Mechanical Circulatory and Respiratory Support

Shaun Gregory,John Fraser,Michael Stevens

• Publisher: Academic Press
• Year: 2017
• ISBN:
  9780128104927
• Topic: Technology & Engineering
• Subtopic: Biomedical Science
• Index: Technology & Engineering

Mechanical Circulatory and Respiratory Support is a comprehensive overview of the past, present and future development of mechanical circulatory and respiratory support devices. Content from over 60 internationally-renowned experts focusses on the entire life-cycle of mechanical circulatory and respiratory support – from the descent into heart and lung failure, alternative medical management, device options, device design, implantation techniques, complications and medical management of the supported patient, patient-device interactions, cost effectiveness, route to market and a view to the future.

This book is written as a useful resource for biomedical engineers and clinicians who are designing new mechanical circulatory or respiratory support devices, while also providing a comprehensive guide of the entire field for those who are already familiar with some areas and want to learn more. Reviews of the most cutting-edge research are provided throughout each chapter, along with guides on how to design new devices and which areas require specific focus for future research and development.

• Covers a variety of disciplines, from anatomy of organs and evolution of cardiovascular devices, to their clinical applications and the manufacturing and marketing of devices
• Provides engineering and clinical perspectives to assist readers in the design of a market appropriate device
• Discusses history, design, usage, and development of mechanical circulatory and respiratory support systems

Part 1

Heart Failure and Nondevice Treatment

Chapter 1

Descent into heart and lung failure

Maithri Siriwardena⁎; Eddy Fan^{†,‡ ⁎} Critical Care Research Group, Intensive Care Unit, The Prince Charles Hospital, Brisbane, QLD, Australia
^† Interdepartmental Division of Critical Care Medicine University Health Network/Mount Sinai Hospital, Toronto, ON, Canada
^‡ Extracorporeal Life Support Program, University Health Network, Toronto, ON, Canada

Abstract

Mechanical circulatory and respiratory support is a rapidly expanding field. Available devices can potentially completely accomplish the primary function of the heart and lung, i.e., the transport of oxygen and nutrients to cells and the maintenance of perfusion pressure. If oxygenation and tissue perfusion are compromised, multiorgan dysfunction ensues and is potentially irreversible in established cases.

Depending on the acuity and severity of the pathological state encountered and despite the timely introduction of pharmacological and ventilatory support, selected cases of cardiorespiratory failure require such measures. This may take the form of short-term support such as intra-aortic balloon pumps, short-term ventricular assist devices, extracorporeal membrane oxygenation, or long-term ventricular assist devices.

The effective design and use of such advanced therapies require a thorough understanding of normal cardiorespiratory anatomy, physiology, and pathophysiology and is, therefore, reviewed in this chapter.

Keywords

Cardiorespiratory failure; Pathophysiology; Cardiac anatomy; Cardiac physiology; Respiratory physiology

Acknowledgment

The authors would like to thank Dr. Bradley Smith, staff anesthetist at St Vincent's Hospital, Sydney, for his contribution to this chapter.

Introduction

The primary role of the heart and lung is transport of oxygen and nutrients to cells. In health, both allow the transport of oxygen from the atmosphere to the alveolar capillary membranes and efficiently to cells in different organs, with variable rates of oxygen consumption according to widely varying demands. This chapter aims to cover basics in cardiac and respiratory anatomy and physiology and give the reader a brief overview of pathology and treatment options.

The cardiac portion focuses primarily on left ventricular (LV) dysfunction since this is the primary cause of pathology. More emphasis is given to LV systolic dysfunction or heart failure (HF) with reduced ejection fraction (HFrEF) than diastolic dysfunction. Despite having similar prevalence, morbidity, and mortality, HF with preserved ejection fraction (HFpEF) is still incompletely understood and is without effective treatment options that meaningfully alter survival.

The causes and management of respiratory failure are summarized. The main form of support in respiratory failure remains humidified supplemental oxygen and mechanical ventilatory support. The respiratory portion introduces the reader to two scenarios, acute severe asthma and acute respiratory distress syndrome (ARDS), where effective treatment with mechanical ventilation alone may not be sufficient.

Cardiac Anatomy and Physiology

The heart is a mediastinal structure encased in a fibrous pericardial sac consisting of the parietal and visceral pericardium. A small amount of pericardial fluid decreases the resistance for normal translational motion of the heart during contraction (systole) and relaxation (diastole). The heart consists of left and right sides, with each side containing a ventricle and an atrium.

