ards overview

Acute Respiratory Acute Respiratory Distress SyndromeDistress Syndrome

(ARDS)(ARDS)

Presented by Melinda C. JordanPresented by Melinda C. Jordan

Acute Respiratory Acute Respiratory Distress SyndromeDistress Syndrome

Sudden, progressive form of acute respiratory failureCharacterised by:

Severe dyspneaHypoxaemia↓ Lung complianceDiffuse pulmonary infiltrates

Sudden, progressive form of acute Sudden, progressive form of acute respiratory failurerespiratory failureCharacterised by:Characterised by:

Severe Severe dyspneadyspneaHypoxaemiaHypoxaemia↓↓ Lung complianceLung complianceDiffuse pulmonary infiltratesDiffuse pulmonary infiltrates

Clinical Conditions Associated with Clinical Conditions Associated with the development of ARDSthe development of ARDS

SepsisSepsisSevere TraumaSevere TraumaPulmonary contusionPulmonary contusionPneumoniaPneumoniaNear drowningNear drowningMassive transfusionMassive transfusionFat embolismFat embolism

AetiologyAetiology and Pathophysiologyand Pathophysiology

Develop from a variety of direct or indirect lung injuriesExact cause for damage to alveolar-capillary membrane not knownPathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems

Develop from a variety of direct or Develop from a variety of direct or indirect lung injuriesindirect lung injuriesExact cause for damage to alveolarExact cause for damage to alveolar--capillary membrane not knowncapillary membrane not knownPathophysiologic changes of ARDS Pathophysiologic changes of ARDS thought to be due to stimulation of thought to be due to stimulation of inflammatory and immune systemsinflammatory and immune systems

Pathophysiology of ARDSPathophysiology of ARDS

Fig. 66Fig. 66--99

AetiologyAetiology and and PathophysiologyPathophysiology

Phases:Phases:ExudativeExudativeProliferativeProliferativeFibroticFibrotic

AetiologyAetiology and Pathophysiologyand PathophysiologyExudative phase

1-7 days after direct lung injury or host insultNeutrophils adhere to pulmonary microcirculation

Damage to vascular endotheliumIncreased capillary permeability

Results in leakage of H2OProteinInflammatory chemical

ExudativeExudative phasephase11--7 days after direct lung injury or host 7 days after direct lung injury or host insultinsultNeutrophils adhere to pulmonary Neutrophils adhere to pulmonary microcirculationmicrocirculation

Damage to vascular endotheliumDamage to vascular endotheliumIncreased capillary permeabilityIncreased capillary permeability

Results in leakage of Results in leakage of H2OH2OProteinProteinInflammatory chemicalInflammatory chemical

OedemaOedema Formation in Acute Formation in Acute Respiratory Distress SyndromeRespiratory Distress Syndrome

Fig. 66Fig. 66--88

A,A, Normal alveolus and Normal alveolus and pulmonary capillary pulmonary capillary

B, Interstitial B, Interstitial oedemaoedema occurs occurs with increased flow of fluid with increased flow of fluid into the interstitial space into the interstitial space

C, Alveolar C, Alveolar oedemaoedema occurs occurs when the fluid crosses the when the fluid crosses the bloodblood--gas barriergas barrier

Aetiology and PathophysiologyAetiologyAetiology and Pathophysiologyand Pathophysiology

Alveolar cells type 1 and 2 are damagedSurfactant dysfunction → atelectasis

Hyaline membranes line alveoliContribute to atelectasis and fibrosis

Lungs become less compliant

Alveolar cells type 1 and 2 are damagedAlveolar cells type 1 and 2 are damagedSurfactant dysfunction Surfactant dysfunction →→ atelectasisatelectasis

Hyaline membranes line alveoliHyaline membranes line alveoliContribute to atelectasis and fibrosisContribute to atelectasis and fibrosis

Lungs become less compliantLungs become less compliant


↑ WOB↑ RR ↓ Tidal volume

Produces respiratory alkalosis from increase in CO2 removal↓ CO and tissue perfusion

↑↑ WOBWOB↑↑ RR RR ↓↓ Tidal volumeTidal volume

Produces respiratory alkalosis from increase in Produces respiratory alkalosis from increase in COCO22 removalremoval↓↓ CO and tissue perfusionCO and tissue perfusion


Proliferative phase1-2 weeks after initial lung injuryInflux of neutrophils, monocytes, and lymphocytesFibroblast proliferationLung becomes dense and fibrousLung compliance continues to decrease

