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ADV PHARM TEST 3 > HTN > Flashcards

HTN Flashcards

1
Q

Clinical practice guidelines for normal BP? What is normal BP?

A

<120/80

  • Promote optimal lifestyle habits
  • reassess in 1 yr
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2
Q

Clinical practice guidelins for elevated BP? What is elevated BP?

A

120-129/ <80

  • Non-pharmacologicla therapy
  • Reassess in 3-6 mo
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3
Q

Clinical practice guidliens for Stage 1 HTN? What classifies as stage 1 HTN?

A

bp 130-139/ 80-89

  • Is patient clniical ASCVD or estimated 10 y CVD risk >10%
    • yes
      • non pharmacological therapy and BP lowerin g meds
      • reassess in 1 mo
        • BP goal met?
          • yes- reassess in 3-6 min
          • no- assess and optimize adherence to therapy and consider intensification of therapy
    • No
      • non pharmacologicla therap
      • reassess in 3-6 mo
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4
Q

What classifies as Stage 2 HTN? Clinical Practice Guidelines?

A

>140/90

  • non pharmacologicla therapy and BP lowering meds
  • reassess in 1 mo
  • Bp goal met?
    • yes- reasses in 3-6 mo
    • no- assess and optimize adherence to therapy. consider intensification of therapy
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5
Q

What physiologically influences BP?

A
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6
Q

What are the various sites of action for anti-HTN?

A
  1. Brainstem- alpha 2 receptors
    • clonidine
    • methyldopa
  2. sympathetic ganglia- not as popular because influence both SNS and PSNS
    • mecamylamine
    • trimethapran
  3. Adrenergic terminals- would deplete ALL adrenergic terminals, of vesicales with NT; can cause unwanted s/e such as depression
    • guanethidine
    • reserpine
  4. Cardiac B1 receptors
    • Propranolol
    • metoprolol
    • other B blocker
  5. Vascular alpha 1 receptors
    • Prazosin
    • Terazosin
    • Labetalol
  6. Vascular smooth muscle
    • hydralazine
    • minoxidil
    • nitroprusside
    • diazoxide
    • CCB
    • Thiazides
  7. Renal Tubules- Decrease amt Na/H2O reabsorption
    • thiazide diuretics
    • furosemide
    • K sparing diuretics
  8. Components of the RAAS- huge component is decreasing tone RAAS
    • 8A- receptors on juxtaglomerular cells- propranolol, metoprolol
    • 8B- Renin- aliskiren
    • 8C- ACE- Captopril, enalapril
    • 8D- ANGII Receptor- losartan, valsartan
    • 8E - Aldosterone receptors- eplerenone, spironolactone
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7
Q

RAAS system and role in BP modulation?

A
  • Renin+ angiotensinogen–> ANG I–> (via ACE)–> ANG II–> SNS activity, tubular NaCl reabsorption and K excretion, adrenal cortex to make aldosterone, arterialar vasoconstriction, ADH secretion
  • Renin works to maintain tissue perfusion through increase ECF volume and increase BP
  • Renin is secreted by the Juxtaglomerular Apparatus
    • renin is the rate-limiting step
    • released when less NaCl delivery to juxtaglomerular apparatus or when renal baroreceptors sense decreased flow
    • beta 1 receptors on renal tubules also stimulated by circulating NE/Epi
    • release renin when dry and BP too low
  • Results in 1) vasoconstriction & 2) Na+ retention
  • Renin-angiotensin system is synergistic with SNS by increasing the release of noradrenaline from the sympathetic nerve terminals
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8
Q

Role of ACE inhibitors to treat HTN?

A
  • First line therapy
    • HTN
    • CHF
      • Post-MI to reduce CHF progression
    • Mitral Regurgitation
  • Delay progression of renal disease
    • More effective in diabetic patients- ACE inhibitors in DM can delay renal dysfunction
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9
Q

MOA ACE inhibitors?

A
  • Mechanism of Action: Block the conversion of angiotensin I to angiotensin II in the vascular endothelium
    • Via an interaction with the zinc ion of angiotensin converting enzyme (peptidyl-dipeptidase)
    • Fall in arterial pressure
    • Reduced cardiac work load
  • Get less ANGII and subsequent fall in BP
    • ​vasodilation
    • decrease blood volum
    • decrease cardiac and vascular remodeling
    • potassium retention
    • fetal injury
  • ACE inhibitors also block bradykinin
    • get vasodilation, cough and rare angioedema
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10
Q

What is effect on ANG II on BP? What receptor does ANG II bind to?

