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2-Pharm Exam 3 > Antihypertensive Vasodilators > Flashcards

Antihypertensive Vasodilators Flashcards

1
Q

Review nitric oxide (NO) pathway.

A
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2
Q

What is a side effect of inhaled NO?

A
  • NO Toxicity
  • Inhaled NO increases methemoglobin levels (usually modest)
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3
Q

What can occur with d/c of inhaled NO therapy?

A

Rebound hypoxemia or pulmonary HTN may occur with sudden discontinuing inhaled therapy (must wean inhaled NO slowly)

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4
Q

What can happen when given NO in patients with LV dysfunction/failure?

A

Can precipitate acute left heart failure and pulmonary edema when given in presence of LV dysfunction/failure

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5
Q

What is NO toxicity?

A
  • NO oxidized to NO2 especially with high oxygen concentrations
  • NO2 is a pulmonary toxin
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6
Q

Why is it important to continuously monitor inspired NO and NO2 concentrations?

A

NO Toxicity

Important to continuously monitor inspired NO and NO2 concentrations during inhaled therapy (inhaled NO delivery system should have this)

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7
Q

What are examples of nitrodilators?

A
  • Sodium Nitroprusside
  • Nitroglycerin
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8
Q

What is the target of Sodium Nitroprusside (SNP)?

A

Direct-acting nonselective peripheral vasodilator

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9
Q

What is the effect of Sodium Nitroprusside (SNP)?

A
  • venous and arterial smooth muscle
  • lacks effect on nonvascular smooth muscle or cardiac muscle
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10
Q

What is the onset of Sodium Nitroprusside (SNP)?

A

Immediate onset & administered by continuous IV infusion

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11
Q

What is the MOA of Sodium Nitroprusside (SNP)?

A

IV SNP infusion interacts w/oxyhemoglobin and dissociates immediately to form methemoglobin while releasing cyanide & NO

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12
Q

What does released NO from Sodium Nitroprusside (SNP) cause?

A
  • released NO activates GC in vascular smooth muscle
  • increased cGMP
  • inhibits calcium entry into vascular smooth muscle cells
  • vasodilation
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13
Q

What is the metabolism of Sodium Nitroprusside (SNP)?

A

SNP interacts with the Fe in oxyhemoglobin to yield methemoglobin and an unstable SNP radical

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14
Q

What does an unstable SNP radical from Sodium Nitroprusside (SNP) metabolism breakdown into?

A

which breaks down into 5 cyanide ions; 1 ion forms cyanomethemoglobin (non-toxic)

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15
Q

What happens to the remaining CN molecules from Sodium Nitroprusside (SNP) metabolism?

A
  • The remaining CN molecules are converted to thiocyanate by way of rhodanese enzyme
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16
Q

What can be used to treat cyanide toxicity?

A

Rhodanese also uses exogenous thiosulfate as a sulfur donor to treat cyanide toxicity

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17
Q

Sodium Nitroprusside (SNP) metabolism: When is Thiocyanate eliminated from the body?

A

Thiocyanate is eliminated in the urine (3-7 days)

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18
Q

What is the dose of Sodium Nitroprusside (SNP)?

A

O.3 mcg/kg/min IV infusion titrated

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19
Q

What is the max dose of Sodium Nitroprusside (SNP)?

A

a max of 10 mcg/kg/min (not to infuse max rate longer than 10 min)

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20
Q

What needs to be present Sodium Nitroprusside (SNP) infusion?

A

Need arterial line

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21
Q

What occurs with Sodium Nitroprusside (SNP) doses over 2 mcg/kg/min?

A

place patient at risk for cyanide toxicity

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22
Q

What HR change can occur with Sodium Nitroprusside (SNP)?

A

Baroreceptor mediated tachycardia with increased myocardial contractility can oppose vasodilatory effect

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23
Q

What effect does Sodium Nitroprusside (SNP) have on venous return and CO?

A

Decreased venous return but increase in CO may result due to reflex sympathetic activity and afterload reduction

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24
Q

What effects occur with Sodium Nitroprusside (SNP) administration in LV failure?

A

SNP decreases SVR, pulmonary vascular resistance, & right atrial pressure

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25
Q

Why must caution with Sodium Nitroprusside (SNP) be used in the presence of myocardial ischemia?

A
  • Implicated in “coronary steal” phenomenon
  • SNP can also decrease diastolic BP
  • decrease coronary perfusion pressure & decrease coronary blood flow
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26
Q

What effect does Sodium Nitroprusside (SNP) have on renal function?

A
  • May result in decreased renal function (from low BP)
  • Increase renin (blood pressure overshoot when D/C’d)
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27
Q

What effect does Sodium Nitroprusside (SNP) have on liver?

A

Does not effect hepatic blood flow changes or hepatic injury

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28
Q

What impact can occur with Sodium Nitroprusside (SNP) and cerebral system?

