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USMLE STEP 2 and 3 > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

Acute Coronary Syndrome (ACS) includes … ?

A
  • Unstable angina (UA)
  • Non-ST segment elevation (NSTEMI)
  • ST segment elevation MI (STEMI)
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2
Q

The distinction between UA and NSTEMI is based entirely on

A

cardiac enzymes, unstable angina lacks biomarkers while NSTEMI has elevated biomarkers.

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3
Q

Why is UA is more of a historical term?

A

With more widespread use of high-sensitivity troponin testing, UA is a rare diagnosis since virtually all cases of ACS will have an elevation in this biomarker.

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4
Q

What is shared between both UA and NSTEMI?

A

Both UA and NSTEMI lack ST-segment elevations, differentiating them from STEMI

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5
Q

When patients present with suspected ACS, what is the overall priority?

A

The priority in clinical care is differentiating and managing NSTEMI versus STEMI.

vvvvvvvvvvv

MI occurs in NSTEMI and STEMI, and is defined as an elevation in a cardiac biomarker with evidence of acute myocardial ischemia.

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6
Q

What is the oxygen demand in patients with UA, and how does this drive management?

A

The overall oxygen demand is unchanged in unstable angina (UA), but the supply is decreased due to reduced resting coronary blood flow (as opposed to stable angina where the demand is increased). UA is significant because it indicates stenosis via thrombosis, hemorrhage, or plaque rupture. UA may lead to total occlusion of a coronary vessel and has a higher risk of Ml and death than stable angina, therefore patients with this diagnosis should be hospitalized.

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7
Q

What is the morality rate for MI?

A

30% (about 1/2 are in the prehospital setting).

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8
Q

Most cases of MI are due to …. ?

A

Acute coronary thrombosis.

vvvvvvvvvvv

MI is due to necrosis of myocardium as a result of an interruption of blood supply. Atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel.

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9
Q

What are the five classes of MI?

A
  • Type 1 MI: Plaque rupture with thrombus
  • Type 2 MI: A supply-demand mismatch with oxygen delivery
  • Type 3 MI: Typical MI suspected, but death occurs without testing the blood for cardiac biomarkers
  • Type 4 Ml: Ml associated with PCI
  • Type 5 MI: Ml associated with CABG
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10
Q

What are the most common clinical features of ACS?

A
  • Chest pain (intense substernal pressure sensation)
  • Radiation to neck, jaw, arms, or back, commonly to the left side
  • Some patients may have epigastric discomfort
  • Other symptoms include dyspnea, diaphoresis, weakness, fatigue, nausea and vomiting, sense of impending doom, syncope, and even sudden cardiac death (usually due to ventricular fibrillation).
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11
Q

What are the other causes of sudden cardiac death and how can these be prevented?

A

Unexpected death due to cardiac causes within 1 hour of symptom onset, most commonly due to lethal arrhythmia (eg, ventricular fibrillation). Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary channelopathies (eg, long QT syndrome, Brugada syndrome). Prevent with implantable cardioverter-defibrillator.

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12
Q

The chest pain associated with ACS is commonly described as … ?

A

often described as a “crushing” pain, like “an elephant standing on chest”

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13
Q

What is similar about the chest pain seen in ACS with stable angina? What is different about this pain?

A

Similar to angina pectoris in character and distribution but much more severe and lasts longer.

vvvvvvvvvvvvv

Unlike in angina, pain may not respond to nitroglycerin.

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14
Q

Up to how many patients with ACS can be asymptomatic or have atypical symptoms? Which patient population is at risk for this?

A

Can be asymptomatic in up to one-third of patients; painless infarcts or atypical presentations are more likely in postoperative patients, the elderly, diabetic patients, and women.

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15
Q

The setting of ACS, the EKG should be repeated every … ?

A

15 to 30 minutes to evaluate for dynamic changes

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16
Q

What are the markers for ischemia/infarction on the EKG evaluating for ACS?

A
  • Peaked T-waves
  • T-wave inversions
  • ST-elvations
  • Q-waves
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17
Q

ST-depressions in continuous leads is … ?

