1

Acknowledgment

Pursuing a book is a both painful and enjoyable experience. It is just like

climbing a high peak, step by step, accompanied with hardships, frustration,

encouragement and trust and with so many people help. When I found myself at the top

enjoying the beautiful scenery, I realized that it was, in fact, teamwork that got me there.

Though it will not be enough to express my gratitude in words to all people helped me.

Above all, thank to Allah the Glorious, and the compassionate for helping me

and giving me the strength to accomplish this work. To him I present this work,

please God accept it pure for your face and forgive me for all the bad things I have

ever done.

My deepest thanks, appreciation and profound gratitude to supervisors of this

work

Assist. Prof. Dr. Hanaa Y. Hashem

Assistant Professor of Medical-Surgical Nursing & Director of the Quality Assurance

Unit Faculty of nursing, Cairo University.

Dr. Mahmoud M. Alsagheir

Lecturer of Anesthesia and Intensive Care, Faculty of Medicine - Al- Azhar University

Dr. Mohammed Salah

Resident of Anesthesia and Intensive Care Assigned Doctor for Pain Management,

Nizwa Hospital – Sultanate Oman.

In addition, I would like to thank every person who helped me to fulfill this

book even if I forget to write his or her name.

Maha Salah

2

Dedication

To The Soul of My Father

Who always stood behind me and knew I would succeed. Gone now but never

forgotten. I will miss him always and love him forever.

To My Mother

Whatever I am is due to your hard work, prays and love

To My Brothers, Sister & Close friends

Those are my great support

Thanks for all they did.

3

LIST OF CONTENTS

Chapter Page

Acknowledgment………………...…………………………… 1

Dedication…………………………………………………….. 2

List of Contents…………………………………..…………… 3

List of Abbreviations…………………………..……………… 5

Abstract……………………………………………………….. 6

I INTRODUCTION……...……………………………….......... 7

II CLINICAL PATHWAY…………………………………........ 10

Definition of Clinical Pathway 11

Synonyms 11

Characteristics of Clinical Practice Guidelines 12

Clinical Pathways Aim 12

Clinical Pathways Benefits 13

Four Components of a Clinical Pathway 15

Guidelines for the Development and Implementation 16

Development and implementation strategies 16

Potential Problems and Barriers to the Introduction of

Clinical Pathways 18

Challenges faced for Implementation 19

Discontinuing the Clinical Pathway 19

Keys to pathway success 20

III ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS).. 21

History 22

Definition 28

The Origin 28

4

Risk Factors 29

Risk Factors Predictive of Mortality 29

Causes 30

Pathophysiology 31

Consequences 37

Complications 38

IV MEDICAL and NURSING MANAGEMENT of ARDS 39

1. Conventional therapy 41

2. Supportive therapy 47

3. Non-Conventional Therapy 50

V DEVELOPED CLINICAL PATHWAY FOR ARDS

PATIENTS 57

VI REFERENCES 62

5

LIST OF ABBREVIATIONS

AECC American-European Consensus Conference

ALI Acute Lung Injury

ARDS Acute Respiratory Distress Syndrome

ARPs Anticipatory recovery pathways

CMV Controlled Mandatory Ventilation

CP Clinical Pathway

CPAP Continuous Positive Airway Pressure

DIC Disseminated Intravascular Coagulation

FiO2 Friction of Inspired Oxygen

HIV Human Immune Deficiency Virus

HTN Hypertension

ICU Intensive Care Unit

I:E Inspiration : Expiration

ION Inhaled Nitric Oxide

P Plat Plateau Pressure

PAC Pulmonary Artery Catheter

PaO2 Partial Pressure of Arterial Blood Oxygen

PAOP Pulmonary artery occlusion pressure

PBW Predicted Body Weight

PEEP Positive end-expiratory pressure

PH Power of Hydrogen Ions

RR Respiratory Rate

SIRS Systemic Inflammatory Response Syndrome

SpO2 Saturation of Peripheral Oxygen

TRALI Transfusion Related Acute Lung Injury

VILI Ventilator Induced Lung Injury

VT Tidal Volume

6

Abstract

Acute respiratory distress syndrome (ARDS) represents a complex clinical

syndrome and carries a high risk for mortality. The severity of the clinical course,

the uncertainty of the outcome, and the reliance on the full spectrum of critical care

resources for treatment mean that the entire health care team is challenged.

Researchers and clinicians have investigated the nature of the pathological process

and explored treatment options with the goal of improving outcome. Through this

application of research to practice, we know that some previous strategies have been

ineffective, and innovations in mechanical ventilation, sedation, nutrition, and

pharmacological intervention remain important research initiatives.

