Cardiovascular Conditions · 7 min read
Acute Coronary Syndromes
Acute coronary syndromes (ACS) result from a sudden reduction in coronary blood flow, most often from atherosclerotic plaque rupture or erosion with platelet activation and thrombus formation. A type 1 MI is this atherothrombotic event; a type 2 MI reflects supply–demand mismatch without acute plaque rupture (tachyarrhythmia, anemia, hypotension, hypoxemia, coronary spasm). Myocardial infarction requires a rise and/or fall of cardiac troponin with at least one value above the 99th-percentile upper reference limit plus clinical evidence of ischemia; high-sensitivity assays allow rapid rule-in or rule-out protocols at 0 and 1–3 hours.
| Syndrome | ECG | Troponin | Pathology | Strategy |
|---|---|---|---|---|
| Unstable angina | Normal, transient ST depression, or T-wave inversion | Not elevated | Partial or transient occlusion; no necrosis | Antiplatelet, anticoagulant, risk-guided invasive strategy |
| NSTEMI | ST depression, T-wave inversion, or normal | Rise/fall above 99th percentile | Partial occlusion with necrosis (often subendocardial) | Risk-stratify (GRACE, TIMI); invasive timing by risk |
| STEMI | New ST elevation in ≥2 contiguous leads meeting voltage criteria (or posterior equivalent) | Rises (do not wait for it) | Complete occlusion; transmural injury | Emergent reperfusion |
ECG Criteria for STEMI
- New ST elevation at the J point in ≥2 contiguous leads of ≥1 mm in all leads other than V2–V3.
- In V2–V3: ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, ≥1.5 mm in women regardless of age.
- Posterior MI: ST depression V1–V3 with ST elevation ≥0.5 mm in V7–V9. RV MI: ST elevation ≥1 mm in V4R.
- A new or presumed-new LBBB alone is no longer a STEMI equivalent; apply Sgarbossa criteria and clinical context (ongoing ischemic pain, hemodynamic instability).
| Pattern | ECG Finding | Significance |
|---|---|---|
| Sgarbossa (LBBB or ventricular paced rhythm) | Concordant ST elevation ≥1 mm; concordant ST depression ≥1 mm in V1–V3; or discordant ST elevation that is excessive relative to the S wave (ST/S ratio ≥25%, modified criteria) | Acute occlusion despite baseline conduction abnormality; activate cath lab |
| Wellens pattern | Deep symmetric or biphasic T-wave inversion in V2–V3, often pain-free | Critical proximal LAD stenosis; avoid stress testing; early angiography |
| De Winter pattern | Upsloping ST depression with tall symmetric T waves in precordial leads | Proximal LAD occlusion; treat as STEMI equivalent |
| ST elevation in aVR with diffuse ST depression | aVR elevation ≥1 mm plus widespread ST depression | Left main or multivessel ischemia; high risk |
Presentation
Classic ischemic pain is substernal pressure or heaviness radiating to the arm, neck, or jaw with diaphoresis, dyspnea, and nausea. Atypical presentations — isolated dyspnea, fatigue, epigastric discomfort, nausea, or syncope — are more frequent in women, older adults, and patients with diabetes or chronic kidney disease, and they contribute to delays. A 12-lead ECG within 10 minutes of arrival is required for any suspected ACS; repeat it every 15–30 minutes if the first is nondiagnostic and symptoms persist.
Initial Management
Reperfusion Targets
Primary PCI is the preferred reperfusion strategy for STEMI within 12 hours of symptom onset when first-medical-contact (FMC)-to-device time can be met. When PCI cannot be achieved within 120 minutes of FMC, give fibrinolytic therapy (tenecteplase, alteplase, or reteplase) within 30 minutes of arrival, then transfer to a PCI-capable center: rescue PCI if reperfusion fails (less than 50% ST-segment resolution at 60–90 minutes, persistent pain, or instability), otherwise routine angiography within 2–24 hours (pharmacoinvasive strategy). Primary PCI is also indicated beyond 12 hours with ongoing ischemia, cardiogenic shock, or acute severe HF, regardless of delay.
