STEPUP Cardiovascular System: Ischemic Heart Disease - Myocardial Infarction Flashcards

1
Q

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?

A

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

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2
Q

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?

A

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

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3
Q

What fraction of patients may have asymptomatic MI? What type of patients does asymptomatic MI usually present in?

A

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

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4
Q

What are some symptoms other than chest pain or epigastric discomfort in MI patients?

A

1) Dyspnea
2) Diaphoresis
3) Weakness, fatigue
4) Nausea and vomiting
5) Sense of impending doom
6) Syncope

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5
Q

What is a complication of MI?

A

Sudden cardiac death - usually due to ventricular fibrillation (Vfib)

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6
Q

How do you diagnose MI using ECG?

A

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

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7
Q

What two parts of a presentation strongly suggest acute MI?

A

1) The combination of substernal chest pain persisting for longer than 30 minutes
2) Diaphoresis

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8
Q

How does right ventricular infarct present? What is it dependent on?

A

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

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9
Q

What percentage of the time does ST segment elevation indicate an infarction? What percentage of the time does ST segment depression indicate infarction?

A

1) 75% of the time

2) 25% of the time

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10
Q

What ECG changes are expected in an anterior myocardial infarct and in what leads?

A

1) ST segment elevation in V1-V4 (acute/active)

2) Q waves in leads V1-V4 (late change)

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11
Q

What ECG changes are expected in a posterior myocardial infarct and in what leads?

A

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

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12
Q

What ECG changes are expected in a lateral myocardial infarct and in what leads?

A

Q waves in leads I and aVL (late change)

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13
Q

What ECG changes are expected in an inferior myocardial infarct and in what leads?

A

Q waves in leads II, III, aVF (late change)

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14
Q

What are the two categories on infarcts?

A

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

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15
Q

What is the current diagnostic gold standard for myocardial injury?

A

Cardiac enzymes

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16
Q

What is the most important enzyme test to order? When does it increase, peak, and return to normal?

A

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

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17
Q

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?

A

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

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18
Q

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?

A

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

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19
Q

When are cardiac enzymes drawn? What does a higher peak and longer enzyme level elevation indicate?

A

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

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20
Q

In MI, what agents are the only ones shown to reduce mortality?

A

1) Aspirin
2) Beta blockers
3) ACE inhibitors

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21
Q

What forms of cardiac monitoring should be done for a patient with acute MI?

A

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

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22
Q

What are the three forms of treatment for acute MI?

A

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

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23
Q

What are forms of medical therapy for acute MI?

A

1) Aspirin
2) Beta blockers
3) ACE inhibitors
4) Statins
5) Oxygen
6) Nitrates
7) Morphine sulfate
8) Heparin

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24
Q

How does aspirin help in MI treatment?

A

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

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25
Q

How do beta blockers help in MI treatment?

A

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

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26
Q

How do ACE inhibitors help in MI treatment?

A

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

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27
Q

How do statins help in MI treatment? What did the PROVE IT-TIMI 22 trial show?

A

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

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28
Q

How does oxygen help in MI treatment?

A

May limit ischemic myocardial injury

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29
Q

How do nitrates help in MI treatment?

A

1) Dilate coronary arteries (increase supply)
2) Venodilation (decrease preload and thus demand)
3) Reduce chest pain, although not as effective as narcotics

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30
Q

How does morphine sulfate help in MI treatment?

A

1) Analgesia

2) Causes venodilation, which decreases preload and thus oxygen requirements

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31
Q

How does heparin help in MI treatment? What form of heparin is perferred and why?

A

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

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32
Q

When is revascularization for MI most benefitial? When should it be considered?

A

1) Benefit highest when performed early (within 90 minutes of hospital arrival)
2) In all patients with MI

33
Q

What are options for revascularization?

A

1) Thrombolysis
2) PCI
3) CABG

34
Q

What are benefits of PCI over thrombolysis for MI? What should be chosen in patients with a delayed presentation?

