PART 1: Introduction and History of Autonomic Nervous System Monitoring
CHAPTER 1:
Introduction to Parasympathetic and Sympathetic Monitoring
This introductory section starts with a review of the “Old School” information commonly taught in medical school, including the anatomy of the autonomic nervous system (ANS) and its two branches, the parasympathetic and sympathetic nervous systems; the biochemistry of the ANS; general physiology associated with the two ANS branches; and methods of measuring the ANS. Measuring the ANS includes older noninvasive measures and the newer method to be the basis of this book. This section concludes by answering the “So What?” question behind the development of a newer method of measuring the ANS, specifically, a general introduction to why it is important to specifically measure the parasympathetic and sympathetic nervous systems, independently (in a mathematical sense) and simultaneously. The newer method removes many of the assumptions and approximations required by the older methods, improving specificity, sensitivity, reliability, and repeatability and thereby improving patient outcomes.
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CHAPTER 2:
History of Parasympathetic and Sympathetic Monitoring
Historically, heart rate variability (HRV) has been recognized as the primary method for noninvasive monitoring of the autonomic nervous system (ANS), including its parasympathetic and sympathetic branches. HRV, however, is a single independent measure of heartbeat intervals (HBI). Yet the ANS is a system with two independent components. As a measure of a system with two independent components, HRV fails a fundamental law of mathematics. Therefore, it is merely a gross measure of total ANS function. More recently, beat-to-beat blood pressure (btbBP) has been developed in an attempt to better specify sympathetic activity. Again, btbBP fails the fundamental law of math. It is still just based on HBIs and therefore a gross measure of the ANS. More information is needed. This information historically came in the form of symptoms. Yet, as was introduced in the previous chapter, symptoms often are late in the progression of autonomic dysfunction and also often require assumption. MIT and Harvard researchers understood that a second, independent measure was required to clear the ambiguity and the need for assumption. These researchers determined and validated that the second measure is respiratory activity. This chapter introduces the history of confusion caused by HRV and perpetuated by btbBP and resolves the issue with the second independent measure of respiratory activity.
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CHAPTER 3:
Drawbacks of Heart Rate Variability Analysis and Application of Parasympathetic and Sympathetic Monitoring
In this chapter, the failure of heart rate variability and beat-to-beat blood pressure is delineated and the solution to their failings (P&S monitoring) is introduced and developed. The chapter compares graphically spectral analysis of HRV with the spectral analysis method associated with P&S monitoring. The method of spectral analysis, the Fourier transform, is developed and demonstrated and applied to both HRV and P&S monitoring. This is to demonstrate how spectral analysis quantifies the respective measurement, enabling the primary care physician to assess their patient’s ANS. The shortcomings of the Fourier transform when applied to biological, especially autonomic, signals are then elucidated and their solution in the form of wavelet transforms is introduced and developed. In conclusion, the two transform techniques are then compared graphically.
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PART 2: Validation and General Evaluation of the Autonomic Nervous System
CHAPTER 4:
Validation and General Evaluation of Parasympathetic and Sympathetic Monitoring
Part II provides validations of the P&S monitoring method. This chapter bases P&S validation on comparisons with HRV-alone techniques in response to rest, deep breathing, head-up postural change (stand), clinical examples and in an outcomes study. It ends with a short treatise on past completed validation studies and summarizes how these studies also demonstrate that the methods reduce morbidity and mortality risk, thereby improving patient outcomes.
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CHAPTER 5:
Autonomic (Parasympathetic and Sympathetic) Assessment
The clinical ramifications of the differences between P&S monitoring and HRV alone are explored as the differences pertain to the Autonomic Assessment itself. Through this, the format, justification, and contraindication of the clinical autonomic assessment are discussed. The six phases of the clinical autonomic assessment are based on the Ewing challenges, including rest, deep breathing, Valsalva, head-up postural change (standing), and the intervening baselines. The resting phase (initial baseline) enables the patient to be their own control allowing for results on the first assessment. The assessment fulfills the American Diabetes Association’s recommended tests to assess autonomic function, including blood pressure and EKG responses to the Ewing challenges. The unique to P&S monitoring finding of parasympathetic excess (PE) in response to Valsalva or stand is introduced with its clinical implications.
