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Pharm 2 > Vasodilators, Negative Inotropes > Flashcards

Vasodilators, Negative Inotropes Flashcards

1
Q

What is the definition of idiopathic hypertension?

A

Related to overactivity of the ANS and an interaction with the RASS. Along with factors related to sodium homeostasis and intravascular volume.

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2
Q

In the development of idiopathic hypertension, what occurs first? and it leads to what?

A

First, SVR is normal, but CO increases which increases BP.

SVR increases eventually increases to stop high BP from being transmitted to the capillary bed where it would affect cell homeostasis.

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3
Q

What is the primary cause of perioperative hypertension?

A

Increased sympathetic discharge with systemic vasoconstriction

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4
Q

What are the 4 types of vasodilators?

A
  1. Direct smooth muscle dilation
  2. Alpha-1 Antagonists
  3. Alpha-2 Agonists
  4. A.C.E. Inhibitors
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5
Q

Afterload is improved by vasodilation of which vessels?

A

Arterial dilation

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6
Q

Preload is improved by vasodilation of which vessels?

A

Venous dilation

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7
Q

T/F: Pure venodilators are optimal in providing afterload reduction and pure arteriole dilators are not available?

A

False; Pure venodilators technically do not exist and arteriole dilation would cause reduction in afterload.

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8
Q

What other hemodynamic effects might be seen with vasodilator administration?

A
  1. Reflex increase in HR to maintain CO.

2. Redistribution of coronary blood flow (some improve, some cause coronary steal).

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9
Q

What percent of coronary artery perfusion occurs during systole?

A

10-20%. 70-90% occurs during diastole.

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10
Q

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

A

True

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11
Q

Describe coronary steal:

A

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.

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12
Q

What are three examples of direct vasodilators?

A
  1. Hydralazine
  2. Nitroglycerine
  3. Sodium Nitroprusside
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13
Q

What receptor does hydralazine stimulate?

A

Hydralazine Receptor

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14
Q

Once the hydralazine Receptor is activated, what happens?

A

It is G protein coupled and has 2nd messenger pathways which amplify the signal. GC (Guanilate Cyclase) changes GTP to cGMP.

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15
Q

What action does cGMP perform?

A

It blocks calcium absorption and slows down the influx of calcium which promotes relaxation.

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16
Q

What CV effects will be seen with hydralazine administration?

A
  1. Reflex increase in HR
  2. Renin activity- fluid retention
  3. Can even see peripheral edema
  4. Decreased BP and SVR
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17
Q

Will diastolic or systolic pressure be decreased more with hydralazine administration?

A

Diastolic>Systolic

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18
Q

Hydralazine may also cause hyperpolarization of smooth muscle cells by influx of what electrolyte?

A

Potassium.

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19
Q

Does hydralazine increase or decrease myocardial oxygen demand and why?

A

It increases and leads to ischemia d/t an increase in HR.

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20
Q

Which patients should hydralazine be avoided in?

A

CAD, increased ICP, Lupus

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21
Q

Side effects of hydralazine to be concerned with?

A

Anemia, agranulocytosis, nasal congestion, muscle cramps, edema, Hydralazine-Induced Lupus

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22
Q

What is the dose, onset, and duration of hydralazine?

A

10-20mg IV
Onset 30min
Duration 4-6hrs

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23
Q

Advantages of hydralazine?

A
  1. Maintains/increases cerebral blood flow

2. Increased CO and SV

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24
Q

Disadvantages of hydralazine?

A
  1. Reflex tachycardia
  2. Sodium/water retention
  3. Long duration of action
  4. Tachyphylaxis with monotherapy.
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25
Q

What is Sodium Nitroprusside broken down into?

A

1 Nitrous Oxide and 5 Cyanide molecules.

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26
Q

Ultimately, what are the effects of Nitroglycerine and Sodium Nitroprusside on smooth muscle?

A

Relaxation. This is achieved via Nitric Oxide promoting GC (guanilate cyclase) which converts GTP to cGMP

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27
Q

What effect dose nitroglycerine have on smooth muscle?

A

Causes release of Nitric Oxide which dilates primarily veins, but has some arterial dilation.

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28
Q

What CV effects can be seen with nitroglycerine administration?

A
  1. Decreased peripheral vascular resistance
  2. Decreases Venous return
  3. Decreased Myocardial oxygen consumption

(Overall, reduces workload of the heart).

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29
Q

What effect does NTG have on coronary vessels?

