Ventilatory management of Acute Hypercapnic Respiratory Failure

Ventilatory Management of Acute Hypercapnic Respiratory Failure

DR. VITRAG SHAH SECOND YEAR FNB RESIDENT,

DEPARTMENT OF CCEM, SGRH, DELHI

MODERATOR DR.VINOD SINGH

vitrag24-www.medicalgeek.com

Acute Hyperapnic Respiratory Failure

• COPD

• Asthma

• Cystic fibrosis (CF)

• Non-CF Bronchiectasis

• Restrictive lung disease – NMD & CWD

• Obesity Hypoventilation syndrome (OHS)


Outline • Respiratory mechanics in COPD • DHI & AutoPEEP • Ventilatory goal & strategy • Indication & Contraindication of NIV • NIV setup & optimizing NIV • Indication of IMV • Ventilator settings & it’s implications • Weaning • PSV, NAVA & PAV • Approach to Patient-ventilator asynchrony • Extubation • Role of ECCO2R & Heliox • Prognosis • Differences in management of AHRF in etiologies other than COPD • Key points • References


Respiratory mechanics in COPD

Airway

Obstruction

Resistance

Dynamic Hyperinflation

Work Of Breathing

Expiratory Flow

Limitation

Intrinsic PEEP

COPD Exacerbation





DHI without airflow limitation

• Rapid respiratory rate

• High tidal volume

• Inspiratory time more than expiratory time

• Small bore endotracheal and ventilatory tubes


Diagnosis of DHI

1. Slow filling of manual ventilator bag

2. Capnography trace not reaching plateau

3. Expiratory flow not reaching zero in flow-time/volume graph

4. Measure intrinsic PEEP (PEEPi)


AutoPEEP Mechanisms

1. Hyperinflation with dynamic airway collapse (DAC) – e.g. COPD

2. Hyperinflation without DAC – e.g. Severe Asthma exacerbation

3. Contraction of expiratory muscle which increases Palv above Patm – e.g. During exercise


AutoPEEP measurement



Occult AutoPEEP

• Standard AutoPEEP measurement doesn’t reflect pressure in lung areas behind obstructed airways at end-expiration.

• Occult AutoPEEP is suspected when low measured AutoPEEP but high Plateau pressure & evidence of hyperinflation on Chest X-Ray.


Ventilatory Goal

• Treatment principle is to support gas exchange and correct lung mechanics

• Ventilatory Goal : - To improve gas exchange - Reduce dynamic hyperinflation

- Increase Expiratory Time , Increase Inspiratory Flow rate - Decrease MV (TV, RR) - Application of PEEP (Not in Asthma) - Treat bronchospasm

- Rest to the respiratory muscles & decrease WOB - Better patient ventilator synchrony - Prevention of barotrauma - Minimizing cardiovascular effects


Ventilatory Strategy

• NIPPV is the first choice

• Assist control ventilation

• Target pH, not pCO2

• Optimize respiratory mechanics

• Optimum sedation

• Early weaning

• Extubation with NIPPV


0


Mechanism of benefit in NIV

• Applied EPAP offsets PEEPi resulting from expiratory airflow obstruction.

• IPAP augments tidal volume for any given respiratory effort leading to unloading of respiratory muscles, decreased WOB, decreased RR, and improvements in alveolar ventilation which improves gas exchange


Indication of NIV • Patients with pH between 7.30 and 7.25 • Non-responders to medical therapy having PaO2 <50

mmHg, PaCO2 >80–90 mmHg, pH ≤7.2, with following: Sick but not moribund Able to protect airway Conscious and cooperative Haemodynamically stable No excessive respiratory secretions Few co-morbidities

• Patients who have declined intubation • As a weaning facilitator & shorten IMV duration • Post extubation respiratory failure • Domiciliary NPPV for patients with recurrent

admissions. vitrag24-www.medicalgeek.com

RECOMMENDED ALGORITHM Noninvasive ventilation in acute exacerbations of COPD

M.W. Elliott, Eur Respir Rev 2005



Optimizing NIV delivery

• Leak should always be minimised by mask adjustment and/or by changing the mask type

• Head flexion is avoided, particularly in sleep.

