Cardiopulmonary effects of fentanyl in conscious dogs and dogs sedated with a continuous rate infusion of medetomidine

Medetomidine is a relatively new sedative analgesic in dogs and cats but some precautions are required when using it. It is a potent alpha 2-adrenoceptor agonist and stimulates receptors centrally to produce dose-dependent sedation and analgesia and receptors centrally and peripherally to cause marked bradycardia and decrease the cardiac output. While hypotension occurs frequently, higher doses of the sedative can raise the blood pressure due to an affect on peripheral receptors. Slowing of the respiratory rate is a frequent effect of medetomidine with some dogs showing signs of cyanosis. Other actions that follow medetomidine use are slowing of gastrointestinal motility, hypothermia, changes to endocrine function and, occasionally, vomiting and muscle twitching. The clinical use of medetomidine in dogs and cats is discussed. Recommended dose rates are presented along with precautions that should be taken when it is used alone for sedation, as an anaesthetic premedicant or in combination with ketamine, propofol or opioids. Hypoxaemia occurs frequently in dogs given medetomidine and propofol. The actions of medetomidine can be rapidly reversed with the specific alpha 2-adrenoceptor antagonist, atipamezole, which is an advantage because undesirable and sedative actions of medetomidine can be terminated.

The alpha 2-adrenergic agonist dexmedetomidine decreases not only heart rate, myocardial contractility, and oxygen demand, but also cardiac output (Q). To investigate whether this reduction in Q could critically impair perfusion of individual organs, we studied the effect of dexmedetomidine on nutrient blood flow to the heart, brain, kidney, spleen, skin, intestine, liver, and arteriovenous anastomoses using the radioactive microsphere technique. Studies were conducted in 14 dogs with an open chest and anesthetized with either chloralose/urethane (CU) or fentanyl/halothane (FH), to create different baseline conditions. Hemodynamic variables, organ blood flow, arterial and mixed venous oxygen, and lactate content were measured before and after administration of 0.1, 1, and 10 micrograms/kg dexmedetomidine intravenously (IV). After 10 micrograms/kg dexmedetomidine Q decreased in both groups by 50%. The decrease in blood flow varied greatly between the organs. While flow through arteriovenous anastomoses and skin decreased by 70% to 90%, renal blood flow decreased by 30%, cerebral blood flow only when baseline blood flow was high (FH dogs), and left ventricular blood flow only in the CU group, where the largest decrease in hemodynamic variables occurred. Oxygen consumption decreased only in CU dogs, but so did arterial lactate levels. These data indicate that dexmedetomidine causes considerable redistribution of Q, predominantly reducing blood flow to less vital organs and shunt flow.