The polipnea is a clinical sign and symptom consisting of increasing frequency and inspiratory volume during breathing. It is produced by the association of two symptoms (tachypnea and hyperpnea) due to the stimulation of the respiratory center. As a result of a given stimulus, the breaths become faster and deeper.
Under normal conditions, the respiratory rate of an adult ranges between 16 and 20 breaths per minute. The depth of inspiration will determine the volume of lung air at a given time. Inspiratory volume corresponds to about 500 milliliters of air — about 7 ml per kilogram of weight — and is part of the tidal volume.
Polypnea is an alteration of the normal respiratory process. The process of respiration depends on the concentration of oxygen and carbon dioxide in the blood; this represents a stimulus. Specific receptors of the nervous system recognize the stimulus and, consequently, activate respiratory movements.
A decrease in the partial pressure of oxygen (hypoxemia) is one of the stimuli that can trigger polypnea. The symptom is a response to oxygen demand, expressed in increased respiration and inspiration rates.
Any process that lowers oxygen levels in the blood will affect the normal respiratory pattern, occasionally producing polypnea. Treatment should be instituted to eliminate the cause, thus restoring both respiration and oxygen concentration.
Polypnea is a symptom associated with the alteration of the normal respiratory pattern. It is characterized by an increase in the respiratory rate with a deep and prolonged inspiration. This is due to the need to enter oxygen because it is diminished, which is called hypoxia.
There is a causal relationship between respiratory pathologies and polypnea. To the respiratory symptoms that are part of the polypnea and accompany it, the symptoms of the triggering pathologies are added. The symptoms that can be described frequently are the following:
– Tachypnea or increased respiratory rate above 20 breaths per minute.
– Hyperpnea, which consists of a slow and deep inspiration followed by a prolonged expiration.
– Subcostal and intercostal pulling, due to muscle contraction due to the use of respiratory accessory muscles.
– Perioral cyanosis and acrocyanosis. Cyanosis is the bluish coloration in the mouth or extremities as a result of tissue hypoxia.
– Tachycardia. The increase in heart rate is a compensatory mechanism that guarantees blood perfusion in cases of hypoxia.
Hypoxia or hypoxemia is a stimulus capable of producing the increase in respiratory rate and inspiratory volume that characterizes polypnea. Understanding the origin of the symptom implies understanding the respiratory control mechanisms.
The function of the respiratory system is to guarantee the supply of oxygen to the body and eliminate carbon dioxide, in addition to regulating body pH.
Breathing is an involuntary act, with a voluntary component depending on the control pathway at the level of the nervous system .
Respiration, from the autonomic point of view, depends on three elements (receptors, control centers and effectors), which respond in a coordinated way to specific stimuli.
These stimuli can be changes in pH and the partial pressures of oxygen and carbon dioxide (PO 2 and PCO 2 , respectively).
The receptors will be able to capture the stimulus and send the information to the control centers located in the pons or in the peripheral nerve ganglia.
Once the information is processed, the effectors (respiratory muscles) are activated that generate a response according to the received stimulus.
Respiratory dysfunction given by tachypnea and hyperpnea means disturbance anywhere from the lungs to the cerebral cortex .
In 1874 a German physician named Adolph Kussmaul described a type of breathing present in diabetic patients with ketoacidosis. This breathing was fast and deep at the same time, establishing a breathing pattern named after the doctor who described it.
Kussmaul respiration or acidotic respiration is a clear example of polypnea. The observation made by the German doctor served as a starting point to relate metabolic acidosis with changes in the respiratory pattern.
Thus, disease states including acidosis can trigger the symptom. Polypnea occurs as a compensatory respiratory response to the state of acidosis.
The presence of polypnea in acidosis is a compensatory response. The decrease in the pH of the imbalance acts as a stimulus that determines deeper and faster breathing. The objective is to increase the supply of oxygen, PO 2 and decrease PCO 2.
The lack of insulin in type 1 diabetes means that glucose cannot be metabolized. Then, the body carries out energy metabolism from lipids, which leads to acidosis. The compensatory respiratory pattern change is the same for all acidosis.
This pathology consists of an obstructive pattern with air trapping, which prevents the normal entry of oxygen and the expulsion of CO 2 . The increase in PCO2 activates the compensatory mechanism.
Other clinical states that can produce polypnea are:
– Acute bronchitis and pneumonia.
– Chronic obstructive pulmonary disease or COPD.
– Respiratory insufficiency of any cause.
– Respiratory distress of the infant or adult.
– Shock of any cause.
– Infections and sepsis.
– Head trauma, with cerebral edema.
– Intoxications or poisonings.
– Multi-organ failure.
Correction of the causes that produce polypnea is the main goal of treatment. The symptom is produced by an alteration of the homeostasis of the organism, for which it must be restored.
The severity of the pathology causing changes in the respiratory pattern will require hospitalization of the patient. The clinical evaluation and complementary tests will lead to the cause and, consequently, the appropriate therapy will be established. Treatment of polypnea is general and specific.
– Hospitalization of the patient.
– Semi-sitting position to facilitate breathing.
– Vital signs monitoring.
– Parenteral hydration.
– Continuous moist oxygen.
– Nebulization or aerolization if necessary
– Endotracheal intubation and mechanical ventilation will be necessary according to the severity of the clinical picture.
It is the treatment of the triggering pathologies of the respiratory clinical picture. The purpose will be to eliminate the cause and restore the patient’s health status.
– Antibiotic therapy for infectious pathologies.
– Steroids, especially in bronchial inflammatory processes such as asthma.
– Sodium bicarbonate to treat acid-base imbalances, such as metabolic acidosis.
– The use of inhalers and nebulotherapy will be indicated mainly in asthma and COPD.
– Respiratory physiotherapy.
- WebMD medical reference (Reviewed by Robinson, J. 2018). Types of Breathing Problems, Explained. Recovered from webmd.com
- Admin in respiratory diseases (sf). Polypnea and Hyperpnea: Definition, Causes, Symptoms and Treatment. Recovered from scopeheal.com
- Hhp team (2016). Polypnea in adults and children, what is it and what can it be a symptom of? Recovered from hhp.es
- García C, L; Rodríguez R, O; Rodríguez C, OB (2010). Regulation of respiration: morphofunctional organization of its control system. Recovered from bvs.sld.cu
- Mitchell, RA; Berger, AJ (1975). Neural regulation of respiration. Abstract retrieved from ncbi.nlm.hih.gov
- (Abstract) Kilburn, KH (1965). Tachypnea and Hyperpnea: Signs of Compensatory Ventilation. Recovered from annals.org
- Boynton de S, L. (2002, last rev 2016). Breathing difficulties. Recovered from alsa.org
- Murat, A (2017). Respiratory failure. Recovered from emedicine.medscape.com
- Harman, EM (2017). Acute respiratory distress syndrome. Recovered from emedicine.medscape.com
- (sf) Acidosis (Acidoses). Recovered from symptom.com