A

NSTEMI

vvvvvvvvvvvv

ST depressions may have STEMI equivalents when there is an ST elevation in aVR and depressions exist in 6 leads.

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18
Q

Seeing a pattern on an EKG from an anterior lead is …

A

an STEMI equivalent (de Winter T wave).

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19
Q

ST-depressions indicate infarction ___% of the time.

A

25%

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20
Q

ST depressions in V2 and V3 (with concerning posterior ECG), this would be … ?

A

an STEMI equivalent.

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21
Q

T-wave inversions in continuous leads is … ?

A

NSTEMI

vvvvvvvvv

These are sensetive but not specifc.

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22
Q

Peaked T waves tend to be an indication of ischemic changes (early or late) in ACS?

A

Early

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23
Q

What occurs to the T-waves a few hours after in the progression of ACS?

A

Inversion

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24
Q

After T-wave inversion, what occurs to T-waves?

A

ST elevation

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25
Q

ST elevations indicate infarction ___% of the time?

A

75%

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26
Q

ST elevations need to be in ______ contiguous leads.

A

2

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27
Q

How is an ST-elevation to be defined in terms of the amount of elevation?

A

1 small box = 1 mm = 0.1 mV

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28
Q

What is the exception for the ST elevations with V2 and V3?

A

The amount of elevation needs to be at least:

0.15 mV in females

0.2 mV in males older than 40

0.25 mV in males younger than 40

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29
Q

After the initial MI, what feature tends to occur on the EKG?

A

Q-waves

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30
Q

For patients with an initial normal troponin, it should be repeated in

A

3 to 6 hours

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31
Q

What are the areas impacted with NSTEMI and STEMI?

A

NSTEMI: subendocardial (inner 1/3 to 1/2 of myocardium)
STEMI: transmural

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32
Q

ST elevations in V1 to V4 are from an ______ infarction.

A

anterior wall

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33
Q

ST elevations in V1 to V2 are from an ______ infarction.

A

Septal

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34
Q

ST elevations in V3 to V4 are from an ______ infarction.

A

Apical

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35
Q

ST elevations in V5 to V6 are from an ______ infarction.

A

Lateral

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36
Q

Leads I and aVL are for the _______ portion of the heart.

A

Lateral

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37
Q

The inferior heart is analyzed with leads _____. ______. and ______.

A

II, III, aVF

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38
Q

A posterior wall MI will show … ?

A

ST depressions in V1-V3 (PDA)

39
Q

For inferior wall MIs, what is the initial medical management?

A

IV fluids and atropine.

40
Q

In MI, which vessels are most commonly infarcted?

A

LAD > RCA > circumflex

41
Q

Cardiac troponin I rises after …. ?

A

4 hours

42
Q

When does troponin peak?

A

24 hours

43
Q

Troponin will remain elevated for … ?

A

7 to 10 days following infarction

44
Q

Which cardiac marker is useful in diagnosing reinfarction following acute MI?

A

CK-MB

vvvvvvvvvvvv

CK-MB increases after 6–12 hours (peaks at 16–24 hr) and is predominantly found in myocardium but can also be released from skeletal muscle.

45
Q

What occurs hystologically in the initial stages of myocadial infarction?

A

coagulative necrosis

46
Q

What cell begins to invade 1 to 3 days following myocadial infarction?

A

PMNs

47
Q

What cell begins to invade 3 to 14 days following myocadial infarction?

A

Macrophages

48
Q

When does scar tissue develop following myocardial infarction?

A

2 weeks to several months

49
Q

What is the inital work-up for patients with supected ACS?

A

Initial approach: all patients should, at minimum, include a brief history and physical, lab testing (including cardiac biomarkers, especially high-sensitivity troponin if available), and an ECG. A bedside ultrasound can also be useful to evaluate cardiac function and regional wall motion abnormalities. Obtain a CXR. Establish continuous cardiac monitoring, IV access for electrolyte repletion, and provide oxygen (if SpO2 is < 90%).

