Gas Exchange PDF

Gas Exchange Learning Objectives Notice the risk factors for impaired gas exchange Recognize when an individual has compromised gas exchange Provide appropriate nursing and collaborative interventions for optimizing gas exchange Discuss the role of hemoglobin in transport of oxygen t...

Gas Exchange Learning Objectives Notice the risk factors for impaired gas exchange Recognize when an individual has compromised gas exchange Provide appropriate nursing and collaborative interventions for optimizing gas exchange Discuss the role of hemoglobin in transport of oxygen throughout the body Identify signs of impaired perfusion caused from a pulmonary embolism Discuss the physiological processes of COPD that lead to impaired ventilation 4 Essential components for Effective Gas Exchange Mechanics of breathing Perfusion Ventilation > lungs have to be working Transport > think about hemoglobin Gas Exchange Process Is performed automatically by the lungs and respiratory system > don’t have to think> involuntarily How it works ○ The air, containing oxygen and other gasses, comes into the body through the lungs ○ In the lungs, the oxygen is moved into the bloodstream and carries through the body ○ Red blood cells collect the carbon dioxide and transport it back to the lungs, where it leaves the body when we exhale Alveoli > the exchange of oxygen and carbon dioxide occurs in the alveoli Pulmonary venule > carries oxygenated blood to the heart Pulmonary arteriole > carries deoxygenated blood from the heart Ventilation-Perfusion ratio (V-Q ratio) Measure of the effectiveness of gas exchange Ratio of the amount of air reaching the alveoli to the amount of blood reaching the alveoli Can be measured with a ventilation-perfusion scan (VQ scan) Normal = 4:5 ○ Alveoli receive 4 L/ min of air, capillaries supply blood at 5L/ min ○ Must match as closely as possible for proper gas exchange judgment The lungs have a built-in compensatory mechanism that attempts to match blood flow and ventilation: where there is little ventilation, pulmonary arterial vessels constrict Pulmonary artery vasoconstriction leads to redistribution of blood flow to better-ventilated areas of the lungs Aspiration occurs in straight right bronchus > aspiration pneumonia Mucociliary Apparatus Inhaled particles such as dust,pollen, and pathogens are trapped by the mucus and removed from air passages Upward motion of the cilia moves the mucus from the bronchioles up to the throat where it is swallowed > so no longer in danger of going to lungs  Smoking paralyzes the mucociliary apparatus and inhaled particles stimulate smokers to forcibly cough to mobilize mucus Failure to remove excess particles from the respiratory system increases the risk of infection Oxyhemoglobin Oxygen combines loosley with the heme portion of hemoglobin to form oxyhemoglobin The most important function of hemoglobin is to combine with oxygen in the lungs and then release oxygen to the peripheral tissues It then collects carbon dioxide from the tissues and carries it back to the lungs to be excreted The percentage of hemoglobin saturated with oxygen can be measured using a pulse oximeter If the pressure of oxygen in the arterial blood (PO2) stays within the 90 to 100 mmHg range, hemoglobin remains maximally saturated with oxygen and tissues remain oxygenated Erythropoietin Erythropoietin which is responsible for the stimulation of red blood cell (RBC) production is secreted by the kidneys in response to low oxygen levels in the bloodstream Any condition that causes hypoxia, such as cardiac disease, lung disease, or change in the atmospheric pressure, will stimulate erythropoietin Erythropoietin then stimulates the bone marrow to produce more RBCs that can carry oxygen to the tissues How it goes ○ Low oxygen in arteria blood > kidneys secret erythropoietin > erythropoietin stimulates bone marrow > bone synthesizes erythrocytes > which turns into red blood cells > which increases oxygen carriage in the blood Substances Vital for healthy Red Blood Cells (RBCs) Protein Iron Vitamin B12 Folic acid Breaking Down Hemoglobin Hemoglobin = heme and globin Heme consist of iron and a protein called porphyrin The synthesis of hemoglobin is highly