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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2920_Библиотеки_им_академика_М_И_Перельмана
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analysis at least once a day. The patient may
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need X-ray studies and further blood work to
determine the cause of absent bowel sounds.
After mechanical obstruction and intraabdominal sepsis have been ruled out as the
cause of absent bowel sounds, give the patient
drugs to control pain and stimulate peristalsis.
P
EDIATRIC POINTERS
Absent bowel sounds in children may result
from Hirschsprung’s disease or intussusception,
both of which can lead to life-threatening obstruction.
G
ERIATRIC POINTERS
Older patients with a bowel obstruction that
doesn’t respond to decompression should be
considered for early surgical intervention to
avoid the risk of bowel infarct.
BOWEL SOUNDS, HYPERACTIVE
Characteristics of bowel
sounds
The sounds of swallowed air and fluid moving through the GI tract are known as bowel
sounds. These sounds usually occur every 5
to 15 seconds, but their frequency may be
irregular. For example, bowel sounds are
normally more active just before and after a
meal. They may last less than 1 second or
up to several seconds.
Normal bowel sounds can be character-
ized as murmuring, gurgling, or tinkling.
Hyperactive bowel sounds can be characterized as loud, gurgling, splashing, and rushing; they’re higher pitched and occur more
frequently than normal sounds. Hypoactive
bowel sounds are softer or lower in tone and
occur less frequently than normal sounds.
101
Bowel sounds, hyperactive
Sometimes audible without a stethoscope, hyperactive bowel sounds reflect increased intestinal motility (peristalsis). They’re commonly
characterized as rapid, rushing, gurgling waves
of sounds. (See Characteristics of bowel sounds.)
They may stem from life-threatening bowel obstruction or GI hemorrhage or from GI infection,
inflammatory bowel disease (which usually follows a chronic course), food allergies, or stress.
(See Hyperactive bowel sounds: Causes and asso-
ciated findings, page 102.)
EMERGENCY INTERVENTIONS After
detecting hyperactive bowel sounds, quickly
check vital signs and ask the patient about associated symptoms, such as abdominal pain, vomiting, and diarrhea. If he reports cramping abdominal pain or vomiting, continue to auscultate for
bowel sounds. If bowel sounds stop abruptly, suspect complete bowel obstruction. Prepare to assist
with GI suction and decompression and to give
I.V. fluids and electrolytes, and prepare the patient
for surgery.
If the patient has diarrhea, record its frequency,
amount, color, and consistency. If you detect excessive watery diarrhea or bleeding, prepare to
administer an antidiarrheal, I.V. fluids and electrolytes and, possibly, blood transfusions.
GENDER CUE Homosexual males who
report acute diarrhea and who have negative
fecal ova and parasite cultures may be infected
with chlamydial proctitis not associated with lymphogranuloma venereum. Because rectal cultures
will probably be negative, treatment with tetracycline is appropriate.
H
ISTORY AND PHYSICAL
EXAMINATION
If you’ve ruled out life-threatening conditions,
obtain a detailed medical and surgical history.
Ask the patient if he has had a hernia or abdominal surgery because these may cause mechanical intestinal obstruction. Does he have a history
of inflammatory bowel disease? Also, ask about
recent episodes of gastroenteritis among family
members, friends, or coworkers. If the patient
has traveled recently, even within the United
States, was he aware of any endemic illnesses?
In addition, determine whether stress may
have contributed to the patient’s problem. Ask
about food allergies and recent ingestion of unusual foods or fluids. Check for fever, which suggests infection. Having already auscultated, now
gently inspect, percuss, and palpate the abdomen.
M
EDICAL CAUSES
◆ Crohn’s disease. Hyperactive bowel sounds
usually arise insidiously in Crohn’s disease. Associated signs and symptoms include diarrhea,
cramping abdominal pain that may be relieved
by defecation, anorexia, low-grade fever, abdominal distention and tenderness and, in
many cases, a fixed mass in the right lower
quadrant. Perianal and vaginal lesions are common. Muscle wasting, weight loss, and signs of
dehydration may occur as Crohn’s disease progresses.
