The Association of Lung Distention, PEEP and Biventricular Failure

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 H(2)O 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 .m (2) +/- 0.35 to 2.19 L/min m(2) +/- 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 H(2)O, 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 H(2)O of PEEP, the mean cardiac index fell in these animals from 2.36 L/min. m(2) +/- 0.26 to 1.47 L/min.m(2) +/- 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 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.     

Arterial and mixed venous blood acid-base balance during hypoperfusion with incremental positive end-expiratory pressure in the pig

The authors sought to determine how hypoperfusion influences acid-base balance in arterial and mixed venous blood. In anesthetized, ventilated pigs (n = 12), we determined hemodynamics, O2 uptake, CO2 output, dead-space ventilation, arterial and mixed venous blood acid-base balances, and lactate concentrations during graded reductions in cardiac output by incremental positive end-expiratory pressure (PEEP, 0-20 cm H2O). Cardiac output decreased from 3.2 +/- 0.2 (mean +/- SEM) to 1.2 +/- 0.1 L/min at 20 cm H2O PEEP. Oxygen delivery declined more than O2 uptake did by 60% +/- 2% and 27% +/- 2%, respectively. The decrease in CO2 output (by 21% +/- 2%) was less than that in O2 uptake. Fractional dead-space ventilation increased. At a slight increase in carbon dioxide tension (PCO2) of 4 +/- 1 mm Hg, pH decreased in arterial blood from 7.54 +/- 0.01 to 7.47 +/- 0.02 mmol/L, and standard bicarbonate decreased from 30.3 +/- 0.5 to 27.5 +/- 0.6 mmol/L. The decrease in standard bicarbonate exceeded the increase in blood lactate concentrations. At a similar decrease in standard bicarbonate, the decrease in pH was larger (P less than 0.005) in mixed venous blood than in arterial blood owing to a larger increase in PCO2 (from 40 +/- 2 to 50 +/- 2 mm Hg, P less than 0.005). The changes were reversed after discontinuing PEEP. The authors conclude that ischemia after incremental PEEP results in tissue metabolic acidosis with superimposed respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of positive end-expiratory pressure ventilation on peripheral tissue perfusion evaluated by measurements of tissue gases and pH. An experimental study in pigs with oleic acid lung injury.

Measurements of subcutaneous oxygen tension (PscO(2)), subcutaneous carbon dioxide tension (PscCO(2)) and subcutaneous pH (pHsc) were used for evaluation of peripheral oxygenation in pigs subjected to oleic acid-induced lung injury during ventilation with increasing levels of positive end-expiratory pressure (PEEP). Lung injury resulted in a decrease of arterial oxygen tension (PaO(2)) from 93 to 37 mm Hg (p<0.01) with maintained cardiac output. PscO(2) decreased from 45 to 17 mm Hg (p<0.01) and pHsc from 7.47 to 7.39 (p<0.05), and PscCO(2) increased from 46 to 59 mm Hg (p<0.05). Increase of PEEP level between 5 and 20 cm H(2)O resulted in a continuous increase of PaO(2) from 45 to 145 mm Hg and a decrease of cardiac output from 4.1 to 2.0 liters/min (p<0.01). PscO(2) increased up to a PEEP level of 15 cm H(2)O, reaching 26 mm Hg. Further increase of PEEP level up to 20 cm H(2)O resulted in an increase of PscCO(2) from 65 to 71 mm Hg (p<0.05) and a decrease of pHsc from 7.31 to 7.29 (p<0.05). In conclusion: measurements of tissue gases and pH can be used to evaluate optimum peripheral tissue oxygenation during titration of PEEP level. Whether these measurements can be used as the only indicator to guide therapy in an individual case remains to be studied.     

