Correlation of blood gas and pH changes with arrhythmiasduring exercise in patients with chronic lung disease

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Authors Howe, Helen Serena, 1942-

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COREELATION OP BLOOD GAS AND pH CHANGES WITH ARRHYTHMIAS DURING EXERCISE IN PATIENTS

WITH CHRONIC LUNG DISEASE

byHelen Serena Howe

A Thesis Submitted to the Faculty of theCOLLEGE OF NURSING

In Partial Fulfillment of the Requirements For the Degree ofMASTER OF SCIENCE

In the Graduate CollegeTHE UNIVERSITY OF ARIZONA

1 9 7 6

STATEMENT BY AUTHOR.

This thesis has been submitted in partial ful­fillment of requirements for an advanced degree at The : University of Arizona and is deposited in the Uni­versity Library to be made available to borrowers under­rules of the Library.

Brief quotations from this thesis are allowable without special permission, provided that accurate acknowledgment of source is made. Requests for permis­sion for extended quotation from or reproduction of this manuscript in whole or in part may be granted by the . head of the major department or the Dean of the Graduate College when in his judgment the proposed use of the material is in the interests of scholarship. In all other instances, however, permission must be obtained from the author.

SIGNED:

APPROVAL BY THESIS DIRECTOR This thesis has been approved on the date shown below:

AsWcigfce Professor of Nursing

ACKNOWLEDGMENTS

The author wishes to express her appreciation to her committee: Miss Gayle Traver» Chairman; Mrs„ KarenSechrist; and Dr. Ronald Knutson. Also to Dr. Bertron Groves for interpretation of the electrocardiograms. Acknowledgment is also made to the employees of the Pulmonary Function Laboratory at The University of Ari­zona Medical Center for their assistance.

This study was supported in part by a grant from the American Lung Association,

ill

TABIS OF CONTENTS

LIST OF TABLES a o o « » o o « » » o o » » o » LIST OF ILLUSTRATIONS .ABSTRACTa o a o # o O C O O O O o O O O O O O

INTRODUCTION, 6 © O O 6 O O O O O O O O O o o

Purpose of the Study Significance of the Problem Conceptual Framework Hypotheses

O O 0 O O O O O 0 O O o o o o o o o

O O O 0 6 0 0 0 0 0

o e O O O O O O O O O O O O O O

2e REVIM OF THE LITERATURE O O O O d O O O O O O

Exercise Training „ 0 » .. » 0 = 0 a » „ «■ Arrhythmias and Chronic Lung Disease, , , Arrhythmias With Exercise Arterial Blood G-as Changes With Exercise,

METHODOLOGY O o o O 0 O O o ® 0 0.0 o o c.o o

Population and Sample Data Collection Method

O O O 0 . 0 o o O o o

o o o o o o o o o o

PRESENTATION AND ANALYSIS OF DATA o e o o o o

Characteristics of the Sample . , , , , „ Levels of Exercise, , , , , , , , , , , , Electrocardiographic Findings , , , , , ,

Arterial Blood Gas Findings . , , , » Blood Pressure, Pulse Rate and

' Respiratory Rate,Analysis of Data

O O O O 0 6 O O

O O O O 0 0 o o o o o o o

DISCUSSION OF FINDINGS 6 0 0 0 0 0 0 0 0 O O O

o o a 6 0 6 6 0 o o o oArrhythmias , ,Correlation of FEV^ to Arterial Oxygen

Tension Changes , , . , , . , , , , , Correlation of Heart Rate to Arterial

Oxygen Tension Changes,Shortness of Breath O O 0 . 0 0 0 0

O O O O O o 0 0 0 o o

IV

Pagevi

viiviii

123

8810

15161616181820202222232828293031

TABLE OP OOHTEMTS— Continuedv

PageRecovery Period « , = „ a 0 0 „ , 0 0 eo » 31Conelus ions * e * » @ © @ @ » » o . © o <> o « 31Recoromendations for Further Study 0 . » . = 32

SUl ' I MARY o 0 6 0 o ' o o o e o o o o o o o 0 0 0 0 3^1“"

APPENDIX As SUBJECT'S CONSENT8 . . . . . . . . ; 36APPENDIX Bs DATA COLLECTION FORM « « « » « »' , 38APPENDIX Cs CLASSIFICATION OF ARRHYTHMIAS. . . 39REFERENCES . . . . . . . . . . . . . . . . . o . i}.l

LIST OF TABLES

Table Page10 Characteristics of the Sample Including

Diagnosis, Age, Sex, Electrocardiogram,FEY-,, FEVi/VC ratio. Vital Capacity (VC),VC Percent Predicted, FEV1 PercentPredicted, Height and Weight „ . „ „ o 19

2a Rest, Exercise and Post Exercise pH, BloodGases, Blood Pressure, Pulse, Respiratory Rate, Cardiac Rhythm and Exercise Level0 „ 21

vi

LIST OF ILLUSTRATIONS

F ig u re

10 Relationship Between Resting FBVj end PaOpChanges W ith E xerc ise 0 0 , 6 0 0 0 0 0 0

2e Relationship Between Change in Heart Rate andN Change in PaOg From Rest to Exercise, » »

3o Relationship Between Change in RespiratoryRate and Change in PaOg From Rest to Peak

vii

ABSTRACT

Eight patients with chronic lung disease were monitored with an electrocardiogram while having rest and exercise blood gas studiese Exercise was terminated when the subject was unable to continue due to shortness of breathe Arterial blood gas studies were done at rest, during exercise, and five minutes post exercise» Pulse rate, blood pressure, and respiratory rate were monitored at three-minute intervals „ Only two patients had arrhyth­mias (PVC *s) which decreased during exercise althoughtheir PaO fell below 50 torr„ One other subject had a 2PaO2 below 50 torr during exercise but had no arrhythmias„ Only two patients, neither of whom had arrhythmias, had pH values below 7,35 at any time during the study. All patients complained of being short of breath at peak exer­cise but only three patients had a PaOg below JO torr at that time. Pulse rate, respiratory rate, and FEV^ did not correlate with the PaOg, The five-minute post exercise values showed the PaOg above pre-exercise levels, but the pulse and respiratory remained elevated.

