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PleasingVibraphone

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Far Eastern University

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respiratory disorders medical nursing critical care healthcare

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NCM 118 MEDICAL-SURGICAL NURSING...

NCM 118 MEDICAL-SURGICAL NURSING LEC / PROF. E. SALAVANTE MIDTERMS TOPIC OUTLINE 3 Categories Fall of the Abnormal Side of Ventilation/Perfusion I. Critical Care: The Adult Client with Respiratory Disorder Balance II. Chest and Lower Respiratory Tract Disorder a. Pneumonia Low Ventilation-Perfusion Ratio (Shunts) b. Aspiration Pneumonia c. Ventilator-Associated Pneumonia d. Pleural Effusion e. Chronic Obstructive Pulmonary Disease (COPD) f. Asthma g. Pulmonary Edema h. Pulmonary Embolism COPD i. Acute Respiratory Distress Syndrome (ARDS) j. Respiratory Failure o Chronic bronchitis – overproduction of mucus III. that obstructs the airways. o Emphysema – destruction of the alveolar CRITICAL CARE: THE ADULT CLIENT WITH RESPIRATORY walls, making it impossible for the alveoli to DISORDER recoil. Mechanics of Ventilation Pneumonia – accumulation of mucus Surface tension of alveolar fluid Atelectasis – collapse of the alveoli o To prevent alveolar collapse Tumor Compliance of the lungs – the ability of lungs to stretch Mucus Plug – nagbabara ‘yung airway gawa ng mucus. and expand The problem is in the alveoli. There is an obstruction o The factors that help in lung compliance are from the alveoli blocking the air from entering. elastic fibers and surface tension. o We need to understand the anatomical High Ventilation-Perfusion Ratio (Dead Space) structure. Intact ang chest wall, no trauma kasi kapag may disruption sa chest wall, it will lead to a difference in the pressure gradient ▪ Pressure Gradient – the lungs having negative pressure vs the outside having positive. The difference between the pressure creates a vacuum effect (in and out ang Pulmonary embolism* – nagkakameron ng obstruction hangin). sa pulmonary artery that could lead to pulmonary o Another factor is the degree to which oxygen infarction is being delivered. Every time the oxygen is Pulmonary infarction – because of pump failure being delivered, the pressure inside must be Cardiogenic shock – kapag may arrythmia considered as it has maximum capacity. There is a blockage in the capillary flow Airway resistance The pressure gradient might not be enough, thus creating dead space. V/Q Balance: Normal Ratio Silent Unit Pneumothorax – vessel injury, progressive pleural The balance between what we can have through the accumulation, pulmonary edema process of diffusion – the exchange between oxygen ARDS – there is overflowing pulmonary edema and carbon dioxide, and perfusion – the delivery of the oxygenated blood. The bottom line of the 3 is Hypoxemia 1 body to experience fever and chills kasi your body is working to protect you from the infection. Bed rest is important para reduce ang workload ni patient o Explain what activities are allowed and not allowed. Clinical Manifestations Typical – strep. Pneumoniae (60 w/ comorbidity), H. influenzae type B (elderly) Atypical Pneumonia – S. Aureus, M. Pneumoniae (older children and younger adults), L. pneumophila Medical Management Antibiotics Hydration How to determine hypoxemia: Nutrition o With the use of pulse oximetry Rest to decrease the workload o ABG* - more accurate Nebulization The best indicator of a hypoxic state in the body: o Level of consciousness* Nursing Management o Skin discoloration Administer oxygen o Use of accessory muscles Monitor RR (labored respiration, cyanosis, cold, clammy skin) CHEST AND LOWER RESPIRATORY TRACT DISORDER Encourage deep breathing and coughing technique PNEUMONIA o Inhale through the nose para mag-expand Inflammation of lung parenchyma ang lungs, then exhale through the mouth. Community-acquired Semi-Fowlers position Origin: community, hospital, bacterial, viral, fungal, CPT, suctioning, pulse