Mixed Venous Blood Gases Research Articles

Effect of furosemide on fully established low pressure pulmonary edema

It has been shown that furosemide, via nondiuretic vascular effects, reduces pulmonary shunt and lung water during the development of oleic acid permeability edema. We studied this effect in a fully established stable model of oleic acid permeability edema. Sixteen anesthetized mongrel dogs, mechanically ventilated with a F IO 2 of 0.5, were studied 24 hr after induction of pulmonary capillary leak by intraveneous oleic acid (0.06 cc/kg). After stabilization of pulmonary capillary wedge pressure (PCWP) in the range of 0.5–3 mm Hg., bilateral ureteral ligation was performed. Furosemide (2 mg/kg) was then administered intravenously to eight dogs (treated group). An equivalent volume of saline was given to eight control dogs (control group). Pulmonary artery (PAP) and capillary wedge pressures (PCWP), thermodilution cardiac output ( Q t), thermal dye lung water (LW), venous admixture ( Q va/ Q t), arterial and mixed venous blood gases ( P a O 2, MVO 2) were then measured at hourly intervals for 4 hr. During this period of time, central hemodynamics (PCWP, PAP, Q t) remained stable in both groups. Indices of gas exchange and edema formation ( Q va/ Q t, LW, P a O 2) did not change significantly in either control or treated animals. We conclude that furosemide, previously shown to reduce pulmonary shunt and lung water in the early phase of oleic acid permeability edema, does not have any effect once the pulmonary injury is well-established.

CENTRAL VENOUS BLOOD OXYGEN SATURATION

Accurate and relatively simple monitoring is essential in managing patients with multiple injuries, and becomes particularly important when there is substantial occult blood loss. Tachycardia, said to occur following a 15% blood loss, is generally regarded as the first reliable sign of hemorrhage. However, heart rate is a nonspecific parameter which is affected by factors other than changing intravascular volume. The purpose of this study was to evaluate available means of monitoring volume status and to identify the parameter which is the earliest and most reliable indication of blood loss. Sixteen mongrel dogs were anesthetized and bled by increments of 3% of their total blood volume until the onset of sustained hypotension or a 25% blood loss. All dogs were monitored with a Swan-Ganz catheter and an arterial line. Vital signs, full hemodynamic parameters, and arterial and mixed venous blood gases were measured after each 3% blood loss. Statistical analysis of the data demonstrated that only Cardiac Index and Mixed Venous Oxygen Saturation showed linearity as function of measure blood loss. Linear regression analysis generated r values that ranged from 0.85-0.99 with a mean of 0.95 for Mixed Venous Oxygen Saturation; r values for Cardiac Index ranged from 0.39-0.98 with a mean of 0.85. Furthermore, all dogs had increased tissue oxygen extraction after 3-6% blood loss. Because Central Venous Blood Oxygen Saturation mirrors Mixed Venous Oxygen Saturation and is easily and rapidly measured, we extended our study by repeating all of the previously measured parameters, with the addition of CVP blood gases in an unanesthetized animal model.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the effects of combined or separate alpha- and beta-blockade in the treatment of hypertension in the acute stage of myocardial infarction

We have assessed the benefit of separate or combined alpha- and beta-receptor blockade in the treatment of 33 patients suffering from acute (< 48 hr) myocardial infarction complicated by sustained (> 6 hr) systolic hypertension (systolic blood pressure > 150 mm Hg). Eight patients have been treated with metoprolol, 7 with phentolamine and 18 with labetalol. We evaluated the effects of these drugs on hemodynamics and arterial and mixed venous blood gases. The patients were divided into two groups on the basis of the pulmonary wedge pressure. The first group had a pressure > 15 mm Hg. It included 9 patients treated with labetalol (1.8 mg/min for 1 hr) and 7 others with phentolamine (0.6 mg/min for 1 hr). The wedge pressure in the second group was < 13 mm Hg. Nine patients in this group had been treated with labetalol (2.1 mg/min for 1 hr) and 8 others with metoprolol (0.2 mg/kg in 15 min). Labetalol normalized the blood pressure in both groups within 1 hr as did phentolamine. Metoprolol did not significantly reduce either the systolic or the diastolic pressures. The high wedge pressures in the first group were reduced by both labetalol and phentolamine. The cardiac index was increased following phentolamine administration while it was reduced by labetalol. In the group with low wedge pressure, labetalol and metoprolol induced a slight but significant reduction in cardiac index but the pulmonary wedge pressures were significantly increased for metoprolol only. The rate-pressure product was very significantly decreased by labetalol and metoprolol but not by phentolamine. The emergency treatment of systemic hypertension occurring in the setting of acute myocardial infarction would thus appear to be best achieved by combined alpha- and beta-blockade rather than with either pure alpha- or pure beta-blockade. Phentolamine, however, would be a good drug in the presence of a reduced cardiac index.

