Vasoconstrictors - Week 1 Flashcards
2 hemodynamic effects of vasoconstrictors
Increase arterial resistance and after load (increase SVR and MAP)
Increase venous return (increase preload and CO)
Reflex changes of vasoconstrictors include:
- decreased HR
- decreased conduction
- occasionally decreased contractility
non cardiac effects of vasoconstrictors
- bronchodilation
- glycogenolysis
- insulin, renin, and pituitary hormone
- CNS stimulation (low lipid solubility)
indications for vasoconstrictors
- decreased arterial resistance (HoTN)
- CPR
- Anaphylactic shock
- intracardiac R –> L shunts
- hypovolemia
2 types of HoTN
Iatrogenic and Physiologic
What is the goal of using vasoconstrictors in CPR?
To restore perfusion pressure to vital organs (used in conjunction w other appropriate cardiac drugs)
Name 4 complications/contraindications for vasoconstrictors
- can worsen LV failure
- can exacerbate RV failure
- can decrease renal blood flow
- can mask hypovolemia
Epi stimulates which receptors?
alpha 1, Beta 1, and Beta 2
Epi is the most potent activator of ________ receptors. it is ______x more potent than NE.
Alpha 1
2-10
How does epidural increase the following processes:
- lipolysis
- glycogenolysis
- insulin secretion
lipolysis - increases
glycogenolysis - increases
secretion of insulin - decreases
T/F Epi decreases blood sugar in response to surgical stress.
False - episode increases the blood sugar
Does epi decrease renal blood flow even in the absence of changes in systemic BP?
yes.
Name 2 renal effects of epi
- potent renal vasoconstrictor (a1 effect)
- stimulates renin release (indirect effect)
What is the physiological effect of low doses (1-2 mcg/min) of epi?
Predominantly B2 stimulation
Compare the alpha effects to the B2 effects of low dose epi, and what is the net effect on SVR and MAP?
a1 receptors in skin, mucosa, and hepatorenal system are stimulated
B2 receptors in sk musc are stimulated
Net effect:
- decreased SVR (distribution of blood to sk muscle)
- MAP remains the same (essentially)
What are the physiological effects of intermediate doses of epi (4 mcg/min)
- receptor stimulated:
- effect on HR, contractility, and CO
- effect on automaticity
Predominantly B1 stimulation
- increased HR, contractility, and CO
- increased automaticity (may lead to dysrhythmias)
What would be considered high dose epinephrine, and what receptor predominates at this dose?
> 10 mcg/min
Alpha 1
Epinephrine is the most potent activator of Alpha 1 receptors. It is a potent vasoconstrictor of the ______, ______, and ______ vascular beds with no significant effect on _______ _______. It is therefore used to maintain ________ and _______ perfusion
vasoconstrictor of cutaneous, splanchnic, and renal beds
little effect on cerebral arterioles
used to maintain myocardial and cerebral perfusion
Can reflex bradycardia occur w epinephrine?
Yes.
What is racemic epi, and what does it do?
moisture of levo- and dextrorotary isomers
constricts edematous mucosa
What are 3 indications for racemic epi?
- severe croup
- post-extubation airway edema
- traumatic airway edema
Racemic epi tx lasts _______ minutes. The pt should be observed for ___ hrs after tx to watch for _____.
30-60 min
2 hrs
rebound
What are the CNS of epi?
There aren’t any.
What are 8 side effects of epi?
- hyperglycemia
- mydriasis
- plt aggregation
- sweating
- HA
- tremor
- nausea
- arrhythmias
What 5 things should be monitored on a pt who has received/is receiving epinephrine?
- BG
- RR
- O2 sats
- HR
- BP
How does NE affect:
- SBP
- DBP
- MAP
increases all three my adjusting SVR (alpha 1 effects)
NE is a potent vasoconstrictor of ______, _______, and _______ vascular beds. What are the implications for each?
