STEMI Flashcards
(201 cards)
1
Q
What ECG criteria define STEMI in leads V2–V3?
A
A: ST elevation ≥2 mm in men or ≥1.5 mm in women.
2
Q
What ECG criteria define STEMI in other contiguous leads?
A
A: ST elevation ≥1 mm in at least two contiguous chest or limb leads.
3
Q
What finding in leads V1–V3 may indicate a posterior STEMI?
A
A: Isolated or most prominent ST depression ≥0.5 mm.
4
Q
What is the ST elevation cutoff in posterior leads (V7–V9)?
A
A: ≥0.5 mm.
5
Q
Can ST elevation <1 mm still indicate myocardial injury?
A
A: Yes, if the clinical setting or morphology suggests ischemia.
6
Q
What distinguishes ischemic ST elevation from benign early repolarization?
A
A: Morphology, context, associated features (Q waves, T waves).
7
Q
How does STEMI typically appear on ECG over time?
A
A: It evolves into Q waves and T-wave inversion.
8
Q
Does STEMI always lead to Q waves?
A
A: No, some STEMIs do not generate Q waves.
9
Q
Can NSTEMIs have Q waves?
A
A: Yes, though less commonly.
10
Q
When do troponins typically begin to rise after infarction?
A
A: Within 3 hours.
11
Q
What percent of MIs are completely silent?
A
A: ~12.5%.
12
Q
What percent present with atypical symptoms (e.g., dyspnea, malaise)?
A
A: ~12.5%.
13
Q
In which patients are silent or atypical MIs more common?
A
A: Elderly and diabetic patients.
14
Q
Within how many hours of symptom onset is emergent reperfusion indicated?
A
A: Within 12 hours (class I), possibly up to 24 hours (class IIa for PCI).
15
Q
Is reperfusion indicated if symptoms have resolved but ST elevation persists?
A
A: Yes.
16
Q
What is the goal door-to-balloon (DTB) time for PCI-capable hospitals?.
A
A: ≤90 minutes
17
Q
What is the goal FMC-to-device time for transferred patients?.
A
A: ≤120 minutes
18
Q
When should fibrinolytics be considered instead of PCI?
A
A: If PCI cannot be performed within 120 minutes and the patient presents within 12 hours.
19
Q
Are patients presenting >24 hours after symptom onset candidates for emergent PCI?
A
A: Usually no, except for specific indications (e.g., cardiogenic shock, ongoing pain).
20
Q
Should patients with cardiogenic shock always undergo PCI?
A
A: Yes, regardless of delay.
21
Q
Should PCI be favored in late presenters (3–12 hours)?
A
A: Yes.
22
Q
How effective is PCI in SVG occlusion compared to fibrinolytics?
A
A: PCI: 50–70% TIMI 3 flow; fibrinolytics: 25–50%.
23
Q
What are the benefits of reperfusion after 3–12 hours?
A
Prevents remodeling, improves scar turgor, reduces mortality.
24
Q
Patient with prior MI and persistent ST elevation with Q waves: STEMI?
A
A: Probably not; compare to old ECG and consider echo.
25
Patient with chest pain for 8 hours, Q waves and ST elevation: Reperfuse?
A: Yes. Q waves do not preclude reperfusion.
26
Chest pain resolved, but ST elevation persists: Reperfuse?
A: Yes, within 24 hours.
27
Pain and ST elevation resolve after nitrates: Reperfuse?
A: Not emergently; consider early angiography
28
ST elevation <1 mm but ischemic morphology: Reperfuse?
A: Yes, if ischemia occurred <24 hours ago.
29
Q waves and T-wave inversion without ST elevation: Reperfuse?
A: PCI preferred, but not emergently.
30
What are the two key criteria for emergent PCI?
A: (1) Persistent ST elevation <24 h after pain onset; (2) Persistent pain >24 h even if ST elevation resolved.
31
What does concordant ST deviation in LBBB suggest?.
A: STEMI (high specificity >95%)
32
What is Sgarbossa’s criterion for STEMI?
A: Concordant ST elevation ≥1 mm or ST depression ≥1 mm in V1–V3.
33
What does extreme discordance (ST elevation >25% of QRS) suggest?
