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KLowe Pharm 2 > Lecture 2-Antihypertensives, Negative Inotropes, Negative Chronotropes > Flashcards

Lecture 2-Antihypertensives, Negative Inotropes, Negative Chronotropes Flashcards

1
Q

This type of hypertension is related to overactivity of the ANS and an interaction with the renin-angiotensin system, along with factors related to sodium homeostasis and intravascular volume

A

Idiopathic hypertension

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2
Q

Primary cause of perioperative hypertension is increased ___ (sympathetic/parasympathetic) discharge with systemic vaso___

A

Increased sympathetic discharge with systemic vasoconstriction

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3
Q

Potential complications related to perioperative hypertension include CVA, MI, ischemia, LV dysfunction, arrhythmias, increased suture tension, hemorrhage, pulmonary edema, cognitive dysfunction—T/F?

A

True

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4
Q

Vasodilators are classified according to their predominate effect on the circulation—arterial dilators reduce ___

A

Afterload

Most vasodilators are arterial vasodilators

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5
Q

Vasodilators are classified according to their predominate effect on the circulation—venodilators reduce ___

A

Preload

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6
Q

Vasodilators act primarily to cause systemic vasodilation—T/F?

A

True

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7
Q

Pure arteriole dilators cause minimal effect on preload—T/F?

A

True—arteriole dilators affect afterload

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8
Q

“Pure” venodilators are not available—T/F?

A

True—NTG acts primarily on the venous circulation but also affects arterioles

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9
Q

Balanced vasodilators (i.e.: SNP) decrease afterload and preload—T/F?

A

True

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10
Q

Hemodynamic effects of vasodilators—reflex increase in ___

A

Heart rate—baroreceptors pick up on vasodilation in the periphery, resulting in a reflex tachycardia

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11
Q

Hemodynamic effects of vasodilators—redistribution of ___ blood flow; NTG may improve ___ circulation; other vasodilators may cause coronary ___

A

Coronary blood flow; NTG may improve collateral circulation; other vasodilators may cause coronary steal

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12
Q

What is coronary steal?

A

Stealing blood flow away from ischemic areas, making coronary artery disease/ischemia even worse. Can occur with use of vasodilators

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13
Q

70-90% of coronary artery perfusion to the LV occurs during ___ (systole/diastole)

A

Diastole

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14
Q

Aortic ___ (systolic/diastolic) pressure governs perfusion

A

Aortic diastolic pressure

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15
Q

In the presence of ischemic heart disease, collateral arteries are maximally dilated and coronary perfusion is largely pressure dependent—T/F?

A

True

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16
Q

Beta blockers/calcium channel blockers reduce myocardial oxygen demand and improve myocardial oxygen use—T/F?

A

True

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17
Q

What is this phenomenon?—narrowed coronary arteries are always maximally dilated to compensate for the decreased blood supply; dilating the other arterioles causes blood to be shunted away from the coronary vessels

A

Coronary steal

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18
Q

Vasodilators and coronary perfusion pressure—in the myocardium, ___ (what vasodilator?) dilates both epicardial conductance and intramyocardial resistance vessels; in the presence of CAD, this vasodilator shunts blood away from ischemic zones

A

SNP—sodium nitroprusside

This increases coronary steal and makes ischemia even worse

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19
Q

Vasodilators and coronary perfusion pressure—___ (what vasodilator?) preferentially dilates conductance vessels and directs more blood toward ischemic zones

A

NTG

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20
Q

(3) vasodilator medications that we use:

A
  • Hydralazine
  • Nitroglycerine (NTG)
  • Sodium nitroprusside (SNP)
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21
Q

Hydralazine is a direct acting ___ (arterial/venous) vasodilator; it alters ___ metabolism and movement

A

Arterial vasodilator; it alters calcium metabolism and movement

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22
Q

Hydralazine ___ (increases/decreases) HR, contractility, renin activity, fluid retention, CO, and SV

A

Increases

Reflex tachycardia results from drops in BP

Stimulates the RAAS system as pressures begin to drop, leading to increased renin activity/fluid retention

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23
Q

Hydralazine ___ (increases/decreases) BP—it decreases ___ BP more than ___ BP; ___ (increases/decreases) SVR

A

Decreases BP—it decreases diastolic BP more than systolic BP; decreases SVR

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24
Q

Hydralazine acts on a specific receptor—T/F?

A

False—does not act on a specific receptor

Hydralazine acts through a second messenger pathway with cyclic GMP as the second messenger protein; results in an increase in cyclic GMP which reduces afterload (arterial vasodilator)

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25
Q

Hydralazine ___ (increases/decreases) myocardial oxygen demand, leading to ischemia

A

Increases myocardial oxygen demand

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26
Q

Hydralazine should be avoided in patients with ___, increased ___, and ___…why?

A

CAD, increased ICP, and lupus

Avoid in CAD because Hydralazine can cause reflex tachycardia, resulting in ischemia

Avoid with increased ICP d/t fluid shifts (stimulates RAAS system, leading to increased renin/fluid retention)

Avoid in lupus—interesting side effect with lupus—will see positive ANA [antinuclear antibody] titers in 5-10% of patients treated with Hydralazine; patients won’t get butterfly rash or organ damage but will get arthralgias and painful components of lupus from hydralazine

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27
Q

Hydralazine CNS side effects—___ache, ___ness, ___ from increased ICP

A

Headache, dizziness, tremor from increased ICP

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28
Q

Hydralazine CV side effects—___tations, ___ina, ___cardia, ___ from vasodilation

A

Palpitations, angina, tachycardia, flushing from vasodilation

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29
Q

Hydralazine GI side effects—___xia, ___/___, ___ pain, paralytic ___

A

Anorexia, nausea/vomiting, abdominal pain, paralytic ileus

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30
Q

Hydralazine other side effects—___ia, ___osis, ___ congestion, muscle ___, ___ from activation of RAAS system

A

Anemia, agranulocytosis, nasal congestion, muscle cramps, edema from activation of RAAS system

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31
Q

Hydralazine pharmacokinetics—onset ___ mins (IV and PO); peak ___-___ mins (IV and PO); duration ___-___ hours (PO), ___-___ hours (IV); half life ___-___ hours (IV and PO); metabolized in ___, excreted by ___; highly ___ bound

A

Onset 30-60 mins (IV and PO); peak 30-60 mins (IV and PO); duration 4-6 hours (PO), 2-6 hours (IV); half life 3-7 hours (IV and PO); metabolized in liver, excreted by kidney; highly protein bound

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32
Q

Hydralazine is good for acute BP management—T/F?

