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6 Shock

Kenneth W. Burchard,. M.D.



insult that can progress even when suffkient oxygen is

delivered. Such conditions as severe hemorrhage and
cardiac malfunction were recognized throughout the
century as etiologies of inadequate oxygen d,elivery. The
recognition that the primary toxins of cellular injury are
endogenous (the products of tissue injury or the conse-
quent inflammatory response) rather than exogenous
(endotoxin) emerged primarily over the last two
decades. Tissue injury and the associated inflammatory
response result in the production or activation of cellu-
lar molecules (i.e., cytokines, superoxide radicals,
prostaglandins, adhesion factors) that promote local cel-
lular activation, tissue repair, and host defenses. How-
ever, sometimes this local response incites similar
responses in cells that are distant from the primary
insult. The result is systemic inflammaHon that can
cause organ malfunCtion and shock.
Simultaneously, during the last two decades, experi-
mental and clinkal studies showed that these two
mechanisms of cellular injury are not competitive or
exclusive, but are most often additive during shock
states. Simply stated, hypoperfusion begets inflamma-
tion, and inflammation begets hypoperfusion. The clini-
Traditional descriptions of shock often use systolic cian must be alert to this association and must approach
hypotension « 90 nun Hg) as the defining variable. each patient who has the manifestations of total body
According to this criterion, classifkation schemes that cellular malfunction with the dual goals of carefully
use categories such as hypovolemic, septic, cardiogenic, assessing the circulation for oxygen delivery and care- .-
and neurogenic shock are common. However, certain fully assessing the state of inflammation for cell toxicity.
etiologies of hypotension (i.e., neurogenk vasodilation Restoring excellent circulation and treating severe
after spina] cord injury) do not necessarily cause signif- inflammation are the primary tenets for managing the
kant cellular or organ injury. In addition, cellular and patient with shock.
organ injury may develop without hypotension reach- This chapter describes the pathophysiology that links
ing 90 mm Hg. Therefore, definitions of shock based on hypoperfusion with inflammation and provides clinical
systolic blood pressure are potentially misleading and guidelines for recognizing hypoperfusion and severe
narrow in scope. inflammaHon and managing these two mechanisms of
A broader definition of shock is a condition in which cellular injury.
total body cellular metabolism is ma]functiona], When
treated aggressively, this cellular metabo]k dysfunction
is reversible. When allowed to continue, however, shock Normal PhysioloW of the Circulation
results in cellular death, organ damage, and eventual and of Inflammation
During the 20th century, many theories were devel- The main function of the circulation is to deliver oxy-
oped to explain this cellular injury and death (i.e., dis- gen to the capilJaries. The determinants of total body
orders of the circulation, disorders of the nervous sys- oxygen delivery are listed with other commonly meas-
tem, toxemia). By 1950, two competing theories were ured or calculated hemodynamic variables in Table 6-1.
predominant: (1) shock is secondary to inadequate oxy- As the formula for oxygen delivery shows, the pul-
gen delivery; (2) shock is secondary to a toxic cellular monary component is limited to providing adequate

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94 Essentialsof General Surgery

Table 6-1. Hemodynamic and Oxygen Delivery Variables Table 6-2. Determinants of Ventricular Function

