What is the major immediate complication of Intubation/commencement of ventilation?



    Intubation and positive pressure ventilation is usually complicated by hypotension, vasodilators are avoided and the patient treated with fluids and vasopressors.

Many of my most unpleasant memories of intensive care feature the aftermath of endotracheal intubation. The patient’s blood pressure inevitably falls, due to loss of compensatory vasoconstriction (in a truly hypovolemic patient) and reduction in cardiac output associated with commencement of mechanical ventilation.

Most critically ill patients are in a state of compensated shock: they are hypovolemic, but vasoconstrict and increase their heart rate to maintain cardiac output. The application of  a vasodilator will reverse this process, and reduce the blood pressure, by reducing peripheral resistance. The second element of blood pressure, the cardiac output (BP = CO x PR) also drops due to an increase in intrathoracic pressure. Normally most of the venous return to the heart occurs during inspiration, due to the negative pressure in the thorax, which sucks fluid into it. When positive pressure is applied to the airway, the reverse occurs and the patients left ventricular filling volume, the preload, reduces, lowering the stroke volume and the cardiac output. The treatment for loss of vascular tone is vasoconstrictors. The treatment for lowered stroke volume is fluid boluses.

Always have an intravenous fluid drip running and be prepared to run in a liter or more of fluid quickly. In addition, have an ampule of phenylephrine (a selective alpha adrenoceptor agonist) at hand to reverse vasodilatory hypotension