Vasopressors Flashcards
Dobutamine
(mechanism of action)
♦ Inotrope ♦
♦ Stimulates
beta 1+++++ = ⇡ heart rate and stroke volume (inotropy/chronotropy) = increased cardiac output
beta 2+++ vasodilates arteries = decreased SVR (afterload)
alpha 1 + vasoconstriction of arteries = increased SVR (afterload)
(if heart is already working as hard as it can, the secondary effect may be dominant, causing a drop in blood pressure)
⇔used alone, effect unpredictable⇔
Dobutamine
(onset / duration)
♦ Onset 1 - 2 minutes
(may take up to 10 min for peak effect)
Dobutamine
(side effects)
Tachycardia
Ventricular Ectopy / Palpitations
Headache
Nausea/Vomiting
Hypertension/Hypotension
Dobutamine
(indications)
Cardiogenic Shock associated with Hypotension
(as an add-on or secondary med)
Dobutamine
(contraindications)
Hypersensitivity
* use with caution in pt’s with AMI, unstable angina, or severe CAD, as dobutamine can intensify or extend myocardial ischemia
Dobutamine
(adult dose)
2 - 20 mcg/kg/min IV/IO
Dobutamine
(pediatric dose)
2 - 20 mcg/kg/min IV/IO
Dobutamine
(pregnancy safe)
Class C
No adequate or well-controlled studies have been conducted in pregnant women. Use dobutamine during pregnancy only when the expected benefits clearly outweigh the potential risks to the fetus
Dopamine
(mechanism of action)
Stimulates:
beta 1 ++++ inotrophy / chronotropy = increased cardiac output
beta 2 ++ vasodilate arteries = decreased SVR (afterload)
alpha 1 +++ → vasoconstriction = increased SVR (afterload)
(stronger effect on cardiac output than it does on SVR [afterload])
Dopamine
(onset and duration)
Onset 2 - 5 mins
Duration < 10 min (after stopping infusion)
Dopamine
(side effects)
Tachydysrhythmias / Ectopy
Headache
Angina
Nausea/Vomiting
Dopamine
(indications)
Cardiogenic Shock associated with Hypotension
Dopamine
(contraindications)
♦ Hypovolemic Shock where Complete Fluid Resuscitation has NOT Occurred
♦ Uncorrected Tachydysrhythmias or V-fib
Dopamine
(adult dose)
2 - 20 mcg/kg/min IV/IO
1600 mcg/mL concentration
- ♦ 1-5 mcg/kg/min - mainly affects renal arteries*
- ♦ 5-20 mcg/kg/min - inotropic / chronotropic and systemic vasoconstriction*
Dopamine
(pediatric dose)
2 - 20 mcg/kg/min IV/IO
1600 mcg/mL concentration
(same as adult)
Dopamine
(pregnancy safe)
Class C
Use is recommended only if clearly needed and the benefit outweighs the risk to the fetus.
Epinephrine Infusion
(mechanism of action)
Stimulation of:
beta 1++++ ⇡ heart rate and stroke volume = increased cardiac output
beta 2+++ vasodilation of arteries = decreased SVR (afterload)
alpha1+++++ pure vasoconstriction of arteries = increase in SVR (afterload)
- (indirectly causes coronary artery vasodilation)*
- (dose for dose, Epi will increase cardiac output MORE than Norepi)*
- (Epi + Dopamine will increase cardiac output BUT maintain SVR, which increases MAP)*
- (Norepi will increase SVR AND maintain cardiac output, which increases MAP)*
Epinephrine
Push Dose Pressor
(onset / duration)
Onset < 1 min
Duration +/- 5 - 10 min
Epinephrine
(side effects)
Palpitations
Hypertension
Dysrhythmias
Anxiety
Tremors
Epinephrine
(indications)
V - Fib / Pulseless V - Tach
Asystole / PEA
Anaphylaxis
Bronchospasm
Hypotension
Epinephrine
(contraindications)
None Listed
Epinephrine
Anaphylactic Shock / Allergic Reaction
(adult dose)
♦ 0.3 – 0.5 mg 1:1,000 solution IM
♦ May be repeated every 20 minutes up to three times for a total of 4 doses
♦ If patient is hemodynamically unstable, administer 1:10,000 solution up to 0.5mg IO/IV.
Titrate to effect.
