Sequential Organ Failure Assessment (SOFA) score

Model for end-stage liver disease score(MELD)

—MELD(Model for end-stage liver disease) score   
計算公式：

 MELD Score = (0.957 * ln(Serum Cr) + 0.378 * ln(Serum Bilirubin) + 1.120 * ln(INR) + 0.643 ) * 10 (if hemodialysis, value for Creatinine is automatically set to 4.0)

the 3 month mortality is: [6]

—40 or more — 71.3% mortality

—30–39 — 52.6% mortality

—20–29 — 19.6% mortality

—10–19 — 6.0% mortality

—<9 — 1.9% mortality

Source from http://en.wikipedia.org/wiki/Model_for_End-Stage_Liver_Disease

Pre-operative usage of molecular adsorbent re-circulating system (MARS)

—MARS（Molecular Adsorbent Recycling System）

是一種新型人工肝臟支持系統，目的為延長等待時間增加急性肝衰竭患者接受肝臟移植手術的機會。該系統將血液引流到體外，血液的毒素經由特殊的透析膜，被另一側循環的白蛋白溶液吸附帶走，經過透析、活性碳吸附、樹脂吸附，乾淨的白蛋白溶液再循環重複使用。其毒素移除效果好，不良反應少。處理後的乾淨血液回輸患者體內，每次治療約需6至8小時，一般治療期間需每天或每2天洗1次，不過費用高昂，每洗1次約需15至20萬元，健保並未給付。

CTP(Child-Turcotte-Pugh)

Measure	1 point	2 points	3 points
Total bilirubin, μmol/l (mg/dl)	<34 (<2)	34-50 (2-3)	>50 (>3)
Serum albumin, g/l	>35	28-35	<28
PT INR	<1.7	1.71-2.30	> 2.30
Ascites	None	Mild	Moderate to Severe
Hepatic encephalopathy	None	Grade I-II (or suppressed with medication)	Grade III-IV (or refractory)

Points	Class	One year survival	Two year survival
5-6	A	100%	85%
7-9	B	81%	57%
10-15	C	45%	35%

source from: http://en.wikipedia.org/wiki/Child-Pugh_score

Cuff-leak test for the diagnosis of upper airway obstruction in adults: a systematic review and meta-analysis

Maria Elena Ochoa, Maria del Carmen Marı´n, Fernando Frutos-Vivar, Federico Gordo, Jaime Latour-Pe´rez, Enrique Calvo, Andres Esteban   

Intensive Care Med (2009) 35(7):1171-9

報告者：廖瑞琪 101.12.19

Abstract

Purpose:

To evaluate, in adults, the diagnostic accuracy of the cuff-leak test for the diagnosis of upper airway obstruction secondary to laryngeal edema and for reintubation secondary to upper airway obstruction.

Methods:

Systematic review without language restrictions based on electronic databases and manual review of the literature up to December 2008. When appropriate, a random-effects meta-analysis and meta-regression (Moses’ method) were performed.

Results:

Upper airway obstruction was the outcome in nine studies with an overall incidence of 6.9%. There was significant heterogeneity among studies. The pooled sensitivity was 0.56 (95% confidence interval: 0.48–0.63), the specificity was 0.92 (95% CI: 0.90–0.93), the positive likelihood ratio was 5.90 (95% CI: 4.00–8.69), the negative likelihood ratio was 0.48 (95% CI: 0.33–0.72), and the diagnostic odds ratio was 18.78 (95% CI:7.36–47.92). The area under the curve of the summary receiver-operator characteristic (SROC) was 0.92 (95% CI: 0.89–0.94). Only three studies have evaluated the accuracy of the cuff-leak test for reintubation secondary to upper airway obstruction. Overall incidence was 7%. The pooled sensitivity was 0.63 (95% CI: 0.38–0.84), the specificity was 0.86 (95% CI: 0.81–0.90), the positive likelihood ratio was 4.04 (95% CI:2.21–7.40), the negative likelihood ratio was 0.46 (95% CI: 0.26–0.82), and the diagnostic odds ratio was 10.37 (95% CI: 3.70–29.13).

Conclusions:

A positive cuff-leak test (absence of leak) should alert the clinician of a high risk of upper airway obstruction.

