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S5 - Anesthesia Pharm II - Test 2 > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Main concern of antihypertensives + anesthesia is due to interference with which system?

A

Interference with SNS activity
Resulting in orthostatic hypotension, or exaggerated hypotension

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2
Q

What are reasons for hypotension during anesthesia that may be exaggerated when patient has taken an antihypertensive

A
  • Hypovolemia
  • Position change
  • Decreased venous return related to positive pressure ventilation
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3
Q

Which catecholamine may be depleted when a surgical patient is on antihypertensives?

A

Norepinephrine

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4
Q

How might a patient taking antihypertensives respond to indirect sympathomimetics like ephedrine?

A

Minimal response due to depletion of norepinephrine

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5
Q

Which drugs may a surgical patient on antihypertensives have an exaggerated response to? Why?

A

Direct sympathomimetics, due to no counter balancing of beta2

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6
Q

Why were antihypertensives always withheld before surgery before the mid 1970’s

A

Due to their myocardial depressant nature
The drugs then caused severe perioperative lability

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7
Q

What do we know now about patients with HTN taking beta-blockers prior to surgery?

A

May improve outcomes of patients with hypertension

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8
Q

Antihypertensives should be taken the morning of surgery except for what drugs?

A

Diuretics

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9
Q

Benefits of taking most antihypertensives the morning of surgery?

A

Fewer alterations in BP and HR
Fewer arrhythmias

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10
Q

Beta-blockers effect on HR and contractility

A

Negative chronotropic and inotropic effect

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11
Q

What receptors does Labetalol work on?

A

Combined alpha1 and beta adrenergic blcoker

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12
Q

Effect of Labetalol on HR, contractility, and vessel tone

A

Negative inotropic and chronotropic
Vasodilation

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13
Q

Which is more potent?
Labetalol vs beta-blockers or phentolamine

A

Beta-blockers or phentolamine

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14
Q

Two Alpha1 adrenergic blocking drugs
How do they reduce blood pressure?

A

Prazosin and phentolamine
Vasodilation

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15
Q

Two centrally acting alpha2 adrenergic agonists
How do they decrease blood pressure?

A

Clonidine and dexmedetomidine
Decrease sympathetic outflow

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16
Q

Neurogenic control of vasomotor tone through SNS

A

Cortex–> hypothalamus –> vasomotor center –> sympathetic ganglia –> adrenergic nerves –> adrenergic receptors (alpha1 and beta 2) –> calcium channels

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17
Q

Neurogenic control of vasomotor tone through PNS

A

Cortex –> hypothalamus –> PNS ganglia –> cholinergic receptors –> endothelium –> EDRF (NO)

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18
Q

Where do diuretics work in the body?

A

Kidney tubules and vascular smooth muscle

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19
Q

Where do ACE-inhibitors work in the body?

A

Kidney tubules, angiotensin receptors on vessels, and adrenal medulla

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20
Q

Where do beta-blockers work in the body?

A

B-adrenoreceptors on heart and juxtaglomerular cells that release renin

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21
Q

How do ACE inhibitors work?

A

Inhibit ACE in plasma and vascular endothelium to block conversion of angiotensin I to angiotensin II

Prevents vasoconstriction effect of angiotensin II and stimulation of SNS

Also causes decreased aldosterone

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22
Q

What effect do ACE inhibitors have on aldosterone?
What are the effects?

A
  • Decreased aldosterone
  • Causes decreased Na and water retention
  • Increased potassium retention
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23
Q

Advantage of ACE inhibitors vs beta blockers and diuretics

A

minimal side effects

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24
Q

Indications of ACE inhibitors

A
  • Hypertension in diabetes
  • CHF
  • Mitral regurg (F, F, V)
  • Development of CHF (regression of LVH)
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25
Q

In which patients are ACE-inhibitors contraindicated?

A
  • Renal artery stenosis
  • their renal perfusion is highly dependent on angiotensin II
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26
Q

Where is angiotensin I converted to angiotensin II?

A

Lungs

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27
Q

There is great controversy on whether to continue your ACE inhibitor the morning of surgery. If you patient does, what should you absolutely be prepared for during their surgery?

