respiratory failure Flashcards

1
Q

what all is measured in an ABG

A
  • Oxygen tension (PaO2)
  • Oxyhemoglobin saturation (SaO2)
  • Carbon dioxide tension (PaCO2)
  • Acidity (pH)
  • Bicarbonate concentration (HCO3)
  • Can also request Methemoglobin, carboxyhemoglobin and hemoglobin levels if needed
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2
Q

what should be done prior to an arterial blood gas

A

assess palmar circulation with a modified allens test

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3
Q

what is Arterial oxygen Saturation (SaO2)

A

the proportion of RBCs with hemoglobin bound to O2

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4
Q

how is SaO2 typically measured

A

pulse oximetry

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5
Q

what is normal SaO2

A

Level below 95% considered abnormal but needs to be below 89% to qualify for home O2 per Medicare guidelines

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6
Q

what is the best marker of oxygenation

A

arterial oxygen tension (PaO2)

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7
Q

what is arterial oxygen tension (PaO2) a measurement of?

A

unbound oxygen that is dissolved in plasma

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8
Q

what is considered abnormal arterial oxygen tension (PaO2)

A

considered abnormal if les than 80mmHg but must be 55 or less to qualify for home oxygen.

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9
Q

what is the best marker of adequate ventilation

A

carbon dioxide tension (PaCO2)

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10
Q

what is normal PaCO2

A

Considered abnormal if above 45mmHg or below 35mmHg

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11
Q

what is the strongest buffer in the body and how is it regulated

A

Bicarbonate, regulated by kidneys

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12
Q

How long does it take bicarbonate to buffer blood acidity

A

3-5 days to reach full effect

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13
Q

what system is used to regulate body pH

A

carbonic acid/bicarbonate buffering system

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14
Q

what chemical links the respiratory and kidney pH regulating system

A

carbonic acid

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15
Q

what is the A-a gradient

A

the ratio of alveolar oxygen level to arterial oxygen tension (PaO2) levels in the capillaries

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16
Q

what would a normal A-a gradient suggest in a patient who is hypoxic

A

Hypoventilation
Low inspired O2

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17
Q

what would a elevated A-a gradient suggest in a patient who is hypoxic

A

V/Q mismatch
Shunt
Impaired diffusion

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18
Q

what are the 3 steps to interprettnig an ABG

A
  1. is acidemia or alkalemia present?
  2. is the cause respirtory (assess PaCO2)
  3. is the cause metabolic? (assess bicarb)
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19
Q

interpret
pH = 7.32
PaCO2 = 52
HCO3 = 19

A

mixed respiratory and metabolic acidosis

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20
Q

interperet
pH = 7.34
PaCO2 = 50
HCO3 = 31

A

respiratory acidosis with incomplete metabolic compinsation

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21
Q

Interperet:
pH = 7.38
PaCO2 = 24
HCO3 = 19

A

metabolic acidosis with complete respiratory compensation

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22
Q

Interperet:
pH = 7.46
PaCO2 = 42
HCO3 = 31

A

metabolic alkalosis with no compensation

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23
Q

Interperet:
pH = 7.39
PaCO2 = 41
HCO3 = 25

A

normal blood gas

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24
Q

Interperet:
pH = 7.42
PaCO2 = 51
HCO3 = 33

A

metabolic alkalosis with complete respiratory compensation

  • remember the body does not over compensate so the cause is in the same direction as the blood pH
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25
Q

what are possible causes of respiratory acidosis

A
  • Airway obstruction
  • Lung disease
  • Chest wall disease
  • Neuromuscular disease
  • Primary brain injury (ex. CVA, trauma), sleep apnea, drugs causing sedation like opioids.
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26
Q

what are possible causes of respiratory alkalosis

A
  • Voluntary hyperventilation
  • Involuntary hyperventilation (anxiety states, asthma exacerbation, CNS disease)
  • Lung disease causing hyperventilation (remember back to PE lecture)
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27
Q

what are causes of metabolic acidosis

A
  • bicarbonate loss (diarrhea, biliary drainage)
  • increased acid load (lactic acidosis, Ketoacisosis, ingestion)
  • impaired acid excretion (renal failure, adrenal insufficiency)
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28
Q

what is the next step ater determining that your primary disorder is metabolic acidosis

A

calculate the anion gap

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29
Q

what is an anion gap

A

measures difference between cations and anions using the formula below

I dont think we have to know the formula!

