patho quiz 4 heart disease.txt

inability of the heart to eject the blood delivered to it by the venous system. Congestive heart failure may involve any of the four chambers.

:results from increased congestion of venous circulation

results from inadequate cardiac output

• Left side failure is characterized by the inability to pump oxygenated blood to the systemic circulation. Common causes include:
• o Systemic hypertension
• o Mitral or aortic valve disease
• o Ischemic heart disease
• o Primary disease of the myocardium

• Right side failure is characterized by the inability to effectively accept blood from the venous circulation or to deliver blood to the pulmonary circulation. Common causes include:
• o Left ventricle failure  results in failure of heart to accept blood from pulmonary circulation
• o Pulmonary thromboembolism  blockage of the pulmonary artery or its branches

muscle wall increases in thickness without increase in chamber size  adaptation to increase in pressure load (hypertension, valvular stenosis [stuck valves])

muscle wall increases in thickness and chamber size- adaptation to increase in volume load (valvular regurgitation [leaky valve] or abnormal shunts)

• Dyspnea (breathlessness)  left side pulmonary edema and congestion
• Soft tissue edema  right side
• Muscle fatigue (not enough oxygen)
• Enlarged heart (hypertrophy from trying to pump too much)
• Irregular heart beat and rhythm (arrythmia)
• Lung rales (characteristic sounds from lung edema)

Ischemic heart disease refers to a group of related syndromes resulting from myocardial ischemia- an imbalance between cardiac blood supply (perfusion) and myocardial oxygen demand. In most cases, IHD is caused by a narrowing of the coronary arteries by atherosclerosis. This disease is also commonly termed coronary heart disease or coronary artery disease.

• Angina pectoris (chest pain)
• Acute myocardial infarction
• Chronic IHD with congestive heart failure
• Sudden cardiac death

• Acute plaque changes can result in IHD
• Coronary artery vasoplasm/vasoconstriction can result in IHD

blood flow to cardiac muscle cannot keep pace with increased demand for cardiac function

increased exertion and sress

coronary artery spasm

occurs at rest

progressive narrowing of coronary arteries that may precede MI

Increased frequency of chest pain and more intense attacks

development of an area of myocardial necrosis caused by local ischemia

• Most common cause is coronary artery thrombosis
• Necrosis begins within 20-30 minutes of occlusion
• Area of necrosis (infarction) reaches full size within 3-6 hours
• Location and size of infarct is dependent on the site of the occlusion (chich coronary artery and how distal)

• First 30 minutes: no gross and microscopic change, reversible
• 30 min-4 hour: no gross and microscopic change, irreversible process begins
• 4hr: a sequential process of cell death, hemorrhage, edema, coagulation, fibrosis
• It takes > 2 months to complete the scarring

• Severe crushing substernal chest pain. In 10-15% of patients the MI is preceded by unstable angina not relieved by nitroglycerin
• Rapid, weak pulse and shortness of breath. This is associated with decreased blood pumping capacity

elevated within 2-4 hrs after an MI and peak at 24-48 hours after. It returns to normal 72 hrs after

elevated within 2-4 hrs after an MI and peak at 48 hours. They remain elevated for 4-7 days after.

• Cardiogenic shock and pulmonary congestion and edema due to impaired left ventricle function
• Arrythmias
• Myocardial rupture can occur 3-7 days after infarction due to heart wall weakening
• Progression to chronic ischemic heart disease associated with congestive heart failure

Hypertensive heart disease is characterized by left ventricular hypertrophy (thickening of the muscle wall with no increase in chamber volume. It is an adaptive change to permit the increased pumping pressure the heart is required to generate in response to systemic vascular hypertension

• Hypertrophoc myocardium is poorly perfused by capillaries and is in a state of chronic ischemia. This stimulated mild inflammation and deposition of fibrous material that impairs contraction and relaxation and can ultimately lead to heart failure.
• Chronic ischemic state also sensitizes tissue to ischemic damage by cardiac infarction
• Hypertension increases the risk of atherosclerosis
• Combination leads to increased incidence of MI and increased severeity of ischemic damage by MI

• the failure of a valve to open completely, thereby obstructing forward flow
• It is typically the consequence of valve calcification or scarring
• It demands additional pumping pressure by the heart. This leads to concentric hypertrophy of the heart

• the failure of a valve to close completely, thereby permitting reverse blood flow
• It is typically the consequence of valve destruction or distortion of the supporting structures
• It demands additional pumping volume by the heart. This leads to eccentric hypertrophy of the heart

(a type of valvular heart disease)

• Hypersensitive immune reaction to group A strep
• Antibodies against group A strep cross-react with normal cellular proteins causing ADCC and inflammatory damage

• irreversibly deformity of one or more cardiac valves
• Leads to stenosis (more common) or incompetence
• Pulmonary congestion
• Hypertrophy of right ventricle and atrium
• Concentric hypertrophy of left atrium
• Chronic aortic valve stenosis
• Increased pressure load on left ventricle
• Concentric hypertrophy
• Left ventricle failure

• Acute rheumatic carditis  inflammatory changes in all 3 layers of the heart
• " Aschoff bodies (heart muscle)
• " Fribrinous pericarditis (pericardium)
• " Endocardium inflammation
• " Mitral and aortic valves
• " Minor; does not contribute to valvular dysfunction

Valve is characteriscally Floppy, Incompetent

progressive hypertrophy, dilation, contractile dysfunction

myocardial hypertrophy, abnormal diastolic filling, powerful contractions

decrease in ventricular compliance--> impaired ventricular filling

viral infection, alcohol abuse, toxic insult, inheretid mutations

genetic mutations

heart is enlarged and flabby, thrombi and emboli develop, ineffective contraction, leads to CHF, need transplant

Increased pulmonary venous pressure, exertional dyspnea, ventricular arrythmia

CHF, pulmonary congestion, right side failure