NUR 833 Ch. 20 Vasodilators.docx

Systemic HTN stage 1: 130/80 to 139/89 stage 2: ≥ 140/90 essential/primary HTN is most common no clear pathophysiology HTN is a major risk factor for CV dz: atherosclerosis HF stroke renal dz secondary HTN—less common mgmt. of primary HTN: lifestyle modifications (diet, exercise, weight reducti...

Systemic HTN stage 1: 130/80 to 139/89 stage 2: ≥ 140/90 essential/primary HTN is most common no clear pathophysiology HTN is a major risk factor for CV dz: atherosclerosis HF stroke renal dz secondary HTN—less common mgmt. of primary HTN: lifestyle modifications (diet, exercise, weight reduction, smoking cessation, salt restriction) + meds thiazide diuretic → initial therapy monitor K+ ways to decrease pressure: dec volume out of vasculature (will decrease the pressure) diuretics increase Na excretion (Water follows sodium) dec vascular tone (vasodilation) receptors to vasodilate NO, DA-1 control of vascular tone: anesthesia implications: Pre-existing conditions and routine medications Assess status of systemic hypertension Routine meds Evaluation by managing physician How often do you see your physician? Date of last visit? Recent changes in status or medications and results? Control of hypertension What is typical blood pressure? Acute medications given in perioperative period to reduce systemic and pulmonary pressures Choices? Treatment algorithm looking for red flags systemic HTN diagnosis and staging: know diastolic pressure = pressure that must be overcome by ao valve to get blood out if in hypertensive crisis, do not take to the OR unless emergency case. chronic HTN—new “normal” may not be 120/80, could be 130/90 keep BP within 20% of the pt’s “normal” evidence supporting this is controversial typical mgmt. of essential HTN: Essential Hypertension Alteration in Lifestyle or Diet Smoking Cessation Weight Reduction Physical Activity Salt Restriction Medications Initial Therapy Thiazide diuretic (increased sodium excretion) decreases volume Monitor K+ Labs: decreased K? Meds: supplemental K? Monotherapy CCB: direct vasodilation with few side effects ACE inhibitor: POTENT ATN; targets RAAS; inhibition of Angiotensin II production; few side effects Angiotensin II receptor blocker (ARB): POTENT ATN; targets RAAS; Blockade of Angiotensin II receptor; few side effects Beta Blocker: inferior stroke protection in pts older than 60; greater potential for side effects essential HTN—no notable (dz) cause not linked to cause result of RAAS: normally causes vasoconstriction if blocking, Na+ excretion and water following decreases volume if on > 2 drugs to target BP automatic ASA 3 according to CMS, thiazide diuretics count as an antihypertensive medication. typical mgmt. of secondary HTN: tx of underlying cause medication for HTN here, HTN is a side effect of the dz process. Specific Antihypertensive Drugs & Anesthesia antihypertensive therapy should be continued until the time of surgery HTN patients are likely on the following as a primary treatment: Thiazide diuretics (Supplemental K?) CCB ACE inhibitors ARB Beta Blockers ”Add-ons” (combination therapy) Goal is to antagonize the SNS Centrally acting Alpha 2 agonists Peripheral alpha 1 blocker Alpha/Beta blocker Dopamine 1 agonist Nitric oxide vasodilators Anesthesia Consideration ATN therapy should be continued up until the time of surgery; easier to manage a well-controlled hypertensive patient. Beta-Adrenergic Blockers not routinely used as first-line tx for HTN side effects are not ideal: fatigue, depression, impotence indicated for long-term tx of CAD and HF Less commonly used as first line agents for tx of HTN Caution in patients older than 60 y/o due to safety profile Side effects: Fatigue, depression, and impotence Indicated for long-term treatment CAD Heart failure Anti-hypertensive action in the above patients Mechanism of Action cardiac selective—specific to beta-1 nonselective—equal affinity for beta-1 and beta-2 beta blockers w/ intrinsic sympathomimetic activity: pindolol, acebutolol less bradycardia, less likely to unmask LV dysfunction less likely to produce vasospasm less likely to exacerbate PVD NSAIDs weaken the antihypertensive effects of beta blockers nonselective—propranolol cardioselective (b1)—acebutolol, atenolol, metoprolol, bisoprolol low-moderate dosing unlikely to cause bronchospasm, decreased peripheral blood flow, or mask hypoglycemia preferred in pulmonary dz, IDDM, symptomatic PVD nonselective beta blockers with a-1 blocking activity: