Is your patient at risk?
RESPONDING TO SHOCK STAT
CE Offering, 3 ANCC/AACN Contact Hours
SALLY RUSSELL, RN,C, CS, MN
You know that acuity levels are rising in medical/surgical units. Because of that, you have to rethink the type of crises you may have to handle.
Take hypovolemia, for example. Emergency, trauma, and critical care nurses assume their patients are hypovolemic until they know otherwise, so they take steps to prevent hypovolemic shock.
But patients in almost any unit can become hypovolemic. So even if you don't work in the emergency department, trauma unit, or critical care unit, you have to be prepared to recognize and manage hypovolemia and prevent hypovolemic shock.
You're probably already familiar with the classic signs of hypovolemic shock -- decreasing blood pressure, increased pulse and respiratory rates, pale and clammy skin, decreased urine output, and restlessness or confusion. They alert you to investigate further but, unfortunately, they're also relatively late developments. Once they appear, you know the prognosis is poor unless you act quickly.
Meet your patients
Knowing which patients are at risk can be tricky -- hypovolemic shock can occur for so many reasons. Three typical medical/surgical patients illustrate this point.
Philip Jensen, 41, has been admitted with traumatic injuries suffered in a car accident. After a quick assessment and treatment in the emergency department, he underwent surgery to remove his lacerated spleen. He lost approximately 1,500 ml of blood, which was replaced during surgery.
As you do your initial assessment, you note that Mr. Jensen is lethargic but oriented to time and place. His skin is pale, moist, cool, and clammy; his mucous membranes, dry and light pink. You check his vital signs: pulse, 102; blood pressure, 108/66; respirations, 24; and temperature, 99° F (37.2° C). Mr. Jensen is N.P.O. An intravenous (I.V.) solution of 0.9% sodium chloride is infusing at 125 ml/hour, and a nasogastric (NG) tube has evacuated 50 ml of greenish fluid.
David Astley, 51, developed chronic hepatitis 8 years ago after receiving a contaminated blood transfusion. He's been admitted with jaundice and worsening ascites. His distended abdomen is hard and tight on palpation. You also note fresh striae. And he has 3 + pitting edema in his sacral and thigh areas.
Mr. Astley's skin is cool and dry, he's alert and oriented to place and self but not time, and he's restless. His vital signs are: pulse, 110; blood pressure, 112/70; respirations, 28; and temperature, 98.4° F (36.9° C).
An I.V. of 5% dextrose in 0.45% sodium chloride is infusing at 75 ml/hour. Although he says he's thirsty, he refuses the clear liquids you offer because he says "nothing tastes right."
Susan Forester, 83, was admitted with acute small-bowel obstruction caused by adhesions from surgery 6 months ago. An NG tube has evacuated 1,200 ml of a brownish, fecal-smelling liquid. Mrs. Forester also vomited several times before coming to the hospital.
Since she was admitted a few hours ago, her urine output has totaled 50 ml -- and the urine is very concentrated. She's receiving an infusion of 0.9% sodium chloride at 100 ml/hour. Her vital signs are: pulse, 100; blood pressure, 130/64; respirations, 24; and temperature, 99° F (37.2° C). She's also confused.
All three patients are hypovolemic, although their clinical pictures and histories are very different. You don't yet have enough evidence to determine whether they're headed toward hypovolemic shock, so you'll need to be alert to subtle changes that signal an impending crisis.
Actual vs. relative hypovolemia
Philip Jensen, you'll recall, lost 1,500 ml of blood. This is the classic picture of actual, or true, hypovolemia, which occurs when fluid is lost from the intravascular space and the body. Hemorrhage, burns, vomiting, diarrhea, and severe sodium loss are the most common causes. Patients will lose weight and have dry skin and mucous membranes, poor skin turgor, narrowed pulse pressure (the difference between the systolic and diastolic pressures), decreased systolic pressure, and a diminished level of consciousness.
David Astley, who has jaundice and worsening ascites, is typical of patients who suffer relative hypovolemia, also called third-spacing. Fluid is lost from the intravascular space but not from the body. Patients who've been burned, for example, experience dramatic third-spacing. Because of increased capillary permeability, fluid easily travels across vascular membranes. The same is true of patients in septic shock.
