hypovolemia in shock due to acute myocardial...

8
Hypovolemia in Shock Due to Acute Myocardial Infarction By HENRY S. LOEB, M.D., RAYMOND J. PIETRAS, M.D., JoHN R. TOBIN, JR., M.D., AND ROLF M. GUNNAR, M.D. SUMMARY Twelve patients with the clinical features of shock following acute myocardial infarction were treated with low molecular weight dextran (LMWD) as a plasma volume expander. Two of the patients had elevated central venous pressures (CVP), and neither responded favorably to plasma volume expansion. The remaining 10 patients had CVPs under 7 mm Hg prior to dextran infusion; five survived. Each survivor re- sponded favorably to dextran infusion manifested by an increase in arterial pressure and cardiac index. The average increase in CVP in these patients was 1.0 mm Hg per 100 ml of dextran infused. The other five patients died either without recovering from shock or in chronic cardiac failure. These patients failed to show a significant increase in arterial pressure or cardiac index after dextran infusion; CVP increased by an average of 1.9 mm Hg per 100 ml infused. Hypovolemia must be considered in all patients in whom clinical evidence of shock develops as a complication of acute myocardial infarction, and if the CVP is normal or low, plasma volume expansion should be undertaken with caution. Increase in arterial pressure and evidence of improved cardiac index with little rise in CVP indicate a good response to the infusion and ex- cellent prognosis for survival. Additional Indexing Words: Central venous pressure Dextran Pulmonary arterial pressure Cardiac index HYPOVOLEMIA is not considered to be a basic defect in shock associated with acute myocardial infarction and has seldom been recognized as an early complication. However, through routine monitoring of the CVP, we have been made aware of the frequency of this defect in patients in whom circulatory insufficiency or shock develops after acute myocardial infarction. Because hypovolemia is easily treated, some investiga- From the Department of Adult Cardiology and the Hektoen Institute for Medical Research of the Cook County Hospital; the Section of Cardiology, Depart- ment of Medicine, University of Illinois College of Medicine, Chicago, Illinois; and the Department of Medicine of the Loyola University Stritch School of Medicine, Hines, Illinois. Supported in part by Grant HE-08834, from the National Institutes of Health, U. S. Public Health Service. Circulation, Volume XL, November 1969 tors have advocated plasma volume expansion of all patients in whom shock develops after myocardial infarction.' On the other hand, the potential hazards of such therapy in the presence of severe myocardial damage has caused us to attempt to establish some guidelines for using plasma volume expanders in these patients. We have conducted hemo- dynamic studies on 40 patients with circula- tory insufficiency or shock complicating acute myocardial infarction. We report here the clinical and hemodynamic responses to low molecular weight dextran (LMWD) in 12 of these patients, 10 of whom had control CVPs of less than 7 mm Hg (10 cm H20). Methods Patients were selected for study because they presented the clinical features of shock (obtunda- tion, weak pulses, cold extremities, and oliguria) following acute myocardial infarction. Mean 653 by guest on June 23, 2018 http://circ.ahajournals.org/ Downloaded from

Upload: vukhanh

Post on 16-May-2018

216 views

Category:

Documents


1 download

TRANSCRIPT

Page 1: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

Hypovolemia in Shock Due to AcuteMyocardial Infarction

By HENRY S. LOEB, M.D., RAYMOND J. PIETRAS, M.D., JoHN R. TOBIN, JR., M.D.,

AND ROLF M. GUNNAR, M.D.

SUMMARYTwelve patients with the clinical features of shock following acute myocardial

infarction were treated with low molecular weight dextran (LMWD) as a plasmavolume expander. Two of the patients had elevated central venous pressures (CVP),and neither responded favorably to plasma volume expansion. The remaining 10 patientshad CVPs under 7 mm Hg prior to dextran infusion; five survived. Each survivor re-

sponded favorably to dextran infusion manifested by an increase in arterial pressure

and cardiac index. The average increase in CVP in these patients was 1.0 mm Hg per

100 ml of dextran infused. The other five patients died either without recovering fromshock or in chronic cardiac failure. These patients failed to show a significant increasein arterial pressure or cardiac index after dextran infusion; CVP increased by an

average of 1.9 mm Hg per 100 ml infused. Hypovolemia must be considered in allpatients in whom clinical evidence of shock develops as a complication of acutemyocardial infarction, and if the CVP is normal or low, plasma volume expansion shouldbe undertaken with caution. Increase in arterial pressure and evidence of improvedcardiac index with little rise in CVP indicate a good response to the infusion and ex-

cellent prognosis for survival.

