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Emergencies Resulting from Pulmonary Diseases & Disorders EMS Professions Temple College Pulmonary Diseases & Disorders Pulmonary Disease & Conditions may result from: – Infectious causes – Non-Infectious causes Adversely affect one or more of the following – Ventilation – Diffusion – Perfusion Pulmonary Diseases & Disorders The Respiratory Emergency may stem from dysfunction or disease of (examples only): – Control System • Hyperventilation • Central Respiratory Depression • CVA – Thoracic Bellows • • • • • Chest/Diaphragm Trauma Pickwickian Syndrome Guillian-Barre Syndrome Myasthenia Gravis COPD Pulmonary Diseases & Disorders The Respiratory Emergency may affect the upper or lower airways Upper Airway Obstruction – – – – – – Tongue Foreign Body Aspiration Angioneurotic Edema Maxillofacial, Larnygotracheal Trauma Croup Epiglottitis Respiratory Emergencies: Causes Lower Airway Obstruction – – – – Emphysema Chronic Bronchitis Asthma Cystic Fibrosis Pulmonary Diseases & Disorders The Respiratory Emergency may stem from Gas Exchange Surface Abnormalities – – – – – – Cardiogenic Pulmonary Edema Non-cardiogenic Pulmonary Edema Pneumonia Toxic Gas Inhalation Pulmonary Embolism Drowning Pulmonary Diseases & Disorders Problems with the Gas Exchange Surface Pulmonary Edema Pulmonary Edema: Pathophysiology A pathophysiologic condition, not a disease – Fluid in and around alveoli – Interferes with gas exchange – Increases work of breathing Two Types – Cardiogenic (high pressure) – Non-Cardiogenic (high permeability) Pulmonary Edema High Pressure (cardiogenic) • AMI • Chronic HTN • Myocarditis High Permeability (non-cardiogenic) • Poor perfusion, Shock, Hypoxemia • High Altitude, Drowning • Inhalation of pulmonary irritants Cardiogenic Pulmonary Edema: Etiology Left ventricular failure Valvular heart disease – Stenosis – Insufficiency Hypertensive crisis (high afterload) Volume overload Increased Pressure in Pulmonary Vascular Bed Pulmonary Edema High Permeability – Disrupted alveolar-capillary membrane – Membrane allows fluid to leak into the interstitial space – Widened interstitial space impairs diffusion Non-Cardiogenic Pulmonary Edema: Etiology Toxic inhalation Near drowning Liver disease Nutritional deficiencies Lymphomas High altitude pulmonary edema Adult respiratory distress syndrome Increased Permeability of Alveolar-Capillary Walls Pulmonary Edema: Signs &Symptoms Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea Noisy, labored breathing Restlessness, anxiety Productive cough (frothy sputum) Rales, wheezing Tachypnea Tachycardia Management of Non-Cardiogenic Pulmonary Edema Position Oxygen PPV / Intubation – CPAP – PEEP IV Access; Minimal fluid administration Treat the underlying cause – Diuretics usually not helpful; May be harmful Transport Adult Respiratory Distress Syndrome AKA: Non-cardiogenic pulmonary edema A complication of: – – – – – – – – Severe Trauma / Shock Severe infection / Sepsis Bypass Surgery Multiple blood transfusions Drug overdose Aspiration Decreased compliance Hypoxemia ARDS Pathophysiology A condition resulting from severe illness or injury and associated with a high mortality rate – – – – – – Increased permeability Pulmonary edema Surfactant destruction Atelectasis Decreased compliance Hypoxemia ARDS Presentation History – Recent hx of severe illness or injury – Often already being treated for underlying cause Exam Findings – – – – Dyspnea Evidence of pulmonary edema Poor oxygenation Decreased lung compliance ARDS Management Airway Management – Endotracheal intubation – Suction Mechanical Ventilation – PEEP ECG Monitoring Treat underlying cause – May require vasopressors for shock Pneumonia Pneumonia Fifth leading cause of death in US Group of Specific infections Risk factors – Cigarette smoking – Exposure to cold – Extremes of age • young • old Pneumonia Inflammation of the bronchioles and alveoli – Products of inflammation (secretions, pus) add to respiration difficulty Gas exchange is impaired Work of breathing increases May lead to – – – – Atelectasis Sepsis VQ Mismatch Hypoxemia Pneumonia: Etiology Viral Bacterial Fungi Protozoa (pneumocystis) Aspiration Presentation of Pneumonia Shortness of breath, Dyspnea Fever, chills Pleuritic Chest Pain, Tachycardia Cough – Green/brown sputum May have crackles, rhonchi or wheezing in peripheral lung fields – Consolidation – Egophony Management of Pneumonia Treatment mostly based upon symptoms – – – – – – Oxygen Rarely is intubation required IV Access & Rehydration B2 agonists may be useful Antibiotics (e.g. Rocephin) Antipyretics