25- IMV 2 .pptx

Inavsive mechanical ventilation 2
WHO Health Emergencies program (WHE)

Learning objectives
At the end of this lecture, you will be able to:
• Manage mechanically ventilated patient with ARDs, Asthma , COPD.
• Know Respiratory Care, Setup, & Monitoring.

Choosing a mode of mechanical ventilation depends on:
• The reason it is required.
• The underlying disease process.
• In general, AC is used as the initial mode for a patient needing invasive mechanical ventilation.
Choosing a mode and initial ventilator settings

A previously healthy 46-year-old woman presents to the hospital and reports a cough, sputum production,
and a fever of 4 days’ duration. An admission chest radiograph reveals a developing infiltrate in the left
lower lobe. The man is admitted to the general ward and started on antibiotics for community-acquired
pneumonia. Less than 24 hours later, the patient continues to deteriorate and requires oxygen at 15 L/min
om mask bag. He is not in obvious respiratory distress; however, pulse oximetry reveals severe hypoxemia
(83% to 89% on supplemental oxygen, 10 L/min). Sputum cultures pending , and a new chest radiograph
reveals new, diffuse bilateral alveolar infiltrates. The patient is intubated because of worsening hypoxemia.
• What initial ventilator settings would you use for this patient?
• What steps should be taken to minimize barotrauma during ventilation?
• What parameters should be measured and monitored?
Case study

ARDS is a heterogenous disease
VT diverted from injured units to over distend healthier units
Source: https://www.futuremedicine.com/doi/10.2217/17455111.2.3.301

• The primary goal of mechanical ventilation is to prevent ventilator-induced lung injury (VILI).
Mechanical ventilation
Source: NEJM.org
• Barotrauma e.g., pneumothorax.
• Volutrauma.
• Atelectrauma.
• Biotrauma.
• Oxygen toxicity.

The ventilator settings should be adjusted to ensure adequate gas exchange without causing ventilator-induced
lung injury (VILI).
The factors that promote VILI are:
1. Hyperinflation during inspiration induced by large VTs and high end-inspiratory pressures.
2. Alveolar collapse during expiration and repeated alveolar opening and closing during each breath promoted
by low pressures during expiration. (atelectrauma).
3. Driving pressure (plateau pressure – PEEP) was a major determinant of outcome driving (> 14 cm H2 O was
associated with poor outcomes). In addition, , it has been suggested that the mechanical power transferred to
the respiratory system from the ventilator plays a key factor in VILI. This means that not only the strain
(change in lung volume) but both high flow and respiratory rate are potentially harmful to the lungs.

Target of mechanical ventilation (lung protective ventilation):
1. Low VTs.
2. High PEEP levels.
3. Strict monitoring of plateau pressure to avoid exceeding 30 cm H2O.
Oxygenation:
• No studies have shown that increasing PaO2 improves outcome.
• SpO2 between 94% and 98% may improve outcomes compared to conventional therapy maintaining
SpO2 around 97%.

VILI can be reduced by Lung protective stratgy

• Intubation should not be delayed.
Respiratory indications:
• RR>35-40 breaths/min and there are clinical signs of respiratory distress.
• Severe hypoxemia defined as PaO2 < 60 mm Hg or SpO2 < 90% despite high FiO2.
• Respiratory acidosis.
• Copious secretions.
• Other indications for intubation.
Non-respiratory indications:
• Altered consciousness.
• The occurrence of shock.
Invasive mechanical vetilation
Indications for invasive mechanical ventilation:

• Volume-controlled ventilation (VCV) is the most commonly used mode of ventilation in ICU.
• No data to demonstrate a difference in outcomes between VCV and pressure-controlled ventilation
(PCV).
• In both VTs and end-inspiratory plateau pressure should be limited and continuously monitored.
• The main advantage of VCV is respiratory mechanics monitoring.
Which mode of MV is better for ARDS

1. VCV
How to monitor plateau pressure

Source: Plateau pressure during pressure control ventilation
Simone Sosio , Giacomo Bellani 2019
2. PCV by inspecting the flow signal.
If end-inspiratory flow is nil the pressure set at the
ventilator in PCV is the plateau pressure.
If it is still positive, a resistive pressure is included, which
can be calculated by performing an end-inspiratory
occlusion manually.
The end-inspiratory plateau pressure cannot exceed the
set inspiratory pressure in PCV.
How to monitor plateau pressure?