Additional Indexing Words:Central venous pressureDextran

Pulmonary arterial pressure Cardiac index

HYPOVOLEMIA is not considered to be abasic defect in shock associated with

acute myocardial infarction and has seldombeen recognized as an early complication.However, through routine monitoring of theCVP, we have been made aware of thefrequency of this defect in patients in whomcirculatory insufficiency or shock developsafter acute myocardial infarction. Becausehypovolemia is easily treated, some investiga-

From the Department of Adult Cardiology and theHektoen Institute for Medical Research of the CookCounty Hospital; the Section of Cardiology, Depart-ment of Medicine, University of Illinois College ofMedicine, Chicago, Illinois; and the Departmentof Medicine of the Loyola University StritchSchool of Medicine, Hines, Illinois.

Supported in part by Grant HE-08834, from theNational Institutes of Health, U. S. Public HealthService.

Circulation, Volume XL, November 1969

tors have advocated plasma volume expansionof all patients in whom shock develops aftermyocardial infarction.' On the other hand, thepotential hazards of such therapy in thepresence of severe myocardial damage hascaused us to attempt to establish someguidelines for using plasma volume expandersin these patients. We have conducted hemo-dynamic studies on 40 patients with circula-tory insufficiency or shock complicating acutemyocardial infarction. We report here theclinical and hemodynamic responses to lowmolecular weight dextran (LMWD) in 12 ofthese patients, 10 of whom had control CVPsof less than 7 mm Hg (10 cm H20).

MethodsPatients were selected for study because they

presented the clinical features of shock (obtunda-tion, weak pulses, cold extremities, and oliguria)following acute myocardial infarction. Mean

653

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 2: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

LOEB ET AL.

intra-arterial pressure (measured prior to vaso-pressor therapy) was less than 80 mm Hg in allbut three patients. These three each had historicaland clinical evidence of pre-existing hypertension.In addition, at the onset of clinical shock thesethree patients had blood pressures (obtained bythe cuff method) that were significantly less thanon admission. The diagnosis of acute myocardialinfarction was verified by necropsy in threepatients and by history, electrocardiogram, orserum enzyme changes in all.The decision to expand intravascular volume in

10 of the patients was based on the findings of anormal or low CVP (under 7 mm Hg). In twopatients although the CVP was slightly elevated(10.5 and 12 mm Hg), volume expansion wasattempted in the hope that a further increase inventricular filling pressure might improve cardiacoutput. It should be emphasized that the majorityof our patients with circulatory insufficiency orshock after acute myocardial infarction have hadelevated control CVPs, and thus the question ofplasma volume expansion has not arisen.

Patients were studied at the bedside or in aspecially equipped study unit. Arterial pressure(MAP) and CVP were measured with atransducer through catheters threaded into thecentral aorta and superior vena cava or rightatrium after surgical exposure of the rightbrachial vessels. Cardiac output (CO) wasmeasured by the indicator-dilution method bymeans of indocyanine green injected through theCVP catheter and sampling from the centralaortic catheter. Values for CO were obtained byaveraging two to five indicator-dilution curvesand were corrected for body surface area (CI).We have found this method to be reproducibleto + 5% when done in rapid succession on thesame patient. Pressure pulses, dilution curves,and a standard electrocardiogram lead wererecorded on a photographic recorder. Systemicvascular resistance (SVR) was calculated as

follows: SVR_ MAP-CVP.CO

Immediately after control measurements LMWDwas given in an amount averaging 580 ml(range 200 to 1,000) at an average infusion rateof 7.6 ml per minute (range 4.4 to 12.0). Allmeasurements were repeated within a fewminutes after completion of the LMWD infusion.Infusions of norepinephrine (in two patients) andisoproterenol (in one patient) were continued ata constant rate throughout the LMWD studyperiod. One patient received 10 mg of morphinesulfate during the time LMWD was beinggiven.