ProliferativeProliferative phasephase11--2 weeks after initial lung injury2 weeks after initial lung injuryInflux of neutrophils, monocytes, and Influx of neutrophils, monocytes, and lymphocyteslymphocytesFibroblast proliferationFibroblast proliferationLung becomes dense and fibrousLung becomes dense and fibrousLung compliance continues to decreaseLung compliance continues to decrease

AetiologyAetiology and Pathophysiologyand Pathophysiology

Hypoxaemia worsensThickened alveolar membrane

Causes diffusion limitation and shunting

If reparative phase persists, widespread fibrosis resultsIf phase is arrested, fibrosis resolves

HypoxaemiaHypoxaemia worsensworsensThickened alveolar membraneThickened alveolar membrane

Causes diffusion limitation and shuntingCauses diffusion limitation and shunting

If reparative phase persists, widespread If reparative phase persists, widespread fibrosis resultsfibrosis resultsIf phase is arrested, fibrosis resolvesIf phase is arrested, fibrosis resolves

AeAetiologytiology and Pathophysiologyand PathophysiologyFibrotic phase

2-3 weeks after initial lung injuryLung is completely remodeled by sparsely collagenous and fibrous tissues

↓ Lung complianceReduced area for gas exchange

Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis

Fibrotic phaseFibrotic phase22--3 weeks after initial lung injury3 weeks after initial lung injuryLung is completely remodeled by sparsely Lung is completely remodeled by sparsely collagenous and fibrous tissuescollagenous and fibrous tissues

↓↓ Lung complianceLung complianceReduced area for gas exchangeReduced area for gas exchange

Pulmonary hypertension Pulmonary hypertension Results from pulmonary vascular destruction Results from pulmonary vascular destruction and fibrosisand fibrosis

Clinical ProgressionClinical Progression

Some persons survive acute phase of lung injury

Pulmonary oedema resolves Complete recovery

Some persons survive acute phase of Some persons survive acute phase of lung injurylung injury

Pulmonary Pulmonary oedemaoedema resolves resolves Complete recoveryComplete recovery

Clinical ProgressionClinical Progression

Survival chances are poor for those who enter fibrotic phase

Requires long-term mechanical ventilation

Survival chances are poor for those who Survival chances are poor for those who enter fibrotic phaseenter fibrotic phase

Requires longRequires long--term mechanical ventilationterm mechanical ventilation

Clinical ManifestationsClinical ManifestationsClinical Manifestations

Initial presentation often insidiousMay only exhibit dyspnea, tachypnea, cough, and restlessnessAuscultation may be normal or have fine, scattered cracklesMild hypoxaemiaChest x-ray may be normal

Oedema may not show until 30% increase in lung fluid content

Initial presentation often insidiousInitial presentation often insidiousMay only exhibit dyspnea, tachypnea, May only exhibit dyspnea, tachypnea, cough, and restlessnesscough, and restlessnessAuscultation may be normal or have fine, Auscultation may be normal or have fine, scattered cracklesscattered cracklesMild Mild hypoxaemiahypoxaemiaChest xChest x--ray may be normalray may be normal

OedemaOedema may not show until 30% increase in may not show until 30% increase in lung fluid contentlung fluid content

Clinical ManifestationsClinical Manifestations

Symptoms worsen with progression of fluid accumulation and decreased lung complianceEvident discomfort and WOBPulmonary function tests reveal decreased compliance and lung volume

Symptoms worsen with progression of Symptoms worsen with progression of fluid accumulation and decreased lung fluid accumulation and decreased lung compliancecomplianceEvident discomfort and WOBEvident discomfort and WOBPulmonary function tests reveal Pulmonary function tests reveal decreased compliance and lung volumedecreased compliance and lung volume

Clinical ManifestationsClinical ManifestationsAs ARDS progresses

Increasing TachypneaDiaphoresis Cyanosis Pallor Decreases in sensoriumChest x-ray termed whiteout or white lung due to consolidation

As ARDS progressesAs ARDS progressesIncreasing Increasing TachypneaTachypnea

Diaphoresis Diaphoresis Cyanosis Cyanosis Pallor Pallor Decreases in Decreases in sensoriumsensoriumChest xChest x--ray termed whiteout or white lung ray termed whiteout or white lung due to consolidation due to consolidation

Clinical ManifestationsClinical ManifestationsClinical Manifestations

If prompt therapy not initiated, severe hypoxaemia, hypercapnea, and metabolic acidosis may ensueMechanical Ventilation may be required to prevent profound hypoxaemia

