Respiratory Emergencies PDF

OUTLINE There is a natural steroid produced I. Respiratory Distress a. Status Asthmaticus by the body, but...

OUTLINE There is a natural steroid produced I. Respiratory Distress a. Status Asthmaticus by the body, but since you are given b. COPD steroids, the intrinsic source stops c. Pneumonia producing the natural steroid. That's II. Acute Pulmonary Edema why tapering doses must be done III. Pneumothorax to let the body slowly buildup the IV. Pulmonary Embolism production of the steroid from an intrinsic source. Respiratory Distress Acute respiratory distress syndrome (ARDS) is a Ingestion of aspirin and/or related drugs in life-threatening lung injury that allows fluid to leak into aspirin-sensitive patient the lungs. Breathing becomes difficult and oxygen cannot get into the body. Most people who get ARDS Clinical Manifestations are already at the hospital for trauma or illness. - Labored respirations, with increased effort on (American Lung Association - www.lung.org) exhalation ○ expiratory wheeze Signs and Symptoms Distended neck and face veins Severe shortness of breath Labored and rapid breathing that is not usual ○ bc of the pressure exerted into the systemic Cough circulation (vena cava) Chest discomfort Fatigue (d/t effort of breathing), headache, irritability, Tachycardia dizziness, impaired mental functioning ○ bumaba O2 = compensatory mechanism to ○ from hypoxia pump more blood CO2 doesn’t go out d/t Confusion and extreme fatigue bronchoconstriction → O2 di Causes pumapasok ng maayos Sepsis (most common cause of ARDS) Muscle twitching, somnolence, diaphoresis Severe pneumonia (affecting all five lobes of the ○ from continued carbon dioxide retention lungs) Heart failure and death from suffocation (Cor Coronavirus disease 2019 (COVID-19) pulmonale) Head, chest or other major injury (accidents, such as falls or car crashes, can damage the lungs or the Chest X-Ray portion of the brain that controls breathing) Breathing in harmful substances Hyperinflation Other conditions and treatments (asthma, allergic reactions / anaphylaxis, BT reaction, prematurity) A. Status Asthmaticus Severe form of asthma; airway obstruction is unresponsive to conventional therapy; Does not respond to primary medications Lasts >24 hrs pag marami black, that’s air Medical emergency, an extreme form of asthma branches are not present in the exacerbation characterized by hypoxemia, film hypercarbia, and secondary respiratory failure. X-ray doesn’t really show definite Contributing Factors signs of asthma, but signs can be Infection identified like hyperinflation Overuse of tranquilizers (CNS depressant) Nebulizer abuse (builds tolerance) ○ depresses respiratory centers Dehydration Inhalation of air pollutants Noncompliance in taking medications Sudden reduction in corticosteroids (should taper doses before discontinuing) ○ with steroids: negative feedback mechanism 1 bbg | 2025  Occupational exposures Pneumothorax Clinical Manifestations Chronic cough Shortness of breath with ADLs (dyspnea) Coughing up sputum (phlegm or mucus) Wheezing or chest tightness Fatigue Unable to take a deep breath Respiratory Restriction Barrel chest – hyperinflated lungs d/t enlarged terminal bronchioles ○ increased pressure inside → need more space → thoracic cage increases → barrel chest ○ Ineffective breathing pattern due to lack of respiratory effort aeb no recoil of chest/ limited movement of chest that pleural white lin Alveoli Changes Mediastinal shift ○ Alveoli lose their elasticity with COPD and become enlarged, forming large air spaces Pulmonary called bullae; reduces surface area and Edema impairs lung function Bronchospasm ○ The muscle surrounding the airways can become contracted and tight, which causes narrowing and reduced airflow. Chronic Inflammation and Irritation ○ The bronchial tubes become inflamed and irritated, which causes thickening of the all white is the interstitial fluid passages and excess mucus, leading to airway obstruction and DOB Impaired gas exchange B. COPD ○ alveolar damages result in less function with Chronic Obstructive Pulmonary Disease – the exchange of oxygen and carbon dioxide; Smoker’s Disease leading to symptoms like SOB and fatigue A condition caused by damage to the airways or other Chest X-Ray parts of the lung that blocks airflow and makes it hard costophrenic angle – flat to breathe narrowed bronchial trees Group of conditions characterized by continued lung lining above scapula increased resistance to expiratory airflow. A person diaphragm is flattened with COPD may have: clavicle - pantay ○ Excessive secretion of mucus and chronic hyperinflated lungs infection within the airways (bronchitis - cardiac silhouette- the heart should have at least ⅓ of the width of the entire thorax chronic, long-term) ○ An increase in size of air spaces distal to the terminal bronchioles, with loss of alveolar walls and elastic recoil of the lungs (emphysema) ○ There may be an overlap of these conditions. “Pink-puffers” Lower terminal airways Contributing Factors History of childhood respiratory infections Smoking / vaping Smoke exposure from coal or wood burning stove C. Pneumonia (indoor / outdoor pollutants) Inflammatory process involving the terminal airways Exposure to secondhand smoke and alveoli. People with a history of asthma Primarily caused by infectious agents such as People who have underdeveloped lungs bacteria, viruses and other foreign bodies. Age 40 and older as lung function declines with age 2 bbg | 2025  Air sacs fill up with fluid or pus, causing symptoms Depression of the central nervous system (from such as a cough, fever, chills and trouble breathing. drugs – including alcohol, head injury) predispose the ○ Intact alveoli → becomes filled with fluid → patient to pneumonia. impaired gas exchange Persons over 65 have a high mortality rate, even Lowest terminal airways with appropriate antimicrobial therapy. Predisposing Factors Clinical Manifestations The organism gains access to the lungs through Bacterial Pneumonia aspiration of oropharyngeal contents, by inhalation of Sudden onset; shaking chill; rapidly rising fever respiratory secretions from infected individuals, via (39.5-40.5 C) the bloodstream, or from direct spread to the lungs ○ elderly px may not manifest fever anymore from surgery or trauma. usually confusion (sepsis) Cough productive of purulent sputum ○ never event: pag naintubate for a different Pleuritic chest pain aggravated by respiration / problem, dapat hindi magkapneumonia coughing Patients with bacterial pneumonia usually have an Tachypnea (24 - 45/min) accompanied by respiratory underlying disease that impairs host defense; more grunting, nasal flaring, use of accessory muscles of often pneumonia arises from endogenous flora of the respiration person whose resistance has been altered or from Rapid bounding pulse aspiration of oropharyngeal secretions. Chest X-Ray When bacterial pneumonia occurs in a healthy Pneumonia- chest is expanded, may white person, there usually is a history of preceding viral consolidate? illness. COVID19 – broken glass effect Pneumonia may be divided into three groups: ○ Community-acquired (CAP), due to a number of organisms, namely Streptococcus pneumoniae; AIDS ○ Hospital or nursing home acquired (nosocomial or HAP) due primarily to gram-negative bacilli and staphylococci; a ○ In the immunocompromised person. Immunocompromised patients (those receiving CURB Criteria for CAP corticosteroids; those with cancer; those being treated with chemotherapy or radiotherapy; those undergoing organ transplantation = immunosuppressants) have an increased chance of developing overwhelming infection. A wide variety of pulmonary infections may develop in patients receiving immunosuppressive drugs (aerobic and anaerobic gram-negative bacilli, Staphylococcus, Nocardia, fungi, Candida, viruses [including cytomegalovirus], Pneumocystis carinii, reactivation of tuberculosis, and others). Any condition interfering with normal drainage of the lung will predispose the person to pneumonia (e.g., cancer of the lung). Postoperative patients may develop bronchopneumonia, since anesthesia impairs respiratory defenses and decreases diaphragmatic movement. ○ extubating patients → spirometry in bedside to exercise breathing of post op patients ○ within 24 hours – px must be able to change positions ○ within 48 hours – px can ambulate ○ dapat after 24hrs, make sure px to mobilize progressively: upo, dangling feet, go to chair, walk in the room ○ give pain relief if may post-op pain 3 bbg | 2025  ○ nag kakaroon ng imbalance sa o2 and co2 = lack of O2 sa body (ineffective breathing pattern is 2nd Nursing diagnosis) Diagnostics Medical history, physical examination Chest X-ray Echocardiogram (suspected valvular disease) Measurement of pulmonary artery wedge pressure (PAWP) by Swanz-Ganz catheter (differentiates etiology of pulmonary edema-cardiogenic or altered alveolar-capillary membrane) Blood cultures (suspected infection) Cardiac enzymes (suspected MI) Chest X-Ray Acute Pulmonary Edema A feature of many conditions of diverse etiology. The effects on lung mechanics and gas exchange make it one of the common causes of respiratory failure. Pulmonary edema is most often due to: ○ increased microvascular hydrostatic Noncardiogenic Cardiogenic pressure, associated with left-sided or bilateral cardiac failure (cardiogenic edema) obliterated all of the lungs is ○ hypervolemia (excessive fluid therapy), may costophrenic angle d/t covered with fluid wet sounds fluid always acute shifting of fluid pero wlaang excess fluid sa body. No costophrenic angle always up to lung apex emergency situation Causes elevated, intact Heart disease (acute LV failure, MI, AS, severe mitral diaphragm valve disease, hypertension, CHF) mas maraming tubig ○ bumubula ung bibig dahil sa pulmonary heart is really enlarged edema - suction