VENTILATORY STRATEGIES IN INFLUENZ-A H1N1, ASSOCIATED ARDS

DR ARVIND KHARE Associate Professor

Department of Anaesthesia,J.l.N. Medical College,

AJMER

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PULMONARY COMPLICATIONS The majority of H1N1 patients presented with rapidly progressive hypoxemia (ARDS),

Primary viral pneumonia

Secondary bacterial pneumonia

Exacerbation of COPD and bronchial asthma

croup/bronchiolitisin the pediatric population

EXTRA-PULMONARY COMPLICATION central nervous system (e.g., septic encephalopathy) kidneys (e.g.,acute renal failure), gastrointestinal system (e.g. organ ischemia

Myocarditis and Pericarditis

. Reye Syndrome

Fatigue (persists for weeks)

COMPLICATINS OF H1N1 FLU

Whats the problem in ARDS• ARDS is a serious disease that initially presents

as an acute lung lesion it is characterized by• damage the parenchyma of the lungs • Thickened diffusion membrane• Inflamed exudate-filled alveoli• Collapsed bronchioles• Massive intra pulmonary shunt• non-cardiogenic pulmonary edema- arising

from an increase in the permeability of the alveolar capillary membrane of the lung

cause alterations in pulmonary compliance, and high inspiratory pressure is then required to open the collapsed alveoli

ARDS associated with influenza A H1N1,the following criteria must be fulfilled

•A- Acute onset ((1 to 3 days)•R- Pao2/Fio2 ratio </= 200•D- Bilateral diffuse infiltrates on chest radiography consistent S- PA wedge pressure(Swan Ganz) </=18 mm Hg other criteria based on clinical symptoms andgasometrical tests Pao2 <60 mmHg or a FiO 2 >50% , lack of left ventricle dysfunction in echo cardiographic examination

DIAGNOSIS OF ARDS

Ventilatory failure

Inability of the pulmonary system to maintain proper removal of CO2 result into hypercapnia ultimately lead to Oxygenation failure

Acute ventilatory failure• sudden increase of PaCO2>50 mmHg with respiratory acidosisPH<7.3 • Eg; COPD

Impending ventilatory failure Excessive ventilatory work load may lead to muscle fatigue & lead to ventilatory &

oxygenation failure . Gradual increase of PaCO2>50 mmHg with respiratory acidosisPH<7.3 Eg.ARDS

•

Ventilatory failure

• Hypoventilation –paco2 >45mmHg=COPD

• V/Q mismatch/Dead space ventilation=pulmonary embolism=respond to o2 therepy

• Intrapulmonary shunting/Wasted perfusion= shunt>20%= Atelectasis= Refractory hypoxemia

• Diffusion defect= impaired gas exchange through alveolar capillary membrane = interstial pulmonary edema

Assesment of Impending ventilatory failure

Severe hypoxemia- Pao2<60mmHg on 50%Fio2 Pao2<40mmHg on any Fio2 intrapulmonary shunting {p(A-a)o2}>450 on 100% Fio2RR=labored respiratory pattern >35/minMinute ventilation>10 l/minVital capacity<15 ml/kgMaximum inspiratory pressure< -20 cm H2oPH <7.3(progressive acidosis&hypoventilation)Paco2 >50mmHg

Fraction of Inspired Oxygen[FIO2]

The percent of oxygen concentration that the patient is receiving from the ventilator. ---- Between 21% & 100%

Initially a patient is placed on a high level of- 60% or 100% FIO2 until arterial blood gases can document adequate oxygenation Goal – to achieve PaO2 > 60mmHg or Sao2 >90%

After stabilization of the patient Fio2 may be set=<50% to avoid O2 induced lung injury Subsequent changes in FIO2 are based on ABG Pao2 [80-100mmHg] maintain an SaO2 of greater than 90%Oxygen toxicity -is a concern when an FIO2 of greater than 60% is required for more than 25 hours. 1.. Absorption atelectasis, 3..Accentuation of hypercapnia, 2. Airway injury 4. Parenchymal injury