carvedilol, labetalol alpha-blocking properties results in less bradycardia and negative inotropic effects compared to “pure” beta blockers alpha blocking properties → orthostatic hypotension Side Effects bradycardia heart block CHF bronchospasm claudication masking of hypoglycemia sedation impotence abrupt discontinuation → angina or MI avoid nonselective beta blockers in asthma selective beta blockers are safe in asthma and COPD diabetics: beta blockers increase risk of hypoglycemia they blunt ANS responses that would warn of hypoglycemia IV Beta-Blockers metoprolol, propranolol, labetalol (a-1/nonselective beta blocker), esmolol (short-acting; metabolized by plasma esterases) labetalol: b to a ratio is 3:1 (oral); 7:1 (IV) Alpha-1 Receptor Blockers prazosin, terazosin, doxazosin → oral, selective post-synaptic alpha-1 antagonists result in vasodilation on arterial and venous vasculature absence of presynaptic alpha-1 blocker leaves the normal inhibitory effect on NE release from nerve endings unlikely to elicit reflex increases in CO and renin release oral phenoxybenzamine & IV phentolamine → nonselective alpha blockers also block presynaptic alpha-2 receptors used in mgmt. of pheochromocytoma prazosin—tx of essential HTN decreases afterload in pts with CHF useful in preop prep in pts with pheochromocytoma relieves vasospasm of Raynaud’s tx of BPH Pharmacokinetics nearly completely metabolized 60% bioavailability after oral admin → substantial first-pass hepatic uptake T ½: 3 hours; prolonged in CHF but not in renal dysfunction metabolized in liver CV Effects dec SVR without causing reflex tachycardia or increased renin activity these side effects do occur w/ hydralazine & minoxidil dec vascular tone → dec CO & venous return Side Effects SE of prazosin: vertigo fluid retention orthostatic hypotension dry mouth sexual dysfunction nasal congestion nightmares urinary frequency lethargy NSAIDs interfere with antihypertensive effects of prazosin. epidural—exaggerated hypotension d/t alpha-1 blockade that prevents compensatory vasoconstriction in unblocked parts of the body dec SVR may not respond to a-1 agonism by phenylephrine may need epi to increase SVR & BP prazosin + beta blocker → potential for refractory hypotension during regional anesthesia d/t blunted response to b-1 & a-1 agonists Alpha-2 Agonists Mechanism of Action Pharmacokinetics CV Effects Side Effects Rebound HTN Other Clinical Uses Alpha-1 Blockers and Alpha-2 Agonists Alpha 1 blockers: For tx of HTN, used almost exclusively for pheochromocytoma Phenoxybenzamine Alpha 2 agonists: For HTN, Clonidine used to tx severe HTN and in renin-dependent disease. May also be used in neuraxial anesthesia Side effects: sedation, rebound HTN with abrupt discontinuation. Continue Clonidine up until time of surgery. Angiotensin-Converting Enzyme Inhibitors and Angiotensin II Receptor Blockers better safety profile free of CNS effects—depression, insomnia, sexual dysfunction free of other adverse effects—CHF, bronchospasm, bradycardia, PVD exacerbation no rebound HTN ACE inhibitors—most effective in treating HTN secondary to increased renin production first-line tx in those with systemic HTN, CHF, mitral regurg safer for diabetics delay progression of diabetic renal dz Potent with few side effects Side effects: cough, upper respiratory congestion, allergic-like symptoms (“kinin” response) May see exaggerated hypotension during induction of anesthesia. American College of Cardiologists/ AHA suggest it is “reasonable” to continue drugs until time of surgery. may see exaggerated hypotension on induction May see hypoglycemia. Increases insulin sensitivity Caution in pts with diabetes. ACE inhibitors allow Na+ excretion and vasodilation. Angiotensin II Receptor Blockers (ARBs) Losartan, Candesartan, Valdesartan May see exaggerated hypotension during induction of anesthesia. Increased Na+ excretion, decreased volume, vasodilation. Exaggerated hypotension on induction Mechanism of Action angiotensin II normally binds to cell membrane receptor AT1 → leads to increased release of Ca2+ from SR → vasoconstriction ACE inhibitor decreases generation of angiotensin II → leads to decreased vasoconstriction decreases plasma levels of aldosterone → less sodium and water retention ACE inhibitors block the breakdown of bradykinin (endogenous vasodilator)—contributes to their antihypertensive effects ACE inhibitors reduce activation of LDL receptors → results in decreased LDL cholesterol concentrations