A
  • Angiotensin II is a potent vasoconstrictor responsible for arterial smooth muscle constriction
  • Angiotensin II
    • Main action mediated via AT-1 G-protein coupled receptor.
      • Signaling results in increased Ca2+ release from the SR
  • AT-1 receptor effects
    • Generalized vasoconstriction (especially in the afferent arterioles of renal glomeruli)
    • Increased norepinephrine release
    • Proximal tubular reabsorption of Na+
    • Secretion of aldosterone from adrenal cortex
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11
Q

Examples of ace inhibitors?

A
  • Highly Potent with minimal side effects
  • Good patient compliance (end in -pril)
    • Captopril- [Capoten]
    • Enalapril- [Vasotec]
    • Ramipril- [Altace]
    • Benazepril- [Lotensin]
    • Lisinopril- [Zestril, Prinivil]
    • Moexipril- [Univasc]
    • Quinapril- [Accupril]
    • Fosinopril- [Monopril]
    • Trandorapril- [Mavik]
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12
Q

S/E of ace inhibitors? Drug interaction? contraindications

A
  • S/E
    • prolonged hypotension intra op (prohibit taking on AM of sx)
    • granulocytopenia
    • angioedema d/t bradykinin
    • persistent cough d/t bradykinin
    • hyperkalemia (esp CRI)
  • Drug interaction: NSAIDs antagonize its effects, other anti-HTN additive effect
    • NSAIDs inhibit prostaglandin, which is a vasodilator. Giving NSAIDS stop vasodilation, kind of working against ACE vasodilation.
  • Contraindication
    • pregnancy
    • renal artery stenosis patients may develop renal failure due to impaire efferent arteriole constriction
      • renal artery stenosis patients rely on efferent vasoconstriction to maintain GFR
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13
Q

ACE inhibitor pharmacologic effects?

A
  • all affect venous and arterila system evenly
  • enalapril and ramipril are prodrugs
    • peak times can be 4-8 hours after dose, with duration lasting 18-30 hours (enalapril) or 24-60 hours (ramipril)
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14
Q

MOA Angiotensin II Receptor Blockers? S/E? Contraindications?

A
  • Angiotensin II (AT1) receptor antagonists
  • MOA: Competitive binding to inhibit the action of angiotensin II at its receptor
    • Blocks the vasoconstrictive actions of angiotensin II without effecting ACE activity
    • results in decreased peripheral vasoconstriction
  • Side effects similar to ACE inhibitors
    • No significant bradykinin accumulation (avoid cough side effect)
  • Contraindication:
    • renal artery stenosis
    • pregnancy
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15
Q

Examples ARBS?

A
  • Losartan-[Hyzaar, Cozaar]
  • Valsartan- [Diovan]
  • Irbesartan- [Avalide, Avapro]
  • Candesartan- [Atacand]
  • Telmisartan- [Micardis]
  • Eprosartan- [Teveten]
  • Olmesartan- [Benicar]
  • Tasosartan- [Verdia]
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16
Q

MOA hydralazine? Dose?

A
  • direct arterial vasodilator, second- line
    • reserved for cases not responding and in pregnancy
    • used in OR frequently when beta blockers are contraindicated
  • Vasodilation through activation of guanylate cyclase (interferes with action of IP3 mediated calcium release from SR) and hyperpolarization
  • Produces direct relaxant effect on vascular smooth muscle and decrease in SVR
    • arteries > veins
    • Alter Ca2+ transport in vascular smooth muscles
  • Dosage 2.5-10mg IV
    • 10-20minutes peak, can last up to 6hrs
      • ​be careful/patient when titrating hydralazine
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17
Q

Pharmacokinetic hydralazine?

A
  • Extensive hepatic first pass metabolism
  • Onset 15 minutes give slowly
  • Elimination ½ time 3 hours
  • After IV < 15% appears unchanged in the kidney
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18
Q

S/E Hydralazine?