ResultsTwo patients, one of whom was receiving

isoproterenol throughout the study period,had control CVPs over 7 mm Hg and did notrespond to LMWD by significant increases inCI, urine flow, or evidence of clinicalimprovement. Although one patient had amodest rise in MAP (14 mm Hg) afterLMWD, his ultimate recovery from shock wasunrelated to plasma volume expansion, and helater died of refractory cardiac failure. Theother patient failed to recover from shock.Both of these patients had massive myocardialinfarction demonstrated at necropsy.The remaining 10 patients all had normal or

low CVPs (less than 7 mm Hg) beforeinfusion of LMWD and were divided into twogroups on the basis of survival. Five of thesepatients (group A) showed marked clinicalimprovement and increased urine flow (aver-age increase being 1.7 ml per minute) afterreceiving LMWD. These patients all survivedtheir illness and were eventually dischargedfrom the hospital. Four of the remaining fivepatients (group B) failed to show clinicalimprovement or significant increases in urineflow after receiving LMWD, and none ofthese five survived to be discharged from thehospital, although two recovered from shockonly to die later of cardiac failure.Comparison is made between the two

groups to determine if additional criteriacould aid in the early selection of thosepatients in shock after acute myocardialinfarction who can be expected to benefitfrom plasma volume expansion.

Certain clinical differences between the twogroups were apparent. The average age ofgroup A patients was 48 (range 42 to 52)years, whereas group B patients averaged 69(range 50 to 85) years. None of the group Apatients were known to have had previousmyocardial infarction, whereas two patients ingroup B had histories and electrocardiographicevidence of previous infarction. Inferior wallinfarction was present in three of the fivegroup A patients, and anterior infarctionoccurred in four of the five group B patients.The degree of serum enzyme elevation didnot, however, differ between the groups.Although a probable cause for hypovolemia

Circulation, Volume XL, November 1969

654

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 3: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

HYPOVOLEMIA IN SHOCK

Table 1Hemodynamic Status in Graups A and B

Patient

Group A A.F.M.G.H.S.B.M.E.G.

Mean ± SD

LMWD Infusionvolume rate

Age (ml) (ml/min)

425243524948

500100010004501000790

9.65.88.38.34.8

7.4 i 1.8

MAP(mm Hg)

103*85t6089t66

78 i 15

Control

CVP(mm Hg)

1.5001

0.50.7 + 0.7

After LMWD

CI MAP CVP(L/min/m2) (mm Hg) (mm Hg)

1.92.52.32.52.1

2.2 4 0.2

12092929793

99 4 11

4.59.57.08.08.0

7.4 4 1.7

Group B-V.B.A.P.K.W.

(NE) A.W.(NE) J.A.

Mean ± SD

735085806070

400500500200500420

6.77.75.54.4

11.97.2 ± 2.6

6162639066

68 4± 10

6.51.504.50

2.5 ± 2.6

2.13.93.21.93.6

2.9 i 0.8

4853788869

67 ± 15

(NE) Received norepinephrine at constant infusion rate throughout study period.* Admission blood pressure 190/140 (cuff) fell to 100/70 (cuff) before study.t Admission blood pressure 110/80 (cuff) fell to 85/60 (cuff) before study.I Admission blood pressure 150/110 (cuff) fell to 40 systolic by palpation before study.

could be found in all group A patients, in onlyone group B patient was it possible toestablish a possible reason for hypovolemia.Group A also differed from group B in

terms of hemodynamic status both before andafter LMWD infusion (table 1). BeforeLMWD infusion hypotension was less markedin group A than in group B patients; afterinfusion, each group A patient showed an

increase in MAP averaging 18±10 mm Hg(mean + SD), whereas only one group Bpatient responded to LMWD with a signifi-cant increase in MAP; the average change forgroup B was a fall of 1 + 10 mm Hg.CVP increased in all patients during infu-

sion of LMWD; however, when changes inCVP were related to the amount of LMWVDinfused, group A patients increased their CVPby a mean of 1.0 0.4 mm Hg per 100 ml ofLMWD infused, significantly less than the1.9 0.3 mm Hg per 100 ml for patients ingroup B (P<0.02).Circulation, Volume XL, November 1969

Values for heart rate prior to LMWD were

not significantly different between the groupsand tended to be slightly lower after infusionof LMWD in most patients in both groups.

