Chapter 2.

1 Shock
Principles and Practice of Emergency Medicine
CHAPTER 2 CAR!"#ASC$%AR S&STEM 'A!%$RE A( SH"C)
1 Shock
Max Harry Weil and Eric C. Rackow
Introduction
Hemodynamic Mechanisms of Shock
INR!"#CI!N
Shock is a clinical syndrome characteri*ed +y protracted prostration, pallor, coolness and moistness of the skin,
collapse of the s-perficial .eins, alteration of mental stat-s, and s-ppression of -rine formation. The +asic defect that
-nderlies shock is a red-ction in effecti.e perf-sion of tiss-es /ith decreased o0ygen deli.ery to the capillary +ed. The
systolic arterial press-re is -s-ally less than 12 mm Hg or has declined +y more than 32 mm Hg from a pre.io-s
hypertensi.e le.el. A 4normal5 +lood press-re may reflect e0cessi.e .asoconstriction e.en /hen +lood flo/ is critically
red-ced.
Shock may +e regarded as a hemodynamic defect of s-ch se.erity that deli.ery of o0ygen is not ade6-ate to
meet the meta+olic needs of the tiss-es
718. 9iochemical dist-r+ances follo/ ischemic in:-ry to tiss-es. These incl-de the li+eration of lysosomal en*ymes,
histamine, serotonin, kallikrein, and prostaglandins; alterations in +lood clotting /ith cons-mption coag-lopathies and
disseminated intra.asc-lar coag-lation; red-ction in retic-loendothelial acti.ity; and the release of protein +reakdo/n
prod-cts, especially -ric acid, -rea, and creatinine. Acidemia from an e0cess of these acids, as /ell as lactic and
pyr-.ic acid, fatty acids, ketones, and amino acids, ens-es. Signs of diff-se in:-ry appear, incl-ding increases in
ser-m transaminase and lactic dehydrogenase. !ndocyanine green clearance +y the li.er is impaired, reflecting a
decrease in hepatocell-lar f-nction. <hen intracell-lar o0ygen is critically red-ced, mitochondrial f-nction and the
regeneration of high=energy phosphate compo-nds are impaired
728. Cell-lar mem+rane permea+ility is increased, and the sodi-m=potassi-m p-mp is damaged. Accordingly, intracell-lar
potassi-m is red-ced, sodi-m concentration is increased, and the cell s/ells. !ntracell-lar acidosis and lysosomal
lysis /ith release of lysosomal hydrolases initiate a-todigestion of cell parenchyma /ith -ltimate cell death
7>8. !mpairment of aero+ic meta+olism triggers a less efficient anaero+ic path/ay of energy prod-ction /ith acc-m-lation
of lactic acid, /hich has +een correlated /ith se.erity and s-r.i.al 7?,3,@,A and B8 7'ig. 2C1.18.
<e +elie.e that the lactate concentration c-rrently ser.es as the +est single meas-rement of the presence and the
se.erity of shock states 718.
HEM!"$N%MIC MECH%NISMS !& SH!C'
The hemodynamic mechanisms of shock are +est .ie/ed in relationship to the f-nctional components of the
cardio.asc-lar system.
The first component is the total .ol-me of +lood contained /ithin the .asc-lar compartment.
The second component is the heart, /hich ser.es as the p-mp pro.iding hydra-lic po/er for circ-lation.
The third component is the resistance circ-it, /hich incl-des arteries and arterioles, thro-gh /hich +lood tra.els to the
capillary e0change +eds.
The fo-rth component is the capillary +ed, /hich is the site of n-trient e0change and fl-id filtration +et/een the
intra.asc-lar and interstitial fl-id compartments. 9lood flo/ and fl-id filtration thro-gh these capillary +eds are reg-lated
+y h-moral and ne-rogenic controls on the precapillary arterioles and postcapillary .en-les.
The postcapillary .en-les are the fifth component, ser.ing as a site for .eno-s pooling.
The si0th component is the .eno-s capacitance +ed, /hich is the primary storage reser.oir, accommodating -p to B2D of
the total +lood .ol-me. Changes in .eno-s capacitance ser.e to increase or decrease the circ-lating +lood .ol-me and,
therefore, the preload, /hich may +e represented as the .eno-s ret-rn of +lood to the heart.
The metarterioles are the se.enth component. These .essels +ridge the resistance .essels and the postcapillary .eno-s
+eds, +ypassing the capillary circ-it, and ser.e as 4sh-nts.5
The mainstream channels are the eighth component, cond-cting +lood to and from the heart.
Hemodynamic mechanisms of shock are related to the dysf-nction of one or more components of the system 7Ta+le 2C
1.18.
Altho-gh a single hemodynamic a+normality may initiate the lo/=flo/ state, the progression of shock is typically
related to the com+ined effect of se.eral ca-ses. 'or instance, a critical red-ction in intra.asc-lar .ol-me acco-nts for
hypo.olemic shock, +-t progression of the shock state is also related to increased arterial and .en-lar resistance, .eno-s
pooling, cardiac fail-re, and intra.asc-lar coag-lation /ith .asc-lar o+str-ction. !n cardiogenic shock, factors that may
acco-nt for the progression of shock incl-de hypo.olemia, distri+-ti.e defects associated /ith increased arteriolar and
.en-lar resistance, and e.en o+str-cti.e defects from throm+osis and em+oli*ation.
Circ-latory competence and o0ygen deli.ery to the tiss-es is maintained +y an integrated f-nctioning of the
cardio.asc-lar system, incl-ding 7128 the heart, /hich ser.es as a p-mp; 7118 the arterial tree, as the resistance +ed,
/hich ser.es as the cond-it that deli.ers +lood to the capillaries thro-gh /hich meta+olites are e0changed; 7128 the lo/=
press-re .eins as the ret-rn system, /hich also ser.es as the capacitance +ed; and 71>8 the +lood .ol-me.
Shock is classified asE 7a8 hypo.olemic, 7+8 cardiogenic, 7c8 o+str-cti.e, 7d8 or distri+-ti.e 7Ta+le 2C1.28. The primary
defect -nderlying all ac-te circ-latory fail-re is red-ction of effecti.e +lood flo/ /ith inade6-ate tiss-e perf-sion. %actic
acid acc-m-lates +eca-se of anaero+ic meta+olism and can pro.ide a 6-antitati.e meas-re of perf-sion fail-re and
o0ygen deficit. P-lmonary hydrostatic press-re and colloid osmotic press-re are important in the prod-ction of p-lmonary
edema. <hen ca-sed +y left .entric-lar fail-re, p-lmonary edema represents a form of shock that may e.en re6-ire fl-id
repletion to restore the effecti.eness of inotropic and .asodilator dr-gs.
