Sequential cardiopulmonary variables of infants and children in septic shock

Sequential cardiopulmonary variables were analyzed in 32 infants and children with septic shock. Variables were staged by a system based on therapeutic efforts to control blood pressure. There were 14 survivors and 18 nonsurvivors. Systemic circulation variables (MAP, cardiac index [CI], systemic vascular resistance index [SVRI], wedge pressure [WP], left cardiac work index [LCWI]) and pulmonary circulation variables (mean pulmonary artery pressure [MPAP], pulmonary vascular resistance index [PVRI], CVP, right cardiac work index [RCWI]) were similar in survivors and nonsurvivors. Pulmonary variables (intrapulmonary shunt [Qsp/Qt], fraction of inspired oxygen [FIO2], Pao2, PaCO2) revealed significantly more dysfunction in nonsurvivors than survivors during the postresuscitation (PR) and middle (M) shock stages. Even though oxygen delivery was equivalent in survivors and nonsurvivors, nonsurvivors demonstrated decreased oxygen utilization variables (oxygen consumption [Vo2], arteriovenous oxygen content difference [C(a-v)O2], O2 extraction index, core temperature) during the resuscitation (RS) and PR stages.     

静脉注射乌拉地尔对扩张型心肌病心衰患者急性血液动力学效应

目的　探讨乌拉地尔对扩张型心肌病心力衰竭患者急性血液动力学效应。方法　扩张型心肌病心力衰竭患者 15例 ,静脉注射乌拉地尔 2 5mg ,应用Swan Ganz漂浮导管测量用药前、用药 10、3 0、60、90min右心房压 (RAP)、肺动脉压(PAP)及肺毛细血管楔压 (PWP) ,采用热稀释法同步测量心排血量 (CO ) ,无创袖带法同步测量外周动脉收缩压 (SBP)、舒张压 (DBP)、平均压 (MAP) ,心脏监护系统记录心率 (HR) ,计算心脏指数 (CI)、外周血管阻力指数 (SVRI)、肺血管阻力指数 (PVRI)、左心室每搏作功指数 (LVSWI) ,并进行临床观察。结果　与用药前相比 ,用药 10minDBP、MAP、MPAP、PWP、SVRI、PVRI开始降低 (P <0 .0 5 ) ,CO、CI、LVSWI开始增加 (P <0 .0 1) ;用药 3 0minDBP、MAP、MPAP、PWP、SVRI、PVRI降低最明显 (P <0 .0 5 ) ,CO、CI、LVSWI增加最明显 (P <0 .0 1) ;用药 60minDBP、MAP、MPAP、PWP、SVRI、PVRI开始上升 ,CO、CI、LVSWI开始下降 (P <0 .0 5 ) ;用药 90minDBP、MAP上升至用药前水平 (P >0 .0 5 ) ,MPAP、PWP、SVRI仍低于用药前水平 ,CO、CI、LVSWI下降至用药前水平 ;用药后各时刻HR、SBP、RAP无显著变化。所有病人均无不良反应。结论　乌拉地尔可明显改善扩张型心肌病心力衰竭患者急性血液动力学参数     

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.     

Experience with phenylephrine as a component of the pharmacologic support of septic shock

