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Anti-hypertensives Flashcards

1
Q

Angiotensin Converting Enzyme (ACE) Inhibitors

Use

A
  • 1st line therapy: HTN, CHF (Post-MI to reduce CHF progression), Mitral Regurgitation
  • Delay progression of renal disease → More effective in diabetics
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2
Q

Ang II normal physiology effects

A
  • Ang II is potent vasoconstrictor: arterial smooth muscle constriction
    • Main action mediated via AT-1 G-protein coupled receptor
      • Signaling = ↑ Ca2+ release from SR
  • AT-1 receptor effects
    • Generalized vasoconstriction (esp afferent arterioles of renal glomeruli)
    • ↑ NE release
    • Proximal tubular Na+ reabsorption
    • Secrete aldosterone from adrenal cortex
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3
Q

ACE Inhibitors

MOA

A
  • MOA: Block conversion of ang I to ang II in vascular endothelium
    • Via interaction w/ zinc ion of ACE (peptidyl-dipeptidase)
    • ↓ arterial pressure
    • ↓ cardiac work load
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4
Q

ACE Inhibitors

Side Effects

A
  • Highly potent & minimal side effects → good pt compliance
  • Side Effects:
    • Prolonged hypotension intra-op (do NOT take AM of surgery!)
    • Granulocytopenia
    • Hyperkalemia (esp CRI)
    • Angioedema
    • Persistent cough
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5
Q

ACE Inhibitors

Drug Interactions

A
  • NSAIDs antagonize effects
  • Other anti-hypertensives additive effect
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6
Q

ACE Inhibitors

Contraindications

A
  • Pregnancy
  • Renal artery stenosis pts may develop renal failure d/t impaired afferent arteriole constriction
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7
Q

Angiotensin II Receptor Blockers (ARBs)

MOA

A
  • Angiotensin II (AT1) receptor antagonists
  • MOA: Competitive binding to inhibit action of ang II at its receptor
    • Blocks vasoconstrictive actions of ang II w/out effecting ACE activity = ↓ peripheral vasoconstriction
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8
Q

Angiotensin II Receptor Blockers (ARBs)

Side Effects

A
  • Similar to ACEI’s but no significant bradykinin accumulation = no cough side effect
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9
Q

Angiotensin II Receptor Blockers (ARBs)

Contraindications

A

Pregnancy, Renal artery stenosis

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10
Q

Hydralazine

MOA/Dose

A
  • Vasodilation through activation of guanylate cyclase (interferes w/ action of IP3 mediated Ca++ release from SR) and hyperpolarization
  • Produces direct relaxant effect on vascular smooth muscle & ↓SVR
    • arteries > veins
    • Alter Ca2+ transport in vascular smooth muscles
  • Dose 2.5-10 mg IV
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11
Q

Hydralazine

Clinical Uses

A
  • In combo w/ BB and diuretic
  • Also, used in CHF (combo w/ isosorbide mononitrate)
  • Limits increased SNS activity
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12
Q

Hydralazine

Pk

A
  • Extensive hepatic first pass metabolism
  • After IV < 15% appears unchanged in kidney
  • Onset: 15 min, give slowly
  • Peak: 10-20 min
  • DOA: up to 6 hrs
  • E½t = 3 hrs
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13
Q

Hydralazine

Side Effects

A
  • Angina w/ EKG changes
    • DBP reduced >SBP
  • Reflex ↑HR, SV, CO
  • Tolerance & Tachyphylaxis
  • Na+ & H2O retention
  • Lupus-like syndrome
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14
Q

Minoxidil

MOA

A
  • KATP channel opener → hyperpolarization (↓VG-Ca2+ channel activity) & vasodilation
  • Directly relaxes arteriolar smooth muscle; little effect on venous capacitance
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15
Q

Minoxidil

Clinical Use

A
  • In combo w/ BB (offset reflex tachycardia) & diuretic (offset Na+ & H2O retention)
  • Treat most severe forms of HTN d/t: renovascular dz, renal failure, transplant rejection
  • Topically used to treat baldness (side effect hirsutism)
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16
Q

