Hemodynamic spectrum of “dominant” right ventricular infarction in 19 patients

Hemodynamic Spectrum of “Dominant” Right Ventricular Infarction in 19 Patients

ELWYN BERNARD

A.

LLOYD, J.

BM,

GERSH,

BCh

MB,

FACC BRIAN M. KENNELLY,

ChB,

MB, ChB,

DPhil,

PhD,

FACC

Cape Town, South Africa

From the Department of Medicine, University of Cape Town and Cardiac Clinic, Groote Schuur Hospital, Cape Town, South Africa. Manuscript received April 14, 1981; revised manuscript received June 15, 1981, accepted June 22, 1981. Address for reprints: Bernard J. Gersh. MD, Division of Cardiovascular Diseases and internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905.

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In 19 patients right ventricular infarction was diagnosed on the basis of electrocardiographic features of acute inferior infarction and clinical evidence of elevation of systemic venous pressure and an absence of pulmonary congestion. Right heart catheterization documented elevated right ventricular end-diastolic pressure (mean 15.5 mm Hg) and commensurate right atrial pressure (mean 14.9 mm Hg). In all patients the pulmonary capillary wedge pressure (mean 13.2 mm Hg) was exceeded or equaled by the right ventricular end-diastolic pressure, suggesting a disproportionate reduction in right ventricular compliance or contractile function, or both. Thirteen patients were hypotensive (systolic blood pressure less than 100 mm Hg on admission), including six patients with cardiogenic shock. Right ventricular infarction is an uncommon and potentially reversible cause of cardiogenic shock; yet, in the experimental model, isolated right ventricular damage is relatively well tolerated. To identify the factors associated with systemic hypotension, data from patients with and without compromised systemic hemodynamic function were compared. In hypotensive patients, the right ventricular end-diastolic pressure was significantly higher (16.6 versus 12.6 mm Hg; p
Although isolated right ventricular infarction is rare,l associated right ventricular damage is increasingly recognized as a determinant of the overall hemodynamic profile in patients with transmural infarction of the left ventricle.2-g It has also become evident that the sequelae of right ventricular infarction encompass a wide spectrum ranging from minimal hemodynamic impairment to cardiogenic shock. The importance of this diagnosis lies in the potential reversibility of shock, as emphasized in the original report by Cohn et a1.2 Yet, in the experimental model,lO-l5 isolated right ventricular damage is hemodynamically well tolerated

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TABLE I Clinical and Hemodynamic Characteristics of 19 Patients With Right Ventricular Infarction* & Sex

ECG Infarct Site

56F 46M 62M 62M 53M 70M 71F 62F 49M 49M 54M 73M 57M 56M 55M 67M 62M 46M 69M

Inf Inf Inf Inf Inf Inf Inf Inf Inf Inf Inf Inf, post Inf, lat Inf Inf Inf Inf Inf Inf

Age (yr) Case 1 : 4 : 6 1: 11 :z :z 16 17 18 19 Mean f SD Range

Systemic BP 1 IO/90 140/110 120/70 130180 1 10180 120190 60140 90170 90160 90160 80150 70140 90150 90160 80150 70140

Pressures (mm Hg) RVSP

RVEDP

::

::

:;

148

:2

:: 14

z;

1; 5

:s 16 16

:;

;: 24 22

:6” 14

:: 16 14 16

:: 29

:: 16 14

:f

ii:: 40/+

PCWP

RAP

:r!i

Z8

:t

:;

:: 20

:z

::

:: 16

:: 20

:r!I 30

:;