administration of ACE inhibitors as prodrugs increases oral bioavailability prior to hepatic metabolism enalapril → prodrug of the active ACE inhibitor enalaprilat conversion altered in hepatic dz captopril, lisinopril → not prodrugs ARBs produce antihypertensive effects by blocking vasoconstrictive actions of angiotensin II don’t affect ACE activity Side Effects side effects of ACE inhibitors: cough upper resp. congestion rhinorrhea allergic-like symptoms decreased GFR caution use in renal dysfunction hyperkalemia (dec production of aldosterone) greatest risk in CHF with renal insufficiency) resp. distress—give 0.3-0.5 mL 1:1,000 dilution epinephrine subQ angioedema → life-threatening complication of ACE inhibitors side effects of ARBs: do not inhibit breakdown of bradykinin no cough Preoperative Mgmt. ACE inhibitors and ARBs may cause adverse circulatory effects during anesthesia should be dc’d 12-24 hrs before surgery (??) Specific Agents oral ACE inhibitors: captopril, enalapril, lisinopril, ramipril lisinopril & ramipril → longer DOA captopril common ARBs: losartan, irbesartan, candesartan, olmesartan, valsartan all have a relatively long DOA no IV admin neprilysin inhibitor + valsartan (sacubitril + valsartan) neprilysin: circulating enzyme that metabolizes vasoactive peptides, including bradykinin, enkephalins, substance P, and the natriuretic peptides Calcium Channel Blocking Drugs inhibit Ca2+ influx through voltage-gated L-type calcium channels in vascular smooth muscle arterial specific; little to no effect on venous circulation dihydropyridines: nifedipine, amlodipine, nicardipine, clevidipine nondihydropyridines: verapamil, diltiazem less potent vasodilators negative inotropic & chronotropic effects limited use in cardiac dz mostly used for antiarrhythmics dihydropyridines are potent vasodilators safe in HF & conduction defects nicardipine & clevidipine—IV infusions rapid titration short half-lives side effects: potential reflex tachycardia & negative inotropy inhibit hypoxic pulmonary vasoconstriction → worsens V/Q mismatch be aware of this rapidly reversed with discontinuation nicardipine: hypertensive emergency tx hepatic metabolism clevidipine: metabolized by plasma esterases to inactive metabolites do not have to adjust dose for renal or hepatic impairment injectable emulsion caution in pts with defective lipid metabolism contraindicated in severe aortic stenosis → lowers coronary perfusion pressure; precipitates myocardial ischemia Arterial specific, little action on venous system. Target L-type calcium channels Does not require concurrent sodium restriction Effective in elderly, African Americans, and salt sensitive patients Two classes: Dihydropyridine Nifedipine, amlodipine, nicardipine, clevidipine Potent vasodilators Relatively safe to use in heart failure and conduction defects. Nicardipine IV: HTN emergencies Non-dihydropyridine Verapamil and Diltiazem Less potent vasodilators, but also negative inotropic and chronotropic Used more for antiarrhythmic patients Limited in cardiac disease **know which drugs fall into each class Phosphodiesterase Inhibitors phosphodiesterases (PDEs): broad family of 11 isoenzymes that mediate the breakdown of intracellular cAMP and cGMP PDE3 inhibitors: amrinone, milrinone PDE5 inhibitors: sildenafil, tadalafil, vardenafil inhibiting PDE causes vascular smooth muscle relaxation PDE3 inhibitors also cause positive inotropy by mobilizing intracellular calcium milrinone: IV PDE3 inhibitor inhibits breakdown of cAMP and cGMP in myocardial cells and vascular smooth muscle combined inotropy and vasodilation beneficial in short-term tx of HF excreted by kidneys T ½: 2-4 hrs increased in kidney dysfunction (up to 20 hours if on CRRT) PDE5 inhibitors selectively inhibit the breakdown of cGMP. more so in vascular smooth muscle than in CV sites lots of PDE5 in the lungs → these drugs are great for pulmonary vasodilation also good for erectile dysfunction only available orally modest systemic vascular effects; when combined with other vasodilators, they can cause a significant reduction in BP Inhibits breakdown of cAMP and cGMP. Two relevant classes: PDE 3 inhibitors Milrinone and Amrinone Vascular smooth muscle relaxation (systemic vasodilation) Positive inotropy on intracellular calcium mobilization cAMP and cGMP Milrinone is drug of choice for IV r/t safety profile PDE 5 inhibitors Sildenafil, Tadalafil, Vardenafil Vascular smooth muscle relaxation cGMP only; selective; more in vascular than CV sites