Relation between plateau pressure and mortality rate

Adjustment of ventilatory settings
1. Adjustment of VT.
2. Adjustment of PEEP.
3. Adjustment of flow rate.

1. Adjustment of VT:
The VT should be adjusted to 6 ml/kg predicted body weight.
It has been shown that a high driving pressure exceeding 14 cm H2 O was
associated with poor outcomes.
know whether or not VT should be reduced below 6 ml/kg to decrease the
driving pressure.
To estimate predicted body weight:
Males: 50 + 2.3 (height in inches –60) or 50 + 0.91 (height in cm – 152.4).
Females: 45.5 + 2.3 (height in inches –60) or 45.5 + 0.91 (height in cm – 152.4).

• PEEP is the airway pressure at the end of expiration:
• recruits atelectatic lung to prevent atelectrauma.
• Challenge is in determining “how much PEEP” for the heterogenous ARDS lung.
• High PEEP levels around 15 cm H2 O may improve survival in ARD.
• The methods used to adjust PEEP in these trials were either to follow a PEEP/FiO2 table
or to maintain plateau pressure below 28-30 cm H2O.
2. Adjustment of PEEP:

• Set PEEP corresponding to severity of oxygen impairment:
• Titrate the FiO2 to the lowest value that maintains target SpO2 88–93%.
• Set corresponding PEEP, based on individual.
• Higher PEEP for moderate-severe ARDS.
Source: www.ardsnet.org

• When high PEEP levels are used ,be cautious:
• Earlier application of low tidal volume and the appropriate level of PEEP will minimize risk.
• Hypotension due to decreased venous return to right heart.
• Over-distension of normal alveoli and possible ventilator-induced lung injury and increase in
dead space ventilation.

During VCV, flow rate around 60 L/min usually suffices to meet the patient’s ventilatory demand
and this setting can be used as a default value.
3. Adjustment of flow rate:

Mechanical Ventilation in Acute Respiratory Distress
Syndrome summary (LPV)
Goals:
• PaO2: 55-80 mm Hg (7.3-10.7 kPa).
• Pplat: ≤30 cm H2O.
• VT: 4-6 mL/kg PBW.
• pH: >7.15 is acceptable.
1. Start with Assist-Control with VT of 8 mL/kg PBW.
2. Decrease by 1 mL/kg over the next 4 hours until VT of 4-6 mL/kg is reached.
3. If Pplat is >30 cm H2O, decrease VT by 1 mL/kg until VT is 4 mL/kg or arterial pH reaches 7.15.
4. If using VT of 4 mL/kg and Pplat is <25 cm H2O, VT can be increased by 1 mL/kg until Pplat is 25
cm H2O or VT is 6 mL/kg.

Mechanical Ventilation in Acute Respiratory Distress
Syndrome summary (LPV)
5-If a Pplat of ≤30 cm H2O has been achieved with a VT >6 mL/kg and a lower VT is clinically problematic
(i.e., need for increased sedation), it is acceptable to maintain the higher VT.
6- Initiation of PEEP in Acute Respiratory Distress Syndrome.
• Initiate PEEP at 5 cm H2O and titrate up in increments of 2-3 cm H2O.
• Full recruitment effect may not be apparent for several hours.
• Monitor blood pressure, heart rate, and PaO2 or pulse oximetry during PEEP titration.
• Optimal PEEP settings are typically 8-15 cm H2O.

A 31-year-old man with a history of asthma is intubated and admitted to
the ICU for an acute asthma exacerbation. Peak airway pressure on
admission was 42 cm H2O, and Pplat was 24 cm H2O immediately after
intubation; however, 6 hours later, peak airway pressures have arisen to 53
cm H2O while the Pplat has remained the same.
• What is the likely etiology of her high peak airway pressures in the
setting of unchanged plateau pressures?
• What adjunctive therapies, in addition to ventilator support, does this
patient need to reduce the elevated airway pressures?
Case study

Pathophysiology of acute exacerbation of
COPD and asthma
• Dynamic hyperinflation.
• Respiratory muscle dysfunction.
• Inefficient gas exchange.
• Cardiovascular abnormalities.

