Right Ventricular Infarction

9 Buckley RH, Schiff Rl, Amos DB: Blocking of autologous and homologous leukocyte response by human alloimmune plasma: Possible in vitro correlates of enhancement. J. Immunol 108:34-44, 1972 10 Hellstrom KE, Hellstrom I: Lymphocyte-mediated cytoxicity and blocking serum activity to tumor antigens. Adv Imrnunol18:209-277, 1974 11 Adcock EW, Teasdale T, August CS, et al: Human chorionic gonadotropin: Its possible role in maternal lymphocyte suppression. Science 181:845-847, 1973 12 Guttman R: Radiotherapy in locally advanced cancer of the breast. Cancer 20:1046-1050, 1967

Right Ventricular Infarction* DanielS. Raabe, ]r., M.D., 00 and Andrew C. Chester, B.A.t Serial hemodynamic measurements were made in a pa-

laboratory features of each case. 5 Factors arguing against this pulmonary lesion being a second primary bronchogenic cancer were the patient's age, sex, and nonsmoking history and the histopathologic comparability of the metastatic and primary lesions. Finally, metastasis to the brain from the breast, although unusual, 8 seemingly occurred here. The reason for the early unusual spread of this young woman's cancer remains speculative. Pregnancy may have played a role. The serum of pregnant women is found to contain as yet undefined factors which nonspecifically depress lymphocyte-mediated immune responses that are active in defense against neoplasia. 9 - 11 The initial low dose of radiotherapy to regional nodal stations may have contributed to earlier metastasis. 12 In contrast to 1971, present-day management of cancer of the breast probably would include adjunctive chemotherapy after mastectomy, with the hope of preventing late metastasis. This case represents an interesting addition to the list of primary malignant neoplasms metastasizing to major airways. REFERENCES

1 Greenberg BE, Young JM: Pulmonary metastasis from occult primary sites resembling bronchogenic carcinoma. Dis Chest 33:496-505, 1958 2 King DS, Castleman B: Bronchial involvement in metastatic pulmonary malignancy. J Thorac Surg 12:305-315, 1943 3 Higginson JF: A study of excised pulmonary metastatic malignancies. Am J Surg 90:241-252, 1955 4 Trinidad S, Rosenblatt L, Rosenblatt R: Bronchogenic carcinoma simulated by metastatic tumors. Cancer 16: 1521-1529, 1963 5 Case records of the Massachusetts General Hospital: Case 13. N Engl J Med 286:713-719, 1972 6 Braman S, Whitcomb M: Endobronchial metastasis. Arch Intern Med 35:543-547, 1975 7 Kennedy P, Stockman C, Smith F: Endobronchial metastasis from cervical cancer: A case report. Gynecol Oncol 4 :340-344, 1976 8 Holland JF, Frei E III: Cancer Medicine. Philadelphia, WB Saunders Co, 1973

96 RAABE, CHESTER

tient with a massive infarction of the right ventricle complicated by cardiogenic shock, right ventricular fallure, and tricuspid insufficiency. A favorable hemodynamic response was obtained by reducing afterload with administration of sodium nitroferricyanide (nitroprusside) while maintaining preload with infusion of ftuids.

ventricular infarction is uncommon, with an R ight incidence at autopsy of 15 percent in patients with

myocardial infarction. 1 In most cases, right ventricular infarction is discovered only upon microscopic examination of the heart and is almost always accompanied by left ventricular infarction; however, in rare instances, infarction of the right ventricle may predominate, producing a unique clinical and hemodynamic picture. 2 CASE REPoRT

A 49-year-old white woman was admitted to a local hospital with an eight-hour history of nausea, vomiting, chills, and shortness of breath without pain in the chest. Physical examination revealed an obese, tachypneic white woman without obtainable blood pressure. The skin was cold and clammy, with mottled cyanosis. The lungs were clear, and the findings from cardiac examination were described as normal. The electrocardiogram showed atrial fibrillation and an acute inferior myocardial infarction. A chest x-ray film showed cardiomegaly, with clear pulmonary fields. An infusion of dopamine was started, and the blood pressure rose to 110/70 mm Hg. The central venous pressure was 24 mm Hg. The urinary output was poor and did not increase after the rapid infusion of 300 ml of physiologic saline solution and intravenous administration of 40 mg of furosemide. Eight hours later, the patient was transferred to the Medical Center Hospital of Vermont, Burlington. On admission the blood pressure was 110/80 mm Hg without administration of pressor substances, and the pulse rate was 75 beats °From the Departments of Medicine and Pathology, College of Medicine, University of Vermont, Burlington. Assistant Professor of Medicine. tFellow in Pathology. Reprint requests: Dr. Raabe, Mary Fletcher Unit, Medical Center Hospital of Vennont, Burlington 05401 0 0

CHEST, 73: 1, JANUARY, 1978

Table }-Hemodynamic Data /rom Patient wilh Ri«ht Yenlricular ln/aretion -

--

Data

. ...

