ACUTE MEDICAL EMERGENCIES - PART 2 potx

SUMMARY Airway control and ventilation are essential prerequisites for successful resuscitation. Airway obstruction should be recognised and managed immediately. Endotracheal intu- bation remains the best method of securing and controlling the airway, but requires addi- tional equipment, skill and practice. The ultimate aim is to ventilate the patient with greater than 95% oxygen. Occasionally, when all other methods of ventilation have failed, a surgical airway may be required as a life saving procedure. TIME OUT 4.1 Take a break and list the clinical features of airway obstruction. Key point Suction must not be applied directly to the tracheal tube or surgical airway, as this will result in life threatening hypoxia and dysrhythmias AIRWAY ASSESSMENT 37 04-AcuteMed-4-cpp 28/9/2000 3:33 pm Page 37 This Page Intentionally Left Blank CHAPTER 5 Breathing assessment OBJECTIVES After reading this chapter you will be able to: ● understand the physiology of oxygen delivery ● describe a structured approach to breathing assessment ● identify immediately life threatening causes of breathlessness ● describe the immediate management of these patients. INTRODUCTION The acutely breathless patient is a common medical emergency that is distressing for both the patient and the clinician. Often the effort required for breathing makes it virtu- ally impossible for the patient to provide any form of medical history and questioning may only make the situation worse. Information should be sought from any available source. The clinician’s skills will help to determine the underlying cause and dictate appropriate management. Immediately life threatening causes of breathlessness Airway ● Obstruction Breathing ● Acute severe asthma ● Acute exacerbation of chronic obstructive pulmonary disease (COPD) ● Pulmonary oedema ● Tension pneumothorax Key point Breathlessness can result from a problem in breathing (B), circulation (C), and disability (D) 39 Reading: 45 minutes 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 39 Disruption of oxygen delivery is a fundamental process in these conditions.Therefore it is important to understand the mechanisms that maintain their integrity in health. PRIMARY ASSESSMENT AND RESUSCITATION Relevant physiology Oxygen delivery The normal respiratory rate is 14–20 breaths per minute.With each breath 500 ml of air (6–10 litres per minute) are inhaled and exhaled.This air mixes with alveolar gas and, by diffusion, oxygen enters the pulmonary circulation to combine mainly with haemoglobin in the red cells.The erythrocyte bound oxygen is transported via the systemic circulation to the tissues where it is taken up and used by the cells. Consequently the delivery of oxygen (DO 2 ) to the tissues depends on: ● concentration of oxygen reaching the alveoli ● pulmonary perfusion ● adequacy of pulmonary gas exchange ● capacity of blood to carry oxygen ● blood flow to the tissues. Concentration of oxygen reaching the alveoli The two most important factors determining the amount of oxygen reaching the alveoli are: ● the fraction of inspired oxygen (FiO 2 ) ● ventilation. Providing supplementary oxygen to a person increases the number of oxygen mole- cules getting to the alveoli. Consequently common medical practice in dealing with ill patients is to use various types of oxygen masks so that the fraction of inspired oxygen is increased. However, the effectiveness of this procedure depends on the lungs’ ability to draw the inspired gas into the alveoli.The mechanism for transporting inspired air to, and expired gas from, the alveoli is called ventilation (V). As ventilation is essential for life it is sub- ject to several regulatory processes which are summarised in the box. The normal ventilatory volumes and rates are summarised in Figures 5.1 and 5.2. The normal resting respiratory rate is 15 (range 14–20) breaths per minute. The amount of air inspired per breath is called the tidal volume and is equivalent to Key components in regulating ventilation Brain stem medullary respiratory centre Receptors pulmonary stretch chemoreceptors for CO 2 , O 2 , H + Vagus and phrenic nerves increased ventilation Respiratory muscles chest wall and diaphragm Mechanics air passages compliant lungs and chest wall ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 