HEMODYNAMIC IN- · 6 Model P-23A, Statham Laboratories, Beverly Hills, Calif. 7 Designed and built...

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HEMODYNAMIC ALTERATIONS IN ACUTE MYOCARDIAL IN- FARCTION. I. CARDIAC OUTPUT, MEAN ARTERIAL PRES- SURE, TOTAL PERIPHERAL RESISTANCE, "CENTRAL" AND TOTAL BLOOD VOLUMES, VENOUS PRES- SURE AND AVERAGE CIRCULATION TIME ' 2 By EDWARD D. FREIS, HAROLD W. SCHNAPER, ROBERT L. JOHNSON,3 AND GEORGE E. SCHREINER (From the Cardiovascular Research Laboratory, Georgetown Hospital, the Department of Medicine, Georgetown University School of Medicine, and tile Veterans Administration Hospital, Washington, D. C.) (Submitted for publication June 18, 1951; accepted August 20, 1951) Despite its importance little is known of the hemodynamic abnormalities which accompany acute myocardial infarction in man. Aside from clinical observations, the measurement of venous pressure (1) and total blood volume (1, 2), few systematic studies have been carried out in clinical cases. The reason for this has been the impossi- bility of subjecting such acutely ill patients to diffi- cult or time-consuming technical procedures. However, recent studies (3, 4) indicated that the values for cardiac output obtained with the Hamil- ton dye injection method were not significantly dif- ferent from those obtained with the intravenous catheterization method using the Fick principle. It seemed probable, therefore, that the Hamilton dye method suitably modified could be used to de- termine cardiac output at the bedside in acutely ill patients. This report describes the changes ob- served using the dye injection method and other procedures in a series of cases with myocardial in- farction as compared to a group of normal sub- jects and hypertensive patients. METHODS Fourteen hemodynamic studies were carried out in 11 patients with acute myocardial infarction, eight determi- 1 Supported in part by research grants from the National Heart Institute, U. S. Public Health Service, The Squibb Institute for Medical Research, New Brunswick, N. J. and Irwin Neisler & Co., Decatur, Ill. Presented in part at the Southern Society for Clinical Research, Jan. 19, 1952. 2 Sponsored (in part) by the VA and published with the approval of the Chief Medical Director. The statements and conclusions published by the authors are a result of their own study and do not necessarily reflect the opinion or policy of the Veterans Administration. nations in seven normal male medical students, and five in a similar number of hypertensive patients. It was es- sential in the cases of acute myocardial infarction to carry out the experimental procedures rapidly at the bedside and without serious disturbance to the patient. For this reason the dye inj ection method of Hamilton and col- leagues (5) as modified by Werko and associates (4) was used for determining cardiac output. After novo- cainizing the skin and making a small incision through the dermis with a scalpel blade, a 15 gauge Robb type needle 5 cm. in length 4 was inserted into the femoral artery. This permitted excellent flows of 2 to 3 cc. of blood per second while the rate of flow could be controlled by the stopcock which forms a part of the hub of this needle. Despite the large size there was little difficulty with hematoma formation when the puncture site was com- pressed for 20 minutes after removing the needle. The dye was inj ected into the central circulation by means of polyethelene tubing (1.12 mm. inner diameter),5 previously sterilized by soaking in 1 to 1,000 aqueous zephiran solution. After nicking the novocainized skin over an antecubital vein situated on the medial aspect of the arm, a 13 gauge needle was introduced into the vein and using sterile precautions the polyethelene tubing was inserted through the needle to a level calculated to be midway between the axilla and the center of the sternum. The catheter always was advanced several inches further and then retracted to be certain that it was not in a venous tributary. Since the placement could not be determined by fluoroscopy it was decided not to attempt to reach the right auricle since in the process the catheter might pass over into the jugular or opposite subclavian veins. Fol- lowing placement of the catheter the 13 gauge needle was removed and an 18 gauge needle inserted into the end of the catheter a distance of 1 inch. Every effort was made to carry out these procedures calmly and quietly and towels were so draped that the patient could not see the insertion of the needles. The "team" of investigators was trained so that two men 3 Captain, MC, U.S.A.F. 4 Becton, Dickinson & Company, Rutherford, N. J. 5Clay-Adams Company, Inc., New York, N. Y. 131

Transcript of HEMODYNAMIC IN- · 6 Model P-23A, Statham Laboratories, Beverly Hills, Calif. 7 Designed and built...

Page 1: HEMODYNAMIC IN- · 6 Model P-23A, Statham Laboratories, Beverly Hills, Calif. 7 Designed and built by Mr. Robert Wood, Tacoma Park, Md. 8 Visocardiette, Sanborn Co., Boston, Mass.

