2. INTRODUCTION
Refers to the use of artificial methods for delivery of gases into and
out of the lungs for oxygenation and CO2 removal.
Historically, there is evidence of use of artificial respiration since
biblical times, use of fire bellows in 15th century and negative pressure
ventilators in 1800s and early 1900s.
Positive pressure ventilation as a clinical modality was first used in
1950s at the Massachusets General Hospital during the polio
epidemic in Europe and USA
Numerous advancements have led to the use of highly sophisicated
ventilators across a wide range of patients making it a cornerstone in
the treatment of critically ill patients.
3. INDICATIONS
Due to the associated risks and complications, and
the question of weaning; the decision to initiate
mechanical ventilation can be a tricky one.
The indications may be classified in various ways,
but the clinician’s judgement is of paramount
importance.
The indiacations may broadly be classified as either
ventilatory failure and oxygenation failure.
4. VENTILATORY FAILURE
Inability of lungs to remove adequate
CO2.
Hypercapnia (increased PaCO2) and
consequent respiratory acidosis is the
primary feature.
Hypoxemia (low PaO2) may be
secondary, but responds well to
supplemental oxygen.
May be caused by various mechanisms
like
Hypoventilation
Persistent V/Q mismatch
Persistent intrapulmonary shunt
Persistentdiffusion defect
HYPOVENTILATION may be caused by
CNS depression, neuromuscular
diseases, airway obstruction etc.
Clinically characterised by reduced
alveolar ventilation and raised PaCO2
Minute alveolar ventilation = Va x RR
DIFFUSION DEFECT refers to impaired
gas exchange between the alveoli and
pulmonary capillaries.
Decreased O2 gradient P(A-a)O2 – High
altitude, smoke inhalation
Thickening of A-C membrane – Edema,
secretions
Dec. surface area of A-C membrane –
Emphysema, fibrosis
6. OXYGENATION FAILURE
Refers to hypoxemia not responsive to moderate to high levels
of supplemental oxygen.
Caused by the same mechanisms as discussed above, but
more in severity.
Hypoxemia refers to low oxygen content in blood.
PaO2 values of less than 60 mm Hg is moderate hypoxemia, less the
40 mm hg is considered severe hypoxemia. (Normal : 80-100 mm Hg)
Hypoxia refers to reduced O2 in the organs and tissues.
7. CLINICAL CONDITIONS
1. James MM et al. Mechanical Ventilation. Surg
Clin North Am 2012;92(6)
Acute respiratory /
ventilatory failure
Impending respiratory /
ventilatory failure
Low output states
Purposeful
hyperventilation
It is the primary indication of mechanical
ventilation.
Early institution of mechanical ventilation is
associated with reduced complications and
mortality. [1]
Objective criteria for initiating mechanical
ventilation are: pH<7.30, PaCO2 > 50mm
Hg and severe hypoxemia (PaO2 < 40
mm Hg) despite supplemental O2.
Clinical signs such as apnea/ bradypnea
and cynaosis can aid in the diagnosis.
8. ACUTE RESPIRATORY FAILURE - CAUSES
1. Primary ventilatory failure
CNS depression:
narcotics, sedatives,
alcohol
Neuromuscular
disorders: poliomyelitis,
transverse myelitis,
myasthenia, MND, GBS,
spinal trauma, snake
bite, tetanus
Comatose patients:
Stroke and neurological
diseases, head injury
etc. (GCS < 8, loss of
gag reflex,
hypoventilation)
2. Acute pulmonary disease, eg.
Fulminant pneumonia, ARDS
3. Fulminant pulmonary oedema
4. Major pulmonary embolism
5. Major atelectasis
6. Acute exacerbation of COPD/
Asthma non responsive to
therapy
7. Chest trauma: Flail chest,
Pneumothorax, Haemothorax
8. Respiratory fatigue in critically ill
9. IMPENDING VENTILATORY FAILURE
Condition when the patient can maintain marginally normal
blood gases at the expense of increased work of breathing.
It can progress to hypercapnia, acidosis and hypoxemia due to
respiratory muscle fatigue.
Early intervention can prevent complications like major organ
failure due to hypoxemia and acidosis.
Several objective parameters have been described for ease of
diagnosis and institution of therapy.
10. ASSESMENT OF IMPENDING FAILURE
Parameter Limit
Tidal Volume <3-5 ml/kg
Respiratory Rate > 25-35 breaths/min
Minute Ventilation >10 ml/min
Vital Capacity < 15 ml/kg
Maximum inspiratory pressure < 20 cm of H2O (> 25 cm of H2O
correlates with VC of 15ml/kg
PaCO2 Increasing trend over a period of time to
more than 50 mm Hg
Clinical Signs Poor chest movement, tachypnea,
tachycardia, accessory muscle use,
11. CLINICAL CONDITIONS
Acute airflow obstruction:
Asthma, COPD, epiglotittis,
laryngospasm/bronchospas
m
Rapidly progressive
pulmonary parenchymal
disease: ARDS, pneumonia
Cardiac conditions: CHF,
Acute Coronary Event,
Congenital Heart Disease.
