nursing diagnosis of left ventricular failure in acute

NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE

IN ACUTE MYOCARDIAL INFARCTION

by

Alfred Bobby Miller

A thesis submitted to the faculty of The University of Utah in partial fulfillment of the requirements

for the degree of

Master of Science

College of Nursing

The University of Utah

December 1979

THE UNIVERSITY OF UTAH GRADUATE SCHOOL

SUPERVISORY COMMITTEE APPROVAL

of a thesis submitted by

Alfred Bobby Miller

I have read this thesis and have found it to be of satisfactory quality for a master's degree.

f1ut ell 1f11 i

! ) i /�/C' (;�

, Dale Maeona K. Jacobs Chairman. Supervisory Commillcc

I have read this thesis and have found it to be of �atisfactory quality for.

a master's degree.

d ' A:' FM.7 /1 77 . / / v. . . P / ,.. " '\ .. / ' I ' , ' 4,'

Dale

Member, Supen isory Commillcc

THE UNIVERSITY OF UTAH GRADUATE SCHOOL

FINAL READING APPROVAL

To the Graduate Council of The University of Utah:

I have read the thesis of Alfred Bobby Miller in its

final form and have found that (I) its format, citations, and bibliographic style are

consistent and acceptable; (2) its illustrative materials including figures, tables, and

charts are in place; and (3) the final manuscript is satisfactory to the Supervisory

Committee and is ready for submission to the Graduate School.

Dale

Member. Supervisory Commiltee

Approved for the Major Department .""

)

Approved for the Gradu3te Council

ABSTRACT

A new mode of therapy has recently been advocated for the treatment

of left ventricular failure (L VF) due to acute myocardial infarction (AMI).

This therapy involves the use of vasodilator drugs., Current literature

places little emphasis on the clinical findings of the effects of vasodilators.,

This is especially true of nursing literatureo

Registered nurses (RN) i.n coronary care units (CCU) throughout the

country are responsible for the monitoring and administration of vaso

dilator therapy., The majority of RNs use hemodynamic measurements as

their only data to administer vasodilators. It is a well-known fact that

electronic equipment utilized to obtain hemodynamic measurements can

produce inaccurate data., Several medical studies exist which document

the relationships between clinical findings and hemodynamic measurements

during L VF due to AML

Providing adequate care requires the RN to acquire appropriate

skills and be capable of correlating these skills with all available data"

The investigator theorized that a properly prepared RN could assess,

diagnose and place patients, with LVF due to AMI, into clinical and

hemodynamic subsets for purposes of management.,

A continuous measurement experimental design as described by

Drew (1976) was utilized., The subject population consisted of 30 patients

with AMI. The investigator utilized multiple assessments on each subject

while providing a continuous measurement of the subjects' clinical progress

throughout medical therapy 0

The majority of subjects (23) did not require hemodynamic

monitoring. Correlation of clinical and hemodynamic subsets for those

subjects who were monitored is not consistenL A significant percentage

(26.6%) of the subject population were less than 50 years of age 0 Therapeutic

regimes could not be compared because of the physicians' reluctance to

record appropriate data.

Appropriately prepared RNs are capable of performing cardio

vascular assessments while obtaining a sound clinical data base upon which

to arrive at a nursing diagnosis. Utilizing the subset classification system,

the RN could begin management of patients with LVF due to AMI on a regular

basis. This may reduce the number of fatalities due to L VF c

v

TABLE OF CONTENTS

Page

ABSTRACT 0 ••• ix

LIST OF TABLES .. viii

ACKNOWLEDGMENTS. • ix

NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE IN ACUTE MYCARDIAL INFAR CfION . .,. ,. ,. 1

Current Nur sing Practice,. .. • • ,. . .. 2

LITERATURE REVIEW. .. . .. . • .. .. 0 ,. ,. ,. ,. ,. ,. ,. ,. 5

Pathophysiological Considerations in Left Ventricular Thera PY 0 • 0 • 0 0 • • .. • • • 0 0 " • 0 0 • 5

Clinical Assessment of Cardiopulmonary Function.. 0 ,. ,. 0 ,. 11 Hemodynamic Monitoring of Cardiopulmonary Function,. ,. 12 Subset Classification and Hemodynamic. ,. • .. .. • ,. ,. ,. ,. 13 Sodium Nitroprusside Therapy.. • . .. • • .. • .. ,. .. • . 0 16 Conceptual Framework 0 0 • 0 ,.,. ,. ,. • ,. 18 Statement of the Problem . . ,. • . ,. ,. ,. ,. 24 Overall Purpose. ,. ,. ,.

METHOD 0 0 0 • • 0 0 0 0 0 • "" 0 Q 0 0 0 0 0 0 ., 0 0 0' Q 0

Setting ,. Subject,. . ,. ,. • Design,. • Procedure. ,. . . ,. ,. • ,. ,. ,. . ,. • • . . • ,. ,. ,. 0 • • •

RESULTS AND DISCUSSION c ,. ,. ,. ,. ,. ,. ,. ,. ... 0 ,. • 0 ,.

Results 0 0 0 0 0 0 0 '" 0 • 0 0 0 0 0 0 0 0 0 0 0 0 0

Discussion.. ,. .. . . ,. 0 ,. ,. • • ,. ,. ,. ,. 0 0 ,. ,. 0 •

26

27

27 27 27 28

30

30 38

Appendices Page

A. PHYSICIAN NOTIFICATION. • 43

B. PATIENT INFORMATION" " 44

C. CLINICAL ASSESSMENT. 0 0 • • • • 0 " " 45

D. HEMODYNAMIC MEASUREMENTS .• o Q 46

E 0 SUMMA R Y. • • " 0 • • • " • • • . . 47

F. OPERATIONAL DEFINITIONS. 77

BIBLIOGRAPHY. . • " " . . " " . " . 78

VITA . . • • . • . . " . " . " " . " . . . " . • • . 82

vii

Table

1.

20

LIST OF TABLES

Characterization of Patients with Acute Myocardial Infarction Clinical Subset. . . . . " 0 0 • 0 • 0

Characterization of Patients with Acute Myocardial Infarction Hemodynamic Subset 0 0 0 0 0 0 0 0 0

30 Clinical Subjects with Number of Clinical Assess-

40

50

6.

m. en ts 0 It 0 0 0 0 0 0 0 0 0 0 !OJ 0 0 0 0 0 0 0 It

Hemodynamic Subsets with Number of Hemodynamic Measurements . 0 0 0 0 • 0 0 0 0 • 0 0 .. 0 0 0 •

Comparison Matrix of Clinical and Hemodynamic Subset Classification 0 0 0 0 0 • 0 0 0 0 0 0 0

Classification of Hemodynamic Measurement by Range and Average. • 0 0 0 0 0 0 • • 0 0 0

Page

31

32

34

37

37

39

ACKNOWLEDGMENTS

The investigator wishes to thank the supervisory committee mem

bers for their cooperation and patience during the development of this

study 0 Particular appreciation of Ms 0 Liz Close, RN, MSN, and Dr.

Steven Klausner, M .. D", for their efforts in the initial preparation and

continuing development of the study is warranted.

I also wish to thank my wife Margaret for her eternal patience,

understanding and support during this study.

NURSING DIAGNOSIS OF LEFT VENTRICULAR FAILURE

IN ACUTE MYOCARDIAL INFARCTION

A new mode of therapy has recently been advocated for the treatment

of left ventricular failure (L VF) due to acute myocardial infarction (AMI).

The new therapy involves after load reduction with the use of vasodilator

drugs; the major drug utilized is sodium nitroprusside (SNP). Afterload is

clinically defined as the resistance, or impedence, to ejection of the blood

from the heart during systole 0 Current literature emphasizes the use of

vasodilators, especially SNP(Awan, Vera, Demaria, Amsterdam & Mason,

1976; Chatterjee, Parmley, Ganz, Forrester, Walinsky, Crexells & Swan,

1973; Chiariello, Gold, Leinbach, Davis & Maroko, 1976; Cohn, 1973;

Franciosa, Guiha, Limas, Rodriguera & Cohn, 1972; Guiha, Cohn, Miku

lic, Franciosa & Limas, 1974; Moskowitz, 1975; Parmley, Chatterjee,

Charuzi & Swan, 1974; Rowe & Henderson, 1974; Ziesche & FranciO,sa,

1977). Authors generally report hemodynamic effects of an increase in

stroke volume. A decrease in pulmonary wedge pressure (PWP) contributes

to increased cardiac output (CO), which together with an increase in stroke

volume indicates improved left ventricular function.

Sodium nitroprusside (SNP) has been in existence for many years

and its hemodynamic effects were first reported by Johnson in 1929. Page~

Corcoran and Koppany began more intense research with SNP in 1955. As

modern technology progressed and more advanced pressure monitoring

equipment became available, interest in SNP became increasingly intense,

with a considerable number of studies being reported in the 1970' s . SNP

therapy is now routinely prescribed by the physician with dosage depen

dent upon the desired hemodynamic responses 0 Little or no emphasis, to

augment hemodynamic measurements, is placed on the physical assess ~

ment of the patient (Awan et a1o, 1976; Chatterjee et a1. ~ 1973; Chiariello

et a1., 1976; Franciosa et a1., 1972; Guiha et a1o, 1974; Moskowitz, 1975;

Parmley et a1., 1974; Rowe & Henderson, 1974; Ziesche & Franciosa,

1977). It has been the experience of this investigator that the registered

nurse (RN) assigned to the coronary care unit is responsible for titrating

SNP dosages to achieve the desired hemodynamic effects .. Moskowitz

(1975) also reports titration of SNP to be a regularly performed RN duty 0

Current Nursing Practice

Throughout the country nursing is becoming increasingly involved

in various treatment modalities.. In small community hospitals RNs do

not have the benefit of full time physician coverage when monitoring

patients with L VF due to AMI. The RNs generally responsible for SNP

and other therapies have access to physicians on a limited basis. The

RN therefore must correlate the hemodynamic measurements with the

cardiovascular assessment to validate treatment effectiveness and

achieve favorable therapeutic results.

2

In large medical centers where the RN may rely on house physi

cians to determine the course of therapy, the RN must still be capable of

obtaining a clinical data base 0 Utilizing such data may alert the R N

to a deterioration of the patient and provide a check on invasive moni ~

toring devices. This investigator has noted that often the RN uses only

the hemodynamic measurements derived from arterial and balloon -tipped

·flotation catheters (Swan -Ganz) to evaluate the patiene s physiological

response to ordered therapeutic modalities 0 It is unusual to observe an

RN perform a cardiovascular assessment consisting of inspection, per

cussion' palpation and auscultation of the heart and lungs to determine if

the clinical findings correlate with the findings of hemodynamic measure~

menta

Current nursing education and literature provide the technique and

methodology for performing cardiovascular assessment 0 This places

the responsibility to perform assessments, on which therapeutic deci

sions are based, within the domain of nursing practice (Adler, 1977;

Delaney, 1975; Gordon, 1976; Mechner, 1976; Mechner, 1977; Silver

man, 1971; Tanner, 1977). Current nursing literature does not, how

3

ever, document the relationships between clinical findings and hemodynalnic

measurements as do certain medical studies (Chatterjee & Parmley, 1977;

Forrester, Diamond, Chatterjee & Swan, 1976; Forrester ~ Diamond &

Swan, 1977).