1\49 2.7 1 l-18

I:“5 3.7 11-20

24804 6.4 17-40

:; 13.2

Pressor Aoents

Fluid Loadina

:: No No No No Yes Yes Yes Yes No No No No No No Yes No No

,“: Yes No Yes No Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes

5Z

Electrocardiographic criteria of transmural infarction were present in all but two patients (Cases 2 and 11),in whom the diagnosis was nontransmural infarction. Six patients (Cases 2,4, 7, 8, 13 and 16) had S-T segment elevation in leads VI to Vs, suggesting associated septal infarction. One patient (Case 7) died with cardiogenic shock complicated by a cerebrovascular accident. All other patients survived to leave the hospital (hospftal mortality rate 5.3 percent). Another patient (Case 13) sustained a cerebrovascular accident and had substantial residual neurologic disability. + Diastolic pressures were not recordable in these three patients. BP = blood pressure; ECG = electrocardiogram; Inf = inferior; lat = lateral; PCWP = pulmonary capillary wedge pressure; post = posterior; RAP = right atrial pressure; RVEDP = right ventricular enddiastolic pressure; RVSP = right ventricular peak systolic pressure; SD = standard deviation, l

without the development of cardiogenic shock. Indeed, surgical bypass of the right ventricle is successfully used in the management of certain forms of congenital heart disease and does not result in cardiogenic shock.16J7 This retrospective study reports the hemodynamic and clinical findings and the long-term follow-up data in 19 patients with right ventricular infarction. An attempt was made to identify those factors associated with systemic hypoperfusion and shock by comparing data from patients with and without compromised systemic hemodynamic function. Methods The computerized records of all patients with acute myocardial infarction who were admitted to the coronary care unit between January 1976 and March 1979 were examined. Nineteen patients met the criteria for inclusion in this study. Patients:

The following criteria were used to identify patients with suspected right ventricular infarction: (1) electrocardio-

graphic features of acute inferior and inferoposterior myocardial infarction, (2) serum creatine kinase values more than twice the upper limit of normal, (3) clinical evidence of dominant right heart failure demonstrated by elevation of jugular venous pressure without clinical or radiologic evidence of left ventricular failure, and (4) hemodynamic confirmation based on elevation of the right ventricular end-diastolic pressure to values greater than or equal to the pulmonary capillary wedge pressure.2 Some patients who were initially thought to fulfill the criteria for right ventricular infarction subsequently responded to fluid administration with the development of frank left ventricular failure. These patients were considered to have biventricular infarction and were excluded from this analysis of patients with “dominant” right ventricular infarction. Diagnostic procedures: Right-sided intracardiac pressures were measured with the use of flow-directed balloon

TABLE II Incidence of Electrocardiographic

Conduction Disturbances (19 patients) Atrioventricular

lmolantation of Temporary Pacemaker Group’

n

Sinus Bradycardia or Sinus Arrest %

n

Block

2nd Degree %

n

Complete %

n

%

Groups were determined according to systolic blood pressure on admission: group I, more than 100 mm Hg; group II, less than 100 mm Hg. + One patient had atrial fibrillation with an irregular but slow ventricular response. l

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ET AL.

15

(=ii

RA ~~~~,~

hmHg)

r

FIGURE 1. Case 18. Representative pressure records from a patient with right ventricular infarction. Right atrial (R.A.), right ventricular (R.V.) and pulmonary capillary wedge pressures were recorded sequentially. Right atrial pressure is elevated, with a prominent y descent. (The accompanying electrocardiographic tracing is not shown, but the timing of the y descent was established at the time of analysis.) Right ventricular end-diastolic pressure is elevated and exceeds pulmonary capillary wedge pressure. A “dip and plateau” pattern in the right ventricular diastolic pressure waveform is noted. In this patient, equalization of diastolic pressures of left and right heart is not present. The patient was very hypotensive, with a radial arterial systolic pressure of approximately 50 mm Hg.

‘ifl so

40

RADIAL ARTERY 40 hm H@)

30 R.V. (mHg)

20

20

catheters inserted at the bedside under pressure-monitoring control. The left ventricular end-diastolic pressure was assumed to equal the mean pulmonary capillary wedge pressure. Pressures were recorded with the use of Ailtech transducers and were displayed on Electrodyne monitors.

