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Biomedical subjects

M R Pinsky

Publications and source records attributed to M R Pinsky.

At least 145 records · Page 8Linked to original sources
PubMed1988

Effect of positive-pressure ventilatory frequency on regional pleural pressure.

Regional lung ventilation is modulated by the spatiotemporal distribution of alveolar distending forces. During positive-pressure ventilation, regional transmission of airway pressure (Paw) to the pleural surface may vary with ventilatory frequency (f), thus changing interregional airflow distribution. Pendelluft phenomena may result owing to selective regional hyperventilation or phase differences in alveolar distension. To define the effects of f on regional alveolar distension during positive-pressure ventilation, we compared regional pleural pressure (Ppl) swings from expiration to inspiration (delta Ppl) and end-expiratory Ppl over the f range 0-150 min-1 in anesthetized, paralyzed, close-chested dogs with normal lungs. We inserted six pleural balloon catheters to analyze Ppl distribution along three orthogonal axes of the right hemithorax. Increases in regional Ppl were synchronously coupled with inspiratory increases in Paw regardless of f. However, at a constant tidal volume and percent inspiratory time, end-expiratory Paw and Ppl increased in all regions once a f threshold was reached (P less than 0.01). Supradiaphragmatic delta Ppl were less than in other regions (P less than 0.05), but thoracoabdominal binding abolished this difference by decreasing thoracoabdominal compliance. We conclude that the distribution of forces determining dynamic regional alveolar distension are temporally synchronous but spatially asymmetric during positive-pressure ventilation at f less than or equal to 150/min.

Animals↗
PubMed1988

Flow resistance of expiratory positive-pressure systems.

We measured the flow-resistance of five commercially available 10 cm H2O expiratory positive-pressure (EPP) valves (n = five per valve type) at bias flows of between 0 and 2,000 ml/s. We found that individual valves of each type and manufacturer functioned similarly. Different valve types, however, functioned differently: with one type, system pressure was higher than rated (p less than 0.05), and with another type, system pressure was significantly flow-dependent (p less than 0.01). The remaining types of valves had no flow-resistive properties and maintained a system pressure of 10 cmH2O. We conclude that system pressure is not similar in all continuous positive airway pressure (CPAP) systems using bias flow and EPP valves. The work of breathing imposed by CPAP circuits will be increased in systems whose EPP valves have flow-dependent properties.

Airway Resistance↗
PubMed1987

Do periodic hyperinflations improve gas exchange in patients with hypoxemic respiratory failure?

Prolonged artificial ventilation may result in worsening gas exchange and pulmonary compliance in patients with otherwise normal lungs. Prolonged hyperinflations to 40 cm H2O can completely reverse deterioration of gas exchange and compliance in such patients. Similar efforts have effectively recruited atelectatic lung regions in critically ill patients. Less aggressive hyperinflations have not improved lung function in patients with abnormal lungs with hypoxemia. However, sustained exaggerated hyperinflations may successfully open collapsed lung units in these patients when standard recruitment techniques fail. We compared periodic hyperinflations of 40 cm H2O lasting 15 to 30 sec associated with body positioning (directed recruitment [DR]) to standard bag-sigh-suctioning (BSS) for their effects on gas exchange and pulmonary compliance in 16 stable surgical ICU patients with hypoxemic respiratory failure of 24-h duration or longer. Patients were sequentially alternated between DR and BSS (group 1, BSS followed by DR; group 2, DR followed by BSS). Neither technique, alone or in sequence, resulted in a sustained (greater than or equal to 5 min) improvement or deterioration in either gas exchange or pulmonary compliance. We conclude that neither BSS nor DR reliably affects gas exchange or compliance in patients with established hypoxemic respiratory failure.

Blood Gas Analysis↗
PubMed1987

Effects of positive end-expiratory pressure on hepatic blood flow and performance.

