Peculiarities of the physical examination of the patients with pathology of respiratory organs, laboratory tests and instrumental diagnostics of pulmonary disorders

 

 

Management of the patients with pulmonary insufficiency.

 

 

 

The main clinical syndromes in case of respiratoty diseases are:

bronchial obstruction, bronchial spasm, inflammatory syndrom, pulmonary infiltration, diffuse lung injury, pulmonary insufficiency.

Thay will be discussed in certain parts of methodological instructions.

 

PULMONARY FUNCTION TESTS

Pulmonary function testing has progressed from simple spirometry to sophisti­cated physiologic testing over the past decade. This chapter will attempt to survey the major clinically applicable tests available and then will attempt to identify their role in clinical management, including recommendations for ordering tests.

In the normal respiratory system, the volume and pattern of ventilation are initiated by neural output from the respiratory center in the medulla of the brain-stem. This output is influenced by afferent information from several sources, in­cluding higher centers in the brain, carotid chemoreceptors (PaO₂), central chemoreceptors (Paco2 [H⁺]), and neural impulses from moving tendons and joints. Nerve impulses travel via the spinal cord and peripheral nerves to the intercostal and diaphragmatic muscles where appropriate synchronous contrac­tion generates negative intrapleural pressure. If the resulting inspiration is trans­mitted through structurally sound, unobstructed airways to patent, adequately perfused alveoli, then O₂ and CO₂ are respectively added to and removed from mixed venous blood. This feedback mechanism of control of breathing is nor­mally very sensitive, so that alveolar ventilation is kept proportional to the meta­bolic rate and the arterial blood gas tensions are maintained within a very narrow range.

Malfunction of the respiratory system at any point in this pathway can result in deviation from this normal range, and consequent respiratory insufficiency. A disturbance at a given point can often be specifically measured if available tests and known patterns of pathophysiologic disturbances are understood. This chap­ter discusses tests of pulmonary function.

Static Lung Volumes (see Fig. 1)

The vital capacity (VC or “slow VC”) is the maximum volume of air that can be expired slowly and completely after a full inspiratory effort. This simply per­formed test is still one of the most valuable measurements of pulmonary function. It characteristically decreases progressively as restrictive lung disease increases in severity, and, along with the diffusing capacity, can be used to follow the course of a restrictive lung process and its response to therapy.

The forced vital capacity (FVC) is a similar maneuver utilizing a maximal forceful expiration. This is usually performed in concert with determination of expiratory flow-rates in simple spirometry (see Dynamic Lung Volumes and Flow Rates, below).

The (slow) VC can be considerably greater than the FVC in patients with air­ways obstruction. During the forceful expiratory maneuver, terminal airways can close prematurely (i.e., before the true residual volume is reached), and the distal gas is “trapped” and not measured by the spirometer.

Functional residual capacity (FRC) is physiologically the most important lung volume because it incorporates the normal tidal breathing range. It is defined as the volume of air in the lungs at the end of a normal expiration when all the respiratory muscles are relaxed. It is determined by the balance between the elas­tic forces (stiffness) of the chest wall, which tend to increase lung volume, and the elastic forces of the lungs, which tend to reduce it. These forces are normally equal and opposite at about 40% of total lung capacity (TLC). Changes in the elastic properties of the lungs or of the chest wall result in changes in the FRC. The loss of elastic recoil of the lung seen in emphysema results in an increase in the FRC. Conversely, the increased lung stiffness of pulmonary edema, interstitial fibrosis, and other restrictive lung processes results in a decreased FRC. Kyphoscoliosis leads to a decrease in FRC and in the other lung volumes because the stiff, noncompliant chest wall restricts ventilation.

 

table 1. PULMONARY FUNCTION ABBREVIATIONS

 

 

The FRC has 2 components, the residual volume (RV), the volume of air remain­ing in the lungs at the end of a maximal expiration, and the expiratory reserve volume (FRC = RV + ERV).

The RV normally accounts for about 25% of the TLC. It changes with the FRC with 2 exceptions. In restrictive lung diseases, RV tends to remaiearer to nor­mal than other lung volumes (shown in fig. Ib). In small airways diseases, presumably because premature closure of the airways leads to air trapping, the RV may be elevated while the FRC and FEV₁ remaiormal.

TLC equals the VC + the RV. In obstructive airways disease, RV increases more than does TLC, resulting in some decrease in VC, particularly in severe disease.

In obesity the ERV is characteristically diminished because of a markedly de­creased FRC and a relatively well-preserved RV.

fig la. Normal. RV = 25% of  TLC; FRC = 40% of TLC. FEV₁ = > 75% of FVC: FEV3 = > 95% of FVC.

fib. lb. Restrictive disease. Lung volumes are all diminished, the RV less so than the FRC, VC. and TLC. FEV₁ is normal or greater thaormal. Tidal breathing is rapid and shallow.

Fig. lc. Obstructive disuse. RV and FRC are increased. TLC is also increased, but to a lesser degree, so that VC is decreased. There is prolongation of expiration. FEV, = < 75% of VC. Note the “emphysematous notch.”

Fig. 1. Spirograms and lung volumes.

 

Dynamic Lung Volumes and Flow Rates

Dynamic lung volumes reflect the nonelastic properties of the lungs, primarily the status of the airways. The spirogram (see Fig. la) records lung volume against time on a water or electronic spirometer during an FVC maneuver. The FEV₁ is the volume of air forcefully expired during the first second after a full breath and normally comprises > 75% of the VC. The mean maximal expiratory flow over the middle half of the FVC (MMEF_25-75%) is the slope of the line that intersects the spirographic tracing at 25% and 75% of the VC. The MMEF is less effort-dependent than is the FEV₁ and is a more sensitive indicator of early air­ways obstruction.

Airway caliber (and therefore flow) is directly related to lung volume, being greatest at TLC, and decreasing progressively to RV. During a  forced expiratory maneuver, the airways become further narrowed because of positive intrathoracic pressure. This “dynamic compression of the airways” limits maximum expiratory flow rates. The opposite effect is seen during an inspiratory maneuver, wheega­tive intrathoracic pressure tends to maintain the caliber of the airways. The differ­ences in airway diameter during inspiration and expiration thus result in greater flow rates during inspiration than expiration during much of the breathing cycle (see Fig. 2a). In chronic obstructive pulmonary disease (COPD) and asthma, prolongation of expiratory flow rates is further exaggerated because of airway narrowing (asthma), loss of structural integrity of the airways (bronchitis), and loss of lung elastic recoil (emphysema). In fixed obstruction of the trachea or larynx, flow is limited by the diameter of the stenotic segment rather than by dynamic compression, resulting in equal reduction of inspiratory and expiratory flows.

In restrictive lung disorders, the increased tissue elasticity tends to maintain airway diameter during expiration so that, at comparable lung volumes, flow rates are often greater thaormal. (Tests of small airways function, however, may be abnormal—see below.)

Retesting of pulmonary function after inhalation of a bronchodilator aerosol (e.g., isoproterenol) provides information about the reversibility of an obstructive process (i.e., asthmatic component). Improvement in VC and/or FEV₁(L) of > 10% is usually considered a significant response to a bronchodilator.

The maximal voluntary ventilation (MW) is determined by encouraging the pa­tient to breathe at maximal tidal volume and respiratory rate for 12 seconds; the amount of air expired is expressed in L/min. The MW generally parallels the FEV₁ and can be used as a test of internal consistency and as an estimate of patient cooperation (MW = FEV₁[L] X 40). The MW decreases with respira­tory muscle weakness and may be the only demonstrable pulmonary function abnormality in moderately severe neuromuscular disease. The MW is considered an important preoperative test as it reflects the severity of airways obstruction as well as being an index of the patient’s respiratory reserves, muscle strength, and motivation.

Flow-Volume Loop (see Fig. 2). The disadvantage of the simple measurements discussed above is that they fragment the complex dynamic interrelationships of flow, volume, and pressure into simple dimensions for arbitrary measurement. The continuous analysis of these parameters during forced respiratory maneuvers is more physiologic and can be more revealing. An analogy in cardiology is the additional information obtained by vectorcardiography above that provided by the conventional ECG. For the flow-volume loop the patient breathes into an electronic spirometer and performs a forced inspiratory and expiratory VC maneuver while flow and volume are displayed continuously on an oscilloscope. The shape of the loop reflects the status of the lung volumes and of the airways throughout the respiratory cycle and can be diagnostic. Characteristic changes are seen in restrictive and in obstructive disorders. The loop is especially helpful in the assessment of laryngeal and tracheal lesions. It can distinguish between fixed (e.g., tracheal stenosis) and variable (e.g., tracheomalada, vocal cord paralysis) obstruction. Fio. 30-2 illustrates some characteristic flow-volume loop abnormalities.

 

Lung Mechanics

Airway resistance (raw) can, with the help of a body plethysmograph, be directly measured in the laboratory by determining the pressure required to produce a given flow. More commonly, however, it is inferred from dynamic lung volumes and expiratory flow rates more easily obtainable in the clinical laboratory.

Static lung compliance (cstat) is defined as volume-change/unit of pressure-change and reflects lung elasticity or stiffness. This requires the use of an esophageal balloon and is seldom utilized in the clinical laboratory. Lung compliance is inferred by the resultant changes in static lung volumes (see Fig. 3).

Maximal inspiratory and expiratory pressures reflect the strength of the respira­tory muscles. These are measured by having the patient forcibly inspire and ex­pire through a closed mouthpiece attached to a pressure gauge. Maximal pressures are reduced ieuromuscular disorders (e.g., myasthenia gravis, muscu­lar dystrophy, Guillain-Barre syndrome).

Diffusing Capacity (DLco) DLco is defined as the number of ml of CO absorbed/min/mm Hg. It is deter­mined by having the patient inspire maximally a gas containing a known small concentration of CO, hold his breath for 10 seconds, then slowly expire to RV. An  aliquot of alveolar (i.e., end-expired) gas is analyzed for CO and the amount absorbed during that breath is then calculated. It is generally agreed that an abnormally low DLco is not due to physical thickening of the alveolar-capillary membrane alone, but probably reflects abnor­mal ventilation/perfusion (V/Q) in diseased lungs. DLco is low in processes that destroy alveolar-capillary membranes; these include emphysema and interstitial inflammatory fibrotic processes. The DLco also tends to be diminished in severe anemia (less Hb available to bind the inhaled CO) and will be artifactually low­ered if the patient’s Hb already is occupied by CO (e.g., smoking within several hours prior to the test). The DLco increases with increases in pulmonary blood flow as occurs during exercise and also in mild (interstitial) congestive heart fail­ure (increase in blood flow to the usually poorly perfused lung apices).

 

 

 

Fie. 2c. COPD, asthma. Though all flow-rates are diminished, ex­piratory prolongation predominates, and MEF « MIF.

