PATIENT MONITORING
Final Objective: On completion of this module you will know about the appropriate use of monitoring and possible complications.
Enabling Objective: To achieve this goal, you should be able to:
Reference Reading:
Monitoring helps the anaesthetist to support and control vital organ function during anaesthesia. In order to control any physiological variable the anaesthetist must be able to measure the variable and change it if required.
Early detection of adverse events or trends during anaesthesia will result in the prevention of more serious problems. Anaesthetic disasters may not be due to a single factor. Anaesthetic disasters may be due to a combination of events, none of which on its own seems important.
Monitors are more accurate than human observation. They free the anaesthetist’s hands to perform other tasks and monitors also allow the anaesthetist to assess more than one parameter at a time.
Not all patients require the same type or intensity of monitoring. What is used will depend upon a variety of factors including:
The Association of Anaesthetists of Great Britain and Ireland state, “that continuous monitoring of ventilation and circulation is essential. This may be performed by the use of the human senses augmented, where possible, by the use of monitoring equipment”.
The Association of Anaesthetists of Great Britain and Ireland has core standards of monitoring wherever a patient is anaesthetised. These include:
MONITORING THE ANAESTHETIC EQUIPMENT.
It is essential that the anaesthetist check all equipment before anaesthetising a patient.
Oxygen supply. All oxygen supplies (cylinder or piped oxygen) must be monitored by a pressure gauge. The use of an oxygen analyser with an audible alarm is essential. Ideally, anaesthetic machines should have an anti-hypoxic device.
If at all possible, a vapour analyser should be used whenever a volatile anaesthetic agent is given.
Breathing systems must be monitored by observation for leak or disconnections. Capnography provides early recognition of these problems and is therefore an essential part of routine monitoring. When positive pressure ventilation is given, airway pressure alarms must be used to detect excessive pressure and also to warn of disconnections and leaks.
MONITORING THE PATIENT.
During anaesthesia, the patient’s physiological state and depth of anaesthesia need continual assessment. Monitoring devices supplement clinical observations. Appropriate clinical observations may include pulse rate and volume, mucosal colour, pupil size, response to surgical stimuli, sweating, and movement of the chest wall and/or reservoir bag. The anaesthetist should also listen to breath sounds and measure urine output and blood loss. A stethoscope must always be available.
CARDIOVASCULAR SYSTEM
Blood Pressure should be measured on all patients. The frequency and accuracy of blood pressure monitoring will depend on the severity of patient disease and the likelihood of surgery or anaesthesia causing cardiovascular instability. It may be measured directly or indirectly.
Indirect blood pressure measurement is used in the majority of anaesthetics and is based on the gradual deflation of a pneumatic cuff placed around a limb, usually the upper arm. A cuff with a width that is 40% of the arm circumference must be used and the internal bladder should encircle at least half the arm and be positioned over the artery. If the cuff is too small for the arm, the blood pressure will be over estimated. If the cuff is too large, the blood pressure will be under estimated. The cuff is inflated to above systolic pressure.
The simplest and least accurate measurement of blood pressure is to feel for a pulse whilst the cuff is slowly deflated. Listening to the Korotkoff sounds provides a more accurate measure of blood pressure. The Korotkoff sounds are due to changes in turbulent flow. The pressure at which the first sound is heard as the cuff is deflated (phase1) is the systolic pressure. With further deflation the sound characteristics change (phase 2 & 3), then become muffled (phase 4) and finally disappears (phase 5). The diastolic pressure is usually taken as phase 4 or 5.
Auscultation of the Korotkoff sounds is difficult in theatre and there may be errors including observer errors, problems with the stethoscope, inaccurate pressure monitor, incorrect cuff size and placement, and if peripheral blood flow is reduced.
Automated non-invasive devices (e.g Dinamap) minimize errors and usually provide consistent and reliable readings. An electric pump inflates the cuff which then undergoes controlled deflation. A computer controlled pressure transducer detects arterial wall motion and calculates systolic, diastolic and mean arterial pressure. The measured diastolic pressure is the least accurate of the 3 pressures recorded. The mean arterial pressure is the most accurate.
Direct blood pressure measurement with an intra-arterial line is more accurate, provides continuous measurements and allows easy blood sampling. A cannula is inserted into a peripheral artery and connected to a transducer that converts pressure into an electrical signal. This is then amplified and displayed both as a waveform and a blood pressure. Direct arterial monitoring has the risks of haemorrhage, infection and distal ischaemia.
The pulse provides the anaesthetist with information on the heart rate, rhythm and peripheral perfusion. The pulse must be frequently or continuously assessed. It can be monitored by direct palpation of a peripheral artery or by detecting pulsatile flow through peripheral tissue (pulse oximetry). As cardiac output falls, increasing vasoconstriction (attempting to maintain arterial pressure) reduces the volume of the pulse and with extreme vasoconstriction the peripheral pulse may not be palpable.
The electrocardiogram (ECG) monitors heart rate and rhythm. Acute changes in blood potassium and calcium concentration andmyocardial ischaemia can be detected. The ECG does not monitor cardiac output. It is possible to have an almost normal ECG with almost no cardiac output. With the standard three-limb ECG the electrodes are placed on the right shoulder, left shoulder and left lower chest. Lead II is chosen so that the ECG looks from right shoulder to lower left chest. This is equivalent to lead II on a 12 lead ECG and is a good monitor of rate and rhythm but a poor monitor of ischaemia. Moving the right shoulder electrode to the manubrium and the left arm electrode to the left 5 intercostal space on the anterior axillary line (heart apex) and choosing lead I on the monitor will allow monitoring of the lateral part of the heart. This lead is a much better monitor of myocardial ischaemia (CM5).
