Ischemic Heart Disease Flashcards
ischemia
refers to a lack of oxygen due to inadequate perfusion, which results from an imbalance between oxygen supply and demand
Narrowing of the coronary artery lumen can cause
- hypertension -> hypertrophy
- increased work load -> heart failure
- formation of a thrombus -> MI
risk factors for ischemic heart disease
smoking, hypertension, obesity, diabetes, hypercholesterolemia; some reversal of disease process with elimination of risk factors
Other associated problems with ischemic heart disease
thromboemboli, particularly from valvular vegetations; coronary artery spasm (cocaine); coronary arteritis; increased work load or decreased oxygen delivery of any cause; anomalous origin of the left coronary artery; chest trauma
Ischemia results from
oxygen supply/oxygen demand mis-match
Mechanism of ischemic injury
inadequate 02 delivery; occlusive disease; myocardial injury
most common cause of decreased perfusion
progressive stenosis with or without associated formation of thrombus
Other causes of decreased perfusion
thromboembolus, vasospasm, vasculitis, hyperperfusion secondary to hypovolemia
Causes of decreased oxygenation
anemia, carbon monoxide, congenital heart disease, asphyxia, lung disease
Important underlying principles of atherosclerosis
no specific correlation between the extent of stenosis and type or severity of ischemic heart disease; rapidity of decreased perfusion, tendency of thrombus formation
Critical event in atherosclerosis
abrupt mismatch of perfusion to demand
Decreased ability to meet an increase in demand once stenosis reaches
75%
coronary artery thrombus usually occurs
in the first 2 cm of the coronary vessel of LAD or left circumflex; occurs in the proximal and distal 1/3 of the right coronary artery
coronary artery thrombus formation usually results from
rupture of fissure of plaque with platelet aggregation, release of TXA2
Vasospasms are associated with
adrenergic stimulation, local factors (NO, endothelin, platelet factors including thromboxane)
Vasospasms have a clear association with
stress, excitement; more MI’s occur between 6AM and noon
Vasospasms may be mediated by
hypertension, increased platelet activity
conductance vessels and major sites of atherosclerosis
epicardial coronary vessels
Intramyocardial coronary vessels
resistance vessels (major determinant of autoregulation and flow)
Area at greatest risk for ischemia
subendocardium
What happens to myocytes with a decrease in O2
cells switch to anaerobic glycolysis within minutes; glucose is broken down into lactate; pH is reduced; impaired cell membrane function results in leakage of potassium and uptake of sodium
When does reversible injury become irreversible injury in the heart?
after 40 minutes of hypoxia
Irreversible injury results in
necrosis and permanent loss of functional myocardium; may be diffuse as in acute MI or may involve slow loss of cells or groups of cells over time
Morphological characteristics of reversible injury
“stunned myocytes”; mitochondrial swelling, relaxation of myofibrils, distortion of cristae
Morphological characteristics of irreversible injury
chronic loss of individual myocytes, particularly in the subendocardial region; coagulative necrosis; apoptosis; area eventually becomes fibrotic
Gross appearance of an MI
early: pallor +/- hyperemic border
3 to 7 days: hyperemic border with central, yellow-brown softening; possible hemorrhage
after 1 week: replacement with red-brown, depressed, scarred areas; scar appears grey and fiber-like
Microscopic appearance of an MI
evolution of many stages beginning with necrosis of myocytes, inflammation, infiltration with inflammatory cells, clean up of necrotic debris, replacement of myocardium with scar tissue
Reperfusion injury
additional myocyte injury with free radical formation, influx of Ca2+, hemorrhage; characterized by the presence of contraction bands in damaged myocytes
Critical mismatch in an MI
when intramyocardial vessels are maximally dilated, coronary flow becomes the main determinant of the flow of oxygen; an increase in demand or temporary decrease in flow results in symptomatic ischemia
chest pain in an MI
crushing pain over sternum radiating to left arm or back; usually not sharp of fluctuating; severe pain is accompanied by sweating, nausea, and vomiting
diaphoresis
shortness of breath, sweating, nausea - usually signs of severe cardiac pain or insufficiency
Troponin I and Troponin T
cardio specific and sensitive; increase along with CMB and stay elevated up to 7 days
Creatinine kinase (MB isozyme)
MB isoenzyme is highly specific and sensitive marker; peaks at 12-24 hours; number of hours needed to peak correlates with infarct size
Lactic dehydrogenase
peaks later and remains elevated (rises after 24 hours; peaks in 3-6 days, may not return to normal for 2 weeks)
Causes of an MI
- pre-existing coronary disease + thrombus formation
- coronary spasm
- sudden loss of vascular volume
- hemopericardium/cardiac tamponade
Most MIs are precipitated by what?
by a ruptured atherosclerotic plaque and subsequent thrombus formation
where do thrombi usually form
within first few cm of vessel distribution (near ostia for right and left main coronaries, just distal to bifurcation for LAD, RC, and circumflex)
Why are the characteristic features of inflammation in an MI delayed by 24-48 horus?
inflammation is initiated at borders and the process must migrate into the (usually large) necrotic area
First visual signs of inflammation with an MI (within first 24 hours)
edema and separation of fibers at the margins
hallmarks of coagulative necrosis
loss of nuclei and hypereosinophilic fibers
describe the progression of the histopathologic features in an MI
coagulative necrosis (loss of nuclei and hypereosinophilic fibers) -> neutrofils migrate -> 2-4 days until cellular infiltrate become prominent -> subacute phase with macrophages and lymphocytes -> fibrosis occurs over next several weeks -> replacement of myocardium with fibrous scar
Tissue weakest and most vulnerable to rupture after
4-5 days
Early complications of an MI
dysfunctional heart muscle; arrhythmias; extensions of the infarct
Late complications of an MI
aneurysm/dilatation; ventricular rupture (septal or free wall); mural thrombus; pericardial effusion/pericarditis; papillary muscle infarction with mitral insufficiency
EKG changes with ischemia
inversion of the T wave; more severe, displacement of the ST segment; transient ST-segment depression reflexts subendocardial ischemia; transient ST-segment elevation suggests transmural ischemia; ischemia may induce ventricular arrhythmias
What might a stress test elicit on an EKG
may elicit ST segment changes even in the absence of symptomatic angina; a positive result indicates CAD in 98%
EKG changes in Prinzmetal’s angina
ST segment may be strikingly elevated
EKG changes with an MI
Q waves or loss of R waves; subendocardial may only show ST segment changes; total occlusion results in ST-segment elevation and most individuals develop Q-waves; a minority that present without ST-segment elevation may develop Q-waves
perfusion studies are indicated in
- patients with chronic stable or unstable angina who are severely symptomatic despite medical therapy
- patients with troublesome symptoms that present diagnostic difficulties
- patients with signs of severe ischemia regardless or presence of symptoms
Treatment for angina
lifestyle changes; treat risk factors; treatment of underlying conditions; nitrates; beta blockers; calcium channel blockers; aspirin; platelet adhesion blockers
Goal of myocardial infarction treatment
prevent fatal arrhythmias and re-establish blood flow to myocardium
diagnose infarction with
12-lead EKG
Management/Treatment of an MI
increase oxygenation; establish airway and IV access; aspirin; anti-arrhythmics; re-establish blood flow
Ways to re-establish blood flow in an MI
angiography; PCI; fibrinolysis (most effective within 30 min)
