Acute Respiratory Distress Syndrome

(ARDS)

Prepared by Wajeeha Nabulsi, Ghassan Zakarni

Supervised by Dr. Aidah Abu Elsoud Alkaissi
An-Najah National University
Faculty of Nursing
12/24/15

Another Names for ARDS

Da Nang Lung
Transfusion Lung
Post Perfusion Lung
Shock Lung
Traumatic Wet Lung
Posttraumatic Failure
Posttraumatic Pulmonary Insufficiency
Wet lung
White Lung
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HISTORICAL PERSPECTIVES

Described by William Osler in the 1800s

Ashbaugh, Bigelow and Petty, Lancet 1967
12 patients
pathology similar to hyaline membrane disease in
neonates

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ORIGINAL DEFINITION

Acute respiratory distress

Cyanosis refractory to oxygen therapy
Decreased lung compliance
Diffuse infiltrates on chest radiograph
Difficulties:
lacks specific criteria
controversy over incidence and mortality

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REVISION OF DEFINITIONS

1988: four-point lung injury score

Level of PEEP
PaO
2 / FiO2 ratio
Static lung compliance

Degree of chest infiltrates

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1994 CONSENSUS

Acute onset
may follow catastrophic event
Bilateral infiltrates on chest radiograph
PAWP < 18 mm Hg

Two categories:

Acute Lung Injury - PaO2/FiO2 ratio < 300

ARDS - PaO2/FiO2 ratio < 200

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INCITING FACTORS
Shock
Aspiration of gastric contents
Trauma
Infections
Inhalation of toxic gases and fumes
Drugs and poisons
Miscellaneous

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STAGES

Acute, exudative phase

rapid onset of respiratory failure after trigger
diffuse alveolar damage with inflammatory cell infiltration
hyaline membrane formation
capillary injury
protein-rich edema fluid in alveoli
disruption of alveolar epithelium

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STAGES
Subacute, Proliferative phase:
persistent hypoxemia
development of hypercarbia
fibrosing alveolitis
further decrease in pulmonary compliance
pulmonary hypertension

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STAGES

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nn
Chronic phase
obliteration of alveolar and bronchiolar spaces and pulmonary capillaries
Recovery phase
gradual resolution of hypoxemia
improved lung compliance
resolution of radiographic abnormalities
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MORTALITY
40-60% Deaths due to:
multi-organ failure
Sepsis

Mortality may be decreasing in recent years

better ventilatory strategies
earlier diagnosis and treatment

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PATHOGENESIS
Inciting event
Inflammatory mediators
Damage to microvascular endothelium
Damage to alveolar epithelium
Increased alveolar permeability results in alveolar
edema fluid accumulation

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PATHOGENESIS

Target organ injury from hosts inflammatory response and

uncontrolled liberation of inflammatory mediators

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Localized manifestation of SIRS

Neutrophils and macrophages play major roles
Complement activation
Cytokines: TNF-, IL-1, IL-6
Platelet activation factor
Eicosanoids: prostacyclin, leukotrienes, thromboxane
Free radicals
Nitric oxide

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PATHOPHYSIOLOGY

Abnormalities of gas exchange

Oxygen delivery and consumption

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Cardiopulmonary interactions
Multiple organ involvement
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ABNORMALITIES OF GAS
EXCHANGE
Hypoxemia: HALLMARK of ARDS
Increased capillary permeability
Interstitial and alveolar exudate
Surfactant damage
Decreased FRC
Diffusion defect and right to left shunt

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ARDS

Is defined as a distinct form of acute respiratory failure that

results from diffuse pulmonary injury of various causes

characterized by:
- diffuse alveolar
- capillary wall injury
- increased alveolar- capillary permiability
- noncardiogenic pulmonary edema
- hyaline membrane formation, and atelectasis

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Pathophysiology

The physiologic reaction of all body tissues sometimes

results in pathologic changes in the lung

Asystemic insults causes low tissue perfusion and

cellular hypoxia

Consequently, peripheral tissues are deprived of

essential nutrients, and intracellular metabolic
derangements result

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Pathophysiology

Certain chemical factors such as prostaglandins, clotting

factors, lysosomal enzymes, activated complement, or
histamine are released into the systemic circulation