Lower Tidal VolumeIndication of lower TV=• increase airway pressure -ARDS ,Pulm. edema• Increase lung

compliance=Emphysema[ COPD]- decreasing TV 100-200 ml reduces expiratory

time requirement & help to prevent air trapping

Adverse effect of low TV=• Ac hypercapnia,• Acidosis

Respiratory Rate• An optimal method for setting the respiratory rate is intended to

provide Eucapneic ventilation• An initial RR between 10 and 12 breaths per minute

RR=MV/TV• If CO2 production is more or increased Physiological dead space RR should increase & not increase TV- because high TV can cause

high airway pressure

• What should be New Ventilator rate? If Patient RR is 10 paco2 is 60&, desired Paco2 is 40mmHg New rater =Rate*Paco2/ desired Paco2 = =10*60/40=600/40=15/min

Inspiratory Time: Expiratory Time(I:E Ratio)

I:E ratio: the fractional proportion of time spent on each phase of the respiratory cycle. The normal I:E ratio is 1:2 I:E ratio: depand on flow rate- if flow rate increase = I time& delivered TV will be decrease =I:E Ratio would be increase

Eg Asthma/COPD =1:3, 1:4, If . flow rate decrease = = I time& delivered TV will be increase = I:E Ratio would decrease

Eg S ARDS/ALI ,Pulm..Edema= 1:1,2:1

Using I time to to desire Ratio[1:3] = if RR=16/Min [=60/16=3.75/sec]

I time=time for each breath*[I ratio/sum of I:Eratio] =3.75*[1/1+3] =0.93 sec I time require to desire Ratio[1:3 •

Physiology of PEEP• Re inflates collapsed alveoli and maintains

alveolar inflation during exhalationPEEP

Decreases alveolar distending pressure

Increases FRC by alveolar recruitment

Improves ventilation

Increases V/Q, improves oxygenation, decreases

work of breathing Recruit lung

Collapse/ atelectosis/ ARDS

Increases Surface area for gas exchangeOpens the collapsed lung

Collapsed alveoli

After PEEP

PEEP

PEEPDuring the H1N1 pandemic, high levels of PEEP were often used to achieve

adequate oxygenation (SpO2 88–90%) high PEEP is applied to counteract Low VT ventilation effects by recruiting

non aerated lung. PEEP levels as high as 24 cm H20 can be usedOptimal PEEP -the lowest PEEP level leading to the best oxygenation or

compliance status without causing cardiopulmonary side effects At 10 cm H2o- Pao2 is 83 mmHg/ compliance is 43 ml/cm H2o At 12 cm H2o- Pao2 is 79 mmHg/ compliance is 41 ml/cm H• Adverse effect -High PEEP levels carry the potential for significant

hemodynamic• Adverse effects, including decreased venous return and right ventricular

dysfunction

Permissive Hypercapnia-

• Intentional hypoventilation by reducing TV to 4-7 ml /kg• aims to limit plateau pressure<35 cm H2o and is generally tolerated until

arterial pH declines to 7.15• Side effect-• Intentional hypoventilation may cause co2 retention- lead to

acidosis,CNS dysfunction,intra cranial hyper tension neuro muscular weakness,cardio vascular impairment

• THAM[ tromethamine]• is a non bicarbonate buffer lower the CO2 & increase the bicarbonate

level.it is prefereble to bicarbonate in patient who are being hypoventilated intentionaly

Dose=0.3*BW[kg] *base deficit[meq/lit]

Vent settings to improve <ventilation>Vent settings to improve <ventilation>

• Respiratory rate• Max RR at 35 breaths/min • Efficiency of ventilation decreases

with increasing RR• Decreased time for alveolar emptying

• TV• Goal of 10 ml/kg• Risk of volutrauma

• Other means to decrease PaCO2• Reduce muscular activity/seizures• Minimizing exogenous carb load• Controlling hypermetabolic states

• Permissive hypercapnea• Preferable to dangerously high RR and

TV, as long as pH > 7.15

RR and TV are adjusted to maintain VE and PaCO2

• I:E ratio (IRV)• Increasing inspiration time will

increase TV, but may lead to auto-PEEP

• PIP• Elevated PIP suggests need for

switch from volume-cycled to pressure-cycled mode

• Maintained at <45cm H2O to minimize barotrauma

• Plateau pressures• Pressure measured at the end of

inspiratory phase• Maintained at <30-35cm H2O to

minimize barotrauma

Routine use of NIV should be avoided.