viii

CHAPTER 1

INTRODUCTION

In 1958 Corazza and Pastor published their retro­spective study of 122 patients with chronic cor pulmonale demonstrating that there was a significant incidence of cardiac arrhythmias in these patients. Since then, arrhythmias in patients with chronic pulmonary disease have been of interest to physicians and nurses. Studies have shown significant arrhythmias in patients with chronic lung disease, particularly during acute exacerbation of the disease. Many of the arrhythmias shown to exist are con­sidered "major" arrhythmias, as defined by Hudson, Kurt and Petty (1973)j which are treated in other clinical situa­tions such as post myocardiad infarction but are not "always treated in the patient with chronic lung disease.

The mechanism for cardiac arrhythmias in chronic pulmonary disease is not known. It probably includes many factors such as hypoxemia, acidemia, digitalis therapy, bronchodilator therapy and electrolyte imbalance (Ayres and Mueller 1973).

Activity of the patient with chronic lung disease may be limited since work increases the metabolic rate which increases the tissue demand for oxygen. To compen­sate for the increased demand the individual must increase

■ ■ ■ i ■ ' "

; ■ aeffective ventilation* The patient with chronic lung disease may be unable to increase effective ventilation adequately to meet the metabolic demand and may, therefore, develop hypoxemia, hypercapnia, and/or acidemia. All of these may precipitate cardiac arrhythmias (Armstrong et al. 1966).

Bellet (1971) listed exercise among the causes of arrhythmias in cor pulmonale. He states that nduring exercise there is arise in pulmonary arterial pressure, increased hypoxia, carbon dioxide retention, rand some de­gree of relative coronary insufficiency" (p. 766). He also states, "after exercise, electrocardiographic changes, including arrhythmias, have been observed in patients with cor pulmonale" (p. 766).

■Purpose of the StudyThe.purpose of the study was to monitor the cardiac

rhythm of patients with chronic lung disease undergoing exercise testing to determine if there was a significant number of arrhythmias in these patients during physical exercise„ This study also was done to determine if the incidence of arrhythmias correlated with levels of hypox­emia, hypercapnia and respiratory acidosis. Blood pressure and pulse rate were also monitored to determine if these simple clinical observations could be used as tools to an­ticipate and prevent the occurrence of arrhythmias.

3The forced expiratory volmm in one second (FEV^)

and the FEV^ vital capacity (100 x FEV]_/VC) ratio were also considered as. possible observations to assist in prediction of arrhythmia occurrence during exercise test­ing.

Significance of the ProblemPatients with chronic respiratory disease have

been shown to benefit from exercise training. The trained patient with chronic pulmonary disease can perform a measured exercise test at a lower respiratory rate, pulse rate, minute ventilation, oxygen consumption and carbon dioxide production than when untrained (Thomas and Valabhji 1969, Zehnam. and Phillip 1973)° Since the increased abil­ity to exercise allows the patient to have a more active life at less energy cost, exercise is considered a part, of the total, care for the patient with chronic lung disease.

The potential problem of increased incidence of arrhythmias during exercise is of importance to the nurse for the nurse may be the person instructing the patient in exercise therapy. The patient must be encouraged to remain active but concurrently the nurse must know to what level exercise, can be safely prescribed. If noninvasive methods such as pulse rate, blood pressure, FEVi, and/or FEVi/VC ratio can be used to predict the occurrence of

arrhythmias, the nurse will be better prepared for compli cations o

Conceptual Framework As metabolism Increases„ the tissue oxygen con­

sumption increases thereby demanding that a larger amount of oxygen be delivered to the tissues„ This increased demand for oxygen can be supplied in one. of three ways:

1. A more efficient distribution of blood flow to working muscles effected partly by vasodi- lation;

2. An increase in cardiac output which is accomplished by an increased stroke volume, and/or an increased heart rate;

3. An increase in oxygen uptake by the lungs, both by increasing the alveolar ventilation and apparent pulmonary diffusing capacity (Armstrong et al„ 1966, Jones 1967, Zehnam and Phillip 1973).

If these adaptations do not keep pace with metabolism and if the demand for oxygen exceeds its local supply, then the tissue oxygen tension falls and an increased propor­tion of energy production is diverted into pathways which do not require oxygen (Jones 1967).

The person with pulmonary disease may have all three mechanisms impaired but usually the respiratory system is chiefly affected.

Pulmonary disease affects pulmonary function adversely either by reducing the ventilatory capacity,'usually because of the obstructive air­way disease or by interfering with the. ability

5of the lungs to arterlallze mixed venous bloodor a combination of both of these (Armstronget al. 1966,, p. 90).

When physical exercise is pushed beyond the capability of the body to provide the necessary oxygen, anaerobic metabolism occurs. A small amount of energycan still be released to the cells by glycolysis, for thechemical reaction in the glycolytic breakdown of glucose to pyruvic acid requires only small amounts of oxygen.The two end products of the glycolytic reaction are pyruvic acid and hydrogen ions. These two end-products react with each other to form lactic acid which diffuses out of the cell into the extracellular fluid. The lactic acid so produced reacts with bicarbonate in the blood liberating carbon dioxide which is excreted by the lungs. (Corazza and Pastor 1958). This anaerobic metabolism in muscle is therefore accompanied by an Increase in carbon dioxide production. The increase in carbon dioxide may be handled by normal lung function but if the lung function is inadequate, as in chronic lung disease, carbon dioxide retention occurs. Concurrently» the muscle continues to demand more oxygen to sustain the physical work and an increase (above resting) amount of oxygen is extracted from the blood perfusing the contracting mucles (Armstrong et al. 1966). If the cardio-pulmonary system cannot in­crease the oxygen content delivered, hypoxemia results.

