Oxygen Insufficiency

OXYGEN INSUFFICIENCY

INTRODUCTION When there is an inadequate supply of oxygen to tissue its called hypoxia which causes an impairment or reduction in partial pressure of oxygen, inadequate oxygen transport, or the inability of the tissues to use oxygen. When the oxygen carrying capacity of the blood is reduced, it prevents the blood from being adequately oxygenated and results in tissue death. Severe hypoxia oxygen deficiency causes reduced human body function and brain death. INSUFFICIENCY It is the inability to perform properly an allotted function. 1) Pulmonary insufficiency Insufficiency of the pulmonary valve, permitting blood to flow into the right ventricle of the heart 2) Respiratory insufficiency Failure to adequately provide oxygen to cells of the body and to remove excess carbon dioxide from them APPLICATION Acute tracheobronchitis: is an acute inflammation of the mucous membranes of the trachea and the bronchial tree, often follows infection of the upper respiratory tract. Pneumonia: is an inflammation of the lung parenchyma that is caused by a microbial agent. Pulmonary tuberculosis: is an infectious disease that primarily affects the lung parenchyma. Lung abscess: is a localized necrotic lesion of the lung parenchyma containing purulent material that collapses and forms a cavity. Pleurisy: is inflammation of both layers of the pleurae (parietal and visceral) Pleural effusion: is a collection of fluid in the pleural space. Empyema: is an accumulation of thick, purulent fluid within the pleural space, often with fibrin development and a loculated (walled-off) area where infection is located. Pulmonary edema: is an abnormal accumulation of fluid in the lung tissue and/or alveolar space. Acute respiratory failure: is a fall in o2 tension (Pao2) to less than 50 mm Hg (hypoxemia) and a rise in arterial co2 tension to greater than 50 mm Hg (hypercapnia). Pulmonary embolism: is the obstruction of the pulmonary artery or one of its branches by a thrombus that originates somewhere in the venous system or in the right side of the heart.

PHYSIOLOGY Air moves in and out of the lungs for the same basic reason that any fluid, that is, a liquid or a gas, moves from one place to another, because its pressure in one place is different from that in the other place. Or stated differently, the existence of pressure gradient (a pressure difference) causes fluid to move. This means that a fluid moves from the area where its pressure is higher to the area where its pressure is lower. Under standard conditions, air in the atmosphere exerts a pressure of 760mm Hg. Air in the alveoli at the end of one expiration and before the beginning of another inspiration also exerts a pressure of 760 mm Hg. When atmospheric pressure is greater than pressure within the lung, air flows down this gas pressure gradient. Then air moves from the atmosphere into the lungs. In other words, inspiration occurs and vice-versa. Respiratory system performs its function by facilitating life-sustaining processes such as 1) Oxygen transport 1

Oxygen is supplied to and co2 is removed from cells by the circulating blood. Cells are in close contact with capillaries whose thin walls permit easy passage or exchange of o2 and co2. The movement of co2 occurs by diffusion. 2) Respiration After these tissue capillary exchanges, blood enters the systemic veins and travels to the pulmonary circulation. Movement of air in and out of the airways (ventilation) continually replenishes the o2 and removes the co2 from the airways in the lung. This whole process of gas exchange between the atmospheric air and blood and between the blood and the cells of the body is called respiration 3) Ventilation During inspiration, air flows from the environment into the trachea, bronchi, bronchioles and alveoli. During expiration, alveolar gas travels the same route in reverse. Physical factors that govern air flow in and out of the lungs are collectively referred to as the mechanics of ventilation and include • Air pressure variances Air flows from a region of higher pressure to a region of lower pressure. During inspiration, movement of the diaphragm and other muscles of respiration enlarge the thoracic cavity and thereby lower the pressure inside the thorax to a level below that of atmospheric pressure. As a result, air is drawn through the trachea and bronchi into the alveoli. During normal expiration, the diaphragm relaxes and the lungs recoil, resulting in a decrease in the size of the thoracic cavity. The alveolar pressure then exceeds atmospheric pressure and air flows from the lungs into the atmosphere. • Airway resistance Any process that changes the bronchial diameter or width affects airway resistance and alters the rate of air flow for a given pressure gradient during respiration. • Compliance A measure of the elasticity, expandability and distensibility of the lungs and thoracic structures is called compliance. CONTROL OF RESPIRATION • • •

