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69 Cards in this Set
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Characterized by presence of airflow obstruction
Caused by emphysema or chronic bronchitis or both Generally progressive May be accompanied by airway hyperreactivity May be partially reversible 4th leading cause of death in U.S Exposure to tobacco smoke is the Primary cause of COPD in the U.S. |
COPD
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Abnormal permanent enlargement of the air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles without obvious fibrosis |
emphysema
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Presence of chronic productive cough for
3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded |
chronic bronchitis
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Cigarette Smoking most significant cause of COPD
Clinically significant airway obstruction develops in 15% of smokers 80% to 90% of COPD deaths in the U.S. are related to tobacco smoking More than one out of every five deaths in the U.S. is the result of cigarette smoking Approximately 4000 chemicals and gases are inhaled into the lungs when smoking Nicotine acts as a stimulant to the sympathetic nervous system Compounds problems in a person with CAD ¯ Ciliary activity -can't clear mucous well Possible loss of ciliated cells Increased HR and BP-peripheral vasoconstriction |
COPD
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Production of mucus -more mucus and smaller airway to clear secretions
Reduction in airway diameter Increased difficulty in clearing secretions Abnormal dilation of the distal air space Alveolar wall destruction Stimulatory effect of nicotine increases the heart’s demand for O2 |
Cellular hyperplasia
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Carbon monoxide-from smoking
¯ O2 carrying capacity Impairs psychomotor performance and judgment Involuntary smoke exposure (secondhand smoke) associated with: ¯ Pulmonary function Risk of lung cancer Mortality rates from ischemic heart disease |
COPD
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Major contributing factor to the aggravation and progression of COPD
Recurring infections occur more in people with COPD Recurring infections impair normal defense mechanisms |
COPD infection
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protein normally stop prolytic enzyme from being so rough on lungs
a-Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD AAT deficiency accounts for < 1% of COPD in the U.S. AAT is a produced by the liver and normally found in the lungs Leads to premature emphysema Emphysema results in lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages Level of AAT is controlled by a pair of autosomal codominant genes People with this type of emphysema are primarily of northern European origin |
COPD heredity
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Some degree of emphysema is common
Gradual loss of elastic recoil Lungs become rounded and smaller Loss in alveolar supporting structures Loss of intraalveolar septum decreases number of functional alveoli Thinner alveolar walls contribute to loss of septal tissue and alveolar capillaries Arterial O2 levels decrease Thoracic cage changes from osteoporosis and calcification of costal cartilages decrease compliance of chest wall; increase work of breathing |
COPD and Aging
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Hyperinflation of alveoli
Destruction of alveolar walls Destruction of alveolar capillary walls Narrowed airways Loss of lung elasticity Destruction of alveolar walls allow to breathe in but not out so have air trapping so can't exhale as efficiently as should d/t loss of lung elasticity and narrowed airways Two types: Centrilobular Panlobular |
emphysema patho
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ones closer to bronchus are ones trapping air
Respiratory bronchioles enlarge Walls are destroyed Bronchioles become confluent Often associated with chronic bronchitis More common than panlobular |
Centrilobular emphysema
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)-all alveoli are trapping air
Affects bronchioles, alveolar ducts and sacs, and alveoli Progressive loss of lung tissue ¯ Alveolar-capillary surface area Usually found in persons with AAT deficiency |
Panlobular emphysema
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Difficult to distinguish the two types
Two types may exist at the same time |
severe emphysema
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Small bronchioles become obstructed as a result of mucus
Smooth muscle spasm Inflammatory process Collapse of bronchiolar walls Recurrent infectious processes lead to increased production and stimulation of neutrophils and macrophages |
emphysema
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Proteolytic enzymes released by neutrophils and macrophages
Destruction of alveolar tissue ® Inflammation Exudate formation Edema Elastin and collagen are destroyed Results in no pull or traction on the walls of the bronchioles Air goes into the lungs but is unable to come out on its own and remains in the lung Causes bronchioles to collapse Trapped air ® hyperinflation and overdistention-air is trapped d/t lack of recoil. air can't get out b/c of bad airways As more alveoli collapse, blebs and bullae may develop-bleb=airfilled space Surface area for O2 diffusion in the blood decreases Compensation is done by increasing respiratory rate to increase alveolar ventilation Hypoxemia usually develops late in disease as more air comes in bronchioles collapse causing less airspace |
