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Risks and Complications of
Mechanical Ventilation
Ewan C. Goligher MD PhD
Assistant Professor of Medicine, University of Toronto
Attending Physician, MSICU, Toronto General Hospital
Scientist, Toronto General Hospital Research Institute
Disclosures
• Conflicts of Interest
– Equipment from Timpel
– Equipment and personal fees from Getinge
Modern Mechanical Ventilation Saves Lives
Lassen HCA Lancet 1953
West JB JAP 2005
Risks and Complications
• Hemodynamic effects
• Ventilation-induced lung injury
• Ventilator-induced diaphragm dysfunction
Hemodynamics: Heart-Lung Interactions
Venous return
Hemodynamics: Right Ventricle
Venous return
Hemodynamics: Right Ventricle
Jardin et al Intensive Care Med 2007
Hemodynamics: Right Ventricle
Repessé et al Chest 2015
Hemodynamics: Left Ventricle
Ventilation-Induced Lung Injury
Webb & Tierney ARRD 1974
0
14
45
Ventilation-Induced Lung Injury
Slutsky & Ranieri NEJM 2013
Ventilation-Induced Lung Injury
Slutsky & Ranieri NEJM 2013
Ventilation-Induced Lung Injury
volume at or below 6 ml per kilogram, a high PEEP,
and permissive hypercapnia. The mortality rate at
28 days was significantly lower with protective ven-
tilation than with conventional ventilation (38%
vs. 71%). There was also significantly less clini-
cal barotrauma and a significantly higher rate of
weaning from ventilation in the protective-venti-
lation group. Although some criticized this study
for the high mortality rate in the conventional-ven-
tilation group, the patients studied were extremely
ill (with failure of a mean of 3.6 organs per pa-
tient).
In a subsequent, larger study by the Acute Re-
spiratory Distress Syndrome Network (ARDSNet),
jor goal of the ventilatory strategy was to keep the
plateau airway pressure below 30 cm of water;
therefore, the group that underwent ventilation at
6 ml per kilogram of predicted body weight is of-
ten referred to as the low-stretch group. The low-
stretch strategy was associated with a significantly
lower mortality rate (31%, vs. 40% with ventilation
at 12 ml per kilogram of predicted body weight).
Therefore, the best available evidence is for a ven-
tilation strategy using a tidal volume of 6 ml per
kilogram of predicted body weight for patients
with acute lung injury or ARDS.
Three other small, randomized trials, per-
formed during the same period, failed to demon-
Figure 2. Conventional Ventilation as Compared with Protective Ventilation.
This example of ventilation of a 70-kg patient with ARDS shows that conventional ventilation at a tidal volume
of 12 ml per kilogram of body weight and an end-expiratory pressure of 0 cm of water (Panel A) can lead to alveolar
overdistention (at peak inflation) and collapse (at the end of exhalation). Protective ventilation at a tidal volume
of 6 ml per kilogram (Panel B) limits overinflation and end-expiratory collapse by providing a low tidal volume
and an adequate positive end-expiratory pressure. Adapted from Tobin.18
Ventilation-Induced Lung Injury
Ventilator
Abdomen
PL = Pairway - Ppleural
Monitoring
Lung-Protective Ventilation
• Aim for lower tidal volumes in patients with ARDS
– Vt ≤6-8 ml/kg predicted body weight
• Minimize the pressure applied to the lung
– Driving pressure ≤15 cm H2O
– Plateau pressure ≤30 cm H2O
• Avoid excessive respiratory efforts
– Pocc <15 H2O
– P0.1 <3.5 cm H2O
Ventilator-Induced Diaphragm Dysfunction
Introduction
are generally provided with positive-pressure
l ventilation when their own ventilatory capa-
outstripped by the demands imposed by various
tes (Fig. 1). Positive-pressure mechanical ven-
necessary delays in this withdrawal process increase the
complication rate of mechanical ventilation (eg, pneumo-
nia, discomfort) and drive up cost. Aggressiveness in re-
moving ventilatory support, however, must be balanced
against the risks of prematurely withdrawing that support,
including difficulty in re-establishing the artificial airway,
elationship between patient capabilities and demands. When demands outstrip the capabilities, the balance swings to the left
evel of ventilatory support is required. As the patient recovers, the balance shifts rightward. The clinical challenges during this
-fold: (1) recognize when ventilatory assistance is no longer necessary, and (2) provide appropriate levels of assistance until that
T ! compliance of the lungs and thorax. Raw ! airway resistance. V̇A ! alveolar ventilation. V̇CO2
! carbon dioxide production.
en consumption. V̇D ! dead-space volume. (Adapted from Reference 1.)
