this presentation is toalking about the Sympathomimetic drugs which are agents which in general mimic responses due to stimulation of sympathetic nerves. These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing norepinephrine and epinephrine (mediators of the sympathoadrenal system) levels. These drugs are used clinically to treat glaucoma, anaphylactic shock, chronic obstructive pulmonary disease, hypotension, hypertension, heart failure, nasal congestion, premature labor, attention-deficit/hyperactivity disorder, narcolepsy, and acute or chronic asthma. The α or β adrenergic antagonists block or attenuate the effect of sympathomimetics on α or β receptors. Alpha blockers are used clinically to treat hypertension and benign prostatic hyperplasia. Beta blockers are used clinically to treat ischemic heart disease, essential hypertension, cardiac arrhythmias, congestive heart failure, glaucoma, hyperthyroidism, surgical removal of pheochromocytoma, nonparkinsonian tremor, migraine headache (prophylaxis), and a wide variety of anxiety situations.

1. Dr. Ahmed Abu-Draz
RH ICU consultant

2. 
Classification
Vasopressor and
Inotropes
Catecholamines
Non-
catecholamines

3. Catecholamines

4. 
Nervous system

5. 
Autonomic nervous system

6. 
Autonomic nervous system

7. 
Adrenergic receptors

8. 
Adrenergic receptors

10. 
 MAP = CO X SVR Vasopressors
CO = HR X SV
Preload contractility Afterload
Inotropic
Inotropes vs. vasopressors

12. C.V effects of
Vasopressors

13. 
 It is a potent α1-adrenergic receptor agonist with
modest β-agonist activity, lead to powerful
vasoconstrictor with less potent direct inotropic
properties.
 It mainly increase:
 Systolic.
 Diastolic
 Pulse pressure
 Coronary blood flow.
 It has minimal impact in the CO.
Noradrenaline

14. 
 It is a potent synthetic α-adrenergic activity and
virtually no affinity for β-adrenergic receptors.
 Used primarily as a rapid bolus for immediate
correction of sudden severe hypotension.
 It has virtually no direct heart rate effects, although it
has the potential to induce significant baroreceptor-
mediated reflex rate responses after rapid alterations
in MAP
Phenylephrine

15. C.V effects of
Inotropes

16. 
 It has high affinity for β1, β2, and α1-receptors
present in cardiac and vascular smooth muscle.
 β adrenergic effects are more pronounced at low
doses and α1-adrenergic effects at higher doses.
 Coronary blood flow is enhanced.
 Arterial and venous pulmonary pressures are
increased
Adrenaline

17. 
 A synthetic catecholamine with a strong affinity for
both β1- and β2-receptors (ratio 3:1).
 It has potent inotrope with weaker chronotropic
activity.
 At a dose up to 15mcg/kg/min, it has mild
vasodilation effect.
 Vasoconstriction progressively dominates at higher
infusion rates.
 It significantly increases myocardial oxygen
consumption.
Dobutamine

18. 
 It is a potent, nonselective, synthetic β-adrenergic
agonist with very low affinity for α-adrenergic
receptors.
 It has powerful chronotropic and inotropic effects.
 It has potent systemic and mild pulmonary
vasodilator effects.
 It has a net neutral impact on CO.
Isoproterenol

19. 
 an endogenous central neurotransmitter.
 It is the immediate precursor to norepinephrine in
the catecholamine synthetic pathway.
 It acts on dopaminergic and adrenergic receptors.
 At low dose (< 3mcg/kg/min), It stimulate the
dopaminergic D1 and D2 receptors in the cerebral,
renal, mesenteric and vasculature tissues leading to
vasodilation and increased blood flow to these
tissues.
Dopamine

20. 
 At intermediate doses (3-10 mcg/kg/min), it weakly
binds to β1-adrenergic receptors leading to increased
cardiac contractility and chronotropy, with a mild
increase in SVR.
 At higher doses (10 to 20 mcg/kg/min), stimulate
α1-adrenergic receptor leading to vasoconstriction.
Dopamine

22. Non
Catecholamines

23. 
Phosphodiesterase Inhibitors

24. 
 PDIs are potent inotropes and vasodilators.
 PDI improve diastolic relaxation.
 PDI reduce:
 Preload.
 Afterload.
 SVR.
 Milrinone is the most commonly used PDI
Phosphodiesterase Inhibitors

