- Acts primarily directly at alpha-1-adrenoreceptors (phospholipase C → IP3 → increased calcium)
- To a lesser extent acts on beta 1>beta 2 effects

Predominant mechanism is via direct acting B1 stimulation (increased cAMP) and retains a small amount of B2 effects

Low doses: β - ↑ino+chronotropy
increased MVO2
Higher doses: 1 -
peripheral vasocontriction.
↑systolic/diastolic pressures
may cause reflex bradycardia

Detail:
CVS
- Increased SVR leading to increased SBP/DBP/MAP
- Increased afterload - leading to increased myocardial oxygen consumption, slight decrease in cardiac output and may lead to reflex bradycardia (through beta-1 effects limit this)
- Coronary artery vasodilation increased coronary O2 delivery
- Pulmonary vascular resistance is increased
- Excessive doses may lead to limb or organ ischaemia
- Extravasation may lead to tissue necrosis

CNS
- Generally improves cerebral blood flow by way of improved CPP more than it decreases CBF by cerebral vasoconstriction

Renal/GU
- Decreases renal blood flow
- Causes uterine constriction (may lead to fetal asphyxia)

GIT:
- Decreased splanchnic blood flow

Metabolic
- Less hyperglycaemia/acidosis, although it may decrease insulin secretion

composite of α and β actions.
Mostly β1 effect: ↑ ino+ chrono tropy and MVO2.
Mild β2 eff¬ects.

Detail:

CVS
- Beta1 effects lead to increased SA node activation (increased chronotropy), increased dromotropy and increased inotropy, thereby increasing cardiac output (inotropy greatest)
- Coronary artery vasodilator
- Beta-2 activity tends to decrease LVEDP and SVR, contributing to increased CO and cardiac index
- Increased MVO2
- Increased risk of arrhythmias (especially at doses >10mcg/kg/min)
- Should be avoided in patients with cardiac outflow obstruction (AS, tamponade)

Resp
- Modest pulmonary vasodilation
- Inhibits HPV

Renal- Increased RBF due to increased CO may occur

IV only
Clear Solution 1:1000
8-12 mcg/min uptitrated to effect
onset / duration immediate / 1-2 minutes

IV, dose starts at 5mcg/kg/min uptitrate to
e¬ffect, max 40mcg/kg/min

doesn’t cross the BBB

Small vd

0.2L/kg

Rapidly metabolised into adrenaline by MAO (Uptake 1, Nv terminal)
COMT (Uptake 2 circulation)

25% removed in the lungs

via COMT then gluruonidation hepatically

urine as inactive metabolites (84-96%)

urine as inactive metabolites

2 minutes

2 minutes

Excessive doses cause severe hypertension
Reduced flow to organs
splanchnic
renal
Issues with increased MVO2 and IHD

1. Arrhythmias (especially at doses >10mcg/kg/min)
2. Arrest in fixed output patients (AS, tamponade)
3. Increased MVO2
4. Eosinophilic myocarditis in prolonged infusion

ADRENERGIC

ADRENERGIC

Used to treat hypotension due to decreased SVR

1. Inotropic support in low cardiac output secondary to MI, cardiac surgery, cardiomyopathy
2. Cardiac stress testing

Is a naturally occurring catecholamine released in post ganglionic SNS, medulla (20:80 Adr)

synthetic catechol derivative of isoprenaline

Level 1

Level 3

Alpha and beta adrenergic receptor activity

the + enantiomer is a potent α1 antagonist
and β1 agonist, the -ve enantiomer has
opposite effects on α1 causing agonism and
is less potent (10%) β1 agonist.

injectable solution only, 1mg/mL in 2 mL vials diluted in 5D or NS.
CVC only due to risk of extravasation associated necrosis

Is a racemic mixture. White
powder for reconstitution(250mg) or Clear fluid 12.5mg/ml in 20ml vials.
Should not be
mixed with alkaline solutions (HCO3)

IV infusion- 0.05-0.5mcg/kg. Through a central line diluted with glucose or saline.

IV Infusion
Dose range 0.5-40mcg/kg/min. Response within 2 minutes