The cardiac, muscle needs oxygen as all muscles do and it is sensitive to the lack of oxygen or the increase of carbon dioxide. Hypoxemia and hypercapnia can effect the automaticity of the cardiac cell. Special cells in the SA node, atria, bundle of His, and Perkinje fibers do not remain polarized as do most cardiac cells, but con­stantly leak current and spontaneously depolarize, Hoff­man and Cranefield (196^) call these "automatic cells,"The rate of the spontaneous depolarization of such cells is increased by hypoxemia.

The effects of hypercapnia on the heart include direct depression of conduction through the AV junction and indirect effects due to vagal poten­tiation. Conduction is particularly depressed when hypercapnia causes a marked fall in pH (Bellet 1971, P. 86),

Hypoxemia and acidemia can both lead to cardiac arrhythmias. The patient who has pulmonary disease is more likely to have these problems for the ability to respond to increased oxygen need is not present. During exercise, hypoxemia and acidemia may develop or, if pres­ent at rest, become more severe in the patient with chronic lung disease. If hypoxemia or acidemia is severe enough, cardiac arrhythimas may be developed.

Hypotheses1. Those patients who have a decrease in arterial

oxygen tension below 50 mm Hg with exercise will have a

. . - 7significantly greater incidence of arrhythmias than those with an arterial oxygen tension above 50 mm Hg„

2, Those patients who have a decrease in pH to levels below 7.35 with exercise will have a significantly greater incidence of arrhythmias than those who do not exhibit such a change in pH„

CHAPTER 2

EBVIEW OF THE LITERATURE.

A summary of the literature pertinent to exer­cise training, cardiac arrhythmias in patients with chronic pulmonary disease, and incidence of arrhythmias occurring with exercise will be presented.

Exercise Training Patients with chronic illnesses were often told

to decrease their activity so as not to add stress to their already poorly functioning systems„ The decreased activity made them less and less able to do any type of activity. Pierce, Taylor, and Archer (1964) noted that their patients with chronic lung disease who continued to be active remained in relatively better health for a. longer period of time than the patients with chronic lung disease who were more sedentary. This observation prompted them to investigate the use of exercise training. They studied nine patients with severe obstructive pulmonary disease, gradually increasing their daily amount of exer­cise. They found that after the exercise training period all, nine patients were able to do the same exercise as in the pre-training period with decreased heart rate, res­piratory rate, minute ventilation, oxygen consumption,

8

9and carbon dioxide production. He also noted that the trained patient had a more rapid return of the above param­eters to resting levels after cessation of exercise.

Petty et al„ (19&9) study of 182 patients who in­creased their exercise tolerance after physical retraining demonstrated that patients with chronic airway obstruc­tion can improve and sustain exercise tolerance. These 182 patients were followed over a two-year period. They also showed a decrease oxygen uptake for a given level of exercise.

Pierce, Paez, and Miller (1965) noted that patients who developed premature ventricular contractions or severe hypoxemia while exercising were unable to profit from the previous exercise programs. They then studied four pa­tients with severe emphysema who had premature ventricu­lar contractions or hypoxemia which limited their exercise ability. These patients exercised while using portable oxygen. The exercise training caused the same change of physiological functions in these patients as in the study of Pierce et al. (1964).

These studies show that exercise training will help most patients with chronic airway obstruction. It helps the patients to increase their level of activity although they have irreversible airway disease.

Arrhythmias and Chronic Lung DiseaseThe Incidence of arrhythmias occurring with chronic

lung disease was considered very infrequent until Corazza and Pastor (1958) showed that 31 percent of.the patients with chronic lung disease had one or more types of arrhyth­mias. The chart review method was used. The types of arrhythmias found were: frequent (more than six per min­ute) premature beats of ventricular, atrial and nodal origin; supraventricular tachycardia (atrial and nodal, atrial flutter and fibrillation, slow nodal rhythm) and prolonged A.V conduction.

Thomas and Valabhji (19&9) found atrial tachy­cardia to be the most common arrhythmia. They noted that many patients with lung disease have multiple arrhythmias. Goldberg et al. (i960) in the study of 37 patients having paroxysmal atrial tachycardia with block found a high incidence (25 percent) of pulmonary disease in that popu­lation.

Hudson et al. (1973) found in their study that 4-7 percent of the patients with chronic airway obstruction and acute respiratory failure had major supraventricular or ventricular arrhythmias. Atrial tachycardia was the most common, but ventricular arrhythmias (mainly premature ventricular contractions) were seen.

The frequency of arrhythmias reported in patients with chronic lung disease varies from 7 percent (Thomas

11and Valabhji 1969) to 47 percent (Hudson et al„ 1973),The difference In reported Incidence could be due to the severity of the pulmonary disease or the undiagnosed com­bination of pulmonary disease with coronary heart disease (Petty, Hudson, and Neff 1973),

The preceding studies were done by reviewing 12 lead electrocardiograms taken on hospitalized, patients with pulmonary disease. Electrocardiograms taken daily only record electrical activity for 1/500 of the 24-hour period. The brevity of the electrocardiogram may be a major fact accounting for the difference in reported occurrence of arrhythmias for most arrhythmias are found to be Intermittent. In order to overcome this problem, Holford and Hithoefer (1973) did a study on 35 hospital­ized patients with the diagnosis of chronic obstructive pulmonary disease. These patients were monitored continu­ously for 72 hours. The study showed that all but three of the patients studied had arrhythmias. The arrhythmias in 57 percent of the cases were considered clinically sig­nificant and would require treatment in usual standard practice. In only 31 percent of the patients were arrhyth­mias detected by routine 12 lead electrocardiogram taken just prior to the start of the 72-hour monitoring period.

