respiratory failure & mechanical ventilation

Respiratory Failure & Respiratory Failure & Mechanical Mechanical VentilationVentilation

Dr Sigal Sviri Medical ICU

ContentsContents

Definitions in respiratory failure Oxygen therapy Non-invasive ventilation Indications for intubation Technique Modes of Ventilation (pros and cons) Evaluating & Monitoring ventilated

patients Ventilation in clinical situations Weaning from mechanical ventilation

Acute respiratory failure

Acute respiratory failure can be defined as the relatively sudden onset of failure of the respiratory system to carry out its major functions (i.e the adequate delivery of oxygen into and adequate removal of CO2 from the arterial blood) to a degree that cause a threat to life.

A syndrome marked by abnormal physiologic functions that can be caused by a variety of disease processes.

Respiratory Failure

Hypercarbic – type II (reduced ventilation)

Hypoxic type I (reduced gas exchange)

Mixed

Respiratory FailureRespiratory Failure –– Failure to adequately maintain gas

exchange:

Respiratory Failure

Failure to oxygenate Failure to ventilate

LUNG FAILURE CNS AirwaysPeripheral nerves

Alveolar component

Blood vessels

Multiple Systems are Involved in Successful Ventilation

Ventilation Failure

CNS- reduced drive:

Neuromuscular:

Musculoskeletal:

Airways:

Narcotic overdose CVA, ICH, SAH Head trauma Guillain-Barre Myasthenia gravis Spinal cord injury Kyphoscoliosis Flail chest Hemo/pneumothorax Upper airway

obstruction/edema Asthma/COPD

Causes of Respiratory Failure

Alveoli & Capillaries:

Pneumonia Pulmonary edema ARDS Interstitial lung dis Pulmonary

Embolism

Gas exchange

PaO2 = 150PCO2 = 0.4

PaO2 = 106PaCO2 = 40

PaO2 = 40

PaCO2 = 46

PaO2 =100

PaCO2 = 40

DefinitionsDefinitions

Dead space Shunt Compliance Resistance Work of breathing FRC

V/Q Ratio

The balance between pulmonary ventilation and capillary blood flow.

Under normal conditions ventilation and perfusion are matched and V/Q=1.

Dead space and shunt are examples of V/Q mismatch.

V/Q Ratio

West zones of the lung

(PA > Pa > Pv)

(Pa > PA > Pv )

(Pa > Pv > PA )

V/Q Mismatch

DEAD SPACE (V/Q > 1.0)

Anatomic dead space. The volume of the lung (including the mouth, pharynx, larynx, trachea, bronchi, artificial tubing) which is not involved in gas exchange.

Physiological dead space.Anatomical dead space plus alveolar dead space.Alveolar dead space – areas in the lung which are ventilated but not perfused (VQ mismatch)

DEAD SPACE (V/Q>1)יותר אוורור מאשר פרפוזיה

In normal lungs, dead space (Vd) accounts for 20-30% of total ventilation (Vt):

Vd/Vt=0.2-0.3 Increased Vd/Vt causes hypoxemia and

hypercapnea. Hypercapnea is significant when

Vd/Vt>0.5.

Vd = PaCO2-ETCO2Vt PaCO2

DEAD SPACE

Lung apices Emphysema Positive pressure Hypovolemia Shock Decreased blood

flow

DEAD SPACE (V/Q>1)

Dead space ventilation

increases:

ירידה בתפוקת הלב

(heart failure, pulmonary

embolism).

הרס מבנה האלבאולים

(emphysema)

ניפוח יתר של האלבאולים

(positive pressure ventilation)

VQ MISMATCH SHUNT (V/Q<1)

Blood does not participate in gas exchange:

True shunt – anatomical shunt between right & left heart

Physiologic shunt: איזוריםבריאה שאינם מאווררים

Capillary blood flow to areas of shunt does not participate in gas exchange and does not equilibrate with alveolar gas.

Venous admixture (V/Q<1)פחות אוורור מאשר פרפוזיה

Partial occlusion Venous admixture –

דם לא מחומצן חוזר מהריאות ומתערבב עם דם מחומצן

Because there is some ventilation, increasing FiO2 minimally increases PaO2 (shunt<50%).

