COPD and Anesthesia
Vesicular Breath Sounds
Heard at the periphery of the lungs. Quiet, low-pitched, rustling sound. Inspiratory phase – louder and longer than expiration; no distinct pause between inspiration and expiration (Fig. 2.5). Vesicular breath sounds originate in larger airways; in their passage through normal lungs the intensity and frequency of the sounds are decreased since normal lung parenchyma transmits sounds poorly.
Bronchial Breath Sounds
Bronchial breathing is characterized by breath sounds that are high-pitched with a hollow or blowing quality similar to those heard over the trachea and larynx during tidal breathing. The breath sounds are of similar length and intensity in both inspiration and expiration and have a characteristic pause between. (Fig. 2.5)Bronchial breath sounds are found whenever normal lung tissue is replaced by uniformly conducting tissue, whether through consolidation, fibrosis or collapse and the relevant major bronchus is patent.
Musical high-pitched sounds associated with airway narrowing. Polyphonic, when airflow obstruction is diffuse, as in asthma or bronchitis; Monophonic, when the airflow obstruction is localized, as in foreign body or tumor obstruction. However, in severe airflow obstruction, silent chest will be an ominous sign.
Short, explosive sounds, often described as bubbling or clicking noises; produced by sudden changes in the gas pressure related to sudden opening of the previously closed small airways. Late inspiratory crackles heard at the lung bases indicate delayed airway opening as occurs in pulmonary edema or fibrosing alveolitis.
Characteristic of pleural inflammation and occurs at a stage when there is usually pain. Described as creaking or rubbing character; do not change in character after coughing (as against crepitations); associated with localized pain; often during both inspiration and expiration.
If right sided pressures are sufficiently high, neck veins may elevate instead of collapse with inspiration.
The oxygen cascade describes the process of declining oxygen tension from atmosphere to mitochondria (figure 2-6). Oxygen moves down the pressure or concentration gradient from a relatively high level in air, to the levels in the respiratory tract and then alveolar gas, the arterial blood, capillaries and finally the cell. The PO2 reaches the lowest level (4-20 mm Hg) in the mitochondria (structures in cells responsible for energy production). This decrease in PO2 from air to the mitochondrion is known as the oxygen cascade and the size of any one step in the cascade may be increased under pathological circumstances and may result in hypoxia. If PO2 value falls below 1-2 mm Hg then aerobic metabolism stops and anaerobic metabolism sets in and this is referred to as Pasteur Point.
The Bohr equation is used to quantify the ratio of physiological dead space to the total tidal volume, and gives an indication of the extent of wasted ventilation. It is stated as follows:
Note that physiological dead space differs from anatomical dead space (as measured by Fowler’s method) as it includes alveolar dead space.
The Shunt equation quantifies the extent that venous blood bypasses oxygenation in the capillaries of the lung.
Qs /QT = (Cc’O2 −CaO2 ) / (Cc’O2 − CvO2)
Alveolar-arterial gradient (A-a gradient)
The Alveolar-arterial gradient (A-a gradient), is a measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen. It is used in diagnosing the source of hypoxemia.
A-a gradient = P O − P O where:
PAO2 = alveolar PO2 (calculated from the alveolar gas equation).
PaO2 = arterial PO2 (measured in arterial blood)
A normal A-a gradient is less than 10 mmHg, but can range from 5–20 mm Hg. Normally, the A-a gradient increases with age. For every decade a person has lived, their A-a gradient is expected to increase by 1 mm Hg.
Causes of increased Alveolar-Arterial gradient:
Increased areas of low V/Q ratios
Low mixed venous tension
Decreased cardiac output
Increased oxygen consumption
Decreased hemoglobin concentration.
Smoking and Anesthesia
Effects of smoking
Increases sputum production (mucous hypersecretion)
Decreases ciliary activity
Increase synthesis and release of elastolytic enzymes from alveolar macrophages
Increases epithelial permeability
Immunoregulatory function of macrophages is changed
Changed pulmonary surfactant
Airway irritation/small airway reactivity (activation of sensory endings located in the central airways, whichis primarily caused by nicotine).
