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Biomedical subjects

M R Pinsky

Publications and source records attributed to M R Pinsky.

At least 19 recordsLinked to original sources
PubMed1992

Outcome of intensive care of the "oldest-old" critically ill patients.

OBJECTIVE: To determine the short-term and long-term outcome of critically ill "oldest-old" (greater than or equal to 85 yrs) patients. DESIGN: Retrospective chart review and follow-up telephone interview. SETTING: ICUs at a tertiary care hospital. METHODS: The medical records of all patients greater than or equal to 85 yrs of age admitted to the ICUs during 1988 were reviewed. Demographic information, severity of illness, major interventions, mortality rate, and hospital charges were examined. A follow-up telephone interview was conducted to determine the quality of life and mortality rate after discharge. RESULTS: Of 34 patients greater than or equal to 85 yrs of age admitted to the ICU, 21 (62%) survived to discharge from the hospital, and 13 (62%) of these 21 patients were discharged to home. Mean +/- SD hospital charges were $34,738 +/- 34,366. Seventeen of the 21 patients were contacted for long-term follow-up, and ten of these patients were alive at a mean follow-up time of 18 +/- 10 months (range 1 to 32). Eight of the ten patients described their quality of life as fair or good. CONCLUSION: These findings suggest that age alone may be an inappropriate criterion for allocation of ICU resources.

Aged↗
PubMed1992

Continuous monitoring of right ventricular volume changes using a conductance catheter in the rabbit.

To assess the reliability of conductance (G) catheter for evaluating right ventricular (RV) volume changes, a miniature (3.5F) six-electrode catheter was developed and tested in 11 New Zealand rabbit hearts. In five animals the heart was excised; in six it was left in the thorax. RV conductance was recorded while the RV was filled with blood in 0.25-ml steps at different left ventricular (LV) volumes. Linear correlation of measured conductance vs. reference volumes was computed. RV conductance was highly correlated with reference volume [correlation coefficient (r) ranging from 0.991 to 0.999]. Slope of regression lines was not significantly affected by LV volume variations in 1-ml steps or by acute conductance changes of structures surrounding the heart, whereas the intercept was affected only by the 0- to 1-ml LV volume change. In four rabbits, RV conductance changes during a cardiac cycle [stroke volume- (SV) G] were compared in vivo with electromagnetic flow probe-derived estimates of SV (SVem) as stroke volume was varied by graded inferior vena caval occlusion. SV-G correlated well with SVem (r ranging from 0.92 to 0.96). This correlation persisted after the thorax was filled with saline; however, significant differences were found in individual slopes (P < 0.001). These results show that the conductance catheter has a potential to reliably monitor in vivo relative RV volume changes in small-animal hearts.

Anesthesia↗
PubMed1992

Effect of positive end-expiratory pressure on right ventricular function in humans.

The effect of positive end-expiratory pressure (PEEP) on right ventricular (RV) function in humans is complex. Previous studies have been limited in their interpretation by not defining either pericardial pressure (Ppc) or RV volumes. Accordingly, we measured RV volumes and pressures and Ppc as PEEP was increased from zero to 15 cm H2O in 12 patients after thoracotomy, using a pulmonary arterial catheter equipped with a rapid responding thermistor that allowed measurement of RV ejection fraction (ef), while Ppc was measured via a pericardial balloon catheter. RV end-diastolic volume (EDV) was estimated as the ratio of stroke volume (SV) to RVef, whereas RV end-systolic volume (ESV) was estimated as RV EDV-SV. Right atrial pressure (Pra) was defined as end-diastolic pressure, and pulmonary arterial pressures (Ppa), both peak and mean, were used as end-systolic pressures. PEEP increased Ppc, Pra, and lung compliance (Cl). Cardiac output also decreased but not significantly. Neither mean nor peak systolic Ppa, nor RVef was significantly altered by PEEP. There was no relation between either RV filling pressure (Pra-Ppc) and EDV or the change in RV filling pressure and EDV, although EDV varied significantly as PEEP varied for individuals (p less than 0.05). Similarly, there was no relation between Ppa and ESV when either mean or peak Ppa values relative to Ppc were used. The relations between EDV and both SV and RVef were weak (r = 0.54 and 0.55, respectively). RVef varied inversely with ESV (r = -0.77), although it showed no relation to transmural peak Ppa (r = 0.28).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Effects of a closed tracheal suction system on ventilatory and cardiovascular parameters.