Effective Pulmonary Vasodilators; also effective as erectile dysfunction drug Oral preparation only No concurrent administration with NTG (life-threatening hypotension) No calcium available to help out PDE Inhibitors: inhibiting breakdown of cAMP PDE3—heart PDE5—more in vascular system than in heart PDE inhibitors: for smooth muscle relaxation, it causes SR to reabsorb calcium, resulting in systemic vasodilation. Nitric Oxide & Nitrovasodilators Nitric Oxide (NO) NO is a chemical messenger in various biological systems. modulates CV tone, regulates platelets, functions as a NT in the CNS relaxes GI smooth muscle regulates immune fx inhalation admin → relaxes pulmonary arterial vasculature NO synthesis: NO synthetase acts on L-arginine to make NO. NO diffuses into precapillary resistance arterioles to induce guanylate cyclase to increase cGMP concentration → results in vasodilation as a therapeutic agent, NO affects pulmonary circulation but not systemic circulation d/t rapid uptake by Hgb nitrovasodilators (nitrates and nitroprusside) work by generating NO throughout the vasculature Nitro-vasodilators work through the generation of nitric oxide throughout the vasculature. Nitric Oxide—lives in endothelial cells of blood vessels Chemical messenger of the nitro-vasodilators 3 functions: modulates CV tone, platelet regulation, neurotransmitter function in the CNS Relevant A&P diagram Inhaled NO affects pulmonary circulation: Pediatric lung injury: infants or newborns with persistent pulmonary HTN Adult “off label”: Severe Pulmonary HTN with R heart dysfunction; transplants Increases in methemoglobin levels Other preparations work through the generation of NO in vasculature. NTG, SNP Inhaled NO affects pulmonary circulation NO in smooth muscle interferes w/ how actin and myosin connect. how to activate NO? mechanical shearing vasoactive amines histamine several other factors if we can get NO from endothelium to smooth muscle vasodilation Nitric Oxide: Endogenous Physiology NO lives in endothelial cells Messenger NO is released in response of many factors that result in vasodilation Steps: Ach binds to vascular endothelial receptor Ca ions are released from endogenous storage vesicle Ca ions combine with Calmodulin- messenger protein Ca-Calmodulin complex binds with and activates NO synthase NO synthase then catalyzes a reaction (arginine + O2 into citrulline + NO) NO molecule diffuses out of endothelial cell and into vascular smooth muscle cell NO binds with and activates guanylyl cyclase Guanylyl cyclase converts inactive GTP into active cGMP cGMP then causes dephosphorylation of MLCK (myosin light chain kinase) MLCK causes a dissociation of actin and myosin filaments Relaxation (if in vessels dilation) Nitric Oxide Donor Physiology Organic nitrates (NTG) Diffuse into smooth muscle cell (RNO2) NO molecule from NTG mimics function of endogenous NO at this point. body recognizes NTG as its own NO Organic nitrates (SNP/Nipride) Release RNO2 into blood. Converts to NO in the blood. *extra step w/ Nipride Diffuses into smooth muscle cell. NO molecule mimics function of endogenous NO at this point. Nitric Oxide as a Pulmonary Vasodilator inhaled NO → pulmonary arterial vasodilation proportional to the degree of pulmonary constriction less effect on pulmonary vascular resistance if pulmonary vascular tone is not increased (ex.: pulmonary HTN other than the primary type) dilates alveolar vessels to improve oxygenation via improving V/Q matching pediatrics—only approved use; pediatric lung injury adults—off label use; mgmt. of severe pulmonary HTN in the setting of acute R HF Toxicity inhaled NO increases methemoglobin levels—NO combines w/ Hgb discontinuation of NO may lead to life-threatening rebound arterial hypoxemia and pulmonary HTN wean slowly NO is oxidized to NO2 NO2 is a pulmonary toxin inhaled NO can lead to acute L HF and pulmonary edema (d/t increased pulmonary blood flow) Nitrodilators SNP & IV NTG are most widely used. generate NO → augments cGMP in vascular smooth muscle (arteries & veins) → vasodilation nitric oxide donors or nitrodilators: nitroprusside (SNP) organic nitrates NTG isosorbide Sodium Nitroprusside (SNP) direct-acting nonselective peripheral vasodilator that causes relaxation of arterial and venous vascular smooth muscle 44% cyanide by weight water-soluble lacks significant effects on nonvascular smooth muscle and on cardiac muscle onset: almost immediate duration: transient (requires continuous IV admin) made up of a