Pulmonary Diseases Pulmonary Diseases Disorders n Pulmonary Disease

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Pulmonary Diseases

Pulmonary Diseases

Pulmonary Diseases & Disorders n Pulmonary Disease & Conditions may result from: – Infectious

Pulmonary Diseases & Disorders n Pulmonary Disease & Conditions may result from: – Infectious causes – Non-Infectious causes n Adversely affect one or more of the following – Ventilation – Diffusion – Perfusion

Pulmonary Diseases & Disorders n The Respiratory Emergency may stem from dysfunction or disease

Pulmonary Diseases & Disorders n 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 n The Respiratory Emergency may affect the upper or lower

Pulmonary Diseases & Disorders n The Respiratory Emergency may affect the upper or lower airways n Upper Airway Obstruction – – – Tongue Foreign Body Aspiration Angioneurotic Edema Maxillofacial, Larnygotracheal Trauma Croup Epiglottitis

Respiratory Emergencies: Causes n Lower Airway Obstruction – – Emphysema Chronic Bronchitis Asthma Cystic

Respiratory Emergencies: Causes n Lower Airway Obstruction – – Emphysema Chronic Bronchitis Asthma Cystic Fibrosis

Pulmonary Diseases & Disorders n The Respiratory Emergency may stem from Gas Exchange Surface

Pulmonary Diseases & Disorders n 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 Diseases & Disorders Problems with the Gas Exchange Surface

Pulmonary Edema

Pulmonary Edema

Pulmonary Edema: Pathophysiology n A pathophysiologic condition, not a disease – Fluid in and

Pulmonary Edema: Pathophysiology n A pathophysiologic condition, not a disease – Fluid in and around alveoli – Interferes with gas exchange – Increases work of breathing n Two Types – Cardiogenic (high pressure) – Non-Cardiogenic (high permeability)

Pulmonary Edema n High Pressure (cardiogenic) • AMI • Chronic HTN • Myocarditis n

Pulmonary Edema n High Pressure (cardiogenic) • AMI • Chronic HTN • Myocarditis n High Permeability (non-cardiogenic) • Poor perfusion, Shock, Hypoxemia • High Altitude, Drowning • Inhalation of pulmonary irritants

Cardiogenic Pulmonary Edema: Etiology n n Left ventricular failure Valvular heart disease – Stenosis

Cardiogenic Pulmonary Edema: Etiology n n Left ventricular failure Valvular heart disease – Stenosis – Insufficiency n n Hypertensive crisis (high afterload) Volume overload Increased Pressure in Pulmonary Vascular Bed

Pulmonary Edema n High Permeability – Disrupted alveolar-capillary membrane – Membrane allows fluid to

Pulmonary Edema n 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 n n n n Toxic inhalation Near drowning Liver disease

Non-Cardiogenic Pulmonary Edema: Etiology n n n n 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 n n n n n Dyspnea on exertion Paroxysmal nocturnal

Pulmonary Edema: Signs &Symptoms n n n n n 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 n n n Position Oxygen PPV / Intubation –

Management of Non-Cardiogenic Pulmonary Edema n n n Position Oxygen PPV / Intubation – CPAP – PEEP n n IV Access; Minimal fluid administration Treat the underlying cause – Diuretics usually not helpful; May be harmful n Transport

Adult Respiratory Distress Syndrome n n AKA: Non-cardiogenic pulmonary edema A complication of: –

Adult Respiratory Distress Syndrome n n 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

Pneumonia

Pneumonia

Pneumonia n n n Fifth leading cause of death in US/Canada Group of Specific

Pneumonia n n n Fifth leading cause of death in US/Canada Group of Specific infections Risk factors – Cigarette smoking – Exposure to cold – Extremes of age • young • old

Pneumonia n Inflammation of the bronchioles and alveoli – Products of inflammation (secretions, pus)

Pneumonia n Inflammation of the bronchioles and alveoli – Products of inflammation (secretions, pus) add to respiration difficulty n n n Gas exchange is impaired Work of breathing increases May lead to – – Atelectasis Sepsis VQ Mismatch Hypoxemia

Pneumonia: Etiology n n n Viral Bacterial Fungi Protozoa (pneumocystis) Aspiration

Pneumonia: Etiology n n n Viral Bacterial Fungi Protozoa (pneumocystis) Aspiration

Presentation of Pneumonia n n Shortness of breath, Dyspnea Fever, chills Pleuritic Chest Pain,

