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CCP Semester 2: The Path Of Shame > CCP 208 Designing Ventilation Strategies > Flashcards

CCP 208 Designing Ventilation Strategies Flashcards

1
Q

CCP approach to establishing Mech Vent

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Am I adequately oxygenating (PaO2)
  2. Am I ventilating appropriately (PaCO2)
  3. Am I on safe ground
  4. What is my current acid-base status
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2
Q

4 types of hypoxia

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A
  1. hypoxic
  2. hypemic
  3. stagnant
  4. histotoxic
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3
Q

5 causes of hypoxemia

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A
  1. V/Q mismatch
  2. Diffusion impairment
  3. Shunt (think right to left shunt)
  4. Hypoventilation
  5. Decreased partial pressure of inspired oxygen (think high altitude)
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4
Q

causes of hypoxemia with normal A-a

A
  1. Hypoventilation

2. Decreased partial pressure of inspired oxygen (think high altitude)

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5
Q

causes of hypoxemia with high/wide A-a

A
  1. V/Q mismatch
  2. Diffusion impairment
  3. Shunt (think right to left shunt)
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6
Q

The bicarbonate-carbonic acid buffering system equation

A

CO2 + H2O ⇌ H2CO3 ⇌ HCO3- + H+

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7
Q

Oxygen extraction ratio

A

O2ER = VO2 / DO2 = (SaO2-SvO2) / SaO2

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8
Q

Oxygen delivery equation (DO2)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

DO2 = CO x CaO2 (mL/min/m2)

CaO2 = (1.34 X Hgb X SaO2) + (0.003 X PaO2)

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9
Q

equation of motion for the respiratory system

A

muscle pressure (Pmusc) + ventilator pressure (Pvent) = (elastance x volume) + (resistance x flow)

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10
Q

causes of increased airway resistance

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. bronchospasm
  2. ETT problems (too small/kinked/bitten/flexed/obstructed)
  3. mucus plugging/secretions
  4. water in HME
  5. blocked exhalation valve
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11
Q

causes of decreased lung compliance

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. ARDS
  2. atelectasis
  3. abdominal distention (abdominal HTN)
  4. CHF
  5. consolidation
  6. fibrosis (pulmonary fibrosis)
  7. hyperinflation
  8. pneumothorax
  9. pleural effusion
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12
Q

Functional Residual Capacity (FRC)

what is it and why is it important

this is very esoteric 🧙

A

simply, FRC is the volume of air present in the lungs at the end of passive expiration

Why is FRC important ?

  1. At optimized FRC, the work to inflate the lungs is the lowest, as the inward and outward lung compliances are balanced
  2. compliance of lung depends on both elastic recoil of lung tissue and outward expansion of chest wall. ↓ in either of these result in a ↓ FRC
  3. The FRC results in an O2 reserve, the residual air volume in the lungs allows for O2 exchange. ↑ FRC = ↑ oxygenation “time under the curve”
  4. ↓ lung volumes result in ↓ FRC. Low lung volumes result in less alveolar tension pulling the lung airways open, and the airway narrowing results in ↑ airway resistance
  5. A ↓ FRC can result in shunts and atelectasis. This occurs when the FRC ↓ below the closing capacity of the lung; the volume at which the respiratory bronchioles collapse
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13
Q

Transpulmonary pressure

A

the difference between the alveolar pressure and the intrapleural pressure in the pleural cavity

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14
Q

pulmonary shunt

A

the passage of deoxygenated blood from the right side of the heart to the left without participation in gas exchange in the pulmonary capillaries

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15
Q

Ventilation perfusion mismatch or “V/Q defects”