OBJECTIVE: To evaluate the use of the selective alpha 1-adrenergic receptor agonist phenylephrine in the hemodynamic support of patients with septic shock. DESIGN: Retrospective analysis of clinical use of phenylephrine. SETTING: Surgical ICU in a university hospital. PATIENTS: Thirteen patients with septic shock (diagnosed by defined criteria) requiring pharmacologic support for the treatment of hypotension. INTERVENTIONS AND MAIN RESULTS: All patients underwent invasive hemodynamic monitoring followed by volume resuscitation and inotropic support to reverse flow-dependent oxygen consumption and lactic acidosis. Patients with persistent hypotension (mean arterial pressure [MAP] less than 65 mm Hg) and vasodilation (systemic vascular resistance index [SVRI] less than 1500 dyne.sec/cm5.m2 received phenylephrine at iv infusion rates of 0.5 to 9 micrograms/kg.min to maintain MAP greater than 70 mm Hg. MAP, SVRI, left ventricular stroke work index, and stroke volume index were significantly (p less than .05) increased after phenylephrine administration and at the time of highest oxygen consumption (VO2). Cardiac index was unchanged initially but increased at the time of highest VO2 (p less than .05). Pulmonary artery occlusion pressure and heart rate were unchanged. Average baseline VO2 increased from 145 to 200 mL/min.m2 and oxygen delivery (DO2) increased from 447 to 597 mL/min.m2 during phenylephrine treatment (p less than .05). Blood lactate concentrations decreased and urine output increased significantly (p less than .05), while serum creatinine concentrations remained unchanged during phenylephrine therapy. CONCLUSIONS: Treatment with phenylephrine was associated with beneficial hemodynamic effects when used to maintain perfusion, while increasing DO2 and VO2 in patients with septic shock.     

Cardiovascular adjustments and gas exchange during extreme hemodilution in humans

OBJECTIVE: To examine the cardiovascular adjustments and pattern of gas exchange that occur during hemodilution. DESIGN: Nonrandomized prospective study. SETTING: Operating room in a university hospital. PATIENTS: Seven patients undergoing elective aortocoronary artery bypass surgery. INTERVENTIONS: Before initiating cardiopulmonary bypass, the patients' hematocrit levels were decreased to approximately 15%. This hemodilution was done by removing a sufficient amount of autologous blood from the aortic cannula and replacing it with a sufficient amount of crystalloid solution. After the discontinuation of cardiopulmonary bypass, measurements were made at a hematocrit of approximately 15%. Then, after autologous blood infusion, measurements were made at a hematocrit of 20%, followed by more blood infusion to approximately 25% with repeat measurements. MEASUREMENTS AND MAIN RESULTS: The following measurements were made before hemodilution and then at all three levels of hemodilution: heart rate, mean arterial pressure (MAP), right atrial pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. From these measurements, the following derived variables were calculated: cardiac index, systemic vascular resistance, and pulmonary vascular resistance. From measurements of arterial oxygen content, mixed venous oxygen content, and cardiac output, intrapulmonary shunt (Qsp/Qt), oxygen uptake (VO2), oxygen extraction ratio, and oxygen delivery (DO2) were derived. The MAP was lowest (57 +/- 3 [SD] vs. 92 +/- 3 mm Hg) at the lowest hematocrit. The cardiac index was highest (4.0 +/- 0.3 vs. 2.3 +/- 0.6 L/min.m2) at the lowest hematocrit. DO2 was lowest at the lowest hematocrit but VO2 remained constant at all levels of hematocrit. The oxygen extraction ratio increased as hematocrit decreased. With progressive increases in hematocrit, DO2 increased and Qsp/Qt decreased. CONCLUSIONS: The data suggest that, during hemodilution, tissue autoregulation of VO2 and utilization are not impaired, but gas exchange function (Qsp/Qt) is impaired.     

High-frequency jet ventilation versus intermittent positive-pressure ventilation

Airway pressures and cardiorespiratory variables were compared for conventional ventilation (CV) and high-frequency jet ventilation (HFJV), at a similar fraction of inspired O2 (FIO2), positive end-expiratory pressure (PEEP) and PaCO2 in 11 ICU patients. For CV and HFJV, respectively, peak (PAP) and mean airway pressures (Paw) were 15.4 and 9.1 mm Hg and 4.4 and 5 mm Hg. Cardiac index (CI) was 2.54 and 2.60 L/min X m2, total systemic vascular resistance index (SVRI) 2846 and 2923 dyne X sec/cm5 X m2, PaO2 207 and 149 torr, and Qsp/Qt 7% and 11%. HFJV decreased significantly PAP and was less likely to produce pulmonary barotrauma. Cardiac indices were not different, indicating that this variable may be affected by Paw. HFJV neither increased nor decreased CI at similar PEEP and PaCO2 as compared to CV. The decrease in PaO2 and increase in Qsp/Qt may be due to small inspired gas volumes potentiating microatelectasis. On the basis of this study, we recommend initiating HFJV at FIO2 of 0.9 and PEEP of 5 cm H2O, and monitoring both PAP and Paw.     