HEMODYNAMICALTERATIONS IN ACUTEMYOCARDIALIN-FARCTION. I. CARDIAC OUTPUT, MEANARTERIAL PRES-

SURE, TOTAL PERIPHERAL RESISTANCE, "CENTRAL"ANDTOTAL BLOODVOLUMES,VENOUSPRES-

SUREAND AVERAGECIRCULATIONTIME ' 2

By EDWARDD. FREIS, HAROLDW. SCHNAPER,ROBERTL. JOHNSON,3 ANDGEORGEE. SCHREINER

(From the Cardiovascular Research Laboratory, Georgetown Hospital, the Department ofMedicine, Georgetown University School of Medicine, and tile Veterans Administration

Hospital, Washington, D. C.)

(Submitted for publication June 18, 1951; accepted August 20, 1951)

Despite its importance little is known of thehemodynamic abnormalities which accompanyacute myocardial infarction in man. Aside fromclinical observations, the measurement of venouspressure (1) and total blood volume (1, 2), fewsystematic studies have been carried out in clinicalcases. The reason for this has been the impossi-bility of subjecting such acutely ill patients to diffi-cult or time-consuming technical procedures.However, recent studies (3, 4) indicated that thevalues for cardiac output obtained with the Hamil-ton dye injection method were not significantly dif-ferent from those obtained with the intravenouscatheterization method using the Fick principle.It seemed probable, therefore, that the Hamiltondye method suitably modified could be used to de-termine cardiac output at the bedside in acutely illpatients. This report describes the changes ob-served using the dye injection method and otherprocedures in a series of cases with myocardial in-farction as compared to a group of normal sub-jects and hypertensive patients.

METHODS

Fourteen hemodynamic studies were carried out in 11patients with acute myocardial infarction, eight determi-

1 Supported in part by research grants from the NationalHeart Institute, U. S. Public Health Service, The SquibbInstitute for Medical Research, New Brunswick, N. J.and Irwin Neisler & Co., Decatur, Ill.

Presented in part at the Southern Society for ClinicalResearch, Jan. 19, 1952.

2 Sponsored (in part) by the VA and published with theapproval of the Chief Medical Director. The statements andconclusions published by the authors are a result of theirown study and do not necessarily reflect the opinion orpolicy of the Veterans Administration.

nations in seven normal male medical students, and fivein a similar number of hypertensive patients. It was es-sential in the cases of acute myocardial infarction to carryout the experimental procedures rapidly at the bedsideand without serious disturbance to the patient. For thisreason the dye inj ection method of Hamilton and col-leagues (5) as modified by Werko and associates (4)was used for determining cardiac output. After novo-cainizing the skin and making a small incision throughthe dermis with a scalpel blade, a 15 gauge Robb typeneedle 5 cm. in length 4 was inserted into the femoralartery. This permitted excellent flows of 2 to 3 cc. ofblood per second while the rate of flow could be controlledby the stopcock which forms a part of the hub of thisneedle. Despite the large size there was little difficultywith hematoma formation when the puncture site was com-pressed for 20 minutes after removing the needle.

The dye was inj ected into the central circulation bymeans of polyethelene tubing (1.12 mm. inner diameter),5previously sterilized by soaking in 1 to 1,000 aqueouszephiran solution. After nicking the novocainized skinover an antecubital vein situated on the medial aspect ofthe arm, a 13 gauge needle was introduced into the veinand using sterile precautions the polyethelene tubing wasinserted through the needle to a level calculated to bemidway between the axilla and the center of the sternum.The catheter always was advanced several inches furtherand then retracted to be certain that it was not in a venoustributary. Since the placement could not be determinedby fluoroscopy it was decided not to attempt to reach theright auricle since in the process the catheter might passover into the jugular or opposite subclavian veins. Fol-lowing placement of the catheter the 13 gauge needle wasremoved and an 18 gauge needle inserted into the endof the catheter a distance of 1 inch.

Every effort was made to carry out these procedurescalmly and quietly and towels were so draped that thepatient could not see the insertion of the needles. The"team" of investigators was trained so that two men

3 Captain, MC, U.S.A.F.4 Becton, Dickinson & Company, Rutherford, N. J.5Clay-Adams Company, Inc., New York, N. Y.

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E. D. FREIS, H. W. SCHNAPER, R. L. JOHNSON, AND G. E. SCHREINER

would insert the catheter while another placed the Robbneedle in the femoral artery. After some practice theseprocedures could be carried out in less than 10 minutes.Following this, the central venous pressure was meas-ured through the catheter using a water manometer andthe arterial pressure was measured using a strain gaugemanometer,6 a carrier-wave type amplifier 7 and singlechannel recorder.8 Mean arterial pressure was determinedby electronic integration of the pulse wave.

