Sympathomimetics Flashcards
Adrenaline presentation and uses
Clear solution containing 0.1-1mg/mL for administration as a bolus in asystole or anaphylaxis or an infusion in the critically ill with circulatory failure.
May also be nebulised in to upper airwaywhere its vasoconstrictor properties will temporarily reduce swelling associated with acute upper airway obstruction.
Adrenaline effects
CVS - effects vary according to dose. When administered at low dose infusion beta effects predominate = Increased CO, myocardial 02 consumption
At high doses by infusion or when given as a 1mg bolus during cardiac arrest alpha 1 effects predominate causing a rise in systemic vascular resistance.
Also used in conjunction with local anaestethetics to proeduce vasoconstriction prior to incision in surgery
Respiratory - Potent bronchodilator effects via b2 receptors. Also increases pulmonary vascular resistance
Metabolic - increases BMR. Raises plasma glucose by stimulating glycogenolysis (liver and skeletal muscle). Glucagon secretion and lactate are also raised. Sodium reabsorption is increased by direct stimulation of tubular Na transport and by stimulating renin (therefore AT2 and aldosterone)
Adrenaline kinetics
Not given orally due to inactivation by liver and GI mucosa. Therefore given IV, subcut or IM.
Metabolised by monoamine oxidase (MAO) and catechol -methyl transferase (COMT) within the liver, kidney and blood to inactive metabolites which are excreted in the urine. Short half-life (about 2 minutes) due to rapid metabolism
Noraderenaline presentation and uses
Presented as a clear solution containing 0.2-2mg/mL noradrenaline acid tartrate. Used as an IV infusion (dose range 0.05-0.5mcg/kg/min) to increase systemic vascular resistance
Noradrenaline effects
CVS - infused norad causes peripheral vasoconstriction, increases systolic and diastolic BP and may cause reflex brady. Pulmonary vascular resistance may increase and venous return is increased due to venoconstriction (caution in right heart failure). Such a potent vasconstrictor it can cause organ / digit ischaemia, renal arteriolar constriction - oliguria and renal failure.
Extravasation can cause tissue necrosis.
Splanchnic - renal and hepatic blood flow falls due to vasoconstriction
Interactions - Should be used in caution in patients taking MAOIs as effects of norad may be exaggerated and prolonged.
Noradrenaline kinetics
For edogenously released norad, uptake 1 describes active uptake back in to nerve terminal where it is metabolised by MAO (COMT not present in sympathetic nerves) or recycled. This is the main mechanism by which norad is inactivated.
Uptake 2 describes diffusion away from the nerve (less important). Reaches the circulation and is metabolised by COMT to inactive metabolites excreted in urine. Short half life (2 min).
Dopamine presentation and uses
Presented as a clear, colourless solution containing 200-800mg in 5mL. Used to improve haemodynamic parameters and urine output.
Dopamine effects
CVS - depend on rate of infusion. 0.5-3mcg/kg/min D1 and D2 effects predominate - vasodilation, decreased MAP, increased splanchnic blood flow. 3-10 B1 dominates, increased contractility, heart rate, cardiac output. >10 alpha 1 dominates - increased SVR, venous return
Respiratory - infusions of dopamine attentuate the response of the carotid body to hypoxia. PVR increased.
Splanchnic - dopamine vasodilates mesenteric vessels via D1 receptors. Increased urine output however this may be due to inhibition of na reabsorption, improved CO and BP.
CNS - dopamine modulates extrapyramidal effects and inhibitis secretion of prolactin from pit gland
GIT - causes nausea and vomiting (likely due to D2 receptor in medulla. Gastric transit time also increased.
Interactions - like norad effects can be significantly exaggerated or prolonged by MAOI.
Dopamine kinetics
Administered IV. Acts within 5min and has a duration of 10min.
Metabolism via MAO and COMT in the liver, kidneys and plasma to inactive compounds which are excreted in the urine.
