RESPIRATORY FAILURE

INTRODUCTION The term respiratory failure, is used to describe inadequate gas exchange by the respiratory system, with the result that arterial oxygen and/or carbon dioxide levels cannot be maintained within their normal ranges. A drop in blood oxygenation is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. The normal reference values are: oxygen PaO2 greater than 80 mmHg and carbon dioxide PaCO2 less than 45 mmHg . DEFINITION
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. (LEWIS) Respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg.

Acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status. Blood gases Table 14-1: Blood gas values (ranges) from healthy persons at rest. - Normal mean tensions for mixed venous blood and for alveolar air are shown below. PaO2 : PaCO2: Base Excess: pHa : PAO2 : PACO2 : Mean PvO2 : Mean PvCO2 : 10-13 kPa (75-95 mmHg) 4.8-6 kPa (36-45 mmHg), Zero 7.35-7.45 (ie,[H+] = 35-44 nM) 10 - 13.3 kPa (75-100 mmHg) 4.8-6 kPa (36-45 mmHg). Mean: 5.3 kPa (40 mmHg), 6 kPa (45 mmHg) 6.1 kPa (46 mmHg)

Types Type 1 (HYPOXEMIC RESPIRATORY FAILURE) / OXYGENATION FAILURE

Type 1 respiratory failure is defined as hypoxemia without hypercapnia, and PaCO2 may be normal or low. It is defined as PaO2 of 60 mmHg or less when the patient is receiving an inspired O2 concentration of 60% or greater. The basic defect in type 1 respiratory failure is failure of oxygenation characterized by: PaO2 low (< 60 mmHg) PaCO2 normal or low CAUSES Respiratory system

interstitial lung diseases: ARDS, pneumonia, emphysema. Toxic inhalation (smoke inhalation) Hepatopulmonary syndrome (low resistance flow rate ,v/q mismatch) Massive pulmonary emboli,fat emboli Pneumothorax Hemothorax

Cardiac system

Anatomic shunts: right-to-left shunt (VSD )

Cardiogenic pulmonary edema Shock ( decreased CO ,decreasing blood flow through pulmonary vasculature) CHF ( decreased CO)

Type 2 (HYPERCAPNIC RESPIRATORY FAILURE /VENTILATORY FAILURE)

Type 2 respiratory failure is caused by increased airway resistance; both oxygen and carbon dioxide are affected. Defined as the build up of carbon dioxide levels (PaCO2) above normal. (>45mmHg) in combination with academia (pH< 7.45). primary problem is inufficient CO2 removal. causes include: Respiratory system Asthma COPD Cystic fibrosis

CNS :-- :-- Diseases affecting the nerves and muscles that "signal" the lungs to inflate or deflate

Brin stem infaction Sedative and narcotic overdose e.g., (morphine, benzodiazepines) that suppress respiration.Spinal cord injury Sever head injury

CVA

Chest wall Thorasic trauma (eg flail chest ) Kyphoscoliosis :-- which make the lungs less efficient at filling and emptying Pain Massive obesity Neuromuscular system Myasthenia gravis Polyneuropathy Acute myopathy Toxic ingestion ALS Phrenic nerve injury GBS Poliomyelitis Muscular dystrophy Multiple sclrrosis decreased Increased decreased

PaO2 PaCO2 pH

The basic defect in type 2 respiratory failure is characterized by:

Type III Respiratory Failure (Combined Oxygenation and Ventilatory Failure): Combined respiratory failure It shows features of both arterial hypoxaemia and hypercarbia (decrease in PaO2 and increase in PaCO2). Assessment based on alveolar gas equation shows an increase in PAO2 PaO2 difference, venous admixture and Vd/VT. In theory, any disorder causing Type I or Type II respiratory failure can cause Type III respiratory failure. Common causes of Type III respiratory Failure: 1. Adult respiratory distress syndrome (ARDS) 2. Asthma 3. Chronic obstructive pulmonary disease

Acute hypercarbic respiratory failure is characterizedby a patient with no, or minor, evidence of pre-existingrespiratory disease and arterial blood gas tensions will showhigh PaCO2, low pH, and normal bicarbonate. Acute on chronic hypercarbic respiratory failure ischaracterized by an acute deterioration in an individual with significant pre-existing hypercarbic respiratory failure, high PaCO2, low pH, and high bicarbonate.

Chronic hypercarbic respiratory failure is characterized by the evidence of chronic respiratory disease, high PaCO2, normal pH and high bicarbonate. The causes of respiratory failure are diverse. PATHOPHYSIOLOGY

Physiology of gas exchange

Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. Following diffusion into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of

hemoglobin contains 4 sites for combination with molecular oxygen, 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen. The quantity of oxygen combined with hemoglobin depends on the level of blood PaO2. This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear but has a sigmoid-shaped curve with a steep slope between a PaO2 of 10 and 50 mm Hg and a flat portion above a PaO2 of 70 mm Hg. The carbon dioxide is transported in 3 main forms: (1) in simple solution, (2) as bicarbonate, and (3) combined with protein of hemoglobin as a carbamino compound. During ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial PO2 difference. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused while others are overperfused. The optimally ventilated alveoli that are not perfused well are called high V/Q units (acting likedead space), and alveoli that are optimally perfused but not adequately ventilated are called low V/Q units (acting like ashunt).

Pathophysiologic mechanisms that cause hypoxemic respiratory faiuure are 1. 2. 3. 4. Ventilation perfusion mismatch Shunt Diffusion limitation Hypoventilation Ventilation perfusion mismatch (V/Q mismatch) V/Q mismatch is the most common cause of hypoxemia. In normal lung volume of blood perfusing the lungs each minute (4-5L) is appx equal to the amount of fresh gas that reaches the alveoli each minute (4-5L) . In a perfectly matched system each portion of lung would receive 1ml of air for each 1ml of blood. ie V/Q is 1:1. In real situation normally there is some mismatch ,at the apex V/Q ratio is >1 (more ventilation than perfusion).at the midpoint it is nearly 1,and at the base it is <1. Many diseases and conditions alter V/Q ratio and thus causes V/Q mismatch.

V/Q is decreased in conditions like

increased secreations are present in airway :--COPD,pneumonia mucus plug in airway bronchospasm is present (asthma) alveolar collapse (atelectasis) pain :--unreleived pain interferes with chest and abdominal wall movement,compromising lung ventilation. Also pain increases muscle and motor tension,producing muscle rigidity and it causes systemic vasoconstrction and activation of the stress response and it increases o2 consumption and co2 production.this results in limited airflow to alveoli. Pulmonary emboli Dead space ,no perfusion due to obstruction of the pulmonary capillary.

