Right ventricular infarction with hemodynamic decompensation due to transient loss of active atrial augmentation: Successful treatment with atrial pacing

792 Brief communications

Right ventricular infarction with hemodynamic decompensation due to transient loss of active atrial augmentaiion: Successful treatment with atrial pacing Jeffrey M. Isner, M.D.,* Gary P. Fisher, M.D., Albert A. Del Negro, M.D., and Jeffrey S. Borer, M.D.** Bethesda, Md., and

Washington, D.C.

Fig. 2. Preoperative

M-mode echocardiogram showing asymmetrically thickened ventricular septum (KS) with respect to left ventricular (LV) free wall and a small LV cavity. RV = right ventricular.

Fig. 3. Heart cut in a “long-axis” fashion showing walls of the right (RV) and left (LV) ventricles ventricular septum (KS) to be very thick and the cavity to be small. The two white arrows indicate the of the operative vs incision and excision.

the and LV line

constriction or restriction, the mechanism by which the HC caused these hemodynamic alterations is uncertain but probably related to decreased LV diastolic compliance.

REFERENCES

Cohn J, Effat H, Goodwin JF, Oakley CM, Steiner RE: Hypertrophic obstructive cardiomyopathy. Br Heart J z&16, 1964. Goodwin JE: Congestive and hypertrophic cardiomyopathies: A decade oi study. Lancei i:731, i970. Braunwald E. Lambrew CT. Rockoff SD. Ross J. Morrow AG: Idiopattii hypertriphic’subaortic ate&& I. i deacription of the disease based upon an analysis of 64 patienta. Ciiculation 29 (suppl IV):& 1, 1964. McReynolds, RA, Roberta WC: The intramural coronary arteries in hypertrophic cardiomyopathy. Am J Cardiol 35:I54,

1975.

Right ventricular (RV) myocardial infarction (MI) may complicate up to 25% of cases of left ventricular (LV) inferior M1.l If RV hemodynamic decompensation is severe, LV underfilling may result in inadequate systemic perfusion. Therapy in such cases consists chiefly of vohrme administration aimed at increasing RV filling pressure (FP) and thereby augmenting RV cardiac output (CO). The importance of preserving active and synchronous right atria1 (RA) pump in RVMI, however, has not been previously discussed. In the patient described in this report, appropriately timed atria1 contraction was demonstrated both spontaneously and by transvenous atria1 pacing to be the critical factor that preserved right-sided contribution to LVFP and thereby maintained adequate systemic perfusion following acute (A) MI of the RV and LV. A 63-year-old man, admitted because of chest pain, had ECG (Fig. 1, a) pathologic Q waves in inferior leads and serial serum creatine phosphokinase MB isoenzymes documenting evolving AMI. Initially he was mildly hypertensive (130/W mm Hg) in normal sinus rhythm (NSR) at 80 bpm with distended neck veins but clear lung fields. However, 12 hours later he suddenly became hypotensive (64/50 mm Hg) with junctional rhythm (JR) and ventricular rate 68 bpm (Fig. 1, b). Two doses of 0.5 mg atropine failed to restore NSR or increase JR rate. Swan-Ganz catheter recorded pressures (mm Hg) of RA (mean) 14, RV 20/14, pulmonary artery (PA) 20/2, and PA occlusion pressure (PAOP) (mean) 2. Systemic blood pressure (SBP) was unchanged by intravenous dopamine and 5 L of normal saline. NSR spontaneously returned at 76 bpm with PAOP 10 mm Hg and SBP IO5/70 mm Hg, Shortly thereafter, JR recurred at 48 bpm with SBP 60 mm Hg and PAOP 3 mm Hg; SBP then became inaudible by Doppler examination despite reinstitution of dopamine (25 mcg/kg/min). Atropine, 1.0 mg intravenously, restored NSR with Doppler BP 100 mm Hg. Six minutes later, From the Pathology and Cardiology Branches, Blood Institute; and the Division of Cardiology, Georgetown University Hospital. Received Reprint Ce&er,

l Prwent **Pr=esent

for publication

May

14, 1981; accepted

National Heart, Lung and Department of Medicine, June

requesta: Jeffrey M. Isner, M.D., Tufts-New 171 Harrison Ave., Boaton, MA 02111. address: addrew

0002-8703/81/100792

Tufta-New

England

New York

Hospital

+ 03$00.30/O

Medical (Come!&

Center, New

0 1981 The

4, 1981. England

Medical

Boston. York

City.

