NU2ICU Inotropes & Vasopressors in ICU

NU2ICU V3 logo

Inotropes and Vasopressors

What is an inotrope?
Inotropes are drugs that change the force of your heart’s contractions. There are 2 kinds of inotropes: positive inotropes and negative inotropes. Positive inotropes strengthen the force of the heartbeat (increase contractility). Negative inotropes weaken the force of the heartbeat.

ALL Inotropes and Vasopressors require their own lumen on a CVC or own dedicated large bore jelco access unless otherwise authorised or as is accepted practice in your unit.

The IV line will be clearly identified and will have its injection port (if present) occlusively taped to prevent accidental bolusing. 

Please refer to your own hospitals dilution and usage protocols – these are not one size fits all drugs

INOTROPES

1st Line Agent 2nd Line Agents
Septic Shock Noradrenaline Vasopressin
Adrenaline
Heart Failure Dobutamine Milrinone
  Dopamine
Cardiogenic Shock Noradrenaline
  Dobutamine
Anaphylactic Shock Adrenaline Vasopressin
Cardiac Arrest Adrenaline Adrenaline
General non cardiac / hypotension Metaraminol (bridging until CVC access) Adrenaline
                   Receptor Physiology
Receptor   Location Effect
Alpha-1 Adrenergic   Vascular wall ↑ Vasoconstriction (SVR)
     Heart ↑ Duration of contraction without

↑ chronotropy

Beta Adrenergic Beta-1 Heart ↑ Inotropy and chronotropy
  Beta-2 Blood vessels ↑Vasodilation
Beta-3 Adipose tissues ↑ fat breakdown ↑ body heat

Alpha-1, Beta-1, and Beta-2 adrenergic receptors induce vasoconstriction, inotropy plus chronotropy, and vasodilation, respectively (dose dependant)

 

Hang on… what is chronotropy?

This is the effect of making impulses like those that trigger heart beats faster  (Greek; Chronos = time)

 

ADRENALINE

  • adrenaline acts by binding to a variety of adrenergic receptors. It is a non-selective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, and β3.
  • adrenaline’s binding to these receptors triggers a number of metabolic changes.
  • binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis in muscle.
  • β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland and increased lipolysis by adipose tissue.

Adrenaline stimulates the heart to increase contractility / output; raises the systolic blood pressure; lowers diastolic blood pressure; relaxes bronchial spasm and mobilises liver glycogen causing hyperglycemia.

Organ Effects
Heart Increases heart rate
Lungs Increases respiratory rate
Systemic Vasoconstriction or vasodilation
Liver Stimulates glycogenolysis
Systemic Triggers lipolysis
Systemic Muscle contraction

 

The best thing is that Coronary arteries have only β2 receptors, which cause vasodilation in the presence of adrenaline so during cardiac arrest increases vasocontriction, cardiac excitablity and helps the oxygenation of the heart itself!

 

In ICU

Presentation – 1mg /ml ampule

  • 6mg diluted to 100mls total in 5% dextrose (or equivalent if larger volume required)
  • remove 6 mls 5% dextrose from the bag prior to adding

Adrenaline

  • start ~ 3mls/hr titrate to ordered effect (ie MAP ≥ 70mmHg)

Can be given peripherally (but not for long)

 

In ALS

Presentation – 1mg / 10ml premix syringe or 1mg /ml ampule

  • 1mg diluted to 10mls total in 5% dextrose or 0.9% saline

Dose – 1mg Adrenaline bolus followed by 20ml fluid bolus (if given peripherally) and CPR

Freq – every second loop of CPR (4 minutes)

IV, Intra-osseous or via ETT

 

NORADRENALINE

  • noradrenaline acts by binding to a variety of adrenergic receptors. It is a non-selective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, and β3.
  • noradrenaline gives essentially the same effects as adrenaline but is much more vasoactive than bronchoactive
  • usually causes less chronotropy but increases the risk of organ ischaemia

At high doses every inotrope adds to the same risks of ischaemia to organs and tissues

 

In ICU (can vary)

Presentation – 4mg / 2ml ampule

  • 6mg diluted to 100mls total in 5% dextrose (or equivalent if larger volume required)
  • remove 6 mls 5% dextrose from the bag prior to adding

Noradrenaline

  • start ~ 3mls/hr titrate to ordered effect (ie MAP ≥ 70mmHg)

Can NOT be given peripherally (can but shouldn’t)