V/Q is increased in conditions like ;-- factors that affect perfusion unit of V/Q

Management :-- Administration of 100% oxygen eliminates all of the low V/Q units, thus leading to correction of hypoxemia. by Hypoxemia increases minute ventilation chemoreceptor stimulation.

Shunt
Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. There are 2 types of shunt :-Anatomical shunt :-- exists in normal lungs because of the bronchial and thebesian circulations, accounting for 2-3% of shunt.it occurs when blood passes through an anatomic channel and in the heart. A right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac origin. Hypercapnia generally does not develop unless the shunt is excessive (>60%).

Intra pulmonary shunt :-- occurs when blood flows through pulmonary capillaries without participating in gas exchange. It is seen in conditions where the alveoli is flll with blood. (ARDS,pneumonia, pulmonary edema) When compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by oxygen administration. They may require mechanical ventilation and a high fraction of inspired o2 (Fio2 ) to improve gas exchange.Because
1. blood passes from right-to-left without passing through the lung(Anatomical shunt )

2. alveoli are filled with fluid which prevent gas exchange.(intra pulmonary shunt)

Diffusion limitation It occurs when gas exchange across the alveolar capillary membrane is compromised by a process that thickens (fibrosis ) or destroys the membrane,it slows the gas transport (pulmonary fibrosis,interstitial lung disease and ARDS) Also caused by certain conditions that affect pulmonary vascular bed (emphysema,recurrent pulmonary emboli) Occurs more during exercise than at rest because during exercise blood move rapidly through the lung so transit time is increased ,RBC are in the lung for shorter time,decreasing the time for diffusion of o2 across the alveolar capillary membrane.the classical sign of diffusion limitation is hypoxemia that is present during exercise but not at rest

Alveolar Hypoventilation
It is a generalised decrease inventilationthat result in an increase in the PaCO2 and a consequent decrease in the PaCO2. Hypoventilation is characterized by hypercapnia and hypoxemia. Hypoventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles or chest wall dysfunction As ventilation decreases below 4-6 L/min, PaCO2 rises

precipitously. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient. Primarily it is a mechanism of hypercapnic respiratory failure it is mentioned here because it can also cause hypoxemia. Interrelationships of mechanisms Hypoxemic respiratory failure is caused by combination of 2 or more of the above .eg :--in case of acute respiratory failure secondary to pneumonia may have combination of V/Q mismatch (because of inflammation ,edema and hypersecreation of exudates with in the bronchioles and terminal respiratory unit obstruct the airways) and shunt(fill the alveoli with exudates. Pathophysiologic mechanisms that cause hypecapnic respiratory faiuure are Imbalance between ventilator supply and ventilator demand.:--Ventilatory supply is maximum ventilation (gas flow in and out of lungs) that the patient can sustain without developing respiratory musclr fatigue.ventilatory demand is amount of ventilation needed to keep the PaCO2 with in the normal limits. Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). So an individual with normal normal lung function can engage in strenuous exercise ,results in increased co2 production without an elevation of PaCO2 .But patient with emphysema do not have this advantage in response to exercise or metablic demand. Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing. When ventilator demand exceeds ventilatory supply ,the PaCO2 can no longer sustained with in normal limits and hypercapnia occurs. It is also called ventilator failure because the primary problem is the inability of the respiratory system to ventilate out sufficient CO2 to maintain a normal PaCO2. MECHANISMS OF LIMITATIONS IN VENTILATORY SUPPLY
1. Abnormalities of airways and alveoli :-- asthma (bronchospasm ,edema of the

bronchial mucosa and plugging of small airways with secreations reduces airflow .so work of breathing increase causing respiratory muscle fatigue decrease in PaO2 and an increase in PaCO2) ,emphysema,chronic bronchitis and cystic fibrosis are results in airflow obstruction and air trapping. 2. Abnormalities of the CNS :-- occur due to overdose with narcotic or with other respiratory center depressents(it may suppress the drive to breathe.so respiration slowed and CO2 excreation is insufficient.resulting in increased PaCO2.) brain infarction and head injury( medulla cannot alter the RR in response to the change in PaCO2) and spinalcord injuries(that limit innervations to respiratory muscle. 3. Abnormalities of the chest wall :--in conditions like flail chest, fractures(rib),soft tissue injury,pain (prevent the normal rib cage expansion because of pain mechanical restriction and muscle spasm results in inadequate gas exchange), kyphoscoliosis ( the change in spinal configuration compresses the lung and prevent the normal expansion of the chest wall), massive obesity (wt of chest and abdominal contents may limit the lung expansion) causes respiratory failure cause these are limit the lung expansion or diaphragmatic movement and consequently gas exchange. 4. Neuromuscular conditions :--GBS,muscular dystrophy ,multiple sclerosis(because of underlying neuromuscular conditions respiratory muscle weakness or paralysis occurs,preventing normal CO2 excretion.dysfunction may br slowly progressive [muscular dystrophy ,multiple sclerosis],progressive with no potential of recovery [ALS],rapid with good expectation of recovery[GBS] or stable for extended periods

of time[ Poliomyelitis,myasthenia gravis].in case of cerviacal cord injury and phrenic nerve injury neural control is lost ,preventing the use of diaphragm ,the major muscle for respiration .sothe patient inspires a smaller TV,which predisposes to an increase in PaCO2.

