Chapter 5. Therapeutic Approach to the Hypotensive Patient

Shock is circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption). Such tissue hypoperfusion is associated with decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is classified into four categories based on etiology: (a) hypovolemic, (b) cardiogenic, (c) distributive (eg, neurogenic and anaphylactic), and (d) obstructive.

Factors that influence the clinical presentation of a patient in shock include 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 readily apparent (eg, acute myocardial infarction, trauma, gastrointestinal [GI] bleeding, or anaphylaxis). It is not uncommon for the patient to present with nonspecific symptoms (eg, generalized weakness, lethargy, or altered mental status). A targeted history of the presenting symptoms and previously existing conditions (eg, cardiovascular disease, GI bleeding, adrenal insufficiency, or diabetes) will aid in identifying the cause and guide the initial treatment of shock. Drug use (prescribed and nonprescribed) is an essential element of the initial history. Medication use may be the cause or a contributing factor to the evolution of shock. For example, diuretics can lead to volume depletion and cardiovascular medications (eg, β-blockers) can depress the pumping action of the heart. The possibility of drug toxicity and anaphylactic reactions to medications also should 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 hyperthermia or hypothermia may be a result of endogenous factors (eg, infections or hypometabolic states) or exogenous causes (eg, environmental exposures). The heart rate is typically elevated; however, bradycardia may be present with many conditions, such as excellent baseline physiologic status (young athletes), intraabdominal hemorrhage (secondary to vagal stimulation), cardiovascular medication use (eg, β-blockers and 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 be seen. As shock progresses, hypoventilation, respiratory failure, and respiratory distress syndrome may occur.

Shock is usually, but not always, associated with systemic arterial hypotension, with a systolic blood pressure (BP) below 90 mm Hg. The insensitivity of blood pressure to detect global tissue hypoperfusion has been repeatedly confirmed. Thus, shock may occur with a normal blood pressure, and hypotension may occur without shock. Early in shock, the systolic and diastolic BPs may initially be normal or elevated in response to a compensatory mechanism 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 these vital sign abnormalities, other cardiovascular manifestations may include neck vein distention or flattening and cardiac dysrhythmias. A third heart sound (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 longstanding 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 the hemoglobin level is less than 5 grams/dL), altered temperature, and delayed capillary refill.

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

The clinical presentation and presumed etiology of shock will dictate the diagnostic studies, monitoring modalities, and interventions used. 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 used 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 potential. No single laboratory value is sensitive or specific for shock. 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. The following are helpful in this assessment: subcostal cardiac view, inferior vena cava view, parasternal long-axis cardiac view, apical four-chamber cardiac view, right upper quadrant abdominal view, pelvic view, and abdominal aorta view.

Continuous monitoring of vital signs should be instituted in all patients. Additionally, modalities such as pulse oximetry, 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.

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 central venous pressure 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 (eg, rupture ectopic pregnancy, or occult intraabdominal or pelvic bleeding) in the 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.

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, best obtained through endotracheal intubation, is indicated. Remember that 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.

2. All patients should receive supplemental high-flow oxygen. If mechanical ventilation is used, neuromuscular 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 PaCO2 of 35 to 40 mm Hg.

3. Circulatory hemodynamic stabilization begins with IV access through large-bore peripheral venous lines. Central venous access aids in assessing volume status (preload) and monitoring ScvO2. US guidance has proven helpful with these procedures. Central venous access is the preferred route for the long-term administration of vasopressor therapy. The Trendelenburg position does not improve cardiopulmonary performance compared with the supine position, and it may worsen pulmonary gas exchange and predispose to aspiration. Passive leg raising above the level of the heart with the patient supine can be effective. Early surgical consultation is indicated for internal bleeding. Most external hemorrhage can be controlled by direct compression. Rarely will clamping or tying off of vessels be needed.

4. The type, amount, and rate of fluid replacement remain areas of controversy. There is no difference in survival comparing crystalloid with colloid resuscitation. Crystalloid solutions continue to be recommended because of the increased cost of colloid agents. Most use isotonic crystalloid intravenous fluids (0.9% NaCl, Ringer lactate) in the initial resuscitation phase. Due to the increased cost, lack of proven benefit, and potential for disease transmission (with FFP), the routine use of colloids (5% albumin, purified protein fraction, fresh-frozen plasma [FFP], and synthetic colloid solutions [hydroxyethyl starch or dextran 70]) is questionable. Standard therapy in the hemodynamically unstable patient is 20 to 40 mL/kilogram given rapidly (over 10 to 20 min). Because only about 30% of infused isotonic crystalloids remain in the intravascular space, it is recommended to infuse approximately 3 times the estimated blood loss in acute hemorrhagic shock. However, the benefits of early and aggressive fluid replacement in these trauma patients remain unproven as do the benefits of permissive hypotension.

5. 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 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/mm3 or lower; administer 6 units initially. FFP is indicated if the prothrombin time is prolonged beyond 1.5 seconds; administer 2 units initially. Trauma patients requiring transfusion of multiple units of packed RBCs should receive FFP and platelets early in ratios that approach 1:1:1 in order to address the accompanying coagulopathy that will likely be present. The use of fresh whole blood has also been advocated and may be the most effective approach for such patients. The potential need for FFP and platelet transfusions should be considered early and reassessed frequently in an effort to detect and limit the adverse effects of trauma-induced coagulopathy.

6. Vasopressors are used after appropriate volume resuscitation has occurred and there is persistent hypotension. Possible choices include: dobutamine 2.0 to 20.0 micrograms/kilogram/min, dopamine 5.0 to 20.0 micrograms/kilogram/min, and norepinephrine 0.5 to 30.0 microgram/min.

7. 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/kilogram/h, CVP 8 to12 mm Hg, MAP 65 to 90 mm Hg, and ScvO2 > 70% during ED resuscitation of septic shock significantly decreases mortality.

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

9. Early surgical or medical consultation for admission or transfer is indicated.