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Inotropes are the most commonly prescribed group of cardiotropic drugs. The use of each drug varies widely depending on local practice and the patient's condition. In general the following rules should be followed where possible before instituting inotropic support.
Systolic Blood Pressure <90 mmHg or MAP <60Despite these definitions, we often quote mean arterial blood pressure (MAP) as being more relevant to organ perfusion. A MAP of >60 mmHg would be considered adequate in most instances.
When hypotension is deemed to exist, assess organ perfusion:
This simple concept is in practice very difficult to perform accurately. In the intensive care unit there are a number of ways to assess intravascular volume status although each has shortcomings.
Clinical assessment of fluid status including JVP
Variation of arterial waveform characteristics with ventilatory cycle
Measurement of CVP
Right heart catheterization
Calculation of intrathoracic blood volume and extrapolation to extra vascular lung water using the PiCCO monitor
Except in very clear-cut cases (ie gross fluid overload or cardiac failure), in a situation where there is doubt as to the patients fluid status, a trial of fluid administration should be considered.
Only once the above steps have been considered should inotrope therapy be considered. No single inotrope (or mixture of inotropes) has been shown to be superior to another. There is marked inter-individual variation in response to a chosen inotrope, due to:
Qualitive and quantitive changes in adrenergic receptor kinetics in both acute illness (sepsis) and chronic conditions (heart failure)
Underlying variability in disease state (ie cardiogenic shock, sepsis, Hypovolaemia)
They may increase cardiac afterload and thus cardiac wall stress.
In selected patients with hypotension refractory to high doses of catecholamine's, the co-administration of physiological doses of intravenous steroid has been beneficial.
This practice is not routine in the Christchurch Intensive Care and may not be practiced without prior consultation with senior staff.
Dopamine / adrenaline / noradrenalin: For ease of application many claim these three agents have an -adrenergic action in low dose and a progressive -effect in increasing doses. Each however has a characteristic feature worth noting.
Dopamine: in low doses (2.5 g / kg / min) has a direct diuretic effect which may result in increased urine volume, there is no evidence of a renal sparing or protective effect.
Adrenaline: is a useful / agonist, however it does have significant 2-effect which may result in unwanted metabolic effects (hyperglycaemia, excess lactate production unrelated to organ perfusion).
Noradrenaline: is generally held to have a predominant -effect and is therefore useful as an inotrope-vasopressor, particularly in septic shock.
Dobutamine: a synthetic inotrope, does not have significant -effects (may have some myocardial -effect) and is therefore useful in increasing heart rate and stroke volume, but may cause a paradoxical fall in blood pressure due to peripheral -adrenergic activity.
Adrenaline and Noradrenaline: infusions should be started at 1-5mls / min and titrated to response. Infusions of these agents require 3-5 minutes to achieve steady state. Changes in rate more frequently than every 3-5 minutes (unless in an emergency) should be discouraged as it may lead to a "roller-coaster" effect.
Milrinone: not commonly used in the intensive care unit, but may be indicated in isolated patients. Phosphodiesterase inhibitors increase cAMP by non-adrenergic mechanisms. They result in:
Increased myocardial contractility
Systemic and pulmonary vasodilatation (often requires co-administration of a vasopressor / noradrenalin)
Improved diastolic relaxation (useful in patients with diastolic heart failure).
The relatively long half-life of this agent requires forethought before administration, as its action is not easily reversed, and titration of infusions to effect cannot be effected rapidly.
ReferenceFriedrich JO, Lapinsky SE. New evidence for old therapies in catecholamine-dependant septic shock. Intensive Care Med 2001;27:787-790.
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