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ULY CLINIC
ULY CLINIC
11 Septemba 2025, 07:28:58
Hyperpnea (Increased Respiratory Effort)
Hyperpnea refers to an increase in the depth and/or rate of breathing that is sustained over time. It may present as:
Normal rate with increased depth (tidal volume >7.5 mL/kg)
Increased rate (>20 breaths/min) with normal depth
Both increased rate and depth
Hyperpnea differs from sighing, which involves intermittent deep breaths. It may occur voluntarily (e.g., stress relief, labor) or involuntarily due to metabolic, psychiatric, neurologic, or respiratory disorders. Hyperventilation, often a consequence of hyperpnea, leads to respiratory alkalosis (arterial pH >7.45, PaCO₂ <35 mm Hg). Kussmaul’s respirations, a form of compensatory hyperpnea, occur in response to metabolic acidosis.
Pathophysiology
Metabolic acidosis: Loss of bicarbonate ions through diarrhea, GI drainage, or ureterosigmoidostomy stimulates deep breathing to normalize pH.
Central neurogenic hyperventilation: Brain stem injury (midbrain or upper pons) increases rate and depth of respirations.
Hypoxemia: Pulmonary conditions (pneumonia, edema, COPD, pneumothorax) trigger compensatory hyperpnea.
Ketoacidosis: Diabetic, alcoholic, or starvation-induced ketoacidosis causes Kussmaul respirations.
Renal failure: Uremic acidosis stimulates hyperpnea, sometimes accompanied by uremic frost and electrolyte disturbances.
History and Physical Examination
Assess level of consciousness (LOC).
Inquire about recent illnesses, infections, drug ingestion (e.g., aspirin, salicylates), diabetes, renal disease, pulmonary disorders, or gastrointestinal fluid losses.
Observe respiratory pattern: rate, depth, ability to speak, use of accessory muscles, intercostal or abdominal retractions.
Inspect for cyanosis, diaphoresis, dehydration, or signs of infection.
Vital signs: note fever, blood pressure, heart rate, and oxygen saturation.
Auscultate heart and lungs for crackles, wheezing, or abnormal heart sounds.
Medical Causes
Cause | Key Findings | Distinguishing Features |
Head injury / Central neurogenic hyperventilation | Fast, deep breathing; loss of consciousness; facial/head trauma; abnormal pupillary reaction | Indicates brain stem injury; possible increased ICP (bradycardia, widened pulse pressure) |
Metabolic acidosis | Deep, labored breathing; nausea, vomiting, diarrhea; dehydration | Compensatory hyperpnea (Kussmaul’s respirations) |
Diabetic ketoacidosis | Polydipsia, polyphagia, polyuria; fruity breath; hypotension; thready pulse | Hyperpnea is life-threatening; requires insulin, fluids, electrolytes |
Alcoholic / Starvation ketoacidosis | Vomiting, dehydration, acetone odor; alert patient; normal glucose in alcoholic ketoacidosis | Abrupt onset of Kussmaul respirations in alcoholics |
Uremia / Renal failure | Oliguria/anuria; uremic frost; nausea; pruritus; neurologic symptoms | Hyperpnea occurs secondary to metabolic acidosis |
Hypoxemia | Dyspnea, cough, cyanosis, decreased breath sounds | Often due to pulmonary pathology (pneumonia, pulmonary edema, COPD) |
Hyperventilation syndrome | Episodic hyperpnea with anxiety, dizziness, paresthesia | Respiratory alkalosis without primary metabolic disorder |
Shock | Hypotension, tachycardia, weak pulse, cool/clammy skin | May be hypovolemic, cardiogenic, septic, or anaphylactic; compensatory hyperpnea |
Other causes
Drugs/toxins: salicylates, acetazolamide, methanol, ethylene glycol.
Severe infections causing lactic acidosis (sepsis).
Special considerations
Monitor vital signs and oxygen saturation continuously.
Be prepared for immediate intervention: IV fluids, blood transfusions, vasopressors, ventilatory support.
Order arterial blood gas analysis and blood chemistry tests.
Identify underlying cause promptly to prevent cardiovascular or neurologic deterioration.
Patient counseling
Instruct patients on monitoring blood glucose, especially in diabetics.
Advise avoidance of alcohol and respiratory irritants.
Provide dietary guidance and instructions to prevent infection.
Offer support for alcohol cessation if applicable.
Pediatric pointers
Causes are similar to adults (metabolic, neurologic, respiratory).
Most common metabolic cause in children is diarrhea-induced acidosis.
Infants may develop Kussmaul respirations due to inborn errors of metabolism.
Prompt intervention is critical to prevent respiratory or cardiovascular collapse.
References
Hayward, J. (2011). Common genetic conditions in primary care. Pulse, 26, 824–825.
McCahon, D., Holder, R., Metcalfe, A., Clifford, S., Gill, P., Cole, T., … Wilson, S. (2009). General practitioners’ attitudes to assessment of genetic risk of common disorders in routine primary care. Clinical Genetics, 76, 544–551.
