Recognition and Treatment of Right Ventricular Myocardial Infarction

Recognition and Treatment of Right Ventricular Myocardial Infarction

     Thirty to 50% of patients experiencing an inferior wall infarct may also have involvement of the right ventricle. Right ventricular infarctions seldom exist alone; they are almost always seen with an inferior infarct. The coronary artery involved is usually an occluded right coronary artery (RCA).

     The proximal segment of the RCA supplies the sinoatrial (SA) node and the right atrial wall; the middle segment supplies the lateral and inferior right ventricle (RV); and the posterior portion of the left ventricle, the inferior septum, inferior left ventricular wall and atrioventricular (AV) node are perfused by the distal segment of the RCA. A few patients (10%) may have a right ventricle that is supplied by the circumflex artery.

     When the inferior wall of the left ventricle is deprived of blood through RCA occlusion, it is reasonable to ask whether the right ventricle is also involved, since an RVI can present distinct treatment challenges for the paramedic.1

     In the early days of EMS, cardiac monitors were not standard equipment on all ambulances. In those services without cardiac monitors, myocardial infarctions were recognized through history and physical exam, and some MIs were missed. When monitors became available, most were three- or four-lead and were used for dysrhythmia recognition only. Medics were trained in dysrhythmia recognition and treatment, but not in 12-lead interpretation. The ability to recognize a myocardial infarction in the field through ECG monitoring came much later.

     Chest pain was treated with high- flow oxygen, nitroglycerin and morphine. Paramedics did not realize that nitroglycerin and morphine could complicate care in patients with RVI.

     Most ambulances are now equipped with 12-lead monitors and defibrillators, which also provide capnography, blood pressure monitoring and pulse oximetry, and 12-lead ECG monitoring is now standard of care for prehospital emergency services.2

     Paramedics are usually required to maintain current American Heart Association Advanced Cardiac Life Support training, and most have now been exposed, at least minimally, to 12-lead ECG monitoring and interpretation.

     The emphasis on cardiac care in the field has evolved from dysrhythmia recognition and treatment only to recognition and treatment of an evolving MI.

     Medics see more evolving MIs than fatal dysrhythmias, and they must be able to diagnose the regions of the heart affected and treat patients appropriately.

     A 2002 study among emergency physicians and cardiologists revealed that a high percentage (76%) of cardiologists believed acquisition and transmission of 12-lead ECGs by paramedics is beneficial, and half believed that it is beneficial for paramedics to be able to interpret 12-lead ECGs in the field.3

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     While there is no evidence that early recognition of RVI by paramedics results in improved survival, some believe that early intervention in RVI can be important in morbidity and mortality in these patients.4 Research led by emergency physician Steven Moye found that early fibrinolysis in patients with left and right ventricular infarcts could improve their chances of survival.5 Although, since that study, emphasis has shifted from fibrinolysis to other therapies like stenting, it would seem that early recognition can be beneficial.

     The right ventricle may recover more quickly than left ventricular tissue, possibly due to its relatively low workload and collateral perfusion from the left coronary artery.5

     With the advent of prehospital 12-lead ECGs, paramedics are first taught to recognize ST segment changes along with abnormal T waves and Q waves, and to recognize lateral, inferior, posterior and anterior infarcts, and combinations of those.

     The implications of standard management techniques, such as administration of nitroglycerin and other vasodilators in RVI patients, have only recently been addressed in paramedic education.

     It is important to recognize the signs of a right ventricular infarct because treatment differs significantly between patients with an RVI and those with other infarct sites.

     The traditional field treatment for an MI is aspirin and oxygen, with nitroglycerin and morphine for pain (often referred to as MONA). Some services now administer angiotensin converting enzyme (ACE) inhibitors, clopidogrel, and beta-blocking drugs as well.6

     Patients were given high-flow oxygen for years, although some authors have recently cast doubt on the routine use of high-flow oxygen in myocardial infarctions and called for controlled studies to evaluate its effectiveness as opposed to low-flow oxygen.7 American Heart Association guidelines no longer recommend high-flow oxygen, except when hypoxia is present; however, there is no evidence that hypertherapeutic oxygen harms when used in the field.

     Nitroglycerin has been the mainstay of treatment for ischemic chest pain, followed by IV opioids when adequate nitroglycerin therapy does not reduce the pain.

