Caring for the Perioperative Patient E-Book

Paul Wicker

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: Essential Clinical Skills
• Sprache: Englisch

Seitenzahl: 565

Veröffentlichungsjahr: 2013

Beschreibung

Caring for the Perioperative Patient is a practical, evidence-based and innovative book that identifies and discusses the essential core skills and knowledge required by perioperative practitioners to care for their patients.  Divided into two sections, the first explores core perioperative issues, such as pharmacology, communication, homeostasis, and equipment.  The second part of the book looks at more specific perioperative practice issues, including enhanced competence, patient preparation, and care of the patient during anaesthesia, surgery, and recovery. 

This updated new edition is skills-focused and uses examples of techniques or procedures to illustrate how skills can be applied in perioperative practice.  It is essential reading for nurses or operating department practitioners (ODPs) who perform scrub, circulating, anaesthetic and recovery roles whilst caring for perioperative patients, as well as nursing and ODP students working in perioperative care.

• New edition of a successful text for perioperative practitioners and students
• Emphasises holistic patient centred care
• Focused on key skills and knowledge required by practitioners
• Explores the evidence-base for safe and effective practice

Leseprobe

Contents

Foreword

Preface

CORE ISSUES

PERIOPERATIVE PRACTICE

Acknowledgements

Section 1: Core Issues

1 Perioperative Homeostasis

LEARNING OUTCOMES

INTRODUCTION

PRINCIPLES OF HOMEOSTASIS

WATER AND ELECTROLYTE HOMEOSTASIS

THE CARDIOVASCULAR SYSTEM

THE RESPIRATORY SYSTEM

TRAUMA AND WOUND HEALING

REFERENCES

2 Managing Perioperative Equipment

LEARNING OUTCOMES

INTRODUCTION

DUTIES OF THE EMPLOYER

DUTIES OF THE EMPLOYEE

ANAESTHETIC EQUIPMENT

ANAESTHETIC MONITORING EQUIPMENT

SURGICAL EQUIPMENT

REFERENCES

3 Perioperative Pharmacology

LEARNING OUTCOMES

PRINCIPLES OF PHARMACOLOGY

PHARMACOKINETICS AND PHARMACODYNAMICS

MAJOR CHANNELS OF DRUG ADMINISTRATION

DRUGS USED DURING PERIOPERATIVE INTERVENTIONS

ANAESTHESIA

CONCLUSION

REFERENCES

4 Perioperative Communication

LEARNING OUTCOMES

PATIENT COMMUNICATION

PATIENT ADVOCACY

PATIENT CONSENT

ACCOUNTABILITY

DOCUMENTATION

CLINICAL SUPERVISION

INFORMATION TECHNOLOGY WITHIN THE NHS

TEAMWORK

THE PERIOPERATIVE TEAM

CHANGE MANAGEMENT

CLINICAL GOVERNANCE

CONCLUSION

REFERENCES

5 Managing Perioperative Risks

LEARNING OUTCOMES

RISK ASSESSMENT

ACCIDENTAL HAZARDS

WASH HANDS

MAINTENANCE OF EQUIPMENT

MANUAL HANDLING

PRESSURE AREAS/ULCERS

RADIATION HAZARDS

TEMPERATURE CONTROL

CHEMICAL HAZARDS

LATEX ALLERGY

BIOLOGICAL HAZARDS

ORGANISATIONAL HAZARDS

INFECTION CONTROL

DEEP VEIN THROMBOSIS (DVT)

CONCLUSION

REFERENCES

Section 2: Perioperative Practice

6 A Route to Enhanced Competence in Perioperative care

LEARNING OUTCOMES

INTRODUCTION

ROLE OF THE PERIOPERATIVE PRACTITIONER

ENHANCED PERIOPERATIVE COMPETENCIES

PORTFOLIO OF CORE COMPETENCIES FOR ANAESTHETIC ASSISTANTS

CONCLUSION

ACKNOWLEDGEMENT

NES PERIOPERATIVE WORKING PARTIES

REFERENCES

FURTHER READING AND RESOURCES

7 Preoperative Preparation of Perioperative Patients

LEARNING OUTCOMES

INTRODUCTION

PREOPERATIVE PREPARATION

PREOPERATIVE ASSESSMENT

CARE PATHWAYS

DIAGNOSTIC SCREENING

PREOPERATIVE INVESTIGATIONS

REDUCING POSTOPERATIVE COMPLICATIONS

CONCLUSION

REFERENCES

8 Patient Care During Anaesthesia

LEARNING OUTCOMES

INTRODUCTION

GENERAL ANAESTHESIA

ANAESTHETIC EQUIPMENT

MAINTENANCE AND EMERGENCE FROM ANAESTHESIA

REGIONAL ANAESTHESIA

LOCAL ANAESTHESIA, LOCAL INFILTRATION AND NERVE BLOCKS

SEDATION

THE PAEDIATRIC PATIENT

THE PREGNANT PATIENT: CAESAREAN SECTION

THE ELDERLY PATIENT

CONCLUSION

REFERENCES

9 Patient Care during Surgery

LEARNING OUTCOMES

INTRODUCTION

INFECTION CONTROL IN THE PERIOPERATIVE ENVIRONMENT

POSITIONING THE PATIENT

SURGICAL SKILLS

REFERENCES

10 Patient Care During Recovery

LEARNING OUTCOMES

ROLE OF THE RECOVERY PRACTITIONER

KEY CLINICAL SKILLS

REFERENCES

Index

Paul and Joy would like to dedicate this book to:

Our teachers, our students, our colleagues, our friends

Kate, Mairi and Neil Wicker

Barry and Nicola O’Neill

Beth Lynch

Anne Mottram

This edition first published 2010First edition published 2006© 2010 Paul Wicker and Joy O’Neill

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Library of Congress Cataloging-in-Publication Data

Wicker, Paul.

Caring for the perioperative patient/Paul Wicker and Joy O’Neill. – 2nd ed. p.; cm.

Includes bibliographical references and index.

ISBN 978-1-4051-8850-0 (pbk.: alk. paper) 1. Operating room nursing. 2. Preoperative care. 3. Postoperative care. I. O’Neill, Joy. II. Title.

[DNLM: 1. Perioperative Care–nursing. 2. Perioperative Nursing–methods. WY 161 W636c 2010]

RD32.3.W53 2010

617’.917–dc22

2009049072

A catalogue record for this book is available from the British Library.

Set in 9 on 11 pt Palatino by Toppan Best-set Premedia Limited

1 2010

Foreword

In recent years the NHS has seen unprecedented change, resulting in significant healthcare improvement for patients and increased career opportunities within the NHS and its partners. These developments in innovative and advancing levels of practice are also reflected across Europe and many parts of the world.

The dynamic pace of this change has presented significant challenges for clinicians as they endeavour to acquire high-level clinical skills and deliver care while adapting to many new ways of working.

The UK NHS has had to respond dramatically to the changing demographics of its workforce and to high-level policy to drive down waiting times for patients and to increase the capacity for surgery. The perioperative workforce has been at the forefront of such changes and has had to undergo significant transformation in the way it works, crossing traditional healthcare boundaries. The aspirations of health professionals, structured NHS career frameworks, pay modernisation, working practice legislation, advancing levels of practice and the skills escalator concept of skills progression all contribute to the complexity of delivering care to patients.

