Mechanical ventilation with permissive hypercapnia increases intrapulmonary shunt in septic and nonseptic patients with acute respiratory distress syndrome

OBJECTIVE: To compare the effects of conventional mechanical ventilation with low-volume, pressure-limited ventilation (LVPLV) and permissive hypercapnia on ventilation-perfusion (V/Q) distributions in patients with acute respiratory distress syndrome. We hypothesized that the advantageous cardiopulmonary effects of LVPLV would be greater in patients with sepsis than in those without sepsis. PATIENTS AND INTERVENTIONS: Twenty-two patients with acute respiratory distress syndrome were studied (group 1: 12 patients with hyperdynamic sepsis; group 2: 10 nonseptic patients). Intrapulmonary shunt (Qsp/Qt) (percentage of cardiac output), perfusion of "low" V/Q areas (percentage of cardiac output), ventilation of "high" V/Q areas (percentage of total ventilation [VE]), and deadspace ventilation (percentage of VE) were calculated from the retention/excretion data of six inert gases. Data were obtained during conventional mechanical ventilation and during LVPLV. MEASUREMENTS AND MAIN RESULTS: In group 1, LVPLV increased PaCO(0)rom 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 61 +/- 12 torr (8.1 +/- 1.6 kPa). Qsp/Qt increased from 28 +/- 16% to 36 +/- 17%, whereas Pao2 (84 +/- 15 torr [11.1 +/- 2.0 kPa] vs. 86 +/- 21 torr [11.5 +/- 2.8 kPa]) and Qt (10.6 +/- 2.3 vs. 11.5 +/- 2.5 L x -1) remained unchanged and PVO(2) (40 +/- 4 [5.3 +/- 0.5 kPa] vs. 49 +/- 6 torr [6.5 +/- 0.3]) increased. In group 2, LVPLV increased PaCO(2) from 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 63 +/- 11 torr (8.4 +/- 1.5 kPa). For Qsp/Qt (24 +/- 9% to 34 +/- 16%), the increase was not significant, whereas Qt (7.4 +/- 1.8 vs. 10.2 +/- 2.2 L x -1), PVO(2)(38 +/- 4 torr [5.1 +/- 0.5 kPa] vs. 50 +/- 6 mm Hg [6.7 +/- 0.8 kPa]), and PaO(2) (89 +/- 16 torr [11.9 +/- 2.1 kPa] vs. 98 +/- 19 torr [13.1 +/- 2.5 kPa]) increased. In both groups, the scatter of perfusion distribution (log SDQ) was greater than expected for normal subjects but was not different between the groups or altered by the treatments. CONCLUSIONS: In patients with acute respiratory distress syndrome, LVPLV with permissive hypercapnia, tended to increase Qsp/Qt, without a concomitant decrease of PaO(2). This occurs because, although atelectasis and increased shunt result from the low ventilatory volume, the effects on PaO(2) are offset by increased PVO(2) resulting from the hypercapnic stimulation of cardiac output. This result was independent of the presence or absence of sepsis.     

Right ventricular response to high-dose almitrine infusion in patients with severe hypoxemia related to acute respiratory distress syndrome

OBJECTIVE: To evaluate the effects of high-dose almitrine infusion on gas exchange and right ventricular function in patients with severe hypoxemia related to acute respiratory distress syndrome (ARDS). DESIGN: Prospective study. SETTING: Medicosurgical intensive care department (ten beds). PATIENTS: Nine patients with ARDS and severe hypoxemia (PaO2/FIO2 ratio, <150 torr [20 kPa]). INTERVENTION: High-dose almitrine infusion (16 microg/kg/min for 30 mins). MEASUREMENTS AND MAIN RESULTS: Gas exchange and hemodynamic parameters were recorded before and after almitrine infusion. Right ventricular function was evaluated by using a fast response thermistor pulmonary artery catheter that allowed measurement of right ventricular ejection fraction and calculation of right ventricular end-diastolic and end-systolic volumes. Almitrine did not significantly alter arterial oxygenation and intrapulmonary shunt. Almitrine increased mean pulmonary arterial pressure (MPAP) from 31 +/- 4 to 33 +/- 4 mm Hg (p < .05), pulmonary vascular resistance index from 353 +/- 63 to 397 +/- 100 dyne x sec/ cm5 x m2 (p < .05), and right ventricular end-systolic volume index from 71 +/- 22 to 77 +/- 21 mL/m2 (p < .05); almitrine decreased right ventricular ejection fraction from 36% +/- 7% to 34% +/- 8% (p < .05). Stroke volume index and cardiac index did not change. The almitrine-induced changes in right ventricular ejection fraction were closely correlated with the baseline MPAP (r2 = .71, p < .01). CONCLUSION: In patients with severe hypoxemia related to ARDS, high-dose almitrine infusion did not improve arterial oxygenation and impaired the loading conditions of the right ventricle. The decrease in right ventricular ejection fraction induced by almitrine was correlated with the baseline MPAP. Thus, high-dose almitrine infusion may be harmful in ARDS patients with severe hypoxemia and pulmonary hypertension.     

