CV pharm PPT

Question 1

What is the result of beta-1 agonism?

Answer 1

increased inotropy

increased chronotropy

increased cardiac output

Question 2

What is the result of beta-2 agonism?

Answer 2

peripheral vasodilation (decreasing afterload)

bronchodilation

Question 3

What is the result of alpha-1 agonism?

Answer 3

skin, mesenteric, hepatorenal constriction

leading to an increase in afterload

Question 4

Epinephrine infusion starting dose?

Answer 4

0.01 - 0.02 mcg/kg/min

(to a max of 0.3 mcg/kg/min)

(4 mg in 250 mL D5W or NS = 16 mcg/mL)

Question 5

Epinephrine pings on what adrenergic receptors?

Answer 5

beta-1 and beta-2 (with low doses of 0.01 - 0.04 mcg/kg/min)

alpha-1 (with higher doses, up to 0.3 mcg/kg/min)

Question 6

Why can an epinephrine infusion cause mild hypokalemia?

Answer 6

d/t the increased activity of the Na/K pump, silly muppet…

Question 7

Norepinephrine infusion starting dose?

Answer 7

0.01 - 0.02 mcg/kg/min

(to a max of 0.3 mcg/kg/min)

(4 mg in 250 mL D5W or NS = 16 mcg/mL)

Question 8

Norepinephrine pings on what adrenergic receptors?

Answer 8

beta-1 and beta-2 (beta-1 > beta-2)

alpha-1 (potent effect!)

Question 9

Is norepinephrine a good first line drug for low cardiac output in cardiopulmonary bypass?

Answer 9

hell yeah it is. use that shit!

Question 10

Milrinone is what class of drug?

Answer 10

a phosphodiesterase inhibitor

Question 11

What do phosphodiesterase inhibitors do?

Answer 11

phosphodiesterase breaks down cyclic-AMP within the cell.

with inhibition, you have the cAMP building up.

in cardiac muscle this leads to increased inotropy.

in vascular smooth muscle this causes vasodilation.

(may selectively dilate pulmonary greater than the systemic system)

good times…

Question 12

Will milrinone work in the presence of a beta-blocker?

Answer 12

yes.

phosphodiesterase inhibitors are considered “back-door” drugs.

they work within the cell, not at the receptor site outside the cell.

Question 13

Milrinone loading dose?

Answer 13

50 - 75 mcg/kg over 10 minutes

Question 14

Milrinone infusion starting dose?

Answer 14

0.375 - 0.75 mcg/kg/min

20 mg in 100mL = 200mcg/mL

Question 15

Is milrinone recommended with MI patients?

Answer 15

not at all

Question 16

Nipride infusion starting dose?

Answer 16

0.25 - 0.5 mcg/kg/min

(max dose 10 mcg/kg/min)

(50 mg in 250 mL D5W or NS = 200 mcg/mL)

Question 17

How does nipride work?

Answer 17

it is a direct nonselective arterial and venous smooth muscle dilator (arterial > venous). because of this, it decreases both preload and afterload.

(direct NO donor, activates guanylyl cyclase, increases cGMP, inhibits Ca++, vascular smooth muscle relaxation)

Question 18

Can nipride inhibit hypoxic pulmonary vasoconstriction?

Answer 18

yes, yes it can

Question 19

How does cyanide toxicity occur with nipride? (quick and dirty)

Answer 19

nipride interacts with oxyhemoglobin, releasing cyanide and NO, and turns the oxyhemoglobin into methemoglobin

Question 20

Cyanide toxicity causes what?

Answer 20

tissue hypoxemia and anearobic metabolism

cyanide toxicity can occur at rates > 2 mcg/kg/min

Question 21

What does amiodarone do?

Answer 21

inhibits K+ channels, prolonging action potentials and repolarization

(per the PPT, it also blocks alpha receptors, beta receptors, K+ channels, and Ca++ channels)

(d/t K+ and Ca++ blockade, there are some minor negative inotropic and potent vasodilating effects)

Question 22

Amiodarone is used to treat what?

Answer 22

SVT, VT, and A-fib

by depressing AV node and accessory tracts

Question 23

Two side effects of amiodarone. (per the PPT)

Answer 23

pulmonary alveolitis

prolonged QT interval

Question 24

What is lidocaine used to treat?

Answer 24

PVCs and V-tach

Question 25

What does lidocaine do?

Answer 25

decreases AV node and bundle conduction

Question 26

What are toxic lidocaine plasma levels and what can happen?

Answer 26

plasma concentration > 5 mcg/mL - seizures

plasma concentration > 10 mcg/mL - CNS depression, apnea, cardiac arrest

Question 27

What is nitric oxide used for?

Answer 27

relaxation of the pulmonary vascular smooth muscle.

treatment of cor pulmonale.

decreases PAP and RV afterload.

Question 28

Nitric oxide dose?

Answer 28

2 - 40 ppm

rapidly inactivated by Hgb

Question 29

Can nitric oxide improve V/Q mismatching in ARDS patients?

Answer 29

yes

Question 30

What is prostacyclin (PGI2) used for?

Answer 30

as a potent vasodilator

IV doses to reduce PAP often cause systemic hypotension

Question 31

Which is cheaper, nitric oxide or prostacyclin?

Answer 31

prostacyclin

Question 32

Heparin, random facts, go! (3)

Answer 32

• increases antithrombin III
• doesn’t cross the placenta
• CPB minimum dose is 300 units/kg (ACT minimum of 400 or 90 - 120 seconds)

Question 33

How many units equal one milligram?

Answer 33

100 units / mg

Question 34

Angiomax, random facts, go! (3)

Answer 34

• direct thrombin inhibitor
• half life of 25 minutes (this is short)
• eliminated by proteolysis

Question 35

Argatroban, random facts, go! (4)

Answer 35

• direct thrombin inhibitor
• less potent than bivalirudin
• pump load 0.05 mg/kg
• IV load 0.1 mg/kg

Question 36

Dobutamine, fun facts! (3-ish)

Answer 36

• partially selective beta-1, with some beta-2 action
• < 5 mcg/kg/min - predominant B-1 and B-2 agonism, leading to increased CO and decreased afterload
• > 5 mcg/kg/min - B-1 and A-1 stimulation, leading to increased CO and stable afterload

Question 37

Dopamine! (5)

Answer 37

• precursor to norepi
• stimulates: Dop 1, Dop 2, B1, B2, A1
• low dose: 0.5 - 3 mcg/kg/min (increase pee)
• moderate dose: 3 - 10 mcg/kg/min (increase pump)
• high dose: > 10 mcg/kg/min (increase press)

Question 38

IABP, what does it do? (3)

Answer 38

• inflates with helium during diastole
• increases coronary perfusion
• deflates before AV opening, decreasing afterload

Question 39

What does using an IABP accomplish? (2)

Answer 39

• increases myocadial O2 supply (diastolic augmentation)

- decreases myocardial O2 demand (reduces afterload)