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MRS. S.KAMALI KIRUBA
MSC (N),MEDICAL SURGICAL NURSING
ASSOCIATE PROFESSOR
GANGA COLLEGE OF NURSING
COIMBATORE
ANATOMY
PHYSIOLOGY OF
RESPIRATION
 Respiration is exchange of gases
between an organism and its
environment.
 In humans the respiratory and
circulatory system cooperate the
transport of gases to the cells.
INTRODUCTION
 Acute respiratory distress syndrome
(ARDS) is a life-threatening condition
of seriously ill patients, characterized
by poor oxygenation, pulmonary
infiltrates, and acuity of onset. On a
microscopic level, the disorder is
associated with capillary endothelial
injury and diffuse alveolar damage.
DEFINITION
ARDS is an acute diffuse, inflammatory lung
injury, leading to increased pulmonary vascular
permeability, increased lung weight, and loss of
aerated lung tissue…[with] hypoxemia and
bilateral radiographic opacities, associated with
increased venous admixture, increased
physiological dead space and decreased lung
compliance.
BERLIN-2012
Acute respiratory distress syndrome (ARDS) is a
life-threatening lung condition that prevents
enough oxygen from getting to the lungs and into
the blood.
ETIOLOGY
DIRECT LUNG INJURY
COMMON CAUSES:
Aspiration of gastric contents
or other substances
Viral/ bacterial
pneumonia
DIRECT LUNG INJURY
LESS COMMON CAUSES:
Chest trauma
Embolism: fat, air, amniotic
fluid, thrombus
Radiation
pneumonitis
Inhalation of toxic substances
INDIRECT LUNG INJURY
COMMON CAUSES
Sepsis( gram –negative infection) Severe massive trauma
INDIRECT LUNG INJURY
Cardiopulmonary bypassAcute pancreatitis
Opioid drug overdose Severe head injury
LESS COMMON CAUSES
Con ….
Disseminated intravascular
coagulation
Multiple blood transfusions
Anaphylaxis
Shock states
PATHOLOGICAL STAGES OF ARDS
PATHOLOGICAL STAGES OF ARDS
Exudative (acute) phase (0-4
days)
PATHOLOGICAL STAGES OF ARDS
Exudative (acute) phase (0-4 days)
Characterized by accumulation in the
alveoli of excessive fluid, protein
and inflammatory cells that have
entered the air spaces from the alveolar
capillaries. The exudative phase unfolds
over the first 2 to 4 days after onset of
lung injury.
PATHOLOGICAL STAGES OF ARDS
Proliferative phase(4-8 days)
Connective tissue and other structural
elements in the lungs proliferate in
response to the initial injury. Under a
microscope, lung tissue appears
densely cellular. Also, at this stage,
there is a danger of pneumonia sepsis
and rupture of the lungs causing
leakage of air into surrounding areas.
PATHOLOGICAL STAGES OF
ARDS
Fibrotic phase(>8days)
During this stage, the lung reorganizes
and recovers. Lung function
may continue to improve for as long as
6-12 months and sometimes longer,
depending on the precipitating condition
and severity of the injury. It is important
to remember that there may be and
often are different levels of pulmonary
recovery amongst individuals who suffer
from ARDS.
PATHOPHYSIOLOGY
CLINICAL MANIFESTATION
EARLY SIGN / SYMPTOMS
 Dyspnea
 Low BP
 Confusion
 Extreme tiredness
 Change in patient’s behavior
Mood swing
Disorientation
Change in LOC
 If pneumonia is causing ARDS
Cough & fever
CLINICAL MANIFESTATION
LATE SIGN/ SYMPTOMS
 Severe difficulty in breathing (labored, rapid
breathing, shortness of breath)
 Tachycardia
 Cyanosis
 Thick frothy sputum
 Metabolic acidosis
 Abnormal breathing sounds like crackles
 Decreased PaCO2 with respiratory alkalosis
 Decreased PaO2
DIAGNOSTIC FINDING
REFRACTORY HYPOXEMIA
PaO2<50 mmHg on FIO2> 40% with PEEP>5cm
H2O
PaO2/FIO2 ratio <200
CHEST X-RAY
New bilateral interstitial and alveolar infiltrates
PULMONARY ARTERY WEDGE PRESSURE
< 18 mm Hg and no evidence of heart failure
PREDISPOSING CONDITION
Identification of a predisposing condition for ARDS
within 48 hr of clinical manifestation
MANAGEMENT
MANAGEMENT
1. Respiratory therapy
a. O2 administration
b. prone positioning
c. Lateral rotation therapy
d. Positive pressure ventilation with PEEP
e. Permissive hypercapnia
f. Alternative modes of mechanical
ventilation : pressure support ventilation,
pressure release ventilation, pressure
control ventilation, inverse ratio ventilation,
high frequency ventilation.
