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Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso > Vasodilators PPT part 2 > Flashcards

Vasodilators PPT part 2 Flashcards

1
Q

ACE I are free of many SE’s associated with other antihypertensive drugs including:

A
  • depression
  • insomnia
  • sexual dysfunction
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2
Q

AE’s such as HF, bronchospasm, bradycardia, and exacerbation of PVD are not seen with:

A

ACE inhibitors

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3
Q

Are metabolic changes induced by diuretic therapy (hypokalemia, hyponatremia, and hyperglycemia) observed in ACE I?

A

No!

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4
Q

Do ACE inhibitors see the same rebound htn as clonidine users?

A

nope!

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5
Q

ACE inhibitors have been established as first line therapy for pts with: (3)

A
  • CHF
  • Mitral regurgitation
  • Systemic HTN
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6
Q

ACE inhibitors are more effective and possibly safer than other antihypertensive drugs in the tx of

A

HTN in diabetics

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7
Q

there is evidence that ACE I delay the progression of

A

diabetic renal disease

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8
Q

ACE I have been shown to provide survival benefit to pts who (2 types):

A
  1. have suffered a MI

2. with HF

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9
Q

Angiotensin II binds to a specific cell membrane receptor:

This Receptor ultimately leads to:

A
  • AT1

- increased release of Ca+ from SR to produce vasoconstriction

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10
Q

Decreased generation of angiotensin II due to the administration of an ACE inhibitor results in

A

-reduced vasoconstrictive
effects

-decreased plasma concentrations of aldosterone resulting in less sodium and water retention

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11
Q

ACE I also block the breakdown of

A

bradykinin

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12
Q

Bradykinin is what? what does it do?

A
  • an endogenous vasodilator

- contributes to the antihypertensive effects of ACE I

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13
Q

How are ACE I like statins?

A

they reduce LDL activation thus reducing plasma concentrations of LDL

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14
Q

What ACE I is a PRODrug?

A

Enalapril

-the prodrug of the active ACE I, enalaprilat

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15
Q

Conversion of enalapril may be altered in patients with?

A

Hepatic dysfuntion

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16
Q

Captopril and lisinopril are not:

A

Prodrugs

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17
Q

The major difference among various clinically used ACE I is in:

A

duration of action

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18
Q

Name the most common SE of ACE I:

A
  • cough
  • Rhinorrhea
  • Upper Respiratory congestion
  • allergic-like symptoms
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19
Q

What patient type more frequently experiences the cough associated with ACE I?

A

Women

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20
Q

If RD develops, prompt tx of what is advised?

A

Epi (0.3-0.5mL of a 1:1,000 dilution) Subcutaneously

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21
Q

A potentially life-threatening complication of tx with ACE I is?

A

Angioedema

*an EMERGENCY!

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22
Q

ACE Inhibitors may decrease what in patients being treated with ACE I:

A

GFR

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23
Q

Who would you use ACE I with caution in?

What patients are not recommended for tx with ACE I?

A
  • caution in pre-existing renal dysfunction

- not rec. for patients with renal artery stenosis

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24
Q

The risk of hyperkalemia is greatest in patient’s with what RF’s?

What causes the hyperkalemia with ACE I?

A

Recognized RF - CHF with renal insufficiency

-Hyperkalemia is possible d/t decreased production of ALDOSTERONE

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25
Q
  1. Due to adverse effects to the circulatory system during anesthesia in pts chronically treated with ACE I, what is the recommended discontinuation timeline?
  2. What happens with GA? 3. How would you tx this?
A

1-D/C 12-24hrs before anesthesia and surgery.

2- exaggerated HYPOtension

3- responsive to cystalloid fluid infusion and/or admin of a catecholamine or vasopressin

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26
Q

What did Dr. Hammon say was the issue with stopping ACE I 12-24h before surgery?

A

it’s still likely in the pt’s system

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27
Q

ACE I may increase sensitivity to:

A

insulin (and hypoglycemia)

*concern w/DM

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28
Q

Is there evidence that the incidence of hypoglycemia is great in diabetics being treated with ACE I for control of HTN?

A

no

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29
Q

Name the only IV ACE I:

and a few notes about it

A

enalaprilat

  • there’s little published to guide its use in this setting. Not used as a gtt. Dosing rec’s are for intermittent injection.
  • has a less predictable onset and DOA as well as antihypertensive action than short-acting direct vasodilators
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30
Q

Angiotensin II Receptor inhibitors produce antihypertensive effects by blocking the:

A

vasoconstrictive actions of angiotensin II w/o affecting ACE activity

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31
Q

Common Angiotensin II R-inhibitors are:

A
  • candesartan
  • losartan
  • valdesartan

*All have relatively long DOA; once/twice daily dosing

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32
Q

Name the IV angiotensin II R-inhibitor agent

A

there is no iv agent available

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33
Q

Angiotensin II R-inhibitors have similar SE profile to?

