shock in the emergency department

CONCEPTS, COMPONENTS, AND CONFIGURATIONS

Shock in the Emergency Department

Robert F. Wilson, MD Jacqueline A. Wilson, RN

Dennis Gibson, BA William J. Sibbald, MD

Detroit, Michigan

S h o c k c o n t i n u e s to b e a s s o c i a t e d w i t h a h i g h m o r t a l i t y r a t e p r i m a r i l y b e c a u s e o f d e l a y s in d i a g n o s i s a n d t h e r a p y . To d i a g n o s e s h o c k e a r l y , a n d t h e r e b y i n c r e a s e t h e c h a n c e s o f r e v e r s a l b e f o r e t h e r e is e x t e n s i v e d e t e r i o r a t i o n o f v i t a l o r g a n s , one s h o u l d l o o k fo r a n y d e c r e a s e in p u l s e p r e s s u r e , u r i n e o u t p u t , u r i n e s o d i u m c o n c e n t r a t i o n , a l e r t n e s s o r a n y in- c r e a s e in u r i n e o s m o l a r i t y , t a c h y p n e a o r t a c h y c a r d i a . S y s t o l i c h y p o t e n - s ion, o l i g u r i a , m e t a b o l i c a c i d o s i s a n d a c o l d c l a m m y s k i n a r e l a t e s i g n s of s h o c k . T h e p a t h o p h y s i o l o g y o f e a r l y h y p o v o l e m i c s h o c k i n c l u d e s h y p e r v e n t i l a t i o n , v a s o c o n s t r i c t i o n , c a r d i a c s t i m u l a t i o n , f l u id sh i f t s i n to t h e v a s c u l a r s y s t e m a n d p l a t e l e t a g g r e g a t i o n . L a t e s h o c k is c h a r a c - t e r i z e d b y l y s o s o m a l b r e a k d o w n , s u b s e q u e n t r e l e a s e of k i n i n s (espe- c i a l l y b r a d y k i n i n ) , i m p a i r e d ce l l m e t a b o l i s m a n d o r g a n f u n c t i o n , f l u id sh i f t s o u t o f t h e v a s c u l a r s y s t e m b e c a u s e of c a p i l l a r y e n d o t h e l i a l d a m - a g e a n d i n t r a v a s c u l a r c o a g u l a t i o n . T h e p r i m a r y c a u s e o f s h o c k s h o u l d n o t b e n e g l e c t e d in f a v o r o f t r e a t i n g s igns , s y m p t o m s , a n d l a b o r a t o r y d a t a . T h e r e s u s c i t a t i o n f r o m t h e s h o c k p r o c e s s i t s e l f i n v o l v e s c o r r e c t i o n o f p a t h o p h y s i o l o g i c c h a n g e s , b a s e d on o b j e c t i v e t r e n d s a n d r e s p o n s e s r a t h e r t h a n i s o l a t e d m e a s u r e m e n t s . A s u g g e s t e d o u t l i n e o f t h e r a p i e s in o r d e r o f t h e i r u s e i n c l u d e s : 1) c o r r e c t i o n of t h e p r i m a r y p r o b l e m ; 2) v e n t i l a t i o n a n d o x y g e n ; 3) f l u i d - l o a d i n g ; 4) i n o t r o p i c a g e n t s ; 5) cor - r e c t i o n o f a c i d - b a s e a n d e l e c t r o l y t e a b n o r m a l i t i e s ; 6) s t e r o i d s ( " p h y s i o - l og i c " o r " p h a r m a c o l o g i c " doses) ; 7) v a s o p r e s s o r s ( e s p e c i a l l y in e l d e r - ly , s e v e r e l y h y p o t e n s i v e p a t i e n t s ) ; 8) v a s o d i l a t o r s (if e x c e s s v a s o - c o n s t r i c t i o n ) ; 9) d i u r e t i c s (if o l i g u r i c in s p i t e of t h e above ) , a n d 10) h e p - a r i n (if DIC). T h e m o s t c o m m o n errors are 1) l a t e d i a g n o s i s ; 2) i n a d e - q u a t e c o n t r o l o f t h e p r i m a r y p r o b l e m s ; 3) i n a d e q u a t e f l u i d l o a d i n g ; 4) d e l a y e d v e n t i l a t o r a s s i s t a n c e , a n d 5) e x c e s s i v e r e l i a n c e on a n d u s e o f v a s o p r e s s o r s a n d d i u r e t i c s .

Wilson RF, Wilson JA, Gibson D, Sibbald WJ: Shock in the emergency department. JACEP 5:678-690, September 1976. shock, hypovolemic . . . septic; acid base balance, abnormalities; alkalosis, metabolic . . . respiratory; acidosis, metabolic.., respiratory.

From the Department of Surgery, Wayne State University School of Medicine and Shock Unit, Detroit General Hospital.

Supported by the Detroit General Hospi- tal Research Corporation and Michigan

Association for Regional Medical Pro- grams. Grant #75-6-25.

Address for reprints: Robert F. Wilson, MD, Professor of Surgery, Wayne State University, School of Medicine, 540 E. Canfield, Detroit, Michigan 48201.

Page 678 Volume 5 Number 9

INTRODUCTION

Shock cont inues to be a problem f r equen t ly t r e a t e d wi th ~too l i t t le , too l a t e " a n d c o n t i n u e s to be associated wi th a high mor ta l i t y rate. E a r l y d iagnos i s and rap id , aggressive therapy , based on t rends and responses de tec ted by se r ia l objective measurements , seem to offer the only reasonable chance, for m a n y critically-il l and in jured pat ients . Emergency physic ians are at a pa r t i cu l a r disad- vantage because they mus t diagnose and begin t he rapy wi th l i t t le previous da ta or cl inical information. This paper will discuss a few of the more pe r t inen t aspects of shock tha t may help the emergency s taff unders tand shock p a t h o p h y s i o l o g y , m a k e an ea r ly d iagnos is and develop an or- derly, def in i t ive approach to t reat- ment.

DEFINITION

For m a n y y e a r s , p h y s i c i a n s thought of shock in very mechanist ic t e r m s , c l a s s i f y i n g i t s complex pathophysiologic processes as though t h e y were p l u m b i n g p rob lems , ie, abnormal i t i e s in the pump, the p~pes, or the fluid in the pipes. Such com- p a r i s o n s m a y be h e l p f u l in un- d e r s t a n d i n g hypovo lemic and car- d iogenic shock. However , i t is in- c r e a s i n g l y a p p a r e n t t h a t most pa- t i en t s wi th ea r ly sept ic shock, and some with acute myocard ia l infarc- t ion (AMI) shock, do not have the cold, c l ammy skin, poor t issue perfu-

September 1976 J ~ P

sion, low cardiac output and exces- sire vasoconstriction so long considered characteristic of all shock_

When we began to measu re the cardiac output in pat ients with early septic shock, we found tha t most pa- t ien ts had e i the r an i nc rea sed or normal ca rd iac o u t p u t and a low total p e r i p h e r a l v a s c u l a r res is- tance.1, 2 Those with low cardiac output, excessive vasoconstr ict ion and cold, c lammy skin usual ly had been in shock for several hours and had complicating hypovolemia or, occa- s ional ly , a ca rd iac a b n o r m a l i t y . When hypovolemia was corrected in these pa t i en t s , the cardiac Output rose rap id ly to normal , or higher , levels.

Nevertheless, the concept that all shock is associated with poor tissue perfusion persists. Adherents to this theory3,4 point out that, even though early septic shock may be associated with a normal or high cardiac output and warm, dry skin, there is still a perfusion problem because much of the cardiac output may be diverted through arter iovenous fistulas ra ther than through the n u t r i e n t capillaries where it is needed. Al though high oxygen concentrat ions in the venous blood of such pat ients suggests tha t this may be t rue , it appears t h a t anatomic s h u n t i n g t h r o u g h arteriovenous fistulas is not the basic problem. On the contrary, there is evidence that , in sepsis, the problem is increased physiologic shun t ing due to abnormali t ies involving the capillary and cell m e m b r a n e s and cell metabol ism. 5-7 E v e n though blood may be p a s s i n g t h r o u g h n u t r i e n t capil laries in large quant i t i es , the cells are unable to use the oxygen, glucose and other nu t r ien t s brought to them_ Thus, al though there may be increased anatomic s h u n t i n g in sepsis, the ma in problem appears to be inc reased physiologic s h u n t i n g that has now been demonstrated in the lungsS, 9 and kidneys. 1°

C o n s e q u e n t l y , shock shou ld be considered a problem due to, or as- socia ted wi th , a b n o r m a l c e l l u l a r metabolism, in most ins tances the result of poor t issue perfusion, but perhaps also the result of other factors, such as sepsis. The advantage of t h i n k i n g of shock in b iochemica l terms is that , i n m a k i n g the diag-

~ ) September 1976

nosis, the emphasis is switched from the c a r d i o v a s c u l a r changes ( t ha t may occur late) and to the biochemical changes (that often occur earlier).

DIAGNOSIS

Once the word ~'shock" is men- t ioned, pe r sonne l seem to be gal- vanized into action, and observation and t r e a t m e n t of the p a t i e n t are rapidly intensified. Regardless of the t r ea tmen t up to tha t time, it invar- iably improves after the diagnosis of shock. For th i s a nd a n u m b e r of o the r r ea sons , e a r l y d i a g n o s i s great ly increases the chance of re- versing the shock process before ex- tensive deteriorat ion of the vital organs. Unfo r tuna te ly , the most frequent cri teria used to diagnose shock - - systolic blood pressure less t han 80 mm Hg, severe oliguria, metabolic acidosis and evidence of poor t issue pe r fus ion (cold, c l a m m y s k i n and clouded sensorium) - - are extremely variable and are often not detected unt i l late. If the diagnosis is delayed unt i l all, or most, of these signs are present , p a r t i c u l a r l y in septic pa- t ients, the chances of successful out- come are greatly reduced.

Blood Pressure

The blood pressure can be considered to consist of the diastolic pressure, which co r r e l a t e s w i th the amount of vasoconstriction present; the pulse pressure (the difference between the systolic and diastolic pressures) , p r i m a r i l y r e l a t e d to the s t roke vo lume and r ig id i ty of the aorta and its larger branches, and the systolic pressure, determined by a combinat ion of these factors.

Pulse pressure. Of the three men- tioned, the pulse pressure is the most important . Although cardiac output and stroke volume tend to decrease with age, the pulse pressure rises because of the increas ing stiffness of the aor ta and its la rger branches . Despite this and the fact tha t it var- ies great ly from pa t ien t to pat ient , changes in an i nd iv idua l pa t i en t ' s pulse pressure often correlate well with changes in stroke volume.

Changes with hemorrhage. In hypovolemic shock major decreases in stroke volume and, hence, pulse pressure, often occur long before any s ignif icant fall in systolic pressure.

