Acute Cardiac Care E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 790

Veröffentlichungsjahr: 2013

Beschreibung

Acute Cardiac Care provides nurses with a comprehensive understanding of the current practice and principles underlying the care and management of acute cardiac conditions. It addresses the management of acute coronary syndromes (ACS) with an emphasis on evidence-based pharmacological management, cardiac emergencies (cardiac arrest, arrhythmia, acute pulmonary oedema, cardiogenic shock), current diagnostic and interventional modalities for the management of ACS, including risk stratification, and the ethical, political, social and economic factors that impact upon the provision of acute cardiac services in Australia and the UK.

Edited by renowned academics and clinicians in the field, this practical text will encourage nurses to think critically about evidence and management of acute coronary conditions, and provide a guide on how and where to look for up-to-date evidence and guidelines.

KEY FEATURES:

• A comprehensive and practical guide to the current practice and principles underlying the nursing care of acute cardiac conditions
• Edited by leading authorities in the field with a wealth of experience in acute cardiac care and resuscitation
• Has an emphasis on evidence-based practice, encouraging nurses to critically think about their practice
• Contains learning objectives, key points and activities and further reading guidelines

Leseprobe

Contents

Contributors

Foreword

Preface

1 Mechanics of the Cardiovascular System

Overview

Basic heart anatomy

The cardiac cycle

Cardiac output

Conclusion

2 Regulation of Cardiac and Vascular Function

Overview

Central nervous system regulation of the cardiovascular system

Vasomotor control

Baroreceptors

Chemoreceptors

Humoral control

Electrolytes

Conclusion

3 Cardiac Electrophysiology

Overview

Cardiac cells

The action potential

The action potential in non-pacemaker cells

The cardiac conduction system

The electrocardiogram

Conclusion

4 The Coronary Circulation

Overview

The coronary circulation

The left main coronary artery

The LAD artery

The LCX or CX artery

The right coronary artery

Collateral circulation

Microvascular circulation

Coronary venous circulation

5 Risk Factors for Cardiovascular Disease

Overview

Classification of risk factors for CVD

Biomedical risk factors

Behavioural risk factors

Psychosocial risk factors

Conclusion

6 Populations at Risk

Overview

Risk factors for CVD

Clarifying risk

Risk assessment tools

Populations at increased risk

Targeting treatment

Using what we know

Conclusion

7 Evidence-Based Practice

Overview

The need for change

Evidence-based practice

Barriers to the evidence

Conclusion

8 Ethics of Research in Acute Cardiac Care

Overview

Evidence-based medicine and clinical trials

Informed consent for trial participation

What is an ethical dilemma?

Genetic research

Considering an offer for the unit to participate in a clinical trial

Ethical issues in marketing and pricing of new pharmaceutical agents

Conclusion

9 Cardiovascular Assessment

Overview

Health history

Physical examination

Conclusion

10 Electrocardiogram Interpretation

Overview

Normal sequence of depolarisation and repolarisation

Theoretical basis of electrocardiography

Determining the cardiac axis

Determination of heart rate and electrocardiographic intervals

Chamber enlargement

Bundle branch block

ECG changes related to myocardial ischaemia and infarction

Obtaining a 12-lead ECG

Conclusion

11 Cardiac Monitoring

Overview

ECG monitoring systems and lead formats

Indications for arrhythmia monitoring

Nursing considerations in the care of the patient with ECG monitoring

12 Laboratory Tests

Overview

Generic laboratory tests

Electrolytes

Renal function

Glucose measurement

Lipid profiles

Complete blood examination

Clotting screen

Biochemical markers

Markers of myocardial necrosis

Cardiac natriuretic peptides

C-reactive protein

Conclusion

13 Diagnostic Procedures

Overview

Chest X-ray

Cardiac catheterisation (angiogram)

Echocardiography

Stress testing

Magnetic resonance imaging

Computerised tomography

Electrophysiology studies

Conclusion

14 Sudden Cardiac Death

Overview

Definitions

Burden of disease and risk factors for SCD

Sudden death in the young (including athletes)

Structural abnormalities

Cardiomyopathies and SCD

Genetic syndromes and SCD

Conclusion

15 Out-of-Hospital Cardiac Arrest and Automated External Defibrillation

Overview

Out-of-hospital cardiac arrest

Hazards to the victim and rescuer

Recognition of cardiac arrest and BLS

Automated external defibrillation

Conclusion

16 Ethical Issues in Resuscitation

Overview

Guiding ethical principles in resuscitation

Futility

Rights of the individual versus the needs of society

Patient perceptions of resuscitation

Introducing the DNR conversation

Witnessed resuscitation

Withdrawal of treatment

Organ donation

Training and research with the newly dead

17 Pathogenesis of Acute Coronary Syndromes

Overview

Acute coronary syndrome

Atherosclerosis

Endothelial dysfunction

Plaque disruption

Inflammation

Thrombosis

Vasoconstriction

Conclusion

18 Presentations of Acute Coronary Syndromes

Overview

Angina pectoris

Stable angina

The acute coronary syndromes

Global trends in ACS presentations

Clinical history in ACS

Physical examination in ACS patients

The 12-lead electrocardiogram in ACS

Cardiac markers in ACS

Clinical assessment and risk stratification in ACS

Conclusion

19 Risk Stratification in Acute Coronary Syndromes

Overview

Introduction

Risk stratification

Risk stratification guidelines

Risk scores

Chest pain units

Conclusion

20 Reducing Time to Treatment

Overview

Benefits of early reperfusion

Identifying and addressing delays

Conclusion

21 Reperfusion Strategies

Overview

Pathogenesis of STEMI

Principles of reperfusion strategies

Options for reperfusion

Strategies for reducing treatment time delays

Detecting and managing failed reperfusion

Preventing and detecting re-occlusion

Conclusion

22 Adjunct Pharmacological Agents in Acute Coronary Syndromes

Overview

Anti-ischaemic therapies

Antiplatelet and anticoagulant therapy

Inhibitors of the renin-angiotensin-aldosterone system

Statins

Conclusion

23 Arrhythmias

Overview

Basic electrophysiology

Mechanisms of arrhythmia generations

Cardiac monitoring

Rhythm interpretation

Determining the rhythm

Tachyarrhythmias

Asystole

Treatment of arrhythmias

Conclusion

24 In-Hospital Resuscitation

Overview

Introduction

Prevention: systems for identifying patients at risk of cardiac arrest

Early recognition and management of critically ill patients

In-hospital resuscitation

Working within your scope of practice

Audit and data collection

Conclusion

25 Acute Heart Failure

Overview

Introduction

Establishing the diagnosis

Management specifics

Refractory AHF

Dignity, communication and preventing complications: ‘back to basics’

Managing chronic heart failure better to reduce the need for re-hospitalisation

Conclusion

26 Convalescence

Overview

Introduction

Assessment and identification of patient needs

High risk groups

Promoting self-management in the convalescent phase

Particular concerns of spouses and family members

Accommodating convalescence and discharge planning following an acute cardiac event

Models of intervention to facilitate convalescence and secondary prevention

Nursing strategies to promote convalescence

Palliative care

Conclusion

27 Discharge Planning and Secondary Prevention

Overview

Discharge planning

Secondary prevention

Provision of secondary prevention

Components of secondary prevention

Cardio-protective drug therapy

Challenges in secondary prevention

Conclusion

Index

This edition first published 2010

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Library of Congress Cataloging-in-Publication Data

Acute Cardiac Care: A Practical Guide for Nurses/edited by Angela M. Kucia, Tom Quinn.

p. ; cm.

