ANNEMI BESTBIER
BLOG #8
3 Apr 2021, 09:50
- Compile a table, listing the major effects on every system (cardiovascular, CNS, renal, hepatic and uterus) for all the inhalation anaesthetics. This table is important when it comes to the selection of drugs in certain individuals
|
INHALATION DRUG |
CV EFFECT |
CNS EFFECT Decreases metabolic activity of the brain |
RESPIRATORY EFFECT Bronchodilating properties |
RENAL EFFECT |
HEPATIC EFFECT |
UTERUS EFFECT |
|
Nitrous oxide |
Depresses myocardial cardiac function in [ ] dependent manner |
Weak anesthetic Potent analgesic Amnesia |
Pure N2O-hypoxia Use with O2 or air Nonpungent |
Alters tubular function & increases urinary output |
Not metabolised by human tissues |
Little effect |
|
Desflurane |
Less cardiac contractility depression than halothane and enflurane. Vasodilation with minimal effect on cardiac output. Increases HR |
Faster induction and recovery than isoflurane. Increased cerebral blood flow and intracranial pressure |
Strong smell, irritates airways. If used as induction drug it causes cough, shortness of breath and laryngospasm |
Decrease GF and urine flow |
[ ] dependent decrease in portal BF that parallels with decline in CO |
Uterine muscle relaxant. |
|
Sevoflurane |
Vasodilation with minimal effect on cardiac output |
Increased cerebral blood flow and intracranial pressure |
Less irritating on airways than desflurane. Bronchodilating |
Decrease renal blood flow and GF rate which decreases urine production |
[ ] dependent decrease in portal BF that parallels with decline in CO. Undergoes metabolism, chemically unstable |
Uterine muscle relaxant |
|
Isoflurane |
Vasodilation with minimal effect on cardiac output. Increases HR |
Faster induction and recovery than halothane |
Potent depressant effect strengthened because of potent skeletal muscle relaxing effect |
Decrease GF and urine flow |
[ ] dependent decrease in portal BF that parallels with decline in CO |
Uterine muscle relaxant |
|
Enflurane |
Depress normal cardiac contractility |
Fast, smooth induction can sometimes cause convulsions. NOT suitable for epileptics |
More depressant than Halothane |
Decrease GF and urine flow |
[ ] dependent decrease in portal BF that parallels with decline in CO |
Uterine muscle relaxant |
|
Halothane |
Depress normal cardiac contractility. Decreases BP, sensitized myocardium to catecholamines |
Medium rate of onset and recovery, very soluble. Stadium ii absent |
Non pungent. Bronchodilating No saliva, bronchial secretions or cough |
Decrease GF and urine flow |
Hepatotoxic (rare, unpredictable) |
Decrease muscle contractions- external twisting of baby |
Name the major acute toxic effects of the inhalation drugs
extensions of effects on brain, heart/vasculature and lungs. Drug interactions are additive with other CNS depressants with agents such as opioids and sedative hypnotics.
nephrotoxicity- metabolism of enflurane and sevoflurane
hematotoxicity- prolonged exposure to nitrous oxide decreases methionine synthase activity that could lead to megaloblastic anemia. Al inhaled anesthetics can produce carbon monoxide that in turn reduces oxygen delivery.
malignant hyperthermia- heritable genetic disorder of skeletal muscle that occurs in susceptible individuals exposed to volatile anesthetics. Succinylcholine ( depolarizing muscle relaxant) may also trigger this.
hepatotoxicity (halothane hepatitis)-hepatic dysfunction most likely cause by hypovolemic shock, infection conferred by blood transfusion or other surgical stresses rather than volatile anesthetic toxicity. Small subset exposed to halothane can develop hepatic failure (rarely) happens. Free radical formation or initiated immune response is believed to cause hepatocellular damage.
Katzung, B.G., 2018. Basic & Clinical Pharmacology. 14th ed. United States of America: McGraw-Hill Education.
Brand, L. 2021. General Anesthetics. Study Unit 5[PowerPoint Presentation]. Unpublished lecture notes on eFundi, FKLG 312. Potchefstroom, NWU.