right ventricular infarction: …right ventricular dysfunction in the setting ofright...

British Heart Journal, I974, 36, 941-944.

Right ventricular infarction: a haemodynamic diagnosis'

Michael Rotman, Norman B. Ratliff, and John HawleyFrom the Division of Cardiology of the Department of Medicine and the Department of Pathology,Duke University Medical Center, Durham, North Carolina, 27710, U.S.A.

Right ventricular infarction is a rarely recognized clinical entity. This report describes a patient who perishedwith a massive right ventricular infarction. The pathogenesis of right ventricular infarction is discussed.Haemodynamic studies in this patient suggest that an increase of right atrial mean pressure relative to anychange in pulmonary artery diastolic pressure may be a strong haemodynamic indicator of right ventricularinfarction.

The incidence of right ventricular infarction, basedon necropsy studies, has been reported to be be-tween 2 and 13 per cent of patients dying fromcoronary heart disease (Bean, I938; Wartman andHellerstein, I948). In a recent pathological studyfrom our institution (Ratliff and Hackel, I974) thefrequency of right ventricular infarction in associa-tion with left ventricular infarction was 34 per cent(35 of I02). Right ventricular infarction is onlyrarely recognized clinically and there are no agreedelectrocardiographic criteria of this entity. The pur-pose of this report is to describe a patient who ex-pired with a massive right ventricular infarction.Haemodynamic studies in this patient before hisdeath revealed findings thought to be compatiblewith acute right ventricular failure.

Case reportA 6r-year-old man presented to the emergency room on27 September I97I at 7.oo am with a 9-hour history ofdizziness, shortness of breath, and severe substernalchest pain. While in the emergency room he was notedto have a blood pressure of 5o/o nunHg. An electro-cardiogram taken at that time revealed ST segmentelevation in leads II, III, and aVF, and first-degree heartblock. No previous history of chest pain, myocardial in-farction, hypertension, diabetes mellitus, or pulmonarydisease was obtained.The patient was transferred to the coronary care unit.

Physical amination revealed a blood pressure of 88/6ommHg, a pulse of 88 beats/min, and a respiratory rate of40 per minute. The skin was cool, but was not dia-phoretic. There was pronounced distension ofthe jugularveins with tall 'A' waves. The lungs were clear. Examina-tion of the heart showed an apex impulse in the fifth

1 This work was supported in part by grants from the USPHS.

intercostal space, 5 cm to the left of the midsternal line.No abnormal praecordial activity was noted. The heartsounds were distant and an S4 gallop was heard at theapex. mination ofthe abdomen was normal except forright upper quadrant tenderness. Peripheral oedema wasabsent.On admission the patient's haemoglobin was 9.4 gl

I00 ml and the white blood cell count was 22,900/mm3with a shift to the left. The serum levels were: sugar i8omg/boo ml, BUN 26 mg/ioo ml, Na 127 mEq/l., K 6-7mEq/l., Cl 89 mEq/l.,and CO2Of Io mm/l. Blood gases onnasal oxygen revealed a pH of 7-36, P02 of I59 mmHg, aPco2 of II mmHg, and bicarbonate of 6 mEq/l. Serialenzymes and electrocardiograms were compatible with anevolving diaphragmatic myocardial infarction. Radio-graphic evaluation revealed mild left ventricular enlarge-ment and absent pulmonary congestion.A Swan-Ganz flow-directed catheter (Ganz et al.,

I970) was used to obtain right-sided cardiac pressures.The pressures were measured with a Hewlett-Packardtransducer (No. I28oC) and recorded on a Hewlett-Packard multichannel oscillograph. A point io cm abovethe bed or catheterization table was used as zero refer-ence. Cardiac output was measured by the dye-dilutiontechnique using indocyanine green. Dye curves wererecorded on a Waters densitometer (No. XP-302) andwere calibrated using known quantities of dye in thepatient's blood. The cardiac outputs were calculated bythe method of Thompson et al. (I964). Arterial andvenous oxygen samples were measured on an Instru-mentation Laboratories CO-Oximeter (No. I82). Thehaemodynamic data are presented in the Table. Theinitial study on 27 September 197I at I.00 pm revealed aright atrial mean pressure of I8 mmHg and a pulmonaryartery diastolic pressure of 14 mmHg. The cardiac indexwas 3-I I./min per ma and the AV 02 difference was 6-9vol per cent. Subsequent data continued to show a pro-nounced discrepancy between the right atrial meanpressure and the pulmonary artery diastolic pressure.There was progressive haemodynamic deterioration with

