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Cardiac Pathophysiology

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Pericarditis

• Often local manifestation of another disease

• May present as:

– Acute pericarditis

– Pericardial effusion

– Constrictive pericarditis

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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

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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

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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.

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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

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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

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• 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.

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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

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Treatment

• Pericardiocentesis

• Treat pain

• Surgery if cause is aneurysm or trauma

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Constrictive (chronic) pericarditis

• Years ago, synonymous with T.B.

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

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• 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:

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Symptoms and Signs

• Exercise intolerance

• Dsypnea on exertion

• Fatigue

• Anorexia

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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

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Treatment

• Drugs and diet

– Digitalis

– Diuretics

– Sodium restriction

• Surgery to remove restrictive pericardium

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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

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Dilated cardiomyopathy

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

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Hypertrophic Cardiomyopathy

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

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Restrictive cardiomyopathy

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

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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)

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• 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.

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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

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Aortic Stenosis

• Three common causes:– Rheumatic heart disease -Streptococcus

infection – damage by bacteria and auto-immune response

– Congenital malformation– Degeneration resulting from calcification

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• Blood flow obstructed from LV into aorta during systole

Causes increased work of LV→ LV dilation & hypertrophy as

compensation→ prolonged contractions as

compensationFinally heart overwhelmed

• → increased pressures in LA, then lungs, then right heart

Aortic Stenosis

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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

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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

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• 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

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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

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Aortic Regurgitation

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

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• 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

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Clinical manifestations• Widened pulse pressure

• Prominent carotid pulsations and throbbing peripheral pulses

• Palpitations

• Fatigue

• Dyspnea

• Angina

• High-pitched or blowing heart sound during diastole

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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

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• 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

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Clinical Manifestations

• Weakness and fatigue

• Dyspnea

• Palpitations

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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

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Clinical manifestations

• Palpitations

• Tachycardia

• Light-headedness, syncope, fatigue, weakness

• Chest tightness, hyperventilation

• Anxiety, depression, panic attacks

• Atypical chest pain

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• Once considered to be a psychiatric malady

• 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

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Management

• 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

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General Treatment for Valve disorders

• Antibiotics for Strep

• Anti-inflammatories for autoimmune disorder

• Analgesics for pain

• Restrict physical activity

• Valve replacement surgery

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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

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Ischemic Heart Disease

• 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.

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Coronary Artery Disease• Any vascular disorder that narrows or

occludes the coronary arteries.

• Most common cause is atherosclerosis

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• 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.

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Risk Factors• Hyperlipidemia

• Hypertension

• Diabetes mellitus

• Genetic predisposition

• Cigarette smoking

• Obesity

• Sedentary life-style

• Heavy alcohol consumption

• Higher risk for males than premenopausal women

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Myocardial Ischemia• 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

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• 20 minutes after blockage–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

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Clinical Manifestations

• May hear extra, rapid heart sounds

• ECG changes:

– T wave inversion

– ST segment depression

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Chest Pain• 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

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• Due to :– Accumulation of lactic acid in myocytes or– Stretching of myocytes

• Three types of angina pectoris:– Stable, unstable and Prinzmetal

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Stable angina pectoris

• 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

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Prinzmetal angia pectoris(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

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Unstable Angina pectoris

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

• May indicate a progression to M.I.

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Silent Ischemia

• Totally asymptomatic

• May be due abnormality in innervation

• Or due to lower level of inflammatory cytokines

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Treatment• 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

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blockers:

– Block sympathetic input, so

– Decrease heart rate, so

– Decrease oxygen demand

• Digitalis

– Increases the force of contraction

• Calcium channel blockers

• Antiplatelet agents (aspirin, etc.)

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Surgical treatment

• Angioplasty – mechanical opening of vessels

• Revascularization – bypass

– Replace or shut around occluded vessels

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Myocardial infarction

• Necrosis of cardiac myocytes– Irreversible– Commonly affects left ventricle– Follows after more than 20 minutes of

ischemia

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Structural, functional changes• Decreased contractility

• Decreased LV compliance

• Decreased stroke volume

• Dysrhythmias

• Inflammatory response is severe

• Scarring results –– Strong, but stiff; can’t contract like healthy

cells

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Clinical manifestations• 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)

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• Blood test show several markers:– Leukocytosis– Increased blood sugar– Increased plasma enzymes

• Creatine kinase• Lactic dehydrogenase• Aspartate aminotransferase (AST or

SGOT)

– Cardiac-specific troponin

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ECG changes

• Pronounced, persisting Q waves

• ST elevation

• T wave inversion

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Treatment

• 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