Lecture 7: Respiratory Failure Flashcards

1
Q

What does an ABG measure?

A
  • PaO2 (Oxygen tension)
  • SaO2 (Oxyhemoglobin saturation)
  • PaCO2 (CO2 tension)
  • pH
  • HCO3 (Bicarb concentration)

Additional tests cinlude methemoglobin, carboxyhemoglobin, and hemoglobin levels.

The little a means arterial, whereas a big A means alveolar.

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2
Q

What wrist test is used to test for ABG viability?

A

Modified allen test, which checks for collateral circulation of the radial and ulnar arteries.

Only checking patency of ulnar side, normal is both sides.

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3
Q

What are CIs to ABG?

A
  • Severe PAD in wrist
  • Active Raynaud’s
  • Failure of modified allen test
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4
Q

What is SaO2?

A

Proportion of RBCs with hemoglobin bound to O2.

Pulse ox measurement

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5
Q

What is the preferred measurement to look at for ventilation?

A
  • Ventilation is best marked by PaCO2.
  • Oxygenation is best marked by PaO2.
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6
Q

What are the 3 causes of an increased A-a gradient?

A
  • V/Q mismatch
  • Shunt
  • Impaired diffusion

Helps to determine the cause of hypoxemia

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7
Q

What could result in hypoxemia even if the A-a gradient is normal?

A
  • Hypoventilation
  • Low inspired O2
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8
Q

What measurement in an ABG suggests respiratory acidosis? Alkalosis?

A
  • Acidosis: PaCO2 > 45
  • Alkalosis: PaCO2 < 35
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9
Q

Determine the acid-base disorder currently present.

pH = 7.32
PaCO2 = 52
HCO3 = 19

A

Mixed acidosis

No compensation present

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10
Q

Determine the acid-base disorder currently present.

pH = 7.34
PaCO2 = 50
HCO3 = 31

A

Respiratory acidosis with incomplete compensation.

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11
Q

Determine the acid-base disorder currently present.

pH = 7.38
PaCO2 = 24
HCO3 = 19

A

Metabolic acidosis with complete compensation.

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12
Q

Determine the acid-base disorder currently present.

pH = 7.46
PaCO2 = 42
HCO3 = 31

A

Metabolic alkalosis with incomplete compensation.

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13
Q

Determine the acid-base disorder currently present.

pH = 7.39
PaCO2 = 41
HCO3 = 25

A

Normal

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14
Q

Determine the acid-base disorder currently present.

pH = 7.42
PaCO2 = 51
HCO3 = 33

A

Metabolic alkalosis with complete compensation.

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15
Q

What are the primary causes of respiratory acidosis?

A
  • Airway obstruction
  • Lung disease
  • Chest wall disease
  • Neuromuscular disease
  • Primary brain injury

Things causing you to not breathe out enough.

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16
Q

What are the primary causes of respiratory alkalosis?

A
  • Voluntary hyperventilation
  • Involuntary hyperventilation (anxiety, asthma exacerbation, CNS disease)
  • Lung disease resulting in hyperventilation (PE)

Things causing you to breathe out too much CO2.

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17
Q

What are the 3 primary etiologies for metabolic acidosis?

A
  1. Bicarb loss
  2. Increased acid load
  3. Impaired acid excretion
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18
Q

What does elevated anion gap imply?

A

There are anions that we cannot measure.

= Na + K - (HCO3 + Cl)

Examples: lactic acidosis, ketoacidosis, acute renal failure, and toxic acids.

Normal gap is typically < 12.

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19
Q

What is MUDPILES?

A
  1. Methanol
  2. Uremia (BUN > 60)
  3. DKA
  4. Paracetamol (Acetaminophen)
  5. Isoniazid, Iron
  6. Lactic acidosis
  7. Ethylene glycol
  8. Salicylates (ASA)

Causes of anion gap metabolic acidosis

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20
Q

If there is no anion gap present, what are the most likely etiologies?

A
  • Diarrhea
  • Renal tubular acidosis

Loss of bicarb or decreased H+ excretion

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21
Q

What are the 3 primary etiologies for metabolic alkalosis?

A
  • Volume contraction (losing fluid that mostly has Na in it)
  • Loss of HCl
  • Hypokalemia
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22
Q

What characterizes acute lung injury? (ALI)

A

Acute, severe hypoxia with a non cardiogenic cause.

ARDS is the most severe form of an ALI.

Usually due to non-cardiogenic pulmonary edema. (AKA not pulmonary edema 2/2 HF)

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23
Q

What is the most common cause of ARDS?

A

Sepsis

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24
Q

What is the pathologic hallmark of ARDS?

A

Diffuse, alveolar damage due to pro-inflammatory cytokines.

Pathognonomic

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25
Q

Describe the pathophysiological effects of ARDS on lung interstitium and alveoli.