Hypertonic Saline as a Resuscitation Solution in Hemorrhagic Shock

To determine the effect of resuscitation with hypertonic saline on extravascular lung water, seven adult sheep were endotracheally intubated; mean arterial pressure (MAP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), and central venous pressure (CVP) were monitored. A 5-French, thermistor-tipped catheter was used to measure extravascular lung water (EVLW). Colloid oncotic pressure (COP), serum electrolytes and osmolality, and arterial and mixed venous blood gas tensions were measured. The COP-PCWP gradient and the shunt fraction (Qsp/Qt) were calculated. After baseline measurements, the animals were bled to an MAP of 50 mm Hg (blood volume removed, 16.2 +/- 3.6 ml/kg), which was maintained for 30 min, measurements then being repeated. Three percent sodium chloride solution was infused at 500 ml/15 min until two of three parameters--cardiac output (CO), PCWP, or MAP--were restored to baseline values. Data were recorded again and then 60 min later. No shed blood was reinfused. The total volume of hypertonic saline infused was 39 +/- 19 ml/kg. Pulmonary artery pressure did not vary throughout the study. PCWP, MAP, and CO were significantly lower than baseline (P less than 0.05) 30 min after bleeding but all except MAP returned to baseline with resuscitation. Throughout the study, EVLW did not vary despite a COP-PCWP gradient less than 4 mm Hg. Serum sodium levels and serum osmolality were significantly above baseline values after resuscitation. In this animal model of hemorrhagic shock, infusion of hypertonic saline effected resuscitation without compromising cardiopulmonary function or increasing EVLW.

Arterial oxygenation and oxygen transport during exercise in patients with chronic obstructive pulmonary disease.

Twenty patients with chronic obstructive pulmonary disease (COPD) walked on the treadmill until symptoms limited further exercise. Ventilation, pulmonary gas exchange, arterial and mixed venous blood gas and haemodynamic variables were measured during steady state. It was not possible to predict from any resting cardiopulmonary variables (including static lung function tests) which patients would develop a decline in arterial PO2. In spite of variable PvO2 values at symptom-limited exercise, a good correlation was obtained between arterial haemoglobin saturation with oxygen and the venous admixture fraction. The directional change in PaO2, however, did not always follow that of the total oxygen transport to the tissues as gauged by either the PvO2 or the efficiency of oxygen delivery (oxygen flux/oxygen consumption) when expressed as a percentage of the value predicted for the level of exertion. This was due to the variable and unpredictable response of the cardiac output on exercise. It is concluded that there is a need to assess each patient individually both at rest and on exercise when evaluating arterial oxygenation and oxygen transport. The pattern of exercise-induced change in these oxygen indices is not predictable from resting data and they may even follow opposite directional trends.

Blood gas, cardiopulmonary, and urine electrolyte reference values in the pregnant yellow baboon (Papio cynocephalus).

We measured urine sodium and potassium; respiratory rate, lung water, and arterial and mixed venous blood gases; adult and fetal heart rates; hematocrit, plasma sodium and potassium; cardiac output; and arterial, pulmonary artery, central venous, and pulmonary wedge pressures in 13 clinically normal, pregnant yellow baboons (papio cynocephalus). Arithmetic means, standard deviations, and coefficients of variation were calculated to develop reference values; in addition, the 95% confidence limits for ranges were established and regression analyses were performed to determine relationships between parameters. Comparison of derived data with those from published values for nonpregnant baboons indicated differences similar to those seen when examining pregnant and nonpregnant humans.

