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Vasopressors raise blood pressure mainly by constricting arterioles (raising systemic vascular resistance). Inotropes raise cardiac output by making the heart contract more forcefully. Many drugs do both, and the balance changes with dose. Perfusion pressure is judged by mean arterial pressure (MAP); most adults with shock are started at a target of MAP 65 mmHg.
| Receptor | Location | Effect when stimulated |
|---|---|---|
| Alpha-1 | Vascular smooth muscle | Vasoconstriction → ↑SVR, ↑BP |
| Beta-1 | Heart | ↑Contractility, ↑heart rate, ↑conduction (more oxygen demand, more dysrhythmias) |
| Beta-2 | Bronchi, skeletal muscle vessels | Bronchodilation, vasodilation; also raises glucose and lactate, shifts potassium into cells |
| Dopamine-1 | Renal and mesenteric vessels | Vasodilation (no proven kidney protection) |
| Vasopressin V1 | Vascular smooth muscle | Vasoconstriction by a non-adrenergic pathway — still works when acidosis blunts catecholamines |
Vasopressors support pressure while the cause is treated. They do not replace volume, source control, bleeding control, or revascularization.
| Drug (generic) | Main receptor action | Key use | Key point |
|---|---|---|---|
| Norepinephrine (noradrenaline) — prototype vasopressor | Alpha-1 > beta-1 | First-line in septic shock; cardiogenic shock with hypotension; neurogenic shock | Titrated in mcg/min or mcg/kg/min to MAP |
| Vasopressin | V1 | Added to norepinephrine in septic shock rather than escalating norepinephrine further | Fixed low dose (commonly 0.03 units/min), often added when norepinephrine reaches about 0.25–0.5 mcg/kg/min |
| Epinephrine (adrenaline) | Beta at low dose; alpha rises with dose | Anaphylaxis (IM first; IV infusion if refractory); added in septic shock when MAP is still inadequate on norepinephrine plus vasopressin; cardiac arrest; bradycardia | Raises glucose and lactate — a rising lactate on epinephrine may not mean worse perfusion |
| Phenylephrine | Pure alpha-1 | Short-term hypotension (e.g., during anesthesia); when tachydysrhythmias limit other drugs | Reflex bradycardia; can lower cardiac output |
| Dopamine | Dose-dependent D1 → beta-1 → alpha-1 | Selected bradycardia; not first-line in shock | More dysrhythmias than norepinephrine; "renal-dose" dopamine does not protect the kidneys |
| Angiotensin II | AT1 receptor | Refractory vasodilatory shock | Thrombosis — needs VTE prophylaxis |
| Dobutamine — prototype inotrope | Beta-1 | Low cardiac output with poor perfusion (cardiogenic shock, acute decompensated HF, septic shock with cardiac dysfunction) | Commonly 2–20 mcg/kg/min; tachycardia, may drop BP |
| Milrinone | PDE-3 inhibition | Low-output HF, including clients on beta blockers | Hypotension; accumulates in kidney failure (dose reduction) |
| Drug | Key adverse effects |
|---|---|
| All alpha-agonists (norepinephrine, epinephrine, phenylephrine, dopamine) | Tissue ischemia (fingers, toes, gut, kidneys), extravasation necrosis, hypertension, reflex bradycardia (phenylephrine), headache |
| Beta-agonist activity (epinephrine, dopamine, dobutamine) | Tachycardia, dysrhythmias, myocardial ischemia, anxiety, tremor; epinephrine → hyperglycemia, high lactate, hypokalemia |
| Vasopressin | Digital, skin, and mesenteric ischemia; decreased cardiac output; hyponatremia is possible |
| Dobutamine | Tachycardia, ventricular ectopy, hypotension, angina; rarely hypersensitivity (eosinophilic) myocarditis with prolonged use |
| Milrinone | Hypotension, ventricular dysrhythmias, thrombocytopenia, headache |
| Angiotensin II | Arterial and venous thrombosis |
Dopamine (and older norepinephrine) labels carry a boxed warning on extravasation, naming phentolamine as the antidote; current norepinephrine labels keep this as a warning. Adrenergic IV infusions are high-alert medications.
Listed in priority order.
Most clients are critically ill; teach the client if awake, and the family:
| Problem | Findings | Action |
|---|---|---|
| Excess dose (programming or concentration error) | Severe hypertension, headache, tachydysrhythmias, chest pain, pulmonary edema | Stop or reduce infusion; catecholamines have half-lives of about 2 minutes, so effects fade quickly; notify provider |
| Extravasation of an alpha-agonist | Blanching, cold, hard, painful skin → necrosis | Stop, phentolamine infiltrated per protocol (within 12 hours is the usual label window), elevate, document |
| Vasopressin extravasation | Ischemia | Phentolamine is not a specific antidote (non-alpha drug); stop and follow protocol |
| Digital or mesenteric ischemia | Dusky digits, abdominal pain, rising lactate | Report; reassess MAP target and doses |
| Milrinone excess | Prolonged hypotension (half-life about 2–3 hours, longer in kidney failure) | Stop infusion, supportive care, vasopressor if needed |
| Dobutamine-induced dysrhythmia | Tachycardia, ventricular ectopy | Reduce or stop; short half-life |
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