A

1) Several studies have shown enhanced survival and lower rates of recurrent MI and intracranial bleeding when PCI performed by skilled personnel is chosen over thrombolysis
2) For patients with a delayed presentation, fibrinolysis alone may be a better option

35
Q

When is urgent/emergent CABG typically performed? When is it almost never performed?

A

1) Only in the setting of mechanical complications of an acute MI, cardiogenic shock, life-threatening ventricular arrhythmias, or after failure of PCI
2) It is almost never performed in the acute setting on a stable patient

36
Q

What word can be used to describe the effects of clopidogrel in the setting of aspirin? When should clopidogrel be used in the setting of revascularization? How long should dual antiplatelet therapy with aspirin and clopidogrel be continued for after a bare metal stent placement and after a drug-eluting stent?

A

1) Evidence suggests that benefits of clopidogrel is additive to the effects of aspirin
2) Clopidogrel therapy should be initiated in all patients who undergo PCI and receive a stent
3) Dual antiplatelet treatment with aspirin and clopidogrel should continue for at least 30 days in patients who receive a bare metal stent, and at least 12 months in patients who receive a drug-eluting stent

37
Q

What is cardiac rehabilitation? How does cardiac rehabilitation affect symptoms and survival?

A

1) Cardiac rehabilitation is a physician-supervised regimen of exercise and risk factor reduction after MI
2) Shown to reduce symptoms and prolong survival

38
Q

What did the CAPRICORN trial show?

A

It showed that the beta blocker carvedilol reduces risk of death in patients with post-MI LV dysfunction

39
Q

What medical treatments are indicated in patients with MI?

A

1) Oxygen
2) Nitroglycerin
3) Beta-blockers
4) Aspirin
5) Morphine
6) ACE inhibitor
7) IV Heparin

40
Q

What is the most helpful laboratory test to measure if patients have a recurrent infarction on the same hospital admission?

A

CK-MB is most helpful laboratory test to detect this if patient develops recurrent chest pain

41
Q

What is the preferred treatment for STEMI if it can be performed expeditiously and by skilled personnel? In what patients is it also preferred in?

A

1) Percutaneous Coronary Intervention, so long as it can be performed within 90 minutes (door to balloon time)
2) Also preferred in patients with contraindications for thrombolytic therapy; no risk of intracranial hemorrhage

42
Q

What did the PAMI trial show?

A

PAMI trial showed that PTCA reduces mortality more than t-PA

43
Q

When is thrombolytic therapy useful to use?

A

For patients who present later and for those in whom PCI is contraindicated

44
Q

When should thrombolytic therapy ideally be given?

A

Early treatment is crucial to salvage as much of the myocardium as possible

1) Administer as soon as possible up to 24 hours after the onset of chest pain
2) Outcome is best if given within the first 6 hours

45
Q

What is an indication for thrombolytic therapy?

A

ST segment elevation in two contiguous ECG leads in patients with pain onset within 6 hours who have been refractory to nitroglycerin

46
Q

What thrombolytic is the first choice? What are alternatives?

A

1) Alteplase has been shown to have the best outcomes amongst thrombolytic medications, and is the first choice in many centers, despite its high costs
2) Alternatives include streptokinase, tenecteplase, reteplase, lanoteplase, and urokinase

47
Q

What is the main reason to initiate therapy with thrombolytics/angioplasty in the ED setting?

A

Whether there is ST segment elevation on ECG

48
Q

What are absolute contraindications to thrombolytic therapy?

A

1) Trauma: Recent head trauma or traumatic CPR
2) Previous stroke
3) Recent invasive procedure or surgery
4) Dissecting aortic aneurysm
5) Active bleeding or bleeding diathesis

49
Q

How frequently is coronary artery bypass grafting (CABG) in comparison to PCI or thrombolytic therapy? What are benefits of CABG? When is it the procedure of choice?

A

1) Less often used than the other two in the acute setting
2) Benefits of CABG include low rates of event-free survival and reintervention-free survival
3) It remains the procedure of choice in patients with severe multivessel disease and complex coronary anatomy

50
Q

What are complication categories for acute MI?

