Why it's important to identify right ventricular infarct

A right-sided 12-lead EKG can identify signs of a right ventricular infarct to guide patient care decisions


Article updated July 27, 2017 

You contact medical control and report that you are transporting a 40-year-old male who was playing walleyball when he began experiencing a new onset of 8/10 level chest pain radiating to his left arm. The patient is alert and oriented, but is in severe distress. His vital signs are otherwise normal.

A 12-lead EKG shows ST elevation is present in leads II, III, aVF and V4r.

Transport time is about 20 minutes.

Two large bore IVs have also been initiated at a TKO rate. You inform the physician that you would like to administer nitroglycerin, but are concerned about the right ventricular involvement and preload dependency.

The medical control physician recommends that you give the patient a 250 mL fluid bolus prior to the administration of nitrates and suggests you be prepared to administer another liter to maintain a systolic blood pressure above 90mm Hg and to monitor the patient's lung sounds for changes. The physician then asks you to report any changes prior to your arrival and that the cath lab team is being paged.

Sudden cardiac arrest

Upon arrival at the ED, the patient becomes pulseless and apneic. The EKG monitor shows ventricular fibrillation. While you prepare to defibrillate the patient, your partner finds the "Code Blue" button near the ambulance entrance and yells out for assistance.

You administer four defibrillations interspersed with CPR and the patient returns to a perfusing rhythm just as a cot is wheeled into the cardiac arrest room. The cardiologist is already in the area and begins to prepare his team for the patient.

Within minutes, lab tests are ordered, blood is drawn, a stat chest EKG is taken, and the patient is taken to the cath lab. The patient goes into cardiac arrest three more times before his angioplasty is performed. The patient’s coronary artery disease is so advanced that the cath lab inserts an intra-aortic balloon pump and prepares him for coronary artery bypass grafting, while another team is paged to prepare the operating room/suite.

Right ventricle infarction

The EKG Club experts created this case for these learning objectives: 

  • Basic: Differentiating between inferior, anterior, septal and lateral leads.
  • Intermediate: Identification of right ventricular infarct and the treatment modalities.
  • Advanced: Identification of the culprit artery in the STEMI patient.

The response and treatment to this case was performed exceptionally well. Educating the patient and obtaining his consent for transport to a more distant but better equipped hospital, set into place a chain of events that likely resulted in his successful outcome. 

Identifying the patient's RVI also may have avoided a needless negative outcome. Had you given nitroglycerin and morphine liberally to this RVI patient, it could have resulted in severe hypotension.

During cardiac ischemia and infarction, the heart is especially reliant on preload for producing adequate cardiac output. The ventricles are much more efficient when preloaded during diastole, the moment at which the heart itself also is perfused. When the right ventricle is stunned from infarction, it is even more reliant on the preload to ensure the left ventricle is preloaded. Without this, the blood pressure will plummet. Administering nitroglycerin to a patient that is preload-dependent could result in severe hypotension which may prevent any blood from circulating in the coronary arteries. 

Initiating two large bore IVs is beneficial for delivering such a rapid bolus. Even though the patient deteriorated into ventricular fibrillation, was defibrillated, had angioplasty, had a balloon pump inserted, followed by open heart surgery, there was still a positive outcome.

Here are some additional teaching points for this case:

  • Approximately 50 percent of patients with acute inferior myocardial infarctions will not have precordial ST-depression or "reciprocal changes." These patients have the best overall outcome of all the subgroups of IMI patients. They have less myocardial damage, lower rates of heart failure, cardiogenic shock and dysrhythmias.
  • One study found the sum of ST-depression in V1-V6 to be an independent risk factor for increased 30-day mortality. For every 0.5mV of ST-depression, mortality increased by 36 percent. In this large study, the sum of precordial ST-depression was a more powerful predictor of outcome than the amount of inferior-lead ST-elevation.
  • The right coronary artery is the infarct-related artery in about 70 percent of all IMIs independent of reciprocal changes.  When there is maximal ST-depression in leads V1-V3 versus V4-V6, left circumflex artery occlusion is more prevalent. When maximal precordial ST-depression occurs in V4-V6 as opposed to V1-V3, this is more commonly associated with multi-vessel CAD. These patients require more aggressive treatment, such as CABG and PTCA, despite an apparently successful initial thrombolytic treatment. 
  • Right ventricular infarctions complicate up to 50 percent of all IMIs.  The ED diagnosis of RV infarction is often suggested by these clinical findings: hypotension, clear lung fields, and JVD. However, up to 60 percent of patients with RV infarction will not have hemodynamic compromise and the clinical triad described is found to have a sensitivity of 10-25 percent.
  • There is a 31 percent in-hospital mortality rate when RV infarction complicates IMI versus 6 percent without RV infarction.  It is believed that this increased mortality rate is due to an increased incidence of sustained VT and VF, as the right ventricle may be more dysrhythmogenic than the left ventricle.
  • Although posterior infarction is classically associated with IMI, the left coronary artery supplies the posterior wall of the LV in 10-20% of the population.  These patients have the posterior descending artery branch off the left circumflex instead of the right coronary artery. 

References:
Rotondo N, et al. Electrocardiographic manifestations: acute inferior wall myocardial infarction. Journal of Emergency Medicine: 2004;26: 433-40. 

PB Berger and TJ Ryan. Inferior myocardial infarction. Circulation 1990: 401-411. 

Peterson ED, et al.  Prognostic significance of precordial ST segment depression during inferior myocardial infarction in the thrombolytic era: results in 16,521 patients. Journal of The American College of Cardiology: 1996;28: 305-12.

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