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Hyperpnea

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 frequency).

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. Of course, hyperpnea may also accompany strenuous exercise, and voluntary hyperpnea can promote relaxation in patients experiencing stress or pain — for example, females in labor.

Hyperventilation, a consequence of hyperpnea, is characterized by alkalosis (arterial pH above 7.45 and Paco₂ below 35 mm Hg). In central neurogenic hyperventilation, brain stem dysfunction (such 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 to metabolic acidosis. Under these conditions, it’s known as Kussmaul’s respirations. (See Kussmaul’s respirations: A compensatory mechanism.)

Act Now: Carefully examine the patient with hyperpnea for related signs of life-threatening conditions, such as increased intracranial pressure (ICP), metabolic acidosis, diabetic ketoacidosis, and uremia. Be prepared for rapid intervention. (See Managing hyperpnea, page 174.)

Assessment

History

If you’ve ruled out a life-threatening condition, confirmed that the patient’s level of consciousness (LOC) permits, and determined that hyperpnea isn’t interfering with his ability to speak, obtain his history. Has he experienced any recent illnesses or infections, such as severe diarrhea or an upper respiratory tract infection? Ask about ingestion of aspirin, other drugs, or chemicals, and about inhalation of drugs or chemicals. Is he excessively thirsty or hungry? Does he have a history of diabetes mellitus, renal disease, or a pulmonary condition?

Physical examination

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 him for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), restlessness, and anxiety — 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, and examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient’s heart and lungs.

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.

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 ICP 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 pneumotho-
rax — 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 commonly 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 or may not 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 ecchymoses. 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 or 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 and ethylene glycol, found in antifreeze solutions.

Nursing 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 vasopressor drugs for hemodynamic stabilization, as ordered, and prepare to give ventilatory support. Prepare the patient for arterial blood gas analysis and blood chemistry studies.

Patient teaching

Teach the patient how to monitor his blood sugar level. Stress the importance of compliance with diabetes therapy, if applicable. Provide information on fluids and foods the patient should avoid. Discuss pulmonary hygiene and teach the patient ways to avoid respiratory infections. Emphasize the importance of abstinence from alcohol; refer to support groups or other resources that can assist, if indicated.

Pictures

Book Source Details

• Book Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series
• Author(s): Springhouse
• Year of Publication: 2007
• Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2007 Lippincott Williams & Wilkins.

Other Book Chapters Related to Orthopnea

Read excerpts from these other book chapters related to Orthopnea:

Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2008 Williams & Wilkins.

More About Causes of Orthopnea

• Back to symptom: Orthopnea: Introduction (review 41 causes)
• Next Book Extract About Orthopnea: Respirations, stertorous (Signs & Symptoms: A 2-in-1 Reference for Nurses)
• All Book Extracts: All Online Book Extracts for Orthopnea

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More About This Book: Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-624-5

 » Next page: Respirations, stertorous (Signs & Symptoms: A 2-in-1 Reference for Nurses)

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