Therapeutic Approach to the Hypotensive Patient

Over 1 million patients in shock present to emergency departments each year. Shock occurs when circulation is insufficient to meet the resting metabolic demands of the tissues. Such tissue hypoperfusion is associated with decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is classified into four categories based on etiology: (1) hypovolemic, (2) cardiogenic, (3) distributive (e.g., neurogenic anaphylaxis), and (4) obstructive.

Clinical Features

Factors that influence the clinical presentation of a patient in shock include the etiology, duration, and severity of the shock state as well as the underlying medical status of the patient. Often the precipitating cause of shock may be readily apparent [e.g., acute myocardial infarction, trauma, gastrointestinal (GI) bleeding, or anaphylaxis]. It is not uncommon for the patient to present with nonspecific symptoms (e.g., generalized weakness, lethargy, or altered mental status). A targeted history of both the presenting symptoms and previously existing conditions (e.g., cardiovascular disease, GI bleeding, adrenal insufficiency, or diabetes) will aid in identifying the cause and guide the initial treatment of shock. Drug use (both prescribed and nonprescribed) is an essential element of the initial history. Medication use may be either the cause or a contributing factor to the evolution of shock. For example, diuretics can lead to volume depletion, and cardiovascular medications (e.g., beta blockers and digoxin) can depress the pumping action of the heart. The possibility of drug toxicity and anaphylactic reactions to medications should also be considered.
Assessment of vital signs is a routine part of the physical examination; however, no single vital sign or value is diagnostic in the evaluation of the presence or absence of shock. The patient’s temperature may be elevated or subnormal. The presence of hyper- or hypothermia may be a result of endogenous factors (e.g., infections or hypometabolic states) or exogenous causes (e.g., environmental exposures). The heart rate is typically elevated; however, bradycardia may be present with many conditions, such as intraabdominal hemorrhage (probably secondary to vagal stimulation), cardiovascular medication use (e.g., beta blockers or digoxin), hypoglycemia, and preexisting cardiovascular disease.
The respiratory rate is frequently elevated early in shock. Increased minute ventilation, increased dead space, bronchospasm, and hypocapnia may all be seen. As shock progresses hypoventilation, respiratory failure, and respiratory distress syndrome may occur.
The systolic and diastolic blood pressures (BP) may initially be normal or elevated in response to compensatory mechanisms such as tachycardia and vasoconstriction. As the body’s compensatory mechanisms fail, BP typically falls. Postural changes in BP, commonly seen with hypovolemic states, will precede overt hypotension. The pulse pressure, the difference between systolic and diastolic BP measurements, may be a more sensitive indicator. The pulse pressure usually rises early in shock and then decreases before a change in the systolic BP is seen.
In addition to the abovementioned vital sign abnormalities, other cardiovascular manifestations may include neck vein distention or flattening, and cardiac dysrhythmias. An S3 may be auscultated in high-output states. Decreased coronary perfusion pressures can lead to myocardial ischemia, decreased ventricular compliance, increased left ventricular diastolic pressures, and pulmonary edema.
Decreased cerebral perfusion leads to mental status changes such as weakness, restlessness, confusion, disorientation, delirium, syncope, and coma. Patients with long-standing hypertension may exhibit these changes without severe hypotension. Cutaneous manifestations may include pallor, pale or dusky skin, sweating, bruising, petechiae, cyanosis [may not be evident if severe anemia (hemoglobin level less than 5 g/dL) is present], altered temperature, and decreased capillary refill.
GI manifestations resulting from low flow states may include ileus, GI bleeding, pancreatitis, acalculous cholecystitis, and mesenteric ischemia. In an effort to conserve water and sodium, levels of aldosterone and antidiuretic hormone are increased. This results in a reduced glomerular filtration rate, redistribution of blood flow from the renal cortex to the renal medulla, and oliguria. In sepsis, a paradoxical polyuria may occur and be mistaken for adequate hydration.
Early in shock a common metabolic abnormality is a respiratory alkalosis. As the shock state continues and compensatory mechanisms begin to fail, anaerobic metabolism occurs, leading to the formation of lactic acid and resulting in a metabolic acidosis. Other metabolic 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 utilized. The approach to each patient must be individualized; however, frequently performed laboratory studies include complete blood count; platelet count; electrolytes, blood urea nitrogen, and creatinine determinations; prothrombin and partial thromboplastin times; and urinalysis. Other tests commonly utilized are arterial blood gas, lactic acid, fibrinogen, fibrin split products, D-dimer, and cortisol determinations; hepatic function panel; cerebrospinal fluid studies, and cultures of potential sources of infection. A pregnancy test should be performed on all females of childbearing age. Other common diagnostic tests include radiographs (chest and abdominal), electrocardiograms, ultrasound or computed tomography scans (chest, head, abdomen, and pelvis), and echocardiograms.
Continuous monitoring of vital signs should be instituted in all patients. In addition to commonly monitored parameters such as pulse, blood pressure, respiratory rate, and temperature, other modalities, such as pulse oximetry, end-tidal CO2, central venous pressure (CVP), central venous O2 saturation, cardiac output, and calculation of systemic vascular resistance, may be indicated.
A search to determine the etiology of the shock must be undertaken. Lack of response to appropriate stabilization measures should cause the clinician to evaluate the patient for a more occult cause. First the physician must be certain that the basic steps of resuscitation have been carried out appropriately. Consider whether or not the patient has been adequately volume resuscitated. Early use of vasopressors may elevate the CVP and mask the presence of continued hypovolemia. Ensure that all equipment is connected and functioning appropriately. Carefully expose and examine the patient for occult wounds. Consider less commonly seen diagnoses, such as cardiac tamponade, tension pneumothorax, adrenal insufficiency, toxic or allergic reactions, and occult bleeding (e.g., rupture of ectopic pregnancy, or occult intraabdominal or pelvic bleeding) in a patient who is not responding as expected.
Please refer to the other chapters in this book regarding the evaluation of the specific forms of shock.