emphysema
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mucus secreting glands overproducing in trachea and bronchi-normal alveoli
Hyperplasia of mucus-secreting glands in the trachea and bronchi Increase in goblet cells Disappearance of cilia-no cilia to get rid of extra mucus Chronic inflammatory changes and narrowing of small airways Altered function of alveolar macrophages leading to increased bronchial infections Frequently airways are colonized with microorganisms Excess amounts of mucus are found and may occlude small bronchioles |
Chronic bronchitis patho
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Alveolar structures and capillaries are normal-but airways get thicker
Chronic inflammation Primary pathologic mechanism in causing changes Causes vasodilation, congestion, mucosal edema Mucous glands become hyperplasic -alveolar walls full of mucus Causes narrowing of airway lumen and diminished airflow |
chronic bronchitis patho
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Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema Mucus is a physical barrier to ventilation Tendency to hypoventilate and retain CO2 Frequently patients require O2 both at rest and during exercise Peribronchial fibrosis may also result from the healing process secondary to inflammation Cough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretions Bronchospasm frequently develops Usually more common with history of smoking or asthma |
chronic bronchitis patho
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can have emphysema for years before dyspnea becomes significant
Dyspnea Progresses in severity Patient will first complain of dyspnea on exertion and progress to interfering with ADLs and rest Minimal coughing with no to small amounts of sputum Overdistention (barrel chest) of alveoli causes diaphragm to flatten and AP diameter to increase Patient becomes chest breather, relying on accessory muscles Ribs become fixed in inspiratory position Patient is characteristically underweight even when the patient has adequate calorie intake Protein-calorie malnutrition with loss of lean muscle mass and subcutaneous fat |
Emphysema
Clinical Manifestations |
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Earliest symptoms:
Frequent, productive cough during winter Frequent respiratory infections Bronchospasm can occur at end of paroxysms of coughing Cough usually exacerbated by respiratory irritants or cold air Dyspnea on exertion History of smoking is almost always present Normal weight or heavyset Ruddy appearance Hypoxemia and hypercapnia Result from hypoventilation and airway resistance in addition to problems with alveolar gas exchange Cyanosis Hemoglobin may reach 20 g/dl or more-causes ruddy appearance body produces more RBCs-polycythemia |
Emphysema
Clinical Manifestations |
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Cor pulmonale-right sided heart failure
Pulmonary hypertension-causes heart failure d/t HTN Acidosis Polycythemia Right side of the heart must increase to push blood into the lungs Right-sided heart failure develops Subsequent intravascular volume expansion b/c blood can't be pumped to lungs Systemic venous congestion Heart sound changes to the second heart sound, right-sided ventricular diastolic S3 gallop, and early ejection click along left sternal border Distended neck veins Hepatomegaly with upper quadrant tenderness Ascites Epigastric distress Peripheral edema Weight gain |
COPD complications
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Acute exacerbations of chronic bronchitis
Acute respiratory failure Can be caused by cor pulmonale or discontinuation of bronchodilator or corticosteroid medication- R.sided heart failure b-adrenergic blockers may exacerbate respiratory failure in patient with asthmatic component Indiscriminate use of sedatives and narcotics may suppress respiratory drive and lead to respiratory failure Peptic ulcer disease and GERD-occur with steroids pt. is on. Pneumonia |
COPD complications
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Chest x-rays early in the disease may not show abnormalities-later will show flat diaphram and larger airspace
History and physical exam Pulmonary function studies Spirometry Typical findings include reduced FEV(forced expiratory velocity) /FVC(forced vital capacity) and increased residual volume and total lung capacity-d/t air trapping Ratio of < 70% suggests presence of obstructive lung disease |
COPD diagnostic studies
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ABGs
¯ PaO2-d/t decreased area for gas exchange PaCO2 d/t air trapping making you acidotic ¯ pH respiratory acidosis Bicarbonate level found in late stages COPD b/c can't compensate anymore |
COPD diagnostic studies
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Exercise test to determine O2 saturation in the blood and pulse oximetry
ECG can show signs of right ventricular failure Goal: increased ventilation-reduce complication |
COPD diagnostic studies
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Smoking cessation
Accelerated decline in pulmonary function slows and function usually improves Most significant factor in slowing the progression of the disease |
COPD collaborative care
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Bronchodilators
¯ Airway resistance and hyperinflation Reduction in dyspnea and in FEV Given as maintenance therapy b-adrenergic agonists MDI or nebulizer Preferred route of administration Inhaled anticholinergics 1st line ex: albuterol, atrovent Minimal side effects-increased HR, stimulates beta receptors on SNS, headaches, tremors-dry mouth headache, dry cough Best taken on a regular basis |