RESPIRATORY MECHANICS IN THE PATIENT WHO IS WEANING FROM THE VENTILATOR
De Troyer and Loring, Handbook of Physiology
Ventilator-Induced Diaphragm Dysfunction
The new engl and jour nal o f medicine
AUTHOR:
FIGURE:
4-C
RETAKE
SIZE
ICM
CASE
EMail Line
Revised
REG F
1st
2nd
3rd
Levine
1 of 4
ARTIST: ts
Control
Case
Fiber Size
Slow Myosin
Heavy Chain
Fast Myosin
Heavy Chain
B
A
D
C
F
E
50 µm
50 µm
50 µm
50 µm
50 µm
50 µm
Figure 1. Comparison of Representative Case and Control Diaphragm-Biopsy
Specimens with Respect to Fiber Size.
The slow-twitch and fast-twitch fibers in the case specimens (Panels A, C,
and E) are smaller than those in the control diaphragms (Panels B, D, and F).
Panels A and B (hematoxylin and eosin) show that neither inflammatory
6000
5000
4000
3000
1000
2000
0
P=0.001
P=0.0
100
80
60
40
20
P=0.11
P=0.1
Control (N=
Case (N=14)
Levine et al N Engl J Med 2008
Control specimen Resistive loading specimen
Ventilator-Induced Diaphragm Dysfunction
Reid et al. J Appl Phys 1994
Goligher et al. AJRCCM 2015
Ventilator-Induced Diaphragm Dysfunction
Monitoring
Diaphragm-Protective Ventilation
• Minimize duration of passive ventilation
• Aim for resting effort level
– Clinical trials awaited
• Lung protection > diaphragm protection
Summary: Risks and Complications
• Hemodynamic effects
• Ventilation-induced lung injury
• Ventilator-induced diaphragm dysfunction
EWAN.GOLIGHER@UTORONTO.CA
Questions?

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Wed risks and-complications_of_mv

  • 1. Risks and Complications of Mechanical Ventilation Ewan C. Goligher MD PhD Assistant Professor of Medicine, University of Toronto Attending Physician, MSICU, Toronto General Hospital Scientist, Toronto General Hospital Research Institute
  • 2. Disclosures • Conflicts of Interest – Equipment from Timpel – Equipment and personal fees from Getinge
  • 3. Modern Mechanical Ventilation Saves Lives Lassen HCA Lancet 1953 West JB JAP 2005
  • 4. Risks and Complications • Hemodynamic effects • Ventilation-induced lung injury • Ventilator-induced diaphragm dysfunction
  • 7. Hemodynamics: Right Ventricle Jardin et al Intensive Care Med 2007
  • 10. Ventilation-Induced Lung Injury Webb & Tierney ARRD 1974 0 14 45
  • 13. Ventilation-Induced Lung Injury volume at or below 6 ml per kilogram, a high PEEP, and permissive hypercapnia. The mortality rate at 28 days was significantly lower with protective ven- tilation than with conventional ventilation (38% vs. 71%). There was also significantly less clini- cal barotrauma and a significantly higher rate of weaning from ventilation in the protective-venti- lation group. Although some criticized this study for the high mortality rate in the conventional-ven- tilation group, the patients studied were extremely ill (with failure of a mean of 3.6 organs per pa- tient). In a subsequent, larger study by the Acute Re- spiratory Distress Syndrome Network (ARDSNet), jor goal of the ventilatory strategy was to keep the plateau airway pressure below 30 cm of water; therefore, the group that underwent ventilation at 6 ml per kilogram of predicted body weight is of- ten referred to as the low-stretch group. The low- stretch strategy was associated with a significantly lower mortality rate (31%, vs. 40% with ventilation at 12 ml per kilogram of predicted body weight). Therefore, the best available evidence is for a ven- tilation strategy using a tidal volume of 6 ml per kilogram of predicted body weight for patients with acute lung injury or ARDS. Three other small, randomized