שיפור בחמצון עד רמה מסויימת

SHUNT (V/Q=0)מצב אבסולוטי

Areas of NO ventilation (fully collapsed lung)

Causes : Occlusion of small airways (asthma) Alveoli are filled with fluid (pulmonary

edema, ARDS, pneumonia) The alveoli are collapsed (atelectasis) Blood is unchanged (PaO2 is 40 mmHg) The hypoxemia CANNOT be corrected by

increasing FiO2 Well ventilated areas cannot compensate

because Hb is fully saturated Adequate oxygenation can only be

established by restoring ventilation by recruitment and PEEP

V/Q MISMATCH

V/Q mismatch: summary

חמצן100%תגובה ל-

בנוכחותSHUNT אין תיקון מלא של החמצון בתגובה

קטןSHUNTלחמצן אלא אם כן ה-

בנוכחותVQ MISMATCH או ירידה בדיפוזיה, חמצן יתקן

באופן מלא או חלקי תלוי בחומרת המצב

בלבד, חמצן תמיד יתקן את החמצון היפוונטילציהבנוכחות

אך אינו הטיפול המומלץ!

Pulmonary vasoconstriction

The lung can improve shunt by vasoconstriction of blood vessels in less ventilated areas

May cause pulmonary hypertension

FRC- Functional Residual Capacity

The amount of air remaining in the lungs after a normal quiet expiration (i.e. expiratory reserve volume + residual volume).

If lung volumes are less than FRC, work of breathing is increased.

Recognizing Respiratory Failure

Vital Capacity - The volume of gas that can be forcefully exhaled after maximal inspiratory effort.

Vital Capacity -Reflects patient’s strength and reserve.

Compliance

Distensibility (flexibility) of the lung (& chest wall) during inspiration

The change in volume caused by a change in pressure

COMPLIANCE - The distensibility of the lung

The normal lung+thorax compliance of an adult

is

100 mL/cm H20.

When the compliance is low, more pressure will

be needed to deliver a given volume of gas to a

patient.

Peak pressures will be high!

Compliance = change in volume change in pressure in mL/cm H20.

Decreased compliance occurs in:

ARDS, pulmonary edema, pneumonia, atelectasis, pleural effusion, pulmonary fibrosis and interstitial lung disease.

•Emphysema is a typical

cause of increased lung

compliance.

V/P CurveV/P Curve

RESISTANCE- The resistance of the airways to flow


Obstruction/narrowing of the airways and resistance to the flow of air

The flow of air causes high pressure


The normal value for an adult is around 0.5 - 1.5 cm H20/L/sec

Increased airway resistance occurs in: asthma, COPD (acute), emphysema with airway collapse, mucus plugging, endobronchial obstruction either from tumors or foreign bodies, blocked tube.

Resistance = change in pressure flow in cm H20/L/second

Restrictive lungs

דלקת ריאותבצקת ריאותתמטמחלת ריאות אינטרסטיציאליתARDSעודף משקל ניכרחזה אויר

Obstructive lung disease

אסטמהCOPDאמפיזמה

Work of Breathing

Energy requirements of intercostal muscles and diaphragm.

Increased resistance, reduced compliance, rapid shallow breathing increase work of breathing.

Increased work of breathing may cause lactic acidosis and fatigue.

Mechanical ventilation should decrease the work of breathing.

Recognizing Respiratory Recognizing Respiratory FailureFailure

Use clinical judgment: Dyspnea Tachypnea Accessory muscles Shallow breathing Speech dyspnea Sweating Cyanosis Decreased

consciousness

Respiratory Rates

Normal Respiratory Rates in Adult 12 – 20 / min

The very important prognostic sign of respiratory failure: RR- tachypnea.

A normal rate excludes respiratory dysfunction, but tachypnea > 40 will usually lead to fatigue.

Factors Affecting Respiratory Rate:

Fever Anxiety Pain Insufficient oxygen Insufficient breath Sleep Anesthesia/ opiates drugs Acid-base balance


Arterial Blood Gases – Always assess PaO2 in relation to FiO2. Look at trend.

FiO2 may be difficult to assess in non-ventilated patients.

Use Venturi masks, accurate flows.