COPD drug therapy
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¯ Airway resistance and hyperinflation
Reduction in dyspnea and in FEV Given as maintenance therapy |
bronchodilators
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MDI or nebulizer
Preferred route of administration |
b-adrenergic agonists
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Minimal side effects-increased HR, stimulates beta receptors on SNS, headaches, tremors-dry mouth headache, dry cough
Best taken on a regular basis 1st line ex: albuterol, atrovent |
Inhaled anticholinergics
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Raises PO2 in inspired air
Treats hypoxemia Classified as high- or low-flow systems Simple Face Mask for Oxygen Administration Plastic Face Mask with Reservoir Bag for Oxygen Administration Humidification is commonly used because O2 has a drying effect on the mucosa Nebulizers provide humidified O2 |
O2 therapy
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Deliver flows (15 to 20 L/min) of warm, humidified air through a nasal cannula or a transtracheal cannula
Increases exercise tolerance |
vapotherm
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Combustion
CO2 narcosis-stop drive to breathe O2 toxicity Absorption atelectasis Infection |
complications of oxygen therapy
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Improved prognosis
Improved neuropsychologic function Increased exercise intolerance Decreased hematocrit Reduced pulmonary hypertension Benefit of therapy should be evaluated when patient’s condition has stabilized Short-term home O2 may be indicated for persisting hypoxemia after discharge Long-term O2 therapy Patients may receive O2 only during exercise and/or sleep Periodic reevaluations are necessary for the patient who is using chronic supplemental O2 every 30 to 90 days |
chronic O2 therapy at home
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Nasal cannula
Regular O2-conserving Reservoir cannula Store O2 in a small reservoir during exhalation and can reduce flow requirements by 50% Encourage patient to remain as active as possible |
oxygen delivery systems
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Lung volume reduction surgery
Lung transplantation Single lung is most common technique Prolongs life Improves functional capacity Enhances quality of life Rejection and effects of immunosuppressive therapy are obstacles |
surgical therapy
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Breathing retraining
Pursed-lip breathing-inhale through nose; exhale w/lips pursed (like whistling) Prolongs exhalation and prevents bronchiolar collapse and air trapping Diaphragmatic breathing Focuses on using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rate Can be achieved by assuming semi- Fowler’s position and placing one hand on the abdomen and the other on the chest and observing which moves Lay back in semifowlers one hand on abdomen and one on chest-abd. out when inhale and hand on stomach should rise |
respiratory therapy
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Huff coughing-cough during exhalation-helps clear secretions
Can easily be taught May help clear secretions ineffective coughing patterns do not |
effective coughing
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Postural drainage-uses gravity to rid secretions
Percussion Vibration Helps bring secretions into larger, more central airways Postural drainage Uses gravity to assist in bronchial drainage Drainage positions are determined by involved areas of lung |
Chest physiotherapy
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-hands cupped and loosen secretions
Performed in the appropriate postural drainage position Hands in a cup-like position, creating an air pocket between the patient’s chest and the hand Hollow sound should be heard with flexion and extension of the wrist Facilitates movement of thick mucus Should not be performed over kidneys, sternum, spinal cord, or any tender area |
percussion
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Tensing the hand and arm muscles repeatedly
Pressing mildly with the flat of the hand on the affected area while the patient slowly exhales a deep breath Facilitates movement of secretions to larger airways Mild vibration tolerated better than percussion Flutter mucus clearance device-used more with patients wtih CF Handheld device Provides expiratory pressure treatment for patients with mucus-producing conditions Works by vibrating the airways, loosening the mucus from airway walls Intermittently increases interbronchial pressure, helping to maintain the patency of the airway Accelerates expiratory airflow Used in place of CPT in patients where it is contraindicated |
vibration
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should breathe slow and deep with meds-cough when done
Powered by a compressor air or O2 generator Medication is nebulized depending on factors such as droplet size |
Aerosol-nebulization therapy
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Full stomachs press on diaphragm causing dyspnea and discomfort
Difficulty eating and breathing at the same time leads to inadequate amounts being eaten Decrease dyspnea and conserve energy Rest at least 30 minutes prior to eating-right up until meals Use bronchodilator Select foods that can be prepared in advance Patient should eat 5-6 small meals to avoid feeling bloated (caused by swallowing air) Avoid foods that require a great deal of chewing Avoid exercises and treatments 1 hour before and after eating Avoid gas-forming foods High-calorie, high-protein diet is recommended Supplements Avoid high carbohydrate diet to prevent increase in CO2 load Fluids (intake of 3L/day) should be taken between meals |