40 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 40 7–8 ml/kg body weight (or 500 ml for the 70 kg patient). Therefore the amount of air inspired each minute, the minute volume, can be calculated by multiplying the respi- ratory rate by the tidal volume (15 × 500 ml) to produce a value of 7·5 l/min. The tidal volume (500 ml) is distributed throughout the respiratory system but only 350 ml (70%) mixes with alveolar air. The remainder (150 ml) occupies the airways that are not involved in gas transfer. This volume is referred to as the anatomical dead space . In addition, there are certain areas within the lungs which are also not involved with gas transfer because they are ventilated but not perfused. The volume produced by the combination of these areas and the anatomical dead space is called the total or physiological dead space . In healthy individuals these two dead spaces are virtually identical because ventilation and perfusion are well matched. BREATHING ASSESSMENT 41 Figure 5.1 Normal ventilatory volumes as measured by spirometry Tidal volume 500 ml Minute volume 7.5 I/min Alveolar ventilation 5250 ml/min V/Q = 0 Pulmonary blood flow Anatomical dead space 150 ml Rate / breaths 15/min Alveolar gas 3000 ml Pulmonary capillary blood 70 ml 5500 ml/min Volumes Flows Figure 5.2 Normal volumes and flows 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 41 It follows that the amount of air reaching the alveoli, i.e. the alveolar ventilation, can be calculated from: respiratory rate × (tidal volume – anatomical dead space) Using data from Figure 5.2, this corresponds to 15 × (500 – 150) = 5250 ml/min. However rapid shallow respiration causes a marked reduction in alveolar ventilation because the anatomical dead space is fixed i.e. 30 × (200 – 150) = 1500. This is demon- strated further in Table 5.1 where the effect of different respiratory rates can be seen. Table 5.1 The effect of respiratory rate on alveolar ventilation Finally it is important to be aware of a crucial volume known as the functional resid- ual capacity (FRC) (2·5–3·0 l). This is the amount of air remaining in the lungs at the end of a normal expiration. As 350 ml of each tidal volume is available for gas transfer, fresh alveolar air will only replace 12–14% of the functional residual capacity. The FRC therefore acts as a large reservoir, preventing sudden changes in blood oxygen and car- bon dioxide concentration. Pulmonary perfusion At rest the cardiac output from the right ventricle is delivered to the pulmonary circulation at approximately 5·5 l/min. As alveolar ventilation is 5·25 l/min, the ventilation:pulmonary perfusion ratio is equal to 0·95 (5·25/5·5). The pressures in the pulmonary vascular bed are low (around 20/9 mm Hg) and there- fore affected by posture. As a result there are differences in blood flow to different lung regions, contributing to the physiological dead space. In the upright position, basal alveoli are well perfused but poorly ventilated. Consequently, in these areas, venous blood comes into contact with alveoli filled with low concentrations of oxygen and so less oxygen can be taken up. This effect is minimised in healthy individuals by pulmonary vasoconstriction which diverts blood to areas of the lungs that have better ventilation. There are also direct links between the right and left side of the heart. These normally allow 2% of the right ventricle’s output to bypass the lungs completely and are collec- tively known as the physiological shunt. As the blood in this shunt has had no contact with the alveoli, its oxygen and carbon dioxide concentrations will remain the same as those found in the right ventricle. Pulmonary gas exchange Oxygen continuously diffuses out of the alveolar gas into the pulmonary capillaries with carbon dioxide going in the opposite direction. The rate of diffusion is governed by the following factors: ● partial pressure gradient of the gas ● solubility of the gas ● alveolar surface area ● alveolar capillary wall thickness. Respiratory rate (/min) 10 20 30 Tidal volume (ml) 600 400 200 Anatomical dead space (ml) 150 150 150 Alveolar ventilation (ml/min) 4500 5000 1500 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 42 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 42 The lungs are ideally suited for diffusion as they