MANAGEMENT
2. Supportive therapy
a. Identification and treatment of
underlying causes
b. Hemodynamic monitoring
c. Maintenance of nutrition
d. Medication administration
e. IV fluid administration
I. Respiratory therapy
O2 ADMINISTRATION
O2 administered by face mask or
cannula
Monitor SPO2
I. Respiratory therapy
SUPINE TO VOLLMAN PRONE
POSITION
I. Respiratory therapy
LATERAL ROTATION THERAPY BED
I. Respiratory therapy
MECHANICAL VENTILATION:
Maintain FIO2 at 60% greater to maintain the
PaO2 at 60 mm Hg or greater.
PEEP is typically applied with FIO2 0f 60% or
less.
ARDS with higher level of PEEP 10-20 cm
H2O be used.
I. Respiratory therapy
ECMO & ECCO2R
ECCO2 Removal pass blood across a gas
exchanging membrane outside the body and
then return oxygenated blood back to the
body.
2. Supportive therapy
Maintain cardiac output and tissue
perfusion
Maintain hemodynamic monitoring
IABP monitor -BP
MEDICAL SUPPORTIVE THERAPY
2. Supportive therapy
MAINTENANCE OF NUTRITION
Parenteral Nutrition Enteral Feeding
2. Supportive therapy
BLOOD TRANSFUSION
Packed RBC may be administered to increase
Hb and increase O2 carrying capacity of the
blood.
2. Supportive therapy
FLUID REPLACEMENT
 Fluid replacement with crystalloids or
colloids.
2. Supportive therapy
MEDICATION
Inotropic/vasopressor medication
Antibiotics
Anti-inflammatory drugs
Diuretics
Drugs to raise blood pressure
Anti anxiety
Sedation / Analgesia
Inhaled drugs( Bronchodilators)
COMPLICATION
 INFECTION
Catheter related infection
Hospital – Acquired pneumonia
Sepsis (bacteremia)
 RESPIRATORY COMPLICATION
O2 toxicity
Pulmonary barotrauma(pneumothorax,
pneumomediastinum, subcutaneous
emphysema)
Pulmonary emboli
Pulmonary fibrosis
Ventilator associated pneumonia
COMPLICATION
 GASTROINTESTINAL COMPLICATION
Paralytic ileus
pneumoperitoneum
Stress ulceration and hemorrage
Hypermetabolic state, dramatically increased
nutrition requirements
 RENAL COMPLICATION
Acute renal failure
 CARDIAC COMPLICATION
Dysrhythmias
decreased cardiac output
COMPLICATION
 HEMATOLOGIC COMPLICATION
Anemia
Disseminated intravascular coagulation
Thrombocytopenia
 ENDOTRACHEAL TUBE INTUBATION COMPLICATION
Laryngeal ulceration
Tracheal malacia
Tracheal stenosis
Tracheal ulceration
 CENTRAL NERVOUS SYSTEM/ PSYCHOLOGIC
COMPLICATION
Delirium/ Sleep deprivation
Posttraumatic stress disorder
NURSING DIAGNOSIS
NURSING DIAGNOSIS
 Ineffective breathing pattern related to
decreased lung compliance, decreased energy
as characterized by dyspnea, abnormal ABGs,
cyanosis and use of accessory muscle.
 Impaired gas exchange related to diffusion
defect as characterized by hypoxia,
hypercapnia, tachycardia and cyanosis.
 ineffective protection related to positive pressure
ventilation, increased secretions as
characterized by crepitus, altered chest
excursion, abnormal ABGs and restlessness.
NURSING DIAGNOSIS
 Impaired physical mobility related to monitoring
devices, mechanical ventilation and medication
as characterized by imposed restriction of
movement, decreased muscle strength and
limited range of motion..
 Risk for impaired skin integrity related to
prolonged bed rest, prolonged intubation and
immobility
 Knowledge deficit related to health condition and
treatment modalities as characterized by
frequency of questions posted by patient.