What do they not do?

A
  • ACE I
  • the do not inhibit breakdown of bradykinin

–> (one of the benefits of ACE I that make it generally a preferred first line therapy)

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34
Q

A major difference b/w ACE and ARBs is:

A

ARBs do not cause cough

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35
Q

What percentage of pts tx with ACE I may not tolerate it d/t cough?

A

more than 10%

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36
Q

D/t hypotension following induction/anesthesia in pts treated with ARBs, some recommend these drugs be discontinued:

A

on the day before surgery

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37
Q

These are historically the vasodilators most widely used by anesthesia providers

A 
Sodium nitroprusside (SNP) and 
IV nitroglycerin

*“nitrodilators”

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38
Q

SNP and Nitroglycerin work through the generation of:

Which then augments ____ in ____ ____ ____, both arteries and veins, leading to _____.

A
  • NO
  • cyclic cGMP in vascular smooth muscle,
  • vasodilation
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39
Q

Nitroprusside (SNP) is a

A

direct acting, Nonselective peripheral vasodilator that causes relaxation of arterial and venous vascular sm

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40
Q

SNP lacks significant effects on -

A

nonvascular smooth muscle and on cardiac muscle

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41
Q
  1. SNP onset of action is:
  2. equipotent on:
  3. its duration is:
A
  1. almost immediate
  2. arteries and veins,
  3. transient- requiring continuous IV administration to maintain a therapeutic effect
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42
Q

SNP necessitates careful titration of dosage as provided by continuous infusion devices and frequent monitoring of systemic blood pressure, often by intraarterial monitoring due to it’s:

A

extreme potency

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43
Q

SNP interacts with oxyhemoglobin, dissociating immediately and forming

A

methemoglobin while releasing cyanide and NO

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44
Q

Once released, NO activates the enzyme :

Resulting in increased:

A
  • guanylate cyclase (present in vascular smooth muscle)

- intracellular concentrations of cGMP

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45
Q

cGMP inhibits

A

calcium entry into vascular smooth muscle cells and may increase calcium uptake by the smooth endoplasmic reticulum to produce vasodilation.

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46
Q

What is the active mediator responsible for the direct vasodilating effect of SNP

A

NO

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47
Q

SNP spontaneously generates this product, thus functioning as a prodrug

A

NO

*(in contrast to Nitroglycerin, -organic nitrate-which requires trio-containing compound to generate NO)

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48
Q

Metabolism of SNP begins with the transfer of an electron from the iron of oxyhemoglobin to SNP, yielding

A

methemoglobin and an unstable SNP radical

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49
Q

The unstable SNP radical promptly breaks down, releasing all

A

five cyanide ions,

50
Q

The unstable SNP radical promptly breaks down, releasing all five cyanide ions, one of which reacts with :

and forms?

A

one of which reacts with methemoglobin to form cyanomethemoglobin.

51
Q

The remaining free cyanide ions are available to rhodanese enzyme in the liver and kidneys for conversion to

A

thiocyanate

52
Q

Rhodanese uses thiosulfate ions as sulfur donors, and most adults can detoxify approximately:

A

50 mg of SNP using existing sulfur stores

53
Q

What is the issue when the SNP level is > 50mg?

A

cyanide toxicity

54
Q

S/S associated with Cyanide Toxicity

A

red nose

red face

55
Q

What remains in dynamic equilibrium with free cyanide and is nontoxic?

A

Cyanomethemoglobin

56
Q

SNP Dose:

A
  • The initial dose: 0.3 µg/kg/minute IV
  • maximum rate of 10 µg/kg/minute IV,

-maximum rate not to be infused longer than 10 minutes.

57
Q

SNP infusion rates of greater than ______ result in dose-dependent accumulation of cyanide and the risk of cyanide toxicity must be considered

A

2 µg/kg/minute IV

58
Q

There is no evidence that SNP exerts what type of effect on the heart

A

inotropic or chronotropic effects on the heart

59
Q

SNP may increase the area of damage associated with a myocardial infarction through a phenomenon called

A

“coronary steal.”

*SNP dilates resistance vessels in nonischemic myocardium, resulting in diversion of blood flow away from ischemic areas where collateral blood vessels are already maximally dilated

60
Q

Baroreceptor-mediated reflex responses to SNP-induced decreases in systemic blood pressure manifest as

A

tachycardia and increased myocardial contractility

*These reflex-mediated responses may oppose the blood pressure–lowering effects of SNP.

