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CCP Semester 2: The Path Of Shame > CCP 215 Respiratory Emergencies > Flashcards

CCP 215 Respiratory Emergencies Flashcards

1
Q

Berlin criteria for ARDS

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

1) PF ratio < 300
2) Bilateral opacities on CXR not fully explained by effusions, lung collapse, or nodules.
3) Respiratory failure not fully explained by cardiac failure.
4) Pulmonary insult within 1 week.

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2
Q

pathogenesis of VAP

A

1) Microaspiration of upper respiratory tract and GI aspirations (80%)
2) Biofilm colonization. This is why we don’t routinely flush the ETT when suctioning

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3
Q

VAP prevention bundle

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A 
H - HOB up
O - Oral care 
S - Sub/supra glottic suctioning (hourly) 
E - Earliest possible Extubation 
S - Safe ICU nutrition
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4
Q

CCP staged approach to refractory hypoxemia

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Increase FiO2 to 1.0 (increased diffusion gradient)
  2. Optimize PEEP (increased mean airway pressure)
  3. Increase RR (increased mean airway pressure)
  4. Increase tidal volume
  5. paralyze
  6. Switch to pressure control mode
  7. Increase Ti time (draw out your inspiratory time)
  8. Recruitment manoever
  9. Prone patient
  10. ECMO
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5
Q

What are the 5 causes of hypoxemia?

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

1) Hypoventilation
2) V/Q mismatch
3) shunt (anatomic or physiologic)
4) Diffusiona abnormalities
5) Decreased FiO2

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6
Q

trans-pulmonary plateau pressure equation

A

Pplat - Pleural Pressure (Pes at end inspiration)

Ideal Ptp plat = < 25

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7
Q

trans-pulmonary peep pressure equation

A

Peep - Pleural Pressure (Pes at end expiration)

Ideal Ptp peep = 0

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8
Q

What is driving pressure, when is it used and what value would you want it be below?

A

Driving pressure = Pplat - applied PEEP

Optimal driving pressure in ARDS <15 cmH2O

If you increase your PEEP and driving pressure decreases, then additional alveoli have been recruited

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9
Q

gold standard radiological test for determining the presence of pulmonary embolism

A

CT-PA (CT pulmonary angiogram)

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10
Q

state the rule for expected compensation (PCO2:HCO3-) in a patient who is chronically hypercapneic (chronic respiratory acidosis secondary to COPD, for example)

A
  1. With chronic respiratory acidosis, the kidneys respond by retaining HCO3 (renal compensation)
  2. Use the β€œ10-4” rule (PCO2:HCO3-) to determine appropriate compensation
  3. For every 10mmHg rise in PCO2 above the baseline (chronic CO2 retention), there should be an expected compensatory rise in HCO3- by 4 mmol/L
  4. For example: A chronic PCO2 of 60mmHg should have an expected bicarbonate of 32 mmol/L
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11
Q

typical findings on CXR associated with PE

A
  1. CXR is neither sensitive nor specific for PE
  2. used to assess for differential diagnostic possibilities such as pneumonia and pneumothorax
  3. In late PE CXR may show small areas of infarcted lung
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12
Q

classic case ECG findings associated with PE

A
  1. sinus tachycardia
  2. incomplete or complete right bundle branch block (right heart strain pattern)
  3. prominent R wave in lead V1 (right heart strain pattern)
  4. right axis deviation (right heart strain pattern)
  5. T-wave inversion in the right precordial leads +/- the inferior leads (right heart strain pattern)
  6. SIQIIITIII pattern (right heart strain pattern)
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13
Q

explain the relationship between the D-Dimer test and pulmonary embolism

A
  1. negative D-dimer has almost 100% negative predictive value (virtually excludes PE) = no further testing is required
  2. positive D-dimer is seen with PE but has many other causes and is, therefore, non-specific: it indicates the need for further testing if PE is suspected

NEGATIVE DIMER = NO PE
POSITIVE DIMER = MAYBE A PE

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14
Q

the three subcategories of pulmonary embolism

A
  1. Massive PE
  2. Sub-massive PE
  3. Low Risk PE
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15
Q

Alternative radiologic testing modality to CT-PA for diagnosis of PE

A
  1. V/Q (ventilation/perfusion) scan
  2. Described as a scintigraphic examination of the lung that evaluates pulmonary vasculature perfusion and segmental bronchoalveolar tree ventilation
  3. Performed by sensing the gradient of diffusion of a test gas across the alveolar membrane
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16
Q

Virchow’s triad

A
  1. Hypercoagulability
  2. Vascular stasis
  3. Endothelial injury/dysfunction
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17
Q

Types of DVT which are β€œhigh risk” for PE

A
  1. Popliteal vein and up

2. Any DVT at the level of the knee and upwards

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18
Q

Pertinent lab findings in PE

A
  1. D-dimer (non-specific marker of clot degradation)
  2. Troponin (dilation of the RV and stretching of the myocardium)
  3. stress-induced leukocytosis
  4. Elevated serum lactate (global perfusion/badness)
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19
Q

define β€œmassive PE” aka β€œhigh-risk PE”

A
  1. Hemodynamically unstable PE β†’ hypotension
  2. SBP <90 mmHg or a drop in SBP of β‰₯40 mmHg from baseline for a period >15 minutes
  3. hypotension that requires vasopressors or inotropic support
  4. not explained by other causes such as sepsis, arrhythmia, LV dysfunction from AMI, or hypovolemia
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20
Q

define β€œsub-massive PE” aka β€œintermediate-risk PE”

A
  1. PE that does not meet the definition of hemodynamically unstable PE
  2. Acute PE without systemic hypotension (SBP >90 mmHg) but with either RV dysfunction or myocardial necrosis
  3. RV dysfunction is characterized by RV dilation, elevated BNP, ECG changes indicative of ischemia or β€œstrain pattern”, elevated cardiac troponin
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21
Q

