01Approach to the Critical Patient/attcp43

Immediate stabilization

›Time-critical actions

›Stop nitrates and diuretics immediately if RVMI suspected

›Nitrates are Class III (harm) per ACC/AHA in RV infarction

›Sublingual NTG can precipitate cardiovascular collapse

›IV access: two large-bore peripheral IVs

›Cardiac monitor, continuous pulse oximetry

›12-lead ECG plus right-sided leads (V3R, V4R) immediately

›Aspirin 325 mg chewed immediately

›Heparin per standard STEMI protocol

›P2Y12 inhibitor per institutional STEMI pathway

Hemodynamic targets

›Volume resuscitation strategy

›NS 250-500 mL bolus aliquots targeting SBP >90 mmHg

›Reassess after each bolus with clinical exam and bedside echo

›Avoid excessive volume — worsens RV dilation and causes septal shift

›Target MAP >65 mmHg to maintain coronary perfusion pressure

›Norepinephrine for refractory hypotension

›Dobutamine 2-20 mcg/kg/min if volume loading fails

›Rhythm management

›Atropine 0.5-1 mg IV for HR <50 bpm or symptomatic bradycardia

›Transcutaneous pacing if atropine refractory

›AV sequential pacing preferred over ventricular pacing alone

›Prompt DC cardioversion for atrial fibrillation with hemodynamic compromise

›Loss of atrial kick is poorly tolerated in RV failure

Escalation triggers

›Cardiogenic shock recognition

›Refractory hypotension despite 1-2 L volume loading

02History/hx63

Presenting symptoms

›Chest pain characteristics

›Substernal pressure or squeezing

›Radiation to jaw, left arm, or back

›Onset, duration, severity, response to rest or NTG

›Diaphoresis

›Vagotonic symptoms common with inferior and RV MI

›Nausea and vomiting

›Dyspnea

›Typically without orthopnea or PND (distinguishes from LV failure)

›Lightheadedness or near-syncope

›NTG history

›Profound hypotension after sublingual NTG is a diagnostic clue for RVMI

›Symptom timeline relative to NTG administration

›Number of doses taken prior to arrival

Alarm features

›High-risk symptoms

›Syncope or near-syncope

›AV block or bradyarrhythmia concern

›Low output state

›Palpitations

›VT or atrial fibrillation in setting of RV ischemia

›AF poorly tolerated due to atrial kick dependence

›Altered mental status

›Cardiogenic shock with end-organ hypoperfusion

›Cerebral hypoperfusion

Risk factors

›Standard CAD risk factors

03Physical Exam/exam53

Vital signs

›Hemodynamic profile

›Blood pressure

›Hypotension SBP <90 mmHg present in 25-50% with hemodynamically significant RVMI

›BP discrepancy between arms suggests aortic dissection mimic

›Heart rate

›Bradycardia: sinus bradycardia or AV block from RCA-SA/AV node involvement

›Tachycardia may be absent due to vagotonic physiology

›Respiratory rate

›Tachypnea if cardiogenic shock or concomitant LV failure

›Normal rate with clear lungs supports isolated RVMI

›Oxygen saturation

›Hypoxemia suggests right-to-left shunting through PFO or concomitant LV failure

›Clear lungs with preserved SpO2 supports isolated RV pattern

Classic signs

›Jugular venous pressure

›Elevated JVP or JVD: hallmark finding

›Kussmaul sign: JVP rises with inspiration (paradoxical, highly specific)

›Hepatojugular reflux positive

›Clear lung fields on auscultation

›Distinguishes from LV-predominant cardiogenic shock

›Pulmonary edema suggests concomitant LV dysfunction

›Right-sided gallop

›S3 or S4 at left lower sternal border

›Increases with inspiration (right-sided origin)

›Peripheral perfusion

›Cool, clammy extremities

›Low output cardiogenic shock

04Differential Diagnosis/ddx53

Life-threatening mimics

›Cardiac tamponade

›ICD-10 I31.9

›Similarities: JVD, hypotension, elevated venous pressure

›Distinctions: pulsus paradoxus, muffled heart sounds, pericardial effusion on echo

›Hemodynamics of RVMI more closely resemble constrictive pericarditis than tamponade

