CrmieAL Can Muoicrse Copyright © 1975 hy The Wiliams & Wikins Co Prmiedin USA Hemodynamic patterns in shock and critically ill patients S. A. VILLAZGON, MD; U. A. SIERRA, MD; S. F. LOPEZ, MD; M. A. ROLANDO, MD Nine variables were studied in 56 pati hemodynamic patterns of critically ill and shock pa- tients. The variables were central venous pressure, mean arterial pressure, heart rate, cardiac index, left ventricular stroke work, stroke index; total peripheral resistance, arteriovenous oxygen difference, and oxy- gen consumption. We observed six patterns; three with low cardiac index (hypodynamic) and three with cardiac index (hyperdynamic), Group IA: Low cardiac index with increased central ‘enous pressure and arteriovenous oxygen differences associated with myocardial infarction, cardiac insuffi- ciency, and postoperative cardiac surgery: Group IB: Low cardiac index with normal arteriove- nous oxygen difference associated with myocardial infarction or hypovolemia. Group IC: Low cardiac index and decreased arterio- venous oxygen difference in patients with hypodynamic septic shock. Group IID: High cardiac index and increased arte- riovenous oxygen difference in patients with sepsis and stable hemodynamic conditions. Groups IE and LIF: Increased a index and From the Department of Intensive Care, Hospital Espa, Mexico City, D.F., Mexico. Dr. Villazon is Chairman of the Intensive Care Unit and on the surgical staff of Hospital Espafo Dr. Sierra isthe attending staff physician ofthe Intensive Care Unit Dr. Lopez is a member of the junior staff of the Intensive Care Unit, Dr. Rolando is Assistant Professor of Mathematics and Associ- ate Professor of Internal Medicine. 215 normal or increased arteriovenous oxygen difference in septic patients, who were hemodynamically unstable or in shoe ‘These hemodynamic observations were found to be useful for understanding physiological compensations, for deciding on therapy, and in evaluating the effective- ness of therapy. ‘The primary function of the circulatory system is to deliver oxygen and nutrients to peripheral tissues for cellular metabolism. Healthy resting adults have oxy- gen consumption of 150 ml/min/m? with cardiac index of 3.0 liters/min/w®, and arteriovenous oxygen difference of 5 ml/100 ml."? Carlsten and Grinby® observed that trained athletes reached oxygen con- sumptions of over 1500 ml/min/m; in these instances, CI* increased to 10-12 liters/min/m? and av DOs increased to 15 ml/100 ml. Circulatory adjustments also occur with age, as metabolism and oxygen consumption are less than normal in the elderly. In healthy persons between 70 and 80 years of age, Brandfonbrener and Landownet found that CI averaged 2.36 liters/min/m?; VO,, * The abbreviations used aie: Cl, cardiac index; av DOs, arteriovenous oxygen difference: VO,, oxygen consumption (in ddexed, TPR, total peripheral resistance, HB, hemoglobin; MAP, mean arterial pressure; HR, heart rate; CVP. central venous pees: sure; LVSW, le ventricular stroke work: Sl,216 CRITICAL CARE MEDICINE 90 100 mi/min/M® av DO,, 4.3 ml/100 ml; total peripheral resistance, 1600 dyne/see/em* Normal subjects undergoing hyperoxygenization have decreased C1 and oxygen consumption associ ‘ated with proportional increases in TPR.* Voluntary hyperventilation, sufficient to reduce PaCO, to 50% of its basic value, was accompanied by a 2 liter/min/ M? rise in Cl, and a drop of 23 mm Hg in mean ar- terial pressure, and 45% of TPR.* In 1963, Roy and Col? studied 51 patients with chronic anemia caused by ankylostomiasis. The hemoglobin levels varied between 1.5 and 6.5 g (average 3.7). An inverse correlation between the Hb and Cl was observed in these cases: CI was over 5 liters/min/s; VO, was 140 ml/min/M?, the av DO was 2.25 ml/100 mi, Alkalemia, acidemia, hypoxia, and other factors are able to alter circulatory dynam- ies in normal subjects." The state of shock is usually defined as a hemody- namic condition characterized by poor tissue perfu- sion, cellular hypoxia, and damage to vital organs.