Transcript Cardiac Pathophysiology

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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Outcome depends on how fast fluid
accumulates.
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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.
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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
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Exercise intolerance
Dsypnea on exertion
Fatigue
Anorexia
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Clinical manifestations
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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
– 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
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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 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
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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
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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
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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
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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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