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CHAPTER 6:
Parasympathetic and Sympathetic Testing
This chapter begins the rest of the book, in that it turns the readers’ attention from the theoretical and developmental issues behind P&S monitoring and begins the focus of applying P&S monitoring clinically. It is a general overview of the additional information that is available from P&S monitoring and Autonomic Assessment. In this chapter, we describe the data that are collected, what clinical reporting is produced, and how to utilize and interpret the reports. Again, within the theme of an overview, orienting the reader to what will come, these are general interpretation guidelines, the specifics, including disease-specific applications, will come later. Included in this chapter is how P&S monitoring may be synergistic with other tests. In general, two questions are asked: are the sympathetics managed, and are the parasympathetics balanced, relative to the sympathetics, to promote health and minimize risk? The chapter starts with a general answer to the inevitable “So what?” response, which is more specifically answered throughout the remainder of the book in relation to specific diseases.
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CHAPTER 7:
Interpreting Parasympathetic and Sympathetic Results
The interpretation algorithm presented in this chapter only assesses the patient’s ANS. It has no “knowledge” of the patient or patient history. It assumes an otherwise healthy individual. While multiple ANS symptoms may be demonstrated simultaneously, they must all must be considered together and together with the patient’s history in mind. The software can diagnose the ANS, but not the ANS in light of the patient’s history. This is where the physician’s experience and knowledge of the specific patient history, physical examination, laboratory data, and other pertinent diagnostic tests are needed. The report from many physicians is that the software only highlights autonomic dysfunction. The true interpretation comes when these highlights are applied to the specific patient history, etc. Only then are appropriate therapy plans developed and is the physician ready to speak with the patient.
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CHAPTER 8:
Possible Therapy Options
There are two sets of possible therapy options presented here and discussed throughout this book: pharmaceutical and non-pharmaceutical. At rest there are only four autonomic imbalances. Contrary to the “seesaw” model of the ANS taught in medical school, one side low is not always the same as the other side high. This is only typical in healthy individuals. Treating patients as if it were often does not lead to improved outcomes. The four states should be treated separately, but with the “seesaw” still in mind, when more therapy is needed. For example, it is often not recommended to attempt to treat by directly increasing parasympathetic activity. So to effect an increase in the parasympathetics, we treat to decrease the sympathetics. However, this only works so long as the therapy does not drive HR and BP too low and cause fatigue and other dysfunction. During the dynamic states (i.e., in response to challenges) therapy is even more directed. Lastly, the therapy options included are only to treat the ANS. They assume an otherwise healthy individual. While some therapies can be additive to treat multiple ANS symptoms simultaneously, all therapy must be considered with the patient’s history in mind. The software can diagnose the ANS, but not the ANS in light of the patient’s history. This is where the physician’s knowledge of the patient and experience is needed. After all is reviewed in context, the physician can then target and tailor therapy more precisely.
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CHAPTER 9:
Cardiovascular Autonomic Neuropathy: Risk Factor or Risk Indicator
This chapter discusses some more recent articles regarding risk factors and inflammation. There is a significant body of evidence that associates cardiovascular autonomic neuropathy (CAN) with most risk factors and with inflammation. It is known that CAN is associated with increased morbidity and mortality risk. The associations with traditional and nontraditional, as well as modifiable and nonmodifiable, risk factors, including inflammation, have historically made CAN a difficult diagnosis, especially since the perception has been that CAN is not treatable. This chapter concludes by explaining that this perception is not correct and discusses, generally, possible treatment modalities. Within the community of P&S monitoring, CAN has become an important diagnosis to document as early as possible to help avoid increased morbidity and mortality risk that leads to greater medication loads and hospitalization rates, causing greater healthcare costs.
