Respiratory patterns: Difference between revisions
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Latest revision as of 23:58, 29 July 2020
Respiratory Patterns |
Classification |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]
Overview
Normal breathing is consisted of inhalation (sucking the air into the lungs) followed by exhalation (blowing the air out of the lungs). Every exhalation is followed by an automatic pause of about 2 second, before the next inhalation. Normal respiratory rate in a healthy adult is 12-20 per minutes. There are some conditions that may cause variation in rate and depth of respiration. Tachypnea is defined as increase in rate and decrease in depth of breathing. Bradypnea is a decrease in number of breath to less than 8-10 per minute in adults and 16 per minute in infants. Apnea is the respiratory arrest for couple of seconds. Cheyne-Stokes respiration is recurrent central apneustic episodes during sleep. Biot's respiration is a kind of slow respiration pattern with periodic increasing 10-20 respiration per minute, without crescendo–decrescendo pattern. Apneustic respiration is prolonged inspiration arrest followed by inadequate expiration. Agonal breathing is slow, very shallow irregular respirations. Kussmaul's respiration is a deep, sighing respiration with normal or slow rate. Sighing respiration is a normal physiologic reaction of human body to fatigue and emotional changes.
Eupnea
- Normal breathing is consisted of inhalation (sucking the air into the lungs) followed by exhalation (blowing the air out of the lungs).
- Every exhalation is followed by an automatic pause of about 2 second, before the next inhalation.
- Inhalation is an active process using diaphragm muscles, despite exhalation which is a passive process.
- Eupnea is the normal pattern of breathing with a rate of 10-12 per minute, each cycle is composed of:[1]
- Inhalation for 1.5-2 seconds
- Exhalation for 1.5-2 seconds
- Spontaneous stop of 2 seconds
- The main characteristics of eupnea are as following:[2]
- Slow
- Regular
- Nasal inhalation, oral exhalation
- Diaphragmatic
- Effortless
- Clear auscultation:
Normal respiratory rate in every age group is as following:
Age group | Normal respiratory rate (Breath number per minute) |
---|---|
Infants | 30 to 60 |
1 to 3 years | 24 to 40 |
3 to 6 years | 22 to 34 |
6 to 12 years | 18 to 30 |
12 to 18 years | 12 to 16 |
Tachypnea
- Tachypnea is increased rate and decrease depth of breathing.
Decreased plasma oxygen (hypoxemia) | Increased plasma CO2 (respiratory acidosis) | Decreased pulmonary compliance | Increased airway resistance | ||||||||||||||||||||||||||||||||||||||||||||
Carotid body | Medullary chemoreceptors | Pulmonary or muscle mechanoreceptors | Airway receptors | ||||||||||||||||||||||||||||||||||||||||||||
Tachypnea | |||||||||||||||||||||||||||||||||||||||||||||||
The main causes of tachypnea are classified into pulmonary, cardiovascular, hematologic, and metabolic pathophysiologies.[4]
Bradypnea
- Bradypnea is defined as decrease in respiratory rate to less than 8-10 per minute in adults and 16 per minute in infants.
- Mostly in bradypnea the exhalation phase is increased.
- The depth of breathes and tidal volume may be increased during bradypnea episodes.
- The main pathophysiology of bradypnea includes:[5]
- Desensitization of the medullary responses to PCO2
- Reduction in respiratory neuronal activity
- Inhibition of neural transmission within the respiratory center
- Neuronal damage to the brain stem
- The main causes of bradypnea are as following:[6]
Causes | Other | ||
---|---|---|---|
Drugs | Opioids | Heroin | Can become worse when used along with: |
Codeine | |||
Hydrocodone | |||
Morphine | |||
Oxycodone | |||
Toxins | Sodium azide |
| |
Carbon monoxide | |||
Other drugs | Sedatives |
| |
Anesthetics | |||
Systemic disease | Lung diseases | Emphysema | - |
Chronic bronchitis | |||
Severe asthma | |||
Pneumonia | |||
Pulmonary edema | |||
Thyroid | Hypothyroidism | - | |
Neuromuscular | Guillain-Barré syndrome |
| |
Amyotrophic lateral sclerosis (ALS) |
Apnea
- Apnea is the respiratory arrest for couple of seconds.
