Swine flu-management
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Transcript of Swine flu-management
VENTILATORY STRATEGIES IN INFLUENZ-A H1N1, ASSOCIATED ARDS
DR ARVIND KHARE Associate Professor
Department of Anaesthesia,J.l.N. Medical College,
AJMER
2
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
33
34
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