Failure of the respiratory system to return to the elastic equilibrium volume (PEEPi)
In COPD and asthma consequences is sever and may lead to hypotension and can be life-threatening.
Causes leading to DH are:
• High expiratory airway resistance, combined with expiratory flow limitation.
• Low elastic recoil (emphysema).
• High ventilatory demands
• Short expiratory time due to tachypnoea.
Dynamic hyperinflation (DH)

Consequences of dynamic hyperinflation during
acute exacerbation of COPD and asthma
• Always consider hyperinflation in the mechanically
ventilated patient with hypotension, especially if
obstructive lung disease is present.
• Briefly disconnect the ventilator and hypotension
will rapidly improve

Airflow obstruction increases the work of breathing
• No auto- PEEP (PEEPi).
• Minimal inspiratory pressure change
required (‘trigger’ work) to initiate inspiration .
• With auto- PEEP (PEEPi).
• Pressure change required t o initiate inspiration
(‘trigger’ work) is evidently increased
• Alveolar pressure and flow curves during spontaneous breathing
Source : SARI ToolKit 2nd Edition

• Relieve excessive dyspnoea
• Improve gas exchange
• Sustain alveolar ventilation
• Unload respiratory muscles
Mechanical ventilatory goals in Asthma And COPD:

Non-invasive mechanical ventilation (NIMV) in COPD
Physiological effects NIMV failure
Decreased work of breathing Counterbalance
PEEPi Improve gas exchange.
Worsening pH and/or respiratory rate after 2-4
hours of BiPAP therapy Failure to tolerate BiPAP.
Deterioration in mental status.
Inability to manage secretions.
Hypotension.
Uncorrected hypoxaemia.
No change in both pH and respiratory rate at 2-4
hours.

Non-invasive mechanical ventilation (NIMV)
Physiological effects NIMV failure
• May have a direct bronchodilating effect.
• Minimise dynamic hyperinflation by
offsetting intrinsic PEEP Recruit collapsed
alveoli.
• Improve ventilation/perfusion mismatch.
• Reduces the work of breathing.
• Tachypnoea RR >25/min.
• Tachycardia 110/min.
• Use of accessory muscles of respiration.
• Hypoxia with a PF ratio >200 mmHg.
• Hypercapnia with PaCO2>45 mmHg / 6kPa.
• FEV1 <50% predicted

Non-invasive mechanical ventilation In COPD and
Asthma Practical aspects:
• The patient must be seated and reassured.
Choose a face mask appropriate for patient’s face shape/size.
BiPAP (IPAP/ EPAP) is the preferred initial mode:
Titrate PEEP by increments of 1–2 cmH2O according to patient’s comfort (observe and assess
ineffective triggering attempts)
Titrate IPAP by increments of 2 cmH2O to patient’s comfort, respiratory rate (≤25/min) and tidal
volume (6–8 mL/kg), avoid total airway pressure above 20 cmH2O.

Proposed initial settings in controlled modes in patient with severe obstruction:
• Tidal volume <6 mL/kg.
• Respiratory rate 10 to 14 per minute.
• Inspiratory flow 70 to 100 L/min.
• Consider the application of low level of PEEP (<5 cmH2O).
Invasive mechanical ventilation

The main principles to decrease dynamic hyperinflation in patients on controlled
modes are:
1. Providing controlled hypoventilation : the most effective measure to DH , Achieved By:
• Decreasing dead space (using a heated humidifier (HH) instead of heat and moisture filter)
• Decreasing in CO2 production (by avoiding hyperthermia, reduction of carbohydrate intake
and providing adequate sedation and analgesia).
Decreasing dynamic hyperinflation in patients
on controlled modes

2. Prolongation of the expiratory time :
• Increasing peak inspiratory flows.
• Shortening inspiratory time.
• Eliminating inspiratory pause time.
3. Decrease resistance to expiratory flows.
Decreasing dynamic hyperinflation in patients on
controlled modes

Respiratory Care, Setup, & Monitoring
Ventilator Setup (prior to connecting patients)
• Inspect all equipment for cleanliness or damage.
• Review circuit orientation, filters, & heat & humidification system.
• Ensure gas supply connected.
• Perform machine self-test with new patient and per manufacture
(ensure leak test included).
• Confirm initial settings and alarms.

Ventilator Performance
Perform Full Status Check q4h: (PIP, Pplat, VT , FiO2, auto-PEEP, Alarms, SpO2, ETCO2 in
addition to routine ICU monitoring).
• Evaluate vent & patient within 1h of ventilator settings changes.
• Wipe down ventilator with approved disinfection qShift.
Contingency Planning
• Ensure manual (i.e. bag valve resuscitator) ventilation device is operational and at beside along
with a face mask and PEEP valve.