Safe use of PEEP in patients with severe head injury

Thirty-three patients with severe head trauma were studied to determine whether the use of positive end-expiratory pressure (PEEP) would cause an increase in intracranial pressure (ICP). Changes in ICP induced by PEEP were then correlated with a panel of physiological variables to try to explain these changes. Mean ICP increased from 13.2 +/- 7.7 mm Hg (+/- standard deviation) to 14.5 +/- 7.5 mm Hg (p less than 0.005) due to 10 cm H2O PEEP, but the eight patients with elevated baseline ICP experienced no significant increase. Cardiac output and venous admixture (Qs/Qt) declined significantly, while central venous pressure, peak inspiratory pressure, functional residual capacity, and arterial pCO2 increased significantly due to PEEP. Blood pressure and cerebral perfusion pressure were unchanged. The change in ICP due to PEEP correlated significantly with a combination of cardiac output, peak inspiratory pressure, Qs/Qt, and changes in blood pressure and arterial pCO2 due to PEEP, indicating that the effect of PEEP on ICP could be largely explained by its effect on hemodynamic and respiratory variables. No patient deteriorated clinically due to PEEP. It is concluded that 10 cm H2O PEEP increases ICP slightly via its effect on other physiological variables, but that this small increase in ICP is clinically inconsequential.     

Abnormalities in organ blood flow and its distribution during positive end-expiratory pressure.

Current evidence is inconclusive regarding the possibility that positive end-expiratory pressure (PEEP) redistributes flow and may be directly responsible for systemic organ dysfunction. This study tests the hypothesis that PEEP may induce abnormalities in the distribution of cardiac output (CO). Eight anesthetized dogs were studied during (1) 0 cm H2O PEEP (Z1), (2) 15 cm H2O PEEP (P), (3) Z2, and (4) bleeding (B) to reduce the CO to the same level as P. At each of the four periods, a different 15 mu radiolabelled microsphere was injected into the left atrium. Another four dogs were used to varify that each type of microsphere had the same flow distribution. CO fell from 3.1 liters/min to 1.9 during P (P smaller than 0.01) and to 2.0 during B (P smaller than 0.01). Mean arterial pressure (MAP) declined from 102 to 83 mm Hg (P smaller than 0.01) and 86 mm Hg (P smaller than 0.01(, respectively. Left atrial pressure (LAP) rose from 5.0 to 7.9 mm Hg during P (P smaller than 0.01) and fell during B to 2.7 mm Hg. c0 and its distribution were the same during Z1 and Z2. P caused selective reductions in hepatic (52%), adrenal (25%), and bronchial (24%) blood flows (P smaller than 0.01). In contrast, total flow to these organs during B was the same as during Z. Total renal flow was unchanged by P or B, but the cortical:medullary flow ratio increased during P from 24 to 49 (P smaller than 0.01) and was unchanged by B. P induced a decrease in fundal nucosal flow as compared with Z (P smaller than 0.01). Total coronary flow fell from 100 to 64 ml/min during both P and B (P smaller than 0.01). P led to a selective fall in subendocardial flow (67 ml/min X 100 gm) as compared with B (82.5 ML/MIN X 100 gm, P smaller than 0.01) as well as in the subendocardial:subepicardial flow ratio (1.069 vs. 1.112 ml/min X 100 gm, P smaller than 0.05). It is likely that the higher left ventricular filling pressure (LAP) during P as compared with during B compressed the endocardium and induced relative ischemia. Similarly the high airway pressure during P may have impeded bronchial mucosal flow. The causes and consequences of the other P-induced variations in flow are speculative.     