Circulatory overload – transfusions and infusions Drug hypersensitivity; allergy; poisoning POCUS Ultrasound / Echocardiogram showing B-line Lung injuries – smoke inhalation, shock lung, pulmonary embolism or infarct CNS injuries – stroke, head trauma Infection and fever-infectious pneumonia (viral, bacterial, parasitic) Post-cardioversion, post-anesthesia, post-cardiopulmonary bypass Narcotic overdose Clinical Manifestation B-line is generated by UTZ resembling water Coughing and restlessness during sleep (premonitory ○ B-line – like rays of light symptoms) ○ all of it is fluid Extreme dyspnea and orthopnea – patient usually uses accessory muscles of respiration with retraction Echocardiogram of intercostal spaces and supraclavicular areas Cough with varying amounts of white or pink-tinged frothy sputum ○ nasira ung capillaries/ alveoli= nagbleed= pink sputum Noisy breathing – inspiratory and expiratory wheezing and bubbling sounds Cyanosis with profuse perspiration Distended neck veins (d/t excess fluid) Tachycardia (compensatory mechanism) Precordial pain (if pulmonary edema s/t to MI) Mitral valve pliable → regurgitation of fluid Extreme anxiety and panic 4 bbg | 2025  LV does not close properly meaning maraming laman Chest X-Ray sa loob = congestion Pneumothorax Air in the pleural space occurring spontaneously from injury or disease. In patients with chest trauma, it is usually the result of a laceration to the lung parenchyma, tracheo-bronchial tree, or esophagus The patient’s clinical status depends on the rate of air leakage and size of wound. Seldom complain of chest pain compressed to the lung Assessment Hyperresonance; diminished breath sounds ○ bc of the air present Reduced mobility of affected half of thorax Rarely presents as chest pain except when trauma is the cause ○ Tactile fremitus – kung saan may pneumothorax – dun may gumagalaw SOB Asymmetric breathing Types mediastinal shift to the left bc right lung is being Spontaneous Pneumothorax compressed by pleural space = may lead to Tension Pneumothorax hypotension Spontaneous Pneumothorax May occur in healthy individuals; usually d/t rupture of a subpleural bleb of the lung ○ Treatment is generally non-operative if pneumothorax is not too extensive; needle aspiration or chest tube drainage may be necessary to achieve re-expansion of collapsed lung ○ Surgical intervention (thoracotomy) is advised for patients with recurrent spontaneous pneumothorax ○ Pleurodesis – lalagyan ng talcum powder dun sa pleural space, para induce ng whole chest collapses = flail chest due to multiple rib inflammation, magstick yung pleura, para no fractures space for fluid build-up = downside, may pain si px Pulmonary Embolism Refers to the obstruction of one or more pulmonary Tension Pneumothorax arteries by a thrombus (or thrombi) or originating Buildup of air under pressure resulting in interference usually in the deep veins of the legs or in the right with filling of both the heart and lungs side of the heart, which becomes dislodged and is Mas common ito sa ph specially post op patients carried to the lungs. ○ clinical picture is one of air hunger, agitation, Pulmonary Infarction – necrosis of lung tissue that hypotension, and cyanosis; there is an acute can result from interference with blood supply. threat to life hypotension - due to the Predisposing Factors compression of the heart Stasis; prolonged immobilization Concurrent clinical phlebitis Management ○ DVT Immediate insertion of a chest tube drain to allow air Previous heart (CHF or MI) or lung disease to escape (chest tube then connected to ○ complains impending doom feeling under-water-seal suction). Injury to vessel wall - endothelial injury Use thoracentesis for emergency decompression of Coagulation disorders pleural space until tube thoracostomy can be Metabolic, endocrine, vascular, or collagen disorders accomplished. ○ Diabetic px Malignancy Advancing age; estrogen therapy COVID 19 - hypercoagulability 5 bbg | 2025 Diagnostic Evaluation Emergency Management (Massive Pulmonary Embolism) Physical findings: clinical signs and symptoms are Goal: To stabilize the cardiorespiratory system elusive ○ Administer O2 to relieve hypoxemia, ABG – systemic arterial hypoxemia d/t perfusion respiratory distress, and cyanosis abnormality of the lung ○ Establish IV access drugs / fluids Radioisotope lung scans (V/Q or SPECT/CT) – ○ Vasopressors, inotropic agents (dopamine) perfusion scan investigates regional blood flow to and/or antidysrhythmic agents may be determine presence of perfusion defects; ventilation indicated to support circulation if the patient scan may be done in patients with large perfusion is unstable defects. ○ Continuous cardiac monitoring – to WOF RV Pulmonary angiogram (most definitive) failure (rapid onset) Contrast phlebography or impedance phlebography – ○ Small doses of IV morphine (PRN) are given for DVT to relieve anxiety, to alleviate chest CT angiography – only