CVS 1 Flashcards
Cardiac hypertrophy: the compensatory response due to pressure overload?
Concentric. Increased wall thickness; reduced cavity diameter.
The heart has to pump harder to overcome the systemic pressure.
Cardiac hypertrophy: compensatory response due to volume overload?
Hypertrophy with dilation; increased ventricular diameter.
Too much blood in the heart would mean the heart harder to eject blood from the chamber.
Some causes of pressure overload in the heart?
systemic hypertension –> LV hypertrophy
pulmonary hypertension –> RV failure
Characterized by Diminished CO and/or damming back of blood in the venous system.
Heart failure, congestive heart failure
Most common cause of CHF
systolic dysfunction
Major s/sx of systolic dysfunction:
pulmonary congestion
Causes of diastolic dysfunction:
LV hypertrophy, amyloid deposition, contrictive pericardits
restrictive conditions –> reduced compliance
Left-sided HF in lungs presents with:
acute: congestion and edema
chronic: with heart failure cells
Left-sided HF in kidneys:
decreased renal blood flow –> activation of RAAS –> hydrostatic pressure increases –> peripheral and pulmonary edema
Left-sided HF in brain:
hypoxic encephalitis
Right-sided HF in liver:
nutmeg liver, chronic passive congestion
centrilobular necrosis, sclerosis
Right-sided HF in spleen:
congestive splenomegaly
Right-sided HF in heart:
RV hypertrophy/dilatation
Right-sided HF in kidneys:
congestion
Right-sided HF in brain:
hypoxic encephalopathy
Patient presents with pulmonary edema, dyspnea, and orthopnea?
Describe the heart failure
Left-sided
Heart failure results in nutmeg liver, hepatojugular reflex, edema
right-sided
Manifestations/syndromes of ischemic heart disease:
- Acute MI
- Angina
- Chronic IHD
- Sudden cardiac death
70% of a coronary artery lumen occluded with atherosclerotic plaque:
critical stenosis
Causes of non-atheromatous coronary arterial occlusion
embolism dissecting aneurysm vasospasm congenital anomaly trauma
Most common form of angina pectoris
Stable AP
Chest pain with progressive, recurrent pain at rest
Unstable AP
Chest pain secondary to vasospasm at rest
Prinzmetal AP
Chest pain secondary to atherosclerosis
Stable
Chest pain with ST depression
Stable AP
Unstable AP
Chest pain associated with acute plaque change with superimposed partial thrombosis or vasospasm
Unstable AP
Chest pain with thrombosis but no necrosis
Unstable AP
Chest pain with exertion
Stable AP
Chest pain with ST elevation
Prinzmetal’s AP
Sequence of coronary artery thrombosis
Tear/fissure collagen exposed extrinsic pathway (coagulation) activated platelets release factors causing vasospasm occlusive thrombosis
Indicator of irreversible damage in MI
sarcolemmal membrane damage
Time it takes for irreversible damage in MI
20-40 minutes
Gross changes 0-18 hours after MI
None
Yellow pallor in heart is seen how long after MI?
1-7 days
Vague pallor in heart is seen how long after MI?
18-24 hours
White scar is seen in heart how long after MI?
months
Central pallor with hyperemic border seen how long after MI?
7-28 days
Dark mottling or tigering effect is seen how long after MI?
12-24 hours
How long post-infarct is this microscopic change seen: wavy myocyte fiber
1-4 hours
How long post-infarct is this microscopic change seen: neutrophilic infiltrate
1-4 days (within 1 week macrophages and neutrophils)
How long post-infarct is this microscopic change seen: granulation tissue
7-28 days
How long post-infarct is this microscopic change seen: macrophages
4-7 days (within 1 week macrophages and neutrophils)
How long post-infarct is this microscopic change seen: coagulative necrosis
4-24 hours
What pathologic form of MI is associated with diffuse stenosing coronary artery atherosclerosis without thrombosis and acute plaque change?
subendocardial
What pathologic form of MI is associated with chronic atherosclerotic obstruction, acute plaque change, and superimposed complete thrombosis?
transmural
Type of infarct with greater necrosis
transmural
Type of infarct with ST depression?
subendocardial
Type of infarct with ST elevation and pathologic Q waves?
transmural
Characteristic MI microscopic change seen 12 hours post-infarct:
hyper-eosinophilia with surrounding congestion
First change seen (electron microscope):
myofibril relaxation
glycogen loss
mitochondrial swelling
ECG feature in MI
new Q waves
Cardiac proteins seen an hour after MI, peaking at 16 hours
troponin I
troponin T
Most specific protein marker in MI?
Troponin I
CK-MB is also found in
skeletal muscle
