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• 51 year old gentleman was BIBA to A&E after his wife found him collapsed and
unconscious at home on the early hours of Wednesday
• He had a background history of obesity, epistaxis and trismus, but was otherwise
independent and well.
• On admission at 9.00am, the patient’s GCS was 3/15
• Observations:
• Apyrexial, BP 213/120, HR 45, Sats 92% (air), RR 18
• Blood gases (on admission):
• FiO2 21%, pH 7.216, pO2 8.11, pCO2 6.46, Hb 101, SO2 76.4, k 3.5, Na 143, Glu 14, Lact
2.7, BE -2.2, HCO3 20.4
• The ITU registrar was called to assist with the patient’s airway upon admission to A&E.
She noted he was producing copious amounts of pink fluid which required
suctioning, but managed to intubate and ventilate him.


PULMONARY OEDEMA • Definition: an increase in extravascular fluid in the lungs. which occurs when transudation or exudation exceeds the capacity of lymphatic drainage • Key pathophysiological mechanisms: • Imbalance of Starling’s forces of fluid movement across a capillary membrane • Increased permeability of the capillary-alveolar barrier • Impaired lymphatic clearance mechanisms • Clinical consequences: Fick’s law of gas exchange .

PHYSIOLOGY: STRUCTURE OF THE ALVEOLAR-CAPILLARY UNIT • Pulmonary capillary endothelial cells abut one another in a fairly loose fashion • gap junctions are ~ 5 nm wide. alveolar epithelial cells meet at tight junctions ~ 1 nm wide. and permit the passage of moderately large protein molecules • However. and are virtually impermeable to protein (DeFouw 1983) • Epithelial Na & Cl ion channels on the apical membrane of alveolar epithelial cells – facilitate water reabsorption from alveolar airspace into interstitium .

pulmonary venous capillaries lack this protective system  any increase in left ventricular pressure will be easily transmitted to the pulmonary capillaries . there is small balance favouring transudation of fluid into the interstitium (this is greater in most dependent area of the lung) • Lymphatics drain fluid from the interstitium into the systemic circulation at a rate of ~10ml/hr • The interstitial space and lymphatics can accommodate an increase in fluid of ~ 500 ml with an increase of pressure of only ~ 1.5 mmHg • Arteriolar vasomotor tone can regulates the transmission of flow & pressures to the capillary bed • However.-4) – (30-15) = 19 – 15 = 4mmHg • Overall. PHYSIOLOGY: THE STARLING’S LAW OF THE CAPILLARY • Starling’s Law of the Capillary: • Flow = (Pc – Pif) – (πc-πif) • P = hydrostatic pressure • Π = oncotic pressure • Under normal conditions: • Flow = (15.

there is small balance favouring membrane of alveolar epithelial cells facilitate water transudation of fluid into the interstitium reabsorption from alveolar spaces Pulmonary lymphatics drain fluid from the interstitium into the systemic circulation at a rate of ~10ml/hr. BALANCE OF OEDEMA PROMOTING VS SUPPRESSING PHYSIOLGOICAL MECHANISMS SUPPRESSING PROMOTING Alveolar epithelial gap junctions are narrow and Pulmonary capillary gap junctions are fairly wide impenetrable to proteins through which proteins can leak through Epithelial Na & Cl ion channels on the apical Overall. and have significant capacity to drain excess insterstitial fluid Arteriolar vasomotor tone can regulates the Pulmonary venous capillaries lack this protective transmission of flow & pressures to the capillary bed system  increaess in left ventricular pressure will be easily transmitted to the pulmonary capillaries .