A
  • Increases cerebral blood flow/cerebral blood volume
  • Can raise ICP with those with decreased intracranial compliance
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29
Q

What are increases in ICP from Sodium Nitroprusside (SNP) offset with?

A

Offset with hypocarbia and hyperoxia

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30
Q

When can maximum increases in ICP from Sodium Nitroprusside (SNP) be seen?

A

Maximal increases in ICP when SBP < 30%

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31
Q

When should Sodium Nitroprusside (SNP) be used cautiously?

A

Caution with carotid stenosis, patients with inadequate cerebral blood flow

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32
Q

What respiratory and ventilatory effects can be seen with Sodium Nitroprusside (SNP)?

A

Decreases in PaO2 by attenuating the homeostatic process of hypoxic pulmonary vasoconstriction (HPV) and resulting in shunting (VQ mismatch)

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33
Q

What can bee added to reverse the respiratory effects from Sodium Nitroprusside (SNP)?

A

Adding PEEP may reverse vasodilator-induced decrease in PaO2

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34
Q

What coagulation effects can be seen with Sodium Nitroprusside (SNP)?

A

Increase intracellular cGMP inhibits platelet aggregation and may increase bleeding bleeding time with infusion rates > 3 mcg/kg/min (reversible)

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35
Q

When does cyanide toxicity occur?

A

Cyanide toxicity may occur when the IV Sodium Nitroprusside (SNP) infusion rate is >2mcg/kg/min

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36
Q

How does cyanide toxicity occur?

A
  • Prolonged or high infusion rates can cause cyanide radical accumulation which bind to tissue cytochrome oxidase and prevents oxidative phosphorylation (part of the cellular respiration process)
  • Occurs with Sodium Nitroprusside (SNP)
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37
Q

What can cyanide toxicity lead to (3)?

A

Leads to tissue anoxia, anaerobic metabolism and lactic acidosis

38
Q

When is cyanide toxicity is seen?

A

Suspect when tachyphylaxis is seen and with rates > 2 mcg/kg/min along with lactic acidosis and increase in mixed venous O2 (tissues aren’t able to use O2) d/t paralysis of cytochrome oxidase activity

39
Q

What acid base disturbance can occur with cyanide toxicity?

A

Metabolic acidosis d/t anaerobic metabolism in the tissues

40
Q

What are side effects of awake patients with cyanide toxicity?

A

Awake patients: CNS dysfunction (mental status changes, seizures)

41
Q

What is the treatment of cyanide toxicity?

A

D/C Sodium Nitroprusside (SNP) and administer 100% O2

42
Q

What medications should be adminsitered for cyanide toxicity?

A
  • Sodium bicarbonate
  • Hydroxocobalamin (vitamin B12a)
  • For severe toxicity: Sodium nitrate
43
Q

Cyanide toxicity: Why is sodium bicarbonate administered?

A

Sodium bicarbonate administered to correct metabolic acidosis

44
Q

Cyanide toxicity: What is the components of Sodium thiosulfate administration?

A
  • 150 mg/kg IV over 15 min: first-line tx
  • acts as a sulfur donor to convert cyanide to thiocyanate which is non-toxic
45
Q

What is the first line treatment for cyanide toxicity?

A
  • Sodium thiosulfate 150 mg/kg IV over 15 min
  • Hydroxocobalamin (vitamin B12a)
46
Q

Cyanide toxicity: What is the components of Hydroxocobalamin (vitamin B12a) administration?

A
  • 5gm initial dose; also first-line tx
  • 2nd dose depends on clinical response
  • binds cyanide to form cyanocobalamin (vitamin B12)
  • expensive drug
  • may produce reddish discoloration of skin & mucous membranes, and interfere with co-oximetry blood gas analysis
47
Q

What is the treatment of severe cyanide toxicity treatment?

A
  • Sodium nitrate 5mg/kg slow IV
  • converts Hb to methemoglobin which cyanide reacts with to form cyanomethemoglobin (non-toxic)
48
Q

What is cyanide toxicity associated with?

A

Sodium Nitroprusside (SNP)

49
Q

What is the clearance of Thiocyanate?

A

Slowly cleared by the kidneys (elimination 1/2 time 3-7 days)

50
Q

What is the components of Thiocyanate toxicity?

A

Rare, less toxic than free CN

51
Q

When is Thiocyanate toxicity seen?

A
  • Seen with prolonged infusions 2-5mcg/kg/min
  • 7-14 days with normal renal function
  • 3-6 with reduced function
52
Q

What is the symptoms of thiocyanate toxicity?

A

fatigue, tinnitus, N/V

53
Q

What is the neurotoxicity symptoms of thiocyanate toxicity?

A

hyperreflexia, confusion, psychosis, miosis, seizures, coma

54
Q

Where does Nitroglycerin (NTG) act?