Beneficial effects of helium:oxygen versus air:oxygen noninvasive pressure support in patients with decompensated chronic obstructive pulmonary disease

OBJECTIVE: To test the hypothesis that, in decompensated chronic obstructive pulmonary disease (COPD), noninvasive pressure support ventilation using 70:30 helium:oxygen instead of 70:30 air:oxygen could reduce dyspnea and improve ventilatory variables, gas exchange, and hemodynamic tolerance. DESIGN: Prospective, randomized, crossover study. SETTING: Medical intensive care unit, university tertiary care center. PATIENTS: Nineteen patients with severe COPD (forced 1-sec expiratory volume of 0.83+/-0.3 l) hospitalized in the intensive care unit for noninvasive pressure support ventilation after initial stabilization with noninvasive pressure support for no more than 24 hrs after intensive care unit admission. INTERVENTIONS: Noninvasive pressure support ventilation was administered in the following randomized crossover design: a) 45 min with air:oxygen or helium:oxygen; b) no ventilation for 45 min; and c) 45 min with air:oxygen or helium:oxygen. MEASUREMENTS AND MAIN RESULTS: Air:oxygen and helium:oxygen decreased respiratory rate and increased tidal volume and minute ventilation. Helium:oxygen decreased inspiratory time. Both gases increased total respiratory cycle time and decreased the inspiratory/total time ratio, the reduction in the latter being significantly greater with helium:oxygen. Peak inspiratory flow rate increased more with helium:oxygen. PaO2 increased with both gases, whereas PaCO2 decreased more with helium:oxygen (values shown are mean+/-SD) (52+/-6 torr [6.9+/-0.8 kPa] vs. 55+/-8 torr [7.3+/-1.1 kPa] and 48+/-6 torr [6.4+/-0.8 kPa] vs. 54+/-7 torr [7.2+/-0.9 kPa] for air:oxygen and helium:oxygen, respectively; p<.05). When hypercapnia was severe (PaCO2 >56 torr [7.5 kPa]), PaCO2 decreased by > or =7.5 torr (1 kPa) in six of seven patients with helium:oxygen and in four of seven patients with air:oxygen (p<.01). Dyspnea score (Borg scale) decreased more with helium:oxygen than with air:oxygen (3.7+/-1.6 vs. 4.5+/-1.4 and 2.8+/-1.6 vs. 4.6+/-1.5 for air:oxygen and helium:oxygen, respectively; p<.05). Mean arterial blood pressure decreased with air:oxygen (76+/-12 vs. 82+/-14 mm Hg; p<.05) but remained unchanged with helium:oxygen. CONCLUSION: In decompensated COPD patients, noninvasive pressure support ventilation with helium:oxygen reduced dyspnea and PaCO2 more than air:oxygen, modified respiratory cycle times, and did not modify systemic blood pressure. These effects could prove beneficial in COPD patients with severe acute respiratory failure and might reduce the need for endotracheal intubation.     

Gastric tonometry in patients with cardiogenic shock and intra-aortic balloon counterpulsation

OBJECTIVE: To study the course of gastric regional PCO2 (PrCO2) in patients with cardiogenic shock requiring intra-aortic balloon (IAB) counterpulsation and the prognostic value of PrCO2 in this patient population. DESIGN: A prospective, observational clinical study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: Twenty-six consecutive patients with cardiogenic shock requiring mechanical support with an IAB counterpulsation undergoing mechanical ventilation INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULT: Hemodynamic variables, tonometric variables, arterial blood gases, and arterial lactate were assessed before insertion of IAB (baseline), and 1, 2, 3, 8, 16, 24, and 48 hrs thereafter. A subset of these patients (n = 14) were studied just before and 1, 8, 24, and 32 hrs after IAB removal; 12/26 patients (46.2%) died. Cardiac index increased from baseline to 1 hr after insertion of IAB (1.7 +/- 0.3 to 2.6 +/- 0.8 L/min/m2, p < .05). PrCO2 did not change between admission (47 +/- 13 torr [6.3 +/- 1.7 kPa]) and 8 hrs after placement of IAB but increased to 63 +/- 22 torr (8.4 +/- 2.9 kPa) at 16 hrs (p < .05) without any further alteration until 48 hrs. CO2 gap showed a similar pattern with 15 +/- 11 torr (2.0 +/- 1.5 kPa) at baseline and an increase to 28 +/- 22 torr (3.7 +/- 2.9 kPa) 16 hrs later. PrCO2 and CO2 gap remained at high levels (59 +/- 11 torr [7.7 +/- 1.5 kPa] and 22 +/- 10 torr [2.9 +/- 1.3 kPa], respectively), before IAB removal without further improvement or deterioration thereafter. PrCO2 values showed no difference between survivors and nonsurvivors at any time point. CONCLUSION: Patients with cardiogenic shock developed high PrCO2 within the first 24 hrs, which reflects gastric mucosal ischemia. Persistently high levels of PrCO2 were indicative for prolonged hypoperfusion of the gut. Gastric tonometry failed to discriminate between survivors and nonsurvivors.     