In 197^ Kleiger and Senior reported a study done on ambulatory patients with clinical and spirometrie evidence of chronic obstructive pulmonary disease. The

12patients were monitored over ten; hours with Holter moni­toring. (Long term electrocardiographic monitoring re­corded on tape which is later scanned for arrhythmias.)The results showed that 84- percent of . the 25 patients had some disturbance of rhythm, ?2 percent ventricular and 52 percent atrial arrhythmias. The incidence of arrhyth­mias in these patients resembles the incidence of ar­rhythmias in a comparable age group following myocardial infarction.

Studies done to determine the reason for arrhyth­mias in chronic lung disease patients demonstrate that hypoxemia, hypercapnea and acidosis play a role. Ayres and Mueller (1973) found that anesthetized dogs who were subjected to rapidly produced hypoxemia showed conduction disturbances and idioventricular rhythm as the atrial oxygen tension fell below 50 torr . They state evidence that acute respiratory acidosis with mild hypoxemia can precipitate ventricular arrest.' In a study of myocardial infarction patients, Ayres and Grace (1969), showed that severe arrhythmias (ventricular and supraventricular) can be produced by hypoxemia or acidemia.

Bellet in his textbook. Clinical Disorders of the Heart Beat (1971), states from his own observations that one of the causes of arrhythmias in cor pulmonale is exercise. Arrhythmias occur during exercise because "there is a rise in pulmonary arterial pressure, Increased

13hypoxia,, carbon dioxide retention and some degree of rela­tive coronary artery Insufficiency" (p. 766).

Arrhythmias With Exercise Arrhythmias produced by exercise have been well

studied in efforts to diagnose covert coronary heart disease through non-invasive methods. These studies have included efforts to determine when arrhythmias can be con­sidered a normal varient and when they may be dangerous. Following is a review of the literature on arrhythmias occurring with exercise stress testing.

Helfant et al. (1974) in their study of 60 pa­tients undergoing both exercise testing and coronary arteriography found 38 patients who had precipitation of or increase in premature ventricular contractions with exercise. Of these 22 were shown to have coronary heart disease with coronary arteriograms. Therexwere another 22 patients in whom premature ventricular contractions de­creased with exercise; only six of these were shown to have coronary heart disease on cardiac catherizatlon. ,

McHenry et al, (1972) studied 650 men of the Indi­ana State Police Force during maximimal exercise stress testing on a treadmill. Of these 561 were normal, having no clinical evidence of cardiovascular disease, and 89 had definite or suspected cardiovascular disease. Unifocal and isolated premature ventricular contractions were

14commonly found In the normal Individuals when the heart rate increased above 150 per minute usually at the end of maximal stress or in the early recovery period. The fre­quency was age-related, occurring in 29 percent of those under age 35 and in 43 percent of those 45 and over. Mul­tifocal premature ventricular contractions were rarely encountered in any age group, and.there was only one in­stance of ventricular tachycardia. The men in the cardio­vascular disease group developed a much higher frequency of multifocal premature ventricular contractions and episodes, of ventricular tachycardia.

Guenter (1975) reports that in 16 healthy men who were exercised under hypoxic conditions (breathing 10 per­cent oxygen) there were no cardiac arrhythmias. It is of Interest that two individuals who had occasional prema­ture ventricular contractions at maximal exercise breathing room air had no premature ventricular contractions at similar heart rates while hypoxemic.

The preceding study by Guenter points to the fact that increased Incidence of arrhythmias associated with exercise is not a common occurrence in patients without cardiac disease. This study also appears to agree with the previously discussed study of arrhythmias in patients with chronic lung disease. As Petty et al. (1973) com­mented, the presence or absence of coronary heart disease

■ 15in the patient with chronic lung disease may account for the wide variations in reported incidence of arrhythmias.

Arterial Blood Gas Changes with Exercise

During graded exercise stress testing, individuals with normal cardie-pulmonary system keep their arterial oxygen tension and carbon dioxide tension within normal limits, Whipp and Wasserman (1969) showed that five healthy men maintained relatively steady arterial oxygen tension values up to 9. maximal level of work. After reaching 60 percent of maximal work the arterial carbon dioxide tension progressively decreased,

Guenter (1975) found that 16 men who progressed through exercise to maximal heart rate breathing room air dropped their mean arterial oxygen tension from 79 torr at rest to 7^ torr at maximal exercise. This change was associated with a decrease in mean arterial carbon dioxide tension from 30 torr to 28 torr and a decrease in pH from 7.45 to 7.38,

These findings demonstrated that the individual with adequate lung function can maintain arterial blood gas tension within the range of noraal while exercising. Exercise stress testing becomes a helpful tool in diag­nosing the severity of chronic lung disease, detecting the presence of cardiac arrhythmias, and determining what advice to give the patient about daily exercise.

CHAPTER 3

METHODOLOGY

In this chapter the sample selection, the method for protection of human rights, and data collection method is presented.

Population and Sample All adult patients (over 20) who were referred to

the pulmonary function laboratory of a university medical center for rest and exercise blood gas studies were con­sidered, The patients were interviewed and the purpose of the study explained. If the patient was willing to participate in the study he was asked to sign the consent form approved by the Human Rights Committee (Appendix A), Additional data concerning additional lung or cardiac\ disease were obtained from the subject or his medical record (Appendix B),

Data Collection Method In keeping with the routine of the pulmonary

function laboratory, the patients were asked to choose the speed and grade at which they wished to walk on the treadmill. This speed was considered to be consistent with the level of exercise they were able to do in activ­ities of daily living.