A

condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen

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16
Q

Physiologic right to left shunt

A

exist when non-ventilated alveoli are perfused

  1. atelectasis
  2. pneumonia
  3. acute respiratory distress syndrome

as opposed to anatomic shunt which would be d/t something like a VSD

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17
Q

diffusion limitation

A
  1. movement of oxygen from alveolus → pulmonary capillary impaired
  2. usually d/t alveolar and/or interstitial inflammation and fibrosis (pulmonary fibrosis)

don’t get this confused with V/Q mismatch, it is a distinct clinical entity

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18
Q

right to left shunt

A

deoxygenated blood flowing from right side of the heart to left side of the heart without being oxygenated via the lungs

could be d/t an ASD/VSD, could be pulmonary

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19
Q

Goals of NIPPV

A
  1. Decrease WOB (unload respiratory muscles)
  2. Increase FRC
  3. Improve atelectatic recruitment
  4. Improve lung compliance
  5. Improve oxygenation
  6. Decrease LV preload, decrease LV afterload, improve cardiac output, improve forward flow
  7. PEEP matching for autoPEEP
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20
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 is a caution
  8. Maxillofacial injury
  9. Intractable vomiting
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21
Q

Adverse effects of NIPPV

A
  1. Local skin damage around bridge of nose
  2. Mask leak
  3. Eye and mouth irritation from mask leak air flow
  4. Sinus pain and sinus congestion
  5. Claustrophobia
  6. Mild gastric distention
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22
Q

simplified equation of motion of the respiratory system

A

Ventilation Pressure = Elastic Pressure + Resistive Pressure

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23
Q

effects of PEEP on the RV

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. decreased RV venous return (decreased RV preload)
  2. increased pulmonary vascular resistance due to vascular compression (increased RV after load)
  3. increased RV dilation, leading to a leftward shift in the intraventricular septum
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24
Q

effects of PEEP on the LV

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. decreased LV preload from decreased RV output
  2. decreased LV SV d/t bulging of the ventricular septum from RV dilation
  3. decreased LV afterload
  4. decreased LV preload and decreased LV dilation
  5. decreased myocardial oxygen demand
  6. increased pressure gradient from thorax to periphery
  7. increased hydrostatic displacement of alveolar edema
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25
Q

Summary of effects of PEEP on the heart

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Net effect of PEEP on CO depends on RV/LV function, preload, after load, and ventricular interdependence
  2. In RV failure/RV preload dependence, moderate to high PEEP (5-15 cmH2O) may decrease RV CO
  3. In after load-dependent states (such as LV failure) moderate-to-high PEEP (10 to 15 cmH2O) may improve CO
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26
Q

Triggering variable

A

initiates the delivery of a breath (e.g. flow or pressure)

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27
Q

Control variable

A

algorithm that determines the delivered pressure during mechanical inspiration (e.g. volume or pressure)

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28
Q

Cycling off variable

A

signal for terminating the pressure delivery (e.g. time, pressure, flow)

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29
Q

causes of Increased Airway Resistance

A
  1. Asthma (e.g. bronchospasm)
  2. Obstruction or kinking in ETT
  3. Excessive airway secretions
  4. Clogged HME filter
  5. Small-bore ETT
  6. High flow rate
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30
Q

causes of Decreased Compliance

A
  1. ARDS
  2. Pulmonary fibrosis
  3. Abdominal distention
  4. Pneumonia
  5. Pleural effusion (e.g. heart failure)
  6. Pneumothorax
  7. Atelectasis
  8. Bronchial intubation
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31
Q

decreased compliance (pip/plat)

A

Increased PIP

Increased Pplat

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32
Q

increased resistance (pip/plat)

A

Increased PIP

Normal/Unchanged Pplat

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33
Q

ARDS Berlin definition

A
  1. Acute, within 1 week of a known risk factor
  2. Bilateral opacities on CXR
  3. Respiratory failure not purely of cardiac origin
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34
Q

Berlin ARDS staging

A
  1. Mild. P/F ratio 200-300, PEEP >5 cmH2O
  2. Moderate. P/F ratio 100-200, PEEP >5 cmH2O
  3. Severe. P/F ratio <100, PEEP >5 cm H2O
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35
Q

ARDSnet lung protective protocol

A

Starting at 6 mL/kg PBW Reduced stepwise by 1 mL/kg PBW to maintain plateau pressure < 30 cmH 2 O

