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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