Respiratory Flashcards

1
Q

<p>4 causes of hypoxia </p>

A

<p>1. Low PaO@

2. Anemia or abnormal hemoglobin
3. Low cardiac output states
4. Inability to use delivered oxygen ie. cyanide toxicity</p>

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2
Q

<p>6 physiological mechanisms of hypoxemia </p>

A

<p>1. Low inspired partial pressure of O2

2. Hypoventilation
3. Ventilation/perfusion mismatch
4. Shunt - intrapulmonary vs. intracardiac
5. Low mixed venous oxygen saturations
6. Diffusion abnormality </p>

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3
Q

<p>Etiologies of decreased lung compliance</p>

A
<p>pneumonia
pneumothorax 
atelectasis
mainstem intubation
obesity
pulmonary fibrosis
ARDS
congestive heart failure
abdominal distension, compartment syndrome
kyphoscoliosis 
</p>
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4
Q

<p>Causes of increased lung compliance </p>

A

<p>emphysema
open chest
flail chest </p>

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5
Q

<p>Contraindications of NIPPV </p>

A

<p>1. hemodynamic instability/shock

2. decreased LOC/unable to protect airway
3. inadequate respiratory drive
4. high risk aspiration (UGIB, SBO)
5. facial trauma/burns/surgeries (unable to wear mask)
6. upper airway obstruction
7. inability to clear secretions
8. agitated, uncooperative patient </p>

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6
Q

<p>Indications for NIPPV </p>

A

<p>1. Cardiogenic pulmonary edema

2. AECOPD
3. Others controversial: pre-oxygenation, asthma </p>

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7
Q

<p>Complications of NIPPV </p>

A

<p>pressure necrosis of skin
damages to eyes
claustrophobia </p>

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8
Q

<p>Benefits of PEEP </p>

A

<p>prevent end expiratory collapse of alveoli
recruit non or poorly ventilated alveoli
creates hydrostatic forces that move fluid from airway to interstitium (helps with gas exchange) </p>

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9
Q

<p>Complications of PEEP </p>

A

<p>overinflation and barotrauma
decreased preload
</p>

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10
Q

<p>Relative contraindications of PEEP </p>

A
<p>hypotension
right heart failure
R->L intracardiac shunt
increased ICP
hyperinflation
asymmetric or focal lung disease
bronchopleural fistula </p>
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11
Q

<p>How do you detect auto-PEEP (breath stacking) </p>

A

<p>Clinical: patients fight the vent, dysynchronous
Expiratory sounds heard throughout expiratory phase up until inspiration
Expiratory hold maneuver </p>

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12
Q

<p>What is the definition of ARDS (Berlin 2012) </p>

A

<p>Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week.
1. Bilateral opacities consistent with pulmonary edema must be present on a chest radiograph or computed tomographic (CT) scan. These opacities must not be fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules.
2. The patient’s respiratory failure must not be fully explained by cardiac failure or fluid overload. An objective assessment (eg, echocardiography) to exclude hydrostatic pulmonary edema is required if no risk factors for ARDS are present.
3. A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2). The severity of the hypoxemia defines the severity of the ARDS:
•Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O.
•Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200 mmHg, on ventilator settings that include PEEP ≥5 cm H2O.
•Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilators setting that include PEEP ≥5 cm H2O.</p>

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13
Q

<p>What is the dosing of norepinephrine (levophed) </p>

A

<p>0.01-3 mcg/kg/min for infusion

| Once you exceed 0.3-0.4, start thinking about other causes of shock </p>

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14
Q

<p>What is the dosing of push dose epi and how do you make it? </p>

A

<p>Take 1:10,000 cardiac epi from crash card. 100 mcg/mL
Mix 1 cc with 9 cc of NS = 10 mcg/mL
Duration 5-10 min
Give 0.5-2 mL q2-5 min (5-20 mcg) </p>

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15
Q

<p>What is the dosing of push dose phenyl and how do you make it? </p>

A

<p>Take 1 mL of phenyl (10 mg/mL), mix in 100 cc bag of NS
= 100 mcg/mL
Duration 10-20 min
Give 0.5-2 mL q2-5 min (50-200 mcg) </p>

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16
Q

<p>What are the 4 evidence based interventions for supportive treatment of ARDS?</p>

A

<p>1. Lung protective ventilation status

2. Keep lungs dry (avoid pulmonary edema)
3. Neuromuscular blockade
4. Proning </p>

17
Q

<p>What are the 4 mechanisms of ventilator associated lung injury?</p>

A

<p>1. Volutrauma

2. Barotrauma
3. Aletectrauma
4. Biotrauma</p>

18
Q

<p>Name 5 pulmonary and non-pulmonary causes of ARDS</p>

A
<p>Pulmonary:
1. Aspiration
2. Infection/pneumonia
3. Heart failure
4. Pulmonary vasculitis
5. Lung transplantation
Non-pulmonary:
1. Massive trauma
2. Non-pulmonary sepsis
3. TRALI, massive transfusion
4. Burns
5. Pancreatitis 
6. Drug induced </p>
19
Q

What are 4 mechanisms of decreased central venous oxygen saturation?