Use of a counterpulsation balloon as a substitute for the pulmonic valve: a new application

An inflatable, 3-ml balloon positioned within the distal right ventricular outflow tract was used to restore pulmonic valve function in 8 dogs that had undergone open-chest valvectomy. Balloon inflation and deflation were accomplished with a counterpulsation console. Valvectomy produced loss of the pulmonic incisura, a decrease in pulmonary artery diastolic pressure (PADP; mean +/- standard error) (9.5 +/- 1.3 versus 4.4 +/- 0.6 mm Hg, p less than 0.01), and an increase in pulmonary artery pulse pressure (PAPP) (8.6 +/- 0.7 versus 19.1 +/- 1.9 mm Hg, p less than 0.01) without significantly affecting forward cardiac output (CO) (1,750 +/- 110 versus 1,880 +/- 230 ml/min, p is not significant). Properly timed counterpulsation restored the pulmonic incisura, raised the PADP from 6.1 +/- 0.8 to 9.5 +/- 0.8 mm Hg (p less than 0.01), lowered the PAPP from 15.1 +/- 1.4 to 10.6 +/- 1.0 mm Hg (p less than 0.01), and raised the forward CO from 1,850 +/- 260 to 1,920 +/- 260 ml/min (p less than 0.01). The injection of glass beads, 40 to 150 microns in diameter, into the right ventricular outflow tract increased pulmonary vascular resistance from 383 +/- 87 to 730 +/- 150 dyne . sec cm-5 (p less than 0.05) and decreased forward CO from 1,850 +/- 260 to 1,570 +/- 230 ml/min (p less than 0.05). Following this injection, counterpulsation again restored the pulmonic incisura, raised the PADP from 9.3 +/- 1.4 to 16.0 +/- 1.8 mm Hg (p less than 0.01), lowered the PAPP from 25.0 +/- 2.5 to 18.2 +/- 2.5 mm Hg (p less than 0.01), and raised the forward CO from 1,570 +/- 230 to 1,720 +/- 220 ml/min (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of positive end-expiratory pressure (PEEP) after pneumonectomy in dogs

Little is known regarding the hemodynamic effect of positive end-expiratory pressure (PEEP) following pneumonectomy. To investigate this, 9 mongrel dogs underwent PEEP before and after lung resection. With the chest closed, the dog anesthetized, and partial pressure of carbon dioxide constant, PEEP was added in increments of 2 mm Hg until the animal's condition became hemodynamically unstable. At each level of PEEP, aortic, pulmonary, left atrial, and central venous pressures were monitored while aortic flow (cardiac output) was determined with an electromagnetic probe and airway pressure was measured with a Millar catheter in the respiratory tubing. Pneumonectomy was then performed, PEEP was again sequentially added, and the same measurements were recorded. Both before and after pneumonectomy, a strong positive linear correlation exists between the level of PEEP and pulmonary vascular resistance (PVR) (r greater than 0.74; p less than 0.05). Also, there is a high negative linear correlation between the level of PEEP and cardiac output (r greater than -0.76; p less than 0.05). At 0 mm Hg of PEEP, the PVR is higher after pneumonectomy than before (p less than 0.02). The incremental elevation in PVR persists after pneumonectomy at each level of PEEP, and in 5 of the 9 dogs the slope of the linear regression line relating PVR to PEEP was steeper following resection (p less than 0.05), thereby demonstrating an exaggerated effect of PEEP on PVR. In addition, all animals had a lower cardiac output at each comparable level of PEEP following pneumonectomy (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial natriuretic factor may mediate the renal effects of PEEP ventilation