A

False—not good for acute BP management because it takes ~30 mins to kick in, peak effect in 60 mins

Pros = lasts longer

Cons = tachycardia and fluid shifts

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33
Q

Nitroglycerine causes a release of ___ for ___ (specific/non-specific) relaxation of vascular smooth muscle

A

Causes a release of nitric oxide for non-specific relaxation of vascular smooth muscle

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34
Q

Nitroglycerine dilates ___ > ___

A

Veins > arteries

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35
Q

Nitroglycerine ___ (increases/decreases) PVR, venous return, and myocardial oxygen consumption

A

Decreases

Venous dilation = decreased venous return, reducing preload

Decreased venous return = pooling of blood/edema in lower extremities

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36
Q

Nitroglycerine relaxes ___ vessels and relieves ___ spasms

A

Relaxes coronary vessels and relieves coronary spasms

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37
Q

What is an advantage of using nitroglycerine?

A

It preferentially shifts blood flow to areas that need it—don’t have coronary steal like you do with SNP

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38
Q

NTG non-cardiac effects—dilates ___ vessels (caution in patients with increased ___); decreased ___ blood flow with decreased BP; dilates ___ vessels and reduces ___ vascular resistance

A

Dilates meningeal vessels (caution in patients with increased ICP); decreased renal blood flow with decreased BP; dilates pulmonary vessels and reduces pulmonary vascular resistance

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39
Q

Pharmacokinetics of NTG—onset ___ min; duration ___-___ min; half life ___-___ min

A

Onset 1 min; duration 3-5 min; half life 1-4 min

Much faster onset than hydralazine, much shorter duration

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40
Q

Nitroglycerine/SNP are good for acute BP management, unlike hydralazine—T/F?

A

True

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41
Q

Metabolism of NTG—metabolized by ___ in the ___

A

Glutathione nitrate reductase in the liver

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42
Q

Metabolism of NTG—nitrite ion oxidizes ___ to ___

A

Hemoglobin to methemoglobin

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43
Q

What is a risk of using nitroglycerin in patients at risk for developing anemia? (i.e.: patients with CKD or CLD)

A

If you have a patient at risk for developing anemia (i.e.: patients with CKD or CLD), the more the methemoglobin builds up from NTG metabolism into nitrite ions, the less O2 delivery and higher risk for ischemia

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44
Q

Tolerance with NTG—tolerance in ___ (arterial/venous) vessels can occur with chronic NTG administration

A

Tolerance in arterial vessels can occur with chronic NTG administration, but not in the venous vessels

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45
Q

Tachyphylaxis can occur with NTG over time—T/F?

A

True—can start to lose effect in arterial vessels

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46
Q

NTG CNS side effects—___ache, appre___, ___ vision, ___go, ___ness, ___ness

A

Headache, apprehension, blurred vision, vertigo, dizziness, faintness

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47
Q

NTG CV side effects—___ hypotension d/t vaso___ and ___ of blood in the periphery, ___tations, ___ (increased/decreased) heart rate, ___cope

A

Postural hypotension d/t vasodilation and pooling of blood in the periphery, palpitations, increased heart rate, syncope

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48
Q

NTG GI side effects—___/___, ___ pain, ___ mouth

A

Nausea/vomiting, abdominal pain, dry mouth

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49
Q

NTG other side effects—___hemoglobinemia, ___ from vasodilation, ___, ana___, ___ and ___ edema (potentially d/t fluid shifts)

A

Methemoglobinemia, flushing from vasodilation, rash, anaphylaxis, oral and conjunctival edema (potentially d/t fluid shifts)

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50
Q

Warnings/contraindications with NTG—___ inhibitors; ___ glaucoma; ___ trauma, cerebral ___; severe ___; ___tension

A

PDE5 inhibitors (used to treat erectile dysfunction/pulmonary HTN); narrow angle glaucoma; head trauma, cerebral hemorrhage; severe anemia; hypotension

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51
Q

If you give NTG with PDE5 inhibitors, it can lead to fatal ___

A

Fatal hypotension

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52
Q

Advantages of NTG—___ (rapid/slow) onset; ___ (short/long) duration; coronary vaso___; ___ (increased/decreased) myocardial O2 consumption; no major ___; no coronary ___; reduced ___ vascular resistance

A

Rapid onset; short duration; coronary vasodilation; decreased myocardial O2 consumption; no major toxicities; no coronary steal; reduced pulmonary vascular resistance

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53
Q

Disadvantages of NTG—decreased ___ (systolic/diastolic) BP; reflex ___cardia; possible ___tension; variable efficacy; ___phylaxis

A

Decreased diastolic BP; reflex tachycardia; possible hypotension; variable efficacy; tachyphylaxis

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54
Q

Within 3-5 days of NTG use—___hemoglobinemia; intrapulmonary ___; prolonged ___ time

A

Methemoglobinemia; intrapulmonary shunting; prolonged bleeding time

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55
Q

NTG is best used to treat ___

A

Emergent HTN—fast onset, short duration, and easy to titrate

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56
Q

SNP directly vasodilates ___ and ___

A

Arteries and veins

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57
Q

SNP ___ (increases/decreases) BP with slight ___ (increase/decrease) in HR; ___ (increases/decreases) cerebral blood flow and ICP; ___ (increases/decreases/maintains) renal blood flow; ___ (increases/decreases) myocardial O2 demand

A

SNP decreases BP with slight increase in HR; increases cerebral blood flow and ICP; maintains renal blood flow, slight reduction; decreases myocardial O2 demand

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58
Q

What occurs with abrupt discontinuation of SNP?—___cardia and ___tension

A

Reflex tachycardia and hypertension

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59
Q

SNP pharmacokinetics—onset less than ___; peak ___-___ min; duration ___-___ min; half life ___ to ___ days

A

Onset less than 1 min; peak 2-3 min; duration 5-10 min; half life 2.7 to 7 days

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60
Q

Even though SNP has a much longer half life than NTG, the risk of toxicity is low because it doesn’t actually exert its effects for a full 7 days—T/F?

A

True

Half life of NTG = 1-4 min

Half life of SNP = 2.7 to 7 days

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61
Q

SNP CNS side effects—___lessness, appre___, muscle ___, ___ache, ___ness

A

Restlessness, apprehension, muscle twitching, headache, dizziness

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62
Q

SNP CV side effects—profound ___tension, ___tations, fluctuations in ___, ___ discomfort

A

Profound hypotension, palpitations, fluctuations in heart rate, retrosternal discomfort

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63
Q

SNP GI side effects—___/___, ___ pain

A

Nausea/vomiting, abdominal pain

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64
Q

SNP other side effects—nasal ___; ___ (increased/decreased) serum creatinine with ___/___ doses; ___/___ toxicity that can lead to ___ via ___

A

Nasal stuffiness, increased serum creatinine with higher/longer doses; thiocyanate/cyanide toxicity that can lead to end organ damage via hypoxia

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65
Q

SNP warnings/contraindications—congenital optic ___; ___volemia; compensatory ___tension (i.e.: AV shunting, aortic coarctation); ___ (increased/decreased) ICP; severe ___/___ impairment

A

Congenital optic atrophy; hypovolemia; compensatory hypertension (i.e.: AV shunting, aortic coarctation); increased ICP; severe renal/hepatic impairment

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66
Q

Why should SNP be avoided in severe renal/hepatic impairment?

