Handbook for
Acute Care
Handbook for
Physical Therapists
Second Edition
Jaime
C.
Paz, M.S., P.T.
Assistant Clinical Specialist, Department of Physical Therapy, Northeastern University, Boston; Adjunct Faculty Member, Department of Physical Therapy, Simmons College, Boston; Adjunct Physical Therapist, Care Group Home Care, Belmont, Massachusetts
Michele P. West, M.S., P.T.
Physical Therapist, Inpatient Rehabilitation, Rehabilita tion Services, Lahey Clinic, Burlington, Massachusetts
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Library of Congress Cataloging-ill-Publication Data Paz, Jaime C.,
1966-Acute care handbook for physical therapists I Jaime c. Paz, Michele P. West.-2nd ed. p. ;cm.
Includes bibliographical references and mdex.
ISBN· 13, 978·0·7506·7300·6 ISBN· 10, 0·7506·7300·1
I. Medicine-Handbooks, manuals, etc. 2. Hospital care-Handbooks, manuals, ere. I. West, Michele P., 1969-11. lide.
[DNLM: I . Acute Discase-rherapy-Handbooks. 2.1mensive Care-Handbooks. WB 39 PJ48a 20021
RC55 .1'375 2001 6 I 6-<1c2 I
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To Nay and Tay, words can't convey my love and gratitude To my little "ieee, Alex, who has give" everyone a reason to smile And to the delicate balance o( li(e, let's not (orgot what is tntly important
J. P.
With (OIId memories o( Nana and Cookie
To jim, thank you (or your love, patience, and encouraging smile ... now we can go out and play!
Contributing Authors ix Contributing Artists XI Preface XIII Acknowledgments xv 1. Cardiac System 1 Seall M . Col/ills 2. Respiratory System 89
Michele P. West and jaime C . Paz
3. Musculoskeletal System 159
Michele P. West and james j . Caydos
4. Nervous System 259
Michele P. West
5. Oncology 331
Susan Polich
6. Vascular System and Hematology 363
Michele 1'. West and jaime C. Paz
7. Burns and Wounds 435
Michele P. West, Kimberly KllowltOll, alld Marie jarrell-Cracious 8. Gastrointestinal System 501 jaime C. Paz 9. Genirourinary System 557 jamie C. Paz 10. Infectious Diseases 605
jaime C. Paz alld V. Nicole Lombard
VIlI CONTENTS 11. Endocrine System 649 Jaime C. Paz 12. Organ Transplantation 697 Jellnifer Lee H,mt Appendices
I-A. Medical Record Review 745
Michele P. West
I-B. Acute Care Setting 749
Michele P. West
D. Fluid and Electrolyte Imbalances 763
Susan Polich and Jaime C. Paz
ill-A. Medical-Surgical Equipment in the Acute Care Setting 769 Eileen F. Lang
ill-B. Mechanical Ventilation 811
Sean M. Collins
ill-G. Circulatory Assist Devices 829
Jaime C . Paz
IV. Pharmacologic Agents 839
Jaime C. Paz and Michele P. West
V. Effects of Anesthesia 871
Michele P. West
VI. Pain Management 877
Jaime C. Paz
YD. Amputation 887
Jason D. Rand and Jaime C. Paz
Vll!. Postural Drainage 897
Michele P. West
lX. Functional Tests 901
Jellnifer A . Silva and Jaime C. Paz
X. Physical T herapy Considerations for Patients
Who Complain of Chest Pain 921
Michele P. West
Scan M. Collins, M.S., P.T., C.C.S.
Department of Physical T herapy, University of Massachusetts, Lowell; Adjunct Physical Therapist, Department of Rehabilitation Services, Lowell General Hospital, Lowell, Massachusetts
James J. Gaydos, M.S., P.T.
Senior Physical Therapisr, Department of Inpatient Acute Care, New England Baptist Hospital, Boston
Marie Jarrell-Gracious, P.T.
Owner, Specialty Care, Mokena, Illinois Jennifer Lee Hunt, M.S., P.T.
Physical Therapist, Rehabilitation Services, Lahey Clinic, Burlington, Massachusetts
Kimberly Knowlton, P.T.
Clinical Lead Physical Therapist, Rehabilitation Services, University of Massachusetts Memorial Medical Center, Worcester
Eileen f. Lang, P.T.
Senior Physical Therapist, Rehabilitation Services, Lahey Clinic, Burl ington, Massachusetts
x CONTRIBUllNG AlITHORS
V. Nicole Lombard, M.S., P.T.
Staff Physical Therapist, Department of Physical Therapy, New England Baptist Hospital, Boston
Jaime C. Paz, M.S., P.T.
Assistant Clinical Specialist, Department of Physical Therapy, North eastern University, Boston; Adjunct Faculty Member, Department of Physical Therapy, Simmons College, Boston; Adjunct Physical Thera pist, Care Group Home Care, Belmont, Massachusetts
Susan Polich, P.T., M.T.(A.S.C.P.l, M.Ed.
Assistant Clinical Specialist, Department of Physical Therapy, North eastern University, Boston; Adjunct Instruccor, Physical Therapist Assis tant Program, Community College of Rhode Island, Newport; Physical Therapist, Sturdy Memorial Hospital, Attleboro, Massachusetts Jason D. Rand, P.T.
Physical Therapist, Inpatient Physical Therapy Services, Winthrop Universiry Hospital, Mineola, New York
Jennifer A. Silva, M.S., P.T.
P hysical Therapist, Outpatient Rehabilitation Center, South Shore Hospital, South Weymouth, Massachusetts
Michele 1'. West, M.S., P.T.
Physical Therapist, Inpatient Rehabilitation, Rehabilitation Services, Lahey Clinic, Burlington, Massachusetts
Sean M. Collins, M.S., P.T., C.C.S.
Department of Physical Therapy, University of Massachusetts, Lowell; Adjunct Physical Therapist, Department of Rehabilitation Services, Lowell General Hospital, Lowell, Massachusetts
Barbara Cocanour, Ph.D.
Department of Physical Therapy, University of Massachusetts, Lowell
Marybeth Cuaycong
Graduate Student, Department of Physical Therapy, Northeastern University, Boston
Peter L. Scotch, M.A.
English Teacher, Byram Hills High School, Armonk, New York Michele P. West, M.S., P.T.
Physical Therapist, Rehabilitation Services, Lahey Clinic, Burlington, Massachusetts
Peter P. Wu
Graduate Student, Department of Physical Therapy, Northeastern Universiry, Boston
Preface
Acute Care Handbook for Physical Therapists was originally devel oped to provide clinicians with a handy reference for patient care in the hospital serring. It was created primarily for physical therapy stu dents and clinicians unfamiliar with acute carc. Because of the positive comments and feedback to the first edition, this second edition was written to serve the same purpose with updated information, including the following:
• A revision of all chapters and appendices with expanded infor
mation on new technologies, medical-surgical innovations, clinical tips, and guidelines to physical therapy management
• A new chapter on organ transplantation
• Updated information on common medications, including a new
pharmacologic agents appendix
• New appendices, such as Acute Care Setting and Functional Tests Additionally, the ralents of new contributors have given this edition a broader perspective on clinical practice in the acute care setting. Last, language that is consistent with the Guide to Physical Therapist Prac tice is used throughout all the chapters and appendices.