Nervous control Chemical control Mechanical control

RESPIRATORY CENTER: Lies in Medulla oblongata & Pons of the Brain Stem Respiratory center can be divided into 3 areas on the basis of their function; a) The medullary rhythmicity area in the medulla oblongata b) The pneumotaxic area in the pins c) The apneustic area also in the pons a) Medullary Rhythmicity Area Its function is to control the basic rhythm of the respiration. Their are inspiratory and expiratory areas within it. During quiet breathing, inhalation lasts for about 2 seconds and exhalation lasts for about 3 seconds. Nerve impulses generated in the inspiratory area establish the basic rhythm of breathing. While the inspiratory area is active, it generates nerve impulses. The impulses propagate to the external intercostal 2

muscles via intercostals nerves and to the diaphragm via the phrenic nerve. When the impulses reach the diaphragm and external intercostals muscles, the muscles contract and inhalation occurs. At the end of the 2 seconds, the inspiratory area becomes inactive and nerve impulses cease. With no impulses arriving, the diaphragm and the external intercostal muscles relax for about 3 seconds, allowing passive elastic recoil of the lungs and thoracic wall. Then the cycle repeats. The neurons of the expiratory area remain inactive during quiet breathing. However, during forceful breathing, nerve impulses from the inspiratory area activate the expiratory area. Impulses from the expiratory area cause contraction of the internal intercostal and abdominal muscles, which decrease the size of the thoracic cavity and causes forceful exhalation. b) Pneumotaxic area Although the medullary rhythmicity area control the basic rhythm of the respiration, other sites in the brain stem help coordinate the transition between inhalation and exhalation. One of these sites is the pneumotaxic area in the upper pons, which transmits inhibitory impulses to the inspiratory area. The major effect of these nerve impulses is to help turn off the inspiratory area before the lungs become too full of air. In other words, the impulses shorten the duration of inhalation. c) Apnuestic area Another part of the brain stem that coordinates the transition between inhalation and exhalation is the apneustic area in the lower pons. This area sends the stimulatory impulses to the inspiratory area that activate it and prolong inhalation. The result is a long deep inhalation. REGULATION OF THE RESPIRATORY CENTRE Cortical influences on respiration Because the cerebral cortex has connections with the respiratory centre, we can voluntarily alter our pattern of breathing. Voluntary control is protective because it enables us to prevent water or irritating gases from entering the lungs. The ability to not breathe, however is limited by the buildup of CO2 and H+ in the body. When Pco2 and H+ concentrations increase to a certain level, the inspiratory area is strongly stimulated, nerve impulses are sent along the phrenic and intercostal nerves to inspiratory muscles, and breathing resumes, whether the person wants it or not. Chemoreceptor regulation of respiration There are sensory neurons that are responsive to chemicals called chemoreceptors. Chemoreceptors in two locations monitors levels of CO2, H+ and O2 and provide input to the respiratory center. Central chemoreceptors are located in or near medulla oblongata in the CNS. They respond to changes in H+ concentration or Pco2 or both, in cerebrospinal fluid. Peripheral chemoreceptors are located in the aortic bodies, clusters of chemoreceptors located in the wall of the arch of the aorta and in the carotid bodies, which are oval nodules in the wall of the arch of the left and right common carotid arteries, where they divide into the internal and external carotid arteries. Normally, the Pco2 in arterial blood is 40 mm Hg. If even a slight increase in Pco2 occurs- a condition called hypercapnia or hypercarbia- the central chemoreceptors are stimulated and resond vigorously to the resulting increase in H+ level. The peripheral chemoreceptors also are stimulated by both the high Pco2 and the rise in H+. IN addition, the peripheral chemoreceptors respond to the deficiency of O2. when PO2 IN arterial blood falls from a normal level of 100 mm Hg but is still above 50 mm Hg , the peripheral chemoreceptors are stimulated. LUNG VOLUMES