Epinephrine
Anaphylactic Shock / Allergic Reaction
(pediatric dose)
♦ 0.01 mg/kg 1:1,000 IM max 0.5 mg
→ may repeat q 20 mins for a total of 4 doses
♦ Hemodynamically Unstable → 1:10,000 0.01 mg/kg
up to 0.5 mg IV/IO titrate to effect
Epinephrine
(pregnancy safe)
Class C
Epinephrine is only recommended for use during pregnancy when benefit outweighs risk.
Norepinephrine (Levophed)
(mechanism of action)
Stimulates:
beta 1+++ ⇡ HR and stroke volume = increased cardiac output
beta 2++ vasodilation of the arteries = decreased SVR (afterload)
alpha 1+++++ vasoconstriction of the arteries = increased SVR (afterload)
(stronger effect on SVR than on cardiac output)
(increases SVR while maintaining or slightly increasing cardiac output)
(good broad spectrum vasoactive agent when it’s unclear what is going on)
Norepinephrine (Levophed)
(onset / duration)
Norepinephrine (Levophed)
(side effects)
Tissue Hypoxia
Brardycardia (increase in afterload from α-1 stimulation results in a reflex bradycardia)
Anxiety
Headache
Respiratory Difficulty
Extravasation Necrosis
Norepinephrine (Levophed)
(indications)
>>Hypotension<<
»Septic Shock«
Norepinephrine (Levophed)
(contraindications)
♦ Hypotension From Blood Volume Deficits
♦ Mesenteric or Peripheral Vascular Thrombosis
Norepinephrine (Levophed)
(adult dose)
2 - 20 mcg/min IV/IO
Titrate every 3 - 5 mins
Norepinephrine (Levophed)
(pediatric dose)
0.1 - 2 mcg/kg/min
Titrate every 3 - 5 mins
Norepinephrine (Levophed)
(pregnancy safe)
Category C
Use is recommended only if clearly needed and the benefit outweighs the risk
(Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans)
Phenylephrine (Neo-Synephrine)
(mechanism of action)
♦ Pure α-1 adrenergic receptor agonist
♦ Increases SVR (afterload) =** increased MAP, and **total peripheral vascular resistance
Effect on cardiac output depends on preload-responsiveness versus the ability of the heart to handle increased afterload.(example, a patient with systolic heart failure and volume overload, added preload won’t help, whereas the heart may be unable to tolerate afterload – so the net effect is to reduce the cardiac output. Alternatively, for a patient who is preload-responsive with a stronger ejection fraction, phenylephrine could cause a net increase in cardiac output.)
Phenylephrine (Neo-Synephrine)
Push Dose Pressor
(onset / duration)
Onset < 1 min
Duration +/- 10 - 20 min
Phenylephrine (Neo-Synephrine)
(side effects)
♦ Hypertension
♦ Bradycardia (as mean arterial pressure increases, vagal activity also increases, resulting in reflex bradycardia)
♦ Headache
♦ Dizziness
♦ Dysrhythmias
(**also causes vasoconstriction of coronary arteries**)
Phenylephrine (Neo-Synephrine)
(indications)
♦ Hypotension
♦ Neurogenic Shock
♦ Spinal Shock (below level of T-6)
(preferred PD pressor in presence of tachycardia)
Phenylephrine (Neo-Synephrine)
(contraindications)
>> Hypovolemia <<
Phenylephrine (Neo-Synephrine)
(adult infusion dose)
40 - 180 mcg/min IV/IO
Phenylephrine (Neo-Synephrine)
(pediatric infusion dose)
0.1 - 0.5 mcg/kg/min
Phenylephrine (Neo-Synephrine)
(pregnancy safe)
Category C
Should be given to a pregnant woman only if the potential benefit justifies the potential risk to the fetus.