Chapter 2.2 ShockE Clinical Treatment
Principles and Practice of Emergency Medicine
CH%(ER ) C%R"I!*%SC#+%R S$SEM &%I+#RE %N" SH!C'
) Shock, Clinical reatment
-eor.e R. Schwart/0
Hy1o2olemic Shock
Specific "rgan !n.ol.ement in Shock and Treatment to Red-ce !schemic amage
Prehospital Assessment and Sta+ili*ation
Clinical Presentations of Shock
Ca-ses and Classification
Hypo.olemic Shock
Cardiogenic Shock
Septic Shock
"+str-cti.e Shock
Anaphylactic Shock
!nitial Management of Shock
%a+oratory and "ther Proced-res
Therape-tic Regimens
Miscellaneo-s Treatments
H$(!*!+EMIC SH!C'
(e-roh-moral Responses
The response to hypo.olemic hypotension in an other/ise healthy person is reprod-ci+le 7'ig. 2C2.18. A fall in +lood
.ol-me initiates increased acti.ity from the carotid and aortic arch +aroreceptors, and from mechanoreceptors /ithin the
right atri-m. A ne-roh-moral response is initiated that incl-des increased sympathetic ner.o-s system acti.ity /ith direct
cardiac stim-lation and peripheral .asoconstriction, increased pit-itary release of adrenocorticotropic hormone 7ACTH8
and antidi-retic hormone 7AH8, increased adrenocortical release of epinephrine and cortisol, and increased renin=
angiotensin=aldosterone secretion. The net effect is an integrated response to maintain +lood press-re and +lood .ol-me.
<ith se.ere hypo.olemia, ho/e.er, these compensatory mechanisms are ineffecti.e and organ f-nction deteriorates.
"ther hormones +esides catecholamines ha.e .asoacti.e properties and are released into the circ-lation d-ring shock.
!mm-ne system factors prod-cing inflammation are also released 718. The res-lt alters myocardial f-nction, clotting
mechanisms, and increase inflammatory response to name :-st a fe/. A loss of more than >2D of plasma .ol-me
threatens immediate s-r.i.al and elicits a profo-nd +ody reaction as descri+ed pre.io-sly.
Ca-ses of shock determine +ody response. 'or e0ample, infarcted myocardi-m is largely -nresponsi.e to adrenergic
stim-lation, and cardiac stim-lation is there+y limited as an early compensatory mechanism d-ring cardiogenic shock.
Peripheral .asoconstriction, /hich may +e -sef-l d-ring hypo.olemic shock, can +e co-nterprod-cti.e d-ring cardiac
shock, especially in the presence of an already /eakened myocardi-m, +y increasing cardiac afterload. Alternati.ely,
d-ring septic shock, peripheral .asoconstriction is often a+sent or ineffecti.e, and myocardial dysf-nction is the res-lt of
coronary hypoperf-sion or circ-lating depressant factors.
S(ECI&IC !R-%N IN*!+*EMEN IN SH!C' %N" RE%MEN ! RE"#CE ISCHEMIC "%M%-E
<hen coronary perf-sion is compromised, as it is d-ring systemic hypotension, especially /ith -nderlying coronary
disease, cardiac f-nction s-ffers. Myocardial depressant factors may also +e present in some forms of shock 72,>8, and
cardiac o-tp-t can +e compromised +y dysrhythmias ca-sed +y coronary ischemia, hypo0emia, adrenergic stim-lation,
dr-g to0icities, hypo0emia, or acidosis.
!n the a+sence of coronary stenosis, myocardial necrosis per se 7as e.idenced +y release of the M9 fraction of creatine
kinase, troponin !, or electrocardiographic ST=segment ele.ation and F /a.e de.elopment8 is -n-s-al in shock. Rather,
-nless shock is of cardiac origin, the heart -s-ally plays a participatory role in /hich it is -na+le to compensate f-lly for
arterial hypotension ca-sed +y hypo.olemia, .asodilation, or other factors.
"rdinarily, cere+ral perf-sion is kept relati.ely constant o.er a /ide range of perf-sion press-res. E.ent-ally, ho/e.er,
cere+ral perf-sion decreases if perf-sion press-re falls +elo/ a+o-t @2 to A2 mm Hg. 9rain f-nction can also +e
significantly affected +y regional decreases in perf-sion imposed +y -nderlying cere+ro.asc-lar disease.
Renal '-nction and T-+-lar (ecrosis
"lig-ria is a cardinal manifestation of shock. !n fact, the diagnosis sho-ld +e serio-sly 6-estioned if olig-ria is not present.
(e.ertheless, the pathogenesis of shock=related olig-ria is comple0. !t is not simply ca-sed +y renal hypoperf-sion.
Red-ced cardiac o-tp-t, sympathetic stim-lation, circ-lating catecholamines, angiotensin, and locally prod-ced
prostaglandins all contri+-te to renal afferent arteriolar .asoconstriction and to the redistri+-tion of +lood flo/ a/ay from
cortical glomer-li to/ard the med-lla. The net effect of these changes is a decrease in glomer-lar filtration rate.
These refle0 responses, all of /hich ca-se olig-ria can also +e altered +y therapy 7e.g., the -se of .asoconstricting
catecholamines8 and +y in:-ry to the nephron. Three pathologic changes are fre6-ently o+ser.edE t-+-lar necrosis /ith
+ack=diff-sion of glomer-lar infiltrate, t-+-lar o+str-ction +y casts or other cell-lar de+ris, and t-+-lar epithelial damage
/ith conse6-ent interstitial edema and t-+-lar collapse.
This mi0t-re of refle0 responses and primary ischemic damage may e0plain the .aria+le response to therapy for olig-ria.
<hen afferent arteriolar .asoconstriction predominates, dopamine, in lo/ doses, may help to preser.e -rine o-tp-t +y
opposing .asoconstriction. As pathologic changes occ-r, intra.asc-lar .ol-me e0pansion com+ined /ith a loop di-retic or
mannitol may diminish t-+-lar o+str-ction +y maintaining -rine flo/. "nce o+str-ction or t-+-lar necrosis is present,
treatment +ecomes +asically conser.ati.e, s-pported +y dialysis, /hile cell-lar repair and reco.ery take place.
