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Acute Respiratory Distress Syndrome (ARDS)

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Acute Respiratory Distress Syndrome (ARDS) Prepared by Wajeeha Nabulsi, Ghassan Zakarni Supervised by Dr. Aidah Abu Elsoud Alkaissi An-Najah National University – PowerPoint PPT presentation

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Title: Acute Respiratory Distress Syndrome (ARDS)


1
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

2
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

3
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

4
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

5
REVISION OF DEFINITIONS 
  • 1988 four-point lung injury score
  • Level of PEEP
  • PaO2 / FiO2 ratio
  • Static lung compliance
  • Degree of chest infiltrates

6
1994 CONSENSUS 
  • Acute onset
  • may follow catastrophic event
  • Bilateral infiltrates on chest radiograph
  • PAWP lt 18 mm Hg
  • Two categories
  • Acute Lung Injury - PaO2/FiO2 ratio lt 300
  • ARDS - PaO2/FiO2 ratio lt 200

7
INCITING FACTORS 
  • Shock
  • Aspiration of gastric contents
  • Trauma
  • Infections
  • Inhalation of toxic gases and fumes
  • Drugs and poisons
  • Miscellaneous

8
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

9
STAGES 
  • Subacute, Proliferative phase
  • persistent hypoxemia
  • development of hypercarbia
  • fibrosing alveolitis
  • further decrease in pulmonary compliance
  • pulmonary hypertension

10
STAGES 
  • 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

11
MORTALITY 
  • 40-60 Deaths due to
  • multi-organ failure
  • Sepsis
  • Mortality may be decreasing in recent years
  • better ventilatory strategies
  • earlier diagnosis and treatment

12
PATHOGENESIS 
  • Inciting event
  • Inflammatory mediators
  • Damage to microvascular endothelium
  • Damage to alveolar epithelium
  • Increased alveolar permeability results in
    alveolar edema fluid accumulation

13
PATHOGENESIS 
  • Target organ injury from hosts inflammatory
    response and uncontrolled liberation of
    inflammatory mediators
  • Localized manifestation of SIRS
  • Neutrophils and macrophages play major roles
  • Complement activation
  • Cytokines TNF-a, IL-1b, IL-6
  • Platelet activation factor
  • Eicosanoids prostacyclin, leukotrienes,
    thromboxane
  • Free radicals
  • Nitric oxide

14
PATHOPHYSIOLOGY 
  • Abnormalities of gas exchange
  • Oxygen delivery and consumption
  • Cardiopulmonary interactions
  • Multiple organ involvement

15
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

16
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17
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

18
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

19
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

20
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

21
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

22
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

23

24
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

25
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26
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

27
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

28
Implementation and evaluation1. 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

29
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

30
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 (gt0.50)
    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

31
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)

32
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

33
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.

34
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

35
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

36
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

37
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)

38
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

39
If there is evidence for impaired tissue
oxygenation, the sequence of managementCardiac
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

40
If there is evidence for impaired tissue
oxygenation, the sequence of managementBlood
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

41
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)

42
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

43
Specific Therapies1. 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)

44
Specific Therapies2. 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

45
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

46
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

47
Specific Therapies
  • 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

48
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.

49
Prone positioning
  • Prone therapy assists pts with ARDS by reducing
    the ventilation\perfusion mismatch

50
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
Kinetic Therapy
51
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

52
Oscillator High Frequency Ventilation
53
Extracorporeal respiratory support
  • 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.

54
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55
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

56
Nursing care plan patient with ARDS
  • 2- Ineffective breathing pattern related to
    deceased complain
  • Interventions Nursing
  • Maintain ventilator settings as ordered.
  • Assist patient to use relaxation techniques.
  • Sedate patient as ordered.

57
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.

58
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
  • Monitor temperature.
  • Monitor leukocytes and albumin
  • Assess nutritional status.

59
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.

60
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.

61
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.

62
  • Ghassan Zakarni
  • Wajeeha Nabulsi
  • Thank You
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