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Symptomatic hypotension, venous oximetry and outpatient hemodialysis

Dissertation
Author: H. Paul Smith
Abstract:
Problem statement . Symptomatic hypotension is the most common complication during hemodialysis. It can induce cardiac arrhythmias and predisposes patients to coronary, splanchnic, and/or cerebral ischemic events. Non-invasive intermittent blood pressure measurement is used to identify hypotension during dialysis, yet it is a post-facto indicator of intravascular hypovolemia. Continuous monitoring of central venous oxygen saturation (ScvO2) may offer an innovative approach to early detection of symptomatic hypotension during outpatient hemodialysis. Aims . The overall aim of this study is to determine whether ScvO2 is related to changes in systolic blood pressure (SBP) and acute signs and symptoms in outpatients undergoing hemodialysis. The specific aims of this study are to determine the: (1) change in ScvO2 as fluid is removed during outpatient hemodialysis; (2) relationship between ScvO2 and changes in systolic blood pressure during hemodialysis; (3) association between percent change in ScvO2 and acute signs and symptoms during hemodialysis; (4) association between the percent change in SBP and acute signs and symptoms during hemodialysis; and (5) change in ScvO2 in patients without symptomatic hypotension compared to those with symptomatic hypotension. Methods . In this prospective observational study, data were collected from adult hemodialysis outpatients with a central line dialysis catheter. ScvO2, blood pressure, blood volume change, total fluid removed and acute signs and symptoms were recorded during one week of consecutive hemodialysis treatments. Descriptive statistics, multi-level regression and multi-level negative binomial regression models were utilized to analyze data. Findings . Subjects (n=39) were mostly African American (49%) and White (28%) with a mean age of 60±17 years. There was a statistically significant linear and quadratic change in ScvO2 during hemodialysis and the change trajectory was significantly greater in those patients with symptomatic hypotension. ScvO2 was significantly associated with SBP and acute signs and symptoms. Acute symptoms associated with hypotension occurred in 38% of patients and 24% of dialysis treatments. Conclusion . ScvO2 may be used by dialysis nurses to guide therapeutic interventions to avoid symptomatic hypotension in the outpatient setting. Further research is warranted to replicate these findings and broaden our understanding of strategies to mitigate hypotensive symptoms.

TABLE OF CONTENTS Copyright……………………………………………………………………………...…..ii Acknowledgements and Dedication…………………………………………………..….iii Abstract……………………………………………………………………………….…..iv Table of Contents…………………………………………………………………………vi List of Tables……………………………………………………………….………….....ix List of Figures………………………………………………………………………...…...x CHAPTER 1 – INTRODUCTION Statement of the Problem and Significance……...………………………….…….2 Study Aims……………………………………………………………..…………3

CHAPTER 2 – CONCEPTUAL FRAMEWORK AND REVIEW OF LITERATURE Introduction………………………………………………….…………….………5 Circulatory Physiology: Basic Concepts of Volume, Pressure and Flow…………5 Volume………………………………………………………….….….…..6 Pressure……………………………………………………………...…….7 Flow………………………………………………………………….……8 Normal Oxygen Delivery and Consumption………………………………….....10 Oxygen Delivery………………………………………………………....10 Oxygen Consumption……………………………………………………11 Oxygen to Assess Flow…………………………………………………..12 Venous Oxygen Saturation Monitoring………………………………………….13 The Process of Hemodialysis and the Dialysis Patient…………………….…….16 The Process of Hemodialysis………………………………………….....16 The Dialysis Patient……………………………………………………...18 Plasma Refilling to Maintain Volume…………………...……....19 Peripheral Vascular Resistance to Maintain Pressure……..……..20 Cardiac Output to Maintain Flow………………………..………20 Oxygen Delivery and Consumption During Hemodialysis……………….….….21 Ischemia During Hemodialysis………………………………………………..…23 Cardiac Ischemia………………………………………………..……..…23 Splanchnic Ischemia………………………………………………..……24 Cerebral Ischemia………………………………………………………..24 Signs and Symptoms During Hemodialysis…………………….…….…………26 Early Studies of Symptoms Associated With Hemodialysis…………….26 Prevalence of Acute Signs and Symptoms During Hemodialysis……….27 Hypotension…………………………………………….……..…33 Muscle Cramps………………………………………………..…34 Nausea and Vomiting…………………………………….……....36 vi