nutritional therapy
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Health History
Exposure to chemical pollution Respiratory irritants Recurrent respiratory infections Medications Smoking Family history of respiratory disease |
nursing assessment COPD
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Weight loss or gain
Inability to perform ADLs Fatigue Swelling of the feet Progressive dyspnea Recurrent cough, sputum Constipation, gas, bloating Insomnia, sitting up to sleep |
nursing assessment COPD
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Rapid, shallow breathing
Inability to speak Pursed-lip breathing Wheezing, rhonchi, crackles Use of accessory muscles Arrhythmias Cor pulmonale Ascites Barrel-chest Abnormal ABGs |
nursing assessment COPD
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Ineffective airway clearance
Impaired gas exchange Imbalanced nutrition: less than body requirements Disturbed sleep pattern Risk for infection |
nursing diagnosis COPD
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Return of baseline respiratory function
Ability to perform ADLs Relief from dyspnea No complications related to COPD Knowledge and ability to implement long- term regimen Overall improved quality of life |
Nursing Management
Planning Goals COPD |
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STOP SMOKING!!!
Avoiding or controlling exposure to occupational and environmental pollutants and irritants Early detection of small-airway disease Early diagnosis of respiratory tract infections Awareness of family history of COPD and AAT deficiency Health care workers should avoid smoking while caring for patients, as odor is offensive to patients |
health promotion COPD
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watch for complications
Required for complications like pneumonia, cor pulmonale, and acute respiratory failure Once crisis is resolved, assess degree and severity of underlying respiratory problem |
acute intervention COPD
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Pulmonary rehabilitation-often very effective-structured prgram can attend
Control and alleviate symptoms of pathophysiologic complications of respiratory impairment Teach patient how to achieve optimal capability in carrying out ADLs Physical therapy Nutrition Education |
ambulatory and home care COPD
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Activity considerations
Exercise training of upper extremities to help improve function and relieve dyspnea Alternative methods of ADLs explored Encourage patient to sit while performing activities Coordinated walking Slow, pursed-lip breathing After exercise, wait 5 minutes before using b-adrenergic agonist MDI Keep diary of activity to see progress Sexual activity Plan during part of day when breathing is best Slow, pursed-lip breathing Refrain from activity after eating or other strenuous activity Do not assume dominant position Do not prolong foreplay Sleep Nasal saline sprays Decongestants Nasal steroid inhalers Long-acting theophylline Decreases bronchospasm and airway obstruction |
ambulatory and home care COPD
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Psychosocial considerations
Guilt Depression Anxiety Social isolation Denial Dependence Use relaxation techniques and support groups Discourage moving to places above 4000 ft. No significant benefit to moving to a different climate |
psychological considerations COPD
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Expected outcomes
Normal breath sounds Effective coughing Return of PaO2 to normal range for patient Improved mental status Maintenance of normal body weight Normal serum protein levels Feeling of being rested Improvement in sleep pattern Awareness of need to seek medical attention Behaviors minimizing risk of infection No infection |
nursing management COPD
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Not disease, a condition caused by something else
Results from inadequate gas exchange Insufficient O2 transferred to the blood Hypoxemia-not enough O2 to tissues (PaO2 < 60mmHg on 60% O2) Inadequate CO2 removal Hypercapnia-can't get rid of CO2 (PaCO2 > 45mmHg and pH < 7.35) Not a disease but a condition Result of one or more diseases involving the lungs or other body systems Classification: Hypoxemic respiratory failure Hypercapnic respiratory failure |
Acute respiratory failure
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Causes: tramua, emphysema, asthma, pulmonary edema, pneumonia
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hypoxemic respiratory failure
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PaO2 of 60 mm Hg or less
Inspired O2 concentration of 60% or greater |
hypoxemic respiratory failure
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Causes: COPD, drug overdose, CNS disease, MS, gamorea
PaCO2 above normal (>45 mm Hg) Acidemia (pH <7.35) |
Hypercapnic Respiratory Failure
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V/Q mismatch-V=ventilation Q=perfussion should be equal. Air in alveoli & blood going into alveolus
COPD-ventilation-makes alveoli walls collapse Pneumonia-ventilation-mucus & infection in way of air exchange Asthma-ventilation Atelectasis-ventilation Pulmonary embolus-perfussion |
causes hypoxemic respiratory failure
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Shunt-blood goes through heart but doesn't get oxygenated.