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CHAPTER 10:
Normal Data
Chapter 10 presents a series of normal patients. Normal is defined as an individual not currently prescribed with medication with autonomic assessment responses that are within age- and baseline-adjusted, published, normal limits; this includes a couple of octogenarians. This chapter includes the method by which the physician can have quality assurance regarding the clinical assessment results. Since the physician does not have to be in the room when the autonomic test is administered, this method provides the physician a level of assurance that the data are valid. The chapter concludes with discussion on specificity, sensitivity, reliability, and reproducibility.
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CHAPTER 11:
Medical Specialties’ View of Autonomic System Measurements
This short chapter presents the seminal articles that provide the basis for the patients for whom Autonomic Assessment is recommended. The articles are from the medical leadership, including the American Academy of Family Practitioners, American Academy of Neurology, American Diabetes Association, and American Heart Association. The articles identify which diseases or disorders lead to autonomic neuropathy. We know that autonomic neuropathy is late in the progression and leaves few therapy options. We know that autonomic dysfunction is treatable, but is asymptomatic. Therefore, the leadership articles lead to the conclusion that the disease or disorder itself is the “symptom” indicating the need for autonomic assessment. This avoids the issue of screening. So, as long as the patient has been diagnosed with a chronic condition that is identified in the literature as leading to autonomic neuropathy, then they are recommended for periodic Autonomic Assessment.
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PART 3: Assessment and Management of the Parasympathetic and Sympathetic Nervous Systems
CHAPTER 12:
The Progression of Autonomic Dysfunction in Chronic Disease
Normally, when we are born, we are born with as healthy an ANS as we will have: our resting response is in the middle of the gray area on the baseline response plot. When we are no longer breathing, there is no power in either ANS branch: our resting response is at the bottom left corner of the baseline response plot. The middle diagonal line connecting the two points, the perfect balance line, turns out to be the slowest path from birth to death. This means that the ANS will decline, even if we live a “perfectly healthy life.” As will be demonstrated, chronic disease accelerates this decline. Fortunately, as has been demonstrated in the previous chapter, establishing and maintaining proper balance for the individual can return the patient to a “normal” decline, slowing the progression of autonomic dysfunction as much as possible, minimizing morbidity and mortality risk. Note that the progression plots are not from numbers of patients followed from birth; they are composite plots from large populations of subjects covering the ages. Albeit balance has become the key to promoting and maintaining health and minimizing morbidity and mortality risk. These plots demonstrate the difference between normal aging balance and disease balance.
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CHAPTER 13:
Autonomic Dysfunction Versus Neuropathy
Unfortunately the “autonomic neuropathy” has inherited the misperception that it is not treatable. While this may be true due to a lack of sufficient information, it is no longer the case. This then begs the question, when does autonomic dysfunction become autonomic neuropathy. While neuropathy may now be treatable, given more information, it still leaves the physician with few therapy options. Autonomic dysfunction has more therapy options but is asymptomatic. In this chapter, we will discuss a recent study to highlight the difference between autonomic neuropathy and dysfunction, and provide another approach to differentiating stages of autonomic decline. There is actually two schools of thought: five stages of decline or six. The six stages of decline include a brief second stage which is early in the progression. It is not often observed. However, it may provide the insight needed to understand the etiology of high BP or hypertension secondary to many chronic diseases.
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CHAPTER 14:
General Autonomic Disorders
This chapter discusses “general” autonomic disorders. These are autonomic disorders that may be present regardless of the primary disease or disorder or age or stage. Included is the association between autonomic dysfunction and inflammation. Recent evidence indicates that the two are linked and that treating one helps to relieve the other. The etiology of inflammation may provide additional insight into the processes contributing to the progression of autonomic dysfunction.
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PART 4: Internal Medicine
CHAPTER 15:
Geriatrics
Part IV begins the specialty-specific applications of P&S monitoring. The first specialty is presented in internal medicine. In this chapter, the first section under internal medicine presents applications in geriatrics. P&S monitoring is contrasted with Holter monitoring. Outcomes are discussed in geriatric heart failure, and the benefits of “more parasympathetic activity” at rest are discussed in detail. Too much more resting parasympathetic activity is associated with depression, and depression is known to elevate mortality risk in heart disease patients. However, a little more parasympathetic activity is known to be cardioprotective. Historically, the difficulty was titrating to “a little more.” In other words, is it possible to quantify “a little more”? The study that answers this question is included. Like the Lipid Hypothesis in the 1990s, simply demonstrating that having “a little more” resting parasympathetic activity is beneficial is not enough. It must be demonstrated that titrating to establish and maintain “a little more” improves outcomes. These results are described as well.