Bronchitic disease: Increased pulmonary compliance; barrel chest; flattened diaphragm; incomplete passive
emptying leading to gas trapping ÂÂVentilation-perfusion mismatch: Large areas of dead space ventilation and venous admixture and hencecarbon dioxide elimination is inefficient. ÂÂSympathomimetic effect of nicotine on heart (may be
Increased carbon monoxy hemoglobin (CO-Hb), as high as 8–10% (normal 1%) – can cause impaired gas exchange (Other effects of carbon monoxide: over- estimation of oxygen saturation by pulse oximeter, negative inotropic effects)
Smoker’s polycythemia: Increased CO-Hb shifts oxygen- dissociation curve to left; as P50 reduces, the resultant tissue hypoxia can stimulate production and release of erythropoietin. Further, plasma volume reduces. Therefore hematocrit increases.
2–6 fold increased risk of developing postoperative pneumonia
Increased risk of head and neck cancer; may cause airway management issues
2 fold risk of developing peripheral vascular disease ÂÂSome components of cigarette smoke stimulate hepatic enzymes, which can alter postoperative analgesic requirements
Usually associated with essential hypertension and cerebrovascular accidents.
A way to measure the amount a person has smoked over a long period of time. It is calculated by multiplying the number of packs of cigarettes smoked per day by the number of years the person has smoked. (National Cancer Institute definition of pack year)
For example, 1 pack year is equal to smoking 20 cigarettes per day for 1 year, or 40 cigarettes per day for half a year, and so on. .
Number of pack years = (Packs smoked per day) × (years as a smoker); or
Number of pack years = (number of cigarettes smoked per day × number of years smoked)/20
For example: A patient who has smoked 15 cigarettes a day for 40 years has a (15 × 40)/20 = 30 pack year smoking history.
Possible risks of stopping smoking immediate preoperatively
Development of hypersecretion and bronchospasm
Increased incidence of deep vein thrombosis (DVT)
(Management options: Anxiolytics, bronchodilators, anticoagulants).
Beneficial effects of smoking cessation and time course
The key beneficial effects are summarized in Table 2.23.
Chronic bronchitis causes enlargement of mucous secreting glands in the trachea and bronchi. It is defined as ratio between the thickness of the submucosal mucous secreting glands (AB) and the thickness between the epithelium and cartilage that covers the bronchi (CD) as given in Figure 2.7.
A normal Reid index is less than 0.4 and is increased in chronic bronchitis. Hyperplasia and hypertrophy of mucous glands as in chronic bronchitis causes them to be present at deeper levels in the bronchial wall and thicker in size, thus increasing the Reid Index beyond the normal value.
The Haldane effect is a property of hemoglobin first described by the Scottish physician John Scott Haldane. Deoxygenation of the blood increases its ability to carry carbon dioxide; this property is the Haldane effect. Conversely, oxygenated blood has a reduced capacity for carbon dioxide.
Patients with COPD who have had a cardiorespiratory arrest and have been pronounced dead after failed resuscitation have spontaneously recovered once resuscitation is stopped. Anesthesiologists must be very aware of the possibility of dynamic hyperinflation whenever general anesthesia is induced in a patient with emphysema. Even seemingly low levels of positive airway pressure in these patients, such as those generated by bag-mask ventilation during induction of anesthesia, can lead to severe hyperinflation with secondary impairment of cardiac venous return leading to hypotension and even cardiac arrest. This hemodynamic effect is exacerbated in the presence of decreased intravascular volume and vasodilating anesthetic agents. An extremely difficult differential diagnosis arises when one of these patients ‘‘crashes’’ during positive pressure ventilation. The diagnostic dilemma is to differentiate between tension pneumothorax and dynamic hyperinflation. The choice is not always obvious and the definitive treatments are very different. Unilateral changes in chest auscultation, tracheal deviation and the presence of known bullae favor pneumothorax and the need for decompression. In the absence of these clues it is best to stop ventilation and let the patient breath out passively to atmosphere while beginning pharmacologic resuscitation. With hyperinflation there will be a gradual return of circulation, but it is not immediate. If there is no improvement after one minute of apnea the assumption should be pneumothorax and chest drains should be placed.
