Coronary artery disease (CAD) affects 16.8 million people worldwide annually, and about half are noted to have a known history of CAD.4
Inferior wall myocardial infarctions (MI) are most commonly caused by an occlusion of the posterior descending artery via the right coronary artery, which is seen in 80% of the population. In the other 20%, it is seen as an occlusion in the circumflex artery.1 MIs affect about 3 million people worldwide, and cause about 1 million deaths in the U.S. annually.2 In 2013, about 40-50% of all MIs were inferior in nature, and it was noted that inferior MIs have a better prognosis compared to other MIs; 2% vs. 9% mortality.1 Recent studies have shown this number to increase to about 12%, especially with right ventricular involvement.3
The main treatment for any coronary occlusion is immediate reperfusion; the preferred involves Percutaneous Coronary Intervention (PCI). According to the American Heart Association (AHA), the gold standard is to allow for door to balloon time within 90 minutes. In the cases of not being in a PCI capable facility, thrombolytics can be administered within 30 minutes of contact with the patient. This standard has not changed in over 20 years. Outside of reaching metrics, when else should thrombolytics be considered? In both scenarios below, acute decompensation was a key driver that pushed providers to give thrombolytics, even while being in a PCI capable center. Although outcomes were different, this may be something to consider in our acute occlusive myocardial infarction (OMI) patients if their courses change while still under our care.
Case Presentation 1
A 69-year-old female with a past medical history of hypertension (HTN), diabetes (DM), questionable history of congestive heart failure (daily lasix and metoprolol), presenting with worsening shortness of breath at night. Per family, the patient has been having trouble breathing for the last week, worse when lying down at nighttime. Denies any new symptoms that made them come to the ED that night. The patient reported no other associated symptoms of dizziness, chest pain, nausea, vomiting, changes in urinary habits. Vitals on arrival remarkable for hypotension (80s systolic) but on repeat normotensive, respiratory rate of 35, saturating 90% on room air. On examination, the patient appeared in mild respiratory distress, but clear in all lung fields. EKG on arrival show normal sinus, questionable depressions in the lateral leads. Initial management included placing the patient on Bi-Level Positive Airway Pressure (BIPAP). Initial bedside echocardiogram demonstrated grossly preserved ejection fraction with no concern for myocardial hypokinesis, mild B lines were seen with a plump IVC.
Labs collected on arrival demonstrated: BUN/Creatinine 85/5.6, glucose 320, potassium 5.2, CO2 9, Anion Gap 23, BHB 0.4. Cardiac labs noted with a trop of 353, BNP >70000. Venous blood gas, pH 7.2, pCO2 27, lactate 4.4, HCO3 11. Patient appeared to be in an Anion Gap Metabolic Acidosis likely secondary to impending DKA vs. Uremia vs. Lactic acidosis vs. AKI/CKD with no known history of renal disease, no history of hemodialysis discussion or use in the past.
One hour into the visit, the patient began to have chest pain and was noted to be hypotensive on one read with systolic in the 80s, MAPs ranging between 50-60s. The patient’s blood pressure was varying during this time, at times normotensive, but majority of hypotensive with MAPs in the 50s. A repeat EKG was conducted showing mild ST elevations in leads II, III, aVL with reciprocal ST depressions in aVL, V4-V5. Serial EKGs confirmed these findings, and STEMI code was called. The patient at this time was consented for emergent PCI, loaded with antiplatelet therapy, heparin, and aspirin, but continued to be hypotensive. At this time, the patient was started on vasopressor and inotropic support with epinephrine infusion, later escalated to Norepinephrine to stabilize prior to catheterization.
The Cardiology team notified the ED team that cardiac cath lab was down, and the patient required transfer to a tertiary center to allow for catheterization. Cardiology initiated transfer and an ambulance would be there shortly to pick up the patient.
At this time, the patient continued to decompensate, with worsening hypotension, worsening tachypnea, diaphoresis, and vomiting.
In light of the peri-code inferior MI, now unstable for transfer, about 1.5 hours into the patient’s ER visit, a decision was made to give thrombolytics; 50 mg of tenecteplase was administered. The decision to intubate for airway protection was made after pushing thrombolytics, as the patient was not hemodynamically stable prior to this intervention and there was hope of some clinical improvement after thrombolysis. The patient did not immediately worsen after thrombolytics, and was intubated in one attempt successfully. Repeat bedside echocardiograms demonstrated worsening global hypokinesis. Patient’s course continued to worsen, hypotension continued, leading to additional vasopressin, phenylephrine, and milrinone infusions. Sodium bicarbonate infusion was added to address the metabolic acidemia, along with treatment for questionable sepsis vs. other etiologies.