The provision of education to health professionals giving perioperative care has also undergone significant change, with much more cross-profession delivery of core skills, increased e-learning opportunities and the development of nationally led Advanced Practitioner programmes. This education and exposure to hands-on learning is against a backdrop of increasing workload and advances in technology that now support clinical intervention.

Clinical input for trainees is a vital component in the education of our perioperative workforce, but both students and teachers within the many specialisms that encompass perioperative practice need access to a knowledge base that is modern, comprehensive and fit for purpose. The publication of such a clinically based and up-to-date resource is well overdue, and this book promises to fill that gap.

This text is well structured for easy reference and lends itself to detailed underpinning of knowledge, while at the same time being suitable for use as a quick reference guide. I am confident that it will fulfill a need for both learners and teachers within perioperative care.

Mary Moore

Associate Director, National Orthopaedic Project

Department of Health, London

Preface

Perioperative care has been through a number of changes and has now developed into a truly patient-centred, holistic, evi­dence-based speciality that offers practitioners challenges and opportunities that are rarely seen outside the perioperative environment. Perioperative practitioners are defined in this book as nurses or operating department practitioners (ODPs) who perform scrub, circulating, anaesthetic and recovery roles whilst caring for perioperative patients.

The pressures brought about by initiatives such as the NHS Plan, Clinical Governance and Agenda for Change mean that the care of the patient undergoing surgery is now carried out by many different professionals. Old technique-centred practice has given way to a patient-centred, evidence-based approach. A diverse and challenging perioperative environment has there­fore developed with subsequent challenges for the practitioners who work there.

The purpose of this book is to identify and discuss the essen­tial core skills and knowledge required by perioperative practi­tioners to care for their patients. It is primarily aimed at the period following registration but before the development of advanced perioperative skills, such as those displayed by advanced practitioners. As such it is also a source of informa­tion for nursing and ODP students working in perioperative care.

This evidence-based and innovative book has been written to embrace the changes in the perioperative role. It is skills-orien­tated and uses examples of techniques or procedures to illus­trate how those skills can be applied in perioperative practice. It refers to practitioners rather than nurses or ODPs to ensure the inclusion of all practitioners working in the perioperative environment.

This book is arranged in two sections: Core Issues and more specific Perioperative Practice.

CORE ISSUES

Chapter 1 describes the practitioner’s role in the delivery of therapeutic interventions required because of the anatomical and physiological influences of anaesthesia and surgery. The chapter reviews the concept of homeostasis in the context of holistic perioperative care and identifies the impact of anaesthe­sia and surgery on the systems of the body. Topics include principles of perioperative homeostasis, fluid balance, cardio­vascular homeostasis, the respiratory system, wound healing and trauma.

Chapter 2 discusses the overall management of perioperative equipment with specific reference to the most common types currently in use in the perioperative environment. There is an emphasis on the safe use and maintenance of anaesthetic and surgical equipment.

Chapter 3 discusses the implications of the use of various drugs on perioperative care. There is a discussion on the metab­olism of drugs, and the uses, administration and side effects of common perioperative drugs. Drugs included in this chapter include opiates, muscle relaxants, analgesics, local anaesthetic agents, general anaesthetic agents and antiemetics.

Chapter 4 considers ways to enhance communication in the perioperative environment. There is an exploration of impor­tant aspects of communication in relation to perioperative patients to ensure safe and effective care. There is also reference to the different roles of the perioperative practitioner within the perioperative team. Topics include perioperative patient check­lists, patient advocacy, consent, clinical governance, change management, principles of record keeping and NHS and patient agencies.

Chapter 5 looks at risk management in the perioperative envi­ronment. It explores the main principles of risk management and identifies some of the common perioperative risks to patients. Topics include discussion on specific perioperative risks, such as infection control, pressure area care, deep vein thrombosis prophylaxis, inadvertent hypothermia, latex allergy and smoke inhalation.

The following chapters explore the indicators further and discuss some of the important skills and knowledge displayed by practitioners in anaesthesia, surgery and recovery.

PERIOPERATIVE PRACTICE

Chapter 6 presents the competencies associated with the role of the perioperative practitioner. It is based on the work carried out by NHS Education Scotland (NES) working parties in 2001–2002 and 2006–2008. This chapter presents a discussion of perioperative competencies and their associated indicators for perioperative practitioners and also specifically anaesthetic assistants. The indicators are measurable markers of the achieve­ment of the competencies and are provided as examples of the competencies that practitioners develop in specific clinical areas.

Chapter 7 considers the role of the practitioner in the preoperative preparation of perioperative patients. It explores the techniques and methods of perioperative assessment and the role of the perioperative practitioner in preoperative visiting and care planning. Topics include selection of patients for surgery, assessment of patient’s condition, common concurrent diseases, illnesses and conditions, and preoperative planning to prevent intraoperative and postoperative complications.

Chapter 8 explores the skills and knowledge required by anaesthetic practitioners in the assistance of the establishment and maintenance of anaesthesia. It discusses the different types of anaesthesia, many of the clinical techniques used in anaes­thesia and the role of the anaesthetic practitioner in the anaes­thetic team. Topics include patient care during different types of anaesthesia, airway management and patient monitoring.

Chapter 9 discusses the roles of the scrub and circulating practitioners. It explores some of the clinical techniques that practitioners use during surgery and the part that the practitio­ner plays within the surgical team. Content includes discussion on surgical scrubbing, haemostasis, wound closure, positioning the patient and wound care.

Finally, Chapter 10 considers unique aspects of the role of the recovery practitioner and the main clinical techniques used in recovery. Content includes discussion on the principles of patient care after clinical intervention, patient assessment, airway maintenance, pain management and discharge criteria in postoperative patients. Topics also include common postoperative complications such as nausea and vomiting, shock, hypothermia and airway complications.

We hope that you enjoy using this book to enhance your practice and that it helps you to provide optimum patient care.

Joy O’Neill and Paul Wicker

Readers’ note: Every effort has been made to check the accuracy of drug and product information, and clinical content. However, readers should check the manufacturer’s product information and local workplace policies and protocols before undertaking any intervention.

Acknowledgements

We would like to say thank you to several people for helping us to produce this book. For help with the first edition, we would like to say thank you to Caroline MacDonald, Joanne Wildman and Linda Faulkener for their help reviewing the book proposal. We also thank all the people who have read, reviewed, edited and commented on our work as it has devel­oped, including Rachel Astle, Janet Bidwell, Samantha Mills, Caroline Macdonald, Amanda Clarke, Andrew Clancy, Robert Hughes, Jonathon Kenworthy, Shahid Mirza, Mujahid Zaheer, Janet Barrie, Brian Allsop for the photographs, Beth Lynch for help with the illustrations, and all our colleagues at work. Finally thank you to Beth Knight for her confidence in us and for the role she has played in helping us to achieve our goal.

For help with the second edition, we would also like to thank Adele Nightingale, Jill Ferbrache, Felicia Cox, Africa Bocos, Teresa Hardcastle, Chris Wiles, Victoria Mason and Bernard Pennington.

Section 1

Core Issues

1

Perioperative Homeostasis

Paul Wicker

LEARNING OUTCOMES

 Understand homeostasis.