A

Because you need the liver to breakdown cyanide (byproduct of SNP)

Thiocyanate is a byproduct of cyanide metabolism and is broken down by the kidneys

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67
Q

Thiocyanate/cyanide toxicity presentation—___tension; ___ vision; ___gue; metabolic ___osis; ___ skin; absence of ___; ___ heart sounds

A

Hypotension; blurred vision; fatigue; metabolic acidosis; pink skin; absence of reflexes; faint heart sounds

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68
Q

Risk of thiocyanate/cyanide toxicity increases with doses over ___mcg/kg/min, > ___ days of therapy

A

Doses over 4 mcg/kg/min, > 2 days of therapy

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69
Q

Thiocyanate levels—therapeutic = ___-___ mcg/ml; toxic = ___-___ mcg/ml; fatal > ___ mcg/ml

A

Therapeutic = 6-29 mcg/ml

Toxic = 35-100 mcg/ml

Fatal > 200 mcg/ml

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70
Q

Cyanide levels—normal is < ___ mcg/ml, < ___ mcg/ml for smokers; toxic > ___ mcg/ml; fatal > ___ mcg/ml

A

Normal is < 0.2 mcg/ml, < 0.4 mcg/ml for smokers

Toxic > 2 mcg/ml

Fatal > 3 mcg/ml

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71
Q

Thiocyanate/cyanide toxicity—what happens? ___ binds to hemoglobin very quickly; iron in hemoglobin cannot bind to ___ when cyanide is bound; patients can die of ___ dysfunction because they are ___ and no ___ exchange is occurring

A

Cyanide binds to hemoglobin very quickly; iron in hemoglobin cannot bind to oxygen when cyanide is bound; patients can die of multiorgan dysfunction because they are hypoxic and no oxygen exchange is occurring

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72
Q

What is one distinct feature in patients with thiocyanate/cyanide toxicity?

A

Can smell almonds on patient’s breath

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73
Q

SNP—treatment of cyanide toxicity—___ infusion; administer ___; correct ___

A

Stop SNP infusion; administer 100% oxygen; correct metabolic acidosis

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74
Q

SNP—treatment of cyanide toxicity—sodium thiosulfate donates a ___ group to remove ___/___ molecules from hemoglobin so that hemoglobin can bind to ___

A

Sodium thiosulfate donates a sulfate group to remove thiocyanate/cyanide molecules from hemoglobin (they will bind to the sulfate instead) so that hemoglobin can bind to oxygen

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75
Q

SNP—treatment of cyanide toxicity—hydroxocobalamin is a precursor to vitamin ___; binds ___ molecules

A

Precursor to vitamin B12; binds cyanide molecules

Can consider Vitamin B12 for treatment of cyanide toxicity as well

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76
Q

SNP—treatment of cyanide toxicity—3% sodium nitrite has become a medication of last resort because it causes ___ and can worsen ___

A

Has become a medication of last resort because it causes anemia and can worsen ischemia

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77
Q

SNP advantages—___ onset, ___ (short/long) duration, ___ (increased/decreased) myocardial O2 demand

A

Immediate onset, short duration, decreased myocardial O2 demand

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78
Q

SNP disadvantages—reflex ___cardia; ___ toxicity; intrapulmonary ___; precipitous drop in ___ is possible; ___degradation; ___hemoglobinemia; coronary ___; enhanced ___; cerebral vaso___

A

Reflex tachycardia; cyanide toxicity; intrapulmonary shunting; precipitous drop in BP is possible; photodegradation; methemoglobinemia; coronary steal; enhanced bleeding; cerebral vasodilator

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79
Q

Always use ___ for CAD patients, not ___

A

NTG for CAD patients, not SNP

Because NTG does not cause coronary steal and SNP does, which further worsens ischemia

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80
Q

Alpha 1 receptor activation—increases intracellular ___; smooth muscle ___ (contraction/relaxation); peripheral vaso___; broncho___; ___ (inhibits/stimulates) insulin secretion; ___ (inhibits/stimulates) glycogenolysis and gluconeogenesis; ___ (mydriasis/miosis); GI ___ (contraction/relaxation)

A

Increases intracellular calcium; smooth muscle contraction; peripheral vasoconstriction; bronchoconstriction; inhibits insulin secretion; stimulates glycogenolysis and gluconeogenesis; mydriasis; GI relaxation

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81
Q

Alpha 2 receptor activation ___ (stimulates/inhibits) neuronal firing in the CNS and peripheral NS; results in ___tension, ___cardia, ___ation, ___gesia

A

Inhibits neuronal firing in the CNS and peripheral NS; results in hypotension, bradycardia, sedation, analgesia

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82
Q

Alpha 2 receptor activation—effects on other organs—___ (increased/decreased) salivation and secretions; ___ (increased/decreased) GI motility; ___ (stimulates/inhibits) renin release; ___ (increases/decreases) GFR; ___ (increases/decreases) sodium and water secretion; ___ (increased/decreased) insulin release

A

Decreased salivation and secretions; decreased GI motility; inhibits renin release; increases GFR; increases sodium and water secretion; decreased insulin release

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83
Q

Phenoxybenzamine (Dibenzyline) is a ___

A

Nonselective alpha antagonist—it irreversibly binds to alpha 1 and alpha 2 receptors

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84
Q

Main use of phenoxybenzamine (dibenzyline)—long-term preoperative treatment to control the effects of ___

A

Pheochromocytoma

“Chemical sympathectomy”

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85
Q

Other uses of phenoxybenzamine (dibenzyline)—relieve ischemia in ___; ___ to improve flow

A

Relieve ischemia in PVD; BPH to improve flow (was used before flomax, rapaflo, and hytrin came around)

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86
Q

Effects of phenoxybenzamine (dibenzyline)—reduced ___ to reduced ___; secondary increases in ___ due to ___ blockade can increase ___ and ___

A

Reduced peripheral vascular resistance (PVR) to reduced BP; secondary increases in NE due to alpha 2 blockade can increase HR and CO (beta 1 effects)

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87
Q

Phenoxybenzamine (dibenzyline) does not cross the BBB—T/F?