16

17An Indwelling arterial needle was inserted per-

cutaneously in the radial or brachial artery by the physician. The needle was secured and the arm placed on an arm board to prevent dislodging the needle from the artery. At 12 lead resting electrocardiogram was taken and two telemetry electrodes applied to the chest in a lead two position. After a five-minute rest an arterial blood sample was drawn, a one minute rhythm strip ob­tained , and the blood pressure taken. The patients were then allowed to walk on the treadmill until they requested to stop. Just before stopping the exercise another blood sample was drawn. The cardiac rhythm was continuously visually monitored with a permanent recording and the blood pressure, pulse rate, and respiratory rate were recorded every three minutes during exercise and the rest period.

All arterial blood samples were analyzed for oxygen tension (PaOg), carbon dioxide tension (PaCOg), J oxygen saturation (SaOg) and pH on a Coming, Radiometer or Instrumentation Laboratory arterial blood analyzer.The electrocardiogram and rhythm strips were reviewed by a cardiologist and the arrhythmias identified and clas­sified according to the criteria in Appendix G.

CHAPTER 4

PRESENTATION AND ANALYSIS OF DATA

This chapter presents the characteristics of the sample in the study. The data from the rest, exercise and post exercise measurements of arterial blood gas studies, cardiac rhythm, pulse rate, respiratory rate, and their analysis are included.

Characteristics of the SampleDuring the six months when data were being col­

lected, seven patients were scheduled for rest and exercise blood gas studies. They all consented to partic­ipate and were included in the study. The eighth subject was reviewed retrospectively with previously collected data.

The subject group included four males and four females ranging in age from 33 to 63 with a mean age of 49, Five subjects bad a diagnosis of chronic obstructive pulmonary disease, the others had diagnoses of sclero­derma (subject 4), asthma (subject 1), and dyspnea on exertion (subject 6), The FEV^ ranged from 0,7 to 3.3 with a mean of 1.58 liters. The FBVj/VC ratio ranged from 30 to 98 percent with a mean of 60 percent (Table 1).

18

Table 10 Characteristics of the Sample Including Diagnosis* Age* Sex* Electro cardiogram* FEV_ * FEV^/VC Ratio* Vital Capacity (VC), VC Percent Predicted* Percent Predicted* Height and Weight

Subleot Diagnosis Age Sex Height Weight PEVi FBV-, PEV, % VO - VO % Eleetrooardiogram .(inches) (lbs) VC Predicted Predicted

1 Asthma 37 ■ M 67 l80 2.8 65% 74% 4.3. 92% Within normal limits2 EmphysemaBronchitis 59 M 67 125 0.7 30% ■ 24% 2.4 60% . Right axis with PVCs3 . Bronchitis 62- P 62 120 1.4 59% 62% 2.3 89% Within normal limits

V Sclero­derma 41 P 67 118 0.9 98% 33% 1.0 28% • Abnormal— non­specific ST segment changes,5 Bronchitis

Bronchi-ectesis 48 F . 63 125 1.3 58% 49% 2.1 73% ' Within normal limits6 Dyspnea on Exertion 33 M 71 195 3.3 73% . 80% 4.5 : 87% Within normal limits7 Broncho-ectesis 63 M 66 150 1.0 39% 38% . 2.8 73%

Abnormal— sugge s t i ve of old true Posterio: MI8 COPD Bron­chitis 53 P 67 120 1.2 58% 46% 2.0 67% ' . Rot recorded

20Levels of Exercise .

The duration of exercise and the grade and speed of the treadmill differed for each subject (Table 2).The grade ranged from 0 to 10 percent with a mean of 7 percent. The speed ranged from 1 to 5 miles per hour with a mean of 2„7 miles per hour and the distance walked ranged from 106 yards to 1355 yards with an average of4-73 yards „

Electrocard1ographlc Pindings The resting 12 lead electrocardiogram was within

normal limits on four subjects (1, 3, 5, 6). Subject 2 had a right axis deviation and multiple premature ventric­ular contractions. Subject 4- had abnormal nonspecific ST segment changes. Subject 7 had an abnormal electro­cardiogram suggestive of an old true posterior myocardial infarction. Subject 8 did not have a resting 12 lead electrocardiogram done before exercise but did have a resting rhythm strip (Table 1).

All the subjects showed sinus rhythm on the rest­ing rhythm, strip. Two subjects (2 and 8) had multiple (above 10 per minute) premature ventricular contractions at rest which with exercise decreased.to three per minute. The rest of the subjects in the group had sinus tachy­cardia when exercised with no ectopic rhythms. On all subjects the resting post exercise rhythm strip showed

’Table 2„ Rest, Exercise and Post Exercise pH, Blood Gases, Blood Pressure, Pulse, Respiratory Rate, Cardiac Rhythm and Exercise Load

Blood Gases , - Exercise-Load, APatient . Blood Respira- Cardiac ' .Number Stage pH Pa02 PaCOg Sa02 Pressure Pulse tory Rate Rhythm Grade MPH Yards

1 Rest . : 7.43 70 31 96# 130/90 64 16 Sinus BradyExercise 7-32 79 30 96# 170/90 150 36. Sinus Tach 10# 3.5 986Post Exercise 7.32 77 26 96# 120/70 100 30 Sinus Tach

2 Rest 7.46 62 38 91# 140/80 . 80 20 Sinus with26 PVC/minExercise . 7.45 41 43 77# 180/70 110 30" Sinus Tach 6# 2 1062 PVC/minPost Exercise 7.45 65 40 94# 150/90 100 24 Sinus Tach21 PVC/min

3 Rest 7.39 68 31 95# 150/70 80 20 SinusExercise 7.39 74 31 97# 160/80 140 " 34 Sinus Tach 10# 2 13551PVC ■Post Exercise 7.39 74 29 97# 140/60 110 26 ' Sinus Tach

