vasopressors presentation_final
TRANSCRIPT
VasopressorsRasha Sarhan, MSC, B.Sc.Pharm, Pharm D Candidate
Shock
Shock
ObjectivesDefine shock.
Define and interpret various hemodynamic parameters [mean arterial pressure (MAP), preload, afterload, Cardiac output (CO)].
List types, causes, and symptoms of shock.
Describe the pharmacology, doses and use of vasopressors.
Explain practical issues with using vasopressors.
Apply knowledge to a patient with a shock syndrome
Shock
A state of cellular and tissue hypoxia due to
reduced oxygen delivery and/or increased
oxygen consumption or inadequate oxygen
utilization.
SBP < 90 mmHg or reduction of > 40 mmHg
with perfusion abnormalities* despite
adequate fluid resuscitation.
* End organ hypoperfusion (lactic acidosis, oliguria,
mental status deterioration).
Preload (PCWP)
Represents the amount
of blood available to the
left ventricle for pumping
and is influenced by
venous return to the left
atrium.
Normal = 12 - 18 mmHg
Dry < 12 mmHg
Wet > 18 mmHg
Afterload (SVR)
Represents the ventricular wall
tension required for expulsion
of ventricular blood volume
into the aorta during
contraction.
Normal = 1000 - 1600 dynes-sec/m2
Arterial dilation < 800 dynes-sec/m2
Arterial constriction > 1800 dynes-sec/m2
Definitions
MAP = 1/3 SBP + 2/3 DBP
MAP = CO X SVR
CO = HR X SV
The stroke volume is
determined by:
Preload
Afterload
Myocardial contractility
SVR is
determined by:
Vessel length
Blood viscosity
Vessel tone
Shock Symptoms
Hypotension
Tachycardia
Abnormal mental status
Cool clammy cyanotic skin
Metabolic acidosis
oliguria
Shock
Classification & Etiology
• Hypovolemic: (hemorrhagic, Non-hemorrhagic).
• Cardiogenic: (MI, cardiomyopathy, arrhythmia).
• Distributive: (septic, non-septic).
• Obstructive:
• Pulmonary Vascular: [Pulmonary embolus, severe pulmonary
hypertension (PAH)].
• Mechanical: (Tension pneumothorax, pericardial tamponade,
constrictive pericarditis, restrictive cardiomyopathy).
Hypovolemic Hemorrhagic Trauma, GI bleed (e.g., varices, peptic
ulcer)
Non-
hemorrhagic
Gastrointestinal losses, skin losses; renal
losses, hypoaldosteronism, third space
losses.
Cardiogenic Cardiomyopathy MI, HF exacerbation, cardiac arrest,
hypotension, cardiopulmonary bypass,
advanced septic shock, myocarditis.
Arrhythmia fibrillation, flutter, reentrant tachycardia,
complete heart block.
Mechanical Severe aortic or mitral valve insufficiency.
Distributive Septic Infection ( Gram +ve , Gram –ve, viral,
fungal, parasite, mycobacterium)
Inflammatory shock –SIRS; neurogenic
shock, anaphylactic shock, drugs and toxins,
endocrine shock.
Non-Septic
Obstructive Pulmonary
vascular
Pulmonary embolism (PE), Pulmonary artery
hypertension (PAH).
Mechanical Tension pneumothorax (trauma, iatrogenic,
ventilator-induced), pericardial tamponade,
constrictive pericarditis, restrictive
Hypovolemic Shock
Goal is to increase preload (PCWP) by
replacing fluid loss with blood, crystalloid,
or colloid.
Cardiogenic Shock
Goal is to increase cardiac output
(CO) with inotropic pharmacotherapy
(dobutamine) and reduce afterload
(SVR) with vasodilators.
Septic Shock
Goal is to increase preload (PCWP) with
fluid replacement (crystalloid, then
colloid), then increase afterload (SVR)
with vasopressor (e.g. dopamine,
norepinephrine, phenylephrine,
vasopressin).
Neurogenic Shock
Goal is to increase afterload (SVR)
with vasopressor (e.g. phenylephrine,
norepinephrine).
Combined ShockPatients with pancreatitis or sepsis have distributive shock but may have hypovolemic and cardiogenic component.
Patients with cardiomyopathy may present with cardiogenic shock and hypovolemic shock.
Patients with severe traumatic injury may have hemorrhagic and distributive shock
Patients with spinal cord injury can have distributive and cardiogenic shock.
Vasopressors Goals of Therapy
PCWP = 8 to 12 mm Hg ( up to 15 mm Hg in
specific patients).
MAP ≥ 65 mm Hg.
Mixed venous Oxygen saturation (SvO2) ≥ 65%.
Central venous Oxygen saturation (ScvO2) ≥
70%.
Lactate Clearance ≥ 20%.
Receptors
α 1 β 1 β 2 Dop V1 V2
CO − − − −
Preload
(PCWP)
− − − − − −
Afterload
(SVR)
−
Urine
output
− −
Dopamine (Dop)
• Receptors: D1, D2, β1, α1*
• Use:
• At (3 to 10 mcg / Kg/ min), increases CO in cardiogenic shock.
• At (10 to 20 mcg / Kg/ min), increases afterload (SVR) and urine output in septic shock.
• Dose: 1 to 20 mcg / kg/ min.