As a member of the health care team, the physical therapist is often expected to understand hospital protocol, safety, medical-surgical
"lingo," and the many aspects of patient care from the emergency room setting, to the intensive care unit, to the general ward. This handbook is therefore intended to be a resource to aid in the interpre tation and understanding of the medical-surgical aspects of acute care.
Each chapter in this edition of Acute Care Handbook (or Physical Therapists discusses a major body system. The chapters include the following:
• A review of basic structure and function
• An overview of the medical-surgical evaluation of a patient admitted to the hospital, including diagnostic procedures and labo ratory tests
• A review of pathophysiology that emphasizes signs and symp
toms of specific diseases and disorders
• Guidelines for physical therapy intervention
Clinical Tips appear throughout each chapter. These helpful hints are intended to maximize safety, quality, and efficiency of care. These clin ical rips are suggestions from the editors and contributors that, from clinical experience, have proved to be valuable in acclimating thera pists to the acute care setting.
Appendices provide information to complement topics presented in the cha pters.
It is important to remember that all of the information presented in this book is intended to serve as a guide to stimulate independent critical thinking within the spectrum of medical-surgical techniques and trends. Developing and maintaining a rapport with the medical-surgical team is highly recommended, as the open exchange of information among pro fessionals is invaluable. We believe this new edition of Acute Care Handbook (or Physical Therapists can enhance the clinical experience by providing valuable information while reviewing charts, preparing for therapy intervention, and making clinical decisions in the acute care setting.
j.p.
Acknowledgments
We offer sincere gratitude to the following people:
Leslie Forman and Butterworth-Heinemann for their confidence in creating a second edition of this work.
Jennifer Rhuda for her editOrial expertise and resourcefulness. Shannon Riley at Silverchair for her graceful editing down the home Stretch.
The contributOrs-we couldn't have completed this project without you.
The many patients, whose lives have enriched ours, both clinically and personally.
Personal thanks from Jaime to the following:
Tallie, for all your love, support and continuous encouragement. couldn't have made it without you. Mahal kita.
The students, both at Northeastern University and Simmons College, who give me one of the best reasons to get up in the morning. Jennifer Katz and Cindy Dubois for your research assistance.
My colleagues and mentors, who continually inspire me to become a better educator and clinician.
And to my extended family, whom I need to see a lot more of now that this is all over: Rory and Jane; John and Alex; Vic, Karen, Anna, and Little Vic; Steve, Jennifer, ChristOpher, and Aidan; Peter, Sally, and Hannah; Rick, Cheryl, Andrew, and Lauren; Mark, Gina, Ben jamin, and Nicholas.
Personal thanks from Michele to the following:
My family and friends, who offered encouragement throughout the publishing process, including Mom and Dad, Marie, Heather, Tracee, Lynn, IGm J., Betsy, Kelly, Kelli, Kim P., Julie, and Bill.
Nana and Cookie, for reminding me to find the grandparent in each patient.
My husband, Jim, for teadling me more computer skills than I ever wanted to know.
My laser printerlfaxlcopier, I couldn't have done this withour you! My colleagues and patients, who inspire me to become a better clinician.
My fellow Lahey inpatient physical therapists, for bearing with me rhrough the completion of rhis manuscript.
Lena, for cooking me dinner when I didn't have time.
Heather Hayden, M.S., P.T., and Kelly Madden, M.S., P.T., for your helpful suggestions and manuscripr review.
Carol Spencer, Medical Librarian, Cattell Memorial Library, Lahey Clinic, for your research assistance.
Acute Care
Handbook for
Cardiac System
Sean M. Collins
Introduction
1
Physical therapists in acute care faci lities commonly encounter patients with cardiac system dysfunction as either a primary morbidity or comorbidity. Based on current estimates, 59,700,000 Americans have one or more types of cardiovascular disease (CVD), making the preva lence rate for men and women 20% ' In 1 997, CVD ranked first among all disease categories and accounted for 6, 1 45,000 inpatient admissions.' In the acute care setting, the role of the physical therapist with this diverse group of patients remains founded in examination, evaluation, intervention, and discharge planning, for the purpose of improving functional capacity and minimizing disabiliry. The physical therapist must be prepared to safely accommodate for the effects of dynamic (pathologic, physiologic, medical, and surgical intervention) changes into his or her evaluation and intervention.
The normal cardiovascular system provides the necessary pumping force to circulare blood through the coronary, pulmonary, cerebral,
and systemic circulation. To perform work, such as during functional rasks, energy demands of the body increase, therefore increasing the oxygen demands of the heart. A variery of pathologic states can create
2 Acme CARE HANDBOOK FOR PHYSICAL THERAPISTS
impairments in the cardiac system's ability to successfully meet these demands, ultimately leading to functional limitations. To fully address these functional limitations, the physical therapist must understand normal and abnormal cardiac function, clinical tests, and medical and surgical management of the cardiovascular system.
The objectives of this chapter are to provide the following:
1 . A brief overview of the Structure and function of the
cardio-vascular system
2. An overview of cardiac evaluation, including physical exami-nation and diagnostic testing
3. A description of cardiac diseases and disorders, including clinical findings and medical and surgical management
4. A framework on which to base physical therapy evaluation and intervention in patienrs with CVD
Structure
The heart and the roots of the great vessels ( Figme 1 - 1 ) occupy the peri cardium, which is located in the mediastinum. The sternum, the costal cartilages, and the medial ends of the third to fifth ribs on the left side of the thorax create the anterior border of the mediastinum. It is bordered inferiorly by the diaphragm, posteriorly by the vertebral column and ribs, and laterally by the pleural cavity (which contains the lungs).' Specific cardiac structures and vessels and their respective functions are outlined in Tables 1 - 1 and 1-2.
Note: The mediastinum and the heart can be displaced from their normal positions with changes in the lungs secondary to various dis orders. For example, a tension pneumothorax will shift the mediasti num away from the side of dysfunction (see Chapter 2 for further description of pneumothorax).
Function
The cardiovascular system must adjust the amount of nutrient and oxy gen rich blood pumped out of the heart (cardiac output [CO]) to meet the wide spectrum of daily energy (metabolic) demands of the body.
Superior Vena ClIVI Sinus Node Branch
-/---<
rush' "n'''''
--+-Right Coronary Art,,>,Inferior Vena CO'"
--J+-=�,
Pulm��", Art,,,,... ->'''''',w
BranchBranches
A..\\-·�." "'''I
BranchPostcnOf Dcscmdlng Art,,,,
".,
1:;;;
..
=-
____ Pulmonary Artery Left Atrium Ldt Main Coronary ArterylsI Diagonal Branch Left Venuicle 2nd Diagonal Branch
\r--#o+--
Left AnteriorDescending Artery
Apical Branches
Figure 1-1. Anatomy of the right coronary artery and Jeft coro,wry artery, including left maiu, left auterior descending, and left circumflex coronary arteries. (Reprinted with permissioll (rom R C Becker. Chest Pain: The Most
Common Complaints Series. Boston: Butterworth-Heinemann, 2000;26-28.)