Includes bibliographical references and index.

ISBN 978-1-4051-6361-3 (pbk.: alk. paper)

1. Heart—Diseases—Nursing. I. Kucia, Angela M. II. Quinn, Tom, 1961–[DNLM: 1. Heart Diseases—nursing. 2. Critical Care. WY 152.5 A189 2010]

RC674.A28 2010

616.1′20231—dc22

2009006627

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

1 2010

Contributors

D. Barrett, RN, BA (Hons), PG Dip., PG Cert., is a Lecturer in Nursing in the Faculty of Health and Social Care, University of Hull, UK.

J.F. Beltrame, BSc, BMBS, PhD, FRACP, is Associate Professor and a National Heart Foundation Research Fellow at The University of Adelaide and a Senior Consultant Cardiologist at The Queen Elizabeth Hospital and Lyell McEwin Health Service, Adelaide, South Australia.

L. Belz, RN, Grad. Dip. Health Sc., is the Charge Nurse of the Coronary Care Unit at Auckland City Hospital, Auckland, New Zealand.

E. Birchmore, BN, MNP, Grad. Dip. Coronary Care, MRCNA, MACNP, is a Heart Failure Nurse Practitioner at The Queen Elizabeth Hospital, Adelaide, South Australia.

P. Davidson, RN, BA, MEd, PhD, is Professor and Director of the Centre for Cardiovascular & Chronic Care, Curtin University of Technology and St Vincent’s Hospital, Sydney, New South Wales.

A. Day, RN (USA), RGN (UK), MSc, PGCE, BSc (Hons), is a Senior Lecturer in Emergency Nursing, and a member of the Applied Research Group on Pre-hospital, Emergency and Cardiovascular Care in the Faculty of Health and Life Sciences at Coventry University, UK.

D. Evans, MNS, PhD, is a Senior Lecturer and Program Director for Higher Degrees by Research in the School of Nursing and Midwifery, University of South Australia in Adelaide, South Australia.

B. Greaney, RGN, PG Dip., PGCE, MA(Ed), is a Senior Lecturer in Critical Care Nursing, and a member of the Applied Research Group on Pre-hospital, Emergency and Cardiovascular Care in the Faculty of Health and Life Sciences at Coventry University, UK.

P. Gregory, BSc (Hons), PGCE, Paramedic, is a Senior Lecturer in Paramedic Science, and a member of the Applied Research Group on Pre-hospital, Emergency and Cardiovascular Care in the Faculty of Health and Life Sciences, Coventry University, UK.

J.D. Horowitz, MBBS, BMedSci (Hons), PhD, FRACP, is Professor and Director of Cardiology at The Queen Elizabeth Hospital, and a Professor of Cardiology at the University of Adelaide, Adelaide, South Australia.

L. Jesuthasan, MBBS, BMedSci, FRACP, is a Staff Specialist in Cardiology at the Queen Elizabeth Hospital, Adelaide, South Australia.

K. Mishra, MBBS, MD, MRCP (UK), FRACP (Cardiology), is a Staff Specialist in Cardiology at the Lyell McEwin Hospital, Adelaide, South Australia.

C. Oldroyd, RGN, PGCE, RNT, Bsc (Hons), MSc, is a Senior Lecturer in Cardiac Nursing, and a member of the Applied Research Group on Pre-hospital, Emergency and Cardiovascular Care in the Faculty of Health and Life Sciences, Coventry University, UK.

C. Ryan, BN, MNSc, is an Emergency Nurse Practitioner at The Queen Elizabeth Hospital, Adelaide, South Australia.

J. Smith, RN, BA (JUr), MHSc, is a Senior Project Officer in the Aboriginal and Torres Strait Islander Program with the National Heart Foundation of Australia, Adelaide, South Australia.

S.A. Unger, MBBS, FRACP, PhD, is a Staff Cardiologist and the Director of Nuclear Medicine at The Queen Elizabeth and Lyell McEwin Hospitals and as Senior Lecturer at the University of Adelaide, Adelaide, South Australia.

T. Wachtel, RN, MN, Grad. Cert. HD Nursing, MRCNA, is a Lecturer in Nursing and Clinical Coordinator in the School of Nursing and Midwifery, Flinders University, Renmark Campus, South Australia.

R. Webster, RN, BSc (Hons), MSc, is a Senior Nurse for Education and Practice Development for the Cardio-Respiratory Directorate, University Hospitals of Leicester, UK.

P. Whiston, RN, Grad. Dip. Coronary Care, is a Clinical Practice Consultant in the Coronary Care Unit at The Queen Elizabeth Hospital, Adelaide, South Australia.

B.F. Williams, NZRGON MHSc (Hons), is a Research Manager, Pacific Clinical Research Group (PCRG), Sydney, Australia.

C.J. Zeitz, MBBS, PhD, FRACP, OstJ, is Co-Director of Medicine and Emergency Clinical Services, and Director of Interventional Cardiology at the Queen Elizabeth Hospital in Adelaide, and Associate Professor of Rural and Indigenous Cardiovascular Health at the Spencer Gulf Rural Clinical School in Whyalla, South Australia.

Foreword

As the editors of this book cogently remind us, cardiovascular disease touches the lives of virtually everyone. Nurses are invariably at the forefront, working in collaboration with doctors and other health professionals, in providing acute cardiac care, including prevention and rehabilitation, to patients and their families. They have a professional duty to ensure that the care they give is safe and of a high quality and is informed by the best evidence. This requires them keeping up to date with the rapid developments in science and technology, changes in health policy and planning and increased expectations of the profession and the public whom they serve: a major challenge to busy nurses working in cardiac care settings.

Acute Cardiac Care, edited by two authorities in the field, with contributions from recognised experts (nurses, doctors and a paramedic) from both sides of the world, is therefore a welcome resource that will help meet this challenge. It is certainly a practical guide for nurses, presenting in a highly readable way, the essential topics that pertain to acute cardiac care. Each chapter begins with an overview, learning objectives and key concepts, is interspersed with key points and concludes with learning activities, pertinent references and resources and suggested further reading. It deserves to be in the library of every clinical setting where nurses care for patients with acute cardiac conditions.

David R Thompson BSc, MA, PhD, MBA, RN, FRCN, FAAN, FESCProfessor of Cardiovascular NursingSchool of MedicineUniversity of LeicesterLeicesterUK

July 2009

Preface

Cardiovascular diseases touch the lives of millions of people – patients, their families and friends, together with those who provide and plan care, and those responsible for planning and funding care: in essence, all members of society.

Great advances in scientific knowledge have accumulated since the advent of the cardiac care unit (CCU) in the 1960s, stimulated by the work of a British cardiologist, Professor Desmond Julian, who undertook pioneering work in the UK and Australia that changed the paradigm of care for patients with acute myocardial infarction. Much literature has accumulated on the key role nurses played in the development of the CCU in its formative years, and continue to do so in the present day.

