Oxygenation, Ventilation And Ventilator Management In The First 24 Hours
Ventilator Management
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Transcript of Ventilator Management
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Ventilator Management
Michael Schmitz, DO, MS
Emergency Medicine/Internal Medicine
October 10, 2007
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Objectives: To review differences in ventilator modes To review how to interpret ventilator settings
and readings
To discuss the protocol for assessing a
ventilated patient who is in distress
To review the pathophysiology of the
obstructive lung diseases To discuss guidelines for ventilator settings for
patients with obstructive lung disease
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25
0.6
14
5050
5
18
0.58
BUY EASY TIGER by RYAN ADAMS
*
*
*
*
*
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Nomenclature
A/C 600/14/50%/+5
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Volume Cycled Ventilation
A/C Ventilation
SIMV
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Pressure Cycled Ventilation
Pressure Support
(PSV)
Airway Pressure
Release (APRV)
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Flow Rate / I:E Ratio Flow Rate: a measure of the rate of delivery of
oxygen through the system to the patient.
(usually 60 liters per minute)
I:E Ratio: a measure of total inspiratory time toexpiratory time. (1:3) is ideal
Inspiratory time = Tidal Volume / Inspiratory flow
An increase in flow rate will shorten inspiratory time anddecrease I:E
Insufficient flow rates contribute to patient dyspnea
Insufficient expiratory time increases mean airwaypressure, the likelihood of barotrauma and auto-PEEP.
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Trigger Mode/Sensitivity Trigger Mode- (A/C)
Most common is pressuretriggering; the patient must
generate a sufficient NE
Tnegative airway pressure inorder to receive a breath
Sensitivity- the set
negative pressure thepatient must overcome toopen the demand valveand trigger a breath
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Flow Pattern
Constant (square)
Decelerating (ramp)-possibly better in
COPD
Sinusoidal
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PEAK VS. PLATEAU PRESSURES
Peak Pressure:Pressure at the end of inspiration.
Determined by inflation volume, airway resistance
and the elastic recoil of the lungs and chest wall
Plateau Pressure: Measured when airflow is
stopped. It is directly proportional to the elasticity of
the lungs and chest wall
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PEAK VS.
PLAT
EAUP
RESSURES
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**
*
25
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Positive End-Expiratory
Pressure
PEEP: an elevation in
alveolar pressure
above atmospheric
pressure at the end ofexhalation
Extrinsic PEEP(ePEEP): applied
through a mechanical
ventilator
ACV without PEEP
ACV with PEEP
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Positive End-Expiratory Pressure
improves gas exchange by
opening small airways inthe dependent lung zonesand distributing inspiredgas homogeneously.
decreases expiratory flow
limitation and dynamichyperinflation.
decreases oxygenconsumption
Physiologic:(3-5 cm H20) overcomes the decreasein functional residual capacity due to endotracheal
intubation (glottis has been bypassed):
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Positive End-Expiratory
PressureSupraphysiologic PEEP:(>5 cm H20)
Offsets auto-PEEP in patients with obstructivelung disease
Improves oxygenation in patients with hypoxemicrespiratory failure
Improves oxygenation and cardiac performancein patients with cardiogenic pulmonary edema
Caution in: focal lung disease, pulmonary embolism,hypotension, patients with increased ICP, hypovolemia,bronchopleural fistula
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Positive End-Expiratory
Pressure
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Auto-P
EEP
Intrinsic PEEP(iPEEP, aka occult, vent-
associated) occurs because of incompleteventilation: Initiating a new breath prior to
complete exhalation causes air-trapping
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Auto-P
EEP
Causes: high minute
volume ventilation,
expiratory flow
limitation or increasedexpiratory resistance
Hypoxemia,
hypotension and
barotrauma can occur
as a result
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Auto-PEEP
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PEEP
Applying PEEP can decrease the magnitude of
negative pressure that the patient must generate to
trigger the ventilator, which reduces work done by
the muscles of inspiration
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Consequences of MV Positive pressureventilation preferentiallyinflates the more compliant,non-dependent upper lung
zones Uneven gas distribution
contributes to barotraumaand auto-PEEP, with apreference for damaging
normal alveoli Occurs in ARDS, asthma
and chronic interstitial lungdisease
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Consequences of MV Barotrauma causes
damage to adjacent
alveoli via stretching andshearing forces.
High peak airway
pressures are directly
correlated with
barotrauma
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Consequences of MV Complications of
alveolar rupture can be
devastating: Pulmonary interstitial
emphysema
Pneumomediastinum
SQ Emphysema Pneumothorax
Pneumoperitoneum
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Ventilator Synchrony
Setting the ventilator to cycle with the patients respiratory
rhythm
Requires close patient monitoring
Try to prevent ineffective triggering
Adjust oxygen flow rate in proportion to tidal volume
* may increase peak airway pressure Adequate sedation is critical
Any increased sense of effort (fatigue vs. forced exhalation) on the
part of the patient contributes to sensation of dyspnea
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CaseP
resentation 65 year-old man BIBEMS
c/o increasing dyspnea
over3 days associated with
temperature of100.3 andincrease in thickened,
green sputum. He has a
history of emphysema, is
on home oxygen and hasbeen using his inhalers
without relief.