A: Possible STEMI, but lower specificity.
34
Are upright T waves >50% of QRS in LBBB concerning?
A: Yes, may indicate STEMI.
35
Why is LBBB challenging for STEMI diagnosis?
A: Because ST changes may be masked or mimicked by the LBBB.
36
Is a new LBBB a STEMI equivalent?
A: Not by itself; needs ischemic symptoms and supporting ECG findings.
37
How often is STEMI present in new LBBB with ischemic symptoms?
A: ~10%.
38
What is the next step if STEMI is suspected but uncertain in LBBB?
A: Urgent bedside echo; look for wall motion abnormalities.
39
In LBBB, what does anterior/apical akinesis suggest?
.
A: Acute ischemia
40
What does global hypokinesis suggest in LBBB?
A: Chronic cardiomyopathy
41
What is the "STEMI Equivalent" pattern in posterior MI).
A: ST depression in V1–V3 (reciprocal change
42
What’s the significance of "Q-wave MI"?.
A: Often denotes a larger, transmural infarct
43
What’s the significance of ST resolution with pain resolution?
A: May indicate spontaneous thrombolysis (~15% of STEMIs).
44
What is the best lead to detect RV infarction?
A: V4R.
45
What is the target "diagnosis-to-device" time in ESC guidelines?
A: ≤120 minutes.
46
What is the absolute mortality benefit of fibrinolytics if given within the first hour of STEMI onset?
A1: 6.5% absolute mortality reduction (50% relative reduction) – "golden hour."
47
What is the mortality benefit of fibrinolytics in the second hour after STEMI onset?
A2: 4% absolute mortality reduction.
48
What is the mortality benefit between 3–6 hours after STEMI onset?
A3: ~3% absolute mortality reduction (~25% relative).
49
What is the mortality benefit between 6–12 hours after STEMI onset?
A4: ~2% absolute mortality reduction
50
What is the benefit of fibrinolytics beyond 12 hours of STEMI onset?
A5: Marginal and questionable.
51
In which high-risk STEMI subgroups is the fibrinolytic benefit more striking?
A6: Anterior STEMI, STEMI with bundle branch block, high-risk score (tachycardia, hypotension).
52
Why is fibrinolysis less beneficial in elderly patients?
A7: Higher bleeding risk and extensive CAD reduce efficacy.
53
What is the recommended TNK dose in patients ≥75 years?
A8: Half-dose TNK (ESC class IIa).
54
What defines successful fibrinolysis at 60–90 minutes?
A9: ≥50% ST-segment resolution (ideally 70%) and chest pain resolution.
55
What rhythm is highly specific for reperfusion?
A10: Accelerated idioventricular rhythm (AIVR).
56
What is TIMI 3 flow?
Normal flow and full perfusion – associated with best outcomes.
57
What does TIMI 2 flow indicate?
Full vessel perfusion but slow flow (microvascular obstruction or residual narrowing).
58
What is "no-reflow" and when is it used?
TIMI 0–2 flow post-PCI without mechanical obstruction; not used with fibrinolysis.
59
How does streptokinase differ from alteplase (r-tPA)?
Streptokinase affects systemic fibrinogen; r-tPA is fibrin-specific and has a short half-life (~6 min).
60
Why is heparin needed after r-tPA infusion?
A15: To prevent recurrent thrombosis due to short drug half-life.
61
Which fibrinolytic has the highest fibrin specificity and longest effect?
Tenecteplase (TNK) – 14x fibrin specificity, 120-minute duration.
62
What was the main finding of the GUSTO trial?
A17: r-tPA reduced mortality by 1% vs. streptokinase, but with increased ICH (by 0.25%).
63
What benefit is seen by bypassing ED and going directly to cath lab?
A38: DTB reduced by 20 minutes (~33%).
64
What is the maximum acceptable additional transport time to a PCI center?
A37: ≤45–60 minutes.
65
What do guidelines recommend regarding bypassing non-PCI hospitals?
A36: Triage STEMI patients directly to PCI centers (Class I ACC/ESC).
66
What is the preferred prehospital STEMI strategy where PCI isn’t available?