General ly the diastolic p ressurer i ses in i t ia l ly due to intense sympathoad- r e n a l s t i m u l a t i o n 11 so tha t , even though the stroke volume and pulse pressure decreasel the systolic pressure ma y be m a i n t a i n e d . ,Because vasoconstriction can only increase :to a cer ta in max imum, continued blood loss will eventual ly result in a ra ther rapid fall of both the systolic and d ia s to l i c p r e s s u r e s . In o the rwi se no rma l pat ients , the systolic pressure often is ma in ta ined unt i l a blood volume deficit of 15% to '25% has de- Veloped. Thus, in the average 70 kg ma n with a normal blood volume of 5000 ml, a rapid blood loss of 500 ml to 1000 ml of blood may cause some decrease in the pulse pressure. The systolic pressure often does not fall u n t i l 1000 to 1500 ml .or more of blood has been lost.

It m igh t be well to different ia te blood volume loss from blood volume deficit. If a pat ient lost 1500 ml of blood over one hour's time, about 400 to 600 ml of fluid might move from the in ters t i t ia l space into the vascular, space du r ing tha t hour to par- t ial ly correct hypovolemia. Thus, the ac tua l blood volume deficit migh t only be 900 to 1100 ml.

Unobtainable cuff blood pressure. Because emergency staff mus t rely on the sphygmomanometer to obtain blood pressure , it is i m p o r t a n t to point out several potential errors associated with this technique. While a p p r o x i m a t e l y 90% to 95% of pa- t i e n t s w i th an u n o b t a i n a b l e cuff blood pressure have a low systolic blood pressure, usual ly less t h a n 50 mm Hg, the r e m a i n i n g 5% to 10% may have a normal , or even elevated, i n t r a - a r t e r i a l pressure. Apparen t ly the stroke volume, ra ther than systolic pressure, is more impor tant in de te rmin ing when Korotkoffs sounds are best heard. Thus, pat ients with an unobta inable cuff blood pressure, if their vessels are intact, almost invar iable have a low stroke volume and severe vasoconstriction, The use of vasopressors in such patients, par- t icular ly when the blood pressure is normal or high, may be extremely deleterious.

Another clue tha t stroke volume is fal l ing occurs when the clinician, try- ing to obtain a cuff blood pressure, begins to have trouble hear ing the

Volume 5 Number 9 Page 679

sounds, or only hears them intermit- tently, and obtains widely different blood pressure read ings w i t h each measurement_

In t ra -ar t e r ia l blood pressure . If there is difficulty obta in ing a consis- tent, clear, cuff blood pressure and t he r e is no i m p r o v e m e n t w i th therapy, an i n t r a - a r t e r i a l ca theter should be inserted. It is ext remely i m p o r t a n t to a c c u r a t e l y and fre- q u e n t l y follow blood p r e s s u r e changes when t r e a t i n g pa t i en t s in shock. The changes and t rends are more i m p o r t a n t t h a n an i so la ted value.

The radial ar tery is general ly the p r e f e r r ed s i te for i n t r a - a r t e r i a l catheter insert ion because of its ac- c e s sab i l i t y . D i g i t a l i s c h e m i a has been extremely rare in our experience. Not only does an in t ra-ar te r ia l l ine provide more accu ra t e blood pressure values, but it also provides a ready source for blood gas determi- nations. If a t ransducer for measur- ing the in t ra -ar te r ia l blood pressure is no t a v a i l a b l e , t he m e a n blood pressure can be measured with in- t ravenous extension tubes connected much like a central venous pressure monitor. Every 5.3 inches above the mid-axil lary l ine is equivalent to 10 mm Hg mean ar ter ial pressure.

Urine Output Correlat ion wi th cardiac output.

The ur ine output (without diuretics) is an extremely impor tan t measurement , pa r t i cu l a r l y in hypovolemic patients. Often a reasonable correla- t ion exists between it and renal blood flow, which, in turn, is dependent on cardiac output. Renal blood flow during h y p o v o l e m i a sh i f t s from the outer renal cortex to the medul lary portions of the kidney. Since renal vasoconstriction is greater than that in other v i ta l organs, when rena l perfusion is adequate, almost certain- ly blood flow to the brain, hear t and liver is adequate. For this reason we connect extension tub ing to the Foley catheter so as to permit the observa- t ion of ur ine dripping, drop-by-drop, into a closed collection system. Usu- ally about 15 drops/ml are present in the tub ing and, thus, u r ine output can be e s t i m a t e d on a m i n u t e to m i n u t e basis and changes i n - r e n a l p e r f u s i o n wi l l be de tec ted m u c h sooner.


Urine flow in sepsis. Although the ur ine output may be helpful in de- tecting fluid deficits, sepsis has been sho w n to h a v e u n i q u e effects on rena l funct ion which can resul t in very deceptive findings. A small, but increasing, number of severely septic pat ients with an inappropriate, ap- p a r e n t l y ob l iga to ry , p o l y u r i a are being seen. TM In spite of a relat ive hypovo lemia , these p a t i e n t s may have an hourly ur ine output exceeding 100 to 200 ml. At the same time, they have of ten been g iven large volumes of fluid, are often edematous and have a high central venous pressure. Rales can usual ly be heard and the chest x-ray film frequently shows evidence of severe pu lmona ry con- gestion or ear ly pu lmonary edema. U n d e r such c i r c u m s t a n c e s , the polyuria appears to be appropriate, and it is assumed that fluid in take should be drast ically reduced. How- ever, if f luid is severely restr ic ted unde r such c i rcumstances , wi thout close, c o n t i n u e d o b s e r v a t i o n , the blood pressure and ur ine output may sudden ly fall. Un les s f luid is immed ia t e ly a d m i n i s t e r e d to restore adequate perfusion, the shock and oliguria may be very difficult to correct and the pat ient 's chance of survival is decreased_

Urine sodium concentration. When it is difficult to est imate intravascu- lar volume and organ perfusion, the f r e q u e n t m e a s u r e m e n t of u r i n e sodium concentra t ion may be helpful. If it falls rapidly, or is less t han 10 to 20 mEq/liter, the kidneys are functioning, but are not being satis- factorily perfused. A urine- to-serum osmolarity ratio of greater than 2-1 is also a re l iab le index of reduced rena l perfusion. A l though reduced renal blood flow under such circumstances may occasionally be due to decreased cardiac ou tput r e su l t ing from intr insic myocardial disease, in most instances it is due to hypovolemia.

Acid-Base Changes

Respiratory alkalosis. The classic acid-base abnormal i ty in shock has g e n e r a l l y b e e n cons ide red to be metabol ic acidosis. However, it is

n o w recognized tha t early shock is charac te r ized by a r e sp i ra to ry alkalosis, par t icular ly if sepsis is present.12,13 Endotoxin in the cerebrospi-

nal fluid is a powerful s t imulus to ven t i l a t ion . Therefore, ear ly blood gas analyses in these pat ients gener- ally reveals a low PCO2, a normal HCO3 and an elevated pH_ Patients with t rauma, shock or sepsis tend to hypervent i la te and often have min- u te vo lumes t h a t exceed 11/2 to 2 t imes normal . The ini t ia l respiratory alkalosis is general ly not a compen- s a t o r y m e c h a n i s m b u t r a t h e r a nonspecific response: If, however, the effects of the t rauma, shock or sepsis are no t i m m e d i a t e l y r emedied , me tabo l i c acidosis u l t i m a t e l y develops, causing the pa t ien t to hypervent i la te even more as a compensatory mechamsm.

Thus, tachypnea is a valuable sign tha t an otherwise stable pa t ient is gett ing sicker. The corollary of this is also true: early hypervent i l a t ion is such a f requen t accompan imen t of shock and sepsis tha t if such a pa- t ient is not hypervent i la t ing, the incidence of la ter respiratory failure is r a t h e r h igh and one m u s t search carefully for a serious abnormal i ty of the central nervous system, airway, lungs, chest wall or diaphragm.

Metabolzc acidosis. As shock progresses, local changes in ce l lu la r m e t a b o l i s m resu l t in the develop- men t of metabolic acidosis. This occurs, first, in t race l lu lar ly and, then, at the capil lary level. As the process c o n t i n u e s , the m e t a b o l i c acidosis may be detected in venous blood from the i n v o l v e d a reas and f ina l ly , somewhat later, in the ar ter ial sys- tern. By the t ime a signif icant base def ic i t is p r e s e n t in the a r t e r i a l blood, the process is quite advanced. Alterat ions in cell membrane poten- t i a l and i n t r a c e l l u l a r pH usua l l y occur ra ther early, not infrequently hours before changes are apparent in the ar ter ia l bloo d ~as samples.

In e a r l y phases of me tabo l i c acidosis, often the acid-base abnormal i ty can be corrected by improving t i s sue pe r fus ion . La te r , however , sodium b ica rbona te may be necessary, par t icular ly if the ar ter ial pH falls below 7.20. If metabolic acidosis continues to progress, the amount of bicarbonate needed for correction increases almost geometrically.

Combined metabolic and respiratory acidosis. If the pa t ien t in severe shock lives long enough, a combined


respi ra tory and metabol ic acidosis will develop. O r d i n a r i l y the lungs excrete carbon dioxide easily. Termi- ually, however, the lungs may become so bad ly damaged tha t they canno t p r o p e r l y excre te ca rbon dioxide and the PCOe begins to rise back to, and then f inal ly above, nor- real. Thus, in the very f inal stages of shock, blood gas analyses will often show an elevated PCO2, low HCOa and very low pH. If this combined acidosis is al lowed to develop, the prognosis is poor.

Tissue Perfusion

Pulse pressure. Blood flow and tissue per fus ion are more i m p o r t a n t than blood pressure in the shock patient. Al though cardiac ou tput de~ terminat ions may be helpful in this regard, m a n y hospitals do not have the equipment for such studies. One can, however, follow the stroke volume to a cer ta in extent by observing changes in pulse pressure and noting the ease with which the pulse can be palpated. In an ind iv idua l pat ient , changes in pulse pressure general ly reflect changes in the stroke volume and, thus, are a much better indica- tion of blood flow than the systolic pressure.

Sk in changes. If the skin is cold and c lammy and these changes are generalized, the pa t ient probably has a low cardiac output and a high total peripheral vascu la r res i s tance secondary to in tense sympathoadrenal stimulation. However, many pat ients with early nonhypovolemic sepsis or acute myocard ia l in fa rc t ion (AMI) have warm, dry skin and no apparent vasoconst r ic t ion . In the septic patient, vasodilat ion may be part ial- ly due to re leased vasoact ive substances such as bradykinin . In AMI shock, lack of vasoconstriction may be due to abnormal , or pathologic, reflexes or ig ina t ing from the ische- raic myocardium.1445

Mentation. A cloudy sensorium or increas ing l e tha rgy should also be considered a sign of poor tissue per- fusion_ Not i n f r equen t ly , it is the first sign of sepsis.