ferrous ion center complexed with 5 cyanide moieties Direct acting; nonspecific actions (arteries and veins dilation) Monitoring (indication for arterial line) Metabolism biproduct is cyanide Initial dose is 0.3 mcg/kg/minute Max rate is 10 mcg/kg/min Rates greater than 2 mcg/kg/min may result in accumulation of cyanide. Protect from light with aluminum foil covering CV (tachycardia, increased myocardial contractility, “coronary steal” reflex) Renal (decreased renal function, do not discontinue abruptly) Hepatic (largely maintained) Cerebral (increases CBF and CBV; caution with increased ICP pts) Pulmonary (Decreases in PaO2 d/t hypoxic pulmonary vasoconstriction, add PEEP) Hematological (inhibits platelet aggregation, increases bleeding time) Mechanism of Action interacts with oxyhemoglobin; dissociates immediately to form methemoglobin and releases cyanide and NO NO activates the enzyme guanylate cyclase → results in increased intracellular cGMP cGMP inhibits calcium entry into vascular smooth muscle cells and increases calcium uptake by SER to produce vasodilation functions as a prodrug Metabolism begins w/ transfer of an electron from the iron of oxyhemoglobin to SNP → yields methemoglobin and an unstable SNP radical unstable SNP radical rapidly breaks down → releases all 5 cyanide ions one cyanide ion reacts with methemoglobin → forms cyanomethemoglobin the remaining free cyanide ions are available to rhodanese enzymes in the liver and kidneys to be converted to thiocyanate Dose and Administration monitor BP continuously w/ arterial line initial dose of SNP: 0.3 mcg/kg/min max dose: 10 mcg/kg/min should not run longer than 10 min infusion rates > 2 mcg/kg/min → cyanide accumulation Organ-Specific Effects CV baroreceptor-mediated reflex responses include tachycardia & increased contractility improves LV ejection and increases peripheral SNS activity → increases CO in LV failure, SNP decreases SVR, PVR, RAP no direct inotropic or chronotropic effects coronary steal → SNP may increase the area damaged from MI SNP dilates resistance vessels in nonischemic myocardium, which diverts blood flow away from ischemic areas where collateral vessels are already maximally dilated decreases diastolic BP → may lead to myocardial ischemia d/t decreased coronary perfusion pressure and coronary blood flow Renal decreased systemic BP → renal dysfunction if BP drops, renin will be released (will be a rebound effect if SNP discontinued) Hepatic no changes Cerebral SNP increases cerebral blood flow and cerebral blood volume if pt has decreased intracranial compliance, this may increase ICP may not have enough time for autoregulation (BP drops fast while ICP increases d/t SNP) Pulmonary decreases PaO2 weakens hypoxic pulmonary vasoconstriction adding PEEP may reverse vasodilator-induced decreases in PaO2 Hematologic increased intracellular cGMP inhibits platelet aggregation infusion at rates > 3 mcg/kg/min may result in decreased platelet aggregation and increased bleeding time Toxicity Cyanide Toxicity occur if infusion rate > 2 mcg/kg/min (when cyanide accumulates) increased cyanide leads to tissue anoxia, anaerobic metabolism & lactic acidosis treatment: discontinue 100% O2 sodium thiosulfate 150 mg/kg over 15 min if severe cyanide toxicity, give sodium nitrate 5 mg/kg Thiocyanate Toxicity rare thiocyanate is cleared by kidneys very slowly (T ½ 3-7 days) symptoms: fatigue, tinnitus, nausea, vomiting symptoms of neurotoxicity: hyperreflexia, confusion, psychosis, miosis may see seizures, coma Methemoglobinemia Clinical Use use has declined used for hypertensive emergencies, aortic & cardiac surgery, HF HF: affects preload and afterload Nitrates NTG—organic nitrate that acts on venous capacitance vessels and large coronary arteries to produce peripheral pooling of blood and decreased cardiac ventricular wall tension as the dose of NTG is increased, there is relaxation of arterial vascular smooth muscle can produce pulmonary vasodilation most common use: SL or IV for angina d/t atherosclerosis or vasospasm of the coronary arteries Mechanism of Action generates NO which stimulates the production of cGMP to cause peripheral vasodilation NTG requires the presence of thio-containing compounds, unlike SNP NTG is not recommended in pts w/ hypertrophic obstructive CM, severe ao stenosis → venous pooling will lead to syncope Organic nitrate Venous capacitance vessels and coronary arteries Peripheral pooling of blood and decreased cardiac ventricular wall tension. Larger