Pneumonia: Management MD follow-up for labs, cultures & Rx Transport considerations – – – – Elderly have significant co-morbidity Young have difficulty with oral medications ED vs PMD office/clinic Transport in position of comfort Would an anticholinergic like Atrovent be useful in managing pneumonia? Pulmonary Embolism Pulmonary Embolism ~ 50,000 deaths / year – ~5% of all sudden deaths – <10% of all PE result in death Pulmonary Embolism: Pathophysiology Something moving with flow of blood passes through right heart into pulmonary circulation It reaches an area too narrow to pass through and lodges there Part of pulmonary circulation is blocked Blood: – Does not pass alveoli – Does not exchange gases Pulmonary Embolism (PE) A disorder of perfusion Combination of factors increase probability of occurrence – Hypercoagulability – Platelet aggregation – Deep vein stasis Embolus usually originates in lower extremities or pelvis Pulmonary Embolism (PE) Risk factors – Venostasis or DVT – Recent surgery or trauma • Long bone fractures (lower) – – – – Oral contraceptives Pregnancy Smoking Cancer Pulmonary Embolism: Etiology Most Common Cause = Blood Clots Vessel Wall Injury Virchow’ sTriad Hypercoagulability Venous Stasis Pulmonary Embolism: Etiology Other causes – – – – – Air Amniotic fluid Fat particles (long bone fracture) Particulates from substance abuse Venous catheter Pulmonary Embolism: Signs & Symptoms Small Emboli – – – – – – – – Rapid Onset Dyspnea Tachycardia Tachypnea Fever Episodic = Showers Evidence or history of thrombophlebitis Consider early when no other cardiorespiratory diagnosis fits Pulmonary Embolism: Signs & Symptoms Larger Emboli – – – – – – Small Emboli S/S plus: Pleuritic pain Pleural rub Coughing Wheezing Hemoptysis (rare) Pulmonary Embolism: Signs & Symptoms Very Large Emboli – – – – – – Preceded by S/S of Small & Larger Emboli plus: Central chest pain Distended neck veins Acute right heart failure Shock Cardiac arrest Pulmonary Embolism: Signs & Symptoms There are NO assessment findings specific to pulmonary embolism Pulmonary Embolism: Management Management based on severity of Sx/Sx Airway & Breathing – High concentration O2 – Consider assisting ventilations – Early Intubation Circulation – IV, 2 lg bore sites • Fluid bolus then TKO; Titrate to BP ~ 90 mm Hg – Monitor ECG Rapid transport PE Management Thrombolytics – Aspirin & Heparin (questionable if any benefit) Rapid transport to appropriate facility – Embolectomy or thrombolytics at hospital (rarely effective in severe cases due to time delay) – Poor prognosis when cardiac arrest follows Pulmonary Embolism If the patient is alive when you get to them, that embolus isn’t going to kill them. But the next one they throw might! Pleurisy Inflammation of pleura caused by a friction rub – layers of pleura rubbing together Commonly associated with other respiratory disease Presentation of Pleurisy Sharp, sudden and intermittent chest pain with related dyspnea – Possibly referred to shoulder – May or with respiration Pleural “friction rub” may be audible” May have effusion or be dry Pleurisy Management – Based upon severity of presentation – Mostly supportive Pulmonary Diseases & Disorders Problems with Airway Obstructions Obstructive Airway Diseases Obstructive Airway Disease Asthma Emphysema Chronic Bronchitis Obstructive Airway Diseases Asthma experienced by ~ 4 - 5 % of US population – Mortality rate increasing Factors leading to Obstructive Airway Diseases – Smoking – Exposure to environmental agents – Genetic predisposition How does this differ from “COPD”? Obstructive Airway Disease Exacerbation Factors – Intrinsic • Stress (especially in adults) • URI • Exercise – Extrinsic • • • • Cigarette Smoke Allergens Drugs Occupational hazards Obstructive Airway Disease General Pathophysiology – Specific pathophysiology varies by disease – Obstruction in bronchioles • Smooth muscle spasm (beta) • Mucous accumulation • Inflammation – Obstruction may be reversible or irreversible Obstructive Airway Disease General Pathophysiology – Obstruction results in air trapping • Bronchioles usually dilate on inspiration • Dilation allows air to enter even in presence of “obstruction” • Bronchioles tend to constrict on expiration • Air becomes trapped distal to obstruction Lower Airway Disease Chronic Obstructive Pulmonary Disease Emphysema Chronic Bronchitis (Rarely Asthma may result in COPD) COPD: Epidemiology Most common chronic lung disease 14.8 million cases in U.S. 4th leading cause of death 110,000 deaths annually Emphysema Type A COPD Emphysema: Definition Destruction of