4 Rest 7.46 77 31 97# 90/70 95 36 Sinus ; . •Exercise 7.47 72 31 97# 110/90 120 38 Sinus Tach ' 10# 1.25 106Post Exercise 7.Il4 81 30 98# .100/76. 100 _______26_____ Sinus Tach

5 Rest 7.44 77. 28 97# 125/85 90. 20 SinusExercise 7.41 74 23 96# 140/90 110 30 Sinus Tach 5# 3 158Post Exercise 7.43 87 23 130/85 ' 100 24 Sinus Tach6 Rest 7.42 81 36 97# 130/80 ' 8 75 20 Sinus

Exercise 7,37 71 35 94# 140/80 150 32 Sinus Tach VI0H 5 246Post Exercise 7.33. 98 31 98# 130/80 100. ■..30 Sinus Tach7 Rest 7.40 49 44 90# 98/60 90 20 Sinus

Exercise 7.36 37 46 76# 120/80 130 28 Sinus Tach 0 25' 475Post Exercise T3J 53 39 91# 100/70 100 20 Sinus Tach8 Rest 7.48 64 36 93# 96 Sinus10 PVC/minExercise 7.48 47 35 ,85# 130 Sinus Tach .10# 2 3523 PVC/minPost Exercise 100 Sinus Tach

22sinus tachycardia with no arrhythmias except for subjects 2 and 8 who had a return of their premature ventricular contractions.

Arterial Blood Gas FindingsThe resting PaOg ranged from 4-9 to 81 torr with

a mean of 68.5 torr. During exercise the PaC>2 ranged from 39 to 79 torr with a mean of 64 torr. Following a 5- minute rest period post exercise the PaOg ranged from 4? to 98 torr with a mean of ?6 torr (Table 2).

The resting PaCOg ranged from 28 to 44 torr with a mean of 34.4 torr. During exercise the PaCOg ranged from 23 to 46 torr with a mean of 34 torr. Five minutes post exercise the PaCOg ranged from 23 to 40 torr with a mean of 31 torr (Table 2).

The pH ranged from 7.39 to 7.48 with a mean of 7.44. at rest. During exercise the pH range was 7.32 to 7.48 with a mean of 7.40. Five minutes post exercise the pH ranged from 7.32 to 7.45 with a mean of 7.39 (Table 2).

Blood Pressure., pulse Hate and Respiratory RateThe.resting systolic blood pressure ranged from

90 to 150 mm Hg. with a mean of 123 mm Eg, while the diastolic range was 60 to 90 mm Hg with a mean of 76 mm Hg, During exercise the systolic blood pressure ranged

23from 110 to 180 mm Eg with a mean of 145 mm Eg, while the diastolic blood pressure ranged from 70 to 90 mm Eg with a mean of 82, Following a 5-minute rest period post exercise the systolic blood pressure ranged from 100 to 150 mm Eg with a mean of 124 mm Eg and the diastolic blood pressure ranged from 60 to 90 mm Eg with a mean of 75 mm. Eg.

The resting pulse rate ranged from 64 to 95 per minute* with a mean of 84. During exercise the pulse rate increased and ranged from 110 to 150 per minute, with a mean of 130. The pulse rate following a 5-minute rest post.exercise ranged from 100 to 110 per minute with a mean of 101.

The resting respiratory rate ranged from 16 to 36 per minute with a mean of 22. During exercise the respiratory rate ranged from 28 to 38 per minute with a mean of 32. After a 5-minute rest period post exercise the respiratory rate ranged from 20 to 36 per minute with a mean of 27.

Analysis of DataThe first hypothesis that those subjects who have

a decrease in arterial oxygen tension below 50 torr with, exercise will have a significantly greater incidence of arrhythmias than those with an arterial oxygen tension above 50 torr was rejected. No arrhythmias developed nor

24was there an increase in arrhythmias during exercise even when the PaOg fell below 50 torr. In fact, the number of premature ventricular contractions present at rest in two subjects (2 and 8) decreased during exercise„

The second hypothesis that those subjects who have a decrease in pH to levels below 7-35 with exercise will have a significantly greater incidence of arrhythmias than those whose pH does not fall to such low levels was also rejected. Only two subjects (1 and 6) had a pH below 7.35 as a result of exercise and neither of these had any cardiac arrhythmias -

In order to further evaluate the data several correlations were done to determine relationship between clinical findings and changes in PaOg between rest and exercise. The FEV- was correlated with the change in PaOg using Pearson Product Moment Correlation Coeffici­ent (Ferguson 1959). The r was 0,4 which was nonsig­nificant at the .05 level one tail test (see Fig. 1 for a scattergram of this relationship).

The correlation coefficient was determined between the change in pulse rate and paOg and also between the change in respiratory rate and PaOg from rest to exercise. The r was 0-5 in the first correlation and 0.54 in the second. Neither was significant at the0.05 level one tail test (see Figs. 2 and 3 for a scat­tergram of these relationships).

25FEV*3.83.63.4

* 3.23.02.8 *2.62.4 2.22.0!:!1.4 *

* 1.2* 1.0

* 0.8* 0.6

0.40.20

O GO XO _r%- CM O O CM VO GO Oh h h h h c x .v o ^ - c m ^ v o c o h h h h h c m

Change PaOg

Fig. 1. Relationship Between Resting FEV^ and PaOg Changes with Exercise.

*

26

Heart Rate Change 9085 *80

* 75. 65 60 , *55

. 1 .

