Accompanied by his daughter, George Moran, age 81, comes to the emergency department looking frail and weak. His vital signs are: blood pressure, 82/40 mm Hg; heart rate 130 beats/minute and regular; and oral temperature, 98.6°F (37° C). He weighs 125 lb (57 kg )—5 lb (2.3 kg) less than his normal weight. On inspection, you detect poor skin turgor and dry mucous membranes; on palpation, you note his abdomen is tender but not distended. As ordered, you obtain blood samples and send them to the laboratory immediately.
Although Mr. Moran is lethargic, he’s able to answer questions when you try to obtain his history. He states he has had nausea, vomiting, and watery diarrhea for the last 2 days and that he fell earlier today when getting up from a chair. His daughter adds that several family members have had the “stomach flu” lately.
When laboratory results come back, you note an elevated white blood cell count, high blood urea nitrogen level, and borderline-low creatinine level (0.8). Other values are normal.
Synthesizing this information with the history and assessment findings, you begin to suspect Mr. Moran has suffered GI tract volume loss leading to hypovolemic shock. His shock index (heart rate divided by systolic blood pressure) is 1.59—significantly higher than the normal range of 0.5 to 0.7.
Knowing that quick action is critical, you immediately place an 18G I.V. line in Mr. Moran’s left antecubital vein and, as ordered, begin to infuse Ringer’s lactate at 250 ml/hour.
A perilous plunge in perfusion
Hypovolemic shock occurs when circulatory volume drops significantly. As in other types of shock, systemic reduction in tissue perfusion leads to decreased oxygen delivery. Unless the initial process is reversed, prolonged oxygen deprivation causes cellular hypoxia and metabolic waste accumulation, leading to multisystem organ failure and death. Fortunately, early recognition of hypovolemic shock and aggressive treatment can dramatically improve the patient’s outcome.
Hypovolemic shock most commonly results from blood loss. Decreased renal function puts the elderly at higher risk for this type of shock. Children also are at greater risk due to their higher proportion of body water.
In hypovolemia, decreased fluid volume reduces blood return to the heart, causing a decline in preload (the volume of blood remaining in the left ventricle at the end of diastole). As preload falls, cardiac output drops.
To compensate for low cardiac output, the heart rate speeds up and systemic vascular resistance (SVR) increases. Increased SVR in turn boosts cardiac output, increases tissue perfusion pressure, and triggers catecholamine release. Blood volume rises as interstitial fluid shifts to the intravascular spaces and the liver and spleen release stored red blood cells (RBCs). These changes activate the renin-angiotensin-aldosterone system, which promotes sodium and water retention in an effort to raise systolic pressure. Urine output then declines.
If blood loss continues, compensatory mechanisms maintain perfusion to vital tissues by shunting blood away from nonvital organs. Decreased perfusion leads to cellular injury in the catabolic state. If the process isn’t reversed, cellular death follows. Also, the glucose level rises as insulin loses its ability to control the processes triggered by lactic acidosis. With the body in a state of oxygen debt, anaerobic metabolism produces lactic acid, directly reflecting poor perfusion and oxygen debt in later shock stages. In uncorrected hypovolemic shock, loss of buffering ability leads to acidosis (pH below 7.35).
Assessment and diagnosis
As with Mr. Moran, the patient’s history may provide important information. After obtaining a thorough history of the present illness, conduct a general physical assessment, including blood pressure, pulse, temperature, oxygenation, urine output, mental status, and pain level.
To quickly assess fluid volume, think of the “hose and toes” theory: Fluid volume is sufficient if the “hose” (kidney) is producing adequate urine and the toes are pink in light-skinned patients or brown in dark-skinned patients.
Expect to draw blood samples for a complete blood count, which may suggest or help rule out infection and certain other conditions. Hemoglobin and hematocrit values may indicate bleeding; during treatment, they provide a baseline for gauging the patient’s response to blood transfusions or other replacement fluids. Also draw blood for typing and screening. If the patient has anemia with acute blood loss, make sure blood is crossmatched.
Other useful studies may include a liver profile, arterial blood gas analysis, and measurement of lactic acid, fibrinogen and fibrin split products, and cardiac enzyme levels. Calculating the shock index may be useful, too; in acute hypo-volemia, the index rises. The physician may order an ECG to evaluate cardiac rhythm and a chest X-ray to look for evidence of pneumonia or heart failure.
Early intervention is crucial to a positive outcome. Hypovolemic shock calls for rapid volume resuscitation to restore homeostasis. Ensure the ABCs of basic resuscitation—airway, breathing, and circulation. The underlying cause of shock must be treated as well.
