mechanical ventilation
TRANSCRIPT
MECHANICAL VENTILATION IN ICU
Moderator: Sir Prof. L Deban Singh
Presenter: Dr. Shikhar More
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.
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.
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
VENTILATORY FAILURE
Ventialtion Perfusion (V/Q) mismatch: Deadspace ventilation Intrapulmonary shunting
• Reduced cardiac output: CHF• Low pulmonary perfusion : embolism, Vasoconstriction
•ARDS, pneumonia (consolidation), pulmonary edema , atelectasis, interstitial lung disease• Prevented by the normal reflex hypoxic pulmonary vasocinstriction
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.
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.
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
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.
ASSESMENT OF IMPENDING FAILUREParameter 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, diaphoresis, cyanosis
CLINICAL CONDITIONS
Acute airflow obstruction: Asthma, COPD, epiglotittis, laryngospasm/bronchospasm
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)
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
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
BASICS OF MECHANICAL VENTILATORS
PHASE VARIABLES There are four distinct phases of ventilator breath
Four parameters can be controlled or manipulated during each phase: Volume, Pressure, Flow, Time.
Expiration – Inspiration
•Trigger
Inspiration
•Limit, Control
Inspiration - Expiration
•Cycle
Expiration
•Baseline
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.
FIG: PRESSURE TRIGGER
FIG: FLOW TRIGGER
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.
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).
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)
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.
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.
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.
VOLUME VS PRESSURE CONTROL
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
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
(Assisted)
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
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
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.
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.
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
DUAL CONTROL MODESMODE 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• Uses sophisticated algorithms to decide RR, TI , I:E, Paw limits.•Adjusts mandatory frequency, VT in response to patients spontaneous efforts to keep MV constant
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.
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
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 ;
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; 20072. Kaplan LJ et al, CritiCare; 20013. Rathgeber J et al, EurJAnaesthesiol;
1997
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
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
PEEP
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
PCV
SLOW ADEQUATE OVERSHOOT
PRESSURE VOLUME LOOPS
MANAGEMENT OF MECHANICAL VENTILATION
Strategies to improve ventilation
STRATEGIES TO IMPROVE OXYGENATION
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 managementiv. Assesment of sedation
and analgesic needsv. Meet the patient’s
nutritional needs
vi. Suction appropriatelyvii. Assesment Infection
preventionviii. Maintain
haemodynamic stabilityix. Check for possibility of
weaningx. Educate the patient and
the family
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
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
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 requirementFewer days on MV, ICUFewer days of deleriumLower mortality , lower costs
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
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
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
HME Filter
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
CLOSED SUCTION
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)
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
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
COMMON WEANING PROCEDURES
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)
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
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
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
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
ARDS – DEFINITION, DIAGNOSIS AND MANAGEMENT
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 mismatchDIRECT 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)
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;303:865-73.
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]
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
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
REFERENCES1. Clinical Application of Mechanical Ventilation – David W Chang, 4 th
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
“…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
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