The injection of T-1824 9 in 0.5 per cent solution andcollection of samples from the femoral artery were car-ried out according to method of Werko and associates(4). Following this the arterial pressure was measuredagain and additional arterial samples were withdrawnat 10, 15, and 20 minutes for determination of totalplasma volume. In order to minimize hemolysis all sam-ples were collected in parafined tubes containing a dropof dried heparin. Hemolyzed samples (rarely obtained)were discarded. The average circulation time and cen-tral blood volume were determined according to themethod of Hamilton and co-workers (5). It was recog-nized that this method was not precise because of thevariable contribution of blood from other large veins en-tering the right heart (6). However, it seemed thatlarge discrepancies could be determined by this methodespecially since comparisons were made with normal andhypertensive controls who \\ere studied using the samemethods.

RESULTS

It was apparent that the hemodynamic changesfound in cases of myocardial infarction varied withthe clinical state of the patient. For this reasonthe cases have been divided into three groups: (1)mild, (2) moderately severe and severe and (3)cardiogenic "shock." The basis of such differen-tiation was made on clinical grounds. The mildcases were those who exhibited little or no evi-dence either of shock or of congestive heart failureand made a rapid and uneventful recovery. Themoderately severe and severe group exhibited defi-nite evidence of circulatory embarrassment, par-ticularly prostration, and manifestations of conges-tive heart failure. The cardiogenic shock casesall were severely ill exhibiting extreme prostra-tion, frequently with mental confusion as well asthe clinical appearance of shock. All of the lattercases terminated fatally during the acute episode.

6 Model P-23A, Statham Laboratories, Beverly Hills,Calif.

7 Designed and built by Mr. Robert Wood, TacomaPark, Md.

8 Visocardiette, Sanborn Co., Boston, Mass.9William Warner Co., New York, N. Y.

Mean Arterial Pressure, Cardiac Output, HeartRate, Stroke Volume and Total Peripheral

Resistance

In the normal group the mean pressure in thefemoral artery ranged from 63 to 93 mm. Hg (av-erage 84 mm. Hg), while in the hypertensive pa-tients the average was 145 mm. Hg with a range of104 to 189 mm. Hg (Table I). The mean arterialpressures in the cases with myocardial infarctionwere as follows: in the mild group the average was95 mm. Hg (range 85 to 113 mm. Hg), in themoderately severe and severe cases it was 89 mm-n.Hg (range 68 to 120 mm. Hg) and in the patientswith cardiogenic shock the average was 79 mm.Hg (range 73 to 88 mm. Hg). Extreme hypo-tension was not observed in the patients withcoronary occlusion even in those cases who ap-peared clinically to be in "shock" and who laterdied.

Cardiac outputs were unusually high in the nor-mal subjects, the mean cardiac index being 4.0 +

0.81 L. per min. (Table I). The high values prob-ably were due to the fact that all were healthy.young male individuals. These subjects were notunduly apprehensive as evidenced by the averageheart rate of 64 per minute. In the hypertensivepatients, who were more comparable in age to thecases with myocardial infarction, the mean car-diac index was 3.2 ± 0.4 L. In the patients withcoronary occlusion the cardiac output was withinthe normal range in the mild cases, but was abnor-mally low in the cases exhibiting shock. The meancardiac index in the mild group was 3.4 ± 0.8 L.per milm., in the moderately severe and severe pa-tients 2.9 ± 0.3 L. per min.. and in the shockgroup 1.8 ± 0.4 L. per min.

The heart rate usually was increased in the pa-tients with myocardial infarction but there wasconsiderable variation from patient to patient. Theaverage in the mild cases was 92 beats per minuteand the range 64 to 124. In the moderately severeand severe group the heart rate ranged between 85and 122 per minute (average 101), and in the casesexhibiting shock, it ranged from 74 to 160 perminute with an average of 128. Thus, in generalthe heart rate increased with increasing severityof the infarction.

The stroke volume was unusually high in thenormal subjects averaging 118 ± 16 cc. In the

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HEMODYNAMICALTERATIONS IN MYOCARDIAL INFARCTION

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E. D. FREIS, H. W. SCHNAPER, R. L. JOHNSON, AND G. E. SCHREINER

c.c. PER STam

STROKEVOLUMEFOLLOWINGINFARCTION

1.IID.Ed.JA. T.R D& F.Me. R.E. F.Me. P.C G.Ma HM

MILD MODERATELYSEVERE CARDIOGENICAND SEVERE SHOCK

FIG. 1. RELATIONSHIP BETWEEN SEVERITY OF DISEASE AND DEGREE OFREDUCTIONOF STROKEVOLUMEIN THE PATIENTS WITH ACUTE MYOCARDIALINFARCTION

hypertensives the mean stroke volume was 73 +

11 cc. and in the patients with myocardial infarc-tion of mild degree the mean was 76 ± 14 cc.Stroke volume was slightly reduced in the moder-ately severe and severe group averaging 50 ± 9cc., while in the patients with the shock syndromethere was a marked reduction of stroke volume to27 ± 7 cc. (Table I, Figure 1).