Results Clinical data: The clinical features of the 19 patients with right ventricular infarction are summarized in Table I. There were 16 men and 3 women; their average age was 58.6 years (range 41 to 75). Nine patients had a history of chronic angina pectoris (duration longer than 1 year); three of the nine had a documented previous myocardial infarction, and one had had previous coronary bypass surgery. All 19 patients had electrocardiographic evidence of an acute inferior myocardial infarction (transmural in 17 and nontransmural in 2). Associated direct posterior infarction was evident electrocardiographically in one patient and lateral infarction in another. In six patients additional S-T segment elevation was noted in electrocardiographic leads Vi to V3, suggesting associated septal involvement.18 The severity of the systemic hemodynamic disturbance at the time of admission can be assessed from data in Table I. Six patients were normotensive on

TABLE III Summary of Hemodynamic Data (19 patients)

Pressures(mm Hg) Group

Systolic BP

l

RAP

RVEDP

RVSP

PCWP

I (6 cases) Mean f SD Range II (13 cases) Mean f SD Range D

122 1:;-140 73 4A890

12.8 1.3 11-14

12.8 1.3 11-14

23.8 1%32

9.7 3.3 5-14

15.9 1.6 14-18 <0.02

16.8 1.9 14-20
30.5

14.8

2:-40 <0.03

1?318 <0.05

Groups determined according to systolic blood pressure on admission: group I, more than 100 mm Hg; group II. less than 100 mm Hg. Comparisons between groups I and II were made by using a two sample t test. BP = blood pressure; PCWP = pulmonary capillary wedge pressure; RAP = right atrial pressure; RVEDP = right ventricular end-diastolic pressure: RVSP = right ventricular peak systolic pressure; SD = standard deviation. l

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admission, and 13 (68 percent) were hypotensive (systolic blood pressure less than 100 mm Hg). In the six patients (32 percent) whose systolic blood pressure was persistently less than 80 mm Hg, a clinical diagnosis of cardiogenic shock was made on the basis of systemic hypoperfusion and oliguria. Conduction disturbances within the first 24 hours were noted in 17 of the 19 patients (Table II). Sinus bradycardia or sinus arrest was noted in eight patients, Wenckebach atrioventricular (A-V) block in seven patients, and complete A-V block in four patients. In nine patients (47 percent) the conduction disturbance was treated by implantation of a temporary pacemaker. Conduction disturbances, including complete A-V block, were more severe in patients with hypotension (Table II), and implantation of a temporary pacemaker was confined to this group. Hemodynamic data (Table I): Right heart catheterization was performed within 1 to 6 hours of admission in 15 patients and approximately 24 hours after admission in 4 patients. Mean right heart filling pressures were elevated; the mean right atria1 pressure was 14.9 mm Hg (range 11 to la), and the mean right ventricular end-diastolic pressure was 15.5 mm Hg (range 11 to 20). The mean right ventricular peak systolic pressure was 28.4 mm Hg (range 17 to 40). The mean pulmonary capillary wedge pressure was normal (mean 13.2 mm Hg, range 5 to 18). The index of the ratio of the right ventricular end-diastolic pressure to the pulmonary capillary wedge pressure was 1 or more in all patients, according to previously stated hemodynamic criteria of right ventricular infarction.2 A typical pressure record is illustrated in Figure 1, which demonstrates right heart filling pressures exceeding the pulmonary capillary wedge pressure. The right ventricular diastolic pressure had a “dip and plateau” pattern.5Jg Patients were separated into two groups (groups I and II) according to whether the systolic blood pressure was greater or less than 100 mm Hg on admission, Table III summarizes the hemodynamic data by group and shows that patients who were hypotensive had significantly higher values for right atria1 pressure (15.9 versus 12.8 mm Hg, p <0.02), right ventricular enddiastolic pressure (16.8 versus 12.8 mm Hg, p
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right ventricular peak systolic pressure (30.5 versus 23.8 mm Hg, p <0.03) and pulmonary capillary wedge pressure (14.8 versus 9.7 mm Hg, p <0.05). In both groups the pulmonary capillary wedge pressure was within the “optimal” range for acute myocardiai infarctionzO but was nevertheless higher in hypotensive than in normotensive patients. A wedge pressure of 15 mm Hg or greater was noted in 6 (46 percent) of the 13 patients in group II and in none of the patients in group I. Figure 2 illustrates the significant correlation (r = 0.895, p
Discussion Noninvasive radionuclide echocardiographic techniques7-sfz1 coupled with autopsy data3 have established that the right ventricle is frequently involved in acute myocardial infarction. Our study illustrates the wide clinical spectrum of right ventricular infarction, which may uncommonly contribute to a profound systemic hemodynamic disturbance but often is clinically “silent,” apart from a disproportionate elevation in jugular venous pressure.22 Hemodynamic concepts: In all of our patients, right heart filling pressure was equal to or greater than pulmonary capillary wedge pressure (the latter reflecting left ventricular filling pressure). That a disproportionate elevation in right heart filling pressure could be a consequence of right ventricular infarction has been suspected for years, 23 but pathophysiologic confirmation awaited the study by Cohn et al2 in 1974. In the absence of chronic lung disease or pulmonary embolism, disproportionately elevated right heart filling pressure in the setting of acute infarction could be the result of an impairment in right ventricular contractility or compliance, or both. The relatively low wedge pressure in comparison with that normally found in acute myocardial infarction20 is likely the consequence of an in-