Prognostic value of hemodynamic indices in patients with sepsis after fluid resuscitation

BACKGROUNDSepsis usually causes hemodynamic abnormalities. Hemodynamic index is one of the factors to identify the severity of sepsis and an important parameter to guide the procedure of fluid resuscitation. The present study investigated whether the assessment of hemodynamic indices can predict the outcomes of septic patients undergoing resuscitation therapy.AIMTo evaluate the prognostic value of hemodynamic indices in patients with sepsis after fluid resuscitation.METHODSA retrospective study was conducted in 120 patients with sepsis at Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University between October 2016 and October 2019. All patients were treated with sodium chloride combined with dextran glucose injection for fluid resuscitation. Patients’ hemodynamic parameters were monitored, including heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI), mean arterial pressure (MAP), central venous pressure (CVP), and central venous oxygen saturation. The prognostic value of hemodynamic indices was determined based on the prognosis status.RESULTSDuring fluid resuscitation, 86 patients developed septic shock and 34 did not. Ninety-nine patients survived and 21 patients died at 28 d after the treatment. Heart rate, CI, mean arterial pressure, SVRI, and CVP were higher in patients with septic shock and patients who died from septic shock than in non-shock patients and patients who survived, and central venous oxygen saturation was lower in patients with shock and patients who died than in non-shock patients and the survivors (P < 0.05). When prognosis was considered as a dependent variable and hemodynamic parameters was considered as independent variables, the results of a logistic regression analysis showed that CI, SVRI, and CVP were independent risk factors for septic shock, and CI was an independent risk factor for 28-d mortality (P < 0.05).CONCLUSIONHemodynamic indices can be used to evaluate the prognosis of septic patients after fluid resuscitation.     

连续性血液净化对感染性休克患者血流动力学及氧合指数的影响

目的观察连续性血液净化(CBP)对感染性休克患者血流动力学及氧合指数的影响。方法我科确诊的25例感染性休克患者行CBP治疗及脉搏波形心排量监测(PICCO)72小时,治疗前和治疗后1、2、6、12、24、48、72小时分别测量持续心排量指数(CCI),外周血管阻力指数(SVRI)等血流动力学参数,同时检测动脉血气分析计算氧合指数,记录心率(HR)、有创平均动脉压(MAP)及去甲肾上腺素(NA)剂量的变化。结果治疗前、后血流动力学指标MAP、CCI、SVRI及氧合指数(OI,PaO2/FiO2)均有明显的改善(P0.05),在48及72小时改善尤为明显(P0.01),同时伴随去甲肾上腺素剂量的下降。结论 CBP可改善感染性休克患者血流动力学参数及氧合指数。     

终末期肝衰竭患者肝脏移植术后血流动力学变化

目的 :观察终末期肝衰竭患者肝脏移植术后的血流动力学变化。方法 :5例终末期肝衰竭患者行肝脏移植手术 ,监测其手术后 3日内中心静脉压 (CVP)、肺动脉压 (PAP)、肺小动脉楔压 (PAWP)、心排血量 (CO)和平均动脉压 (MAP)等参数的变化。结果 :患者术后进入 ICU当时的 MAP、肺毛细血管楔压 (PCWP)和 CVP均明显低于正常参考值 ,心率 (HR)显著增快 ;术后 3日内经过积极扩容 ,MAP、PCWP和 CVP显著升高(P均 <0 .0 1)。入 ICU后 8小时内的心脏指数 (CI)轻度降低 ,但与术后 2 4、4 8小时的 CI值比较均无显著性差异 (P均 >0 .0 5 )。入室后 8小时内的外周血管阻力指数 (SVRI)、肺血管阻力指数 (PVRI)轻度降低 ;术后 3日内上述指标逐渐恢复正常。结论 :终末期肝衰竭患者肝移植术后血流动力学不稳定 ,出现明显的血容量不足表现 ,如不及时纠正可能导致脏器灌注不足 ,乃至器官功能衰竭 ,因此 ,密切监测其血流动力学的变化 ,估计其血容量不足状态并予充分纠正 ,是肝移植患者安度围手术期的关键     