Urine output is usually measured in severe illness, major surgery, prolonged surgery or when large blood loss is expected. Measurements should be made at least hourly; aiming for a urine output of at least 1 ml/kg/h. Correcting blood pressure and hypovolaemia are the first steps in treating poor urine output.
Blood loss should be frequently estimated. Unfortunately visual estimation of surgical blood loss often underestimates blood loss. Anaesthetists must look at blood in suction bottles, in surgical swabs and packs, on surgical drapes and on the floor. Anaesthetists should investigate how much blood can be in the surgical packs or swabs used in their hospitals. A large (45cm) surgical pack may contain between 150 and 350 ml when completely wet. To learn the capacity of packs and swabs used in their hospital, anaesthetists should weigh them dry and when soaked with water. The difference in weight in grams will be an estimate of the volume of blood in mls.
RESPIRATORY SYSTEM
Pulse oximetry and end tidal capnography have greatly increased the anaesthetist’s ability to ensure adequate oxygenation and ventilation. They are essential monitors and must be used whenever available, however the anaesthetist should also continually observe the patient’s colour, auscultate the chest and observe chest movements for rate, depth and symmetry of breathing.
The oxygen reserves of the body are very limited and life-threatening hypoxemia can develop rapidly within minutes and with few initial clinical signs. Pulse oximetry is an easy to use, non-invasive, continuous real time monitor of a patient’s level, (percentage) of oxygenated haemoglobin (Hb). It is important to note that whilst the oxygen saturation is a very important component of tissue oxygenation, it is in fact only one component of a range of factors that determine the overall oxygen delivery to the tissues.
The total oxygen delivery (or “oxygen flux”) to the tissues is determined by the following equation:
Oxygen delivery = (cardiac output) x (oxygen content of the blood).
Oxygen content of the blood = oxygen carrying capacity of Hb + dissolved oxygen
Oxygencarrying capacity of Hb = 1.39 x Hb gm / 100 mls blood x % saturation.
Dissolved oxygen = 0.3 ml / 100 ml at PaO2 of 100 mmHg
Therefore, in summary, adequate tissue oxygenation depends not only on the PaO2, but also on an adequate cardiac output, and haemoglobin level.
Thepulse oximeter consists of a probe, containing two light emitting diodes (LED) and a photodetector, which can be applied across the tip of a digit or earlobe such that light is transmitted through the tissue. The LEDs transmit red light at two different wavelengths (660 nm and 940 nm) that are absorbed in different amounts by oxyhaemoglobin and deoxyhaemoglobin. The intensity of transmitted light reaching the photodetector is converted into an electrical signal. This information is processed and the absorption due to the tissues and venous blood, which is constant, is subtracted from the total amount. The remaining absorption is due to the pulsatile arterial blood. The information is displayed both as waveform and a number. Pulse oximeters are usually accurate to +/- 2% over the range of 70-100% and reasonable in the range of 55-70% but below 55% are not accurate.
Hb Saturation PaO2 (mmHg) Clinical Correlation
100% > 250 Breathing 40% oxygen.
97% 95-100 PaO2 in the young and healthy breathing room air.
96% 80 PaO2 in the elderly breathing room air.
93% 70 Lower limit of PaO2 in the elderly breathing room air.
90% 60 Definition of respiratory failure
85% 50 Cyanosis may be visible below this level.
75% 40 Mixed venous blood
32% 20 Coronary sinus blood.
Note that a saturation of 90%, represents the beginning of the steep descent of the oxygen-haemoglobin dissociation curve. Within this region, even small decreases in the SaO2 will represent a profound decrease in the PaO2. It is the PaO2 that determines the flow of oxygen down the “oxygen cascade” from alveoli to mitochondria. For this reason a saturation level below 90% represents imminent respiratory failure.
It is important to be aware of the normal limitations as well as the pathological and technical factors that may reduce the accuracy of these instruments.
As mentioned above whilst giving a reading for a patient’s oxygenation status, the adequacy of the total oxygen delivery to the tissues is not necessarily determined, as this will further depend on functional haemoglobin levels and the cardiac output. A normal SaO2 reading especially in cases of increased inspired oxygen concentrations will not necessarily indicate an adequate ventilatory effort. Hypoventilation may not become apparent till late because of a falsely reassuring SaO2 reading.
There are pathological factors that limit the use of pulse oximeters. Anaemia will reduce the oxygen carrying capacity of the blood, but the recorded SaO2 will remain unaltered. With carbon monoxide poisoning there may be normal readings despite severe tissue hypoxia. With Methaemoglobinaema the pulse oximeter may only read about 85%. Factors that shift the oxygen dissociation curve will make interpretation of results more difficult and if there is a poor peripheral perfusion, readings may be inaccurate. Motion will cause artefacts and some nail polishes may interfere with readings.
Capnography is the measurement of expired carbon dioxide by infrared light absorption. In a healthy person the concentration of carbon dioxide in alveolar (end-tidal carbon dioxide) gas is similar to the concentration in arterial blood (end tidal carbon dioxide is approximately 5 mmHg lower). The gap between arterial and end tidal carbon dioxide is increased (end tidal carbon dioxide falls) in sick patients with increased dead space.
Capnography is an important non-invasive monitor that provides information about carbon dioxide production (metabolism), pulmonary and systemic circulation, alveolar ventilation, respiratory patterns and elimination of carbon dioxide from the anaesthetic breathing system.
Capnography has been shown to be effective in the early detection of adverse events. Capnography and pulse oximetry together could help in the prevention of 93% of avoidable anaesthesia mishaps.
Clinical uses of capnography include:
TEMPERATURE.
Anaesthesia and surgery commonly cause changes in the patient’s temperature. Hypothermia, results from a combination of anesthetic-induced impairment of thermoregulatory control, a cool operating room environment, and factors unique to surgery and anaesthesia that promote excessive heat loss. Available data suggest that inhibition of normal thermoregulatory defenses contributes more to hypothermia than does cold exposure. Much core hypothermia results from altered distribution of body heat rather than from an imbalance between metabolic heat production and heat loss.
