Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 12  |  Issue : 2  |  Page : 143-148

Noninvasive positive pressure ventilation in acute hypercapnic respiratory failure


Department of Pulmonology and Critical Care, Assiut University, Assiut, Egypt

Date of Submission23-Jul-2017
Date of Acceptance29-Jul-2017
Date of Web Publication23-May-2018

Correspondence Address:
Khaled Hussein
Department of Pulmonology and Critical care, Assiut University, Assiut, 71111
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejb.ejb_65_17

Rights and Permissions
  Abstract 

NPPV is well established in the management of acute on chronic hypercapnic respiratory failure secondary to acute exacerbation of COPD (AECOPD), obesity hypoventilation syndrome, and restrictive thoracic disorders. Because of its design, success depends largely on patient cooperation and acceptance. The most commonly used interfaces in acute hypercapnic respiratory failure are oronasal masks. During noninvasive ventilation patients respiratory system is maintained throughout the whole respiratory cycle at a constant pressure higher than the atmospheric pressure, usually termed the positive end-expiratory pressure (PEEP). Pressure support ventilation (PSV), is the most famous mode of partial ventilatory support that during spontaneous inspiratory efforts imposes a set level of positive pressure in a patient with intact respiratory drive. Bilevel positive airway pressure (BiPAP) include PSV during inspiration and EPAP during expiration. The highest pressure reached during inspiration is called inspiratory positive airway pressure (IPAP) which equal PSV + EPAP.

Keywords: chronic obstructive pulmonary disease, noninvasive positive pressure ventilation, obesity hypoventilation syndrome


How to cite this article:
Hussein K. Noninvasive positive pressure ventilation in acute hypercapnic respiratory failure. Egypt J Bronchol 2018;12:143-8

How to cite this URL:
Hussein K. Noninvasive positive pressure ventilation in acute hypercapnic respiratory failure. Egypt J Bronchol [serial online] 2018 [cited 2018 Aug 17];12:143-8. Available from: http://www.ejbronchology.eg.net/text.asp?2018/12/2/143/233043


  Acute hypercapnic respiratory failure of chronic obstructive pulmonary disease Top


Noninvasive positive pressure ventilation (NPPV) is a well-established technique used in the management of acute hypercapnic respiratory failure secondary to acute exacerbation of chronic obstructive pulmonary disease (AECOPD) [1], as shown in [Figure 1].
Figure 1 Acute exacerbation of COPD with respiratory failure is the commonest indication for NPPV.

Click here to view



  Physiological rationale of noninvasive positive pressure ventilation in acute exacerbation of chronic obstructive pulmonary disease Top


As shown in [Figure 2], the upward yellow arrow mentions the effect of continuous positive airway pressure or PEEP to counterbalance intrinsic positive end-expiratory pressure (PEEP) (decrease work of breathing with better trigger) [1]. The downward yellow arrow mentions the effect of pressure support to unload respiratory muscles and improving ventilation (decrease PaCO2).
Figure 2 Flow chart for physiological rationale of application of NPPV in acute hypercapnic respiratory failure of COPD.

Click here to view



  Indications of noninvasive positive pressure ventilation Top


NPPV should be started when pH is below 7.35 after standard medical treatment including oxygen therapy ([Figure 3]) [2]. pH plays an important role for selection of location of admission and for decision of intubation as in the following:
  1. pH higher than 7.35: prophylactic use of NPPV and no benefit versus conventional therapy.
  2. pH from 7.25 to 7.35: mandatory use of NPPV in emergency department or respiratory ward but not ICU with excellent prognosis.
  3. pH below 7.25: mandatory use of NPPV and mandatory admission to ICU with good prognosis.
  4. pH below 7.20: expect the need for intubation and chance for successful NPPV is decreased.
  5. pH below 7.10: NPPV is contraindicated and intubation is mandatory.
Figure 3 Flow chart for the application of NPPV in acute exacerbation of COPD, according to the severity of respiratory acidosis.

Click here to view



  Modes of noninvasive positive pressure ventilation in acute exacerbation of chronic obstructive pulmonary disease Top


There are main and accessory modes of NPPV:
  1. The main mode acts during inspiration to augment spontaneous breathing such as pressure support (PSV), proportional assist, or volume assured pressure support (VAPS).
  2. Accessory mode uses either expiratory positive airway pressure (EPAP) or pressure control ventilation (timed mode or T).