Item Definition Normal Preload

CVP Central venous pressure; 5-15 mm Hg Contractility
CVP = RAP; in the absence Heart rate
of tricuspid valve disease,
LAP Left atrial pressure; in the 5-15 mm Hg
absence of mitral valve
disease, LAP = LVEDP
PCWP Pulmonary capillary wedge 5-15 mm Hg
pressure; PCWP = LAP,
except sometimes with high
PEEP levels
MAP Mean arterial pressure, mm a0-90 mm Hg
Hg; MAP = DP + 1/3 (SP DP) -
CT Cardiac index; CI = CO/m2 2.5-3.5 Uminlni
51 Stroke index; SI = SV/m2 BSA 35-40 mLlbeat/m'
SVR Systemic vascular resistance; 1000-1500
SVR = (MAP - CVP) x ao dyne-sec!cm~
PVR Pulmonary vascJlar resistance; 10D-400 dyne-sec!
PVR = (MAP - PAOP) x ao cmf
20 vol % lVFP
Ca02 Arterial oxygen content
(vol %); CaO, = 1.39 x Hgb Figure 6-1 Expected hemodynamic response in severe left
Sa02 + (PaO, x 0.0031) ventriculardysfunction to administration of diuretics (D), inotropic
Mixed venous oxygen content 15 vol %
drugs (I),vasodilators (V),and a combination of vasodilators and
(vol %); CiiO = 1.39 x Hgb x inotropics (V + I). SV, stroke volume. LVFp, left ventricular filling
Sii02 + (PiiO, x 0.0031) pressure. F, failure.
Arterial venous O. content 3.5-4.5 vol %
difference; CIa :. ii)O, =
CaO, - CVO,(vol %)
Op 0, delivery; O.D = CO x 900-1200 mUmin and sometimes it is more useful to use the logic associ-
CaO, x 10; 10 = factor to ated with alterations in venous return physiology. This
convert mL 0/100 mL blood logical application of one circulatory physiologyversus
to mL OIL blood
250 mUmin
another (physio-Iogic) is described in more detail in the
O. consumption; O.C =
hypoperfusion section.
'ICaO, - CliO,) x' CO x 10
Ventrjcular Physiology
BSA. body surface area 1m2). CO. cardiac output. DP. diastolic pressure. lVEDP, The major determinants of ventricular performance
left ventricular end-diastolic pressure. PaO., PAOP. pulmonary artery occlusion
pressure. PEEP, positIve end = expiratory pressure, arterial PO, (mm Hg). PYO.,
are listed in Table 6-2. PreJoad is the magnitude of myo-
mixed venous PO.. RAP. right atrial pressure. RVEDP. right ventricular end-diaf' cardial stretch, the stimulus to muscle contraction that is
toJic pressure. Sa6.. arterial oxygen saturation (%). SVO., mixed venous oxygen described by the Frank-Starling mechanism (Fig-
saturation. SP, systolic pressure. SV, stroke volume.
ure 6-1), wherebv increased stretch leads to increased
contraction untij the muscle is overstretched (com-
monly recognized clinically as congestive heart failure;
arterial oxygen saturation (~ 90% saturation is usually see the hypoperfusion section). Preload is most appro-
present when PaO: ~ 60 mm Hg). This goal is usually priately measured as end-diastolic volume. Because
readily achieved with modem respiratory therapy. volume is not easily measured clinically, the direct pro-
Hemoglobin is frequently increased with transfusion. portion between ventricular volume and ventricuJar
Usua]]y, the most difficult component to treat is cardiac end-diastolic pressure allows the measurement of pres-
output. The determinants of cardiac output are organ- sure (measured as central venous pressure (CVP) for the
ized by both the variables that affect ventricular func- right side of the heart and pulmonary capillary wedge
tion and the variables that affect venous return. or pulmonary artery occlusion pressure (PAOP) for the
Depending on clinical circumstances, sometimes it i~ left side of the heart] to estimate volume.
more useful to use the logic associated with alterations Ventricular afterload is determined primarily by the
in ventricular physiology to enhance the circulation, resistance to ventricular ejection that is present in either

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6 : Shock 9S

Table 6-3. Factors That Affect Myocardial Contractility Table 6-4. Faclors That Alter Venous Return Variables