Hypoxic Pulmonary Vasoconstriction
Hypoxic pulmonary vasoconstriction was first described by Von Euler and Liljestrand in 1946. HPV helps to improve
V/Q matching by reducing perfusion of poorly oxygenated lung tissue. HPV is active in the physiologic range (PaO2 40 to 100 mm Hg in the adult) and proportional to the severity of the hypoxia. Low partial pressure of oxygen results in inhibition of potassium currents, leading to membrane depolarization and calcium entry through L-type calcium channels. Extracellular calcium entry, plus calcium release from the sarcoplasmic reticulum, culminates in smooth muscle contraction, primarily in small resistance pulmonary arteries with a diameter less than 500 μm. The primary stimulus for HPV appears to be the alveolar PaO2; however, the mixed venous PvO2 also is involved.
The commonly reported factors affecting HPV are summarized in the Table 2.24.
Apart from potent inhaled agents, other drugs and maneuvers used during anesthesia may also have an inhibitory effect on regional or whole-lung HPV. Factors associated with an increase in pulmonary artery pressure antagonize the effect of increased resistance caused by HPV and result in increased flow to the hypoxic region. Such indirect inhibitors of HPV include mitral stenosis, volume overload, thromboembolism, hypothermia, vasoconstrictor drugs, and a large hypoxic lung segment. Direct inhibitors of HPV include infection, vasodilator drugs such as nitroglycerin and nitroprusside, hypocarbia, and metabolic alkalemia. All these potential inhibitors should be considered when evaluating a patient for hypoxemia during thoracic surgery.
Denotes right ventricular hypertrophy and eventual failure resulting from pulmonary disease and attendant hypoxia or from pulmonary vascular disease.
The key factors leading to pulmonary hypertension in COPD are:
Mechanical compression of capillaries by distended lung units; and
Hypoxic pulmonary vasoconstriction.
Pulmonary Function Tests
1. Tests of Mechanical Function
a. Spirometry: VC, FVC, FEV1, IC, maximum inspiratory and expiratory flow rates
b. Static lung volumes
c. Respiratory mechanics
Respiratory muscle strength
i. Maximum inspiratory and expiratory mouth pressures
ii. Maximum transdiaphragmatic pressure (Pdi max)
Elastic recoil of lungs and chest wall Respiratory resistances
Bronchial provocation testing
2. Tests of Gas Exchange
a. Blood gas analysis
b. Carbon monoxide-diffusing capacity (transfer factor)
3. Assessment of Respiratory Control
Measurements of the ventilatory responses to hypercapnia and hypoxia
4. Exercise Assessment
The Six-Minute Walking Test.
1. Tests of Mechanical Function
Spirometry is the timed measurement of dynamic lung volumes during forced expiration and inspiration to quantify how effectively and how quickly the lungs can be emptied and filled (Fig. 2.8). Spirometry is used to establish baseline lung function, evaluate dyspnea, detect pulmonary disease, monitor effects of therapies used to treat respiratory disease, evaluate respiratory impairment, evaluate operative risk, and perform surveillance for occupational-related lung disease. The measurements usually made are the vital capacity (unforced and/or forced – VC, FVC), forced expiratory volume in one second (FEV1) and the ratio of these two volumes (FEV1/FVC). The flow volume loop also may be plotted (Fig. 2.9). Additionally, one can measure the maximum expiratory flow over the middle 50% of the vital capacity (FEF25–75%) which is a sensitive index of small airway function. A further spirometric measure undergoing renewed interest is that of inspiratory capacity (IC) which is the maximum volume of air that can be inspired from the end of quiet expiration (FRC) to total lung capacity (TLC). IC is reduced when hyperinflation is present or develops dynamically, e.g. during exercise in COPD patients. Measures of forced maximal flow during expiration and inspiration flow can also be made, either absolutely, e.g. peak expiratory flow (PEF) or as a function of volume thus generating a flow volume curve, the shape of which also contains information of diagnostic value.