Developed Clinical pathway is multidisciplinary plans of best clinical practice

for this specified groups of patients that aid in the coordination and delivery of high

quality care. They are a documented sequence of clinical interventions that help a

patient to move, progressively through a clinical experience to a desired outcome.

Although there is a lot of heterogeneity in patients with ARDS, this

suggested developed clinical pathway with alternatives was built depended on a lot

of researches and evidence based medicine and nursing practices which may

be helping these patients to improve outcomes, quality of life and decrease mortality.

7

HAPTER I

8

CHAPTER I

INTRODUCTION

Clinical pathways are multidisciplinary plans (or blueprint for a plan of care)

of best clinical practice for specified groups of patients with a particular diagnosis

that aid in the coordination and delivery of high quality care. They are a documented

sequence of clinical interventions that help a patient with a specific condition or

diagnosis move, progressively through a clinical experience to a desired outcome.

Predominantly, they are management tools and clinical audit tool that are based on

clinical information developed in other guidelines or parameters. They are specific

to the institution using them. Originally, critical pathways began with admission and

ended with discharge from the hospital. Today, they are usually interdisciplinary in

focus, merging the medical and nursing plans of care with those of other disciplines,

such as physical therapy, nutrition, or mental health. They provide opportunities for

collaborative practice and team approaches that can maximize the expertise of

multiple disciplines. Clinical pathways have four main components; a timeline, the

categories of care or activities and their interventions, intermediate and long term

outcome criteria, and the variance record (to allow deviations to be documented and

analyzed). They differ from practice guidelines, protocols and algorithms as they are

utilized by a multidisciplinary team and have a focus on the quality and co-ordination

of care (Audimoolam, Nair, Gaikwad, & Qing, 2005).

Acute respiratory distress syndrome (ARDS) represents a complex clinical

syndrome and carries a high risk for mortality. The severity of the clinical course,

the uncertainty of the outcome, and the reliance on the full spectrum of critical care

resources for treatment mean that the entire health care team is challenged. Since the

9

1960s, researchers and clinicians have investigated the nature of the pathological

process and explored treatment options with the goal of improving outcome.

Through this application of research to practice, we know that some previous

strategies have been ineffective, and innovations in mechanical ventilation, sedation,

nutrition, and pharmacological intervention remain important research initiatives

(Morton & Fontaine, 2014).

Acute Lung Injury (ALI)/ Acute Respiratory Distress Syndrome (ARDS) are

affecting both medical and surgical patients. Despite great advances in

understanding the pathogenesis of disease mortality rate is still high. Mortality rates

ranges between (30-50 %), although some trials had demonstrated lower mortality

rates (25 -30 %). Prevention of long-term disabilities must be a priority of care. Even

survivors of ARDS usually experience long ICU stay, hospital stay and several co-

morbidities & require prolonged rehabilitation time until of full recovery.

Restoration of normal activities ranges between 6 months to 12 months. Nearly half

of survivors had neurocognitive impairment & decrease quality of life that persist at

least 2 years. ALI/ARDS not only represent great impact on ICU but on nation's

economics as well (Sole, Klein, & Moseley, 2013).

A key role for the critical care nurse is early detection and prevention of

ARDS. Therefore, with respect to ARDS, it is essential that critical care nurses be

knowledgeable about risk factors, assessment tools and protocols, and prevention

strategies. ARDS is at the extreme end of a continuum of hypoxic acute lung injury

(ALI) that results in respiratory failure. In 1994, the American-European Consensus

Conference members issued definitions of ALI and ARDS that are widely used by

researchers today (Morton & Fontaine, 2014).

10

11

CHAPTER II

CLINICAL PATHWAY

Definition of Clinical Pathway:

“Clinical Pathways" (CP) is multidisciplinary plans of best clinical practice

for specified groups of patients with a particular diagnosis that aid the co-ordination

and delivery of high quality care. They are both, a tool and a concept, which embed

guidelines, protocols and locally agreed, evidence-based, patient-centered, best

practice, into everyday use for the individual patient” (Kinsman, Rotter, James,

Snow, & Willis, 2010).

A mapping of a patients’ condition that organizes, sequences and times the

major interventions of nursing staff, physicians and other departments for a

particular case type, subset or condition (Rotter , Kinsman, James , Machotta , &

Gothe , 2010).

