Michal E. Douglas

Ventilatory pattern, intrapleural pressure, and cardiac output.

Continuous positive-pressure ventilation may decrease cardiac output. However, a few reports have separated the effects of positive and end-expiratory pressure (PEEP) from those of mechanical ventilation. Ten surgical patients requiring mechanical ventilatory support had catheters inserted for measurement of right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), intrapleural, radial artery, airway, and atrial filling pressures, and cardiac output. All patients breathed spontaneously between mechanical breaths delivered every 30 seconds by intermittent mandatory ventilation (IMV). Measurements were made with 0, 5, and 10 cm H2O PEEP, and during intermittent positive-pressure ventilation (IPPV) with 12 breaths/min without PEEP. Airway pressure (Paw), intrapleural pressure, RAP, and PAOP were increased by PEEP and IPPV. Intrapleural pressure increased most during IPPV (p less than 0.001). Atrial filling pressures and cardiac output were unaffected by PEEP but decreased during IPPV (p less than 0.001). Patients receiving IMV maintained negative intrapleural pressure, atrial filling pressure, cardiac output and, therefore, O2 delivery, regardless of PEEP level. The authors conclude that patients requiring mechanical respiratory support, with or without PEEP, may maintain better cardiopulmonary function when allowed some spontaneous ventilatory activity.

Renal function and cardiovascular responses during positive airway pressure.

The authors determined cardiovascular, renal, and hormonal responses to increased airway pressure during continuous positive-pressure ventilation (CPPV) and continuous positive airway pressure (CPAP). Nine healthy, hydrated laboratory swine had appropriate catheters placed to allow for measurement of intra-pleural, aortic, inferior vena caval, and left ventricular end-diastolic pressures; cardiac output; and urinary flow. Samples of arterial blood were analyzed for oxygen and carbon dioxide tensions, pH, plasma vasopressin, osmolality, and creatinine and sodium concentrations. Urine was analyzed for osmolality and creatinine and sodium concentrations, and volume was recorded. Intrapleural pressure was subtracted from left ventricular end-diastolic pressure to calculate transmural pressure, a reflection of left ventricular filling pressure. Glomerular filtration rate and urinary free-water and osmolal clearances were also calculated. Expiratory left ventricular filling pressure was decreased equally by CPAP and CPPV. However, inspiratory left ventricular filling pressure and cardiac output were decreased by CPPV only. Urinary flow and glomerular filtration rate were decreased equally by CPAP and CPPV. Sodium excretion was decreased and plasma vasopressin increased by CPPV, but not by CPAP. Urinary free water and osmolal clearances were not changed by either ventilatory pattern. Although many of the renal-function variables were affected similarly by CPPV and CPAP, these alterations were not influenced solely by cardiac output or vasopressin, because only CPPV depressed cardiac output and increased vasopressin levels.

Assessment of cardiac filling pressure during continuous positive pressure ventilation.

Before and after 10 dogs were near-drowned with fresh water, cardiac filling pressures were measured during spontaneous respiration, controlled mechanical ventilation with ambient expiratory airway pressure, continuous positive-pressure ventilation (CPPV) with 20 ml H2O PEEP, and CPPV alone. Pulmonary arterial occlusion and left ventricular end diastolic pressures were measured and compared. Intrapleural pressure was subtracted from values for each of these pressures to calculate respective transmural filling pressures. Mechanical ventilation and CPPV each decreased thoracic venous return, but only CPPV increased pulmonary arteriolar resistance. The increase of both airway pressure and pulmonary arteriolar resistance, in turn, increased both right atrial and pulmonary arterial occlusion pressures, but decreased left ventricular filling. Thus, measurement of pulmonary arterial occlusion pressure alone did not allow accurate assessment of cardiac filling pressure. The authors found that measurement of intrapleural pressure was necessary to obtain an accurate reflection of left ventricular filling pressure during CPPV. Momentary interruption of CPPV to measure any pressure was of no value in assessing vascular filling and caused pulmonary edema in several animals. Therefore, the authors recommend that vascular pressures be measured and evaluated without interruption of positive airway pressure.

A randomized trial of the traditional sitting position versus the hamstring stretch position for labor epidural needle placement.

BACKGROUND: Anecdotal and experimental evidence suggest that a sitting position with maximum knee extension, hip adduction, and forward lean (hamstring stretch position) may produce better reversal of the lumbar lordosis than a traditional sitting position. METHODS: In a randomized trial during initiation of epidural labor analgesia, we compared the traditional versus hamstring stretch positions. The primary outcome was the number of needle-bone contacts. RESULTS: The groups were equivalent with respect to the number of needle-bone contacts. CONCLUSIONS: The hamstring stretch position is equivalent to the traditional sitting position in terms of the number of needle-bone contacts encountered when placing labor epidural needles.

