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Pharm II > Vasodilators and Antihypertensives > Flashcards

Vasodilators and Antihypertensives Flashcards

1
Q

What are some reasons for perioperative hypertension?

A 
Inadequate anesthesia
Airway manipulation
Hypercarbia
Hypoxia
Medications
Aortic cross clamp
Hypervolemia
Hypothermia
Pain
Pre-existing disease states
Type of procedure being performed
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2
Q

What is the primary cause for perioperative hypertension?

A

Increased sympathetic discharge with systemic vasoconstriction

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3
Q

What are come complications from perioperative hypertension?

A 
CVA
MI
Ischemia
LV dysfunction
Arrhythmias
Increased suture tension
Hemorrhage
Pulmonary edema
Cognitive dysfunction
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4
Q

Idiopathic hypertension accounts for how much of all hypertension?

A

95%

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5
Q

For idiopathic hypertension, the renin-angiotensin system is important in ___, but not for ___

A

Control

Development

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6
Q

How does idiopathic hypertension develop?

A

Initially, SVR is normal, increased BP is due to increased CO
SVR increases to prevent the increased BP from being transmitted to the capillary bed where it would affect cell homeostasis

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7
Q

Do most systemic vasodilators increase or decrease resistance in the pulmonary circulation?

A

Decrease

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8
Q

What is the mechanism of action for vasodilators?

A 
Direct smooth muscle dilatation (production of intracellular NO, calcium channel blockers)
Alpha-1 antagonists (prazosin and labetalol)
Ganglionic blockers (trimethaphan)
Alpha-2 agonists (clonidine, alpha-methyldopa)
ACE inhibitors (captopril and enalapril)
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9
Q

How are vasodilators classified?

A

According to their predominate effect on the circulation:

  • Arterial dilators (resistance circulations)
  • Venodilators (capacitance circulation)
  • Balanced vasodilators
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10
Q

How do arterial dilators work?

A

Dilate the arterial resistance circulation, decrease afterload and enhance CO when myocardial contractility is impaired. Most arterial vasodilators work on systemic and pulmonary arterioles

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11
Q

How do venodilators work?

A

Dilate the venous capacitance circulation and decrease preload, pulmonary congestion, and edema

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12
Q

How do balanced vasodilators work?

A

Dilate the arterial and venous systems and decrease preload and afterload

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13
Q

What are some examples of arterial dilators?

A

Hydralzine
ACE inhibitors
Nicardipine

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14
Q

What is an example of a balanced dilator?

A

Nitroprusside

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15
Q

What is an example of a venodilator?

A

Nitroglycerine

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16
Q

What are the primary effects of vasodilators?

A

Act primarily to cause systemic vasodilatation and decrease afterload

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17
Q

T/F: Pure arteriole dilator causes maximal effects on preload

A

False, causes minimal effects of preload

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18
Q

Are there pure venodilators?

A

No, not available

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19
Q

What is the only “pure” pulmonary vasodilator?

A

Inhaled NO

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20
Q

What are the indications for vasodilators?

A 
Hypertension
Low CO (must maintain preload)
Valvular insufficiency
Coronary and cerebral vasospasm
Pulmonary hypertension
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21
Q

When does the LV get perfused?

A

70-90% of the coronary artery perfusion to the LV occurs during diastole

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22
Q

What governs perfusion?

A

Aortic diastolic pressure

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23
Q

In the presence of ischemic heart disease, the ___ ___ are maximally dilated and coronary perfusion is largely ___ dependent

A

Collateral arteries

Pressure

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24
Q

What is the formula for coronary perfusion pressure?

A

Transmyocardial gradient (TMG) = Aortic diastolic pressure (ADP) - LVEDP or PCWP

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25
Q

What is 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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26
Q

Which drugs can help treat myocardial ischemia?

A

Nitroglycerine
Calcium channel blockers
Sodium nitroprusside

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27
Q

How does Nitroglycerine work?

A

Venodilation decreases venous return and filling pressures

  • Relative increase in coronary perfusion pressure facilitates subendocardial and collateral blood flow
  • Wall tension and myocardial O2 demand decrease
  • Mild arteriolar dilatation may decrease BP and cause a reflex increase in HR
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28
Q

How do calcium channel blockers work for myocardial ischemia?