arterial hypoxaemia develops PaCO2 remains normal. usually terminal • Increased pulmonary blood flow .* the above diagnostic criteria are present severe arterial hypoxaemia & a large PA-aO2 gradient develops • Imbalance of Starling’s Forces [Flow = (Pc – Pif) – (πc-πif) ] PaCO2 becomes slightly elevated CXR shows characteristic bilateral infiltrates • Increased Pc hydrostatic pressures (Haemodynamic pulmonary oedema) CT decreases. vasopressors 4.Cardiogenic (LV failure. the lungs are stiff and PAWP increases • Absolute hypervolaemia – overtransfusion. anaemia. renal failure artificial ventilation is usually instituted if not already present • Relative pulmonary hypervolaemia – postural effects. exercise (rarely) massive bilateral consolidation with unremitting hypoxaemia • PaO2 is usually £ 50 mmHg Raised pulmonary venous pressures .0drugs (histamine) • Reduced Pc oncotic pressures VD increases and normocapnia can only be maintained by a large VM. . MVwith disease). High altitude Fat embolus Pancreatitis Amniotic fluid embolus Diabetic coma Radiation Massive blood transfusion Bleomycin DIC Nunn 3rd Ed. often 10-20 l/min • Critically ill patients • Cirrhosis not all patients progress through all of these stages and the disease may resolve at any stage serial observations of the CXR and PA-aO2 gradient are the best indicators • Nephrotic syndrome • Increased permeability of the capillary-alveolar barrier (non-cardiogenic pulmonary oedema or ARDS ) • Direct injury Predisposing Conditions • Indirect injury Direct injury Indirect injury • Impaired lymphatic clearance mechanisms Pulmonary contusion Septicaemia • Tumour Gastric / other aspiration Shock / prolonged hypotension • Infection Near-drowning Non-thoracic major trauma Toxic gas / vapour inhalation Cardiopulmonary bypass • Surgery Certain infections Head injury • Miscellaneous: Neurogenic. a FIO2 = 1.left/right shunt. aO2 usually lasts ~ 24/24 2. or subnormal PATHOPHYSIOLOGICAL CAUSES OF there are only minor abnormalities on CXR the is an increase in lung water & QT usually lasts ~ 24-48/24 PULMONARY OEDEMA 3. dysrhythmias.

further facilitating flow in minimizing the thickness of the ti Alveolar number and surface adolescence (See Table below). This is denoted thei schematically Fick’s law of diffusion statesanalysis thattha net d o tissue is proportional to the area o • FICK’S LAW 1) Diffu proportional to the thickness of th 2) Diffu • diffusion of gas across a sheet of contains 300-500 million alveoli a between 50 and 100 square meter tissue is proportional to the area of membranes in the body! In additi the sheet and inversely proportional close association between the alve to the thickness of the tissue. A Therefore. further improves the efficiency of • C = concentration lung. The intimate association be vasculature can bring the blood to • D = Diffusion co-efficient for a gas alveoli. PULMONARY OEDEMA LUNG STRUCTURE FACILITATES GAS-EXCHANG GAS DIFFUSION ACROSS THE ALVEOLI DIFFUSION OF OXYGEN AND CARBON DIOXIDE In our earlier discussion of the structure and function of the Oxygen and carbon dioxide move exchanging between unit of thetoair the lung is designed and facilitate theofblO diffusion driving force for this diffusion being the pressure gradient across area available for diffusion and by having a thin membrane separati blood in the pulmonary capillaries. remains constant an 1) Length of the diffusion path (thickness) 2) Surface Area have a limited capac 3) Concentration Gradient • Alveolar Ventilation • Pulmonary Blood Flow 4) Diffusion Coefficient for O 2 and CO2 . net gas exchange is dependent upon. CLINICAL MANIFESTATIONS OF diffusion of air within this region of the lungs is very rapid occurring of this dramatic reduction in air velocity is that inhaled dust and poll alveoli.

maintain alveolar ventilation minimiz • Clinical sign: Increased work of breathing/ Alve Dyspnoea adolesce . Th compliance vasculat • This results in increased work of breathing . to alveoli. • Stage 1: Interstitial pulmonary oedema LUNG STRUCTURE FACILITAT • Excessive fluid enters into the interstitium Oxygen and carbon dioxide move b •  increases ”thickness” in Fick’s equation driving force for this diffusion being the pr • Lymphatic system becomes distended and tries Fick’s la to compensate but fails to completely drain tissue is excess interstitial fluid proporti • Increased interstitial pressures can cause contains capillary narrowing between •  increases ”thickness” in Fick’s equation membra • Lung compensates by recruiting more alveolar. close ass capillary units further i • Increase in interstitial fluid  reduced lung lung. diffusion of air within this region of the lun of this dramatic reduction in air velocity is STAGES OF PULMONARY OEDEMA alveoli.

relatively normal gases • Mechanism: Stimulation of J-receptors • sensory nerve endings of the vagus nerve which are present in the alveolar walls and are in close contact with pulmonary capillaries. • When stimulated they result in a reflex comprising of hyperventilation. bradycardia and hypotension . STAGES OF PULMONARY OEDEMA • Stage 2: Crescenteric alveolar filling • Interstitial oedema increases further and there is passage of fluid into the alveoli • This first appears as crescents in the angles between adjacent septa • The centre of the alveoli and most of the alveolar walls remain clear • So gas exchange remains little affected and the PA-aO2 gradient remains small • Clinical manifestation: Tachypnoea.