Vital capacity (VC): The maximum volume of gas that can be exhaled following maximal inspiration. In addition to body habitus, VC is also dependent on respiratory muscle strength and chest–lung compliance. Normal VC is about 60–70 ml/kg.
Measuring vital capacity as an exhalation that is as hard and as rapid as possible provides important information about airway resistance. The ratio of the forced expiratory volume in 1s (FEV1) to the total forced vital capacity (FVC) is proportional to the degree of airway obstruction. Normally, FEV1/FVC is 80%. Whereas both FEV1 and FVC are effort dependent, forced midexpiratory flow (FEF25–75%) or Maximum Midexpiratory Flow rate (MMF25–75%) is effort independent and may be a more reliable measurement of obstruction.
It is routine practice to quantify the degree of reversibility of an obstructive defect by measuring spirometry before and after the administration of a bronchodilator. Generally, an improvement in FEV1 of 200 mL or more infers significant reversibility when the baseline FEV1 is <1.5 L as does an improvement of >15% when the FEV1 is >1.5 L.
Improvement in IC may occur due to an increase in TLC and/or to a reduction in FRC with lessening of hyperinflation. IC may improve significantly without change in FEV1 in patients with “irreversible” airflow obstruction in COPD. Furthermore, changes in IC following bronchodilator correlate better than other spirometric indices with improvement in dyspnea and exercise performance.
Similarly, the shape of the expiratory flow-volume curve (Fig. 2.10) varies between obstructive ventilatory defects where maximal flow rates are diminished and the expiratory curve is scooped out or concave to the X axis, and restrictive diseases where flows may be increased in relation to lung volumes. Reduction of maximal expiratory flow as residual volume is approached is suggestive of obstruction in the peripheral airways. A plateau of inspiratory flow may result from a collapsible extrathoracic airway whereas inspiratory and expiratory flows are both limited for fixed lesions. Maximal expiratory flow is selectively reduced for collapsible intrathoracic airway obstruction.
When PEF is measured repeatedly and plotted against time (e.g. morning and evening values by asthmatic patients) the pattern of the graph can be of great value in identifying particular aspects of the patient’s disease. Typical patterns are i) the “morning dipper” pattern of some asthmatics due to a fall in the early morning hours and ii) fall in PEF during the week with improvement on weekends and holidays which occurs in occupational asthma. Isolated falls in PEF in relation to specific allergens or trigger factors can help to identify and quantify these for the doctor and patient. A downward trend in PEF and an increase in its variability can identify worsening asthma.
b. Static Lung Volumes
Static lung volumes and capacities are determined using methods in which airflow does not play a role, so that flow- resistance has no influence. There are four volumes (tidal volume Vt, inspiratory reserve volume (IRV), expiratory reserve volume (ERV), and residual volume (RV)) and four capacities (total lung capacity (TLC), vital capacity (VC), inspiratory capacity (IC), and functional residual capacity (FRC) (Fig. 2.11). VC and its subdivisions may be measured with simple devices, such as spirometers. Because RV is not part of respired volume it (and capacities including it) must be measured by gas dilution, body plethysmography or graphic methods.
Tidal volume (Vt): The amount of air that moves into the lungs with each inspiration (or the amount that moves out with each expiration).
Inspiratory reserve volume (IRV): The air inspired with a maximal inspiratory effort in excess of the tidal volume.
Expiratory reserve volume (ERV): The volume expelled by an active expiratory effort after passive expiration.
Residual volume (RV): The air left in the lungs after a maximal expiratory effort.