Prehospital fibrinolysis with early transfer – reduces mortality (CAPTIM, STREAM).
67
When should glycoprotein IIb/IIIa inhibitors be used?
During PCI, not before.
68
Is enoxaparin appropriate in early PCI post-fibrinolysis?
No.
69
Are ticagrelor/prasugrel appropriate with early PCI (<24h)?
No – only if PCI is >24 hours later.
70
What percent of fibrinolysis cases need rescue PCI?
~35.
71
When should fibrinolytics be given before transfer?
If DTB >120 minutes expected
72
When is transfer for PCI preferred over fibrinolytics?
If predicted DTB <120 minutes.
73
What is pharmacoinvasive therapy?
Fibrinolysis at non-PCI center followed by PCI within 2–24 hours.
74
What dose of TNK is used in elderly STEMI patients in the STREAM trial?
Half-dose TNK.
75
Why is PCI preferred over fibrinolysis in elderly patients (>75)?
More mortality benefit with PCI; fibrinolytics have higher bleeding risk.
76
How does every 30-minute DTB delay affect mortality?
Increases mortality by 0.5–1%.
77
What is the TIMI 3 flow rate with primary PCI vs. fibrinolytics?
PCI ~95%; Fibrinolytics ~55–60%.
78
What is the incidence of new-onset AF after MI?
~10%.
79
What does monomorphic VT suggest?
Large scar; increased in-hospital and long-term mortality.
80
What does polymorphic VT suggest?
Active ischemia; increased short-term mortality.
81
What defines late VF?
VF >48 hours post-MI, without HF/shock.
82
How is dynamic LVOT obstruction treated?
β-blockers and α-agonists (avoid inotropes, diuretics, and IABP).
83
What is the mechanism of LVOT obstruction post-MI?
Apical akinesis with basal hyperkinesis → systolic anterior motion (SAM) of mitral valve.
84
What type of MI is associated with dynamic LVOT obstruction?
Anterior MI, especially in women.
85
What is the treatment for leaflet tethering MR?
Revascularization, vasodilators, and IABP; surgery if no improvement.
86
What is the operative mortality for mitral valve replacement in papillary muscle rupture?
20–40%
87
What is seen on PCWP in acute MR?
Giant V wave.
88
What right heart cath finding is diagnostic of VSR?
≥7% oxygen step-up between RA and RV.
89
What distinguishes VSR from MR clinically in shock?
VSR murmur is loud with a thrill; MR murmur may be faint due to equalized pressures.
90
What is the most common mechanical complication post-STEMI?
Free wall rupture.
91
What is the pathophysiology of VSR?
Severe left-to-right shunt causing hypotension and LV volume overload.
92
What distinguishes papillary muscle rupture from tethering on echo?
Rupture shows flail leaflet and chordae; tethering shows restricted posterior leaflet.
93
Which papillary muscle is most commonly ruptured post-MI and why?
The posterior papillary muscle due to single blood supply from PDA.
94
What are two types of mitral regurgitation mechanisms after MI?
Papillary muscle rupture and posterior leaflet tethering.
95
When is myocardial rupture most frequent in reperfusion era?
Within the first 24 hours.
96
When do mechanical complications of STEMI most commonly occur?
Within the first 14 days, with peaks at 24 hours and 3–5 days.
97
What adjunct therapy can be used for RV shock with pulmonary HTN?
Inhaled nitric oxide (NO).
98
What is the inotrope/vasopressor of choice in RV shock?.
Norepinephrine
99
What is the ideal RA pressure for stroke volume optimization in RV MI?
10–14 mmHg (13–18 cm H₂O).
100
How should fluids be administered in RV shock?
Cautiously in 500 ml boluses while monitoring RV size and SBP/pulse pressure response.
101
What is the usual culprit artery in RV infarction?
Proximal RCA (~96%)
102
What % of inferior MIs have RV involvement?
30%.
103
How is pulmonary edema treated in acute MI without shock?
Low-dose IV furosemide (20–40 mg) + low-dose IV NTG.
104
How should pacing be approached in cardiogenic shock with bradycardia?
Temporary pacing to >80 bpm.
105
What medications are used for inotropic support in cardiogenic shock?
