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__NOTOC__
__NOTOC__
{{Cyanosis}}
{{Cyanosis}}
{{CMG}}; {{AE}} {{MAD}}
{{CMG}}; {{AE}} {{Sara.Zand}} {{MAD}}


==Overview==
==Overview==
In every neonate presented with cyanosis and shock, [[congenital heart disease]] dependent on [[patency ductus arteriosus]] should be considered. The physiologic constriction of [[ductus arteriosus]] after birth in a [[neonate]] whose [[pulmonary blood flow]] or [[aortic blood flow]] is dependent on [[PDA]] leads to [[shock]] and [[collapse]] in the [[neonate]]. Infusion of [[prostaglan]] in such a [[neonate]] is life-saving and keeps [[patency ductus arteriosus]]. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock  due to [[low cardiac output state]] and [[peripheral vasoconstriction]] lead to disappearing of [[cyanosis]].
In every neonate presented with cyanosis and shock, [[congenital heart disease]] dependent on [[patency ductus arteriosus]] should be considered. The physiologic constriction of [[ductus arteriosus]] after birth in a [[neonate]] whose [[pulmonary blood flow]] or [[aortic blood flow]] is dependent on [[PDA]] leads to [[shock]] and [[collapse]] in the [[neonate]]. Infusion of [[prostaglan]] in such a [[neonate]] is life-saving and keeps [[patency ductus arteriosus]]. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock  due to [[low cardiac output state]] and [[peripheral vasoconstriction]] lead to disappearing of [[cyanosis]].
== Medical therapy ==
*The mainstay of therapy for [[cyanosis]] is the treatment of underlying causes of [[cyanosis]].
* In cyanotic [[congenital heart disease ]] whether the flow is dependent on patency ductus arteriosus, infusion of  [[prostaglandin]] E1  is recommended.
* In the setting of pulmonary disease such as [[pneumonia]], [[pleural effusion]], treatment of underlying disease and [[oxygen]] therapy are advised.
* In the setting of low cardiac output state such as [[pulmonary thromboembolism]] and [[ cardiogenic shock]], management of thrombotic events and [[oxygen]] supplement therapy is recommended.
* In [[methemoglobinemia]] discontinuing the medications related disorder and administration of [[methylene blue]] is recommended.