Fig. 2d. Fixed obstruction of upper airway (e.g., trachea! ste­nosis, bilateral vocal cord paralysis, goiter). Top and bottom of loop are flattened so that the configuration approaches that of a rectangle. The fixed obstruction limits flow equally during inspiration and expiration, and MEF = MIF.

 

Fig. 2a. Vocal cord paralysis, unilateral vocal cord pathology results in variable extrathoracic obstruction. The plateau of flow-limita­tion Is seen on inspiration as paralyzed vocal cord is drawn passively inwards. Expiration is normal, and MEF > MIF.

Fig. 2f. Fixed obstruction of one main bronchus. Alveoli from the unob­structed lung empty early, with rapid expiratory flow-rates. Latter half of expiratory limb of loop reflects the second more slowly-emptying populations of alveoli on ob­structed side. This patient had a focal wheeze over left parasternal area, and was found to have a bulky carcinoma partially obstructing left main bronchus.

 

Distribution of Ventilation

The distribution of ventilation is studied by continuously recording the concen­tration of expired N2 at the mouth following a single maximal inspiration of 100% 0₂. If the distribution of ventilation is normal (i.e., the majority of alveoli fill and empty synchronously), there should be a < 2% increase in N concentration be­tween 750 and 1250 ml of expired breath (see fig. 4). A > 2% change implies asynchronous emptying of alveoli, which most commonly is due to airways obstruction. A more direct though more complex study involves lung scanning after the inhalation of radioactive xenon gas.

Peripheral “Small” Airways Studies

raw and FEV measurements reflect primarily the condition of the large air­ways. In the normal lung, bronchi < 2 mm in diameter contribute < 10% of the total airways resistance, yet their aggregate surface area is large. Disease affecting primarily the smaller airways can be very extensive and yet not affect the raw or any tests dependent on this such as the FEV₁. This is true of early obstructive lung disease and probably also of interstitial granulomatous, fibrotic, or inflammatory disorders. The status of the small airways is reflected by the MMEF and by expiratory flows in the last 25 to 50% of the FVC, best determined from the flow-volume loop (see fig. 2a). More complex and sophisticated tests of small airways function have been devised. These include frequency-dependent changes in lung compliance (dynamic compliance), closing volume, and closing capacity. The latter can be determined by a modification of the N washout technic (see Distribution of Ventilation, above, and fig. 3), but in general, measurement of these more complex tests adds little to those more readily available (see above) and has little place in the clinical laboratory.

Control of Breathing

Recent emphasis on the clinical importance of obstructive sleep apnea and central hypoventilation (pickwickian syndrome) has brought the study of the con­trol of breathing to the clinical physiology laboratory.

Hypoxic drive (function of the carotid chemoreceptors) can be studied by plot­ting the ventilatory response to progressive decrements in inspired O₂.

CO₂ sensitivity (function of the central, medullary chemoreceptors) is reflected by the ventilatory response to progressive increments in inspired CO₂.

Expired Volume (L)                                                        

 

fig. 4. Distribution of ventilation, and closing volume. The numbered phases of expiration refer to deadspace gas (I), mixed deadspace and alveolar gas (II), alveolar gas (III), and “airway closure” (IV). Normally, the CV is less than the FRC in both supine and sitting positions and all airways are open during tidal breathing. As the CV increases with progressive disease of the airways, more and more of the dependent airways become closed during part or all of tidal breathing, contributing to hypoxia. The % rise iitrogen (W between 750 and 1250 ml of expired gas is a reflection of the distribution of ventilation (see text).

 

Central and obstructive sleep apnea can be distinguished by monitoring respi­ration during sleep. An ear oximeter monitors Ch saturation. A CO₂ electrode placed in a nostril monitors Pco₂ and also serves as an indicator of air flow. Chest wall motion is monitored by a strain gauge or by impedance electrodes. In ob­structive sleep apnea, air flow at the nose ceases despite continued excursion of the chest wall, 02 saturation drops, and Pco₂ increases. In central apnea, chest wall motion and air flow cease simultaneously.

 

How to Order and Interpret Pulmonary Function Tests

A “complete” set of pulmonary function tests in a good clinical laboratory includes determination of all lung volumes (VC, FRC, RV, TLC), spirometry (FVC, FEV₁, MMEF), diffusing capacity, flow-volume loop, MW, and of maxi­mum inspiratory and expiratory pressures. This extensive testing is tiring, time-consuming, expensive, and ofteot necessary for adequate clinical assessment.

Any physician who evaluates patients with pulmonary disorders should have access to simple spirometry in the office. Simple spirometry is the backbone of pulmonary function evaluation and usually provides sufficient information. A number of inexpensive electronic spirometers are now available capable of mea­suring VC, FEV₁, and PEF. The procedure is readily taught to both patient and operator and yields permanent, reproducible, and accurate data. While spirom­etry alone may not permit specific diagnosis, it can differentiate between obstruc­tive and restrictive disorders and permits estimation of the severity of the process.

With a few simple guidelines, a great deal of useful information can be gathered from the simple spirogram. A low VC in association with normal flow rates ordi­narily suggests restrictive disease (see Fig. Ib). COPD and asthma have the characteristic exponentially decreasing flows seen in fig. 30-Ic. In the patient with predominant emphysema, the airways can be intrinsically normal, and ex­piratory flow is limited by dynamic compression of the airways because of the loss of elastic supporting tissues. A finite amount of time is necessary for the airways (wide open at TLC) to snap shut after the onset of the FVC maneuver. Thus a transient of rapid flow is often reflected by a notch at the beginning of the tracing. The spirogram in Fig.Ic shows such an “emphysematous notch”, and sug­gests that there has been substantial loss of lung elastic recoil; i.e., there is a significant component of emphysema present. In very severe COPD, expiratory flow can be so prolonged as to appear almost linear on visual analysis of the spirographic tracing. Since lung volume is a major determinant of airway caliber, the slope of the spirogram should continuously decrease from TLC to RV. A truly linear decrease in flow from TLC to RV is pathognomonic of fixed obstruction of the larynx or trachea (e.g., tracheal stenosis or tumor). The limitation to maximal flow here is no longer dynamic compression of airways but a fixed area of narrow­ing in the large airway.

The spirogram can occasionally be misleading in asthma because it may mimic restrictive disease if there is severe obstruction predominating in the smaller air­ways. Total occlusion of the airways precludes any air flow and much gas is trapped distally, thus underestimating the VC. The larger airways are patent, so the overall raw is not much increased and the FEV₁ is normal.

 

table 2. CHARACTERISTIC CHANGES IN PULMONARY FUNCTION IN SEVERAL DISORDERS

 

* Distinctive features. fN – normal. # –COPD. $– tracheal stenosis.

 

TABLE 3. CHARACTERISTIC CHANGES IN PULMONARY FUNCTION IN RESTRICTIVE AND OBSTRUCTIVE DISEASE OF VARYING SEVERITY

 

N — normal; R — rest; E — exercise.

 

The severity of COPD and the potential for response to bronchodilator can be adequately assessed by simple spirometry (± flow-volume loop) before and after inhalation of bronchodilator. Simple spirometry with determination of the FVC, FEV₁, and MW usually suffices as a general preoperative screen and should be performed in all smokers > 40 and in all patients with respiratory symptoms prior to chest or abdominal surgery. The response to treatment during an exacerbation of asthma can and should be monitored by portable (bedside) spirometry or by serial measurement of peak expiratory flow rates.

Patients with suspected laryngeal or tracheal pathology are adequately and specifically studied by a flow-volume loop (see Fig. 2d).

If weakness of the respiratory muscles is suspected, the MW, maximal inspiratory and expiratory pressures, and VC are the appropriate tests.

Full tests should be requested when the clinical picture (history, physical ex­amination, chest x-ray) does not coincide with the data obtained by simple spirometry, or when more complete characterization of an abnormal pulmonary process is desired. They are indicated prior to thoracotomy or extensive abdomi­nal surgery (particularly in the patient with known or suspected pulmonary im­pairment) and to document the severity of interstitial pulmonary disorders. Periodic VCs and Dlco₂ usually suffice to follow the course of a restrictive pro­cess.

The following tables are intended as general guides to the interpretation of pulmonary function tests. table 2 illustrates several simple patterns of pul­monary function abnormality. These are not necessarily mutually exclusive; a patient may have a combination of disorders (e.g., restrictive and obstructive disease), which complicates the interpretation. table 3 details the expected changes in pulmonary function in restrictive and obstructive disorders of varying severity.

 

Peakfluorymetry– method of estimation of peak expiratory flow (PEF, L/sec) by portable device usually used by patients to estimate the changes of bronchial obstruction.

CHEST RADIOGRAPHY

Chest radiography is often the initial diagnostic study performed to evaluate patients with respiratory symptoms but it can also provide the initial evidence of disease in patients who are free of symptoms Perhaps the most common example of the latter situation is the finding of one or more nodules or masses when the radiograph is performed for a reason other than evaluation of respiratory symptoms

A number of diagnostic possibilities are often suggested by the radiographic pattern. A localized region of opacification involving the pulmonary parenchyma can be described as a nodule (usually <6 cm in diameter) a mass (usually >= 6 cm in diameter) or an infiltrate Diffuse disease with increased opacihcation is usually characterized as having an alveolar an interstitial or a nodular pattern In contrast increased radiolucency can be localized as seen with a cyst or build or generalized as occurs with emphysema The chest radiograph is also particularly useful for the detection of pleural disease especially if manifested by the presence of air or liquid in the pleural space An abnormal appearance of the hilus and/or the mediastinum can suggest a mass or enlargement of lymph nodes

A summary of representative diagnoses suggested by these common radiographic patterns is presented in Table

Additional Diagnostic Evaluation Further information for clarification of radiographic abnormalities is frequently obtained with computed tomographic scanning of the chest. This technique is more sensitive than plain radiography in detecting subtle abnormalities and can suggest specific diagnoses based on the pattern of abnormality Alteration in the function of the lungs as a result of respiratory system disease is assessed objectively by pulmonary function tests and effects on gas exchange are evaluated by measurement of arterial blood gases or by oximetry.  As part of pulmonary function testing quantitation of forced expiratory flow assesses the presence of obstructive physiology which is consistent with diseases affecting the structure or function of the airways such as asthma and chronic obstructive lung disease Measurement of lung volumes assesses the presence of restrictive disorders seen with diseases of the pulmonary parenchyma or respiratory pump and with space occupying processes within the pleura.