Prostaglandin contribute to vasodilation, capillary

permeability, pain and fever, which accompany cell injury

Changes in the vessel walls and disturbances in blood

flow increase platelet function, causing adhesiveness
and aggregation

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Pathophysiology

Lysosomal enzymes from neutrophils increase

vascular permeability and cause tissue damage

Histamine is released from platelets, mast cell, and

basophils and cause arterial vasodilation and
enhanced permiability of capillaries and venules

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Pathophysiology

Neutrophils and other inflammatory mediators can

thus gain access to the lung parenchyma and carry on
the inflammatory process
The inflammation then produces the lung injury,
Severe ventilation-perfusion mismatching occurs
Alveolar collaps of the inflammatory infiltrate, blood
fluid and surfactant dysfunction
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Pathophysiology

The lung compliance becomes markedly decreased

(stiff lung)

The blood returning to the lung for gas exchange is

pumped through the nonventilated, nonfunctioning
areas of the lung, causing a shunt to develop

The blood interfacing with nonfunctioning alveoli and

gas exchange is markedly impaired, resulting in
severe refractory hypoxemia

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Clinical Features of ARDS

The earliest clinical signs of ARDS include

tachypnea and progressive hypoxemia

Within 24 hours, the chest x-ray begins to

reveal bilateral pulmonary infiltrates

Progression to mechanical ventilation often

occurs in the first 48 hours of the illness

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Common conditions that

predispose to ARDS

Aspiration (gastric secretion, drowning, hydrocarbons)

Intracranial hypertension
Haemetologic disorders (disseminated intravascular
coagulopathy (DIC) , Massive transfusion of blood
products, cardiopulmonary bypass
Prolonged inhalation of high concentration of oxygen,
smoke, or corrosive substances
Shock (any cause)
Catheter sepsis, drugs

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Common conditions that

predispose to ARDS

Localized infection (bacterial, fungal, viral pneumonias),

Trauma (pulmonary contusion, multiple fracture, head
injury)
Major surgery
Metabolic disorders (Pancreatitis, uremia)
Urosepsis,
amniotic fluid embolism
Long bone fracture
Fat or air embolism
Systemic sepsis

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Implementation and evaluation

1. Fluid therapy

Hypoalbuminemic patients should receive coloids whereas

all other patients should receive crystalloid fluids to
decrease the pulmonary congestion

The patients pulmonary capillay wedge pressure (PCWP) is

kept as low as possible as long as the cardiac output and
tissue perfusion can be maintained at normal levels

Maintenance of the PCWP at 10-15 mm Hg provides

adequate, but not excessive intravascular volumes

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Maintaining tissue oxygenation

The fractional concentration of inspired oxygen

(FiO2) should be kept at 50% or lower to minimize the
risk of oxygen toxicity

An SaO2 above 90% should be sufficient to maintain

oxygen delivery to peripheral tissues

If the FiO2 cannot be reduced to below 60% external

PEEP is added to help reduce the FiO2 to nontoxic
levels

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2. Maintaining Tissue Oxygenation

The goal of O2 therapy is to administer the lowest

possible oxygen concentration to sustain a mixed venous
oxygen greater than 40 mm Hg

Positive end expiratory pressure (PEEP) is indicated for

use in patients who are being ventilated mechanically with
high FiO2 (>0.50) and who have a PaO2 of less than 65 mm
Hg

The purpose of PEEP in ARDS is to minimize alveolar

collapse and small airway closure and reduce interstitial
edema and total extravascular
lung water
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2. Maintaining Tissue Oxygenation

Initial levels of PEEP should be in the range of 5-10 cm

H2O

Small increments of PEEP are added until the optimal

level is reached

The best meaurement available for evaluating tissue

oxygenation at the bedside are systemic oxygen uptake
(VO2 [oxygen consumption]), venous lactate level, and
gastric intramucosal PH ( measure directly by gastric
tonometry)

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2. Maintaining Tissue Oxygenation

Tissue oxygenation is considered to be inadequate if whole

body VO2 is less than 100 ml/minute/m2 , venous lactate is
greater than 4 mmol/L, or gastric intramucosal PH is less
than 7.32

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3. Drug Therpy

Morphine for sedating mechanically ventilated pat, who

are restless, fearful and experiencing tachypnea

Pancuronium bromide (pavulon ) neuroblocking agent to

paralyze completely the voluntary respirations of the patient

Possible sedatives are:

lorazepam (ativan), midazolam (versd), haloperidol (haldol),
propofol (diprivan), and short-acting barbiturates.