If the RN is to continue to accept responsibility for management

of complex therapy in patients with LVF due to AMI, then she must be

capable of providing adequate care to the patient. This responsibility

requires that the RN is able to: 1) perform a cardiovascular assessment,

2) utilize the assessment data and hemodynamic measurements to form a

clinical data base, and 3) arrive at a therapeutic decision which is con

sistent with that of the physiciano

4

LITERATURE REVIEW

Pathophysiological Considerations in Left Ventricular Therapy

Recent nursing literature discusses left ventricular failure (LVF),

its pathophysiology and symptomology in a clear, concise manner (Foster,

1974; Tanner, 1977). Foster (1974) reports the effects of medications,

electrolytes, endocrine disor.ders and autonomic nervous system dis-

turbances on the failing heart.

The major effects of medications on the heart are described as:

1) inotropic, 2) chronotropic, and 3) dromotropic; also, the author briefly

discusses the cardiac effects of potentiation of one medication by another 0

Electrolyte imbalances may be caused by hypoxemia, acidosis, decreased

serum calcium and decreased magnesium levels 0 These alterations give

rise to arrhythmias and directly affect myocardial contractility 0 A notable

omission from Foster's discussion of electrolyte imbalance is that of hypo-

kalemia. This is a common electrolyte imbalance seen in patients treated

with diuretics. This omission is readily corrected by the works of several

other authors who fully discuss the difficulty (del Bueno, 1975; Haughey &

Sica, 1977; Reed, 1978, pp. 84-85 and 87)0 Foster (1974) briefly discusses

endocrine disorders such as: 1) hypothyroidism, 2) pheochromacytomas,

and 3) adrenal crisis G Though the listed disorders are not discussed in

6

detail, they do provide incentive for a further review of literature.

Foster (1974) discusses the role of the autonomic nervous system

in detaiL Patients with severe pain as often experienced during AMI

demonstrate evidence of vagal stimulation causing brachycardia and hypo

tension. Emotional responses such as anxiety produce enhanced sympathetic

stimulation manifested by sinus tachycardia and a rise in blood pressure

(BP) •

The diagnostic methodology reported by Foster (1974) is applicable

to this study and for usage by the nurse in the coronary care unit. Guidelines

are provided for the purpose of performing a cardiovascular assessment

allowing the RN to arrive at a reliable assessment of left ventricular

function.. Emphasis for a nursing diagnosis is placed on: 1) history, 2)

a physical assessment consisting of observable patient data, clinical

examinations, laboratory findings, and 3) data from the physician's assess=

ment.. The clinical evaluation is regarded as a continual and essential pro~"

cess that is necessary to determine the patient's response to therapy"

Tanner (1977) provides diagnostically useful information that is

based on the symptomology observed in patients developing heart failure ..

Meltzer and Dunning (1972) report that heart failure is the major cause of

death in patients admitted to coronary care units with AML The improve

ment in the nurse's ability to diagnose and treat death =producing arrhythmias

is reported by Tanner (1977) to have eliminated arrhythmias as the major

cause of death for patients with AMI who are hospitalized in ceus. The

7

author supports the concept that R Ns can also fulfill a similar role in

reducing the number of deaths from heart failure. The RN, knowing that

certain compensatory mechanisms occur following AMI, can assess and

evaluate symptoms which are related to the compensatory mechanisms and the

associated changes in cardiovascular hemodynamics 0

Tanner (1977) attributes the symptoms of heart failure to its effect

on: 1) the heart itself, 2) the lungs, and 3) the degree of peripheral per

fusion. For purposes of this discus sion, only the symptoms attributed to

acute left ventricular failure will be considered"

In discussing symptomology related to heart and blood vessel function

Tanner (1977) begins with pathophysiological changes that occur within a

short period of time following a decrease in cardiac output (CO). Stimula

tion of the sympathetic nervous system produces an increase in heart rate

concurrent with inhibition of the parasympathetic nervous system"

Initial autonomic activation results in an increase in CO 0 Tachy

cardia, defined as a persistent heart rate of greater than 100 beats per

minute, as a symptom by itself is not evidence of L VF but may be due to

increased sympathetic tone from other disease processes ..

Pulsus alternans, one regular beat followed by a weaker beat during

normal sinus rhythm, may occur in LVF and is due to variations in the

strength of myocardial contraction with a decreased amount of blood being

ejected during the weaker beat. Winthrobe (1974) reports that the weaker

beat is probably the result of shorter myocardial fibers at the end of

diastole, therefore causing les s blood to be ejected during systole.,

Auscultation of the failing heart may reveal abnormal sounds,

termed gallop sounds, which occur after the second normal heart sound

(S2). The first gallop, S3' best heard over the apex of the heart, occurs

early in diastole and is associated with the period of rapid ventricular

filling. Its presence indicates a relative increase in the volume of blood

that is being injected into the left ventricle (volume overload). Another

gallop sound, S4' is heard during ventricular filling toward the end of

diastole. This sound is believed to be caused by decreased compliance of

the left ventricular wall due to ischemia. A combination of both S3 and S4

sounds is termed a summation gallop and may occur during tachycardia

when diastole is shortened and the two sounds merge.,

8

Dilation and hypertrophy of the heart may result if the myocardium

cannot eject the entire volume of blood from the left ventricle during systole 0

According to the Frank-Starling Law, the greater the end diastolic volume~

the stronger the contraction of the myocardial fiber within limits <> The fail =

ing heart will compensate by this method to a maximum sacromere length

of 2.2 microns. Once this point is reached, the heart cannot distend further

to increase its stroke volume. Prolongation of this compensatory mechanism

results in irreversible cardiac dilatation" The heart can also increase its

muscle mass and hyperthrophy to compensate for a decreased stroke volume Q

Clinical assessments to determine hypertrophy and dilatation are the point of

maximum impulse (PMI), the chest X -ray and the electrocardiogram"

9

Although Tanner (1977) discusses clinical findings common to the

respiratory system that occur with LVF, West (1974) gives a more con

cise report.. West (1974) states that an increase in end diastolic volume

causes an increase in left ventricular pressures which in turn causes the

pressure in the left atrium and pulmonary veins to elevate" As a result,

pressures in the pulmonary capillaries exceed critical levels and fluid

croses the alveolar epithelium into the alveolar spaces, causing pulmonary

edema" This may occur when the pressure in the pulmonary capillaries

exceeds 25 mm Hg" Pulmonary edema may be seen on chest X -ray with

rales heard as a late sign" Depending upon the amount of fluid involved,

increasing dullness to percussion can be utilized to outline areas of fluid

in the lungs or periphery. If an individual has been bedridden for several

days, rales may be due to the pooling of fluids at the bases of the lungs

because of inactivity. Rales due to pulmonary congestion of a cardiac origin

are usually heard in the lung bases initially and are defined as fine and

crepitant. The auscultated height of the rales in the lungs may correlate

with the severity of the congestion"

Another early symptom related to pulmonary venous congestion

and elevated left ventricular filling pressure is difficult or labored breath =

ing" This usually manifests initially only upon exertion and eventually as

the pulmonary congestion increases, it is present even at rest.. Orthopnea

also occurs during acute, LVF and it is thought to be caused by the follow~

ing mechanism.. While a person is upright, blood is pooled in the lower

10

extremities because of gravitational forces and upon reclining, pooled blood

returns to the right heart, effectively increasing the circulating blood

volume. With increased blood volume» intravascular pressure rises

which can subsequently lead to more fluid being forced into the interstitial

spaces of the lung, causing decreased distensibility of the lung with

increased difficulty in breathing 0 Coughing» another diagnostic clue

reported by West (1974) usually starts as dry and nonproductive and pro

gresses to productive hemoptysis as hydrostatic pressures in the pulmonary

capillaries become great enough to rupture blood vessels 0 Depending upon

the fragility of the blood vessels hemoptysis may occur with hydrostatic

pressures in excess of 28 mm Hg (West, 1974).

Various other symptoms are associated with LVF 0 Many commonly

seen symptoms are due to a decreased CD and blood flow to vital organs.

Tanner (1977) reports cheyne-stokes respirations, manifest by alternating

periods of hypo and hyper ventilation, may occur as a late symptom of LVF ~

Guyton (1976) states that the mechanism of causation is disordered cyclic

changes in the oxygen (02) and carbon dioxide (C02) tensions in arterial

blood initiated by a low CO2 , Such variable 02 and CO2 levels may be due

to decreased circulation times Q Clinical signs and symptoms such as

decreased blood pressure, fatigue~ weakness, restlessness and oliguria

are also evidenced in acute phases of L VF 0

As stated earlier, a fall in CO stimulates the sympathetic nervous

system 0 Tanner (1977) reports that in the kidney this results in

11

constriction of afferent arterioles.. A decrease in the glomerular filtration

rate results in diminished urine output 0 The decreased blood flow to the

kidney activates the renin-angiotensin cycle. Angiotensin, a potent vaso

constrictor, causes further reduction in renal blood flow 0 The author

states that the signs of fatigue, weakness and restlessness are probably

due to the decreased blood flow to the skeletal muscles e

Tanner (1977) addressed the most common symptoms seen with

LVF. The presentation is logical, easily understood, and includes some

pathophys iology as sociated with L VF. The di scussion provides incentive

for further study of advanced literature so that LVF may be thoroughly

understood and appropriately managed ..

Clinical Assessment of Cardiopulmonary Function

Silverman (1971) reported a program directed at increasing the

registered nurse's (R N) ability to obtain a clinical data base consisting of a

detailed history and a cardiovascular examinationo The information obtained

was recorded in the patient's chart, using the problem ~oriented method ..

The purpose of the program reported by Silverman was to provide a broader

data base to enable the physician to follow the patient's progress throughout

each shift. Comparisons could also be made by the nurse to assess the

patient's progress on succeeding shifts .. Silverman (1971) reported that

some physicians initially respond to the project with reluctance because

the clinical findings and charting were done on the Physician's Note section

12

of the patient's chart.