A

All are coronary and systemic vasodilators
May produce myocardial depression
Useful to treat coronary vasospasm

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29
Q

What are some adverse effects to vasodilators?

A
  • Acute hypotension in hypovolemic patients
  • Older patients more sensitive to vasodilatation because of an attenuated baroreceptor reflex and impaired reflex tachycardia
  • Rebound hypertension when abruptly discontinued
  • Hypoxemia from reversal of hypoxic pulmonary vasoconstriction
  • Increased CBF, increased ICP, and decreased CPP in patients with a closed head injury or intracranial hypertension
  • Salt and water retention
  • Adverse effects on MvO2
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30
Q

What are the nitrovasodilators?

A

Nitric oxide

SNP and NTG

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31
Q

___ spontaneously generates NO while ___ requires a cofactor to release NO in smooth muscle

A

SNP

NTG

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32
Q

SNP receives an electron from oxyhemoglobin and dissociates immediately releasing,

A

Methemoglobin
NO
5 cyanide molecules

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33
Q

How does NO work?

A

Activates guanylyl cyclase leading to the formation of cGMP in vascular smooth muscle cells. cGMP inhibits calcium entry into smooth muscle cells and produces vasodilitation

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34
Q

What are the effects of nitric oxide?

A

Vasodilator
Relaxes other smooth muscle
Increases blood flow to parts of the lung exposed to NO and decreases pulmonary vascular resistance

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35
Q

What are the clinical application for NO?

A

Hypoxic respiratory failure
Pulmonary artery hypertension
Cardiopulmonary resuscitation

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36
Q

How do you administer NO?

A

Inhalation as a gas
Dosed in ppm
-NO is stored as a compressed gas that is mixed with nitrogen: 100 or 800 ppm. Dose: 18 ppm

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37
Q

What is the toxicity and adverse interactions for NO?

A
  • React with oxygen to form nitrogen dioxide (NO2): pulmonary irritant that can decrease lung function
  • Can induce the formation of methemoglobin: hemoglobin that cannot bind to oxygen
  • Monitor NO2 and methemoglobin levels during administration
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38
Q

What is an alternative strategy to NO?

A

PDE (isoform 5) inhibitors

  • Inhibit PDE that degrades cGMP in vascular smooth muscle
  • Results in the prolongation of the duration of NO-induced cGMP elevations
  • Approved for the treatment of PAH
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39
Q

How does SNP act as a balanced vasodilator?

A
  • Direct action on vascular smooth muscle
  • Decreased MAP and MPP
  • Decreases LA and LV filling pressures
  • Decreased afterload promotes forward flow in MR and AI
  • May dilate coronary arteries (coronary steal)
  • No direct myocardial depression
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40
Q

Does SNP increase or decrease cerebral blood flow and ICP?

A

Increase

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41
Q

What happens with abrupt discontinuation of SNP?

A

Reflex tachycardia and hypertension

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42
Q

Does SNP cause and increase or decrease in renal blood flow?

A

Decrease

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43
Q

What is the dose for SNP?

A
  • Start with 0.1-0.2 mcg/kg/min IV
  • Recommended max dose 0.5 mg/kg/hr (8-10 mcg/kg/min) for 10 mins
  • Over 2-4 mcg/kg/min, add a second drug (BB, trimethopham)
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44
Q

What are some misc. facts about administration of SNP?

A
  • Requires placement of aline
  • May be administered peripherally
  • Protect from light
  • Mix in D5W
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45
Q

What are the pharmacokinetics of SNP?

A
  • Onset: <1 min
  • Duration: 5-10 mins
  • Peak: 2-3 mins
  • Half life: 2.7-7 days
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46
Q

What are the CNS side effects of SNP?

A 
Restlessness
Apprehension
Muscle twitching
HA
Dizziness
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47
Q

What are the CV side effects of SNP?

A

Profound hypotension
Palpitations
Fluctuations in HR
Retrosternal discomfort

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48
Q

What are some other side effects of SNP?

A 
N/V
Abdominal pain
Nasal stuffiness
Increased serum creatinine
Thiocyanate/cyanide toxicitiy
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49
Q

What are the advantages to using SNP?