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30
Q

what does an increased anion gap suggest

A

the presence of anions that cannot be measured

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31
Q

what is the mnemonic used to remember the causes of anion gap in matabolic acidosis

A

MUD PILES

M- methanol intake
U - uremia (BUN>60)
D- diabetic ketoacidosis

P-paracetamol (tylenol)
I - Isoniazid, iron
L - Lactic acidosis
E - Ethylene glycol
S - salicylates (ASA)

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32
Q

what is the cause of non-anion gap acidosis

A

loss of bicarbonate or decreasd H+ excretion such as during:
- diarrhea
- renal tubular acidosis

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33
Q

what are causes of metbaolic alkalosis

A
  • volume contration (dehydration, over diuresis)
  • loss of hydrochloride (vomiting, gastric suctioning, antacid use)
  • hypokalemia
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34
Q

what is acute lung injury

A

clinical and radiographic changes that cause respiratory failure in the critically ill patient

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35
Q

what characterizes acute lung injury

A

acute severe hypoxia that is not due to the heart

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36
Q

what is the most severe form of acute lung injury

A

ARDS

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37
Q

what is ARDS

A

Acute hypoxemic respiratory failure following a systemic or pulmonary insult without evidence of heart failure

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38
Q

what are some examples of causative events in ARDS

A
  • sepsis (MC, 1/3)
  • shock
  • aspiration pna
  • drugs/OD
  • long contusion
  • toxic inhalation
  • multiple transfusions
  • near-drowing
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39
Q

what is the pathogenesis of acute lung injury

A

pro-inflammatory cytokines cause damage and injury mainly at the capillary and alveolar cells

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40
Q

what is the pathological hallmark for acute lung injruy

A

diffuse alveolar damage

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41
Q

what is the pathology of ARDS

A

Lung injury causes excess fluid to accumulate in both the interstitium and alveoli which causes the following:
- Impaired gas exchange
- Decreased compliance
- Increased pulmonary arterial pressure
- decreased surfactant

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42
Q

what is the diagnostic cirteria for ARDS

A
  • acute onset within 1 week of clinical insult
  • BIL pulm infiltrates
  • resp failure not explained by HF or fluid overload
  • PaO2/FIO2 ratio < 300mmHg
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43
Q

How is the severity of ARDS determined

A
  • mild - PaO2/FIO2 ratio between 200-300mmHg
  • Moderate-PaO2/FIO2 ratio between 100-200mmHg
  • Severe - PaO2/FIO2 ratio less than 100mmHg
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44
Q

what are clinical findings in ARDS

A
  • rapid onset dyspnea
  • SOB
  • tachypnea
  • intercostal retractions
  • crackles on exam
  • hypoxemia unresponsive to supp O2
  • could see multiple organ failure
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45
Q

what does imaging show in ARDS

A

CXR - diffuse or patchy BIL infiltrates that rapidly progress but SPARE the costophrenic angles

  • air bronchograms are seen in 80% of patients!!
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46
Q

what differential diagnosis must you exclude when a patient has ARDS

A

cardiogenic pulmonary edema
pneumonia

47
Q

what is treatment for ARDS

A

treat underlying condition
treat secondary condition (sepsis)
supportive care

48
Q

How do you treat hypoxemia in ARDS

A
  • requires tracheal intubation and ventilation
  • supplemental O2 required
  • efforts to keep FlO2 less than 60% to avoid O2 toxicity
49
Q

what is PEEP

A

positive end expiratory pressure - used to prevent alveolar collapse

50
Q

what level of PEEP should be used

A

the lowest effective level

51
Q

what can develop when administering PEEP

A
  • Auto-PEEP can develop which can decrease venous return, reduce cardiac output and potentially cause hypotension
  • barotrauma can also occur
52
Q

how does PEEP affect outcome

A

Has been shown to improve hemodynamic outcomes but not shown to improve mortality

