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==Overview==
==Overview==
== Initial management of neonantal 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]].
* Newborns with cyanosis require adequate tissue perfusion and oxygenation.
* An infant who fails the hyperoxia test and does not have persistent pulmonary hypertension of the newborn or a chest radiograph consistent with lung disease is likely to have a cyanotic CHD. 
* Monitoring of oxygen level and tissue perfusion is necessary.
* An adequate airway should be established immediately, mechanical ventilation may be needed in case of failed spontaneous respiration. 
* Initiating oxygen therapy with 40–60% O2 is sufficient. Exposures to hyperoxia increases oxidative stress and damage lung parenchymal and vascular function.
* In case of a minimal response to oxygen, cardiac disease should be suspected and need for PGE1 should be discussed.
* Cardiac diseases are dependent on a patent ductus to maintain systemic blood flow. 
* Oxygen may increase pulmonary blood flow and decrease systemic blood flow.
* Placement of secure intravenous and intraarterial catheters is most easily accomplished via the umbilical vessels.
* Inotropic agents such as dopamine or dobutamine may be necessary to correct '''hypotension'''.
* An isovolumetric partial exchange transfusion should be performed with saline to reduce the hematocrit in cases of severe '''polycythemia'''.
* Maintenance a '''blood glucose''' > 55 mg/dL should be considered.  
* '''Acidosis''' should be corrected with infusions of sodium bicarbonate.
* '''Hypocalcemia''' should be corrected based on the ionized calcium.
* Broad spectrum antibiotics should be initiated (ampicillin and gentamicin).
* Closure of the ductus arteriosus can precipitate rapid clinical deterioration with significant life-threatening changes.
* Infants with ductal-dependent lesions are at increased risk for death and significant morbidity unless interventions are initiated to maintain patency of the ductus arteriosus for ductal-dependent lesions, ensure adequate mixing of deoxygenated and oxygenated blood, or relieve obstructed blood flow.
* The initial dose is dependent on the clinical setting, as the risk of apnea, one of the major complications of prostaglandin E1 infusion, is dose dependent
* If the ductus is known to be large in a patient with duct-dependent physiology, the initial dose is 0.01 mcg/kg per minute. This scenario typically is seen in patients with echocardiographic confirmation of a large PDA who are cared for in a tertiary center that provides treatment for neonates with cyanotic heart disease.
* If the ductus is restrictive or the status of the ductus is unknown, the initial dose is 0.05 mcg/kgper minute. This is the standard dose used in patients who require transport to a center with expertise in the care of neonates with cyanotic heart disease.
* The dose of prostaglandin can be increased as needed to a maximum dose of 0.1 mcg/kg per minute.
* Complications of prostaglandin E1 infusion include hypotension, tachycardia, and apnea [8]. As a result, a separate reliable intravenous catheter must be in place to provide fluids for resuscitation. Intubation equipment should be immediately available because apnea can occur at any time during infusion.  


== 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/or slow the ventricular response.
* 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. When possible, 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 ====
== Medical therapy ==
* 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 ==
*The mainstay of therapy for [[cyanosis]] is the treatment of underlying causes of [[cyanosis]].
* If surgical intervention is not available, treatment is mostly [[palliative]]
* In cyanotic [[congenital heart disease ]] whether the flow is dependent on patency ductus arteriosus, infusion of  [[prostaglandin]] E1  is recommended.
** Anticoagulants
* In the setting of pulmonary disease such as [[pneumonia]], [[pleural effusion]], treatment of underlying disease and [[oxygen]] therapy are advised.
** Pulmonary vasodilators such as [[bosentan]]
* 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.
** PGE 5 inhibitor
* In [[methemoglobinemia]] discontinuing the medications related disorder and administration of [[methylene blue]] is recommended.
** 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 ==
== Medical therapy of [[Cyanosis]] ==
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. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily.
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="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>