61
Q

(with SNP) Although decreased venous return would tend to decrease cardiac output, the net effect is often an increase

A

in cardiac output d/t reflex-mediated increases in peripheral sympathetic nervous system activity combined w/ decreased impedance to left ventricular ejection

62
Q

SNP-induced decreases in systemic blood pressure may result in decreases .

A

in renal function

63
Q

Release of renin may accompany blood pressure decreases produced by SNP and contribute to blood pressure ______ when the drug is discontinued.

A

overshoots

64
Q

**To prevent blood pressure overshoots after discontinuation of SNP we should consider:

A

**Pretreatment with a competitive inhibitor of angiotensin II

65
Q

**SNP increases cerebral :

A

blood flow and cerebral blood volume.

In patients with decreased intracranial compliance, this may increase intracranial pressure (greater than the increase produced by nitroglycerin).

66
Q

In patients with decreased intracranial compliance, SNP may:

A

increase intracranial pressure (greater than the increase produced by nitroglycerin).

67
Q

does nitro or SNP have a greater effect on increasing ICP?

A

SNP

68
Q

It is likely that the rapidity of systemic blood pressure decrease produced by SNP exceeds the capacity of the cerebral circulation to

A

autoregulate its blood flow such that intracranial pressure and cerebral blood flow change simultaneously but in opposite directions

69
Q

decreasing blood pressure slowly over 5 minutes with SNP in the presence of hypocarbia and hyperoxia negates the

A

increase in intracranial pressure that accompanies the rapid infusion of nitroprusside

70
Q

Patients with known with these conditions should probably not be treated with SNP:

A
  • inadequate cerebral blood flow as associated with :
  • dangerously increased intracranial pressure
  • or carotid artery stenosis
71
Q

Clinical evidence of cyanide toxicity may occur when the rate of IV SNP infusion is greater than:

A

2 µg/kg/minute or when sulfur donors and methemoglobin are exhausted, thus allowing cyanide radicals to accumulate.

72
Q

Clinical evidence of cyanide toxicity may occur when the rate of IV SNP infusion is greater than 2 µg/kg/minute or when :

A

sulfur donors and methemoglobin are exhausted, thus allowing cyanide radicals to accumulate.

73
Q

Regardless of the SNP infusion rate or total administered dose, cyanide toxicity should be suspected in any patient requiring an increasing dose especially more than ______ or in a previously ____________________.

A
  • 2 µg/kg/minute or

- in a previously responsive patient who becomes less or unresponsive to the drug.

74
Q

In awake patients, what may occur? (side effect)

A

CNS dysfunction (mental status changes, seizures) may occur.

75
Q

CNS dysfunction (mental status changes, seizures) may occur in

A

awake patients receiving an SNP infusion

76
Q

If cyanide toxicity is severe, with deteriorating hemodynamics and metabolic acidosis, the recommended treatment is (and dose):

Why? What does this do?

A
  • slow IV administration of sodium nitrate,
  • 5 mg/kg.

-Sodium nitrate converts hemoglobin to methemoglobin, which acts as an antidote by converting cyanide to cyanomethemoglobin

KNOW THIS

77
Q

Sodium nitrate converts hemoglobin to

A

methemoglobin

78
Q

methemoglobin, acts as an antidote by

A

converting cyanide to cyanomethemoglobin

79
Q

this acts as an antidote by converting cyanide to cyanomethemoglobin

A

methemoglobin

80
Q

What converts hemoglobin to methemoglobin?

A

sodium nitrate,

  • 5 mg/kg
  • slow IV administration
81
Q

Appearance of tachyphylaxis in a previously sensitive patient in association with metabolic acidosis and increased mixed venous Po2 in a pt with a SNP gtt indicates what?

A

cyanide toxicity

KNOW THIS

82
Q

Suspected cyanide toxicity mandates immediate:

A
  • discontinuation of SNP and -100% O2 despite normal O2 sat
  • NaHCO3 to correct Met Acidosis
  • sodium thiosulfate

KNOW THIS

83
Q

**a recommended treatment for cyanide toxicity is:

dose if known

A

**-Sodium bicarbonate to correct metabolic acidosis
-Sodium thiosulfate:
150 mg/kg IV over 15 mins

KNOW THIS

84
Q

Another treatment is for cyanide toxicity is:

A

methylene blue
1 to 2 mg/kg IV, over 5 mins

to facilitate the conversion of methemoglobin to hemoglobin

85
Q

methylene blue helps facilitate the conversion of

A

methemoglobin to hemoglobin

86
Q

Thiocyanate Toxicity is clinically:

Why?

