Transcript Pulmonary edema

Pulmonary Diseases
Pulmonary Diseases & Disorders
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Pulmonary Disease & Conditions may result
from:
– Infectious causes
– Non-Infectious causes
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Adversely affect one or more of the following
– Ventilation
– Diffusion
– Perfusion
Pulmonary Diseases & Disorders
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The Respiratory Emergency may stem from
dysfunction or disease of (examples only):
– Control System
• Hyperventilation
• Central Respiratory Depression
• CVA
– Thoracic Bellows
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Chest/Diaphragm Trauma
Pickwickian Syndrome
Guillian-Barre Syndrome
Myasthenia Gravis
COPD
Pulmonary Diseases & Disorders
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The Respiratory Emergency may affect the
upper or lower airways
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Upper Airway Obstruction
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Tongue
Foreign Body Aspiration
Angioneurotic Edema
Maxillofacial, Larnygotracheal Trauma
Croup
Epiglottitis
Respiratory Emergencies: Causes
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Lower Airway Obstruction
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Emphysema
Chronic Bronchitis
Asthma
Cystic Fibrosis
Pulmonary Diseases & Disorders
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The Respiratory Emergency may stem from
Gas Exchange Surface Abnormalities
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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
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A pathophysiologic condition, not a
disease
– Fluid in and around alveoli
– Interferes with gas exchange
– Increases work of breathing
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Two Types
– Cardiogenic (high pressure)
– Non-Cardiogenic (high permeability)
Pulmonary Edema
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High Pressure (cardiogenic)
• AMI
• Chronic HTN
• Myocarditis
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High Permeability (non-cardiogenic)
• Poor perfusion, Shock, Hypoxemia
• High Altitude, Drowning
• Inhalation of pulmonary irritants
Cardiogenic Pulmonary Edema:
Etiology
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Left ventricular failure
Valvular heart disease
– Stenosis
– Insufficiency
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Hypertensive crisis (high afterload)
Volume overload
Increased Pressure in Pulmonary Vascular Bed
Pulmonary Edema
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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
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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
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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
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Position
Oxygen
PPV / Intubation
– CPAP
– PEEP
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IV Access; Minimal fluid administration
Treat the underlying cause
– Diuretics usually not helpful; May be harmful
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Transport
Adult Respiratory Distress Syndrome
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AKA: Non-cardiogenic pulmonary edema
A complication of:
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Severe Trauma / Shock
Severe infection / Sepsis
Bypass Surgery
Multiple blood transfusions
Drug overdose
Aspiration
Decreased compliance
Hypoxemia
Pneumonia
Pneumonia
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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
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Inflammation of the bronchioles and alveoli
– Products of inflammation (secretions, pus) add to
respiration difficulty
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Gas exchange is impaired
Work of breathing increases
May lead to
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Atelectasis
Sepsis
VQ Mismatch
Hypoxemia
Pneumonia: Etiology
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Viral
Bacterial
Fungi
Protozoa (pneumocystis)
Aspiration
Presentation of Pneumonia
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Shortness of breath, Dyspnea
Fever, chills
Pleuritic Chest Pain, Tachycardia
Cough
– Green/brown sputum
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May have crackles, rhonchi or wheezing in
peripheral lung fields
– Consolidation
– Egophony
Management of Pneumonia
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Treatment mostly based upon symptoms
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Oxygen
Rarely is intubation required
IV Access & Rehydration
B2 agonists may be useful
Antibiotics (e.g. Rocephin)
Antipyretics
Pneumonia: Management
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MD follow-up for labs, cultures & Rx
Transport considerations
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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
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~ 50,000 deaths / year/ US
– ~5% of all sudden deaths
– <10% of all PE result in death
Pulmonary Embolism:
Pathophysiology
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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)
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A disorder of perfusion
Combination of factors increase probability of
occurrence
– Hypercoagulability
– Platelet aggregation
– Deep vein stasis
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Embolus usually originates in lower
extremities or pelvis
Pulmonary Embolism (PE)
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Risk factors
– Venostasis or DVT
– Recent surgery or trauma
• Long bone fractures (lower)
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Oral contraceptives
Pregnancy
Smoking
Cancer
Pulmonary Embolism: Etiology
Most Common Cause = Blood Clots
Vessel Wall Injury
Virchow’
sTriad
Hypercoagulability
Venous Stasis
Pulmonary Embolism: Etiology
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Other causes
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Air
Amniotic fluid
Fat particles (long bone fracture)
Particulates from substance abuse
Venous catheter
Pulmonary Embolism: Signs & Symptoms
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Small Emboli
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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
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Larger Emboli
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Small Emboli S/S plus:
Pleuritic pain
Pleural rub
Coughing
Wheezing
Hemoptysis (rare)
Pulmonary Embolism: Signs & Symptoms
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Very Large Emboli
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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
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Management based on severity of Sx/Sx
Airway & Breathing
– High concentration O2
– Consider assisting ventilations
– Early Intubation
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Circulation
– IV, 2 lg bore sites
• Fluid bolus then TKO; Titrate to BP ~ 90 mm Hg
– Monitor ECG
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Rapid transport
PE Management
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Thrombolytics
– Aspirin & Heparin (questionable if any benefit)
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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
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Inflammation of pleura caused by a friction
rub
– layers of pleura rubbing together
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Commonly associated with other respiratory
disease
Presentation of Pleurisy
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Sharp, sudden and intermittent chest pain
with related dyspnea
– Possibly referred to shoulder
– May  or  with respiration
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Pleural “friction rub” may be audible”
May have effusion or be dry
Pleurisy
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Management
– Based upon severity of presentation
– Mostly supportive
Pulmonary Diseases & Disorders
Problems with Airway
Obstructions
Obstructive Airway Diseases
Obstructive Airway Disease
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Asthma
Emphysema
Chronic Bronchitis
Obstructive Airway Diseases
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Asthma experienced by ~ 4 - 5 % of
Canadian population
– Mortality rate increasing
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Factors leading to Obstructive Airway
Diseases
– Smoking
– Exposure to environmental agents
– Genetic predisposition
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How does this differ from “COPD”?