A

Relaxation of coronary vessels and relieves spasm (Pritzmetal angina).

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30
Q

What are the non-cardiac effects of NTG?

A
  1. Dilates minigeal vessesl (caution with inc ICP).
  2. Decreased RBF with dec BP
  3. Dilates pulmonary vessels.
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31
Q

What is dose, onset, and duration of NTG?

A

0.5mcg/kg/min, onset 1 min, duration 3-5

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32
Q

How is NTG metabolized?

A

By Glutathione Nitrate Reductase in the liver.

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33
Q

Nitrite Ion oxidizes Hgb into what?

A

Methemoglobin.

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34
Q

T/F: Tolerance in venous vessels occurs with chronic administration, but not in arterial vessels?

A

False; venous vessels do not, arterial vessel become tolerant.

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35
Q

5 contraindications for Nitroglycerine?

A
  1. PDE5 inhibitors
  2. Narrow angle glaucoma
  3. Head trauma, cerebral hemorrhage
  4. Severe anemia
  5. Hypotension.
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36
Q

What is the issue co-administration of NTG and PDE5 Inhibitors?

A

Severe hypotension (even death).

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37
Q

Advantages of NTG?

A
  1. Rapid onset and short duration
  2. Coronary dilation
  3. Dec. myocardial O2 consumption
  4. No major toxicities
  5. No coronary steal
  6. Reduced PVR
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38
Q

Disadvantages of NTG?

A
  1. Dec diastolic BP
  2. Reflex tachycardia
  3. Possibly HoTN
  4. Variable efficacy
  5. Tachyphylaxis
  6. Methemoglobinemia
  7. Intrapulmonary shunting
  8. Prolonged bleeding time
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39
Q

What vessels does Sodium Nitroprusside dilate?

A

Both arteries and veins

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40
Q

What can be seen with abrupt discontinuation of Sodium Nitroprusside?

A

Reflex tachycardia and hypertension

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41
Q

Is there an increase or decrease in myocardial O2 demand with SNP?

A

Overall reduction

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42
Q

What is the dose, onset, and duration of SNP?

A

Dose 0.5-10mcg/kg/min
Onset <1min
Duration 5-10min

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43
Q

Side effects of SNP?

A

Cyanide toxicity, increased serum creatinine

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44
Q

Contraindications of SNP?

A
  1. Congenital optic atrophy
  2. Hypovolemia
  3. Compensatory HTN (AV shunting, aortic coarctation)
  4. Inc ICP
  5. Severe renal/hepatic impairment
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45
Q

How does cyanide toxicity present? (7)

A
  1. Hypotension
  2. Blurred vision
  3. Fatigue
  4. Metabolic acidosis
  5. Pink skin
  6. Absence of reflexes
  7. Faint heart sounds

(breathe smells like almonds)

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46
Q

Do smokers have a higher or lower tolerance for cyanide levels?

A 
Higher tolerance (<0.4mcg/ml)
Non-smokers <0.2mcg/ml
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47
Q

What are two risk factors for cyanide toxicity with SNP administration?

A
  1. Doses over 4mcg/kg/min

2. >2 days of therapy

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48
Q

What is treatment of cyanide toxicity from SNP?

A
  1. Stop infusion
  2. Admin 100% oxygen
  3. Correct metabolic acidosis
  4. Admin 3% Sodium Nitrite IV
  5. Admin Sodium Thiosulfate
  6. Consider Vit B12 administration
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49
Q

Which two methods of administration are available for Sodium Thiosulfate?

A

Prophylaxis or treatment

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50
Q

SNP advantages:

A
  1. Immediate onset
  2. Short duration
  3. Reduced myocardial O2 demand
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51
Q

SNP disadvantages:

A 
Reflex tachycardia.
Cyanide toxicity.
Intrapulmonary shunting.
Precipitous drop in BP
Methemoglobinemia
Coronary steal.
Cerebral vasodilator
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52
Q

MOA of Alpha Antagonists?

A

Blocks alpha-1 receptor from converting Inositol triphosphate into a contraction

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53
Q

Which alpha antagonist irreversibly binds to the receptor?

A

Phenoxybenzamine (dibenzyline)

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54
Q

In what situations is phenoxylbenzamine used?

A

Long term preoperative control of pheochromocytoma (chemical sympathectomy).
and in BPH to improve flow

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55
Q

Since phenoxybenzamine is a non-selective alpha antagonist, what are signs/symptoms you will see with administration?

