How Long Can a Copd Patient Live on a Ventilator

Indian J Anaesth. 2022 Sep; 59(9): 589–598.

Mechanical ventilation in patients with chronic obstructive pulmonary disease and bronchial asthma

Syed Moied Ahmed

Department of Anaesthesiology and Critical Care, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh, Bharat

Manazir Athar

Department of Anaesthesiology and Critical Care, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh, Bharat

Abstract

Chronic obstructive pulmonary illness (COPD) and bronchial asthma oftentimes complicate the surgical patients, leading to post-operative morbidity and mortality. Many authors take tried to predict mail service-operative pulmonary complications but not specifically in COPD. The aim of this review is to provide recent evidence-based guidelines regarding predictors and ventilatory strategies for mechanical ventilation in COPD and bronchial asthma patients. Using Google search for indexing databases, a search for articles published was performed using various combinations of the following search terms: 'Predictors'; 'mechanical ventilation'; COPD'; 'COPD'; 'bronchial asthma'; 'contempo strategies'. Boosted sources were as well identified by exploring the chief reference list.

Keywords: Bronchial asthma, chronic obstructive pulmonary disease, heliox, mechanical ventilation, adventure

INTRODUCTION

Chronic obstructive pulmonary illness (COPD) is a disease spectrum that includes bronchitis and emphysema. Information technology is condign a major health and economical trouble worldwide; in 1990, it was the 6th most common cause of death which is expected to exist tertiary most mutual crusade by 2020. Mortality associated with asthma is also substantial with 1–8 deaths per lakh worldwide; nevertheless, the bodily magnitude of the problem in our state is not known.[1] Then, it is advisable to optimise these patients pre-operatively to avoid complications in the mail-operative period as many times mechanical ventilation tin be more of a problem than a solution. Ventilating a COPD patient is often hard because the disease may not have a reversible component. Further, quantification and management of dynamic hyperinflation (DH) at bedside is very difficult. In due course of time, it is becoming a major health problem as more and more than number of patients with obstructive disease are presenting for surgeries.[ii]

Obstructive lung disease

Obstructive lung diseases primarily include disorders of the airways such as COPD, asthma, bronchiectasis and bronchiolitis.[3]

PHYSIOLOGICAL CHANGES IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE RELEVANT TO MECHANICAL VENTILATION

Expiratory flow limitation

Information technology is the master physiologic alteration in COPD and is overcome past increasing the inspiratory flow and lung volume. Although the load is expiratory the compensation is essentially inspiratory, this combined with loftier respiratory drive leads to development of inspiratory musculus fatigue which is of fundamental pathophysiological importance in the development of acute respiratory failure (ARF) in these patients.

Dynamic hyperinflation and auto-positive end-expiratory pressure level

The airflow obstruction, low elastic recoil, high ventilatory demand and brusque expiratory time result in air trapping and consequent DH. In COPD patients with ARF, DH is the main factor explaining the increased intrathoracic force per unit area, increased piece of work of breathing (WOB), ventilator dependency and weaning failure.[4,v] According to the waterfall theory, increasing force per unit area downstream from the site of small airway closure or plummet should non decrease expiratory flow until the downstream water (external positive end-expiratory pressure level [PEEP]) reaches the disquisitional pressure [Figure 1].[4] So, The external PEEP should be kept below 75% to 85% of machine-PEEP to avoid any worsening of hyperinflation or circulatory compromise.[6,7] Determination of dynamic pulmonary hyperinflation is, however, non easy to perform in an ICU. It requires insertion of an oesophageal balloon and assessment of the abdominal muscles that can be recruited during expiration.[eight] It has been shown, though, that changes in inspiratory chapters (IC) replicate that of hyperinflation, the greater the IC, the lower the terminate-expiratory lung volume assuming a constant total lung capacity.[ix,10]

