Hemodynamic monitoring in acute myocardial infarction JOHN A. CAIRNS,* MD, FRCP[C], FACC

The main cause of in-hospital death in patients with acute myocardial infarction is the "power failure syndrome". Hemodynamic monitoring provides precise and current data on the filling and output* status of the left ventricle and, when indicated, the right ventricle. The information obtained is used to determine the hemodynamic status more precisely than is possible from conventional clinical assessment. It permits categorization of patients by hemodynamic status; the hemodynamic subset classification of Forrester, Diamond and Swan is a powerful tool in guiding therapy and establishing prognosis in individual patients. In addition to guiding the initiation of therapy, hemodynamic monitoring is useful in the continuing assessment of potent and complex treatment. This therapy is directed at resolving hemodynamic derangements without unfavourably altering the myocardial oxygen supply-demand relationship. Specific clinical indications for hemodynamic monitoring may include confusing or complicated clinical situations in which diagnostic problems exist, complicating mechanical derangements, severe congestive heart failure, cardiogenic shock and clinical research in acute myocardial infarction. La principale cause des deces hospitaliers chez les patients frappes d'infarctus du myocarde est le "syndrome de perte de puissance". La surveillance h6modynamlque assure des donnees precises et actuelles sur l'etat de remplissage et de debit du ventricule gauche et, quand cela est indique, du ventricule droit. L'information obtenue est utilisee pour determiner le statut hemodynamique avec plus de precision qu'il n'est possible par l'evaluation clinique conventionnelle. Cela permet Ia classification du patient selon son statut hemodynamique; Ia classification hemodynamique de Forrester, Diamond et Swan est un puissant instrument permettant d'orienter le traitement et d'etablir le pronostic chez chacun des patients. En plus d'orienter Ia mise en route du traitement, Ia surveillance hemodynamique est utile . l'6valuation continue d'un traitement puissant et complexe. Ce traitement est oriente vers Ia resolution des perturbations hemodynamiques sans que le rapport de fourniture et de Ia demande d'oxygene du myocarde ne soit altere d6favorablement. Les indications cliniques specifiques de Ia surveillance hemodynamique peuvent comprendre des situations cliniques deroutantes ou complexes ou ii existe des problemes de diagnostic, des derangements mecaniques qui compliquent Ia situation, l'insuffisance cardiaque congestive grave, le choc cardiogene et Ia recherche clinique dans l'infarctus aigu du myocarde.

The management of the electrical complications of acute myocardial infarction has accounted for most of the reduction of in-hospital mortality accomplished by coronary care units in the past 15 years. However, an in-hospital mortality of 12% to 18% persists. This is *A.istant professor, department of medicine, McMaster University and director, intensive care and coronary care units, McMaster University Medical Centre Reprint requests to: Dr. John A. Cairns, Division of cardiology, McMaster University Medical Centre, 1200 Main St. W, Hamilton, Ont. L8S 4J9

almost exclusively the result of mechanical dysfunction that gives rise to the "power failure syndrome", which is characterized by severe congestive heart failure and cardiogenic shock.1 It is primarily to the problem of these mechanical consequences of myocardial infarction that hemodynamic monitoring is directed. Recently there has been increased awareness of the dynamic nature of acute myocardial infarction. It is now recognized that the patient admitted with an infarction has a significant mass of myocardium that has not yet become necrotic but is at risk of doing

..*2.3 This so-called border zone is thus particularly sensitivc to any unfavourable alteration in the myocardial oxygen supply-demand relationship; hence, therapy undertaken to alleviate the mechanical consequences of acutc myocardial infarction should be aimed not only at improving myocardial performance but also at favourably altering the oxygen supply-demand relationship so as to avoid extension of the area of necrosis. Purpose of hemodynamic monitoring The purpose of hemodynamic monitoring is to obtain accurate knowledge of cardiovascular function from precise and current data on the filling and output status of the heart. Since acute myocardial infarction produces regional cardiac dysfunction, thereby disturbing the normal relations between right and left ventricular filling, central venous pressure measurements give little useful information about the status of the left ventricle and may be misleading in some instances.4 Acute myocardial infarction is a clinical condition in which accurate assessment of left ventricular function is most important. One achieves this by placing a balloon flotation catheter in the pulmonary artery to measure the pulmonary capillary wedge pressure (PCW) and the cardiac output (CO) by thermodilution or other techniques. Additional information may be gained by recording the right atrial pressure so as to assess right ventricular function, and the intraarterial pressure so as to assess the perfusion pressure of vital organs, particularly the heart, brain and kidneys. The potential gains provided by hemodynamic monitoring must be weighed against the risks; this point is further discussed elsewhere in this symposium.