But cardiac nursing is not solely about what happens on the CCU. We believe that nurses are crucial to improved prevention, care and rehabilitation of cardiovascular disease. Whether in the emergency department, cardiac care unit, catheter laboratory, cardiac surgical ward, or in the community setting, or as researchers, managers or policy makers, nurses have opportunities to make a real difference.

As two cardiac nurses with a combined total of more than half a century of experience in acute care, research and policy, we have worked with colleagues with a wide range of experience and knowledge from across our two countries to produce what we hope will be a key resource for nurses embarking on studies of this exciting and constantly evolving arena of practice, and serve as a stimulating source of continuing professional development for more experienced colleagues.

We are grateful to all our contributors for their expertise and commitment, and to Magenta Lampson, Senior Commissioning Editor and Rachel Coombs, Development Editor, Nursing, for their invaluable assistance in bringing this project to fruition.

We dedicate this book to our partners, with thanks for their love and support, and look forward to spending more time with them than we have had in the past 2 years while we’ve been nursing this book!

Angela KuciaAdelaide, South Australia

Tom QuinnSurrey, UK.

1

Mechanics of the Cardiovascular System

B. Greaney & A.M. Kucia

Overview

The cardiovascular system consists of two primary components: the heart and blood vessels. The lymphatic system also has a cardiovascular exchange function but does not contain blood. This chapter will highlight the mechanics of the cardiovascular system and present an overview of the essential elements and structures involved in the flow of blood through the venous and arterial systems. It will also highlight how abnormalities in the mechanics of the cardiovascular system can result in degrees of cardiac disease states.

Learning objectives

After reading this chapter, you should be able to:

Identify the anatomical location of the heart and its basic function.Identify the key structures within the heart, which are involved in the flow of blood through the heart and identify their specific function.Define the term ‘cardiac cycle’ and explain the key physiological changes that occur in the heart during this process.Define the terms ‘cardiac output’ (CO) and ‘stroke volume’ (SV), and explain their physiological significance in relation to the cardiac cycle.Define the terms ‘preload’, ‘afterload’ and ‘contractility’, and explain their physiological impact upon myocardial contraction.

Key concepts

Cardiac cycle; cardiac output; cardiac chambers; cardiac valves; layers of the heart

Basic heart anatomy

The human heart is essentially a muscular pump which delivers blood containing oxygen, nutrients and other vital elements to the body tissues and major organs. The structure and location of the heart was described by Henry Gray in 1918. It is conical in shape, about the size of a human fist and weighs between 230 and 340 g in an adult. The heart is located in the mediastinum, with one-third lying to the right of the sternum and two-thirds to the left. The top of the heart is known as the base, and this is located behind the sternum; the bottom of the heart, known as the apex, is located in the fifth intercostal space in the mid-clavicular line. The heart is a four-chambered structure – the upper chambers known as the right and left atria, the lower two chambers known as the right and left ventricles, with right and left-sided chambers divided by the septum.

The bulk of the heart’s wall is the myocardium, which is a thick contractile mass of cardiac muscle cells. It is the myocardium that provides the force of contraction to move blood out of the ventricles at the end of each cardiac cycle. The heart is surrounded by the pericardium, which is comprised of two principal layers that surround and protect the heart. The outer layer is known as the fibrous pericardium, which is made up of tough and fibrous connective tissue. This layer provides both protection and anchorage for the heart. The second layer, the serous pericardium, is a thinner, more delicate layer and forms two distinct layers around the heart. The outer parietal layer is adhered to the inner side of the fibrous pericardium, whilst the inner visceral layer, also known as the epicardium, is adhered tightly to the myocardium. Between these two layers there exists a potential space termed the pericardial cavity. Within this cavity is a very thin film of serous fluid known as pericardial fluid, which is normally between 15 and 35 mL in volume (Spodick 1997). The key function of this fluid is to reduce friction between the pericardial layers as the heart contracts. The inner layer lining the heart is a continuous sheet of squamous epithelium, continuing into the tunica intima of blood vessels, and is known as the endocardium.

The heart is divided into four chambers: two upper atria and two lower ventricles. These chambers are separated by a set of heart valves termed the atrioventricular (AV) valves; the tri-cuspid valve separates the right atrium (RA) and right ventricle (RV) and the bicuspid valve or mitral valve separates the left atrium (LA) and left ventricle (LV) (Figure 1.1a). Attached to each AV valve are two structures: the chordae tendinae and the papillary muscles. These two structures are adhered to the walls of each ventricle (Figure 1.1a). Their function is to prevent the valve cusps inverting or swinging upward into the atria during ventricular systole. The key function of the heart valves is to permit the flow of blood in one direction only as it flows through the heart.

The heart can be viewed functionally as two pumps serving the pulmonary and systemic circulations. The pulmonary circulation refers to the flow of blood within the lungs that is involved in the exchange of gases between the blood and the alveoli. Deoxygenated blood returns to the RA via the inferior and superior vena cavae. It then passes through the tricuspid valve to the RV before entering the pulmonary circulation via the pulmonary artery, where gases are exchanged. The pulmonary artery has a pulmonary valve or semi-lunar valve which opens and closes during contraction and relaxation of the heart, again having a similar function to the AV valves, allowing the flow of blood in one direction only (Figure 1.1). The systemic circulation consists of all the blood vessels within and outside of all organs excluding the lungs. Once oxygenated, the blood returns to the LA via the pulmonary veins and then passes through the mitral valve into the thicker-walled left ventricle, which ejects the oxygenated blood through the aortic valve into the aorta and into the systemic circulation. The aorta also has a valve, the aortic valve, which prevents the back-flow of blood during myocardial contraction (Figure 1.1a).

The cardiac cycle

In simple terms, the heart is a pump that receives blood from the venous system at low pressure and generates pressure through contraction to eject the blood into the arterial system. The mechanical action of the heart is created by a synchronised contraction and relaxation of the cardiac muscle, referred to as systole and diastole. The actual mechanical function of the heart is influenced by pressure, volume and flow changes that occur within the heart during one single cardiac cycle.

When the heart muscle contracts (systole) and relaxes (diastole), sequential changes in pressure are produced in the heart chambers and blood vessels, which result in blood flowing from areas of high pressure to areas of lower pressure. The valves prevent backflow of blood. Under normal conditions, this cycle will take place in the human heart between 60 and 100 times per minute.

Figure 1.2a demonstrates the seven phases of the cardiac cycle.

Figure 1.1 Gross anatomy of the heart.

Source: From Aaronson and Ward (2007).

Phase 1: Atrial systole

Atrial systole begins after a wave of depolarisation passes over the atrial muscle. Atrial depolarisation is represented by the P wave on the electrocardiograph (ECG). As the atria contract, pressure builds up inside the atria forcing blood through the tricuspid and mitral valves into the ventricles. Atrial contraction causes a small increase in proximal venous pressure (in the pulmonary veins and vena cavae). This is represented by the ‘a’ wave of the jugular venous pulse, which is used to measure jugular venous pressure (JVP) (Klabunde 2005).

Blood flows from the RA across the tricuspid valve into the RV.

Blood flows from the LA through the mitral valve into the LV.