102 BOWEL SOUNDS, HYPERACTIVE
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SIGNS & SYMPTOMS
Hyperactive bowel sounds:
Causes and associated findings
Major associated signs and symptoms
Common
causes
Crohn’s disease
Food
hypersensitivity
Gastroenteritis
GI hemorrhage
Mechanical
intestinal
obstruction
Ulcerative colitis
(acute)
◆ Food hypersensitivity. Malabsorption—
typically lactose intolerance—may cause hyperactive bowel sounds. Associated signs and
symptoms include diarrhea and, possibly, nausea and vomiting, angioedema, and urticaria.
◆ Gastroenteritis. Hyperactive bowel sounds
follow sudden nausea and vomiting and accompany “explosive” diarrhea. Abdominal cramping
or pain is common, often after a peristaltic
wave. Fever may occur, depending on the
causative organism.
◆ GI hemorrhage. Hyperactive bowel sounds
provide the most immediate indication of persistent upper GI bleeding. Other findings include
hematemesis, coffee-ground vomitus, abdominal distention, bloody diarrhea, rectal passage
of bright red clots and jellylike material or melena, and pain during bleeding. Decreased urine
output, tachycardia, and hypotension accompany blood loss.
◆ Mechanical intestinal obstruction. Hyper-
active bowel sounds occur simultaneously with
cramping abdominal pain every few minutes in
Abdominal
distention
Abdominal pain
Anorexia
•
•
•
••
•
•
•• •
•
••• •
Constipation
Diarrhea
Fever
Nausea
Perianal lesions
Rectal
bleeding
Vomiting
••
•
•
•
•
•
•
•
••
•
patients with mechanical intestinal obstruction—
a potentially life-threatening disorder. Bowel
sounds may later become hypoactive and then
disappear. Nausea and vomiting occur earlier
and with greater severity in small-bowel obstruction than in large-bowel obstruction. In
complete bowel obstruction, hyperactive
sounds are also accompanied by abdominal distention and constipation, although the part of
the bowel distal to the obstruction may continue to empty for up to 3 days.
◆ Ulcerative colitis (acute). Hyperactive bowel
sounds arise abruptly in patients with ulcerative
colitis and are accompanied by bloody diarrhea,
anorexia, abdominal pain, nausea and vomiting, fever, and tenesmus. Weight loss, arthralgia, and arthritis may occur.
S
PECIAL CONSIDERATIONS
Prepare the patient for diagnostic tests, which
may include endoscopy to view a suspected lesion, barium X-rays, or stool analysis.
Weight loss
•
BOWEL SOUNDS, HYPOACTIVE
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103
P
EDIATRIC POINTERS
Hyperactive bowel sounds in children usually
result from gastroenteritis, erratic eating habits,
excessive ingestion of certain foods (such as
unripened fruit), or food allergy.
P
ATIENT COUNSELING
Explain prescribed dietary changes to the patient. These may range from complete food and
fluid restrictions to a liquid or bland diet. Because stress often precipitates or aggravates
bowel hyperactivity, teach the patient relaxation
techniques such as deep breathing. Encourage
rest and restrict the patient’s physical activity.
Bowel sounds, hypoactive
Hypoactive bowel sounds, detected by auscultation, are diminished in regularity, tone, and
loudness from normal bowel sounds. In themselves, hypoactive bowel sounds don’t herald
an emergency; in fact, they’re considered normal during sleep. However, they may portend
absent bowel sounds, which can indicate a lifethreatening disorder.
Hypoactive bowel sounds result from decreased peristalsis, which, in turn, can result
from a developing bowel obstruction. The obstruction may be mechanical (as from a hernia,
tumor, or twisting), vascular (as from an embolism or thrombosis), or neurogenic (as from
mechanical, ischemic, or toxic impairment of
bowel innervation). Hypoactive bowel sounds
can also result from the use of certain drugs,
abdominal surgery, and radiation therapy.
H
ISTORY AND PHYSICAL
EXAMINATION
After detecting hypoactive bowel sounds, look
for related symptoms. Ask the patient about the
location, onset, duration, frequency, and severity
of any pain. Cramping or colicky abdominal
pain usually indicates a mechanical bowel obstruction, whereas diffuse abdominal pain usually indicates intestinal distention related to
paralytic ileus.
Ask the patient about any recent vomiting:
When did it begin? How often does it occur?
Does the vomitus look bloody? Also, ask about
any changes in bowel habits: Does he have a
history of constipation? When was the last time
he had a bowel movement or expelled gas?