Dizziness…………………………………………...….……..…..38 Summary………………………………………………………..….…….……....39 CHAPTER 3 – METHODS Study Design……………………………………..…………..…………...……..40 Sample and Setting……………………………….………..…………………….40 Study Variables and Measures…………………….……..………………………40 Data Collection Procedure………………………….…..…………………..……45 Data Analysis………………………………………...…………………………..46 Aim 1………………………………………..………………...…………47 Aim 2………………………………………………………….…………48 Aim 3…………………………………………………………………….48 Aim 4…………………………………………………….………………49 Aim 5…………………………………………………………………….49

CHAPTER 4 – RESULTS Sample Characteristics…………………..……………………………………….50 Physiologic Measures and Treatment Start………………………………………52 Total Fluid Removed and Percent Change in Physiologic Variables……..…..…52 Hypotensive Events Associated with Acute Symptoms……………………..…..53 Acute Signs and Symptoms………………………………………….…………..54 Timing, Severity and Distress of Acute Symptoms…………………..………….55 Aim 1: ScvO2 Change over Time…………………………………..……………57 ScvO2 Change over Time by Clinic……………………………………..59 Aim 2: ScvO2 Change over Time Related to SBP…………………..…….…….62 Aim 3: ScvO2 Change and Acute Signs and Symptoms……………………...…65 Aim 4: SBP Change and Acute Signs and Symptoms……………………….…..67 Aim 5: ScvO2 Change over Time by Symptom Status……………………….....68 CHAPTER 5 – DISCUSSION Interpretation and Significance of the Study Results………….…………………73 ScvO2 Change over Time……………………………………….……….73 ScvO2 Change over Time Related to SBP………………………………75 ScvO2 Change and Symptomatic Hypotension…………..……………...76 SBP Change and Symptomatic Hypotension…………….………………77 Occurrence of Acute Symptoms………………………………………....78 Severity and Distress of Acute Symptoms……………….……………...79 Strengths and Limitations…………………………………………..…………....81 Implications for Nursing and Future Research………………………..…………82 References……………………………………………………………………..……..….84 Appendix A Crit-Line III™ with Sensor Clip……………………………………….....103 vii

Appendix B: Hct-based Blood Volume Monitor……………………………………….104 Appendix C: Acute Symptom Data Collection Form…………………………………..105 Appendix D: ELSEVIER Permission to Reprint……………………………………….106 Publishing Agreement………………………………………………………………..…108

viii

LIST OF TABLES 2-1 Frequency of Signs and Symptoms during Hemodialysis, 1980 – 1990………...30 2-2 Frequency of Signs and Symptoms during Hemodialysis, 1996 – 2007………...32 3-1 Study Variables and Associated Instruments………………………………….…41 4-1 Baseline Demographic and Clinical Characteristics…………………………..…51 4-2 Mean Physiologic Measures at Treatment Start.............................................…...52 4-3 Mean Change in Physiologic Variables During Dialysis……………….……….53 4-4 Symptom Frequencies…………………………………………………...……….55 4-5 Timing, Severity and Distress of Acute Symptoms………………………….…..55 4-6 Parameter Estimates: ScvO2 regressed on time30 and day………………...……57 4-7 Variance Components: ScvO2 regressed on time30 and day……………………58 4-8 Parameter Estimates: ScvO2 on time30 and day by clinic ……………….……..60 4-9 Variance Components: ScvO2 on time30 and day by clinic .........................…...61 4-10 Parameter Estimates: ScvO2 regressed on time30 with baseline SBP………..…63 4-11 Variance Components: ScvO2 regressed on time30 with baseline SBP………...64 4-12 Multi-level NBR: Predicting a Symptom from ScvO2 % Change………...…….66 4-13 Multi-level NBR: Predicting a Symptom from SBP % Change…………………67 4-14 Baseline Demographic and Clinical Characteristics by Symptom Status……….68 4-15 Physiologic Measures by Symptom Status……………………………………....69 4-16 Parameter Estimates: ScvO2 regressed on time30 by symptom status…………..70 4-17 Variance Components: ScvO2 regressed on time30 by symptom status……...…71

