Ischemic heart dz Flashcards
What is ischemic heart dz?
Results from insufficient perfusion to meet the metabolic demands of myocardium
Disruption of what arteries mainly result in ischemic heart disease?
Coronary arteries
Blood to myocardium is supplied by the coronary arteries, so any disruption of coronary flow may result in ischemia
What can ischemia result in?
MI
Angina pectoris
Chronic ischemic heart dz, with heart failure
Sudden cardiac death
What is the leading cause of death in the US? What is it associated with?
Ischemic heart disease
> 90% of cases are secondary to atherosclerosis
- chronic vascular occlusion
- acute plaque change = thrombus
What is angina pectoris?
Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce MI
What are the clinical variants Angina Pectoris?
Stable angina
Prinzmetal variant angina
Unstable (or “crescendo”) angina
Describe stable angina.
Stenotic occlusion of coronary artery
“Squeezing” or burning sensation, relieved by rest or vasodilators
Induced by physical activity, stress
Describe Prinzmetal variant angina.
Episodic coronary artery spasm, relieved with vasodilators
Unrelated to physical activity, HR, or BP
Describe unstable (or “crescendo”) angina.
Frank pain, increasing in frequency, duration, & severity; at progressively lower levels of physical activity, eventually even at rest
Usually rupture of atherosclerotic plaque, with partial thrombus
~50% may have evidence of myocardial necrosis, acute MI may be imminent
90% of all MIs are caused by ____. What are some other causes?
Atheromatous plaque
Embolus
vasospasm
ischemia secondary to vasculitis, shock, hematologic abnormalities
What is a classic presentation of MI?
Prolonged CP (>30 min)
- crushing, stabbing, squeezing, tightness
- radiating down left arm, or left jaw
Diaphoresis
Dyspnea
Nausea-vomiting
Up to 25% asymptomatic
*side note: info based on studies primarily w/ men
The location, size, & features of an acute MI depend on what?
Site, degree, & rate of occlusion of the artery
Size of area perfused
Duration of occlusion
Metabolic & oxygen needs of the area at risk
Extent of collateral blood flow
Presence of arterial spasm
Describe ATP and lactate levels in relation to ischemia.
ATP levels decline as Lactate levels increase
- ATP levels to 50% = 10 min
- ATP levels to 10% = 40 min
As lactate levels rise you see the onset of irreversible injury (20-40 min)
Describe the frequency at which the coronary vessels are affected and which region of the heart do the affect.
LAD (40-50%)
-Apex, LV anterior wall, anterior 2/3 of septum
RCA (30-40%)
-RV free wall, LV posterior wall, posterior 1/3 of septum
LCX (15-20%)
-LV lateral wall
Describe how irreversible injury to the heart progresses overtime.
Within the first 24 hrs:
- dark mottling
- waviness of fibers –> edema, hemorrhage –> pyknosis, hypereosinophilia, neutrophilic infiltrate
Within 7 days:
- Yellow-tan infarct
- coagulation necrosis –> disintegration of dead myocytes by macrophages; dying neutrophils
Within 14 days:
- Red-gray infarct
- well-developed phagocytosis, granulation tissue at margin –> well-established gt with new blood vessels & collagen
Within 2 mo:
-increased collagen w/ decreased cellularity –> dense collagenous scar
What changes to the heart are seen within the first 24 hours of an acute MI?
Coagulative necrosis
Pyknotic nuclei
Loss of cross striations
What changes to the heart are seen within 1-3 days of an acute MI?
Loss of striations
Neutrophilic infiltration
What is reperfusion?
Restoring blood flow to an area of ischemia and impending infarction
Attempt to limit infarct size by rescuing at risk myocardium
How can you undergo reperfusion?
Thrombolysis
Angioplasty
Stent placement
CABG (coronary artery bypass graft)
Why would you order labs to diagnose an MI?
Measure blood levels of proteins that leak out of irreversibly damaged myocytes
What are the most useful proteins to test for MI? Which is the most sensitive and specific? What does it do?
Cardiac specific Troponins T and I (cTnT and cTnI)
MB fraction of creatinine kinase (CK-MB)
Most sensitive and specific = troponins
-proteins that regulate ca-mediated contraction of cardiac and skeletal muscle
Describe the changes in troponin levels during an MI.
Troponins I and T are NOT normally detectable in circulation
Following MI, levels being to rise at 3-12 hours
- cTnT peak at 12-48 hrs
- cTnI peak at 24 hrs
What is CK? Elaborate on the MB designation.
Creatine Kinase - enzyme expressed in brain, myocardium, and skeletal muscle; dimer composed of 2 isoforms = M and B
MM = predominantly in cardiac and skeletal muscle BB = brain, lung, and other tissue
MB = localized to cardiac muscle (considerable lesser amounts in skeletal)
CK-MB = sensitive by NOT specific (can rise in skeletal m injury)
How do CK-MB levels change during MI?
Begins to rise within 3-12 hours of onset of MI
Peaks at 24 hrs, returns to normal within 48-72 hrs
Briefly describe cardiac enzyme level changes over time.
Elevation of CKMB, cTnI & T = 3-12 hrs
Both peak at 24 hrs
CK-MB normal within 3 days
cTnI = 5-10 days
cTnT = 5-14 days
What are some complications of an MI?
Arrhythmia Contractile dysfunction Fibrinous pericarditis Myocardial rupture Infarct expansion Ventricular aneurysm
Describe how arrhythmia is a complication of an MI.
Half of all MI death occur within 1 hour of onset, and are usually secondary to an arrhythmia
Can be long-term complication of MI, depending on site and extent of lesion
Can result form permanent damage to conducting system or from myocardial irritability following infarct
Describe how contractile dysfunction is a complication of an MI.
Dependent on size of infarct and associated loss of function
Describe how myocardial rupture is a complication of an MI. What are the risk factors?
Typically requires transmural infarct
2-4 days post MI, when inflammation and necrosis have weakened the wall
Risk factors = older, large transmural anterior MI, first MI, absence of LV hypertrophy
Describe how infarct expansion is a complication of an MI.
Muscle necrosis –> weakening, stretching, and thinning of wall
Mural thrombus often seen
Describe how ventricular aneurysm is a complication of an MI
Late complication of large transmural infarcts with early expansion
Composed of thinned wall of scarred myocardium
Also associated with mural thrombus
Rupture does not usually occur
