Anesthesia for COPD

pulmonary function tests

pulmonary function tests

1. spirometry

spirometry is used to measure how much air can be taken in and out as wellas how fast air can move also in and out.
the spirometry is used for the following 3 tests:

• flow volume loops

flow volume loops provide a graphical illustration of a patient`spirometric efforts. flow is plotted against volume to display a contiuous loop from inspiration to expiration.
the loops show FVC and FEV1.
FEV1/ FVC is normally 80%.

COPD: decrease in expiratory flow rate at any giving lung volume, invrease in residual volume.
restrictive disease; decrease in all lung volumes.
fixed large airway ostruction: plateau in both ispiratory and expiratory cycles.
variable extrathoracic obstruction: plateau in the inpiratory limb.

• The severity of the abnormality might be graded as follows:
• May be a physiologic variant: Predicted FEV₁ ≥100%
• Mild: Predicted FEV₁ <100% and ≥70%
• Moderate: Predicted FEV₁ <70% and ≥60%
• Moderately severe: Predicted FEV₁ <60% and ≥50%
• Severe: Predicted FEV₁ <50% and ≥34%

case discussion

hi, here I post this case for open discussion. let us think together and try to answer these questions. I am waiting for your valuable contributions.


A 56-year-old coal miner requires sigmoid colectomy for carcinoma. He has a home nebuliser. His FEV1 is 0.68 litres, and he has 3% reversibility with salbutamol.

Observations/examination Shortness of breath 50 yards. 
Wheezy chest 
Respiratory rate 30/min 
Non-productive cough 
Chest X-ray: bullous lung disease and prominent pulmonary arteries 
ECG: normal 
Saturations: 93% on air. PO2 12 kPa; PCO2 4.5 kPa 
No FBC 
No electrolytes 

Drugs 
He is currently taking 2.5 mg prednisolone (the dose was recently reduced) 

Questions 1. Summarise the case. 
2. What are the main issues? 
3. How would you optimise this patient preoperatively? 
4. What is the likely cause of his COPD? 
5. Present the chest X-ray. 
6. What are the chest X-ray findings in pulmonary hypertension? 
7. Present the ECG. 
8. What ECG findings might you find? 
9. What are the ECG changes seen in heart strain (left and right)? 
10. What are the criteria for pathological Q waves? 
11. What is respiratory failure? 
- Give blood gas definitions of type 1 and 2 respiratory failure 
12. What are blue bloaters and pink puffers? 
- Which is this patient? 
13. How would you anaesthetise this man? 

ArticleDate:20070524 

lung function

Understanding lung function is vital for both intensivists and anaesthetists. Normal lung physiology is unfortunately extremely complex, and this complexity is further enhanced in sick lungs! Lacking smart and well-programmed supercomputers to simulate normal lung physiology, we tend to rely on gross over-simplification. The relationship between our current understanding of how lungs function, and what actually happens is perhaps similar to the relationship between counting on one's fingers and advanced matrix algebra! Unfortunately, many of the fruitful analogies that we use have been turned into dogma!

In most textbooks, you will encounter a vast array of "laws", which examination candidates in particular are encouraged to regurgitate, often with minimal understanding. For the record, here are some of them:-

A List of Laws Note that this mildly formidable table is mainly for reference purposes. The wise reader will skip over it, and come back from time to time. All equations are discussed in a friendly fashion in the body of the text! Those we are on "first name" terms with (Henry, Charles & Graham) will be used less extensively!
Name	Equation	Meaning
Boyle's Law	P.V = K	In a container filled with gas, if you decrease the volume, the pressure will correspondingly increase, and vice versa.
Dalton's Law		In a mixture of gases, each gas behaves as if it were on its own: it exerts a partial pressure that is independent of that exerted by other gases in the mixture.
Hooke's Law	L   T	The change in length of a spring is proportional to the tension exerted on the spring.
Laplace's Law	P = 2.T/r	The pressure inside a bubble exceeds the pressure outside the bubble by twice the surface tension, divided by the radius. In other words, the smaller a bubble, the more the pressure inside it exceeds the pressure on the outside.
Poiseuille's Law	R = 8.L.eta/(pi.r4)	Where laminar flow occurs, the resistance to flow decreases with the fourth power of the radius - if you double the radius, the resistance decreases sixteen times! Resistance also depends on the eta, (the viscosity of the gas or fluid), as well as the length of the tube being assessed (L). Note that with turbulent flow, things are completely different - we can't even talk about "resistance" as the drop in pressure is not directly related to flow, but to flow squared!
The Fanning Equation	P  1 / r5	With turbulent flow, for any particular flow rate, pressure drop depends on the fifth power of the radius of the tube.
Fick's Law	Vgas  A * P / L	Gas transfer through a membrane is proportional to membrane surface area (A) and partial pressure gradient across the membrane(P), and inversely proportional to thickness (L).
Graham's Law	D  sol / MW0.5	Diffusion of molecules is inversely proportional to the square root of their molecular weight, and directly proportional to their solubility.
Henry's Law		The number of molecules of gas dissolved in solution is proportional to the partial pressure of the gas.
Charles' Law	V = K'. T	As the temperature of an amount of gas increases, so does its volume (maintaining a constant pressure). We can combine this with Boyle's law to get: PV = nRT Where n is the number of moles of gas, and R is a constant, the universal gas constant. At standard temperature and pressure, a mole of gas occupies 22.4 litres. The actual value for CO2 and N2O is about 22.2 litres.
Reynold's number	linear gas velocity * diameter * density / viscosity	Reynold's number is dimensionless. Turbulence occurs if Reynold's number is over 1000, and flow is entirely turbulent if it exceeds 1500.