Mechanical ventilation with PEEP decreases urine output and urinary sodium excretion. Observed changes in cardiac output, renal blood flow, renin release, and antidiuretic hormone (ADH) secretion do not adequately explain the renal effects of PEEP. Altered release of atrial natriuretic factor (ANF), which is natriuretic and diuretic, may complete this explanation. The following hypothesis was tested: a PEEP-induced decrease in transmural right atrial pressure decreases ANF release, and this mechanism mediates subsequent alterations in renal function. Seven female mongrel dogs were anesthetized with halothane and their lungs ventilated mechanically for three consecutive 40 min periods of 0 PEEP, 10 cmH2O PEEP, and 0 PEEP. Addition of 10 cmH2O PEEP during mechanical ventilation decreased right atrial dimension and transmural right atrial pressure while intracavitary right atrial pressure was increased. Urine output was significantly decreased during PEEP, as were absolute and fractional excretion of sodium and osmolar clearance. PEEP ventilation resulted in a consistent and significant decline in plasma ANF concentration (82 +/- 11 to 62 +/- 11 pg/ml, P less than 0.05). Hemodynamic parameters, renal function, and ANF concentration returned to control values after cessation of PEEP. A second series of experiments in five dogs demonstrated a close temporal relationship between changes in atrial dimension or atrial transmural pressure, plasma ANF concentration, and urine output or sodium excretion. The results of this study demonstrate that PEEP-induced decreases in atrial distension resulted in decreased ANF release, which may mediate, in part, the antinatriuretic and antidiuretic effects of PEEP.     

Experimental cardiac tamponade with a myocardial wound: the effect of rapid intravenous infusion of saline.

In order to demonstrate that the evolution of cardiac tamponade from a ventricular wound is different from that without myocardial wounding, the effects of a rapid infusion of saline solution on hemodynamic behavior and pericardial pressure (PP) were evaluated in dogs with cardiac tamponade caused by ventricular perforation (group C), animals without cardiac tamponade (group A), and animals with cardiac tamponade induced by infusion of saline into the pericardium (group B). We found that blood pressure (BP) increased from 107.5 +/- 15.5 mm Hg to 126 +/- 4 mm Hg in group A; increased from 64.5 +/- 17.9 mm Hg to 117.5 +/- 22.17 mm Hg in group B; and increased from 60.75 +/- 46.5 mm Hg to 76 +/- 14.4 mm Hg in group C. Central venous pressure (CVP) increased from 3.75 +/- 0.96 cm H2O to 9.5 +/- 3.3 cm H2O in group A; increased from 8 +/- 2.4 cm H2O to 16.25 +/- 3.1 cm H2O in group B; and rose from 7.75 +/- 2.6 cm H2O to 20.66 +/- 5.03 cm H2O in group C. Cardiac output (CO) increased from 3.9 +/- 1.2 L/min to 18.93 +/- 3.96 L/min in group A; increased from 1.23 +/- 0.3 L/min to 5.4 +/- 1.7 L/min in group B; and increased from 1.8 +/- 0.66 L/min to 3.53 +/- 1.31 L/min in group C.(ABSTRACT TRUNCATED AT 250 WORDS)     

Continuous positive airway pressure versus positive end-expiratory pressure in respiratory distress syndrome.

The hemodynamic and respiratory effects of spontaneous ventilation with continuous positive airway pressure (CPAP) and mechanical ventilation with positive end-expiratory pressure (PEEP) were compared in nine patients who had adult respiratory distress syndrome. These patients were capable of maintaining spontaneous ventilation (tidal volume above 300 ml. and PaCO2 below 45 torr). Arterial and mixed venous blood gases, cardiac output, oxygen delivery and consumption, pulmonary artery pressure, and pulmonary wedge pressure were measured in 11 instances, with each patient on 5 or 10 cm. H2O CPAP or PEEP, and in nine instances, with each patient on the ventilator but without PEEP (O PEEP). During CPAP, when compared to PEEP at the same level of end-expiratory pressure, mean PaO2 increased significantly (p less than 0.05) and mean physiological shunt decreased (p less than 0.05). In nine of 11 instances, cardiac output was higher on CPAP than on a corresponding level of PEEP. Thus CPAP was more effective than the same amount of PEEP in improving arterial oxygenation by the lung without adversely affecting cardiac output.     