Pressure support ventilation

This mode is a part of S or S/T modes, where S is the spontaneous mode and is called bilevel positive airway pressure and includes PSV during inspiration and EPAP during expiration ([Figure 4]). The highest pressure reached during inspiration is called inspiratory positive airway pressure (IPAP), which equal PSV+EPAP [3].
Figure 4 Pressure, flow, and volume tracers during pressure support.

Click here to view


On the contrary, S/T ([Figure 5]) is S mode plus T mode. T mode is delivered only if patient failed to initiate trigger within a time governed by backup rate.
Figure 5 Different parameters for setting S/T mode.

Click here to view


Benefits of expiratory positive airway pressure

  1. Counterbalance auto PEEP.
  2. Maintain patency of upper airways at the end of expiration.
  3. Helps CO2 wash from exhalation port and decrease its rebreathing.


How to set S/T mode

  1. EPAP: 5–7 cmH2O.
  2. Set pressure support at least 8 cmH2O and increased in increments of 2 cmH2O every 30 min targeting tidal volume of 8 ml/kg and SPO2 above 90%.
  3. IPAP is preferred not exceeding 20 cmH2O to prevent gastric insufflation.


Proportional assist ventilation

The second common mode used in acute exacerbation of COPD ([Figure 6]).
  1. It is proportional to patient effort by delivering volume assist and flow assist according to elastance and resistance [4]. Thus, pressure, volume, and flow are variable from breath to breath as shown in below figure.
  2. It is indicated if there is good triggering, otherwise S/T is indicated.
Figure 6 Pressure, flow, and volume tracers during proportional assist ventilation.

Click here to view


Volume assured pressure support

  1. A recent dual mode with target tidal volume (average VAPS) or target alveolar ventilation (intelligent VAPS).
  2. It is thought to augment alveolar ventilation with enhanced CO2 wash and improved acidosis.



  Monitoring during noninvasive positive pressure ventilation Top


  1. Continuous:
    1. SpO2.
    2. ECG.
    3. Respiratory rate.
  2. Intermittent:
    1. Arterial blood gases.
    2. Leaks.
    3. Patient–ventilator synchrony.



  Acute hypercapnic respiratory failure of obesity hypoventilation syndrome Top


In the Western world, the prevalence of obese patients in ICUs is increasing. Additionally, morbid obesity has dramatic consequences on pulmonary function. Therefore, respiratory physicians and intensivists are more likely to manage a larger number of acute hypercapnic respiratory failure (AHRF) episodes in patients with a BMI of at least 30 [5]. Cor pulmonale is a major cause of ICU admission, which requires mechanical ventilation with higher mortality in obese compared with nonobese patients. It is, therefore, surprising that experience of AHRF in obese patients has rarely been reported in the literature and, consequently, evidence-based guidelines remain to be established. There are cumulating reports that suggest that NPPV plays a key role in the treatment of obese patients with AHRF [6].

Physiological rationale of noninvasive positive pressure ventilation in obesity hypoventilation syndrome

To control upper airways obstruction and overcome the respiratory muscle load, a high EPAP and high inspiratory driving pressure are required.

Specifically, the EPAP should set to optimise respiratory mechanics by modifying lung volume and the operating position on pressure volume curve as well as overcoming upper airways obstruction (reduce work of breathing) [7].

IPAP should be titrated to ensure satisfactory chest wall excursion with supplemental oxygen achieving target saturation from 90 to 92% [7].

Modes of noninvasive positive pressure ventilation in obesity hypoventilation syndrome

The optimal ventilatory mode is pressure support, using turbine-driven ventilators or ICU ventilators. A backup frequency rate is required in most cases, owing to the likelihood of sleep central apneas [8].

If a single circuit is used, it should be equipped with an expiratory valve or an intentional calibrated leak [7]. In this previous case, a slight expiratory positive pressure is required to limit CO2 rebreathing. Clinical series show that obesity hypoventilation syndrome (OHS) patients with AHRF require high levels of inspiratory positive pressures (often 22 cmH2O) owing to low thoracic compliance in this disease [8].