• Patient–ventilator asynchrony may be caused by mask leak, insufficient or excessive IPAP, inappropriate setting of Ti or Te, high levels of intrinsic PEEP or excessively sensitive triggers.



Duration of NIV in COPD

• Time on NIV should be maximised in the first 24 h depending on patient tolerance and/or complications.

• NIV use during the day can be tapered in the following 2–3 days, depending on pCO2 self-ventilating, before being discontinued overnight.

• NIV can be discontinued when there has been normalisation of pH and pCO2 and a general improvement in the patient’s condition


Predictor of NIV failure • Glasgow Coma Score <11 • Acute physiology and chronic health evaluation (APACHE) II

score ≥29, • Respiratory rate ≥30 • pH <7.25

• After two hours of NIV, a pH <7.25 further increased the

likelihood of need for intubation from 70 to 90 percent

• A bedside scoring system, BAP-65 (elevated BUN, altered mental status, pulse >109 beats/min, age >65 years), that uses signs of respiratory distress, along with other risk factors, has been found to predict the need for mechanical ventilation in patients with acute exacerbations of COPD


Indication of IMV

*pH<7.25 has been suggested as a level below which IMV should be considered and <7.15 as the level that IMV is indicated (following initial resuscitation and use of controlled oxygen). These patients should be intubated based on the severity of respiratory distress rather

than any absolute value of PaCO2 or RR followed by 24 h of full ventilatory support to rest the fatigued respiratory muscles.


Intubation

• Anaesthesia can be provided using ketamine, propofol or fentanyl with midazolam. Before induction, fluid status has to be optimised in these patients as haemodynamic collapse can occur due to increased DH and PEEPi.

• If a patient becomes hypotensive after intubation that is not responding to fluid, ventilator can be disconnected and if the BP improves, a manual squeeze of the thoracic cage can be performed to reduce DH which can be appreciated on SpO2 tracings as huge respiratory swings


Ventilator initiation

• Ventilation should be adjusted based on the degree of DH and Auto-PEEP and not PaCO2.

• There are only three factors that determine auto-PEEP: (1) Minute ventilation, (2) I: E ratio & expiratory time constants, (3) Expiratory flow

• Of these, minute ventilation is the most important factor which causes DH. Hence, when ventilating patients with COPD, a smaller VT, slow RR, high peak flow should be used with an aim to target normal pH and not PaCO2


Initial settings

Mode ACV TV 6-8 ml/kg RR 10-15

Target MV 115 ml/kg

I:E ratio 1:3-1:5

Flow 60-100 L/min

Square wave form

(Constant flow)

PEEP 50-80% of iPEEP

<10- 12

(Zero in Asthma)

FiO2 : To target SpO2 88-92%,

(>96% in Asthma)

PaO2 >60mmhg

Target pH : 7.2-7.4

Pplt <30

In PSV - Trigger

Flow (Preffered): 2L

Pressure : -1 to -2cm

Cycling : >35%

Controlled modes should be used as briefly as possible to avoid disuse atrophy of respiratory muscles and unnecessary prolongation of the period of mechanical ventilation. vitrag24-www.medicalgeek.com

Measures to reduce DHI & AutoPEEP

• Reduce ventilatory demand and minute ventilation (TV & RR), Optimum sedation and analgesia

• Prolonged expiratory time

• Increase inspiratory flow rate

• Apply Extrinsic PEEP

• Adjust trigger sensitivity

• Reduce airflow resistance by bronchodilators and steroids

Deep sedation should be used when required and N-M blockers should be avoided as this patients are prone to difficult weaning and it contributes to CIN/CIM


Expiratory time

• It is important to note that recent research suggests that there is a plateau in expiratory flow after a certain point, so increasing the expiratory time above a certain value has limited benefit. In general, after about 4 seconds of expiration there is nominal gain in reducing hyperinflation.


