start of inhalation sedation. The reservoir bag should then be observed and appropriate adjustments to the fl ow rate made as appropriate. It is usually possible for a person to inhale further air above the tidal volume. The volume inhaled over and above the tidal volume is called the inspiratory reserve volume (IRV). At the end of a normal exhalation, a person can forcefully breath out; this is forcibly expelled air from the lungs and is called the expiratory reserve volume . The total volume of air that can be expired after a maximum inspiration (TV + IRV + ERV) is known as the vital capacity (VC), and is about 4.5 l for an adult. Only a small amount of this capacity is used in normal breathing. After maximum respiratory effort approximately 1.5 l of air, the residual volume (RV), remains in the lungs. The total lung capacity is around 6 l (TV + IRV + ERV + RV).
The effi ciency of gaseous exchange in the lungs can be seriously impaired by several diseases, such as asthma, bronchitis and emphysema. Patients who smoke may have a reduced arterial oxygen saturation, increased bronchial secretions, a persistent cough and reduced lung function. Expiration is a relatively passive process; inspiration is an active event dependent on muscle activity. In an asthma attack breathing out is diffi cult because the bronchi are constricted (narrowed) and wheezing occurs. When the upper airway is partially obstructed, paradoxical or see - saw respiration occurs. The accessory muscles of respiration become active in respiration in an attempt to increase the volume of the thorax.
Control of r espiration
The rate and depth of respiration is controlled by the respiratory (ventilation) centre which is situated in the brain. Breathing can be altered by chemical and nervous control.
There are chemoreceptors situated in the aorta and carotid arteries and the respiratory centre. They are sensitive to a rise in the level of circulating carbon dioxide (CO 2 ), a drop in blood pH or reduced levels of circulating oxygen (O 2 ). Stretch receptors, situated in the lungs and respiratory muscles, can stimulate the vagus nerve to inhibit inspiration.
Emotions can also affect breathing by infl uencing the higher centres of the brain.
An increased partial pressure of carbon dioxide ( Pa C O 2 ) ( hypercapnia ) is a more sig- nifi cant and sensitive stimulus for respiration than hypoxia; a low Pa O 2 will cause an increase in ventilation rate but this is far less dramatic than the hypercapnic drive. The hypoxic drive is a back - up mechanism, but it may assume importance in patients with chronic lung disease. Medicines that are CNS depressants, including benzodiazepines, can reduce the respiratory drive and reduce chemoreceptor sensitivity.
Oxygen d issociation c urve
Oxygen is essential to maintain life; when tissues become hypoxic (low oxygen levels) they die. For example, when a coronary artery becomes blocked with a thrombus an area of the myocardium (heart muscle) fails to receive oxygen. This results in a myocardial infarct (an area of dead tissue), also called a heart attack or a coronary. When the tissues of the brain are deprived of oxygen for more than three minutes irreversible brain damage occurs. In a sedated patient there is an increased risk of hypoxia because sedative
Partial pressure of oxygen in mm Hg Venous blood
0 20 40 60 80 100
Arterial blood 100
75
50
25
0
Oxygen saturation (%)
Figure 4.2 The oxygen dissociation curve showing the relationship between the partial pressure of oxygen ( Pa O 2 ) and the percentage saturation of haemoglobin with oxygen ( Sa O 2 ). The shape of the oxygen dissociation curve favours the loading of haemoglobin with oxygen in the lungs and the release of oxygen in the tissues. (Adapted from Mallett and Dougherty, 2000 .)
drugs have the potential to cause respiratory depression. Hypoxaemia is defi ned as a low Pa O 2 in the blood; this may be caused by pulmonary disease, cardiovascular collapse drug overdose or airway obstruction by a foreign body.