* Based on Wigger’s classical experiments on hemor thagic shock,"® this condition was considered to be a state of low flow with an increased TPR. As knowl- cedge of the pathophysiology of shock has expanded, it was seen that this view did not cover all types. Patients with traumatic or septic shock have normal or elevated cardiac output": and there are different hemodynamic patterns with various metabolic and clinical conditions;'*""* moreover, hemody- namic events are markedly different in the early, middle, and late periods of shock." Thus, in patients who are critically ill or in shock, there is a diversity of factors that influence the hemodynamic responses from the initiating pathological processes to therapy, age. adaptation to hyperoxia, and anemia, and com- pensatory mechanisms. For these reasons, frequent hemodynamic measurements are needed for physio- logical evaluation and for treatment. * The pres- ent report summarizes hemodynamic measurements which we have made in the Intensive Therapy Unit at the Espaiiol Hospital, Mexico City. This report describes the various hemodynamic patterns ob- served in patients who were critically ill or in shock MATERIALS AND METHODS A study was made of 56 critically ill patients, 42 males and 14 females. Ages varied between 21 and 91 years with an average age of 57. Methods employed for hemodynamic evaluation were previously de- scribed in detail."* Percutaneous catheterization of femoral artery with a 16 angiocath allowed continuous recording of arterial pressure. CVP was taken by plastic, radiopaque catheters placed by percutaneous puncture in the right atrium through the internal jugular vein, Cardiac output was determined by the November-December, 1975 indicator dilution method as described by Hamilton.* Indocyanine green dye was used as indicator: the curves were mude in duplicate. The curves were analyzed by the planimetric method proposed by Cohn-Del Guercio."? but in patients with cardiac insufficiency and myocardial infarction, we used Dow's system modified by Oriol.™* Immediately after the dilution curves, blood was taken from cach catheter for blood gas-pH analysis with an TL 113. Hb content was determined by the cyanomethemoglobin method; oxygen saturations were calculated by Severinghaus nomogram Patients were classified as hypodynamic if the CL was less than 2.5 liters/min/?, and hyperdynamic if over 3.5 liters/min/M?. After this first differentiation, they were subdivided into three groups according to variations of TPR and the av DO, differences as follows. I. Hypodynamic (decreased CI) (Fig. 1). A. In- creases in both TPR and av DO,, B. Increased TPR with relatively normal av DO,, C. Relatively normal TPR and av DO;. II, Hyperdynamic (increased CI) (Fig. 2). D. In: creased VO, supplied by increased CI and av DO, there was reduced TPR. E. Increased VO, and LVSW, normal av DO,, and decreased TPR. F. Decreased VO,, av DO,, and TPR Since some of the groups had many patients in overt hypotensive shock, subsets were made for groups 1A, 1B, AND IIF to compare and constrast the differences between these states within each group. Shock was considered to be present when the MAP was below 70 mm Hg and there was oliguria of tess than 20 ml/hour without renal insufficiency. Recently Siegel" ** reported physiological charac- teristics of shock patients from different causes by deviations from the normal of 9 variables. We carried out a similar study with various variables: C1, LVSW, SI, HR, av DO,, TPR, MAP, CVP, and VO,, Circular diagrams were made with the mean of these rine variables in order to illustrate the physiological alterations by comparison with the normal range To quantify the relative change in each variable, 1/10 the normal range was considered as one diviation unit. When an index was less than normal, it was taken as a negative and when it was greater then normal, positive. In each group the algebraic sum of all the variables was determined with these units RESULTS, We found that all patients with uncomplicated myocardial infarction, congestive cardiac failure (or insufficiency), and hypovolemia had decreased cardiac output; they comprised the larger proportion of hypodynamic groups (IA and IB). In contrast, the patients in group IC and most of the patients with hyperdynamic states (group 11) had infections: oneVol. 