== Medical therapy of [[Cyanosis]] ==
== Medical therapy of [[Cyanosis]] ==
<ref name="CucereaSimon2016">{{cite journal|last1=Cucerea|first1=Manuela|last2=Simon|first2=Marta|last3=Moldovan|first3=Elena|last4=Ungureanu|first4=Marcela|last5=Marian|first5=Raluca|last6=Suciu|first6=Laura|title=Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit|journal=The Journal of Critical Care Medicine|volume=2|issue=4|year=2016|pages=185–191|issn=2393-1817|doi=10.1515/jccm-2016-0031}}</ref>
The mainstay of therapy is treatment of underlying causes of [[cyanosis]].<ref name="CucereaSimon2016">{{cite journal|last1=Cucerea|first1=Manuela|last2=Simon|first2=Marta|last3=Moldovan|first3=Elena|last4=Ungureanu|first4=Marcela|last5=Marian|first5=Raluca|last6=Suciu|first6=Laura|title=Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit|journal=The Journal of Critical Care Medicine|volume=2|issue=4|year=2016|pages=185–191|issn=2393-1817|doi=10.1515/jccm-2016-0031}}</ref>
<ref name="HenretigGribetz2011">{{cite journal|last1=Henretig|first1=Fred M.|last2=Gribetz|first2=Bruce|last3=Kearney|first3=Thomas|last4=Lacouture|first4=Peter|last5=Loveiov|first5=Frederick H.|title=Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia|journal=Journal of Toxicology: Clinical Toxicology|volume=26|issue=5-6|year=2011|pages=293–301|issn=0731-3810|doi=10.1080/15563658809167094}}</ref><ref name="TisiWolfe1970">{{cite journal|last1=Tisi|first1=G M|last2=Wolfe|first2=W G|last3=Fallat|first3=R J|last4=Nadel|first4=J A|title=Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion.|journal=Journal of Applied Physiology|volume=28|issue=5|year=1970|pages=570–573|issn=8750-7587|doi=10.1152/jappl.1970.28.5.570}}</ref><ref name="Austin1973">{{cite journal|last1=Austin|first1=John H. M.|title=Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs|journal=Investigative Radiology|volume=8|issue=5|year=1973|pages=315–321|issn=0020-9996|doi=10.1097/00004424-197309000-00003}}</ref><ref>{{cite journal|doi=10.1164/rccm.201503-0584OC.}}</ref>
<ref name="HenretigGribetz2011">{{cite journal|last1=Henretig|first1=Fred M.|last2=Gribetz|first2=Bruce|last3=Kearney|first3=Thomas|last4=Lacouture|first4=Peter|last5=Loveiov|first5=Frederick H.|title=Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia|journal=Journal of Toxicology: Clinical Toxicology|volume=26|issue=5-6|year=2011|pages=293–301|issn=0731-3810|doi=10.1080/15563658809167094}}</ref><ref name="TisiWolfe1970">{{cite journal|last1=Tisi|first1=G M|last2=Wolfe|first2=W G|last3=Fallat|first3=R J|last4=Nadel|first4=J A|title=Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion.|journal=Journal of Applied Physiology|volume=28|issue=5|year=1970|pages=570–573|issn=8750-7587|doi=10.1152/jappl.1970.28.5.570}}</ref><ref name="Austin1973">{{cite journal|last1=Austin|first1=John H. M.|title=Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs|journal=Investigative Radiology|volume=8|issue=5|year=1973|pages=315–321|issn=0020-9996|doi=10.1097/00004424-197309000-00003}}</ref><ref>{{cite journal|doi=10.1164/rccm.201503-0584OC.}}</ref><ref name="SmedleyGrocott2013">{{cite journal|last1=Smedley|first1=Tom|last2=Grocott|first2=Michael PW|title=Acute high-altitude illness: a clinically orientated review|journal=British Journal of Pain|volume=7|issue=2|year=2013|pages=85–94|issn=2049-4637|doi=10.1177/2049463713489539}}</ref>
 
'''<span style="font-size:85%">'''Abbreviations:'''
'''<span style="font-size:85%">'''Abbreviations:'''
'''d-TGA:''' [[ dextro-Transposition of great arteries]];
'''d-TGA:''' [[ dextro-Transposition of great arteries]];
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{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Causes of [[cyanosis]]!![[CHD]] dependent on [[PDA]]!![[CHD]]  with severe restriction of [[pulmonary blood flow]]!![[CHD]] with severe restriction of [[systemic blood flow]]!![[CHD]] due to bidirectional shunt!![[Methemoglobinemia]]!![[PTE]]!![[Cardiogenic shock]]!![[ARDS]]!![[Acute mountain sickness]]!![[Pulmonary edema]]
!Causes of [[cyanosis]]!![[CHD]]  with severe restriction of [[pulmonary blood flow]]!![[CHD]] with severe restriction of [[systemic blood flow]]!![[CHD]] due to bidirectional shunt!![[Methemoglobinemia]]!![[PTE]]!![[Cardiogenic shock]]!![[ARDS]]!![[Acute mountain sickness]]
|-
|-
|Example||Example||
 
||'''Note'''||
*[[Pulmonary atresia]]
*[[Pulmonary atresia]]
*[[Tricuspid atresia]]
*[[Tricuspid atresia]]
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*[[Coarctation aorta]]
*[[Coarctation aorta]]
*[[Interrupted aortic arch]]
*[[Interrupted aortic arch]]
*[[Left hypoplastic syndrome]]
*[[Hypoplastic  left heart syndrome]]