Presentation of Pneumonia n n Shortness of breath, Dyspnea Fever, chills Pleuritic Chest Pain, Tachycardia Cough – Green/brown sputum n May have crackles, rhonchi or wheezing in peripheral lung fields – Consolidation – Egophony

Management of Pneumonia n Treatment mostly based upon symptoms – – – Oxygen Rarely

Management of Pneumonia n Treatment mostly based upon symptoms – – – Oxygen Rarely is intubation required IV Access & Rehydration B 2 agonists may be useful Antibiotics (e. g. Rocephin) Antipyretics

Pneumonia: Management n n MD follow-up for labs, cultures & Rx Transport considerations –

Pneumonia: Management n n 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

Pulmonary Embolism n ~ 50, 000 deaths / year/ US – ~5% of all

Pulmonary Embolism n ~ 50, 000 deaths / year/ US – ~5% of all sudden deaths – <10% of all PE result in death

Pulmonary Embolism: Pathophysiology n n Something moving with flow of blood passes through right

Pulmonary Embolism: Pathophysiology n n 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) n n A disorder of perfusion Combination of factors increase probability

Pulmonary Embolism (PE) n n A disorder of perfusion Combination of factors increase probability of occurrence – Hypercoagulability – Platelet aggregation – Deep vein stasis n Embolus usually originates in lower extremities or pelvis

Pulmonary Embolism (PE) n Risk factors – Venostasis or DVT – Recent surgery or

Pulmonary Embolism (PE) n 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’ s.

Pulmonary Embolism: Etiology Most Common Cause = Blood Clots Vessel Wall Injury Virchow’ s. Triad Hypercoagulability Venous Stasis

Pulmonary Embolism: Etiology n Other causes – – – Air Amniotic fluid Fat particles

Pulmonary Embolism: Etiology n Other causes – – – Air Amniotic fluid Fat particles (long bone fracture) Particulates from substance abuse Venous catheter

Pulmonary Embolism: Signs & Symptoms n Small Emboli – – – – Rapid Onset

Pulmonary Embolism: Signs & Symptoms n 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 n Larger Emboli – – – Small Emboli S/S

Pulmonary Embolism: Signs & Symptoms n Larger Emboli – – – Small Emboli S/S plus: Pleuritic pain Pleural rub Coughing Wheezing Hemoptysis (rare)

Pulmonary Embolism: Signs & Symptoms n Very Large Emboli – – – Preceded by

Pulmonary Embolism: Signs & Symptoms n 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: Signs & Symptoms There are NO assessment findings specific to pulmonary embolism

Pulmonary Embolism: Management n n Management based on severity of Sx/Sx Airway & Breathing

Pulmonary Embolism: Management n n Management based on severity of Sx/Sx Airway & Breathing – High concentration O 2 – Consider assisting ventilations – Early Intubation n Circulation – IV, 2 lg bore sites • Fluid bolus then TKO; Titrate to BP ~ 90 mm Hg – Monitor ECG n Rapid transport

PE Management n Thrombolytics – Aspirin & Heparin (questionable if any benefit) n Rapid

PE Management n Thrombolytics – Aspirin & Heparin (questionable if any benefit) n 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

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 n Inflammation of pleura caused by a friction rub – layers of pleura

Pleurisy n Inflammation of pleura caused by a friction rub – layers of pleura rubbing together n Commonly associated with other respiratory disease

Presentation of Pleurisy n Sharp, sudden and intermittent chest pain with related dyspnea –

Presentation of Pleurisy n Sharp, sudden and intermittent chest pain with related dyspnea – Possibly referred to shoulder – May or with respiration n n Pleural “friction rub” may be audible” May have effusion or be dry

Pleurisy n Management – Based upon severity of presentation – Mostly supportive

Pleurisy n Management – Based upon severity of presentation – Mostly supportive

Pulmonary Diseases & Disorders Problems with Airway Obstructions

Pulmonary Diseases & Disorders Problems with Airway Obstructions

Obstructive Airway Diseases

Obstructive Airway Diseases

Obstructive Airway Disease n n n Asthma Emphysema Chronic Bronchitis

Obstructive Airway Disease n n n Asthma Emphysema Chronic Bronchitis

Obstructive Airway Diseases n Asthma experienced by ~ 4 - 5 % of Canadian

Obstructive Airway Diseases n Asthma experienced by ~ 4 - 5 % of Canadian population – Mortality rate increasing n Factors leading to Obstructive Airway Diseases – Smoking – Exposure to environmental agents – Genetic predisposition n How does this differ from “COPD”?