PEEP Benefits of PEEP: 1. Decrease inspiratory threshold, so less WOB 2. Stenting collapsible airways, so increasing expiratory flow rates


Waterfall over dam concept in COPD


PEEP

• In contrast to COPD patients, applying PEEP during total ventilatory support of a patient who has DH with fixed airflow obstruction due to severe asthma and without airway collapse may produce potentially dangerous increases in lung volume, airway pressure and intrathoracic pressure, causing circulatory compromise.

• Although some clinical studies have reported improved airway function (without untoward effects) with continuous positive airway pressure or with NIV and PEEP among patients with acute asthma, the use of PEEP during total ventilatory support of a patient with acute asthma is controversial.


When to wean

• Cause of exacerbation treated • Hemodynamically stable • Absense of major organ failure • Optimum acid base & electrolyte balance • MV <15 L • RR <30 • TV >325ml • Dynamic compliance >22 • Static compliance >33 • RSBI <105 • MIP > -15


Daily SBT

<100

Mechanical Ventilation

RR > 35/min Spo2 < 90% HR > 140/min Sustained 20% increase in HR SBP > 180 mm Hg, DBP > 90 mm Hg Anxiety Diaphoresis

30-120 min

PaO2/FiO2 ≥ 200 mm Hg PEEP ≤ 5 cm H2O Intact airway reflexes No need for continuous infusions of vasopressors or inotrops

RSBI

Extubation* No

> 100

Rest 24 hrs

Yes

Stable Support Strategy Assisted/PSV

24 hours

Low level CPAP (5 cm H2O), Low levels of pressure support (5 to 7 cm H2O) “T-piece” breathing

*If good sensorium, cough and swallowing present vitrag24-www.medicalgeek.com

Weaning • Inability to wean is invariably associated with a worse

prognosis and prolonged ventilation. • Marginal respiratory mechanics and continued presence

of auto-PEEP make weaning difficult in COPD patients. • Factors that increase resistance such as size, secretions,

kinking of the tube and the presence of elbow-shaped parts or a HME in the circuit have to be optimised to promote early weaning.

• Patients of cor pulmonale may require small dose of inotrope, diuretics and low fluid strategy during weaning

• Role of tracheostomy is uncertain, but due to marginal respiratory mechanics, it is also expected to help in weaning


Weaning Mode • PSV, PAV, NAVA, Extubation f/b NIPPV

• Pressure support ventilation is the most common

mode used in weaning

• Key determinants of PSV Triggering of the ventilator Pressurization slope and inspiratory flow, Level of PS Cycling


Trigger

• Flow rather than pressure trigger preffered as it reduce the incidence of asynchrony & WOB.

• Main determinants affecting workload associated with triggering are : – Magnitude of change required (Optimized by increasing

sensitivity & setting PEEP)

– Delay between onset of inspiratory effort & ventilator response (Optimized by NAVA)

• During NIV, leak can cause autotrigger and asynchrony

• Highest possible sensitivity should be set, without auto-triggering



Rise time / Slope

• During PS, the slope of pressurization, that is, the incremental increase in Paw per time unit, can be adjusted on most ventilators . The steeper the slope, the faster Paw will rise to its target value. The steeper the slope the lower the WOB.

• But comfort is lowest at both the lowest and highest pressurization rates.

• >100ms and, if a patient exhibits discomfort, to increase the time up to 200 ms.


Level of PS • Avoid both insufficient support leading to

increased respiratory muscle load and excessive support bearing the risk of worsening dynamic hyperinflation and PEEPi by insufflation of high tidal volume in obstructive patients

• A high level of PS can worsen the delayed cycling phenomenon & increase in leak

• Empirically, PS can be titrated on the expiratory tidal volume (approximately 8 to 10 ml/kg, the lowest value being preferred in NIV) and the patient’s respiratory rate, which should remain below 30/minute.



Cycling

• The transition from inspiration to expiration, known as cycling, occurs when instantaneous inspiratory flow (V′insp) decreases to a predetermined fraction of peak inspiratory flow (V′insp/V′peak), often referred to as an ‘expiratory trigger’ (ET)

• Delayed cycling has been shown to occur mostly in patients with obstructive airways disease

• On many ventilators, the cutoff value of ET is pre-determined, usually at a default setting of 0.25

• Higher the ET, decrease magnitude of delayed cycling & better synchrony.