Transcutaneous PCO2 monitoring on adult patients in the ICU and the operating room

Studies were performed on 44 patients who were monitored continuously with transcutaneous carbon dioxide (PtcCO2) sensors. The patients were monitored intermittently with arterial and mixed venous blood gases and full hemodynamic and oxygen transport data. Twenty of the studies were performed intraoperatively. A total of 411 data sets revealed a correlation coefficient, r, between arterial and transcutaneous PCO2 of 0.80 when the patients were not in low flow shock, i.e., cardiac index (CI) greater than 1.5 L/min x M2. On the basis of these data, the authors have found the normal arterial-transcutaneous carbon dioxide gradient, delta CO2, (delta CO2 = PtcCO2 -- PaCO2) to be 23 +/- 11 torr. The PtcCO2 monitor was found to be a valuable trend monitor of arterial CO2 tensions of adults during adequate cardiac function in the ICU and the operating room. Twenty-four data sets were collected while 3 patients were monitored during severe shock (CI less than 1.5 L/min x M2). PtcCO2 trended inversely with changes in CI during shock and did not follow PaCO2 (r = --0.85). During shock, delta CO2 = 61 %/- 25 torr. The severity of shock could be roughly determined by comparing the PtcCO2 values with arterial CO2 tensions.     

Effects of perfusion pressure on tissue perfusion in septic shock

OBJECTIVE: To measure the effects of increasing mean arterial pressure (MAP) on systemic oxygen metabolism and regional tissue perfusion in septic shock. DESIGN: Prospective study. SETTING: Medical and surgical intensive care units of a tertiary care teaching hospital. PATIENTS: Ten patients with the diagnosis of septic shock who required pressor agents to maintain a MAP > or = 60 mm Hg after fluid resuscitation to a pulmonary artery occlusion pressure (PAOP) > or = 12 mm Hg. INTERVENTIONS: Norepinephrine was titrated to MAPs of 65, 75, and 85 mm Hg in 10 patients with septic shock. MEASUREMENTS AND MAIN RESULTS: At each level of MAP, hemodynamic parameters (heart rate, PAOP, cardiac index, left ventricular stroke work index, and systemic vascular resistance index), metabolic parameters (oxygen delivery, oxygen consumption, arterial lactate), and regional perfusion parameters (gastric mucosal Pco2, skin capillary blood flow and red blood cell velocity, urine output) were measured. Increasing the MAP from 65 to 85 mm Hg with norepinephrine resulted in increases in cardiac index from 4.7+/-0.5 L/min/m2 to 5.5+/-0.6 L/min/m2 (p < 0.03). Arterial lactate was 3.1+/-0.9 mEq/L at a MAP of 65 mm Hg and 3.0+/-0.9 mEq/L at 85 mm Hg (NS). The gradient between arterial P(CO2) and gastric intramucosal Pco2 was 13+/-3 mm Hg (1.7+/-0.4 kPa) at a MAP of 65 mm Hg and 16+/-3 at 85 mm Hg (2.1+/-0.4 kPa) (NS). Urine output at 65 mm Hg was 49+/-18 mL/hr and was 43+/-13 mL/hr at 85 mm Hg (NS). As the MAP was raised, there were no significant changes in skin capillary blood flow or red blood cell velocity. CONCLUSIONS: Increasing the MAP from 65 mm Hg to 85 mm Hg with norepinephrine does not significantly affect systemic oxygen metabolism, skin microcirculatory blood flow, urine output, or splanchnic perfusion.     

Bulk diffusion apnea test in the diagnosis of brain death.

OBJECTIVE: To assess the efficacy of bulk diffusion in maintaining oxygenation during apnea testing for brain death. DESIGN: Case series. SETTING: ICU in a primary care hospital. PATIENTS: Twenty-four consecutive patients with suspected brain death. Most patients suffered cerebral trauma from vehicular accidents. INTERVENTION: Patients were preoxygenated with an FIO2 of 1.0 and were maintained during apnea testing with bulk flow of an FIO2 of 1.0 at 40 to 60 L/min in adults and 15 L/min in children. The pre-apnea PaCO2 was between 35 to 45 torr (4.7 to 6.0 kPa) in all patients. MAIN OUTCOME MEASURES: Twenty-three patients completed the test. Five patients had a PaO2 < 100 torr (< 13 kPa) during the 10-min ventilator withdrawal time period. MAIN RESULTS: No patient breathed spontaneously during the apnea test. Twenty-two patients achieved a PaCO2 > 60 torr (> 8 kPa). One patient had a postapnea PaCO2 of 59 torr (7.8 kPa). The test was stopped in one patient who became hypotensive. CONCLUSIONS: The bulk diffusion technique has several advantages, including ease of performance over other methods of supplying oxygen during apnea testing, but this method does not prevent hypoxemia in patients with lung disease.     

Airway pressure release ventilation in a neonatal lamb model of acute lung injury

