during a few hours; after a period of quiescence it reappears. Pleural friction persists for a week and over in dry pleurisy of tuberculosis etiology and pleurisy with effusion at the stage of resorption. Pleural friction sounds can be heard in some patients for years after pleurisy because of large cicatrices and roughness of the pleural surfaces.
The point over which pleural friction can be heard depends on the focus of inflammation. Most frequently it is heard in the inferolateral parts of the chest, where the lungs are most mobile during respiration. In rare cases this sound can be heard over the lung apices, when they are affected by tuberculosis with involvement of the pleural membranes.
If the inflammatory focus is localized in the pleura adjacent to the heart, pleuropericardial friction sound may be heard during both inspiration and expiration, and also during cardiac systole and diastole. As distinct from cardiac murmurs, this noise is best heard at the height of a deep inspiration because at that time the pleural surfaces come in closer contact with the pericardium.
Pleural friction sounds can be differentiated from fine bubbling rales and crepitation by the following signs: (1) the character of rales is altered or rales can disappear for a short time after coughing, while pleural friction sound does not change in these conditions; (2) when a stethoscope is pressed tighter against the chest, the pleural friction sound is intensified, while rales do not change; (3) crepitation is only heard at the height of inspiration, while pleural friction sound is heard during both inspiration and expiration; (4) if a patient moves his diaphragm in and out while his mouth and nose are closed, the sound produced by the friction of the pleura due to the movement of the diaphragm can be heard, while rales and crepitation cannot because there is no air movement in the bronchi.
Succusion (Hippocratic) sound. This is the splashing sound heard in the chest of a patient with hydropneumothorax, i.e. when serous fluid and air are accumulated in the pleural cavity. The sound was first described by Hippocrates, hence the name. The sound can be identified by auscultation: the physician presses his ear against the chest of the patient and then shakes the patient suddenly. The splashing sounds are sometimes heard by the patient himself during abrupt movements.
The so-called falling-drop sound (gutta cadens) can be heard by auscultation. It can occur in large cavities of the lungs or at the base of the pleural cavity which contain liquid pus or air as the patient changes his posture from recumbent to upright position or vice versa. Tenacious liquid containing pus sticks to the surface of the cavity and as the patient changes his position it gathers in drops which fall one after another into the liquid (sputum or pus) accumulated at the bottom.
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Bronchophony
This is the voice conduction by the larynx to the chest, as determined by auscultation. But as distinct from vocal fremitus, the words containing sounds “V” or “ch” are whispered during auscultation. In physiological conditions, voice conducted to the outer surface of the chest is hardly audible on either side of the chest in symmetrical points. Exaggerated bronchophony (like exaggerated vocal fremitus) suggests consolidation of the pulmonary tissue (which better conducts sound waves) and also cavities in the lungs which act as resonators to intensify the sounds. Bronchophony is more useful than vocal fremitus in revealing consolidation foci in the lungs of a patient with soft and high voice.
Examination of lung ventilation
The indices of lung ventilation are not constant and depend not only on the pathological conditions of the lungs or bronchi, but also on the patient's constitution, physical fitness, height, weight, sex, and age. The data obtained during examination of the patient are therefore assessed by comparing them with the data that might be expected from a person with the given physical properties. These data are calculated by special nomograms and formulas that have been compiled from basal metabolism indices.
Measuring respiratory capacity
Various indices are used to characterize lung ventilation. The so-called volumes of the lungs are most popular but they are not accurate enough.
1.The respiratory volume (RV) is the volume of air inspired and expired during normal breathing. It is 500 ml on the average varying from 300 to 900 ml. Of this volume, about 150 ml is the physiological dead-space volume of air (PDSV) which is present in the larynx, trachea, and bronchi, but which does not participate in art air to warm and moisten it, which makes residual air physiologically important.
2.The expiratory reserve volume (ERV) (1500-2000 ml). This is the
volume of air which can be expired by maximum effort after completion of a normal expiration.
3.The inspiratory reserve volume (IRV) (1500-2000 ml). This is the volume of air that can be inspired after a normal inspiration.
4.The vital capacity (VC) is found by summation of the IRV and ERV
and the respiratory volume (3700 ml on the average). This is the greatest volume of air that can be expired from the lungs after a maximum inspiration. The vital capacity of the lungs can be calculated by multiplying the tabulated (optimal) volume of basal metabolism by an empirically found factor 2.3. The deviation from the expected (optimum) vital capacity calculated by this method should not exceed ± 15 per cent.
5. The residual air volume (RAV) (1000-1500 ml) is the air that remains in the lungs after maximum expiration.
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6. The total lung capacity (TLC) is the sum of the RV, ERV and IRV, and RAV. It is about 5000-6000 ml.
Respiratory volumes can be used to assess possible compensation of respiratory insufficiency by increasing respiratory depth at the expense of expiration and inhalation and residual volume.
Normal respiratory volume is about 15 per cent of the vital lung capacity; expiratory and inspiratory air volumes are 42-43 per cent (inspiratory air usually slightly exceeds expiratory air volume); residual air is about 33 per cent of the vital capacity of the lungs. The VC slightly decreases in patients with obstructive hypoventilation, while expiratory and residual air volumes increase at the expense of decreased inspiratory air. RAV (especially the RAV: TLC ratio) increases in some cases to 50 per cent of the TLC (in lung emphysema, bronchial asthma, to a lesser degree in aged persons). VC in patients with hypoventilation also decreases because of the decreased IRV, while the RAV changes only insignificantly.
Spirography gives more reliable information on respiratory volumes. A spirograph can be used not only to measure various respiratory volumes but also some additional ventilation characteristics of intensity of lung ventilation such as the respiratory volume, minute volume, maximum ventilation of the lungs, and the volume of forced expiration.