Shock of any etiology: Low
PA pressure leads to V/Q
mismatch, poor tissue
oxygenation. MV provides
high FiO2, decreased work
of breathing and O2
consumption.
Drugs: Organophosphates,
paraquat, opioids, Amanita
mushrooms etc
High risk postoperative
patients (obese, upper-
abdominal/ thoracic surgery)
12. PURPOSEFUL (THERAPEUTIC) HYPERVENTILATION
Conditions with raised ICP – head injury, neurosurgery, SOLs
To reduce cerebral oedema after CPR or CVA
Has been shown to be of benefit over only a short period of
time (24 hours), not instituted within 8 hrs of injury
13. EFFECTS OF POSITIVE PRESSURE
VENTILATION
System Effect
Respiratory / Pulmonary mPaw, alveolar and pleural pressures
Cardiovascular • intrathoracic pressure - venous return - CO and SV
• BP during inspiration ( reverse pulsus paradoxus),
opposite in hypovolaemic patients.
• CVP is increased with PEEP, normal or less with PPV
•Effects are more pronounced with use of PEEP
Renal Decreased CO – Decreased GFR – Reduced filtration and
urine output
Hepatic Reduced hepatic blood flow with PEEP (32% decrease with
PEEP of 20 cm H2O
Gastrointestinal/
Abdominal
• Increase in Intra abdominal pressure – impaired
circulation
• Erosive oesophagitis, stress related mucosal damage
Neurologic Prolonged hyperventilation (>24 hrs) may cause cerebral
hypoxia due to left shift of O2 Hb dissociation curve and
hypophosphatemia
15. PHASE VARIABLES
There are four distinct phases of ventilator breath
Four parameters can be controlled or manipulated during each
phase: Volume, Pressure, Flow, Time.
• TriggerExpiration –
Inspiration
• Limit, ControlInspiration
• CycleInspiration -
Expiration
• BaselineExpiration
16. TRIGGER VARIABLE
Determines the start of inspiration.
Time trigger:
Breath is delivered once the preset time interval has elapsed.
If RR is 12/min, the ventilator will deliver breath every 5 secs. (60s /
12 = 5), irrespective of patient effort or requirement.
Pressure Trigger:
Breath is delivered once preset negative pressure is generated by
patients’ spontaneous effort.
Values of -1 to -5 cm of H20 (below end-expiratory pressure) is
acceptable.
Flow Trigger:
Breath is delivered when patients’ inspiratory flow reaches a specific
value.
More sensitive than pressure trigger to detect inspiratory effort, hence
less inspiratory work.
18. Limit Variable:
Normally, volume, pressure and flow all rise above their baseline
values during ventilator supported breath.
If one or more variable is not allowed to rise beyond a preset value
during inspiratory time, it is called limit variable.
Inspiration does not end at the preset value, but the variable is held
fixed at that value during inspiration.
Cycle Variable:
Inspiration ends when a specific cycle variable is reached – pressure,
volume, flow or time cycle)
Baseline Variable:
Expiratory time = Interval between start of expiration and start of
inspiration.
Variable that is controlled during expiratory time is baseline variable;
most commonly it is pressure.
PEEP and CPAP are applied to the baseline pressure variable.
19. CONTROL VARIABLE
The primary target achieved by the ventilator during inspiration:
pressure, volume, flow and time.
Volume and pressure control are used most often, flow and time
are indirectly controlled.
Most of the classic ventilator modes can be either volume
controlled or pressure controlled, newer modes (ASV, PRVC)
have dual control.
Control may itself act as the cycle variable (VCV)or a separate
cycle may be used (PCV).
20. VOLUME CONTROL
• The ventilator delivers a pre set tidal volume.
• Pressures may vary with changes in resistance and compliance, but
volume remains constant.
• Volume may be measured by displacement of piston or bellows, or by
electronically computing in relation to flow. ( Vol = Flow rate x Time)
• Inspiration ends when the pre set volume is reached, or after certain
time elapses (inspiratory hold)
21. Advantages Disadvantages
Predictable
regulation of TV,
MV
Higher incidence
of barotrauma,
volutrauma and
VILI esp in ARDS
and ALI
Better control
over PaCO2 than
PC
During assisted
breath, flow rates
may be
insufficient
leading to dys-
synchrony and
auto PEEP
Settings:
VT , RR, Flow/ Time and
FiO2.
VT set at 6 – 12 ml/kg IBW
RR = 10 – 15 bpm
FiO2 lowest possible to
achieve oxygenation
I:E – 1:2 – 1:4
Flow rate is a measure of
I:E, can be set separately in
some models.
Monitoring and alarms:
• PIP and PPlat relates to compliance.
Cstatic = Vt /Pplat – PEEP
Cdyn = Vt/ PIP – PEEP
• High pressure alarm set at 5 – 10 cm above ventilating pres.
• Low pressure alarm 5 – 10 cm H20 belowventilating pres.
• Low pressure and volume alarms signify leak in system.
22. PRESSURE CONTROL
Provides pre set pressure to the airways, not exceeding the set
level irrespective of changes in compliance and resistance.
VT is variable, dependent on compliance, Raw , set pressure and
patient effort.
Once the preset pressure is achieved, a plateau is created
using ventilaor or patient generated flow.