perihilar haze. mem close furth STAGES OF PULMONARY OEDEMA lung. ”bat wing” oedema. THE GENERATION OF A PRE . while A others. large cardiac sillhouette. • Coarse inspiratory crackles • X-ray: Kerley-B lines. pulmonary vascular congestion. b/l fluffy air-space shadowing. normo or hypocapnea.e. the venous flow to the lung goes past alveoli without coming into contact with alveolar air • Clinical manifestations: • Hypoxia. Pleural effusions. vascu • Stage 3: Alveolar flooding alveo minim • some alveoli become totally flooded with fluid. frequently adjacent show only crescentic filling adole • No gas exchange can occur in completed flooded alveoli •  Further increase in ”thickness” in Fick’s equation •  Reduced “area” in Fick’s equation – as functioning alveolar membranes are reduced •  this results in alveolar shunting causing venous admixture i.

hypercapnia may result from interference with gas I 2 subsequ exchange effect o unmask • Tachypneoa also stimulated by J-receptor reflex a typica left. STAGES OF PULMONARY OEDEMA • Why is there normocapnoea/hypocapnea despite chemore hypoxia? more do respons • CO2 is 23 times more soluble than O2 in plasma and for any chemore given partial pressure gradient. Alv the insp . chemore These c • If PaO2 become severe (<60mmHg or 8kPa). then hypoxic changes ventilatory drive kicks in stimulated by peripheral 500 mm chemoreceptors (located in carotid bodies) between • if patients with severe oedema are treated with a high hypoxia FI O2 . it will diffuse 23 x 0.85 (diffusion ventilati bodies a coefficient) = 20 times faster than O2.

STAGES OF PULMONARY OEDEMA • Stage 4: Airway flooding • Fluid floods the alveolar spaces and extends to the airways  effectively blocks air passages preventing any meaningful gas exchange and is rapidly fatal unless treated .


NEUROGENIC PULMONARY OEDEMA • Definition: The rapid onset (mins-hours) of pulmonary oedema secondary to an injury to the central nervous system (CNS) and typically associated with raised intracranial pressure (ICP) • It is a diagnosis of exclusion • Causes: • Cerebral haemorrhage (SAH – most common cause) • TBI • Epileptic seizures • Embolic stroke • Blocked VP shunt .

particularly when associated with ischaemia. • Pulmonary effects: pulmonary venous vasoconstriction  rapid elevation in pulmonary capillary hydrostatic pressure •  imbalance of Starling’s forces  transudation of fluid into interstitium •  mechanical stress injury to endothelium (when Pc pressures >24mmHg)  inflammatory response + exudation of fluid • Cardiovascular effects: •  increased systemic arterial resistance •  tachycardia •  increased venous return •  increased CO & SVR  HTN •  these can all precipitate cardiac stunning  superadded cardiogenic oedema •  hypovolaemia can arise through the lung and third spaces due to the raised systemic capillary pressure • Other effects: Neurogenic diabetes insipidus can arise secondary to TBI or less commonly cerebral haemorrhage •  can worsen hypovolaemia . NEUROGENIC PULMONARY OEDEMA • Pathophysiology: • CNS injury  excessive stimulation of sympathetic nervous system • Anatomical site of CNS discharge not exactly known: Animal data suggest that the presence of blood and inflammatory mediators in the hypothalamus and medulla oblongata is pivotal.

RAISED ICP  CUSHING REFLEX • Raised ICP  Cerebral areteriolar compression when ICP > MAP  cerebral ischaemia • Stage 1: • RICP  Sympathetic nervous sytem  vasoconstriction + tachycardia + increased venous return  increased CO & SVR  hypertension • Stage 2: • HTN  Baroreceptors in aortic arch  stimulate vagus nerve in response to HTN  bradycardia .

to achieve SaO2 94-98% • NIV • RCEM recommend NIV should be considered in all patients with cardiogenic pulmonary oedema. • Commence PEEP at 5-7cmH20 and increase to 10 as tolerated – be weary of increasing PEEP too much .g. • Supplementary high-flow oxygen .35 & RR>20/min • Non-Invasive Positive Pressure Ventilation (NIPPV) is the NIV of choice in pulmonary oedema (especially if cardiogenic) • Can use either BiPAP or CPAP – no signfiicant differences in efficacy • But there is a reluctance to recommend BiPAP as standard treatment because a previous study indicated an increased incidence of myocardial infarction during treatment when compared with CPAP (Mehta et al 1997). especially if pH <7. • Suction secretions • BREATHING • Position the patient e. sit the patient up • Patient positioning should be considered as an early intervention since it can have an immediate effect on oxygenation and symptoms of breathlessness (O’Driscoll et al 2008). INVESTIGATIONS & MANAGEMENT • AIRWAYS • The presence of pink frothy sputum indicates severe acute pulmonary oedema.