Pre-Operative Risk Factors Predict Post-Operative Respiratory Failure after Liver Transplantation

Ching-Tzu Huang., Horng-Chyuan Lin, Shi-Chuan Chang, Wei-Chen Lee   

PLoS ONE 2011,6(8): e22689

報告者：郭小萍 101.12.12

Abstract

Objective:

Post-operative pulmonary complications significantly affect patient survival rates, but there is still no conclusive evidence regarding the effect of post-operative respiratory failure after liver transplantation on patient prognosis. This study aimed to predict the risk factors for post-operative respiratory failure (PRF) after liver transplantation and the impact on short-term survival rates.

Design:

The retrospective observational cohort study was conducted in a twelve-bed adult surgical intensive care unit in northern Taiwan. The medical records of 147 liver transplant patients were reviewed from September 2002 to July 2007. Sixty-two experienced post-operative respiratory failure while the remaining 85 patients did not.

Measurements and Main Results:

Gender, age, etiology, disease history, pre-operative ventilator use, molecular adsorbent re-circulating system (MARS) use, source of organ transplantation, model for end-stage liver disease score (MELD) and Child-Turcotte-Pugh score calculated immediately before surgery were assessed for the two groups. The length of the intensive care unit stay, admission duration, and mortality within 30 days, 3 months, and 1 year were also evaluated. Using a logistic regression model, post-operative respiratory failure correlated with diabetes mellitus prior to liver transplantation, preoperative impaired renal function, pre-operative ventilator use, pre-operative MARS use and deceased donor source of organ transplantation (p<0.05). Once liver transplant patients developed PRF, their length of ICU stay and admission duration were prolonged, significantly increasing their mortality and morbidity (p<0.001).

Conclusions:

The predictive pre-operative risk factors significantly influenced the occurrence of post-operative respiratory failure after liver transplantation.

Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients (Review)

Blackwood B, Alderdice F, Burns KEA, Cardwell CR, Lavery G, O’Halloran P

The Cochrane Library 2011, Issue 7

報告者：林美妙 101.12.5

A B S T R A C T

Background

Reducing weaning time is desirable in minimizing potential complications from mechanical ventilation. Standardized weaning protocols are purported to reduce time spent on mechanical ventilation. However, evidence supporting their use in clinical practice is inconsistent.

Objectives

To assess the effects of protocolized weaning from mechanical ventilation on the total duration of mechanical ventilation for critically ill adults; ascertain differences between protocolized and non-protocolized weaning in terms of mortality, adverse events, quality of life, weaning duration, intensive care unit (ICU) and hospital length of stay (LOS); and explore variation in outcomes by type of ICU, type of protocol and approach to delivering the protocol.

Search methods

We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2010), MEDLINE (1950 to 2010), EMBASE (1988 to 2010), CINAHL (1937 to 2010), LILACS (1982 to 2010), ISI Web of Science and ISI Conference Proceedings (1970 to 2010), Cambridge Scientific Abstracts (inception to 2010) and reference lists of articles. We did not apply language restrictions.

Selection criteria

We included randomized and quasi-randomized controlled trials of protocolized weaning versus non-protocolized weaning from mechanical ventilation in critically ill adults.

Data collection and analysis

Three authors independently assessed trial quality and extracted data. A priori subgroup and sensitivity analyses were performed. We contacted study authors for additional information.

Main results

Eleven trials that included 1971 patients met the inclusion criteria. The total duration of mechanical ventilation geometric mean in the protocolized weaning group was on average reduced by 25% compared with the usual care group (N = 10 trials, 95% CI 9% to 39%, P = 0.006); weaning duration was reduced by 78% (N = 6 trials, 95% CI 31% to 93%, P = 0.009); and ICU LOS by 10% (N = 8 trials, 95% CI 2% to 19%, P = 0.02). There was significant heterogeneity among studies for total duration of mechanical ventilation (I² = 76%, P < 0.01) and weaning duration (I² = 97%, P < 0.01), which could not be explained by subgroup analyses based on type of unit or type of approach.

Authors’ conclusions

There is some evidence of a reduction in the duration of mechanical ventilation, weaning duration and ICU LOS with use of standardized protocols, but there is significant heterogeneity among studies and an insufficient number of studies to investigate the source of this heterogeneity. Although some study authors suggest that organizational context may influence outcomes, these factors were not considered in all included studies and therefore could not be evaluated.

Massive Pulmonary Hemorrhage After Pulmonary Thromboendarterectomy

Anesthesia and Analgesia 2004 vol. 99 no. 3672-675

Figure 1. A general algorithm for the approach to postcardiopulmonary bypass (CPB) pulmonary hemorrhage. PEEP = positive end-expiratory pressure; FFP = fresh frozen plasma; PAP = positive airway pressure.

