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Vasopressors and Inotropes

Critical Care Lecture Series

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Objectives

What are the different classes of shock and give examples of each. Discuss how to investigate and the management principles behind each of the causes of shock. What are the different crystalloids and colloids available for resuscitation? Have knowledge of the mechanism of action of commonly used vasopressors and inotropes, including dopamine, dobutamine, milnerone, levophed, phenylephrine, epinephrine, vasopressin Discuss adverse events associated with the above agents.

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Is My Patient in Shock?

Definition of shock

Inadequate end organ perfusion leading to inadequate oxygen delivery

N.B. a patient in shock does not have to be hypotensive

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Treatment of Shock
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Basic

Resuscitation: ABCDEs

A: Airway establishment B: Breathing: control WOB C(a): Circulation Optimization C(b): Control O2 consumption D: Delivery of O2 adequately E Extraction of O2

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Fluid resuscitation
Very important. Therapy with least detrimental effects Fluid therapy may be beneficial in any type of shock

Even cardiogenic shock/pulmonary edema

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Fluid Resusitation

Must test the patient

Give volume and look for response/improvement Always start with NS of RL ? Need blood

Must always look for the effect of treatment

Re-evaluate patient after fluid If no improvement, and no adverse effects, repeat If adverse effect, needs inotropes/vasopressor if still in shock

Too much: pulmonary edema (O2 sats)

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A: Airway establishment
Indications for intubation: 1. Failure of oxygenation or ventilation 2. Failure to protect airway 3. Condition present or procedure needed that will require intubation shock is an indication for intubation Hypotension common after intubation

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B: Breathing: control WOB


Respiratory muscles are significant consumers of oxygen Control will allow better O2 delivery to other tissues Sedation after intubation

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C(a): Circulation Optimization


Most causes of shock require some volume re-expansion even cardiogenic shock - Starling curve Crystalloid as good as colloid Vasopressors ineffective if hypovolemic

double edged sword

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C(b): Control O2 consumption


Reduce hyper-adrenergic state Analgesia/sedation/muscle relaxation temperature

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D: Delivery of O2 adequately
Follow sats (keep > 92%) ? Transfusion (Hbg >80-100) Lactate SmvO2

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E: Extraction of O2
O2 must get from lungs to Hbg to tissues O2 extraction important in some types of shock

Cyanide, MetHbg, SEPSIS

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ABCDEs: Summary
A: Airway establishment: 02,biPap, ETT

B: Breathing: control WOB: Sedation, analgesia


C(a): Circulation Optimization: fluids, inotropes, pressors C(b): Control O2 consumption: sedation, temp control, seizure control

D: Delivery of O2 adequately: Hbg, fluid, pressor, inotropes


E: Extraction of O2: R/O cyanide, metHbg, sepsis

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Vasopressors

Many different pressors/inotropes Need to understand how they work to use effectively If choose wrong one, or use inappropriately, can harm the patient

Adrenergic precipitation of arrhythmias Drive the heart too fast resulting in decreased filling time and decreased stroke volume Vasoconstriction of splachnic circulation and coronary arteries Inotropes may make certain patients hypotensive

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Vasopressors
1 agonist/stimulation: chronitropic, inotropic 2 agonist/stimulation: vasodilation, bronchodilation : vasoconstriction D: increases renal blood flow

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Vasopressors and inotropes: the chart (everything you need to know)


Normal

Need CO

Need nothing

Blood pressure Low Need

BP and CO
Low

Need BP
Normal

Cardiac Output

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Dopamine
Dopaminergic, Beta, Alpha: ranges ? Dopa: 1-5 ug/kg/min

? Renal flow Inoptropy/chronotropy Vasoconstriction

Beta: 5-10 ug/kg/min

Alpha: >10 ug/kg/min

Major use: increasing HR, ? bp

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Dobutamine
Beta (little alpha) Inotropic/chronotropic 2-20 ug/kg/min Major use: Systolic dysfunction Caveat: can/will decrease MAP

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Milrinone
Used as an inotrope Mechanism of Action

Side Effects

Phosphodiesterase inhibitor decrease the rate of cyclic AMP degradation increase in cyclic AMP concentration leads to enhanced calcium influx into the cell, a rise in cell calcium concentration, and increased contractility
can also cause vasodilatation but tends to have less chronotropy than dobutamine 5-15 minutes

Onset of action

Duration

Dose

Half life of approximately 2 hours (so its gonna last a while


Loading dose: 50 mcg/kg administered over 10 minutes followed by 0.375 mcg/kg/minute

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Phenylepherine
Pure alpha agonist Vasoconstrictor with no effect on inotropy/chronotropy 0.2-3.0 ug/kg/min Major use: non-cardiogenic hypotension

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Norepinepherine
Alpha and Beta 0.02-3.0 ug/kg/min Major Use: when you need A&B

? Drug of choice for septic shock

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Epinepherine
Alpha and Beta 0.01 1.0 ug/kg/min Major Use: when you need A&B

resuscitation

Vasopressors and inotropes


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Normal Blood pressure Low

Dobutamine Milrinone
Dopamine Levophed Epinepherine Or Dobutamine/phenyl

nothing Phenylepherine Levophed (dopamine)


Normal

Low

Cardiac Output

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Overview of the Management of Shock

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Case Study
65 yo male presents to ED Complaining of cough and feeling very unwell HR 120, BP 100/60, RR 30, temp 39 Is this patient in shock? What investigations What treatment would you start?

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Case Study
The patients BP drops to 90/50, what would you do now? Would you start pressors? Which one?

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Case Study

The patient is on 0.8ug/kg/min of levophed through a femoral line. Why might the patient not be responding to the vasopressors? What measurement would be helpful in improving this mans MAP?

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Case Study

The patient has been resuscitated, now has a BP of 110/90. HR 65. His JVP is 12. His lactate continues to rise however. He is also anuric. Is this patient in shock? What is your management now?

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Summary

Shock can be the consequence of decreased SVR, decreased CO or both. Management of shock should be tailored to the physiologic state of the patient of the patient. Drugs are available to augment SVR, HR, afterload and contractility. Remember to optimize preload and consider the oxygen carrying capacity of the blood.