According to Silverman (1971, po 380), an extensive backgroupd in

anatomy , physiology, pathophysiology, electTocardiography, clinical

pharmacology and physical diagnosis enabled the nurse to perform a

complete and accurate cardiopulmonary assessment. Several advantages

to nursing involvement in the constant and. in -depth management of patients

are apparent: 1) a sound basis for evaluation of nursing care is provided

in the charted records, 2) immediate identification of problems in educa-

tional preparation or misinterpretation of data is possible which allows

for corrective feedback, and 3) a source of highly reliable physiological

data is readily available to the physician (Silverman, 1971) 0

A conspicuous omission in the Silverman (1971) report was that the

author did not convey whether nurses were included in the decision making

process of formulating a plan for therapy 0 The RNs were trained and

utilized to gather and report data utilized to gather and report data utilized

by the physician, however? no other involvement of the RN is reportedo

Hemodynamic Monitoring of Cardiopulmonary Function

Hemodynamic monitoring of patients with left ventricular failure

(LVF) associated with AMI became common practice only in the 1970so

Many studies (Awan et ala ~ 1976; Chatterjee et ala? 1972; Chiariello

et aL, 1976; Cohn, 1973; Franciosa et aL, 1972; Parmley et {iI., 1974;

Rowe & Henderson, 1974; Ziesche & Franciosa, 1977) have been conducted

13

utilizing the balloon -tipped flow directed catheter (Swan -Ganz) and record-

ing devices to describe the effects of various medications on the hemo-

dynamics of the cardiopulmonary system. The primary focus of these

studies has been to manipulate the pulmonary artery pressure (PAP),

pulmonary wedge pressure (PWP), cardiac output (CO) and cardiac index

(CI) ~ The authors generally agree that these parameters can be desirably

altered with the use of vasodilator therapy ~ and for patients experiencing

acute LVF associated with AMI, desired values for the PWP are commonly

between 15-18 mm Hg. with the CI greater than 2.2 l/min/m2 (Forrester

et al o , 1976, 1977). The major criticism of these studies is that they are

hemodynamically oriented while providing the reader with little or no

clinical findings which may be useful to assess the hemodynamic response

obtained.

Subset Classification: Clinical and Hemodynamic

As nursing becomes more sophisticated, professional nurses are

seeking greater responsibilities 0 Gordon (1976) describes nursing diagnosis

as:

Description of actual or potential health problems, which nurses, by virtue of their education and experience, are capable and licensed to treaL (po 1299)

The registered nurse who functions in the role of diagnostician must be

knowledgeable of the physiologic reasons for clinical symptoms usually

seen following acute myocardial infarction and must be knowledgeable

14

the hemodynamic response of the cardiovascular system 0

Gordon (1976) states that the end product of nursing diagnosis is

the placement of the patient in one or more diagnostic categories for the

purpose of determining therapy. She did not attempt to broaden this

concept into specific specialty fields of nursing.

Several studies have attempted to classify the degree of loss of

LVF in AMI on the basis of clinical and hemodynamic parameters (Chatter-

jee & Parmley, 1977; Forrester et al.q 1976, 1977) 0 The patients in such

studies were clinically categorized on the basis of physical assessment

and invasive hemodynamic measurements 0 Forrester et al. (1976, 1977)

categortzed the hemodynamic responses and clinical findings commonly

found in patients experiencihg AML In Forrester's et a1.. (1977) scheme,

both hemodynamic and clinical findings are divided into four subsets with

a parallel relationship existing between the corresponding subseL

A sample of the classification system as utilized by Forrester

et a10 (1977, po 139) is as follows~

Subsets

Hem odynam ic

HI) PWP less than 18 mm Hg 0

and CI greater than 2 02 l/min/m2

H2) PWP greater than 18 mm Hg.

H3) CI less than 202 l/min/m2

Cli.nical

Cl) No pulmonary congestion or peripheral hypoperfusion

C2) Pulmonary congestion present

C3) Peripheral hypoperfusion present

H4) PWP greater than 18 mm Hg 0

and CI less than 2.2 1/min/m2

C4) Both pulmonary congestion and peripheral hypoperfusion present

The study by Chatterjee and Parmley (1977) does not include subsets

equivalent to the clinical and hemodynamic classifications of Forrester

et a10 (1977). Forrester et a10 (1977~ p. 137) report that by utilizing

their classification system, patterns may be established which aid in the

prognosis and treatment following AMI. The authors further report that

15

even with accurate equipment nothing can substitute for the bedside cHnical

examination.

Forrester et a1. (1977) with the use of clinical subsets, were able

to predict the hemodynamic subset with approximately 83% accuracy.

This means that 83% of the time the actual hemodynamic measurement

corresponded with that predicted by the clinical finding" Terms for the

study used in the clinical subset classification scheme were carefully

defined" Peripheral hypoperfusion was defined as the presence of:

1) decreased skin temperature, 2) mental confusion, and 3) oliguria in

conjunction with arterial hypoperfusion or sinus tachycardia with the

patient breathing room air before sedation. Mental state p skin tempera-

ture and color were determined subjectively. Oliguria was defined as

urine output of less than 40 cc/hr" Arterial hypoperfusion was indicated

if the systolic blood pressure was less than 100 mm Hg 0 and sinus

tachycardia was defined as a heart rate of more than 125 beats/minute.

Pulmonary congestion was considered present if auscultatory findings

16

revealed rales over the posteriobasal chest and radiographic findings were

positive for pulmonary congestiono

Forrester et aL (1977) also discuss several classes of medica-

tions utilized for therapy in patients and identify their effects on CO

and PWPo The hemodynamic effects of the drug classes are as follows:

Class

Inotropics Diuretics Vasodilators Beta -adrenegic

blockers

CO PWP

Unchanged or Increased Unchanged or Decreased Unchanged Decreased Increased Decreased Decreased Unchanged or Increased

Utilizing the above guidelines, medical therapy was tailored to the patient's

subset classification 0 For example, if a patient is assigned to clinical

subset C4 and hemodynamic subset H4, the patient will have a decreased

CI and an increased PWP Q Vasodilators would be the medication of choice

as these medications increase CD and decrease PWP 0 The author s contend

that in patients with AMI, prime consideration should be given to correcting

the abnormal hemodynamics Q

The studies by Forrester et aL (1976, 1977) are complete when

considering the factors of hypoperfusion and pulmonary congestiono These

studies demonstrate that it is possible to interrelate clinical findings and

hemodynamic responses in patients with L VF due to AML

Sodium Nitropruss ide Therapy

It has been this investigator i s experience that the major vasod)l

currently used in the treatment of LVF associated with AMI is sodium

nitroprusside (SNP). Of the many studies related to the use of vasodi-

1ators two are of prime importance to the nursing management of SNP

therapy 0

Moskowitz (1975) discusses vasodilator therapy in general with a

specific section related to SNP.. The author reports hemodynamic changes

associated with SNP therapy as increased CO and decreased PWP 0 Infor

mation relevant to nursing implications contributed by Moskowitz are:

1) an emphasis for careful history taking, 2) the need for continuous

monitoring of hemodynamics to maintain the PWP between 15 -18 mg Hgo

without inducing hypotension, 3) patient activities that may potentiate the

effects of SNP, and 4) precautions utilized in preparation of SNP for intra

venous infusion. Unfortunately, the report is not primarily concerned

with associated changes in the clinical findings and is therefore narrow

in scope 0

Ziesche and Franciosa (1977) in their article also do not provi.de

the reader with useful clinical data by which to assess SNP therapy.

Their major contribution is concerned with the administration of SNP.

They provide information in a clear concise manner which enables the

reader to understand the administration and evaluation of SNP utilizing

hemodynamic measurements.. Included in their report is a cornplete

reference table for the titration scheduling of SNP dosage (Ziesche &

Franciosa, 1977, p. 101)0

17

The literature on left ventricular failure and SNP therapy reveals

that a core of valuable information is available to the RN involved in the

care and management of the patient with LVF associated with AMI.

Clinical data may be utilized as the RN desires, however ~ it has been

the experience of this investigator that the majority of RNs use only bits

and pieces of clinical informationo An extensive review of literature

revealed no centralized, succinct report on the synthesis of clinical

and hemodynamic data designed for and by RNs. Thus~ it may be diffi

cult to arrive at a nursing diagnosis and determine appropriate therapy

for patients undergoing treatment of LVF due to AMI.

Although most of the available literature on clinical and hemo

dynamic responses to vasodilator therapy is physician oriented, it can be

understood by the professional nurse 0 By synthesiz ing information con ~

cerning the pathophysiology of AMI, clinical signs and symptoms of LVF

and the involved hemodynamics, the professional nurse can arrive at a

nursing diagnosis 0 Utilizing a classification system such as that pre =

pared by Forrester et al. (1977) the RN could manage patients with L VF

associated with AMI within more complete parameters 0

Conceptual Framework

18

The professional registered nurse must possess an adequate under

standing of the relationship between clinical findings and the hemodynamic

function of the myocardium to adequately assess the pathophysiology of

acute myocardial infarction. The RN must also possess understanding of

the physiological effects of vasodilators on this relationship. The follow

ing discussion is based on the model in Figure 1 designed by the investi

gator which depicts a relationship between key factors associated with

vasodilator therapy and management 0 The arrows serve as a guide to

direct the reviewer's attention toward the clinical and hemodynamic

aspects of the pathophysiology that occurs during AMI, L VF and vaso

dilator therapy. The relationships within the model have been explained

in the review of literature. Each of the four parts of Figure 1 relate to

one of the four clinical and hemodynamic subsets suggested by Forrester

et a 1. (1 977) •

19

The clinical findings and hemodynamic alterations associated with

acute myocardial infarction (AMI) are attributed to the extent of myocardial

damage during the infarction process (Netter~ 1974)0 The patient with an

uncomplicated AMI (see Figure I-A) may exhibit few or no abnormal

clinical findings from the infarction process"

SNP reduces the impedence against which the heart must eject blood

during systole.. This results in a larger volume of blood ejected without

an increase in myocardial workload (see Figure 1 =D)~ therefore, myo=

cardial oxygen consumption remains the same or improves due to reduced

workload. This decreases the possibility of injury or necrosis to the myo

cardium adjacent to the infarction site in the ventricle (Armstrong~ Walker,

Burton & Parker, 1975; Chatterjee et aL, 1973; Chiariello et aL, 1976;

Classification:

Assessment:

Therapy:

Legend:

HI) PWP < I8mm Hgo -(; ,... CI) CI > 202 I/min/m2

~ HI) Hemodynamic mea- ~CI)

surements of: 1) PWP < I8mm Hg. 2) CI > 202 I/min/m2

t HI) Monitor for digression+> CI)

to other subsets

PWP - Pulmonary Wedge Pres sure CI - Cardiac Index CXR - Chest X-Ray M - Murmur AMI - Acute Myocardial Infarction

No complications

1 No pulmonar y congestion or peri phera 1 hypo~' perfusion present

l Assess for di= gres sion to other subsets

Figure 1 =A 0 AMIg Hemodynamic Alterations (H) and Clinical Findings (C)

20

21

Classification: H2) PWP > 18mm Hg 0 lIII(;oo(;~-7""> C2) Pulmonary co nge s -

1 tion present

Assessment: H2) PWP > 18mm Hg 0 ,II(; .... C2) 1 0 Rales~ rhonchi or when hemodynamic measurements completed

wheezes present 2" CXR positive for

interstitial or alveoli pulmonary edema

3" S3' S4' and M may be present

40 Respirations may be slow & deep or rapid & shallow

Therapy: H2) Diuretics to in - 011( .. C2) 1 Q Rales, rhonchi or crease or stabilize CO

Legend: PWP - Pulmonary Wedge Pressure CI - Cardiac Index CXR - Chest X -Ray M Murmur AMI - Acute Mycardial Infarction

wheezes may decrease

2" CXR shows decrease in interstitial or alveolar pulmonary edema

30 S3~ S4 and M may decrease until gone

40 Respirations may return toward nor mal rate and depth

Figure I-Bo AMI~ Hemodynamic Alterations (H) and Clinical Findings (C)

22

Classification: H3) CI < 2.2 1/min/m2 ~ C3) Peripheral hypoperfusion present

Assessment:

Therapy:

t H3) CI< 2,,2 1/min/m2 ~ C3) 1" Decrease in urine

when hemodynamic output measurements com ~ 2" Skin: cool, clammy pleted 3" Mental obtundation

1 may be present

4. Hypotension systolic 100mm Hg"

H3) Inotropic Agents to ~ C3) 1.. Skin may be warm/ 1" Increase or dry

stabilize CO 2.. Mental state returns 2. Decrease or

stabilize PWP 3.. Volume replace

ment to possibly increase PWP and CO if PWP is normal or low and CO is decreased

toward normal 3" Urine output exceeds

40 ml/hr. when averaged over 24 hr .. period

4.. Systolic BP increase to greater than 100 mm Hg.