Synonyms

Critical Pathway

Anticipatory recovery pathways (ARPs)

Integrated Care Pathways,

Multidisciplinary pathways of care ( MPCs),

Pathways of Care,

Care Maps,

Collaborative Care Pathways

Anticipated Recovery Path

Managed care plans

Care track

Clinical Practice Guidelines and Clinical Pathways; (components of clinical

protocols)

12

Characteristics of Clinical Practice Guidelines

Explicitly identify, appraise and summarize the best evidence about

prevention, diagnosis, prognosis, therapy, harm, and cost-effectiveness

Identify the range of potential decisions and provide the physicians with the

evidence which, when added to individual clinical judgment and patient's

values and expectations, will help them their own decisions in the best interest

of the patient.

Evidence-based medicine is the conscientious, explicit and judicious use of

current best evidence in making decisions about the care of individual

patients. This is the source for the clinical practice guidelines (Goldszer, et

al., 2004).

Clinical Pathways aim to have…

The right people

Doing the right things

At the right time

In the right place

With the right outcome

All with attention to the patient experience

To compare planned care with care actually given

13

Clinical Pathways Benefits:

a. General Benefits:

The pathway is a great tool for communicating to co-workers

To improve patient care

To maximize the efficient use of resources

To help identify and clarify the clinical processes

To support clinical effectiveness, clinical audit and risk management

Enhances interdisciplinary collaboration

Eliminate prolonged lengths of stay arising from inefficiencies, allowing

better use of resources

Reduce mistakes, duplication of effort

Improve the quality of work for service providers

Improve communication with patients as to their expected course of treatment

Identify problems at the earliest opportunity and correct these promptly

Facilitate quality management and an outcomes focus

b. Specified Benefits:

For Caregiver and Client

Improved quality and coordination of care

Improved clinical outcomes

Reduced practice variations

Increased use of Best Practice

Improved communication and information transfer across multi-disciplinary

teams and organizations

14

For Organization

Support the introduction of evidence-based medicine and use of clinical

guidelines

Support clinical effectiveness, risk management and clinical audit

Improve multidisciplinary communication, teamwork and care planning

Can support continuity and co-ordination of care across different clinical

disciplines and sectors

Provide explicit and well-defined standards for care

Reduce variations in patient care (by promoting standardization)

Support training

Optimize the management of resources

Can help ensure quality of care and provide a means of continuous quality

improvement

Support the implementation of continuous clinical audit in clinical practice

Support the use of guidelines in clinical practice

Improve communications between different care sectors

Disseminate accepted standards of care

Provide a baseline for future initiatives

Not prescriptive: don't override clinical judgment

Expected to help reduce risk

Expected to help reduce costs by shortening hospital stays (Dy, et al., 2005)

15

Components of a Clinical Pathway

1. A Timeline,

2. Categories of care or activities and their interventions,

3. Intermediate and long-term outcome criteria,

4. Variance record

Time Line

Pre-admission

Admission

Procedure

Post-operative

Discharge

Variance Record

Any mandatory or checked optional intervention that was not done.

An abnormal finding

An unmet outcome within the time frame

So, look for common variances to improve pathway and improve compliance.

Reasons for Variance

Patient’s clinical condition

Patient’s social situation

Associated diagnoses

Changing technology or techniques

Clinician’s discretion

Consultation and internal system services

External issues: primary care, home health care.

16

Guidelines for the Development and Implementation of Clinical

Pathway

Educate and obtain support from medical and nursing staff, and establish a

multidisciplinary team.

Identify potential obstacles to implementation.

Use quality improvement methods and tools.

Determine staff interest and select clinical pathways to develop.

Collect clinical pathway data and medical record reviews of practice patterns.

Conduct literature review of clinical practice guidelines.

Develop variance analysis system and monitor the compliance with

documentation on Clinical Pathways.

Use a pilot clinical pathway for 3 to 6 months; revise as needed (Audimoolam,

Nair, Gaikwad, & Qing, 2005).

Development and Implementation Strategies of Clinical Pathway

1. Select a Topic

Topic of high-volume, high-cost diagnoses and procedures.

For example:- Critical pathway development for cardiovascular diseases and

procedures

2. Select a Team

Active physician participation and leadership is crucial

Representatives from all disciplines

17

3. Evaluate the Current Process of Care

Key to understanding current variation

A careful review of medical records

Identify the critical intermediate outcomes, rate-limiting steps, and high-cost

areas on which to focus.

4. Evaluate Medical Evidence and External Practices

Evaluate the literature to identify evidence of best practices

In the absence of evidence, comparison with other institutions, or

"benchmarking," is the most reasonable method to use.

