through ↑TPR
May be transient bradycardia due to baroreceptor feedback upon infusion initiation.
↑Pulmonary vascular resistance. ↑coronary artery flow by an indirect mechanism (stimulates NA release)

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

CVS:
- Increased SVR leading to an increase in diastolic and systolic BP
- Reflex bradycardia may occur despite B1 effects
- It has positive inotropic effects but cardiac output is more likely to decrease as a result of increased afterload
- Coronary artery blood flow increases as an indirect mechanism
- Increased PVR

CNS:
- Doesn’t cross BBB
- Causes cerebral vasoconstriction but increases CPP

Renal/GU
- Renal vasoconstriction but re-established renal perfusion pressure in hypotension
- Uterine contraction and reduces uterine blood flow

Metabolic
- Inhibits insulin release and increases lipolysis
- May increase VO2

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

IV. BA 100%
0.1-0.2mg boluses titrated to BP
onset / dur imm / up to 20 mins

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

limited data on pharmacokinetics

doesn’t cross the BBB

Hepatic

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

25% removed in the lungs

Unknown

urine as inactive metabolites (84-96%)

short

2 minutes

Caution should be exercised in patients with pulmonary hypertension. May cause
severe hypertension in some patients

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

ADRENERGIC

ADRENERGIC

short term correction of BP in the setting of regional anaesthesia and off label for short term BP correction

Used to treat hypotension due to decreased SVR

synthetic noncatecholamine with both direct and indirect
sympathomimetic actions.

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

Level 2

Level 1

both direct and indirect
sympathomimetic actions. It acts mainly via alpha1/2 adrenoceptors to cause
vasoconstriction but also has some minor beta activity.

Alpha and beta adrenergic receptor activity

clear solution 10mg/mL in one mL vials and usually diluted to
10mg in 10ml or 20ml

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

IV boluses or infusion

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