Intermittent Mandatory Ventilation and Weaning

Oxygen, PEEP, and mechanical ventilatory therapy should be administered to patients in varying amounts and should be removed gradually and independently. The method of determining optimal PEEP, oxygen, and ventilation is not unlike that recommended for many other therapies. Nine years of prospective evaluation have demonstrated the numerous clinical advantages of this technique, and relatively few complications have been associated with it. Reduced FIO2 may promote resistance to atelectasis and allow rapid discontinuation of mechanical ventilation and PEEP. Similarly, optimal levels of PEEP may improve matching of ventilation and perfusion and assist lung mechanics so that FIO2 and mechanical ventilation may be reduced. Minimal mechanical ventilatory support eliminates iatrogenic respiratory alkalosis, and weaning from ventilatory support may be initiated early. This, in turn, minimizes the detrimental effects of mechanical ventilation on acid-base balance and cardiovascular function, as well as lessening barotrauma. We think that this approach has simplified the clinical management of patients with compromised repiratory function and decreased their mortality.

Cardiopulmonary effects of intermittent mandatory ventilation.

IMV is a combination of spontaneous and mechanical ventilation. For numerous reasons, IMV is potentially more advantageous than conventional techniques. By maintaining spontaneous breathing, mechanical augmentation can be titrated to adjust alveolar minute ventilation levels to normal, thereby decreasing the incidence of respiratory alkalemia. There are major differences between the cardiopulmonary effects of IMV and conventional mechanical ventilation. Spontaneous inspiration decreases Ppl and results in better distribution of inspired gas, a better V/Q, and less physiological dead space. In addition, transmural filling pressures, venous return, and cardiac output are more normal than during conventional mechanical ventilation. Maintenance of spontaneous ventilation lowers mean Paw and pulmonary vascular resistance. If venous admixture occurs, it can be minimized by titrating PEEP. Thus, more effective therapy for hypoxemia is possible. If spontaneous breathing is to persist and be efective, work-of-breathing must be minimized. This can be accomplished best when a continuous flow of gas provides optimal CPAP to maintain FRC and to minimize the effects of decreased compliance without depressing cardiac function.

Comparison of assisted and controlled mechanical ventilation in anesthetized swine.

We compared assisted mechanical ventilation with controlled mechanical ventilation with and without PEEP in 10 anesthetized swine. Catheters were placed to measure airway, intrapleural, and blood pressures; Pao2 and Paco2; arterial pH; total minute ventilation; and mixed exhaled oxygen and carbon dioxide tensions. We calculated the ratio of physiological dead space to tidal volume, alveolar minute ventilation, co2 production, Vo2, and RQ. We found no clinically or statistically significant difference between assisted and controlled ventilation.

Brain tissue pressure measurement during sodium nitroprusside infusion.

The effect of an acute 25% decrease in mean arterial pressure (MAP) produced by sodium nitroprusside (SNP) infusion on mean intracerebral and cerebral perfusion pressures was examined in 7 swine with intracranial hypertension. All animals were anesthetized (a-chloralose), paralyzed (pancuronium bromide), orotracheally intubated and mechanically ventilated to maintain normocapnia. An epidural balloon was incrementally inflated to produce the desired brain tissue pressure (BTP) which was measured by an intracerebral microtransducer implanted contralat-eral to the balloon. MAP was measured from the carotid artery; cerebral perfusion pressure (CPP) was calculated as: MAP - BTP. During mildly (14 ± 1 (se) mm Hg) or moderately (37 ± 3 mm Hg) increased BTP, SNP infusion further increased BTP (17 ± 1 and 44 ± 3 mm Hg, respectively) (p < 0.05). During severely increased BTP (70 ± 4 mm Hg), SNP decreased BTP (53 ± 4 mm Hg, p < 0.05). Despite this variable BTP, CCP consistently decreased during SNP infusion. BTP and supratentorial subarachnoid cerebrospinal fluid pressure correlated closely; however, the supratentorial subarachnoid pressure consistently underestimated BTP. These findings suggest that estimation of BTP obtained from subarachnoid screw-type devices may not accurately record the pressure within cerebral tissue and the SNP should not be administered to patients with known or suspected intracranial hypertension unless an intracranial (either BTP or subarachnoid) pressure is being monitored.