Renal, mesenteric, and cutaneous
- Renal - decreased RBF –> oliguria
- Mesenteric - mesenteric infarct
- Cutaneous - periph hypo perfusion –> gangrene of digits
T/F: NE is a potent alpha agonist that produces intense arterial AND venous vasoconstriction in ALL vascular beds and LACKS bronchodilating effects.
True
T/F: NE is primarily an a1 agonist, and any B1 effects are overshadowed by a1 effects.
True.
The B2 effects are virtually non-existent. However, it can still cause arrhythmias r/t the B1 effects.
How do high and low doses of NE affect CO?
Low doses - CO increases
High doses - CO may decrease b/c of increased after load and baroreceptor-mediated reflex bradycardia. Refractory HoTN is also a possibility.
How do the metabolic effects of NE compare to the metabolic effects of epi?
Fewer metabolic effects w NE (B/c it doesn’t have the B2 effects as much)
Larger doses of NE may have metab effects.
What is the effect of dopamine at 5 mcg/kg/min?
It causes NE to be released, contributing to cardiac stimulation (precursor)
What is the effect of dopamine at 10 mcg/kg/min?
alpha effects begin to predominate
At what dose of dopamine do the Alpha receptor effects definitely predominate?
> 20 mcg/kg/min
How does dopamine effect the pulm status?
It. doesn’t.
What are the CNS effects of dopamine:
- IV
- Increased dopamine
- Decreased dopamine
- D2 inhibition
- IV dopamine - none, it doesn’t cross the BBB
- increased dopamine - mania
- decreased dopamine - schizophrenia, ADHD, PD
- D2 inhibition - decreased prolactin secretion
What 5 things should be monitored in a pt on dopamine?
- BP
- HR
- MAP
- UOP
- Mental status
T/F: All catecholamines are sympathomimetics, but no tall sympathomimetics are catecholamines.
True
What type of drug is ephedrine, and what are the clinical implications?
Synthetic noncatecholamine
It still works on the sympNS, but it isn’t metabolized by COMT, and it is not recycled. Therefore, it is entirely dependent on MAO for metabolism.
Ephedrine has direct and indirect actions, but its principle effect is ______.
indirect
Beta stimulation by ephedrine may evoke ________, particularly in a ________ ________.
Arrhythmias
Sensitized myocardium
What is the principle mechanism of ephedrine?
increased myocardial contractility
How do the Beta 1 effects of the ephedrine combine with the release of NE caused by ephedrine to increase CO?
Nepi: venoconstriction > arteriolar constriction –> increased preload
B1: increased HR and contractility
combination leads to increased CO
Does ephedrine increase both SBP and DBP as a result of the increased CO?
Yes
Explain how tachyphylaxis occurs w repeated dosing of ephedrine.
A2 in the CNS senses too much NE so it stops making NE. If NE is not available, it will not be released in response to ephedrine.
How does ephedrine affect uterine blood flow and bronchial smooth muscle?
preserves or increases UBF
Bronchial smooth musc relaxant (direct effect)
T/F: Ephedrine is similar to epinephrine, but the BP response is less intense and lasts longer.
True.
It lasts longer because it has no reuptake and is metabolized by MAO only. this makes it last longer than a normal catecholamine.
Does ephedrine cross the BBB?
Yes. Therefore, high doses can cause psychosis.
Side effects of ephedrine
- HTN
- insomnia
- urinary retention
- HA
- weakness
- tremor
- palpitations
- psychosis
What 4 things should be monitored in a pt receiving ephedrine?
- BP
- pulse
- UOP
- mental status
How are ephedrine OD and extravasation treated?
Supportive therapy
What type of drug (structurally) is phenylephrine?
synthetic non-catecholamine
Which does phenylephrine increase more, preload or after load?
preload
Phenylephrine increases PVR when:
CO is adequate
Phenylephrine may be used to improve _____ _____ _____ w/o _____ side effects
coronary perfusion pressure
chronotropic
Is phenylephrine safe for preggo pts?
Yes.