     The rationale for giving nitroglycerin has been that it will vasodilate both sides of the systemic circulation, reducing both preload (venous return) and afterload (forward systemic resistance), which reduces the workload on the heart and therefore oxygen and glucose consumption. It is also thought to vasodilate the coronary circulation, which improves coronary artery circulation, both direct and collateral, increasing oxygen and glucose delivery to ischemic tissues. However, nitroglycerin cannot do anything to correct complete obstruction from ruptured plaques or platelet aggregations (clots).

     The American Heart Association's Handbook of Emergency Cardiovascular Care, Guidelines CPR-ECC 2005 states that nitroglycerin is contraindicated in RVI.8

     The rationale for giving morphine is that by making the patient pain-free, endogenous catecholamine release and vasoconstriction (Alpha-1 effect) will be lessened, and the workload on the heart will be decreased; however, morphine causes histamine release, and histamine is a vasodilator. Vasodilation can lower venous return and preload to the damaged right ventricle, thus affecting cardiac output.

     Morphine has been shown to increase infarct size9 and lessen blood flow through coronary arteries by as much as 13%.10 Some have questioned the efficacy of morphine in MI, but the American Heart Association still grants it a Class IC classification with the stated precaution: "Use with caution in right ventricular infarction."11

     The right ventricle is not designed to provide systemic circulation. Its purpose is to pump blood through the lungs and pulmonary circuit. Thus, the pressures it is required to produce are less, and it has a thinner wall than the left ventricle, which must pump blood throughout the body.

     Its functional abilities are dependent upon preload, or the volume of venous return to the heart, principally during diastole, since veins do not have muscular walls to keep blood moving as do the arteries. The right atria and ventricle have relatively little "suction" from contractions to pull blood into them.

     So a reduction in venous return will result in diminished pumping pressure by the right ventricle, diminished pulmonary circulation, diminished left ventricular filling, diminished cardiac output, diminished systemic blood pressure and, if not corrected, possible dysrhythmias, shock and death.12,13

     If one understands that heart muscle, or myocardium, is perfused by the coronary artery system, and that the coronary arteries primarily fill with blood during diastole and are dependent upon pressures in the aorta immediately after the left ventricle contracts, one can easily understand that a drop in stroke volume as a result of lessened preload will eventually result in a drop in coronary artery filling pressures. If there is an obstruction in one or more of the coronary arteries, the blood supply to myocardial tissue will be further compromised, since collateral circulation (blood flow through arterial branches not affected by the obstruction) is dependent upon adequate filling pressures.

     Aside from questions about area of infarct, any patient who presents with chest pain, shortness of breath, unexplained hypotension, abdominal pain, back pain in the scapular or subscapular region, epigastric pain, neck or jaw pain, generalized weakness, syncope, complaint of tightness in the chest, nausea, vomiting, sweating (even in hyperthermic environments) that is unusual, and any other presentation that is systemically abnormal, should get an immediate 12-lead ECG. If 12-lead monitoring is available, failure to use it with such patients could result in liability.

     Cardinal signs of RVI are unexplained hypotension, distended jugular veins with Kussmaul's sign (increased jugular vein pressure on inspiration) and clear lung sounds;14 however, in the prehospital environment, it may be difficult to recognize these signs. The 12-lead ECG can be diagnostic, although not always. Some patients do not show ECG changes that are easy to recognize early in the evolution of an MI. Nevertheless, a 12-lead ECG should be done as soon as possible in patients with the above stated indications.15

     A 12-lead tracing that shows ST segment elevation in any of the inferior leads (II, III or aVF), or relative ST segment depression in V2 or V3 compared with lead V1, should immediately trigger acquisition of a right-sided 12-lead. With RVI, the ECG may also show an acute anterior Q-wave pattern in leads V1 through V3.16 A significant Q wave is one that is >¼ the length of the following R wave, or wider than 0.03 seconds. (One small block on the ECG equals 0.04 seconds.)

     What is the significance of a right ventricular MI? The treatment of patients with RVI is different from non-RVI patients. If they are treated with nitroglycerin, they may experience sudden and dramatic hypotension from vasodilation.

     To acquire a regular left-sided 12-lead ECG, do the following:

     Begin by locating the patient's angle of Louis, which is the bony horizontal ridge between the upper part of the sternum, or manubrium, and the body of the sternum. From there, move your finger to the right into the depression between the second and third ribs. This is the second intercostal space. Work your finger down space by space until you reach the fourth intercostal space and place the normal V1 lead there, just to the right of the border of the sternum. Then, place V2 just across the sternum on the left margin, in the fourth intercostal space. Skip V3, move down and place V4 in the fifth intercostal space, midclavicular line. It is important to trace the midclavicular line down from the clavicle, which normally bisects the left nipple in males. Place V3 halfway between V2 and V4. Continue to palpate the fifth intercostal space and place V5 at the anterior axillary line and V6 in the mid-axillary line, still in the fifth intercostal space.