Waterfall phenomenon and its relation with critical force per unit area

Types of car-positive cease-expiratory pressure and their measurement

Static auto-positive stop-expiratory pressure

It is measured just in patients without active respiratory effort using the stop-expiratory occlusion on the ventilator. The auto-PEEP is then calculated by subtracting the external PEEP from the total PEEP [Figure ii].[11]

Expiratory hold manoeuvre to approximate machine-positive end-expiratory pressure level

Dynamic automobile-positive end-expiratory pressure

Information technology is measured by simultaneous recording of airflow and airway pressure level at end-expiration. In spontaneously breathing patients, machine-PEEP is determined by simultaneously recording oesophageal force per unit area and airflow tracings. Information technology is measured at end-expiration as the negative deflection of oesophageal pressure to the betoken of aught flow. It is less than the static car-PEEP because it reflects the terminate-expiratory pressure of the lung units with short time constants and rapid expiration while units with long time constants are still emptying.

Diagnosis of dynamic hyperinflation

1. Slow filling of manual ventilator purse

2. Capnography trace non reaching plateau

3. Expiratory menses non reaching naught in period-time/volume graph [Figures ​ 3 and ​ iv]

   

   Generation of auto-positive end-expiratory pressure

   

   Air trapping in menstruation-volume loop

4. Measure intrinsic PEEP (PEEPi).[12]

Management Allowing more than time for exhalation

Reduce the respiratory charge per unit (RR) or I: East ratio (typically to ane:3–i:v) to allow more fourth dimension for exhalation and reduce breath stacking. However, this will result in low infinitesimal ventilation causing hypercapnia, hypoxia or acidosis. This leads to increased pulmonary vascular resistance and worsened haemodynamic instability. If this is a business organization, a college inspiratory flow rate with high peak pressures tin be utilised, but this places the patient at increased take a chance of barotrauma.

Awarding of positive terminate-expiratory pressure level

The utilise of external PEEP in ventilated patients with COPD has theoretical benefits past keeping small airways open up during late exhalation, so potentially reducing PEEPi or auto PEEP. Additionally, information technology has been seen that if external PEEP is kept below PEEPi, no significant increase in alveolar pressure and cardiovascular compromise occurs.[thirteen]

Treatment of bronchospasm

Gas flow in small-scale airways may be severely compromised by bronchospasm, which commonly occurs at induction of anaesthesia or during airway instrumentation. It should be treated promptly either by inhaled bronchodilators or by deepening anaesthesia with propofol or increased concentrations of inhalation anaesthetics.

PREDICTORS OF POST-OPERATIVE VENTILATION IN PATIENTS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE OR BRONCHIAL ASTHMA

Predicting post-operative pulmonary complications (PPCs) remains a claiming for most of the researchers. Although many studies have attempted to predict PPCs, they were not specifically for COPD patients. Patients with COPD are unambiguously at an increased run a risk for PPCs. A recent review estimated the incidence of unadjusted PPCs every bit xviii.2% in COPD patients undergoing surgery.[14] Increasing severity of COPD confers greater run a risk, from 10% with mild-to-moderate disease to 23% in patients of the severe disease.[fifteen]

Show shows that history and physical examination are poor predictors of airway obstacle and its severity. Even so, the presence of history of >55-pack-year smoking, wheezing on auscultation and patient cocky-reported wheezing can be considered predictive of airflow obstacle, defined as post-bronchodilator forced expiratory volume 1 (FEV1)/forced vital capacity < 0.lxx.[2] Spirometry is useful to identify airflow obstruction in symptomatic patients, merely its utility in patients without respiratory symptoms is questionable. Smokers with normal spirometry have simply a four% risk of PPC.[16] Symptomatic patients with FEV1 < 60% predicted will benefit from inhaled treatments but evidence does not support treating asymptomatic, regardless of the risk factors and airflow obstruction.[2] However, unlike in pulmonary resection, there is no cut-off value of FEV1 or any other spirometric index to consider these patients unsuitable for surgery.