 Discuss fluid and electrolyte balance in the perioperative patient.

 Describe the structure, function and regulation of the cardiovascular and respiratory system.

 Describe blood pressure regulation.

 Discuss the implications of the metabolic response and the stages of wound healing.

INTRODUCTION

Teamwork is the focus of good perioperative practice. Nowhere is teamwork more obvious than within the human body itself, where the close and efficient functioning of all the individual parts is essential for survival.

The purpose of this introductory chapter is to set the context of perioperative care and to identify links between the patient’s anatomy and physiology, and perioperative care. Everything that happens to the perioperative patient during surgery and anaesthesia has an effect on his or her anatomy and physiology. This makes it important to understand the internal maintenance and control of the body’s systems, and the external control through medical interventions.

The human body is a complex system of parts which can protect itself against major changes to its own internal environment. It does this by preserving a fine balance between all its major organs and systems, by maintaining fluids and electrolytes, blood pressure and oxygenation between particular limits to ensure efficient functioning. Every part of the system is related: for example, the lungs absorb oxygen which is transported by the blood to muscles such as the heart, allowing it to beat and maintain blood pressure. The blood pressure in turn pushes the oxygenated blood around the body to the tissue cells. The blood then progresses back to the lungs where it supplies the lung tissue itself, as well as going on to provide a further source of oxygenated blood to all the cells of the body.

The term homeostasis is often used to refer to the maintenance of a constant environment. In perioperative care; however, it is better to see homeostasis as a dynamic process that results in a peak state for the body under existing circumstances (Clancy et al. 2002). Hence, for example, blood pressure may or may not be maintained at preoperative levels during the peri-operative experience, and during surgery a low blood pressure may be helpful to reduce bleeding, ensuring a bloodless field. However, the main principles of control still hold true – maintaining an ideal environment for body processes to take place under current circumstances. The aim of medical interventions, as external homeostatic controllers, is to support the body’s natural ability to maintain this dynamic homeostatic environment.

The topics associated with homeostasis are huge and this chapter will highlight selected areas of interest and relate them to clinical issues raised later in the book. This chapter therefore, describes some of the ways in which the human body maintains equilibrium, how anaesthesia and surgery affect this balance and how medical interventions support the return to normal homeostasis. Finally, this chapter will look at the human body’s response to stress and the process of wound healing.

PRINCIPLES OF HOMEOSTASIS

To maintain homeostasis naturally, the body needs to:

detect and analyse changes;

take measures to address the changes;

evaluate the effect of measures taken.

Control mechanisms carry out these processes, acting as receptors (detecting the changes), analysers (interpreting the changes) and effectors (acting on the changes to minimise, maximise or regulate them). These mechanisms detect changes in normal values and try to bring them back to within the normal homeostatic range. An example of this system is the acid–base balance, where the buffer systems (described later in this chapter) act in unison to maintain the pH of body fluids within a normal range of around 7.35–7.45. Under normal circumstances, the body’s buffer systems are able to maintain this balance; however, during illness, disease or because of trauma such as surgery or anaesthesia, the body may need support from external controls (medical interventions) to regain equilibrium.

Most of the body’s own control mechanisms work through negative feedback – a change occurs to the body’s environment and then mechanisms to cancel the changes are activated. Blood glucose regulation, for example, involves either the release of insulin to lower blood glucose or the release of glucagon to raise it. In either case, blood sugar levels are brought back to within the normal range.

Occasionally the control mechanisms work through positive feedback and a control mechanism to promote changes is activated – for example, blood clotting, where the blood undergoes changes that allow it to clot and therefore reduce blood loss. Once the need has passed, the blood then returns to its normal state.

Internally, the organs act as both independent and interactive homeostatic controllers. This topic goes beyond the scope of this book. However, in the perioperative patient, several systems are specifically important because they are critical to the patient’s immediate survival and are also the target of many perioperative interventions. Fluid and electrolyte balances are important perioperative considerations because of the potential for blood loss and possible hypovolaemia. Medical interventions that support the effects of blood and fluid loss, and help maintain electrolyte balance, therefore, merit consideration. The regulation of the respiratory and cardiovascular systems is also crucial in both the long and the short term. The aim of many anaesthetic functions is to control these systems to provide the optimum physiological environment during surgery.

Table 1.1 Terminology associated with fluid compartments.

WATER AND ELECTROLYTE HOMEOSTASIS

Table 1.1 describes the fluid compartments of the body. Total body water is distributed among all the fluid compartments of the body. Of the 40 litres present in a 68kg (150 lb) male, 65% is intracellular and 35% is extracellular. Extracellular fluid is composed of 25% tissue fluid, 8% blood plasma and lymph, and 2% transcellular fluid such as cerebrospinal fluid (CSF) and synovial fluid.

Osmosis is the main process that distributes fluid throughout these compartments (Watson & Fawcett 2003). The term ‘osmolarity’ refers to the concentration of solutes (such as potassium) in the solution (such as water). Osmosis is a special form of diffusion which involves the passage of water across a selectively permeable cell membrane that is freely permeable to water but not freely permeable to solutes. This process aims to equalise the concentrations of the solution on each side of the membrane. In osmosis, water will flow across a membrane toward the solution that has the higher concentration of solutes, because that is where the concentration of water is lowest (Figure 1.1). A solution with a high osmolarity has high osmotic pressure.

Fig. 1.1 Osmosis.

An important effect of the movement of ions and water across cell membranes is the development of an electrical charge across the membrane. The resting potential is the charge across the membrane of an undisturbed cell. When the cell is stimulated, the electrical charge may be increased, causing an ‘action potential’. In nerves, for example, this represents the movement of information away from the cell body and down the nerve. In muscles, the action potential causes the contraction of muscle fibres.

Other methods which the cell uses to transport water and electrolytes include:

filtration, which is a passive process where hydrostatic pressure (blood pressure) forces fluid and solutes across a membrane barrier;

carrier-mediated transport, which involves specialised cell proteins binding to ions or organic substances, facilitating their entry to or exit from the cell;

vesicular transport, which involves the movement of materials within small membranous sacs or vesicles.

Fluid balance

A person is in a state of fluid balance when water gain equals water loss; for example, a water intake of 2.5 litres a day, taken in by food and drink, is balanced by water loss via routes such as faeces, expired air, sweat and urine.

Fluid intake is mainly controlled by the thirst centre in the hypothalamus which generates the sensation of thirst. Water output is regulated by varying urine volume. This system is mainly controlled by the antidiuretic hormone (ADH), but also to a lesser extent by aldosterone and atrial natriuretic factor (ANF). Blood osmolarity is maintained because both sodium and water are either retained or excreted.

Changes in the osmotic pressure exerted by plasma influence the release of ADH. High osmotic pressure (i.e. dehydration) leads to release of ADH; low osmotic pressure (i.e. hydration) reduces excretion of ADH. This system is so efficient that under normal conditions water balance is maintained to within 2% of the normal homeostatic range (Clancy et al. 2002).

