Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Emergency Medicine > Approach to Dyspnea in the ED > Flashcards

Approach to Dyspnea in the ED Flashcards

You may prefer our related Brainscape-certified flashcards:
Royal College: Emergency Medicine 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Chronic cardiopulmonary diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Steroid use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
  • Angioedema
  • FB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
  • Acrocyanosis
  • Signs of fluid overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the goal PaO2 and oxygen saturation?

A
  • PaO2 aboe 60 mmHg or O2 saturation >90%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which patients would have lower oxygen goals?

A
  • Chronic lung disease (CO2 retainers) due to risk of respiratory depression if chronic hypercapnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are upper airway emergencies?

A
  • Croup
  • Bacterial tracheitis
  • Airway foreign body
  • Epiglottitis
  • Retropharyngeal abscess
  • Peritonsillar abscess
  • Laryngotracheomalacia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Stridor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the MC cause of stridor in neonates?

A
  • Laryngotracheomalacia: weak larynx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Who should an airway foreign body be considered in?

A

All children who present with respiratory complaints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the MC age for airway foreign body?

A

1-3 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Classic presentation of bronchial FB

A
  • Unilateral wheezing
  • Decreased breath sounds
25
Q

Imaging for airway foreign body

A
  • 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
Q

Evidence of radiolucent FB may present with what on CXR?

A
  • 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
Q

How can you tell if a coin is in trachea or esophagus?

A
  • Circular face on AP/PA –> esophagus
  • Circular face on lateral –> trachea
28
Q

Management of airway foreign body causing complete airway obstruction

A
  • 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
Q

Management of airway foreign body if partial airway obstruction

A
  • Bronchoscopy under general anesthesia
30
Q

Clinical presentation of croup

A
  • Prodrome: cough, coryza, and mild fever
  • Inspiratory stridor
  • Barking seal-like cough
  • Hoarseness
  • Respiratory distress
  • Fever
31
Q

Mild vs moderate vs severe croup

A
  • 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
Q

Imaging of croup

A
  • Soft tissue neck x-ray showing:
  • Subglottic haziness
  • Narrowing of superior trachea in steeple sign with normal epiglottis
33
Q

Management of croup

A
  • 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
Q

Discharge criteria for croup

A
  • 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

Must meet all!!

35
Q

Indications for admission of croup

A
  • Persistent stridor at rest
  • Persistent tachypnea
  • Persistent retractions
  • Persistent hypoxia
  • > 2 doses of nebulized epi needed

Only needs to meet one!!

36
Q

Clinical presentation of bacterial tracheitis

A
  • 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
Q

Diagnostics for bacterial tracheitis

A
  • 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
Q

Management of bacterial tracheitis

A
  • Intubation and mechanical ventilation
  • Vancomycin + Ampicillin/Sulbactam (Unasyn) or ceftriaxone (Rocephin)
  • FQ substituted for beta-lactam if allergy is present
  • Consult pulmonology
39
Q

What is the role of the kidneys in acid-base balance?

A
  • 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
Q

What is the role of the lungs in acid-base balance?

A
  • 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
Q

What is an ABG?

A

Serologic test that measures acidity, oxygen, and carbon dioxide in the arterial blood

42
Q

What is assessed in an ABG?

A
  • 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
Q

What are types of acid-base disorders?

A
  • Acidosis: pH <7.35
  • Alkalosis: pH >7.45
44
Q

What are representations of organ system dysfunction in acid-base disorders?

A
  • Metabolic: HCO3 increased (alkalosis) decreased (acidosis)
  • Respiratory: PaCO2 increased (acidosis) decreased (alkalosis)
45
Q

How do you know whether an organ system is compensating?

A

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
Q

What is the pathophysiology of respiratory acidosis?

A

Alveolar hypoventilation

47
Q

Acute causes of respiratory acidosis

A
  • Head trauma
  • Chest trauma
  • Lung disease
  • Excess sedation
48
Q

Chronic causes of respiratory acidosis

A
  • 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
Q

If patient is at risk of respiratory depression from loss of respiratory drive what should be done?

A

Still don’t withold oxygen if severely dyspneic!
Monitor for apnea or hypoventilation

50
Q

Treatment of respiratory acidosis

A
  • Increase minute ventilation
  • Bronchodilators with small amounts of O2
  • Invasive ventilation assistance
51
Q

Pathophysiology of respiratory alkalosis

A
  • Alveolar hyperventilation
  • Decrease in CO2 –> decreased H+ resulting in imbalance of cations and anions
  • Negatively charged proteins bind Ca2+ leading to ionized hypocalcemia
52
Q

Etiologies of respiratory alkalosis

A
  • CNS tumors or stroke
  • Infections
  • Pregnancy
  • Hypoxia and toxins
  • Anxiety
  • Pain
  • Iatrogenic overventilation on mechanical ventilators
53
Q

Treatment of respiratory alkalosis

A

Treatment of underlying condition

Emergency Medicine (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions