Exam II: Cardiovascular Drugs Flashcards
Endogenous catecholamines: (3)
___, ___, ___
[Sympathomimetics and agonists]
Epinephrine, norepinephrine, dopamine
Synthetic catecholamines
___, ___
[Sympathomimetics and agonists]
Isoproterenol, dobutamine
Synthetic noncatecholamines
___, ___, ___
[Sympathomimetics and agonists]
Ephedrine, amphetamine, phenylephrine
Selective alpha2-adrenergic agonists
___, ___
[Sympathomimetics and agonists]
Clonidine, dexmedetomidine
Selective beta2-adrenergic agonists
___, ___, ___
[Sympathomimetics and agonists]
Albuterol, terbutaline, ritodrine
Cardiac stimulation (increased ___ and __, contractility, susceptibility to ectopy)
[Sympathetic NS Activation – fight or flight]
HR and BP
Broncho___
[Sympathetic NS Activation – fight or flight]
dilation
Vasoconstriction (decreased flow to ___, ___, ___)
[Sympathetic NS Activation – fight or flight]
skin, GI tract, renal
Vasodilation (improved blood flow to ___)
[Sympathetic NS Activation – fight or flight]
skeletal muscle
CNS stimulation – increased ___ (except ___)
[Sympathetic NS Activation – fight or flight]
cognition, alpha2
Increased blood ___
[Sympathetic NS Activation – fight or flight]
sugar
Lipolysis – breakdown of___
[Sympathetic NS Activation – fight or flight]
lipids
Glycogenolysis – splitting up of ___ in the liver, yielding ___
[Sympathetic NS Activation – fight or flight]
glycogen, glucose
___rate of coagulation
[Sympathetic NS Activation – fight or flight]
Increased
Look at Table 13.2 in Nagelhout, p. 167 to see agonist, blocker, cholinergic agonists, and anticholinergic effects.
[Sympathetic NS Activation – fight or flight]
Look at Table 13.2 in Nagelhout, p. 167 to see agonist, blocker, cholinergic agonists, and anticholinergic effects.
Look at Table 13.2 in Nagelhout, p. 167 to see agonist, blocker, cholinergic agonists, and anticholinergic effects.
Look at Table 13.2 in Nagelhout, p. 167 to see agonist, blocker, cholinergic agonists, and anticholinergic effects.
Used to____ contractility or ___ vascular tone after sympathetic blockade caused by ___anesthesia
[Clinical use: Sympathomimetics]
increase, increase, regional
Used to___ or ___blood pressure (to prevent tissue ischemia) during the time required to correct for hypovolemia or ____anesthesia
[Clinical use: Sympathomimetics]
increase or maintain, excessive inhaled
Used to relax ___of asthmatic
[Clinical use: Sympathomimetics]
bronchoconstriction
Used to manage ___phylaxis
[Clinical use: Sympathomimetics]
ana—
Used to prolong ___ anesthesia
[Clinical use: Sympathomimetics]
regional
Direct
Bind to receptors and activate them directly (___ and ___)
[Direct versus Indirect]
catecholamines and phenylephrine
Indirect
Cause the release of norepinephrine from ___sympathetic nerve endings (___)
[Direct versus Indirect]
postganglionic, amphetamine
Indirect
___ the reuptake of norepinephrine to make more in circulation (___, ___)
[Direct versus Indirect]
Block, cocaine, tricyclic antidepressants)
Indirect agent might not be effective if patient has a ___, or depletion of ___.
[Direct versus Indirect]
denervation injury, neurotransmitter
The greater the concentration of the sympathomimetic, the ___ the number of receptors in tissues or ___response.
[Tachyphylaxis]
lower, decreased
Example:
Increased concentration of norepinephrine results in ___adrenergic receptors on cell membranes.
[Tachyphylaxis]
fewer
Example:
Chronic treatment with Albuterol (beta2 agonist) causes the number of receptors to___.
[Tachyphylaxis]
decrease
Desensitization – define– Can happen rapidly – within only ___.
[Tachyphylaxis]
rapid reduction in response to hormones and neurotransmitters despite continuous exposure. hours
Down-regulation is different from desensitization in that ____ (example: rebound tachycardia)
receptors are destroyed and new receptors must be created before a return to baseline.
