Alterations In Respiration Part 2 Flashcard

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Recognize early clinical signs of respiratory distress

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Restlessness, agitation, apprehension, confusion*** Increased work of breathing (tachypnea, tachycardia, increased BP, use of accessory muscles)** Decrease in SPO2; delayed capillary refill Cyanosis is a LATE sign

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Recognize early clinical signs of respiratory distress

Emphysema patho

smoking - attraction of inflammatory cells & decreased alpha 1 antitrypsin activity (leads to destruction of elastin fibers in lung*, then to emphysema) - release of elastase - action inhibited by alpha 1 antitrypsin & decreased alpha 1 antitrypsin - inherited alpha 1 antitrypsin deficiency - *destruction of elastin fibers in lung* - emphysema

Describe the etiology for a barrel chest in emphysema

Loss of lung elasticity results in hyperinflation of lungs with increased chest diameter. With loss of lung elasticity and hyperinflation of the lungs, the airways often collapse during expiration because pressure in surrounding lung tissues exceeds airway pressure. Air becomes trapped in the alveoli and lungs, producing an increase in the AP dimensions of the chest.

Discuss how the diagnosis of COPD is made relative to pulmonary function testing

Using a spirometer to diagnosis COPD also measures: forced vital capacity (FVC), forced expiratory volume in 1 second (FEV)*. Typical findings of chronic lung disease patients when using a spirometer: Decreased FEV1, reduced FEV1/FVC ratio (<70%)*, increased residual volume, increased total lung capacity.

Recognize normal ABG values for COPD patients

Hypercapnia (increased CO2), respiratory acidosis, metabolic alkalosis Also, hypoxemia, cor pulmonale (right sided heart failure), and cyanosis develops (imbalance between ventilation and perfusion)

Relate risk factors for pulmonary embolus to Virchow's triad and discuss nursing interventions aimed at prevention.

Immobility Previous DVT Recent surgery Previous CVA, SCI Malignancy Smoking Obesity Virchow's Triad Venous stasis (bedrest - immobility) Hypercoagulability (dehydration) Vascular wall damage (surgery) Prevention: use of anticoagulants (sometimes contraindicated with post-op patients). Surgical interruption of the vena cava or insertion of a filter to prevent emboli from traveling to the lung (more extreme situations). IPC booties to prevent DVT. Anticoagulant therapy to decrease likelihood of DVT, thromboembolism, and fatal pulmonary embolism after surgical procedures.

Describe the pathophysiology of pulmonary embolus and the most important signs and symptoms

Emboli released from DVT travels towards heart and lungs. Lodge in the pulmonary vasculature. Vasoconstriction - increased pulmonary artery pressures. Increased workload for right ventricle - right sided heart failure. Hypotension from decreased CO and shock can result. Most important S&S - sudden dyspnea, chest pain.

Give examples of common ventilation and perfusion problems. Know that a PE is a perfusion defect

Pulmonary embolus (V>Q) = mismatch Atelectasis (Q>V) = "dead space" = "shunt"

Define pleural effusion - definition/treatment

Abnormal collection of fluid in the pleural cavity as a result of a disease process (perfusion deficit)* Patho- main: increased capillary pressure, increased capillary permeability, decreased colloid osmotic pressure. other: increased negative intrapleural pressure, impaired lymphatic drainage Treatment - treat the cause -- thoracentesis (aspiration of fluid from the pleural space - used in Dx and Rx), chest tube - both used to drain fluid.

Define pneumothorax - definition/treatment . Differentiate between traumatic/spontaneous

Accumulation of air in the pleural cavity. Partial or complete collapse of the lung. Breach in the lung or pleura, allows air to enter the pleural space and the lung or a portion of the lung collapses. Treatment - supplemental O2. Evacuation of the air from the pleural space. Chest tube insertion - 2nd intercostal space midclavicular line. Placed to chest drainage system that provides water-seal and suction. Spontaneous - air-filled bleb on the surface of the lung ruptures, allowing atmospheric air from the airways to enter the pleural space. Traumatic - caused by penetrating or non-penetrating chest injuries, most commonly fractured or dislocated ribs that penetrate the pleura.

Discuss the pathophysiology and causes of atelectasis

Incomplete lung expansion* Patho - decreased ciliary function - secretion retention - airway obstruction - impaired cough reflex - hypoventilated alveoli - hypoxemia - acute respiratory failure Causes: inadequate ventilation, mucus plug, external compression by fluid, mass, exudate Most common cause: not taking deep breaths after surgery.

Explain why we don't give high concentrations of oxygen to COPD patients

Outside of being in the hospital, they need to be use to atmospheric oxygen and their lungs need to be trained to live with that environment. Giving high concentrations of oxygen to a CPOD patient will decrease their strength to breath in hard enough for the adequate oxygen they need.

Asthma patho

allergen - mast cells (& eosinophils - high WBC of IgE) - bronchospasm (which leads to airflow limitation) & infiltration of inflammatory cells - airway inflammation - airflow limitation & increased airway responsiveness (leads to bronchospasm) - edema, impaired mucociliary function, and epithelial injury.

Bronchitis patho

Bronchitis - chronic productive cough for 3 months in 2 consecutive years. Hypersecretion of mucus in large airways. Hypertrophy of submucosal glands in trachea and bronchi. Increase goblet cells and excess mucus production in small airways**

Clinical manifestation in asthma

cough - dry * wheezing chest tightness * prolonged expiration tachycardia tachypnea dyspnea

Diagnostic tests for asthma

ABG pulmonary function test determination of allergens - skin testing CBC

COPD - chronic bronchitis vs emphysema

CB - obstruction of airways caused by chronic inflammation and fibrosis of bronchial wall hypertrophy of submucosal glands with *hyper-secretion of mucus (classic sign)* with excessive bronchial secretions Emphysema - enlargement of air spaces cased by destruction of alveolar walls and capillary beds. Loss of alveolar tissue - decreased surface area for gas exchange. Loss of elastic lung fibers - airway collapse, air trapping. Retained CO2

Acute Respiratory Failure

Rapidly occurring inability of the lungs to maintain adequate oxygenation of blood and/or impairment of CO2 elimination. ** inadequate gas exchange

Causes of acute hypoventilation

atelectasis, oversedation, respiratory muscle fatigue, neuromuscular disorders, COPD paCO2 > 45 = hypercapnea

Causes of Oxygenation Failure

atelectasis pneumonia pulmonary edema ARDS COPD pneumothorax paO2 < 60 mm Hg = hypoxemia

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