oximetry immunocompromised host (HIV, cancer, SLE, multi- High caloric, high protein diet in SFF organ failure), aspiration, VAP – inflammation will Increased fluid intake 3L/day happen. Administer medications (antipyretics, bronchodilators, Inflammation comes with mucus, then comes cough mucolytics, expectorants) reflex. Avoid exposure Look at the age, si px ba ay immunocompromised? Ang cough ba niya ay weak or strong? Is he bedridden? ASPIRATION PNEUMONIA Mababa ba ang LOC or GCS niya? Inhalation of oropharyngeal secretions and or stomach Pneumonia ay nanggagaling sa infection. It produces contents into the lungs. mucus with a weak cough and accumulation of mucus. Risk Factors Pathophysiology Seizure activity o Decreased level of consciousness from trauma, drug or alcohol intoxication, excessive sedation, or general anesthesia Nausea and vomiting in the patient with a decreased level of consciousness Stroke Swallowing disorders Cardiac arrest Silent aspiration o There is no control in the airway kaya lahat sila ay at risk for aspiration. Pathophysiology and Etiology Loss of protective airway reflexes NG tube feedings May fever and chills kasi the body is undergoing Patients under anesthesia systemic inflammatory response. It is normal for the The effects of aspiration depend on the following: 2 o Particulate matter Inflammatory response. Tingnan if nilalagnat si patient. o Anaerobic bacterial aspiration Kapag tumataas ang WBC, watch out na for signs of o Gastric juice infection and inflammation. Check if the patient underwent weaning. Management Goal: prevent aspiration Maintain the elevation of the head of the bed at 30-45 degrees. Avoid gastric over-distention. Use cuffed ET with inline or subglottic suctioning. ET pressure should be at least 20 cm H2O. Avoid unplanned extubation and reintubation. Regular oral care with an antiseptic solution. Orotracheal over nasotracheal intubation. Rinse reusable respiratory equipment with sterile water. Remove condensate from ventilatory circuits. Charge circuit only when using visibly soiled or malfunctioning. Store and disinfect respiratory therapy equipment properly. VENTILATOR-ASSOCIATED PNEUMONIA 3 Mechanisms by which V.A.P. Develops Nursing Management Aspiration of secretions Assessment: airway obstruction, risk factors for o Nagpakain habang nakahiga ang patient, aspiration, development of fever, foul-smelling nagpakain kahit hindi chineck ang patency or sputum, and congestion placement. O2 therapy Colonization of the aerodigestive tracts Clearing the airway o Every time ang patient na kakain siya, iaassess o Proper positioning muna ang abdomen if hyper- or hypoactive o Checking NGT patency ang bowel movements. Pwede o Proper suctioning magregurgitate or VAP. Contaminated equipment Complications o Hindi nagpapalit ng gamit (madumi) Immunocompromised patients SLE patients Diagnostic Tests CA patients Chest X-ray ABG PLEURAL EFFUSION Laryngoscopy Collection of fluid in pleural space Bronchoscopy Secondary to diseases Effusion can be clear, bloody, or purulent Pathophysiology Etiology Either transudative or exudative. Occurs as a complication of another disorder. Pathophysiology 3 o Chronic productive cough lasting 3 months for at least 2 consecutive years. Emphysema o The abnormal distention of air spaces beyond the terminal bronchioles with destruction of the walls of the alveoli. Asthma is reversible, chronic bronchitis and emphysema are irreversible. Pathophysiology General Management Treat underlying cause Thoracentesis o Kapag marami ang nakukuha sa thoracentesis, mag-CTT na or ihook sa 3-way bottle system o Ang normal ay tidaling pero kapag continuous bubbling sa water seal, refer immediately kasi baka may leak, blockage, or kink. If may inflammation, si goblet cells ay active na o Kapag nabasag ang chamber, ilagay sa isang magproduce ng plema. container with sterile water immediately Wala pang gumagaling sa COPD pero namamanage. (dapat nasa bedside na). o Kapag tumigil ang tidaling, possible