Intensity of lung ventilation
1.The minute volume (MV) is calculated by multiplying the respiratory volume by respiratory rate; it is about 5000 ml on the average. More accurately the MV can be determined by a Douglas bag or using a spirograph.
2.The maximum lung ventilation (MLV) is the amount of air that can
be handled by the lungs by maximum effort of the respiratory system. It is determined by spirometry during deepest breathing at a rate of 50 r/min; normal ventilation is 80-200 1/min. According to Dembo, the predicted value of the maximum ventilation is the vital capacity of the lungs multiplied by 35 (MLV = VC x 35).
3. The respiratory reserve (RR) is determined by the formula RR = MLV - MV. In norm the RR exceeds the MV by at least 15-20 times. In healthy persons the RR is 85 per cent of the MLV, while in patients with respiratory insufficiency it decreases to 60 per cent or lower. This value shows the reserves of a healthy person by which he ensures adequate ventilation under considerable loads, or of a patient with respiratory insufficiency by which he may compensate for significant insufficiency by increasing the minute respiratory volume.
All these tests help study lung ventilation and its reserves, which are important when heavy work is done or there are respiratory diseases.
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Mechanics of the respiratory act
The study of this mechanics is necessary for determining changes in the inspiration to expiration ratio, the respiratory efforts at various respiratory phases, and other indices.
1.The forced expiratory vital capacity (FEVC). According to VotchalTiffeneau this is determined like the vital capacity except that the forced expiration should be performed as fast as possible. The FEVC is 8-11 per cent (100-300 ml) lower than the VC in healthy persons, mainly due to the increased resistance of fine bronchi to the passage of air. When this resistance increases due to bronchitis, bronchospasm, emphysema, etc., the difference may be as great as 1500 ml and more. The volume of forced expiration per minute is also determined. In healthy persons it is more than 75.0 per cent of the VC (average 82.7%).
2.The forced inspiratory vital capacity (FIVC) is determined during
forced inspiration at a maximum speed. It does not change in emphysema non-aggravated by bronchitis but decreases in obstructed patency of the airways.
3. Pneumotachymetry and peakflowmetry are the technique used for measuring peak velocities of air streams in forced inspiration and expiration and is intended to determine the condition of bronchial patency.
Types of disordered lung ventilation
Depending on the cause and mechanism of developing respiratory insufficiency, three types of disordered lung ventilation are distinguished: obstructive, restrictive and mixed (combined).
The obstructive type is characterized by difficult passage of air through the bronchi (because of bronchitis, bronchospasm, contraction or compression of the trachea or large bronchi, e.g. by a tumour, etc.). Spirography shows marked decrease in the MLV and FEVC, the VC being decreased insignificantly. Obstruction of the air passage increases the load on the respiratory muscles. The ability of the respiratory apparatus to perform additional functional load decreases (fast inspiration, and especially expiration, and also rapid breathing become impossible).
Airflow obstruction is usually determined by forced expiratory spirometry - the recording of exhaled volume against time during a maximal expiration. Normally, a full forced expiration takes between 3 and 4 sec, but when airflow is obstructed, it takes up to 15 or even 20 sec and may be limited by breath-holding time. The normal forced expiratory volume in the first second of expiration (FEV1) is easily measured and accurately predicted on the basis of age, sex, and height. The ratio of FEV1 to forced vital capacity (FEV1/FVC, or index of Tiffeneau) normally exceeds 0.75 (75%), in bronchial obstruction FEV1/FVC <0.7 (70%).
The restrictive type of ventilation disorder occurs in limited ability of the lungs to expand and to collapse, i.e. in pneumosclerosis, hydroand
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pneumothorax, massive pleural adhesions, kyphoscoliosis, ossification of the costal cartilages, limited mobility of the ribs, etc. These conditions are in the first instance attended by a limited depth of the maximum possible inspiration. In other words, the vital capacity of the lungs (VC) decreases together with the maximum lung ventilation (MLV), but the dynamics of the respiratory act is not affected: no obstacles to the rate of normal breathing (and whenever necessary, to significant acceleration of respiration) are imposed.
The mixed, or combined type includes the signs of the two previous disorders, often with prevalence of one of them; this type of disorder occurs in long-standing diseases of the lungs and the heart.
Examination of patients with diseases of circulatory system:
Subjective examination. Objective examination of circulatory system: survey and palpation of region of the heart and large vessels. Measuring arterial (blood) pressure
Inquiry
Complaints
Patients with diseases of the heart usually complain of dyspnea, i.e. distressing feeling of air deficit. Dyspnea is a sign of the developing circulatory insufficiency, the degree of dyspnea being a measure of this insufficiency. When questioning the patient, it is therefore necessary to find out the conditions under which dyspnea develops. At the initial stages of heart failure, dyspnea develops only during exercise, such as ascending the stairs or a hill, or during fast walk. Further, it arises at mildly increased physical activity, during talking, after meals, or during normal walk. In advanced heart failure, dyspnea is observed even at rest. Cardiac dyspnea is caused by some factors which stimulate the respiratory centre.
Attacks of asphyxia, which are known as cardiac asthma, should be differentiated from dyspnea. An attack of cardiac asthma usually arises suddenly, at rest, or soon after a physical or emotional stress, sometimes during night sleep. It may develop in the presence of dyspnea. In paroxysmal attacks of cardiac asthma, the patient would usually complain of acute lack of air; respiration becomes stertorous, the sputum is foamy with traces of blood.
Patients often complain of palpitation. They feel accelerated and intensified heart contractions. Palpitation is determined by the increased excitability of the patient's nerve apparatus that controls heart activity. Palpitation is a sign of affection of the heart muscle in cardiac diseases such as myocarditis, myocardial infarction, congenital heart diseases, etc., it may
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