Table: Major Respiratory Diagnoses with Common Chist Radiography Patterns

Solitary circumscribed density nodule (<6 cm) or mass (>= 6 cm)

 Primary or metastatic neoplasm

Localized infection (bacterial abscess mycobacterial or fungal infection)

Wegener’ s granulomatosis (one or several nodules)

Rheumatoid nodule (one or several nodules)

Vascular malformation

 Bronchogenic cyst

 

Localized opacification (infiltrate)

Pneumonia (bacterial, atypical, mycobacterial or fungal infection)

Neoplasm

Radiation pneumonitis

Bronchiolitis obliterans with organizing pneumonia

Bronchocentric granulomatosis

Pulmonary infarction

 

Diffuse interstitial disease

Idiopathic pulmonary fibrosis

 Pulmonary fibrosis with systemic rheumatic disease

 Sarcoidosis

Drug induced lung disease

 Pneumoconiosis

Hypersensitivity pneumonitis Infection (Pneumocystis, viral pneumonia)

Eosinophilic granuloma

 

Diffuse alveolar disease

Cardiogenic pulmonary edema

Acute respiratory distress syndrome

Diffuse alveolar hemorrhage

Infection (Pneumocyitis viral or bacterial pneumonia)

Sarcoidosis

 

Diffuse nodular disease.

 Metastatic neoplasm

Hematogenous spread of infection (bacterial mycobacterial fungal)

Pneumoconiosis

Eosinophilic granuloma

 

Sputum Examination.

Examination of the sputum remains the mainstay of the evaluation of a patient with lung inflammation. Unfortunately expectorated material is frequently contaminated by potentially pathogenic bacteria that colonize the upper respiratory tract (and sometimes the lower respiratory tract) without actually causing disease This contamination reduces the diagnostic specificity of any lower respiratory tract specimen In addition it has been estimated that the usual laboratory processing methods detect the pulmonary pathogen in fewer than 50% of expectorated sputum samples from patients with bacteremic S pneumomae pneumonia This low sensitivity may be due to misidentification of the a hemolytic colonies of S pneumonie as nonpathogenic a hemolytic streptococci ( normal flora ) overgrowth of the cultures by hardier colonizing organisms or loss of more fastidious organisms due to slow transport or improper process ing In addition certain common pulmonary pathogens such as an aerobes mycoplasmas chlamydiae Pneumocystis mycobacteria fungi and legionellae cannot be cultured by routine methods.

Since expectorated material is routinely contaminated by oral an aerobes the diagnosis of anaerobic pulmonary infection is frequently inferred Confirmation of such a diagnosis requires the culture of an aerobes from pulmonary secretions that are uncontammated by oropharyngeal secretions which in turn requires the collection of pulmonary secretions by special techniques such as transtracheal aspiration (TTA) transthoracic lung puncture and protected brush via bronchoscopy These procedures are invasive and are usually not used unless the patient fails to respond to empirical therapy

Gram s staining of sputum specimens screened initially under low power magnification (10X objective and 10X eyepiece) to deter mine the degree of contamination with squamous epithelial cells is of utmost diagnostic importance In patients with the typical pneumonia syndrome who produce purulent sputum the sensitivity and specificity of Gram s staining of sputum minimally contaminated by upper respiratory tract secretions (>25 polymorphonuclear leukocytes and < 10 epithelial cells per low power field) m identifying the pathogen as S pneumomae are 62 and 85% respectively Gram s staining in this case is more specific and probably more sensitive than the accompanying sputum culture The finding of mixed flora on Gram s staining of an uncontammated sputum specimen suggests an anaerobic infection Acid fast staining of sputum should be undertaken when mycobacterial infection is suspected Examination by an experienced pathologist of Glemsa stained expectorated respiratory secretions from patients with AIDS has given satisfactory results in the diagnosis of PCP The sensitivity of sputum examination is enhanced by the use of monoclonal antibodies to Pneumocystis and is diminished by prior prophylactic use of inhaled pentamidine. Blastomycosis can be diagnosed by the examination of wet preparations of sputum. Sputum stained directly with fluorescent antibody can be examined for Legionella but this test yields false negative results relatively often Thus sputum should also be cultured for Legionella on special media

Expectorated sputum usually is easily collected from patients with a vigorous cough but may be scant in patients with an atypical syndrome in the elderly and in persons with altered mental status If the patient is not producing sputum and can cooperate respiratory secretions should be induced with ultrasonic nebulization of 3% saline. An attempt to obtain lower respiratory secretions by passage of a catheter through the nose or mouth rarely achieves the desired results m an alert patient and is discouraged usually the catheter can be found coiled in the oropharynx.

In some cases that do not require the patient s hospitalization an accurate microbial diagnosis may not be crucial and empirical therapy can be started on the basis of clinical and epidemiologic evidence alone This approach may also be appropriate for hospitalized patients who are not severely ill and who are unable to produce an induced sputum specimen Use of invasive procedures to establish a microbial diagnosis carries risks that must be weighed against potential benefits However the decision to initiate empirical therapy without an evaluation of induced sputum should be undertaken with caution and in the case of hospitalized patients should always be accompanied by the culture of several blood samples The ability to understand the cause of a poor response to empirical antimicrobial therapy may be compromised by the lack of initial sputum and blood cultures Establishing a specific microbial etiology in the individual patient is important for it allows institution of specific pathogen directed antimicrobial therapy and reduces the use of broad spectrum combination regimens to cover multiple possible pathogens Use of a single narrow spectrum antimicrobial agent exposes the patient to fewer potential adverse drug reactions and reduces the pressure for selection of antimicrobial resistance Emergence of antimicrobial resistance is a type of adverse drug re action unlike others because it is contagious. In addition establishing a microbial diagnosis can help define local community outbreaks and antimicrobial resistance patterns.

In case of allergic process many eossinophils are found microscopically, frequently arranged in sheets. Eosinophilic granules from disrupted cells may be seen throughout the sputum smear. Elongated dipyramidal crystals (Charcot-Leyden) originaiting from from eosinophils are commonly found.

In case of lung cancer is possible to evaluate the atypical cells.

PLEURAL EFFUSION

Essentials of Diagnosis

•     Dyspnea if effusion is large; may be asymptomatic.

•     Pain of pleurisy often precedes the pleural effu­sion.

•     Decreased breath sounds, flatness to percussion, egophony.

•     The underlying cardiac or pulmonary disease may be the major source of symptoms and signs.

•         X-ray evidence of pleural fluid.

General Considerations

Any fluid collection (transudate or exudate) in the pleural space constitutes a pleural effusion. Numerous disease processes of inflammatory, circulatory, and neoplastic origin can cause pleural effusion. Every effort should be directed toward the diagnosis of the primary disease. “Idiopathic” pleural effusion often proves to be of tuberculous origin.

Clinical Findings

A. Symptoms and Signs: There may be no symptoms. Chest or shoulder pain may be present at onset, especially when fibrinous pleuritis precedes the effusion. Dyspnea may be mild or, with large or rap­ idly forming effusions, severe. Cardiac failure may be associated with effusion. Fever, sweats, cough, and expectoration may occur, depending upon the underly­ing cause.

Physical findings include decreased motion of the chest and decreased to absent vocal fremitus on the side of the fluid, flat percussioote and decreased to absent breath sounds over the fluid, and egophony (e-to-a sound) at the upper level of the fluid. With large effusions, the mediastinum shifts away from the fluid (as shown by displacement of the trachea and the cardiac apex), although underlying atelectasis may result in a shift toward the fluid. Signs resembling those of consolidation (dullness, bronchial breath sounds, bronchophony) are occasionally elicited over the fluid, presumably as a result of compression of the underlying lung by large, rapidly forming effusions.

B.            X-Ray and Sonographic Findings (picture 1-6, figure 3-5) : Three hundred milliliters or more must be present before fluid can be demonstrated by x-ray. Obliteration of the costophrenic angle is the earliest sign. Later, a homogeneous triangular density with a concave medial border extends upward to the axilla; other borders are formed by the lateral chest wall and the diaphragm. The mediastinum shifts away from the fluid (displaced heart and tracheal air shadow). The mobility of the fluid shadow, which ‘ ‘pours” into dependent areas of pleural space when the patient is placed on the involved side, may aid in the demonstration of small effusions. An atypical distribution of fluid along the interlobar fissures or in loculated areas may be noted.

Picture 1 In this patient there is an obvious right upper lung field opacification which on later work-up was determined to be a primary cancer. Note that the right lower lung field is clear and that the right diaphragm and lateral costophrenic angle seem sharp though it would seem peculiar that the right diaphragm should seem so high. Although pleural effusions are usually expected to blunt the costophrenic angle, occasionally a “subpulmonic” effusion may mimic the surface of the diaphragm which is the case here. When the decubitus film is obtained note the substantial amount of fluid that layers out.

 

Picture 2. Sonographic images of normal pleura and chest wall using a 5- to 10-MHz linear scanner

(A) Transverse image through the intercostal space. The chest wall is visualized as multiple layers of echogenicity representing muscles and fascia. The visceral and parietal pleura appear as echogenic bright lines that glide during respiration (gliding sign). Reverberation echo artifacts beneath the pleural lines imply an underlying air-filled lung. (B) Longitudinal image across the ribs. Normal ribs are seen as hyperechoic chambered surfaces (arrowheads) with prominent acoustic shadows beneath the ribs. Pp, parietal pleura; Pv, visceral pleura; L, lung.

Figure 3. Sonographic appearance of pleural effusion

(A) Pleural effusion is presented as an echo-free space between the visceral and parietal pleura. Compressive atelectasis of the lung may be seen in a huge effusion. (B-E) The effusion can be subclassified as anechoic (B), complex nonseptated (C), complex septated (D), and homogenously echogenic (E). Note the movable echogenic spots within the complex nonseptated effusion, and the floating strands and septa within the complex septated effusion (arrowheads). (F) The presence of a consolidation is suggestive of parapneumonic effusion. (G) Pleural effusion associated with pleural nodules or nodular thickenings is characteristic of malignant effusion. PE, pleural effusion; D, diaphragm; RLL, right lower lung; L, lung; T, pleural tumor.

 

Figure 3. Ultrasound (US) images of pleural thickening and pleural tumors

Figure 4. Extension of inflammatory diseases (A, B) or tumors (C, D) to the pleura

(A) Ultrasound (US) shows a chest wall abscess in a patient with liver cirrhosis as an ill-defined lesion with soft-tissue echogenicity that extends to the pleura. Puslike material was obtained with transthoracic aspiration under US guidance, which yielded Aeromonas hydrophila. (B) US shows an irregular and hypoechoic parenchymal lesion with involvement of the pleural cavity. Nocardiosis was proved microbiologically after transthoracic biopsy of the lesion under US guidance. (C) US shows a parenchymal tumor with posterior echo enhancement (PEE). Note that both of the visceral and parietal pleural lines are intact, fulfilling the criteria of ultrasound pattern 1 of Sugama et al.. The respiratory movement of the tumor should be preserved in real-time US. (D) US shows a peripheral mass that extends beyond the pleura. The visceral pleural line is cut off, and the respiratory movement of the tumor is disturbed in real-time US. Invasion of the pleural cavity by the tumor is evident. A, abscess; P, pleura; L, lung; T, tumor; Pv, visceral pleural; Pp, parietal pleura.

