Systemic Oxygen Transport Research Articles

Effects of phenylephrine on the sublingual microcirculation during cardiopulmonary bypass

The objective of the present study was to investigate sublingual microvascular blood flow and microcirculatory haemoglobin oxygen saturation (Smc(O(2))) during cardiopulmonary bypass (CPB) using constant systemic blood flow but different perfusion pressures achieved by phenylephrine administration. Fifteen patients undergoing coronary artery bypass grafting were enrolled in this pilot study. Systemic haemodynamics, oxygen transport variables, arterial and mixed venous blood gas analysis, and microcirculatory variables were determined after initiation of general anaesthesia, during CPB (systemic blood flow=2.4 litre m(-2)), after increasing perfusion pressure by 20 mm Hg with a continuous infusion of phenylephrine, and after termination of phenylephrine infusion. CPB immediately resulted in a significant (P<0.05) decrease in systemic oxygen transport without alterations in sublingual microcirculatory blood flow and Smc(O(2)). Increasing perfusion pressure from 47 (SD 9) to 68 (7) mm Hg using phenylephrine=1.4 (1.0) microg kg(-1) min(-1) resulted in a significant decrease in sublingual small vessel blood flow (from median 2.5 to 1.8 arbitrary units) representing mostly capillary blood flow, but not in medium-sized vessels (median 3 to 2.8 arbitrary units). Concurrently, global tissue blood flow from 110 (54) to 197 (100) perfusion units and Smc(O(2)) increased from 72 (11)% to 84 (7)%, suggesting significant microcirculatory blood flow shunting in vessels with diameters >25 microm. Our data demonstrate that an increased perfusion pressure produced by phenylephrine at constant CPB flow may decrease microcirculatory blood flow in the sublingual mucosal microcirculation due to microvascular blood flow shunting.

Comparison of cardiac, hepatic, and renal effects of arginine vasopressin and noradrenaline during porcine fecal peritonitis: a randomized controlled trial

IntroductionInfusing arginine vasopressin (AVP) in vasodilatory shock usually decreases cardiac output and thus systemic oxygen transport. It is still a matter of debate whether this vasoconstriction impedes visceral organ blood flow and thereby causes organ dysfunction and injury. Therefore, we tested the hypothesis whether low-dose AVP is safe with respect to liver, kidney, and heart function and organ injury during resuscitated septic shock.MethodsAfter intraperitoneal inoculation of autologous feces, 24 anesthetized, mechanically ventilated, and instrumented pigs were randomly assigned to noradrenaline alone (increments of 0.05 μg/kg/min until maximal heart rate of 160 beats/min; n = 12) or AVP (1 to 5 ng/kg/min; supplemented by noradrenaline if the maximal AVP dosage failed to maintain mean blood pressure; n = 12) to treat sepsis-associated hypotension. Parameters of systemic and regional hemodynamics (ultrasound flow probes on the portal vein and hepatic artery), oxygen transport, metabolism (endogenous glucose production and whole body glucose oxidation derived from blood glucose isotope and expiratory 13CO2/12CO2 enrichment during 1,2,3,4,5,6-13C6-glucose infusion), visceral organ function (blood transaminase activities, bilirubin and creatinine concentrations, creatinine clearance, fractional Na+ excretion), nitric oxide (exhaled NO and blood nitrate + nitrite levels) and cytokine production (interleukin-6 and tumor necrosis factor-α blood levels), and myocardial function (left ventricular dp/dtmax and dp/dtmin) and injury (troponin I blood levels) were measured before and 12, 18, and 24 hours after peritonitis induction. Immediate post mortem liver and kidney biopsies were analysed for histomorphology (hematoxylin eosin staining) and apoptosis (TUNEL staining).ResultsAVP decreased heart rate and cardiac output without otherwise affecting heart function and significantly decreased troponin I blood levels. AVP increased the rate of direct, aerobic glucose oxidation and reduced hyperlactatemia, which coincided with less severe kidney dysfunction and liver injury, attenuated systemic inflammation, and decreased kidney tubular apoptosis.ConclusionsDuring well-resuscitated septic shock low-dose AVP appears to be safe with respect to myocardial function and heart injury and reduces kidney and liver damage. It remains to be elucidated whether this is due to the treatment per se and/or to the decreased exogenous catecholamine requirements.