||
||
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|| Complication of exposue to some drugs such as [[nitrites]] and [[aniline]] leading to [[dizziness]] , [[coma]], chocolate-brown discoloration of [[blood]] samples, [[respiratory distress]] [[seizures]] and [[myocardial ischemia]]   
|| Complication of exposue to some drugs such as [[nitrites]] and [[aniline]] leading to [[dizziness]] , [[coma]], chocolate-brown discoloration of [[blood]] samples, [[respiratory distress]] [[seizures]] and [[myocardial ischemia]]   
|| [[Hypoxia]] due to V/Q  mismatch, low [[cardiac out-put]] state, acute [[ right ventricular dilation]] and increased [[pulmonary vascular resistance]]
|| [[Hypoxia]] due to V/Q  mismatch, low [[cardiac out-put]] state, acute [[ right ventricular dilation]] and increased [[pulmonary vascular resistance]]
|| Example ||  
|| [[Cyanosis]], [[olyguria]], [[altered mental status]]  ||  
*SpO2/FiO2 <315, No PEEP requirement  
*SpO2/FiO2 <315, No PEEP requirement  
||Example|| Complication of [[pneumonia]], [[non cardiogenic shock]], [[drug overdose]], [[trauma]]|| Example
*Complication of [[pneumonia]], [[non cardiogenic shock]], [[drug overdose]], [[trauma]]
||Leakage of large molecules  into alveolar space  leading rich protein [[pulmonary edema]]
|-
|-
| '''Mechanism of [[cyanosis]]''' || Example|| [[ Hypoxia]] and [[cyanosis]] due to constriction of the [[ductus arteriosus]] after birth and dependency of the [[Pulmonary circulation]] on the [[patency of the ductus arteriosus]]||[[Cyanosis]],[[systemic hypoperfusion]], [[circulatory collapse]], [[metabolic acidosis]], [[shock]] due to constriction ductus arteriosus and dependency systemic circulation on  [[PDA]] after birth  ||  Constriction of [[PDA]] after birth leading decreased systemic circulation due to mixing of [[pulmonary]] and [[systemic blood flow]] via [[PDA]]
| '''Mechanism of [[cyanosis]]''' || [[ Hypoxia]] and [[cyanosis]] due to constriction of the [[ductus arteriosus]] after birth and dependency of the [[Pulmonary circulation]] on the [[patency of the ductus arteriosus]]||[[Cyanosis]],[[systemic hypoperfusion]], [[circulatory collapse]], [[metabolic acidosis]], [[shock]] due to constriction ductus arteriosus and dependency systemic circulation on  [[PDA]] after birth  ||  Constriction of [[PDA]] after birth leading decreased systemic circulation due to mixing of [[pulmonary]] and [[systemic blood flow]] via [[PDA]]
||  
||  
*[[Oxidative sresss]] , [[methemoglobin]] level > 10 % total [[hemoglobin]]  
*[[Oxidative sresss]] , [[methemoglobin]] level > 10 % total [[hemoglobin]]  
* [[Cyanosis]] refractory to [[oxygen]] therapy,  
* [[Cyanosis]] refractory to [[oxygen]] therapy,  
  ||
  ||
*[[V/Q mismatches]]  due to small airway constriction in both nonperfused and nonembolized areas of [[lung]], reduced [[surfactant]] production, development of [[pulmonary edema]] and [[atelectasis]]
*[[V/Q mismatches]]  due to small airway constriction in both nonperfused and nonembolized areas of [[lung]], reduced [[surfactant]] production, [[pulmonary edema]], [[atelectasis]]
*Right to left shunt via [[PFO]] leading [[central cyanosis]]
*Right to left shunt via [[PFO]] leading [[central cyanosis]]
* Low cardiac output state due to [[right ventricular dilation]] and increased [[PVR]] leading to [[peripheral cyanosia]]
* Low [[cardiac output]] state due to [[right ventricular dilation]] and increased [[PVR]] leading to [[peripheral cyanosia]]
|| Example|| Increased alveolar vascular permeability, interstitial and alveolar [[pulmonary
|| Low [[cardiac output]] state due to [[myocardial infarction]] and [[pump failure]] leading to  vasoconstriction and [[peripheral cyanosis]]||  
edema]].|| Example|| Example||
*Increased alveolar vascular permeability
*Interstitial and alveolar [[pulmonary edema]]
 