A
  1. Excess fluid accumulates in both interstitium and alveoli.
  2. Impaired gas exchange
  3. Decreased compliance
  4. Increased pulmonary arterial pressure
  5. Reduction in production of surfactant.

Surfactant reduces surface tension.

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26
Q

What is the diagnostic criteria for ARDS?

A
  1. Acute onset within 1 week of clinical insult
  2. Bilateral pulmonary infiltrates (r/o PNA)
  3. Respiratory failure not fully explained by HF or volume overload.
  4. PaO2/FiO2 ratio < 300 mm Hg

Normal FiO2 is around 21%.

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27
Q

What determines ARDS severity?

A
  1. Mild = PaO2/FiO2 ratio is 200-300 mm Hg
  2. Mod = PaO2/FiO2 ratio is 100-200 mm Hg
  3. Severe = PaO2/FiO2 ratio < 100 mm Hg
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28
Q

What are the clinical findings often associated with ARDS?

A
  • SOB, tachypnea, intercostal retractions and crackles.
  • Marked hypoxemia
  • Multiple organ failure
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29
Q

What do CXRs tend to show for ARDS?

A
  • Diffuse or patchy bilateral infiltrates that spare the costophrenic angles.
  • Heart size should be normal w/ no effusions.
  • Air bronchograms in 80% of patients. (Not diagnostic)
30
Q

What is the treatment for ARDS?

A
  • Treating the underlying condition that led to ARDS.
  • Treat any secondary condition (such as sepsis)
  • Supportive care
31
Q

What is the treatment for hypoxemia 2/2 ARDS?

A
  • Ventilator
  • Supplemental O2 to maintain PaO2 > 55 mm Hg.
  • Keep FiO2 < 60% to prevent O2 toxicity.
32
Q

What is PEEP and what is it used for?

A
  • Positive end-expiratory pressure
  • Prevents alveolar collapse

Ideally, lowest PEEP possible that is effective.

33
Q

What can auto-PEEP lead to?

A
  • Decreased venous return
  • Reduced cardiac output
  • Hypotension

If we keep building pressure within our chest, then we have a smaller pressure gradient between our chest and our heart, so less venous return.

Improves hemodynamic outcomes but not mortality.

34
Q

What is prone positioning and what is the purpose?

A

Laying flat will shift the lungs, recruiting different alveoli and making the heart press less against the left lung.

35
Q

What is the only treatment that has been shown to reduce mortality in ARDS?

A

Volume controlled ventilation with low tidal volume ventilation (LTVV)

Prevents alveoli from overexpanding

Can result in permissive hypercapnia

36
Q

What is respiratory failure in a nutshell?

A

Inability of the lungs to meet the metabolic demands of the body.

37
Q

What is Type 1 respiratory failure?

A

Lungs fail to provide adequate oxygenation of the blood (PaO2 < 60 mm Hg)

Hypoxemic respiratory failure, also the MC.

Oxygenation is impaired, but ventilation is normal.

38
Q

What are the causes of hypoxemic respiratory failure?

A
  • Decreased inspired O2 tension (PIO2)
  • V/Q mismatch (COPD)
  • Diffusion limitation (Fibrosis)
  • Intrapulmonary shunts (PNA, atelectasis, CHF, ARDS)
  • Heart/Lung/Blood disorders

PIO2 is partial pressure of inspired oxygen, which decreases in high altitudes. (thinner air)

39
Q

What do focal infiltrates on a CXR + hypoxemic respiratory failure suggest for etiologies?

A
  • Atelectasis
  • Pneumonia
40
Q

What do diffuse infiltrates on CXR + hypoxemic respiratory failure suggest for etiologies?

A
  • Cardiogenic pulmonary edema
  • Non-cardiogenic pulmonary edema
  • Interstitial PNA or fibrosis
  • Infectious (bilateral PNA)
41
Q

What is type 2 respiratory failure?

A
  • Defect in ventilation, AKA inability to eliminate CO2 properly.
  • PaCO2 > 50 mm Hg
  • Hypercapnic respiratory failure

Also hypoxemic, but PaCO2 is far more elevated.

pH is variable due to bicarb buffering.

42
Q

What are the primary causes of hypercapnic respiratory failure?

A
  • Respiratory center dysfunction (medulla)
  • Drug OD, CVA, tumor
  • Central hypoventilation
  • Neuromuscular diseases (polio, myasthenia gravis, spinal injuries, GBS)
  • Chest wall/pleural diseases
  • Upper airway obstruction
  • Peripheral airway disorder

GBS = guillain barre syndrome

43
Q

What is acute on chronic respiratory failure?

A

A patient with chronic CO2 retention acutely worsens, resulting in rising CO2 and low pH.

Acute hypercapnic respiratory failure

Arterial pH is often low.

44
Q

What are the slight differences between hypoxemia vs hypercapnia?

