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Respiratory Flashcards

1
Q

What three inputs control the respiratory pattern in the conscious patient?

A
  • pH of CSF surrounding medulla/midbrain (CO2 crosses BBB easily)
  • PaCO2 level from peripheral chemoreceptors
  • PaO2 level from peripheral chemoreceptors
  • The cortex has a mild inhibitory influence on the respiratory centres, hence why stroke patients can develop Cheyne-Stokes.
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2
Q

Who have worse outcomes. ARDS patients from a systemic source, or pulmonary source?

A

If ARDS is the result of pulmonary disease (aspiration, pneumonia), they have worse mortality rates than those who develop ARDS from something like sepsis.

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3
Q

What are the three main physiological consequences of developing ARDS?

A
  • Impaired diffusion/gas exchange
  • Decreased lung compliance
  • Increased pulmonary artery pressures
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4
Q

What P:F ratios define mild, moderate and severe ARDS?

A

Mild: 200-300 (27% mortality)
Moderate: 100-200 (32% mortality)
Severe: <100 (45% mortality)

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5
Q

What is the P:F ratio and what is normal?

A

It’s the patient’s PaO2 divided by the FiO2 they were receiving at the time of the ABG.

N: 400-500

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6
Q

Normally, only a small volume of fluid is allowed into the pulmonary interstitium in order to keep the alveoli dry. The mechanisms that maintain this are:

A
  • Oncotic gradient
  • Interstitial lymphatics can return a large volume
  • Tight alveolar-epithelial junctions prevent leakage (sigma factor)
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7
Q

List some pro-inflammatory cytokines and their role in ARDS:

A

TNF-a, IL-1, IL-6, IL-8

They recruit neutrophils to the lungs where they become activated and release toxic mediators (O2 species, proteases) that damage the capillary endothelium and alveolar epithelium. This results in permeability and loss of oncotic gradient. Lymphatics overrun. Surfactant washed out->atelectasis.

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8
Q

Most common causes of ARDS

A 
Sepsis
Pneumonia
Aspiration
Blood transfusions (TRALI)
Trauma (lung contusion, fat embolus)
Drugs (ASA, cocaine, opioids, TCAs)
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9
Q

Broadly speaking, what is the definition of ARDS?

A

Bilateral lung infiltrates with hypoxemia despite a PEEP of at least 5 cmH2O, and no other explanation.

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10
Q

What is the A-a gradient?

A

‘A’ denotes alveolar oxygenation while ‘a’ denote arterial oxygenation (PaO2).
Calculate the PAO2 and get the PaO2 from an ABG.

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11
Q

What does increasing FiO2 do to the A-a gradient.

A

It increases it.

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12
Q

How does hypoventilation affect oxygenation?

A

Both PaCO2 and PACO2 build up causing displacement of O2 from the alveoli. O2 can’t diffuse into bloodstream until CO2 is forced out since there isn’t a strong enough concentration gradient for CO2 to dissipate into atmosphere.

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13
Q

What is Winter’s formula?

A

Expected PaCO2 = (HCO3 x 1.5) + (8 +/-2)

PaCO2 > Cal PCO2 = Superimposed respiratory acidosis
PaCO2 < Cal PCO2 = Superimposed respiratory alkalosis

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14
Q

In the setting of SCI, what vital capacity should you consider intubating?

A

Anything less than 20cc/kg

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15
Q

Oxygenation requires these three processes:

A

Concentration gradient
Surface area
Cardiac output

A reduced wall thickness also helps

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16
Q

Does PEEP recruit alveoli?

A

No, it simply maintains it. A lack of PEEP, however, can collapse the FRC.

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17
Q

Does PFO shunt blood from right to left or left to right? Why?

A

Mostly, it shunts blood from left to right because the LA has higher pressures than the RA.
In the setting of pulmonary HTN, this process can be reversed.

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18
Q

What is HPVC and what does it lead to?

A

Hypoxic Pulmonary Vasoconstriction

Leads to pulmonary hypertension

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19
Q

What is the equation to measure compliance?

A

Delta V divided by Delta P

Think cowgirl. V over P

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20
Q

There are three types of compliance:

A

Pulmonary (atelectasis)
Thoracic (Burns, MSK)
Extra-thoracic (ACS)

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21
Q

How can you estimate deadspace using an ABG?

A

A difference greater than 10mm/Hg between the PaCO2 and the EtCO2.
*This could also be seen in low cardiac outputs.

