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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

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Pericarditis
Pericarditis

  • Often local manifestation of another disease

  • May present as:

    • Acute pericarditis

    • Pericardial effusion

    • Constrictive pericarditis


Acute pericarditis
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


Symptoms
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, restlessness, irritability, anxiety, weakness and malaise


Signs
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.


Treatment
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


Pericardial effusion
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


Outcome depends on how fast fluid accumulates
Outcome depends on how fast fluid accumulates.

  • 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.


Clinical manifestations
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


Treatment1
Treatment

  • Pericardiocentesis

  • Treat pain

  • Surgery if cause is aneurysm or trauma


Constrictive chronic pericarditis
Constrictive (chronic) pericarditis

  • Years ago, synonymous with T.B.

  • Today, usually idiopathic, or associated with radiation exposures, rheumatoid arthritis, uremia, or coronary bypass graft


Pathophysiology
Pathophysiology:

  • 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


Symptoms and signs
Symptoms and Signs

  • Exercise intolerance

  • Dsypnea on exertion

  • Fatigue

  • Anorexia


Clinical manifestations1
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


Treatment2
Treatment

  • Drugs and diet

    • Digitalis

    • Diuretics

    • Sodium restriction

  • Surgery to remove restrictive pericardium


Cardiomyopathies
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


Dilated cardiomyopathy
Dilated cardiomyopathy

↓ C.O.; ↑ thrombi formation ; ↓ contractility, and mitral valve incompetence, arrhythmias Tx: relieve symptoms of heart failure, decrease workload, and anticoagulants; transplants


Hypertrophic cardiomyopathy
Hypertrophic Cardiomyopathy

C.O. is normal,↑ inflow resistance, and mitral valve incompetence, arrhythmais and sudden death.


Restrictive cardiomyopathy
Restrictive cardiomyopathy

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


Disorders of the endocardium valvular dysfunction
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)


Cardiac pathophysiology


Both types of valve disorders
Both types of valve disorders: aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Aortic stenosis
Aortic Stenosis aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • Three common causes:

    • Rheumatic heart disease -Streptococcus infection – damage by bacteria and auto-immune response

    • Congenital malformation

    • Degeneration resulting from calcification


Aortic stenosis1
Aortic Stenosis aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Clinical manifestations2
Clinical manifestations aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Mitral stenosis
Mitral Stenosis aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Cardiac pathophysiology

  • By causing LA to become pump: aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Clinical manifestations3
Clinical Manifestations aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

  • 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


Aortic regurgitation
Aortic Regurgitation aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.

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


Cardiac pathophysiology


Clinical manifestations4
Clinical manifestations relaxation.

  • Widened pulse pressure

  • Prominent carotid pulsations and throbbing peripheral pulses

  • Palpitations

  • Fatigue

  • Dyspnea

  • Angina

  • High-pitched or blowing heart sound during diastole


Mitral regurgitation
Mitral Regurgitation relaxation.

  • 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


Cardiac pathophysiology

  • Causes blood to flow simultaneously to aorta and back to LA. relaxation.

  • 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


Clinical manifestations5
Clinical Manifestations relaxation.

  • Weakness and fatigue

  • Dyspnea

  • Palpitations


Mitral valve prolapse
Mitral Valve Prolapse relaxation.

  • 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


Clinical manifestations6
Clinical manifestations relaxation.

  • Palpitations

  • Tachycardia

  • Light-headedness, syncope, fatigue, weakness

  • Chest tightness, hyperventilation

  • Anxiety, depression, panic attacks

  • Atypical chest pain


Cardiac pathophysiology

  • Once considered to be a psychiatric malady relaxation.

  • May have an autonomic dysfunction in which large quantities of catecholamines are produced.

  • May be a normal variant

  • Can see:

    • chorda rupture

    • ventricular failure

    • systemic emboli and sudden death

  • actually associated with minimal morbidity and mortality


  • Management
    Management relaxation.

    • Echocardiography for diagnosis

    • Related to degree of regurgitation

    • Antibiotics before invasive procedures

    •  blockers to relieve syncope, severe chest pain, or palpitations

    • Avoid hypovolemia

    • Surgical repair


    General treatment for valve disorders
    General Treatment for Valve disorders relaxation.

    • Antibiotics for Strep

    • Anti-inflammatories for autoimmune disorder

    • Analgesics for pain

    • Restrict physical activity

    • Valve replacement surgery


    Heart failure
    Heart failure relaxation.

    • 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


    Ischemic heart disease
    Ischemic Heart Disease relaxation.

    • Coronary Artery Disease (CAD), myocardial ischemia and myocardial infarction are progression of conditions that impair the pumping ability of the heart by depriving it of oxygen and nutrients.


    Coronary artery disease
    Coronary Artery Disease relaxation.

    • Any vascular disorder that narrows or occludes the coronary arteries.

    • Most common cause is atherosclerosis


    Cardiac pathophysiology

    • The arteries that supply the heart are the first branches off the aorta

    • Coronary artery disease decreases the blood flow to the cardiac muscle.

    • Persistent ischemia or complete occlusion leads to hypoxia.

    • Hypoxia can cause tissue death or infarction, which is a “heart attack,” which accounts for about one third of all deaths in U.S.