ix

x

LIST OF FIGURES 2-1 Pressure and Flow………………………………….……………………………...9 2-2 Normal Hgb-O2 Dissociation Curve…………………………………………….11 4-1 Plot of Predicted Values: ScvO2 regressed on time30…………………………..59 4-2 Plot of Predicted Values: ScvO2 regressed on time30 by Clinic………………...62 4-3 Plot of Predicted Values: ScvO2 regressed on time30 with baseline SBP………65 4-4 Plot of Predicted Values: ScvO2 regressed on time30 by symptom status……...72

CHAPTER 1 INTRODUCTION There are over 341,000 people in the United States with end-stage renal disease (ESRD) who are dependent on dialysis for survival (United States Renal Data Systems, 2009). Hemodialysis is performed three to four times per week to remove wastes that cannot be excreted due to end-organ kidney disease. Basically, hemodialysis involves exposing patient blood to a semi-permeable membrane to allow wastes and fluid to be removed from the body. The rate of fluid removal is preset by the dialysis prescription and nurses monitor patient responses to fluid removal using blood pressure (BP), heart rate (HR) and subjective complaints. These parameters reflect intravascular hypovolemia and associated end-organ ischemia. The number of people requiring dialysis continues to increase annually. Between 2005 and 2006, the greatest increase in number of these patients occurred among those age 45 – 64 and 65 – 74, at 6.1, and 3.5 percent respectively (United States Renal Data Systems, 2009). The emergence of the baby boomers into a senior population will contribute to the rapid growth of the overall dialysis population, with projections exceeding 600,000 dialysis dependent patients by the year 2020 (United States Renal Data Systems, 2009). The most common causes of ESRD are diabetes and hypertension, significantly increasing the risk of cardiovascular complications and mortality (National Kidney Foundation Kidney Early Evaluation Program, 2006). Patients with kidney disease experience symptoms associated with both their comorbid conditions and dialysis treatment. Hemodialysis is associated with physiologic responses and symptoms which 1

negatively impact patients’ health and quality of life (Al-Arabi, 2006). Consequently, most patients on dialysis are vulnerable to ischemia related to cardiovascular instability and symptomatic hypotension (Santoro, 2006). Statement of the Problem and Significance Hypovolemia of the intravascular compartment through ultrafiltration is the most common complication of hemodialysis and results in the occurrence of symptomatic hypotension in 10 to 50 percent of dialysis treatments (Henrich, 1999; Hosslie, 2005; Schreiber, 2001). In a survey of 422 registered nurses working in hemodialysis units across the country, more than two-thirds (69%) stated that dialysis hypotension occurs several times a week to daily (Thomas-Hawkins, Flynn, & Clarke, 2008). Symptomatic hypotension during hemodialysis is a well-documented cause of patient discomfort as well as early termination of dialysis therapy (DeOreo, 1997; Rocco & Burkart, 1993). Hypotension that occurs during dialysis treatments can induce cardiac arrhythmias, predispose patients to coronary, splanchnic, and/or cerebral ischemic events, and is associated with end-organ damage and increased mortality (Jakob, Ruokonen, Vuolteenaho, Lampainen, & Takala, 2001; National Kidney Foundation Kidney Disease Outcomes Quality Initiative, 2005b; Shoji, Tsubakihara, Fujii, & Imai, 2004). Recent clinical practice guidelines established by the National Kidney Foundation (2005a) define symptomatic hypotension as a decrease in systolic blood pressure (SBP) of 20 mm Hg or a decrease in mean arterial pressure (MAP) of 10 mm Hg associated with symptoms. These acute symptoms include muscle cramps, nausea, vomiting, dizziness or fainting, abdominal discomfort, yawning, sighing, restlessness, and anxiety (National Kidney Foundation Kidney Disease Outcomes Quality Initiative, 2005a). In 2