If Plateau pressure <25 cmH20, TV increased by
1 mL/kg PBW until plateau pressure > 25 cmH2O

Minimal tidal volume 4 mL/kg
Maximum tidal volume 8 mL/kg
Minimal arterial pH 7.15

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36
Q

respiratory effects of prone ventilation

A
  1. recruitment of dorsal lung → increased lung compliance
  2. stiffening of chest wall → decreased chest wall compliance
  3. overall respiratory system compliance varies case-by-case
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37
Q

circulatory effects of prone positioning

A
  1. increased intrathoracic pressure leads to decreased RV preload
  2. decreased trans pulmonary pressure leads to reduced RV after load
  3. overall RV cardiac output varies case-by-case
38
Q

summary of prone positioning

A
  1. Optimizes V/Q matching by increased blood flow to the dependent lung
  2. Reduced atelectasis
  3. Facilitates secretion drainage
  4. Less lung deformation
  5. Increased FRC as abdomen less likely to distend when in prone position
  6. Decreased Transpulmonary pressure
  7. More uniform alveolar ventilation
39
Q

Volutrauma

A

Ventilation at high lung volumes

40
Q

Barotrauma

A

Misnomer. Not due to high airway pressures but

also associated with high lung volumes

41
Q

Atelectrauma

A

Repetitive opening and closing of terminal units

42
Q

Biotrauma

A

Biological response to VILI

43
Q

Pleural pressure surrogate

A

Esophageal pressure

44
Q

Ptp Pplat

A

Inspiratory hold and in a no-flow state transduce the Pes at the same point in time

Ptp Pplat = pPlat - Pes * 1.36 (to convert mmHG to cmH2O)

Desired Value: <25 cm H2O

Adjust VT to achieve this value

45
Q

Ptp PEEP

A

Expiratory hold and in a no-flow state transduce the Pes at the same point in time

Ptp PEEP = (Auto PEEP + Applied PEEP) – Pes * 1.36 (to convert mmHG to cmH2O)

Desired Value: 0–10 cm H2O

Adjust PEEP to achieve this value

46
Q

Sequential approach to refractory hypoxemia

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Increase FiO2
  2. Increase PEEP
  3. Paralyze patient
  4. Increase RR
  5. Pressure control (square waveform)
  6. Lengthen out I-time
  7. Recruitment maneuver
  8. Prone positioning

*Don’t forget to consider a fluid bolus to improve West Zone physiology

47
Q

factors contributing to development of autoPEEP in mechanically ventilated patients

A
  1. RR too high (not enough time to exhale)
  2. Minute volumes are too high
  3. Bronchospasm
  4. ETT too small
  5. Mucus plug in ETT
48
Q

Effects of PPV on neurological system

A
  1. high PEEP levels → decreased cerebral venous drainage → worsening ICP
  2. pH changes → changes in cerebral blood flow
  3. Changes in cerebral pH can impact respiratory centre in brainstem → variable respiratory effort
49
Q

Effects of PPV on respiratory system

A
  1. possible VILI (barotrauma, volutrauma, biotrauma, atelectrauma)
  2. Over-distention of alveoli will increase PVR → VQ mismatch/shunt
50
Q

Effects of PPV on GI/GU systems

A
  1. possible GI bleeding from “stress ulceration”
  2. Impaired renal blood flow and possible AKI due to decreased CO (pre-renal azotemia)
  3. Gut ischemia may cause translocation of bacteria (abdominal sepsis)
  4. Decreased CO may cause Liver dysfunction (hypoalbuminemia, coagulopathy)
51
Q

Effects of PPV on the immune system

A
  1. May induce pulmonary inflammation (biotrauma)

2. Translocation of tracheal bacteria promoting infection (VAP)

52
Q

the three goals of mechanical ventilation

A
  1. Oxygenate adequately
  2. Ventilate appropriately
  3. Optimize pH
53
Q

How does increasing the PEEP actually reduce the Pplat in some patients?

