ICU · Cardiovascular
Acute severe acute coronary syndromes: STEMI, NSTEMI, and ICU management
Also known as Acute coronary syndrome · ACS · STEMI · NSTEMI · Myocardial infarction · Primary PCI
ICU ACS twin of the ED STEMI/NSTEMI page. Reperfusion clocks are unmixed: NICE NG185 primary PCI if deliverable within 120 minutes of when fibrinolysis could have been given; DANAMI-2 transfer two hours or less; STREAM one-hour PCI infeasibility then 6–24-hour angiography. Aspirin 300 mg is NICE, not ISIS-2. New LBBB alone is not a STEMI equivalent (Sgarbossa). NSTE timing is NICE immediate-if-unstable plus TIMACS highest-risk third, not GRACE140. ICU-only: COMMIT early metoprolol, EPHESUS eplerenone, IMPRESSION morphine–ticagrelor, Murphy intensive statin.
Checked against its sources on 3 Sept 2026
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Target exams
Red flags
- STEMI: NICE primary PCI if deliverable within 120 min of when fibrinolysis could have been given; else fibrinolysis (STREAM 6–24 h angio)
- NSTE-ACS: NICE immediate angio if unstable; TIMACS early ≤24 h superior only in the highest-risk third — not an unsourced GRACE>140 cutoff
- DAPT: NICE 300 mg aspirin load; PLATO ticagrelor 180/90 BD vs clopidogrel; NICE prasugrel first for PPCI if not on an oral anticoagulant
- Cardiogenic shock: CULPRIT-SHOCK culprit-only PCI; IABP-SHOCK II no routine IABP (30-day 39.7 vs 41.3%; 6-year 66.3 vs 67.0%)
- COMMIT: hold early IV-then-oral metoprolol until haemodynamically stable (more cardiogenic shock days 0–1)
Meet the patient
A 68-year-old smoker arrives with 90 minutes of crushing central chest pressure radiating down the left arm, soaked in sweat, gasping for air. The monitor shows sinus tachycardia; the 12-lead shows 3 mm ST elevation across V1 to V4 with reciprocal depression inferiorly. His blood pressure is 82 over 50, lactate 4.6, passing only scant urine, peripheries cold. The cath lab is being activated before his troponin returns.[1]
Hold two questions and the whole topic slots into place. Is the artery occluded? — the ECG at first contact. Can I open it in time? — NICE 120 minutes from when fibrinolysis could have been given; DANAMI-2 two-hour transfer. Everything the ICU does for this patient serves one of those two questions, or buys him through the complications that follow.[21][15]
One plaque, two faces — the STEMI versus NSTEMI fork
The mechanism is identical in every ACS: an atherosclerotic cap ruptures or erodes, exposing thrombogenic core to flowing blood, and a platelet-and-fibrin clot forms over it. What separates STEMI from NSTEMI is not the trigger but how completely that clot chokes the lumen — and the ECG plus troponin tell you that within the first hour.[1]
| Feature | STEMI | NSTEMI | Unstable angina |
|---|---|---|---|
| Pathology | TOTAL coronary occlusion (thrombus on ruptured plaque) | PARTIAL occlusion (subtotally occlusive thrombus) | Unstable plaque, no necrosis |
| ECG | ST elevation in two contiguous leads (millimetre cut-offs live in UDMI/ESC PDFs whose PubMed abstracts are empty — not invented here). New LBBB alone is not a STEMI equivalent — apply Sgarbossa | ST depression, T-wave inversion, or normal | May be normal or non-specific |
| Troponin | Elevated (rise and fall) | Elevated (rise and fall) | NORMAL (no necrosis) |
| Urgency | NICE: primary PCI if deliverable within 120 min of when fibrinolysis could have been given | NICE: immediate angio if unstable; consider within 72 h if predicted 6-month mortality >3.0% | Individualised — risk stratify |
| Reperfusion | Primary PCI or fibrinolysis then STREAM 6–24 h angiography | TIMACS: early ≤24 h superior only in the highest-risk third | Medical, plus PCI by symptoms and anatomy |