Pulmonary gas exchange and central hemodynamics at rest and during exercise in patients with chronic obstructive pulmonary disease.

Right-heart catheterization and ergometry with arterial and mixed venous blood gas analysis were performed in 27 patients with a wide range of chronic obstructive pulmonary diseases. The purpose of the examination was to evaluate the risk in patients for lung surgery or to detect additional heart diseases. Patients who developed exertional hypoxia (group 1) were compared with others who did not (group 2). In all patients the steady-state maximal workload was determined by ventilatory dysfunction. Both groups had normal values for mixed venous pO2 and normal increase of the circulatory parameters during exercise. The patients with exertional hypoxia differed from the others in that they showed no decrease of venous admixture and alveolar-arterial oxygen gradient. In addition, these patients had increasing pCO2 values at rest compared with exercise, indicating alveolar hypoventilation and ventilation-perfusion mismatching. Because of the good correlation of the absolute values of FEV1 (forced expiratory volume in 1 s) with pulmonary artery pressures, parameters of gas exchange and working capacity, this lung function parameter seems to have a central role in predicting the functional state of patients with chronic obstructive disease. Ergometry and blood gas analysis should be performed in addition because these values cannot be predicted with the calculated postoperative FEV1.

Blood respiratory properties in pigeons at high altitudes: effects of acclimation.

Many birds thrive at high altitudes where environmental temperatures are low. Previous studies have shown that tolerance of and acclimation to hypoxia involve cardiopulmonary and hematological adaptations. We investigated blood respiratory properties during exposure to simulated high altitude (hypobaric hypoxia) and low temperature in unanesthetized resting pigeons (Columbia livia, mean mass 0.38 kg). A control group (C) and a group acclimated to 7 km above sea level (ASL) in a hypobaric chamber at 25 degrees C (HA group) were used. All were acutely exposed to altitudes through 9 km ASL at 5 or 25 degrees C. Arterial and mixed venous blood gas tensions and O2 and CO2 content during steady state decreased with increased altitude, whereas blood lactate increased in both groups at both temperatures. Acute high-altitude exposure did not affect hematocrit, hemoglobin concentrations, or O2 carrying capacity, but at any altitude these were all greater in HA than in C birds. At 5 degrees C blood pH increased with altitude in controls but remained unchanged in HA birds. At 25 degrees C in both groups mean intracellular pH did not change, averaging 6.97, whereas extracellular (venous) pH increased with altitude. At the highest altitudes tissue O2 extraction was virtually complete in both groups. Acclimation changed blood O2 and CO2 combining properties in ways likely to improve gas transport at high altitudes. The previously unreported shifts in blood respiratory and acid-base properties with acclimation indicate that innate extrapulmonary adaptations contribute to avian hypoxia tolerance.

Evidence for Adenosine Triphosphate Degradation in Critically-Ill Patients

Alterations of cellular energy metabolism may provide important markers during the clinical course of critically ill patients. To determine whether adenosine triphosphate (ATP) degradation occurs in critically ill patients, we measured levels of adenosine, inosine, hypoxanthine, and xanthine in 18 patients and seven control subjects. The mean concentration of hypoxanthine (3.8 microM) in the critically ill patients was elevated (p less than 0.01) compared to that of our control population (0.1 microM). A subgroup of seven critically ill patients had levels of hypoxanthine, xanthine, or inosine higher than those of any member of the control group. This subgroup was characterized by a lower systolic blood pressure, an increased requirement for vasopressors, and a markedly decreased survival rate when compared to the other critically ill patients. Arterial and mixed venous blood gas values were not helpful in predicting survival and did not correlate with levels of ATP degradation products. In two patients who showed subsequent clinical improvement, the initially elevated levels of hypoxanthine and xanthine returned to normal. This study indicates that critically ill patients have elevated levels of ATP degradation products. These increased levels may indicate cellular hypoxia.