Minoxidil

Pk

A
  • Orally active
  • Very potent; activity via active sulfate metabolite
  • 90% oral dose absorbed from GI tract
  • 10% of drug recovered unchanged in urine
  • Peak levels = 1 hr
  • E½t = 4 hrs
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17
Q

Minoxidil

Side Effects

A
  • Marked ↑ in HR & CO
  • ↑ plasma concentration of NE and Renin
    • Compensatory retention of Na+ & H2O
      • Weight gain, Edema
      • Pulmonary HTN, Pericardial effusion or tamponade
  • Hypertrichosis
  • Abnormal EKG: Flat or inverted T wave, ↑ voltage of QRS complex
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18
Q

Sodium Nitroprusside (SNP)

MOA

A
  • Direct acting, nonselective peripheral vasodilator
  • Relaxation of arterial & venous vascular smooth muscle
  • Lacks significant effects on non-vascular smooth muscle and cardiac muscle
  • MOA:
    • SNP interacts with oxyhemoglobin
      • dissociates immediately to form
        • Methemoglobin
        • Releasing Nitric Oxide (NO) and cyanide
    • NO activates guanylate cyclase (in the vascular muscle) = ↑ cGMP
      • cGMP inhibits Ca++ entry into vascular smooth muscle & increases uptake of Ca++ into smooth ER → Results in vasodilation via NO
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19
Q

Sodium Nitroprusside (SNP)

Effects

A
  • CV:
    • Direct venous & arterial vasodilation, ↑ venous capacitance d/t ↓VR
    • ↓SBP, SVR, PVR
    • Baroreceptor reflex = ↑HR
    • ↑contractility
    • Intracoronary steal in MI- damanged areas
  • CNS: ↑CBF, ICP
  • Pulmonary: Attenuate hypoxic vasoconstriction
  • Blood: ↑intracellular GMP→ inhibit platelet aggregation = ↑bleed time
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20
Q

Sodium Nitroprusside (SNP)

Metabolism

A
  • Transfer of electron from 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)
  • Remainder metabolized in liver and kidney; converted to thiocyanate
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21
Q

Sodium Nitroprusside (SNP)

Dosage

A
  • 0.3 mcg/kg/min – 10 mcg/kg/min IV
  • > 2.0 mcg/kg/min ↑risk toxicity
  • Do not infuse max dose >10 min
  • Onset: Immediate
  • DOA: Short
  • Need continuous IV admin to maintain therapeutic effect
  • Extremely potent: use A-line
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22
Q

Sodium Nitroprusside (SNP)

Dosing for different clinical uses

A
  • Controlled hypotension: 0.3-0.5 mcg/kg/min not to exceed 2 mcg/kg/min
  • HTN crises:
    • Infusion 1-2 mcg/kg IV can be given as bolus
    • Infusion not to exceed 10 mcg/kg/min
  • Cardiac disease:
    • ↓ LV afterload, useful for MR, AR, heart failure
    • Consider coronary steal
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23
Q

Sodium Nitroprusside (SNP)

Cyanide Toxicity

A
  • Cyanide Toxicity: toxicity occurs due to effects of high plasma concentrations of thiocyanate
    • At rates >2 mcg/kg/min for long periods
    • Suspect when pt starts demonstrating resistance to hypotensive effects or a previous responsive patient who is unresponsive (tachyphylaxis) at rates >2-10 mcg/kg/min
    • May precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis
    • Caution in pregnancy
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24
Q

Treatment of SNP-Related Cyanide Toxicity

A
  • Immediately d/c SNP
  • 100% O2 despite normal O2 sat
  • Sodium bicarbonate to correct metabolic acidosis
  • Sodium thiosulfate 150 mg/kg over 15 min
    • Acts as sulfur donor to convert cyanide to thiocyanate
  • Sodium nitrate 5 mg/kg if severe toxicity
    • Converts hgb → metHgb, which coverts cyanide to cyanometHgb
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25
Q