CLINICAL FEATURES
Specific symptoms Respiratory

HYPOXEMIC RESPIRATORY FAILURE

Dyspnea, :--an uncomfortable sensation of breathing, often accompanies respiratory failure. Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of dyspnea central cyanosis. :-- a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL.. Tachypnoea :--increases the respiratory rate in an effort to blow off accumulated co2 Prolonged expiration (I:E 1:4,1:3) Intercostal muscle retraction Use acessory muscle for respiration Paradoxic chest wall movement

Nonspecific symptoms Cerebral :-- Severe hypoxaemia produces marked cellular hypoxia and
affects most adversely central nervous Anxiety, Restlessness, Agitation Mental confusion Disorientation Confusion Decreased level of consciousness Coma Somnolence . Myoclonus seizures cardiovascular systems :-- The cellular hypoxia depresses myocardial functions Tachycardia and Hypertension :--in response to myocardial hypoxia sympathetic system activated ,results in increased peripheral vascular resistance results in increases the cardiac output &elevated blood pressure.In respons to severe and unrelieved hypoxia, marked depression of mycarditun occurs, ultimately resulting in progressive drop in blood pressure and circulatory failure. Hypotension (late)

Arrhythmias.:-- Severe hypoxia adversely affects the heart also by increasing its ectopic irritability, and thereby may result in various types of arrhythmias

Skin

Cool ,clammy Diaphoretic

Other

Metabolic acidosis ;-- The cellular hypoxia resulting from severe hypoxaemia leads to anaerobic metabolism with consequent production of large amounts of lactic and pyruvic acids. The resulting metabolic acidosis has a narcotic effect and further depresses central nervous system Fatigue . Polycythemia is a complication of long-standing hypoxemia

HYPERCAPNIC RESPIRATORY FAILURE

specific
Respiratory Dyspnea decreased RR or rapid rate with shallow respiration
decreased TV decreased minute ventilation Non specific

CEREBRAL ; dilatation of cerebral vessels produces headache, restlessness, muscle twitchings, flapping tremors and even convulsions. Papilloedema may also occur and (coupled with headache) may mimic intracranial space occupying lesion. The depressant action on the nervous system initially results in a varying degree of confusion, impaired memory, disturbance in sleep and behaviour and flapping tremors.
Morning headache Disorientation Progressive somnolence Coma

CARDIAC Carbondioxide is a very potent vasodilator and produces generalised dilationof vessels. The patient therefore develops full and bounding pulse, flushed facies and warm sweating hands. Arrythmia Hypertension :-- Hypotension may, however, be more than compensated by stimulation of sympathetic nervous system as a result of both hypoxia and hypercapnia; Tachycardia

NEUROMUSCULAR Muscle weakness Decrease DTR Tremer Seizures OTHER

Tripod position :--initially have bradypnea ,and increase respiratory rate in an effort to blow off accumulated co2.the position that the patient assume is an indication of the effort associated with breathing.the patient may able to lie down (mild distress),be able to lie down but prefer to sit (moderate distress)or unable to breathe unless sitting upright9severe distress) . a common position is to sit with the arm propped on the overbed table ,this position is called tripod position (it decreases the work of breathing ,because propping the arm increases the A-P diameter of the chest and changes pressure in the thorax. Pursed lip breathing:--this causes an increase in SaO2 because it slows the respiration, allows more time for expiration and prevent the small bronchioles from collapsing, thus facilitating air exchange. Number of pillows ;-- Number of pillows the patient requires to breath ,it may be documented as 1 ,2 ,3 or 4 pillow orthopnea

Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis. Both confusion and may occur in respiratory failure. Myoclonus and seizures may occur with severe hypoxemia. Polycythemia is a complication of long-standing hypoxemia. Pulmonary hypertension frequently is present in chronic respiratory failure. Alveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of the affected smooth muscles and narrowing of the pulmonary arterial bed. The increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure. This, in turn, causes enlargement of the liver and peripheral edema. The entire sequence is known as cor pulmonale. Criteria for the diagnosis of acute respiratory distress syndrome Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis) Radiologic appearance - Three-quadrant or 4-quadrant alveolar flooding Lung mechanics - Diminished compliance (< 40 mL/cm water) Gas exchange - Severe hypoxia refractory to oxygen therapy (PaO2/FIO2 < 200) Normal pulmonary vascular properties - Pulmonary capillary wedge pressure of less than 18 mm Hg

Diagnostic studies

A complete blood count :-- anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure. A Blood chemistry :--Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function. Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase with a normal troponin I may indicate myositis, which occasionally can cause respiratory failure. In chronic hypercapnic respiratory failure, serum thyroid-stimulating hormone should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure. Chest radiography is essential ;-- distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult. Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS). Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected. The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest acute respiratory distress syndrome (ARDS). Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure. it also may detect dysrhythmias resulting from severe hypoxemia and/or acidosis.

Chest radiograph

Echocardiography

Other Tests Patients with acute respiratory failure generally are unable to perform pulmonary function tests (PFTs). However, PFTs are useful in the evaluation of chronic respiratory failure.

Normal values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. A decrease in FEV1 -to-FVC ratio indicates airflow obstruction, whereas a reduction in both the FEV1 and FVC and maintenance of the FEV1 -to-FVC ratio suggest restrictive lung disease. Respiratory failure is uncommon in obstructive diseases when the FEV1 is greater than 1 L and in restrictive diseases when the FVC is more than 1 L.

MANAGEMENT Respiratory therapy

Mechanical Ventilator

Endotracheal intubation and mechanical ventilation may be required. Respiratory stimulants such as doxapram may be used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote such as naloxone or flumazenil will be given.
Mechanical ventilation is used for 2 essential reasons: (1) to increase PaO2 (2) to lower PaCO2.

Ventilator

Right heart catheterization This remains a controversial issue in the management of critically ill patients. Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, adequacy of volume resuscitation, and systemic oxygen delivery remain, right heart catheterization should be considered. Measurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema. The pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function. Extracorporeal Membrane Oxygenator (ECMO)

The extracorporeal membrane oxygenator (ECMO) is essentially an artificial lung. It is an appropriately cased artificial membrane which is attached to the patient externally (extracorporeally), through a vein or artery. Although the best substitute for a diseased lung that cannot handle gas exchange adequately is a healthy human lung, such substitution is often not possible. Circulating the patient's blood through the ECMO offers another approach. Gas exchange using ECMO keeps the patient alive while the damaged lungs have a chance to heal. ECMO seems to be an effective option in some infants with respiratory failure when treatment with mechanical ventilation fails.
Pharmacologic Therapy
Antibiotics help when infections (sepsis) as well as pneumonia are involved in respiratory failure.