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MEASUREMENT

TIDAL VOLUME INSPIRATORY RESERVE VOLUME

EXPIRATORY RESERVE VOLUME

SYMBOL NORMAL VALUE TV

IRV

ERV

RESIDUAL VOLUME RV

500mL

3000mL

DESCRIPTION THE VOLUME OF AIR INHALED EXHALED WITH EACH BREATH.

AND

THE MAXIMUM VOLUME OF AIR THAT CAN BE INHALED AFTER A NORMAL INHALATION.

1100mL

THE MAXIMUM VOLUME OF AIR THAT CAN BE EXHALED FORCIBLY AFTER A NORMALEXHALATION

1200ml

THE VOLUME OF AIR REMAINING IN THE LUNGS AFTER A MAXIMUM EXHALATION

LUNG CAPACITIES

MEASUREMENT

SYMBOL NORMAL VALUE VC

VITAL CAPACITY

THE MAXIMUM VOLUME OF AIR EXHALED FROM THE POINT OF MAXIMUM INSPIRATION VC=TV+IRV+ERV

INSPIRATORY CAPACITY

THE MAXIMUM VALUE OF AIR INHALED AFTER NORMAL EXPIRATION IC=TV+IRV

IC

FUNCTIONAL RESIDUAL CAPACITIY FRC

4600mL

DESCRIPTION

3500mL

THE VOLUME OF AIR REMAINING IN THE LUNGS AFTER A NORMAL EXPIRATION 2300mL

FRV=ERV+RV

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TOTAL CAPACITY

LUNG TLC

5800ml

THE VOLUME OF AIR IN THE LUNGS AFTER A MAXIMUM INSPIRATION TLC=TV+IRV+ERV+RV

FUNCTIONS AFFECTING RESPIRATORY FUNCTION 1. 2. 3. 4.

Physiological Factors Developmental Factors Behavioral Factors Environmental Factors

(a) SIGN AND SYMPTOMS Following are the some of the major sign and symptoms of respiratory disease: 1) 2) 3) 4) 5) 6) 7) 8)

Dyspnea Cough Sputum production Chest pain Wheezing Clubbing of the fingers Hemoptysis Cyanosis

1) DYSPNEA DEFINITION Dyspnea is a condition characterized by shortness of breath or difficult or labored breathing, sometimes accompanied by pain. The intensity of the condition varies from mild to severe, as does the number of episodes a person with dyspnea may experience. The condition can be extremely frightening for patients, though it is typically not life-threatening. CLINICAL MANIFESTATIONS Symptoms of dyspnea can occur when a person is completely at rest as well as during periods of intense exercise. Although shortness of breath remains the primary symptom, the following symptoms may also accompany dyspnea: • • • • • • •

difficult or labored breathing feeling of suffocation inability to get enough air Tightness in the chest A distressed anxious expression Dilated nostrils Protrusion of the abdomen and expanded chest 5

• •

Gasping Cyanosis

CAUSES Dyspnea is caused by insufficient oxygenation of the blood resulting from disturbances in the lungs, low oxygen pressure of air, circulatory disturbances and hemoglobin deficiency. •

Cancerous Causes: Cancerous causes can include a tumor blocking the trachea or bronchus or a tumor that prevents the lungs from fully expanding to take in enough air. People with lung cancer commonly experience dyspnea.

•

Cardiac and Pulmonary Causes: Most causes of dyspnea have roots in a cardiac or pulmonary disorder. Cardiac or pulmonary causes include an accumulation of fluid in either the lung tissue (pleural effusion) or around the heart itself (pericardial effusion).