SNP: Other Toxicity

A
  • Thiocyanate Toxicityz; Rare → thiocyanate cleared by kidney in 3-7 days
    • Less toxic than cyanide
    • Symptoms: N/V, tinnutis, fatigue, CNS hyperreflexia, confusion, psychosis, miosis, seizure, coma
  • Methemoglobinemia: Rare
    • Consider as differential diagnosis in pts w/ impaired oxygenation despite adequate CO and arterial oxygenation
  • Phototoxicity
    • SNP should be mixed w/ 5% glucose in water and protected from exposure to light.
    • SNP is converted to aquapentacyanoferrate in presence of light and release of hydrogen cyanide occurs
    • Wrap solution/tubing in foil or dark plastic bag
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26
Q

Nitroglycerin (NTG)

MOA

A
  • Organic Nitrate
  • Acts on venous capacitance vessels and large coronary arteries
  • Administered IV, SL, PO, transdermal ointment
  • MOA:
    • Similar to SNP
      • Generates NO through a glutathione-dependent pathway which involves glutathione S-transferase
      • Requires presence of thio-containing compound to generate NO
      • Generation of NO then stimulates cGMP to cause peripheral vasodilation.
      • E½t = 1.5 min
    • Methemoglobinemia
      • Nitrite metabolite oxidizes ferrous ion in Hgb to ferric form which leads to formation of methgb.
      • Caution w/ high doses
      • Treat w/ methylene blue 1-2 mg/kg IV over 5 min to reconvert methgb to hgb
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27
Q

Nitroglycerin (NTG)

Systemic Effects

A
  • Tolerance → limitation of use of nitrates; seen after 24 hrs of sustained treatment
  • CNS: Vasodilation = ↑ ICP headache
  • CV:
    • Venodilation = ↓ VR, ↓ L&R VEDP, ↓ CO
    • No change or only slight ↑ HR
    • No change SVR
    • ↑ coronary blood flow to ischemic subendocardial areas (opposite of SNP)
  • Pulmonary:
    • ↓ PVR and Bronchial dilation → inhibits hypoxic pulmonary vasoconstriction
  • Coagulation: Inhibits platelet aggregation → Dose-related prolonged bleeding time
  • GI: Relaxes smooth muscles of GI tract
28
Q

Nitroglycerin (NTG)

Clinical Uses

A
  1. Angina
  2. Cardiac Failure
  3. Controlled hypotension (less than SNP)
29
Q

Nitroglycerin (NTG)

Clinical Uses

Angina & Cardiac Failure

A
  • Angina:
    • Venodilation and ↑ venous capacitance ↓VR to heart which ↓RVEDP & LVEDP
    • ↓ myocardial O2 requirements
  • Cardiac failure:
    • ↓ preload
    • Relieve pulm edema
    • Limits damage of MI
30
Q

Nitroglycerin (NTG)

Clinical Uses

Controlled hypotension

A
  • Less potent than SNP
  • Start: 10-20 mcg/min (3-6 mL/hr)
  • Titrate: ↑5-10 mcg/min every 5-10 min
  • Usual dosage: 50-200 mcg/min (max 500 mcg/min)
    • Not recommended in cranial surgery prior to opening dura
  • Sphincter of Oddi Spasm treatment: Can bolus 200 mcg at a time (1cc)
    • Spasm can occur during laparoscopic cholecystectomy or w/ opioid use
31
Q

Isosorbide Dinitrate

A
  • Oral nitrate: used to treat angina pectoris and in combo w/ hydralazine to treat CHF
  • PO: well absorbed from GI tract, DOA = 6 hrs
  • Sublingual DOA = 2 hrs
  • Works predominantly on venous circulation, improves regional distribution of myocardial blood flow in CAD pts
  • SE include: orthostatic hypotension
  • Active metabolite- isosorbid-5-mononitrate more active than parent compound
32
Q

Trimethaphan

A
  • Ganglionic blocker & peripheral vasodilator.
  • Rapid onset/must be given IV continuous drip 10-200 mcg/kg/min IV
  • Blocks ANS signals (both SNS & PSNS) between pre-ganglionic and post-ganglionic neurons; relaxes capacitance vessels
  • ↓ BP, CO, SVR
  • Can have ↑ HR d/t PSNS blockade, not because of reflex
  • Mydriasis, ↓ GI activity, urinary retention
33
Q