used when other dx tests are discomfort (which improve ventilation), and not working to ease adaptation to mechanical ventilator, if this is necessary V/Q Scan ○ Carry out pulmonary angiography, priority problem: make sure thrombus is removed and hemodynamic measurements, ABG to that oxygenation is improved determination, etc. you need to make more oxygen bc the remaining tissues need to get oxygenated, bc if you do not give enough o2, lalaki yung area Normal V (alveolar ventilation) value is around 4 L/min Normal Q (perfusion) value is around 5 L/min Normal V/Q Ratio: ⅘ or 0.8 ○ V/Q > 0.8 – ventilation exceeds perfusion blood clots, heart failure, emphysema, or damage to the pulmonary capillaries may cause this ○ V/Q < 0.8 – perfusion exceeds ventilation aspiration, blockage of bronchi by a foreign object, pneumonia, severe asthma, pulmonary edema, or COPD Subsequent Management (Massive Pulmonary Embolism) Anticoagulation (for clinically stable patient) HEPARIN (IV) first line stops further thrombus formation and extends the clotting time of the blood; both an anticoagulant and antithrombotic ○ IV loading dose usually followed by continuous pump or drip infusion or given intermittently every 4-6 hrs ○ Dosage adjusted to maintain the activated partial thromboplastin time at 1.5 - 2 times the pre-treatment value (if value was normal) 6 bbg | 2025  Ineffective breathing pattern r/t ○ Protamine sulfate may be ○ chronic airflow limitation (bronchospasm) given to neutralize heparin in the event of severe Ineffective airway clearance r/t bleeding. ○ bronchospasm, increased mucus production, ineffective cough, possible Oral used for follow-up anticoagulant bronchopulmonary infection Anticoagulation therapy after heparin therapy has (WARFARIN) been established; interrupts the Potential for respiratory infection r/t coagulation mechanism by ○ compromised pulmonary function interfering with the vitamin K-dependent synthesis of Altered nutrition (less than body requirements) r/t prothrombin and factors VII, IX, ○ increased work of breathing and X ○ air swallowing Note: Dosage is controlled by ○ medication effects monitoring serial tests of ○ impaired gastrointestinal function (bloating; prothrombin time; desired reflux) prothrombin time is 1.2 - 1.5 times ○ depression control value monitor aptt every 3 days Activity intolerance r/t compromised pulmonary function resulting in shortness of breath and fatigue Oral has more advantages over Anticoagulation warfarin, including: Sleep pattern disturbance r/t hypoxemia and (Novel Oral ○ more predictable hypercapnia Anticoagulant pharmacokinetics which [NOAC]) eliminate the need for Impaired individual coping r/t stress of living with routine aPTT monitoring chronic disease ○ rapid onset of action ○ shorter half-life Risk for aspiration r/t breathing difficulties ○ fewer drug and food interactions Knowledge deficit of how to live with chronic obstructive pulmonary disease Characteristics: Anxiety (specify level: mild, moderate, severe, panic) Acute Pulmonary Edema Impaired gas exchange r/t ○ excess fluid in the lungs ○ acute pulmonary obstruction resulting to reduced ventilation (V/Q mismatch) Ineffective breathing pattern r/t Thrombolytic Enzyme ○ airflow limitation brought about by fluid Thrombolytic agents (urokinase; streptokinase) may accumulation be used in patients with massive pulmonary embolism; effective in lysing recently formed thrombi; Anxiety (specify level: mild, moderate, severe, panic) improve circulatory and hemodynamic status r/t sensation of suffocation and fear Administer IV in a loading dose followed by constant infusion Pneumothorax Newer clot-specific thrombolytics (tissue type Acute pain (only if there is) r/t plasminogen activator [t-PA], acylated plasminogen, ○ presence of air in the thoracic cavity streptokinase activator complex, single-chain ○ chest injury urokinase) ○ activate plasminogen only w/i thrombus itself Impaired gas exchange r/t rather than systematically ○ ventilation and perfusion imbalance (V/Q ○ minimize occurrences of generalized mismatch) fibrinolysis and subsequent bleeding ○ reduced functional lung tissue due to compression Nursing Diagnoses Ineffective breathing pattern r/t Respiratory Distress ○ limited / asymmetrical lung expansion Impaired gas exchange r/t ○ airway compression brought about by ○ increased alveolar-capillary permeability, mediastinal shift / tracheal deviation interstitial edema, and decreased lung compliance ○ chronic pulmonary obstruction (V/Q abnormalities) 7 bbg | 2025  Pulmonary Embolism Ineffective breathing pattern r/t increase in alveolar dead space and possible changes in lung mechanics from embolism Altered tissue perfusion r/t decreased blood circulation (lungs) Pain (pleuritic) r/t ○ congestion ○ possible pleural effusion ○ possible lung infarction Anxiety r/t ○ dyspnea ○ pain ○ seriousness of condition Knowledge deficit of current condition and long-term treatment 8 bbg | 2025