The alveoli of the lungs are surrounded with capillaries and this is where pulmonary gas exchange occurs. Oxygen and carbon dioxide diffuse across the alveolar - capillary walls by diffusion. Oxygen is carried around the body by haemoglobin, which is found in the red blood cells. Haemoglobin has a great affi nity with oxygen and when com- bined to it is called oxyhaemoglobin. The amount of oxygen in the tissues is termed the oxygen tension or the partial pressure of oxygen ( Pa O 2 ), and is now measured in kilopascals (kPa). It used to be measured in millimetres of mercury (mmHg). The rela- tionship between the Pa O 2 and the percentage saturation of haemoglobin with oxygen is not linear – this is clear from the oxygen dissociation curve (Figure 4.2 ); the line is described as having a sigmoid or ‘ S ’ shape. The top of the graph is fairly fl at and this represents what happens in the lungs; even if the partial pressure of oxygen in the alveoli falls, a high percentage saturation of haemoglobin is maintained. The steep part of the curve represents the Pa O 2 levels found in the tissues. In the tissues, a small fall in Pa O 2 will cause a larger percentage fall in the saturation level of haemoglobin, therefore oxygen is released in areas of low oxygen tension. Thus the sigmoid shape of the oxygen saturation curve ensures that the red blood cell haemoglobin combines with oxygen in the lungs (areas of high partial pressures of oxygen) and releases oxygen when in the tissues.
Pulse o ximetry
Pulse oximetry is a non - invasive method of electromechanically monitoring arterial oxygen saturation ( S aO 2 , sometimes shown as S pO 2 ). Pulse oximetry enables the operator to detect the early onset of hypoxia during procedures involving conscious sedation.
Visual signs of cyanosis will only be detected by a skilled operator when the S aO 2 falls below 85%. The use of a pulse oximeter will enable the clinician to be aware of any impairment of oxygenation before cyanosis develops. Patients will normally have oxygen saturation levels of 96 – 100%.
Pulse oximeters have the following features.
■ A probe with a light - emitting diode and a photosensor (usually a fi nger probe; toe and ear probes are available but they are thought to be less reliable).
■ A digital display window showing the pulse rate and the percentage S aO 2 of the haemoglobin. Many units also have a graphic display where the patient ’ s pulse pressure is shown in a plethysmographic waveform (this is not an ECG (electrocar- diogram) tracing).
■ Audible alarms for the pulse and oxygen saturation programmed to activate when critical values are reached. These levels can be reset, for example the pulse alarm settings will need to be altered for a marathon runner who has a resting pulse rate of 48.
■ Battery back - up in case of power failure.
Pulse oximetry combines the principles of spectrophotometry with plethysmography.
Spectrophotometry uses light absorption and emission to measure a change in the con- centration of oxyhaemoglobin. There is a change in colour in red blood cells as they gain or lose oxygen, consequently oxygenated and deoxygenated blood transmit and absorb different amounts of light. One side of the probe emits light of two different wavelengths (one red and one infra - red) that passes through the tissue of the fi nger and is received by a photodetector on the other side of the probe. A microprocessor analyses the signals received and sends the percentage S aO 2 to the digital display. Plethysmography uses light absorption technology to reproduce waveforms produced by the pulsatile fl ow of blood.
Cardiac c ycle
Knowledge of the cardiac cycle is essential to understand blood pressure and the electri- cal activity of the heart. The cardiac cycle, shown in Figure 4.3 , lasts approximately 0.8 seconds in a person at rest and represents the contraction and relaxation phases of the heart. The systolic (contraction) phase, also referred to as systole , commences with the atria contracting, forcing blood from the atria into the ventricles. The ventricles then contract and eject the blood into the aorta and pulmonary arteries. The walls of the aorta expand to take much of the expelled blood and so act as a reservoir. The intra - cardiac pressure falls as the heart enters the relaxation or diastolic phase of the cycle. During
diastole the atrioventricular valves are open and the ventricles fi ll up with blood from the atria.