OBJECTIVE: To determine if airway pressure release ventilation (APRV) is feasible in a neonatal animal model with acute lung injury. DESIGN: Nonrandomized, repeated, bracketed measures. SETTING: University research laboratory. SUBJECTS: Seven neonatal sheep (5.6 +/- 0.6 kg), less than 10 days of age. INTERVENTIONS: Acute lung injury was induced by oleic acid infusion and cardiorespiratory profiles were compared during spontaneous ventilation at ambient airway pressure, continuous positive airway pressure (CPAP), APRV, and conventional positive-pressure ventilation (PPV). MEASUREMENTS AND RESULTS: Oleic acid resulted in acute lung injury with stable cardiorespiratory status during the 3-hr study period. Mean airway pressure (Paw) was comparable for all three positive-pressure modes (CPAP 13.4 +/- 1.5, APRV 13.5 +/- 1.4, PPV 13.9 +/- 1.4 cm H2O, NS). After acute lung injury, CPAP increased arterial oxygenation compared with spontaneous ventilation (77.3 +/- 6.9 vs. 57.7 +/- 4.2 torr [10.3 +/- 0.9 vs. 7.7 +/- 0.6 kPa], p less than .05), and this increase was maintained during APRV (73.3 +/- 5.6 vs. 77.3 +/- 6.9 torr [9.8 +/- 0.7 vs. 10.3 +/- 0.9 kPa], NS). Alveolar ventilation was increased by APRV compared with CPAP (PaCO2 29 +/- 1 vs. 41 +/- 2 torr [3.9 +/- 0.1 vs. 5.4 +/- 0.3 kPa], p less than .05) without impairment of cardiovascular performance (cardiac output 1.18 +/- 0.16 vs. 1.20 +/- 0.17 L/min, NS). To achieve ventilation equivalent to APRV during PPV, peak Paw was greater (36.4 +/- 3.2 vs. 19.7 +/- 1.7 cm H2O, p less than .05) and cardiac output (0.94 +/- 0.11 vs. 1.18 +/- 0.16 L/min, p less than .05) and mean arterial pressure (91 +/- 7 vs. 96 +/- 6 mm Hg, p less than .05) were decreased during PPV compared with APRV. CONCLUSIONS: In this neonatal laboratory model of acute lung injury, APRV maintained oxygenation and augmented alveolar ventilation compared with CPAP. Compared with PPV, APRV provided similar ventilation and oxygenation, but at lower peak Paw than PPV, without compromising cardiovascular performance.     

Effects of epinephrine on intestinal oxygen supply and mucosal tissue oxygen tension in pigs

OBJECTIVE: To study the effects of increasing dosages of epinephrine given intravenously on intestinal oxygen supply and, in particular, mucosal tissue oxygen tension in an autoperfused, innervated jejunal segment. DESIGN: Prospective, randomized experimental study. SETTING: Animal research laboratory. SUBJECTS: Domestic pigs. INTERVENTIONS: Sixteen pigs were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension was measured by using Clark-type surface oxygen electrodes. Microvascular hemoglobin oxygen saturation and microvascular blood flow (perfusion units) were determined by tissue reflectance spectrophotometry and laser-Doppler velocimetry. Systemic hemodynamics, mesenteric-venous acid-base and blood gas variables, and systemic acid-base and blood gas variables were recorded. Measurements were performed after a resting period and at 20-min intervals during infusion of increasing dosages of epinephrine (n = 8; 0.01, 0.05, 0.1, 0.5, 1, and 2 microg x kg(-1) x min(-1)) or without treatment (n = 8). In addition, arterial and mesenteric-venous lactate concentrations were measured at baseline and at 60 and 120 mins. MEASUREMENTS AND MAIN RESULTS: Epinephrine infusion led to significant tachycardia; an increase in cardiac output, systemic oxygen delivery, and oxygen consumption; and development of lactic acidosis. Epinephrine significantly increased jejunal microvascular blood flow (baseline, 267 +/- 39 perfusion units; maximum value, 443 +/- 35 perfusion units) and mucosal oxygen tension (baseline, 36 +/- 2.0 torr [4.79 +/- 0.27 kPa]; maximum value, 48 +/- 2.8 torr [6.39 +/- 0.37 kPa]) and increased hemoglobin oxygen saturation above baseline. Epinephrine increased mesenteric venous lactate concentration (baseline, 2.9 +/- 0.6 mmol x L(-1); maximum value, 5.5 +/- 0.2 mmol x L(-1)) without development of an arterial-mesenteric venous lactate concentration gradient. CONCLUSIONS: Epinephrine increased jejunal microvascular blood flow and mucosal tissue oxygen supply at moderate to high dosages. Lactic acidosis that develops during infusion of increasing dosages of epinephrine is not related to development of gastrointestinal hypoxia.     

Venous hypercarbia associated with severe sepsis and systemic hypoperfusion

We studied 37 patients with severe sepsis and systemic hypoperfusion to assess changes in PvCO2. Before fluid administration, the cardiac index (CI) was 2.64 +/- 0.14 L/min.m2. The PvCO2 was 38 +/- 1 torr and mixed venous pH was 7.32 +/- 0.02. The venous-arterial CO2 tension gradient (P[v-a]CO2) was 6 +/- 1 torr. After fluid administration, the CI increased to 3.45 +/- 0.14 L/min.m2 (p less than .001) and the P(v-a)CO2 decreased to 5 +/- 1 torr. The correlation between the change in CI and the change in P(v-a)CO2 was r = .42, p less than .01. P(v-a)CO2 was elevated in 19 (51%) patients before fluid administration (P[v-a]CO2 greater than 6 torr) (hypercarbic group). The P(v-a)CO2 gradient in this group was 9 +/- 1 compared with 4 +/- 1 torr in 18 patients with a normal P(v-a)CO2 gradient (p less than .001) (normocarbic group). PvCO2 was 41 +/- 2 torr in the hypercarbic group compared with 35 +/- 2 torr in the normocarbic group (p less than .05). No difference was noted in PaCO2. Venous arterial pH and HCO3- gradients were of greater magnitude in the hypercarbic group, -0.05 +/- 0.003 and 2.4 +/- 0.3 mEq/L compared to -0.02 +/- 0.004 (p less than .001) and 1.1 +/- 0.2 mEq/L (p less than .001), respectively. CI in the hypercarbic group was 2.3 +/- 0.2 compared to 3.0 +/- 0.2 L/min.m2 in the normocarbic group (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of adrenergic-receptor blockade and ligation of spleen vessels on the hemodynamics of dogs injected with scorpion venom