The heart's ability to pump blood depends on the following characteristics3:
• Automaticity-the ability to initiate its own electrical impulse
4 AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 1-1. Primary Structures of the Hearr Structure Pericardium Epicardium Myocardium Endocardium Right atrium Tricuspid valve Right ventricle Pulmonic valve Left atrium Mitral valve Left ventricle Aortic valve Description
Double-walled sac of elas tic connective tissue, a fibrous outer layer and serous inner layer Outermost layer of car
diac wall, covers sur face of heart and great vessels
Central layer of thick muscular tissue Thin layer of endothe
liurn and connective tissue
Heart chamber
Atrioventricular valve between right atrium and ventricle Hearr chamber
Semilunar valve between right ventricle and pulmonary arrery Heart chamber
Atrioventricular valve between left atrium and ventricle Heart chamber
Semilunar valve between left ventricle and aorta
Function
Prorects against infection and trauma
Protects against infection and trauma
Provides major pumping force of the venrricles
Lines [he inner surface of hearr, valves, chordae rendineae, and papillary muscles Receives blood from venous
system and is a primer pump for the right ventri cle
Prevents back flow of blood from right ventricle to atrium during ventricular systole
Pumps blood to pulmonary circulation
Prevents back flow of blood from pulmonary artery to right ventricle during diastole Acts as a reservoir for blood
and primer pump for left ventricle
Prevents backflow of blood from left ventricle to atrium during ventricular systole
Pumps blood to systemic circu lation
Prevents backflow of blood from aorta to left ventricle during ventricular diastole
Table 1-1. Continued Structure Chordae tendineae Papillary muscle Description Tendinous attachment of atrioventricular valve cusps to papillary muscles
Muscle that connects chordae tendineae to floor of ventricle wall
Function
Prevents valves from everting into atria during ventricular systole
Constricts and pulls on chordae tendineae to prevent eversion of valve cusps dur ing ventricular systole
• Conductivity-the ability to transmit electrical impulse from
cell to cell within the heart
• Contractility-the ability to stretch as a single unit and then
passively recoil while actively contracting
• Rhythmicity-the abiliry to repeat the cycle in synchrony with
regularity
Table 1-2. Great Vessels of the Heart and Their Function
Structure Description Function
Aorta Primary artery from the left ven- Ascending aorta delivers tricle that ascends and then blood to neck, head,
descends after exiting the heart and arms.
Descending aorta deliv-ers blood to visceral and lower body tissues.
Superior Primary vein that drains into the Drains venous blood
vena cava right atrium from head, neck, and
upper body.
Inferior Primary vein that drains into the Drains venous blood
vena cava right atrium from viscera and lower
body.
Pulmonary Primary artery from right Carries blood to lungs.
6 AarrE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Cardiac Cycle
Blood flow throughout the cardiac cycle depends on circulatOry and cardiac pressure gradients. The right side of the heart is a low pressure system with little vascular resistance in the pulmonary arter ies, whereas the left side of the heart is a high-pressure system with high vascular resistance from the systemic circulation. The cardiac cycle is the period from the beginning of one contraction, starting with sinoatrial (SA) node depolarization, to the beginning of the next contraction. Systole is the period of contraction, whereas diastole is the period of relaxation. SystOle and diastOle can also be categorized into atrial and ventricular components:
1 . Atrial diastole is the period of atrial filling. The flow of blood is directed by the higher pressure in the venous circulatory system.
2. Atrial systole is the period of atrial emptying and
cOntrac-tion. Initial emptying of approximately 70% of blood occurs as a result of the initial pressure gradient between the atria and the ventri cles. Atrial contraction then follows, squeezing our the remaining 30%.3 This is commonly referred to as the atrial kick.
3. Ventricular diastole is the period of ventricular filling. It initially
occurs with ease; then, as the ventricle is filled, atrial contraction is neces sary to squeeze the remaining blood volume into the ventricle. The amount of stretch placed on the ventricular walls during diastOle, referred to as left ventricular end diastolic pressure (LVEDP), influences the force of contraction during systOle. (Refer to description of preload in the section Factors Affecting Cardiac Output.)
4. Ventricular systole is the period of ventricular contraction.
The initial contraction is isovolumic (meaning it does nOt eject blood), which generates pressure necessary to serve as the catalyst for rapid ejection of ventricular blood. The left ventricular eiectiOlt fraction
(EF) represents the percent of end diastOlic volume ejected during sys tOle and is normally approximately 60%.3
Cardiac Output
CO is the quantiry of blood pumped by the heart in 1 minute. It can also be described relative to body mass as the cardiac index, the
amount of blood pumped per minute per square meter of body mass. Regional demands for tissue perfusion (based on local metabolic needs) compere for systemic circularion, and roral CO adjusts ro meet these demands. Adjustment ro CO occurs with changes in hearr rate (HR)
(chronotropic) or stroke volume (SV) (inotropic).· Normal resting CO is approximarely 4-8 liters per minute, and normal cardiac index is approximately 2.5-4.0 liters per minute per meter'·' (with a resting HR of 70 beats per minute [bpml, resring SV is approximately 71 ml/beat). The maximum value of CO represents the functional capacity of the circulatory system to meet the demands of physical activity.
CO (liters per minute) = HR (bpm) x SV (liters)
Facrors Affecting Cardiac Output
Preload
Preload is the amount of tension on the ventricular wall before it con tracts. It is related ro venous return and affects SV by increasing left ventricular end diastolic volume as well as pressure and therefore con
traction J This relationship is explained by the Frank-Starling Mecha
nism and is demonstrated in Figure 1-2.
Frank-Starli/lg Mechanism
The Frank-Starling mechanism defines the normal relationship between length and tension of the myocardium,s The greater the stretch on the myocardium before systole (preload), the stronger the ventricular contraction. The length-tension relationship in skeletal muscle is based on the response of individual muscle fibers; however, relationships between cardiac muscle length and tension consist of the whole heart. Therefore, length is considered in terms of volume; tension is considered in terms of pressure. A greater volume of blood returning to the hearr during diastole equates ro greater pressures generated initially by the heart's con tractile elements. Ultimately facilitated by elastic recoil, a greater volume of blood is ejected during systole. The effectiveness of this mechanism can be reduced in pathologic situations.4
Afterload
Afterload is the force against which a muscle must contract to ini tiate shortening.s Within the ventricular wall, this is equal to the
S1"Olk SWill of tIM Myocudl".:
Tht lour bns prowk an eumple of how tbt contrxtiIt .�It of Iht myocanJl\lDI InfluIonca Iht rNtiondUp bftWftft LVEDV and vmtritWM pmornwn.
�
OI .. lo!!, Stak of tM Myol:lrdhun Ldl VmtriclILIr Endmati.,!!, Vol ... ' {LVEDyt «: ... , � of Myocard.i...
