269 STEMI Flashcards

1
Q

Classification of Myocardial infarction. Troponin I positive. Post 2 vessel stentt

A

Tupe 4A: PCI
Type 4B: Stent Thrombosis
Type 5: CABG

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2
Q
Not associated with CAD
A. Age
B. Inflammation
C. Systemic huper
D. Metabolic syndrome
A

Age

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3
Q

OASIS 7. Superior to placebo in STEMI not receiving reperfusion therapy

A

Fondaparinux

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4
Q

Less common presentations of STEMI

A
Loss of consciousness
Confusional state
Sensation of profound weakbess
Appearance of arrhythmia
Evidence of peripheral embolism
Unexplained drop in arterial pressure
Breathlessness
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5
Q

Pain in STEMI typically radiates in what areas but never in what area?

A

Pain may radiate to occipital area but not below umbilicus and the trapezius

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6
Q

Temporal stages in STEMI

A

Acute: hours to days
Healing: 7-28 days
Healed: more than 29 days

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7
Q

*Pathologic change in myocardial infarction 24 hours from onset

A

band necrosis

*still to find actual page in Harrison

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8
Q

CK rises within and returns to normal by?

A

CK rises in 4 to 8 hours and returns to normal by 48 to 72 hours

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9
Q

Cardiac Troponin remains elevated for how long after STEMI

A

7 to 10 days

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10
Q

Universally present in STEMI on cardiac imaging

A

Abnormalities in wall motion

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11
Q

ECG findings candidate for reperfusion

A

ST segment elevation at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads

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12
Q

Time from FMC to device time in PCI capable hospital

A

less than 90 minutes

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13
Q

Door in Door out time from non PCI capable hospital

A

less than 30 minutes

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14
Q

FMC to device time in non PCI capable hospital

A

less than 120 minutes

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15
Q

When to administer fibrinolysis when anticipated FMC to device is long

A

within 30 minutes of arrival

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16
Q

Reason why glucocorticoids and NSAIDS not given to STEMI patients

A

They can impair infarct healing and increase risk of myocardial rupture

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17
Q

Treatment of choice of ventricular tachycardia if heart failure is present

A

Digoxin

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18
Q

Cause of LV wall rupture

A

*Few hours from myocardial infarction

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19
Q

When goes LV aneurysm occur in patients with STEMI

A

Weeks to months after STEMI

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20
Q

Dykinesia or local expansile paradoxical wall motion; composed of scar tissue; most common location

A

ventricular aneurysm; apical aneurysm is most common

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21
Q

Class 1 A recommendation for …

A

Sustained Vtach
Recurrent chest pain
*from exam; still to find actual Harrison page

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22
Q

Pivotal diagnostic and Triage tool because it is at the center of the decision pathway for management

A

12 Lead ECG

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23
Q

Stages of STEMI

A

Acute few hours to 7 days
Healing 7- 28 days
Healed more than 29 days

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24
Q

Laboratory test for confirmation of STEMI

A

ECG
Serum cardiac biomarkers
Cardiac imaging
Nonspecific indices of tissue necrosis and inflammation

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25
Q

Why does slowly developing high grade coronary artery stenoses do not typically precipitate STEMI

A

development of rich collateral network over time

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26
Q

what causes STEMI in most cases

A

atherosclerotic plaque becomes disrupted and conditions favor thrombogenesis

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27
Q

characteristic of plaque prone to rupture

A

rich lipid core and thin fibrous cap

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28
Q

the amount of myocardial damaged caused by coronary occlusion depends on what factors

A
  1. territory supplied 2. whether or not the vessel becomes totally occluded 3. duration of coronary occlusion 4. quantity of blood supplied by collateral vessels 5. demand of oxygen of the myocardium whoes blood supply has been limited 6. endogenous factors that produce spontaneous lysis of occlusive thrombus 7. adequacy of myocardial perfusion in the infarct zone when flow is restored in occluded epicardial coronary artery
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29
Q

most common presenting symptom in STEMI

A

pain

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30
Q

cluster where STEMI often commence

A

morning within a few hours of awakening

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31
Q

typical pain in STEMI

A

central portion of the chest and or epigastrium and on occasion it radiates to the arms

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32
Q

pain in STEMI can radiate as high as where but not below the what?