Obtain a detailed medical and surgical history
of any conditions that may cause mechanical
bowel obstruction, such as an abdominal tumor
or hernia. Does the patient have a history of severe pain; trauma; conditions that can cause
paralytic ileus such as pancreatitis; bowel inflammation or gynecologic infection, which may
produce peritonitis; or toxic conditions such as
uremia? Has he recently had radiation therapy
or abdominal surgery, or ingested a drug such
as an opiate, which can decrease peristalsis and
cause hypoactive bowel sounds?
After the history is complete, perform a careful physical examination. Inspect the abdomen
for distention, noting surgical incisions and obvious masses. Gently percuss and palpate the
abdomen for masses, gas, fluid, tenderness, and
rigidity. Measure abdominal girth to detect any
subsequent increase in distention. Also check
for poor skin turgor, hypotension, narrowed
pulse pressure, and other signs of dehydration
and electrolyte imbalance, which may result
from paralytic ileus.
M
EDICAL CAUSES
◆ Mechanical intestinal obstruction. Bowel
sounds may become hypoactive after a period
of hyperactivity. The patient may also have
acute colicky abdominal pain in the quadrant of
obstruction, possibly radiating to the flank or
lumbar region; nausea and vomiting (the higher
the obstruction, the earlier and more severe the
vomiting); constipation; and abdominal distention and bloating. If the obstruction becomes
complete, signs of shock may occur.
◆ Mesenteric artery occlusion. After a brief
period of hyperactivity, bowel sounds become
hypoactive and then quickly disappear, signifying a life-threatening crisis. Associated signs
and symptoms include fever; a history of colicky
abdominal pain leading to sudden and severe
midepigastric or periumbilical pain, followed by
abdominal distention and possibly bruits; vomiting; constipation; and signs of shock. Abdominal rigidity may appear late.
◆ Paralytic (adynamic) ileus. Bowel sounds
are hypoactive and may become absent in this
disorder. Associated signs and symptoms include abdominal distention, generalized discomfort, and constipation or passage of small,
liquid stools and flatus. If the disorder follows
acute abdominal infection, fever and abdominal
pain may occur.
O
THER CAUSES
◆ Drugs. Certain classes of drugs reduce in-
testinal motility and thus produce hypoactive
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bowel sounds. These include opiates such as
codeine, anticholinergics such as propantheline
bromide, phenothiazines such as chlorpromazine, and vinca alkaloids such as vincristine.
General or spinal anesthetics produce transient
hypoactive sounds.
◆ Radiation therapy. Hypoactive bowel
sounds and abdominal tenderness may occur
after irradiation of the abdomen.
◆ Surgery. Hypoactive bowel sounds may oc-
cur after manipulation of the bowel. Motility
and bowel sounds in the small intestine usually
resume within 24 hours; colonic bowel sounds,
in 3 to 5 days.
S
PECIAL CONSIDERATIONS
Frequently evaluate the patient with hypoactive
bowel sounds for indications of shock (thirst;
anxiety; restlessness; tachycardia; cool, clammy
skin; weak, thready pulse), which can develop if
peristalsis continues to diminish and fluid is lost
from the circulation.
Be alert for the sudden absence of bowel
sounds, especially in postoperative and hypokalemic patients because they’re at increased
risk for paralytic ileus. Monitor the patient’s
vital signs and auscultate for bowel sounds
every 2 to 4 hours.
Severe pain, abdominal rigidity, guarding,
and fever, accompanied by hypoactive bowel
sounds, may indicate paralytic ileus from peritonitis. If these signs and symptoms occur, prepare for emergency interventions. (See “Bowel
sounds, absent,” page 99.)
The patient with hypoactive bowel sounds
may require GI suction and decompression, using a nasogastric or intestinal tube. If so, restrict
the patient’s oral intake. Then elevate the head
of the bed at least 30 degrees, and turn the patient on his right side to facilitate passage of the
tube through the GI tract.
Remember not to tape an intestinal tube to
the patient’s face. Ensure tube patency by
watching for drainage and properly functioning
suction devices. Irrigate the tube and closely
monitor drainage.
Continue to administer I.V. fluids and electrolytes, and send a serum specimen to the laboratory for electrolyte analysis at least once a
day. Recognize that the patient may need X-ray
studies, endoscopic procedures, and further
blood work to determine the cause of hypoactive bowel sounds.
