Hyperpnea
Hyperpnea: Excerpt from Professional Guide to Signs & Symptoms (Fifth Edition)
Hyperpnea indicates increased respiratory effort for a sustained period—a normal rate (at least 12 breaths/minute) with increased depth (a tidal volume greater than 7.5 ml/kg), an increased rate (more than 20 breaths/minute) with normal depth, or increased rate and depth. This sign differs from sighing (intermittent deep inspirations) and may or may not be associated with tachypnea (increased respiratory rate).
The typical patient with hyperpnea breathes at a normal or increased rate and inhales deeply, displaying marked chest expansion. He may complain of shortness of breath if a respiratory disorder is causing hypoxemia, or he may not be aware of his breathing if a metabolic, psychiatric, or neurologic disorder is causing involuntary hyperpnea. Other causes of hyperpnea include profuse diarrhea or dehydration, loss of pancreatic juice or bile from GI drainage, and ureterosigmoidostomy. All these conditions and procedures cause a loss of bicarbonate ions, resulting in metabolic acidosis. Hyperpnea may also accompany strenuous exercise, and voluntary hyperpnea can promote relaxation in patients experiencing stress or pain—for example, women in labor.
Hyperventilation, a consequence of hyperpnea, is characterized by alkalosis (arterial pH above 7.45 and partial pressure of carbon dioxide [Pco2] below 35 mm Hg). In central neurogenic hyperventilation, brain stem dysfunction (as results from a severe cranial injury) increases the rate and depth of respirations. In acute intermittent hyperventilation, the respiratory pattern may be a response to hypoxemia, anxiety, fear, pain, or excitement. Hyperpnea may also be a compensatory mechanism in metabolic acidosis. Under these conditions, it’s known as Kussmaul’s respirations. (See Kussmaul’s respirations: A compensatory mechanism.)
History and physical examination
If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly and effectively. (See Managing hyperpnea, page 442.) However, if the patient’s condition isn’t grave, first determine his level of consciousness (LOC). If he’s alert (and if his hyperpnea isn’t interfering with speaking), ask about recent illnesses or infections; ingestion of aspirin or other drugs or chemicals; or inhalation of drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or any pulmonary conditions. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?
Next, observe the patient for clues to his abnormal breathing pattern. Is he unable to speak, or does he speak only in brief, choppy phrases? Is his breathing abnormally rapid? Examine the patient for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), anxiety, and restlessness—all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient supply of oxygen. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient’s vital signs, including oxygen saturation, noting fever. Also, examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient’s heart and lungs.
Medical causes
Head injury
Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation. Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle’s sign; an absent doll’s eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and widening pulse pressure.
Hyperventilation syndrome
Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia
Many pulmonary disorders that cause hypoxemia—for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax—may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis
Alcoholic ketoacidosis (occurring most often in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul’s respirations begin abruptly and are accompanied by vomiting for several days, fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul’s respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may have a history of diabetes mellitus. Other clinical features include fruity breath odor; orthostatic hypotension; rapid, thready pulse; generalized weakness; decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul’s respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure
Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul’s respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymosis. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis
A severe infection may cause lactic acidosis, resulting in Kussmaul’s respirations. Other findings include tachycardia, fever or a low temperature, chills, headache, lethargy, profuse diaphoresis, anorexia, cough, wound drainage, burning on urination, confusion or change in mental status, and other signs of local infection.
Shock
Potentially life-threatening metabolic acidosis produces Kussmaul’s respirations, hypotension, tachycardia, narrowed pulse pressure, weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain, arrhythmias, and signs of heart failure (in cardiogenic shock); high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). Onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs
Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul’s respirations. So can ingestion of methanol or ethylene glycol, found in antifreeze solutions.
Special considerations
Monitor vital signs, including oxygen saturation, in all patients with hyperpnea, and observe for increasing respiratory distress or an irregular respiratory pattern signaling deterioration. Prepare for immediate intervention to prevent cardiovascular collapse: Start an I.V. line for administration of fluids, blood transfusions, and vasopressors for hemodynamic stabilization, as ordered, and prepare to give ventilatory support. Prepare the patient for arterial blood gas analysis and blood chemistry studies.
Pediatric pointers
Hyperpnea in children indicates the same metabolic or neurologic causes as in adults and requires the same prompt intervention. The most common cause of metabolic acidosis in children is diarrhea, which can cause a life-threatening crisis. In infants, Kussmaul’s respirations may accompany acidosis due to inborn errors of metabolism.
Pictures
Book Source Details
- Book Title: Professional Guide to Signs & Symptoms (Fifth Edition)
- Author(s): Springhouse
- Year of Publication: 2006
- Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2006 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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