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    Left vs. right ventricular MI: Which is it?

    RN/MCPHU Home Study Program

    Left vs. right ventricular MI: Which is it?

    CE credit is no longer available for this article. (Expired May 2004)

    Originally posted May 2002

    Left vs. right ventricular MI: Which is it?


    KIMBERLEY LITTON is a clinical specialist in the coronary care unit at Allegheny General Hospital, Pittsburgh.

    KEY WORDS: acute myocardial infarction (AMI), left, right coronary arteries, left anterior descending (LAD) artery, left circumflex (LCx) artery, ST segment elevation, ST segment depression, right ventricular AMI, left ventricular AMI

    Learn how to spot the clues—quickly and accurately—that distinguish a right ventricular myocardial infarction from a left one. Giving the right treatment depends on it.

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    Each year over 1.5 million Americans suffer an acute myocardial infarction (AMI).1 Up to 500,000 victims die, half of them before even reaching the hospital.1 Early treatment can limit myocardial damage and improve the chances of survival.

    For that reason, American Heart Association guidelines require that a targeted history, physical assessment, and 12-lead EKG be obtained within the first 10 minutes of an AMI patient's arrival in the ED. Life-saving treatments should be started within the first 20 to 30 minutes.1,2

    That leaves little time to determine if the infarction is affecting the right ventricle or the left. Yet giving a patient with a right ventricular AMI the interventions recommended for a left ventricular AMI—or vice versa—could prove harmful.2

    Nurses are in a pivotal position to help determine the type of AMI a patient is suffering and thus guide both swift and accurate treatment decisions. This article will show you how to use EKG and clinical findings to pinpoint the site of an infarction. We will then review treatment guidelines for AMI and specific nursing interventions for a right vs. a left infarction.

    Left ventricle is most vulnerable to injury

    The heart relies heavily on the generous supply of oxygenated blood delivered by the coronary arteries for its proper function. In the majority of people, the right coronary artery supplies blood primarily to the right atria, right ventricle, the sinoatrial (SA) and atrioventricular (AV) nodes, the posterior one-third of the septum, and the posterior wall of the left ventricle.

    The left coronary artery divides into the left anterior descending (LAD) artery and the left circumflex (LCx) artery. The LAD supplies most of the blood feeding the anterior wall of the left ventricle, apex, most of the conduction system below the AV node, and the anterior two-thirds of the septum. The LCx supplies the lateral wall of the left ventricle, left atria, and part of the posterior portion of the left ventricle.

    Because the major branches of the right and left coronary arteries line the grooves between the ventricles and atria, there is much overlap and individual variation in anatomy. Communication—that is, anastomosis—is common among the branches and occurs particularly during periods of ischemia, giving rise to collateral circulation. However, blockage in any one of the major vessels will most often cause damage in the left rather than the right ventricle.

    Nearly 70% of all AMIs involve some or part of the left ventricle.2 This happens, in part, because the left ventricle is larger, has the most muscle mass, requires more oxygen to function, and therefore is most sensitive to oxygen supply and demand.3 The left ventricle also shows more resistance to subendocardial perfusion than the right ventricle, and it receives most of its blood supply only during diastole.4 Depending on which area of myocardium is affected, AMIs of the left ventricle are classified as anterior, lateral, posterior, or inferior wall infarcts (or a combination of those areas).

    The right ventricle is less susceptible to infarcts because it functions at lower pressure and volume and has thinner walls, which require less oxygen to function.4 In addition, the right ventricle is perfused during both systole and diastole, giving it a larger supply of blood and enabling it to extract oxygen during periods of increased stress.

    When damage occurs to either ventricle, however, telltale signs can be found on the EKG

    Zero in on ST segment elevation

    On EKG, the ST segment elevation alone is the most sensitive indicator of the location of an infarction, even though other changes may be evident.

    ST segment elevation reflects the area of injury and is the first sign of coronary artery occlusion. The ST segment will be elevated in leads facing the injured wall, with reciprocal changes, or ST depression, in the leads opposite the injury. Knowing where to look for ST elevation can help you locate an AMI's site, as summarized below and in the "Where's the blockage? EKG findings give key clues" table.