have both a large alveolar surface area (approximately 50 m 2 ) and a thin alveolar capillary wall. It is also easy to understand why gas exchange would be compromised by a reduction in the former (e.g. pneumothorax) or an increase in the latter (e.g. interstitial pulmonary oedema). Gases move passively down gradients from areas of high to low partial pressure. The partial pressure of oxygen in the alveoli ( PAO 2 ) is approximately (13·4kPa),100mmHg whereas that in the pulmonary artery is (5·3 kPa) 40 mm Hg. In contrast the gradient for carbon dioxide is only small, with the alveolar partial pressure being (5·3 kPa) 40 mm Hg compared with (6·0 kPa) 46 mm Hg in the pulmonary artery. However, carbon dioxide passes through biological membranes 20 times more easily than oxygen.The net effect is that, in health, the time taken for exchange of oxygen and carbon dioxide is virtually identical. Although alveolar ventilation, diffusion and pulmonary perfusion will all affect the alveolar PO 2 (PAO 2 ) and hence the arterial PO 2 (PaO 2 ), the most important factor in determining the PaO 2 is the ratio of ventilation to perfusion. Ventilation:perfusion ratio To understand this concept it is helpful to divide each lung into three functional areas: apical, middle, and basal (Figure 5.3). Remember that the overall ratio of ventilation to perfusion is nearly one (0·95). Figure 5.3 Three different ventilation (V) perfusion (Q) ratios (a) normal ventilation with reduced perfu- sion; (b) normal ventilation with normal perfusion; (c) reduced ventilation with normal perfusion The apical segment is well ventilated, but unfortunately poorly perfused. Therefore, not enough blood is available to accept all the alveolar oxygen, however, the red cells that are available are fully laden (saturated) with oxygen. Thus, the unused oxygen is simply dissolved in the plasma. V/Q < normal High CO 2 content High CO 2 content Low O 2 content Low O 2 content V/Q = normal High CO 2 content High O 2 content Low O 2 content Low CO 2 content V/Q > normal High CO 2 content Low O 2 content Slightly > normal O 2 content Very low CO 2 content BREATHING ASSESSMENT 43 (a) (c) (b) 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 43 The middle segment has ventilation and perfusion perfectly matched. Alveolar oxygen diffuses into, and is correctly balanced by, the pulmonary capillary blood ensuring that the red cells are fully saturated. The remaining small amount of oxygen is dissolved in plasma. The basal segment alveoli are well perfused, but poorly ventilated. All the available oxygen is bound to red cells but they are not fully saturated, i.e. there is spare oxygen car- rying capacity.This is similar to the physiological shunt as described earlier. The oxygen content of blood at point X (Figure 5.4) depends on the mixture of blood coming from all three parts of the lung. The final value is not simply the mid point between a and c. This is because the small amount of additional oxygen dissolved in the plasma cannot offset the massive decrease in oxygen content produced by the incom- pletely saturated haemoglobin molecules in part c.Therefore the oxygen content is much lower than half way between the values of a and c. Figure 5.4 Mixed blood returning from three sites at point X V/Q = normal (from (b)) V/Q > normal (from (a)) Low CO 2 content Slightly increased O 2 content V/Q < normal (from (c)) High CO 2 content Very low O 2 content Normal CO 2 content Low O 2 content X Key point An area of lung with a high V:Q ratio cannot offset the fall in oxygen content produced by an area of lung with a low V:Q ratio Tip In the basal segment ventilation is reduced when compared to perfusion, i.e., the V:Q ratio < 1 Tip In the middle segment ventilation and perfusion are matched, i.e., the V:Q ratio = 1 Tip In the apical segment there is more ventilation than perfusion, i.e., the V:Q ratio > 1 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 44 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 44 Oxygen content of arterial blood The oxygen content of haemoglobin (Hb) going to tissues depends on the: ● saturation of haemoglobin with oxygen ● haemoglobin concentration ● oxygen carrying capacity ● oxygen dissolved in plasma. Haemoglobin is a protein comprising four subunits, each of which contains a haem molecule