A

They will become hypotensive

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28
Q

Most common side effects of ACE-inhibitors
What causes these?

A
  • Cough, upper respiratory congestion, rhinorrhea allergic symptoms
  • Potentiation of kinins and inhibition of breakdown of bradykinins
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29
Q

Two potentially life-threatening side effects of ACE-inhibitors

A

Angioedema and hyperkalemia

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30
Q

How to treat angioedema with ACE-inhibitors

A
  • Epinephrine 0.3-0.5 ml of 1:1,000 dilution (assuming this is IM?)
  • FFP: 2-4 units to replace deficient enzyme
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31
Q

What causes hyperkalemia with ACE inhibitors?
Who is it more common in?

A

Decreased production of aldosterone
More common in CHF with Renal insufficiency

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32
Q

2 ACE-inhibitors

Which is available IV route?

A
  • Captopril (Capoten)
  • Enalapril (Vasotec) - IV option
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33
Q

Which ACE-inhibitor is available IV?

IV dose?

A

Enalapril (Vasotec)

0.625- 1.25 mg

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34
Q

Angiotensin receptor blocking drug

What drugs are these simlar to?

A

Losartan (Cozaar)

Similar to ACE-inhibitors

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35
Q

Compare onset and duration of Captopril (capoten) and enalapril (vasotec)

A

Captopril has faster onset and shorter duration than enalapril

Captopril: Onset 15 mins and duration 6-10 hours

Enalapril: Onset 1 hour and duration 18-30 hours

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36
Q

Between the two ACE-inhibitors discussed, which one does not cause rash and pruritis side effect and rarely causes angioedema?

A

Enalapril

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37
Q

Effects of captopril on CO, SVR, HR, and electrolytes

A
  • Decreased SVR (especially in renal)
  • CO and HR not effected
  • Baroreceptor sensitivity is reduced so you do not see increased HR with decreased BP
  • May cause hyperkalemia due to blocking of aldosterone release
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38
Q

MOA of losartan (cozaar)

A

Blocks binding of angiotensin II to receptors

Type AT1- found in vascular smooth muscle to prevent vasoconstriction and aldosterone release

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39
Q

What drug showed 25% in stroke risk reduction when compared with atenolol

A

Losartan (Cozaar)

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40
Q

Entresto is a combination of what two drug classes

A

ARB + neprilysin inhibitor

*also can combine losartan (cozaar) with a thiazide diuretic

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41
Q

3 classifications of calcium channel blockers

A
  1. phenylalkylamines
  2. 1,4 dihydropyridines
  3. benzothiazepines
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42
Q

MOA of phenylalkylamines

Name the drug in this class

A

MOA: occludes the calcium channel

Verapamil

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43
Q

MOA of dihydropyridines

Name the 3 drugs in this class

A

Act on arterial vascular smooth muscle cells to cause vasodilation

Nifedipine, nicardipine, nimodipine

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44
Q

MOA of benzothiazepines

Drug in this class

A

Blocks calcium channels in AV node

Diltiazem (cardizem)

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45
Q

General MOA of Calcium channel blockers

A

Bind to alpha1 subunit of slow L-type calcium ion channels to block Calcium from entering cardiac and vascular smooth muscle cells (particularly in arteries

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46
Q

Two main effects of reduction of calcium in heart and nodal tissue

A
  1. Fails to activate myosin which reduces contraction
  2. Slows depolarization of SA and AV nodal tissue
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47
Q

Effects of ca++ channel blockers on HR, contractility, nodal tissue, vessels

A

Negative inotropic and chronotropic

Decreased SA node activity and slowed conduction through AV node

Vasodilation and deceased BP

Relaxes coronary artery vasospasm (in complement to nitrates)

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48
Q

4 main uses of calcium channel blockers

A
  1. Coronary artery vasospasm
  2. Unstable angina pectoris
  3. Chronic stable angina
  4. Essential hypertension
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49
Q

Which class of calcium channel blcoker carries increased risk?