Bronchodilators, for example, theophylline compounds, to relieve bronchospasm. Aminophylline. This is a potent bronchodilator and should be given

initially in a loading dose of 5-6 mg/kg IV over 10-15 minutes. This may be repeated every 8-12 hours as required provided the systolic pressure is adequate (over 100 mm Hg) every time the drug is administered
sympathomimetic agents (albuterol, metaproterenol, isoproterenol), anticholinergics (ipratropium bromide), corticosteroids, reverse bronchoconstriction and reduce tissue inflammation. Eg:--methylprednisolone. In cases with moderate degree of

respiratory failure, oral corticosteroid therapy in the form of prednisolone 20-40 mg daily in divided doses in usually adequate.
Diuretic :--furosemide Digitalis, improve cardiac output, and drugs which increase blood pressure in shock can improve blood flow to the tissues. Anxiolytics

Liquefaction of Secretions. Attempt should be made to liquefy the secretions in the respiratory passages by ensuring adequate fluid intake and proper humidification of the inspired gas. Acetylcystine (Airbron) is a useful mucolytic agent and can be aerosolized in a dose of 3-5 ml of 20 percent solution four times a day. If tracheostomy has been done, the dnig is better instilled directly through the tracheostomy opening in a dose of 1-2 ml of a ten percent solution every 3-4 hours. Respiratory Stimulants. The use of respiratory stimulants in respiratory failure is controversial. The two commonly used drugs are nikethamide (Coramine) and Micoren. Both drugs not only stimulate the respiratory centre but also produce

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NURSING MANAGEMENT Nursing Assessment 1. Obtain history from the client as to the onset and progression of symptoms. 2. Assess respirations for dyspnea and pain that increases with inspiration. 3. Assess for headache, confusion, restlessness, and increased heart rate. 4. Assess sputum for quantity and characteristics. Nursing Diagnosis Goals 1. Prevent avoidable injury. 2. Maintain effective airway clearance and gas exchange. 3. Increase comfort. 4. Reduce anxiety. 5. Maintain adequate nutritional status. 6. Increase understanding of the disease process, its treatment, and prevention Impaired gas exchange related to loss of functioning lung tissue and inadequate ventilation/perfusion ratio as evidenced by laboured breathing

Ineffective Breathing Pattern related to damage of alveolar capillary membrane as evidenced by Dyspnea ,Crackles ,Cough
Ineffective airway clearance related to excessive secreations as evidencd by rhonchi ,crackles etc

Risk for decreased cardiac output related to mechanical ventilation

Ineffective tissue perfusion: Cardiopulmonary related to decreased CO as evidenced by multiple organ failure. Risk for impaired skin integrity related to prolonged bed rest Risk for infection related to impaired immune mechanisms as evidenced by decreased immune tolerance Ineffective individual coping related to sudden change in life style

Anxiety related to oxygen deprivation as evidenced by expression of patient Fatigue related to oxygen deprivation as evidenced by expression of patient Fear related to air hunger and mechanical ventilation as evidenced by expression of patient Impaired physical mobility related to activity intolerance Impaired verbal communication related to breathing difficulty

Nursing Assessment

Assess respirations: note quality, rate, pattern, depth, and breathing effort. Both rapid, shallow breathing patterns and hypoventilation affect gas exchange. Shallow, "sighless" breathing patterns postsurgery (as a result of effect of anesthesia, pain, and immobility) reduce lung volume and decrease ventilation. Assess lung sounds, noting areas of decreased ventilation and the presence of adventitious sounds. Assess for signs and symptoms of hypoxemia: tachycardia, restlessness, diaphoresis, headache, lethargy, and confusion. Assess for signs and symptoms of atelectasis: diminished chest excursion, limited diaphragm excursion, bronchial or tubular breath sounds, rales, tracheal shift to affected side. Collapse of alveoli increases physiological shunting. Assess for signs or symptoms of pulmonary infarction: cough, hemoptysis, pleuritic pain, consolidation, pleural effusion, bronchial breathing, pleural friction rub, fever. Monitor vital signs. With initial hypoxia and hypercapnia, blood pressure (BP), heart rate, and respiratory rate all rise. As the hypoxia and/or hypercapnia becomes more severe, BP may drop, heart rate tends to continue to be rapid with arrhythmias, and respiratory failure may ensue with the patient unable to maintain the rapid respiratory rate. Assess for changes in orientation and behavior. Restlessness is an early sign of hypoxia. Chronic hypoxemia may result in cognitive changes such as memory changes. Monitor ABGs and note changes. Increasing PaCO2 and decreasing PaO2 are signs of respiratory failure. As the patient begins to fail, the respiratory rate will decrease and PaCO2 will begin to rise. Some patients, such as those with COPD, have a significant decrease in pulmonary reserves, and any physiological stress may result in acute respiratory failure. Assess skin color for development of cyanosis. For cyanosis to be present, 5 g of hemoglobin must desaturate. Monitor chest x-ray reports. Chest x-rays may guide the etiological factors of the impaired gas exchange. Keep in mind that radiographic studies of lung water lag behind clinical presentation by 24 hours.

Monitor effects of position changes on oxygenation (SaO2, ABGs, SVO2, and end-tidal CO2). Putting the most congested lung areas in the dependent position (where perfusion is greatest) potentiates ventilation and perfusion imbalances. Assess patients ability to cough effectively to clear secretions. Note quantity, color, and consistency of sputum. Retained secretions impair gas exchange.

Plan of action
1. Provide a quiet, supportive environment. 2. Assess, record, and report all deviations from baseline evaluation and document complaints of increased discomfort and difficulty breathing. 3. Encourage bed rest in semi to high Fowler position, allow frequent uninterrupted rest periods in between therapeutic interventions. 4. Monitor vital signs, breath sounds, heart sounds, neurological status, and signs of hypoxia every 1 to 2 hours depending on status acuity. 5. Monitor need for suctioning secretions when client is unable to clear on his own. 6. Administer prescribed bronchodilators, be alert for potential side effects. 7. Prepare the client and family for intubation and mechanical ventilation. 8. Monitor arterial blood gases (ABGs). 9. Stabilize the endotracheal (ET) tube for comfort and assess skin integrity around mouth for irritation. 10. Suction via ET tube as needed, evaluate lung sounds and quality of mechanical ventilation. 11. Monitor renal status for fluid imbalance, assess intake and output with quality and quantity of urine. 12. Assure that the client maintains adequate nutritional status, whether by parenteral nutrition (TPN) or tube feedings as prescribed by physician. 13. Turn every 2 hours to prevent skin breakdown, hemostasis, and pooling of pulmonary secretions. 14. Provide emotional support to the client and family members.

15. Provi Therapeutic Interventions

Maintain oxygen administration device as ordered, attempting to maintain oxygen saturation at 90% or greater. This provides for adequate oxygenation.