improves ventilation-perfusion relationships. corrects hypoxia and hypercapnia • Positive intrathoracic pressure  decreased pre-load and afterload (but be careful not to increase afterload) . INVESTIGATIONS & MANAGEMENT • Beneficial effects of NIPPV: • Recruits alveoli • Increases Functional Residual Capacity • Allows breathing to be on more compliant part of the lung’s pressure-volume curve •  decreases work of breathing.

• Permissive hypercapnia should not be used in the presence of raised ICP or only permitted if ICP monitoring is in place. pressure-limited ventilation. prophylactic hyperventilation in traumatic brain injury associated with worse outcomes” (Muizelaar et al 1991) • So aim for eucappnia • High-frequency oscillation ventilation may aid the treatment of refractory hypoxaemia. • But hypocapnia can also be harmful “Early. • Lung-protective strategies include: smaller VTs. . permissive hypercapnia. as it can cause cerebral vasodilatation and further worsen ICP. Also in setting of CNS injury. INVESTIGATIONS & MANAGEMENT • BREATHING: Invasive ventilation in the setting of pulmonary oedema • Ventilation should prevent hypoxaemia and avoid iatrogenic lung injury which patients with ARDS are at higher risk of developing. • Care should be taken. however. • Any patient with raised ICP should be ventilated according to neuroprotective parameters which may conflict with optimal ventilation for pulmonary oedema. that high PEEP does not impair cardiac function. high PEEP can increase ICP further. inverse-ratio ventilation • Initial tidal volumes should be 6–7 ml kg−1 utilising PEEP to aid clearance of the oedema and maintain alveolar recruitment.

Coag. INVESTIGATIONS & MANAGEMENT • CIRCULATION • ECG. Blood gas. BNP. Bedside echocardiogram. Troponin. LFTs. Blood cultures • Catheterisation and careful fluid input-output monitoring • Pharmacological management . U&Es. CRP. CXR • Vascular access • Blood tests: FBC.

Also can worsen cerebral vasospasm. hyponatraemia. counteracts increased effects of RAAS in cardiogenic pulmonary oedema • But limited benefits in RCTs • Also. INVESTIGATIONS & MANAGEMENT • CIRCULATION • Pharmacological management: • Vasodilators .reduces systemic venous and arteriolar vascular resistance and hence both pre-load and afterload  reduces cardiac workload • Nitrate infusion commence at a rate of 10-20mcg/min increasing every 3-5min by 5-10 mcg/min as needed and as BP allows • Contraindications: aortic stenosis. evidence of harmful effects (hypotension. IV dobutamine at 2-3mcg/kg/min) • not routinely recommended in cardiogenic pulmonary oedema as lack of evidence but may be required if cardiogenic shock develops OR signs of end-organ failure OR in neurogenic pulmonary oedema where myocardial stunning may develop .g. systolic BP <90mmHg • Loop Diuretics – reduces pre-load by increases diuresis + venodilator effect • Theoretically. dehydradation) at high doses • The ESC Guidelines advocate small intravenous boluses of furosemide at 20-40mg for patients with CPO and symptoms of fluid overload or congestion • High dose diuretics should be used with caution and only in those with evidence of fluid overload and a history of long term diuretic use • Note diuretics should be avoided in neurogenic pulmonary oedema where DI can arise post- cerebral injury. so should be avoided in patients with SAH • Inotropes (e.

2. INVESTIGATIONS & MANAGEMENT • DISABILITY • People with acute pulmonary oedema will be distressed • Small doses of opiates (e.g. the risks of depressing an already compromised respiratory system should be considered (Skinner and McKinney 2011) • NICE (2014) recommended that opiates should not be routinely given to people in acute cardiogenic pulmonary oedema • E: Treat underlying cause .5mg IV morphine) can be given to reduce anxiety + reduce pre-load + can produce mild vasodilatation (and thus reduce afterload) • Although opiate analgesia may be required to control pain or distress. reading/cardiology/ • https://www.blogspot.5/pulmonary-oedema • • oedema/ • http://adultemergencymedicine. USEFUL RESOURCES • Nunn’s Applied Respiratory Physiology: Chapter 29 • Neurogenic pulmonary oedema: oedema/ .derangedphysiology.