Increased Decreased Increased venous return

Increased MSP
Increased vascular volume
Catecholamines Catecholamine depletion and receptor Increased vascular tone
External compression
Inotropic drugs Alpha and beta blocker~ Trendelenburg position (increased MSP in lower extremities and
Calcium channel blocker~
Increased preload Decreased preload Decreased CVP
Overstretching of myocardium Hypovolemia
Decreased afterload Increased afterload Negative pressure respiration
Severe inflammationand ischemia Decreased venous resistance
Decreased venous constriction
Negative pressure respiration
Diminished venous return
Decreased MSP
the pulmonary (pulmonary vascular resistance) or sys-
Increased CVP
temic arterial tree (systemic vascular resistance). With Intracardiac
constant preload, increased afterload diminishes ven- Congestive heart failure
tricu1ar ejection, and decreased afterload augments ejec- Cardiogenic shock
tion (see Figure 6-1). Tricuspid regurgitation
Contractility is the force of contraction under condi. Right heart failure
tions of a predetermined prel,oad or afterload. Factors Extracardiac
that increase and decrease contractility are listed in Positive pressure respiration
Table 6-3. A change in contractility, like a change in PEEP
afterload, results in a different cardiac funchon curve Tension pneumothorax
(see Figure 6-1). Cardiac tamponade
Increased abdominal pressure
The combined influence of increasing contractility Increased venous resistance
and decreasing afterload to improve ventricular func- Increased thoracic pressure
tion is also shown in Figure 6-1. Positive pressure respiration
Heart rate is directly proportional to cardiac output PEEP
(not to cardiac muscle mechanics) until rapid rates Increased abdominal pressure
diminish ventricular filling during diastole. Tension pneumothorax
Increased abdominal pressure
Venous Return Ascite~
Bowel distension
Venous return is described by the following formula: Tension pneumoperitoneum
MSP CVP - Intraabdominal hemorrhage
VR = RV + RA/19 Retroperitoneal hemorrhage

where MSP = mean systemic pressure, CVP = centra] MSP, m6sn systemIC pr6ssure. CVP, cenlral venous pressure.
end-expiratory pressur6.

venous pressure (right atria] pressure), RV = venous

resistance, and RA = artena] resistance.
The division of arterial resistance by 19 was formu-
lated by Guyton in 1973 using both calcu]ations and
empirical observation. As might be expected, alterations Physiology of Inflammation
in arterial resistance have much less effect on venous The normal response to tissue injury is essential for
return than alterations in venous resistance, as indicated restoring normal tissue function and wound healing.
in the formula. The initia] response to tissue damage by trauma is
Mean systemic pressure (MSP) is not the same as b]eeding and coagulation. This response is less likely,
mean arterial pressure. MSP is the pressure in small but not impossible, with tissue damage from ischemia
veins and venules. This pressure must be higher than or infection. Platelet activation results in the release of
CVP in the periphery so that blood can flow from the important chemoattractants [i.e., platelet-derived
periphery to the thorax. Venous resistance occurs pri- growth factor (PDGF), transforming growth factor-~
marily in the ]arge veins in the abdomen and thorax. (TGF-j3»).
Arteria] resistance occurs mostly in the arterioles. Damaged blood vessels initially vasoconstrict, but.
Factors that alter venous return variables are listed in this constriction is soon fo)]owed bv vasodj]ation and
Table 6-4. Surgical patients frequently have diseases or increased capj))ary permeabiJity secondary to the action
therapeutic interventions that may inhibit venous of agents such as prostaglandin _~~,prostacyclin, hista-
return. mine, serotonin, and kinins. when blood flow is
-. --. .'-'----- _.. h .._

96 Essentialsof General Surgery

present, this vascular response resuJts in the accumula- such mediators as IL-J, TNF, PDGF, TGF-/3, TGF-a, and
tion' of protein-rich edema fluid (exudate). White cells fibroblast growth factor.
adhere to these damaged, leaky vessels. For instance, fibroblast migration and angiogenesis
Attracted by chemoattractants (e.g., PDGF), poly- begin next. Fibroblasts are influenced by IL-l, TNF,
morphonuclear cells (PMNs) are the first white ceUs to PDGF, TGF-/3, TGF-a, insulin-like growth factor, and
migrate to the inflammatory site (within minutes if the epidermal growth factor (EGF). Angiogenesis is influ-
circulation is good). PMNs phagocytize dead tissue and enced by TNF, TGF-/3, TGF-a, and EGF. The combined
foreign objects. Opsonins and preformed antibodies process of fibrobl,ast proliferation and capillary budding
may assist in the removal of bacteria. PMNs produce produces granulation tissue that is friable and bleeds
proteases and intraceUular oxygen radicals that are crit- easily.
ical for beneficial PMN activity. Besides proteases and Fibroblasts produce collagen. This process usually
oxygen radicals, PMNs can also release interleukin-J accelerates 5 days after tissue damage occurs. CoUagen
(IL-J), or endogenous pyrogen. IL-J mediates tempera- synthesis is influenced by !L-l, TNF, PDGF, TGF-/3, and'
ture elevation through the thermoregulatory center and EGF.
also stimulates other inflammatory activity (e.g., migra- A summary of ceUular activity in' inflammation is
tion of macrophages). Another cytokine, interleukin-8 shown in Tables 6-5 and 6-6. '
(JL-8), is a potent PMN attractant that is produced by
many cell types after incubation with IL-J and the
cytokine tumor necrosis factor (TNF). Incubation ~erfusion States
involves the in vitro juxtaposition of ceUs with a sub-
stance of interest in a physiologic environment that sup- Hypoperfusion is a decrease in total body or regional
ports cell survival. If the cells respond to the substance, blood flow that is suffjcient to result in cellular mal-
then the effect can be assayed in this controUed, isolated function or death. Hypoperfusion is the primary mech-
milieu. The PMNs last only for a period of hours. anism that is responsible for inadequate oxygen deliv-
Within hours, tissue macrophages and circulating ery; the immediate effects of hypoperfusion on cell
monocytes are attracted by such substances as PDGF, viability are secondary to the interruption of oxidative
TGF-/3, and IL-J; they migrate into the injured area, and metabolism.
last for days to 'weeks. The continuing 'inflammatory I
process is largely regulated by macrophages through The Neurohumoral Response
to Hypoperfusjon '