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4. Preventing Iatrogenic Injury

Ventilator management

There is now considerable evidence indicating that the

large tidal volume used during conventional mechanical
ventilation (10 to 15 ml/kg) can damage the lungs

The pathologic changes in ARDS are not distributed

uniformly throughout the lungs

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4. Preventing Iatrogenic Injury

Ventilator management

Recognition of the risk of lung injury at high inflation

volumes and pressures had led to an alternative strategy
where peak inspiratory pressures are kept below 35 cm H2O
by using tidal volume of 7-10 ml/kg

According to this strategy, mechanical ventilation is started

at inflation volumes of 10 ml/kg

If the resulting peak inspiratory pressure (PIP) is above 35

cm H2O, the inflation volume is reduced in increments of 2
ml/kg until PIP falls below 35 cm H2O

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5. Reducing Lung Water

The two measures that are advocated for

reducing lung water are diuretics and PEEP

Unfortunately , neither measure is likely to be

effective in ARDS
The application of PEEP does not reduce
extravasascular lung water in ARDS

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5. Reducing Lung Water

Diuretics

The use of diuretics to minimize or reduce fluid overload

seems a more reasonable measure, but only when renal
water excretion is impaired (otherwise the best way to
prevent fluid overload is to maintain an adequate cardiac
output)

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Positive End-Expiratory
Pressure

In fact, high levels of PEEP can actually increase

lungwater

This latter effect may be the result of alveolar

overdistension, or may be the result of PEEP-induced
impairment of lymphatic drainage from the lungs

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If there is evidence for impaired tissue

oxygenation, the sequence of management

Cardiac Output

If the cardiac output is inadequate (e.g. A cardiac

index below 3L/min/m2 and CVP or wedge pressures
are not elevated, volume infusion is indicated

If volume infusion is not indicated, dobutamine is used

to augment the cardiac output

Dopamine should be avoided because of its propensity

to constrict pulmonary vein

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If there is evidence for impaired tissue

oxygenation, the sequence of management

Blood Transfusion

Transfusion is often recommended to keep the Hb above

10 g/dL.

In fact, given the propensity for blood transfusion to cause

ARDS
It seems wise to avoid transfusing blood products in ARDS

If there is no evidence of inadequate tissue oxygenation,

there is no need to correct anemia

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A brief summary of the

available studies- Steroids

High-dose methylprednisolone (30 mg/ kg) I.V every 6

hours for 4 doses) given to patients within 24 hours of the
diagnosis of ARDS has not improved outcome or reduced
mortality

In fact, one study showed a higher mortality associated

with steroid therapy in ARDS (Bone 1987)

Secondary infection are increased in patients receiving high

dose methyl-prednisolone for ARDS (Bone 1987)

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A brief summary of the

available studies- Steroids

High-dose methylprednisolone (2-3 mg/kg/day) given to

25 patients with late ARDS (2 weeks duration) resulted in a
beneficial response in 21 patients and an 86% survival in
the responders (Meduri 1994)

This study suggests a possible role for steroids late in the

course of ARDS, but corroborative evidence is required

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Specific Therapies
1. Surfactant

Aerosolized surfactant has proven effective in

improving outcomes in the neonatal form of respiratory
distress syndrome, but it has not met with similar
success in adults with ARDS (Anzueto 1996)

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Specific Therapies
2.