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.

1. Aggressive airway control, often involving endotracheal intubation, is indicated.
2. All patients should receive supplemental high-flow oxygen. The tachypnea that often accompanies shock adds to oxygen consumption and therefore may contribute to lactic acid production.
3. 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 of tourniquets is discouraged. All patients require adequate venous access. Cannulation of peripheral veins with large-bore catheters usually provides an adequate route for providing fluid resuscitation. For monitoring and treatment purposes (e.g., long-term vasopressors or pacemakers), however, central venous access may be necessary.
4. Volume replacement. The type, amount, and rate of fluid replacement remain areas of controversy. Most utilize isotonic crystalloid intravenous (IV) fluids (0.9% NaCl, Ringer’s lactate) in the initial resuscitation phase. Use of colloids [5% albumin, purified protein fraction, fresh-frozen plasma (FFP), and synthetic colloid solutions (hydroxyethyl starch or dextran 70)] continue to be advocated by some. Due to the increased cost, lack of proven benefit, and potential for disease transmission (with FFP), the routine use of colloids is questionable. Standard therapy in the hemodynamically unstable patient typically has been 20 to 40 mL/kg given rapidly (over 10 to 20 min). Since only about 30 percent of infused isotonic crystalloids remain in the intravascular space, it is recommended to infuse approximately three times the estimated blood loss. However, the benefits of early and aggressive fluid replacement in the ED or prehospital setting remain unproven. Studies have suggested that rapid fluid administration may contribute to ongoing hemorrhage by both mechanical effects and dilution of clotting factors. While it is not appropriate to totally withhold fluids, some amount of “underresuscitiation” (i.e., maintaining mean arterial BP around 70 mmHg) may be beneficial until surgical control of the bleeding site can be accomplished. Blood remains the ideal resuscitative fluid. Ideally, fully cross-matched blood is preferred. If the clinical situation dictates more rapid intervention, type-specific, type O (Rh negative to be given to females of childbearing years), or autologous blood may be utilized. The decision to use platelets or FFP should be based on clinical evidence of impaired hemostasis and frequent monitoring of coagulation parameters. Platelets are generally given if there is ongoing hemorrhage and the platelet count is 50,000 or less; FFP is indicated if the prothrombin time is prolonged more than 1.5. The pneumatic antishock garment is no longer recommended in the treatment of shock but may be used to splint and control bleeding of the lower extremities.
5. Vasopressors are utilized after appropriate volume resuscitation has occurred and there is persistent hypotension. American Heart Association recommendations based on blood pressure determinations are dobutamine 2.0 to 20.0 µg/(kg/min) for systolic BP over 100 mmHg, dopamine 2.5 to 20.0 µg/(kg/min) for systolic BP 70 to 100 mmHg, and norepinephrine 0.5 to 30.0 µg/min for systolic BP under 70 mmHg.
6. Acidosis should be treated with adequate ventilation and fluid resuscitation. Sodium bicarbonate (1 meq/kg) use is controversial. If it is used, it is given only in the setting of severe acidosis refractory to the abovementioned methods.
7. Early surgical or medical consultation for admission or transfer is indicated.