Arterial blood gas (ABG) analyses are not indicated unless the patient's history suggests arterial hypoxaemia or astringent enough COPD that one suspects CO_two retention. Then, the ABG should exist used in essentially the same manner as one might use pre-operative PFTs, that is, to await for reversible affliction or to define the severity of the illness at its baseline. Defining baseline PaO₂ and PaCO₂ is peculiarly important if i anticipates postal service-operatively ventilating a patient who has severe COPD.[17] In general, various independent risk factors [Table one] and run a risk indices take been developed that can be used to predict PPCs.[15,18,19,20,21,22]

Table one

Contained risk factors for post-operative pulmonary complications

Unremarkably USED Chance INDICES FOR PREDICTING RISKS OF Postal service-OP PULMONARY COMPLICATIONS IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND ASTHMA

1. Score for prediction of post-operative respiratory complications (SPORC).[18] Risk factors and the corresponding scores (in brackets) are American Social club of Anesthesiologists score ≥3 (3), emergency procedure, (iii) loftier risk-service, (2), congestive heart failure (2), and chronic pulmonary affliction (1).

   (Probability of reintubation: 0 points = 0.1%; 1–3 points = 0.4%; four–6 points = 1.6%; 7–11 points = 6.4%)

2. Respiratory failure risk alphabetize:[23]

   1. Blazon of surgery

   2. Emergency

   3. Albumin (<30 g/Fifty)

   4. Blood urea nitrogen > 30 mg/dl

   5. Functional dependency

   6. COPD

   7. Age

   Probability of respiratory failure (PRF): Course 1 (≤x points) =0.5%; Class 2 (11–19 points) =2.ii%; Class 3 (20–27 points) =v%; Form 4 (28–40 points) =11.6%; Class 5 (>40 points) =30.5%

3. PRF risk calculator: Available online at http://www.surgicalriskcalculator.com/prf-risk-estimator.[20]

4. Cardiopulmonary take chances index.[24]

MECHANICAL VENTILATORY SUPPORT IN OBSTRUCTIVE PULMONARY DISEASE

Using current evidence, non-invasive positive-pressure ventilation (NPPV) is the showtime line of handling for these patients, just invasive positive-pressure level ventilation may also be required in patients who have more than astringent affliction. One major crusade of the morbidity and mortality arising during mechanical ventilation in these patients is excessive DH with PEEPi, which severely increases the WOB. The main goals of mechanical ventilation are to improve pulmonary gas exchange and to rest compromised respiratory muscles sufficiently to recover from the fatigued state.

Strategies to meliorate pulmonary gas substitution

The hypoxaemia of obstructive air diseases is basically due to one of the 3 general causes: Shunt, ventilation/perfusion abnormalities (Five/Q mismatching) and diffusion defects [Table 2]. In general, individuals with astute exacerbations of COPD have a greater degree of ventilation defect (causing hypercapnia) than chronic patients who mainly develop perfusion defect (causing hypoxia). Nonetheless, hypoxic vasoconstriction and collateral ventilation in chronic patients decrease the expected V/Q mismatch.[25] So, managing the crusade is of prime number importance in the treatment of hypoxaemia of COPD. Moreover, evidence shows beneficial effects of controlled breathing techniques such every bit active expiration, slow and deep breathing, pursed-lips breathing, relaxation therapy, specific body positions and inspiratory muscle training. Diaphragmatic breathing has non been shown to be beneficial.[26]

Table 2

Factors affecting pulmonary gas exchange

Strategies to rest compromised respiratory muscles and reduce the piece of work of breathing

In patients with COPD and asthma, a state of loftier respiratory bulldoze and poor mechanical advantage cause inspiratory musculus fatigue that tin can exist improved by decreasing respiratory load, increasing muscular competence and providing mechanical ventilatory support [Table 3].