3, No. 6 HYPODYNAMIC STATE 1B TOTAL GROUP Hn patient had terminal hepatic insulficiency (Figs. / and 2, Table 1), Hypodynamic States Low cardiac and stroke index with high TPR, CVP, and av DO, values were found in patients of group IA: these patients were found to have myocardial infarc tion, postoperative cardiac conditions, and hypovo- emia, The major differences between groups [A and IB were that group IA patients had higher av DO, and Villazén et al HEMODYNAMIC PATTERNS. 217 HYPODYNAMIC STATE IA TOTAL GROUP ton HYPODYNAMIC STATE Ic Diagrams of nine variables in the three hypodynamic groups, The two concentric circles correspond to the range of normality and the ular dark lines tothe average value obtained foreach variable VO. than did those in group 1B. Group 1A, in contrast to the septic, group IC, patients had higher TPR, av DOz, and VO, than did those of the latter group. The diagnosis and ages of group 1B did not differ greatly from those of IA. There was no increase in av DO,, and consequently VO; was diminished, The C1 and other variables were less altered in relation to the normal In group IC, the patients had sepsis and their average age was greater, There was absent TPR218 CRITICAL CARE MEDICINE HYPEROYNAMIC STATE GROUP TE November-December, 1975 HYPERDYNAMIC STATE at) 002 HYPERDYNAMIC GROUP nF TOTAL GROUP Fig. 2—Diagrams of nine variables which show the meun value of exch variable of the theee hyperdynamic groups. compensation for the decreased flow, but marked tachycardia and very low VOa. The other variables were similar to those of [A and 1B (Table 1). Hyperdynamic States All of the hyperdynamic patients except one had severe infections. There were no differences between the three hyperdynamic groups in regard to age and primary diagnosis (Table 1, Fig. 2). Group IID had increased Cl, decreased TPR, and increused av DOs, This permitted greater VO,, perhaps sufficient to satisfy the increased tissue demands produced by the infection. It was observed that this group maintained normal CVP, MAP, and LVSW; tachycardia was related to the febrile process. The greatest number of patients was in group HIF. Generally, there were higher Cl and lower TPR in the patients of group ILF. The striking findings in group IID was increased av DO, and VO,; values of both of these variables were low in group LIF patients, Hypotensive Shock Half of the patients in group IA were in hypoten- sive shock at the time of the studies: they had de- creased TPR and LVSW. Cl and SI were also less but not significant (Fig. 3). In group IB three pa- tients with MI were clinically in shock but had similar hemodynamic changes, The primary diseases were similar in patients with septic hypodynamic and hyperdynamic shock. TheVol. 3, No. 6 Villazén et al HEMODYNAMIC PATTERNS. 219 former were slightly older and had lower LVSW, These changes reflect hemodynamic responses to the MAP, Cl, SI, and VO, but higher MAP, TPR, and stress of illness and various interrelated mechanisms av DO; (Fig. 4). including cardiac performance, sympathetic-adrenal responses, peripheral oxygen metabolism, pulmonary eens function, etc. These factors are also greatly influenced Various hemodynamic alterations may be found in patients who are critically ill or in a state of shock se of cardiac output typically gives ‘Table 1: Data from patients studied piven us mean & S.D. Number cr TPR ww DO, to, HR se wimy eh mila CV LYSW MAP hy Grow pans “amy afi nu qty tg) cms) ent) “i Group 1A — hk 8 akeagt ee THa2L ae das Had ae a) totale Nat WTS MDI Wet TN ats oath sls toes rau tee mse IH a2? Ma Was Me el as ED cope Tomek A203) tsa Bab bas es ae as ee Nate 2 vert tid sik Sti Mik omie Bik sin Shock raat 9 97038 toa ns A2e0H Ha Set el a LG AD aug ic ine W122 Mai? Wa Ted 6 a Tek Sa et 7 ase) oem 104L7 A oad ema aT at Shc et 3AM a0d NBT 39409 HSA Sas Ed ed Ha Seek Grip Toh Sat SBame 22410 Hos 944 Hae ae a Mame Navn $ GSES SII Btat tein Stl Bim Bl AI meta Shok rat Met eI 25409 Haak Ha Maw BAD aD HYPODYNAMIC GROUP HYPODYNAMIC STATE IA 1A SHOCK NO SHOCK ¢ et « a 4, @ Fig. 3—Diagrams which show the mean value for each variable of the group IA patients with shock (left) and without shock (right).220 CRITICAL CARE MEDICINE ci Top a 002 Fig. 4—Diagrams of nine variables in which the data from the hhypodynamic septic shock group are compared with those of the hhyperdiynamic septic shock group. rise to sympathetic-adrenal responses with secretion of catecholamines and cortisol, antidiuretic hormone (vasopressin), and aldosterone.