50
Q

What is the inital medical management for patients with ACS entail?

A
  1. High dose ASA (162-325 mg)
  2. Sublingual nitroglycerin
  3. Dual anti-platlet agent (clopidogrel, ticagrelor, prasugrel)
  4. Heparin bolus (UFH, bivalirudin, enoxaparin)
  5. Beta-blocker (cardioselective; metroprolol or atenolol
  6. High intesity statin
  7. ACE inhibitor
  8. morphine (only if chest pain is unrelieved by nitrates)
51
Q

When is reperfusion (coronary angiography) performed for NSTEMI?

A

Immediate PCI for shock, severe CHF, ventricular arrhythmias, or structural complications. Otherwise this is done within 24-48 hours depending on TIMI or GRACE stratifications.

52
Q

Which ionotrope is provided for cardiogenic shock in the setting of ACS?

A

dobutamine.

53
Q

When is nitroglycerin avoided?

A

Inferior wall MI (leads II, III, or aVF).

54
Q

Should patients with heart failure get nitrates in the acute setting of ACS?

A

Nitroglycerin decreases cardiac preload and is indicated for the relief of persistent chest pain in patients with ACS as well as for alleviation of pulmonary edema in those with ADHF and hypertension. It is generally contraindicated in patients with right ventricular myocardial infarction as it may cause severe hypotension in such patients, but not in cases of heart failure. Patients with heart failure and ACS can receive nitrates, but only if they are not hypotensive (SBP <90 mmHg) and do not have contraindications such as right ventricular infarction.

55
Q

Can patients who take sildenafil be given nitrates for ACS in the acute setting?

A

No.

56
Q

What can patients get for chest pain if nitrates are contraindicated?

A

morphine

57
Q

What is the purpose of heparin bolus in ACS?

A

limits thrombus expansion

58
Q

Do you provide DAPT to patients with NSTEMI?

A

Patients with NSTEMI or unstable angina, P2Y12 inhibitor therapy is often held until after coronary angiography in case the atherosclerotic coronary anatomy indicates the need for coronary artery bypass grafting.

59
Q

What are the DAPT doses for ACS?

A

Clopidogrel 300 mg
Ticagrelor 180 mg
Prasugrel 60 mg

60
Q

What is the purpose of statin therapy in ACS?

A

Stabilizes atherosclerotic plaque

vvvvvvvvvvvv

High-intensity statin therapy (eg, atorvastatin, rosuvastatin) is indicated in all patients with ACS (eg, goal of lowering serum LDL to approximately 50 mg/dL) with beneficial effects thought due to plaque stabilization, reduction of inflammation, and atherosclerosis regression. Intolerance of a previous trial of simvastatin is not a contraindication to therapy. Following the acute period, close monitoring and various other strategies (eg, every-other-day dosing, reduction of statin intensity (eg, pravastatin]) should be implemented to try to achieve a tolerable statin regimen if patients were intolerant.

61
Q

What is the preferred anticoagulation in the acute setting of ACS for patients undergoing cath?

A

Heparin or bivalirudin

62
Q

What is the preferred anticoagulation in the acute setting of ACS for patients NOT undergoing cath?

A

Enoxaparin or fondaparinux

63
Q

For unstable angina and NSTEMI, which anticoagulant is preferred?

A

Enoxaparin

In the ESSENCE trail, the risk of death, recurrence, and need for re-vascularization was lower than Heparin treated patients following a sequence of 14 days, 30 days and 1 year.

64
Q

What is the duration of anticoagulation treatment for ACS?

A

48 hours.

65
Q

When are beta-blockers held for ACS?

A

Contraindicated in cardiogenic shock, bradycardia, or signs of heart failure (JVD or pulmonary crackles).

66
Q

Which beta blocker has shown a reduction in death in patients with post-MI LV dysfunction?

A

Carvedilol (CAPRICORN trial)

67
Q

When fibrinolysis considered in the medical management of ACS?

A

In STEMI patients after symptoms occur (within 12 hours), and PCI is not able to be performed within 120 mins, provide thrombolytic therapy (alteplase) within 30 mins.