Carbon dioxide—a complex gas in a complex circulation: Its effects on systemic hemodynamics and oxygen transport, cerebral, and splanchnic circulation in neonates after the Norwood procedure

Carbon dioxide is suggested to increase oxygen delivery after the Norwood procedure. We sought to quantitatively define the effects of stepwise increases in arterial carbon dioxide tension on systemic oxygen transport and cerebral and splanchnic circulation after the Norwood procedure. Seven sedated, paralyzed, and mechanically ventilated neonates were studied after the Norwood procedure. Arterial carbon dioxide tension increased from 40-50-60 mm Hg using inspired carbon dioxide. Each step was 30 minutes. Pulmonary and systemic blood flow, vascular resistance, and oxygen delivery were calculated with the measurement of oxygen consumption and blood gases and pressures from the aorta, superior vena cava, and pulmonary vein. Plasma epinephrine and norepinephrine were measured. Cerebral and splanchnic oxygen saturations were measured by near-infrared spectroscopy, and cerebral blood flow velocity was measured by transcranial Doppler. Stepwise increase in arterial carbon dioxide tension was associated with a decrease in systemic vascular resistance (P < .001) and an increase in systemic blood flow (P < .01) and oxygen delivery (P < .0001), but not with significant changes in total pulmonary vascular resistance and pulmonary blood flow. Cerebral oxygen saturation increased (P < .0001), and splanchnic oxygen saturation decreased (P < .01). Oxygen consumption decreased (P < .01), and epinephrine and norepinephrine increased (P < .01 and .05). Moderate hypercapnia increases systemic blood flow because of its effect on systemic vascular resistance after the Norwood procedure. The increase in systemic blood flow is primarily a consequence of increased cerebral blood flow that compromises splanchnic circulation. The decrease in oxygen consumption improves oxygen transport, but the increase in catecholamines may be undesirable. Clinical use of carbon dioxide aiming to improve oxygen delivery should be with caution.

Abstract 2597: Aortic Atresia Is Associated with an Inferior Postoperative Systemic, Cerebral and Splanchnic Oxygen Transport Status in Neonates with Hypoplastic Left Heart Syndrome after the Norwood Procedure

Aortic atresia (AA) has been identified as a risk factor for mortality after the Norwood procedure. We compared postoperative systemic and regional (cerebral and splanchnic) oxygen transport profiles in neonates with hypoplastic left heart syndrome with or without AA after the Norwood procedure. Systemic oxygen consumption (VO 2 ) was measured using respiratory mass spectrometry postoperatively for 72 hrs in 17 neonates (n=9 in AA group and 8 in non-AA group). Arterial, superior vena cava, and pulmonary venous blood gases and pressures were measured at 2– 4 hr intervals to calculate cardiac output (CO), systemic vascular resistance (SVR), oxygen delivery (DO 2 ) and oxygen extraction ratio (ERO 2 ). Cerebral (ScO 2 ) and splanchnic (SsO 2 ) oxygen saturations were measured using near infrared spectroscopy. The doses of dopamine, vasopressin (up to 0.0008 unit/kg/min), phenoxybenzamine and milrinone were noted. When compared to non-AA group, AA group had lower CO (p=0.03), higher systolic arterial blood pressure (p=0.01) and SVR (p=0.002), lower DO 2 (p=0.07), VO 2 (p=0.003) and ScO 2 during the first 30 to 40 hrs. There was no significant difference in SsO 2 (p=0.12, n=7 in AA group and 3 in non-AA group). Despite a similar ERO 2 (p=0.5), AA group had higher lactate over 72 hrs (p=0.01). AA group received higher doses of vasopressin (p=0.005) and milrinone (p&lt;0.0001), lower doses of dopamine (p=0.07), with similar use of phenoxybenzamine. Furthermore, VO 2 negatively correlated with vasopressin (p=0.05), positively correlated with milrinone (p=0.03) and dopamine (p&lt;0.0001). When including the drugs, the inferior status in all the oxygen transport variables remained, and additionally adversely correlated with vasopressin (p from &lt;0.0001 to 0.06), except for ScO 2 that positively correlated with dopamine, but not with other drugs. Aortic atresia is associated with an inferior status of systemic, cerebral and splanchnic oxygen transport in neonates after the Norwood procedure. Aggressive use of vasopressin worsens systemic and splanchnic oxygen transport status. Postoperative management strategies should be directed to improve both systemic and regional oxygen transport in this special group of patients.

