Cardiovascular Drugs Flashcards
P wave in EKG
first positive deflection
what does P wave represent?
atrial depolarization
QRS complex in EKG
3 waves in one:
- if 1st wave is downward then called Q wave
- 1st upward wave is called R wave
- if there is a downward wave after R wave, it’s called S wave
what does Q wave represent on EKG?
septal depolarization
what does QRS complex on EKG represent?
ventricular depolarization and implies contraction
what does T wave on EKG represent?
re-polarization of ventricles
you should be aware of T waves that what?
- deflect downward
2. are tall and pointy
volume-pressure diagram
- mitral valve opens
- end-systolic volume at 50 mL in left ventricle
- end-diastolic volume at 120 mL in left ventricle
- mitral valve closes (when ventricular pressure > atrial pressure)
- isovolumetric contraction
- aortic valve opens at 80 mm Hg (b/c ventricular pressure > aortic pressure)
- period of ejection
- aortic valve closes at 100 mm Hg (b/c aortic pressure > ventricular pressure)
- isovolumetric relaxation
period of contraction on volume-pressure diagram
- ventricular pressure rises as contraction begins
- initially the pressure is not sufficient to open aortic valve
- no emptying occurs
how much pressure is required to push open aortic valve according to volume-pressure diagram?
pressure >80 mm Hg
what percent of blood is ejected in first 1/3 of ejection period on volume-pressure diagram?
70%
what percent of blood is ejected in remaining 2/3 of ejection period on volume-pressure diagram?
30%
what causes period of relaxation on volume-pressure diagram?
- ventricles relax quickly
- blood in aorta pushes back and closes aortic valve
- ventricles continue to relax, but the volume doesn’t change
- also when left ventricle is perfused
when is the left ventricle perfused?
during isovolumetric relaxation
in what phase does cardiac cell depolarizes?
phase 0
what happens to membrane during phase 0 (depolarization)?
becomes more positive causes fast Na channels to open and sodium rushes in
what happens when membrane potential reached +20mV in phase 0 (depolarization) of cardiac cell?
fast sodium channels close
in what phase does cardiac cell repolarize?
phase 1 and 3
what happens after fast sodium channels close in phase 1 (initial repolarization)?
cell begins to repolarize and potassium channels open causing potassium ions to flow out
in what phase does cardiac cell plateaus?
phase 2
what happens after slow calcium channels open in phase 2 (plateau)?
potassium channels remain open
what happens when potassium channels remain open during phase 2 (plateau)?
net balance of membrane charge causing repolarization to be temporarily delayed
in what phase of cardiac muscle action potential does slow calcium channels close?
phase 3 (rapid repolarization)
what happens after slow calcium channels close during phase 3 (rapid repolarization)?
potassium channels stay open and potassium rushes out causing cell to repolarize
phase 4 (resting membrane potential)
cell membrane averages -90 mV
Ohm’s law
V = I x R
V = voltage I = current R = resistance
how is Ohm’s law applied to hemodynamics?
P = F x R
P = pressure = mean arterial pressure (MAP) F = flow = cardiac output (CO) R = resistance = systemic vascular resistance (SVR)
Ohm’s law and hemodynamics
MAP = CO x SVR
how can blood pressure (MAP) be raised?
- increasing HR
- increasing SV
- increasing SVR
location of alpha 1 adrenergic receptors
vasculature
actions of alpha 1 adrenergic receptors
vasoconstriction
locations of alpha 2 adrenergic receptors
- brain
2. nerves
actions of alpha 2 adrenergic receptors
- sedation
2. sympathetic inhibitions
locations of beta 1 adrenergic receptors
heart
actions of beta 1 adrenergic receptors
- inotrophy
- chronotropy
- dromotropy
locations of beta 2 adrenergic receptors
- lung
2. vasculature
actions of beta 2 adrenergic receptors
- bronchodilation
2. vasodilation
effect of alpha adrenergic receptors
- mydriasis
- increase glycogenolysis
- decrease insulin secretion
- lipolysis
- vasoconstriction
effect of beta adrenergic receptors
- bronchodilation
- increase inotropy
- increase chronotropy
- increase automaticity
- vasodilation
parent compound of catecholamine
beta phenylethylamine
catechol group consists of what?
hydroxyl substitution on #3 and #4 carbons on benzene ring of beta phenylethylamine
T/F: drugs that have a catechol group are often called “catecholamines” and are usually vasoactive
true
effect of hydroxyl substitutions on catecholamine
increase beta and alpha activity
amine substitutions on catecholamine has what effect?
larger substitutions increases beta activity but no or smaller substitution (i.e.-CH3) gives less beta activity
effect of side chain distance on catecholamine
- length increases sympathomimetic activity
2. substitution increases duration of action
dopamine is a naturally occurring what?
sympathomimetic
where is dopamine synthesized?
in kidney
dopamine bind to which receptors?
- alpha 1
- beta 1
- delta 1
T/F: dopamine can also be a central neurotransmitter (“feel good” neurotransmitter)
true
at low levels, dopamine binds to D1 and causes what?
increased renal flow
at moderate levels, dopamine binds to which receptor?
beta 1
what happens when dopamine binds to B1 receptor at moderate levels?
increases BP and HR
at high levels, dopamine binds to which receptor?
alpha 1
what happens when dopamine binds to a1 receptors at high levels?
causes vasoconstriction
epinephrine is a naturally occurring what?
sympathomimetic
epinephrine is synthesized, stored and released by what type of cells in response to what?
chromaffin cells in adrenal medulla in response to stress
non-selective epinephrine binds to which receptors?
- alpha 1
- beta 1
- beta 2
effects of non-selective epinephrine
- vasoconstriction
- increased inotropy
- increased chronotropy
- bronchodilation
- mast cell stabilization
uses of epinephrine
- cardiac arrest
- anaphylaxis
- asthma
how much epinephrine should be given to pts under cardiac arrest?
1 mg every 3-5 minutes
how much epinephrine is given to pedo patients undergoing anaphylaxis?
150 mcg
how much epinephrine is given to adult patients undergoing anaphylaxis?
300 mcg
how much epinephrine is given to patients for asthma?
11.25 mg nebulized racemic epi
norepinephrine is a naturally occurring what?
sympathomimetic
where is norepinephrine synthesized?
adrenal medulla and sympathetic neurons
what is the primary post-ganglionic adrenergic neurotransmitter?
norepinephrine
where does norepinephrine bind predominantly at?
alpha 1 but also beta 1
effect of norepinephrine
causes intense increase in systemic vascular resistance
catecholamine synthesis pathway
phenylalanine –> L-tyrosine –> L-dopa –> dopamine –> norepinephrine –> epinephrine
phenylephrine is a synthetic what?
non-catecholamine
where does phenylephrine bind?
alpha 1
effect phenylephrine
- causes intense vasoconstriction
- increase preload and blood pressure
- reflex bradycardia (can cause asystole)
T/F: phenylephrine must be diluted before use
true
ephedrine is synthetic what?
non-catecholamine
where does ephedrine bind?
- alpha 1
- beta 1
- beta 2
effect of ephedrine
tachphylaxis because of norepinephrine depletion
when is ephedrine contraindicated?
with MAOIs (phenezine/Nardil)
digoxin
cardiac glycoside
effect of digoxin
increases contractility by inhibiting Na+K+ATPase which causes increase in intracellular Ca2+
what was digoxin traditionally used for?
heart failure and ventricular control in patients with a-fib
T/F: digoxin has an extremely low therapeutic index and is not used much anymore
true
signs of digoxin toxicity
- confusion
- vomiting
- anorexia
- blurry vision
- arrhythmias