Oxygenation

PaO2/FiO2

Normal on 21% O2:100 / 0.21 =~ 500Shunt on 100% O2100 / 1.0 = 100

PaO2/FiO2 < 300 = Acute lung injury

Oxygenation PaO2/FiO2

A-a gradient:

Normal < 10 mmHg, or Age/4 +4 May be normal in hypercapnea

(hypoventilation)

A-a gradient= PAO2-PaO2

PAO2=FiO2(700-47)-PaCO2/0.8

Oxygenation A-a gradient:

FiO2 – 0.21, PaCO2 – 40 mmHg, PaO2 – 50 mmHg

What is the A-a Gradient?


PAO2=FiO2(760-47)-PaCO2/0.8

Oxygenation A-a gradient:

FiO2 – 0.21, PaCO2 – 60 mmHg, PaO2 – 70 mmHg

What is the A-a Gradient?


PAO2=FiO2(760-47)-PaCO2/0.8

Oxygenation

PaO2<70 mmHg on high flow O2, and increased A-a gradient are markers of severe hypoxemia and shunt.

Oxygen-Dissociation Oxygen-Dissociation CurveCurve

Factors reducing O2 Sat reliability

and accuracy

Reduced blood flow • Vasoconstriction • Hypotension • Blood Pressure cuff on arm

with sensor • Hypothermia Severe Anemia Carboxyhemoglobin. Intense Ambient lighting. Nail varnish may cause

falsely low readings . Poorly adherent probe Excessive motion (shivering)

Hypoxemia

Four mechanisms of hypoxemia: Hypoventilation Diffusion impairment Shunt VA/Q mismatch

Respiratory failure All can contribute VA/Q mismatch most

important

Hypercapnea

Arterial Blood Gases – PaCO2 reflects ventilation.

The trend is more important Acidosis represents an acute rise of CO2. A normal PaCO2 in a tachypneic asthmatic is

worrying. A high PaCO2 may be normal in COPD patients.

Increased dead space will worsen PaCO2.


Inspiratory Force – Measuring forced inspiratory and expiratory pressures against a closed airway.

Reflects neuromuscular strength and respiratory drive.

Also valuable predictor in weaning.

MIP<-20 represents severe weakness.


Bedside technique

Physiologic measurement

Normal value

Moderately abnormal (intensive care)

Severely abnormal (intubate)

Observation

Respiratory rate (per min)

12-2025-35>40

SpirometryVital capacity (ml/kg)

65-7515-30<15

ABG (astrup)

PaO2 mmHgPaCO2

75-10035-4545-60

<70>65 pH<7.25

A-a gradient

On room air10-2050-200>250

PressureNegative inspired (cmH2O)

75-10025-50<20

Treating respiratory failure Oxygen therapy Non-invasive ventilation Invasive mechanical

ventilation

Oxygen therapy Oxygen may be

toxic! Oxygen therapy

has a dose Each apparatus

has a spectrum of FiO2

Use as instructed

Oxygen Therapy

O2 by Nasal Cannula

FiO2 increases by 4% for every liter increment in flow

Greater than 6L is not tolerated

O2 by Venturi Mask

Allows administration of exact concentrations of oxygen from 24% to 50%

Non-rebreather Non rebreather mask

has a one way valve Expiratory air is not

inhaled Patient receives

100% oxygen from reservoir

May cause “absorption atelectasis”

Mechanical ventilation

Non Invasive ventilation Invasive ventilation

NINPVCuirass

Ventilation

NIPPVCPAPBIPAP

Pressure ControlPressure ControlPCPS

Volume ControlVolume ControlSIMVCMVA/CASV

Non-Invasive ventilation

CPAP PS + PEEP BiPAP Negative pressure (Cuirass)

Non-invasive ventilation

External positive or negative pressure

Non-invasive Improves gas exchange

without intubation May improve work of

breathing May aid extubation May prevent atelectasis Acute or Chronic

Non-invasive positive pressure ventilation (NiPPV)

Positive pressure through a mask Major Indications:- COPD Exacerbation

(prevent intubation)- Pulmonary edema- Sleep apnea

(improve quality of life & survival)

- Muscle weakness (delay mechanical ventilation)

- Flail chest (stabilize chest wall)

- Weaning

Patient Selection At least two of the following criteria

should be present: 1. Respiratory distress with dyspnea 2. Use of accessory muscles of

respiration 3. Respiratory rate >25/min 4. ABG shows pH <7.35 or PaCO2

>45mmHg or PaO2/FiO2 <200

Non-invasive positive pressure ventilation (NPV)

