Borchers Andrea Ann (ed.) Handbook of Signs & Symptoms 2015

irritation with catheter removal may cause edema or spasms of the detrusor muscle and the external urethral sphincter, thereby blocking urine outflow.

Drugs. Parasympatholytics, anticholinergics, ganglionic blockers, sedatives, anesthetics, and opiates can produce urine retention and bladder distention.

Special Considerations

Monitor the patient’s vital signs and the extent of bladder distention. Encourage the patient to change positions to alleviate discomfort. He may require an analgesic.

Prepare the patient for diagnostic tests (such as endoscopy and radiologic studies) to determine the cause of bladder distention. You may need to prepare him for surgery if interventions fail to relieve bladder distention and obstruction prevents catheterization.

Patient Counseling

Teach the patient to use Valsalva’s maneuver or Credé’s method to empty the bladder. Explain how to stimulate voiding.

Pediatric Pointers

Look for urine retention and bladder distention in infants who fail to void normal amounts. (In the first 48 hours of life, infants excrete about 60 mL of urine; during the next week, they excrete about 300 mL of urine daily.) In males, posterior urethral valves, meatal stenosis, phimosis, spinal cord anomalies, bladder diverticula, and other congenital defects may cause urinary obstruction and resultant bladder distention.

REFERENCES

James, N., Hussain, S., Hall, E., et al. (2010). Results of a 2 × 2 phase III randomized trial of synchronous chemoradiotherapy (CRT) compared to radiotherapy (RT) alone and standard vs. reduced high volume RT in muscle invasive bladder cancer (MIBC) (BC2001 CRUK/01/004). International Journal of Radiation Oncology, Biology, Physics, 78(3), S2–S3.

James, N. D., Hussain, S. A., Hall, E., et al. (2012). Radiotherapy with or without chemotherapy in muscle-invasive bladder cancer. New England Journal of Medicine, 366(16), 1477–1488.

Blood Pressure Decrease[Hypotension]

Low blood pressure refers to inadequate intravascular pressure to maintain the oxygen requirements of the body’s tissues. Although commonly linked to shock, this sign may also result from a cardiovascular, respiratory, neurologic, or metabolic disorder. Hypoperfusion states especially affect the kidneys, brain, and heart and may lead to renal failure, a change in the patient’s level of consciousness (LOC), or myocardial ischemia. Low blood pressure may be drug induced or may accompany diagnostic tests — most commonly those using contrast media. It may stem from stress or change of position — specifically, rising abruptly from a supine or sitting position to a standing position (orthostatic hypotension).

Normal blood pressure varies considerably; what qualifies as low blood pressure for one person may be normal for another. Consequently, every blood pressure reading must be compared against the patient’s baseline. Typically, a reading below 90/60 mm Hg, or a drop of 30 mm Hg from the baseline, is considered low blood pressure.

weight loss, fever, and tachycardia. The patient may also have hyperpigmentation of fingers, nails, nipples, scars, and body folds; pale, cool, clammy skin; restlessness; decreased urine output; tachypnea; and coma.

Alcohol toxicity. Low blood pressure occurs infrequently; more commonly, alcohol toxicity produces distinct alcohol breath odor, tachycardia, bradypnea, hypothermia, a decreased LOC, seizures, a staggering gait, nausea, vomiting, diuresis, and slow, stertorous breathing.

EXAMINATION TIP Ensuring Accurate Blood Pressure

Measurement

When taking the patient’s blood pressure, begin by applying the cuff properly, as shown here.

Then, be alert for these common pitfalls to avoid recording an inaccurate blood pressure measurement.

Wrong-sized cuff. Select the appropriate-sized cuff for the patient. This ensures that adequate pressure is applied to compress the brachial artery during cuff inflation. If the cuff bladder is too narrow, a false-high reading will be obtained; too wide, a false-low reading. The cuff bladder width should be about 40% of the circumference of the midpoint of the limb; bladder length should be twice the width. If the arm circumference is less than 13” (33 cm), select a regular-sized cuff; if it’s between 13” and 16” (33 to 40.5 cm), a largesized cuff; if it’s more than 16”, a thigh cuff. Pediatric cuffs are also available.

