Term
|
Definition
| primary effect on site 1 (decrease sympathetic outflow from vasomotor centers in CNS) |
|
|
Term
|
Definition
| primary effect on site 1 (decrease sympathetic outflow from vasomotor centers in CNS) |
|
|
Term
|
Definition
| Primary mechanism: adrenergic (ß1 and 2) receptor inhibitor. Contributes to effect on site 1 (decrease sympathetic outflow from vasomotor centers in CNS). Contributes to action at ganglion (site 3) |
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Term
|
Definition
| Primary mechanism: depresses pre-synaptic, adrenergic transmission at nerve ending (site 3). Contributes to effect on site 1 (decrease sympathetic outflow from vasomotor centers in CNS) |
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Term
|
Definition
| Primary mechanism on Site two (inhibition of sympathetic outflow from ganglia) |
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Term
|
Definition
| primary: alpha1 and 2 adrenergic inhibitor. Site 4 (adrenergic receptor inhibitor) |
|
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Term
|
Definition
| primary: alpha1 and 2 adrenergic inhibitor. Site 4 (adrenergic receptor inhibitor) |
|
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Term
|
Definition
| primary mechanism: alpha1 adrenergic receptor inhibitor. Site 4 |
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Term
|
Definition
| primary mechanism: beta1 and 2 and alpha1 adrenergic receptor inhibitor (site 4) |
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|
Term
| Direct acting vasodilators: list all |
|
Definition
| Hydralazine, minoxidil, nitroprusside, diazoxide, CCBs |
|
|
Term
| Functional vasodilators: list all |
|
Definition
| ACE-I (captoPRIL, enalaPRIL, lisinoPRIL, xx-PRIL). ARB (loSARTAN, ValSARTAN). Renin inhibitor (aliskirin). D1 receptor agonist (fenolDOPam) |
|
|
Term
| What are the ABCDs of HTN therapy? |
|
Definition
| ACEI, ARB, alpha blockers; Beta blocker, CCB, Diuretic |
|
|
Term
| What is the general flow of HTN perscription? |
|
Definition
| Monotherapy, then add second drug (one of the first two drugs should be diuretic), then increase dose, then modify combination (but keep diuretic), then add additional drug. Remember that the drugs should have different targets and toxicities. |
|
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Term
|
Definition
| choloTHIAZIDE, hydrochloroTHIAZIDE, polyTHIAZIDE, chlorthalidone |
|
|
Term
| What are the non-thiazides of similar action? |
|
Definition
|
|
Term
|
Definition
| SOA = primarily the DISTAL tubule. MOA: reduces NACl (inhibits co-transporter) and therefore REDUCES WATER REABSORPTION |
|
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Term
|
Definition
| A: oral, D: M:requires active secretion into renal tubule via ORGANIC ACID PATHWAY E: kidney |
|
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Term
|
Definition
| Dose related therefore use lowest effective dose. HYPOKALEMIC (ARRHYTHMOGENIC), hypochloremic, ALKALOSIS. hyponatremia, hyperglycemia, hyperuricemia (gout), increased Triglycerides and total cholestereal (LDL) therefore increased CV disease. Chronic use: impotence. |
|
|
Term
|
Definition
| furosemide (lasix), bumetanide (bumex), torsemide (demadex), ethacrynic acid (edecrin) |
|
|
Term
| Loop diuretics: SOA and MOA |
|
Definition
| SOA: THICK ASCENDING LIMB of loop of Henle; MOA: INHIBITION OF K+, NA+ AND Cl- reabsorption (cotransporter). |
|
|
Term
|
Definition
| A: oral, D: M: E: renal excretion. ACTIVE SECRETION VIA ORGANIC ACID PATHWAY into tubule is NECESSARY for therapeutic effects |
|
|
Term
| Compare Loop Diuretics to Thiazides |
|
Definition
| Loop Diuretics are more efficacious and faster acting but have a shorter uration than thiazides. |
|
|
Term
| Loop Diuretics: Side Effects |
|
Definition