“Almost too potent” as TC says

What are the increased risks?

A

Dihydropyrimidine derivatives (nifidepine)

Increased risks:

  • CV complications (hypotension, strokes, MI)
  • Perioperative bleeding, GI hemorrhage
  • Development of cancer (compared to beta-blockers, ACE-Is)

Anyone know if this just applies to nifedipine or all 3 of them?

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50
Q

Verapamil is a deriverate of ________

A

Papaverine

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51
Q

How does verapamil affect contractility, HR, conduction, and vasculature?

A
  • Decreased contractility
  • Decreased HR
  • Decreased conduction through AV node
  • Relaxation of vascular smooth muscle, coronary arteries
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52
Q

Uses of Verapamil

A

Treatment of SVT and HTN

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53
Q

metabolism of Verapamil for IV and PO forms

Elimination 1/2 life

A

IV: 70% renal, 15% bile

Oral: nearly complete hepatic

6-10 hours

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54
Q

Effect of combining verapamil and volatiles

A

Additive myocardial depressant and vasodilation effects, even in normal LV function

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55
Q

which drug vasodilates coronary and peripheral arteries even better than verapamil?

A

Nifedipine

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56
Q

Effects of nifedepine on vessels, BP, contractility

A

Vasodilation of coronary and peripheral arteries

Decreased BP

Directly decreased contractility, chronotropic, and dromotropic effects

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57
Q

Explain effects of nifedipine on HR

A

Directly decreases chronotopic (HR)

However, indirectly may cause baroreceptor mediated increase in HR that may outweigh direct decrease

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58
Q

Metabolism of nifedipine

Elimination half life

A

Hepatic

2-5 hours

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59
Q

Uses of nifedipine

A
  • Angina
  • Especially coronary artery vasospasm
  • Hypertension emergencies
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60
Q

Contraindications/caution/reasons to stop nifedepine

A
  • Severe hypotension (duh?)
  • MI
  • Cerebrovascular ischemia
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61
Q

Side effects of nifedipine

A
  • Flushing
  • Headache
  • Vertigo
  • Hypotension
  • may cause renal dysfunction
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62
Q

What can occur from abrupt discontinuation of nifedipine

Soooo should you take it the day of surgery?

A

Coronary artery vasospasm

TC says take it the morning of surgery because that would be bad during surgery

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63
Q

Which Calcium channel blocker has the greatest vasodilating effects, especially on coronary arteries?

Does this drug affect conduction?

A

Nicardipine (Cardene)- selective arterial vasodilator

Does not effect SA or AV node and has minimal myocardial depressant effects

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64
Q

Which Calcium channel blocker is incompatible with LR?

A

Cardene

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65
Q

Concentration and dose of cardene

A

25 mg in 240 ml solution (0.1 mg/ml)

Start at 5 mg/hr (50 ml/hr) and titrate by 2.5 mg/hr every 5-15 mins to a max of 15 mg/hr

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66
Q

3rd generation dihydropyride

Fast or slow onset?

Bolus or titratable?

A

Clevidipine (cleviprex)

Rapid onset

Titrable

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67
Q

Which calcium channel blocker is a lipid emulsion?

What is the max dose and why is it important to know?

A

Clevidipine (cleviprex)

Max dose is 32 mg/hr because of risk of increased triglycerides

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68
Q

Which calcium channel blocker would be useful in patient with severe organ dysfunction? Why?

A

Clevedipine

Because it is metabolized by plasma and tissue esterases independent of organs

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69
Q

Calcium channel blocker used to treat vasospasms related to subarachnoid hemorrhage

What unique property allows this

A

Nimodipine (Nimotop)

Highly lipid soluble allows it to cross BBB

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70
Q

Potential adverse effect of Nimodipine if intracranial compliance is a concern

A

Increase in ICP can occur due to vasodilation

71
Q

Is nimodipine short term or long term use?

Dosage forms available

A

Short term use (~21 days)

PO form only makes it a realy pain in the butt apparently

72
Q

Which calcium channel blocker is given more for conduction issues?

how does it work?