Slow cuff deflation, causing venous congestion in the extremity. Don’t deflate the cuff more slowly than 2 mm Hg/heartbeat because you’ll get a false-high reading.

Cuff wrapped too loosely, reducing its effective width. Tighten the cuff to avoid a falsehigh reading.

Mercury column not read at eye level. Read the mercury column at eye level. If the column is below eye level, you may record a false-low reading; if it’s above eye level, a false-high reading.

Tilted mercury column. Keep the mercury column vertical to avoid a false-high reading. Poorly timed measurement. Don’t take the patient’s blood pressure if he appears anxious or has just eaten or ambulated; you’ll get a false-high reading.

Incorrect position of the arm. Keep the patient’s arm level with his heart to avoid a falselow reading.

Cuff overinflation, causing venospasm or pain. Don’t overinflate the cuff because you’ll get a false-high reading.

Failure to notice an auscultatory gap (sound fades out for 10 to 15 mm Hg, then returns). To avoid missing the top Korotkoff sound, estimate systolic pressure by palpation first. Then, inflate the cuff rapidly — at a rate of 2 to 3 mm Hg/second — to about 30 mm Hg above the palpable systolic pressure.

Inaudibility of feeble sounds. Before reinflating the cuff, have the patient raise his arm to reduce venous pressure and amplify low-volume sounds. After inflating the cuff, lower the patient’s arm; then, deflate the cuff and listen. Alternatively, with the patient’s arm positioned at heart level, inflate the cuff and have the patient make a fist. Have him rapidly open and close his hand 10 times before you begin to deflate the cuff, and then listen. Make sure to document that the blood pressure reading was augmented.

Anaphylactic shock. Following exposure to an allergen, such as penicillin or insect venom, a dramatic fall in blood pressure and narrowed pulse pressure signal anaphylactic reaction. Initially, anaphylactic shock causes anxiety, restlessness, a feeling of doom, intense itching (especially of the hands and feet), and pounding headache. Later, it may also produce weakness, sweating, nasal congestion, coughing, difficulty breathing, nausea, abdominal cramps, involuntary defecation, seizures, flushing, change or loss of voice due to laryngeal edema, urinary incontinence, and tachycardia.

Anthrax (inhalation). Anthrax is an acute infectious disease that’s caused by the gram-positive, spore-forming bacterium Bacillus anthracis. Although the disease most commonly occurs in wild and domestic grazing animals, such as cattle, sheep, and goats, the spores can live in the soil for many years. The disease can occur in humans exposed to infected animals, tissue from infected animals, or biological warfare. Most natural cases occur in agricultural regions worldwide. Anthrax may occur in the cutaneous, inhalation, or GI form.

Inhalation anthrax is caused by inhalation of aerosolized spores. Initial signs and symptoms are flulike and include fever, chills, weakness, cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial signs and symptoms. The second stage develops abruptly with rapid deterioration marked by fever, dyspnea, stridor, and hypotension, generally leading to death within 24 hours. Radiologic findings include mediastinitis and symmetric mediastinal widening.

Cardiac arrhythmias. With an arrhythmia, blood pressure may fluctuate between normal and low readings. Dizziness, chest pain, difficulty breathing, light-headedness, weakness, fatigue, and palpitations may also occur. Auscultation typically reveals an irregular rhythm and a pulse rate greater than 100 beats/minute or less than 60 beats/minute.

Cardiac contusion. With cardiac contusion, low blood pressure occurs along with tachycardia and, at times, anginal pain and dyspnea.

Cardiac tamponade. An accentuated fall in systolic pressure (more than 10 mm Hg) during inspiration, known as paradoxical pulse, is characteristic in patients with cardiac tamponade. This disorder also causes restlessness, cyanosis, tachycardia, jugular vein distention, muffled heart sounds, dyspnea, and Kussmaul’s sign (increased venous distention with inspiration).

Cardiogenic shock. A fall in systolic pressure to less than 80 mm Hg or to 30 mm Hg less than

the patient’s baseline because of decreased cardiac contractility is characteristic in patients with cardiogenic shock. Accompanying low blood pressure are tachycardia, narrowed pulse pressure, diminished Korotkoff sounds, peripheral cyanosis, and pale, cool, clammy skin. Cardiogenic shock also causes restlessness and anxiety, which may progress to disorientation and confusion. Associated signs and symptoms include angina, dyspnea, jugular vein distention, oliguria, ventricular gallop, tachypnea, and a weak, rapid pulse.