Expiration occurs once a pre set inspiratory time has elapsed.
PCV is thus time/patient triggered, pressure limited and time
cycled.
23. Advantages Disadvantages
Avoids over
distention and
VILI,esp in
ALI/ARDS
VT and MV are
variable,
decrease in
worsening
conditions
Adequate flow:
less flow dys-
synchrony & auto
PEEP
May promote
hypoventilation
Time cycled:
recruitment of
alveoli
May cause
increase in
PaCO2
Settings
Pressure - <30 cm H2O
RR – 10-15 bpm
I:E ratio: 1:2 - 1:4
Inspiratory time and flow
rate depend on I:E ratio
and RR
•Monitoring and alarms:
•Low Volume alarm: Set at the minimum acceptable VT for the patient,
signifies increased resistance or decreased compliance (in VCV signifies
leak)
•Low pressure alarm: Set at ~10 cm H2O below patients ventilation
pressure, signifies leak in the system.
25. BASIC MODES OF VENTILATION
“Perhaps no other word in the mechanical ventilation lexicon is
more used and less understood than ‘mode’ “ – Chatburn RL,
JRespirCare 2007
Beier et al have suggested a complete mode description to
include
1. Description of breath sequence
(mandatory/spontaneous/assisted/continuous/ intermittent)
2. Control and limit variables within and between breaths (P, Vol, F, T)
3. Description of adjunctive control algorithms
26. CONTROLLED VS ASSISTED VENTILATION
Controlled breaths are time
triggered breaths.
Patient cannot initiate breath
sequence, irrespective of
effort.
May be volume or pressure
targeted
Patient cannot control RR, VT
or Paw
Assisted breaths are
triggered by patients’ effort.
(Flow/ Pressure)
Once breath is initiated, pre
set VT or Paw attained by the
ventilator.
Patient can control RR but
not VT or Paw
28. CONTROLLED MANDATORY VENTILATION
Also called continuous
mandatory ventilation.
Time triggered, V or P limited
and F or T cycled
Patient has no control over
breathing
Approprite use of sedatives and
muscle relaxants.
Decreases work of breathing
and O2 cost of breathing if
properly instituted.
Indications:
Initiation of MV, to avoid dys-
synchrony, ‘fighting’ or bucking.
Tetanus/ seizure
Extensive chest trauma
Disadvantages:
Regardless of effort, patient
cannot initiate flow –
psychological burden
Due to sedation and paralysis,
potential for apnea if accidental
disconnection
Cannot be used for weaning
29. ASSIST / CONTROL MODE
Breaths may be time triggered
or patient triggered (P, Flow)
Each time a breath is triggered
a pre set VT or Paw is delivered
Patient can control RR but not
VT or Paw
If patients RR in less than the
clinician set value, time
triggered breath is delivered
Primarily indicated during
initiation of full ventilatory
support and in pts with stable
respiratory drive
Advantages:
Very small WOB, if correct trigger
sensitivity is set.
Allows patient to control MV
(through RR) to normalise PaCO2
Disadvantages:
Alveolar hyperventilation
Respiratory alkalosis
Higher pH and lower PaCO2
compared to IMV [1]
Contraindications:
Irregular RR
Cheyne – Stokes respiration
Hiccoughs
Brainstem injury
30.
31. INTERMITTENT MANDATORY VENTILATION
John Downs and colleagues
described this revolutionary
mode in 1973.
Allowed patient to breathe
spontaneously between
controlled mandatory breaths.
Many publications have
described the pro’s and con’s
to this approach
The con’s have been
addressed in newer modes
like SIMV and PSV and IMV is
not an option in most modern
ventilators.
Advantages:
More physiological control over
MV and Paw
Minimal cardio-vascular side
effects of PPV
Can be used during weaning.
Disadvantages:
‘Breath Stacking’ – When
mandatory breath delivered on
top of spontaneous breath,
dangerous rise in Vol and Paw .
Partial WOB done by the
patient
High resistance during
spontaneous breath through
ETT.
32. SYNCHRONISED IMV
Mandatory breaths are ‘sychronised’
with patient effort.
Mandatory breaths may be time
triggered (poor RR) or patient
triggered (good RR)
Thus, mandatory breaths my be
assisted or controlled.
Mandatory breaths can be set as
volume controlled or pressure
controlled.
Synchronisation window: Time
interval just prior to time trigger when
the ventilator is sensitive to patient
effort, and assisted breath is
delivered. It varies in different
manufacturers but 0.5 sec before
time trigger is representative.
The problem of ‘breath stacking’
and dys-synchrony was
addressed by SIMV.
But, problems of WOB and Raw
during spontaneous breath
persisted.
This is tackled with use of
Pressure Support as adjunct.
Inspiratory flow is provided to
maintain a pressure plateau if
inspiratory effort is sensed.
Breath is terminated once
patients inspiratory flow declines
below a set limit.
Thus, patient triggered, pressure
limited, flow cycled assisted
ventilation.
SIMV and spontaneous mode
always used with PSV in modern
practice.
33.
