Antihypertensives Flashcards

1
Q

Many patients present to the OR on various ________

A

HTN agents

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2
Q

What is the drug classes commonly used to treat hypertension? (4)

A

thiazide diuretics, CCB (dihydropyridine), ACE-I, ARB, beta-blocker

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3
Q

Patients with systemic HTN can be sensitive to anesthetic agents; challenging for anesthesia provider: ________

A

Roller coaster anesthetics

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4
Q

What is the continuation of antihypertensive meds for surgery? When is this not the case?

A

Antihypertensive meds are continued up to time of surgery; held for severe bradycardia or hypotension

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5
Q

What antihypertensive medications must be held prior to surgery?

A

Ace inhibitors the exception: commonly held 12-24 hrs before surgery (patients can develop refractory hypotension intraoperatively

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6
Q

What are some medications that can cause refractory hypotension intraoperatively when given with ACE inhibitors?

A

sometimes minimal effect using ephedrine or phenylephrine; vasopressin effective)

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7
Q

When are β-Adrenergic Receptor Blockers indicated?

A

Indicated in long-term tx of patients w/ CAD & HF

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8
Q

What is the classification for β-Adrenergic Receptor Blockers?

A

Classified as nonselective or cardioselective

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9
Q

When are cardioselective β-Adrenergic Receptor Blockers prefered?

A

cardioselective drug preferred in pulmonary disease, IDDM, & symptomatic PVD

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10
Q

What are general side effects of β-Adrenergic Receptor Blockers?

A

bradycardia, heart block, CHF, bronchospasm, claudication, masking hypoglycemia, sedation, impotence, abrupt withdrawal issues

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11
Q

What is the use of metoprolol?

A

Metoprolol used to control HR (cardioselective)

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12
Q

What is MOA of labetalol?

A

: nonselective beta and alpha-1 adrenergic blocker

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13
Q

What is the use of labetalol in anesthesia?

A

used to tx hypertensive emergencies & type B aortic dissections

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14
Q

What is the onset of labetalol?

A

Onset 1-5 min

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15
Q

What is the clinical half life of labetalol?

A

clinical half-life 1-4 hrs

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16
Q

What are the side effects of Labetalol?

A
  • Less reflex tachycardia and less negative inotropy
  • Decreases HR d/t beta-blocking activity
  • Orthostatic hypotension
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17
Q

What is the use of esmolol?

A

control HR and blunt sympathetic responses that are episodic during an anesthetic (ideal anesthetic drug, quick on-quick off)

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18
Q

What is the target receptors of Prazosin, terazosin, doxazocin?

A

peripheral-acting, oral, selective postsynaptic a-1 adrenergic receptor blockers

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19
Q

What is the effect of Prazosin, terazosin, doxazocin?

A

arterial & venous vasodilation

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20
Q

What is the MOA of phenoxybenzamine and phentolamine?

A

(nonselective alpha blockers) by not affecting presynaptic α-2 receptors

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21
Q

What is the affect of phenoxybenzamine and phentolamine?

A

no reflex increase in CO or renin

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22
Q

What is the use of Prazosin?

A

used for HTN, afterload reduction for CHF and alpha blockade in preop management of pheochromocytoma (”a before b”)

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23
Q

What is Prazosin most commonly used for in males?

A

HTN in males with BPH

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24
Q

What are the side effects of Prazosin?

A

orthostatic hypotension, vertigo, fluid retention

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25
Q

What medications can interfere with the anti-HTN effects of Prazosin?

A

NSAIDS may interfere with anti-HTN effects

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26
Q

What can be exaggerated when Prazosin and epidurals? What is the treatment? What can occur when combined with BB?

A
  • Hypotension with epidural may be exaggerated
  • Phenylephrine may not be effective; may require epinephrine
  • When combined with B-blockers could result in refractory hypotension
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27
Q

What is the receptors targets of Clonidine?

A

central acting, partial α2- adrenergic agonist

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28
Q

What is the effect of Clonidine?

A

d/t decreased sympathetic output from the CNS

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29
Q

What is the clinical use of Clonidine?

A

Tx of patients w/severe HTN

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30
Q

What is the formularies of Clonidine?