Ultimately, the patient became bradycardic, pulseless prior to transfer, and ROSC was not achieved.
Case Presentation 2
A 70-year-old Punjabi-speaking male with past medical history significant for CAD and NSTEMI (10/2017) s/p PCI of the dRCA, HTN, HLD, and DM who presented to the emergency department with complaints of 1 hour of sudden onset substernal, crushing chest pain, and shortness of breath that awoke him from sleep. Patient’s son was present and helped translate and provide history. He noted the patient felt well during the day and had a few beers during a Super Bowl party. He denies vomiting and vision changes since the onset of symptoms, but the patient was too uncomfortable to provide further details.
Per EMS, the patient was given aspirin 325 mg en route to the hospital. On presentation, the patient was initially hypertensive at 191/94 and tachycardic to 134, but on repeat blood pressure 140/82, afebrile, saturating 100% on room air with no respiratory distress. Initial examination showed an uncomfortable appearing, mildly diaphoretic patient. Lung fields were clear to auscultation and cardiac auscultation showed tachycardia, but was otherwise unremarkable with no lower extremity edema. Initial bedside echocardiogram demonstrated preserved EF with no large global hypokinesis, lungs had no b lines and the IVC had respiratory variation.
Initial EKG showed normal sinus rhythm notable for ST elevation in lead AVR and ST depressions in anterior leads V2, V3, V4 and lateral leads V5 and V6.
Cardiology was consulted immediately upon this ECG, and recommended to initiate treatment with plavix loading dose, heparin bolus and drip, admission to Cardiac Critical Unit (CCU). Before medication could be initiated, the patient was found to be standing at bedside with difficulty breathing, rales bilaterally, and B lines on ultrasound. Repeat blood pressure was again elevated with systolics in the 190s. Patient was helped back into bed and given versed for increasing agitation likely secondary to difficulty breathing, oxygen saturations were in the 70s. Started on bipap and high dose nitroglycerin therapy at 300 mcg/min for concern of Sympathetic Crashing Pulmonary Edema (SCAPE) in the setting of possible OMI. After 5 minutes, the patient’s vitals started slowly improving with oxygen into the low 80s and blood pressure 174/95; he remained diaphoretic and the ECG demonstrated worsening ischemia with evolving STEMI concerns.
Cardiology bedside activated Cath Lab but would not be available for one hour, later to find out the lab was not functioning. Family at bedside agreed for thrombolysis for STEMI without emergent PCI capability. The patient was given 50 mg TNKase, remained on bipap and high dose nitroglycerin infusion. The patient was further optimized prior to intubation with oxygen saturations consistently 100%, blood pressure remained elevated but improving slowly. The decision again was made to intubate after thrombolytics for the concern of further deterioration if the patient was not optimized prior to intubation.
Patient was intubated on one single attempt with notably frothy secretions, and placed on propofol for sedation. Nitroglycerin drip was continued, lasix given, and the patient later had resolution of hypertension and SCAPE concerns and nitroglycerin was discontinued. Serial EKGs showed improvement in AVR ST elevation and ST depressions, though persistent, much improved upon transport to CCU.
The patient went for non-emergent cardiac catheterization later in the day and was found to have severe triple vessel disease: 95% stenosis of the proximal LAD, 90% stenosis of the proximal RCA, and 100% stenosis of the RPDA with left to right collaterals. The patient was then transferred to another facility for surgical evaluation for Coronary Artery Bypass Graft vs. high risk PCI management.
The patient went for high risk PCI, LAD was stented, and he followed up with his primary care doctor 3 weeks after this initial emergency visit.