Prior to LMWD, CI averaged 2.2 + 0.2L/min/m2 for group A and 2.9 0.8 L/min/m2 for group B. After LMWD infusion every

group A patient had increased CI by at least0.7 L/min/m2, with an average increase of 1.5+ 0.9 L/min/m2. Only two patients in group Bshowed significant increases in CI afterLMWD, and the average increase for all fivepatients was 0.1 0.8 L/min/m2.

Left ventricular pressure was measuredbefore infusion of LMWD in two patients,one in each group, by passing a catheterretrograde across the aortic valve. Thesepatients are presented in some detail.

Case 1

A.F., a 42-year-old Negro man with a pasthistory of hypertension and anginal pain was

admitted after 4 days of increasingly severe

CL(L/min/m2)

2.63.55.53.93.4

3.8 ± 1.0

16.58.0

14.07.57.5

10.7 4± 3.8

1.72.74.22.24.5

3.1 ± 1.1

655

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 4: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

LOEB ET AL.

anterior chest pain unrelieved by rest. Onadmission the patient complained of severe chestpain and required morphine. Blood pressure was190/140, and the pulse was 80 and regular.Cardiac enlargement and a presystolic gallopwere present. There was no evidence of conges-tive failure. The electrocardiogram showedchanges typical of an acute inferior wallinfarction, and serial enzymes were confirmatory.The patient was given reserpine, and his bloodpressure decreased to 120/80. He continued tocomplain of severe chest pain and 2 days afteradmission atrial fibrillation with a rapid ven-tricular response occurred. Electrocardiographicchanges suggested extension of the originalinfarct with involvement of the posterior basalleft ventricle. Although there was no evidence ofcardiac failure, digoxin was given to control therapid ventricular rate. The patient began tocomplain of nausea and vomiting, which per-sisted. Four days after admission blood pressureby cuff was found to be 100/70 mm Hg. Thepulse was weak, and the extremities were coldand clammy. Urine flow was 30 ml per hour.Hemodynamic measurements revealed a CVP

of 1.5 mm Hg and a left ventricular end-diastolicpressure (LVEDP) of 4.5 mm Hg. MAP was 103mm Hg but the pulse pressure was only 32 mmHg. CI was 1.9 L/min/m2. The patient was given500 ml of LMWD, and the CVP increased byonly 3 mm Hg. During this infusion MAP rose to120 mm Hg, pulse pressure increased to 48 mmHg, and CI to 2.6 L/min/m2. Urine flowincreased to 170 ml per hour, and upon returningto the ward blood pressure by the cuff methodwas 140/90 mm Hg. A few days later sinusrhythm returned spontaneously. Recovery wasuneventful, and upon discharge the patient wasasymptomatic and did not require digitalis.Comment. In this patient circulatory insuffi-

ciency was clearly related to hypovolemia due toinadequate fluid intake, diaphoresis, and vomit-ing. However, until the CVP was measured,hypovolemia was unrecognized. The normalLVEDP, his rapid improvement when givenvolume, and his subsequent course all attest tothe fact that myocardial failure following acutemyocardial infarction was not the cause of thecirculatory insufficiency.Case 2

A.P., a 50-year-old Negro man, was admittedfor severe substernal pain. The patient had beenhospitalized 3 months previously for acutemyocardial infarction. For 5 years prior to this hehad been treated for hypertension. He had beenasymptomatic for 2 months, and this wasinterrupted by the onset of chest pain 2 daysbefore admission. On admission, the patient wasalert and complained of chest pain. Blood

pressure was 90/60 mm Hg, pulse 130 perminute, and temperature 101.6 F. The lungswere clear. Cardiac enlargement and a "summa-tion" gallop were present. An electrocardiogramshowed evidence of an old anterolateral andrecent inferior myocardial infarction. Hemody-namic studies were initiated shortly after admis-sion. After the catheters had been inserted, thepatient developed rigors and a further elevationof temperature to 106 F. The catheters werechanged, and when the rigors had subsided,measurements were made. CVP, which had been7 mm Hg, fell to 1.5 mm Hg; however, LVEDPremained elevated at 24 mm Hg. MAP was 63mm Hg and CI was 3.9 L/min/m2. When 700 mlof LMWD had been infused, the CVP hadincreased to 10.5 mm Hg, MAP had fallen to 56mm Hg, and CI had fallen to 2.6 L/min/m2. Thetemperature had fallen to 101.8 F. The patient wasrapidly digitalized, and this resulted in a rise inMAP and CI, while CVP and HR fell. Thepatient's condition stabilized; however, during theremainder of his hospital course he complained ofsevere dyspnea and orthopnea, which remainedrefractory to vigorous medical therapy until hedied in cardiac failure 2 weeks after admission.Comment. The patient had severe cardiac

damage from at least two myocardial infarctions.Although CVP was low after an apparent pyrogenreaction, LVEDP was markedly elevated. Plasmavolume expansion was accompanied by anelevation in CVP but MAP and CI fell, indicatingthat hypovolemia was not responsible for thepatient's circulatory insufficiency. Digitalization,which had been withheld at first because of thelow CVP, clearly resulted in hemodynamicimprovement.