A
  • Angina with EKG changes
    • DBP reduced >SBP- potential impairment coronary perfusion
  • Reflex Increase HR, SV, CO
  • Tolerance & Tachyphylaxis
  • Sodium and H20 retention- from compensatory action of aldosteron from drop in BP. May need to give BB and diuretic with hydralazine
  • Systemic lupus like syndrome

Clinically used in combination with BB and diuretic

  • Limits the increased SNS activity
  • Also, used in CHF (combined with isosorbide mononitrate)
    • speicfically helpful in black patients not traiditonally responding to BP meds
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19
Q

Minoxidil MOA and use?

A

Mechanism of Action

  • KATP channel opener: resulting in hyperpolarization (decreased voltage-gated Ca2+ channel activity) and vasodilation
  • Directly relaxes the arteriolar smooth muscle little effect on venous capacitance
  • Orally active
  • Very potent; activity via active sulfate metabolite

Clinically used (2nd line drug with severe forms HTN)–refractory HTN, if patient on this drug, do thorough cardiac w/u)

  • To treat the most severe forms of hypertension due to
    • renovascular disease
    • renal failure
    • transplant rejection
  • used in combination with beta-blocker (offset reflex tachycardia and compensatory aldosterone activation) & diuretic (to offset sodium and water retention)
  • Topical formulation used to treat baldness (side effect hirsutism)
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20
Q

Pharmacokinetics minoxidil?

A
  • Pharmacokinetics
  • 90% oral dose absorbed from the GI tract
  • Peak levels in 1 hour
  • E ½ t 4 hours
  • 10% of drug is recovered unchanged in the urine
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21
Q

S/E Minoxidil?

A
  • Marked increase in HR &CO
  • Increased plasma concentration of NE and Renin
    • Compensatory retention of Na and H20 (aldosterone mediated)
    • Weight gain
    • Edema
    • Hypertrichosis
    • Pulmonary HTN
    • Pericardial effusion or cardiac tamponade
  • Can have abnormal EKG-
    • Flat or inverted T wave, increased voltage of the QRS complex
22
Q

Sodium Nitroprusside Use?

A
  • Direct acting, nonselective peripheral vasodilator
    • most potent vasodilator we use in OR
  • Relaxation of arterial & venous vascular smooth muscle
  • Lacks significant effects on non-vascular smooth muscle and cardiac muscle
23
Q

MOA Sodium Nitroprusside (SNP)

A
  • SNP interacts with oxyhemoglobin
    • dissociates immediately to form
      • Methemoglobin
      • Releasing Nitric Oxide (NO) and cyanide
      • (One good guy and 2 bad guys made…)
  • Nitric Oxide activates guanylate cyclase (in the vascular muscle) thus increasing cGMP
  • cGMP inhibits calcium entry into vascular smooth muscle & increases uptake of Ca2 into the smooth endoplasmic reticulum.
  • Results in vasodilation via NO
    • ​good for pheochromocytoma with extremely high, difficult to control BP
24
Q

EFFECTS of SNP?

A
  • ­CV:
    • ­Direct venous and arterial vasodilation, increased venous capacitance due to decreased venous return
    • ­Baroreceptor mediated reflex responses increased HR
    • ­decrease SBP, decrease SVR, decreasePVR, ­increase contractility,
    • causes an intracoronary steal in areas of damage associated with MI- .loosing preferential flow to ischmic areas during MI. can worsen an MI. main difference between nitrate (NTG) and sodium nitroprusside. NTG maintains preferential blood flow during ischemia
  • ­CNS:
    • Increase CBF, and ICP.
  • ­Pulmonary:
    • ­ Attenuation of hypoxic vasoconstriction.
      • problematic in patient in supine with single lung ventilation, won’t have the HPV to maintain ventilation to “good” lung
  • ­Blood:
    • ­ Increases in intracellular GMP–> inhibit platelet aggregation and bleeding time.
25
Q

Sodium Nitroprusside dosage? onset, doa?

A
  • 0.3ug/kg/min - 10ug/kg/min IV
  • >2.0ug/kg/min increased risk toxicity
  • max dose should not be infused for >10 minutes
  • Immediate onset
  • Short duration of action
  • Requires continuous IV administration to maintain therapeutic effect
  • Extremely potent: use A-line

SNP is good choice if someone accidently gave too much NE, helps to dilate arteries.

26
Q

Metabolism of Sodium Nitroprusside?

