Lecture 4 Flashcards
(38 cards)
Unstable Angina Pectoris
- unexpected chest pain due to ischemia
- transientive secclusion (<10 min)
- followed by spontaneous thrombolysis
Myocardial Infarction
- persisting vessel occlusion ( >60 min)
- resulting in death of myocardial muscle cells
Difference between Unstable Angina Pectoris and Myocardial Infarction
disruption of myocyte membrane
Types of Angina
Stable and Unstable
Stable Angina
- more common form
- occurs at given activity level or level of mental stress
- fibrous cap not ruptured
Unstable Angina
- new onset
- unpredictable
- fibrous cap ruptures
- may lead to heart attack
History of Myocardial Infarction affected:
16 million Americans
History of Angina affected
~9 million Americans
New acute coronary syndrome affects
785,000/year
Recurrent incidents affect
470,000/year
Silent Myocardial Infarction affects:
195,000/year
Total costs for heart diseases in 2007
177.5 billion
Coronary Circulation supplies
myocardium with Oxygen
Coronary Circulation in Coronary Arteries
-off the root of aorta RIGHT CORONARY ARTERY ---RCA ---right atrium and ventricle LEFT CORONARY ARTERY ---splits ------anterior descending -----------LAD ------circumflex artery -----------LCx ---left atrium and ventricle
Coronary Blood Flow (Blood Flow and Metabolism)
- rest
- —60-90ml/min/100 g
- exercise
- —-5-6 times higher
ATP Generation
- mostly aerobic
- myocardial oxygen uptake
- –rest: 8 - 10 ml/min/100 g
- –exercise: 2 - 3 times higher
- –indirect indicator: RPP
Ischemia
-O2 supply < O2 demand
ISCHEMIC CASCADE
- stiffness of left ventricle
- systolic dysfunction
- localized hypokinesis
- left ventricle ejection fraction decreases
- arrhythmia
- angina pectoris
SILENT ISCHEMIA
risk factors of atherosclerosis
- age
- male sex
- family history and genetics
- smoking
- pre-diabetes and diabetes
- obesity
- metabolic syndrome
- hypertension
- dyslipidemia
- physical inactivity
- psycho-social factors
- homocysteine
- c-reactive protein
- inflammatory protein
- fibrinogen
Pathophysiology of Atherosclerosis [PROGRESSIVE]
- Endothelial dysfunction
- LDL-C accumulation and oxidation in arterial wall
- Injury and inflammation
- Monocyte binding and entry into cell
- Monocyte differentiation into macrophage
- Macrophage engulfs oxidized LDL and creates foam cell
- plaque maturation and calcification
Trigger for Myocardial Infarction
- exertion
- emotional stress
- sympathetic activation [heart rate variability and prognosis]
- surgery causing blood loss
Pathophysiology of Myocardial Infarction
- plaque rupture rulceration in coronary artery
- –bifurcations
- thrombosis (blood clotting)
- blood flow acculsion
- necrosis of downstream myocardium
- –protein synthesis
- —-cardiac tropinin
- dysrhythmia
- –ventricular fibrillation
- –ventricular tachycardia
- potentially death
Complications of Acute Myocardial Infarction
- arrythmias
- conduction abnormalities
- cardiogenic shock
- infarct extension or expansion
- myocardial rupture
- new mitral valve regurgitation
- pericardial effusion and pericarditis
- post-infarction syndrome
- left ventricular mural thrombus
Prognosis of Acute Myocardial Infarction
Factors associated with poor prognosis
- LIVEF < 5 METs
- evidence of extensive myocardial ischemia during exercise or pharmacologic stress testing
- having survived sudden cardiac death
- servere non-revascularized CAD
Protocols from Prognostic GXT-Predischarge
- <7 days post myocardial infarction
- sub maximal before discharge
- termination
- —HRpeak: 120-130
- —70% age-predicted HRmax
- —achieving 5 METs