Table 3

Factors affecting respiratory musculus efficiency

Office OF Non-INVASIVE POSITIVE-PRESSURE VENTILATION IN TREATING OBSTRUCTIVE PULMONARY DISEASE PATIENTS

NPPV has been accustomed widely equally the ventilatory manner of the starting time selection in treating obstructive airway affliction patients with respiratory failure. It provide a pregnant reduction in endotracheal intubation and thereby its complications (e.g., ventilator-associated pneumonia, tracheal and laryngeal complications) if considered early in the grade of the affliction.[27,28,29,30,31]

Mechanism of activity of non-invasive positive-pressure level ventilation

Expiratory positive airway force per unit area (EPAP) applied offsets PEEPi resulting from expiratory airflow obstruction [Figure 5]. Inspiratory positive airway force per unit area (IPAP) augments tidal volume for whatsoever given respiratory effort leading to less mechanical disadvantage, decreased RR, decreased WOB and improvements in ventilation (generally reduced PaCO₂).[32]

(a) Waterfall phenomenon-negative pressure level required to trigger the ventilator breath is reduced on awarding of external positive end-expiratory pressure level, (b) consequence of practical positive terminate-expiratory pressure on triggering-extrinsic positive stop-expiratory force per unit area of 5 cm H₂O reduces the work of breathing from level A to level B by offsetting the auto-positive end-expiratory pressure in this chronic obstructive pulmonary disease patient with trigger sensitivity of ii cm H_twoO

Indications for non-invasive positive-pressure level ventilation

1. Patients with pH between 7.30 and vii.25

2. Non-responders to medical therapy having PaO_ii <fifty mmHg, PaCO₂ > 80–ninety mmHg, pH ≤7.2, with following:

   1. Sick but not moribund

   2. Able to protect airway

   3. Witting and cooperative

   4. Haemodynamically stable

   5. No excessive respiratory secretions

   6. Few co-morbidities

3. Patients who have declined intubation

4. Every bit a weaning facilitator

5. Domiciliary NPPV for patients with recurrent admissions.

Technique of non-invasive positive-pressure ventilation[33,34]

Initial settings

• Pressure level support (PS) mode at 10 cm H₂O of IPAP and v cm H_iiO EPAP

• Pressures <8 cm/four cm H_iiO (IPAP/EPAP) not advised as this may be inadequate

• Conform (IPAP and/or EPAP) to achieve tidal volume of 5–seven ml/kg.

Adjustment on the basis of arterial blood gas analysis

• Increase IPAP by 2 cm H₂O if persistent hypercapnia

• Increase IPAP and EPAP by ii cm H_twoO if persistent hypoxaemia

• Maximal IPAP express to 20–25 cm H_twoO (avoids gastric distension, improves patient condolement)

• Maximal EPAP limited to ten–15 cm H_iiO. It can be increased past looking at the number of missed breaths

• FiO₂ to be adjusted to everyman level with an adequate pulse oximetry value

• Backup RR 12–16 breaths/min

• If the patient is not able to trigger, accept big leaks that lead to automobile-cycling with PS, the patient may be switched over to force per unit area controlled mode. Proportional assistance ventilation (PAV) tin besides been used with promising results.

Predictors of successful trial of not-invasive ventilation (ane–2 h)

1. Decrease in PaCO_two >viii mmHg

2. Improvement in pH >0.06

3. Correction of respiratory acidosis.

Predictors of failure

1. Severity of illness

   • Acidosis (pH <7.25)

   • Hypercapnia (>lxxx and pH <7.25)

   • Astute physiology and chronic health evaluation Two score college than 20

2. Level of consciousness[34,35]

   • Neurologic score/Kellye–Matthay score >4 (stuporous, arousal but after vigorous stimulation, inconsistently follows commands)

   • Encephalopathy score >3 (major defoliation, daytime sleepiness or agitation)

   • Glasgow Blackout Scale score <8

3. Failure of improvement with 12–24 h of non-invasive ventilation (NIV)

Indications for invasive mechanical ventilation

Major criteria (any 1 of the following)[36,37]

• Respiratory abort

• Loss of consciousness

• Psychomotor agitation requiring sedation

• Haemodynamic instability with systolic claret pressure (BP) <lxx or > 180 mmHg

• Heart rate <50 beats/min with loss of alertness

• Gasping for air.