C. V. Mosby

Co.

vohmle 102 Number 6

Brief

communications

793

Fig. 1. Sequential ECGs from the patient presented. a, Initial ECG on admission shows NSR and pathologic Q waves and T wave inversions in leads II, III, and aVp consistent with inferior MI. b, ECG during initial hemodynamic decompensation reveals JR with normal QRS duration. c, ECG following insertion of coronary sinus pacemaker documents successful atria1 pacing (pacing artifact best seen in leads I, II, III, aVp, and VX). however, JR recurred at 55 bpm with Doppler BP 66 mm Hg and dopamine was given (20 mcg/kg/min). His rhythm and hemodynamic status remained refractory to atropine, increasing doses of dopamine, and continued infusion of normal saline. Because the patient’s perfusion pressure appeared dependent on active and properly timed atria1 contraction, atria1 pacing was instituted. A No. 6760 Medtronic transvenous pacing catheter was inserted into the coronary sinus and atria1 pacing at 75 bpm was begun (Fig. 1, c). SBP immediately rose to 120/75 mm Hg with PA pressure 26/12 mm Hg which was maintained without pressor agents during pacing. The patient was weaned from atria1 pacing 3 days later. Following discontinuation of pacing, he remained in NSR and was discharged on the thirtieth hospital day without further complications. Radionuclide angiography performed at g-month followup examination demonstrated mild RV dilatation and hypokinetic RV apex (Fig. 2) consistent with RVMI. The syndrome of RVMI accompanying LVMI is characterized by (1) LV inferior wall MI, (2) RV dilatation, and (3) elevation of RVFP in excess of LVFP. The latter criterion, first established by Cohn et al. in 1974,* has been shown to be specific for associated RVMI in the absence of pericardial or valvular heart disease.l In our patient, ECG changes and enzyme elevations confirmed LV inferior wall MI, and the high RVFP greatly exceeded the subnormal LVFP, consistent with RVMI. Treatment of choice for this syndrome consists of administration of fluids sufficient to increase RV stroke volume (SV)3; the expected increase in RV CO is designed to increase LV CO by

Fii. 2. Systolic and diastolic frames from 99m-technetium albumin gated cardiac blood pool scan performed 9 months following MI. Both RV and LV are dilated and hypokinetic. augmenting LVFP, thus restoring adequate systemic perfusion. In our patient, volume administration, as well as institution of pressor agents, failed to result in adequate systemic perfusion. Recovery of stable active atria1 mechanism, however, produced improved LVFP and normal SBP. The critical importance of normal synchronous atria1 transport function was demonstrated repeatedly as SBP dropped to hypotensive levels during periods of JR, and then immediately returned to normal levels upon either spontaneous return to NSR or treatment with transvenous atria1 pacing. In the setting of hypocontractile and noncomplaint RV, end-diastolic RA contraction may augment RV CO in two ways. First, it transiently increases RV end-diastolic myocardial fiber length, resulting in improved RV CO by the Frank-Starling mechanism. Because acute myocardial ischemia or MI is generally associated with marked reduc-