--------- ·---

.

- - - - - - - - - - - - - --33 hr 100 hr

0 hr

4 hr

None

2 L of physiologic saline solution

Mean systemic arterial pressure, mm Hg

82

79

80

72

84

Mean right atrial pressure, mm Hg

18

20

21

20

20

Mean pulmonary arterial pressure, mm Hg

22

23

26

24

25

Mean pulmonary capillary wedge pressure, mmHg

14

20

23

20

19

Drug administered

Cardiac index, L/min/sq m

L23

L28

23 hr

Sodium nitro- Sodium nitroferricyanide, ferricyanide, 200,.g/min lOO,.g/min

L58

L86

None

L89

Stroke index, ml/min/sq m

13

17

20

23

29

Left ventricular stroke work index, gm-m/sq m

12

13

16

16

26

Right ventricular stroke work index, gm-m/sq m Systemic vascular resistance, dyne sec/em·' Pulmonary vascular resistance, dyne sec/em·'

0.70

1.36

L25

L97

2,438

2,155

1,755

1,312

1,595

305

110

89

101

125

per minute. The veins in the neck were distended, with "v" waves noted. The lungs were clear. The heart was not enlarged, and the first and second heart sounds were normal. A loud third heart sound was heard at the lower left sternal border, along with a grade 2/6 systolic ejection murmur in the same area. Neither the murmur nor the third heart sound varied with respiration. The edge of the liver was palpable 12 em below the right costal margin and was tender but not pulsatile. An inferior myocardial infarction was confirmed by serial electrocardiographic and enzyme changes. In addition, there was laboratory evidence of hepatic necrosis, mild disseminated intravascular coagulation, and acute renal failure. An echocardiogram done on the second day of hospitalization revealed an increased right ventricular end-diastolic internal diameter ( 2.4 em/sq m ) and paradoxical septal motion. A How-directed, balloon-tipped thermodilution catheter was positioned in the pulmonary artery for the measurement of pulmonary arterial and pulmonary capillary wedge pressures (Table 1) _ Because of the low cardiac index and relatively low mean pulmonary capillary wedge pressure, 2L of physiologic saline solution was given over a period of four hours, with a resultant rise in the mean right atrial pressure and mean pulmonary capillary wedge pressure without any change in the cardiac index or stroke work index. Unloading therapy with sodium nitroferricyanide (nitroprusside ) was then begun, while fluids were infused at a rate sufficient to maintain the mean pulmonary capillary wedge pressure at 18 to 20 mm Hg. Concomitant with this therapy, there was a rise in the cardiac index and right ventricular stroke work index, indicating improved right ventricular performance. Therapy with sodium nitroferricyanide was discontinued on the fifth day of hospitalization, at which time the patient's hemodynamic status was stable. Hemodialysis was instituted because of persistent renal failure. On the sixth day of hospitalization, while undergoing dialysis, the patient developed frequent premature ventricular contractions that were not suppressed

CHEST, 73: 1, JANUARY, 1978

0.70

by therapy with lidocaine, and her cardiac rhythm deteriorated into ventricular fibrillation. Resuscitation was unsuccessful. At autopsy the heart weighed 470 gm. There was a recent transmural infarction involving the posterior left ventricle, the posterior one-third of the interventricular septum, and the posterior and lateral walls of the right ventricle, including the inferior right ventricular papillary muscle ( Fig 1 ) . In addition, an old subendocardial infarction of the lateral left ventricular wall was present. All of the coronary arteries were diffusely involved with moderate to severe atherosclerosis. The right coronary artery was totally occluded by an atheromatous plaque and recent thrombus at the acute margin of the heart. DISCUSSION