L-arginine and endothelin receptor antagonist bosentan counteract hemodynamic effects of modified hemoglobin

Pyridoxalated hemoglobin polyoxyethylene conjugate (PHP), a nitric oxide scavenger, causes systemic and pulmonary vasoconstriction in normal and septic sheep. We studied the effect of L-arginine and the endothelin-1 (ET-1) antagonist bosentan on the PHP response to determine whether the PHP-induced vasoconstriction resulted predominantly from the action of ET-1 or solely from removal of NO. After 24 h of carrier solution (nonseptic sheep), sheep received PHP (20 mg/kg/h; n = 5), PHP plus L-arginine (at 28 h, 100 mg/kg bolus and 500 mg/kg for 1 h) plus bosentan (at 32 h, 10 mg/kg; n = 6), and only L-arginine and bosentan (n = 5). These protocols were repeated after 24 h of Pseudomonas aeruginosa (S, 6x10(6) colony-forming units/kg/h). PHP induced vasoconstriction in septic and nonseptic sheep for the duration of its infusion. In nonseptic sheep, neither L-arginine nor bosentan significantly lowered systemic (SVRI) and pulmonary (PVRI) vascular resistance and did not antagonize the PHP-induced vasoconstriction. During sepsis, SVRI fell and cardiac index (CI) rose. L-arginine and bosentan further decreased SVRI (L-arginine: 34+/-2%*, p<.05; bosentan: 35+/-5%*, p<.05) and PVRI (L-arginine: 28+/-2%*, p<.05; bosentan: 33+/-7%*, p<.05) and increased CI (L-arginine: 29+/-4%*, p<.05; bosentan: 11+/-5%, NS). Both agents antagonized the PHP-induced vasoconstriction lowering SVRI (L-arginine: 29+/-3%*, p<.05; bosentan: 26+/-5%*, p<.05) and PVRI (L-arginine: 27+/-4%*, p<.05; bosentan: 32+/-4%*, p<.05) to levels before PHP administration. Plasma ET-1 levels increased during sepsis (from 9.8+/-.2 to 15.6+/-.7* pg/mL, p<.05) and fell during PHP infusion (to 9.7+/-1.6* pg/mL, p<.05). In nonseptic sheep, ET-1 levels decreased during PHP (from 8.5+/-.6 pg/mL to 5.9+/-.6*, p<.05). Bosentan increased ET-1 levels 2.7 times higher in septic than in nonseptic sheep. We conclude that during sepsis, the NO scavenger PHP unmasks an underlying ET-1 mediated vasoconstriction, and its effect is antagonized by L-arginine and bosentan.     

Respiratory index/pulmonary shunt relationship: quantification of severity and prognosis in the post-traumatic adult respiratory distress syndrome

The relationship between the respiratory index (RI = alveolar-arterial oxygen gradient [P(A-a)O2] normalized by PaO2) and the pulmonary shunt (Qsp/Qt) has been examined in 929 studies from 240 critically ill post-traumatic patients. Of these, 88 patients (443 studies) were individuals who developed post-traumatic adult respiratory distress syndrome (ARDS) and 152 were patients (486 studies) who did not develop ARDS. This study demonstrates that the RI to Qsp/Qt [RI/(Qsp/Qt)] relationship was significantly (p less than .0001) increased in patients who developed fatal ARDS compared with those who did not develop ARDS, or with those whose ARDS resolved. Because of the increased oxygen consumption (VO2) in ARDS patients in association with their severe limitations in gas exchange (RI) and increased Qsp/Qt, surviving ARDS patients had a significant increase in the cardiac index which resulted in a higher oxygen delivery to VO2 ratio. ARDS patients showed significant (p less than .0001) evidence of increased pulmonary vascular tone, correlated with the increase in the RI/(Qsp/Qt) relationship. In addition, those patients with high RI/(Qsp/Qt) also had increased right ventricular (RVSW) to left ventricular work (LVSW) ratios which were shown to be a direct function of the rise in RI. This increase in both RVSW/LVSW and RI/(Qsp/Qt) ratios was significantly (p less than .0001) correlated with an increased mortality. Thus, the RI/(Qsp/Qt) relationship, which can be obtained from arterial and mixed venous blood gases and saturations only, can be used to predict the severity of the ARDS process as well as important pulmonary vascular and right ventricular overload consequences.     

