ABSTRACT
Background:Monitoring of cardiac preload by determination of pulmonary artery occlusion pressure (PAOP) has been traditionally used to guide fluid therapy to optimize cardiac output (CO). Since factors such as intrathoracic pressure and ventricular compliance may modify PAOP, volumetric estimators of preload have been developed. The PiCCO system is able to measure CO and intrathoracic blood volume (ITBV) by transpulmonary thermodilution. Aim: To compare a volumetric (ITBV) versus a pressure (PAOP) determination to accurately estimate cardiac preload in severely ill patients. Patients and Methods: From June 2001 to October 2003, 22 mechanically ventilated patients with hemodynamic instability underwent hemodynamic monitoring with pulmonary artery catheter (PAC) and PiCCO system. ITBV index (ITBVI), PAOP and CI were measured simultaneously by both methods. One hundred thirty eight deltas (D) were obtained from the difference of ITBVI, PAOP, CI-PAC and CI-PiCCO between 6-12 am and 6-12 pm. Linear regression analysis of DITBVI versus Ð CI-PiCCO and Ð PAOP versus DCI-PAC were made. Results: Mean age of patients was 60.8 ± 19.4 years. APACHE II was 23.9 ± 7. Fifteen patients met criteria for acute respiratory distress syndrome (ARDS). Delta ITBVI significantly correlated with DCI-PiCCO (r=0.54; 95% confidence interval = 0.41-0.65; p <0.01). There was no correlation between DPAOP and Ð CI-PAC. Conclusion: ITBVI correlated better with CI than PAOP, and therefore it seems to be a more accurate estimator of preload in unstable, mechanically ventilated patients.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Blood Volume/physiology , Cardiac Output/physiology , Critical Illness , Monitoring, Physiologic/methods , Pulmonary Wedge Pressure/physiology , Hemodynamics/physiology , Prospective Studies , Stroke Volume/physiologySubject(s)
Humans , Female , Pregnancy , Lactation , Pregnancy , Adrenal Cortex Hormones , Analgesics/administration & dosage , Anesthetics, Local/administration & dosage , Anticonvulsants , Antidepressive Agents , Hypnotics and Sedatives/administration & dosage , Narcotics/administration & dosage , Pregnancy ComplicationsABSTRACT
The immune response is partly regulated by the nervous system, that involves endogenous opioids, stimulating or depressing immune responses. Opioids modulate immune response by indirect and direct mechanisms. Indirect modulation occurs when the activation of opioid receptors within the nervous system modifies the activity of neuroendocrine axes or neurotransmission pathways. Direct modulation results from the effects of opioids on immune system cells. This requires the expression of membrane opioid receptors in these cells. Immunomodulating effects of morphine would be a result of the integration of indirect and direct effects. In animal models, morphine transiently depresses cellular and humoral immunity. In humans, morphine has similar effects; however, the real impact of morphine administration on the immune response in clinical situations in not yet known
Subject(s)
Humans , Immune System/drug effects , Narcotics/pharmacology , B-Lymphocytes/drug effects , B-Lymphocytes/immunology , T-Lymphocytes/drug effects , T-Lymphocytes/immunology , Morphine/pharmacology , Adjuvants, Immunologic/pharmacology , Killer Cells, Natural , Killer Cells, Natural/immunology , Narcotics/immunology , Immune ToleranceABSTRACT
General anesthesia is defined by reversible unconsciousness, lack of response to noxious stimuli, and amnesia, induced by chemical agents. Mechanisms underlying the anesthetic effect are not known. The most prevalent belief was that anesthetic drugs acted on the lipid cell membranes, based on the correlation between oil solubility and anesthetic potency. Later, it has been proposed that anesthetic agents act on specific proteins of the cellular membrane of neurons. Voltage-gated ionic channels are inhibited by anesthetic agents, being some subtypes more sensitive. Clinical concentration of anesthetic agents inhibit or stimulate excitatory or inhibitory neurotransmitter receptors, respectively. Specific receptor agonists and antagonists modify this effect. Intercellular channels (gap junctions) are also affected by anesthetic agents through direct interaction with some of their protein subunits. Thus, anesthesia would result from combined effects on specific proteins acting on neural cell excitability as well as transmission and propagation of nerve impulses