Hemodynamic response to positive end-expiratory pressure following right atrium-pulmonary artery bypass (Fontan procedure)

Thirteen patients were studied in the early postoperative period to determine the hemodynamic response to increasing levels of positive end-expiratory pressure (PEEP) following right atrium-pulmonary artery bypass (Fontan procedure). Hemodynamic data and arterial oxygen and carbon dioxide tensions were measured without PEEP and with PEEP = 3, 6, 9, and 12 cm H2O. Cardiac index decreased progressively with increasing levels of PEEP compared to PEEP = 0 (cardiac index = 2.7 +/- 1.2 L/min/m2), and the decrease was significant at PEEP = 9 (cardiac index = 2.2 +/- 0.8 L/min/m2, p less than 0.05) and 12 cm H2O (cardiac index = 2.0 +/- 0.7 L/min/m2, p less than 0.05). Both arterial oxygen tension and pulmonary vascular resistance index increased significantly at all levels of PEEP studied compared to PEEP = 0. Significant positive trends were demonstrated for arterial oxygen tension and pulmonary vascular resistance index and a significant negative trend was shown for cardiac index with increasing PEEP. Heart rate, right atrial pressure, left atrial pressure, mean arterial blood pressure, and arterial carbon dioxide tension did not change significantly nor consistently with increasing PEEP. From these data it appears that PEEP is an effective means of raising arterial oxygen tension after right atrium-pulmonary artery bypass. A progressive fall in cardiac index occurs with increasing PEEP, and the fall becomes significant at PEEP greater than 6 cm H2O. The fall in cardiac index appears to be mediated by a significant rise in pulmonary vascular resistance index.     

Hemodynamic consequences of PEEP in seated neurological patients--implications for paradoxical air embolism

In order to better understand the hemodynamic consequences of the use of positive end-expiratory pressure (PEEP) in patients in the seated position, 11 patients undergoing neurosurgical operations were monitored with radial arterial and thermistor-tipped Swan-Ganz catheters both before and during 10-cm H2O PEEP. Significant (P less than 0.05) reductions in cardiac output (15%), stroke volume (15%), and mean arterial pressure (14%) occurred with the introduction of PEEP, while pulmonary vascular resistance increased 47% and right atrial pressure (RAP) increased from 3.6 +/- 0.7 SEM mm Hg to 8.9 +/- 0.9 SEM mm Hg (P less than 0.05). Pulmonary capillary wedge pressure (PCWP) did not increase significantly during PEEP. RAP exceeded PCWP in only two patients before PEEP, but RAP exceeded PCWP in seven patients during PEEP. We conclude that PEEP is potentially detrimental during operations in the seated position because it not only impairs hemodynamic performance, but might predispose patients with a probe-patent foramen ovale to the risk of paradoxical air embolism.     

The Effect of High Pressure on Microporous Membrane Oxygenator Failure

A retrospective study to determine the relationship between early microporous membrane oxygenator (MMO) failure and blood pressure at the MMO outlet (Pmo) was conducted using data collected with 19 dogs (22 +/- 1 kg, mean +/- SEM) undergoing routine normothermic cardiopulmonary bypass. Because gas flow was maintained at a high level, it could not be used to control CO2 exchange. Instead, blood PCO2 was controlled by adding CO2 to the sweep gas. Blood PO2 was controlled as suggested by the manufacturer, by adjusting the %O2 in the gas phase (g). Blood flow was 2575 +/- 54 ml/min; Pmo ranged from 173 to 790 mm Hg; and hematocrit was 33 +/- 1%. O2 exchange was calculated from blood gas parameters. Changes in the diffusion potential of O2 (delta PO2) and CO2 (delta PCO2) and MMO performance (P, taken as oxygen exchange normalized to a diffusion potential of 100 mm Hg) indicated MMO failure. Initial values, taken within 60 min of bypass initiation, were compared to final values taken at 226 +/- 9 min of bypass. Despite higher final delta PO2 (411 +/- 9 vs. 538 +/- 19 mm Hg, p less than 0.0001 paired t-test) and delta PCO2 (18.6 +/- 2.4 vs. 30.5 +/- 4.7 mm Hg, p less than 0.0017), arterial blood PO2 decreased (159 +/- 15 to 89 +/- 6 mm Hg, p less than 0.0005) and PCO2 increased (36.4 +/- 1.5 to 46.1 +/- 3.0 mm Hg, p less than 0.0039), and the performance decreased [24.5 +/- 1.1 to 20.1 +/- 0.7 (ml/min)/(100 mm Hg), p less than 0.0001].(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15 degrees, 30 degrees, and 60 degrees. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15 degrees (a fall of -4.5 +/- 1.6 mm Hg, p less than 0.001) and 30 degrees (a fall of -6.1 +/- 3.5 mm Hg, p less than 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60 degrees, the mean ICP increased to -3.8 +/- 9.3 mm Hg of baseline, while the CPP decreased -7.9 +/- 9.3 mm Hg (p less than 0.02), and the cardiac index also fell -0.25 +/- 0.28 liters/min/sq m (p less than 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15 degrees or 30 degrees) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0 degrees) or higher (60 degrees) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.     