Consequences of delayed cycling


PAV & NAVA

• Both modes are designed to reduce patient effort in response to changes in ventilatory demand.

• PAV generates respiratory support as a proportion of the total pressure needed to inflate the respiratory system.

• During PAV, the total pressure needed to inflate the respiratory system is obtained by automatic and repeated calculations of resistance and compliance via short end-inspiratory occlusions. This is why leaks impede proper PAV functioning.


NAVA

• When NAVA is used, the inspiratory trigger does not depend on airway flow detection; rather, gas delivery starts when electrical activity in the diaphragm is detected.

• The inspiration ends at a predetermined percentage of peak EMG activity: 70% of the peak if EADi values are higher than 1.5 μV. If EADi is lower than 1.5 μV, then the inspiration ends at a 40% of the peak.

• Unlike PAV, the trigger mechanism in NAVA is not affected by leaks or PEEPi.


PAV & NAVA : Conclusion

• NAVA improved patient–ventilator synchrony by reducing triggering and cycling delays in comparison to PSV. In any case, despite the theoretical promise of PAV and NAVA, data published to date are insufficient to claim that either mode is superior to conventional modes such as PSV in terms of major clinical outcomes (i.e., duration of MV, length of ICU stay).


NIV in Weaning



Extubation

• Successful extubation is defined as the absence of the need for ventilatory support for 48 h.

• Patients receiving post-extubation NIV (see below) are classified as ‘weaning in progress’.



Role of ECCO2R

1. If, despite attempts to optimise IMV using lung protective strategies, severe hypercapnic acidosis (pH<7.15) persists

2. When ‘lung protective ventilation’ is needed but hypercapnia is contraindicated, for example, in patients with coexistent brain injury (Grade D)

3. For IMV patients awaiting a lung transplant


Role of Helium/Oxygen

• The percentage of oxygen in heliox should be at least 20% to prevent hypoxia, and no more than 40% for heliox to show clinically significant effect

• As airway turbulence is dependent on density, heliox having a lower density decreases the airway resistance and, therefore, the WOB particularly in situations associated with upper airway obstruction.

• Due to conflicting literature, Heliox should not be used routinely in the management of AHRF (Grade B).


Prognosis

• The mortality of patients with COPD who are mechanically ventilated for acute respiratory failure is high (37 to 64 percent). Factors that portend a poor prognosis in this population include failure to respond to noninvasive ventilation, the presence of multiorgan failure and the presence of virulent pathogens such as Pseudomonas and Aspergillus species cultured from airway secretions.


Differences in management of AHRF due to etiologies other than COPD


Acute Asthma

• NIV should not be used in patients with acute asthma exacerbations and AHRF (Grade C).

• Acute (or acute on chronic) episodes of hypercapnia may complicate chronic asthma. This condition closely resembles COPD and should be managed as such (Grade D).


Non-CF bronchiectasis

• In patients with non-CF bronchiectasis and AHRF, controlled oxygen therapy should be used.(Grade D)

• In patients with non-CF bronchiectasis, NIV should be started in AHRF using the same criteria as in AECOPD (Grade B).

• In patients with non-CF bronchiectasis, NIV should usually be tried before resorting to IMV in those with less severe physiological disturbance


Cystic fibrosis

• In patients with CF, controlled oxygen therapy should be used in AHRF (Grade D).

• In patients with CF, NIV is the treatment of choice when ventilatory support is needed (Grade C).

• In patients with CF, specialised physiotherapy is needed to aid sputum clearance (Grade D).

• In patients with CF, a mini-tracheostomy combined with NIV may offer greater chance of survival than resorting to IMV. (Grade D)


Restrictive lung diseases (NMD and CWD)

• Controlled oxygen therapy should be used in patients with NMD or CWD and AHRF (Grade D).

• NIV is the ventilation mode of choice because patients with NMD or CWD tolerate it well and because extubation from IMV may be difficult.

• NIV should almost always be trialled in the acutely unwell patients with NMD or CWD with hypercapnia. Do not wait for acidosis to develop (Grade D).