The mean total peripheral resistance for thenormal subjects was 925 + 225 dynes cm.-5 sec.and for the hypertensives was 1,875 + 250 dynescm.-5 sec. In the patients with myocardial in-farction of mild degree the total peripheral re-sistance was 1,175 ± 100 dynes cm.-5 sec. How-ever, it was slightly increased in the moderatelysevere and severe group being 1,325 + 250 dynescm.-5 sec. and strikingly increased in the cardio-genic shock cases, averaging 2,050 ± 450 dynescm.-5 sec.

"Central" Venous Pressutre, Average CirculationTime, "Central" Blood Volume and Total

Blood VolutmeThe "central" venous pressure measured in the

region of the subclavian or innominate veins aver-aged 90 mm. HO (range 70 to 117 mm.) in thepatients with mild coronary occlusion. In the pa-tients with moderately severe or severe myocardial

infarction the venous pressure varied between 81and 160 mm. H2O (average 120 mm. H.,O). Theaverage venous pressure for the cardiogenic shockcases was 115 mm. H20 (range 90 to 140 mm.).

The average circulation time was 22.1 + 4.5sec. in the normal subjects, 24.8 + 4.2 sec. in thehypertensive cases, and 25.4 ± 8.7 sec. in the pa-tients with myocardial infarction of mild degree.The circulation time was prolonged in the moresevere cases being 33.6 ± 4.1 sec. in the patientswith moderately severe or severe attacks, and44.5 +- 21 seconds in the cardiogenic shock group.

The "central" blood volume was not significantlydifferent in the various groups, the average valuesbeing as follows: 2.8 L. in the normal subjects,2.4 L. in the hypertensive patients, 2.7 L. in the pa-tients with mild coronary occlusion, 2.9 L. in themoderately severe and severe group, and 2.3 L. inthe patients with cardiogenic shock.

The total blood volume tended to be slightly re-duced in the cases of severe myocardial infarctionbut the differences were not sufficiently marked tobe significant in view of the small series of patientsand there was considerable overlapping of indi-vidual values. The total blood volume ranged be-tween 2.3 and 4.2 L. per sq. ni. surface area (av-erage 3.2 L.) in the normal subjects. In the hy-pertensives the average was 3.2 L. and the range

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HEMODYNAMICALTERATIONS IN MYOCARDIALINFARCTION

2.6 to 3.9 L. The total blood volumes in the pa-tients with myocardial infarction were as follows:average 3.0 and range 2.6 to 3.4 L. per sq. m. in themild group, average 2.8 and range 2.4 to 3.5 L. inthe moderately severe and severe group, and av-erage 2.7 and range 2.3 to 3.5 L. per sq. m. in thecardiogenic shock patients.

In patient F. McC. the typical picture of cardio-genic shock developed three days after the infarc-tion and two days after the original studies (TableI and Figure 2). Hence, it was possible to com-pare the values obtained prior to and after the de-velopment of the shock-like state. In the intervalbetween the tests, the electrocardiogram indicatedextension of the infarct while the arterial pressurehad fallen from hypertensive to hypotensive levels.The most striking change in this patient was thereduction of stroke volume from 51 to 28 cc. Thevenous pressure increased from 84 to 115 mm.H2O and the heart rate from 122 to 160 beats perminute. Unfortunately during the shock phase itwas impossible to thread the catheter into an armvein. The femoral vein was entered and the cath-eter tip placed in the neighborhood of the rightauricle. Hence, the measurements of average cir-

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culation time and central blood volume weren'tcomparable in the two determinations.