Is pulmonary gas exchange during exercise in hypoxia impaired with the increase of cardiac output?

During exercise in humans, the alveolar-arterial O(2) tension difference ((A-a)DO(2)) increases with exercise intensity and is an important factor determining the absolute level of oxygen binding to hemoglobin and therefore the level of systemic oxygen transport. During exercise in hypoxia, the (A-a)DO(2) is accentuated. Using the multiple inert gas elimination technique it has been shown that during exercise in acute hypoxia the contribution of ventilation-perfusion inequality to (A-a)DO(2) is rather small and in the absence of pulmonary edema intrapulmonary shunts can be ruled out. This implies that the main mechanism limiting pulmonary gas exchange is diffusion limitation. It is presumed that an elevation of cardiac output during exercise in acute hypoxia should increase the (A-a)DO(2). However, no studies have examined how variations in cardiac output independently affect pulmonary diffusion with increases in exercise intensity. We have consistently observed that during steady-state, submaximal (100-120 W) exercise on the cycle ergometer in hypoxia the lung can accommodate an increase in cardiac output of approximately 2 L x min(-1) without any significant effect on pulmonary gas exchange. This result contrasts with the predicted effect of cardiac output on (A-a)DO(2) using the model of Piiper and Scheid, and thus indicates that an elevation of cardiac output is not necessarily accompanied by a reduction of mean transit time and (or) diffusion limitation during submaximal exercise in acute hypoxia. It remains to be determined what is the influence of changes in cardiac output per se on pulmonary gas exchange during high-intensity exercise.

Response to Letters Regarding Article, “Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure: A Pilot Study”

We appreciate the contribution of Dr Schranz and colleagues to the development of the hybrid procedure for single ventricle palliation and their insightful comments regarding our recent article.1 The hybrid procedure with bilateral pulmonary banding and arterial duct stenting was designed as a minimally invasive alternative to a Norwood procedure. By avoiding cardiopulmonary bypass and the consequent ischemia-reperfusion injury and systemic inflammatory response, we hypothesized that we would find minimally altered systemic hemodynamic and oxygen transport status as compared with the well-documented hemodynamic derangements associated with the Norwood procedure.2 We evaluated the hybrid strategy through analysis of dispassionate and objective data and, to our knowledge, our study represents the only published hemodynamic assessment of this strategy. As noted in our article, the patterns of hemodynamic alterations after hybrid procedures were more complex than might have been anticipated. Although the data are precise, Dr Schranz and colleagues appear to be concerned that these data may not accurately represent all hybrid procedures. Our intuition (without data) would suggest that this may be so and, consequently, we will endeavor to obtain another dataset in the future to determine whether the early position of this cohort on our learning curve was an important modulator of …

Letter by Phillips Regarding Article, “Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure: A Pilot Study”

To the Editor: I want to compliment Li et al on a very unique study1 evaluating oxygen consumption and delivery during the first 72 hours postoperatively in patients with hypoplastic left heart syndrome treated by either the Norwood procedure (n=13) or the hybrid procedure (n=6). The study design was excellent; however, it is my opinion that there are several problems with the study and the conclusions drawn by the authors. The hybrid procedure, which is generally used by most centers, involves placement of bilateral branch pulmonary artery bands and a stent in the patent ductus arteriosus either by a transpulmonary approach2 (Columbus) or percutaneous approach3 (Giessen). The need …

Letter by Schranz et al Regarding Article, “Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure: A Pilot Study”

To the Editor: We appreciate the novel technique applied by Li et al1 to assess continuously the hemodynamics and oxygen transport after the Norwood (n=13) and hybrid (n=6) procedures. The results obtained and the conclusions drawn, however, may be misleading in terms of the hybrid procedure in general. In most centers, the hybrid procedure is usually not performed as described here by Li et al but is instead a minimally invasive alternative to a Norwood stage I or Sano modification.2–4 The hybrid approach performed in our center in Giessen, Germany, consists of an operation in which bilateral pulmonary bands are placed through an open chest approach in the shortest amount of time possible with …

The influence of systemic hemodynamics and oxygen transport on cerebral oxygen saturation in neonates after the Norwood procedure