Anatomic shunt-septal defect-blood R--> L side heart Intrapulmonary shunt-pulmonary capillaries with no gas exchange Extreme V/Q mismatch |
causes hypoxemic respiratory failure
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Diffusion limitation-problem in ARDS
Severe emphysema Recurrent pulmonary emboli-no gas diffusion d/t thicker walls Pulmonary fibrosis-thick alveoli & perfussion cant' take place Hypoxemia present during exercise |
cause hypoxemic respiratory failure
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Alveolar hypoventilation
Restrictive lung disease CNS disease Chest wall dysfunction Neuromuscular disease |
causes hypoxemic respiratory failure
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Interrelationship of mechanisms
Combination of two or more physiologic mechanisms |
causes hypoxemic respiratory failure
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getting rid of CO2 is problem; gets enough O2
Airways and alveoli-obstuction and airtrapping can't get rid of CO2 Asthma Emphysema Chronic bronchitis Cystic fibrosis |
cause of hypercapnic respiratory failure
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getting rid of CO2 is problem; gets enough O2
Imbalance between ventilatory supply and demand Airways and alveoli-obstuction and airtrapping can't get rid of CO2 Asthma Emphysema Chronic bronchitis Cystic fibrosis Central nervous system-suppress drive to breathe not breathing off CO2 Drug overdose Brainstem infarction Spinal cord injuries Chest wall-can't expand fully-don't have unresticted movement so can't breathe out fully. Flail chest Fractures Mechanical restriction Muscle spasm Neuromuscular conditions Muscular dystrophy Multiple sclerosis |
Hypercapnic Respiratory Failure
Etiology and Pathophysiology |
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Major threat is the inability of the lungs to meet the oxygen demands of the tissues or tissue can't use oxygen you are getting
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tissue oxygen needs
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Sudden or gradual onset-sudden onset poorly tolerated
A sudden ¯ in PaO2 or rapid in PaCO2 is a serious condition When compensatory mechanisms fail, respiratory failure occurs Signs may be specific or nonspecific- decreased LOC, restlessness Severe morning headache-d/t increased CO2, vasodilation & more blood in head causing HA Cyanosis- Late sign Tachycardia and mild hypertension Early signs Consequences of hypoxemia and hypoxia Metabolic acidosis and cell death ¯ Cardiac output Impaired renal function- d/t decreased O2 to kidneys Specific clinical manifestations Rapid, shallow breathing pattern as you decompensate it will slow down Tripod position Dyspnea Pursed-lip breathing Retractions Change in I:E ratio |
Clinical manifestations respiratory failure
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Physical assessment--crackles, absent lung sounds, rubs
ABG analysis- increased CO2, decreased O2 Chest x-ray-COPD, pneumonia, trauma CBC ECG Serum electrolytes Urinalysis V/Q lung scan Pulmonary artery catheter (severe cases) cultures-sputum, blood |
Diagnostic studies respiratory failure
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Nursing Assessment
Past health history-TB, pneumonia, COPD Medications Surgery Tachycardia Fatigue Sleep pattern changes Headache Restlessness |
nursing assessment and management respiratory failure
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