Small Criteria (whatever 2 of the following)

• RR >35 breath/min

• Worsening acidaemia or pH <7.25

• PaO₂ <forty mmHg or PaO₂/FiO_two <200 mmHg despite oxygen

• Decreasing level of consciousness.

SECURING AIRWAY

These patients should be intubated (based on the severity of respiratory distress rather than whatsoever absolute value of PaCO₂ or RR) followed by 24 h of full ventilatory support to residue the fatigued respiratory muscles. Controlled modes should be used equally briefly equally possible to avoid disuse cloudburst of respiratory muscles and unnecessary prolongation of the menstruation of mechanical ventilation.

Anaesthesia tin 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 subsequently intubation that is not responding to fluid, ventilator can be disconnected and if the BP improves, a manual squeeze of the thoracic muzzle can be performed to reduce DH which can be appreciated on SpO₂ tracings as huge respiratory swings.[38]

VENTILATION IN A PASSIVE PATIENT

Ventilation should be adjusted based on the degree of DH and Motorcar-PEEP and not PaCO₂. At that place are just three factors that determine auto-PEEP: (one) Minute ventilation, (two) I: Due east ratio, (3) expiratory time constants. Of the three factors, minute ventilation is the near of import factor which causes DH. Hence, when ventilating patients with COPD, a smaller V_T, slow RR, high height menstruum should be used with an aim to target normal pH and not PaCO₂ (permissive hypercapnia).

Initial settings

• Set FiO_two to target SpO₂ of 88–92%

• Mode-assist command ventilation (preferred)/intermittent mandatory ventilation (IMV ± PS)

• V_T - 8 ml/kg, RR - 12–14/min, I: E ratio = 1:3 or more than depending on expiratory time abiding calculation, flow rate-eighty–100 L/min, peak inspiratory pressure (PIP) of < 40–45 cm H₂O and Pplat < 30 cm H₂O is acceptable

• Adjust the trigger usually by − 1 to 2 cm H_iiO for force per unit area and two Fifty/min for flow. If trigger is sensitive, respiratory alkalosis may occur while besides 'difficult' a trigger volition increment WOB

• PEEP setting start at v cm H_twoO, and keep a watch at Pplat or PIP and haemodynamics. Low levels of PEEP improve synchrony and reduce the WOB from level A to level B by off-setting the auto-PEEP in COPD patients [Effigy 5]. This beneficial effect of PEEP is the most evident in patients who have flow limitation during tidal expiration and could be probably due to reduction in the lung heterogeneity.[ane]

VENTILATION IN SPONTANEOUS PATIENT

• PS/PC manner/PAV

• PS to generate 8 ml/kg of V_T, minimal trigger-flow or pressure, height catamenia of 80–100 L/min

• PEEP can be added starting at 5 cm H₂O in increments of 2 cm H₂O

• Observe the WOB, RR and missed breaths in flow versus fourth dimension scalar which testify a decrease in RR and no missed breaths

• Monitor PIP and Pplat, if there is any increase in these pressures-reduce PEEP. Rarely more than x cm H₂O PEEP is required

• Expiratory sensitivity can be set much above the default setting of 25%

• If the patient is still non synchronising, other causes similar fever, pain, etc., have to be looked for and in case no other cause is establish, sedation can be used.

EXACERBATION OF SEVERE ASTHMA

In add-on to standard recommendation for NPPV in all situations, the specific recommendations for patients with acute/severe bronchial asthma are:

• Current literature favour relatively small V_T (6–ten ml/kg), higher inspiratory flow (fourscore–100 L/min) with PIP < 40–45 cm H₂O and Pplat < 25–thirty cm H_iiO, to preserve expiratory time and minimise hyperinflation, barotrauma and hypotension [Figure 6]. The RR should be 8–12 breaths/min to accomplish the least possible hyperinflation (auto-PEEP <10 cm H₂O) and to maintain pH in an adequate range, if possible

  

