What is the definition, relevant anatomy, etiology, signs, symptoms, diagnosis, and management of inferior STEMI (ST-Elevation Myocardial Infarction) in an adult patient with a history of cardiovascular disease or risk factors?

Inferior STEMI: Comprehensive CVICU Guide

Definition

Inferior ST-Elevation Myocardial Infarction (STEMI) is acute myocardial necrosis caused by complete thrombotic occlusion of the right coronary artery (RCA) in 85% of cases or left circumflex artery (LCx) in 15%, presenting with ST-segment elevation ≥1 mm in contiguous inferior leads (II, III, aVF). 1, 2

Relevant Anatomy and Physiology

Coronary Territory

• The RCA supplies the inferior wall of the left ventricle, the right ventricle in most patients, and the inferior interventricular septum 2
• The RCA provides blood flow to the sinoatrial node in 60% of patients and the atrioventricular node in 90% of patients 3
• The LCx supplies the inferior-lateral wall when it is the culprit vessel 2

Right Ventricular Involvement

• RV infarction complicates 30-50% of inferior STEMIs and carries 25-31% in-hospital mortality 4
• The RV is a thin-walled, compliant chamber that depends heavily on adequate preload for cardiac output 4
• Acute RV dilation causes increased intrapericardial pressure with pericardial restraint, interventricular septal shift toward the left ventricle, and reduced LV preload 4

ECG Localization

• ST elevation in lead III exceeding lead II predicts RCA culprit with 94% sensitivity and 85% positive predictive value 2
• ST elevation in lead II exceeding lead III predicts LCx culprit with 94% specificity 2

Etiology and Pathophysiology

Thrombotic Mechanism

• Plaque rupture or erosion with subsequent thrombosis causes complete coronary occlusion in the majority of cases 1
• Platelet adhesion and aggregation initiate mural thrombus formation, while fibrin stabilizes the early platelet thrombus 3
• The thrombotic response is dynamic—thrombosis and clot lysis occur simultaneously with vasospasm, causing intermittent flow obstruction and distal embolization 3

Myocardial Necrosis Timeline

• Myocardial necrosis begins 15-30 minutes after complete coronary occlusion and progresses from subendocardium to subepicardium in a time-dependent "wave-front phenomenon" 3
• In 25-30% of patients undergoing primary PCI, initial angiography shows a patent infarct-related artery due to spontaneous lysis 3

Signs & Symptoms

Classic Presentation

• Chest pain or discomfort lasting >10-20 minutes, not fully responsive to nitroglycerin, with radiation to neck, lower jaw, or left arm 3
• Associated symptoms include diaphoresis, nausea, vomiting, and dyspnea 3
• Approximately one-third of patients experience symptoms other than chest pain, particularly the elderly, women, and diabetics 3

Atypical Presentations

• In elderly patients, fatigue, dyspnea, faintness, or syncope are common presentations 3
• Epigastric or interscapular pain may occur 3

Physical Examination Findings

• Pallor, sweating, and evidence of autonomic nervous system activation 3
• Hypotension or narrow pulse pressure 3
• Irregularities of pulse, bradycardia (common with inferior STEMI), or tachycardia 3
• Third heart sound and basal rales if LV involvement 3

Typical CVICU Presentation

Clinical Triad of RV Infarction

• Hypotension, clear lung fields, and elevated jugular venous pressure in the setting of inferior MI—though this triad has sensitivity <25% 4
• Kussmaul's sign (paradoxical rise in jugular venous pressure with inspiration) is a key clinical indicator 4

Hemodynamic Profile

• Low cardiac output with elevated right atrial pressure but normal or low pulmonary capillary wedge pressure 3, 4
• Systolic blood pressure may be 70-100 mmHg with signs of shock 3

Arrhythmias

• Bradycardia and high-degree AV block occur frequently due to RCA supplying the AV node in 90% of patients 3
• Ventricular arrhythmias may occur 3

Diagnosis & Evaluation

12-Lead ECG (Primary Diagnostic Tool)

• A 12-lead ECG must be obtained and interpreted within 10 minutes of presentation 3
• ST-segment elevation ≥1 mm in two contiguous inferior leads (II, III, aVF) establishes the diagnosis 3
• If initial ECG is not diagnostic but clinical suspicion remains high, repeat ECGs at 5-10 minute intervals or use continuous 12-lead ST-segment monitoring 3

Right Ventricular Lead Assessment

• In all patients with inferior STEMI, obtain right precordial lead V4R immediately—ST-segment elevation ≥1 mm in V4R is the single most predictive finding for RV infarction 3, 4
• This finding may resolve within 10 hours of symptom onset, making early recording crucial 4

Echocardiography

• Patients with inferior STEMI and hemodynamic compromise should undergo echocardiography to screen for RV infarction (Class I, Level B) 3
• Echocardiography identifies regional wall-motion abnormalities within minutes of coronary occlusion 3
• Useful for diagnosing mechanical complications (papillary muscle rupture, ventricular septal rupture, free wall rupture) 3

Cardiac Biomarkers

• Elevated CK-MB and troponins confirm myocardial necrosis, but do not wait for biomarker results to initiate reperfusion treatment 3

