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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
4
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
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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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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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
Dilated cardiomyopathy
Hypertrophic Cardiomyopathy
Restrictive cardiomyopathy
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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
25
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
26
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
27
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
28
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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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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Clinical Manifestations
Weakness and fatigue
Dyspnea
Palpitations
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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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Management
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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
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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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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
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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
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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Decreased contractility
Decreased LV compliance
Decreased stroke volume
Dysrhythmias
Inflammatory response is severe
Scarring results
Strong, but stiff; cant contract like healthy
cells
60
Clinical manifestations
Sudden, severe chest pain
Similar to pain with ischemia, but stronger
Not relieved by nitrates
Radiates to neck, jaw, shoulder, left arm
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Cardiac-specific troponin
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ECG changes
Pronounced, persisting Q waves
ST elevation
T wave inversion
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Treatment