Provide comfort measures as needed. SemiFowler’s position offers the best relief for the
patient with paralytic ileus. Sometimes, getting
the patient to ambulate can reactivate the sluggish bowel. However, if the patient can’t tolerate ambulation, range-of-motion exercises or
turning from side to side may stimulate peristalsis. Turning the patient from side to side also
helps move gas through the intestines.
P
EDIATRIC POINTERS
Hypoactive bowel sounds in a child may simply
be due to bowel distention from excessive swallowing of air while the child was eating or crying. However, be sure to observe the child for
further signs of illness. As with an adult, sluggish bowel sounds in a child may signal the onset of paralytic ileus or peritonitis.
Bradycardia
Bradycardia refers to a heart rate of less than
60 beats/minute. It occurs normally in young
adults, trained athletes, and elderly people as
well as during sleep. It’s also a normal response
to vagal stimulation caused by coughing, vomiting, or straining during defecation. When bradycardia results from these causes, the heart rate
rarely drops below 40 beats/minute. However,
when it results from pathologic causes (such as
cardiovascular disorders), the heart rate may be
slower.
By itself, bradycardia is a nonspecific sign.
However, together with such symptoms as chest
pain, dizziness, syncope, and shortness of
breath, it can signal a life-threatening disorder.
(See Differential diagnosis: Bradycardia, pages
106 and 107.)
H
ISTORY AND PHYSICAL
EXAMINATION
After detecting bradycardia, check for related
signs of life-threatening disorders. (See Manag-
ing severe bradycardia.) If bradycardia isn’t accompanied by untoward signs, ask the patient if
he or a family member has a history of a slow
pulse rate because this may be inherited. Also,
find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he’s
taking and if he’s complying with the prescribed
schedule and dosage. Monitor vital signs, temperature, pulse rate, respirations, blood pressure, and oxygen saturation.
EMERGENCY INTERVENTION
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Managing severe bradycardia
BRADYCARDIA
105
Bradycardia can signal prolonged exposure to
cold; head or neck trauma; or a life-threatening
disorder when accompanied by pain, shortness of breath, dizziness, syncope, or other
symptoms. In such patients, quickly take vital
signs. Connect the patient to a cardiac monitor, and insert an I.V. catheter. Depending on
the cause of bradycardia, you’ll need to
administer fluids, atropine, steroids, or thyroid
medication. If indicated, insert an indwelling
urinary catheter. Intubation, mechanical ventilation, or placement of a pacemaker may be
necessary if the patient’s respiratory rate falls.
If appropriate, perform a focused evaluation
to help locate the cause of bradycardia. For example, ask about pain. Viselike pressure or
crushing or burning chest pain that radiates to
the arms, back, or jaw may indicate an acute
M
EDICAL CAUSES
◆ Cardiac arrhythmias. Depending on the
type of arrhythmia and the patient’s tolerance of
it, bradycardia may be transient or sustained
and benign or life-threatening. Related findings
include hypotension, palpitations, dizziness,
weakness, syncope, and fatigue.
◆ Cardiomyopathy. Cardiomyopathy is a po-
tentially life-threatening disorder that may
cause transient or sustained bradycardia. Other
findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.
◆ Cervical spinal injury. Bradycardia may
be transient or sustained, depending on the
severity of the injury. Its onset coincides with
sympathetic denervation. Associated signs and
symptoms include hypotension, decreased
body temperature, slowed peristalsis, leg paralysis, and partial arm and respiratory muscle
paralysis.
◆ Hypothermia. Bradycardia usually appears
when the core temperature drops below 89.6° F
(32° C). It’s accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and
confusion leading to stupor.
◆ Hypothyroidism. Hypothyroidism causes se-
vere bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity
to cold. Related signs include cool, dry, thick
skin; sparse, dry hair; facial swelling; periorbital
myocardial infarction (MI); a severe headache
may indicate increased intracranial pressure.
Also ask about nausea, vomiting, or shortness
of breath—signs and symptoms associated
with an acute MI and cardiomyopathy. Observe the patient for peripheral cyanosis, edema, or jugular vein distention, which may indicate cardiomyopathy. Look for a thyroidectomy
scar because severe bradycardia may result
from hypothyroidism caused by failure to take
thyroid hormone replacements.
If the cause of bradycardia is evident, provide supportive care. For example, keep the
hypothermic patient warm by applying blankets, and monitor his core temperature until it
reaches 99⬚ F (37.2⬚ C); stabilize the head and
neck of a trauma patient until cervical spinal
injury is ruled out.
edema; thick, brittle nails; and confusion leading to stupor.