    The following are typical findings of ST segment elevation associated with a specific wall injury. Keep in mind, though, that there can always be exceptions to the rule.

    Anterior wall AMI. An occlusion of the left coronary artery or its branches results primarily in injury to the anterior wall of the left ventricle. Anterior wall AMIs tend to be large and cause the most damage to the myocardium. An occlusion of the left main portion of the left coronary artery (before it branches), for example, can result in a massive infarction involving not only the anterior wall of the left ventricle, but the interventricular septum and lateral wall as well. ST segment elevation of a left main infarction is seen in leads V1 through V6.5 An occlusion of the LAD can result in ST segment elevation of leads V1 through V4, also known as an anteroseptal AMI, because the zone of injury involves the anterior wall and the anterior portion of the septal wall. ST segment elevation in leads I, aVL, and V3 through V6 indicate an occlusion of the LAD, causing an anterolateral infarction.

    Lateral wall AMI. An occlusion of the LCx or the diagonal branches of the LAD results in an infarction of the lateral wall of the left ventricle. ST elevation in leads I and aVL indicate a high lateral infarct, while ST segment elevation in V5 and V6 indicates a lower lateral, or apical, infarct. Lateral infarctions rarely occur alone and are often associated with anterior wall or inferior wall AMIs.5

    Posterior wall AMI. Because a 12-lead EKG looks at only the front of the heart, no leads will face an injury to the posterior walls. But reciprocal changes, or ST depression, in leads V1 through V3 accompanied by tall R waves in those leads indicate an occlusion of the posterior descending artery.6,7

    A posterior wall AMI is confirmed by ST segment elevation in leads V7 through V9, the leads placed on the patient's back in the fifth intercostal space beginning at the left posterior axillary line.6

    Inferior wall AMI. ST segment elevation in leads II, III, and aVF usually indicates blockage in the artery supplying the inferior wall of the left ventricle. The infarction often stems from an occlusion of the distal portion of the right coronary artery; however, up to 50% of all inferior wall AMIs are associated with an occlusion of the proximal portion of the right coronary artery, which can result in significant damage to the right ventricle.2

    Right ventricular AMI. The best way to determine if the right ventricle has suffered severe damage is to place leads on the right side of the chest in the mirror image position of the left precordial leads (V1R through V6R), as shown in the "Lead placement for right-sided EKG" box. ST segment elevation of 1 mm or more in V3R through V6R—particularly in V4R—confirms right ventricular AMI.1-6

    Look for these clinical signs

    Along with an EKG, a patient's clinical signs can help you distinguish between a left vs. a right AMI. Consider the following:

    Left ventricular AMI. Clinical signs of an infarction of the left ventricle may include tachycardia, hypertension, and dyspnea. Damage to the left ventricle compromises the heart's ability to send oxygen-rich blood to the rest of the body. The drop in cardiac output stimulates sympathetic compensation, which results in tachycardia and increased blood pressure from circulating catecholamines.7

    In patients with congestive failure, dyspnea results from pulmonary congestion, as the injured left ventricle is unable to eject its contents and as blood flowing in from the lungs has nowhere to go. Patients typically have a third or fourth heart sound and may develop mitral regurgitation.

    The stretch on the atria from congestive failure can cause atrial fibrillation, atrial flutter, or supraventricular tachycardia. Damage to the His-Purkinje system can give rise to a new-onset bundle-branch block, a sign that reflects a significant loss of left ventricular myocardium.5 If a patient with a left ventricular AMI is hypotensive, the infarction is a large one, and cardiogenic shock is likely to follow.

    Right ventricular AMI. Suspect a right ventricular AMI in all patients who present with an inferior wall AMI.2,4 Typical signs of an inferior wall infarction include hypotension, bradycardia, nausea, vomiting, hiccoughing, and the urge to defecate as the result of parasympathetic stimulation from increased vagal tone. Ischemia of the SA or AV nodes or the bundle of His can also cause bradycardia or first-, second- (Mobitz I or Mobitz II), or third-degree heart block.

    Look for the classic triad of distended neck veins, clear lungs, and hypotension—the signs of a right ventricular infarction.4 These signs emerge as the right heart loses its ability to handle systemic venous return. Right atrial pressure rises and jugular vein distention occurs without pulmonary congestion. When the compromised right ventricle can't eject its contents, cardiac output drops, leaving the left ventricle in a state of relative hypovolemia.