Legend: PWP - Pulmonary Wedge Pressure CI ~ Cardiac Index CXR - Chest X-Ray M - Murmur AMI - Acute Myocardial Infarction

Figure I-C. AMI, Hemodynamic Alterations (H) and Clinical Findings (C)

Classification: H4) PWP > 18mm Hg.. C4) CI < 2.2 1/min/m2 ~

J

Both pulmonary congestion and peripheral hypoperfusion present

23

J H4) PWP > 18mm Hg. ~ C4) 10 Rales, rhonchi,

and CI < 2.2 1/min/m2 wheezes may be Assessment:

when hemodynamic measurements are completed

present 20 CXR positive for

effusions or other signs of pulmonary

3 0 S3' S4 or M may be present

40 Respirations may be slow & deep or rapid & shallow

5" Decrease in urine output

6 0 Skin: cool, clammy 7.. Mental obtundation

ma y be present

Therapy: H4) Vasodilators and diuretics to:

~ ~ C4) 1 .. Rales, rhonci,

10 decrease PWP toward normal

2. Increase CIabove 202 1/min/m2

3.. Inotropic agents may be utilized to increase BP caus ing increased perfusion to vital organs

Legend: PWP ~ Pulmonary Wedge Pressure CI - Cardiac Index CXR - Chest X -Ray M - Murmur AMI - Acute Myocardial Infarction

wheezes begin to appear

2.. CXR shows decrease of effusions/ ederna

3. S3~ S4 and M begin to disappear

4. Respirations return toward normal rate and depth

5.. Urine output in =

creases to 40 ml/hr x 24 hr. period

Figure I-D. AMI, Hemodynamic Alterations (H) and Clinical Findings (C)

Cohn, 1973; DaLuz, Forrester & Wyatt, 1975; Franciosa et aI., 1972;

Guiha et al., 1974; Parmley et aI., 1974; Rowe & Henderson, 1974;

Schlant, Tsagaris & Robertson, 1962; Ziesche & Franciosa, 1977) 0

24

As a result of the increased CO several clinical findings can be

expected to occur (see Figure 1-D)o Depending upon the patient response

to SNP, therapy may be dramatic and occur within minutes 0 The blood

pressure may remain the same, decrease or increase slightly. Heart

sounds such as S3 and S4 may gradually disappear because the ventricle

may become less distended and arterial filling may not be as rapid. There

will be less hydrostatic pressure exerted on the pulmonary circulation

because of increased CD. Rales may begin to disappear and pulmonary

congestion will decrease, allowing respirations to slow and become less

difficult (Forrester et al., 1976, 1977; Foster, 1974; Tanner, 1977)0

The effects of SNP therapy are closely related and dependent upon

the physiological state of the myocardium 0 Titration of SNP to produce

the desired effects and improve the physiological state is variable 0 SNP

therapy is a dynamic treatment mitigated by concomitant clinical findings

and hemodynamic responses 0

Statement of the Problem

The registered nurse (RN) in the coronary care unit (CCU) is

responsible for constant physiological and electrocardiographic monitoring

of the patient who has incurred an acute myocardial infarction (AMI) ~

25

Physiological monitoring includes responses to various therapeutic regimes Q

A survey of 22 medical records of patients with AMI for episodes of hypoper

fusion and pulmonary congestion (as defined by Forrester et alo, 1976,

1977) which involved hundreds of entries on nursing and progress notes,

revealed that the majority of R Ns do not record their clinical findings 0

Of approximately 50 episodes of hypoperfusion and pulmonary con

gestion, verified by recorded hemodynamic measurements, only six

assessments of the cardiopulmonary system were recorded. In general,

it was not unusual to find recorded increases in the pulmonary wedge

pressure (PWP) from 15 mm Hg. to 30 mm Hg. or greater in less than 2 -3

hours. The RN caring for the patient continued to increase the SNP infu

sion rate without reporting the findings of a clinical assessment which

would substantiate the l1emodynamic measurements ..

Fallibility of electronic equipment utilized in hemodynamic moni ~

toring is well acknowledged (Adams, 1976; Forrester et aL, 1977; LalU,

1978; Woods, 1976). This investigator, in agreement with others (Adams 9

1976; Lalli, 1978· Woods, 1976), have found the cause of inaccuracy to

be mainly due to improper calibration of the monitoring equipment ..

Forrester et ala (1977) indicates that although hemodynamic monitoring

may be accurate, nothing substitutes for the bedside clinica1 assessment

and its findings 0 If the RN is to continue to be responsible for immediate

care of the AMI patient and the administration of medical therapeutic

regimes, she must be capable of performing a physical assessment of

the cardiopulmonary system. This is particularly important when SNP

or vasodilators are administered 0 Correlation of clinical findings to

the hemodynamic measurement is essential for safe care 0 Review of

nursing and progress notes by this investigator revealed that the RN is

either: 1) unwilling to obtain or record data of physical findings, or 2)

not able to correlate clinical findings with hemodynamic measurements.

Overall Purpose

The purpose of the study is to determine if the registered profes

sional nurse who has successfully completed an approved course of study

consisting of cardiovascular anatomy, physiology, pathophysiology,

electrocardiography, cardiac pharmacology and physical diagnosis can

in accordance with Forrester's et al. (1977) subset classification para-

meters:

1. Utilize an obtained clinical data base to determine the appro =

priate clinical subset for each subjecL

2. Utilize known hemodynamic measurements to determine the

appropriate hemodynamic subset for each subject.

30 Determine a therapeutic regime which would approximate that

of the physician.

26

METHOD

Setting

This study was conducted in the coronary care unit (CCU) of a 580-

bed hospital in Salt Lake City, Utah 0 The CCU has a total of 12 beds. All

beds can be monitored from the central nursing station for arrhythmias 0

The nursing care for all subjects was provided by the staff of the CCU.

Subjects

The sample of 30 subjects was selected from the population of all

patients admitted to the coronary care unit, arriving in a predetermined

time period, who exhibited electrocardiographic and serum changes con

sis tent with acute myocardial infarction. Exclusions included:

1) Those declining to participate in the study.

2) Those already receiving SNP therapy 0

Design

This study is an exploratory continuous measurement research

design as described by Drew (1976, p. 37) 0 It does not meet the criteria

of baseline or multibaseline designs because treatment is begun immedi c~

ately which precludes the establishment of baseline data.

Procedure

Consent

Within 48 hours following admission the patient was interviewed to

obtain consent. If the patient was not capable of giving an informed con

sent, his/her immediate family was contacted to provide consent for

participation in the study. Attending physicians were contacted regarding

each subject and cooperation obtained (see Appendix A).

Medical History and Assessment

After the consent had been obtained and the physician informed, a

detailed history was obtained by the investigator. Emphasis was placed

on cardiopulmonary factors"

Following the history, the investigator performed a cardiopul

monaryassessment, using the physical examination techniques and pro

cedures advocated by Alder (1977) and other authorities (DeGowin &

DeGowin, 1976; Judge & Zuidema, 1968; Mechner, 1976, 1977; Prior &

Silverstein, 1973) A minimum of three cardiopulmonary assessments,

performed at approximately 24-hour intervals, were completed by the

investigator for each subjecto Two subjects expired before this pro

cedure could be completed 0

Hemodynamic Measurements

Each hemodynamically monitored subject was connected to the

following equipment: a) Bently Manufacturing Company Model 800

28

Transducter, b) Gould Manufacturing Company Brush Recorder Model

2200, c) Hewlett-Packard bedside and central monitoring oscilloscopes,

d) General Data Corporation Model 3300 computer with Hewlett-Packard

terminal oscilloscope.. Hemodynamic measurements were made by the

CCU staff nurses using unit procedures 0 The investigator performed a

cardiopulmonary assessment in immediate conj unction with hemodynamic

measurements recorded during the study.

Data Acquisition

29

All data was recorded on the appropriate collection forms (see

Appendices A, B, C, D, E). The investigator utilizing staff and self

gathered data, assigned the subject to clinical and hemodynamic subsets"

The investigator then developed a therapeutic regime and following each

cardiopulmonary assessment recorded his findings on the Patient Assess

ment Form (see Appendix C). If the physician had completed an assess

ment within three to four hours of the investigator's assessment a

comparison of the investigator's therapeutic regime and the physician's

regime was made by the investigator. This comparison was also recorded

on the appropriate form (see Appendix D). All data was summarized by

the investigator on the Summary Form (see Appendix E) g

RESULTS AND DISCUSSION

Results

Statistics

The descriptive nature of this study necessitated measures of

central tendency, mean and standard deviation be utilized. Raw score

and percentiles were utilized to describe the subject's assignment to subset

cIa s sifica tion.

Findings

Clinical Subsets. Table 1 describes the common characteristics of

all 30 subjects assigned to clinical subsets developed by Forrester et al.

(1976, 1977). Assignment to clinical subsets is as follows: 1) Cl no pul

monary congestion or peripheral hypoperfusion, 2) C2 pulmonary congestion

present, 3) C3 peripheral hypoperfusion present, 4) C4 both pulmonary con

gestion and peripheral hypoperfusion present.

The majority (63%) of the subjects were assigned to Cl. This is

consistent with previous experience of the investigator 0 Forrester et al.

(1977) also report that the majority of subjects fall into this subseL The

authors fail to report, however, if more than one assessment was done on

each subject.