na may COPD Acute Exacerbations: Triggers and Signs/Symptoms kink or blockage. Kapag walang kink or blockage pero tumigil pa rin ang tidaling, it means na nakakapag-expand na ang lungs (can be verified thru CXR). Pleurodesis o Kapag ready na tanggalin ‘yung tube pero makapal pa rin ang pleural space, do pleurodesis to create a physiologic adhesion. Chest tube insertion Nursing Management Maintain normal breathing pattern Fowler’s position Assist with thoracentesis and/or pleurodesis Pain management Care of chest tube Oxygen therapy Exacerbation is the worsening of the disease or an increase in its symptoms. Need to ask if may previous hospitalization, vaccines, o Laging 2x or 3x ang symptoms. living conditions (saan nakatira, populated ba What triggers acute exacerbation? masyado), proper ventilation of air. o Environmental pollutants/exposure to the We start antibiotics once nakuha na ang culture para allergens mamodify pa ang ibibigay na antibiotic. ▪ Smoking ▪ Pollution CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) ▪ Underlying infections Also known as chronic airway limitation (CAL). What is the first line of management? Diseases that cause airflow obstruction and are not o Bronchodilators first, then oxygenation. fully reversible. If the doctor orders oxygen therapy, what will you Chronic Bronchitis prepare or consider? 4 o Monitor oxygen saturation o ABG o Appropriate oxygen delivery – low flow oxygen via nasal cannula or simple mask. ▪ Kasi need to release ang carbon dioxide. Pwede ba si patient iswitch sa higher dosage ng oxygen? o Yes, but check the ABG first. Diagnostic and Laboratory Tests Chest x-ray shows hyperinflation and increased broncho vascular markings Pulmonary Function Test – increased RV, decreased VC ABG – acidosis and alkalosis with O2 reduction Sputum – reveals the causative agent of infection ECG – right ventricular hypertrophy and arrhythmias Critical Pulse oximetry - decreased O2 saturation o Absence of wheezing kasi may airway CBC – increased Hb obstruction na. Alpha 1 antitrypsin deficiency Spirometry Clinical Assessment MILD MODERATE SEVERE Breathless Walking Talking At rest Management Talks in Sentences Phrases Words Avoid air pollutants Alertness May be agitated Usually agitated Agitated Stop smoking (most common cause) RR Inc Inc >30 Accessory (-) (+) (+) Adequate hydration to loosen secretion Wheeze Audible Audible Audible w/o Chest physiotherapy stethoscope Nebulizer to loosen secretions Pulse 120 Low O2 Antibiotics for infection Diagnostic and Laboratory Tests Bronchodilators to relieve spasms ABG – respiratory acidosis Steroids for inflammation Pulmonary Function Test – expiratory volume is Diuretics for edema decreased Surgery Chest X-ray – hyperinflation from air trapping Patient underwent left pneumonectomy Sputum Exam – increased viscosity or C&S to identify o Turn the patient to the unaffected side para infecting agent makapag-expand ‘yung unaffected side ng CBC count – increase eosinophils lungs. Wala naman kasi makakapag-expand Serum Theophylline – therapeutic range is 10-20 sa affected side. ug/mL Patient underwent left lobectomy ECG – to detect side effects of bronchodilators o Turn to the unaffected side para makapagheal Skin testing – to identify specific allergens ‘yung affected side. Pulse oximetry – O2 saturation is decreased ASTHMA Management Clinical Manifestations Avoid precipitating factors Classical signs of asthma Increase fluid intake and adequate nutrition/non- o Wheezing allergenic diet o Dyspnea Desensitization to specific antigen o Cough Oxygen therapy Labored breathing Orthopneic position Prolonged exhalation Environmental modification Engorged neck veins Health education Critical sign: Status asthmaticus – nonresponsive sa treatment. o Absence of wheezing – total shutdown Tingnan ang hypoxic levels niya, check if the px is a candidate for intubation. Pathophysiology Medications: Bronchodilators – reduce bronchial edema o Theophylline 5 o Aminophylline o Epinephrine o Albuterol o