If prompt therapy not initiated, severe If prompt therapy not initiated, severe hypoxaemiahypoxaemia, hypercapnea, and , hypercapnea, and metabolic acidosis may ensuemetabolic acidosis may ensueMechanical Ventilation may be required Mechanical Ventilation may be required to prevent profound to prevent profound hypoxaemiahypoxaemia

ComplicationsComplications

Nosocomial pneumoniaStrategies for prevention

Infection control measuresElevating HOB 45 degrees or more to prevent aspiration

Nosocomial pneumoniaNosocomial pneumoniaStrategies for preventionStrategies for prevention

Infection control measuresInfection control measuresElevating HOB 45Elevating HOB 45 degreesdegrees or more to prevent or more to prevent aspirationaspiration

ComplicationsComplicationsComplications

BarotraumaRupture of overdistended alveoli during mechanical ventilationTo avoid, ventilate with smaller tidal volumes

Results in higher PaCO2

“Permissive hypercapnia”

BarotraumaBarotraumaRupture of overdistended alveoli during Rupture of overdistended alveoli during mechanical ventilationmechanical ventilationTo avoid, ventilate with smaller tidal To avoid, ventilate with smaller tidal volumesvolumes

Results in higher PaCOResults in higher PaCO22

““Permissive hypercapniaPermissive hypercapnia””

ComplicationsComplicationsComplications

Volu-pressure traumaOccurs when large tidal volumes used to ventilate noncompliant lungs

Alveolar fractures and movement of fluids and proteins into alveolar spaces

Avoid by using smaller tidal volumes or pressure ventilation

VoluVolu--pressure traumapressure traumaOccurs when large tidal volumes used to Occurs when large tidal volumes used to ventilate noncompliant lungsventilate noncompliant lungs

Alveolar fractures and movement of fluids and Alveolar fractures and movement of fluids and proteins into alveolar spacesproteins into alveolar spaces

Avoid by using smaller tidal volumes or Avoid by using smaller tidal volumes or pressure ventilationpressure ventilation


Stress ulcersBleeding from stress ulcer occurs in 30% of patients with ARDS on PPVManagement strategies include correction of predisposing conditions, prophylactic antiulcer agents, and early initiation of enteral nutrition

Stress ulcersStress ulcersBleeding from stress ulcer occurs in 30% Bleeding from stress ulcer occurs in 30% of patients with ARDS on PPVof patients with ARDS on PPVManagement strategies include correction Management strategies include correction of predisposing conditions, prophylactic of predisposing conditions, prophylactic antiulcer agents, and early initiation of antiulcer agents, and early initiation of enteral nutritionenteral nutrition


Renal failureOccurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapniaMay also be caused by nephrotoxic drugs used for infections associated with ARDS

Renal failureRenal failureOccurs from decreased renal tissue Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, oxygenation from hypotension, hypoxemia, or hypercapniaor hypercapniaMay also be caused by nephrotoxic drugs May also be caused by nephrotoxic drugs used for infections associated with ARDSused for infections associated with ARDS

Nursing AssessmentNursing AssessmentHistory of lung disease, Smoking Restlessness AgitationPale, cool, clammy or warm, flushed skinShallow breathing with increased respiratory rate Use of accessory muscles

History of lung disease, Smoking History of lung disease, Smoking Restlessness Restlessness AgitationAgitationPale, cool, clammy or warm, flushed Pale, cool, clammy or warm, flushed skinskinShallow breathing with increased Shallow breathing with increased respiratory rate respiratory rate Use of accessory musclesUse of accessory muscles

Nursing AssessmentNursing Assessment

Tachycardia progressing to bradycardia Extra heart sounds Abnormal breath soundsHypertension progressing to hypotension

Tachycardia progressing to bradycardia Tachycardia progressing to bradycardia Extra heart sounds Extra heart sounds Abnormal breath soundsAbnormal breath soundsHypertension progressing to Hypertension progressing to hypotensionhypotension

Nursing AssessmentNursing Assessment

Somnolence, confusion, deliriumChanges in pH, PaCO2, PaO2, SaO2

Decreased tidal volume, FVCAbnormal x-ray

Somnolence, confusion, deliriumSomnolence, confusion, deliriumChanges in pH, PaCOChanges in pH, PaCO22, PaO, PaO22, SaO, SaO22

Decreased tidal volume, FVCDecreased tidal volume, FVCAbnormal xAbnormal x--rayray