Figure 5A. Ultrasound findings in patients with pleuritic chest pain and partial pneumothorax

(A) Ultrasound (US) findings in a patient with pleuritic chest pain. The grayscale US reveals irregularity and interruption of the pleura. (B, C) Sonographic features in a patient with partial pneumothorax. Real-time US of the healthy side of the chest (B) shows normal gliding of the visceral and parietal pleura with respiration. On the other side with partial pneumothorax (C), the gliding sign of the pleura is absent in real-time US. Markedly enhanced comet-tail reverberation artifacts are seen compared with the US image of the healthy side. P, pleura; L, lung; Pv, visceral pleura; Pp, parietal pleura.

 

 

Picture 5B. Lateral X-ray of  chest with pleural effusion A-effusion B- pleural cavity

 

 

Picture 6 Transudative pleural effusions are formed wheormal hydrostatic and oncotic pressures are disrupted. Exudative pleural effusions occur when pleural membranes or vasculature are damaged or disrupted therefore leading to increased capillary permeability or decreased lymphatic drainage.

C. Thoracentesis: This is the definitive diagnos­tic procedure. It demonstrates conclusively the pres­ence of fluid and provides samples for study of physical characteristics, protein content, cells, and infectious agents. Thoracentesis should be done care­ fully to avoid introducing infection and puncturing the visceral pleura.

1.   Removal of fluid for examination-Remove 50-1000 mL. Use a 3-way stopcock to avoid introduction of air. Care must be exercised to avoid contaminat­ing the pleural space.

2. Pleural fluid examination-(Specimen must be fresh.) A specific gravity of more than 1.015 or protein of more than 3 g/dL usually indicates an exuda­tive fluid. More reliable indicators include a ratio of    pleural fluid protein to serum protein greater than 0.5; a fluid LDH to serum LDH ratio of more than 0.6; or a pleural fluid LDH of more than 200IU, especially if all 3 conditions are present.  

A stained smear should be examined for the detec­tion of organisms and the nature of the cellular content. Collect a specimen in an anticoagulant tube for cell count. Cultures on appropriate media are indicated for all fluids from unexplained pleural effusions to dem­onstrate the presence of tubercle bacilli, other bacteria, or fungi. Cy tologic examination of the remaining fluid should be done if a neoplasm is suspected.

Lactic dehydrogenase (LDH) levels are fre­quently increased in effusions due to cancer. Chylous effusions usually signify interruption of the thoracic duct by cancer.

D. Pleural Biopsy: This procedure has become very simple and valuable as a result of the development of better biopsy needles (eg, Abrams’ needle) that permit thoracentesis and removal of one or more tissue specimens with the same needle. Pleural biopsy is indicated whenever the diagnosis is in doubt. If the tissue is not diagnostic, several more specimens should be taken. If pleural fluid examination and needle biopsy do not yield a diagnosis, open pleural biopsy must be considered. A portion of the biopsy material should be cultured.

Treatment

A. Postpneumonic and Other Sterile Effusions: Remove readily obtainable fluid by multiple thoracentesis, at daily intervals if necessary. Removal of more than 1000 mL initially is not advisable. Reexamine subsequent fluid specimens to rule out empyema if the pleuritis does not respond to treatment.

B. Tuberculous Effusion: Uncomplicated pleural effusion due to tuberculosis is treated essen­ tially as minimal pulmonary tuberculosis. A course of isoniazid plus one of the other major antituberculosis drugs is recommended. Many patients with untreated tuberculous effusions develop pulmo­nary tuberculosis later, usually within 5 years.

Removal of all readily available fluid by thoracentesis is advisable to minimize later pleural fibrosis. When high fever persists for longer than 2 weeks, hematogenous dissemination should be sus­pected.

C. Effusions Due to Malignant Tumors: These tend to reaccumulate rapidly and require frequent re­moval. An attempt should be made to control the re-formation of fluid by irradiation of the hemithorax or by the use of intrapleural tetracycline or cytotoxic agents.

Prognosis

The prognosis is that of the underlying disease.

HYDROTHORAX

The term hydrothorax generally denotes the pres­ence of a collection of serous fluid having a specific gravity of less than 1.015 or a protein content of less than 3 g/dL (transudate). The most common cause is congestive heart failure, but lymphatic obstruction and obstruction of the superior vena cava or vena azygos may also cause hydrothorax. The not unusual finding of hydrothorax in hepatic cirrhosis with ascites (6%) is explained by observations of ready transfer of radioiodine-labeled albumin from the peritoneal to the pleural spaces. The initial examination of the pleural fluid should be as described above.

The fluid should be removed by thoracentesis when it causes dyspnea.

The prognosis is that of the underlying disease.

HEMOTHORAX

Hemothorax (pooling of blood in a pleural space) is most commonly due to trauma but may also follow tumor, tuberculosis, and pulmonary infarction. The physical findings are the same as those of pleural effusion. Military experience has shown that early removal of all blood from the pleural space is desira­ble. If this cannot be accomplished by thoracentesis, an intercostal tube with water-seal drainage is indi­cated. If bleeding continues, thoracotomy is indicated. Great care must be taken during aspiration to avoid bacterial contamination of the pleural cavity. Surgical removal of residual blood clots may be necessary.

 

PLEURAL EMPYEMA (Nontuberculous)

Acute infection of the pleural space may result from (1) direct spread from adjacent bacterial pneumonia, (2) postsurgical infection, (3) post-traumatic (including thoracentesis)infection. Underly­ing chronic obstructive pulmonary disease or broncho-genie carcinoma is frequently present. The availability of early and specific therapy for these conditions has made empyema an uncommon disease. However, the mortality rate remains high (50% in some series). The incidence of anaerobic infection appears to be increas­ing. Hospital-acquired infections have a more serious prognosis.

The clinical findings are often obscured by the primary underlying disease. Pleural pain, fever, and ‘ ‘toxicity” after clinical improvement of the primary disease, in association with physical and x-ray signs of pleural fluid, are characteristic. Thoracentesis reveals a frankly purulent exudate from which the causative organism may be cultured. Empyema, like lung ab­scess, may become chronic, with a prolonged course and little tendency to spontaneous resorption (espe­cially in bronchiectasis and tuberculosis).

The key to nonsurgical treatment of acute em­pyema is early diagnosis. Any collection of fluid oc­curring in the course of pulmonary inflammatory disease should be removed at once. If pus is present, a specimen should be obtained for Gram staining and cultures, including cultures for anaerobic organisms. Specimens for anaerobic culture must be collected without exposure to air and must be placed into suit­able transport media immediately. (Coagulase-positive Staphylococcus aureus and gram-negative bacilli are the most common aerobic bacteria causing empyema; Bacteroides and peptostreptococci are the most frequently encountered anaerobic organisms.) The empyema should be aspirated as completely as possible. Some early localized empyemas can be treated by thoracentesis and antibiotic therapy alone. Any large or loculated empyema should be drained immediately via an intercostal tube. Open thoracotomy is sometimes required to ensure adequate drainage.

As soon as specimens have been obtained for culture, parenteral antibiotic treatment should be started with penicillin, 600,000 units intramuscularly every 6 hours, or, alternatively, cephalothin, 8 g intra­venously daily. When the pus has a foul odor or the empyema is thought to be secondary to an intra-abdominal infection, chloramphenicol, 50 mg/kg daily orally, should be added to the initial treatment. The object is to obliterate the empyema space as soon as possible. Irrigations with saline through the catheter may be necessary. Chronic empyema usually results from inadequately treated acute empyema or from a bronchopleural fistula. Surgical drainage with or with­out decortication is usually necessary.

 

PLEURAL PUNCTION

Pleural punctioormally is done under the local anesthesia. For this purposes 0,5 – 1,0 % solution of Novocain infiltration of chest tissues is used. First of all anesthesia of skin is done (so called “lemon cover”). After that, changing the needle on “muscular” one is done the anesthesia of muscles. Pleural punction is performed by third needle connected with syringe by rubber or silicone tube. After the punction of pleural cavity the content of it is aspirated. When the syringe is full for prevention of ear income to pleura the transmitter (rubber or silicone tube) is closed by assistant. The syringe is disconnected. It content transmitted to sterile tube for histological and bacteriological analysis.

After the effusion aspiration from pleural cavity it is necessary to infuse the antimicrobal remedies for prevention of infection complications. After the finish of manipulation the needle is removed and the skin is sterilized by alcohol. After the estimating of effusion amount it transmitted to laboratory study.

 

CLOSED TUBE THORACOTOMY

(Tube Drainage)

Indications: Pneumothorax, spontaneous and traumatic, is the condition most commonly treated with tube drainage. Massive and recurrent pleural effusions unmanageable by needle aspiration also require this treatment; the etiology may be infection, malignancy, chylothorax, etc. Other indications are empyema, hemo­thorax, and hemopneumothorax.

Contraindications: Adhesions which may prevent introduction of the tube, clot­ted hemothorax, and/or empyema with pachypleuritis preclude successful tube drainage and require a thoracotomy.

Procedure: The location is chosen for introduction of the tube. For pneumothorax, the anterior chest wall, 2nd or 3rd intercostal space, midclavicular line is used. For pleural effusion, hemothorax, empyema, etc., the axillary line is pre­ferred in the 5th mid or posterior intercostal space. The skin and the intercostal space are infiltrated with 2% procaine or similar agent, a small incision is made, the intercostal muscles are separated, and the tube is introduced through a trocar or directly with the aid of a clamp. The tube is sutured to the skin and connected to an underwater drainage system. Sometimes drainage is promoted by the use of a pump that can generate up to 20 cm H₂O negative pressure.

Complications: Bleeding from an intercostal vessel injured by the trocar, subcu­taneous emphysema if the side holes of the drainage tube are not properly placed inside the pleural space, infection of the local skin site, and pain are common.

THORACOSCOPY

Indication: To obtain a biopsy from a peripheral lesion of the lung or pleura under direct vision through a mediastinoscope or similar instrument.

Contraindications: Adhesions, central location of the lesions to be biopsied, bleeding tendency, or air leak.

Procedure: Under general anesthesia, the location is chosen in the anterior or lateral chest wall according to the location of the lesion. A small incision is made in the skin and the intercostal muscles. A mediastinoscope or a bronchoscope is introduced to explore the pleura and the lung. A biopsy is taken through the instrument with a forceps. The lung is then reinflated. Usually, a tube for drainage is left after the procedure.