A

False—crosses the BBB

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88
Q

Phenoxybenzamine (dibenzyline) CNS side effects—___ation, ___ssion, ___ness, ___gy, ___ache

A

Sedation, depression, tiredness, lethargy, headache

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89
Q

Phenoxybenzamine (dibenzyline) GI side effects—___/___

A

Nausea/vomiting

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90
Q

Phenoxybenzamine (dibenzyline) CV side effects—___tension, ___cardia, ___mias

A

Postural hypotension, tachycardia, arrhythmias

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91
Q

Phenoxybenzamine (dibenzyline) pharmacokinetics—half life ___ hours; duration of action ___ days; route of administration ___

A

Half life 24 hours; duration of action 4 days; route of administration PO

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92
Q

May see up regulation of alpha receptors with phenoxybenzamine (dibenzyline)—T/F?

A

True—because it is a nonselective alpha antagonist—blocks alpha 1 and alpha 2 receptors

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93
Q

Phentolamine is a ___

A

Nonselective alpha antagonist—blocks alpha 1 and alpha 2 receptors just like phenoxybenzamine

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94
Q

Phentolamine uses—hypertension secondary to ___; ___ withdrawal hypertension; ___ dysfunction; ___ of catecholamines

A

Hypertension secondary to pheochromocytoma; clonidine withdrawal hypertension; erectile dysfunction; extravasation of catecholamines

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95
Q

Phentolamine pharmacokinetics—half life ___ minutes; onset ___-___ minutes IM, ___ IV

A

Half life 19 minutes; onset 15-20 minutes IM, immediate IV

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96
Q

Oral alpha 1 antagonists are ___ (selective/non-selective)

A

Selective

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97
Q

Alpha 1 antagonists end in -___

A

-zosin or -osin

Examples = prazosin (minipres); terazosin (hytrin); doxazosin (cardura); tamsulosin (flomax); silodosin (rapaflo); afluzosin (uroxatral)

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98
Q

What did Cochrane review demonstrate about the use of Alpha 2 agonists and risk of cardiac complications after surgery?

A

Alpha 2 agonists had no effect on reducing cardiac complications after surgery—specifically, they had no effect on overall mortality, cardiac mortality, and prevention of MI

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99
Q

Alpha 2 agonists and cardiac complications—monitor patients for excessive ___ and ___

A

Excessive hypotension and bradycardia

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100
Q

Clonidine is a ___ (central/peripheral) acting alpha-___ ___ that leads to inhibition of ___ (sympathetic/parasympathetic) outflow

A

Clonidine is a central acting alpha-2 agonist that leads to inhibition of sympathetic outflow

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101
Q

Clonidine affinity for alpha 2 over alpha 1 receptors is ___:___

A

220:1

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102
Q

Clonidine ___ (increases/decreases) the release of sympathetic neurotransmitters, ___ (stimulates/inhibits) renin release

A

Decreases the release of sympathetic neurotransmitters, inhibits renin release

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103
Q

Clonidine can be administered orally and by patch, as well as by IV, intrathecal, and epidural—T/F?

A

True

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104
Q

Clonidine actions/effects—___ (increases/decreases) HR, BP, CO, and SVR

A

Decreases

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105
Q

Baroreceptor reflexes are preserved in patients on clonidine—T/F?

A

True

106
Q

Abrupt cessation of clonidine may lead to rebound ___

A

Rebound hypertension

Clonidine blocks NE from binding to alpha 2 receptors, so there is an upregulation of alpha receptors; with abrupt discontinuation, there is a risk for accelerated HTN, because all of the NE that was blocked now binds to the upregulated receptors—can push systolic pressures into the 200s

107
Q

If patient has been on clonidine for 6 days or more, abrupt discontinuation will cause accelerated HTN—T/F?

A

True

108
Q

Clonidine withdrawal occurs with ___ discontinuation; due to ___; manifestations include excessive ___tension, ___cardia, ___lessness, ___mnia, ___ache, ___ea

A

Abrupt discontinuation; due to NE; manifestations include excessive hypertension, tachycardia, restlessness, insomnia, headache, nausea

109
Q

Patients are at risk for clonidine withdrawal if they have taken clonidine for at least 6 days—T/F?

A

True

110
Q

Clonidine pharmacokinetics—rapidly and completely absorbed from PO dosing with peak in ___-___ minutes; patch takes about ___ days to reach full potential; half life ___-___ hours

A

Peak in 60-90 minutes; patch takes about 2 days to reach full potential; half life 9-12 hours

111
Q

Clonidine side effects—___siness, ___ness, ___ mouth, ___stasis

A

Drowsiness, dizziness, dry mouth, orthostasis

112
Q

Caution using clonidine in patients with severe ___ insufficiency, ___ disturbances, recent ___/___, ___

A

Severe coronary insufficiency, conduction disturbances, recent MI/CVA, CKD

Because clonidine decreases HR, BP, CO, and SVR

113
Q

It is recommended to give clonidine via epidural route for the perioperative period—T/F?

A

False—not recommended

114
Q

Clonidine effects on anesthesia—___ (increases/decreases) propofol and thiopental requirements; can be used as an alternative to ___ for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia; supplement to ___

A

Decreases propofol and thiopental requirements; can be used as an alternative to nitrous for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia; supplement to regional blocks

115
Q

Dexmedetomidine (precedex) is a relatively ___ (selective/non-selective) alpha-___ ___ used for continuous IV ___ in the ICU

A

Relatively selective alpha-2 agonist used for continuous IV sedation in the ICU (package insert says it should be used as a continuous infusion for < 24 hours)

116
Q

Precedex affinity for alpha 2 over alpha 1 receptors = ___:___

A

1620:1

117
Q

Precedex maintains ___ stability in intubated or extubated patients; patients are ___ and ___ when stimulated; sedation resembles natural ___

A

Precedex maintains respiratory stability in intubated or extubated patients; patients are arousable and alert when stimulated; sedation resembles natural sleep

118
Q

Precedex may be useful for ___ sedation, i.e.: sedation for awake ___ intubation, during ___ anesthesia or other procedures

A

Procedural sedation, i.e.: sedation for awake fiberoptic intubation, during regional anesthesia or other procedures

119
Q

Precedex allows patients to maintain ___ respirations; sedation is more like natural ___; has some ___ effects, no ___ effects

A

Maintain spontaneous respirations; sedation is more like natural sleep; has some analgesic effects, no amnesic effects

120
Q

Precedex is safe for use by nonanesthesia providers—T/F?

A

True

121
Q

There are no studies regarding the safety of precedex use in children—T/F?