34. Settings:
1. SIMV + PS – VCV
VT - 6-12 ml/kg IBW
RR – 10 – 15 bpm
I:E – 1:2 – 1:4
FiO2 – titrated to PaO2
PS: PIP – Pplat (min 5 cm
H2O
High pressure alarm
Low pressure/ vol alarm
2. SIMV + PS – PCV
Pressure - < 30 cm H2O
Low pressure alarm
Low volume alarm
Advantages Disadvantages
Maintains
respiratory
muscle strength/
avoids atrophy
May provide false
sense of
improvement of
lung function
Reduces V/Q
mismatch
Desire to wean
too early and
failed weaning.
Decreases mean
airway pressure
Facilitates
weaning
P.S: Increases VT
, decreases
patients’ RR,
decreases WOB
35. DUAL CONTROL MODES
MODE DESCRIPTION
VOLUME ASSURED
PRESSURE SUPPORT
(VAPS; Bird Ventilators)
• Initially, ventilator delivers a patient or time triggered P.C /
P.S breath.
• Set pressure level is reached soon, and the delivered Vol
is compared with pre set volume.
• If, volume is adequate, breath is a PCV/ PSV breath and
terminated
•If volume is low, it switches to VC mode and delivers the
rest of the volume (Dual control within a breath)
PRESSURE
REGULATED VOLUME
CONTROL(SIEMENS),
ADAPTIVE PRESSURE
CONTROL (GALILEO),
AUTOFLOW (DRAGER
EVITA)
• Achieve volume support while keeping PIP lowest possible
• Ventilator gives a trial breath and calculates Pplat &
compliance
• Pressure gradually increased till it reaches set VT .
• PIP is kept at lowest by altering the flow rate and
inspiratory time in response to changing compliance or Raw
• Dual control breath to breath
ADAPTIVE SUPPORT
VENTILATION (ASV;
HAMILTON GALILEO)
• Clinician enters body weight and desired M.V %
• Ventilator calculates dead space and required M.V from
weight
• Uses test breaths to calculate compliance, Raw , intrinsic
PEEP
36. OTHER MODES
MODE DESCRIPTION
Inverse Ratio Ventilation (IRV) • Longer inspiratory time; I:E – 2:1 – 4:1
•Beneficial in ARDS by – reducing
intrapulmonary shunt, reduced deadspace
ventilation, Better V/Q matching
• Higher mPaw - more chances of
barotrauma
•May worsen pulmonary edema
•Requires sedation and paralysis
Automatic Tube Compensation (Drager
Evita)
• Can be applied to all other modes
•Compensates for the airflow resistance of
artificial airway
• Appropriate pressure is delivered during
inspiration and expiration, changes with
respect to Raw and flow requirements
Neumerous other modes have been described such as Automode, Volume Ventilation
Plus, Volume Support, Pressure Support Volume Guarantee etc which are similar to or
combination of the above discussed modes.
37. NEWER MODES
Name Description
Proportional Assist Ventilation + • Clinician only sets the % of WOB that the
ventilator should do.
• Compliance and resistance information is
collected every 4-10 breaths, F and V data
collected every 5 ms to know the patients’
demands.
• No target flow, volume or pressure
•Initially started at 80% WOB, then weaned
back to stabilise.
Neurally Adjusted Ventilatory Assist (NAVA) • Uses electrical signals from the
diaphragm as trigger in addition to flow/
pressure
• Signals measured trans-oesophagally
with use of a cathater ( doubles as Ryle’s
Tube)
• Clinician can set the level of amplification
of the signal – NAVA level
38. AIRWAY PRESSURE RELEASE VENTILATION
Relatively new mode of ventilation, available on the Drager
Sevina 300.
Described as continuous positive airway pressure (CPAP) with
regular, brief, intermittent releases in airway pressure.
The baseline Paw is set to a higher level and ventilation (CO2
removal) occurs by decreasing the Paw to lower level, opposite
of conventional ventilation.
In addition, spontaneous breaths are allowed throughout the
cycle.
I:E ratio is inverse, i.e longer TI than TE ;
39.