Dobutamine (SBP >80), norepinephrine (SBP <80 or low SVR).
106
What trial showed the benefit of early revascularization in cardiogenic shock?
The SHOCK trial.
107
What defines LV-related cardiogenic shock?
Low perfusion signs + pulmonary edema + CI ≤2.2 L/min + PCWP ≥15 mmHg.
108
What ECG pattern suggests RV infarct in inferior MI?
ST elevation in right-sided leads (V4R).
109
What percent of MI-related cardiogenic shock patients have inappropriately low or normal SVR?
Over 25%.
110
What is a key difference between cardiogenic shock in chronic HF vs. acute MI?
An EF tolerated in chronic HF (e.g., 30%) may cause cardiogenic shock in acute MI due to lack of adaptive mechanisms.
111
What is the definition of cardiogenic shock?
Sustained SBP <90 mmHg for ≥30 min with signs of hypoperfusion (oliguria <30 ml/h, cold extremities, altered mentation, lactate >2 mmol/L).
112
What was the main finding of the OAT trial regarding PCI performed 1–28 days after MI (especially Q-wave STEMI)?
Late PCI in patients with totally occluded infarct-related arteries (TIMI 0/1) provided no benefit and was associated with more reinfarctions.
113
What were the inclusion characteristics in the OAT trial?
Totally occluded infarct-related artery (TIMI 0 or 1)
Akinetic/dyskinetic wall
One- or two-vessel CAD
No recurrent angina or severe ischemia
No shock or class III–IV HF
114
When is late PCI (>24 h) indicated for a totally occluded artery?
Only if the patient has:
Persistent/recurrent angina (low threshold)
Severe ischemia on stress testing
Persistent HF after initial therapy
115
When is emergent PCI (Class I) indicated in STEMI?
<12 hours from symptom onset
Cardiogenic shock
Acute severe HF (Killip III–IV)
116
What is the ACC recommendation for PCI 12–24 hours post-MI?
Class IIa (benefit likely exceeds risk). ESC uses 48-hour cutoff.
117
Is PCI >24 h after MI indicated for a totally occluded artery with no ischemic symptoms?
No, it's Class III (harm) per OAT trial.
118
What is the ESC’s cutoff time to avoid routine PCI of occluded artery in asymptomatic patients?
48 hours.
119
When can a submaximal stress test be done post-STEMI?
On day 4.
120
When is a maximal (symptom-limited) stress test appropriate post-STEMI?
Between 5–14 days.
121
When is stress testing NOT used post-MI?
In NSTEMI, if planning for invasive strategy, as the myocardium is still salvageable.
122
When is routine PCI recommended after successful fibrinolysis?
3–24 hours post-lysis (Class IIa ACC, Class I ESC).
123
What is the recommendation for PCI of a non-occluded infarct artery >24 hours post-STEMI?
Class IIb – may benefit due to viable myocardium
124
What proportion of totally occluded arteries spontaneously recanalize in the first 24 hours?
Approximately 35%.
125
What is the definition of “no reflow”?
Poor microvascular flow despite open epicardial vessels (TIMI 0–2 flow after PCI).
126
What percent of patients achieve TIMI 3 flow after primary PCI?
Approximately 95%.
127
What percent of TIMI 3 flow patients achieve full ST-segment resolution (cellular reperfusion)?
Only ~60%.
128
What therapies are used for no-reflow?
Intracoronary vasodilators, GP IIb/IIIa inhibitors (GPI), and IABP.
129
What is the key difference between ischemia and viability?
I
schemia = worsens with stress, improves with revascularization.
Viability = preserved uptake at rest, may or may not benefit from revascularization.
130
Did viability predict benefit from late PCI in OAT?
No.
131
What did the SWISSI-2 trial show?
In patients with stress-induced ischemia and 1–2 vessel CAD, PCI reduced CV events by 70%.
132
What percentage of STEMI patients have multivessel CAD?
A: 50–60%.
133
When is staged non-culprit PCI preferred?
Within the same hospitalization or within 45 days, especially for critical stenoses (>90%).
134
When should CABG be delayed post-MI?
Preferably 3–7 days, especially in large infarcts.
135
When should CABG be delayed for RV infarction?