RVSP (mm Hg)

ET AL.

.

*... . *.

25 2.

INFARCTION-LLOYD

. 15 10 5

: 0

5

10

20

15

25

30

PCWP (mm Hg)

FIGURE 2. Scatter diagram of right ventricular peak systolic pressure (RVSP) and pulmonary capillary wedge pressure (PCWP) in 19 patients. The correlation coefficient is 0.895 (p
adequate left ventricular preload resulting in part from a reduction in right heart output.2,24v25 Hemodynamie similarity between right ventricular infarction and constrictive pericarditis: Attention has been drawn to the potential diagnostic problem created by the hemodynamic similarity between constrictive pericarditis and right ventricular infarction.5Js The “dip and plateau” waveform of right ventricular diastolic pressure (Fig. 1) may simulate pericardial disease, particularly when accompanied by equalization of diastolic pressure in both ventricles. These findings are not surprising and are readily explicable. First, equilibration of diastolic pressure may be expected in the absence of an effective right ventricular contraction.26 This pressure configuration is also seen in patients with restrictive cardiomyopathy27 when right ventricular compliance is decreased, as is the case in right ventricular infarction. The restraining effect of the pericardium, which acutely dilates by only about 20 percent,28 may also contribute to the restrictive pressure waveform, because acute dilatation of the right ventricle is common in right ventricular infarction.3 The transient nature of the restrictive pattern in the right heart chambers may result from a rapid improvement in right ventricular function with a reduction in cavity size,2g,3o or conceivably may be influenced by gradual stretching

TABLE

IV

Clinical Management (19 patients)

in Right Ventricular

Infarction

Group’

Therapeutic Interventions Fluid administration Vasopressor agents Digitalis Temporary pacemaker

(6 clses) n %

(13 clLs.es) n %

:

33

13

:

330 0

z 9

100 39” 69

Groups determined according to systolic blood pressure on admission: group I, more than 100 mm Hg; group II, less than 100 mm Hg.

