Cardiac Patophysiology

8/10/2019 Cardiac Patophysiology

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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 respiratorymovements 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 andsinus tachycardia

Friction rub(sandpaper sound) may be

heard at cardiac apex and left sternalborder and is diagnosticfor pericarditis

(but may be intermittent)

ECG changes reflect inflammatoryprocess 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 constrictivepericarditis


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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 paradoxusB.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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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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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

DiureticsSodium 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, andmitral 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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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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Both types of valve disorders:

Cause increased cardiac work, and

increased volumes and pressures in thechambers.

This leads to chamber dilation and

hypertrophy. Chamber dilation and myocardial

hypertrophy are compensatorymechanisms to increase the pumpingcapability of the heart.

Eventually, the heart fails from overwork


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Aortic Stenosis

Three common causes:

Rheumatic heart disease -Streptococcus

infectiondamage by bacteria and auto-

immune response Congenital malformation

Degeneration resulting from calcification


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Blood flow obstructed from LV into aorta during

systoleCauses increased work of LV

LV dilation & hypertrophy as

compensationprolonged contractions as

compensation

Finally heart overwhelmed

increased pressures in LA, then lungs, thenright heart

Aortic Stenosis


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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 valvesbecome 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 LAinto lung

pulmonary congestion

lung tissue changes to accommodateincreased 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 ofpulmonary 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) oratherosclerosis


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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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Mitral Regurgitation

Causes: mitral valve prolapse, rheumaticheart disease, infective endocarditis,

connective tissue disorders, and

cardiomyopathy Permits backflow of blood from the LV

into the LA during ventricular systole

Loud pansystolicmurmur that radiatesinto the back and axilla


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Causes blood to flow simultaneously toaorta and back to LA.

Both LV and LA pump harder to movesame 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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Weakness and fatigue

Dyspnea

Palpitations


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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 areproduced.

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

DefinitionWhen 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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Coronary Artery Disease

Any vascular disorder that narrows oroccludes the coronary arteries.

Most common cause is atherosclerosis

The arteries that supply the heart are the first


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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.

Risk Factors


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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

Myocardial Ischemia


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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 cellElectrolyte imbalances

Loss of contractibility


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20 minutes after blockage

Myocytes are still viable, so

If blood flow is restored, and increasedaerobic metabolism, and cell repair,

Increased contractility

About 30-45 minutes after blockage, if norelief

Cardiac infarct & cell death


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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 (anginapain)

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

Prinzmetal angia pectoris


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Prinzmetal angia pectoris

(Variant angina)

Caused by abnormal vasospasm ofnormal 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 ofsympathetic 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

T


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Treatment

Pharmacologically manipulate bloodpressure, heart rate, and contractility to

decrease oxygen demands

Nitrates dilate peripheral bloodvessels 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

Angioplastymechanical opening of

vessels

Revascularizationbypass

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; cant contract like healthy

cells



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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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ECG changes

Pronounced, persisting Q waves

ST elevation

T wave inversion


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Cardiac Patophysiology