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942 Rotman, Ratliff, and Hawley

TABLE Haemodynamic data: a rise in right atrialpressure relative topulmonary artery diastolic pressureis noted on all three observations

Date 27.9.71 28.9.71Time I.00 pm 9.30 am* 5.30 pm

Pressures (mmHg)Right atrium a=2i (i8) (i6) (22)

V=I7Right ventricle 25/5-I4Pulmonary artery 25/14 (i6) I8/8 (I3) 25/9 (I7)Pulmonary

arterywedge (I2) (9)

Radial artery 92/64 (76) 84/60 84/36 (54)Cardiac index

(1./min per m2) 3-I 2.7Stroke index

(ml/beat per M2) 30 27AV 02 difference

(vol %) 6-9 7.8Heart rate

(beats/min) 100 95 I05

* The patient was treated with an isoprenaline drip on 27 and28 September. Isoprenaline was discontinued at the time ofthe observations indicated at 9.30 am on 28 September.

a fall in cardiac and stroke index as well as blood pres-sure. During the first 24 hours in hospital the patient re-sponded to therapy which included nasal oxygen, an iso-prenaline drip, and intermittent doses of intravenousfrusemide, bicarbonate, and digitalis. Over the final 12hours gradual deterioration occurred with a decrease inurinary output and an altered sensorium in spite oftherapy with intravenous glucagon and noradrenaline. At6.oo pm on 28 September 1971 the patient suffered arespiratory and cardiac arrest with ventricular fibrillationand could not be resuscitated.At necropsy the heart was enlarged, weighing 475 g.

The right atrial appendage contained a well-fixed muralthrombus. The right ventricle was moderately dilatedand the trabeculae carneae flattened. The left atrial andleft ventricular cavities were not remarkable. There was arecent transmural infarct at the base of the heart involv-ing the posterior left ventricular wall and the posteriorthird of the interventricular septum. The infarctextended transmurally from endocardium to epicardiumin the left ventricle and completely across the septum.The infarct also extended posteriorly into the thinnedright ventricular wall for a distance of 5.5 cm, and wellaround to the lateral margin of the right ventricle (Fig.).The right coronary artery was dominant and its orificewas narrowed by approximately 75 per cent. The sino-atrial nodal artery originated about i cm distal to theorifice and was patent. There were multiple narrowedatheromatous lesions along the course of the rightcoronary artery with a point of 85 per cent narrowing3 cm from the coronary orifice and a second narrowed

point of about 85 per cent narrowing in the posteriorpart of the right coronary artery 8 cm from the coronaryorifice. In addition to the old atherosclerotic narrowing,the right coronary artery was completely occluded by arecent thrombus that filled the lumen from the coronaryorifice to just i to 2 cm proximal to its posterior descend-ing branch. The main left coronary artery was modera-ely involved by old atherosclerosis that narrowed thelumen by about 50 per cent. The left anterior descendingand left circumflex coronaries were severely stenosed byold atheromatous plaques.

DiscussionTo understand the pathogenesis of right ventricu-lar infarction the normal vascular supply of the rightventricle and the distribution of the right coronaryartery must be considered. Farrer-Brown (I968)studied the vascular patterns of the myocardium ofthe right ventricle in 5o human hearts. He foundthat the right coronary artery supplied all the rightventricular free wall except the anterior marginwhich was supplied by branches of the left anteriordescending. The posterior descending branch of theright coronary artery supplied the posterior wall ofthe right ventricle as well as in the majority of heartsthe diaphragmatic and posterior surface of the leftventricle. The right marginal artery of the rightcoronary supplied the lateral wall of the rightventricle. A pattern of perfusion with both branch-ing and straight type arteries was found in thedistribution of the right coronary artery, similar tothe pattern of the left coronary artery. The leftcoronary artery was an important source of bloodsupply to the right side via a number of branches,the most important of which was the left anteriordescending branch.The most complete clinical and pathological cor-