I_
[
V_ Rttum we Atnal Contribution ID VmlriNL1r filII,. (Atnal Kid:J S)'mpithtuc T ant utecholaminn foror.FftqUftlC)' Relation """"" . ....,. AnoDa/Hyptrc:&pnlal """"" l.osI of MyocardIum lnlnnlit� Elutldty 01 MyocardJum upKity of Ventrkwn 0._Toul lSIood Volunv Pumpof�IMUkIes Body fUslllOn lntnothorildl: � lntnopmcardilll'rtulm V_Tent
Figure 1-2. Factors affecting left ventricular function. (Adapted from E Braunwal. J Ross, E Somlenblick. et al. Mechanisms of Contraction of the Normal and Faili,lg Heart {2nd ed}. Boston: Little, Brown, 1 976.}
QO
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�
'" '"�
z "g
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tension developed across its wall during systo le. The most promi nent force contributing to afterload in the heart is SP, specifically vascular compliance and resistance. BP affects aortic valve opening and is the most obvious load encountered by the ejecting ventricle. An example o f afterload is the amount of pressure in the aorta at the time of ventricular systo le.3
Cardiac Conduction System
A schematic of the cardiac conduction system and a normal electrocar diogram (ECG) are presented in Figure 1 -3. Normal conduction begins in the SA node and travels t1uoughout the atrial myocardium (atrial depolarization) via intranodal pathways to the atrioventricular (AV) node, where it is delayed momentarily. It then travels to the bundle o f His, to the bundle branches, to the Purkinje fibers, and finally to the myocardium, resulting in ventricular contraction.6 Disturbances in
con-Sinoatrial ___
-A::
;::-
�:;--�
node Atrioventricular node Bundle of His--+/1---'<'<\
Area 1 R�tpa"of---��---
�
ventricular discharge Q waveI
--4h
Area2 Second part of P Q S T ventricular dischargeFigure 1-3. Schematic representation of the sequence of excitation in the
heart. (\'(lith permission from M \'(Ialsh. A Crumbie. S Reveley. Nurse Practi tioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heine man, 1999;99.)
10 AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
duction can decrease CO (refer to the discussion of rhythm and con duction disturbances in the Pathophysiology section)?
Netlral lnptlt
The SA node has its own inherent rate. Neural input can, however, influence HR, HRV, and contractility through the autonomic nervous system.J•s
Parasympathetic system (vagal) neural input generally decelerates cardiac function, thus decreasing HR and contractility. Parasympa thetic input travels through the vagus nerves. The right vagus nerve pri marily stimulates the SA node and affects rate, whereas the left vagus nerve primarily stimulates the AV node and affects AV conduction.J,8
Sympathetic system neural input is through the thoracolumbar sympathetic system and serves to increase HR and augment ventricu lar contractility, thus accelerating cardiac function.3
Endocrine Input
In response to physical activity or stress, a release in catecholamines increases HR, contractility, and peripheral vascular resistance for a net effect of increased cardiac function.' Refer to Table 1-3 for the cardiac effects of hormones.
Local Input
Tissue pH, concentration of carbon dioxide (C02), concentration of oxy gen (02)' and metabolic products (e.g., lactic acid) can affect vascular tone.' During exercise, increased levels of CO2, decreased levels of 02' decreased pH, and increased levels of lacric acid ar the tissue level dilate local blood vessels and therefore increase CO distribution to thar area.
Cardiac Reflexes
Cardiac reflexes influence HR and contractility and can be divided into three general categories: baroreflex (or pressure), Bainbridge reflex (or stretch), and chemoreflex (or chemical reflexes).
Table 1-3. Cardiac Effects of Hormones
Hormone Primary Site Stimulus Cardiac Effect
Norepinephrine Adrenal Stress/exercise Vasoconstriction
medulla
Epinephrine Adrenal Stress/exercise Coronary artery
medulla vasodilation
Angiotensin Kidney Decreased arte- Vasoconstriction, rial pressure increases blood
volume
Vasopressin Posterior Decreased arte- Potem vasoconstriaor
pituitary rial pressure
Bradykinin Formed by Tissue damage! Vasodilation,
polypep- inflammation increased
capil-tides in lary permeabiliry
blood when activated
Histamine Throughout Tissue damage Vasodilation,
tissues of increased
capil-body lary permeability
Atrial natri- Atria of heart Increased atrial Decreased blood
uretic pep- stretch volume
tides
Aldosterone Adrenal Angiotensin II Increases blood cortex (stimulated) by volume, kidneys
hypovolemia excrete more or decreased potassium
renal perfusion
Source: Data from AC Guyton.JE Hall. Textbook of Medical Physiology (9th cd).
Phil-adelphia: Saunders, 1996.
Baroreflexes are activated through a group of mechanoreceptors located in the heart, great vessels, and intrathoracic and cervical blood vessels. These mechanoreceptors are most plentiful in the walls of the internal carotid arteries.] Mechanoreceptors are sensory recep tors that are sensitive co mechanical changes, such as pressure and Stretch. Activation of the mechanoreceptors by high pressures results in an inhibition of the vasomotor center of the medulla that increases vagal stimulation. This chain of events is known as the baroref/ex and results in vasodilation, decreased HR, and decreased contractility.
12 ACUTE CARE HANDBOOK ';OR PHYSICAL THERAPISTS
Mechanoreceptors located in the right atrial myocardium respond to stretch. With an increased volume in the right atrium, there is an increase in pressure on the atrial wall. This reflex, known as the Bail1bridge reflex, stimulates the vasomOtor center of the medulla, which in turn increases sympathetic input and increases HR and contractility.) Respiratory sinus arrhythmia, an increased HR during inspiration and decreased HR during expira tion, may be facilitated by changes in venous return and SV caused by changes in thoracic pressure induced by the respiratory cycle. At the beginning of inspiration, when thoracic pressure is decreased, venous return is greater, and therefore there is a greater stretch on the atrial wall .'
Chemoreceptors located on the carotid and aortic bodies have a primary effect on increasing rate and depth of ventilation in response to CO, levels, but they also have a cardiac effect. Changes in CO, during the respiratory cycle may also result in sinus arrhythmia.3
Coroltary Perfusiolt
For a review of the major coronary arteries, refer to F igure I - I . Blood is pumped to the large superficial coronary arteries during ventricular systole. At this time, myocardial contraction limits the flow of blood to the myocardium; therefore, myocardial tissue is actually perfused during diastole.
Systemic Circulatiolt
For review of the primary anatomic structures and distribution of the systemic circulation, refer to F igure ] -4. Systemic circulation is affected by roral peripheral resistance (TPR), which is the resis tance to blood flow by the force created by the aorta and arterial system. Two factors that contribute to resistance are ( 1 ) vasomotor tone, in which vessels dilate and constrict, and (2) blood viscosity, in which greater pressure is required to propel thicker blood. Also called systemic vasClilar resistaltce, TPR and CO influence blood pressure (BP).3 This relationship is illustrated in the following equation:
Upper Systemic Circulation __
//6�
Superior Vena Cava 7"'-_
Anenes
Inferior Vena Cava Liver Circulation
Intestinal Circulation
Lower Systemic Circulation
Figure 1-4. Schematic of systemic circulation. (Draw'J by Barbara Cocanoll"
Ph.D., University of Massachusetts, Lowel1, Department of Physical Therapy.)
Cardiac Evaluation
Cardiac evaluarion consists of patient history, physical examina tion (which consists of observation, palpation, BP measurement, and heart sound auscultation), laboratory rests, and diagnostic procedures.