Cholera. This acute infection, caused by the bacterium Vibrio cholerae , may be mild with uncomplicated diarrhea or severe and life threatening. Cholera is spread by ingesting contaminated water or food, especially shellfish. Signs include abrupt watery diarrhea and vomiting. Severe fluid and electrolyte loss leads to thirst, weakness, muscle cramps, decreased skin turgor, oliguria, tachycardia, and hypotension. Without treatment, death can occur within hours.

Diabetic ketoacidosis. Hypovolemia triggered by osmotic diuresis in hyperglycemia is responsible for the low blood pressure associated with diabetic ketoacidosis, which is usually present in patients with type 1 diabetes mellitus. It also commonly produces polydipsia, polyuria, polyphagia, dehydration, weight loss, abdominal pain, nausea, vomiting, breath with fruity odor, Kussmaul’s respirations, tachycardia, seizures, confusion, and stupor that may progress to coma.

Heart failure. With heart failure, blood pressure may fluctuate between normal and low readings. However, a precipitous drop in blood pressure may signal cardiogenic shock. Other signs and symptoms of heart failure include exertional dyspnea, dyspnea of abrupt or gradual onset, paroxysmal nocturnal dyspnea or difficulty breathing in the supine position (orthopnea), fatigue, weight gain, pallor or cyanosis, sweating, and anxiety. Auscultation reveals ventricular gallop, tachycardia, bilateral crackles, and tachypnea. Dependent edema, jugular vein distention, increased capillary refill time, and hepatomegaly may also occur.

Hyperosmolar hyperglycemic nonketotic syndrome (HHNS). HHNS, which is common in the patient with type 2 diabetes mellitus, decreases blood pressure — at times dramatically — if he loses significant fluid from diuresis due to severe hyperglycemia and hyperosmolarity. It also produces dry mouth, poor skin turgor, tachycardia, confusion progressing to coma, and, occasionally, generalized tonic-clonic seizure.

Hypovolemic shock. A fall in systolic pressure to less than 80 mm Hg or 30 mm Hg less than the patient’s baseline, secondary to acute blood loss or dehydration, is characteristic in hypovolemic shock. Accompanying it are diminished Korotkoff sounds, a narrowed pulse pressure, and a rapid, weak, and irregular pulse. Peripheral vasoconstriction causes cyanosis of the extremities and pale, cool, clammy skin. Other signs and symptoms include oliguria, confusion, disorientation, restlessness, and anxiety.

Hypoxemia. Initially, blood pressure may be normal or slightly elevated, but as hypoxemia becomes more pronounced, blood pressure drops. The patient may also display tachycardia, tachypnea, dyspnea, and confusion and may progress from stupor to coma.

Myocardial infarction (MI). With MI, a life-threatening disorder, blood pressure may be low or high. However, a precipitous drop in blood pressure may signal cardiogenic shock. Associated signs and symptoms include chest pain that may radiate to the jaw, shoulder, arm, or epigastrium; dyspnea; anxiety; nausea or vomiting; sweating; and cool, pale, or cyanotic skin. Auscultation may reveal an atrial gallop, a murmur and, occasionally, an irregular pulse.

Neurogenic shock. The result of sympathetic denervation due to cervical injury or anesthesia,

neurogenic shock produces low blood pressure and bradycardia. However, the patient’s skin remains warm and dry because of cutaneous vasodilation and sweat gland denervation. Depending on the cause of shock, there may also be motor weakness of the limbs or diaphragm.

Pulmonary embolism. Pulmonary embolism causes sudden, sharp chest pain and dyspnea accompanied by a cough and, occasionally, a low-grade fever. Low blood pressure occurs with a narrowed pulse pressure and diminished Korotkoff sounds. Associated signs include tachycardia, tachypnea, a paradoxical pulse, jugular vein distention, and hemoptysis.