doses of NTG: arterial wall relaxation primarily works on venous vessels Pulmonary vasodilation = systemic arterial vasodilation Uses Angina (vessel spasm or artherosclerosis) Controlled hypotension (good for keeping pt hypotensive) Contraindications Hypertrophic obstructive cardiomyopathy Severe AS stenotic outlet requires pressure Routes SL, oral, IV Indications to use NTG: any surgery that presses on baroreceptors (carotids) Route of Admin SL tablet transdermal—5-10 mg over 24 hours IV infusion Pharmacokinetics T ½ of 1.5 min large Vd (tissue uptake) Methemoglobinemia nitrite metabolite → can oxidize ferrous ion in Hgb to the ferric state → causes methemoglobinemia high doses of NTG may cause methemoglobinemia in pts w/ hepatic dysfunction Tolerance dose and duration dependent Clinical Use tx of myocardial ischemia tx of volume overload in R HF (reduces preload) systemic antihypertensive preferential effect on veins rather than arteries Isosorbide Dinitrate oral nitrate used for angina prophylaxis and for preload reduction (HF) similar effects of NTG well absorbed from GI tract no first-pass metabolism dose of 60-120 mg lasts up to 6 hours metabolite: isosorbide-5-mononitrate → more active than parent compound orthostatic hypotension Hydralazine direct systemic arterial vasodilator hyperpolarizes smooth muscle cells activates guanylate cyclase to vasorelax not recommended in CAD or myocardial ischemia causes reflex SNS stimulation that increases HR and contractility (increases O2 demand) effective afterload reduction limited long-term use d/t systemic autoimmune syndromes drug-induced lupus antineutrophil cytoplasmic antibody-associated vasculitis Direct systemic arterial vasodilator Activates guanidine cyclase, hyperpolarizes smooth muscle cells. Reflex increase in HR and myocardial contractility (usually short-lived), caution in patients with myocardial ischemia or coronary disease. don’t want to increase demand without increasing supply Slightly delayed IV onset wait 10-15 min before redosing Order of meds to dec BP: Esmolol (beta) Labetalol (alpha-beta) Hydralazine (direct arterial vasodilator) Fenoldopam DA type 1 receptor agonist causes systemic arterial dilation by increasing cAMP increases renal blood flow and UOP increases splanchnic blood flow d/t the density of DA-1 receptors in this location IV use only onset: rapid T ½ of 10 min baroreflex-mediated increases in HR and plasma catecholamines adverse effects: increased IOP not good for glaucoma Works on DA-1 receptors in the kidneys End result: causes dilation in the renal arteries decreases resistance to increase UOP, RBF works in splanchnic vessels too Short-term tx of HTN Diuretics first-line oral tx of essential HTN thiazide diuretic usually prescribed first loop diuretics (furosemide, bumetanide) reserved for pts where thiazides are not effective ex.: renal failure, HF not vasodilators thiazide and loop diuretics → K+ loss require supplementation watch Mg too aldosterone antagonists—“potassium-sparing” diuretics less potent than loop diuretics good for HF in combination with ACE inhibitors Perioperative Control of HTN Preoperative Cardiovascular Status? HTN? Control? Physician? How often do you visit? Last visit? Med changes? Usual BP? Meds? Last dose? Two or more Anti-HTN drugs (ASA III)? 12 lead EKG? METs? Physical Assessment? Clinical Predictors of Increased Risk? risk vs. benefit DECISION: Can this patient be optimized for surgery? Preoperative drug preparation? Further testing and preparation? May need cardiac consult. labs, 12-lead EKG Clinical Predictors of Increased Perioperative CV Risk Cardiac Risk Stratification of Noncardiac Surgical Procedures NYHA Functional Classification of Heart Failure **see attachment on Canvas** METs Metabolic equivalents (METs) are a measure of metabolic cost – a physiological benchmark used to track exercise intensity.  METs are classified as the ratio of metabolic rate (as expressed as rate of energy consumption) against a given physical activity task. One MET is defined as the amount of oxygen consumed while sitting at rest and is equal to 3.5 ml of O² per kg body weight, per min One MET is essentially the amount of energy produced relative to body mass whilst at rest. You are expending 1 MET of energy reading this PowerPoint slide. Intraoperative Tx of HTN Anesthesia depth: does it match what’s needed? Postop: pain control--opioids may need pharmacological agent for BP control if not related to pain, consult admitting physician