Another ventilatory mode in these patients is flow-preset mode that allows a better control of delivered volumes. AHRF in obese patients is one of the last medical situations where pressure support may be less effective than flow-preset modes [9]. After discharge, most OHS patients are managed with nocturnal bilevel NPPV without additional oxygen.

Noninvasive positive pressure ventilation settings in obesity hypoventilation syndrome

  1. EPAP set at 8–10 cmH2O aiming SpO2≥90%.
  2. IPAP set at 18–24 cH2O aiming pH ≥7.35 and tidal volume 8–10 ml/kg of ideal body weight [10].
  3. Inspiratory time limit 1.4 s.



  Acute hypercapnic respiratory failure of restrictive thoracic disorders Top


Patients with severe kyphoscoliosis and acute respiratory failure exhibit marked decrease of pulmonary compliance but, contrary to in COPD, increase in airway resistance, and intrinsic PEEP seem to play only a secondary role [11]. Because cough is not impaired like in neuromuscular diseases (NMD), secretion management is not so critical in this context, and management of ARF may be easier [11].

In neuromuscular disorders (NMD) ([Figure 7]), the normality of the respiratory function requires the integrity of three main respiratory muscles: (i) inspiratory muscles, responsible for ventilation; (ii) expiratory muscles, involved in the ability to cough; and (iii) bulbar muscles, which protect against the risk of aspiration [12]. Acute NMD (such as Guillain–Barre’s syndrome) together with the ICU acquired NMD are the most frequent NMD associated with ARF [13].
Figure 7 Pathophysiology of muscle weakness in neuromuscular disease.

Click here to view


Concerning the mode of NPPV, it is preferable to use volume-cycled ventilators in assist control, with high tidal volumes, for sufficient lung expansion and to allow air-stacking for coughing. This can be performed during the day using a mouthpiece and at night with a nasal or oral interface [12].

When patients with amyotrophic lateral sclerosis under home mechanical ventilation need to be hospitalized because of ARF, there are some technical as well as ethical aspects that need to be considered. It needs to be confirmed if all noninvasive respiratory aids were optimized at home, if the patient has refused tracheostomy, if bulbar impairment is severe, and if the risk of aspiration is high. Lung function status, previous to the decompensation, can be helpful in the decision making [14].

Another issue is when nonbulbar patients with NMD are intubated because of failure of noninvasive ventilation or because of a more-conventional approach. In this context, it is a common attitude to gradually reduce the support of the ventilator until the patient is weaned [15]. Unfortunately patients with NMD with a pre-existing respiratory dysfunction often fail to wean off invasive ventilation and are almost invariably tracheostomized [14].

Noninvasive positive pressure ventilation in patients with an acute pneumothorax

For patients with NMD, or any other condition in which the risk of acute pneumothorax is high who require NPPV [16], the following strategies can be used:
  1. Insert chest drain.
  2. Use pressure preset, pressure limited ventilator to reduce peak airway pressure.
  3. Use the lowest IPAP and EPAP settings that are comparable to arterial blood gas tensions and symptoms.
  4. Temporarily withdraw NPPV.



  Contraindications of noninvasive positive pressure ventilation Top


The boundaries for the use of NPPV continue to expand. NPPV is not appropriate in well-documented end-stage disease or when several co-morbidities are present.

There are no absolute contraindications, although a number of them have been suggested. In part, these ‘contraindications’ have been determined by the fact that they were exclusion criteria for the controlled trials [1]. It is therefore more correct to state that NPPV is not proven in these circumstances rather than that it is contraindicated.

Whether NPPV is contraindicated or not must depend on individual circumstances. For instance, if invasive ventilation is not considered appropriate but NPPV would be acceptable, there is nothing to be lost by a trial of NPPV and there are no contraindications [2].

