Editorials - October 15, 1999 - American Academy of Family Physicians

Editorials

Treatment of Right Ventricular Infarction

ASSAD MOVAHED, M.D.
East Carolina University School of Medicine
Greenville, North Carolina

See article in this issue.

Right ventricular infarction may occur in isolation or with acute inferoposterior left ventricular myocardial infarction. In fact, right ventricular infarction occurs in as many as 30 to 50 percent of patients who have an acute inferior myocardial infarction, and it is hemodynamically significant in approximately one half of these patients. Because the treatment of right ventricular infarction differs from that of the more common left ventricular infarction, it is important for clinicians to be aware of the condition and intervene accordingly.^1-5

Classically, right ventricular infarction presents as acute inferior infarction, hypotension and elevated jugular venous pressure, with clear lung fields. However, these findings are seen in fewer than 25 percent of patients with acute right ventricular infarction. Therefore, hemodynamic data, along with an electrocardiogram or echocardiogram/radionuclide angiogram, should be obtained early to confirm the diagnosis.^5-8 In this issue of American Family Physician, Horan and Flowers⁹ describe the diagnosis of right ventricular infarction.

The correct diagnosis is critical in the management of patients who present with low cardiac output and low arterial pressure in the setting of acute myocardial infarction. Right ventricular infarction lowers the compliance of the right ventricle, leading to a reduction in right ventricular filling and a decrease in right ventricular stroke volume. As a result, left ventricular filling and stroke volume would diminish, causing a decrease in arterial pressure. Severe right ventricular dysfunction may be associated with cardiogenic shock. In such cases, conventional treatment may be deleterious. The initial therapy for a patient with acute right ventricular infarction who has hypotension is volume expansion, with the use of normal saline to increase filling of the right ventricle. This will in turn increase filling of the underfilled left ventricle and increase cardiac output.^10,11

In some patients with acute right ventricular infarction, volume loading causes dilatation of the right ventricle, which could compromise left ventricular output, because the added pressure in the pericardium does not allow the left ventricle to fill. To avoid this complication, hemodynamic monitoring may be necessary. Positive inotropic support must be considered if the cardiac output does not improve following volume loading.

The administration of dobutamine lowers pulmonary vascular resistance and therefore reduces right ventricular afterload, improving cardiac function.¹²Dobutamine can be started at 5 µg per kg per minute, and the dose may be titrated up to 20 µg per kg per minute if required. Diuretics and nitrates, which reduce preload, can diminish cardiac output and induce significant hypotension in the presence of right ventricular infarct. They must be used with caution in this setting.

Patients with inferior myocardial infarction who have associated right ventricular infarction have an increased risk of early morbidity and mortality. Early reperfusion using thrombolytic therapy or primary percutaneous transluminal coronary angioplasty (PTCA) may reduce infarct size and improve the short-term survival in many of these patients.¹³ In patients with right ventricular infarction, the use of thrombolytic therapy is associated with a 4.2-fold lower incidence of in-hospital mortality and a 2.4-fold lower rate of complications.¹⁴In patients with right ventricular infarction, complete reperfusion of the right coronary artery with PTCA resulted in the dramatic recovery of right ventricular function and an improved clinical outcome. However, unsuccessful reperfusion was associated with a high in-hospital mortality rate.¹⁵

Despite the potentially life-threatening acute hemodynamic effects of right ventricular infarction, most patients have spontaneous early hemodynamic improvement and subsequent recovery of right ventricular function. The prognosis after right ventricular infarction is related to the degree of coexisting left ventricular dysfunction. Patients who survive the acute phase tend to show more clinical and hemodynamic improvement of the right ventricle than of the left, in part because of the lower right ventricular muscle mass and the presence of coronary blood flow to the right ventricle during both systole and diastole.^10,12

Dr. Movahed is director of nuclear cardiology and professor of medicine and radiology in the Department of Medicine, Section of Cardiology, East Carolina University School of Medicine in Greenville, N.C.

Address correspondence to Assad Movahed, M.D., East Carolina University, Brody Medical Sciences Building, Greenville, N.C. 27858-4354.

REFERENCES

Cohn JN, Guiha NH, Broder MI, Limas CJ. Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol 1974;33:209-14.

Isner JM, Roberts WC. Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Am J Cardiol 1978;42: 885-94.

Sharpe ND, Botvinick EH, Shames DM, Schiller NB, Massie BM, Chatterjee K, Parmley WW. The noninvasive diagnosis of right ventricular infarction. Circulation 1978;57:483-90.