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CHAPTER 16:
Depression
Depression is associated with parasympathetic excess (PE), whether at rest or during Valsalva or stand. Typically, Valsalva or stand PE is associated with unstable patients, including difficult to control BP, blood glucose, or hormone level, and stand PE can mask sympathetic withdrawal (SW) which is associated with orthostatic dysfunction. In cases of depression, Valsalva or stand PE often involves depression with anxiety, high BP, pain, or hyperactivity, i.e., bipolar, manic depression, anxiety, hypertension with depression, chronic regional pain syndrome, fibromyalgia, chronic fatigue, or attention-deficit disorder with or without hyperactivity. Physiologically, the PE amplifies the sympathetic response, causing a seemingly normal individual at rest to react excessively. Since the sympathetic nervous system is the reactionary nervous system, it should not be surprising that the Valsalva or stand PE is the primary autonomic disorder. Treating the PE enables the sympathetics to react less excessively, normalizing those responses, thereby normalizing BP or other responses. Stand PE masking SW helps to document and treat dizzy hypertensives. Resting PE is associated with clinical or subclinical depression and is the PE that elevates mortality risk in heart disease patients.
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CHAPTER 17:
Gastroenterology
The parasympathetic nervous system uniquely controls the gastrointestinal (GI) tract. In the upper GI tract, GERD is possible in two ways: either as a parasympathetic insufficiency (leading to gastroparesis) causing food to collect, causing the acid to back up into the esophagus, or as a parasympathetic excess causing an overactive stomach, splashing the acid up into the esophagus. In the lower GI tract, parasympathetic insufficiency leads to lower motility leading to constipation, and parasympathetic excess leads to excess motility leading to diarrhea. Most GI medications, especially those that affect motility, are direct or indirect anticholinergics.
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PART 5: Cardiology
CHAPTER 18:
Arrhythmia
Part V moves into cardiology. This chapter considers arrhythmia. It looks at atrial fibrillation as a possible model of arrhythmia and discusses the interpretation of ANS assessment results that include high-quality arrhythmia. While traditional HRV is contraindicated for arrhythmia, P&S monitoring, as shown in the atrial fibrillation trail is not. This is the result of the more specific measures of P and S activity. Where HRV alone uses spectral analysis windows for low and high frequencies that are of different widths, the window widths for P&S monitoring are significantly more well matched. For P&S monitoring, the matched windowing enables greater noise rejection, where the arrhythmia is treated as (relatively) broad-spectrum noise. With improved noise rejection, arrhythmic records may still be interpreted. For records with arrhythmia in only one or two phases, like with pacing activation, consider the arrhythmia as a symptom, given the stimulus being presented in that phase of the assessment.
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CHAPTER 19:
Heart Diseases
This chapter considers heart diseases, beginning with the P&S association with sudden cardiac death. Included are coronary artery disease, congestive heart failure, and cardiovascular diseases with depression. The ValHeft and COMET studies are revisited with P&S monitoring, and ranolazine improvements in P&S responses and cardiac outcomes are presented. The basic premise is that the heart, a special muscle, is not unlike other muscles. It is controlled by nerves, the P&S nerves. Documenting P&S responses to disease helps to guide therapy for the individual patient. Documenting the individual’s P&S responses to therapy helps to determine patient compliance and guide titration and selection for the individual. As is demonstrated, P&S monitoring provides more information promoting improved outcomes.
