Understand the therapeutic goal for treating hypertension
HTN can be treated by:
Know the basic mechanisms of action for each class of drugs and relate the action to the cardiovascular effects (particularly on blood volume, vascular tone and cardiac function).
Another view: b -blockers in the b 1 block will CO which will ¯ BP, in the kidneys b 1 block will renin release which will AII which will TPR which will ¯ BP and AII also will stimulation of aldosterone and ADH which will Na+ and H2O retention which will Blood volume which will CO. a 1 in the VSM block will cause vasodilation thus a in TPR. When there is an in SNS stimulation, both a 1 and b 1 are mediated by a 1 stimulation neurally in the carotid sinus (baroreceptors) to the medulla. b -blockers will block the b 1 response but not the a 1 response so an in SNS stim will cause an in TPR only without the concurrent in HR and contractility
3 types of b -blockers: nonselective – which doesn’t discriminate btw different subtypes of b -blockers. Propranolol is the prototype. It blocks b 1 and b 2 so you would see a in CO and blood volume and possible bronchial vasoconstriction. These drugs are contraindicated in pts with asthma for that reason. They are also contraindicated in pts with Type I DM or who are susceptible to hypoglycemia since there are b 2 receptors in the liver which are stimulated by hypoglycemia and if blocked will not then mediate the glycogenolysis necessary to bring up the serum glucose level to normal. Selective b 1 Blocker such as atenolol block b 1 only and thus only affect the b 1 receptors in the © and kidneys and don’t affect the b 2 receptors in the lungs or liver. Partial agonists like pindolol have ISA or intrinsic sympathomimetic activity which means they still will have some sympathomimetic activity of in HR and contractility and an in TPR, although because they are only a partial agonist will not have as great of an effect than the intrinsic agonist of NE or epi. The partial agonist will compete for the sites and can block the response some but these are not recommended or highly utilized drugs. Full Agonists like labetolol will block a 1 , b 1, and b 2 which will then block all the hemodynamic effects.
Know the clinical problems associated with each class of antihypertensive drug (especially as they relate to the mechanisms of action).
1. Diuretic – Loop = hypokalemia, electrolyte imbalance. Loop – block the reabsorption of salts so stimulate the loss of calcium by stimulating secretion. Another problem is that the kidneys now sense the high Na+ in the collecting tubules so will try to reabsorb some of it which then exchanges K+ for the Na+ so you get hypokalemia. The thiazides also can cause hypokalemia and hyperuricemia. The K+- sparing ones are too ineffective to be used alone. Mannitol can have a rebound effect. Caution should be used with all diuretics not to deplete the blood volume too low and cause hypotension!
2. b -blockers- cause hypotension, may decrease libido and cause impotence drug-induced sexual dysfunction which can pt compliance with taking the meds. Abrupt withdrawal may cause rebound HTN probably as a result of upregulation of b receptors. May also produce bradycardia, CHF, brochospasm.
3. ACE Inhibitors – adverse effects are hypotension in hypovolemic states and hyperkalemia. Angioedema is a rare but potentially life threatening reaction. Because of the risk of angioedema and 1st dose syncope, ACE inhibitors are administered in the MD’s office with close observation. Reversible renal failure can occur in pts with severe renal artery stenosis. ACE inhibitors are fetotoxic and should not be used in pregnant women.
4. Ca+2 channel blockers – have infrequent side effects which include constipation, dizziness, h/a, fatigue by way of a decrease in BP. Verapamil should be avoided in treating pts with CHF due to the negative inotropic effects.
5. Direct a 1 blocker- this will block the typical SNS response from postural changes so postural hypotension is a huge concern since the baroreceptor response is blocked by the a 1 mediated SNS response.
6. a 2 agonist- sedation is a side effect but no effect of respiratory depression, can also block the normal SNS induced tachycardia and TPR from low BP associated with anesthetic use!
Know which class of drugs may have significant interactions with anesthetics
and what are the potential toxicities. For example, know the clinical uses,
mechanisms of action, toxicities and ways of minimizing toxicities of
SNP had the toxicity of cyanide poisoning. It is a 6-coordinate iron salt which when broken down binds to the RBC as cyano-met-Hgb and cyanide in its free form (Cn-) which is toxic. It is metabolized in the liver then excreted in the kidney. Cyanide concentrations may precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis. SNP is used because when it is metabolized you free up a nitric oxide molecule, which is a potent vasodilator. Cn- is released however when the NO is freed. Treatment for cyanide poisoning is the following:
Last updated 04/10/00 12:26 PM
Return To The MNA 2001 Homepage