Septic shock. Initially, septic shock produces fever and chills. Low blood pressure, tachycardia, and tachypnea may also develop early, but the patient’s skin remains warm. Later, low blood pressure becomes increasingly severe — less than 80 mm Hg or 30 mm Hg less than the patient’s baseline — and is accompanied by narrowed pulse pressure. Other late signs and symptoms include pale skin, cyanotic extremities, apprehension, thirst, oliguria, and coma.

Vasovagal syncope. Vasovagal syncope is the transient loss or near loss of consciousness following stressful, painful, or claustrophobic experiences. It’s characterized by low blood pressure, pallor, cold sweats, nausea, palpitations or slowed heart rate, and weakness.

Other Causes

Diagnostic tests. Diagnostic tests include the gastric acid stimulation test using histamine and X-ray studies using contrast media. The latter may trigger an allergic reaction, which causes low blood pressure.

Drugs. Calcium channel blockers, diuretics, vasodilators, alphaand beta-adrenergic blockers, general anesthetics, opioid analgesics, monoamine oxidase inhibitors, anxiolytics (such as benzodiazepines), tranquilizers, and most I.V. antiarrhythmics (especially bretylium tosylate) can cause low blood pressure.

Special Considerations

Check the patient’s vital signs frequently to determine if low blood pressure is constant or intermittent. If blood pressure is extremely low, an arterial catheter may be inserted to allow close monitoring of pressures. Alternatively, a Doppler flowmeter may be used.

Normal Pediatric Blood Pressure

Hypertension has been reported to be two to three times more common in women taking hormonal contraceptives than those not taking them. Women age 35 and older who smoke cigarettes should be strongly encouraged to stop; if they continue to smoke, they should be discouraged from using hormonal contraceptives.

Elevated blood pressure may develop suddenly or gradually. A sudden, severe rise in pressure (exceeding 180/110 mm Hg) may indicate life-threatening hypertensive crisis. However, even a less dramatic rise may be equally significant if it heralds a dissecting aortic aneurysm, increased intracranial pressure, myocardial infarction, eclampsia, or thyrotoxicosis.

Usually associated with essential hypertension, elevated blood pressure may also result from a renal or endocrine disorder; a treatment that affects fluid status, such as dialysis; or a drug’s adverse effect. Ingestion of large amounts of certain foods, such as black licorice and cheddar cheese, may temporarily elevate blood pressure. (See Pathophysiology of Elevated Blood Pressure.)

Sometimes, elevated blood pressure may simply reflect inaccurate blood pressure measurement. (See Ensuring Accurate Blood Pressure Measurement , page 96.) However, careful measurement alone doesn’t ensure a clinically useful reading. To be useful, each blood pressure reading must be compared with the patient’s baseline. Also, serial readings may be necessary to establish elevated blood pressure.

Pathophysiology of Elevated Blood Pressure

Blood pressure — the force blood exerts on vessels as it flows through them — depends on cardiac output, peripheral resistance, and blood volume. A brief review of its regulating mechanisms — nervous system control, capillary fluid shifts, kidney excretion, and hormonal changes — will help you understand how elevated blood pressure develops.

Nervous system control involves the sympathetic system, chiefly baroreceptors and chemoreceptors, which promotes moderate vasoconstriction to maintain normal blood pressure. When this system responds inappropriately, increased vasoconstriction enhances peripheral resistance, resulting in elevated blood pressure.

Capillary fluid shifts regulate blood volume by responding to arterial pressure. Increased pressure forces fluid into the interstitial space; decreased pressure allows it to be drawn back into the arteries by osmosis. However, this fluid shift may take several hours to adjust blood pressure.

Kidney excretion also helps regulate blood volume by increasing or decreasing urine formation. Normally, an arterial pressure of about 60 mm Hg maintains urine output. When pressure drops below this reading, urine formation ceases, thereby increasing blood volume. Conversely, when arterial pressure exceeds this reading, urine formation increases, thereby reducing blood volume. Like capillary fluid shifts, this mechanism may take several hours to adjust blood pressure.

Hormonal changes reflect stimulation of the kidney’s renin-angiotensin-aldosterone system in response to low arterial pressure. This system affects vasoconstriction, which increases arterial pressure, and stimulates aldosterone release, which regulates sodium retention — a key determinant of blood volume.