• Monitoring: Blood pressure (BP); Heart rate (HR); urine output, renal function, serum glucose, CO, PCWP, and SVR.
Dobutamine (Dob)
• Receptors: β1, β2, α1
• Use: Increase CO and decrease
afterload in cardiogenic shock.
• Dose: 1 to 20 mcg / kg/ min.
• Monitoring: BP, ECG, renal function,
urine output, CO, PCWP, and SVR.
Norepinephrine (Nepi)
• Receptors: α1, β1, β2
• Use: Increase afterload (SVR) in septic and neurogenic shock.
• Dose: 8 to 20 mcg / min.
• Monitoring: BP, HR, CO, urine output, infusion site for extravasation or necrosis.
Epinephrine (Epi)
• Receptors: α1, β1, β2
• Use: Increase afterload (SVR) in
neurogenic shock or as an add on in
septic shock.
• Dose: 1 to 10 mcg / min.
• Monitoring: BP, HR, continuous cardiac
monitoring, serum lactate, site of
infusion for blanching/extravasation.
Phenylephrine (Phen)
• Receptors: α1
• Use: Increase afterload (SVR) in
neurogenic shock, or as salvage - add on
- to other vasopressors.
• Dose: 100 to 180 mcg / min.
• Monitoring: BP, HR, CO, local skin
blanching, extravasation.
Vasopressin (Vas)
• Depleted in septic shock
• Receptors:
1. Vascular V1 receptors: Cause vasoconstriction.
2. Renal V1 and V2 receptors: Increases GFR and net increase urine output.
3. Pituitary gland V3: Increase serum cortisol.
• Dose: 0.02 to 0.04 units / min.
• Monitoring: Fluid input, urine output, HR, BP, skin blanching.
Vasopressors Pharmacology
Dop Dob Nepi Epi Phen Vas
α1✚ ✚✚ ✚✚✚ ✚✚✚ ✚✚✚ 0
β1✚ ✚✚✚ ✚✚ ✚✚ 0 0
β20 ✚✚✚ ✚⁄✚✚ ✚✚ 0 0
D1,D2✚✚ 0 0 0 0 0
V1, V20 0 0 0 0 ✚
Dose1 to 20
mcg/kg/min
1 to 20
mcg/kg/min
8 to 20
mcg/mi
n
1 to 10
mcg/min
100 to 180
mcg/min
0.02 to 0.04
units/min
Vasopressor IV Infusion Chart
Medication Indication BolusInitialIVinfusion
Titration
Usualdose
Maximumdose/duration
Diluent/Line
DobutamineDecreasedcardiac
outputNoBolus
0.5to1mcg/Kg/min
By2.5
mcg/kg/minAccordingto
response~
every5min
2to20
mcg/
kg/min
҂Upto40
mcg/Kg/
min
NS/D5W/LR
DoNotaddSod
Bicarbonate
PeripheralDobutamine
PostcardiacArrestACLS
5to10
mcg/Kg/min
0.5to1
mcg/Kg/min
2to20mcg/
kg/min
DopamineCardiogenic/septicShock,CHF/renal
failureNoBolus 2to5mcg/kg/min
5to10mcg/kg/minincrements
¥Upto20-50
mcg/kg
/min
NS/D5W
DoNotaddSod
Bicarbonate
CentralLine
Epinephrine3
Hypotension/SepticShockorasanaddontoother
vasopressors
NoBolus₠0.1to0.5
mcg/Kg/min
0.05to0.2
mcg/kg/minute
every10-15mintotarget
MAP
1to10
mcg/min
€Upto10
mcg/min
NS/D5W
CentralLine
Epinephrine
Asystole/pulselessarrest
ACLS
1mgIVorI.O.
Give1mgevery3to5minuntilreturnof
spontaneouscirculation.
Upto0.2
mg/Kg(totaldose)
InBBand
CCBoverdose
NS/D5W/
LR
Central
Line*2.5mgendotracheal Dilutein5to10mlNSorsterilewater
Epinephrine Anaphylaxiso mgIV
over5min
5to15mcg/min
Norepinephrine4Levophed®
Hypotension/Shock
NoBolus 8to12mcg/min
Titrateto
desiredresponseby
2mcg/min
1to
4mcg
/min
Upto20mcg/min
NS/D5W
Central
Line
SummaryTypes of Shocks: hypovolemic, Cardiogenic, Septic, neurogenic.
Hypovolemic Shock: goal is to increase preload with fluids1st.
Cardiogenic Shock: goal is to increase cardiac output (CI) with dopamine (1-10μg /Kg/min), or dobutamine.
Septic Shock: goal is to increase preload with fluids1st , then increase afterload with, dopamine, norepinephrine, phenylephrine, or vasopressin.
Neurogenic Shock: goal is to increase afterload with norepinephrine, phenylephrine.
SummaryNepi is the initial vasopressor, 8 to 20 μg / min.
Dop alternative to Nepi in patients with low CO or HR. Dop
receptor effect is dose dependent, 1 to 20 μg / kg / min.
Dob used in patients with cardiogenic shock 1 to 20 μg / kg /
min.
Epi used as an add on to increase MAP, 1 to 10 μg / min.
Vasopressin used as an add on to Nepi to increase MAP,
0.03 Unit / min.
Phen used in neurogenic shock or as an add on to increase
MAP, 100-180 μg / min.