For patients who should be ambulatory, provide extension tubing or portable oxygen apparatus. These promote activity and facilitate more effective ventilation. Position with proper body alignment for optimal respiratory excursion (if tolerated, head of bed at 45 degrees). This promotes lung expansion and improves air exchange. Routinely check the patients position so that he or she does not slide down in bed. This would cause the abdomen to compress the diaphragm, which would cause respiratory embarrassment. Position patient to facilitate ventilation/perfusion matching. Use upright, high-Fowlers position whenever possible. High-Fowlers position allows for optimal diaphragm excursion. When patient is positioned on side, the good side should be down (e.g., lung with pulmonary embolus or atelectasis should be up). Pace activities and schedule rest periods to prevent fatigue. Even simple activities such as bathing during bed rest can cause fatigue and increase oxygen consumption. Change patients position every 2 hours. This facilitates secretion movement and drainage. Suction as needed. Suction clears secretions if the patient is unable to effectively clear the airway. Encourage deep breathing, using incentive spirometer as indicated. This reduces alveolar collapse. For postoperative patients, assist with splinting the chest. Splinting optimizes deep breathing and coughing efforts. Encourage or assist with ambulation as indicated. This promotes lung expansion, facilitates secretion clearance, and stimulates deep breathing. Provide reassurance and allay anxiety:

Have an agreed-on method for the patient to call for assistance (e.g., call light, bell). Stay with the patient during episodes of respiratory distress.

Anticipate need for intubation and mechanical ventilation if patient is unable to maintain adequate gas exchange. Early intubation and mechanical ventilation are recommended to prevent full decompensation of the patient. Mechanical ventilation provides supportive care to maintain adequate oxygenation and ventilation to the patient. Treatment also needs to focus on the underlying causal factor leading to respiratory failure. Administer medications as prescribed. The type depends on the etiological factors of the problem (e.g., antibiotics for pneumonia, bronchodilators for COPD, anticoagulants/thrombolytics for pulmonary embolus, analgesics for thoracic pain).

Education/Continuity of Care
Explain the need to restrict and pace activities to decrease oxygen consumption during the acute episode. Explain the type of oxygen therapy being used and why its maintenance is important. Issues related to home oxygen use, storage, or precautions need to be addressed. Teach the patient appropriate deep breathing and coughing techniques. These facilitate adequate air exchange and secretion clearance. Assist patient in obtaining home nebulizer, as appropriate, and instruct in its use in collaboration with respiratory therapist. Refer to home health services for nursing care or oxygen management as appropriate.

Conclusion Acute respiratory failure is a process that, if not recognised and treated early, can be fatal. Many patients are at risk for a variety of reasons so the key element is early recognition, assessment and management.Treating acute respiratory failure and any respiratory disease needs a multidisciplinary, collaborative approach. Nurses are in an ideal position to assess patients risk of developing respiratory failure, to monitor them, and evaluate their care and coordinate a multidisciplinary approach

ACUTE RESPIRATORY DISTRESS SYNDROME INTRODUCTION Patients developing ARDS are critically ill, often with multisystem organ failure, and they may not be capable of providing historical information. Typically, the illness develops within 12-48 hours after the inciting event, although, in rare instances, it may take up to a few days.With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen. History Since World War I, it has been recognized that some patients with nonthoracic injuries, severe pancreatitis, massive transfusion, sepsis, and other conditions develop respiratory distress, diffuse lung infiltrates, and respiratory failure, sometimes after a delay of hours to days. Ashbaugh et al described 12 such patients in 1967, using the term adult respiratory distress syndrome to describe this condition. American-European Consensus Conference (AECC) on acute respiratory distress syndrome (ARDS). The term acute respiratory distress syndrome was used instead of adult respiratory distress syndrome because the syndrome occurs in both adults and children. DEFINITION The AECC defined ARDS as an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema. (AECC) ARDS is characterised by increased permeability of the alveolar capillary membrane,diffuse alveolar damage and the accumulation of proteinaceous pulmonary edema. (HARRISON) ARDS is the sudden and progressive form of acute respiratory failure in which alveolar capillary membrane becomes damaged and more permeable to intravascular fluid,resulting in dyspnea ,hypoxemia refractory to supplemental o2 redused lung compliance and diffuse pulmonary infiltrates. (LEWIS) Acute respiratory distress syndrome (ARDS) is characterized by the development of acute dyspnea and hypoxemia within hours to days of an inciting event, such as trauma, sepsis, drug overdose, massive transfusion, acute pancreatitis, or aspiration. In many cases, the inciting event is obvious, but, in others (eg, drug overdose), it may be harder to identify (NET) INCIDENCE Age ARDS may occur in people of any age. Its incidence increases with advancing age,306 cases per 100,000 person-years in those between the ages of 75 and 84 years. Sex For ARDS associated with sepsis and most other causes, no differences in the incidence between males and females appear to exist. However, in trauma patients only, the incidence of the disease may be slightly higher among females.

Genetic factors A study by Glavan et al examined the association between genetic variations in the FAS gene and ALI susceptibility. PREDISPOSING FACTORS Direct Lung Injury Common causes

viral or bacterial Pneumonia Aspiration of gastric contents or other substance Pulmonary contusion Chest truma Embolism:--fat,air,amniotic fluid Near-drowning Toxic inhalation injury O2 toxicity Radiation pneumonitis

Less common causes

Indirect Lung Injury Common causes Sepsis (gram ve infection) Severe trauma Less common causes

Multiple bone fractures Flail chest Head trauma Burns Multiple blood transfusions Drug overdose with narcotics (heroin) 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 to development of ARDS. Pancreatitis Post-cardiopulmonary bypass Anaphylaxis DIC Shock cigarette smoking alcohol use. Staging

In the 1980s, Murray and coworkers developed a lung injury scoring system, which has proven helpful in clinical research on ARDS. This system was based on the following 4 parameters: Severity of consolidation based on chest radiograph findings

Severity of hypoxemia based on the PaO2/FIO2 ratio Lung compliance level of PEEP required

Pathophysiology
Compensatory Mechanisms in presence of respiratory failure: The response to hypoxaemia depends on the ability of the patient to recognize the hypoxemic state and then to increase cardiac output and minute ventilation to improve the situation. Peripheral chemoreceptors located in the arch of aorta and at the bifurcation of carotid artery send afferent signals to the brain.Rate This Article:

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The pathophysiological changes in ARDS are divided into 3 phases 1 Injury or exudative phase :--occures 1-7 days after initial lung injury This phase results from direct injury to alveolar capillary membrane or host insult.neutrophils adhere to the pulmonary microcirculation ,causing damage to the vascular endothelium and increased capillary permeability. This will cause interstitial edema.fluid from the interstitial space crosses the alveolar epithelium and enters the alveolar occurs space.alveolar edema occurs when the fluid crosses the blood-gas barrier. Alveolar type1 and type 2 cells which produce surfactant are damaged by changes caused by ARDS.in addition to further fluid and protein accumulation this damage results in surfactant dysfunction.the main function of surfactant is to maintain alveolar stability by decreasing alveolar surface tension and preventing alveolar collapse .decreased synthesis of surfactant and inactivation of existing surfactant cause the alveoli to become collapse.it will decrease lung compliance,compromise gas exchange,and contributes to hypoxemia.in this stage hyaline membrane begins to line the alveoli. hyaline membrane is composed of necrotic cells,protein and fibrin and lies adjacent to the alveoli wall. This hyaline membrane contribute to the development of fibrosis and atlectasis.the primary pathophysiologic changes in this phase are interstitial and alveolar edema (non cardiogenic pulmonary edema.) and atletasis. The patient may generate high air way pressure to inflate stiff lung.as a compensatory mechanism juxtacapillary receptors in the stiff lung parenchyma(J reflex) cause an increase in RR and decrease in TV.this breathing pattern increase co2 removal ,producing respiratory alkalosis.as the atlectasis , pulmonary edema or shunt increases compensation fails and results in hypoventilation decreased CO and decreased tissue o2 perfution eventually occurs . 2 Reparative or proliferative phase :-- occures 1-2 weeks after initial lung injury In this phase there is an influx of neutrophils ,monocytes ,lymphocyte and fibroblast proliferation as a part of the inflammatory response. This phase is complete when the diseased lung become characterised by dense,fibrouse tissue.increased pulmonary vascular resistance and pulmonary hypertension may occure in this stage.because fibroblast and inflammatory cells destroys the pulmonary vasculature.lung compliance is continues to decrease as a result of interstitial fibrosis.hypoxemia worson because of thickend alveolar membrane, causing diffusion limitation and shunting.if this phase persist wide spread fibrosis result.if it is arrested,the lesion resolved. 3 Fibrotic phase ;-- occurs 2-3 weeks after initial lung injury

This phase is also called late phase of ARDS .here the lung is completely remodelled by sparsely collagenous and fibrous tissue.there is diffuse scaring and fibrosis,resulting in decreased lung compliance.in addition surface area of gas exchange is slightly reduced because the interstitium is fibrotic and therefore hypoxemia continues.pulmonary hypertension result from pulmonary vascular destruction and fibrosis. CLINICAL FEATURES Physical findings often are nonspecific and include febrile or hypothermic. Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. SKIN :--Cyanosis of the lips and nail beds may occur. Pallor may be present Lungs :-- may reveal bilateral rales. Rales may not be present despite widespread involvement. Because the patient is often intubated and mechanically ventilated, decreased breath sounds over 1 lung may indicate a pneumothorax or endotracheal tube down the right main bronchus. tachypnea, dyspnoea,cough and restlessness are the initial symptom.chest auscultation may reveal fine scattered crackles.as progresses intercostals and suprasternal retraction may be seen. ABG :--mild hypoxemia nd respiratory alkalosis (due to hypoxemia and stimulation of juxta capillary receptors. CNS ;--changes in sensorium,decreased mentation Manifestations of the underlying cause (eg, acute abdominal findings in the case of ARDS caused by pancreatitis) are present. Infection :--In a septic patient without an obvious source, pay careful attention during the physical examination to identify potential causes of sepsis. Carefully examine sites of intravascular lines, surgical wounds, drain sites, and decubitus ulcers for evidence of infection. Cardiac :--Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, tachycardia, cardiac murmurs and gallops, hepatomegaly, and edema. DIAGNOSIS

1. 2. 3.

Arterial blood gas analysis :-- hypoxemia (reduced levels of oxygen in the blood),Respiratory alkalosis.normal or decreased PaCO2 Refractory hypoxemia :-- PaO2 <50mmhg on FIO2 >40% with PEEP >5 cm water ,PaO2/FIO2 <200 complete blood count may be taken. The number of white blood cells is increased in sepsis. Thrombocytopenia may be observed in septic patients in the presence of disseminated intravascular coagulation (DIC). Von Willebrand factor (VWF) may be elevated in patients at risk for ARDS and may be a marker of endothelial injury. Chest x-ray will show the presence of fluid in the lungs. cest x ray often termed as whiteout or white lung.because bilateral interstitial and alveolar infiltrates and consolidation are wide spread throughout lungs,leaving few recognizable air spaces.

CT scan of the chest may be required only in some situations (routine chest x-ray is sufficient in most cases). CT scanning is more sensitive than plain chest radiography in detecting pulmonary interstitial emphysema, pneumothoraces and pneumomediastinum, pleural effusions, cavitation, and mediastinal lymphadenopathy. Echocardiogram (an ultrasound of the heart) may help exclude any heart problems that can cause fluid build-up in the lung. Monitoring with a pulmonary artery catheter may be done to exclude a cardiac cause for the difficulty in breathing. Pulmonary artery wedge pressure 18mmof hg or less Bronchoscopy (a procedure used to look inside the windpipe and large airways of the lung) may be considered to evaluate the possibility of lung infection. PaO2/FIO2 <200 despite increased FIO2 by mask cannula or endotracheal tube are hallmark of ARDS. Hepatic - Liver function abnormalities may be noted in either a pattern of hepatocellular injury or cholestasis. Cytokines - Multiple cytokines, such as interleukin (IL)1, IL-6, and IL-8, are elevated in the serum of patients at risk for ARDS. Open lung biopsy is reserved for cases when diagnosis is difficult ot establish

TREATMENT Medical Treatment for ARDS Persons with ARDS are hospitalized and require treatment in an intensive care unit. No specific therapy for ARDS exists.
1.

