Respiratory patterns: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 4: Line 4:


{{CMG}}; {{AE}} {{EG}}
{{CMG}}; {{AE}} {{EG}}
{{SK}}
==Overview==
==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]]. Tachypnea is increased rate and decrease depth of [[breathing]]. [[Bradypnea]] is decreased count 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 respirations|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 [[Respiration|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 ==
== Eupnea ==
Line 13: Line 11:
* Every [[exhalation]] is followed by an automatic pause of about 2 second, before the next [[inhalation]].
* 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.
* [[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:
* [[Eupnea]] is the normal pattern of [[breathing]] with a rate of 10-12 per minute, each cycle is composed of:<ref name="pmid14637316">{{cite journal |vauthors=St -John WM, Paton JF |title=Defining eupnea |journal=Respir Physiol Neurobiol |volume=139 |issue=1 |pages=97–103 |date=December 2003 |pmid=14637316 |doi= |url=}}</ref>
** [[Inhalation]] of 1.5-2 seconds
** [[Inhalation]] of 1.5-2 seconds
** [[Exhalation]] of 1.5-2 seconds
** [[Exhalation]] of 1.5-2 seconds
** Spontaneous stop of 2 seconds
** Spontaneous stop of 2 seconds
* The main characteristics of eupnea are as following:
* The main characteristics of eupnea are as following:<ref name="pmid18322090">{{cite journal |vauthors=Ruangkittisakul A, Schwarzacher SW, Secchia L, Ma Y, Bobocea N, Poon BY, Funk GD, Ballanyi K |title=Generation of eupnea and sighs by a spatiochemically organized inspiratory network |journal=J. Neurosci. |volume=28 |issue=10 |pages=2447–58 |date=March 2008 |pmid=18322090 |doi=10.1523/JNEUROSCI.1926-07.2008 |url=}}</ref>
** Slow
** Slow
** Regular
** Regular
Line 53: Line 51:
* Tachypnea is increased rate and decrease depth of [[breathing]].
* Tachypnea is increased rate and decrease depth of [[breathing]].


<div style="text-align: center;">'''The main pathophysiology of tachypnea is as following:'''</div>
<div style="text-align: center;">'''The main pathophysiology of tachypnea is as following:'''<ref name="pmid171314692">{{cite journal| author=Browne GW, Pitchumoni CS| title=Pathophysiology of pulmonary complications of acute pancreatitis. | journal=World J Gastroenterol | year= 2006 | volume= 12 | issue= 44 | pages= 7087-96 | pmid=17131469 | doi= | pmc=4087768 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17131469  }}</ref></div>


{{family tree/start}}
{{family tree/start}}
Line 63: Line 61:
{{family tree/end}}
{{family tree/end}}


