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Treatment depends on prompt diagnosis and an accurate appraisal of inciting conditions Initial management consists of basic life support with an assessment of the patient s airway, breathing, and circulation This may entail airway intubation and mechanical ventilation Ventilatory failure should be anticipated in patients with a severe metabolic acidosis in association with shock Mechanical ventilation along with sedation and paralysis can decrease the oxygen demand of the respiratory muscles and allow improved oxygen delivery to other hypoperfused tissues Intravenous access and fluid resuscitation should be instituted along with cardiac monitor-
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Volume replacement is critical in the initial management of shock Hemorrhagic shock is treated with immediate efforts to achieve hemostasis and rapid infusions of blood substitutes, such as type-specific or type O negative packed red blood cells (PRBC) or whole blood, which also provides extra volume and clotting factors Each unit of PRBC or whole blood is expected to raise the hematocrit by 3% Hypovolemic shock secondary to dehydration is managed with rapid boluses of isotonic crystalloid, usually in 1 liter increments Cardiogenic shock in the absence of fluid overload requires smaller fluid challenges usually in increments of 250 mL Septic shock usually requires large
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tors Amrinone or milrinone are phosphodiesterase inhibitors that can be substituted for dobutamine These drugs increase cyclic AMP levels and increase cardiac contractility, bypassing the -adrenergic receptor For vasodilatory shock when increased vasoconstriction is required to maintain an adequate perfusion pressure, -adrenergic agonists such as phenylephrine and norepinephrine are generally used Although norepinephrine is both an -adrenergic and -adrenergic agonist, it preferentially increases mean arterial pressure over cardiac output The initial dose is 05 1 mcg/min as an intravenous infusion, titrated to maintain the systolic blood pressure to at least 80 mm Hg The usual maintenance dose is 2 4 mcg/min (maximum dose is 30 mcg/min) Patients with refractory shock may require dosages of 8 30 mcg/ min Epinephrine, also with both -adrenergic and adrenergic effects, may be used in severe shock and during acute resuscitation Initially, give 1 mcg/min as a continuous intravenous infusion; the usual dosage range is 2 10 mcg/min IV Dopamine has variable effects according to dosage At low doses (2 3 mcg/kg/min) stimulation of dopaminergic and -agonist receptors produces increased glomerular filtration, heart rate, and contractility At higher doses (> 5 mcg/kg/min), -adrenergic effects predominate, resulting in peripheral vasoconstriction Recent studies have suggested some advantages to norepinephrine over dopamine at high doses Vasopressin (antidiuretic hormone or ADH) is gaining widespread acceptance in the treatment of distributive or vasodilatory shock Vasopressin causes peripheral vasoconstriction via V1 receptors located on smooth muscle cells and attenuation of nitric oxide (NO) synthesis and cGMP, the second messenger of NO The rationale for using low-dose vasopressin in the management of septic shock include the relative deficiency of vasopressin in late shock and the increased sensitivity of the systemic circulation to the vasopressor effects of vasopressin Vasopressin also potentiates the effects of catecholamines on the vasculature and stimulates cortisol production Several small clinical trials have demonstrated improvement in hemodynamic parameters and urinary output with vasopressin use but no clinical study has yet demonstrated improved survival Several studies have reported reduced catecholamine requirements with vasopressin administration At this time, it is unclear if vasopressin should be administered at a low fixed dose (001 004 units/min) or titrated according to blood pressure as with the use of conventional catecholamine vasopressors Higher doses of vasopressin decrease cardiac output and may put patients at greater risk for splanchnic and coronary artery ischemia Terlipressin is a synthetic long-acting analogue of vasopressin that increases blood pressure at the expense of cardiac index and oxygen consumption but may be an effective rescue therapy in patients with catecholamine resistant septic shock NO plays an important role in the vasodilatation associated with septic shock Endotoxin and inflammatory cytokines induce a calcium independent NO synthase that results in a sustained production of NO The NO pathway
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volumes of fluid for resuscitation as the associated capillary leak releases fluid to the extravascular space Meta-analyses of studies of critically ill heterogenous populations comparing crystalloid and colloid resuscitation (with albumin) indicate no benefit of colloid over crystalloid solutions, and some have suggested a trend toward increased mortality with albumin Clinical trials and meta-analyses have also found no difference in mortality between trauma patients receiving hypertonic saline (75%) and those receiving isotonic crystalloid More positive results were found with hypertonic saline plus dextran with an increase in survival over patients managed with isotonic saline, particularly in patients with traumatic brain injury Large-volume resuscitation with unwarmed fluids produces hypothermia, which must be treated to avoid hypothermia-induced coagulopathy
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