A

True

122
Q

Precedex may reduce post-op opiate use by as much as ___ and can be used to reduce post-op ___

A

By as much as half and can be used to reduce post-op shivering

123
Q

Precedex adverse effects—___/___, ___, ___ia

A

Nausea/vomiting, fever, hypoxia

124
Q

Precedex BOLUS adverse effects—___tension, ___cardia

A

Hypertension, bradycardia

125
Q

Clinically significant bradycardia and sinus arrest has been seen in young, healthy volunteers with high vagal tone when bolused with precedex—T/F?

A

True

126
Q

Precedex INFUSION adverse effects—___tension

A

Hypotension

127
Q

Safety precautions for precedex—exercise caution in patients with advanced heart ___ or severe ___ dysfunction; significant ___cardia and sinus ___ are possible, especially with high vagal tone or rapid bolus

A

Exercise caution in patients with advanced heart block or severe ventricular dysfunction; significant bradycardia and sinus arrest are possible, especially with high vagal tone or rapid bolus

128
Q

Less than 1% of patients have respiratory adverse events with continuous precedex infusion—T/F?

A

True

129
Q

As per the package insert, do not give precedex > 24 hours continuous infusion—T/F?

A

True

130
Q

Methyldopa (aldomet) is initially thought to act as a false transmitter in the periphery (alpha-methyl-NE)—T/F?

A

True

131
Q

Alpha-methyl-NE (methyldopa/aldomet) is almost as potent as NE—T/F?

A

True

132
Q

In the CNS, methyldopa (aldomet) is further metabolized to alpha-methyl___

A

Alpha-methylepinephrine

133
Q

Alpha-methylepinephrine (metabolite of methyldopa) acts at alpha-___ receptors to decrease ___ outflow

A

Acts at alpha-2 receptors to decrease sympathetic outflow

134
Q

Methyldopa is used to treat ___

A

Hypertension during pregnancy, usually third trimester

135
Q

RAAS review

A
  • Renin is released by the kidneys in response to low BP/decreased renal perfusion
  • Angiotensinogen released by the liver converts renin into angiotensin I
  • ACE (angiotensin converting enzyme) released by the lungs converts angiotensin I to angiotensin II
  • Angiotensin II is a potent vasoconstrictor—increases BP
  • Angiotensin II stimulates the adrenal cortex to release aldosterone, which results in sodium/water retention, H+/K+ excretion
  • Angiotensin II stimulates the pituitary gland to release ADH—increases water reabsorption
136
Q

Angiotensin II participates in cardiac remodeling; it slows down cardiomegaly/ischemia that occurs from longstanding CV disease—T/F?

A

True

137
Q

ACE inhibitors are predominantly ___ (arterial/venous) vasodilators

A

Arterial vasodilators

138
Q

ACE inhibitors treat CHF and MR by ___ (preload/afterload) reduction; are used post-___; have improved outcomes in ___

A

Treat CHF and MR by afterload reduction; are used post-MI; have improved outcomes in DM

139
Q

ACE inhibitors are the antihypertensive of choice for patients with ___

A

Chronic illnesses

140
Q

ACE inhibitors effect on renal function—biphasic effect depending on baseline BP—if patient is baseline ___tensive, decreased renal vascular resistance improves RBF and GFR

A

If patient is baseline hypertensive, decreased renal vascular resistance improves RBF and GFR

141
Q

ACE inhibitors effect on renal function—biphasic effect depending on baseline BP—if patient is baseline ___tensive, if BP is decreased, renal function may deteriorate because compensatory efferent arteriolar constriction mediated by angiotensin II is blocked and decreased glomerular filtration pressure and GFR may result in acute hyperkalemia

A

If patient is baseline hypotensive…

142
Q

ACE inhibitors should be avoided in patients with significant ___ dysfunction or renal artery ___

A

Should be avoided in patients with significant renal dysfunction or renal artery stenosis

143
Q

Constriction of the efferent arteriole is mediated by ___; with ACE inhibitors, the kidney can’t regulate its own blood flow via constriction of the ___ arteriole; this leads to further vaso___/___perfusion of the kidney and massive reduction in ___

A

Angiotensin II; with ACE inhibitors, the kidney can’t regulate its own blood flow via constriction of the efferent arteriole; this leads to further vasodilation/hypoperfusion of the kidney and massive reduction in GFR

144
Q

ACE inhibitors end in -___

A

-pril

145
Q

ACE inhibitors—enalaprilat (vasotec) IV—defer or avoid if there is ___ or ___ postoperatively

A

Hemodynamic instability or renal insufficiency postoperatively

146
Q

Respiratory side effects of ACE inhibitors—___, ___, and ___ are most common side effects; ___ is a serious side effect; ___kalemia, ___mias

A

Cough, congestion, and rhinorrhea are most common side effects; angioedema is a serious side effect; hyperkalemia, arrhythmias

147
Q

It is not safe to d/c ACE inhibitors without tapering—T/F?

A

False—it is safe to d/c without taper

CHF, bronchospasm, hypokalemia, hyponatremia, and rebound hypertension NOT seen with abrupt withdrawal

148
Q

Angioedema from ACE inhibitors can lead to ___ compromise

A

Airway compromise

149
Q

Caution using ACE inhibitors in ___ failure and ___kalemia; these effects are reversible with withdrawal of the drug

A

Acute renal failure and hyperkalemia

150
Q

ACEI ___ (have/have not) demonstrated fetal morbidity and mortality

A

Have

151
Q

It is safe to use ACEIs during pregnancy—T/F?

A

False—do NOT use at all during pregnancy

152
Q

ACE inhibitors and perioperative issues—prolonged ___tension can occur in patients being treated with ACE inhibitors and undergoing general anesthesia

A

Prolonged hypotension

153
Q

Risk of ___ in the intra- and postoperative periods in patients on ACEIs or ARBs; ___tension and ___volemia seem to contribute to this risk

A

Risk of acute renal failure in the intra- and postoperative periods in patients on ACEIs or ARBs; hypotension and hypovolemia seem to contribute to this risk

154
Q

What should patients on ACEIs or ARBs do the day of surgery?

A

Hold medication on the day of surgery

155
Q

Preop ACEIs in CABG patients may contribute to significant reduction in glomerular perfusion pressure and postop acute renal failure; the risk is especially high if large blood or fluid shifts occur—T/F?

A

True

156
Q

There is loss of the compensatory mechanism of constriction of the efferent arteriole in people taking ACE inhibitors; acute renal failure can occur with hypotension because they don’t have this compensatory mechanism available—T/F?