Tension pneumothorax during extracorporeal membrane oxygenation

Life-threatening tension pneumothorax in neonates on extracorporeal membrane oxygenation (ECMO) has been associated with an increase in arterial oxygen tension and a decrease in peripheral perfusion, followed by a decrease in ECMO flow with progressive hemodynamic deterioration. To investigate this triad, chest tubes were placed bilaterally in 9 dogs to allow injection of air to produce tension pneumothorax. Six dogs were subsequently placed on standard venoarterial ECMO before the reinduction of tension pneumothorax. Measured values included arterial pulse pressure, inferior vena cava pressure, systemic arterial blood gases, peripheral arterial oxygen saturation, mixed venous oxygen saturation, and left heart cardiac output. Oxygen delivery was calculated from directly measured values. Each of the 6 dogs on ECMO demonstrated the triad of increased arterial oxygen tension (92 +/- 7 to 325 +/- 20 mm Hg; p less than 0.05), decreased peripheral perfusion (as evidenced by a decrease in pulse pressure from 55 +/- 4 to 31 +/- 5 mm Hg; p less than 0.05), and decreased mixed venous oxygen saturation (71% +/- 3% to 22% +/- 2% saturation; p less than 0.05) followed by a lower ECMO flow with progressive hemodynamic deterioration (oxygen delivery decreased from 285 +/- 11 to 111 +/- 12 mL/min; p less than 0.05). Aspiration of the intrathoracic air allowed return to baseline ECMO flow and hemodynamic stability in all dogs. The triad of increased arterial oxygen tension and decreased peripheral perfusion (as evidenced by a lower arterial pulse pressure and lower mixed venous oxygen saturation) followed by decreased ECMO flow with progressive hemodynamic deterioration consistently appears when tension pneumothorax occurs on ECMO.     

Depression of myocardial ATPase activity by plasma obtained during positive end-expiratory pressure

Dogs treated with 15 cm H2O positive end-expiratory pressure (PEEP) invariably show a decrease in cardiac output (CO). Plasma that is obtained from PEEP-treated dogs and applied to an isometrically contracting rat papillary muscle results in a significant depression of the peak developed tension. The present study evaluates the nature of the circulating negative inotropic agent with respect to its action on the coupling of myocardial energy production and contraction. PEEP plasma was found to depress Ca++-ATPase activity (P less than 0.025) when incubated with cardiac subfractions obtained from dog and rat myofibrils, sarcolemma, and sarcoplasmic reticulum. No change in Mg++-ATPase activity was observed. The declines in Ca++-ATPase activity correlate significantly with decreases in left ventricular stroke work, stroke volume, and CO during PEEP treatment. The decrease in Ca++-ATPase with PEEP plasma also correlates with a decrease in developed tension of a rat papillary muscle bathed with PEEP plasma. There were no changes in CO in animals who were simply anesthetized; plasma from these animals did not alter developed tension or ATPase. These observations suggest that PEEP plasma and serum contain a negative inotropic agent(s) that may reduce contractility by Ca++-ATPase inhibition.     

Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow.

The effects of increased intra-abdominal pressure (IAP) on intestinal blood flow were studied in eight anesthetized pigs. Mesenteric artery blood flow (MABF), intestinal mucosal blood flow (IMBP), tonometric intramucosal pH (pHi), mean BP (MAP), cardiac output (CO), and pulmonary artery wedge pressure (PAWP) were measured as IAP was raised to 10, 20, 30, and 40 mm Hg by infusing lactated Ringer's solution (LR) into the peritoneal cavity. The MAP was kept constant with IV LR. Cardiac output fell slightly from 5.4 +/- 1.1 at baseline to 4.0 +/- 1.2 L/min at an IAP of 40 mm Hg (p less than 0.05). An IAP of 20 mm Hg caused significant decreases in MABF (73% +/- 22% of baseline) (p less than 0.05) and IMBF (61% + 12% of baseline) (p less than 0.05). These changes became progressively greater as the IAP was increased to 40 mm Hg. The pHi fell to 6.98 +/- 0.14 at 40 mm Hg IAP (p less than 0.01), indicating severe mucosal ischemia. Thus increased IAP can cause severe intestinal ischemia, which may be more important than the cardiac, pulmonary, and renal changes usually described.     

Effects of ventriculoperitoneal shunt removal on cerebral oxygenation and brain compliance in chronic obstructive hydrocephalus

OBJECT: The pathophysiology of shunt malfunction has not been fully examined, probably because of the paucity of appropriate animal models. Using a canine model of chronic obstructive hydrocephalus, the effects of shunt placement and removal on physiological parameters were evaluated. METHODS: Fifteen dogs, nine in which chronic hydrocephalus was induced and six controls, were used in the experiment. Thirteen weeks after the induction of hydrocephalus, intracranial pressure (ICP), tissue and cerebrospinal fluid O2 saturation, response to hyperventilation, and brain compliance at low (5-15 mm Hg) and high (15-25 mm Hg) pressures were measured (untreated stage). Following this procedure, ventriculoperitoneal shunts were implanted in the dogs suffering from hydrocephalus. Two weeks later, the same series of measurements were repeated (shunted stage), following which the shunt systems were removed. One week after shunt removal, the last measurements were obtained (shunt-removed stage). All dogs underwent magnetic resonance imaging four times: before induction of hydrocephalus and before each measurement. All dogs with hydrocephalus also had ventriculomegaly (1.42 +/- 0.89 ml before induction of hydrocephalus compared with 3.4 +/- 1.64 ml 13 weeks after induction, p = 0.0064). In dogs in the untreated hydrocephalus stage, ICP remained within the normal range (8.33 +/- 2.60 mm Hg)--although it was significantly higher than that in the control group (5 +/- 1.41 mm Hg, p = 0.014). Tissue O2 saturation in the dogs in the hydrocephalus group (26.1 +/- 5.33 mm Hg) was lower than that in the dogs in the control group (48.7 +/- 4.27 mm Hg, p < 0.0001). After the dogs underwent shunt placement, significant improvement was observed in their ICP (5.22 +/- 2.17 mm Hg, p = 0.012) and tissue O2 saturation (35.2 +/- 6.80 mm Hg, p = 0.0084). However, removal of the shunt reversed these improvements back to the preshunt status. Hyperventilation induced significant decreases in ICP and O2 saturation at every measurement time and induced a significant decrease in tissue O2 saturation during the shunted stage, but not during the untreated and shunt-removed stages. Brain compliance measured at high pressure demonstrated a significant gradual decrease at every measurement. CONCLUSIONS: In chronic obstructive hydrocephalus, shunt placement improves ICP and cerebral oxygenation as well as the response to hyperventilation in the tissue. Shunt removal reverses these improvements back to levels present during the untreated stage. The decrease in brain compliance may be one of the factors responsible for symptoms in shunt malfunction.     

Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance

BACKGROUND: Positive end-expiratory pressure (PEEP) can be effective in improving oxygenation, but it may worsen or induce intracranial hypertension. The authors hypothesized that the intracranial effects of PEEP could be related to the changes in respiratory system compliance (Crs). METHODS: A prospective study investigated 21 comatose patients with severe head injury or subarachnoid hemorrhage receiving intracranial pressure (ICP) monitoring who required mechanical ventilation and PEEP. The 13 patients with normal Crs were analyzed as group A and the 8 patients with low Crs as group B. During the study, 0, 5, 8, and 12 cm H2O of PEEP were applied in a random sequence. Jugular pressure, central venous pressure (CVP), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral compliance, mean velocity of the middle cerebral arteries, and jugular oxygen saturation were evaluated simultaneously. RESULTS: In the group A patients, the PEEP increase from 0 to 12 cm H2O significantly increased CVP (from 10.6 +/- 3.3 to 13.8 +/- 3.3 mm Hg; p < 0.001) and jugular pressure (from 16.6 +/- 3.1 to 18.8 +/- 3.2 mm Hg; p < 0.001), but reduced mean arterial pressure (from 96.3 +/- 6.7 to 91.3 +/- 6.5 mm Hg; p < 0.01), CPP (from 82.2 +/- 6.9 to 77.0 +/- 6.2 mm Hg; p < 0.01), and mean velocity of the middle cerebral arteries (from 73.1 +/- 27.9 to 67.4 +/- 27.1 cm/sec; F = 7.15; p < 0.001). No significant variation in these parameters was observed in group B patients. After the PEEP increase, ICP and cerebral compliance did not change in either group. Although jugular oxygen saturation decreased slightly, it in no case dropped below 50%. CONCLUSIONS: In patients with low Crs, PEEP has no significant effect on cerebral and systemic hemodynamics. Monitoring of Crs may be useful for avoiding deleterious effects of PEEP on the intracranial system of patients with normal Crs.     

When should the hypoplastic right ventricle be used in a Fontan operation? An experimental and clinical correlation

Eight anesthetized dogs underwent closure of the tricuspid valve and a Fontan procedure, and the right ventricular cavity was reduced in stepwise fashion. There was an increase in right atrial pressure from 9.3 +/- 2.2 to 14.1 +/- 2.4 mm Hg (p less than 0.001), a decrease in pulmonary artery pulse pressure from 10.8 +/- 2.2 to 6.8 +/- 2.2 mm Hg (p less than 0.01), and a decrease in cardiac index from 2.7 +/- 0.3 to 2.2 +/- 0.2 L/min/m2 (p less than 0.001) when the ventricular size was dropped from 50% to 25% of normal. The difference between mean pulmonary artery pressure and mean right atrial pressure, which reflects the positive stroke work index of the ventricle, disappeared once the right ventricular cavity was reduced to 25% of normal (15.0 +/- 6.1 versus 14.1 +/- 2.4 mm Hg; p = not significant). Experimental results were correlated with postoperative catheterization data from 19 patients with tricuspid atresia who had the Fontan operation. Mean right atrial pressure was 18 +/- 4.6 mm Hg and cardiac index was 2.35 +/- 0.65 L/min/m2 in patients with a direct atrium-pulmonary artery anastomosis or an atrioventricular anastomosis with a right ventricular cavity less than 30% of normal versus 13 +/- 3.2 mm Hg and 3.42 +/- 0.46 L/min/m2 for those with an atrioventricular connection and a right ventricular cavity greater than 30% of normal (p less than 0.05 and p less than 0.02, respectively). The right ventricle enlarged from 27% +/- 6% of normal preoperatively to 35% +/- 10% of normal on follow-up (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)