1 / 79

Cardiac Pathophysiology

Cardiac Pathophysiology. Pericarditis. Often local manifestation of another disease May present as: Acute pericarditis Pericardial effusion Constrictive pericarditis. Acute Pericarditis. Acute inflammation of the pericardium

tanith
Télécharger la présentation

Cardiac Pathophysiology

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Cardiac Pathophysiology

  2. Pericarditis Often local manifestation of another disease May present as: Acute pericarditis Pericardial effusion Constrictive pericarditis

  3. Acute Pericarditis Acute inflammation of the pericardium Cause often unknown, but commonly caused by infection, uremia, neoplasm, myocardial infarction, surgery or trauma. Membranes become inflamed and roughened, and exudate may develop

  4. Symptoms: Sudden onset of severe chest pain that becomes worse with respiratory movements and with lying down. Generally felt in the anterior chest, but pain may radiate to the back. May be confused initially with acute myocardial infarction Also report dysphagia (difficulties swallowing), restlessness, irritability, anxiety, weakness and malaise

  5. Signs Often present with low grade fever and sinus tachycardia Friction rub(sandpaper sound) may be heard at cardiac apex and left sternal border and is diagnostic for pericarditis (but may be intermittent) ECG changes reflect inflammatory process through PR segment depression and ST segment elevation.

  6. Treatment Treat symptoms Look for underlying cause If pericardial effusion develops, aspirate excess fluid Acute pericarditis is usually self-limiting, but can progress to chronic constrictive pericarditis

  7. Pericardial effusion Accumulation of fluid in the pericardial cavity May be transudate May be exudate May be blood Not clinically significant other than to indicate underlying disorder, unless: Pressure becomes sufficient to cause cardiac compression – cardiac tamponade

  8. If development is slow, pericardium can stretch If develops quickly, even 50 -100 ml of fluid can cause problems When pressure in pericardium = diastolic pressure, get ↓ filling of right atrium, ↓ filling of ventricles, ↓ cardiac output → circulatory collapse. Outcome depends on how fast fluid accumulates.

  9. Clinical manifestations Pulsus paradoxus – B.P. higher during expiration than inspiration by 10 mm Hg Distant or muffled heart sounds Dyspnea on exertion Dull chest pain Observable by x-ray or ultrasound

  10. Treatment Pericardiocentesis Treat pain Surgery if cause is aneurysm or trauma

  11. Constrictive (chronic) pericarditis Years ago, synonymous with T.B. Today, usually idiopathic, or associated with radiation exposures, rheumatoid arthritis, uremia, or coronary bypass graft

  12. Fibrous scarring with occasional calcification of pericardium Causes parietal and visceral layers to adhere Pericardium becomes rigid, compressing the heart →↓ C.O. Stenosis of veins entering atria Always develops gradually Pathophysiology:

  13. Symptoms and Signs Exercise intolerance Dsypnea on exertion Fatigue Anorexia

  14. Clinical manifestations Weight loss Edema and ascites Distention of jugular vein (Kussmaul sign) Enlargement of the liver and/or spleen ECG shows inverted T wave and atrial fibrillation Can be seen on imaging

  15. Treatment Drugs and diet Digitalis Diuretics Sodium restriction Surgery to remove restrictive pericardium

  16. Cardiomyopathies Disorders of the heart muscle Most cases idiopathic Many due to ischemic heart disease and hypertension. Three categories: Dilated ( formerly, congestive) Hypertrophic Restrictive Heart loses effectiveness as a pump

  17. Dilated cardiomyopathy AKA: congestive, ↓ C.O.; ↑ thrombi formation, slow blood flow ; ↓ contractility, and mitral valve incompetence, arrhythmias

  18. Treatment: relieve symptoms of heart failure, decrease workload, and anticoagulants; transplants

  19. Hypertrophic Cardiomyopathy Often inherited, C.O. is normal,↑ inflow resistance, and mitral valve incompetence, arrhythmais and sudden death.

  20. Chest pain • Dizziness • Fainting, especially during exercise

  21. major cause of death in young athletes who seem completely healthy but die during heavy exercise

  22. The goal of treatment is to control symptoms and prevent complications

  23. Restrictive cardiomyopathy Reduced diastolic compliance of the ventricle. C.O. is normal or↓;↑ formation of thrombi, dilation of left atrium, and mitral valve incompetence.

  24. Disorders of the Endocardium:Valvular dysfunction Endocardial disorders damage heart valves Changes can lead to : Valvular Stenosis = too narrow Valvular Regurgitation = too leaky (or insufficiency or incompetence)

  25. Valves that are most often affected are the mitral and aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve. Heart Murmur – sound caused by turbulent blood flow through damaged valves.

