Chest Pain Flashcards
Define Ischemia
-Absence of adequate oxygenated blood to meet metabolic demands of tissue
Define Angina pectoris
-chest pain induced by myocardial ischemia
Define Typical Angina Pectoris
- Chest pain increases w/ exercise
- Deceases w/ rest
- Retrosternal dull pain
- Radiation to arm, neck and jaw
Define Atypical Angina Pectoris
- Some qualities consistent w/ angina
- Some qualities not consistent: location, quality, duration
Define non-anginal chest pain
- No features of myocardial ischemia
- Sharp focal pain
- Pleuritic: increases w/ inspiration or coughing
- Lasts hours
- Unaffected by exertion
Define stable angina
- Not new chest pain
- Reliable occurs w/ only a certain level of exercise
- Relieved by rest
Define Unstable angina
- New chest pain
- Occurs at lower work loads
- Occurs at rest
- Acute coronary syndrome
Define Acute Coronary Syndrome
- Unstable angina
- Or acute myocardial infarction
Define Myocardial Infarction
- Death of myocardial tissue
- Due to prolonged ischemia
- Severe ischemia >20m
- Loss of contractile function permanent in necrotic zone
- Pain less than 1-2h b/c damage to sensory nerves
Pathophysiology of angina pectoris and myocardial ischemia
- Chest pain signals ischemia
- Myocardium recieveing too little blood flow from coronaries
- Decreased phosphates from oxidative metabolism -> decreased contraction and leakage of negative ions
- Loss of contractility causes SOB, fatigue, and decreased BP
- Ion leakage causes increase/decrease ST segment
- Release of metabolites such as adenosine stimulate local sensory nerves causing pain
Role of myocardial O2 consumption in chest pain
- Increases ventricular systole wall stress, contractility and HR all lead to increased O2 Consumption
- Exercise causes increased HR, systolic LV pressure, and contractility
- Vasodilators released and increase coronary flow 4x
- In stable angina coronary arteries are narrowed and decrease max coronary flow
- Eventually flow cannot increase enough to keep up with demand and causes ischemia
- Exercise after a meal hastens increase HR, BP, and O2 use
- Post-prandial angina
Role of Fixed Coronary obstructions in chest pain
-Fixed obstructions caused by athromatous build up
<50% obstruction has no effect
50%-70%: max flow decreased and ischemia w/ exercise
90% obstruction causes angina at rest (Angina decubitus)
-occlusions can be mitigated by collateral channels
Effects of Variable Coronary Obstructions
- Coronary artery spasms
- Worsen fixed obstructions
- Cause fluctuations in level of exercise needed to induce angina
- Vasospastic angina develops unpredictably
- Treat w/ vasodilators such as nitroglycerine
Conditions that decrease O2 supply to myocardium
- Anemia and hypoxemia: O2 poor blood worsens angina
- Tachycardia shortens diastole, therefore shortens time for coronary filling
- CHF causes increased ventricular pressure that compresses the coronary arteries
- Myocardial hypertrophy causes increased ischemia b/c coronary flow no longer matches the size of the muscle
- Aortic stenosis causes hypertrophy
Timeline for morphological changes in MI
- If immediate death then no changes
- 12h: dark mottling on myocardium
- 1-3d: infarcted area is yellow/tan; Neutrophils most prominent
- 3-7d: soft central area w/ hyperemic border; macrophages most prominent
- 10-14d: granulation tissue replaces phagocytosis
- weeks-months: progressive collagen deposition and scar