A

Acts on venous capacitance vessels and large coronary arteries

55
Q

What does Nitroglycerin (NTG) produce?

A
  • produce peripheral pooling of blood
  • decreases cardiac ventricular wall tension
  • larger doses relax arterial vascular smooth muscle
56
Q

What is the clinical indications for Nitroglycerin (NTG)?

A

SL or IV in tx of myocardial ischemia or vasospasm, volume overload/HF, controlled hypotension

57
Q

How does Nitroglycerin (NTG) help with HF?

A

Decreases preload

58
Q

What is the MOA Nitroglycerin (NTG)?

A

Administration generates NO which stimulates production of cGMP to cause peripheral vasodilation

59
Q

What does Nitroglycerin (NTG) require?

A

NTG requires a glutathione-dependent pathway involving glutathione and glutathione S-transferase to biotransform nitrate group in NTG into NO

60
Q

When is Nitroglycerin (NTG) not recommended?

A

severe aortic stenosis or hypertrophic obstructive cardiomyopathy

61
Q

What is characteristics of Nitroglycerin (NTG) SL route?

A
  • limited hepatic first-pass
  • peak plasma concentration achieved in 4 min
62
Q

What is the elimination half time of Nitroglycerin (NTG)?

A

half-time 1.5 min

63
Q

What is the dose of Nitroglycerin (NTG) for controlling BP?

A

10-200 mcg/min (approximately 0.1 to 3 mcg/kg per minute)

64
Q

What is a side effect of Nitroglycerin (NTG)?

A
  • Risk of methemoglobinemia at high doses
65
Q

What is the nitrate metabolite of NTG capable of?

A

oxidizing ferrous ion in hemoglobin to the ferric state with production of methemoglobinemia

66
Q

What is the tolerance to Nitroglycerin (NTG)?

A
  • dose-dependent & duration dependent
  • usually seen within 24 hrs of sustained treatment
67
Q

What is recommendation to reversing Nitroglycerin (NTG) tolerance?

A

a drug-free interval of 12-14 hours recommended to reverse tolerance (NTG or other nitrates)

68
Q

What is hydralazine?

A

Direct systemic arterial vasodilator

69
Q

What is the MOA of Hydralazine?

A

Hyperpolarizes smooth muscles cells, activates guanylate cyclase to produce vasorelaxation

70
Q

What is the side effect of Hydralazine?

A

Can result in reflex tachycardia

71
Q

What population should hydralazine be used carefully?

A

careful with CAD/ischemia, lupus syndrome w/ long term use

72
Q

What is the anesthesia use of Hydralazine?

A

Tx of elevated BP with low HR

73
Q

What is the dose of Hydralazine?

A

Administered as bolus doses (eg, 2.5 mg), which may be repeated every 5 minutes up to 20 mg

74
Q

What are disadvantage of Hydralazine?

A

include relatively slow onset compared with other IV antihypertensive agents, with a less predictable antihypertensive response

75
Q

What is the onset of Hydralazine?

A

5–20 min

76
Q

What is the peak of Hydralazine?

A

15–30 min

77
Q

What is the duration of Hydralazine?

A

2–6 hr

78
Q

What is the MOA of Fenoldopam?

A

Dopamine type-1 agonist resulting in systemic arterial dilation by increasing cAMP

79
Q

What is the effects of Fenoldopam?

A
  • Increases renal and splanchnic blood flow & increases UOP
80
Q

When is Fenoldopam indicated?

A

It is indicated for patients undergoing cardiac surgery and aortic aneurysm repair because of its antihypertensive and renal-sparing properties

81
Q

What is the side effects of Fenoldopam?

A

Reflex tachycardia and increased IOP

82
Q

What is the dose of Fenoldopam?

A

0.05–0.3 mcg/kg/min

83
Q

What is the first line oral agent for Diuretics?

A

First-line oral agents used for essential HTN

84
Q

What diuretics are the first line choice?

A

Thiazide drugs first-line

85
Q

When are loop diuretics are used for HTN?

A

loop diuretics reserved for patients w/renal insufficiency or HF

86
Q

What are examples of loop diuretics?

A

furosemide, bumetanide

87
Q

What is the side effect of loop diuretics?

A

Both result in K+ loss – monitor serum K+ & magnesium, may require supplementation

88
Q

Diuretics: ___________ with IV furosemide

A

Venodilating effects

89
Q

What are the properities of Diuretics?

A

Aldosterone antagonists “K+ sparing” used with ACE inhibitors

90
Q

What is an example of Aldosterone antagonists diuretics?

A

Example: Spironolactone

91
Q

What is the MOA of Aldosterone antagonists?

A

Blocks the effects of aldosterone which block the reabsorption of Na+ & excretion of K+ which leads to decrease in BP and fluid overload

2-Pharm Exam 3 (14 decks)

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