alveolar walls Distention of pulmonary air spaces Loss of elastic recoil Destruction of gas exchange surface Emphysema: Incidence Male > females Urban area > rural areas Age usually > 55 Emphysema:Etiology Smoking – 90% of all cases – Smokers 10x more likely to die of COPD than non-smokers Environmental factors Alpha – 1 antitrypsin deficiency – hereditary – 50,000 to 100,000 cases – mostly people of northern European descent Emphysema: Pathophysiology Decreased surface area leads to decreased gas exchange with blood Loss of pulmonary capillaries & hypercapnia lead to – increased resistance to blood flow which leads to • pulmonary HTN • right heart failure (cor pulmonale) Emphysema: Pathophysiology Loss of elastic recoil leads to increased residual volume and CO2 retention – Air Trapping – Hyperinflation – Hypercapnia -> pulmonary vasoconstriction -> V/Q mismatch Emphysema: Signs and Symptoms Increasing dyspnea on exertion Non-productive cough Malaise Anorexia, Loss of weight Hypertrophied respiratory accessory muscles Emphysema: Signs and Symptoms Increased Thoracic AP Diameter (Barrel Chest) Decreased lung/heart sounds Hyperresonant chest Emphysema: Signs and Symptoms Lip pursing on exhalation Clubbed fingertips Altered blood gases – Normal or decreased PaO2 – Elevated CO2 Cyanosis occurs LATE in course of disease PINK PUFFER Chronic Bronchitis Type B COPD Chronic Bronchitis: Definition Increased mucus production for > 3 months for > 2 consecutive years Recurrent productive cough Chronic Bronchitis: Incidence Males > females Urban areas > rural areas Age usually > 45 Chronic Bronchitis: Etiology Smoking Environmental irritants Chronic Bronchitis: Pathophysiology Mucus plugging/inflammatory edema Increased airflow resistance leads to alveolar hypoventilation Alveolar hypoventilation leads to – hypercarbia – hypoxemia Chronic Bronchitis: Pathophysiology Hypoxemia leads to – increased RBC’s w/o oxygen which leads to • cyanosis Hypercarbia leads to – pulmonary vascular constriction which leads to • increased right ventricular work which leads to • right heart failure which may progress to • cor pulmonale Chronic Bronchitis: Signs and Symptoms Increasing dyspnea on exertion Frequent colds of increasing duration Productive cough Weight gain, edema (right heart failure) Rales, rhonchi, wheezing Bluish-red skin color (polycythemia) Headache, drowsiness (increased CO2) Chronic Bronchitis: Signs and Symptoms Decreased intellectual ability Personality changes Abnormal blood gases – Hypercarbia – Hypoxia Cyanosis EARLY in course of disease BLUE BLOATER COPD Assessment Findings Chronic condition acute episode S&S of work of breathing and/or hypoxemia – – – – – Use of accessory muscles Increased expiratory effort Tachycardia, AMS, Cyanosis Wheezing, Rhonchi, LS Thin, red/pink appearance Saturation usually normal in emphysema COPD: Management Causes of Decompensation – Respiratory infection (increased mucus production) – Chest trauma (pain discourages coughing or deep breathing) – Sedation (depression of respirations and coughing) – Spontaneous pneumothorax – Dehydration (causes mucus to dry out) COPD: Management Airway and Breathing – – – – Sitting position or position of comfort Calm & Reassure Encourage cough Avoid exertion Oxygen – Don’t withhold – Maintain O2 saturation above 90 % TRUE HYPOXIC DRIVE IS VERY RARE COPD: Management Ventilation – Avoid intubation unless absolutely necessary • near respiratory failure • exhaustion Circulation – IV TKO – Titrate fluid to degree of dehydration • 250 cc trial bolus – Excessive fluid may precipitate CHF – Monitor ECG COPD: Management Drug Therapy – Obtain thorough medication history – Nebulized Beta 2 agonists • Albuterol • Terbutaline • Metaproterenol • Isoetharine COPD: Management REMEMBER All bronchodilators are potentially arrhythmogenic COPD: Management Drug Therapy – Ipratropium (anticholinergic) by SVN – Terbutaline (beta-2 agonist) by MDI, SQ or IV – Corticosteroids (anti-inflammatory agent) by IV COPD: Management Drug Therapy – Aminophylline (methylxanthine) • • • • Little evidence of benefit in acute management Is arrhythmogenic Produces toxicity easily 2 to 3 hours to peak effect – Magnesium sulfate • Also with little supportive evidence – Antibiotics COPD: Management Avoid – Sedatives • Restlessness = hypoxia – Antihistamines • Dry secretions, decrease LOC – Epinephrine • Myocardial ischemia, arrhythmias – Intubation • difficult to wean off ventilator Reversible Obstructive Airway Disease Asthma Asthma: Definition Lower airway hyper-responsiveness to a variety of stimuli Diffuse reversible airway obstruction