›Equalized filling pressures in tamponade

›RV free wall hypokinesis identifies RVMI on echo

›Massive pulmonary embolism

›ICD-10 I26.01

›RV dilation, hypotension, elevated JVP, clear lungs

›ECG: S1Q3T3, sinus tachycardia vs inferior ST elevation in RVMI

›McConnell sign on echo: RV free wall hypokinesis with apical sparing

›CTPA confirms PE

›RV free wall hypokinesis diffuse in RVMI, not sparing apex

›Acute aortic dissection

›ICD-10 I71.00

›Type A can cause coronary malperfusion mimicking inferior STEMI

›Pulse deficits, BP arm discrepancy, tearing pain, widened mediastinum

›CT aorta or TEE to exclude before thrombolytics

›Anticoagulation and thrombolytics are contraindicated in dissection

Other cardiac causes

›LV-predominant cardiogenic shock

›ICD-10 I21.09

›Pulmonary edema distinguishes from isolated RVMI

›Anterior or extensive inferior MI with LV involvement

›Combined RVMI plus LVMI carries highest mortality

›Multivessel CAD pattern

05Laboratory Tests/lt59

Core cardiac biomarkers

›High-sensitivity troponin

›Elevated in RVMI as component of inferior STEMI

›Serial measurements at 0 and 3 hours for trend

›Magnitude of elevation correlates with infarct size

›Kinch and Ryan NEJM 1994: troponin elevation confirms myocardial necrosis

›Right-sided troponin rise confirms RV involvement

›Sensitivity superior to CK-MB alone

›BNP or NT-proBNP

›Elevated with significant RV dysfunction

›Prognostic marker in acute RV failure

›Serial levels guide response to therapy

›BNP >100 pg/mL in context of RV failure supports hemodynamic compromise

›NT-proBNP thresholds age-adjusted

›Houston et al. NEJM 2023 biomarker data

Metabolic and perfusion labs

›Lactate

›Marker of tissue hypoperfusion in cardiogenic shock

›Lactate >=2 mmol/l indicates compromised perfusion

›Serial lactate to assess response to resuscitation

›Lactate >4 mmol/l associated with higher mortality

›Repeat within 1-2 hours if elevated

›Clearance target >10% per hour with resuscitation

›Comprehensive metabolic panel

›Potassium and magnesium

›Hypokalemia and hypomagnesemia increase arrhythmia risk

›Target K+ >4.0 mmol/l and Mg2+ >1.0 mmol/l in acute MI

›Creatinine and eGFR

06Diagnostic Tests/dt81

Scoring Systems

›ACS risk stratification tools

›GRACE score

›Age, heart rate, SBP, creatinine, Killip class, cardiac arrest, ST deviation, troponin

›GRACE >140 = high risk; interventional strategy within 24 hours

›Online calculator available

›TIMI risk score for STEMI

›Age, heart rate, SBP, Killip class, weight, anterior ST elevation or LBBB, time to treatment

›Higher TIMI score correlates with 30-day mortality

›Primarily used for fibrinolytic decision in resource-limited settings

›Killip classification

›Class I: no signs of heart failure

›Class II: S3, bilateral crackles <50% of lung fields

›Class III: pulmonary edema

›Class IV: cardiogenic shock

›RVMI hemodynamic severity stratification

›Mild: RV wall motion abnormality, hemodynamically stable, no arrhythmias

›Moderate: hypotension responsive to volume, transient bradyarrhythmias

›Severe: cardiogenic shock refractory to fluids, requires inotropes or MCS

MRI

›Cardiac MRI role in RVMI

›Gold standard for RV infarct size quantification

›Late gadolinium enhancement maps ischemic territory

›Edema imaging identifies area at risk vs necrosis

›Microvascular obstruction assessment

›No-reflow zone after primary PCI

›Microvascular obstruction predicts poor recovery and adverse remodeling

›RV function quantification

›RV ejection fraction and volumes

›RV free wall strain analysis

›Timing considerations

›Typically performed post-acute phase (days to weeks after PCI)

›Not indicated in emergency setting for acute management decisions

›Stiermaier et al. Heart 2020: CMR frequency and prognostic impact of RV involvement