$rine that is prod-ced d-ring shock often reflects these pathophysiologic changes in the kidney. <hen refle0
.asoconstricting mechanisms predominate 7hypo.olemic and cardiogenic shock8, the -rine is largely free of salt and
highly concentrated. !n contrast, /hen ischemic damage is prominent, t-+-lar f-nction, salt retention, and -rine osmolality
decrease. E.en so, -rine chemistries are not highly specific, and ca-tion m-st +e -sed to a.oid o.erinterpretation.
"smotic agents 7e.g., mannitol or di-retics Gf-rosemideH8 ha.e +een -sed +ased on animal e0periments sho/ing
protection against ischemic in:-ry. <hile proof of o-tcome impro.ement is still lacking /e s-ggest the -se of osmotic
agents to increase -rine flo/.
"ther "rgan SystemsE Heart, %-ngs, %i.er, I-t
"ther organ systems are affected +y shock. P-lmonary edema is common d-ring shock, and may +e the res-lt of cardiac
fail-re, o.erly aggressi.e intra.asc-lar .ol-me e0pansion, or increased p-lmonary .asc-lar permea+ility 7?8. <ith hepatic
ischemia 74shock li.er58, characteristic en*ymes 7ser-m gl-tamic=o0aloacetic transaminase GA%TH and ser-m gl-tamic=
pyr-.ate transaminase GASTH8 are released. "ccasionally, an o+str-cti.e pict-re /ith ele.ated +ilir-+in and alkaline
phosphatase predominates.
!schemic in:-ry to the g-t is manifested primarily +y interstitial fl-id se6-estration, hemorrhage, or necrosis of the m-cosal
lining. $lcer formation /ith e0sang-inating hemorrhage can occ-r, often se.eral days after normal hemodynamic f-nction
has +een restored. The ischemic lesions that de.elop in the g-t -s-ally are most prominent in the stomach, /ith the rest
of the gastrointestinal tract less fre6-ently affected. 9reakdo/n of the g-t epitheli-m also creates a portal for entry of
+acteria or other deleterio-s +acterial prod-cts.
(REH!S(I%+ %SSESSMEN %N" S%3I+I4%I!N
The most important o+ligation of field personnel is to recogni*e that shock or a preshock state is present. !n.aria+ly, this
assessment +egins /ith acc-rate .ital signs. A com+ination of systolic +lood press-re less than 12 mm Hg, com+ined /ith
either +radycardia or tachycardia and an altered mental stat-s, sho-ld +e considered shock -ntil pro.en other/ise.
Altho-gh .irt-ally all patients in shock ha.e an impaired le.el of conscio-sness, in preshock states these changes can +e
s-+tle. <hen shock is associated /ith peripheral .asoconstriction, the skin /ill feel cool and clammy, and capillary refill
/ill +e prolonged 7J2 seconds8. <ith fe.er or sepsis, this sign may not +e present. <ith hypo0emia, cyanosis may +e
apparent, +-t only if s-fficient red-ced hemoglo+in is present.
"nce shock is recogni*ed, treatment depends greatly on se.erity and the -nderlying ca-se. Se.erity can +est +e :-dged
in the field +y the effects on cardiac and +rain f-nction. !f mental stat-s is reasona+ly normal and electrocardiographic
manifestations of ischemia are a+sent, aggressi.e therapy can -s-ally +e deferred -ntil arri.al at the hospital. "ther/ise,
some form of res-scitation sho-ld +e attempted immediately, if possi+le, as indicated +y the most likely ca-se.
Certain meas-res are rele.ant to any patient.
1.Ens-re ade6-ate gas e0change
2.All patients sho-ld recei.e s-pplemental o0ygen.
>.Those in respiratory distress or /ith inade6-ate .entilatory effort sho-ld +e int-+ated thro-gh the trachea, if possi+le or
other/ise aided /ith .entilation -ntil E arri.al.
?.#eno-s access sho-ld +e attempted. Place one or t/o large=+ore 71B ga-ge or larger8 peripheral intra.eno-s catheters
if transport /ill not +e delayed. !f cardiogenic shock can +e e0cl-ded /ith confidence 7for instance, /hen tra-ma or
hemorrhage is the o+.io-s ca-se8, start intra.eno-s fl-ids, especially if the neck .eins are flat. A +alanced isotonic salt
sol-tion sho-ld +e inf-sed at a rapid rate. A c-rrent contro.ersy in.ol.es /hether rapid inf-sions may increase +leeding
7?A8. After arri.al in the emergency department, these rates can +e ad:-sted as appropriate.
The patient sho-ld +e kept /arm /ith +lankets, especially if am+ient temperat-res are lo/ or the patient is shi.ering.
"+.io-sly, gross e0ternal hemorrhage sho-ld +e stopped if possi+le. The time spent in the field, ho/e.er, sho-ld +e kept
to a minim-m. o not persist in prolonged -ns-ccessf-l attempts at int-+ation or intra.eno-s catheteri*ation. $s-ally t/o
or three attempts at either proced-re determine the likely feasi+ility of additional effort.
C+INIC%+ (RESEN%I!NS !& SH!C'
9eca-se perf-sion is directly related to press-re, a fall in systemic +lood press-re is a cardinal manifestation of shock
7Ta+le 2C2.18. Changes in regional .asc-lar resistance can, ho/e.er, compensate for modest decreases in perf-sion
press-re, there+y maintaining perf-sion to .ital organs. Th-s, a fall in arterial press-re can +e a har+inger of potential
shock, as /ell as a common manifestation of shock itself, +-t a 4normal5 +lood press-re is still possi+le d-ring the early
phases of compensated shock 74preshock58. !ndeed arterial hypotension can often +e treated +efore .ital organ
dysf-nction is clinically o+.io-s. This pres-ma+ly pre.ents irre.ersi+le organ dysf-nction or at least ameliorates its
se.erity.
An acc-rate +lood press-re is necessary /hen treatment is initiated, especially to a.oid false lo/ readings. Peripheral
.asc-lar disease, tachycardia /ith a small p-lse press-re, and irreg-lar rhythms s-ch as atrial fi+rillation can ca-se the
a-sc-ltatory +lood press-re to +e -nderestimated. oppler de.ices often, +-t not al/ays, impro.e press-re detection.