=== The main causes of tachypnea are classified into [[pulmonary]], [[cardiovascular]], [[hematologic]], and [[metabolic]] pathophysiologies. ===
=== The main causes of tachypnea are classified into [[pulmonary]], [[cardiovascular]], [[hematologic]], and [[metabolic]] pathophysiologies.<ref name="pmid20807157">{{cite journal |vauthors=Yurdakök M |title=Transient tachypnea of the newborn: what is new? |journal=J. Matern. Fetal. Neonatal. Med. |volume=23 Suppl 3 |issue= |pages=24–6 |date=October 2010 |pmid=20807157 |doi=10.3109/14767058.2010.507971 |url=}}</ref> ===
{| class="wikitable"
{| class="wikitable"
! colspan="2" |Causes
! colspan="2" |Causes
Line 152: Line 150:
** Inhibition of [[neural]] transmission within the [[respiratory center]]
** Inhibition of [[neural]] transmission within the [[respiratory center]]
** [[Neuronal]] damage to the [[brain stem]]
** [[Neuronal]] damage to the [[brain stem]]
* The main causes of bradypnea are as following:
* The main causes of bradypnea are as following:<ref name="pmid11943527">{{cite journal |vauthors=Flisberg P, Jakobsson J, Lundberg J |title=Apnea and bradypnea in patients receiving epidural bupivacaine-morphine for postoperative pain relief as assessed by a new monitoring method |journal=J Clin Anesth |volume=14 |issue=2 |pages=129–34 |date=March 2002 |pmid=11943527 |doi= |url=}}</ref>
{| class="wikitable"
{| class="wikitable"
! colspan="3" |Causes
! colspan="3" |Causes
Line 227: Line 225:
* [[Apnea]] is the [[respiratory arrest]] for couple of seconds.
* [[Apnea]] is the [[respiratory arrest]] for couple of seconds.
* The most common form of [[apnea]] in generally healthy people is [[obstructive sleep apnea]].
* The most common form of [[apnea]] in generally healthy people is [[obstructive sleep apnea]].
* The [[pathophysiology]] of [[sleep apnea]] are as following:
* The [[pathophysiology]] of [[sleep apnea]] are as following:<ref name="urlObstructive Sleep Apnea - National Library of Medicine - PubMed Health">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024431/ |title=Obstructive Sleep Apnea - National Library of Medicine - PubMed Health |format= |work= |accessdate=}}</ref>
<small>
<small>
{{family tree/start}}
{{family tree/start}}
Line 243: Line 241:
{{family tree/end}}
{{family tree/end}}
</small>
</small>
* The main causes of [[apnea]] include:
* The main causes of [[apnea]] include:<ref name="pmid26336596">{{cite journal| author=Spicuzza L, Caruso D, Di Maria G| title=Obstructive sleep apnoea syndrome and its management. | journal=Ther Adv Chronic Dis | year= 2015 | volume= 6 | issue= 5 | pages= 273-85 | pmid=26336596 | doi=10.1177/2040622315590318 | pmc=4549693 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26336596  }}</ref>
** [[Obstructive sleep apnea]]
** [[Obstructive sleep apnea]]
** [[Opioid toxicity]]
** [[Opioid toxicity]]
Line 271: Line 269:
* Cheyne-Stokes [[respiration]] is recurrent central [[Apneustic respirations|apneustic episodes]] during [[sleep]].
* Cheyne-Stokes [[respiration]] is recurrent central [[Apneustic respirations|apneustic episodes]] during [[sleep]].
* [[Tidal volume]] is in crescendo-decrescendo manner during Cheyne-Stokes [[respiration]].
* [[Tidal volume]] is in crescendo-decrescendo manner during Cheyne-Stokes [[respiration]].
* Cheyne-Stokes [[respiration]] is almost always due to congestive heart failure, contributed with:
* Cheyne-Stokes [[respiration]] is almost always due to congestive heart failure, contributed with:<ref name="pmid7723977">{{cite journal |vauthors=Nachtmann A, Siebler M, Rose G, Sitzer M, Steinmetz H |title=Cheyne-Stokes respiration in ischemic stroke |journal=Neurology |volume=45 |issue=4 |pages=820–1 |date=April 1995 |pmid=7723977 |doi= |url=}}</ref>
** [[Orthopnoea|Orthopnea]]
** [[Orthopnoea|Orthopnea]]
** [[Paroxysmal nocturnal dyspnea]]
** [[Paroxysmal nocturnal dyspnea]]
Line 294: Line 292:
</small>
</small>
</small>
</small>
* Cheyne-Stokes respiration is mostly secondary to [[heart failure]], but can be associated with following conditions:
* Cheyne-Stokes respiration is mostly secondary to [[heart failure]], but can be associated with following conditions:<ref name="pmid1509783">{{cite journal| author=Lieber C, Mohsenin V| title=Cheyne-Stokes respiration in congestive heart failure. | journal=Yale J Biol Med | year= 1992 | volume= 65 | issue= 1 | pages= 39-50 | pmid=1509783 | doi= | pmc=2589377 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1509783  }}</ref>


[[image:Cheyne Stokes.jpg|thumb|500px|Cheyne-Stokes respiration pattern - By Sav vas (Own work), via Wikimedia Commons<ref name="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0, <"https://commons.wikimedia.org/wiki/File%3ABreathing_abnormalities.svg"></ref>]]
[[image:Cheyne Stokes.jpg|thumb|500px|Cheyne-Stokes respiration pattern - By Sav vas (Own work), via Wikimedia Commons<ref name="https://creativecommons.org/licenses/by-sa/3.0">CC BY-SA 3.0, <"https://commons.wikimedia.org/wiki/File%3ABreathing_abnormalities.svg"></ref>]]
Line 326: Line 324:
<br>
<br>