The possible contraindications for NPPV can be summarized as follow:
  1. Facial trauma/burns.
  2. Recent facial, upper airway, or upper gastrointestinal tract surgery.
  3. Fixed obstruction of the upper airway.
  4. Inability to protect airway.
  5. Cardiorespiratory arrest.
  6. Uncontrolled life-threatening arrhythmia.
  7. Hemodynamic instability.
  8. Severe co-morbidity.
  9. Coma.
  10. Vomiting and hematemesis.
  11. Bowel obstruction.
  12. Undrained pneumothorax


NPPV may be used, despite the presence of these contraindications (except for facial trauma/burn, and fixed obstruction of the upper airway), provided contingency plans for tracheal intubation have been made, or if it is to be the ‘ceiling’ of treatment in patients who are not candidates for intubation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Elliott MW. Non invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease: do not think twice, its alright. Am J Respir Crit Care Med 2012; 185:121–123.  Back to cited text no. 1
    
2.
Ambrosino N, Vaghegginni G. Non invasive ventilation in acute care settings: where are we? Eur Respir I 2008; 31:874–886.  Back to cited text no. 2
    
3.
Austin MA. Effect of high flow oxygen on mortality of chronic obstructive pulmonary disease patients in pre hospital setting: randomized controlled trial. BMJ 2010; 341:5426.  Back to cited text no. 3
    
4.
Colombo D. Physiologic response to varying levels of pressure support and neurally adjusted ventilatory assist in patients with acute respiratory failure. Intensive Care Med 2008; 34:2010–2018.  Back to cited text no. 4
    
5.
El-Solh A, Sikka P, Bozkanat E, Jaafar W, Davies J. Morbid obesity in the medical ICU. Chest 2001; 120:1989–1997.  Back to cited text no. 5
    
6.
Jubber AS. Respiratory complications of obesity. Int J Clin Pract 2004; 58:573–580.  Back to cited text no. 6
    
7.
Cuvelier A, Muir JF. Acute and chronic respiratory failure in patients with obesity hypoventilation syndrome: a new challenge for noninvasive ventilation. Chest 2005; 128:483–485.  Back to cited text no. 7
    
8.
Cuvelier A, Muir JF. Obesity-hypoventilation syndrome and noninvasive mechanical ventilation: new insights in the Pickwick papers? Chest 2007; 131:7–8.  Back to cited text no. 8
    
9.
Pastores SM. Morbidly obese patients with acute respiratory failure: don’t reach for the endotracheal tube yet!. Crit Care Med 2007; 35:956–957.  Back to cited text no. 9
    
10.
Mokhlesi B, Kryger MH, Grunstein RR. Assessment and management of patients with obesity hypoventilation syndrome. Proc Am Thorac Soc 2008; 5:218–225.  Back to cited text no. 10
    
11.
Conti G, Rocco M, Antonelli M. Respiratory system mechanics in the early phase of acute respiratory failure due to severe kyphoscoliosis. Intensive Care Med 1997; 23:539–544.  Back to cited text no. 11
    
12.
Benditt JO. The neuromuscular respiratory system physiology, pathophysiology, and a respiratory care approach to patients. Respir Care 2006; 51:829–837.  Back to cited text no. 12
    
13.
Hughes RA, Wijdicks EF, Benson E, Cornblath DR, Hahn AF, Meythaler JM. Supportive care for patients with Guillain-Barre’s syndrome. Arch Neurol 2005; 62:1194–1198.  Back to cited text no. 13
    
14.
Farrero E, Prats E, Povedano M, Martinez-Matos JA, Manresa F, Escarrabill J. Survival in amyotrophic lateral sclerosis with home mechanical ventilation: the impact of systematic respiratory assessment and bulbar involvement. Chest 2005; 127:2132–2138.  Back to cited text no. 14
    
15.
Servera E, Sancho J, Zafra MJ, Catala A, Vergara P, Marin J. Alternatives to endotracheal intubation for patients with neuromuscular diseases. Am J Phys Med Rehabil 2005; 84:851–857.  Back to cited text no. 15
    
16.
Seneviratne J, Mandrekar J, Wijdicks EF, Rabinstein AA. Noninvasive ventilation in myasthenic crisis. Arch Neurol 2008; 65:54–58.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Acute hypercapni...
Physiological ra...
Indications of n...
Modes of noninva...
Monitoring durin...
Acute hypercapni...
Acute hypercapni...
Contraindication...
References
Article Figures

 Article Access Statistics
    Viewed228    
    Printed24    
    Emailed0    
    PDF Downloaded87    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]