addition to these acute symptoms, dialysis patients experience a plethora of chronic, often co-occurring signs and symptoms during and in between dialysis sessions. Common chronic symptoms include fatigue, pain, itching and thirst (Janssen, Spruit, Wouters, & Schols, 2008; Murtagh, Addington-Hall, & Higginson, 2007). The primary monitoring parameters during dialysis are limited to intermittent BP and HR measurements and the patient’s subjective complaints (National Kidney Foundation Kidney Disease Outcomes Quality Initiative, 2005a, 2005b, 2006b). While often used to monitor circulatory competence, changes in BP and HR reflect the later stages of circulatory failure and not the adequacy of the circulation to meet the metabolic demands of the tissues (Cordtz, Olde, Solem, & Ladefoged, 2008; Shoemaker, 1996). The primary purpose of the circulatory system is to deliver oxygen to the tissues to maintain viability, yet the movement and utilization of oxygen in patients experiencing symptomatic hypotension during hemodialysis has not been well investigated. Recent advances in hemodialysis technology allow continuous measurement of blood oxygen saturation during a dialysis session. Monitoring of venous blood oxygen saturation is utilized routinely in critical care as an early indicator of hemodynamic instability, including impending hypotension, but has not been fully explored in patients undergoing outpatient hemodialysis.

Study Aims The overall aim of this study is to determine whether central venous oxygen saturation (ScvO2) is related to changes in SBP and acute signs and symptoms in outpatients undergoing hemodialysis.

3

The specific aims of this study are to determine: 1. the change in ScvO2 as fluid is removed during hemodialysis; 2. the relationship between ScvO2 and changes in SBP during hemodialysis; 3. the association between percent change in ScvO2 and acute signs and symptoms during hemodialysis; 4. the association between the percent change in SBP and acute signs and symptoms during hemodialysis; 5. the change in ScvO2 among patients with no symptomatic hypotension compared to those with symptomatic hypotension.

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CHAPTER 2 CONCEPTUAL FRAMEWORK AND REVIEW OF LITERATURE

Introduction The reasons for symptomatic hypotension during hemodialysis are multifactoral, but primarily due to intravascular hypovolemia and decreased cardiac output from too rapid of fluid removal during the dialysis procedure (Daugirdas, 1991). Care of the chronic dialysis patient requires an understanding of the physiologic mechanisms and the various treatment and patient related factors associated with symptomatic hypotension. This chapter will discuss circulatory physiology, oxygen delivery and consumption, the process of hemodialysis and the physiologic responses to hemodialysis related to the dialysis patient. A review of the literature pertaining to ischemic signs and symptoms during hemodialysis will also be presented. Circulatory Physiology: Basic Concepts of Volume, Pressure, and Flow The primary role of the circulatory system is the delivery of dissolved gases and other molecules for nutrition, growth, and repair (Boron & Boulpaep, 2005). The normal heart, blood, and vessels are highly integrated and during everyday activities are able to adapt or compensate to meet the oxygen requirements of organs and cells. The body’s ability to compensate, however, may be challenged under conditions of advanced age, physiologic stress such as trauma or illness, and cardiovascular disease. An understanding of basic circulatory physiology is necessary in order to contextualize what occurs in patients undergoing hemodialysis. The most important characteristics of the circulation are volume, pressure, and flow (Smith & Kampine, 5

1990). These core concepts are interrelated and provide a foundation for understanding one of the primary functions of the circulation: the movement and utilization of oxygen. Volume The total blood volume is the sum of formed elements which include red cells, white cells, and platelets, in a liquid medium called plasma. The plasma is the non-cellular part of the blood and communicates continuously with the interstitial fluid through the pores of the capillary membranes. The percentage of the blood that is cells is called the hematocrit. Therefore, if a person has a hematocrit of 40, this means that 40 percent of the blood volume is cells and the remainder is plasma. The cells occupy about 40 percent of the total blood volume and the plasma volume occupies about 60 percent of the total blood volume. These percentages can vary considerably in different people, depending on sex, weight, and other factors (Guyton & Hall, 2000). In healthy individuals, the plasma volume is maintained by a complex balance between fluid intake and urinary and gastrointestinal output. The total blood volume in a normal adult ranges from 70 to 75 ml / kg of body weight. Therefore, a 70 kg adult has a total blood volume of about 5000 ml with 3000 ml of the total as plasma volume and about 2000 ml as red cell mass (Guyton & Hall, 2000). A person’s total blood volume is not uniformly distributed throughout the body. About two-thirds of the total blood volume is normally in the venous system, about one-sixth is in the arteries, and the remaining is in the heart and pulmonary circulation (Boron & Boulpaep, 2005).