OBJECTIVE: To determine whether patients ventilated in the assist-control mode experienced a change in oxygenation, respiratory rate, inspiratory:expiratory ratio, heart rate, blood pressure or acid-base balance when suctioned with a closed tracheal suction system. DESIGN: A quasi-experimental, within-subject, repeated-measures design was used. SUBJECTS: 18 patients ventilated on a fraction of inspired oxygen of 0.47 +/- 0.17 and 2.3 +/- 5.0 cm H2O positive end-expiratory pressure. INTERVENTIONS: Two suction passes were performed, with measurements at baseline, immediately after the first suction pass, immediately before the second suction pass, immediately after the second suction pass, 2 minutes after the second suction pass and 5 minutes after the second suction pass. No hyperoxygenation was used. RESULTS: Significant differences were seen over time for arterial oxygen saturation, respiratory rate and inspiratory:expiratory ratio. Arterial oxygen saturation decreased to less than 90% in four subjects (range 88% to 89%), with a maximum fall of 9%. No significant differences were seen for heart rate, blood pressure, partial pressure of carbon dioxide, bicarbonate, time to nadir (lowest arterial oxygen saturation) or recovery time. CONCLUSIONS: Subjects ventilated in the assist-control mode and suctioned with a closed tracheal suction system did not experience significant changes in cardiovascular or acid-base parameters when suctioned without hyperoxygenation. Although most subjects did not become desaturated, four subjects experienced desaturation at one or more intervals. To prevent desaturation, hyperoxygenation should be used before and after suctioning with a closed tracheal suction system.

Aged↗
PubMed1992

Cardiovascular response in canine endotoxic shock: effect of ibuprofen pretreatment.

Ibuprofen pretreatment increases arterial pressure and reduces mortality in endotoxic dogs. The increase in arterial pressure may be caused by increases in arterial resistance, arterial sphincter tone, or both. Thus it is not clear if ibuprofen pretreatment prevents the hemodynamic effects of endotoxemia or merely masks such effects by producing concomitant increases in arterial resistance. Accordingly, this study was performed to determine the effects of ibuprofen pretreatment on arterial pressure-flow relations and other measures of cardiovascular function in a canine model of endotoxic shock. In 19 pentobarbital-anesthetized and splenectomized, closed-chest dogs, biventricular stroke volumes were measured with electromagnetic flow probes, and intrathoracic vascular and pleural pressures were measured with catheters. Instantaneous venous return curves (see Pinsky MR, J Appl Physiol 56:765, 1984) were generated during positive-pressure ventilation, and steady-state arterial pressure-flow relations, left ventricular function, peripheral vascular compliance, oxygen consumption/oxygen delivery ratio, and arterial blood lactate levels were measured during two sequential volume loading and removal (20 ml/kg) sequences. All but two dogs received a bolus infusion of Escherichia coli endotoxin (2 mg/kg) between the two fluid challenge runs. Eleven of the 17 endotoxic dogs also received ibuprofen (15 mg/kg) immediately before the initial fluid challenge. Ibuprofen pretreatment abolished all hemodynamic effects of endotoxin, whereas in the untreated group endotoxin caused decreases in calculated arterial outflow pressure and in peripheral vascular capacitance. Oxygen consumption remained constant despite changes in oxygen delivery in the nonendotoxic dogs and in the ibuprofen-pretreated dogs, whereas oxygen consumption covaried with oxygen delivery in the endotoxic dogs not pretreated with ibuprofen. Arterial lactate levels were higher after endotoxin infusion (2.1 +/- 0.5 to 3.1 +/- 0.6 mmol/liter; P less than 0.05 pre- to postvolume) but were not different between treatment groups. These data suggest that ibuprofen alters many, but not all, of the hemodynamic effects of endotoxin infusion in the dog.

Acidosis↗
PubMed1992

Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation.

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.

Adult↗
PubMed1991

Interleukin-6 administration has no acute hemodynamic or hematologic effect in the dog.