ANF is a peptide released by walls of the cardiac atrium in response to high sodium chloride (NaCl) concentration, high extracellular fluid volume or high blood volume. ANF inhibits NaCl reabsorption in the distal convoluted tubule and cortical collecting duct of the kidneys. It also dilates the afferent glomerular arteriole and constricts the efferent glomerular arteriole. This increases the glomerular filtration rate, which increases NaCl excretion, raises urinary filtration rate and therefore increases the rate of urine production.

Volume depletion (hypovolaemia) is a loss of total body water volume when osmolarity remains normal. Vomiting, diarrhoea, burns, haemorrhage or renal failure can cause this. Addison’s disease results in dehydration leading to loss of total body water volume with an associated rise in osmolarity. This condition can also be caused by lack of drinking water, diabetes, profuse sweating or diuretics. Infants are more vulnerable to this condition.

Electrolyte balance

The balance of major electrolytes such as sodium (Na+), potassium (K+), calcium (Ca2+), hydrogen (H+) and bicarbonate is essential to ensure homeostasis and the proper functioning of the body’s processes (Saladin 2009).

Maintaining electrolyte and water balance are three major hormones: ADH, which promotes water retention independently of Na+ and K+ concentration; aldosterone, which promotes retention of water and Na+, and secretion of K+; and ANF which increases NaCl secretion.

Electrolyte metabolism

Sodium and potassium

Sodium and potassium levels are critical to homeostasis because of their many roles. These two electrolytes contribute to maintaining membrane potentials, a major role of the sodium–potassium pump. Sodium is also responsible for 90–95% of osmolarity of extracellular fluid (ECF) and potassium is the primary cation in intracellular fluid (ICF).

The normal sodium intake of around 3–7 g/day exceeds the 0.5 g/day needed for survival. Normal blood level ranges are:

Na

+

, 130–145 mmol/litre;

K

+

, 3.5–5.5 mmol/litre.

The homeostasis of water, sodium and potassium levels occurs by various linked systems:

aldosterone/ANF;

ADH;

oestrogen/progesterone;

salt craving.

Intercalated cells in the collecting duct of the kidneys also control potassium levels (Saladin 2009).

Calcium

ECF contains a low concentration of calcium; however calcium exerts great influence on the body systems. Low calcium concentration increases the excitability of cells and in muscle cells this may lead to tetany. High concentrations of calcium ions make the cells less excitable and may lead to symptoms such as muscle weakness and bowel stasis. Other roles of calcium include skeletal mineralisation, muscle contraction, exocytosis (release of substances such as hormones from the vesicles of certain tissue cells) and blood clotting. Blood levels of 2.25–2.9 mmol/litre are normal.

Calcitonin is a hormone that takes part in calcium and phosphorus metabolism and affects bone deposition and resorption. Low intracellular Ca2+ levels influences calcitonin. The thyroid gland produces most calcitonin.

Phosphate

Phosphate is concentrated in ICF and variations in levels are well tolerated. Roles include being an ingredient of nucleic acids, phospholipids and some enzymes and coenzymes such as adenosine triphosphate. Phosphate also activates enzymes in metabolic pathways and buffers pH. Maintenance and control of phosphate homeostasis is by tubular reabsorption in the kidneys.

Chloride

Sodium and chloride homeostasis are linked. Chloride preserves osmolarity of ECF and plays a part in stomach acid production. The so-called ‘chloride shift’ (influx of chloride ions into cells) helps to maintain pH and electrical neutrality within cells. Chloride has a strong attraction to Na+, K+ and Ca2+, and is retained or secreted with Na+ by the kidneys.

Acid–base balance

The acid–base balance is a critical part of homeostasis – the normal pH range of ECF (including blood) is 7.35–7.45. Several processes within the body affect acid–base balance maintenance. For example, normal metabolism produces substances such as lactic acids, phosphoric acids, fatty acids, ketones and carbonic acids, which all affect pH. Even absorption of acidic foods may alter blood pH (Saladin 2009). Maintenance of acid–base balance is through buffer systems in the blood, respiration and renal systems.

Blood-based buffers

The blood itself contains three buffering systems that help to stabilise pH – the bicarbonate buffer, the phosphate buffer and the protein buffer. The bicarbonate buffering system works through the association and disassociation of carbon dioxide, water, hydrogen, carbonic acid and bicarbonate, according to the following formula:

One molecule of carbon dioxide (CO2) combines with one molecule of water (H2O) to become one molecule of carbonic acid (H2CO3). The release of hydrogen ions from the carbonic acid increases the acidity of blood.

The carbonic acid molecule is not especially stable and will break down in one of two ways. The carbonic acid molecule may break down back to carbon dioxide and water; the equation moves to the left, resulting in alkalosis. Alternatively it could break down into one molecule of bicarbonate and one hydrogen ion and the equation moves to the right, resulting in acidosis. The chemical reactions have the effect of equalising the levels of bicarbonate/hydrogen and carbon dioxide/water – so regulating the balance between alkalinity and acidity.

The phosphate buffer system works as follows:

Again, an increase in hydrogen ions increases acidity.

The protein buffer system works because the acidic side groups of protein molecules release hydrogen ions (increasing acidity) and amino side groups bind hydrogen ions (increasing alkalinity).

Respiratory buffer

The second main buffering system is a bicarbonate buffer within the respiratory system. This system is nearly three times more powerful as a buffer system than blood. The process is the same as the bicarbonate system in blood.

Renal buffer

The third and most powerful buffer system to adjust pH is renal control. The renal tubules secrete H+ into urine and this secretion involves chemical processes using ammonium chloride and phosphate. The pH of urine affects the pH of blood by the diffusion of hydrogen ions through the membranes of the renal tubules into the kidney’s capillaries (Saladin 2009).

Acidosis and alkalosis

Increasing acid or a significant loss of bicarbonate results in acidosis. H+ ions diffuse into cells where they are buffered by the protein buffer system, and simultaneously K+ ions are driven into the ECF. The result is membrane hyperpolarisation, which affects, for example, muscle and nerve cells function. Alkalosis is essentially the opposite of this: H+ ions diffuse out of the cells, K+ ions diffuse in and the membrane becomes hypopolarised.

Acidosis has several possible causes, for example carbon dioxide retention (leading to increased carbonic acid); ketone or organic acid production (such as ketoacidosis or lactic acidosis); the use of acidic drugs; or renal failure resulting in the inadequate excretion of H+ ions. The patient may suffer symptoms of headache, blurred vision, fatigue and weakness.

Metabolic alkalosis may be the result of various conditions including, for example, inadequate generation of metabolic acids, overuse of antacids or severe vomiting. Symptoms may include weakness, muscle cramps and dizziness.

Perioperative implications of fluid and electrolyte balance

Various factors present during anaesthesia and surgery can lead to water imbalances which must either be controlled by the body systems or supported through medical interventions (Heitz & Horne 2004).

Preoperative fasting, while necessary to reduce the risk of aspiration of stomach contents during induction or recovery from anaesthesia, may also result in dehydration in elderly, young or sick patients.

Surgery may have a significant effect on water balance because of rapid changes in water level and distribution. High blood loss, for example, and resulting hypovolaemia can be quickly fatal. Hypovolaemia can also develop because of acute renal failure following disruption of perfusion of the kidneys, respiratory losses during ventilation or insensible losses through sweating because of postoperative pyrexia or disturbances in temperature. Other reasons include blood loss from wound drains, loss of peritoneal fluid and loss by vomiting, diarrhoea and evaporation by exposed moist tissues.