o&ber,1@81

794

Brief communications

heckan

tion in myocardial compliance,4 passive atria1 contribution to RVFP is unlikely to produce an optimally “stretched” RV. Previous investigators have demonstrated that in the setting of acute ischemia or MI of the LV, the potential contribution of active left atria1 (LA) contraction to LV SV may be as high as 56%.3 When impaired systemic perfusion is the result of ischemic and noncompliant LV and associated loss of LA contraction, however, LVFP is generally elevated in the absence, as well as in the presence, of active LA contraction.s In our patient, LVFP was subnormal in absence of active atria1 contraction. The improved systemic perfusion that resulted from restoration of active atria1 contraction in our patient is therefore more likely to have resulted from improved RVFP with consequent increase in RV CO and secondary improvement in LVFP, rather than from primary LVFP improvement due to restored LA contraction RA contraction may also augment RV CO by a second mechanism. If pressure generated by RA contraction exceeds PA diastolic pressure, as it did in the present patient, the force of RA contraction alone may be sufficient to open the pulmonic valve before the onset of RV systole. The RA thus acts as an auxiliary but independent right-sided pumping chamber. Echocardiographic confirmation of this latter mechanism has been demonstrated in a 14year-old girl with congenital RV hypoplasia (Uhl’s anomaly): a naturally-occurring model for RVMI. The critical importance of preserving an active and synchronous RA contraction in patients with RVMI has potential therapeutic implications. First, patients in whom atria1 fibrillation (AF) accompanies RVMI with hemodynamic decompensation should be considered candidates for emergency electrical cardioversion. In at least one such patient reported previously, death was preceded for several days by prolonged hemodynamic decompensation associated with protracted AF.’ Second, in patients like the one in the present report in whom accelerated junctional or ventricular pacemaker usurps the sinus pacemaker but in whom AV conduction remains intact, attempts to restore physiologic atria1 function should be quickly and aggressively pursued. Administration of intravenous atropine may be effective in restoring NSR, aIthough in the present patient this was successful on only one occasion, and in that instance only transiently. Under such circumstances, transvenous physiologic atria1 pacing, either from the RA appendage or coronary sinus, may produce substantial CO increment. Finally, patients with RVMI appear to be at increased risk for development of complete heart block (CHB)2; this is because patients with RVMI have severe narrowing of the coronary artery supplying the posterior wall of the heart,l the same artery which gives rise to the AV nodal artery. In those patients with RVMI in whom hemodynamic decompensation is associated with CHB refractory to atropine therapy, ventricular pacing is likely to have deleterious hemodynamic consequences.8 In contrast, um of sequential AV pacemaker may provide significant hemodynamic improvement.

Chamberlain

et al3

have

previously

demon-

Howl Joum.sl

strated the utility of sequential AV pacing in improving CO in treating CHB complicating AMI. Although hemodynamic data were not available to determine how many of the nine patients reported by Chamberlain et al. had associated RVMI, eight of the nine patients had either acute

or healed

MI

involving

the

inferior

LV

wall.

REFERENCES

1.

2.

3.

4.

5.

6.

Isner JM, Roberts WC: Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Frequency, location, associated findings, and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. Am J Cardiol42885, 1978. Cohn JN, Cuiha NH, Broder MI, Limas CJ: Right ventricular infarction. Clinical and hemodynamic features. Am J Cardiol33:209, 1974. Rigo P, Murray M, Taylor DR: Right ventricular dysmnction detected by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 52:268, 1975. Bristow JD, Van Zee BE, Judkins MP: Systolic and diastolic abnormalities of the left ventricle in coronary artery disease. Studies in patients with little or no enlargement of ventricular volume. Circulation 42219, 1970. Rahimtoola SH, Ehsani A, Smno MZ, Loeb HS, Rosen KM, Gunnar RM: Left atria1 transport function in myocardial infarction. Importance of its booster pump function. Am J Med 59:686, 1975 French JW, Baum D, Popp RL: Echocardiographic findings in Uhl’s anomaly. Demonstration of diastolic pulmonary valve onenina. Am J Cardiol36z349. 1975. Raabe DS, Chester AC: Right ventricular infarction. Chest 73:96, 1978. Johnson AD, Laiken SL, Engler RL: Hemodynamic comnromise associated with ventriculoatrial conduction followmg transvenous pacemaker placement. Am J Med ti75, 1978. Chamberlain DA, Leinbach RC, Vassaux CE, Kastor JA, DeSanctis RW, Sanders CA: Sequential atroventricular pacing in heart block complicating acute myocardiai infarction. N Engl J Med 23%577, 1970.

Control of ventricular preexcitatfon z+nd associated arrhythmias by encainide Dan M. Roden, M.D., Henry J. Duff, M.D., R. Kirby Primm, M.D., Marvin W. Kronenberg, and Raymond L. Woosley, M.D., Ph.D.

M.D.,

Nashville, Tenn.

From the Divisicms of Clinical Pharmacology and Canliology, Departmeriti of Medicine and Pharmacology, Vanderbilt Univemity 8chool of Medicine. This work was supported by granta from the Genmal Clinical Research Center Program of the Division of F&search Ftesources, National Institutes of Health (5MOl RR-95) and from the United Statea public Health Service Nos. GM 15431, GM 07569, HL 22oO4, and HL 07411. Fteceiwd for publication Apr. 6, 1981; accepted May 10,198l. Reprint requestsz D. M. Roden, M.D., Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232. f032-8703/81/100794

+ 04$00.40/O

0 1981 The

C. V. Mosby

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