Ar t e r iovenous oxygen dif ference. Trends in cardiac output may also be i nd i ca t ed by c h a n g e s in the arteriovenous (AV) oxygen differences. If t he AV oxygen d i f fe rence is greater t han 6 vol% and is increas-

ing, the cardiac ou tpu t is about 4 li ter/rain or less and falling. In contrast, if the AV oxygen difference is less t han 3 vol% and decreasing, the cardiac ou tput is about 8 l i t e r /min and rising• Even without calculat ing

• )

AV oxygen differences, one can esti- mate changes in cardiac output . If venous blood from a CVP catheter or a pu lmonary artery becomes darker because it is less sa tura ted with oxygen, blood flow to the t i s sues has been reduced. On the other hand, if the venous blood becomes brighter, the cardiac output is probably rising.

I t must be emphasized repeatedly that single levels or isolated deter- minations of any parameter may be deceptive: it is the changes, te, the trends and responses, that tell what is happening.

Urine. As ment ioned earlier, if the urine output and ur ine sodium concentrat ion are fall ing and ur ine os- molari ty is rising, it can be assumed that there is inadequate renal perfusion, usual ly due to hypovolemia_

PATHOPHYSIOLOGY Early Shock

Ventilation. In ear ly hypovolemic shock, even after minor trauma,1647 hypervent i la t ion is usual ly seen and minu te vent i la t ion is often 11/2 to 2 t imes normal. Al though tidal volume is reduced, the respiratory rate is increased two to three fold and provides much of the increased ventilation. Such changes are nonspecific, however, and may occur wi th any stress_ As a result of hypervent i la- ti0n, the PCO2 frequently falls to 25 to 35 mm Hg or lower. Init ial ly, the ar ter ial PO2 may r ema in near normal in spite of mild-moderate lung damage because of hypervent i la t ion. If a pa t ient with increas ing sepsis or early shock is not hypervent i la t ing, some th ing is wrong. The pa t i en t ' s chance of d e v e l o p i n g r e s p i r a t o r y failure, if t r ea tmen t is inappropriate, is increased.

Vasoconstriction_ S t i m u l a t i o n of the s y m p a t h e t i c ne r vous sys tem's a -ad rene rg ic receptors result in arter ia l vasoconstr ict ion, par t icu la r ly in those tissues, such as the skin and kidneys, tha t are more res is tant to hypoxia and ischemia. Initially, this Vasoconstriction is beneficial because it diverts blood to those organs that

cannot tolerate an inadequate blood flow for more t h a n a few minutes , such as the hear t and the brain. As- sociated with arteriolar vasoconstric- t ion is a s u b s t a n t i a l r educ t ion in vascular capacity due to narrowing of the larger veins. Since about 60% of the pat ient ' s systemic blood volume is present in the larger (capaci- tance) veins, this reduction in vascular capacity is one of the most impor- ran t compensatory mechanisms for tolerat ing volume defects as high as 15% to 25% without hypotension.

Pa t i en t s given narcotics, particu- l a r l y m o r p h i n e , fo l lowing severe t r auma will occasionally have a sudden drop in blood pressure. In retro- spect, it is usual ly clear tha t such pa- t ients were hypovolemic but a significant amoun t of vasoconstriction was m a i n t a i n i n g blood pressure at rela- t ively normal levels. Narcotics and vasodilators not only interfere with, or inhibi t , ar ter iolar vasoconstriction but also increase vascular capacity by 1 to 2 liters or more, which can cause a sudden , severe , r e l a t i v e hypovolemia to develop. As a conse- qnence, before any narcotic is given to a pa t ient with t r auma or sepsis, it should be ascer ta ined tha t the pa- t ient is not hypovolemic and an in- t ravenous line should be established for rapid infusion of blood or fluid if the blood pressure does fall. More- over, if there is any question about the s ta tus of the pat ient 's cardiovascular or respiratory systems, and if narcotics appear to be necessary, it is preferable to adminis ter them in- t ravenously in mult iple small doses.

Cardiac s t imulat ion . St imu la t i on of the•-adrenergic receptors results in a faster hear t rate (chronotropic effect), an increased force of myocardial con t r ac t i on ( inotropic effect), s l ight vasod i l a t ion of the ske le ta l muscle arteries and venous constriction. The net result is improved tissue circulation. This is an impor tant part of defense agains t shock and pa- t ients who fail to develop an appro- pr ia te tachycard ia seem to have a poor prognosis. Excessive B st imula- tion, par t icular ly in septic patients, may: cause the pa t ient to develop an a r rhy thmia before other signs of in- c reas ing sepsis or septic shock become evident, is If the pulse rate is slow, increasing it to 90-110/minute

J ~ P September 1976 Volume 5 Number 9 Page 681

us ing isoproterenol , a t rop ine or a t empora ry t r a n s v e n o u s pacemaker may be of Value by increas ing cardiac output.

Fluid shifts. Whenever hypovolemia or hypotension in i t i a l ly develop, fluid tends to move, often rapidly, from the in ters t i t ia l space im to the v a s c u l a r space. In y o u n g heal thy soldiers in Viet Nam, 19 this shift was found to exceed one liter in the first hour_ It occurs, according to the F r a n k - S t a r l i n g hypothesis, because the colloid osmotic pressure, at least init ial ly, is normal whereas the f i l t ra t ion pressure at the ar ter iolar end of the .capillaries is reduced, not 0nly because of decreased a r te r ia l blood pressure but also because of increased arter iolar vasoconstriction in the precapillary area. As the inter- s t i t ia l space becomes depleted and the plasma proteins are progressively d i lu ted by the i n t e r s t i t i a l fluid t h a t has moved i n t o the v a s c u l a r space, the shift of fluid from the in- terst i t ial to the in t ravascular space decreases.

Ear ly in sepsis, capillary permea- bili ty may increase so tha t the fluid shift i s qu ick ly reversed from the vascular space into the in te r s t i t i a l fluid space. Consequently, septic pa- t ients often require more fluid and become 'more edematous t han other p a t i e n t s w i t h s i m i l a r degrees of hypotension_

Platelet aggregation. Another in- c reas ing ly recognized phenomenon occuring in ear ly shock is p la te le t aggregation.. 2° This can result in in- t e r f e r e n c e w i th local micro- c i r c u l a t o r y blood flow s ince the platelet aggregates, or the vasoactive substances they release, may occlude small vessels. These aggregates may also form emboli tha t can migrate to the lungs, where they may be an impor tant factor in the development of the respiratory failure seen during, or following, prolonged shock.

L a t e S h o c k ~

Lysosomal breakdown_ If shock is a l lowed to pe r s i s t in to its l a t e r s tages , s eve r a l d i s a s t r o u s pa tho : physiologic changeS associated with the r progressive deteriorat ion in cel- lu la r and o r g a n f u n c t i o n :begin. Dur= ing the past several years increas- i n g - a t t e n t i o n has b e e n ;paid to a


group of in t race l lu lar vacuoles called lysosomes, occasionally referred to as " i n t r a c e l l u l a r s tomachs ," par t icular ly in phagocytes, because bacte- r ia or par t ic les t a k e n in by these cells are usual ly ~'digested" or broken down in the lysosomes. These vacuoles contain a number of powerful enzymes and ther l imi t ing membrane a r o u n d t h e m of ten b r e a k s down rapidly with shock, sepsis, or t r auma r e su l t i ng in a release of these enzymes into the cell and the blood s t r e a m. The p ro t eo ly t i c e nz yme s from the lysosomes may be particu- larly active and can convert inactive k i n i n o g e n s [which are vasoac t ive polypeptides combined wi th a protein, usual ly an a - 2 globulin) into active k in ins by enzymatical ly split- t i n g off t he protein_ F r o m a t h e r a p e u t i c s t a n d p o i n t , m a s s i v e doses of steroids can stabilize lysosomes, r e d u c i n g the r e l e a se of lysosomal enzymes and vasoactive substances.

Vasoactive polypeptides. The best known of those k i n i n s re leased in shock is bradykinin , which is one of the most potent vasodilators known. This v a s o d i l a t o r p r o b a b l y causes much of the skin f lushing that occurs with alcoholism, sepsis, pancreat i t is and the carcinoid syndrome. Another vasoactive polypeptide, referred to as ~ 'myocardia l d e p r e s s a n t fac tor" (MDFI, comes p r i m a r i l y f rom ischemic p a n c r e a s a nd m a y cause s p l a n c h n i c v a s o c o n s t r i c t i o n wi th subsequent depression of myocardial act ivi ty_ 21 A l t h o u g h some inves - t i g a t o r s doub t the p r e s e n c e of MDF; 22 previous bioassays done here suggest tha t shock, sepsis and pan- creatitis cause the formation and/or release of mul t ip le vasoactive substances, some of which almost cer- ta in ly have a de t r imenta l effect on cardiac function.

Induced histamine. A d d i t i o n a l microcirculatory changes are caused by h is tamine produced at the cellular level in response to injury. This "induced" h i s t a m i n e , u n l i k e ~'pre- formed" his tamine, which is stored in mast cells, is not inhibi ted or blocked by ant ihis tamines_ The presence of induced h is tamine was inferred from studies showing tha t damaged, or ischemic, t i s sues have an increased quant i ty of hist idine decarboxylase,

which converts inactive hist idine to active his tamine. 2a

Impaired cell metabolism. As the shock process continues, there is increasing dis turbed cel lular metabo, lism. E n e r g y for the cell comes from a var ie ty of sources, one of impor, tance in shock is the conversion of glucose to pyruvate . Al though this process m a y occur anae rob ica l l y , it resul ts in formation of only two moles of ATP~from each mole of glucose. If there is not enough oxygen present to combine with the hydro- converted to acetyl-CoA, can then e n t e r the Krebs cycle where it is broken down into carbon dioxide and hydrogen. The hydrogen ions enter the electron t ranspor t system where they combine with oxygen to form water with the eventual release of 38 moles of ATP from each mole of glucose. If there is not enough oxygen present to combine with the hydrogen, as m a y occur in shock, the Krebs cycle gr inds to a hal t . The pyruvate is then converted to lactate• The accumulat ion of lactate and lactic acid is the m a i n cause of the metabolic acidosis of shock. •

We are seeing more severely septic pat ients who do not have a metabolic acidosis, in spite of a reduced oxygen consumpt ion . 24 Fu r the rmore , some s e v e r e l y sep t ic p a t i e n t s develop metabolic a lkalosis as well as res- p i ra tory alkalosis, a l ready present because of hypervent i la t ion. The resu l t an t combined alkalosis may be difficult to correct. A possible expla- na t ion for this metabolic alkalosis is tha t the anaerobic metabolism that forms p y r u v a t e f rom.g lucose may also be impaired by products of infection. Therefore, pyruvate and lactate cannot accumulate.