The ages of subjects classified in clinical subsets ranged between

35-81 years, the mean age was 60-62 years. This is consistent with data

Table 1

Characterization of Patients with Acute Myocardial Infarction Clinical Subset

31

I II III IV Total

Patients 19 S 3

Age: Range 35-S1 43~SO 46-74 Mean 60.S9 62.62 60.23 Standard Division 7.S 7.9 7.7

Sex: Female 2 1 1 Male 17 7 2

History: Previous MI 3 2 2 Previous CHF 2 1

CHF - Congestive Heart Failure MI - Myocardial Infarction

reported by Forrester et ale (1977). A clinically significant percentage

30

4 26

7 3

(26.6%,) of the subjects were under 50 years of age. Forrester et al. (1977)

did not report this parameter. The study population included four

subjects (13.3%,). This differs from the percentage of 21.5% as reported

by Forrester et aL (1977, Table I, p. 13S). The larger population or the

time frame of the study reported by Forrester et al. (1977) may account

for this difference. Patient histories reveal only seven subjects (23. 3%,)

with previous infarctions and three subjects (10%,) with a previous history

of congestive heart failure.

32

Hemodynamic Subsets. During the study period only seven subjects

were hemodynamically monitored 0 Table 2 describes the cornmon charac-

teristics of these subjects assigned to hemodynamic subsets 0 The hemo-

dynamic measurements, obtained by staff RNs assigned to the CCU so that

internal bias would not skew findings, were used to assign patients to a

particular subset as outlined in Figure 1. The hemodynamic subsets are

defined as follows: 1) HI normal hemodyanmic measurements, 2) H2 puI=

monary wedge pressure (PWP) greater than 18 mm Hg., 3) H3 a cardiac

index (CI) of less than 2.2 l/min/m2.

The ages of subjects classified in hemodynamic subsets ranged

between 43-76 years, the mean age was 55-61 years .. This is consistent

with Forrester et ala (1977). A clinically significant percentage (42.85%)

Table 2

Characterization of Patients with Acute Mycardial Infarction Hemodynamic Subset

I II III IV Total

Patients 1 2 1 3 7

Age: Range 59 43-76 61 44=75 Mean 59 59.5 61 55 Standard Deviation 5.45 4 .. 28

Sex: Female 1 1 2 Male 1 1 1 2 5

History: Previous MI Previous CHF 1 1

'---CHF - Congestive Heart Failure MI - Mycardial Infarction

33

were under 50 years of age. There were two female subjects (28.5%).

Only one subject (14.2%) reported a previous history of congestive heart

failure and none had a previous history of AMI. This sample is too small

to compare with Forrester et al. (1977).

Clinical Subjects. Table 3 represents the categorized results of

clinical assessments completed by this investigator. Since no study could

be found which reports multiple assessment and placement into clinical sub

sets as defined by Forrester et al. (1977) the percentages reported by the

investigator cannot be compared with other findings at this time. Because

of the large number of clinical assessments accomplished (137) a compari~

son was made with Forrester et ale (1977) data (see Figure 2).

The most striking difference occurs when comparing clinical subset

C4. Approximately 10.2% of the assessments completed by the investigator

placed subjects into category C4. Forres ter et ala (1977) report approxi ~

mately 33.5% in this subseL Clinical subset C3 is another area of striking

difference, with this investigator reporting 2.189% of the assessments in

this category. Forrester et al. (1977) report approximately 1005% in

clinical subset C3. These differences may be attri.buted to the lack of

high acuity subjects available during this study. Also, Forrester et ala

(1977) report their study was approximately 5 years in length. The large

time difference may have allowed Forrester et al. (1977) to be more

selective and choose only patients with expected high acuities. Other

factors such as different medical regimes or the time frame before

34

Table 3

Clinical Subjects with Number of Clinical Assessments

Subsets Total Subjects # I II III IV Assessments

1 3 3 2 3 3 3 4 3 3 5 4 4 6 4 4 7 1 1 8 8 8 9 6 1 1 1 9

10 5 5 11 5 5 12 3 3 13 4 4 14 3 2 1 6 15 3 3 16 3 3 17 2 2

18 5 5 19 4 4 20 3 1. 1 5 21 1 1 2 22 4 5 9 23 4 4 24 4 4 25 3 2 5 26 4 4 27 1 2 3 28 1 10 11

29 2 5 7 30 5 5 31 1 2 3

Total 72 48 3 14 137

35

initiation of therapy may have also contributed to this difference. Due to

a lack of data these factors cannot be evaluated. It can be reported that

the investigator's clinical as ses sments concluded the maj ority (52.5%)

of the subjects were placed in clinical subset Cl, no complications.

Forrester et al. (1977) report approximately 37% in this category. This

data clinically supports the contention that Forrester et ale (1977) had

access to patients with higher acuities.

100

90

80 -'-.. '-..

~ '-..

rJ) '-.. ~ 70 '-.. ~

~ '-.. '-.. Q) '-.. '-..

8 '-.. '-.. rJ) '-.. '-.. rJ) 60 '-.. '-.. Q) '-.. '-.. rJ) '-.. '-.. rJ) '-.. '-..

~ 50 '-.. - '-.. '-.. "" "H '-.. "" 0 '-.. '-.. '-.. '-... H 40 '-.. --- ......... Q) '-.. '-.. '-.. ..0 '-.. '-.. '-..

8 '-.. '-.. ........... '-.. '-.. '-.. ::l 30 '-.. '-.. Z '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-..

20 '-.. '-.. '-.. '-.. '-..

~ '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. =:t r- '-.. 10 '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. '-.. r '-.. '-.. '-.. '-..

~ 1::::--'-.. '-..

Cl C2 G .. C4

Legend Miller Study

II / IIII Forrester et ale (1977)

Figure 2. Comparison of Clinical Subjects

36

Hemodynamic Subjects. Only seven subjects required hemodynamic

monitoring during the study, however, initial planning required ten sub

jects in this category., The sporadic occurrence of these subjects rendered

it impossible to obtain the required data. By using multiple hemodynamic

assessments it was possible to accomplish 33 assessments on the 7 subjects

obtained., If a single assessment had been made~ 7 would not constitute a

clinically significant number for analYSiS" Multiple assessments also

allowed the investigator to assess the subject over the acute phase of the

medical regime. When compared with Forrester et al. (1977), who

accomplished only one assessment per subject, this produces a more

clinically significant evaluation of the medical regime. By utilizing multiple

assessments the 33 assessments obtained would be significant for clinical

analysis.

Table 4 summarizes the placement of subjects within the four hemo

dynamic subsets. The difference in numbers of the hemodynamic measure

ments between the two studies (33 vs. 200) does not allow for statistical

comparison. This investigator reports a relatively even distribution of

subjects within the hemodynamic subset classification system.

Table 5 demonstrates a comparison of the clinical and hemodynamic

subsets of all subjects who were hemodynamically monitored. The clinica 1

subset did not correlate with the hemodynamic subset on 19 comparisons

(57%). The discrepancy in correlation between clini.cal and hemodynamic

subset classification is due in large part to the MPWP which were less

37

Table 4

Hemodynamic Subsets with Number of Hemodynamic Measurements

Subsets Total Patient # I II III IV Assessments

14 1 1 2 4

17 1 1 2

22 3 1 5 9

24 2 2

26 4 4

28 2 2 1 2 7

30 1 4 5

Total 7 9 8 9 33

Table 5

Cornparison Matrix of Clinical and Hemodynamic Subset Classification

Hemodl:namic Subsets Total Clinical Subsets I II III IV Assessments

I 1 1 2

II 19 7 8 1 3 38

III

IV 13 1 7 5 26

Total 33 7 9 8 9 66

38

than 18mm Hg in 13 comparisons.

Table 6 classifies the raw data secured from subjects who were

hemodynamically monitored. It displays the range and average of the

cardiac index (CI) and the mean pulmonary wedge pressure (MPWP). This

data indicates that hemodynamic monitoring was appropriate in all but one

subject. Raw data for all subjects from which subset classifications were

made is displayed in Appendix E.

Progress Notes. Physician Progress Notes were reviewed for the

following data: 1) time of day, 2) recording of hemodynamic measurements,

3) clinical findings, and 4) planned therapeutic regimes. Progress notes

for comparison purposes, were deficient in three areas: 1) they consistently

failed to provide the time of clinical assessment, 2) hemodynamic measure

ments were recorded on only 2 occasions, and 3) a recorded planned thera

peutic regime was not consistently available. Thus, it was not possible

to perform a significant comparison of the investigator's therapeutic

regime with that of the physicians.

Discussion

Since no study utilizing mUltiple clinical assessments of subjects who

have developed left ventricular failure due to acute myocardial infarction

with subsequent assignment to clinical and hemodynamic subsets could be

found, this study could not be compared with similar studies 0

39

Table 6

Classification of Hemodynamic Measurements by Range and Average

Total Patient # CI (L/min/m2) MPWP (mm Hg) Measurements

14 Range 1 .. 79-2.15 13-26 4 Average 1.99 21025

17 Range 2.03-2.54 20-22 2 Average 2.28 21

22 Range 1.83 -2 .56 12-16 9 Average 2.116 14.25

24 Range 2.65-2.75 14 ... 15 2 Average 2.7 14.5

26 Range 2.45-206 19-25 4 Average 2.51 22

28 Range 1.6-2022 12-27 7 Average 2.1 20.14

30 Range 1014-2.02 15-21 5 Average 106 19

Summary Range 1.14-2.75 12-27 33 Average 2.11 18.63

40

Limitations

Certain aspects of the study posed limitations that had not been

anticipated. The time frame for the study did not allow a large patient

population. The methodology for performing hemodynamic measurements

was not controlled. In an attempt to limit internal bias, the investigator

decided it would be more appropriate not to know the hemodynamic

measurements prior to completing a cardiopulmonary assessmenL This

placed the responsibility for hemodynamic measurements upon the nursing

staff of the CCU. It was subsequently determined that each RN did not

accomplish the hemodynamic measurements with the same technique.

For example, some R Ns did not calibrate the transducer at each measure ~

menL This may have introduced error into recorded values for hemo~

dynamic measurements. This may have attributed to some of the differ

ences when clinical and hemodynamic subsets did not correlate (see Table

5).

The investigator utilized both subjective and objective data when

assigning subjects to clinical and hemodynamic subsets. The subjective

data may have resulted in some internal bias when assigning subjects to

subsets a

1m plications

Cardiopulmonary assessments in conjunction with hemodynamic

measurements are not routinely performed by nursing 0 If the professional

RN were to assume this function on a regular basis the number of fatalities

41

due to left ventricular failure might be reduced. Since the advent of SNP

therapy, nursing has been accomplishing the management of SNP therapy

on the basis of hemodynamic measurements alone. Nursing has not

taken into account the {X)ssibility of equipment malfunction or improper

technique while accomplishing hemodynamic measurements, and sub-

sequently used clinical data to expand the data base on which critical

judgments are made. The opportunity to improve nursing care is both

pos sible and neces sary to improve patient care 0

In clinical settings where hemodynamic monitoring is accomplished

expectations of the R N are high 0 Experience and the study results has

shown that the highly skilled RN, is capable of and can achieve competence

in performing cardiopulmonary assessments and hemodynamic measure-

ments. However, to achieve the desired level of competence there needs

to be a planned course of instruction with expected skills to be demon-

strated 0 A logical method to provide incentive to learn advanced skills

would be a clinical ladder in which the clinical unit defined competencies

to be achieved at each leveL The most advanced level could require the

RN perform a complete and accurate cardiopulmonary assessment in

conjunction with hemodynamic measurement.