199 OXYGEN CONSUMPTION (VO2) AND TISSUE METABOLISM IN THE HYPOXIC LAMB

The observation has been made in the newborn (NB) animal that a fall in VO2 with alveolar hypoxia is not always accompanied by acidosis, suggesting that there is primarily a reduction in non-essential oxidative metabolism. To test this hypothesis we compared the metabolic consequences of an induced reduction in VO2 in conscious NB and older lambs. Seven lambs with chronic aortic and pulmonary arterial catheters were studied at < 7 days, at 1 mo. and at 2–3 mos. Sequential measurements were made at FIO2 = .21, .16, .12 and .08 obtaining: arterial and mixed venous blood gases, hemoglobin (Hb) concentrations, %HbO2, lactate (L), VO2, and CO2 production (VCO2). Base deficit (BD), cardiac output, systemic O2 transport (SOT) and R (VCO2/VO2) were calculated. All data were compared to measurements at FIO2 .21. In all groups when SOT fell sufficiently with hypoxia there was a fall in VO2. This occurred at a higher SOT in the NB (15 mlO2/min/kg) than lambs 2–3 mos (10 ml)2/min/kg). Δ L (L-L@control) consistently increased at all ages to ≥ 3 mMol/L whenever V)2 decreased to ≤ .7 × control VO2. Like L, BD and R increased significantly with a fall in VO2. Therefore we found that a comparable decrease in VO2 is attended by evidence of anaerobic metabolism at all ages; the major age related difference was the higher critical SOT at which this occurred in the newborn. Thus, the newborn does not seem to be less susceptible than the older subject to the impairment of oxidative metabolism caused by alveolar hypoxia.

Thromboxane interaction with cardiopulmonary dysfunction in graded bacterial sepsis.

The relationship between plasma levels of thromboxane A2, radioimmunoassayed as thromboxane B2 (TxB), and cardiopulmonary dysfunction in graded bacterial sepsis was investigated. Five adult female pigs under anesthesia were intubated and allowed to breathe room air spontaneously. Femoral arterial, venous, and pulmonary artery catheters were inserted. After a 60-minute control period Aeromonas hydrophila (1.0 X 10(9)/ml) was infused intravenously at 0.2 ml/kg/hr, gradually increasing to 4.0 ml/kg/hr over 4 hours. Arterial and mixed venous blood gases, hemodynamic measurements, and TxB plasma concentrations were obtained during the control period, at 10, 20, 30, 45, and 60 minutes and at 30-minute intervals thereafter. Cardiac index increased significantly from control at 20 minutes, remained above control levels for 1 hour, and then declined to significantly low values at 150 minutes. TxB was increased from control at 20 minutes, rising to four times control at 120 minutes. Mean arterial pressure, pulmonary capillary wedge pressure, left ventricular stroke work, paO2, and pvO2 decreased significantly during the experiment. Pulmonary artery pressure and pulmonary vascular resistance increased significantly. Changes in TxB were significantly cross-correlated with changes in cardiac index, pulmonary vascular resistance, stroke volume, left ventricular stroke work, and paO2. TxB elevations led the cross-correlated variables by 0 to 60 minutes. Pulmonary vascular resistance cross-correlated with mean arterial pressure and cardiac index. TxB is increased early in graded bacterial sepsis. Changes in TxB appear to precede impaired cardiopulmonary function. The data suggest that TxB is involved in the detrimental hemodynamic effects of early septicemia.

Cardiorespiratory effects of pneumatic trousers in critically ill patients.

