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Session 2 CMCardio4
CM- Cardio -4- ACS myocardial infarction
| Question | Answer |
|---|---|
| what are the primary determinants of myocardial oxygen demand | heart rate, contractility and ventricular wall tension. Increase one of these and increase oxygen demand |
| What is myocardial ischemia | when myocardial oxygen demand exceeds myocardial oxygen supply |
| What governs myocardial oxygen supply | coronary blood flow and ability of myocardium to extract oxygen from the blood delivered to it |
| Would increasing hearts ability to extract oxygen be a good treatment for ischemia | theoretically yes but hearts efficiency in extracting oxygen is near maximal efficiency so not much potential to increase oxygen extraction to counter increased oxygen demand |
| how much of an increase in coronary blood flow can you see in coronary vasodilation | increases several fold in normal subjects most do to arteriolar level dilation |
| what are causes of myocardial ischemia that prevent normal vasodilation | coronary arterial stenosis, and endothelial dysfunction. Coronary blood flow can no longer increase proportional to rising oxygen demand=ischemia |
| what are likely causes of ischemia that occur when oxygen demand hasn't risen but coronary blood flow drops | -coronary artery spasm -rapid evolution of underlying atherosclerotic plaque -intermittent microvascular plugging by platelet aggregates |
| if the ischemic episode is symptomatic what is it called | angina pectoris- many episodes are silent though |
| do silent ischemic attacks or symptomatic angina pectoris indicate a worse prognosis for patients with prior MI or Angina | they both have same importance in patients with diagnosed coronary disease |
| what does acute coronary syndrome describe | spontaneous presentation of acute ischemic heart disease |
| What types of coronary ischemia fall under acute coronary syndrome | Unstable angina Non-ST-segment elevation M.I. (non-Q-wave M.I.) ST segment elevation M.I. (Q-wave M.I.) |
| what does the extent and location of the infarct depend on | anatomic distribution of occluded vessel, presence of additional stenotic lesions, adequacy of collateral circulation |
| occlusion of what coronary vessel will lead to infarction of anterior left ventricle and interventricular septum | anterior descending branch of Left Coronary artery |
| occlusion of what coronary vessel will lead to infarction of anterolateral or posterolateral infarction | Left Circumflex artery |
| occlusion of what coronary vessel will lead to infarction of postero-inferior portion of left ventricle and generally invovles right ventricular myocardium if obstruction is proximal | Right Coronary Artery |
| on the ECG what part of the heart do leads II, III and AVF refelect | inferior |
| on the ECG what part of the heart do lead I, AVL and V4 through V6 reflect | lateral |
| on the ECG what part of the heart do leads V1 through V6 reflect | anterolateral. |
| What do tall R waves in v1-3, st depression in V1-3 and st elevation in II and III relate to in the heart | posterior wall MI |
| What percent of MI's are silent | 50% |
| what are the essentials of dx of acute MI | sudden development of prolonged >30min anterior chest discomfort w/ possible arrythmias hypotension shock or cardiac failure can be painless though and masquerade as acute congestive heart failure syncope stroke shock |
| If your patient has chest pain what 4 steps are you going to take | get a hx do a PE get and EKG Run labs |
| what is one of the classical s/s of heart attack | sweating, anxiety and chest pains |
| If some one is having an Acute MI what are you likely going to see on the EKG | st elevation or depression evolving Q wave symmetric T wave inversion |
| what labs are you going to look at | creatine kinase-MB Troponin T Topnonin I Imaging showing segmental wall motion abnormalities |
| what do MI's develop from | result from prolonged ischemia generally from a coronary thrombus at a preexisting atherosclerotic plaque site |
| What are very rare causes of MI's | prolonged vasospasm inadequate myocardial blood flow from hypotension excessive metabolic demand |
| What are rare causes of MI's | embolic occlusion w/o plaque vasculitis aortic root or coronary artery dissection aortitis |
| What illicit drug can cause infarction | cocaine |
| how does the tissue necrosis start in MI | begins with hypoxia and then results from accumulation of deleterious metabolites |
| What are the many ways an MI can present | M I can be typical, sudden, silent, subtle, new onset, or accelerated, atypical, or mimicking. |