Surgery also has an effect on other systems of the body, especially the endocrine system, which can lead to changes in the homeostasis of water and electrolytes. For example, ADH is released because of hypotension, blood loss or dehydration, leading to water retention. Adrenaline (epinephrine) is released because of surgical stress and can lead to sodium and water retention by the kidneys (Clancy et al. 2002).

Management of the water balance is necessary because of these perioperative challenges. Fluid balance charts are the most common means of recording and estimating the fluid needs of patients. Consumed or infused fluids are matched against fluid losses such as urine output, exudates from wounds or blood loss. Weighing swabs during surgery gives an estimate of the volume of blood loss. The continuing assessment of patients to guard against dehydration or overhydration is therefore essential during all phases of their care (Hatfield & Tronson 2008).

Conditions such as renal depression, blood loss, vomiting or diarrhoea are likely to affect the perioperative electrolyte balance. Vomiting in particular leads to the loss of Na+, Cl– and K+ ions, and gastric acids, leading to metabolic alkalosis. Anaesthetic drugs, such as morphine can stimulate vomiting, and so antiemetics (such as metoclopramide, cyclizine or ondansetron) are often administered concurrently. The problems of unproven efficacy and sometimes serious side effects of antiemetics have led to alternatives such as acupressure and acupuncture being evaluated in some areas (Abraham 2008).

Diarrhoea is common following abdominal surgery for various reasons, such as the use of enemas, use of antiemetic drugs, and following trauma or excision of the large or small bowel. When there is diarrhoea the bowel secretes several litres of fluid a day, which is high in bicarbonate, and may therefore lead to metabolic acidosis and overall electrolyte loss (Waugh & Grant 2004).

Intravenous replacement

The perioperative infusion of fluid and blood products supports homeostasis. Using fluid replacement therapies it is possible to influence the water and electrolyte content of the fluid compartments to achieve the desired result. It is important to realise that surgery and anaesthesia may have altered the body’s needs either permanently, because of anatomical and physiological changes, or temporarily during the recovery phase and period of return to normality. The continuing assessment of the patient’s needs is part of the science of anaesthesia and is beyond the scope of this book. However, following diagnosis and establishment of the patient’s requirements, fluid and electrolyte replacement therapy will involve the practitioner in the use of colloids, crystalloids and blood products.

Colloids are plasma expanders – they selectively increase fluid in plasma while having a small effect on the intracellular compartments. Colloids include the protein-based gelatin (Gelofusine) and the carbohydrate-based dextran. They work by increasing or restoring the colloid pressure of plasma, resulting in increased fluid movement into the intravascular space. Infusion provides a short-term increase in plasma volume and their effects reduce as they are excreted.

Crystalloid infusions provide electrolytes and water, and support both intracellular and extracellular compartments. Crystalloids can be hypertonic, hypotonic or isotonic. Hypertonic solutions draw water out of cells, causing them to shrink. Mannitol is an example of such an infusate that shrinks brain cells and reduces pressure inside the cranium. Hypotonic solutions draw water into cells causing them to swell. There is a potential danger of lysis, where the cell membranes burst, and therefore it is rare to use hypotonic solutions. Cells suspended in an isotonic solution would neither increase nor decrease in size because the osmotic pressure of the fluid inside the cells is equal to that outside the cells. Isotonic solutions are widely used because they support both the intracellular and extracellular compartments.

Isotonic solutions, such as saline 0.9%, dextrose 5% and Hartmann’s solution, have an osmotic pressure similar to that of plasma and therefore move between the compartments in a similar way to normal body fluids. In hypovolaemia, isotonic crystalloids, the most common of which is sodium chloride 0.9% (normal saline), replace fluid in the intravascular compartment and will slowly diffuse into the intracellular space.

Dextrose 5% is a solution of glucose in water. At a concentration of 5% it has an equal osmolarity to body fluids and so on infusion it remains largely in the intravascular compartment since it cannot diffuse rapidly into the cells. However, the body’s normal metabolic processes use up the glucose, leaving behind water, which is hypotonic. Intracellular volume increases as this water is drawn into the cells. Dextrose 5% is therefore effective at increasing both extracellular and intracellular fluid. The 25 g of glucose in 0.5% solution also provides a little energy – roughly equivalent to two chocolate biscuits per 500 ml!

Hartmann’s solution provides a more complex mix of electrolytes, which closely resembles that of extracellular fluid, except for the presence of lactate rather than the bicarbonate normally found in blood. Other less common infusates include potassium chloride infusion, combinations such as dextrose/saline infusions and hyper/hypotonic variations of these solutions, such as 2.5% sodium chloride (Hatfield & Tronson 2008).

THE CARDIOVASCULAR SYSTEM

For the body to stay alive, each of its cells must receive a continuous supply of nutrition and oxygen. Simultaneously, the body removes carbon dioxide and other materials produced by the cells. The body’s circulatory system – the heart and blood vessels – continuously support this process of nutrition delivery and waste removal. The circulatory system pumps blood from the heart to the lungs to receive oxygen. Blood then returns to the heart to be pumped throughout the body and then returns to the heart to begin again. The lymphatic system, which is an important constituent of the circulatory system, collects interstitial fluid and returns it to the blood. The cardiovascular system and the respiratory system are linked and could be seen as interlocking and interdependent systems. They are jointly responsible for carrying oxygen from the air to the bloodstream and tissues, and expelling the waste product of carbon dioxide.

Fig. 1.2 Anatomy of an artery and a vein.

Arteries and veins

Both arteries and veins consist of three major layers called ‘tunica’ (Figure 1.2). Endothelium lines the inner layer of the vessel, the tunica intima. The tunica media is the middle layer, which is much thicker in arteries and contains an extra thick layer of smooth muscle that can constrict to reduce the diameter of the vessel. Blood vessels have an outer layer called the tunica adventitia. Arteries use smooth muscle contractions to alter their internal diameter, which increases or decreases the resistance to the flow of blood provided by pressure from the heart. Smooth muscle in veins can only contract weakly and so there are one-way valves that aid the flow of blood. Squeezing veins, by contracting muscles (such as calf muscles in the leg), produces blood flow through the one-way valves. Venous pressure is low in comparison with arterial pressure because the blood has lost the pressure exerted by the heart after moving through the smaller blood vessels and capillaries.

Arteries carry blood loaded with oxygen and nutrients away from the heart to all parts of the body. The only exception to this rule is the pulmonary artery which in fact carries deoxygenated blood from the heart to the lungs. Eventually arteries divide into smaller arterioles and then into even smaller capillaries, the smallest of all blood vessels. The network of tiny capillaries is where the exchange of oxygen and carbon dioxide between blood and body cells takes place.

The return of blood via the heart to the lungs for reoxygenation is of equal importance. Capillaries join to form venules and then veins, which flow into larger main veins, until finally they deliver deoxygenated blood back to the heart.

The heart

The heart consists mainly of cardiac muscle which works like a pump and contracts automatically (without conscious thought) to send blood to the lungs and the rest of the body. The heart consists of four chambers: each half of the heart consists of an upper chamber (called the atrium) and a larger lower chamber (called the ventricle). The major blood vessels entering and leaving the heart are shown in Figure 1.3.