NIV should not be use in H1N1 respiratory failure.poor ventilator support rapid progression of hypoxemia, unable to secure an airway hemodynamic instability high failure rate NIV misguided & might worsen the prognosis because this disease is known

to progress quickly from ARF to ARDS,

CONVENTIONAL TRADITIONAL VENTILATION

CONVENTIONAL TRADITIONAL VENTILATION IN H1N1 FAILURE VT of 12 mL/kg minimum PEEP guided by the FIO2 goal PPLAT 50 cmH20.

• Aim= large tidal volumes would recruit atelectatic lung. Drawback=. large tidal volume - ventilation created regional over distension . Barotrauma -Small changes in volume causes large changes in alveolar

pressure which lead to barotrauma in poor compliance atelectatic lung Excessive alveolar distension led to neutrophil activation and increased

cytokine release,and thus greater ventilator-induced lung injury (VILI

Lung protective ventilation strategy

for the ARDS “lung protective ventilation” with low

tidal volume– Aim PaO2 = 55-80 mmHG– Tidal volume of ONLY 6ml/kg– Pplat to be kept under

35cmH2O – PEEP titrated based on FiO2

• pH to be kept over 7.30 (Permissive hypercapnia )

• goal SpO2 88-90%.& • - ANY ventilator mode

ACUTE RESPIRATORY MANAGEMENT IN ARDS (ARMA) lung-protective ventilation strategy • low tidal volume - limit the trans pulmonary driving pressure in diseased lungs • PEEP is titrated to counteract the atelectasis lung that invariably occurs with a

low VT strategy plateau pressure was allowed to not more than 35 cm H2O.

Benefit• There was a significant improvement in pulmonary compliance, gas exchange, and

weaning rate in the group• Less regional over distension-& barotrauma• requires a shorter duration of Mechanical ventilation• improves survival rates& reduces the mortality rate

Permissive hypercapnia-

• Intentional hypoventilation by reducing TV to 4-7 ml /kg• aims to limit plateau pressure<35 cm H2o and is generally tolerated until

arterial pH declines to 7.15• Side effect-• Intentional hypoventilation may cause co2 retention- lead to

acidosis,CNS dysfunction,intra cranial hyper tension neuro muscular weakness,cardio vascular impairment

• THAM[ tromethamine]• is a non bicarbonate buffer lower the CO2 & increase the bicarbonate

level.it is prefereble to bicarbonate in patient who are being hypoventilated intentionaly

Dose=0.3*BW[kg] *base deficit[meq/lit]

Which mode is your choice ?

VOLUME CONTROL-PRESSURE CONTROL-

CHOICE- PRESSURE CONTROL VENTILATION

ADVANTAGE

• The inspiratory pressure, RR, I:E ratio may be selected

• guarantees desire pressure • Once pressure plateau is

created & maintained for a preset inspiratory time

Allows limitation of peak inspiratory pressures(PIP)

Decelerating flow pattern lower PIP for same TV

Pitfalls Does not guarantee minute

ventilation tidal volume may change

suddenly as patient’s compliance changes

Potential hyper- or hypoventilation with lung resistance/compliance changes

• No participation of patient • patient requires sedation

Pressure control ventilationWhy better than volume control in– low compliance lung/ARDS – -have increased airflow resistance

– VCV require high PIP& flow – to maintaining adequate oxygenation & ventilation may lead to excessive inspiratory

pressures may causes Barotrauma Square wave(constant) flow pattern results in higher PIP for same tidal volume

What happened in volume control?