  Pressure-time curve indicating increased airway resistance. Peak inspiratory pressure increases whereas Pplat remains same

• In contrast to COPD patients, applying PEEP during full 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 level, causing circulatory compromise. Although some clinical studies have reported improved airway role (without untoward effects) with continuous positive airway pressure or with NIV and PEEP amid patients with acute asthma, the use of PEEP during full ventilatory support of a patient with acute asthma is controversial

• Moreover, because the degree of variability in auto-PEEP on a breath-to-breath basis can be loftier in asthmatic patients receiving mechanical ventilation, the addition of applied PEEP without considering the breath-to-breath variability tin lead to lung overdistention. Therefore, PEEP should be used cautiously in asthmatic patients undergoing mechanical ventilation and titrated in real time

• Controlled hypoventilation appears to improve the clinical outcome of patients who have status asthmaticus. When reduction of DH is an issue and provided that there is no intracranial hypertension and overt haemodynamic instability, acceptance of moderate acidaemia (pH ≥ seven.2) is reasonable.

Office OF HELIOX THERAPY IN OBSTRUCTIVE AIRWAY DISEASE

Heliox was introduced in 1934 for the handling of airway obstacle.[39] 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. Moreover, heliox is also found to improve the deposition of aerosolised bronchodilators with a superior particle retention in the lung.[40]

The percentage of oxygen in heliox should be at least xx% to prevent hypoxia, and no more than twoscore% for heliox to show clinically significant issue.[40] Information technology has been shown to reduce DH past xv% that will probably place the respiratory muscles at a better mechanical advantage and subtract the WOB.[41] Indeed, a significant reject in VCO_ii was also noted supporting a reduced WOB leading to modest simply significant fall in the PaCO₂.[42] It also enhances exercise tolerance, at least at abiding work charge per unit, and thus tin can be useful to increment the level of physical training in patients of obstructive airway disease.[43] Notwithstanding, due to presence of conflicting literature, heliox therapy which is costly and cumbersome is not warranted for stable COPD patients at rest with moderate to severe affliction, but could exist effective as an adjuvant therapy to raise the efficacy of medical handling. So, further research to identify the COPD patients potentially able to do good from this blazon of therapy is required.[42,43]

WEANING

An aggressive policy toward weaning is justified in COPD patients because an disability to wean is invariably associated with a worse prognosis and prolonged ventilation. It begins when the precipitating cistron of the respiratory failure is partially or totally reversed. Marginal respiratory mechanics and continued presence of car-PEEP brand weaning difficult in COPD patients. Hence, factors that increase resistance such as size, secretions, kinking of the tube and the presence of elbow-shaped parts or a heat and moisture exchanger in the circuit have to be optimised to promote early weaning. Furthermore, patients of cor pulmonale may require pocket-size dose of inotrope, diuretics and low fluid strategy during weaning.

Weaning can exist done with PS mode along with spontaneous breathing trials (SBTs). Sequential weaning (early extubation followed by NPPV) is found to be good alternative in patients showing failed SBTs.[44,45] On the reverse, role of tracheostomy is uncertain, but due to marginal respiratory mechanics, it is also expected to help in weaning.

SUMMARY

Ventilatory back up is a lifesaving procedure in acute exacerbation of COPD and asthma. The therapeutic goals are to meliorate gas exchange, unload ventilatory pump and to relieve respiratory distress. Nowadays, NPPV is regarded as the commencement line of treatment while invasive ventilation is reserved for life-threatening respiratory failure. However, information technology tin can cause considerable increase in morbidity and mortality if not used properly. Therefore, information technology is necessary to take a good agreement of pathophysiology, mechanics and design of menses obstruction and DH to provide the near suitable ventilation to these patients. The ventilatory graphics (flow, force per unit area and volume) of the well-nigh of the mod ventilators becomes a valuable tool in these situations and assistance in early diagnosis and management of the patient'south condition earlier it becomes clinically overt.

Financial support and sponsorship

Nada.

Conflicts of interest

There are no conflicts of interest.

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613406/

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