The aorta is the largest artery in the body. It extends upward from the left ventricle of the heart, arches over the heart to the left, and descends just in front of the spinal column. The first portion of the aorta is the ascending aorta, which curves into the arch of the aorta. Three major arteries originate from the aortic arch: the brachiocephalic artery (which then branches into the right common carotid artery and the right subclavian artery), the left common carotid artery and the left subclavian artery.

The cardiac cycle

Each heartbeat consists of a ‘cardiac cycle’. As the heart relaxes, both atrium chambers fill with blood: deoxygenated blood comes into the right side from the superior and inferior vena cava, and oxygenated blood returns to the left side from the lungs via the pulmonary veins. The heart valves open and the atria contract (systole) and force the blood into the ventricles. The ventricles then contract to pump the deoxygenated blood through the pulmonary valve into the lungs and the oxygenated blood through the aortic valve into the body’s main circulatory system. The atria relax once more (diastole) and fill with blood to restart the cycle. As the valves slap shut to prevent the blood’s backflow, they make a noise described as the ‘lub–dub’ sound of a heartbeat (Tortora 2008).

Fig. 1.3 The heart.

Conduction of impulses within specialised muscle tissue in the heart itself largely controls this process. The sinuatrial node, found in the right atrium, starts an impulse which spreads throughout the atrium, causing atrial contraction. It then arrives at the atrioventricular (AV) node which ‘forwards’ it to the bundles of His and the Purkinje fibres, spreading the signal throughout the ventricles, which cause these parts to contract. The intrinsic properties of these nodes normally control the rate of heartbeat; however, the autonomic nervous system (producing emotions such as anxiety or fear) and hormones such as thyroxine and adrenaline (epinephrine) also influence the rate of the heartbeat. The electrical activity of the heart produces the signals that can be picked up by electrocardiographs.

This outline of the cardiovascular system serves only to show the complexity of the system. Reference to texts on anatomy and physiology are essential for a full understanding of this system (e.g. Tortora 2008).

The cardiovascular system delivers oxygen and nutrients to the cells of the body, and removes waste products. This system is inextricably linked to the survival of the patient and is thus vitally important in perioperative care (Clancy et al. 2002). Two important areas for the perioperative patient will now be considered – interpreting cardiac rhythms and the homeostasis of blood pressure.

The electrocardiogram

The electrocardiogram (ECG) measures the electrical changes of the heart as it goes through the cardiac cycle. It is therefore useful for diagnosis of abnormal cardiac rhythms and other cardiac pathology. Therefore, ECG machines provide early warning of cardiac problems during anaesthesia and surgery.

Normal sinus rhythm (NSR)

The sinus node produces an electrical impulse that launches a normal heart rhythm. This signal radiates through the right and left atrial muscles, producing electrical changes represented by the P-wave on the ECG. The electrical impulse stimulates the atria causing them to contract. This contraction of cardiac muscle is known as systole. The electrical impulse then continues to travel into and through specialised cardiac tissue known as the AV node, which conducts electricity at a slower pace, and forwards the impulse into the ventricles causing ventricular systole. The slower conduction rate will create a pause (PR interval) before stimulation of the ventricles. The pause between atrial and ventricular systole allows blood to empty into the ventricles from the atria before ventricular contraction, which propels blood out towards the aorta and the pulmonary artery. The QRS complex of waves on the ECG represents ventricular contraction. The T-wave follows, representing the electrical changes in the ventricles as they are relaxing. The QRS complex hides the electrical changes produced by atrial relaxation. The cardiac cycle then repeats itself after a short pause (Jevon & Ewens 2002).

Fig. 1.4 ECG of a single cardiac cycle.

Therefore, a cardiac cycle is represented on an ECG by P-waves which are followed after a brief pause by a QRS complex, then a T-wave (Figure 1.4).

Normal sinus rhythm (Figure 1.5) suggests that the rhythm produced by the sinus node is travelling through the tissues of the heart in a normal fashion and rate. The normal range of heart rate varies by individual and is influenced by factors such as age, health, body mass index, fitness and emotional state. An adult’s heart rate is around 60–80 beats per minute at rest. A newborn infant may have a heart rate up to 150 beats per minute, while a child of 5 years old may have a heart rate of 100 beats per minute.

Fig. 1.5 Normal sinus rhythm.

Fig. 1.6 Tachycardia.

Tachycardia

Sinus tachycardia is a fast heart rate which occurs with a normal heart rhythm (Figure 1.6). This means that although the impulses producing the heartbeats are normal, they are occurring at a faster pace. This occurs because of conditions such as shock and drug actions, as well as exercise, excitement, anxiety or as a reaction to stress.

Supraventricular tachycardia (SVT)

This is an abnormal heart rhythm because the sinus node does not produce the impulse stimulating the heart, which instead comes from tissues around the AV node. Rapid generation of these abnormal electrical impulses leads to a heartbeat that may reach up to 280 beats per minute (Figure 1.7).

Ventricular tachycardia is similar; however, it results from abnormal tissues in the ventricles producing a rapid and irregular heart rhythm. Poor cardiac output usually accompanies this rapid heart rhythm and can therefore be significant during surgery.

Fig. 1.7 Supraventricular tachycardia.

Fig. 1.8 Atrial flutter.

Atrial flutter

This abnormal rapid heart rhythm arises because the impulse which arises from the abnormal tissue in the atria bypasses the AV node. Without the dampening effect of the AV node, the impulse is repeated rapidly, resulting in the faster abnormal rhythm (Figure 1.8).

Sinus bradycardia

Sinus bradycardia presents as a slow heart rate with a normal sinus rhythm (Figure 1.9). It is usually benign, although in some circumstances it may need treatment, for example when caused by stimulation of the vagus nerve during surgery. It is also a result of using medications such as beta-blockers (see Chapter 3).

Atrioventricular block (AVB)

This abnormal rhythm occurs because of a block in conduction between the sinus node and the AV node. There are various types of AV block depending upon the mechanism of block. For example, second-degree heart block occurs when some signals from the atria do not reach the ventricles, resulting in ‘dropped beats’ (Figure 1.10). Third-degree or complete AV block results in a total lack of atrial impulses passing through the AV node and the ventricles therefore create their own rhythm. This rhythm is usually extremely slow and so the heartbeat must be raised to within the normal range with a pacemaker.

Fig. 1.9 Sinus bradycardia.

Fig. 1.10 Atrioventricular block.

Premature atrial contraction (PAC)

The sinoatrial node fires early, causing the atria to contract early in the cycle, resulting in an irregular rhythm (Figure 1.11).

Premature ventricular contraction (PVC)

The AV node fires early, causing the ventricles to contract early in the cycle, resulting in an irregular rhythm (Figure 1.12).

Atrial fibrillation

This is a result of many sites within the atria firing electrical impulses in an irregular fashion, causing irregular heart rhythm (Figure 1.13). This abnormal heart rhythm is unusual in children.

Fig. 1.11 Premature atrial contractions.

Fig. 1.12 Premature ventricular contractions.

Fig. 1.13 A trial fibrillation.

Asystole

Asystole represents the lack of electrical activity of the heart and therefore the ending of heartbeats. Note the absence of a completely straight line which signals continuing residual electrical activity (Figure 1.14).

