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Anesthesia Pharm > Week 4 - Antihypertensives: Vasodilators > Flashcards

Week 4 - Antihypertensives: Vasodilators Flashcards

1
Q

When could you see HTN in the OR?

A
  • Pain/Tourniquet Pain
  • Intubation
  • On incision
  • Induction
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2
Q

What two physiologic factors determine blood pressure?

A

Cardiac Output and Total Peripheral Resistance

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3
Q

What physiologic factors determine cardiac output?

A

Heart rate (epi/SNS - increase PSNS - decrease)

Stroke Volume

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4
Q

What physiologic factors determine stroke volume?

A

Contractility (epi/SNS - increase PSNS - decrease)

Venous Return

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5
Q

What physiologic factors determine venous return?

A
  • Venous Tone (epi/SNS - increase)
  • Blood volume

(renal retention affects blood volume — aldosterone, ADH, SNS - increase ANP - decrease)

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6
Q

What physiologic factors determine total peripheral resistance?

A

Circulating Factors (angiotensin II, epi, NE - increase)
Innervation (alpha1 - increase / beta1 - decrease)
Viscosity
Local Regulators (Endothelin/O2 - increase — NO, H+, Adenosine, PG, Bradykinin - decrease)

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7
Q

What are the different classifications of antihypertensives?

A

Diuretics (Thiazide, Loop, & K sparing)
Agents that block production/action of angiotensin (ACE/ARBs)
Sympatholytic (Beta/Alpha blockers)
Direct Vasodilators (Nitric oxide donors)
Calcium channel blockers

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8
Q

What is the mechanism of action for ACE inhibitors?

A

Block the conversion of angiotensin I to angiotensin II in the pulmonary endothelial tissue

Angiotensin II is a POTENT vasoconstrictor and stimulator of the SNS

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9
Q

What are side effects of ACE inhibitors?

A 
Cough
Angioedema!
Rash
ARF
Hyperkalemia
Taste disturbance
Can cause fetal morbidity and should be avoided during pregnancy
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10
Q

What are the benefits of ACE inhibitors?

A

Free of CNS side effects of other HTN drugs
No insomnia or sexual dysfunction
No bronchospasm
Good to use in CHF (no beta blocking effects)
Don’t see decrease HR, worsening PVD, metabolic derangements, or rebound HTN

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11
Q

When are ACE inhibitors the first line drug of choice?

A

HTN
CHF
Mitral Regurgitation

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12
Q

What are the effects of Captopril?

A

Competitive inhibition of ACE
Oral (comparatively shorter acting)

Antihypertensive Effects:

  • Reduce SVR: prominent in the kidneys, cerebral and coronary autoregulation are maintained
  • Orthostatic HoTN and reflex tachycardia do NOT occur
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13
Q

What are the side effects of Captopril?

A

Rash/Pruritis 10%
Angioedema (face, mouth, larynx)
Loss of taste 2-4%
NSAIDS antagonize effects of ACE inhibitors
Hyperkalemia (especially with impaired renal fxn)
Granulocytopenia

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14
Q

Describe Enalopril and Enaloprilat

A 
Enalopril = Prodrug
Enaloprilat = active
ACE inhibitor (Effects resemble those of Captopril  - reduce SVR)
Active form lacks sulfhydril which may be responsible for adverse effects of captopril
IV preparation (-at) allows for periop continuation
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15
Q

What are examples of ACE inhibitors?

A

Captopril, Enalopril, Lisinopril, Fosinopril, Benazepril, Quinapril, Ramipril

(-pril)

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16
Q

What are angiotensin II receptor antagonists (ARBs)? Give examples of drugs in this category

A

Competitive inhibition at sites of angiotensin II action (AT-1 receptors)

Also cause fetal morbidity
Not shown to be superior to ACEIs (reduce all-cause mortality/hospitalization in pts with HF when used in addition to ACEIs)

Losartan, Candesartan, Irbesartan, Olmesartan, Valsartan
(-sartan)

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17
Q

Do you hold ACE inhibitors and ARBs pre-op?

A

It is up for debate but there is literature out there supporting risk of hypotension if not held

-General rule is to hold because it can cause refractory hypotension (resistant to other meds)

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18
Q

What is the mechanism of action of Calcium Channel Blockers?

A

inhibit calcium influx through the voltage-sensitive L-type calcium channels in vascular smooth muscle

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19
Q

What is the MOA for the Dihydropyridine class of Ca++ blockers? What drugs?

A

Nifedipine, Amlodipine, Nicardipine, Clevidipine

Vasodilate: prevent Ca++ influx by modulating the shape of the opening of the channel (peripheral arterioles, not veins)

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20
Q

What is the MOA for the Nondihydropyridine class of Ca++ blockers? What drugs?