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22
Q

Is peri-bronchial cuffing and air bronchograms found in CXRs a sign of consolidated or atelectic parenchyma?

A

Consolidated

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23
Q

Early ABx for pneumosepsis:

Remember, Strep-A can cause your pneumoseptic patient to go from 0 to 50mcg/min of levophed in a hurry, but early ABx can improve mortality significantly!

A

Ceftriaxone
Azithromycin
Piptaz (if they’re sick)
Vancomycin + Miropenim + anti-fungal (if they’re dying in front of you)

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24
Q

When fluid resuscitating sepsis, what indicators can you use to determine adequacy?

A
  • Passive leg raise
  • IVC diameter/collapsibility <50%
  • Lactate < 4.0?
  • Delta P <10%
  • Urine output > 80mL/hr
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25
Q

Berlin criteria for ARDS:

A
  • Acute onset (<1wk)
  • Bilateral lung opacities on CXR not explained by other pathology
  • Decreased P:F ratio, despite at least 5cmH2O PEEP
  • Not explained by HF (BNP/ECG) or volume overload
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26
Q

Goals for treating ARDS patients:

A

Target PaO2 > 80 for flight, > 60 for ground

  • Prevent volutrauma (4-8mL/kg with PLATs < 30)
  • Prevent cyclic atelectasis (PEEP)
  • Prevent O2 toxicity/nitrogen washout (PEEP ladder)
  • Prevent biotrauma (ET cuff pressure, suction)
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27
Q

Oxygenation strategies for failing ARDS patients:

A
  1. Sedate and paralyze (reduce O2 demand)
  2. ACV with increased FiO2
  3. PC with increased PEEP
  4. Inverse ratio ventilation with increased Ti
  5. Lung recruitment maneuvers
  6. Prone ventilation
  7. Don’t forget suction, ETT placement, PTXs
  8. V-V ECMO
    * Don’t forget to consider a fluid bolus to turn WZ I into WZ II or III.
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28
Q

What are the main causes of ARDS?

A

Pulmonary: CAP, aspiration

Systemic: Sepsis, trauma, TRALI, pancreatitis

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29
Q

What is the sigma factor?

A

The sigma factor is what keeps the epithelial junctions together in the face of hydrostatic pressure. An acute reaction to injury is transient loss of sigma factor. This allows fluid and protein to escape into the interstitial space, reversing the oncotic gradient and leading to hypoalbumenia and edema. Most ICU patients are edemous and have an albumin level of approx 20 upon admittance.

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30
Q

Does oxygenation occur during inspiration or exhalation?

A

Both… Except in COPD/asthma when bronchioles collapse on expiration. Also, this is what contributes to elevated CO2 levels. As this builds up, CO2 displaces O2 from alveoli since it has a higher gradient and oxygenation fails as well.

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31
Q

Treatment for COPD exacerbation:

A
  • Oxygen to target SpO2 to 88-94%
  • Bronchodilators (ventolin, atrovent)
  • Steroids (prednisone or methylpred)
  • Consider ABx
  • CPAP (PEEP matching)
  • Paralyze and intubate, put in pressure control
  • Pop them off the vent in peri-arrest situations to allow long exhale
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32
Q

What is the reasoning as to why asthmatics are so dangerous to intubate?

A

Asthmatics rely on active exhalation to force air out. If you intubate them, they must rely on passive exhalation which will likely kill them.
*COPDers, on the other hand, have their shitty lung architecture splinted open by PEEP which actually helps them.

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33
Q

Asthma treatment:

A
  • Bronchodilators (salbutamol, atrovent)
  • Steroids
  • ZEEP to 3cm/H2O
  • Ketamine
  • MgSO4
  • Epinephrine
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34
Q

DDx for peri-arrest COPD/asthmatics:

A
  • DOPE
  • Airway obstruction
  • Tension PTX
  • Hyperinflation
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35
Q

Discuss the hemodynamics of PE…

A
  • Decreased pulm flow = increased RV afterload and decreased LV preload. Cardiac output is reduced.
  • Bulging RV distends septum into LV, further worsening CO.
  • Less CO + increased RA pressure = bad coronary blood flow gradient. RV becomes hypoxic and stiff. RV contractility worsens.
  • Patient tries to compensate with tachycardia.
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36
Q

If PE patients are RV preload dependant, why not bolus them?

A
  • Yes, hypotension will kill PE patients, but increasing RA pressure will only worsen Ohm’s law (coronary gradient).
  • Consider Milrinone or vasopressin to improve BP.
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37
Q

What will worsen RV afterload and kill PE patients?