A

radiate as high as the occipital area but not below the umbilicus

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33
Q

differentials of the pain in STEMI

A

acute pericarditis, pulmonary embolism, acute aortic dissection, costochondritis, and gastrointestinal disorders

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34
Q

True or false. Radiation of discomfort to the trapezius is not seen in patients with STEMI

A

True.

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35
Q

Proportion of painless STEMI is greater in what subset of patients

A

elderly, patients with diabetes mellitus

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36
Q

less common presentation of STEMI

A

loss of consciousness, confusional state, sensation of profound weakness, appearance of an arrhythmia, evidence of peripheral embolism or a merely unexplained drop in arterial pressure

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37
Q

duration of substernal chest pain and diaphoresis that strongly suggest STEMI

A

more than 30 mins

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38
Q

manifestation of anterior infarction

A

sympathetic nervous system hyperactivity like tachycardia and or hypertension

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39
Q

manifestation of inferior infarction

A

parasympathetic hyperactivity like bradycardia and or hypotension

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40
Q

True or false. In patients with anterior wall infarction, an abnormal systolic pulsation casued by dyskinetic bugin fo the infarcted myocardium amy develop in the periapical area within the first days of the illness and then may resolve

A

True.

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41
Q

decline in systolic pressure in patients with transmural infarction

A

systolic pressure declines by 10-15 mmHg from the preinfarction state

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42
Q

True or false. Most patients initially presenting with ST segment elevation ultimately evolve Q waves on the ECG

A

True.

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43
Q

Levels of cardiac troponin may remain elevated for how many days after STEMI

A

7-10 days

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44
Q

CK rises within how many hours and generally returns to normal by how many hours

A

CK rises within 4-8 hrs and generally returns to normal by 48-72 hr

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45
Q

True or false. Nonspecific reaction to myocardial injury is associated with polymorphonuclear leukocytosis with WBC count reaching levels of 12,000- 15, 000/ uL

A

True.

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46
Q

Elevated WBC and ESR may occur for how long in STEMI

A

leukocytosis for 3-7 days, and ESR may remain elevated for 1-2 weeks

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47
Q

universally present on cardiac imaging for patient with STEMI

A

abnormalities of wall motion

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48
Q

True or false. Although perfusion scanning is extremely sensitive, it cannot distinguish acute infarcts from chronic infarcts

A

True.

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49
Q

technique to detect MI on high resolution cardiac MRI

A

late enhancement

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50
Q

two general classes of complications for STEMI

A

electrical complications (arrhythmias) and mechanical complications (pump failure)

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51
Q

most common cause of death in the first 24 hr of STEMI

A

ventricular fibrillation

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52
Q

greatest cause of delay for the treatment of STEMI

A

onset of pain and patient’s decision to call for help

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53
Q

criteria for AMI

A

detection of a rise and or fall of cardiac biomarker values, symptoms of ischemia, new ST wave changes of new LBBB, development of pathologic Q waves on ECG, imaging evidence of new loss of viable myocardium, or new regional wall motion abnormality, identification of intracoronary thrombus by angiography or autopsy

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54
Q

AMI in PCI

A

cTn 5x in patients with normal baseline or rise of cTn values 20% from baseline if elevated

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55
Q

AMI in CABG

A

cTn 10x in patient with normal baseline

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56
Q

Criteria for prior myocardial infarction

A

any one of the ff. 1. pathologic Q waves with or without symptoms in the absence of nonischemic causes 2. imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of nonischemic cause, 3. pathologic findings of a prior MI

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57
Q

goal of initiating PCI

A

Within 120 mins of first medical contact

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58
Q

Classification of Myocardial infarction. Spontaneous

A

Type 1

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59
Q

Classification of Myocardial infarction. Secondary to an ischemic imbalance

A

Type 2

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60
Q

Classification of Myocardial infarction. Resulting in death when biomarker values are unavailable