Impaired Organ Function. With i n c r e a s i n g i m p a i r m e n t of cell metabolism, organ function also begins to deteriorate. If the in tes t ine is ischemic or damaged, bacter ia and bacterial products may enter the circulat ion through, or across, the intest inal mucosal barrier. In the liver, the hepatocytes may be damaged and energy production decreases. The re- t iculoendothelial system may also be impai red , dec reas ing the pa t ien t ' s a b i l i t y to cope wi th b a c t e r i a and bacterial products. In the lungs, the p u l m o n a r y c a p i l l a r y e n d o t h e l i u m


may become damaged, resul t ing in a p rog re s s ive ly severe i n t e r s t i t i a l edema and congestive atelectasis, re- (lected by a r i s ing alveolar-ar ter ia l oxygen difference. Kidney damage resul ts in a dec reas ing c r ea t i n ine clearance, even when the ur ine output is good. The stomach has severe mucosal ischemia, which can later result in gastric erosions and stress bleeding. 2~ Cerebra l func t ion may rapidly deteriorate and confusion is often one of the earl iest signs of sepsis. E v e n w h e n card iac o u t p u t is normal, Or increased, cardiac func- t ion cu rves m a y d e m o n s t r a t e an e lement of myocard ia l dysfunct ion before other hemodynamic changes become apparent.

Fluid Shifts

In tracel lu lar edema. The f luid shifts in late shock are opposite to those found early, and tend to cause s i g n i f i c a n t h y p o v o l e m i a . The so called ~'sodium pump," which main- tains low sodium concentra t ions of 10 to 12 mEq/l i ter inside the cell in spite of s o d i u m c o n c e n t r a t i o n of 135 to 142 mEq/l i ter in the extracellular fluid, depends on active (energy-mediated) cellular metabolism to funct ion. In damaged or ischemic cells, this process breaks down. As a consequence, sodium begins to diffuse into the cells and potassium, which normal ly has a concentrat ion of about 130 to 150 mEq/l i ter inside the cell, diffuses out into the ex- t r a c e l l u l a r f lu id . Because w a t e r tends to follow the sodium the cells begin to swell, pul l ing fluid from the extracellular fluid space, resul t ing in an increas ing tendency to hypovolemia in late shock, regardless of its original cause.

Capillary endothelial damage. As shock, or sepsis progresses, the capil- Jary e n d o t h e l i a l cells, which nor- really are th in , flat and fit t ight ly agains t each other, beg in ,to swell and separate, leaving progressively e n l a r g i n g i n t e r c e l l u l a r c a p i l l a r y spaces. 26 Fluid can then escape at an increasing rate from the capillaries into the in ters t i t ia l space. As these spaces enlarge, increas ing ly larger part icles , i n c l u d i n g p ro t e in mole- cules and eventua l ly red blood cells, can pass through the capillary wall. The capil lary leak, together with the in t race l lu la r edema, may resul t in

J ~ P September 1976

fluid leaving the circulation, even in re la t ive ly hypovolemic pat ients , at rates exceeding 200 ml/hr. Such a leak, seen early in severe sepsis, is so characteristic tha t any pat ient who requires more than 200 m l of fluid per hour , b e y o n d r e p l a c e m e n t of m e a s u r e d e x t e r n a l f lu id losses to m a i n t a i n vital signs, should be considered septic un t i l proven otherwise.

[ntravascular coagulation. As in- c r e a s i n g q u a n t i t i e s of vasoac t ive substances and acid metabolites accumulate in the capillaries, the precapillary sphincters in some vascular beds become para lyzed and dilate, resul t ing in s tagnat ion and pooling of blood in the peripheral microcircu- lation. This, together with hypovolemia caused by the fluid shifts out of the " leaking" capil lar ies , causes a progressive decrease and slowing in effective circulat ion in the affected vascular beds. This s tagnation, with the local capil lary chemical changes, causes increas ing red cell aggrega- t ion and in t ravascu la r clotting. If serial coagulation tests are performed, a progress ive drop in the p la te le t count and the plasma concentrat ions of fibrinogen, Factor V, Factor VIII and p r o t h r o m b i n ma y be found. Since these are "consumed" by the in t ravascular coagulation, this process is often referred to as a "con- sumptive coagulopathy."

The concentrat ions of the clotting factors may be extremely variable in crit ically ill and injured patients_ Se- rial clott ing studies are impor tant in such p a t i e n t s be c a use t hey ma y demonstra te significant trends long before all laboratory values are abnormal or the clinical picture characteristic of disseminated in t ravascular coagula t ion (DIC) develops. By the t ime DIC is c l in ica l ly reflected in t r o u b l e s o m e b l e e d i n g from needle puncture sites, surgical wounds and mucosal surfaces, the concentrat ions of the clott ing factors are extremely low_ At this point, the problem is dif- flcult to correct.

Monitoring

• Blood pressure : i n t r a - a r t e r i a l l ine if necessary

• Hear t rate and rhy thm (cardio- scope)

• R e s p i r a t o r y ra te , also n o t i n g depth

• C e n t r a l venous pressure (also p u l m o n a r y wedge p ressure in selected cases)

• Ur ine output (ml/hr and sodium concent ra t ions and/or osmolarity)

• Serial blood gases and electro- lytes

Close observat ion for t rends and responses is needed to identify pa- t ients who are get t ing into t rouble when the a b n o r m a h t y can st i l l be easily corrected. However, since all p a t i e n t s c a n n o t be e x t e n s i v e l y studied, clinical judgement is necessary. Wi th experience, it becomes easier to recognize those who need closest observation.

It is impor tant tha t such pat ients be monitored objectively and almost continously. Wherever possible, the observations should be put in numbers and "graphed." Rapid scanning of columns of numbers does not help r e c o g n i t i o n of sub t l e changes . Graph ic record ings of v i ta l s igns, par t icular ly blood pressure, are ex- t r e m e l y he lpfu l in d e m o n s t r a t i n g t rends in the pulse pressure. Fur- thermore, the responses of critically ill pa t ients are extremely variable. Single or isolated measurements are of less v a l u e t h a n t r e n d s or responses.

TREATMENT Primary Process

In t r ea t ing pat ients in shock, par- t i cu la r ly in the emergency department, it is impor tant to a t tempt to d e l i n e a t e the p r i m a r y process or cause. There is a tendency to treat signs, symptoms and laboratory data while forgett ing etiology. Although on occasion it is necessary to t reat shock pat ients without knowing the ini t ia l cause, a strong effort should always be made to establish an accurate diagnosis. Left uncorrected for more t h a n a few hours , problems such as i n t r a - a bdomina l abscesses, necrotic bowel, a ruptured spleen, or a ruptured ectopic pregnancy, have an ex t r eme ly high mor ta l i ty rate, regardless of how well the cardiovascu la r , r e s p i r a t o r y and me tabo l i c changes are corrected.

Correction of Pathophysiologic Changes/Ventilation and Oxygen

Need for increased ventilation. The

Volume 5 Number 9 83

first priority is to ensure adequate venti lat ion. Adequate vent i la t ion in the pat ient with severe sepsis shock or t r a u m a is of ten 11t2 to 2 t imes no rma l or more_ In such pa t ien ts , "normal" vent i la t ion should be considered inadequate, ie, if the pat ient with severe sepsis, shock, or t r auma is not h y p e r v e n t i l a t i n g , one m u s t suspect t ha t there is a s i gn i f i c an t v e n t i l a t o r y problem invo lv ing the brain, airway, chest wall, d iaphragm or lungs. Vigorous efforts should be made to diagnose and correct the abnormali ty. In many hospitals in Viet Nam, r e s p i r a t o r y f a i l u re was the mos t c o m m o n cause of d e a t h in wounded soldiers who could get to a hospital.2% 28 A s imi la r experience has been noted in our cri t ically ill and injured patients.

If the p a t i e n t is comatose or lethargic, it may be easy to inser t an orotracheal or nasotracheal tube to begin early vent i la tory assistance. If the pat ient is awake and alert, however, good topical anesthesia to the nose and airway and expertise in the technique of inser t ion is necessary to inse r t the tube a t r a u m a t i c a l l y . In general, nasotracheal tubes are better tolerated t han orotracheal tubes, but since they are longer and nar- rower, it is more difficult to suction thick or copious secretions. Some pa- t ients may not tolerate an oral tube u n l e s s s eda t ed or pa r a lyzed wi th drugs_

If vent i la tor assistance is required, volume-cycled resp i ra tors are preferred because they will del iver a consistently high t idal volume, 12 to 15 ml/kg body weight, which may be necessary to prevent or correct the diffuse microatelectasis tha t may develop. These pat ients are put on a respirator pr imar i ly to m a i n t a i n opti- mal vent i la t ion of alveoli and to pre- ven t or correct atelectasis. Mainte- nance of normal blood gas values is only a secondary consideration. Pre- ven t ion or correct ion of congestive atelectasis in the pat ient with severe t rauma, sepsis or shock usual ly requires much greater t idal volumes and m i n u t e v e n t i l a t i o n t h a n is needed to m a i n t a i n n o r m a l blood •gases.

While high t idal volumes are fa- vored, the inf la t ion pressure ~s kept to less t han 40 cm I-hO, if possible, to


decrease any risk of pneumothorax. When forced, however, to use infla- t ion pressures of 50 or more cm I-I20, we find ~'prophylactic" chest tubes may be of value, par t icular ly when the pat ient has had chest t r auma or previous pu lmonary disease. If pul- m o n a r y f u n c t i o n is poor, or dete- riorates in spite of the high tidal volumes, gradual ly add up to 3 to 10 cm I-I20 positive end expiratory pressure (PEEP). If blood p ressure fal ls by more t h a n 5 to 10 m m Hg w h e n PEEP is added, it can be assumed that the pa t ien t is hypovolemic and addit ional fluids or blood should be given. 29 If the pa t ien t is b rea th ing spontaneously and if lower t idal volumes are used, then much greater PEEP (up to 20 to 30 cm I-hO pressure) can be employed us ing a tech- n ique sometimes referred to as in- t e r m i t t e n t m a n d a t o r y v e n t i l a t i o n (IMV).

A slow respiratory rate, preferably 12 to 16/minute is desirable and mul- t ip le s m a l l doses of i n t r a v e n o u s m o r p h i n e , d i a z e p a m ( V a l i u m ) or Pavulon may be needed. In rare in- s t ances , i t m a y be n e c e s s a r y to paralyze the pa t ien t us ing succinyl- choline or curare. These drugs can be d a n g e r o u s w h e n the p a t i e n t is h y p o t e n s i v e or h y p o v o l e m i c a nd should be avoided if at all possible. If the respiratory rate cannot be con- trolled, high t idal volumes combined with the rapid respiratory rate can cause a severe respiratory alkalosis. Because of our reluctance to reduce tidal volume, we will inser t as much as 300 ml of dead space between the respirator and the pa t i en t to raise the PCO2 into the range of 30 to 35 mm Hg.