Obstructive Airway Disease n Exacerbation Factors – Intrinsic • Stress (especially in adults) •

Obstructive Airway Disease n Exacerbation Factors – Intrinsic • Stress (especially in adults) • URI • Exercise – Extrinsic • • Cigarette Smoke Allergens Drugs Occupational hazards

Obstructive Airway Disease n General Pathophysiology – Specific pathophysiology varies by disease – Obstruction

Obstructive Airway Disease n 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 n General Pathophysiology – Obstruction results in air trapping • Bronchioles

Obstructive Airway Disease n 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

Lower Airway Disease

Chronic Obstructive Pulmonary Disease Emphysema Chronic Bronchitis (Rarely Asthma may result in COPD)

Chronic Obstructive Pulmonary Disease Emphysema Chronic Bronchitis (Rarely Asthma may result in COPD)

COPD: Epidemiology n n n Most common chronic lung disease 4 th leading cause

COPD: Epidemiology n n n Most common chronic lung disease 4 th leading cause of death many deaths annually

Emphysema Type A COPD

Emphysema Type A COPD

Emphysema: Definition n n Destruction of alveolar walls Distention of pulmonary air spaces Loss

Emphysema: Definition n n Destruction of alveolar walls Distention of pulmonary air spaces Loss of elastic recoil Destruction of gas exchange surface

Emphysema: Incidence n n n Male > females Urban area > rural areas Age

Emphysema: Incidence n n n Male > females Urban area > rural areas Age usually > 55

Emphysema: Etiology n Smoking – 90% of all cases – Smokers 10 x more

Emphysema: Etiology n Smoking – 90% of all cases – Smokers 10 x more likely to die of COPD than non -smokers n n Environmental factors Alpha – 1 antitrypsin deficiency – hereditary – 50, 000 to 100, 000 cases – mostly people of northern European descent

Emphysema: Pathophysiology n n Decreased surface area leads to decreased gas exchange with blood

Emphysema: Pathophysiology n n 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 n Loss of elastic recoil leads to increased residual volume and CO

Emphysema: Pathophysiology n Loss of elastic recoil leads to increased residual volume and CO 2 retention – Air Trapping – Hyperinflation – Hypercapnia -> pulmonary vasoconstriction -> V/Q mismatch

Emphysema: Signs and Symptoms n n n Increasing dyspnea on exertion Non-productive cough Malaise

Emphysema: Signs and Symptoms n n n Increasing dyspnea on exertion Non-productive cough Malaise Anorexia, Loss of weight Hypertrophied respiratory accessory muscles

Emphysema: Signs and Symptoms n n n Increased Thoracic AP Diameter (Barrel Chest) Decreased

Emphysema: Signs and Symptoms n n n Increased Thoracic AP Diameter (Barrel Chest) Decreased lung/heart sounds Hyperresonant chest

Emphysema: Signs and Symptoms n n n Lip pursing on exhalation Clubbed fingertips Altered

Emphysema: Signs and Symptoms n n n Lip pursing on exhalation Clubbed fingertips Altered blood gases – Normal or decreased Pa. O 2 – Elevated CO 2 n Cyanosis occurs LATE in course of disease PINK PUFFER

Chronic Bronchitis Type B COPD

Chronic Bronchitis Type B COPD

Chronic Bronchitis: Definition n n Increased mucus production for > 3 months for >

Chronic Bronchitis: Definition n n Increased mucus production for > 3 months for > 2 consecutive years Recurrent productive cough

Chronic Bronchitis: Incidence n n n Males > females Urban areas > rural areas

Chronic Bronchitis: Incidence n n n Males > females Urban areas > rural areas Age usually > 45

Chronic Bronchitis: Etiology n n Smoking Environmental irritants

Chronic Bronchitis: Etiology n n Smoking Environmental irritants

Chronic Bronchitis: Pathophysiology n n n Mucus plugging/inflammatory edema Increased airflow resistance leads to

Chronic Bronchitis: Pathophysiology n n n Mucus plugging/inflammatory edema Increased airflow resistance leads to alveolar hypoventilation Alveolar hypoventilation leads to – hypercarbia – hypoxemia

Chronic Bronchitis: Pathophysiology n Hypoxemia leads to – increased RBC’s w/o oxygen which leads