25. 
 The nonapeptide vasopressin (antidiuretic hormone) is
primarily stored in the posterior pituitary gland.
 It exerts its circulatory effects through V1and V2
receptors.
 V1a stimulation mediates constriction of vascular
smooth muscle.
 Vasopressin cause increase :
 SVR.
 Vagal tone.
 Vascular sensitivity to norepinephrine further augments
its pressor effects.
Vasopressin

26. 
 It has a neutral or inhibitory impact on CO.
 The pressor effects of vasopressin are relatively
preserved during hypoxic and acidotic conditions,
which commonly develop during shock of any
origin.
Vasopressin

27. 
 CSA are a recently developed class of inotropic
agents.
 The most common CSA is levosimendan.
 These agents have a dual mechanism of action:
 Calcium sensitization of contractile proteins.
 The opening of ATP-dependent potassium channels.
 CSA cause:
 Increase cardiac contractility (inotropic effect).
 Reduce the SVR (vasodilation effect).
Calcium-Sensitizing Agents

28. Vasopressor and
inotropes usage
in shock

29. 
 Shock is characterized by inadequate tissue perfusion,
resulting in life-threatening impairment of oxygen and
nutrient delivery.
 Types of shock:
 Septic Shock.
 Cardiogenic Shock.
 Hemorrhagic Shock.
 Neurogenic Shock.
 Vasopressors should only be initiated with/after adequate
resuscitation is provided with crystalloids, colloids, and or
blood products.
Shock

30. 
 Low-dose dopamine should not be used for renal
protective effects.
 Norepinephrine is the first line agent when vasopressors
are indicated.
 Epinephrine, phenylephrine and vasopressin should not
be used as first line agents.
 If hypotension persists despite the use of norepinephrine,
vasopressin or epinephrine should be added to current
vasopressor therapy.
Septic Shock

31. 
 Dobutamine may be initiated in combination with
norepinephrine in patients with myocardial
dysfunction.
 Dopamine can be used as an alternative vasopressor
agent to norepinephrine only in highly selected
patients.
Septic Shock

32. 
 Vasopressors and/or inotropes may be initiated
earlier in cardiogenic shock with clinical evidence of
volume overload.
 In low output cardiogenic shock, dobutamine may
be initiated in combination with norepinephrine.
 Milrinone/levosimendan can be used as alternative
to dobutamine in specific occasion.
Cardiogenic Shock

33. 
 Vasopressors/inotropes are not recommended in the
initial stabilization of hemorrhagic shock.
 Permissive hypotension may be employed until
bleeding is controlled in patients requiring emergent
surgical intervention.
 If hypotension persists despite adequate blood and
fluid resuscitation and surgical intervention, consider
other etiologies for shock and an appropriate
vasopressor.
Hemorrhagic Shock.

34. 
 Due to the physiologic nature of neurogenic shock,
vasopressors may be initiated earlier to avoid
volume overload.
 Norepinephrine should be first line agent once
vasopressors are indicated.
 Phenylephrine should be avoided in most patients
due to unopposed alpha activity that can result in
reflex bradycardia.
Neurogenic Shock

35. 
 The American College of Cardiology/American
Heart Association guidelines for management of
hypotension complicating AMI suggest:
 the use of dobutamine as a first-line agent if systolic
blood pressure ranges between 70 and 100 mm Hg in
the absence of signs and symptoms of shock.
 Dopamine is suggested in patients who have the same
systolic blood pressure in the presence of symptoms of
shock
Cardiogenic Shock Complicating Acute
Myocardial Infarction

36. 
 The deliberate combination of dopamine and
dobutamine at a dose of 7.5 mcg/kg/min of each
was shown to improve hemodynamics and limit
important side effects compared with either
individual agent administered at 15 mcg/kg/min.
 When response to a medium dose of dopamine or
dopamine/ dobutamine in combination is
inadequate, or the patient’s presenting systolic blood
pressure is 70 mm Hg, the use of norepinephrine has
been recommended.
Cardiogenic Shock Complicating Acute
Myocardial Infarction