53
Q

what other treatment is used in ARDS

A
  • Prone positioning
  • Volume controlled ventilation with Low Tidal Volume Ventilation (LTVV) – resulted in 10% reduction in mortality over standard therapy
  • Strategies to decrease O2 consumption include appropriate use of sedatives, analgesics and antipyretics
54
Q

what are the outcomes of ARDS

A
  • Mortality ranges 30-40% and increases to 90% when associated with sepsis
  • Median survival is 2 weeks
  • Most survivors are left with chronic pulmonary symptoms
55
Q

what is respiratory failure

A

Inability of the lungs to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or CO2 elimination

56
Q

what is type 1 respiratory failure

A

Type 1 – lungs fail to provide adequate oxygenation of the blood (PaO2 <60mmHg)

57
Q

what causes T1 RF

A

Caused by diseases that interfere with O2 exchange, but ventilation is maintained
Occurs when significant intrapulmonary shunting or V/Q mismatch is present

58
Q

what are causes of hypoxemic respiratory failure

A
  • Decreased inspired O2 tension (↓PIO2)
  • V/Q mismatch (COPD)
  • Diffusion limitation (fibrosis)
  • Intrapulmonary shunt
  • disorder of heart, lungs, blood
59
Q

what are possible etiologies of T1 RF if a normal CXR ois observed

A

COPD
Intracardiac shunt (right to left)
Pulmonary embolism

60
Q

if there are focal infiltrates on the CXR, what is likely the etiology of hypoxemic respiratory failure (T1)

A

Atelectasis
Pneumonia

61
Q

if there are diffuse infiltrates on the CXR, what is likely the etiology of hypoxemic respiratory failure (T1)

A
  • Cardiogenic pulmonary edema
  • Noncardiogenic pulmonary edema (ARDS)
  • Interstitial pneumonitis or fibrosis
  • Infectious (bilateral pneumonia)
62
Q

What is the MC type of respiratory failure

A

type 1

63
Q

what is type 2 respiratory failure

A

defect in ventilation where Hypoxemia is always present but PaCO2 is elevated >50mmHg

64
Q

what are causes of hypercapnic respiratory failure

A
  • respiratory center dysfunction
  • drug overdose, CVA, tumor
  • central hypoventilation
  • neuromsucular disease (polio, spinal injury, myasthenia gravis)
  • chest wall/pleural disease
  • upper airway distrcution
  • peripheral airway disorder
65
Q

What is the cause of low arterial pH in type 2 LF

A
  • sedative drug overdose
  • acute muscle weakness (MG)
  • severe lung disease
  • acute on chronic RF
66
Q

what is Acute on chronic respiratory failure and what causes it?

A
  • Occurs in patients with chronic CO2 retention who acutely worsen and have rising CO2 and low pH
  • Caused by respiratory muscle fatigue in some cases
67
Q

what are s/s of hypoxemia

A
  • dyspnea
  • cyanosis
  • restless/anxious
  • confusion/delerium
  • tachypnea, tahcycardia, HTN
  • temor
68
Q

what are s/s of hypercapnia

A
  • dyspnea and HA
  • peripheral and conjunctival hyperemia
  • tachycardia, tachypnea, HTN
  • impaired conciousness
  • papilledema
  • asterixis
69
Q

What is the treatment for hypercapnia

A
  • specific therapy directed toward the underlying disease (ex. abx for pna)
  • respiratory supportive care to maintain adequate gas exchange
  • general supportive care
70
Q

what is the main goal in acute hypoxemic respiratory failure

A

ensuring adequate oxygenation!

keeping O2 sat>90% or PaO2 >60mmHg

71
Q

what can restoring oxygenation in chronic hypercapnia patients cause (rarely)

A

hypoventilation.

However, oxygen therapy should never be withheld for fear of causing progressive respiratory acidosis.

72
Q

what are the oxygen delivery methods

A

Nasal cannula
Nasal catheter
Simple mask
Partial rebreather mask
Non rebreather mask
Venturi mask
Oxygen tent

73
Q

for every liter increase in O2, FiO2 increases by how much?

A

4%

74
Q

what are the pros and cons of nasal cannula

A

pros:
- common and inexpensive
- does not interfere with eating or talking, well tolerated

cons:
- higher flow rates can dry out the nasal mucosa fast
- dependent on how much patients inhale through the nose

75
Q

what is considered high flow vs low flow in nasal cannula

A

Low flow: 1-6 L/min (FiO2 of 24% to 44%)
High flow: up to 10 L/min

(note: remember room air is about 20% FiO2, so you add 4% per liter)

76
Q

what is a nasal catheter and why is it not used very often?

