(ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS

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Definition * Noncardiac pulmonary edema ٠ ‏عالت 165211210157 01 متتده1 لل‎ * Complication of hospitalized patients - Serious med-surg problem - May not be lung related - Mortality remains 50-60% 2 دك 12/25/24 

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Pathophysiology * Frequently associated - Low perfusion * Single organ * Multi-organ (MODS) * Total body system (shock) ٠ Etiology: Severe CNS Disorder, Trauma, CVA, Inc. CSF. * Hallmark of ARDS - Hypoxia دك 12/25/24 

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Pathophysiology * Other characteristics - Severe dyspnea - Diffuse bilateral ‏عمط[‎ 12/25/24 15 3 

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Pathophysiology * Injury to lungs (Scoring) Abnormal gas exchange Intrapulmonary shunting Reduced lung compliance Decreased surfactant activity . Amt. of Infiltrates on CXR. . Degree of Hypoxemia. . Amount of PEEP. . Static Lung Compliance. 15 na 12/25/24 

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Pathophysiology * Physiologic alterations - Injury to pulmonary endothelium and alveolar epithelium causes increase in lung permeability. - Fluid leaks into interstitial spaces causing pulmonary edema. - INCIDENCE AND PREVALENCE دك 12/25/24 

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Pathophysiology * Physiologic alterations - Injury to Type II pneumocytes, causes increase in surface tension and atelectasis - Alveolar-capillary membrane damage, inflammation occurs, 2 decreasing gas exchange دك 12/25/24 

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Pathophysiology * American-European Consensus Conference (1994) Defines ARDS 25: 1. PaO,/FiO, <200; 2. Bilat. Infiltrates; 3. PCWP <18mm Hg (or more easily understood, no clinical evidence of L Atrial HTN). دك 12/25/24 

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Pathophysiology * Results of physiologic alterations - Ventilation-perfusion anomalies - Decreased lung compliance - Increase work of breathing دك 12/25/24 

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Etiology * No single exogenous or endogenous precipitating factor> Multiple causes. * Exact causative mechanism is unknown * Direct and Indirect Causes دك 12/25/24 

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11 Etiology * Many conditions associated - Most common * Non pulmonary © eou- Te) E 2 - Trauma * Pulmonary related ۳ - AIDS/PCP - Near drowning - Pulmonary embolism دك 12/25/24 

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Etiology * Other conditions - Amniotic fluid embolism - Bowel infarction - Drug abuse - Multiple fractures - Heat stroke - Peritonitis - Multiple blood transfusions دك 12/25/24 

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Clinical manifestations * Acute respiratory failure - Change in Personality, disorientation, dec. LOC. - Initial Dyspnea w/ Hyperventilation (Tachypnea) - Grunting respirations - Cyanosis - 1107 - Retractions 13 دك 12/25/24 

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Clinical manifestations * Dry cough * Diaphoresis * Crackles, Rhonchi, and Bronchial 50۰ * Vitals Signs - Fever - Hypotension - Tachycardia (dysrhythmias) ¢ Altered sensorium * PaCO2 dec.> Resp. Alkalosis (initial); * Lactic Acid> Met. Acidosis (later) دك 12/25/24 

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Diagnostic studies * Radiologic - CXR * Diffuse, bilateral infiltrates ا ل 5 ‎Hypoxemia‏ * تا ا ‎alkalosis‏ 12/25/24 

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16 Phases of ARDS ¢ Phase I - Client exhibits dyspnea and tachypnea ¢ Support client with oxygenation * Phase 2 - Increasing pulmonary edema * Mechanical ventilation support دك 12/25/24 

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Phases of ARDS * Phase 3 - Progressive refractory hypoxemia * Maintain oxygenation ¢ Prevent complications ¢ Phase 4 - Pulmonary fibrosis pneumonia * Chronic problem * Maybe ventilator dependent 17 دك 12/25/24 

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Management * Vent. Settings should be Lung- Protective. * Unconventional Modes (High Frequency Ventilation, Pressure-Controlled Ventilation, and Inverse-Ratio Ventilation) have failed to demonstrate efficacy and are not standard acceptable Tx. 18 دك 12/25/24 

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Nursing diagnosis 9۹2 * Impaired gas exchange ¢ Altered nutrition ¢ Depression ¢ Decreased cardiac output * Knowledge deficit دك 12/25/24 

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Interventions * Assess - Sputum production - Oxygenation - Heart sounds - Lung sounds - Urinary output - Cardiac rhythm دك 12/25/24 

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Interventions * Monitor - ABGs - Pulse oximetry - Ventilator settings - Fluid maintenance * Teach - Ventilator - Lines 21 دك 12/25/24 

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Medical management * Medications - Diuretics - Anti anxiety - Neuromuscular blocking agents - Analgesics - Antibiotics - Dopamine - Corticosteroids دك 12/25/24 

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Management * Possible Prone Positioning (Vollman, 1997). * F/E Balancing: Monitor R Arterial Pressure (RAP) and Pulmonary Artery Diastolic (PAD) Pressure. * Nutrition: ARDS increases nutritional requirements by 1.5 to 2 9۹ 24 دك 12/25/24 

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Management ¢ Psychosocial Support * Complications of ARDS: 1. Heart failure 2. Acidosis 3. Hyper- hypo- kalemia 4. De- over- hydration 5. Pulmonary embolism دك 12/25/24 

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Management ۰ ‏تاووتته ممنلتجن0‎ * Prognosis: ٠. 216 ‏مالالا .وخط‎ 760057“ typically return to * GI bleed ‏تممه لو نامام‎ * Renal failure lung function. Studies of ARDS 0 months- 4 years after lung injury show a ۱۱۱۱۱۱۰۰ pulmonary function. 26 دك 12/25/24 

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)_ 03/16/25 LBS 1 Definition • Noncardiac pulmonary edema • A form of respiratory failure • Complication of hospitalized patients – Serious med-surg problem – May not be lung related – Mortality remains 50-60% 03/16/25 LBS 2 Pathophysiology • Frequently associated – Low perfusion • Single organ • Multi-organ (MODS) • Total body system (shock) • Etiology: Severe CNS Disorder, Trauma, CVA, Inc. CSF. • Hallmark of ARDS – Hypoxia 03/16/25 LBS 3 Pathophysiology • Other characteristics – Severe dyspnea – Diffuse bilateral infiltrates 03/16/25 LBS 4 Pathophysiology • Injury to lungs (Scoring) – Abnormal gas exchange – Intrapulmonary shunting – Reduced lung compliance • 1. 2. 3. 4. 03/16/25 Decreased surfactant activity Amt. of Infiltrates on CXR. Degree of Hypoxemia. Amount of PEEP. Static Lung Compliance. LBS 5 Pathophysiology • Physiologic alterations – Injury to pulmonary endothelium and alveolar epithelium causes increase in lung permeability. – Fluid leaks into interstitial spaces causing pulmonary edema. – INCIDENCE AND PREVALENCE 03/16/25 LBS 6 Pathophysiology • Physiologic alterations – Injury to Type II pneumocytes, causes increase in surface tension and atelectasis – Alveolar-capillary membrane damage, inflammation occurs, substances gather at site of injury decreasing gas exchange 03/16/25 LBS 7 Pathophysiology • American-European Consensus Conference (1994) Defines ARDS as: 1. PaO2/FiO2 <200; 2. Bilat. Infiltrates; 3. PCWP <18mm Hg (or more easily understood, no clinical evidence of L Atrial HTN). 03/16/25 LBS 8 Pathophysiology • Results of physiologic alterations – Ventilation-perfusion anomalies – Decreased lung compliance – Increase work of breathing 03/16/25 LBS 9 Etiology • No single exogenous or endogenous precipitating factor Multiple causes. • Exact causative mechanism is unknown • Direct and Indirect Causes 03/16/25 LBS 10 Etiology • Many conditions associated – Most common • Non pulmonary – Gram (-) sepsis – Trauma • Pulmonary related – – – – 03/16/25 Aspiration AIDS/PCP Near drowning Pulmonary embolism LBS 11 Etiology • Other conditions – – – – – – – Amniotic fluid embolism Bowel infarction Drug abuse Multiple fractures Heat stroke Peritonitis Multiple blood transfusions 03/16/25 LBS 12 Clinical manifestations • Acute respiratory failure – Change in Personality, disorientation, dec. LOC. – Initial Dyspnea w/ Hyperventilation (Tachypnea) – Grunting respirations – Cyanosis – Pallor – Retractions 03/16/25 LBS 13 Clinical manifestations • Dry cough • Diaphoresis • Crackles, Rhonchi, and Bronchial Sounds. • Vitals Signs – Fever – Hypotension – Tachycardia (dysrhythmias) • Altered sensorium • PaCO2 dec. Resp. Alkalosis (initial); • Lactic Acid Met. Acidosis (later) 03/16/25 LBS 14 Diagnostic studies • Radiologic – CXR • Diffuse, bilateral infiltrates • Laboratory – ABGs • Hypoxemia • Respiratory alkalosis 03/16/25 LBS 15 Phases of ARDS • Phase I – Client exhibits dyspnea and tachypnea • Support client with oxygenation • Phase 2 – Increasing pulmonary edema • Mechanical ventilation support 03/16/25 LBS 16 Phases of ARDS • Phase 3 – Progressive refractory hypoxemia • Maintain oxygenation • Prevent complications • Phase 4 – Pulmonary fibrosis pneumonia • Chronic problem • Maybe ventilator dependent 03/16/25 LBS 17 Management • Vent. Settings should be LungProtective. • Unconventional Modes (High Frequency Ventilation, Pressure-Controlled Ventilation, and Inverse-Ratio Ventilation) have failed to demonstrate efficacy and are not standard acceptable Tx. 03/16/25 LBS 18 Nursing diagnosis • Anxiety • Impaired gas exchange • Altered nutrition • Depression • Decreased cardiac output • Knowledge deficit 03/16/25 LBS 19 Interventions • Assess – – – – – – Sputum production Oxygenation Heart sounds Lung sounds Urinary output Cardiac rhythm 03/16/25 LBS 20 Interventions • Monitor – ABGs – Pulse oximetry – Ventilator settings – Fluid maintenance • Teach – Ventilator – Lines 03/16/25 LBS 21 Medical management • Ventilator – IMV – PEEP • Fluid control – Swan Ganz line 03/16/25 LBS 22 Medical management • Medications – – – – – – – Diuretics Anti anxiety Neuromuscular blocking agents Analgesics Antibiotics Dopamine Corticosteroids 03/16/25 LBS 23 Management • Possible Prone Positioning (Vollman, 1997). • F/E Balancing: Monitor R Arterial Pressure (RAP) and Pulmonary Artery Diastolic (PAD) Pressure. • Nutrition: ARDS increases nutritional requirements by 1.5 to 2 times. 03/16/25 LBS 24 Management • Psychosocial Support • Complications of ARDS: 1. 2. 3. 4. 5. Heart failure Acidosis Hyper- hypo- kalemia De- over- hydration Pulmonary embolism 03/16/25 LBS 25 Management • • • • Cardiac arrest DIC GI bleed Renal failure 03/16/25 • Prognosis: Pts. Who recover typically return to relatively normal lung function. Studies of ARDS survivors from 9 months- 4 years after lung injury show a mild restrictive pulmonary function. LBS 26