Expect to insert a large-bore (18G or larger) peripheral I.V. line or a central access catheter for fluid administration; a multiple-lumen line aids delivery of fluids and I.V. medications. Choice of replacement fluid depends on the type of volume lost.
Colloids and crystalloids
Colloids, whose molecules are too large to pass through semipermeable membranes, provide volume of higher osmolarity than crystalloids and help prevent fluid shifts. Staying mostly within the intravascular compartment, they maintain plasma colloid osmotic pressure. Examples include blood and blood products, such as packed red blood cells (PRBCs), whole blood, fresh frozen plasma, hetastarch, and albumin.
If the patient has lost blood from surgery or trauma, be prepared to administer PRBCs, which lend oxygen-carrying capacity without adding excessive volume. Fresh frozen plasma helps expand intravascular volume and restore deficient clotting factors, whereas whole blood increases volume and boosts oxygen-carrying capacity. If the patient has thrombocytopenia, expect to give platelet transfusions.
Crystalloids, such as normal saline solution and Ringer’s lactate, have smaller molecules than colloids and can penetrate semipermeable membranes. The clinician may order 2 to 3 L of a crystalloid to help maintain fluid and electrolyte balance. Lactated Ringer’s solution is isotonic and provides buffering to counteract the effects of acidosis. Normal saline solution is helpful for a patient who hasn’t lost RBCs.
Because crystalloids distribute from the intravascular space throughout the entire extracellular space, they must be administered in large volumes to treat hypo-volemic shock. Avoid giving
dextrose-containing crystalloids, which may increase the serum glucose level. (Tight glycemic control promotes healing.)
Vasopressors aren’t a first-line treatment for hypovolemic shock. Normally, they cause contraction of the peripheral vasculature, which leads to shunting of blood to vital organs; however, when volume is low, this mechanism isn’t effective. Nonetheless, if aggressive volume resuscitation doesn’t improve blood pressure, vasopressors may be given in addition to I.V. fluids.
Be aware that I.V. fluids increase the patient’s risk of heart failure. During fluid administration, be sure to assess breath sounds, heart rate, and oxygenation and monitor fluid intake and output.
Other nursing interventions
Expect to administer oxygen and ventilatory support, if needed, to support tissue perfusion. To optimize blood pressure, position the patient flat or in Trendelenburg’s position to increase venous return from the legs. But be aware that such positioning heightens the risk of aspiration. Hypovolemia itself reduces gut perfusion; decreased blood flow to the stomach can increase the risk of gastric residuals, reflux, and aspiration. So if the patient’s receiving enteral nutrition, discontinue tube feedings temporarily.
Also, low perfusion puts the patient at higher risk for pressure ulcers. Although skin condition isn’t a high priority during fluid resuscitation, you can take steps to help reduce pressure surface by obtaining a low air-loss mattress and making sure the patient doesn’t lie on a moist, hard surface for extended periods.
Unless volume is restored and bleeding is halted, coagulopathies may develop—and fluid resuscitation can worsen these. Hypovolemic shock also may cause other complications, including:
- systemic infection from use of a large-bore I.V. line for fluid resuscitation
- transfusion reaction if blood transfusions are given
- hypothermia, which may follow trauma, surgery, or infusion of massive amounts of I.V. fluids. Hypothermia may worsen acidosis, so be sure to keep the patient warm. If body temperature drops, warm I.V. fluids externally, apply warm blankets or external warming devices, or increase room temperature.
Promoting an optimal outcome
For a patient in hypovolemic shock, a successful outcome hinges largely on prompt diagnosis and aggressive treatment. Prognosis varies with such factors as how early treatment begins and the degree of shock; in severe shock, death may occur despite immediate treatment.
Elderly patients are particularly likely to have a poor outcome. Mr. Moran, though, was one of the lucky ones. After 2 hours of fluid resuscitation, his blood pressure increased, his heart rate slowed, and his indwelling urinary catheter had collected about 100 ml of output. He’ll be admitted shortly to a general medical unit, where he’ll continue to receive I.V. fluids, but at a lower rate. Thanks largely to nursing expertise and quick action, he was able to avoid disaster. O
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Margaret M. Ecklund, MS, RN, CCRN, APRN-BC, is a Clinician VI/Nurse Practitioner in Pulmonary Medicine at Rochester General Hospital in Rochester, N.Y. Christine R. Ecklund, BSN, RN, is a Staff Nurse at Beth Israel Deaconess Medical Center in Boston, Mass.