Body tissues produce heat in proportion to their metabolic rates. The brain and major organs in the trunk are the most metabolically active tissues and generate more metabolic heat than muscle at rest. The human body can very roughly be described as having a core thermal compartment and a peripheral compartment. Physically, the core compartment consists of the well-perfused organs of the trunk and head. Temperatures within the core compartment rarely differ by more than a few tenths of a degree centigrade. The peripheral compartment consists of the arms and legs.
Nearly all patients administered general anaesthesia become hypothermic, typically by 1–3°C depending on the type and dose of anesthesia, amount of surgical exposure, and the ambient temperature. Hypothermia develops with a characteristic pattern. Core temperature decreases rapidly, 1–1.5°C during the first hour. This initial hypothermia is followed by 2 or 3 h of a slower, linear, decrease in core temperature. Finally, patients enter a plateau phase during which core temperature remains constant. Each segment of this typical hypothermia curve has a different cause.
The initial decrease in core temperature is due to redistribution of heat. General anaesthesia reduces the vasoconstriction threshold to well below core temperature, thus inhibiting centrally medicated thermoregulatory vasoconstriction. Most anaesthetics cause direct (peripheral) vasodilatation. Vasodilatation allows core heat, which is no longer constrained to the central thermal compartment, to flow down the temperature gradient into peripheral tissues. This internal redistribution of body heat decreases core temperature and proportionately increases the temperature of peripheral tissues; it does not, however, represent any net exchange of heat to the environment, and body heat content remains constant. Of course any systemic cooling that occurs simultaneously will increase core hypothermia.
The extent to which induction of general anaesthesia induces redistribution hypothermia in individual patients depends on a number of factors. Among the most important is the patient’s initial body heat content. Core temperature remains essentially normal even in warm environments. However, body heat content increases as peripheral tissues absorb heat; after a number of hours in a sufficiently warm environment, peripheral tissue temperature approaches core temperature. Because flow of heat needs a temperature gradient, redistribution is limited when peripheral and core temperatures are similar and increased when peripheral temperature is low. Patients should not come to theatre cold.
The second portion of the hypothermia curve is a relatively slow, linear decrease in core temperature. It results simply from heat loss exceeding metabolic heat production. During general anaesthesia heat loss increases and the metabolic rate is reduced by 15–40%.
The major cause of heat loss is radiation, accounting for approximately 60%. The remaining heat loss is largely convective. Conductive heat loss is usually unimportant. Respiratory evaporative heat loss accounts for 10% and evaporative heat loss from large surgical incisions can be substantial.
A passive plateau results when metabolic heat production equals heat loss. However, several factors complicate the situation during anaesthesia and surgery: (1) Anaesthesia significantly decreases metabolic heat production. (2) Heat loss may be abnormally high because of a relatively cool operating room environment, administration of cool intravenous and irrigating fluids, ventilation with cold dry gas, and evaporative and radiation losses from within surgical incisions. (3) Behavioral compensations are not available to unconscious patients, and autonomic responses are impaired, at least until patients become quite hypothermic.
Postoperative return to normothermia occurs when brain anaesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anaesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2–5 h, depending on the degree of hypothermia and the age of the patient.
The anaesthetist should attempt to limit hypothermia. Patients should be brought to theatre warm. Fluids, especially blood should be warmed, gases should be humidified and exposed areas covered. The operating theatre should not be cold.
The adverse effects of hypothermia are proportional to the reduction in the patient’s temperature. For every 1° C fall in temperature, the metabolic rate is reduced by 10%. Hypothermia also reduces cardiac output and reduces the binding of oxygen to haemoglobin. This results in reduced oxygen delivery to organs. Hypothermia also reduces the activity of platelets and interferes with coagulation. There is an increased risk of wound infection. Drug metabolism is reduced. The MAC of inhalation agents are decreased and the duration of muscle relaxants increased. Postoperative shivering may increase oxygen consumption by 400%. These patients may be at risk of myocardial ischaemia.
PREVENTION OF INJURIES IN THE ANAESTHETISED PATIENT.
General and regional anaesthesia removes many of the body’s protective mechanisms and patients are at risk of injury. The anaesthetist must recognise the risks and is responsible for prevention.
Anaesthetised patients are at risk of nerve injuries and tissue injury (eyes, teeth, bones and joints, and burns.) Anaesthetised patients cannot protect themselves from trauma or burns. Objects should not be unnecessarily passed over the patient. Hot liquid and equipment must be kept away.
An anaesthetised patient is at risk of ocular injuries ranging from corneal abrasions to retinal ischaemia. Corneal abrasions are due to direct trauma (surgical drapes, facemask, fingers etc) in combination with decreased tear production due to general anaesthesia. The patient’s eyes should be gently taped shut. The tape should not be pushed onto the eyelids. Special care is required in the prone position where direct pressure on the eye may result in retinal ischaemia.
POSITIONING
Correct positioning of the surgical patient provides the best surgical access to the operative site, reduces bleeding, prevents pressure damage to skin, nerves, joints and muscles, minimises adverse cardiac and respiratory problems, and provides good access for the anaesthetist.
All positions carry some risk to the patient and this is greatly increased when anaesthetised. Some positions have specific physiological changes and complications associated with them.
Patients may be at an increased risk because of diseases such as diabetes, arthritis or osteoporosis, and because of old age.
Patients may be transferred and positioned on the operating table after they are anaesthetised. Moving an anesthetised patient requires great care and cooperation. All staff must understand their role and responsibility. The anaesthetist should be in charge, coordinating the movement and controlling the patient’s head and neck. All intravenous lines, catheters, endotracheal tubes etc must be well secured to the patient and free to move.