Dell'Italia LJ, Starling MR, O'Rourke RA. Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med 1983;99:608-11.

Starling MR, Dell'Italia LJ, Chaudhuri TK, Boros BL, O'Rourke RA. First transit and equilibrium radionuclide angiography in patients with inferior transmural myocardial infarction: criteria for the diagnosis of associated hemodynamically significant RV infarction. J Am Coll Cardiol 1984;4:923-30.

Erhardt LR, Sjogren A, Wahlberg I. Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction. Am Heart J 1976;91:571-6.

Robalino BD, Whitlow PL, Underwood DA, Salcedo EE. Electrocardiographic manifestations of right ventricular infarction. Am Heart J 1989;118:138-44.

Jugdutt BI, Sussex BA, Sivaram CA, Rossall RE. Right ventricular infarction: two-dimensional echocardiographic evaluation. Am Heart J 1984;107: 505-18.

Horan LG, Flowers NC. Right ventricular infarction: how cardiac management differs from usual. Am Fam Physician 1999;60:1727-34.

Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994;330:1211-7.

Goldstein JA, Vlahakes GL, Verrier ED, et al. Volume loading improves low cardiac output in experimental right ventricular infarction. J Am Coll Cardiol 1983;2:270-8.

Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol 1996;28: 1328-1428.

O'Rourke RA. Treatment of right ventricular infarction: thrombolytic therapy, coronary angioplasty or neither (editorial)? J Am Coll Cardiol 1998;32:882-4.

Zehender M, Kasper W, Kauder E, Geibel A, Schonthaler M, Olschewski M, Just H. Eligibility for and benefit of thrombolytic therapy in inferior myocardial infarction: focus on the prognostic importance of right ventricular infarction. J Am Coll Cardiol 1994;24:362-9.

Bowers TR, O'Neill WW, Grines C, Pica MC, Safian RD, Goldstein JA. Effect of reperfusion on biventricular function and survival after right ventricular infarction. N Engl J Med 1998;338:933-40.

Dyspepsia: Relief Not Yet Beyond Belief

DAVID S. GREENBAUM, M.D.
Michigan State University
East Lansing, Michigan

See article in this issue.

The magnitude of dyspepsia is obvious; up to 40 percent of adults in the Western world have frequent episodes and, in the United States, 2 to 5 percent of primary care visits are for this condition.^1-3 The cost of relevant prescription drugs alone is over $1.3 billion annually in the United States, and the cost of over-the-counter medications is probably at least as much. Yet, despite its prevalence, we are relatively ignorant of the etiology. The symptom of dyspepsia should no longer evoke a differential diagnosis that primarily considers ulcer disease, gallbladder problems, gastritis and "nerves." As Bazaldua and Schneider³ indicate in their article in this issue of American Family Physician, with the exception of clear-cut gastroesophageal reflux disease (GERD), we cannot rely on the complaint of dyspepsia alone to help us diagnostically.

Because of the ready accessibility of endoscopy and the discovery of Helicobacter pylori and its relationship to peptic ulcer disease, our perception of dyspepsia has changed and, like many things in life, it appears to be more complex than we had anticipated. Most patients with dyspepsia have normal findings on endoscopy.¹ The majority of patients colonized with H. pylori are asymptomatic, and patients with dyspepsia have the same or slightly higher colonization rates as persons without symptoms. There are poor correlations between symptoms and histologic gastritis, secondary to H. pylori or other causes, and response of symptoms following H. pylori eradication is unpredictable and relatively small.

Bazaldua and Schneider³ give short shrift to functional or nonulcer dyspepsia which, as they point out, is the most frequent cause of dyspepsia. Their reticence is somewhat understandable in light of the uncertain pathophysiology and, as yet, generally unsatisfactory treatment. Nevertheless, progress is slowly being made in understanding and treating nonulcer dyspepsia. Although motility disturbances were considered the most likely etiology in the recent past, gastric or duodenal hypersensitivity, or both, now appears to more probably account for most symptoms.^4,5 There may be an absence of normal postprandial gastric fundus relaxation associated with abnormal antral distension, but this was found in less than one half of subjects tested in one study.⁶

Although this disorder of relaxation could be primary, it could also be secondary to increased resistance to duodenal filling. Delayed duodenal clearance and hypersensitivity to acid may account for nausea in some patients.⁷ The hyperalgesia is site-specific and, as with other functional gastrointestinal disorders, these patients have normal somatic pain thresholds. The associated higher frequency of psychiatric disorders may reflect health-care seeking behavior, response to chronic illness and an intrinsic component of the visceral disorder.^8,9 Proton pump inhibitors, prokinetic agents, antidepressants, newer kappa opioid agonists and behavioral therapy all appear to be effective in some patients. The high placebo response rate should be viewed as an important part of management.