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Precise determination of hemodynamic classification

The clinical assessment always precedes and dictates the advisability of hemodynamic monitoring. Clinical manifestations of left ventricular dysfunction (rales, dyspnea, tachypnea and roentgenographic abnormalities) reflect an elevated PCW, whereas signs of hypoperfusion (decreased blood pressure, decreased urine output, cool and clammy skin, and mental confusion and obtundation) reflect a decreased CO. Forrester, Diamond and Swan5 have demonstrated that early in the course of acute myocardial infarction the clinical assess-

ment of the filling and output functions of the left ventricle is relatively good. However, among the patients they assessed, 25% of those with an elevated PCW and 15% of those with a low CO had insufficient clinical evidence for diagnosis of these derangements. Deficiencies of clinical assessment may become more marked once interventions are begun and time has passed; this has been discussed in this symposium by Holder. An example is the phase lag in chest roentgenographic findings as compared with actual left atrial pressure.6 Accurate and current information is only obtainable by hemodynamic monitoring.

Table I-Clinical and hemodynamic subsets in acute myocardial infarction Clinical status

Hemodynamic status* Pulmonary Peripheral Subset congestion hypoperfusion Cl (I/mm. rn-2) PCW (mm Hg) Absent Absent > 2.2 < 18 II Present Absent > 2.2 . 18 Ill Absent Present ( 2.2 < 18 IV Present Present . 2.2 . 18 *CI = cardiac index; PCW = mean pulmonary capillary wedge pressure.

Classification of patients from clinical evaluation has been a practice of physicians for many years. Such classification has been subjective and qualitative but has been formalized by various workers. .' These approaches have some value in the initial assessment of patients with acute myocardial infarction but are not precise or responsive enough to guide the management of individual patients. The simple subset classification of Forrester and colleagues'0 (Table I) is clinically relevant. These workers initially divided patients into four subsets on the basis of the clinical findings of pulmonary congestion and peripheral hypoperfusion. Hemodynamic evaluation was then performed and the patients were classified into four analogous hemodynamic subsets. Correct hemodynamic subset classification was predicted from clinical criteria in 70% of the patients. This classification is a powerful tool in assessing outcome as well as in selecting and monitoring appropriate therapy. Thus, patients in subset I, who have relatively normal hemody-

30

20

B

pcw 10 I I I

I

I0 LV Volume

PCW

Table Il-Expected effects of various drugs employed in the management of acute myocardial infarction* Myocardial oxygen Hemodynamic change Drugs

Cl

PCW

Diuretics

4.--.

4.

Demand Effect

Mechanism

4. -. 4. if 4. heartsize

Digoxin

1-

4.-.

Norepinephrine

I -.

I -.

Dopamine, 2-4 pg/kg. mm

1 --.

-. 4.

1 4.

Dopamine, >4pg/kg*min

1--.

1--.

1

Isoproterenol

1

4.

1

Vasodilators

I -.

4.

4.

Propranolol

4.

4. -*

4. I I

4.ifheartsize4. I if I contractility exceeds 4. heart size I heart rate, 4. contractility, I SVR 1 contractility 4. secondary to diuresis and 4. preload 4. heart rate, I contractility, I SVR 1

1 I heart rate, 4. contractility 4. PCW, 4. SVR

4. 4. 4. heart rate, 4. contractility 1 1 heart size *SVR = systemic vascular resistance; ADP = arterial diastolic pressure.

Supply (coronary flow) Effect

-*4. I -*1

Mechanism

4. if 4. Cl 4. if transmyocardial gradient I by 4. PCW

4. ifCl I and/orPCW 4.

4.

1 ADP, I Cl

1

1 Cl

I

I ADP, I Cl

I secondary to I Cl I 4.--* 4. secondary to 4. ADP and I heart rate -. 14. 1 if transmyocardial gradient I and I Cl; 4. if 4. ADP> 4.PCW --.