•

Non-Cancerous Illnesses and Infections: Many non-cancer-related illnesses or infections can also cause dyspnea, including: o anemia o anxiety o asthma o cardiomyopathy o chronic bronchitis o chronic obstructive pulmonary disease (COPD) o congestive heart failure o emphysema o pneumonia o pulmonary edema o renal insufficiency

DIAGNOSIS There is no specific way to measure dyspnea, as the severity and symptoms can vary. However, in order to form a diagnosis, a health care provider will most likely begin by giving you a physical examination. The exam may involve an assessment of the health of your cardiac, respiratory and renal systems. Your doctor might also check your musculoskeletal and skin status. This helps to identify possible causes of dyspnea. Finally, some laboratory testing may be needed, including:    

a complete blood count an electrocardiogram (ECG) an evaluation of the oxygen and carbon dioxide levels in the blood Chest X-rays.

Based on the test results, additional testing may be needed. RELIEF MEASURES  Assess for airway patency and a complete respiratory assessment is performed to identify additional sign and symptoms of respiratory distress. 6

 Arterial blood gas values are obtained if indicated and oxygen saturation is monitored.  The patient is placed in high fowler position.  Oxygen and medications are administered in severe cases and the patient’s response is evaluated and documented. 1) COUGH DEFINITION A forceful and sometimes violent expiratory effort preceded by a preliminary inspiration. Cough results from irritation of the mucus membrane anywhere in the respiratory tract. CLINICAL SIGNIFICANCE Cough may indicate serious pulmonary disease. The nurse needs to evaluate the character of the cough.  Dry cough-----a cough unaccompanied by sputum production.  Moist cough--- a cough accompanied by production of mucus or exudates. The time of coughing is also noted.  Coughing at night time may herald the onset of left-sided heart failure or bronchial asthma.  A cough in the morning with sputum production may indicate bronchitis.  Coughing after food intake may indicate aspiration of material into the tracheobronchial tree. 3) SPUTUM PRODUCTION A patient who coughs long enough almost invariably produces the sputum. CLINICAL SIGNIFICANCE  A profuse amount of purulent sputum (thick and yellow, green or rust-colored) or a change in color of the sputum probably indicates the bacterial infection.  Thin, mucoid sputum frequently results from viral bronchitis.  A gradual increase of sputum over time may indicate the presence of chronic bronchitis or bronchiectasis.  Pink-tinged mucoid sputum suggests a lung tumor.  Profuse, frothy, pink material, often welling up into the throat, may indicate pulmonary edema.  Foul-smelling sputum and bad breath point to the presence of a lung abcess, bronchiectasis or an infection caused by anaerobic organisms. RELIEF MEASURES  If the sputum is too thick for the patient to expectorate, it is necessary to decrease its viscosity by increasing its water content through adequate hydration (drinking water) and inhalation of aerolized solutions, which may be delivered by any type of nebulizer.  Adequate oral hygiene.  Stop smoking. 2) CHEST PAIN

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Chest pain or discomfort may be associated with pulmonary or cardiac disease. Chest pain associated with pulmonary conditions may be sharp, stabbing and intermittent or it may be dull, aching and persistent. The pain is usually felt on the side where the pathologic process is located. CLINICAL SIGNIFICANCE Chest pain may occur with pneumonia, pulmonary embolism with lung infarction and pleurisy. It also may be a late symptom of bronchogenic carcinoma.