- The most common form of apnea in generally healthy people is obstructive sleep apnea.
- The pathophysiology of sleep apnea are as following:[7]
Apnea | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sleep disturbances | ↓O2, ↑CO2, ↓pH | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Excessive motor activity | Loss of deep sleep Sleep fragmentation | Brain malfunction | Severe CO2 retention | Systemic vasoconstriction | Pulmonary vasoconstriction | Vagal bradycardia Ectopic cardiac pulses | Decreased pulmonary pressure Increased cardiac afterload | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Restless sleep | Excessive daytime fatigue | Chronic hypoventilation | Systemic hypertension | Pulmonary hypertension | Unexplained nocturnal death | Left heart failure | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Intellectual deterioration | Right heart failure | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Personality change | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Behavioral disorder | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
To read more about sleep apnea, click here.
- The main causes of apnea include:[8]
Cheyne-Stokes Respiration
- Cheyne-Stokes respiration is recurrent central apneustic episodes during sleep.
- Tidal volume has crescendo-decrescendo pattern during Cheyne-Stokes respiration.
- Cheyne-Stokes respiration is almost always due to congestive heart failure, contributed with:[9]
- Patients with congestive heart failure who have already Cheyne-Stokes respiration pattern, would have more mortality rate.[10]
Hypoxemia | Pulmonary vein congestion | Pulmonary C fibers stimulation | Spontaneous arousal | Increased circulating noradrenaline | Decreased cardiac output | Increased cardiac chamber size | Increased blood volume | Hyperventilation during day and night | Restrictive ventilatory defect | Decreased CO2 transfer capacity | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Peripheral chemoreceptor stimulation | Increased pulmonary vagal efferent activity | Increased sympathetic activity | Circulatory delay | Decreased total body CO2 | Decreased total body O2 | Increased pulmonary capillary wedge pressure | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Hyperventilation | Length of the apnea-hyperpnea cycle | Crescendo-decrescendo respiratory pattern | Decreased blood gas buffering capacity | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Cheyne-Stokes respiration | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
- Cheyne-Stokes respiration is mostly secondary to heart failure, but can be associated with following conditions:[12]
Biot's Respiration
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- Camille Biot, in 1878 distinguished Biot's respiration from Cheyne-Stokes, named it “rhythme meningitique”.
- Biot's respiration is a kind of slow respiration pattern with periodic increasing 10-20 respiration per minute, without crescendo–decrescendo pattern.
- Accelerations are different in a patient with Biot's respiration:[14]
- Short and incomplete
- Long and deep
- Often interrupted by gasps
- The periods are different in length, ended to a sigh just before the pause.
- The main causes of Biot's respiration include:[15]
- Pontine lesions
- Damage to the medulla oblongata
- Stroke
- Trauma
- Pressure on the medulla (uncal or tentorial herniation)
- Prolonged opioid abuse
Apneustic Respiration
- Apneustic respiration is first described in 1888 by Marckwald as prolonged inspiration arrest followed by inadequate expiration.
- The rate of apneustic breathing is about 1.5 breath per minute.
- The main causes of apneustic respiration include:[16]
- Congenital brain-stem abnormalities
- Upper pons damage secondary to:[17]
- Severe brain injury
- Ketamine (temporary)
- Phenobarbital
- Apneustic respiration almost always carries a poor prognosis
Agonal Respiration
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- Agonal breathing is slow, very shallow irregular respirations.
- Agonal breathing is resulted from anoxic brain injury.
- The main causes of agonal breathing include:[18]
- The pathophysiology of agonal respiration in decreased blood flow to the brain, which causes gasps.
Kussmaul's Respiration
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- The most important type of disturbed respiratory pattern; Kussmaul's respiration was first described by Adolf Kussmaul in 1874, as "air hunger".[19]
- Kussmaul's respiration is a deep, sighing respiration with normal or slow rate.
- The main pathophysiology of Kussmaul's respiration is increased tidal volume without increasing respiratory rate.
