is mostly on symptom management. Drug therapy of beta blockers or can use calcium channel blockers but not recommended for severe. Surgery myotomy myectomy or alchol ablation. Implanted cardioverter defibrillator.
What is arrhythmogenic right ventricular dysplasia? Dilated Cardiomyopathy?
ARVD or ARVC is a heart muscle disease that primarily affects the right ventricle, leading to various rhythm disturbances, particularly ventricular tachycardia, and potentially to heart failure. is inherited disorder. Second leading cause of sudden cardiac death in young athletes.
Mani - is characterized by progressive loss of myocytes, with partial or complete replacement of the right ventricular muscle with adipose or fibrofatty tissue. It is precipitated by an exercise induced discharge of catecholamines. Usually are palpitations, syncope, cardiac arrest. May include abd pain and mental confusion.
Treatment - aimed at prevention of sudden cardiac death, It can’t be cured radiofrequency ablation but needs to be repeated, Implantable cardioverter - defibrillator. Final options ventriculotomy or heart transplant
Dilated DCM is common cause of heart failure and leading cause of implantation. 33% are genetic the rest are infection, toxins, alcoholism, chemo, metals, and other disorders. It is characterized by progressive cardiac dilation and contractile dysfunction usually with concurrent hypertrophy.
Mani - Related to heart failure, dyspnea, orthopnea, reduced exercise capacity. Stasis of blood in the walls of the heart chamber can lead to thrombus and systemic emboli. Secondary mitral valve regurgitation and abn cardiac rhythms. Death can occur suddenly.
Treatment - Diuretics, beta blockers to reduce HR, afterload reducing agents and ACE inhibitors. Anticoagulant and antiarrhythmic drugs. Biventicular pacemaker an implantable cardioverter - defibrillator. Cardiac transplant. Average survival rate of less then 50% if no surgery in 5 years.