Although pneumatic antishock trousers (PT) are widely used in prehospital and emergency care, little is known about their cardiorespiratory effects in critically ill patients. To examine this issue, we measured hemodynamic and oxygen metabolism variables in ten critically ill patients. All patients were studied with PTs uninflated, after five minutes of PT inflation to 40 mm Hg, and five minutes after PT deflation. Significant increase in mean arterial pressure, systemic vascular resistance, and pulmonary artery pressures were present after PT inflation. No significant changes in cardiac index, stroke index, arterial or mixed venous blood gas values, or oxygen delivery were found. There was a downward trend in VO2 that was on the border of statistical significance. Regression analysis of cardiorespiratory variables on blood volume demonstrated no physiologic effects of external counterpressure in hypovolemic, hypervolemic, or normovolemic patients. We concluded that PT inflation increases BP through its effects on peripheral resistance. No significant autotransfusion effect was present, and there was a suggestive impairment in oxygen metabolism.

Time course and responses of sustained hypoxic pulmonary vasoconstriction in the dog.

The stability of the pulmonary blood pressure and flow response to alveolar hypoxia (hypoxic pulmonary vasoconstriction or HPV) was studied in six pentobarbital anesthetized, mechanically ventilated open-chested dogs. Aortic and left pulmonary artery blood flows; systemic and pulmonary arterial, central venous, left atrial, and airway pressures; hemoglobin; arterial and mixed venous blood gases were measured. The right lung was ventilated continuously with 100% oxygen, while the left lung was ventilated alternately with 100% O2 ( prehypoxia control phase), an hypoxic gas mixture containing 4% O2, 3% CO2, balance N2 for 4 h, or 100% O2 (post-hypoxia control phase). Hypoxic ventilation of the left lung resulted in an immediate and sustained decrease in left lung blood flow (QL%) from 39.0 +/- 1.8% (mean +/- SE) to 9.9 +/- 3.6% at 15 min of hypoxic ventilation. QL% remained decreased and did not vary significantly during the 4 h of hypoxia. Venous admixture correspondingly was increased and PaO2 decreased by hypoxic ventilation and did not vary significantly during the 4 h of hypoxia. All variables returned to control levels upon reestablishing ventilation with 100% O2. While the maximal reduction in QL% with left lung hypoxic ventilation was identical to that observed during atelectasis previously in our laboratory, the time course of the response was different. The response to hypoxia was maximal by 15 min, however, QL% decreased more slowly during atelectasis, where the maximal reduction was observed by 60 min. The present study therefore demonstrated that hypoxic ventilation of the left lung yielded an immediate and sustained decrease in left lung blood flow for 4 h. The stability of the HPV response probably was accounted for by the lack of such confounding factors as respiratory alkalosis, severe systemic hypoxemia, and increased cardiac output.

Assessment of out-of-hospital resuscitation

The best method for employment of phased chest and abdominal compression–decompression (Lifestick™) cardiopulmonary resuscitation (CPR) has yet to be determined. Of particular concern with using this technique is the combining of ventilation with the phased compressions and decompressions. Twenty domestic swine (50±1 kg) were equally divided into four groups. Following 10 min of untreated VF, CPR was begun. Group 1 received Lifestick™ (LS) CPR with only passive ventilation (‘passive’); Group 2 received LS-CPR with synchronized positive pressure ventilations (ppv) at a chest compression ratio of 15:2 (15:2 S); Group 3 had LS-CPR with synchronized ppv at 5:1 (5:1 S); and Group 4 received LS-CPR with asynchronous ppv at 5:1 (5:1 A). Endpoints included hemodynamics, blood gases, minute ventilation, and 24 h outcome. Asynchronous ventilation (5:1 A) had significantly worse hemodynamics including aortic and right atrial systolic, aortic diastolic, and coronary perfusion pressures than the other groups (P<0.05). Passive ventilation had the poorest arterial and mixed venous blood gases (P<0.05), but did not differ from 15:2 S in minute ventilation produced (8 vs 10 l/min). No differences in outcome were seen. The ventilation technique combined with LS-CPR can make a significant difference in hemodynamics as well as ventilation. Optimizing other forms of basic and advanced cardiac life support through different ventilation methods deserves new consideration, including a re-examination of the current single rescuer recommendation of a 15:2 ratio. Optimal ventilation strategy when using the LS device at 60 compressions per min appears to be 5:1 S. Such data is important for conducting clinical trials with this new CPR adjunct.