RELIEF MEASURES  Analgesic medications  NSAIDs  A regional anesthetic block may be performed to relieve extreme pain. 3) WHEEZING Wheezing is often the major finding in a patient with bronchoconstriction or airway narrowing. It is heard with or without a stethoscope, depending on its location. Wheezing is a high-pitched, musical sound heard mainly on expiration. RELIEF MEASURES  Oral or inhalant bronchodilator medications 4) CLUBBING OF THE FINGERS It is a sign of lung disease found in patients with chronic hypoxic conditions, chronic lung infections and malignancies of the lung. This finding may be manifested initially as sponginess of the nailbed and loss of the nailbed angle. 7) HEMOPTYSIS DEFINITION It is defined as expectoration of blood from the respiratory tract. It is a symptom of both pulmonary and cardiac disorders. The onset is usually sudden, and it may be intermittent or continuous. THE COMMON CAUSES ARE  Pulmonary infection  Carcinoma of lung  Abnormalities of the heart or blood vessels  Pulmonary artery or vein abnormalities  Pulmonary emboli and infarction 9) CYANOSIS 8

DEFINITION Cyanosis is the bluish coloration of the skin and is a very late indicator of the hypoxia. The condition is caused by a deficiency of o2 and an excess of co2 in the blood. Hence, the presence or absence of the cyanosis is determined by the amount of unoxygenated hemoglobin in the blood. Cyanosis appears when there is 5g/dLof unoxygenated Hb. TREATMENT  To remove the underlying cause  Artificial respiration together with oxygen inhalation.

ACUTE RESPIRATORY FAILURE DEFINITION Respiratory failure is a sudden life-threatening deterioration of the gas exchange function of the lung. It exists when the exchange of o2 for co2 in the lungs cannot keep up with the rate of oxygen consumption and co2 production by the cells of the body. Acute Respiratory failure is defined as a fall in o2 tension (Pao2) to less than 50 mm Hg (hypoxemia) and a rise in arterial co2 tension to greater than 50 mm Hg (hypercapnia).

PATHOPHYSIOLOGY Common causes of ARF can be classified into 4 categories: a) Decreased respiratory drive It may occur with severe brain injury, large lesions of the brain stem, use of sedative medications, and metabolic disorders such as hypothyroidism. These disorders impair the normal response of chemo receptors in the brain to normal respiratory stimulation. b) Dysfunction of the chest wall The impulses arising in respiratory center travel through the nerves that extend from the brain stem down the spinal cord to receptors in the muscles of respiration. Thus, any disease or disorder of nerves, muscles or neuromuscular junction involved in respiration seriously affects ventilation and may ultimately lead to ARF. c) Dysfunction of the lung parenchyma Pleural effusion, hemothorax, pneumothorax, and upper airway obstruction are conditions that interfere with ventilation preventing expansion of the lung. These conditions which may cause respiratory failure usually are produced by an underlying lung disease, pleural disease, or trauma and injury. Other diseases include pneumonia, pulmonary embolism and pulmonary edema. d) Other causes 9

In the post-operative period, especially after thoracic or abdominal surgery, inadequate ventilation and respiratory failure may occur because of several factors like due to the effects of the anesthetic agents, analgesics and sedatives, which may effect respiration leading to hypoventilation. CLINICAL MANIFESTATIONS Earlier signs are, • Restlessness • Fatigue • Headache • Dyspnea • Air hunger • Tachycardia • Increased blood pressure As the hypoxemia progresses, more obvious signs may be present, including • Confusion • Lethargy • Tachycardia • Tachypnea • Central cyanosis • Diaphoresis And finally, • Respiratory arrest Physical findings are • Use of assessory muscles • Decreased breath sounds NURSING DIAGNOSIS 1) Impaired gas exchange and airway clearance related to excessive mucus production, retained secretions and inflammation. GOAL: To maintain patent airway. 2) Acute chest pain related to pleural inflammation. GOAL: To reduce pain. 3) Activity intolerance related to dyspnea and hypoxemia. GOAL: To improve activity level of the patient.

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4) Anxiety related to feeling of suffocation. GOAL: To reduce anxiety. 5) Disturbed sleep pattern related to dyspnea. GOAL: To improve the sleep pattern. 6) Deficit knowledge regarding prevention of respiratory tract infections, treatment regimen, GOAL: To provide knowledge to the patient.