To investigate the possible hemodynamic effects of interleukin-6 (IL-6), a single dose of 15 mcg/kg of recombinant IL-6 isolated from Escherichia coli was injected intravenously in six pentobarbital-anesthetized dogs. After 30 min, saline infusion was performed to maintain the pulmonary artery balloon-occluded pressure at baseline level. The animals were observed for up to 5 hours. No other hemodynamic alteration was observed than a gradual decline in cardiac output attributed to anesthesia. Hematologic variables, blood glucose, and total serum proteins were also constant. IL-6 levels were markedly elevated in the blood, but no tumor necrosis factor activity was detected. Thus a primary role for IL-6 in the early cardiovascular alterations associated with septic shock seems unlikely.

Animals↗
PubMed1991

Flow redistribution during progressive hemorrhage is a determinant of critical O2 delivery.

O2 consumption (VO2) of anesthetized whole mammals is independent of O2 delivery (DO2) until DO2 declines to a critical value (DO2c). Below this value, VO2 becomes O2 supply dependent. We assessed the influence of whole body DO2 redistribution among organs with respect to the commencement of O2 supply dependency. We measured DO2, VO2, and DO2c of whole body, liver, intestine, kidney, and remaining carcass in eight mongrel dogs during graded progressive hemorrhage. Whole body DO2 was redistributed such that the organ-to-whole body DO2 ratio declined for liver and kidney and increased for carcass. We then created a mathematical model wherein each organ-to-whole body DO2 ratio remained approximately constant at all values of whole body DO2 and assigned organ VO2 to predicted organ DO2 by interpolation and extrapolation of observed VO2-DO2 plots. The model predicted that O2 supply dependency without redistribution would have commenced at a higher value of whole body DO2 for whole body (8.11 +/- 0.89 vs. 6.98 +/- 1.16 ml.kg-1.min-1, P less than 0.05) and carcass (6.83 +/- 1.16 vs. 5.06 +/- 1.15 ml.kg-1.min-1, P less than 0.01) and at a lower value of whole body DO2 for liver (6.33 +/- 1.86 vs. 7.59 +/- 1.95, ml.kg-1.min-1, P less than 0.02) and kidney (1.25 +/- 0.64 vs. 4.54 +/- 1.29 ml.kg-1.min-1, P less than 0.01). We conclude that redistribution of whole body DO2 among organs facilitates whole body O2 regulation.

Animals↗
PubMed1991

Renal O2 consumption during progressive hemorrhage.

Most mammalian tissues regulate O2 utilization such that O2 consumption (VO2) is relatively constant at O2 delivery (DO2) higher than a critical value (DO2c). We studied the relationship between VO2 and DO2 of kidney and whole body during graded progressive exsanguination. The relationship between whole body VO2 and DO2 was biphasic, and whole body VO2 decreased by 5.6 +/- 14.4% (P = NS) from the initial value to the value nearest whole body DO2c. Kidney DO2 decreased in direct proportion to whole body DO2 such that the average R2 value describing the linear regression of kidney DO2 vs. whole body DO2 was 0.94 +/- 0.02. The relationship between kidney, like whole body, VO2 and DO2 appeared biphasic; however, kidney VO2 decreased by 63.3 +/- 10.4% (P less than 0.0001) from the initial value to the value nearest kidney DO2c. Renal O2 extraction ratio was relatively constant over a wide range of kidney DO2, whereas whole body O2 extraction ratio increased progressively at all whole body DO2 values as whole body DO2 decreased. However, final values of O2 extraction ratio were indistinguishable for whole body (0.86 +/- 0.1) and kidney (0.86 +/- 0.06) (P = NS). We conclude that the pattern of kidney and whole body VO2 response to decreasing DO2 differs during hemorrhage, particularly in the range of DO2 normally associated with tissue wellness.

Animals↗
PubMed1991

Monitoring the effect of CPAP on left ventricular function using continuous mixed-blood saturation.

The hypothetic benefit of CPAP on cardiac performance and on a reduction in VO2 was tested in a patient before heart transplantation after acute myocardial infarction using continuous SvO2 monitoring. The CPAP added to inotropic support (enoximone plus dobutamine) and intraaortic balloon pumping dramatically increased SvO2 in relation to both an increase in cardiac output and a decrease in VO2 secondary to respiratory work reduction, validating the initial hypotheses.