Full Face mask Nasal Mask

Positive pressure ventilation at home

Non-invasive positive pressure ventilation (NPV)

Advantages Keeps alveoli open Recruits more alveoli Improves compliance Improves

oxygenation and shunt

Prevents atelectasis Improves failing LV

Disadvantages May reduce venous

return May cause

hypotension Barotrauma Expiratory resistance Increased ICP

Contraindications to Contraindications to NIPPVNIPPV

Cardiac or respiratory arrest Medically unstable ( hypotension, cardiac

ischaemia, arrhythmia ) GI bleeding, vomiting Severe upper airway obstruction Unable to protect airway, risk of aspiration Excessive secretions Uncooperative or agitated Facial trauma, burns or surgery Anatomical abnormalities interfering with mask

fit

Negative Pressure Ventilation First ventilators to be developed Initially termed “body ventilators” or

“iron lung” Used mainly in Polio epidemic in 1950’s Negative pressure on chest and

abdomen Air enters mouth because if pressure

gradient (physiologic)

Iron Lung

ICU in the 50’s

New Cuirass ventilators

Cuirass ventilators

A see through plastic cuirass is placed on the chest

Positive and Negative pressure exerted

Used in mainly in neuro-muscular diseases, hypoventilation and as an option for patients who do not tolerate PPV

Negative pressure Negative pressure ventilationventilation

Advantages Used mainly in patients with

reduced muscle strength May improve secretion

mobilisation May be used in patients with

reduced respiratory drive (Ondine’s curse etc)

More physiological Reduces need for tracheostomy Less atelectasis, infections,

complications

Disadvantages May cause pressure

sores Noisy May be hard to tolerate

for long periods of time Inadequate for severe

weakness or poor compliance

Good patient selection required

The decision to use mechanical ventilation

To improve hypoxemia To improve respiratory acidosis To reduce excessive work of breathing

The decision to ventilate is based on an

evaluation of anticipated benefits and possible risks.

Indications for invasive mechanical ventilation

Inadequate oxygenation (PaO2 < 50mmHg RA) or 70mmHg after supplemental oxygen.

Inadequate ventilation (PaCO2 > 50mmHg + acidosis)

Fatigue (RR> 35/min) Inability to maintain airway Inability to clear secretions and cough Muscle weakness (MIP< -25, VC < 10 ml/kg) Shock (acidosis) Therapeutic (sedation, raised ICP)

Endotracheal Intubation

In adults use 6.5-8.5 mm tube

Technique

Head position – pillow under head

Oral Nasal

What to prepare Endotracheal tube – check cuff Laryngoscope - check Suction catheter and rigid

suction – check Oxygen source, Ambu with

oxygen, mask Lubricant 10 ml syringe Tape Magill forceps Stylet

What to prepare

For nasotracheal intubation:

Hot water –tip only Ephedrine drops Local anesthetic Magill forceps

Procedure may be blind, patient awake and sitting/supine

Immediate complications Hypoxia (during intubation) Misplacement (right bronchus,

esophagus) Trauma (larynx, pharynx, trachea, teeth) Hypotension (dehydration, sedation,

positive pressure) Bradycardia (vagal stimulation) Hypoxia due to V/Q mismatch Vomiting & aspiration

Monitoring Cuffs

Cuffs allow ventilation without leak and prevent aspiration

Overinflation causes pressure on tracheal wall, tracheal dilation, tracheomalacia, granuloma, erosions and bleeding, tracheo-esophageal fistula.

Cuff pressure should be less than 25 cm H2O Cuff pressure should be as low as possible to enable its

purpose with minimal damage Minimal occlusive volume – Sufficient air in cuff to

prevent air leak Use high volume-low pressure cuffs Measure cuff pressure regularly

Endotracheal Endotracheal IntubationIntubation

ORAL Emergency airway

Larger tube Less resistance Less kinking Easier to insert

Less comfortable Patient may bite on tube Oral hygiene difficult Tube less secure

NASAL Elective intubation Cervical spine injury

Oral trauma/surgery More comfortable Good oral hygiene Less gagging Less sedation

More difficult to place Smaller tube Epistaxis or

turbinectomy Sinusitis, otitis media C/O in basal skull

fracture

Indications

Advantages

Disadvantages

Spontaneous vs Positive Spontaneous vs Positive Pressure ventilationPressure ventilation

In spontaneous respiration contraction of respiratory muscles causes negative pressure in the chest.