A

Verapamil and Diltiazem

Antiarrhythmics
-less potent vasodilators, negative inotropic and chronotropic activity limiting their use in pts with cardiac disease

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21
Q

What is the mechanism of action and the uses of Verapamil?

A

Synthetic derivative of papaverine — Ca++ channel Blocker (Nondihydropyridine)
Bind to alpha1 subunit in the open state and physically blocks the channel

Uses:

  • SVT (direct negative ino-, chrono, dromotropic effects)
  • Angina/Essential HTN (vasodilation w/o reflex tachy)
  • Maternal/Fetal tachyarrythmias and premature labor
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22
Q

What are the side effects of Verapamil?

A
  • Depressed AV node, negative chronotrope at SA
  • Negative inotrope on muscle cells
  • Moderate vasodilation on coronary and systemic arterial system
  • Decreased SVR, little effect on capacitance (veins) vessels
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23
Q

What is the mechanism of action of Diltiazem and its effects/uses?

A

Ca++ Channel Blocker (Nondihydropyridine) — Benzothiazepine
Acts on alpha1 subunit of the L-type Ca++ channel predominately in the SA node (acts on alpha1 subunit with an unknown mechanism)

Has peripheral vasodilating effects
Minimal myocardial depressant effects (less interaction with beta-adrenergic antagonists

Uses: SVT and HTN
Side effects are similar to Verapamil

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24
Q

What are the effects of Nifedipine?

A

Ca++ Channel Blocker (Dihydropyridine)

  • Significant coronary and arterial dilating properties
  • Little or no depressant effect on SA/AV nodes at vasodilatory doses
  • Peripheral dilation –> baroreceptor - mediated reflex tachycardia
25
Q

What are the uses, dose, and side effects of Nifedipine?

A

Ca++ Channel Blocker (Dihydropyridine)

Uses: Angina (especially printz metals) and HTN emergencies
Dose: 10-20 mg PO TID
Side Effects: Flushing, vertigo, headache (peripheral edema, HoTN, paresthesias, skeletal muscle weakness less common), renal dysfunction

26
Q

What are the effects and uses of Nicardipine?

A

Ca++ Channel Blocker (Dihydropyridine)

  • Available IV for continuous infusion
  • Some selectivity for coronary vessels — Increased coronary flow
  • Little negative inotropic effect

Uses: angina, HTN crisis in OR (decreases BP –> increases CO, HR, and EF)
*Used a lot in Neuro cases (continuous Nicardipine infusion to control BP after evacuation of acute cerebral hemorrhage)

27
Q

What is the mechanism of action and the effects and uses of Amlodipine?

A

Ca++ Channel Blocker (Dihydropyridine)
Modulates the shape of the Ca++ channel

-Coronary and peripheral vasodilation
-Less reflex tachycardia
-Slow rate of absorption and prolong effect
Uses: HTN and coronary angiospasm
-Once daily dosing of amlodipine is of particular appeal

28
Q

What antihypertensive agent is particularly successful in treating HTN in the elderly, African Americans, and Salt-sensitive patients?

A

Calcium Channel Blockers

29
Q

What is Nimodipine?

A

Analog of Nifedipine

ONLY PO not IV

  • Selective for large cerebral vessels
  • Used post neurosurgery for cerebral vasospasm and cerebral protection after global cerebral ischemia
30
Q

What are the anesthetic implications for Ca++ Blockers?

A

Anesthetics: negative inotropic effects, depressant effects on the SA node, and peripheral effects and volatiles are similar

  • Volatiles have Ca++ antagonist effects
  • Adverse CV changes more likely with heart block or LV dysfunction
  • Caution with halothane (accentuated depression)
31
Q

What effect does Ca++ Blockers have on Neuromuscular Blocking Agents?

A

Potentiate the effects of both DMRs and NDMRs

Reversal may be impaired due to diminished presynaptic release of ACh

32
Q

What effect does Ca++ Blockers have on Local Anesthetics?

A

Verapamil has LA properties and may increase the risk of toxic reactions during regional anesthesia

33
Q

What happens if Dantrolene is administered in the presence of Ca++ Blockers?

A

The administration of Dantrolene in the presence of Ca++ blockers may result in increased potassium levels and CV collapse

Invasive monitoring and frequent serum K+ levels are recommended in pts treated with both drugs

34
Q

What is the physiologic function of endogenous Nitric Oxide?

A

it is a gas that acts as a chemical second messenger in the maintenance of CV tone, platelet regulation, immune regulation, GI smooth muscle relaxation and as a possible effector molecule for volatile anesthetics

  • has 1/2 time of <5seconds (localized action)
  • Binds to heme (inactivated by Hgb
  • NO2 is a product of NO/O2 interaction which is a pulmonary toxin
35
Q

What is the effect of inhaled nitric oxide?