Effects of oral hydralazine on gas exchange in patients with cor pulmonale

Vasodilators lower total pulmonary vascular resistance in some patients with pulmonary hypertension, but If vasodilators worsen arterial oxygenation in cor pulmonale, as they do in some patients with left ventricular failure, the benefits of a decrease in vascular resistance would be offset by a lack of change or a deterioration in systemic oxygen delivery. Measurement was made of arterial and mixed venous blood gases, minute ventilation, shunt fraction, alveolar-arterial oxygen difference, pulmonary arterial pressures, and cardiac output before and four hours after a single dose of hydralazine, 75 mg orally, in six patients (Group I) and before and after 48 hours of hydralazine, 50 to 75 mg orally, every six hours In 10 patients (Group II). Cardiac output increased 36 percent in Group I and 48 percent in Group II. In both groups total pulmonary vascular resistance decreased (8.0 ± 2.8 to 6.1 ± 2.6 units in Group I, p < 0.01; 9.7 ± 3.7 to 5.6 ± 2.1 units in Group II, p < 0.01). Arterial P O 2 increased significantly both in Group I (61 ± 8 to 67 ± 10 torr, p < 0.05) and Group II (50 ± 13 to 54 ± 13, p < 0.05); however shunt fraction and alveolar-arterial oxygen difference were unchanged. The ratio of dead space to tidal volume decreased slightly in both groups, and minute ventilation increased significantly. Systemic oxygen delivery was increased by 39 and 51 percent in Groups I and II, respectively. Thus, gas exchange may be preserved or improved when hydralazine is used in the treatment of cor pulmonale.

Influence of mixed venous oxygen tension (PVO2) on blood flow to atelectatic lung.

The influence of mixed venous oxygen tension (PVO2) on blood flow to the atelectatic left lung was studied at normal and reduced cardiac outputs (CO) using extracorporeal veno-venous bypass in six pentobarbital anesthetized, mechanically ventilated dogs. Aortic and left pulmonary artery flows; airway, left atrial, central venous, pulmonary, and systemic arterial pressures; hemoglobin, arterial, and mixed venous blood gases were measured. The blood flow reduction observed in atelectasis was altered by the PVO2. Approximately 50% of blood flow was diverted away from atelectatic lung when PVO2 was low (24 +/- 2 mmHg) or normal (46 +/- 2 mmHg) (mean left lung blood flow [QL%] was 23.2 +/- 4.6% with low PVO2 and 19.0 +/- 3.4%, with normal PVO2). When PVO2 was increased to greater than 100 mmHg, diversion of blood flow away from atelectatic lung did not occur and QL% was nearly the flow expected for normoxic ventilated left lung (mean QL% = 40.4 +/- 5.9%). Shunt (QS/QT%) was significantly greater when PVO2 was high than when it was normal or low (mean QS/QT% = 51.7 +/- 5.6%, 31.0 +/- 3.1%, 26.0 +/- 3.4% with high, normal, and low PVO2, respectively). Mean PaO2 was significantly greater when PVO2 was high than when PVO2 was normal or low, despite the increase in QL% and QS/QT% (PaO2 = 327 +/- 25 mmHg, 220 +/- 32 mmHg, 115 +/- 21 mmHg with high, normal, and low PVO2, respectively). A 40% reduction in cardiac output significantly decreased transmural pulmonary artery pressure but did not affect PaO2, QS/QT%, or QL%.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of clenbuterol hydrochloride on certain respiratory and cardiovascular parameters in horses performing treadmill exercise