A
  1. Reduced SVR
  2. Reduced BP
  3. Secondary increase in NE due to alpha 2 blockade can increase HR and CO
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56
Q

What are uses for phentolamine?

A
  1. HTN secondary to pheochromocytoma
  2. Clonidine withdrawal HTN
  3. Erectile dysfunction
  4. Extravasation of catacholamines
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57
Q

Which medications may not have the same level of effect when a patient is on an Alpha 1 antagonist?

A

Alpha 1 Agonists like phenylephrine or norephinephrine

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58
Q

What medication can be administered to potentially see a reduction in post-op delirium?

A

Precedex

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59
Q

Cochrane Review on Alpha 2 Agonists concluded that…?

A

Overall mortality, cardiac mortality, and MI are all reduced with clonidine use peri-operatively.

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60
Q

What is clonidine’s affinity for Alpha 2 vs Alpha 1 receptors?

A

Alpha-2 220:1

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61
Q

What two main results are seen from clonidine adminsitration?

A
  1. Decrease release of sympathetic neurotrasmitters

2. Inhibits renin release

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62
Q

T/F: Clonidine cessation must be done abruptly as to not produce down-regulation of receptors?

A

False; Abrupt cessation of clonidine may lead to rebound HTN. This withdrawal is very common and is significant

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63
Q

Why/how does clonidine withdrawal occur?

A

Up-regulation occurs because Alpha 2 agonism means less NE “floating around”. Body begins to produce more Alpha 1 Receptors in response.

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64
Q

How many days of therapy are required before abrupt cessation of clonidine leads to withdrawal?

A

Usually 6 or more.

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65
Q

How quickly does peak effect of PO clonidine take?

A

60-90 mins

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66
Q

Which patients should clonidine be avoided?

A

Severe coronary insufficiency.
Conduction disturbances.
Recent MI, CVA.
CKD

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67
Q

During withdrawal from clonidine, which medication can be given to correct HTN/tachycardia?

A

Coreg or labetolol

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68
Q

What effects on anesthesia administration does clonidine have?

A
  1. Reduces propofol/thiopental requirements
  2. Alternative to N2O for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia
  3. Supplement of regional blocks
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69
Q

What is Precedex’s affinity for a given Alpha receptor?

A

Alpha 2>Alpha 1 1620:1

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70
Q

Which patients can clinically significant bradycardia and sinus arrest be seen in with precedex use?

A

Young, healthy patients with high vagal tone

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71
Q

Will you more likely see HTN or HoTN with bolus of precedex?

With infusion?

A

Bolus=HTN

Infusion=Hypotension

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72
Q

MOA of methyldopa?

A

Acts as a “false” neurotransmitter and is apart of a negative feedback loop. Falsely makes the body think it is breaking down into NE, but it isnt.
Further, it is broken down from Alpha-methyl-NE to Alpha-methyl-epinephrine which acts at alpha 2 receptors to decrease sympathetic outflow

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73
Q

What are uses for methyldopa?

A

treatment of HTN during pregnancy

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74
Q

What are side effects of methyldopa?

A
  1. Sedation, H/A, dizzy
  2. Fluid retention
  3. Orthostasis/bradycardia
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75
Q

MOA of ACE Inhibitors

A

By inhibiting Angiotensin converting enzyme which ultimately stops angiotensin I from converting to angiotensin II

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76
Q

Ultimately, how do ACE inhibitors decrease BP?

A

Predominantly arterial vasodilation because angiotensin II is not binding to arterial receptors

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77
Q

Uses of ACE Inhibitors?

A
  1. Treat CHF and MR by afterload reduction

2. Increase CO without excessive decrease in preload

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78
Q

If a patient is Normotensive and an ACE inhibitor is administered, what is the effect on renal function?

A

Renal function may deteriorate because compensatory efferent arteriolar constriction mediated by angiotensin II is blocked and decreased GFR may result in acute hyperkalemia

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79
Q

Which two patients is an ACE inhibitor the anti-HTN drug of choice?

A
  1. DMII

2. Renal failure

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80
Q

What are the side effects of ACE Inhibitors?

A
  1. Respiratory (cough, congestion, rhinorrhea)

2. Angioedema

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81
Q

T/F: ACE Inhibitors and methyldopa are the only two anti-HTN medications safe to use in pregnancy?

