A Pharm- summer 1- cardiac
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. What would you like to do?
____________, treating _____ prob.
Vasopressors: Increase ________, and ________ and treat ____ problem
- VASCULAR tone
- treat PIPE problem
Relaxation of cardiac myocytes occurs when _____ ____ channels close.
INOtropy: ________ of intracellular Ca2+ and ________. (IQT)
- Max Tension developed
CHRONOtropy: _____ of Ca2+ delivery.
Rate of __________. (CRC^2)
LUSItropy: _________ of
intracellular Ca2+. _______ of __________. (LRR)
- Rate of Relaxation
An increase in cAMP in heart cell will increase ______ release. What are two drugs that use this pathway?
β- Agonists mechanism of action? Main method?
- stimulate adenylate cyclase, ^ cAMP.
B2 increases what?
- Smooth muscle vasodilation (pulm)
A1 causes what effect?
Epi has _____ fx on B1, B2, a1. side fx include:
What two drugs have higher a than B fx?
Norepi side fx:
intense SVR increase can cause CO drop
Dobutamine side fx:
Isoproteronol is a _____ __ _______. side fx include what three things?
- Pure B agonist.
- Significant TACHY, ARRHYTMIA, drop SVR.
Phosphodiesterase Inhibitors mechanism of action:
prevent cAMP breakdown.
PDE’s breakdown cyclic nucleotides (____, ____) and are ________ __________ that ACTIVATE PROTEIN KINASES and OPEN ___ ________.
- camp, cgmp
- second messengers
- PROTEIN KINASES
- ION CHANNELS
PDE3 A receptors found where?
CARDIOVASCULAR SYSTEM and PLATELETS
PDE3 B receptors found where? activated by?
PDE3 INHIBITORS: What two areas are effected by these drugs?
- Cardiac myocytes: ^ cAMP = ^ Ca2+, increase contractility
- Vascular tissue: ^ cyclic nucleotides, smooth muscle relaxation, Decrease PA pressure and SVR
what are 3 PDE-I drugs?
How is Enoximone excreted?
Why is NOREPI 1st line of support? What can be added is systolic function is poor?
- some + inotropy, maintain perfusion pressure
- Epi, dobutamine, PDE-I
T or F, second messenger in a receptors of vasculature is cAMP? Do they cause Ca2+ release?
What are the non-catecholamine sympathomimetics? (3) PME
- Phenylephrine- pure direct a agonist
- Methoxamine- direct direct a agonist
- Ephedrine- indirect
What are the 2 pure direct a agonists?
how does Ephedrine work?
causes Norepi release from neurons
T or F, Ephedrine has some B2 activation? Is it direct? What prolongs ephedrine? How much is excreted unchanged from the kidney? Does it affect uterine vasc resistance?
Vasopressin: a ___-______________ vasopressor. No __ receptors involved, vasoconstriction due to ___ receptors. Second messenger system is utilized, and Ca2+ release causes vasoconstriction- T or F?
Where are the following receptors located?
AVP main role is not ___ _____ _____. levels increase by 2-3X with _____. Levels decrease following ___
Vasopressin side effects and what causes them:
- Intense vasoconstriction = Myocardial ischemia, decreased CO, mesenteric ischemia
- less effect on pulmonary vasculature
why can Vasopresson be beneficial with pulmonary HTN?
Less of an effect on pulmonary vasculature
Conventional Inotropes are ______ __________.
“Calcium Sensitizers” work at the interaction
of_______/____ or response to ____ binding.
Why the fact that calcium sensitizers don't increase calcium possibly a benefit?
- Less arrythmogenic
- Do not increase O2 consumption
Calcium Sensitizers are _________ with other agents.
What are the Calcium Sensitizer drugs? (3)
What is Methylene Blue mechanism? what are side fx of high doses?
- Block GC activation by NO, leading to LESS vasodilation.
- High doses = hyperbilirubinemia/ hemolytic anemia
What causes a higher change in VO2? Milrinone or Levosimendan?
What would you like to do?
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