OBJECTIVE: In dogs, scorpion venom evokes a rapid increase in cardiac output (CO) that decreases below baseline level in 1 hr. The changes in CO have recently been shown to be related to the effect of the venom on venous return. In the present study, we tested the hypothesis that changes in determinants of venous return are secondary to sympathoadrenal stimulation evoked by the venom, which causes splenic contracture in the first stage of envenomation leading to increased mean circulatory pressure (MCP) and CO. Persistence of adrenergic response is the main factor leading to the second stage of envenomation, characterized by an increase in resistance to venous return (Rv) and a decrease in CO. DESIGN: Repeated measures, prospective study in dogs. SETTING: University-affiliated research laboratory. SUBJECTS: Mixed-breed dogs injected with scorpion venom. INTERVENTIONS: The effects of alpha- and beta-adrenergic-receptor blockade (blockade group, n = 9 dogs) and effects of ligation of spleen vessels (spleen ligation group, n = 11 dogs) following intravenous injection of scorpion venom from Leiurus quinquestriatus (0.05 mg/kg) were tested on the determinants of venous return and compared with the effects of scorpion venom alone (control group, n = 6 dogs). MEASUREMENTS AND MAIN RESULTS: Scorpion venom in the control group caused a marked increase in CO from 2.9+/-0.2 SD L/min to 6.5+/-2.2 L/min (p<.001) and MCP from 8.7+/-2.7 torr (1.2+/-0.35 kPa) to 21.6+/-1.4 torr (2.9+/-0.19 kPa) (p<.001) within 5 mins after venom injection. Cardiac output and MCP markedly decreased at 60 mins to 1.8+/-0.3 L/min (p<.001) and 7.3+/-3.8 torr (1.0+/-0.5 kPa) (p<.05), respectively. Rv did not change at 5 mins but increased from 196+/-50 dyne x sec/cm5 to 335+/-102 dyne x sec/cm5 (p<.01) at 60 mins. Adrenergic-receptor blockade attenuated the increase of CO and MCP at 5 mins, from 2.1+/-0.5 L/min to 2.7+/-1 L/min (p<.001) and from 5.6+/-2.0 torr (0.8+/-0.27 kPa) to 7.5+/-2.3 torr (1.0+/-0.31 kPa) (p<.05), respectively. By 60 mins, both CO and MCP returned to baseline, while Rv was not affected and was maintained at 204+/-158 dyne x sec/cm5. Ligation of spleen vessels prevented a CO increase at 5 mins and it was maintained at baseline value (2.5+/-0.6 L/min). However, MCP increased from 7.9+/-0.5 torr to 12+/-1.3 torr (p<.05). At 60 mins, CO decreased to 1.6+/-0.7 L/min (p<.01) while MCP returned to baseline. The changes in MCP were accompanied by significant increases of Rv from 152+/-24 dyne x sec/cm5 to 383+/-93 dyne x sec/cm5 (p<.001) at 5 mins, and 510+/-175 dyne x sec/cm5 (p<.01) at 60 mins. CONCLUSIONS: The changes in CO and MCP following scorpion venom injection in dogs are in part related to sympathetic stimulation. Adrenergic-receptor blockade attenuated the initial inotropic effect of the venom and completely prevented a late decrease in CO and MCP. The increase in Rv is the most important factor for late decrease in CO, and results from persistent adrenergic-receptor stimulation. In addition, an Rv increase apparently expresses vasoconstriction and redistribution of blood flow. The initial increase in CO and MCP is explained mainly by adrenergic-receptor effects on the spleen leading to augmented circulatory blood volume.     

Acute respiratory failure after cardiac surgery: clinical experience with the application of continuous arteriovenous hemofiltration

Hemodynamic and oxygen measurements were obtained before and during 24 h of continuous arteriovenous hemofiltration (CAVH) in 36 postoperative cardiac surgery patients with severe acute pulmonary failure. During the first 6 h, the low mean arterial pressure averaged only 50 +/- 7 mm Hg; PaO2 was 90 torr on an inspired oxygen fraction of 0.86 +/- 0.03; and lactic acid was 10.5 +/- 6 mmol/L. Of the 34 patients recovering from shock within 12 h, only 24 (67%) were hospital survivors. Cardiac index, oxygen availability index, oxygen consumption, and PaO2 increased during CAVH. This treatment decreased serum levels of the myocardial depressant factor, thus allowing catecholamine support to be reduced. We conclude that CAVH eliminates cardiopulmonary toxic substances partly responsible for shock. Our patients' improved hemodynamic and respiratory function suggests that CAVH may be useful in postoperative cardiac surgery patients with respiratory and hemodynamic failure.     