A
  • PEEP
  • Hypoxic pulmonary vasoconstriction
  • So you’re kinda damned if you do, and damned if you don’t. Good luck!
38
Q

You tPA a PE, what will be your first likely indicator that hemodynamics are improving?

A

Heart rate slows down. Conversely, if your patient’s heart rate speed up, the PE is likely worsening…or they’re now bleeding to death.

39
Q

Since hypercarbia causes pulmonary vasoconstriction, what is one drug you could consider when intubating a PE patient?

A

-One amp of NaHCO3-

40
Q

Treatment for a peri-arrest PE patient…

A
  • tPA

- Epi infusion if tPA is unavailable

41
Q

You have a patient that is metabolic/respiratory acidosis. What is the first step in interrupting the cycle of badness?

A

Try to improve their PaO2.

-Hypercarbia won’t kill patients right away but hypoxia will. The pH will eventually turn around once the PaO2 starts to improve, even if the PaCO2 is getting worse.

42
Q

Does a recruitment maneuver potentially improve oxygenation or ventilation?

A

Both. It increases surface area for gas exchange of both O2 and CO2.

43
Q

What did the FACTT trial prove?

A

That patients with ALI/ARDS that had a CVP < 4 had fewer ventilator days, improved lung function and fewer ICU days than those who received a liberal fluid balance approach.

44
Q

What did the ARDSnet trial prove?

A

That a lung protective ventilation strategy using low tidal volumes (<6ml/kg) was much better for patients with ALI/ARDS.

45
Q

What did the ALVEOLI trial recommend?

A

There is no difference in outcome in ARDS patients that received high or low PEEP (with PLAT < 30). They still recommend to try high PEEP, but if it doesn’t improve oxygenation, reduce PEEP.

46
Q

What was the LOVS trial about?

A

To see if high PEEP/recruitment maneuvers/low tidal volume ventilation strategy in combination would reduce mortality over low tidal volume ventilation only. This “open lung ventilation strategy” showed some benefit.

47
Q

An ABG should always be interpreted with what parameters?

A

Respiratory rate and tidal volumes.

ie. A PaCO2 of 40 is abnormal if the patient is breathing at 33/min.

48
Q

Before you prone an ARDS patient, what is one piece of diagnostics you should look at?

A

CT Scan will show if the consolidation is in the posterior/inferior portion of the lungs. If it is, this patient will benefit from lying prone.

49
Q

What is the one condition where you can use tPA when the the diagnosis of PE is only presumptive and a CT hasn’t been completed?

A

Cardiac arrest

50
Q

Contraindications for recruitment maneuver:

A
  • Right heart syndromes
  • COPD
  • PTXs
  • Hypotension
  • Brain injury
51
Q

Worth saying again… ARDS mgmt strategies:

A
  • Reduce O2 demand
  • <6mL/kg of TV
  • Permissive hypercapnia (keep pH > 7.15)
  • PEEP ladder
  • Drop esophageal ballon, monitor PLATs (keep <25)
  • Paralyze, deeply sedate and switch to pressure control
  • Inverse ratio vent
  • Recruitment maneuver
  • Prone the patient
52
Q

Perform a recruitment maneuver

A
  • Make sure patient is paralyzed
  • Switch to pressure mode
  • Prolong I-time
  • Crank Pip to 40 (~25 + 15 of PEEP)
  • Clamp tube at end of inspiration and silence alarm
  • Modify vent to settings for post maneuver
  • Monitor Vte for signs of improved compliance
53
Q

What’s the percentage of of right lung ventilation vs left lung?

A

60/40

54
Q

What percentage of perfusion do the two lower lobes receive compared to the rest of the lungs?

A

60-70%

55
Q

Briefly describe the West Zones:

A

1) Too much alveolar pressure compresses capillary, creating deadspace ventilation.
2) Some ventilation, some perfusion (systole only)
3) This is the best V/Q matching.
* Over-ventilating a healthy alveoli will cause it to compress the vasculature and turn a WZ 3 into a WZ1! Blood could then be shunted to an unhealthy alveoli.

56
Q

Generally, there are two ways to turn a West Zone 1 into a West Zone 2 or 3.

A
  • Increase pressure within the vasculature (fluid bolus, proning)
  • Decrease pressure within the alveoli (lower Pip/PEEP)
57
Q

You’re looking at a CXR and the costophrenic angles are fully blunted. This is a sign of pleural effusion, but what volumes are associated with these CXR findings?

