THERAPUTIC APPROACH TO THE HYPOTENSIVE PATIENT

Shock is circulatory insufficiency that creates an imbalance between tissue oxygen supply and demand.

Tissue hypoperfusion is associated with decreased venous O₂ content and metabolic acidosis.

Shock is classified into four categories based on etiology: (a) hypovolemic, (b) cardiogenic, (c) distributive (eg, neurogenic and anaphylactic), and (d) obstructive.

CLINICAL FEATURES

The clinical presentation will depend on the etiology, duration, and severity of the shock state and the underlying medical status of the patient.

Often the precipitating cause of shock may be apparent; however, nonspecific symptoms are not uncommon.

A targeted history of the presenting symptoms and existing conditions including drug use (prescribed and nonprescribed) is an essential. Drug toxicity and anaphylactic reactions should be considered.

Assess vital signs; however, no single vital sign or value is diagnostic.

The body temperature may be normal, elevated, or subnormal. Hyper- or hypothermia may be a result of endogenous factors or exogenous causes.

Cardiovascular: The heart rate is typically elevated; however, bradycardia may be present, often seen with fit individuals, cardiovascular drug use, hypoglyc-emia, and preexisting cardiovascular disease. Shock is usually, but not always, associated with arterial hypotension, with a systolic blood pressure (BP) below 90 mm Hg. However, shock may occur with a normal blood pressure, and hypotension may occur without shock.

Cardiovascular: pulse pressure. Early in shock, BP may be normal or elevated in response to compensatory mechanisms. As these mechanisms fail, BP typically falls. In hypovolemia, postural changes often precede overt hypotension. The pulse pressure may be an earlier and more sensitive indicator.

Cardiovascular: neck veins. Other cardiovascular manifestations may include neck vein distention or flattening and cardiac dysrhythmias. Decreased coronary perfusion pressures can lead to myocardial ischemia, decreased ventricular compliance, increased left ventricular diastolic pressures, and pulmonary edema.

Respiratory. The respiratory rate is frequently elevated early. As shock progresses, hypoventilation, respiratory failure, and respiratory distress syndrome may occur.

Decreased cerebral perfusion leads to mental status changes such as weakness, restlessness, confusion, disorientation, delirium, syncope, and coma.

Cutaneous manifestations may include pallor, pale or dusky skin, sweating, bruising, petechiae, cyanosis, altered temperature, and delayed capillary refill.

GI manifestations resulting from low flow states may include ileus, GI bleeding, pancreatitis, acalcu-lous cholecystitis, and mesenteric ischemia.

Renal manifestations. Aldosterone and antidiuretic hormone are increased resulting in a reduced glomer-ular filtration rate and oliguria. In sepsis, a paradoxical polyuria may occur and be mistaken for adequate hydration.

Metabolic manifestations. Respiratory alkalosis is common early. As the shock state continues and compensatory mechanisms begin to fail, anaerobic metabolism occurs, leading to the formation of lactic acid and metabolic acidosis. Other abnormalities that may be seen are hyperglycemia, hypoglycemia, and hyperkalemia.

DIAGNOSIS AND DIFFERENTIAL

The clinical presentation and presumed etiology of shock will dictate the diagnostic studies, monitoring modalities, and interventions.

The patient approach must be individualized; however, frequently performed laboratory studies include complete blood count, platelet count, serum lactate levels, electrolytes, blood urea nitrogen, and creati-nine determinations; prothrombin and partial throm-boplastin times; and urinalysis.

Other tests commonly used are arterial blood gas, fibrinogen, fibrin split products, D-dimer, and Cortisol determinations; hepatic function panel; cerebros-pinal fluid studies; and cultures of potential sources of infection.

A pregnancy test should be performed on all females of childbearing potential.

Other common diagnostic tests include radiographs (chest and abdominal), electrocardiographs, computed tomography scans (chest, head, abdomen, and pelvis), and echocardiograms. Beside US may also help determine the etiology of shock.

Continuous monitoring of vital signs should be instituted. Additionally, modalities such as pulse oxime-try, end-tidal CO₂, central venous pressure, central venous O₂ saturation, cardiac output, and calculation of systemic vascular resistance and systemic oxygen delivery may be indicated.

Lack of response to appropriate stabilization should lead to a search for more occult causes. Be certain that basic resuscitation have been carried out including adequate volume replacement. Early use of vasopressors may elevate the central venous pressure and mask the presence of continued hypo-volemia. Ensure that all equipment is functioning appropriately.

Expose and examine for occult wounds.

Consider less commonly seen diagnoses, such as cardiac tamponade, tension pneumothorax, adrenal insufficiency, toxic or allergic reactions, and occult bleeding (eg, ruptured ectopic pregnancy, or occult intraabdominal or pelvic bleeding).

EMERGENCY DEPARTMENT CARE AND DISPOSITION

The goal of the interventions is to restore adequate tissue perfusion in concert with the identification and treatment of the underlying etiology.

Aggressive airway control, best obtained through endotracheal intubation, is indicated. Remember associated interventions such as medications (ie, sedatives can exacerbate hypotension) and positive pressure ventilation may reduce preload and cardiac output and may contribute to hemodynamic collapse.

All patients should receive supplemental high-flow oxygen. If mechanical ventilation is used, neuromus-cular blocking agents should be used to decrease lactic acidosis from muscle fatigue and increased oxygen consumption. Arterial oxygen saturation should be restored to >93% and ventilation controlled to maintain a Pa_CO2 of 35 to 40 mm Hg.

Circulatory hemodynamic stabilization begins with IV access through large-bore peripheral venous lines. Central venous access aids in assessing volume status (preload) and monitoring S_cvO2. US guidance has proven helpful with these procedures. Central venous access is the preferred route for the long-term administration of vasopressor therapy.

Early surgical consultation is indicated for internal bleeding.

Most external hemorrhage can be controlled by direct compression. Rarely, clamping or tying off of vessels may be needed.

Use isotonic crystalloid intravenous fluids (0.9% NaCl, Ringer’s lactate) in the initial resuscitation phase. Standard therapy is 20 to 40 mL/kg given rapidly (over 10–20 minutes). Only about 30% of infused isotonic crystalloids remain in the intravascular space; therefore, it is recommended to infuse three times the estimated blood loss in acute hemorrhagic shock.

The benefits of early and aggressive fluid replacement in these trauma patients remain unproven as do the benefits of permissive hypotension.

Blood remains the ideal resuscitative fluid. When possible, use fully cross-matched PRBCs. If the clinical situation dictates more rapid intervention, type-specific, type O (rhesus negative to be given to females of childbearing years) may be used. The decision to use platelets or fresh frozen plasma (FFP) should be based on clinical evidence of impaired hemostasis and frequent monitoring of coagulation parameters.

Vasopressors are used after appropriate volume resuscitation, and there is persistent hypotension.

The goal of resuscitation is to maximize survival and minimize morbidity using objective hemodynamic and physiologic values to guide therapy. A goal-directed approach of urine output >0.5 mL/kg/h, CVP 8 to 12 mm Hg, MAP 65–90 mm Hg, and S_cv02 >70% during ED resuscitation of septic shock significantly decreases mortality.

Acidosis should be treated with adequate ventilation and fluid resuscitation. Sodium bicarbonate (1 mEq/kg) use is controversial. Use only in the setting of severe acidosis refractory to above-mentioned methods. Correct only to arterial pH 7.25.