Post-ral Changes in 9lood Press-re
Post-ral changes in +lood press-re and heart rate can +e helpf-l in detecting mild to moderate degrees of hypo.olemia
738. "rthostasis normally ca-ses the systolic press-re to decrease slightly, the diastolic press-re to increase or stay
-nchanged, and the p-lse rate to increase +y less than 12 to 22 +eats per min-te. <ith hypo.olemia, a fall in diastolic
+lood press-re greater than 13 to 22 mm Hg /hen the patient is sitting or standing is almost al/ays a+normal, especially
if accompanied +y an increase in p-lse rate greater than 22 to >2 +eats per min-te. Significant di**iness or
lightheadedness on sitting or standing, e.en in the a+sence of significant p-lse and +lood press-re changes, is still
consistent /ith hypo.olemia, +eca-se some patients maintain +lood press-re at the e0pense of cardiac o-tp-t. Changes
in systolic +lood press-re are more .aria+le and th-s less helpf-l in e.al-ating orthostasis. !n contrast, dangero-s
hypo.olemia is essentially e0cl-ded if significant di**iness or changes in +lood press-re or p-lse fail to occ-r on the
patientKs ass-ming the standing position.
Shock Affecting 9rain, Heart, and )idney
The +rain, heart, and kidneys are the .ital organs most often affected +y shock. Therefore, red-cing the effect of shock on
these organs is the key to treatment. The se.erity of organ dysf-nction and clinical presentation, ho/e.er, .aries /ith
pre.io-s le.els of organ f-nction, compensatory mechanisms, and ca-se.
The most common clinical manifestation of cere+ral dysf-nction is an ac-te change in mental state, .arying from mild
changes in mental ac-ity to frank coma. 'ocal ne-rologic deficits are not e0pected. <hen they are present, an associated
primary ne-rologic pro+lem sho-ld +e ass-med.
The most common presentation of cardiac dysf-nction is tachycardia. The p-lse is fre6-ently 4thready,5 indicating a lo/
cardiac stroke .ol-me. <ith coronary ischemia, more comple0 rhythm dist-r+ances may occ-r, and these can also impair
cardiac f-nction. As the heart fails, left .entric-lar end=diastolic press-re rises, -ltimately ca-sing p-lmonary edema and
respiratory fail-re. The most common clinical symptoms of coronary hypoperf-sion are chest pain and dyspnea; physical
signs incl-de the appearance of a dyskinetic apical cardiac imp-lse, a ne/ third or fo-rth heart so-nd, a ne/ m-rm-r of
mitral reg-rgitation 7representing papillary m-scle dysf-nction8, and p-lmonary crackles. Electrocardiographic signs 7ST=T
/a.e changes8 of myocardial ischemia can also +e e0pected. "ccasionally, shock can res-lt from mitral .al.-lar
dysf-nction or papillary m-scle r-pt-re 7@8.
Skin Changes
<hen the skin is poorly perf-sed, its temperat-re falls and its color changes. "ften skin color is pale and d-sky,
representing oligemia and .eno-s pooling of +lood desat-rated of o0ygen. <ith concomitant hypo0emia, frank cyanosis
can +e present. Sympathetic ner.o-s system stim-lation, a compensation for hypotension, ca-ses s/eat gland
hypersecretion. The res-lt is the fre6-ently o+ser.ed cool, clammy skin of shock. !n addition, other skin manifestations
can occ-r. 'or instance, diff-se erythroderma in a menstr-ating /oman s-ggests the to0ic shock syndrome. Cell-litis,
erysipelas, or fasciitis may +e +oth the ca-se or res-lt of sepsis. $rticaria or angione-rotic edema may signify
anaphylactic shock. The presence of petechial hemorrhages or ecchymoses may indicate disseminated intra.asc-lar
coag-lation 7!C8 or, more rarely, meningococcemia. Em+olic lesions may indicate endocarditis.
P-lmonary dysf-nction is common and -s-ally represents p-lmonary edema from either increased hydrostatic press-res
7e.g., cardiac shock8 or increased .asc-lar permea+ility 7e.g., septic shock8. -ring anaphylactic shock, -pper air/ay
o+str-ction may res-lt from s/elling of the tong-e or laryn0 7manifested +y stridor8 and lo/er air/ay o+str-ction from
+ronchospasm 7manifested +y /hee*ing8. <hee*ing can also occ-r in p-lmonary edema.
%i.er fail-re is occasionally prominent, as e.idenced +y either hyper+ilir-+inemia or the release of li.er en*ymes. <hen
shock is ca-sed +y infection hyperglycemia and fe.er are -s-ally present; parado0ically, hypothermia can also occ-r.
Meta+olic 7lactic8 acidosis is ca-sed +y tiss-e hypo0ia and anaero+ic meta+olism, often complicated +y hepatic
dysf-nction and inade6-ate lactate meta+olism. The se.erity of acidosis .aries greatly and is poorly correlated /ith
o-tcome /hen all forms of shock are considered.
!n s-mmary, conf-sion, tachycardia, arterial hypotension, and olig-ria are the most common early manifestations of +rain,
cardiac, and kidney dysf-nction, respecti.ely, d-ring shock. More se.ere degrees of shock res-lt in coma, myocardial
ischemia, and p-lmonary edema. Meta+olic acidosis and arterial hypotension are fre6-ent, especially /hen shock is
se.ere, +-t are not prere6-isites for diagnosis. "ther physical signs depend on the -nderlying ca-se, the le.el of organ
f-nction +efore the onset of shock, and the effecti.eness of compensatory mechanisms.
C%#SES %N" C+%SSI&IC%I!N
A -sef-l /ay to classify shock 7Ta+le 2C2.28 is +y the primary ca-se of the circ-latory dist-r+ance prod-cing arterial
hypotension and the effects 7Ta+le 2C2.>8. Many cases of shock o.erlap more than one category. !n other cases, the
circ-latory dist-r+ance is comple0, -ncertain, or -nkno/n. This o-tline is a .ariant of the terms hypo.olemic, cardiogenic,
o+str-cti.e, or distri+-ti.e.
H$(!*!+EMIC SH!C'
Hypo.olemic shock prod-ces the prototypical hemodynamic pict-re of shock. !t is characteri*ed +y marked decreases in
cardiac filling press-res and a conse6-ent decrease in stroke .ol-me. Cardiac o-tp-t is partially maintained +y a
compensatory tachycardia. Refle0 increases in peripheral .asc-lar resistance and myocardial contractility initially
maintain perf-sion to the +rain and heart. <hen +lood loss e0ceeds 22 to 23D of the intra.asc-lar .ol-me 7a+o-t 1 %8,
ho/e.er, these compensatory mechanisms are no longer effecti.e. The decrease in cardiac o-tp-t ca-ses decreased
o0ygen transport to peripheral tiss-es. The arterio.eno-s o0ygen content difference /idens as o0ygen e0traction
increases, +-t e.ent-ally tiss-e hypo0ia and lactic acidosis s-per.ene. Treatment m-st foc-s on restoring .ol-me, red
cells, and perf-sion.
