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

Via selective PDE3 inhibition which causes
decreased cAMP breakdown intracellularly
and hence increased Ca

This improves myocardial contractility and improves cAMP-dependent protein phosphorylation leading to vascular smooth muscle relaxation.

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
- Positive inotrope, leading to increased cardiac output. CI increases 30%
- PCWP decreases 20%, with improved lusotropy
- SVR and MAP decrease
- May increase AV nodal conductance, accelerating arrhythmias in atrial fibrillation or flutter

Resp: Decreased PVR

GU: UO and GFR may increase in response to increased CO

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

IV only

Small vd

small vd

0.2L/kg

0.4 L/kg

via COMT then gluruonidation hepatically

minimally hepatic

urine as inactive metabolites

excretion is in the urine, mostly as
unchanged drug, dose adjustment
in renal failure

2 minutes

2 hours

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

may be proarrhythmogenic causing SVT and
VT. Have been shown to worsen outcomes
in acute on chronic heart failure

ADRENERGIC

NON-ADRENERGIC

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

used in severe refractory heart failure and
for short periods post cardiac surgery

synthetic catechol derivative of isoprenaline

selective phosphodiesterase inhibitor

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.

PDEIII Inhibition: Improves myocardial contractility, 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)

is a yellow solution, stored at room temperature, should not be given with HCO3 or frusemide

pKA of 9.67 and pH of 6.35

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

IV
50mcg/kg loading dose over 10min (optional)
0.375mcg/kg/min-0.75mcg/kg/min