A

Immediate onset
Short duration
Reduced myocardial O2 demand

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50
Q

What are the disadvantages to using SNP?

A 
Reflex tachycardia
Cyanide toxicity
Intrapulmonary shunting
Precipitous drop in BP is possible
Photodegradation
Methemogloninemia
Coronary steal
Enhanced bleeding
Cerebral vasodilator
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51
Q

What is the hyperdynamic response to SNP?

A

Progressive widening of the arterial pulse pressure

Increase in HR

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52
Q

How do you treat the hyperdynamic response to SNP?

A

BB to suppress reflex tachycardia, narrow the pulse pressure and be able to treat the hypertension with a lower dose of SNP

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53
Q

What is the metabolism of SNP?

A

Can break down to 5 cyanide molecules:

  • CN can react with methemoglobin to form cyanomethemoglobin
  • CN can be converted to thiocyanate in the liver or kidneys by the rhodanase enzyme (requires thiosulfate)
  • CN may inactivate cytochrome oxidase in cells (changes cells from aerobic to anaerobic metabolism)
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54
Q

Toxicity of SNP depends on what?

A
  • How rapid the drug is given (max dose should not be infused for longer than 10 mins)
  • Total amount given: > 2 mcg/kg/min can lead to accumulation of cyanide and cyanide toxicity
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55
Q

When does cyanide intoxication occur?

A

When the detoxification pathways are overwhelmed by the rapid administration of SNP. CN enters the cell and binds and inactivated Fe3 cytochrome oxidase and blocks cellular use of oxygen (cytotoxic anoxia)

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56
Q

What is acute cyanide toxicity associated with?

A

Tachyphylaxis
Increasing SvO2
Metabolic acidosis
Cardiac dysrhythmias

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57
Q

How does thiocyanate/cyanide toxicity present itself?

A 
Hypotension
Blurred vision
Fatigue
Metabolic acidosis
Pink skin
Absence of reflexes
Faint heart sounds
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58
Q

What are the therapeutic, toxic and fatal doses of thiocyanate?

A

Therapeutic: 6-29 mcg/ml
Toxic: 35-100 mcg/ml
Fatal: >200 mcg/ml

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59
Q

What are the normal, toxic and fatal doses of cyanide?

A

Normal: 2 mcg/ml
Fatal: > 3 mcg/ml

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60
Q

How do you treat cyanide toxicity?

A

Stop infusion, administer 100% O2
Give bicarb
Administer 3% sodium nitrite 4-6 mg/kg slowly IV
Administer sodium thiosulfate 150-200 mg/kg IV over 15 mins

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61
Q

T/F: Thiocyanate cannot be removed with dialysis

A

False, can be removed with dialysis

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62
Q

Methemoglobin reductase converts what?

A

Methemoglobin to hemoglobin

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63
Q

How much methemoglobin is produced with a SNP dose of 1 mg/kg?

A

10% methemoglobin

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64
Q

How do you convert methemoglobin back to hemoglobin?

A

Methylene blue 1-2 mg/kg IV over 5 mins

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65
Q

What are the side effects of methemoglobin?

A
  • HA, NV, palpitations, abd pain

- Worsening intrapulmonary shunt

66
Q

Thiocyanate inhibits the uptake and binding of iodine and may cause what with chronic use?

A

Hypothyroidism

67
Q

SNP reverses what?

A

Hypoxic pulmonary vasoconstriction

68
Q

T/F: thiocyanate is a metabolite

A

True

69
Q

NTG requires what to release NO?

A

A cofactor such as a cysteine (a thiol)

70
Q

NTG increases ___ blood flow relative to ___ blood flow

A

Endocardial

Epicardial

71
Q

Does NTG dilate or constrict meningeal vessels?

A

Dilate, caution with increased ICP

72
Q

Does NTG increase or decrease renal blood flow?

A

Decreases renal blood flow with decrease in systemic BP

73
Q

What are the indications of NTG?

A

Ventricular failure
Hypertension
Ischemic heart disease

74
Q

How is NTG metabolized?

A

Metabolized by glutathione nitrate reductase in the liver

Nitrite ion oxidizes Hgb to methemoglobin

75
Q

How does the body build a tolerance to NTG?

A

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

76
Q

What is the IV dose of NTG?

