Danos no NTS poderiam aumentar a permeabilidade pulmonar como mecanismo adicional. Muroi et al. Todos os pacientes foram tratados de acordo com protocolos universalmente reconhecidos. Quase todos os pacientes necessitaram de catecolaminas na fase aguda.
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Traditionally, pulmonary oedema has been divided into cardiogenic left ventricular and non-cardiogenic causes. The non-cardiogenic causes include a wide range of diseases, for example, pulmonary oedema caused by the acute lung injury—adult respiratory distress syndrome ALI—ARDS spectrum of pathology, and pulmonary oedema arising from increased pulmonary capillary pressure hydrostatic pulmonary oedema.
Trying to classify the causes of pulmonary oedema, however, understates the degree of inter- action between the various components involved and it is probable that pulmonary oedema results from the interactions of dysfunction affecting the left ventricle, the pulmonary capillary endothelium, intravascular osmotic and oncotic pressures, and right side of the heart. In any case, the term hydro- static pulmonary oedema is reserved for oedema developing due to, for example, brain injury, airway obstruction, and high altitude, and refers to oedema forming because of increased transcapil- lary pressure within the pulmonary vasculature.
Neurogenic pulmonary oedema NPO is the most frequently encountered manifestation of hydrostatic pulmonary within critical care environments and is often fatal. Where it does not cause death, it may exacerbate secondary brain injury. This article will outline the physi- ology regulating extravascular lung water and the pathological processes which disrupt this before discussing NPO and other causes of hydrostatic pulmonary oedema. Physiology Pulmonary capillary structure Pulmonary oedema forms at the pulmonary capillary network, a branching vascular tree arising from the pulmonary artery which goes through 16—18 branches before the formation of the capillaries which then feed into the pul- monary venous network.
The wall of the capillary is intermeshed with the cells and the extracellular matrix of the alveo- lus to form the blood—gas barrier and is extra- ordinarily thin, around 0. Consequently, high pulmonary pressures are damaging to the blood—gas interface. Key points Pulmonary oedema which arises due to increased pulmonary capillary pressure, in the absence of left ventricular failure, is hydrostatic pulmonary oedema.
Neurogenic pulmonary oedema NPO is the most frequent manifestation of hydrostatic pulmonary oedema and develops after a severe neurological insult. NPO forms due to a combination of increased pulmonary capillary pressure and stress fracture disruption of the pulmonary capillary basement membrane. Similar pathophysiological processes include negative pressure pulmonary oedema, high-altitude pulmonary oedema, and pulmonary oedema in hypertensive crises.
All rights reserved. For Permissions, please email: journals. The hydrostatic pressure i. An important detail is the transalveolar pressure. In reality, it is probably a combination of all three. Neurogenic pulmonary oedema Pathophysiology NPO is characterized by sudden onset respiratory failure after an injury to the central nervous system CNS and typically associated with raised intracranial pressure ICP. Subarachnoid haemorrhage SAH is the most frequently associated neurological insult.
It may also be associated with traumatic brain injury, epileptic seizures, embolic stroke, neurological endo- vascular procedures, and raised ICP due to blocked VP shunts. Fig 1 Fluid regulation in the lung. The interstitial hydrostatic pressure Pif 25—0 mm Hg is negative or zero in health but when positive, i. The alveolar sodium— potassium ATPase acts to remove water from the alveolar space. B The net movement out of the capillary is described as Pc—Pif and the net force pulling water into the capillary is Pc—Pif.
A value of zero indicates free passage of the solute across the membrane. Increased pulmonary vascular pressure The CNS discharge increases sympathetic nervous system tone and circulating catecholamine release.
The anatomical location where the centrally mediated vasoconstriction arises from is uncertain. The structures are thought to include the A1 cat- echolaminergic neurones in the caudal ventrolateral medulla, the dorsal motor vagus nucleus, the tractus solitarius, and the posterior hypothalamus.
This results in a dramatic increase in pulmonary and systemic vascular resistance PVR, SVR , cardiac contractility until cardiac dysfunction supervenes, see below , and tachycardia.
There is a concomitant mechanical stress injury to the pulmon- ary capillary basement membrane which occurs at pressures as low as 24 mm Hg. It is initially a protein and cell poor transudate, but it progresses to contain abundant plasma proteins and cells.
The combination of increased SVR and PVR causes increased demands on the myocardium to maintain output and when associ- ated with tachycardia, there is a critical impairment of myocardial oxygen delivery due to increased transmural pressure and decreased diastolic time. This can result in reversible myocardial stunning or overt myocardial injury and may be associated with a spectrum of pathology ranging from simple ECG changes, to tro- ponin rises, infarction,5 and structural changes such as Tako-subo cardiomyopathy.
