The Breathless Heart: Apneas in Heart Failure

Description

This book systematically focuses on central sleep apneas, analyzing their relationship especially with heart failure and discussing recent research results and emerging treatment strategies based on feedback modulation. The opening chapters present historical background information on Cheyne-Stokes respiration (CSR), clarify terminology, and explain the mechanics and chemistry of respiration. Following a description of the physiology of respiration, the pathophysiology underlying central apneas in different disorders and particularly in heart failure is discussed. The similarities and differences of obstructive and central apneas are then considered. The book looks beyond the concept of sleep apnea to daytime CSR and periodic breathing during effort and contrasts the opposing views of CSR as a compensatory phenomenon or as detrimental to the failing heart. The diagnostic tools currently in use for the detection of CSR are thoroughly reviewed, with guidance on interpretation of findings. The book concludes by describing the various forms of treatment that are available for CSR and by explaining how to select patients for treatment. Preface References Contents 1: Historical Background and Glossary of the Apnea Phenomenon 1.1 Introduction 1.2 From Hippocrates to Hunter, Cheyne and Stokes: Watching the Ill Breathing 1.3 Between Nineteenth and Twentieth Century: The Golden Age of Physiology 1.4 From the Birth of Sleep Medicine to the Rediscovery of PB/CSR in Heart Failure 1.5 Appendix: A Brief Dictionary of Breathlessness References 2: Mechanics and Chemistry of Respiration in Health 2.1 Introduction 2.2 Functional Pulmonary Anatomy and Mechanics of Ventilation 2.2.1 Functional Pulmonary Anatomy 2.2.1.1 Pulmonary Volumes 2.2.1.2 Respiratory Muscles 2.2.1.3 Pulmonary Circulation 2.2.2 The Mechanical Substrate of Respiration 2.2.2.1 Resistances Elastic Resistances Non-elastic Resistances Turbulent Flux Resistances 2.2.2.2 Pulmonary, Thoracic and Thoracopulmonary Compliances 2.2.2.3 The Intrapleural Pressure 2.3 Pulmonary Gas Exchange 2.3.1 Alveolar Structure, Surfactant and Alveolar Gas Exchange 2.3.2 The Ventilation to Perfusion Ratio in Physiological and Pathological Conditions 2.3.3 Modulation of Gas Transport by Haemoglobin 2.3.3.1 CO2 Transportation 2.4 Central Control of Ventilation 2.5 Functional Architecture of Chemoreceptive Control of Ventilation 2.5.1 Peripheral Chemoreceptors 2.5.2 Central Chemoreceptors 2.5.3 Key Features of Chemoreflexes 2.5.3.1 Hypoxic Ventilatory Response (Fig. 2.3) 2.5.3.2 Hypercapnic Ventilatory Response (Fig. 2.4) 2.5.3.3 Integration of Central and Peripheral Chemoreflexes References 3: Hypopneas and Apneas as Physiological and Pathological Phenomena Throughout the Life Span 3.1 Introduction 3.2 Pediatric Apneas and Sudden Infant Death Syndrome 3.2.1 Definition 3.2.2 Epidemiology 3.2.3 Clinical Presentation, Risk Factors, and Complications 3.2.4 Pathophysiology 3.2.5 Treatment 3.3 Diverse Central Apneas in Physiological and Pathological Conditions 3.3.1 Idiopathic Central Sleep Apnea 3.3.1.1 Definition 3.3.1.2 Epidemiology and Clinical Presentation 3.3.1.3 Pathophysiology 3.3.1.4 Treatment 3.3.2 Apneas at High Altitude 3.3.2.1 Definition 3.3.2.2 Clinical Presentation 3.3.2.3 Pathophysiology 3.3.2.4 Treatment 3.3.3 Periodic Breathing in Neurological Diseases 3.3.3.1 Definition 3.3.3.2 Epidemiology and Clinical Presentation 3.3.3.3 Pathophysiology 3.3.3.4 Treatment 3.3.4 Periodic Breathing and Kidney Failure 3.3.4.1 Definition 3.3.4.2 Epidemiology 3.3.4.3 Clinical Implications and Complications 3.3.4.4 Pathophysiology 3.3.4.5 Treatment 3.3.5 Periodic Breathing and Pulmonary Hypertension 3.3.5.1 Definition 3.3.5.2 Epidemiology and Risk Factors 3.3.5.3 Clinical Implications and Complications 3.3.5.4 Pathophysiology 3.3.5.5 Treatment 3.4 Obstructive Sleep Apnea 3.4.1 Definition 3.4.2 Epidemiology and Risk Factors 3.4.3 Clinical Implications and Complications 3.4.4 Pathophysiology 3.4.5 Treatment References 4: Pathophysiology of Central Apneas in Heart Failure 4.1 Introduction 4.2 Introduction to Mathematical Modelling 4.3 Mathematical Basis Behind the Instability Loop Theory 4.4 History of Mathematical Modelling and Periodic Breathing 4.4.1 Horgan and Lange Model (1962) [21] 4.4.2 Longobardo Model (1966) [10] 4.4.3 Grodins Model (1967) [20] 4.4.4 The Mackey-Glass Model (1977) [33] 4.4.5 The Khoo Model (1982) [12] 4.4.6 The Carley and Shannon Model (1988) [44] 4.4.7 The Francis Model (2000) [14] References 5: The Importance of Visceral Feedbacks: Focus on Chemoreceptors 5.1 Introduction 5.2 Chemoreflex Overactivity, Ventilatory Instability, and Sympatho-vagal Imbalance 5.2.1 Clinical Correlates of Enhanced Chemosensitivity in CHF 5.2.2 Mechanisms of Increased Chemoreflex Sensitivity in CHF 5.2.3 From Enhanced Chemosensitivity to PB/CSR 5.2.4 Chemoreflex Overactivity and Autonomic Deregulation 5.3 Altered Baroreceptor and Ergoreceptor Sensitivities: Contributors to Autonomic Dysfunction and Ventilatory Instability? 