A

Initial: 0.5 mcg/kg/min (we use 5 mcg/min)
Titrate to desired hemodynamic response
Small IV bolus dose for uterine relaxation

77
Q

What is the sublingual dose of NTG?

A

0.3-0.8 mg (bypasses a lot of first-pass effects)

78
Q

What is the pharmacokinetics of NTG?

A

Onset: 1 min
Duration: 3-5 mins
Half-life: 1-4 mins

79
Q

What are the adverse effects of NTG?

A 
Postural hypotension
Tachycardia
HA
Dizziness
Weakness
Methemoglobinemia
80
Q

What are the contraindications to using NTG?

A 
PDE5 inhibitors
Narrow angle glaucoma
Head trauma, cerebral hemorrhage
Severe anemia
Hypotension
81
Q

What are the advantages to using NTG?

A 
Rapid onset
Short duration
Coronary vasodilator
Decreased myocardial O2 consumption
No major toxicities
No coronary steal
Reduced PVR
82
Q

What are the disadvantages to using NTG?

A 
Decreased diastolic BP
Reflex tachycardia
Possible hypotension
Variable efficacy
Tachyphylaxis
Methemoglobinemia
Intrapulmonary shunting
Prolonged bleeding time
83
Q

How does Hydralazine work?

A

Direct-acting dilator of vascular smooth muscle due to hydralazine-related interference with calcium ion transport

84
Q

What does Hydralazine do clinically?

A 
Decreases SVR (decreases dBP more than sBP)
Increases CO HR and SV
Effect on arterioles greater than veins so minimal risk for orthostatic hypotension
85
Q

Does rebound hypertension occur with hydralazine?

A

No but ICP increases significantly

86
Q

What are the advantages to Hydralazine?

A

Maintains/increases cerebral blood flow

Increased CO and SV

87
Q

What are the disadvantages to hydralazine?

A 
Reflex tachycardia
Reduced pressor response to ephedrine
Drug interactions
Sodium and water retention (increases renin activity)
Longer duration of action
88
Q

What are the CNS side effects to Hydralazine?

A

HA
Dizziness
Tremor
Vertigo

89
Q

What are the CV side effects to Hydralazine?

A 
Palpitations
Angina
Tachycardia
Flushing
Reflex tachycardia
90
Q

What are the GI side effects to Hydralazine?

A 
Anorexia
NV
Abd pain
Paralytic ileus
Diaphoresis
91
Q

What other side effects can occur with Hydralazine?

A 
Anemia
Agranulocytosis
Nasal congestion
Muscle cramps
Edema
Sodium and water retention
92
Q

Who do you want to avoid Hydralazine with?

A

Patients with CAD, increased ICP, lupus

93
Q

What is the dose of Hydralazine?

A

5-20 mg IV

94
Q

What are the pharmacokinetics of Hydralazine?

A

Onset: 10-20 mins
Peak: 30-60 mins
Duration: 3-6 hrs
Half-life: 3-7 hours

95
Q

T/F: Tachyphylaxis does not occur with hydralazine

A

False, tachyphylaxis may occur

96
Q

Activation of alpha 1 receptor increases intracellular calcium causing what?

A

Smooth muscle contraction
Peripheral vasoconstriction
Bronchoconstriction

97
Q

What else does activation of alpha 1 receptor do?

A

Inhibits insulin secretion (stimulates glycongeloysis and gluconeogenesis)
Mydriasis
GI relaxation

98
Q

Alpha 2 receptor activation inhibits neuronal firing in the CNS and PNS causing what?

A

Hypotension
Bradycardia
Sedation
Analgesia

99
Q

What else does alpha 2 receptor activation do?

A

Decreased salivation and secretions
Decreased GI motility
Inhibit renin release, increase GFR, increased NA and H2O secretion
Decreased insulin release

100
Q

What are some of the alpha1 antagonists?

A

Phentolamine
Phenoxybenzamine
Prozosin (minipres)

101
Q

How do alpha1 antagonists work?

A

Block the effect of endogenous catecholamines on arterial and venous constriction

102
Q

What are some side effects of alpha1 antagonists?

A

Hypotension
Nasal congestion
Orthostasis

103
Q

How does Phentolamine work?