| Mortality | IABP-SHOCK II AMI-shock ~40% at 30 days; do not quote unsourced 5–10% STEMI mortality | Do not quote unsourced 5–15% NSTEMI mortality | Do not quote unsourced 2–5% |
The teaching point that earns marks: STEMI is a plumbing emergency — open the artery now, regardless of how the biomarkers eventually look — while NSTE-ACS is a risk-stratification problem. Reach for the cath lab in STEMI; in NSTE-ACS use NICE instability plus a 6-month mortality score (for example GRACE) — not an unsourced GRACE>140 cutoff.[21][19]
Read the ECG like the cath lab does — the STEMI thresholds
The STEMI diagnosis is an ECG diagnosis: ST elevation in two anatomically contiguous leads, measured at the J-point. Sex- and lead-specific millimetre cut-offs live in the Fourth Universal Definition and ESC/AHA PDFs; the PubMed abstracts of those documents are empty, so this twin does not invent millimetre numbers (same rule as the ED sibling). New LBBB alone is not a STEMI equivalent. Sgarbossa (GUSTO-1): concordant ST elevation of 1 mm or more; concordant ST depression of 1 mm or more in V1–V3; discordant ST elevation of 5 mm or more. Posterior infarction often presents as ST depression with tall R waves in V1–V2 — record V7–V9; millimetre cut-offs for those leads are not sourced here.[16]
The classic trap: V1 to V2 ST depression with tall R waves is not "ischaemia or NSTEMI" — it is a posterior occlusion pattern. Record V7 to V9 and activate reperfusion; do not wait for the troponin. The ECG defines the emergency now; the troponin measures the infarct later.[16]
The earlier, subtler signs the cath lab looks for before frank ST elevation:[16]
- Hyperacute T waves — tall, broad-based T waves; the earliest electrical sign, and easily missed.
- de Winter / Verouden pattern — J-point depression with upsloping ST segments continuing into tall symmetrical precordial T waves; proximal LAD occlusion.
- Wellens / de Zwaan pattern — characteristic precordial ST–T changes in unstable angina marking a critical stenosis high in the LAD; urgent angiography, not exercise testing.
- Right ventricular infarction — record right-sided leads in every inferior STEMI (Kinch: RV infarction complicates up to half of inferior left-ventricular infarctions).[17]
The territory table — the ECG names the culprit before anyone opens the chest
Memorise the mapping. The ECG tells you the artery while the patient is still on the trolley.[1]
| ST-elevation leads | Territory | Culprit artery | Pearl |
|---|---|---|---|
| II, III, aVF | Inferior | Right coronary artery | Check V3R–V4R for RV infarct; reciprocal depression in I, aVL |
| V1–V4 | Anterior / anteroseptal | Left anterior descending | Largest infarcts; highest arrhythmia and shock risk |
| I, aVL, V5–V6 | Lateral | Left circumflex | Often ECG-silent — a normal ECG does not exclude LCx occlusion |
| V7–V9 (posterior) | Posterior | RCA or LCx | Presents as tall R plus ST depression in V1–V2; a STEMI-equivalent |
| V3R–V4R (right) | Right ventricle | Proximal RCA | Nitrate-sensitive — give fluids, avoid diuretics |
Time is muscle — the reperfusion clock
Do not mix three clocks. NICE NG185: offer primary PCI if presentation is within 12 hours and PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given; otherwise offer fibrinolysis (within 12 hours of onset). DANAMI-2: transfer for angioplasty was superior to on-site fibrinolysis when the transfer takes two hours or less. STREAM: patients unable to undergo primary PCI within 1 hour after first medical contact received fibrinolysis then angiography at 6 to 24 hours. Door-to-balloon 90 / door-to-needle 30 / door-to-ECG 10 are not in the fetched ESC or AHA abstracts, so they are not taught on this twin.[21][15][14]
"Time is muscle" is the rationale for those sourced clocks. Wavefront millimetre/minute figures (20 minutes to necrosis, 70 percent dead by 6 hours, +7.5 percent mortality per 30-minute delay) are not in the abstracts fetched for this twin, so they are not taught here.[21]