Peripheral nerves may be damaged by stretch, compression, ischaemia or metabolic changes. Damage may be temporary (90%) with recovery occurring within weeks, or permanent. Reduce stretch/compression on nerves by careful positioning and padding. Tourniquet time should be less than 2 hours.
Pressure sores will occur if excessive pressure is applied to a relatively small area of skin, especially if there is also decreased peripheral perfusion. As for nerve damage, the incidence of pressure sores may be reduced by careful positioning/padding and regular observation.
Overextension or flexion of a joint may cause joint, tendon and muscle damage. Patients with suspected joint disease should have their range of movement assessed before anaesthesia.
In the supine position the main nerves at risk are:
The Trendelenburg position is often used to describe any head down position. This position has several physiological effects that may harm the patient including increased venous return, increased intracranial pressure, increased intraocular pressure, increased intragastric pressure and an increased risk of passive regurgitation. The anaesthetist must consider protecting the airway of patients with other risk factors for aspiration with an endotracheal tube.
The lithotomy position will increase venous return. The common peroneal nerve may be damaged by the lithotomy pole resulting in foot drop and sensory loss to the dorsal surface of the foot and antero-lateral lower leg. Both legs should be moved together to minimise damage to pelvic ligaments. Extreme flexion of the hip joint can cause damage by stretching of the sciatic and obturator nerves. Calf compression may predispose to venous thromboembolism and compartment syndrome.
The prone position may be especially dangerous. Usually an anaesthetised patient is turned from supine to prone. This puts the patient at significant risk. There must be sufficient number of people to gently and slowly move the patient. The anaesthetist must be in charge of the positioning and control the movement of the head and neck. Once turned the anaesthetist must carefully assess the risk of pressure damage and nerve damage. The neck must not be hyper-extended nor hyper-flexed. There must be no pressure on the eyes. The endotracheal tube must not be kinked. There should be padding below the pelvis and the chest wall to allow free movement of the abdomen with respiration. The shoulders are at risk of hyperextension.
Macroglossia and oropharyngeal swelling can occur in the sitting position from excessive flexion of the head and neck causing obstruction to venous drainage. It has also been reported in the prone position.
Usually, cardiac index is reduced with a reduction in stroke volume but unchanged heart rate. Mean arterial pressure is maintained by an increase in systemic vascular resistance. The inferior vena cava is at risk of compression.
The functional residual capacity (FRC) is reduced by 40% when a patient goes from the awake upright position to the anaesthetised supine position. In the anaesthetised prone position the reduction in FRC is only 12% and there is an improvement in ventilation/perfusion (V/Q) matching leading to improved oxygenation.
All nerves commonly damaged during anaesthesia are at risk in the prone position, though the incidence of damage is less, and there are some nerves that are only damaged in the prone position. These rare peripheral nerve injuries include the supra-optic, phrenic, recurrent laryngeal and mental nerves.
Postoperative visual loss (POVL) after non-ocular surgery in any position is relatively rare but 60% of cases of POVL followed the prone position. The two injuries most commonly described are ischaemic optic neuropathy and central retinal artery occlusion. The most obvious aetiology is the effect of direct external pressure on the eye causing an increase in intraocular pressure that may lead to retinal ischaemia and visual loss.
POVL can occur with out direct pressure, usually by ischaemic optic neuropathy. The oxygenation of the optic nerve is dependent on the adequate perfusion pressure (i.e. the difference between the mean arterial pressure and intraocular pressure or venous pressure, whichever is greater). Increased intraocular pressure occurs in the prone position.
SELF-ASSESSMENT QUESTIONS
1. Draw the appearance of common arrhythmias that may occur intra-operatively. For each, list common causes and treatment.
2. Draw and explain a normal capnograph pattern. Draw and explain other possible patterns.
3. How may hypothermia be reduced?
4. Why is an adequate saturation reading a poor monitor of adequate ventilation?
5. List the potential usefulness of capnography.
ASSIGNMENT
Discuss what you consider to be the minimum standard of monitoring that must always be used for all anaesthetised patients. What other monitoring should ideally be available?
Chapter title CASE STUDIES
Case 7.1
Bayanaa is about to undergo a laparoscopic cholecystectomy. She is 60 years old and has been a heavy smoker. Her father died at a young age of cardiac disease. She denies any symptoms of chest pain but is a little short of breath on exertion. You plan to do a general anaesthetic.
Question 1
What standard monitoring is indicated for Bayanaa?
Question 2
You consider her to be at increased risk of myocardial ischemia. How will you change your standard monitoring to enable detection of intraoperative ischaemia?
Question. 3
Immediately after intubation of the trachea, the capnograph displays a carbon dioxide concentration of zero. What are the potential causes and outline your next step?
Question 4
You correct the problem but during the operation, you notice that the baseline capnogram is elevated and does not return to zero. What are the possible causes?
Question 5
The saturation reading shortly after arriving to the recovery room is 90%. How will you manage her?
Final Objective: On completion of this module you will know about the appropriate use of monitoring and possible complications.
Enabling Objective: To achieve this goal, you should be able to:
- List the core standards of monitoring during anaesthesia.
- Describe how anaesthetic monitors work, when to use them and potential errors.
- Describe the potential problems caused by the patient’s position during surgery.
- Describe the control of body temperature and the adverse effects of hypothermia.
Reference Reading:
- Developing Anaesthesia page 53, 147
Monitoring helps the anaesthetist to support and control vital organ function during anaesthesia. In order to control any physiological variable the anaesthetist must be able to measure the variable and change it if required.
Early detection of adverse events or trends during anaesthesia will result in the prevention of more serious problems. Anaesthetic disasters may not be due to a single factor. Anaesthetic disasters may be due to a combination of events, none of which on its own seems important.
Monitors are more accurate than human observation. They free the anaesthetist’s hands to perform other tasks and monitors also allow the anaesthetist to assess more than one parameter at a time.
