Temporary physiologic pacing in inferior wall acute myocardial infarction with right ventricular damage

May 1, 1987

Temporary Physiologic Pacing in Inferior Wall Acute Myocardial Infarction with Right Ventricular Damage MURRAY F. MATANGI, MB, ChB, FRACP, FRCPC

A

trioventricular (AV) sequential pacing for chronic complete heart block is clearly superior in both the laboratory animal and in humans.le3 The importance of AV synchrony in patients with acute myocardial infarction (AMI) is not well appreciated. Some investigators suggest that AV synchrony is extremely important in patients with inferior AMI, right ventricular (RV) dysfunction and nonsinus bradyarrhythmias.J-6 The predominantly used pacing mode in such patients is ventricular demand pacing with aggressive fluid loading.7 A canine model of right coronary artery occlusion, septal damage and complete heart block conclusively showed that addition of AV synchrony improves mean arterial pressure 29% and cardiac output 34% .* This study compares the hemodynamics of ventricular demand and atria1 or AV sequential pacing in 5 patients with inferior AMI, RV dysfunction and nonsinus bradyarrhythmias.

THE AMERICAN

TABLE I

JOURNAL

OF CARDIOLOGY

Volume 59

1207

Patient Characteristics

Pt

Age (~0 8 Sex

1 2 3 4 5

71M 65M 61F 71F 60M BP = blood pressure;

Admission BP (mm Hs)

Rhythm Disturbance Nodal Nodal CHB Nodal CHB CHB = complete

86160 80180 70136 90152 90160

heart block

Initially pacing was ventricular using the VW mode at a rate 5 to 10 beats/min above the underlying atrial rate for patients in complete heart block or 5 to 10 beats/min above the underlying ventricular rate for those in a nodal rhythm. After a IO-minute stabilization period, systemic pressures, pulmonary pressures, right atrial pressure, pulmonary artery wedge pressure and cardiac output was determined. The pacing mode was then changed to atrial, A00 pacing for patients in a nodal rhythm or AV sequential, DVI pacing for patients with complete heart block. For DVI pacing the AV interval was set at 150 ms. AtriaJ capture was considered present when atrial pacing was followed by a definite p wave recognized on the rest electrocardiogram. After a further 10-minute stabilization period the hemodynamic values were The 5 patients had all sustained an inferior AMI again recorded. At the end of this study the patients and nonsinus bradyarrhythmias refractory to intravewere placed in the pacing mode that gave them the nous a&opine. A11 required temporary transvenous best hemodynamic results. pacing. Patients had hypotension (systolic arterial Values are mean f standard deviation. A z-tailed pressure 100 mm Hg or less) and clinical evidence of paired t test was used to detect differences between RV dysfunction. The latter was manifested by an ele- the means of the results for the 2 pacing modes. A p vated jugular venous pressure without pulmonary con- value <0.05 was considered significant. gestion either clinically or by chest radiography. AJJ Patient characteristics are summarized in Table I. patients were monitored using an arterial line, a AJJ patients had clinical evidence for shock and RV Swan-Ganz catheter and either an atrial bipolar pac- infarction. The hemodynamic results are recorded in ing electrode with a ventricular bipolar pacing elec- Table II. Results for cardiac output and systolic arteritrode or an AV pacing catheter specifically designed aJ pressure are shown in Figures 1 and 2. Hemodyfor temporary physiologic pacing. Patients were studied if they had an elevated right atrial pressure [at least 10 mm Hg) without a marked elevation of the pulmonary artery wedge pressure (20 mm Hg or less]. The pressure tubing and transducers were flushed and reset at 0 before each set of recordings. AJJ pressure recordings were obtained with the patient in the supine position. The transducers were zeroed in the midaxillary position. Cardiac output was recorded in triplicate using the thermodilution method. If the cardiac output varied by more than 10% or the cardiac output curves obtained were unsatisfactory, another 2 50 cardiac outputs were determined. The mean of the PC 0.005 1 r 3 or 4 correct cardiac output measurements was 01 calculated. DVI/AOO

VVI

PACING From the LJnivcrsity of Saskatchewan and Plains Health Centre, 4500 Wascana Parkway, Regina, Saskatchewan Canada, S4S 5W9. Manuscript received December 8, 1986; revised manuscript received January 23, 1987, accepted January 24, 1987.