Systemic hemodynamics, gastric intramucosal PCO2 changes, and outcome in critically ill burn patients

OBJECTIVES: To define the hemodynamic and gastric intramucosal PCO2 (PiCO2) changes during the first 48 hrs after burn trauma and to analyze their relationship with outcome. DESIGN: Prospective, observational study in a cohort of consecutively admitted critically ill burn patients. SETTING: Intensive care burn unit in a university hospital. PATIENTS: Forty-two patients with burns covering >20% of body surface area or inhalation injury. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients were monitored with an oximetric pulmonary arterial catheter and a gastric tonometer to measure PiCO2. The difference between arterial and gastric mucosal PCO2 (P[i-a]CO2) was considered indicative of gastric mucosal hypoxia. Hemodynamic and PiCO2 measurements were performed during the first 48 hrs after admission. Patients suffered burns covering 36.1% +/- 14.3% (mean +/- SD) and 45.3% +/- 21.9% of body surface area (survivors and nonsurvivors, respectively). All patients were successfully resuscitated by conventional standards. Nonsurvivors (n = 16) died a median of 17 days after admission. In univariate analysis, the presence of shock during the resuscitation phase, age, mixed venous pH, P[i-a]CO2, right atrial pressure, pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, systemic and pulmonary vascular resistance, left ventricular stroke work index, mixed venous oxygen saturation, and systemic oxygen delivery, consumption, and extraction ratio, measured over the first 12 hrs after admission, were significantly (p < .05) different between survivors and nonsurvivors. These differences disappeared after 12 hrs after admission. Multivariate analysis identified age, percentage body surface area burned, and oxygen delivery index (6 hrs after admission) as factors independently associated with a poor outcome. P[i-a]CO2 (12 hrs after admission) was significantly greater in patients with than in those without inhalation injury (17 +/- 13 torr [2.26 +/- 1.73 kPa] vs. 6 +/- 10 torr [0.79 +/- 1.33 kPa]; p = .005). Patients with a P[i-a]CO2 difference (6 hrs after admission) > or =10 torr (1.33 kPa) had a mortality rate of 56% vs. 25% of those patients with <10 torr (p = .044). CONCLUSIONS: Our data indicate that there are hemodynamic and biochemical changes that occur early after burn trauma that are associated with prognosis after an apparently successful resuscitation. Particularly, a hemodynamic profile characterized by systemic acidosis, low systemic blood flow, and systemic and pulmonary vasoconstriction early after trauma is associated with a poor outcome. Additionally, intestinal mucosal acidosis occurs after burn trauma, is influenced by inhalation injury, and is a variable related to outcome.     

Titrating positive end-expiratory pressure therapy in patients with early, moderate arterial hypoxemia

A prospective randomized study to compare two physiologic end-points for titrating positive end-expiratory pressure (PEEP) was performed in patients with early, moderate arterial hypoxemia after surgery or trauma. All patients initially received 5 cm H2O of PEEP. In group 1 patients, PEEP was increased only if PaO2 decreased below 65 torr on an inspired oxygen fraction (FIO2) of 0.45. PEEP was then added in 2- to 3-cm H2O increments until PaO2 again was above 65 torr. Group 2 patients were treated with incremental PEEP until the PaO2/FIO2 ratio was greater than 300 or physiologic shunt (Qsp/Qt) was less than 0.20. All therapy other than PEEP was similar in the two groups. There were no statistically significant differences in entry PaO2 (mean 85 +/- 11 [SD] and 87 +/- 11 torr in groups 1 and 2, respectively), and Qsp/Qt was 0.22 in each group. Five (28%) of 18 patients in group 1 and 19 (95%) of 20 patients in group 2 received more than 5 cm H2O of PEEP. Between groups 1 and 2 there were no statistically significant differences in days intubated (3.4 +/- 3 vs. 5.3 +/- 5, respectively), ICU days (5.3 +/- 3 vs. 6.6 +/- 5), hospitalization days (26 +/- 24 vs. 28 +/- 24), incidence of pulmonary barotrauma (0/18 vs. 1/20), ICU mortality (22% vs. 20%), or overall mortality (33% vs. 25%). The number of blood gas analyses and cardiac output measurements, and the total hospital charges were also similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation

OBJECTIVES: We noticed that in some patients after cardiac surgery, when flow triggering was used, cardiogenic oscillation might be autotriggering the ventilatory support. In a prospective study, we evaluated the degree of cardiogenic oscillation and the frequency rate of autotriggering. We suspected that autotriggering caused by cardiogenic oscillation was more common than clinically appreciated. DESIGN: Prospective, nonrandomized, clinical study. SETTING: Surgical intensive care unit in a national heart institute. PATIENTS: A total of 104 adult patients were enrolled after cardiac surgery. INTERVENTIONS: During the study period, patients were paralyzed and ventilated with intermittent mandatory ventilation at a rate of 10 breaths/min, pressure support of 10 cm H2O, and flow triggering with a sensitivity of 1 L/min. MEASUREMENTS AND MAIN RESULTS: Because the patients would not be able to breathe spontaneously, we counted pressure-support (PS) breaths as instances of autotriggering. Then, we classified the patients into two groups according to the number of PS breaths: an "AT group" (PS breaths of >5/min) and a "non-AT group" (PS breaths of < or =5/min). If autotriggering occurred, we decreased the sensitivity so autotriggering disappeared (threshold triggering sensitivity). The intensity of cardiogenic oscillation was assessed as the flow and airway pressure at the airway opening. A total of 23 patients (22%) demonstrated more than five autotriggered breaths/min. During mechanical ventilation, the inspiratory flow fluctuation caused by cardiogenic oscillation was significantly greater in the AT group than in the non-AT group (4.67+/-1.26 L/min vs. 2.03+/-0.86 L/min; p<.01). The AT group also showed larger cardiac output, higher ventricular filling pressures, larger heart size, and lower respiratory system resistance than the non-AT group. As the inspiratory flow fluctuation caused by cardiogenic oscillation increased, the level of triggering sensitivity also was increased to avoid autotriggering. In the AT group with 1 L/min of sensitivity, the respiratory rate increased (19.9+/-2.7 vs. 10+/-0 breaths/min, p<.01), Paco2 decreased (30.8+/-4.0 torr [4.11+/-0.36 kPa] vs. 37.6+/-4.3 torr [5.01+/-0.57 kPa]; p < .01), and mean esophageal pressure increased (7.7+/-3.0 vs. 6.9+/-3.0 cm H2O; p<.01) compared with the threshold triggering sensitivity. CONCLUSIONS: Autotriggering caused by cardiogenic oscillation is common in postcardiac surgery patients when flow triggering is used. Autotriggering occurred more often in patients with more dynamic circulation. Autotriggering caused respiratory alkalosis and hyperinflation of the lungs.     