Primary physiological complications of ARDS

A
  1. Impaired diffusion/gas exchange (shunt/VQ mismatch)
  2. Decreased pulmonary compliance
  3. Pulmonary hypertension
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22
Q

different treatment options for massive PE

A
  1. Systemic thrombolysis for acute PE in any centre
  2. Catheter directed thrombolysis (CDT) for patients who have had a cardiac arrest
  3. Mechanical thrombectomy for pregnant patients or those in large centres
  4. Systemic anticoagulation to support the clot breakdown and prevent further growth over a period of days
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23
Q

Correlation between PaO2 and hypoxic pulmonary vasoconstriction

A
  1. At PaO2 of 83 mmHg (oxygen saturation of around 95%) we start to see hypoxic pulmonary vasoconstriction
  2. At an SaO2 of 92% (PaO2 64 mmHg) pulmonary vasoconstriction would be about 20-30% of maximum
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24
Q

West lung zone 1

A

UPPER LUNG

  1. alveolar pressure is higher than arterial or venous pressure
  2. PA > Pa > Pv
  3. Alveolar pressure exceeds pulmonary arterial and venous capillary pressure
  4. Little gas exchange takes place
  5. Blood flow is limited and probably cyclical (i.e. only systolic, and dependent on the phase of the respiratory cycle)
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25
Q

West lung zone 2

A

MIDDLE

  1. arterial pressure is higher than alveolar and venous, a relationship which changes during the respiratory cycle
  2. Pa > PA > Pv
  3. Pulmonary arterial pressure exceeds alveolar pressure
  4. Alveolar pressure exceeds pulmonary venous pressure
  5. Blood flow is therefore dependent on the gradient between alveolar and pulmonary arterial pressure
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26
Q

West lung zone 3

A

BOTTOM

  1. both arterial and venous pressure are higher than alveolar
  2. Pa > Pv > PA
  3. Both pulmonary arterial and pulmonary venous pressure exceeds alveolar pressure
  4. Flow is proportional to the gradient between pulmonary arterial and pulmonary venous pressure
  5. Blood flow to this zone exceeds the blood flow to all the other zones
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27
Q

West lung zone 4

A
  1. the interstitial pressure is higher than alveolar or pulmonary venous pressure
  2. Pa > Pi > Pv > PA
  3. the space where flow is reduced because the calibre of the extra-alveolar vessels is narrowed by the increased interstitial pressure
  4. the bulk of atelectatic or oedematous lung at the base of the chest cavity, where interstitial fluid pressure exceeds pulmonary venous pressure
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28
Q

How does PPV relate to the concept of West’ lung zones

A
  1. increased positive alveolar pressure can push blood out of the lung, creating more Zone 1 (deadspace) ventilation through increasing PVR
  2. Microscopically, alveolar capillaries appeared compressed and flattened by PEEP (increased PVR)
  3. positive pressure ventilation of a volume-depleted patient can be expected to do this
  4. A fluid bolus will increase intravascular volume, turn Zone 1 lung units into Zone 2 lung units

this is your classic β€œzone of over-distention” duck billed waveform you get on PV loop

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29
Q

preferred glucocorticoids in asthma/COPD exascerbation

A
  1. Methylprednisone

2. Prednisone

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30
Q

core features of COPD exacerbation

A
  1. Hypercapnia
  2. Hypoxemia
  3. Increase in dyspnea
  4. Increase in sputum volume and/or viscosity
  5. Increase in sputum purulence
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31
Q

core principles of mechanical ventilation in asthmatics

A
  1. Low PEEP or zEEP so as to avoid dynamic hyperinflation and worsening autoPEEP
  2. keep the respiratory rate low (to allow increased time for exhalation). don’t worry about matching their intrinsic rate pre-intubation
  3. High flow (in order to allow for a prolonged expiratory phase)

some other thoughts off the top of my head. you shouldn’t need a high FiO2 in these patients. Oxygenation generally isn’t the problem. That being said, after you tube them it’s probably best to get them started on an FiO2 of 1.0 and titrate down as needed

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32
Q

what is the pathogenesis behind chronic opportunistic pulmonary bacterial infections in asthma and COPD

A
  1. increased prevalence of sputum production
  2. impaired ability to adequately clear sputum/secretions
  3. Sputum provides an ideal medium for bacterial growth, β†’ pulmonary infection
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33
Q

what is the benefit of inhaled corticosteroids versus systemic in asthmatics and COPD

A

inhaled corticosteroids exert a local effect rather than systemic, thus avoiding some of the deleterious side effects of chronic usage of systemic steroids

an example of this would be long term PO prednisone use in COPD’ers. they get all sorts of deleterious side effects affecting bones (osteoporosis), skin (thinning of hair), eyes (cataracts), immune system (opportunistic infections) and digestive system.

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34
Q

describe the β€œ90/60” rule correlating SpO2 to PaO2

A

An SpO2 of 90% is approximately correlated to a PaO2 of 60 mmHg

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35
Q

describe which lobe of the lung is most often affected by aspiration

A

The right lower lung lobe is the most common site of infiltrate formation due to the larger caliber and more vertical orientation of the right mainstem bronchus

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36
Q

describe which lobe of the lung is most often affected by pneumonia

A

The right middle lung lobe is the most common site of pneumonia formation due to the proximity to the trachea (micro aspiration)

when we use the term β€œaspiration” we are usually talking about MACRO aspiration, ie, inhaling a bunch of your own vomit.

most pneumonia’s form from MICRO aspiration. ie an old person or a person with shitty oral hygiene has micro aspiration events as they sleep causing translocation of bacteria and a right mid lobe pneumonia