In another patient (J. V.) the determinationswere repeated approximately two months afterthe myocardial infarction when he had completelyrecovered (Table I). This patient was criticallyill during the acute episode manifested by pul-monary edema, dyspnea and orthopnea. Follow-ing recovery the mean arterial pressure fell mark-edly from 103 to 74 mm. Hg while the cardiacoutput rose slightly from 5.0 to 5.8 L. per minute.The stroke volume, however, increased markedlyfrom 36 to 73 cc. This was due in most part tothe marked elevation of heart rate to 140 beatsper minute during the acute episode which fellon recovery to 80 per minute. There also was astriking reduction in total peripheral resistancefrom 1,650 to 1,020 dynes cm.-5 sec. The ve-nous pressure also fell from 144 to 74 mm. H20,while the average circulation time became some-what reduced from 29.6 to 24.9 seconds. How-ever, despite the high venous pressure and evi-dence of cardiac failure at the time of' the acuteattack, the central blood volume was not signifi-cantly changed, being 2.4 L. initially and 2.6 L.

FIG. 2. CUTTINGS TAKEN FROM TRACINGS OF FEMORALARTERIAL PRES-SURE AND ELECTROCARDIOGRAMSIN PATIENT F. MCC., A WHITE MALE, AGE58 YEARS, WITH ACUTE MYOCARDIALINFARCTION

During the interim between the first and second determinations the pa-

tient developed the clinical picture of "shock." See text for further details.

..: ::

'ROCARDIOGRAMIII aVR aVL.VF J1OR'.O aVL oVF

V2 V3 V4 V5 V6 VI V2 V3 V4 V5 V6

DAY AFTER INFARCT 3 DAYS AFTERONE

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E. D. FREIS, H. W. SCHNAPER, R. L. JOHNSON, AND G. E. SCHREINER

after recovery. The total blood volume also re-mained essentially unchanged.

DISCUSSION

The disturbances in cardiovascular hemody-namics observed in the patients with myocardialinfarction varied with the severity of the attack.The mild cases failed to exhibit significant abnor-malities. In the patients with cardiogenic shockthe most marked disturbances were the serious re-duction of the stroke volume of the heart and themarked increase in total peripheral resistance.The moderately severe and severe cases formed anintermediate group between the mild and the shockpatients so far as hemodynamic abnormalities wereconcerned. Thus, the severity of the attack asjudged by clinical observations appeared to becorrelated directly with the degree of depressionof stroke volume.

Since the central blood volume was not signifi-cantly reduced it seemed reasonable to concludethat the depression of stroke output was due to fail-ure of the heart as a pump and not to hypovolemia.These observations are in agreement with similardata obtained by Mendlowitz, Schauer and Gross(7) in dogs subjected to ligation of coronary ar-teries. In addition, Gilbert, Aldrich and Ander-son, utilizing techniques similar to those used inthe present study, found a reduction of cardiac out-put in two of three patients with acute myocardialinfarction (8).

On the basis of the observed data the sequence ofhemodynamic events following severe myocardialinfarction appeared to be as follows: if the infarctionwas extensive or if it involved a previously dam-aged myocardium there was diminished contrac-tility and hence a failure of stroke output. Theconsequent reduction of arterial pressure imimedi-ately resulted in the activation of neurogenic re-flexes and possibly other compensatory mecha-nisms which produced an increase in total periph-eral resistance and tach-cardia. Thus, the he-modynamic response was not unlike the compen-sated phase of hypovolemic shock (9), except thatthe disturbance was due to ineffectual contractionof the myocardium rather than to blood loss.

This interpretation of the hemodynamic altera-tions accompanying myocardial infarction are inessential agreement with the classical studies ofWiggers and his colleagues on experimental cor-onary occlusion in animals. In his review of this

work (10) Wiggers points out that the infarctedsegment balloons out rather than contracts duringsystole. In some animals this is compensated forby an increase in diastolic ventricular volume withstretching of the muscle fibers and hence an in-creased contraction of the uninvolved portions ofthe myocardium. In others, however, this com-pensatory mechanism is insufficient to restore thecardiac output to normal. In these cases the ar-terial pressure falls progressively while the ven-tricles, atria, pulmonary vessels, and veins fill withblood.

Wiggers further states that, "the similarity ofclinical syndromes following coronary occlusionand loss of blood or plasma is due to the fact that inboth cases, cardiac output is decreased, but fordifferent reason, hypovolemia in the case of shockdue to blood loss and failure of the contractilecapacity of the ventricle in the case of myocardialinfarction. One of the consequences of loweringarterial pressure is that moderator vascular re-flexes operate to cause generalized vasoconstric-tion . . . and constriction of skin reservoirs incases of coronary occlusion . . . merely tends tointensify the engorgement and adds to the volumeof blood that the defective mlyocardiuim cannotmove."