Basic Ideas

Atmospheric oxygen arose as a toxic by-product of the very first photosynthetic organisms, which were possibly quite similar to today's blue-green algae. Smarter organisms rapidly learned to use this oxygen, and minimise its toxic effects. When they possibly unwisely decided to abandon their individual identities and co-operate to form multicellular organisms, and moved onto land, then their problems really began! They needed:

1. Ways of acquiring atmospheric oxygen in large quantities;
2. A method to transport this O₂ to distant, oxygen- starved cells;
3. Processes for removal of carbon dioxide, the principal metabolic waste product.

All of these are more-or-less adequately fulfilled by the tightly entwined cardiovascular and respiratory systems. The respiratory system is a marvellous, efficient pump for passing air over the capillary bed of the lung, where oxygen moves into the blood and CO₂ is removed from the blood. The inefficient and failure-prone cardiovascular system then takes over, finally distributing oxygen to oxygen-hungry cells throughout the body. The inefficiency with which this occurs can be seen if we look at the oxygen cascade, which documents the changes in partial pressure of oxygen from inspired air down to the mitochondrion where the oxygen is actually used. Oxygen moves down a gradient, from a partial pressure of about 160mmHg in the atmosphere, down to about 4-20mmHg in the mitochondrion! The steps are:

Inspired oxygen	160 mmHg
Alveolar oxygen	~ 120 mmHg
Oxygen in the blood	~ 100 mmHg
Oxygen at tissue level	~ 4-20 mmHg

Considering these in more detail we find:

1. Atmospheric pressure at sea level is about 760mmHg, and the concentration of oxygen is 20.95%. Using Dalton's Lawwe calculate that in dry, inspired air, the partial pressure of oxygen is 159mmHg. Unfortunately, air within the lungs is 100% saturated with water. We need to re-think! If we know that the partial pressure of water vapour at 37 degrees Celsius is 47mmHg, we can work out that the partial pressure of the remaining gases is (760 - 47)mmHg. We'll call this barometric pressure that excludes water vapour pressure the 'dry barometric pressure', or P_Bdry. Applying Dalton's law yet again, we determine that the inspired PO₂ is therefore actually 149mmHg, once the air has become fully hydrated in the nose. Let's abbreviate the inspired PO₂ to PiO₂. But wait a bit..
   
2. Oxygen is taken up in the lung! This will decrease the amount of oxygen in the alveolar air. The decrease will be directly related to the amount of oxygen taken up, and inversely related to the alveolar ventilation. In other words, the greater the alveolar ventilation, the less the effect of this oxygen uptake on the fraction of oxygen in the alveolar air. This is an expression of the "universal alveolar air equation". We say:
   
   
   alveolar PO2     ~     P_Bdry * (FiO2 - fractional O2 uptake)
   
   Where the fractional O2 uptake is equal to: O2 uptake / alveolar ventilation
   
   We may abbreviate alveolar PO2 to P_AO2. Thus:
   
   
   P_AO2    ~    P_Bdry * (FiO2 - O2 uptake / alveolar ventilation)
   
   
   Note that this is only approximate - differences between inspired and expired volumes will affect the estimate. In addition, if you guessed that P_AO2 fluctuated with each breath, you would be correct, but this variation is normally only about 3mmHg. 
   (There are more convenient ways of estimating P_AO2, although many of these are fairly inaccurate!) Plugging values into the above, we might get something like:
   
   P_AO2 = (760 - 47) * ( 0.2095 - 250/5000)
   
   Where the true barometric pressure is 760mmHg - the partial pressure of water vapour at 37 degrees is 47mmHg, the inspired oxygen concentration is 20.95%, the oxygen consumption is say 250 ml/minute, and the alveolar ventilation is 5 litres/minute. This gives us a P_AO2 of about 114 mmHg. We rush on, inexorably down the oxygen cascade!
   
