respiratory failure & mechanical ventilation
DESCRIPTION
Respiratory Failure & Mechanical Ventilation. Dr Sigal Sviri Medical ICU. Contents. Definitions in respiratory failure Oxygen therapy Non-invasive ventilation Indications for intubation Technique Modes of Ventilation (pros and cons) Evaluating & Monitoring ventilated patients - PowerPoint PPT PresentationTRANSCRIPT
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Respiratory Failure & Respiratory Failure & Mechanical Mechanical VentilationVentilation
Dr Sigal Sviri Medical ICU
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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
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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.
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Respiratory Failure
Hypercarbic – type II (reduced ventilation)
Hypoxic type I (reduced gas exchange)
Mixed
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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
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Multiple Systems are Involved in Successful Ventilation
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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
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Causes of Respiratory Failure
Alveoli & Capillaries:
Pneumonia Pulmonary edema ARDS Interstitial lung dis Pulmonary
Embolism
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Gas exchange
PaO2 = 150PCO2 = 0.4
PaO2 = 106PaCO2 = 40
PaO2 = 40
PaCO2 = 46
PaO2 =100
PaCO2 = 40
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DefinitionsDefinitions
Dead space Shunt Compliance Resistance Work of breathing FRC
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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.
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V/Q Ratio
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West zones of the lung
(PA > Pa > Pv)
(Pa > PA > Pv )
(Pa > Pv > PA )
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V/Q Mismatch
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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)
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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
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DEAD SPACE
Lung apices Emphysema Positive pressure Hypovolemia Shock Decreased blood
flow
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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)
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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.
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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
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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
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SHUNT
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V/Q MISMATCH
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V/Q mismatch: summary
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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!
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Pulmonary vasoconstriction
The lung can improve shunt by vasoconstriction of blood vessels in less ventilated areas
May cause pulmonary hypertension
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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.
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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.
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Compliance
Distensibility (flexibility) of the lung (& chest wall) during inspiration
The change in volume caused by a change in pressure
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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.
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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.
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V/P CurveV/P Curve
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RESISTANCE- The resistance of the airways to flow
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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
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RESISTANCE- The resistance of the airways to flow
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
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Restrictive lungs
דלקת ריאותבצקת ריאותתמטמחלת ריאות אינטרסטיציאליתARDSעודף משקל ניכרחזה אויר
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Obstructive lung disease
אסטמהCOPDאמפיזמה
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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.
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Recognizing Respiratory Recognizing Respiratory FailureFailure
Use clinical judgment: Dyspnea Tachypnea Accessory muscles Shallow breathing Speech dyspnea Sweating Cyanosis Decreased
consciousness
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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.
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Factors Affecting Respiratory Rate:
Fever Anxiety Pain Insufficient oxygen Insufficient breath Sleep Anesthesia/ opiates drugs Acid-base balance
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Recognizing Respiratory Failure
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.
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Oxygenation
PaO2/FiO2
Normal on 21% O2:100 / 0.21 =~ 500Shunt on 100% O2100 / 1.0 = 100
PaO2/FiO2 < 300 = Acute lung injury
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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
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Oxygenation A-a gradient:
FiO2 – 0.21, PaCO2 – 40 mmHg, PaO2 – 50 mmHg
What is the A-a Gradient?
A-a gradient= PAO2-PaO2
PAO2=FiO2(760-47)-PaCO2/0.8
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Oxygenation A-a gradient:
FiO2 – 0.21, PaCO2 – 60 mmHg, PaO2 – 70 mmHg
What is the A-a Gradient?
A-a gradient= PAO2-PaO2
PAO2=FiO2(760-47)-PaCO2/0.8
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Oxygenation
PaO2<70 mmHg on high flow O2, and increased A-a gradient are markers of severe hypoxemia and shunt.
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Oxygen-Dissociation Oxygen-Dissociation CurveCurve
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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)
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Hypoxemia
Four mechanisms of hypoxemia: Hypoventilation Diffusion impairment Shunt VA/Q mismatch
Respiratory failure All can contribute VA/Q mismatch most
important
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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.
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Recognizing Respiratory Failure
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.