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Pressure Blood pressure is the force exerted by the blood against any unit area of the vessel wall, and is measured in millimeters of mercury (mmHg) (Guyton & Hall, 2000). Vascular tone is maintained by smooth muscle cells and is regulated by a complex balance between the cardiopulmonary and pressoreceptor reflexes, the autonomic and sympathetic nervous systems, and vasoactive hormones such as the renin-angiotensin system (Hollenberg, Kavinsky, & Parrillo, 1999; Sato et al., 2001; Smith & Kampine, 1990; Ushioda et al., 1983). Because of the structure and relative elasticity of the circulatory system, there is an inverse relationship between volume and pressure in the arteries and veins (Smith & Kampine, 1990). Though the venous system normally contains about four times more blood volume than the arterial system, the internal pressure in the large arteries is normally about 120/80 mm Hg in contrast to 10 mm Hg at the venous end of the capillaries (Smith & Kampine, 1990). All blood vessels contain varying proportions of smooth muscle, elastin, and collagen and the arteries are thicker and have large amounts of elastin as compared to veins. The thicker and elastin rich arteries allow them far greater ability to sustain pressure energy in contrast to the thin-walled venous system. The difference in the volume/pressure characteristics of arteries and veins have been described as their ‘distensibility’, or the percent increase in volume that is necessary to create a unit pressure change (Guyton & Hall, 2000). The distensibility of the circulatory system is influenced not only by the thickness and composition of the vessel wall, but also by the degree of filling of the vessel. The distensibility of a normal artery is reduced under conditions of high pressure, such as volume overload. Veins on the other hand, 7

have much lower pressures and much greater distensibility which is why they are able to store 25 to 30 times the volume of the arterial system. Distensibility of the circulatory system is altered by age, disease, autonomic stimulation, and various medications (Boron & Boulpaep, 2005; Smith & Kampine, 1990). Flow Blood flow is characterized by the moving stream of blood in the circulation, as the term “flow” is the displacement of volume per unit of time (Boron & Boulpaep, 2005). Blood flow through a vessel is determined by the pressure gradient, or the pressure difference of the blood between the two ends of a vessel, and the vascular resistance within that vessel (Guyton & Hall, 2000). The flow of blood in the vascular system can be calculated by the following formula: ¨P = F * R in which ¨P is the pressure difference (gradient) between the two ends of the vessel, F is blood flow, and R is the resistance. This calculation is based on Ohm’s law, where the pressure difference (¨P) between an upstream point (P1) and a downstream site (P2) is equal to the product of the flow (F) and the resistance (R) (Figure 2-1).

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Figure 2-1. Pressure and Flow: The flow (F) between a high-pressure point (P1) and low- pressure point (P2) is proportional to pressure difference (¨P). From Boulpaep, E. L. (2003). Integrated Control of the Cardiovascular System. In Medical Physiology: Update Edition (p. 426). With permission.

Normal blood flow delivered by the heart is the quantity of blood that passes a given point in the circulation in a given period of time and is expressed in milliliters per minute or liters per minute (Guyton & Hall, 2000). Blood flow in the circulation of an adult person at rest is about 5000 ml / minute and is called the cardiac output, which is the product of the heart rate times the stroke volume (Guyton & Hall, 2000). Blood flow is dependent not only on the degree of vascular resistance from the vessel diameter, but also the viscosity of the blood (Boron & Boulpaep, 2005). Viscosity is the resistance to flow due to the friction of molecules in a moving stream of liquid (Boron & Boulpaep, 2005). The viscosity of normal blood is about three times as great as the viscosity of water (Guyton & Hall, 2000). The relative viscosity of whole blood depends on the concentration of cells (hematocrit) in relation to the plasma volume. As red cell volume increases (such as after a blood transfusion) or the plasma volume decreases (such as during dehydration), blood becomes more hemoconcentrated. This 9

