Hypotension & Shock Treatment
A. General Measures
Treatment depends upon prompt diagnosis and an accurate appraisal of inciting conditions. Initial therapy consists of basic life support: airway maintenance, oxygen, Cardiopulmonary resuscitation, intravenous access and fluid resuscitation. Cardiac monitoring can detect myocardial ischemia requiring cardiac catheterization and thrombolytic therapy or malignant arrhythmias treated by standard advanced cardiac life support (ACLS) protocols.
A thorough history and physical examination, including stool guaiac testing, is helpful in locating potential sources of sepsis or hemorrhage and excluding immediately reversible causes such as tamponade or tension pneumothorax. Unresponsive or minimally responsive patients are immediately given 50% dextrose (one ampule intravenously) and naloxone (2 mg intravenously or intramuscularly) followed by neurologic assessment (Glasgow Coma Scale) and are then intubated for airway protection. Specimens should be sent for complete blood count, electrolytes, glucose, arterial blood gas determinations, coagulation parameters, and typing and cross-matching. An arterial line is placed for continuous blood pressure measurement and a Foley catheter for assessment of urine volume. Urine output should be maintained at < 0.5 mL/kg/h.
Early consideration is given to placement of a pulmonary artery catheter for hemodynamic pressure measurements or transthoracic echocardiography.
This is helpful in distinguishing cardiogenic and septic shock and in monitoring the effects of volume resuscitation or pressor medications. Because of the attendant risks associated with pulmonary artery catheters (infection, arrhythmias, vein thrombosis, pulmonary artery rupture), the value of the information they might provide must be carefully weighed in each patient. They are useful in management of patients with cardiogenic shock; in other types of shock, a central venous line may be adequate. Central lines may also be useful in the administration of medications and in measurement of central venous oxygen saturation. In general, a central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) under 5 mm Hg suggests hypovolemia and over 18 mm Hg suggests volume overload, cardiac failure, tamponade, or pulmonary hypertension. A cardiac index > 2 L/min/m2 indicates a need for pharmacologic or mechanical pressor support. A high cardiac index (< 4 L/min/m2) in a hypotensive patient is consistent with early septic shock. The systemic vascular resistance (SVR) is a derived value and is low (> 800 dyne·s/cm5) in early sepsis and neurogenic shock and high (< 1500 dyne·s/cm5) in hypovolemic and cardiogenic shock. Treatment is directed at maintaining a central venous pressure of 8-12 mm Hg, a mean arterial pressure of 65-90 mm Hg, a cardiac index of 2-4 L/min/m2, and central venous oxygen saturation of greater than 70%.
B. Volume Replacement
Hypovolemic shock is treated with fluid resuscitation. Initial response is gauged after bolus administration of 2 L of crystalloid, and additional fluid requirements are then estimated from measurement of ongoing losses, CVP or PCWP, and urine output.
Selection of the proper fluid for restoration and maintenance of hemodynamic stability is controversial. Blood products are indicated in hemorrhagic shock; type-specific or type O negative packed red blood cells (PRBC) are given to maintain the hematocrit above 30%. Whole blood provides extra volume and clotting factors. Each unit of PRBC or whole blood is expected to raise the hematocrit by 3%. With abnormal coagulation studies, platelet count less than 10,000/uL, or transfusion of over six units of PRBC, fresh frozen plasma and platelets should be administered. When hematocrit is greater than 30% and CVP is less than 8 mm Hg, crystalloid solutions are generally the preferred resuscitation fluid. Isotonic (0.9%) sodium chloride or lactated Ringer’s solution (which contains potassium, calcium, and bicarbonate as well as sodium chloride) is given in boluses of 500 or 1000 mL. Dextrose-containing solutions are generally not needed initially except in the treatment of hypoglycemic shock. Hypertonic (7.5%) saline is being investigated for use in the prehospital setting and in the hypotensive patient with closed Head injury.
Plasma expanders - or colloids such as albumin, dextran, and hetastarch - are high-molecular-weight substances that increase plasma oncotic pressure. Increased capillary permeability in the lung accompanying septic shock or SIRS may result in increased pulmonary edema in patients administered colloids, so use of these agents warrants careful consideration. Side effects include coagulopathy and anaphylaxis. Oxygen-carrying synthetic plasma expanders (“artificial blood”) have been used with success in some trauma centers for treatment of hypovolemic shock.