The 3 Major Classes of Ca2+ Channel Blockers

A
  1. Dihydropyridines
    • Nifedipine (Procardia, Adalat)
    • Amlodipine (Norvasc)
    • Nicardipine (Cardene)
    • Felodipine
  2. Phenylalkylamines
    • Verapamil
  3. Modified Benzothiazepines
    • Diltiazem
34
Q

The 3 Major Classes of Ca2+ Channel Blockers

Their actions

A

The 3 major chemical classes bind the alpha-1 subunit of L-type VGCaC at distinct/different sites and work allosterically to inhibit Ca entry into myocardial & vascular smooth muscle cells

35
Q

Ca2+ Channel Blockers: Voltage Sensitive L-type Ca2+ Channel Non-competitive Antagonists

MOA

A
  • Block entry of Ca2+(All classes)
    • Cardiac muscle: ↓inotropic effect, ↓contractility
    • Coronary vascular dilation (good choice in variant angina)
    • Systemic arterial dilation (artery > veins) → ↓afterload → ↓ wall tension and BP
  • Slow Ca2+ channel recovery (Phenylalkylamines)
    • SA node: chronotropic effect, HR↓
    • AV node: dromotropic effect, decrease conductivity, HR↓
36
Q

Ca Channel Blockers

Anesthetic Specific Drug Interactions

A
  • Myocardial depression & vasodilation with VA’s
  • Potentiate NMB’s
  • Verapamil contraindicated w/ Beta blockers
  • Verapamil ↑ risk LA toxicity
  • Verapamil & Dantrolene can cause hyperkalemia d/t slowing of inward movement of K+ ions → can result in cardiac collapse
37
Q

Ca Channel Blockers

Drug interactions General

A
  • Digoxin: CCBs can ↑ plasma concentration of digoxin by decreasing its plasma clearance
  • H2 antagonists: Ranitidine and Cimetidine alter hepatic enzyme activity and could ↑ plasma levels of CCB
38
Q

Can CCB’s toxicity be reversed?

A

Yes. May be reversed with IV admin of Ca++ or dopamine.

39
Q

Nifedipine

MOA

A
  • Dihydropyridine derivative
  • Primary site of action is peripheral arterioles
    • Coronary and peripheral vasodilator properties > verapamil
    • Little to no effect on SA or AV node (esp. w/ baroreceptor responses)
    • ↓SVR, BP
    • Reflex tachycardia
    • Can produce myocardial depression in pts w/ LV dysfunction or on BB’s
40
Q

Nifedipine

Pk

A
  • 90% PB/near complete hepatic metabolism/ metabolites excreted in urine
  • IV, oral or sublingual
  • PO onset = 20 min
  • PO peak = 60-90 min
  • E½t = 3-7 hrs
41
Q

Nifedipine

Clinical Uses

A
  • Angina pectoris
  • HTN
42
Q

Verapamil

MOA

A
  • Synthetic papaverine derivative
  • Its levoisomer is specific for slow Ca++ channel
  • Primary site of action is AV node
    • Depresses AV node
    • Negative chronotropic effect on SA node
    • Negative inotropic effect on myocardial muscle
    • Moderate vasodilation on coronary & systemic arteries
43
Q

Verapamil

Pk

A
  • 90% PB (presence of other agents such as lidocaine, diazepam, propranolol ↑ its activity)
  • PO almost completely absorbed w/ extensive hepatic first pass metabolism (PO dose 10X higher than IV)
  • Active metabolite: Norverapamil
  • PO peak = 30-45 min
  • IV peak = 15 min
  • E½t = 6-12 hrs
44
Q

Verapamil

Clinical Uses

A
  • Vasospastic Angina pectoris
  • Hypertrophic cardiomyopathy
  • Maternal & fetal tachydysrhythmias
  • Premature onset of labor
  • SVT
  • HTN
45
Q