| OVERZEALOUS TREATMENT (as in edema): Dehydration, hypotension, marked hypokalemic, hypochloremic, alkalosis |
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|
Term
| Potassium-sparing diruetics: list and general info |
|
Definition
| Spironolactone (Aldolactone), Eplerenone (Inspra), Triampterene (Dyrenium), Amiloride (Midamor). |
|
|
Term
| potassium-sparer: SOA and MOA |
|
Definition
| SOA: late distal tubule and cortical collecting duct. MOA: generally decrease Na reabsorption more specifically: Competitive antagonist of aldosterone (spironolactone, eplerenone), Decrease membrane permeability to sodium (triampterene, amiloride). |
|
|
Term
| Compare Spirolactone to triampterene or amiloride |
|
Definition
| Spirolactone has slower onset (2-3 days) but longer duration of action and produces more diureses than triampterene or amiloride. |
|
|
Term
| Potassium sparer: side effects |
|
Definition
| HYPERKALEMIA. spironolactone gives steroid-like effects (gynecomastia, amenorrhea) that can be minimized by using eplerenone |
|
|
Term
| what are the most frequently used diuretics in chronic HTN? how does dose differ between treating HTN and edema? |
|
Definition
| thiazides. Flat dose reponse curve = dose for HTN <<< dose for edema |
|
|
Term
| If a patient has decreased renal function or resistant "psuedotolerance" due to vasodilators, what is the diuretic class of choice? |
|
Definition
|
|
Term
| How and when are K+ sparers used? |
|
Definition
| Rarely used without another diuretic class. Used to PREVENT HYPOKALEMIA. may also provide SOME ADDITIONAL DIURESIS and MINIMIZES TENDENCY FOR ALKALOSIS. Exception: Spirolactone has been used effecitely as monotherapy. |
|
|
Term
| Describe the general sequence of action of diuretics in MOA |
|
Definition
| first decrease in extracellular fluid causes CO to decrease and TPR to increase (reflex). TPR decreases, CO approaches, but does not reach, pre-treatment levels. This is clled adaptation or reverse autoregulation. Natriuresis is essential for antiHTN effect. |
|
|
Term
| When would you prescribe a diuretic? |
|
Definition
| monotheraphy in uncomplicated HTN, as a second drug to attenuate the "psuedo" tolerance d/t salt and water retention that develops with other HTN drugs. |
|
|
Term
| List the types of agents altering Sympathetic tone |
|
Definition
| alpha receptor antagonists, beta receptor antagonists, competitive alpha and beta antagonists, agents affecting adrenergic nerve endings, agents working through central mechanisms, Alpha 2 agonists |
|
|
Term
| Do alpha receptor antagonists work on alpha 1 or 2? |
|
Definition
|
|
Term
| List the alpha1 receptor antagonists |
|
Definition
| Prazosin (minipres), Terazosin (hytrin), Doxazosin (cardura) |
|
|
Term
| alpha 1 receptor antagonist: MOA |
|
Definition
| MOA: reduces TPR --> increase in sympathetic (HR). Increase venous capacitance,. AFFECTS BOTH ARTERIES AND VEINS. Prazosin = functional vasodilator. TPR remains reduced. HR returns to control. |
|
|
Term
| a1 receptor antagonist: ADME |
|
Definition
| A: rapidly absorped D: M: liver E: ; note: usually takes several weeks to attain maximal decrease in BP |
|
|
Term
| a1 receptor antagonist: Side Effects |
|
Definition
| Salt and water retention (Tx with diuretic); First dose phenomenon (orthostatic hypotension, syncope) with 1st or increased dose. occurs more in patients on diuretics, BB, or volume depleted. Tx: maintenance dose/2, give at bedtime during start or increase of dose. |
|
|
Term
| a1 receptor antagonist: uses |
|
Definition
| monotherapy; +diuretic to minimize psuedotolerance; +diuretic+BB ; (functional vasodilator +diuretic + BB = TPR, NaCl & H20 rentetion and CO are all reduced. |
|
|
Term
| Which Beta blockers are B1 vs B1 and B2 |
|
Definition
| A-M = B1 (cardioselective); N-Z= B1 and 2. They all end in -olol |