Shock index: a re-evaluation in acute circulatory failure.

STUDY OBJECTIVE: To evaluate the relationship between the shock index SI (ratio of heart rate to systolic arterial pressure) and cardiac function and oxygen transport in an experimental model of hemorrhage and clinical septic shock. METHODS AND RESULTS: This study was conducted in a hypovolemic circulatory failure model; 40% hemorrhage in the anesthetized pig and normovolemic hyperdynamic septic patients in the intensive care unit (ICU). Hemodynamic and oxygen transport variables were measured and their relationships to SI was examined. SI was inversely related to blood loss, cardiac index (CI), stroke volume (SV), mean arterial pressure (MAP) and left ventricular stroke work (LVSW) (r = -0.73, -0.75, -0.89 and -0.75, respectively P less than 0.01) following hemorrhage in the anesthetized pig. Oxygen transport variables, i.e. oxygen delivery (DO2) and mixed venous oxygen saturation (SvO2P) (r = -0.68 and -0.74, respectively, P less than 0.01) were also inversely related to the SI. Oxygen consumption (VO2) increased initially with increasing SI and fell when SI was greater than 3.0. In clinical septic shock and following blood volume expansion, the SI was not correlated to CI, SVI, MAP or systemic vascular resistance (SVR) (r = -0.01, -0.47, -0.34 and -0.14, respectively, P-value NS) but was inversely related to LVSWI (r = -0.68, P less than 0.01). There were no relationships between the SI and oxygen transport variables (DO2, SvO2) (r = -0.02 and -0.17, P-value NS) in septic shock. CONCLUSION: SI provides a non-invasive means to monitor deterioration or recovery of LVSW during acute hypovolemic and normovolemic circulatory failure and its therapy. SI may be of limited value in the assessment of systemic oxygen transport and response to therapy in clinical shock.     

休克患者血浆肾上腺髓质素与血管阻力变化的关系

目的：观察休克患者血浆肾上腺髓质素（ＡＤＭ）与血管阻力变化,探讨其在休克病理生理过程中的作用。方法：应用放射免疫方法检测４６ 例休克患者血浆ＡＤＭ 浓度,无创胸导生物电阻抗方法测定平均动脉压（ＭＢＰ）、全身血管阻力（ＳＶＲＩ）和心排指数（ＣＩ）。结果：休克组治疗前血浆ＡＤＭ 浓度明显高于正常对照组（Ｐ＜０．０１）;感染性休克组高于非感染性休克组（Ｐ＜ ０．０５）;死亡组高于存活组（Ｐ＜ ０．０５）;感染性休克组ＳＶＲＩ较其他组明显降低,而ＣＩ较正常组略高,其他休克组则明显降低（Ｐ＜ ０．０５）。结论：ＡＤＭ 与血管阻力变化相关,并参与了休克的病理生理过程。     

Cardiorespiratory responses to fluid administration in peritonitis

Intravascular volume expansion was studied in 59 critically ill patients with a wide variety of sepsis and in a small group of 12 patients with peritonitis; either 500 ml of 5% albumin solution or 2 units of packed red blood cells were given over a 60-min period. During the 2-h period after volume loading, significant increases in mean arterial pressure (MAP), pulmonary capillary wedge pressure (WP), central venous pressure (CVP), and oxygen consumption (VO2) were observed. One hour after fluid administration MAP had risen from 72 +/- 16 (SD) at baseline to 78 +/- 17 mm Hg (p less than .01), WP from 9 +/- 5 to 16 +/- 7 mm Hg (p less than .05), CVP from 7 +/- 4 to 9 +/- 4 mm Hg (p less than .05) and VO2 from 132 +/- 19 to 148 +/- 31 ml/min X m2 (p less than .01). Improvement in VO2 after volume loading is consistent with the concept that circulatory problems in sepsis result in less VO2 than is needed and that intravascular volume expansion in normovolemic septic patients may improve peripheral perfusion as measured by oxygen uptake.     