A

1) Pump failure (CHF)
2) Arrhythmias
3) Recurrent infarction (extension of existing infarction or reinfarction of a new area)
4) Mechanical complications
5) Acute pericarditis
6) Dressler syndrome (“postmyocardial infarction syndrome”)

51
Q

What is the most common cause of in-hospital mortality?

A

Pump failure (CHF)

52
Q

If CHF is mild as a complication of acute MI, how is it treated? What may severe CHF as a complication of acute MI lead to? What may be indicated to do at this point?

A

1) Treat medically with ACE inhibitor and diuretic
2) May lead to cardiogenic shock
3) Invasive hemodynamic monitoring may be indicated

53
Q

What are the different types of arrhythmias that can develop post-MI?

A

1) Premature ventricular contractions (PVCs)
2) Atrial fibrillation (AFib)
3) Ventricular tachycardia (VT)
4) VFib
5) Accelerated idioventricular rhythm
6) Paroxysmal supraventricular tachycardia (PSVT)
7) Sinus tachycardia
8) Sinus bradycardia
9) Asystole
10) AV block

54
Q

How do you treat premature ventricular contractions (PVCs) post-MI?

A

Conservative treatment (observation) indicated; no need for antiarrhythmic agents

55
Q

How do you treat sustained ventricular tachycardia (VT)?

A

Sustained VT requires treatment: If patient is hemodynamically unstable, electrical cardioversion is indicated. If patient is hemodynamically stable, start antiarrhythmic therapy (IV amiodarone)

56
Q

How do you treat VFib?

A

Immediate unsynchronized defibrillation and CPR are indicated

57
Q

How do you treat accelerated idioventricular rhythm?

A

Does not affect prognosis; no treatment needed in most cases

58
Q

What may sinus tachycardia post-MI be caused by? Why is it bad to have? How do you treat it?

A

1) May be caused by pain, anxiety, fever, pericarditis, medications, etc.
2) Worsens ischemia (increases myocardial oxygen consumption)
3) Treat underlying cause (analgesics for pain, aspirin for fever, etc.)

59
Q

When does sinus bradycardia occur in relation to MI? Why may it be beneficial to have? What is the treatment?

A

1) A common occurrence in early stages of acute MI, especially right-sided/inferior MI
2) May be a protective mechanism (reduces myocardial oxygen demand)
3) No treatment is required other than observation. If bradycardia is severe or symptomatic (hemodynamic compromise), atropine may be helpful in increasing HR

60
Q

What is bad about asystole? How do you treat it? What if asystole is the cause of cardiac arrest?

A

1) Very high mortality
2) Treatment should begin with electrical defibrillation for VFib, which is more common in cardiac arrest and may be difficult to clearly differentiate from asystole
3) If asystole is clearly the cause of arrest, transcutaneous pacing is the appropriate treatment

61
Q

What is AV block associated with? What types of AV block do not require therapy?

A

1) Associated with ischemia involving conduction tracts

2) First-degree and second-degree (type I) blocks do not require therapy

62
Q

What is done for second degree (type II) and third degree heart blocks that can improve prognosis in the setting of an anterior MI? What about for inferior MI?

A

1) Prognosis is dire in the setting of an anterior MI - emergent placement of a temporary pacemaker is indicated (with later placement of a permanent pacemaker)
2) In inferior MI, prognosis is better, and IV atropine may be used initially. If conduction is not restored, a temporary pacemaker is appropriate

63
Q

What is a recurrent infarction?

A

1) Extension of existing infarction
or
2) Reinfarction of a new area

64
Q

What occurs to both short-term and long-term mortality in the setting of recurrent infarction?

A

Increased mortality

65
Q

Why is diagnosis often difficult in recurrent infarction? Are troponin levels useful to measure? Why may CK-MB be a good marker to detect recurrent infarction? What finding on EKG within the first 24 hours after infarction would make you suspect recurrent infarction?

