CH8 - Cardiac Pathology Flashcards
What is ischemic heart disease (IHD)?
Group of syndromes related to myocardial ischemia
What is the leading cause of death in the US?
ischemic heart disease (IHD)
What is ischemic heart disease (IHD) usually due to?
atherosclerosis of coronary arteries, which decreases blood flow to the myocardium
What are the risk factors for IHD?
They are similar to those of atherosclerosis; incidence increases with age.
What is stable angina?
chest pain that arises with exertion or emotional stress.
What is stable angina due to?
atherosclerosis of coronary arteries with > 70% stenosis;
Why does stable angina arise with exertion?
decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion
What does stable angina represent?
reversible injury to myocytes (no necrosis)
How does stable angina present?
As chest pain lasting < 20 minutes that radiates to the left arm or jaw, diaphoresis, and shortness of breath
What does the EKG show in stable angina?
ST-segment depression due to subendocardial ischemia
What is stable angina relieved by?
rest or nitroglycerin
What is unstable angina?
chest pain that occurs at rest.
What is unstable angina usually due to?
rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
What does unstable angina represent?
reversible injury to myocytes (no necrosis)
What does the EKG show in unstable angina?
ST-segment depression due to subendocardial ischemia
What is unstable angina relieved by?
Nitroglycerin
In unstable angina there is a high risk of what?
progression to myocardial infarction
What is prinzmetal angina?
episodic chest pain unrelated to exertion.
What is prinzmetal angina due to?
coronary artery vasospasm
What does prinzmetal angina represent?
reversible injury to myocytes (no necrosis)
What does the EKG for prinzmetal angina show?
ST-segment elevation due to transmural ischemia.
What is prinzmetal angina relieved by?
nitroglycerin or calcium channel blockers
What is myocardial infarction?
Necrosis of cardiac myocytes
What is myocardial infarction usually due to?
rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
In addition to atherosclerotic plaque what are some other causes of myocardial infarction?
coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (e.g., Kawasaki disease).
What are the clinical features for myocardial infarction?
include severe, crushing chest pain (lasting > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea; symptoms are not relieved by nitroglycerin.
In myocardial infarction what does the infarction usually involve?
the left ventricle (LV); right ventricle (RV) and both atria are generally spared.
What artery is most commonly involved artery in MI?
LAD; left anterior descending artery ? 45% of cases
What does occlusion of the left anterior descending artery (LAD) lead to?
infarction of the anterior wall and anterior septum of the LV
What does occlusion of right coronary artery (RCA) lead to?
infarction of the posterior wall, posterior septum, and papillary muscles of the LV;
What is the 2nd most commonly involved artery in MI?
RCA, right coronary artery
What does occlusion of the left circumflex artery lead to?
infarction of lateral wall of the LV.
What does the initial phase of infarction lead to?
subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction);
What does the EKG show for the initial phase of infarction?
(subendothelial infarction) ST-segment depression.
After the initial phase of infarction, what does continued or severe ischemia lead to?
transmural necrosis involving most of the myocardial wall (transmural infarction)
What does the EKG show in transmural infarction?
ST-segment elevation
What do the laboratory tests detect for myocardial infarction?
elevated cardiac enzymes.
What is the most sensitive and specific marker (gold standard) for Ml?
troponin I
What are the troponin I levels after 2-4 hours?
Levels rise 2-4 hours after infarction
When do troponin I levels peak?
at 24 hours
When do troponin I levels return to normal?
By 7-10 days.
What is CK-MB is useful for?
detecting reinfarction that occurs days after an initial MI
When do creatine kinase MB (CK-MB) levels rise?
4 - 6 hours after infarction
When does creatinine kinase MB levels peak?
They peak at 24 hours
When does creatinine kinase MB levels return to normal?
by 72 hours.
What does treatment for myocardial infarction include?
1) Asprin 2) Supplemental O2 3) Nitrates 4) beta-blockers 5) ACE inhibitor 6)Fibrinolysis or angioplasty
How does aspirin and/or heparin help treat MI?
limits thrombosis
How does supplemental 02 help treat MI?
minimizes ischemia
How do nitrates help treat MI?
vasodilate coronary arteries
How does beta-blockers help treat MI?
slows heart rate, decreasing O2 demand and risk tor arrhythmia
How does ACE inhibitors help treat MI?
decreases LV dilation
How does fibrinolysis or angioplasty help treat MI?
opens blocked vessel
What happens in fibrinolysis or angioplasty post-MI?
it opens bloced vessel; 1) contraction band necrosis 2) reperfusion injury
What is contraction band necrosis?
After fibrinolysis or angioplasty post-MI there is reperfusion of irreversibly damaged cells resulting in calcium influx, leading to hypercontraction of myofibrils
What is reperfusion injury?
After fibrinolysis or angioplasty post-MI, the return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes
< 4 hours from time of infarction what are the gross and microscopic changes?
No gross changes, and no microscopic changes
What are the complications < 4 hours from time of infarction?
Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
4-24 hours from time of infarction what are the gross and microscopic changes?
[Gross] Dark discoloration and [microscopic] Coagulative necrosis
What are the complications from 4-34 hours from the time of infarction?
arrhythmia
1-3 days from time of infarction what are the gross and microscopic changes?