N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin

Inhibitors of nitric oxide synthase (NOS) have been reported to increase mean arterial pressure in animal models of sepsis and recently have been given to patients in septic shock. However, controlled studies to determine the effects of these agents on cardiovascular function and survival in awake animal models of sepsis have not been reported. To examine the therapeutic potential of NOS inhibition in septic shock, we challenged canines with endotoxin (2 or 4 mg/kg i.v.) and treated them with either normal saline or N omega-amino-L-arginine (10 or 1 mg/kg/h), the most specific inhibitor available for the isoform of NOS implicated in septic shock. Endotoxemic animals treated with N omega-amino-L-arginine (n = 11) had higher systemic and pulmonary vascular resistance indices (SVRI and PVRI, p less than or equal to 0.033) and decreased heart rates (p = 0.009), cardiac indices (CI, p = 0.01), oxygen delivery indices (p = 0.027), and oxygen consumption indices (p = 0.046) compared with controls (n = 6). Moreover, N omega-amino-L-arginine increased mortality rates after endotoxin challenge (10 of 11 vs. 1 of 6 controls, p = 0.005). Administration of L-arginine did not improve survival or alter the cardiopulmonary effects of N omega-amino-L-arginine, which suggests that inhibition of NOS may not have been competitive. In normal animals, N omega-amino-L-arginine alone (n = 3) increased SVRI (p = 0.0008) and mean arterial pressure (p = 0.016), and decreased CI (p = 0.01) compared with saline-treated controls (n = 3), but, at the high dose, also produced neuromuscular rigidity and seizure-like activity that was not apparent in the endotoxemic model. Thus, the mortality rate from endotoxemia increased either because of NOS inhibition per se or because of properties unique to N omega-amino-L-arginine, or both.     

Unreliability of oxygen tension-based indices in reflecting intrapulmonary shunting in critically ill patients

Measurement of intrapulmonary shunting (Qsp/Qt), a widely used method for monitoring disturbances of pulmonary oxygen transfer in critically ill patients, involves calculation of arterial and mixed venous oxygen contents. In circumstances where mixed venous blood samples are not readily available, oxygen tension-based indices such as the alveolar to arterial oxygen tension differences (P[A-a]O2), arterial oxygen tension to alveolar oxygen tension ratio (PaO2/PAO2), PaO2 to FIO2 ratio (PaO2/FIO2) and respiratory index (RI) are widely utilized to reflect Qsp/Qt. Oxygen content-based indices such as the estimated shunt are not as widely utilized as the oxygen tension indices. In 75 critically ill patients in whom a pulmonary artery catheter was being utilized to augment clinical care, comparisons were made between Qsp/Qt and P(A-a)O2, PaO2/PAO2, PaO2/FIO2, RI, and estimated shunt to determine which index best reflected Qsp/Qt. Correlations between Qsp/Qt and estimated shunt were good (r = .94) and poor for the P(A-a)O2 (r = .62), PaO2/PAO2 (r = .72), PaO2/FIO2 (r = .71), and RI (r = .74). We conclude that there are no real substitutes for venous oxygen contents in critically ill patients. When pulmonary artery blood is not available for analysis, oxygen tension-based indices are unreliable reflectors of Qsp/Qt while the estimated shunt, an oxygen content-based index, provides a more reliable reflection of Qsp/Qt.     

