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Pre-hospital ketamine -Is there anything it can’t do?
Per P. Bredmose Director of Training Consultant in Prehospital and retrieval medicine Consultant anaesthetist/intensivist Air Ambulance Department Oslo University Hospital
@VikingOne_
@VikingOne_No conflicts of interest
Plan
Ketamine How do we use it - «ketamine staircase» What are the pitfalls?
«Do not try this at home....»
Forms
R – ketamine (racemic)
S – ketamine
Know YOUR local drug form
High dose dissociation
Graded use...
Ketamine starway to full dissociation....
Dose Range
0.1 mg/kg iv
3 mg/kg iv
(to 10 mg/kg IM)
Smaller doses for sedation
Hypnosis FIRST Then dissociation
For the co-operating awake patient
BZ Propofol
RSI
«Upper-end» doses for RSI !
BEWARE : Titrated to patient physiology
Adult: 30-300 mg iv !!
THINK and BE AWARE !
CONFLICT
Ketamine RSI for the compromised patient
Why on f..k earth use benzodiazepines/propofol to block endogenous symphathetic response ???
Agitated patient
GET CONTROL
IV IM
Head Injury
YES you can do it...
That’s fine! --------------------------------------------- Continued anaesthesia
YES
Barking MAD ONES
SAFE transport of psychiatric patients when needed
+
BZ/Propofol
YES
Asthma
YES
Really sick babies
Sepsis Congenital heart disease Diaphragmatic Hernias
Cardiomyopathy
YES
YES
However...
Apnoea
Short lasting apnoea
Sick patients:Longer lasting apnoea !!
Beware
Reduced stroke volume Cardiac depressant
Increases mainly BP via alfa-receptors Constriction and tachycardia
Anaesth Intensive Care 1997 Jun;25(3):255-9.
• Following sedation with midazolam (0.15 +/- 0.07, mg.kg-1.h-1) and sufentanil (0.88 +/- 0.33 microgram.kg-1.h-1), patients with impaired left ventricular function (left ventricular ejection fraction area 30 +/- 7%) were randomly assigned to receive ketamine (2.5 +/- 0.9 mg.kg-1.h-1) and midazolam (Group A) or remained on sufentanil/midazolam (Group B). Haemodynamic measurements were performed throughout the first 24 hours after randomization. In group A cardiac index decreased by 21% (P = 0.01), mean arterial pressure increased by 13% (P = 0.01), mean pulmonary artery pressure by 14% (P = 0.04), pulmonary capillary wedge pressure by 20% (P = 0.03), and systemic vascular resistance index by 38% (P < 0.001). No significant cardiovascular effects were observed in Group B. Neither group had significant changes of exogenous catecholamine requirement. In conclusion, ketamine exhibits potential negative cardiovascular effects in patients with catecholamine-dependent heart failure. Therefore, ketamine should not be considered a first line drug for longterm sedation of patients with impaired left ventricular function.
Impaired LV Sedation with KETAMINE and MIDAZOLAM
BP (MAP) ↑ 13 %
----- ----- ----- -----
Cardiac index ↓ 21 %
PAP MAP ↑ 14 %
Wedge pressure 14 %
SVRI ↑↑ 38 %
Reduced CO Increased wordload
ROSC
Tachycardia ↓ Diastolic time ↓ Coronary perfusion ↑↑ Myocardial demand...
Sub Arachnoid Hemorrhage
BP 188/129
Don’t go there !
HYPERTENSIVE PATIENTS
And the team..
Warn team Warn others Warn family Warn hospital
Ketaminised patients look different.....
In conclusion....
Be familiar with your drug Know and acknowledge physiology Dose depending on patient Be familiar with your drug
1. Hypertensive patients 2. ROSC 3. Remember info to those around you
Pre-hospital ketamine Is there anything it can’t do?
Well....there are certainly things where it seems to be less optimal
But under many circumstances it is brilliant !!
Pre-hospital ketamine -Is there anything it can’t do?
Per P. Bredmose Director of Training Consultant in Prehospital and retrieval medicine Consultant anaesthetist/intensivist Air Ambulance Department Oslo University Hospital
@VikingOne_
?Thank you!