Pressure in the atria falls and the AV valves float upward. Ventricular volumes are now at their maximum (around 120mL) and this is known as end diastolic volume (EDV). Left ventricular end diastolic pressure (LVEDP) is approximately 8–12 mmHg; right ventricular end diastolic pressure (RVEDP) is usually around 3–6 mmHg. A fourth heart sound (S4) may be heard in this phase if ventricular compliance is reduced, such as happens with ventricular hypertrophy, ischae-mia or as a common finding in older individuals.

Figure 1.2 Cardiac cycle.

Source: From Aaronson and Ward (2007).

Key point

Ventricular filling occurs passively before the atria contract and depends upon venous return. Atrial contraction normally accounts for only around 10% of ventricular filling, when the body is at rest. However, at high heart rates (such as during exercise), there is a shortened period of diastole where passive filling normally occurs. Under these conditions, atrial contraction is more important and can contribute up to 40% of ventricular filling. Enhanced ventricular filling due to atrial contraction is sometimes referred to as the ‘atrial kick’ (Klabunde 2005).

Phase 2: Isovolumetric contraction

This phase is represented by the QRS complex on the ECG. The ventricle depolarises and initiates contraction of the myocytes, resulting in a rapid increase in ventricular pressure. This rise in pressure causes the AV valves to close. Closure of the AV valves generates the first heart sound (S1). A split S1 may be heard as mitral valve closure precedes tricuspid valve closure by around 0.04 of a second, although usually only one sound can be heard through a stethoscope. The time between closure of the AV valves and opening of the semilunar valves is known as isovolumetric contraction because there is no change in the volume of blood in the ventricle at this stage, although the ventricle contracts and becomes more spheroid in shape. The pressure in the LV becomes maximal at this stage and is termed dp/dt (maximal slope of the ventricular pressure tracing/time) (Klabunde 2005).

Phase 3: Rapid ventricular ejection

When the ventricular pressure exceeds that of the aorta (around 80 mmHg) and pulmonary arteries (around 10 mmHg) the aortic and pulmonary valves open and blood is ejected out of the ventricles. The LV has a thick muscular wall that allows it to generate high pressures during ventricular contraction. Maximal outflow velocity occurs early in the ejection phase, so the highest aortic and pulmonary artery pressures are reached at this time (Klabunde 2005).

Blood is ejected from the RV across the pulmonic valve and into the pulmonary artery to the pulmonary circulation.

Blood is ejected from the LV across the aortic valve and into the aorta to the systemic circulation.

Between 70 and 90 mL of blood is ejected with each stroke (stroke volume), but about 50 mL remains in each ventricle. The residual amount of blood left in the ventricle is known as the endsystolic volume (ESV). Stroke volume thus is the difference between EDV and ESV. Around 60% of the total volume of the ventricle is ejected in each cycle. To work out the ejection fraction of the ventricle, divide the stroke volume by the EDV. The normal left ventricular ejection fraction (LVEF) is above 55% (Klabunde 2005).

Key point

In the healthy heart, no heart sounds should be heard during the ejection phase of the cardiac cycle. The presence of sounds during ejection indicates valvular disease or intracardiac shunts (Klabunde 2005).

Phase 4: Reduced ventricular ejection

The ventricle relaxes and the rate of ejection begins to fall, although kinetic or inertial energy continues to propel the blood forward into the aorta. This phase coincides with ventricular repolarisation, which occurs approximately 150–200 ms after the QRS complex and appears as the T wave on the ECG. Atrial pressure starts to rise during this phase due to venous return (Klabunde 2005).

The RA receives blood from the systemic circulation via the inferior and superior vena cavae at a low pressure (approximately 0–4 mmHg).

After circulating through the lungs, blood returns to the heart via the four pulmonary veins into the LA. The pressure in the LA is usually between 8–12 mmHg.

Phase 5: Isovolumetric relaxation

In this phase, the pressure in the ventricles continues to fall and when the point is reached where the pressure is less in the ventricles than that in the outflow tracts (aorta and pulmonary veins), the aortic and pulmonary valves close abruptly, causing a second heart sound (S2). Aortic and pulmonary artery pressures fall slowly due to a combination of stored energy in the elastic walls of these vessels which controls pressure and flow, and because forward flow is impeded by systemic and pulmonic vascular resistance as blood is distributed through the systemic and pulmonary circulations (Klabunde 2005).

Key point

As the aortic valve closes before the pulmonic valve, there is a physiological splitting of the S2 sound and this may be heard with a stethoscope. Closure of the aortic and pulmonary valves result in a characteristic notch in aortic and pulmonary artery pressure tracings (Figure 1.2a). The aortic notch is important in setting timing for intra-aortic balloon counterpulsation.

Phase 6: Rapid ventricular filling

Low pressures in the heart allow blood to passively return to the atria. When the ventricular pressure falls below the atrial pressure, the AV valves open and the ventricles fill quickly. Blood flows into the atria and ventricles throughout diastole with the rate of filling decreasing as the amount of blood in the chambers distends the walls. About 70% of ventricular filling occurs passively at this time.

Key point

No prominent heart sounds should be heard at this time. If a third heart sound (S3) is heard during ventricular filling in adults, it may indicate tensing of the chordae tendinae and AV ring, often associated with ventricular dilation. It is a normal finding in children.

Phase 7: Rapid ventricular filling

There is no clear demarcation as to when this phase begins, but this is a stage during diastole when passive ventricular filling is near completion. As the ventricles fill, they become less compliant, causing intraventricular pressure to rise and the rate of ventricular filling starts to fall. Immediately following this phase, atrial systole occurs following firing of the sino-atrial node.

Key point

At slow heart rates, diastole is lengthened, resulting in increased filling time. In rapid heart rates, there is less filling time. This would compromise CO, if not for compensatory mechanisms.

Cardiac output

CO is an important index of cardiac function, and refers to the amount of blood that is ejected with each contraction (stroke volume) multiplied by heart rate (HR):

At typical resting values, if the heart rate is 75 beats/min and the stroke volume is 70 mL/beat, the CO should equal 5.25 L/min. Therefore the body’s total volume of blood (4–6 L/min) passes through the body each minute (Saladin 2001).

CO never remains at a constant rate: any factor that alters stroke volume or heart rate will alter CO and it can vary significantly according to normal physical exercise as well as impaired cardiac function. Other factors such as preload, afterload and contractility (inotropy) will indirectly affect CO.

Preload is defined as the actual stretch or tension on the ventricular myocardium prior to contraction (Totora & Gabowski 2002). The greater the preload on the myocardium (the larger the amount of blood that has filled the heart during diastole), the greater the contraction will be. A simple analogy to explain this concept is that the further you stretch an elastic band prior to releasing it, the further it will recoil. The same principle applies here: the greater the stretch or tension on the myocardium, the greater the force of contraction. When venous return to the heart increases, ventricular filling and preload also increase. The Frank Starling Law of the Heart (Starling’s Law) asserts that the more the ventricle is filled with blood during diastole (EDV), the greater the volume of blood that will be ejected (stroke volume) during the ensuing systolic contraction. Thus, altered preload is a mechanism by which the force of contractility can be affected (Klabunde 2005).

Contractility, also known as inotropy, is the ability of a cardiac myocyte to alter its tension development independently of preload changes (Klabunde 2005). Contractility is affected by autonomic innervation and circulating catecholamines (adrenaline, noradrenaline), and additionally changes in afterload and heart rate can augment contractility. A number of pharmacological agents positively or negatively affect contractility. Agents that affect contractility are called positive or negative inotropes, depending upon whether they increase or decrease contractility. Loss of myocardial contractility results in heart failure.