|| [[Central cyanosis]] due to alveolar [[hypoxia]] , [[pulmonary vasoconstriction]], [[ pulmonary hypertension]]
|-
|-
|'''Treatment''' ||Example||[[Prostaglandin]] E1 ||[[Prostaglandin ]] E1||[[Prostaglandin]] E1||
|'''Treatment'''||[[Prostaglandin]] E1 ||[[Prostaglandin ]] E1||[[Prostaglandin]] E1||
*[[Methylenblue]] infusion  
*[[Methylenblue]] infusion  
* Hyperbaric [[oxygen]] therapy  
* Hyperbaric [[oxygen]] therapy  
*[[Ascorbic acid]]
*[[Ascorbi:c acid]]
||  
||  
*[[Anticoagulant therapy]]
*[[Anticoagulant therapy]]
Line 71: Line 89:
*[[ Mechanical thrombectomy]]
*[[ Mechanical thrombectomy]]


||Example||
||[[Coronary revascularization ]]||
*[[Extracorporeal membrane oxygenation]]
*[[Extracorporeal membrane oxygenation]]
*[[High-frequency oscillatory ventilation]]
*[[High-frequency oscillatory ventilation]]
*[[Neuromuscular blocking agents]]
*[[Neuromuscular blocking agents]]
*Intravenous β-2 agonist ([[Salbutamol]])||
*Intravenous β-2 agonist ([[Salbutamol]])
||
*Descent
*Supplement [[oxygen]] therapy
*Portable hyperbaric chamber
*[[Nifedipine]]
|}
|}
==Respiratory distress syndrome==
===Surfactant therapy===
*Exogenous [[surfactant]] replacement therapy is effective in reducing [[RDS]] [[mortality]] and [[morbidity]] in [[preterm]] infants.
*It may be natural or synthetic surfactants.
*Natural surfactants have been shown to be more efficient with lower inspired oxygen concentration and ventilator pressures, decreased mortality, and lower rate of RDS complications in preterm infants.
*All patients with RDS, and intubate and administer surfactant to those with persistent severe [[Respiratory failure|respiratory distress]] (defined as requiring a fraction of inspired oxygen [[[FiO2]]] of 0.40 or higher to maintain [[oxygen saturation]] above 90 percent or who are [[Apnea|apneic]].
*If the infant maintains adequate respiratory efforts and has an [[FiO2]] requirement less than 0.30, no additional doses of surfactant are needed.
*[[Endotracheal intubation]] has been the standard technique of surfactant administration.
==Ebstein's anomaly==
*Control of the heart rhythm with antiarrhythmic drugs: Ebstein's anomaly may present with an [[AV nodal reentrant tachycardia]] with associated [[pre-excitation]].
*Among these patients, the preferred pharmacological treatment agent is [[procainamide]].
*Since AV-blockade may promote conduction over the [[accessory pathway]], drugs such as [[beta blockers]], [[Calcium channel blocker|calcium channel blockers]] and [[digoxin]] are contraindicated. If there is [[atrial fibrillation]] with pre-excitation, treatment options include [[procainamide]], [[flecainide]], [[propafenone]], [[dofetilide]] and [[ibutilide]] since these medications slow conduction in the [[accessory pathway]] <nowiki/>causing the tachycardia and should be administered before considering electrical [[cardioversion]]. Intravenous [[amiodarone]] may also convert [[atrial fibrillation]] and slow the ventricular response.
*[[Inotrope|Inotropic]] agents and [[diuretics]] for [[heart failure]].
*[[Anticoagulation]] in patients with [[atrial fibrillation]] and [[paradoxical embolization]] Tricuspid valve repair is indicated in patients in which there is symptoms or deteriorating exercise capacity, [[cyanosis]] (oxygen saturation less than 90%), [[paradoxical embolism]], progressive [[cardiomegaly]] on chest x-ray or progressive [[right ventricular dilation]] or reduction of right ventricular systolic function.
*Repair is favored over replacement. [[Warfarin]] is recommended for patients with Ebstein’s anomaly with a history of paradoxical embolus or [[atrial fibrillation]].
==Coarctation of aorta==
====Preoperative====
*[[Beta blockers]] are the treatment of choice.
*Caution should be taken as too much control of [[hypertension]] in upper limb can cause hypotension in [[lower limbs]].
*Surgical treatment of the lesion should not be delayed for the correction of [[hypertension]]. 
====Postoperative====
*Immediate post operative hypertension - use short-term vasodilators for e.g. [[sodium nitroprusside]], or intravenous beta-blockers like [[esmolol]].
*Long-term antihypertensive post surgery
