Acute Respiratory Distress Syndrome.pdf

ACUTE RESPIRATOR Y DISTRESS SYNDROME Presented by Omar AL-Rawajfah, RN, PhD  Lecture Outlines Etiology and Pathophysiology – Definition – Systemic inflammatory response syndrome – Precipitating causes of ARDS – Mediator of sepsis, ARDS – Stages Asse...

ACUTE RESPIRATOR Y DISTRESS SYNDROME Presented by Omar AL-Rawajfah, RN, PhD  Lecture Outlines Etiology and Pathophysiology – Definition – Systemic inflammatory response syndrome – Precipitating causes of ARDS – Mediator of sepsis, ARDS – Stages Assessment – Neurologic – Respiratory – Cardiovascular Nursing diagnoses Collaborative management – Airway management – Mechanical ventilation – Pharmacotherapy – Fluid and nutritional therapy 2  Etiology and Pathophysiology Acute Lung Injury (ALI): a syndrome characterized by non-cardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemia ARDS: is the most sever form of ALI ARDS: a syndrome of inflammation and increased permeability associated with a constellation of clinical, radiologic, and physiologic abnormalities unexplained by elevations in left atrial or pulmonary capillary pressure 3  Etiology and Pathophysiology Clinically ARDS is defined by: – PaO2/FIO2 < 200 mmHG (normally > 300mm Hg) – Bilateral infiltration of lungs – Pulmonary Artery Occlusive Pressure (PAOP) < 18 mmHg (normally 5-15mm Hg) – Alveolar damage ARDS is characterized by the following criteria:[ – lung injury of acute onset, within 1 week of an apparent clinical insult and with progression of respiratory symptoms – bilateral opacities on chest imaging not explained by other pulmonary pathology (e.g. pleural effusion, pneumothorax, or nodules) – respiratory failure not explained by heart failure or volume overload – decreased arterial PaO2/FiO2 ratio: mild ARDS: ratio is 201 - 300 mmHg moderate ARDS: 101 - 200 mmHg severe ARDS: ≤ 100 mmHg 4  Systemic Inflammatory Response Syndrome SIRS: is an overly aggressive host defense response to insult or tissue damage in the body The local injury response becomes total-body response Most SIRS patients have bacterial infection SIRS may be associated with trauma, hypoxia, pneumonitis, burns, tissue necrosis, & sever peripheral vascular disease – Fever more than 38C or hypothermia less than 36 – HR > 90, RR > 20 PaCO2 < 32, WBC > 12,000 Inflammatory cytokines produce in response to injury have negative effect in lung healing The hallmark of ARDS is accumulation of protein-rich fluid in the alveoli and interstitial spaces 5  Precipitating causes of ARDS Direct pulmonary insults – Aspiration of GI contents – Inhalation of toxic substance – Diffuse pneumonia – Pulmonary contusion – Pulmonary embolism – End stage COPD – O2 toxicity Indirect pulmonary insults – Sepsis – Multiple trauma – Burn – Anaphylaxis – Tissue necrosis – Disseminated intravascular coagulation (DIC) – Cardiopulmonary bypass 6 Causes of ARDS NEJM 2000;342,18:1334-1349  Pathophysiology The damage to the endothelial lining of the alveolar-capillary membrane increases its permeability Shifting of the fluids and proteins into the alveoli inactivates surfactant result in alveolar collapse V/Q mismatch is occurred because of the blood passing through the lungs without gas exchange This condition is manifested by deterioration of oxygenation in spite of increased O2 supply In the process of lung healing, fibrosis and scarring further dispute gas exchange 8  Mediators of Sepsis, ALI & ARDS Components of the host defense response: Inflammation – Vasodilatation, increased capillary permeability – Clotting within the interstitial space – Migration of granulocytes and monocytes to the tissue – Release of bradykinin, histamine, prostaglandines Modulation of Immune Response – Tumor Necrosis Factor (TNF) and Interleukin-1 are stimulated by bacterial endotoxin and cause fever – Neutrophils attack the damaged pulmonary capillaries endothelial lining result in organ damage in other organ system – Arachidonic acid, thromboxane, & prostacyclcin believed to cause pulmonary hypertension, and smooth muscle construction 9 Components of the host defense response Coagulation – Microthrombi and fibrin disposition – Intravascular coagulation decrease the size of available pulmonary vascular beds – Tissue repair – Regeneration of native parenchymal cells and filling the gaps with fibroblastic tissue creates persistent problem with gas exchange – Fibroblastic tissue decrease the lung compliance – It is believed that progression of fibroproliferation to pulmonary fibrosis is the responsible for 15-40% of death with ADRS Activation of hypothalamic-pituitary-adrenal axis – Stress responses → release of catecholamines – Increased vascular tone 10 11 12  Stages of ARDS Phase 0: injury stage  First 12 h  Diagnosis is difficult because the signs are subtle.  The patient exhibits increased dyspnea and tachypnea.  