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Pharmacology > Periph Vasodilators > Flashcards

Periph Vasodilators Flashcards

1
Q

What do peripheral vasodilators facilitate?

A

Forward flow in AR, MR or HF

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2
Q

When do we use peripheral vasodilators?

A

For controlled hypotension and to treat hypertensive ccrisis

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3
Q

Two most common peripheral vasodilators we use?

A

Nipride and NTG

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4
Q

Approximately what is the goal MAP in cases that use controlled hypotension?

A

70

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5
Q

When would we NOT use controlled hypotension?

A

Severe CVD, SCI or TBI. They all really need perfusion.

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6
Q

Where does nipride lack significant effects?

A

nonvascular smooth muscle and cardiac muscle (DOES NOT DILATE THE CORONARIES)

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7
Q

Does nipride relax arterial or venous?

A

Both

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8
Q

Is nipride direct or indirect and selective or nonselective?

A

Direct acting

Non selective

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9
Q

What is the MOA of nipride?

A

Nipride interacts with oxyhemoglobin which dissociates immediately to form methemoglobin and the release of NO and cyanide. NO activates the guanylate cyclase (in the vascular muscle) increasing cGMP. cGMP inhibits calcium entry into the vascular smooth musle but increases the uptake of Ca into the sER. RESULTS IN VASODILATION!

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10
Q

How is nipride metabolized?

A

The transfer of an election from Fe to nipride yields metHgb and an unstable nipride radical where all 5 cyanide ions are released. One of these cyanide ions reacts with metHgb to form cyano-methemoglobin. The remainder of cyanide ions are metabolized in the liver and kidney are are converted to thiocyanate which is cleared by the kidney.

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11
Q

Why do we care about the metabolism of nipride?

A

Cyanide toxicity.

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12
Q

When can cyanide toxicity occur?

A

At rates over 2mcg/kg/min for long periods.

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13
Q

When do we start to suspect cyanide toxicity?

A

When a patient starts demonstrating resistance to effects, previous responsive patient could now be unresponsive at rates over 2-10mcg/kg/min.

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14
Q

Why is cyanide toxicity so bad?

A

The cyanide ion interferes with the tissues ability to uptake oxygen which may precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis (see a lactate like 10 instead of the normal 1-3)

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15
Q

What can occur as a result of cyanide toxicity?

A

CNS dysfunction, mental status changes and seizures.

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16
Q

How do we treat cyanide toxicity?

A

Immediately discontinue nipride, 100% FiO2 admin despite their O2 sat. Sodium bicarb to correct metabolic acidosis. Sodium thiosulfate acts as a sulfur donor to convert cyanide to thiocyanate. Sodium nitrate 5mg/kg if severe toxicity (converts hemoglobin to metHgb which converts cyanide to cyanomethemoglobin).

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17
Q

Do we worry about thiocyanate toxicity?

A

It is rare seeing as thiocynate (which is the result of the livers conversion of a cyanide ion) is cleared by the kidney in 3 to 7 days. It is less toxic than cyanide.

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18
Q

What are some symptoms of thiocyanate toxicity?

A

N/V, tinnitus, fatigue, CNS hyperreflexia, confusion, psychosis, miosis, seizure and coma.

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19
Q

What about methemoglobinemia?

A

It is also rare but should be considered as a differential diagnosis in patients with impaired oxygenation despite adequate CO and arterial oxygenation.

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20
Q

What happens when nipride is exposed to light?

A

With continuous exposure to light nipride is converted to aquapentacyanoferrate in the presence of light and the release of hydrogen cyanide.

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21
Q

What should nipride be mixed in?

A

5% glucose in water.

22
Q

What is the dose of nipride?

A

0.3mcg/kg/min-10mcg/kg/min IV

23
Q

The max dose of nipride should not be infused for greater than how long?

A

10 minutes.

24
Q

What is the onset and DOA of nipride?

A

Immediate onset and a short duration of action.

25
Q

What considerations do we have regarding the use of nipride?

A

Requires a continuous IV administration to maintain a therapeutic effect. Extremely potent use and aline.

26
Q

What kind of affects does nipride have on the CV system?

A

Direct venous arterial vasodilation, decreased venous capacitance and decreased preload. We can see a baroreceptor mediated reflex in HR. We decrease our SBP, SVR, PVR while we increase contractility. There is an intracoronary steal in areas of damage associated with MI.

27
Q

What is coronary steal?