Mr. Astley's peritoneum is filled with a protein-rich fluid that draws fluid from the vascular and intracellular spaces. This fluid accumulation is increasing, indicated by the fresh striae. And because he also has pitting edema in his sacral and thigh areas, you suspect that fluid is escaping from vessels.
Initially, you aren't concerned about Mr. Astley's blood pressure -- until you review his chart and discover that he's usually hypertensive. The latest reading in his doctor's office was 186/92. If you hadn't checked, you would have missed a clue to hypovolemia. Mr. Astley is thirsty too. That's another indicator of hypovolemia that you might miss.
Susan Forester has a combination of actual and relative fluid loss, which is typical of acute small-bowel obstruction. Initially, gastrointestinal secretions accumulate because they can't get past the obstruction. So water isn't reabsorbed by the large intestines and returned to the vascular space. This is relative loss because the fluid hasn't left the body -- it's still in the small bowel. Actual loss doesn't occur until the patient begins vomiting or an NG tube evacuates the fluid.
In Mrs. Forester's case, the acute small-bowel obstruction first caused third-spacing into the gastrointestinal lumen (relative hypovolemia). Then, at home, she began to vomit. The NG tube inserted in the hospital removed even more fluid (actual hypovolemia). She's begun to exhibit early signs and symptoms of hypovolemia: decreased output of increasingly concentrated urine, apparent confusion, and a diastolic blood pressure of 64, which is low for someone her age.
With a patient like Philip Jensen, David Astley, or Susan Forester, you'd do a head-to-toe assessment at the first sign of trouble, even if the first sign is just your gut feeling that something isn't right. These assessments are critical -- the longer the diagnosis and interventions are delayed, the poorer the overall prognosis will be.
¥ Neurologic system. The brain, as you know, is very sensitive to decreasing oxygen levels. So you can learn a lot about the blood's ability to supply oxygen by assessing the patient's level of consciousness. Ask him his name, where he is, and why he's there. Also observe for restlessness, agitation, or lethargy.
Compare your results with the baseline assessment to see if anything has changed. And check for laboratory results that indicate metabolic or electrolyte abnormalities.
The baseline assessment is crucial. Suppose, for example, you didn't know how well Mrs. Forester was oriented previously. Because of her age, you might assume she's confused because of other health problems. So you'd miss an important clue to a developing problem.
If you don't have a baseline assessment, discuss the patient's usual mental status with the family. Or if the patient had been transferred from another facility, call the nursing staff there to get more information. (The transfer sheet may say what a patient can do but not how well oriented he is.)
¥ Cardiac system. Expect to take the patient's vital signs as often as every 5 minutes -- you might use a noninvasive automatic vital signs monitor if one is available. Expect to see a compensatory increase in the heart rate as the blood pressure decreases. Keep a careful record so you can watch the overall picture -- trends give a better indication of the patient's status than any single reading.
Also watch for changes in the pulse pressure. A narrowing in the pulse pressure, an early symptom of hypovolemic shock, reflects a decrease in stroke volume and peripheral vasoconstriction.
Frequently assess the radial pulse (and periodically check the brachial, pedal, and popliteal pulses), noting its rate, strength, and regularity. Correlate it with the apical pulse.
You'll know your patient is getting into trouble when the peripheral pulses become harder to detect. As the systolic blood pressure (and blood volume) drops below 80 mm Hg, you'll lose the radial pulse. So you'll have to correlate the apical pulse with the more central pulses, such as the brachial or femoral pulses.
¥ Respiratory system. Assess the patient's airway patency. Then note the respiratory rate, the depth and ease of respirations, whether chest wall expansion is equal bilaterally, and whether the patient is using accessory muscles during inspiration. But don't rely solely on your examination findings -- ask the patient if he's having trouble breathing. Some patients say they feel they aren't getting enough air even if they don't seem to be having any difficulty. Use a pulse oximeter for a more accurate assessment of what's really happening to your patient.
Auscultate the lungs to check whether fluid is shunting into lung tissue. Be especially alert for crackles, which would indicate fluid in the smaller airways of the lung parenchyma. Gurgles (fluid) and wheezing (narrowing) are clues to obstruction of the larger airways, although they would be late findings of fluid accumulation.