results in an increase in viscosity of the blood and as hematocrit increases, the relative viscosity increases disproportionately. For example, an increase of 10 in the hematocrit from the level of 40 will increase the viscosity about 25% and an increase of 20 to the level of 60 will increase viscosity about 60% (Smith & Kampine, 1990). Normal Oxygen Delivery and Consumption Oxygen Delivery More than 98% of oxygen is transported bound to hemoglobin with less than two percent dissolved in plasma (Boron & Boulpaep, 2005). Hemoglobin is normally present in a concentration of 14 to 15 g/dl of whole blood (Smith & Kampine, 1990). If blood is fully saturated with oxygen (100%), one gram of hemoglobin can combine with 1.34 ml of oxygen so that blood with a hemoglobin concentration of 15 g/dl will then have a maximum oxygen carrying capacity of 20.1 ml / dl (Guyton & Hall, 2000). The amount of oxygen that combines with each unit of hemoglobin is dependent primarily on the partial pressure of oxygen, and to a lesser extent, pH, PC02, blood temperature, or the presence of chronic lung disease (Smith & Kampine, 1990). The normal relationship between oxygen and hemoglobin is best depicted using the hemoglobin-oxygen (Hgb- O2) dissociation curve (Figure 2-2).

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Figure 2-2. A normal Hgb-O2 dissociation curve, assuming 15g Hgb/dl. The y axis on the right shows O2 content. The y axis on the left, gives the percentage of Hgb saturation. (Hgb = hemoglobin). From Boulpaep, E. L. (2003). Integrated Control of the Cardiovascular System. In Medical Physiology: Update Edition (p. 659). With permission.

The Hgb-O2 dissociation curve represents the “S-shaped” relationship between the hemoglobin saturation (%), the partial pressure of O2 (PO2) (mmHg), and the oxygen content in the blood (ml O2/dl of blood). At low P02 values, increases in P02 produce small increases in oxygen saturation and reduced oxygen content in the blood. At moderate P02 values, the amount of bound oxygen increases more steeply with increases in PO2. Lastly, the curve flattens out at high PO2 values as the hemoglobin saturates even more, maximizing the oxygen content in the blood. Oxygen delivery to the organs and tissues is determined by several factors, including not only the concentration of Hgb in the blood and its oxygen saturation, but also the cardiac output, and the efficiency with which the O2 is “unloaded” to the tissues. Consequently, despite the presence of a normal PO2, a patient’s O2 delivery may be 11

inadequate if the patient is anemic, hypovolemic, or has a reduced cardiac output (Dudell, Cornish, & Bartlett, 1990; Guyton & Hall, 2000). Oxygen Consumption Oxygen is consumed in the tissues to maintain cellular metabolism and energy production and can be measured indirectly by the difference between arterial oxygen content and venous oxygen content (Bauer, Reinhart, & Bauer, 2008). Normally, oxygen delivery is four to five times the oxygen consumption (Dudell et al., 1990), and approximately 20 – 25% of the oxygen delivered is utilized, and the rest remains in the venous blood. If the hemoglobin of the arterial blood is 100% saturated, normal venous hemoglobin saturation will be 75% to 80% saturated. An abrupt decrease in venous oxygen saturation is caused by a decrease in delivery or an increase in consumption. Tissue oxygenation is determined by a balance between the rate of oxygen transport in the blood to the tissues and the rate at which the oxygen is used by the tissues to meet cellular metabolic demand (Guyton & Hall, 2000). Without evidence of venous oxygen saturation, cardio-respiratory monitoring based solely on the measurement of heart rate, blood pressure, and arterial oxygen saturation alone provides little information on tissue and cellular oxygenation (Bauer et al., 2008). Oxygen to Assess Flow Oxygen can be used to measure blood flow. In 1870, Fick explored the relationship between cardiac output, global oxygen demand and oxygen extraction and discovered the principle that total uptake or release of any substance by an organ is the product of blood flow to the organ by the difference between the arterial content and the venous content of the substance (Fick’s principle) (Vandam & Fox, 1998). For example, according to the 12