Diagnosis of respiratory insufficiency. The best method of t rea t ing respiratory fai lure is to prevent it. Unfor tunate ly , clinical evidence of a respiratory abnormal i ty is frequently not apparent un t i l it is so severe that it is difficult to correct. Serial blood gas analyses may be especially helpful.

Although more a t ten t ion is paid to the ar ter ial PO2 than to the PCO2, unless it is very low or greater t han 45-50 mm Hg, the lat ter is an impor- t an t indicator of adequacy of ventilation. The PCO2 provides evidence as to what the PO2 should be, particu-

larly if the pat ient is b rea th ing room air. Most pat ients with severe sepsis, t r a u m a or shock will hyperventi late and their PCCh will be 35 mm Hg or less. If the PCO2 is 40 mm Hg or higher, there may be a problem with the central nervous system, airway, chest wall or lungs.

When ar ter ia l PCO2 falls because of hypervent i ia t ion, the alveolar and arterial PO2 should rise by an almost equivalent amount. In other words, if a n o r m a l a d u l t w i t h an a r t e r i a l PCO2 of 40 mm Hg and PO2 of 80 m m Hg s u b s e q u e n t l y hype rven t i - lates and reduces his PCO~ to 25 mm Hg, his a r te r ia l PO2 should rise to a b o u t 95 m m Hg. One way to monitor such changes is to measure, or c a l c u l a t e the a l v e o l a r - a r t e r i a l oxygen difference (A-aDO2).

In hea l thy young adults breathing room air, the A-aDO~ is about 10 mm Hg and in h e a l t h y midd le - aged adults, it averages 10 to 20 m m Hg. Unfor tunate ly , in shock patients, the A-aDCh on room air is often much higher . For example, it is no t un- usual to see a pa t ient in early shock or sepsis who has a pH of 7.50, a PO2 of 70 mm Hg, an oxygen saturat ion of 94% and a PCO2 of 25 m m Hg. These blood gases would be considered sa t i s fac tory . However, if the A-aDO2 is considered, it can be seen immediate ly tha t significant abnormal i ty exists.

The A-aDO2 can be eas i ly esti- ma ted in mos t p a t i e n t s w i th l~re- v ious ly n o r m a l l ungs l i v i n g at or near sea level by adding the arterial PO2 and PCO2 on room air and sub- t rac t ing the sum from 145. Thus, if the pa t ient has a PO2 of 70 m m Hg and a PCO2 of 25 m m Hg, the esti- mated A-aDO2 would be 145-(70+25) or about 50 mm Hg. If the A-aDO2 on room air is r i s ing rapidly or exceeds 50 to 55 m m Hg, vent i la tory assis- t ance w i th a r e sp i r a to r should be considered.

We have noted an in teres t ing em- p i r ica l f i n d i n g in p a t i e n t s wi th a normal or high cardiac ou tput and previous ly n o r m a l lungs. The percentage of physiologic s h u n t i n g or arteriovenous admixture in the lung is a p p r o x i m a t e l y e q u a l to the A-aDO2 on room air minus 15. Thus, pat ients with an A-aDO2 difference of 50 mm Hg on room air, on the av-


erage, will have a physiologic shunt of about 35% in their lungs, ie, ap- proximately 35% of the blood going through the lungs is not completely oxygenated. Normal ly , the physiologic shun t is considered to be about 3% to 8% and if the shun t is r i s ing p rogress ive ly or exceeds 40%, ag- gress ive v e n t i l a t o r y a s s i s t ance is indicated_

Oxygen. E v e n if v e n t i l a t i o n is adequate, v i r tua l ly all shock pat ients will benefi t from the adminis t ra t ion of oxygen. Oxygen exchange may become impai red very quickly and if the cardiac output is decreased, tissue oxygenat ion may be total ly in- adequate_ Consequently, v i r tua l ly all shock pat ients should be given oxygen to m a i n t a i n an ar ter ial PO2 of at least 100 mm Hg dur ing the ini t ia l 4 to 6 hours of resusci tat ion. At this stage, we are not concerned about oxygen toxicity. If possible, we will give 100% 02 with a respirator, or face mask, p a r t i c u l a r l y if there is any evidence of myocardial ischemia. Later, after the pat ient ' s cardiovascular s ta tus has stabilized, a t tent ion can be directed to any potential pulmonary problems resu l t ing from the prolonged inha la t ion of high concen- t rat ions of oxygen_

Fluids. By far the most effective t r ea tment for all types of shock, par- t i cu la r ly fol lowing t r a u m a , is the early and aggressive adminis t ra t ion of fluids. In the injured patient, volume replacement is begun with 2 to 3 li ters of a balanced electrolyte solution given over 20 to 30 minutes. If addit ional fluid is needed to main- ta in adequate v i ta l signs, blood is adminis tered ra ther l iberal ly to keep the hemoglobin at 12.5 to 14.0 gin/ 100ml. We have found that the pa- t ients with hemoglobin levels in the range of 12.5 to 14.0 gm/100ml tend to m a i n t a i n a be t te r i n t r a v a s c u l a r volume, have a lower incidence of respiratory failure and are more apt to survive.

If the blood pressure in a recently in jured p a t i e n t does not r e t u r n to normal following the adminis t ra t ion of the balanced electrolyte solution, the pa t ien t is probably losing blood rapidly and emergency surgical control of the bleeding may be required.

Our choice of in i t ia l fluids is Ring- er's lactate solution. However, if the pat ient is in severe shock or is se-

~ P September 1976

verely cirrhotic, a buffered electro- lyre solution without lactate may be preferable. Such a solution can easily be made by adding one to two ampules of sodium bicarbonate to a liter of 0.9% saline.

I f the p a t i e n t ' s s e r u m p r o t e i n levels are very low, such as occurs with severe cirrhosis, plasma or al- bumi n may be given to help main- t a in a more normal colloid osmotic pressure in the blood_ However, the use of such colloids, par t icular ly al- bumin , is controversial_ In shock, especially if associated with sepsis, the a lbumin may move rapidly into the p u l m o n a r y i n t e r s t i t i a l space drawing water with it, increasing the tendency to respiratory failure.

If the p a t i e n t r equ i res mu l t i p l e t r a n s f u s i o n s , f resh frozen p l a s m a may have addit ional value because i t can help restore many of the clotting factors (except platelets) tha t are de- f ic ient in ~old" b a n k blood. When m a s s i v e t r a n s f u s i o n s are used, warming of the blood may help to reduce the incidence and severity of at- r h y t h m i a s a nd use of the n e w e r blood filters may help decrease the incidence of acute respiratory failure s e c o n d a r y to e m b o l i z a t i o n to the lungs of aggregates tha t have formed in the t ransfused blood.

We have avoided the use of low molecular weight dex t ran (LMWD) in acutely injured pat ients because (1) a l though it does not increase clot- t ing times, it may increase bleeding from raw surfaces, (2) we have seen a few severe allergic reactions following its use, and (3) dextran, particu- lar ly the p repara t ions wi th h igher molecular weight, may interfere with typing and cross-matching unless the red cells are washed with saline.

The amoun t of fluid given is de- t e rmined by many factors, including blood pressure, pulse rate, u r i n a r y o u t p u t ; s k i n pe r fu s ion , a nd the n u m b e r and loca t ion of a ny ra les tha t persist in spite of efforts to prevent or correct atelectasis. If the pa- t ient is in severe shock or does not respond promptly to therapy, a central venous pressure (CVP) catheter should be inserted and the CVP response to fur ther f luid adminis t ra - t ion checked carefully.

Many factors affect the CVP level and, therefore, its response to fluid

load is much more impor tan t t han the actual level. ~° The CVP in critically ill and injured pat ients is ex- t remely variable and frequently cor- relates poorly with the pat ient 's fluid needs. A number of patients, particu- larly those with sepsis or respiratory failure who have had a CVP above 20 to 25 cm I-hO, have had a rela- t ively low pulmonary wedge pressure (PWP) and have responded to a fluid challenge with an increased cardiac ou tpu t and improved t issue perfusion. The use of high tidal volumes and P E E P may increase the CVP and PWP by 5 to 10 cm I-hO or more. The CVP may also rise, or be high if the pa t ien t is receiving vasopressors because the ar ter ial vasoconstriction i n c r e a s e s the r e s i s t a n c e a g a i n s t which the hear t must pump tending to reduce ca rd iac output_ The increased venous constriction may also reduce vascular capacity, increasing venous re turn . to the heart.

If the CVP rises abrupt ly as fluid is given, the rate of fluid adminis t ra- t i o n s h o u l d be decreased , or the fluids stopped u n t i l the CVP falls back near the basel ine levels. Fre- quent use of CVP catheter for drawing blood may adverse ly affect its function. The column of fluid should fall abrupt ly and fluctuate well with respirators before it can be considered reliable. X-ray confirmation of ca the ter posi t ion is also impor t an t p a r t i c u l a r l y if i t is i n s e r t e d per- cutaneously into the subclavian vein. A l t e rna te in t r avenous lines should be used for the adYr~inistration of blood or colloid solutions.

In most instances, the functions of the r ight and left ventricles are quite s imi lar so tha t changes in the CVP, which reflect f i l l ing pressures in the r ight heart, correlate fairly well with changes in the PWP, which more ac- curately reflects left ventr icular fill- i ng p r e s su r e . In a n u m b e r of instances, however, the CVP and PWP may be quite disparate. For example, following an acute myocardial infarction, the pa t i en t may have an iso- la ted acute left ven t r i cu la r fa i lure with a low CVP and high PWP. On the other hand, pat ients with severe sepsis or respiratory failure not in- f requent ly have a high CVP and a low PWP.

The S w a n- G a nz catheter , a soft


balloon-tipped, flow directed catheter, is used for obta in ing the PWP. ~1 After inser t ion via a cutdown or per- cutaneously, the catheter position as i t is a d v a n c e d is d e t e r m i n e d by moni tor ing pressure recordings. Use of the S w a n - G a n z c a t h e t e r to monitor PWP is par t icular ly impor- t an t in pat ients with shock due to an acute myocardial infarction. We have had five such pat ients who developed pulmonary edema with CVP of less t han 5 cm I-hO. Another possible in- dication for ob ta in ing the PWP is a h igh CVP in pa t i en t s wi th severe sepsis or r e s p i r a t o r y f a i l u r e and hypotension.

One diff icul ty in m e a s u r i n g the PWP is tha t accurate recording gen- erally requires an electronic pressure monitor. Since it is a low pressure system, frequent recal ibrat ion of the equipment is mandatory. In general, a PWP less t h a n 10 mm Hg suggests hypovolemia and PWP of 20 mm Hg or h igher is an ind i ca t ion of f luid overload and/or left vent r icular failure. As with the CVP, however, the response of the PWP to a fluid challenge is much more informative than the level itself•

Use of blood volume de t e rmina - tions to guide the rate or amount of fluid adminis t ra t ion has been found to be very deceptive in our experience. The range of normal for blood v o l u m e s is r a t h e r l a rge a n d one s tandard deviat ion from the normal a v e r a g e s a b o u t 10%. The a c t u a l blood vo lume , moreove r , is no t near ly as impor tan t as the relation- ship between the blood volume and vascular capacity.