Table 6-5. Normal Inflammation Total body hypoperfusion usually manifests as a

reduction in cardiac output. The most frequently stud-
ied models of total body hypoperfusion cause a reduc-
Event Cells Responsible tion in cardiac output from loss of volume (hypo-
volemic hypoperfusion) or loss of cardiac function
Coagulation Platelets (cardiogenic hypoperfusion). Either of these etiologies
Early inflammation Polymorphonuclear leukocytes (firstfew may result in the neurohumoral response shown in
hours) Table 6-7.
Later inflammation Monocytes (days) macrophage~ The clinicaUy apparent effects of this neurohumoral
Collagen and Fibroblasts (maximumdeposition response are tachycardia (epinephrine, norepinephrine,
mucopolysaccharide 7-10 days) dopamine), vasoconstriction (norepinephrine, arginine
Capillary budding Endothelial cells (maximum7-10 days)

Table 6-7. Neurohumoral Response to Hypoperfusion

Table 6-6. Functions of Inflammatory Cells
Increased Decreased
Cells Function
Epinephrine '
Platelets Coagulation, release PDGF, IL-1 Norepinephrine Thyroxine
Polymorphonuclear Phagocytosis, especially microbes, release Dopamine Triiodothyronine
leukocyte~ IL-1, IL-8 Glucagon Luteinizinghormone
Macrophage Phagocytosis; stimulate fibroblast migration Renin Testosterone
and growth; stimulate endothelial cell
Angiotensin Estrogen
migration and growth; release FGF, PDGF,
IL-1, TNF, TFG-p, TGF-o Argininevasopressin Follicle-stimulatinghormone
Fibroblast Collagen deposition Adrenocorticotropichormone
Endothelialcells Capillary budding Cortisol
PDGF, platelet-derived growth tac1or. Il, interleukin. FGF, fibroblast growth fac- Growth hormone
tor, TNF, tumor necrosis fac1or. TGF, transforming growth fac1or,
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6 : Shod 97
" -

