Respiratory patterns: Difference between revisions
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==Overview== | ==Overview== | ||
== Eupnea == | == Eupnea == | ||
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== Kussmaul's Respiration == | == Kussmaul's Respiration == | ||
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== References == | == References == | ||
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Revision as of 16:05, 5 March 2018
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Respiratory Patterns |
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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]
Synonyms and keywords:
Overview
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:
- Inhalation of 1.5-2 seconds
- Exhalation of 1.5-2 seconds
- Spontaneous stop of 2 seconds
- The main characteristics of eupnea are as following:
- 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.
The main pathophysiology of tachypnea is as following:
| 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.
Bradypnea
- Bradypnea is decreased count of breath 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:[1]
- 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:
| 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:
| 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 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
- The main causes of apnea include:
Cheyne-Stokes Respiration
- Cheyne-Stokes respiration is recurrent central apneustic episodes during sleep.
- Tidal volume is in crescendo-decrescendo manner during Cheyne-Stokes respiration.
- Cheyne-Stokes respiration is almost always due to congestive heart failure, contributed with:
- Patients with congestive heart failure who have already Cheyne-Stokes respiration pattern, would have more mortality rate.[2]
The main pathophysiology of Cheyne-Stokes respiration pattern is as following:[3]
| 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:
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:[5]
- 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:
- 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
- Congenital brain-stem abnormalities
- Upper pons damage secondary to:[6]
- 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:
- 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, is first described by Adolf Kussmaul in 1874, as "air hunger".
- 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.
- Main causes of Kussmaul's respiration include:
 |
- 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
References
- ↑ 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.
- ↑ 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.
- ↑ 4.0 4.1 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.
- ↑ 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.