A
  • Transfer of an electron from the Iron (Fe) of oxyhemoglobin to SNP yields
  • metHGb and an unstable SNP radical where all 5 cyanide ions are released.
  • One of these cyanide ions reacts with metHGb to form cyano-methemoglobin (nontoxic)
  • the remainder are metabolized in the liver and kidney
    • converted to thiocyanate
27
Q

Clinical uses of SNP?

A
  • Clinical uses
  • Controlled hypotension:
    • 0.3-0.5ug/kg/min not to exceed 2 ug/kg/min
  • Hypertensive crises:
    • infusion 1-2ug/kg IV can be given as bolus
    • Infusion not to exceed 10 mcg/kg/min
  • Cardiac disease:
    • decreases LV afterload, benefits management of MR or AR, CHF, and heart failure.
    • Consider coronary steal
28
Q

Cyanide toxicity with SNP? Treatment?

A
  • At rates >2ug/kg/min for long periods
  • Suspect when the pt starts demonstrating resistance to hypotensive effects or a previous responsive patient who is unresponsive (tachyphylaxis) at rates >2-10 ug/kg/min
  • May precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis
  • Caution in pregnancy

Treatment:

  • Immediate discontinuation of SNP
  • 100% 02 administration despite normal oxygen saturation
  • Sodium bicarbonate to correct metabolic acidosis
  • Sodium thiosulfate 150mg/kg over 15 minutes
    • Sodium thiosulfate acts as a sulfur donor to convert cyanide to thiocyanate (less toxic)
  • Sodium nitrate 5mg/kg if severe toxicity
    • Converts hemoglobin to metHgb which coverts cyanide to cyanometHemoglobin
29
Q

Other toxicities related to SNP besides cyanide toxicity?

A

Thiocyanate Toxicity

  • Rare as thiocyanate is cleared by the kidney in 3-7 days
  • Less toxic than cyanide
  • Symptoms include:
    • N/V, tinnutis, fatigue, CNS hyperreflexia, confusion, psychosis, miosis seizure and coma

Methemoglobinemia

  • Rare
  • Should be considered as a differential diagnosis in patients with impaired oxygenation despite adequate cardiac output and arterial oxygenation

Phototoxicity

  • SNP should be mixed w/ 5% glucose in water and be protected from exposure to light.
  • With continuous exposure to light SNP is converted to aquapentacyanoferrate in the presence of light and the release of hydrogen cyanide
  • Wrap the solution and tubing in foil or dark plastic bag.
30
Q

NTG class, main effect?

A
  • Organic Nitrate
  • Acts on venous capacitance vessels and large coronary arteries
  • Administered IV, SL, PO, transdermal ointment
31
Q

MOA NTG? What can form from nitrite metabolite?

A

Similar to SNP

  • Generates NO through a glutathione-dependent pathway which involves glutathione S-transferase
  • Requires the presence of thio-containing compound to generate NO
  • Generation of NO then stimulates cGMP to cause peripheral vasodilation.
  • Elimination ½ time is 1.5 minutes

Methemoglobinemia

  • Nitrite metabolite oxidizes ferrous ion in Hgb to ferric form which leads to formation of metHgb.
  • Caution with high doses
  • MetHemoglobinemia can be treated with methylene blue 1-2mg/kg IV over 5min to reconvert metHgb to Hgb.
32
Q

CV Effects NTG?

A

CV:

  • Venodilation,
  • Decrease venous return,
  • Decrease L and R ventricular end diastolic pressure,
  • Decrease CO,
  • No change or only slight increase in HR
  • No change in SVR
  • Increase in coronary blood flow to ischemic subendocardial areas (opposite of SNP)

Tolerance

  • Tolerance is a limitation of the use of nitrates
  • Seen after 24 hours of sustained treatment
33
Q

CNS, Pulm, coag, GI effects NTG?

A

CNS:

  • Vasodilation
  • Increased ICP headache

Pulmonary:

  • Decreased PVR,
  • Bronchial dilation
  • Inhibits Hypoxic pulmonary vasoconstriction

Coagulation:

  • Dose related prolonged bleeding time
  • Inhibits platelet aggregation

GI:

  • Relaxes smooth muscles of GI tract
34
Q

Clinical Uses NTG?