Ischemic brain injury is an important morbidity in neonates after the Norwood procedure. Its relationship to systemic hemodynamic oxygen transport is poorly understood. Sixteen neonates undergoing the Norwood procedure were studied. Continuous cerebral oxygen saturation was measured by near-infrared spectroscopy. Continuous oxygen consumption was measured by respiratory mass spectrometry. Pulmonary and systemic blood flow, systemic vascular resistance, oxygen delivery, and oxygen extraction ratio were derived with measurements of arterial, and superior vena cava and pulmonary venous gases and pressures at 2- to 4-hour intervals during the first 72 hours in the intensive care unit. Mean cerebral oxygen saturation was 66% +/- 12% before the operation, reduced to 51% +/- 13% on arrival in the intensive care unit, and remained low during the first 8 hours; it increased to 56% +/- 9% at 72 hours, still significantly lower than the preoperative level (P < .05). Postoperatively, cerebral oxygen saturation was closely and positively correlated with systemic arterial pressure, arterial oxygen saturation, and arterial oxygen tension and negatively with oxygen extraction ratio (P < .0001 for all). Cerebral oxygen saturation was moderately and positively correlated with systemic blood flow and oxygen delivery (P < .0001 for both). It was weakly and positively correlated with pulmonary blood flow (P = .001) and hemoglobin (P = .02) and negatively correlated with systemic vascular resistance (P = .003). It was not correlated with oxygen consumption (P > .05). Cerebral oxygen saturation decreased significantly in neonates during the early postoperative period after the Norwood procedure and was significantly influenced by systemic hemodynamic and metabolic events. As such, hemodynamic interventions to modify systemic oxygen transport may provide further opportunities to reduce the risk of cerebral ischemia and improve neurodevelopmental outcomes.

Adverse Effects of Dopamine on Systemic Hemodynamic Status and Oxygen Transport in Neonates After the Norwood Procedure

Adverse Effects of Dopamine on Systemic Hemodynamic Status and Oxygen Transport in Neonates After the Norwood Procedure

Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure: A Pilot Study

Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure: A Pilot Study

Dexmedetomidine Alters the Cardiovascular Response During Infra-Renal Aortic Cross-Clamping in Sevoflurane-Anesthetized Dogs

Some properties of the volatile anesthetics, such as vasodilatation and myocardial depression, combined with the sympathetic inhibition that α2-agonists can produce, may determine hemodynamic alterations during aortic surgery. The interaction between dexmedetomidine (DEX), an α2-agonist, and sevoflurane during aortic surgery is unknown. We studied the effects of DEX on hemodynamics and systemic oxygenation during aortic cross-clamping (Aox) and unclamping (UAox) in sevoflurane-anesthetized dogs. Twenty dogs were anesthetized with sevoflurane and were randomly assigned to two groups prior to Aox and UAox: control, n = 10, received saline infusion only, and DEX (1 μg.kg−1 load followed by 1 μg.kg−1.h−1 infusion), n = 10. Hemodynamic and oxygenation variables were measured at baseline, after saline or DEX loading dose, 20 and 40 min after Aox, and 20 and 40 min after UAox. After DEX administration, heart rate, cardiac index (CI) and systemic oxygen transport index (DO2I) were lower than in control group. Aox increased mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both groups, but the effects were greater with DEX. CI, heart rate, and DO2I were lower, while central venous pressure (CVP) and pulmonary artery occlusion pressure were higher in DEX compared to control. After UAox, MAP, CVP and SVRI were maintained higher in DEX in relation to control. We conclude that in sevoflurane-anesthetized dogs DEX alters the cardiovascular response during aortic surgery.

Comparison of the Profiles of Postoperative Systemic Hemodynamics and Oxygen Transport in Neonates After the Hybrid or the Norwood Procedure

