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

i) ↑myofilament Ca sensitivity by binding to Cardiac trop C in Ca-dependent manner.
ii) Vasodilation through opening of ATP-sensitive K channels
iii) selective PDE-III inhibition at higher conc - inotropy

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

CVS:
- Increased cardiac output without increasing MVO2
- Causes coronary and peripheral vasodilation → anti-ischaemia and anti-stunning effects

GU:
Increased GFR and UO secondary to increased CO

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

IV only

Small vd

small vd

98% protein binding.
Peak concentration after 48 hrs

0.2L/kg

0.2 L/kg

via COMT then gluruonidation hepatically

Intestinal bacteria OR1896 active metabolite

Hepatic conjugation

urine as inactive metabolites

excretion renal and fecal. Cardiac Effects 2-7 days

2 minutes

1 hour (70hr for active metabolite)

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

Interference with potassium channels causes an increase in the QTc- theoretical ↑risk of arrhythmias. May cause hypotension. Caution should be exercised in
patients with renal or hepatic impairment.

ADRENERGIC

NON-ADRENERGIC

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

short term management of severe acute heart failure

synthetic catechol derivative of isoprenaline

Ca sensitizer and PDE-III inhibitor
selectively

Level 3

Level 3

Level 1

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.

Increases Myofilament Ca sensitivity, vasodilation

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)

in IV form only - clear yellow solution 2.5mg/mL in 5 and 10ml vials

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

IV, loading dose of 6 to 24 mcg/kg over 10 minutes
then continuous infusion of 0.05-0.2 mcg/kg/min