Afterload is defined as the force or pressure against which the ventricular myocardium must push prior to contraction (Totora & Grabowski 2003). This force or pressure is constantly present in the arteries as arterial blood pressure. Therefore, any increase in systemic blood pressure will result in the left ventricular myocardium having to contract more forcefully to eject its volume of blood. Any increase in the pressure of the pulmonary circulation, such as pulmonary oedema, or the presence of any physical obstruction to the pulmonary circulation, such as lung scar tissue, will result in the right ventricular myocardium having to contract more forcefully. In the long term, this increased workload for the myocardium will eventually result in the abnormal enlargement of the myocardium (hypertrophy), which may in turn lead to heart failure.

Key point

The myocardium requires oxygen to regenerate adenosine triphosphate (ATP) that is hydrolysed to produce energy during contraction and relaxation. Any change to the force or frequency of contraction will have an effect on myocardial oxygen consumption (MVO2). Imbalances in the supply and demand of oxygen to the myocardium may result in myocardial ischaemia or infarction.

Conclusion

This chapter has provided you with an overview of anatomical and physiological underpinnings underlying much of the assessment and nursing care of the patient with a cardiovascular disorder. When next you check a patient’s heart rate or blood pressure, or listen to their heart sounds, consider in detail the anatomical and physiological determinants of those measures.

Learning activities

There are a number of interactive online websites where you can test your knowledge of cardiac anatomy and physiology. The Columbia University Medical Center Department of Surgery in New York has some great heart animations and information at http://www.columbiasurgery.org/pat/cardiac/anatomy.html

The Texas Heart Institute at St Luke’s Episcopal Hospital Heart Information Center likewise has some good cardiovascular information and animations at http://texasheart.org/HIC/Anatomy/index.cfm

References

Aaronson, P.I. & Ward, J.P.T. (2007). The Cardiovascular System at a Glance3E. Wiley Blackwell, Oxford.

Gray, H. (1918). Anatomy of the Human Body. Lea & Febiger, Philadelphia.

Klabunde, R. (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins, Philadelphia.

Saladin, K.S. (2001). Anatomy & physiology: The Unity of Form & Function. McGraw Hill, New York.

Spodick, D.H. (1997). Pericardial macro- and micro-anatomy: A synopsis. In: D.H. Spodick, (ed.), The Pericardium: A Comprehensive Textbook. Marcel Dekker, New York, pp. 7–14.

Totora, G.J. & Grabowski, S.R. (2003). Principles of Anatomy and Physiology, 10th edn. John Wiley & Sons, New Jersey.

Useful Websites and Further Reading

Klabunde, R.E. (2007). Cardiovascular physiology concepts. Retrieved online 4th October 2007 from http://www.cvphysiology.cm/

Rogers, J. (1999). Cardiovascular physiology. Retrieved online 4th October 2007 from http://www.nda.ox.ac.uk/wfsa/html/u10/u1002_01.htm

2

Regulation of Cardiac and Vascular Function

B. Greaney & A.M. Kucia

Overview

Regulation of cardiac and vascular function is somewhat complex and involves autonomic nerves and circulating hormones. You will hear this referred to as ‘neurohumoral control of the cardiovascular system’. These mechanisms control cardiac output, blood pressure and local control of blood flow in response to physiological requirements and in the setting of an adverse clinical event such as trauma, disease or stress. In turn, neurohumoral control is influenced by sensors that monitor blood pressure (baroreceptors), blood volume (volume receptors), blood chemistry (chemoreceptors) and plasma osmolarity (osmoreceptors). These sensors work together to maintain arterial pressure at a level that is adequate for organ perfusion (Klabunde 2005). This chapter reviews the mechanisms involved in neurohumoral controls of the cardiovascular system.

Learning objectives

After reading this chapter, you should be able to:

Describe the components of the autonomic nervous system that relate to cardiac function.Describe the effects of sympathetic and parasympathetic stimulation on the cardiovascular system.Discuss the function of baroreceptors in the regulation of arterial pressure.Discuss the function of chemoreceptors in the regulation of respiratory activity and arterial pressure.List the chemicals that can stimulate the heart and cardiovascular system and describe their negative and positive effects.

Key concepts

Neurohumoral control; sympathetic and parasympathetic nervous system; baroreceptors; chemoreceptors; blood pressure regulation

Central nervous system regulation of the cardiovascular system

The central nervous system (CNS) controls the autonomic regulation of cardiovascular function. Autonomic refers to functions of the nervous system that are not under voluntary control (such as regulation of heart rate). The heart is innervated by both parasympathetic and sympathetic nerve fibers. These fibers together play a vital role in the control of heart rate and contractility, as well as Regulation of blood pressure. These nerve fibres are conveyed directly to the heart from the cardiovascular centre located in the medulla oblongata of the brain, which is the main region for nervous system regulation of the heart and blood vessels (Totora & Grabowski 2003). Parasympathetic innervation is associated with the cardioinhibitory centre of the cardiovascular centre, and sympathetic innervation is associated with the cardioacceleratory centre (also known as cardio-stimulatory centre) of the cardiovascular centre.

The cardio inhibitory centre sends signals via parasympathetic fibers in the vagus nerve to the sino-atrial (SA) and atrio-ventricular (AV) nodes, conduction pathways, myocytes and coronary vasculature. The right vagus nerve predominantly innervates the SA node, and the left vague nerve innervates the AV node and ventricular conduction system. Nerve fibers in the parasympathetic nervous system are cholinergic, which means they release acetylcholine. Acetylcholine binds to muscarinic receptors which are specifically associated with vagal nerve endings in the heart, resulting in negative chronotropy (decreased heart rate); negative inotropy decreased contractility, more so in the atria than the ventricles) and negative dromotropy (decreased conduction velocity).

The cardioacceleratory centre sends signals by way of the thoracic spinal cord and sympathetic cardiac accelerator nerves to the SA node, AV node and myocardium. These nerves secrete nore-pinephrine, which binds to β-adrenergic receptors in the heart. The term ‘pressor’ is sometimes used to describe the responses associated with sympathetic stimulation on the heart, which are positive chronotropy (increased heart rate); positive inotropy (increased contractility, more so in the atria than the ventricles) and positive dromotropy (increased conduction velocity).

Key point

It is important to note that despite this continual regulation of the heart, the SA and AV nodes are autorhythmic: they fire at their own intrinsic rate (see Chapter 3 for further detail). Therefore, if Para-sympathetic and sympathetic nerve fibers to these nodes were severed, the heart would continue to beat at its own intrinsic rate. Parasympathetic activity, or vigil tone, is the dominant controlling factor of heart rate and it inhibits the nodes to a normal rate of 70–80 beats per minute (bum). Maximum vigil stimulation can reduce the heart rate to as low as 20 bpm (Saladin 2001). In clinical situations, where a patient’s heart rate has become dangerously low due to myocardial infarction, ischaemia or other reasons, the drug atropine, a vagal nerve blocker, may be used to block vagal stimulation on the heart, allowing sympathetic nerve fibres to be the dominant nervous stimulus, producing an increase in the heart rate. Parasympathetic activity in the heart inhibits sympathetic activity and vice versa (Klabunde 2005).

