A. Hypovolemic Shock
The treatment goals for hypovolemic shock are restoration of intravascular volume and prevention of further volume loss. Therapy of hypovolemic shock should be targeted to reestablish normal blood pressure, pulse, and organ perfusion. For initial resuscitation, either colloid or crystalloid fluids are effective if given in sufficient volume. Subsequently, the fluid that is used should replace the fluid that has been lost. For example, blood products may be needed to replace blood loss (Chapter 9), and crystalloid should be used for vomiting and dehydration. For hypotension, the crystalloid of choice is normal saline or lactated Ringer’s solution because of the osmolality needed to restore intravascular volume. In large volume resuscitation, however, normal saline infusion may produce hyperchloremic metabolic acidosis. Vasoactive medications should be considered only as a temporizing measure
while fluid resuscitation is ongoing or when hypotension persists despite adequate volume
resuscitation. CVP monitoring may help to guide fluid resuscitation in patients without significant heart or lung disease.
B. Distributive Shock
The initial approach to the patient with septic shock is restoration and maintenance of adequate intravascular volume. Obtaining cultures and prompt institution of appropriate antibiotics are essential, as are other interventions to control the infection (removal of catheter, surgery, drainage, debridement). Early goal-directed therapy using CVP monitoring and measurement of ScVO2 has been shown to reduce mortality in severe sepsis and septic shock (Figure 7-1).
Figure 7-1. Protocol for Resuscitation of Hypovolemic and Distributive Shock
Abbreviations: MAP, mean arterial pressure; SVO2/ScVO2 = mixed or central venous oxygenation saturation aWhere infection is possible
Volume expansion can be initiated with isotonic crystalloid or colloid solutions. Vasodilation and diffuse capillary leaks are common in septic shock, and fluid requirements may be large. If the patient with septic shock remains hypotensive despite adequate fluid resuscitation, dopamine or
norepinephrine is recommended as the initial vasoactive drug. Low-dose vasopressin or epinephrine can be considered for patients who fail to respond adequately to first-line vasoactive agents, but these agents have not been shown to improve survival. Dobutamine should be considered in patients with adequate blood pressure who have hypoperfusion and low cardiac output with adequate ventricular preload. Reversible myocardial dysfunction with ventricular dilation and decrease in ejection fraction frequently occurs in septic shock. An initial MAP <65 mm Hg may require initiation of vasoactive pharmacologic therapy until fluid resuscitation is optimized. Corticosteroids
(hydrocortisone 200-300 mg in 24 hours administered as boluses or continuous infusion) should be considered in patients with septic shock when the blood pressure is poorly responsive to fluids and vasoactive medications. Anaphylactic shock is treated with volume resuscitation and subcutaneous epinephrine. In circumstances of very low blood pressure and poor peripheral perfusion, titrated intravenous epinephrine is indicated. Acute adrenal insufficiency is treated with volume therapy, intravenous corticosteroids, and vasoactive medications, if needed (Chapter 12). See Chapter 9 for information about the management of neurogenic shock.
C. Cardiogenic Shock
The primary goal in treating cardiogenic shock is to improve myocardial function. Arrhythmias should be treated promptly. Reperfusion by percutaneous intervention is the treatment of choice in cardiogenic shock due to myocardial ischemia (Chapter 10). Diastolic dysfunction during
myocardial ischemia may decrease ventricular compliance and elevate the left ventricular filling pressures, falsely indicating adequate preload. Therefore, a cautious trial of fluid administration may be warranted (250-mL bolus amounts). When blood pressure is decreased in cardiogenic shock, initial therapy with a single agent that has inotropic and vasopressor effects (eg, norepinephrine or dopamine) is indicated. Severely hypotensive patients (systolic arterial pressure <70 mm Hg) should be treated with norepinephrine to rapidly raise the systolic arterial pressure. The addition of an intravenous inotrope, such as milrinone or dobutamine (or dopexamine, which is available in some countries), may be considered to augment myocardial contractility after blood pressure stabilizes, with the goal of decreasing vasopressor therapy. If moderate hypotension is not responsive to initial therapy, consultation should be sought for steps such as intra-aortic balloon counterpulsation or left/right ventricular assist devices.
The elevated afterload (SVR) may also impair cardiac output if it is a primary hemodynamic
alteration, as occurs in chronic congestive heart failure. Often in acute cardiogenic shock, the SVR is secondarily elevated to maintain vascular perfusion pressure. Treatment aimed primarily at reducing afterload with a vasodilator, such as nitroprusside, should be initiated very cautiously and only in patients with hypoperfusion accompanied by adequate blood pressure.
Afterload and preload reduction should be avoided in cardiac failure when hypotension is present.
When cardiac failure is characterized by low cardiac output, normal or elevated blood pressure, and hypoxemia due to high pulmonary capillary pressure, reduction of preload and afterload is helpful in improving hypoxemia. High pulmonary capillary pressure is diagnosed clinically. Preload reduction is accomplished with loop diuretics (furosemide or bumetanide) and venodilators (nitroglycerin and morphine), whereas afterload reduction is accomplished with arterial vasodilators (angiotensin- converting enzyme inhibitors or, occasionally, nitroprusside). If the blood pressure can be increased to normal levels with inotropes, then the cautious addition of afterload and preload reduction is feasible in the presence of low cardiac output or high pulmonary capillary pressure.
D. Obstructive Shock
In the patient with obstructive shock, relief of the obstruction is the treatment of choice. Additionally, maintenance of intravascular volume is vitally important. Fluid resuscitation may improve the
patient’s cardiac output and hypotension temporarily. Inotropes or vasopressors have a minimal role in the management of obstructive shock, and these agents provide only temporary improvement, if any.
Pulmonary embolus is a common cause of obstructive shock. Treatment is centered on fluid resuscitation to maintain cardiac output and prompt anticoagulation to prevent clot propagation (Chapter 13). Thrombolytic therapy or thrombectomy is needed in rare cases of refractory cardiac collapse. If cardiac tamponade is present, pericardiocentesis may be lifesaving. Tension
pneumothorax must be treated promptly by needle decompression and subsequent tube thoracostomy (Appendix 8).
Diuretics and venodilators should be avoided in obstructive shock.