During a second attempt at separation from CPB, PEEP 10 cm H₂O was applied; phenylephrine 10 mg and vasopressin 20 U diluted to 10 mL with normal saline were administered via the endotracheal tube;

pulmonary thromboendarterectomy (PTE); cardiopulmonary bypass (CPB)

Alveolar hemorrhage associated with lupus nephritis

Jornal de Pneumologia

Print version ISSN 0102-3586

J. Pneumologia vol.29 no.6 São Paulo Nov./Dec. 2003

CASE REPORT

Ricardo Henrique de Oliveira Braga Teixeira^I; Marcel Hiratsuka^II; Flávia Calderini Rosa^II; Rogério Souza^III; Carlos Roberto Ribeiro de Carvalho^IV

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ABSTRACT

Alveolar hemorrhage leading to respiratory failure is uncommon. Various etiologies have been reported, including systemic lupus erythematosus, which generally presents as pulmonary-renal syndrome. It is believed that the pathogenesis of microangiopathy is related to deposits of immune complexes that lead to activation of cellular apoptosis. We report two cases of alveolar hemorrhage and respiratory failure, both requiring mechanical ventilation. The two cases had opposite outcomes after pharmacological therapy. In one of the cases, the presence of anti-glomerular basement membrane antibodies demonstrates the multiplicity of physiopathological mechanisms that may be involved. This multiplicity of mechanisms provides a possible explanation for the heterogeneous responses to the available treatments.

Key words: Lupus erythematosus systemic/etiology. Lupus nephritis/etiology. Respiratory insufficiency/complications.

---

Abbreviations used in this paper:
GBM – Glomerular basement membrane
SLE – Systemic lupus erythematosus
PEEP – Positive end-expiratory pressure
ICU – Intensive care unit

Introduction

Diffuse alveolar hemorrhage leading to respiratory failure is uncommon. Various etiologies have been reported, including infections, inhaled toxins, coagulation disorders, Goodpasture’s syndrome, microscopic polyangiitis and Wegener’s granulomatosis, as well as various types of collagenosis, such as scleroderma and systemic lupus erythematosus (SLE).^(1,2)

Pulmonary-renal syndrome is characterized by the occurrence of both alveolar hemorrhage and glomerular nephritis and is frequently associated with the presence of antineutrophil cytoplasmic antibodies or anti-glomerular basement membrane (anti-GBM) antibodies. The type of injury, (alveolar, glomerular or both) determines the evolution and prognosis of the syndrome.⁽¹⁾

A diagnosis of alveolar hemorrhage is made through the identification of acute pulmonary symptoms. Such symptoms include hemoptysis, new alveolar infiltrate (seen in chest radiographs), lower concentrations of hemoglobin and the presence of blood or hemosiderin-laden macrophages in bronchoalveolar lavage fluid, although diagnosis can be made in the absence of some of these symptoms.^(1,3)

In SLE patients, diffuse alveolar hemorrhage is quite uncommon, occurring in only about 2% of cases, and is often associated with higher mortality rates. In most cases, concomitant renal involvement is also observed.⁽³⁾

We report 2 cases of lupus nephritis-related alveolar hemorrhage treated between June and August of 2002 in the respiratory intensive care unit (Respiratory ICU, Hospital das Clínicas, University of São Paulo School of Medicine).

 Case reports

Case 1

The patient was an 18-year-old female patient who, due to cutaneous and articular symptoms, had been diagnosed 2.5 years prior with SLE, for which she was being treated with 250 mg of chloroquine/day.

Without consulting a physician, the patient suspended her medication at 1 month prior to admission, consequently developing progressive dyspnea (even during minimal exertion) and muscle weakness. In addition, 4 days before admission, she began to suffer from diuresis. She was taken to the emergency service after an acute attack of dyspnea.

The patient presented with intense pulmonary discomfort, tachypnea (30 breaths per minute), and hypoxemia (88% oxygen saturation in room air). She claimed to have no expectoration. A chest radiograph revealed bilateral alveolar infiltrate and small pleural effusions (Figure 1A). Laboratory tests showed anemia, normal leucocyte counts, impaired renal function and evidence of active inflammation. Since there was no clear evidence of infection, alveolar hemorrhage was suspected.