- Compensating metabolic acidosis
- Stimulation of the respiratory center which is located in the brain stem by low serum pH
- Lowering of the partial pressure of CO2 in the alveoli
- Hyperventilation
- In primary stages of acidosis, breathes are rapid and shallow, while they become deeper and slower in the later stages, which are called Kussmaul's respirations.[20]
- Main causes of Kussmaul's respiration include:[19]
- Heart failure
- Liver failure
- Chronic alcohol overuse
- Cancers
- Seizures
- Intense overuse of muscles (overexertion)
- Prolonged low blood sugar levels
- Prolonged elevated blood sugar levels
- Toxic ingestions
Sighing Respiration
- Sighing respiration is a normal physiologic reaction of human body to fatigue and emotional changes.
- Sigh is the elongated, often noisy expiration after inspiration of considerable amounts of air.
- Dyspnea and shortness of breath are commonly contributed to sighing respiration.
- Lack of efficient inspiration and expiration for several seconds is the main basic for sighing respiration.
- The most common causes of sighing respiration are anxiety and depression syndromes.[21]
Sigh syndrome manifestations[22] |
---|
Recurrent deep inspiration, between other normal breathings, by a prolonged and often noisy expiration. |
Generally shallow respiration. |
Patients sense the breathing as obstructive, weightened, and tough. |
Some severe episodes may trigger ample stress. |
Spontaneous episodes, without remarkable trigger or provocation. |
The duration varies from few days to several weeks. |
Without interruption of normal speech. |
Not presented during sleep. |
No relation with physical activity level. |
Self limited, without need to urgent care. |
References
- ↑ St -John WM, Paton JF (December 2003). "Defining eupnea". Respir Physiol Neurobiol. 139 (1): 97–103. PMID 14637316.
- ↑ Ruangkittisakul A, Schwarzacher SW, Secchia L, Ma Y, Bobocea N, Poon BY, Funk GD, Ballanyi K (March 2008). "Generation of eupnea and sighs by a spatiochemically organized inspiratory network". J. Neurosci. 28 (10): 2447–58. doi:10.1523/JNEUROSCI.1926-07.2008. PMID 18322090.
- ↑ Browne GW, Pitchumoni CS (2006). "Pathophysiology of pulmonary complications of acute pancreatitis". World J Gastroenterol. 12 (44): 7087–96. PMC 4087768. PMID 17131469.
- ↑ Yurdakök M (October 2010). "Transient tachypnea of the newborn: what is new?". J. Matern. Fetal. Neonatal. Med. 23 Suppl 3: 24–6. doi:10.3109/14767058.2010.507971. PMID 20807157.
- ↑ Leung, Alexander K. C.; Schmitt, Marcus; Thomas, Christie P.; Sunderkötter, Cord; Schiller, Meinhard; Schwarz, Thomas; Berneburg, Mark; Kohlschütter, Alfried; Cerroni, Lorenzo; Direskeneli, Haner; Calamia, Kenneth; David, Gloria L.; Zeldin, Darryl C.; Schütte, Bärbel; Denson, Lee A.; Erhardt, Andreas; Kubitz, Ralf; Häussinger, Dieter; Sealey, Wendy M.; Mock, Donald M.; Wolf, Barry; Schumacher, Johannes; Propping, Peter; Metze, Dieter; Leung, Alexander K. C.; Wong, Andrew L.; Berneburg, Mark; Schwarz, Thomas; Hengstschläger, Markus; High, Whitney A.; Shroyer, Kenneth R.; McCready, M. Elizabeth; Bulman, Dennis E.; Afzal, Ali R.; Everman, David B.; Stoll, Claude; Darcan, Sukran; Kou, Yu Ru; Lin, You Shuei; Suzuki, Yoichi; Tada, Keiya; Leung, Alexander K. C.; Kupka, Susan; Dietmaier, Wolfgang; Hartmann, Arndt; Hennekam, Raoul C. M.; Belperio, John A.; Keane, Michael P.; Smith, M. Iain; Strieter, Robert M.; Molfino, Nestor A.; Sciandra, Francesca; Rossenbacker, Tom; Priori, Silvia G.; Senzolo, Marco; Triantos, Christos; Samonakis, Dimitrios; Cholongitas, Evangelos; Burroughs, Andrew K.; Mura, Marco; Braun-Falco, Markus; Hofmann, Silke; Bruckner-Tuderman, Leena (2009). "Bradypnea": 241–243. doi:10.1007/978-3-540-29676-8_246.