◆ Increased intracranial pressure (ICP).
Bradycardia occurs as a late sign of increased
ICP along with rapid respiratory rate, elevated
systolic pressure, decreased diastolic pressure,
and widened pulse pressure. Associated signs
and symptoms include persistent headache,
projectile vomiting, decreased level of consciousness (LOC), and fixed, unequal, and possibly dilated pupils.
◆ Myocardial infarction (MI). Sinus bradycar-
dia is the most common arrhythmia associated
with an acute MI. Accompanying signs and
symptoms of an MI include an aching, burning,
or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric
area; nausea and vomiting; cool, clammy, and
pale or cyanotic skin; anxiety; and dyspnea.
Blood pressure may be elevated or depressed.
Auscultation may reveal abnormal heart
sounds.
O
THER CAUSES
◆ Diagnostic tests. Cardiac catheterization
and electrophysiologic studies can induce temporary bradycardia.
◆ Drugs. Beta-adrenergic blockers, some cal-
cium channel blockers, cardiac glycosides,
topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics,
(Text continues on page 108.)
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Differential diagnosis: Bradycardia
History of present illness
Focused physical examination: Vital signs; thyroid, cardiovascular,
neurologic, and pulmonary systems
Cardiac arrhythmia
Signs and symptoms
◆ Bradycardia (transient or
sustained)
◆ Hypotension
◆ Palpitations
◆ Dizziness or syncope
◆ Nausea
◆ Weakness or fatigue
◆ Pallor
Diagnosis: Laboratory tests
(arterial blood gas analysis,
complete blood count, cardiac enzymes, electrolytes,
glucose), electrocardiogram
(ECG), 24-hour Holter monitoring
Treatment: Medication
(antiarrhythmic, vagolytic),
pacemaker
Follow-up: Referral to cardiologist
Cardiomyopathy
Signs and symptoms
◆ Bradycardia (transient or
sustained)
◆ Dizziness or syncope
◆ Edema
◆ Jugular vein distention
◆ Fatigue
◆ Orthopnea
◆ Dyspnea
◆ Peripheral cyanosis
◆ Chest pain
Diagnosis: Drug screen,
electrolytes, imaging studies
(chest X-ray, echocardiogram), ECG, cardiac catheterization
Treatment: Medication
(antiarrhythmics, diuretics,
angiotensin-converting enzyme inhibitors); oxygen
therapy; limited activity;
low-fat, low-salt diet
Follow-up: Referral to cardiologist
Cervical spine injury
Signs and symptoms
◆ Bradycardia (transient or
sustained)
◆ Hypotension
◆ Hypothermia
◆ Slowed peristalsis
◆ Leg paralysis
◆ Partial arm paralysis
Diagnosis: History of trauma, imaging studies (computed tomography [CT]
scan, magnetic resonance
imaging [MRI] of spine)
Treatment: Spine stabilization, corticosteroids
Follow-up: Transfer to
spinal injury center
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Hypothyroidism
Signs and
symptoms
◆ Fatigue
◆ Constipation
◆ Weight gain
◆ Cold sensitivity
◆ Cool, dry, thick skin
◆ Sparse, dry hair
◆ Alopecia
◆ Facial swelling
◆ Periorbital edema
◆ Thick, brittle nails
◆ Neck swelling
◆ Goiter
Diagnosis: Thyroid
studies, ECG
Treatment: Thyroid
hormone replacement
Follow-up: Return
visits every 4 to 6
weeks until thyroidstimulating hormone
level is normal, then
every 6 months
Myocardial
infarction
Signs and
symptoms
◆ Chest, back, or ab-
dominal pain
◆ Shortness of breath
◆ Cough
◆ Dizziness
◆ Nausea and vomit-
ing
◆ Diaphoresis
◆ Anxiety
Diagnosis: Laboratory
tests (isoenzymes,
troponin I and T),
imaging studies
(angiography, echocardiogram), ECG,
cardiac catheterization
Treatment: Medication (aspirin, nitrates,
analgesics, thrombolytics, anticoagulants,
beta-adrenergic
blockers, vasopressors), oxygen therapy,
angioplasty, coronary
artery bypass graft
Follow-up: Referral
to cardiologist; return
visit 3 to 6 weeks after hospitalization,
then every 3 months
Hypothermia
Signs and
symptoms
◆ Temperature be-
low 89.6° F (32° C)
◆ Shivering
◆ Peripheral
cyanosis
◆ Muscle rigidity
◆ Bradypnea
◆ Confusion and
stupor
Diagnosis: Temperature, ECG
Treatment: Establishment of ABCs
(airway, breathing,
circulation), temperature monitoring, warm I.V.