Unlike the condition seen in congestive heartfailure, the total blood volume tended to be slightlyreduced and the central blood volume was not in-creased. This occurred even in those patientswith elevations of venous pressure and, hence, thelatter phenomenon cannot be ascribed to heart fail-ure alone. The venous pressure, however, ap-peared to correlate with the total peripheral re-sistance, usually being high in the patients withelevated total peripheral resistances. These ob-servations suggest that in addition to peripheralarterial constriction there also was venoconstric-tion. Elevation of venous pressure can be obtainedin normal individuals following drugs which in-crease total peripheral resistance such as angio-tonin (11) and norepinephrine (12). It seemsnot unlikely, therefore, that the increase in venouspressure observed in coronary occlusion is at leastin part a reflection of the overall increase of totalperipheral resistance.

It was surprising to find that the mean pres-sure as measured in the femoral artery was notusually significantly below normal in these pa-tients, many of whom appeared to be in shock

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HEMODYNAMICALTERATIONS IN MYOCARDIALINFARCTION

I I I I Al e~~~~~~V`RoVL aVF

_ ~~~~~~~~~~~~. .

VI V2 V3 V4 V5 v6,

1ii4 !! tA.': _~~~~~~~~~~~~~~liFIG. 3. CUTTINGS FROM ELECTROCARDIOGRAMAND PHOTOGRAPHOF THE

HEARTOF PATIENT G. McK., A WHITE MALE, AGED 54 YEARS WHOEx-HIBITED CARDIOGENIC SHOCK

The electrocardiogram is consistent with a diagnosis of acute anteroseptalinfarction and intraventricular block, R.B.B.B. type. The photograph dis-closes extensive infarction and thinning of the left ventricular myocardiumand "ballooning" of the intraventricular septum into the cavity of the rightventricle. See Table I for hemodynamic data.

clinically in that they were pale, mentally dulledand had weak and rapid pulses. Yet most of thepatients who were judged to be in shock by clini-cal observations exhibited pressures in the femoralartery not markedly lower than in the normalsubjects. The mean pressure as recorded directlyfrom the femoral artery in shock due to skeletaltrauma or blood loss is much lower, varying be-tween 40 and 60 mm. Hg depending on the severityof the shock (13), as compared to an averagevalue of 79 mm. Hg in the present series diagnosedclinically as being in cardiogenic "shock."

However, the level of arterial pressure probably

was maintained at barely normal levels by meansof the marked increase in total peripheral resist-ance. If the stroke volume fell further or per-sisted at low levels for long periods, eventually alimit would have been reached when the com-pensatory mechanisms of vasoconstriction andtachycardia could no longer compensate. Thisevent apparently occurred in the case of G. McK.whose initial determination soon after the infarc-tion revealed a mean arterial pressure of 88 mm.Hg despite a stroke volume of only 22 cc. How-ever, two days later the mean arterial pressure hadfallen to 73 mm. Hg with a stroke volume of 20

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E. D. FREIS, H. W. SCHNAPER, R. L. JOHNSON, AND G. E. SCHREINER

cc. It would appear in this case that the compen-satory mechanisms began to fail after several days.A similar sequence seemed to have occurred alsoin patient F. McC.

One of the most puzzling aspects of the shock-like state accompanying acute myocardial infarc-tion has been the presence on the one hand of theclinical features of hypovolemic shock, and on theother, of hypervolemic heart failure. Thus, thepatient may exhibit at the same time pallor, mod-erate hypotension, and a thready pulse and alsomay have a high venous pressure, pulmonaryedema, dyspnea and orthopnea. These discrepan-cies, however, can be fitted into a comprehensiveschema. It is well known that if in hypovolemicshock the combination of low stroke volume andintense peripheral vasoconstriction is allowed topersist, there is fluid retention and eventuallyedema, i.e., the so-called lower nephron nephrosissyndrome (14) associated with a reduction of re-nal blood flow and glomerular filtration rate (15).

It seems possible that a similar sequence mayoccur in acute myocardial infarction. Initially inthis condition there is a shock-like state whereasthe signs of congestive heart failure occur char-acteristically several days following the infarc-tion ( 1 ). This pattern is similar to that observedin the lower nephron syndrome. However, in thepatients with coronary occlusion, the signs of con-gestive heart failure are greatly exaggerated be-cause of defective myocardial contractility. Theadministration of blood or plasma to such patientsshould only add to the insult since there is nodeficiency of central blood volume but rather afailure of output. In G. McK., an attempt wasmade to transfuse the patient intra-arterially.The rapid administration of blood resulted almostimmediately in increased dyspnea and substernalpain. The transfusion was stopped and the pa-tient recovered. Further attempts at transfusingeven small amounts of blood produced the samesymptoms and, after 200 cc. had been adm-ninis-tered, the attempt to transfuse this patient wasabandoned. Several other subjects claimed thatthey derived definite relief of substernal pain anddyspnea following the cardiac output determina-tion which entailed the withdrawal of 100 to 150cc. of blood.