A
  1. Recruitment maneuvers and PEEP can recruit atelectatic lung tissue and improve lung compliance
  2. This will decrease intrathoracic pressures and lower Pplat
54
Q

how does pressure mode allow for more “time under the curve”

A
  1. Pressure mode has a square waveform which allows for more uniform gas distribution
  2. It dissipates pressure evenly throughout the alveoli
55
Q

You’ve successfully recruited lung tissue in an ARDS patient. Now you need to suction their airway. What must one be aware of?

A
  1. Suctioning will potentially collapse their PEEP

2. may need to do a lung recruitment maneuver after the suction

56
Q

5 prerequisites to make someone a candidate for NIPPV

A
  1. Conscious and spontaneously breathing
  2. Protecting their airway
  3. Managing their secretions
  4. Appropriate seal
  5. Physiology to support it (not in shock or impending shock)

Can they handle it for the duration of the flight

57
Q

process for calculating if you have recruitable lung tissue using an esophageal balloon

A

Calculate trans-pulmonary PEEP (PtpPEEP).

  1. The value should be 0-10
  2. Anything less than 0 is sheer trauma
  3. Anything greater than 10 is baro/volutrauma.
  4. Ptp PEEP = (Auto PEEP + Applied PEEP) – Pes * 1.36 (to convert mmHg to cmH2O)
58
Q

process for calculating if your plateau pressures are “safe” using an esophageal balloon

A

Calculate trans-pulmonary plateau pressure (Ptp Pplat)

  1. Ptp Pplat = pPlat - Pes * 1.36 (to convert mmHg to cmH2O)
  2. Desired Value: <25 cm H2O
  3. Adjust Vt to achieve this value
59
Q

process for performing a recruitment maneuver

A
  1. Paralyze
  2. Switch to pressure control
  3. Prolong I-time
  4. Increase PIP to desired level
  5. Clamp tube on end-inspiration and hold for desired timeframe
  6. Dial in new vent settings with increased PEEP
  7. Monitor for changes
60
Q

Mech Vent strategy for obstructive lung disease

A
  1. High Flow (80-100lpm)
  2. Prolonged expiratory time (I:E of at least 1:3)
  3. Lower RR (10 to 14 frequency, monitor capnographic waveform)
  4. Lower Vt (Keep tidal volumes below 8mL/kg)
  5. Allow permissive hypercapnia; target pH instead
  6. Lung protection (Keep Pplat <30cmH2O)
  7. Monitor autoPEEP carefully
  8. Ongoing bronchodilator therapy
61
Q

DOPES mnemonic for rapid decompensation while on mechanical ventilation

A
  1. Displaced ETT
  2. Obstructed ETT
  3. Pneumothorax
  4. Equipment failure
  5. Stacked breaths
62
Q

How to reduce autoPEEP

A
  1. Change vent settings (increase flow, decrease RR, decrease Vt)
  2. Reduce patient-ventilator demand (fever, pain, anxiety)
  3. Reduce airway resistance (suction ETT, bronchodilators, larger ETT)
  4. disconnect circuit, let patient fully exhale passively
63
Q

Effects of PPV on the RV

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Increased intrathoracic pressure is transmitted to central veins and the RA → decreased RV preload
  2. Increased alveolar pressure → increased PVR → increased RV afterload
  3. increased RV afterload and decreased RV preload → decreased RV stroke volume
64
Q

Effects of PPV on the LV

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Decreased RV CO → decreased pulmonary venous pressure → decreased LV preload
  2. Decreased LV afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
  3. Decreased LV stroke volume
65
Q

patient cohorts in whom NIPPV bears the best evidence

A
  1. Acute COPD exacerbation
  2. Acute cardiogenic pulmonary edema
  3. Pneumonia/bronchiolitis in pediatric patients
66
Q

contraindications to NIPPV

A
  1. Pending cardiac or respiratory failure
  2. Need for immediate intubation
  3. Inability to protect airway
  4. Significant facial trauma or abnormality preventing facial mask
  5. Recent facial or gastric/esophageal surgery
  6. Excess secretions or high risk for vomiting (relative)
  7. Significantly altered mental status or inability to cooperate (relative)
67
Q

