An expression of circulatory failure with inadequate cellular oxygen utilization.
A common process in critical care, affecting one third of patients in the ICU.
Diagnosis based on clinical hemodynamic and biochemical signs.
Associated with systemic arterial hypotension, but the magnitude maybe moderate, especially in patients with chronic hypertension.
Typically associated with systolic pressures of less than 90 mm Hg or the mean to arterial pressure of less than 70 mm Hg with associated tachycardia.
Associated with clinical signs of tissue hypoperfusion apparent in the skin that is cold and clammy with vasoconstriction and cyanosis.
Associated with decreased urine output of less than 0.5 mls per kilogram of body weight per hour.
Associated with neurologic changes of altered mental state including obtundation, confusion and disorientation.
Hyperlactemia is usually present, a reflection of abnormal cellular oxygen metabolism.
Normal blood lactate when millimoles per liter, but is increased to greater than 1.5 mmol per liter in acute circulatory shock.
Results from four mechanisms: hypovolemia with loss of fluid, cardiogenic factors such as acute myocardial infarction, end-stage cardiomyopathy, advanced valve disease, cardiac arrhythmias, or myocarditis, obstruction including pulmonary embolism, tension pneumothorax, cardiac tamponade, or distributive factors such as severe sepsis or anaphylaxis with the release of cytokines.
Hypovolemia, cardiogenic factors, and obstruction are associated with low cardiac output and inadequate oxygen transport.
In distributive shock the major abnormalities are associated with decreased systemic vascular resistance and altered oxygen extraction.
In distributive shock the cardiac output is usually high.
Patients with acute circulatory shock often have multiple mechanisms as above.
Septic shock is a form of distributive shock and is the most common type of shock experienced by patients in the ICU.
Cardiogenic shock and hypovolemic shock are the next most common types of circulatory shock in the ICU.
Obstructive shock is the least common type of circulatory shock experienced in the ICU.
In a study of 1600 patients with shock the distribution of shock was: septic shock occurred and 62% of patients, cardiogenic shock 16%, hypovolemic shock 16% and other types of distributed shock 4%, and obstructive shock 2% (De Backer D et al).
Type of shock can be established by history , physical exam and clinical evaluation.
Shock following trauma is usually hypovolemia, related to bleeding.
Cardiogenic shock or distributive shock may occur alone or in combination.
Clinical examination for cardiogenic shock includes skin color, body temperature, evaluation for peripheral edema, and assessment of jugular venous distention.
Echocardiographic evaluation is essential in the presence of shock to access the presence of a pericardial effusion, measurement of left and right ventricle size and function, assess respiratory variation in vena cava dimensions and calculation of the aortic velocity time integral, a measure of stroke volume.
Treatment requires adequate hemodynamic support to prevent worsening organ dysfunction and failure.
Treatment resuscitation starts before the exact cause is established and must be initiated rapidly.
When the cause is identified it should be corrected, such as control of bleeding, thrombolysis for pulmonary embolus and antibiotics for septic shock.
Monitoring for arterial blood pressure and blood sampling is helpful with the insertion of an arterial catheter.
Center venous catheter placement for infusion of fluids and the administration of vasoactive agents is essential
Resuscitation components include ventilation, fluid resuscitation and administration of vasoactive agents.
Oxygen is delivered immediately to increase oxygenation and to prevent pulmonary hypertension.
Pulse oximetry is often unreliable due to peripheral vasoconstriction, and serial blood gas monitoring is often required.
Mechanical ventilation support is primarily through the placement of an endotracheal tube because masks often fail and the patients frequently will have respiratory and cardiac arrests.
Mechanical tracheal intubation should be performed in nearly all patients with severe shortness of breath, hypoxemia, or persistent acidemia.
Mechanical ventilation reduces oxygen demand of respiratory muscles, decreases left ventricular afterload by increasing intrathoracic pressure.
Following placement of mechanical ventilation, and abrupt decrease in blood pressure suggests hypovolemia and decreasing venous return.
Fluid therapy improves microvascular bloodflow, increases cardiac output, and is an essential part of the treatment of any form of shock.
Even patients with cardiogenic shock may benefit from fluids, since active acute edema can result in decrease in vascular volume.
Fluid resuscitation is carefully monitored to prevent excess fluid from being administered.
The objective for fluid resuscitation is for cardiac output to become preload-independent.
Patients should receive a fluid challenge to determine the actual response to the administration of fluids, while limiting the risks of adverse effects.
Crystalloid fluids are the first choice of therapy because they are well-tolerated and inexpensive.
In patients with hypoalbuminemia, albumin may be a reasonable fluid choice for resuscitation.
Typical fluid administration rate for fluid challenge is an infusion of 300-500 mL over 20-30 minutes.
Fluid challenge is to increase systemic blood pressure, decrease heart rate, or increase urine output.
The most serious complication of fluid resuscitation is the development of pulmonary edema.