V a s c u l a r c a p a c i t y can c h a n g e rapidly with vasoconstriction or vasod i l a t i on . For example , v a s c u l a r

• capacity may be reduced up to 25% by vasoconstriction and with vasodilation, vascular capacity may be in- c reased by 40% to 50% or more. Blood volume d e t e r m i n a t i o n s wi th r a d i o i o d i n a t e d s e r u m a l b u m i n (RISA) are par t icular ly deceptive in shock because tl~e normal RISA dis- appearance rate of 8% per hour may be increased to as high as 30% to 35% in pat ients with shock or severe sepsis_

Acid-base therapy. Most acid-base problems in shock will improve spontaneously if adequate vent i la t ion and


t issue perfusion are provided.

The bicarbonate deficit can be cal- culated by considering the bicarbonate space to be equal to 30% to 50% of the body weight, with the larger f igure app l i cab le to base def ic i ts greater t han 15 mEq/li ter . Thus, a base deficit of 10 mEq/l i ter in a 70 kg ma n can general ly be corrected with about 210 mEq of bicarbonate. If the base deficit in the same pat ient were 18 mEq/liter, however, it might take 630 mEq of bicarbonate or more to correct the deficit.

Only half the base deficit is corrected at a t ime, general ly at a rate not exceeding 3 to 5 mEq/minute . If the pa t ient has a combined acidosis, he is most l i ke ly in the t e r m i n a l phases of shock. In such pa t ien ts , bicarbonate may be ineffective, and TRIS buffer may be required_

Inotropic Agents Digoxin. The r e is m u c h con-

t r ove r sy over the f u n c t i o n a l capabilities of the heart in critically ill and injured patients. In our opinion, all pa t ients who remain in shock despite adequate fluid admin i s t r a - t ion have some e lement of hear t failure and should be digitalized. Since la rge doses of d igox in m a y cause splanchnic vasoconstriction, mult iple smal l i n t r a ve nous doses should be administered.

In the p a t i e n t w i th an acu te myocardial infarction, the use of di- gi tal is prepara t ions is very contro- versial_14, ~2 Al though these drugs may improve myocard ia l funct ion, they also increase myocardial oxygen demands and may s igni f icant ly increase the incidence and severity of ar rhythmias .

The amoun t of digoxin needed in shock pa t i en t s is var iab le and, although use of an EKG response is not the best method to regulate dosage, it may be the only way to obtain some reasonab le idea of its effect. Some shock may be adequate ly digitalized us ing half the usual dosage.

Dopamine. Although dopamine has only been avai lable for general clinical use for a short time, it has become our choice of positive inotropic agents in the t r ea tment of shock. In smal l doses it may increase r e na l and sp lanchnic blood flow wi thout

s ignif icant change in cardiac output or blood pressure . In slightly larger doses, d o p a m i n e m a y i n c r e a s e pe r iphera l vasocons t r ic t ion bu t its inotropic effects are usua l ly s t rong enough to also increase cardiac output .~ , ~4 This is in sharp contrast to vasopressor drugs such as norepi- n e p h r i n e (Levophed) a n d m e t a r a - minol (Aramine), which usual ly reduce cardiac output because of the excessive vasoconstriction they produce. However , as the a m o u n t of dopamine infused is increased, its vasoconst r ic t ive proper t ies become more d o m i n a n t and cardiac output may fall. If dopamine is admin i s - tered too rapidly, troublesome tach- y a r r h y t h m i a s occasionally will develop.

Epinephrine. Epinephr ine is used by some clinicians' when a combina- t ion of an inotropic agent and vasoconstrictor might be of benefit. In our own e x p e r i e n c e , however , dopamine tends to produce a more uniform response and a bet ter rise in cardiac ou tput with much less tendency to dangerous dysrhythmias.

Calcium. A d m i n i s t r a t i o n of calcium should be considered when any shock p a t i e n t is g iven m u l t i p l e t r a n s f u s i o n s . U n d e r such c i rcumstances, the citrate may reduce the ionized calcium level in the blood to the point of impai r ing cardiovascular funct ion. Consequen t ly , a gra m of calcium chloride is given after every 2 to 4 uni ts of blood in pat ients with pe r s i s t en t hypotension_ Ord inar i ly ca l c ium can be r a p i d l y mobi l ized when the ionized calcium levels fall because of the citrate in the stored blood. In shock, however , ca lc ium mobilization may be impaired.

Isoproterenol. In the unusua l shock pat ient with a slow pulse rate, isoproterenol in doses of 1 to 2 mg per minute may be helpful_ If the pulse ra te exceeds 120/minute , however, isoproterenol is cont ra indica ted because it is not apt to improve cardiac output and is more l ikely to cause da nge r ous t a c h y a r r h y t h m i a s . Iso- proterenol should not be given to pc- t ients with an acute myocardial infarction or pu lmonary embolus because it m a y inc rease myocard ia l oxygen demands much more t h a n it increases coronary blood flow.

Glucagon_ The use of glucagon is

September 1976 J ~ F )

controversial and we rarely use this drug except as a last resort_ How- ever, in about 20% to 30% of the patients in whom we have used it in large doses (4 mg bolus and then 10 mg per hour by constant in t ravenous infusions), it has produced some, although temporary, improvement. Re- const i tu t ion of glucagon should be done hourly, as it rapidly loses its po- tency at room temperature .

Steroids Small ("physiologic") doses. Al-

though i t has been a s s u m e d t h a t virtually all pat ients with shock respond with increased secretion of ad- renocortical hormones, in our own studies we have seen severa l patients who have not increased their blood cortisol levels and who have not responded to adrenocorticotropic hormone (ACTH). Because of the possibility tha t subcl inical adrena l insufficiency may be present, all pa- t ien ts w i th shock u n r e s p o n s i v e to usual t h e r a p y should be g iven at least 200 mg of hydrocor t isone by rapid in t ravenous injection.

No pat ient is allowed to die in shock without getting at least 200 mg of hydrocortisone rapidly intra- venously.

This is par t icu lar ly impor tan t in patients, such as those with chronic severe rheumatoid arthri t is , who are likely to have been given steroids for prolonged periods in the past. A few patients who do not respond to other therapy, when given this amount of hydrocor t isone, may improve dra- matically.

Massive (pharmacologic) doses. Al- though there is genera l agreement that "physiological" doses of steroids are beneficial and, indeed, necessary in p a t i e n t s w i t h a d r e n a l insuf f i - ciency, the use of massive steroids in shock is extremely controversial.35, 36 Much evidence exists to suggest tha t massive steroids can be valuable in experimental shock by restoring cell and capil lary membrane permeabil- ity 37 and by improving cardiovascular f u n c t i o n 3s and c e l l u l a r me ta - bolism. 3s,4° However, there are no good double-b l ind prospective clinical s tudies to conclusively demon- s t ra te t h e i r va lue . N e v e r t h e l e s s , inves t iga tors 41-4G have described a humber of pa t i en t s who appear to have improved d r a m a t i c a l l y af ter


massive steroids in doses equivalent to 50 to 150 mg of hydrocortisone per ki logram body weight. In a previous clinical study, us ing the equivalent of 50 mg of hydrocortisone per kilo- g ram body weight , we noted t h a t massive steroids tend to "normalize" cardiac o u t p u t and the total peripheral resistance. 47 Pat ients with a low card iac o u t p u t and excess ive vasoconstr ic t ion seemed to develop somewhat higher cardiac output and somewhat less vasoconstr ict ion. In contrast, pat ients with a high cardiac o u t p u t a nd v a s o d i l a t i o n e i t h e r showed no change or had a drop in cardiac output and rise in peripheral v a s c u l a r r e s i s t a n c e . U s i n g doses equiva lent to 150 mg hydrocortisone per k i log ram, most p a t i e n t s have shown some vasodilation even if they are already somewhat vasodilated.

Our presen t massive steroids reg- i m e n cons i s t s of g iv ing , i n t r a v e - nously, a complete dose over 10 to 15 minutes and again in 4 to 6 hours, whiie ob ta in ing objective studies before, 30 minu tes and two hours after each dose. If any improvemen t occurs, the dose is repeated every 4 to 6 hours as needed but seldom beyond 24 to 48 hours. We have found no definite cl inical difference between methylprednisolone succinate (Solu- medrol), 30 mg/kg and dexametha- sone phosphate (Decadron), 6 mg/kg.

There is no quest ion in our minds that the earl ier the massive steroids are given, the better the response. As soon as it appears tha t the pat ient is not l ikely to improve with rapid aggressive s tandard therapy, massive steroids are indicated. Since the response to steroids is often quite sub- tle, it may not be recognized unless ca re fu l objec t ive s t ud i e s are performed before and after adminis t ra- tion of the drug. If improvement is noted, bu t the pat ient 's condition de- teriorates again later, the doses may be repeated every 4, 6, or 8 hours, but the massive steroids are discon- t i n t e d after 24 to 48 hours. Used in this manner , we have seen no com- plications from massive steroids.

Vasopressors. In general, vasopressors can be considered po ten t i a l ly lethal drugs, only to be given as a temporary measure when there appears to be no other rapidly effective m e t h o d of r e s t o r i n g an a d e q u a t e

coronary or cerebral blood flow. They should not be adminis tered un t i l an adequate t r ial with venti lat ion, oxygen, fluids, acid-base correction, inotropic agents, and steroids has been given.

The le thal i ty of the vasoconstrictors has been well demonstrated in our l abora tory (R. F. Wilson, MD, unpub l i shed data). Norep inephr ine in doses of 5 mcg/kg/min given for one hour to hea l thy dogs almost uni- formly causes death wi thin 24 hours. If, however, mass ive steroids were given before, or small amounts of a vasod i l a to r such as p h e n t o l a m i n e (Reg i t i ne ) were g iven wi th the norepinephrine, most of the an imals survived.

Large, c o n t i n u i n g doses of vasopressors can cause almost complete occlusion of arterioles with resu l tan t cessa t ion of blood flow to progressively larger t issue areas. Addition of a vasodilator may take some of the '~edge" off the sever i ty of the vas- o c o n s t r i c t i o n . A d m i n i s t r a t i o n of n o r e p i n e p h r i n e in hypovo lemia is p a r t i c u l a r l y l e t h a l and is ap t to cause complete ar ter iolar occulsion. As a consequence , vasocons t r ic tor d rugs s h o u l d n e v e r be gi.ven to hypovo lemic p a t i e n t s except very t r ans ien t ly to m a i n t a i n coronary perfusion in elderly pat ients while other t r e a t m e n t is be ing in i t i a ted . Fur- thermore, a vasodilator or massive s teroids should p robab ly be g iven with, or before, the vasopressors to reduce the excessive vasoconstriction tha t might otherwise result.