or narrowing Airway inflammation Asthma: Incidence 50% onset before age 10 33% before age 30 “Asthma” in older patients suggests other obstructive pulmonary diseases Risk Factors – Family history of asthma – Perinatal exposure to airborne allergens and irritants – Genetic hypersensitivity to environmental allergens (Atopy) Asthma Diagnosis – H&P, Spirometry – Hx or presence of episodic symptoms of airflow obstruction – airflow obstruction is at least partially reversible – alternative diagnoses are excluded Asthma Commonly misdiagnosed in children as – – – – Chronic bronchitis Recurrent croup Recurrent URI Recurrent pneumonia Asthma Often triggered by: – – – – – Cold temperature Respiratory Infections Vigorous exercise Emotional Stress Environmental allergens or irritants Exacerbation – Extrinsic common in children – Intrinsic common in adults Asthma Pathophysiology Asthma triggered Bronchial smooth muscle contraction Increased mucus production – Bronchial ‘plugging’ – Relative dehydration Alveolar hypoventilation – Ventilation Perfusion Mismatch – CO2 retention – Air ‘Trapping’ Asthma: Pathophysiology Bronchospasm Bronchial Edema Increased Mucus Production Asthma: Pathophysiology Asthma: Pathophysiology Cast of airway produced by asthmatic mucus plugs Asthma: Pathophysiology Difficulty exhaling – chest hyperinflation Poor gas exchange – hypoxia – hypercarbia Increased respiratory water loss – dehydration Asthma: Types Type 1 Extrinsic – – – – – – Classic allergic asthma Common in children, young adults Seasonal in nature Sudden brief attacks Major component is bronchospasm Good bronchodilator response Asthma: Types Type 2 Extrinsic Asthma – – – – – Adults < 35 Long term exposure to irritants More inflammation than Type 1 Extrinsic Does not respond well to bronchodilators Needs treatment with corticosteroids Asthma: Types Intrinsic Asthma – – – – Adult > 35 No immunologic cause Aspirin sensitivity/nasal polyps Poor bronchodilator response Asthma: Signs and Symptoms Onset of attacks associated with “triggers” Dyspnea Non-productive cough Tachypnea Expiratory wheezing Accessory muscle use Retractions Asthma: Signs and Symptoms Absence of wheezing IMPENDING RESPIRATORY ARREST! Asthma: Signs and Symptoms Tachycardia Pulsus paradoxus in severe attacks Anxiety, restlessness (hypoxia) progressing to drowsiness, confusion (hypercarbia) Asthma: Signs and Symptoms Lethargy, confusion, suprasternal retractions RESPIRATORY FAILURE Asthma: Signs and Symptoms Early Blood Gas Changes – Decreased PaO2 – Decreased PaCO2 WHY? Asthma: Signs and Symptoms Later Blood Gases – Decreased PaO2 – Normal PaCO2 IMPENDING RESPIRATORY FAILURE Asthma: Signs and Symptoms Still Later Blood Gases – Decreased PaO2 – Increased PaCO2 RESPIRATORY FAILURE Asthma: Risk Assessment Prior ICU admissions Prior intubation >3 ED visits in past year >2 hospital admissions in past year >1 bronchodilator canister used in past month Use of bronchodilators > every 4 hours Chronic use of steroids Progressive symptoms in spite of aggressive Rx Asthma: Management Airway Breathing – Sitting position or position of comfort – Humidified O2 by NRB mask • Dry O2 dries mucus, worsens plugs – Encourage coughing – Consider intubation, assisted ventilation • Impending respiratory failure • Avoid if at all possible Asthma: Management Circulation – IV TKO – Assess for dehydration – Titrate fluid administration to severity of dehydration • Trial bolus of 250 cc – Monitor ECG, Pulse Oximetry Asthma: Management Obtain medication history Consider – Overdose – Dysrhythmias Asthma: Management Nebulized Beta-2 agents – – – – Albuterol Terbutaline Metaproterenol Isoetharine Nebulized anticholinergics – Ipratropium – Atropine IV Corticosteroid – Methylprednisolone Asthma: Management Rarely used – Questionable efficacy, Potential Complications – Magnesium Sulfate (IV) – Methylxanthines • Aminophylline (IV) Asthma: Management Subcutaneous beta agents – Epinephrine 1:1000 q 30 minutes up to 3 doses • Adult – 0.3 to 0.5 mg SQ • Pediatric – 0.1 to 0.3 mg SQ – Terbutaline • Adult - 0.25 mg SQ q 30 minutes up to 2 doses • Pediatric -SQ or IV infusion usually begun @ 0.17 mcg/kg/min POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE Asthma: Management Use EXTREME caution in giving two sympathomimetics or two doses to same patient Monitor ECG Asthma: Management Avoid – Sedatives • Depress respiratory drive – Antihistamines • Decrease LOC, dry secretions – Aspirin • High incidence of allergy Asthma: Management Continuous Monitoring & Frequent Reassessment Need for transport? Destination? Asthma: Management Transport