A

Diltiazem

Blocks calcium channels in the AV node

73
Q

Uses of diltiazem

A

SVT, angina pectoris

74
Q

Dose of diltiazem

Elimination of diltiazem

A

Dose 0.25 mg/kg IV over 2 mins

May repeat in 15 mins if needed

Elimination: 60% in bile and 35% in urine

75
Q

Which calcium channel blocker may be used to decrease HR significantly for off-pump CABG?

A

Diltiazem

76
Q

Name some drugs that may interact with calcium channel blockers

A
  • Volatiles
  • NMB
  • Local anesthetics
  • Potassium replacement
  • dantrolene (with verapamil)
  • Digoxin
77
Q

Reaction between Calcium channel blockers and volatiles

A

Additive myocardial depression, especially with pre-existing LV dysfunction

78
Q

Calcium channel blockers effect on NMB

Why?

What drug is this similar to?

A

Potentiates/ prolongs both depolarizing and non-depolarizine NMB

Calcium ions are needed to release acetylcholine at the NMJ

similar to mycin antibiotics

79
Q

Why do calcium channel blockers increase risk of LAST?

A

Inhibition of NA ion movement via Na channels

80
Q

How do Ca channel blockers increase risk of hyperkalemia with K replacement?

A

Inhibition of K moving into cell

81
Q

Potential adverse effect of combining verapamil + dantrolene

A

hyperkalemia

82
Q

Effect of calcium channel blockers on digoxin

A

Increased digoxin plasma concentration

Decreases its clearance

83
Q

Uses for vasodilators

A
  • hypertension
  • induce controlled hypotension
  • encourage LV stroke volume
84
Q

effects of vasodilators

A
  • decreased BP
  • decrease SVR
  • decrease VR and CO
85
Q

How do nitrovasodilators work?

A

Cause both pulmonary and systemic vasodilation by producing nitric oxide

More specifically, nitric oxide increases intracellular cGMP causing smooth muscle relaxation resulting in decreased intracellular calcium

Similar to effect of cAMP from beta2 stimulation

86
Q

How can nitric cause pulmonary vasoconstriction specifically

A

can be inhaled in the gaseous state

87
Q

Effect of essential hypertention on endogenous nitric oxide

A

Decreased NO release

88
Q

Effect of septic shock on endogenous NO

A

Excessive NO release

89
Q

Effect of atherosclerosis on endogenous NO

A

Decreased NO causing platelet aggregation and vasoconstriction

90
Q

Effect of cirrhosis on endogenous NO

A

Excessive production of NO

Responsible for hyperdynamic state (decreased SVR, increased CO)

91
Q

CV effects of NO

A
  • Release from NO from endothelial cells due to shear stress and pulsatile arterial flow
  • Regulates baseline SVR and PVR
  • Impacts distribution of CO
  • Autoregulation- increased NO production with decreased oxygenation
92
Q

Which produces more NO, arteries or veins?

Impact?

A

Arteries

This is why the IMA remains patent longer than saphenous vein grafts

93
Q

Pulmonary effects of NO

A

Bronchodilation

Selective dilation of vessels to ventilated alveoli

94
Q

Platelet effects of NO

A

inhibits platelet activation, aggregation, and adhesion (antithrombotic)

95
Q

Nervous systom effects of NO

A

Neurotransmitter in the brain, spinal cord, and peripheral nervous system

  • may be involved in antinociception and anesthetic effects
96
Q

GI effects of NO

A

Produces relaxation of smooth muscle in the GI tract

97
Q

Immune response of NO

A

Produced in response to activation of macrophages

  • Can damage bacteria, fungi, and protozoa
98
Q

Anesthetic effects of NO

A
  • NO involved in excitatory neurotransmission
  • Anesthetics suppress formation of NO to decrease excitatory neurotransmission and enhance GABA inhibitor effects
  • NO synthase inhibitors have dose-dependent reduction in MAC
99
Q

What populations is NO approved for use?

A

Neonates- has decreased use of ECMO

Use in adults is off label

100
Q

Nipride is a direct acting vasodilator

Does it dilate arterial, venous or both?

