Comparative cardiovascular and pulmonary effects of sedatives and anesthetic agents and anesthetic drug selection for the trauma patient

Abstract

Objective: To integrate and compare the effects of tranquilizer/sedatives and anesthetic drugs on various parameters of cardiovascular function in normal dogs and in dogs stressed by hypovolemia, anemia, and endotoxemia, and to discuss the relative merits and appropriate precautions of anesthetic drugs with respect to specific patient physiologic complications. Data sources: Personal data and experiences in conjunction with veterinary and human clinical and research studies. Human and veterinary data synthesis: Drugs that produce calming, sedation, muscle relaxation, analgesia, and loss of consciousness have the potential to produce marked cardiorespiratory effects particularly in hemorrhaged, hypovolemic‐traumatized animals. Acute but key cardiovascular components that are affected by sedative and anesthetic drugs include heart rate and rhythm, venous return (preload), systemic vascular resistance (afterload), and myocardial contractile (inotropic) and relaxation (lusitropic) properties. In addition, all sedative and anesthetic drugs alter or depress normal baroreceptor reflex activity, thereby inhibiting or eliminating the animal's normal physiologic response to decreases in arterial blood pressure and predisposing to tissue hypoperfusion, decreased oxygen delivery, and oxygenation. Oxygen delivery needs to be adequate to meet the metabolic (oxygen) requirements of the patient. Decreases in oxygen delivery to tissues increases oxygen extraction, thereby maintaining tissue oxygenation (supply‐independent oxygen consumption phase) until compensatory processes reach their limit and any further decrease in oxygen delivery causes a decrease in oxygen consumption (supply‐dependent oxygen consumption phase). The critical oxygen delivery that defines the transition between these 2 phases is generally higher in the anesthetized state than in the awake state. The effect of anesthetics on critical oxygen delivery at comparable anesthetic dosages is pentobarbital=ketamine>alfentanil>etomidate=propofol>inhalational anesthetics. Anesthetics generally decrease oxygen consumption from the awake, baseline state; exceptions are ketamine and ether. Ketamine, however, increases oxygen delivery and oxygen extraction. Conclusions: The transition from the awake to the anesthetized state is a huge imposition on the physiology of animals and, therefore, should be accomplished with great care and proper vigilance. Rapid, ‘crash’ induction of anesthesia should be avoided in hypotension‐prone animals and slow, prolonged induction should be avoided in animals with respiratory disorders. It is not recommended to implement an unfamiliar protocol in critical patients, even if it might be pharmacologically preferable. Familiarity with an anesthetic drug is a very important reason for its selection.

Respostas cardiorrespiratória e metabólica do propofol nas formulações em emulsão lipídica ou microemulsão em gatas

“…O posicionamento do sensor pediátrico do BIS foi adaptado da metodologia utilizada por GUERRERO & NUNES (2003) …”

Avaliação metabólica e hemodinâmica de dois protocolos de sedação prolongada em cães

“…A anestesia normalmente diminui a DO 2 (Haskins, 2006), possivelmente pela ação dos fármacos na redução do IC ou, ainda, pela redistribuição de eritrócitos e consequente diminuição da hemoglobina circulante e da CaO 2 (Costa et al, 2013). Porém, Haskins (2006) O pH arterial (7,32±0,06 no GMF e 7,31±0,03 no GCM) e o venoso misto (7,29±0,07 no GMF e 7,26±0,06 no GCM) estavam levemente abaixo dos valores de referência no momento basal (Ha et al, 2013), devido aos maiores valores da PaCO 2 , de 47,9±6,6 no GMF e de 49,6±4,9mm/Hg no GCM nesse momento, possivelmente pela respiração espontânea sob anestesia geral inalatória, a qual pode promover depressão respiratória dose-dependente (Galloway et al, 2004). Com o início da VM, os valores de pH e de PaCO 2 permaneceram dentro da faixa aceitável para animais anestesiados (pH 7,35-7,45mm/Hg e PaCO2 35-45mm/Hg), não havendo diferença entre grupos em nenhum momento do estudo.…”

“…A PaO 2 permaneceu entre 160 e 200mm/Hg, valores esperados para a FiO 2 padronizada em 40%, sem diferenças entre momentos ou entre grupos. A PvmO 2 diminui 20% no GMF e 25% no GCM, levando a diminuição da SvmO 2 em 14% no GCM e em 15% no GCM, em relação ao basal (79,6±2,6% no GMF e 81,2±2,7% no GCM) devido ao aumento da TEO 2 , que ocorreu em ambos os grupos (Haskins, 2006). Taxas de SvmO 2 acima de 74% têm sido associadas com melhor prognóstico em pacientes críticos (Conti-patara et al, 2012), porém a diminuição da taxa metabólica e de VO 2 promoveu adequação da necessidade fisiológica, não provocando hipoxemia.…”

Validation of acute traumatic coagulopathy in an ovine model of trauma and haemorrhage

“…However the use of animals for trauma research also has limitations. The ethical necessities of sedation and anesthesia alter the compensatory physiologic responses to injury and have an unknown effect on the overall response observed (210,211). Animals are also genetically distinct from humans and demonstrate differences in coagulation assay parameters, coagulation factor concentrations and platelet function that may alter susceptibility to ATC (58-60).…”

“…The lack of catecholamine release by the trauma animals in this thesis suggests that the ethical necessities of sedation and anaesthesia may have significantly altered the compensatory physiological responses to injury (211), impacting on the overall response that was observed. In contrast to human trauma patients who simultaneously experience tissue injury and uncontrolled haemorrhage, this thesis applied standardised insults in a staggered fashion to control the degree of trauma and haemorrhage experienced by the animals.…”