The patient was transferred to the ICU and submitted to non-invasive ventilation. Intubation was considered necessary due to her worsening condition. Bronchoalveolar lavage was performed and cultures obtained. The cultures tested negative, which is indicative of alveolar hemorrhage. The ventilation was adjusted to allow up to 22 cm H₂O of positive end-expiratory pressure (PEEP), with partial response in the oxygenation. Intravenous methylprednisolone was administered as pulse therapy and the chloroquine was maintained. Since the patient did not respond, she was submitted to plasmapheresis for 3 days, and cyclophosphamide was introduced for immunosuppression. After new episodes of bleeding, gamma globulin was administered. However, none of these procedures had any effect on the bleeding episodes, which continued to occur every 3 to 7 days.

Upon admission, the patient had presented compromised renal function, evidenced by disproportionately increased levels of creatinine (urea = 60 mg/dL; creatinine = 2.1 mg/dL). This condition worsened over the course of treatment, despite fluid replacement and the previously described immunosuppression therapy. From day 42 onward, the patient required dialysis. On day 61 of treatment, intracranial hypertension was detected, and computer tomography scans revealed a large area of ischemia in the right cerebral hemisphere, with intense edema and mid-line shift. The patient underwent decompressive craniectomy, but died during the immediate post-operative period.

Case 2

A 40-year-old female patient had, 17 years earlier, been diagnosed with SLE. Since then, she had been suffering from malar erythema, serositis and arthritis in both the large and small joints. In addition, she had developed renal involvement, including proteinuria and reduced creatinine clearance (40 mL/min). During that time, a renal biopsy was performed, revealing membranous and mesangial glomerulopathy.

Her renal function continued to deteriorate until 5 years prior to her admission to our hospital, at which time partial improvement was achieved through the use of pulse therapy with cyclophosphamide. A regime of mycophenolate mofetil was initiated 2 years later (3 years prior to being admitted to our hospital).

At 1 month before admission to our hospital, her renal function worsened. Proteinuria, dyslipidemia, generalized edema (anasarca), and anuria were all increased and she required hospitalization. Pulse therapy with methylprednisolone was administered, to no effect. She was then given pulse therapy with cyclophosphamide. Again, there was no improvement, and a program of hemodialysis was initiated.

Upon admission to our facilities, the patient presented progressive dyspnea and decreased hemoglobin, as well as alveolar infiltrate in the chest radiograph (Figure 2A). After hemoptysis and a drop in arterial saturation, as well as a severe episode of tachypnea, were observed, the patient was transferred to the ICU. She was intubated and submitted to bronchoscopy with bronchoalveolar lavage, which revealed bleeding. Cytological examination of the bronchoalveolar lavage fluid revealed hemosiderin-laden macrophages, confirming the diagnosis of alveolar hemorrhage.

While in the ICU, ventilation was set at 18 cm H₂O of PEEP and a tidal volume of 6 mL/kg, and there were not other bleeding episodes. Ventilation was maintained for 5 days and there was a rapid improvement in her respiratory pattern. She was then extubated and ventilation was maintained through use of an oxygen mask in combination with periods of non-invasive ventilation. Until the patient was discharged from the ICU, she was under monotherapy with prednisone.

Discussion

Although SLE-related alveolar hemorrhage is quite uncommon (found in only 2% of lupus patients), the prognosis is always negative and the mortality rate is between 70 and 90%.^(1,4) Histological studies have shown that, in about 70% of pulmonary biopsies, there is little inflammatory activity and a predominance of hemorrhagic characteristics, whereas, in the remaining 30%, histological changes are compatible with neutrophilic capillaritis or diffuse alveolar damage.⁽⁴⁾

In approximately 75% of SLE-related alveolar hemorrhage cases, immunocomplex deposits have been observed in the alveolar wall.⁽⁴⁾ However, other histological studies have shown that most cases are characterized by hemorrhage involving minimal inflammation (with neutrophilic capillaritis in only 7% of cases).⁽⁵⁾

Under electron microscopy, immunocomplex deposits, characteristic of class IV lupus nephritis, are seen in the alveolar wall. In cases involving renal microangiopathy, such deposits are found in the subendothelial region of the glomerular capillary basement membrane. In the literature, most cases of renal microangiopathy have been attributed to class III or IV lupus nephritis. Evidence of microangiopathy is uncommon in class II (mesangial) or V (membranous) lupus nephritis, except when an increase in SLE activity leads to impaired renal function.^(3,4)

In our study, both patients presented an acute reduction in renal function. In order to evaluate autoimmunity in these 2 patients, we measured titers of anti-glomerular basement membrane (anti-GBM) antibodies, which are associated with Goodpasture’s syndrome and are considered to be one of the most prevalent indicators of pulmonary-renal syndrome.

