This document provides an overview of inotropes and vasoactive drugs, explaining how they work to increase cardiac output by enhancing contractility, heart rate, preload, and manipulating vascular resistance through their effects on adrenergic receptors and other mechanisms. It discusses various drugs like adrenaline, noradrenaline, dobutamine, vasopressin, GTN, and others, explaining their receptor targets, clinical applications, and nursing considerations for safe administration. The goal is to help nurses better understand these important hemodynamic medications and feel more confident in their use.

1. Uppers, Downers and
Squeezers
INOTROPES AND VASOACTIVE DRUGS

2. Aim and Objective
 Functional overview of how inotropes and vasoactive
drugs work.
 Explore nursing considerations.
 Discuss case examples.
 Hopefully end up feeling more confident.

3. It’s all about the Oxygen
 For tissues to be oxygenated, 3 factors need
to be considered:
 1) Oxygen transfer across the alveolar-capillary
membrane
 2) Oxygen attachment to haemaglobin
 3) Adequate cardiac output (CO) to move the
oxyhaemaglobin compound to the tissues – this is
what we are talking about!

4. Two Limbs to Oxygenation

5. To increase CO we can…
1) Enhance circulating volume through fluid
resuscitation (increasing preload)
2) Enhancing myocardial contractility with inotropes
(their inotropic effect)
3) Manipulating heart rate with inotropes (their
chronotropic effect)

6. Remember
Cardiac output (CO) =
Heart Rate (HR) x Stroke Volume (SV)

7. Measuring Cardiac Output
 How do we commonly evaluate?
 How complex is this?

8. Blood Pressure
BP = CO x Total Peripheral Resistance
Simple enough right???

9. Remember this?

10. Stroke Volume
 Complex beast affected by preload, afterload and
contractility.
 Confused???

11. How does this stay balanced?
Parasympathetic down regulates and Sympathetic up regulates.

12. A&P

13. It’s all about the Receptors
Table 1. Adrenergic receptor sites (SNS)
Receptor Actions Locations
α ↑SVR Coronary arterioles
↑Blood pressure Vascular smooth muscle
↓Insulin release
β1 ↑Heart rate Sinoatrial node
↑Contractility Myocardium
β2 ↑Contractility Coronary arterioles
↓SVR Bronchial smooth muscle
Atrioventricular node
Vascular smooth muscle
DA Vasodilation Kidney
Mesentery
Heart
SVR =systemic vascular resistance. DA = Dopaminegic

14. Important terms – Agonist

15. Important terms - Antagonist

16. Important terms – Partial Agonist

17. Ok take a breather!

18. How do we treat this stuff?
http://www.youtube.com/watch?v=HMGIbOGu8q0

19. Let’s talk drugs!
In the context of the SNS, drugs:
Mimic or impair (stimulate or block)
 Directly (agonist or antagonist)
 Indirectly
- releasing endogenous Norad (metaraminol,
ephedrine at a1)

20. Let’s talk drugs!
In the context of the PNS,
drugs work on:
 Nicotinic and
muscarinic receptors
with Ach as
neurotransmitter
 M2 heart

21. Atropine - PNS
 Anticholinergic drug – works as a competitive
antagonist in muscarinic receptors (M2 = Heart)
 Blocks slow – down signals to the heart.

22. Adrenaline - SNS
 Non-selective b and
a agonist
 +inotrope and
chronotrope
 Vasodilates at low
dose, constricts at
high dose
 Bronchial smooth
muscle relaxant
 Use in asthma?

23. Noradrenaline - SNS
 Acts predominantly on
alpha-receptors and beta-
receptors in the heart.
 Causes peripheral
vasoconstriction (alpha-
adrenergic action) and a
positive inotropic effect on
the heart and dilatation of
coronary arteries (beta-
adrenergic action).
 Why is it important to
assess adequate fluid
loading?

24. Dobutamine - SNS
 Direct acting inotropic whose primary
activity results from stimulation of the
beta-receptors of the heart while
producing comparatively mild
chronotropic, hypertensive,
arrhythmogenic and vasodilative effects.
 It does not cause the release of
endogenous noradrenaline as does
dopamine
 Used for heart failure for the above
reasons
 250mg vials

25. Vasopressin (ADH)
 increase resorption of water by the renal
tubules
 Cause contraction of smooth muscle of the
gastrointestinal tract and of all parts of the
vascular bed, especially the capillaries,
small arterioles and venules, with less
effect on the smooth musculature of the
large veins.
 20IU/ml

26. Metaraminol - SNS
 Increases both systolic and diastolic blood
pressure.
 The pressor effect begins one to two
minutes after intravenous injection, and
lasts about 20 minutes to one hour.
 Positive inotropic effect on the heart and
has a peripheral vasoconstrictor action.
 Potent sympathomimetic – alpha agonist
effects, mild beta 1 effects.