¥ Renal system. Urine output is a direct indicator of cardiac output, the amount of blood the heart ejects each minute. The kidneys receive 25% of cardiac output, so if the urine volume drops acutely, you can assume that cardiac output has dropped as well. To monitor urine output, obtain an order to catheterize the patient. Use a urine meter to measure the urine output hourly, and immediately call the doctor if the volume falls below 30 ml/hour. Also, you might need to obtain urine samples for sodium, specific gravity, and acetone testing as often as every 4 hours.
¥ Gastrointestinal tract. Assess bowel sounds frequently. Expect to hear hypoactive bowel sounds if the patient's fluid volume is low enough to cause hypoxia to the mucosa. Bowel sounds can also reflect the disorder causing hypovolemia (such as ascites or bowel obstruction).
¥ Neurosensory system. Ask about pain and pressure sensations. Is a specific area painful? The answer could tell you where a hemorrhage is occurring.
For example, a patient who's bleeding into his abdomen may complain of back pain if he's lying on his back. Or a patient who's just had a specific procedure, such as a femoral arterial puncture, may have neurosensory changes in the affected arm or leg. After a femoral arterial puncture, for example, a patient who's bleeding into the groin might begin to feel numbness or coolness in his toes. Remember, too, that a vague feeling of unease or impending doom may precede shock.
¥ Skin. The skin and mucous membranes will be pale if the patient has either actual or relative blood loss. Patients with relative loss might appear normal, although some color change usually occurs because of decreased perfusion and compensatory peripheral vasoconstriction (an attempt to maintain blood in the central circulation). Cyanosis, an extremely late sign of hypoxia, indicates a poor prognosis.
Typically, a hypovolemic patient's skin will be cool because of the lack of perfusion. But that's not an absolute rule: The patient's skin could be cool normally. And don't be fooled into thinking the patient is fine if his skin is warm -- another pathology could be raising the temperature.
Skin turgor can generally be used to assess skin, but not always in elderly patients: The fluid loss that's part of the normal aging process can cause changes in skin turgor. So assess the mucous membranes for more valuable information about hydration. Normally, they're moist and pink. Or assess skin turgor over the sternum, not on the arms and legs. Also, check for weight changes.
How you can intervene
Hypovolemia isn't caused by a problem with the heart's pumping ability but with the amount of vascular volume available to be pumped by the heart.
The body's compensatory mechanisms attempt to take over when vascular volume drops. The baroreceptors in the aortic arch and the carotid arteries are the major stimuli for this attempt. These baroreceptors react to varying fluid pressure by sending signals to autonomic regulatory centers in the central nervous system, causing vessels to constrict or dilate.
Your nursing interventions will center on supporting the compensatory mechanisms. Start by placing the patient in a supine position with his legs elevated. (If this worsens his respiratory difficulty, raise the head of the bed 30 to 45 degrees.) This will promote venous blood return to the heart, improving cardiac output and perfusion to vital organs.
If the patient's head were below heart level, pressure on the baroreceptors in the aortic arch and carotid arteries would increase, causing them to send signals consistent with elevated blood pressure. This would also increase the patient's respiratory problems and anxiety.
The patient may be unable to maintain a patent airway if his level of consciousness is impaired. So be alert for respiratory changes and keep an oral or nasal airway handy in case problems develop. Turn him on his side if you're concerned about aspiration.
A patient who's hypovolemic needs supplemental oxygen to meet his body's high metabolic demand. If you can't reach the patient's doctor for an order, follow your institution's standing orders for low-flow oxygen (but continue trying to reach the doctor because a higher oxygen level would be better). Also keep in mind that the doctor may order intubation and mechanical ventilation or a continuous positive airway pressure meter to deliver a higher oxygen level than can be given through nasal prongs or a regular mask.
Continue the cardiac assessments you began earlier. An electrocardiogram may be needed to determine if the patient's heart has been affected.
Be prepared to administer large amounts of fluids, maybe even blood products. (See Using Fluids to Treat Hypovolemic Shock) If venous access isn't already established, insert two 16- to 18-gauge catheters. You may have to use two smaller catheters at first if the patient's vessels are severely constricted. Or the doctor may insert a central venous catheter after peripheral access is established (or if peripheral access isn't possible) to evaluate fluid status and the response to fluid challenges.
Once the I.V. fluids are infusing, carefully monitor intake and output. Watch, too, for signs of fluid overload (moist respirations, respiratory distress, and increased central venous pressure and jugular venous distension), which could easily occur if fluid is replaced faster than the body can tolerate it.