Indications of Thrombolytics
Thrombolytic therapy is indicated for ST-segment elevation myocardial infarction (STEMI) when primary percutaneous coronary intervention (PCI) is unavailable within 120 minutes of first medical contact. This is considered most effective when administered within the first 3 hours of symptom onset. Even if PCI is not feasible, thrombolytics can be considered up to 12 hours of contact. Candidates for thrombolysis must have ST-segment elevation in at least two contiguous leads or a new left bundle branch block (LBBB) with a high suspicion of infarction. Prompt administration, ideally within 30 minutes of hospital arrival, improves outcomes by restoring coronary perfusion.9
However, thrombolytics are contraindicated in patients with high bleeding risks, such as those with a history of hemorrhagic stroke, active internal bleeding, recent major trauma or surgery, or severe uncontrolled hypertension (>180/110 mmHg). While thrombolysis is an important alternative to PCI, patients should be transferred to a PCI-capable center for further evaluation and possible rescue PCI if thrombolysis fails.9
Management of Inferior MI/Cardiogenic Shock
Cardiogenic shock is a life-threatening condition, causing decreased end organ perfusion due to lack of cardiac output. The main cause of cardiogenic shock is cardiac dysfunction secondary to acute myocardial infarction. Patients may be noted to have hypotension; however, recent studies have even noted that hypotension may not always be noted. Decreased cardiac output is the main driver for this type of shock.5
Inotropic agents may be required to increase cardiac contractility, or vasoactive support for hypotension. First line of vasopressors may be norepinephrine, followed by vasopressin. Epinephrine also has some utility in cases when the above fails, and systemic resistance continues to be low as well as having an added inotropic effect. Phenylephrine is alternatively preferred by some cardiologists for hypotension.
Dobutamine is another common agent that can be used as an adjunct. Dobutamine is known as an inodilator; acting as a beta agonist, it increases heart rate but also inhibits cAMP breakdown leading to vasodilation. The idea of vasodilation is important, as it counteracts the compensatory mechanism of vasoconstriction seen with decreased cardiac output; this increases afterload, leading to worsening cardiac output. Adding this agent can help maintain cardiac output, which is essential in cardiogenic shock while knowing these side effects. In similar fashion, milrinone can also be added with the known side effect of hypotension as well. Milrinone works via inhibiting phosphodiesterase-3, which is found specifically at the cardiac myocytes. This in turn increases cAMP, leading to increased cardiac contractility and lusitropy; the perfect inotropic agent adding in both systole and diastole. And even works distally to help with vasodilation.7 Studies have shown both these agents have no different effects on morbidity and mortality when used in the setting of cardiogenic shock.8
If all fails, these patients may require ECMO or further mechanical circulatory support including an intra-aortic balloon pump to help further decompress cardiac function and improve coronary perfusion. Patients in cardiogenic shock are associated with a mortality rate of 50%. Emergency physicians need to recognize this disease process as early intervention is crucial for patient outcomes.
Conclusion
Managing cardiogenic shock in the emergency setting requires a rapid, systematic approach to stabilize hemodynamics and address the underlying cause. Emergency medicine physicians play a crucial role in early recognition, initiation of vasopressor and inotropic support, and coordination of advanced therapies such as mechanical circulatory support and percutaneous coronary intervention (PCI). When PCI is unavailable, thrombolytic therapy serves as a critical alternative in cases of cardiogenic shock secondary to acute myocardial infarction, though its risks must be carefully weighed against its benefits. The decision to administer thrombolytics requires thorough patient evaluation, considering contraindications and the urgency of reperfusion. Ultimately, a multidisciplinary approach, integrating emergency, cardiology, and critical care teams, is essential to optimizing survival and improving patient outcomes in cardiogenic shock.
References
- Warner MJ, Tivakaran VS. Inferior Myocardial Infarction. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
- Mechanic OJ, Gavin M, Grossman SA. Acute Myocardial Infarction. [Updated 2023 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
- Hu M, Lu Y, Wan S, Li B, Gao X, et al; China Acute Myocardial Infarction Registry Investigators. Long-term outcomes in inferior ST-segment elevation myocardial infarction patients with right ventricular myocardial infarction. Int J Cardiol. 2022 Mar 15;351:1-7.
- Gul F, Parekh A. Multivessel Disease. [Updated 2023 Feb 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
- Bae DH. Optimal Inotrope and Vasopressor Therapy in Cardiogenic Shock. J Cardiovasc Interv. 2025 Jan;4:e9.
- Jung RG, Stotts C, Gupta A, Prosperi-Porta G, Dhaliwal S, et al. Prognostic factors associated with mortality in cardiogenic shock—a systematic review and meta-analysis. NEJM Evidence. 2024. 3(11).
- Ayres JK, Maani CV. Milrinone. [Updated 2023 Aug 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
- Mathew R, Di Santo P, Jung RG, Marbach JA, Hutson J, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021. Aug 5;385(6):516-525.
- Antman EM, et al. ACC/AHA guidelines for the management of patients with st-elevation myocardial infarction—executive summary. Circulation, vol. 110, no. 5, 3 Aug. 2004, pp. 588–636.