Complications: Most are due to bleeding or air leak from the location of the biopsy. Infection of the pleural space in the course of the procedure is uncommon except when infected lesions are biopsied.

FIBERBRONCHOSCOPY

Direct visual examination of the tracheobronchial tree using a flexible tube (flexi­ble bronchoscope; fiberbronchoscope) containing light-transmitting glass fibers that return a magnified image (picture 7-8). Fiberbronchoscopes range in external diameter from 3 to 6 mm; the proper diameter depends on the size of the patient. The small caliber of the instrument makes it possible to enter segmental bronchi and to visualize subsegmental bronchi. The central channel of the scope is 2 to 2.5 mm in diameter and is used to aspirate secretions, to give anesthetic agents, to obtain brush or forceps biopsies, and to introduce bronchographic contrast material. It is also possible to obtain uncontaminated cultures through the channel. Lavage fluid, such as saline, acetylcysteine, and heparin can be introduced through the channel. Cuffing of the scope makes it possible to lavage a lobe via its lobar bronchus.

Diagnostic indications: It is used to explore the cause of an unexplained persis­tent cough, wheeze, or hemoptysis, or unresolved pneumonia or atelectasis, espe­cially in a male smoker above age 30. The flexible bronchoscope is used for small hemoptysis, i.e., blood-tinged sputum or small quantities of blood; for large he­moptysis, rigid bronchoscopy is used. Fiberoptic bronchoscopy is also used to perform transbronchial lung biopsy and/or bronchial lavage in diffuse lung dis­ease of obscure etiology, to investigate paralysis of the recurrent laryngeal or phrenic nerves, to search for the origin of positive cytology obtained from sputum or endobronchial aspiration or of any other suggestion of lung tumor, to deter­mine the state of the tracheobronchial tree after acute inhalation injury, to deter­mine the anatomy of the endobronchial tree, to visualize a bronchiectatic area, and postoperatively to evaluate the stump of a resected bronchus.

Therapeutic indications: Attempt to open atelectasis; attempt to drain lung ab­scess; assist a weakened patient to raise secretions; performing extensive suction through an endotracheal or tracheostomy tube; removal of certain foreign bodies;

perform lung lavage after aspiration of add or alkaline material especially; and identification of acute laryngeal obstruction to direct treatment. For removal of large amounts of secretions or foreign bodies, a rigid bronchoscope is generally preferred.

Contraindications depend, in part, on the clinical state. A few, such as an intrac­table bleeding disorder or severe cardiopulmonary failure, are usually absolute contraindications. But even in bleeding disorders, temporary correction of the defect by transfusion may sometimes allow enough time for visualization of the airways, although biopsy is avoided. An uncooperative patient can be made trac­table by preoperative medication or general anesthesia. Cardiac arrhythmias, especially bradyarrhythmias, are contraindications unless they can be brought under control by premedication.

Procedure

The patient to be bronchoscoped fasts for at least 8 h before the procedure is done. P-A and lateral chest x-rays should be done within 24 h of the procedure Clotting function should be known to be normal within 24 h of the procedure. Patients with a history of cardiac disease or arrhythmias or > 50 yr of age should be monitored using the ECG.

Premedication consists of atropine average dose 1 mg s.c. and morphine or valium in appropriate dose. Topical anesthesia is accomplished with 2 or 4% lidocaine by first spraying the mouth, throat, and tongue and then through the nose. The patient inhales with each spray and, after one nostril is well sprayed, the other is anesthetized. A nasal Catheter is then placed through the least opeostril to the level of the uvula and O₂  4 to 6 L/min is given throughout the procedure.

Before inserting the fiberbronchoscope, lidocaine jelly is used as a lubricant to protect both the patient’s mucosa and the fiberbronchoscope from abrasion. The scope may be inserted through the nose providing there is no block, and through the mouth providing a simple curved endotracheal tube is used both as guide and protection for the instrument. The fiberbronchoscope is advanced to the epiglottis and anesthesia of the glottis is completed through the bronchoscope. Additional anesthetic is administered through the fiberbronchoscope as sensitive areas are reached by injecting 1 to 2 ml of the agent through the open channel. It is impor­tant to avoid excessive anesthetic agent because of the increasing prospect of untoward reactions as dosage increases.

Insertion of the fiberbronchoscope through endotracheal tubes or tracheostomy tubes that are already in place is quite easy; the main concern is to ensure adequate ventilation of the patient while the procedure is going on. Attachments are available to enable ventilation to proceed during the examination.

The entire procedure can be done under general anesthesia if necessary. Even then topical anesthesia of the glottic structures is advised to minimize the possi­bility of laryngospasm during or after the procedure is completed.

Complications: The main complications include laryngospasm, cardiac arrhyth­mias (cardiac arrest is a particular threat in asthmatic patients), hemorrhage due either to biopsy or to injury of the bronchial mucosa by the bronchoscope, pneumothorax secondary to bronchial biopsy, arterial hypoxemia due either to ob­struction of a major bronchus by the bronchoscope or to spillover in the course of bronchial lavage, allergic reactions either to premedication or to anesthetic agent, urinary retention or respiratory depression due to premedication, bronchospasm due to irritation of the mucosa by the bronchoscope, and infections of the tra-cheobronchial tree and lung introduced during the procedure.

One complication is potentially useful for cytologic or microbiologic studies— the almost invariable mild bronchitis that follows the procedure increases sputum production for a few days.

Since the patient’s swallowing and cough reflexes are depressed for an hour or so, care must be taken to prevent aspiration by abstaining from eating or drinking for a few hours after the procedure.

Picture 7 Bronchoscopy. General view.

 

Picture 8 Bronchoscopy view.

Some  more info about Dronchoscopy you may find here:

http://dpi.radiology.uiow http://dpi.radiology.uiowa.edu/nlm/app/atlas/welcome2.htmla.edu/nlm/app/atlas/welcome2.html

MEDIASTINOSCOPY

Indications: The prime indication is the need to biopsy a tumor of the upper mediastinum or to determine whether lymph node metastases have occurred. In systemic diseases (e.g., Hodgkin’s disease or lymphoma) both primary diagnosis and staging of the process may be achieved by mediastinoscopy and biopsy.

Contraindications: Superior vena cava syndrome, aneurysm of the aortic arch, and primary tuberculosis of the lung with lymph node involvement are the major conditions that militate against performing this operation. If the indication is urgent enough for the procedure to be performed, even these conditions are not absolute contraindications.

Procedure

Under general anesthesia in supine position with the neck extended, a trans­verse incision is made in the suprastemal notch. ^Because of anatomic limitations imposed by the aortic arch and the fascial compartments, the operator has easiest access to structures on the right side, particularly those in the same plane as the trachea and anterior to it. The mediastinoscope is introduced, the dissection is performed in the pretracheal fascia and extended under direct vision to the re­gional lymph nodes, where biopsy is performed. At the close of the procedure, the fascia and skin are sutured without drainage.

Complications are rare. Pneumothorax may occur if the pleura is opened. Local bleeding may be a problem, especially if superior vena caval obstruction exists. Infection is unusual. Arrhythmias may occur if the pericardium and the heart are touched.

MEDIASTINOTOMY

Indications: The same indications apply as for mediastinoscopy. This procedure is used to biopsy areas that cannot be reached by mediastinoscopy, especially the left side of the mediastinum, the subaortic glands, and structures at or below the level of the hili.

Contraindications are the same as for mediastinoscopy (see above).

Procedure

Under general anesthesia, the patient is placed in the supine position. A para-sternal incision is made above the 3rd rib. The cartilage is excised. The approach is extrapleural. If a deeper approach is needed, a mediastinoscope is used. If the pleura is inadvertently entered during the procedure, drainage is established by leaving a catheter in the pleural space at the end of the procedure.

A lung biopsy may be performed through this approach. If indicated, the inci­sion can be extended into a full thoracotomy for better exploration or excision.

Complications: Pneumothorax, bleeding from vessels such as the internal mam­mary arteries, intercostal arteries, etc., and infection occur infrequently.

 

PULMONARY INSUFFICIENCY, (RESPIRATORY FAILURE)

Pulmonary insufficiency or some degree of respiratory failure occurs when the exchange of respiratory gases between the circulating blood and the ambient atmo­sphere is impaired. The terms are used synonymously though the term respiratory failure generally refers to more severe lung dysfunction. The gaseous composition of arterial blood with respect to 0₂ and C0₂ pressures is normally maintained within restricted limits; pulmonary insufficiency occurs when the Pao₂ is < 60 mm Hg and the Paco₂ is > 50 mm Hg, but pulmonary insufficiency or respiratory failure may be manifested by a reduced Pao₂, with a normal, low, or elevated Paco2.

There are 3 pathogenic categories of diseases of the respiratory apparatus: (1) those manifested mainly by airways obstruction; (2) those largely affecting the lung parenchyma but not the bronchi; and (3) those in which the lungs may be anatomically intact but the regulation of ventilation is defective because of abnor­mal musculoskeletal structure and function of the chest wall or primary dysfunc­tion of the CNS respiratory center. The etiology and mechanisms of disease leading to the physiologic disturbances in each of these categories may differ, but the pattern of physiologic disturbance of lung function is quite similar. Lists the most commonly recognized chronic lung disorders in these catego­ries. These and acute disorders (e.g., pulmonary edema, pneumonia, shock lung) which may lead to pulmonary insufficiency.

 

DISORDERS CAUSING CHRONIC PULMONARY INSUFFICIENCY:

PATHOGENIC CLASSIFICATION

1. Airways Obstruction

Chronic bronchitis (figure 1)

Emphysema

Cystic fibrosis (mucoviscidosis) (figure 2)

Asthma

2. Abnormal Pulmonary Interstitium (Pulmonary Alveolitis, Interstitial Fibrosis)

Sarcoidosis

Pneumoconiosis

Progressive systemic sclerosis

Rheumatoid lung

Disseminated carcinoma

Idiopathic fibrosis (Hamman-Rich syndrome)

Drug sensitivity (hydralazine, busulfan, etc.)

Hodgkin’s disease

Systemic lupus erythematosus

Histiocytosis

Radiation

Leukemia (all cell types)

3. Alveolar Hypoventilation Without Primary Bronchopulmonary Disease

Functional: Sleep, chronic exposure to CO₂, metabolic alkalosis Anatomic abnormal respiratory center (Ondine’s curse), abnormal chest cage (kyphoscoliosis, fibrothorax) Disordered neuromuscular function: Myasthenia gravis, infectious potyneuritis, muscular dystrophy, poliomyelitis, polymyositis Obesity. Hypothyroidism.

Figure 1.  X-ray of patient with chronic bronchitis (COPD) and respiratory failure. The signs are characteristic to main disease.