Patiellt History
In addition to the general charr review presented in Appendix I-A,
pertinent information about patients with cardiac dysfunction that should be obtained before physical examination includes the following'· 10-12:
• Presence of chest pain (see Appendix X for an expanded
14 ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS
1. Location, radiation
2. Character and quality (crushing, burning, numbing, hot) and frequency
3. Angina equivalents (what the patient feels as angina, e.g., jaw pain, shortness of breath, dizziness, lightheadedness, dia phoresis, burping, nausea, or any combination of these) 4. Aggravating and alleviating factors
5. Precipitating factors
• Medical treatment sought and its outcome • Presence of palpitations
• Presence of cardiac risk factors (Table 1-4) • Family history of cardiac disease
Table 1-4. Cardiac Risk Faccors Major Independent Risk FactOrs Smoking Hypertension Elevated serum cholesterol, roral (and LDLI Decreased high
density lipopro tein cholesterol Diabetes mellitus Advancing age
Predisposing Risk Factors Physical inactivity Obesity
Body mass index >30 kglm'
Abdominal obesity (waist hip ratio)
Men >40 in.
Women >35 in.
Family history of prema ture heart disease Psychosocial factors Ethnic characteristics LDL = low-density lipoprotein.
Conditional Risk Factors
Elevated triglycerides Small LDL parricles Elevated homocysteine Elevated lipoprotein (a)
Elevated inflammatory markers
C-reactive protein Fibrinogen
Source: Data from SM Grundy, R Pasternak, P Greenland, et al. Assessment of cardio vascular risk by use of multiple-risk-factOr assessmenr equations: a statement for healthcare professionals from the American Heart Association and the American Col lege of Cardiology, Circulation 1999; 100: 1481-1492.
o History of dizziness or syncope
o Previous myocardial infarction (MI), cardiac studies, or procedures
Clinical Tip
• When discussing angina with a patient, use the patient'S terminology. If the patient describes the angina as "crush ing" pain, ask the patient if he or she experiences the crushing feeling during treatment as opposed to asking the patient if he or she has chest pain.
o The common medical record abbreviation for chest pain is CPo
Physical Exam;1Iatio1l
Observation
Key components of the observation portion of the physical examina tion include the following··7:
1 . Facial color, skin color and rone, or the presence of diaphoresis 2. Obvious signs of edema in the extremities
3. Respiratoty rate
4. Signs of trauma (e.g., paddle burns or ecchymosis from car diopulmonary resuscitation)
5. Presence of jugular venous distention, which results from the backup of Auid into the venous system from right-sided CHF (Figure 1-5)
a. Make sure the patient is in a semirecumbent position (45 degrees).
b. Have the patient turn his or her head away from the side being evaluated.
c. Observe pulsations in the internal jugular neck region. Pulsations are normally seen 3-5 em above the sternum.
Pul-1 6 ACUTE CARE HANDBOOK FOR PHYSICAL TI-IERAPISTS
CaroHd artery
In1ernal jugular veJn External Jugular vein
Sternal angle
Figure 1-5. Measurement of iugular venous distention (J VPJ. The J VP read ing is the maximum height, in centimeters, above the sternal angle at which venous pulsations are visible.
sations higher than this or absent pulsations indicate jugular venous distention.
Palpation
Palpation is the second component of the physical examination and is used to evaluate and identify the following:
• Pulses for circulation qua�ty, HR, and rhythm (Table 1-5, Figure 1-6) • Exttemities for pitting edema bilaterally (Table 1-6)
Clinical Tip
• When palpating HR, counting pulses for 1 5 seconds and multiplying by 4 is sufficient with normal rates and rhythms. [f rates are faster than 1 00 bpm or slower than 60 bpm, they should be palpated for 60 seconds. If the rhythm is irregularly irregular (e.g., during atrial fibrilla tion) or regularly irregular (e.g., premature ventricular contractions [PVCs]), auscultation of heart sounds should be performed to identify the apical HR for a full minute.
Table 1-5. Pulse Amplitude Classification and Pulse Abnormalities Scale o 1+ 2+ 3+ 4+ Abnormality Pulsus alternans Bigeminal pulses Pulsus paradoxus
Pulse Amplitude Classification
Degree Absent pulse Diminished pulse Normal pulse Moderately increased Markedly increased (boundlllg)' Description No pulse-no circulation Reduced stroke volume and ejec
tion fracrion, Increased vascular resistance
Normal resting conditions, no pathologies
Slightly increased stroke volume and ejection fraction
Increased stroke volume and ejec tion fraction, can be diminished with vasoconstriction
Pulse Abnormalities Palpation
Regular rhythm With strong pulse waves alternaring with weak pulse waves
Every mher pulse is weak and early
Reduction in strength of the pulse with an abnormal decline in blood pressure during inspiration
Description
Indicates left ventricular failure when present at normal heart rares
Due ro preventricular contractions (bigeminy)
May be caused by chronic obstruc tive lung disease, pericarditis, pulmonary emboli, restrictive cardiomyopathy, and cardio genic shock
·Corrigan's pulse IS a houndmg pulse viSible in the carotid artery rhat occurs with aor lIC rcgurgltallon.
Source: Data from SL Woods, ES SivaraJian-Froelichcr. S Underhill-Morzer (eds). Car· dlac NurSing (4th cd). Philadelphia: Lippincott, 2000.
In these cases, palpation of pulse cannot substitute for ECC analysis ro moniror the patient'S rhythm, but it may alert the therapist to the onset of these abnormalities.
• Use caution in palpating pulses, as manual pressure on the
1 8 ACUTE CARE HANDBOOK FOR PHYSICAL TIIFRAI'ISTS
\1Il--- Carotid Pulse
Brachial Pullse·---�I/I.jrll
Radial P"II,.,.---f.I!'
II
1\\ 1foK+--
Popliteal Pulse(posterior knee)
U--- Pedal Pulse
Figure 1 ·6. Arterial pulses. (Draw" by Barbara Cocauour, Ph.D., U"iversity
Table 1-6. Pirring Edema Scale Scale Degree 1 + Trace Slighr 2+ Mild 0-{}.6 em 3+ Moderare 0.6-1.3 em 4+ Severe 1.3-2.5 em
EID = easily identified depression.
Description
Barely perceprible depression Easily idenrified depression (EID)
(skin rebounds in <15 secs) EID (rebound 15-30 sees) EID (rebound >30 sees)
Sources: Dara from SL Woods, ES Sivarajian Froelichcr, 5 Underhill-Moner (cds). Cardiac Nursing (4th cd). Philadelphia: Lippincott, 2000; and EA Hillegass, HS Sadowsky (cds). Essentials of Cardiopulmonary Physical Therapy (2nd cd). Philadelphia: Saunders, 2001.
B)ood Pressure
BP measurement with a sphygmomanometer (cuff) and ausculta tion is an indirect, noninvasive measurement of the force exerted against the arterial walls during ventricular systole (systolic blood
pressure [SBPJ) and during ventricular diastole (diastolic blood
pressure). BP is affected by peripheral vascular resistance (blood
volume and elasticity of arterial walls) and CO. Table 1-7 lists normal BP ranges. Occasionally, BP measurements can only be performed on certain limbs secondary ro the presence of condi tions Stich as a percutaneous inserted central catheter,
arteria-Table 1-7. Normal Blood Pressure Ranges
Age 8 yrs Agel2 yrs Adulr Borderline hypertension Hypertension Normal exer cise Systolic 85-1 14 111m Hg 95-'135 mm Hg 100- 140 mm Hg 140-150 mm Hg >150 mm Hg
Increases during rime and wirh increased load or intensity
Diastolic 52-85 mOl Hg 58-88 mm Hg 60-90 mm Hg 90-100 mm Hg > 100 mm Hg ,,) O mm Hg
Sources: Data from SL Woods, ES Sivarajian Froelicher, S Underhill-Moner (cds). Car diac Nursing (4th cd). Philadelphia: Lippincott, 2000; :md LS Bickley. Bate's Guide to Physical Examination and Hisrory Taking (7th cd). Philadelphia: Lippincon, 1999.