The cardiovascular centre receives both neural and chemical input from many sources. Stimuli such as exercise, anxiety, fear, pyrexia and pain will act upon the cardiovascular centre via higher centres in the brain such as the cerebral cortex, the limbic system and the hypothalamus. A number of specific mechanisms exist at various locations in the body which control and regulate the heart and vascular system in response to such factors. Sudden fear or emotion, for example, may cause vagal stimulation resulting in bradycardia, loss of vascular tone and fainting (vasovagal syncope) (Klabunde 2005).

Vasomotor control

As described, the CNS plays an important role in regulating systemic vascular resistance (SVR) and cardiac function which in turn influence arterial blood pressure. The distribution of blood, as well as the control of arterial blood pressure, can be influenced by factors that control changes in the diameter of blood vessels. The vasomotor centre controls sympathetic activation of the vascular system and is located in the medulla of the brain. Sympathetic activation causes an impulse outflow via sympathetic fibers that terminate in the smooth muscle tissue of both resistance (arteries and arterioles) and capacitance (veins and venules) vessels, causing constriction. This increases SVR and thus arterial blood pressure.

Baroreceptors

Arterial blood pressure is regulated through a negative feedback system which uses pressure sensors, known as baroreceptors, located in the carotid sinus and aortic arch and the bifurcation of the subclavian artery (Bridges 2005). These baroreceptors are sensitive to changes in pressure or stretch in the vessels walls where they are located. They are also sensitive to the rate of pressure change and to a steady (mean) pressure.

Figure 2.1 Physiological changes to cardiac output associated with body position change.

To understand how baroreceptors function, let us consider what happens in the physiologic circumstance of when a person suddenly changes from a reclining position to one of standing as in Figure 2.1.

In addition to arterial baroreceptors, there are stretch receptors located at the veno-atrial junctions of the heart that respond to atrial filling and contraction (Klabunde 2005). Low-pressure baroreceptors are located in the atria, ventricles, pulmonary artery and veins that are sensitive to changes in transmural pressure in these chambers or vessels.

Learning activity

Carotid sinus massage is sometimes used to abort some forms of supraventricular tachycardia. Considering the action of baroreceptors, how do you think this works?

Clinical states such as hypovolaemia may result in the vascular system recruiting blood from the reservoirs found in the venous plexuses and sinuses in the skin and abdominal organs, especially the liver and spleen (Thibodeau & Patton 2007). Blood can be shifted quickly out of these reservoirs to arteries that supply heart and skeletal muscles when increased activity demands.

Key point

Stimulation of certain mechanoreceptors (sensory receptors that respond to mechanical pressure or distortion), and chemoreceptor’s, in the heart and coronary arteries can result in a vitally mediated triad of bradycardia, apnoea and hypotension (Bridges 2005) known as the Bezold–Jarisch reflex. This happens commonly when dye is injected into the coronary arteries during coronary angiography or during ischaemia/reperfusion involving the infero-posterior wall of the left ventricle.

Chemoreceptors

Chemoreceptors are specialised cells that have a significant role in the regulation of respiratory activity to maintain arterial blood PO2, PCO2 and pH within a physiologic range (Klabunde 2005). These receptors are sensitive to small changes in oxygen levels but are more sensitive to abnormal carbon dioxide and hydrogen ion levels in the blood plasma. Abnormal levels of any of these substances trigger the chemoreceptors to send impulses to the cardiovascular centre. In response, the cardiovascular centre increases sympathetic stimulation to the smooth muscle of arterioles and veins, bringing about vasoconstriction and a subsequent increase in arterial blood pressure and heart rate, thus improving tissue perfusion. Peripheral chemoreceptors are located in the aortic arch (known as the aortic bodies) and in the carotid arteries (known as the carotid bodies), and are responsive to hypoxaemia (decreased arterial PO2), hypercapnia (increased arterial PCO2) and hydrogen ion concentration (acidosis). Central chemoreceptors are located within the medulla of the brain (central chemoreceptors) and are responsive to hypercapnia and acidosis but not directly to hypoxia (Klabunde 2005). Stimulation of these receptors leads to hyperventilation and sympathetic activation causing vasoconstriction in most vascular beds except those of the brain and heart (Bridges 2005). Although the chemoreceptor reflex results in an increase in arterial blood pressure, this rise will be mediated by the baroreceptor response.

Key point

Central and peripheral chemoreceptor responses may be enhanced in heart failure patients, resulting in increased sympathetic activation which may contribute to sleep apnoea in those patients and is associated with a poor prognosis (Javaheri 2003; Narkiewicz & Somers 2003).

Humoral control

There are a number of naturally produced chemicals (humoral substances) in the body that significantly effect the action of the heart and vascular system. These can have both positive and negative effects. These include circulating catecholamines, the renin-angiotensin-aldosterone system (RAAS), atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) (vasopressin). Other substances such as thyroxine, oestrogen, insulin and growth hormone also have direct or indirect effects on the cardiovascular system (Klabunde 2005). Epinephrine (adrenalin) and norepinephrine (noradrenalin) are classed as non-steroid hormones called catecholamines and are particularly potent cardiac stimulants. They are secreted by the adrenal medulla and cardiac accelerator nerves in response to arousal, stress (physical or emotional) and exercise (Saladin 2001) and are associated with the body’s ‘fight and flight’ reflex. Epinephrine accounts for about 80% of the adrenal medullas secretion, the other 20% is norepinephrine (Thibodeau & Patton 2007). When secreted into the bloodstream, epinephrine prepares the body to respond to an acute stressor by increasing the supply of oxygen and glucose to the brain and muscles, while suppressing other non-emergency bodily processes such as digestion (fight or flight mechanism). It binds to numerous adrenergic receptors (β1, β2, α1 and α2) throughout the body, although it has a greater affinity for (β-adrenoreceptors than α-adrenoreceptors. Therefore, when plasma levels of epinephrine are low, it will bind preferentially to (β- adrenoreceptors. This is important to know because heart rate, inotropy and dromotropy are mainly mediated by (β1-adrenoreceptors (Klabunde 2005). Low dose epinephrine binds to (β2-adrenoreceptors in skeletal muscle and splanchnic arterioles, triggering vasodilation. However, when epinephrine binds with α-adrenergic receptors that are found in smooth muscle in the walls of blood vessels, it causes vasoconstriction. Blood pressure is increased due to the resulting increase in cardiac output and SVR.

Key point

When epinephrine is administered exogenously, its effects are dose related. Low dose epinephrine stimulates the (β-adrenoreceptors resulting in vasodilation and increased heart rate and contractility. Higher doses stimulate the α-adrenoreceptors, increasing vascular resistance and blood pressure. Thus, if the intent of epinephrine administration is vasoconstriction, it is important to administer a large enough dose to achieve this effect (Bridges 2005).

Circulating norepinephrine transiently increases heart rate and increases β1-adrenoreceptor-mediated inotropy. It causes vasoconstriction in most systemic arteries and veins (α1 and α2 adrenoreceptors). The overall effect is increased cardiac output and SVR leading to an increase in arterial blood pressure. The initial increase in heart rate is not sustained due to activation of baroreceptors which cause vagal-mediated slowing of heart rate (Klabunde 2007).