|
|
Term
| Intrinsic Sympothomimetic Activity |
|
Definition
| weak, partial agonist activity. Seen in acebutolol and pindolol |
|
|
Term
| What are the long acting BB? |
|
Definition
| atenolol and nadolol. Long activing because they have little to no liver metabolism |
|
|
Term
| What are the sequence of effects on CV by BB |
|
Definition
| 1. decrease HR and contractility --> decreased CO 2. TPR increases 3. TPR returns to pre-treatment or decreases.||| Decrease in Renin Release --> less salt and water retention. |
|
|
Term
|
Definition
| inhibition of renin release. depress CNS outflow (not all the same solubility into CNS). decreased neurotransmitter (NE) release. Adaptive changes to reduction in CO include a decrease in resistance. Reverse autoregulation. |
|
|
Term
|
Definition
| A: oral absorption D: M: first pass liver (except nadolol and atenolol). wide variation = titers necessary to individualize dose! E: |
|
|
Term
|
Definition
| B1: CHF, Bradycardia, AV block, B2: bronchospams, hypoglycemia, aggravates peripheral vascular disease. CNS: depression, nightmares, hallucinations. decreased HDL and increased triglycerides. withdrawal. Sexual dysfunction |
|
|
Term
|
Definition
| monotherapy. +diuretic. +diuretic and vasodilator (propranolol + thiazide + hdyralazine = decreased CO, NaCl & H20 retention & TPR) |
|
|
Term
|
Definition
| competitive alpha1, beta1, beta2 adrenoreceptor. Beta>alpha |
|
|
Term
| Low dose propranolol + low dose prazosin acts as |
|
Definition
| comptetitive antatonist of both alpha and beta receptors. propranolol is (b1>b2); prazosin is alpha1 |
|
|
Term
| what are the CV effects of coptetitive antagonist of alpha and ß receptors? |
|
Definition
| decrease in CO (d/t b1 receptors), TPR (d/t alpha 1 receptors) and therefore BP. |
|
|
Term
| Side effects of both alpha and ß receptor antagonist |
|
Definition
|
|
Term
| How do you prescribe competitive antagonists of both alpha and beta receptors? |
|
Definition
| usually w/ a diuretic but can be monotherapy. |
|
|
Term
| what agent affects adrenergic nerve endings? |
|
Definition
| Resperine: depletes neuronal stores of all catecholamines (NE, EPI, serotonin, DA). both centrally and peripherally. |
|
|
Term
|
Definition
| binds irreversibly to neuronal storage vesicles and prevents accumulation and storage of catecholamines which leads to depletion of neurotransmitter stores. |
|
|
Term
|
Definition
| decreases CO (HR & SV). Decreases TPR. Decreases sympathetic tone to the heart (decreased CO, and arteries (decreases TPR) and veins. orthostatic hypotension |
|
|
Term
|
Definition
| A: D: high lipid solubility = wide distribution includying CNS and long duration M: E: |
|
|
Term
| Side effects of Reserpine |
|
Definition
| Na+and H20 Retention (treat with diuretic). PS predominance results in diarrhea, cramps, increased gastric acid secretion. Sedation and severe DEPRESSION (CNS). orthostatic hypotension. sexual dysfunction. |
|
|
Term
| How should you prescribe reserpine? |
|
Definition
| NOT as monotherapy -- NEED To add a DIURETIC. Reserpine +diuretic +vasodilator = decreased TPR and CO, Decreased H20 and NaclRetention + decreased TPR) |
|
|
Term
| what kind of agents work primarily through central mechanisms? |
|
Definition
|
|
Term
| List the alpha2 receptor agonists |
|
Definition
|
|
Term
|
Definition
| Decreases CO (HR &SV), concomitant with decrease in TRP. Decreases venous return (relaxes capacitance) |
|
|
Term
|
Definition
| "prodrug". Metabolized to alpha methyl NE in CNS. stimulation of alpha2 receptors in CNS leads to a decreased in sympathetic outflow. |
|
|
Term
|
Definition
| A: variable D: CNS storage of active metabolites M: minimal liver but must be activated in CNS E: |
|
|
Term
| Side effects of Methyldopa |
|
Definition