68
Q

PCI is ideally performed within _____ mins of presentation of ACS.

A

90

69
Q

When are NSTEMI patients revascularized?

A

New HF, cardiogenic shock, persistent angina despite medical therapy, ventricular arrhythmias, or high risk patients (TIMI or GRACE stratification).

70
Q

What factors does the TIMI score use to stratify patients?

A
  1. Cardiac markers
  2. ST deviation
  3. Age older than 65
  4. Risk factors for CAD (DM, HTN, smoking, dyslipidemia, fam hx)
  5. Used ASA within 5 days
  6. 1 or more episodes of angina at rest within 24 hours
  7. Chest pain with unstable vitals

2 points or more –> stress test
3 points or more –> cath lab

71
Q

What medications are continued following re-vascularization following ACS?

A
  1. DAPT (ASA and P2Y12 inhibitor)
  2. BBs
  3. Nitrates
  4. Statins
  5. ACE inhibitor
72
Q

Patients with UA or NSTEMI who are treated conservatively should undergo a … ?

A

Stress test (prior to discharge).

73
Q

Which medications are known to decrease mortality following MI?

A

ACE inhibitor, BBs, and ASA.

74
Q

Drug eluting or bare metal stents require at least ____ months of DAPT

A

6 to 12 months

75
Q

What is used to provoke variant or Prinzmetal angina?

A

Variant or Prinzmetal angina involves transient coronary spasm that usually is accompanied by a fixed arteriolosclerotic lesions but can also occur in normal coronary arteries. Episodes of angina occur at rest (classically occurs at night) and is associated with ventricular arrhythmias. The Hallmark is transient ST segment elevation, not depression, on EKG during chest pain. Coronary angiography is the definitive test that displays coronary spasms when the patient is given IV ergonovine or acetylcholine to provoke spasms. The treatment is with vasodilators such as calcium channel blockers and nitrates. Risk factor modifications include smoking cessation and lowering of lipid levels.

76
Q

What is the most common cause of inpatient mortality in the setting of acute MI complications?

A

Pump failure is the most common cause of in hospital mortality in the setting of acute ACS. If mild, treat medically with an ace inhibitor or a diuretic. If severe this may lead to cardiogenic shock and invasive hemodynamic monitoring or support with tropes or devices may be indicated.

77
Q

How are premature ventricular contractions (PVCs) treated in the context of complications of acute MI?

A

PVCs are treated conservatively with observation

78
Q

Can atrial fibrillation occur as a complication of acute MI?

A

Yes this is a common arrhythmia that occurs in the setting of ACS

79
Q

What is the most common cause of death within 24 hours following myocardial infarction?

A

Ventricular arrhythmias, these can occur at any time following a myocardial infarction (MI).

80
Q

How is VT in the setting of ACS managed?

A

Sustained ventricular tachycardia (VT) requires treatment.

If the patient is hemodynamically unstable:
-with a pulse, perform synchronized cardioversion.
-pulseless, perform defibrillation (unsynchronized cardioversion or direct current countershock [DCCS]).

If the patient is hemodynamically stable:
-initiate antiarrhythmic therapy, typically with amiodarone.

81
Q

How is VF in the setting of ACS managed?

A

Unsynchronized defibrillation.

82
Q

How is bradycardia in the setting of ACS managed

A

This is a common occurrence in early stages of acute MI especially following a right sided or inferior MI. There is no treatment required other than observation. If bradycardia is severe or symptomatic give atropine.

83
Q

Which arrhythmia maybe difficult to differentiate and has a very high mortality in the setting of ACS?

A

Asystole.

The treatment should begin with electrical defibrillation for V fib which is more common in cardiac arrest and may be difficult to clearly differentiate from Asystole. If Asystole is clearly the cause of arrest perform transcutaneous pacing.

84
Q

How are AV blocks managed in the setting of ACS?