5. Determine the Critical Pathway Format

The format of the pathway include a task-time matrix

spectrum of pathways of the medical record used as a simple checklist

6. Document and Analyze Variance

The most important processes in the critical pathway

Identification of factors the key features in process improvement

Variance in clinical pathways is a result of the omission of an action or the

performance of an action at an inappropriate (often, a late) time.

18

For example: length of stay in the intensive care unit

Potential Problems and Barriers to the Introduction of Clinical

Pathways

May appear to discourage personalized care

Risk increasing litigation

Don't respond well to unexpected changes in a patient's condition

Suit standard conditions better than unusual or unpredictable ones

Reluctance to change

Require commitment from staff and establishment of an adequate

organizational structure

Problems of introduction of new technology

May take time to be accepted in the workplace

Need to ensure variance and outcomes are properly recorded, audited and

acted upon (Goldszer, et al., 2004).

19

Challenges Faced the Implementation of Clinical Pathway

Difficulties in engaging senior clinicians and persuading them to participate

in the procedure of designing and implementation of the clinical pathways

(e.g. engaging a cardiologist or neurologist in the process)

Problems in finding a common meeting time across disciplines, and getting

the multidisciplinary staff involved in the use of the clinical pathways for the

training for their effective use and learning their importance in the clinical

practice

Discontinuing the Clinical Pathway

The pathway will be discontinued whenever:

The patient’s primary diagnosis changes

The patient’s condition significantly worsens

The patient fails to meet clinical outcomes for 24-48 hours

To discontinue the pathway, a progress note (SOAP) is written by the Medical

doctor outlining the patient’s new plan of care and new orders. A new nursing

plan of care is also written. The pathway is then filed in the patient record.

20

Keys to Clinical pathway success

Make pathways part of your quality program.

Ensure strong collaboration between all relevant disciplines, with a strong

medical lead.

Select appropriate medical conditions in making pathways.

Base the pathway orders on best available evidence / best practice.

Collect and analyze variances and involve the staff in interventions to

decrease variances.

Incorporate adherence to pathway policies in performance appraisal of all

staff members.

Conclusion

A Clinical Pathway is thus a road map for a patient as well as for the treatment

team, which supports an Effective In-patient Care.

21

22

CHAPTER III

ACUTE RESPIRATORY DISTRESS SYNDROME

History:

Year History

1967 The first description of ARDS consisted of a case series of 12

patients with the acute onset of dyspnea, tachypnea, severe

hypoxemia, chest radiographic abnormalities, and decreased lung

compliance.

It Called Adult Respiratory Distress Syndrome

(Bernard , 2005)

1975 With the increased availability of pulmonary artery catheterization in

ICUs, ARDS was recognized as:

Non-cardiogenic form of pulmonary edema

With accumulation of both protein and cells in the alveoli

The presence of normal left atrial pressures.

(Bernard , 2005)

1980 Subsequently, several ARDS definitions were used that required at

least four basic clinical features,

1. Hypoxemia (varying severity).

2. Decreased respiratory system compliance.

3. Chest radiographic abnormalities.

4. Pulmonary artery occlusion pressure (PAOP) = 18 mmHg or

less using a Pulmonary Artery Catheter (PAC).

(Bernard , 2005)

23

1983 Other Names:

Adult hyaline-membrane disease

Adult respiratory insufficiency syndrome

High output respiratory failure

Congestive atelectasis

Hemorrhagic lung syndrome

Stiff-lung syndrome

Shock lung

White lung

1988 Murray and colleagues proposed a lung injury score that was based

on four components

1.Chest radiograph,

2. Hypoxemia.

3.Positive end-expiratory pressure.(PEEP)

4. Respiratory system compliance.

(Bernard , 2005)

1994

Subsequently, the American-European Consensus Conference

(AECC) had a goal of bringing “clarity and uniformity to the

definition of ARDS” The diagnostic criteria for ARDS were

1. ARDS = Pao2/Fio2 ≤ 200.

2. Bilateral infiltrates on chest radiograph.

3. Pulmonary artery occlusion pressure ≤18 mmHg or no clinical

evidence of left atrial hypertension.

(Bernard , 2005)

24

1994

25

1994

A: Normal chest X-ray.

B: Abnormal chest X-ray with consolidation from pneumonia in the

right lung, middle or inferior lobe (white area, left side of image).