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of the pericardium. It is possible that relative pericardial restriction in itself may contribute to the low cardiac output in some patients with right ventricular infarction.“’ Role of associated left ventricular dysfunction: The concepts mentioned offer a rational explanation for the hemodynamic derangements observed in this and other studies of right ventricular infarction but do not explain the profound systemic disturbance noted in severe cases of right ventricular infarction as opposed to the right ventricular damage found in experimental and surgical situations.10,17 In our study, patients with right ventricular infarction were separated into two groups according to the presence or absence of systemic hypotension. The moderate but significant increase in right heart filling pressure in the hypotensive patients is likely the result of more extensive right ventricular dysfunction. In addition, the pulmonary wedge pressure was significantly higher in hypotensive patients, and values greater than 15 mm Hg were confined to this group. It would appear that in some patients with dominant right ventricular infarction (whose right ventricular end-diastolic pressure was equal to or greater than pulmonary wedge pressure) an additional impairment of left ventricular function is an important determinant of systemic blood pressure. An explanation of the deleterious effect of elevations of left ventricular end-diastolic pressure and wedge pressure on right ventricular performance lies in the concept that in the absence of pulmonary embolism or chronic lung disease the wedge pressure approximates the pulmonary arterial diastolic pressure,32 which in turn influences right ventricular afterload.33*34 The right ventricular peak systolic pressure is a function of right ventricular afterload, and this pressure was significantly higher in hypotensive than in normotensive patients (Table III). The relation between the pulmonary capillary wedge pressure and right ventricular afterload is emphasized by the correlation illustrated in Figure 2. The difference in wedge pressure between the two groups, although statistically significant, was small (mean 5.1 mm Hg) but may be consequential, because the right ventricle is ill adapted to compensate for increased afterload. It has a large surface area in contrast to volume, and the free wall is thin in contrast to the high resistance left ventricular chamber.36 Starr et a1.15 in 1943 suggested that a normal left ventricle and normal pulmonary vasculature were necessary to maintain the circulation in the presence of right ventricular dysfunction, and this was further stressed in 1979 by Cohn.26 Other support for the critical role of associated left ventricular dysfunction in patients with right ventricular infarction arises from extensive experimental evidence suggesting that the intact left ventricle may assist right ventricular ejection.11-15 There is speculation and some evidence that motion of the interventricular septum, either by bulging paradoxically into the right ventricle or by shortening the apex to base axis, could be responsible for the generation of right ventricular pressures despite substantial damage to this

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chamber.10p35,37 In a large autopsy study,” transmural infarction of the posterior ventricular septum was invariably found in cases of right ventricular infarction. Septal motion in clinical right ventricular infarction has not been systematically studied to our knowledge and requires further clarification. In a radionuclide study reported in 1979, Berger et a1.38 pointed out that in the presence of right ventricular ischemia, the left ventricle contributes to normal right ventricular function. Clinical management and hospital mortality: The relatively low hospital mortality rate in our series (5.3 percent) differs from previous reports2,5,25 of less favorable results. This difference probably reflects a different patient population because 6 of our 19 patients were normotensive and only 6 fulfilled the clinical criteria for cardiogenic shock. Understandably, other series incorporating patients primarily in this high risk group have reported less favorable results. Nevertheless, five of our six patients with cardiogenic shock survived to leave the hospital. A further stimulus to the aggressive diagnosis and management of this condition is evidence that right (as opposed to left) ventricular function may improve rapidly after the initial acute ischemic insUlt.zsJc The mainstay of therapy is fluid administration, with the intention of increasing right heart output and left ventricular preload. Ours was a highly selected series of patients with “dominant” right ventricular infarction, in that patients whose wedge pressure was elevated to more than 20 mm Hg by fluid administration were considered to have biventricular infarction and were excluded from the series. Although this definition of acute “dominant” right ventricular infarction is arbitrary, it is clinically relevant as a basis for selecting specific therapeutic interventions and particularly for rejecting inappropriate treatments, specifically the use of diuretic agents, that further reduce ventricular preload.26 If fluid administration alone fails, the administration of inotropic agents appears logical. Our data are inconclusive on this point because the study was retrospective and therapy uncontrolled. That vasodilator agents might be an added rational therapeutic option is suggested by our data. Theoretically, these drugs, by increasing left ventricular ejection, could also augment right ventricular output by reducing right ventricular afterload, either through a direct action on the pulmonary vascular resistance or secondary to a decrease in left heart filling pressure.3gT40 It is feasible that the “flat” part of the ventricular function curve is operative in patients with severe right ventricular dysfunction in whom fluid replacement alone does not substantially increase right ventricular stroke work, and that therapy should be directed toward maintaining adequate right and left ventricular filling (volume loading) in addition to administering agents that directly or indirectly reduce right and left ventricular afterload. We have subsequently encountered three additional patients in whom treatment with fluid administration and inotropic agents failed to maintain an initial improvement. Although adequate right heart preload was maintained with fluids, the addition of