A

False; ACE Inhibitors are CONTRAINDICATED in pregnancy

82
Q

Two major outcomes of Hollman et al 2018?

A
  1. Overall 30% increase in risk of HoTN associated with continued ACEI preoperatively
  2. Patients that withheld 24hrs prior had lower incidence of all-cause death, stroke, MI
83
Q

Which medications when given with ACE inhibitors decrease the anti-HTN effects of the ACEI?

A

NSAIDs and ASA because they effect the way the afferent arteriole constricts and dilates

84
Q

What class of drug is Cozaar (losartan)?

A

Angiotensin II Receptor Antagonist (ARB).

85
Q

What other medication class are ARBs most alike in SE profile and use?

A

A.C.E. Inhibitors

86
Q

What three major locations do Calcium Channel Blocks typically work?

A

Peripheral smooth muscle, Cardiac Smooth muscle, and SA/AV nodes

87
Q

What electrolyte is the driving force for action potentials in the pacemaker cells?

88
Q

What are the 3 primary actions of Calcium Channel Blockers?

A
  1. Negative Inotropic effect
  2. Negative dromotropic effect (AV conduction mostly)
  3. Vasodilation of systemic, splanchnic, coronary, and pulmonary beds
89
Q

What are the two classes of Calcium Channel Blockers?

A
  1. Dihydropyridines

2. Non-Dihydropyridines (Phenylalkylamines and Benzothiazines)

90
Q

What are 3 examples of Dihydropyridine Calcium Channel Blockers?

A
  1. Nifedipine
  2. Nicardipine
  3. Amlodipine
91
Q

How do dihydropyridine Calcium channel blockers lower BP?

A

Pure arterial vasodilators, but with minimal reflex tachycardia

Also have minimal negative inotropic and dromotropic effects

92
Q

Do Dihydropyridines have any effect on Ca+ channels in the heart?

A

No, hence why there is no change in HR

93
Q

Nicardipine is a ___ specific vasodilator

94
Q

What is a unique feature of nicardipine?

A

There is no coronary steal syndrome, so it has favorable myocardial O2 supply/demand

95
Q

What is the onset of nicardipine?

A

Less than minute

96
Q

What is the DOA of nicardipine?

A

15-20 mins

97
Q

What is the dose of nicardipine to attenuate the hypertensive response to intubation?

A

0.5mg to 1mg boluses

Give 1mg/min to achieve a systolic arterial pressure decrease of up to 30mmHg or until 5mg has been administered

98
Q

How does nicardipine compare to nitro and SNP?

A
  • longer DOA compared to nitro

- slower onset and offset than SNP

99
Q

Why is nicardipine useful for IV control of HTN in the PACU and ICU?

A
  • Easier to use with less swings in BP bc of longer half life
  • No rebound hypertension with withdrawal (actually with any CCB)
  • Reflex tachycardia <10 bpm
  • Prolonged duration of action may be a benefit postop
100
Q

Advantages of nicardipine

A
  • Dose dependent arterial vasodilation
  • no aterial cath,
  • no coronary steal
  • cerebral and coronary vasodilation
  • minimal effects on contractility/ conduction
  • mild natriuretic effect
101
Q

Disadvantages of nicardpine

A
  • May accumulate (this can actually be a good thing per Emily)
  • Variable DOA
  • Hypotension
  • Venous irritation
  • May cause tachycardia
102
Q

Clevdipine is a _____

A

Dihydropyridine

103
Q

MOA of Clevidine

A

Vasodilation reduces PVR (arteriole specific)

104
Q

Is Clevidine is long acting or short actin?

A

Ultra-short acting

105
Q

Onset, peak, DOA of Clevipine

A

Onset < 5 min
Peak 10 min
Duration 10-20 min

Quickly cleared after administration due to half life of 1 min

106
Q

The dose of Clevidipine can be double every ___

A

90 seconds

107
Q

Once a vial of Clevidipine is open, use within ____

A

12 hours ( due to being in a lipid emulsion like propofol

108
Q

What has a faster onset, Clevidipine or Nicardipine?

A

Nicardipine

109
Q

Advantages of Clevidine

A
  • Reduced need for other antihypertensives
  • Reliable control
  • No dose adjustments for renal/hepatic disease
  • Ready to use vial
  • No sig myocardial depression
  • No effect on preload
  • Low potential for drug interactions
110
Q

Disadvantages of Clevidpine

A
  • Lipid emulsion (no more that 1 L or 21 mg/h recommended)
  • Continuous monitoring required,
  • Contraindicated with egg and soy bean allergy, pancreatitis, and HLD
111
Q

Verapamil is ____ CCB

A

phenylalkylamine

112
Q

Verapamil is a potent _____

A

negative inotrope, dromotrope, and vasodilator

113
Q

What are 3 uses of Verapamil?

