STEPUP Cardiovascular System: Ischemic Heart Disease - Myocardial Infarction Flashcards
What is MI? What is it most commonly due to? What is the mortality rate and when do deaths occur in relation to hospitalization? What is associated with MI?
1) Necrosis of myocardium as a result of interruption of blood supply (after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis)
2) Most cases are due to acute coronary thrombosis: Atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel
3) MI is associated with a 30% mortality rate; half of the deaths are prehospital
4) Most patients with MI have a history of angina, risk factors for CAD, or history of arrhythmias
Describe the chest pain associated with MI. Where does it radiate? How does it differ from angina pectoris? What other type of discomfort can patients with MI have?
1) Intense substernal pressure sensation; often described as “crushing” and “an elephant standing on my chest”
2) Radiation to neck, jaw, arms, or back, commonly to the left side
3) Similar to angina pectoris in character and distribution but much more severe and lasts longer. Unlike in angina, pain typically does not respond to nitroglycerin
4) Some patients may have epigastric discomfort
What fraction of patients may have asymptomatic MI? What type of patients does asymptomatic MI usually present in?
1) Can be asymptomatic in up to one-third of patients
2) Painless infarcts or atypical presentations more likely in postoperative patients, the elderly, diabetic patients, and women
What are some symptoms other than chest pain or epigastric discomfort in MI patients?
1) Dyspnea
2) Diaphoresis
3) Weakness, fatigue
4) Nausea and vomiting
5) Sense of impending doom
6) Syncope
What is a complication of MI?
Sudden cardiac death - usually due to ventricular fibrillation (Vfib)
How do you diagnose MI using ECG?
Markers for ischemia/infarction include:
1) Peaked T waves - occur very early and may be missed
2) ST segment elevation - indicates transmural injury and can be diagnostic of an acute infarct
3) Q waves - evidence for necrosis (specific) - q waves are usually seen late; typically not seen acutely
4) T-wave inversion is sensitive but not specific
5) ST segment depression: Subendocardial injury
What two parts of a presentation strongly suggest acute MI?
1) The combination of substernal chest pain persisting for longer than 30 minutes
2) Diaphoresis
How does right ventricular infarct present? What is it dependent on?
1) Inferior ECG changes
2) Hypotension
3) Elevated jugular venous pressure
4) Hepatomegaly
5) Clear lungs
6) Preload dependent - do NOT administer nitrates or diuretics as will cause cardiovascular collapse
What percentage of the time does ST segment elevation indicate an infarction? What percentage of the time does ST segment depression indicate infarction?
1) 75% of the time
2) 25% of the time
What ECG changes are expected in an anterior myocardial infarct and in what leads?
1) ST segment elevation in V1-V4 (acute/active)
2) Q waves in leads V1-V4 (late change)
What ECG changes are expected in a posterior myocardial infarct and in what leads?
1) Large R wave in V1 and V2
2) ST segment depression in V1 and V2
3) Upright and prominent T waves in V1 and V2
What ECG changes are expected in a lateral myocardial infarct and in what leads?
Q waves in leads I and aVL (late change)
What ECG changes are expected in an inferior myocardial infarct and in what leads?
Q waves in leads II, III, aVF (late change)
What are the two categories on infarcts?
1) ST segment elevation infarct: Transmural (involves entire thickness of wall); tends to be larger
2) Non-ST segment elevation infarct: Subendocardial (involves inner one-third to one-half of the wall); tends to be smaller, and presentation is similar to USA - cardiac enzymes differentiate the two
What is the current diagnostic gold standard for myocardial injury?
Cardiac enzymes
What is the most important enzyme test to order? When does it increase, peak, and return to normal?
1) Troponins (Troponin I and T)
2) Increases within 3 to 5 hours and returns to normal in 5 to 14 days; reaches a peak in 24 to 48 hours
How does sensitivity and specificity for troponins differ from CK-MB? When should serum level of troponins be obtained? When can troponin I be falsely elevated?
1) Greater sensitivity and specificity than CK-MB for myocardial injury
2) Obtain serum levels of either troponin T or I on admission, and again every 8 hours for 24 hours
3) Troponin I can be falsely elevated in patients with renal failure; thus following trend of levels is important
When does CK-MB increase, peak, and return to normal? When does it have the highest sensitivity and specificity? When should total levels be measured? When is it most helpful to measure?