** Arterial pressure is maintained by peripheral vasoconstriction; the latter also redistributes cardiac output and may lead to decreased tissue perfusion, especially inthe splanchnic area, skeletal muscle, skin and kidney. Cellular dam- age which may arise is related to the disparity between ‘oxygen supply and demand, the degree of anaerobic metabolism, and the liberation of lactate acid. The rapidity of the fall in cardiac output, the age of Patients, the primary and associated clinical factors, and therapy may modify these responses Group IA patients had decreased cardiac output with increased av DO, and subnormal VO,. This group was composed of patients with cardiogenic Problems, except four who had hypovolemia. The latter were differentiated from the rest of the group only by CVP, which was found to be low; without these patients, the average CVP of the group would have been much higher. The main characteristic of this group appears to be the maintenance of tissue perfusion despite the high peripheral vasoconstriction required to maintain near normal blood pressure. They had a greater capacity for oxygen extraction November-December, 1975 which, to a certain extent, maintained near normal ‘oxygen consumption. In this group, patients who were in shock had slightly decreased CI and slightly decreased WO,. It is difficult to evaluate whether this decreased VO. was sufficient for the tissue require- ments. The rapid decrease in C1 was associated with pronounced increases in av DO, and the maintenance of near normal VO; The hypodynamic group with decreased av DO, (IC) is of special interest (Fig. 2). These patients were in septic shock; the decrease of Cl and TPR was less than the other groups. Patients had very low VO, with high CVP, tachycardia, and decreased LVSW and SI ‘The causes of this hemodynamic problem involve multiple factors including associated diseases, hy- poxia, acidosis, direct action of endotoxin or other bacterial products, and perhaps ¢ myocardial depres- sant factor.?* There are three common hemodynsmie patterns in septic patients: (a) increased demands which elevate CI and VO, (IID); (b) inability to increase Cl or TPR due to associated illness such as myocardial damage: (c) increased output with interferences in peripheral oxygen extraction resulting in ineffective flow (TIF). A major difference between patients with and without infection was the TPR which was decreased in all four groups of septic patients as compared with hypovo- lemic or cardiogenic shock. The patterns of the septic patients support the theory that in septic shock there is interference with peripheral O, extraction’. #*** from (a) precapillary arteriovenous communications by nutritive capillaries; (b) preferential passage of arte- rial blood flow through nonnutritive capillaries: (c) shift to the left of the Hb dissociation curve with decreased 2-3 DPG.%*# (d) alteration of the cellular respiratory mechanisms,#** etc. Presumably, the reduced VOs is related to decreased flow or factors that reduce effective tissue perfusion The hyperdynamic hypotensive shock patients were all in group LIF. One of the primary characteristics of septic shock was a disproportionate drop in resistance; possible causes include: (a) reduced response to pre capillary sphincters because of endotoxin blocking; (b) opening of precapillary communications; (c) re- duced calcium which alters vascular responsiveness to catecholamines, * ete Data presented in this report suggest six common hemodynamic patterns. Deviation from the standard values, based on normal ranges, can be used as an alarm to initiate preventive clinical treatment to avert shock, Repeated measurements of these variables before and after therapy will quantify the therapeutic efficacy. In some instances, therapeutic failure may justify the addition of desperate measures, such as intra-aortic counterpulsation for cardiogenic shockVol. 