== Raynaud's phenomenon ==
'''<span style="font-size:85%">'''Abbreviations:'''
* Drug treatment is normally with a [[calcium channel blocker]], frequently [[nifedipine]] to prevent arterioconstriction. It has the usual side effects of headache, flushing, and ankle [[edema]], and patients often stop treatment, preferring the symptoms of Raynaud's to the symptoms of the drug.
'''d-TGA:''' [[ dextro-Transposition of great arteries]];
* The extract of the [[Ginkgo biloba]] leaves (Egb 761, 80mg) reduces symptoms in two weeks.
'''PDA:''' [[Patent ductus arteriosus]] ;
* There is some evidence that [[Angiotensin II receptor antagonist|Angiotensin II receptor antagonists]] (often [[Losartan]]) reduce frequency and severity of attacks.
'''ASD:''' [[Atrial septal defect]];
* In intractable cases, [[sympathectomy]] and infusions of [[Prostaglandin|prostaglandins]], e.g. [[prostacyclin]], may be tried, with [[amputation]] in exceptionally severe cases.
'''VSD:''' [[Ventricular septal defect]];
* Alpha-1 adrenergic blockers such as prazosin can be used to control Raynaud's vasospasms under supervision of a health care provider.
'''TOF:''' [[Tetralogy of fallot]];
* In a study published in the November 8, 2005 issue of ''Circulation'', [[sildenafil]] (Viagra) improved both microcirculation and symptoms in patients with secondary Raynaud's phenomenon resistant to vasodilatory therapy. The authors, led by Dr Roland Fries (Gotthard-Schettler-Klinik, Bad Schönborn, Germany), report: "In the present study, capillary blood flow was severely impaired and sometimes hardly detectable in patients with Raynaud's phenomenon. Sildenafil led to a more than 400% increase of flow velocity."
'''CHD:''' [[Congenital heart disease]];
* Two separate gels combined on the fingertip (somewhat like two-part [[epoxy]], they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds. Tucker, A.T. et al., ''The Lancet'', Vol. 354, November 13, 1999, pp..
'''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]];
</span>
<br>
{| class="wikitable sortable"
|-
!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]]
|-


== Peripheral vascular disease ==
||'''Note'''||
*[[Pulmonary atresia]]
*[[Tricuspid atresia]]
*[[Tetralogy of Fallot]] with [[pulmonary atresia]]
||
*[[Severe AS]]
*[[Coarctation aorta]]
*[[Interrupted aortic arch]]
*[[Hypoplastic  left heart syndrome]]


=== Medical Therapy for Acute Occlusion ===
||
* Urgent measures should be taken to ensure blood flow and protect the limb:
*[[TGA]]
** ICU admission
*[[Truncus arteriosus]]
** Administration of [[heparin]] for [[anticoagulation]]
*[[Double outlet right ventricle]]
** Electrolytes, acid- base and renal status monitoring
|| 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]] 
** Limb status monitoring and frequent assessment of the need for fasciotomy.
|| [[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]]  ||
*SpO2/FiO2 <315, No PEEP requirement
*Complication of [[pneumonia]], [[non cardiogenic shock]], [[drug overdose]], [[trauma]]
||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]]
||
*[[Oxidative sresss]] , [[methemoglobin]] level > 10 % total [[hemoglobin]]
* [[Cyanosis]] refractory to [[oxygen]] therapy,
||
*[[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]]
* Low [[cardiac output]] state due to [[right ventricular dilation]] and increased [[PVR]] leading to [[peripheral cyanosia]]
|| 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]]