27. Ephedrine – SNS
Stimulates both alpha and beta-adrenergic
receptors indirectly and also releases endogenous
noradrenaline from its storage site (particularly
observed in the substantia nigra).
Often used in OT due to strong direct evidence
base lying in anaesthetic hypotension.

28. Phenylephrine - SNS
Used mostly in OT
Produces vasoconstriction that lasts longer than that of
adrenaline and ephedrine.
Responses are more sustained than those to adrenaline,
lasting 20 minutes after intravenous and as long as 50
minutes after subcutaneous injection.
Its action on the heart opposite to adrenaline and
ephedrine, in that it slows the heart rate and increases
the stroke output, producing no disturbance in the
rhythm
Powerful postsynaptic alpha-receptor stimulant with
little effect on the beta-receptors of the heart.
A singular advantage of this drug is the fact that repeated
injections produce comparable effects.

29. GTN – Direct Vasoactive
 Glyceryl trinitrate produces a dose related
dilation of both arterial and venous beds.
 Decreases venous return to the heart,
reducing left ventricular end diastolic
pressure and pulmonary capillary wedge
pressure (preload).
 Arteriolar relaxation reduces systemic
vascular resistance and arterial pressure
(afterload).
 Also dilates the coronary arteries, although
this effect is short-lived.

30. These are also out there
 Some less frequently used drugs

31. Dopamine - SNS
 Stimulates alpha, beta and dopamine receptors.
 Precursor to noradrenaline chemically
 At infusion rates of 0.5 to 2 microgram/kg/minute,
dopamine receptors are selectively activated and blood
pressure either does not change or decreases slightly.
 Causes renal and mesenteric vasodilatation - Renal plasma
flow, glomerular filtration rate and sodium excretion usually
increase.
 At infusion rates of 2 to 10 microgram/kg/minute, beta1-
receptors are activated and cardiac output and systolic
blood pressure increase.
 The total peripheral resistance is relatively unchanged
because of peripheral vasoconstriction (alpha effect) and
muscle vasodilatation (beta effect).
 At infusion rates above 10 microgram/kg/minute, alpha-
receptors are activated, causing vasoconstriction, and both
systolic and diastolic pressures increase
 200mg Ampoules

32. Isoprenaline
Acts on the heart, smooth muscle of bronchi,
skeletal muscle vasculature and gastrointestinal
tract.
Increases cardiac output due to its positive
inotropic and chronotropic actions and by
increasing venous return.
Also lowers peripheral vascular resistance.
The rate of discharge of cardiac pacemakers is
increased.
Great option in complete heart block.

33. Milrinone
Selective phosphodiesterase inhibitor which has
positive inotropic and vasodilatory activity.
Milrinone improves hemodynamics and
biventricular function in patients with
ventricular dysfunction by increasing stroke
volume index, increasing left ventricular
contractility, producing pulmonary vasodilation.
Used in heart failure due to minimal
chronotropic effect

34. Sodium Nitroprusside (SNP) – Direct Vasoactive
Potent relaxation of vascular smooth muscle and
consequent dilatation of peripheral arteries and
veins.
Non-selective compared to GTN .

35. Levosimendan
Developed for the treatment of decompensated heart
failure and is used intravenously when patients with
heart failure require immediate initiation of drug
therapy.
It increases the sensitivity of the heart to calcium, thus
increasing cardiac contractility without a rise in
intracellular calcium.
Exerts its effect by increasing calcium sensitivity of
myocytes by binding to cardiac troponin C in a calcium-
dependent manner.
It also has a vasodilatory effect, by opening adenosine
triphosphate (ATP)-sensitive potassium channels in
vascular smooth muscle to cause smooth muscle
relaxation.

36. Ok…….
 Inotropic drugs are potentially dangerous so
be very thorough checking.
 Vascular access needs to be spot on.
 On central line always endeavour to use
distal, brown lumen (in furthest)
 Wear gloves when preparing.
 Know what the drug does and why we use
it.
 Don’t EVER make a mistake with
inotropes!!!