fluids, warming
blanket, treatment
of underlying cause
(if physiologic)
Follow-up: Return
visit 2 weeks after
hospitalization
Intracranial
hypertension
Signs and
symptoms
◆ Bradypnea or
tachypnea
◆ Widened pulse
pressure
◆ Persistent head-
ache
◆ Projectile vom-
iting
◆ Fixed, unequal,
or dilated pupils
◆ Decreased level
of consciousness
Diagnosis: Imaging studies (CT
scan, MRI)
Treatment: Treatment of underlying
cause, medication
(osmotic diuretics,
barbiturates), ventilatory support
Follow-up: Referral to neurologist
or neurosurgeon
Other causes: beta-adrenergic blockers ◆ cardiac glycosides ◆ cardiac surgery ◆ diagnostic tests
(cardiac catheterization, electrophysiologic studies)
mine sulfate
◆ sympatholytics ◆ topical miotics
◆ quinidine and other antiarrhythmics ◆ some calcium channel blockers ◆ suctioning
◆ failure to take thyroid replacements ◆ prota-
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and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may
cause bradycardia.
◆ Invasive treatments. Suctioning can induce
hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or
damage to conduction tissues, causing bradycardia.
S
PECIAL CONSIDERATIONS
Continue to monitor vital signs frequently. Be
especially alert for changes in cardiac rhythm,
respiratory rate, and LOC.
Prepare the patient for laboratory tests,
which can include complete blood count; cardiac enzyme, serum electrolyte, blood glucose,
blood urea nitrogen, arterial blood gas, and
blood drug levels; thyroid function tests; and a
12-lead electrocardiogram. If appropriate, prepare the patient for 24-hour Holter monitoring.
P
EDIATRIC POINTERS
Heart rates are normally higher in children than
in adults. Fetal bradycardia—a heart rate of less
than 120 beats/minute—may occur during prolonged labor or complications of delivery, such
as compression of the umbilical cord, partial
abruptio placentae, and placenta previa. Intermittent bradycardia, sometimes accompanied
by apnea, commonly occurs in premature infants. Bradycardia rarely occurs in full-term infants or children. However, it can result from
congenital heart defects, acute glomerulonephritis, and transient or complete heart
block associated with cardiac catheterization or
cardiac surgery.
G
ERIATRIC POINTERS
Sinus node dysfunction is the most common
bradyarrhythmia in the elderly. Patients with
this disorder may cite fatigue, exercise intolerance, dizziness, or syncope as their chief complaint. If the patient is asymptomatic, no intervention is necessary. Symptomatic patients,
however, require careful scrutiny of their drug
therapy. Beta-adrenergic blockers, verapamil,
diazepam, sympatholytics, antihypertensives,
and some antiarrhythmics have been implicated;
symptoms may clear when these drugs are discontinued. Pacing is usually indicated in patients with symptomatic bradycardia lacking a
correctable cause.
Bradypnea
Commonly preceding life-threatening apnea or
respiratory arrest, bradypnea is a pattern of regular respirations with a rate of fewer than
10 breaths/minute. This sign may result from
neurologic or metabolic disorders or a drug
overdose, all of which depress the brain’s respiratory control centers. (See Understanding how
the nervous system controls breathing.)
EMERGENCY INTERVENTIONS Depend-
ing on the degree of central nervous system
(CNS) depression, a patient with severe bradypnea may require constant stimulation to breathe.
If the patient seems excessively sleepy, try to
arouse him by shaking him and instructing him
to breathe. Quickly take the patient’s vital signs.
Assess his neurologic status by checking pupil
size and reactions and by evaluating his level of
consciousness (LOC) and his ability to move his
extremities.
Connect the patient to an apnea monitor, keep
emergency airway equipment available, and be
prepared to assist with intubation and mechanical
ventilation if spontaneous respirations cease. To
prevent aspiration, position the patient on his side
or keep his head elevated 30 degrees higher than
the rest of the body, and clear his airway with suction if necessary.