Epinephrine
Asystole / PEA / V-fib / V-Tach
(adult dose)
1 mg 1:10,000 solution IO/IV every 3 – 5 minutes
until ROSC
Epinephrine
Bradycardia / Medical Hypotension
(adult dose)
Set drip at 0.5 – 10 mcg/min IO/IV
Epinephrine
Push Dose
(adult and pediatric dose)
♦ Push Dose 5 - 20 mcg / 0.5 - 2 mL q 2 - 5 min
Epinephrine
Push Dose Mixing Instructions
(adult and pediatric)
Mixing
Take 10 mL syringe with 9 mL NS. Draw up 1 mL (0.1 mg) of 1:10,000 Epi from a pre-mixed vial. (concentration is 10 mcg/mL)
OR
Take 1 mL 1:1,000 Epi and mix in a 100 mL bag of NS
(resulting concentration is also 10 mcg/mL 1:1,000 Epi
Epinephrine
Reactive Airway Disease
(adult dose)
0.3 mg 1:1,000 solution IM
Epinephrine
Reactive Airway Disease
(pediatric dose)
0.1 mg/kg 1:1,000 solution IM
Phenylephrine (Neo-Synephrine)
Push Dose
(adult and pediatric dose)
50 - 200 mcg (0.5 - 2 mL)
q 2 - 5 min
Phenylephrine (Neo-Synephrine)
Push Dose
(mixing instructions)
Take a 3mL syringe, draw up 1 mL Phenylephrine with 10 mg/mL concentration
Inject this into a 100 mL bag NS
Resulting concentration is 100 mcg/mL
Alternatively
take 1 mL 1:1,000 Epi and mix into 100 mL bag NS
= 10 mcg/mL Epi 1:100,000 concentration
Examples of Inotrope Medications Include
Digoxin - increased contractility
Dopamine - increased contractility
(also increases heart rate)
Dobutamine - increased contractility
(also increases heart rate)
Milrinone - increased contractility
When is Dopamine useful?
Hypotension likely caused by vasodilation due to cardiac arrest, anaphylaxis, or sepsis, or when the heart is not contracting hard enough or fast enough.
Must give fluids FIRST
Also used in heart block and bradycardia in order to help maintain blood pressure and increase the heart rate.
NOT first-line in sepsis or anaphylaxis.
Problems Associated With Dopamine
♦ Ionotropic effects can cause increased oxygen demand / increased contractility can cause HTN
♦ Chronotropic effects can cause dysrhythmias if multiple pacemaker cells are stimulated at once
♦ Abdominal pain/nausea/vomiting come from vasoconstriction in the gastrointestinal system
Cardiogenic Shock =
Pump Failure/Sick Heart
(low stroke volume from low ejection fraction or MI that is impairing ejection fraction)
Cardiogenic Shock Effects on
CO/SVR/CVP
Cardiac output: Decreased
Afterload (SVR): Increased
Preload (CVP): Increased (JVD, Pulmonary edema)
Cardiogenic Shock Treatment Goal
Increase cardiac output AND Decrease SVR (afterload)
¤ (Be careful - decreasing SVR (afterload) in an already sick heart/hypotension may reduce pressure even further)
Phenylephrine is not a good choice for cardiogenic shock because?
Phenylephrine is alpha only (⇡ SVR)
(Afterload (SVR) is already increased, further increases in afterload (SVR) may worsen stroke volume, leading to a further reduction in cardiac output)
Why would Epi not be the best first-line med choice for cardiogenic shock?
Epi has strong beta-1 (inotropic/chronotropic) stimulation, increases cardiac output but maintains afterload (SVR)
(ie. increased myocardial oxygen demand to an already stressed heart compared to norepi)
Is Phenylephrine a Good Choice for Use in Cardiogenic Shock?
Why?
NO
Phenylephrine is pure Alpha which causes arterial constriction. (increased afterload/SVR)
Since SVR (afterload) is already increased due to the shock state, increasing SVR (afterload) more, may worsen stroke volume, leading to a further reduction in cardiac output.
Distributive Shock Effects on
CO/SV/SVR
(ie. sepsis / anaphylaxis)
Cardiac Output: decreased/normal, or slightly increased
Stroke Volume: decreased, or no change
SVR (afterload): decreased
Heart Rate: increased
(decreased afterload and preload = decreased stroke volume and cardiac output)
Distributive Shock is Caused by?
Inflammation making the blood vessels “leaky”, causing fluid to leak into the interstitial spaces
(preload is the most sensitive to volume changes)
The inflammation of the arterial system initiates histamine release causing dilation of the peripheral arteries which decreases afterload and then preload.
Decreased preload ⇢ causes a decrease in stroke volume ⇢ decreased stroke volume causes an increase in HR in attempt to maintain cardiac output.
What Is The First Intervention When Treating Septic Shock?
Volume Expansion
ie. Fluid Bolus
30mL/kg
(the first thing affected due to hypovolemia is preload)