At least 4 weeks, to allow RV recovery.
136
When is early ICD placement indicated?
For sustained VT/VF occurring beyond 48h post-MI.
137
Why is early ICD placement (within 40 days) not recommended?
Does not reduce overall mortality; EF may improve; high-risk patients often die of other causes.
138
When is an ICD indicated post-MI for primary prevention?
EF ≤35% at ≥40 days post-MI.
139
By how much can EF improve with each remodeling drug?
Up to 5%.
140
What are the two causes of EF improvement after MI?
Recovery from myocardial stunning and reverse remodeling with ACE-I/β-blockers/aldosterone antagonists.
141
What cardiac enzymes peak after STEMI, and when?
Troponin I: 50–300 ng/ml at 24h; CK: 2500–5000 U/L at 18–24h.
142
Criteria for early discharge (48–72h) post-STEMI?
Successful PCI, age <70, no arrhythmias, no HF, 1–2 vessel disease, no major comorbidities.
143
How long should a STEMI patient be monitored in CCU?
12–24 hours.
144
What is the glucose target in STEMI patients?
≤180 mg/dL.
145
What is the high-dose statin regimen in STEMI?
Atorvastatin 80 mg or rosuvastatin 20 mg.
146
When should NTG be avoided?
SBP <100 mmHg, HR <50 or >100 bpm, or suspected RV infarct.
147
When is IV nitroglycerin indicated in STEMI?
After SL NTG fails and if patient has angina, HTN, or HF.
148
What did the PARADISE-MI trial show about sacubitril-valsartan?
Not superior to ACE-I post-MI with low EF.
149
Is IV ACE-I recommended in acute MI?
A: No, due to risk of hypotension.
150
Contraindications to ACE-I initiation in STEMI?
SBP <100 mmHg, acute renal failure, or 30 mmHg drop from baseline.
151
When should ACE-I be initiated in MI?
Within first 24h if stable (not hypotensive or in shock).
152
When are β-blockers initiated in HF/LVEF <40% patients?
>24h post-MI, titrated slowly (e.g., carvedilol 6.25 mg BID, as in CAPRICORN trial).
153
When should β-blockers be avoided acutely in STEMI?
Killip class ≥ II, SBP <120 mmHg, HR >110, age >70, bradycardia <60 bpm, AV block, asthma, or low output.
154
Which P2Y12 inhibitors are avoided within 24h of fibrinolytics?
Prasugrel, ticagrelor, and clopidogrel 600 mg.
155
What is enoxaparin dosing in fibrinolytic-treated STEMI?
30 mg IV, then 1 mg/kg SQ Q12h (dose adjusted in elderly and renal impairment).
156
Duration of anticoagulation in standalone fibrinolysis?
At least 48h, preferably throughout hospitalization.
157
Which anticoagulant is associated with the lowest bleeding risk in this context?
Fondaparinux.
158
What is the UFH protocol with fibrinolytics?
60 units/kg IV bolus (max 4000 units), then 12 units/kg/h infusion; adjust Q6h to PTT 1.5–2x normal.
159
What antiplatelet therapy is given with fibrinolytics in STEMI?
Aspirin 325 mg + Clopidogrel (300 mg if <75 y/o, 75 mg if ≥75 y/o).
160
How does bivalirudin compare to UFH in PCI?
Comparable ischemic and bleeding risk; bivalirudin has higher acute stent thrombosis risk unless followed by 1–4h high-dose infusion.
161
What is the UFH dose in the ED for STEMI?
60 units/kg, max 4000 units.
162
What did the ATLANTIC trial show about prasugrel pre-cath loading?
No benefit over loading during PCI.
163
Which ADP-receptor antagonists are preferred in STEMI?
Ticagrelor and prasugrel.
164
What is a “transient” or “aborted” STEMI?
Spontaneous or lysis-induced reperfusion with minimal biomarker rise (CK-MB <2x normal).
165
What is the initial fluid management post-arrest?
1–2 liters isotonic fluid, followed by dopamine or norepinephrine if needed.
166
What is the blood pressure goal post-arrest?
Systolic BP >90 mmHg, mean BP >70 mmHg in first 6 hours associated with better neurological outcomes.