This patient initially had an acute inferior myocardial infarction complicated by cardiogenic shock, right-sided congestive heart failure, and tricuspid insufficiency. Right ventricular failure and cardiogenic shock have been noted in most published cases of right ventricular infarction. Rotman et al2 reported the findings in a 61year-old man with cardiogenic shock and right ventricular failure following acute inferior myocardial infarction. Autopsy showed infarction of the posterior left ventricular wall and interventricular septum and of the posterior and lateral walls of the right ventricle. Cohn et aP described six patients with inferior myocardial infarction and right ventricular failure, five of whom initially were in cardiogenic shock. Right ventricular involvement was confinned at autopsy in two patients and was assumed in the others on the basis of similar clinical and hemodynamic findings; however, this high incidence of congestive heart failure and shock in patients

RIGHT VENTRICULAR INFARCTION 97

POSTERIOR

ANTERIOR FIGURE 1. Cross section of heart through right and left ventricles (left), with diagrammatic representation ( right) . There is extensive fresh infarction of lateral and posterior walls of right ventricle ( RV) and posterior third of interventricular septum (dark areas). Area of fresh infarction extends into posterior left ventricle ( LV). Healed intramural infarction of posterior and lateral walls of left ventricle is also present (light areas). Papillary muscle infarction cannot be seen at this cross-sectional level.

with right ventricular infarction may be due to the selection of patients, rather than to the natural course of right ventricular infarction. Rigo et al 4 have described right ventricular enlargement on scintiphotographs in six of 14 patients with inferior myocardial infarction without shock, and echocardiographic studies by Gomez et al5 have shown an increase in the right ventricular internal diameter and paradoxical septal motion in six of nine patients with inferior myocardial infarction. These patients also had high mean right atrial pressure ( 11 mm Hg) in the face of a normal mean pulmonary capillary wedge pressure ( 10 mm Hg). These authors 4 • 5 concluded that right ventricular infarction or ischemia or both are frequently present in patients with inferior myocardial infarction without shock or congestive heart failure. Initial hemodynamic measurements revealed an elevated mean right atrial pressure, normal mean pulmonary capillary wedge pressure, and markedly diminished cardiac index and stroke work index (Table 1). This combination of elevated mean right atrial pressure with normal mean pulmonary capillary wedge pressure has been noted in all cases of right ventricular infarction in which these measurements have been made."· 3 Therapy with volume loading increased both the mean right atrial pressure and mean pulmonary capillary wedge pressure, but there was no significant change in the left or right ventricular stroke work indices or the cardiac index, indicating a flat curve for the ventricular function of both left and right ventricles. Because of the poor response to therapy with volume loading, a reduction in afterload with administration of sodium nitroferricyanide was initiated, while preload was maintained by infusion of fluids. This resulted in an improvement in right ventricular stroke work index and

98 RAABE, CHESTER

an increase in both the mean pulmonary arterial pressure and the cardiac index (Table 1). By decreasing impedance to right ventricular ejection, therapy with sodium nitroferricyanide allowed for improved right ventricular emptying and an increase in right ventricular cardiac output and right ventricular stroke work index. As shown in Table 1, therapy with sodium nitroferricyanide, produced vasodilatation in both the systemic and pulmonary arterial beds. This is in agreement with data in experimental canine infarction in which administration of sodium nitroferricyanide produced an equivalent decrease in both systemic vascular resistance and pulmonary vascular resistance.6 Therapy with sodium nitroferricyanide has been shown to improve left ventricular function and survival 7 in patients with left ventricular acute myocardial infarction. It is probable that the beneficial effects of therapy with sodium nitroferricyanide on left ventricular function in acute myocardial infarction are due to a combination of reduction in afterload and a decrease in myocardial ischemia, although this latter effect is controversial. 8 The improvement in right ventricular function noted in our patient treated with sodium nitroferricyanide suggests that these mechanisms are operative in right ventricular, as well as left ventricular, infarctions. Cohn et a)3 also reported that one of their patients with right ventricular infarction and cardiogenic shock responded to therapy with sodium nitroferricyanide, although no hemodynamic data were provided. The pressure contours were of interest. The right atrial and right ventricular pressures were identical, with a large "v" wave in the right atrium and the configuration of a diastolic dip and plateau in both chambers (Fig 2). After therapy with volume loading, the mean right atrial pressure, right ventricular end-diastolic pressure, pulmo-

CHEST, 73: 1, JANUARY, 1978

-

.....

.04111C (•

•"

.'

....

• L

•...