vasopressin, angiotensin), diaphoresis (norepineph- Elevated levels of lactic acid, with low pyruvate levels,
rine), oliguria with sodium and water conservation characterize anaerobic gyJcolysis as the primary means
ladrenocorticotropic hormone (ACTH), cortisol, aldo- of ATPproduction in anaerobic states.
"terone, arginine vasopressin], and hyperglycemia (epi- Besides an elevation in lactic acid, cell membrane
nephrine, glucagon, cortisol, insufficient insulin). This function may be impaired by decreased intracellular
activaHon of the neuroendocrine system may preserve ATP production and from a circulating protein that can
blood flow to vital organs (heart, lungs, brain) while depolarize cell membranes. Possibly as a result of such
diminishing flow to less vital organs (kidneys, gastroin- cell membrane alterations, sodium and calcium can
testinal tract). In this way, it preserves or increases move into cells, with water following the sodium.
intravascular volume by limiting urine output. This Sequestration of wate!: in cells can cause a deficit in
response is more homeostatic under conditions of hypo- extracellular fluid, which may accentuate the fluid
volemic hypoperfusion compared with cardiogenic requirements during resuscitation.
hypoperfusion, in which tachycardia, vasoconstriction,
and sodium and water retention may aggravate rather
than diminish hypoperfusion by decreasing ventricular Etiologies, Diagnosis, and Management
filling time, increasing afterload, and increasing myo- ~erfuslon States .
cardial stretch, respectively.
The primary etiologies of hypoperfusion states in
The Effects of Hypoperfusion surgical patients are decreased venous return and
on Inflammation decreased myocardial functi<;m(Table6-8).
The most clearly documented association of hypo-
perfusion with inflanunation is the effect of ischemia Decreased Venous RetUrn: Hypovolemia
followed by reperfusion. Clinically, this effect is most Hypovolemia is the most common etiology of
obvious in patients with isolated limb ischemia (com- decreased venous return secondary to decreased MSP.
partment syndrome) and in some patients with 10ca1- Common etiologies of hypovolemia are listed in
ized intestinal ischemia. However, severe systemic Table 6-9. Hypovolemia is the most conunon cause of
hypoperfusion may cause a similar response in many hypotension.
tissues, particularly the gastrointestinal tract.
The mechanism that is responsible for ischemia I
reperfusion injury appears to require both local and sys- Table 6-8. Etiologiesof Hypoperfusion
temic factors. A complex interaction of oxygen free rad-
icals, thromboxane, leukotrienes, phospholipase A" and Decreased venous return
leukocytes pamcipates in both regional and total body Hypovolemia
alterations in capillary permeability and organ function. Pericardialtamponade
Anatomic and physiologic damage to the intestine, Tension pneumothorax
limb, kidney, liver, and lung may occur after reperfu- Increased abdominal pressure
sion, even when a specific organ (i.e., lung) was not ini- Bowelobstruction
tially"hypoperfused. Because PMNs are potent produc- Tension pneumoperitoneum
ers of oxygen free radicals, these cells are central to this Massive bleeding
pathophysiology. Diagnosticlaparoscopy
The potential for severe inflammation to develop Pneumatic antishock garment
during, rather than after, hypoperfusion is less well
documented and more controversial. Some experimen- Positiveend-expiratory pressure
tal studies showed an increase in inflanunatory media- Decreased myocardialfunction
tors and cellular activity during hemorrhagic hypoper- Congestive heart failure
fusion. Others did not show this increase. Cardiogenic shock
In clinical hypoperfusion, particularly with trauma, it
is difficult to separate tissue injury that is secondary only
to hypoperfusion from damage from other mechanisms
(e.g., a direct blow). Again, whatever the cause, hypo- Table 6-9. Common Etiologies of Hypovolemia
perfusion and inflammation conunonly occur together.
Severe inflammationor infection
The Effects of Hypoperfusion
on Ce]]ular Metabohsm Trauma
The classic effectof hypoperfusion on cellular metab- Pancreatitis or other causes of peritonitis
olism is anaerobic metabolism caused by an oxygen Burns
deficit. The reduction in adenosine triphosphate (ATP) Vomitingor other intestinal losses
production that occurs secondary to the loss of mito- Excess diuresis
chondrial function can result in inadequate energy to Inadequate oral intake
meet ce]]uJar needs, with cell death as a consequence.