A
  • inserted through nostril with the end of catheter resting in the oropharynx
  • not used because its uncomfortable
  • has to be changed to the other nostril every 8 hours
77
Q

what is a simple face mask and when is it used? when should it NOT be used?

A
  • Has vents on both sides to allow room air to enter and exhaled CO2 to escape
  • Used when increased O2 delivery is needed for short periods (less than 12 hours)
  • Never use less then 5 L/min as patient may rebreathe most of their own air and become hypoxemic/hypercapnic
78
Q

what is the delivery rate of a simple flow mask

A

Delivers FIO2 of 40 to 60% at flow rates of 5 L/min to 8 L/min respectively

79
Q

what is a rebreather mask?

A

O2 reservoir bag that allows the patient to rebreathe the first 1/3 of exhaled air (dead space air)

80
Q

what is the delivery rate of a partial rebreather mask?

A
  • Delivers FiO2 of 35% to 60% at a flow rate of 6 L/min to 10 L/min respectively
  • It increases FIO2 by recycling expired O2
81
Q

what is a non rebreather mask

A

Mask with two one-way valves prevent the following:
- Entrance of room air during inspiration
- Retention of exhaled gases during expiration

82
Q

what is the delivery rate for a non-rebreather mask

A

Delivers the highest FiO2 possible 95% at a flow rate of 10-12 L/min

83
Q

what is a venturi mask?

A

A mask that mixes room air with precise amount of oxygen so you can dial in the FiO2. The size of the port and oxygen flow rate determine the FiO2

84
Q

what is the delivery rate of a venturi mask

A

Delivers FiO2 varying from 24% up to 60% at flow rates of 4 L/min to 10 L/min

85
Q

what is a face tent

A

Designed for patients who cannot wear a mask or nasal cannula (examples: facial surgery or trauma)

86
Q

what are oxygen hoods?

A

used in infants! rigid plastic domes that enclose the infants heads

87
Q

what is a oxygen tent?

A

plastic canopy that supplies humidified O2

88
Q

what is noninvasive positive airway ventilation (NPPV)

A

the first line therapy in COPD patients with hypercapnic respiratory failure who can:
- Protect their own airway
- Handle their own secretions
- Tolerate the BPAP mask
Reduces intubation rates and amount of ICU stay

89
Q

what is a Bilevel Positive Airway Pressure machine? who is it most commonly used in?

A

AKA a BiPAP

Delivers preset inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP)

MC used in patients with COPD, conditions causing resp muscle weakness, and obesity hypoventilation

90
Q

what is a continuous positive airway pressure machine? who is it MC used in?

A
  • supplies a continuous level of positive airway pressure throughout respiratory cycle
  • no additional pressure above CPAP level is provided
  • MC used in patients with sleep apnea or cardiogenic pulmonary edema
91
Q

what is the caveat of a BiPAP and CPAP

A

patients must INITIATE each breath on most machines

92
Q

what are indications for intubation?

A
  • Hypoxemia despite supplemental O2
  • Upper airway obstruction
  • Unable to protect airway or clear secretions
  • Acute hypercapnia that does not quickly respond to noninvasive ventilation (CPAP or BiPAP)
  • Progressive fatigue, mental status changes, tachypnea, or use of accessory muscles
  • Apneas
93
Q

what is the preferred intubation method and why?

A

Orotracheal intubation is preferred since easier, faster and less traumatic than nasotracheal

94
Q

How do you assure intubation has been properly placed?

A
  • Auscultate the lungs to verify both lungs are being ventilated
  • Position of the tip of the endotracheal tube should be positioned at the level of the aortic arch and verified by CXR
  • Cuff pressure should not exceed 20mmHg to minimize tracheal injury
95
Q

When is mechanical ventilation used and what are its beneits?

A
  • Used for acute or chronic respiratory failure when there is insufficient oxygenation or ventilation, or both. can fully or partially replace spontaneous breathing
  • benefits are:
  • Improved gas exchange
  • Decreased work of breathing
  • More precise titration of oxygen needs
96
Q

what are the 3 types of breaths that we learned ( we will elaborate on each of these!)