I. DIAGNOSTIC EVALUATIONS • PULMONARY FUNCTION TEST (PFT) PFT is performed to assess respiratory function and to determine the extend of dysfunction. Such tests include measurements of lung volumes, ventilatory function and the mechanics of breathing, diffusion and gas exchange. • ARTERIAL BLOOD GAS STUDIES Measurements of blood pH and of arterial O2 & CO2 tensions are obtained when managing patients with respiratory problems and in adjusting oxygen therapy as needed. The arterial oxygen tension indicates the degree of oxygenation of blood and the arterial CO2 tension indicates the adequacy of alveolar ventilation. Alveolar blood gas studies aid in assessing the ability of lungs to reabsorb or excrete bicarbonate ions to maintain to normal body Ph • PULSE OXIMETRY It is a non-invasive method of continuously monitoring the o2 saturation of hemoglobin. A probe or sensor is attached to the fingertip, forehead, earlobe or bridge of the nose. The sensor detects changes in oxygen saturation levels by monitoring high signals generated by the oxieter and reflected by blood pulsing through the tissue at the probe. Normal SpO2 values are 98% to 100%. Values less than 85% indicate that the tissues are not receiving enough oxygen. • CULTURES Throat cultures may be performed to identify organisms responsible infection in the respiratory tract. Nasal swabs may also be performed for the same purpose. • SPUTUM STUDIES Sputum is obtained to identify pathogenic organisms and to determine whether malignant cells are present. •

IMAGING STUDIES  Chest X-ray  Computed tomography  Magnetic resonance imaging  Fluoroscopic studies  Pulmonary angiography 11

• ENDOSCOPIC PROCEDURES  Bronchoscopy  Thoracoscopy •

THORACENTESIS

•

BIOPSY

OXYGEN INHALATION Patient with respiratory dysfunctions are treated with oxygen inhalations to relieve anoxemia or hypoxemia. The normal amount of oxygen in the arterial blood should be in the range of 80 to 100 mm Hg. If it falls below 60mm Hg, irreversible physiologic effects may occur. Thus, it is urgent to correct anoxemia promptly. Indications for oxygen therapy • Cyanosis Cyanosis is defined as the bluish coloration of the skin nail beds and mucus membranes, resulting from a decreased amount of oxygen in the hemoglobin of the blood. • Breathlessness or labored breathing It may be caused by certain diseases such as asthma, emphysema, pulmonary embolism, coronary thrombosis and in other cardiac insufficiencies. •

An environment low in oxygen content e.g., high altitudes

• Anemia It is the deficiency of either quality or quantity of the red corpuscles in the blood giving rise to the symptoms of anoxemia. •

Diseases or conditions in the alveoli of the lungs that interfere with the exchange of oxygen across the alveolar-capillary membranes e.g., atelectasis, pneumonectomy, thoracoplasty etc.

• Poisoning Poisoning with chemicals or that alter the tissue’s ability to utilize oxygen, e.g. cyanide poisoning. •