Discussion

Although hypovolemia is not present in themajority of patients with acute myocardialinfarction, it should be searched for in allpatients in whom shock or circulatory insuffi-ciency-develops. From our data, measurementof the CVP and, when nornal or low, CVPmonitoring during a careful therapeutic trialof plasma volume expansion are safe andpractical methods for identifying those pa-tients able to respond to volume expansion.When the CVP is elevated above normal

(above 7 mm Hg), volume administrationalone is unlikely to result in significanthemodynamic improvement. These patientsusually have severe myocardial damage andfail to increase cardiac output when given

Circulation, Volume XL, November 1969

656

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 5: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

HYPOVOLEMIA IN SHOCK

intravenous infusions. If plasma volume ex-pansion is to be attempted in such patients, itmust be done with extreme caution.When the CVP is not elevated and yet the

patient shows evidence of circulatory insuffi-ciency or shock following acute myocardialinfarction, hypovolemia must be suspected.Under these circumstances, a therapeutic trialof plasma volume expansion is indicated. Afavorable response to fluid administration canbe recognized by an increase in arterialpressure, pulse volume, and urine flow ac-companied by clinical improvement. The CVPwill remain low or increase minimally. Thepatients in group A (responding well tovolume expansion) showed a mean rise inCVP of only 1.0 mm Hg per 100 ml of LMWDadministered, and the highest was only 1.5mm Hg per 100 ml infused. This responseis most likely to be seen in younger pa-tients with minimal myocardial damage andindicates an excellent prognosis. When, how-ever, fluid administration results in a rapidincrease in the CVP and shock or circulatoryinsufficiency persists, severe myocardial dam-age is probably present. The patients ingroup B (poor response to volume expan-sion) had a mean rise in the CVP of 1.9mm Hg per 100 ml of LMWD infused, andthe least rise was 1.3 mm Hg per 100 ml.These patients were elderly, had lower initialblood pressures than group A patients, andhad clinical or postmortem evidence, or both,of severe myocardial damage.Although we did not measure total blood

volume in our patients, others have foundnormal or slightly reduced blood volumes inpatients with shock after acute myocardialinfarction.2-4 It is likely that the hemodynamicalterations present in the shock patientprohibit the use of standard normal values forblood volume in determining the need forfluid administration.5' 6We have used the CVP and its response to

plasma volume expansion as a guide to fluidtherapy. This type of therapeutic trial andmonitoring has been proved to be of greatvalue in other types of shock.A9 It should bestressed that in addition to intravascularCirculation, Volume XL, November 1969

volume, the CVP is influenced by changes invenous tone and by changes in the complianceof the right ventricle. Under conditions ofincreased venous tone or decreased rightventricular compliance, or both, the CVPmight be normal in spite of an inadequateintravascular volume.3

Since myocardial infarction usually involvesthe left ventricle, and since a sudden rise inLVEDP during fluid administration can pre-cipitate acute pulmonary edema, it is impor-tant to determine the relation between theCVP and LVEDP. Increases in CVP havebeen shown to reflect increases in LVEDPduring experimental volume overload.10 Cohn,and associates" have made simultaneousmeasurements of the CVP and LVEDP innine patients with acute myocardial infarctionand shock, and in none did LVEDP risewithout a concomitant rise in CVP. We havemade a similar observation in 23 patients withvarious types of shock in whom we havemeasured CVP and LVEDP during plasmavolume expansion.12 Although in the twopatients presented here LVEDP was notmeasured following LMWD, the rapid rise inthe CVP in the patient whose initial LVEDPwas elevated supports the contention that,even in acute myocardial infarction, monitor-ing the CVP is a safe guide for a trial ofplasma volume expansion.