98 Essentialsof General Surgery

Severe hypoperfusion secondary to hypovolemia 10% loss of blood volume (560 mL, approximately the
(i.e., hypovolemic shock) was studied most frequently amount donated for transfusion) produces little, if any,
in experimental and clinical hemorrhage. Hemorrhagic disturbance. A 20% loss may cause tachycardia and
shock not only diminishes venous return, but also may orthostatic hypotension. A 30% loss may produce
cause cardiovascular alterations (Table 6-10). Cellular hypotension while the patient is supine. However, a
effects (other than lactic acidosis from anaerobic glycol- patient may be normotensive when supine, even with
ysis) are listed in Table 6-11. As mentioned earlier, greater loss of blood volume (Table6-12).
ischemia-induced local and systemic inflammation Agitation, tachypnea, and peripheral vasoconstric-
have also been described. tion are common with any etiology of hypoperfusion.
The metabolic and toxic phenomena associated with Hypotension, however, most commonly occurs second-
hypovolemic shock, even without severe inflammation, ary to hypovolemia. Hypotension as a result of disrup.'
result in loss of plasma and interstitial volume beyond tion of intrinsic cardiac function (cardiogenic shock) is
what is accounted for by the primary disease process much less common (discussed later). Congestive heart
(i.e., hemorrhage, vomiting). Migration of interstitial failure, a distinct clinical entity from cardiogenic shock,
fluid into cells and increased capillary permeability are frequently causes increased blood pressure.
implicated as mechanisms. The neck veins are not distended unless hypo-
volemia is accompanied by an extracardiac increase in
Physical Examination in Hypovolemic central venous pressure (tension pneumothorax, peri-
Hypoperfusion cardial tamponade, severe effort during expiration,
In the patient who has hypovolemia, vital signs and increased abdominal pressure). An S gallop is not usu-
physical findings show evidence of hypoperfusion
ally present. An etiology of hypovo emia may also be
roughly in proportion to the degree of hypovolemia. A apparent (open wound with hemorrhage, distended
abdomen, femur and pelvic fractures).
Table 6-10. Cardiovascular Effects of Hemorrhagic Shock Common Laboratory Aids
Hypovolemic hypoperfusion that is severe enough to
Decreased venous return
cause hypotension is associated with metabolic acidosis
Increased systemic vascular resistance that is recognized either from serum electrolytes or,
Decreased ventricular contractility more precisely, arterial blood gases. Elevated serum
Decreased ventricular compliance blood urea nitrogen (BUN) and creatinine levels that are
Increased atrial contractility indicative of renal malfunction are common. CVP and
Transcapillary refill of water to restore plasma volume PAOP are low, as are cardiac index and oxygen delivery.
Intravascular protein replenishment from preformed extravascular Other tests (e.g., hemoglobin level, other serum
protein chemistries, radiographic studies) are usually used to
determine the etiology of hypovolemic hypoperfusion
rather than to document the severity of the perfusion
Table 6-11. Cellular Effects of Hemorrhagic Shock

Treatment of Hypovolemia
Diminished transmembrane potential difference
Increased intracellular sodium In the patient who has severe hypovolemic hypoper-
Decreased intracellular adenosine triphophate
fusion, the circulation must be restored simultaneously
with. diagnostic and therapeutic interventions to correct

Table 6-12. Hemodynamic Effects of IntravascularVolume Loss in Supine Subjects

Blood Skin Urine

Amount Rate Pressure Pulse Mentation Vasoconstriction Output

10% 5 min NL Nl NL Nl NL
$10% 1 hr NL NL NL NL NL
20% 5min J. l' NL l' J.
20% 1 hr NL l' NL NL J.
30% 5min J.J. i1' .1 i1' J..1
30% 1 hr J. 1 .1 l' .1
50% 5min U.! ii1 J..! iii U.!
50% 1 hr J..! i1 J..! i1' .u
NL. normal.

_ h____ ___ ___._____________

6 : Shock 99 t_.'