›Contraindications

›Unstable hemodynamics

›Non-MRI compatible implants or devices

›Claustrophobia without sedation capacity

CT

›CT coronary angiography

›Not the primary tool in STEMI with RVMI

›Invasive coronary angiography is diagnostic and therapeutic

›CTA may be used if diagnosis is uncertain and PE or dissection must be excluded

›Sensitivity and specificity for CAD >95% in elective setting

›Limited data in acute STEMI context

›Calcium scoring and plaque characterization as secondary findings

›CT aorta

›Indicated when aortic dissection cannot be excluded

›Type A dissection can cause coronary malperfusion mimicking inferior STEMI

›BP discrepancy between arms, tearing pain, widened mediastinum

›Sensitivity 100%, specificity 98% for aortic dissection

›ACEP Level B recommendation for CT aorta in dissection workup

›Excludes dissection before thrombolytics or anticoagulation in equivocal cases

›CT pulmonary angiography

›If PE cannot be excluded by ECG, troponin, and echo

›Sensitivity 83-100%, specificity 89-97%

›McConnell sign on echo may guide urgency of CTPA vs catheterization lab

›Contrast and renal function considerations

›Creatinine assessment before iodinated contrast

›Volume preloading in RVMI patients who need CTPA

Ultrasound

›Point-of-care echocardiography

›RV dilation

›RV:LV end-diastolic diameter ratio >0.6 in parasternal short axis

›RV area greater than LV area in apical four-chamber view

›RV free wall hypokinesis or akinesis

›Regional wall motion abnormality in RCA territory

›Diffuse vs regional pattern distinguishes RVMI from PE (McConnell sign)

›Interventricular septal bowing toward LV

›D-shaped LV in parasternal short axis

›Indicates RV pressure or volume overload

›IVC plethora

›Dilated IVC with blunted respiratory variation

›Reflects elevated right atrial pressure

›LVEF assessment

›Preserved LVEF with RV dysfunction: isolated RVMI pattern

›Reduced LVEF: concomitant LV involvement

›Pericardial effusion screen

›Cardiac tamponade exclusion

›Diastolic chamber collapse confirms hemodynamic tamponade

›Valvular assessment

›Tricuspid regurgitation severity

›New MR or VSD: mechanical complication

›ACEP Level B recommendation for bedside echo in suspected RVMI

›Goldstein et al. JACC 2024: echo central to diagnosis and management

07Disposition/dispo47

Level of care

›CCU/ICU indications

›Hemodynamic instability

›SBP <90 mmHg, MAP <65 mmHg

›Vasopressor or inotrope requirement

›High-degree AV block

›Second or third degree AV block

›Temporary pacemaker in place

›Ventricular arrhythmias

›VT or VF episodes

›Antiarrhythmic therapy initiated

›Cardiogenic shock

›Mechanical circulatory support in place

›Escalating support requirements

›Telemetry or step-down

›Hemodynamically stable post-PCI

›No arrhythmias on monitoring

›Volume-responsive hypotension corrected

›Preserved or mildly reduced LVEF post-reperfusion

›Stable vital signs off vasopressors

›No mechanical complications

Observation is not appropriate

›All confirmed RVMI patients require inpatient admission

›Risk of arrhythmia, AV block, or hemodynamic collapse

›Continuous cardiac monitoring mandatory

›Telemetry minimum for stable patients

›High-degree AV block may develop after initial presentation

›Occurs in 10-15% of inferior STEMI

08Treatment/t123

Immediate interventions

›Reperfusion therapy

›Primary PCI: treatment of choice for all RVMI

›Successful reperfusion dramatically reduces arrhythmias and in-hospital mortality

›Goldstein et al. JACC 2024: reperfusion is cornerstone of RVMI management

›Target door-to-balloon time <90 minutes for direct presentations

›First medical contact to balloon <120 minutes including transfers

›Catheterization lab activation from ED simultaneously with resuscitation

›Fibrinolytic therapy if PCI not available within 120 minutes

›Alteplase 15 mg IV bolus then 0.75 mg/kg over 30 min then 0.5 mg/kg over 60 min

›Tenecteplase single weight-based bolus

›Transfer to PCI center after fibrinolysis (pharmaco-invasive strategy)