Cardiotonic Agents↗
PubMed1990

Regional oxygen delivery in oxygen supply-dependent states.

Assessment of the adequacy of systemic O2 delivery (DO2) is central in the evaluation of critically ill patients, but estimates of systemic DO2 do not assess the effectiveness of regional DO2 to all vascular beds whose functions may require different degrees of blood flow depending on their metabolic and functional demands. The oxygen supply-consumption curve includes a supply-independent portion, which represents the reserve capacity of the body to maintain oxygen consumption (VO2) despite inadequate increases in DO2, and a supply-dependent portion, which represents the physiologic adaptation that occurs once DO2 is unable to meet the metabolic demands of the body. Experiments in dogs revealed that when systemic DO2 was progressively reduced, blood flow was maintained in the vital organs (heart and brain) and redistributed away from the kidneys and liver, enhancing the ability of the whole organism to use oxygen efficiently. Disease states and iatrogenic conditions that alter this vasoregulatory process may directly impair organ system function.

Animals↗
PubMed1990

Effect of positive end-expiratory pressure on hypoxic pulmonary vasoconstriction in the dog.

We studied the effects of uni- and bilateral positive end-expiratory pressure (PEEP) on pulmonary artery pressure-flow (Ppa/Q) relationships during unilateral hypoxia in anesthetized dogs. A bronchial divider was inserted, the right lung was ventilated with 100% O2, and the left lung was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Left lung blood flow (QL) and aortic flow (QT) were measured by electromagnetic flow probes. Simultaneous Ppa/Q relations for both lungs, with Q on the ordinate, were obtained by altering QT via an arteriovenous fistula and an inferior vena cava occluder. Ppa/Q slopes (delta Q/delta Ppa) and extrapolated zero-flow Ppa intercepts (Pzf) were obtained by linear regression analysis. Bilateral PEEP increased Pzf for both lungs (P less than 0.01) but did not alter delta Q/delta Ppa of either lung. Unilateral PEEP decreased ipsilateral blood flow (P less than 0.001) and increased Pzf for the ipsilateral lung (P less than 0.05). Left lung PEEP did not affect the slope of the left lung Ppa/Q relationship (delta QL/delta Ppa). Hypoxic ventilation of the left lung decreased QL (P less than 0.001), increased Pzf (P less than 0.05), and decreased delta QL/delta Ppa (P less than 0.001). Neither uni- nor bilateral PEEP altered this flow diversion away from the left lung or the reduction in delta QL/delta Ppa with left lung hypoxia. We conclude that PEEP and alveolar hypoxia increase pulmonary vascular resistance at different loci, such that their effects are additive. A net increase in 10 cmH2O of PEEP does not inhibit the pulmonary vascular response to regional alveolar hypoxia.

Animals↗
PubMed1990

Effect of synchronous increase in intrathoracic pressure on cardiac performance during acute endotoxemia.

In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min after infusion of 1 mg/kg Escherichia coli endotoxin (serotype 055:B5) and then after 2 mg/kg propranolol at both low (less than 10 mmHg) left ventricular filling pressure (LVFP) and high (greater than 10 mmHg) LVFP. Ventricular function curves, aortic pressure-flow (P-Q) relationships, and venous return (VR) curves were analyzed. We found that endotoxin did not alter VR curves but shifted the aortic P-Q curves to the left with pressure on the x-axis (P less than 0.05). Volume loading increased SV (P less than 0.01) because of a rightward shift of the VR curve. No specific differences occurred with either sync or async HFJV during endotoxin, presumably because of preserved VR and shifted aortic P-Q. The lack of cardiac cycle-specific effects of ITP appears to be due to the selective endotoxin-induced changes in peripheral vasomotor tone that counterbalance any depressed myocardial contractility.

Adrenergic beta-Antagonists↗
PubMed1990

Hemodynamic effects of synchronous high-frequency jet ventilation in mitral regurgitation.