Transcutaneous and liver surface PO2 during hemorrhagic hypotension and treatment with phenylephrine

Transcutaneous PO2 (PtcO2) and liver surface PO2 (PIO2) were measured in six mongrel dogs during hemorrhagic shock, normotensive shock, and volume resuscitation. Normotension was produced during extreme hypovolemia by an infusion of phenylephrine. PtcO2 and PlO2 were compared to each other and to hemodynamic and oxygen transport variables. PtcO2 and PlO2 correlated well with cardiac index (CI) r = .71 and .86, respectively; n = 60) and with each other (r = .79; n = 60). Heart rate, mean arterial pressure (MAP), and PaO2) correlated less with PtcO2 or PlO2. During the normotensive shock period, PtcO2, PIO2, CI, oxygen delivery (DO2), and oxygen consumption (VO2) were all severely decreased, while PaO2 and MAP were normal and lactic acid concentrations were elevated. It was concluded that PtcO2 follows changes in PlO2 during hypotensive and normotensive low cardiac output shock in mongrel dogs. Low PtcO2 values are associated with low values of PlO2, DO2, VO2, and rising lactic acid concentrations in dogs. These animal data imply that low PtcO2 values encountered in clinical monitoring during anesthesia and surgery may correspond to decreased blood volume, blood flow, and PlO2.     

Reduced venous admixture in hemorrhagic hypovolemia: maintenance of arterial oxygenation by selective pulmonary vascular collapse

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p less than .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p less than .05) and an increase in mean VD/VT from 0.39 to 0.54 (p less than .05). Arterial Hgb saturation (Sao2) increased from 88 +/- 7% to 90 +/- 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p less than .001). VD/VT had an inverse correlation with cardiac output (r = -.90), MAP (r = -.82), Qsp/Qt (r = -.83), MPAP (r = -.77), and Svo2 (r = -.92, p less than .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios.     

Oxygen tensions and oxyhemoglobin saturations in the assessment of pulmonary gas exchange

We studied the theoretical basis for continuous monitoring of pulmonary gas exchange using arterial and mixed venous oximetry by examining the mathematical relationships between the calculated venous admixture (Qsp/Qt) and the ventilation-perfusion index, which is derived from oxyhemoglobin saturations. We compared this relationship with that between Qsp/Qt and its commonly used estimates: inspired oxygen concentration to arterial blood oxygen tension ratio, arterial to alveolar oxygen tension ratio, and alveolar-arterial oxygen tension difference. The relationship between Qsp/Qt and the oxygen tension-based indices is nonlinear and substantially influenced by changes in inspired oxygen concentration and arteriovenous oxygen content difference. Therefore, it is inaccurate within the clinically acceptable range of arterial blood oxygenation. In contrast, calculation of ventilation-perfusion index from arterial and mixed venous blood oxyhemoglobin saturations provides a linear estimate of Qsp/Qt that is minimally affected by alterations in inspired oxygen concentration or oxygen uptake and, therefore, will allow accurate continuous assessment of pulmonary gas exchange.     

Peripheral vascular resistance in septic shock: its relation to outcome

To support the concept that patients who die of septic shock have a persistent defect in peripheral vascular tone irrespective of cardiac index (CI), a retrospective study was undertaken of 42 patients with documented septic shock. From the patient records, the single lowest CI (t=2) measured after initial values (t=1) with concomitantly obtained haemodynamic and metabolic variables was taken. Group 1 consisted of 21 survivors and group 2 of 21 patients, who had died in shock. Initial haemodynamic and metabolic variables were comparable between the groups, reflecting shock with a hyperdynamic circulation and lactic acidemia. At t=2, median CI measured 3.21·min^-1·m^-2 in both groups, but mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) were higher in group 1 than 2 (p<0.0005). Changes in arterial blood lactate levels also differed significantly. The rankcorrelation between CI and SVRI at t=2 was significant in group 1 (r _s=-0.69, p<0.005) but not in group 2 (r _s=-0.34). Our data suggest that when CI decreases in septic shock, patients with a fatal outcome have less capability to augment vascular resistance than survivors. Hence, peripheral vascular failure, even if complicated by inability to maintain an elevated CI, may be a major haemodynamic determinant of mortality in septic shock.