40. Advantages:
Lower Paw for given VT compared
to VCV, IMV [1]
Better PaO2/ FiO2 in ARDS
compared to conventional modes
[1]
Maintaining Paw helps in
recruitment of alveoli, limits lung
injury by repeated expansion,
collapse and stretch
Maintains cardiovascular status
better as compared to VCV, PCV,
IRV [2]
Requires lesser sedation and
paralysis[3]
Disadvantages:
Cannot be used in patient’s
requiring sedation for
management like head inury
Limited availibility
Limited data on conditions other
than ARDS/ ALI
Settings:
PHIGH : <35 cm H2O
Plow: 0 – 5 cm H2O
THIGH : 4-6 secs
TLOW : 0.5 – 1 sec (0.8 sec)
To improve oxygenation:
Increase PHIGH or THIGH
Prone position
To improve ventilation (CO2
removal:
Increase PHIGH and decrease
T HIGH to increase MV
Increase TLOW by 0.1 sec
increments
Decrease sedation
1. Daoud EG AnnThoracMed; 2007
2. Kaplan LJ et al, CritiCare; 2001
3. Rathgeber J et al, EurJAnaesthesiol;
1997
41. POSITIVE END EXPIRATORY PRESSURE (PEEP)
Elevation of baseline Paw above
atmospheric pressure
Not a standalone mode of
ventilation, used as adjunct to other
modes
When applied to spontaneous
breathing patients, it is called CPAP
Increases FRC, results in
recruitment and prevents collapse
of alveoli, i.e better V/Q match
Lowers the distention pressure of
alveoli and facilitates oxygenation
and oxygenation
Indications:
Refractory hypoxemia (PaO2< 60
mmHg with FiO2> 50%
Intrapulmonary shunt – atelectasis
etc
Decreased FRC and compliance –
ALI/ ARDS
Hazards of PEEP:
Lowers venous return, CO
Barotrauma (PEEP>10 cm H2O)
Increased CVP, ICP
Decreased hepatic perfusion, bowel
perfusion
Decreased renal perfusion, GFR
and overall excretory function
42. Continuous positive airway
pressure (CPAP)
PEEP applied to spontaneous
breathing patient
Requires eucapnic ventilation
by the patient
Can be applied via ETT, face
mask, nasal mask
In neonates nasal CPAP is
method of choice
Less adverse effects than
PEEP because of
spontaneous rather than PPV
Bilevel positive airway
pressure (BiPAP)
Independent positive
pressures to inspiration (IPAP)
and expiration (EPAP)
IPAP provides pressure
support during inspiration and
EPAP helps in recruitment and
FRC
Generally via non invasive
methods, prevents intubation
in chronic diseases
Initially IPAP – 8 cm H2O,
EPAP – 4 cm H2O; maybe
increased or decreased in 2cm
44. VENTILATOR GRAPHICS ANALYSIS
Scalars:
Pressure vs time
Volume vs time
Flow vs time
Uses:
Confirm mode functions
Detect Auto-PEEP
Detect asynchrony
Asses and adjust triggers
Calculate WOB
Assesment of bronchodilator
therapy
Equipment malfunction
Detect leaks
Decide adequacy of inspiratory
time and rise time
Loops:
Flow vs volume
Pressure vs volume
Uses:
Changes in compliance and
resistance
WOB and work of triggering
Inspiratory area calculations
Lung overdistention
Assesment of bronchodilator
therapy
Adequacy of flow rates
53. PATIENT CARE DURING ONGOING
MECHANICAL VENTILATION
i. Review communications –
From patient to medical
staff and between doctors
and nurses
ii. Check and confirm modes,
settings and alarms
iii. Airway management
iv. Assesment of sedation and
analgesic needs
v. Meet the patient’s
nutritional needs
vi. Suction appropriately
vii. Assesment Infection
prevention
viii. Maintain haemodynamic
stability
ix. Check for possibility of
weaning
x. Educate the patient and the
family
54. PAIN AND ANALGESIA
Patel SB et al. Sedation and Analgesia in the Mechanically
Ventilated Patient. Am J Respir Crit Care Med 2012; 185(5)
Pain is a frequent symptom of
mechanically ventilated
patient
It may be due to intubation
and ventilation itself, due to
disease conditions or due to
movement and adjustment to
tubes and lines.
Pain may be significant and
can initiate elements of the
stress response
Pain is reported by upto 60 %
patients while on ventilator.
Assesment of pain is
dependent on the ability of
patients’ to communicate
The Neumeric Rating Scale
or Visual Analog Scale have
been validated
The Behavioral Pain Scale,
Critical Care Pain
Observation Tool and Non
Verbal Pain Scale are other
tools that have been tested
with varying results
55.
56. SEDATION
Patel SB et al. Sedation and Analgesia in the Mechanically
Ventilated Patient. Am J Respir Crit Care Med 2012; 185(5)
Analgesia alone may be enough
in some patients, others may
require additional seation
Sedation reduces patient
discomfort, improves
synchronicity and decreases O2
consumption and WOB
But, also associated with
delayed weaning,
haemodynamic laibility and
respiratory depression
Intermittent boluses as well as
continuous infusion may be
used.
Infusions may have prolonged
action after discontinuation and
accumalation of metabolites
Daily ‘wake-up’ and assesment
for weaning is recommended.
Neumerous tools such as the
Ramsay Sedation Scale(RAS),
Sedation Agitation Scale (SAS)
and Richmond Agitation
Sedation Scale etc may be
employed
57.
58. CHOICE OFDRUG
AUTHORS DRUGS COMPARED OUTCOME
Carrer et al.(100 postsurgical
patients)
Ramifentanyl + morphine vs
morphine alone
R+M more effective
Dahaba et al (40 patients) Ramifentanyl vs morphine R more effective, more rapid
wake up and extubation
Muellejans et al (152 cardiac,
general surgical and medical
pts)
Ramifentanyl vs fentanyl Ramifentanyl requires lesser
sedatives, but more
painafterward
Muellejans et al (80 cardiac
surgery pts)
Ramifentanyl + propofol vs
fentanyl + midazolam
R + P: Fewer days on MV,
fewer days in ICU
Pohlman el at Lorazepam vs midazolam Lorazepam: more rapid wake
up
Swart et al Lorazepam vs midazolam Lorazepam: more effective
sedation and more cost
effective
Grounds et al, Aitkenhead et al,
Ronan et al, Kress et al
Propofol vs Midazolam Propofol more effective
sedation, fewer days on MV,
more rapid wale up
Venn et al, Herr et al,
Pandharipande et al,
Riker et al, Dasta et al,
Shehabi et al
Dexmedetomidine Vs Various
(placebo, propofol, midazolam,
lorazepam)
Dexmedetomidine:
Lesser analgesic requirement
Fewer days on MV, ICU
Fewer days of delerium
Lower mortality , lower costs
59. NUTRITION
Protein Energy Malnutrition, common in
critically ill patients results in diminished
strength and endurance.