[gross] Yellow pallor, [microscopic] Neutrophils
What are the complications for 1-3 days from time of infarction?
Fibrinous pericarditis presents as chest pain with friction rub
What does fibrinous pericarditis present as?
chest pain with friction rub
4-7 days from time of infarction, what are the gross and microscopic changes?
[gross] Yellow pallor, [Microscopic] Macrophages
What are the complications 4-7 days from time of infarction?
Rupture of ventricular free wall, interventricular septum, or papillary muscle
What does rupture of ventricular free wall lead to?
cardiac tamponade
What does rupture of interventricular septum lead to?
shunt,
What does rupture of papillary muscle lead to?
mitral insufficiency
1-3 weeks from time of infarction, what are the gross and microscopic changes?
[gross] Red border emerges as granulation tissue enters from edge of infarct, [microscopic] Granulation tissue with plump fibroblasts, collagen, and blood vessels
Months from time of infarction, what are the gross and microscopic changes?
[gross] White scar, [microscopic] Fibrosis
What are the complications for 1 Month from the time of infarction?
Aneurysm, mural thrombus, or Dressier syndrome
What is sudden cardiac death?
Unexpected death due to cardiac disease, occurs without symptoms or <1 hour after symptoms arise
What is sudden cardiac death usually due to?
fatal ventricular arrhythmia
What is the most common etiology for sudden cardiac death?
acute ischemia; 90% of patients have preexisting severe atherosclerosis.
What are the less common causes for sudden cardiac death?
mitral valve prolapse, cardiomyopathy, and cocaine abuse
What is chronic ischemic heart disease?
Poor myocardial function due to chronic ischemic damage (with or without infarction);
What does chronic ischemic heart disease progress to?
congestive heart failure (CHF)
What is congestive heart failure?
Pump failure; divided into right- and left-sided failure
What are the causes of left-sided heart failure?
ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy
What are the clinical features for left-sided heart failure due to?
decreased forward perfusion and pulmonary congestion.
What are the clinical features for left-sided heart failure?
1) decreased perfusion and pulmonary congestion 2) activation of rennin angiotensin system
In left-sided heart failure what does pulmonary congestion lead to?
pulmonary edema.
In left-sided heart failure why is there paroxysomal nocturnal dyspnea?
Its due to increased venous return when lying flat
In left-sided heart failure, pulmonary edema results in what?
dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles
How can left-sided heart failure lead to intra-alveolar hemorrhage?
Small, congested capillaries may burst, leading to intraalveolar hemorrhage
In left-sided heart failure what is intra-alveolar hemorrhage marked by?
hemosiderin-laden macrophages (heart-failure cells)
In left sided heart failure how are the kidneys involved?
Decreased flow to kidneys leads to activation of renin-angiotensin system
In left sided heart failure does the kidney affect the rennin angiotensin system?
Fluid retention exacerbates CHF
What is the main treatment for left sided heart failure?
treatment is ACE inhibitor.
What is right-sided heart failure most commonly due to?
left-sided heart failure;
Aside from left sided heart failure what are some other important causes for right sided heart failure?
Left to-right shunt and chronic lung disease (cor pulmonale)
What are the clinical features for right sided heart failure due to?
congestion
What are the clinical features for right sided heart failure?
- Jugular venous distension 2. Painful hepatosplenomegaly with characteristic nutmeg liver; may lead to cardiac cirrhosis 3. Dependent pitting edema
In right sided heart failure what is the dependent pitting edema due to?
increased hydrostatic pressure
What are the congenital heart defects?
Arise during embryogenesis
When do congenital heart defects usually arise?
usually weeks 3 through 8
In what percentage of live births do you see congenital heart defects?
seen in 1% of live births
Most congenital heart defects are?
sporadic.
Congenital heart defects often result in?
shunting between left (systemic) and right (pulmonary) circulations.
Defects with left-to-right shunting
may be relatively asymptomatic at birth, but the shunt can eventually reverse
What does increased flow through the pulmonary circulation result in?
hypertrophy of pulmonary vessels and pulmonary hypertension.
What does increased pulmonary resistance eventually result in?
reversal of shunt
What does the reversal of shunt in congenital defects with left to right shunt lead to?
late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing.
What do defects with right-to-left shunting usually present as?
cyanosis shortly after birth.
What is ventricular septal defect (VSD)?
Defect in the septum that divides the right and left ventricles
What is the most common congenital heart defect?
ventricular septal defect (VSD)
What is ventricular septal defect (VSD) associated with?
fetal alcohol syndrome
What does ventricular septal defect (VSD) result in?
left-to-right shunt,
What determines extent of shunting in ventricular septal defect (VSD)?
size of defect and age at presentation
What happens with small defects in ventricular septal defect (VSD)?
they are often asymptomatic
What happens with large defects in ventricular septal defect (VSD)?
can lead to Eisenmenger syndrome
What is the treatment for ventricular septal defect (VSD)?
involves surgical closure; small defects may close spontaneously
What is atrial septal defect?
Defect in the septum that divides right and left atria;
What is the most common type of atrial septal defect?
It is ostium secundum (90% of cases)
What type of atrial septal defect is type is associated with Down syndrome?
Ostium primum
What does atrial septal defect result in?
left-to-right shunt and split S2 on auscultation