 

DOBUTAMINE

  • dobutamine is used to treat acute heart failure, such as which occurs during cardiac surgery or in cases of septic or cardiogenic shock on the basis of its positive inotropic action
  • dobutamine can be used in cases of congestive heart failure to increase cardiac output. It is indicated due to depressed contractility. It is not useful in ischemic heart disease because it increases heart rate and therefore increases myocardial oxygen demand
  • primary side effects include those commonly seen for β1 effects, such as hypertension and arrhythmia, however it can cause hypotension also
  • used with caution in atrial fibrillation as it has the effect of increasing the atrioventricular (AV) conduction

 

In ICU (can vary)

Presentation – 500mg ampule

  • 500mg diluted to 100mls total in 5% dextrose or 0.9% saline
  • start ~ as ordered or 3mls/hr titrate to ordered effect (ie MAP ≥ 70mmHg)

Can be given peripherally but via CVC for longer term in preferable

Other drugs you may come across include Milrinone (an inhibitor of PDE3 – increasing intracellular calcium causing vasodilation and increased myocardial contractility) and Levosimendan (it sensitises troponin-C to calcium and  acts on potassium channels in smooth muscle to cause vasodilation) both of these are very selective drugs in their application in the ICU

VASOPRESSORS IN ICU

So whats is a Vasopressor?

Vasopressors are a class of drug that cause vasoconstriction (increase Systemic Vascular Resistance) and thereby elevate MAP.   Vasopressors differ from inotropes, which increase cardiac contractility; however, many drugs have both effects

 

VASOPRESSIN

  • low concentration; usually released when body is dehydrated and causes the kidneys to urine volume
  • high concentrations; raises blood pressure by inducing moderate vasoconstriction
  • vasopressin infusion is used as a second line of management in patients not responding to high dose of inotropes

 

In ICU (can vary)

Presentation – 20u ampule

  • 20u added to total volume 20mls total in 5% dextrose or 0.9% saline
  • start ~ as ordered or 1- 3mls/hr titrate to ordered effect (ie MAP ≥ 70mmHg)

Slow wean in 0.5 increments due to low volume

Wean before other inotropes (unless specific order)

Should NOT be given peripherally

 

METARAMINOL

  • metaraminol is a potent sympathomimetic amine used in the “bridging” prevention and treatment of hypotension. It is an α1-adrenergic receptor agonist (vasoconstrictor) with some β effect
  • usually given in 0.5 – 1.0 mg (1ml) bolus
  • usually only as an infusion or boluses while achieving CVC access for inotropes

 

In ICU (can vary)

Presentation – 5mg/10ml premix syringe

  • Contains 0.5mg / ml
  • Bolus as ordered to ordered effect (ie MAP ≥ 70mmHg)

Should NOT be given peripherally in long term

 

Inotropic Nursing Considerations

  • always titrate to achieve effect as ordered
  • if large increases in trends (>5ml/hr or as discussed with your TL) inform your Team Leader or Shift Coordinator
  • never ever, ever run out of medication
  • chart as ordered if in ml/hr then ml/hr, if mcg/kg/min then mcg/kg/min etc
  • label lines / occlude injection ports
  • observe for side effects – peripheral ischaemia, tachycardia, increasing organ dysfunction (↑ lactate) etc
  • NEVER use a alligator or quick release clip, always luer lock vasoactive connections
  • change bags as required if unsure of how to maintain infusion during flask / bag change ask your Access or TL
  • if a line change is due consult your T/L about how to maintain infusion rates
  • increase or decrease at 2 minute intervals – we need to achieve the target pressure ASAP
  • if infusion ceased remove line and aspirate lumen and discard drug/blood syringe contents then flush with 0.9% saline so removing drug to avoid accidental bolus

One more thing…

Dromotropic

derives from the Greek word “dromos”, meaning running a race.  A dromotropic agent is one which affects the conduction speed in the AV node, and subsequently the rate of electrical impulses in the heart. Agents that are dromotropic are often (but not always) inotropic and chronotropic. For example, parasympathetic stimulation is usually negatively dromotropic, inotropic, and chronotropic.

NOTE – dosages are suggested only – see your local clinical guidelines for concentrations, rates and indications

REFERENCES

Oh’s Intensive Care Manual 7th Edition 2014 by Andrew Bersten, Neil Soni

The ICU Book 4th Edition 2015 by Paul L Marino