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sodium nitroprusside greatly improved the hemodynamic status in the two patients who survived but was without effect in the third patient, who died. Clinical implications: Although the diagnosis of right ventricular infarction can be suspected clinically and confirmed hemodynamically, its importance lies in the identification of those patients with systemic hypoperfusion, because this condition may be reversible with specific therapeutic interventions. The relatively favorable short-term prognosis is an incentive to the aggressive diagnosis and management of right ventricular infarction. This disease incorporates many shades of a spectrum, ranging from,the rare entity of isolated right ventricular infarction to infarction of both ventricles, in which extensive damage to the left ventricle may overshadow and conceal the hemodynamic sequelae of right ventricular infarction. Conversely, the dynamics of right ventricular infarction may mask as-

INFARCTION-LLOYD

ET AL.

sociated left ventricular failure by reducing left heart preload. For these reasons, hemodynamic monitoring and a therapeutic trial of fluid administration are indispensable as a guide to treatment in patients with functionally significant right ventricular damage after acute infarction. In this series of patients, who fulfilled the criteria of “dominant” right ventricular infarction, the elevation of the pulmonary capillary wedge pressure in those patients with hypotension emphasizes that right ventricular infarction should not be considered an isolated disease of the right ventricle but rather the result of a critical interaction between both ventricles.

Acknowledgment We acknowledge the constructive criticism of this article given by Jay N. Cohn, MD, Minneapolis, and the special secretarial assistance of Deborah Peck.

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26. 27.

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30.

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313. 31. Goldstein JA, Vlahakes GJ, Verrier ED, Schiller N, Tyberg JV, Chatterjee K. Mechanism of low output in experimental right ventricular infarction (abstr). Am J Cardiol 1981;47:437. 32. Rahimtoola SH, Loeb HS, Ehsani A, et al. Relationship of pulmonary artery to left ventricular diastolic pressures in acute myocardial infarction (abstr). Clin Res 1972;20:392. 33. Bergel DH, Mllnor WR. Pulmonary vascular impedance in the dog. Circ Res 1965;16:401-15. 34. Reuben SR, Swadling JP, Gersh BJ, Lee G de J. Impedance and transmission properties of the pulmonary arterial system. Cardiovasc Res 1971;5:1-9. 35. Rushmer RF. Cardiovascular Dynamics. 4th ed. Philadelphia: WB Saunders, 1976:89-99. 36. Stool EW, Mullins CB, Leshin SJ, Mitchell JH. Dimensional

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changes of the left ventricle during acute pulmonary arterial hypertension in dogs. Am J Cardiol 1974;33:868-75. Fixler DE, Monroe GA, Wheeler JM. Hemodynamic alterations during septal or right ventricular ischemia in dogs. Am Heart J 1977;93:210-5. Berger HJ, Matthay RA, Davies RA, Zaret BL, Gottschalk A. Comparison of exercise right ventricular performance in chronic obstructive pulmonary disease and coronary artery disease: noninvasive assessment by quantitative radionuclide angiocardiography. Invest Radio1 1979;14:342-53. Rowe GG, Henderson RH. Systemic and coronary hemodynamic effects of sodium nitroprusside. Am Heart J 1974;87:83-7. Raabe DS Jr, Chester AC. Right ventricular infarction. Chest 1978:73:96-g.

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