| postive Coomb's test (10-30%). hemolytic anemia (5% of +coombs). dry mouth. sedation. DECREASED MENTAL ACUITY |
|
|
Term
| Prescription pattern of methyldopa |
|
Definition
| REQUIRES DIURETIC or combination with DIURETIC+VASODILATOR. (decrease CO, TPR, Nacl+H2O retention, tpr). Drug of choice for persistent HTN during pregnancy. |
|
|
Term
| what is the Drug of choice in persistent HTN that develops during pregnancy. what are alternatives? |
|
Definition
| Methyldopa. Alternatives: hydralazine and labetalol. |
|
|
Term
| Clonidine and guanafacine MOA |
|
Definition
| Alpha 2 receptor agonist in CNS. Causes decreased in sympathetic outflow from CNS. Alpha2 stimulation of periphery of unknown importance |
|
|
Term
| CV effects of Clonidine and guanafacine |
|
Definition
| lowers BP by decreasing both CO (HR and SV) and TPR |
|
|
Term
|
Definition
| A: 70-80%, available via patch; D: M: 50%; E: |
|
|
Term
| Side effects of Clonidine and guanafacine |
|
Definition
| withdrawal syndrome (increased sympathetic activity, rebound HTN) when clonidine is rapidly discontinued. sedation and dry mouth |
|
|
Term
| Pattern of use of clonidine and guanafacine |
|
Definition
| use with diuretic or diuretic+vasodilator. |
|
|
Term
| first dose phenomenon is associated with what HTN med? |
|
Definition
| alpha1 receptor antagonists, especially in patients who are taking diuretics, beta blockers or who are already volume depleted. |
|
|
Term
|
Definition
| https://spreadsheets.google.com/ccc?key=0Ar1HwrS70Eb7dEpXOGU4OEhMN3hyaHE1Z3c2T20tSUE&hl=en&authkey=COSU8ekC |
|
|
Term
| List the vasodilators. How are they usually used? |
|
Definition
| Hydralazine (apresoline). Minoxidil (loniten). CCBs. ACE-I. ARB. Renin inhibitors. usually used in 3 drug combination except CCBs that can be used alone |
|
|
Term
|
Definition
| MOA: direct acting smooth muscle (SOA) relaxant. 1º effects resistance vessels (arteries) little/no effect on capacitance vessels (veins). |
|
|
Term
|
Definition
| BP increased due to reduction in TPR. Reflex increase in HR and SV, renin release, and pseudotolerance |
|
|
Term
|
Definition
| A: absorbed well D: M: intestine and liver = rapid therefore, metabolite may be effector. Need to see if patient is a fast or slow metabolizer and adjust dose accordingly |
|
|
Term
| Side effects of hydralazine |
|
Definition
| drug induced LUPUS SYNDROME, especially in SLOW ACETYLATORS (more than 200 mg/day) |
|
|
Term
|
Definition
| NEVER USE ALONE (reflex activation of sympathetic system d/t Na and H2O retention. usually +diuretic+sympathetic depressant. Hydralazine+diuretic+propranolol is effective (decrease TPR, NaCl/H2Oretention, CO). Used in elderly as second agent (+diuretic) d/t blunted baroreceptor reflex. safe alternative to methyldopa in prego HTN |
|
|
Term
| minoxidil (Loniten) MOA and CV effects |
|
Definition
| MOA: arterial smooth muscle relaxant; CV: decreases TPR then BP resulting in tachycardia so need to pair with sympathetic depressant. extensive salt and water retention (treat with loop diuretic) |
|
|
Term
| Minoxidil (Loniten) ADME and Side effects |
|
Definition
| A: good, D: may accumulate in smooth muscle, prolonging duration M: first pass liver metabolism. active metabolites. Side effects: hypertrichosis and hyperpigmentation (active ingredient in rogaine). pericardial effusions in patient with renal insufficiency. |
|
|
Term
|
Definition
| RESERVED for patients with SEVERE HTN who are resistant to other regiments. +LOOP DIURETIC+BETA BLOCKER. (decrease TPR, Decrease retention, decrease CO) |
|
|
Term
| What are the three distinct groups of CCBs? |
|
Definition
| Phenylalkylamines (verapamil), Benzothiazepines (diltiazem), Dihydropyridines (end in dipine) |
|
|
Term
|
Definition