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Antioxidant

Neutrophil-mediated tissue injury may play an important

role in the pathogenesis of ARDS, it is no surprise that
there is conciderable interest in the possible role of
antioxidants as a specific theray for ARDS

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3. Nitric oxide

Nitric oxide can improve oxygenation and reduce

pulmonary artery pressures in ARDS, mortality is
unchanges (Lunn 1995)

Nitric oxide is a pulmonary vasodilator, which inhaled

crosses the alveolar membrane and acts locally on the
pulmonary vasculature, dilating vessels and increasing
blood flow

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3. Nitric oxide

Has the effect of improving ventilation/perfusion

(V/Q) matching and therefore gas exchange as
the blood flow is only increased in the ventilated
areas

as soon as it enters the blood, nitric oxide is

bound to haemoglobin and has no further
systemic (i.e. Hypotensive) effect

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Therapies

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Numerous pharmacological RX are underinvestigation

to stop the cascade of events leading to ARDS
Neutrrophil inhibitors
Interleukin-1 receptor antagonist
Pulmonary specific vasodilator
Surfactant replacement therapy
Antisepsis agents

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prone position
Study shows that prone positioning
significantly improves oxygenation in
about 65% of patients. This allows nurses
to reduce the percentage of inspired
oxygen and positive end-expiratory
pressure.

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Prone positioning

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Prone therapy assists pts with ARDS by

reducing the ventilation\perfusion mismatch

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Kinetic Therapy
Can help improve clinical outcomes and lower overall
cost of care. By continuously rotating critically ill
patients from side-to-side to at least 40, Kinetic
Therapy helps prevent and treat pulmonary
complications as ARDS

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High frequency oscillation

High frequency ventilation incorporates techniques

using ventilation frequencies of greater than 60 breath
per minute and tidal volumes between 1 and 5 ml/kg

Arapidly oscillating gas flow is created by a device

that acts like a woofer on aloudspeaker, producing a
high frequency rapid change in direction of gas flow

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Oscillator High Frequency Ventilation

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Extracorporeal respiratory
support

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The process involves the machine taking the

blood without oxygen, the "blue" blood from the
right side of the heart, and pumping it through the
artificial lung, the oxygenator. Once the blood is
oxygenated, or "red," it is warmed before
returning to the patient.

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Nursing care plan

patient with ARDS
Nursing diagnose:
1- impaired gas exchange related to alveolar- capillary
membrane changes
Nursing interventions:

Auscultate lungs for crackles (rales).

Evaluate arterial and mixed venous blood gas analyses.

Observe for changes in awareness, orientation, and behavior.

Monitor ECG and dysrhythmias
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Nursing care plan

patient with ARDS
2- Ineffective breathing pattern related to

deceased complain

Interventions Nursing

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Maintain ventilator settings as ordered.

Assist patient to use relaxation techniques.
Sedate patient as ordered.

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Nursing care plan

patient with ARDS
3- Ineffective airway clearance related to pulmonary
and interstitial edema.
Nursing Interventions:
Assess characteristics of secretions such as
quantity, color, consistency, and odor.
Assess patient's hydration status by monitoring
skin turgor, mucous membranes, tongue, and
intake and output over 24 hours.
Monitor sputum, gram stains, and culture and
sensitivity reports.
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Nursing care plan

patient with ARDS
4- high risk for infection related to decreased pulmonary function,
possible steroid therapy, and ineffective airway clearance
Nursing interventions:

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Monitor temperature.
Monitor leukocytes and albumin
Assess nutritional status.

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Nursing care plan

patient with ARDS
5- Altered nutrition: less than body requirements related to
inadequate intake secondary hypoxia and fatigue
Nursing interventions:
Assess dietary habits and needs.
weigh patient weekly.
Enterable feeding is the first consideration, parenteral
nutrition may required.
Measure fluid intake and output.
Auscultat bowel sounds.
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Nursing care plan

patient with ARDS
6- Fear related to suffocation, being on

mechanical
ventilation, uncertainty of prognosis, and inability to
verbally communicate.

Nursing interventions
Validate sources of fear with patient.
Assess patient's perception of unmet need and
expectations.
Assist patient to identify coping skills used
successfully in the past.
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Nursing care plan

patient with ARDS
7- knowledge deficit related to follow-up and home care.
Nursing interventions:
teach the patient the following:
Adaptive breathing techniques.
The importance of turning, coughing, and deep
breathing.
The importance of not fighting the ventilator, and
relaxing to permit maximum ventilation.
The importance of periodic rest periods.
The name, dosage, time, of administration, and side
effects of all medications.
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