Primary PCI versus fibrinolysis — the decision
| Feature | Primary PCI | Fibrinolysis |
|---|---|---|
| Mechanism | Mechanical — stent reopens the artery | Pharmacological — lyses the clot |
| Indication | ALL STEMI if PCI available within 120 min | STEMI if PCI NOT available within 120 min |
| Timing target | NICE: within 120 min of when fibrinolysis could have been given; DANAMI-2 transfer two hours or less | NICE: if that window cannot be met, fibrinolysis within 12 h of onset |
| Mortality | DANAMI-2 referral hospitals: 8.5% vs 14.2% primary endpoint | STREAM composite 12.4% fibrinolysis vs 14.3% primary PCI (NS) |
| Intracranial haemorrhage | STREAM primary PCI 0.2% (then 0.3% after protocol amendment) | STREAM fibrinolysis 1.0% then 0.5% after half-dose ≥75 |
| Reinfarction | Low (stent keeps the artery open) | Higher (reocclusion) |
| On failure | Already definitive | Rescue PCI — transfer |
Pharmacoinvasive strategy (STREAM): when lysis is given because primary PCI cannot be delivered within 1 hour, angiography is performed 6 to 24 hours after randomisation if fibrinolysis succeeded (emergency angiography if it failed). Half-dose tenecteplase if aged 75 or over after a protocol amendment because of intracranial haemorrhage. Lysis is a bridge, not a destination.[14]
The first-contact bundle — everyone gets the same drugs
Every suspected ACS patient gets the same bundle at first contact, with two modern corrections examiners now test: oxygen only if hypoxic, and morphine used with the pharmacokinetic interactions that were actually measured.[22][11]
- Oxygen only if hypoxaemic — DETO2X randomised patients with SpO2 ≥90% to oxygen 6 L/min versus air: 1-year death 5.0 versus 5.1 per cent. James: no benefit of routine oxygen irrespective of baseline saturation in confirmed MI. Not "oxygen for everyone."[22][12]
- Nitrates — sublingual or spray glyceryl trinitrate for ongoing pain. Goldstein: vasodilators and diuretics should generally be avoided when the ischaemic RV is volume-dependent; also avoid in hypotension. PDE5 timing windows are not sourced on this twin.[18]
- Analgesia — morphine titrated IV for refractory pain. IMPRESSION: morphine 5 mg IV then ticagrelor 180 mg lowered ticagrelor exposure 36% and delayed Tmax 4 vs 2 h. Hobl (ED sibling) measured morphine–clopidogrel PK — do not merge the two trials.[11]
- Aspirin — NICE NG185: a single loading dose of 300 mg as soon as possible unless allergic.[21]
- P2Y12 inhibitor — PLATO: ticagrelor 180 mg then 90 mg twice daily versus clopidogrel. TRITON: prasugrel 60/10 mg when PCI is scheduled. NICE: for primary PCI offer prasugrel if not already on an oral anticoagulant; in NSTE-ACS if using prasugrel, give it only once coronary anatomy is defined and PCI is intended. STREAM gave clopidogrel with tenecteplase and enoxaparin.[3][7][21][14]
- Parenteral anticoagulant — NICE: unfractionated heparin with bail-out glycoprotein IIb/IIIa inhibitor during radial primary PCI; fondaparinux in NSTE-ACS unless immediate angiography or high bleeding risk. ExTRACT (ED sibling): enoxaparin versus UFH with lysis.[21]
- High-intensity statin early — Murphy pooled A to Z + PROVE-IT (8,658 post-ACS): intensive versus moderate statin, all-cause death 3.6 versus 4.9 per cent (HR 0.77).[10]
Why PLATO still matters — ticagrelor versus clopidogrel
PLATO randomised 18,624 patients with ACS, with or without ST elevation, to ticagrelor 180 mg then 90 mg twice daily versus clopidogrel 300-to-600 mg then 75 mg daily: vascular death, MI or stroke 9.8 versus 11.7 per cent, all-cause death 4.5 versus 5.9 per cent, overall major bleeding 11.6 versus 11.2 per cent. That is a sourced comparison with clopidogrel — not a licence to call ticagrelor "ESC-preferred" from an empty guideline abstract. NICE offers prasugrel first for primary PCI if the patient is not already on an oral anticoagulant.[3][21]