A

True

157
Q

Toronto 2011 study on ACE inhibitors

A

Found no difference between taking ACEI vs. holding it before surgery; patients on ACEI had lower 30 day mortality post procedure

158
Q

Roshanov et al Anesthesiology 2017 study on ACE inhibitors

A

Holding ACEIs/ARBs the morning of surgery reduced death/stroke/myocardial injury by 18% and hypotension by 20%

159
Q

Hollmann et al Anesth Analg. 2018 study on ACE inhibitors

A

No difference if withheld the day of surgery; higher rates of hypotension in those who continued the medication, but no significant increase in mortality found

160
Q

ACC and AHA recommend ___ (continuing/not continuing) for major non-cardiovascular surgery; ___ (continue/do not continue) for cardiovascular surgery

A

Recommend continuing ACEIs for major non-cardiovascular surgery; do not continue for cardiovascular surgery

161
Q

ACEIs have increased hypotensive effects with ___, ___, and ___

A

Diuretics, vasodilators, and anesthetics

162
Q

ACEIs + NSAIDs/ASA interaction—reduce anti___ effect, increased risk of ___kalemia and ___ failure

A

Reduce antihypertensive effect, increased risk of hyperkalemia and acute renal failure

163
Q

For patients on ACEIs, check fluids for ___ (what electrolyte?)

A

Potassium

164
Q

Angiotensin II receptor antagonists end in -___

A

-sartan

I.e.: losartan (cozaar), irbesartan (avapro)

165
Q

Angiotensin II receptor antagonists have the same hemodynamic effects and uses as ___

A

ACEIs

166
Q

Angiotensin II receptor antagonists have ___ (more/less) cough/angioedema than ACEIs

A

Less

167
Q

Angiotensin II receptor antagonists are available ___

A

PO, no IV available yet

168
Q

Angiotensin II receptor antagonists have a similar side effect profile and considerations with anesthesia as ACEIs—T/F?

A

True

169
Q

Other RAS medications—aliskiren (tekturna) is a ___

A

Direct renin inhibitor

170
Q

Other RAS medications—sacubitril/valsartan (entresto); combination medication—sacubitril is a ___ inhibitor that reduces ___ peptide degradation; valsartan is an ___

A

Sacubitril is a neprilysin inhibitor that reduces natriuretic peptide degradation; valsartan is an angiotensin II receptor blocker (ARB)

171
Q

How do calcium channel blockers work?—they block ___ channels that move ___ into the cell; need this for ___/___; by blocking, less ___ = more ___

A

They block calcium channels that move calcium into the cell; need this for contraction/constriction; by blocking, less calcium = more relaxation

172
Q

Functions of calcium—signal transduction in the ___, ___; muscle contraction—___ muscle, ___ muscle, ___ walls; ___ health; ___ cascade

A

Signal transduction in the CNS, heart; muscle contraction—smooth muscle, cardiac muscle, vessel walls; bone health; clotting cascade

173
Q

Calcium channel blockers primary actions—negative ___ effect; negative ___ effect; vasodilation of ___, ___, ___, and ___ beds

A

Negative inotropic (force of contraction) effect

Negative dromotropic (speed of conduction in the AV node) effect (AV conduction block)

Vasodilation of systemic, splanchnic, coronary, and pulmonary beds

174
Q

Calcium channel blockers—dihydropyridines end in -___

A
  • dipine

i. e.: nifedipine (adalat/procardia); nicardipine (cardene); amlodipine (norvasc)

175
Q

Dihydropyridine CCBs are pure ___ (arterial/venous) vasodilators, but with minimal ___; they have minimal negative ___/___ effects

A

Pure arterial vasodilators, but with minimal reflex tachycardia (usually < 10 bpm); they have minimal negative inotropic/dromotropic effects

176
Q

Nicardipine is a potent vasodilator of ___, ___, and ___ circulations without important negative ___ or ___ effects

A

Potent vasodilator of systemic, coronary, and cerebral circulations without important negative inotropic or dromotropic effects

177
Q

Nicardipine is a/an ___ (arteriole/venous) specific vasodilator

A

Arteriole

178
Q

Nicardipine has no ___, which allows for favorable myocardial oxygen supply/demand

A

No coronary steal syndrome

179
Q

Nicardipine is useful for IV control of ___tension in the PACU or ICU

A

Hypertension

180
Q

Nicardipine has ___ (slower/faster) onset and offset than SNP; has ___ (more/less) swings in BP; no rebound ___ with withdrawal; reflex tachycardia is usually < ___ bpm; ___ (short/long) duration of action may be a benefit postop

A

Nicardipine has a slower onset and offset than SNP; has less swings in BP; no rebound hypertension with withdrawal; reflex tachycardia is usually < 10 bpm; long duration of action may be a benefit postop

181
Q

Advantages of nicardipine—dose dependent ___ (arterial/venous) vasodilation; ___ (does/does not) cause coronary steal; cerebral and coronary vaso___; minimal effects on ___/___; mild ___ effect

A

Dose dependent arterial vasodilation; does not cause coronary steal; cerebral and coronary vasodilation; minimal effects on contractility/conduction; mild natriuretic effect

182
Q

Disadvantages of nicardipine—may ___; ___ (predictable/variable) duration of action; ___tension; ___ irritation; may cause ___cardia

A

May accumulate; variable duration of action; hypotension; venous irritation; may cause tachycardia

183
Q

Clevidipine is an IV ___; ___pyridine; vasodilation reduces ___ vascular resistance; ___ (arteriole/venous) specific

A

IV calcium channel blocker; dihydropyridine; vasodilation reduces peripheral vascular resistance; arteriole specific

184
Q

Clevidipine is cleared much ___ (slower/faster) than nicardipine

A

Much faster than nicardipine—half life of 1 min

185
Q

Disadvantages of clevidipine—___ emulsion; contraindicated with ___ and ___ allergy, ___titis, and hyper___

A

Lipid emulsion; contraindicated with egg and soy bean allergy, pancreatitis, and hyperlipidemia

186
Q

Verapamil is part of the ___ class

A

Phenylalkylamine class

187
Q

Verapamil is a potent negative ___trope, ___trope, and vaso___

A

Potent negative inotrope, dromotrope, and vasodilator

188
Q

Verapamil is used for aortic ___; conversion of atrial re-entry ___arrhythmias; coronary artery ___

A

Verapamil is used for aortic stenosis; conversion of atrial re-entry tachyarrhythmias; coronary artery vasospasm (Prinzmetal angina)

189
Q

70% of verapamil is excreted via ___; 20-30% of verapamil is excreted via ___/___

A

70% of verapamil is excreted via urine; 20-30% of verapamil is excreted via bile/feces