It is possible to precipitate pulmonaryedema in the presence of a normal CVP inpatients with acute myocardial infarction byadding small amounts of fluid, and, therefore,measurement of LVEDP is the ideal methodfor monitoring this form of therapy. However,the CVP measurement can easily be madeand, if used as a dynamic measurement, canreflect directional changes in LVEDP ifaddition of volume is the only therapeuticchange being made.12 The catheter can also beused to withdraw fluid, should pulmonaryedema develop.A normal SVR in spite of a reduced CI has

been frequently observed in patients withshock due to acute myocardial infarction.2 1 14The mechanism for this absence of compensa-tory vasoconstriction is unclear; however, a

657

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 6: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

LOEB ET AL.

similar mechanism might cause a decreasein venous tone and low CVP in patientshaving normal or elevated blood volumes.Although our patients in groups A and Bhad similar values for SVR, it is possiblethat reduced venous tone was partly responsi-ble for normal or low CVPs in some of ourgroup B patients. Group A patients, however,responded well to fluid therapy, and wepostulate that hypovolemia was the majorcause for their low CVPs and circulatoryinsufficiency.The incidence of hypovolemia complicating

acute myocardial infarction is probably low,and the routine administration of significantvolume loads to all patients with shock doesnot seem justified. The use of vasodilatoragents coupled with plasma volume loadinghas been advocated;'5 however, this form oftherapy has yet to be evaluated clinically andshould be reserved for those patients whoalthough manifesting clinical signs of shock,are able to maintain adequate intra-arterialpressures in spite of vasodilator therapy.Langsjoen and associates'6 have reported a

reduced mortality in patients with acutemyocardial infarction treated with low mo-

lecular weight dextran. Therapy in thesepatients was designed to reduce intravascularsludging rather than to expand intravascularvolume, and the rate of administration was

significantly less than in our patients. Theyhave postulated correction of undetectedhypovolemia as contributing to improvedsurvival in these patients. Since we did notcompare our infusions with equal amounts ofdextrose or saline solution infusions, it isimpossible for us to know whether the dextransolution had any effect in addition to itscontribution to plasma volume.

Allen and others'7 reported hypovolemia tobe present in 20% of patients with cardiogenicshock. Although this figure corresponds closelyto our own experience, it has undoubtedlybeen inflated by exclusion of patients present-ing with profound shock due to rapidlyprogressing pump failure, since such patientsfrequently do not survive long enough forhemodynamic measurements to be obtained.

There are many mechanisms by whichhypovolemia can develop after acute myocar-dial infarction:

1. Inadequate fluid intake is common, andparenteral fluid administration is frequentlykept at a minimum for fear of precipitatingcardiac failure.

2. Excessive loss of fluids may occur be-cause of fever and diaphoresis, the use ofpotent diuretics for pulmonary edema, and asa result of nausea and vomiting secondary topain or drugs.

3. A shift of fluid from the intravascular tothe extravascular compartments, or trappingof red cell aggregates in various capillary bedsmay result in a reduced effective circulatingblood volume. This is most likely to occur inpatients who remain vasoconstricted for pro-longed periods, either from compensatorymechanisms or from the use of various pressoragents.'8 Also, acute acidosis following tempo-rary circulatory arrest may result in suddenmarked loss of intravascular volume.

4. In addition to the primary illness,associated illnesses such as sepsis or gastroin-testinal bleeding may cause hypovolemia inpatients with acute myocardial infarction and,if unrecognized, may lead to a decrease incoronary flow and extension of the myocardialdamage.

References1. NIXON, P. G. F., IKROM, H., AND MORTON, S.:

Cardiogenic shock treated with infusion ofdextrose solution. Amer Heart J 73: 843,1967.

2. SMITH, W. W., WICKLER, N. S., AND Fox, A. C.:Hemodynamic studies of patients with myocar-dial infarction. Circulation 9: 352, 1954.

3. FREWs, E. D., ScHNAPER, H. W., JOHNSON, R. L.,AND ScHREINNm, G. E.: Hemodynamic altera-tions in acute myocardial infarction: I. Cardiacoutput, mean arterial pressure, total peripheralresistance, "central" and total blood volumes,venous pressure and average circulation time. JClin Invest 31: 131, 1952.