• In patients with NMD or CWD, NIV should be considered in acute illness when vital capacity (VC) is known to be <1 L and RR >20, even if normocapnic (Grade D).

• In patients with NMD or CWD, consider controlled ventilation as triggering may be ineffective (Grade D).

• In NMD or CWD, unless escalation to IMV is not desired by the patient, or is deemed to be inappropriate, intubation should not be delayed if NIV is failing (Grade D).


NIV failure in NMD

• In patients with NMD or CWD, intolerance of the mask and severe dyspnoea are less likely to cause NIV failure. Bulbar dysfunction makes NIV failure more likely.

• Deterioration in patients with NMD or CWD may be very sudden. Difficulty achieving adequate oxygenation or rapid desaturation during a break from NIV are important warning signs.


IMV strategy in NMD and CWD

• Patients with NMD usually require low levels of PS.

• Patients with chest wall deformity usually require higher levels of PS.

• PEEP in the range of 5–10 is commonly required to increase residual volume and reduce oxygen dependency in both patient groups.


Obesity hypoventilation syndrome

• Controlled oxygen therapy should be used in patients with OHS and AHRF (Grade D).

• In patients with OHS, NIV should be started in AHRF using the same criteria as in AECOPD (Grade B).

• NIV is indicated in some hospitalised obese hypercapnic patients with daytime somnolence, sleep disordered breathing and/or right heart failure in the absence of acidosis.


NIV settings and placement in OHS

• High inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) settings are commonly required in patients with OHS (eg, IPAP>30, EPAP>8).

• Volume control (or volume assured) modes of providing NIV may be more effective when high inflation pressures are required.


NIV failure in OHS

• Fluid overload commonly contributes to ventilatory failure in patients with OHS, and its degree is easily underestimated.

• Forced diuresis may be useful.


IMV strategy in OHS

• In patients with OHS, pressure controlled MV is recommended initially.

• In patients with OHS, high PEEP settings may be needed to recruit collapsed lung units and correct hypoxaemia.

• In patients with OHS, a forced diuresis is often indicated.



Key points

• The overall goals of treatment should be to provide adequate gas exchange while minimizing hyperinflation , unload respiratory muscles and administering aggressive therapy to reduce airway inflammation and bronchoconstriction.

• Primary cause of respiratory failure should be treated. • NPPV is regarded as the first line of treatment while invasive

ventilation is reserved for life-threatening respiratory failure. • MV should be adjusted to pH , not pCO2. • The ventilatory graphics (flow, pressure and volume) of the modern

ventilators becomes a valuable tool & assist in early diagnosis and management of the patient’s condition before it becomes clinically overt.

• Weaning from MV is typically difficult in these patients, and factors amenable to pharmacological correction (such as increased bronchial resistance, tracheobronchial infections, and heart failure) are to be systematically searched and treated.

• In selected patients, early use of NIV may hasten the whole process of weaning.


1. Davidson AC, Banham S, Elliott M, et al. Thorax 2016;71:ii1–ii35 - BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults

2. Ahmed SM, Athar M. Mechanical ventilation in patients with chronic obstructive pulmonary disease and bronchial asthma. Indian J Anaesth 2015;59:589-98

3. Jolliet, Philippe, and Didier Tassaux. "Clinical review: patient-ventilator interaction in chronic obstructive pulmonary disease." Critical Care 10.6 (2006): 1-6.

4. Parrilla, Francisco José, et al. "Ventilatory strategies in obstructive lung disease." Seminars in respiratory and critical care medicine. Vol. 35. No. 4. 2014.

5. Reddy, Raghu M., and Kalpalatha K. Guntupalli. "Review of ventilatory techniques to optimize mechanical ventilation in acute exacerbation of chronic obstructive pulmonary disease." International journal of chronic obstructive pulmonary disease 2.4 (2007): 441

6. Medoff, Benjamin D. "Invasive and noninvasive ventilation in patients with asthma." Respiratory care 53.6 (2008): 740-750

7. Gilman B Allen, MD et al “Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease” UpToDate


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Ventilatory management of Acute Hypercapnic Respiratory Failure