Chronic Bronchitis: Pathophysiology n Hypoxemia leads to – increased RBC’s w/o oxygen which leads to • cyanosis n 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 n n n n Increasing dyspnea on exertion Frequent

Chronic Bronchitis: Signs and Symptoms n n n n 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 CO 2)

Chronic Bronchitis: Signs and Symptoms n n Decreased intellectual ability Personality changes Abnormal blood

Chronic Bronchitis: Signs and Symptoms n n Decreased intellectual ability Personality changes Abnormal blood gases – Hypercarbia – Hypoxia Cyanosis EARLY in course of disease BLUE BLOATER

COPD Assessment Findings n n Chronic condition acute episode S&S of work of breathing

COPD Assessment Findings n n Chronic condition acute episode S&S of work of breathing and/or hypoxemia – – – n Use of accessory muscles Increased expiratory effort Tachycardia, AMS, Cyanosis Wheezing, Rhonchi, LS Thin, red/pink appearance Saturation usually normal in emphysema

COPD: Management n Causes of Decompensation – Respiratory infection (increased mucus production) – Chest

COPD: Management n 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 n Airway and Breathing – – n Sitting position or position of

COPD: Management n Airway and Breathing – – n Sitting position or position of comfort Calm & Reassure Encourage cough Avoid exertion Oxygen – Don’t withhold – Maintain O 2 saturation above 90 % TRUE HYPOXIC DRIVE IS VERY RARE

COPD: Management n Ventilation – Avoid intubation unless absolutely necessary • near respiratory failure

COPD: Management n Ventilation – Avoid intubation unless absolutely necessary • near respiratory failure • exhaustion n Circulation – IV TKO – Titrate fluid to degree of dehydration • 250 cc trial bolus – Excessive fluid may precipitate CHF – Monitor ECG

COPD: Management n Drug Therapy – Obtain thorough medication history – Nebulized Beta 2

COPD: Management n Drug Therapy – Obtain thorough medication history – Nebulized Beta 2 agonists • Albuterol • Terbutaline • Metaproterenol • Isoetharine

COPD: Management REMEMBER All bronchodilators are potentially arrhythmogenic

COPD: Management REMEMBER All bronchodilators are potentially arrhythmogenic

COPD: Management n Drug Therapy – Ipratropium (anticholinergic) by SVN – (beta-2 agonist) by

COPD: Management n Drug Therapy – Ipratropium (anticholinergic) by SVN – (beta-2 agonist) by MDI, SQ or IV – Corticosteroids (anti-inflammatory agent) by IV

COPD: Management n Avoid – Sedatives • Restlessness = hypoxia – Antihistamines • Dry

COPD: Management n Avoid – Sedatives • Restlessness = hypoxia – Antihistamines • Dry secretions, decrease LOC – Epinephrine • Myocardial ischemia, arrhythmias – Intubation • difficult to wean off ventilator

Reversible Obstructive Airway Disease Asthma

Reversible Obstructive Airway Disease Asthma

Asthma: Definition n Lower airway hyper-responsiveness to a variety of stimuli Diffuse reversible airway

Asthma: Definition n Lower airway hyper-responsiveness to a variety of stimuli Diffuse reversible airway obstruction or narrowing Airway inflammation

Asthma: Incidence n n 50% onset before age 10 33% before age 30 “Asthma”

Asthma: Incidence n n 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 n Diagnosis – H&P, Spirometry – Hx or presence of episodic symptoms of

Asthma n 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 n Commonly misdiagnosed in children as – – Chronic bronchitis Recurrent croup Recurrent

Asthma n Commonly misdiagnosed in children as – – Chronic bronchitis Recurrent croup Recurrent URI Recurrent pneumonia

Asthma n Often triggered by: – – – n Cold temperature Respiratory Infections Vigorous

Asthma n Often triggered by: – – – n Cold temperature Respiratory Infections Vigorous exercise Emotional Stress Environmental allergens or irritants Exacerbation – Extrinsic common in children – Intrinsic common in adults

Asthma Pathophysiology n n n Asthma triggered Bronchial smooth muscle contraction Increased mucus production

Asthma Pathophysiology n n n Asthma triggered Bronchial smooth muscle contraction Increased mucus production – Bronchial ‘plugging’ – Relative dehydration n Alveolar hypoventilation – Ventilation Perfusion Mismatch – CO 2 retention – Air ‘Trapping’