    One caveat: An isolated right ventricular AMI is rare. The EKG findings associated with it may mimic an anteroseptal AMI, namely ST segment elevation in leads V1 through V3. Placing the right precordial leads and finding ST elevation, particularly in V4R, may confirm the diagnosis. This is partly why it's known as a pseudoanteroseptal MI. Observations following angioplasty have shown this to be true. They have also shown that the ST segment suppression of precordial leads associated with a right ventricular AMI occurs only with a concomitant inferior wall MI.

    The bottom line: Maintain a high index of suspicion in patients with ST segment elevation in V1 through V3 who also demonstrate significant hemodynamic instability. In addition, as a safeguard to help prevent missing a right ventricular infarction, obtain a right-sided EKG on all patients with an inferior wall AMI and on those with ST segment elevation in leads V1 through V3 that raises a high index of suspicion of a right ventricular infarction.1

    Steps that limit the damage in AMI

    When a patient arrives with an AMI, the primary goals are to restore the blood flow of the blocked artery and limit the damage from the infarction. The following are typical interventions; practices at individual hospitals may differ.

    On admission, according to your hospital's protocol and doctor's orders, assess the patient, get an EKG STAT, administer supplemental oxygen, and implement continuous cardiac monitoring.

    Next, start an IV and have the patient chew one 325 mg tablet of aspirin (or four 81 mg tablets of so-called "baby aspirin") immediately. Never give enteric-coated aspirin; it takes longer to be absorbed. You may give clopidogrel bisulfate (Plavix) or ticlopidine HCl (Ticlid) to patients allergic to aspirin.1

    You'll draw blood for serial cardiac enzymes, electrolytes, complete blood count, partial thromboplastin time (PTT), prothrombin time (PT-INR), magnesium, and a baseline lipid profile. Anticipate administering thrombolytics such as alteplase (Activase), reteplase (Retavase), or tenecteplase (TNKase) to restore blood flow to the blocked artery of patients for whom this is indicated. Alternatively, emergent angioplasty or intracoronary stent placement may be ordered, with or without a glycoprotein IIb/IIIa receptor blocker such as abciximab (ReoPro) or eptifibatide (Integrilin) to inhibit platelet aggregation.

    Hemodynamically unstable patients may require monitoring with a pulmonary artery catheter, as well as mechanical ventilation and, in the sickest patients, an intraaortic balloon pump for support. Some patients may require dopamine HCl (Intropin, Dopastat) or dobutamine HCl (Dobutrex) for inotropic support and transvenous pacing to abort lethal arrhythmias.

    For patients with left ventricular AMI, intervention is aimed at reducing the myocardial workload, managing pain, and minimizing the risk of pulmonary edema. The mainstay of treatment is nitroglycerin (if the systolic blood pressure is greater than 90 mm Hg), and/or morphine sulfate, both to reduce preload and manage pain. Fluid restriction and diuretics are given to control pulmonary congestion.

    IV heparin is indicated for the first 24 to 48 hours and may be continued longer in patients who develop atrial fibrillation, or who have a known left ventricular thrombus or a large anterior wall MI. Early beta-blocker therapy is indicated, but not if the patient has significant hypotension, heart block, bronchospasm, or heart failure.

    For patients with right ventricular AMI, treatment involves aggressive fluid resuscitation, which may include infusing one to two liters of 0.9 normal saline over a short time frame. The purpose is to raise the preload and right ventricle filling pressure and to maximize the contractility and blood flow from the right ventricle into the left.

    If fluids do not correct the failure, dobutamine is given to enhance contractility, reduce afterload, and increase the forward flow of blood to boost the cardiac output.7 Preload reducing agents such as morphine sulfate, diuretics, and nitrates should be avoided. Meperidine HCl (Demerol) may be used in place of morphine for pain control.7

    Patients who have both a left and a right ventricular AMI should be treated as if they have a right ventricular AMI because a failing right ventricle can't provide sufficient volume to the left ventricle to maintain cardiac output. Treating this patient strictly as you would treat one with a left ventricular AMI would hasten cardiogenic shock.4

    Clearly, mistaking a left for a right ventricular AMI—or vice versa—can spell disaster. Honing your skills for recognizing clues to the location of an AMI can help minimize that risk by shortening the time it takes to make a treatment decision. That will speed the time to appropriate therapy and can substantially reduce the damage an AMI can cause.