relative study of right ventricular infarction wasdescribed by Wade (I959). He reviewed the patho-logical studies of ii cases and added io additionalcases previously reported. The clinical descriptionin 7 of his cases revealed the presence of right-sidedcongestive failure in 5. The electrocardiogramshowed a diaphragmatic or posterior infarction in allcases. In contrasting the group of patients withright ventricular infarction with those with leftventricular infarction, some interesting differenceswere noted. Those patients with right ventricularinfarction had a higher incidence of multiple infarc-tions, right-sided mural thrombi, pulmonary embol-ism, pericarditis, right ventricular hypertrophy, andchronic pulmonary disease. Examination of thecoronary arteries revealed a 'severe' right coronaryocclusion in all cases and 'moderate to severe' in-volvement in at least one or both remaining maincoronary branches in most of the cases. The site of



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FIG. A complete cross-section of the heart near the base of the heart. The acute myocardialinfarction involved the posterior third of the interventricular septum and the posterior andposterolateral walls of the right ventricle. The arrows delineate the extent of the infarction. Theinfarcted myocardium is pale and contains extensive areas of haemorrhage. Haemorrhage isparticularly evident in the left side of the posterior interventricular septum, in the subendo-cardial myocardium of the posterior wall of the left ventricle, and through the full thickness ofthe posterior wall of the right ventricle. The infarction is transmural in both left and rightventricle. Note the dilatation of the right ventricle and the thinning of the infarcted rightventricle, interventricular septum, and left ventricle. (A=anterior, P=posterior, R=right,L= left.)

infarction in the right ventricle was posterior in I8cases and anterior in 3. The great proportion of theinfarcts were transmural. The pathological dataobtained in our patient conform to the findingsnoted by Wade.The lower incidence of right ventricular infarc-

tion when compared to involvement of the leftventricle is probably due to a number of factors.These include: the lower metabolic requirements ofthe right ventricle since it is a low pressure chamber,the pattern of coronary flow in the right coronaryartery being both diastolic as well as systolic, therate and extent of collateral vessel developmentnoted in experimental studies of right coronaryartery occlusions when compared to occlusion of theleft anterior descending, and the available collateral

vessels from the left coronary system (Gregg, I950;Wiggers, I954; Farrer-Brown, I968; Ramo et al.,I970). The pathogenesis of right ventricular infarc-tion from pathological data in man (Wade, I959) andfrom experimental data in the pig (Peter et al., I972)thus includes a severe degree of coronary athero-sclerosis and the development of right ventricularhypertrophy.

Acute myocardial infarction predominantly in-volves the left ventricle. Since right ventricularfunction does not parallel changes in left ventricularfunction in the setting of acute infarction, the use ofmean right atrial pressure or central venous pressureis not a reliable guide in determining the fillingpressure of the left ventricle (Rapaport andScheinman, I969; Hamosh and Cohn, I971;



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944 Rotman, Ratliff, and Hawley

Forrester et al., I971). More recent studies haveshown that the level of pulmonary artery diastolicpressure is highly correlated with the filling pressureof the left ventricle (Kaltman et al., I966; Sapru,Taylor, and Donald, I968; Falicov and Resnekov,1970; Hamosh and Cohn, 1971).A number of haemodynamic studies revealed a

group of patients where the level of right atrial meanpressure was raised relative to any change in pul-monary artery diastolic pressure or left ventricularend-diastolic pressure (Fluck et al., I967; Lassers etal., I970; Hamosh and Cohn, I97i). Acute diaphrag-matic or posterior myocardial infarctions werepresent in all these patients. In 5 of these patientsstudied pathologically, definite infarction of theright ventricle was seen in 4 and obstructive lungdisease in i. Thus the pronounced increase in rightatrial mean pressure relative to any change in pul-monary artery diastolic pressure noted in our patientand other patients with diaphragrnatic or posteriormyocardial infarctions may be a manifestation ofright ventricular dysfunction in the setting of rightventricular infarction.There are certain clinical clues to the diagnosis of

right ventricular infarction. These include a patientwith a diaphragmatic or posterior infarction,associated with conditions that may have led to im-paired right ventricular function, and the finding ofright ventricular failure out of proportion to leftventricular failure. Though these clues may lead toa suspicion of right ventricular infarction thehaemodynamic alterations described should increasethe objectivity and accuracy in the diagnosis ofacute right ventricular infarction.