Air flows, at atmospheric pressure into the lungs.

Positive pressure ventilation is non-physiologic (positive pressure in the chest).

Expiration is passive to atmospheric pressure or PEEP.

Approaches to ventilation

Full ventilatory support – Mechanical ventilation in which the ventilator performs all the work of breathing (WOB).

Partial ventilatory support – Both the ventilator and the patient contribute to ventilation and WOB.

Ventilation Modes

Modes of VentilationModes of Ventilation

Controlled Mandatory Assisted

spontaneous Ventilator settings

Modes of controlled ventilation

CMV- Controlled Mechanical Ventilation

A/C – Assist-Control Ventilation

SIMV- Synchronized Intermittent Mandatory Ventilation

Modes of assisted spontaneous ventilation

PS – Pressure Support ventilation VS – Volume Support ventilation ASV – Adaptive Support ventilation

Volume controlled ventilation

Lungs are inflated to a predetermined volume.

Tidal volume is constant, despite changes in compliance or resistance in the lung, which will cause changes in peak pressure.

Pressure controlled ventilation

Lungs are inflated to a predetermined pressure.

Tidal volume is variable, depending on changes in compliance or resistance in the lung.

Volume changes in pressure controlled ventilation

Controlled Mechanical Controlled Mechanical Ventilation - CMVVentilation - CMV

Full ventilatory support.

Patient cannot trigger ventilator.

Patient receives a set number of breaths at a set tidal volume (TV).

Controlled Mechanical Controlled Mechanical Ventilation - CMVVentilation - CMV

Indications: Patient with minimal or no respiratory

effort CNS depression (brain, spinal cord) Drug overdose Neuromuscular dysfunction Anesthesia and paralysisPatient cannot trigger the ventilator, needs

to be sedated.

Assist-Control Assist-Control VentilationVentilation

The ventilator delivers a preset number of breaths and tidal volume (TV).

The patient can trigger the ventilator.

With each triggered breath, the preset tidal volume is delivered.

The only work the patient has to perform is to trigger the ventilator.

Assist Control

A/C - What do you set?

Rate – Minimum No of breaths Tidal volume- in EACH breath FiO2 - Lowest Flow - How quickly volume goes in (Ti) PEEP – End Expiratory Pressure Trigger sensitivity –What patient

needs to do to trigger a spontaneous inspirium

Assist-Control Ventilation

Indications Normal drive but muscles

are too weak to perform WOB.

Pulmonary pathology is too severe and WOB is too high for respiratory muscles.

Tachypneic patient with asynchrony with ventilator on other modes.

Disadvantages Causes

hyperventilation Respiratory alkalosis High peak pressures Tendency for

intrinsic PEEP Hemodynamic

instability because of high pressures

CMV vs A/C

SIMV - SIMV - Synchronized Synchronized Intermittent Mandatory Intermittent Mandatory

VentilationVentilation

Intermittent Mandatory Intermittent Mandatory VentilationVentilation- - IMVIMV

The patient receives a preset number of breaths and TV.

Mandatory breaths are delivered at a set time.

The patient can trigger spontaneous breaths.

The volume in spontaneous breaths depends on patient effort and strength. Spontaneous TV is variable.

The is no synchrony between patient & mandatory breaths.

IMV vs SIMVIMV vs SIMV

Synchronized Intermittent Synchronized Intermittent Mandatory Ventilation - Mandatory Ventilation -

SIMVSIMV

Developed to improve patient synchrony with ventilator.

Same as IMV but mandatory breaths are synchronized with patient’s spontaneous breaths.

If the patient makes an inspiratory effort, the mandatory breath will be delivered at that time.

If the patient does not make an inspiratory effort, the ventilator will deliver the breath at the intended time.

Spontaneous breaths occur in-between mandatory breaths.

Tidal volume depends on effort and strength.

SIMVSIMV

Advantages Improved patient

comfort Prevents breath

stacking and increased pressures.