Positive end-expiratory pressure (PEEP) may impair extrapulmonary organ function. However, the effects of PEEP on the liver are unclear. We tested the hypothesis that at a constant cardiac output (CO), PEEP does not induce changes in hepatic blood flow (QL) and parenchymal performance. In splenectomized, close-chested canine preparations (group I, n = 6), QL was derived as hepatic outflow using electromagnetic flow probes (QLemf), and hepatic performance was defined by extraction and clearance of indocyanine green (ICG). In a noninvasive model (group II, n = 7), the effects of PEEP on hepatic performance alone were similarly analyzed. Measurements were taken during intermittent positive-pressure ventilation (IPPV1), after addition of 10 cmH2O PEEP to IPPV (PEEP1), during continued PEEP but after return of CO to IPPV1 levels by intravascular volume infusions (PEEP2), and after removal of both PEEP and excess blood volume (IPPV2). Phasic inspiratory decreases in QLemf present during positive-pressure ventilation were not increased during either PEEP1 or PEEP2. Mean QLemf decreased proportionately with CO during PEEP1 (P less than 0.05), but was restored to IPPV1 levels in a parallel fashion with CO during PEEP2. The ICG pharmacokinetic responses to PEEP were complex, with differential effects on extraction and clearance. Despite this, hepatic performance was not imparied in either group. we conclude that global QL reductions during PEEP are proportional to PEEP-induced decreases in CO and are preventable by returning CO to pre-PEEP levels by intravascular volume infusions. However, covarying changes in blood volume and hepatic outflow resistance may independently modulate hepatic function.

Animals↗
PubMed1987

Ventricular assist by cardiac cycle-specific increases in intrathoracic pressure.

Changes in intrathoracic pressure can influence cardiac performance by altering ventricular loading conditions. Since ventricular loading, both from systemic venous return (preload) and from left ventricular wall stress (afterload), varies during the cardiac cycle, we reasoned that appropriately placed, phasic, cardiac cycle-specific (synchronous) increases in intrathoracic pressure might augment ventricular ejection in acute ventricular failure. Recent studies in animals suggest that synchronous increases in intrathoracic pressure during systole increase ejection. We compared the hemodynamic effect of synchronous increases in intrathoracic pressure with similar increases delivered at random in the cardiac cycle in patients with congestive cardiomyopathy (n = 9). Intrathoracic pressure was estimated by measuring esophageal pressure. High-frequency jet ventilation (HFJV) synchronized with the electrocardiogram (synchronous HFJV) was compared with HFJV at a fixed frequency within 15 percent of the heart rate (asynchronous HFJV) and with intermittent positive-pressure breathing (IPPB) (tidal volume = 10 ml/kg; f = 15). All forms of ventilation resulted in the same mean airway pressure and esophageal pressure. Mean pulmonary arterial occlusion pressure and arterial pressure were constant in all conditions. Cardiac output was greater with synchronous HFJV than with either IPPB or asynchronous HFJV (4.5 +/- 0.7 L/min compared with 3.5 +/- 0.7 and 3.4 +/- 0.6 L/min [mean +/- SE], respectively; p less than 0.05). Mixed venous oxygen saturation covaried with cardiac output (p less than 0.05), such that calculated oxygen consumption remained constant for all conditions. We conclude that synchronous HFJV augments cardiac output more efficiently than do similar increases in intrathoracic pressure delivered randomly in the cardiac cycle.

Adult↗
PubMed1987

Cardiovascular responses to acute loading with nifedipine alone and nifedipine plus propranolol during inhalation anesthesia in monkeys.

The cardiovascular effects of the administration of nifedipine and nifedipine combined with propranolol were examined in 15 monkeys during 0.75 and 1.25 MAC of anesthesia with isoflurane, enflurane, or halothane. Hemodynamic variables measured included heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP), maximum rate of increase of the Left ventricular pressure (max LV dP/dt), and thermodilution cardiac output (CO). The infusion of nifedipine at a rate adequate to produce therapeutic blood levels during 0.75 MAC with each anesthetic decreased MAP and SVR, but had no effect on cardiac index (CI), max LV dP/dt, or HR. Increasing the anesthetic concentration from 0.75 to 1.25 MAC during nifedipine administration decreased HR and MAP in all groups and decreased CI with halothane and enflurane, but not with isoflurane. Addition of propranolol by infusion in amounts adequate to produce 75% beta-adrenergic blockade caused a further depression of CI, max LV dP/dt, HR, and MAP. However, the hemodynamic depression was significantly greater with halothane and enflurane than with isoflurane. Intravenous administration of calcium chloride (10 mg/kg) after calcium channel and beta-adrenergic blockade only partially reversed the hemodynamic depression that occurred with all three anesthetics. It was concluded that acute loading with nifedipine with and without propranolol exerts a greater cardiovascular depressant effect during enflurane or halothane anesthesia than during isoflurane anesthesia. The myocardial depressant effects of nifedipine and propranolol myocardial depressant effects of nifedipine and propranolol may be synergistic with the depressant effects of potent inhalation anesthetics.