Learning activity

β-blockers are drugs that bind to β-adrenoceptors, blocking the ability of norepinephrine and epinephrine to bind to these receptors. The first generation of β-blocking drugs were ‘non-selective’ – what does this mean and what disadvantage does this have?

Second generation β-blockers are said to be more ‘cardioselective’ – what does this mean and which beta blockers are ‘cardioselective’?

Third generation β-blockers have vasodilator actions through blockade of α-adrenoreceptors. Which drugs are included in this class?

Arginine vasopressin (AVP), commonly known as antidiuretic hormone (ADH), is a peptide hormone produced in the hypothalamus and stored in the posterior pituitary gland, and is mainly released into the bloodstream (and some directly into the brain) in response to increased plasma osmolality (detected by osmoreceptors in the hypothalamus). AVP may also be secreted in response to decreased blood volume or blood pressure (detected by baroreceptors), but this is a less sensitive mechanism than osmolality. AVP causes the kidneys to conserve water (but not sodium) by concentrating the urine and reducing urine volume, and elevates blood pressure through vasoconstriction.

Natriuretic peptides are hormones that are involved in the homeostatic regulation of blood pressure, volume and electrolytes. Atrial natriuretic peptide (ANP) is released from the walls of the atria, and brain (B-type) natriuretic pep-tide (BNP) from the walls of the ventricles in response to increased stretch or hormonal stimuli (angiotensin II, catecholamines, glucocorticoids, endothelin 1). C-type natriuretic peptide (CNP) is distributed throughout the heart, brain, lungs, kidneys and endothelin and is released in response to stress. Natriuretic peptides increase excretion of sodium and water and inhibit sodium reabsorption, thereby reducing blood pressure. They also inhibit activation of the RAAS.

Key point

Evidence from clinical trials suggests that short-term administration of intravenous BNP (nesiritide) may be effective in improving haemodynamic function and reducing symptoms of acute decompensate heart failure (Mills et al. 1999; Colucci et al. 2000; Keating & Goa 2003), although a trend towards an increase in early mortality in nesiritide-treated patients has raised some safety concerns (Aaronson & Sackner-Bernstein 2005).

The RAAS is a hormone system that has a role in regulating long-term blood pressure and extracellular fluid volume. A number of hormones and enzymes which are significant in the RAAS cause both vasodilatation and vasoconstriction, and therefore influence arterial blood pressure in specific clinical and associated disease states.

The RAAS has a cascade effect (Figure 2.2) that is triggered by rennin release from the kidney in response to sympathetic nerve activation (acting via β1-adrenoceptors); renal artery hypotension (caused by systemic hypotension or renal artery stenosis) or decreased sodium delivery to the distal tubules of the kidney (Klabunde 2007). When rennin is released into the bloodstream, it acts upon a circulating substrate, angiotensinogen, which through the process of proteolytic cleavage becomes angiotensin I. Angiotensin converting enzyme, found mainly in vascular endothelium in the lungs, converts angiotensin I to angiotensin II. Angiotensin II is a powerful substance that causes vasoconstriction in the resistance vessels leading to increased SVR and arterial pressure and stimulates the adrenal cortex to release aldosterone which acts on the kidneys to increase sodium and fluid retention. It also stimulates the posterior pituitary to release AVP (ADH) which acts on the kidneys to increase fluid retention, stimulates Renin-angiotensin-aldosterone system thirst centers within the brain and enhances sympathetic adrenergic function by facilitating the release of from nor epinephrine sympathetic nerve endings and inhibiting its reuptake. The net effect of this cascade is to maintain blood pressure and volume. Natriuretic peptides modulate the function of the RAAS and have an important counter-regulatory influence (Klabunde 2007).

Figure 2.2 The renin-angiotensin-aldosterone system (RAAS).

Source: Reproduced from Rad (2006). Copyright 2006.

Learning activity

Knowledge of the RAAS pathway is necessary in understanding the action of drugs used to treat heart failure and hypertension, as the RAAS is often the target of therapeutic manipulation in treating these conditions. Review the drugs used to treat hypertension and heart failure and their actions on the RAAS.

Electrolytes

Potassium, sodium and calcium have an influence on heart rate and rhythm through their role in action potentials (see Chapter 3 Elevated blood levels of potassium and sodium decrease heart rate and the contractility of the heart, but a moderate increase in extracellular and intracellular calcium levels increases both heart rate and contractility (Totowa & Grabowski 2003). Potassium also appears to induce vasodilatation, though its specific role in vasoregulatory processes has not yet been fully elucidated (Berne & Levy 2001).

Conclusion

This chapter has provided an overview of the regulation of cardiovascular function. The processes and mechanisms by which the cardiovascular system is regulated are many and complex. It is important for nurses to have a broad understanding of these mechanisms in order to recognise any disturbance in neurohumoral control that might compromise the patient, and also to understand the actions of a number of pharmacological substances that are utilised to therapeutically manipulate neurohumoral processes.

3

Cardiac Electrophysiology

B. Greaney & A.M. Kucia

Overview

This chapter outlines the anatomy and physiology of the conduction system of the heart and the vital role it plays in the overall function of the heart. An understanding of cardiac electrophysiology will provide a basis for interpretation of the 12-lead electrocardiogram (ECG), and the impact that myocardial ischaemia and other metabolic derangements have upon the 12-lead ECG. This chapter will also facilitate an understanding of the electrophysiological basis of arrhythmia generation, the pharmacological actions of certain classes of medications and the underlying physiological concepts related to defibrillation and cardioversion.

Learning objectives

After reading this chapter, you should be able to:

Describe the structure and function of cardiac myocytes and autorhythmic cells.Describe the process of action potentials within the myocardium.Name the key components of the heart’s conduction system.Describe the specific anatomical location of the key components of the heart’s conduction system.Relate the specific electrophysiological events in the cardiac cycle to the generation of ECG waveforms.

Key concepts

Electrophysiology; automaticity; contractility; action potential; cardiac conduction system

Cardiac cells

When referring to the electrophysiology of the heart, we are describing the overall electrical activity within the myocardium, which plays a vital role in the overall effective function of the heart. The conduction system is made up of a series of specific structures within the myocardium, which are still essentially part of the cardiac muscle, but are modified enough in their structure and function to be significantly different from ordinary cardiac muscle (Thibodeau & Patton 2007). The main function of the cardiac cells is to contract. Contraction is initiated by electrical changes within the cardiac cells making up the cardiac muscle (myocardium). The myocardium is mainly composed of muscle cells that can be classified into two types: contractile cells that account for around 99% of cardiac cells, and autorhythmic cells that account for the remaining 1%.

Contractile cells (myocytes) have an elongated structure and are connected to adjacent cells by intercalated discs. Gap junctions between the cells allow electrical (ionic) conduction to pass between neighbouring cells, allowing the heart to contract as a single unit. The myocyte cell membrane (sar-colemma) contains long, tubular invaginations called transverse T tubules that extend in-between myofibrils to facilitate rapid calcium influx during depolarisation. Cardiac myocytes are composed of bundles of myofibrils that contain sarcomeres, the basic contractile units of the myocyte, which are aligned with each other and separated by Z lines. Sarcomeres are composed of thick and thin filaments – myosin and actin, respectively – which are important in myocardial contraction. Using adenosine triphosphate (ATP) for energy, filaments of actin chemically link and unlink with those of myosin, resulting in cardiac contraction and relaxation. Between the actin strands are rod-shaped proteins known as tropomyosin to which the troponin complex is attached at regular intervals (see Figure 1.1a). The troponin complex is responsible for the regulation of actin–myosin function and is made up of three subunits: troponin-T (TN-T), troponin-C (TN-C) and troponin-I (TN-I).