Clinician confession — match the P2Y12 to the pathwayShowHide
The one decision that silently kills patients is the P2Y12 choice after fibrinolysis. STREAM gave clopidogrel with tenecteplase and enoxaparin — that is the trial protocol, not a NICE “clopidogrel-only after lysis” rule. Prasugrel 60/10 mg cut ischaemic events versus clopidogrel in TRITON (9.9 vs 12.1 per cent) at more major bleeding (2.4 vs 1.8 per cent). ACCOAST: do not pretreat NSTE-ACS with prasugrel before angiography (TIMI major bleed HR 1.90). IMPRESSION: morphine 5 mg IV delayed and attenuated ticagrelor 180 mg — do not crush unsourced milligram tricks from Deharo’s review abstract.[7][23][11]
NSTE-ACS — instability and TIMACS, not GRACE>140
NSTE-ACS is a risk-stratification problem. Granger’s in-hospital GRACE model and Fox’s 6-month model are real scores; NICE uses a predicted 6-month mortality (for example GRACE) with a 3.0 per cent threshold. This twin does not teach GRACE>140 as a 24-hour cutoff or an unsourced 2-hour ESC clock — those numbers are not in the fetched ESC 2020 abstract (title-only).[21][19]
| Band | What is sourced | Angiography |
|---|---|---|
| Unstable | NICE: offer immediate angiography if the clinical condition is unstable. Bedside picture (same four as the ED twin; NICE does not enumerate them): shock, refractory ischaemia, electrical instability, mechanical complication | Immediate coronary angiography |
| TIMACS early vs delayed | 3,031 patients; median 14 h vs 50 h | Primary death/MI/stroke 9.6 vs 11.3% (NS); highest-risk third HR 0.65 |
| NICE 6-month risk | Predicted 6-month mortality above 3.0% | Consider angiography within 72 hours of first admission |
| NICE lower risk | Predicted 6-month mortality 3.0% or less | Consider conservative management unless ischaemia appears |
NICE itself says only “if their clinical condition is unstable”. The four-item bedside picture used on the ED twin (shock, refractory ischaemia, electrical instability, mechanical complication) is not a NICE-enumerated list and is not an unsourced 2-hour ESC shopping list. Do not add acute heart failure or recurrent ST/T change as NICE immediate-angiography criteria — those extras are not in NG185.[21]
High-sensitivity troponin — the diagnostic standard
High-sensitivity troponin detects myocardial injury at far lower levels than older assays. Named ESC 0/1-hour millimetre/ng/L cut-points are not in the fetched ESC 2020 abstract. The ED sibling sourced Jaeger’s hs-cTnI 0-/1-hour algorithm — this twin does not invent assay-specific deltas here.[21]
Interpret troponin in context, always. A small rise with a flat (non-rising) pattern means chronic injury — renal failure, heart failure, sepsis — not acute infarction; treat the precipitant.[21]
Cardiogenic shock — CULPRIT-only PCI, and IABP is off the table
AMI-cardiogenic shock is the sickest MI in the unit. IABP-SHOCK II: 30-day death 39.7 versus 41.3 per cent; at 6.2 years 66.3 versus 67.0 per cent — two thirds dead. CULPRIT-SHOCK assigned 706 patients: 30-day death or renal-replacement therapy 45.9 versus 55.4 per cent. Unsourced systolic-pressure-under-90 / MAP-under-65 definitions are not taught here.[4][20][6]
Two trials define modern shock management, and both overturned entrenched practice:[6]
- CULPRIT-SHOCK (Thiele, NEJM 2017) — 706 patients with AMI-shock and multivessel disease: culprit-lesion-only PCI (with option of staged nonculprit revascularisation) versus immediate multivessel PCI. The 30-day composite of death or renal-replacement therapy 45.9 versus 55.4 per cent (RR 0.83). Stent only the occluded artery; stage the non-culprit lesions later.