These observations are in agreement with thoseof Boyer who in a review of cardiogenic shock

(16) concluded that, "The bulk of evidence bothdirect and theoretical is overwhelmingly in favorof the concept that shock in myocardial infarctionis largely, and probably solely, a manifestation ofheart failure. . . Indeed pulmonary edema mayconstitute a more immediate threat to life (by low-ering the oxygen content of the blood) than doesshock, and venesection may occasionally be life-saving." Stead and Ebert withdrew 500 and 650cc. of blood, respectively, from two patients withmyocardial infarction and shock with no evidentharmful effects (17).

The hypovolemia and terminal heart failure ob-served in animals in the late stages of hemorrhageshock (18) no doubt lead to an insufficient coro-nary circulation as pointed out by Corday and hisco-workers (19), but is not at all comparable tothe hemodynamic situation existing in myocardialinfarction. Corday and associates ligated coro-nary vessels and found that if the animals werethen bled to shock levels, the non-contractile zoneof myocardium became larger. Transfusion inthis instance improved the contractility of theischemic area. However, this experimental situ-ation cannot be directly related to the patient withcoronary occlusion since as determined by thepresent study there is no deficiency of centralblood volume but rather a failure of the ventricleto expel the normal amount of blood presentedto it.

The compensatory mechanisms activated by thereduction of stroke volume aid in the maintenanceof aortic pressure and hence of coronary bloodflow; but they also may have harmful conse-

quences on the course of the disease, by addingextra burdens to an already damaged heart.Such deleterious influences include (1) an eleva-tion of total peripheral resistance thereby increas-ing the work of the heart, (2) tachycardia whichalso adds to the work of the heart and results ina less effective stroke output, (3) increased veno-

constriction resulting in increased venous fillingpressure in the presence of a failing heart, and (4)a fluid retention syndrome secondary to renalvasoconstriction. It seems possible that such a se-ries of compensatory reactions teleologically de-signed to tide a wounded animal over an emergencysituation may be harmful in the patient with aweakened myocardium ldue to coronary occlusion.

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HEMODYNAMICALTERATIONS IN MYOCARDIALINFARCTION

SUMMARYAND CONCLUSIONS

The hemodynamic abnormalities associated withsevere myocardial infarction were a reduction ofcardiac output, especially stroke volume, an in-crease of total peripheral resistance, heart rate.central venous pressure and average circulationtime, a slight and possibly insignificant reductionof total blood volume and an essentially normalcentral blood volume. The less severe cases didnot exhibit these abnormalities.

It is suggested that the initial change after an

extensive infarction is a reduction of stroke volumedue to the myocardial insult. This is followed bya series of compensatory mechanisms character-ized by generalized, intense vasoconstriction prob-ably including venoconstriction, and by tachycar-dia producing a clinical picture resembling shock.Such intense vasoconstriction in the presence ofa reduced stroke volume may be followed by a

fluid retention syndrome which, in the presence

of a defective myocardium, results in congestiveheart failure as well as the shock-like state. Thesecompensatory reactions to a reduced stroke vol-ume appear beneficial in that by raising aorticpressure they aid in the maintenance of coronary

blood flow, but they also seem detrimental in thatthey add in various ways to the work load of an

already damaged heart.

CASE SUMMARIES

H. B.-A 60 year old white male dentist developed in-creasing substernal oppression seven hours prior to ad-mission to the hospital. This was associated with pro-

fuse seating but there was no dyspnea. The lungs were

clear and the heart sounds were of good quality. Theelectrocardiogram was within normal limits on the dayof admission but the next day disclosed changes con-

sistent with a recent posterior myocardial infarction.Recovery was uneventful.

L. B.-A 56 year old colored male was admitted to thehospital complaining of substernal pain of three hoursduration. He had been hospitalized two years previouslyfor a "heart attack." The lungs were clear and therewas no dyspnea or orthopnea. The electrocardiogramwas consistent with a recent posterior myocardial infarc-tion. Recovery was uneventful.

J. W.-This 45 year old white male had experiencedangina intermittently for two months. On the day ofadmission while pushing his car he developed substernalpain lasting for six hours. Aside from apprehension thephysical examination was not remarkable. The electro-cardiogram disclosed the pattern of fresh anterolateralmyocardial infarction. He made an uneventful recovery.

J. S.-A 37 year old male developed severe squeezing

pain in the substernal area 11 hours before admission tothe hospital. For the two months preceding this episodethere had been angina on exertion. The patient was palebut the heart sounds were of good quality and the lungswere clear. The electrocardiogram indicated a recent,anteroseptal infarction. Recovery was uneventful.

