Dr Bronwyn Avard, July 2010

 To understand the basic physiology of shock  To understand the pharmacodynamics and pharmacokinetics of vasoactive drugs used in ICU  To know the indications for the administration of different inotropes and vasopressors in the critically ill patient  To know the complications of administering these vasoactive drugs, and relevant patient care issues

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SHOCK

 Cardiac output = stroke volume x heart rate amount of blood ejected from the ventricle in systole depends on : - preload - afterload - contractility

 Cardiac output = stroke volume x heart rate › Preload = end-diastolic ventricular volume › Afterload = resistance against which ventricle contracting › Contractility = strength of muscle activity  Cardiac index = cardiac output / BSA

 Oxygen delivery = cardiac output x arterial oxygen content stroke volume x heart rate preload afterload contractility [haemoglobin] x SaO 2

 Blood pressure = cardiac output x systemic vascular resistance

 Hypovolaemic  Cardiogenic  Distributive / vasodilatory  Obstructive

 Inotropes  Vasopressors

global oxygen delivery cardiac output arterial oxygen content mean arterial pressure cardiac output systemic vascular resistance

 Adrenaline  Noradrenaline  Dobutamine  (Dopamine)  Metaraminol  Phenylephrine  Ephedrine

 aka ephinephrine  Low dose = ↑ heart rate & contractility  High dose = vasoconstriction

Adrenaline infusion 0.01mcg/kg/minute HR 110 bpm MAP 70mmHg Warm peripherally Infusion increases to 0.03mcg/kg/minute HR now 150bpm MAP now 65mmHg Cool peripherally WHY?

As heart rate rises, less time available for cardiac filling, hence stroke rate falls MAP falls rather than rising as you would have expected

 aka norepinephrine  Low doses = mainly ↑ HR & SV  High doses = mainly vasoconstriction

Nordrenaline infusion 0.05mcg/kg/minute MAP 55mmHg Warm peripherally As infusion increases Cool peripherally Lactate rising WHY?

Vasoconstriction caused by higher dose noradrenaline redistributes blood flow to essential organs Even though MAP rises, splanchnic perfusion falls & rising lactate can indicate gut ischaemia

 Acts on both beta 1 and 2 receptors  Net effects are › Increased contractility › Increased heart rate › Mild vasodilation  Effect on MAP variable and not always predictable – may increase or decrease

76 year old woman post NSTEMI HR 84bpm MAP 64mmHg Cool peripherally Begun on dobutamine 7.5mcg/kg/minute MAP falls to 60mmHg WHAT WOULD YOU DO?

She was probably vasoconstricted prior to infusion. Beginning dobutamine caused vasodilatation hence MAP fell. Fluid bolus or noradrenaline would be appropriate.

mcg/kg/min = rate (mL/h) x concentration (mcg/mL) weight (kg) x 60

mcg/kg/min = rate (mL/h) x concentration (mcg/mL) Weight (kg) x 60 You are caring for a 60 year old man, weighing approximately 90kg, admitted after a non-ST elevation myocardial infarction. He is receiving adrenaline at 5mL/h. The 100mL bag has 8mg adrenaline in it. What dose of adrenaline is he receiving ? (in mcg/kg/min)

ANSWER : 0.07 mcg/kg/min

mcg/kg/min = rate (mL/h) x concentration (mcg/mL) weight (kg) x 60 mcg/min = concentration (mg/mL) x 1000 x rate (ml/h) 60

mcg/min = concentration (mg/mL) x 1000 x rate (mL/h) 60 You are looking after a 25 year old woman who has been admitted with sepsis. She has 6mg noradrenaline in 100mL bag of normal saline, which is running at 5mL/hour. How many mcg/minute is she receiving?

ANSWER : 5mcg/min This is why we use the concentration of 6mg/100mL as the “mL/h” equals “mcg/min” (she was on 5mL/h noradrenaline)

 Adrenaline  Noradrenaline  Ephedrine  Metaraminol  Phenylephrine

 Inotropes : › Milrinone › Levosimenden  Vasopressor : › Vasopressin

 Accurate measurement of vital signs & invasive blood pressure  Check vasoactive drugs at start of shift  Ideally administered centrally  Labelling critical  Change bag every 24 hours

 Local necrosis with extravasation  Tachycardia & arrhythmias  Increased myocardial oxygen consumption  Ischaemia of gut &/or extremities

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