Flashcards in General anesthetic Deck (25):
What is the state of "general anesthesia?"
• Loss of consciousness
• Suppression of reflexes
• Skeletal muscle relaxation
What is balanced anesthesia?
There is no single drug that can achieve all the desired goals of anesthesia. In balanced anesthesia there are several drugs used in combination to produce the anesthetic state.
• Gases -N2O
• Volatile halogenated hydrocarbons
**used for maintenance of anesthesia after administration of the IV agent
• Increase perfusion of brain.
• Cause bronchodilation.
• Decrease minute ventilation.
• Potency correlates with liposolubility.
• Rate of onset inversely correlates to blood
• Recovery is due to redistribution from the brain.
MOA of inhaled anesthetics?
Direct interaction with ligand-gated ion channels - positive modulation of GABAa and glycine receptors as well as inhibition of nicotinic receptors.
MAC (minimum alveolar concentration)?
Concentration tat results in immobility in 50% of pts when exposed to a noxious stimulus such as surgical incision. It is expressed as a % of the alveolar gas mixture.
MAC is low for potent anesthetics and large for less potent agents. - the smaller the MAC, the lower the ED50 and the more potent
MAC values are additive -- NO (high - so needs to be combined with other substances), Methoxyflurane (low)
The potency of an anesthetic can be predicted form its liposolubility. This can be predicted by the partition coefficient [oil:gas]. This measures how much the solution likes to go into the oil vs the air. As oil:gas increases, MAC decreases.
Ratio of the concentrations of a compound in one solvent to the concentration in another solvent. This is just comparing the solubility of an anesthetic in oil vs gas.
Potency of an anesthetic increases as its liposolubility increases - MAC decreases, partition coefficient increases.
-high potency, slower onset b/c it is more soluble
Transfer of anesthetic from the alveolar air to the blood and then the brain. Rate depends on...
• Solubility of the anesthetic [can be estimated by partition coefficient of blood:air of anesthetic - the higher the solubility in blood, the more will be dissolved and the less it wants to escape the blood so it reaches the brain less quickly -- in contrast an anesthetic with low blood:gas, the faster the onset of anesthesia -- NO has fast onset (low solubility), Halothane of Methoxyflurane has slow onset (high solubility)]
• Its concentration in the inspired air [up the pt, increase respiration rate, etc] - increase in anesthetic concentration increases the rate of induction
• Pulmonary ventilation rate [up to the surgeon b/c they can ventilate the pt at different speeds] - increase in ventilation rate, increase rate of induction
• Pulmonary blood flow [property of the pt] - depends on cardiac output, if blood flow increases, there is slower rate of induction so you need more anesthetic due to larger volume of blood
• Arteriovenous concentration gradient - difference b/t concentration of anesthetic in arterial and venous blood reflects the solubility of the anesthetic in the tissues - uptake by tissues slows down onset and recovery
Elimination of anesthetic?
Reverse process of uptake - if there is high tissue solubility it will act as depot retaining the anesthesia
Methoxyflurane - give for a long time, there is high solubility in blood/tissue so it remains int he system for a very long time
NO - give for a long time, but not very soluble so it is eliminated in the blood quickly
Anesthetic effects on cardiovascular system?
-Depress normal cardiac contractility
-Decrease mean arterial pressure
-Halothane and enflurance reduce MAP via myocardial depression rather than vascular resistance effect
-Isoflurance, desflurance, sevoflurane reduces MAP by producing vasodilation rather than effecting myocardial output -- better for pts with impaired myocardial function
-N2O lowers blood pressure less than other inhaled anesthetics
-Halothane sensitizes the myocardium to circulating catecholamines which may lead to ventricular arrhythmias -- there is less of an effect on isoflurane, sevoflurane, and desflurane
Anesthetic effect on Respiratory system?
• Volatile anesthetics are bronchodilators.
• Isoflurane and desflurane are pungent: not
suitable in patients with bronchospasm.