Not all patients require the same type or intensity of monitoring. What is used will depend upon a variety of factors including:
- The current and past health of the patient
- The type of operation
- The anaesthetic technique used
- The equipment available and the preference of the anaesthetist.
The Association of Anaesthetists of Great Britain and Ireland state, “that continuous monitoring of ventilation and circulation is essential. This may be performed by the use of the human senses augmented, where possible, by the use of monitoring equipment”.
The Association of Anaesthetists of Great Britain and Ireland has core standards of monitoring wherever a patient is anaesthetised. These include:
- The anaesthetist must be present and care for the patient for the entire time the patient is anaesthetised.
- Monitoring devices must be attached before induction and their use continued until the patient has recovered from the anaesthetic.
- The same standards of monitoring for general anaesthesia apply for sedation and regional anaesthesia.
- A summary of information provided by the monitoring devices should be recorded on the anaesthetic record. Core data (heart rate BP, SaO2) should be recorded at intervals no longer than 5 minutes.
- The anaesthetist must ensure that all monitoring equipment is checked before use and that all alarms are working and appropriately set.
MONITORING THE ANAESTHETIC EQUIPMENT.
It is essential that the anaesthetist check all equipment before anaesthetising a patient.
Oxygen supply. All oxygen supplies (cylinder or piped oxygen) must be monitored by a pressure gauge. The use of an oxygen analyser with an audible alarm is essential. Ideally, anaesthetic machines should have an anti-hypoxic device.
If at all possible, a vapour analyser should be used whenever a volatile anaesthetic agent is given.
Breathing systems must be monitored by observation for leak or disconnections. Capnography provides early recognition of these problems and is therefore an essential part of routine monitoring. When positive pressure ventilation is given, airway pressure alarms must be used to detect excessive pressure and also to warn of disconnections and leaks.
MONITORING THE PATIENT.
During anaesthesia, the patient’s physiological state and depth of anaesthesia need continual assessment. Monitoring devices supplement clinical observations. Appropriate clinical observations may include pulse rate and volume, mucosal colour, pupil size, response to surgical stimuli, sweating, and movement of the chest wall and/or reservoir bag. The anaesthetist should also listen to breath sounds and measure urine output and blood loss. A stethoscope must always be available.
CARDIOVASCULAR SYSTEM
Blood Pressure should be measured on all patients. The frequency and accuracy of blood pressure monitoring will depend on the severity of patient disease and the likelihood of surgery or anaesthesia causing cardiovascular instability. It may be measured directly or indirectly.
Indirect blood pressure measurement is used in the majority of anaesthetics and is based on the gradual deflation of a pneumatic cuff placed around a limb, usually the upper arm. A cuff with a width that is 40% of the arm circumference must be used and the internal bladder should encircle at least half the arm and be positioned over the artery. If the cuff is too small for the arm, the blood pressure will be over estimated. If the cuff is too large, the blood pressure will be under estimated. The cuff is inflated to above systolic pressure.
The simplest and least accurate measurement of blood pressure is to feel for a pulse whilst the cuff is slowly deflated. Listening to the Korotkoff sounds provides a more accurate measure of blood pressure. The Korotkoff sounds are due to changes in turbulent flow. The pressure at which the first sound is heard as the cuff is deflated (phase1) is the systolic pressure. With further deflation the sound characteristics change (phase 2 & 3), then become muffled (phase 4) and finally disappears (phase 5). The diastolic pressure is usually taken as phase 4 or 5.
Auscultation of the Korotkoff sounds is difficult in theatre and there may be errors including observer errors, problems with the stethoscope, inaccurate pressure monitor, incorrect cuff size and placement, and if peripheral blood flow is reduced.
Automated non-invasive devices (e.g Dinamap) minimize errors and usually provide consistent and reliable readings. An electric pump inflates the cuff which then undergoes controlled deflation. A computer controlled pressure transducer detects arterial wall motion and calculates systolic, diastolic and mean arterial pressure. The measured diastolic pressure is the least accurate of the 3 pressures recorded. The mean arterial pressure is the most accurate.
Direct blood pressure measurement with an intra-arterial line is more accurate, provides continuous measurements and allows easy blood sampling. A cannula is inserted into a peripheral artery and connected to a transducer that converts pressure into an electrical signal. This is then amplified and displayed both as a waveform and a blood pressure. Direct arterial monitoring has the risks of haemorrhage, infection and distal ischaemia.
The pulse provides the anaesthetist with information on the heart rate, rhythm and peripheral perfusion. The pulse must be frequently or continuously assessed. It can be monitored by direct palpation of a peripheral artery or by detecting pulsatile flow through peripheral tissue (pulse oximetry). As cardiac output falls, increasing vasoconstriction (attempting to maintain arterial pressure) reduces the volume of the pulse and with extreme vasoconstriction the peripheral pulse may not be palpable.
The electrocardiogram (ECG) monitors heart rate and rhythm. Acute changes in blood potassium and calcium concentration andmyocardial ischaemia can be detected. The ECG does not monitor cardiac output. It is possible to have an almost normal ECG with almost no cardiac output. With the standard three-limb ECG the electrodes are placed on the right shoulder, left shoulder and left lower chest. Lead II is chosen so that the ECG looks from right shoulder to lower left chest. This is equivalent to lead II on a 12 lead ECG and is a good monitor of rate and rhythm but a poor monitor of ischaemia. Moving the right shoulder electrode to the manubrium and the left arm electrode to the left 5 intercostal space on the anterior axillary line (heart apex) and choosing lead I on the monitor will allow monitoring of the lateral part of the heart. This lead is a much better monitor of myocardial ischaemia (CM5).