C%R"I!-ENIC SH!C'
Cardiogenic shock occ-rs if more than ?2D of the left .entricle is in.ol.ed in ac-te infarction 7A8. Clinically, signs of
peripheral .asoconstriction are prominent, p-lmonary congestion is fre6-ent, and olig-ria is .irt-ally al/ays present. The
complications of myocardial infarction also prod-ce characteristic signs. Cardiac r-pt-re into the pericardial sac can
prod-ce classic signs of tamponade. Septal r-pt-re can prod-ce the classic m-rm-r and thrill of a .entric-lar septal
defect. Papillary m-scle or chordae tendineae r-pt-re can prod-ce f-lminant mitral reg-rgitation and p-lmonary edema.
Emergency echocardiography can confirm poor left .entric-lar f-nction and can help e0cl-de s-rgically correcta+le
mechanical lesions, /hich may +e contri+-ting to the pict-re of shock 7@8. Throm+yolytics are -sef-l if myocardial
infarction is the ca-se. #ario-s +ypass ad:-ncts are e0perimental. Medications to impro.e heart fail-re are not -s-ally
effecti.e. Mortality is still high, regardless of treatment.
Right #entric-lar !nfarction and Shock
An important .ariant of cardiogenic shock is that d-e to right .entric-lar 7-s-ally inferior /all8 myocardial infarction, since
treatment differs markedly from that indicated for left .entric-lar infarction 7B8. Clinically, the l-ngs are clear despite the
presence of :-g-lar .eno-s distention. "ccasionally, )-ssma-lKs sign 7:-g-lar .eno-s distention d-ring inspiration8 may
+e o+ser.ed. Hemodynamic findings are .aria+le, +-t fre6-ently incl-de ele.ated right atrial press-re compared /ith the
/edge press-re, ele.ated right .entric-lar diastolic press-re, and decreased p-lmonary artery press-re. The cardiac
o-tp-t is decreased and, not infre6-ently, e6-ali*ation of .asc-lar and .entric-lar end=diastolic press-res is present. !n
this case, pericardial tamponade m-st +e e0cl-ded. Again, emergency echocardiography can help /ith this determination,
/hile also demonstrating decreased right .entric-lar f-nction. %eft .entric-lar contractility may +e normal or a+normal,
depending on /hether it is affected +y ischemia, too. <hen right .entric-lar dysf-nction is present, a p-lmonary perf-sion
or .entilation perf-sion scan may +e necessary to e0cl-de p-lmonary em+ol-s. <ith p-lmonary em+oli*ation, ho/e.er,
p-lmonary hypertension almost in.aria+ly accompanies shock.
The main foc-s in treating hypotension accompanying right .entric-lar infarction is to maintain right .entric-lar filling
press-re and preload /ith intra.asc-lar .ol-me e0pansion. %eft .entric-lar filling press-re sho-ld +e -sed along /ith
meas-rements of cardiac o-tp-t as an end point for f-rther fl-id administration. 9eca-se the dilated right .entricle may
ca-se the sept-m to +-lge into the left .entricle and, therefore, change left .entric-lar diastolic compliance 74.entric-lar
interdependence58, ho/e.er, little change in cardiac o-tp-t may occ-r despite an increase in the p-lmonary artery /edge
press-re. !f .ol-me inf-sion is not s-fficient to restore hemodynamic f-nction to normal, inotropic therapy sho-ld +e -sed.
The inotropic agents of choice, s-ch as do+-tamine or dopamine, do not increase p-lmonary .asc-lar resistance.
SE(IC SH!C'
Septic shock is ca-sed +y the presence of infectio-s agents or their prod-cts in the +lood stream. Iram=negati.e
organisms are responsi+le for the ma:ority of cases. Iram=positi.e +acteria, f-ngi, and .ir-ses, ho/e.er, are all capa+le
of prod-cing a clinical syndrome indisting-isha+le from that d-e to Iram=negati.e +acteria. A -sef-l definition of septic
shock isE sepsis=ind-ced hypotension despite ade6-ate fl-id challenge /ith systolic +lood press-re less than 12 mm Hg
or red-ction of more than ?2 mm from +aseline along /ith organ perf-sion a+normalities 71,128.
Sepsis and septic shock are not identical. Sepsis is +est considered as the host response to +acteremia, endoto0emia, or
other +yprod-cts of +acteria in the +lood. This host response is characteri*ed +y clinical feat-res s-ch as fe.er,
tachycardia, tachypnea, and respiratory alkalosis. Meta+olic a+normalities 7e.g., +oth hypoglycemia and hyperglycemia,
as /ell as acidosis and hypocalcemia8 are also common in sepsis 7@8. 9acteremia or a locali*ed infectio-s site 7e.g., an
a+scess8 are common, +-t to0ic shock syndrome may not demonstrate so-rce 711,12,1> and 1?8, altho-gh caref-l search
is -s-ally re/arding. 9e/are of -n-s-al ca-ses s-ch as postsplenectomy sepsis, sepsis in sickle cell disease patients
and pse-domonas sepsis /ith or /itho-t the skin changes of ecthyma gangrenos-m 7-s-ally teeming /ith +acteria8.
Meningococcal sepsis is partic-larly aggressi.e and re6-ires rapid treatment.
Septic shock is often descri+ed, in its initial phases, as a hyperdynamic state /ith a high cardiac o-tp-t, normal to lo/
cardiac filling press-res, and decreased systemic .asc-lar resistance 713,1@8. !ndeed, a hyperdynamic circ-lation in a
patient /ith shock is s-fficiently characteristic of sepsis in /hich an empirical +road spectr-m anti+iotic therapy sho-ld +e
immediately initiated along /ith fl-id res-scitation and occ-lt so-rces of infection e0cl-ded. "ccasionally, a hyperdynamic
pict-re is associated /ith other ca-ses of shock, incl-ding se.ere hepatic dysf-nction, hyperthyroidism, and tra-ma.
!n the terminal stages of septic shock, cardiac f-nction deteriorates and the hemodynamic pattern often resem+les that of
cardiogenic shock 71A8.