dependent on the availability of iron A deficiency in iron results in a lack of hemoglobin in each red blood cell and results in low oxygen carrying capacity of the blood Red blood cells > heme + globin > iron + porphyrin > biliverdin > bilirubin > jaundice Exemplars Chronic obstructive pulmonary disease (COPD) Pulmonary Embolus (PE) Iron deficiency anemia Chronic Obstructive Pulmonary Disease (COPD)  Characterized by an increase in resistance to airflow from the trachea and large bronchi to the terminal and respiratory bronchioles Combination of chronic bronchitis, emphysema, and hyperreactive airway disease Impaired ventilation Causes ○ Combination of environmental factors and genetics ○ Environmental risk factors Smoking > number 1 risk factor Dust and chemical exposure, combat exposure Secondhand smoke exposure ○ Genetic predisposition Alpha-1 antitrypsin (AAT) deficiency > affects liver and lungs Chronic Bronchitis in COPD Characteristic features > hypersecretion of mucus in the large and small airways, hypoxia, and cyanosis Excessive mucus creates obstruction to inspiratory airflow that inhibits optimal oxygenation Unable to get air INTO the lungs Diagnosis occurs when ○ Cough for 3 months out of the year for 2 consecutive years Distinguishing characteristic ○ Airflow obstruction caused by mucus Pathophysiology Cascade of Chronic Bronchitis Chronic inhalation of irritants leads to resistance of small airways Results in severe V/Q imbalance ○ Decrease in arterial oxygenation ○ Chemoreceptors become insensitive to chronic high CO2 ○ Respiratory drive changes from CO2 to low PO2 focus Don’t want to give them oxygen sends body a signal that they don’t need to provide anymore oxygen Diminished respiratory drive ○ Hypoventilation ○ Hypoxia drives respiration ○ Can’t give too much O2 as it will decrease respiratory drive Chronic hypoxia ○ Kidneys produce erythropoietin ○ Stimulate bone marrow to produce excessive RBCs (erythropoiesis) = polycythemia ○ Leads to pulmonary arterial vasoconstriction = pulmonary hypertension ○ Causes right sided heart failure > cor pulmonale Hgb levels are high ○ Goal to draw more O2 to cells but unable to End result cyanosis > blue bloater Clinical Manifestations of Chronic Bronchitis  Productive cough, recurrent cough, high sputum production Dyspnea Cyanosis Use of accessory muscles to breathe > ribs Pulmonary hypertension Elevated Hgb Peripheral edema Rhonchi, weezing Right Sided heart failure, liver engorgement, cardiac enlargement Chest x ray shows hyperinflation increased bronchovascular markings ABG - decreased PaO2 and normal or increased PaCO2 (hypercapnia) Pulse oximetry - low SpO2 Hypoxia, respiratory acidosis, digital clubbing Emphysema Characteristic findings ○ Air trapping - over distention of alveoli with trapped air Obstructs expiratory airflow Loss of elasticity of alveoli High concentration of CO2 in lungs ○ Cannot get air OUT Pathophysiology Cascade of Emphysema Recurrent inflammation release proteolytic enzymes ○ Causes irreversible enlargement of airspaces distal to terminal bronchioles Results in destruction of elastic fibers ○ Loss of elastic recoil in lungs ○ Expiratory narrowing of small airways ○ Airflow obstruction Enlarged airspaces destroy alveolar walls ○ Reduced surface for gas exchange ○ Hypoxia drives respiration ○ Dyspnea on exertion Chronic hypercapnia Hgb levels are high ○ Goal to draw more O2 to cells but unable to End result: hyperventilation to force air out and CO2 retention (pink puffer) ○ Barrel shaped chest ○ Prolonged expiration Accessory muscles used for inspiration, abdominal muscles used to force out air Clinical Manifestations of Emphysema Lungs less compliant Dyspnea on exertion, orthopnea Barrel shaped chest > other parts of body thin Prolonged expiration  ○ Accessory muscles used for inspiration, abdominal muscles used to force air out Decreased breath sounds Hyperinflation with flattened diaphragm on chest x ray Minimal V/Q mismatch and hyperventilation keeps ABG’s until late in disease Higher CO2 retention (pink) , minimal cyanosis Pursed lip breathing Hyperresonance on chest percussion Thin appearance Anxious, speaks in short jerky sentences Chronic Bronchitis Emphysema Mucus and edema