The RN who achieves this level would then be considered clinically

competent to administer and manage patients receiving vasodilator therapy

for left ventricular failure due to acute myocardial infarction.

ISR:

42

R ecommenda tions

The pertinence of clinical data could be increased if the following

gUidelines had been included in the methodology: 1) that the physicians

who participated utilized the same recording technique as the investigator,

and 2) that all RNs accomplished hemodynamic measurements utilizing

the same technique 0

These guidelines would have provided to the investigator a more

valid and reliable data base of clinical informationo Future studies,

embodying these recordings, would provide a core of clinical data useful

for determining the extent to which the competent, highly skilled R N is

capable of managing patients with left ventricular failure 0

APPENDIX A

PHYSICIAN NOTIFICATION

Dr"

Your cooperation and permission are requested in a study designed to increase the effectiveness of nursing care provided in the coronary care unit" has been contacted and has consented to participate in this study"

The study involves the patient receiving a cardiopulmonary assess =

ment consisting of auscultation of the heart and lungs with palpation of the trunk and peripheral pulses" The number of assessments conducted will be determined by the severity of the patient's conditiono

This study is being conducted by Alfred Be Miller, RN and is being supervised by Dr. Frank Yanowitz, M .. D 0 and Dr" Steven Klausner, MoD" of the Cardiology Department of LDS Hospital 0 This study has been reviewed by the University of Utah Review Committee for Research with Human Subjects and the LDS Hospital Research and Human Rights Committee" These committees have determined that the patient will be at Low or No Risk during the study.. A copy of the study proposal is on file with each committee ..

Questions can be directed to Alfred B" Miller, RN or Dr. Yanowitz 9

MoDo and Dr 0 Klausner, M"D"

Thank you for your cooperation 0

Alfred B" Miller J RN Principal Investigator

Permis sion is granted , denied --------------~ -------------

Dr. --------------------------------------

APPENDIX B

PATIENT INFORMATION

1. Name 2. Number --------------------------3. Age ---- 4. Sex 5. Race ----- 6. Weight __ kgo

7. Height 8. Allergies ----- ----------------------------------

9. Date of AMI -----11. Enzyme Levels:

Date/Time

CPK

LDH

SGOT

12.. Family History:

130 Chief Complaint:

14. Review of System:

10. Location of AMI --------------------

--

--

Normals

9.0~10600

90.0-21000

10 0 0=4500

APPENDIX C

CLINICAL ASSESSMENT

DATE/TIME

MEDICATIONS:

VITAL SIGNS:

TREATMENTS/RESPONSE:

ASSESSMENT:

Subjective

Objective Heart Lungs Vessels Skin

Assessment

Plan

APPENDIX D

ca.t.a/!!.::e HEMODYNAMIC MEASUREMENTS

2~O I I I

2)0

210

190 ,! 1-

1'70

150

HR 1;0

BP 110

90

10

50

)0

7

6

.;

CO 4-

C! J

2

1

50

I?A SiD ~ t1P~ S"IR JO

20

10

SNP I j I !!Iq;/kg

Subject # 1

Date Time H d emo lynamlcs

HR BP CO CI PA MP\tVP SVR

Clinical S1 S2 S3 S4 Rales Rhonchi Wheezes Output

Skin Color Temp Moist Dry

l 64 1140/98

n1 n1 0

0 + 0-5'

2:i.iO

nl warm

0

+ Mental State

APPENDIX E

SUMMARY

60 60 ll6/86 140/90

!

nl n1 ! nl n1 -0 0

0 0

+ + I 0 -

0

~ lj

17RO 850

n1 nl warm warm

-0 0

+ +

Obttmd. ~f ____ ~ ____ 4-____ ~ __ ~ ____ -+ ____ ~ ____ ~ __ ~ ____ ~ Nonnal ~[_+~ __ ~+ __ ~~+ __ ~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ __ ___

Subsets Clin. ~_C~1 __ ~C~1:...-+-~C~1~ __ -I-__ -I-_--+ __ -+-__ -t-_--t Hemo. ~ ____ ~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ ____ ~ __ ~ ____ ~

Subject # 2


HR BP CO CI PA MPWP SVR

Clinical Sl S2 S3 S4 Rales Rhonchi Wheezes Output

Skin

I 80 1160/98 I

nl nl 0

+ +LR

+ 11873cc

48

86 86 170174 96/74

nl nl nl nl 0' 0 0' 0 I

+ R L +R L

+R 0' l612~c l1520cc

~~f.~ I wa:~ I wa:~ r::tt I I I I I I Mental State

Obtund.' ~----~----+---~~--~----+---~-----Ir----T----~ Nanna 1 ~.~+L-~~+~~_+~~ ____ ~ __ ~ ____ ~ ____ . __________ ~ Subsets

Clin. Hemo.

I Cl C1

Subject # 4

Date 14/28/7814/28/7814/30/71 Time ! 0830 . 1200 . 1030 _ Hemodvnamics

HR BP CO CI PA MP\VP SVR


Skin

t 60 --;);:)

lS4/76 i 124/7C I

I

nl nl nl nl () ()

() 0

+RT + R T

1"'\" n 0" 0

1102 1230

i 58 122/80

nl nl (1

0

i+ R ('5'

0

1400

gf.~ I w:m I w:~m I w:~ I Mental State

~~:~i I + +! + Subsets

49

I

I

I I

r

I I

I I I I

Clin. I Cl Cl I Cl Hemo. ~ ____ ~ ____ ~ ____ ~ __ ~ ____ ~ __ ~~ __ ~ ____ ~ __ ~

Subject # 5



Clinical SI S2 S3 S4 Rales Rhonchi Wheezes Output


Mental State

54 112./64

nl nl 5' 5' 0" 0" 0"

2~8cc

nl warm

+

I I

50

'" 48 72 74

110/80 108/78 120/68

nl nl nl i nl nl nl 5' 5" 5' 5" 5" 5' 0" 0" 0" 0" 0" 0" 0 0 0

2714cc t1648cc

nl nl nl twarm warm warm

+ + +

Obtund. ~----~----+---~----~----+---~----~----T---~ Normal . + + + +

Subsets Clin: ~~C~l~~~C~l~~C~l~~C~l __ ~ __ -+ ____ ~ __ ~ ____ ~ ____ ~ Hemo. L ____ ~ ____ ~ __ ~~--~----~--~ ____ ~ ____ ~--~

Subject # 6

Date Time H d erno lynam lCS



Skin

84 )124/70 I

nl nl 0 +

rt-L R 0' 0

7098

51

88 80 83 88/68 102/80 104/7:

nl nl nl I I

nl nl nl i 0 0 n + + +

f+- L R + L R H-LR 0 0 0' 0 0' 0'

3917 3306

~?~ ~~~01W~cll~~cll:Lcll I I II I Mental State

Obtund. 1~--~----~----4-----~---+----+---~I-----r--~ Normal . + + + + .

Subsets Clin. ~~C~l~~~C~l~ __ C~l~~C~l __ ~ __ -+ ____ ~ __ ~ ____ ~ ____ ~ Herno. ~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ __ ~

Subject # 7

Date Time

15/3/781 . 0930

H emodynamlcs HR BP CO CI PA MPWP SVR


j 80 194/60 I

nl nl 0 + + 0

a

52

I I

I

I

Skin

~p ~~l:~n;m~1 ~I~I-.·~I~I~I~I~I ~I Mental State

Obtund. II-_.l-! -~--+--4--+--+-+-I-+-----1 Nonnal L. ~+~~.~ __ ~ ____ ~ ____ ~ __ ~ ____ ~ __ ~ _____ ~ ____ ~

Subsets Clin. Hemo. I Cl I

Subject #8

Date Time H d erno lynamlcs



) 100 1130J98 I

nl nl 0" 0

+

+ 2478

I

1


cyanotic warm

+ Mental State

100 1 94 120/7R' 132/78

nl nl nl nl 0 -0

+ faint + faint + +

+ + 1739 1750

cyarrOC cyarrOC ~l/wrm warm +

+ +

53

100 100 9Q 103 100 104170 100/80 100/70 104/76 104/64

I

nl nl nl nl nl nl nl nl nl nl - 0 - - 0 0 0 0

+ faint + faint ± faint + faint + faint 0 + + + +

1:50 I 736

I + + +

1303 1611 --

Ojaroic cyanic cyanotic C)8Jtti.c cyanic warm rnarm rnarm warm warm

+ + + + +

Obttmd. I~ ____ ~ ____ ~ __ ~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~ Normal . + + + + + + + +

Subsets CUn. I C2 C2 C2 C2 C2 C2 C2 C2

Hemo. :====::========::==========:====:==========:====:

Subject # 9

Date Time Hemodvnamics


Clinical S1 S2 S3 S4 Ra1es Rhonchi Wheezes Output


! 64 i124/80 [

t I I I

nl nl 0 ()

0-0

0 1650

nl warm sliQ"ht

Mental State

88 100 146 124/72 120/80 98/54

nl nl nl nl nl nl 0 0 0 0 n 0" n 01' 0 t-

0 0 0 -0 0 0

1525 650 1600

nl nl nl warm warm warm

+ + +

54

120 94 120 80 82 104/68 L04/68 130/80 106/70 L20/80

I I

nl nl I nl nl nl nl nl nl nl nl -0 + + 0 0

0 0 0 -0 0

o of' o. 0" ,t- o 0 0 0 0 0

0 0 0 0 0

300 1401 1334 1550

nl nl nl nl nl warm warm warm warm warm

sli,ght

+ + + +

Obtund. ~ ____ ~ ____ ~ __ ~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~ Normal . + + + + + + + + +

Subsets Clin. I C1 C1 IC4mildi Cl C3 C2 Cl Hemo. ...1-_-_-_;;;..; _~ _-:.-_-_...;; _-_-.... ~ _;..;;; _.;;;.;_~...;..;,""",,,,,"::::::::::::::::::::::::::::::~ ....