The choice of vasopressors may be impor tant . Agents such as phenyl- ephrine (Neo-synephrine) and meth- oxamine (Vasoxyl), which have only a per iphera l vasoconstr ictor effect, can effectively raise blood pressure but at the same t ime can cause severe r educ t i ons in cardiac o u t p u t and t issue perfusion. 41 Vasopressors such as norep inephr ine (Levophed) and me ta ramino l (Aramine), which are p r e domi na n t l y vasoconstrictors with some cardiac effect, genera l ly cause less of a drop in cardiac output. With norepinephrine , the smaller the dose used per minute , the less vasoconstrictor effect produced relat ive to the ca rd iac effect; wi th l a r g e r doses, the vasoconstrictor effect becomes more and more dominant .


Our cur ren t choice of vasopressor solution for ra i s ing the blood pressure, if none of the previously men- tioned therapy ( including dopamine) has been effective, is four ampules of Levophed and two ampules of phen- tolamine (Regitine) in 500 ml of 5% g lucose - in -wate r . Reg i t ine in th is dosage may prevent excessive vasoconstr ic t ion bu t it does not significant ly a l ter the cardiac ou tpu t or peripheral vascular resistance_ Fur- thermore, if the Levophed should ex- t ravasate into the tissue around the vein, the phento lamine prevents the local necrosis which can resul t from the excessive vasoconstrictor effect. In i n s t ances w h e n the p a t i e n t al- r e ady seems exces s ive ly vasocons t r ic ted , the c o n c e n t r a t i o n of Reg i t ine may be increased to two a m p u l e s for each a m p u l e of Levophed.

The o p t i m a l blood p r e s s u r e in shock is v a r i a b l e . C o n s e q u e n t l y , close o b s e r v a t i o n of the p a t i e n t ' s CNS ac t iv i ty , e l e c t r o c a r d i o g r a m s (EKG) and ur ine output is required to properly regulate the dose of vasopressors and inotropic agents. One technique that may be helpful is to raise the blood pressure to "normal" or sl ightly higher levels with a vasopressor and note the pat ient ' s alert- ness, E K G and u r i n e output . The blood p ressure is t h e n al lowed to g r a d u a l l y fal l , u n t i l a c h a n g e is noted in any of these pa ramete r s . This blood pressure is then considered to be the basal one. The dose of vasopressor is regulated to m a i n t a i n the p ressure 10 to 20 m m h ighe r t han the basal level.

The re is some q u e s t i o n a s to whether vasopressor drugs are ever required in young patients, particu- larly following t rauma. However, in older pat ients with signif icant coro- n a r y or cerebra l a r t e r i a l s tenosis , where flow m a y be p r e s s u r e - dependent and may require normal or h i g h e r p res su res , vasopressors may be used temporar i ly to correct hypotension while other, more defi- nitive, t r ea tmen t is being inst i tuted.

It may be impor tan t to keep the mean ar ter ial blood pressure in pa- t ients with 70% to 80% coronary artery occlusion at about 75 to 85 mm Hg whi l e c o r r e c t i n g the p r i m a r y problem. In those without coronary a r t e r y d i sease , r a i s i n g the blood


pressure usual ly results in a fall in cardiac ou tpu t and an increase in myocardia l oxygen demand tha t is greater t han the increase in coronary blood flow. However, in pat ients with significant coronary disease, ra is ing the mean blood pressure to 75 mm Hg may increase coronary blood flow more t h a n it increases myocardia l oxygen d e m a n d s a n d the ca rd iac output may rise_ Rais ing the mean blood pressure above .85 mm Hg in such patients, however, often causes a d i s p r o p o r t i o n a t e i n c r e a s e in myocardial oxygen needs and a fall in cardiac output.

Even small changes in the amount of vasopressors delivered may cause wide f luctuat ions of vital signs. Use of mechanical devices helps to ensure a c o n s t a n t i n f u s i o n at the proper rate. No medications used to main- t a i n n o r m a l v i t a l s igns should be adminis tered through the CVP hne because of the i n t e r m i t t e n t rate of infusion that resul ts while the CVP is being measured_

Vasodilators. If the pa t ient shows evidence of excessive vasoconstric- t ion a nd poor t i s sue pe r fus ion in spite of all t h e r a p y and his blood pressure is no rma l or high, a vasodilator may, on occasion, be helpful. These agents should not be used in p a t i e n t s who are hypovolemic because vasodilators may increase vascular capacity by up to 2 to 3 liters, m a k i n g the p a t i e n t e v e n more hypovolemic and resul t ing in sudden severe h y p o t e n s i o n . In sp i te of adequate volume, vasodi la tors will often cause the blood pressure to fall by at least 5 to 10 m m Hg. If the pa- t ient is already hypotensive, such. a drop in blood pressure may seriously j e o p a r d i z e c o r o n a r y a nd c e r e b r a l blood flow, par t icular ly if these yes- sels have a 70% to 80% occlusion t h a t m a k e s flow t h r o u g h t h e m pressure-dependent.

Al though pa t i en t s with sepsis or cirrhosis who appear to be vasodilated may have isolated areas of vasoconstr ic t ion in some vi ta l organs, the use of vasodilators in such pa- t ien ts has resul ted in an increased morta l i ty rate_4S, 49 It appears to be safe to use v a s o d i l a t o r s i n vas- oconstricted pat ients and to use vasoconstrictors in vasodilated patients_ However, it appears to be much more

dangerous to use vasodilators in vasodilated pa t i en t s and vasoconstrictors in pa t i en t s who a l ready show evidence of severe vasoconstriction.

Of the various vasodilators avail- able , we pre fe r c h l o r p r o m a z i n e (Thoraz ine) i n m u l t i p l e s m a l l in- t ravenous doses beg inn ing with 1 to 2 mg every three to five minutes . We increase the dose un t i l an adequate improvement in skin perfusion and ur ine output is noted. In many pa- t ients, par t icular ly those with excessive vasoc0nstrictlon, massive doses of steroids may produce signif icant vasodilation and an improvement in cardiac o u t p u t due l a rge ly to the peripheral effects of the drug.

Diuretics. If the ur ine output is not a d e q u a t e a f t e r a l l t he a fo remen- tioned therapy and the extracellular volume has been restored, diuretics m a y be t r ied . The mos t effect ive method for ob ta in ing a satisfactory ur ine output, however, is to adminis- t e r a d e q u a t e f lu ids . If t he u r i n e output is s t i l l less t h a n 40 to 50 ml/ hour , 5 to 10 mg of f u r o s e m i d e (Lasix) in t ravenous ly may be used. The dose is then doubled every 15 minutes un t i l at least 50 to 100 ml of u r i n e / h o u r is o b t a i n e d or u n t i l a s ing le dose of 500 to 1000 mg is reached. Use of 40 to 80 mg of Lasix as the in i t i a l dose can occasionally cause excessive diuresis resu l t ing in severe catastrophic hypovolemia.

If more t h a n 20 mg of furosemide is g iven w i t hou t adequa t e resul t s and the pa t ient does not appear overloaded or in congestive hear t failure, a test dose of 10 to 20 gm of mannito! is often used coincident With the progressive Lasix therapy. If ol iguria persists, we assume tha t the patient is in renal failure and t rea t him ac- cordingly_ Such a si tuation, however, makes the t r e a t m e n t of shock ex- t remely difficult, if not impossible. Ol igur ic r e n a l fa i lure , in spite of dialysis therapy, has been associated w i th m u c h h i g h e r m o r t a l i t y ra te than nonoliguric renal failure.

Antibiot ics_ P a t i e n t s w i t h prolonged shock have decreased resistance to infection. The mucosal barrier in the intest ine, because of ira- paired cell metabolism, may become inc reas ing ly permeable to bacter ia a nd b a c t e r i a l p roduc t s . The re- t i c u l o e n d o t h e l i a l sys tem, par t icu-

September 1976 ~ ] ~ )

larly in the poorly perfused liver, may be less effective. Consequently, these pa t i en t s are closely observed for any sign of infection. At the ear- liest indicat ion of an infection or septic focus, antibiotics are begun, after we first ob ta in appropria te smears and cultures.

The choice of antibiot ics will de- pend upon which par t of the body is most l ikely to be the source of infection and on current hospital bacterial sensitivities. For infections involving the per i toneal cavity following disease or t r a u m a to the distal small bowel or colon, our preferred regimen now consists of a combinat ion of gen- tamicin for g ram-nega t ive aerobes, p e n i c i l l i n or a m p i c i l l i n for en- terococci a n d c l i n d a m y c i n for anaerobes, pa r t i cu la r ly Bacteroides fragilis.

Heparin. V a r y i n g degrees of in- t ravascula r coagula t ion can be assumed to be present in most pat ients with severe, pe r s i s t en t shock, par- ticularly if the pa t ient is septic. Only a small percentage, however, present with the full-blown clinical syndrome of DIC. If serial coagula t ion studies reveal a progressive reduction in the platelet count and in the concentration of Factor V, Factor VIII, fibrinogen and prothrombin, we recommend that h e p a r i n t r e a t m e n t be b e g u n immed ia t e ly . The fu l l -b lown syndrome with bleeding from mult iple areas, if allowed to develop, is extremely difficult to correct.

T rea tment of DIC includes (a) re- versal of the pr imary septic or shock process (the most difficult par t of the treatment), (b) hepar in in full dosage and (c) rep lacement of clot t ing factors if troublesome bleeding is occur- ring. In our opinion, heparin, to be effective in DIC, should only be given in a loading dose of 5,000 to 10,- 000 uni ts by rapid in t ravenous injection followed by a constant infusion of 500 to 1500 uni ts per hour to main- tain a th rombin or clotting t ime 21~ to 3 t imes normal or par t ia l throm- boplastin t ime of 7 0 to 80 seconds. The clott ing factors can be replaced with fresh, frozen p la sma and the platelet coun t can be ra i sed wi th platelet concentrates.

Mechan ica l ass is tance. If cardiogenic shock pers is ts in spite of adequate vent i la t ion, oxygen, fluids,


ac id -base co r rec t ion , i no t rop i c agents, steroids, vasopressors or vasodilators, and control of ar rhythmias , it can be assumed that the persis t ing shock is due to "power failure" because of inadequa te func t ion ing of 40% to 70% of' the left ven t r i cu la r myocardium. If severe hypovolemia is present, much smaller infarcts can cause shock_ If power failure persists for more t h a n two hours , the mortal i ty rate approaches 100% and m e c h a n i c a l suppor t of c i r c u l a t i on wi th c a r d i o p u l m o n a r y bypass or coun te rpu l sa t ion should be consid- ered_

If i n t r a - a o r t i c ba l loon p u m p i n g (IABP) is begun before further cardiovascular and other organ function has i r reversibly deteriorated, up to a th i rd of the pa t i en t s may improve s u f f i c i e n t l y to t e r m i n a t e IABP wi th in 2d hours. A second thi rd may improve temporari ly, but cannot be taken off the IABP. Under such cir- cums t a nc e s , a n g i o g r a p h i c s tud ies should be performed to determine if the pat ient has a mechanical cardiac problem or major coronary occlusion that can be surgically corrected. Al- though cardiac surgery under such c i rcumstances is associated with a high mor ta l i ty rate, these pa t ien ts have no other chance of survival.