2. 3. Respiratory therapy supplemental oxygen positioning strategies mechanical respirator and oxygen administration :-

by face mask, nasal cannula are inadequate.mask with high flow system that deliver high o2 concentration are used . moniter pulse oxymetry to assess effectiveness of o2 therapy.

mechanical ventilation Tracheostomy The treatment of ARDS itself is medical. However, as previously noted, surgical intervention may be required for some of the underlying causes of ARDS. In patients requiring prolonged mechanical ventilation, tracheostomy is eventually necessary. positioning strategies:-1. prone positioning ;-- show marked improvement in PaO2 (PaO2 70 mmhg in

supine,PaO2 90 mmhg in prone). In this position air filled ,nonatelectic alveoli in the anterior portion of the lung become dependent.perfusion may be better matched with ventilation, causing less v/q mismatch. 2. Lateral rotation therapy :-- purpose is to provide continuous ,slow, side to side turning of the patient by rotating the actual bed frame.lateral movement of the bed maintained for 18 of every 24 hrs to simulate postural drainage andhelp to mobilize

pulmonary secreation .this type of bed may contain vibrator pack to provide chest physical therapy .base line RR,rhythm,,breath sounds,ABG and SpO2 obtained before therapy and continued throughout therapy Medications for ARDS The following drugs may be administered:
Antibiotics to treat infection

Anti-inflammatory drugs, such as corticosteroids, to reduce inflammation in the lungs in the late phase of ARDS or sometimes if the person is in septic shock Diuretics to eliminate fluid from the lungs
Drugs to counteract low blood pressure that may be caused by shock

Anti-anxiety drugs to relieve anxiety Inotropic ;--dopamine, dobutamine Inhaled drugs administered by respiratory therapists to open up the airways (bronchodilators) Packed RBC may be administred to increase Hb if < 9-10 g/dl Fluid balance
Intravenous fluids are given to provide nutrition and prevent dehydration, and are

carefully monitored to prevent fluid from accumulating in the lungs (pulmonary edema). PAWP kept as low as possible with out impairing CO to limit pulmonary edema. Patient may placed in mild fluid restriction ,diuretic are used as necessary. Nutritional Support Institution of nutritional support after 48-72 hours of mechanical ventilation usually is recommended. Enteral nutrition via a feeding tube is preferable to IV hyperalimentation unless it is contraindicated because of an acute abdomen, ileus, GI bleeding, or other conditions. A low-carbohydrate high-fat enteral formula including anti-inflammatory and vasodilating components (eicosapentaenoic acid and linoleic acid) along with antioxidants has been demonstrated to improve outcome in ARDS. Activity Restriction Patients with ARDS are on bed rest. Frequent position changes should be started immediately, as should passiveand, if possible, activerange-of-motion activities of all muscle groups. Elevation of the head of the bed to a 45 angle is recommended to diminish the development of VAP. Invasive Hemodynamic Monitoring Because the differential diagnosis of ARDS includes cardiogenic pulmonary edema, hemodynamic monitoring with a pulmonary artery (Swan-Ganz) catheter may be helpful in selected cases for distinguishing cardiogenic from noncardiogenic pulmonary edema. The pulmonary artery catheter is floated through an introducer that is placed in a central vein, usually the right internal jugular or subclavian vein. With the balloon inflated, the catheter is advanced with continuous pressure monitoring. This allows measurement of right atrial pressure, right ventricular pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure (PCWP). PCWP lower than 18 mm Hg is usually consistent with noncardiogenic pulmonary edema, although other factors, such as a low plasma oncotic pressure, may allow cardiogenic pulmonary edema to occur at lower pressures.

Prevention of ARDS Because aspiration is a risk factor for ARDS, taking appropriate measures to prevent aspiration, such as elevation of the head of the bed, may prevent some cases of ARDS Prognosis Until the 1990s, most studies reported a 40-70% mortality rate for ARDS. However, 2 reports in the 1990s, suggested much lower mortality rates, in the range of 30-40%.Possible explanations for the improved survival rates may be better understanding and treatment of sepsis, recent changes in the application of mechanical ventilation, and better overall supportive care of critically ill patients. Note that most deaths in ARDS patients are attributable to sepsis (a poor prognostic factor) or multiorgan failure rather than to a primary pulmonary cause, although the recent success of mechanical ventilation using smaller tidal volumes may suggest a role of lung injury as a direct cause of death. Mortality in ARDS increases with advancing age. The study performed in King County, Washington, found mortality rates of 24% in patients between ages 15 and 19 years and 60% in patients aged 85 years and older. The adverse effect of age may be related to underlying health status.

Complications
Respiratory complications ;- high mean airway pressures; thus, barotrauma may occur. Patients present with pneumomediastinum, pneumothorax, or both. Other potential complications that may occur in these mechanically ventilated patients include accidental extubation and right mainstem intubation. If prolonged mechanical ventilation is needed, patients may eventually require tracheostomy. With prolonged intubation and tracheostomy, upper airway complications may occur, most notably postextubation laryngeal edema and subglottic stenosis. O2 toxicity,pulmonary emboli,pulmonary fibrosis GIT ;--paralytic ileus,pneumo peritoneum,stress ulseration and hemorrhage. Stress ulcer prophylaxis is indicated for these patients. Anemia may be prevented by the use of growth factors (epopoietin). Renal :--Renal failure is a frequent complication of ARDS, particularly in the context of sepsis. Renal failure may be related to hypotension, nephrotoxic drugs, or underlying illness. Fluid management is complicated in this context, especially if the patient is oliguric. Cardiac complication ;--arrythmias ,decreased CO Haematological complications : -anemia ,DIC, Thrombocytopenia Multisystem organ failure, rather than respiratory failure alone, is usually the cause of death in ARDS. ET intubation complication :--laryngeal ulseration ,tracheal malacia.tracheal stenosis, tracheal ulceration Infections :-- include urinary tract infection (UTI) related to the use of urinary catheters and sinusitis related to the use of nasal feeding and drainage tubes. Patients may also develop Clostridium difficile colitis as a complication of broad-spectrum antibiotic therapy. Patients with ARDS, because of the extended intensive care unit (ICU) stay and treatment with multiple antibiotics, may also develop infections with drug-resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE). Nosocomial pneumonia, and sepsis. Because patients with ARDS often require prolonged mechanical ventilation and invasive hemodynamic monitoring, they are at risk for serious nosocomial infections, including ventilator-associated pneumonia (VAP) and line sepsis. The incidence of VAP in ARDS patients may be as high as 55% and appears to be higher than that in other populations requiring mechanical ventilation. Preventive strategies

including elevation of head of the bed, use of subglottic suction endotracheal tubes, and oral decontamination. Functional impairment :-- primarily related to muscle wasting and weakness. Corticosteroid treatment and use of neuromuscular blockade are risk factors for muscle weakness and poor functional recovery. difficulty weaning from mechanical ventilation. Strategies to facilitate weaning, such as daily interruption of sedation, early institution of physical therapy, attention to maintaining nutrition, and use of weaning protocols, may decrease the duration of mechanical ventilation and facilitate recovery. NURSING MANAGEMENT
Nursing diagnosis for Acute respiratory distress syndrome ARDS