E.en /hen cardiac o-tp-t is ele.ated d-ring septic shock, cardiac f-nction and peripheral perf-sion are still a+normal
72,>,1B,118. A+normalities in systolic f-nction are characteri*ed +y decreases in stroke .ol-me and e:ection fraction.
E0perimentally, a+normalities in myocardial contractility ha.e +een demonstrated. These a+normalities may +e ca-sed +y
the presence of 4myocardial depressant factors,5 or coronary ischemia. 9eca-se contractility may sometimes +e
a+normal, increasing preload 7e.g., /ith intra.asc-lar .ol-me e0pansion8 may not al/ays increase stroke .ol-me +-t may
instead e0acer+ate p-lmonary edema. A+normalities in .entric-lar compliance 7diastolic dysf-nction8 also occ-r in septic
shock.
A significant decrease in systemic .asc-lar resistance, often o-t of proportion to any increase in cardiac o-tp-t, is
common in septic shock and may +e responsi+le for refractory hypotension in many patients.
!n general, in most forms of shock, tiss-e o0ygen cons-mption remains independent of o0ygen deli.ery as tiss-e o0ygen
e0traction increases. !n septic shock, ho/e.er, o0ygen cons-mption appears to +e directly proportional to o0ygen
deli.ery. The clinical implications of this oft=repeated finding, ho/e.er, are still -ncertain.
!3SR#CI*E SH!C'
Se.eral ca-ses of shock present /ith signs of ele.ated right=sided cardiac filling press-res +-t no e.idence of p-lmonary
edema, s-ggesting normal left=sided filling press-res. These incl-de right .entric-lar infarction 7see pre.io-s description8,
p-lmonary em+ol-s, tamponade, and tension pne-mothora0.
P-lmonary em+ol-s is -s-ally characteri*ed +y the s-dden onset of chest pain, tachypnea, tachycardia, ele.ated :-g-lar
.eno-s press-re, hypo0ia, and at times hemoptysis. !n se.ere cases, p-lmonary artery o+str-ction res-lts in p-lmonary
hypertension and e.en ac-te right heart fail-re. !n patients /ith other/ise normal cardiop-lmonary systems, shock
ca-sed +y p-lmonary em+oli only occ-rs /hen at least @2 to A3D of the p-lmonary circ-lation is o+str-cted. <ith
-nderlying cardiop-lmonary disease, lesser degrees of o+str-ction can ca-se shock.
Cardiac tamponade can occ-r ac-tely as the res-lt of +l-nt or penetrating tra-ma, or de.elop chronically in a more s-+tle
fashion, as the res-lt of pericarditis, renal fail-re, or a malignant pericardial eff-sion. Symptoms depend largely on the
primary disease process. <ith chest tra-ma, ac-te cardiac tamponade is s-spected in any patient /ho presents /ith
9eckKs triadE ele.ated neck .eins, shock, and m-ffled or distant heart so-nds. !n the more chronic e.ol-tion of cardiac
tamponade, a fre6-ently present sign is p-ls-s parado0-s. The patient also de.elops symptoms of right heart fail-re /ith
peripheral edema, dyspnea, .eno-s congestion, and tachycardia. The chest radiograph demonstrates cardiomegaly /ith
a /idened trans.erse diameter and a glo+-lar appearance of the cardiac silho-ette. An echocardiogram confirms the
diagnosis of pericardial eff-sion and can s-ggest the possi+ility of hemodynamic em+arrassment. Periocardiocentesis is
the re6-ired treatment.
Tension pne-mothora0 7often associated /ith assisted .entilation8 can also ca-se shock /ith distended neck .eins. !n
tension pne-mothora0, ho/e.er, there are no +reath so-nds on the affected side, and the mediastin-m is shifted, /ith
displacement of the trachea a/ay from that side. Tension pne-mothora0 ca-ses shock +y decreasing +lood ret-rn to the
right heart. Treatment can range from rapid needle decompression to t-+e thoracostomy.
%N%(H$+%CIC SH!C'
Anaphylactic shock can occ-r /hen a pre.io-sly sensiti*ed indi.id-al is e0posed to a specific antigen. Atopic persons are
partic-larly at risk. Parenterally administered dr-gs, especially penicillins, cephalosporins, and iodinated contrast media,
are common offenders. The hemodynamic manifestations of anaphylactic shock incl-de decreased +lood press-re,
cardiac o-tp-t, preload 7primarily from .enodilation8, and occasionally systemic .asc-lar resistance. The latter may not +e
apparent -ntil after fl-id res-scitation. <hen systemic .asc-lar resistance is decreased, the hemodynamic pict-re may +e
conf-sed /ith sepsis. The ca-se is -nclear, +-t is -s-ally attri+-ted to .asoacti.e mediators. !n contrast to other forms of
hypo.olemic shock, .asodilation prod-ces /arm skin, and increased permea+ility prod-ces peripheral edema. Rapid
re.ersal re6-ires adrenaline, fl-id s-pport, corticosteroids, and antihistamines.
INII%+ M%N%-EMEN !& SH!C'
Most patients /ith f-lly de.eloped shock re6-ire tracheal int-+ation and mechanical .entilatory s-pport, e.en if ac-te
respiratory fail-re per se 7diagnosed /ith arterial +lood gases8 is not yet present. Tracheal int-+ation is also indicated if
mental stat-s changes makes protection of the air/ay -ncertain, or if inade6-ate respiratory compensation for a
meta+olic acidosis is life=threatening 7'ig. 2C2.28.
Theoretically, tilting a patient into the head=do/n 7Trendelen+-rg8 position di.erts +lood .ol-me into the central circ-lation,
increasing cardiac filling and a-gmenting stroke .ol-me. Recent st-dies, ho/e.er, ha.e failed to demonstrate significant
redistri+-tion of +lood .ol-me centrally. 'or this reason, and +eca-se the head=do/n position can ca-se /orsened gas
e0change and e.en /orsened cardiac f-nction, -se of the Trendelen+-rg position in the emergency management of
shock can no longer +e ro-tinely recommended. !f any s-ch meas-re is desira+le, it is s-fficient to simply raise the
patientKs legs a+o.e the le.el of the heart.