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CHAPTER 20:
Hypertension
This chapter discusses hypertension. The sympathetic nervous system mediates baroreceptor reflex, which medicates blood pressure. Chronic elevations in sympathetic activity lead to elevations in blood pressure which may lead to hypertension. Elevations in sympathetic activity may be a primary autonomic condition or it may be secondary to a parasympathetic excess. This differentiation helps to differentiate between primary hypertensive disorders and labile or difficult to control hypertension, sometimes known as autonomically mediated hypertension. The difficulty in control may be due to a hidden parasympathetic excess thwarting therapy by being exacerbated by the therapy. Another possible form of secondary hypertension is as a reflex to orthostatic dysfunction. These patients are those whose dizziness is exacerbated when their BP is reduced and whose BP is exacerbated when their dizziness is relieved. P&S monitoring provides more information to document and manage hypertension.
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PART 6: Endocrinology
CHAPTER 21:
Diabetes
Diabetes has been discussed several times throughout the book. It is arguably one of the most researched chronic diseases regarding autonomic dysfunction. This body of data provides a strong basis for the systemic ways, in part via the autonomic nervous system, that diabetes affects multiple organ systems. This helps as a basis for a model of the autonomic effects of chronic disease in general and therefore as an example of many of the effects of autonomic dysfunction, due to chronic disease, on comorbidities and symptoms secondary to autonomic dysfunction. In this section we focus on diabetes specifically and hypoglycemia effects on the ANS.
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CHAPTER 22:
Other Diseases in Endocrinology
Because diabetes is one of the most researched diseases regarding the autonomic nervous system and due to its near epidemic conditions, other endocrine diseases are often overlooked. This is unfortunate, especially given the intimate relationship between the ANS and the endocrine system. Virtually, all hormones are at least neuromodulators and some serve as neurotransmitters. This relationship often makes these “other” endocrine diseases (the title is in no way meant to be de minimis) some of the more interesting diseases to diagnose and treat. Unfortunately, at this time, we only have significant amounts of data to discuss hypothyroid and estrogen dysfunction. In many cases, establishing and maintaining P&S balance helps to maintain a more normal endocrine function. However, the challenge is in the fact that changes, due to therapy, in the functioning of the ANS and the endocrine system are on different time scales and treating one affects the other. As a result, the physician and the patient must treat one and wait to see the response in the other, treat the other, and wait again. This “seesawing” back and forth may happen three or more times over 18 or more months before a final equilibrium is reached. Examples are included.
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PART 7: Neurology
CHAPTER 23:
Dizziness
In general, there are four conditions that directly lead to dizziness or lightheadedness: vestibular dysfunction, arrhythmia, orthostatic dysfunction, and syncope. Only the last three may involve the autonomic nervous system. Which, by the way, is the main reason for augmenting vestibular testing with autonomic testing in geriatrics, where there is rarely a single cause for dizziness. Ultimately, all three non-vestibular causes of dizziness involve marginal or poor perfusion of the brain due to decreased of insufficient blood flow to the brain. It has been our experience that a significant number of people (about 40 % of those reporting dizziness or lightheadedness) are simply dehydrated. Dehydration is most often due to a lack of proper daily hydration; too many sugary (including sugar substitutes), caffeinated, or alcoholic drinks; or excessive use of diuretics. Preclinical or subclinical orthostatic dysfunction, and perhaps preclinical syncope, may not yet actually involve dizziness or lightheadedness. Rather, due to marginal brain perfusion, it often involves afternoon fatigue, headache, reduced cognitive function, and evening edema. These may also be signs of insufficient volume or in appropriate volume distribution. The autonomics are not the only reason for dizziness. Vascular function (“lazy” walls or damaged valves in the veins) and cardiac function (damaged valves, holes in walls, or carotid or renal artery stenoses) may also be involved. If autonomic responses to head-up postural change are normal or autonomic therapy, after at least 3 months, is not sufficient, additional testing may be indicated to also treat the end organ(s).