The amount of air inspired per minute (pulmonary ventilation, respiratory minute volume) is normally about 6l (500 ml/breath × 12 breaths/min). The maximal voluntary ventilation (MVV), or, as it was formerly called, the maximal breathing capacity, is the largest volume of gas that can be moved into and out of the lungs in 1 minute by voluntary effort. The normal MVV is 125-170 l/min.
Normal values for these lung volumes, and names applied to combinations of them, are shown in Table 2.25.
Two broad categories of abnormality in lung volumes are seen in association with respiratory disease: restriction and over-inflation. Restriction is seen with decreased compliance of lungs (e.g. pulmonary fibrosis) or chest wall (e.g. kyphoscoliosis). This pattern is, in general, associated with a uniform reduction in TLC, RV and VC. Over-inflation is seen with airway narrowing, either extrinsic (due to loss of elastic support) as in emphysema, or intrinsic (due to disease directly affecting the airway wall), such as in asthma. These conditions are usually associated with an increase in TLC (particularly emphysema) and a disproportionate increase in RV and FRC, so that VC and IC are decreased. Mixed restrictive and obstructive patterns may occur. Respiratory muscle weakness affecting both inspiratory and expiratory muscles may be associated with a decrease in TLC and increase in RV, again decreasing VC.
c. Respiratory Mechanics
Respiratory mechanics entails examination of the forces involved in the act of breathing. The “active” forces generated by inspiratory muscles are opposed by “passive” forces generated by elastic recoil of the lungs and the chest wall (which increase with increasing volume), resistance to air, and tissue-flow (which increase with increasing flow), and (much less importantly) inertia.
Respiratory Muscle Strength
i. MaximumInspiratoryandExpiratoryMouthPressures: reflect the force generating capacity of inspiratory and expiratory muscles respectively
ii. Maximum Transdiaphragmatic Pressure (Pdi Max): reflects the strength of the diaphragm.
Elastic Recoil of Lungs and Chest Wall
Elastic recoil is usually measured in terms of compliance (C), which is defined as the change in volume divided by the change in distending pressure. Compliance measurements can be obtained for either the chest, the lung, or both together. In the supine position, chest wall compliance (CW) is reduced because of the weight of the abdominal contents against the diaphragm. Measurements are usually obtained under static conditions, i.e. at equilibrium. (Dynamic lung compliance [Cdyn,L], which is measured during rhythmic breathing, is also dependent on airway resistance). Lung compliance (CL) is defined as CL = Change in lung volume/ Change in transpulmonary pressure.
CL is normally 150–200 mL/cm H2O. A variety of factors, including lung volume, pulmonary blood volume, extravascular lung water, and pathological processes such as inflammation and fibrosis, affect CL.
Chest wall compliance (Cw) = Change in chest volume/ Change in transthoracic pressure where transthoracic pressure equals atmospheric pressure minus intrapleural pressure.
Normal chest wall compliance is 200 mL/cm H2O. Total compliance (lung and chest wall together) is 100 mL/cm H2O and is expressed by the following equation:
During quiet breathing (awake) the mouth, pharynx, larynx and trachea account for 20–30% of total airway resistance. The major sites of remaining airway resistance are the lobar, segmental and subsegmental airways, up to about the 7th generation. Because of their high total cross-sectional area, the numerous small (<2mm diameter) peripheral airways normally contribute less than 20% of total airway resistance.
Assuming laminar flow, resistance (in cm H2O/l/s) = pressure gradient (in cm H2O) divided by flow (in l/s). Normal value for an adult is around 0.5 – 1.5 cm H2O/l/sec while in states of disease this value may be 100 cm H2O/l/ sec or higher.
Bronchial Provocation Tests
Bronchial provocation testing identifies and char- acterizes airway hyperresponsiveness. Bronchial hyperresponsiveness refers to an exaggerated response to a bronchoconstrictor and is reflected by an increased sensitivity to the stimulus. The bronchoconstrictive stimuli used are pharmacological agents (histamine, methacholine), physical stimuli (non-isotonic aerosols, cold/dry air, exercise) and specific sensitizing agents (allergens, occupational sensitisers).