A

Both

101
Q

Onset and duration of nitroprusside

Considerations?

A

Rapid onset (60-90 seconds)

Short duration

Requires infusion and titration

Needs to be on pump (not roller clamp) and patient needs art line

102
Q

Dose of Nitroprusside

Max dose

A

0.25-1 mcg/kg/min up to 5 mcg/kg/min

BUT Max infusion dose is 2 mcg/kg/min to prevent cyanide toxicity??

103
Q

MOA of nitroprusside

A

Reacts with hemoglobin to form methemoglobin and release cyanide and NO which causes vasodilation

104
Q

Why can nitroprusside cause cyanide toxicity?

A

Nipride is 44% cyanide

During metabolism five cyanide ions are released

105
Q

Who is more susceptible to cyanide toxicity

A
  • Infusion dose >2 mcg/kg/min
  • Children or young adults due to baroreceptor reflexes causing SNS stimulation requiring larger dose
  • In pregnancy, fetus is more at risk
  • If the drug is not protected from light, it can breakdown into cyanide
106
Q

How long is nitroprusside safe for when protected from light?

A

24 hours

107
Q

S/S of cyanide toxicity

A
  • Tissue anoxia
  • Anaerobic metabolism
  • Lactic acidosis
  • Unresponsive to previously therapeutic doses
  • Increased MvO2 due to inability of tissues to use O2
  • CNS dysfunction, seizures
108
Q

Treatment for cyanide toxicity

A
  • Stop infusion
  • 100% O2
  • May need to use a different anti-hypertensive
  • Sodium bicarb to correct acidosis
  • Sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate
109
Q

Nipride is a coronary artery vasodilator

In a good or bad way?

A

BAD- Can cause coronary steal

Potential for preferential blood flow to bigger vessels

110
Q

CV effects of nitroprusside

A
  • Direct arterial and venous dilation
  • Decreased BP, SVR
  • Indirect increase in HR and contractility (reflex)
  • May have increased CO due to heart pumping agianst lower afterload
  • Coronary artery vasodilation (steal)
  • Decrease in diastolic blood pressure
111
Q

CNS effects of nitroprusside

A
  • Increased CBF and CBV
  • If decreased compliance can dangerously increase ICP
112
Q

With nitroprusside, when are ICP increases maximal

When are they maintained normal

A

Maximal ICP increase if MAP decreases <30%

Maintained if MAP decreases >30%

113
Q

How to prevent increase in ICP with nipride/SNP

A

Influse slowly to lower BP over 5 minutes

Along with hyperoxia and hypocarbia

Also could just wait until dura is open

114
Q

Contraindications to nitroprusside

A

Increased ICP and inadequate CBF

Patients with carotid artery stenosis

115
Q

Pulmonary effects of nitroprusside

How to treat

A
  • Decrease in PaO2
  • Alteration of hypoxic pulmonary vasoconstriction
  • More of an issue in healthy lungs than COPD patients (develop vascular changes to prevent)

Treatment: add PEEP

116
Q

What dose of nipride can inhibit platelet aggregation?

Is it clinically significant?

A

Dose >3 mcg/kg/min

Not clinically significant

117
Q

Which drug used for deliberate hypotension is most likely to maintain cerebral perfusion?

(not 100% sure this is what this means but we will go with it)

A

Nitroprusside

118
Q

Why is nitroprusside good for hypertensive emergencies?

A
  • effective no matter the cause so good for inital temporary treatment until you can figure something else out
  • Onset, titration, and offset are all quick
119
Q

Use of nitroprusside in cardiac diseases

A
  • MR
  • AR
  • CHF
  • MI with LV failure (but may combine with inotrope)
120
Q

use of nitroprusside in aortic surgery

A
  • to treat HTN related to cross-clamping

SOS idk what this means but- may cause spinal cord ischemia related to distal hypotenion and something about the artery of adamkiewicz

121
Q

Use of nitroprusside at the end of cardiac surgery

A
  • Used in the rewarming period to caue vasodilation to distribute warmth to periphery
  • To treat pulmonary HTN after valve replacement
122
Q

Nitroglycerine vasodilates

Arteries, veins, both?