167
When may fibrinolytics be appropriate after cardiac arrest?
After return of spontaneous circulation in a patient with STEMI.
168
What does preserved LV function with akinetic or dilated RV suggest?
Massive pulmonary embolism (PE).
169
Q: How does survival change with delay to defibrillation in VF patients?
Decreases by 7–10% for each minute of delay.
170
From which arteries do the sinus nodal and AV nodal arteries usually originate?
Sinus nodal artery: proximal RCA (60%) or LCx (40%); AV nodal artery: dominant RCA (90%) or dominant LCx (10%).
171
What causes early (<24 hours) sinus bradycardia and AV block in inferior MI?
Increased vagal tone.
172
What causes AV block beyond 24 hours in inferior MI?
Ischemia and edema of the AV node.
173
Is the AV node prone to infarction?
A: No, it is resistant to ischemia and almost never infarcts.
174
How does AV block due to nodal ischemia present on ECG?
First-degree AV block, second-degree type I AV block, or complete AV block with junctional rhythm (40–100 bpm).
175
What is the approximate incidence of complete AV block in inferior MI?
About 4–5%, mostly on the first day.
176
What is the treatment for AV block occurring in the first 24 hours of inferior MI?
Atropine if hemodynamically unstable.
177
Does atropine work for AV block occurring after 24 hours in inferior MI?
No, it typically does not; aminophylline may help
178
When is temporary pacing required in inferior MI with AV block?
Only in cases of shock, heart failure, or low-output signs
179
Which artery supplies the bundle branches and fascicles?
Left anterior descending artery (LAD).
180
What type of AV block is seen in anterior MI?
Hisian or infra-Hisian AV block, often preceded by bundle branch blocks.
181
What is the incidence and prognosis of high-degree AV block in anterior MI?
~1-2% incidence; associated with very high mortality (>50% pre-reperfusion).
182
What is the pacing indication for high-grade AV block in anterior MI?
Transvenous pacing for any high-grade block, permanent pacing if persistent infranodal block
183
What is the most common new intraventricular block in STEMI?
Left anterior fascicular block (LAFB)
184
What supplies the right bundle and left anterior fascicle?
Single arterial supply from LAD (first septal branch).
185
Why is it difficult to infarct the left bundle branch?
It has a dual blood supply (LAD septal branches and AV nodal artery).
186
In which MI types are RBBB and LAFB commonly seen?
Anterior MI, and also inferior MI with severe LAD disease.
187
What does new bundle branch block (BBB) signify in acute MI?
More extensive infarction and higher mortality (2–3x increase).
188
Does NSTEMI have the same mortality as STEMI?
Yes, same short- and long-term mortality but lower in-hospital mortality.
189
What is the risk of progression to complete AV block from acute BBB?
20% for BBB, 25–40% for bifascicular blocks.
190
When is temporary pacing indicated for new BBB or bifascicular block?
If occurring in anterior MI.
191
What defines dyskinesis in the LV?
A myocardial segment moves outward during systole (paradoxical motion)
192
How does an LV aneurysm differ from dyskinesis?
Aneurysm protrudes during both systole and diastole, forms a thin-walled myocardial pocket.
193
What is the treatment to prevent embolization from LV thrombus?
Warfarin anticoagulation for at least 3 months.
194
What imaging is best for detecting LV thrombus?
MRI (more sensitive than echo).
195
Q: When does LV thrombus typically form?
3–6 days post-MI; some form within 24 hours.
196
In which MI type is LV thrombus most common?
Anteroapical MI.
197
What is Dressler syndrome?
An autoimmune pericarditis occurring 1–8 weeks post-MI with fever and effusions.
198
What drugs are contraindicated in post-MI pericarditis?
NSAIDs (except high-dose aspirin is allowed).
199
When does post-infarction pericarditis usually develop?
In the first 1–2 days after MI.
200
How can echo distinguish LV aneurysm from pseudoaneurysm?
Pseudoaneurysm has a narrow neck with neck-to-diameter ratio <0.5 and turbulent to-and-fro flow.
201
What is an LV pseudoaneurysm?
A myocardial rupture sealed by pericardium and thrombus, without myocardium in the wall.