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37
Q

two factors that increase the risk of pneumonia from aspiration

A
  1. Poor oral hygiene. poor oral hygiene leads to increased pathogenicity of oral micro aspirations
  2. PPI therapy. PPI therapy alkalinizes the gastric acid, creating an ideal environment for bacteria that thrive in alkalotic environments
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38
Q

define pulmonary-renal syndrome

A
  1. describes the occurrence of renal failure in association with respiratory failure
  2. characterised by autoimmune-mediated rapidly progressive glomerulonephritis (RPGN) and diffuse alveolar haemorrhage (DAH)

whatever the fuck that means

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39
Q

treatment considerations for massive hemoptysis/ pulmonary hemorrhage

A
  1. Early intubation
  2. Consider unilateral lung isolation with selective intubation of the β€œgood lung” and lung β€œisolation” of the bad lung
  3. Dependent positioning. Trendelenburg with β€œbad side” down (theoretical belief to minimize reflux of blood into normal lung)
  4. High PEEP to improve V/Q matching
  5. If major pulmonary haemorrhage target SBP <140 mmHg
  6. Consider IV TXA. If patient is not intubated and can tolerate it, consider nebulizer TXA
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40
Q

management considerations for pulmonary contusion

A
  1. Conservative fluid resuscitation to prevent further capillary leakage
  2. Consider diuresis to reduce hydrostatic pressure
  3. ABX not usually req’d for pneumonitis assoc. with pulmonary contusion
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41
Q

management considerations for flail chest

A
  1. PPV or CPAP to stabilize/fixate the segment

2. Analgesia to promote appropriate breathing mechanics

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42
Q

criteria for β€œmassive hemothorax”

A
  1. Immediate return of blood of β‰₯ 1500mL when the chest tube is inserted
  2. bleeding β‰₯ 200mL/hr for 2-4 hours
  3. Rapid accumulation of β‰₯ 1500mL blood in chest or β‰₯ 1/3 of patient’s total blood volume in chest
  4. Indicates need for urgent thoracotomy
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43
Q

what direction should the chest tube point in a pneumothorax

A

apical

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44
Q

criteria for β€œmassive hemoptysis”

A
  1. β‰₯50cc blood in single cough or
  2. β‰₯600ml in 24 hours or
  3. Needs transfusion
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45
Q

key items to document and report to TA with respect to a chest tube

A
  1. Location/size (gauge, intercostal space, angle, number of tubes)
  2. How is it secured
  3. What is draining and what are its characteristics (pleural-e-vac, hooked up to suction, rate, colour, consistency, volume, etc)
  4. How is it draining/is it draining
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46
Q

what does a continuous bubbling in the pleura-vac indicate

A
  1. Continuous communication with leaking air
  2. potential broncho-pleural fistula or
  3. potential air leak in the system
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47
Q

iatrogenic ways to worsen a broncho-pleural fistula

A
  1. aggressive PPV

2. over suctioning/aggressive suction on the pleur-evac

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48
Q

when would a clinician choose a β€œpig-tail” catheter over a traditional chest tube for drainage of the chest

A
  1. A pig-tail may be used when draining small amounts of air or thin fluid, such as small pleural effusions
  2. For major trauma or frank blood a traditional chest tube is preferred
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49
Q

define pleural empyema

A
  1. a collection of pus in the pleural cavity caused by microorganisms, usually gram-positive bacteria
  2. Usually occurs within the context of a pneumonia
  3. May also occur following injury, or chest surgery
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50
Q

differentiate between an uncomplicated (simple) and complicated parapneumonic (pleural) effusion

A
  1. Complicated pleural effusions: bacterial invasion into the pleural space, with evidence of evidence of micro-organism invasion by culture or Gram stain
  2. uncomplicated effusion (simple) does not contain evidence of micro-organisms
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51
Q

describe β€œLight’s Criteria” for evaluating pleural effusions

A
  1. clinical decision making rule which can be used to determine the type of a patient’s pleural effusion and thus its etiology
  2. provides a systematic, validated approach to evaluating pleural fluid studies
  3. differentiates transudates and exudates using serum/pleural protein and LDH measurements
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52
Q

what is the purpose for β€œdraining” a pleural effusion

A
  1. Obtains a diagnosis by culture
  2. Relieve pressure in the hemi-thorax
  3. Reduces bacterial load and medium
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53
Q

define β€œtransudative” fluid

A
  1. fluid which occurs due to increased hydrostatic pressure or low plasma oncotic pressure

β€œshifting” of fluid

54
Q

define β€œexudative” fluid

A
  1. fluid which occurs due to inflammation and increased capillary permeability
  2. β€œleakage” of fluid
55
Q

differentiate between transudative vs exudative pleural effusion

A
  1. transudative effusion would arrive from circumstances owning to increased hydrostatic pressure or low plasma oncotic pressure. Examples include: CHF, Cirrhosis, nephrotic syndrome, hypoalbuminemia
  2. transudative effusion would arrive from circumstances owning to inflammation and increased capillary permeability. examples include: pneumonia, cancer, TB, certain autoimmune conditions

can be differentiated with Light’s Criteria

56
Q

What are the primary causes of massive pulmonary hemmorhage (actual legit pulmonary hemorrhage, not undifferentiated hemoptysis)

A
  1. Bronchiectasis
  2. Tumours/CA
  3. AVM’s
57
Q

primary causes of hypotension in an asthmatic

A
  1. AutoPEEP
  2. Tension pneumothorax

beware of the potential for iatrogenic PTX in these guys from overzealous bagging/mechanical ventilation

58
Q

describe negative pressure pulmonary edema

A
  1. Diaphragm descends, creates negative pleural pressure during spontaneous inspiration
  2. This β€œpulls” on the alveoli (trying to create a positive Palv) but is unable to expand them with air due to fixed obstruction (laryngospasm, choking, etc)
  3. The subsequent negative alveolar pressure (negative Palv) draws fluid from the adjacent pulmonary capillaries into the alveoli
59
Q

concerning signs in the crashing, un-intubated asthmatic patient

A
  1. Normal/Rising PaCO2 in the setting of tachypnea (worsening respiratory acidosis indicates patient is no longer compensating)
  2. Hypoxemia (asthma is NOT an oxygenation problem. if asthmatics start de-sat’ing, you know they are going down the shitter)
  3. Silent chest
  4. Visibly fatiguing/becoming somnolent
60
Q

describe obstructive atelectasis

A
  1. Obstructive atelectasis is the most common type of atelectasis
  2. a form of lung collapse that is due to obstruction of the airways supplying a lung segment or lobe
  3. results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed
  4. can be seen in dense, consolidated pneumonia

big shitty mucous plug clogs up a chunk of lung, air can’t get in or out, the distal lung collapses and becomes shitty and atelectatic

