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Health care providers are charged with the primary goal of optimizing the oxygenation, ventilation, and 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, and the ability to administer medications endotracheally can be lifesaving.

The ET route of medication administration was first reported in 1857 for the alveolar absorption of curare in dogs.1 This was followed in 1884 by the observation that ET instilled salicylates appeared in the urine.2 The ET application of strychnine, atropine, chloral hydrate, and potassium iodide was studied in 1897.2 The first suggestion to use the ET route for the therapy of pulmonary disease was made in 1915.3 This idea resulted in a study in 1937 that recommended the use of inhaled epinephrine in asthmatics.4 The rapidity of pulmonary absorption was eventually used for resuscitation purposes. In 1967, the equality of the ET, intravenous (IV), and intracardiac routes of epinephrine administration in the resuscitation of hypoxia-induced cardiorespiratory arrest in dogs was demonstrated.5 This study prompted the routine use of the ET route for medication administration in emergent clinical situations.

The ideal drug delivery system to the lungs does not yet exist. It would have the following characteristics. Medications are aerosolized to a fine mist to increase the absorption through the alveoli. Avoid adherence of medication to the ET tube. Delivery to the lungs and not the bronchi, trachea, or ET tube. No risk of splash-back. No need to stop compressions or ventilations of cardiopulmonary resuscitation (CPR). We have achieved some of these characteristics.


Most experiments involving ET medication administration have been conducted on subjects with normal cardiovascular function. There are still many questions remaining about the utility of this route in patients with cardiopulmonary arrest. The alveolar-capillary membrane is a highly absorptive surface. Numerous factors can undermine this potential. These include reduced pulmonary blood flow (e.g., less than 30% of normal during CPR), ventilation-perfusion mismatch, and compromised alveolar absorption (e.g., from pulmonary edema) in cardiopulmonary arrest.6-8

ET-administered medications are absorbed in a protracted manner during a cardiopulmonary arrest. This is termed the “depot effect” and is observed in laboratory and clinical experiments.6 A study of 2 mg/kg ET lidocaine in nonarrest patients revealed a biphasic pattern of absorption, with an initial immediate peak and a second higher peak approximately 24 minutes later.9 Plasma lidocaine levels were still measurable 120 minutes after instillation.9 The relatively low initial and subsequent extended plateau of plasma medication levels is also exhibited by the ET administration of atropine, epinephrine, and vasopressin.6,10 Local vasoconstriction induced by epinephrine may further contribute to this “depot effect.”11

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