190
Q

Diltiazem (cardizem) is part of the ___ class

A

Benzothiazine class

191
Q

Diltiazem (cardizem) is used as a ___ agent in a-fib/atrial tachycardia versus a ___ agent like verapamil

A

Diltiazem (cardizem) is used as a rate-control agent in a-fib/atrial tachycardia versus a conversion agent like verapamil

192
Q

Diltiazem drug interactions—CYP ___ (inhibitor/inducer)

A

Inhibitor

193
Q

Review of CCBs—which CCB is this describing?—potent negative inotrope and negative dromotrope; mild vasodilator; useful in the treatment of vasospastic angina and essential hypertension

A

Verapamil

194
Q

Review of CCBs—which CCB is this describing?—fits between verapamil (phenylakylamine) and dihydropyridines in action; less negative inotropic/dromotropic effects than verapamil but more than dihydropyridines; mild vasodilator like verapamil

A

Diltiazem

195
Q

Review of CCBs—which CCB is this describing?—virtually pure arterial vasodilator; lack clinically significant negative inotropic and dromotropic effects

A

Dihydropyridines—nifedipine, nicardipine, amlodipine

196
Q

CCBs—dihydropyridines may cause ___ from a reflex ___cardia d/t ___ (arterial/venous) vasodilation

A

May cause palpitations from a reflex tachycardia d/t arterial vasodilation

197
Q

CCBs—non-dihydropyridines may cause ___cardia

A

Bradycardia

198
Q

Which CCB mostly causes cough?

A

Nifedipine

199
Q

Verapamil and diltiazem ___ (enhance/worsen) myocardial oxygen balance by ___ reduction and/or negative ___tropic effect; they increase O2 delivery through coronary vaso___

A

Enhance myocardial oxygen balance by afterload reduction and/or negative inotropic effect; they increase O2 delivery through coronary vasodilation

200
Q

Dihydropyridine vasodilators may ___ (enhance/worsen) MvO2 (myocardial oxygen consumption) by causing diastolic ___tension and reflex ___cardia

A

Worsen MvO2 by causing diastolic hypotension and reflex tachycardia

201
Q

Which dihydropyridine does not cause reflex tachycardia to a great extent and thus does not worsen MvO2 as much as other dihydropyridine vasodilators?

A

Nicardipine

202
Q

CCBs ___ (increase/decrease) reperfusion injury after ischemia

A

Decrease

203
Q

CCBs effect on renal function—___ (increase/decrease) renal blood flow and GFR; induce a ___

A

Increase renal blood flow and GFR; induce a naturesis

204
Q

CCB benefits on renal function can be reversed if they cause hypotension because reflex catecholamine release and angiotensin activation lead to decreases in RBF and GFR—T/F?

A

True

205
Q

Overall, CCB effects on renal function are not significantly beneficial or detrimental—T/F?

A

True

206
Q

CCBs should be continued up to the time of surgery without risk of significant drug interactions—T/F?

A

True

207
Q

CCBs may potentiate the effects of ___ agents

A

Neuromuscular blocking agents

208
Q

CCBs block ___-type calcium channels in the CV system; by blocking this type of calcium channel, more NDNMB may bind to ___-type channels that affect ACh calcium mediated release (and thus prolonging the block)

A

L-type calcium channels in the CV system; by blocking this type of calcium channel, more NDNMB may bind to P-type channels that affect ACh calcium mediated release (and thus prolonging the block)

209
Q

CCBs—anesthetic considerations—they may enhance ___tensive, CV ___, vaso___ effects of anesthetics and analgesics

A

They may enhance hypotensive, CV depressant, vasodilating effects of anesthetics and analgesics

210
Q

Clevidipine reduces ___; what post-op issues can this cause?

A

Reduces gastric emptying—post-op can cause nausea/vomiting, aspiration

211
Q

Diltiazem can increase sedative effects of ___

A

Midazolam

212
Q

Beta receptor activation—beta-1 ___ (increases/decreases) HR, conduction velocity, myocardial contractility

A

Increases HR, conduction velocity, myocardial contractility

213
Q

Beta receptor activation—beta-2–stimulation leads to smooth muscle ___; peripheral vaso___; ___ (increases/decreases) BP; broncho___; ___ (increases/decreases) insulin secretion; ___ (increases/decreases) glycogenolysis, gluconeogenesis; ___ (increases/decreases) GI mobility

A

Smooth muscle relaxation; peripheral vasodilation; decreases BP; bronchodilation; increases insulin secretion; increases glycogenolysis, gluconeogenesis; decreases GI mobility

214
Q

Beta blockers ___ (increase/decrease) cardiac output; ___ (increase/decrease) renin release; ___ (do/do not) vasodilate

A

Decrease cardiac output (HR and contractility); decrease renin release; do NOT vasodilate

215
Q

Advantages of beta blockers over vasodilators—no reflex ___cardia or ___ of pulse pressure; improved ___ through decreased HR and contractility; intrinsic anti___ activity

A

No reflex tachycardia or widening of pulse pressure; improved MvO2 through decreased HR and contractility; intrinsic antiarrhythmic activity

216
Q

Pure beta blockers vasodilate—T/F?

A

False—pure beta blockers do NOT vasodilate

217
Q

Labetalol and carvedilol do not vasodilate—T/F?

A

False—they are alpha/beta blockers, so they do vasodilate

Pure beta blockers do NOT vasodilate

218
Q

Classifications of beta blockers—beta selectivity—beta-1 selective beta blockers (metoprolol, atenolol, acebutolol, bisoprolol, esmolol) ___ (increase/decrease) velocity of AV conduction, HR, contractility, renin release, and lipolysis

A

Decrease

219
Q

Classifications of beta blockers—beta selectivity—non-selective beta blockers (propranolol, nadolol, timolol, pindolol, carteolol) block both ___ and ___ receptors; action at beta-2 receptor causes broncho___, peripheral vaso___, and ___ (increased/decreased) glycogenolysis

A

Block both beta 1 and beta 2 receptors; action at beta-2 receptor causes bronchoconstriction, peripheral vasoconstriction, and decreased glycogenolysis

220
Q

What two beta blockers have combined alpha 1 and non selective beta effects?

A

Labetalol and carvedilol

221
Q

What two beta blockers are the top choices to treat cocaine OD or Clonidine withdrawal?

