inotropes are drugs that increase the force and velocity of myocardial contraction resulting in increased contractility and stroke volume, and therefore cardiac output.
vasopressors increase vascular tone, resulting in raised mean arterial pressure (MAP), and systemic vascular resistance.
inotropes and vasopressors are used in the Mx of shock such as sepsis / septicaemia
the ideal inotrope would be one that increases stroke volume without an increase in myocardial oxygen consumption or arrhythmias but as they usually work by increasing intracellular calcium (an exception is levosimendan), they are usually arrhythmogenic and usually increase myocardial oxygen consumption.
most agents have varying effects depending upon their dose given the variation in their activity on the various receptors
effects may also occur due to reflex actions, eg. reflex bradycardia with lowered cardiac output may occur with agents that cause hypertension.
choice of agent
it would seem dopamine has fallen out of favour in all shock states, but particularly so in septic sock following the SOAP study published in 20061)
septic shock
traditionally noradrenaline is 1st line with addition of dobutamine as 2nd line (controversial), and argipressin (vasopressin / ADH) for cas unresponsive to catecholamines.
it would seem adrenaline is as effective but tends to be withdrawn more frequently due to metabolic effects, in particular, there appears to be more splanchnic vasoconstriction than with equipotent doses of noradrenaline or dopamine in patients with severe shock.
it would seem vasopressin is as effective as noradrenaline
acute decompensated heart failure
inotropes may increase mortality
cardiogenic shock
unclear as to the best agents, although AHA seems to still recommend dopamine for moderate hypotension and noradrenaline for severe hypotension despite lack of evidence
inotropic agents
adrenaline
aka epinephrine is the US
an endogenous sympathomimetic agent which stimulates all adrenoceptors including alpha and beta types.
infusion results in positive inotropy, positive chronotropy (increased heart rate), and a significant increase in MAP, although beta-2 stimulation of skeletal muscle vascular beds causing vasodilatation may actually cause a fall in MAP.
it can potentiate arrhythmias, increases myocardial work and oxygen demand.
it's alpha-1 vasocontrictive actions (vasopressor) may result in reduced peripheral, pulmonary, renal and splanchnic perfusion and may contribute to a lactic acidosis.
it's significant beta 2 adrenergic agonists actions enhance glycogenolysis and triglyceride breakdown resulting in an hyperglycaemia resistant to insulin and increased lactic acid production.
primarily used in refractory heart failure or cardiogenic shock but avoided a sole agent in septic shock due to the risk of hypotension from the vasodilatation.
unlike dopamine, it does not selectively cause renal vasodilatation.
a synthetic sympathomimetic agent which acts mainly on beta-1 adrenoceptor but with beta-2 agonist actions and some alpha-1 actions as well (the (-) isomer is an agonist at alpha-1 whereas the (+) isomer is an antagonist at alpha-1 with net effect being vasodilation)
it is useful in reducing after load in low cardiac output states such as post-MI or post-op cardiac surgery.
it can be used in Mx of sepsis / septicaemia in combination with noradrenaline or high dose dopamine to reduce the after load that these agents induce via their alpha-1 actions.
C/I in patients with idiopathic hypertrophic subaortic stenosis
an endogenous sympathomimetic agent, its main action is as a alpha-1 agonist with beta-1 agonist actions and little beta-2 agonist actions (thus no skeletal muscle vasodilation nor the glucose metabolism effects as with adrenaline)
variable effect on HR and cardiac output:
low doses often result in vagal reflex reduction in HR accompanying the rise in MAP, and thus cardiac output may even fall.
it's alpha-1 vasocontrictive actions (vasopressor) may result in reduced peripheral, pulmonary, renal and splanchnic perfusion.
a synthetic sympathomimetic agent which acts mainly on beta-1 adrenoceptor but with significant beta-2 agonist actions
actions are thus mainly chronotropic and inotropic but its skeletal muscle vasodilation and resultant decrease in MAP limits its use mainly to Mx of severe bradycardia or heart block.
result in inotropy with improved diastolic relaxation (lusitropy), and vasodilation, thus reduced after load making them theoretically useful in right heart failure, and for heart failure in patients on beta adrenergic blockers