A

Type 3

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61
Q

Classification of Myocardial infarction. Related to PCI

A

Type 4a

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62
Q

Classification of Myocardial infarction. Related to stent thrombosis

A

Type 4b

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63
Q

Classification of Myocardial infarction. Related to CABG

A

Type 5

64
Q

when hypoxemia is present how to give oxygen supplementation

A

oxygen nasal prong or face mask 2-4 L/min for the first 6-12 h after infarction

65
Q

in addition to diminishing or abolishing chest discomfort, it also capable to decreasing myocardial oxygen demand and increasing myocardial oxygen supply

A

nitroglycerin

66
Q

how to reverse hypotension from ingestion of nitrates and PDE5 inhibitor

A

atropine

67
Q

very effective analgesic for pain associated with STEMI

A

morphine

68
Q

when is nitrates avoided

A

SBP less than 90 mmHg and in whom there is clinical suspicion of RV infarction

69
Q

True or false. Morphine also has a vagotonic effect and may cause bradycardia or advanced degrees of heart block esp in patients with inferior infarction

A

True.

70
Q

conditions prior to giving metoprolol IV

A

HR more than 60 bpm, SBP more than 90 mmHg, PR interval less than 0.24 s

71
Q

how to give metoprolol IV

A

5 mg every 2-5 mins for a total of 3 doses

72
Q

how to transition to metoprolol oral

A

50 mg every 6h for 48 hr then 100 mg every 12 hr

73
Q

contraindication to oral beta blocker therapy

A
  1. signs of heart failure 2. low output state 3. increased risk of heart failure 4. PR more than 0.24 s, 2nd or 3rd degree heart block, active asthma or reactive airway disease
74
Q

True or false. Unlike beta blockers, calcium antagonist are of little value in the acute setting

A

True.

75
Q

ECG of STEMI

A

2 mm in two contiguous precordial leads and 1 mm in adjacent limb leads

76
Q

true or false. In the absence of ST segment elevation, fibrinolysis is not helpful and evidence even suggesting that it may be harmful

A

True

77
Q

why are glucocorticoids and NSAIDs avoided in patients with STEMI

A

they can impair infarct healing and increase risk of myocardial rupture

78
Q

When is PCI generally preferred over fibrinolysis

A

diagnosis is in doubt, cardiogenic shock is present, bleeding risk is increased, symptoms have been present for at least 2-3 hr

79
Q

why is PCI done when the symptoms has already been present for 2-3 hrs

A

clot is mature and less easily to be lysed by fibrinolytic drugs

80
Q

when should fibrinolysis ideally be initiated

A

Within 30 mins of presentation

81
Q

what is the principal goal of fibrinolysis

A

prompt restoration of full coronary arterial patency

82
Q

fibrinolytic agents approved by US FDA

A

tpa, streptokinase, tenecteplase and reteplase

83
Q

what is the mechanism of action of these fibrinolytic agents

A

promote the conversion of plasminogen to plasmin which subsequently lyses fibrin thrombi

84
Q

Meaning of TIMI score 0

A

complete occulusion of the infarct related artery

85
Q

Meaning of TIMI score 1

A

some penetration of the contrast media beyond point of obstruction

86
Q

Meaning of TIMI score 2

A

perfusion of the infarct vessel into the distal bed but flow is delayed compared to that of normal

87
Q

Meaning of TIMI score 3

A

full perfusion of the infarct vessel with normal flow

88
Q

What is the TIMI goal of reperfusion therapy

A

TIMI 3

89
Q

more effective than streptokinase at restoring full perfusion

A

tpa, rpa, TNK

90
Q

how to give tpa

A

15 mg bolus followed by 50 mg IV over the first 30 mins then 35 mg over the next 60 mins