(Neo used to be taboo, and ephedrine was the drug of choice. But Neo is actually just as good as ephedrine, if not better. Neo has also been associated w better fetal acid-base status than ephedrine)
3 alternative uses for phenylephrine
- drug induced priapism
- mydriatic agent
- nasal decongestant
Phenylephrine decreases ______ and ______ blood flow and increases ______ and ______.
decreases renal and splanchnic
increases pulm art resist and pressure
T/F: although phenylephrine does cause reflex bradycardia, it doesn’t not directly cause dysrhythmias.
True
T/F: phenylephrine is like NE but less potent and longer lasting.
True.
It lasts longer because it is not reuptaken and recycled. It is only metabolized by MAO.
What 4 things should be monitored in a pt receiving phenylephrine?
- BP
- HR
- ABG
- CVP
What posterior pituitary hormones increase BP?
Arginine vasopressin (AVP) (Pitressin)
DDVAP (Desmopressin)
Oxytocin (Pitocin)
What are the ratios of Antidiuretic : Vasopressor effects of the following drugs:
- Arginine vasopressin
- Oxytocin
- DDAVP
antidiuretic: vasopressor effects
- AV 100:100
- Oxytocin 1:1
- DDAVP 1200:0.39
Vasopressin stimulates vascular _______ receptors causing intense arterial vasoconstriction.
V1a
Vasopressin increases the permeability of cell membranes resulting in the passive reabsorption of water via the _____ receptors in the renal _________.
V2
collecting ducts
Vasopressin is used to preserve _________ homeostasis in pts w _______.
cardiocirculatory homeostasis
advanced vasodilatory shock
Vasopressin is good for pts who:
- conventional vasopressor therapy has failed or the pt is resistant to it
- experience adverse effects of conventional vasopressor therapy
T/F: Unlike catecholamines, effects of arginine vasopressin are preserved during hypoxia and severe acidosis.
True
3 Advantages of vasopressin over epinephrine
- epi increases myocardial O2 consumption, contributing to the risk of developing post-resuscitation MI and arrhythmias
- catecholamines may not work as well in an acidic environment associated w CPR
- in animal studies, vasopressin is associated w:
- better blood flow to vital organs
- better delivery of cerebral O2
- better chance of resuscitation and better neurologic outcome
(human data is lacking)
T/F: Vasopressin is at least as effective as epi, may have fewer adverse effects than epi, and therefore is a reasonable alternative to epi in the tx of cardiac arrest.
True, esp if pt is highly acidic
adverse effects/drug interactions of vasoconstrictors
- cardiac dysrhythmias (beta stimulation)
- pure alpha agonists can activate baroreceptor reflex mediated bradycardia and possibly decrease CO
- antihypertensives may decrease the pressor response to indirect acting drugs or enhance the response to direct acting drugs (denervation hypersensitivity)
How do tricyclic antidepressants and MAOI’s interact w vasoconstrictors?
What are the anesthetic implications?
- increase availability of endogenous NE
- exaggerated response w indirect acting agents
- worse in the first 14-21 days of therapy (then down regulation of receptors occurs)
- ok to continue these drugs in the period period
- use a decreased dose of direct acting drugs
How does cocaine interact w vasoconstrictors?
How is acute toxicity best managed?
- interferes w re-uptake of catecholamines –> both exogenous and endogenous catecholamine effects are enhanced
- produces central and peripheral sympathetic stim –> vasoconstriction, tachycardia, and arrhythmias
- acute toxicity may best be managed w adrenergic blockade (Labetalol w a and B effects)
How do natural weight loss products interact w vasoconstrictors?
How soon before surgery should a pt stop taking the product?
- they may contain ma Huang (ephedra) which contains ephedrine, pseudoephedrine
- long term use results in tachyphylaxis from depletion of endogenous catecholamines stores –> peri-op hemodynamic instability and cv collapse
- stop product at least 24 hrs prior to surgery
What drug should be used to treat extravasation from vasoconstrictors? How does it work?
Phentolamine
- alpha 1&2 antagonist
- peripheral vasodilator
- treats skin necrosis 2* to NE, dopamine, and epi