2. Tests of Gas Exchange
a. Blood Gas Analysis
Blood gas analyzers measure oxygen partial pressure (PaO2), carbon dioxide partial pressure (PaCO2)and hydrogen ion activity (pH) in arterial blood and also calculate indices of bicarbonate concentration, base excess, and oxygen saturation.
b. CO Diffusing Capacity - (Transfer Factor)
The carbon monoxide diffusing capacity (TLCO) or transfer factor of the lung is a measurement of the rate of transfer of CO from inspired gas to pulmonary capillary blood. Its units are ml/min/mm Hg driving pressure. TLCO is therefore not a capacity but a conductance, the inverse of a resistance. It is used primarily to ascertain the health of the alveolar-capillary membrane, or gas exchange surface of the lung, and in specific circumstances it is helpful as a diagnostic aid or to follow disease progression. The transfer of CO from the inspired gas to capillary blood is a relatively complex process, the rate of transfer usually being limited by the properties of the alveolar-capillary membrane and the capillary blood “sink” on the other side.
3. Assessment of Respiratory Control
Ventilatory drive is influenced by a variety of factors including conscious state, volition, emotion, arterial pH, PCO2 and PO2 (via chemoreceptors), mechanoreceptors in the chest wall and lungs, and irritant receptors in the airways. Furthermore, the translation of ventilatory drive into ventilation is a function of the integrity of neural pathways, strength and efficiency of respiratory muscles, and magnitude of the mechanical loads with which those muscles cope, which increase with restrictive or obstructive respiratory diseases.
The most commonly performed of these tests are measurements of the ventilatory responses to hypercapnia and hypoxia. Hypercapnic responses assess the relationship between ventilatory output and arterial CO2 concentration (usually estimated from end-tidal PCO2) in the presence of normoxia. Hypoxic responses assess the relationship between ventilatory output and arterial O2 concentration (usually estimated from pulse oximetry) in the presence of a stable arterial PCO2.
4. Exercise Assessment
Cardiopulmonary exercise testing enables a standardized measurement of aerobic capacity and oxygen reserve. The anaerobic threshold (AT) is an objective measurement of cardiac function that is independent of patient effort. AT is the point at which the rate of rise of CO2 output becomes greater than the rate of rise of VO2, which indicates anaerobic metabolism has begun to supplement aerobic metabolism. Electrocardiogram evidence of ischemia or AT <11 ml/min/kg has been associated with increased postoperative mortality. VO2 <20ml/kg/min also correlates with increased rates of postoperative cardiopulmonary complication.
When formal cardiopulmonary exercise testing is unavailable, a simple measurement of exercise capacity can be obtained by assessing the number of flights of stairs a patient is able to climb. In general terms, patients who can climb 5 flights of stairs will have a VO2 max >20 ml/kg/min. Conversely, patients who cannot climb 1 flight of stairs will have a VO2 max <10 ml/kg/ min. Two fights are approximately 12-15 ml/kg/min. The inability to climb 2 flights of stairs correlates with an increased rate of postoperative cardiopulmonary problems, as well as increased length of hospital stay.
An incremental protocol, with gradually increasing work levels to a symptom limited maximum, allows the interrelation of the measured variables to be observed throughout the normal work range. The Six-Minute Walking Test (6 MWT) is the most standardized of cardiopulmonary exercise tests and is currently in widespread use. With the 6-MWT the instructions to the patient are to “walk as far as you can during 6-minutes”. The 6MWT is self-paced, and a patient is probably less likely to push himself beyond his endurance or through angina or other pain. The primary measurement is the total distance walked. Secondary measures can include fatigue and dyspnea, measured with a modified Borg or visual analog scale. Arterial oxygen saturation can also be measured via pulse oximetry, as long as the oximeter is portable and not heavy.