Metaproterenol o Terbutaline Corticosteroids – anti-inflammatory and immunosuppressive effect o Hydrocortisone o Methylprednisolone Mast Cell Stabilizers – inhibits degranulation of Mast cells o Cromolyn Sodium o Nedocromil Sodium SRS-A Inhibitors – inhibits production o Zafirlukast (Accolate) o Montelukast (Singulair) ‘Yung alveoli wall may transcapillary pressure gradient Asthma Acute Exacerbation: Pathogenesis and Treatment kaya napupunta ‘yung water from the capillary to the interstitium going to the alveoli, which leads to pink frothy sputum kasi nagmix na ang mucus at water sa alveoli. Clinical Manifestations Dyspnea on exertion Air hunger Central cyanosis, anxiety, agitation Cough with foamy, frothy sputum Crackles in lung bases, tachycardia General Management (Medical) Reduce extravascular fluid o Diuretics Improving gas exchange and myocardial function o Digoxin o Morphine PULMONARY EDEMA Correcting underlying disorder Abnormal accumulation of fluid in lung tissue/alveolar o High concentration of O2 via nasal cannula space. o Assisted ventilation Due to or secondary to the backup of blood into the o Diuretics pulmonary vasculature, hypervolemia, and increased o Positive inotropic such as Digoxin intravascular pressure in the lung. o Morphine Conditions that lead to pulmonary edema o Heart failure PULMONARY EMBOLISM o Chronic kidney failure Obstruction of the pulmonary artery by a thrombus. o Pneumonia Virchow’s triad o Anasarca – severe buildup of fluids in the o Hypercoagulable state tissues o Vessel injury ▪ Caused by hypertension, once Pathophysiology: Negative Pressure Pulmonary Edema nagkameron ng damage, it leads to thrombus o Venostasis gawa ng or leads to immobility o Deep venous thrombosis o Homan’s sign - a physical test where dorsiflexion of the foot causes calf pain. Managament o Umbrella filter o Pampatunaw ng thrombus o Embolectomy 6 Risk Factors Management Associated with trauma, prolonged immobility Subsequent Management Most common origin: deep veins of the leg o Anticoagulation and Thrombolysis o IV Heparin Pulmonary Infarction o Oral coagulation (coumadin) Refers to the necrosis of the lung tissue that can result o Streptokinase from the interference with blood supply. Surgical Management o Embolectomy Pulmonary Embolism: Pathogenesis and Clinical Findings o Interruption of the vena cava ▪ Ligation, clipping, insertion of umbrella filter Umbrella Filter If the Patient is in a Critical State Notify the RAPID RESPONSE TEAM D-dimer – definitive laboratory test used to detect the Elevate the head of the bed degree of embolism. Administer oxygen Pulmonary edema + pulmonary embolism = ARDS Check V/S and lung sounds ABG Etiology Prepare to administer heparin therapy Predisposing factors Document o Stasis of blood PT/PTT test before heparin therapy (thrombi stabilizer) o Concurrent phlebitis Proper positioning o Injury to the vessel wall o Elevate HOB kapag may blood clot. o Coagulation disorders o Kapag air embolism, decrease the HOB, dapat Obstruction reverse Trendelenburg – away from the heart. Hemodynamic Consequences o Increased pulmonary vascular resistance ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) o Increased RV workload to maintain Noncardiogenic pulmonary edema pulmonary blood flow Sudden and progressive pulmonary edema o RVF Unresponsive to O2, with decreasing lung compliance o Decreased CO, BP Nalulunod ang lungs ni patient sa fluid o Shock Px is unresponsive to O2 Diagnostic Test and Procedures Pathophysiology of ARDS ABG Chest x-ray V/Q Scan Pulmonary Angiogram Management for Massive Pulmonary Embolism Goal: stabilize cardio-respiratory status Administer O2 Start an IV line Vasopressors, inotropic agents, and antidysrhythmic agents, morphine ECG, pulmonary angiography, ABG, hemodynamic measurements Microvascular obstruction – pulmonary embolism Surfactant defect 7 o Exacerbation diseases Steroids to reduce inflammation o COPD NaHCO3 to reverse acidosis o Pneumonia Antibiotics o Asbestosis Hypoxia/hypoxemia – oxygenation, PEEP – helps the alveoli from collapsing. Alveolar Changes in ARDS Reduce anxiety – use sedatives Hypotension – elevate ang foot To relieve pressure from the back, use a proning position. This receives more alveoli for gas exchange. o Mas nakaka-expand ang lungs o Less pressure sa heart RESPIRATORY FAILURE An alteration in the function of the respiratory system that causes the PaO2 to fall below 50 mmHg and causes the PCO2 to rise above 50 mmHg (hypoxemia and hypercapnia) Acute RF – hypoxemia and hypercapnia with acidemia/acidosis. Occurs rapidly in minutes. o Acidotic pH Chronic RF – hypoxemia and hypercapnia with normal ARDS: Pathogenesis and Clinical Findings pH. Occurs over a long period from months to years. Allows activation of compensatory mechanism. o Normal pH Definitive test - ABG Pathophysiology and Etiology Oxygenation failure o Decrease in PaO2 and normal or decreased PaCO2 ▪ Etiology: cardiogenic pulmonary edema, ARDS o Primary problem: hypoxemia o Alveolar- capillary membrane damage o Hypocapnia results from hypoxemia and decreased pulmonary compliance o Change in compliance – increased ventilation o Permeable ang alveoli kaya pabagsak lahat. Compensatory stage (manage the patient immediately) Decreased perfusion. o Tachypnea Ventilatory failure with normal lungs o Tachycardia o Decrease in PaO2, increase in PaCO2, decrease in pH Clinical Manifestations ▪ Etiology: insufficient respiratory Initial – severe dyspnea, retraction of ICS, bibasilar center activity and insufficient chest crackles, and rhonchi wall function Decreased LOC o Primary problem: alveolar hypoventilation Pink frothy sputum o Hypercapnia Late – severe hypoxemia – hypotension, decreased o Acidemia – results from a combination of CO2 urine output, acidosis, arrhythmias and H2O Oliguria o Hypoxemia – consequence of hypercapnia o Healthy lungs but the problem is in the General Management neurotoxic center, brain, chest Treat the cause and prevent hypoxemia ▪ Head trauma O2, nebulization, chest physiotherapy ▪ CNS depression Suctioning ▪ Flail chest ETT with mechanical ventilator; PEEP to improve ▪ Open pneumothorax oxygenation ▪ Trauma in the chest Fluids and vasopressors to maintain blood pressure o Alveolar hypoventilation Sedatives and narcotics to minimize restlessness Ventilatory failure with intrinsic lung disease Vecuronium (neuromuscular blocking agent) o Decrease in PaO2 and decrease in pH 8 ▪ Etiology: CAL, severe asthma, cystic o Prepare to assist in intubation and mechanical fibrosis ventilator initiation. o Primary problem: acute exacerbation or chronic progression of previously existing lung disease resulting in CO2 retention o Hypercapnia o Acidemia o Hypoxemia o Problem with lungs and ventilatory failure ▪ Severe asthma, cystic fibrosis, CAL, COPD ▪ Chronic respiratory failure ▪ Tumor formation ▪ Acute exacerbation worsens the underlying condition. Signs and Symptoms Hypoxemia – restlessness, dyspnea, agitation, disorientation, confusion, delirium, LOC Hypercapnia – headache, dizziness, confusion Tachypnea Accessory muscle use Asynchronous respirations Diagnostics ABG analysis Pulse oximetry Procedures to determine the underlying cause or primary disorders (CBC, electrolytes, chest x-ray, urinalysis, ECG, sputum, and blood cultures) General Management O2 therapy Bronchodilators and corticosteroids Diuretics Mechanical ventilation General rule (umbrella management): ano ba ang underlying cause? Correct the underlying disease Nursing Assessment Breath sounds: diminished or absent breath sounds, crackles, wheezing, and rhonchi LOC Signs of hypoxia Analyze ABG* - important Nursing Management Focus on improving gas exchange and maintaining airway clearance o Administer antibiotics, cardiac meds, and diuretics as ordered. o Administer O2. o Provide measures to prevent atelectasis and promote chest expansion and secretion clearance. o Perform chest physiotherapy, and suctioning as needed. o Monitor I&O strictly. 9

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