Ischemic heart disease Flashcards Preview

Cardio II Midterm > Ischemic heart disease > Flashcards

Flashcards in Ischemic heart disease Deck (10)
Loading flashcards...
1

Clinical presentation of angina pectoris

-Paroxysmal and recurrent attacks of substernal or precordial chest discomfort
-Silent ischemia is common in geriatrics or diabetics
-Stable: deep, poorly localized pressure, squeezing or burning sensation that is relieved by rest or vasodilators
-Prinzmetal: unrelated to physical activity, heart rate or BP. Responds to vasodilators

2

Pathogenesis of angina pectoris

-Caused by transient myocardial ischemia that is insufficient to induce myocyte necrosis

-Pain is a consequence of ischemia induced release of adenosine, bradykinin and other molecules
-Caused by decreased perfusion, increased demand, and coronary arterial pathology

-Stable: imbalance of coronary perfusion relative to myocardial demand. Triggers are physical activity, emotional excitement or psychological stress.

-Prinzmetal: uncommon. From coronary artery spasm

-Unstable: increasingly frequent, prolonged or severe angina precipitated by lower levels of physical activity or at rest. Caused by the disruption of an atherosclerotic plaque. Half have myocardial necrosis

3

Clinical course of MI

-Reversible injury within 20-30 minutes of onset
Contractile dysfunction: some type of left ventricular failure
-Arrhythmias: myocardial irritability that cause sinus brady, a fib, heart block, tachy, ventricular premature contractions, ventricular tachy, v fib
-Myocardial rupture: transmural necrosis weakens the wall and happens within 2 to 4 days
-Risk factors for rupture: over 60, first MI, transmural and anterior MI, absence of LVH, preexisting HTN
-Ventricular aneurysm: late complication of transmural infarcts when the myocardium has become scarred
-pericarditis: 2 to 3 days after: Dressler syndrome
-Infarct expansion
-Mural thrombosis
-Papillary muscle dysfunction
-Progressive late heart failure
-Postinfarct complications depend on size, location and fraction of wall
-Non-infarcted segments undergo ventricular remodeling of hypertrophy and dilation

4

Diagnosis of MI

-Diagnosed by clinical symptoms, lab tests, and EKG changes
-Chest pain, sweating, nausea and vomiting, dyspnea from pulmonary congestion
-Blood levels of cTnT and cTnI and CK-MB are diagnostic markers
-Troponins I and T are not normally found in circulation but begin to rise at 3-12 hours. Troponin T peaks at 12-48. Troponin I max at 24 hours.
-Creatine kinase: brain, myocardium and skeletal muscle. MB is specific for the heart
-CK-MB rises within 3-12 hours and peaks at 24. Returns to normal at 48 to 72

5

Treatment of MI

Therapy: morphine, reperfusion, aspirin, heparin, nitrates, beta blockeers, antiarrhythmics, ACE inhibitors, oxygen

6

Pathogenesis of MI

-Coronary arterial occlusion: plaque undergoes hemorrhage or rupture, platelets adhere and form a microthrombi, vasospasm, tissue factor starts coagulation cascade, thrombus expands to occlude the vessel
-This sequence is why coronary revascularization and clot busting works

-Other mechanisms: vasospasm due to drugs, emboli from left atrium, ischemia without detectable or significant coronary atherosclerosis and thrombosis

-With prolonged vascular compromise, there is myocardial death

-Area at risk: the region of the heart supplied by occluded artery
-Severity and duration
-Myocardial contractility ceases within a minute
-Reversible ultrastructural changes: myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling
-Earliest detectable feature is disruption of the sarcolemmal membrane (what allows the blood testing for injury)
-Transmural: occlusion of an epicardial vessel. Chronic atherosclerosis, acute plaque change, superimposed thrombis
-Subendocardial: most vulnerable area. Inner third of the ventricular wall. If the clot is lysed before full thickness. From global hypotension, this is circumferential
-Multifocal microinfarction: involves small intramural vessels. Microemboli, vasculitis, or vascular spasm. Epi or drugs. Can cause sudden cardiac death
-Transmural=STEMI
-subendocardial=NSTEMI

7

Morphology of MI

-Ischemia is the worst in the subendocardium
-“wavefront” of cell death that progressively goes more towards transmural
-Morphology depends on: location severity and rate of obstruction, size of the vascular bed, duration of occlusion, metabolic needs, collateral circulation, vasospasm, HR, rhythm, O2 sat
-Half thickness in 2 to 3 hours. Full thickness in 6 hours
-Patterns: transmural, subendocardial (most vulnerable), Multifocal (microthrombi)
-Nearly all contain a portion of the left ventricle
-Entire zone of the occluded coronary artery
-Left anterior descending: anterior wall of the left ventricle near septum
-Right coronary: inferior/posterior wall of left ventricle
-Left circumflex: lateral wall of left ventricle
-Irreversibly injured cells have contraction bands
-Early: Usually are not apparent grossly. Stained w/ triphenyltetrazolium chloride
-12 to 24 hrs: reddish-blue area of discoloration
-10 dayrs to 2 weeks: Vascularized granulation tissue
-Weeks: covered by a fibrous scar
-Wavy fibers develop at the edge of the infarct
-Myocytolysis occurs at the edge of the infarcts
-Macrophages remove the necrotic myocytes in 3 to 7 days
-Highly vascularized granulation tissue is there from 1 to 2 weeks and then is replaced by fibrous tissue after
-Scarring is advanced by week 6
-Heal from the margins towards the center

8

Reperfusion after MI

restoration of blood flow. Salvages cardiac muscle and limits infarct size. Preeminent objective. Thrombolysis, angioplasty, stent, CABG.
-Reperfusion benefits depend on: rapidity of resolution, extent of restoration
-Reperfused infarcts are usually hemorrhagic
-Reperfusion can trigger arrhythmias and damage on the original ischemia
-Oxidative stress, calcium overload and inflammatory cells
-Reperfusion causes hemorrhage, endothelial swelling, and damage to cells. Up to 50% of infarct size can be due to reperfusion
-Stunned myocardium: prolonged cardiac failure from short-term ischemia that lasts days
-Hibernation: decreased metabolism and function following ischemia

9

Pathogenesis of chronic ischemic heart disease

-Progressive congestive heart failure due to accumulated ischemic myocardial damage
-Usually from prior MI
-Due to functional decompensation of hypertrophied non-infarcted myocardium
-Severe obstructive coronary artery disease may cause this as well

10

Morphology of chronic ischemic heart disease

Cardiomegaly w/ LVH and dilation
-stenotic coronary atherosclerosis is usually present
-Healed infarcts generally seen
-patchy fibrous thickening and mural thrombi present
-Myocardial hypertrophy, diffuse subendocaridal vacuolization and fibrosis