Antithrombotic therapy

›Aspirin

›325 mg loading dose chewed immediately

›81 mg daily maintenance thereafter

›Class I recommendation ACC/AHA

›P2Y12 inhibitor

›Ticagrelor 180 mg loading dose then 90 mg twice daily

›Preferred over clopidogrel per current guidelines

›Contraindicated with prior hemorrhagic stroke

›Clopidogrel 600 mg loading dose then 75 mg daily

›Alternative if ticagrelor unavailable or contraindicated

›Prasugrel 60 mg loading then 10 mg daily if no prior stroke or TIA

›DAPT duration: minimum 12 months post-STEMI

›Extended DAPT beyond 12 months per bleeding and ischemic risk assessment

›Anticoagulation

›Unfractionated heparin IV

›60 units/kg bolus (max 4000 units) then 12 units/kg/h (max 1000 units/h)

›aPTT target 50-70 seconds

›Bivalirudin 0.75 mg/kg IV bolus then 1.75 mg/kg/h during PCI

›Alternative with lower bleeding risk

›Dose reduce in renal impairment

›Enoxaparin 30 mg IV bolus then 1 mg/kg SC every 12 hours

›Avoid or dose reduce if eGFR <30 mL/min/1.73m2

Volume resuscitation

›IV fluid strategy

›NS 250-500 mL bolus aliquots

›Reassess hemodynamic response after each bolus

›Bedside echo to assess RV size and septal position

›Target SBP >90 mmHg with careful titration

›Avoid >1-2 L without hemodynamic response assessment

›Excessive volume worsens RV dilation and LV filling via pericardial constraint

›Balanced crystalloid acceptable alternative to NS

›No clear superiority data specific to RVMI

›Avoid hypotonic fluids

Vasopressors and inotropes

›Dobutamine

›First-line inotrope if volume loading fails to restore cardiac output

›Starting dose 2-5 mcg/kg/min IV infusion

›Titrate by 2-5 mcg/kg/min every 10-30 minutes

›Maximum dose 20 mcg/kg/min

›Monitor for tachycardia and arrhythmia at higher doses

›Goldstein et al. JACC 2024 and Kinch Ryan NEJM 1994 support dobutamine first-line

›Norepinephrine

›Refractory hypotension to maintain coronary perfusion pressure

›Starting dose 0.01-0.1 mcg/kg/min IV infusion

›Titrate to MAP >65 mmHg

›Maximum dose 1-3 mcg/kg/min in cardiogenic shock

›Arterial line for accurate titration

›Consider vasopressin 0.03-0.04 units/min as norepinephrine-sparing agent

›Milrinone

›Alternative inotrope for refractory RV failure

›Loading dose 50 mcg/kg over 10 minutes (often omitted to avoid hypotension)

›Maintenance 0.375-0.75 mcg/kg/min IV infusion

›Systemic vasodilation risk

›May require concurrent vasopressor

›Dose reduce significantly in renal impairment

Rhythm management

›Bradyarrhythmia management

›Atropine 0.5-1 mg IV for HR <50 bpm or symptomatic bradycardia

›Repeat every 3-5 minutes to total 3 mg

›Class I recommendation for symptomatic sinus bradycardia post-MI

›Transcutaneous pacing if atropine refractory

›Rate 60-80 ppm starting output

›Titrate to capture threshold plus 10 mA safety margin

›Transvenous pacemaker for sustained high-degree AV block

›AV sequential pacing preferred over ventricular pacing

›Atrial kick preservation critical in RV failure

›Atrial fibrillation management

›DC cardioversion if hemodynamically compromised

›Biphasic 200 J synchronized cardioversion

›Sedation before cardioversion

›Rate control if stable and not compromised

›Digoxin 0.25-0.5 mg IV loading; avoid beta-blockers and diltiazem acutely

›Amiodarone 150 mg IV over 10 minutes then 1 mg/min infusion x 6h then 0.5 mg/min x 18h

Mechanical circulatory support

›Escalation pathway for refractory shock

›Intra-aortic balloon pump (IABP)

›For mild hypotension with LV component

›Counter-pulsation augments diastolic perfusion

›Percutaneous RVAD (e.g., Impella RP)

›Severe isolated RV failure with preserved LV

›Decompresses RV and augments forward flow

›Biventricular mechanical support

›Concurrent Impella RP (RV) and Impella CP or 5.5 (LV)