61
Q

what is the most common pathogen responsible for CAP

A
  1. Streptococcus pneumoniae (gram-positive cocci, Responds to Ceftriaxone)
62
Q

Mechanism behind hypoxemia in PE

A
  1. Ischemic alveolar cells stop producing surfactant
  2. Atelectasis ensues
  3. no gas exchange occurs from the resulting shunt effect
63
Q

common gram positive cocci strains of pneumonia

A
  1. Streptococcus pneumoniae

2. Staphylococcus aureus

64
Q

common β€œatypical” strains on pneumonia

A
  1. Chlamydophila pneumoniae
  2. Legionella pneumophila
  3. Mycoplasma pneumoniae
65
Q

the six anatomic regions leading to type 2 respiratory failure

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Medulla
  2. Diaphragm
  3. Pleural space
  4. Chest wall
  5. Airway
  6. Lungs
66
Q

causes of type 2 respiratory failure originating in the medulla (CNS control of breathing)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. drugs
  2. stroke
  3. hemorrhage
  4. ischemia
  5. metabolic
  6. structural lesions
67
Q

causes of type 2 respiratory failure originating in the diaphragm (muscle problem)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. SCI
  2. inflammation to C3-5 (osteomyelitis, for example)
  3. phrenic nerve malfunction
  4. GBS (phrenic nerve)
  5. myasthenia gravis (motor end plate)
  6. hypophosphatemia
  7. diaphragmatic myositis (muscle fibres)
68
Q

causes of type 2 respiratory failure originating in the pleural space

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. effusions

2. tension PTX

69
Q

causes of type 2 respiratory failure originating in the chest wall

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. obesity
  2. pregnancy
  3. kyphosis/scoliosis
  4. burns (eschar)
70
Q

causes of type 2 respiratory failure originating in the airway (tracheal problem)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. airway obstruction (mass, foreign body)
  2. congenital esophageal atresia (EA)
  3. tracheoesophageal fistula (TEF)
71
Q

causes of type 2 respiratory failure originating in the lungs (small airways problem)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. COPD

2. asthma

72
Q

Causes of hypercapneic respiratory failure

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. CNS control of breath
  2. tracheal problems
  3. Chest wall problems
  4. Muscle problems
  5. Pleural space problems
  6. Small airway problem
73
Q

Benefits of prone positioning

πŸ”₯πŸ”₯πŸ”₯MEGA PEARLπŸ”₯πŸ”₯πŸ”₯

A
  1. Optimizes VQ matching (more blood to dependent lung segments)
  2. Reduces atelectasis
  3. Facilitates drainage of secretions
  4. Less lung deformation
  5. Increased FRC
  6. Decreased transpulmonary pressures
  7. Increased uniform ventilation
74
Q

4 types of VILI

A
  1. volutrauma
  2. barotrauma
  3. biotrauma
  4. atelectotrauma
75
Q

benefits of NIPPV

A
  1. increased oxygenation
  2. increased end organ perfusion of oxygen
  3. increased ventilation
  4. decreased work of breathing
  5. potentially avoids intubation
76
Q

Contraindications to NIPPV

A
  1. Cardiac arrest
  2. Respiratory arrest
  3. Unable to protect airway
  4. Upper airway obstruction with foreign bodies
  5. Untreated or loculated pneumothorax found on imaging
  6. SHOCK
  7. Post GI surgery (caution)
  8. Maxillofacial injury
  9. Intractable vomiting
77
Q

CCP approach to mech vent (what you should ask yourself ANY time you approach a mechanically ventilated patient)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅
πŸ”₯πŸ”₯πŸ”₯MEGA PEARLπŸ”₯πŸ”₯πŸ”₯

A
  1. Am I adequately oxygenating (PaO2)
  2. Am I ventilating appropriately (PaCO2)
  3. Am I on safe ground (oxygenation + ventilation + hemodynamics)
  4. Current acid/base status
78
Q

causes of cardio-pulmonary shunt

A
  1. alveoli getting filled with shit (think pneumonia/ARDS)
  2. atelectasis (lotta shit can cause atelectasis)
  3. intrapulmonary vascular shunt (PE or vascular compression from overdistention from PEEP)
  4. intracardiac shunt (VSD/PFO)
79
Q

harmful effects of patient-ventilator dyssynchrony

A

1) increased O2 consumption
2) potential for Muscle/diaphragmatic injury
3) V/Q Mismatch
4) Dynamic hyperinflation
5) worsening acid-base status

legit though don’t let your patient become dysynchronous with the vent, they will get super fucked up real quick. try to match what they want, if you can’t do that sedate them, if you can’t do that paralyze them

80
Q

pathophysiology of pulmonary hypertension

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. The pulmonary vascular bed is normally a high-flow, low-pressure system. When there is an increase in the PVR, the RV cannot adapt as well as the LV, β†’ RV dilation
  2. When faced with an acute increase in PVR, the RV can only generate systolic pressures up to 40-50 mm Hg
  3. With gradual, chronic changes, the RV systolic pressure can become equal to systemic pressures, up to 80-110 mmHg
  4. Volume overload, pressure overload, and dilation eventually lead to tricuspid regurgitation
  5. Normally, the RV is perfused in both systole and diastole, given the low RV pressures. Upon increased pressures within the RV, the wall tension leads to decreased RCA perfusion and eventual RV ischemia
  6. RV failure can develop with PH progression or an acute or chronic insult, particularly one that decreases RV perfusion or further increases PVR. This is why hypotension, decreasing RCA perfusion, or hypoxemia, hypercapnia, or positive-pressure ventilation can be so detrimental.
  7. The relationship between the RV and LV cavities is known as interventricular dependence. When the RV bulges with volume and pressure overload into the LV, the LV has decreased filling
  8. The RV is a conical structure and contracts in systole against the interventricular septum. Distortion of the RV not only decreases LV filling but also further decreases effective RV contractility
81
Q