Asthma: Pathophysiology Bronchospasm Bronchial Edema Increased Mucus Production

Asthma: Pathophysiology Bronchospasm Bronchial Edema Increased Mucus Production

Asthma: Pathophysiology

Asthma: Pathophysiology

Asthma: Pathophysiology Cast of airway produced by asthmatic mucus plugs

Asthma: Pathophysiology Cast of airway produced by asthmatic mucus plugs

Asthma: Pathophysiology n Difficulty exhaling – chest hyperinflation n Poor gas exchange – hypoxia

Asthma: Pathophysiology n Difficulty exhaling – chest hyperinflation n Poor gas exchange – hypoxia – hypercarbia n Increased respiratory water loss – dehydration

Asthma: Types n Type 1 Extrinsic – – – Classic allergic asthma Common in

Asthma: Types n 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 n Type 2 Extrinsic Asthma – – – Adults < 35 Long

Asthma: Types n 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 n Intrinsic Asthma – – Adult > 35 No immunologic cause Aspirin

Asthma: Types n Intrinsic Asthma – – Adult > 35 No immunologic cause Aspirin sensitivity/nasal polyps Poor bronchodilator response

Asthma: Signs and Symptoms n n n n Onset of attacks associated with “triggers”

Asthma: Signs and Symptoms n n n n 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 Absence of wheezing IMPENDING RESPIRATORY ARREST!

Asthma: Signs and Symptoms n n n Tachycardia Pulsus paradoxus in severe attacks Anxiety,

Asthma: Signs and Symptoms n n n 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 Lethargy, confusion, suprasternal retractions RESPIRATORY FAILURE

Asthma: Signs and Symptoms n Early Blood Gas Changes – Decreased Pa. O 2

Asthma: Signs and Symptoms n Early Blood Gas Changes – Decreased Pa. O 2 – Decreased Pa. CO 2 WHY?

Asthma: Signs and Symptoms n Later Blood Gases – Decreased Pa. O 2 –

Asthma: Signs and Symptoms n Later Blood Gases – Decreased Pa. O 2 – Normal Pa. CO 2 IMPENDING RESPIRATORY FAILURE

Asthma: Signs and Symptoms n Still Later Blood Gases – Decreased Pa. O 2

Asthma: Signs and Symptoms n Still Later Blood Gases – Decreased Pa. O 2 – Increased Pa. CO 2 RESPIRATORY FAILURE

Asthma: Risk Assessment n n n n Prior ICU admissions Prior intubation >3 ED

Asthma: Risk Assessment n n n n 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 n n Airway Breathing – Sitting position or position of comfort –

Asthma: Management n n Airway Breathing – Sitting position or position of comfort – Humidified O 2 by NRB mask • Dry O 2 dries mucus, worsens plugs – Encourage coughing – Consider intubation, assisted ventilation • Impending respiratory failure • Avoid if at all possible

Asthma: Management n Circulation – IV TKO – Assess for dehydration – Titrate fluid

Asthma: Management n Circulation – IV TKO – Assess for dehydration – Titrate fluid administration to severity of dehydration • Trial bolus of 250 cc – Monitor ECG, Pulse Oximetry

Asthma: Management n n Obtain medication history Consider – Overdose – Dysrhythmias

Asthma: Management n n Obtain medication history Consider – Overdose – Dysrhythmias

Asthma: Management n Nebulized Beta-2 agents – Salbutamol n Nebulized anticholinergics – Ipratropium –

Asthma: Management n Nebulized Beta-2 agents – Salbutamol n Nebulized anticholinergics – Ipratropium – Atropine n IV Corticosteroid – Methylprednisolone n Combination – Flovent/etc

Asthma: Management n Rarely used – Questionable efficacy, Potential Complications – Magnesium Sulfate (IV)

Asthma: Management n Rarely used – Questionable efficacy, Potential Complications – Magnesium Sulfate (IV) – Methylxanthines • Aminophylline (IV)

Asthma: Management n Subcutaneous beta agents – Epinephrine 1: 1000 q 30 minutes up

Asthma: Management n Subcutaneous beta agents – Epinephrine 1: 1000 q 30 minutes up to 3 doses • Adult – 0. 3 mg SQ/IM • Pediatric – 0. 1 to 0. 3 mg SQ/IM POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE

Asthma: Management n n Use EXTREME caution in giving two sympathomimetics or two doses

Asthma: Management n n Use EXTREME caution in giving two sympathomimetics or two doses to same patient Monitor ECG

Asthma: Management n Avoid – Sedatives • Depress respiratory drive – Antihistamines • Decrease

Asthma: Management n Avoid – Sedatives • Depress respiratory drive – Antihistamines • Decrease LOC, dry secretions – Aspirin • High incidence of allergy

Asthma: Management n n Continuous Monitoring & Frequent Reassessment Need for transport? Destination?