A
  • Aortic Stenosis and IHSS
  • Conversion of atrial re-entry tachyarrhythmias
  • Coronary artery vasospasm (Prinzmetal angina)
114
Q

What 2 big side effects of Verapamil?

A
  • Lower extremity edema

- Constipation

115
Q

Diltiazem is a ____ CCB

A

Benzothiazine

116
Q

In regards to action, where does Diltiazem fit with phenylakylamine and dihydropyrdinces?

A

Right in b/w them

117
Q

What is Diltiazem used for?

A
  • Rate control of fib and atrial tachycardia vs a conversion agent such as verapamil
118
Q

Describe the dosing of IV Diltiazem

A
  • Dose 20mg IV bolus over 2 min
  • If no response, in 15 min give 25mg IV over 2 min
  • Infusion 10-20mg/hr.
119
Q

Verapamil vs Diltiazem vs Dihydropyridnes

A

VERAPAMIL:

  • Potent negative inotrope and negative dromotrope
  • Mild vasodilator
  • Useful in the treatment of vasospastic angina and essential hypertension.

DILTIAZEM(Cardizem®):

  • Fits between verapamil (phenylakylamine) and dihydropyridines in action
  • Less negative inotropic and dromotropic effects than verapamil but more than dihydropyridines.
  • Mild vasodilator like verapamil

DIHYDROPYRIDNES:

  • Virtually pure arterial vasodilator
  • Lack clinically significant negative inotropic and dromotropic effects.
120
Q

Which CCB’s have the the most potent vasodilation effect?

A

NIcarpdine and Nifedipine

121
Q

Do Nicardipine and Nifedipine have any effect on negative inotropy and AV block?

122
Q

Which CCB has the most potent negative isotropy and AV block effects?

A

Verapamil

Diltiazem is 2nd

123
Q

Do Diltiazem and Verapamil have any effect any vasodilation?

A

Yes, but mild

124
Q

Is constipation more common with dihydropyramines (DHP) or non-dihydropyramines (NDHP)?

125
Q

Adverse CNS effects of CCB’s

A
  • Dizziness,
  • HA
  • Fatigue
  • Insomnia
  • Nervousness
126
Q

Adverse CV effects of CCB’s

A
  • Flushing,
  • Edema,
  • Palpitations (DHP)
  • Bradycardia (NDHP)
127
Q

Adverse Respiratory effects of CCB’s

A
  • Nasal congestion
  • Dyspnea
  • Cough (nifedipine mostly)
128
Q

Adverse GI effects of CCB’s

129
Q

Other adverse effects of CCB’s

A
  • Arthralgias/joint stiffness,

- Itching

130
Q

When would give a NDHP vs a DHP CCB?

A

NDHP is given when you want the HR to come down, not given just for BP control. If that’s the case, just give DHP

131
Q

How do Verapamil and Diltiazem enhance myocardial O2 balance?

A
  • Decreasing myocardial oxygen consumption by afterload reduction and/or negative inotropic effect.
  • Increasing O2 delivery through coronary vasodilation.
132
Q

How do DHP CCB’s effect myocardial O2 balance?

A

Dihydropyridine vasodilators may worsen MvO2 by causing diastolic hypotension and reflex tachycardia (except nicardipine).

133
Q

T/F

CCB decrease reperfusion injury after ischemia

134
Q

Are there any significant benefits of CCB’s on the kidneys

A

No, they are not nephroprotective

135
Q

What are the effects of CCB’s on renal function?

A

Increase RBF and GFR and induce a naturesis

Benefits can be reversed if they cause hypotension, reflex catecholamine release and angiotensin activation leading to decreases in RBF and GFR

136
Q

What are the recommendations of CCB and surgery

A

Continue up to the time of surgery without risk of significant drug interactions

137
Q

CCB’s ___ the effects of neuromuscular blocking agents

A

Potentiate

138
Q

What are some anesthetic considerations with CCB’s?