26

2005 The Delphi Definition of ARDS

27

2012 The Berlin Definition of ARDS (Ranieri, et al., 2012)

Bilateral Opacities

A: Normal chest x-ray

B: Bilatral Alveolar infiltration (opacities)

(Koh , 2014)

A B

28

Definition:

• Acute Lung Injury (ALI)/ Acute Respiratory Distress Syndrome (ARDS) are

clinical devastating syndrome that characterized by:

The Origin of ARDS:

• The origin is unclear

• It is result of severe inflammatory process

29

Risk Factors for ARDS:

Direct (Respiratory) Non-Direct (Not respiratory)

• Aspiration of Gastric Content

• Pneumonia

• Fat Embolism

• Near Drowning

• Neurogenic Pulmonary Edema

• Oxygen Toxicity

• Chest or Lung Trauma

• Chest Radiation

• Sepsis

• Transfusion Related Acute Lung

Injury (TRALI)

• Multisystem Trauma

• Cardiopulmonary Bypass

• Anaphylaxis

• Disseminated Intravascular

Coagulation (DIC)

• Eclampsia

• Fracture Pelvic or Long Bones

• Leukemia

• Pancreatitis

• Sever Burn

• Non-Cardiogenic shock

(ARON & FARGO, 2012)

Risk Factors Predictive Of Mortality:

• Liver dysfunction/ cirrhosis

• Sepsis

• Non pulmonary organ dysfunction

• Age > than 65

• Organ transplantation

• HIV

• Active malignancy

• Chronic alcoholism. (Moazed & Calfee, 2014)

30

Causes for ARDS:

31

32

Pathophysiology

(Morton & Fontaine, 2014)

33

1- Acute Exudative Phase:

A. Basement membrane disruption

Type I pneumocystis destroyed

Type II pneumocystis preserved

B. Surfactant deficiency

Inhibited by fibrin

Decreased type II cell production

Impaired surfactant function (Inactivated)

C. Microatelectasis / alveolar collapse

Interstitial edema

Necrosis capillary endothelial cell

Alveolar cell + fibrin + plasma Protein together form hyaline membrane

(after 24-48h)

Normal & Injured Alveoly during Acute Phase

34

Clinical Manifestation of Acute Phase:

• Early (24 – 48hrs)

- Initial dyspnea with hyperventilation

- Retraction & use of accessory muscles

- Cough, breathlessness, fatigue & diaphoresis

- Cyanosis, pallor

• Late (after 48hrs) Due to worsening hypoxemia

- Fever, hypotension, tachycardia & refractory hypoxemia

- Crackles & rhonchi lung sounds

- Agitation, anxiety & confusion

2. Fibroproliferative phase:

• Type II Pneumocystis Proliferate

• Differentiate Into Type I Cells

• Reline Alveolar Walls

• Regeneration Of Capillary Endothelial Cells

• Fibroblast Proliferation

• Interstitial/Alveolar Fibrosis

• Lymphocytic Infiltration

• Collagen Deposition

35

3. Fibrotic phase:

• Characterized by:

• Local fibrosis

• Vascular obliteration

• Repair process:

• Resolution or fibrosis depending on

• Timing of intervention and management

Fibroproliferative & Fibrotic phase

36

Fibroproliferation Phase Clinical Manifestation:

Late signs & symptoms

• Severe difficulty in breathing i.e., labored, rapid breathing.

• Shortness of breath.

• Tachycardia

• Cyanosis (blue skin, lips and nails)

• Think frothy sputum

• Respiratory alkalosis

• Abnormal breath sounds, like crackles

• Respiratory Acidosis (Sole, Klein, & Moseley, 2013)

Time Course of ARDS:

37

Pathophysiology of ARDS

Consequences:

• Impaired gas exchange leading to severe hypoxemia - ventilation-perfusion

mismatch, increase in physiologic dead-space

• Decreased lung compliance – due to the stiffness of poorly lung

• Pulmonary HTN – 25% of patients, due to hypoxic vasoconstriction, Vascular

compression by positive airway compression, airway collapse and lung

parenchymal destruction

• Impaired gas exchange leading to severe hypoxemia - ventilation-perfusion

mismatch, increase in physiologic dead-space

• Decreased lung compliance – due to the stiffness of poorly lung

• Pulmonary HTN – 25% of patients, due to hypoxic vasoconstriction, Vascular

compression by positive airway compression, airway collapse and lung

parenchymal destruction (Chio, 2010)

38

Complications

• Common Complications:

• Nosocomial Pneumonia

• Barotrauma

• Renal Failure

• Other Complications:

• O2 Toxicity

• Stress Ulcers

• Tracheal Ulceration

• Blood Clots Leading To Deep Vein Thrombosis

• Pulmonary Embolism.

