Cardiotonic Agents The Script

Front 1

what 2 factors are involved in stroke volume?

Back 1

systolic function (inotropic) and diastolic function (lusitropic)

Front 2

what 4 things are involved in systolic function?

Back 2

1. contractility
2. ejection fragment
3. preload
4. afterload

Front 3

what is a positive inotropic agent?

Back 3

one that allows for greater relaxation

Front 4

how does hypertension effect the diastolic function of stroke volume?

Back 4

hypertrophic stiff heart cannot relax as well (negative lusitropy)

Front 5

what is a normal ejection fragment?

Back 5

50-60%

Front 6

what are 4 compensatory mechanisms in compensated LOCHF in the temporal order that they act?

Back 6

1. Frank-Starling's Law
2. Sympathetic Activation
3. Renin-Angiotensin-Aldosterone System
4. Myocardial Hypertrophy

Front 7

What are the signs and symptoms of compensated LOCHF?

Back 7

you don't see any! it is compensated!

Front 8

What are the signs and symptoms of decompensated LOCHF?

Back 8

1. Pulmonary Edema
2. Systemic Edema
2. Palpitations
3. Cardiomegaly

Front 9

What differentiates the NYHA functional classification of heart disease?

Back 9

I. No physical limitations
II. Limitations in physical activity
III. Marked limitation
IV. Can't do physical activity. Symptoms present at rest. Will die 6-12 mo.

Front 10

What are some non-pharmacological treatments of LOCHF?

Back 10

limit salt and water, limit emotional stress, decrease physical activity

Front 11

How do venodilators and diuretics treat LOCHF?

Back 11

decrease preload

Front 12

how do vasodilators, endothelin antagonists, and RAS antagonists treat LOCHF?

Back 12

decrease afterload

Front 13

what are 2 ways to block the RA system?

Back 13

ACE Inhibitors
AT1 Receptor Antagonists

Front 14

antidote for beta blocker toxicity?

Back 14

glucagon - binds different site on the receptor and causes Gs signalling. doesnt have to compete like giving NE would

Front 15

do beta 1 agonists help inotropy or lusitropy?

Back 15

both!

Front 16

how do beta 1 agonists cause positive inotropic and lusitropic functions?

Back 16

pos inotropic
1. phosphorylate calcium channels and increase calcium entry

lusitropic
1. phosphorylate phospholamban
removes calcium from cell, allowing faster relaxation

2. phosphorylates troponin I which causes the dissociation of troponin C and calcium, allowing removal of crossbridges and faster relaxation

Front 17

4 classes of cardiotonic (positive inotropic) drugs used in the treatment of CHF

Back 17

a. Cardiac Glycosides
b. Sympathomimetic amines (short term)
c. Phosphodiesterase inhibitors
d. Calcium-sensitizing Drugs

Front 18

What are the effects of cardiac glycosides?

Back 18

a. Increases myocardial contractility

b. Decreases heart rate via baroreceptor reflex

c. Increases vasomotor tone (although BRR causes overall decrease in vasomotor tone!)

d. Increases urinary sodium and water excretion (inhibits renal tubular Na,K-ATPase)

e. Stimulates certain areas of CNS

Front 19

why can cardiac glycosides lead to arrhythmias?

Back 19

they decrease intracellular K

Front 20

effect of cardiac glycosides on Na / water balance?

Back 20

inhibit renal Na/K ATPase and increase renal Na / H2O excretion

Front 21

why is slowing the heart rate down with cardiac glycosides good?

Back 21

LOCHF pts have such a high heart rate that slowing their heart down increases SV and increases CO, making it more efficient

Front 22

how do cardiac glycosides help with edema?

Back 22

they increase sodium and water excretion

Front 23

what electrophysiological effects do cardiac glycosides have?

Back 23

Direct - effect of the pump
(decreased K and increased Ca)
Indirect - effect of vagal reflex

1. SA Node - direct and indirect
decrease in automaticity and HR

2. AV node -direct and indirect
increase in ERP and decrease in CV.
can cause heart blocks

3. His-Purkinje - (direct)
decrease in CV and increase in automaticity

Front 24

Where do cardiac glycosides caused decreased conduction velocity? increased conduction velocity?

Back 24

mostly decreased conduction velocity due to vagal stimulation and the effects of the pump

**exception - in the atria, cardiac glycocides decrease effective refractory period and can cause atrial tachycardia

Front 25

What kind of arrythmias can cardiac glycosides cause?

Back 25

1. atrial tachycardia
2. ventricular arrhythmias -

Front 26

Why does the PR interval prolong with cardiac glycosides?

Back 26

conduction velocity is slowed

Front 27

4 major cardiac glycoside toxicities

Back 27

1. Cardiotoxicity
a. heart blocks
b. sinus arrhythmia and atrial tachycardia (esp in young ppl)
c. PVC
d. Ventricular Tachycardia and/or Fibrillation
2. GI disturbances
3. Neurological problems
4. Vision disturbances

Front 28

1st,2nd,3rd degree heart blocks

Back 28

1st - prolonged QR interval
2nd - missed QRS
3rd - atria and ventricles contract independently

Front 29

how to treat cardiac glycoside toxicity in a patient with a potassium deficiency, heart block, and PVC's. v fib?

Back 29

potassium supplement
atropine for heart block
lidocaine for PVC's
defibrillator

Front 30

ACE inhibitor effect on bradykinin?

Back 30

they block a kinase which allows bradykinin to go up leading to vasodilation and the coughing s/e

Front 31

S/E of sympathomimetic amines for LOCHF

Back 31

tachycardia, cardiac demands
PVR, arrhythmias, and etc
- short acting

Front 32

how do cardiac glycosides cause atrial tachycardia?

Back 32

they decrease the ERP in the atria

Front 33

how do cardiac glycosides cause ventricular arrhythmias?

Back 33

increase automaticity in the His-Purkinje fibers

Front 34

how can cardiac glycosides cause heart blocks?

Back 34

at the av node, they increase ERP and decrease CV

Front 35

which two ions contribute to arrhythmias caused by cardiac glycosides

Back 35

the decreased K and increased Ca

Front 36

how does electrolyte balance contribute to drug interactions with cardiac glycosides?

Back 36

drugs that affect K and Ca will have an additive effect