Cardiovascular ppts Flashcards by Victor Ogoti

Primarily Arterial Relaxation

Hydralazine

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Greater effect on Venous Relaxation

Nitroglycerin

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Venous & Arterial Relaxation

Sodium Nitroprusside

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MOA of:
Sodium Nitroprusside
Nitroglycerin
Hydralazine

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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Sodium Nitroprusside:
Onset?
Duration?

Onset within seconds

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

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

Decreases preload afterload and filling pressures

Increases cardiac output and stroke volume

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

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

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What is the starting dose of Sodium Nitroprusside

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

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Infusion rates of __________ is rarely exceeded when using Sodium Nitroprusside

3 mcg/kg/min

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

5 mcg/kg/min

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Maximum recommended infusion rate of Sodium Nitroprusside is

10 mcg/kg/min

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How is Sodium Nitroprusside Reconstituted?

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

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

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One cyanide ion binds with _________ to form cyanmethemoglobin

methemoglobin

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

thiocyanate

Liver

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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

renal

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thiosulfate B12.

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Cyanide toxicity results when ______________________

metabolic pathway is quantitatively overwhelmed

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

500 mcg/kg

2 mcg/kg/min

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

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

What are the treatments of cyanide toxicity

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.

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

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

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

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

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

decrease

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

redirection increase

At higher concentrations of nitroglycerin, ________ dilation also can occur

Arterial vasodilation

IV Nitroglycerin has an onset and duration of action of:

Onset 1-2 minutes | Duration 10 minutes

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

liver 3 minutes

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 ________

ST-segment elevation MI (STEMI).

Nitroglycerin infusions are usually started at _____ and titrated to effectiveness

10-20 mcg/min

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

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

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

narcotic

Generally nitroglycerin is mixed how?

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

Epi is used to treat

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

Beta-1 produces:

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

EPi Beta 2 stimulation results in?

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

Dose dependent effects of Epinephrine

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

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

``` 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

Hydralazine elimination half-life

~ 1 hour

Hydralazine metabolism

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.

Calcium Channel Blockers Proven to be useful in treatment of?

``` Angina HPTN arrhythmias Peripheral vascular disease Esophageal spasm Cerebral vasospasm Controlled hypotension ```

All CCB have negative ________and _____ actions

inotropic and chronotopic

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

4 antiarrhythmics

Depolarization of the SA and AV nodes is dependent on?

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

Diltiazem is effective with

Atrial Tachycardia (Verapamil is effective too) WPW Controlling Ventricle responses to A-Fib/Flutter