Weakness of respiratory muscles like
diaphragm and SCM lead to poor
pulmonary performance, SOB, fatigue
and decreased response to hypoxia
Malnutrition also affects the immune
system, more susceptibility to infection
Low magnesium associated with muscle
weakness, hypophosphatemia – delayed
weaning
Recommended that nutritional therapy
start latest by 3rd day of MV, within 24 hrs
in malnurished patients
Protien requirements range from 1.2 – 2
g/kg/day; higher in burns, severe trauma
and obese patients
60. 1. Martindale RG et al. Guidelines for the provision and assessment of nutrition support therapy in the adult
critically ill patient. Crit Care Med 2009; 37(5)
2. Canadian Practice Guidelines for nutrition support in mechanically ventilated, critically ill patient . Journal
of Parenteral and Enteral Nutrition 2003; 27(5)
Whenever possible, Enteral
Nutrition should be the method of
choice.
EN maintains gut integrity, lesser
infections, more nutrients
delivered and better immunity
‘Refeeding syndrome’ – large shift
of fluid and electrolytes after
institution of EN, caution in shock
patients, obese and prolonged
NPO
Serum pre-albumin, BUN, Na, K,
Mg, P may be reflective of
nutrition status
Addition of vitamins (thiamine),
supplements like fish oil (omega 3
and 6 - better outcome in ARDS),
arginine, glutamate etc may be
considered
Tolerance of EN should be
assesed, pain, distention,
reflux, non-passage of flatus,
abnormal Xray abd
Residual volumes on aspiration
are used as indicator – 150-200
ml taken as cutoff, newer
evidence suggests as much as
500 ml may be tolerable
Prokinetics are recommended,
dietary fibre, laxatives,
probiotics may be used
PN used only when EN is not
possible, inadequate or
contraindicated
PN associated with more
metabolic, electrolyte and
infectious complications; higher
cost, gut atrophy
61. CARE OF VENTILATOR CIRCUIT
Circuit compliance:
Higher circuit compliance may
result in lowe effective tidal
volumes
Circuit Patency:
Condensation of moisture from
expired gases is the biggest
threat to patency
Heated wire circuits, in-line water
trap and HME filters are
commonly used for this purpose
Frequency of circuit change:
Frequent circuit change for
infection control is not
recommended
Some recommend circuit change
only if visibly soiled
Others have recommended
weekly change of circuit
Patency of ET tubes:
Secretions (low humidification)
Kinking (patient positioning)
Patient biting ETT
Malfunction of ETT cuff
HME Filters:
Temporary humidification devices
Placed between circuit and patient
Absorbs heat and moisture during
exahalation (CaCl2, AlCl2) and
transfers back during inspiration
May colonise bacteria – anti-
bacterial filter
Large amount of secretions, very
high MV and aerosol delivery are
potential problems
63. REMOVAL OF SECRETIONS
AARC Clinical Practice Guidelines. Endotracheal suctioning to
mechanically ventilated patients with artificial airways. Respir
Care 2010;55(6)
Repeated removal of
secretions are necessary at
times
Pooled secretions may cause:
Poor gas exchange
Higher airway pressures
Obstruction of ETT
Patient coughing, restlessness
Higher spontaneous RR
Suction only when secretions
present – not routinely
Use of saline or mucolytic
solution either in aerosol or
direct instillation can aid in
suctioning, but may be a
source of infection – not
routinely recommended
Combined with recruitment
maneuvers and chest
physiotherapy
Use of closed suction unit as
far as practicable.
Use of closed suction unit as
far as practicable.
Pre-oxygenation prior to
suction procedure to prevent
desaturation
Suction catheter should not
occlude more than 50% of
lumen of ETT
Duration of suctioning limited
to less than 15 seconds
65. WEANING FROM MECHANICAL VENTILATION
Weaning is the process of withdrawl of ventilatory
support, ultimately resulting in a patient breathing
spontaneously and being extubated.
Transfer of WOB to the patient from the ventilator.
Weaning Success:
Absence of need of ventilatory support 48 hrs following
extubation.
The patient is able to pass a Spontaneous Breathing
Trial (SBT).