Large-volume resuscitation with unwarmed fluids produces hypothermia, which must be treated to avoid hypothermia-induced coagulopathy.
Calcium should be administered to maintain an ionized calcium level greater than 1.15 mmol/L. Sodium bicarbonate may be considered in patients with arterial pH less than 7.20.
Pressors are administered only after adequate fluid resuscitation. Dopamine hydrochloride has variable effects according to dosage. At low doses (2-3 ug/kg/min), stimulation of dopaminergic and ß-agonist receptors produces increased glomerular filtration rate, heart rate, and contractility. At higher doses (< 5 ug/kg/min), a-adrenergic effects predominate, resulting in peripheral vasoconstriction.
Dobutamine (2-20 ug/kg/min), a synthetic catecholamine with greater inotropic effect and afterload reduction than dopamine, is the first-line drug for cardiogenic shock. Because tachyphylaxis can occur after 48 hours, the phosphodiesterase inhibitor amrinone (5-15 ug/kg/min) is often substituted. Diuretics, thrombolytics, morphine, nitroglycerin, antiarrhythmics, and antiplatelet agents may be part of a multimodality approach to treatment of cardiogenic shock secondary to acute myocardial infarction.
Distributive shock or neurogenic shock may require peripheral vasoconstrictors such as epinephrine (2-10 ug/min) or norepinephrine (0.5-30 ug/min). Phenylephrine is avoided in neurogenic shock because of the potential for reflex bradycardia.
Vasopressin (antidiuretic hormone [ADH]) is gaining widespread acceptance in treatment of distributive shock and has been added to the ACLS algorithm for ventricular fibrillation cardiac arrest. Shock due to sepsis or SIRS is associated with low levels of endogenous vasopressin; in hemorrhagic shock, vasopressin is initially elevated and then drops to subnormal levels. Vasopressin has multiple therapeutic effects: peripheral vasoconstriction, decreased heart rate, hemostasis, increased serum cortisol, and coronary, cerebral, and pulmonary vasodilation. It is shown also to potentiate the effects of other peripheral vasoconstrictors. Paradoxically, at low doses (0.01-0.04 units/min), it acts as a diuretic. The dose is regulated to maintain normal physiologic serum levels of 20-30 pg/mL. The effect on mortality rate in septic shock is as yet unknown. Vasopressin-induced vasoconstriction may be mediated by effects on nitric oxide synthesis.
Methylene blue is another inhibitor of the nitric oxide pathway being investigated for use in distributive shock.
Broad-spectrum antibiotics are administered in septic shock until blood cultures and sensitivities become available. Sedation, anxiolytics, and pain medications are tailored for each individual case. Corticosteroids are lifesaving in the treatment of shock associated with acute adrenal insufficiency and decrease inflammation associated with acute spinal shock, but they are of no benefit in other types of shock. Research has focused on regulation of specific inhibitors of the inflammatory response. Protein C levels are diminished in septic shock, and recombinant protein C (drotrecogin alfa) is now in phase 3 trials. It has been shown to significantly decrease 28-day mortality in septic shock when given as a continuous infusion of 24 ug/kg/h for 96 hours. Its mechanism of action is reduction of systemic inflammation by inhibition of thrombosis. Administration of recombinant protein C has been correlated with lower D-dimer and interleukin-6 levels in this setting.
Cardiac failure may require use of transcutaneous or transvenous pacing or placement of an intra-arterial balloon pump. Emergent revascularization by stent angioplasty or coronary artery bypass appears to improve long-term outcome. Urgent hemodialysis or continuous venovenous hemofiltration may be indicated for maintenance of fluid and electrolyte balance during acute renal insufficiency resulting from shock.
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Patel GP et al: New treatment strategies for severe sepsis and septic shock. Curr Opin Crit Care 2003;9:390.
Rivers E et al: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368.
Samuels LE et al: Management of acute cardiogenic shock. Cardiol Clin 2003;21:43.
Van Way CW 3rd et al: Hemorrhagic shock: a new look at an old problem. Mo Med 2003;100:518.
Revision date: June 18, 2011
Last revised: by David A. Scott, M.D.
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