A

1) Cardiac enzymes are already elevated from the initial infarction
2) Troponin levels remain elevated for a week or more, so are not useful here
3) CK-MB returns to normal faster, and so a reelevation of CK-MB after 36 to 48 hours may be due to recurrent infarction
4) If there is repeat ST segment elevation on ECG within the first 24 hours after infarction, suspect recurrent infarction

66
Q

What are mechanical complications of acute MI?

A

1) Free wall rupture
2) Rupture of interventricular septum
3) Papillary muscle rupture
4) Ventricular pseudoaneurysm
5) Ventricular aneurysm

67
Q

How severe is a free wall rupture post-MI and when does it occur? What is the mortality rate? What does it usually lead to? What is the treatment?

A

1) A catastrophic, usually fatal event that occurs during the first 2 weeks after MI (90% within 2 weeks, most commonly 1 to 4 days after MI)
2) 90% mortality rate
3) Usually leads to hemopericardium and cardiac tamponade
4) Treatment: Hemodynamic stabilization, immediate pericardiocentesis, and surgical repair

68
Q

How severe is a rupture of interventricular septum and what is the treatment? When does it usually occur? What is the likelihood of survival correlated to?

A

1) Greater potential for successful therapy than with a free wall rupture, although this is also a critical event; emergent surgery is indicated
2) Occurs within 10 days after MI
3) Likelihood of survival correlates with size of defect

69
Q

What does a papillary muscle rupture cause and how does this present? What test should be done is papillary muscle rupture is suspected? What treatment is needed?

A

1) Produces mitral regurgitation (presents with new murmur)
2) If suspected, obtain an echocardiogram immediately
3) Emergent surgery is needed (mitral valve replacement is usually necessary), as well as afterload reduction with sodium nitroprusside or intra-aortic balloon pump (IABP)

70
Q

What is a ventricular pseudoaneurysm? What test is best for detecting it? Why is it a surgical emergency?

A

1) Incomplete free wall rupture (myocardial rupture is contained by pericardium)
2) Bedside echocardiogram may show the pseudoaneurysm
3) Ventricular pseudoaneurysms tend to become a free wall rupture

71
Q

What types of ACS is heparin used for? What is it not used for?

A

1) Heparin is used for USA and MI (both NSTEMI and STEMI)

2) It is NOT used for stable angina

72
Q

What test should all patients initially treated conservatively for USA/NSTEMI undergo before leaving the hospital and why?

A

A stress test to determine the need for angiography (which in turn determines the need for angioplasty or CABG)

73
Q

Patients who suffer an acute MI have what level risk for a stroke during the next 5 years? What increases this risk?

A

1) High risk

2) The lower the EF and the older the patient, the higher the risk of stroke

74
Q

What is the most common cause of death in the first few days after MI?

A

Ventricular arrhythmia (either VT or VFib)

75
Q

After an MI, what should all patients be discharged home on?

A

1) Aspirin
2) Beta-blocker
3) Statins
4) ACE inhibitor

76
Q

What is a key difference between a complication of ventricular pseudoaneurysm and ventricular aneurysm? What are ventricular aneurysms associated with? What may be protective in the setting of a ventricular aneurysm? What treatment may be appropriate in selected patients?

A

1) Ventricular aneurysm rarely ruptures (in contrast to pseudoaneurysms)
2) Associated with a high incidence of ventricular tachyarrhythmias
3) Medical management may be protective
4) Surgery to remove aneurysm may be appropriate in selected patients

77
Q

What caused the incidence of acute pericarditis to decrease? What is the treatment? What medications are contraindicated and why?

A

1) The incidence has decreased sharply since the introduction of revascularization techniques
2) Treatment consists of aspirin (which is already standard in treatment of MI)
3) NSAIDs and corticosteroids are contraindicated (may hinder myocardial scar formation)

78
Q

What is Dressler syndrome (postmyocardial infarction syndrome)? What is the most effective therapy?

A

1) Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occurring weeks to months after an MI
2) Aspirin. Ibuprofen is a second option