A

Oral and transdermal use

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31
Q

What is the clinical effects of Clonidine?

A

Affects systolic more than diastolic, maintains homeostatic CV reflexes (no orthostatic hypotension or hypotension during exercise)

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32
Q

What id the MOA of Clonidine?

A

Clonidine binds to α2 receptors in medullary vasomotor center to decrease SNS outflow

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33
Q

What effect does Clonidine and anesthetics have?

A

Decreases anesthetic requirements by modifying K+ channels in CNS (decreases MAC by nearly 50%)

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34
Q

What impact does neurxial administration have with Clonidine?

A

inhibits nociceptive neuron firing and spinal substance P release

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35
Q

What is the side effects of Clonidine?

A

sedation and xerostomia (dry mouth)

36
Q

What is the effects of Clonidine that is abruptly withdrawal? What is this treated with?

A

Rebound HTN with abrupt discontinuation- better treated with hydralazine, SNP or labetalol (given the alpha blockade), restart clonidine

37
Q

What is true about Clonidine and DEX?

A

Both clonidine and DEX reduce the sympathetic hyperactivity following ETOH and opioid withdrawal

38
Q

Overview of commonly used antihypertensive drugs.

A
39
Q

Describe the Renin-Angiotensin-Aldosterone Pathway.

A
40
Q

What is the MOA of ACE Inhibitors?

A

Decrease the production of angiotensin II by inhibiting the activity angiotensin-converting enzyme

41
Q

What does Angiotensin II produce?

A

produces vasoconstriction through release of Ca++ from SR in vascular smooth muscle

42
Q

What do ACE Inhibitors prevent?

A

prevent breakdown of bradykinin

43
Q

What is bradykinin?

A

an endogenous vasodilator

44
Q

What are side effects of ACE Inhibitors?

A

cough (most common), upper respiratory congestion, rhinorrhea

45
Q

Why do allergy-like symptoms occur with ACE Inhibitors?

A

d/t inhibiting breakdown of bradykinin

46
Q

What is the life threatening side effects of ACE Inhibitors?

A

ANGIOEDEMA

47
Q

What are the effects of ACE Inhibitors?

A

Decreases GFR; caution with renal dysfunction, renal artery stenosis

48
Q

What is the electrolyte abnormality associated with ACE Inhibitors?

A

Hyperkalemia (from decreased aldosterone); highest risk in patients with CHF or renal insufficiency

49
Q

What effect do ACE Inhibitors have on the kidneys?

A

Decreased renal perfusion and increase sympathetic activity result in increase in renin

50
Q

What do ACE Inhibitors lack?

A

The agents lack many of the CNS side effects seen with the other centrally acting anti-HTN agents

51
Q

What do ACE Inhibitors treat?

A

Treat systemic HTN, CHF, mitral regurg.

52
Q

What do ACE Inhibitors delay?

A

Delay progression of diabetic renal disease

53
Q

Why do ACE Inhibitors need to be held before anesthesia?

A

Common to hold these agents 12-24 hrs before surgery due to profound hypotension following induction

54
Q

Profound hypotension from ACE Inhibitors associated with anesthesia can be treated with?

A

May be responsive to crystalloids, catecholamine or vasopressin administration

55
Q

What are examples of ACE inhibitors?

A
  • Benazepril (Lotensin)
  • Captopril
  • Enalapril (Vasotec)
  • Fosinopril
  • Lisinopril (Prinivil, Zestril)
  • Moexipril
  • Perindopril
  • Quinapril (Accupril)
  • Ramipril (Altace)
  • Trandolapril
56
Q

What is the MOA of Angiotensin II Receptor Blockers (ARB’s)?

A

Block the vasoconstrictive effects of angiotensin II without blocking ACE activity

57
Q

Angiotensin II Receptor Blockers (ARB’s): Similar anti-HTN and treatment regimen as __________

A

ACE inhibitors

58
Q

What is differ with Angiotensin II Receptor Blockers (ARB’s) then with ACE inhibitors?