Considerations – How severe is the episode? – Is the patient improving? – How extensive (invasive) were the required therapies? – What does he/she normally do after treatment? – Medical Control or PMD consult Drug Delivery Methods: Review MDI vs. MDI w/ spacer vs. SVN vs. SQ injection Status Asthmaticus Asthma unresponsive to beta-2 adrenergic agents Status Asthmaticus Oxygen (humidified if possible) Nebulized beta-2 agents Nebulized Ipratropium Corticosteroids IV or SQ terbutaline or epinephrine Aminophylline (controversial) Magnesium sulfate (controversial) Intubation – Caution with PPV Golden Rule ALL THAT WHEEZES IS NOT ASTHMA Pulmonary edema Pulmonary embolism Allergic reactions COPD Pneumonia Foreign body aspiration Cystic fibrosis Lower Airway Disease Cystic Fibrosis Cystic Fibrosis: Definition Inherited metabolic disease of exocrine glands and sweat glands Primarily affects digestive, respiratory systems Begins in infancy Cystic Fibrosis: Etiology Autosomal recessive gene Both parents must be carriers Incidence – Caucasians--1:2000 – Blacks--1:17,000 – Asians--very rare Cystic Fibrosis: Pathophysiology Obstruction of pancreatic, intestinal gland, bile ducts Over-secretion by airway mucus glands – mucous plugs Excess loss of sodium chloride in sweat Cystic Fibrosis: Recognition History Airway obstruction, chronic cough – Recurrent respiratory infections – May be oxygen-dependent Diffuse Wheezing Frequent, foul-smelling stools Salty taste on skin Intolerance of hot environments Cystic Fibrosis: Management Position of comfort Oxygen Suctioning Nebulized Beta agonists – May not be very helpful but worth attempting if absence of contraindications Assisted ventilation Lower Airway Disease Neoplasms of the Lung Neoplasms of the Lung 150,000 cases Usually occurs between ages of 55 and 65 Most die within one year 20% only local lung involved 25% spread to lymphatic system 55% result in distant metastatic cancer Neoplasms of the Lung Prevention – Centered on prevention of smoking in youths – Then, cessation in current smokers – Avoid environmental hazards (e.g. asbestos) Neoplasms of the Lung Presentation – – – – Respiratory Difficulty progressing to Distress Cough, Hemoptysis Hoarseness or voice change Dysphagia Management of Neoplasms of the Lung Supportive care based upon presentation – Oxygen – Consider presence of advance directives or DNR • Patient’s wishes • Family discussions • MD prognosis – If appropriate • • • • Assist ventilations or Intubate IV access & rehydration Bronchodilators Analgesia for pain (small, slow doses) Hyperventilation Syndrome Hyperventilation Syndrome Brady Textbook Correction, Vol. 3, p. 57 – Table 1-4: These are NOT Causes of hyperventilation syndrome A diagnosis of EXCLUSION!!! An increased ventilatory rate that – DOES NOT have a pathologic origin – Results from anxiety Remains a real problem for the patient Hyperventilation Syndrome: Pathophysiology Tachypnea or hyperpnea secondary to anxiety Decreased PaCO2 Respiratory alkalosis Vasoconstriction Hypocalcemia Decreased O2 Release to Tissues Hyperventilation Syndrome: Signs & Symptoms Symptoms – Light-headedness, giddiness, anxiety – Numbness, paresthesias of: • Hands • Feet • Circumoral area – – – – Cold hands, feet Carpopedal spasms Dyspnea Chest pain Hyperventilation Syndrome: Signs & Symptoms Signs – – – – Rapid breathing Cool & possibly pale skin Carpopedal spasm Dysrhythmias • Sinus Tachycardia • SVT • Sinus arrhythmia – Loss of consciousness and seizures (late & rare) Hyperventilation Syndrome: Management Thorough assessment to rule out physiologic causes – Rule out head injury, metabolic acidosis Metabolic acidosis and increased ICP can cause rapid breathing that mimics hyperventilation syndrome! Hyperventilation Syndrome: Management Oxygen based upon presentation Reassurance & Patience – Coach breathing rate – CAUTION: Rebreathing into bag or NRB Monitoring – ECG – Pulse oximetry Hyperventilation Syndrome: Management Educate patient & family – Consider possible psychopathology especially in “repeat customers” Transport occasionally required – If loss of consciousness, carpopedal spasm, muscle twitching, or seizures occur: • Monitor EKG • IV TKO • Transport Hyperventilation Syndrome Serious diseases can mimic hyperventilation Hyperventilation itself can be serious Pulmonary Infectious Diseases Laryngotracheobronchitis (Croup) Common syndrome of infectious upper airway obstruction Viral infection – parainfluenza virus Subglottic Edema – larynx, trachea, mainstem bronchi Usually 3 months to 4 years of age Croup: Signs & Symptoms Gradual onset (several days) – Often