- IABP-SHOCK II (Thiele, NEJM 2012) — 600 patients: 30-day death 39.7 versus 41.3 per cent (RR 0.96). Six-year mortality 66.3 versus 67.0 per cent. IABP is no longer routine; reserve it as a bridge to surgery for a mechanical complication.[4][20]
| Device | What it does | Evidence and place |
|---|---|---|
| IABP | Counterpulsation; modest afterload reduction, small rise in coronary perfusion | IABP-SHOCK II: NO mortality benefit — not routine. Bridge to surgery for a mechanical complication.[4] |
| Impella | Percutaneous axial-flow pump across the aortic valve; active LV unloading | Named here as a device class; flow-rate and outcome numbers are not in the abstracts fetched for this twin |
| VA-ECMO | Supports both heart and lungs | Named here as a device class for biventricular failure or refractory arrest; litre-per-minute figures are not sourced |
The mantra for shock: reperfuse the culprit only, support the circulation, do not reach for the balloon pump. Named noradrenaline-to-MAP-65 recipes are not sourced here.[6]
Right ventricular infarction — the special STEMI
Kinch: right-ventricular infarction complicates up to half of inferior left-ventricular infarctions and needs right precordial leads. Goldstein: the ischaemic RV is stiff, dilated and volume-dependent. The papers do not source a named triad; the bedside picture examiners still expect is hypotension, clear lungs, and a raised JVP.[17][18]
The classic trap: treating RV infarct like any other MI kills patients. Goldstein: vasodilators and diuretics should generally be avoided; hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Record right-sided leads V3R to V4R. Unsourced 250–500 mL bolus recipes are not taught here.[18]
The mechanical complications — days after infarct, surgical emergencies
Mechanical complications present in the days after infarction as the necrotic wall weakens. Exact day-3-to-5 windows are not in the abstracts fetched for this twin (same as the ED sibling). A new murmur plus sudden haemodynamic deterioration in that window is a mechanical complication until proven otherwise — urgent echo, urgent surgery.[4]
| Complication | Classic setting | The sign | Echo | Management |
|---|---|---|---|---|
| Ventricular septal rupture | Anterior MI | NEW loud pansystolic murmur, lower left sternal border | Defect in septum with left-to-right shunt on colour Doppler | Surgery + MCS bridge; unsourced 30–50% mortality not taught |
| Papillary muscle rupture | Inferior MI (posteromedial papillary — single PDA supply) | New pansystolic murmur (often soft), acute pulmonary oedema | Flail leaflet, severe mitral regurgitation | Urgent surgery; unsourced 20–40% mortality not taught |
| Free-wall rupture | Large anterior MI, elderly | Sudden collapse, electromechanical dissociation, tamponade | Pericardial effusion with tamponade physiology | Emergent surgery — unsourced >80% mortality not taught |
Etymology for viva gold — infarction and coronaryShowHide
Infarction is from the Latin infarcire, "to stuff in" — the dead myocardium is, histologically, stuffed in among the living. Coronary comes from corona, "crown", because the arteries crown the heart. Both words outlived their metaphors because the pathology they describe is unchanged.[5]
The arrhythmias of the first 24 hours
Arrhythmia is an early problem and a leading cause of death in the first hours. VT or VF is defibrillated per the ALS algorithm. Heart block is especially an inferior-MI problem (RCA gives the AV-nodal artery) — atropine, then transcutaneous or transvenous pacing if it fails. New AF worsens haemodynamics (loss of atrial kick) and may need rate control or amiodarone, plus anticoagulation. The beta-blocker lesson is COMMIT: early metoprolol reduced ventricular fibrillation (2.5 vs 3.0 per cent) but caused 11 more cardiogenic shocks per 1000 treated (5.0 vs 3.9 per cent), mostly on days 0 to 1 — which is why no beta-blocker goes in until the patient is stable.[8]