After the Norwood procedure, early postoperative neonatal physiology is characterized by hemodynamic instability and imbalance of oxygen transport that is commonly attributed to surgical myocardial injury and a systemic inflammatory response to cardiopulmonary bypass (CPB). Because the Hybrid procedure (arterial duct stenting and bilateral pulmonary artery banding) avoids CPB, cardioplegic arrest, and circulatory arrest, we hypothesized that the Hybrid procedure is associated with superior postoperative hemodynamics and oxygen transport. Oxygen consumption (VO2) was continuously measured using respiratory mass spectrometry for 72 hours after Hybrid (n=6) and Norwood (n=13) procedures. Arterial, superior vena cava, and pulmonary venous blood gases and pressures were measured at 2- to 4-hour intervals to calculate systemic and pulmonary blood flows (Qs, Qp), and systemic vascular resistance (SVR), total pulmonary vascular resistance including pulmonary arterial band or B-T shunt (tPVR), cardiac output (CO), oxygen delivery (DO2), and oxygen extraction ratio (ERO2). Rate-pressure product was calculated as heart rate x systolic arterial pressure. When compared with the Norwood procedure, the early postoperative Hybrid patients had lower CO, higher SVR, and higher Qp:Qs ratios. In addition, the DO2 and VO2 were both lower in the Hybrids with higher ERO2 and lactate levels. This early postoperative pattern reversed after 48 hours. Although Hybrid procedure avoids CPB and cardioplegic arrest, the early hemodynamic profile is not superior to the Norwood in terms of cardiac output and control of pulmonary blood flow. These data strongly suggest that a "hands off" approach to postoperative care in Hybrid patients may not be appropriate in patients with preoperative diminished myocardial function; and in such patients a Norwood-derived management strategy (afterload reduction and inotropic support) should be considered.

Atrial Septostomy in Treatment of End-Stage Right Heart Failure in Patients With Pulmonary Hypertension

Right ventricular (RV) failure is the main cause of death in patients with pulmonary hypertension (PH). Balloon atrial septostomy (BAS) is believed to relieve symptoms of PH by increasing systemic flow and reducing RV preload. Fourteen BAS procedures were performed in 11 patients (5 men and 6 women; mean [+/- SD] age, 33 +/- 12 years) with RV failure in the course of PH that was refractory to conventional treatment. BAS consisted of a puncture of the interatrial septum and subsequent dilatations with balloons of increasing diameter in a step-by-step manner. After BAS, the mean oxygen saturation of aortic blood decreased (before, 93 +/- 4%; after, 84 +/- 4%; p = 0.001), while mean cardiac index increased (before, 1.54 +/- 0.34 L/min/m(2); after, 1.78 +/- 0.35 L/min/m(2); p = 0.001), resulting in a positive trend for mean systemic oxygen transport (before, 270 +/- 64 mL/min; after, 286 +/- 81 mL/min; p = 0.08). Pulmonary vascular resistance (PVR) slightly increased immediately after the procedure, and this rise inversely correlated with mixed venous blood partial oxygen pressure both before BAS (r = -0.69; p = 0.009) and after BAS (r = -0.64; p = 0.018). Mean functional class improved from 3.2 +/- 0.4 to 2.6 +/- 0.7 (p = 0.03) after 1 month. At follow-up (mean time to follow-up, 8.1 +/- 6.2 months; range, 0.8 to 20.2 months), seven patients died and two underwent lung transplantation. There was no difference in the survival rate compared to that obtained from National Institutes of Health equation. A significant size reduction in the created defect was observed in six patients, requiring repeat BAS procedures in three cases. The current BAS technique improves cardiac index and functional class without significant periprocedural complications, except for a transient increase in PVR related to acute desaturation of mixed venous blood. At long-term follow-up, a high incidence of spontaneous decrease in orifice size has been observed.

Systemic and Myocardial Oxygen Transport Responses to Brain Death in Pigs

Background Brain death is associated with profound disturbances of systemic and myocardial oxygen transport, but little is known regarding the acute response of systemic oxygen consumption (VO 2). Methods Brain death was induced in 6 pigs (30.6 ± 3.0 kg) by balloon inflation into the cranial cavity. VO 2 was continuously measured by respiratory mass spectrometry. Blood pressures and gases were measured from the aorta, superior vena cava, and coronary sinus, with arterial epinephrine and norepinephrine, prior to brain death, at 1, 10, and 90 minutes after brain death. Cardiac output (CO), systemic vascular resistance (SVR), oxygen delivery (DO 2), oxygen extraction (EO 2), and myocardial oxygen (mEO 2) and lactate extractions (mE 1ac) were calculated. Left ventricular contractility was assessed by micromanometer tipped catheters. Results VO 2 increased from 4.8 ± 0.9 to 6.3 ± 0.9 mL/min/kg 1 minute after brain death ( P < .001), and subsequently decreased to below baseline at 90 minutes ( P < .001). Left ventricular contractility, CO, and DO 2 increased 1 minute after brain death ( P < .001), followed by a rapid decrease to baseline within 10 minutes ( P < .001). SVR and EO 2 decreased after brain death ( P < .01) and remained low. Lactate remained unchanged. mE 1ac decreased after brain death despite a decrease in mEO 2 ( P < .01), and returned to baseline at 90 minutes. Conclusions The initial surge in VO 2 after brain death is offset by the greater increase in DO 2, thus tissue perfusion remains adequate. The lower than baseline VO 2 and SVR at the end of the study period may indicate general metabolic and hemodynamic compromise. The information regarding the profound metabolic alterations imposed by brain death may have implications for management of brain death donors.