91
Q

how to give streptokinase

A

1.5 MU IV over 1 hr

92
Q

how to give rPa

A

10 MU bolus over 2-3 mins then 10 MU bolus 30 mins after

93
Q

how to give TNK

A

0,53 mg/kg over 10 s

94
Q

contraindication to use of fibrinolytic agents

A

history of crebrovascular hemorrhage at any time, nonhemorrhage stroke or cerebrovascular event within the past year, BP more than 180/110 mmHg, suspicion of aortic dissection and active internal bleeding

95
Q

relative contraindication of fibrinolytic agents

A

INR more than 2, less than 2 weeks invasive or surgical procedure, more than 10 mins cardiopulmonary resuscitation, known bleeding diasthesis, pregnancy, hemorrhage ophthalmic condition, active peptic ulcer disease, severe hypertension that is currently under adequate control

96
Q

because of risk of an allergic reaction, patients should not receive streptokinase if the agent had been received within the preceding

A

5 days to 2 years

97
Q

most frequent and potentially most serious complication of fibrinolytic agents

A

hemorrhage

98
Q

cardiac catheterization and coronary angiography should be carried out after fibrinolytic therapy if there is

A
  1. failure of reperfusion (persistent chest pain and ST segment elevation more than 90 mins) 2. coronary artery re occlusion ( re elevation of ST segments or recurrent chest pain)
99
Q

True or false. Patient who have confirmed STEMI but low risk (no persistent chest pain, no CHF, no hypotension or no cardiac arrhythmias) may be transferred out to coronary care unit within 24 hours

A

True.

100
Q

STEMI patient should be kept on bed rest for how long

A

First 6-12 hrs

101
Q

what is the activity of STEMI patient within the first 24 hrs

A

upright position and dangle legs over side of the bed, then sitting in a chair

102
Q

when can STEMI patient start ambulating in room

A

by the second or third day

103
Q

after day 3, what is the goal distance of ambulating in STEMI patients

A

185 ms (600 ft) at least 3x a day

104
Q

what is the diet of STEMI patient

A

NPO or clear liquids only in the first 4-12 hrs

105
Q

what is the calorie for fat and cholesterol in STEMI patient

A

less than 30% of calories as fat and cholesterol less than 300 mg/day

106
Q

what is the proportion of carbohydrates in STEMI patients

A

50-55% of total calories

107
Q

what the choice and dose of sedation in STEMI patient

A

Diazepam 5 mg or oxazepam 15-30 mg or lorazepam 0.5- 2 mg given three to four times a day

108
Q

what is the goal of anticoagulation therapy

A

maintain patency of the infarct related artery in conjunction with reperfusion strategy and to reduce tendency to thrombosis

109
Q

how is UFH administered in STEMI

A

initial bolus of 60 U/kg then 12 U/kg per hour

110
Q

what is the goal APTT during the maintenance therapy of UFH

A

1.5 – 2 times the control value

111
Q

Individuals who are for prolonged therapy with anticoagulatnts

A

anterior location of infarct, severe LV dysfunction, heart failure, history of embolism, mural thrombbus, atrial fibrillation

112
Q

how long should individuals with increased risk of systemic or pulmonary thromboembolism receive anticoagulant

A

full therapeutic levels of LWH or UFH then 3 months of warfarin

113
Q

what is the mechanism of ACEI leading to reduced mortality in STEMI

A

reduction in ventricular remodeling after infarction

114
Q

how long should ACEI be given

A

indefinitely

115
Q

contraindication to ARBs in STEMI patients

A

creatinine more than 2.5 in male and more than 2.0 in female or hyperkalemia of more than 5.0 meq/L

116
Q

how long can a patient be on intravenous nitroglycerin

A

24-48 hrs

117
Q

refers to the series of changes in shape, size and thickness in both the infarcted and noninfarcted segments in the left ventricle

A

ventricular remodelling

118
Q

medications to the prescribed in patients with ejection fraction of less than 40% regardless of whether or not heart failure is present

A

ACEI or ARB

119
Q

primary cause of in hospital death from STEMI

A

pump failure

120
Q

most common clinical signs of pump failure

A

S3 and S4 gallop sounds and pulmonary rales

121
Q

Killip I

A

no signs of pulmonary or venous congestion

122
Q

Killip II

A

moderate heart failure as evidence by rales at the lung bases, S3 gallop, tachypnea, signs of failure of the right side of the heart,