A

Venous > arterial

  • only vasodilates arterial at elevated doses
123
Q

MOA of nitroglycerine

A
  • Produces NO which causes peripheral vasodilation
124
Q

Routes of nitroglycerine

A

IV, sublingual, transdermal

Sublingual- onset 4 minutes

Transdermal - sustained protection from MI

125
Q

Special considerations with nitroglycerine infusion

A

Requires special tubing and glass bottles to prevent absorption into plastic

126
Q

Elimination 1/2 life of nitroglycerine

A

1.5 minutes

So requires infusion

127
Q

AE of nitroglycerine

A

May cause production of methemoglobin when the nitrite metabolite oxidizes the ferrous ion in hemoglobin

128
Q

Treatment of methemoglobinemia with nitroglycerine

A
  • Methylene blue 1-2 mg/kg IV over 5 minutes to convert back to hemoglobin
129
Q

At what dose of nitroglycerine can arterial vasodilation occur

A

>2 mcg/kg/min

130
Q

Which is more potent, nipride or nitroglycerine?

A

Nipride

131
Q

Effects of nitroglycerin on vessels

A
  • Venous dilation (and arterial >2 mcg/kg/min)
  • Decreased venous return, LVEDP, RVEDP
  • Dilates larger conductance vessels of coronary circulaiton
  • Relaxes pulmonary vessels
132
Q

Does nitroglycerine cause coronary steal?

A

No

Provides better flow to ischemic areas

133
Q

Smooth muscle effects of nitroglycerine

A
  • Relaxes bronchial smooth muscle
  • Relaxes biliary tract smooth muscles (sphincter of Oddi)
  • Relaxes esophageal muscles
  • Relaxes uterine and ureteral smooth muscle
134
Q

Which is more likely to cause increased ICP, nitroglycerine or nipride?

A

More likely with nipride but both can cause

135
Q

Effect of nitroglycerine on platelet

A

inhibits aggregation

136
Q

Clinical uses of nitroglycerine

A
  • Angina pectoris
  • Cardiac failure
  • Acute hypertension
  • Deliberate hypotension
137
Q

Effect of nitroglycerine on angina

A
  • Decrease CMRO2 and vasodilates coronary arteries to ischemic areas

Decreases size of MI

138
Q

Effect of nitroglycerine on cardiac failure

A
  • Decrease preload and relieve pulmonary edema
139
Q

Consideration with use of nitroglycerine for acute hypertension in pregnant mom

A

Better for maternal patient during C-section with no effects on fetus

140
Q

Use of nitroglycerine for deliberate hypotension compared to SNP

A

Less potent than SNP

Less decrease in DBP than SNP

Decrease is more related to intravascular volume

141
Q

Uses of isosorbide dinitrate

A
  • Prophylaxis of angina pectoris (chronic)
  • Prolonged antianginal effect
  • Increases exercise tolerance up to 6 hours
142
Q

Vasodilation with isosorbide dinitrate

arteries, veins, or both?

A

Venous > arterial

143
Q

Does isosorbide dinitrate cause steal?

A

No, redirects blood flow to ischemic areas

144
Q

Isosorbide is given to what patients preop

A

CABG

TC says maybe to vasodilate their saphenous but she doesnt really know ?

145
Q

Vasodilation with hydralazine

Arterial, venous, or both?

A

Arterial > venous

Dilates coronary, cerebral, renal, splanchnic, and pulmonary vessels

146
Q

MOA of hydralazine

A

Interference with calcium ion transport

147
Q

Hydralazine effect on BP, HR, SV, and CO

Possible adverse effect

A

Decreases diastolic more than systolic (so not good for coronary perfusion)

Increases HR both directly and baroreceptor mediated

Increases SV and CO

Can cause MI, prevent with Beta-blocker

148
Q

Onset and duration of hydralazine

A
  • 10 -20 minutes (TC says be patient)
  • Duration 2-4 hours but very unpredictable
149
Q

Hydralazine metabolism

A

Mostly hepatic

150
Q

Side effects of hydralazine

(more with chronic use)

A
  • Lupus like autoimmune syndrome
  • Peripheral neuropathies
  • Vertigo
  • Diaphoresis
  • Nausea
  • Tachycardia - uncommon
151
Q

What may offset benefit of decreased BP with trimethorphan

A

Increased HR

152
Q

Effects of trimethorphan

A
  • Ganglion blocker- blocks ANS reflexes
  • Vasodilation of venous capacitance vessels
  • Decreases CO, SVR
  • Blocks receptors for acetylcholine
153
Q

What is adenosine and what is its role?