Asthma: Management n n Continuous Monitoring & Frequent Reassessment Need for transport? Destination?

Asthma: Management n Transport Considerations – How severe is the episode? – Is the

Asthma: Management n 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

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 Asthma unresponsive to beta-2 adrenergic agents

Status Asthmaticus n n n n Oxygen (humidified if possible) Nebulized beta-2 agents Nebulized

Status Asthmaticus n n n n 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 n n n n Pulmonary edema

Golden Rule ALL THAT WHEEZES IS NOT ASTHMA n n n n Pulmonary edema Pulmonary embolism Allergic reactions COPD Pneumonia Foreign body aspiration Cystic fibrosis

Lower Airway Disease Cystic Fibrosis

Lower Airway Disease Cystic Fibrosis

Cystic Fibrosis: Definition n Inherited metabolic disease of exocrine glands and sweat glands Primarily

Cystic Fibrosis: Definition n Inherited metabolic disease of exocrine glands and sweat glands Primarily affects digestive, respiratory systems Begins in infancy

Cystic Fibrosis: Etiology n n n Autosomal recessive gene Both parents must be carriers

Cystic Fibrosis: Etiology n n n Autosomal recessive gene Both parents must be carriers Incidence – Caucasians--1: 2000 – Blacks--1: 17, 000 – Asians--very rare

Cystic Fibrosis: Pathophysiology n n Obstruction of pancreatic, intestinal gland, bile ducts Over-secretion by

Cystic Fibrosis: Pathophysiology n n Obstruction of pancreatic, intestinal gland, bile ducts Over-secretion by airway mucus glands – mucous plugs n Excess loss of sodium chloride in sweat

Lower Airway Disease Neoplasms of the Lung

Lower Airway Disease Neoplasms of the Lung

Hyperventilation Syndrome

Hyperventilation Syndrome

Hyperventilation Syndrome n Brady Textbook Correction, Vol. 3, p. 57 – Table 1 -4:

Hyperventilation Syndrome n Brady Textbook Correction, Vol. 3, p. 57 – Table 1 -4: These are NOT Causes of hyperventilation syndrome n n A diagnosis of EXCLUSION!!! An increased ventilatory rate that – DOES NOT have a pathologic origin – Results from anxiety n Remains a real problem for the patient

Hyperventilation Syndrome: Pathophysiology Tachypnea or hyperpnea secondary to anxiety Decreased Pa. CO 2 Respiratory

Hyperventilation Syndrome: Pathophysiology Tachypnea or hyperpnea secondary to anxiety Decreased Pa. CO 2 Respiratory alkalosis Vasoconstriction Hypocalcemia Decreased O 2 Release to Tissues

Hyperventilation Syndrome: Signs & Symptoms n Symptoms – Light-headedness, giddiness, anxiety – Numbness, paresthesias

Hyperventilation Syndrome: Signs & Symptoms n Symptoms – Light-headedness, giddiness, anxiety – Numbness, paresthesias of: • Hands • Feet • Circumoral area – – Cold hands, feet Carpopedal spasms Dyspnea Chest pain

Hyperventilation Syndrome: Signs & Symptoms n Signs – – Rapid breathing Cool & possibly

Hyperventilation Syndrome: Signs & Symptoms n 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 n Educate patient & family – Consider possible psychopathology especially in

Hyperventilation Syndrome: Management n Educate patient & family – Consider possible psychopathology especially in “repeat customers” n 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

Hyperventilation Syndrome Serious diseases can mimic hyperventilation Hyperventilation itself can be serious

Pulmonary Infectious Diseases

Pulmonary Infectious Diseases

Laryngotracheobronchitis (Croup) n n Common syndrome of infectious upper airway obstruction Viral infection –

Laryngotracheobronchitis (Croup) n n Common syndrome of infectious upper airway obstruction Viral infection – parainfluenza virus n Subglottic Edema – larynx, trachea, mainstem bronchi n Usually 3 months to 4 years of age

Croup: Signs & Symptoms n Gradual onset (several days) – Often begins with Sx

Croup: Signs & Symptoms n Gradual onset (several days) – Often begins with Sx of URI – May begin with only low grade fever n n Hoarseness Cough – “Seal Bark Cough” – “Brassy Cough” n Nocturnal episodes of increased dyspnea and stridor