›Biventricular failure pattern

›VA-ECMO

›Profound cardiogenic collapse with refractory hypoxemia

›Bridge to recovery or durable MCS decision

›Team-based decision with advanced heart failure and perfusion

Contraindicated treatments

›Medications to avoid in RVMI

›Nitroglycerin

›Class III (harm) ACC/AHA in RV infarction

›Reduces preload, precipitates cardiovascular collapse

›Diuretics

›Reduce preload, worsen RV hemodynamics

›Contraindicated unless significant LV failure with pulmonary edema also present

›Morphine

›Venodilator effect reduces preload

›Cautious use; may exacerbate hypotension

›Acute beta-blockade

›Avoid with bradycardia or hemodynamic instability

›Can initiate once hemodynamically stable in recovery phase

Secondary prevention

›Post-reperfusion medications

›High-intensity statin

›Atorvastatin 40-80 mg daily or rosuvastatin 20-40 mg daily

›Start in-hospital; Class I recommendation

›ACE inhibitor or ARB

›Ramipril 1.25-10 mg daily titrated

›Beneficial in all post-MI patients with reduced LVEF or diabetes

›Beta-blocker

›Initiate once hemodynamically stable

›Metoprolol succinate 25-200 mg daily or carvedilol 3.125-25 mg twice daily

›Hold in acute setting with bradycardia or cardiogenic shock

›Eplerenone or spironolactone

›If LVEF <40% with symptoms of HF or diabetes

›Eplerenone 25-50 mg daily

›Monitor potassium and renal function

09Special Populations/sp72

Pregnancy

›Pregnancy considerations in RVMI

›Increased plasma volume and cardiac output during pregnancy

›Normal hemodynamic changes may mask or modify RVMI presentation

›JVP elevation baseline in pregnancy complicates interpretation

›Acute MI in pregnancy rare: incidence approximately 6.2 per 100,000 deliveries

›Peripartum period highest risk

›Coronary artery dissection most common mechanism in young pregnant women

›ECG interpretation

›Leftward axis shift is normal in pregnancy

›Right-sided leads still diagnostic for RVMI

›Treatment modifications

›Primary PCI preferred over fibrinolysis

›Fibrinolytics relatively contraindicated in pregnancy (bleeding risk)