Although you wouldn't immediately deal with gastrointestinal problems, continue to auscultate bowel sounds. Blood is shunted away from the gastrointestinal tract in extreme hypovolemia. Ischemic changes in the organs will set the stage for complications, such as gastric ulcerations or sepsis.
Skin care is important too. The patient is at risk for skin breakdown because of poor perfusion, moisture from the clamminess caused by shock, edema from third-spacing, and immobility.
Keep the patient covered with a light blanket to decrease shivering. But be alert for vasodilation -- if the patient's skin is warm and dry, you've added too many layers.
Any patient who's at risk for hypovolemic shock is going to be scared. Let him know what's going on, and periodically reassure him. By maintaining a calm manner, you can prevent panic, which would put more stress on the patient's already-stressed body. Also, include the family in your updates, and allow them to visit whenever possible (even if visits are short).
How are your patients faring?
What happened with Philip Jensen, David Astley, and Susan Forester?
Because of his traumatic injuries, Mr. Jensen quickly became hypovolemic. During your initial assessment, you found that he was pale, cool, clammy, and oriented though lethargic. His mucous membranes were dry, and you found no evidence of blood loss (his dressings were dry and his abdomen was soft and flat with no distension on palpation or back pain). His vital signs, particularly his blood pressure, pointed to hypovolemic shock.
The doctor decided to increase Mr. Jensen's infusion of 0.9% sodium chloride to 150 ml/hour. (Depending on his hemoglobin and hematocrit levels, he might have needed blood products as well.) Over the next 3 hours, Mr. Jensen became less lethargic. His skin was cool but no longer clammy, his blood pressure had increased to 128/78, his heart rate was 90, and his respirations were 20. He'll be continually observed for signs of a recurrence.
Mr. Astley's care was more complex -- his hypovolemia was caused by liver disease, not overt blood loss. His decreased blood pressure and increased pulse rate were early signs of hypovolemia.
As the evening went on, you noted that his respiratory effort was increasing -- he was using his accessory muscles to breathe and grunting on inspiration because of abdominal fluid pressing on his diaphragm. His urine output also dropped to 30 ml/hour. You knew he was at high risk for hypovolemic shock as more fluid was pulled into his abdomen from the intravascular space (osmolality of fluid in the peritoneal cavity is generally higher than that of serum in patients with liver disease).
Mr. Astley's doctor ordered 25% albumin to replace the albumin in his serum and pull fluid back into the vascular space from the peritoneum. This increased his vascular volume without increasing peripheral edema. If his respiratory distress continues, the doctor may perform a paracentesis.
Although Mr. Astley's vital signs improved during your shift, they didn't return to his preshock level, and his urine output remained low. His prognosis was guarded, and he may remain hypovolemic for some time.
Mrs. Forester was quickly approaching hypovolemic shock. While awaiting surgery, she was still experiencing actual and relative fluid loss. Her low urine output indicated that her kidneys weren't well perfused, and her blood pressure (particularly her diastolic pressure) was lower than normal for an 83-year-old woman. She'd been restless, pulling at her NG tube.
As ordered, you increased her infusion of 0.9% sodium chloride to 125 ml/hour and switched from continuous to low intermittent NG suctioning; this decreased the amount of fluid evacuated each hour. Potassium replacement therapy will be ordered based on her serum chemistry results. When she received preoperative medication, she was more alert and her urine output had increased. The higher fluid intake had no effect on her respiratory or cardiovascular status.
No one wants to care for three patients who are at risk for hypovolemic shock at the same time. And, fortunately, you probably won't ever have to.
Understanding why hypovolemic shock occurs and which patients are at risk will give you an edge in heading it off. That doesn't mean you can relax. But it can help you get through your shift with confidence.
Burrell, L.: Adult Nursing in Hospital and Community Settings. East Norwalk, Conn., Appleton & Lange, 1992.
Chowdry, P.: Pathophysiology and Practical Applications. Dubuque, Iowa, William C. Brown, 1993.
Flavell, C.: "Combating Hemorrhagic Shock," RN. 57(12):26-31, December 1994.
Metheny, N.: Fluid and Electrolyte Balance: Nursing Considerations, 2nd edition. Philadelphia, J.B. Lippincott Co., 1992.
Phillips, L.: Manual of I.V. Therapeutics. Philadelphia, F.A. Davis, 1993.
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