**Monotherapy with [[beta-blockers]]
**[[ACE inhibitors]] or [[angiotensin II antagonists]] may be added if hypertension continues with beta-blocker monotherapy.
==Eisenmenger syndrome==
*If surgical intervention is not available, treatment is mostly [[palliative]]
**Anticoagulants
**Pulmonary vasodilators such as [[bosentan]]
**[[Prostacyclin]] may improve pulmonary artery pressure and may improve length of life
**Antibiotic [[prophylaxis]] to prevent [[endocarditis]]
**[[Bloodletting|Phlebotomy]] to treat [[polycythemia]]
**Maintaining proper fluid balance
**These measures can prolong lifespan and improve quality of life
==Methemoglobinemia==
*[[Methemoglobinemia]] is treated with supplemental oxygen and [[methylene blue]] 1% solution (10mg/ml) 1-2mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline.
*[[Methylene blue]] restores the iron in [[hemoglobin]] to its normal ([[reduced]]) oxygen-carrying state. This is achieved through the [[Enzyme induction|enzyme inducing]] effect of [[methylene blue]] on levels of diaphorase II ([[NADPH]] [[methemoglobin reductase]]).
*Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as [[methylene blue]], to 5 times its normal level of activity.
==Peripheral cyanosis treatment==
===Raynaud's phenomenon===
*Drug treatment is normally with a [[calcium channel blocker]], frequently [[nifedipine]] to prevent artery constriction.
*It has the usual side effects of [[headache]], flushing, and ankle [[edema]], and patients often stop treatment, preferring the symptoms of [[Raynaud's disease|Raynaud's]] to the symptoms of the drug.
*The extract of the [[Ginkgo biloba]] leaves reduces symptoms in two weeks.
*There is some evidence that [[Angiotensin II receptor antagonist|Angiotensin II receptor antagonists]] (often [[Losartan]]) reduce frequency and severity of attacks.
*In intractable cases, [[sympathectomy]] and infusions of [[Prostaglandin|prostaglandins]], e.g. [[prostacyclin]], may be tried, with [[amputation]] in exceptionally severe cases.
*Alpha-1 adrenergic blockers such as [[prazosin]] can be used to control Raynaud's [[Vasospasm|vasospasms]] under the supervision of a healthcare provider.
===Peripheral vascular disease===
*Urgent measures should be taken to ensure blood flow and protect the limb:
**ICU admission
**Administration of [[heparin]] for [[anticoagulation]]
**Electrolytes, acid-base and renal status monitoring
**Limb status monitoring and frequent assessment of the need for fasciotomy.
*If the limb is not immediately threatened:
**Continue treatment with [[thrombolytic]] therapy for 14 days.
*If the limb ischemia is critical:
**Consider percutaneous transluminal angioplasty
**Consider surgery: thromboembolectomy, bypass grafting
*Send sample for pathologic examination ([[myxoma]] may be present)
=====<u>Cilostazol</u>=====
*[[Cilostazol]] is a [[Phosphodiesterase inhibitors|phosphodiesterase III inhibitor]].
*[[Cilostazol]] is not administered to all PAD cases but rather to selected cases where regular walking program has failed to improve the walking time and capacity.
*It is contraindicated in [[congestive heart failure]].
*Side effects:
**[[Headache]]
**[[Diarrhea]]
**Gastric upset
**[[Palpitation|Palpitations]]
**[[Dizziness]]
===Endovascular Revascularization Modalities===
*PTAC
*[[Stent|Stents]]
*Atherectomy
*Laser
*Cutting balloons
*Thermal [[angioplasty]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
[[Category:Up-To-Date]]
{{WS}}
[[Category:Primary care]]

Latest revision as of 20:12, 29 January 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Mohammed Abdelwahed M.D[3]

Overview

In every neonate presented with cyanosis and shock, congenital heart disease dependent on patency ductus arteriosus should be considered. The physiologic constriction of ductus arteriosus after birth in a neonate whose pulmonary blood flow or aortic blood flow is dependent on PDA leads to shock and collapse in the neonate. Infusion of prostaglan in such a neonate is life-saving and keeps patency ductus arteriosus. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock due to low cardiac output state and peripheral vasoconstriction lead to disappearing of cyanosis.