• • • i* 20

15 ' 1 0' .• 50

O 00 xo -ti" <X1 O O CX! -zj- VO co oCM r—I rH i—1 rH rH CO VO -CT CM CM VO CO r—i !—i [—I I—1 I—i CMI I I I I I I I I I + + + + + + + + + IChange in PaOg

Pig. 2. Relationship Between Change in Heart Rate and Change in PaOg Prom Rest to Exercise

2?Change in Respiratory Rate

2220 *

181614 *

* 12# * 10

* 86 4

* ' ■ 2 0

O 00 \0 (MO O CM -d" xO 00 OC MHHHHH00 x O - d " C M I I I I I I I I I I + + ! + + + 4- + t + +

Change in PaOgPig. 3. Relationship Between Change in Respiratory

Rate and Change in PaC^ From Rest to Peak Exercise. — Data for subject. 8 is not Included because data was obtained retrospectively.

CHAPTER 5

DISCUSSION OF FINDINGS

In this chapter, a discussion of the findings is presented, including the conclusions and recommenda­tions for further investigation.

ArrhythmiasIn three subjects the arterial oxygen tension

fell below 50 torr during exercise. Two (2 and 8) of these three had arrhythmias which consisted of multiple premature ventricular contractions at rest. In both cases when they exercised the frequency of premature ventricu­lar contractions decreased as the pulse rate increased. During the rest period after exercise the heart rate decreased and the frequency of premature ventricular con­tractions increased to pre-exercise levels. It appears that the increased heart rate suppressed the ectopic foci responsible for the premature ventricular contractions.The decrease in the ectopic rhythm with exercise would most likely indicate that neither subject had significant coronary artery disease. This conclusion would agree with the findings of Helfant at al. (1974) that patients who had a decrease In ectopic rhythms during exercise had a lower percentage of coronary heart disease than those who

28

29had an increase in ectopic rhythms„ The third subject (?) whose arterial oxygen tension fell below 50 torr during exercise had no cardiac arrhythmias before or during exer­cise.

Although the sample is small the data suggest that a decrease in PaOg to 39 torr in itself is not enough to cause cardiac arrhythmias. This finding would agree with Guenter’s (1975) study of 16 healthy men who, while exercising under hypoxic conditions, had no cardiac arrhythmias even with a mean arterial oxygen tension of 31 torr.

Ayres and Mueller (1973) found that a combination of hypoxemia and acidemia precipitated ventricular arrhythmias and arrest. None of the subjects in this study exhibited this combination Of abnormality. Possibly it is the combination of hypercapnia, hypoxemia and aci­demia that causes increased arrhythmias in the patient with chronic lung disease rather than hypoxemia alone.

Correlation of FEV-, to Arterial Oxygen Tension Change's"

Measuring the FEV^ is one of the methods of test­ing for presence, and' degree of lung disease. As the ability to force the air out of the lungs decreases, ability to increase effective ventilation also decreases, The person with chronic lung disease may not be able to

30increase the oxygen tension of the "blood to meet the In­creased demands of the working muscle. The muscle extracts increased amounts of oxygen from the blood and the oxygen tension falls.

The data from this study failed to demonstrate a correlation between the level of FEV^ and the change in paOg during exercise. The lack of correlation is most likely due to the fact that besides lung function, cardiac function and. muscle training are Important in determining the patients' ability to tolerate exercise. All three mechanisms must be considered in predicting the patients' change in PaC^ with exercise.

Correlation of Heart Rate to Arterial Oxygen Tension

ChangesAlthough the correlation between heart rate change

and change in arterial, oxygen tension from rest to exer­cise is not statistically significant (Fig. 2) the scat- tergram shows a slight relationship. This trend could be important if it could be shown that part of the reason for the patients' decrease in arterial oxygen tension with exercise is that the cardiac output cannot be ade­quately increased. Further study would have to be done to determine if the limiting factor is primary heart disease or cardiac hypoxia secondary to lung disease.

' 31Another possible Interpretation is that the pa­

tients with the least change in heart rate were also the ones who exercised the shortest.amount of time. The prob­lem may have been just not enough time at the increased work load for an adequate cardiac response.

Shortness of Breath All the subjects complained of being short of

breath at the peak of exercise but only three subjects had arterial oxygen tensions below 70 mm Hg. The shortness of breath with normal arterial oxygen tension shows that there are factors, other than hypoxemia, which cause the sensation of shortness of breath.

Recovery Period All the patients, after a five-minute rest period

post exercise, still had pulse and respiratory rates above their pre-exercise levels. At that time, although they were not in any obvious distress and stated they were re­covered, their cardiac and pulmonary functions had not yet returned to pre-exercise levels. The elevated pulse and respiratory rate infers that the oxygen debt is not totally repaid.

ConclusionsNeither hypoxemia or pH changes in themselves can

be used to predict the development of or increase in

32cardiac arrhythmias during exercise„ With rejection of the original hypotheses, pulse rate, respiratory rate, and FEV^ were also analyzed to see if nurses could predict a drop in PaOg by these parameters. No correlation existed between any one parameter and a fall in PaOg.

All subjects also experienced shortness of breath regardless of their exercise.level and their PaOg.Nurses, therefore, cannot use any one measure alone to prescribe the amount of exercise or to anticipate a change in PaOg or pH.

It was apparent that five minutes rest post exer­cise was not a sufficient recovery period. Patients had not reached resetting parameters by this time although they subjectively felt recovered. A longer rest period is necessary before the nurse encourages additional exercise.

Recommendations for Further Study Because of the limitations and findings of the

present study, it is recommended future studies should be designed including the following:

1. A larger sample size of homogenous diagnosis and standardized exercise.

2. Monitoring of the patients with a three-channel electrocardiograph recorder to determine if

33there are any ST segment changes during exercise when and if hypoxemia occurs,

3. Monitoring of arterial blood gas changes fre­quently during rest and exercise to determine if changes, have a correlation with time.

4. Monitoring for a longer period of time following exercise to determine the.length of time neces­sary for the heart rate and respiratory rate to return to pre-exercise values.