5.3.1 Baroreflex Depression, Sympatho-Vagal Imbalance, and PB/CSR 5.3.2 Ergoreflex Overactivity and PB/CSR During Exercise References 6: The Apneas Before and After Heart Failure 6.1 Obstructive Sleep Apnea Before and After Heart Failure 6.1.1 Prevalence 6.1.2 Definitions 6.1.3 Hemodynamics 6.1.4 Severity 6.1.5 Metabolic and Cardiovascular Effects 6.1.6 Relationships with Heart Failure 6.1.7 Arrhythmia Risk 6.1.8 Arteriosclerosis 6.2 Treating Obstructive Sleep Apnea Before and After Heart Failure 6.2.1 Effects on Blood Pressure 6.2.2 Antiarrhythmic Effects 6.2.3 Inflammation and Metabolic Effects 6.2.4 Use in Heart Failure 6.3 Central Sleep Apnea in Heart Failure 6.3.1 Pathophysiology 6.3.2 Relationships with Heart Failure 6.4 Treating Central Sleep Apnea in Heart Failure 6.4.1 Continuous Positive Airway Pressure 6.4.2 Adaptive Servo Ventilation 6.4.3 Phrenic Nerve Stimulation References 7: Not Only Sleep Apnea: The “Awake” Apneas of the Failing Heart 7.1 Epidemiology and Clinical Predictors of Abnormal Breathing Patterns During Daytime in Heart Failure 7.2 Prognostic Value of Abnormal Breathing Patterns During Daytime in Heart Failure 7.3 Pathophysiological Mechanisms of Periodic Breathing During Wakefulness 7.4 Effects of Sleep on Ventilatory Control and Stability 7.5 Sleep or Awake Apneas? 7.6 Periodic Breathing and Body Position References 8: Exertional Oscillatory Ventilation and Central Sleep Apnea in Heart Failure: Siblings, Cousins, or What Else? 8.1 Definition of Exertional Oscillatory Ventilation 8.2 Prevalence of Exercise-Induced EOV 8.3 Physiology of Exercise-Induced Periodic Breathing in Heart Failure 8.4 Sleep Disorders in HF Patients with EOV 8.5 Prognostic Role of Exercise-Induced Periodic Breathing References 9: To Breathe, or Not to Breathe: That Is the Question 9.1 Introduction 9.2 To Take Arms Against a Sea of Troubles and by Opposing End Them. Periodic Breathing as a Compensatory Phenomenon. The Naughton’s Hypothesis (Hyperpnea Versus Apnea; Beneficial Effects on Hemodynamics, Ventilation and Other) 9.2.1 Is Really Cheyne-Stokes Respiration Detrimental? 9.2.2 Is Cheyne-Stokes Respiration Compensatory? 9.2.3 To Die, to Sleep: Periodic Breathing Is Bad for You (Detrimental Effects on Hemodynamics, Neurohormonal Activation, and Prognostic Value of Apneas in Heart Failure) References 10: Diagnostic Tools: The Easier, the Better 10.1 Introduction 10.2 Standard PSG 10.3 “Ambulatory” Sleep Recordings 10.3.1 Home Polysomnography 10.3.2 CR Monitoring 10.3.3 Single or Double Channel Recordings 10.4 Short-term In-lab Polygraphy References 11: Diagnostic Tools: Messages from Implanted Devices (Pacemakers as Diagnostic Tools) 11.1 Introduction 11.2 Automatic Detection of SA in Implantable Devices 11.2.1 Boston Scientific Technology 11.2.2 LivaNova Technology 11.2.2.1 Abnormal Breathing Pattern Identification 11.2.2.2 Calculation of the AHI References 12: Targeting and Treating Apneas 12.1 Introduction 12.2 How Should We Treat Apneas? Treating Downstream: CPAP Versus Servo-ventilation 12.2.1 Noninvasive Mechanical Ventilation 12.2.2 Types of Noninvasive Ventilation 12.2.2.1 Continuous Positive Airway Pressure (CPAP) 12.2.2.2 Auto-CPAP 12.2.2.3 Bi-level Positive Airway Pressure (BIPAP) 12.2.2.4 Adaptive Servo-assisted Ventilation 12.2.3 NIV in OSA Syndrome 12.2.4 NIV in Central Apneas 12.3 How Should We Treat Apneas? Treating Upstream: Which Target? (Chemoreflex, Hemodynamics, Others) 12.3.1 Drugs 12.3.1.1 HF Therapies and Inotropes 12.3.1.2 Acetazolamide 12.3.1.3 Theophylline 12.3.1.4 Benzodiazepines 12.3.2 Gas Administration 12.3.2.1 Oxygen 12.3.2.2 Carbon Dioxide 12.3.3 Devices and Surgery 12.3.3.1 Overdrive Pacing, Cardiac Resynchronization Therapy, and Dynamic Pacing 12.3.3.2 Heart Transplantation, Valve Surgery, and Ventricular Assist Devices 12.3.3.3 Chemoreflex Modulation or Demolition? 12.4 When Should We Treat Apneas? When Should We Not? Conclusive Remarks References 13: Novel Tools for Treating Central Apneas 13.1 Introduction 13.2 Feasibility Trial of Transvenous Phrenic Nerve Stimulation 13.3 Description of the Fully Implantable remedē® System and Pilot Trial of Phrenic Nerve Stimulation 13.4 Design of the remedē® System Pivotal Trial References 14: Breathless Heart: Final Remarks References