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Course Handbook SAAD National Course in Conscious Sedation for Dentistry COURSE HANDBOOK Society for the Advancement of Anaesthesia in Dentistry Introduction The handbook which follows has been produced to complement our National Courses, and so reflect the syllabi set out in current national guidance. We have designed our courses to help provide both dental and medical participants who are ‘new starters’with the necessary knowledge, skills and attitudes ahead of supervised clinical practice with an approved supervisor. This is a mandatory requirement prior to independent clinical practice. The focus of our courses is to ensure that all members of the clinical team are able to deliver safe and effective conscious sedation for their patients who require it, such as those with high levels of anxiety, during potentially unpleasant and distressing surgical procedures or in other situations that might require conscious sedation as an adjunct. The provision of effective pain and anxiety control as part of an agreed and consented treatment plan is a great attribute. In the UK, both the General Dental Council and the Department of Health consider conscious sedation to be an integral and fundamental aspect of the modern practice of dentistry. For those who are already employing sedation in their practice, we hope our courses provide a useful update and stimulus to further advancement. I do hope you will enjoy the course and find this handbook useful. Stephen Jones President of SAAD 1 Editors Leah Adams and Zahra Shehabi Acknowledgments The editors would like to thank the SAAD Faculty for their contributions to this handbook. 2 Table of Contents 1. Anatomy and physiology 4 2. Principles of pharmacology 10 3. Patient assessment and treatment planning 20 4. Local analgesia: tips and techniques 24 5. Intravenous sedation with midazolam 29 6. Inhalational sedation (Relative Analgesia) 35 7. Monitoring 41 8. Management of sedation related complications 47 9. Paediatric sedation techniques 50 10. Alternative sedation techniques 56 11. Sedation for medically compromised patients 61 12. Psychological approaches 67 13. Legal and ethical issues 74 14. Standards of good practice 80 3 1 Anatomy and Physiology Introduction It is important for the sedationist, dental nurses, therapists and hygienists to understand the principles of cardiovascular and respiratory anatomy and physiology in order to appreciate the changes made to these systems by the administration of sedative drugs. CARDIOVASCULAR ANATOMY AND PHYSIOLOGY The circulatory system comprises the: • heart • arteries • arterioles • capillaries • veins Its main function is to deliver oxygen and other cellular nutrition to the tissues while removing the waste products: carbon dioxide and water. The heart acts as two separate pumps working in parallel. The right heart pumps venous blood to the lungs, where oxygen is taken up and carbon dioxide given up (pulmonary circulation). The left heart pumps blood to the tissues/organs where it gives up oxygen and takes up carbon dioxide (systemic circulation). Coronary circulation The myocardium receives its arterial blood supply via the left and right coronary arteries and their branches. The sinoatrial node (SAN) and atrioventricular node (AVN) are mainly supplied by the right coronary artery (90%), with the remainder supplied by the left circumflex artery. Venous drainage is via the coronary veins which drain into the right atrium. Nerve supply to the heart The heart has an autonomic nerve supply. The sympathetic supply is via cardiac branches of the sympathetic trunk while the parasympathetic supply is via cardiac branches of the vagus nerve. Under resting conditions, the heart is under vagal tone (this reduces the heart rate). Stimulation of the sympathetic system is part of the normal response to fear, producing increased heart rate and force of myocardial contraction. Average adult resting heart rate = 70-80 beats per minute Average heart rate for a small child = 130 beats per minute 4 Tachycardia (defined as a heart rate of > 100/min) and bradycardia (defined as a heart rate of < 60/min) can occur in the absence of pathology e.g. the tachycardia associated with exercise and anxiety; the bradycardia associated with sleep. Electrical conduction system The sinoatrial node (SAN) is the origin of the impulses responsible for normal heart rhythm (‘sinus rhythm’). The atrioventricular node (AVN) regulates the frequency of conduction to the ventricles - the delay in conduction between the SAN and AVN allows the ventricles to fill with blood as they depolarise, prior to ventricular contraction. From here the bundle of His fibres radiate out into the Purkinje network. Heart valves and chambers There are four heart chambers: • right atrium • right