Ventilatory support by tracheal gas insufflation and chest vibration during bronchoconstriction

OBJECTIVE: To determine whether chest wall vibration with tracheal gas insufflation during bronchoconstriction maintains gas exchange at lower airway and intrathoracic pressures than those that occur during positive pressure ventilation. DESIGN: Prospective study. SETTING: Experimental laboratory. SUBJECTS: Six anesthetized, paralyzed mongrel dogs (mean weight, 24.7+/-3.8 kg). INTERVENTIONS: Dogs were ventilated by two methods: mechanical ventilation (7 breaths/min, 25 mL/kg tidal volume); and tracheal oxygen insufflation at 0.15 L x kg(-1) x min(-1) delivered with external chest wall vibration (29 Hz, 2 mm amplitude) of the dependent hemithorax. Bronchoconstriction was induced by methacholine infusion adjusted to double and quadruple the baseline airway resistance. Proximal mean airway pressure was kept equal for both modes of ventilation. MEASUREMENTS AND MAIN RESULTS: Airway pressure and flow, esophageal pressure, hemodynamic variables (cardiac output, systemic and pulmonary arterial pressures, pulmonary artery occlusion pressure) and gas exchange variables (PaO2, PaCO2, pH, shunt fraction, VO2) were measured. Peak airway pressure was lower (p < .05) with insufflation and vibration than with mechanical ventilation by 83.6% at baseline resistance, by 76.9% at twice baseline resistance, and by 76.8% at four times baseline resistance. Peak esophageal pressure was lower (p < .05) during insufflation with vibration by 68.5% at baseline resistance, by 87.5% at twice baseline resistance, and by 107% at four times baseline resistance. During insufflation with vibration, mild hypercapnia (PaCO2 58+/-3 torr (7.7+/-0.4 kPa) and pH 7.28+/-0.02) developed with moderate bronchoconstriction; more profound respiratory acidosis (PaCO2 137+/-41 torr (18.2+/-5.5 kPa) and pH 6.87+/-0.11) developed with severe bronchoconstriction. CONCLUSIONS: Tracheal gas insufflation with chest vibration supports gas exchange with permissive hypercapnia only during moderate, not severe, bronchoconstriction. Gas exchange was achieved at lower airway and intrathoracic pressures than those that developed during mechanical ventilation. The alveolar hypoventilation that occurred during insufflation with vibration indicates impaired CO2 elimination and suggests increased resistance to CO2 transport. This ventilation technique may confer therapeutic advantages over mechanical ventilation in the treatment of asthma.     

Small intestine intramucosal PCO(2) and microvascular blood flow during hypoxic and ischemic hypoxia

OBJECTIVE: To determine whether small intestine intramucosal PCO(2) and mucosal blood flow changes would be different between ischemic and hypoxic hypoxia. DESIGN: Randomized animal experiment. SETTING: Research laboratory. SUBJECTS: Anesthetized, mechanically ventilated, and surgically instrumented pigs. INTERVENTIONS: Systemic oxygen delivery was lowered in a stepwise manner to decrease it beyond critical oxygen delivery by lowering either FIO(2) or blood volume. MEASUREMENTS AND MAIN RESULTS: In hypoxic hypoxia pigs (n = 6), arterial oxygen concentration and oxygen delivery decreases were achieved by progressively reducing arterial PO(2) while cardiac index remained unchanged. In ischemic hypoxia pigs (n = 5), oxygen delivery reduction was achieved by progressively reducing cardiac index while arterial PO(2) remained unchanged. In control pigs, oxygen delivery remained unchanged. The lowest oxygen delivery measured in both hypoxia and ischemia experiments was 3.60 +/- 0.26 vs. 2.93 +/- 0.77 mL x kg(-1) x min(-1), respectively (p =.23). At the lowest oxygen delivery level, differences between ischemic hypoxia and hypoxic hypoxia experiments were observed for arterial lactate concentration (468 +/- 308 vs. 1070 +/- 218 mmol/L, respectively; p =.03), mixed venous arterial PCO(2) difference (10 +/- 7 vs. 4 +/- 2 torr, respectively; p =.04), and small intestine mucosal blood flow (6.2 +/- 2.1 vs. 15.7 +/- 7.4 perfusion units, respectively; p =.02). Small intestine intramucosal-arterial difference was higher in ischemic hypoxia than in hypoxic hypoxia (52 +/- 15 vs. 31 +/- 12 torr, respectively; p =.03). CONCLUSION: Small intestine intramucosal PCO(2) increases may indicate systemic oxygen uptake supply limitation in ischemic and hypoxic hypoxia related to conditions of mucosal flow stagnation and CO(2) generation.     

