Shock

Introduction

Shock is an acute state of inadequate perfusion of critical organs that can lead to death if therapy is not optimal. Shock is defined as systolic blood pressure (SBP) less than 90 mm Hg or reduction of at least 40 mm Hg from baseline with perfusion abnormalities despite adequate fluid resuscitation.

CLINICAL PRESENTATION

• Patients with hypovolemic shock may have thirst, anxiousness, weakness, lightheadedness, dizziness, scanty urine output, and dark yellow urine.
• Signs of more severe volume loss include tachycardia (>120 beats/min), tachypnea (>30 breaths/min), hypotension (SBP<90mm of Hg)
• Serum sodium and chloride concentrations are usually high with acute volume depletion. The blood urea nitrogen (BUN): creatinine ratio may be elevated initially, but the creatinine increases with renal dysfunction. Metabolic acidosis results in elevated base deficit and lactate concentrations with decreased bicarbonate and pH.
• Complete blood cell count (CBC) is normal in absence of infection. In hemorrhagic shock, the red cell count, hemoglobin, and hematocrit will decrease
• Urine output is decreased to less than 0.5 to 1 mL/h. With more severe volume depletion, dysfunction of other organs may be reflected in laboratory testing (e.g., elevated serum transaminases levels with hepatic dysfunction).

DIAGNOSIS And Monitoring

Noninvasive and invasive monitoring and evaluation of medical history, clinical presentation, and laboratory findings are important in establishing the diagnosis and assessing mechanisms responsible for shock. Findings include hypotension (SBP 100 beats/min), and low urine output less than 20ml/hr.

• Pulmonary artery (Swan–Ganz) catheter can be used to determine central venous pressure (CVP), pulmonary artery pressure (PAP), cardiac output (CO), and pulmonary artery occlusion pressure (PAOP).
• Renal function can be assessed grossly by hourly measurements of urine output, but estimation of creatinine clearance based on isolated serum creatinine values may be inaccurate. Decreased renal perfusion and aldosterone release result in sodium retention and thus low urinary sodium (<30mEq/L).

TREATMENT

Goals of Treatment: The goal during resuscitation from shock is to achieve and maintain mean arterial pressure (MAP) above 65 mm Hg while ensuring adequate perfusion to critical organs. The ultimate goals are to prevent further disease progression with subsequent organ damage and, if possible, to reverse organ dysfunction that has already occurred

FLUID RESUSCITATION FOR HYPOVOLEMIC SHOCK

• Crystalloids: Isotonic (or near isotonic) crystalloid solutions (0.9% sodium chloride or lactated Ringer solution) are the initial fluids of choice. The choice between normal saline and lactated Ringer solution is based on clinician preference and adverse effect concerns. Crystalloids can be rapidly and easily administered, are compatible with most drugs, and have low cost. Their disadvantages include the need to use large fluid volumes and the possibility that dilution of oncotic pressure may lead to pulmonary edema. Crystalloids are administered at a rate of 500 to 2000 mL/h, depending on severity of the deficit, degree of ongoing fluid loss, and tolerance to infusion volume. Usually, 2 to 4 L of crystalloid normalizes intravascular volume.
• Colloids: Hydroxyethyl starch, dextran, and albumin possess the theoretical advantage of prolonged intravascular retention time compared with crystalloid solutions. However, colloids are expensive and have been associated with fluid overload, renal dysfunction, and bleeding. In 2013, the U.S. Food and Drug Administration (FDA) analyzed data from randomized controlled trials, meta-analyses, and observational studies and concluded that hydroxyethyl starch is associated with increased mortality and renal injury requiring renal replacement therapy in critically ill adult patients, including patients with sepsis and those admitted to the intensive care unit (ICU). The FDA concluded that the solutions should not be used in these patient populations and added a boxed warning to the labeling describing the risk of mortality and severe renal injury.
• Blood products: Some patients require blood products (whole blood, packed red blood cells, fresh frozen plasma, or platelets) to ensure maintenance of O2 -carrying capacity, as well as clotting factors and platelets for blood hemostasis.

PHARMACOLOGIC THERAPY FOR SHOCK

• Hypovolemic shock: Inotropic agents and vasopressors are generally not indicated in initial treatment of hypovolemic shock (if fluid therapy is adequate), because the body’s compensatory response is to increase CO and peripheral resistance to maintain BP.
• Septic shock: Initial hemodynamic therapy for septic shock is administration of IV fluid (30 mL/kg of crystalloid), with the goal of attaining CVP 8 to 12 mm Hg or 15 mm Hg in mechanically ventilated patients or patients with abdominal distention or preexisting ventricular dysfunction. Crystalloids are preferred over colloids unless patients are at risk for adverse events from redistribution of IV fluids to extravascular tissues or are fluid restricted.

✓ Norepinephrine is the preferred initial vasopressor in septic shock not responding to fluid administration.

✓ Epinephrine may be added in cases where there is suboptimal hemodynamic response to norepinephrine.

✓ Phenylephrine may be tried as the initial vasopressor in cases of severe tachydysrhythmias.

✓ Dobutamine is used in low CO states despite adequate fluid resuscitation pressures.

✓ Vasopressin may be considered as adjunctive therapy in patients who are refractory to catecholamine vasopressors despite adequate fluid resuscitation.

• Corticosteroids can be initiated in septic shock when adrenal insufficiency is suspected, when vasopressor dosages are escalating, or when weaning of vasopressor therapy proves futile. Adverse events are few because corticosteroids are administered for a short time, usually 7 days. Acutely, elevated BUN, white blood cell count, and glucose may occur. In general, treatment of septic shock with corticosteroids improves hemodynamic variables and lowers catecholamine vasopressor dosages with minimal to no adverse effect on patient safety.