3. In a healthy young adult breathing air, the gradient from alveolus to capillary is minimal - under 15mmHg. In the 'normal' elderly person, this may rise to 37mmHg! (One convenient estimate of this gradient is simply 4 + age/4 mmHg)! In the critically ill, this alveolar/arterial oxygen difference may be hundreds of millimetres of mercury. Nevertheless, even in the normal young individual we still take a small step down, to an arterial partial pressure of oxygen (P_aO2) of about 100mmHg.
   
   Another useful estimate for PaO2 at sea level (in healthy subjects breathing air) is given as:
   
   
   PaO2    = 102 - 0.33 * (age in years)
   
   This is expressed in mmHg, and we stress that the confidence limits for this estimate are fairly wide: +- 10mmHg.
   
4. The big drop comes at the tissue level, where the PO2 within the mitochondrion has been estimated to be as low as 4-20mmHg! In some normally functioning cells this PO2 may even drop to 1mm Hg!
   Perhaps this is the PO2 that our ancient unicellular ancestors first found that they could effectively use, and there has been no (heh) pressure to subsequently change, or perhaps this low PO2 is a trade-off related to the number of capillaries needed to support the tissues, but we know one thing, and that is that we could sure use a bigger tolerance margin in critically ill patients!

source: http://www.anaesthetist.com/icu/organs/lung/Findex.htm#lungfx.htm

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

COPD is characterized by the progressive development of airway limitation that is not fully reversible.

The term COPD encompasses chronic bronchitis and emphysema.

     Chronic bronchitis is defined as the presence of a productive cough for more than 3 months for more than 2 successive years.

     Chronic bronchitis follows prolonged exposure of the airways to non specific irritant and characterized by hypersecretion of mucous and inflammatory changes in the bronchi.

     Pulmonary emphysema is defined as enlargement of air spaces and destruction of lung parenchyma, loss of lung elasticity, and closure of small airways. Obstruction to expiratory airflow can also lead to the formation of bullae with compression of the adjacent lung tissues.

Diagnostic and Clinical Features

A chronic productive cough and progressive exercise limitation are the hallmarks of persistent expiratory airflow obstruction.

Patient with predominant chronic bronchitis present with chronic productive cough, whereas patient with predominant emphysema complain of dyspnea

                                                           Chronic bronchitis                                           emphysema

Mechanism of airway             decreased airway lumen due                         loss of elastic recoil of the

Obstruction                              to mucous and inflammation                         lung

Dyspnea                                    moderate                                                           severe

FEV₁                                            decreased                                                          decreased

PaO2                                          marked decrease                                              moderate decrease

                                                    (blue bloater)                                                    (pink buffer)

PaCO2                                        increased                                                            normal - decrease

Diffusing Capacity                    normal                                                                decreased

HT                                               increased                                                            normal

Corpulmonale                           marked                                                                mild

Prognosis                                   poor                                                                     good

Pulmonary Function tests

Pulmonary Function tests reveal

1.       Decrease in FEV₁ / FVC ration

2.       Decrease in F. expiratory flow

3.       Increase in RV and normal to increase FRC, TLC

Chest Radiography

Radiologic abnormalities may be minimal but it meight show

·         Hyperlucency and hyperinflation

·         Flattening of the diaphragm

·         Very vertical cardiac silhouette

·         Emphasematous bullae

ABG

ABG can be used to categorize patient with COPD as

Pink buffers

PaO2 usually high than 60mmHg and PaO2 is normal

Individual characterized as pink buffers are typically thin and free of signs of right heart failure and have severe emphysema.

Blue bloaters

PaO2 usually less than 60mmHg and

PaCO2 chronically increased to more than 45mm

Blue bloater typically exhibit cough and sputum production

Consequences of these two Arterial BIood  Gas pattern

Blue bloater:

Arterial hypoxemia and respiratory acidosis lead to increase in pulmonary vascular resistance with resultant pulmonary  hypertension.

Chronic pulmonary hypertension cause right ventricular hypertrophy and failure (Cor pulmonale) arterial hypoxemia also cause secondary erythrocytosis.

Pink buffers:

Loss of pulmonary cap. Vascular bed decrease

Lung diffusing capacity.

Since paO2 is only mildly decrease, pulmonary V.C. is minimal and erythrocytosis does not occur.

Spirometric Classification of COPD

0:     at risk        normal spirometry

                           Chronic sympt

                           FEV₁ / FVC    ˂   70%

I:     mild            FEV₁ ≥ 80% of predicted

                           with or without chronic symptoms

II:    moderate FEV₁ / FVC  ˂ 70%

                          50% ˂ FEV₁  ˂ 80%

                          with or without symptoms

III: severe                       FEV₁ / FVC ˂ 70%

                                        FEV₁  30-50% of predicted

                                        With or without chronic symptoms

IV:  very severe             FEV₁ / FVC  ˂  70%

                                        FEV₁  ˂  30%

                                        FEV₁  ˂  50% + chronic respiratory failure

Treatment of COPD

1.       Cessation of smoking and supplemental O2

2.       Drug therapy

-          Bronchodilator, β agonist, anticholinergic, antibiotics

3.       Lung volume reduction surgery

Anesthetic management of patient with COPD

Preoperative management

The history and physical examination of patient with COPD provide more accurate assessment of the likelihood of post-op pulmonary complications.