| decrease membrane conducance through L-type, potential dependent (or voltage gated), calcium selective channels in vascular smooth muscle (artery>>>vein) and/or cardiac muscle leading to decreased TPR d/t vascular relaxation and/or myocardial depression (Decreased CO) |
|
|
Term
| Explain the cardiovascular pharmacodynamis of the CCB |
|
Definition
| In the heart (SOA): inhibition of Ca++ entry (MOA) results in negative inotrpic, chronotropic and dromotropic actions. In blood vessels (SOA), inhibition of Ca++ entry (MOA) results in vasodilation, primary site is artery>>>veins. |
|
|
Term
| Does verapamil or diltiazem have greater myocardial depressant effects? |
|
Definition
| verapamil = phenylalkylamine |
|
|
Term
| Rank the effect of CCB types on blood vessels from greatest to least. |
|
Definition
| nifedimpine (DHP) >verapamil (phenylalkylamine) =diltiazem (Benzothiazepine) |
|
|
Term
| What are the CV effects of CCBs? |
|
Definition
| reflex tachycardia that resolves over several weeks as BP decreases. ( not as much with diliazem or verapamil b/c they are myocardial depressors). Not as much Na+ retention. May have some diuretic protperties. Can be used as monotherapy in patients with low renin or AA patients |
|
|
Term
|
Definition
| A: effective orally (verapamin=nifedipine>diltiazem). D: highly bound to plasma proteins M: first pass liver, some active metabolites (verapamil>diltiazam) short half life so either give frequently or use extended release formulation E: by Kidneys |
|
|
Term
|
Definition
| related to therapeutic effects: vascular effects seen most with DHPs (hypotension, dizziness, flushing, reflex tachycardia, peripheral edema). Cardiac: negative inotropism --> myocardial depression (CHF). SA or AV nodal depression --> decreased HR and conduction blocks (arrhythmias). Cardiac side effects seen more with verapamil and diltiazem. GI: constipation with verapamil. |
|
|
Term
|
Definition
| monotherapy; +diuretic; +diuretic+sympathetic depressant other than an alpha blocker. (decreased TPR+decreased NaCl&H2O retention+decreased CO) or (decreased TPR and CO + decreased NaCl and H2O retention) |
|
|
Term
|
Definition
| inhibit angiotensin converting enzyme thereby inhibit formation of Angiotensin II (vasoconstrictor). prolong action of bradykinin (vasodilator) because ACE breaksdown braydikinin. Reduced AII = reduced aldosterone secretion --> less salkt and water retention. |
|
|
Term
| What are the CV effects of ACE-Inhibitors? |
|
Definition
| reduction in BP d/t decreased TPR "functional vasodilator" with less reflex tachycardia or water retention. Not effective as monotherapy in AA patients. |
|
|
Term
| What are the ADME of ACE-Inhibitors? |
|
Definition
| A: orally effective M: liver, some are prodrugs (enalapril) E: Kidney |
|
|
Term
| Side effects of ACE-Inhibitors |
|
Definition
| loss of sense of taste, hypotension, hyperkalemia, neutropenia and proteinuria with renal disease, persistent non, productive cough with crhonic use, DO NOT SURE WHEN PREGO. angioedema, rash. |
|
|
Term
|
Definition
| monotherapy; +diuretic; +diuretic+sympathetic depressant. (decrease TPR, and salt and water retention) or (decrease TPR, salt and water, CO and/or TPR) |
|
|
Term
|
Definition
| MOA: blocks binding of angiotensin II to type I angiotensin II receptors. SOA: blood vessels, heart and kidney |
|
|
Term
|
Definition
| all end in -sartan. Losartan, candesartan... |
|
|
Term
|
Definition
| all end in -PRIL. Captopril (Capoten), enalapril (Vasotec), lisinopril (prinvil) |
|
|
Term
|
Definition
| decrease in BP d/t reduced TPR. Relaxes BOTH resistance and capacitance vessels (functional vasodilator). Less salt and water retention because aldosterone secretion is reduced. |
|
|
Term
|
Definition
| lower incidence of, hyperkalemia, and cough than in ACE-inhibitors. neutropenia and proteinuria with renal disease, DO NOT SURE WHEN PREGO. angioedema, rash. loss of sense of taste, hypotension |