H
ISTORY AND PHYSICAL
EXAMINATION
Obtain a brief history from the patient, if possible, or from whoever accompanied him to your
facility. Ask if he’s experiencing a drug overdose
and, if so, try to determine which drugs he took,
how much, when, and by what route. Check his
arms for needle marks, indicating possible drug
abuse. You may need to administer I.V. naloxone, an opioid antagonist.
If you rule out a drug overdose, ask about
chronic illnesses, such as diabetes and renal
failure. Check for a medical identification
bracelet or card that identifies an underlying
condition. Also ask whether the patient has a
history of head trauma, brain tumor, neurologic
infection, or stroke.
M
EDICAL CAUSES
◆ Diabetic ketoacidosis. Bradypnea occurs
late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may
experience Kussmaul’s respirations. Associated
signs and symptoms include decreased LOC,
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109
Understanding how the
nervous system controls breathing
Stimulation from external sources and from higher brain centers acts on respiratory centers in the
pons and medulla. These centers, in turn, send impulses to the various parts of the respiratory
system to alter respiratory patterns.
Respiratory center
Cortex
Expiratory center
Pons
Nose and throat
Medulla
Cervical nerves
Thoracic nerves
Trachea and
bronchi
Lungs
Diaphragm
Intercostal
muscles
fatigue, weakness, fruity breath odor, and oliguria.
◆ Hepatic failure. Occurring in end-stage he-
patic failure, bradypnea may be accompanied by
coma, hyperactive reflexes, asterixis, a positive
Babinski’s reflex, fetor hepaticus, and other
signs.
◆ Increased intracranial pressure (ICP). A
late sign of increased ICP—a life-threatening
condition—bradypnea is preceded by decreased
LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late
medullary strangulation.
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Respiratory rates in
children
This graph shows normal respiratory rates
in children, which are higher than normal
rates in adults. Accordingly, bradypnea in
children is defined according to age.
35
30
25
20
BREATHS/MINUTE
15
cause bradypnea. Use of any of these drugs with
alcohol can also cause bradypnea.
S
PECIAL CONSIDERATIONS
Because a patient with bradypnea may develop
apnea, check his respiratory status frequently
and be prepared to give ventilatory support if
necessary. Don’t leave the patient unattended,
especially if his LOC is decreased. Keep his bed
in the lowest position and raise the side rails.
Obtain blood for arterial blood gas analysis,
electrolyte studies, and possibly a drug screen.
Ready the patient for chest X-rays and possibly
a computed tomography scan of the head.
Administer prescribed drugs and oxygen. Avoid
giving the patient a CNS depressant because it
can exacerbate bradypnea. Similarly, give oxygen
judiciously to a patient with chronic carbon dioxide retention, which may occur in chronic obstructive pulmonary disease, because excess oxygen therapy can have a negative effect.
When dealing with slow breathing in hospitalized patients, always review all drugs and
dosages given during the last 24 hours.
P
EDIATRIC POINTERS
Because respiratory rates are normally higher in
children than in adults, bradypnea in children is
defined according to age. (See Respiratory rates
in children.)
10
< 1 2 4 6 8 10 12 14 16 18
AGE IN YEARS
◆ Renal failure. Occurring in end-stage renal
failure, bradypnea may be accompanied by
seizures, decreased LOC, GI bleeding, hypotension or hypertension, uremic frost, and diverse
other signs.
◆ Respiratory failure. Bradypnea occurs in
end-stage respiratory failure along with
cyanosis, diminished breath sounds, tachycardia, mildly increased blood pressure, and decreased LOC.
O
THER CAUSES
◆ Drugs. An overdose of an opioid analgesic
or, less commonly, a sedative, barbiturate, phenothiazine, or another CNS depressant can
G
ERIATRIC POINTERS
When administering drugs to elderly patients,
keep in mind that they have a higher risk of developing bradypnea secondary to drug toxicity.
That’s because many of them take several drugs
that can potentiate this effect or have other conditions that predispose them to it. Warn older
patients about this potentially life-threatening
complication.
P
ATIENT COUNSELING
Alert patients who regularly take an opioid—for
example, those with advanced cancer or sickle
cell anemia—that bradypnea is a serious complication, and teach them to recognize early
signs of toxicity, such as nausea and vomiting.
Also, try to identify patients who may be abusing these drugs.
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