begins with Sx of URI – May begin with only low grade fever Hoarseness Cough – “Seal Bark Cough” – “Brassy Cough” Nocturnal episodes of increased dyspnea and stridor Croup: Signs & Symptoms Evidence of respiratory distress – Tracheal tugging – Substernal/intercostal retractions – Accessory muscle use Inspiratory stridor or respiratory distress may develop slowly or acutely Croup: Management Usually requires little out of home treatment Calm & Prevent agitation!!! Moist cool air - mist Humidified O2 by mask or blowby Do Not Examine Upper Airways!!! Croup: Management If in respiratory distress: – Racemic epinephrine via nebulizer • Decreases subglottic edema (temporarily) • Necessitates transport for observation for rebound – IV TKO - ONLY if severe respiratory distress – Transport Bronchiolitis Pathophysiology – Viral Disease resulting in inflammation of the lower airways – Usually caused by RSV Typically affects children 6 - 18 months old (15% of all children < 2 years old) Usually occurs in the winter or early spring Bronchiolitis: Presentation Usually – – – – – – less than 18 months during the winter or early spring wheezing mild to moderate respiratory difficulty no asthma history associated with other viral symptoms • • • • runny nose sneezing cough low grade fever Bronchiolitis: Management Usually require little out of home treatment Oxygen, mask or blowby Nebulized Bronchodilators if respiratory distress – May not respond well or at all Transport Epiglottitis Bacterial infection (Hemophilus influenza ) Edema of epiglottis (supraglottic) – partial upper airway obstruction Typically affects 3-7 year olds Epiglottitis: Presentation Age: 3-7 years of age – can occur in adults – can occur in infants Rapid onset & progression – – – – – Fever Severe sore throat Dysphagia Muffled voice Drooling Epiglottitis: Presentation Respiratory difficulty – Stridor – Usually in an upright, sitting, tripod position Child may go to bed asymptomatic and awaken during the night with – sore throat – painful swallowing – respiratory difficulty Epiglottitis: Management Immediate life threat (8-12% die from airway obstruction) Do NOT attempt to visualize airway Allow child to assume position of comfort – AVOID agitation of the child!!! – AVOID anxiety of the healthcare providers!!! O2 by high concentration mask Epiglottitis: Management If respiratory failure is eminent: – IV TKO ONLY if eminent or respiratory arrest – Be prepared to take control of airway • Intubation equipment with smaller sized tubes • Needle cricothyrotomy & jet ventilation equipment Rapid but calm transport – Appropriate facility Upper Respiratory Infection Common illness Rarely life-threatening Often exacerbates underlying pulmonary conditions May become more significant in some patients – Immunosuppressed – Elderly – Chronic pulmonary disease Upper Respiratory Infection Prevention – Avoidance is nearly impossible • Too many potential causes • Temporarily impaired immune system – Best prevention strategy is handwashing • Covering of mouth during sneezing and coughing also helpful Pathophysiology of URI Wide variety of bacteria and viruses are causes – Normal immune system response results in presentation 20-30% are Group A streptococci Most are self-limiting diseases Presentation of URI Symptoms – – – – Sore throat Fever Chills HA Signs – Cervical adenopathy – Erythematous pharynx – Positive throat culture (bacterial) Management of URI Usually requires no intervention Oxygen if underlying condition has been exacerbated Rarely, pharmacologic interventions are required – Bronchodilators – Corticosteroid Occasionally, transport required – Key question: Destination? Central Respiratory Depression Respiratory Depression: Causes Head trauma CVA Depressant drug toxicity – – – – Narcotics Barbiturates Benzodiazepines ETOH Respiratory Depression: Recognition Decreased respiratory rate (< 12/min) Decreased tidal volume Decreased LOC Look, Listen, Feel If you can’t tell whether a patient is breathing adequately... Use Your Stethoscope THEY PROBABLY AREN’T Respiratory Depression: Management Airway – Open, clear, maintain – Consider endotracheal intubation The need to VENTILATE is not the same as the need to INTUBATE Respiratory Depression: Management Breathing – Oxygenate, ventilate – Restore normal rate, tidal volume Oxygen alone is INSUFFICIENT if Ventilation is INADEQUATE Respiratory Depression: Management Circulation – Obtain vascular access – Monitor EKG (Silent MI may present as CVA) Manage Cause – Check Blood Sugar – Consider Narcan 2mg IV push if S/S suggest narcotic overdose Intubate if can not