A

At least 500mL.

58
Q

Welp, fuck! This seems like a fucked up equation… How do you determine the PAO2 in the setting of hypoxemic respiratory failure?

A

PAO2 = FiO2 (PB - PH2O) - (PaCO2/R)

  • PB: barometric pressure
  • PH2O: humidity
  • R: constant
59
Q

List the 5 causes of hypoxemic respiratory failure. Hint: Low FiO2 environment isn’t one of them…. Don’t tell that to the guys in the mine.

A

1) Hypoventilation
2) Shunt
3) V/Q mismatch
4) Low barometric pressure
5) DO2/VO2 mismatch (won’t cause hypoxemia on its own)

60
Q

How do you determine if there is a DO2/VO2 mismatch?

A

Get an SvO2 from a CVC. It might be inaccurate in the setting of sepsis, propofol infusions, liver failure and cyanide poisoning due to mitochondrial dysfunction.

61
Q

When assessing hypercarbic respiratory failure, what 6 areas must guide your approach?

A
  1. Medulla - (drugs, stroke, hemorrhage, ischemia, metabolic)
  2. Diaphragm - (SCI, inflammation to C3-5, phrenic nerve malfunction, GBS, myasthenia gravis, hypophosphatemia, myosotis)
  3. Pleural space - (effusions, PTX)
  4. Chest wall - (obesity, pregnancy, kyphosis)
  5. Airway - (obstruction)
  6. Lungs - (COPD, asthma)
62
Q

What are the four types of pneumonia?

A
  1. CAP - typical (GPC/GNC) and atypical
  2. Nosocomial/HAP/VAP (GNR)
  3. Aspiration
  4. Immunocompromised
63
Q

The patient’s pneumonia culture comes back as gram-positive cocci. What should you be prepared for?

A

A fucking bomb to go off! This patient is going to crash hard. Get your fluids ready and be ready to go up to 50mcg/min of Levophed in a hurry (< 2 hours).

ABx is preferably 3rd generation Beta Lactam cephalosporins such as Ceftriaxone (2g).

64
Q

So, you figured out that gram positive cocci pneumonias (strep P., Group A strep, Staph A.) react well to third generation Beta Lactams, but what about atypical pneumonias (chlamydia, legionella, mycoplasma)?

A

No. Give any suspected CAP 500mg Azithromycin q.d. to treat the atypical agents and 2g Ceftriaxone to treat the typical agents. Worry about the gram stain and cultures at the receiving center.

65
Q

What’s the most common bacterial agent of typical CAP?

A

Strep Pneumoniae (gram-positive cocci, responds to Ceftriaxone)

66
Q

Ahhh, this again. A common theme is that hypoxemia in PE isn’t actually caused by decreased perfusion. What’s Myp’s take on it?

A

Ischemic alveolar cells stop producing surfactant. Atelectasis ensues and then no gas exchange occurs from the resulting shunt effect.

67
Q

Treatment for PE:

A

A PE can really only be diagnosed with CT angio. If highly suspicious (ECG, D-dimer, tachycardia, clear CXR, hemoptysis, dyspnea) then consult ETP and give tPA. There must be signs of RV dysfunction and shock.

Otherwise, best to treat with LMWH/UFH.

68
Q

Signs of impending doom with a crashing asthmatic patient:

A
  • Normal PaCO2 in the setting of tachypnea
  • Hypoxemia
  • Quiet chest
  • Too tired/SOB to speak
69
Q

Asthma Tx:

A
  • Tx infection or any precipitating factor
  • Salbutamol (5-10mcg/min IV) or atrovent
  • Steroids (1mg/kg methylprednisone)
  • Mg++
  • Epinephrine
  • Ketamine, fentanyl, rocuronium if you have to intubate
70
Q

Ventilation strategies for asthma exacerbation:

A
  • Large ETT
  • ACV, so you can trend Pips
  • Long I:E, high flow, decreased RR
  • Permissive hypercapnia (> 7.10)
  • Keep patient paralyzed and cool to reduce CO2 production
  • Consider fluid
  • Consider ECMO
  • Base PEEP off of VTe
71
Q

You’re ventilating an asthmatic patient. How do you pick the right amount of PEEP?

A

Look at the patient’s VTes. If they don’t match the ACV, then consider increasing PEEP in order to splint the airways open. If it gets worse, go the other way.