Effects of ventilation and nonventilation on pulmonary venous blood gases and markers of lung hypoxia in humans undergoing total cardiopulmonary bypass

OBJECTIVE: To assess the effects of lung oxygenation and ventilation vs. lung collapse on pulmonary markers of lung hypoxia. DESIGN: A prospective, nonrandomized, nonblinded comparative study. SETTING: University department of anesthesiology and cardiothoracic surgery. SUBJECTS: Twelve adult patients undergoing coronary bypass grafting requiring total cardiopulmonary bypass. INTERVENTIONS: Single lung ventilation during total cardiopulmonary bypass (tidal volume, 150 mL; respiratory rate, 6 breaths/min; inspiratory oxygen fraction, 0.5) while the contralateral lung was allowed to collapse completely without oxygenation. MEASUREMENTS AND MAIN RESULTS: At the beginning and at the end of total cardiopulmonary bypass (duration, 59-65 mins), blood was aspirated from the right and left pulmonary veins and the radial artery for measurement of blood gases and concentrations of endothelin-1, big-endothelin, thromboxane B2, lactate, and lactate dehydrogenase. Nonventilation during total cardiopulmonary bypass compared with ventilation resulted in lower pulmonary venous P(O2) values (57+/-15 torr [7.6+/-2.0 kPa] vs. 103+/-23 torr [13.7+/-3.1 kPa]) and higher thromboxane B2 concentrations (488+/-95 pg/mL vs. 434+/-92 pg/mL). The concentrations of endothelin-1, big-endothelin, lactate, and lactate dehydrogenase in the pulmonary veins did not differ significantly between nonventilated and ventilated lungs. CONCLUSIONS: Development of pulmonary tissue hypoxia during 1 hr of nonventilation and cardiopulmonary bypass with completely inhibited pulmonary arterial blood flow is unlikely, suggesting that enough oxygen is stored in or is provided to the collapsed lung. Thus, nonventilation during total cardiopulmonary bypass does not appear to contribute to postoperative respiratory dysfunction by causing pulmonary tissue hypoxia. These results, however, do not exclude that mechanical factors of ventilation might benefit the lung during cardiopulmonary bypass.     

Splanchnic perfusion during hemodialysis: evidence for marginal tissue perfusion.

OBJECTIVE: Splanchnic perfusion may be compromised during hemodialysis because of hypovolemia, inflammatory response, and blood flow redistribution. The aim of this study was to assess the response of splanchnic blood flow and oxygen transport to hemodialysis. DESIGN: A prospective clinical study. SETTING: A mixed medical-surgical intensive care unit in a university hospital. PATIENTS: Nine patients with acute renal failure. INTERVENTIONS: A 4-hr period of hemodialysis. MEASUREMENTS AND MAIN RESULTS: Systemic (via a pulmonary artery catheter), hepatosplanchnic, and femoral (via dye dilution) blood flow and gastric mucosal Pco2 were measured before, during, and 2 hrs after hemodialysis. During hemodialysis, despite unchanged arterial blood pressure, cardiac output and stroke volume decreased from 3.0 +/- 1.0 L/m2/min (mean +/- sd) to 2.3 +/- 0.7 L/m2/min (p =.02), and from 38 +/- 16 mL/m2/min to 28 +/- 12 mL/m2/min (p =.01), respectively. Splanchnic but not femoral blood flow decreased from 0.9 +/- 0.3 L/m2/min to 0.7 +/- 0.2 L/m2/min (p =.02). The blood flows returned to baseline values after dialysis without need for therapeutic interventions. Gastric mucosal-arterial Pco2 gradients were high before dialysis (35 +/- 23 torr [4.6 +/- 3.1 kPa]) and did not change. Renin but not atrial natriuretic peptide concentration increased during hemodialysis from 13 +/- 13 microg/L to 35 +/- 40 microg/L and decreased afterward to baseline values (13 +/- 13 microg/L; p =.01). Whereas interleukin 6 tended to decrease, tumor necrosis factor alpha increased during hemodialysis from 74 +/- 24 pg/mL to 86 +/- 31 pg/mL and continued to increase after hemodialysis to 108 +/- 66 pg/mL (p =.022). CONCLUSION: Hemodialysis and fluid removal in normotensive patients with acute renal failure may result in a reduction of systemic and splanchnic blood flow that is undetectable using traditional clinical signs. In contrast to what is observed in hypovolemia, the changes in regional blood flow are rapidly reversible after hemodialysis.     

Mechanisms producing hypoxemia during hemodialysis

Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary gas exchange, and dialyzer gas exchange. During use of acetate as a dialysate buffer, PaO2 decreased to 80 +/- 6.8 torr, whereas during use of the bicarbonate buffer oxygen tension remained at 92 +/- 4.9 torr or greater. Hypoventilation and microembolism were not sufficient to explain the degree of hypoxemia during acetate dialysis. Hypoxemia occurred only after the 1st exposure to acetate; neither an instantaneous change to bicarbonate nor stopping dialysis restored oxygen tension to normal. We conclude that a pharmacologic action of acetate adversely affects lung function, aggravating the decreased alveolar oxygen tension (PAO2) due to hypoventilation. Hypoxemia was not present when bicarbonate was used. Acetate buffer should not be used for dialysis in patients with unstable cardiovascular or respiratory systems.