classic Fick equation, cardiac output equals the oxygen consumption (VO2) divided by the difference between the arterial and venous oxygen content (Mahutte et al., 1994): Q(VO2) = ___ ______VO2 ___________ 13.4Hgb (SaO2 – SvO2) where Q(VO2) denotes cardiac output, VO2 the oxygen consumption, Hgb the hemoglobin, SaO2 the arterial oxygen saturation, and SvO2 the venous oxygen saturation. For the whole body circulation, the input flow is the arterial oxygen delivery to the tissues, and the output flow is measured by the venous oxygen return to the heart (Caille & Squara, 2006). There is extensive evidence that oxygen is the most flow-dependent blood constituent because it has the largest extraction ratio and the net O2 transported is the amount consumed by the tissues and may be easily and repeatedly measured (Shoemaker, 1987). Oxygen transport is strongly related to survival or death, and therefore circulatory function should be evaluated in terms of oxygen consumption and oxygen delivery. To better understand the physiologic concepts associated with oxygen delivery and consumption during illness, it is important to review the research of cardiac and trauma patients using venous oxygen saturation monitoring. Venous Oxygen Saturation Monitoring Venous oxygen saturation is the balance between arterial oxygen supply and tissue oxygen demand with a normal value between 60 – 80% (Guyton & Hall, 2000). Venous oxygen saturation decreases when systemic oxygen delivery has been compromised or when systemic oxygen demands increase (Rivers, Ander, & Powell, 2001). Venous 13

oxygen saturation monitoring or venous oximetry allows for a global assessment of oxygen supply and demand, and is used as a prognostic, diagnostic and therapeutic tool in critically ill patients experiencing sepsis, trauma, hemorrhagic shock, and cardiac dysfunction (Reinhart & Bloos, 2005). The critical care literature makes reference to mixed venous oxygen saturation and central venous oxygen saturation. The differences between them lie in where these measurements are obtained. Mixed venous oxygen saturation (SvO2) is obtained from the pulmonary artery using a pulmonary artery catheter, necessitating an intensive care environment. Central venous oxygen saturation (ScvO2) is obtained at the junction of the superior vena cava and the right atrium using a central venous catheter, which is widely feasible in most clinical settings. Both provide a measure of oxygen returning to the heart and lungs. The relation between mixed and central venous oxygen saturation in animal and human models has been studied and reviewed extensively (Rivers, Ander et al., 2001). These two indices are highly correlated when viewed serially, with r values ranging from .85 to .99 (Dueck, Klimek, Appenrodt, Weigand, & Boerner, 2005; Goldman, Klughaupt, Metcalf, Spivack, & Harrison, 1968). A large body of literature has been published regarding the use of both mixed (SvO2) and central (ScvO2) venous oxygen saturation as early indicators of hemodynamic instability in multiple critical care settings. In an early study of patients with myocardial infarction (n=31), Goldman, et al. (1968) demonstrated that as myocardial function deteriorates, ScvO2 falls. In this study, they demonstrated that clinical signs of heart failure were usually present when the ScvO2 was <60% (p < 0.001) and that when the ScvO2 was <45%, myocardial dysfunction had progressed to a shock state (p < 0.001). 14

In addition, early research in cardiac surgery demonstrated the usefulness of SvO2 as an early marker of cardiac deterioration (de la Rocha, Edmonds, Williams, Poirier, & Trusler, 1978; Muir, Kirby, King, & Miller, 1970). Jamieson, et al. (1982) evaluated the usefulness of SvO2 monitoring as an index of cardiac output and overall tissue perfusion in high-risk cardiac surgery patients (n= 20). The results indicated that satisfactory mixed venous oxygen saturation (> 65%) correlated with normal hemodynamic measurements including cardiac output and cardiac index (r > .95), and that a fall in SvO2 of more than 10% was noted before a fall in the mean blood pressure, increase in heart rate, or change in other hemodynamic measures (p < 0.05). Their findings also demonstrated however, that a decrease in measured ScvO2 occurs with fever, pain, shivering, increased work of breathing, and interventions or procedures. Scalea, et al (1988) investigate the use of multiple hemodynamic parameters to identify the earliest and most reliable indicator of blood loss in the canine model (n=16). Using Swan-Ganz catheters and arterial lines, they collected vital signs and full hemodynamic parameters including arterial and mixed venous blood gases. After bleeding the dogs in increments of 3% of their total blood volume, only cardiac index and SvO2 showed linearity as a function of measured blood loss (r = .85, and .99 respectively). Scalea, et al (1990) then investigated trauma patients (n=26) with an injury mechanism suggesting blood loss, but who were deemed stable after initial evaluation. They found that ScvO2 was more reliable and sensitive to acute blood loss than blood pressure, pulse, pulse pressure, urine output, and central venous pressure (r = 0.436, p < 15

