What to expect:
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Describe the receptors involved in vascular tone control.
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List the effects of common pressors on systemic vascular resistance (SVR) and cardiac output (CO).
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Choose appropriate pressors in hypotension and shock.
Control of Vascular Tone
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Vasoconstrictors: Epinephrine, norepinephrine, angiotensin II, vasopressin (ADH), sympathetic norepinephrine, endothelin.
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Vasodilators: ANP, BNP, bradykinin, histamine, nitric oxide, adenosine.
Catecholamines
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Endogenous: Dopamine → Norepinephrine → Epinephrine (biosynthetic chain from phenylalanine).
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Synthetic: Dobutamine, phenylephrine (not true catecholamine), isoproterenol.
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Structural differences → different hemodynamic effects.
Receptor Actions
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α1: Vasoconstriction → ↑ SVR.
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β1: Inotropy (↑ contractility) & chronotropy (↑ HR) → ↑ CO.
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β2: Vasodilation → ↓ SVR.
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(α2, β3 not clinically relevant here).
Key Catecholamines
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Norepinephrine: Strong α1, minor β1, no β2 → ↑ SVR, mild ↑ CO.
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Epinephrine: Strong β1, β2; minor α1 → ↑ CO, vasodilation at low doses; at high doses α1 dominates → ↑ BP.
Dose-Dependent Effects
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Receptor selectivity changes with dose (e.g., epinephrine, dopamine).
Classification of Pressors
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Vasopressors (↑ SVR): Phenylephrine.
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Inotropes (↑ CO): Dobutamine, milrinone (PDE inhibitor).
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Both: Norepinephrine, epinephrine, dopamine.
Clinical Use by Shock Type
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Septic shock:
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1st line → Norepinephrine.
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Alternative → Phenylephrine (only if arrhythmias, high CO, or other agents fail).
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Refractory → Add vasopressin or epinephrine.
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Cardiogenic shock:
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Traditional → Dobutamine ± dopamine.
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Alternative → Norepinephrine ± dobutamine (controversial, post-SOAP II trial).
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Hypovolemic shock:
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Primary → IV fluids (pressors not routine).
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Pressors only if collapse imminent while fluids infusing.
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Mixed/uncertain shock:
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Norepinephrine often chosen; sometimes epinephrine or dopamine.
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Special Notes
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Phenylephrine caution: Pure vasoconstrictor; avoid if myocardial dysfunction suspected.
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SOAP II Trial (1700 pts, dopamine vs norepi):
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No overall mortality difference.
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Cardiogenic subgroup → norepi seemed better (less arrhythmia risk).
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Flawed design (high dopamine dose, mixed use of dobutamine).
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Bottom line: Trial shouldn’t change cardiogenic shock management.
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Evidence Summary
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No clear mortality benefit of one pressor over another.
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Choice depends on:
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Clinical scenario (shock type).
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Physician experience.
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Side effects, drug interactions.
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Availability & cost.
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Key Takeaway:
Pressors are selected based on underlying shock physiology. Norepinephrine is the most widely used first-line agent, but no single drug has proven mortality.
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