* If the limb is not immediately threatened:
||  [[Central cyanosis]] due to alveolar [[hypoxia]] , [[pulmonary vasoconstriction]], [[ pulmonary hypertension]]
** Continue treatment with thrombolytic therapy for 14 days.
* If the limb ischemia is critical:
|-
** Consider percutaneous transluminal angioplasty
|'''Treatment'''||[[Prostaglandin]] E1 ||[[Prostaglandin ]] E1||[[Prostaglandin]] E1||
** Consider surgery: thromboembolectomy, bypass grafting
*[[Methylenblue]] infusion
* Send sample for pathologic examination ([[myxoma]] may be present)
* Hyperbaric [[oxygen]] therapy  
*[[Ascorbi:c acid]]
||
*[[Anticoagulant therapy]]
*[[Fibrinolytic]] therapy in case of [[ collapse]] and [[shock]]
*[[ Mechanical thrombectomy]]


==== Reduction in Modifiable Cardiovascular Risk Factors[edit | edit source] ====
||[[Coronary revascularization ]]||
* [[Diabetes]] control
*[[Extracorporeal membrane oxygenation]]
* [[Hypertension]] treatment
*[[High-frequency oscillatory ventilation]]
* Dyslipidemia treatment
*[[Neuromuscular blocking agents]]
* [[Smoking]] cessation
*Intravenous β-2 agonist ([[Salbutamol]])
 
||
==== Improvement of the Walking Ability[edit | edit source] ====
*Descent
 
*Supplement [[oxygen]] therapy
===== Exercise Rehabilitation[edit | edit source] =====
*Portable hyperbaric chamber
* A regular walking program four times a week for six month results in an average of 6.5 minutes improvement in the walking time.
*[[Nifedipine]]
* It opens up collateral circulation.
|}
* It reduces cardiovascular mortality.
* It improves quality of life.
 
===== Cilostazol[edit | edit source] =====
* Cilostazol is a phosphodiesterase III inhibitor.
* It is FDA approved.
* 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]]
 
==== The Choice of the Revascularization Intervention Based on TASC Classification[edit | edit source] ====
''For detailed information regarding the TASC classification, click [[Peripheral arterial disease classification|here]].''
 
===== Iliac Lesions[edit | edit source] =====
* Endovascular revascularization is the intervention of choice in patients with TASC type A iliac lesions.
** TASC type A iliac lesions is defined as a single stenosis less than 3 cm of the common iliac artery or external iliac artery (unilateral/bilateral).
* Surgical revascularization is the intervention of choice in patients with TASC type D iliac lesions.
** TASC type D iliac lesions is defined as either one of the following:
*** Diffuse, multiple unilateral stenoses involving the common iliac artery, external iliac artery, and common femoral artery (usually more than 10 cm long)
*** Unilateral occlusion involving both the common iliac artery and external iliac artery
*** Bilateral external iliac artery occlusions
*** Diffuse disease involving the aorta and both iliac arteries
*** Iliac stenoses in a patient with an abdominal aortic aneurysm or other lesion requiring aortic or iliac surgery.
* As for TASC type B iliac lesions and TASC type C iliac lesions, the choice between endovascular and surgical revascularization requires the evaluation of the percentage of artery stenosis.
 
===== Femoral Lesions[edit | edit source] =====
* Endovascular revascularization is the intervention of choice in patients with TASC type A femoropopliteal lesions.
** TASC type A femoropopliteal lesions is defined as a single stenosis less than 3 cm of the superficial femoral artery or popliteal artery.
* Surgical revascularization is the intervention of choice in patients with TASC type D femoropopliteal lesions.
** TASC type D femoropopliteal lesions is defined as complete common femoral artery or superficial femoral artery occlusions or complete popliteal and proximal trifurcation occlusions.
* As for TASC type B femoropopliteal lesions and TASC type C femoropopliteal lesions, the choice between endovascular and surgical revascularization is not definite.
 
=== Endovascular Revascularization Modalities[edit | edit source] ===
* PTAC ( Percutaneous transluminal angioplasty)
* [[Stent|Stents]]
* Atherectomy
* Laser
* Cutting balloons
* Thermal angioplasty
* Fibrinolysis/Fibrinectomy


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
 
[[Category:Up-To-Date]]
{{WH}}
[[Category:Primary care]]
{{WS}}
[[Category: (name of the system)]]

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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