 

Figure 2.  X-ray of patient with cystic fibrosis and respiratory failure. The signs are characteristic to main disease.

 

Pathophysiologic Changes in Airways Obstruction

The diseases in this category induce an abnormally high resistance to airflow in the bronchial tree. The causes vary with the etiology but include secretions, bron­chial mucosal edema, bronchial smooth muscle spasm, or structural weakness of bronchial wall supports. An abnormally high effort, and therefore energy expendi­ture, is required for ventilation to produce the necessary pressure differences be­tween the mouth and alveoli during expiration and inspiration. The high resistance to airflow can profoundly affect the gas exchanging function of the lung in the alveoli by disturbing the distribution of ventilation to various parts of the lung with respect to regional perfusion by mixed venous blood.

The ventilation/perfusion ratio must be close to 1 for Pao2; and Paco₂  to remaiormal (80 to 100 mm Hg for Pao₂; 40 ± 4 mm Hg for Paco₂). Paco2 is below normal if there is high alveolar ventilation for the level of perfusion; high regional perfusion with respect to ventilation reduces 0₂ tension and content of pulmonary capillary blood, a more dire occurrence. The mixing of blood from such over-perfused regions with blood from regions with a normal ventilation/perfusion ratio causes hypoxemia, which is determined quantitatively by the proportion and composition of blood mixing with the normally oxygenated blood. A true shunt of 50% of mixed venous blood (0₂; saturation 75%) mixing with a similar proportion of fully oxygenated blood results in an Sao2 of 87% or a Pao2 of 53 mm Hg. Hypercapnia or a high Paco2 will not occur as long as regions of the lung are over-ventilated with respect to the regional perfusion (a high ventilation/perfusion ratio) so that C02 is expelled from the blood in large volumes and the regional capillary Pco2 is below the normal 40 mm Hg. The net mixed Paco2 remains normal in the presence of persistent hypoxemia. Arterial hypercapnia develops when total ventilation or regional ventilation is depressed so that regional hyperventilation sufficient to maintain the Paco2 at normal cao longer occur. Hyper­capnia may occur with exacerbations of bronchitis, pneumonia, or status asthmaticus, or suppression of total pulmonary ventilation due to pharmacologic depression of the respiratory center by such agents as codeine, morphine, barbitu­rates, or other sedatives.

The characteristic changes in lung volumes and ventilatory tests in intrathoracic airways obstruction are (1) reduced VC, (2) increased RV and FRC so that TLC may be normal or increased, and (3) reduced MW, FEV₁, and airflow rates on expiration at all phases of the forced expiratory volume.

 

Diffuse Interstitial Fibrosis and Alveolitis

The pattern of physiologic abnormality in these diseases is strikingly different from that in airways obstruction. VC is reduced, usually with reduced RV, so that TLC is also reduced. However, tests of airways obstruction (e.g., the FEV₁ and the MW) are usually normal. The Paco2 is usually normal and often below nor­mal because of hyperventilation, and is almost never elevated. The Pao2, however, is mildly to moderately reduced at rest and more markedly reduced during exercise. The hypoxemia is caused by ventilation/perfusion imbalance and diffusion limitation by the structurally abnormal alveolar capillary membrane or by reduc­tion in the total lung area for diffusion. Lung diffusing capacity for CO2 or O2 is characteristically low at rest and during exercise.

Unlike the case in obstuctive lung diseases, the major mechanical abnormality is increased lung stiffness (reduced lung compliance) with normal airway resist­ance. Ventilatory drive is also increased, frequently causing hyperventilation at rest and during exercise, with associated hypocapnia. The reduced lung compli­ance and the increased ventilatory drive and hypoxemia contribute to dyspnea, the outstanding symptom in this group of diseases.

 

Alveolar Hypoventilation Without Primary Bronchopulmonary Disease

Alveolar hypoventilation of this type occurs when pulmonary structure is intact but the regulatory function of ventilation in relation to whole body metabolism is disturbed. The pathognomonic manifestation of this imbalance between ventila­tory and metabolic function is an elevated Paco2 (normal = 40 ± 4 mm Hg) and a concomitantly reduced PaO2 (PaO2 falls as alveolar Pco2 rises). Ventilation/perfu­sion imbalances are usual in addition to alveolar hypoventilation. The alveolar to arterial 02 tension difference is therefore increased, contributing further to arte­rial hypoxemia. Sometimes (e.g., in central depression of the respiratory center), the elevated Paco2 also results from a total alveolar hypoventilation; other times (e.g., in obesity and severe kyphoscoliosis), elevated Paco2 may result from both ventilation/perfusion imbalance and reduced overall alveolar ventilation.

The pathologic basis of alveolar hypoventilation in the presence of normal lung structure (see table ) vanes from weakness or paralysis of the ventilatory muscles (as in myasthenia gravis and infectious polyneuritis) to acquired or con­genital damage to the medullary respiratory center. In most cases except obesity, lung compliance and airway resistance are unimpaired and voluntary hyperventi­lation usually markedly improves blood gas composition.

 

Consequences of Respiratory Failure

Depressed arterial and tissue O2 tensions affect the cellular metabolism of all organs and, if severe, can cause irreversible damage in minutes. In addition, even moderate (< 60 mm Hg) alveolar hypoxia over days or weeks can induce pulmo­nary arteriolar vasoconstriction and increased pulmonary vascular resistance which leads to pulmonary hypertension, right ventricular hypertrophy (cor  pulmonale), and eventually right ventricular failure.

Elevated arterial and tissue CO2 tensions, however, affect mainly the CNS and the acid-base balance. Paco2 elevations, usually > 70 mm Hg, are associated with marked cerebral vasodilation, increased CSF pressure, and changes in sensorium ranging from confusion to narcosis. Papilledema occurs at these levels of hypercapnia when they persist for many days; it is reversed on lowering of the Paco2.

Ventilatory responsiveness to CO2 as a stimulus to breathing is diminished by persistent hypercapnia, largely due to the increase in blood and tissue buffers resulting from the generation of bicarbonate by the kidney in response to the elevated Paco2. The increased buffering capacity which also occurs in the CNS diminishes the decrease in pH which occurs with increases in plasma and tissue C02 levels. The contribution of pH to the ventilatory stimulus of CO2 is therefore diminished. This can be seen in the relationship between pH, bicarbonate concen­tration, and Paco2 in the Henderson-Hasselbalch equation. This effect on ventila­tory responsiveness is reversed when the Paco2 returns to normal.

Sudden rises in Paco2 occur much faster than compensatory rises in extracellu­lar buffer base; this causes marked acidosis (pH < 7.3), which additionally contributes to pulmonary arteriolar vasoconstriction, reduced myocardial contractility, hyperkalemia, hypotension, and cardiac irritability. This type of acidosis is rapidly reversed by increasing alveolar ventilation by mechanical hy­perventilation if necessary and rapidly lowering Paco2 to normal levels.

 

Clinical classification of pulmonary insufficiency

Stage I– the breastlessness occurred in case of usual physical activity that previously didn’t course it (running, going upstears). Hemoglobin saturation by O₂ no less than 80%.

Stage II– the breastlessness occurred in case of low physical activity (walking on plain surface). Hemoglobin saturation by O₂ near about 60– 80%.

Stage III– the breastlessness occurred in rest. Hemoglobin saturation by O₂ less than 60%.

 

Pulse oxymetry

Objective measures of monitoring for hypoxaemia include pulse oximetry. This is a good bedside monitor if its limitations are recognised. It is a continuous and non-invasive monitor. Its principal limitation is that, in patients who are receiving supplemental oxygen, it will not reliably detect hypoventilation. Hypoventilation must, in the clinical environment, usually be confirmed by measurement of the PaCO2 by arterial blood gas analysis.

Infrequently, inadequate oxygenation with normal oxygen saturation may occur in cases with very gross anaemia or in situations where the cells are unable to utilise oxygen such as severe sepsis or cyanide poisoning. Mixed venous oxygen saturation measurements may be helpful in these situations but this is only practical in an intensive care setting with a pulmonary artery catheter in situ. Inaccurate readings may also be obtained in patients who have high carboxyhaemoglobin or methaemoglobin concentrations, high concentrations of endogenous or exogenous pigments such as bilirubin or methylene blue as well as with cold extremities and movement artifact.

In most circumstances, the trend in oxygen saturation is more important than the value per se as this can indicate whether the patient is responding to therapy or deteriorating.

Arterial blood gases

This is the ‘gold standard’ monitor of ventilation. Arterial blood gases are needed to obtain accurate data, in particular, evidence of hypoventilation (raised PaCO2) as a reason for hypoxaemia. Arterial blood gases may also give an indication of the metabolic effects of clinically important hypoxaemia. Formal blood gas analysis may also afford accurate estimates of carboxyhaemoglobin and methaemoglobin, the former being particularly important in patients rescued from fires. However, a blood gas is a painful, invasive and intermittent procedure that is time consuming in the setting of a busy ward.

A spectrum of treatments exist for the hypoxic patient. These range from supplemental oxgyen therapy and simple measures such as altering posture. Even sitting a patient up improves FRC, compared with the patient lying down. Physiotherapy can be useful, but most specifically in those patients with copious airways secretions. If the patient is still hypoxic after these ward-based treatments, measures such as continuous positive airway pressure, non-invasive ventilation or invasive ventilation may be required, usually in the setting of an intensive care unit.

 

Therapy of Respiratory Failure

The detection of respiratory failure from any cause and its therapy depend on analysis of arterial blood Po2, Pco2. and pH; faculties for such analyses are essential for effective therapy.

When the Paco2 is not elevated and only hypoxemia exists, the therapy of respi­ratory failure may be different than when both blood gas abnormalities are pres­ent. All available technics for reducing airways obstruction (i.e., bronchodilators, tracheal suction, moisturization, and chest physiotherapy) may be required in the treatment of respiratory failure. Ultimate recovery demands recognition of every factor leading to respiratory failure and use of therapeutic agents that can reverse these factors while the patient receives respiratory support by mechanical ventila­tion and high O2  mixtures.

Oxygenation: The concentration of enriched O2 selected to overcome hypoxe­mia should be the lowest concentration that will provide an acceptable Pao2. Inspired O2 concentrations exceeding 80% have significant toxic effects on the alveolar capillary endothehum and bronchi and should be avoided unless neces­sary for the patient’s survival. Concentrations of inspired O2 of < 60% are well tolerated for long periods without manifest toxicity. Most patients tolerate a Pao2 > 55 mm Hg quite well. However, Pao2 values in the range of 60 to 80 mm Hg are most desirable for adequate delivery of 0₂ to tissues and prevention of increases in pulmonary artery pressure from alveolar hypoxia. Pao2 values between 55 and 80 mm Hg are acceptable. For pulmonary insufficiency resulting from ventila­tion/perfusion imbalances as associated with obstructive lung disease or with combined diffusion limitation and ventilation/perfusion imbalance, inspired O2 concentrations of > 40% are usually not required. Most patients with these types of physiologic dysfunctions receive adequate oxygenation with 25 to 35% inspired O2. Such concentrations can be given readily by face masks designed to deliver specific concentrations at the mouth, or by nasal cannulas. With face masks, the flow of O2 required for a given percentage is predetermined by the mask design.