ReferencesBean, W. B. (1938). Infarction of the heart: III. Clinical

course and morphological findings. Annals of InternalMedicine, 12, 71.

Falicov, R. E., and Resnekov, L. (I970). Relationship of thepulmonary artery end-diastolic pressure to the leftventricular end-diastolic and mean filling pressures inpatients with and without left ventricular dysfunction.Circulation, 42, 65.

Farrer-Brown, G. (I968). Vascular pattern of myocardium ofright ventride of human heart. British Heart3'ournal, 30,679.

Fluck, D. C., Valentine, P. A., Treister, B., Higgs, B., Reid,D. N., Steiner, R. E., and Mounsey, J. P. D. (I967). Right

heart pressures in acute myocardial infarction. BritishHeart Journal, 29, 748.

Forrester, J. S., Diamond, G., McHugh, T. J., and Swan,H. J. C. (I97I). Filling pressures in the right and left sidesof the heart in acute myocardial infarction: a reappraisal ofcentral-venous-pressure monitoring. New EnglandJournalof Medicine, 285, I90.

Ganz, W. W., Forrester, J. S., Chonette, D., Donoso, R., andSwan, H. J. C. (I970). A new flow-directed cathetertechnique for measurement of pulmonary artery andcapillary wedge pressure without fluoroscopy (abstract).American Journal of Cardiology, 25, 96.

Gregg, D. E. (I950). Coronary Circulation in Health andDisease. Lea and Febiger, Philadelphia.

Hamosh, P., and Cohn, J. N. (I97I). Left ventricular functionin acute myocardial infarction.Journal of Clinical Investiga-tion, 50, 523.

Kaltman, A. J., Herbert, W. H., Conroy, R. J., and Kossmann,C. E. (I966). The gradient in pressure across the pulmon-ary vascular bed during diastole. Circulation, 34, 377.

Lassers, B. W., George, M., Anderton, J. L., Higgins, M. R.,and Philip, T. (I970). Left ventricular failure in acutemyocardial infarction. American Journal of Cardiology, 25,SII.

Peter, R. H., Ramo, B. W., Ratliff, N., and Morris, J. J., Jr.(I972). Collateral vessel development after right ventricu-lar infarction in the pig. American Journal of Cardiology,29, 56.

Ramo, B. W., Peter, R. H., Ratliff, N., Kong, Y., McIntosh,H. D., and Morris, J. J., Jr. (I970). The natural history orright coronary arterial occlusion in the pig. Comparisonwith left anterior descending arterial occlusion. AmericanJournal of Cardiology, 26, I56.

Ratliff, N. B., and Hackel, D. B. (I974). Studies on rightventricular infarction. Manuscript in preparation.

Rapaport, E., and Scheinman, M. (I969). Rationale andlimitations of hemodynamic measurements in patientswith acute myocardial infarction. Modern Concepts ofCardiovascular Disease, 38, 55.

Sapru, R. P., Taylor, S. H., and Donald, K. W. (I968). Com-parison of the pulmonary wedge pressure with leftventricular end-diastolic pressure in man. Clinical Science,34, 125.

Thompson, H. K., Starmer, C. F., Whalen, R. E., andMcIntosh, H. D. (I964). Indicator transit time consideredas a gamma variate. Circulation Research, 14, 502.

Wade, W. G. (I959). The pathogenesis of infarction of theright ventricle. British Heart3Journal, 21, 545.

Wartman, W. B., and Hellerstein, H. K. (I948). The inci-dence of heart disease in 2000 consecutive autopsies.Annals of Internal Medicine, 28, 41.

Wiggers, C. J. (1954). The interplay of coronary vascularresistance and myocardial compression in regulatingcoronary flow. Circulation Research, 2, 27I.

Requests for reprints to Dr. Michael Rotman, II2Travertine No. B, San Antonio, Texas 782I3, U.S.A.



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