A

Coronary steal (with its symptoms termed cardiac steal syndrome) is a phenomenon where an alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation.[1] It is caused when there is narrowing of the coronary arteries and a coronary vasodilator[2] is used - “stealing” blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.

28
Q

What CNS effects do we see when we use nipride?

A

Increased cerebral blood flow and ICP

29
Q

What pulmonary effects do we see when we use nipride?

A

Attenuation of hypoxic vasoconstriction.

30
Q

What hematological effects do we see with nipride use?

A

Increases in intracellular GMP inhibit platelet aggregation and increase bleeding time.

31
Q

In controlled hypotension what is the dose of nipride that we are not to exceed?

A

2mcg/kg/min

32
Q

In a hypertensive crisis when we can actually bolus nipride (oh dear lord help us all) what is the dose?

A

1-2mcg/kg IV

This just seems like a huge dose. But I guess it’s only about 7 minutes worth.

33
Q

Where does NTG act?

A

on the venous capacitance vessels and large coronary arteries.

34
Q

How can we give NTG?

A

IV, SL, Oral, transdermal ointment.

35
Q

Why can’t a patient be on NTG for 24 hours?

A

They develop a tolerance.

36
Q

What is the MOA of NTG?

A

Similar to nipride. Produce NO through a glutathione-dependant pathway which involves glutathione and glutathione s-transferase. The generation of NO then stimulates cGMP to cause peripheral vasodilation.

37
Q

What is the elimination half time of NTG?

A

1.5 minutes.

38
Q

What can happen with high doses of NTG? When is it more likely.

A

Methemoglobinema when a nitrite metabolite oxidizes a ferrous ion in Hgb to ferric to form which leads to formation of metHgb. More likely in a liver patient.

39
Q

How is methemoglobinemia treated?

A

Methylene blue 1-2mg/kg IV over 5 minutes to convert metHgb to Hgb.

40
Q

What are the CV effects of NTG?

A

Venodilation more than arterial dilation (but remember as doses get higher this could change). Decrease venous return. Decrease L and R ventricular EDP. Decrease in CO. No change or only a slight increase in HR. No change in SVR. Increase in coronary blood flow to ischemic subendocardial areas.

41
Q

What are the CNS effects of NTG?

A

vasodilation and increased ICP headaches.

42
Q

What are the pulmonary effects of NTG?

A

decreased PVR. Bronchial dilation, inhibits hypoxic pulmonary vasoconstriction.

43
Q

What are the heme effects of NTG?

A

Prolonged bleeding time, inhibits platelet aggregation

44
Q

What effect do we see in the GI system with NTG?

A

relaxes the smooth muscles of the GI tract. (they sometimes give one dose for retained placenta to relax the uterus or during sphincter of Oddi dysfunction.

45
Q

Clinical uses of NTG are?

A

Angina where venodilation and increased venous capacitance decreases venous return to the heart which reduces R and L EDPs. Reduces the myocardial O2 demand. In HF NTG decreases preload, relieves pulmonary edema and limits damage of an MI. In controlled hypotension NTG is less potent than nipride.

46
Q

What is the dose of NTG for controlled hypotension? When is it not recommended?

A

4-5mcg/kg/min IV. Not recommended in cranial surgery prior to opening of the dura.

47
Q

What is the dose of NTG for sphincter of oddi spasm? When can this occur?

A

200mcg at one time. Can occur with lap chole

48
Q

Tell me about isosorbid?

A

It is an oral nitrate used for angina pectoris. It is well absorbed from the GI tract with a DOA of 6 hours. SL DOA is 2 hours. Works mostly on the venous circulation, improves regional distribution of myocardial blood flow in patients with CAD. SE include orthostatic hypotension.

49
Q

What is the active metabolite of isosorbid? Why do we care?

A

Isosorbid-5-mononitrate. It is more active than the parent compound.

50
Q

Tell me about dipyridamole?

A

Inhibits platelt aggregation. Interferes with platelet function by potentiating the effect of prostacyclin or by inhibiting phosphodiesterase enzyme activity and increasing intracellular cAMP. Used in Angina and prophylaxis against thromboembolism.

51
Q

Tell me about trimethaphan?

A

It is a ganglionic blocker and peripheral vasodilator. It has a rapid onset and must be given IV continous 10-200mcg/kg/min. Blocks the ANS and relaxes capacitance vessels. Lowers BP, CO and SVR. Can have increased HR because of parasympathetic blockade? SE include mydraiasis, decreased GI activity, and urinary retention.

Pharmacology (23 decks)

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