indications that a patient is “failing” NIPPV

A
  1. increased work of breathing
  2. tachypnea
  3. decreased PaO2/FiO2 ratio
  4. mental status change
  5. no improvement after 1 h of NIPPV
68
Q

initial settings for BiPAP in COPD

A
  1. IPAP 12 cmH2O and EPAP 6 cmH2O.
  2. Wean FiO2 to maintain saturation 88-92%.
  3. Titrate IPAP and EPAP while maintaining at least 5 cmH2O ∆
  4. Titrate up 2 cmH2O q5min prn
  5. If there is no improvement after approximately 1 h, the patient requires intubation
69
Q

initial settings for IPPV in COPD

A
  1. AC-Volume
  2. RR: 10-12 breaths/min
  3. Tidal volume: 6-8 mL/kg IBW
  4. FiO2: 40%.
  5. PEEP: 0-5 cm H2O
  6. Inspiratory flow of 60-80L
70
Q

initial settings for NIPPV in Acute cardiogenic pulmonary edema

A
  1. CPAP 5-10 cmH2O or BiPAP 12/6
  2. Titrate PEEP/FiO2 to maintain saturation >92%
  3. Titrate by 2 cmH2O q5min prn (as tolerated based on patient comfort, vital signs, and respiratory difficulty)
  4. maintain at least 5 cmH2O ∆ if on BiPAP
71
Q

initial settings for IPPV in Acute cardiogenic pulmonary edema

A
  1. AC-Volume
  2. RR: 16-18 bpm
  3. Tidal volume: 6-8 mL/kg IBW
  4. FiO2: 100%
  5. PEEP 5-10 cmH2O
  6. Inspiratory flow of 60 L/min
  7. Titrate PEEP per ARDSnet protocol
72
Q

post intubation mechanical ventilation checklist

A
  1. Initiate waveform capnographic end-tidal CO2 monitoring
  2. Elevate the head of the bed to 30°
  3. Measure the patient to obtain the IBW if not previously done
  4. Check the arterial blood gas approximately 30 min after initiation of IPPV
  5. Ensure patient is appropriately sedated/analgesed
  6. Titrate FiO2 to maintain oxygen saturation of approx 95%
  7. Maintain plateau pressure <30 cm H2O
73
Q

ndications for positive pressure ventilation

A
  1. Hypoxemic respiratory failure (eg, pneumonia, CHF)
  2. Hypercapnic respiratory failure (eg, COPD)
  3. Inability to maintain a patent airway (eg, burns, trauma, stroke, overdose)
  4. Anticipated deterioration of clinical status (shock, metabolic acidosis, worsening TBI)
74
Q

Tidal volume definition

A
  1. The volume of gas delivered during each breathing cycle
75
Q

PEEP definition

A
  1. Airway pressure maintained during expiratory phase
  2. helps to maintain functional residual capacity
  3. works at the alveolar level to “splint open” the airway during expiration.
76
Q

Minute ventilation definition

A
  1. the amount of air breathed per minute

2. respiratory rate × tidal volume

77
Q

Dead space ventilation definition

A
  1. Volume of a breath not participating in gas exchange
78
Q

Alveolar minute ventilation definition

A
  1. the volume of air entering the alveoli per minute
  2. The difference between minute ventilation and alveolar minute ventilation is the dead space ventilation that is wasted from the gas exchange point of view
  3. RR × (tidal volume − volume dead space)
79
Q

Plateau pressure definition

A
  1. Static pressure measured at the end of inspiration
  2. A measure of alveolar overdistention (potential precursor to lung injury)
  3. Patient must be apneic to obtain a reliable measurement
80
Q

describe the Pressure-volume relationship

A
  1. P = V/C (P = pressure, V = volume, C = compliance)
  2. V = P × C (increasing the volume will increase the pressure)
  3. Compliance = tidal volume/(plateau pressure − PEEP)
81
Q