39

40

CHAPTER IV

MEDICAL AND NURSING MANAGEMENT

Objectives:

• Control the original cause

• Achieve adequate oxygenation

• Improve lung function

• Decrease probability of development of ventilator associated lung problems

• Decrease days of mechanical ventilator and length of ICU stay

• Prevent other organ failure

• Reduce mortality

ARDS Already Diagnosed

1. Control of original cause

2. Non-invasive O2 therapy

• Face mask

• Non-rebreathing face mask

• CPAP mask

3. Continuous monitoring of ABG and chest x-ray

If abnormalities start Mechanical ventilation

If normal ranges continue Non-invasive O2 therapy

41

Methods of Therapy:

1- Conventional therapy (Lung Protective Strategy)

2- Supportive therapy

3- Non-conventional therapy (Rescue therapy)

1. Conventional Therapy (Lung Protective Strategy)

ARDSNET

Lung Protective Strategy

• Low tidal volume (VT)

• Low plateau pressure (P Plat)

• Fio2 at non-toxic level (< 60 %)

• Positive end expiratory pressure (PEEP)

PART I: VENTILATOR SETUP AND ADJUSTMENT

Ventilator Mode

• Any mode can be used

• Choose mode & parameters according to severity and patient condition

• Start with Controlled Mandatory Ventilation (CMV)

• Change according to patient response

• Always we use Volume control modes

• Some cases need Pressure control modes (Siegel & Hyzy, 2010)

42

Ventilator Modes

1. Calculate predicted body weight (PBW)

Males = 50 + 2.3 [height (inches) - 60]

Females = 45.5 + 2.3 [height (inches) -60]

2. Select any ventilator mode

3. Set ventilator settings to achieve initial VT

= 8 ml/kg PBW

4. Reduce VT

by 1 ml/kg at intervals ≤ 2 hours until VT

= 6ml/kg PBW.

5. Set initial rate to approximate baseline minute ventilation (not > 35 bpm).

6. Adjust VT

and RR to achieve pH and plateau pressure goals below.

(ARDSNET Clinical Network Mechanical Ventilation Protocol Summary, 2012)

43

OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%

Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP

combinations such as shown below (not required) to achieve goal.

PLATEAU PRESSURE GOAL: ≤ 30 cm H2O

Check Pplat (0.5 second inspiratory pause), at least q 4h and after each change

in PEEP or VT.

If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4 ml/kg).

If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat >

25 cm H2O or VT = 6 ml/kg.

If Pplat < 30 and breath stacking or dis-synchrony occurs: may increase VT in

1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.

44

PH GOAL: 7.30-7.45

Acidosis Management: (pH < 7.30)

If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Maximum set

RR = 35).

If pH < 7.15: Increase RR to 35.

If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH > 7.15,

(Pplat target of 30 may be exceeded). May give NaHCO3

Alkalosis Management: (pH > 7.45) Decrease vent rate if possible.

I: E RATIO GOAL: Recommend that duration of inspiration be < duration of

expiration.

PART II: WEANING

A. Conduct a SPONTANEOUS BREATHING TRIAL daily when:

1. FiO2 ≤ 0.40 and PEEP ≤ 8.

2. PEEP and FiO2 ≤ values of previous day.

3. Patient has acceptable spontaneous breathing efforts. (May decrease vent rate by

50% for 5 minutes to detect effort.)

4. Systolic BP ≥ 90 mmHg without vasopressor support.

5. No neuromuscular blocking agents or blockade.

45

B. SPONTANEOUS BREATHING TRIAL:

If all above criteria are met and subject has been in the study for at least 12 hours,

initiate a trial of UP TO 120 minutes of spontaneous breathing with FiO2 < 0.5 and

PEEP < 5:

1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with PS < 5

2. Assess for tolerance as below for up to two hours.

a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg

b. Spontaneous VT ≥ 4 ml/kg PBW

c. RR ≤ 35/min

d. pH ≥ 7.3

e. No respiratory distress (distress= 2 or more)

Heart Rate > 120% of baseline

Marked accessory muscle use

Abdominal paradox

Diaphoresis

Marked dyspnea

3. If tolerated for at least 30 minutes, consider extubation.

4. If not tolerated resume pre-weaning settings.

(ARDSNET Clinical Network Mechanical Ventilation Protocol Summary, 2012)

46

Ventilator-Induced lung injury (VILI)

Volutrauma Overdistension

Atelectrauma Repeated recruitment and collapse

Bio Trauma Inflammatory mediators

Barotrauma High-pressure induced lung damage

Oxygen Toxic Effect FiO2

Other Medical Strategies for ARDS Management

1- Permissive Hypercapnia

• Hypercapnia and respiratory acidosis are a consequence of this strategy due

to low alveolar pressure and low tidal volume.