Croup: Signs & Symptoms n Evidence of respiratory distress – Tracheal tugging – Substernal/intercostal

Croup: Signs & Symptoms n Evidence of respiratory distress – Tracheal tugging – Substernal/intercostal retractions – Accessory muscle use n Inspiratory stridor or respiratory distress may develop slowly or acutely

Croup: Management n n n Usually requires little out of home treatment Calm &

Croup: Management n n n Usually requires little out of home treatment Calm & Prevent agitation!!! Moist cool air - mist Humidified O 2 by mask or blowby Do Not Examine Upper Airways!!!

Croup: Management n If in respiratory distress: – Racemic epinephrine via nebulizer • Decreases

Croup: Management n 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

Epiglottitis n n n Bacterial infection (Hemophilus influenza ) Edema of epiglottis (supraglottic) –

Epiglottitis n n n Bacterial infection (Hemophilus influenza ) Edema of epiglottis (supraglottic) – partial upper airway obstruction Typically affects 3 -7 year olds

Epiglottitis: Presentation n Age: 3 -7 years of age – can occur in adults

Epiglottitis: Presentation n Age: 3 -7 years of age – can occur in adults – can occur in infants n Rapid onset & progression – – – Fever Severe sore throat Dysphagia Muffled voice Drooling

Epiglottitis: Presentation n Respiratory difficulty – Stridor – Usually in an upright, sitting, tripod

Epiglottitis: Presentation n Respiratory difficulty – Stridor – Usually in an upright, sitting, tripod position n 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) n n Do

Epiglottitis: Management Immediate life threat (8 -12% die from airway obstruction) n n Do NOT attempt to visualize airway Allow child to assume position of comfort – AVOID agitation of the child!!! – AVOID anxiety of the healthcare providers!!! n O 2 by high concentration mask

Epiglottitis: Management n If respiratory failure is eminent: – IV TKO ONLY if eminent

Epiglottitis: Management n 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 n Rapid but calm transport – Appropriate facility

Upper Respiratory Infection n n Common illness Rarely life-threatening Often exacerbates underlying pulmonary conditions

Upper Respiratory Infection n n 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 n Prevention – Avoidance is nearly impossible • Too many potential

Upper Respiratory Infection n 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 n Wide variety of bacteria and viruses are causes – Normal

Pathophysiology of URI n Wide variety of bacteria and viruses are causes – Normal immune system response results in presentation n n 20 -30% are Group A streptococci Most are self-limiting diseases

Presentation of URI n Symptoms – – n Sore throat Fever Chills HA Signs

Presentation of URI n Symptoms – – n Sore throat Fever Chills HA Signs – Cervical adenopathy – Erythematous pharynx – Positive throat culture (bacterial)

Management of URI n n n Usually requires no intervention Oxygen if underlying condition

Management of URI n n n Usually requires no intervention Oxygen if underlying condition has been exacerbated Rarely, pharmacologic interventions are required – Bronchodilators – Corticosteroid n Occasionally, transport required – Key question: Destination?

Central Respiratory Depression

Central Respiratory Depression

Respiratory Depression: Causes n n n Head trauma CVA Depressant drug toxicity – –

Respiratory Depression: Causes n n n Head trauma CVA Depressant drug toxicity – – Narcotics Barbiturates Benzodiazepines ETOH

Respiratory Depression: Recognition n Decreased respiratory rate (< 12/min) Decreased tidal volume Decreased LOC

Respiratory Depression: Recognition n 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 n Airway – Open, clear, maintain – Consider endotracheal intubation The

Respiratory Depression: Management n Airway – Open, clear, maintain – Consider endotracheal intubation The need to VENTILATE is not the same as the need to INTUBATE

Respiratory Depression: Management n Breathing – Oxygenate, ventilate – Restore normal rate, tidal volume

Respiratory Depression: Management n Breathing – Oxygenate, ventilate – Restore normal rate, tidal volume Oxygen alone is INSUFFICIENT if Ventilation is INADEQUATE

Respiratory Depression: Management n Circulation – Obtain vascular access – Monitor EKG (Silent MI

Respiratory Depression: Management n Circulation – Obtain vascular access – Monitor EKG (Silent MI may present as CVA) n Manage Cause – Check Blood Sugar – Consider Narcan 2 mg IV push if S/S suggest narcotic overdose n Intubate if can not find or treat cause