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Recognizing Respiratory Failure
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
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Treating respiratory failure Oxygen therapy Non-invasive ventilation Invasive mechanical
ventilation
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Oxygen therapy Oxygen may be
toxic! Oxygen therapy
has a dose Each apparatus
has a spectrum of FiO2
Use as instructed
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Oxygen Therapy
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O2 by Nasal Cannula
FiO2 increases by 4% for every liter increment in flow
Greater than 6L is not tolerated
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O2 by Venturi Mask
Allows administration of exact concentrations of oxygen from 24% to 50%
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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”
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Mechanical ventilation
Non Invasive ventilation Invasive ventilation
NINPVCuirass
Ventilation
NIPPVCPAPBIPAP
Pressure ControlPressure ControlPCPS
Volume ControlVolume ControlSIMVCMVA/CASV
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Non-Invasive ventilation
CPAP PS + PEEP BiPAP Negative pressure (Cuirass)
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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
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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
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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
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Non-invasive positive pressure ventilation (NPV)
Full Face mask Nasal Mask
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Positive pressure ventilation at home
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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
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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
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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)
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Iron Lung
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ICU in the 50’s
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New Cuirass ventilators
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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
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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
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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.
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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)
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Endotracheal Intubation
In adults use 6.5-8.5 mm tube
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Technique
Head position – pillow under head
Oral Nasal
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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
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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
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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
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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
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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
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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.
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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.
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Ventilation Modes
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Modes of VentilationModes of Ventilation
Controlled Mandatory Assisted
spontaneous Ventilator settings
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Modes of controlled ventilation
CMV- Controlled Mechanical Ventilation
A/C – Assist-Control Ventilation
SIMV- Synchronized Intermittent Mandatory Ventilation
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Modes of assisted spontaneous ventilation
PS – Pressure Support ventilation VS – Volume Support ventilation ASV – Adaptive Support ventilation
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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.
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Pressure controlled ventilation
Lungs are inflated to a predetermined pressure.
Tidal volume is variable, depending on changes in compliance or resistance in the lung.
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Volume changes in pressure controlled ventilation
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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).
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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.
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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.
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Assist Control
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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
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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
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CMV vs A/C
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SIMV - SIMV - Synchronized Synchronized Intermittent Mandatory Intermittent Mandatory
VentilationVentilation
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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.
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IMV vs SIMVIMV vs SIMV
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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.
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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
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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.
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SIMV – What do you set?
Rate (minimum mandatory) Tidal volume FiO2 & PEEP Flow Trigger sensitivity Pressure support:
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SIMV + PS
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Pressure Support - PSPressure Support - PS
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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.
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Pressure SupportPressure Support
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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
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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
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SummarySummary
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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
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Adaptive Support Ventilation - ASV
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
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Adaptive Support Ventilation - ASV
Advantages Automatic weaning “Safe” ventilation Comfortable for
patient Changing lung
physiology leads to changed ventilation !
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Setting the ventilatorSetting the ventilator
FiO2
Tidal Volume Rate Flow (I:E ratio) Trigger sensitivity PEEP High pressure limit Pressure support
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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
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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
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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.
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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).
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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)
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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
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PEEP
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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
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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.
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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
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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.
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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).
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Measuring Intrinsic Measuring Intrinsic PEEPPEEP
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Intrinsic PEEP
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Correcting Auto PEEPCorrecting Auto PEEP
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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
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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.
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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
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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
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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
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How to Ventilate the Patient How to Ventilate the Patient withwith
Reduced ComplianceReduced Compliance
ARDS – Chest x-ray and pathology
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Computerized Computerized TomographyTomography
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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
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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
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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
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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.
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Inverse ratio Inverse ratio ventilationventilation
High Flow
Inverse ratio
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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
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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)
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NITRIC OXIDENITRIC OXIDE
NO
Vasodilation
V/Q mismatch
Open alveoli
HbNO
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Nitric OxideNitric Oxide
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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
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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
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PRONE POSITIONPRONE POSITION
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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.
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Prone PositionProne Position
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How To Ventilate The Patient How To Ventilate The Patient With Increased Airway With Increased Airway
ResistanceResistance
Normal Asthma
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X-ray in obstructive lung disease - hyperinflation
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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)
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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
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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
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Weaning
Methods of weaning include:
Reduce SIMV and Pressure support gradually
T-Piece trial NIV Tracheostomy