Diltiazem

MOA

A
  • Benzothiazepines derivative
  • Primary site of action is AV node
    • 1st line tx SVT
    • HTN
    • Intermediate potency b/t verapamil & nifedipine
    • Minimal CV depressant effects
46
Q

Diltiazem

Pk/Dose

A
  • 70-80% PB/excreted in bile and urine (inactive metab)
  • PO or IV
  • PO onset = 15 min
  • PO peak = 30 min
  • E½t = 4-6 hrs
  • Liver disease may need ↓ dose
  • Dose: 0.25-0.35 mg/kg over 2 min, can repeat in 15 min
  • IV infusion 10 mg/h
47
Q

Diltiazem

Other Clinical Uses

A
  • Similar to verapamil:
    • Vasospastic Angina pectoris
    • Hypertrophic cardiomyopathy
    • Maternal & fetal tachydysrhythmias
48
Q

Nifedipine

Selectivity

49
Q

Verapamil

Selectivity

50
Q

Diltiazem

Selectivity

A

Vascular, Cardiac

51
Q

Nifedipine

Adverse Effects

A
  • Reflexive tachycardia
  • Headache
  • Dizziness, Palpitations
  • Flushing, Hypotension
  • Leg edema
52
Q

Nifedipine

Contraindications/Cautions

A
  • Hypotension
  • Severe aortic valve stenosis
53
Q

Nifedipine

Drug Interactions

54
Q

Verapamil

Adverse Effects

A
  • Hypotension
  • Facial flushing
  • Constipation
  • Nausea
  • Headache
  • Dizziness
  • Gingival hyperplasia
55
Q

Verapamil

Contraindications/Cautions

A
  • Sick sinus syndrome
  • AV block
  • LV dysfunction
  • Digitalis/Quinidine toxicity
56
Q

Verapamil

Drug Interactions

A
  • Beta-blockers
  • Cimetidine
  • Carbamazepine
  • Cyclosporine
  • Digoxin
57
Q

Diltiazem

Adverse Effects

A

“Relatively infrequent”

58
Q

Diltiazem

Contraindications/Cautions

A
  • Sick sinus syndrome
  • AV block
  • LV dysfunction
59
Q

Diltiazem

Drug Interactions

A
  • Beta-blockers
  • Ecainide
  • Cimetidine
  • Cyclosporine
  • Carbamazepine Lithium carbonate
  • Disopryramide
  • Digoxin
60
Q

Centrally Acting Agents

MOA/Site of Action

A
  • MOA: ↓ sympathetic outflow from vasomotor centers in brain stem. Centrally acting selective partial alpha-2 adrenergic agonist
  • Site of action: CNS a2 receptor agonist (clonidine)
61
Q

Centrally Acting Agents

Clinical Uses

A
  • HTN
  • Induce sedation
  • ↓ anesthetic requirements
  • Improve peri-op hemodynamics
  • Analgesia
62
Q

Clonidine

Action/Pk

A
  • Result in:
    • ↓ BP from ↓CO due to ↓HR and peripheral resistance
  • Rebound HTN w/ abrupt cessation
  • Pk
    • Available as PO or transdermal patch
    • 50/50 hepatic metabolism and renal excretion
63
Q

Clonidine

Side Effects

A
  • Bradycardia
  • Lactation in men
  • Impaired concentration
  • Nightmares
  • Depression
  • Sedation
  • EPS
  • Xerostomia (Dry mouth)
  • Vertigo
64
Q

Clonidine

Withdrawal Syndrome

A
  • Occurs in pt taking >1.2 mg/day
  • Occurs 18 hrs after acute d/c of drug
  • Lasts for 24-72 hrs
  • Treatment: rectal or transdermal clonidine
65
Q

Pre-op Continuation of Therapy

Beta Blockers

A

Yes, ↓ peri-op MI

66
Q

Pre-op Continuation of Therapy

CC Blockers

A

Yes, benefits outweigh risks unless severe LV dysfunction

67
Q

Pre-op Continuation of Therapy:

ACEI’s

A

No, withold for 1 dosing interval

Pharm-Spring (7 decks)

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