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CHAPTER 24:
Pain Management
Continuing in neurology, this chapter will address P&S monitoring in pain management. Here we take data from both chronic care and critical care. The majority of the critical care applications will be presented later in that section. Pain is a stressor. The sympathetic nervous system responds to stress. Therefore, sympathetic responses may be used as an objective measure of pain responses, assuming BP is well managed. Given this premise, P&S monitoring in general helps in pain management in four ways: (1) objectively quantifying pain level, (2) differentiating the types of pain, (3) titrating therapy, and (4) documenting rehabilitation. The comorbidities associated with chronic pain are due to the effects of sympathetic excess. Quantitatively assessing sympathetic activity periodically helps to reduce the risk of high BP and hypertension, GI and sleep disorders, urogenital dysfunction, cardiovascular disease, MI, and sudden cardiac death. The last few risks are a main reason for cardiology referral from pain management. While the pain management physician is not ordering an autonomic assessment for the purposes of documenting risk of cardiovascular disease, MI, and sudden cardiac death, it is a natural outcome of the assessment as described elsewhere in this compendium. It is not the intent of the pain management physician to usurp the cardiologist, only to provide the cardiologist with the opportunity to test further and care for their patient. Recently, the field of pain management medicine has welcomed anesthesiologists.
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CHAPTER 25:
Sleep
A third general area of neurology is sleep medicine. The association between sleep medicine and P&S monitoring is very straightforward: daytime sleepiness is associated with parasympathetic excess (PE), and nighttime sleeplessness is associated with sympathetic excess (SE). In this way, P&S monitoring helps to document underlying autonomic involvement which provides more information to guide therapy and improve outcomes. The chapter discusses at length obstructive sleep apnea (OSA). OSA has as its autonomic characteristic, SE. The danger of OSA, as with other chronic conditions that involve SE, is that just treating OSA does not always mean that the SE is relieved. Especially in OSA since the typical therapy is not a sympatholytic. Rather, like pain therapy, CPAP and other typical OSA therapies merely relieve the stress associated with OSA; it does not directly reduce SE, which may leave the patient at continued morbidity or mortality risk. For example, if the patient is a diabetic with hypertension and OSA, the diabetes may involve some SE, the hypertension may involve more SE, and the OSA may involve even more SE. CPAP will only relieve the SE associated with OSA; the SE associated with the other diseases may not be effected and therefore persist. This may be a reason for a significant portion of the OSA patient population experiencing cardiovascular disease even though they are faithful to use CPAP as prescribed.
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CHAPTER 26:
General Neurology
In this chapter, we finish presenting the P&S data we have to date on the remainder of the fields within neurology, including Parkinson’s disease, multiple system atrophy, pure autonomic failure, multiple sclerosis, epilepsy, unexplained seizures, abnormal sweating, and Sörgren’s disease. P&S monitoring, in large part, had its start in cardiology and was significantly promoted in endocrinology (specifically diabetology). However, it is hoped that in bringing more information to light regarding a largely, heretofore, unmeasured portion of the nervous system, neurology will accelerate its growth. The purpose of P&S monitoring is to augment the field of autonomic nervous system monitoring, not to replace anything. P&S monitoring has its role. It is an easy to implement, apply, and utilize tool to assess, treat, and maintain patients who are known to be at risk for autonomic neuropathy before autonomic neuropathy is demonstrated. There is a point beyond which P&S monitoring is no longer effective, because at the level of the heart, there is not enough autonomic function remaining to be measured. It is at this point that traditional autonomic tests, including tilt table, become more effective. Several of the patient types that typically push the limits of P&S monitoring are presented in this section and include patients with advanced Parkinson’s, advanced multiple system atrophy, pure autonomic failure, and severe tremors and movement disorders.
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PART 8: Other Chronic Care Specialties
CHAPTER 27:
Pulmonology
These last chapters under chronic care are no less important than any other; there is just less data currently available in these areas. The hopes are that these areas will grow as P&S monitoring becomes more integrated into these fields of medicine. This chapter will discuss what we have regarding pulmonology, including COPD and asthma. Given the significant use of beta-2 adrenergic agonists utilized for these two diseases and given the fact that there are beta-2 receptors on the heart, it should not be surprising that there is an association between beta-2 adrenergic agonist utilization and eventual heart disease as a comorbidity and eventual mortality risk. The various hypotheses that are currently debated as to the etiology of the greater prevalence of heart disease in COPD and asthma patients all seem to have one thing in common, they all discuss different pathways associated with sympathetic excess (SE). P&S monitoring helps to document SE before changes in other physiologic states (i.e., increased BP, etc.), enabling physicians to intervene earlier, prior to additional symptoms.
