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Emergency Medicine > Approach to Dyspnea in the ED > Flashcards

Approach to Dyspnea in the ED Flashcards

1
Q

Evidence of respiratory distress/failure

A
  • Marked tachypnea and tachycardia
  • Stridor
  • Use of accessory respiratory muscles: sternocleidomastoid, sternoclavicular, intercostals
  • Inability to speak normally as consequence of breathlessness
  • Agitation or lethargy as consequence of hypoxemia
  • Depressed consciousness due to hypercapnia
  • Paradoxical abdominal wall movement: retracts inward with inspiration during diaphragmatic fatigue
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2
Q

What organ system would you want to ask about in the history for dyspnea?

A

Chronic cardiopulmonary diseases

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3
Q

What medication specifically would you want to ask about on clinical evaluation of dyspnea?

A

Steroid use

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4
Q

What would you assess on oral physical exam of someone with dyspnea?

A
  • Angioedema
  • FB
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5
Q

What would you assess in the extremities on physical exam of someone with dyspnea?

A
  • Acrocyanosis
  • Signs of fluid overload
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6
Q

What are the most immediately life-threatening causes of dyspnea?

A
  • Upper airway obstruction: foreign body, angioedema, hemorrhage
  • Tension pneumothorax
  • Pulmonary embolism
  • Neuromuscular weakness: myasthenia gravis, Guillain-Barre syndrome, botulism
  • Fat embolism (trauma –> blood vessel damage)
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7
Q

What are the most common causes of dyspnea?

A
  • Obstructive airway disease: asthma, COPD
  • Decompensated heart failure/cardiogenic pulmonary edema
  • Ischemic heart disease: unstable angina and myocardial infarction
  • Pneumonia
  • Psychogenic
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8
Q

What historical factors would suggest heart failure as the cause for dyspnea?

A
  • History of heart failure, MI, CAD
  • Paroxysmal nocturnal dyspnea
  • Orthopnea
  • Edema
  • Dyspnea on exertion
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9
Q

What PE/diagnostic findings would suggest heart failure as cause of dyspnea?

A

PE
* S3 gallop
* JVD
* Hepatojugular reflex
* S4
* Wheezing
* CXR: pulmonary venous congestion, interstitial edema, alveolar edema, cardiomegaly
* ECG: afib, any abnormal finding

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10
Q

Diagnostic evaluation of dyspnea

A
  • CBC (infection)
  • CMP
  • Peak expiratory flow rate (diff asthma/COPD from other disorders)
  • ABG (if sig hypoxia)
  • EKG (concern of heart)/troponin
  • BNP or N-terminal pro BNP
  • D-dimer (PE)
  • CXR (almost always + try to compare with previous)
  • Bedside point of care ultrasound (diff acute cardiav vs noncardiac)
  • CT scan, CTA, V-Q scan
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11
Q

What can be found on bedside point of care ultrasound that is related to dyspnea?

A
  • Pleural effusion
  • Pneumothorax
  • Pulmonary consolidation
  • Intravascular volume status
  • Cardiac tamponade
  • Cardiac function
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11
Q

General management and disposition of dyspnea

A
  • Initial goal of treatment to maintain oxygenation
  • Once diagnosis is made, treatment focused on underlying diagnosis
  • Most patients who present with hypoxia/hypoxemia require admission
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12
Q

What is the goal PaO2 and oxygen saturation?

A
  • PaO2 aboe 60 mmHg or O2 saturation >90%
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13
Q

Which patients would have lower oxygen goals?

A
  • Chronic lung disease (CO2 retainers) due to risk of respiratory depression if chronic hypercapnia
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14
Q

How can oxygen be administered?

