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Pharm III > Cardiovascular ppts > Flashcards

Cardiovascular ppts Flashcards

1
Q

Primarily Arterial Relaxation

A

Hydralazine

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2
Q

Greater effect on Venous Relaxation

A

Nitroglycerin

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3
Q

Venous & Arterial Relaxation

A

Sodium Nitroprusside

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4
Q

MOA of:
Sodium Nitroprusside
Nitroglycerin
Hydralazine

A

MOA of all 3 agents is believed to be primarily an induced increase in the concentration of vascular nitric oxide (not confirmed with hydralazine)

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5
Q

Sodium Nitroprusside:
Onset?
Duration?

A

Onset within seconds

Duration 1-3 minutes (3-5 minutes and 1-10 minutes)

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6
Q 
How does Sodium Nitroprusside effect:
Preload
Afterload
Cardiac filling pressures
Stroke volume
Cardiac output
A

Decreases preload afterload and filling pressures

Increases cardiac output and stroke volume

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7
Q

Using Nitroprusside contributes to a decreased in myocardial O2 consumption by?

A

Left ventricle volumes are decreased and diminished myocardial wall tension should contribute to a decrease in myocardial oxygen consumption

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8
Q

What is the starting dose of Sodium Nitroprusside

A

0.3 mcg/kg/min an titrated until a response occurs

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9
Q

Infusion rates of __________ is rarely exceeded when using Sodium Nitroprusside

A

3 mcg/kg/min

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10
Q

A top infusion rate of 3 mcg/kg/min is rarely exceeded when using Sodium Nitroprusside. However young, normotensive patients may require up to __________

A

5 mcg/kg/min

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11
Q

Maximum recommended infusion rate of Sodium Nitroprusside is

A

10 mcg/kg/min

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12
Q

How is Sodium Nitroprusside Reconstituted?

A

Reconstitute 50 mg by adding 2—3 ml of D5W injection. Further dilute in 250, 500, or 1000 ml of D5W injection to provide concentrations of 200, 100, or 50 mcg/ml, respectively.

The solution should be discarded after 24 hours.

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13
Q

The chemical structure of sodium nitroprusside contains how many cyanide ions? When are they released?

A

contains five cyanide ions, which are released upon metabolism by plasma hemoglobin

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14
Q

One cyanide ion binds with _________ to form cyanmethemoglobin

A

methemoglobin

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15
Q

One cyanide ion binds with methemoglobin to form cyanmethemoglobin, whereas the other 4 cyanide ions undergo rhodanese-catalyzed conversion to __________ in the __________

A

thiocyanate

Liver

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16
Q

One cyanide ion binds with methemoglobin to form cyanmethemoglobin, whereas the other 4 cyanide ions undergo rhodanese-catalyzed conversion to thiocyanate in the liver, with the thiocyanate undergoing ___________elimination

A

renal

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17
Q

One cyanide ion binds with methemoglobin to form cyanmethemoglobin, whereas the other 4 cyanide ions undergo rhodanese-catalyzed conversion to thiocyanate in the liver, with the thiocyanate undergoing renal elimination. This conversion to thiocyanate requires the cofactor ______.

A

thiosulfate B12.

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18
Q

Cyanide toxicity results when ______________________

A

metabolic pathway is quantitatively overwhelmed

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19
Q

In general, when more than ____ of sodium nitroprusside is administered faster than __, cyanide is generated faster than the patient can eliminate it.

A

500 mcg/kg

2 mcg/kg/min

20
Q

What are the signs/symptoms of cyanide toxicity with sodium nitroprusside?

A

Clinically, the development of metabolic acidosis, increased mixed venous oxygen content, tachycardia, and tachyphylaxis during sodium nitroprusside use are signs of cyanide toxicity

21
Q

What are the treatments of cyanide toxicity

A

Stop the sodium nitroprusside

Administer oxygen

Treat metabolic acidosis

Sodium nitrite 3% at 4-6 mg/kg over 3-5 minutes to promote production of methemoglobin to bind excess cyanide ions.

Sodium thiosulfate at 150-200 mg/kg over 14 min can be administered over 15 minutes and administered every 1 hours as needed.

Vitamin B12

Hydroxocobalamin can be effective (man made B12)

Methylene blue at 1-2 mg/kg may be useful

A new prodrug sulfanegen sodium is being tested.

22
Q

Nitroglycerin has a rapid onset and short duration so it is easily titratable. Nitroglycerin causes a ______ dilation, with an _____ increase in venous capacitance and a resultant ___________ in preload

A

Nitroglycerin causes a venous dilation, with an increase in venous capacitance and a resultant decrease in preload.