Shock and circulatory failure

•

Hemorrhage and air hunger

•

Patients under anesthesia 12

•

Patients who are critically ill

•

Patients with psychologically induced breathlessness

• Asphyxia It is a condition in which there is a lack of oxygen supply to the lungs leading to unconsciousness caused by blocking of the air passages by foreign bodies, drowning, electrical shock, strangulation, inhalation of poisonous gases etc. METHODS OF OXYGEN ADMINISTRATION a) Oxygen by nasal catheter b) Oxygen by mask c) Oxygen tent (a) Oxygen by nasal catheter This is the most common method of administering oxygen to the patients in the hospital wards. The nasal catheter is inserted into the nostril reaching up to the uvula and is held in place by adhesive tapes. The catheter does not interfere with the patient’s freedom to eat, to talk, and o move in bed. Flow of 1 to 4 litres of oxygen will be sufficient to maintain the concentration of 22 to 30% oxygen. (b) Oxygen by mask A variety of face masks that covers the patient’s nose and mouth are available for oxygen administration. If the mask does not fit snugly over the face, oxygen will be lost from the masks. Masks are adventitious for those patients who are unable to breathe through the nose. Flow of 8 to 12 litres will be necessary to maintain the concentration of oxygen 25 to 60%. (c) Oxygen tent An oxygen tent consists of a canopy over the patient’s bed that may cover the patient fully or partially and it is connected to a supply of oxygen. The canopies are transparent and enable the nurse to observe the patient. The lower part of the canopy is tucked under the bed to prevent the escape of oxygen. There are certain advantages and disadvantages for using a oxygen tent. These are:  Oxygen tent provides an environment for the patient with controlled oxygen concentration, temperature regulation and humidity control.  It allows freedom for free movement in bed.  It creates a feeling of isolation.  Since it requires high volume of oxygen (10 to 12 litres per minute) it cannot be made available ordinarily.  Loss of desired concentration occurs each time the tent is opened to provide care for the patient.  There is an increased chance of fire.  It requires much time and to clean and maintain a tent. HAZARDS OF OXYGEN INHALATION a) Infection The use of contaminated equipment can spread infection in the patient. The causative organisms may be present in such places as catheters, tracheostomy or endotracheal tubes, humidifying water and masks. b) Combustion (fire) 13

Oxygen itself does not burn, but it supports combustion. Hence, fire is potential hazard when oxygen is administered. c) Drying of mucus membranes of the respiratory tract If oxygen is administered without sufficient humidity, it causes drying and irritation of the mucus membranes. d) Oxygen toxicity Its symptoms initially start as a tracheal irritation and cough. Others include dryness and irritation of the mucus membrane, substernal pain, nausea and vomiting and formulation of a membrane similar to the hyaline membrane on the alveolar valves, which causes dyspnea. e) Atelectasis Collapse of the alveoli develops as a result of increased oxygen concentrations in the inspired air. Oxygen induced apnea Since the CO2 is completely washed off from the blood by a high concentration of oxygen, the respiratory centre is not stimulated sufficiently. Normally a part of CO2 remaining in the blood, stimulates the respiratory centre. f) Retrolental fibroplasias The hazards of the oxygen therapy may affect the eyes. Retrolental fibroplasias is noted in premature infants who have a high concentration of oxygen inhalation. The infants exposed to high oxygen concentrations which cause an oxygen tension of 200mmHg or more in the blood will develop fibrotic changes behind the lens which impairs light penetration to the retina. The eyes of the adult may also be damaged by the oxygen administration. Ulceration, odema, visual impairment etc. may result from the toxic effects of oxygen on the cornea and the lens of the adult. g) Asphyxia Patients receiving oxygen inhalation by means of masks and closed tents must be protected from the danger of asphyxia resulting from unexpected and unobserved depletion of oxygen cylinders.

REFRENCES

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1. Brunner-Suddharth, Textbook of Medical-Surgical nursing, Edition

10th, Published by Lippincott P: 463-586 2. Sr. Nancy, Stephanies Principles and Practice of Nursing, Fifth Edition,

Published by N. R. Publishing house P: 134-139 3. Potter-Perry, Fundamentals of Nursing, Vol. II, Fifth Edition, Published by Elsevier P: 1132-1134 4. Taylors Lillis Le Mone Lynn, Fundamentals of Nursing, Vol. II, Sixth Edition, Published by Lippincott Williams & Wilkins P-1602-1620 5. Spring House, Nursing Procedures, edition III, P: 462-468 6. Anthony’s Textbook of Anatomy and Physiology, Vol I, Edition XIV, Published by Alison Hiller P: 578-600 7. Taber’s Cyclopedic Medical Dictionary, 18th Edition, Published by

F.A.Davis Company

SEMINAR ON OXYGEN INSUFFICIENCY 15

SUBMITTED BY: Ms. Amandeep Kaur M.Sc. Nursing Roll No. 1

SUBMITTED TO: Ms. N. Juneja Principal ACON, Mukatsar

DATE OF PRESENTATION: Oct.24, 2009

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