We tested the hypothesis that increases in intrathoracic pressure (ITP), by decreasing the pressure gradient for anterograde left ventricular (LV) ejection, should augment cardiac output in acute mitral regurgitation (MR). In a pentobarbital-anesthetized closed-chest canine model, LV stroke volume (SLLV) was measured by integration from an aortic flow probe signal. MR was induced by a regurgitant ring. ITP was elevated over apnea by means of intermittent positive-pressure ventilation (IPPV), asynchronous (asynch) high-frequency jet ventilation (HFJV), and cardiac cycle-specific (synch) HFJV. IPPV resulted in the greatest increase in ITP. MR caused a fall in SVLV and a rise in LV filling pressure that were not altered by IPPV. Compared with IPPV or apnea, both asynch and synch HFJV increased SVLV and reduced LV filling pressures (P less than 0.05). Systolic synch HFJV induced a greater increase in SVLV (32%) than diastolic synch HFJV (26%) despite similar ventilatory settings. Our data suggest that when LV contractility is normal but MR impairs forward flow, cardiac cycle-specific increases in ITP will augment forward flow.

Animals↗
PubMed1990

Effects of D-galactosamine-induced acute liver injury on mortality and pulmonary responses to Escherichia coli lipopolysaccharide. Modulation by arachidonic acid metabolites.

Multiple extrapulmonary organ system failures increase mortality, permeability edema, and alveolar inflammation during gram-negative sepsis because of abnormal regulation of host inflammatory responses. We tested the hypothesis that acute hepatocytic injury induced by the selective hepatotoxin, D-galactosamine (GalN), augments mortality and amplifies pulmonary microvascular permeability to albumin and neutrophilic influx after administering Escherichia coli lipopolysaccharide (LPS) 24 h later by impairing the metabolism of endogenously synthesized products of arachidonic acid. We determined the lung extravascular leak of 125I-human serum albumin measured at multiple time points after LPS and enumerated polymorphonuclear leukocytes (PMNs) in bronchoalveolar lavage fluid (BALF). Because the liver is important in prostaglandin (PG) and leukotriene (LT) metabolism, we measured plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2 (TxB2) in addition to paired plasma BALF concentrations of LTB4 and BALF LTC4 60 min and 24 h after LPS. We further assessed the protective effects of a single 20-mg/kg injection given intraperitoneally (i.p.) of the LTA4 synthetase inhibitor, diethylcarbamazine (DEC). After 400 mg/kg GalN, LPS at 2.5 or 1.25 mg/kg i.p. increased mortality (p less than 0.001), albumin leak 60 and 90 min after LPS (p less than 0.05), plasma 6-keto-PGF1 alpha, TxB2, and LTB4 levels and BALF LTC4 within 60 min (p less than 0.05). LTB4 and LTC4 levels in BALF 24 h later were similarly increased (p less than 0.05) as were bronchoalveolar PMNs (p less than 0.001). DEC improved mortality and albumin leak (p less than 0.001), reduced lung influx of PMNs and peripheral leukocytosis (p less than 0.05), attenuated plasma LTB4 and BALF LTC4 levels 60 min after LPS (p less than 0.05), and decreased BALF LTB4 and LTC4 at 24 h (p less than 0.05), but was associated with higher plasma 6-keto-PGF1 alpha and TxB2 values at 60 min. Changes in eicosanoid levels and modulation of responses by DEC in this model suggest that impaired metabolism of endogenously synthesized leukotriences by the damaged liver underlies these phenomena. We conclude that this mechanism may enhance septic lung injury during acute liver dysfunction.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Measurements of right ventricular volumes during fluid challenge.

The effects of fluid loading on RV function were studied in 41 acutely ill patients monitored with a modified pulmonary artery catheter equipped for measuring RVef. Hemodynamic evaluation was performed before and after infusion of 300 ml of 4.5 percent albumin solution in 30 min. Changes in SI did not correlate with Pra or Ppao but did with RVEDVI. For the entire group, RVef was unchanged (27 +/- 9 vs 27 +/- 9 percent). In the eight patients with an initial RVEDVI greater than 140 ml/m2, the fluid challenge increased Pra and Ppao and reduced LVSWI without any other significant effect. There was no significant correlation between RVEDVI and Pra and only a weak correlation between RVESVI and Ppa. However, there was a highly linear correlation between both RVEDVI and RVESVI and changes in RVEDVI and in RVESVI, suggesting that in the absence of severe pulmonary hypertension RV output is primarily dependent on RV preload.

Acute Disease↗