Asthma treatment pathway

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Oxygen (target SpO2 >90%)
  2. inhaled Ξ²-agonist and anticholinergic (salbutamol + ipratropium)
  3. Systemic corticosteroids (methylprednisolone)
  4. MgSO4 infusion
  5. BiPAP (plus/minus depending how sick they are)
  6. Epinephrine (first IM, then IV. straight to IV if crashing)
  7. Intubation (ketamine induction, consider epi over phenyl for your hemodynamic support agent)
  8. Ketamine infusion therapy (ketamine maintenance of anesthesia)
82
Q

Signs of a severe asthma exacerbation

A
  1. inability to speak in full sentences
  2. tripod positioning
  3. altered mental status or agitation
  4. tachypnea
  5. tachycardia
  6. accessory muscle use
  7. hypoxia
  8. peak flow of <40-50% predicted or best
  9. poor air movement/silent chest
83
Q

asthma definition

A
  1. chronic inflammatory disorder of the lungs characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing.
  2. These episodes are often triggered by stimuli such as allergens, cold weather, or exercise.
84
Q

asthma pathophysiology

A
  1. Asthma is a disease that is characterized by chronic airway inflammation.
  2. Inflammation β†’ airway narrowing, extensive plugging of the airways with mucus and inflammatory infiltrates, airway hyperresponsiveness, hyperinflation, atelectasis, and VQ mismatch
  3. In acute exacerbations, bronchial smooth muscle contraction (bronchoconstriction) occurs rapidly to narrow the airways in response to a variety of stimuli
  4. Airway narrowing β†’ an increase in airway resistance and diminished flow
  5. As resistance increases, the inspiratory muscles must generate more force to offset the increase, β†’ increased WOB and dyspnea
85
Q

β€œfirst-line” treatment for patients with acute asthma exacerbation

A
  1. oxygen
  2. inhaled bronchodilators
  3. ipratropium
  4. systemic steroids
86
Q

β€œsecond line” (adjunctive therapies) for patients with acute asthma exacerbation

A
  1. IV magnesium
  2. systemic beta agonists
  3. Heliox
  4. NIPPV
  5. ketamine infusion therapy
87
Q

β€œthird line” (Rescue therapies) in a patient with a severe, potentially life-threatening asthma exacerbation

A
  1. mechanical ventilation
  2. anesthetic inhalational agents
  3. ECMO
88
Q

MOA for Short-acting Ξ²2-agonists (SABAs) in asthma

A
  1. relaxation of pulmonary smooth muscle
89
Q

side effects of Ξ²2-agonists

A
  1. tachycardia (watch out for hemodynamic/cardiac implications in old folks)
  2. tremors
  3. headache
  4. a transient intracellular shift in potassium, resulting in hypokalemia (typically gonna see a drop in your K+ of approx ~0.5)
90
Q

MOA for IV MgSO4 in asthma

A
  1. rapid smooth-muscle relaxation and bronchodilation
  2. MgSO4 IV has been shown to improve lung function in patients with severe exacerbations and to decrease hospital admissions (NNT = 4!!)
91
Q

MOA for Epinephrine in acute asthma exacerbations

A
  1. Epinephrine has been used for at least 100 years in the treatment of acute asthma exacerbations
  2. Epi’s non-specific Ξ²-agonist properties (Ξ²1 and Ξ²2) cause bronchodilation and concurrent vasoconstriction + decreased mucus production
  3. In adults, IM dosing 0.3-0.5mg, IV dosing is 10-100mcg pushes
92
Q

MOA for Heliox in acute asthma exacerbations

A
  1. Heliox is a titratable mixture of helium and oxygen that promotes a less turbulent airflow through narrowed airways
  2. Helium has a lower molecular density than oxygen or nitrogen, β†’ improved laminar flow
  3. This lower density may reduce the WOB and promote better nebulized drug delivery (heliox-driven nebs)
  4. Heliox may also decrease auto-PEEP, improve VQ matching, enhance the diffusion effect on the elimination of CO2, and ultimately prevent respiratory failure in patients when used early
93
Q

MOA for NIV in acute asthma exacerbations

A
  1. NIV results in direct bronchodilation, which recruits small airways and facilitates the administration of inhaled Ξ²-agonists (in-line neb or MDI’s)
  2. NIV may improve oxygenation, decrease the WOB and fatigue
  3. may prevent intubation in some patients
  4. Essentially, NIV provides rest for the diaphragm
  5. NIV use should not be attempted in agitated patients; patients should not typically be sedated to receive NIV
94
Q

MOA for Ketamine in acute asthma exacerbations

A
  1. Ketamine is a dissociative medication that causes bronchodilation and bronchorrhea, aiding the clearance of mucus plugs
95
Q

decision to intubate the failing asthmatic

A
  1. Progressive deterioration despite maximal therapies, with worsening work of breathing and impending respiratory exhaustion.
  2. Impending cardiopulmonary arrest (suggested by bradycardia, severe respiratory acidosis, very poor air movement, obtundation).
  3. Mental status alteration with inability to protect airway (noting that published case series have reported high success using noninvasive ventilation, even in patients with altered mental status)
96
Q