Assist control – volume cycled

A
  1. Patient is given a full tidal volume breath during each respiration
  2. If the patient triggers another breath before initiation of the next breath, then the patient receives that breath at the full tidal volume
82
Q

High-flow nasal cannula (HFNC)

A
  1. High-flow O2 therapy through a NC is a technique in which heated and humidified oxygen is delivered to the nose at high flow rates
  2. These high flow rates generate low levels of PEEP (3-5cmH2O) in the upper airways, and the FiO2 can be adjusted by changing the fraction of oxygen in the driving gas
  3. Decreases the “dead space” in lungs and washes out CO2 in the upper airways
83
Q

pathophysiology of NIPPV in COPD

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. COPD is an obstructive lung disease that → ventilatory insufficiency, hypercarbia, and respiratory acidosis
  2. BiPAP and CPAP work to reduce the WOB, wash out dead space, and decrease CO2 → increased pH
  3. This occurs by stenting open airways to improve exhalation
  4. decrease in intubation rates (NNT of 4) for early usage of NIPPV in COPD exascerbation
84
Q

discuss the pathophysiology of NIPPV in asthma

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. The exact pathophysiology of asthma is different from COPD, but the respiratory compromise of this obstructive disease is similar
  2. Asthma → significant air trapping and excessive use of respiratory muscles to exhale against smaller airways
  3. The air trapping and intrinsic PEEP makes inhalation difficult and → respiratory muscle fatigue
  4. NIPPV may benefit an asthma exacerbation via offloading the work of inspiratory muscles, a direct bronchodilatory effect (airway “splinting”), allowing improved flow of bronchodilatory agents in the bronchial tree, and improving V/Q matching
  5. Several studies have shown that apply extrinsic PEEP to a patient with asthma decreases dynamic hyperinflation via “PEEP matching”
  6. Initial settings for NIPPV in asthma are similar to COPD
  7. patients who show no improvement or worsen within 1 hr need to be tubed
85
Q

what is the major risk associated with intubation and MV in patients with obstructive lung disease?

A
  1. These patients are at high risk for barotrauma and hemodynamic collapse d/t air trapping → decreased preload
  2. high risk for pneumothorax
  3. ventilator settings should be closely monitored, with the goal of preventing air trapping with resulting barotrauma
  4. These patients must be appropriately sedated to prevent breath stacking, elevated respiratory rates, and the development of auto-PEEP
86
Q

discuss the approach to mechanical ventilation in obstructive lung disease

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Start the patient on AC-V with a lung-protective strategy using a tidal volume of 6-8 mL/kg
  2. A RR of 8-10 bpm is an ideal starting point. The low rate allows more time for exhalation and should prevent air trapping and barotrauma
  3. The low RR will result in some degree of hypercapnia and respiratory acidosis (permissive hypercapnia)
  4. Most patients will tolerate a mild (>7.20) respiratory acidosis very well
  5. To determine the need for rate/volume adjustment, PPlat should be assessed by performing an inspiratory pause
  6. The Pplat should be maintained at <30 cmH2O, and the respiratory rate and Vt should be titrated to maintain a safe plateau pressure (decrease Vt by 1 mL/kg to decrease Pplat if >30 cmH2O per ARDSNet protocol)
  7. FiO2 at 40%, typically no oxygenation problem is present in a purely obstructive disease (target an O2 saturation of 92% or PaO2 60-80 mm Hg)
  8. PEEP should be set at a level of <5 cm H2O (A small amount of PEEP may help offset the added elastic load at the start of inspiration)
  9. I:E ratio should be set at 1:4 to permit an appropriate time for exhalation. This allows for rapid insufflation of the lungs and prolonged expiration, preventing air trapping. The ratio can be increased or decreased as needed based on the Pplat
87
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)
88
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 “true” PEEP)
89
Q

how does one measure “Intrinsic 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)
90
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.
91
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.
92
Q

Assist control – volume cycled:

A

Patient is given a full tidal volume breath during each respiration.

If the patient triggers another breath before initiation of the next breath, then the patient receives that breath at the full tidal volume.

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

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