3, No. 6 REFERENCES t 2 Berne MR, Matthew NL: Cardiovascular Phosiology. St Louis. The Mosby Co., 1972 Barrat-Boyes BG, Wood EH: Cardiac output and relited measurements, pressure values in right heart and associated vessels tether with an analysis ofthe hemodynamic esponse to inhalation of high oxygen mixtucesin healthy subjects. J Clin Med 51:72, 1958 Carlsen A! Grinby G: The Circulatory Response to Muscular Exercive im Man, Springfield I, Charles C-Thomas, 1966 Brandfonbrener M, Landowne M, Shock NW: Changes in cardiac output with age. Circulation 12:587, 1965 Daly WJ. Bondurant S: Effects of oxygen bretthing on heart rate, blood pressure and eardige output under normal men Festing, with feactive hyperemia, and ufter atropine. J Clin Invest 41:126, 1962 Burnum JF, Hickman JB, Melatosh HD: Effect of hypo- ‘apnia on arterial blood pressure. Circulation 9:89, 1954 Roy $B, Bathia ML, Mathus VS, et als Hemodynamic effects ‘of chronic severe anemi, Circulation 28:346, 1963 Richardson DW, Wasserman AJ, Patterson JL: General and regional circulatory responses (0 changes in blood pH and carbon dioxide tension, J Clin Invest 4031, 1961 Sicgel JH, Greenspan M, DelGuereio LR: Abnormal vascular tone, defective oxygen iransport_and myocardial failure in human septic shock. An Sung 165:S04, 1967 Wiggers CJ: Physiology of Shock. New York, Commonwealth Foundation, 1980 Shoemaker WC: Sequential patterns in various etiologies of shock. Surg Gynecol Obst 132:411, 1971 Lopez SF, Sierra A, Maciel LF, etal: Hemodynamic types of hhuman shock, Amuario del Hospiral Espaiol de Mexico. 1971 Villazbn 8, Sierra A, Ferninder GE: Intensive therapy: diagno: sis and physiopathological correlations. Cir crwjanas 39:1283, 1971 Villazbn A, Guevara M, Morales I: Shock, physiopathology and effective eirculitoy blood volume. Prensa Medica 36441 1970 Sierra A:Hemodynamic techniques in the evaluation of the critically il patients. Cir y cirwianos 38:44), 1970 Hamilton WE, Moore JE. Kinsman JM. et al Further analysis, ofthe injection method and changes in hemodynamics under physiological and pathological condition. Amd Physiol 9:53, 1932 Villazén et al—HEMODYNAMIC PATTERNS 21 17, Cohn JD, Del Guercio LRM: Nomogram for rapid calculation af cardiac output atthe bedside. Ann Surg 164:109, 1966 18, Oriol A:Determination of cardiac output; using Dow's formula, J Appl Physiol 22588, 1967 19. Siegel JH, Goldwya RM, Friedman HP: Pattern and process in the evolution of human septic shock. Surgery 70:282, 1971 20, Siegel JH, Farrel BS, Goldwyn MR, el ul) The surgical Implications of physiologic patter in myocardial infarction shock. Surgery 72:126, 1972 21. Oowers RS Renal function and renal fare. WB Saunders Co, 207537, 1964 22, Wangensten SL, Geissinger WT, Lovett WL, et al: Relation ship between splanchnic blood flow and myocasdisl depressant factor inendotoxic shock. Surgery 69:410, 1971 23, Udhoji UM, Weil MH: Hemodynamic and metabolic studies dn shock associated with bacteremia. Ann Intern Med 62:66, 1965 24, Duff JH, Groves AC, McLean APH. et ak: Detective oxygen consumption in septic shock. Surg Grnecol Obst 128 1081 1939 25, Hershey SG, Del Guerico LRM. MeConn R: Septic Shock in ‘Man. Boston, Lite Brown and Co, 1971 26, MeConn R, Del Guerico LRM: Respiratory function of blood in the aculely ill patient and effect of steroids. Ann Surg 1743436, 1971 hires GT, Carrico Chl, Canizaro CP. Shock. Major problems in cinical Surgery. Philadelphia, WB Saunders Co, 1399, 1973 28. Miller RD: The oxygen dissociation curve and multiple tansfa- sions of ACD blood. Clin Anect 9:43, 1972 29. Normick AS, Thal AP: Mechanism forthe high requirements in sepsis and septic shock, nm Surg 170:677, 1969 30, Albrecht M, Clowes GHA’ The ineease of circulatory require- ‘ments in presence of inflammation. Surgery 56: 158, 1968 31. Gump FE, Marin P, Kinney JM: Oxygen consumption and Caloric expenditure in surgical patients, Surg Genecol Obiter 137.499, 1973 32, DePaims R, Coil J, Davis J et sl: Cellular and ultrastructural changes in endotoxemia” A light and electzon microscopic Study: Surgery 62:508, 1967 33. Huckabee WE: Relationships of pyruvate and lactate during anaerobic metabolism: I elfectof breathing low oxygen gases J Chin Invest 37.264. 1988 34, Deysine M, Lieblich M, Aufses AH: Albumin chunges during clinical sept shock, Surg Gynecol Obst 137475, 1973 n.