A

Differ mainly from ACE inhibitors as they do not cause the troublesome cough (since ACE activity not affected, bradykinin is broken down)

59
Q

What is a postop side effect commonly associated with Angiotensin II Receptor Blockers (ARB’s)?

A

Hypotension following surgery similar concern and need to hold preop

60
Q

What are examples of Angiotensin II Receptor Blockers (ARB’s)?

A
  • Azilsartan (Edarbi)
  • Candesartan (Atacand)
  • Eprosartan.
  • Irbesartan (Avapro)
  • Losartan (Cozaar)
  • Olmesartan (Benicar)
  • Telmisartan (Micardis)
  • Valsartan (Diovan)
61
Q

What is the MOA of Calcium Channel Blocking Drugs ?

A

Inhibit calcium influx through voltage-sensitive L-type calcium channels in vascular smooth muscle causing vasodilation

62
Q

What are the two classes of Calcium Channel Blocking Drugs?

A

Dihydropyridine class & Nondihydropyridine class

63
Q

What are examples of Dihydropyridine class of Calcium Channel Blocking Drugs?

A

potent vasodilators (nifedipine, amlodipine, nicardipine, clevidipine)

64
Q

What are examples of Nondihydropyridine class of Calcium Channel Blocking Drugs?

A

verapamil and diltiazem

65
Q

What are the effects of verapamil and diltiazem?

A

less potent vasodilators, both have negative inotropic & chronotropic activity

66
Q

What are the clinical indications of verapamil and diltiazem?

A

antihypertensive and antiarrhythmic activity

67
Q

What is the clinical use of Nicardipine & clevidipine?

A

available as continuous IV infusions for tx of HTN emergencies

68
Q

What are the components of Nicardipine & clevidipine infusions?

A
  • both can be rapidly titrated
  • short half lives
69
Q

What impact is seen with Nicardipine and liver issues?

A
  • hepatic metabolism
  • prolonged half-life & elevated plasma concentrations in pts w/hepatic impairment
70
Q

What is the metabolism of clevidipine?

A

metabolized by plasma esterases to inactive metabolites

71
Q

What is the effect of Clevidipine with hepatic or renal dysfunction?

A

dosing doesn’t have to be adjusted in hepatic or renal dysfunction

72
Q

What is true about Clevidipine?

A

deemed a potent & safe alternative to existing parenteral vasodilators

73
Q

What are the adverse effects of Clevidipine and nicardipine?

A

reflex tachycardia, negative inotropy (as do other CCBs within dihydropyridine class)

74
Q

What Clevidipine and nicardipine inhibit?

A

•Inhibit hypoxic pulmonary vasoconstriction (HPV) – as do other potent vasodilators

75
Q

Clevidipine visually looks like _________

A

Clevidipine

76
Q

When is clevidipine contraindicated? What can this precipitate?

A

relatively contraindicated in severe aortic stenosis d/t lowered coronary perfusion pressure which precipitates myocardial ischemia

77
Q

What are phosphodiesterases (PDEs)?

A

enzymes which mediate the breakdown of intracellular cAMP & cGMP which regulate intracellular calcium

78
Q

What does inhibition of PDE cause?

A

causes vascular smooth muscle relaxation

79
Q

What are the effects of PDE3 inhibition?

A
  • positive inotropy d/t intracellular calcium mobilization
  • combined inotropic & vasodilator actions
80
Q

What is the clinical use of PDE3 inhibitors?

A

tx of heart failure in ICU & OR settings: amrinone, milrinone

81
Q

What are PDE5 inhibitors?

A

sildenafil, tadalafil, vardenafil

82
Q

What is the clinical uses of PDE5 inhibitors?

A

tx pulmonary HTN & erectile dysfunction

83
Q

What is the available forms of PDE5 inhibitors?

A

PO forms

84
Q

What happens when PDE inhibitors are combined with vasofilators?

A

When combined with other vasodilators can be significant BP lowering agents

85
Q

What has been associated with PDE inhibitors and anesthesia?

A
  • Reports of blindness/visual changes after anesthesia
  • Could be related that the ophthalmic and central retinal arteries have an autoregulation of their own blood flow without any autonomic nerve supply
86
Q

What can sildenafil increase?

A

sildenafil also increases IOP