Fig. 1.14 Asystole.

Blood pressure homeostasis

There are two basic mechanisms for regulating blood pressure: short-term mechanisms, which regulate blood vessel diameter, heart rate and contractility; and long-term mechanisms, which regulate blood volume (Clancey et al. 2002).

Nervous control of blood pressure

The sympathetic and parasympathetic nervous systems mainly provide the nervous control of the blood pressure. The vagus nerve provides the parasympathetic nerve supply to the heart. Stimulation of the vagus nerve (e.g. during surgery on the vagus such as a vagotomy) leads to a paradoxical decrease in sympathetic nervous system activity. Blood pressure falls because of vasodilation, a lower heart rate (bradycardia) and lower cardiac output.

Sympathetic nerve fibres stimulate vasomotor fibres within the smooth muscle of arteries, resulting in vasoconstriction; this causes blood pressure to rise. Lack of sympathetic stimulation results in relaxation of the arteries, an increased arterial diameter, and therefore reduces blood pressure.

In the heart, sympathetic activity stimulates the sympathetic cardiac nerves, which results in increased heart rate and contractility, higher cardiac output and increased blood pressure. Simultaneously the vagus (parasympathetic) nerve displays decreased activity.

Hormonal control of blood pressure

Increased sympathetic impulses to the adrenal glands lead to the release of adrenaline (epinephrine) and noradrenaline (nor-epinephrine) into the bloodstream. These hormones act on chemoreceptors to increase heart rate, contractility and vasoconstriction. The effect is slower acting and more prolonged than nervous system control.

Short-term regulation of rising blood pressure

Baroreceptors, specialised areas of tissue which are sensitive to pressure, provide short-term control of rising blood pressure. Rising blood pressure leads to stretching of arterial walls and stimulation of baroreceptors in the carotid sinus, aortic arch and other large arteries of the neck and thorax. The baroreceptors send an increased frequency of impulses to the brain, which leads to increased parasympathetic activity and decreased sympathetic activity. This results in a decreased heart rate and an increase in arterial diameter, which aim to reverse the increasing blood pressure (Jevon & Ewens 2002).

Short-term regulation of falling blood pressure

Falling blood pressure inhibits the baroreceptors, leading to a decrease in impulses sent to the brain. This causes a paradoxical increase in sympathetic activity leading to three effects:

increased heart rate and increased contractility;

increased vasoconstriction;

release of adrenaline (epinephrine) and noradrenaline (nor-epinephrine) from the adrenal glands, which increases heart rate, contractility and vasoconstriction.

The combined effect helps to increase blood pressure.

Long-term regulation of blood pressure

Long-term control of blood pressure is primarily accomplished by altering blood volume. The loss of blood through haemorrhage, accident or donating a pint of blood will lower blood pressure and trigger processes to restore blood volume and therefore blood pressure back to normal. Long-term regulatory processes conserve body fluids by renal mechanisms and stimulate intake of water to normalise blood volume and blood pressures. (See section on water/electrolyte balance pages 5–14.)

Haemorrhage (loss of blood)

When there is loss of blood, blood pressure and blood volume decrease. Juxtaglomerular cells (a small endocrine organ associated with individual nephrons within the kidneys) monitor changes in the blood pressure. If blood pressure falls too low, these specialised cells release the enzyme renin into the bloodstream and launch the renin/angiotensin mechanism. This process consists of a series of steps aimed at increasing blood volume and blood pressure.

The first step of this process is angiotensin I formation. As renin travels through the bloodstream, it binds to an inactive plasma protein, angiotensinogen, activating it to become angiotensin I.

The second step is the conversion of angiotensin I to angiotensin II as it passes through the lung capillaries. Angiotensin II is a vasoconstrictor and therefore raises blood pressure in the body’s arterioles, however, its main effect is on the adrenal gland. Here, in the third step, it stimulates the cells of the adrenal cortex to release the hormone aldosterone.

Aldosterone stimulates increased sodium reabsorption from the tubule cells. The increased sodium levels in the tubules make sodium move into the bloodstream, closely followed by water.

Increase in osmolarity

Dehydration resulting from sweating, diarrhoea or excessive urine flow will cause an increase in osmolarity of the blood and result in a decrease in blood volume and blood pressure. As osmolarity increases there is both a short- and long-term effect. In the long term, the hypothalamus sends a signal to the posterior pituitary to release ADH, which increases water reabsorption in the distal convoluted tubules and collecting tubules of the kidney. Water moves back into the capillaries, decreasing the osmolarity of the blood, increasing the blood volume, and therefore increasing the blood pressure.

A short-term effect of increased osmolarity is the activation of the thirst centre in the hypothalamus. The thirst centre stimulates the individual to drink more water and thus rehydrates the blood and the extracellular fluid, restoring blood volume and therefore blood pressure.

Pharmacology and blood pressure homeostasis

There are many chemicals that influence blood flow and blood vessel diameter and therefore have a direct action on blood pressure. Table 1.2 gives some examples of drugs that act on the cardiovascular system. See Chapter 3 on pharmacology for further discussion of such drugs.

Shock

Shock is a condition that arises from a failure of the circulatory system to deliver oxygen and nutrients to the tissues of the body, and to remove waste products. Before going into shock in detail it is important to understand the relationship between cardiac output, peripheral resistance and blood pressure. Control of blood circulation is through the interaction of blood volume (provided via cardiac output), blood vessel diameter (vasocon-striction – especially peripherally) and the pressure gradient that ‘pushes’ blood through the tissues (blood pressure).

Cardiac output is the volume of blood per minute ejected from the heart. The volume of blood ejected every beat is the stroke volume.

This is the cardiac output for an average heart beating 60 times per minute with a stroke volume per ventricle of 70 ml (so 140 ml total).

Various factors affect stroke volume. For example, low venous return reduces the volume of blood refilling the heart between beats (end-diastolic volume) and therefore reduces stroke volume. Cardiac contractility affects the percentage of blood ejected from the heart on every beat – a strong contraction will empty the heart more efficiently than a weak contraction. A huge variety of factors such as autonomic nervous stimulation, hormones and drugs affect the heart rate.

Table 1.2 Examples of drugs acting on the cardiovascular system.

Drug

Action

Uses

Adrenaline (epinephrine)

α agonist – coronary and peripheralvasoconstriction β agonist– increased heart rate and myocardial contractility

Used in cardiac arrest to stimulate the heart muscles

Isoprenaline, dopamine

β agonist – increased rate and force of heart beat, vasodilation

Cardiogenic shock in infarction or cardiac surgery

Ephedrine

Increases heart rate and myocardial activity. Increases peripheral vasoconstriction

Reversal of hypotension, e.g. from spinal or epidural anaesthesia

Phentolamine

α antagonist – vasodilation and myocardial stimulant. Overall effect of reducing blood pressure

Used as a vasodilator in cardiobypass surgery and in cardiogenic shock

Atenolol

Slows the heart beat and reduces myocardial oxygen demand

Prophylaxis of angina, treatment of dysrhythmias and hypertension

Propranolol (alsooxprenolol and atenolol)

β antagonist – reduces heart rate and output, reduces myocardial oxygen demand

Control of ectopic heartbeats and tachycardia. Reduces incidence of angina

Digoxin

Cardiac glycoside – increases the force of myocardial contraction and reduces conductivity within the atrioventricular (AV) node

Most useful in the treatment of supraventricular tachycardias, especially for controlling ventricular response in persistent atrial fibrillation

Atropine

An antimuscarinic drug which blocks acetylcholine

Prevention and reversal of excessive bradycardia

Peripheral resistance refers to the tissue’s resistance to blood flow. The diameter of blood vessels directly influences the resistance to blood flow – narrow vessels conduct blood at a slower rate than wide vessels. Control of blood vessel diameter occurs at a local tissue level through the release of lactic acid and other metabolites of normal cellular function. These metabolites cause local vasodilatation and therefore reduce peripheral vasoconstriction. Control of peripheral resistance occurs centrally through neural and hormonal activity, in particular the sympathetic nervous system.