1. Boles JM et al. International Consensus Conferences – Weaning from mechanical ventilation. Eur Respir J 2007; 29
2. LermitteJ et al. Weaning from mechanical ventilation. Contin Edu Anesth Crit Care Pain 2005;5(4)
66. ASSESMENT OF READYNESS TO WEAN
1. Boles JM et al. International Consensus Conferences – Weaning
from mechanical ventilation. Eur Respir J 2007; 29
2. LermitteJ et al. Weaning from mechanical ventilation. Contin Edu
Anesth Crit Care Pain 2005;5(4)
General preconditions:
Reversal of primary problem
causing need for mechanical
ventilation
Patient is awake and
responsive
Good analgesia, ability to
cough
No or minimal inotropic
support
Ideally – functioning bowels,
abscense of distention
Normalising metabolic status
Adequate Hb concentration
Objective values:
Minute Ventilation <10l/min
Vital Capacity > 10 ml/kg
RR <35
Tidal volume > 5ml/kg
Max inspiratory pressure <-25
cm H2O
RR /Vt <100 b/min/L
PaCO2 < 50 mmHg
PaO2 > 90 mm Hg at FiO2 0.4
PaO2/ FiO2 > 200
67. WEANING INCICES
Rapid Shallow Breathing Index (RSBI):
Ratio of RR/VT (spontaneous)
Value > 100 suggests potential weaning failure
Patient is allowed to breathe spontaneously for 3 mins, MV is
measured and avg VT over one min is divided by RR
Simplified weaning index:
SWI= FMV (PIP-PEEP)/MIP X PaCO2 MV /40
Used while patients still receiving mechanical supp
SWI < 9/min – 93% weaning success
SWI > 11/ min – 95 % chance of weaning failure
Compliance Rate Oxygenation and Pressure (CROP)
[Cdyn x MIP x PaO2/ PAO2] / F
CROP index > 13 mL/b/min predicts weaning success
69. PROTOCOLISED
WEANING
Various protocols are
published inliterature, with
the aim of standarising
weaning procedure and
shortening the duration of
ventilation
It has been shown in
numerous studies that
protocolised weaning
reduces time on ventilator
and shortens ICU stay
(Dries DJ et al; Jtrauma
2004; 56)
70. VENTILATOR INDUCED LUNG INJURY
Prost DN et al. Ventilator induced lung injury: historical perspectives and clinical implications. Annals of Intensive Care
2011.
Ventilator associated lung injury
(VALI) is acute lung injury that
develops during mechanical
ventilation, termed as VILI of
causation is proved.
Volutrauma:
Areas of atelectasis (dependent),
consolidation, secretion and
heterogenous distribution of disease
(ARDS) and less compliant, air
flows towards the normal alveoli
over distending them.
Increased stretch leading to alveolar
damage, increased permeability,
edema
Prevented by using low VT (6ml/kg)
ventilation.
Atelectrauma:
Repeated expansion and collapse
of alveoli
Shear forces cause disruption of
epithelium and failure of alveolar
membrance
Prevented by PEEP, ‘open lung
concept’ – keep alveoli open
Biotrauma:
Release of inflammatory
mediators from lung tissue.
Inflammation of lung tissue,
surfactant dysfunction
Incidence is 24%, higher in ARDS
Management is same as of ARDS/
ALI – lung protective ventilation
71. VENTILATOR ASSOCIATED PNEUMONIA (VAP)
1. CDC- Ventilator Associated Event Protocol .Jan 2013
2. Guidelines for the management of hosppital aquired,
ventilator associated and healthcare associated
pneumonia. AmJRespirCritCare 2005; 171
Defined as pneumonia occuring
more than 48 hrs after intubation
and mechanical ventilation.
Estimated incidence is 10-25%,
mortality of 33-76%
Early onset (2-5 days) – S.
Pneumoniae, H. Influenzae,
MSSA, E.Coli, Klebsiella, less
severe, minimal mortality
Late onset (> 7 days) – P.
Aeruginosa, Acinetobacter,
MRSA, other MDR pathogens;
higher morbidity and mortality
DIAGNOSIS: Presence of a new
or progressive infiltrate in CXR
plus two of the following:
Fever > 38 C
Leukocytosis/ Leukopenia
Purulent tracheo- bronchial
secretions
Respiratory tract sampling using
BAL, mini BAL, tracheo-bronchial
aspiration for microscopy and
quantitative culture
72. PREVENTION using ‘bundled
approach’ has shown to reduce the
incidence of VAP by as much as 95%
Components may be as:
Appropriate cuff to prevent aspiration
Change of circuit every 7 days/ visible
soiling
HME and suction devices changed daily
ETT with dorsal lumen for sub-glottic
secretions
Elevation of head 30-45%
Strict hand hygiene
Oropharyngeal decontamination –
chlorhexidine, iodine
Sedative vacation; early extubation
Non invasive ventilation
Prophylactic antibiotics are not
recommended by any route
(including aerosol) because of
inconsistency and risk of resistance
TREATMENT
Emperical antibiotic therapy after
sampling.
Choice of antibiotic depends on local
prevalance of organisms and the
patient’s risk for MDR infection.
High risk group incude hospitalisation
> 5 days, antibiotic use in last 90
days, haemo-dialysis, residence in
nursing home
Low risk – Ceftriaxone/ Levo,
ciprofloxacin/ Ampicillin sulbactam/
Ertapenem
High risk –
Antipseudomonal (Cefipime/
Ceftazidime/ carbapenems/ Piperacillin
TZ) +
Fluroquinolone/ Aminoglycoside +
Linezolid/ Vancomycin
73. NON- INVASIVE PPV
NIPPV is the delivery of
mechanical ventilation using
techniques that do not
require tracheal airway
Theoritically, all PPV modes
canbe used in NIPPV; but
mostly used to provide
pressure support during
spontaneous ventilation,
BiPAP, CPAP
Also used as an option for
weaning.