Hemodynamic Monitoring

• Pulmonary artery catheter insertion is a Class I indication for hypotension not responding promptly to initial fluid administration 3, 4
• Target right atrial pressure ≥10 mm Hg and >80% of pulmonary wedge pressure 4
• Optimal left ventricular diastolic filling pressure (pulmonary artery wedge pressure) should be maintained at 14-18 mm Hg 4

Interventions/Treatments: Medical and Nursing Management

Immediate Reperfusion Strategy

Primary PCI (Preferred)

• Primary PCI is the preferred reperfusion strategy if door-to-balloon time can be achieved within 90 minutes 3, 5, 1
• In elderly patients (>70 years), the absolute mortality advantage of PCI over fibrinolysis increases with age, from 1% at age 65 to 6.9% at age >85 years 5
• Early reperfusion reduces mortality from >85% to approximately 60% in shock patients 4

Fibrinolytic Therapy

• If primary PCI cannot be performed within 120 minutes of diagnosis, administer fibrinolysis unless contraindicated 3, 5
• Prehospital fibrinolysis should be started within 30 minutes of EMS arrival if EMS has capability and patient qualifies 3
• Hospital door-to-needle time should be within 30 minutes for patients transported to non-PCI-capable hospitals 3

Antiplatelet and Antithrombotic Therapy

• Administer aspirin 162-325 mg loading dose immediately 5
• Administer P2Y12 inhibitor: ticagrelor 180 mg or prasugrel 60 mg loading dose 5
• Continue dual antiplatelet therapy (DAPT) for 12 months unless excessive bleeding risk 5
• Glycoprotein IIb/IIIa inhibitors (especially abciximab) provide added value in STEMI patients undergoing PCI 6

Management of RV Infarction

Volume Resuscitation (Critical First-Line Therapy)

• Administer intravenous normal saline aggressively—begin with 500-2500 mL bolus, followed by 500 mL/hour—to maintain elevated right-sided filling pressure 4
• This is the single most important initial intervention for RV infarction 3, 4
• Avoid nitrates, diuretics, and vasodilators—these can precipitate catastrophic hypotension 4

Inotropic Support

• Dobutamine 5-20 mcg/kg/min is the preferred inotropic agent when cardiac output fails to increase after adequate volume loading 3, 4
• If systolic blood pressure remains <80 mm Hg despite fluids, initiate dopamine 5-15 mcg/kg/min 3, 4
• For marked hypotension, norepinephrine may be required initially until systolic pressure reaches at least 80 mm Hg, then transition to dopamine 4

Maintaining AV Synchrony

• AV sequential pacing is indicated for symptomatic high-degree heart block unresponsive to atropine—loss of atrial contraction severely compromises RV filling and cardiac output 3, 4
• Treat bradycardia aggressively with atropine if there is evidence of low cardiac output, peripheral hypoperfusion, or frequent premature ventricular contractions (Class I) 4
• Do not use atropine for type II AV block or third-degree AV block with new wide QRS—pacemaker insertion is the treatment of choice 4
• Prompt cardioversion for hemodynamically significant supraventricular tachycardia is essential 4

Mechanical Support

• Intra-aortic balloon counterpulsation is recommended for STEMI patients with low-output state (Class I, Level B) 3
• IABP is recommended when cardiogenic shock is not quickly reversed with pharmacological therapy as a stabilizing measure for angiography and prompt revascularization (Class I, Level B) 3

Nitroglycerin Administration

• Nitroglycerin sublingual, then 10-20 mcg/min IV if systolic blood pressure >100 mm Hg 3
• Contrary to traditional teaching, prehospital nitroglycerin administration to patients with inferior STEMI is not associated with higher rates of hypotension compared to non-inferior STEMI (8.2% vs 8.9%, p=0.73) 7
• However, in confirmed RV infarction, nitrates are absolutely contraindicated 4

ACE Inhibitors

• Short-acting agents such as captopril 1-6.25 mg can be used as second-line therapy after hemodynamic stabilization 3
• For patients with impaired ejection fraction (<40%) or early heart failure, ACE inhibitors should be started within the first 24 hours if no contraindications exist 8

Beta-Blockers

• Avoid IV beta-blockers initially if any signs of heart failure, low output state, or increased cardiogenic shock risk (age >70, systolic BP <120 mmHg) 5

Statin Therapy

• Start high-intensity statin therapy during hospitalization 5

Immediate Nursing Priorities

First 10 Minutes

• Obtain and interpret 12-lead ECG within 10 minutes of arrival 3
• Obtain right precordial lead V4R in all inferior STEMIs 3, 4
• Establish IV access with large-bore catheters 4
• Administer aspirin 162-325 mg (chewed) 5

Continuous Monitoring

• Establish continuous ECG monitoring immediately for at least 48-72 hours to detect life-threatening arrhythmias 4
• Monitor blood pressure, heart rate, oxygen saturation continuously 3
• Monitor for signs of RV infarction: hypotension with clear lungs, elevated JVP, Kussmaul's sign 4