Bazaldua and Schneider³ are to be commended for the concise presentation in Table 6 in their article, presenting the pros and cons relating to the controversies about treatment of H. pylori colonization in dyspeptic patients. However, they do not mention that there is an increased incidence of GERD after eradication of H. pylori and that the alarming increase of adenocarcinoma of the cardia and esophagus may also be related to this intervention.^10,11 The authors favor option 3--testing for and treating H. pylori infections in patients 45 years and younger who have no "alarm" symptoms. Indeed, this approach has considerable support at present.^1,12 However, if a patient responds to eradication treatment, is it because an ulcer was healed, gastritis cured, esophagitis curbed or a placebo effect displayed (which may be over 50 percent in functional gastrointestinal disorders)? The patient's risk is about 20 percent for having an ulcer, 15 percent for esophagitis and 30 to 50 percent for functional dyspepsia.

In quoting from the American Gastroenterological Association Technical Review, Bazaldua and Schneider³ note that the benefits of H. pylori eradication in nonulcer dyspepsia "are likely to be small or nonexistent."¹² In two recent studies, 70 to 80 percent of the patients receiving eradication treatment did not respond.^13,14 The discordant results in these well-performed studies and others demonstrate that there is no easy answer regarding the optimal management of symptomatic functional dyspepsia in patients with H. pylori colonization.

This organism has been around for a long time, and consideration must be given to the fact that it may also have some protective role.¹¹ We should be circumspect as to the possible implications of eliminating it without regard for the long-term negative consequences that ultimately may be greater than the small and unpredictable short-term benefits of treating nonulcer dyspepsia. Management algorithms can be useful guides but should be used with introspection, realizing there are variables too numerous for simplistic solutions to complex problems.¹⁵

Dr. Greenbaum is emeritus professor in the Department of Medicine, College of Human Medicine at Michigan State University in East Lansing, Mich.

Address correspondence to David S. Greenbaum, M.D., Michigan State University, B220 Life Sciences Bldg., East Lansing, MI 48824.

REFERENCES

Fisher RS, Parkman HP. Management of nonulcer dyspepsia. N Engl J Med 1998;339:1376-80.

Friedman LS. Helicobacter pylori and nonulcer dyspepsia (editorial). N Engl J Med 1998;339:1928-30.

Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician 1999;60: 1773-88.

Malagelada JR. The quest for a physiological answer to dyspepsia (editorial). Gastroenterology 1998;115:1586-8.

Fisher RS. Altered visceral perception is responsible for functional (nonulcer) dyspepsia. Practical Gastroenterology May 1999:57-61.

Tack J, Piessevaux H, Coulie B, Caenepeel P, Janssens J. Role of impaired gastric accommodation to a meal in functional dyspepsia. Gastroenterology 1998;115:1346-52.

Samsom M, Verhagen MA, Henegouwen GP, Smout AJ. Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients. Gastroenterology 1999;116:515-20.

Read NW. Functional dyspepsia: a case of indecision. Gastroenterology 1999;116:761-2.

Kapadia CR. The curse of the functional dyspeptic: too sensitive a visceral afferent nervous system. Gastroenterology 1999;116:495-7.

Spechler SJ. Adenocarcinoma of the gastroesophageal junction. Clin Perspectives Gastroenterology March/April 1999;2:95-7.

Blaser MJ. In a world of black and white, Helicobacter pylori is gray (editorial). Ann Intern Med 1999;130:695-7.

Talley NJ, Silverstein MD, Agreus L, Nyren O, Sonnenberg A, Holtmann G. American Gastroenterological Association technical review: evaluation of dyspepsia. Gastroenterology 1998;114: 582-95.

McColl K, Murray L, El-Omar E, Dickson A, el-Nujumi A, Wirz A, et al. Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med 1998;339: 1869-74.

Blum AL, Talley NJ, O'Morain C, van Zanten S, Labenz J, Stolte M, et al. Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med 1998;339:1875-81.

Go MF, Vakil N. Helicobacter pylori infection. Clin Perspectives Gastroenterology May/June 1999;2: 141-53.

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