Less hyperventilation Less muscle atrophy Average mean airway

pressures are lower because of spontaneous breaths

Patient can be weaned

Disadvantages Increased WOB if hard to

open demand valves Increased WOB &

pressures if patient fights ventilator

Insufficient flow during spontaneous breaths may cause air hunger

Increased WOB due to resistance of tube & circuit

Spontaneous TV may be low

SIMV - Indications

Patient has good respiratory drive but increased WOB.

Patient can set own rate to maintain ventilation.

To enable spontaneous muscle activity. To enable gradual weaning.

SIMV – What do you set?

Rate (minimum mandatory) Tidal volume FiO2 & PEEP Flow Trigger sensitivity Pressure support:

SIMV + PS

Pressure Support - PSPressure Support - PS

Pressure Support - PSPressure Support - PS Patients’ spontaneous breaths are

augmented by positive pressure. After patient triggering, PS is held constant

during inspiration. PS is flow cycled – when flow rate reaches

25% of initial flow, inspirium ends. TV is not set, it depends on patient effort,

the level of PS, compliance & resistance. May be used alone or with SIMV.

Pressure SupportPressure Support

Pressure support - Pressure support - IndicationsIndications

Used in spontaneously breathing patients to reduce WOB

Reliable respiratory drive – essential Used for muscle conditioning Used for weaning Good patient tolerance in prolonged

ventilation PS can be adjusted according to rate, TV

and patient comfort If patient is tachypneic – increase PS or

change mode

Pressure supportPressure support

Too slow: Apnea backup

or SIMV

Too fast: Anxiety, pain, rapid shallow breathing – increased work of breathing:

Increase Pressure support,Sedation/analgesia,

Other mode

SummarySummary

Adaptive Support Ventilation - ASV

New generation ventilator

Closed loop ventilation Targeted ventilation

according to patient weight

Set minute volume is achieved with minimal support from ventilator


Ventilator sets target tidal volume & rate which is optimal for the patient

Work of breathing, peak pressure, air trapping is minimal

Ventilation changes breath by breath


Advantages Automatic weaning “Safe” ventilation Comfortable for

patient Changing lung

physiology leads to changed ventilation !

Setting the ventilatorSetting the ventilator

FiO2

Tidal Volume Rate Flow (I:E ratio) Trigger sensitivity PEEP High pressure limit Pressure support

Setting the ventilatorSetting the ventilator

FiO2 - – Fractional inspired oxygen When initiating ventilation use high FiO2

(60-100%). Once patient stable reduce FiO2 according to

SaO2 and/or PaO2. In normal pH and temp,

SaO2 of 90%=PaO2 of 60 mmHg Use minimal FiO2 to achieve PaO2>60mmHg FiO2 > 50% is toxic to the lung

Hazards of O2 therapy

CO2 retention In those with Hypoxic

drive O2 toxicity

High O2conc over time can damage lung

Swollen cap endothelium, replacement of alveolar type I with type II cells, edema; long-term: fibrotic changes

Setting the ventilator Setting the ventilator –– Tidal VolumeTidal Volume

Mechanical ventilation uses high TV to prevent atelectasis.

In the past large TV were used

(10-15 cc/kg) Currently we use TV of 6-10 cc/kg to

prevent volutrauma and barotrauma.

Setting the ventilator Setting the ventilator –– Tidal VolumeTidal Volume

Exhaled TV is used to monitor patient ventilation.

Exhaled TV may be lower than set TV if there is a leak (airway, pleura, circuit).

Expiratory minute volume is the volume the patient received in one minute (L/min).

Setting the ventilator Setting the ventilator –– RateRate

Physiologic respiratory rate: 10-20 bpm

Rate x Tidal volume = minute volume Rate is set according to patient

comfort, PaCO2, pH, tidal volume and patient’s spontaneous rate.

As patient starts to breath, rate may be decreased.

Rate is also set according to lung mechanics (resistance, compliance)

PEEP PEEP –– Positive End Positive End Expiratory PressureExpiratory Pressure

Positive pressure is maintain at the end of expirium.

Usually set at 2-5 cmH2O Prevents alveolar collapse Distends patent alveoli Prevents small airway closure Redistributes lung water from

alveoli to interstitium Increases FRC Improves compliance Decreases shunt Improves oxygenation

PEEPPEEP

Indications Prevent/treat

atelectasis Improve oxygenation Prevent high FiO2 Stabilizes chest wall in

flail chest Increases FRC in

supine position

Contraindications

Acute COPD/Asthma – may cause air trapping and barotrauma.