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The Decision
To Intubate
Initiation of mechanical ventilation in COPD
patients is associated with high patient mortality
and poor potential for weaning
Indications:(E.B.M. vs. clinical gestalt)
Patient failed conservative management
Severe, persistent acidosis
Continued arterial hypoxemia despite initial therapy
Patient fatigue
Altered mental status
Additional major illness (pulmonary embolism, AMI)
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The usual vent settings are applied
Some time passes.
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5
60
0.6
14
50%
*
*
*
*
*
63
3:1
0.24
WARNING: LOW EXHALED VOLUME
*
*
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Respiratory Distress in MV Ventilator: Malfunction or Circuit Leak
Ventilator: Inadequate ventilator settings: Inadequate Tidal volume, FiO2, Flow rate, Positive end
expiratory pressure (PEEP) or over/undersensitivity
Airway:(increased Ppeak-Pplat) ENDOTRACHEAL TUBE MIGRATION, patient biting
tube, balloon cuff leak, deflation or rupture Bronchospasm, increased airway resistance imposed by
heat and moisture exchanger, obstruction by secretions,blood or foreign object
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Respiratory Distress in MV Lungs:(Ppeak-Pplat unchanged or
decreased): pneumonia, atelectasis,pulmonary edema, aspiration of gastric
contents, pneumothorax, pleural effusion,pulmonary embolus,ENDOTRACHEAL TUBE MIGRATION!
Extrapulmonary: Abdominal distension,delerium, anxiety, pain, stroke, seizure
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Respiratory Distress in MV
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What to Do?
Protocol
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*
50
*
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Goals for CO
PD patients
Adequate patient monitoring
Optimize ventilator settings to minimize
excessive work of breathing Assure Synchrony
Detect auto-PEEP and prevent barotrauma
Prevent further respiratory muscle atrophy Intubate using the widest diameterET tube
possible (R = 8nl / r4)
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ObstructiveLung Diseases
Asthma
Chronic bronchitis
Emphysema
Congenital bullous
lung disease
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Pathophys COPD
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Pathophys Emphysema
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VentG
uidelines Emphasis on assisted modes of ventilation
(patient initiated), institution preference for
A/C vs. IMV with PSV (to overcome ET tube)
SIMV: probably causes excess work, b/c of
high resistance circuit but debatable;
requires close patient monitoring
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Vent Guidelines
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VENTGuidelines
Higher flow rates are highly beneficial
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VentG
uidelines
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VentG
uidelines Tidal Volume:5-7 ml/kg
Set Rate: 4 less than spontaneous rate
FiO2: adjust to PaO2 of at least 60 mmHg
Triggering:-1 to -2 cm H2O
Prevent Auto-PEEP with sufficient PEEP
Flow rate: Increase to provide increased expiratory
time (70-90 lpm)
Continue inhaled medications: requires sufficient
tidal volume and inspiratory time
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Pathophys Asthma
Airway narrowing causedby smooth musclecontraction, wall thickeningand increased secretionscombine to reduce air flowrates
Primarily a disease of theAIRWAYS with decreased
elastic recoil of the lungsduring attack
ABG for PaCO2 to identifyrespiratory failure
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Pathophys Asthma
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Vent Settings Asthma Respiratory rate 10 to 14 breaths/min
(allows more time for exhalation)
Tidal volume less than 8 mL/kg Minute ventilation less than 115 mL/kg
Inspiratory flow of 80 to 100 L/min
Extrinsic postive end-expiratory pressureless than 80 percent of the intrinsic PEEP
Continue inhaled medications and steroids
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Vent Settings Asthma Intubate with largest diameter tube possible!(8.0 mm and up)
F
irst priority is to minimize auto-PEEPand keep plateau pressures low!
Lower respiratory rate and tidal volume maybe necessary causing PaCO2 to increase
(permissive hypercapnia) Sedation, then paralysis to force synchrony
Heliox
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Osteopathic Considerations Findings reflect anatomical changes related
to increased lung volumes and impairedventilation
Thoracic Vertebral Dysfunction
Rib Dysfunction (stuck in exhalation)
Diaphram Dysfunction (stuck down)
Law of LaPlace T = Pr Lymphatic obstruction: lymphatic drainage
impaired by positive pressure
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Summary
The need to initiate mechanical ventilation in patients with
obstructive lung disease in the emergency department isassociated with a higher inpatient mortality
Patients with obstructive lung disease require closemonitoring of all physiologic parameters to preventcomplications associated with positive pressure ventilation
Assessing a distressed ventilator dependent patient requiresan organized approach
In general: low tidal volumes, higher flow rates andapplication of a conservative amount ofPEEP are appropriateinitial settings for patients with obstructive lung disease
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References The ICU Book Marino PL, 2nd Edition Respiratory Physiology West JB, 5th Edition
Pulmonary Pathophysiology Grippi MA Textbook of Medical Physiology Guytonand Hall 9th Edition
Chest Radiology Companion Stern EJ,
White CS Harrisons Principles of Internal Medicine 16th
Edition
R f
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References
www.utdol.com :
principles of mechanical
ventilation, alternate modes of
mechanical ventilation,
positive end expiratorypressure, pathophysiologic
consequences of positive
pressure ventilation,
mechanical ventilation in acute
respiratory failure complicatingCOPD, mechanical ventilation
in adults w/ status asthmaticus
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