23
Q

Effects of nitroglycerin on preload, venous capacitance, cardiac filling pressures, myocardial wall tension and myocardial oxygen requirements

A

Nitroglycerin causes a venous dilation, with an increase in venous capacitance and a resultant decrease in preload. This results in lowering cardiac filling pressures, a lessening of myocardial wall tension and ultimately a decrease in myocardial oxygen requirements

24
Q

Nitroglycerin’s primary mechanism of action in the relief of angina is a ______ in preload and cardiac work.

A

decrease

25
Q

Using nitroglycerin can cause some of the larger coronary vessels to become dilated with a resultant ________ and _______ in blood flow to ischemic myocardium.

A

redirection

increase

26
Q

At higher concentrations of nitroglycerin, ________ dilation also can occur

A

Arterial vasodilation

27
Q

IV Nitroglycerin has an onset and duration of action of:

A

Onset 1-2 minutes

Duration 10 minutes

28
Q

Nitroglycerin is extensively metabolized in the _______ and has a half life of _______

A

liver

3 minutes

29
Q

IV nitroglycerin is used for “unloading” of the heart in CHF and MI. Guidelines suggest that IV infusions should be instituted following 3 sublingual doses of 0.4 mg every 5 minutes in patients having an ________

A

ST-segment elevation MI (STEMI).

30
Q

Nitroglycerin infusions are usually started at _____ and titrated to effectiveness

A

10-20 mcg/min

31
Q

Nitrates should be avoided in patient with:
BP of
HR of
Type of infarction

A

BP of < 90 mmHg
HR of < 50 or >100
Type of infarction of: Right ventricle

32
Q

Nitroglycerin has the ability to relax the smooth muscle of the biliary tract and provide relief from _______ induced biliary spasm

A

narcotic

33
Q

Generally nitroglycerin is mixed how?

A

Generally , 50 mg of nitroglycerin is mixed with 250 ml of D5W.

34
Q

Epi is used to treat

A

Anaphylaxis

Cardiopulmonary resuscitation

Treatment of shock with poor tissue O2 delivery and hypotension are combined (this is b/c of its alpha and beta effects)

May be useful as a sympathomimetic agent in patients unresponsive to indirect-acting agents and in those in whom simultaneous Beta 1 (cardiac stimulation) and Beta 2 receptor stimulation (vasodilation).

Dominance of alpha or beta effects is dose related

35
Q

Beta-1 produces:

A

+ inotropic (force of contraction)
+ chronotropic (heart rate)
+ dromotropic (conduction velocity)

36
Q

EPi Beta 2 stimulation results in?

A

Bronchodilation

Vasodilation

Stabilization of mast cells (resulting in decreasing histamine release)

Concurrent alpha stimulation promotes a decrease in bronchial secretion. Net effects are a decrease in airway resistance with an improvement in oxygenation

37
Q

Dose dependent effects of Epinephrine

A

Low Doses 10 mcg/min: The peripheral vasculature promotes the redistribution of blood flow to skeletal muscle, thus producing a decrease in SVR

As doses increase, alpha effects predominates resulting in vasoconstriction and increase in SVR: SBP increases, DBP remains relatively unchanged, Pulse Pressure increases

38
Q

Beta stimulation leads to activation of the renin-angiotensin system and also: to an increase in:

A 
lipolysis
Glycogenolysis
Gluconeogenesis
Ketone production
Lactate release by skeletal muscle 
Insulin secretion is inhibited by an overriding Beta 2 stimulation

Epinephrine induced Beta 2 stimulation also can cause a transient hyperkalemia as potassium follows glucose out of the hepatic cells

This is followed by a longer hypokalemia as Beta 2 stimulation then forces potassium (that is extracellular) into red blood cells

39
Q

Hydralazine elimination half-life

A

~ 1 hour

40
Q

Hydralazine metabolism

A

Hepatic metabolism with renal excretion

Acetylation is partly responsible for the metabolism of hydralazine as well.

Slow acetylators may be more prone to a drug induced lupus syndrome that can result from high serum concentrations during chronic treatment.

41
Q

Calcium Channel Blockers Proven to be useful in treatment of?

A 
Angina
HPTN
 arrhythmias
Peripheral vascular disease
Esophageal spasm
Cerebral vasospasm
Controlled hypotension
42
Q

All CCB have negative ________and _____ actions

A

inotropic and chronotopic

43
Q

CCB are class _______ that block calcium channels, therefore depressing electrical impulses in the SA and AV nodes

A

4 antiarrhythmics

44
Q

Depolarization of the SA and AV nodes is dependent on?

A

the inward flux of calcium during the depolarization phases of the cardiac action potential

45
Q

Diltiazem is effective with

A

Atrial Tachycardia (Verapamil is effective too)

WPW

Controlling Ventricle responses to A-Fib/Flutter

Pharm III (11 decks)

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