The Association of Lung Distention, PEEP and Biventricular Failure JONAH MANNY, M.D.,* MICHAEL T. PATTEN, M.D., PAUL R. LIEBMAN, M.D. AND HERBERT B. HECHTMAN, M.D.

Although positive and expiratory pressure (PEEP) is known to depress the cardiac output, the mechanism remains debated. Two series of experiments were designed to explore this mechanism. In the first study, the application of 15 cm H20 of PEEP to nine anesthetized, ventilated dogs led to a reduction of cardiac index from (mean + one'standard error of the mean) 2.71 L/min m2 + 0.35 to 2.19 L/min m2 ± 0.22 (p < .05) and a drop in mean arterial pressure (MAP) from 117 mm Hg + 8 to 91 mm Hg + 11 (p < .01). The mean net (vascular minus pleural pressure) pulmonary artery pressure (MPAP) rose from 15.3 mm Hg + 1.2 to 20.6 mm Hg ± 1.8 (p < .02). The mean net central venous pressure (CVP) rose from 5.2 mm Hg ± 0.9 to 8.4 mm Hg ± 0.9 (p < .05) and the net pulmonary arterial wedge pressure (PAWP) rose from 6.7 mm Hg ± 0.7 to 9.5 mm Hg ± 0.9 (p < .01). There was a nonsignificant rise in the mean net left atrial pressure (LAP). As PEEP was raised in increments from 0 to 20 cm H20, both LAP and PAWP increased. The rise in PAWP was always greater than the increase in LAP. The difference between PAWP and LAP was strongly correlated with the increase in MPAP (r = 0.98). This relationship was useful in correcting the PAWP during PEEP. The problem of cardiac depression was evaluated in a second series of eight dogs. These animals underwent complete chest wall excision to eliminate any possible direct effects of increased pleural pressure on the heart and great vessels. The absence of the chest wall permitted hyperexpansion of the lungs, particularly with positive end expiratory pressure. At 15 cm H20 of PEEP, the mean cardiac index fell in these animals from 2.36 L/min m2 ± 0.26 to 1.47 L/min m2 + 0.18 (p < .01) and the MAP fell from 105 mm Hg ± 16.2 to 68 mm Hg ± 4.8 (p < .001). The CVP rose from a mean of 5.5 mm Hg ± 0.4 to 8.3 mm Hg ± 0.6 (p < .01) and the LAP rose from 6.3 mm Hg ± 0.8 to 8.0 mm Hg ± 1.1 (p < .05). The MPAP rose from 18.0 mm Hg ± 0.6 to 23.3 mm Hg ± 1.6 (p < .01). Comparison of Group I and II showed a significantly greater depression of *Senior Lecturer of the Department of Surgery, Hadassah Hebrew University Medical Center, Jerusalem, Israel. Address correspondence to: Herbert B. Hechtman, M.D., 721 Huntington Avenue, Peter Bent Brigham Hospital, Boston, Massachusetts 02115. Supported in part by The United States Department of the Army Contract Da-17-76-C-6034 and the National Institute of Health Grant 2-ROI-GM 17366-07-C02. Submitted for publication: March 3, 1977.-

From the Department of Surgery, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts the cardiac output and MAP in the open-chested animals. At the same time LAP was significantly higher. These data strongly suggest that PEEP and particularly pulmonary hyperinflation induce biventricular failure. I N 1924 HUGGETT SHOWED that the application of 5

cm H20 expiratory pulmonary obstruction, now known as positive end expiratory pressure (PEEP) had an adverse effect on cardiac function.12 He observed a decrease in stroke volume without change in pulse rate. This was the first experimental study which demonstrated a relationship between mechanical ventilation and a reduction in cardiac output. Subsequently, Humphreys et al. showed that intermittent positive pressure ventilation (IPPV) was also associated with a fall in cardiac output particularly when high intratracheal pressures were generated. 13 This phenomenon was observed during open thoracotomy. The authors believed that the hemodynamic response was related to a direct pressure effect on the heart and great vessels. In 1948 Cournand et al. reported that PEEP decreased the cardiac output in normal man.4 By the simultaneous measurement of right ventricular and pleural pressure, Cournand demonstrated a direct relationship between the drop in cardiac output and the reduction in net filling pressure of the right ventricle. These data supported the belief that PEEP induced a fall in venous return to the right heart. This mechanism was also supported experimentally by the implantation of pulse ultrasonic flow transducers on the aorta and vena cava of the dog, demonstrating inhibition of venous return following mechanical ventilation which was immediately reflected in the aortic flow.'9 Through the last decade, PEEP has become an im-

