Cardio Mod 5 Flashcards
myocardial infarction
-myocardial cells become ischemic within how many seconds of blood flow occlusion
10 seconds
myocardial infarction-
what is the backup when blood flow initially becomes occluded?
attempt to rely on myoglobin O2 stores for first 6-10seconds
myocardial infarction -
what are the cellular changes as myocardial cells become oxygen deprived
- loss of contractility followed by drop in cardiac output
- conduction abnormalities (EKG changes) leading to dysrhythmias
- anaerobic metabolism is only mechanism to provide energy with lactic acid accumulation
two options after blood flow obstruction
- blood flow restored - return to aerobic metabolism, contractility returns followed by cellular repair
- flow is not restored - then myocardial infarction occurs (damage and potential tissue necrosis)
what is the main cause of myocardial ischemia
atherosclerosis in the form of CAD
initially impairment from MI be only be evident when?
but as time progresses impairment happens when?
- initially under increased demand
2. as pathology impairment becomes evident at low levels of demand (at rest)
other causes of myocardial ischemia - decreased delivery of blood to myocardium
- coronary spasm (prinzmetal angina)
- hypotension
- arrhythmias
- decreased O2 capacity of blood (anemia, hypoxemia, altitude)
other causes of myocardial ischemia - increased demand for O2 by mycardium
- tachycardia and exercise - both more work for the heart
- HTN ( more work to overcome increased afterload)
- cardiac hypertrophy (bigger muscle demands more O2)
- valve dysfunction/disease
- what is stable angina?
- what is happening?
- how long does it last?
- when is the onset? what relieves it?
- transient episode of blood flow impairment in relation to O2 demand of the cardiac muscle
- usually happens with gradual narrowing of the lumen and stable plaque development
- lasts 3-5 min
- onset usually some form of exercise/exertion or stress, relieved with rest
myocardial ischemia
-narrowing of what artery by what percentage will result in impairment of cellular metabolism
coronary artery by >50%
s/s of stable angina
angina pectoris - substernal chest discomfort (heaviness - pressure -pain: all three)
what is silent angina?
-when does it usually happen?
myocardial ischemia that dose not cause obvious s/s
common following conditions/surgical procedures that may impair innervation - ex. heart transplant, CABG, emotional stress, diabetes
acute coronary syndromes - unstable angina
thrombus breaks up before cell death - allows return of blood flow
“reversible MI with no cell damage
**increases likelihood of MI within relative near future (20% of patients with unstable angina will ahve MI or death from MI within 20 days)
what is an MI
thrombus occludes blood flow for prolonged period and causes irreversible cardiac nercrosis
initial pathophys of MI from immediate to 10-20 minutes
- immediate effects?
- accumulation of what due to anaerobic metabolism
- EKG effects
- sympathetic response?
- angiotensin 2 effect?
- metabolic response?
- immediate loss of contractility and dysrhythmia
- lactic acid accumulation - after 6-10 seconds of anaerobic metabolism (mechanism for survival)
- EKG changes within 30-60 seconds (electrolyte changes and lactic acid accumulation alter conduction - dysrhythmia)
- sympathetic - increased catecholamine release (clinical beta blockers)
- angiotensin 2 release - increases BP/cardio exertion,sympathetic response - also increases collagen/scar formation (clinical - ACE inhibitors or angiotensin receptor antagonists
- above processes lead to increase metabolic response = increases glucose & FFA into circulation - 72hr post hyperglycemia