A history of poor exercise tolerance, chronic cough or unexplained dyspnea combined with diminished breath sounds, wheezing and prolonged expiratory phase predict an increased risk of post-op pulmonary complications.

Preop pulmonary Functions  tests

The results of pulmonary function tests and ABG can be useful for predicting pulmonary function after lung resection but they do not reliably predict the likelihood of post-op pulmonary complications after non-thoracic surgery.

Indications for pre-op tests typically include:

1.       Hypoxemia on room air or the need for home oxygen therapy without a known etiology

2.       Bicarbonate more than 33mEq/L or PaCO2 ˃ 50mmHg

3.       History of respiratory failure

4.       Severe shortness of breath due to respiratory disease

5.       Planned pneumonectomy

6.       Determining the response to bronchodilator

7.       Suspected pulmonary hypertension

Risk reduction strategies

1.        Preoperative

-          Encourage cessation of smoking for at least 6 weeks

-          Treat evidence of expiratory airflow obstruction

-          Treat respiratory infection with antibiotics

-          Patient education regarding lung expansion maneuver’s

2.       Intraoperative

-          Use of minimally invasive surgical technique

-          Consider use of regional anesthesia

-          Avoid prolonged surgery ˃ 3 hours

3.       Postoperative

-          Institute lung expansion maneuvers (voluntary deep breathing, incentive spyrometry, CPAP)

-          Maximize analgesia

Acute effects of smoking cessation

The adverse effects of CO on oxygen carrying capacity and effects of nicotine on the cardiovascular system are short lived.

-          The elimination half life of CO2 is approximately 4-6h when breathing room air.

Within 12h after cessation of smoking the PaO2 at which Hb is 50% saturated increase from 22.9 to 26.4mmHg and plasma level of carboxyHb decrease from 6.5% to 1%

-          The sympathomimetic effects of nicotine on the heart are transient, lasting only 20-30mins.

-          Other long term benefits of smoking cessation include: improvement in ciliary function, decrease in sputum production

Intraoperative management

Regional anesthesia is suitable for lower intra-abdominal and lower extremities procedures. However, regional anesthetic techniques that produce sensory anesthesia above T6 are not recommended as they may impair the ventilatory functions requiring active exhalation such as expiratory reserve volume, peak expiratory flow and maximum minute ventilation. Clinically this is manifested as a cough that is inadequate to clear airway secretions.

Loss of proporioception from the chest, and unusual position like lithotomy or lateral position, often accentuate dyspnea in awake patient.

It must be appreciated that COPD patient can be extremely sensitive to the ventilator depressed effects of sedative drugs. When used, it should be given in small incremental doses.

-          General Anesthesia

General anesthesia is often provided with volatile anesthetics. Volatile anesthetics produce bronchodilatation and have ability to be rapidly eliminated through the lung minimizing postop resifual ventilator depression.

Nitrous oxide should be avoided in patient with bullae and patient with pulmonary hypertension. Opioids may be less desirable as they cause prolonged postop respiratory depression.

Ventilation should be controlled with small moderate tidal volume and slow rates to avoid air trapping humidification of inspired gases and use of low gas flow help to keep airway secretion moist.

Arterial CO2 measurement should be used to guide ventilation. Ventilation should be adjusted to maintain a normal arterial pH.

Hemodynamic onitoring should be dictated by any underlying cardiac dysfunction and the extent of surgery.

Postoperative management

Lung expansion maneuvers

They decrease the risk of atelectasis by increasing lung volumes.

They include:

Deep breathing exercises

Chest physiotherapy

Incentive spirometry

Positive pressure breathing techniques

Pain control

Postop. Neuroaxial analgesia with opioids may permit early tracheal extubation, early ambulation, which help to increase FRC and improve oxygenation.

Postoperative neuroaxial analgesia is recommended after high risk thoracic abdominal and major vascular surgery.

Mechanical ventilation

Continued mechanical ventilation during the immediate postop period may be necessary in patient with severe COPD who have undergone major abdominal or intra-thoracic surgery.

FiO2 and ventilator settings should be adjusted to maintain paO2 60-100mmHG and paCO2 in a range that maintains pH at 7.35 – 7.45.

The decision to discontinue mechanical ventilation and tracheal extubation is based on the patient clinical status and indices of pulmonary function.