With nasal cannulas, the flow of 02 can only be estimated. Such estimates require knowledge of the total minute ventilation of the patient in room air and the duration of inspiration and expiration. If the time m both phases of ventila­tion is equal, only half the flow of 100% 02 from the 02 reservoir can be assumed to be delivered to the patient. Thus, for a ventilatory rate of 10 L/min and a 4 L/min flow of 100% 02 through nasal cannulas, the 02 concentration delivered to the patient would be estimated at

If the minute ventilation rises and the 02 flow is unchanged, the inspired concen­tration of O2 decreases. Because of the uncertainties in such estimates (including the admixture of 02 with room air, mouth breathing, varying respiratory rate), the actual Pao2 tension must be monitored regularly to determine the results of ther­apy.

When higher concentrations of 02 must be delivered at the nose and mouth to achieve acceptable Pao2 levels (e.g., in severe pulmonary infection, shock lung, pulmonary edema), concentrations of O2 delivered by nasal cannulas are inadequate and tight-fitting face masks capable of delivering up to 100% inspired O2 may be necessary.

If adequate oxygenation by face mask requires continuous administration of O2 concentrations of more than 80%, tracheal intubation and mechanical ventilation can usually provide adequate oxygenation with a lower concentration of inspired O2, minimizing the risk of O2 toxicity. This provides larger tidal volumes and a more favorable ventilation/perfusion ratio than does spontaneous breathing.

No matter which technic of O2 delivery is used, the patient’s comfort and bron­chial clearance demand that the inspired gas be moisturized by passing it through a water trap.

Managing elevated PaCO2: In airways obstruction or when the ventilatory appa­ratus or its CNS control fails, elevated blood and tissue Pco2, as well as hypoxemia, must be treated. The urgency and necessity of rapid lowering of an abnormally elevated arterial and tissue Poo2 may be questioned when respiratory acidosis is compensated. Elevated Paco2, whatever the primary cause, indicates low alveolar ventilation with respect to body metabolism. A Paco2 even to levels of 70 or 80 mm Hg is generally well tolerated as long as compensated by an increase in buffer base, which keeps arterial pH near normal; the primary consid­eration must always be adequate oxygenation and the state of acidosis of the blood. If supplying enriched 02 during spontaneous ventilation leads to a continuously rising Paco2 and acidosis, then mechanical ventilatory assistance is required to control the Paco2.

Mechanical ventilation: Ionacutely ill patients with respiratory failure, an IPPB apparatus can be applied by a mouthpiece and nose clip or a face mask for intermittent therapy throughout the day. This technic is not effective if respiratory failure is acute and severe. If continuous mechanical ventilatory assistance is re­quired, the patient should have tracheal intubation through either the mouth or nose. Intubation allows easier suctioning and a wide variety of technics of me­chanical ventilation to be applied as required. After the trachea is intubated, the tube may be left in place for as long as 10 to 14 days if necessary before a tracheostomy must be performed or the patient returns to spontaneous ventila­tion. Short-term tracheal intubation without tracheostomy may be adequate for treating acute episodes of respiratory failure due to pulmonary infection, severe left heart failure, pulmonary edema, inadvertent depression of ventilation by sedatives and analgesic agents, uncontrolled bronchospasm, pneumothorax, or combinations of the above.

Any mechanical ventilator, particularly if the driving pressure into the lung is high, may cause reduced venous return to the thorax, reduced cardiac output, and a consequent drop in systemic BP. This is particularly common when inspiratory positive pressures are high, hypovolemia is present, and vasomotor control is inadequate due to drugs, peripheral neuropathy, or muscle weakness.

There are 3 main types of mechanical ventilators for treating acute respiratory failure: (1) pressure-controlled, (2) volume-controlled, and (3) body-tank-type.

Intermittent positive pressure breathing (IPPB) apparatus: Ventilation is induced with a mechanical ventilator which delivers positive pressure during inspiration but allows the pressure in the airway to return to atmospheric pressure during the expiratory phase by spontaneous exhalation (see above). Various kinds of appara­tus will introduce gas into the lungs by delivering the desired inspired mixture at a higher than atmospheric pressure through a face mask, mouthpiece, or intratracheal tube. All have similar features of control and performance. Ventilatory as­sistance is provided only during inspiration; expiration is passive. A slight inspiratory effort by the patient (about 1 cm H₂0 negative pressure) opens a valve that initiates the flow of gas from the apparatus to the lungs. In most types of apparatus, a sensitivity control knob determines the ease with which inspiratory effort initiates inspiratory flow. Flow ceases when the pressure in the mouth or intratracheal tube reaches a positive pressure that has been preset by the pressure control on the apparatus. When inspiratory flow ceases, expiration occurs pas­sively through an expiratory valve. The tidal volume delivered to the patient de­pends on the preset pressure at which the inspiratory flow ceases. Iormal individuals, peak positive pressures of 15 cm H₂0 usually provide tidal volumes of 800 to 1000 ml. If bronchial obstruction, obesity, stiff lungs, or thoracic deformity is present, positive pressures > 20 cm H20 may be required to achieve normal tidal volumes. Newer devices can achieve inspiratory pressures of up to 60 cm H20. Such pressures may be required under circumstances of severely reduced lung compliance or increased airway resistance.

Moisture in the inspired gas or aerosol medications can be delivered by a nebu­lizer connected to the inspired gas flow.

Inspired gas flow rates of about 40 to 60 L/min are usually adequate, even in tachypndc states in which higher thaormal flows are required. Excessively high flow rates may accentuate uneven distribution of inspired gas, especially in bron­chial obstruction, and may result in high positive pressures in the proximal bron­chi before an adequate tidal volume can be introduced. The inspiratory phase may then be unnecessarily short and the tidal volume inadequate for effective gas exchange.

In pressure-controlled ventilators, breathing frequency may be determined by allowing the patient to initiate the inspiratory effort and determine his own rate, or, wheecessary, an automatic frequency control predetermines a rate and will initiate breathing automatically. The frequency control on most apparatus also allows automatic initiation of a tidal volume in a patient breathing spontaneously if a period of apnea longer than a preset duration occurs.

Volume-controlled ventilators: A preset tidal volume is delivered to the patient regardless of the pressure required to deliver the inspiratory volume. Expiration is passive. Controls vary the inspired 02 mixture, inspiration and expiration time, and ventilatory frequency. Humidification and nebulization are provided. These ventilators are particularly useful for maintaining adequate alveolar ventilation regardless of rapid changes in the airway resistance or pulmonary compliance while the patient is being ventilated. Volume-controlled ventilators are in general selected most commonly for ventilatory support in the setting of intensive care.

Tank-type body ventilators: These can be used when ventilation is to be me­chanically maintained for a prolonged period and when tracheostomy or tracheal intubation is not indicated. Such ventilators were commonly used prior to the availability of the mechanical ventilators discussed above. A new type of thoracic ventilator allows the patient to lie in a flexible plastic garment extending from the neck to the thighs with a rigid support overlying the thorax only, leaving the patient’s arms free.

Positive end-expiratory pressure (PEEP): This term refers to ventilation in which a positive pressure is imposed in the airway at the end of expiration. Thus with PEEP, inspiration proceeds by imposing a positive pressure in the airway. After peak pressure and tidal volume are reached, expiration proceeds unobstructed. However, exhalation ceases at a preset expiration pressure that is set by an exha­lation valve sensitive to pressure and placed in the exhalation part of the ventila­tor or tracheal tube. If a Pao2 of 50 to 70 mm Hg cannot be achieved with 60% inspired 02 using positive pressure ventilatory assistance, a continuous PEEP of 3 to 15 cm H20 may be tried to induce further expansion of the lung, improve the ventilation/perfusion ratio, and reduce shunting. Since the procedure is not innocuous and complications are directly related to the magnitude of the endexpiratory pressure, the lowest level of PEEP that achieves an adequate Pao2 should be applied. The major complications of PEEP are decreased venous return, reduced cardiac output, and pneumothorax. Application of PEEP to a severely ill patient is best done by an individual experienced with this technic.

Continuous positive airway pressure (CPAP): In this technic, during spontane­ous breathing, a positive pressure is applied during the entire respiratory cycle (during inspiration and expiration). In this regard, exhalation bears some rela­tionship to pursed-Up breathing. The technic may be applied by a head canopy that controls the ambient airway pressure with or without intubation. When the patient has an intratracheal tube, CPAP can be applied by a specially modified T piece in which a reservoir bag is placed in the expiratory line and the expiratory pressure is controlled by varying the degree of occlusion of the tailpiece of the bag. The term continuous positive pressure breathing (CPPB) is synonymous with CPAP and the term continuous positive pressure ventilation (CPPV) has been used instead of CPPB when ventilation is controlled by a mechanical ventilator rather than spontaneously (picture 1).

 

 

 

 

 

 

 

Picture 1. Continuous Positive Airway Pressure (CPAP) devices maintain open airways in patients who have been diagnosed with Obstructive Sleep Apnea (OSA). This device provides airflow at pressures prescribed by a patient’s doctor during sleep. MedNow carries many different brands of CPAP machines and masks for machines and masks for your individual needs. A Staff Respiratory Therapist will work with you to determine the best CPAP machine and masks for your needs and will be available for any questions or concerns after your initial set-up.

 

Aerosols: When bronchospasm or bronchial edema is a factor, airway resist­ance can be reduced and ventilation/perfusion relationships improved by admin­istering aerosolized bronchodilators. Such solutions may be given by a positive pressure breathing apparatus or by hand or mechanical nebulizers (picture 2).

 

 

 

 

 

 

 

 

Picture 2. The nebulizer is designed for inhalation therapy and treatment of asthma, bronchitis, emphysema and upper respiratory tract disorders. A mouthpiece for adults and children or a mask for infants accompanies the machine

 

Maintenance of clear airways: Clearing of secretions from upper and lower air­ways is crucial to treating respiratory failure. Since alveolar gas is 100% humidi­fied at body temperature, room air or inspired gas delivered from a tank tends to dry out mucous membranes and add to the difficulty of raising secretions. The inspired stream delivered through a positive pressure breathing apparatus must be fully moisturized to ensure reduced viscosity of secretions. This can sometimes be achieved by heated nebulization, which highly moisturizes the inspiratory stream.