CHAPTER 6

’ SUMMARY

The major purpose of this study was to determine if cardiac arrhythmias occur in chronic lung disease patients when they are undergoing a rest and exercise blood gas study. Also investigated was the correlation of incidence of arrhythmias and the degree of hypoxemia, acidemia, or hypercapnia.

Eight patients with intra-arterial catheters in place were monitored while exercising on a treadmill.All the patients exercised at their chosen speed and dura­tion until forced to discontinue exercise due to shortness of breath. Arterial blood gas values were determined at rest, during exercise, and five minutes after termination of exercise. A lead II rhythm strip, blood pressure, and respiratory rate were also recorded.

Three of the patients demonstrated hypoxemia of levels below 50 torr during exercise. Two of these pa­tients' had multiple premature ventricular contractions at rest but the premature ventricular contractions de­creased in number with exercise as the heart rate increased After exercise when the heart rate again approached resting levels, the number of ectopic beats increased. The other

. 34

35patient with an arterial oxygen tension below 50 torr had no arrhythmias at rest or during exercise.

The number of arrhythmias did not increase in any subject so there was no correlation present between hypox­emia or acidemia and arrhythmias.

All of the subjects demonstrated an elevated pulse rate and respiratory rate during exercise. After five minutes rest, these values had not returned to baseline levels even though the arterial oxygen tension had risen to above baseline levels. This finding indicated that a5-minute recovery period was. not sufficient to repay the oxygen debt developed during exercise.

Further study must be done to determine the sig­nificance of the lack of arrhythmias with arterial oxygen tension below 50 torr. Also, further study is needed to determine the amount of time necessary for the heart rate and respiratory rate to return to pre-exercise levels.

APPENDIX A

SUBJECT'S CONSENT.

PROJECT TITLE: Correlation of Blood Gas Changes withArrhythmias During Exercise in Patients with Chronic Lung Disease

Your physician has requested that you undergo a rest and exercise blood gas examination to test how well-: . your lungs function while you are exercising. My research involves watching your heart rate and rhythm while you are walking on the treadmill. I will do this by taping two electrodes to your chest. The electrode is a round patch about 2 inches across which has adhesive on it around a snap-like metal part. The electrode will be attached to a cord which is attached to a special machine which records your heart rhythm. This procedure is simi­lar to the method used to take an EKG (electrocardiogram) which you may have had done before. While you are walking, your heart rhythm will be watched and a permanent record made of it. The heart monitoring should cause you no dis­comfort unless you are allergic to the electrodes in which case you may develop a small reddened area where they were attached. The rest and exercise blood study that your doctor ordered normally takes about 30-45 minutes. With the addition of the heart monitoring portion of the study, the test will take 15-20 minutes longer but there will be no increase in the amount of time you must exercise.

For my research, I will also need to have one more sample of your blood than would normally be drawn in the rest and exercise study. You will not.be charged for the additional blood sample. About 7cc's (1/4 ounce) more blood will be needed and will be taken through the needle already placed in your arm. I will also need information from your chart about your lung function studies and your present medications.

All information received will be used to study the effects of lung disease and exercise on the heart rhythms. This will help nurses and doctors to determine what degree of exercise should be done by the patients with chronic lung disease and the risk of exercise by these patients.

36

37If you decide to participate, your name will be

kept confidential at all times. A code number will be used for your name and your name will appear only on this consent sheet. There will be no added cost to you over and above the cost of the rest and exercise blood gas study. ,

If you desire not to take part in the electro­cardiogram study it will in no way affect the care you receive. You may also withdraw from the study at any time. I will be available to answer any questions now and at any time during the test.

The nature, demands, risks. Subject's Signatureand benefits of the project have been.explained to me as well asthe type of treatment as known and --------- -— --------available and I understand what myparticipation involves. Further- __ ;___;______ _more, I understand that I am free Signature of Parentto ask questions and withdraw from or Legally Authorizedthe project at any time, without Representativeaffecting my medical care.

DateI have carefully explained

to the subject the nature of theabove project. I certify that to '________the best of my knowledge the sub- Investigator's Sig- ject signing this consent form natureunderstands clearly the nature,demands, benefits and risks in- ‘ ____________.______volved in his participation in Datethis study. A medical problem or language or educational bar­rier has not precluded a clear understanding of his/her involve­ment in this project.

APPENDIX B

DATA COLLECTION FOBM

Code Number Age Sex Height _________ _Diagnosis _________ ___________Weight___________ • -

. FEV1/FVC________________Previous History of Heart Disease^___________ ■__Medications:

Name Dose Frequency Last Dose

Stage BP Pulse Resp PQg PCOq pH SaQ^ Bhythm

Before

Durin® i w - ' - ----------------- --------------------------------------- ------ ---------- --------------------------------------------------------------9 min ___________• ___________ ■ ;______ •

3 m i n _____________ ;______After

5 min ______ _____- . ___ ______

38

APPENDIX C

CLASSIFICATION OF ARRHYTHMIAS

I. SupraventricularA.. Tachycardias

1. Sinus - rate above 100.2„ Paroxysmal - included are

AtrialMultifocal Atrial Junctional Atrial Flutter Atrial Fibrillation

B. Bradycardias - Sinus - Below 60 C« Ectopics - above 6/minute

1. PAC * s2. PJC'S

II. VentricularA. Tachycardia - three dr more ventricular beats

in a rowB.' FibrillationC. Ectopics - above 6/minute

1. Unifocal2. Multifocal

III. Conduction DisturbancesA. 1° AV Block - PR interval greater than 0.20B. 2° AV Block

1. Wenchebach2. Mobitz II

39

40C. 3° AV Block D„ Bundle Branch Block

1. Eight2. Left

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Ayres, Stephen E., and William J. Grace. "Inappropriate Ventilation and Hypoxemia, as Causes of Cardiac Arrhythmias," American Journal of Medicine (1969) p. 46.

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41

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