Vasodilators & Nonadrenergic Inotropes Flashcards Preview

Board Review CRNA (Memory Master) > Vasodilators & Nonadrenergic Inotropes > Flashcards

Flashcards in Vasodilators & Nonadrenergic Inotropes Deck (49)
Loading flashcards...
1

**What potential side effect occurs with inamrinone, but not with milrinone?

Inamrinone (Inocor) can produce thrombocytopenia with long-term therapy. Milrinone (Primacor) does not produce any apparent effects on platelets.

2

What are the cardiovascular actions of glucagon? What
second messenger is involved in these responses?

Glucagon increases myocardial contractility (has a positive inotropic effect) and heart rate. The positive inotropic and chronotropic effects of glucagon increase cardiac output. Glucagon increases intracellular levels of cyclic AMP by mechanisms independent of beta-adrenergic receptor stimulation.

3

List three cardiac effects of digitalis.

Digitalis: (1) enhances myocardial contractility, (2) decreases heart rate, and (3) slows impulse propagation through the atrioventricular node. The decreased heart rate and slowed conduction through the atrioventricular node occur because digitalis enhances parasympathetic nervous system activity.

4

What are the two principle clinical uses of digoxin?

Digoxin (digitalis) is used to treat congestive heart failure and to control supraventricular dysrhythmias (atrial tachycardia, atrial flutter, or atrial fibrillation).

5

Digitalis produces its positive inotropic effect by what mechanism?

Digitalis inhibits the sodium-potassium pump. When the sodium-potassium pump is inhibited, sodium accumulates in the cell. As sodium accumulates intracellularly, a sodium-calcium exchange system (sodium out in exchange for calcium in) is accelerated. Hence, calcium accumulates in the cardiac cell. As calcium accumulates in the cardiac cell, contractility increases.

6

In what phase of the cardiac cycle does digitalis work to slow heart rate?

Digitalis works in phase 4. Digitalis decreases automaticity and lowers heart rate. Automaticity is reflected in the slope of phase 4 depolarization. Digitalis decreases phase 4 depolarization by activating the parasympathetic nervous system.

7

What are three signs of digitalis toxicity?

Signs of digitalis toxicity include: (1) atrial or ventricular cardiac dysrhythmias, (2) prolonged PR interval, and (3) gastrointestinal disturbances (anorexia, nausea, and vomiting).

8

What three electrolyte disturbances enhance digitalis toxicity?

Hypokalemia, hypercalcemia and hypomagnesemia are electrolyte disturbances that increase the likelihood of digitalis toxicity.

9

Why does hypokalemia enhance digitalis toxicity?

Hypokalemia allows increased binding of digitalis to the Na= K+ ATPase (pump) in cardiac cells, resulting in an excessive drug effect.

10

Why should hyperventilation be avoided during anesthesia for the patient who is taking digitalis?

Hyperventilation may cause hypokalemia, and hypokalemia increases the likelihood of digitalis toxicity. Plasma potassium concentration decreases 0.5 mEq/L for each 10 mmHg decrease in PaC02.

11

What are five uses of calcium entry blockers?

Calcium channel blockers are used to treat: (1) supraventricular tachydysrhythmias (verapamil); (2) essential hypertension; (3) coronary artery vasospasm (nifedipine and diltiazem); (4) angina pectoris, and (5) cerebral artery vasospasm (nimodipine).

12

How does verapamil effect systemic vascular resistance (SVR) and heart rate?

Verapamil decreases both SVR (by relaxing vascular smooth muscle) and heart rate.

13

Verapamil potentiates the actions of what drugs used in anesthesia?

Verapamil potentiates the actions of nondepolarizing and depolarizing muscle relaxants.

14

Verapamil is contraindicated in what six patient groups?

Verapamil should not be given to patients with (1) Wolff- Parkinson White syndrome, (2) sick sinus syndrome, (3) atrioventricular block, or (4) heart failure. Verapamil should also be avoided or used cautiously in (5) patients on beta blockers, and (6) patients taking digitalis.

15

Why is verapamil a poor choice when treating patients with Wolff-Parkinson-White syndrome?

Verapamil may increase conduction velocity in the accessory tract and increase heart rate excessively.