›Radial access preferred to minimize groin exposure and fetal irradiation

›Antithrombotic therapy

›Aspirin 81 mg daily acceptable in pregnancy

›Heparin (UFH or LMWH) preferred over direct oral anticoagulants

›P2Y12 inhibitors: clopidogrel limited data; ticagrelor not well studied

›Medications to avoid

›Statins: category X, contraindicated

›ACE inhibitors and ARBs: contraindicated in 2nd and 3rd trimester

›Fetal monitoring

›Continuous fetal monitoring during catheterization if viable gestation

›Obstetric and cardiology co-management

›Abdominal shielding during fluoroscopy

Geriatric

›Older adult features

›Atypical presentation more common

›Dyspnea, syncope, confusion may predominate over chest pain

›Silent MI in diabetic and older patients

›Higher prevalence of multivessel CAD

›More complex PCI decisions

›Higher risk of contrast-induced nephropathy

›Baseline functional status

›Frailty assessment: Clinical Frailty Scale

›Goals of care discussion may be needed

›Medication and dosing adjustments

›Renal dosing of heparin and anticoagulants

›Enoxaparin dose reduce if eGFR <30 mL/min/1.73m2

›UFH with aPTT monitoring preferred in severe renal impairment

›Bleeding risk higher with DAPT

›PRECISE-DAPT score for DAPT duration decision

›HAS-BLED score for anticoagulation risk

›Bradyarrhythmia risk higher

›AV conduction disease more prevalent at baseline

›Lower threshold for temporary pacing in older patients

›Outcome considerations

›In-hospital mortality higher in older adults with RVMI

›Age >75 independent predictor of adverse outcomes

›Cardiogenic shock carries greater mortality in older patients

›RV recovery after reperfusion still possible even in older adults

›Reperfusion benefit maintained regardless of age

›Class I recommendation for primary PCI does not have upper age cutoff

Pediatrics

›Pediatric RVMI

›Extremely rare in children and adolescents

›Typically associated with congenital coronary anomalies

›Kawasaki disease with coronary artery aneurysm most common etiology

›Myocarditis as important mimic

›Viral cardiomyopathy with RV involvement

›CMR helpful for differentiation

›Right heart tumors

›Rhabdomyoma, fibroma causing outflow obstruction

›Echo differentiates from RVMI

›Management differences

›Weight-based dosing for antithrombotics

›Aspirin 3-5 mg/kg/day in Kawasaki disease context

›Heparin: loading dose 75 units/kg over 10 minutes then 20 units/kg/h

›Inotropes weight-based

›Dobutamine 2-20 mcg/kg/min

›Milrinone 0.25-0.75 mcg/kg/min

›Pediatric cardiology consultation mandatory

›Congenital anatomy must be understood before intervention

›Transfer to pediatric cardiac center

10Background/b99

Epidemiology

›Frequency of RV involvement

›RVMI complicates up to 50% of inferior MIs

›Results from proximal RCA occlusion in most cases

›Less commonly: left circumflex in left-dominant system

›Stiermaier et al. Heart 2020: CMR-detected RV involvement in acute MI

›RV involvement confirmed in approximately 30-50% of inferior MIs by CMR

›Even isolated right coronary territory MI carries RV dysfunction risk

›Left circumflex and LAD occlusion rarely cause RVMI

›Left-dominant coronary anatomy prerequisite for circumflex-related RVMI

›LAD-related RVMI: atypical, apical RV involvement

›Mortality and morbidity

›In-hospital mortality RVMI with hemodynamic compromise: 25-30%

›vs 6% for inferior MI without RV involvement

›Kinch and Ryan NEJM 1994 landmark data

›Zehender et al. NEJM 1993: RVMI is independent predictor of prognosis

›30-day mortality 31% with ST elevation in V4R vs 9% without

›Major complications: VT/VF, AV block, cardiogenic shock all higher

›1-year mortality approximately 27% with combined right and left CAD

›vs 18% with isolated RCA lesions

›Multivessel disease worsens prognosis substantially

›Incidence and demographics

›RCA is right-dominant in approximately 85% of individuals

›Dominant RCA anatomy prerequisite for typical proximal RCA-related RVMI

›RV receives blood supply almost exclusively from RCA in right-dominant anatomy

›RVMI affects similar age and sex distribution as overall STEMI population

›Mean age of inferior MI approximately 60-65 years

›Higher male predominance

Pathophysiology

›Coronary anatomy

›Proximal RCA occlusion causes RVMI

›RV marginal branches arise from proximal and mid RCA

›Conus branch supplies RV outflow tract

›RV has lower oxygen demand than LV

›Thinner wall, lower systolic pressure

›Better tolerance of brief ischemia

›Dual blood supply theory

›RV receives oxygen from both coronary flow and Thebesian vessels

›Luminal blood supply supplements formal coronary flow

›RV failure mechanism

›RV ischemia causes acute dilation

›Increased RV wall stress reduces subendocardial perfusion

›Vicious cycle: ischemia, dilation, further ischemia

›Interventricular septal dependence

›Failing RV depends on LV-mediated septal contraction for output

›AV sequential pacing preserves septal function via atrial kick

›Pericardial constraint

›RV dilation within fixed pericardial space shifts septum toward LV

›D-shaped LV impairs LV filling and reduces cardiac output

›Reduced RV preload equals catastrophic failure

›Unlike LV, RV is preload-dependent to maintain output

›Nitrates and diuretics remove essential preload reserve

›RV resilience

›RV has remarkable capacity for recovery after reperfusion

›Most patients recover RV function within days to weeks

›Kinch and Ryan NEJM 1994: RV recovery even after prolonged ischemia

›Hibernation and stunning mechanisms

›Acute dysfunction may exceed infarcted territory

›Successful PCI restores stunned but viable myocardium

›Late prognosis favorable after successful reperfusion

›RV function returns to near-normal in most cases

›Long-term mortality 2-3% per year beyond year 1

Therapeutic Considerations

›Preload preservation is the cornerstone of RVMI management

›Fundamentally different from LV failure physiology

›LV failure: reduce preload and afterload

›RV failure: maintain or increase preload, reduce RV afterload

›Nitrates are contraindicated in RVMI

›ACC/AHA Class III (harm) recommendation

›Wilkinson-Stokes et al. EMJ 2023: systematic review and meta-analysis

›Absolute risk increase approximately 3 adverse events per 100 nitrate administrations

