naloxone and Cardiac-Tamponade

Topics: Adult; Anaphylaxis; Cardiac Tamponade; Cardiopulmonary Resuscitation; Emergency Medical Services; Fat Emulsions, Intravenous; Female; Heart Arrest; Humans; Hypothermia; Naloxone; Near Drowning; Percutaneous Coronary Intervention; Pregnancy; Pregnancy Complications, Cardiovascular; Pulmonary Embolism; Water-Electrolyte Imbalance; Wounds and Injuries

Renal sympathetic nerve activity (RSNA) responses to acute cardiac tamponade were studied in conscious rabbits with all reflexes intact (Int) or after either surgical sinoaortic denervation (SAD) or administration of intrapericardial procaine (ip-Pro) or intravenous procaine (iv-Pro). In Int rabbits, the mean arterial pressure (MAP) remained relatively constant until the pericardial volume reached 7. 7 ml, whereas the RSNA increased to 226% [compensated cardiac tamponade (CCT)], then, at a pericardial volume of 9.3 ml, the MAP fell sharply and RSNA decreased to 34% [decompensated cardiac tamponade (DCT)]; 1 min after cessation of pericardial infusion, an intravenous injection of naloxone resulted in increases in both MAP and RSNA. In SAD rabbits, RSNA did not alter throughout CCT and DCT, but increased on injection of naloxone. In ip-Pro rabbits, RSNA increased during CCT but did not decrease during DCT, whereas, in iv-Pro rabbits, the RSNA response was similar to that in Int rabbits. These results indicate that RSNA responses to cardiac tamponade are biphasic, with an increase during CCT and a decrease during DCT. Sinoaortic baroreceptors are involved in mediating the increase in RSNA, whereas cardiac receptors may be involved in mediating the decrease in RSNA. An endogenous opioid may be responsible for the decrease in RSNA seen during DCT.

Topics: Acute Disease; Anesthetics, Local; Animals; Blood Pressure; Cardiac Tamponade; Consciousness; Denervation; Heart; Heart Rate; Kidney; Male; Naloxone; Narcotic Antagonists; Procaine; Rabbits; Reflex; Sympathetic Nervous System

During progressive acute cardiac tamponade (CT) in conscious dogs, cardiac output (CO) falls continuously while arterial blood pressure (BP) is well maintained until an abruptly terminal decline. This response is primarily dependent on alpha-adrenergic mechanisms. During hemorrhagic shock, the opioid receptor blocker naloxone increases CO and BP and improves survival perhaps by reversing an opioid-induced cardiovascular depression. We produced 10 episodes of decompensated CT (DCT; 30% decline in BP) by intrapericardial saline infusion (20 ml/min) in five euvolemic conscious dogs. CT resulted in a decrease in CO and BP from base line (3.79 +/- 0.37 l/min and 89.6 +/- 5.2 mmHg, means +/- SE) to DCT (1.35 +/- 0.15 l/min and 57.5 +/- 3.1 mmHg; P less than 0.05). Naloxone (3 mg/kg iv) given at the onset of DCT resulted in a prompt sustained return of BP to base-line levels (P less than 0.05) with no change in CO. Four more animals were studied before and during naloxone (3 mg/kg iv then 0.3 mg.kg-1.min-1 iv). DCT occurred at a higher intrapericardial pressure (20.1 vs. 18.3 mmHg; P less than 0.025) if CT were induced during naloxone treatment than in its absence. Thus naloxone during DCT promptly reversed hypotension with no change in CO and, if present during induction of CT, naloxone allowed slightly higher levels of intrapericardial pressure to be tolerated. Further studies are needed to determine whether naloxone produced these effects solely by its actions on opioid receptors. This study suggests that the interaction between opioid and adrenergic influences plays a role in causing hypotension during CT.

Topics: Animals; Blood Pressure; Cardiac Tamponade; Dogs; Heart; Hemodynamics; Naloxone