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CHAPTER 28:
Pediatrics
At this point, the book has focused on adult medicine. Applications in pediatric medicine include some of the adult diseases, including diabetes, sleep disturbances, dizziness, seizure, headache, asthma, etc. The main differences are that the ANS, especially the parasympathetic nervous system, is more active in pediatric patients. This greater level of activity often masks underlying autonomic dysfunction or the dysfunction may come and go as the “growth spurts” (development periods) wax and wane. Furthermore, the symptomatology may also change in between the various development periods. In this day of a mobile society, it is often the case that the pediatric patient is not with the same physician throughout their pediatric years and the cyclic nature of the symptoms associated with autonomic dysfunction is often misunderstood. Due to this heightened activity, the normal range for rest (baseline) is 2.0–15.0 bpm2 for both LFa and RFa. Normal values for balance (SB) and stand responses are the same as in adults. The normal values for deep breathing and Valsalva are already age adjusted from 3 years of age. The data that we have and that is different from the adult data include sudden infant death syndrome, pediatric depression-like syndromes (including ADD/ADHD), and familial dysautonomia.
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PART 9: Critical Care
CHAPTER 29:
Critical Care
This chapter will cover several areas of critical care, including anesthesiology, the emergency department, the operating room, and the various intensive care units, highlighting the neonatology intensive care unit in the neonatology section. The original beta-studies that validated P&S monitoring were performed in the critical care arena, including anesthesiology (FG Estafanous, MD, Cleveland Clinic) and pediatric cardiac surgery (WI Norwood, MD, Children’s Hospital of Pennsylvania, University of Pennsylvania). Since the late 1990s P&S monitoring has been validated in the critical care arena under WC Shoemaker, MD, Los Angeles County, and University of Southern California Hospital, specifically in the areas of trauma and sepsis. This chapter will also discuss hypovolemia, hypoxia, heart transplantation, pediatrics, neonatology, and brain and closed head injury.
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PART 10: Sample Studies
CHAPTER 30:
Sample Case Studies
In this chapter, we discuss some common sample case studies, including hypertension with depression, unexplained dizziness, cardiovascular autonomic neuropathy (CAN), sleep apnea, atrial fibrillation, cardiac pathology, diabetes, and depression. It is important to remember that the main goal of autonomic assessment and therapy is not to cure disease. While that may happen, the goal is to slow the progression of autonomic dysfunction and to minimize morbidity and mortality risk. This enables the physician to be more aggressive towards the primary disease and to promote and maintain wellness once the primary disease is controlled. For example, autonomic assessment may not cure heart disease, arrhythmia, COPD, diabetes, or Parkinson’s disease; treating documented autonomic dysfunction will lead to relief from dizziness, depression, secondary hypertension, sleep disorder, etc. This leads to reduced medication load, reducing the potential for conflicting or confounding therapies. This also leads to reduced hospitalization and helps to promote reduced healthcare costs for both the patient and the nation while improving outcomes.
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CHAPTER 31:
Example of Longitudinal Studies
In this chapter, we look beyond the first test and provide sample longitudinal studies. Here we attempt to answer the questions: “Why test?” “How to intervene?” “What are the expected outcomes?” As examples we offer a diabetic and a hypertensive patient as examples.
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PART 11: Why Autonomic (Parasympathetic and Sympathetic) Assessment?
CHAPTER 32:
Summary: General Applications of Parasympathetic and Sympathetic Monitoring
As the last chapter of the book, we summarize it by answering the question, “Why autonomic (P&S) assessment?” Included in the answer are discussions on proactive patient management, individualized therapy titration, documenting outcomes, evidence-based medicine, value-based medicine, comparative effectiveness benefit, PQRI documentation, and improved patient care, and we finish with a look at P&S monitoring in different specialties.
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