Download Heart Diseases

Heart Diseases
Heart Failure
• Decreased contractility power of the heart
• Decreased cardiac output
• Can affect right or left sides of heart
Left-sided heart failure
Causes:
a. Ischemic heart disease (IHD),
b. Systemic hypertension,
c. Mitral or aortic valve disease.
d. Diseases of myocardium
e. Severe anemia
Clinical symptoms
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Fatigue
Exretional Dyspnea (shortness of breathe)
Orthopnea (recumbent position)
Cough
Impairment of renal and cerebral functions
Right sided heart failure
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Causes:
Late consequence of left sided heart failure
Pulmonary hypertension (cor pulmonale)
Pulmonary or tricupid valve stenosis
Left-right shunt
Symptoms
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Systemic venous congestion
Lower limb edema
Hepatomegaly
Splenomegaly
Pericardial effusion
Ascites
Morphology
• Dilated chambers of heart
Ischemic Heart Disease (IHD)
• Also known as Coronary Artery Disease(CAD)
• Decreased oxygen demand to cardiac muscles
• >90% of cases, due to reduced coronary blood
flow secondary to obstructive atherosclerosis
• Other causes: vasospasm, embolus, shock
Clinical Presentation
1) Angina Pectoris ‫ذبحة صدرية‬
2) Myocardial infarction ‫احتشاء عضلة القلب‬
3) Chronic ischemic heart disease
4) Sudden cardiac death
Angina pectoris
• Most patients have “stable, or typical Angina”,
characterized by:
• Squeezing, retrosternal pain
• Intermittent
• Reversible (rest, drugs)
• Short duration (<10 min)
• Preceded by stress
• Atherosclerosis in 70% of coronary arteries
Unstable angina
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Appears at rest
Longer duration
Atherosclerosis occlusion 90%
Commonly precedes myocardial infarction
Prinzmetal Angina
• Also known as variant angina
• Caused by vasospasm
Myocardial Infarction (MI)
• Also known as heart attack
• Can occur at any age but the frequency rises
progressively with increasing age
• Approximately 10% of MIs occur before age 40
• Men are at significantly greater risk than women,
and women tend to be protected against MI
during their reproductive years
• However, menopause women with declining
estrogen is associated with exacerbation of
coronary artery disease and IHD is the most
common cause of death in elderly women
Pathogenesis
• Complete arterial obstruction
• Disease begin with atherosclerotic plaque in arteries,
causing narrowing of the lumen
• External factors, such as hypertension, vasospasm,
adrenergic stress, causes disruption of plaque
• Thrombus forms on the complicated plaque, causing
complete lumen obstruction
• Ischemic necrosis follows to the cardiac territory supplied
by that vessel
• Surge in adrenergic stimulation associated with awakening
and rising may underlie that the incidence of acute MI is
highest in early morning
• 10% of cases results from vasospasm & no atherosclerosis
Cardiac Cathetarization
• Immediate medical intervention (angiography)
can demonstrate the thrombus
• If late (>12 hours), thrombus is demonstrated
in only 60% of cases, due to fibrinolysis
• Early administration of thrombolytics limit the
degree of cardiac infarction
Complications
1. Loss of contractility occurs within a minute of
onset of ischemia and may be reversible
2. Myocyte coagulative necrosis, in severe ischemia
lasting 20 to 40 minutes (if no intervention), can
be fatal if massive (cardiogenic shock)
3. Heart failure
4. Arrhythmia: ventricular fibrillation is responsible
for 90% of mortalities
5. Papillary muscle rupture: results in valve
prolapse
6. Cardiac rupture: results in hemopericardium
7. Mural thrombus
Morphology
The extent of infarction depends on:
1.The size and distribution of the involved vessel
2. The rate of development and the duration of
the occlusion
3. Extent of collateral supply
MI is a white infarction
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Transmural infarctions: Involve > 50% of
the myocardial wall thickness
Subendocardial infarctions : limited to the
inner third of the myocardium
Collateral circulation
• If an atherosclerotic lesion progressively occludes a
coronary artery at slow rate over years, this causes
remodelling of other coronary vessels which may provide a
second compensatory blood flow
• Such collateral perfusion can protect against MI even if the
vessel eventually becomes completely occluded
(alternative way for flow)
• These collaterals normally are closed, gradual narrowing of
one artery allows blood to flow from high to low pressure
areas through the collaterals, therefore; gradual collateral
dilation can provide adequate perfusion to myocardium
• With acute coronary blockage, there is no time for
collateral flow to develop and infarction results
Clinical Symptoms
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Severe crushing retrosternal chest pain that
can radiate to the neck, epigastria, jaw or left
arm
In 10% to 15%, MIs may even be "silent"
infarcts (particularly common in patients with
diabetes mellitus)
Rapid and weak pulse
Nausea and sweating
Dyspnea attributable to resultant acute
pulmonary edema
Diagnosis
• Based on measuring blood levels of macro molecules that leak out of injured myocardial
cells: Cardiac troponins and CK-MB(creatine
kinase) have high specificity and sensitivity for
MI
• Electrocardiogram: specific changes occur in
MI