    Risk factors
    Risk Factors off the aorta

    • Hyperlipidemia

    • Hypertension

    • Diabetes mellitus

    • Genetic predisposition

    • Cigarette smoking

    • Obesity

    • Sedentary life-style

    • Heavy alcohol consumption

    • Higher risk for males than premenopausal women


    Myocardial ischemia
    Myocardial Ischemia off the aorta

    • Myocardial cell metabolic demands not met

    • Time frame of coronary blockage:

      • 10 seconds following coronary block

        • Decreased strength of contractions

        • Abnormal hemodynamics

      • See a shift in metabolism, so within minutes:

        • Anaerobic metabolism takes over

        • Get build-up of lactic acid, which is toxic within the cell

        • Electrolyte imbalances

        • Loss of contractibility


    Cardiac pathophysiology

    • 20 minutes after blockage off the aorta

      • Myocytes are still viable, so

      • If blood flow is restored, and increased aerobic metabolism, and cell repair,

      • →Increased contractility

    • About 30-45 minutes after blockage, if no relief

      • Cardiac infarct & cell death


    Clinical manifestations7
    Clinical Manifestations off the aorta

    • May hear extra, rapid heart sounds

    • ECG changes:

      • T wave inversion

      • ST segment depression


    Chest pain
    Chest Pain off the aorta

    • First symptom of those suffering myocardial ischemia.

    • Called angina pectoris (angina – “pain”)

    • Feeling of heaviness, pressure

    • Moderate to severe

    • In substernal area

    • Often mistaken for indigestion

    • May radiate to neck, jaw, left arm/ shoulder


    Cardiac pathophysiology

    • Due to : off the aorta

      • Accumulation of lactic acid in myocytes or

      • Stretching of myocytes

    • Three types of angina pectoris:

      • Stable, unstable and Prinzmetal


    Stable angina pectoris
    Stable angina pectoris off the aorta

    • Caused by chronic coronary obstruction

    • Recurrent predictable chest pain

    • Gradual narrowing and hardening of vessels so that they cannot dilate in response to increased demand of physical exertion or emotional stress

    • Lasts approx. 3-5 minutes

    • Relieved by rest and nitrates


    Prinzmetal angia pectoris variant angina
    Prinzmetal angia pectoris off the aorta(Variant angina)

    • Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%)

    • Occurs unpredictably and almost exclusively at rest.

    • Often occurs at night during REM sleep

    • May result from hyperactivity of sympathetic nervous system, increased calcium flux in muscle or impaired production of prostaglandin


    Unstable angina pectoris
    Unstable Angina pectoris off the aorta

    • Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing angina

    • May indicate a progression to M.I.


    Silent ischemia
    Silent Ischemia off the aorta

    • Totally asymptomatic

    • May be due abnormality in innervation

    • Or due to lower level of inflammatory cytokines


    Treatment3
    Treatment off the aorta

    • Pharmacologically manipulate blood pressure, heart rate, and contractility to decrease oxygen demands

    • Nitrates dilate peripheral blood vessels and

      • Decrease oxygen demand

      • Increase oxygen supply

      • Relieve coronary spasm


    Cardiac pathophysiology

    •  blockers: off the aorta

      • Block sympathetic input, so

      • Decrease heart rate, so

      • Decrease oxygen demand

    • Digitalis

      • Increases the force of contraction

    • Calcium channel blockers

    • Antiplatelet agents (aspirin, etc.)


    Surgical treatment
    Surgical treatment off the aorta

    • Angioplasty – mechanical opening of vessels

    • Revascularization – bypass

      • Replace or shut around occluded vessels


    Myocardial infarction
    Myocardial infarction off the aorta

    • Necrosis of cardiac myocytes

      • Irreversible

      • Commonly affects left ventricle

      • Follows after more than 20 minutes of ischemia


    Structural functional changes
    Structural, functional changes off the aorta

    • Decreased contractility

    • Decreased LV compliance

    • Decreased stroke volume

    • Dysrhythmias

    • Inflammatory response is severe

    • Scarring results –

      • Strong, but stiff; can’t contract like healthy cells


    Clinical manifestations8
    Clinical manifestations off the aorta

    • Sudden, severe chest pain

      • Similar to pain with ischemia, but stronger

      • Not relieved by nitrates

      • Radiates to neck, jaw, shoulder, left arm

    • Indigestion, nausea, vomiting

    • Fatigue, weakness, anxiety, restlessness and feelings of impending doom.

    • Abnormal heart sounds possible (S3,S4)


    Cardiac pathophysiology

    • Blood test show several markers: off the aorta

      • Leukocytosis

      • Increased blood sugar

      • Increased plasma enzymes

        • Creatine kinase

        • Lactic dehydrogenase

        • Aspartate aminotransferase (AST or SGOT)

      • Cardiac-specific troponin


    Ecg changes
    ECG changes off the aorta

    • Pronounced, persisting Q waves

    • ST elevation

    • T wave inversion


    Treatment4
    Treatment off the aorta

    • First 24 hours crucial

    • Hospitalization, bed rest

    • ECG monitoring for arrhythmias

    • Pain relief (morphine, nitroglycerin)

    • Thrombolytics to break down clots

    • Administer oxygen

    • Revascularization interventions: by-pass grafts, stents or balloon angioplasty