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
16
Q
Hypertrophic caridomyopathy (HCM) 1
A
- Heavy heart w/ very thick ventricular walls and septum (usually septum thicker than walls), may be causing obstruction of outflow tract
- Myocardium is hyper contractile but poorly compliant
- Diastolic filling decreased, diminished chamber size
- Histologically: myocytes are large and hypertrophied, bundles are arranged haphazardly w/ interstitial fibrosis and thickening of vessel walls
17
Q
Hypertrophic caridomyopathy (HCM) 2
A
- Sx include DOE due to pulmonary congestion (secondary to HF), edema/hepatomegaly/ascites, anginal pain (hypertrophied muscle prone to focal ischemia), syncope (fainting) due to decreased CO
- Exam: accentuated apical impulse, mid-systolic murmur due to LV outflow obstruction, holosystolic murmur due to mitral regurg, S4
- Complications: arrhythmias, thromboemboli, endocarditis
- Etiology: many cases familial, w/ mutations involving sarcomeric contractile elements (beta-myosin heavy chain)
- Related to diastolic HF
18
Q
Restrictive cardiomyopathy (RCM) 1
A
- Ventricular stiffness due to fibrosis or infiltration, poorly compliant ventricles impairs filling w/ elevation of venous and pulmonary pressures
- Myocardium is dense, but walls are close to normal size
- Histologically there is patchy or diffuse interstitial fibrosis, often amyloid deposition (apple-green bifringience)
19
Q
Restrictive cardiomyopathy (RCM) 2
A
- Sx: DOE from HF, edema/hepatomegaly/ascites
- Exam: reduced heart sounds, S3/4 most common, mitral regurg present
- Complications: arrhythmias, thromboemboli
- Etiology: amyloidosis most common identifiable cause, idiopathic, familial storage diseases, autoimmune (sarcoidosis)
- Related to diastolic HF
20
Q
Myocarditis 1
A
- Diffuse inflammatory infiltrate in the myocardium in the absence of IHD, HTN, congenital or valvular heart disease
- Viral etiology is suspected, but my accompany any infectious/inflammatory process
- Clinical presentation: acute onset of chest pain, palpitations, fever, dyspnea
- Cardiac findings: LV failure, arrhythmias, systolic murmur (mitral regurg), complete heart block
- Tests: can see leukocytosis, elevated ESR, Tn positive
21
Q
Myocarditis 2
A
- Pathology, gross: heart is dilated, flabby and pale, scattered petechial hemorrhages
- Path, micro: myocardium is infiltrated w/ lymphocytes, plasma cells, and eosinophils, w/ interstitial edema and myocyte necrosis
- Etiology: viral, bacterial, parasites, autoimmune (RA, SLE, Tx rejection, rheumatic fever), toxins (adriamycin, penicillin rxn), sarcoidosis, idiopathic (giant cell)
22
Q
Pericarditis 1
A
- Inflammation of the pericardial surfaces and spaces
- Inflammatory exudate varies w/ cause, can be serous, fibrinous, purulent and hemorrhagic
- Pericardium is infiltrated w/ PMNs and fibrin deposition
- Gross: pericardium is reddened and rough from fibrin, parietal and visceral pericardium lays loosely adherent (bread and butter appearance)
23
Q
Pericarditis 2
A
- Hemorrhagic pericarditis due to TB, uremia (!), or metastatic tumor
- Clinical presentation: chest pain (may be pleuritic), pericardial rub
- Lab: Tn elevated, increase in CRP and ESR
- Etiologies: viral (most common- serous), pyogenic bacterial, TB, CT disease (RA, SLE), chronic renal failure (uremia !)
24
Q
Chronic constructive pericarditis
A
- Occurs when healing of acute pericarditis or a chronic effusion results in obliteration of the pericardial cavity
- Heart encased in thickened fibrotic pericardium
- Follows a slow, indolent course
- Pericardium constricts the chambers, causing impaired filling, leading to ankle edema, ascites, hepatomegaly, pulm edema
- Mostly caused by irradiation, trauma, chronic inflammatory diseases, CA
25
Q
Pericardial effusions
A
- Accumulation of fluid in pericardial space, may be due to inflammation (pericarditis) or non-inflammatory causes (increased hydrostatic pressure)
- Serous: CHF, low albumin, MI
- Serosanguinous: trauma, CA
- Chylous: lymphatic obstruction
- Hemopericardium (may lead to cardiac tamponade): pure blood in pericardial space, due to ruptured Ao aneurysm, rupture of ventricle following MI, trauma
- Cardiac tamponade: blood and other stuff (puss, fluid, gas) in pericardial space