1. Ineffective Breathing Pattern related to damage of alveolar capillary membrane as 2. Impaired gas exchange related to ventilation perfusion mismatch as evidenced by irregular breathing pattern
,cough etc

evidenced by Dyspnea ,Crackles ,Cough

Nursing outcomes

3. Ineffective airway clearance related to excessive secreations as evidencd by rhonchi ,crackles etc 4. Risk for decreased cardiac output related to mechanical ventilation 5. Ineffective tissue perfusion: Cardiopulmonary related to decreased CO as evidenced by multiple organ failure. 6. Risk for impaired skin integrity related to prolonged bed rest 7. Risk for infection related to impaired immune mechanisms as evidenced by decreased immune tolerance 8. Anxiety related to disease process as evidenced by verbalisation of patient 9. Fatigue related to disease process 10. Ineffective individual coping related to sudden change in life style
The patient will maintain adequate ventilation and oxygenation The patient will maintain a patent airway. The patient will maintain adequate cardiopulmonary perfusion The patient will express feelings of reduced anxiety. The patient will remain hemodynamically stable. The patient will verbalize the importance of balancing activity with adequate rest periods. The patient will discuss fears or concerns. The patient will maintain joint range-of-motion and muscle strength. The patient will use alternate means of communication. The patient will use support systems to assist with coping. The patient will maintain skin integrity. The patient will remain free from signs or symptoms of infection.

Nursing Interventions Maintain respiration Respiratory Monitoring: Collection and analysis of patient data to ensure airway patency and adequate gas exchange Oxygen Therapy: Administration of oxygen and monitoring of its effectiveness Airway Management: Facilitation of patency of air passages Exercise Therapy: Use of active or passive body movement to maintain or restore flexibility; use of specific activity or exercise protocols to enhance or restore controlled body movement, etc. Pain Management: Alleviation of pain or a reduction in pain to a level of comfort acceptable to the patient

Cough Enhancement: Promotion of deep inhalation by the patient with subsequent generation of high intrathoracic pressures and compression of underlying lung parenchyma for the forceful expulsion of air Suction the airway Maintaining circulation Hemodynamic Regulation: Optimization of heart rate, preload, afterload, and contractility Cardiac Care: Limitation of complications resulting from an imbalance between myocardial oxygen supply and demand for a patient with symptoms of impaired cardiac function Circulatory Care: Mechanical Assist Devices: Temporary support of the circulation through the use of mechanical devices or pumps Anxiety Reduction

Energy Management: Regulating energy use to treat or prevent fatigue and optimize function Minimizing apprehension, dread, foreboding, or uneasiness related to an unidentified source or anticipated danger Calming Technique: Reducing anxiety in patient experiencing acute distress Security Enhancement: Intensifying a patients sense of physical and psychological safety Exercise Promotion: Facilitation of regular physical exercise to maintain or advance to a higher level of fitness and health Coping Enhancement: Assisting a patient to adapt to perceived stressors, changes, or threats that interfere with meeting life demands and roles Decision-Making Support: Providing information and support for a person who is making a decision regarding healthcare Communication Enhancement: Speech Deficit: Assistance in accepting and learning alternative methods for living with impaired speech Communication Enhancement: Hearing Deficit: Assistance in accepting and learning alternative methods for living with diminished hearing Active Listening: Attending closely to and attaching significance to a patients verbal and nonverbal messages

Maintain nutrition Nutrition Management: Assisting with or providing a balanced dietary intake of foods and fluids Fluid/Electrolyte Management: Promotion of fluid/electrolyte balance and prevention of complications resulting from abnormal or undesired fluid/serum electrolyte levels Maintain skin integrity Skin Surveillance: Collection and analysis of patient data to maintain skin and mucous membrane integrity Pressure Management: Minimizing pressure to body parts Pressure Ulcer Prevention: Prevention of pressure ulcers for a patient at high risk for developing them Infection Protection: Prevention and early detection of infection in a patient at risk Infection Control: Minimizing the acquisition and transmission of infectious agents. Maintain activity

Assess the level of activity restriction Limit activity based on level of distress Assist the patient to do ADLs Take rest in between activities Advise to stop activity when fatigued

RESEARCH STUDY

A study by Lakhal et al determined that respiratory pulse pressure variation fails to predict fluid responsiveness in patients with ARDS.[29] Careful fluid challenges may be a safer alternative. Noninvasive Ventilation Because intubation and mechanical ventilation may be associated with an increased incidence of complications, such as barotrauma and nosocomial pneumonia, noninvasive ventilation by means of a full face mask attached to a ventilator delivering continuous positive airway pressure (CPAP), with or without ventilator breaths or inspiratory pressure support (ie, noninvasive positive pressure ventilation [NIPPV]), may be advantageous in patients with milder ARDS. Noninvasive ventilation has been studied best in patients with hypercapnic respiratory failure caused by chronic obstructive pulmonary disease (COPD) or neuromuscular weakness; however, in a small series of patients with ARDS, the use of this technique may have allowed some patients to avoid intubation. This may be an especially useful approach in immunocompromised patients.

BIBLIOGRAPHY
TEXTS
1. HEITKEMBER LEWIS (2004), Medical surgical nursing; 6th edition 2.

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.Mosby publishers,Missouri.Page:1732-1739 HAWKS BLACK (2002), Medical surgical nursing Clinical management for prospective outcome; 7th edition.Elsevier publication. Page: 2352-2357 WILLIAMS&WILKINS LIPPINCOTT(2005),Pathophysiology A 2- in -1 Reference for nurses;6th edition,Wolters kluwer company, Philadelphia,Page: 234-237 WILLIAMS&WILKINS LIPPINCOTT (2002) Manual of nursing practice;3rd edition; Wolters kluwer company, Philadelphia.Page: 534-544 SHAFERS (1995) Medical surgical nursing5th edition,BI publications,page:-de654-658 DAVIDSONS(2002) Principles and practice of medicine;19th edition,Churchhill Livingstone,Philadelphia; page;1034-1036 BT Basavanthappa(2005) Medical surgical nursing5th edition;Jaypee publishers,Newdelhi; Page: 494-495

JOURNALS
1. The Lancet, Volume 298, Issue 7729, Pages 861-863 2. Indian journal of medical research respiratory volume (3) page: 453-463

1.

WEBSITE www.rand.resp .org

2. www.breathing.org

3. www.niams.nih.gov --