The impaired cardiac function may exacerbate pulmonary oedema i. Secondly, the lung increases the expression and release of cytokines in response to the mechanical insult caused by increased pulmonary capillary pressure which is exacerbated by the barotrauma of mechanical ventilation. NPO typically arises in the presence of associated neuropathol- ogy which may be traumatic, vascular, or due to another cause. It is possible that neurological pathology may be unknown, for example, the development of NPO in a patient who has had a seizure before presentation at hospital.
The diagnostic investi- gations are outlined in Box 1 and the differential diagnoses are shown in Table 1. Clearly, the management of acute neurological pathology will entail measures which may aid man- agement of NPO such as mechanical ventilation; however, aspects of stabilization may also involve steps which are detrimental to NPO such as inter-hospital transfer. The strategy for treatment of NPO is to reverse the pathophysio- logical disturbance while supporting organ function.
The majority of cases will resolve within 24—48 h with appropri- ate treatment; however, some cases may require intensive care for many days. The mortality in this patient group is high and many patients will progress to being candidates for organ donation. Severe NPO will clearly compromise suitability for organ harvest and treatment i.
It should also be inspected for the pres- ence of other causes of respiratory failure such as pneumonia or the consequences of trauma. NPO and a second pathology, for example, traumatic lung contusions, can co-exist. Elevated plasma troponin levels are frequently observed. Pulmonary artery catheter studies show a reduced cardiac index ,2. PCWP may be elev- ated. Clinically related conditions Negative pressure pulmonary oedema NPPO is associated with upper airway obstruction in a spon- taneously breathing patient.
It occurs in 0. Pulmonary oedema is typically described as developing within 2 min of the obstruction. Once the airway is occluded, the spontaneously breathing patient will continue to generate negative intrathoracic pressure which will increase substantially as respiratory distress develops. There is an associated increase in sympathetic tone due to the stress of hypoxia and airway obstruction which increases SVR and elevates pulmon- ary artery pressure.
This is further exacerbated by hypoxic pulmonary vasoconstriction. It is most common in younger patients, presumably because they are able to generate higher negative inspiratory pressures and, arguably, have a higher sympathetic tone and better cardiac func- tion. After recognition of the cause of obstruction, the treatment required ranges from relatively modest support such as brief periods of CPAP for 2 h to positive pressure ventilation over a period of 24 h.
High-altitude pulmonary oedema and exercise-induced pulmonary oedema High-altitude pulmonary oedema HAPE is characterized by the onset of breathlessness or loss of exercise capacity on the second or third day after assent to, or above, m.
Hypoxic Table 1 NPO differential diagnoses. In comparison with the conditions in the table, NPO would generally be associated with a history of neurological insult and very rapid progression of respiratory failure, over 0—6 h. Subsequently, if the level of respiratory support indicates that intubation and mechanical ventilation is required, it should be performed using a technique which will avoid increases in either ICP or systemic arterial pressure yet maintain cerebral perfusion.
Breathing NPO necessitates a protective lung ventilation strategy. Ventilation should prevent hypoxaemia and avoid iatrogenic lung injury. Initial tidal volumes should be 6—7 ml kg21 uti- lising PEEP to aid clearance of the oedema and maintain alveolar recruitment. Care should be taken, however, that high PEEP does not impair cardiac function. Permissive hypercapnia should not be used in the presence of raised ICP or only permitted if ICP monitoring is in place.
High-frequency oscillation ventilation may aid the treatment of refractory hypoxaemia. Prone positioning has been used successfully in the treatment of NPO;10 however, the pres- ence of cervical spine injury may be a relative contraindication.
Circulation The haemodynamic management of NPO is challenging and there is no robust evidence on which to base recommen- dations. With correct interpretation, this may allow modulation of haemodynamic parameters to increase cardiac output, reduce PVR and SVR, and optimize mean arterial pressure and hence cerebral per- fusion pressure.
The precise choice of drugs will depend on the patient, any associated injuries, and pre-existing pathology. The aim of therapy should be to maintain cardiac index at.
Actualidades en terapia intensiva neurológica. Edema pulmonar neurogénico
Neurogenic pulmonary edema is an etiological subtype of non-cardiogenic pulmonary edema. It characteristically presents within minutes to hours following a neurologic insult and usually resolves within 72 hours. The exact pathophysiology of is unclear, but it thought to relate to an adrenergic response leading to increased pulmonary hydrostatic pressure and increased lung capillary permeability 2. On chest radiographs, there are nonspecific, bilateral, rather homogeneous airspace consolidative appearances with an apical predominance is thought to the present in about half of cases 4. Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys.
2010, Número 2
Archivos de Bronconeumologia http: www. Other types of articles such as reviews, editorials, special articles, clinical reports, and letters to the Editor are also published in the Journal. It is a monthly Journal that publishes a total of 12 issues, which contain these types of articles to different extents. All manuscripts are sent to peer-review and handled by the Editor or an Associate Editor from the team. The Journal is published both in Spanish and English. Therefore, the submission of manuscripts written in either Spanish or English is welcome. Translators working for the Journal are in charge of the corresponding translations.