inhibit ventilation Alveoli integrity destroyed, become like overdistended balloons > non recoiling alveoli > retention of air (CO2) Patients cannot get air IN Patients cannot get air out Cyanosis Prolonged exhalation Cough Barrel- shaped chest caused by excessive air in lungs Chronic hypoxia Chest AP diameter = lateral diameter Clubbing of fingers Diaphragm pushed downwards because of excessive air in lungs Chronic hypoxia stimulates pulmonary arterial Chronic hypercapnia (PaCO2) vasoconstriction > right ventricle failure > JVD, ascites, hepatosplenomegaly, ankle edema Blue Bloater Pink Puffer Alveoli Alveoli in chronic bronchitis > shrunken alveoli known as atelectasis Alveoli in emphysema > distended, non recoiling Bronchiectasis All forms of COPD lead to bronchiectasis Structural components of the bronchial wall (cartilage, muscle, and elastic tissue) are destroyed and replaced by fibrous tissue Lose elasticity and ability to clear mucus Airways become irreversibly dilated Leads to build up of thick, purulent mucus ○ Breeding ground for bacteria  ○ Increase illnesses cause more damage Pulmonary Embolism (PE) Occlusion of a portion of the pulmonary arterial bed by a thrombus, embolus, tissue fragment, lipids, or an air bubble Impaired perfusion Pathophysiology of Pulmonary Embolism Thrombus formation ○ Vascular wall damage ○ Venous stasis ○ Hypercoagulability Thrombus loosens or fragments ○ Trauma ○ Clot dissolution ○ Sudden muscle spasm ○ Intravascular pressure changes ○ Change in peripheral blood flow Becomes an Embolus ○ Travels to the right side of the heart and enters lungs via pulmonary circulation Risk factors for Pulmonary Embolism Long term immobility, chronic pulmonary disease , heart failure, atrial fibrillation, thrombophlebitis, polycythemia vera, thrombocytosis, vascular injury, cancer, IV drug abuse Autoimmune hemolytic anemia, sickle cell disease, varicose veins, recent surgery, advanced age, pregnancy, lower extremity fractures or surgery, burns, obesity, hormonal contraceptives Clinical Manifestations Dyspnea, chest pain (sudden sharp) , tachycardia, air hunger, feeling of impending doom, productive cough, blood - tinged sputum, tachypnea (low PCO2) Low grade fever, pleural effusion, leg edema, cyanosis, syncope, distended neck veins, hemoptysis ABG > low PCO2, low PO2, high pH Needs attention immediately > can have clot buster, surgery, mesh net Iron Deficiency Anemia Insufficient delivery of oxygen to the tissues because of an inadequate number of mature, healthy RBCs in the blood due to insufficient iron stores  Impaired transport Pathophysiology of Iron Deficiency Anemia Disorder of oxygen transport where production of Hgb is inadequate due to lack of iron, leading to inadequate RBC formation Comes from ○ Inadequate intake of iron or disorders leading to malabsorption of iron ○ Traumas or surgeries leading to blood loss ○ Pregnancy ○ Cancers ○ Congenital or inherited problems with production or regulation Inadequate number of mature, healthy RBCs in the blood leads to insufficient delivery of oxygen to the tissues Insufficient oxygen delivery to the tissues causes cellular hypoxia and lack of energy Clinical Manifestations of Iron Deficiency Anemia Generalized weakness and fatigue, Pica-craving nonnutritive substances, Koilonychias - dry brittle,ridged nails with concave contours, glossitis = tender, pale, atrophic tongue, cheilitis = cracking at edge of lips, hair loss Pallor of skin, yellowing of eyes, leg cramps, shortness of breath particularly on exertion, tachycardia, palpitations, headache, difficulty concentrating, dizziness, syncope, cope, numb fingertips Diagnosis of Iron Deficiency Anemia Clinical manifestations Lab tests ○ RBC count - typically low ○ Hemoglobin - low ( norm: 14-18 g/dL male, 12-16 g/dL female) ○ Hematocrit - low (norm: 42-52% male, 37-47% female) ○ CBC with differential - determines number, size, and shape of cells ○ Reticulocyte count > determines the number of immature cells present; helps diagnose type Risk Populations for Iron Deficiency Anemia Vegans Women with excessive menstrual bleeding Pregnant woman Elderly Children weaned from breast milk to cow’s milk Teens in growth spurt Persons with chronic slow GI bleeding