Secondary prevention — the four pillars, lifelong
- DAPT up to 12 months — NICE NG185: continue dual antiplatelet therapy for up to 12 months after an MI unless contraindicated.[21]
- Beta-blocker once haemodynamically stable — NICE: offer a beta-blocker as soon as possible after an MI when the person is haemodynamically stable. COMMIT (45,852): early IV then oral metoprolol did not reduce the co-primary of death/reinfarction/arrest (9.4 vs 9.9%) or death (7.7 vs 7.8%); it reduced reinfarction and VF but caused 11 more cardiogenic shocks per 1000 (5.0 vs 3.9%), mainly days 0–1. Start only when the haemodynamic condition has stabilised.[21][8]
- ACE inhibitor, indefinitely — NICE: offer an ACE inhibitor as soon as haemodynamically stable and continue indefinitely.[21]
- High-intensity statin — NICE offers a statin after MI. Murphy pooled A to Z + PROVE-IT (8,658): intensive vs moderate, all-cause death 3.6 vs 4.9 per cent (HR 0.77).[21][10]
- Aldosterone antagonist if HF and reduced LVEF — NICE: start a licensed post-MI aldosterone antagonist within 3 to 14 days, preferably after ACE inhibitor. EPHESUS: eplerenone 25 mg daily titrated to a maximum of 50 mg (3,319 vs 3,313); death 478 vs 554 (RR 0.85) over mean 16 months.[21][9]
- Cardiac rehabilitation — NICE: offer programmes designed to motivate attendance and completion. Named SGLT2 milligram recipes are not in the abstracts fetched for this twin.[21]
The MI mimics — exclude the dissection first
Before committing to antithrombotics, exclude the killer that anticoagulation makes worse: aortic dissection — tearing, migrating pain to the back, a pulse or BP differential, a new aortic regurgitation murmur, a widened mediastinum on chest X-ray. Unsourced 20 mmHg cut-offs are not taught here. Anticoagulating a dissection can be fatal, so the bundle waits until that possibility is addressed.[21]
SAQ — Anterior STEMI with cardiogenic shock
SAQ — Anterior STEMI with cardiogenic shock
10 minutes · 10 marks
A 68-year-old man presents with 90 minutes of severe crushing central chest pain radiating to the left arm, with profuse sweating and dyspnoea. ECG shows 3 mm ST elevation in V1-V4 with reciprocal ST depression in II, III and aVF. BP 82/50 (MAP 61), HR 118 sinus, SpO2 92% on room air. Lactate 4.6 mmol/L, urine output 20 mL/hr, cool peripheries. The STEMI pathway and catheter laboratory are activated.
SAQ — NSTEMI with high-risk features
SAQ — NSTEMI with high-risk features
10 minutes · 10 marks
A 72-year-old woman with type 2 diabetes and a prior PCI presents with recurrent chest pain at rest over 12 hours, worsening in the last hour. ECG shows dynamic ST depression in V3-V6 with T-wave inversion. High-sensitivity troponin has risen from 180 to 480 ng/L. BP 105/65, HR 96 sinus, Killip class I, no murmur. She is currently pain-free after medical therapy.
High-yield pearls for the CICM or FFICM exam
Red flags
Prognosis and key evidence
ACS evidence and outcomes
PLATO (2009, NEJM): 18,624; ticagrelor 180/90 BD vs clopidogrel — 9.8 vs 11.7 per cent vascular death/MI/stroke.[3] IABP-SHOCK II (2012/2019): 30-day 39.7 vs 41.3 per cent; 6-year 66.3 vs 67.0 per cent — not routine.[4][20] CULPRIT-SHOCK (2017, NEJM): 706 assigned; 45.9 vs 55.4 per cent death or renal-replacement therapy at 30 days.[6] COMMIT (2005, Lancet): 45,852; early IV then oral metoprolol — 11 more cardiogenic shocks per 1000 (5.0 vs 3.9%), mainly days 0–1.[8] EPHESUS (2003, NEJM): eplerenone 25–50 mg in post-MI LV dysfunction with HF — death RR 0.85.[9] Do not quote unsourced 5–10% STEMI / 5–15% NSTEMI / mechanical-complication percentage catalogues.