J. V.-This 54 year old male with diabetes mellitus,dyspnea and angina on effort, all of one year's duration,began to have intermittent and then continuous sub-sternal pain radiating to both arms on the day precedingadmission to the hospital. His early clinical course wascharacterized by marked dyspnea and orthopnea withmoist rales at the lung bases, but no hepatomegaly orperipheral edema. Serial electrocardiograms were con-sistent with a diagnosis of recent, subendocardial, antero-lateral infarction as well as old anterolateral infarction.The patient began to improve after the third hospitalday and thenceforth made an uneventful recovery.

T. P.-A 63 year old male, who had suffered withasthma for six years, developed paraesthesias of the leftarm and hand for three weeks and severe continuous sub-sternal pain without radiation for one day prior to admis-sion to the hospital. The patient was dyspneic, mentallydulled and exhibited crackling rales at both lung bases.The electrocardiogram indicated anteroseptal infarction.Several days following admission the patient developeda hemiparesis, which, however, gradually cleared and thefurther course was uneventful.

D. S.-This 64 year old male developed diabetes mel-litus one year ago at which time the electrocardiogram wasinterpreted as indicating "coronary insufficiency." Twodays prior to admission to the hospital he developed crush-ing substernal pain radiating to the left shoulder. Therewas slight dyspnea but the lungs were clear. The elec-trocardiogram indicated recent posterior infarction andAV block with 2 to 1 conduction. On the second hospitalday he developed hypotension, bradycardia and oliguriaand died on the following day. Autopsy was not ob-tained.

R. E.-This 56 year old male, who had mild essentialhypertension and diabetes mellitus for many years, suf-fered a posterior myocardial infarction three years ago.He was admitted to the hospital because of an attack ofpulmonary edema. Response to therapy was slow andwhile convalescing he developed typical anginal pain anda recurrence of congestive heart failure. The electro-cardiogram indicated a recent anteroseptal infarction.The hemodynamic studies were carried out on the sec-ond day of this attack. The patient appeared to recoverfrom this episode but died suddenly five weeks later dur-ing a third attack of angina and acute pulmonary edema.

F. McC.-This 58 year old male had experienced an-gina on effort for the past six months. On the eveningof admission to the hospital he developed squeezing sub-sternal pain accompanied by sweating and dyspnea.There were fine moist rales at both bases and a pleuroperi-cardial friction rub was heard. The electrocardiogramdisclosed posterior and lateral subendocardial infarction.Three days after admission he developed hypotension,extreme prostration, cyanosis, increased pulmonary rales,

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E. D. FREIS, H. W. SCHNAPER, R. L. JOHNSON, AND G. E. SCHREINER

hepatomegaly and oliguria but no orthopnea. He re-mained in this state for an additional 10 days, the bloodnon-protein nitrogen rising gradually during this periodto a level of 210 mg. per cent two days before death.

.No autopsy was performed.P. C.-A 57 year old male suffered a cerebrovascular

accident two years ago and an acute myocardial infarc-tion one year ago. Since the latter lie had frequent boutsof angina particularly at night. On the (lay of admissionhe developed mild but continuous pain in the parasternalarea. On admission he appeared pale with cold handsand feet and was dyspneic and orthopneic. The heartwas enlarged, the lungs moderately congested and theliver edge was palpated 4 cm. below the costal margin.The electrocardiogram revealed the pattern of freshanterolateral infarction. The blood pressure remainedlow, the congestive heart failure increased and the pa-tient died after one week in the hospital. Permission forautopsy was refused.

G. McK.-A 54 year old male who previously had beenin excellent health developed transient substernal paintwo months before admission to the hospital. On themorning of admission he was awakened \vith severe sub-sternal pain radiating to the left arm accomnl)anied by pro-fuse sweating but no dyspnea. On admission he appearedto be in shock with distant heart sounds and fine moistrales at the lung bases. The electrocardiographic changesindicated acute anteroseptal infarction, intraventricularblock (R.B.B.B. type) and frequent interpolated ventricu-lar beats. The clinical course was characterized by in-creasing shock with mental confusion and later delirium.The signs of congestive heart failure, except for dyspnea,never were prominent and there was n1o orthopnea. Theblood nonprotein nitrogen rose gradually to 137 mg. percent and he died six days after admission. Autopsy re-vealed coronary thrombosis left and infarction of the en-tire wall of the left ventricle extending into the inter-ventricular septum. There was also chronic passive con-gestion of the lungs, liver, spleen and gastrointestinaltract.

ACKNOWLEDGMENT

The authors wish to acknowledge the valuable assistancegiven by Dr. Robert Kelley and Mr. Victor R. Landi.

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