Introduction
Respiration is a physiological process involving gaseous exchange between the body and the external environment. A carefully balanced system exists, encompassing various body organs that work harmoniously to facilitate respiration. This intricate network ensures the delivery of an adequate amount of oxygen to body tissues for energy production and the efficient removal of carbon dioxide. Within the central nervous system, specialized respiratory centers integrate neural and chemical input from diverse receptors. These centers then signal the respiratory muscles, ensuring the upper airways remain patent and driving thoracic movements to regulate ventilation level.[1] Additionally, this process plays a crucial role in maintaining the body's acid-base balance.
Although respiration occurs effortlessly and seamlessly, it is susceptible to various abnormalities challenging its efficiency. This activity will explore different respiratory disorders, delving into their pathophysiology and clinical manifestations.
Function
Register For Free And Read The Full Article
- Search engine and full access to all medical articles
- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Function
Respiratory disorders can significantly impact a patient's quality of life. Many respiratory diseases disrupt the normal gas exchange process, reducing oxygen supply to the tissues and causing an accumulation of carbon dioxide. Consequently, individuals experience symptoms like dyspnea, fatigue, and decreased exercise tolerance.[2] To cope, the body activates compensatory mechanisms, often involving an increase in breathing rate or effort to maintain sufficient oxygen levels.
Inflammation of the airways is a protective response against environmental triggers. However, in certain respiratory disorders, such as asthma and chronic obstructive pulmonary disease (COPD), this inflammation can persist chronically, leading to airway damage. A similar occurrence is observed in cases of chronic cough associated with bronchitis.
Individuals affected by respiratory disorders frequently experience fatigue due to the heightened effort required for breathing and the decreased availability of oxygen.[3] When combined with dyspnea, these symptoms can significantly limit a patient's daily activities, exercise capacity, and overall quality of life. Living with a respiratory disorder can also have psychological consequences, leading to anxiety and depression. Patients often struggle with the fear of breathlessness, persistent symptoms, and diminished quality of life. Therefore, implementing appropriate treatment and lifestyle modifications is crucial to enhance the quality of life and prognosis for individuals with respiratory disorders.
Issues of Concern
Disordered respiration can be an uncomfortable and distressing experience for patients. Although specific data regarding its prevalence among ambulatory patients is lacking, the widespread occurrence of cardiac and pulmonary diseases indicates the extensive nature of the condition. Cardiac conditions are among the leading causes of death in the US, often manifesting with dyspnea as a primary symptom.[4] Additionally, obstructive lung diseases, such as asthma and COPD, affect approximately 34 million people in the US, many of whom seek medical assistance to alleviate shortness of breath. However, the actual prevalence is likely underestimated due to the underdiagnosis of COPD.[5] Similarly, asthma presents a significant global challenge, affecting approximately 15% to 20% of individuals in developed countries and about 2% to 4% in less developed countries.