<hen +lood press-re re6-ires immediate treatment 7'ig. 2C2.>8, one m-st choose either a .asopressor agent 7e.g.,
le.arterenol, dopamine8 or intra.asc-lar .ol-me e0pansion 7/ith +lood, +lood s-+stit-tes s-ch as al+-min=containing
sol-tions or hetastarch, or isotonic crystalloid sol-tions8. "ften, a com+ination of a .asopressor /ith a trial of .ol-me
e0pansion is appropriate. The conse6-ences of inade6-ate cere+ral and coronary perf-sion are potentially so disastro-s
that e.ery effort m-st +e made to rapidly restore perf-sion press-re to at least 12 mm Hg systolic or @2 mm Hg mean.
This goal can +e achie.ed rapidly /ith a .asopressor, e.en if shock is ca-sed +y hemorrhage, as long as fl-ids are also
gi.en sim-ltaneo-sly. Altho-gh .asoacti.e agents are least effecti.e /hen intra.asc-lar .ol-me is depleted, their -se can
+e :-stified +y the lethal conse6-ences of prolonged systemic arterial hypotension, namely, irre.ersi+le cere+ral and
cardiac in:-ry. %e.arterenol is the +est initial choice for raising +lood press-re. S-+se6-ently, e.ery attempt m-st +e made
to rapidly decrease the inf-sion rate of the .asopressor, to s/itch to a lo/er 7and less .asoconstricti.e8 effecti.e dose of
dopamine, or to discontin-e .asoacti.e agents altogether 7228.
<ith noncardiogenic forms of shock, especially in the a+sence of p-lmonary edema, intra.asc-lar .ol-me e0pansion
sho-ld +e attempted. The act-al choice of fl-id fre6-ently represents a compromise +et/een /hat is readily a.aila+le and
/hat is re6-ired, +ased on estimated or o+ser.ed losses. !f +lood is the o+.io-s choice for hemorrhage, +-t is not
immediately a.aila+le, a +lood s-+stit-te or isotonic crystalloid sol-tions sho-ld +e gi.en initially. The o-tcome from shock
is pro+a+ly not affected +y the type of sol-tion gi.en d-ring the first ho-rs of res-scitation. "n the other hand, the rate of
administration can critically affect o-tcome. !f it is too slo/, arterial hypotension or .asopressor -se is -nnecessarily
prolonged; if too fast, the risk of p-lmonary edema increases rapidly. (o ar+itrary form-la sho-ld +e adhered to
dogmatically, +-t a reasona+le approach is to administer 322 to A32 m% of a +lood s-+stit-te or 2222 m% of a crystalloid
sol-tion 7normal saline or RingerKs lactate8 d-ring the first ho-r 7not co-nting ongoing losses8. !n hemorrhagic shock, e.en
more rapid administration may +e necessary s-ch as a rapid 322 m% +ol-s 7the 4AT%S5 challenge8. 9lood losses can also
+e occ-lt 7e.g., from internal +leeding after tra-ma or leaking aortic ane-rysm8. 9lood administration may +e -sed to
s-pplement fl-id administration in other forms of shock /hen anemia is present. At all times, the rate of administration
sho-ld +e ad:-sted fre6-ently, -sing changes in +lood press-re, -rine o-tp-t, or e.idence of emerging p-lmonary edema
as important clinical end points. Additional fl-id administration is dictated +y the clinical response to this initial fl-id
challenge, or e.ent-ally +y ne/ information from hemodynamic monitoring 7218.
After this initial period, d-ring /hich maintenance of a minimally accepta+le mean systemic +lood press-re, organ
perf-sion, and a trial of intra.asc-lar .ol-me e0pansion are emphasi*ed, attention m-st +e directed to/ard ac6-iring
additional data, defining the ca-se, and implementing appropriate f-rther specific management.
+%3!R%!R$ %N" !HER (R!CE"#RES
!nitial la+oratory in.estigations sho-ld incl-de ser-m electrolytes, creatinine, and +lood -rea nitrogen; a complete +lood
co-nt and differential; a platelet co-nt, prothrom+in time, and acti.ated partial throm+oplastin time; and, arterial +lood
gases if indicated +y o0imetry. '-rther cardiac en*ymes sho-ld +e taken if there is a chance of cardiogenic shock. A
pregnancy test sho-ld +e performed in all /omen of child+earing age. An electrocardiogram and chest radiograph are
al/ays indicated. "ther st-dies 7e.g., c-lt-res, additional radiographic st-dies8 depend on the circ-mstances and likely
diagnosis.
Monitoring the patient in shock initially incl-des nonin.asi.e determination of .ital signs, p-lse o0imetry cardiac rhythm,
and -rinary o-tp-t. (onin.asi.e monitoring are easy to apply, and are more -sef-l in the emergency setting 71>,1>A8.
<hen hypotension is profo-nd andLor -nresponsi.e to initial res-scitati.e meas-res, in.asi.e hemodynamic monitoring
7arterial and p-lmonary arterial catheteri*ation8 is indicated, +-t sho-ld +e deferred -ntil the patient has +een admitted to
an intensi.e care -nit.
HER%(E#IC RE-IMENS
Choice of 'l-id for #ol-me E0pansion
The type of fl-id to +e administered is a matter of considera+le contro.ersy. espite n-mero-s st-dies, no consistent
e.idence indicates that any fl-id regimen relia+ly affects o-tcome more fa.ora+ly than any other, partic-larly if patients
are closely monitored for impro.ement or complications of therapy. Th-s, fl-id replacement sho-ld incl-de 7altho-gh not
necessarily +e limited to8 the kind of fl-id +eing lost 7e.g., +lood or packed red cells in the case of hemorrhage, crystalloid
sol-tions in the case of diarrhea or e0cessi.e di-retic therapy8. 9lood and colloid=containing sol-tions are more efficient
and often more effecti.e in rapidly e0panding intra.asc-lar .ol-me than are isotonic crystalloid sol-tions. Short=term -se
of +lood or colloid=containing sol-tions is sensi+le for rapid e0pansion of intra.asc-lar .ol-me 7as is often the case in
shock8 /hen o0ygen deli.ery is compromised 721A8. !n practice, patients for /hom a trial of .ol-me e0pansion is
indicated sho-ld recei.e 1 to 2 % of isotonic crystalloid sol-tion or 322 to 1222 m% of a colloid=containing sol-tion 7or
e6-i.alent8, follo/ed +y +lood transf-sions if anemia or hemorrhage is present. S-+se6-ently, colloid is rarely :-stified
+eca-se of the e0pense and the risk of precipitating p-lmonary edema. Additional fl-id administration can +e handled /ith
any com+ination of +lood and crystalloid sol-tions.