attached to a polypeptide chain. The haem molecule contains iron which reversibly binds oxygen; hence it is oxygenated but not oxidised. Each haemoglobin molecule can carry up to four oxygen molecules. Blood has a haemoglobin concentration of approximately 15 g/100 ml, and normally each gram of haemoglobin can carry 1·34 ml of oxygen if it is fully saturated. Therefore the oxygen carrying capacity of blood is: Hb × 1·34 × 1 15 × 1·34 × 1 = 20·1 ml O 2 /100 ml of blood (A value of one indicates that Hb is fully saturated.) This is approximately 60 times greater than the amount of oxygen dissolved in plasma. The relationship between the PaO 2 and oxygen uptake by haemoglobin is not linear, because the addition of each O 2 molecule facilitates the uptake of the next O 2 molecule. This produces a sigmoid shaped oxygen dissociation curve (Figure 5.5). Furthermore, because haemoglobin is 97·5% saturated at a PaO 2 of 100 mm Hg (13·4 kPa) (i.e. that found in the normal healthy state), increasing the PaO 2 further has little effect on oxygen transport. Figure 5.5 Percentage of oxygen saturation of haemoglobin Percentage O 2 oxygen saturation of haemoglobin 97.5 83.5 10 0 0 1.3 6.6 13 PaO 2 (kPa) Key point Nearly all of the oxygen carried in the blood is taken up by haemoglobin with only a small amount dissolved in the plasma BREATHING ASSESSMENT 45 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 45 The affinity of haemoglobin for oxygen at a particular PO 2 (commonly known as the O 2 –Hb association) is also affected by other factors. A decreased affinity means that oxy- gen is more readily released. Thus the oxygen dissociation curve is shifted to the right. This is caused by: ● ↑ hydrogen ion concentration (fall in pH) ● ↑ PaCO 2 ● ↑ concentration of red cell 2,3-diphosphoglycerate (2,3-DPG) ● ↑ temperature. (The opposite of these factors increases the affinity and these will be discussed later.) The normal haemoglobin concentration (as measured by the haematocrit) is usually just above the point at which the oxygen transportation is optimal. Consequently a slight fall in haemoglobin concentration will actually increase oxygen transportation by decreasing blood viscosity. In addition to the oxygen combined with haemoglobin, there is also a smaller amount dissolved in plasma. This amount is directly proportional to the PaO 2 and is approxi- mately 0·003 ml/100 ml blood/mm Hg of PaO 2 . It follows from the description above that the total content of oxygen in blood is equal to the oxygen associated with haemoglobin and that dissolved in plasma. Oxygen blood concentration = (Hb × 1·34 × saturation) + (0·003 × PaO 2 ) For example, in arterial blood with a haemoglobin content of 15 g and a PaO 2 of 100 mm Hg the oxygen content would be: (15 × 1·34 × 97·5%) + (0·003 × 100) = 19·8 ml/100 ml Alternatively, in venous blood with a haemoglobin content of 15 g and a PaO 2 of 40 mm Hg the oxygen content would be: (15 × 1·34 × 75%) + (0·003 × 40) = 15·2 ml/100 ml Airway This has been described in detail in Chapter 4.The following summary contains the rele- vant facts relating to the breathless patient. Assessment Most breathless patients will have a patent airway. The number of words said with each breath is a useful indicator of illness severity and the effects of treatment. If the patient can count to 10 in one breath, then the underlying condition is unlikely to warrant immediate intervention. Occasionally, however, the patient will be severely distressed with stridor, possibly coughing and making enormous but ineffectual respiratory efforts. Stridor is a sinister sign and should be regarded as indicating impending airway obstruc- tion. Resuscitation High flow oxygen (FiO 2 = 0·85) may relieve some of the patient’s distress. If airway obstruction is suspected, immediate review by an anaesthetist is required. If, however, ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 46 05-AcuteMed-5-cpp 28/9/2000 3:38 pm Page 46 [...]