A

rare,

as thiocyanate is 100-fold less toxic than cyanide

87
Q

Thiocyanate is cleared slowly by

A

the kidneys, with an elimination half-time of 3 to 7 days

88
Q

thiocyanate is 100-fold less toxic than

A

cyanide

89
Q

In patients with normal renal function, How many days of SNP infusion in the 2 to 5 µg/kg/minute range may be required to produce potentially toxic thiocyanate blood concentrations?

A

7 to 14 days

1-2 weeks

90
Q

In patients with chronic renal failure who ARE NOT undergoing periodic HD, How many days of a SNP infusion in the 2 to 5 µg/kg/minute range may result in thiocyanate toxicity ?

A

3 to 6 days

91
Q

Adverse effects from methemoglobinemia produced by SNP breakdown are

A

unlikely

even in patients with a congenital inability to convert methemoglobin to hemoglobin (methemoglobin reductase deficiency)

92
Q

Nitroglycerin is an

A

organic nitrate

93
Q

Nitroglycerin is an organic nitrate that acts principally on

A
  • venous capacitance vessels and

- large coronary arteries

94
Q

Nitroglycerin is an organic nitrate that acts principally on venous capacitance vessels and large coronary arteries to produce :

A

peripheral pooling of blood and decreased cardiac ventricular wall tension

95
Q

As the dose of nitroglycerin is increased, there is

A

relaxation of arterial vascular smooth muscle

96
Q

Nitroglycerin can produce pulmonary vasodilation equivalent

A

to the degree of systemic arterial vasodilation.

97
Q

Nitroglycerin can produce pulmonary vasodilation that is _______ to the degree of systemic arterial vasodilation.

A

equivalent

98
Q

A continuous infusion of nitroglycerin can achieve:

A

Controlled hypotension

99
Q

Nitroglycerin, like SNP, generates NO, which stimulates production of

A

cGMP

-to cause peripheral vasodilation

100
Q

nitroglycerin requires the presence of

A

thio-containing compounds.

101
Q

the nitrate group of nitroglycerin is biotransformed to NO through a glutathione-dependent pathway involving

A

both glutathione and glutathione S-transferase

102
Q

the nitrate group of nitroglycerin is biotransformed to

A

NO

nitrous oxide

103
Q

Nitroglycerin is not recommended in patients with:

A
  • hypertrophic obstructive cardiomyopathy
  • severe aortic stenosis
  • venous pooling may be followed by syncope
104
Q

Most frequent administration route of Nitroglycerin is:

A

sublingual

*also available as PO, buccal, or transmucosal tablet; sublingual spray, and a transdermal ointment or patch

105
Q

Special consideration for Nitroglycerin when using a continuous infusion:

A

special iv tubing

  • to decrease absorption of the drug into the plastic
106
Q

Nitroglycerin has an elimination half-time of about :

A

1.5 minutes

107
Q

With Nitroglycerin, There is a large volume of distribution reflecting

A

tissue uptake

108
Q

it has been estimated that only what % of nitroglycerin is present in the plasma?

A

1% of total body nitroglycerin

*d/t large vol of distribution reflecting tissue uptake

109
Q

The nitrite metabolite of nitroglycerin is capable of oxidizing the ferrous ion in hemoglobin to the ferric state with the production of

A

methemoglobin

110
Q

The nitrite metabolite of nitroglycerin is capable of oxidizing the ferrous ion in hemoglobin to the

A

ferric state with the production of methemoglobin

111
Q

In patients with hepatic dysfunction, high doses of nitroglycerin may produce

A

methemoglobinemia

112
Q

with high doses of nitroglycerin methemoglobinemia may be produced in….

A

patients with hepatic dysfunction

113
Q

A limitation to the use of all nitrates is the development of:

A

tolerance to their vasodilating effects.

114
Q

Tolerance to Nitroglycerin is

A

dose-dependent and duration-dependent,

115
Q

Tolerance to nitroglycerin usually manifests

A

within 24 hours of sustained treatment

116
Q

If ischemia occurs during continuous administration of nitroglycerin, responsiveness to the antiischemic effects of the nitrate can usually be restored by

A

increasing the dose

117
Q

A drug-free interval of 12 to 14 hours is recommended to reverse tolerance :

A

to nitroglycerin and other nitrates

118
Q

What is recommended to reverse tolerance to nitroglycerin and other nitrates?

A

A drug-free interval of 12 to 14 hours

119
Q

This may occur during the drug-free interval (from nitrates).

A

Rebound myocardial ischemia

120
Q

Rebound myocardial ischemia may occur

A

during a nitrate drug-free interval.

Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso (17 decks)

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