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portant clinical tool for the treatment of the severe hypoxemia which may accompany acute respiratory failure.1 25'26 Despite the frequent improvement in oxygenation, the associated decrease in cardiac output especially in hypovolemic patients or in those with impaired myocardial function, has limited the wide application of PEEP.9'14 Recent experimental studies confirm Cournand's observation that PEEP leads to a reduction in cardiac output; however, the mechanism of this reduction is debated. Elkins et al., and Qvist et al. suggest that an increase in right ventricle afterload is an important etiologic factor in the induction of right ventricular failure and decreased cardiac output.7'23 The literature is conflicting with regard to the mechanisms responsible for impaired myocardial function with PEEP. Resolution of the problem is difficult in patients treated with PEEP where pleural pressure measurements are usually not available and where the pulmonary arterial wedge pressure may significantly overestimate the true left ventricular end diastolic pressure. 15 This is a report of a series of animal experiments which were conducted to evaluate the relative importance of: venous return, right ventricular and biventricular failure as possible mechanisms for the observed reduction in cardiac output with PEEP. Special attention was directed at developing data which could be applied clinically to correct overestimates in the pulmonary arterial wedge pressure. Methods

Positive end expiratory pressure was applied to two groups of animals: those with intact thoracic cavities and those in whom the entire chest wall had been excised. The major difference between these experimental groups was pleural pressure which rose in animals with intact chests, but remained constant in the group with their chest wall excised. Thus, the great veins of the chest and the heart itself were always exposed to atmospheric pressure in the open chested dog. Materials Two groups of mongrel dogs weighing 23-28 kg were used. Group I consisted of nine dogs which were anesthetized with intravenous pentobarbital, 30 mg/kg, intubated with a cuffed endotracheal tube and ventilated at 15 ml/kg at a rate of 12 using a volume-cycled respirator. The femoral vessels were used for the insertion of an arterial and flow-directed thermister-tipped pulmonary arterial catheter (Instrumentation Laboratory, Lexington, Mass.). A left lateral thoracotomy

Ann. Surg. X February 1978

was done and a left atrial catheter was inserted via the atrial appendage. The anterior mediastinum between the heart and the sternum was resected in order to create one space connecting both pleural cavities. Following hemostasis, the thoracotomy was closed leaving one posterior intercostal tube for drainage. The tube was connected to water seal. A second tube was sutured adjacent to the pericardium. This tube was used to measure intrathoracic pressure after a 50 ml pneumothorax was created by injecting air through the tube. The pneumothorax is required in order to allow transmission of pleural pressure through the catheter.5'17 Mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), mean left atrial pressure (LAP), mean central venous pressure (CVP), mean pulmonary artery wedge pressure (PAWP) and end expiratory intrathoracic-pleuro-mediastinal pressures were measured with strain-gage transducers. Net intrathoracic pressures were derived by subtracting intrathoracic pressure at each point from the measured intravascular pressures. Cardiac outputs (CO) were determined in triplicate by the thermodilution method.27 Cardiac index was calculated from the ratio CO/BSA.* Arterial blood gases and pH were analyzed with standard Clark and Severinghaus electrodes and appropriate minor adjustments made in the tidal volume or the rate of respiration to maintain PaCO2 in the range, 35-42 mm Hg. PEEP was applied by submerging the expiratory port of the respirator under different levels of water. The state of anesthesia and paralysis was maintained by a constant slow infusion of pentobarbital-succinylcholine. Measurements of hemodynamic parameters were done at baseline (O cm H20 PEEP), then 15 cm H20 PEEP and again at 0 cm H20 PEEP. The measurements were done after ten minutes of stabilization at each level of PEEP. This entire cycle, baseline-PEEP-baseline, was repeated three times in each animal. Finally, in order to examine interrelationships between the various intravascular pressures and the magnitude of PEEP, all pressure data were taken as PEEP was raised by 4 cm H20 increments up to 20 cm H20. Net intrathoracic pressures were calculated by subtracting pleural pressure from the measured vascular pressure. Group II consisted of eight dogs which were prepared in a manner similar to Group I. In addition, a wide excision of the entire chest wall was carried out. The lines of excision were the first rib superiorly, the tenth rib inferiorly and the transverse processes posteriorly. The lungs and entire mediastinum were *BSA is body surface area derived from the formula: 0.112 (weight in kg)2/3.26