72
Q

There’s two causes of hypotension in an asthmatic patient:

A
  1. AutoPEEP

2. Tension PTX

73
Q

There are three causes of massive pulmonary hemorrhage:

A
  1. Bronchiectasis
  2. Tumours
  3. AVMs
74
Q

Treatment for massive pulmonary hemorrhage:

A
  • Secure airway
  • Lots of PEEP!
  • SBP < 140
  • Bad lung down
  • TXA?
  • Right mainstem if it’s L sided
75
Q

Where is the most common site for a chest tube to clot?

A

At the level of the dermis. Try breaking up the clot with pressure and milking it down the tube.

76
Q

Radiological indications for a thoracostomy:

A

No PPV: 2cm, or greater

PPV: Even occult PTXs only seen on CT need a tube.

77
Q

Want to figure out if your patient’s lung apices are WZ 1? Try this test…

A

Lay them supine for 3-4 minutes. If their SpO2 climbs, then they are in WZ 1 and would benefit from either a fluid bolus or decrease in PEEP when you sit them back up.

78
Q

What’s the equation to determine the PAO2?

A

PAO2 = FiO2 (PB - PH2O) - (CO2/.8)

Or

PAO2 - .21 (760 - 47) - (40/.8)
PAO2 = 100

79
Q

What are the antibiotics of choice for aspiration pneumonia?

A

Scene aspiration: 2g Ceftriaxone

Hospital aspiration: 4.5g Pip/Tazo q. 6h

80
Q

Why do infectious agents primarily switch from gram positive to gram negative agents after 48 hours in hospital?

A

The oral mucosa is usually gram-positive but because everything in a hospital is covered in feces and patients constantly touch their face and mouths, the bacteria turn to gram-negative agents. Yup, pretty fucking gross!

81
Q

Hospital acquired (>48h in hospital or care home), nonsocomial and ventilator associated pneumonias are all considered gram-negative rod or gram-positive cocci pneumonias. Without worrying about cultures or gram-staining, how are you going to treat?

A

Vancomycin for the gram-positive coverage and meropenem for the gram-negative rods.

82
Q

What are the 5 causes of hypoxemia according to Myp?

A
  1. Hypoventilation
  2. V/Q Mismatch
  3. Shunt
  4. Low PB (Barometric Pressure)
  5. VO2/DO2 Mismatch
83
Q

Describe VO2/DO2 mismatch

A

In times of either heightened metabolic demand (sepsis) or low cardiac output (cardiogenic shock), the cells will cleave off two oxygens from hemoglobin instead of just one. This makes the ScVO2 more like 50% instead of 75%. Not necessarily a cause of hypoxemia by itself, but if there is lung pathology on top of this, it will exacerbate hypoxemia exponentially!

84
Q

So you’re looking at a CXR and the lower lobes look like shit. It’s okay though, because the upper lobes look fine. Right?

A

Wrong, bitch! The upper lobes only receive about 5% of perfusion while the lower lobes receive about 67%. All that blood is going to shitty alveoli and participating in shunt physiology. Your PaO2 is going down, muthafucka!

85
Q

Random facto! Which lobe is most often associated with aspiration? Which one is most often associated with pneumonia?

A

The RLL most often sees aspiration due to angle of the right bronchus and gravity. The RML most often gets infected due to its proximity to the trachea.

86
Q

How does hypoventilation lead to hypoxemia?

A

Without ventilation, CO2 builds up in alveoli. It’s a bully and doesn’t allow oxygen in.

Welcome to Fort Awesome! No O2s allowed!

87
Q

Right to left shunt is something we learned so much about in ACP school. It’s a thing, right?

A

Not really. In order for it to occur, you need an ASD or VSD in the presence of high right sided pressures (pulmonary HTN).

88
Q

So your SpO2 is 90%. About what is your PaO2? What if your SpO2 was 60%

A

90/60 rule, yo!

  • If your SpO2 is 90%, then your PaO2 is about 60mmHg.
  • If your SpO2 is 60%, then your PaO2 is about 30mmHg.
  • This of course is affected by changes to pH, temperature and 2, 3 DPG levels
89
Q

What inotrope/vasopressor can provide some vasodilation?

A

Milrinone

Vasopressin

90
Q

Ultrasound findings that can help determine whether an ARDS patient requires more PEEP and/or prone ventilation.

A

Diffuse B-lines = More PEEP

PLAPS = Prone ventilation

CCP (18 decks)

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