Path: diseases of myocardium and pericardium Flashcards
1
Q
Ischemic heart disease (IHD)
A
- Ischemia causes insufficient O2/nutrient delivery and removal of waste
- Usually due to luminal narrowing from atherosclerosis
- Most common in elderly, much more in men than women
- Contributing factors: smoking, dyslipidemia, lack of exercise, obesity, diabetes
- Manifestations: MI, angina, sudden cardiac death (SCD), CHF
2
Q
Pathogenesis of IHD
A
- 75% of vessel narrowing in 1 or more coronary arteries can cause IHD
- Sx depend on the degree of occlusion and any complications of the plaque, including rupture, thrombosis, hemorrhage or enlargement
- Depending on amount of occlusion after thrombosis, there may be unstable angina, MI, or SCD due to arrhythmia
- Coronary artery vasospasms can further reduce coronary blood flow (athersclerotic segments cannot spasm)
- Ischemia exacerbated by: severe hypotension (shock), increased myocardial O2 demand, hemoglobinopathies
3
Q
Acute MI
A
- Major risk factors same as atherosclerosis/IHD
- Manifestation: crushing retrosternal chest pain radiating to neck, jaw, left arm not relieved by rest or nitrates
- Most MIs are preceded by episodes of angina
- Other Sx: diaphoresis, SOB, lightheadedness, nausea
- ECGs: T wave inversions, STE, Q waves
- Dx using Tn test, Hx and ECG
4
Q
Types of MI
A
- Transmural (most common): usually of the LV and IVS, involving full or close to full thickness of the ventricle wall (worse prognosis)
- Spares the subendocardial myocardium b/c it gets nourished from the blood in the ventricle
- Usually due to LAD infarct
- Subendocardial infarct (less common): often multifocal, inner 1/3-1/2 of ventricular wall (better prognosis)
- Coronary arteries often show diffuse narrowing w/o thrombus
5
Q
Pathophysiology of MI 1
A
- Result from sudden near or complete occlusions, necrosis begins 20-30 min after onset of infarction
- Necrosis first of the subendocardial region, the most poorly perfused region
- Then extends to subepicardial region, reaching full size in 3-6 hrs
6
Q
Pathophysiology of MI 2
A
- Reperfusion in 20-30 min and changes may be reversible (reperfusion w/in 24 hrs causes contraction bands due to Ca influx)
- No observable changes in myocardium until after 4-12 hrs (then acute inflammation, loss of striation, followed by chronic after 7-10 days)
- If fibrosis is present, pt has survived an MI for at least 2 wks
7
Q
Complications of MI 1
A
- Cardiogenic shock: severe hypotension usually in very large infarcts, can lead to mitral regurg, ventricular septal rupture or cardiac tamponade
- Left ventricular failure: due to contractile dysfxn or arrhythmia, may occur acutely or progressively and may be accompanied by pulmonary edema
8
Q
Complications of MI 2
A
- Arrhythmias: most common (in first 3 days), includes ectopic beads, sinus brady/tachycardia, atrial or ventricular fibrillation, heart blocks
- Cardiac rupture: mostly in first week before fibrosis, due to weakening of necrotic myocardium
- Includes formation of false aneurysm (btwn epicardium and parietal pericardium), ventricular wall (cardiac tamponase) or IVS rupture (L-R shunt), papillary muscle rupture (acute mitral regurg and subsequent LV failure)
9
Q
Complications of MI 3
A
- Pericarditis: fibrinous or hemorrhage exudate in pericardium (may be weeks post MI, may be immunologically driven)
- Progressive extension of MI
- Mural thrombus: may embolize to lung, brain, kidney depending on which ventricle it originated from
- Ventricular aneurysm: thinning of ventricular wall results from stretching of the scar tissue, but usually do not rupture (can cause CHF, thromboembolism, arrhythmias)
10
Q
Types of angina
A
- Stable angina: associated w/ exertion, relieved by rest or nitrates
- Variant angina: pain occurs at rest due to vasospasm
- Unstable angina: pain characterized by increased frequency or severity
- UA may precede MI, caused by acute plaque change w/ overlying thrombus, distal embolus, or vasospasm
11
Q
Pathological features of angina
A
- Moderate to severe atherosclerosis of coronary arteries
- Dilation of cardiac chambers
- Multiple areas of myocardial fibrosis
- May see hypertrophy of myocardium
- Microscopic: fibrosis, atrophic and hypertrophic myocytes, vacuolation of myocytes
12
Q
Sudden cardiac death
A
- Not only cardiac in origin, can also be from PE, Ao aneurysm, infection, CNS d/o
- Usually due to arrhythmias
- Causes: CAD, myocardial disease (cadiomyopathies, myocarditis), valvular diseases, conduction system abnormalities
13
Q
Cardiomyopathy
A
-A Dx of exclusion, must be made in the absence of systemic or pulmonary HTN, and IHD, congenital or valvular heart disease
14
Q
Dilated cardiomyopathy (DCM) 1
A
- Most common, characterized by a heavy, enlarged, flabby heart w/ dilated chambers
- Ventricular hypertrophy precedes DCM
- Ventricles contract poorly leading to heart failure
- Histologically there is irregular atrophy and compensatory hypertrophy of the myocardium
- L sided HF: pulmonary edema leading to DOE, orthopnea, fatigue, rales
15
Q
Dilated cardiomyopathy (DCM) 2
A
- R sided HF: JVP distension, bilateral leg edema, ascites, hepatomegaly
- Exam: lateral displacement of apical impulse, M and T regurg, S3/4 audible
- Complications: arrhythmias, thromboemboli, M/T regurg
- Etiologies: idiopathic (mutations involve cytoskeletal proteins), metabolic diseases, toxins (EtOH), neuromuscular (muscular dystrophies), infections, and late pregnancy
- Related to systolic HF
