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36 Cards in this Set

  • Front
  • Back
what 2 factors are involved in stroke volume?
systolic function (inotropic) and diastolic function (lusitropic)
what 4 things are involved in systolic function?
1. contractility
2. ejection fragment
3. preload
4. afterload
what is a positive inotropic agent?
one that allows for greater relaxation
how does hypertension effect the diastolic function of stroke volume?
hypertrophic stiff heart cannot relax as well (negative lusitropy)
what is a normal ejection fragment?
what are 4 compensatory mechanisms in compensated LOCHF in the temporal order that they act?
1. Frank-Starling's Law
2. Sympathetic Activation
3. Renin-Angiotensin-Aldosterone System
4. Myocardial Hypertrophy
What are the signs and symptoms of compensated LOCHF?
you don't see any! it is compensated!
What are the signs and symptoms of decompensated LOCHF?
1. Pulmonary Edema
2. Systemic Edema
2. Palpitations
3. Cardiomegaly
What differentiates the NYHA functional classification of heart disease?
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.
What are some non-pharmacological treatments of LOCHF?
limit salt and water, limit emotional stress, decrease physical activity
How do venodilators and diuretics treat LOCHF?
decrease preload
how do vasodilators, endothelin antagonists, and RAS antagonists treat LOCHF?
decrease afterload
what are 2 ways to block the RA system?
ACE Inhibitors
AT1 Receptor Antagonists
antidote for beta blocker toxicity?
glucagon - binds different site on the receptor and causes Gs signalling. doesnt have to compete like giving NE would
do beta 1 agonists help inotropy or lusitropy?
how do beta 1 agonists cause positive inotropic and lusitropic functions?
pos inotropic
1. phosphorylate calcium channels and increase calcium entry

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
4 classes of cardiotonic (positive inotropic) drugs used in the treatment of CHF
a. Cardiac Glycosides
b. Sympathomimetic amines (short term)
c. Phosphodiesterase inhibitors
d. Calcium-sensitizing Drugs
What are the effects of cardiac glycosides?
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
why can cardiac glycosides lead to arrhythmias?
they decrease intracellular K
effect of cardiac glycosides on Na / water balance?
inhibit renal Na/K ATPase and increase renal Na / H2O excretion
why is slowing the heart rate down with cardiac glycosides good?
LOCHF pts have such a high heart rate that slowing their heart down increases SV and increases CO, making it more efficient
how do cardiac glycosides help with edema?
they increase sodium and water excretion
what electrophysiological effects do cardiac glycosides have?
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
Where do cardiac glycosides caused decreased conduction velocity? increased conduction velocity?
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
What kind of arrythmias can cardiac glycosides cause?
1. atrial tachycardia
2. ventricular arrhythmias -
Why does the PR interval prolong with cardiac glycosides?
conduction velocity is slowed
4 major cardiac glycoside toxicities
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
1st,2nd,3rd degree heart blocks
1st - prolonged QR interval
2nd - missed QRS
3rd - atria and ventricles contract independently
how to treat cardiac glycoside toxicity in a patient with a potassium deficiency, heart block, and PVC's. v fib?
potassium supplement
atropine for heart block
lidocaine for PVC's
ACE inhibitor effect on bradykinin?
they block a kinase which allows bradykinin to go up leading to vasodilation and the coughing s/e
S/E of sympathomimetic amines for LOCHF
tachycardia, cardiac demands
PVR, arrhythmias, and etc
- short acting
how do cardiac glycosides cause atrial tachycardia?
they decrease the ERP in the atria
how do cardiac glycosides cause ventricular arrhythmias?
increase automaticity in the His-Purkinje fibers
how can cardiac glycosides cause heart blocks?
at the av node, they increase ERP and decrease CV
which two ions contribute to arrhythmias caused by cardiac glycosides
the decreased K and increased Ca
how does electrolyte balance contribute to drug interactions with cardiac glycosides?
drugs that affect K and Ca will have an additive effect