• Hypercapnia can be minimized by using the highest respiratory rate and

shortening the ventilator tubing to decrease dead space.

• Help to preserve minute volume in acceptable range and prevent increase of

P plat.

• May give Hco3

Stop Permissive Hypercapnia If:

• Increase intracranial pressure

• Myocardial infarction

• Metabolic acidosis

• Pregnant

• Renal failure

• Cardiovascular problems/Arrhythmia

47

2- Open Lung Ventilation

• A strategy that combines low tidal volume ventilation and high PEEP to

maximize alveolar recruitment by:

• Mitigate alveolar overdistension

• Minimize atelectasis

• Together, decrease the risk of ventilator-associated lung injury

3- Recruitment Maneuvers

• Application of a high level of PEEP (35 to 40 cmH2O) for 40 seconds

• To open the collapsed alveoli (DEJA, et al., 2008)

Adverse effects:

• Hypotension

• Desaturation

2- Supportive Management

1- Hemodynamic management

Early management of any abnormalities in vital signs and hemodynamics.

2- Fluid Management

Conservative fluid strategy

• Negative balance is preferred unless in hypotension and hypovolemia.

• Give colloid or vasopressor rather than crystalloid

• Preliminary data suggests that combination therapy with albumin and

furosemide may improve fluid balance, oxygenation, and hemodynamics

(Koh Y. , 2014).

48

3- Nutritional support

Aim:

• To provide adequate nutrition to meet the patient’s level of metabolism

& reduce morbidity.

Specialized Formula:

• Eicosapentaenoic acid, Gama-linolenic acid & elevated antioxidant.

Effect:

• Reduce mortality

• Improve oxygenation secondary to reduce pulmonary inflammation

• Fewer day on mechanical ventilator

4- Control of blood glucose levels

5- Treatment of nosocomial pneumonia.

6- Pharmacological Management

Medications may be Help

A- Sedatives and neuromuscular block

Sedatives

• Aim: to minimize patient – ventilator asynchrony, prevent self

extubation, promote rest/sleep & decrease anxiety

• Also, use in treatment of hypercapnia

Assess:

• Sedation assessment scale & Delirium assessment scale

49

Neuromuscular Block (Therapeutic Paralysis):

Aim:

• Control ventilation & Promote adequate oxygenation

• Decrease O2 consumption (Raoof, Goulet, Esan, Hess, & Sessler,

2010)

Hazardous:

• Increase risk of prolonged myopathy

N.B.:

NBA improve survival in ARDS patient, decrease ventilator time & didn’t

increase muscle weakness in some population

B- Corticosteroids:

Rationale & Risks:

• Helps by inhibiting neutrophil activation, fibroblast proliferation, and

collagen deposition.

• May increase incidence of severe neuromyopathic events. Subjects started on

steroids 14 days after diagnosis had increased mortality rates (Ariano, 2008).

Evidence:

• Clinical trials show no survival benefits, two small RCT’s show improvement

in oxygenation and lung injury

C- B2 Agonist

• Decreases alveolar-capillary permeability in patients with ARDS, possibly by

simulating alveolar wound repair.

• Reduces the incidence pulmonary edema

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D. Lasix

E. Albumin

F. Low molecular weight Heparin ( Anticoagulant effect & Prophylaxis against

deep venous thrombosis {DVT})

G. Omeprazole – Zantac (Prophylaxis against stress ulcer & gastrointestinal (GI)

bleeding)

(Roch, Hraiech, Dizier, & Papazian, 2013)

3- Non – Conventional Therapy (Alternative Therapy)

(Rescue Therapy)

1- Surfactant Replacement Therapy

Numerous randomized trials have found no clinical benefit from

recombinant surfactant protein C, synthetic surfactant, or freeze-dried

natural animal surfactant in patients with ARDS, despite its benefit in animal

models.

No effect on duration of mechanical ventilation and mortality. The exogenous

surfactant was generally well tolerated.

2- Refractory Hypoxemia

Increasing the I: E ratio by prolonging inspiratory time may improve

oxygenation.

When the inspiratory time is increased, there is an obligatory decrease in

the expiratory time. This can lead to air trapping, auto-PEEP, barotrauma,

hemodynamic instability, and decreased oxygen delivery.

A prolonged inspiratory time may require significant sedation or

neuromuscular blockade.