A

Alpha adrenergic blockade and direct-acting vasodilator

Greater arterial than venous

104
Q

What clinical effects does Phentolamine do?

A

Decreases afterload and preload
Promotes greater EF and CO
Decreases PVR
Used for vasoconstrictor infiltrate

105
Q

What is the dose if phentolamine is used for a vasoconstrictor infiltrate?

A

5-10 mg in 10 ml NSS

106
Q

Does phentolamine increase or decrease airway resistance?

A

Decrease in and improves asthma symptoms

107
Q

What are the uses for phentolamine?

A

Hypertension secondary to pheochromocytoma
Clonidine withdrawal hypertension
Erectile dysfunction
Extravasation of catecholamines

108
Q

What is Phenoxybenzamine (dibenzyline)?

A

Prototype alpha1 antagonist

Irreversibly binds to the receptor

109
Q

What is the use of Phenoxybenzamine?

A

Long-term preop treatment to control the effects of pheochromocytoma (chemical sympathectomy)
Relieve ischemia in PVD
Improve flow in patients with BPH

110
Q

How does Phenoxybenzamine work?

A

Reduced PVR to reduce BP
Secondary increases in NE d/t alpha2 blockade can increase HR and CO
Crosses the BBB

111
Q

What are the side effects of Phenoxybenzamine?

A

CNS: sedation, depression, tiredness, lethargy, HA
GI: N/V
CV: postural hypotension, tachycardia, arrhythmias

112
Q

What are the pharmacokinetics of Phenoxybenzamine?

A

Half-life: 24 hours

Duration of action: 4 days

113
Q

What is Prazosin (minipres)?

A

Oral selective alpha1 antagonist
Peripheral vasodilator (arteries > veins)
Increases HR
Improves urinary flow

114
Q

What is clonidine?

A

Central acting alpha-2 agonists that leads to inhibition of sympathetic outflow
Decreases release of sympathetic neurotransmitters
Inhibits renin release

115
Q

What are the pharmacokinetics of clonidine?

A

Rapidly and completely absorbed from po dosing with peak in 60-90 mins
Half life: 9-12 hours
Patch takes 2 days to reach full potential

116
Q

What are the adverse effects of Clonidine?

A

Drowsiness
Dizziness
Dry mouth
Orthostasis

117
Q

What are the uses for Clonidine?

A

Premedication (sedation, anesthetic sparing effect)
Regional anesthesia
Postop analgesia
Analgesia for labor
Chronic pain
Prevention/treatment of drug withdrawal and postop shivering

118
Q

What are clonidines effects on anesthesia?

A
  • Reduces propofol and thiopental requirements
  • Alternatives to N2O for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia
  • Supplement of regional blocks
119
Q

What are the clinical effects of clonidine?

A

Decreases HR, BP, CO and SVR (baroreceptor reflexes are preserved)

120
Q

Abrupt cessation of clonidine may lead to what?

A

Rebound hypertension

121
Q

Clonidine withdrawal manifests how?

A 
Excessive hypertension
Tachycardia
Restlessness
Insomnia
HA
Nausea
122
Q

Which alpha-2 agonist is almost as potent as NE?

A

Alpha-Methyldopa (Aldomet)

123
Q

What is Alpha-Methyldopa metabolized to?

A

Alpha-methylepinephrine in the CNS which acts at Alpha-2 receptors to decrease sympathetic outflow

124
Q

What is the use of Alpha-Methyldopa?

A

Treatment of hypertension during pregnancy (usually 3rd trimester)

125
Q

What is the dose for Alpha-Methyldopa?

A

500 mg to 2 gm in 4 divided doses po or IV

126
Q

What are the side effects of Alpha-Methyldopa?

A 
Sedation, HA, dizziness
Fluid retention
Orthostatsis, bradycardia
Hepatic necrosis
Dry mouth, diarrhea, NV
Positive coombs test, hemolytic anemia, bone marrow suppression, impotence, rash
127
Q

What are the alpha 2 agonists?

A

Clonidine
Alpha-Methyldopa
Precedex

128
Q

Relatively selective alpha2 agonist for continuous IV sedation in ICU

A

Precedex

129
Q

T/F: Precedex has an analgesic effect

A

False

130
Q

What can Precedex be used for as a preop med?