CONCLUSION
 ARDS is a multi system syndrome – not a
disease
 Hypoxemia, opacities and low lung
compliance
 Three phases: exudative, proliferative and
fibrotic
 Low tidal volume: improves survival
 PEEP: Improves oxygenation
 Recruitment and HFOV: Could be harmful
 Keep them dry and steroids but not past 14
days
 Paralytics and prone position for PaO2/FiO2
< 150
ACUTE RESPIRATORY  DYSTRESS SYNDROME
ACUTE RESPIRATORY  DYSTRESS SYNDROME

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ACUTE RESPIRATORY DYSTRESS SYNDROME

  • 1. MRS. S.KAMALI KIRUBA MSC (N),MEDICAL SURGICAL NURSING ASSOCIATE PROFESSOR GANGA COLLEGE OF NURSING COIMBATORE
  • 2.
  • 4. PHYSIOLOGY OF RESPIRATION  Respiration is exchange of gases between an organism and its environment.  In humans the respiratory and circulatory system cooperate the transport of gases to the cells.
  • 5. INTRODUCTION  Acute respiratory distress syndrome (ARDS) is a life-threatening condition of seriously ill patients, characterized by poor oxygenation, pulmonary infiltrates, and acuity of onset. On a microscopic level, the disorder is associated with capillary endothelial injury and diffuse alveolar damage.
  • 6. DEFINITION ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue…[with] hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance. BERLIN-2012 Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood.
  • 8. DIRECT LUNG INJURY COMMON CAUSES: Aspiration of gastric contents or other substances Viral/ bacterial pneumonia
  • 9. DIRECT LUNG INJURY LESS COMMON CAUSES: Chest trauma Embolism: fat, air, amniotic fluid, thrombus Radiation pneumonitis Inhalation of toxic substances
  • 10. INDIRECT LUNG INJURY COMMON CAUSES Sepsis( gram –negative infection) Severe massive trauma
  • 11. INDIRECT LUNG INJURY Cardiopulmonary bypassAcute pancreatitis Opioid drug overdose Severe head injury LESS COMMON CAUSES
  • 12. Con …. Disseminated intravascular coagulation Multiple blood transfusions Anaphylaxis Shock states
  • 14. PATHOLOGICAL STAGES OF ARDS Exudative (acute) phase (0-4 days)
  • 15. PATHOLOGICAL STAGES OF ARDS Exudative (acute) phase (0-4 days) Characterized by accumulation in the alveoli of excessive fluid, protein and inflammatory cells that have entered the air spaces from the alveolar capillaries. The exudative phase unfolds over the first 2 to 4 days after onset of lung injury.
  • 16. PATHOLOGICAL STAGES OF ARDS Proliferative phase(4-8 days) Connective tissue and other structural elements in the lungs proliferate in response to the initial injury. Under a microscope, lung tissue appears densely cellular. Also, at this stage, there is a danger of pneumonia sepsis and rupture of the lungs causing leakage of air into surrounding areas.
  • 17. PATHOLOGICAL STAGES OF ARDS Fibrotic phase(>8days) During this stage, the lung reorganizes and recovers. Lung function may continue to improve for as long as 6-12 months and sometimes longer, depending on the precipitating condition and severity of the injury. It is important to remember that there may be and often are different levels of pulmonary recovery amongst individuals who suffer from ARDS.
  • 19. CLINICAL MANIFESTATION EARLY SIGN / SYMPTOMS  Dyspnea  Low BP  Confusion  Extreme tiredness  Change in patient’s behavior Mood swing Disorientation Change in LOC  If pneumonia is causing ARDS Cough & fever
  • 20. CLINICAL MANIFESTATION LATE SIGN/ SYMPTOMS  Severe difficulty in breathing (labored, rapid breathing, shortness of breath)  Tachycardia  Cyanosis  Thick frothy sputum  Metabolic acidosis  Abnormal breathing sounds like crackles  Decreased PaCO2 with respiratory alkalosis  Decreased PaO2
  • 21. DIAGNOSTIC FINDING REFRACTORY HYPOXEMIA PaO2<50 mmHg on FIO2> 40% with PEEP>5cm H2O PaO2/FIO2 ratio <200 CHEST X-RAY New bilateral interstitial and alveolar infiltrates PULMONARY ARTERY WEDGE PRESSURE < 18 mm Hg and no evidence of heart failure PREDISPOSING CONDITION Identification of a predisposing condition for ARDS within 48 hr of clinical manifestation
  • 23. MANAGEMENT 1. Respiratory therapy a. O2 administration b. prone positioning c. Lateral rotation therapy d. Positive pressure ventilation with PEEP e. Permissive hypercapnia f. Alternative modes of mechanical ventilation : pressure support ventilation, pressure release ventilation, pressure control ventilation, inverse ratio ventilation, high frequency ventilation.