Unilateral lung disease with hyperinflation of healthy lung.

Hypovolemia – decreases cardiac output

Increased ICP Pneumothorax

Trigger Sensitivity- Trigger Sensitivity- What makes the ventilator open the demand valve

during spontaneous breaths.

Pressure trigger Negative pressure below PEEP the patient has

to make to start inspirium. Sensitivity of -2 cmH2O means the patient has

to make a negative pressure of 2 cm H2O below PEEP.

Lag time between triggering and valve opening The higher the number the more difficult it is to

trigger and the patient may increase WOB or fatigue.

Trigger SensitivityTrigger Sensitivity

Sensitivity too LOW

(high number -4, -5 cmH2O etc)

Sensitivity too HIGH

(low number, -0.5, flow trigger etc)

Pt must work harder Pt ventilator

dysynchrony Pt may be “locked

out”

Auto-cycling Pt – ventilator

dysynchrony

Intrinsic or Auto PEEPIntrinsic or Auto PEEP

The development of end expiratory pressure as a result of insufficient expiratory time.

Causes of intrinsic PEEP: rapid rate, airflow obstruction, inverse ratio ventilation.

If expiratory time is not enough to finish expiration, air will be trapped in the lung and will increase intrathoracic pressure.

Intrinsic or Auto PEEPIntrinsic or Auto PEEP Auto PEEP is not measured routinely by the

ventilator. The suspicion is clinical (hyperinflation,

hypotension, asynchrony with ventilator).

Measuring Intrinsic Measuring Intrinsic PEEPPEEP

Intrinsic PEEP

Correcting Auto PEEPCorrecting Auto PEEP

High Peak PressureHigh Peak Pressure

End inspiratory proximal airway pressure. Function of tidal volume, tube & airway resistance,

lungs and chest wall compliance.

Causes: Tube obstruction / kinking Airway obstruction (secretions) Bronchospasm (COPD, asthma) Decreased compliance (edema, atelectasis, ARDS, pneumonia etc) Asynchronous breathing (coughing) Pneumothorax

High Pressure LimitHigh Pressure Limit

Is the pressure above which the ventilator stops air flow.

Used to protect the lungs from barotrauma. Set at 40-50 cmH2O. DO NOT INCREASE ALARM LIMIT IF

VENTILATOR ALARMS. Call doctor, suction & check for mucus

plugs, check for tube kinking, decrease tidal volume, pneumothorax, treat bronchospasm.

Low pressure/volume Low pressure/volume alarmalarm

Disconnection Cuff leak Tubing leak Partial/complete extubation Intra pleural leak Tidal volume too low Very deep breath by patient

Correcting oxygenation & Correcting oxygenation & ventilationventilation

ProblemABGAdjustment

Excessive oxygenation

PaO2>100 mmHgSaO2 100%

Decrease FiO2Decrease PEEP

Inadequate oxygenation

PaO2<60 mmHgSaO2<90%

Increase FiO2Increase PEEP

Respiratory acidosis

PaCO2> 45 mmHgpH<7.35

Increase TVIncrease rate

Respiratory alkalosis

PaCO2< 35 mmHgpH> 7.45

Decrease TVDecrease rate

Patient-ventilator Patient-ventilator interactionsinteractions

Sedation, anxiety, pain Rapid shallow breathing Work of breathing Adequate triggering Adequate flow Adequate pressure support Auto PEEP Hemodynamic stability with

positive pressure Preload and afterload

reduction in LVF Muscle strength, fatigue,

atelectasis

How to Ventilate the Patient How to Ventilate the Patient withwith

Reduced ComplianceReduced Compliance

ARDS – Chest x-ray and pathology

Computerized Computerized TomographyTomography

How to Ventilate the Patient How to Ventilate the Patient withwith

Reduced ComplianceReduced Compliance

Peak pressures are high with normal ventilation

Small volumes Higher rate Peak pressure < 40 cmH20 Prolonged inspiratory time Decreased flow High PEEP Consider pressure control Inverse ratio

To prevent lung injury

To recruit alveoli

Mode of ventilation

Setting the ventilator Setting the ventilator –– Flow rateFlow rate

Flow = speed in which tidal volume is delivered (L/min)

Normal flow is 40-60 L/min

Insufficient flow will cause “air hunger”

Flow determines inspiratory time

Flow determines I:E ratio

Setting the ventilator Setting the ventilator –– Flow rateFlow rate

High Flow Flow Inspiratory

time Higher peak pressures Required for high

ventilation demand Increases expiratory time Used in obstructive lung

dis

Low Flow Flow Inspiratory

time Decreased peak

pressures Better distribution of gas Used in reduced

compliance

I:E RatioI:E Ratio

Duration of inspirium: Duration of expirium Normal I:E is 1:2 I:E ratio is usually determined by flow rate

and/or inspiratory time (except in pressure control).

