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ULY CLINIC

ULY CLINIC

11 Septemba 2025, 07:28:58

Hyperpnea (Increased Respiratory Effort)

Hyperpnea (Increased Respiratory Effort)
Hyperpnea (Increased Respiratory Effort)
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
  1. Hayward, J. (2011). Common genetic conditions in primary care. Pulse, 26, 824–825.

  2. 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.

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