Urine output is usually measured in severe illness, major surgery, prolonged surgery or when large blood loss is expected. Measurements should be made at least hourly; aiming for a urine output of at least 1 ml/kg/h. Correcting blood pressure and hypovolaemia are the first steps in treating poor urine output.
Blood loss should be frequently estimated. Unfortunately visual estimation of surgical blood loss often underestimates blood loss. Anaesthetists must look at blood in suction bottles, in surgical swabs and packs, on surgical drapes and on the floor. Anaesthetists should investigate how much blood can be in the surgical packs or swabs used in their hospitals. A large (45cm) surgical pack may contain between 150 and 350 ml when completely wet. To learn the capacity of packs and swabs used in their hospital, anaesthetists should weigh them dry and when soaked with water. The difference in weight in grams will be an estimate of the volume of blood in mls.
RESPIRATORY SYSTEM
Pulse oximetry and end tidal capnography have greatly increased the anaesthetist’s ability to ensure adequate oxygenation and ventilation. They are essential monitors and must be used whenever available, however the anaesthetist should also continually observe the patient’s colour, auscultate the chest and observe chest movements for rate, depth and symmetry of breathing.
The oxygen reserves of the body are very limited and life-threatening hypoxemia can develop rapidly within minutes and with few initial clinical signs. Pulse oximetry is an easy to use, non-invasive, continuous real time monitor of a patient’s level, (percentage) of oxygenated haemoglobin (Hb). It is important to note that whilst the oxygen saturation is a very important component of tissue oxygenation, it is in fact only one component of a range of factors that determine the overall oxygen delivery to the tissues.
The total oxygen delivery (or “oxygen flux”) to the tissues is determined by the following equation:
Oxygen delivery = (cardiac output) x (oxygen content of the blood).
Oxygen content of the blood = oxygen carrying capacity of Hb + dissolved oxygen
Oxygencarrying capacity of Hb = 1.39 x Hb gm / 100 mls blood x % saturation.
Dissolved oxygen = 0.3 ml / 100 ml at PaO2 of 100 mmHg
Therefore, in summary, adequate tissue oxygenation depends not only on the PaO2, but also on an adequate cardiac output, and haemoglobin level.
Thepulse oximeter consists of a probe, containing two light emitting diodes (LED) and a photodetector, which can be applied across the tip of a digit or earlobe such that light is transmitted through the tissue. The LEDs transmit red light at two different wavelengths (660 nm and 940 nm) that are absorbed in different amounts by oxyhaemoglobin and deoxyhaemoglobin. The intensity of transmitted light reaching the photodetector is converted into an electrical signal. This information is processed and the absorption due to the tissues and venous blood, which is constant, is subtracted from the total amount. The remaining absorption is due to the pulsatile arterial blood. The information is displayed both as waveform and a number. Pulse oximeters are usually accurate to +/- 2% over the range of 70-100% and reasonable in the range of 55-70% but below 55% are not accurate.
Hb Saturation PaO2 (mmHg) Clinical Correlation
100% > 250 Breathing 40% oxygen.
97% 95-100 PaO2 in the young and healthy breathing room air.
96% 80 PaO2 in the elderly breathing room air.
93% 70 Lower limit of PaO2 in the elderly breathing room air.
90% 60 Definition of respiratory failure
85% 50 Cyanosis may be visible below this level.
75% 40 Mixed venous blood
32% 20 Coronary sinus blood.
Note that a saturation of 90%, represents the beginning of the steep descent of the oxygen-haemoglobin dissociation curve. Within this region, even small decreases in the SaO2 will represent a profound decrease in the PaO2. It is the PaO2 that determines the flow of oxygen down the “oxygen cascade” from alveoli to mitochondria. For this reason a saturation level below 90% represents imminent respiratory failure.
It is important to be aware of the normal limitations as well as the pathological and technical factors that may reduce the accuracy of these instruments.
As mentioned above whilst giving a reading for a patient’s oxygenation status, the adequacy of the total oxygen delivery to the tissues is not necessarily determined, as this will further depend on functional haemoglobin levels and the cardiac output. A normal SaO2 reading especially in cases of increased inspired oxygen concentrations will not necessarily indicate an adequate ventilatory effort. Hypoventilation may not become apparent till late because of a falsely reassuring SaO2 reading.
There are pathological factors that limit the use of pulse oximeters. Anaemia will reduce the oxygen carrying capacity of the blood, but the recorded SaO2 will remain unaltered. With carbon monoxide poisoning there may be normal readings despite severe tissue hypoxia. With Methaemoglobinaema the pulse oximeter may only read about 85%. Factors that shift the oxygen dissociation curve will make interpretation of results more difficult and if there is a poor peripheral perfusion, readings may be inaccurate. Motion will cause artefacts and some nail polishes may interfere with readings.
Capnography is the measurement of expired carbon dioxide by infrared light absorption. In a healthy person the concentration of carbon dioxide in alveolar (end-tidal carbon dioxide) gas is similar to the concentration in arterial blood (end tidal carbon dioxide is approximately 5 mmHg lower). The gap between arterial and end tidal carbon dioxide is increased (end tidal carbon dioxide falls) in sick patients with increased dead space.
Capnography is an important non-invasive monitor that provides information about carbon dioxide production (metabolism), pulmonary and systemic circulation, alveolar ventilation, respiratory patterns and elimination of carbon dioxide from the anaesthetic breathing system.
Capnography has been shown to be effective in the early detection of adverse events. Capnography and pulse oximetry together could help in the prevention of 93% of avoidable anaesthesia mishaps.
Clinical uses of capnography include:
- As an indicator of adequate alveolar ventilation (awake, spontaneous breathing anaesthesia and mechanical ventilation).