PlanningPlanning

Patient with at least 60 mmHg and adequate lung ventilation to maintain normal pH following recovery will have

PaO2 within normal limitsSaO2 >90%Patent airwayClear lungs on auscultation

Patient with at least 60 mmHg and Patient with at least 60 mmHg and adequate lung ventilation to maintain adequate lung ventilation to maintain normal pH following recovery will havenormal pH following recovery will have

PaOPaO22 within normal limitswithin normal limitsSaOSaO22 >90%>90%Patent airwayPatent airwayClear lungs on auscultationClear lungs on auscultation

TreatmentTreatment

Oxygen High flow systems used to maximize O2deliverySaO2 continuously monitoredGive lowest concentration that results in PaO2 60 mmHg or greaterRisk for O2 toxicity increases when FIO2exceeds 60% for more than 48 hours

Oxygen Oxygen High flow systems used to maximize OHigh flow systems used to maximize O22deliverydeliverySaOSaO22 continuously monitoredcontinuously monitoredGive lowest concentration that results in Give lowest concentration that results in PaOPaO22 60 mmHg or greater60 mmHg or greaterRisk for ORisk for O22 toxicity increases when FIOtoxicity increases when FIO22exceeds 60% for more than 48 hoursexceeds 60% for more than 48 hours

TreatmentTreatment

Mechanical ventilationMay still be necessary to maintain FIO2 at 60% or greater to maintain PaO2 at 60 mmHg or greaterPEEP at 5 cm H2O

Opens collapsed alveoli

Mechanical ventilationMechanical ventilationMay still be necessary to maintain FIOMay still be necessary to maintain FIO22 at at 60% or greater to maintain PaO60% or greater to maintain PaO22 at 60 at 60 mmHg or greatermmHg or greaterPEEP at 5 cm HPEEP at 5 cm H22O O

Opens collapsed alveoliOpens collapsed alveoli

TreatmentTreatment

Positioning strategiesTurn from prone to supine position

May be sufficient to reduce inspired O2 or PEEP

Fluid pools in dependent regions of lungMediastinal and heart contents place more pressure on lungs when in supine position than when in prone position

Positioning strategiesPositioning strategiesTurn from prone to supine positionTurn from prone to supine position

May be sufficient to reduce inspired OMay be sufficient to reduce inspired O22 or PEEPor PEEP

Fluid pools in dependent regions of lungFluid pools in dependent regions of lungMediastinalMediastinal and heart contents place more and heart contents place more pressure on lungs when in supine position pressure on lungs when in supine position than when in prone positionthan when in prone position

Medical Supportive TherapyMedical Supportive Therapy

Maintenance of cardiac output and tissue perfusion

Continuous hemodynamic monitoring Arterial catheter

Maintenance of cardiac output and Maintenance of cardiac output and tissue perfusiontissue perfusion

Continuous hemodynamic monitoring Continuous hemodynamic monitoring Arterial catheter Arterial catheter

Medical Supportive TherapyMedical Supportive TherapyMedical Supportive Therapy

Use of inotropic drugs may be necessaryHemoglobin usually kept at levels >9 or 10 with SaO2 >90%

Packed RBCs

Maintenance of fluid balance

Use of inotropic drugs may be Use of inotropic drugs may be necessarynecessaryHemoglobin usually kept at levels >9 or Hemoglobin usually kept at levels >9 or 10 with SaO10 with SaO22 >>90%90%

Packed RBCs Packed RBCs

Maintenance of fluid balanceMaintenance of fluid balance

EvaluationEvaluation

No abnormal breath soundsEffective cough and expectorationNormal respiratory rate, rhythm, and depthSynchronous thoracoabdominal movementAppropriate use of accessory muscles

No abnormal breath soundsNo abnormal breath soundsEffective cough and expectorationEffective cough and expectorationNormal respiratory rate, rhythm, and Normal respiratory rate, rhythm, and depthdepthSynchronous thoracoabdominal Synchronous thoracoabdominal movementmovementAppropriate use of accessory musclesAppropriate use of accessory muscles

EvaluationEvaluation

PaO2 and PaCO2 within normal rangesMaintenance of weight or weight gainSerum albumin and protein within normal ranges

PaOPaO22 and PaCOand PaCO22 within normal rangeswithin normal rangesMaintenance of weight or weight gainMaintenance of weight or weight gainSerum albumin and protein within Serum albumin and protein within normal rangesnormal ranges

ards overview

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