In the obstructed patient use I:E 1:3, 1:4 etc. - increase flow rate, shorten inspiratory time. In the patient with poor compliance use I:E

1:1.5, 1:1 (inverse ratio). - decrease flow rate, prolong inspiratory time.

Inverse ratio Inverse ratio ventilationventilation

High Flow

Inverse ratio

Pressure Control Pressure Control VentilationVentilation

Used in patients with high peak pressures on volume control (low compliance) Volume is given until a preset positive pressure Minimizes volutrauma Causes hypoventilation & permissive hypercapnea Monitor tidal volume Monitor pH (keep pH > 7.2) Watch for significant intrinsic PEEP Requires sedation

Inverse ratio Inverse ratio ventilationventilation

Prolonged inspirium I:E ratio 1:1, 2:1 Allows more time for alveoli to open Gas is more evenly distributed in the lung Peak pressures are lower Mean pressures are higher Short expirium prevents alveolar collapse May cause “intrinsic PEEP” Used in poor compliance states (ARDS)

NITRIC OXIDENITRIC OXIDE

NO

Vasodilation

V/Q mismatch

Open alveoli

HbNO

Nitric OxideNitric Oxide

Nitric Oxide

NO is an endogenous vasodilator Inhaled NO is a selective pulmonary

vasodilator Does not cause systemic vasodilation Redistributes perfusion to ventilated areas Decreases pulmonary artery pressures Reduces shunting & improves oxygenation Improves platelet aggregation Has anti-inflammatory properties

Nitric Oxide Nitric Oxide –– Indications & Indications & AdministrationAdministration

Refractory hypoxemia (ARDS) Acute pulmonary hypertension Respiratory distress syndrome of the newborn Pulmonary hypertension of the newborn Usual dose 10-20 ppm may be increased up to

80 ppm Complications – Nitrogen dioxide

formation which is toxic to the lung (>5ppm)

Methemoglobinemia which can interfere with tissue oxygen delivery (>4%)

Both must be monitored

PRONE POSITIONPRONE POSITION

Prone PositionProne Position

Re-expansion of gravity induced atelectasis Consolidation moves from dorsal to ventral Improvement of V/Q matching +compliance Increased FRC Mobilization of secretions Prone position improves PaO2 but not survival

Watch for ventilator disconnection, kinking, pressure sores, increased peak pressures.

Prone PositionProne Position

How To Ventilate The Patient How To Ventilate The Patient With Increased Airway With Increased Airway

ResistanceResistance

Normal Asthma

X-ray in obstructive lung disease - hyperinflation

Ventilation in asthma (1)Ventilation in asthma (1)

Large tube Maintain adequate sedation /

paralysis Adequate bronchodilation

(continuous or every hour) Check for drug induced

bronchospasm (morphine, inhalations, NSAIDS etc)

Maintain hemodynamics (fluids)

Ventilation in asthma (2)Ventilation in asthma (2)

Prolong the expirium: Low rate High flow I:E ratio > 1:2 Little or no PEEP Watch for intrinsic

PEEP (hemodynamics, chest hyperinflation, agitated patient)

Adjust PEEP for easy triggering

Weaning Weaning – Reduced ventilator support to a

minimum Extubation – Removal of artificial airway

A patient may be weaned from the ventilator but may NOT be ready for extubation !!

E.g - Airway edema, no cough, reduced consciousness etc

Weaning

Methods of weaning include:

Reduce SIMV and Pressure support gradually

T-Piece trial NIV Tracheostomy

respiratory failure & mechanical ventilation

Documents

anatomical dead space

anatomic dead space

physiological dead space

alveolar dead space

shunt shunt vq mismatch

pulmonary ventilation

dead space vd accounts

examples of vq mismatch