Obstructive Airway Disease
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Exacerbation Factors
– Intrinsic
• Stress (especially in adults)
• URI
• Exercise
– Extrinsic
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Cigarette Smoke
Allergens
Drugs
Occupational hazards
Obstructive Airway Disease
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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
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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
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Most common chronic lung disease
4th leading cause of death
many deaths annually
Emphysema
Type A COPD
Emphysema: Definition
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Destruction of alveolar
walls
Distention of pulmonary
air spaces
Loss of elastic recoil
Destruction of gas
exchange surface
Emphysema: Incidence
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Male > females
Urban area > rural areas
Age usually > 55
Emphysema:Etiology
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Smoking
– 90% of all cases
– Smokers 10x more likely to die of COPD than
non-smokers
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Environmental factors
Alpha – 1 antitrypsin deficiency
– hereditary
– 50,000 to 100,000 cases
– mostly people of northern European descent
Emphysema: Pathophysiology
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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
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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
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Increasing dyspnea on exertion
Non-productive cough
Malaise
Anorexia, Loss of weight
Hypertrophied respiratory accessory muscles
Emphysema: Signs and Symptoms
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Increased Thoracic AP
Diameter
(Barrel Chest)
Decreased lung/heart
sounds
Hyperresonant chest
Emphysema: Signs and Symptoms
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Lip pursing on exhalation
Clubbed fingertips
Altered blood gases
– Normal or decreased PaO2
– Elevated CO2
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Cyanosis occurs LATE in course of disease
PINK PUFFER
Chronic Bronchitis
Type B COPD
Chronic Bronchitis: Definition
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Increased mucus production for > 3 months
for > 2 consecutive years
Recurrent productive cough
Chronic Bronchitis: Incidence
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Males > females
Urban areas > rural areas
Age usually > 45
Chronic Bronchitis: Etiology
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Smoking
Environmental irritants
Chronic Bronchitis: Pathophysiology
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Mucus plugging/inflammatory edema
Increased airflow resistance leads to
alveolar hypoventilation
Alveolar hypoventilation leads to
– hypercarbia
– hypoxemia
Chronic Bronchitis: Pathophysiology
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Hypoxemia leads to
– increased RBC’s w/o oxygen which leads to
• cyanosis
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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
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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
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Decreased intellectual ability
Personality changes
Abnormal blood gases
– Hypercarbia
– Hypoxia
Cyanosis EARLY in course of disease
BLUE BLOATER
COPD Assessment Findings
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Chronic condition  acute episode
S&S of  work of breathing and/or hypoxemia
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Use of accessory muscles
Increased expiratory effort
Tachycardia, AMS, Cyanosis
Wheezing, Rhonchi,  LS
Thin, red/pink appearance
Saturation usually normal in emphysema
COPD: Management
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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
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Airway and Breathing
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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
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Ventilation
– Avoid intubation unless absolutely necessary
• near respiratory failure
• exhaustion
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Circulation
– IV TKO
– Titrate fluid to degree of dehydration
• 250 cc trial bolus
– Excessive fluid may precipitate CHF
– Monitor ECG
COPD: Management
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Drug Therapy
– Obtain thorough medication history
– Nebulized Beta 2 agonists
• Albuterol
• Terbutaline
• Metaproterenol
• Isoetharine
COPD: Management
REMEMBER
All bronchodilators are
potentially arrhythmogenic
COPD: Management
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Drug Therapy
– Ipratropium (anticholinergic) by SVN
– (beta-2 agonist) by MDI, SQ or IV
– Corticosteroids (anti-inflammatory agent) by IV
COPD: Management
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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
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Lower airway hyper-responsiveness to a
variety of stimuli
Diffuse reversible airway obstruction or
narrowing
Airway inflammation
Asthma: Incidence
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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
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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
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Commonly misdiagnosed in children as
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Chronic bronchitis
Recurrent croup
Recurrent URI
Recurrent pneumonia
Asthma
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Often triggered by:
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Cold temperature
Respiratory Infections
Vigorous exercise
Emotional Stress
Environmental allergens or irritants
Exacerbation
– Extrinsic common in children
– Intrinsic common in adults
Asthma Pathophysiology
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Asthma triggered 
Bronchial smooth muscle contraction
Increased mucus production
– Bronchial ‘plugging’
– Relative dehydration
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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
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Difficulty exhaling
– chest hyperinflation
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Poor gas exchange
– hypoxia
– hypercarbia
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Increased respiratory
water loss
– dehydration
Asthma: Types
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Type 1 Extrinsic
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Classic allergic asthma
Common in children, young adults
Seasonal in nature
Sudden brief attacks
Major component is bronchospasm
Good bronchodilator response
Asthma: Types
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Type 2 Extrinsic Asthma
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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
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Intrinsic Asthma
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Adult > 35
No immunologic cause
Aspirin sensitivity/nasal polyps
Poor bronchodilator response
Asthma: Signs and Symptoms
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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
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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
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Early Blood Gas Changes
– Decreased PaO2
– Decreased PaCO2
WHY?