     After acquiring the normal left-sided ECG, leave the limb leads and electrodes for V1 and V2 where they are. (Note: Limb leads should be on the limbs, not the chest!) V2 now becomes lead V1R, and V1 becomes V2R. Switch the wires on those two leads accordingly. Place the remainder of the precordial (chest) leads on the right side of the chest in a mirror position from the left-sided 12-lead. Place V4R in the fifth intercostal space, midclavicular line; place V3R halfway between V2R and V4R; place V5R in the right fifth intercostal space, anterior axillary line; and place V6R in the fifth intercostal space, mid-axillary line.

     If the patient has large breasts, place the V3R lead on the breast and V4R and V5R leads below the breast.

     When the strip is printed, write "R" beside the V leads to mark that they are right leads, not left.

     It is important to place electrodes in the correct positions. Many ECG technicians rely on their experience, but that is not reliable. Electrode placement affects the reliability of the ECG, and care must be taken to place them properly. For example, if the limb leads are improperly placed on the chest, this must be noted on the ECG strip, because chest placement of limb leads can affect the tracing, which is important for the physicians interpreting the strip to know. If you change the position of limb leads or any other leads, this must also be written on the strip. Patterns can change if the patient's position is changed between ECGs. For example, moving the patient from a supine to a seated position can cause the tracings to look somewhat different. If the patient's position changed, note that on the strip for the interpreting physician. It is also good practice to leave the electrode pads in place when you transfer the patient to hospital care, since the new caregivers will be easily able to see that a right-sided ECG was done. This is especially helpful if there is commonality of equipment between the prehospital and emergency department providers. Leaving the electrodes in place allows the emergency department to obtain further EKGs from the same lead positions, reducing the chance of errors due to changes in position.

     Run the right-sided EKG just as you would a left-sided EKG, and look for ST elevation in V2R-V6R.

     ST segment elevation in V4R is considered to be diagnostic for right ventricular infarction; however, any ST elevation in the right V-leads 3 through 6 should signal suspicion for a right-sided MI.

     The T wave in V4R usually has a convex or "domed" shape when injury is occurring. Pathological Q waves signal a completed infarct.

     Since the right ventricle is dependent on preload for adequate stroke volume, left ventricular stroke volume and cardiac output, any treatment that involves vasodilation is problematic in a patient with RVI. Fluid infusion is the mainstay of treatment for patients with RVI.

     In the case of an inferior MI with right ventricular involvement, the administration of nitroglycerin and morphine could cause an abrupt drop in blood pressure. Some authorities state categorically that nitroglycerin should be avoided,17,18 while others simply urge extreme caution.19 NTG should not be given without a systolic blood pressure of at least 90. NTG infusion is preferable to tablets or spray, since an infusion can be titrated. Nitroglycerin paste is probably contraindicated due to the unpredictable onset of action and longer duration of effects.

     If NTG is to be used, it should be only according to local protocol. Since field recognition and treatment of RVI is a relatively recent development in prehospital care, some services' protocols may not contain specific orders for RVI patients. However, most will contain the admonishment to use NTG only in the presence of adequate blood pressure. Systems vary in the minimum BP recommendation for NTG use, but NTG should not be given to a hypotensive patient. Prior to NTG administration, obtain IV access. Many practitioners recommend two IV lines in cardiac patients.

     If NTG is administered before an RVI is recognized and hypotension results, fluids should be given. As much as two to three liters of normal saline may be required to restore preload to adequate levels, but less is usually adequate. As always, when administering fluids, lung sounds and oxygenation should be monitored.

     If adequate blood pressure and cardiac output cannot be maintained with fluids alone, dobutamine infusion is the preferred agent in RVI patients with systolic BP of 70–100 mmHg and no signs of shock. Avoid dobutamine when systolic blood pressure is &llt;100 with signs of shock. If dobutamine is not available, dopamine is the drug of choice with hypotension and signs of shock.20

     Symptomatic bradycardias can be treated with atropine up to 3 mg, and AV blocks may require external pacing.

     Transport to the proper cardiac center is of utmost importance. Avoid transport to hospitals that do not have cath lab capability, if possible. Follow regional plans for cardiac care.