Tachypnea is characterized by rapid breathing, with the average breathing rate for adults ranging from 12 to 20 breaths per minute. In newborns, tachypnea signifies a respiratory system issue that can become apparent shortly after birth. It often arises due to impaired fetal lung fluid clearance, resulting in respiratory distress. Transient tachypnea of the newborn is more prevalent in preterm infants, affecting approximately 1 in 100 preterm infants. In full-term infants, transient tachypnea is observed in around 4 to 6 per 1000 infants.[6]
Hypoventilation refers to breathing at a slower and shallower pace than normal, leading to impaired ventilation. This condition ultimately results in hypoxemia and hypercapnia. One example of a disorder associated with hypoventilation is obesity hypoventilation syndrome, characterized by the presence of obesity (body mass index [BMI] ≥30 kg/m²) and daytime hypercapnia (PaCO2 ≥45 mmHg) without any other identifiable cause for hypoventilation. Current estimates indicate that 8% of the adult US population is affected by morbid obesity.[7] Within this group, the prevalence of obesity hypoventilation syndrome is estimated to be between 20% and 30%.[8] The overall prevalence of obesity hypoventilation syndrome ranges from 10% to 20%.[8]
Hypoventilation can also be caused by various neuromuscular disorders, including amyotrophic lateral sclerosis (ALS), diaphragm paralysis, muscular dystrophies such as Duchenne and Becker dystrophies, Guillain-Barré syndrome, and myasthenia gravis.[9] The morbidity and mortality associated with hypoventilation syndromes differ based on their underlying causes. For instance, patients with obesity hypoventilation syndrome are more likely to be admitted to the intensive care unit (ICU) than individuals with similar BMI without hypoventilation.[10]
Clinical Significance
Eupnea refers to normal, unlabored, and regular breathing at rest. Disorders of respiration can stem from abnormalities in any component of the respiratory system, including the airways, alveoli, central nervous system, peripheral nervous system, chest wall, and respiratory muscles. Breathing is influenced by various factors, including blood pH (acidosis or alkalosis), carbon dioxide levels (hypercapnia or hypocapnia), and oxygen levels (hypoxia). The medulla oblongata and pons in the brainstem play a critical role in adjusting the rate and depth of breathing in response to these factors.
Clinically significant abnormal respiration patterns encompass the following:
- Dyspnea is the feeling of difficult or labored breathing, often characterized by a sensation of air hunger or insufficient airflow. Paroxysmal nocturnal dyspnea (PND) is the abrupt onset of severe shortness of breath that occurs during the night, typically waking the patient from sleep.
- Orthopnea is a specific symptom or condition in which patients struggle to breathe when lying flat. Patients with orthopnea typically find relief by sitting upright or adopting a more elevated position, like being propped up with pillows. This condition is often linked with heart failure.
- Cheyne-Stokes respiration (CSR) refers to a cyclical breathing pattern characterized by apnea, followed by a gradual rise in respiratory frequency and tidal volume, and then a subsequent decline in both until the next apneic period occurs.[11] This pattern is commonly observed in patients with heart failure.[12]
- Bradypnea refers to an abnormally slow respiratory rate, notably slower than the average expected breathing rate for an individual at rest. The typical adult respiratory rate at rest ranges between 12 and 20 breaths per minute. Bradypnea is commonly defined as a respiratory rate below 12 breaths per minute in adults, although this reference range may vary slightly based on the information source.
- Tachypnea denotes an abnormally rapid rate of breathing, often defined as a respiratory rate exceeding the normal range for a person's age and physiological condition. The exact threshold for what is considered abnormal or tachypneic can vary, but a common reference point for adults is a breathing rate exceeding 20 breaths/min at rest.
- Hyperpnea involves an increased depth and rate of breathing, typically linked to elevated oxygen demand or metabolic activity. Unlike hyperventilation, which often indicates excessive ventilation out of proportion to metabolic requirements, hyperpnea is a physiological response to factors like exercise, fever, or an increased metabolic rate. During hyperpnea, blood gasses remain within normal ranges.
- Agonal breathing manifests as irregular, gasping, or labored breaths, often resulting from anoxic brain injury. Agonal breathing is often a critical sign of a life-threatening emergency, such as a cardiac arrest. Healthcare professionals or first responders encountering a patient exhibiting agonal breathing should promptly initiate cardiopulmonary resuscitation and call for emergency medical assistance. This breathing pattern indicates the failure of the patient's cardiac and respiratory functions, underscoring the urgency of intervention. Swift intervention significantly enhances the chances of survival and recovery for these patients.
- Apnea signifies a temporary cessation or absence of breathing, with 2 significant types: obstructive sleep apnea (OSA) and central sleep apnea.[13]
- Hyperventilation describes an abnormal increase in breathing rate and depth, leading to decreased CO2 concentration in the blood. Emotional stress, anxiety, panic attacks, fever, or certain medical conditions can trigger hyperventilation. Additionally, chemoreceptor stimulation due to metabolic acidosis can drive this condition.