A
  • Nasal cannula, face mask, or non-rebreather
  • Low flow (allows room air to mix with oxygen): NC (.25 -4lpm) or simple mask (6-10 lpm)
  • High flow (pure oxygen): high flow NC (4 LPM in infants with up to 40 LPM or more in adolescents and adults –> some positive pressure and decreases amount of room air breathed in) or non-rebreather (10-15 lpm)
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15
Q

What is the next step if there is inadequate improvement of hypoxia with O2 therapy?

A
  • Noninvasive ventilation: CPAP or BiPAP
  • Continued decline despite measures: prepare for mechanical ventilation
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16
Q

What are upper airway emergencies?

A
  • Croup
  • Bacterial tracheitis
  • Airway foreign body
  • Epiglottitis
  • Retropharyngeal abscess
  • Peritonsillar abscess
  • Laryngotracheomalacia
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17
Q

What is the MC sign present in patients with upper airway obstruction?

A

Stridor

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18
Q

What is the MC cause of stridor in neonates?

A
  • Laryngotracheomalacia: weak larynx
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19
Q

Who should an airway foreign body be considered in?

A

All children who present with respiratory complaints

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20
Q

What is the MC age for airway foreign body?

A

1-3 years

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21
Q

What are the MC objects and foods to become an airway foreign body?

A
  • Objects: food and toys
    MC foods
  • Peanuts
  • Sunflower seeds
  • Carrots
  • Raisins
  • Grapes
  • Hot dogs

Do not give these to kids!

22
Q

Clinical presentation of airway foreign body

A
  • History of sudden coughing/choking
  • Gagging
  • Stridor
  • Cyanosis
23
Q