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3- High Frequent Oscillation

Patient fully sedated and paralyzed

Increase respiratory rate till 35br/min with low tidal volume

To open collapsed lung and improve lung recruitment

4- Selective Pulmonary Vasodilators Inhaled Nitric oxide (INo)

Improves Oxygenation

- Selective vasodilatation of vessel leading to better ventilation

Improves v/q mismatch.

Reduction in pulmonary artery pressure

- Improves oxygen

- direct smooth muscle relaxation

- Improved RV Fn.

- Reduced capillary leak.

Inhibit platelet aggregation and neutrophil adhesion.

Mortality Benefits – None

5- Partial Liquid Ventilation (Perfluorocarbon )

Mechanism of action

• Reduces surface tension

• Alveolar recruitment – liquid PEEP. Selective distribution to dependent

regions.

• Increases surfactant phospholipid synthesis and secretion.

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• Anti-Inflammatory Properties.

• Improve gas exchange

• Open the dependent alveoli

6- Prone Position:

Effect on gas exchange:

Improve oxygenation

• allow decrease Fio2; PEEP ( Variable - not predictable )

• response rate – 50-70%

• How prone position improve oxygenation

1. Increase in Functional Residual Capacity

2. Improve ventilation of previously dependent regions.

3. Improve in Cardiac output

4. Facilitate clearance of chest secretions

5. Improve lymphatic damage

(Guérin, et al., 2013)

Contraindications

• Unresponsive cerebral hypertension

• Unstable bone fractures

• Left heart failure

• Hemodynamic instability

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• Active intra-abdominal pathology or surgery

• Facial fracture

• Spinal instability

TIMING ARDS > 24 hrs. / 2nd Day

FREQUENCY Usually One Time per Day

DURATION 16 to 20 hrs. /Day. Alternatively, 48h. Prone - 24h. Supine

Outcome:

Improvement Of Oxygenation

No Improvement of Survival.

Complications

• Pressure Sore

• Accident Removal Of ETT; Catheters ; lines

• Arrhythmia

• Reversible Dependent edema (Face, Anterior Chest Wall)

7- Extracorporeal Membrane Oxygenation (ECMO)

• Adaptation of conventional cardiopulmonary bypass technique. Oxygenate

blood and remove CO2 extracorporally.

TYPES

• High-flow venoarterial bypass system.

• Low-flow venovenous bypass system.

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Criteria for treatment with extracorporeal gas exchange

• Fast entry criteria: PaO2 <50 mmHg for >2 h at FiO2 1.0; PEEP > 5 cmH2O

• Slow entry criteria: PaO2 <50 mmHg for >12 h at FiO2 0.6; PEEP > 5

cmH2O

• Maximal medical therapy >48 h

ECMO Complication:

Mechanical Problem:

• Oxygenator failure

• Circuit disruption

• Pump or heat exchanger mal functioning

• Cannula placement /removal

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Patient related:

• Bleeding

• Neurological complications

• Additional organ failure

• Barotrauma, infection, metabolic

Post ARDS:

After ARDS, patient may has:

• Depression (43%)

• Anxiety (48%)

• Post-Traumatic Stress Syndrome (35%)

• Myopathy, neuropathy & cognitive impairment

• Decrease quality of live

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Summery:

Therapeutic modalities to actually treat ARDS have remained elusive. Although

there are multiple potential causes of ARDS, management principles are similar.

Treatment is supportive; that is, contributing factors are corrected or reversed, and

while the lungs heal, care is taken so that treatment does no further damage. The low

tidal volume strategy decreased mortality rate. There is no evidence for the routine

use of corticosteroids in ARDS, and their use should be considered only if other lines

of management failed and not after 14 days of the course of the disease and the use

of beta agonists, anti-inflammatory agents and antioxidant need more studies to rule

out their benefit in management of ARDS.

Also, intermittent sedation for patients with ARDS better than continuous

sedation. On the other hand, the use of muscle relaxants in patients with severe gas

exchange abnormalities (PaO2/FIO2 less than 120 mmhg) is probably safe and

potentially effective. Conservative fluid management is the basic concept in ARDS.

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CHAPTER V

DEVELOPED CLINICAL PATHWAY FOR ARDS PATIENT

Objectives

• Control the original cause

• Achieve adequate oxygenation

• Improve lung function

• Decrease probability of development of ventilator associated lung problems

• Decrease days of mechanical ventilator and length of ICU stay

• Prevent other organ failure

• Reduce mortality

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60

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CHAPTER VI

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