ACUTE RESPIRATORY DISTRESS SYNDROME

ACUTE RESPIRATORY DISTRESS SYNDROME

is a life-threatening reaction to injuries or acute infection to the lung It starts with swelling of tissue in the lungs and build up of fluid in the tiny air sacs that transfer oxygen to the bloodstream. This leads low blood oxygen levels. ARDS is similar infant respiratory distress syndrome, but the causes and treatments are different. ARDS can develop in anyone over the age of one year old. Also known as Adult Respiratory Distress Syndrome, Respiratory Distress Syndrome, The annual incidence of ARDS is 1323 people per 100,000 in the general population The mortality rate varies from 25-40%

CAUSES
Direct injury to the lungs: Chest trauma, such as a heavy blow Breathing smoke, chemicals, or salt water Massive blood transfusion Aspiration of gastric contents Pneumonia Severe inflammation of the pancreas (pancreatitis) Overdoses of alcohol or certain drugs (eg, aspirin, cocaine, opioids, phenothiazines, and tricyclic antidepressants) Lung and bone marrow transplantationwithin few days of a lung transplant, the recipient is prone development of ARDS.

PHASES OF ARDS
Injury or Exudative Phase Occurs approximately 1 to 7 days (usually 24 to 48 hours) after the direct lung injury or host insult. The primary pathophysiological changes that characterize this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis. shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2 termed refractory hypoxemia. Hypoxemia initially cause an increase in respiratory rate, decrease in tidal volume, respiratory alkalosis and an increase in cardiac output.

PHASES OF ARDS
Reparative or Proliferative Phase Begins 1 to 2 weeks after the initial lung injury. During this phase there is an influx of neutrophils, monocytes, lymphocytes and fibroblast proliferation as part of the inflammatory response. The proliferative phase is complete when the diseased lung becomes characterized by dense, fibrous tissue. Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature. Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia. If the reparative phase persists widespread fibrosis results, if it is arrested the lesions resolve

PHASES OF ARDS
Fibrotic or Chronic Phase Occurs approximately 2 to 3 weeks after the initial lung injury.

By this time the lung is completely molded by sparsely collagenous and fibrous tissues.
There is diffuse scarring and fibrosis resulting in decreased lung compliance. The surface area for gas exchange is significantly reduced because the interstitium is fibrotic and therefore hypoxemia continues. Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.

Tests and diagnosis

Chest X-ray. A chest X-ray can reveal which parts of your lungs have fluid in them and whether your heart is enlarged. Computerized tomography (CT). A CT scan combines X-ray images taken from many different directions into cross-sectional views of internal organs. CT scans can provide detailed information about the structures within the heart and lungs Electrocardiogram. This painless test tracks the electrical activity in your heart. It involves attaching several wired sensors to your body. Echocardiogram. A sonogram of the heart, this test can reveal problems with the structures and the function of your heart. Arterial blood gas

Pulmonary function testing shows decreased lung compliance with reduced vital capacity, minute volume, and functional vital capacity Pulmonary artery pressure monitoring shows normal pressures in ARDS, helping distinguish ARDS from cardiogenic pulmonary edema

Signs and Symptoms

Rapid breathing

Feeling like you can't get enough air in your lungs

Low oxygen levels in your blood, which can lead to organ failure

rapid heart rate

abnormal heart rhythms

Confusion
extreme tiredness

Complications
Pulmonary fibrosis Collapsed lung (pneumothorax) Blood clots

Infections
Abnormal lung function Memory, cognitive and emotional problems

Medical History
have recently had conditions that could lead to ARDS History of heart failure

Physical Exam

By auscultation :abnormal breathing sounds, such as crackling

cyanosis on skin and lips

MANAGEMENT
Maintenance of adequate oxygenation, cardiac output, and nutritional support Prevention of secondary pneumonia, other infections, and ventilator induced lung injury. Pharmacological management

Inhaled nitric oxide reduces intrapulmonary shunting and improves oxygenation by dilating blood vessels in better ventilated areas of the lungs. Surfactant therapy it forms a thin layer atop a thin layer of water on the inner surface of the alveolus, reducing the surface tension within the alveoli

Corticosteroid the course of ARDS to improve oxygenation and lung mechanics when fibrotic changes occur

RESPIRATORY THERAPY

Mechanical ventilation The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. Low tidal volume ventilation (LTVV) reduces the damaging, excessive stretch of lung tissue and alveoli NURSING RESPONSIBILITY Some special considerations relate specifically to the type of tube via which the patient is being ventilated (i.e.endotracheal or tracheostomy) and others related to the patient, and theventilator itself

Precaution & Care Tracheobronchial Hygiene: Placement of tube: Chest movement Auscultation Post intubation X-ray

Cuff pressure: If insufficient- Leak Displacement of the tube Aspiration

If high pressure - Tracheal stenosis Desired Pressure - 20-30cm water

 Observe and document

Airway type, size, and

position Character of insertion site Date airway inserted

Pulmonary assessment
Inspection

Palpation Percussion Auscultation Provide oral care prn Reapply ETT tape Monitor for complications Suction as needed

Nursing Diagnoses and Intervention

Decreased Cardiac Output

When PEEP is applied, intrathoracic pressure increases further; this can significantly decrease venous return, ventricular filling, stroke volume, and cardiac output. Monitor and record vital signs, including apical pulse, at least every 2 hours; more frequently immediately following initiation of mechanical ventilation or addition of PEEP. Frequent assessment is vital to detect early signs of decreased cardiac output Assess level of consciousness at least every 4 hours. Altered LOC, confusion, and restlessness are early signs of cerebral hypoxia due to decreased cardiac output.

Monitor pulmonary artery pressures, central venous pressure, and cardiac output readings every 1 to 4 hours. Changes in these measurements may indicate worsening cardiac status