20 ActITE CARE HANDBOOK FOR PHYSICAL TIIERAPlm
venous fistula for hemodialysis, blood clots, scarring from brachial artery cutdowns, or lymphedema (i.e., status-post mastectomy). BP of the upper extremity should be measured ill the following manner:
1 . Check for posted signs, if any, at the bedside that indicate
which arm should be used ill taking BP. BP variations of 5-J 0 mm Hg between the right and lefr upper extremity are considered normal. Patients with arterial compression or obstruction may have differ ences of more than 10-15 mm Hg.12
2. Use a properly fitting cuff. The inflatable bladder should have a width of approximately 40%, and length of approximately 80% of the upper arm circumference. 13
3 . Position the cuff 2.5 em above the antecubital crease.
4. Rest the arm at the level of the heart.
5. To determine how high to inflate the cuff, palpate the radial pulse, inllate until no longer palpable, and nOte this cuff inflation value. Deflate the cuff.
Note: With a patient who is in circulatory shock, auscultation may be too difficult. In these cases, this method can be used to measure the SBP and is recorded as systolic BPfP (i.e., "BP is 90 over palp").13
6. Place the bell of the stethoscope gently over the brachial arrery. 7. Re-inflare rhe cuff to 30-40 mm Hg greater rhan the value in srep 5. Then slowly deflare rhe cuff. Cuff deflation should occur at approximately 2-3 mm Hg per second.13
8. Listen for the onset of tapping sounds, which represents blood flow returning to the brachial arrery. This is the systolic pressure.
9. As the pressure approaches diastolic pressure, the sounds will become muffled and in 5-10 mm Hg will be completely absent. These sounds are referred to as Korotkoff's sounds (Table 1_8). 12.13
Clinical Tip
• Recording pre-, para-, and posrexerrion SP is important in identifying BP responses [0 activity. During recovery from exercise, blood vessels dilate to allow for greater blood flow to muscles. In cardiac-compromised or very
Table 1-8. Kororkoff's Sounds
Phase
2
Sound
First sound heard, faint tapping sound with increasing intensity Start swishing sound
Indicates
Systolic pressure (blood stans to flow through compressed artery).
Because of the compressed artery, blood flow continues to be heard while the sounds change due to the changing compression on the anery.
3 Sounds increase in
4 5
inrensity with a distinct tapping Sounds become muf
ned
Disappearance
Diasrolic pressure in children <13 yrs old and in adults who are exercising, preg nanr, or hyperrhyroid (see phase 5). Diastolic pressure in adults-occurs 5-10
mm Hg below phase 4 in normal adults. In states of increased rate of blood flow, it may be greater than 10 mm Hg below phase 4. In these cases, the phase 4 sound should be used as diasrolic pressure in adults.
Sources: Data from SL Woods, ES Sivarajian-Froelicher, S Underhill-Moner (eds). Car diac Nursing (4th ed). Philadelphia: Lippincott, 2000; and LS Bickley. Bate's Guide to Physical Examination and History Taking (7th ed). Philadelphia: Lippincott, 1 999.
decondirioned individuals, toral CO may nor be able to support this increased flow to the muscles and may lead to decreased Output to vital areas, such as the brain.
• If unable to obtain BP on rhe arm, rhe thigh is an appro
priate alternative, with auscultation at the popliteal artery. • Falsely high readings will occur if the cuff is too small or applied loosely, or if the brachial arrery is lower rhan rhe hearr level.
• Evaluarion of BP and HR in differenr postures can be used to monitor orthostatic hypotension with repeat mea surements on the same arm 1-5 minutes after position changes. The symbols rhar represent parienr posirion are shown in Figure 1 -7.
22 AClJfE CARE HANDBOOK FOR PHYSICAL THERAPISTS
0--Supine Sitting
Figure 1-7. Orthostatic blood pressure symbols.
Standing
• The same extremity should be used when serial BP
recordings will be compared for an evaluation of hemody namic response.
• A BP record is kept on the patient's vital sign flow sheet. This is a good place to check for BP trends throughout the day and, depending on your hospital's policy, to document BP changes during the therapy session.
• An auscultatory gap is the disappearance of sounds between phase 1 and phase 2 and is common in patients with high BP, venous distention, and severe aortic stenosis. Its presence can create falsely low systolic pressures if the cuff is not inflated high enough (which can be prevented by palpating for the disappearance of the pulse prior to measurement), or falsely high diastolic pressures if the therapist stOps measurement during the gap (prevented by listening for the phase 3 to phase 5 transitions). 13
Auscultation
Evaluation of heart sounds can yield information about the patient'S condition and tolerance to medical treatment and physical therapy through the evaluation of valvular function, rate, rhythm, valvular compliance, and ventricular compliance.4 To listen to heart sounds, a stethoscope with both a bell and a diaphragm is necessary. For a review of normal and abnormal heart sounds, refer to Table 1-9. The examination should follow a systematic pattern using both the bell (for low-pitched sounds) and diaphragm (for high-pitched sounds) and should cover all auscultatory areas, as illustrated in
Table 1-9. Normal and Abnormal Heart Sounds Sound Location
5 1 (normal) All areas
52 (normal) All areas
53 (abnormal) Best appreciated
54 (abnormal) Murmur (abnormal) Pericardia I friction rub (abnormal) at apex Best appreciated at apex Over respective valves TIlird or fourth inrercostal space, anrerior axillary line Description
First heart sound, signifies closure of atrioventricular valves and corre sponds to onset of ventricular systole. Second heart sound, signifies closure of
semilunar valves and corresponds with onset of ventricular diastole. Immediately following S2, occurs early
in diastole and represents filling of the ventricle. In young healthy indi viduals, it is considered normal and called a physiologic third sound. In the presence of heart disease, it results from decreased ventricular compliance (a classic sign of conges tive heart failure).
Immediately preceding S l , occurs late in ventricular diastole, associated with increased resistance to ventricu lar filling; common in patients with hypertensive heart disease, coronary heart disease, pulmonary disease, or myocardial infarction, or following coronary artery bypass grafts. Indicates regurgitation of blood
through valves; can also be classified as sysrolic or diastolic ll1llfmurs. Common pathologies resulting in murmurs include mitral regurgita tion and aortic stenosis.
Sign of pericardial innammation (peri carditis), associated with each beat of the hearr, sounds like a creak or leather being rubbed together.
Source: Data from LS Bickley. Bate's Guide to Physical Examination and Hisfory
24 AClITE CARE HAND nOOK FOR I)I·IYSICAL THERAPISTS
Aortic Area
Pulmonic Area
Figure 1-8. Areas for heart sound auscultation. (Drawn by Barbara Cocanour.
Ph.D., University of Massac/msetts, Loweff. Departmel1l of Physical Therapy.)