A
  • HA in hypercapnia
  • Hyperemia in hypercapnia
  • Papilledema & asterixis in hypercapnia

Both share dyspnea, tachycardia, tachypnea, and HTN.

Asterixis is a flapping tremor of the hand.

45
Q

What is the primary goal in treating acute hypoxemic respiratory failure?

A

Adequate oxygenation > 90% SaO2 or PaO2 >= 60 mm Hg.

Do not withhold oxygen for fear of progressive respiratory acidosis.

46
Q

For every liter increase in O2, how much does FiO2 tend to increase?

A

Approximately 4%

2L of O2 starts at around 28% FiO2.

Normal air is 21% FiO2.

47
Q

For a simple face mask, what is the preferred flow rates and why?

A
  • 5-8 L/min
  • Going under 5L/min can cause the patient to rebreathe too much of their own air.

Has vents on the side, unlike a NRB.

Should only be used short term.
Often used in type 1, hypoxemic respiratory failure.

48
Q

What is the main benefit of a partial rebreather mask over a simple mask?

A
  • Increases FiO2 by recycling expired O2.
  • O2 reservoir bag used to recycle dead space air.
49
Q

How high does FiO2 go up to for a NRB?

A

95%

50
Q

What are the one-way valves in a NRB used for?

A
  • Entrance of room air during inspiration
  • Retention of exhaled gases during expiration.
51
Q

What is the primary benefit of a Venturi mask?

A

It can mix RA and oxygen to dial in FiO2 more precisely.

52
Q

What oxygen delivery method would be good for a patient that cannot wear a mask or nasal cannula?

A

Face tent

53
Q

What is the oxygen delivery method for babies?

A

Oxygen hood.

54
Q

What is the first line therapy for COPD patients with hypercapnic respiratory failure and can tolerate a BPAP?

A

Noninvasive positive pressure ventilation. (NPPV)

Pressure ventilation.

Patient must be able to protect their own airway, handle their own secretions, and tolerate a BPAP mask.

55
Q

What is BPAP?

A

Bilevel positive airway pressure, which delivers preset inspiration and expiration positive airway pressure. (IPAP and EPAP)

Essentially, it augments their breathing, but they still breathe on their own.

BPAP = booster

56
Q

What is CPAP?

A
  • Continuous positive airway pressure, mainly for sleep apnea.
  • No additional pressure above CPAP level.

Patient must be able to initiate breathing on their own.

57
Q

When is intubation indicated?

A
  • Hypoxemia despite supplemental O2
  • Upper airway obstruction
  • Unable to protect airway or clear secretions
  • Acute hypercapnia that does not respond quickly to NPPV
  • Progressive fatigue, AMS, weakness
  • Apnea
58
Q

What is the preferred method of intubation?

A

Orotracheal

59
Q

Describe what should be done when first initiating orotracheal intubation.

A
  • Auscultate both lungs to verify ventilation.
  • Verify that ET tube is at the level of the aortic arch.
  • Cuff pressure should be under 20 mm Hg
60
Q

What are the two types of breaths in mechanical ventilation?

A
  • Ventilator-initiated based on a timer.
  • Patient-initiated, in which ventilator detects flow change and assists breath.
61
Q

What is a volume assist breath?

A

Patient initiates, and ventilator provides assistance until set TV is met.

62
Q

What is a volume control breath?

A

Ventilator initiated and terminated once set TV is reached.

63
Q

What is continuous mandatory ventilation mode?

A

Minute ventilation is determined entirely by set RR and TV.

No additional patient effort required.

Most controlled form of mechanical ventilation.

64
Q

What is intermittent mandatory ventilation mode?

A
  • Minimum ventilation set by TV and RR.
  • Patient can increase the minute ventilation by spontaneously breathing as well.

Ensures patient breathes at a minimum.

65
Q

What is synchronized IMV mode?

A

Ventilator will sync with patient effort, preserving better respiratory muscle.

66
Q

What is pressure support ventilation mode?

A
  • Patient triggers each breath.
  • Ventilator simply adjusts the pressure of each breath.

Often used to wean a patient off mechanical ventilation.

Patient needs to provide enough effort to ensure adequate minute ventilation.

67
Q

What is the common PEEP setting and its purpose?

A
  • Commonly set at 5 cm H2O.
  • Prevent alveolar collapse during end expiration.
68
Q

What are the complications of mechanical ventilation?

A
  • Barotrauma (too much TV or PEEP)
  • VAP
  • Trauma (tracheal stenosis, vocal cord dysfunction)

VAP increases by 1% for everyday on a vent ):

Barotrauma includes pneumothorax, subQ emphysema, and pneumomediastinum.

69
Q

What is used to determine lung transplant eligibility?

A

Lung allocation score

Re-evaluated every 3 months.

70
Q

What infections relatively disqualify someone from lung transplant eligibility?

A

Hep B, C, or HIV

Relative contraindications now.