Table Ill-Comparison of oxygen saturation and flow in two patients with new systolic murmurs Papillary muscle rupture Ventricular septal detect Oxygen Oxygen saturation saturation Level (%) Flow (%) Flow Superior vena cava 64 60 Right atrium 65 69 Right ventricle 67 82 Pulmonary artery 67 83 Radial artery 93 95 Cardiac index (I/mm m2). 2.3 5.54 Qp:Qsf 1:1 2.9:1 6Measured by thermodilution. Thus, 5.54 is the pulmonary flow index, which is 2.9 times the systemic flow Index (1.91 l/min* tPulmonary: systemic flow ratio.

hypoperfusion and cardiogenic shock are outlined in Table II. Whatever therapy is selected should be commenced promptly since myocardial necrosis is progressive while shock persists, and the potential for reversibility may disappear quickly. Hemodynamic monitoring is essential to guide therapy, and, although there are many cases in which such monitoring has been a valuable guide for the selection and regulation of therapy with a subsequent favourable result, the overall prognosis of cardiogenic shock remains poor, despite such efforts. Clinical research A variety of potent drugs have been used to decrease myocardial oxygen consumption in an effort to preserve ischemic myocardium; hemodynamic monitoring is required to ensure that unfavourable effects do not occur. Agents such as propranolol,'0 trimethaphan," nitroprusside""' and nitroglycerin given intravenously""3 have been administered in an attempt to limit infarct size under the guidance of hemoSE EKE MR C dynamic monitoring, but such interventions are experimental for the present.TM Monitoring may be useful in assessing the hemodynamic effects of new agents developed for the control of cardiac arrhythmias in acute myocardial infarction. Conclusion a Hemodynamic monitoring in acute myocardial infarction has contributed greatly to our under--PR-standing of the in-hospital course of the disorder, the detection of certain important mechanical complications that have therapeutic relevance and the resolution of confusing clinical problems presenting - - - ---- - - - - - m - - rn in this setting. It provides data that permit the physician to make rational therapeutic choices and guide the subsequent administration of such therapy. Finally, it provides important objective data to guide the direction of future therapeutic FIG. 3-PCW in a patient with severe acute mitral regurgitation (MR). research. as are large regurgitant

tamed perfusion; evidence of hypoperfusion is essential. It is also imCardiogenic shock is defined as portant to rule out other contria state of critically reduced tissue butory causes of hypotension and perfusion resulting from severe left poor perfusion; thus, the diagnosis ventricular dysfunction, usually in of cardiogenic shock implies the the setting of acute myocardial in- correction of ongoing pain, excesfarction. Generally 40% or more sive vagal tone, hypovolemia and of the left ventricular myocardium disturbances of cardiac rhythm. The has been lost.17 Cardiogenic shock aim of therapy here is to improve is defined clinically as a systolic left ventricular function and thus blood pressure of less than 90 mm enhance perfusion without unHg (or a fall in systolic blood pres- favourably altering the myocardial sure greater than 80 mm Hg in a oxygen supply-demand balance. previously hypertensive patient), Possible therapeutic approaches urine output of less than 20 ml/h include attempting to increase coroand evidence of poor tissue perfu- nary perfusion, increasing the heart sion (mental confusion or obtunda- rate when it is inappropriately slow, tion and cool, clammy, mottled augmenting contractility and thereby increasing the CO. It is imporskin).18 Isolated hypotension of this order tant to choose a therapy that does is not by itself enough to establish not augment the CO at the expense the diagnosis of cardiogenic shock, of an inordinate increase in myofor such an arterial pressure is not cardial oxygen demands such as is uncommon in acute myocardial in- produced with the use of isoproterfarction in the face of well main- enol.19 Some of the drugs used in Cardiogenic shock

The a-waves of left atrial contraction are reflected, v-waves of up to 90 mm Hg; this magnitude of v-waves represents acute severe mitral regurgitation in a patient with a left atrium of relatively normal size. The v-waves occur late in the cardiac cycle, at the end of the T-waves, which helps in identifying them. The time lines are one tenth of 1 second apart; the 1 sec designation represents the interval from the onset of the tracing. (Reproduced from Parmley and Chatterjee16 by permission of publisher and authors).

References 1. SwAN HJ, FORRESThR JS, DANZIG

R, et al: Power failure in acute myocardial infarction. Progr Cardicvasc Dis 12: 568, 1970

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2. SOBEL BE, SHELL WE: Jeopardized, blighted, and necrotic myocardium. Circulation 47: 215, 1973 3. Cox JL, MCLAUGHLIN VW, FLOW-

ERS NC, et al: The ischemic zone surrounding acute myocardial infarction. Its morphology as detected by dehydrogenase staining. Am Heart J 76: 650, 1968 4. FORRESTER JS, DIAMOND G, MCHUGH

TJ, et al: Filling pressures in the right and left sides of the heart in acute myocardial infarction. A reappraisal of central-venous-pressure monitoring. N Engi I Med 285: 190, 1971 5. FORRESTER JS, DIAMOND GA, SWAN HJC: Correlative classification of clinical and hemodynamic function after acute myocardial infarction.