| Absolute Contraindications | Relative Contraindications |
|---|---|
| Any prior intracranial hemorrhage | Chronic poorly controlled hypertension, or SBP >180 or DBP >110 mmHg on presentation |
| Known cerebrovascular lesion (AVM) or intracranial malignancy | Ischemic stroke more than 3 months ago, dementia |
| Ischemic stroke within 3 months (except acute stroke within 4.5 h being treated) | Traumatic or prolonged CPR (>10 min), major surgery within 3 weeks |
| Suspected aortic dissection | Internal bleeding within 2–4 weeks; noncompressible vascular punctures |
| Active bleeding or bleeding diathesis (excluding menses) | Pregnancy; active peptic ulcer; current oral anticoagulant use |
| Significant closed-head or facial trauma within 3 months; intracranial or spinal surgery within 2 months | — |
Signs of successful reperfusion include abrupt relief of pain, ≥50% resolution of ST elevation, an early troponin peak, and reperfusion arrhythmias — classically accelerated idioventricular rhythm (wide, regular, 40–100/min), which is benign and should not be suppressed. After fibrinolysis, perform neurologic checks for intracranial hemorrhage (headache, change in level of consciousness, new deficit) and avoid unnecessary punctures.
NSTE-ACS: Timing of Invasive Strategy
| Timing | Indications |
|---|---|
| Immediate (<2 h) | Refractory angina, hemodynamic instability or cardiogenic shock, sustained VT/VF, mechanical complication, acute HF clearly related to ischemia, recurrent dynamic ST changes |
| Early (<24 h) | High-risk features: GRACE score >140, rising troponin consistent with NSTEMI, new or dynamic ST depression |
| Delayed or ischemia-guided | Lower-risk patients; noninvasive testing guides need for angiography |
Right Ventricular Infarction
RV infarction accompanies a substantial proportion of inferior MIs from proximal RCA occlusion. The classic triad is hypotension, elevated JVP/CVP, and clear lung fields, often with Kussmaul sign, bradycardia, and AV block. Because the injured RV cannot generate pressure, LV filling depends on venous return and atrial contraction. Management: IV fluid boluses (with careful reassessment, as overdistension can shift the septum and impair LV filling), avoid nitrates, diuretics, and morphine, maintain AV synchrony (AV sequential pacing for high-grade block), add dobutamine if hypotension persists after preload optimization, and reperfuse urgently.
Mechanical and Other Complications
| Complication | Typical Timing / Setting | Key Findings | Management |
|---|---|---|---|
| Papillary muscle rupture (acute MR) | Days 2–7; usually inferior MI (posteromedial muscle has single blood supply from the PDA) | Sudden flash pulmonary edema, hypotension; murmur may be soft or absent; giant V waves on PAOP tracing | Afterload reduction, IABP or other mechanical support as bridge, emergent surgery |
| Ventricular septal rupture | Days 3–5; anterior or inferior MI | New harsh holosystolic murmur at left sternal border, often with thrill; biventricular failure; O₂ saturation step-up from RA to PA | Afterload reduction, mechanical support, surgical or transcatheter closure |
| Free wall rupture | First week; late presentation, older women, no reperfusion | Sudden chest pain, tamponade, PEA arrest | Pericardiocentesis as bridge, emergent surgery |
| LV aneurysm / LV thrombus | Weeks; large anterior MI | Persistent ST elevation; HF, VT, systemic embolism | Anticoagulation for thrombus; HF therapy |
| Early pericarditis vs Dressler syndrome | Days 1–4 vs weeks to months | Pleuritic pain, friction rub | Aspirin (avoid other NSAIDs and steroids early after MI); colchicine |
| Cardiogenic shock | Usually within first 24–48 h; large anterior MI | Hypotension, cool extremities, oliguria, rising lactate | Emergent revascularization of the culprit, vasopressor/inotrope, mechanical support |
Nursing priorities after reperfusion: continuous ST-segment monitoring for reocclusion, access-site and bleeding surveillance, serial troponin and electrolytes (keep K⁺ ≥4.0 and Mg²⁺ ≥2.0 mg/dL), daily auscultation for new murmurs or rub, and teaching on dual antiplatelet therapy adherence — premature discontinuation is the leading modifiable cause of stent thrombosis. Refer every patient to cardiac rehabilitation.
- New LBBB alone is not a STEMI equivalent; use Sgarbossa criteria and clinical instability.
- FMC-to-device ≤90 min (≤120 min with transfer); if PCI cannot be achieved within 120 min, fibrinolysis within 30 min of arrival.
- RV infarction: fluids, no nitrates or diuretics, maintain AV synchrony.
- A new murmur with sudden pulmonary edema or shock days after MI = mechanical complication; prepare for mechanical support and surgery.
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