Although anti-GBM titers were undetectable in case 1, it must be taken into consideration that the patient had already been treated with pulse corticosteroid therapy, immunosuppressant drugs and plasmapheresis, all of which may have affected titer determination. In case 2, in which the patient presented class V-type renal lesion, anti-GBM titers were significant. Although, histologically speaking, this is not the most common type of SLE-related microangiopathy, progression to the proliferative type is possible, in which case the impaired renal function would be expected.

However, it is still not possible to identify all factors responsible for the lesion related to the alveolar hemorrhage, or for the SLE-related renal microangiopathy. Neither is it possible to identify which factors might be responsible for the different outcomes in both patients, especially for the differing responses to the immunosuppression therapy. However, similarly divergent patient responses have been seen in other forms of vasculitis involving pulmonary complications.⁽⁶⁾

Nevertheless, the use of protective strategies, such as maintaining low tidal volumes and high levels of PEEP during mechanical ventilation, might be fundamental in treating patients with symptoms of severe respiratory insufficiency. In a study involving respiratory distress syndrome patients, including some with leptospirosis-induced alveolar hemorrhage and other forms of pulmonary vasculitis, the use of such ventilation strategies led to lower mortality rates.⁽⁷⁾

Despite the fact that this condition is rare, early diagnosis and the introduction of measures for respiratory system protection might be beneficial in cases of SLE-related alveolar hemorrhage. In addition, greater understanding of the physiopathology of this condition could lead to the development of more effective pharmacological treatments. 

References

1. Bosch X, Font J. The pulmonary-renal syndrome: a poorly understood clinicopathologic condition. Lupus 1999;8:258-62.         [ Links ]

2. Bar J, Ehrenfeld M, Rozenman J, Perelman M, Sidi Y, Gur H. Pulmonary-renal syndrome in systemic sclerosis. Semin Arthritis Rheum 2001; 30:403-10.         [ Links ]

3. Lee JG, Joo KW, Chung WK, Jung YC, Zheung SH, Yoon HJ, et al. Diffuse alveolar hemorrhage in lupus nephritis. Clin Nephrol 2001;55: 282-8.         [ Links ]

4. Hughson MD, He Z, Henegar J, McMurray R. Alveolar hemorrhage and renal microangiopathy in systemic lupus erythematosus. Arch Pathol Lab Med 2001;125:475-83.         [ Links ]

5. Specks U. Diffuse alveolar hemorrhage syndromes.Curr Opin Rheumatol 2001;13:12-7.         [ Links ]

6. Lauque D, Cadranel J, Lazor R, Pourrat J, Ronco P, Guillevin L, et al. Microscopic polyangiitis with alveolar hemorrhage. A study of 29 cases and review of the literature. Groupe d'Etudes et de Recherche sur les Maladies "Orphelines"Pulmonaires (GERM"O"P). Medicine 2000;79: 222-33.         [ Links ]

7. Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338: 347-54.        [ Links ]

Hemorrhaging: Pulmonary hemorrhage (P-Hem) – TheTreatments

Home of Kyle J. Norton for The Better of Living & Living Health   Hemorrhaging is also known as bleeding or abnormal bleeding as a result of blood loss due to internal.external leaking from blood vessels or through the skin.

 I. Classifications of Hemorrhaging
According to the classification from the American College of Surgeons’ Advanced Trauma Life Support (ATLS), Hemorrhaging is divided into 4 classes, depending to the volumes of blood loss and other factors

Classification of hemorrhage

	Class
Parameter	I	II	III	IV
Blood loss (ml)	<750	750–1500	1500–2000	>2000
Blood loss (%)	<15%	15–30%	30–40%	>40%
Pulse rate (beats/min)	<100	>100	>120	>140
Blood pressure	Normal	Decreased	Decreased	Decreased
Respiratory rate (breaths/min)	14–20	20–30	30–40	>35
Urine output (ml/hour)	>30	20–30	5–15	Negligible
CNS symptoms	Normal	Anxious	Confused	Lethargic

Modified from Committee on Trauma. CNS = central nervous system(1a).

II.  Types of hemorrhaging E.4. Treatments 
Treatments depend on the diagnosis of each patient, if the underlined cause is due to medication, then medicine has to be stopped. 