MODE

FIGURE 1. Improvement in systolic arterial pressure (SAP) between ventricular demand (VVI) and atrioventricular sequential (DWAOO) pacing. Verfical bars represent the mean f standard error.

1208

BRIEF REPORTS

TABLE II

Hemodynamic

Results Pressures

PI? (beats/min) Pt 1 2 3 4 5 Mean &SD p Value

SA

(mm Hg) RA

V

AV

V

AV

V

AV

V

AV

V

AV

65 88 81 78 88 80 510

65 88 81 78 88 80 f10

110 120 93 104 106 107 f10

145 130 126 124 122 129 f9

16 15 10 25 20 17 f6

13 14 IO 21 18 15 f4

15 22 17 11 16 16 f4

15 19 12 11 17 14 f4

4.1 4.5 2.8 2.8 2.3 3.3 fl.0

4.9 6.2 3.7 3.9 3.2 4.4 f1.2

1,204 1,269 1,617 1,328 1,727 1,429 f230

1,524 976 1,737 1,326 1,661 1,445 f305

<0.005

<0.05

co

6

L/MIN

5

NS

sequential pacing: CO = cardiac output; NS = not significant; SVR = systemic vascular resistance; V = ventricular pacing.

namics during VW and DVI or A00 pacing at identical rates revealed significant differences favoring the addition of AV synchrony. Systolic arterial pressure increased by 21% (107 f 10 vs 129 f 9 mm Hg, p
2

SVR (dynes s cm-5)

AV

AV = atrioventricular SA = systolic arterial;

3

CO (liters/min)

V

NS

4

PAW

-1 b

1 -

P < 0.005

0 DWAOO

VW

PACING

MODE

FIGURE 2. Improvement in cardiac output (CO) between ventricular demand (VVI) and atrioventricular sequential (DVI/AOO) pacing. Vertical bars represent the mean f standard error.

<0.005

NS

PAW = pulmonary artery wedge; PR = paced rate; RA = right atrial;

systemic vascular resistance between the 2 pacing modes. This study clearly shows the superiority of atria1 or AV pacing over ventricular demand pacing in patients with inferior AMI, RV dysfunction, shock and nonsinus bradyarrhythmias. It confirms the data of other investigator+ and reaffirms the importance of temporary physiologic pacing. All patients with hypotension inferior AMI, RV dysfunction and nonsinus bradyarrhythmias should be given the benefit of temporary AV pacing. 1. Brockman SK. The contribution of atria! systole in complete heart block. Chn Res 1961;9:13. 2. Samet P, Castillo C. Bernstein WH. Hemodynamic consequences of sequential atrioventriculor pacing. Subjects with normal hearts. Am J Cardiol 1968;21:207-211. 3. Leinbach RC, Chamberlain DA, Kastor ]A, Harthorne ]W. Sanders CA. A comparison of the hemodynamic effects of ventricular and sequential A-V pacing in patients with heart block. Am Heart f 1969;78:502-508. 4. Chamberlain DA, Leinbach RC. Vassaux CE, Kastor JA, DeSanctis RW, Sanders CA. Sequential atrioventricular pacing in heart block complicating acute myocardial infarction. N Engl J Med 1970;282:577-582. 5. Haffajee CI. Love J, Gore JM. Alpert JS. Reversibility of shock by atria1 or atrioventricular sequential pacing in right ventricular infarction (absfr]. Am [ Cordial 198z;49:1025. 6. Abraham KA, Brown MA, Norris RM. Right ventricular infarction, bradyarrhythmias. and cardiogenic shock. Importance of atria1 or atrioventricular sequential pacing. Aust NZ J Med 1985;15:52. 7. Cohn JN. Right ventricular infarction revisited. Am r Cardiol 1979;43:666668. 8. Matangi MF, Rysavy J. Shelly W. Eekhoff P. Carlyle PF, Cohn JN. Sequential (DVI] versus ventricular (VVf] Pacing (P] following right coronary artery artery embolization [RCAE] and complete heart block in the dog [obstr). Clin Invest Med 1985:8:B25.