Guillian-Barre´ Syndrome n Autoimmune disease – Leads to inflammation and degeneration of sensory and

Guillian-Barre´ Syndrome n Autoimmune disease – Leads to inflammation and degeneration of sensory and motor nerve roots (demyelination) n Progressive ascending paralysis – Progressive tingling and weakness – Moves from extremities then proximally – May lead to respiratory paralysis (25%)

Guillian-Barre´ Syndrome Management n Treatment based on severity of symptoms – – Control airway

Guillian-Barre´ Syndrome Management n Treatment based on severity of symptoms – – Control airway Support ventilation Oxygen Transport in cases of respiratory depression, distress or arrest

Myasthenia Gravis n n Autoimmune disease Causes loss of ACh receptors at neuromuscular junction

Myasthenia Gravis n n Autoimmune disease Causes loss of ACh receptors at neuromuscular junction – Attacks the ACh transport mechanism at the NMJ n n Episodes of extreme skeletal muscle weakness Can cause loss of control of airway, respiratory paralysis

Myasthenia Gravis Presentation n Gradual onset of muscle weakness – Face and throat –

Myasthenia Gravis Presentation n Gradual onset of muscle weakness – Face and throat – Extreme muscle weakness n n Respiratory weakness -> paralysis Inability to process mucus

Myasthenia Gravis Management n n n Treat symptomatically Watch for aspiration May require assisted

Myasthenia Gravis Management n n n Treat symptomatically Watch for aspiration May require assisted ventilations Assess for Pulmonary infection Transport based upon severity of presentation

Case Studies

Case Studies

Case One n It is 1430 hrs. You are called to a business for

Case One n 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 n Initial Assessment – Airway: Open, maintained by patient – Breathing: Rapid,

Case One n 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 n Vital Signs – P: 126 strong, regular – R: 26 deep,

Case One n Vital Signs – P: 126 strong, regular – R: 26 deep, regular – BP: 130/82 n 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 n History – Allergies: NKA – Medications: Birth control pills – Past

Case One n 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 n n What problem do you now suspect? How would you manage

Case One n n What problem do you now suspect? How would you manage this patient?

Case Two n It is 0530 hours. You are called to a residence to

Case Two n 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 n Initial Assessment – Airway: Inspiratory stridor audible – Breathing: Rapid, shallow,

Case Two n 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 n Vital Signs – P: 130 weak, regular – R: 32 shallow,

Case Two n Vital Signs – P: 130 weak, regular – R: 32 shallow, regular with stridor – BP: 110/70 n 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 n History – – – Allergies: NKA Medications: None Past History: No

Case Two n 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 n n What problem do you now suspect? How would you manage

Case Two n n What problem do you now suspect? How would you manage this patient?

Case Three n At 2330 hrs you are called to a residence to see

Case Three n 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 n Initial Assessment – Airway: Open, maintained by patient, mild stridor audible

Case Three n 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 n Vital Signs – P: 100 weak, regular – R: 30 shallow,

Case Three n Vital Signs – P: 100 weak, regular – R: 30 shallow, labored with stridor – BP: 90/50 n 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 n History – – – Allergies: NKA Medication: Tylenol for fever before

Case Three n 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 n n What problem do you suspect? How would you manage this

Case Three n n What problem do you suspect? How would you manage this patient?

Case Four n At 1945 hours you are dispatched to a “breathing difficulty” at

Case Four n 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 n Initial Assessment – Airway: Open, maintained by patient, difficulty swallowing, voice

Case Four n 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 n Vital Signs – P: 120 strong, regular – R: 26 regular,

Case Four n Vital Signs – P: 120 strong, regular – R: 26 regular, slightly labored – BP: 118/90 n 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 n History – Allergies: No drug allergies; Has experienced itching previously when

Case Four n 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 n n What problem do you suspect? How would you manage this

Case Four n n 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 n At 0130 you are dispatched to an “unconscious person--police on location.

Case Five n 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 n Initial Assessment – Airway: Controllable with manual positioning – Breathing: Very

Case Five n 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 n Vital Signs – P: 70 regular, weak – R: 4 shallow,

Case Five n Vital Signs – P: 70 regular, weak – R: 4 shallow, regular; alcohol odor on breath – BP: 100/70 n 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 n n What problem or problems do you suspect? How would you

Case Five n n What problem or problems do you suspect? How would you manage this patient?