16

Why should verapamil be avoided or used cautiously in the patient taking either a beta blocker (propranolol) or digitalis?

Verapamil and propranolol, or verapamil and digitalis, can produce complete heart block.

17

What are the cardiovascular actions of diltiazem?

Diltiazem is a good coronary vasodilator but a poor peripheral vasodilator. Diltiazem also decreases heart rate.

18

How does nifedipine affect systemic vascular resistance (SVR) and heart rate?

Nifedipine decreases systemic vascular resistance (SVR) and causes a reflex increase in heart rate.

19

When would you use sublingual nifedipine?

Sublingual nifedipine might be used to treat intraoperative myocardial ischemia when hemodynamics are normal.

20

Name four vasodilators that decrease blood pressure by direct effects on vascular smooth muscle independent of alpha or beta receptors.

Direct acting vasodilators are: (1) hydralazine, (2) nitroprusside, (3) nitroglycerin, and (4) diazoxide.

21

Name four vasodilators that decrease blood pressure by direct effects on vascular smooth muscle independent of alpha or beta receptors.

Direct acting vasodilators are: (1) hydralazine, (2) nitroprusside, (3) nitroglycerin, and (4) diazoxide.

22

How do the nitrovasodilators, nitroprusside and nitroglycerin, relax vascular smooth muscle? What substance is produced? What enzyme and what second messenger are involved?

Nitroprusside and nitroglycerin donate nitric oxide (NO). Nitric oxide (NO) activates the enzyme soluble guanylate cyclase, which increases the production of cyclic guanosine monophosphate {cGMP). Cyclic GMP, a second messenger, relaxes vascular smooth muscle, thereby promoting vasodilation and a decrease in blood pressure.

23

What are four contraindications for using sodium nitroprusside?

Avoid nitroprusside if the patient has (1) liver disease, (2) kidney disease, (3) hypothyroidism, or (4) vitamin B-12 deficiency.

24

What are acceptable nitroprusside doses? What are maximum acceptable nitroprusside infusion rates?

The acceptable dose range for IV nitroprusside is 0.25 - 10 mcg/kg/min. Begin IV infusion at 0.5 mcg/kg/min. Acceptable maximum infusion rates are 10 mcg/kg/min for 10 - 15 minutes or 2 mcg/kg/min for 1-3 hours or 0.5mg/kg/hr for chronic infusion.

25

How is cyanide produced?

With high doses of nitroprusside, the ferrous iron of nitroprusside reacts with sulfhydryl groups in red blood cells and releases cyanide.

26

**Sodium nitroprusside contains 5 cyanide ions (CN-) and may cause cyanide toxicity, as you know. What three reactions may cyanide ions (CN-) undergo?

Cyanide ions (CN-) may react in three ways: (1) binding to methemoglobin to form cyanomethemoglobin, (2) reaction with thiosulfate in the liver to produce thiocyandise, catalyzed by rhodanase, and (3) binding to tissue cytochrome oxidase, which interferes with normal oxygen utilization by the tissues.

27

**How do cyanide ions interfere with oxygen utilization at tissue cytochrome oxidase?

Binding of cyanide ions to tissue cytochrome oxidase uncouples oxidative phosphorylation, preventing the formation of ATP.

28

**List the four hallmark signs and symptoms of cyanide toxicity.

Acute cyanide toxicity is characterized by (1) metabolic acidosis (base deficit), (2) cardiac arrhythmias, (3) increased venous oxygen content due to inhibition of cytochrome oxidase and consequent inability of cells to utilize oxygen, and (4) tachyphylaxis.

29

What is the best indicator of cyanide toxicity?

Base deficit may be the best indicator of cyanide toxicity.
The metabolic acidosis accompanying cyanide toxicity “allows the observant practitioner to detect this cellular toxicity.” Arterial blood gases permit determination of the base deficit and hence may most accurately assess cyanide toxicity.

30

How do you know when tachyphylaxis to nitroprusside has occurred?

When a patient is resistant to the hypotensive effects of nitroprusside despite increasing the infusion rate up to 8 micrograms/kg/min, one should suspect cyanide toxicity.