A

Labetalol and carvedilol because they provide both alpha and beta blockade

222
Q

Nadolol is a ___ (short/long)-acting; ___ (selective/nonselective); and is eliminated via the ___

A

Long-acting; nonselective; and is eliminated via the kidney

223
Q

Atenolol is a ___ (short/long)-acting; ___ (selective/nonselective); and is eliminated via the ___

A

Long-acting; selective; and is eliminated via the kidney

224
Q

Propranolol is a ___ (short/long/intermediate)-acting; ___ (selective/nonselective); and is eliminated via the ___

A

Is an intermediate-acting; nonselective; and is eliminated via the liver

225
Q

Metoprolol is a ___ (short/long/intermediate)-acting; ___ (selective/nonselective); and is eliminated via the ___

A

Intermediate acting; selective; and is eliminated via the liver

226
Q

Esmolol is an ___ (ultra short/long)-acting; ___ (selective/nonselective); and is eliminated via ___

A

Ultra short-acting; selective; and is eliminated via red cell esterases

227
Q

Atenolol and nadolol have a ___ (low/moderate/high) lipophilicity

A

Low lipophilicity

228
Q

Metoprolol, Coreg, and labetalol have a ___ (low/moderate/high) lipophilicity

A

Moderate lipophilicity

229
Q

Propranolol has a ___ (low/moderate/high) lipophilicity

A

High lipophilicity

230
Q

Adverse effects of beta blockers—non-selective beta blockers (i.e.: propranolol) can cause vaso___ and worsen ___; can also cause broncho___; caution using non-selective beta blockers in patients with ___

A

Can cause vasoconstriction and worsen PVD; can also cause bronchospasm; caution using non-selective beta blockers in patients with asthma

231
Q

Adverse effects of beta blockers—myocardial ___; decreased contractility could precipitate ___

A

Myocardial depression; decreased contractility could precipitate CHF

232
Q

Adverse effects of beta blockers—life-threatening ___cardia or ___

A

Bradycardia or asystole

233
Q

Adverse effects of beta blockers—___kalemia in patients with ___

A

Hyperkalemia in patients with renal failure

234
Q

Caution using beta blockers with ___ (decreased HR and contractility) and ___ (decreased HR and conduction)

A

Verapamil and digoxin

235
Q

Beta blocker overdose—treat with ___; may need ___, ___, and/or ___ infusion; patient may ultimately need ___

A

Treat with atropine; may need isoproterenol, dobutamine, and/or glucagon infusion; patient may ultimately need pacing

236
Q

Perioperative indications for beta blocker—control intra- and postoperative ___tension and ___cardia; ___ control and/or conversion of SVT, a-fib, and a-flutter; myocardial protection in ___ heart disease; peripheral manifestations of ___thyroidism

A

Control intra- and postoperative hypertension and tachycardia; rate control and/or conversion of SVT, a-fib, and a-flutter; myocardial protection in ischemic heart disease; peripheral manifestations of hyperthyroidism

237
Q

Which beta blocker is effective in limiting hypertension during induction and emergence?

A

Esmolol

238
Q

Contraindications to beta blockers—severe ___cardia; > ___ degree heart block; ___ shock; ___ disease

A

Severe bradycardia; > 1st degree heart block; cardiogenic shock; Raynaud’s disease

239
Q

Caution using nonselective beta blockers in patients with ___/___ because they increase the risk of broncho___

A

Asthma/COPD because they increase the risk of bronchospasm

240
Q

Caution using beta blockers in patients with ___ because they can mask symptoms of ___glycemia

A

In patients with diabetes because they can mask symptoms of hypoglycemia

241
Q

Caution using beta blockers in patients with ___ failure because they can make symptoms even worse

A

Heart failure

242
Q

Propranolol is a ___ (selective/non-selective) beta blocker; it is ___ soluble and can penetrate the ___; it is metabolized in the ___

A

Non-selective beta blocker; it is lipid soluble and can penetrate the CNS; it is metabolized in the liver

243
Q

Esmolol is a beta ___ selective agent; it can blunt the CV response to ___; can control ___ and ___; it is more likely than ___ to convert a-fib to sinus rhythm; can be used to treat intraop/postop ___tension and ___cardia

A

Esmolol is a beta 1 selective agent; it can blunt the CV response to intubation; can control SVT and a-fib; it is more likely than verapamil to convert a-fib to sinus rhythm; can be used to treat intraop/postop hypertension and tachycardia

244
Q

Esmolol has a ___ (slow/rapid) onset and offset; it is metabolized by ___

A

Rapid onset and offset; it is metabolized by red cell esterases

245
Q

Metoprolol is a beta ___ selective agent; approved for the treatment of ___ and acute ___

A

Beta 1 selective agent; approved for the treatment of angina and acute MI

246
Q

Labetalol combines weak alpha blockade with weak non-selective beta blockade—T/F?

A

True

247
Q

Labetalol beta:alpha ratio = ___:___

A

Beta:alpha ratio = 7:1 (5-10:1)

248
Q

Labetalol is a negative ___trope and ___trope with vaso___; it provides effective anti___tensive action

A

Negative inotrope and chronotrope with vasodilation; it provides effective antihypertensive action

249
Q

Labetalol indications—hyperdynamic ___tension—blunts CV response to ___; treatment of aortic ___; tachyphylaxis with ___; intracranial ___tension—does not increase ___

A

Hyperdynamic hypertension—blunts CV response to tracheal intubation; treatment of aortic dissection; tachyphylaxis with SNP; intracranial hypertension—does not increase ICP

250
Q

Beta blockers—negative inotropic effects and conduction delays are potentiated by many general anesthetics—T/F?

A

True

251
Q

Beta blockers should be continued preoperatively—T/F?

A

True

252
Q

Do not stop beta blockers abruptly d/t rebound ___tension and ___cardia

A

Rebound hypertension and tachycardia

253
Q

Beta blockers may mask ___glycemia and ___thyroidism

A

Hypoglycemia and hyperthyroidism

254
Q

Beta blocker overdose—give ___; ___; beta 1 ___; high dose euglycemic ___ therapy; intravenous ___ emulsion

A

Glucagon; atropine; beta 1 agonists; high dose euglycemic insulin therapy; intravenous lipid emulsion

255
Q

There is no data to support use of calcium and sodium bicarb for treatment of beta blocker overdose—T/F?

A

True

256
Q

What antihypertensive medication is favored to use in pregnant patients?

A

Alpha-methyldopa (aldimet)

257
Q

What beta blocker can be used in the 2nd and 3rd trimesters?

A

Labetalol

258
Q

Beta blockers are associated with growth retardation if given during the first trimester of pregnancy—T/F?

A

True

259
Q

What medication class has demonstrated fetal morbidity and mortality in all 3 trimesters?

A

ACE inhibitors

260
Q

Hydralazine may be used during delivery—T/F?

A

True

261
Q

Nifedipine can be used PO but not sublingual in pregnant patients—T/F?

A

True

262
Q

SNP is often used to treat hypertension in pregnancy—T/F?

A

False—rarely used in pregnancy

KLowe Pharm 2 (10 decks)

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