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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
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:
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

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.
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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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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
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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
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workload, and anticoagulants; transplants

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
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incompetence.

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 autoimmune response
Congenital malformation
Degeneration resulting from calcification

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Aortic Stenosis
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
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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; cant 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
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