Increased Airway Resistance Decreased Compliance

PIP

Pplat

PIP

Pplat

A. B.

•A-An increase in airway resistance causes the PIP to increase, but Pplat pressure remains normal.•B-A decrease in lung compliance causes the entire waveform to increase in size. The difference between PIP and Pplat remain normal.

PRVC/APV /AUTOFLOWPressure regulated volume control/ Adaptive pressure

ventilation/ AutoflowPRVC mode can maintained the PIP at 5 cm H2o below the

pressure limit It keep the PIP at lowest level possible by- lowering the peak flow -to reduce the driving pressure increased insp. time - to deliver the target volume in

response to changing airway or complianceDelivers the breath with a decelerating flow pattern that is

thought to be less injurious to the lung…… “the guided hand

Rescue therepy

• Rescue therepy should be considered in patients with persistent hypoxemia, • SpO2 < 88-90% despite conventional ventilation with low tidal volumes

(4-8ml/kg)/adequate PEEP with an FiO2 > 0.8 or plateau pressure > 35 cm H2O• APRV:• Inverse Ratio Ventilation High frequencyventilation (HFV) Extracorporeal membrane oxygenation ventilation in the prone position• Inhaled Nitric Oxide• Sildenafil more appropriate for treatment of ARDS because it improves survival by up to 71%..

APRV [airway pressure release ventilation]

giving a patient two different levels of CPAP (spontaneous breath )Set “high” elevated CPAP(10 cmH2O) is and “low” releasing lowCPAP (0

cmH2O) pressures Length of time at “high” pressure generally greater than length of time at

“low” pressure• By “releasing” to lower pressure, allow lung volume to decrease to FRC

&this periodically facilitate expiration • unlike CPAP it facilitates both oxygenation and removal of carbon

dioxide..

•

Inverse ratio ventilation- IRV IRV is a technique used when conventional mechanical ventilation strategies have

failed reverses this I:E ratio inspiratory time is equal to,( 1:1) or longer than, expiratory

time (upto 4:1). .Indication=ARDS= Inverse I:E ratios are used in conjunction with pressure control to improve oxygenation by overcoming noncompliant lung Recruiting collapsedstiff alveoli Increasing time for gas diffusion preventing alveolar collapse Adverse effect= The increase in mean airway pressure &auto peep in IRV-lead to

increased mean alveolar pressure=Barotrauma • increased mean alveolar pressure leads to higher rate of trans vascular fluid

flow=induce pulmonary edema

High-frequency ventilation (HFV)HFV is time-cycled positive pressure ventilation delivers a high frequency (60–120

breathes per min & small tidal volumes (1.5 mL/kg) that are usually less than the anatomic dead space lower peak pressure, thus better oxygenation with

less barotraumas, Proposed mechanisms of gas exchange include bulk flow, molecular diffusionDifferent modes: High-frequency positive-pressure ventilation HFPPV), High-frequency jet ventilation (HFJV) High-frequency oscillatory ventilation (HFOV)

Prone Positioning

. Proposed mechanisms of action include: Alveolar recruitment improvement in V/Q matching from redistribution of ventilation to dorsal lung

regions, Elimination of the heart’s compressive effects on the lung and Better drainage of respiratory secretions. It is not recommended in Haemodynamically unstable patients as it may interfere with CPR.• Risks include ET obstruction, loss of central vein access during the

manoeuvre• risk of pressure sores. • It is difficult to do in obese patients or in those receiving renal replacement

therapy

Extra-Corporal Membrane Oxygenation• Veno-venous or veno-arterial (VA also provides pump support a’la

cardiopulmonary bypass)• Patients blood is sucked through a membrane which acts as a gas

exchange surface; blood is returned to the lung or to the tissues

SOFA SCORE

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weaning process• It was also noted that once patients improved and the

weaning process should started,• oxygenation was sensitive to small decrements in PEEP. • the best approach was that of watchful waiting with very

small changes made daily to the ventilator settings.• an attempt was made to decrease PEEP 20 cm H2Obefore

weaning FIO2 significantly.