Key point

Troponin-I and troponin-T are released into the circulation when myocytes die – they are measured and used as diagnostic markers of myocardial infarction.

Autorhythmic cells have the ability to generate electrical activity without an external stimulus and are found in the sinoatrial (SA) node, atrioventricular (AV) node, bundles of His and Purkinje fibres.

The action potential

All living cells in the body have an electrical potential across the cell membrane. This can be measured by inserting a microelectrode into the cell and measuring the electrical potential in millivolts (mV) inside the cell relative to that outside the cell. At rest, a ventricular myocyte has a membrane potential of around –90 mV, and this is known as the resting membrane potential (Em). Em is determined by a combination of the concentrations of negatively and positively charged electrons across the cell membrane, the relative permeability of the cell membrane to these ions and the function of the ionic pumps that transport ions across the cell membrane (Klabunde 2005). The primary ions involved in the determination of cell membrane potential are sodium (Na+), chloride (Cl~), potassium (K+) and calcium (Ca++). The cardiac action potential is the electrical activity of the individual cells of the heart that occurs through changes in the cell membrane, permitting the inward and outward flow of ions, resulting in:

depolarisation, which occurs when the interior of the cardiac cell is maximally charged with positive ions; and

Repolarisation, the process of restoration of a cell to its normal resting membrane polarity following depolarisation.

Cardiac action potentials act in a similar manner to other action potentials within the human body, excepting the extended contraction time requirement of the cardiac muscle to effectively move blood through the heart and lungs and into the systemic circulation. The duration of ventricular action potentials range from 200 to 400 ms, compared to 2–5 ms in skeletal muscle cells or 1 ms in a typical nerve cell (Klabunde 2005).

As outlined earlier in this chapter, there are two types of cells in the heart: myocytes (non-pacemaker cells) and autorhythmic (pacemaker) cells. These cells have different action potentials. Non-pacemaker action potentials are triggered by depolarisation currents from adjacent cells, whereas pacemaker action potentials are capable of spontaneous action potential generation, known as automaticity (Klabunde 2005).

Key point

The electrical activity of cardiac myocytes (non-pacemaker cells) is apparent on the ECG. The electrical activity of the specialized conduction tissues (pacemaker cells) are not apparent on the surface ECG because of the relatively small mass of these tissues compared to the myocardium. Pacemaker cells have no true resting potential; instead, they generate regular, spontaneous action potentials.

The action potential in non-pacemaker cells

The action potential in non-pacemaker cells (atrial and ventricular myocytes and Purkinje cells) has five phases, numbered 0–4 (Figure 3.1).

Phase 0 represents the rapid depolarisation phase where the fast sodium channels open and there is a rapid influx of Na

+

into the cell. Calcium moves slowly but steadily into the cell. The membrane potential moves from the negative charge of 85–90 mV to

+

10–20 mV. This creates a gradient with the surrounding cell membranes, allowing the electrical current to flow from the depolarised cell to the surrounding cells, propagating the impulse.

Phase 1 represents an initial repolarisation of the cell caused by opening of special transient outward K

+

channels and the inactivation of the Na

+

channels. Cl

–

ions re-enter the cell.

Phase 2 represents the plateau phase where repolarisation is delayed because of the slow inward movement of Ca

++

through long lasting (L-type) calcium channels.

Key point

L-type calcium channels are blocked by pharmacological L-type calcium channel blockers such as verapamil, diltiazem and dihydropyradines such as nifedipine.

Figure 3.1 Action potential in a cardiac cell.

Phase 3 is the final repolarisation phase. Ca

+

+

channels close and K

+

flows rapidly out of the cell.

Phase 4 refers to the phase where the cell is not stimulated (the resting membrane potential). This phase coincides with diastole. K

+

is restored to the inside of the cell and Na

+

to the outside by active transport through the sodium–potassium pump.

Key point

The ability of the cell to open fast Na+ channels during phase 0 is related to the membrane potential at the moment of excitation. For the cell to be able to open the fast Na+ channels, the resting membrane potential must be at baseline (85–90 mV) and all Na+ channels closed. Excitation opens the Na+ channels, causing a large influx of Na+ ions. If, however, the membrane potential is less negative, some of the fast Na+ channels will not open, resulting in a reduced response to excitation of the cell membrane. In some cases, the cell may not be excitable, and conduction through the heart may be delayed, which increases the risk of arrhythmias.

During phases 0, 1, 2 and part of phase 3, the cell is refractory (unexcitable, unresponsive) to the initiation of new action potentials. This is known as the effective refractory period (ERP). The ERP acts as a protective mechanism in the heart by limiting the frequency of action potentials (and therefore contractions) that the heart can generate, enabling the heart to have adequate time to fill and eject blood. At the end of ERP, the cell is in its relative refractory period, where suprathreshold depolarisation stimuli are required to elicit action potentials (Klabunde 2005).

Learning activity

Potassium is a most important ion in the cardiac action potential. What would you expect to happen to the action potential and heart rhythm in hyperkalemia and hypokalaemia? You may find the following clinical review from the British Medical Journal useful in answering these questions: He, J.F. & MacGregor, G.A. (2001). Beneficial effects of potassium. British Medical Journal, 323:497–501. Retrieved online 17th October 2007 from www.bmj.com/cgi/content/full/323/7311/497

The cardiac conduction system

Cells within the cardiac conduction system are described as autorhythmic or self-excitable, that is to say that they are able to repeatedly and rhythmically generate their own electrical impulses. The conduction system therefore forms a route or pathway for electrical impulses to travel through the myocardium, which in turn will initiate the mechanical contraction of the heart.

The sinoatrial (SA) node is often described as the natural pacemaker of the heart, as this is where initial electrical impulses arise. It is located in the wall of the right atrium just below the opening of the superior vena cava. The SA node at rest generates impulses at an inherent rate of between 60 and 70 impulses per minute (Jones 2006). This rate will increase in response to specific stimuli including exercise, stimulant drugs such as epinephrine, and pyrexia. Additionally, there are specific structures that link the SA node to the left atrium and the atrioventricular (AV) node to ensure rapid propagation of the electrical impulse throughout the atria (Figure 3.2). These structures are termed the internodal tracts over which conduction proceeds more rapidly than in other areas of the atrial myocardium. The conduction of the electrical impulse throughout the right and left atria is seen on the ECG as the P wave and stimulates atrial contraction (Figure 3.3).

Figure 3.2 Atrial conduction.

Source: Reproduced from Meek and Morris (2002). With permission from BMJ Publishing Group Ltd.

Key point

If a rhythm originates from the sinus node at a rate less than 60 bpm, this is known as sinus bradycardia. If a rhythm originates from the sinus node at a rate greater than 100 bpm, this is known as sinus tachycardia.