CK-MB is less commonly used
1) Increases within 4 to 8 hours and return to normal in 48 to 72 hours; reaches a peak in 24 hours
2) When measured within 24 to 36 hours of onset of chest pain, has greater than 95% sensitivity and specificity
3) Levels of total CK and CK-MB should be measured on admission and every 8 hours thereafter for 24 hours
4) Most helpful in detecting recurrent infarction given quicker return to baseline than troponin
When are cardiac enzymes drawn? What does a higher peak and longer enzyme level elevation indicate?
1) Cardiac enzymes are drawn serially - once on admission and every 8 hours until three samples are obtained
2) The higher the peak and the longer enzyme levels remain elevated, the more severe the myocardial injury and the worse the prognosis
In MI, what agents are the only ones shown to reduce mortality?
1) Aspirin
2) Beta blockers
3) ACE inhibitors
What forms of cardiac monitoring should be done for a patient with acute MI?
1) BP and HR: HTN increases afterload and thus oxygen demand, whereas hypotension reduces coronary and tissue perfusion. Both nitrates and morphine can cause hypotension
2) Rhythm strip with continuous cardiac monitor: Watch for dysrhythmias. Note that PVCs can lower stroke volume and coronary artery filling time. A high frequency of PVCs may predict VFib or VT
3) Auscultate the heart (third and fourth heart sounds, friction rub, and so on) and lungs (crackles may indicate LV failure, pulmonary edema)
4) Hemodynamic monitoring (CVP, PCWP, SVR, cardiac index [CI]) with a pulmonary artery catheter is indicated if the patient is hemodynamically unstable. Monitoring is helpful in assessing the need for IV fluids and/or vasopressors
What are the three forms of treatment for acute MI?
1) Admit patient to a cardiac monitored floor (CCU) and establish IV access. Give supplemental oxygen and analgesics (nitrates, morphine)
2) Medical therapy
3) Revascularization
4) Rehabilitation
What are forms of medical therapy for acute MI?
1) Aspirin
2) Beta blockers
3) ACE inhibitors
4) Statins
5) Oxygen
6) Nitrates
7) Morphine sulfate
8) Heparin
How does aspirin help in MI treatment?
1) Antiplatelet agent reduces coronary reocclusion by inhibiting platelet aggregation on top of the thrombus
2) Has been shown to reduce mortality and should be part of long-term maintenance therapy
How do beta blockers help in MI treatment?
1) Block stimulation of HR and contractility to reduce oxygen demand and decrease the incidence of arrhythmias
2) Reduce remodeling of the myocardium post-MI
3) Have been shown to reduce mortality and should be part of long-term maintenance therapy
How do ACE inhibitors help in MI treatment?
1) Initiate within hours of hospitalization if there are no contraindications
2) Have been shown to reduce mortality and should be part of long-term maintenance therapy
How do statins help in MI treatment? What did the PROVE IT-TIMI 22 trial show?
1) Reduce risk of further coronary events
2) Stabilize plaques and lower cholesterol
3) The PROVE IT-TIMI 22 trial showed the superiority of starting atorvastatin 80 mg over other statins before discharging a STEMI patient
4) Should be part of maintenance therapy
How does oxygen help in MI treatment?
May limit ischemic myocardial injury
How do nitrates help in MI treatment?
1) Dilate coronary arteries (increase supply)
2) Venodilation (decrease preload and thus demand)
3) Reduce chest pain, although not as effective as narcotics
How does morphine sulfate help in MI treatment?
1) Analgesia
2) Causes venodilation, which decreases preload and thus oxygen requirements
How does heparin help in MI treatment? What form of heparin is perferred and why?
1) Initiate in all patients with MI; prevents progression of thrombus; however, has not been shown to decrease mortality
2) LMWH, specifically enoxaparin, is preferred over unfractionated heparin, as shown in the ExTRACT TIMI 25 trial as well as a recent meta-analysis. Enoxaparin was shown to decrease the risk of another MI versus unfractionated heparin