trials, per- formed during the same period, failed to demon- Figure 2. Conventional Ventilation as Compared with Protective Ventilation. This example of ventilation of a 70-kg patient with ARDS shows that conventional ventilation at a tidal volume of 12 ml per kilogram of body weight and an end-expiratory pressure of 0 cm of water (Panel A) can lead to alveolar overdistention (at peak inflation) and collapse (at the end of exhalation). Protective ventilation at a tidal volume of 6 ml per kilogram (Panel B) limits overinflation and end-expiratory collapse by providing a low tidal volume and an adequate positive end-expiratory pressure. Adapted from Tobin.18
  • 16. Lung-Protective Ventilation • Aim for lower tidal volumes in patients with ARDS – Vt ≤6-8 ml/kg predicted body weight • Minimize the pressure applied to the lung – Driving pressure ≤15 cm H2O – Plateau pressure ≤30 cm H2O • Avoid excessive respiratory efforts – Pocc <15 H2O – P0.1 <3.5 cm H2O
  • 17. Ventilator-Induced Diaphragm Dysfunction Introduction are generally provided with positive-pressure l ventilation when their own ventilatory capa- outstripped by the demands imposed by various tes (Fig. 1). Positive-pressure mechanical ven- necessary delays in this withdrawal process increase the complication rate of mechanical ventilation (eg, pneumo- nia, discomfort) and drive up cost. Aggressiveness in re- moving ventilatory support, however, must be balanced against the risks of prematurely withdrawing that support, including difficulty in re-establishing the artificial airway, elationship between patient capabilities and demands. When demands outstrip the capabilities, the balance swings to the left evel of ventilatory support is required. As the patient recovers, the balance shifts rightward. The clinical challenges during this -fold: (1) recognize when ventilatory assistance is no longer necessary, and (2) provide appropriate levels of assistance until that T ! compliance of the lungs and thorax. Raw ! airway resistance. V̇A ! alveolar ventilation. V̇CO2 ! carbon dioxide production. en consumption. V̇D ! dead-space volume. (Adapted from Reference 1.) RESPIRATORY MECHANICS IN THE PATIENT WHO IS WEANING FROM THE VENTILATOR De Troyer and Loring, Handbook of Physiology
  • 18. Ventilator-Induced Diaphragm Dysfunction The new engl and jour nal o f medicine AUTHOR: FIGURE: 4-C RETAKE SIZE ICM CASE EMail Line Revised REG F 1st 2nd 3rd Levine 1 of 4 ARTIST: ts Control Case Fiber Size Slow Myosin Heavy Chain Fast Myosin Heavy Chain B A D C F E 50 µm 50 µm 50 µm 50 µm 50 µm 50 µm Figure 1. Comparison of Representative Case and Control Diaphragm-Biopsy Specimens with Respect to Fiber Size. The slow-twitch and fast-twitch fibers in the case specimens (Panels A, C, and E) are smaller than those in the control diaphragms (Panels B, D, and F). Panels A and B (hematoxylin and eosin) show that neither inflammatory 6000 5000 4000 3000 1000 2000 0 P=0.001 P=0.0 100 80 60 40 20 P=0.11 P=0.1 Control (N= Case (N=14) Levine et al N Engl J Med 2008
  • 19. Control specimen Resistive loading specimen Ventilator-Induced Diaphragm Dysfunction Reid et al. J Appl Phys 1994
  • 20. Goligher et al. AJRCCM 2015 Ventilator-Induced Diaphragm Dysfunction
  • 22. Diaphragm-Protective Ventilation • Minimize duration of passive ventilation • Aim for resting effort level – Clinical trials awaited • Lung protection > diaphragm protection
  • 23. Summary: Risks and Complications • Hemodynamic effects • Ventilation-induced lung injury • Ventilator-induced diaphragm dysfunction