• Halothane, sevoflurane and nitrous oxide are nonpungent.
• Volatile anesthetics are respiratory depressants.
• Isoflurane and enflurane are the most depressant.
• N2O is the least depressant.
Anesthetic effect on CNS?
• Inhaled anesthetics increase intracranial pressure.
• Undesirable in patients who already have
increased intracranial pressure because of brain tumor or head injury.
• N2O increases blood flow the least.
• Enflurane at high concentrations may cause tonic clonic movements.
Other effects of anesthetics (other than CV, pulmonary, CNS)?
• N2O exchanges with nitrogen in air-containing
cavities in the body.
• N2O enters the cavity faster than nitrogen
• Therefore, it increases the volume and/or
pressure of the cavity.
• N2O should be avoided in the following clinical
settings: Pneumothorax, Obstructed middle ear, Air embolus, Obstructed loop of bowel, Intraocular air bubble, Pulmonary bulla, Intracranial air
Hepatotoxicity due to anesthetics?
Halothane is a major produces of hepatotoxicity (hepatitis) in some individuals. There is no specific treatment to the hepatitis and a liver transplant may be required.
Nephrotoxicity due to anethestics?
Mainly due to Methoxyflurane - most potent b/c of fluoride released during metabolism
Malignant hyperthermia due to anesthetics?
Fatal autosomal dominant genetic disorder of skeletal muscle triggered by volatile inhaled anesthetics such as halothane or depolarized skeletal muscle relaxants such as succinylcholine. This is a main cause of death due to anesthesia. There is altered control of calcium release from the SR in most cases due to defect in ryanodine receptor gene (RYR1).
The increased calcium concentration causes increased muscle contraction generated heat. There are increased levels of aerobic metabolism producing CO2, and depleting O2 and ATP. A switch then occurs towards anaerobic metabolism producing lactate leading to hyperkalemia and myoglobinuria.
Presents as tachycardia, HTN, severe muscle rigidity, hyperthermia, hyperkalemia, acidosis.
TX - DANTROLENE as it blocks calcium release from SR
What is the treatment of malignant hyperthermia?
Caffeine-halothane muscle contracture test?
Establishes susceptibility to malignant hyperthermia. A muscle sample is removed for the thigh and its response to halothane and caffeine is assessed.
Hematotoxicity due to anesthetics?
• Prolonged exposure to N2O decreases
methionine synthase activity and causes
• Potential occupational hazard for staff
working in poorly ventilated dental
Thiopental and Methohexital?
Ultra-short acting barbiturates used for induction of anesthesia and for short surgical procedures. Their anesthetic effects are terminated by redistribution from the brain to other tissues. Hepatic metabolism is required for elimination from the body.
These medications decrease intracranial pressure, do not produce analgesia, may cause hyperalgesia, as well as laryngospasm, bronchospasm, and chest wall spasms therefore are contraindicated in asthmatic pts.
• Postoperative vomiting is uncommon. Antiemetic.
• Used for induction and maintenance of anesthesia.
• Produces no analgesia.
• Rapidly metabolized in the liver.
• Potent respiratory depressant.
• Reduces intracranial pressure.
• Causes hypotension through decreased PVR.
• Fospropofol: prodrug converted to propofol in vivo.
• Primarily used for anesthetic induction of patients at
risk for hypotension.
• Causes minimal CV and respiratory depression.
• No analgesic effects.
• Reduces intracranial pressure.
• Associated with nausea and vomiting.
• Produces dissociative anesthesia,
characterized by catatonia, amnesia and analgesia, with or without loss of consciousness.
• Mechanism of action may involve blockade of NMDA receptors.
• Only IV anesthetic that possesses both analgesic properties and the ability to produce CV stimulation.
• Increases intracranial pressure.
• Causes sensory and perceptual illusions, and vivid dreams (‘emergence phenomena’).
• Diazepam, midazolam, or propofol reduce the incidence of these phenomena.