Cardiovascular Medications
PICU Resident Talk
Stanford School of Medicine
Pediatric Critical Care Medicine
June 2010
Objectives
After this lesson, the participant will be able to:
• Define inotropy, chronotropy, lusitropy, and
vasopressor.
• List the determinants of BP and CO.
• Describe the receptor/ mechanism of action
of epi, norepi, dopamine, dobutamine,
milrinone, phenylephrine, and nitroprusside.
• List the major side effects of these
medications.
Definitions
• Inotropy—the force of muscle contraction,
most commonly cardiac muscle contraction
• Chronotropy—affecting the heart rate
• Lusitropy—relaxation function of cardiac
muscle and chambers
• Vasopressor—producing a rise in blood
pressure through vasoconstriction
• Why do we use vasoactives/ionotropes?
To improve blood pressure
• Why do we want to improve blood pressure?
To improve oxygen delivery to tissues
• What determines blood pressure?
Where do
cardiovascular
medications work?
Adrenoreceptors
β1 receptors:
α1 receptors:
vasoconstriction
Chronotropy
Inotropy
Vascular Smooth
Muscle
β 2 receptors:
vasodilation
Heart
NO & PDE Inhibitors
PDE3 Inhibitor:
NO → guanalyl cyclase:
vasodilation
Chronotropy
Inotropy
Vascular Smooth
Muscle
PDE3 Inhibitor:
vasodilation
Heart
The meds to choose from….
Dose:
mcg/kg/min
Mechanism /Therapeutic Effects
Adverse Effects
Epinephrine
0.01- 1
β1  ↑ HR, ↑ inotropy
β2  vasodilatation
α1  vasoconstriction  ↑ SVR
Arrhythmia
↑myocardial O2 demand
Norepinephrine
0.01- 1
α1  vasoconstriction  ↑ SVR
β1  ↑ HR, ↑ inotropy
Min β 2 effects
Ischemic injury due to
potent vasoconstriction
↑ afterload
Dopamine
<5
D1 diuresis, natriuresis, renal vasodilatation,
(No proven benefit in preventing AKI or ↓ mortality)
Arrhythmia
↑myocardial O2 demand
5 -10
β1  ↑ HR, ↑ inotropy
>10
α1 effects  vasoconstriction  ↑ SVR
Dobutamine
5-20
β1  ↑ HR, ↑ inotropy
Mild β2, α1 antagonist  vasodilation  ↓ PVR, SVR
Milrinone
0.25 -1
Hypotension
Phosphodiesterase Inhibitor (PDE3 inhibitor):
Myocardial : ↑ cAMP  ↑contractility + ↑lusiotropy Arrhythmia
Vasculature: ↑ cAMP  vasodilatation  ↓ SVR/PVR
Phenylephrine
0.1-5
α1  vasoconstriction  ↑ SVR
Ischemic injury due to
potent vasoconstriction
↑ afterload
Nitroprusside
0.1-4
NO activates guanalyl cyclase (in vasc smooth muscle)
 ↑cGMP  vasodilation
Cyanide toxicity
↑ V/Q mismatch
Arrhythmia
↑myocardial O2 demand
Hypotension
Summary of Key Points
Dopamine
Dobutamine
Epinephrine
Dopamine
Dobutamine
Epinephrine
Norepinephrine
Milrinone
Decrease SVR
Low dose Epi,
Nitroprusside
Milrinone
Dobutamine
Increase SVR
High dose Epi
Norepinephrine
High dose Dopa (>10)
Phenylephrine