A

First and second-degree type one AV blocks do not require treatment, however, second-degree type two and third-degree AV blocks in the setting of an anterior MI requires emergent placement of a temporary pacemaker followed by a permanent pacemaker. An inferior MI the prognosis is better and atropine may be used initially. If conduction is not restored a temporary pacemaker is appropriate. Can use isoproterenol or dopamine while waiting placement of a pacer.

85
Q

When the RCA is implicated in MI what complication tends to occur?

A

Right ventricular failure which can occur at any time following the acute event. Presents with hypotension, elevated JVD, and peripheral edema. Avoid nitroglycerin, watch for AV blocks or bradycardia, and give IV fluids and tropes.

86
Q

Which chamber of the heart is implicated when a patient presents with cardiogenic shock in the setting of ACS?

A

Left ventricular failure. This is usually treated with furosemide, avoidance of beta blockers, and tropes or mechanical support.

87
Q

Fibrinous pericarditis usually occurs at what time following an MI?

A

This usually occurs within one week. The treatment is with ASA. NSAIDs and steroids are NOT indicated because they may hinder myocardial scar formation.

(this also can be treated with addition of colchicine)

88
Q

The patient presents with acute onset of heart failure, low blood pressure, shortness of breath, pulmonary edema, and mitral regurgitation (holosystolic murmur) following an ACS event, what is the underlying cause?

A

Papillary muscle rupture which are occurs within one week of an MI.

The pulmonary wedge pressure will be increased and patients will likely be hypoxic and cyanotic with signs of right right sided heart failure and low O2 stats. This requires diagnosis with an echo (transthoracic) and treatment with surgical repair. Patient will also need after load reduction with nitro peroxide or intra-aortic balloon pump (IABP).

89
Q

A patient presents with a holosystolic murmur at the lower left sternal border after experiencing T wave inversions and leads V1 through V4, what is the underlying cause?

A

This is an interventricular septal rupture which occurs 3 to 10 days following an MI and presents with a hollow systolic murmur and by ventricular CHF. This requires diagnosis with an echo (transthoracic) and treatment with surgical repair. The prognosis and likelihood of survival with this correlates with the size of the defect.

90
Q

A patient has distant heart sounds, JVD, and hypotension following an MI that occurred two weeks ago, what is the underlying cause?

A

This is likely a ventricular wall rupture which occurs within one to two weeks following and MI, most commonly 1 to 4 days. Patient’s present with symptoms of cardiac tamponade and chest pain. This often results in PEA arrest. Diagnosis requires an echo (transthoracic) with pericardiocentesis which can be diagnostic and therapeutic. Definitive treatment is with surgical repair although these patients have a very high mortality rate in this is usually fatal (90%).

91
Q

A patient experiences a stroke two weeks after a myocardial infarction, what is the likely cause?

A

This could be due to a ventricular aneurysm or pseudoaneurysm. This is a free wall rupture contained by scar tissue and pericardium. True aneurysms have dyskinetic left ventricular wall that balloons during systole which increases the risk of thrombus. Patients tend to have Q waves and leads V1 to V4. This is diagnosed with an echo (transthoracic) or angiography and requires surgical repair. True aneurysms do not have a propensity for rupture in contrast to pseudo aneurysms. However true aneurysms have a high incident of ventricular tachyarrhythmias. Medical management maybe protective and involves use of an ace inhibitor with anticoagulation. Surgery to remove the aneurysm may be appropriate in some patients.

92
Q

A patient has diffuse ST elevations, dry cough, shortness of breath, and chest pain that is relieved by leaning forward. The patient also experienced an MI one month ago, what is the likely underlying ideology for the patient’s pain?

A

Dressler syndrome. This is post MI autoimmune pericardial inflammation and is treated with NSAIDs.

(this also can be treated with ASA plus colchicine)

93
Q

A patient experiences dermatologic changes (Levido reticularis), petechiae, and a blue toe, what is the underlying cause?

A

This is blue toe syndrome caused by a crystalized embolus made of cholesterol intends to occur following revascularization following ACS. Patients might encounter renal failure, colonic ischemia, muscle ischemia, and CVA.

USMLE STEP 2 and 3 (139 decks)

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