Key aspects of intubating the critical asthma patient

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. risk of hemodynamic deterioration. High airway pressures often cause hypotension after intubation. Pre-intubation fluid bolus, with an epi-infusion set up and push-dose epi pre-drawn on standby
  2. use a large-bore ETT to reduce airflow resistance, and facilitate bronchoscopy if necessary. (Minimum #8 tube in adults)
  3. Rocuronium over succinylcholine for RSI. Following intubation, it is extremely useful for the patient to be paralyzed briefly. Allows for Interrogation of respiratory mechanics (autoPEEP, plateau pressure), and Determination of a reasonable ventilator setting (without the confounding effect of patient effort)
  4. Avoid avoid aggressive peri-intubation bag-mask ventilation! Aggressive bagging will rapidly precipitate severe gas-trapping in the lungs. Gas-trapping may cause pneumothorax or hypotension.
  5. Have an experienced operator bagging these patients and keep a close eye on things
97
Q

core principles of ventilating an asthmatic

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. target a lung-protective strategy while allowing for permissive hypercapnia. Hypercapnia is well tolerated in asthmatics (who tend to be young, and with good hemodynamic reserves)
  2. Permissive Hypercapnia is the core of safe ventilation in asthma. intentionally allowing the pH to fall is often safer than trying to strictly control it (which would involve more aggressive ventilation with risks of pneumothorax or barotrauma)
  3. Young patients can often tolerate respiratory acidosis with pH <7 surprisingly well. It’s nice to see the pH >7.15 if possible, but we must balance the risks-vs-benefits of more aggressive ventilation vs higher pH
  4. autoPEEP is the main problem. autoPEEP is inevitable with severe asthma. The goal is to minimize it as possible. autoPEEP management depends on increasing the expiratory time or decreasing the tidal volume.
  5. Benefits of set PEEP include the following: [1. May help stent open the airways during exhalation (otherwise the airways may tend to be compressed by adjacent lung tissue). 2. May assist with ventilator triggering. the work of triggering the ventilator is proportional to the difference between the Intrinsic PEEP and the Set PEEP. Increasing the Set PEEP a bit will make it easier for the patient to trigger the ventilator]
  6. slow respiratory rate with normal-ish tidal volumes (10-14 bpm). A slow respiratory rate is essential to avoid autoPEEP. Ideally, tidal volumes should be maintained around 6-8 cc/kg
  7. you shouldn’t need a lot of oxygen. Asthma causes impaired ventilation, but oxygenation should be intact.
    If the patient is requiring >55% FiO2, look for another process going on (e.g., pneumothorax, aspiration, pneumonia, mucus plugging, pulmonary embolism)
  8. β€œSedate to compliance”. Fairly deep sedation is needed initially. Usually a combination of propofol, opioid, and ketamine. Goal is to suppress their respiration enough to synchronize well with the ventilator. In order to ventilate these patient’s effectively they must be synchronized and compliant with the ventilator. May have to paralyze
98
Q

ways to decrease autoPEEP on the ventilator

A
  1. Most effective: Decreasing the respiratory rate.
  2. Decrease the inspiratory time (e.g. using a higher flow rate if you’re using volume-cycled ventilation).
  3. Decreasing the tidal volume (this reduces the amount of gas which must be exhaled)
99
Q

Set PEEP vs Intrinsic PEEP

A
  1. Set PEEP is the amount of PEEP dialed into the ventilator.
  2. Intrinsic PEEP is the actual intrathoracic pressure at end-expiration (the β€œtrue” PEEP)
100
Q

how does one measure β€œIntrinsic PEEP” in mechanically ventilated patients

A
  1. Intrinsic PEEP may be measured by an end-expiratory breath hold maneuver:
  2. At end-expiration the gas flow is stopped. This leads to equilibration between the intrathoracic pressure and the ETT, revealing the intrinsic PEEP.
  3. An end-expiratory breath hold maneuver can be performed accurately only in a patient who is passive on the ventilator (either paralyzed or not triggering the ventilator)
101
Q

how does set PEEP assist with patient-ventilator triggering in autoPEEP

A
  1. In order to trigger a breath from the ventilator, the patient needs to suck the pressure in their lungs down from intrinsic PEEP (autoPEEP) to below the set PEEP.
  2. Thus, the work of triggering the ventilator is proportional to the difference between the Intrinsic PEEP and the Set PEEP.
  3. Increasing the Set PEEP a bit will make it much easier for the patient to trigger the ventilator.
102
Q

discuss the relationship between anatomic and physiologic dead space in mechanical ventilation

A
  1. Dead space is volume which enters the lungs but doesn’t participate in gas exchange.
  2. The amount of dead space is the sum of the anatomic dead space (gas going into and out of the trachea and large bronchi) plus the physiologic dead space (gas going into and out of non-functional alveoli).
  3. The anatomic dead space is roughly fixed, at 1 ml/pound ideal body weight (or ~2.2 ml/kg).
  4. This means ~2 cc/kg of each breath is wasted in ventilating the anatomic dead space (this achieves nothing for the patient)
  5. Some conditions (asthma) may have increased physiologic dead space, causing their total dead space to be relatively high (e.g. ~3 cc/kg)
  6. This means that if the tidal volumes are very low (e.g. 3-4 cc/kg), then the vast majority of ventilation will be wasted!
  7. This may cause the patient to be profoundly hypercarbic – even though the minute ventilation isn’t horribly low.
  8. Maintaining reasonably sized tidal volumes (e.g. at least ~5-6 cc/kg) will ensure some effective ventilation.
103
Q

Acute exacerbation of COPD (AECOPD) treatment algorithm

A
  1. Oxygen (Goal saturation 88-92%)
  2. Beta Adrenergic Agonist (salbutamol)
  3. Anticholinergic/bronchodilator (ipratropium)
  4. Corticosteroids (Methylprednisolone)
  5. Antibiotic coverage
  6. NIPPV (BiPAP or HFNC as tolerated)
  7. Intubation and MV
104
Q

COPD pathophysiology

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Chronic inflammation of the small airways β†’ narrowing and overall reduction of alveoli along with increased mucus production
  2. Alveoli are dilated or destroyed
  3. Patients likely have a history of cigarette smoking, smoke exposure, (occupational/industrial) or alpha-1-antitrypsin deficiency
  4. Nearly 70% of all exacerbations are triggered by a viral or bacterial infection
105
Q

what is the physiology behind hyperoxia VQ mismatch in COPD patients (old school β€œhypoxic drive” concept)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Patients with COPD have shitty lungs. But their whole lung isn’t shitty. Just parts of it. We will call these β€œshitty lung units”
  2. In chronic COPD, patients experience hypoxic pulmonary vasoconstriction, the physiologic process that serves to redirect blood flow away from under-ventilated lung (shitty lung units) in order to optimize the V/Q ratio in the non-shitty lung units (β€œgood lung”)
  3. Administration of excess oxygen causes an increase in ventilation/perfusion mismatch, where blood is shunted to poorly ventilated alveoli (shitty lung units), thereby increasing physiologic dead space and resulting in worsening hypercapnia
106
Q