     Not all heart attacks are the same. Thirty to 50% of patients with inferior MIs have involvement of the right ventricle, usually with an obstruction of the right coronary artery above the first branches.

     The main goals of field treatment for patients with RVI are to maintain preload to the right ventricle, cardiac output, blood pressure, coronary artery filling pressures and prevent shock.

     Because nitroglycerin is a vasodilator, it is contraindicated as standard treatment, or must be given with extreme care. Nitroglycerin should not be given unless specifically authorized by local protocols. Fentanyl may be given instead of morphine, since morphine also causes vasodilation.

     Contrary to the practice of limiting fluids in MI patients without right ventricular involvement, fluids should be given to the RVI patient to maintain cardiac output, blood pressures and coronary artery filling pressures. Normal saline up to 40 ml/kg is the preferred fluid.

     Dobutamine 5–20 mcg/min by infusion is the preferred vasopressor agent if cardiac output cannot be maintained with fluids alone and shock is not present. Dopamine can be used if dobutamine is not available or if shock is present. Atropine and pacing may be used for bradycardias and AV blocks.

     Supplemental oxygen is recommended, and aspirin may be given as usual. Beta-blockers and ACE inhibitors should be given with caution and only in accordance with local protocol in the setting of RVI.

     EMS providers play a special role in early diagnosis and proper treatment of any patient who is having a heart attack. By doing the right things, they can give the RVI patient a better chance for recovery.

Special thanks to Charles Krin, DO, for his advice and help in reviewing this article.


1. Moye S, Carney M, Holstege C, et al. The electrocardiogram in right ventricular myocardial infarction. Am J Emerg Med 23:793–799, 2005.

2. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation: Part I: Introduction to international guidelines 2000 for CPR and ECC: A consensus on science. Circulation 102(8 Suppl): 1–11, 2000.

3. Brainard A, Froman P, Alarcon M, et al. Physician attitudes about prehospital 12-lead ECGs in chest pain patients. Prehosp Disast Med 17(1):33–37, 2002.

4. Zehender M, Kasper W, Kauder E, et al. Eligibility for and benefit of thrombolytic therapy in inferior wall myocardial infarction: Focus on the prognostic importance of right ventricular infarction. J Am Coll Cardiol 24:362–369, 1994.

5. Moye S, op cit.

6. American Heart Association Guidelines for Advanced Cardiac Care, 2005.

7. Beasley R, Aldington S, Weatherall M, Robinson G. Oxygen therapy in myocardial infarction: An historical perspective. J R Soc Med 100:06–0065, 1–4, 2007.

8. American Heart Association Handbook of Emergency Cardiovascular Care, Guidelines CPR-ECC 2005, p. 59.

9. Markiewicz W, Finberg J, Lichtig C. Morphine increases myocardial infarction size in rats. Anesth Analog 61:843–846, 1982.

10. Hilfiker O, Larsen R, Brockschneider B, et al. Morphine in coronary blood flow and oxygen consumption in patients with coronary artery disease. Anesthes 31:371–376, 1982.

11. American Heart Association Handbook of Emergency Cardiovascular Care, Guidelines CPR-ECC 2005, p. 58.

12. Fuster V, et al. Hurst's The Heart, 11th ed., p. 1314–1316. New York, NY: McGraw-Hill Professional, 2004.

13. Horan LG, Flowers NC. Am Fam Phys 60:1721–1734, 1999.

14. Dalton R, Limmer D, Mistovich J, Werman H. Advanced Medical Life Support, 2nd ed., p. 205. Upper Saddle River, NJ: Prentice Hall, 2003.

15. Fuster V, op cit, p. 1315.

16. Horan LG, op cit, p. 1728.

17. Fuster V, op cit, p. 1315.

18. Tintinalli J, et al. Emergency Medicine, 6th ed. , p. 358. American College of Emergency Physicians, New York, NY: McGraw Hill Professional, 2004.

19. Martinez JA. Complications of acute myocardial infarction. Emergency Medicine, July 2003.

20. American Heart Association Handbook of Emergency Cardiovascular Care, Guidelines CPR-ECC 2005, p. 59.

William E. “Gene” Gandy, JD, LP, has been a paramedic and EMS educator for over 30 years. He has implemented a two-year associate’s degree paramedic program for a community college, served as both a volunteer and paid paramedic, and practiced in both rural and urban settings and in the offshore oil industry. He has testified in court as an expert witness in a number of cases involving EMS providers and lectures on medical/legal aspects of EMS. He lives in Tucson, AZ.

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