C1 Cl

Subject # 10


HR t 56 BP i94/60 CO CI PA MPWP SVR



I

Mental State

nl nl 0" 0" ()

0 ()

2300

nl warm

+

+

Cl

68 108/66

nl nl 0" ()

n n n

nl warm

+

I + I I

Cl I

ss

68 62 86 102/70 104/60 110/70

I

nl nl nl I nl nl nl 0" 0" 0" 0 0 0"

n~ n 0'

() 0" 0

n n ()

4130 1300


+ + +

+ + +

Cl Cl Cl

Subject #:11

Date Time H d emo tynamlcs




I 70 [22/80

n1 n1 '0

0' c a 6"

775

n1 warm

+ Mental State

80 I 130/80

n1 n1 0'

6" c E 6"

n1 warm

+

56

93 68 68 122/70 90/60 94/66

I

n1 n1 n1 I n1 n1 n1 0' 5" 6" 6" 5" 6" c s S-() () 0' 6" 6" 6"

1175 1320 300 (pc rtia1 r eport)

n1 n1 n1 warm warm warm

+ + +

Obtund. ~ ____ ~ ____ ~ ____ +-__ ~ ____ -+ ____ ~ __ ~~ __ ~ ____ ~ Normal . + + + + +

Subsets

ain. 1~~C~1~~C~1~t __ ~C~1~I~C~1~~~C~1-+ ____ ~ __ ~~ __ -+ ____ ~ Hemo. ~ ____ ~ ____ ~ _____ . ____ ~ ______________ ~ ________ ~

Subject # 12





i 100 ,

i 104/70 I

!

nl nl 0 Q c 0"

0-

1070

nl warm

+ Mental State

57

88 I 98 112/82 110/70

i I

nl nl i nl nl 0 0 Q Q I ct c j

0' 0'

0- rr 2100 1530

nl nl warm warm

+ +

Obtund. I~----~----~----+---~-----r----+---~~--~----~ Normal . + + +

Subsets Clin. I C1 Cl Cl Hemo • l..,~ _-_-_.;:;;;. _.:;.. _-.L...,!-_-_...; _;;;.: _=-.... -+-_-___ ...:: _:;.:; _-... +-_-_-_-_-.... -+_-_-_-_-_-... +-_-_-_-_-..... -+-_-_-_-_-.... ~-_-_-_-_-..... -1-_-_-_-_-....... --1

Subject #' 13




Skin

) 64 64 ! 100/74 11l2/82 !

nl nl nl nl 0 0 0 0

0 C 0 0

0" 0' 1400 1356

80 70 98/64 104/70

nl nl _nl nl 0 0' 0 0'

C- O' 0 0 0' 0

1420 1560

Color

I~a~ I;a:~ I~a~ ~~ I Temp Moist Dry

Mental State Obtund. I I Normal + + + +

Subsets Clin.

I C1 C1 C1 C1

'I Hemo.

S8

I

I

I I

I I I I I

I

Subject #14


HR !60-150 70 BP i150/120! 88/62 CO CI PA MPWP SVR



i I J

I I

Mental State

I 3 90 2 Ot)

21/8 13

I 25

nl nl nl nl 5" 5" '0 5" 0' C

IT 5" 0' 0

1167

nl nl warm cool

slight +

54 121/78 3 39 1 79

46/22 24 25

nl nl

new 0' c 0' 0'

990

nl warm

dry

59

68 63 65 100/64 108/81 1100/80 3 74 4 08 1 97 ? 15 42/20 44/24

22 26 \

23 24 1

nl nl n1 1 I nl nl nl I 5" ~nterm a I 0" 0 0 I c ct 0' I 0' 5" 0 I 5" 0 0' f

1815 3366 2800 !


dry dry +

Obttmd. ~ ____ ~ ____ ~ __ -+ ____ ~ __ ~~ __ ~ ____ ~ __ -+ ____ ~ Normal . + + + + + +

Subsets Clin. I Cl C4 C2 Cl C2 Hemo. 1-1-_-_-_-_-....1-+_-_-H=3=:~::H=4=::H:..;;..4-_-... -+-_-_-H:2::::::::::::::::::::::: Cl

Subject # 15




Skin

! 51 i 118/72

nl nl 0 0 0 0 0

1140

60

63 ! 64 118/82 110/68

I

nl nl I nl nl ! 0 0 I 0 0 ! + + I 0 0 I 0 0 I

2120 1455 I

~~~ :~lw:_a:~~:_~:_+:lw:_a:~~:_~:_. :~lw:_a:~~:_~:_~:I= __ == __ =:~I_ =-=_=~:I~:-=_=-=:~I=_-==_-=:~I_=-=_=-=:~I= __ ==_~=:I Mental State

Obtund. Normal

Subsets Clin. Hemo ..

C1 C1 C1

Subject # 16

Date Time H d

16/14/78 16/15/7816/ 16/71 i 0600 0800 0815

emo lynamlcs HR BP CO CI PA MPWP SVR

Clinical

S2 S3 S4 Rales Rhonchi Wheezes Output


! 82 1110/82 I

nl nl 0

0 Q 0 +

2025

dusky warm

0 dry

Mental State

92 94 106/68 118/70

nl nl nl nl a 0

0 0 + + 0 n + +"*'

2133 1700

dusky dusky warm warm

0 a dry dry

61

i

Obtund. I~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~ Normal . + + +

Subsets

Clin. 1 C2 C2 I ~2 I H~o. ~==~:=~==:~:.=:~:~.=====~====~====:=====:====:====:

Subject #17




Skin

! 110 i 98./67 I 4 21

2.03 50/20

22 19

nl nl + -

H- Q'r()ss

+

62

96 100/69

4.32 2.54

50/28 20 17 I

.....

nl i I

nl i + -+, I

+

gf.~ 1+1+11111111 Mental State

Obtund. ! I Normal . + ; .

Subsets Clin_! L __ ~C~4~~C~4~1 ____ ~ ____ ~ __ -+ ____ 4-__ ~~ __ ~ ____ i Hemo_ L __ nH~4-L~H~2~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ __ ~ ____ ~

Subject #18


HR i 92 I 84 82 90 BP 1 12Q/88 1114/86 136/90 L48/98 CO CI PA MPWP SVR

Clinical SI 82 S3 84 Rales Rhonchi Wheezes Output


I

Mental State Obtund. Normal

Subsets Clin. Hemo.

I I

f

I

nl nl 5" 0

5" 0 0

1105

nl warm

0

+

Cl

nl nl nl nl nl nl 5" 5" 5"

+ 0' + + 5" 5" 0 0' 0' 0 "0 0

2500 1000 1475


0 5" 0 + + +

Cl Cl Cl

63

I 91 138/96

I

nl I I I

snlit ! 5" 0"

+ 0' I 0

,

nl warm

0 +

Cl

Subject # 19





I 76 1138/88

nl nl 0

0

+ L 0' 0'

305

nl warm

0 +

Mental State

64

52 64 82 124/84 128/88 112/82

1

nl nl nl i !

nl n1 nl 0 0 0 I 0 0 0

+ + + I 0 0 0' '0 0" '0

640 460 1930


0" - 0 0

+ + +

Obtund. ~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~ ____ ~ ____ +-__ ~

Normal . + + + + Subsets

Clin. I C1 C1 I C1 I Cl Hemo. J.... .... _-_-_.:::::. _.=.. _~!-_-_~_~ _=-... +-_-_-_.;;;:: _;.;;;. ...I-t.:~:~=:=:==:====:====~:====:====:

Subject #20





! 97 ,

1114/74 I

nl U1 0' 0'

+ 0

0

425

nl warm

0 +


Subsets Clin. Heme.

Cl

76 102/60

nl nl 0' (5'

+ 0

0

1655

nl !Warm

0 +

C1

85 90 70 94/60 105/70 180/10C

nl nl nl i nl nl nl f

!

0' 0' 0 I I

-t- o + \

+ ~+ "'+ ,

0 0 0

0 0 0

2240 1185 430


- - 0 0 0

+ + +

C31 C2 Cl

C3 -- episode of hypotension and 8-12 hrs. Z .; urine output for that period 230 ml for 16 hr s.

65

i

Subject #21

Date Time Hemodynamics

HR I i B:i I 85

BP 1140.11041 J44/102 CO CI PA MPWP SVR



!

Mental State

split split

5' + 0" 11' 11

nl warm

I J.L +

I

I ! I

1

I

split split

0"

+ + II lL

nl warm

11 ±

66

J 1

i I

I I

Obtood. ~----~---4----~----~---r----rl ----r----r--~ Normal . + + .

Subsets

Qin. ~1~C~1~ __ ~C~34-____ ~ __ -r ____ ~ __ ~I __ --r----T--~ Hemo. L ____ -L ____ ~ __ ~~ __ ~----~--~. ____ ~ ____ ~--~

Subject # 22

Date Time H d erno lynamics

HR f 150 1

BP i 93/68 CO CI PA MPWP SVR




Subsets Clin. Hemo.

4.85 1.98

29/17 13

nl nl + 0 + 5" 0

so

n1 warm

+ 0

95 93 85 107/74 117/79 107/71 4.48 4.79 4.64 1.83 1.96 1.9 34/13 41/17 39/16

15 16 15 18 15 16

nl nl nl nl nl nl + + + 0 0 5"

t+ 't+ 1'+ 5" 5" 5" 0' 0- 0-

RRfl lRO :iSS

nl n1 nl warm warm warm

5" + + 0' 0 0

67

88 93 92 59 66 110/70 108/71 101/66 89/56 89/56 5.61 6.26 6.05 5.24 4.75 2.29 2.56 2.47 2.1 1.94 43/18 41/17 39/12 47/15 48/17

16 15 12 20 15 14 12 12 13 12

nl nl nl nl nl nl nl nl nl nl + + + + + 5" 0' 5" 0 5"

+ + + + + 0 0 I 0' 5" 0' 0- + + + +

1 ?O RJ.O 1qn SR 14

nl nl nl nl nl warm warm warm warm warm + + + + + 0 0 0 0 0

Subject # 23



Clinical Sl S2 S3 S4

1 68 i 136/70 I

nl nl 0 0

a -0

93 126/70

nl nl 0 0 + 0

Rales Rhonchi Wheezes Output 2~513215


Mental State

nl warm

a +

nl warm

0

+

68

90 100 116/60 110/60

i

I

nl nl I nl nl 0 0 a a + a 0 a 0 0

1800 1300

nl nl warm warm

0" 0

+ +

Obtund. I ~~~~~~~--+--~~~~~--~----~--~-----r----~--~ Normal . + + + +

Subsets Qin. ~~C~I~~~C~l~ __ C~l~~C~l __ ~ __ ~ ____ ~ ____ ~ __ ~ ____ ~ Hemo. ~ ____ ~ ____ ~ __ ~ ____ ~ ____ ~ __ ~ __________ ~ __ ~

Subject #24



Clinical SI S2 S3 S4 Rales Rhonchi \Vheezes Output


! 86 i 94/60 I 6 18

2 75 36/18

14 1 :i

n1 nl

5"

+ 0

0' 2065

nl warm

+ 0"

Mental State

69

85 I 80 80 108/71 nO/80 108/74 5 74 2 65 34/13

15 l:i I

n1 n1 nl I n1 nl n1 5" 5" 0' 5" 5" 0' + + + 0"

23~6 12~OO I

0' 2144


0 + + + 5" 0'

Obtund. ~~O~~ __ 5" __ +-_O __ ~~O __ ~ ____ ~ __ ~ ____ ~ ____ +-__ ~ Normal . + + + +

Subsets Clin. I C2 C2 C2 Hemo. :==H::1=:==H:]=:=::=~:::==::::=:=::=:=====:====:====:

C2

Subject #25





! 72 i13RLR2 I

nl nl 0 0' + a-0'

nl warm

a-+

Mental State

88 1112/R2

nl nl 0 0

+ 0 +

685

nl warm

0

+

70

104 92 100 1112/84 110/80 _96lf> 6

I I

nl nl nl I nl nl nl 0 0' a-0 0 0' + a- a- I 0 0 a- I + a- 0

5051 3250 2960


0 0 0

+ + +

a- a- a-+ + +

•C2

1

C1 C1

Subject #26


HR ! 98 BP i 94/62 CO CI PA MPWP SVR

Clinical Sl S2 S3 84 Rales Rhonchi Wheezes Output


I

Mental State

.'1 R 2 4S

47/30 25 22

nl nl + 5" + 5" + 140

nl wm/cl

0 + 0

76 99/6;) 4.0.'1 ? n

38/28 22 17

nl nl + 5" + 5" +

300

nl wm/cl 0 +

0

71

96 100 96/6.'1 94/6.'1 3 R 3 7 2 :; 2 :; 60/24 54/22

19 23 18 17 ,

nl nl i I I

nl nl 1

+ + I 5" 5" I + + 5" 5" + +

12445 520

nl nl wm/c} wm/cl 0 + 0 +

0 0

~~::~i 1~--;--4--+-5"--~-;--+I-;--~----~--~~--~----+---~ Subsets

cun·1 I-----:c:::2~-.::c=2_4_--.....:Hc==22::......,..I-H.;:;;:c22=---1-----lI---~--;-----+---1 Hemo. ~~H~2~~~H~2~~~~.~~~ ____ ~ ________ ~ ___ ~

Subject # 27

Date Time H d emo lynamics




! 56 ,

; 110/74 I

nl nl 0 + + ()

;::;-2320

Iwa~~ Mental State

Obtund.

I [ Normal +

Subsets Clin. I C2 Hemo.

72

56 55 110/70 116/80

I

I 1

I

nl nl I nl nl 0 0 I , + + + 0 () ()

..j.. -;:; I

1550

Iwa~~ I wa~~ I I I I I I I

[ Q + +

C2 C1

Subject #28

Date Time Hemod namics




Mental State

nl nl + 6"

+ 0' 6"

nl warm

+ 6"

nl nl nl nl nl nl + + + 6" 6" 6" + + + 6" 6" 6" 6" 0 6"

2011


+ 0" + (} + 0

73

nl nl i nl nl nl nl nl i nl nl nl + + + + + 6" 0 6" 0' 6"

+ + + + + 6" () 0 0" 0 6" 0 I 0" 0 6"

1510 1755 1210

nl nl nl nl nl warm warm warm warm warm

+ 0 0 0 0

0 + + + +

Obrund. [~----~~~+-~~~~~~--+-~~--~-r----~--~ Normal t

(} 6" 0 6" 6" 6"

I 0

I 0 0

+ + + + + + + + + Subsets

Clin. ~---!---+----;---t-___ -+-~~---r~~+--~ Hemo. .

C2 C21 ~I C2 C2 C2

I C21 C2 C2 HI H3 H4 H4 H2 HI

Subject #29

Date Time H d erno lynamics




! 72 I 1100/60 I

nl nl 0

+ + 0 0'

2170

nl warm

0 +

Mental State

46 60 102/60 98/70

nl nl nl nl 0 0

+ + + + 0 0 0' 0

600

nl nl warm warm

0 0 + +

74

160-214 124 72 56 1~6~( 94/68 l04A)0 98/54

I

nl nl nl ! nl I nl nl nl ! nl 0 0 0 I 0 I

+ + + + + + + 0 0' 0' 0' I 0' 0 0' 0 , (5'

725 1060 1080 1230

nl nl nl nl warm warm warm warm

+ 0 0 0 + + + +