A
  • May enhance hypotensive, CV depressant, and vasodilating effects of anesthetics and analgesics
  • Use adequate hydration to avoid hypotension due to inc fluid requirements
  • Clevidipine reduces gastric emptying
  • Diltiazem inc sedative effects of midazolam
139
Q

How does Diltiazem increase the sedative effect of Midazolam?

A

Diltaizem is a CYP3A4 inhibitor and Midazolam is a CYP3A4 substrate, so may see prolonged DOA of versed and also propofol

140
Q

T/F

Beta blockers cause vasodilation

141
Q

2 actions of beta blockers

A
  • Decrease C.O. (HR and contractility)

- Decrease renin release

142
Q

What are the advantages of beta blockers over vasodilators?

A
  • No reflex tachycardia or widening of pulse pressure
  • Improved MvO2 (decrease HR and decrease contractility)
  • Intrinsic antiarrhythmic activity
143
Q

3 classifications of beta blockers

A
  • Beta-1 selectives (Metoprolol, Atenolol, Acebutolol, Bisoprolol, Esmolol)
  • Non-selective (Propranolol, Nadolol, Timolol, Pindolol, Carteolol)
  • Combined Alpha-1 and non-selective beta(Carvedilol and Labetalol)
144
Q

MOA of beta-1 selective BB’s

A

Decrease velocity of A-V conduction, HR, contractility, renin release and lipolysis

145
Q

MOA of non-selective BB’s

A

Block Beta-1 receptors

Also act at Beta-2 receptor to cause bronchoconstriction, peripheral vasoconstriction and decrease glycogenolysis.

146
Q

Which class of BB’s is useful for cocaine overdose?

A

Combined alpha-1 and non-selective beta

147
Q

What class of BB’s cannot be used in asthmatics?

A

Non-selectives

b/c they cause bronchoconstriction

148
Q

T/F

Propanolol can be used to treat tremors and portal HTN

149
Q

How do beta blockers work at the cellular level?

A

Block beta receptors, which block adenyl cyclase (AC) which block the conversion of ATP to cAMP

150
Q

How are long-acting BB’s metabolized?

A

Glucuronide hepatic biotransformation

Ex. Atenolol and metoprolol XL

151
Q

How are intermediate-acting BB’s metabolized?

A

Rapidly hydroxylated by the liver, 1st pass effect

152
Q

How are short-acting BB’s metabolized?

A

By red cell esterase. These attack esmolol immediately

153
Q

What are the routes of elimination of long-acting, intermediate-acting, and short-acting BB’s?

A

Long-acting: Kidney

Intermediate-acting: Liver

Short-acting: Red cell esterase

154
Q

Why is lipophilicity important for classifying BB’s?

A

BB’s can cause CNS depression

155
Q

What are examples of low lipophilicity BB’s?

A 
Acebutolol
Atenolol
Bisoprolol
Carteolol,
Nadolol
156
Q

What are examples of moderate lipophilicity BB’s?

A

Metoprolol
Pindolol
Coreg
Labetalol

157
Q

What are examples of high lipophilicity BB’s?

A

Propanolol

Penbutolol

158
Q

What happens when you begin to increase the dose of beta blockers?

A

The selecetivity goes away, can cause beta-2 effects

Ex. Loppressor 100mg q8 PO

159
Q

Which BB class has more adverse effects?

A

Non-selective

160
Q

What are the adverse effects of BB’s

A

Non-selective blockade of Beta-2 receptors:

  • Vasoconstriction and worsening PVD
  • Bronchospasm

Myocardial depression:
- Decreased contractility could precipitate CHF

Life-threatening bradycardia or asystole

Hyperkalemia in renal failure

161
Q

What is the treatment for BB overdose?

A
  • Treat with atropine
  • May need Isoproterenol, dobutamine and/or glucagon infusion
  • Could ultimately need pacing
162
Q

Glucagon ____ cAMP

163
Q

What can occur when combining Verapamil and BB’s?

A

Decrease HR and contractility

164
Q

What can occur when combining Digoxin and BB’s?

A

Decrease HR and conduction

165
Q

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

166
Q

what are 4 perioperatve indications for BB’s?

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, AS or IHSS
  • Peripheral manifestations of hyperthyroidism – propranolol given most often for this
167
Q

What are BB contraindications?

A
  • Severe bradycardia
  • > 1st degree heart block
  • Cardiogenic shock
  • Raynaud’s disease
168
Q

What types of patients should BB be used with caution?