A
  1. Decrease in SaO2
  2. Decrease in cardiac output
  3. Decrease in hemoglobin level (O2 carrying capacity)
  4. Increased oxygen consumption (VO2)
20
Q

What do you do if a fresh tracheostomy is dislodged or falls out?

A
NEVER TRY TO PUT IT BACK IN 
Call for help 
Place oxygen face mask, nasal prongs
OPA/NPA as needed 
Try to capture airway from above
21
Q

5 major causes of AECOPD

A
  1. Aspiration
  2. Infection
  3. Heart failure
  4. PE
  5. Dysrhythmias
22
Q

What do you need to consider when extubating a patient?

A
  1. Is the primary indication for intubation resolved?
  2. Does the patient have a reasonable oxygen requirement (ie. FiO2)
  3. Can the patient spontaneously ventilate (passed an SBT) with minimal ventilator support - PEEP 5, PSV 7 to overcome resistance of tube
  4. Tobin score (frequency/TV) s ideal
  5. Cough strength
  6. Presence of cuff leak
  7. Do you anticipate the patient will fail extubation or require re-intubation soon?
23
Q

How does positive pressure ventilation affect preload?

A

Decreases preload by:

  1. decreased venous return (decreases pressure gradient for venous inflow into thorax)
  2. increased pulmonary vascular resistance, impedes RV stroke output (will dilate RV, push into LV, septal shift, decrease LV output by ventricular interdependance)
  3. decreased venous return from pulmonary veins
  4. decreased ventricular distensibility by positive pressure on the outer myocardial surface - leads to reduced ventricular filling in diastole
24
Q

What is the effect of positive pressure ventilation on cardiac output?

A

Reduces ventricular filling during diastole
Enhances ventricular emptying during systole
Net effect depends on if effect on preload or afterload is predominate

Note: if intravascularly deplete, PPV will decrease CO by reducing preload

25
Q

Describe lung protective mechanical ventilation

A

Low tidal volumes (6-8 mL/kg, 4-6 mL/kg in severe cases based on ideal body weight)
Permissive hypercapnea (pH >7.25)
- use RR to help achieve appropriate minute ventilation
Plateau pressure 90%

26
Q

How do you determine static compliance of the thorax?

A

Cstat = Vt/Pplateau
Normal ventilated patient: 50-80 mL/cm H20
Decreased compliance: 10-20 mL/cm H20

27
Q

What is the definition and pathogenesis of obesity hypoventilation syndrome

A

Obesity (BMI >30) and chronic alveolar hypoventilation (PaCO2 >45) during wakefulness in absence of another explanation
A result of obesity, sleep disordered breathing and altered ventilatory control and pulmonary mechanics

28
Q

How do you calculate the expected PCO2 in a metabolic alkalosis?

A

pCO2 = 0.7(HCO3) + 20

29
Q

How do you calculate the expected PCO2 in metabolic acidosis? (Winter’s formula)

A

pCO2 = 1.5(HCO3) + 8

30
Q

What is the compensation rule for chronic respiratory acidosis?

A

change in PCO2 10 = change in HCO3 4

31
Q

DDx of stridor (10)

A
Infectious: epiglottitis, croup, bacterial tracheitis, retropharyngeal abscess, peritonsillar absces
Anaphylaxis
Foreign body
Angioedema
Post extubation edema 
Inhalational/caustic injury 
Subglottic stenosis 
Congenital airway malformations 
Vocal cord dysfunction
32
Q

What are 5 precipitating etiologies of vocal cord dysfunction

A
Asthma
Exercise
Inhalational irritants
Post extubation
Laryngopharyngeal reflux
Psychologic distress
Neurologic injury
33
Q

What are 3 management strategies in acute vocal cord dysfunction

A
  1. Reassurance, voice maneuvers (E’s, panting)
  2. CPAP
  3. Heliox
    * refer for behavioral/speech therapy (SLP)