There are few radiographic changes, there is no evidence of cellular damage. Phase I: Early exudative phase  Alveolar edema with fibrin & leukocytes debris  Damage of type I pneumocytes and endothelial cells Phase II: proliferative phase  Persistent capillary endothelial damage  Type II cell proliferation Phase III: fibroproliferative phase  Also called chronic ARDS  Thickening of the interstitium  Increased number of type 13 II cells and fibrosis Phases of ARDS Phases of ARDS Phases of ARDS Phases of ARDS Phases of ARDS Phases of ARDS  Lung injury score Chest radiograph score (0 – 4) Hypoxemia score (0 – 4) Positive End-Expiratory Pressure (0 – 4) Compliance Score (0 – 4) Total Score – 0: no lung injury – 0.1 – 2.5: mild to moderate lung injury – More than 2.5 severe lung injury 20  Assessment ARDS usually developed 24 – 72 hrs of the insult The assessment should be directed to know the patients at risk for ARDS Neurologic system – Level of consciousness – Restlessness and anxiety – Lethargic and quite behaviors may indicate decompensate quickly Respiratory System – Dyspnea & tachypnea – Cough with think foamy sputum or hemoptysis – Close monitoring of SaO2 – Chest X-ray may be normal within the first 24 hrs then white out or ground glass picture – As the hypoxemia worse cyanosis, pallor, diaphoresis occur – More widespread crackles and wheezes and absent breathing sound over the collapse areas – Early ABG may be alkalotic changed to acidosis after while because of combined respiratory & metabolic acidosis 21 Early stage ARDS 22 Late stage ARDS 23 24  Assessment Cardiovascular System – Tachycardia and dysrhythmias – Cardiac failure is very possible specially for those who had previous cardiac events – Cardiac arrest is possible too – Elevated pulmonary pressure without an increase in vascular volume Nursing Diagnosis – Ineffective airway clearness – Impaired gas exchange – ineffective breathing pattern – Decrease CO – Alter tissue perfusion…. 25  Collaborative Management Airway management – Endotracheal Intubation – Positive pressure ventilation – Consider tracheostomy for intubation more than 7 days Mechanical Ventilation – The goals of MV in ARDS are: Improve gas change and reduce hypoxemia Reliving respiratory distress by reduce the work of breathing Prevent atelectasis Permitting lung and airway healing Avoid complications 26  Collaborative Management Ventilator-Induced Lung Injury – Occurs in ARDS who treated with high pressure and large TV – Because of alveolar collapse and protein leakage small portion of the lung continue to work – In most of case only about one-third of the lung participate in the gas exchange “small lung theory” or baby lung theory” – When this small portion receive full TV and high pressure overdistention and injury occurs in these normal or nearly normal tissue – The goal of the ventilation therapy is to recruit alveoli with PEEP and minimize the ventilator- induced injury 27  Collaborative Management Problem associated with conventional MV – O2 toxicity When O2 percentage is more than 50% for longer than 12-24hr O2 toxicity can cause increased pulmonary micro pulmonary permeability, ↓surfactant production, impedance of tracheal cilia – Hypotension Positive pressure ventilation in all forms increases the intrapulmonary and intrathoracic leading to decreased preload and thus decreased CO – Barotrauma Associated with different conditions such as pneumothorax subcutaneous emphysema – Volutrauma Large shearing force: caused by repeated opening and closing of alveoli with each respiratory cycle May be caused by high peak inspiratory pressure, high PEEP, large TV, high RR 28  Management of ARDS High-frequency Jet Ventilation – Creates a constant airway pressure throughout the respiratory cycle that lower peak airway pressure and allows use of small TV – It need sedation and paralysis – Need special type of ventilators – Need trained nurses Pressure-controlled inverse-ratio – It reveres the normal inspiratory and expiratory time ratio (normally I:E = 1:2 or 1:3) reversed to be 2:1, 3:1, or 4:1 – It allows consistent gas delivery – Allows reduction of FIO2 and PEEP – Need trained nurse with special ventilator settings 29  Management of ARDS Super PEEP – Greater than 15 mmHg – Maintain PaO2 greater than 60mm Hg – Associated with good survivor rate – Barotrauma and hypotension are common side effects – It is well accepted that pressure below 35-50 cm H2O is safe and will not cause lung injury Pressure-controlled without inverse-ratio – Each breath is delivered to reach a preset pressure – Well tolerated by the patient – TV is not constant – In the case of bronchospasm, secretion the preset pressure level reaches the peak quickly→ patient may be under ventilated 30 Additional lung protective techniques Low TV ventilation – Prevents overdistention of normal lung tissue Permissive hypercarpia – Using low TV and limited pressure normally increase the CO2 level – Adult can tolerate higher level of CO2 with few side effects – Mild to moderate acidosis is well tolerated by adult – The metabolic system usually compensate within 1 or 2 days – Moderate acidosis have some positive effect such as increasing the responsiveness to catecholamines Intravascular oxygenation – Direct oxygenation of the blood or direct removal of the CO2 from the blood – Assists the injured lung and reduce the burden on healthy areas 31 Additional lung protective techniques Pharmacologic support – Antioxidants (e.g. Ketoconazole) It is thromoxane A2 synthetase inhibitor Associated with hepatic toxicity, renal toxicity – Steroids Fluid therapy – Negative fluid balance has been beneficial in reducing the associated pulmonary edema and improve the gas exchange – Negative balance can be reached with diuretics – ARDS patient are maintained on the lower end of central venous pressure (i.e 3-5 cm H2O) – Dopamine can be used to compensate the reduction in the CO 32 Additional lung protective techniques Nutrition Body position Use prone position – Contraindication of prone position include: – Hemodynamic instability – Weight over 90kg – Abdominal girth more than 50 inches Preventing of infections – Strict aseptic techniques – Prevent aspiration 33 Questions and answers 34