Interpretation of PFT
Indications for Preoperative Pulmonary Function Tests
Respiratory failure is defined as respiratory dysfunction resulting in abnormalities of oxygenation or ventilation (CO2 elimination) severe enough to threaten the function of vital organs.
In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. Four different types of respiratory failure can be described, based upon these pathophysiologic derangements.
Type I, Acute Hypoxemic Respiratory Failure
Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
Type II, Hypercapnic Respiratory Failure
Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (e.g. asthma, chronic obstructive pulmonary disease [COPD]).
Type III Respiratory Failure
This form of respiratory failure occurs as a result of lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this is also called perioperative respiratory failure. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent lung units. Such atelectasis can be treated by frequent changes in position, chest physiotherapy, upright positioning, and aggressive control of incisional and/or abdominal pain. Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.
Type IV Respiratory Failure
This form occurs due to hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5% of the total cardiac output and O2 delivery. Patients in shock often suffer respiratory distress due to pulmonary edema (e.g. patients in cardiogenic shock), lactic acidosis, and anemia. In this setting, up to 40% of the cardiac output may be distributed to the respiratory muscles. Intubation and mechanical ventilation can allow redistribution of the cardiac output away from the respiratory muscles and back to vital organs while the shock is treated.
Distinctions between Acute and Chronic Respiratory Failure
Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.
The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder.
COPD Assessment Test (CAT) Score
In addition to routine clinical evaluations, a critical step in management is to obtain, from the patients, reliable and valid information on the impact of COPD on their health status. This would include information on daily symptoms, activity limitation and other manifestations of the disease. A standardised patient-centered assessment tool, covering key attributes of COPD health, should facilitate information gathering and improve communication between patient and clinician. In addition to an overall score, an ideal tool should be able to identify specific areas of greater severity to serve as a focal point for targeted management or the evaluation of management goals, thereby improving both the process and the outcome of care.
The Clinical COPD questionnaire (CCQ) was developed in 2003 and contains 10 items with three domains (symptoms, functional and mental state). The CCQ is well validated and has been widely used in research and clinical practice. The CAT was developed later, and was specifically designed to be quick and easy to use. The 8 items of the CAT cover cough, phlegm, chest tightness, breathlessness going up hills/ stairs, activity limitation at home, confidence leaving home, sleep and energy. Good psychometric properties of the CAT have been confirmed in comparison with other measures such as the SGRQ (St George’s Respiratory Questionnaire), the Hospital Anxiety and Depression score, the CCQ (Clinical COPD questionnaire), and different walking tests. The CAT is a reliable measure of overall COPD severity from the patient’s perspective, is independent of tested languages, has an excellent internal consistency, has high agreement between repeated measures in the stable disease phase, and has good discriminative properties between the stable phase and exacerbation, by severity of exacerbation as well as before and after pulmonary rehabilitation.
The CAT will provide clinicians and patients with a simple and reliable measure of overall COPD related health status for the assessment and long-term follow-up of individual patients. It is not a diagnostic tool; its role is to supplement information obtained from lung function measurement and assessment of exacerbation risk. The content and layout of the CAT will allow identification of key areas of health impairment that the clinician can then explore further in the consultation. It has good repeatability and its discriminative properties suggest that it is likely to be sensitive to treatment effects at a group level.
The full questionnaire can be accessed at http://www. catestonline.org/images/pdfs/CATest.pdf (accessed July, 2013). The CAT is made up of 8 items, each scored on a numeric scale of 0 (no impact) to 5 (very severe impact). Each item is weighted equally for the final score, giving a range of CAT scores from 0–40. In general, patients should, therefore, be aiming for a lower score, although exactly what score is achievable will depend on the disease severity of the patient. The optimal state that can be hoped for varies from patient to patient, depending on severity of disease. Therefore, there is no target score representing the best achievable outcome. In general, you and your patient should be aiming for a CAT score lower than or equal to the current one – a change in score of 2 units has been identified by experts involved in developing the test as being clinically relevant.