ventricle • left atrium • left ventricle These are separated by four main valves: • Two atrioventricular valves (tricuspid [left heart]; mitral [right heart]) • Two ventricular outflow valves (aortic; pulmonary) Circulation During systole (atrial and ventricular contraction), blood is pushed through the heart chambers and into the pulmonary and systemic circulation. During diastole the heart muscle is relaxed and the heart fills with blood. Blood returns to the heart from organs and tissues down a pressure gradient with the help of the muscular pump (contraction of calf muscles pushes blood through venous valves) and the respiratory pump (‘bellows’ action of the diaphragm on the inferior vena cava). This venous return is also influenced by other factors such as blood volume and gravity. The circulating blood volume of an adult is 5-6 litres. Cardiac output Cardiac output, the volume of blood circulated in one minute, is approximately 5 litres/min and is dependent on heart rate and stroke volume: Cardiac Output = Heart Rate x Stroke Volume Adult stroke volume is approximately 70mls at rest. It is dependent on end-diastolic pressure after the ventricles have filled with blood (preload) and peripheral resistance (afterload). Increased preload causes increased stretch of cardiac muscle fibres which results in increased force of contraction and increased stroke volume (Starling’s Law of the heart). As blood pressure falls, afterload falls so allowing greater shortening of cardiac muscle fibres, greater power of contraction and a corresponding increase in stroke volume. This system is under neuro-endocrine control and is affected by many drugs e.g.most anaesthetic drugs decrease the contractility of heart muscle. 5 Heart rate is modified by multiple factors, including: • pain and anxiety • vagal tone • endocrine system, e.g. thyroxine, adrenaline • chemoreceptors (hypoxia and hypercarbia) • baroreceptors (sensitive to fall in blood pressure) Blood pressure The pressure generated by blood circulating in the major blood vessels is determined by cardiac output and peripheral resistance. ‘Normal’ blood pressure is 120/70 mmHg. In the management of patients with hypertension, the target clinic blood pressure is 140/80 mmHg (diabetic) or 140/85 mmHg (non-diabetic). Blood Pressure = Cardiac Output x Peripheral Resistance Blood vessel diameter, particularly small vessels, is controlled by the sympathetic nervous system and circulating catecholamines. An increase in sympathetic activity increases vascular tone while a decrease causes vasodilatation. Factors affecting blood pressure HYPERTENSION HYPOTENSION obesity drugs (antihypertensives and antianginals) smoking dehydration high salt/fat intake fitness family history normal pregnancy steroids anxiety recent exercise pregnancy (pre-eclampsia) Arteries, veins and capillaries Arteries carry oxygenated blood from heart to organs in a pulsatile flow. This high-pressure system is a low-volume one, carrying only ~ 20% of circulating blood volume. Veins carry deoxygenated blood back to the heart and are a low-pressure, high-volume system, carrying ~ 75% of circulating blood volume. Gas exchange occurs in the capillary beds. 6 RESPIRATORY ANATOMY AND PHYSIOLOGY The respiratory system comprises: • upper respiratory tract: nose, nasopharynx, larynx • lower respiratory tract: trachea, bronchi • lungs: respiratory bronchioles and alveoli The lungs have a combined surface area of some 500m2 and are directly open to the outside environment. The acinus (branching respiratory bronchioles and clusters of alveoli) is the unit of gas exchange. Blood flows through a rich capillary network intimately related to the acini, so facilitating gas exchange and ensuring that oxygen enters the bloodstream and carbon dioxide is removed. Optimal gas exchange relies on good ventilation and good perfusion of the lung fields. Inspiration and expiration Inspiration is an active process in which muscle contraction works to enlarge the ribcage. The diaphragm is the main muscle of inspiration, assisted by the intercostal muscles. Expiration, however, is usually a passive process of elastic recoil of the lungs and chest wall. Active expiration involves abdominal muscles, diaphragm and intercostal muscles. Lung capacities and volumes These depend on the size of the lungs and thorax and the degree of inspiratory/expiratory effort. Tidal volume is the volume of air moved in one normal breath, usually ~ 500mls. Respiratory rate is ~12 breaths per minute for an adult at rest. Minute volume of ~6 litres/min is the volume of air moved in one minute of normal breathing (this is the volume that the flow rate of an inhalation sedation machine must meet for each patient). Minute Volume = Tidal Volume x Respiratory Rate Vital capacity
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