A

An endogenous nucleotide in all cells

Maintains balance of oxygen supply and demand of heart and all other organs

154
Q

Effects of adenosine

A
  • Dilation of coronary arteries
  • Negative chronotropic
155
Q

MOA of adenosine

A

Stimulation of K channels in supraventricular cells to hyperpolarize atrial cells and slow SA node

Can also stimulate release of NO from endothelial cells

156
Q

Uses of adenosine

A
  • SVT and narrow complex tachycardia (not a fib or v tac)
  • Deliberate hypotension
157
Q

Dose and elimination 1/2 life of adenosine

A

6 mg IV, 12 mg, then 18 (some say repeat 12 mg dose)

Can repeat within 60 seconds

1/2 life 0.6-1.5 seconds

158
Q

Adenosine for deliberate hypotension

Why is it good?

General effects

A

Rapid responsiveness, onset and recovery (must be used as infusion)

Decreases SVR, increases HR, coronary flowincreased, cardiac filling pressures unchanged

220 mcg/kg/min

159
Q

Does adenosine cause coronary steal?

A

Yes

160
Q

Dose of adenosine for deliberate hypotension

Tachyphylaxis?

A

220 mcg/kg/min

No tachypylaxis

161
Q

Effects of adenosine 1 receptor activation

A
  • Slowing of rhythm
  • Negative inotropic
  • Vasoconstriction
  • Bronchoconstriction
  • Sedation
  • Anticonvulsant
  • Decreased neurotransmitter release
162
Q

Effect of Adenosine 2 receptor activation

A
  • vasodilation
  • Bronchodilation
  • Complex stimulant effects
  • Increased neurotransmitter release
  • Platelet aggregation inhibition
163
Q

Effect of nitroglycerine on CO

A
  • CO decreased in normal heart with no CHF
  • CO improved if patient in HF, and pulmonary congestion is relieved
164
Q

Effect of nitroglycerine on BP

A
  • Decreased BP (related more to volume than SNP)
  • Decreased DBP, decreased coronary blood flow
165
Q

Effect of nitroglycerine on HR and contractility

A
  • Baroreceptor reflex tachycardia
  • Increased ionotropic
166
Q

anesthesia challenges for pts with untreated HTN

A

likely to be vasoconstricted, volume depleted, autoregulation shifted higher

167
Q

AEs of Nipride

(table 9-1)

A
  • hypotension
  • N/V
  • apprehension
  • increased cyanide tox with sucky kidneys
168
Q

AEs of labetolol

(table 9-1)

A
  • hypotension
  • heart block
  • heart failure
  • bronchospasm
  • N/V
  • scalp tingling
  • paradoxical pressor response
169
Q

AEs of nitroglycerin

(table 9-1)

A
  • headache
  • N/V
  • beta tolerance with prolonged use (?)
170
Q

AEs of phentolamine

(table 9-1)

A
  • hypotension
  • tachycardia
  • headache
  • angina
  • paradoxical pressor response
171
Q

AEs of hydralazine for treatment of eclampsia

(table 9-1)

A
  • hypotension
  • fetal distress
  • tachycardia
  • headache
  • N/V
  • local thrombophlebitis
172
Q

AEs of nicardipine

(table 9-1)

A
  • hypotension
  • headache
  • N/V
173
Q

to summarize table 9-1:

all the anti hypertensives can cause hypotension (shocker), N/V, and headache

A

:)

S5 - Anesthesia Pharm II - Test 2 (7 decks)

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