1. Immediate treatment
According to the Intensive Care Nursery House Staff Manual immediate treatment of P-Hem should include tracheal suction, oxygen and positive pressure ventilation. To assist in decreasing P-Hem, mean airway pressure should be increased, either by a relatively high PEEP (i.e., 6 to 10 cmH2O) or by high frequency ventilation(15). In the infants, reserachers at suggested that current management of PH in VLBW infants includes ventilatory support using high positive end expiratory pressure, transfusion of blood and blood products to support the circulation and correct any hemostatic or coagulation defects and evaluation and treatment for patent ductus arteriousus (PDA). These strategies are often ineffective in preventing a poor outcome. rFVIIa is effective in controlling life-threatening hemorrhage in patients with hemophilia A and B with inhibitors, and innonhemophiliacs with a variety of inherited or acquired hemostatic defects including platelet disorders, liver disease and von Willebrand’s disease.(15a)

 2. Embolization – Interventional treatment of pulmonary arteriovenous malformations
Acording to the study of Dr. Andersen PE and Dr. Kjeldsen AD. at the Odense University Hospital ”Pulmonary arteriovenous malformations (PAVM) are congenital vascular communications in the lungs.  The generally accepted treatment strategy of first choice is embolization of the afferent arteries to the arteriovenous malformations. It is a minimally invasive procedure and at the same time a lungpreserving treatment with a very high technical success, high effectiveness and low morbidity and mortality. Embolization prevents cerebral stroke and abscess as well as pulmonary haemorrhage and further raises the functional level. Embolization is a well-established method of treating PAVM, with a significant effect on oxygenation of the blood. Screening for PAVM in patients at risk is recommended, especially in patients with HHT(16).

3. Corticosteroids 
There is a report of a patient suffered from acute glomerulonephritis with modest renal impairmentand life-threatening pulmonary hemorrhage. The pulmonary hemorrhage caused severe hypoxia thatnecessitated artificial ventilation. As a last resort, 1 g/day of methylprednisolone was administered intravenously. Rapid cessation of pulmonary hemorrhage ensued with clearing of the lungs fields. the suggestion of large doses of glucocorticosteroids should be administered to patients with life-threatening pulmonary hemorrhage before considering bilateral nephrectomy, especially if the renal function is still adequate. Bilateral nephrectomy is an irreversible approach and, as with massive doses of steroids, has yet to be proved to be a consistently effective mode of therapy(17).

Sources
(1a) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003/table/T1/   
(15) http://www.ucsfbenioffchildrens.org/pdf/manuals/29_PulmHemorrhage.pdf
(15a) http://www.nature.com/jp/journal/v22/n8/full/7210787a.html
(16) http://www.ncbi.nlm.nih.gov/pubmed/21160695 
(17) http://annals.org/article.aspx?articleid=689575 

Positive End-Expiratory Pressure

1. Indications
   1. Pulmonary condition with widespread alveolar collapse
   2. Adult Respiratory Distress Syndrome (ARDS)
      1. PEEP increases lung compliance
      2. PEEP decreases intrapulmonary shunting
      3. Increases PO2 and allows lower FIO2 below 60%
      4. May increase dead space ventilation
         1. Overdistends normal lung
   3. Pulmonary Edema
      1. PEEP allows decrease in FIO2 below 60%
      2. PEEP may increase extravascular lung water
2. Disproved uses of PEEP
   1. Localized Lung Disease (e.g. lobar Pneumonia)
      1. PEEP may worsen Hypoxemia
         1. Overdistends normal lung
         2. Directs blood flow to diseased lung
      2. PEEP not recommended
         1. Unless selectively applied to diseased lung
   2. Prophylactic PEEP
      1. PEEP does not reduce ARDS Incidence
   3. Routine PEEP
      1. PEEP does not appear indiscriminately beneficial
   4. Mediastinal Bleeding
      1. PEEP does not protect against mediastinal bleeding
3. Physiology
   1. PEEP maintains small end-expiratory pressure
      1. Helps to prevent alveolar collapse
      2. Promotes alveolar-capillary gas exchange
   2. Increases lung function parameters
      1. Increases Functional Residual Capacity (FRC)
   3. Increases cardiac output with low airway pressures
      1. May result in increased Oxygen Delivery
4. Dosing
   1. Usual PEEP setting: 5 to 10 cm H2O
5. Complications
   1. Decreased cardiac output
      1. Associated with higher airway pressures
      2. Associated with decreased ventricular filling
   2. Barotrauma
   3. Fluid Retention
   4. Intracranial Hypertension
6. References
1. Marino (1991) ICU Book, Lea & Febiger, p. 375-9

sources from ：http://www.fpnotebook.com/lung/procedure/PstvEndExprtryPrsr.htm