Figure 1-8. Abnormal sounds should be noted with a description of the conditions in which they were heard (e.g., after exercise or dur ing exercise).
Clinical Tip
• Always ensure proper function of stethoscope by tapping the diaphragm before applying the stethoscope to the patient. • Rubbing the stethoscope on extraneous objects can add noise and detract from true examination.
• Auscultation of heart sounds over clothing should be avoided, because it muffles the intensity of both normal and abnormal sounds.
• If the patient has an irregular cardiac rhythm, HR should be determined through auscultation (apical HR). To save time, this can be done during a routine ausculta tOry examination with the stethoscope's bell or diaphragm in any location.
Diagnostic and Laboratory Measures
The diagnostic and laboratory measures discussed in this section pro vide information that is used to determine medical diagnosis, guide interventions, and assist with determining prognosis. The clinical rele vance of each test in serving this purpose varies according to the pathology. This section is organized across a spectrum of least inva sive to most invasive measures. When appropriate, the test results mOst pertinent to the physical therapist are highlighted. Information that bears a direct impact on physical therapy clinical decision mak ing usually includes that which helps the therapist identify indications for intervention, relative or absolute contraindications for interven tion, possible complications during activity progression, and indica tors of performance.
Oximetry
Oximetry (Sa02) is used to indirectly evaluate the oxygenation of a patient and can be used to titrate supplemental oxygen. Refer to Chapter 2 for a further description of oximetry.
Electrocardiogram
ECC provides a graphic analysis of the heart's electrical activity. The ECC is commonly used to detect arrhythmias, heart blocks, and myocardial perfusion. It can also detect atrial or ventricular enlargement. ECC used for continuous monitoring of patients in the hospital typically involves a two- or three-lead system. A lead represents a particular portion or "view" of the heart. The patient'S rhythm is usually displayed in his or her room, in the hall, and at the nurses' station. Diagnostic ECC involves a 1 2-lead anal ysis, the description of which is beyond the scope of this book. For a review of basic ECC rate and rhythm analysis, refer to Table 1-10 and Figure 1-3.
Holter Monitoring
Holter monitoring is 24- or 48-hour ECC analysis. This is per formed to detect cardiac arrhythmias and corresponding symp toms during a patient'S daily activity.12 Holter monitoring is different than telemetric monitoring because the ECC signal is recorded on a tape, and the subsequent analysis follows from this recording.
Indications for Holter monitoring include the evaluation of syn cope, dizziness, shortness of breath with no other obvious cause,
pal-26 AClffE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 1 -10. Electrocardiograph Interpretation
Wave/Segment P wave PR interval QRS complex ST segment QT interval (QTc) T wave Duration (sees) Amplitude (mm) <0. 10 1-3 0.12-1).20 Isoelectric line 0.06-1).10 25-30 (maximum) 0.12 -1/2 co +1 0.42-1).47 Varies 0.16 5-10 mm Indicates Atrial depolarization Elapsed time between atrial
depolarization and ven· tricular depolarization Ventricular depolarization
and atrial repoiariz3tion
Elapsed time between the end of ventricular depo· larization and the begin ning of repolarization Elapsed time between the
beginning of ventricular repoiarization and the end of repolarization
(QT c is corrected for heart rate)
Ventricular repolariz3rion
Sources: Data from RS Meyers (ed). Saunders Manual of Physical Therapy Practice. Philadelphia: Saunders, 1 995; B Aehlen (ed). ACLS Quick Review Study Guide. St. Louis: Mosby, 1 994; and D Davis (ed). How to Quickly and Accurately Mast'er ECG Interpretation (2nd ed). Philadelphia: Lippincott, 1992.
pitations, antiarrhythmia therapy, pacemaker functioning, actlvlty induced silent ischemia, and risk of cardiac complications with the use of heart rate variability (HRV).
Heart Rate Variability
The most common measure of HRV is the standard deviation of all HR intervals during a 24-hour period (SONN).8 HRV has been used in clinical studies to test a variety of health outcomes.8•14-16 In healthy populations, low HRV has been shown to be a risk factor for all causes of cardiac mortality,'7-19 as well as new onset of hypertension.2o Low HRV is also a risk for mortality in patients who have had an MI,21-23 have coronary artery disease,24 or have CHF.25 A classic study performed by Kleiger et al.26 demonstrated a fivefold risk of re-infarction in post-MI patients with an SON (in
milliseconds) of less than 50, when compared to patients with an SDNN of greater than 100.
Telemetric Electrocardiogram Monitoring
Telemetric ECG moniroring provides real time ECG visualization via radiofrequency transmission of the ECG signal ro a moniror. Teleme try has the benefit of Holter monitoring (because there is no hard wire connection of the patient to the visual display unit) as well as the ben efit of the standard ECG monitor attachment, because there is a real time graphic display of the ECG signal.
Clinical Tip
• Some hospitals use an activity log with Holter monitor ing. If 0, be sure to document physical therapy interven
tion on the log. If there is no log, be sure to document time of day and intervention during physical therapy in the medical record.
• The use of cellular phones, although usually prohibited in any hospital, is especially prohibired on a telemetry unit. The cellular phone may interfere with the radio fre quency transmission of the signal.
Complete Blood Cell Count
Relevant values from the complete blood cell count are hematocrit, hemoglobin, and white blood cell counts. Hematocrit refers to the number of red blood cells per 1 00 ml of blood and therefore Auc tuates with changes not only in the total red blood cell count (hemoglobin) but also with blood volume. Elevated levels of hema tocrit (which may be related to dehydration) indicate increased vis cosity of blood that can potentially impede blood Aow to tissues. 12 Hemoglobin is essential for the adequate oxygen-carrying capacity of the blood. A decrease in hemoglobin and hematocrit levels ( 1 0% below normal is called anemia) may decrease activity toler ance or make patients more susceptible to ischemia secondary to decreased oxygen-carrying capacity. "·27 Slight decreases in hema tocrit due to adaptations to exercise (with no change in hemoglo bin) are related to increases in blood volume. The concomitant exercise-related decreases in blood viscosity may be beneficial to post-MI patients.28
28 AClJrE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Elevated white blood cell Counts can indicate that the body is fight ing infection, or they can occur with inflammation caused by cell death, such as in MI. Erythocyte sedimentation rate (ESR), another hematologic test, is a nonspecific index of inflammation and is com monly elevated for 2-3 weeks after MIP Refer to Chapter 6 for more information about these values.
Coagulation Profiles
Coagulation profiles provide information about the c10rting time of blood. Patients who undergo treatment with thrombolytic therapy after the initial stages of MI or who are receiving anticoagulant ther apy owing to various cardiac arrhythmias require coagulation profiles
ro moniror anticoagulation in an attempt to prevent complications,
such as bleeding. The physician determines the patient's therapeutic range of anticoagulation by using the prothrombin time (PT), partial thromboplastin time, and international normalized ratio.17 Refer ro Chapter 6 for details regarding these values and their significance to treatment.