0.005). The linear coefficients were considerably less for all parameters in the clinical study as opposed to the laboratory model due to the lack of a controlled environment in the trauma setting. Despite this, the investigators found that a decrease in ScvO2 reliably predicted blood loss and severity of injuries. Rady, et al. (1996) found that 50% of critically ill patients presenting in shock who were resuscitated to normal vital signs continued to have increased lactate and abnormally low ScvO2, indicating anaerobic metabolism and oxygen debt. These patients required further interventions, giving rise to the clinical use of ScvO2 in the early management of cardiac arrest, the postresuscitation period, trauma and hemorrhage, severe heart failure, severe sepsis and septic shock (Rivers, Ander et al., 2001). These studies are limited by sample size and generalizable only to cardiac and trauma patients. Despite this, however, these findings raise the question of whether venous oximetry would be a useful monitoring tool in complex dialysis patients experiencing large fluid shifts during the dialysis procedure. Of interest is whether ScvO2 monitoring in the dialysis patient could be used to identify physiologic changes that could then be acted upon by nursing staff to prevent symptomatic hypotension. The Process of Hemodialysis and the Dialysis Patient The Process of Hemodialysis Hemodialysis is a substitute process for the filtering functions of the kidney and involves the movement of solutes (waste products) and water across a semi-permeable membrane by diffusion and osmosis (Ahmad, 1999). Clinically, this exchange takes place by exposing the patient’s blood to an artificial membrane outside of the body called an “artificial kidney” or dialyzer. Every dialyzer contains two compartments: the blood 16

Full document contains 119 pages
Abstract: Problem statement . Symptomatic hypotension is the most common complication during hemodialysis. It can induce cardiac arrhythmias and predisposes patients to coronary, splanchnic, and/or cerebral ischemic events. Non-invasive intermittent blood pressure measurement is used to identify hypotension during dialysis, yet it is a post-facto indicator of intravascular hypovolemia. Continuous monitoring of central venous oxygen saturation (ScvO2) may offer an innovative approach to early detection of symptomatic hypotension during outpatient hemodialysis. Aims . The overall aim of this study is to determine whether ScvO2 is related to changes in systolic blood pressure (SBP) and acute signs and symptoms in outpatients undergoing hemodialysis. The specific aims of this study are to determine the: (1) change in ScvO2 as fluid is removed during outpatient hemodialysis; (2) relationship between ScvO2 and changes in systolic blood pressure during hemodialysis; (3) association between percent change in ScvO2 and acute signs and symptoms during hemodialysis; (4) association between the percent change in SBP and acute signs and symptoms during hemodialysis; and (5) change in ScvO2 in patients without symptomatic hypotension compared to those with symptomatic hypotension. Methods . In this prospective observational study, data were collected from adult hemodialysis outpatients with a central line dialysis catheter. ScvO2, blood pressure, blood volume change, total fluid removed and acute signs and symptoms were recorded during one week of consecutive hemodialysis treatments. Descriptive statistics, multi-level regression and multi-level negative binomial regression models were utilized to analyze data. Findings . Subjects (n=39) were mostly African American (49%) and White (28%) with a mean age of 60±17 years. There was a statistically significant linear and quadratic change in ScvO2 during hemodialysis and the change trajectory was significantly greater in those patients with symptomatic hypotension. ScvO2 was significantly associated with SBP and acute signs and symptoms. Acute symptoms associated with hypotension occurred in 38% of patients and 24% of dialysis treatments. Conclusion . ScvO2 may be used by dialysis nurses to guide therapeutic interventions to avoid symptomatic hypotension in the outpatient setting. Further research is warranted to replicate these findings and broaden our understanding of strategies to mitigate hypotensive symptoms.