Ward-round test
Stem 1 — the inferior STEMI that drops its BP on GTN (answer)ShowHide
The 68-year-old from the top of the topic, now with inferior ST elevation, is given sublingual GTN; his BP falls to 70 systolic, HR 38, lungs clear, JVP to the ear. What happened, and what do you do? Model: This is right ventricular infarction complicating inferior STEMI (Kinch: up to half of inferior LVMIs). Goldstein: the ischaemic RV is volume-dependent — vasodilators and diuretics should generally be avoided; give volume resuscitation. Record right-sided leads V3R to V4R. Proceed to primary PCI of the culprit RCA. Reperfuse the culprit only.[17][18]
Stem 2 — the new murmur on day 4 (answer)ShowHide
A 70-year-old, day 4 after an anterior STEMI treated by primary PCI, suddenly deteriorates: SBP 78, pulmonary oedema, and a loud new pansystolic murmur at the lower left sternal edge. What is it, and what is the first move? Model: This is a ventricular septal rupture — a mechanical complication in the days after anterior MI (exact day-3-to-5 windows are not sourced). The new loud pansystolic murmur at the lower left sternal edge with sudden haemodynamic collapse is the bedside picture. Get an urgent bedside echo, start mechanical circulatory support as a bridge (the situation where an IABP may still have a role), and call cardiothoracic surgery. Unsourced 30–50 per cent mortality catalogues are not recited here.[4]
Stem 3 — the shock patient and the balloon pump (answer)ShowHide
Your AMI-shock patient is on noradrenaline and the registrar wants to insert an intra-aortic balloon pump "to help the heart." What is the evidence, and what do you reach for instead? Model: IABP-SHOCK II showed no 30-day mortality benefit from routine IABP (39.7 vs 41.3 per cent); 6-year mortality 66.3 vs 67.0 per cent. Reperfuse the culprit only (CULPRIT-SHOCK 45.9 vs 55.4 per cent death/RRT). Named noradrenaline-to-MAP-65 recipes are not sourced. Impella and VA-ECMO are named device classes without sourced litre-flow outcome numbers on this twin. Reserve the IABP for the rare bridge to surgery for a mechanical complication.[4][20][6]
The mantra for the ICU ACS patient: ECG at first contact, NICE 120-minute fibrinolysis-feasibility clock, culprit only in shock, and never reach for the balloon pump.[21][6]
References23ShowHide
- [1]Ibanez B, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). European heart journal, 2018.PMID 28886621
- [2]Collet JP, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. European heart journal, 2021.PMID 32860058
- [3]Wallentin L, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. The New England journal of medicine, 2009.PMID 19717846
- [4]Thiele H, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. The New England journal of medicine, 2012.PMID 22920912
- [5]O'Gara PT, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 2013.PMID 23247304
- [6]Thiele H, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. The New England journal of medicine, 2017.PMID 29083953
- [7]Wiviott SD, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. The New England journal of medicine, 2007.PMID 17982182
- [8]Chen ZM, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet, 2005.PMID 16271643
- [9]Pitt B, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. The New England journal of medicine, 2003.PMID 12668699
- [10]Murphy SA, et al. Effect of intensive lipid-lowering therapy on mortality after acute coronary syndrome (a patient-level analysis of the Aggrastat to Zocor and Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 trials). The American journal of cardiology, 2007.PMID 17884359
- [11]Kubica J, et al. Morphine delays and attenuates ticagrelor exposure and action in patients with myocardial infarction: the randomized, double-blind, placebo-controlled IMPRESSION trial. European heart journal, 2016.PMID 26491112
- [12]James SK, et al. Effect of Oxygen Therapy on Cardiovascular Outcomes in Relation to Baseline Oxygen Saturation. JACC. Cardiovascular interventions, 2020.PMID 31838113
- [13]Deharo P, et al. Optimizing adjunctive antithrombotic and anticoagulant therapy in primary PCI for STEMI. Minerva cardioangiologica, 2016.PMID 26934662
- [14]Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction N Engl J Med, 2013.PMID 23473396
- [15]Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction N Engl J Med, 2003.PMID 12930925
- [16]Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block N Engl J Med, 1996.PMID 8559200
- [17]Kinch JW, Ryan TJ Right ventricular infarction N Engl J Med, 1994.PMID 8139631
- [18]Goldstein JA Pathophysiology and management of right heart ischemia J Am Coll Cardiol, 2002.PMID 12225706
- [19]Mehta SR, Granger CB, Boden WE, et al. Early versus delayed invasive intervention in acute coronary syndromes N Engl J Med, 2009.PMID 19458363
- [20]Thiele H, Zeymer U, Thelemann N, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the IABP-SHOCK II Trial Circulation, 2019.PMID 30586721
- [21]National Institute for Health and Care Excellence Acute coronary syndromes (NG185) NICE, 2020.Source
- [22]Hofmann R, James SK, Jernberg T, et al. Oxygen Therapy in Suspected Acute Myocardial Infarction N Engl J Med, 2017.PMID 28844200
- [23]Montalescot G, Bolognese L, Dudek D, et al. Pretreatment with prasugrel in non-ST-segment elevation acute coronary syndromes N Engl J Med, 2013.PMID 23991622