Physical therapy technics such as chest percussion several times/day in severely ill patients loosen secretions, allowing their removal by tracheal suction or spon­taneous cough.

Tracheal suction should be performed frequently through the mouth, nose, or tracheal tubes using sterile catheters and following other such precautions to minimize infection. In general, tracheal and lower airways suction without an intratracheal tube or tracheostomy by insertion of the suctioning catheter into the posterior pharynx is usually unsuccessful because of the difficulty of introducing the catheter past the vocal cords. Inadequate removal of secretions is an indica­tion for tracheal intubation, which allows easy access to the upper and lower airways and minimizes the risk of aspiration of stomach contents.

 

SOME DEVICES THAT ARE USEFUL IN PATIENTS

WITH CHRONIC RESPIRATORY FAILURE

Long Term Oxygen Therapy (picture 3) relates to the provision of oxygen therapy for continuous use at home for patients with chronic hypoxaemia (PaO2 at or below 7.3kPa (55mg). The oxygen flow rate must be sufficient to raise the waking oxygen tension above 8 KPa, (60mmHg).

Clincians usually prescribe LTOT where this is needed for at least 15 hours per day. For children this may cover 24 hours per day, but often apply to sleeping periods only.

Ambulatory oxygen may also be indicated in patients on LTOT to facilitate their mobility and quality of life.

Vitalair’s dedicated oxygen concentrator service is there to help and support patients undergoing Long Term Oxygen Therapy. Having a ready supply of oxygen at home will help improve patients’ quality of life, allowing them to enjoy the benefits of living at home.

Vitalair has invested in new concentrator technologies capable of delivering up to 5 litres per minute of therapeutic oxygen in the home. Each unit is known for its high performance, easy maintenance, and unmatched reliability.

Vitalair  (picture 4) has also developed a longer-lasting high capacity cylinder, which can provide up to 20 hours of back-up oxygen supply. The size makes it easier to handle and to store, while the capacity means fewer changeovers are needed when administering oxygen. The permanently live contents gauge allows patients to see how much gas is left in the cylinder at all times.

Since patients only use back-up cylinders very occasionally, we cannot predict when a cylinder replacement is needed.

Picture 3. Patient on Long Term Oxygen Therapy

 

 

Picture 4. The internal auto-recharge power cartridge enables easy movement between AC power outlets without interruption of oxygen therapy and can keep the oxygen flowing for up to 5.1 hours. Long lengths of tangled oxygen tubing are no longer needed to move about the house. The Eclipse means extended travel without the fear of running out of oxygen. Just plug the Eclipse into your auto accessory (lighter) outlet and go as far and as long as you like. 

 

Some devices useful in continuous oxygenating are presented in the table below and picture 5.

 

A Oxygen Concentrator Now you can have the freedom to travel with ease or relax at home in comfort with a portable, reliable and quiet oxygen concentrator. B Devilbiss Pulse Dose Oxygen Conserving Device Pulse dose oxygen conserving technology is on the leading edge of oxygen therapy. Unlike other oxygen regulators that simply limit the flow of oxygen, the Devilbiss Pulse Dose delivers a consistent dose of oxygen at the very moment it is most beneficial. C Portable Compressed Oxygen System Using light weight aluminum cylinders, portable compressed oxygen systems can meet the needs of ambulatory patients or for short trips in the outdoors. D Invacare HomeFill Oxygen System The HomeFill oxygen system allows patients to fill there own high pressure cylinders from a concentrator. The HomeFill is a multi-stage pump that simply and safely compresses oxygen from a specially equipped concentrator into oxygen cylinders.
A Devilbiss 9000D CPAP The quietest CPAP available. Convenient touch keypad control. Operating pressure range. 0, 10, 20, 30 or 45 minute pressure delay options. Push button altitude compensation. Monitors compliance while breathing. Includes travel bag for transporting. B HC220 Fisher & Paykel The HC220 humidified CPAP system offers an adjustable range of warm to heated humidification. Heated humidification with CPAP provides more effective treatment, so you too can have the lifestyle only a good night’s sleep can bring. C Remstar® Plus CPAP System Full featured unit. All-new icon based display. Integrated humidification controls. Easy set-up. Unique new session meter records number of sessions that last more than 4 hours.

 

 

 

 

 

 

Picture  5 Liquid oxygen is another type of oxygen therapy alternative. It consists of a stationary unit that is filled with oxygen that is cooled to below zero then is given to the patient in a comfortable gas form. Liquid oxygen has portable units as well that can be filled from the stationary unit a the patient in a comfortable gas form. Liquid oxygen has portable units as well that can be filled from the stationary unit and carried over the shoulder or strapped to a belt. nd carried

CPAP Moisture Therapy

Apply CPAP Moisture Therapy to facial area where mask meets the skin and inside the the nasal passage before beginning therapy (picture 6).

Repeat this process as often as needed to maintain soft skin and eliminate discomfort from dry/cracking skin.

Technology using CPAP therapy to assist those who have been diagnosed with sleep apnea problems may often result in skin irritation and discomfort in the nasal area. For this reason, CPAP Moisture Therapy may be useful to reduce this trauma.

CPAP Moisture Therapy is offered as a preventative to the skin irritation that may accompany this therapy for sleep apnea and may promote a greater compliance to treatment.

 

 

 

 

 

 

Picture 6. CPAP Moisture Therapy gel

DRY NOSE

The problem with dry nose associated with oxygen delivery by means of plastic cannula has been well documented by care givers at every level for decades.

Nasal dryness as well as other skin dryness can occur apart from the use of oxygen or continuous positive airway pressure (CPAP) devices due to dry climates as well as changing seasons. It may be useful in addressing these issues (picture 7).

 

Picture 7. This is a Non-Petroleum-Based Skin Care Emollient with Aloe Vera, Emu Oil, Vit. A & E to prevent the skin lesions in oxygen therapy.

Oxygen users
Apply RoEzIt Dermal Care before beginning oxygen therapy and at intervals as needed during treatment to lubricate nasal passages, as well as over the ear where friction from tubing may cause discomfort.

Main forms of respiratory insufficiency (according to B. E. Votchal).

1.     Central form – is the result of inhibition of respiratory center (narcosis, drugs, trauma, atherosclerosis, stroke etc.).

2.     Neuro–muscular form – is the result of disturbance of  conduction of signals from central nervous system to muscules (miastenia, poliemielitis etc.).

3.     Thoraco-diafragmal form – is the result of reduction of chest movements (chest degormation, kifoscoliosis etc.).

4.     Pulmonary form – is the result of pulmonary problems:

a)     decrease of pulmonary tissue (pneumonia, tumor);

b)    decrease of pulmonary tissue elasticity (fibrosis);

c)     narrowing of bronchial system (asthma, stenosis).

 

Clinical and instrumental characteristics of main types of ventilation insufficiency: obstructive, restrictive and mixed.

1.     Obstructive type is caused by:

a)     spasm; b) mucous odema; c) hypersecretion; d) scar narrowing;  e) endobronchial tumor; f) external pressuring of bronchus.

Diagnostic crireria: dyspnoe after physical execiesing, dry cough, dry rales. Increasing of expiration period, on spirography– decrease of FEV₁.

2.     Restrictive  type is caused by:

a) fibrosis; b) pleural disorders; c) pleural exudation; d) pneumoconiosis; e) tumors of lungs; f) pulmonectomia.

Diagnostic crireria: on spirography– decrease of VC.

3.     Mixed type: both causes are aviable.

 

 

HYPERBARIC OXYGEN THERAPY      

We can better understand the concepts behind hyperbaric oxygen (HBO) therapy by first gaining an understanding of some basic terms:

Hyperbaric Oxygen Therapy   
Hyperbaric oxygen therapy describes a person breathing 100 percent oxygen at a pressure greater than sea level for a prescribed amount of time—usually 60 to 90 minutes.        

Atmospheric Pressure      
The air we breathe is made up of 21 percent oxygen, 78 percent nitrogen and 1 percent carbon dioxide and all other gases. The air exerts pressure because air has weight and this weight is pulled toward the earth’s center of gravity. This pressure is expressed as atmospheric pressure. Atmospheric pressure at sea level is 14.7 pounds per square inch (psi).     

Hydrostatic Pressure       
As we climb above sea level the atmospheric pressure decreases because the amount of air above us weighs less. When we dive below sea level the opposite occurs (the pressure increases) because water has weight that is greater than air. Thus, the deeper one descends under water the greater the pressure. This pressure is called hydrostatic pressure.       

Atmospheres Absolute (ATA)  
The combination (or the sum) of the atmospheric pressure and the hydrostatic pressure is called atmospheres absolute (ATA). In other words, the ATA or atmospheres absolute is the total weight of the water and air above us.       

Terms Used to Measure Pressure       
We use various terms to measure pressure. HBO therapy involves the use of pressure greater than that found at the earth’s surface at sea level. This is called hyperbaric pressure. The terms or units used to express hyperbaric pressure include millimeters or inches of mercury (mmHg, inHg), pounds per square inch (psi), feet or meters of sea water (fsw, msw), and atmospheres absolute (ATA).     

One atmosphere absolute, or 1-ATA, is the average atmospheric pressure exerted at sea level, or 14.7 psi. Two-atmosphere absolute, or 2-ATA, is twice the atmospheric pressure exerted at sea level. If a physician prescribes one hour of HBO treatment at 2-ATA, the patient breathes 100 percent oxygen for one hour while at two times the atmospheric pressure at sea level. The devices for HBO are presented on pictures 8-9.

 

Picture 8. Hyperbaric oxygen therapy device

 

 

Picture 9. Hyperbaric oxygen therapy device in action

 

While some of the mechanisms of action of HBO, as they apply to healing and reversal of symptoms, are yet to be discovered, it is known that HBO:

1) greatly increases oxygen concentration in all body tissues, even with reduced or blocked blood flow;

2) stimulates the growth of new blood vessels to locations with reduced circulation, improving blood flow to areas with arterial blockage;

3) causes a rebound arterial dilation after HBOT, resulting in an increased blood vessel diameter greater than when therapy began, improving blood flow to compromised organs;

4) stimulates an adaptive increase in superoxide dismutase (SOD), one of the body’s principal, internally produced antioxidants and free radical scavengers; and,

5) aids the treatment of infection by enhancing white blood cell action and potentiating germ-killing antibiotics.

While not new, HBO has only lately begun to gain recognition for treatment of chronic degenerative health problems related to atherosclerosis, stroke, peripheral vascular disease, diabetic ulcers, wound healing, cerebral palsy, brain injury, multiple sclerosis, macular degeneration, and many other disorders Wherever blood flow and oxygen delivery to vital organs is reduced, function and healing can potentially be aided with HBO. When the brain is injured by stroke, CP, or trauma, HBO may wake up stunned parts of the brain to restore function.