Central Nervous System (CNS)
Induction doses of ketamine are generally considered to increase cerebral blood flow (CBF), cerebral metabolism (CMRO2), and intracranial pressure (ICP); however, there is evidence that ketamine administered to anesthetized and mechanically ventilated patients does not increase ICP and has little impact on cerebral hemodynamics. For example, ketamine, in doses up to 5 mg/kg IV, did not increase ICP in intubated, sedated head-injury patients. On electroencephalogram (EEG) ketamine’s effects are characterized by the abolition of alpha rhythm and the dominance of theta activity.
Despite possessing a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements. Systemic vascular resistance and left ventricular end diastolic pressure are normally unchanged. It is important to recognize that critically ill patients may occasionally respond to ketamine with unexpected decreases in blood pressure and cardiac output. This represents depletion of endogenous catecholamines and exhaustion of sympathetic compensatory mechanisms, unmasking ketamine’s direct negative inotropic effects.
Pulmonary and Airway
Ketamine does not produce any significant depression of ventilation when used alone. In addition, upper airway skeletal muscle tone is maintained airway reflexes remain intact. Ketamine also possesses bronchodilatory activity but has been shown to increases salivary and tracheobronchial mucous gland secretions.
Hepatic and Renal Function
Ketamine does not alter any laboratory test that reflects hepatic or renal function.
J Albanèse, S Arnaud, M Rey, L Thomachot, B Alliez, C Martin Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology: 1997, 87(6);1328-34