May delay intubation in
COPD patients
76. Life threatening respiratory
condition characterised by
hypoxemia and stiff lungs.
Stereotypical response to a
number of insults, involves
three phases
Damage to alveolar capillaries
Lung resolution
Fibroproliferative phase
Pulmonary epithelial and
endothelial damage
characterised by
inflammation, apoptosis,
necrosis and increased
permeability.
This inturn laeds to loss of
surfactant, decreased
compllaince and V/Q
mismatch
DIRECT INDIRECT
Pneumonia Non pulmonary sepsis
Aspiration of gastric contents Major trauma
Inhalational Injury Pancreatitis
Pulmonary contusion Severe burns
Drowning Non cardiogenic shock
Drug overdose
Transfusion associated lung injury (TRALI)
77.
78. MANAGEMENT OF ARDS
1. Ventilation with lower tidal volumes as compared with
traditional tidal volumes for ALI/ARDS,The ARDS network,
NEJM 2000;342
2. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy
using low tidal volumes, recruitment maneuvers, and high
positive end-expiratory pressure for ALI/ARDS: a
randomized controlled trial. JAMA 2008;299:637-45.
3. Briel M, Meade M, Mercat A, et al. Higher vs lower positive
end-expiratory pressure in patients with ALI/ARDS:
systematic review and meta-analysis. JAMA 2010;303:865-
Lung protective ventilation
Based on concept that
limiting end inspiratory stretch
may reduce mortality.
Lower VT (4-6 ml/kg) and
PPLAT between 25-30 cm H2O
have been shown to have
mortality benefit compared
with conventional ventilation
(31% vs 40%) [1]
Open Lung approach
Repeated opening and closing
of alveoli can cause further
injury to lungs
Many trials have demonstrated
better PaO2/ FiO2 in patients
with higher PEEP + protective
ventilation, but no mortality
benefit (ALVEOLI, EXPRESS,
Canadian LOV trial[2])
A recent meta-analysis has
concluded that higher PEEP
levels have mortality benefit
only in mod-sev ARDS, not in
mild ARDS[3]
79. 1. Fanelli V, et al. ARDS: new definition, current and future therapeutic options. J Thoracic Dis 2013;5(3)
Non conventional modes
APRV / IRV may allow better
ventilation of dependent and
diseased regions – better V/Q,
oxygenation
Routine widespread use not
recommended due to lack of data
on mortality benefit.
High Frequency Oscillatory
Ventilation delivers very small VT
at a rapid rate (`150/min) – no
mortality benefit, not
recommended as first line
ECMO has been used for
oxygenation, limited by availibility
Non ventilatory measures
Prone position – better
oxygenation, mixed mortality
outcomes
Resticted fluid protocol shown to
have better outcomes vs liberal
fluids
Use of neuromuscular blockers in
forst 24 hrs associated with
reduced mortality
Methylprednisolone in early severe
ARDS reduces mortality
1 mg/ kg IV loading over 30 min
1 mg/kg/day for 14 days
Gradual taper in next 14 days
Fish oil (omega-3 fatty acids) may
have beneficial effects
80. SUMMARY
Mechanical ventilation is an indispensible tool for the intensivist
Whether or not the patient requires ventilator support is a crucial decision to
make
Proper understanding of ventilator function and modes are vital to provide
individualised therapy to a wide range of patients
Ventilator graphics can provide valuable information regarding settings and
pulmonary characteristics
Patient care during critical illness is vital – proper co-ordination between
machines, nurses and doctors
Early weaning is the norm, protocolised weaning should be implemented
VILI and VAP are dreaded complications - prevention is better than cure
ARDS is a ventilatory challenge – large amount of literature available to guide
management
81. REFERENCES
1. Clinical Application of Mechanical Ventilation – David W Chang, 4th
Edition
2. Mechanical Ventilation – Vijay Deshpande, 2nd Edition
3. The ICU book – Paul L. Marino, 4th edition
4. Chatburn RL. Classification of Ventilator Modes. Respir Care 2007;
52(3)
5. www.ardsnet.org
6. www.frca.co.uk – Anaesthesia Tutorial of the Week
7. www.wikipedia.org
8. Ventilator Waveforms – Graphical representation of ventilatory data.
Puritan Bennett
9. Lindgren VA et al. Care for patients on mechanical ventilation. AJN
2005;105
10. Grossbach I et al. Overview of mechanical ventilatory support, and
managent of patient and ventilator related responses. Critical Care
Nurse 2011
11. Girard TD et al. Mechanical ventilation in ARDS – A state of the art
review. CHEST 2007; 131
82. “…an opening must be attempted in the trunk of the trachea, into
which a tube of reed or cane should be put; you will then blow
into this, so that the lung may rise again…and the heart
becomes strong…” - Andreas
Vesalius 1555
THANK YOU