Volume Management

• If hypotension with suspected RV infarction, initiate aggressive IV normal saline bolus 500-2500 mL 4
• Prepare for pulmonary artery catheter insertion if hypotension does not respond promptly to initial fluids 4

Reperfusion Coordination

• Activate catheterization laboratory immediately—target door-to-balloon time <90 minutes 3, 5
• If transfer required for PCI, coordinate emergency transport 3

Potential Complications

Mechanical Complications

Papillary Muscle Rupture

• Presents with acute severe mitral regurgitation and new cardiac murmur 3
• Requires urgent cardiac surgical repair (Class I) 3
• Insert IABP and obtain urgent surgical consultation 3

Ventricular Septal Rupture (VSR)

• Presents with new harsh holosystolic murmur and acute hemodynamic deterioration 3
• Requires urgent cardiac surgical repair with CABG performed at the same time (Class I, Level B) 3
• Insert IABP and obtain prompt surgical referral for almost every patient 3
• Invasive monitoring recommended with judicious use of inotropes and vasodilators 3

Free Wall Rupture

• Presents with sudden hemodynamic collapse, often with electromechanical dissociation 3
• Requires urgent cardiac surgical repair with CABG at the same time (Class I) 3

Cardiogenic Shock

• Occurs in high-risk patients, particularly elderly diabetics with anterior extension 5
• IABP is recommended when shock is not quickly reversed with pharmacological therapy (Class I, Level B) 3
• Early reperfusion is critical 4

Arrhythmic Complications

• High-degree AV block occurs frequently—requires temporary pacing if symptomatic and unresponsive to atropine 3, 4
• Ventricular tachycardia/fibrillation may occur 3
• Atrial fibrillation with rapid ventricular response compromises RV filling 4

Heart Failure

• May develop acutely or subacutely 3
• In RV infarction, pulmonary edema is uncommon unless there is concomitant LV dysfunction 4

Relevant Red Flags & CVICU Tips

Critical Red Flags

RV Infarction Recognition

• Any inferior STEMI with hypotension should be assumed to have RV involvement until proven otherwise 3, 4
• Obtain V4R lead immediately—do not delay 4
• The clinical triad (hypotension, clear lungs, elevated JVP) has low sensitivity—absence does not exclude RV infarction 4

Medication Pitfalls

• Never give nitrates, diuretics, or vasodilators to patients with suspected RV infarction before confirming adequate preload—this can cause catastrophic hypotension 4
• Morphine can cause venodilation and hypotension in RV infarction—use cautiously 4

Volume Management Errors

• The majority of hypotensive MI patients have high LV filling pressures and pulmonary edema, NOT RV infarction—hemodynamic monitoring is crucial to distinguish these 4
• Inadequate volume resuscitation is the most common error in RV infarction management 4

CVICU Tips

Hemodynamic Optimization

• The pressure gradient between right and left atria becomes the critical driving force for pulmonary perfusion in RV infarction 4
• Maintain right atrial pressure ≥10 mm Hg and >80% of pulmonary wedge pressure 4
• If concomitant LV dysfunction increases RV afterload, consider arterial vasodilators only after adequate volume resuscitation and hemodynamic stabilization 4

Pacing Considerations

• AV synchrony is critical in RV infarction—loss of atrial kick can reduce cardiac output by 30-40% 3, 4
• Maintain AV sequential pacing if temporary pacemaker is required 4

Surgical Timing

• After infarction leading to clinically significant RV dysfunction, it is reasonable to delay CABG surgery for 4 weeks to allow recovery of contractile performance (Class IIa, Level C) 3

ECG Interpretation

• ST-segment elevation can have multiple causes including pericarditis, old STEMI with aneurysm, coronary spasm, conduction abnormalities, and early repolarization 3
• In resource-limited settings, assume ST-segment elevation with appropriate chest pain is coronary occlusion and refer to higher level of care 3

Expected Course and Prognostic Clues

Early Phase (0-48 Hours)

• Peak risk for mechanical complications occurs 3-7 days post-infarction 3
• Arrhythmias are most common in first 48 hours 4
• RV function typically begins to recover within 48-72 hours with successful reperfusion 4

Hospital Mortality

• Overall 1-month mortality for STEMI has been reduced to 4-6% in clinical trials with optimal reperfusion and medical therapy 3
• Registry studies show much higher mortality rates (16-25%), suggesting trial patients are lower risk 3
• RV infarction carries 25-31% in-hospital mortality, identifying a high-risk subgroup 4
• Patients on dialysis with STEMI have 21.3% mortality compared to 11.7% for end-stage renal failure not on dialysis 3

Prognostic Factors

• Independent predictors of early death include age, Killip class, time to reperfusion, cardiac arrest, tachycardia, hypotension, anterior infarct location, prior infarction, diabetes mellitus, smoking status, and renal function 3
• Every minute of delay in reperfusion increases myocardial necrosis and mortality risk 5

Long-Term Outcomes

• Substantial numbers of patients experience recurrent cardiovascular events after STEMI despite optimal acute management 1
• Secondary prevention with antiplatelet therapy, statins, ACE inhibitors, and beta-blockers is critical 8, 5
• RV contractile performance typically recovers over 4 weeks in survivors 3