123
Q

Killip III

A

severe heart failure and pulmonary edema

124
Q

Killip IV

A

shock with systolic pressure less than 90 mmHg

125
Q

Mortality rate. Killip I

A

0-5%

126
Q

Mortality rate Killip II

A

10-15%

127
Q

Mortality rate Killip III

A

35-45%

128
Q

Mortality rate Killip IV

A

85-95%

129
Q

infarction of how much of the left ventricle leads to cardiogenic shock

A

more than 40%

130
Q

patients who may benefit from diuresis based on LV filling pressures

A

LV filling pressure more than 22 mmHg and normal cardiac indices

131
Q

patients who may benefit from volume expansion based on LV filling pressure

A

LV filling pressure less than 15 mmHg and reduced cardiac indexes

132
Q

optimal LV filling pressure or pulmonary artery wedge pressure

A

About 20 mmHg

133
Q

True or false. Benefits of digitalis administration to patients with STEMI are unimpressive

A

True.

134
Q

True o false. Nitrates in various forms may be used to decrease preload and congestive symptoms

A

True,

135
Q

True or false. 1/3 of patients with inferior infarction demonstrate at least minor degree of RV necrosis

A

True

136
Q

ST segment elevation in V4R means

A

RV infarction

137
Q

hemodynamic pattern on catheterization in RV dysfucnction

A

steep rigth atrial Y descent, and an early diastolic dip and plateau in RV waveforms

138
Q

True or false. Infrequent sporadic ventricular premature depolarizations occur in almost all patients with STEMI and do not require therapy

A

True.

139
Q

when is pharmacologic therapy in arrhythmias given

A

sustained ventricular arrhythmias

140
Q

True or falsse. Prophylactic antiarrhythmic therapy is contraindicated

A

True.

141
Q

target serum potassium and magnesium in STEMI patient to avoid ventricular fibrillation

A

serum potassium 4.5 mmol/L and magnesium 2.0 mmol/L

142
Q

how to deal with sustained ventricular tachycardia

A

Amiodarone 150 mg over 10 mins followed by infusion of 1.0 mg/min for 6 hr and than 0.5 mg/min

143
Q

if ventricular tachycardia does not stop and there is hypotension, what should be done

A

synchronized cardioversion of 200-300 J

144
Q

what to do if ventricular tachycardia or fibrillation is refractory to electroshock

A

intracardiac epinephrine 1 mg or 10 ml of 1:10,000 dilution or amiodarone 75-150 mg bolus

145
Q

primary response to acute ischemia that occurs during the first 48 hr

A

ventricular fibrillation

146
Q

True or false. Patient who develop ventricular fibrillation after the first 48 hrs have increased mortality rate

A

True.

147
Q

ventricular rhythm with rate of 60-100 beats/min often occurs transiently during fibrinolytic therapy at the time or reperfusion

A

accelerated idioventricular rhythm

148
Q

True or false. AIVR that occurs in association with fibrinolytic therapy is benign and does not presage the development of classic ventricular tachycardia

A

True.

149
Q

most common supraventricular arrhythmia

A

sinus tachycardia

150
Q

if heart failure is absent, alternative to managing supraventricular arrhythmias

A

beta blockers, verapamil or diltiazem

151
Q

what to do if bradycardia is persistent despite atropine

A

electrical pacing

152
Q

True or false. Recurrent or persistent ischemia often heralds extension of the orignal infarct or reinfarction

A

True.

153
Q

how is pericarditis in STEMI managed

A

Aspirin 650 mg 4x a day

154
Q

most common aneurysm post STEMI

A

apical aneurysm

155
Q

usual duration of hospitalization of uncomplicated STEMI

A

3-5 days

156
Q

when can sex be resumed in patients with STEMI

A

After 2 weeks

157
Q

when can STEMI patients return to work

A

Within 2-4 weeks