| Apart from just the tissue necrosis what else does MI infarction mean for the heart possibly | it can mean VF-ventricular fibrillation rupture of the ventricular free wall ventricular septal rupture papillary muscle rupture ventricular muscle rupture ventricular mural thrombus peripheral embolism CVA HF pseudoaneurysm Ventricular dilati |
| If you have a right coronar artery occlusion what can result in the conduction system | The RCA often supplies arteries to the AV node and SA node so occlusion in RCA can lead to AV blocks and SA node dysfunction. frequent in inferior or right sided infarction |
| how are infarctions commonly classified | Q wave and non Q-wave |
| what is a Q wave infarction vs a Non Q wave infarction | a non Q wave infarction is one that still has time to have revascularization techniques done to prevent it from developing into a Q Wave Q wave= infarcted dead tissue |
| what do the size and anatomic location of an infarction influence | acute course early complications long-term prognosis |
| What is premonitory pain | patient give a hx of change in their angina preceding onset of symptoms of MI. IE angina at rest |
| What are some prodromal s/s of MI | fatigue chest discomfort malaise may occure days or hours preceding event |
| When do patients typically feel the pain of MI | mostly at rest. most common in the A.M. Pain is generally more severe than angina builds up rapidly in waves Nitro has little effect and opioids may not relieve the pain |
| Why do you often get hyperglycemia post MI | pancreas doesn't get enough blood flow so it releases less insulin add in catecholamine release that drops insulin secretion and you get hyperglycemia |
| what patients have subtle presentations of MI that may be harder to detect | Elderly and diabetics often only complain of fatigue or weakness may have syncope or near syncope often have altered mental status |
| How are painless infarctions detected | often detected on ECG afterwards and patient doesn't recall ever having an MI |
| What percent of deaths from MI happen before patient gets to the hospital and what is the leading cause | 50% die before they get to the hospital and most die from ventricular fibrillation |
| If MI patient has respiratory distress what might this indicate | heart failure |
| what can appear after the MI and last for several days | a low grade fever |
| why do you get dyspnea pulmonary vascular redistribution interstitial and alveolar pulmonary edema respiratory decompensation hypoxemia after an MI | you get an augmentation of pulmonary pressure that can cause these symptoms |
| What effects can an MI have on the brain | decreases perfusion to brain leading to restlessness psychosis confusion combativeness |
| What are the killip classifications | class I-IV I= absence of rales and S3 II= rales do not clear on coughing over 1/3 or less of lung fields or presence of S3 III= rales do not clear w/ coughing over more than 1/3 of lung fields IV= cardiogenic shock (rales, hypotension and hypoperfusio |
| Why do you listen to the lungs in patient w/ suspected MI | listening for pulmonary edema evidenced by crackles, rales, wheezing or pleural effusions |
| if you hear soft heart sound during PE of suspected MI patient what might that indicate | may indicate left ventricular dysfunction |
| what hard sound is the rule and which one is less common and indicate significant left ventricular dysfunction | S4 atrial gallops are the rule S3 are less common |
| What does a mitral regurgitation murmur heard on PE of suspected MI patient probably indicate | papillary muscle dysfunction or rupture |
| When do pericardial friction rubs typically appear | after the first 24 hours but are uncommon |
| which is more common in MI patient bradycardia or tachycardia | tachycardia |
| What do you see in B/P breathing rate and temperature of MI patient | B/P is elevated unless pulmonary embolism is present then you get Hypotension breathing is tachypenic temp is usually elevated |
| What might you see on fundoscopic exam of MI patient | copper wiring A/V nicking Microaneurysms hemorrhage |
| what might you see in the pulses of an MI patient | pulsus alternans decreased carotid pulse JVD rapid and weak pulses |
| if you hear paradoxical splitting of S2 what might that indicate | LBBB |
| if you hear systolic murmur or thrill what might that indicate | points to ventricular septal rupture |
| how does papillary muscle rupture occur | generally chordiae tendinae or papillary muscle is damage in MI then days later weakens and rupture resulting in new murmur |