Anesthesia, Inhalation↗
PubMed1986

Cardiovascular depression secondary to ionic hypocalcemia during hepatic transplantation in humans.

Cardiovascular function, serum ionized calcium (Ca+2), and serum citrate were measured intraoperatively in patients (n = 9) undergoing orthotopic hepatic homotransplantation. Serum citrate increased 20-fold (P less than 0.0006) following transfusion of citrated blood products in the absence of a functional liver. Serum ionized calcium decreased (P less than 0.003) with concomitant decreases in cardiac index (P less than 0.005), stroke index (P less than 0.004), and left ventricular stroke work index (P less than 0.001). Hemodynamic depression and ionic hypocalcemia were reversed following the administration of CaCl2. In contrast to patients with normal hepatic function, who may tolerate large amounts of citrated blood, patients with end-stage liver disease demonstrate acute ionic hypocalcemia with concomitant hemodynamic depression when receiving citrated blood products during the course of hepatic transplantation.

Calcium Chloride↗
PubMed1986

Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure.

Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.

Animals↗
PubMed1986

Hemodynamic effects of synchronous high-frequency jet ventilation during acute hypovolemia.

We studied the effects of synchronous cardiac cycle-specific high-frequency jet ventilation (HFJV) in pentobarbital-anesthetized, splenectomized, closed-chest dogs to test the hypothesis that phasic inspiratory increases in intrathoracic pressure (ITP) selectively timed to specific periods of the cardiac cycle have different hemodynamic effects during both hypovolemia (acute hemorrhage, 20 ml/kg) and neurogenic vasomotor shock (hexamethonium, 10 mg/kg) than those observed during normovolemic control conditions. Ventricular stroke volumes (SV) were measured by electromagnetic flow probes. The influence of changes in venous return (VR) on the subsequent hemodynamic response to synchronous HFJV was analyzed using instantaneous VR curves (M. R. Pinsky, J. Appl. Physiol. 56:765-771, 1984). During hemorrhage the VR curve was shifted leftward with concomitant reductions in apneic SV (15.4 +/- 3.8 to 11.2 +/- 3.6 ml, mean +/- SD), (P less than 0.01) that were accentuated by HFJV (P less than 0.01), except when the phasic inspiratory increases in ITP during HFJV were timed to occur during late diastole (-4% apneic SV, NS). SV was greater with late diastolic pulses than with other timed synchronous ITP pulses during hypovolemia (P less than 0.01). During ganglionic blockade, arterial pressure decreased (139 +/- 14 to 76 +/- 18 Torr, P less than 0.001), but VR was preserved at control levels, and no significant cardiac cycle-specific HFJV effects occurred. We conclude that SV reductions associated with positive-pressure ventilation during acute hypovolemia are minimized by HFJV synchronized to late diastole but that this effect is preload dependent.

Animals↗
PubMed1985

LV filling pressure during PEEP measured by nadir wedge pressure after airway disconnection.