A
  • Trigger breaths
  • volume assisted breaths (VA)
  • volume control breaths (VC)
97
Q

what is a trigger breath?

A
  • Ventilator-initiated breaths – preset respiratory rate triggered by a timer on ventilator
  • Patient-initiated breaths- patient effort causes flow change which initiates the breath
98
Q

what are volume assist breaths

A
  • Breaths are initiated by the patient with a set inspiratory flow rate
  • Inspiration is stopped when the set tidal volume was delivered
99
Q

what are volume control breaths

A
  • Breaths are ventilator-initiated with a set inspiratory flow rate
  • Inspiration is terminated once the set tidal volume was reached
100
Q

what are the ventilation modes? (we will go into each of these too!)

A
  • continuous mandatory ventilation (CMV)
  • Intermittent mandatory ventilation (IMV)
  • Synchronized IMV (SIMV)
  • pressure support ventilation mode (PSV)
101
Q

what is continuous mandatory ventilation mode?

A
  • Minute ventilation is determined entirely by the set respiratory rate and tidal volume
  • Patient does not initiate additional breaths and does not require any patient effort
  • Patient may be on heavy sedation, pharmacologic paralysis, or in a coma
102
Q

what is intermittent mandatory ventilation mode?

A
  • Clinician determines minimum minute ventilation by setting the respiratory rate and tidal volume
  • The patient can increase the minute ventilation by spontaneously breathing addition breaths
103
Q

what is synchronized IMV mode?

A
  • Variation of IMV
  • Ventilator breaths are synchronized with patient effort
  • Support can range from full support to no support at all
  • Better patient-ventilatory synchrony, preserves respiratory muscle function, greater control over level of support
104
Q

what is pressure support ventilation mode

A
  • Patient must trigger each breath, no set respiratory rate
  • The work of breathing is inversely proportional to the pressure support level
  • Useful when weaning a patient from mechanical ventilation (more comfortable mode that gives patient more control.)
105
Q

what is positive end-expiratory pressure? (PEEP)

A
  • added to ventialtion to prevent alveolar collapse with end expiration
106
Q

what is the pressure used in PEEP

A
  • Usually around a pressure 5cmH20
  • With ARDS (using low tidal volume ventilation) up to 20cmH20 may be used
107
Q

what are the potential complications of PEEP

A
  • Decreased cardiac output
  • Increased risk for barotrauma
  • Possibility of impairing cerebral blood flow (d/t decreased cerebral venous outflow which causes increased intracranial pressure)
108
Q

what are the potential complications of mechanical ventilation

A
  • barotrauma (excessive tidal volumes, PEEP
  • pneumothorax
  • subcutaneous emphysema
  • pneumomediastinum
  • ventilator-associated pneumonia
  • trauma (tracheal stenosis, vocal cord dysfunction)
109
Q

what is the mean survival time after a lung transplant

A

6 years:( thats so crazy.

110
Q

what are the MC diseases that lead to transplants

A
  • COPD
  • Idiopathic pulmonary fibrosis
  • Cystic fibrosis
  • Alpha-1 antitrypsin deficiency
  • Idiopathic pulmonary hypertension
  • Coal Worker’s Pneumoconiosis
111
Q

what are lung transplant recipients chosen based off os

A

the Lung Allocation Score (LAS)

112
Q

what are the general guidelines for lung transplant candidates

A
  • Appropriate age (usually under age 65)
  • Severe lung disease that is progressive
  • Limited life expectancy because of their lung disease
  • Good nutritional status and BMI less than 30
  • Good support system and mentally intact
113
Q

what are contraindications for lung transplant candidacy

A
  • Active smoking (within the past 6 months)
  • Active malignancy in last 2 years
  • Drug or ETOH dependency
  • Significant disease of other organs including CAD and heart failure
  • Untreatable pulmonary or extrapulmonary infection
  • BMI >35
  • Hep B, C or HIV infection (they have become relative contraindications recently)
114
Q

flip for fun

A

WHOO HOOOOO DONE WITH ONE MOREEE. plz enjoy a pic of Rhys’s first UCHOCO!