find or treat cause Thoracic Bellows Malfunction Pickwickian Syndrome Guillian-Barre Syndrome Myasthenia Gravis Pickwickian Syndrome Results from extreme obesity – form of sleep apnea Decreased excursion of chest wall, diaphragm causes – hypoventilation – CO2 retention Pickwickian Syndrome Signs and Symptoms – – – – Headache Drowsiness Inappropriate sleepiness Sleep apnea Treat symptomatically – Assist ventilations as needed Guillian-Barre´ Syndrome Autoimmune disease – Leads to inflammation and degeneration of sensory and motor nerve roots (demyelination) Progressive ascending paralysis – Progressive tingling and weakness – Moves from extremities then proximally – May lead to respiratory paralysis (25%) Guillian-Barre´ Syndrome Self-Limiting – Recovery is spontaneous and complete in 95% of cases – In good outcomes, symptoms clear in 15 to 20 days – Often takes weeks or months Guillian-Barre´ Syndrome Management Treatment based on severity of symptoms – – – – Control airway Support ventilation Oxygen Transport in cases of respiratory depression, distress or arrest Myasthenia Gravis Autoimmune disease Causes loss of ACh receptors at neuromuscular junction – Attacks the ACh transport mechanism at the NMJ Episodes of extreme skeletal muscle weakness Can cause loss of control of airway, respiratory paralysis Myasthenia Gravis Presentation Gradual onset of muscle weakness – Face and throat – Extreme muscle weakness Respiratory weakness -> paralysis Inability to process mucus Myasthenia Gravis Management Treat symptomatically Watch for aspiration May require assisted ventilations Assess for Pulmonary infection Transport based upon severity of presentation Pulmonary Diseases & Disorders Other Causes of Respiratory Emergencies Angioneurotic Edema Allergic reaction – Edema of tongue, pharynx, larynx – NOT the SAME as anaphylaxis Common Causes – Food (seafood or nuts) – Drugs (penicillin or sulfa) – Hymenoptera sting (ants, bees, wasps) Angioneurotic Edema Signs and Symptoms – – – – – – – Itching in palate “Lump in throat” Hoarseness Stridor Coughing Dyspnea Urticaria (hives) Angioneurotic Edema: Management Based upon severity of presentation – – – – Establish airway O2 via NRB IV lg bore TKO Epinephrine • 1:1000 0.3 - 0.5mg SQ • repeat after 20 minutes if needed Angioneurotic Edema: Management Based upon severity of presentation (cont) – Diphenhydramine 25 to 50mg IM/IV – In severe cases, Consider • Positive pressure ventilation • Endotracheal intubation • Surgical airway Spontaneous Pneumothorax Low incidence Many are well tolerated Risk Factors – Males – Younger age – Thin body mass • Marfan’s syndrome – History of Obstructive Airway Disease Presentation of Spontaneous Pneumothorax Symptoms – Sudden SOB – Sudden pleuritic CP Signs – Mild pallor, tachycardia, tachypnea – Decreased lung sounds • usually very localized Increasing pneumothorax presents with more severe S/S Management of Simple Pneumothorax Oxygen based on severity of S/S Assisted ventilation and intubation as needed – May worsen pneumothorax – Rarely needed IV access if severe symptoms are present Position of comfort Transport Case Studies Case One It is 1430 hrs. You are called to a business for a “possible stroke.” The patient is a 20-yearold female complaining of dizziness and of numbness around her mouth and fingertips. What would you like to include in your initial differential diagnosis? Case One Initial Assessment – Airway: Open, maintained by patient – Breathing: Rapid, deep, regular; no accessory muscle use or retractions – Circulation: Radial pulses present, rapid, full; Skin warm, dry; capillary refill < 2 seconds – Disability: Awake, alert, anxious What therapies, if any, would you like to begin? Case One Vital Signs – P: 126 strong, regular – R: 26 deep, regular – BP: 130/82 Physical Exam – Chest: BS present, equal bilaterally; no adventitious sounds – Extremities: Equal movement in all extremities; no weakness; hands cool – Oxygen saturation: 98% Would you like to make any Changes to your therapies or Diff Dx? Case One History – Allergies: NKA – Medications: Birth control pills – Past History: No significant past history; no history of smoking – Last Meal: Lunch 2 hours ago – Events: S/S began suddenly after argument with supervisor Case One What problem do you now suspect? How would you manage this patient? Case Two It is 0530 hours. You are called to a residence to see a child with “a very high fever and difficulty breathing.” The patient is a 6-oldfemale. Mother says the child woke up crying about 2 hours ago. What would you like to include in your differential diagnosis? Case