  26. Both types of valve disorders: Cause increased cardiac work, and increased volumes and pressures in the chambers. This leads to chamber dilation and hypertrophy. Chamber dilation and myocardial hypertrophy are compensatory mechanisms to increase the pumping capability of the heart. Eventually, the heart fails from overwork

  27. Aortic Stenosis Three common causes: Rheumatic heart disease -Streptococcus infection – damage by bacteria and auto-immune response Congenital malformation Degeneration resulting from calcification

  28. Blood flow obstructed from LV into aorta during systole Causes increased work of LV → LV dilation & hypertrophy as compensation → prolonged contractions as compensation Finally heart overwhelmed → increased pressures in LA, then lungs, then right heart Aortic Stenosis

  29. Clinical manifestations Develops gradually Decreased stroke volume Reduced systolic blood pressure Narrowed pulse pressure Heart rate often slow and pulse faint Crescendo-decrescendo heart murmur Angina, dizziness, syncope, fatigue Can lead to dysrhythmias, myocardial infarction, and left heart failure

  30. Mitral Stenosis Most common of all valve disorders Usually the result of rheumatic fever or bacterial endocarditis During healing the orifice narrows, the valves become fibrous and fused, and chordae tendineae become shortened Get decreased flow from LA to LV during filling Results in hypertrophy of LA

  31. By causing LA to become pump: Get increased pulmonary vascular pressures; pressures increase through LA into lung →pulmonary congestion →lung tissue changes to accommodate increased pressures →increased pressure in pulmonary artery →increased pressure in right heart →right heart failure

  32. Clinical Manifestations Atrial enlargement can be seen on x-ray Rumbling decrescendo diastolic murmur, and accentuated first heart sound Dyspnea Tachycardia and risk of atrial fibrillation Other signs and symptoms are of pulmonary congestion and right heart failure

  33. Aortic Regurgitation Caused by acute or chronic lesion of rheumatic fever, bacterial endocarditits, syphilis, hypertension, connective tissue disorder (e.g.Marfan syndrome) or atherosclerosis

  34. Reflux of blood from aorta to LV during ventricular relaxation. Causes LV to pump more blood w/ each contraction → LV hypertrophy LV takes on “globular shape” →increased pressures in LA, lung, right heart

  35. Clinical manifestations Widened pulse pressure Prominent carotid pulsations and throbbing peripheral pulses Palpitations Fatigue Dyspnea Angina High-pitched or blowing heart sound during diastole

  36. Mitral Regurgitation Causes: mitral valve prolapse, rheumatic heart disease, infective endocarditis, connective tissue disorders, and cardiomyopathy Permits backflow of blood from the LV into the LA during ventricular systole Loud pansystolic murmur that radiates into the back and axilla

  37. See the animated

  38. Causes blood to flow simultaneously to aorta and back to LA. Both LV and LA pump harder to move same blood twice →LV hypertrophy and dilation as compensation Compensation works awhile, then see ↓C.O. → heart failure Also →LA hypertrophy → increased pressures through lungs → ↑ pressures in right heart →right heart failure Can see edema, shock

  39. Clinical Manifestations Weakness and fatigue Dyspnea Palpitations

  40. Mitral Valve Prolapse Cusps of valve billow upward into the LA during ventricular systole Mitral regurgitation can occur Most common valve disorder in U.S. Studies suggest an autosomal dominant inheritance pattern Many cases completely asymptomatic Regurgitant murmur or midsystolic click

  41. Clinical manifestations Palpitations Tachycardia Light-headedness, syncope, fatigue, weakness Chest tightness, hyperventilation Anxiety, depression, panic attacks Atypical chest pain

  42. Management Echocardiography for diagnosis Related to degree of regurgitation Antibiotics before invasive procedures Beta blockers to relieve syncope, severe chest pain, or palpitations Avoid hypovolemia Surgical repair

  43. General Treatment for Valve disorders Antibiotics for Strep Anti-inflammatories for autoimmune disorder Analgesics for pain Restrict physical activity Valve replacement surgery

  44. Heart failure Definition – When heart as a pump is insufficient to meet the metabolic requirements of tissues. Acute heart failure 65% survival rate Chronic heart failure Most common cause is ischemic heart disease

  45. Right heart failure • Systemic symptoms • Edema, ascites • Enlarged liver, spleen • Swollen feet, ankles • Nausea • Swollen internal jugular veins

More Related