Vasopressin in vasodilatory shock: hemodynamic stabilization at the cost of the liver and the kidney?

Infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac index and systemic oxygen transport. Whether or not such a vasoconstriction impedes regional blood flow and thus visceral organ function, even when low AVP is used, is still a matter of debate. Krejci and colleagues now report, in this issue of Critical Care, that infusing 'low-dose' AVP during early, short-term, normotensive and normodynamic fecal peritonitis-induced porcine septicemia markedly reduced both renal and portal blood flow, and consequently total hepatic blood flow, whereas hepatic arterial flow was not affected. This macrocirculatory response was concomitant with reduced kidney microcirculatory perfusion, whereas liver micro-circulation remained unchanged. From these findings the authors conclude that the use of AVP to treat hypotension should be cautioned against in patients with septic shock. Undoubtedly, given its powerful vasoconstrictor properties, which are not accompanied by positive inotropic qualities (in contrast with most of the equally potent standard care 'competitors', namely catecholamines), the safety of AVP is still a matter of concern. Nevertheless, the findings reported by Krejci and colleagues need to be discussed in the context of the model design, the timing and dosing of AVP as well as the complex interaction between visceral organ perfusion and function.

Adverse Effects of Dopamine on Systemic Hemodynamic Status and Oxygen Transport in Neonates After the Norwood Procedure

The purpose of this study was to evaluate the effects of dopamine on hemodynamic status and oxygen transport in neonates after the Norwood procedure. Dopamine is widely used to augment cardiac performance and increase oxygen delivery (DO2) in patients after cardiopulmonary bypass (CPB). This might be at the expense of increased myocardial and systemic oxygen consumption (VO2), thus offsetting the improved DO2. This balance is particularly fragile in critically ill neonates. Systemic oxygen consumption was continuously measured with respiratory mass spectrometry in 13 sedated, paralyzed, and mechanically ventilated neonates for 72 h after the Norwood procedure. Arterial, superior vena caval, and pulmonary venous blood gases were measured to calculate pulmonary blood flow (Q(p)) and systemic blood flow (Q(s)), DO2, and oxygen extraction ratio (ERO2). Rate-pressure product was calculated. Dopamine at a dose of 5 microg/kg/min was routinely administered at cessation of CPB and terminated within the first 48 h. Hemodynamic and oxygen transport measures were obtained before and at 100 min after the termination of dopamine. Terminating dopamine was not associated with significant changes in arterial pressure, Q(p), Q(s), or DO2 but was associated with a significant decrease in heart rate (p = 0.003), rate-pressure product (p = 0.03), and VO2 (-20 +/- 11%, p < 0.0001), resulting in a significant decrease in ERO2 (p = 0.01). Dopamine induces a significant increase in VO2 in neonates after the Norwood procedure, and termination is associated with an improved balance of VO2-DO2. These data further emphasize the importance of understanding changes in VO2 as well as DO2 in infants after cardiac surgery.

Indução anestésica após o tratamento do choque hemorrágico: estudo experimental comparando a cetamina e o etomidato

Bleeding causing hemorrhagic shock usually requires surgical treatment under general anesthesia. Anesthetic drugs may further compromise hemodynamics. The objective was to compare the hemodynamic effects of ketamine and etomidate during anesthetic induction in dogs submitted to an experimental model of hemorrhagic shock and resuscitation.Thirty-two mongrel dogs were submitted to a pressure-controlled hemorrhagic shock, resuscitation and anesthetic induction model. After achieving the target pressure of 40 mmHg, they were randomly assigned in two groups according to the resuscitation fluid to be used: NaCl 0.9% (32 mL.kg-1) and NaCl 7.5% (4 mL.kg-1). After volume infusion, these groups were reassigned according to anesthetic drug used: GI) NaCl 0.9% and ketamine; GII) NaCl 7.5% and ketamine; GIII) NaCl 0.9% and etomidate; and GIV) NaCl 7.5% and etomidate. Hemodynamic measurements were obtained at five moments: (M0) baseline; (M1) after bleeding to shock; (M2) after volume expansion; (M3) 5 minutes after anesthetic induction; (M4) 15 minutes after anesthetic induction. Statistical analysis was performed using Student t test and two way ANOVA. Value of p lower than 0.05, was considered significant.After shock, both solutions restored hemodynamics to baseline values. Independently of anesthetic agent or expansion solution used, mean arterial pressure remained unaltered for all groups after induction. Central venous pressure, heart rate, pulmonary capillary wedge pressure and pulmonary vascular resistance index increased significantly after ketamine infusion. Cardiac index, systemic vascular resistance index and oxygen transport variables remained stable in all groups.Etomidate or ketamine were able to maintain hemodynamic stability in dogs undergoing severe hemorrhagic shock treated with NaCl 0.9% or NaCl 7.5%.