Am I Cardiol 39: 137, 1977 6. MCHUGH TJ, FORRESTER JS, ADLER L, et al: Pulmonary vascular congestion in acute myocardial infarction: hemodynamic and radiologic correlations. A flll intern Med 76:

29, 1972 7. PEEL AAF, SEMPLE T, WANG I,

et al: A coronary prognostic index for grading the severity of infarc-

tion. Br Heart 1 24: 745, 1962 8. NoRRIs RM, BRANDT PWT, CAUGHEY DE, et al: A new coronary prognostic index. Lancet 1: 274, 1969 9. SCHEIDT 5, ASCHEIM R, KILLIP T: Shock after acute myocardial infarc-

tion: a clinical and hemodynamic profile. Am J Cardiol 26: 556, 1970 10. FORRESTER JS, DIAMOND G, CHATTERJEE K, Ct al: Medical therapy of acute myocardial infarction by application of hemodynamic subsets.

N Engi J Med 295: 1356, 1404; 1976 11. CREXELLS C, CHATTERJEE K, FORRESTER JS, et al: Optimal level of filling pressure in the left side of the heart in acute myocardial infarction.

N Engi I Med 289: 1263, 1973 12. VARONKOV Y, SHELL WE, SMIRNOV V, et al: Augmentation of serum CPK activity by digitalis in patients

with acute myocardial infarction. Circulation 55: 719, 1977 13. COHN iN, GUIHA NH, BRODER MI, et al: Right ventricular infarction Clinical and hemodynamic features. Am I Cardiol 33: 209, 1974 14. ROTMAN M, RATLIFF NB, HAWLEY J: Right ventricular infarction: a haemodynamic diagnosis. Br Heart I

36: 941, 1974 15. MOSER KM, SHIBEL EM, UNGER KM: Detection of left ventricular failure in patients with adult respiratory distress syndrome. Chest 67: 8, 1975 16. PARMLEY WW, CHATTERJEE K: Con-

gestive

Heart

Failure,

American

Heart Association, Dallas, 1977, p 7 17. PAGE DL, CAULFIELD JB, KASTOR JA, et al: Myocardial changes as-

sociated with cardiogenic shock. N EnglJ Med 285: 133, 1971 18. COHN JN: Shock, in The Heart, A reries and Veins, 4th ed, HURST JW, LOGUE RB, SCHLANT RC, et at (eds), McGraw, New York, 1978, p 716 19. MAROKO PR, KJEKSHUS JK, SOBEL

BE, et al: Factors influencing infarct size following experimental coronary artery occlusions. Circulation 43: 67, 1971 20. GOLD HK, LEINBACH RC, MAROKO PR: Propranolol-induced reduction of signs of ischemic injury during acute myocardial infarction. Am / Cardiol 38: 689, 1976 21. SHELL WE, SOBEL BE: Protection of jeopardized ischemic myocardium by reduction of ventricular afterload. N Engi J Med 291: 481, 1974 22. ARMSTRONG PW, WALKER DC, BURTON JR. et at: Vasodilator therapy in acute myocardial infarction. A

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Combined Meeting of Sydney Australia Royal Australasian College of Surgeons February 24-29, 1980 The Royal Australasian College of Physicians and by invitation The Royal College of Physicians and Surgeons of Canada This unique meeting comprises symposia each morning, breakfast and luncheon sessions, and afternoon meetings of the special sections of the Royal Australasian College of Surgeons and certain special societies of The Royal Australasian College of Physicians. The meeting will be held at the Sydney Hilton and Wentworth Hotels and accommodation has been reserved at both hotels for Canadian delegates. There will be a varied social programme for delegates and associates. For further information please contact:

Mr. Robert A. Davis Associate Director Division of Fellowship Affairs The Royal College of Physicians and Surgeons of Canada 74 Stanley Avenue OTTAWA, Ontario KI M 1 P4, Canada 910 CMA JOURNAL/OCTOBER 6, 1979/VOL. 121