Classic presentation of laryngotracheal FB

A
  • Stridor
  • Hoarseness
  • Complete apnea
24
Classic presentation of bronchial FB
* Unilateral wheezing * Decreased breath sounds
25
Imaging for airway foreign body
* Do not delay lifesaving intervention for imaging * PA and lateral soft tissue neck (tracheal FB) * PA and lateral CXR (bronchial FB): inspiratory and expiratory views assess air trapping * Bronchoscopy: confirms or rules out diagnosis and can be therapeutic to remove FB
26
Evidence of radiolucent FB may present with what on CXR?
* Unilateral obstructive emphysema due to FB obstructing expiration resulting in air trapping and mediastinal shift to opposite side * Focal atelectasis with complete obstructions * Consolidation --> scarring
27
How can you tell if a coin is in trachea or esophagus?
* Circular face on AP/PA --> esophagus * Circular face on lateral --> trachea
28
Management of airway foreign body causing complete airway obstruction
* BLS * Direct laryngoscopy with FB extraction * Orotracheal intubation with dislodgement of FB more distally (if laryngoscopy fails) * If ET intubation fails, needle cricothyroidotomy or emergency tracheostomy * Consult pulmonology for emergent bronchoscopy to remove FB if BLS and laryngoscopy fail
29
Management of airway foreign body if partial airway obstruction
* Bronchoscopy under general anesthesia
30
Clinical presentation of croup
* Prodrome: cough, coryza, and mild fever * Inspiratory stridor * Barking seal-like cough * Hoarseness * Respiratory distress * Fever
31
Mild vs moderate vs severe croup
* Mild: no stridor at rest * Moderate: stridor at rest and mild retractions * Severe: stridor at rest and severe retractions, anxious or agitated appearing, pale/fatigued
32
Imaging of croup
* Soft tissue neck x-ray showing: * Subglottic haziness * Narrowing of superior trachea in steeple sign with normal epiglottis
33
Management of croup
* Standard of care: minimal disturbance, pulse ox monitor, antipyretics * Mild: outpatient, single dose of oral dexamethasone; IM dexamethasone or nebulized budesonide if unable to tolerate oral * Moderate-severe: single dose dexamethasone, nebulized (racemic) epinephrine, humidified oxygen * Heliox (70-80% helium and oxygen 20-30% used as last resort before intubation * Intubation if no response to pharmacotherapy
34
Discharge criteria for croup
* Nontoxic * No signs of dehydration * O2 sat >90% on RA * Reliable caregiver * Observation with improvement for 3 hours after last epi tx * F/U in 24-48 hrs with PCP ## Footnote Must meet all!!
35
Indications for admission of croup
* Persistent stridor at rest * Persistent tachypnea * Persistent retractions * Persistent hypoxia * >2 doses of nebulized epi needed ## Footnote Only needs to meet one!!
36
Clinical presentation of bacterial tracheitis
* More severe respiratory distress than croup * Toxic appearing * Thick mucopurulent secretions result in upper airway obstruction * Sore throat referring to trachea with tenderness on palpation
37
Diagnostics for bacterial tracheitis
* Imaging not clinically necessary: findings similar to croup * Bronchoscopy (after airway is secured) is needed (consult pulm): confirms edema of trachea, therapeutic removal of thick mucopurulent tracheal secretions, C&S to help guide therapy
38
Management of bacterial tracheitis
* Intubation and mechanical ventilation * Vancomycin + Ampicillin/Sulbactam (Unasyn) or ceftriaxone (Rocephin) * FQ substituted for beta-lactam if allergy is present * Consult pulmonology
39
What is the role of the kidneys in acid-base balance?
* Balance HCO3 via retention of secretion * HCO3 = base * Excess HCO3 - alkalosis (increased blood pH) * Low HCO3- acidosis (decreased blood pH) * Compensation in 12-24 hours
40
What is the role of the lungs in acid-base balance?
* CO2 dissolves into carbonic acid in the blood * Excess CO2 will decrease blood pH (acidosis) * Low CO2 will increase pH (alkalosis) * Compensation can occur within minutes
41
What is an ABG?
Serologic test that measures acidity, oxygen, and carbon dioxide in the arterial blood
42
What is assessed in an ABG?
* pH * PaCO2: respiratory component of acid/base regulation * PaO2: amount of O2 dissolved in serum * HCO3: metabolic component of acid/base regulation * O2Sat: oxygen saturation of hemoglobin
43
What are types of acid-base disorders?
* Acidosis: pH <7.35 * Alkalosis: pH >7.45
44
What are representations of organ system dysfunction in acid-base disorders?
* Metabolic: HCO3 increased (alkalosis) decreased (acidosis) * Respiratory: PaCO2 increased (acidosis) decreased (alkalosis)
45
How do you know whether an organ system is compensating?
Whether pH remains normal despite abnormal HCO3 or PaCO2 Can be: * Compensated * Partially compensated * Uncompensated Acute will be uncompensated and chronic will be compensated
46
What is the pathophysiology of respiratory acidosis?
Alveolar hypoventilation
47
Acute causes of respiratory acidosis
* Head trauma * Chest trauma * Lung disease * Excess sedation
48
Chronic causes of respiratory acidosis
* Obesity * COPD * Sleep apnea * If arterial pCO2 exceeds 60 to 70 mmHg, respiratory center may be depressed and stimulation comes from hypoxemia, O2 could leaad to loss of respiratory drive
49
If patient is at risk of respiratory depression from loss of respiratory drive what should be done?
Still don't withold oxygen if severely dyspneic! Monitor for apnea or hypoventilation
50
Treatment of respiratory acidosis
* Increase minute ventilation * Bronchodilators with small amounts of O2 * Invasive ventilation assistance
51
Pathophysiology of respiratory alkalosis
* Alveolar hyperventilation * Decrease in CO2 --> decreased H+ resulting in imbalance of cations and anions * Negatively charged proteins bind Ca2+ leading to ionized hypocalcemia
52
Etiologies of respiratory alkalosis
* CNS tumors or stroke * Infections * Pregnancy * Hypoxia and toxins * Anxiety * Pain * Iatrogenic overventilation on mechanical ventilators
53
Treatment of respiratory alkalosis
Treatment of underlying condition

Emergency Medicine (13 decks)

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