Reversible Causes of So-Called Irreversible Shock

At t imes shock may be so severe or so unresponsive to s tandard therapy, tha t it appears irreversible. Under such circumstances, it is wise to re- eva lua te the pa t i en t to be ce r t a in tha t some revers ible causes of the persis tent shock have not been over- looked. Some of the more f requent t reatable causes of persis tent shock include

• inadequate fluids due to

f a i l u r e to a p p r e c i a t e the amoun t of fluid or blood loss

an incorrect impress ion tha t the pa t ien t is overloaded because:

he either has already been given large amounts of fluid

the CVP is inaccurate or de- ceptively high,

rales (due to atelectasis) are heard_

• i n a d e q u a t e v e n t i l a t i o n or hypoxia

• u n r e c o g n i z e d pneumothorax

• pu lmonary emboli

• cardiac tamponade

• inadequate ly treated sepsis

• acid-base or electrolyte abnormali t ies

• adrenal insufficiency

• hypothermia

• p rev ious pro longed t r e a t m e n t w i t h a n t i h y p e r t e n s i v e d rugs such as reserpine

SUMMARY

Shock s h o u l d be t h o u g h t of in terms of a disorder of cell metabolism rather t han in terms of a simple cir- culatory problem, par t icular ly if sepsis is present. Ear ly diagnosis is es- sen t ia l bu t is usual ly only possible if the problem is ant icipated and frequent , a lmost continuous, objective moni tor ing is performed. Trea tmen t ideally is preventive, and should be based on and guided by objective trends and responses rather than isolated measurements . A logical step- wise a p p r o a c h to t h e r a p y and a check- l is t for r e s i s t a n t cases is of de f imte value , p a r t i c u l a r l y in the emergency depa r tmen t where early diagnosis is often difficult.

REFERENCES

1. Wilson RF, Thal AP, Kindling PH, et al: Hemodynamic measurements in septic shock. Arch Surg 91:121-129, 1965.

2. Wilson RF, Sarver EJ, LeBlanc PL: Factors affecting hemodynamics in clinical shock with sepsis. Ann Surg 174.'939- 943, 1971.

3. Shires GT, Carrico C J, Canizaro PC: Classification and clinical and physiologic manifestat ions of shock, in Shock, Philadelphia, WB Saunders Co, 1973, p 4.

4. Weil MH, Shubin H: General concepts and definitions, in Diagnosis and Treat- ment of Shock, Baltimore, Williams & Wilkins Co, 1967, p 16.

5. Duff J: Cardiovascular changes in sepsis. Heart & Lung, to be published.

6. Finley RJ: The metabolic basis of sepsis in man. Read before the Critical Care Symposium, Wayne State University, De- troit, Michigan, 1976.

7. Schumer W, Nyhus LM: Corticosteroid effect on biochemical parameters of human oligemic shock. Arch Surg 100:405-408, 1970.


8. Wilson RF, Larned PA, Corr JJ , et al: Physiologic shunt ing in the lung in critically ill or injured patients. J Surg Res 12:571, 1970.

9. Wilson RF, Karl A, Asuncion Z, et al: Clinical respiratory failure after shock or t rauma: prognosis and methods of diagnosis. Arch Surg 98:539-550, 1969.

10. Lucas CE, Rector FE, Werner M, et al: Altered renal homeostasis with acute

, sepsis. Clinical significance. Arch Surg 196:444-449, 1973.

11. Bar ron DH: The pressure g rad ien t and pulse in the vascular system, in Ruch TC, Ful ton FJ (eds): Medical Physiology and Biophysics, Philadelphia, WB Saun- ders Co, 1960, p 667.

12. Wilson RF, Gibson DB, Percinel AR, et al: Severe a lkalos is in cr i t ica l ly ill surgical patients. Arch Surg 105:197-203, 1972.

13. Wilson RF: Acid-Base Abnormali t ies in Clinical Shock, Shumer W, Nyhus L (eds): Treatment of Shock: Principles and Practice, Phi lade lph ia , Lea & Febiger, 1974, pp 37-52, chap 3.

14. Gunnar RM, Loeb HS: Use of drugs in cardiogenic shock due to acute myocardial infarction. Circulation 45:1111-1124, 1972.

15. Kuhl L: The t r ea tmen t of cardiogenic shock. Am Heart J 74:578-581, 1967.

16. McCar thy B, M a m m e n E, LeBlanc PL, et al: Subclinical fat embolism: a prospective study of fifty pat ients with ex- t r e m i t y f rac tu res . J Trauma 13:9-16, 1973_

17. Wilson RF, McCarthy B, LeBlanc PL, et al: R e s p i r a t o r y and c o a g u l a t i o n changes af ter uncompl ica ted fractures. Arch Surg 106:395-399, 1973.

18. Kirkpatr ick JR: Cardiac a r rhy thmias - - an ea r ly s ign of sepsis . A m Surg 39:380-382, 1973.

19. Carey LC, Lowery BD, Cloutier CT: H e m o r r h a g i c shock. Curr Probl Surg January , 1971, pp 3-48.

20. Wi l son RF, Robb HJ: P l a t e l e t , hemodynamic, and respira tory changes, in H inshaw LB, Cox BG (eds): Shock, Sepsis, and Trauma. The Fundamental Mechanisms of Shock. 23:145-150, 1972.

21. Lefer AM, S p a t h JA: P a n c r e a t i c h y p o p e r f u s i o n and the p r o d u c t i o n of myocardial depressant factor in hemor- r h a g i c shock. Ann Surg 179:868-876, 1974.

22. Hinshaw LB, Archer LT, Black MR, et al: Myocardial function in shock. Am J Physiol 226:357-366, 1974.

23. Schayer RW: Relationships of stress induced hist idine decarboxylase activity in h i s t a m i n e s y n t h e s i s to c i r cu la to ry homeostas is & shock. Science 131:226- 227, 1960.

24. Wilson RF, Chris tensen C, Ali M, et al: Oxygen consumption in critically-ill surgical pat ients . Ann Surg 176:801-804, 1972.

25. Lucas CE, Sugawa C, Riddle J, et a]: Natura l history and surgical di lemma of "sLress" g a s t r i c b leed ing . Arch Surg 102:266-273, 1971.

26. Wilson JW: Pulmonary factors produced by septic shock: cause or consequence of shock lung? J Reprod Med 8:307-312, 1972.

27. Mar t in AM, Soloway HB, Simmons RL: Pathologic anatomy of the lungs following shock and t r a u m a . J Trauma 8:687-699, 1968.

28. Patterson, in discussion, Gomez AC: Pu lmonary insufficiency in nonthoracic t rauma. J Trauma 8:676-686, 1968.

29. Powers SR, Manna l R, Neclerio M: Physiologic consequences of positive end- expiratory pressure (PEEP) venti lat ion. Ann Surg 178:265-272, 1973.

30. Wilson RF, Sarver E, Birks R: Cen- t ra l venous pressure and blood volume d e t e r m i n a t i o n s in cl inical shock. Surg Gynecol Obstet 132:631-644, 1971.

31. Swan HC, Ganz W, F o r r e s t e r J: Catheter izat ion of the hear t in man with use of a f low-d i r ec t ed b a l l o o n - t i p p e d ca the t e r . N Engl J Med 283:447-451, 1970.

32. Tha l AP: T r e a t m e n t , in Shock: A Physiologic Basis for Treatment. Chicago, Year Book Publishers, 1971, p 251.

33. Loeb HS, Winslow EB, Rohimtoola SA: Acu te h e m o d y n a m i c effects of dopamine in pa t ien ts with shock. Circula- tion 44:163-173, 1971.

34. Wilson RF, Sibbald WJ, J aan imag i JL: Hemodynamic effects of dopamine in critically ill septic patients. J Surg Res 20:163-172, 1976.

35. Glenn TM (ed): Steroids and Shock, Baltimore, Univers i ty Park Press, 1974.

36. Erve PR: Immune response in septm shock: t h e r a p e u t i c i m p l i c a t i o n s , in Schumer W, Nyhus LM (eds): Treatment

of Shock." Principles and Practice, Philadelphia, Lea & Febiger, 1974, p 141.

37. Lillehie RC, Dietzman RH, Movsas S, et al: T rea tmen t of septic Shock. Modern Treatment 4:321-346, 1967.

38. D i e t z m a n RH, E r s e k RA, Lil lehei CW, et al: Low output syndrome: recogni. tion and t rea tment . J Thorac Cardiovasc Surge57:138-150, 1969.

39 Schumer WJ, Moss GS, Nyhus LM: Metabolism of lactic acid in the macacus rhesus monkey in profound shock. Am J Surg 118:200-205, 1969.

40. Schumer WJ, Nyhus LM: Cortico. steroid effect on biochemical parameters of h u m a n o l igemic shock. Arch Surg 100:405-408, 1970.

41. Wilson RF, Ali M, Anand V, et al: The effects of vasoactive agents in clinical septic shock. Brook Lodge Shock Sym- posium. Ams te rdam, Excerpta Mediea, 1972, p 269-281. .-

42. Nishi j ima H, Weil MH, Shubin H, et al: Hemodynamic and metabolic studies on shock associated with gram negative bacteremia. Medicine 52:287-294, 1973.

43. Wilson RF, Chiscano AD, Quadros E, et al: Some observations on 132 patients with septic shock. Anesthesia~Analgesia, 46:751-763, 1967.

44. Wilson l~F, Quadros E, Chiscano A: Some observat ions on 58 pa t ien t s with ca rd iac shock. Anesthesia~Analgesia, 46:764, 1967.

45. Vyden JK, Nagasawa K, Rabinowitz B, et al: Effects of methylprednisolone admin i s t r a t ion in acute myocardial infarction. A m J Cardiol 34-'677, 1974. 46. C r a m p t o n RSI W a g e n s t e e n SL, Lovett WL, et al: Product ion of a myocardial depressant factor in shock following acute myocardial infarction_ Preliminary e v a l u a t i o n of t r e a t m e n t w i t h methyl - prednisolone, abstracted. Am J Cardiol 29:257-258, 1972.

47_ Wilson RF, F i she r RR: The hemodynamic effects of mass ive steroids in shock. Surg Gynecol Obstet 127:769, 1968.

48. Wilson RF, Rizzo J: Hemodynamic changes , t r e a t m e n t and p rognos i s in c l in i ca l shock. Arch Surg 102:21-24, 1971.

49 Fromm S, Wilson RF: Phenoxyben- zamine in h u m a n shock. Surg Gynecol Obstet 129:789-793, 1969.

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shock in the emergency department

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