Random crap

Question 1

Albuterol inhaler mechanism of action?

Answer 1

• mostly selective beta-2 receptor agonist
• While it is recognized that beta-2 receptors are the predominant receptors in bronchial smooth muscle, data indicate that there is a population of beta-2 receptors in the heart existing in a concentration between 10% and 50%. Hence, the possibility of an increased HR with administration.

Question 2

Albuterol dose, peak, and duration?

Answer 2

dose: 2 puffs
peak: 30 - 60 minutes
duration: 4 hours

(no onset time given; probably immediate)

Question 3

What are side effects of albuterol?

Answer 3

• tremor (most common, d/t direct stimulation of beta-2 receptors in skeletal muscles)
• increased HR (d/t either beta-2 stimulation => vasodilation => reflex tachycardia, or direct stimulation on beta-2 receptors located on the heart)
• decrease in arterial oxygenation with acute, severe asthma (d/t reflex relaxation of compensatory vasoconstriction in areas of decreased ventilation when beta-2 agonists are given)
• hypokalemia

Question 4

What is the mechanism behind the lowering of potassium when given large doses of albuterol?

Answer 4

1) albuterol stimulates the release of insulin, which then drives potassium into the cells
2) albuterol stimulates the Na+/K+ pump, causing potassium to shift into cells

(potassium levels can decrease approx. 0.5 - 1 mEq)

(Other sources say: albuterol stimulates the release of glucose => insulin release => insulin stimulates Na/K pump => potassium driven into cell)

Question 5

Uses for beta-2 agonists, such as albuterol…

Answer 5

• relaxation of bronchiole and uterine smooth muscle
  (ie. treatment of acute episodes of asthma; prevention of exercise-induced asthma; COPD; bronchospasm)

(beta-2 agonists in IV form may be given as continuous infusions to stop premature uterine contractions. KNOWLEDGE!!!)

Question 6

Calcium chloride ACLS dose, calcium replacement dose, post-CABG dose, duration?

Answer 6

ACLS dose: 2 - 4 mg/kg

calcium replacement dose: 3 - 6 mg/kg (over 5 - 15 minutes)

post-CABG dose: 5 - 10 mg/kg

duration: 10 - 20 minutes

(no onset or peak times given)

Question 7

Calcium chloride is recognized as what type of drug?

Answer 7

a positive inotropic drug

Question 8

Uses for calcium chloride…

Answer 8

• treatment of cardiac depression that may accompany delivery of volatile anesthetics
• transfusion of citrated blood
• following termination of cardio-pulmonary bypass

Question 9

Sodium Bicarbonate dosing in cardiac arrest, in less urgent forms of metabolic acidosis, and in infants?

Answer 9

cardiac arrest - rapid infusion of one to two 50mL (8.4%) vials every 5 - 10 minutes as needed (not recommended in the ACLS guidelines)

less urgent - 2 - 5 mEq/kg over a four to eight hour period, and may be added to IV fluids

in infants - the 4.2% solution is recommended, at a dose that does not exceed 8 mEq/kg/day.

Question 10

What is sodium bicarbonate used for?

Answer 10

1) increases plasma bicarbonate
2) buffers excess hydrogen ion concentration
3) raises blood pH
4) reverses the clinical manifestations of acidosis.

Question 11

Sodium bicarbonate is contraindicated in which patients?

Answer 11

• patients losing chloride by vomiting or from continuous GI suctioning
• patients receiving diuretics known to produce a hypochloremic alkalosis

Question 12

Sodium bicarbonate should be used cautiously in which patients?

Answer 12

• patients with congestive heart failure
• severe renal insufficiency
• clinical states in which there exists edema with sodium retention

Question 13

Overly aggressive therapy with sodium bicarbonate can result in what two things?

Answer 13

• metabolic alkalosis

- hypernatremia

Question 14

Why has sodium bicarbonate been removed from the ACLS algorithm?

Answer 14

Sodium bicarbonate elevates plasma pH by combining with hydrogen ions to form carbonic acid, which readily dissociates into carbon dioxide and water.

Because carbon dioxide, but not bicarbonate, readily crosses cell membranes and the blood-brain barrier, the resulting arterial hypercapnia will cause intracellular tissue acidosis.

Additionally, increased intra-myocardial carbon dioxide may reduce the possibility of cardiac resuscitation.