4. SHUBIN, H., BRADLEY, E. C., AND WEIL, M.:Hemodynamic and metabolic observationsduring the course of shock complicatingmyocardial infarction. (Abstr.) Circulation 36(suppl. II): 11-237, 1967.

5. THAL, A. P., AND KINNEY, J. M.: On the

Circulation, Volume XL, November 1969

658

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 7: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

HYPOVOLEMIA IN SHOCK

definition and classification of shock. ProgrCardiovasc Dis 9: 527, 1967.

6. WEIL, M. H., SHUBIN, H., A"N ROSOFF, L.:Fluid repletion in circulatory shock: Centralvenous pressure and other practical guides.JAMA 192: 668,1965.

7. JACOBSON, E. D.: A physiologic approach toshock. New Eng J Med 278: 834, 1968.

8. WiLsON, J. N.: Rational approach to themanagement of clinical shock. Arch Surg 91:92, 1965.

9. LOEB, H. S., ET AL.: Haemodynamic studies inshock associated with infection. Brit Heart J29: 883, 1967.

10. HANASHIRO, P. K., Arm WEnu, M. H.: Relation-ship of intracardiac pressures after volumeoverload. (Abstr.) Clin Res 16: 108, 1968.

11. COHN, J. N., KiAERI, I. M., AND TRISTANI, F. E.:Left and right ventricular filling pressuresin clinical shock. (Abstr.) Ann Intern Med 68:1153, 1968.

12. LoEB, H. S., GUNNAR, R. M., PIrARAs, R. J., ANDTOBIN, J. R., JR.: Relationships betweencentral venous and left ventricular fillingpressures prior to and during treatment ofshock. (Abstr.) Amer J Cardiol 23: 125,1969.

13. KuHN, L. A.: Changing treatment of shockfollowing acute myocardial infarction: Aclinical evaluation. Amer J Cardiol 20: 757,1967.

14. GUNNAR, R. M., PiETRAs, R. J., STAVRAKOS, C.,Loim, H. S., AND TOBIN, J. R., JR.: Thephysiologic basis for treatment of shockassociated with myocardial infarction. MedClin N Amer 51: 69, 1967.

15. BLOCH, J. H., PIERCE, C. H., MANAX, W. G., ANDLILLEYHEI, R. C.: Treatment of experimentalcardiogenic shock. Surgery 58: 197, 1965.

16. LANGSJOEN, P. H., FALCONER, H. S., SANCHEZ,S. A., AND LYNCH, D. J.: Observations intreatment of acute myocardial infarction withlow molecular dextran. Angiology 14: 465,1963.

17. ALLEN, H. N., DANZIG, R., AND SWAN, H. J. C.:Incidence and significance of relative hypo-volemia as a cause of shock associated withacute myocardial infarction. (Abstr.) Circula-tion 36: (suppl.) II): II-50, 1967.

18. BoTTICELLI, J. T., TSAGARIS, T. J., AND LANGE,R. L.: Mechanisms of pressor amine depen-dence. Amer J Cardiol 16: 847, 1965.

Circulation, Volume XL, November 1969

659

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from

Page 8: Hypovolemia in Shock Due to Acute Myocardial Infarctioncirc.ahajournals.org/content/circulationaha/40/5/653.full.pdf · HYPOVOLEMIA IN SHOCK Table 1 HemodynamicStatus in Graups AandB

GUNNARHENRY S. LOEB, RAYMOND J. PIETRAS, JOHN R. TOBIN, JR. and ROLF M.

Hypovolemia in Shock Due to Acute Myocardial Infarction

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1969 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.40.5.653

1969;40:653-659Circulation. 

http://circ.ahajournals.org/content/40/5/653located on the World Wide Web at:

The online version of this article, along with updated information and services, is

  http://circ.ahajournals.org//subscriptions/

is online at: Circulation Information about subscribing to Subscriptions: 

http://www.lww.com/reprints Information about reprints can be found online at: Reprints:

  document. and Rights Question and Answer

Permissionsthe Web page under Services. Further information about this process is available in thewhich permission is being requested is located, click Request Permissions in the middle column ofClearance Center, not the Editorial Office. Once the online version of the published article for

can be obtained via RightsLink, a service of the CopyrightCirculationoriginally published in Requests for permissions to reproduce figures, tables, or portions of articlesPermissions:

by guest on June 23, 2018http://circ.ahajournals.org/

Dow

nloaded from