A
  • Asthma/COPD
  • DM
  • CHF
169
Q

What was the prototype non-selective BB?s

A

Propranolol

170
Q

Can propranolol cross the BBB?

A

yes, b/c its lipid soluble

this is why it’s a good drug for people with public speaking anxiety/fear

171
Q

What % of propranolol undergoes metabolism in the liver?

A

70% (undergoes 1st pass effect)

172
Q

What class of BB is esmolol?

A

Beta-1 selective

173
Q

What are 3 intraoperative uses of esmolol?

A
  • Blunt the CV response to intubation
  • Control of SVT and A. Fib.
  • Intraop and postop HTN and tachycardia
174
Q

T/F

Esmolol is more likely than Verapamil to convert fib to SR

175
Q

Is Esmolol’s onset/offest rapid or slow?

A

Rapid, b/c its metabolized by red cell esterases

176
Q

Which BB is approved for the the treatment of angina, acute MI, and HTN?

A

Metoprolol

177
Q

What class of BB is metoprolol?

A

Beta-1 selective

178
Q

What can occur when BB’s and general anesthetics interact?

A

Negative inotropic effects and conduction delays are potentiated by many general anesthetics

179
Q

What can happen if BB’s are stopped abruptly?

A

Rebound HTN and tachycardia

180
Q

What 2 problems can BB’s mask?

A
  • Hypoglycemia

- Hyperthyroidism

181
Q

When a patient is on BB’s, what is the best way to prevent orthostasis?

A

Adequate IVF

182
Q

T/F

If a patient is on BB’s, anticholinesteras may increase bradycardia

183
Q

If a patient develops HTN intraoperatively, what steps should be taken?

A
  1. Check depth of anesthesia
  2. Administer sufficient analgesia
  3. R/O hypercarbia, distended bladder, hyperthermia, hypoxia, thyroid storm, malignant hyperthermia
  4. When vasodilators are used, watch for reflex tachycardia as BP decreases
184
Q

What is the drug of choice for HTN during pregnancy?

A

Alpha-methyldopa

185
Q

Can labetalol be used during pregnancy ?

A

Yes, in 2nd and 3rd trimesters only

Beta blockers are associated with growth retardation in the 1st trimester

186
Q

Can ACEI’s be used for HTN during pregnancy?

A

No

ACEI have demonstrated fetal morbidity and mortality in all 3 trimesters.

187
Q

Can hydralaizne be used during pregnancy?

A

Yes, during delivery

188
Q

What can nifedipine be administered during pregnancy?

A

PO only (not SL)

189
Q

T/F

SNP is regular used to treat HTN during pregnancy

A

False

It is rarely used

190
Q

What is considered a HTN emergency?

A

Acute elevation of SBP > 180 or DBP > 120 with target organ damage

191
Q

What can occur if excessive correction happens for a HTN emergency?

A

Renal, cerebral, and coronary ischemia

192
Q

What is the definition of HTN urgencies?

A

Accelerated, malignant, or perioperative inc in BP without target organ damage

193
Q

T/F

For HTN urgencies, PO therapy is preferred and immediate BP lowering is not required

194
Q

What drug should NOT be used to treat HTN urgencies?

A

IR nifedipine

195
Q

What are 7 examples of target organ damage related to HTN?

A
  1. Encephalopathy
  2. ICH
  3. Unstable angina
  4. Acute MI
  5. Acute LV failure with pulmonary edema
  6. Dissecting aortic aneurysm
  7. Eclampsia
196
Q

T/F

Labetolol does not increase ICP

A

True

This is why its a good choice for ICH patients

197
Q

What is the ratio of beta/alpha blockade with labetalol

A

7:1 (Beta:alpha)

198
Q

What happens if you give labetalol for vasoconstrictor HTN?

A

vasodilation without reflex tachycardia

199
Q

What happens if you give labetalol for hyper dynamic HTN?

A

Beta blocker without reflex vasoconstriction

200
Q

What can occur with giving SNP with labetalol?

A

tachyphylaxis with SNP

201
Q

How should labetalol be administered?

A
  • “Test dose” of “baby dose” 2.5-5mg IV to make sure there isn’t CV collapse.
  • If no change in HR in 5-10 min, progressively double the dose every 5-10 min. to a max. dose of 100mg
  • Dose can be repeated every 2-4 hours.
202
Q

What can occur with labetalol in large doses?

A
  1. Bronchoconstriction

2. Acute hyperkalemia in renal failure

Pharm 2 (19 decks)

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