Asthma: Signs and Symptoms
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Later Blood Gases
– Decreased PaO2
– Normal PaCO2
IMPENDING
RESPIRATORY
FAILURE
Asthma: Signs and Symptoms
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Still Later Blood Gases
– Decreased PaO2
– Increased PaCO2
RESPIRATORY
FAILURE
Asthma: Risk Assessment
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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
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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
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Circulation
– IV TKO
– Assess for dehydration
– Titrate fluid administration to severity of
dehydration
• Trial bolus of 250 cc
– Monitor ECG, Pulse Oximetry
Asthma: Management
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Obtain medication history
Consider
– Overdose
– Dysrhythmias
Asthma: Management
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Nebulized Beta-2 agents
– Salbutamol
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Nebulized anticholinergics
– Ipratropium
– Atropine
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IV Corticosteroid
– Methylprednisolone
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Combination – Flovent/etc
Asthma: Management
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Rarely used
– Questionable efficacy, Potential Complications
– Magnesium Sulfate (IV)
– Methylxanthines
• Aminophylline (IV)
Asthma: Management
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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
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Use EXTREME caution in giving two
sympathomimetics or two doses to same
patient
Monitor ECG
Asthma: Management
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Avoid
– Sedatives
• Depress respiratory drive
– Antihistamines
• Decrease LOC, dry secretions
– Aspirin
• High incidence of allergy
Asthma: Management
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Continuous Monitoring & Frequent
Reassessment
Need for transport? Destination?
Asthma: Management
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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
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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
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Pulmonary edema
Pulmonary embolism
Allergic reactions
COPD
Pneumonia
Foreign body aspiration
Cystic fibrosis
Lower Airway Disease
Cystic Fibrosis
Cystic Fibrosis: Definition
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Inherited metabolic disease of exocrine
glands and sweat glands
Primarily affects digestive, respiratory
systems
Begins in infancy
Cystic Fibrosis: Etiology
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Autosomal recessive gene
Both parents must be carriers
Incidence
– Caucasians--1:2000
– Blacks--1:17,000
– Asians--very rare
Cystic Fibrosis: Pathophysiology
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Obstruction of pancreatic, intestinal gland,
bile ducts
Over-secretion by airway mucus glands
– mucous plugs
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Excess loss of sodium chloride in sweat
Lower Airway Disease
Neoplasms of the Lung
Hyperventilation Syndrome
Hyperventilation Syndrome
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Brady Textbook Correction, Vol. 3, p. 57
– Table 1-4: These are NOT Causes of
hyperventilation syndrome
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A diagnosis of EXCLUSION!!!
An increased ventilatory rate that
– DOES NOT have a pathologic origin
– Results from anxiety
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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
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Symptoms
– Light-headedness, giddiness, anxiety
– Numbness, paresthesias of:
• Hands
• Feet
• Circumoral area
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Cold hands, feet
Carpopedal spasms
Dyspnea
Chest pain
Hyperventilation Syndrome:
Signs & Symptoms
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Signs
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Rapid breathing
Cool & possibly pale skin
Carpopedal spasm
Dysrhythmias
• Sinus Tachycardia
• SVT
• Sinus arrhythmia
– Loss of consciousness and seizures (late &
rare)
Hyperventilation Syndrome:
Management
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Educate patient & family
– Consider possible psychopathology especially
in “repeat customers”
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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)
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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
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Gradual onset (several days)
– Often begins with Sx of URI
– May begin with only low grade fever
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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
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
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
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
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?