    1. Almeda, F. Q., Snell, R. J., & Parillo, J. E. (2001). The contemporary management of acute myocardial infarction. Crit Care Clin, 17(2), 411.

    2. Coven, D., & Pershad, A. "Right ventricular infarction." 2002. www.emedicine.com/med/topic2039.htm (1 Feb. 2002).

    3. Closchesy, J., Breu, C., et al. (1996). Critical care nursing (2nd ed.). Philadelphia: W. B. Saunders.

    4. Horgan, L. G., & Flowers, N. C. (1999). Right ventricular infarction: Specific requirements of management. Am Fam Physician, 60(6),1727.

    5. Goldberger, A. L. "Electrocardiogram in myocardial ischemia and infarction." UpToDate Online 10.1. 2001. www.uptodate.com/html/prcard.htm (1 Feb. 2002).

    6. Lynn-McHale, D. J., & Carlson, K. K. (2001). AACN procedure manual for critical care (4th ed.). Philadelphia: W. B. Saunders.

    7. Bucher, L. (1999). Acute myocardial infarction. In L. Bucher & S. Melander (Eds.), Critical care nursing (1st ed.), (pp. 227 ­ 257). Philadelphia: W. B. Saunders.

    Where's the blockage? EKG findings give key clues


    Site of infarct ST elevation ST depression Possible coronary artery(ies) occluded
    Large anterior wall V1 – V6 II, III, aVF Left main coronary
    Anterior wall
    V1 – V4
    I, aVL, V3 – V6
    II, III, aVF
    II, III, aVF
    Left anterior descending (LAD)
    Lateral wall
    I, aVL II, III, aVF Left circumflex (LCx)
    Lateral wall
    (low, apical area)
    V5 – V6 II, III, aVF LAD, LCx
    Posterior wall V7 – V9 V1 – V3 Posterior descending
    Inferior wall II, III, aVF I, aVL, V5, V6 Right coronary
    Site of infarct ST elevation ST depression Possible coronary artery(ies) occluded
    Inferior wall V3R – V6R
    particularly V4R
    V2 – V4 Right coronary
    (proximal or middle segments)
    (large, isolated right
    ventricular AMI)
    V1 – V3
    (and V4R)
    aVL Significant proximal right coronary
    Sources: 1. Prieto, A., Eisenberg, J., & Thakur, R. K. (2001). Nonarrhythmic complications of acute myocardial infarction. Emerg Med Clin North Am, 19(2), 397. 2. Horgan, L. G., & Flowers, N. C. (1999). Right ventricular infarction: Specific requirements of management. Am Fam Physician, 60(6), 1727. 3. Bucher, L. (1999). Acute myocardial infarction. In L. Bucher & S. Melander (Eds.), Critical care nursing (1st ed.), (pp. 227 ­ 257). Philadelphia: W. B. Saunders. 4. Logeart, D., Himbert, D., & Cohen-Solal, A. (2001). ST-segment elevation in precordial leads: Anterior or right ventricular myocardial infarction? Chest, 119(1), 290.

    Lead placement for right-sided EKG

    The best way to determine if the right ventricle has suffered severe damage is to place leads on the right side of the chest in the mirror image position of the left precordial leads (V1R through V6R), as shown in the figure.



    • V1R: 4th intercostal space (ICS) at left sternal border
    • V2R: 4th ICS at right sternal border
    • V3R: Between V2R and V4R
    • V4R: 5th ICS at right mid-clavicular line
    • V5R: 5th ICS at right anterior axillary line
    • V6R: 5th ICS at right mid-axillary line

    Adapted from: Ellis, K. M. (2002). EKG plain and simple: From rhythm strips to 12-leads. Upper Saddle River, NJ: Prentice Hall.


    Kimberley Litton. Left vs. right ventricular MI: Which is it?. RN 2002;5:36ac5.

    Published in RN Magazine.

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