Five standardbred geldings received intravenous clenbuterol hydrochloride and saline in a crossover experiment to evaluate the effects of clenbuterol on certain cardiorespiratory parameters during and after treadmill exercise. The exercise test consisted of four steps. Step 1 at a speed of 76 m per minute, step 2 at 129 m per minute, step 3 at 190 m per minute and step 4 at 236 m per minute. The duration of each step was two minutes, except step 4 which was four minutes. The treadmill was set at a grade of 19 per cent. Before exercise, 30 minutes after clenbuterol or saline administration, arterial and mixed venous blood gases, mean arterial pressure, mean pulmonary artery pressure, telemetric electrocardiogram and respiratory rate were measured. The measurements were repeated immediately before completion of step 2, step 4 and after one minute, 10 minutes and 30 minutes of recovery from exercise. After clenbuterol administration there was a transient fall in mean arterial pressure, which had returned to control values by 90 seconds. There was no change in mean pulmonary artery pressure. During exercise the heart rate was significantly higher at the end of steps 1 and 4 and after 10 minutes recovery when horses given clenbuterol were compared with those given saline. No adverse effects on the electrocardiogram were demonstrated. Effects of clenbuterol on blood gases included an increase in PaO2 and decrease in PaCO2 one minute after exercise, when compared to saline. It was concluded from the parameters examined that there was no evidence that clenbuterol had any significant untoward effect on the circulatory system of exercising horses.

Cardiovascular response to severe head injury.

The cardiovascular, pulmonary, and metabolic responses to severe head injury were studied clinically in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. Cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases, and arterial and mixed venous epinephrine (E) and norepinephrine (NE) levels were measured serially in 15 patients during the first 3 days after injury. A hyperdynamic state was found, characterized by increased cardiac output, cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting, and increased oxygen delivery and utilization. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Scale score, or computerized tomography findings. It is concluded that a hyperdynamic cardiovascular state occurs after severe head injury, and that it is mediated in part by sympathetic nervous activity. The significance of this state for systemic management of patients with head injury is discussed.

Continuous positive airway pressure is beneficial in treatment of smoke inhalation.

This study demonstrates that continuous positive airway pressure (CPAP) improves pulmonary function after smoke inhalation by dogs. Sixteen dogs were anesthetized with iv sodium pentobarbital. Arterial and mixed venous blood gas tensions; carboxyhemoglobin concentration (COHgb); mean systemic arterial (MAP), mean pulmonary arterial (MPAP), and pulmonary arterial wedge (WP) pressures; heart (HR) and respiratory (f) rates; cardiac output (CO); and airway pressure (Paw) were measured. Intrapulmonary physiologic shunt (Qsp/Qt) and pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. The animals then breathed an aerosol of smoke and were divided randomly into 2 groups. The treatment group breathed spontaneously on 8-torr CPAP whereas the control group continued to breathe spontaneously at ambient pressure. After inhalation of smoke, Qsp/Qt, MPAP, PVR, COHgb, HR, and f rose, whereas PaO2 and MAP fell in untreated animals. When CPAP was applied, PaO2 and Qsp/Qt returned nearly to baseline values. Mean f also was significantly lower in the treated animals. We found that the early institution of CPAP improves oxygen exchange in the lungs after the inhalation of smoke.

The effects of prophylactic expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory airway pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome (ARDS) or if it also affects the resolution of their lung injury. The present investigation was performed to determine whether expiratory positive airway pressure (EPAP), a form of PEEP, is prophylactic in preventing the lung injury induced by oleic acid in dogs or in enhancing its resolution. Arterial and mixed venous blood gases and functional residual capacity (FRC) were measured in 14 pairs of mongrel dogs with indwelling catheters and permanent tracheostomies. One member of each pair was treated with 10 cm H2O EPAP through a valve attached to the tracheostomy tube. Both dogs received 0.06 ml/kg oleic acid intravenously at hour 0. Measurements were made at three, 12, and 24 hours, when EPAP was discontinued, and over the next six days. Five dog pairs were sacrificed at 72 hours; the other surviving animals were sacrificed at 168 hours. FRC was higher at three, 12, and 24 hours in dogs receiving EPAP than in the untreated dogs. The arterial oxygen tension (PaO2) was higher and the venous admixture (Qva/Qt) was lower at three and 12 hours in the dogs receiving EPAP than in the untreated dogs. However, after 24 hours, no differences were noted between the two groups in FRC, PaO2, Qav/Qt, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histology. It is concluded that EPAP improves gas exchange during its administration, but has no demonstrable prophylactic effect on the resolution of lung injury in the oleic acid model of human ARDS.