Pulmonary arterial occlusion pressure (Ppao) may not accurately reflect left ventricular filling pressure (LVFP) during ventilation with positive end-expiratory pressure (PEEP) because increases in pleural pressure (Ppl) increase measured intrathoracic vascular and cardiac chamber pressures relative to atmospheric while decreasing LVFP by decreasing venous return. Steady-state values of Ppao off PEEP are not useful in understanding the hemodynamics on PEEP because of changes in blood volume distribution and ventricular afterload associated with the removal of PEEP. We hypothesized that changes in Ppao immediately after abrupt airway disconnection from PEEP selectively reflect removal of PEEP-associated Ppl changes prior to other physiological changes. In pentobarbital-anesthetized closed-chest dogs, we compared absolute left atrial pressure and left atrial pressure relative to Ppl (Platm) prior to abrupt disconnection from 15 cmH2O PEEP (on-PEEP), with Ppao at its nadir (nadir Ppao) following airway disconnection in three sequential conditions: control (normal), after propranolol-induced acute ventricular failure, and after oleic acid-induced lung injury. For all conditions at low LVFP (less than 9 Torr), nadir Ppao reflects Platm better than on-PEEP Ppao, while at higher LVFP (greater than 9 Torr), on-PEEP Ppao better reflects Platm than nadir Ppao (P less than 0.05). Accurate predictions of on-PEEP Platm can be made using both on-PEEP and nadir Ppao values in a multiple regression equation.

Animals↗
PubMed1985

Determinants of cardiac augmentation by elevations in intrathoracic pressure.

We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. We found that pertubations in mean ITP induced by ventilator adjustments accounted for all observable steady-state hemodynamic changes independent of respiratory frequency, inspiratory time, or phasic respiratory swings in ITP. Changes in ITP were associated with reciprocal changes in both intrathoracic vascular pressures (P less than 0.01) and blood volume (P less than 0.01). When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.

Acute Disease↗
PubMed1984

Instantaneous venous return curves in an intact canine preparation.

The relationship between right atrial pressure (Pra) and venous return describes a venous return curve. Because changes in venous return and right ventricular stroke volume (SVRV) are similar during small tidal volume (VT) breathing, we compared the relationship of SVRV and Pra during positive-pressure ventilation (VT less than 10 ml/kg) in 17 pentobarbital-anesthetized, closed-chest, canine preparations. The SVRV-Pra relationship describes a straight line with a negative slope and a positive mean systemic pressure (Pms)-zero flow intercept (instantaneous Pms). Instantaneous Pms is similar to ventricular fibrillation-induced (stop-flow) Pms (8.1 +/- 0.8 vs. 8.4 +/- 0.7 mmHg, mean +/- SE). With volume infusion, both instantaneous and stop-flow Pms increase to a similar degree (R = 0.9014, P less than 0.001). The effect of opening an arteriovenous fistula is time dependent and variable between dogs, but by 30 s it is associated with an increase in instantaneous Pms (5.2 +/- 3.2 mmHg). Vascular compliance determined by adding and removing blood from the intravascular space displays a curvilinear hysteresis. The instantaneous venous return curve is affected by intravascular blood volume, vasomotor tone, and resistance to venous return. The relationship between SVRV and Pra during small VT breathing define instantaneous venous return curves similar to those described using right-heart bypass preparations.

Animals↗
PubMed1984

Determinants of pulmonary arterial flow variation during respiration.

We characterize the determinants of pulmonary arterial flow ( Qpa ) variation during spontaneous breathing ( SPONT ) and matched tidal volume intermittent positive-pressure breathing (IPPB) in 14 pentobarbital-anesthetized closed-chest canine preparations in which Qpa is measured by an electromagnetic flow probe around the pulmonary artery. Pressures are recorded from the juxtacardiac pleural space (Ppl), right atrium (Pra), and pulmonary artery. Spontaneous inspiratory efforts increase transmural Pra (Pra - Ppl) and right ventricular stroke volume ( SVRV ) but decreases Pra, whereas IPPB inspiration has the opposite effect. However, the relationship between instantaneous changes in SVRV and transmural Pra during SPONT and IPPB define a common "instantaneous" right ventricular (RV) function curve independent of mode of ventilation or phase or respiratory cycle, and this curve is similar to one generated by volume infusion measured at end expiration. Pulmonary vascular resistance changes during ventilation are small (less than 15%) and do not affect RV performance as noted by similar instantaneous RV function curves for SPONT and IPPB with Mueller and Valsalva maneuvers, respectively. Thus variations in Qpa during ventilation represent matched changes in RV filling pressure induced by phasic changes in venous return.

Animals↗