Initial settings for BiPAP in AECOPD

A
  1. Inspiratory positive airway pressure: 8-12 cm H2O (titrate up by 3-5 cm H2O as needed to reduce the work of breathing)
  2. Expiratory positive airway pressure: 4-5 cm H2O
107
Q

What is the difference in salbutamol administration for AECOPD vs Asthma

A
  1. Although aggressive administration of salbutamol in large and serial doses seems to be a common practice, studies have shown that there is no difference in outcomes when patients are treated with higher dosages or continuous treatments in AECOPD.
  2. Therefore, the recommended dose in AECOPD remains at 2.5 - 5 mg.
  3. In AECOPD Administer neb treatments with air rather than oxygen unless the patient is hypoxic. MDI + AeroChamber is preferred d/t the effect of oxygen on hypoxic pulmonary vasoconstriction
  4. In asthma there is proven efficacy for high dose continuous salbutamol neb
  5. Patients with asthma are not predisposed to the chronic remodelling leading to hypoxic pulmonary vasoconstriction, so you can drive your neb with oxygen
108
Q

cycle of death in AECOPD

A

anxiety β†’ tachypnea β†’ dyspnea β†’ gas trapping β†’ anxiety β†’ tachypnea β†’ dyspnea β†’ gas trapping

109
Q

discuss ABX in AECOPD

A
  1. COPD Patients sick enough get critical care should receive antibiotics (even if there is no infiltrate on the chest X-ray)
  2. Patients with COPD have airways which chronically grow a variety of organisms
  3. The goal of ABX therapy is generally to suppress this bacterial growth. narrow-spectrum ABX are fine
  4. Azithromycin is generally first-line
110
Q

oxygen saturation target in COPD

A
  1. target an oxygen saturation of 88-92% (with 85-95% being OK)
  2. Excess oxygen may cause diffuse pulmonary vasodilation, which disrupts VQ matching and increases PaCO2
111
Q

differences in mechanical ventilation for COPD vs Asthma

A
  1. Ventilating COPD patients is generally much easier than ventilating asthmatic patients, despite the fact that both have airflow limitation
  2. COPD patients: Respiratory failure is usually due to a combination of diaphragmatic fatigue and bronchospasm. Once they are on the ventilator, diaphragmatic fatigue isn’t a problem – so ventilation is fairly easy.
  3. Asthmatic patients: Respiratory failure is due primarily to intense bronchospasm with mucous plugging. The degree of airway resistance is more severe, which can create major challenges in ventilator management.
112
Q

blood gas targets in AECOPD, and how to fuck up your patient

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. The best approach is generally to target a pCO2 close to the patient’s baseline value
  2. Many COPD patients have chronic hypercapnic respiratory failure, with a chronic compensatory metabolic alkalosis
  3. If you try to target Ventilation to a normal pCO2 (40mmHg) it will cause alkalemia (pH >7.45) d/t their pre-existing metabolic alkalosis
  4. the kidney will respond to alkalemia by excreting bicarbonate until the serum bicarbonate level is ~24 mEq/L
  5. Stripped of their chronic compensatory metabolic alkalosis, the patient now needs to blow their pCO2 down to ~40 mm in order to achieve a normal pH.
  6. This will increase their WOB, worsening their clinical status
  7. If you don’t know the patient’s baseline CO2, targeting a lowish pH (shoot for pH of roughly ~7.25-7.35) will give you a Mild acidemia which will stimulate the kidney to retain bicarbonate, which keeps the patient near their baseline bicarbonate level
113
Q

adverse effects of oxygen d/t hyperoxia and oxygen toxicity

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

Cellular injury due to increased ROS (reactive oxygen species)

  1. Increased ROS eg superoxide anion, hydroxyl radical, hydrogen peroxide
  2. ROS lead to inflammation and secondary tissue injury / apoptosis
  3. deplete cellular antioxidant defences
  4. react / impair function of intracellular macromolecules
    cell death

Respiratory

  1. pulmonary vasodilation resulting in V/Q mismatch and CO2 retention in COPD
  2. Haldane effect leads to decreased affinity of Hb for CO2 and contributes to CO2 retention in COPD
  3. increased mortality in CO2 retainers from high flow O2 compared with titrated O2 in a prehospital RCT
  4. increased respiratory rate
  5. Denitrogenation of the lungs causing resorption atelectasis
  6. Bronchopulmonary dysplasia: neonates
  7. > 60% O2 causes tracheal irritation, sore throat, substernal pain, pulmonary congestion, decreased VC
  8. Dry nose and mouth, increased susceptibility to mucous plugging
  9. Increased R to L shunt fraction
  10. Accelerated lung injury from bleomycin toxicity and paraquat poisoning
  11. Delay recognition of hypoventilation by SpO2 monitoring during sedation (irrelevant if using ETCO2 monitoring)

Immune

  1. Increased risk of secondary lung infection due to: impaired mucociliary clearance
  2. decreased bactericidal capacity of immune cells

Cardiovascular

  1. Increased mortality post-cardiac arrest with hyperoxia (PaO2>300 mmHg)
  2. Systemic vasoconstriction leading to increased SVR, increased BP, decreased heart rate and decreased cardiac output
  3. Normobaric hyperoxia reduces coronary blood flow by 8 to 29% in normal subjects and in patients with coronary artery disease or chronic heart failure
  4. Increased myocardial infarct size (AVOID study, 2015)
  5. No reduction in myocardial ischemia in the presence of coronary artery disease unless SpO2 <85-90%
  6. Impairs endothelium-mediated vasodilation