Catecholamines
Inactivation by enzymes: (2)
[Metabolism of sympathomimetics]
Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)
Termination of effect influenced more by uptake back into ___ ___ nerve endings
[Metabolism of sympathomimetics]
postganglion sympathetic
Filtration by the ___ of norepinephrine and dopamine
[Metabolism of sympathomimetics]
lungs
Noncatecholamines
Inactivated by ___ only - slower
[Metabolism of sympathomimetics]
MAO
Catecholamines are short-lived due metabolism by ___ and ___
[Metabolism of sympathomimetics]
MAO and COMT
Both ___ and ___ stimulation
Most potent alpha stimulant
alpha1=alpha2; beta1=beta2
Given IV or subq (causes vasoconstriction which slows absorption)
Poorly lipid soluble – lack of cerebral effects
[Epinephrine]
alpha and beta
Most potent ___stimulant
[Epinephrine]
alpha
alpha1=___; beta1=beta2
[Epinephrine]
alpha2, beta2
Given IV or subq (causes ___ which slows absorption)
[Epinephrine]
vasoconstriction
Poorly lipid soluble – lack of ___ effects
[Epinephrine]
cerebral
Uses:
Used to ___absorption and ___ duration of local anesthetics
[Epinephrine]
decrease, prolong
Uses:
Treatment of ana___ reactions
[Epinephrine]
___phylactic
Uses:
Increase myocardial ___
[Epinepherine]
contractility
EpiPen 1:1000 – 0.3 to 0.5 ml = ___ to ___ mg
[Epinepherine]
0.3 to 0.5
CV effects
Low dose (___-___ mcg/kg/min) Beta – 1: increase ___, ___, ___, ___); Beta-2: ___ in DBP due to ___ in SVR (vasodilation in skeletal muscle vessels)
[Epinephrine]
0.01-0.03, HR, BP, CO, Inotropy
decrease, decrease
CV effects
Moderate dose (___-___ mcg/kg/min) Beta-1: increase in ___, ___, ___, ___ (increase in venous return); increase in susceptibility to ___; mixed w Alpha
[Epinephrine]
0.03-0.15, SBP, HR, CO, inotropy, arrhythmias
CV effects:
Large dose (___ mcg/kg/min) both Beta and Alpha-1, but ___predominate: ___ of the skin, mucosa, and hepatorenal vessels (decreased renal blood flow), ___common
[Epinephrine]
> 0.15, Alpha, vasoconstriction, SVT
Net effect of the vascular changes (at low dose) is the distribution of blood flow to the ___and decreased ___, but with ___ renal blood flow.
[Epinephrine]
skeletal muscle, SVR, decreased
___receptors are more sensitive to lower epinephrine doses while effects on ___ receptors predominate at higher doses.
[Epinephrine]
B2, A1
At higher doses, the predominant A activity and resultant vasoconstriction leads to increased ___, which may impede ___ in CO.
[Epinephrine]
afterload, increases
Increase venous return due to high concentration of receptors in ____
[Epinephrine]
venous vasculature.
Respiratory
Smooth muscle relaxed in the bronchi (___)
[Epinephrine]
Beta2
Respiratory
However, if beta antagonist is present, the ___ effect causes bronchoconstriction.
[Epinephrine]
alpha1
Metabolic
most significant effect of all catecholamines – ___
[Epinephrine]
increase in blood glucose
Metabolic:
Beta2 – increases ___ and ___
[Epinephrine]
glycogenolysis and lipolysis
Metabolic:
Alpha2 – inhibits ___ (hyperglycemia)
[Epinephrine]
release of insulin
Electrolytes
Beta2 – stress induced ___ (activation of the ___ on RBCs)
Initial increased K – it follows ___out of hepatic cells
[Epinephrine]
hypokalemia, sodium-potassium pump
glucose
Ocular
___ – contraction of the radial muscles of the iris causes ____; contraction of the ___ causing bulging of the eyes (exophthalmos)
[Epinephrine]
Alpha1, pupil dilation, orbital muscles
GI/GU
Relaxation of ___ ___ muscle
___ – relaxation of the ___ muscle of the bladder; ___ contracts the sphincter muscles
[Epinephrine]
GI smooth, Beta, detrusor, alpha1
Coagulation is accelerated with___ – induces ___ and increases factor V activity
epi, platelet aggregation
Naturally occurring catecholamine released from ___ ___ nerve endings
[Norepinephrine]
postganglionic sympathetic
Potent ___ with ___ agonist effect, but little beta___ effect
[Norepinephrine]
alpha agonist, beta1, 2
alpha1___alpha2; beta1___beta2
[Norepinephrine]
=,»_space;
Clinical use:
Vasoconstrictor to increase ___ and raise ___
[Norepinephrine]
SVR, BP
Infiltration of NE into ___ tissue can cause ___ due to vasoconstriction*
[Norepinephrine]
subcutaneous, necrosis
Infiltration - ___
[Norepinephrine]
phentolamine
CV effects
___ – vasoconstriction of both ___ and ___ vessels of all vascular beds; increased ___, ___, increased* venous return and decreased HR
[Norepinepherine]
Alpha1, arterial and venous, SVR, MAP
CV effects
___ – overshadowed by the above effects causing a decrease in ___, decreased ___, decreased kidney blood flow
[Norepinepherine]
Beta1, CO, tissue perfusion
Respiratory – no ___effects
[Norepinephrine]
beta2
Metabolic – ___ unlikely
[Norepinephrine]
hyperglycemia
At higher doses, decreased___ due to constriction ___ to the capillary bed which causes___of fluid there. Also results in leakage of that fluid into the ____.
[Norepinephrine]
venous return, proximal, trapping, interstitial
Lowering the dose of norepi has been shown to “decrease the ___” – studies raised the legs of the participants to obtain ___ in preload. So ___ vasoconstriction alone did not result in increased preload.
[Norepinepherine]
resistance to venous return, increase, alpha1
Effects of norepinephrine on mean ___ pressure and ___ in human septic shock*
[Norepinepherine]
systemic, venous return
Dose:___ mcg/kg/min
[Norepinepherine]
0.02 -0.4
Low dose: ___ selective – ___ HR, inotropy
[Norepinepherine]
Beta1, increase
High dose: ___, ___, ___ – ___ SVR, BP, but ___ HR (barorec. Reflex)
[Norepinepherine]
Alpha1, Alpha2, Beta1, increase, decreased
Bolus –___ – ___ mcgs (intermittent boluses – less bradycardia than phenylephrine)
[Norepinepherine]
DILUTE, 4-16
Ideal for ___, post ___ with ___ SVR state
[Norepinepherine]
sepsis, CPB, decrease