.;

Oc

I

t

.()4-

40

mmHQ 20

FN

PA

RA

FN/RA

2. Pressure tracings from pulmonary artery ( PA), right ventricle ( RV), and right atrium ( RA). Simultaneous right ventricular and right atrial tracing ( RV/ RA) is also shown. Right ventricular diastolic pressure shows marked pattern of dip and plateau and elevated right ventricular end-diastolic pressure. Diastolic pressures in pulmonary artery, right ventricle, and right atrium are equal. These findings indicate severe restriction to right ventricular filling. There is a large ''v'' wave in right atrium, consistent with tricuspid regurgitation. FIGURE

nary arterial diastolic pressure, and mean pulmonary arterial wedge pressure were equal (Table 1). This equilibrium of pressures plus the pattern of dip and plateau is identical to the hemodynamic picture seen in constrictive pericarditis and restrictive cardiomyopathy, in which How into the nondistensible ventricle ceases in the early to middle portion of diastole at a point corresponding to the onset of the plateau in the pressure contour. 9 Since there was no evidence at autopsy of either restrictive pericardia! or myocardial disease in our patient, it is assumed that the observed pressure contours were caused by a reduction in right ventricular compliance secondary to infarction. Changes in left ventricular compliance have been shown to accompany left ventricular infarction, 10 but the extreme changes in ventricular compliance necessary to produce the type of pattern seen in Figure 2 have never been shown in left ventricular infarction and suggest that right ventricular infarction may produce more severe changes in ventricular compliance than left ventricular infarction. The presence of large "v" waves in the right atrial pressure tracing was consistent with the clinical impression of tricuspid regurgitation due to dysfunction of the right ventricular papillary muscle. At autopsy, this clinical impression was confirmed by the demonstration of infarction of the inferior right ventricular papillary muscle. Acute tricuspid regurgitation secondary to right ventricular infarction has not previously been reported, although Zone and Botti 11 described a 48-year-old white man with tricuspid insufficiency and chronic right ventricular failure two years after an inferior myocardial infarction. CoNCLUSION

The presence of right ventricular failure in a patient with inferior myocardial infarction should suggest the possibility of right ventricular infarction. Hemodynamic evidence of an elevated right ventricular IDling pressure with normal left ventricular filling pressure strengthens that suspicion. Acute tricuspid regurgitation due to dysfunction of the right ventricular papillary muscle can

CHEST, 73: 1, JANUARY, 1978

occur in the setting of right ventricular infarction. Therapy directed towards maintaining adequate left ventricular filling (volume loading) and enhancing ventricular ejection (unloading) has been shown to be effective in a few patients with extensive right ventricular infarction and cardiogenic shock. REFERENCES

1 Wartman WB, Hellerstein HR: The incidence of heart disease in 2,000 consecutive autopsies. Ann Intern Med 28:41-65, 1948 2 Rotman M, Raliff NB, Hawley J: Right ventricular infarction : A hemodynamic diagnosis. Br Heart J 36:941-944, 1974 3 Cohn JN, Guiha NH, Broder Ml, et al: Right ventricular infarction. Am J Cardiol33:209-214, 1974 4 Rigo P, Murray M, Taylor DR, et a! : Right ventricular dysfunction detected by gated scintiphotography in pa.tients with acute inferior myocardial infarction. Circulation 52:268-274, 1975 5 Gomez G, Tresch D, Grismer J, eta!: Hemodynamic and echocardiographic correlation of right ventricular dysfunction in acute myocardial infarction (abstract). Clin Res21:420, 1973 6 Rowe GG, Henderson RH : Systemic and coronary hemodynamic effects of sodium nitroprusside. Am Heart J 87:83-87, 1974 7 Chatterjee K, Swan HJC, Kaushik VS, et a!: Effects of vasodilator therapy for severe pump failure in acute myocardial infarction on short-term and late prognosis. Circulation 53 :797-802, 1976 8 Chiariello M, Gold HK, Leinbach RC, eta!: Comparison between the effects of nitroglycerin and nitroprusside on ischemic injury during acute myocardial infarction ( abstract) . Am J Cardiol37 :127, 1976 9 Gaash WN, Peterson KL, Shabetai R: Left ventricular function in chronic constrictive pericarditis. Am J Cardia! 34 :107-110, 1974 10 Diamond G, Forrester JS: Effect of coronary artery disease and acute myocardial infarction on left ventricular compliance in man. Circulation 45:11-19, 1972 11 Zone DD, Botti RE: Right ventricular infarction with tricuspid insufficiency and chronic right heart failure. Am J Cardiol 37:445-448, 1976

RIGHT VENTRICULAR INFARCTION 99