Ser-m al+-min is a.aila+le in 3 and 23D sol-tions. The former is the form -s-ally -sed to e0pand .ol-me. Al+-min
sol-tions are sta+ili*ed and heat=treated to kill hepatitis .ir-s. Al+-min has no deleterio-s effect -pon hemostasis.
R%(I" #SE !& 3+!!"
Typing and cross matching of +lood cannot al/ays +e achie.ed +efore +lood needs to +e administered, especially if
e0sang-ination is imminent. The +est choice in this sit-ation is type=specific +lood, /hich is prefera+le to " negati.e
7-ni.ersal donor8 +lood +eca-se transf-sing large amo-nts of type " +lood can make s-+se6-ent typing and cross
matching of the patientKs +lood diffic-lt. Ho/e.er, if there is to +e any delay in a hemorrhagic patient, it is +etter to -se the
" negati.e.
!f an additional 13 min-tes are a.aila+le, saline cross matching can +e carried o-t in addition to typing. This permits
determination of the Rh factor and detects strong anti+odies of the minor +lood gro-ps 7e.g., anti=)ell8, a.oiding se.ere
reactions.
<ith massi.e transf-sion, a +lood /armer can help protect the patientKs core temperat-re and the heat=sensiti.e
coag-lation mechanism. A micro/a.e o.en or inc-+ator can +e -sed for this p-rpose /ith crystalloids 7RingerKs lactate
can +e maintained at ?2MC in the emergency department8. 9lood, ho/e.er, m-st +e /armed -sing +lood /armers. T/o
-nits of fresh fro*en plasma and > to ? -nits of platelets may +e necessary after e.ery B -nits of packed cells. C-rrent
practice re6-ires administration only for demonstrated coag-lopathy or la+oratory confirmation. Calci-m gl-conate is
rarely needed -nless the inf-sion rate of +lood is more than A3 to 122 m%Lmin for more than se.eral -nits.
Pharmacologic S-pport of 9lood Press-re
%e.arterenol is the +est choice in hemorrhagic shock, altho-gh dopamine and do+-tamine are the most commonly -sed
inotropic agents in the treatment of cardiogenic shock 7228. opamine is an endogeno-s prec-rsor of norepinephrine, and
has m-ltiple dose=related effects. At lo/ doses, +2 and dopaminergic effects are e.ident, and enhanced +lood flo/ to
renal and splanchnic +eds is prominent. At higher doses, cardiac inotropy is seen; at still higher doses, .asoconstriction
predominates. o+-tamine is a synthetic congener of isoproterenol /ith primarily +1 7cardiac8 +-t also +2 7.asodilatory8
stim-lating properties. !t has little independent .asoconstricti.e or renal .asodilating effect 7Ta+le 2C2.?8.
<hen shock in.ol.es heart fail-re, do+-tamine can often +e -sed to ad.antage. Cardiac o-tp-t is -s-ally increased
/itho-t marked increases in heart rate, and the p-lmonary artery /edge press-re -s-ally falls. A sim-ltaneo-s inf-sion of
lo/=dose dopamine 7N3 OgLkg per min-te8 may enhance renal perf-sion and -rine o-tp-t. o+-tamine and dopamine can
e.en +e -sed in the presence of coronary ischemia if heart rate is not increased significantly.
<hen shock is from ca-ses other than heart fail-re, a .asopressor agent is -s-ally needed if .ol-me replacement does
not correct hypotension. High=dose dopamine may +e -sed in this setting, altho-gh less effecti.e than le.arterenol 72>8.
espite /idespread -se of adrenergic .asopressor agents, +enefits from their -se are not /ell pro.en 72?,238.
"ther dr-gs, incl-ding le.odopa, theophylline, and ne/er agents s-ch as amrinone and milrinone, ha.e potent inotropic
properties that may sometimes +e -sef-l /hen dopamine or do+-tamine is not effecti.e. Amrinone and milrinone are also
.asodilators, /hich may at times contraindicate their -se in shock. The proper role for these dr-gs, primarily in
cardiogenic shock, is not clear.
Red-cing the systemic .asc-lar resistance 74afterload red-ction58 /ith direct=acting .asodilators can +e a .ery effecti.e
means of impro.ing cardiac o-tp-t in heart fail-re, /hen systemic press-res are other/ise normal or e.en ele.ated.
#asodilators, ho/e.er, are e0tremely dangero-s if systemic press-res or cardiac filling press-res are lo/, -nless shock is
ca-sed +y se.ere aortic or mitral .al.-lar reg-rgitation.
(e-rogenic shock res-lts from a se.ere mid+rain or spinal cord in:-ry +y the loss of .asomotor tone thro-gh the
rela0ation of the .asc-lar smooth m-scle. The heart rate is often normal and the periphery /arm and perf-sed. The dr-gs
of choice for +lood press-re s-pport in this setting are the a=adrenergic dr-gsE phenylephrine, metho0amine, and
metaraminol.
MISCE++%NE!#S RE%MENS
A meta+olic lactic acidosis is commonly present /ith shock. Meta+olic acidosis is a kno/n, altho-gh not .ery potent,
myocardial depressant. These factors, ho/e.er, are often -sed as a rationale for recommending aggressi.e treatment of
lactic acidosis 72@8.
The +est treatment of lactic acidosis is -n6-estiona+ly re.ersal of the -nderlying ca-se. Ho/e.er, this is often not an
immediately attaina+le goal. !n s-ch cases, intra.eno-s +icar+onate administration is often gi.en. The /isdom of this form
of treatment has +een 6-estioned 72A8.
High=dose gl-cocorticoids are not effecti.e in the treatment of sepsis or septic shock. The res-lts of t/o large prospecti.e
m-lticenter st-dies ha.e sho/n that early administration of high=dose corticosteroids neither impro.ed patient s-r.i.al nor
pre.ented or re.ersed shock in septic patients. Ho/e.er, in selected cases their -se is /arranted.
"n the other hand, gl-cocorticoids are appropriate if adrenal ins-fficiency may +e present. Stress doses 7122 mg of
hydrocortisone e.ery B ho-rs or its e6-i.alent8 may +e gi.en to patients /ith an impaired adrenal=pit-itary a0is, or those
/ho re6-ire steroids for the treatment of an -nderlying imm-nologic disease 7e.g., .asc-litis8. High=dose steroid
administration has also +een ad.ocated at .ario-s times for cardiogenic and hypo.olemic shock and for ad-lt respiratory
distress syndrome 7ARS8 associated /ith septic shock. (either animal nor clinical st-dies s-pport the -se of steroids in
s-ch patients.