Patients with low PT and partial thromboplastin time are at higher risk of thrombosis, especially if they have arrhythmias (e.g., atrial fibrillation) or valvular conditions (mitral regurgitation) that produce stasis of the blood. Patients with a PT greater than 2.5 times the refer ence range should not undergo physical therapy because of the poten tial for spontaneous bleeding. Likewise, an international normalized ratio of more than 3 warrants asking the physician if treatment should be withheldP
Blood Lipids
Elevated total cholesterol levels in the blood are a significant risk factor for atherosclerosis and therefore ischemic heart disease.29 Measuring blood cholesterol level is necessary ro determine the risk for development of atherosclerosis and to assist in patient educa tion, dietary modification, and medical management. Normal values can be adjusted for age; however, levels of more than 240 mg/dl are generally considered high, and levels of less than 200 mg/dl are con sidered normal.
A blood lipid analysis categorizes cholesterol into high-density lipoprotiens ( HDLs) and low-density lipoproteins (LDLs) and pro vides an analysis of triglycerides.
HDLs are formed by the liver and are considered beneficial because they are readily transportable and do nOt adhere to the intimal walls
of the vascular system. People with higher amounts of HDLs are at lower risk for coronary artery disease.27,29 HDL levels of less than 33 mg/dl carry an elevated risk of heart disease, and a more important risk for heart disease is an elevated ratio of total cholesterol to HDL Normal toral cholesterol to HDL ratios range from 3 to 5."
LDLs are formed by a diet excessive in fat and are related to a higher incidence of coronary artery disease. Low-densiry lipoproteins are nOt as readily transportable, because they adhere to intimal walls in the vascular system .21 Normal LDLs are below 100 mg/dl,"
Triglycerides are fat cells that are free floating in the blood, When not in use, they are stored in adipose tissue. Their levels increase after eating foods high in fat and decrease with exercise. High levels of tri glycerides are associated with a risk of coronary heart diseaseP
Clinical Tip
Cholesterol levels may be falsely elevated after an acute MI; therefore, pre-infarction levels (if known) are used to guide risk factor modification. Values will not return to normal until at least 6 weeks post-M!.
Biochemical Markers
After an initial myocardial insult, the presence of tissue necrosis can be determined by increased levels of biochemical markers. Levels of biochemical markers, such as serum enzymes (creatine kinase [CK), lactate dehydrogenase [LDHJ) and proteins (myoglobin, troponin I and T), can also be used to determine the extent of myocardial death and the effectiveness of reperfusion therapy, In patients presenting with specific anginal symptoms and diagnostic ECG, these biochemi cal markers assist with confirmation of the diagnosis of an M I (Table
1-1 1). Enzymes play a more essential role in medical assessment of the many patients with nonspecific or vague symptoms and inconclu sive ECG changes,30 Such analysis also includes evaluation of isoen zyme levels as wel1,31 Isoenzymes are different chemical forms of the same enzyme that are tissue specific and allow differentiation of dam aged tissue (e,g" skeletal muscle vs, cardiac muscle),
CK (formally called creatille phosphokinase) is released after cell injury or cell death. CK has three isoenzymes. The CK-MB isoenzyme is related to cardiac muscle cell injury or death, The most widely used
30 AClITE CARE HANDBOOK FOR PHYSICAL THERAPISTS
Table 1 - 1 1 . Biochemical Markers
Onset
Enzyme or Normal of Rise
Marker Isoenzyme Value (hrs)
Creatine kinase 55-7 1 3-6 (CK) IU CK-MB 0-3% 4-8 Lactate 1 27 1U 1 2-24 dehydrogenase LDH-I 14-26% 24-72 Troponin T <0.2 �g/ 2-4 (cTnT) liter Troponin I d . 1 pg/ 2-4 (cTnl) liter Myoglobin 3 1-80 1-2 ng/ml Time of Peak Rise 1 2-24 hrs 1 8-24 hrs 72 hrs 3-4 days 24-36 hrs 24-36 hrs 6-9 hrs Return to Normal 24-48 hrs 72 hrs 5- 1 4 days 1 0- 1 4 days 10-14 days 10- 1 4 days 24-36 hrs
Sources: Data from RH Christenson, HME Azzazy. Biochemical markers oC Ihe acute coronary syndromes. Clin Chern 1 998;44: 1855-1 864; and AK Kratz, KB Leq:md Rawski. Normal reference laboratory values. N Engl ] Med 1 998;339: 1 063-1072.
value is the relative ;"dex ( 100%[CK-MBrrotal CKj).30 Temporal measurements of the CK-MB relative index help physicians diagnose MI, estimate the size of infarction, evaluate the occurrence of reperfu sion as well as possible infarct extension. An early CK-MB peak with rapid clearance is a good indication of reperfusion.'2 Values may increase from skeletal muscle trauma, cardiopulmonary resuscitation, defibrillation, and open-heart surgery. Postoperative coronary artery bypass surgery tends to elevate CK-MB levels secondary to cross clamp time. Early postoperative peaks and rapid clearance seem to indicate reversible damage, whereas la[er peaks and longer clearance times with peak values exceeding 50 Ulliter may indicate an ML 12 Treatment with thrombolytic therapy, such as streptokinase or a tis sue plasminogen activaror (tPa), has been shown to falsely elevate the values and may create a second peak of CK-MB, which strongly sug gests successful reperfusion.'2•30
Troponins are essential contractile proteins found in both skeletal and cardiac muscle. Trapollill I is an isorype found exclusively in the myocardium and is therefore 1 00% cardiac specific. Trapollill T is anorher isorype, and alrhough ir is sensirive to cardiac damage, ir also
rises with muscle and renal failure.JO These newer markers are emerg ing as sensitive and cardiac specific clinical indicators for diagnosis of MI and for risk stratification.
Myoglobil1 is an O,-binding heme protein in both cardiac and skele tal muscle. Although myoglobin is good for identifying acute MI in the early stages, skeletal muscle origin needs to be ruled out. One mecha nism of ruling out skeletal muscle damage is a rise in carbonic anhy drase. Carbonic anhydrase only rises with skeletal muscle damage, and irs rise is early, very similar ro myoglobin. Some have advocared a rario of myoglobin and carbonic anhydrase to diagnose acute MI.I2
LDH is also released after cell injury or death. LOH has five isoen
zymes. LOH-I is specific for cardiac muscle injury. Testing for LOH-l is valuable for determining myocardial injury in patients admitted a few days after the initial onset of chest pain, because it takes approxi mately 3 days to peak and may stay elevated for 5-1 4 days .'7
Clinical Tip
• Physical therapy geared toward testing functional
capacity or increasing rhe patient's activity should be with held until CK-M B levels have peaked and begun to fall.
• It is best to await the final diagnosis of location, size,
and rype of MI before active physical therapy treatment. This allows for rest and time for the control of possible post-MI complications.
Arterial Blood Gas Measurements
Arterial blood gas measurement may be used to evaluate the oxygen ation (Pao,), ventilation (Paco,), and pH in patients during acute MI and exacerbations of congestive heart failure (CHF) in certain situa tions (i.e., obvious tachypnea, low Sao,). These evaluations can help determine the need for supplemental oxygen therapy and mechanical ventilatory support in these patients. Oxygen is the first drug pro vided during a suspected MI. Refer to Chapter 2 and Appendix Ill-A for further description of arterial blood gas interpretation and supple mental oxygen, respectively.
Chest Radiography
Chest x-ray can be ordered for patients to assist in the diagnosis of CHF or cardiomegaly (enlarged heart). Patients in CHF have an