... “B” is assessed all breathless patients should have received high flow oxygen (FiO2 = 0·85 at 15 l/min) Do not be concerned about patients who retain CO2 Providing that FiO2 equals 0·85, a rise in PaCO2 will not increase mortality – but untreated hypoxaema will! After the primary assessment has been completed then the FiO2 can be titrated according to the arterial blood gas results or the pulse oximeter... conditions Airway ● Obstruction Breathing ● Acute severe asthma ● Acute exacerbation of chronic obstructive pulmonary disease (COPD) ● Pulmonary pneumothorax ● Tension oedema Circulation ● Shock Therefore it is important to understand the mechanisms that maintain tissue perfusion in health before considering the effects of disrupting the circulation 51 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Relevant... with ischaemic heart disease Although these are many other causes, these will be seen only occasionally in most hospitals 47 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH An idea of the “chance” of meeting such a condition is displayed on an arbitrary scale in the box Causes of acute pulmonary oedema and “chance” of meeting the condition* Cause Ischaemic heart disease Myocardial infarction Cardiac... preexisting cardiac conditions Diuretics 57 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH and angiotensin converting enzyme (ACE) inhibitors are a common cause of this problem in patients with a history of left ventricular failure These drugs should be stopped and fluid replacement titrated against the patient’s clinical condition and central venous pressure Acute severe left ventricular failure The... echocardiography and pericardiocentesis 59 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Figure 6.3 Management of a bradydysrhythmia (UK and European guidelines) Investigations Appropriate investigations at this stage include: ● a full blood count to exclude anaemia (possibly exacerbating left ventricular failure) ● urea and electrolytes for baseline values particularly in patients who are being treated... the history and this will follow the normal “phrased” format (see Chapter 3) Particular attention should be directed at the key features shown in the box Key neurological features ● Define the problem ● Describe the deficit ● Determine the ● Associated symptoms onset pattern extent and duration neurological other 63 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH A comprehensive neurological assessment... that will facilitate differentiation of global and focal neurological disorders 65 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH What to test? There are many ways of assessing the mental state A variation is shown in the box The total score is out of 30 and cognitive impairment is defined as a score of less than 23 Formal assessment of mini mental state Orientation – time, date, day, month, year... to finish an equal distance between your eye and the patient’s eye ● Ensure that the patient continues to look directly into your eye 67 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH The visual pathway with associated lesions is demonstrated in Figures 7.1 and 7 .2 Figure 7.1 Visual pathway with associated lesions Interpretation Monocular defects These usually indicate ocular, retinal or optic nerve... to both asthma and COPD, in acute asthma the inspiratory phase is snatched and expiration is prolonged With chronic airflow limitation, however, the clinical picture ranges widely from a patient with preserved respiratory drive with pursed-lip breathing to one who is cyanosed, lethargic, and mildly dyspnoeic Wheezes may be heard on inspiration, but especially on expiration Acute pulmonary oedema can... cardiac index (CI) is used This is the cardiac output divided by the surface area of the person and hence is measured in litres per square metre Cardiac index = cardiac output/body surface area = 2 8–4 2 l/min/m2 (normal adult) The cardiac output can be affected by: ● ● ● ● preload myocardial contractility afterload heart rate Preload This is the volume of blood in the ventricle at the end of diastole . 150 Alveolar ventilation (ml/min) 4500 5000 1500 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 42 05-AcuteMed-5-cpp 28 /9 /20 00 3:38 pm Page 42 The lungs are ideally suited for diffusion as. will be expelled (Starling’s Law). Therefore, the ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 52 06-AcuteMed-6-cpp 28 /9 /20 00 3:41 pm Page 52 greater the preload, the greater the stroke volume CO 2 content High CO 2 content Low O 2 content Low O 2 content V/Q = normal High CO 2 content High O 2 content Low O 2 content Low CO 2 content V/Q > normal High CO 2 content Low O 2