- As a disconnection alarm
- As a indicator of tracheal/oesophageal intubation
- As an indicator of cardiac output. If cardiac output falls and ventilation remains the same, then end tidal carbon dioxide falls as carbon dioxide is not delivered to the lungs, eg cardiac arrest, hypovolaemia, pulmonary embolus
- As an indicator of a hypermetabolic state eg malignant hyperpyrexia or thyroid storm
- As an indicator of lung disease
- As an early indicator of the return of muscle function after paralysis
TEMPERATURE.
Anaesthesia and surgery commonly cause changes in the patient’s temperature. Hypothermia, results from a combination of anesthetic-induced impairment of thermoregulatory control, a cool operating room environment, and factors unique to surgery and anaesthesia that promote excessive heat loss. Available data suggest that inhibition of normal thermoregulatory defenses contributes more to hypothermia than does cold exposure. Much core hypothermia results from altered distribution of body heat rather than from an imbalance between metabolic heat production and heat loss.
Body tissues produce heat in proportion to their metabolic rates. The brain and major organs in the trunk are the most metabolically active tissues and generate more metabolic heat than muscle at rest. The human body can very roughly be described as having a core thermal compartment and a peripheral compartment. Physically, the core compartment consists of the well-perfused organs of the trunk and head. Temperatures within the core compartment rarely differ by more than a few tenths of a degree centigrade. The peripheral compartment consists of the arms and legs.
Nearly all patients administered general anaesthesia become hypothermic, typically by 1–3°C depending on the type and dose of anesthesia, amount of surgical exposure, and the ambient temperature. Hypothermia develops with a characteristic pattern. Core temperature decreases rapidly, 1–1.5°C during the first hour. This initial hypothermia is followed by 2 or 3 h of a slower, linear, decrease in core temperature. Finally, patients enter a plateau phase during which core temperature remains constant. Each segment of this typical hypothermia curve has a different cause.
The initial decrease in core temperature is due to redistribution of heat. General anaesthesia reduces the vasoconstriction threshold to well below core temperature, thus inhibiting centrally medicated thermoregulatory vasoconstriction. Most anaesthetics cause direct (peripheral) vasodilatation. Vasodilatation allows core heat, which is no longer constrained to the central thermal compartment, to flow down the temperature gradient into peripheral tissues. This internal redistribution of body heat decreases core temperature and proportionately increases the temperature of peripheral tissues; it does not, however, represent any net exchange of heat to the environment, and body heat content remains constant. Of course any systemic cooling that occurs simultaneously will increase core hypothermia.
The extent to which induction of general anaesthesia induces redistribution hypothermia in individual patients depends on a number of factors. Among the most important is the patient’s initial body heat content. Core temperature remains essentially normal even in warm environments. However, body heat content increases as peripheral tissues absorb heat; after a number of hours in a sufficiently warm environment, peripheral tissue temperature approaches core temperature. Because flow of heat needs a temperature gradient, redistribution is limited when peripheral and core temperatures are similar and increased when peripheral temperature is low. Patients should not come to theatre cold.
The second portion of the hypothermia curve is a relatively slow, linear decrease in core temperature. It results simply from heat loss exceeding metabolic heat production. During general anaesthesia heat loss increases and the metabolic rate is reduced by 15–40%.
The major cause of heat loss is radiation, accounting for approximately 60%. The remaining heat loss is largely convective. Conductive heat loss is usually unimportant. Respiratory evaporative heat loss accounts for 10% and evaporative heat loss from large surgical incisions can be substantial.
A passive plateau results when metabolic heat production equals heat loss. However, several factors complicate the situation during anaesthesia and surgery: (1) Anaesthesia significantly decreases metabolic heat production. (2) Heat loss may be abnormally high because of a relatively cool operating room environment, administration of cool intravenous and irrigating fluids, ventilation with cold dry gas, and evaporative and radiation losses from within surgical incisions. (3) Behavioral compensations are not available to unconscious patients, and autonomic responses are impaired, at least until patients become quite hypothermic.
Postoperative return to normothermia occurs when brain anaesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anaesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2–5 h, depending on the degree of hypothermia and the age of the patient.
The anaesthetist should attempt to limit hypothermia. Patients should be brought to theatre warm. Fluids, especially blood should be warmed, gases should be humidified and exposed areas covered. The operating theatre should not be cold.
The adverse effects of hypothermia are proportional to the reduction in the patient’s temperature. For every 1° C fall in temperature, the metabolic rate is reduced by 10%. Hypothermia also reduces cardiac output and reduces the binding of oxygen to haemoglobin. This results in reduced oxygen delivery to organs. Hypothermia also reduces the activity of platelets and interferes with coagulation. There is an increased risk of wound infection. Drug metabolism is reduced. The MAC of inhalation agents are decreased and the duration of muscle relaxants increased. Postoperative shivering may increase oxygen consumption by 400%. These patients may be at risk of myocardial ischaemia.
PREVENTION OF INJURIES IN THE ANAESTHETISED PATIENT.
General and regional anaesthesia removes many of the body’s protective mechanisms and patients are at risk of injury. The anaesthetist must recognise the risks and is responsible for prevention.
Anaesthetised patients are at risk of nerve injuries and tissue injury (eyes, teeth, bones and joints, and burns.) Anaesthetised patients cannot protect themselves from trauma or burns. Objects should not be unnecessarily passed over the patient. Hot liquid and equipment must be kept away.
An anaesthetised patient is at risk of ocular injuries ranging from corneal abrasions to retinal ischaemia. Corneal abrasions are due to direct trauma (surgical drapes, facemask, fingers etc) in combination with decreased tear production due to general anaesthesia. The patient’s eyes should be gently taped shut. The tape should not be pushed onto the eyelids. Special care is required in the prone position where direct pressure on the eye may result in retinal ischaemia.
POSITIONING
Correct positioning of the surgical patient provides the best surgical access to the operative site, reduces bleeding, prevents pressure damage to skin, nerves, joints and muscles, minimises adverse cardiac and respiratory problems, and provides good access for the anaesthetist.