A

Angina:

  • Venodilation and increased venous capacitance decreases venous return to the heart which reduces RVEDP and LVEDP
  • Reduces myocardial oxygen requirements

Cardiac failure:

  • Decreases preload,
  • Relieves pulmonary edema
  • Limits damage of MI

Controlled hypotension:

  • Less potent than SNP
  • Start: 10-20 mcg/min (3-6 ml/hour)
  • Titrate: Increase 5 to 10 mcg/min every 5-10 minutes
  • Usual dosage: 50 to 200 mcg/min (maximum 500 mcg/min)
  • Not recommended in cranial surgery prior to opening the dura

Sphinchter of Oddi Spasm

  • Can occur with Laparoscopic Cholecystectomy or opioid use
  • Can bolus 200ug at a time (1cc)
35
Q

What is isosorbide dinitrate?

A
  • Oral nitrate- used to treat angina pectoris
  • Orally-Well absorbed from the GI tract duration of action 6 hours
  • Sublingual duration of action is 2 hours
  • Works predominantly on venous circulation, improves regional distribution of myocardial blood flow in patients with CAD
  • SE include:
    • Orthostatic hypotension
  • Active metabolite- isosorbid-5-mononitrate
    • more active than parent compound
36
Q

What is trimethaphan?

A
  • Ganglionic blocker & peripheral vasodilator.
  • Rapid onset/must be given IV continuous drip 10-200ug/kg/min IV
  • Blocks the ANS and relaxes capacitance vessels
  • Lowers BP, CO, and SVR
  • Can have increased HR due to parasympathetic nervous system blockade, not because of reflex
  • Mydriasis, decreased GI activity, & urinary retention
    • interfering with PSNS activation
37
Q

What are 3 major classes of CCB? Examples?

A

Dihydropyridines (mainly vascular)

  • ­Nifedipine (Procardia, Adalat)
  • ­Amlodipine (Norvasc)
  • ­Nicardipine (Cardene)
  • ­Felodipine

Phenylalkylamines (mainly cardiac)

  • ­Verapamil

Modified Benzothiazepines (intermed b/w vascular and cardiac)

  • ­Diltiazem
38
Q

CCB MOA?

A
  • CCB- voltage sensitive L-type Ca channel non-competitive antagonists- decrease Ca stimulated Ca release!
  • Block entry of Ca2+(All classes)- relaxation of smooth muscle
    • Cardiac muscle: ↓ inotropic effect, ↓ contractility
    • Coronary vascular dilation (good choice in variant angina)
    • Systemic arterial dilation (artery>veins)–>decrease afterload–> decrease wall tension and blood pressure
  • Slow Ca2+ channel recovery (Phenylalkylamines) (Slow phase 4 depol at heart)
    • SA node: chronotropic effect, HR↓
    • AV node: dromotropic effect, decrease conductivity, HR↓
39
Q

CCB Anesthetic Specific Drug Interactions?

A
  • Myocardial depression & vasodilation with inhalational agents
  • Can potentiate neuromuscular blockers
  • Verapamil contraindicated w/ Beta blockers
  • Verapamil-increases risk of local anesthetic toxicity
    • because you’re already blocking Ca, if you also block Na, risk of dysrhythmia also goes up
  • Verapamil and dantrolene can cause hyperkalemia due to slowing of inward movement of K+ ions can result in cardiac collapse
    • avoid in pt with hx MH because Dantrolene and verapamil= hyperkalemia
40
Q

General drug interaction CCB?

A
  • Digoxin: CCBs can increase the plasma concentration of digoxin by decreasing its plasma clearance
  • H2 antagonists
    • ranitidine and cimetidine alter hepatic enzyme activity and thus could increase plasma levels of CCB
  • Toxicity of CCB
    • may be reversed with IV administration of calcium or dopamine
41
Q

What is verapamil? site of action? clinical uses?

A
  • Synthetic Derivative of papaverine
    • Its levoisomer is specific for the slow calcium channel
  • Primary site of action is the AV node
    • Depresses the AV node
    • Negative chronotropic effect on SA node
    • Negative inotropic effect on myocardial muscle
    • Moderate vasodilation on coronary as well as systemic arteries
  • Clinical Uses
    • SVT
    • Vasospastic Angina pectoris
    • HTN
    • Hypertrophic cardiomyopathy
    • Maternal and fetal tachydysrhythmias
    • Premature onset of labor
42
Q

Who should not receive verapamil?