- Hypoventilation is insufficient ventilation incapable of removing adequate Co2 from the body. Hypoventilation can be a sign of various underlying medical conditions, including respiratory diseases (eg, COPD or sleep apnea), central nervous system disorders, certain medications (eg, opioids), or neuromuscular conditions impairing respiratory muscles.
- Kussmaul respiration, named after the German physician Adolph Kussmaul, manifests as deep, rapid, and difficult breathing. This pattern occurs in conditions causing metabolic acidosis,[14] prompting the body to increase the breathing depth and rate to expel carbon dioxide and reduce blood acid levels. Kussmaul respirations can result from disorders like uremia or toxic ingestions, such as alcohol and salicylates.
- The Biot respiratory pattern, observed by French physician Camille Biot, comprises consistent deep breaths interspersed with apnea due to damage to the pons from stroke, trauma, or uncal herniation. With worsening pons insult, the pattern becomes irregular, eventually deteriorating to ataxic breathing. Additionally, opiate intoxication can trigger the Biot pattern.[15]
- Apneustic breathing is characterized by prolonged, gasping inhalations followed by extremely short and inadequate exhalations. This pattern results from upper pons injury, often due to stroke or trauma, signifying severe brain injury and a poor prognosis. Temporary induction can occur by the administration of ketamine.[16]
- Central neurogenic hyperventilation is persistent hyperventilation resulting from head trauma, brain hypoxia, or inadequate cerebral perfusion, primarily due to the midbrain and upper pons damage. Central neurogenic hypoventilation, on the other hand, occurs when medullary respiratory centers do not respond appropriately to stimuli, occurring with head trauma, cerebral hypoxia, and narcotic suppression. Individuals with traumatic brain injury require careful management to avoid hyperventilation and hypoventilation. This often involves a combination of pharmacological, surgical, and medically induced coma interventions to address raised intracranial pressure.[17][18][19]
Disorders of respiration can lead to various respiratory diseases, which will be only briefly discussed here, as comprehensive activities on these topics are available. For example, in patients with COPD, the onset of hypercapnia is mainly associated with more advanced disease, although its occurrence is inconsistent among patients with similar levels of airflow obstruction. Consequently, individuals with comparable spirometric values might exhibit either the "blue bloater" or the "pink puffer" pattern, characterized by eucapnia and normal oxygen levels.[20][21]
Another example is the Ondine curse, which refers to alveolar hypoventilation due to impaired autonomic ventilation control while maintaining normal voluntary breathing. Classically, individuals with this condition "forget to breathe" during sleep but maintain relatively normal breathing patterns while awake.[22][23] Congenital central hypoventilation syndrome, brainstem tumors or infarcts, and surgical manipulation of the second cervical segment of the spinal cord for intractable pain can cause the Ondine curse.[24]
Enhancing Healthcare Team Outcomes
Improving outcomes for patients with abnormal respirations necessitates a collaborative and interprofessional healthcare approach. A cohesive interprofessional team can enhance patient care, ensure timely interventions, and optimize results. Healthcare professionals, including nurses, respiratory therapists, physicians, and advanced practitioners, must receive training to promptly recognize abnormal respiratory patterns such as tachypnea, bradypnea, and apneustic and irregular breathing.
Effective communication among team members is crucial. Nurses, physicians, respiratory therapists, and specialists must promptly share observations, assessments, and recommendations.[25] Clear and concise documentation of patient assessments and respiratory status changes is essential. Respiratory therapists are crucial in assessing and managing patients with abnormal respirations, offering interventions such as administering oxygen therapy, performing respiratory treatments, and managing mechanical ventilation.
Enhancing healthcare team outcomes for patients with abnormal respirations relies on efficient communication, a collaborative approach, and a commitment to patient-centered care. Healthcare professionals from diverse disciplines must collaborate closely to provide the best possible care for these patients.