~~~~il ~ __ ~~~~~~+-_+~o~~~~~_+~o __ ~~~~~I ___ ~ __ ~1 ----~--~ Subsets

Clin. Hemo.

Subject # 30

Date Time H emodynamics

HR ~ 115 BP li80/114 CO CI PA MPWP SVR




Subsets CUn. Hemo.

2.89 1.80

21 42

nl nl + 0' + 0-n

864

nl warm

+ 0-

117 156/96 3.26 2.02 46/15

20 33

nl nl + 0-+ 0' 0'

nl warm

+ 0-

75

118 127 93 147/85 114/76 113/66

3.16 1.85 2.32 1.96 1.14 1.44

50/20 35/23 44/23 19 20 15 46 37 38 I

nl nl nl i nl nl nl + + + 0- 0- 0-+ + + 0' 0- 0-0- 0" 0-

3422 1273

nl nl nl warm twarm warm

+ + + 0- 0" 0"

Subject :# 31

Date Time H emodynamics



Skin

: 120 1128./88 , I

soUt

nl 0'

solit + 0 IT

IDI0

76

116 120 150/90 126/90

I

soUt ~nlit i

nl nl I 0" 0'

J

I

solit split 1

+ 0 j

0 0' I 0' 0' I

1390 !

Ef.~ ~~I w=!.!::a~~i=m!.!.:l :~: -l-~=..!:.a~=....=~m=~1 =-.:.... t-1~w::..:;:a:~i=m~l=_I~II""""'= _=-= _~-+I=-= -=-= _:+1 =-= -=-= _:Ir-= -=-= _:-1"= -=-= -=-: "1"1 =-= -:-:--tl Mental State

Obtund. ~I ~O'~~~o __ +-~o~~ ____ ~ __ ~--__ ~----r-__ ~ ____ ~ Normal ~.~+ __ ~~+ __ ~_+~~ ____ ~ __ ~ ____ ~ ________ ~ ____ _

Subsets

Clin. ~---...:C2~-4-~C~2---1-_C~1 -+-----+---~----t----t_--___t------Hemo. .

Cardiac Output:

Cardiac Index:

APPENDIX F

OPERATIONAL DEFINITIONS

The amount of blood ejected by the heart expressed in liters/minute ..

The cardiac output divided by the body surface area, expressed in liters/minute/M2, used to normalize cardiac output for body size ..

Pulmonary Artery The pressure in the pulmonary artery, expressed in Pressure: mm Hg"

Pulmonary Wedge The pressure in the pulmonary capillary, expressed Pressure: in mm Hg", usually reflective of left atrial pressure ..

Systemic Vascular The resistance to blood flow in the systemic system Resistance: throughout the cardiac cycle, calculated as mean

Subsets:

Cardiopulmonary Assessment:

arterial pressure - mean right atrial pressure cardiac output

(MAP - RAP) d . W d' h CO an express In 00 unlts, w en

MAP = RAP CO x 80 it is expressed as dynes sec/CMS .

Classification of the physiological state of left ventri ~ cular function. Clinical subsets are defined as the data obtained from the history, physical examination and rc'utine laboratory findings.. Hemodynamic subsets are defined using measured hemodynamic parameters such as CO, CI, PAP, and PWP" In the acute patient, clinical and hemodynamic subsets should correlate to justify their use in directing therapeutic decisions.

Clinical evaluation based on history, physical examina-> tion and routine laboratory findings ..

REFERENCES

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intracardiac monitoring. Nursing

Alder, J. Patient assessrnent: abnormalities of the heart beaL American Journal of Nursing, 1977 ~ 77 (4), 1-26.

Armstrong, P. W., Walker, Do C q Burton, J. R., Parke:r; J. O. Vasodilator therapy in acute myocardial infarction. Circulation, 1975, 52.., 1118-1122.

Awan, N. Aq Miller, R. R.~ Vera, Z., Demaria, A" No~ Amsterdam, Eo A., & Mason, D. T. Reproduction of s -t segment elevation with infusion of nitroprusside in patients with acute myocardial infarction. The American Journal of Cardiology, 1976, 38, 435-439 ..

Chatterjee, K .. , & Parmley, WoW. The role of vasodilator therapy in heart failure. Progress in Cardiovascular Diseases, 1977, 29, 301 =325.

Chatterjee, K., Parmley, W. W., Ganz, W q Forrester? Jq Walinsky, P q

Crexelles, C.? & Swan, H .. J. C. Hemodynamic and metabolic responses to vasodilator therapy in acute myocardial infarction. Circulation, 1973, 48, 1183~1193.

Chiariello, M., Gold~ H. K., Leinbach, R C., Davis, M. A .. , & Maroko, p" R" C,omparison between the effects of nitroprusside and nitroglycerine on ischemic injury during acute myocardial infarction. Circulation, 1976, 54 (5)~ 766 -773.

Cohn, J. No Vasodilator therapy for heart failure 0 Circulation, 1973~ 48, 5 -8"

Da Luz, P. L., Forrester, J. So, & Wyatt, H. Lo Hemodynamic and metabolic effects of sodium nitroprusside on the performance and metabolism of regional ischemic myocardium" Circulation, 1975, 52, 400

DeGowin~ E. L., & DeGowin, R .. L. Bedside diagnostic examination (3rd ed,,). New York: Macmillan» 1976~ 224~459o

79

del Bueno, D. J. Electrolyte imbalance: how to recognize and respond to it.. RN Magazine, Part 1, February 1975, 52 -56, Part 2, March 1975, 54-55"

Delaney, M. T. Examining the chesto Nursing, 1975, 75, 12 -14.

Drew, C. J. Introduction to designing research and evaluation. Sc Louis: Mosby, 1976"

Forrester, J. S., Diamond, Go, Chatterjee, Ko, & Swan, Ho Jo Co Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts) 0 The New England Journal of Medicine, 1976, 295 (24), 1356-13620

Forrester, Jo S., Diamond, G., Chatterjee, K., & Swan, Ho J. CO Medical therapy of acute myocardial infarction by application of hemodynamic subjects (second of two parts). The New England Journal of Medicine, . 1976, 295 (24), 1404 -1413"

Forrester, J" S,,' Diamond, GoA 0' & Swan, H. J. C" Correlative classification of clinical and hemodynamic function after acute myocardial infarction. The American Journal of Cardiology, 1977, 39, 137-1450

Foster, S. B. Pump failure. American Journal of Nursing, 1974, 74 (10), 1830-1834.

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Name

Birthdate

Birthplace

High School

College 1967 -1969

1970-1971

University 1973-1974

1976-1979

Degree 1973

1974

Professional Organizations

Professional Positions

VITA

Alfred Bobby Miller

February 27, 1937

Danville, Pennsylvania

Coal Township High School Shamokin, Pennsylvania

Merced Jr" College Merced, California

Minot State College Minot, North Dakota

University of North Dakota Grand Forks, North Dakota

University of Utah Salt Lake City ~ Utah

A 8 S 0 ~ Merced Jr. College Merced, California

B. S. N.l University of North Dakota Grand Forks, North Dakota

American Association of Critical Care Nurses

Assistant Director of Nursing for Critical Care~ Memorial Hospital of South Bend, Indiana, 1978-Staff Nurse, Coronary Care Unit, LDS Hospital, Salt Lake City, Utah~ 1975=1978; United States Air Force 9

1955-1975

nursing diagnosis of left ventricular failure in acute

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