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LUNG DISTENTION ASSOCIATION

TABLE 1. Hemodvna,nic Effects* of PEEP in Closed Chested Animals (Group I)

PEEP (cm H2O)

Cardiac Index (L/minm2) MAP (mm Hg) MPAP (mm Hg) LAP (mm Hg) CVP (mm Hg) PAWP (mm Hg) Pulse

Baseline 0

TABLE 2. Hemnodvnalnic Events* at Varying Levels of PEEP inl Closedi Chestedi Animilbals (Grouip I) 0

15

PEEP (cm H2O) 2.71 117 15.3 6.8 5.2 6.7 132

± 0.35 ± 8 ± 1.2 ± 1.1 ± 0.9 ± 0.7 ±6

2.19 91 20.6 7.3 8.4 9.5 128

± 0.22t ± 11§ ± 1.8t + 1.2 ± 0.9t + 0.9§ 6

153

2.66 111 14.5 5.1 4.8 5.7 130

± 0.38 + 7 ± 1.5 ± 1.0 ± 0.8 + 0.7 8

* Results are presented as the mean ± one standard error, n = 9. All pressures except MAP are net ie., measured minus pleural pressure. t p < .05 t p < .02 § p < .01. Significance was calculated from the paired t test comparing measurements at 15 cm H2O PEEP to baseline.

exposed to atmosphere. Application of PEEP resulted in a tremendous expansion of the lungs which were no longer confined by the chest wall. The lungs moved forward and away from the heart and mediastinum so that there was no direct pressure exerted on these organs. The body temperature was monitored using the thermister in the pulmonary arterial catheter. It was maintained with external heat. Hemodynamic data were obtained at baseline conditions, 0 cm H,O PEEP, then 15 cm H2O PEEP and again 0 cm H,O PEEP. The same protocol as in Group I was used so that each animal was cycled to 15 cm H2O PEEP on three occasions. The mean ofthe three baselines, PEEP and 0 cm H20 PEEP data points were then used for further calculations and statistical evaluation. The degrees of freedom were always based on the number of animals and not the total number of observations.

MPAP (mm Hg)

0 4 8 12 16 20

14.9 16.1 17.7 18.4 20.3 23.6

± 1.1 ± 1.3 ± 1.6 ± 2.1 ± 1.7 ± 2.1

PAWP (mm Hg)

LAP (mm Hg)

6.3 7.1 7.5 8.4 9.3 10.0

5.9 6.5 6.4 6.9 7.3 7.5

± 0.7 ± 1.0

± 0.9 ± 0.8 ± 0.9 ± 1.2

* Results are presented as the mean All pressures except MAP are net.

+

one

(PAWPLAP) (mm Hg)

± 1.1 ± 1.1 ± 1.2 ± 1.2 ± 1.1 ± 1.4

0.4 0.6 1.1 1.5 2.0 2.5

standard error, n

=

9.

The application of PEEP in increments of 4 cm H,O to closed chested dogs resulted in stepwise elevations of net MPAP, PAWP and LAP (Table 2). The PAWP was higher than LAP at all levels of PEEP (Fig. 1). The discrepancy between these values increased in a linear fashion as PEEP was increased (Fig. 2). After excision of the entire chest (Group II) 15 cm H20 PEEP led to hemodynamic changes (Table 3) which were similar in direction but more marked than those observed in Group I (Table 4, Fig. 3). Thus, the per cent decrease in cardiac index of 33% + 3 SEM 25

MPAP

20

mmHg

Results The application of PEEP to the close chested animals of Group I resulted in a significant depression in cardiac index (CI) from a baseline value of 2.71 L/min m2 + 0.35 SEM* to 2.19 L/min m2 + 0.22 SEM (p < .05, Table 1). There was a concomitant drop in mean arterial pressure (MAP) from 117 mm Hg + 8 SEM to 91 mm Hg± 11 SEM (p

The association of lung distention, PEEP and biventricular failure.

The Association of Lung Distention, PEEP and Biventricular Failure JONAH MANNY, M.D.,* MICHAEL T. PATTEN, M.D., PAUL R. LIEBMAN, M.D. AND HERBERT B. H...
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