References
Horner RL, Bradley TD. Update in sleep and control of ventilation 2006. American journal of respiratory and critical care medicine. 2007 Mar 1:175(5):426-31 [PubMed PMID: 17303896]
Hanania NA, O'Donnell DE. Activity-related dyspnea in chronic obstructive pulmonary disease: physical and psychological consequences, unmet needs, and future directions. International journal of chronic obstructive pulmonary disease. 2019:14():1127-1138. doi: 10.2147/COPD.S188141. Epub 2019 May 24 [PubMed PMID: 31213793]
Level 3 (low-level) evidenceGoërtz YMJ, Spruit MA, Van 't Hul AJ, Peters JB, Van Herck M, Nakken N, Djamin RS, Burtin C, Thong MSY, Coors A, Meertens-Kerris Y, Wouters EFM, Prins JB, Franssen FME, Muris JWM, Vanfleteren LEGW, Sprangers MAG, Janssen DJA, Vercoulen JH. Fatigue is highly prevalent in patients with COPD and correlates poorly with the degree of airflow limitation. Therapeutic advances in respiratory disease. 2019 Jan-Dec:13():1753466619878128. doi: 10.1177/1753466619878128. Epub [PubMed PMID: 31558115]
Level 3 (low-level) evidenceCook DG, Shaper AG. Breathlessness, lung function and the risk of heart attack. European heart journal. 1988 Nov:9(11):1215-22 [PubMed PMID: 3234413]
Level 3 (low-level) evidenceSingh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli BR, Criner GJ, Frith P, Halpin DMG, Han M, López Varela MV, Martinez F, Montes de Oca M, Papi A, Pavord ID, Roche N, Sin DD, Stockley R, Vestbo J, Wedzicha JA, Vogelmeier C. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. The European respiratory journal. 2019 May:53(5):. pii: 1900164. doi: 10.1183/13993003.00164-2019. Epub 2019 May 18 [PubMed PMID: 30846476]
Chowdhury N, Giles BL, Dell SD. Full-Term Neonatal Respiratory Distress and Chronic Lung Disease. Pediatric annals. 2019 Apr 1:48(4):e175-e181. doi: 10.3928/19382359-20190328-01. Epub [PubMed PMID: 30986319]
Hales CM, Fryar CD, Carroll MD, Freedman DS, Aoki Y, Ogden CL. Differences in Obesity Prevalence by Demographic Characteristics and Urbanization Level Among Adults in the United States, 2013-2016. JAMA. 2018 Jun 19:319(23):2419-2429. doi: 10.1001/jama.2018.7270. Epub [PubMed PMID: 29922829]
Mokhlesi B, Tulaimat A, Faibussowitsch I, Wang Y, Evans AT. Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep & breathing = Schlaf & Atmung. 2007 Jun:11(2):117-24 [PubMed PMID: 17187265]
Level 2 (mid-level) evidencePaschoal IA, Villalba Wde O, Pereira MC. Chronic respiratory failure in patients with neuromuscular diseases: diagnosis and treatment. Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia. 2007 Jan-Feb:33(1):81-92 [PubMed PMID: 17568873]
Mokhlesi B, Tulaimat A. Recent advances in obesity hypoventilation syndrome. Chest. 2007 Oct:132(4):1322-36 [PubMed PMID: 17934118]
Level 3 (low-level) evidenceCherniack NS, Longobardo GS. Cheyne-Stokes breathing. An instability in physiologic control. The New England journal of medicine. 1973 May 3:288(18):952-7 [PubMed PMID: 4571351]
Level 3 (low-level) evidenceMittal N, Sykes AV, Malhotra A. A review on the treatment of Cheyne Stokes Breathing in patients with congestive heart failure. Sleep & breathing = Schlaf & Atmung. 2023 Oct:27(5):1939-1940. doi: 10.1007/s11325-023-02790-8. Epub 2023 Feb 6 [PubMed PMID: 36746869]