- ↑ Flisberg P, Jakobsson J, Lundberg J (March 2002). "Apnea and bradypnea in patients receiving epidural bupivacaine-morphine for postoperative pain relief as assessed by a new monitoring method". J Clin Anesth. 14 (2): 129–34. PMID 11943527.
- ↑ "Obstructive Sleep Apnea - National Library of Medicine - PubMed Health".
- ↑ Spicuzza L, Caruso D, Di Maria G (2015). "Obstructive sleep apnoea syndrome and its management". Ther Adv Chronic Dis. 6 (5): 273–85. doi:10.1177/2040622315590318. PMC 4549693. PMID 26336596.
- ↑ Nachtmann A, Siebler M, Rose G, Sitzer M, Steinmetz H (April 1995). "Cheyne-Stokes respiration in ischemic stroke". Neurology. 45 (4): 820–1. PMID 7723977.
- ↑ Hanly PJ, Zuberi-Khokhar NS (January 1996). "Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure". Am. J. Respir. Crit. Care Med. 153 (1): 272–6. doi:10.1164/ajrccm.153.1.8542128. PMID 8542128.
- ↑ Naughton, M T (1998). "Pathophysiology and treatment of Cheyne-Stokes respiration". Thorax. 53 (6): 514–518. doi:10.1136/thx.53.6.514. ISSN 0040-6376.
- ↑ Lieber C, Mohsenin V (1992). "Cheyne-Stokes respiration in congestive heart failure". Yale J Biol Med. 65 (1): 39–50. PMC 2589377. PMID 1509783.
- ↑ 13.0 13.1 CC BY-SA 3.0, <"https://commons.wikimedia.org/wiki/File%3ABreathing_abnormalities.svg">
- ↑ Wijdicks, E. F M (2006). "Biot's breathing". Journal of Neurology, Neurosurgery & Psychiatry. 78 (5): 512–513. doi:10.1136/jnnp.2006.104919. ISSN 0022-3050.
- ↑ Casas-Méndez LF, Lujan M, Vigil L, Sansa G (2011). "Biot's breathing in a woman with fatal familial insomnia: is there a role for noninvasive ventilation?". J Clin Sleep Med. 7 (1): 89–91. PMC 3041627. PMID 21344052.
- ↑ Mador MJ, Tobin MJ (April 1990). "Apneustic breathing. A characteristic feature of brainstem compression in achondroplasia?". Chest. 97 (4): 877–83. PMID 2323256.
- ↑ Wilken, B.; Lalley, P.; Bischoff, A.M.; Christen, H.J.; Behnke, J.; Hanefeld, F.; Richter, D.W. (1997). "Treatment of apneustic respiratory disturbance with a serotonin-receptor agonist". The Journal of Pediatrics. 130 (1): 89–94. doi:10.1016/S0022-3476(97)70315-9. ISSN 0022-3476.
- ↑ Perkin RM, Resnik DB (2002). "The agony of agonal respiration: is the last gasp necessary?". J Med Ethics. 28 (3): 164–9. PMC 1733591. PMID 12042401.
- ↑ 19.0 19.1 Ammons MA, Moore EE, Moore FA (August 1989). "Increased incidence of cardiac contusion in patients with traumatic thoracic aortic rupture". Ann. Surg. 210 (2): 252–4. PMID 2757428.
- ↑ Seth P, Kaur H, Kaur M (2015). "Clinical Profile of Diabetic Ketoacidosis: A Prospective Study in a Tertiary Care Hospital". J Clin Diagn Res. 9 (6): OC01–4. doi:10.7860/JCDR/2015/8586.5995. PMC 4525534. PMID 26266145.
- ↑ Patroniti N, Foti G, Cortinovis B, Maggioni E, Bigatello LM, Cereda M, Pesenti A (April 2002). "Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation". Anesthesiology. 96 (4): 788–94. PMID 11964584.
- ↑ Sody AN, Kiderman A, Biton A, Furst A (January 2008). "Sigh syndrome: is it a sign of trouble?". J Fam Pract. 57 (1): E1–5. PMID 18171560.