Heart Chambers

Right-sided chambers drain deoxygenated blood from the superior and inferior vena cava. The right ventricle (RV) forms the most anterior part of the heart and has a complex three-dimensional structure; in the long axis, it appears triangular but is crescenteric in cross section [1,2].

The RV is composed of the inlet, the free wall, and the infundibulum and has a superficial and deep muscle layer. The superficial layer is circumferential and although the fibers are initially parallel to the atrioventricular (AV) groove, they later run obliquely toward the apex [1]. These are continuous with the superficial fibers of the left ventricle (LV). The deep layer runs longitudinally from the base to the apex. The major vector of contraction of the RV is in this longitudinal plane. The RV wall thickness is only 2–5 mm (compared to LV wall thickness 7–11 mm), and the RV mass is 26±5 g/m² (compared with LV mass 87±12 g/m²). The shape and the relatively thin wall make the RV a highly compliant chamber with the ability to adapt to volume overload but not pressure overload [2,3].

The left-sided chambers drain oxygenated blood from the pulmonary veins and then pump this through the high-pressure peripheral circulation. The LV is a complex, truncated ellipsoid structure that can eject approximately 100 mL of blood at pressures of over 200 mmHg against a relatively noncompliant systemic circulation during exercise [4–6]. It consists of three layers of myofibrils that are arranged in counterwoven helical arrangements with a major vector of contraction being both longitudinal and circumferential [5]. The contribution of torsion or rotational motion is specific to the LV, with the basal segments and apical segments moving in opposite direction. This not only helps to eject blood more efficiently but also allows the storage of energy that can then be released during diastole. The LV can then refill at low filling pressures within as short a time as 100 ms [6]. LV diastolic filling starts later and finishes earlier, with higher filling velocities, compared to the RV. The average end-diastolic volume (EDV) indexed to body surface area (BSA) is less in the LV compared to the RV (66 mL/m² compared with 75 mL/m²); therefore, the LV ejection fraction (EF) is greater than the RVEF (LVEF >50% compared with RVEF 40%–45%) [1,2]. LV stroke work index is approximately five times that of the RV (50±20 g/m² compared with 8±2 g/m²), as it is required to pump into a high resistance systemic circuit (average systemic vascular resistance is 1100 dynes s cm^-5 compared with the average pulmonary vascular resistance of 70 dynes s cm^-5) [1,7,8]. The left and right ventricles are separated by the interventricular septum, which is concave towards the (LV). The pressures and oxygen saturation of each cardiac chamber is summarized in Fig. 1.1.

Fig. 1.1 Pressures and oxygen saturations of each cardiac chamber. Adapted from Hall JE. Guyton and Hall textbook of medical physiology. 13th ed. p. 1 online resource; Mann DL, Zipes DP, Libby P, Bonow RO, Braunwald E. Braunwald's heart disease: a textbook of cardiovascular medicine. 10th ed. p. 1 online resource (xxvii, 1943, 1943 pages); Figure by Yujiro Kawanishi, St Vincent's Hospital, Sydney.

Each side has a thin-walled atrium that acts as a conduit, reservoir, and pump. Atrial myocytes are smaller and have faster repolarization rates and fewer mitochondria than ventricular myocytes. The atria and ventricles act as a functional syncytium with the cardiac myocytes of each chamber interconnected with intercalated discs and gap junctions, which allow the rapid propagation of action potentials, allowing, in turn, synchronized cardiac contraction [9,10]. The efficient pumping of blood depends on the correct electrical activation by excitatory and conductive muscle fibers—namely, the sinus and AV nodes, connected by the internodal tracts, the AV His bundles, and the intraventricular conduction systems [10,11]. Given that the two ventricles anatomically share the interventricular septum, myocardial fibers, and the pericardium, in disease states one ventricle can influence...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Contributors
• Preface
• Acknowledgments
• Part 1: Heart Failure and Nondevice Treatment
• Part 2: Types of Cardiovascular Devices
• Part 3: Pump Design
• Part 4: Implantation and Medical Management
• Part 5: Physiological Interaction Between the Device and Patient
• Part 6: Route to Market (and Staying There!)
• Part 7: Summary
• Index