Ishikawa O, Oks M. Central Sleep Apnea. Clinics in geriatric medicine. 2021 Aug:37(3):469-481. doi: 10.1016/j.cger.2021.04.009. Epub 2021 Jun 4 [PubMed PMID: 34210451]
Shahid W, Khan F, Makda A, Kumar V, Memon S, Rizwan A. Diabetic Ketoacidosis: Clinical Characteristics and Precipitating Factors. Cureus. 2020 Oct 4:12(10):e10792. doi: 10.7759/cureus.10792. Epub 2020 Oct 4 [PubMed PMID: 33154858]
Wijdicks EF. Biot's breathing. Journal of neurology, neurosurgery, and psychiatry. 2007 May:78(5):512-3 [PubMed PMID: 17435185]
Saito Y, Hashimoto T, Iwata H, Takahashi K, Fukumizu M, Sasaki M, Hanaoka S, Sugai K. Apneustic breathing in children with brainstem damage due to hypoxic-ischemic encephalopathy. Developmental medicine and child neurology. 1999 Aug:41(8):560-7 [PubMed PMID: 10479045]
Level 3 (low-level) evidenceHopper K. Respiratory Acid-Base Disorders in the Critical Care Unit. The Veterinary clinics of North America. Small animal practice. 2017 Mar:47(2):351-357. doi: 10.1016/j.cvsm.2016.09.006. Epub 2016 Nov 24 [PubMed PMID: 27890436]
Level 3 (low-level) evidenceHaddad S, Aldawood AS, Alferayan A, Russell NA, Tamim HM, Arabi YM. Relationship between intracranial pressure monitoring and outcomes in severe traumatic brain injury patients. Anaesthesia and intensive care. 2011 Nov:39(6):1043-50 [PubMed PMID: 22165356]
Level 2 (mid-level) evidenceZhou W, Liu W. Hypercapnia and hypocapnia in neonates. World journal of pediatrics : WJP. 2008 Aug:4(3):192-6. doi: 10.1007/s12519-008-0035-5. Epub [PubMed PMID: 18822927]
Lourenço RV, Miranda JM. Drive and performance of the ventilatory apparatus in chronic obstructive lung disease. The New England journal of medicine. 1968 Jul 11:279(2):53-9 [PubMed PMID: 5657011]
Matthews AW, Howell JB. Assessment of responsiveness to carbon dioxide in patients with chronic airways obstruction by rate of isometric inspiratory pressure development. Clinical science and molecular medicine. 1976 Mar:50(3):199-205 [PubMed PMID: 1253530]
Planjar-Prvan M, Krmpotić P, Jergović I, Bielen I. [Central sleep apnea (Ondine's curse syndrome) in medullary infarction]. Acta medica Croatica : casopis Hravatske akademije medicinskih znanosti. 2010 Oct:64(4):297-301 [PubMed PMID: 21688613]
Level 3 (low-level) evidenceMellins RB, Balfour HH Jr, Turino GM, Winters RW. Failure of automatic control of ventilation (Ondine's curse). Report of an infant born with this syndrome and review of the literature. Medicine. 1970 Nov:49(6):487-504 [PubMed PMID: 5286083]
Lim W, Breitling M, Nugent B, Sinha A, Diaz K. A Case of Medullary Infarct Causing Central Alveolar Hypoventilation. Cureus. 2021 Aug:13(8):e17153. doi: 10.7759/cureus.17153. Epub 2021 Aug 13 [PubMed PMID: 34548970]
Level 3 (low-level) evidenceZamjahn JB, Beyer EO, Alig KL, Mercante DE, Carter KL, Gunaldo TP. Increasing Awareness of the Roles, Knowledge, and Skills of Respiratory Therapists Through an Interprofessional Education Experience. Respiratory care. 2018 May:63(5):510-518. doi: 10.4187/respcare.05869. Epub 2018 Jan 23 [PubMed PMID: 29362218]