A

Anxiolytic
Sympatholytic
Analgesic
Sedative

131
Q

What can Precedex be used for intraop?

A 
Reduces the stress response
Improved respirations
Hemodynamic stability
Improves efficacy of anesthetics
Increased recovery time
Less pain meds necessary
132
Q

What does Precedex help with postop?

A

May reduce opiate use by as much as half, reduced postop shivering

133
Q

T/F: Precedex has amnestic effects

A

False

134
Q

What is the dosage of precedex?

A

Bolus 0.5-1 mcg/kg over 5-10 mins (4mcg/mL in 5 ml syringe)

Follow with IV infusion of 0.5-1 mcg/kg/hr

135
Q

What are the adverse effects of precedex?

A

NV
Bolus: HTN, bradycardia
Infusion: Hypotension

136
Q

Which drug is unsafe to administer for >24 hours continuous infusion?

A

Precedex

137
Q

What do ACE inhibitors do?

A

Block the conversion of angiotensin I to angiotensin II preventing vasoconstriction

138
Q

Are ACE inhibitors primarily venous or arterial vasodilators?

A

Arterial vasodilators

139
Q

Risk of acutre renal failure in the intra and postop periods in patients on what?

A

ACEIs or ARBs

140
Q

How do ACE inhibitors work on your renal function if your baseline BP is hypertensive?

A

decreased renal vascular resistance improves RBF and GRF

141
Q

How do ACE inhibitors work on your renal function if your baseline BP is normotensive?

A

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

142
Q

What type of patients do you avoid giving ACEI’s to?

A

Decreased renal function or renal artery stenosis

143
Q

What is the initial dose of Vasotec?

A

1.25 mg IV q 6 hours

144
Q

What are the advantages to ACE inhibitors?

A

Minimal side effects

CHF, bronchospasm, hypokalemia, hyponatremia, and rebound HTN not seen with abrupt withdrawal

145
Q

What are the side effects of ACE inhibitors?

A

Cough
Congestion
Rhinorrhea
Angioedema

146
Q

Is it safe to use ACE inhibitors during pregnancy?

A

No, causes fetal morbidity and mortality

147
Q

What are the angiotensin II receptor antagonists?

A 
Losartan (Cozaar)
Irbesartan (Avapro)
Valsartan (Diovan)
Olmesartan (Benicar)
Telmisartan (Micardis)
Eprosartan (Teveten)
148
Q

What are the advantages of Angiotensin II Receptor Antagonists?

A

Save hemodynamic effects and uses and ACEI
Less cough/angioedema
Available PO, no IV yet

149
Q

What are the types of dopaminergic agonists?

A

DA1 (renal vasodilation and naturesis)
DA2 (presynaptic)–> inhibit NE release and promote vasodilatation. Attenuate the beneficial effects of DA on renal blood flow

150
Q

What is a Dopaminergic agonist?

A

Fenoldopam (Corlopam)

151
Q

What is Colopam?

A

Selective DA1 agonist with moderate affinity for presynaptic alpha2 receptors

152
Q

Does Colopam have any beta or alpha effects?

A

No beta or alpha1 or DA2 effects

153
Q

What do Colopam do clinically?

A

Decreases SVR and renal vasculature resistance resulting in decreased BP and increased LVEF and RBF

154
Q

Does Corlopam increase or decrease RBF?

A

Dose-related increase in RBF. As effective as SNP in controlling BP with the added benefit of increased RBF

155
Q

Is Dopamine or Corlopam more potent?

A

Colopam is 10-100 times more potent than Dopamine

156
Q

What are the uses for Corlopam?

A

Short term (<48 hours) management of severe hypertension

157
Q

T/F: Corlopam is renal protective

A

False, may preserve RBF and UO but NOT renal protective

158
Q

What is the max dose of Colopam?

A

0.5-0.8 mcg/kg/min

Do not bolus!

159
Q

Is an aline required for Corlopam?

A

No, can use a peripheral IV as well

160
Q

What are the cautions with using Corlopam?

A

Dose related tachycardia with infusions >0.1 mcg/kg/min
Hypokalemia may occur
Cost may limit its utility

Pharm II (8 decks)

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