Blood p ressure
Each heartbeat produces a pressure wave in the arterial circulation. Blood pressure (BP) is the force exerted on the blood vessel wall by the blood as it is pumped around the body by ventricular contractions. In younger people the blood vessels are more elastic so the arteries absorb some pressure. There is a tendency for BP to rise with age because the larger arteries become harder and less elastic. During diastole the ventricular pressure drops to zero but the arterial pressure does not; the closure of the aortic valve and resist- ance within the arterial system maintains a diastolic pressure.
The BP of an individual can vary dramatically as it is infl uenced by many factors, such as sounds, talking, recent intake of foods, caffeine, smoking, exertion and arm position.
Age, anxiety and fear can all increase the BP, but the diastolic pressure is less likely to be affected by anxiety than the systolic pressure. Measured in the seated, relaxed patient the normal range of arterial pressures may be taken as 100 – 140 mmHg for the systolic and 60 – 85 mmHg for the diastolic pressure. Systolic reading is written above the diastolic value, e.g. 120/70 mmHg. Ideally the blood pressure should be less than 120/80; however, the systolic reading does increase with age. A raised BP is called hypertension , and patients with a sustained BP of 160/90 mmHg (or greater) should be medically assessed.
Patients who may have isolated systolic hypertension (BP > 160/ < 90 mmHg) should also seek medical advice. It should be remembered that dental anxiety can signifi cantly increase BP, so readings should be repeated. Those with repeatedly high readings should be monitored by their doctor. Undiagnosed or poorly controlled hypertension can cause serious health problems such as hardening and narrowing of the arteries (arteriosclero-
Atrial systole
Ventricular systole Complete
cardiac diastole
0.1 seconds
0.3 seconds 0.4 seconds
Total period of one cycle = 0.8 seconds
Figure 4.3 The cardiac cycle.
sis), a risk of a cerebrovascular accident (a stroke), myocardial infarction (heart attack) and renal damage. Low BP is called hypotension and is usually taken as a systolic BP below 100 mmHg; it does not usually cause serious health problems, but patients may be prone to fainting.
Pulse p oints
A pulse is an impulse transmitted to arteries by the contraction of the left ventricle. The pulse refl ects the heart rate. Pulse points can be found in many peripheral or major arteries; often a pulse can be palpated (felt) when the artery crosses a bony prominence or it can be compressed against fi rm tissue. The radial and brachial are the commonly used superfi cial pulses and are detected in arteries that pass close to the surface of the body. The carotid and femoral pulses are major pulses and are used to assess a collapsed patient. In a baby the brachial pulse is used because the neck is poorly developed making the carotid pulse diffi cult to feel. An average resting pulse rate for an adult is around 80 bpm (range 60 – 100 bpm). Children ’ s pulse rates are faster. When the heart rate is slower than 60 bpm then the patient has a slow heartbeat – or bradycardia . A rapid heart rate of greater than 100 bpm is called tachycardia . A pulse will increase with exertion, anxiety, fear, fever, acute pain and certain illnesses, and decrease during fainting and in certain heart disorders. Elite athletes may have a normal resting pulse of below 60 bpm.
Electrical a ctivity of the h eart
The heart is made up of cardiac muscle cells (fi bres) which branch and network to form the myocardium. The fi bres are arranged to allow a contraction wave to spread quickly across the cardiac muscle; no nerves are involved. The heart contracts regularly because it has areas of specialised tissues that conduct electrical activity in a highly organised manner. The heartbeat originates in the pacemaker or sinoatrial ( SA ) node , situated in the right atrium (Figure 4.4 ). The SA node sends out electrical signals across both atria, causing them to contract simultaneously and expel blood into the ventricles. The electri- cal impulses then reach the atrioventricular node , situated at the junction of the atria and ventricles. From here the electrical impulses travel down the bundle of His (a group of cells that run down the fi brous ventricular septum) towards the apex of the heart. The transfer of electrical activity to the Purkinje fi bres (which fan outwards and upwards into the ventricles) instigates ventricular contraction, which expels blood into the aorta and pulmonary artery.
