PharmacologyTier 2Medical Sciences concept

Catecholamine infusion metabolic effects (lactate, glucose, potassium)

Core concept

Catecholamine infusions produce predictable metabolic derangements that mimic pathology. Recognising them prevents the wrong escalation.

Effect	Receptor	Mechanism
inc Lactate	beta-2	inc skeletal muscle glycogenolysis + glycolysis and inc Na/K-ATPase activity -> aerobic pyruvate overproduction -> type B lactataemia
inc Glucose	beta-2 (+ alpha-2)	inc hepatic glycogenolysis + gluconeogenesis; alpha-2 inhibits insulin secretion; peripheral insulin resistance
dec Potassium	beta-2	inc Na/K-ATPase -> intracellular K shift
dec Phosphate, dec Magnesium	beta-2	Intracellular shift with glycolysis
inc Free fatty acids	beta-1/beta-3	Lipolysis
inc VO2, inc temperature	beta	Thermogenesis

The adrenaline lactate rise is aerobic and benign - it is NOT evidence of tissue hypoperfusion
- Escalating the adrenaline because the lactate is rising is a self-reinforcing error
Distinguish: rising lactate WITH a falling ScvO2, widening base deficit, worsening capillary refill and falling urine output = hypoperfusion. Rising lactate with an improving clinical picture and a rising glucose = the drug.

Vasoactive agents and their metabolic footprints

Agent	Receptors	Metabolic signature
Adrenaline	beta-1 = beta-2 > alpha-1	Marked lactate, glucose, hypokalaemia
Noradrenaline	alpha-1 >> beta-1	Minimal metabolic effect - the reason it is first-line in septic shock
Dobutamine	beta-1 > beta-2	Modest lactate/glucose; tachycardia, vasodilation
Dopamine	Dose-dependent D > beta > alpha	Hyperglycaemia; suppresses TSH and prolactin
Vasopressin	V1	None; reduces catecholamine requirement
Milrinone	PDE3 inhibitor	Hypotension, thrombocytopenia

Magnitudes to expect

Adrenaline infusion: lactate commonly 2-5 mmol/L, rising within 30-60 min of starting or escalating, resolving within hours of weaning
Glucose often >10 mmol/L -> insulin infusion required
Potassium can fall rapidly - check within 1-2 hours of starting or increasing an adrenaline infusion

Other traps

Beta-2 vasodilation in skeletal muscle can lower diastolic BP at low adrenaline doses
Prolonged infusion -> tachyphylaxis (receptor downregulation), tissue ischaemia (digits, mesentery), arrhythmia, stress cardiomyopathy
Extravasation -> tissue necrosis -> phentolamine infiltration
High-dose salbutamol produces the identical picture: lactataemia, hypokalaemia, hyperglycaemia, tremor - and in status asthmaticus the lactate is very commonly the drug rather than the disease

Sepsis: lactate clearance is a resuscitation target, so a drug-induced rise is directly misleading
- Trend the whole picture, not the lactate in isolation
- Noradrenaline is preferred first-line partly because it does not do this
Cardiac surgery and post-arrest: adrenaline infusions routinely produce lactate 3-6 mmol/L with no perfusion deficit
Phaeochromocytoma - endogenous version of the same physiology: hyperglycaemia, lactataemia, weight loss
Check potassium, magnesium and glucose regularly on any catecholamine infusion
Adrenaline in anaphylaxis: the same metabolic effects appear, and a post-adrenaline lactate is expected
Beta-blockade blunts all of these effects - and blunts the response to hypoglycaemia

Vasopressor mechanisms of action
Adrenaline in anaphylaxis - mechanism and timing
Management options for hyperkalaemia (salbutamol uses the same beta-2 shift therapeutically)
Causes of type A vs type B lactic acidosis (metformin, thiamine deficiency, malignancy, HIV/NRTIs, linezolid)
Phaeochromocytoma - investigation and preoperative blockade
Beta-blocker comparative pharmacology
Stress hyperglycaemia and glycaemic control in critical illness

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