Pulmonary, Endotracheal Tube & Circuit Hygiene
• Check cuff pressure and auscultate q12h to avoid over-inflation/leak
(<25 cmH2O); consider 'minimal occluding volume' in peds.
• Check inflation of pilot balloon to ensure it remains inflated.
• Reposition & secure endotracheal tube with skin checks q12h.
• Check ventilator circuit qShift for moisture accumulation (drainage);
change circuit only if damaged or gross contamination (Ventilator
Associated Pneumonia Prophylaxis -VAP PPx).
• Head of bed 30 degrees elevated for pneumonia prophylaxis (VAP
PPx).
• Oral hygiene with mouthwash & suctioning TID (VAP PPx).
• Consider continuous subglottic suctioning or q12h oropharyngeal
suctioning (VAP PPx).

Filters:
• All external filters should be inspected >daily (and after nebs).
• Replace viral filters as frequently as supplies allow in accord with the manufacturer’s
recommendations or if damaged/soiled (may last >1 week)
• For turbine & compressor ventilators, external inlet filters & fan filters must be cleaned at least
monthly. For ventilators that allow, bacterial/viral filters should be placed proximal to external
intake filters.
• Minimize instrumental/filter dead space.

Heat & Humidification:
• Active system: must use distilled or sterile water (~>500mL daily) to avoid infectious risk
and device damage; can be made on site or purchased; check H2O supply q12-24h.
• Passive heat moisture exchanger (HME): Only some HME include pathogen filter
capability; Many manufacturers suggest change q24h, but studies show that an unsoiled HME
in some circumstances can be used for 3-7 days.
Nebs decrease lifespan (and must be given via bypass or with HME removed from circuit).
Monitor for signs of an increased resistance (e.g. increase in PIP but no change in Pplat, or a
prolonged exp flow). Ensure at least 28-30 mgH2O/L efficiency.

Ventilator circuit , filter and humidifier locations
Source : SARI ToolKit 2nd edition

Respiratory Specific Monitoring:
• Continuous pulse oximetry, if unable then spot check as frequently as possible.
• Continuous capnography, if unable then spot check as frequently as possible,
especially after major ventilator settings changes.
• Auscultation performed routinely with checks.
• Skin/Mucosal Assessments qShift.

Abnormal flow waveforms during volume control ventilation

Abnormal pressure waveforms during volume
control ventilation

Factors influencing peak airway pressure

Source : FCCS 7th edition
Abnormal pressure waveforms during volume control ventilation

Complications of Mechanical Ventilation
• Ventilator Induced Lung Injury (VILI).
• Ventilator Induced Diaphragmatic Dysfunction (VIDD).
• Ventilator Associated Pneumonia (VAP).

Hypotension associated with initiation of
mechanical ventilation
A. Tension Pneumothorax.
B. Hemodynamic consequence of Conversion from Negative to Positive Intrathoracic Pressure :
common with dehydration.
C. Auto-PEEP.
D. D. Acute Myocardial Ischemia/Infarction.

Summary
• During mechanical ventilation, a patient must be closely monitored using the ventilator alarm
systems, continuous pulse oximetry, attentive physical assessment, measurement of inspiratory Pplat
(as clinically appropriate), and intermittent arterial blood gases and chest radiographs as needed.
• Guidelines for initiating mechanical ventilation should be carefully followed, with adjustments made
based on patient assessment and monitoring.
• High inspiratory plateau pressures are associated with a higher incidence of ventilator-induced lung
injury and should be maintained below 30 cm H2O.
• Hypotension occurring immediately after initiation of invasive mechanical ventilation should prompt
evaluation for tension pneumothorax, decreased venous blood return because of intrathoracic
pressure, auto-PEEP, or myocardial ischemia.

References :
Clinical care of severe acute respiratory infections – Tool kit COVID-19 adaptation, update 2022 https://www.who.int/p
European Society of Intensive Care Medicine (ESICM) Academy ACE modules
https://academy.esicm.org/course/view.php?id=312
Society of Critical Care Medicine Fundamental Critical Care Support course (FCCS 7th Edition).
• SARI CLINICAL CARE TRAINING
• https://www.futuremedicine.com/doi/10.2217/17455111.2.3.301
• www.ardsnet.org
• Sosio S, Bellani G. Plateau Pressure during Pressure Control Ventilation. abtpn [Internet]. 2019 Oct. 22
;6(1):76-7. Available from: https://journals.aboutscience.eu/index.php/aboutopen/article/view/297

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