Mount Sinai Expert Guides. Группа авторов
Selecting vasoactive therapy
It is critical to understand the physiology of the shock that you are treating, and the receptor targets for each vasoactive medication, so that you can tailor therapy to the particular clinical situation.
Low preload (LVEDP)
In distributive, obstructive, or hypovolemic shock, proper fluid resuscitation is critical to improving blood pressure, cardiac output, and end‐organ perfusion. Monitoring of hemodynamic parameters and filling pressures can be helpful in this setting.
In mixed shock states, invasive hemodynamic monitoring can be useful in determining the predominant mechanism of shock and to customize therapy to the physiology of the patient.
Receptors affected by vasoactive medications
Vasoactive medications often work as agonists or antagonists of adrenergic or parasympathetic receptors. These selected receptors represent the principal targets for vasoactive therapy in the intensive care setting (Table 12.2).
Key principles of vasoactive medication use
Diagnose and understand mechanism causing hypotension:
Physical examination, urine output, laboratory testing, imaging, and invasive hemodynamic monitoring can be important tools to differentiate the nature of the patient’s shock.
Dosage and selection of medication should be titrated to achieve a blood pressure sufficient to maintain end‐organ perfusion, as evidenced by metrics such as mentation, urine output, and blood lactate levels.
Critically ill patients also require frequent re‐evaluation for further hemodynamic insults, response to therapy, or side effects that may require changes in therapeutic strategy.Table 12.2 Action of vasoactive medications.ReceptorLocationActionα‐1 adrenergicVascular smooth muscle (peripheral, renal, coronary)Systemic vasoconstriction – increased SVRα‐2 adrenergicVascular smooth muscle and central nervous systemVasodilation – decreased SVR Sedationβ‐1 adrenergicCardiac muscleIncreased heart rate (chronotropy) and contractility (inotropy) Increased cardiac output Minimal vasoconstrictionβ‐2 adrenergicVascular smooth muscle (peripheral and renal)Vasodilation Reduced SVRDopamine (D1)Vascular smooth muscle (peripheral, renal, splanchnic, coronary, cerebral)Vasodilation in capillary bedsAcetylcholine (ACh)Parasympathetic nervous system (heart, sinoatrial and atrioventricular nodes, GI tract, eyes)Has chronotropic effects on heart Atropine is an antagonist of muscarinic ACh receptors Atropine can stimulate or accelerate AV node conductionPhosphodiesterase 3 (PDE‐3)Cardiac muscle and vascular smooth muscleIncreased contractility (inotropy) and improves diastolic relaxation (lusitropy) VasodilationVasopressin (V1, V2)Vascular smooth muscle and renal collecting ductV1 – stimulation causes vasoconstriction V2 – mediate water reabsorption in renal collecting system
Tailor vasoactive