Neurological

  1. Acute toxicity with hyperbaric 100% O2 causing altered mood, vertigo, LOC, convulsions
  2. Retinopathy of prematurity
  3. Hyperoxia decreases cerebral blood flow by 11 to 33% in healthy adults
  4. Hyperoxia associated with increased mortality in stroke and TBI

Haematological

  1. Prolonged exposure to 100% O2 impairs erythropoiesis
114
Q

lung volumes measured by spirometry

A

Spirometers can measure three of four lung volumes

  1. inspiratory reserve volume
  2. tidal volume
  3. expiratory reserve volume,

Spirometers cannot measure Residual volume

115
Q

Tidal Volume (TV) definition

A
  1. t is the amount of air that can be inhaled or exhaled during one respiratory cycle
  2. The normal adult value is 10% of vital capacity (VC), approximately 300-500ml (6‐8 ml/kg)
116
Q

Inspiratory Reserve Volume (IRV) definition

A
  1. It is the amount of air that can be forcibly inhaled after a normal tidal volume.
  2. IRV is usually kept in reserve, but is used during β€œsigh breaths”.
  3. The normal adult value is 1900-3300ml.
117
Q

Expiratory Reserve Volume (ERV) definition

A
  1. It is the volume of air that can be exhaled forcibly after exhalation of normal tidal volume.
  2. The normal adult value is 700-1200ml.
  3. ERV is reduced with obesity, ascites or after upper abdominal surgery
118
Q

Residual Volume (RV) definition

A
  1. It is the volume of air remaining in the lungs after maximal exhalation.
  2. Normal adult value is averaged at 1200ml (20‐25 ml/kg).
  3. It is indirectly measured from summation of FRC and ERV and cannot be measured by spirometry.
  4. In obstructive lung diseases with features of incomplete emptying of the lungs and air trapping, RV may be significantly high.
  5. The RV can also be expressed as a percentage of total lung capacity and values in excess of 140% significantly increase the risks of barotrauma, pneumothorax, infection and reduced venous return due to high intra thoracic pressures
119
Q

Inspiratory capacity (IC) definition

A
  1. It is the maximum volume of air that can be inhaled following a resting state.
  2. It is calculated from the sum of inspiratory reserve volume and tidal volume.
  3. IC = IRV + TV
120
Q

Total Lung Capacity (TLC) definition

A
  1. It is the maximum volume of air the lungs can accommodate or sum of all volume compartments or volume of air in lungs after maximum inspiration.
  2. The normal value is about 6,000mL (4‐6 L).
  3. TLC is calculated by summation of the four primary lung volumes (TV, IRV, ERV, RV).
  4. TLC may be increased in patients with obstructive defects such as emphysema and decreased in patients with restrictive abnormalities including chest wall abnormalities and kyphoscoliosis
121
Q

Vital Capacity (VC) definition

A
  1. total amount of air exhaled after maximal inhalation.
  2. ~4800mL, varies according to age and body size.
  3. VC = tidal volume + inspiratory reserve volume + expiratory reserve volume.
  4. VC = TV + IRV + ERV.
  5. VC indicates ability to breathe deeply and cough, reflecting inspiratory and expiratory muscle strength.
  6. VC should be 3 times greater than TV for effective cough.
  7. VC is sometimes reduced in obstructive disorders and always in restrictive disorders
  8. VC is used to measure whether or not patients with neuromuscular disorders need to be tubed d/t respiratory muscle fatigue/decline
122
Q

Function Residual Capacity (FRC) definition

A
  1. amount of air remaining in the lungs at the end of a normal exhalation.
  2. calculated by adding together residual and expiratory reserve volumes (FRC = RV + ERV)
  3. normal value is about 1800 – 2200 mL.
123
Q

describe the pulmonary Pressure-volume relationship

A 
P = V/C (P = pressure, V = volume, C = compliance)
V = P Γ— C (increasing the volume will increase the pressure)
Compliance = tidal volume/(plateau pressure βˆ’ PEEP)
124
Q

define and describe Plateau pressure

A

Static pressure measured at the end of inspiration

A measure of alveolar overdistention (potential precursor to lung injury)

Patient must be heavily sedated to obtain a reliable measurement

125
Q

Tidal volume

A

The volume of gas delivered during each breathing cycle

126
Q

PEEP

A

Airway pressure maintained during expiratory phase

helps to maintain FRC and works at the alveolar level to β€œsplint open” the airway during expiration

127
Q

Mild ARDS

A

200 mm Hg [26.60 kPa] < PaO2/FiO2 < 300 mm Hg [39.90 kPa] with PEEP or CPAP >5 cm H2O

128
Q

Moderate ARDS

A

100 mm Hg [13.30 kPa] < PaO2/FiO2 < 200 mm Hg [26.60 kPa] with PEEP >5 cm H2O

129
Q

Severe ARDS

A

PaO2/FiO2 <100 mm Hg [13.30 kPa] with PEEP >5 cm H2O

130
Q

A-a gradient clinical application

A

A-a oxygen gradient = PAO2 - PaO2

PaO2 is measured by ABG, while PAO2 is calculated using the alveolar gas equation: PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 Γ· R)

  1. The A-a gradient is the difference between the oxygen concentration in the alveoli and the arterial blood
  2. Use in patients with hypoxemia of undifferentiated etiology. Measuring the A-a gradient helps narrow down the cause of hypoxemia as either extrapulmonary or intrapulmonary; AKA, to distinguish hypercapnic respiratory failure d/t global hypoventilation (extrapulmonary respiratory failure) from respiratory failure d/t abnormal gas exchange from intrinsic lung disease.
  3. A normal A-a gradient in the setting of an elevated PaCO2 is suggestive of global hypoventilation, whereas a widened gradient suggests that underlying lung disease may be contributing to the measured hypercapnia

CCP Semester 2: The Path Of Shame (20 decks)

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