Two sets of nerves from the autonomic nervous system can affect the heart rate by infl uencing the SA node. The sympathetic nerves increase the heart rate, while the para- sympathetic system, via the vagus nerve, slows the pacemaker down. A vasovagal attack (faint) is when the heartbeat is too slow and the brain receives too little blood with a resultant loss of consciousness.
The electrical events of the cardiac cycle can be detected by an ECG and displayed as a trace on graph paper or a monitor. An ECG waveform displaying normal heart function in sinus rhythm , is shown in Figure 4.5 . Various points of the wave are identifi ed by
letters, starting with the letter P. The whole wave is allocated the letters P, Q, R, S and T (see Figures 4.4 and 4.5 ). The fi rst wave is called the P wave and represents the electrical activity of the atria during atrial contraction. The time it takes for the electrical impulse to travel down the bundle of His from the atria to the ventricles is represented by the P – Q interval. The QRS complex is the spread of electrical activity through the ventricles.
The T wave is the last waveform and represents the preparation (repolarisation) of the ventricles for the next contraction.
Anatomy r elevant to v enepuncture
When sedative drugs are to be administered intravenously an IV cannula needs to be placed securely into a superfi cial vein. The nurse needs to be:
■ familiar with the relevant anatomy and physiology of the common venepuncture sites ■ aware of the criteria used to select a vein and the venepuncture device
Atrioventricular (AV) node
Left ventricle Bundle of His
Purkinje fibres Sinoatrial (SA)
node
T P
S
0 0.8
Time in seconds
P = Atrial depolarisation QRS = Ventricular depolarisation
T = Ventricular repolarisation Q
R
Figure 4.4 The conduction pathway of the heart and a normal ECG trace. (Adapted from Mallett and Dougherty, 2000 .)
Figure 4.5 Waveform of sinus rhythm (Mallett and Dougherty, 2000 ).
■ aware of the potential problems that may be encountered (see Table 4.13 in the section on intravenous sedation)
■ aware of the importance of cross - infection control, including the safe disposal of sharps. Venepuncture has the potential to introduce micro - organisms into what is normally a closed, sterile circulatory system. Therefore, an aseptic technique must be used to place the IV cannula
■ aware of the physical and emotional comfort of the patient
■ able to explain the procedure to a patient and answer questions appropriately.
Dentists only use superfi cial veins of the dorsum (back) of the hand and the forearm for IV access. The main accessible veins are shown in Figures 4.6 and 4.7 and are the metacarpal vein (on the dorsum of the hand) and the median cubital vein (often easier to palpate than to visualise). The cephalic and basilic veins are only occasionally used by dentists for IV access. Venous anatomy is, however, very variable, especially the dorsum of the hands.
The cephalic vein rises from the dorsal vein and runs along the radial border of the forearm until it crosses the antecubital fossa as the median cubital vein. The median cubital vein crosses the brachial artery in the antecubital fossa. As a general rule, arteries tend to be placed more deeply than veins, they have thicker walls, do not tend to collapse and have a pulsatile blood fl ow. The brachial artery usually lies beneath the median cubital vein deep to the biceps tendon. Aberrant positioning of the brachial artery does occur and can result in a superfi cial artery. The operator must take care to avoid intra - arterial cannulation.
Figure 4.6 Dorsum of the hand (Girdler and Hill, 1998 ).
Median cubital vein Basilic vein Cephalic vein Pectoralis minor Deltoid
Biceps tendon Pectoralis major divided and turned medially
Biceps Brachial artery
Medial/ulnar border (a)
Lateral/radial border
(b)
Figure 4.7 (a) Venous anatomy of the arm. (b) Detail of the antecubital fossa showing the biceps tendon lying between the median cubital vein and brachial artery. (Adapted from Ellis, 2002 .)
Recommended t asks
(1) Draw a labelled diagram of the heart. Identify which chambers and vessels trans- port deoxygenated blood.
(2) Draw a diagram of the respiratory system.
(3) Outline the path taken by a red blood cell from the left ventricle to the pulmonary vein. Comment on the variations in oxygen saturation that are likely to occur.