A

Causes pulmonary vasodilation
Usually improves oxygenation by improving ventilation-perfusion matching
Only FDA approved for pediatric use

36
Q

What is the mechanism of action for NitroVasodilating drugs?

A

NO molecule donors at the vascular wall promote vasodilation

Donated NO diffuses through the vascular endothelium to smooth muscle where it (2nd messenger) activates soluble guanylate cyclase –> GTP –> cGMP

37
Q

What is the physiologic effects and dosage of Sodium Nitroprusside?

A

NitroVasodilating Drug – Direct acting, non-selective

Dilates arterial and venous vessels (decreases both preload and afterload)

Onset is immediate
Duration is transient (requires IV infusion)
Dosage = 0.3 to 10 mcg/kg/min (infusion rates >2mcg/kg/min may result in accumulation of cyanide with resultant toxicity)

38
Q

What is the mechanism of action for Sodium Nitroprusside?

A

Interacts with oxyhemoglobin and dissociates immediately to form methemoglobin and release NO

Released NO activates the enzyme guanylate cyclase in smooth muscle resulting in increased concentrations of cGMP

cGMP inhibits Ca++ entry into vascular smooth muscle producing vasodilation

*NO = active mediator of direct vasodilation

39
Q

What is the mechanism of action of Hydralazine?

A

Activates guanylate cyclase to produce direct vascular relaxation

  • Arteriole dilation greater than venous (more effect on afterload)
    • Minimizes risk of orthostatic hypotension
    • Most pronounced in coronary, cerebral, renal, and splanchnic circulations

*often used in combo w/ beta blockers/diuretic therapy to prevent baroreceptor-mediated reflex increases in SNS activity

40
Q

What is the dosing, onset, and duration of Hydralazine?

A

Dosing: 2.5 to 10 mg IV (START SMALL)
Onset: 10 to 20 minutes (wait before redosing)
Duration: 3 to 6 hours

BP response is unpredictable (usually a last resort medication)

41
Q

What are the CV effects of Hydralazine?

A

decreased SVR
decreased DBP more than SBP
increased HR, SV, and CO

42
Q

What are the side effects of Hydralazine?

A 
Sodium/Water retention
Vertigo
Diaphoresis
Nausea
Tachycardia (may evoke ischemia/angina)

Rare = drug fever, anemia, urticaria, polyneuritis, pancytopenia

43
Q

What is the purpose of induced hypotension and potential cases where it is used?

A

It decreases bleeding and improves visualization of the surgical field

Potential Cases = spinal surgery, hip or knee arthroplasty, shoulder arthroscopy, endoscopy, hepatic resection, robotic surgery, and major maxillofacial operations

*beware of pt position!!! (seated position - brain MAP is 10 less than the cuff MAP)

44
Q

How hypotensive is induced hypotension?

A

Patient’s baseline mean arterial pressure (MAP) is reduced by 30% and consequently, the systolic blood pressure values are about 80-90 mmHg and the MAP is reduced to 50-65 mmHg

45
Q

What is the determining factor in the reduction in blood loss in controlled hypotension?

A

In certain techniques, the decrease in cardiac output is the determining factor (remember flow is based on CO so HR and SV also play a part)

In other techniques, it is the fall in MAP

46
Q

What techniques are used for induced hypotension?

A

Deep anesthesia and heavy analgesia (Volatiles - 2-3 MAC, Opioids, Propofol) — typically done first

Standard anesthesia and administration of hypotensive drugs (Sodium Nitroprusside vs Nitroglycerin, beta-blockers, Esmolol infusion, labetalol, metoprolol, nicardipine)

47
Q

What drugs are used to lower blood pressure in the OR?

A

Beta Blockers: generally avoided in pts with acute decompensated HF
-Esmolol, Metoprolol, Labetalol

Calcium Channel Blockers: used cautiously in pts with increased ICP
-Nicardipine, Clevidipine

Direct Vasodilators: generally avoided in pts with increased ICP
-Hydralazine, Nitroglycerin, Nitroprusside

Other Antihypertensives:
-Fenoldopam

48
Q

What is the functional class, bolus/infusion dose, onset, and duration for Esmolol?

A

Beta Blocker – Beta1 selective

Bolus Dose = 10-50mg (may be repeated every 5-15 minutes depending on initial dose, desired effect, and risk for hemodynamic decompensation)
Infusion Dose = 50-300 mcg/kg/min
Onset: 1-2 minutes
Duration: 1/2 life = 9 min

  • rapid onset and very short duration of action
  • clearance is not dependent on renal or hepatic function due to rapid metabolism by plasma esterases
49
Q

What is the functional class, bolus/infusion dose, onset, and duration for Metoprolol?