Blood pressure is also subject to many controls. The higher the pressure gradient the faster blood will flow. The difference between the heart contractions (systole) and the relaxation phase (diastole) produces a pressure gradient. In humans, systolic pressure is normally around 120 mmHg and diastolic pressure is around 80 mmHg. The difference between these two measurements is the pulse pressure and it is this pressure that represents the pressure gradient. Pulse pressure is influenced by a combination of the contractility of the heart, the circulating volume and the peripheral resistance.

Shock, therefore, can be defined as acute circulatory failure leading to inadequate tissue perfusion, resulting in generalised cellular hypoxia and end-organ injury. It is caused by a disruption to the cardiovascular system and inadequate compensation to maintain tissue perfusion (Jevon & Ewens 2002).

Shock can be classified according to its three known causes:

a fault of the heart, which is cardiogenic shock;

a fault of the vascular system, which is distributive shock;

a fault of fluid regulation, which is hypovolaemic shock.

Keeping in mind the previous discussion on blood pressure regulation, it can be seen that hypotension and shock are therefore caused by a problem with heart rate, stroke volume or peripheral resistance.

A clinical approach to shock (Table 1.3) identifies the main clinical problems associated with shock that can be treated by medical interventions such as drugs or surgery:

low blood pressure, because of inadequate cardiac output or low peripheral resistance;

low cardiac output, caused by a problem with heart rate or stroke volume;

heart rate abnormalities – too fast (tachycardia) or too slow (bradycardia);

stroke volume abnormalities, caused by failure to receive blood, failure to eject blood or inadequate volume;

low peripheral vascular resistance, because of inappropriate vasodilation.

Table 1.3 A clinical approach to shock

Hypovolaemic shock

During shock, the body protects itself from hypovolaemia by a series of reflex mechanisms involving the cardiovascular and neurohormonal systems as described previously. The result is a decrease in cardiac output and increased peripheral resistance. The selective shunting of blood occurs to essential organs such as the brain, heart and kidneys, which are further protected by autoregulatory reflexes. This state is ‘compensated shock’ and may occur with up to 20% of blood loss (approximately 1 litre) (University of Pennsylvania 2006).

The clinical signs of compensated shock may be subtle: blood pressure may be normal; there is tachycardia, cold and clammy peripheries, decreased capillary refill; and a widened gap between core and peripheral temperature (Astiz et al. 1993).

As circulating volume decreases (1–2 litres blood loss) blood pressure begins to fall, resulting in increased peripheral vasoconstriction and tachycardia. Blood pressure may become unrecordable and there are signs of end-organ failure (oliguria and confusion) following the loss of more than 40% (2 litres) of circulating volume. The drop in urinary output is a reliable way of identifying progressive loss of circulating volume.

Treatment of hypovolaemic shock

Treatment of shock addresses the cause by replacing lost fluids and supporting the body’s essential systems against the effects of hypovolaemia. Techniques and protocols are constantly being reviewed as new research evidence becomes available.

Replacement of lost fluids by colloids and crystalloids is normally a priority for treating shock. Progressively worsening shock necessitates monitoring of arterial and central venous pressure (CVP) to assess the effects of fluid replacement. The end point of fluid replacement will be: blood pressure within normal limits; urinary output of greater than 1 ml/kg; CVP of over 12 mmHg; and lactate readings of less than 2 mmol/litre (University of Pennsylvania 2006). If the patient remains hypotensive after the volume replacement, then the problem lies with the cardiovascular system which must be supported through medical interventions. Noradrenaline (norepinephrine) and low dosage vasopressin may increase stroke volume, which can be measured with a pulmonary artery catheter or oesophageal Doppler. Dobutamine may be useful at this point to increase the efficiency of the heart pump.

The stroke volume, CVP, pulmonary capillary wedge pressure (PCWP) and venous oxygen saturation may guide fluid resuscitation. Since over-transfusion of patients rarely occurs during shock, non-invasive monitors such as the oesophageal Doppler may provide more rapid and less dangerous measurement of stroke volume. Close monitoring is essential since the patient’s fluid status may change as the body recovers from shock or as the effects of medical interventions progress (Pinsky & Payen 2004)).

THE RESPIRATORY SYSTEM

The respiratory system transports gases between the bloodstream and the outside air. Blood delivers oxygen to the tissues of the body, while carbon dioxide from tissue activity is returned to the lungs. The carbon dioxide waste leaves the body during exhalation.

Breathing is the process of moving air into and out of the lungs. An adult normally breathes from 14 to 20 times per minute, rising to 80 breaths per minute on effort and dropping to 8 or 10 breaths per minute at rest. A child’s rate of breathing at rest is faster than an adult’s at rest, and a newborn baby has a rate of about 40 breaths per minute. In adults the tidal volume (amount of air taken in a normal breath) is about 0.5 litres. The vital capacity (the maximum amount) is about 4.8 litres in an adult male.

The process of breathing comprises two phases, inspiration and expiration. The lungs themselves have no muscle tissue so the ribcage and the diaphragm control their movements.

The diaphragm is a large, dome-shaped muscle that lies just under the lungs, which flattens when stimulated. This expands the volume of the thoracic cavity. The rib muscles also contract on stimulation, pulling the ribcage up and out, also expanding the thoracic cavity. The increased volume of the thoracic cavity creates a partial vacuum which sucks air into the lungs. The diaphragm and rib muscles relax when the nervous stimulation ends, the thoracic cavity shrinks and exhalation occurs.

Conscious control and overriding of the respiratory centre alter the rhythm, for example when singing or whistling, or when holding the breath.

Structure

The respiratory system extends from the nose to the lungs and is divided into the upper and lower respiratory tracts. The upper respiratory tract consists of the nose and the pharynx, or throat. The lower respiratory tract includes the larynx, or voice box; the trachea, or windpipe, which splits into two main branches called bronchi; tiny branches of the bronchi called bronchioles; and finally the lungs. The nose, pharynx, larynx, trachea, bronchi and bronchioles conduct air to and from the lungs. The lungs interact with the cardiovascular system to deliver oxygen and remove carbon dioxide.

Nose and nasal cavity

Capillaries in the nose and nasal cavity warm and humidify the air. Hairs and mucus inside the nasal cavity help to trap dust and other particles to protect the lungs. Stimulation of chemo-receptors inside the nose activates the olfactory nerve which eventually leads to the sensation of smell.

Pharynx