  • 24. MANAGEMENT 2. Supportive therapy a. Identification and treatment of underlying causes b. Hemodynamic monitoring c. Maintenance of nutrition d. Medication administration e. IV fluid administration
  • 25. I. Respiratory therapy O2 ADMINISTRATION O2 administered by face mask or cannula Monitor SPO2
  • 26. I. Respiratory therapy SUPINE TO VOLLMAN PRONE POSITION
  • 27. I. Respiratory therapy LATERAL ROTATION THERAPY BED
  • 28. I. Respiratory therapy MECHANICAL VENTILATION: Maintain FIO2 at 60% greater to maintain the PaO2 at 60 mm Hg or greater. PEEP is typically applied with FIO2 0f 60% or less. ARDS with higher level of PEEP 10-20 cm H2O be used.
  • 29. I. Respiratory therapy ECMO & ECCO2R ECCO2 Removal pass blood across a gas exchanging membrane outside the body and then return oxygenated blood back to the body.
  • 30. 2. Supportive therapy Maintain cardiac output and tissue perfusion Maintain hemodynamic monitoring IABP monitor -BP MEDICAL SUPPORTIVE THERAPY
  • 31. 2. Supportive therapy MAINTENANCE OF NUTRITION Parenteral Nutrition Enteral Feeding
  • 32. 2. Supportive therapy BLOOD TRANSFUSION Packed RBC may be administered to increase Hb and increase O2 carrying capacity of the blood.
  • 33. 2. Supportive therapy FLUID REPLACEMENT  Fluid replacement with crystalloids or colloids.
  • 34. 2. Supportive therapy MEDICATION Inotropic/vasopressor medication Antibiotics Anti-inflammatory drugs Diuretics Drugs to raise blood pressure Anti anxiety Sedation / Analgesia Inhaled drugs( Bronchodilators)
  • 35. COMPLICATION  INFECTION Catheter related infection Hospital – Acquired pneumonia Sepsis (bacteremia)  RESPIRATORY COMPLICATION O2 toxicity Pulmonary barotrauma(pneumothorax, pneumomediastinum, subcutaneous emphysema) Pulmonary emboli Pulmonary fibrosis Ventilator associated pneumonia
  • 36. COMPLICATION  GASTROINTESTINAL COMPLICATION Paralytic ileus pneumoperitoneum Stress ulceration and hemorrage Hypermetabolic state, dramatically increased nutrition requirements  RENAL COMPLICATION Acute renal failure  CARDIAC COMPLICATION Dysrhythmias decreased cardiac output
  • 37. COMPLICATION  HEMATOLOGIC COMPLICATION Anemia Disseminated intravascular coagulation Thrombocytopenia  ENDOTRACHEAL TUBE INTUBATION COMPLICATION Laryngeal ulceration Tracheal malacia Tracheal stenosis Tracheal ulceration  CENTRAL NERVOUS SYSTEM/ PSYCHOLOGIC COMPLICATION Delirium/ Sleep deprivation Posttraumatic stress disorder
  • 39. NURSING DIAGNOSIS  Ineffective breathing pattern related to decreased lung compliance, decreased energy as characterized by dyspnea, abnormal ABGs, cyanosis and use of accessory muscle.  Impaired gas exchange related to diffusion defect as characterized by hypoxia, hypercapnia, tachycardia and cyanosis.  ineffective protection related to positive pressure ventilation, increased secretions as characterized by crepitus, altered chest excursion, abnormal ABGs and restlessness.
  • 40. NURSING DIAGNOSIS  Impaired physical mobility related to monitoring devices, mechanical ventilation and medication as characterized by imposed restriction of movement, decreased muscle strength and limited range of motion..  Risk for impaired skin integrity related to prolonged bed rest, prolonged intubation and immobility  Knowledge deficit related to health condition and treatment modalities as characterized by frequency of questions posted by patient.
  • 41. CONCLUSION  ARDS is a multi system syndrome – not a disease  Hypoxemia, opacities and low lung compliance  Three phases: exudative, proliferative and fibrotic  Low tidal volume: improves survival  PEEP: Improves oxygenation  Recruitment and HFOV: Could be harmful  Keep them dry and steroids but not past 14 days  Paralytics and prone position for PaO2/FiO2 < 150