A

Beta Blocker – Beta1 selective

Bolus Dose = 1-5mg followed by 2.5-15mg every 3-6 hours
Infusion Dose = None
Onset: 1-5 min
Duration: 1/2 life = 3-7 hours Clinical = 1-4 hrs

*commonly used agent to treat suspected myocardial ischemia due to tachycardia with normal or elevated BP

50
Q

What is the functional class, bolus/infusion dose, onset, and duration for Labetalol?

A

Blockade of postsynaptic alpha1 and non-selective beta1/beta2

Bolus Dose = 5-25mg which may be followed by repeated boluses every 10 minutes (300mg max)
Infusion Dose = 0.5-2mg/min (max of 10mg/min)
Onset: 1-5 min
Duration: 1/2 life = 6 hrs Clinical = 1-4 hrs

  • often selected 1st line agent to treat concomitant HTN and tachycardia
  • use cautiously in pts with obstructive or reactive airway disease
  • avoid in hyperadrenergic states (beta blockade can lead to severe HTN when prior alpha1 blockade is incomplete)
51
Q

What is the functional class, bolus/infusion dose, onset, and duration for Nicardipine?

A

Selective dihydropyridine-type Ca++ Blocker (selective arteriolar smooth muscle relaxation)

Bolus Dose = 100-500 mcg
Infusion Dose = 5-15mg/hr
Onset: 2-10 min
Duration: 1/2 life = 2-4 hr Clinical = 30-60 min

  • predominantly arteriolar vasodilator
  • commonly used for neurosurgical pts
52
Q

What is the functional class and bolus/infusion dose for Clevidipine?

A

Selective dihydropyridine-type Ca++ Blocker (selective arteriolar smooth muscle relaxation)

No bolus doses
Infusion Dose = 1-2 mg/hr with rapid titration up to 16mg/hr

  • rapid onset and short duration of action
  • clearance is not dependent on renal or hepatic function due to rapid metabolism by plasma esterases
53
Q

What is the functional class, bolus/infusion dose, onset, and duration for Hydralazine?

A

Highly selective vasodilation of arterial resistance vessels

Bolus Dose = 2.5mg followed by repeated boluses every 5 min to a max of 20mg
Infusion Dose = n/a
Onset: 5-20 min
Duration: 1/2 life = 2-8 hr Clinical = 1-8 hr

  • minimal or no effect on venous circulation
  • relatively slow onset compared w/ other antihypertensive agents
54
Q

What is the functional class, bolus/infusion dose, onset, and duration for Nitroglycerin?

A

Nitrodilator that causes increased release of NO, resulting in smooth muscle relaxation

Bolus Dose = 10-40mcg, may be repeated or followed by infusion
Infusion Dose = 10-200mcg/min or 0.1-3mcg/kg/min
Onset: 1-2 min
Duration: 1/2 life = 1-3 min Clinical = 5-10 min

  • continuous monitoring using an intra-arterial catheter is warranted as soon as feasible, particularly if higher doses are used
  • SL or paste forms of nitro also available
55
Q

What is the functional class and bolus/infusion dose for Nitroprusside?

A

Nitrodilator that directly releases NO, resulting in smooth muscle relaxation

No bolus dose
Infusion Dose = 10-200 mcg/min or 0.1-3mcg/kg/min
Onset: 1-2 min
Duration: 1/2 life = <10 min Clinical = 1-10 min

  • continuous monitoring using an intra-arterial catheter is necessary
  • cyanide accumulation may occur
56
Q

What is the functional class, bolus/infusion dose, onset, and duration for Fenoldopam?

A

Selective agonist for D1 dopamine receptors – binds with moderate affinity to alpha2-adrenoceptors

No bolus dose
Infusion Dose = 0.1 mcg/kg/min titrated up to a max of 1.6 mcg/kg/min
Onset: 5-10 min
Duration: 1/2 life = 5 min Clinical = 30-60 min

  • rarely used in perioperative settings
  • generally avoided in pts with glaucoma or increased ICP
57
Q

What are the four classifications of blood pressure?

A

Normotension <120 and <80 mmHg

Pre-HTN 120-139 or 80-89 mmHg

Stage I HTN 140-159 or 90-99 mmHg

Stage II HTN >160 or >/=100 mmHg

58
Q

Which antihypertensive medications could worsen tachycardia and should be used with caution in a patient with CAD?

A

Hydralazine and Sodium Nitroprusside

*can lead to reflexive tachycardia and worsen the metabolic demand upon the heart

Anesthesia Pharm (18 decks)

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