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Pulmonary Diseases.

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Presentation on theme: "Pulmonary Diseases."— Presentation transcript:

1 Pulmonary Diseases

2 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

3 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

4 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

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

6 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

7 Pulmonary Diseases & Disorders
Problems with the Gas Exchange Surface

8 Pulmonary Edema

9 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)

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

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

12 Pulmonary Edema High Permeability
Disrupted alveolar-capillary membrane Membrane allows fluid to leak into the interstitial space Widened interstitial space impairs diffusion

13 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

14 Pulmonary Edema: Signs &Symptoms
Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea Noisy, labored breathing Restlessness, anxiety Productive cough (frothy sputum) Rales, wheezing Tachypnea Tachycardia

15 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

16 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

17 Pneumonia

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

19 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

20 Pneumonia: Etiology Viral Bacterial Fungi Protozoa (pneumocystis)

21 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

22 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

23 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?

24 Pulmonary Embolism

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

26 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

27 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

28 Pulmonary Embolism (PE)
Risk factors Venostasis or DVT Recent surgery or trauma Long bone fractures (lower) Oral contraceptives Pregnancy Smoking Cancer

29 Pulmonary Embolism: Etiology
Most Common Cause = Blood Clots Vessel Wall Injury Virchow’sTriad Hypercoagulability Venous Stasis

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

31 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

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

33 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

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

35 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

36 PE Management Thrombolytics Rapid transport to appropriate facility
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

37 But the next one they throw might!
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!

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

39 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

40 Pleurisy Management Based upon severity of presentation
Mostly supportive

41 Pulmonary Diseases & Disorders
Problems with Airway Obstructions

42 Obstructive Airway Diseases

43 Obstructive Airway Disease
Asthma Emphysema Chronic Bronchitis

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

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

46 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

47 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

48 Lower Airway Disease

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

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

51 Emphysema Type A COPD

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

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

54 Emphysema:Etiology Smoking Environmental factors
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

55 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)

56 Emphysema: Pathophysiology
Loss of elastic recoil leads to increased residual volume and CO2 retention Air Trapping Hyperinflation Hypercapnia -> pulmonary vasoconstriction -> V/Q mismatch

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

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

59 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

60 Chronic Bronchitis Type B COPD

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

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

63 Chronic Bronchitis: Etiology
Smoking Environmental irritants

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

65 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

66 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)

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

68 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

69 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

71 COPD: Management Ventilation Circulation
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

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

73 REMEMBER All bronchodilators are potentially arrhythmogenic
COPD: Management REMEMBER All bronchodilators are potentially arrhythmogenic

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

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

76 Reversible Obstructive Airway Disease

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

78 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)

79 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

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

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

82 Asthma Pathophysiology
Asthma triggered  Bronchial smooth muscle contraction Increased mucus production Bronchial ‘plugging’ Relative dehydration Alveolar hypoventilation  Ventilation Perfusion Mismatch CO2 retention Air ‘Trapping’

83 Asthma: Pathophysiology
Bronchospasm Bronchial Edema Increased Mucus Production

84 Asthma: Pathophysiology

85 Asthma: Pathophysiology
Cast of airway produced by asthmatic mucus plugs

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

87 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

88 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

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

90 Asthma: Signs and Symptoms
Onset of attacks associated with “triggers” Dyspnea Non-productive cough Tachypnea Expiratory wheezing Accessory muscle use Retractions

91 Asthma: Signs and Symptoms

92 Asthma: Signs and Symptoms
Tachycardia Pulsus paradoxus in severe attacks Anxiety, restlessness (hypoxia) progressing to drowsiness, confusion (hypercarbia)

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

94 Asthma: Signs and Symptoms
Early Blood Gas Changes Decreased PaO2 Decreased PaCO2 WHY?

95 Asthma: Signs and Symptoms
Later Blood Gases Decreased PaO2 Normal PaCO2 IMPENDING RESPIRATORY FAILURE

96 Asthma: Signs and Symptoms
Still Later Blood Gases Decreased PaO2 Increased PaCO2 RESPIRATORY FAILURE

97 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

98 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

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

100 Asthma: Management Obtain medication history Consider Overdose

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

102 Asthma: Management Rarely used Magnesium Sulfate (IV) Methylxanthines
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 mg SQ/IM Pediatric – 0.1 to 0.3 mg SQ/IM POSSIBLE BENEFIT IN PATIENTS WITH VENTILATORY FAILURE

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

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

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

107 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

108 Drug Delivery Methods: Review
MDI vs. MDI w/ spacer vs. SVN vs. SQ injection

109 Asthma unresponsive to beta-2 adrenergic agents
Status Asthmaticus Asthma unresponsive to beta-2 adrenergic agents

110 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

112 Lower Airway Disease Cystic Fibrosis

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

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

115 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

116 Lower Airway Disease Neoplasms of the Lung

117 Hyperventilation Syndrome

118 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

119 Hyperventilation Syndrome: Pathophysiology
Tachypnea or hyperpnea secondary to anxiety Decreased PaCO2 Respiratory alkalosis Vasoconstriction Hypocalcemia Decreased O2 Release to Tissues

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

121 Hyperventilation Syndrome: Signs & Symptoms
Rapid breathing Cool & possibly pale skin Carpopedal spasm Dysrhythmias Sinus Tachycardia SVT Sinus arrhythmia Loss of consciousness and seizures (late & rare)

122 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

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

124 Pulmonary Infectious Diseases

125 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

126 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

127 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

128 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!!!

129 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

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

131 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

132 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

133 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

134 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

135 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

136 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

137 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

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

139 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?

140 Central Respiratory Depression

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

142 Respiratory Depression: Recognition
Decreased respiratory rate (< 12/min) Decreased tidal volume Decreased LOC Use Your Stethoscope Look, Listen, Feel THEY PROBABLY AREN’T If you can’t tell whether a patient is breathing adequately...

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

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

145 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

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

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

148 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

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

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

151 Case Studies

152 What would you like to include in your initial differential diagnosis?
Case One It is 1430 hrs. You are called to a business for a “possible stroke.” The patient is a 20-year-old female complaining of dizziness and of numbness around her mouth and fingertips. What would you like to include in your initial differential diagnosis?

153 What therapies, if any, would you like to begin?
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?

154 Would you like to make any Changes to your therapies or Diff Dx?
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?

155 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

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

157 What would you like to include in your differential diagnosis?
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-old-female. Mother says the child woke up crying about 2 hours ago. What would you like to include in your differential diagnosis?

158 What therapies, if any, would you like to begin now?
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?

159 Would you like to make any Changes to your therapies or Diff Dx?
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?

160 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

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

162 How narrow a Differential Diagnosis can you compile at this point?
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?

163 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

164 Now you can narrow your Diff Dx? To what?
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?

165 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

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

167 What is your differential diagnosis?
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?

168 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

169 What therapies do you want to initiate?
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?

170 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”

171 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?

172 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”.

173 What therapies would you like to begin?
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?

174 Case Five Vital Signs Physical Exam 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

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

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