All positions carry some risk to the patient and this is greatly increased when anaesthetised. Some positions have specific physiological changes and complications associated with them.
Patients may be at an increased risk because of diseases such as diabetes, arthritis or osteoporosis, and because of old age.
Patients may be transferred and positioned on the operating table after they are anaesthetised. Moving an anesthetised patient requires great care and cooperation. All staff must understand their role and responsibility. The anaesthetist should be in charge, coordinating the movement and controlling the patient’s head and neck. All intravenous lines, catheters, endotracheal tubes etc must be well secured to the patient and free to move.
Peripheral nerves may be damaged by stretch, compression, ischaemia or metabolic changes. Damage may be temporary (90%) with recovery occurring within weeks, or permanent. Reduce stretch/compression on nerves by careful positioning and padding. Tourniquet time should be less than 2 hours.
Pressure sores will occur if excessive pressure is applied to a relatively small area of skin, especially if there is also decreased peripheral perfusion. As for nerve damage, the incidence of pressure sores may be reduced by careful positioning/padding and regular observation.
Overextension or flexion of a joint may cause joint, tendon and muscle damage. Patients with suspected joint disease should have their range of movement assessed before anaesthesia.
In the supine position the main nerves at risk are:
- Brachial plexus (excessive abduction and extension of the shoulder, especially if the head is turned away from the abducted arm),
- Ulnar nerve (direct compression in ulnar groove, especially if the hand is supinated, or stretching by acute elbow flexion)
- Radial nerve (arm allowed to hang over the side of the operating table)
- Supraorbital (compression by the facemask).
The Trendelenburg position is often used to describe any head down position. This position has several physiological effects that may harm the patient including increased venous return, increased intracranial pressure, increased intraocular pressure, increased intragastric pressure and an increased risk of passive regurgitation. The anaesthetist must consider protecting the airway of patients with other risk factors for aspiration with an endotracheal tube.
The lithotomy position will increase venous return. The common peroneal nerve may be damaged by the lithotomy pole resulting in foot drop and sensory loss to the dorsal surface of the foot and antero-lateral lower leg. Both legs should be moved together to minimise damage to pelvic ligaments. Extreme flexion of the hip joint can cause damage by stretching of the sciatic and obturator nerves. Calf compression may predispose to venous thromboembolism and compartment syndrome.
The prone position may be especially dangerous. Usually an anaesthetised patient is turned from supine to prone. This puts the patient at significant risk. There must be sufficient number of people to gently and slowly move the patient. The anaesthetist must be in charge of the positioning and control the movement of the head and neck. Once turned the anaesthetist must carefully assess the risk of pressure damage and nerve damage. The neck must not be hyper-extended nor hyper-flexed. There must be no pressure on the eyes. The endotracheal tube must not be kinked. There should be padding below the pelvis and the chest wall to allow free movement of the abdomen with respiration. The shoulders are at risk of hyperextension.
Macroglossia and oropharyngeal swelling can occur in the sitting position from excessive flexion of the head and neck causing obstruction to venous drainage. It has also been reported in the prone position.
Usually, cardiac index is reduced with a reduction in stroke volume but unchanged heart rate. Mean arterial pressure is maintained by an increase in systemic vascular resistance. The inferior vena cava is at risk of compression.
The functional residual capacity (FRC) is reduced by 40% when a patient goes from the awake upright position to the anaesthetised supine position. In the anaesthetised prone position the reduction in FRC is only 12% and there is an improvement in ventilation/perfusion (V/Q) matching leading to improved oxygenation.
All nerves commonly damaged during anaesthesia are at risk in the prone position, though the incidence of damage is less, and there are some nerves that are only damaged in the prone position. These rare peripheral nerve injuries include the supra-optic, phrenic, recurrent laryngeal and mental nerves.
Postoperative visual loss (POVL) after non-ocular surgery in any position is relatively rare but 60% of cases of POVL followed the prone position. The two injuries most commonly described are ischaemic optic neuropathy and central retinal artery occlusion. The most obvious aetiology is the effect of direct external pressure on the eye causing an increase in intraocular pressure that may lead to retinal ischaemia and visual loss.
POVL can occur with out direct pressure, usually by ischaemic optic neuropathy. The oxygenation of the optic nerve is dependent on the adequate perfusion pressure (i.e. the difference between the mean arterial pressure and intraocular pressure or venous pressure, whichever is greater). Increased intraocular pressure occurs in the prone position.
SELF-ASSESSMENT QUESTIONS
1. Draw the appearance of common arrhythmias that may occur intra-operatively. For each, list common causes and treatment.
2. Draw and explain a normal capnograph pattern. Draw and explain other possible patterns.
3. How may hypothermia be reduced?
4. Why is an adequate saturation reading a poor monitor of adequate ventilation?
5. List the potential usefulness of capnography.
ASSIGNMENT
Discuss what you consider to be the minimum standard of monitoring that must always be used for all anaesthetised patients. What other monitoring should ideally be available?
Chapter title CASE STUDIES
Case 7.1
Bayanaa is about to undergo a laparoscopic cholecystectomy. She is 60 years old and has been a heavy smoker. Her father died at a young age of cardiac disease. She denies any symptoms of chest pain but is a little short of breath on exertion. You plan to do a general anaesthetic.
Question 1
What standard monitoring is indicated for Bayanaa?
Question 2
You consider her to be at increased risk of myocardial ischemia. How will you change your standard monitoring to enable detection of intraoperative ischaemia?
Question. 3
Immediately after intubation of the trachea, the capnograph displays a carbon dioxide concentration of zero. What are the potential causes and outline your next step?
Question 4
You correct the problem but during the operation, you notice that the baseline capnogram is elevated and does not return to zero. What are the possible causes?
Question 5
The saturation reading shortly after arriving to the recovery room is 90%. How will you manage her?