›Diuretics worsen hemodynamics in isolated RVMI

›Reserve for cases with concomitant LV failure and pulmonary edema

›Re-evaluate RV vs LV contribution before diuretic initiation

›Reperfusion changes outcomes

›Successful primary PCI dramatically reduces sustained hypotension

›Arrhythmia burden decreases markedly after reperfusion

›In-hospital mortality reduced substantially compared to medical therapy

›Fibrinolysis is acceptable when PCI not available within 120 minutes

›Pharmaco-invasive strategy: thrombolytics followed by routine angiography

›Rescue PCI for failed reperfusion

›RV recovery after PCI is the norm rather than exception

›Weeks of mechanical support may be bridged until native recovery

›Durable MCS rarely needed if RV is isolated culprit

›AV sequential pacing evidence

›Ventricular pacing alone worsens hemodynamics in RVMI

›Loss of atrial kick reduces cardiac output 25-30%

›AV sequential pacing restores atrial contribution

›High-degree AV block in inferior STEMI

›Occurs in 10-15% of inferior STEMI

›Usually reversible after reperfusion

›Often resolves within hours to days post-PCI

›Mechanical circulatory support principles

›IABP: modest benefit mainly when LV component present

›Counterpulsation reduces LV afterload, indirectly aids RV

›Less effective for pure RV failure

›Percutaneous RVAD most effective for isolated RV shock

›Directly unloads RV and maintains pulmonary flow

›Impella RP can be placed at time of PCI

›VA-ECMO bypasses both ventricles

›For biventricular failure and refractory arrest

›Allows time for pharmacologic support and reperfusion to work

11Patient Discharge Instructions/pdi53

copy discharge instructions

›Right ventricular heart attack home care

›All prescribed medications as directed — do not skip doses

›Blood thinners: aspirin and second antiplatelet medication

›Do not stop antiplatelet medications without calling your cardiologist

›Activity: gradual increase per cardiac rehabilitation program

›No driving until cleared by cardiologist (typically 1-2 weeks minimum)

›Avoid heavy lifting more than 5 kg for 4-6 weeks

›Wounds and access sites

›Keep catheter entry site clean and dry

›No prolonged immersion (bath, pool) until fully healed

›Diet

›Low sodium diet: less than 2 g sodium per day

›Heart-healthy Mediterranean-style eating

›Limit saturated fat and processed food

›No nitroglycerin unless your cardiologist has specifically cleared it

›NTG caused dangerous low blood pressure during your hospital stay

›Call 911 for chest pain — do not take NTG at home without clearance

›Warning signs to return to ER immediately

›Chest pain or pressure

›Any new chest pain, even mild

›Do not wait — call 911

›Breathing difficulty

›Sudden shortness of breath at rest

›Unable to lie flat

›Fainting or near-fainting

›Lightheadedness severe enough to lose consciousness

›Palpitations or irregular heartbeat

12References/r45

Guidelines and key sources

›ACC/AHA STEMI guidelines

›Antman et al. Journal of the American College of Cardiology 2004

›ACC/AHA Guidelines for Management of Patients With ST-Elevation Myocardial Infarction

›Primary PCI Class I recommendation, antithrombotic protocols

›Anderson et al. Journal of the American College of Cardiology 2007

›ACC/AHA Guidelines for Unstable Angina/NSTEMI Management

›Risk stratification and anticoagulation guidance

›Wright et al. Journal of the American College of Cardiology 2011

›2011 ACCF/AHA Focused Update for UA/NSTEMI Guidelines

›AHA Scientific Statements

›Konstam et al. Circulation 2018

›Evaluation and Management of Right-Sided Heart Failure

›RV pathophysiology, inotrope selection, MCS guidance

›Damluji et al. Circulation 2021

›Mechanical Complications of Acute Myocardial Infarction

›VSD, free wall rupture, papillary muscle rupture management

›Rosendorff et al. Circulation 2015

›Treatment of Hypertension in Patients With Coronary Artery Disease

›Nitrate and beta-blocker considerations

Landmark trials and studies

›Foundational RVMI studies

›Kinch JW, Ryan TJ. New England Journal of Medicine 1994

›Right Ventricular Infarction: definitive clinical reference

›Volume resuscitation, dobutamine, pacing guidance

›Zehender et al. New England Journal of Medicine 1993

›RVMI as independent predictor of prognosis after inferior MI

›Prognostic impact of ST elevation in V4R

Evidence & Review