* The main causes of Biot's respiration include:
* The main causes of Biot's respiration include:<ref name="pmid21344052">{{cite journal| author=Casas-Méndez LF, Lujan M, Vigil L, Sansa G| title=Biot's breathing in a woman with fatal familial insomnia: is there a role for noninvasive ventilation? | journal=J Clin Sleep Med | year= 2011 | volume= 7 | issue= 1 | pages= 89-91 | pmid=21344052 | doi= | pmc=3041627 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21344052  }}</ref>
** [[Pontine|Pontine lesions]]
** [[Pontine|Pontine lesions]]
** Damage to the [[medulla oblongata]]
** Damage to the [[medulla oblongata]]
Line 342: Line 340:
* Apneustic respiration is first described in 1888 by Marckwald as prolonged [[inspiration]] arrest followed by inadequate [[expiration]].
* Apneustic respiration is first described in 1888 by Marckwald as prolonged [[inspiration]] arrest followed by inadequate [[expiration]].
* The rate of [[Apneustic respirations|apneustic breathing]] is about 1.5 breath per minute.
* The rate of [[Apneustic respirations|apneustic breathing]] is about 1.5 breath per minute.
* The main causes of [[Apneustic respirations|apneustic respiration]] include
* The main causes of [[Apneustic respirations|apneustic respiration]] include:<ref name="pmid2323256">{{cite journal |vauthors=Mador MJ, Tobin MJ |title=Apneustic breathing. A characteristic feature of brainstem compression in achondroplasia? |journal=Chest |volume=97 |issue=4 |pages=877–83 |date=April 1990 |pmid=2323256 |doi= |url=}}</ref>
** [[Congenital]] [[Brain stem|brain-stem]] abnormalities
** [[Congenital]] [[Brain stem|brain-stem]] abnormalities
** Upper [[pons]] damage secondary to:<ref name="WilkenLalley1997">{{cite journal|last1=Wilken|first1=B.|last2=Lalley|first2=P.|last3=Bischoff|first3=A.M.|last4=Christen|first4=H.J.|last5=Behnke|first5=J.|last6=Hanefeld|first6=F.|last7=Richter|first7=D.W.|title=Treatment of apneustic respiratory disturbance with a serotonin-receptor agonist|journal=The Journal of Pediatrics|volume=130|issue=1|year=1997|pages=89–94|issn=00223476|doi=10.1016/S0022-3476(97)70315-9}}</ref>
** Upper [[pons]] damage secondary to:<ref name="WilkenLalley1997">{{cite journal|last1=Wilken|first1=B.|last2=Lalley|first2=P.|last3=Bischoff|first3=A.M.|last4=Christen|first4=H.J.|last5=Behnke|first5=J.|last6=Hanefeld|first6=F.|last7=Richter|first7=D.W.|title=Treatment of apneustic respiratory disturbance with a serotonin-receptor agonist|journal=The Journal of Pediatrics|volume=130|issue=1|year=1997|pages=89–94|issn=00223476|doi=10.1016/S0022-3476(97)70315-9}}</ref>
Line 359: Line 357:
* Agonal [[breathing]] is slow, very shallow irregular [[Respiration|respirations]].
* Agonal [[breathing]] is slow, very shallow irregular [[Respiration|respirations]].
* Agonal [[breathing]] is resulted from [[anoxic brain injury]].
* Agonal [[breathing]] is resulted from [[anoxic brain injury]].
* The main causes of agonal [[breathing]] include:
* The main causes of agonal [[breathing]] include:<ref name="pmid12042401">{{cite journal| author=Perkin RM, Resnik DB| title=The agony of agonal respiration: is the last gasp necessary? | journal=J Med Ethics | year= 2002 | volume= 28 | issue= 3 | pages= 164-9 | pmid=12042401 | doi= | pmc=1733591 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12042401  }}</ref>
** [[Cardiac arrest]]
** [[Cardiac arrest]]
** [[Stroke]]
** [[Stroke]]
Line 374: Line 372:
|{{#ev:youtube|raEKXVfuWTo|500}}
|{{#ev:youtube|raEKXVfuWTo|500}}
|}
|}
* The most important type of disturbed respiratory pattern, [[Kussmaul's respiration]], is first described by Adolf Kussmaul in 1874, as "[[air hunger]]".  
* The most important type of disturbed respiratory pattern, [[Kussmaul's respiration]], is first described by Adolf Kussmaul in 1874, as "[[air hunger]]".<ref name="pmid2757428" />
* Kussmaul's respiration is a deep, sighing [[respiration]] with normal or slow rate.  
* 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]].
* The main [[pathophysiology]] of Kussmaul's [[respiration]] is increased [[tidal volume]] without increasing [[respiratory rate]].
Line 381: Line 379:
*# Lowering of the [[partial pressure]] of [[CO2]] in the [[alveoli]]
*# Lowering of the [[partial pressure]] of [[CO2]] in the [[alveoli]]
*# [[Hyperventilation]]
*# [[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.
* 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.<ref name="pmid26266145">{{cite journal| author=Seth P, Kaur H, Kaur M| title=Clinical Profile of Diabetic Ketoacidosis: A Prospective Study in a Tertiary Care Hospital. | journal=J Clin Diagn Res | year= 2015 | volume= 9 | issue= 6 | pages= OC01-4 | pmid=26266145 | doi=10.7860/JCDR/2015/8586.5995 | pmc=4525534 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26266145  }}</ref>
* Main causes of Kussmaul's respiration include:
* Main causes of Kussmaul's respiration include:<ref name="pmid2757428">{{cite journal |vauthors=Ammons MA, Moore EE, Moore FA |title=Increased incidence of cardiac contusion in patients with traumatic thoracic aortic rupture |journal=Ann. Surg. |volume=210 |issue=2 |pages=252–4 |date=August 1989 |pmid=2757428 |doi= |url=}}</ref>
** [[Diabetic ketoacidosis]]
** [[Diabetic ketoacidosis]]
** [[Renal failure]]
** [[Renal failure]]
Line 405: Line 403:


== Sighing Respiration ==
== 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.<ref name="pmid11964584">{{cite journal |vauthors=Patroniti N, Foti G, Cortinovis B, Maggioni E, Bigatello LM, Cereda M, Pesenti A |title=Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation |journal=Anesthesiology |volume=96 |issue=4 |pages=788–94 |date=April 2002 |pmid=11964584 |doi= |url=}}</ref>
{| class="wikitable"
!Sigh syndrome manifestations<ref name="pmid18171560">{{cite journal |vauthors=Sody AN, Kiderman A, Biton A, Furst A |title=Sigh syndrome: is it a sign of trouble? |journal=J Fam Pract |volume=57 |issue=1 |pages=E1–5 |date=January 2008 |pmid=18171560 |doi= |url=}}</ref>
|-
|Recurrent deep [[inspiration]], between other normal [[Breathing|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 ==
== References ==
<references />
{{reflist|2}}
 
[[Category:Medicine]]
[[Category:Emergency medicine]]
[[Category:Pulmonology]]
[[Category:Cardiology]]
[[Category:primary care]]
[[Category:Up-To-Date]]

Revision as of 17:06, 5 March 2018


Respiratory Patterns
main page

Overview

Classification

Eupnea
Tachypnea
Bradypnea
Apnea
Cheyne-Stokes Respiration
Biot's Respiration
Apneustic Respiration
Agonal Respiration
Kussmaul's Respiration
Sighing Respiration

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. Tachypnea is increased rate and decrease depth of breathing. Bradypnea is decreased count 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 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:[3]
 
 
 
 
 
 
 
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]

Causes Other findings
Pulmonary Asthma
Chronic obstructive pulmonary disease (COPD)
Pneumonia
Congestive heart failure (CHF)
Pneumothorax
Cardiovascular Pericardial effusion
Cardiac Tamponade
Pulmonary embolism
Myocardial infarct
  • Inverted T-wave or depressed/elevated ST-segment
  • Local or generalized wall motion abnormality
Hematologic Anemia
Sickle cell disease
Metabolic Metabolic acidosis
Diabetic ketoacidosis (DKA)

Bradypnea

Causes Other
Drugs Opioids Heroin Can become worse when used along with:
Codeine
Hydrocodone
Morphine
Oxycodone
Toxins Sodium azide
  • Found in automobile airbags
Carbon monoxide
  • Produced from oil or gas furnaces
  • Absorbed by lungs and decrease the blood oxygen level
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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Cheyne-Stokes Respiration

The main pathophysiology of Cheyne-Stokes respiration pattern is as following:[11]


 
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]
Cheyne-Stokes respiration pattern - By Sav vas (Own work), via Wikimedia Commons[13]


Biot's Respiration

P7zvzDUcCCQ|500}}

{{#ev:youtube|REeIL9a0_PM|500}}

  • 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.










Apneustic Respiration

Agonal Respiration

CBMxH4xtE8w|500}}




Kussmaul's Respiration

raEKXVfuWTo|500}}
Kussmaul's respiration pattern - By Sav vas (Own work), via Wikimedia Commons[13]

Sighing Respiration

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

  1. ↑ St -John WM, Paton JF (December 2003). "Defining eupnea". Respir Physiol Neurobiol. 139 (1): 97–103. PMID 14637316.
  2. ↑ 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.
  3. ↑ Browne GW, Pitchumoni CS (2006). "Pathophysiology of pulmonary complications of acute pancreatitis". World J Gastroenterol. 12 (44): 7087–96. PMC 4087768. PMID 17131469.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ "Obstructive Sleep Apnea - National Library of Medicine - PubMed Health".
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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. ↑ 13.0 13.1 CC BY-SA 3.0, <"https://commons.wikimedia.org/wiki/File%3ABreathing_abnormalities.svg">
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ Mador MJ, Tobin MJ (April 1990). "Apneustic breathing. A characteristic feature of brainstem compression in achondroplasia?". Chest. 97 (4): 877–83. PMID 2323256.
  17. ↑ 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.
  18. ↑ 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. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
Retrieved from "https://www.wikidoc.org/index.php?title=Respiratory_patterns&oldid=1451710"