A
  • Should not be given to patients with heart failure severe bradycardia, sinus node dysfunction, or AV node block.
  • Verapamil can precipitate ventricular dysrhythmias in a patient with WPW. Less pronounced effects of vascular smooth muscle so less decrease in BP
43
Q

Pharmacokinetics Verapamil

A
  • 90% protein bound (presence of other agents such as lidocaine, diazepam, propranolol increase­ its activity)
  • Orally almost completely absorbed with extensive hepatic first pass metabolism (PO dose 10X higher than IV)
  • Active metabolite - norverapamil.
  • Oral Peaks in 30-45 minutes/IV 15 minutes
  • E ½ t is 6-12hrs
44
Q

What is nifedipine? uses? site of action?

A
  • Dihydropyridine derivative (vascular selective)
  • Clinical uses
    • Angina pectoris
    • Hypertension
  • Primary site of action is peripheral arterioles
    • Coronary and peripheral vasodilator properties > verapamil
    • Little to no effect on SA or AV node (esp. with baroreceptor responses)
    • Decrease SVR, BP,
    • Reflex tachycardia
    • Can produce myocardial depression in pts with LV dysfunction or on beta blockers
45
Q

Nifedipine pharmacokinetics?

A
  • Pharmacokinetics
  • IV, oral or sublingual
  • Oral –effects in 20 minutes/peaks 60-90 minutes
  • 90%Protein Bound/near complete hepatic metabolism/ metabolites excreted in the urine
  • E ½ t is 3-7hrs
46
Q

Diltiazem? uses? site of action? dose?

A
  • Benzothiazepines derivative- intermediate b/w cardiac and vascular
  • Principle site of action is the AV node
    • 1st line tx SVT
    • HTN
    • Intermediate potency between verapamil & nifedipine
    • Minimal CV depressant effects
  • Other Clinical Uses
    • Similar to verapamil
    • Vasospastic Angina pectoris
    • Hypertrophic cardiomyopathy
    • Maternal and fetal tachydysrhythmias
  • PO or IV
    • Dose is 0.25-0.35mg/kg over 2 minutes can repeat in 15 minutes
    • IV infusion 10mg/h
47
Q

Diltizem pharmacokinetics?

A
  • Oral onset is 15 minutes and peaks in 30 minutes
  • 70-80% protein bound/excreted in the bile and urine (inactive metab)
  • E ½ t is 4-6 hours
  • Liver disease may require a decrease dose
48
Q

What are the effects of verapamil, nifedipine, nicardipine, diltiazem on:

BP?

HR?

Myocardial depression?

SA node drepression?

AV Node conduction?

Coronary artery dilation?

Peripheral artery dilation?

A
49
Q

MOA of centally acting alpha 2 agonists?

A
  • MOA: Reduce sympathetic outflow from vasomotor centers in the brain stem. Centrally acting selective partial alpha-2 adrenergic agonist
  • Site of action: CNS a2 receptor agonist (clonidine)
  • Clinical Uses
    • Hypertension- second line agents because sedative effects as well
    • Induce sedation
    • Decrease anesthetic requirements
    • Improve peri-operative hemodynamics
    • Analgesia
50
Q

Clonidine? s/e?

A

Result in:

  • BP reduction from decreased CO due to decreased HR and peripheral resistance
  • Rebound hypertension with abrupt cessation

Side Effects

  • Bradycardia
  • Sedation
  • Xerostomia (Dry mouth)
  • Impaired concentration
  • Nightmares
  • Depression
  • Vertigo
  • EPS
  • Lactation in men
51
Q

Pharmacokinetics clonidine? withdrawal syndrome?

A

Pharmacokinetics

  • Available as PO or transdermal patch
  • 50/50 hepatic metabolism and renal excretion

Withdrawal Syndrome

  • Occurs in pt on doses of >1.2mg/day
  • Occurs 18 hours after acute discontinuation of drug
  • Lasts for 24-72 hours
  • Treatment rectal or transdermal clonidine
52
Q

Preop continuation HTN therapy?

BB? CCB? ACE?

A

Beta blockers

  • continue
  • bb therapy reduces perioperative MI.
    • document dose within 24 hours!

CCB

  • Continue periop
  • benefits outweight risks unless severe LV dysfunction
    • if worried about EF, hold

ACE

  • NO admin preop
  • withholding for 1 dosing interval

ADV PHARM TEST 3 (5 decks)

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