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Healthcare providers are charged with the primary goal of optimizing the oxygenation, ventilation, and the hemodynamic status of the patient during a resuscitation. In most cases, the first definitive intervention is to secure the airway through endotracheal (ET) intubation. The establishment of access to the systemic circulation soon follows. Vascular access in certain patients can be problematic. In such cases, the ability to administer medications endotracheally can be life saving.
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Bernard first reported the ET route of medication administration in 1857, describing the alveolar absorption of curare in dogs. This discovery was followed by the observation that ET instilled salicylates appeared in the urine (Peiper 1884). In 1897, Washitzky studied the ET application of strychnine, atropine, chloral hydrate, and potassium iodide.1
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The first suggestion for using the ET route for the therapy of pulmonary disease was in 1915.2 This idea evolved, culminating in a study in 1937, which recommended the use of inhaled epinephrine in asthmatics.3 The rapidity of pulmonary absorption was eventually utilized for resuscitation purposes 1967. This study demonstrated the equality of the intratracheal, intravenous (IV), and intracardiac routes of epinephrine administration in resuscitating hypoxia-induced cardiorespiratory arrest in dogs. This study began the utilization of the ET route for medication administration in emergent clinical situations.
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Most experiments involving ET medication administration are conducted on subjects with normal cardiovascular function. Thus, there are still many questions remaining about the utility of this route in patients with cardiopulmonary arrest. While the alveolar-capillary membrane is a highly absorptive surface, numerous factors can undermine this potential. These include reduced pulmonary blood flow (less than 30% of normal during CPR), ventilation–perfusion mismatch, and compromised alveolar absorption (e.g., pulmonary edema and pneumonia) in cardiopulmonary arrest.5–7
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During a cardiopulmonary arrest, ET administered medications are absorbed in a protracted manner. This phenomenon, termed the “depot effect”, is observed in laboratory and clinical experiments.5 Studying ET administered lidocaine (2 mg/kg) in nonarrest patients revealed a biphasic pattern of absorption, an initial immediate peak, and a second higher peak approximately 24 minutes later.8 Plasma lidocaine levels were still measurable 120 minutes postinstillation.8 In addition to the altered physiologic conditions of cardiopulmonary arrest as described above, local vasoconstriction induced by epinephrine may contribute to this “depot effect.”9 The relatively low initial plasma medication levels and then the subsequent extended plateau of plasma medication levels are also exhibited by the ET administration of atropine, epinephrine, and vasopressin.5,10
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The American Heart Association (AHA) suggests an ET medication dose of 2 to 2.5 times the recommended IV dose (Table 9-1).11 The optimal dose of ET administered medications is unknown. While there is a consensus that IV doses given endotracheally result in subtherapeutic plasma levels, the equipotent dose ranges from 3 to 10 times the IV dose in the literature.12...