Circulatory shock
-
To evaluate potential clinical applications of conjunctival (PcjO2) and mixed venous (SvO2) oximeters in the care of surgical patients, we compared continuous measurements of PcjO2 and SvO2 to conventional invasive hemodynamic and oxygen transport variables during normoxia, hyperoxia, hypoxia, hemorrhagic shock, and resuscitation in dogs. During the normoxic control periods, PcjO2 averaged 76% of the arterial oxygen tension (PaO2). During hyperoxia and hypoxia, PcjO2 correlated well with PaO2 values (r = 0.88) but not with mixed venous oxygen tension (PvO2), whereas the SvO2 correlated well with PvO2 (r = 0.88) but not with PaO2 values. ⋯ Both oximeters had in vivo stabilization and 90% response times of less than 2 min. We conclude that both oximetry systems are potentially useful in high-risk surgical patients to provide better cardiorespiratory surveillance and to signal the need for more intensive assessment of hemodynamic stability. This approach may lead to reduced costs from unnecessary invasive procedures as well as reduced morbidity secondary to earlier warning of cardiorespiratory compromise.
-
The hemodynamic and ultrastructural effects of lidocaine HCl pretreatment were assessed on anesthetized rats subjected to acute hemorrhagic shock. After 40 minutes of acute hemorrhagic shock (mean arterial pressure = 40 mmHg), significantly less fluid infusion was needed to return mean arterial pressure to 120 mmHg in lidocaine HCl treated animals as compared to the hemorrhagic shock-untreated group (p less than 0.05). Heart rate was significantly lower in lidocaine treated animals in the immediate post-shock period (p less than 0.05). ⋯ However, in the hemorrhagic shock-untreated group all arterial pressures were still significantly lower than their baseline values (p less than 0.05). Ultrastructural myocardial ischemic changes appeared to be less severe in the lidocaine HCl treated animals. Lidocaine HCl pretreatment improved the response to hemorrhagic shock and reinfusion in this model of hemorrhagic shock.
-
Glucose-insulin-potassium infused (GIK) during endotoxin shock causes increased cardiac output (CO) accompanied by decreased systemic vascular resistance. We have studied the effects of GIK on the distribution of cardiac output with radioactive microspheres to see if this decrease in resistance is equally distributed over all organs. GIK resulted in increased CO and increased flow to heart, splanchnic bed, kidneys, adrenals, and skeletal muscle, but fractional flow to these organs did not change. ⋯ Myocardial and splanchnic oxygen consumption did not change significantly. Oxygen extraction also diminished in these areas after GIK. GIK did not influence serum lactate: In both groups lactate increased significantly.