|
|
Term
|
Definition
| monotherapy; +diuretic; +diuretic+betablocker |
|
|
Term
| Aliskirin (Tekturna): class and MOA, ADME and Uses |
|
Definition
| Renin inhibitor = vasodilator. MOA: inhibits conversion of angiotensinogen to angiotensin I. ADME: orally effective. USE: in combo with diuretic and an ARB (valsartan) |
|
|
Term
| What situations require a prompt reduction in BP? |
|
Definition
| malignant, accelerated HTN; HTN-encephalopathy; HTN-complicated by stroke; dissecting aortic aneurysm; heart failure and cerebrovascular insufficiency; eclampsia; pheochromocytoma or MAO-inhibitor induced HTN |
|
|
Term
| What is the primary concern with HTN urgencies. |
|
Definition
| prevent target organ damage. |
|
|
Term
| what is a caveat in lowering BP in patients with atherosclerosis? |
|
Definition
| don't want to lower it to fast because patients are prone to cerebral or coronary insufficiency |
|
|
Term
| Nitroprusside: MOA, SOA and CV effects? |
|
Definition
| MOA: Direct acting vascular (SOA) relaxant effecting both resistance (afterload) and capacitance (preload) vessels [balanced effort]. Metabolized locally to NO. CV: decreased TPR, decreased CO d/t decreased venous return. Can cause reflex tachycardia. Titrate to desired BP response |
|
|
Term
| Nitroprusside ADME and Side Effects |
|
Definition
| A: NOT ORALLY, IV ONLY! rapid onset and offset. M: metabolized to cyanide in RBC (methylglobinemia, infrequently: cyanide toxicity =acutely). Cyanide metabolized to thiocynate in liver (thiocynate toxicity develops in >72 hrs) |
|
|
Term
| What is the drug of choice in emergencies associated with acute MI or LV failure? |
|
Definition
| Nitroprusside. Alternatives: IV nitroglycerine and IV labetalol |
|
|
Term
| What is diazoxide (hyperstat), when it is it used and how does it work? |
|
Definition
| Non-diuretic, thiazide derivative. Used IV in emergency HTN situations but NOT A FIRST CHOICE. MUST COMBINE WITH DIURETIC for extended use. MOA: direct relaxation of resistance vessels ONLY (SOA). capacitance vessels are uneffected. therefore CV effect is to decrease TPR and therefore BP. Results in reflex tachycardia and salt and water retention. |
|
|
Term
| ADME and SIde effects of Diazoxide (Hyperstat)? |
|
Definition
| A: orally effective but used IV only in blolus or continuous drip.D: 90% bound to albumin M: first pass liver. Side effects: FLUID RETENTION. hyperglycemia, hyperuricemia. NOT A FIRST CHOICE |
|
|
Term
| what are examples of non-selective alpha receptor blocking agents? Side effects? |
|
Definition
| phentolamine (regitine) and phenoxybenzamine (dibenzyline). Used in HTN criss associated with EXCESS OF CIRCULATING CATECHOLAMINES (MAO inhibitor, pheochromocytoma, clonidine withrawal). Pair with a beta blocker to prevent excessive cardiac stimulation. Side effects: reflex tachycardia, orthostatic hypotension, nasal congestion, GI distress and sexual dysfunction. |
|
|
Term
| What is the MOA of the emergency HTN medication that is contraindicated in patients with glaucoma? |
|
Definition
| Fenoldopam is a selective, peripheral dopaminergic (D1) receptor agonist given IV. Lowers pressure while maintaining or increasing renal perfusion pressure. |
|
|
Term
| What agent is used to decrease BP in order to minimize bleeding during surgery? |
|
Definition
| Trimethaphan (Arfonad). MOA: non-depolarizing ganglionic blocking agent (comptetitive ACh inhibitor at nicotinic receptors (sympathetic depressant). Results in decreased CO and TPR. Orthostatic effect on BP causes more dramatic effect to be seen if elevate head of bead. ADME: sulfonium compound (doesn't cross lipid membranes) so IV only. NOT USED MUCH EXCEPT FOR: DISSECTING AORTIC ANEURYSM OR SURGERY. |
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