ANNOTATIONS Am. Heart J. June. 1960

1. De Bakey, >I. E., Hurch, G., lia>., ‘1‘., and Ochsner, ~2.: ‘l‘hc “Uorro~~ing-Lenclillg” Hemo- dynamic Phcnomcnon (Hemomctaliinesia~, 111111. Surg. 126:850, 1947.

2. Sjostrand, ‘1‘. : \‘olume and Distribution of Blood and Their Signilicance in Regnlatinq Circu- lation, I’hysiol. Rev. X3:202, 195.1.

3. Hyman, C., and Winsor, T.: 13lood Flow Redistribution ill the lluman Extremity; The I)i- version Phenomenon, Am. J. Cardiol. 4:566, 1950.

4. Meehan, J. I’.: Personal communication.

Shock Following Myocardial Infarction

The development of shock in acute myocardial illfarrtion produces a hazardous condition with a high mortality rate. It appears that among the factors \vhich affect the prognosis, the duration of shock prior to treatment is of great importance. If rclicf of h>,potension is achieved promptI>- by the use of vasopressor substances, the prognosis a ppcars to be more favorable. Thus, ;Cliller and Moser’ pointed out that only 3 out of 10 patienk survived, in whom shock following myocardial infarction was l;~lown to have been present for o\w 4 hours, whereas IO out of 17 patients treated survived when shock uxs present for lehs than 1 hour. In a series of 30 such patients treated with I-norcpinephrine b>. Sampson and Zipser,’ an immediate survival rate of 67 per cent xvas noted. In this group, the duration of shock before treatment a\-waged 1.8 hours in those who survix-ed, and 4.0 hours in those who died. Griffith alld his assoc.iates,3 in treating shock due to recent m~wxrdial infarction by vasopressor substances and other supplementary means, noted that 60 patients treated within 3 hours of the onset had a mortality rate of onI>- 13 per cent. By contrast, 74 patients who were treated after the I~psc of a .l-hour interxxl showed a mortalit\. rate of 76 per cent.

The classic experiments of \\.iggera’ in animals itldi(xle that profoutltl n1!.ocardial damage and irre\wsiblc circulatory failure develop when hemorrhagic shock ih prolonged for a considerable period of time. Corday and his co-workersj have also presented e\ idence revealing the profound effect of hypotension in reducing myocardial contractility and in decreasing collateral coronary flow. More recently, Savranoglu and associates6 have pointed out that after a period of 60 minutes

ANNOTATIONS

in animals, sustained tissue anosia appeared to produce irreversible damage. Moreover, Calvia ;uld associates7 hu\.e shown that the decreased a\-ailability of m),ocardial oxygen and the decrease ill effcc-ti\ e coronary flo\\- which OKIIW I\-ith falling blood pressures are readily reversible with I-llorcI)iI~ephritle.

The clinical lesson to be learned from these studies in patients and from the laboratory seems clex. The de\-e!opment of shock in acute myocardial infarction produces an acute clinic-al esperi- merit ilr which cur\ ival often is linked to a critical time factor. If effective mean aortic pressure is promptly restored tutyard normal, with an associated ele\.ation in coronary flow and improve- ment in myocxrdial function and c~ollateral flow, the patient ma!- survive the episode. On the c.ontrury, if the shock is unrecognized and treatment is delayed in these patients, irreversible changes may develop in the heart musc.lc, ;tssoc.iated with a high mortality rate, and the frequent tlcvel<lpment trf terminal myocnrdial failure.

The conclusion to Ile tlra\vn from all of this is that the blood pressure and heart rate are two of the parameters which must be followed with the utmost care during the initial hours and days following the de\~elopment of acute myocardial infarction. Constant observation of the patient for clinical signs of shock (such as sweating, pallor, weakness, etc.) is also highly important. The problem is further complicated b!, the fact that many such patients are treated in an oxygen tent and are kept quiet by sedation and analgesics. L-rider such circumstances, there is often a ten- dency to avoid disturbing them to measure their blood pressure and heart rate. U’ith the develop- ment of monitoring de\-ices, it ma). well de\.elop in the future that such patients will generalI> have their blood pressure and pulse recorded automatically, so that warning signals may be flashed if hypotension and/or arrhythmias develop. Such an approach may lead to a further reduction in the mortality rate of patients suffering from acute myocnrdial infarction.

Howard E. Heyer, M.D. Dallas, Teu.

1. Miller, J. :\., and Moser, E. A.: Arterenol Therapy for Shock After Acute Myocardial 111.

2. farction and Pulmonary Embolizationz J.A.M.A. 169:2000, 1959.

Sampson, J. J., and Zipser, A.: Norepinephrme in Shock Following Myocardial Infarction: Influence Iipon Survival Rate and Renal Function, Circulation 9:38, 19.54.

3. Griffith, G. C., Wallace, W. B., Cochran, B., Jr., Nerlich, W. E., and Frasher, W. G.: The Treatment of Shock Associated With Mvocardial Infarction. Circulation 9527. 1954.

4. \I?ggcrs. C. J.: Myocardial Depression in ShoLk: A Survey of Caidiodynamic Studies, AM. HEART J. 33:633, 1947.

5. Corday, E., Bergman, H. C., Schwartz, L. L., Spritzler, K. J., and Prinzmetal, M.: Studies on the Coronary Circulation. IV. The Effect of Shock on the Heart and Its Treat- ment. AM. HEART T. 37560. 1949.

6. Savranoclu. h.. Boucek. 1~ 1.. and Casten. G. G.: The Extent of Revcrsihilitv of Mvrrrardi:ll I%em& in Dogs, A& ‘Hea~r J. 58’:726, 1959.

~.,_._._ .__.

7. Cal\-ia, F. S., Napodano, R., Zurek, R., Pombo, T., and Lyons, R.: The Effects on Myocardial Oxygen Availability of Hemorrhagic Shock and Its Reversal by Various Agents, In- cluding I-Norepinephrine, Clin. Res. 7:18, 1959.