Impact of a Beta-Blocking Agent on Exercise Tolerance in Type 2 Diabetic Patients

Patients with type 2 diabetes without cardiovascular complications present exercise intolerance compared to non diabetic subjects. It has been shown that beta-blocking agents reduce exercise tolerance in the latter. However, it is not known if this medication lowers the already reduced exercise tolerance in type 2 diabetic patients. PURPOSE: To evaluate the impact of a beta-blocking agent on the maximal systemic oxygen transport and exercise tolerance in type 2 diabetic patients. METHODS: A total of 6 sedentary men with type 2 diabetes have been recruited to participate in this study. All patients were treated with oral hypoglycaemic agents and/or diet. The maximal exercise tolerance was evaluated for each subject using an incremental protocol performed on an ergocycle. The subjects were evaluated without (WBB group) and following the intake of a beta-blocking agent for 5 consecutive days (BB group). RESULTS: Per study design, each subject were their own control. The BB group had a lower resting heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP) [(54±3 vs 74±13 bpm; 128±8 vs 135±9 mmHg and 79±5 vs 86±9 mmHg respectively (all p < 0.05)]. At maximal exercise, we observed a 13% reduction in absolute peak oxygen uptake (peak VO2) (2.59±0.49 vs 2.99±0.60 L · min-1;p < 0.05) concomitantly to a 3 5 % and 21 % reduction in maximal HR and SBP respectively [111 ± 10 vs 170±15 bpm; 174±21 vs 220±17mmHg (all p < 0.01)]. Of note, the exercise-induced HR and SBP increase were reduced in the BB group [(58±10 vs 96±19 bpm; 53±15 vs 85±15 mmHg (all p < 0.05)]. Interestingly, the beta-blocking agent lowers maximal ventilation in the BB group compared to the WBB group (100±15 vs 130±18 L · min−1; p < 0.001). CONCLUSIONS: These results suggest that the beta-blocking agent alters the exercise tolerance in patients with type 2 diabetes without cardiovascular complications. With beta-blockers, the systemic oxygen transport might limit maximal exercise tolerance in this population. Finally, this beta-blocking agent appears to have a significant impact on the pulmonary ventilation in these patients.

Poor Circulation, Early Brain Injury, and the Potential Role of Red Cell Transfusion in Premature Newborns

To the Editor .— It is the purpose of this letter to (1) define poor circulation in very premature newborns, (2) discuss the concept of stagnant hypoxia and its relation to early brain injury, and (3) discuss the potential role of adult packed red cell transfusion as an acute intervention for poor circulation. There is no simple definition of poor circulation in newborns. It may be pragmatically described by the presence of 1 of the following: low cardiac output (CO) on echocardiography,1 profound hypotension with capillary refill time of ≥3 seconds,2 or hypoxemia resulting in elevated serum lactate.3 There are a number of different forms of hypoxia, namely, stagnant (inadequate flow), anemic (inadequate hemoglobin concentration), hypoxic (inadequate inspired oxygen), and histotoxic hypoxia. Barcroft first described stagnant hypoxia in 19204 with the sentence “[the] blood is normal but is supplied to the tissues in insufficient quantities.” The principal determinants of systemic oxygen transport are CO, hemoglobin concentration, and hemoglobin saturation.5 Final tissue oxygen extraction depends on the oxygen diffusion gradient, the diffusion distance between the capillary and the cell, and cellular uptake mechanisms. The degree of oxygen extraction varies between tissues but never reaches 100%. When oxygen delivery decreases to …