| What effect may a papillary muscle rupture have on hemodynamics | you get decreased blood flow to organs and back up in lungs leading to fluid in lungs(CHF) |
| why do you want to note peripheral pulses in MI patient | they may be altered later by shock or emboli |
| if you have hypotension in MI patient apart from pulmonary embolism what might it indicate | may indicate ventricular dysfunction due to ischemia in MI may indicate large infarct often involving right ventricular infarct |
| What marker is more sensitive and specific but not as useful for early reinfarction | troponin I and Troponin T |
| What might an echocardiogram let you know | help see if normal wall motion which makes infarction unlikely. Also can show mitral regurgitation or ventricular septal defects |
| when would you order technetium 99m pyrophosphate scintigraphy | order in patients that present several days after MI. It can complesx with calcium in necrotic myocardium and provide hotspot image of infarction |
| how does scintigraphy with thallium-201 show MI damaged tissue | shows regions of diminished perfusion dead myocardium will show as cold spots but doesn't distiguish recent from old damage |
| name at least 5 differential dx that MI could present as | Aortic dissection Esophageal spasm GERD Pericarditis Gastritis P.E. Hiatal hernia Pneumothorax PSYCH Pneumonitis Bursitis Herpes zoster Myalgias Cholecystitis Costochondritis Pancreatitis Cholelithiasis Hepatitis Duodenal/gastric ulcer |
| What drug should be given to patients with definite or suspected MI unless they have an allergy and then what would you give them | Give all patients 325mg of aspirin give clopidogrel if allergic |
| What does MONA stand for | Morphine Oxygen Nitro Aspirin |
| Why do you give anticoagulants in MI patient | help prevent ruccerence of a clot avoid ischemia or future MI's |
| Why give BB to MI patient | lopressor- slows heart rate |
| What drug is glycoprotein IIB and IIIA inhibitor | ReoPro inhibits clotting factors antithrombotic |
| What drug is a direct thrombin inhibitors | Hirudin trying to increase PTT 1.5-2.5 |
| Which drug is a adeosine diphosphate receptor antagonist | plavix can be used as alternative to ASA |
| What is PCTA | precutaneous transluminal coronary angioplasty |
| What is CABG | coronary artery bypass graft |
| why give MI patient thrombolytic therapy | reduces mortalitity limits infarct size in patients with acute MI. Best if initiated within first 3 hours. 50% reduction in mortality rate can be achieved. |
| What type of infarct patient benefits the most from thrombolytic therapy | patient with large anterior infarcation |
| IF you patient does not have ST segment elevation do you want to administer thrombolysis | NO patients DO NOT benefit from thrombolysis and may derive harm if they don't have ST segment elevation |
| what is a major s/e of thrombolytic therapy | small percent of patients have major bleeding complications most seroius is intracranial hemorrhage |
| what are the two therapies recommended for early MI | PCI and thrombolytic therapy |
| what are the absolute contra indications for thrombolytic therapy | previous hemorrhagic stroke strokes or CVA events within 1 year known intracranial neoplasm recent head trauma active internal bleeding suspected aortic dissection major surgery or trauma within last 2 weeks |
| What are the relative contraindications for thrombolytic therapy | blood pressure > 180/110 known bleeding diathesis proliferative diabetic retinopathy prolonged CPR Pregnancy |
| If patient is contra-indicated for thrombolysis what tx would you recommend | PCI- has been shown to be superior to thrombolysis when done by experienced operators. |
| what should be given to relieve pain in MI | nitroglycerine then morphine if nitro doesn't work |
| Studies have shown that giving what IV has improved short term outcome in MI but shouldn't be given to patients in decompensated heart failure | Beta Blockers |
| If patient has low ejection fractions and large infarction or clinical evidence of heart failure what can you give them to improve short and long term survival | ACE inhibitor |
| What can you give prophylatically to patients with sustained ventricular tachycardia to prevent fibrillation | lidocaine |
| what do MI patients have an increased risk of after their infarction | 1.Postinfarction angina 2.Non-Q-wave infarction 3.Heart failure 4.Left ventricular ejection fraction (EF) < 40% 5.Stress-induced ischemia, diagnosed by electrocardiography, scintigraphy, or echo 6.Ventricular ectopy |
Created by:
smaxsmith
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