Indications for extubationIndications for extubation

• Clinical parameters• Resolution/Stabilization of

disease process• Hemodynamically stable• Intact cough/gag reflex• Spontaneous respirations• Acceptable vent settings

• FiO2< 50%, PEEP < 8, PaO2 > 75, pH > 7.25

• General approaches• SIMV Weaning• Pressure Support Ventilation

(PSV) Weaning• Spontaneous breathing trials

with T - piece

No weaning parameter completely accurate when used alone

Numerical Parameters

Normal Range

Weaning Threshold

Tidal volume 5 - 7 ml/kg 5 ml/kgRespiratory rate 14 - 18

breaths/min< 40 breaths/min

Vital capacity 65 - 75 ml/kg 10 ml/kgMinute volume 5 - 7 L/min < 10 L/min

Greater Predictive Value

Normal Range

Weaning Threshold

NIF (Negative Inspiratory Force)

> - 90 cm H2O > - 25 cm H2O

RSBI (Rapid Shallow Breathing Index) (RR/TV)

< 50 < 100 Marino P, The ICU Book (2/e). 1998.

Spontaneous Breathing TrialsSpontaneous Breathing Trials

• Settings• PEEP = 5, PS = 0 – 5, FiO2 < 40%• Breathe independently for 30 – 120

min• ABG obtained at end of SBT

• Failed SBT Criteria• RR > 35 for >5 min• SaO2 <90% for >30 sec• HR > 140• Systolic BP > 180 or < 90mm Hg• Sustained increased work of

breathing• Cardiac dysrhythmia• pH < 7.32

SBTs do not guarantee that airway is stable or pt can self-clear secretions

Causes of Failed SBTs

Treatments

Anxiety/Agitation Benzodiazepines or haldolInfection Diagnosis and txElectrolyte abnormalities (K+, PO4-)

Correction

Pulmonary edema, cardiac ischemia

Diuretics and nitrates

Deconditioning, malnutrition

Aggressive nutrition

Neuromuscular disease Bronchopulmonary hygiene, early consideration of trach

Increased intra-abdominal pressure

Semirecumbent positioning, NGT

Hypothyroidism Thyroid replacementExcessive auto-PEEP (COPD, asthma)

Bronchodilator therapySena et al, ACS Surgery: Principles and Practice (2005).

Ventilator management algorithimVentilator management algorithimInitial intubation• FiO2 = 50%• PEEP = 5

• RR = 12 – 15• VT = 8 – 10 ml/kg

SaO2 < 90% SaO2 > 90%

SaO2 > 90%• Adjust RR to maintain PaCO2 = 40• Reduce FiO2 < 50% as tolerated• Reduce PEEP < 8 as tolerated• Assess criteria for SBT daily

SaO2 < 90%• Increase FiO2 (keep SaO2>90%)• Increase PEEP to max 20• Identify possible acute lung injury• Identify respiratory failure causes

Acute lung injury

No injury

Fail SBT

Acute lung injury• Low TV (lung-protective) settings

• Reduce TV to 6 ml/kg• Increase RR up to 35 to keep

pH > 7.2, PaCO2 < 50• Adjust PEEP to keep FiO2 < 60%

SaO2 < 90% SaO2 > 90%

SaO2 < 90%• Dx/Tx associated conditions

(PTX, hemothorax, hydrothorax)• Consider adjunct measures

(prone positioning, HFOV, IRV)

SaO2 > 90%• Continue lung-protective

ventilation until:•PaO2/FiO2 > 300•Criteria met for SBT

Persistently fail SBT• Consider tracheostomy• Resume daily SBTs with CPAP

or tracheostomy collar

Pass SBT

Airway stableExtubate

Intubated > 2 wks

• Consider PSV wean (gradual reduction of pressure support)

• Consider gradual increases in SBT duration until endurance improves

Prolonged ventilator dependence

Pass SBT

Pass SBT

Airway stable

Modified from Sena et al, ACS Surgery: Principles and Practice (2005).

Who’s Watching the Patient?

BE AWARE PREVENTION IS BETTER THAN CURE