Medical therapy

Medical therapy of Cyanosis

The mainstay of therapy is treatment of underlying causes of cyanosis.[1] [2][3][4][5][6]

Abbreviations: d-TGA: dextro-Transposition of great arteries; PDA: Patent ductus arteriosus  ; ASD: Atrial septal defect; VSD: Ventricular septal defect; TOF: Tetralogy of fallot; CHD: Congenital heart disease; PS: Pulmonary stenosis; PTE: Pulmonary thromboembolism; AS: Aortic stenosis; ARDS: Acute respiratory distress syndrome; PFO: Patent foramen ovale; PVR: Pulmonary vascular resistance; SpO2: Peripheral capillary oxygen saturation.; FiO2: Fraction of inspired oxygen; PEEP: Positive end-expiratory pressure;

Causes of cyanosis CHD with severe restriction of pulmonary blood flow CHD with severe restriction of systemic blood flow CHD due to bidirectional shunt Methemoglobinemia PTE Cardiogenic shock ARDS Acute mountain sickness
Note Complication of exposue to some drugs such as nitrites and aniline leading to dizziness , coma, chocolate-brown discoloration of blood samples, respiratory distress seizures and myocardial ischemia Hypoxia due to V/Q mismatch, low cardiac out-put state, acute right ventricular dilation and increased pulmonary vascular resistance Cyanosis, olyguria, altered mental status Leakage of large molecules into alveolar space leading rich protein pulmonary edema
Mechanism of cyanosis Hypoxia and cyanosis due to constriction of the ductus arteriosus after birth and dependency of the Pulmonary circulation on the patency of the ductus arteriosus Cyanosis,systemic hypoperfusion, circulatory collapse, metabolic acidosis, shock due to constriction ductus arteriosus and dependency systemic circulation on PDA after birth Constriction of PDA after birth leading decreased systemic circulation due to mixing of pulmonary and systemic blood flow via PDA Low cardiac output state due to myocardial infarction and pump failure leading to vasoconstriction and peripheral cyanosis
  • Increased alveolar vascular permeability
  • Interstitial and alveolar pulmonary edema
 Central cyanosis due to alveolar hypoxia , pulmonary vasoconstriction, pulmonary hypertension
Treatment Prostaglandin E1 Prostaglandin E1 Prostaglandin E1 Coronary revascularization

References

  1. ↑ Cucerea, Manuela; Simon, Marta; Moldovan, Elena; Ungureanu, Marcela; Marian, Raluca; Suciu, Laura (2016). "Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit". The Journal of Critical Care Medicine. 2 (4): 185–191. doi:10.1515/jccm-2016-0031. ISSN 2393-1817.
  2. ↑ Henretig, Fred M.; Gribetz, Bruce; Kearney, Thomas; Lacouture, Peter; Loveiov, Frederick H. (2011). "Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia". Journal of Toxicology: Clinical Toxicology. 26 (5–6): 293–301. doi:10.1080/15563658809167094. ISSN 0731-3810.
  3. ↑ Tisi, G M; Wolfe, W G; Fallat, R J; Nadel, J A (1970). "Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion". Journal of Applied Physiology. 28 (5): 570–573. doi:10.1152/jappl.1970.28.5.570. ISSN 8750-7587.
  4. ↑ Austin, John H. M. (1973). "Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs". Investigative Radiology. 8 (5): 315–321. doi:10.1097/00004424-197309000-00003. ISSN 0020-9996.
  5. ↑ . doi:10.1164/rccm.201503-0584OC. Check |doi= value (help). Missing or empty |title= (help)
  6. ↑ Smedley, Tom; Grocott, Michael PW (2013). "Acute high-altitude illness: a clinically orientated review". British Journal of Pain. 7 (2): 85–94. doi:10.1177/2049463713489539. ISSN 2049-4637.
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