Two Initial Assessment – Airway: Inspiratory stridor audible – Breathing: Rapid, shallow, labored – Circulation: Radial pulses present, rapid, weak; skin pale, hot, diaphoretic; capillary refill is 2 seconds – Disability: Awake, alert, obviously frightened and in acute distress What therapies, if any, would you like to begin now? Case Two Vital Signs – P: 130 weak, regular – R: 32 shallow, regular with stridor – BP: 110/70 Physical Exam – HEENT: Flaring of nostrils; accessory muscle use on inspiration; drooling present – Chest: BS present, equal bilaterally; no adventitious sounds – Oxygen saturation: 92% Would you like to make any Changes to your therapies or Diff Dx? Case Two History – – – – – Allergies: NKA Medications: None Past History: No significant past history Last Meal: Dinner at about 1800 hours Events: Awakened with severe sore throat. Has experienced increasing difficulty breathing. Will not eat or drink. Says it hurts to swallow Case Two What problem do you now suspect? How would you manage this patient? Case Three At 2330 hrs you are called to a residence to see a child with “difficulty breathing.” The patient is a 3 year old male. How narrow a Differential Diagnosis can you compile at this point? Case Three Initial Assessment – Airway: Open, maintained by patient, mild stridor audible – Breathing: Rapid, shallow, labored – Circulation: Radial pulses present, weak, regular; Skin pale, warm, moist; Capillary refill <2 seconds – Disability: Awake, sitting up in bed, looks tired and miserable Case Three Vital Signs – P: 100 weak, regular – R: 30 shallow, labored with stridor – BP: 90/50 Physical Exam – HEENT: Use of accessory muscles present; no drooling – Chest: BS present, equal bilaterally with no adventitious sounds. Auscultation difficult because of stridor and barking cough Now you can narrow your Diff Dx? To what? Case Three History – – – – – Allergies: NKA Medication: Tylenol for fever before bedtime Past history: No significant past history Last meal: Dinner around 1800 hours Events: Patient has had “cold” for about 3 days. Reasonably well during day. Awakens around midnight with high-pitched cough that sounds like a dog barking Case Three What problem do you suspect? How would you manage this patient? Case Four At 1945 hours you are dispatched to a “breathing difficulty” at Long John Silver’s. The patient is a 26-year-old female complaining of strange feeling in her mouth and difficulty swallowing. What is your differential diagnosis? Case Four Initial Assessment – Airway: Open, maintained by patient, difficulty swallowing, voice is hoarse – Breathing: Rapid, labored – Circulation: Radial pulses present, strong, regular; Skin “flushed”; Capillary refill < 2 seconds – Disability: Awake, alert, very anxious Case Four Vital Signs – P: 120 strong, regular – R: 26 regular, slightly labored – BP: 118/90 Physical Exam – HEENT: Puffiness around eyes; Lips appear swollen; Mild accessory muscle use – Chest: BS present, equal bilaterally; No adventitious sounds – Urticaria on upper chest, extremities – Oxygen saturation: 94% What therapies do you want to initiate? Case Four History – Allergies: No drug allergies; Has experienced itching previously when eating shrimp – Medications: None – Past history: No significant past history; no history of smoking – Last meal: In progress at time of call – Events: Began to experience itching and difficulty swallowing after eating “fish and chips” Case Four What problem do you suspect? How would you manage this patient? The patient begins to have increased difficulty swallowing, increased anxiety, and increased difficulty breathing. What do you want to do now? Case Five At 0130 you are dispatched to an “unconscious person--police on location.” The patient is a 27-year-old male who is apparently unconscious. The police report they found him lying in an alleyway while they were on routine patrol. He is known to live “on the streets”. Case Five Initial Assessment – Airway: Controllable with manual positioning – Breathing: Very slow, shallow – Circulation: Radial pulses present, weak; Skin pale, cool, moist; Capillary refill 3 seconds – Disability: Unconscious, unresponsive to painful stimuli What therapies would you like to begin? Case Five Vital Signs – P: 70 regular, weak – R: 4 shallow, regular; alcohol odor on breath – BP: 100/70 Physical Exam – – – – – HEENT: Pupils pinpoint, non-reactive Chest: BS present, equal bilaterally Abdomen: Soft, non-tender Extremities: Needle tracks present Blood glucose: 40 mg/dl Case Five What problem or problems do you suspect? How would you manage this patient?