the underlying cause of the hypovolemic state. The cir- mented for increasing the hemoglobin to greater than 10
culatory, metabolic, and toxic effects of hypovolemic g/100 mL, even in patients with little ability to increase
hypoperfusion are best treated by rapid (within minutes) cardiac output. AJthoughhemoglobin concentrations of
restoration of intravascuJar volume, thereby increasing as low as 7 g/100 mL are now considered acceptable for
MSP,venous return, and oxygen delivery.In general, two some acute illnesses, cautious assessment of oxygen
types of fltrld, crysta])oid and co])oid, are used for vol- delivery and consumption variables is recommended if
ume replacement (Table6-13).Red blood cells are effec- a plan to avoid red cell transfusion for such concentra-
tive when needed. After hemorrhage is arrested, the tions is considered advantageous (see section on end-
administration of red cells causes increased cardiac out- points of resuscitation of the circulation).
put, increased oxygen-carrying capacity,and little,if any, Much more controversial than the appropriate use of
leakage of red cells into the interstitium, even in the fi:lce FFPand red blood .cellsare the"iidvantagesand disadvan-
of increased capillary penneability. The primary disad- tages of the various crystaIloid and colloid solutions pre-
vantage of red cell transfusion is the rare risk of infection viouslylisted.Most investigatotSagree that colloidadmin-
with a transmissible disease (e.g., hepatitis C, human istration results in Jess sodium-administration compared
immunodeficiency virus). Also rare is an incompatible with crystalloid solutions arid'less water administration
red cell hemolytic transfusion reaction. Febrile episodes compared with isotonic crystalloid solutions. In addition,
that do not represent true transfusion incompatibility are plasma oncoticpressure is hi~er after the administration
more common, and are most often secondary to anbood- of colloids.Still debated is whether increased total body
ies to the small numbers of white cells that remain in the sodium and water gain are detHmental to organ function
packed red cell unit. Potential advantages and disadvan- after resuscitationof the circWatian.
tages of various resuscitation fltrlds other than red cells When a patient who has hypovolemia is receiving
are shown in Tables6-14and 6-15. largevolumes of crystalloid of colloid and is not respond-
Fresh frozen plasma (FFP)should not be used primar- ing well to therapy (most ~fh;n.seen in severe septic
ily as a colloid. Only when hypovolemia is accompanied shock), dopamine adminis~atiOh. is a logical adjunct.
by bleeding and a deficiency in intrinsic or extrinsic Dopamine increases left ventiic1.ilarfilling pressures as it
coagulation (partial thromboplastin time> 1.5x control, increases cardiac output, probably as a result of constric-
prothrombin time < 50%) should FFP be used. In gen- tion of the veins and decreased venous capacitance. This
eral, red blood cells are used to replace lost red cellsand increase may occur at the expense of increasing myocar-
are administered until the serum hemoglobin dial oxygen demands. Aftet a~equate vascular volume is
approaches 10 g/100 mL. Little advantage is docu- attained,the dopamin'ecanus~~y be discontinued...
Decreased Venous Return:.
Table 6-13. Fluids for Hypovolemia Resuscitation
Pericardia) Tamponade;:'.'"
The primary mechanism lor decreased venous return
Isotonic during pericardial tamponlide is an extra cavitary
Ringer's lactate increase in CVP. The etiolo~~ of tamponade are most
0.9% saline
Hypertonicsaline - .
Red blood cells
Fresh frozen plasma Table 6-15. Colloid Solutions (Other than Red Cells)
Processed human protein Advantages
Low-molecular-weightdextran Less water administered (more resuscitation per milliliter)
Hydroxyethylstarch Lesssodiumadministered ." .
Less decrease in oncotic pressure
Acidbuffer (fresh frozen plasma)
Table 6-14. Crystalloid Solutions Disadvantages
Expensive (albumin,fresh frozen plasma)
Transmissibledisease (fresh frozen plasma)
Isotonic solution advantages Increased interstitialoncotic pressure
Inexpensive Depressed myocardialfunction (albumin:50%reduction in left
Readily available ventricularstroke work index at a pulmonary capillary occlusion
Replenishes epidermal growth factor pressure of 15 mm Hg) ...
Freely mobile across capillaries Depressed immunologicfunction (albumin:decreased
No increase in lung waier immunoglobulins,decreased response to tetanus toxoid)
Isotonic solution disadvantages Delayed resolution of interstitial edema
Rapid equilibration with interstitial fluid Coagulopathy: infrequent in lowdoses (Iow-molecular-weight
Lowers serum oncotic pressure dextran: platelet malfunction; hydroxyethylstarch: decreased
No oxygen carrying capacity factor VIII:cconcentrations; albumin:decreased fibrinogen,
Increase in systemically perfused interstitial fluid decreased prothrombin, decreased factor VIII)

100 Essentialsof General Surgery

commonly chest trauma (penetrating and blunt) and sure, producing an extracavitary increase in CVp, and
bleeding after cardiac surgery. Physical examination increasing venous resistance in abdominal veins.
usually shows evidence of hypoperfusion, along with Increased abdominal pressure may be particularly
distended neck veins, muffled heart sounds, and an detrimental to renal blood flow, but it can cause marked
increased paradoxical pulse (> 15 mm Hg). The electro- total body hypoperfusion despite a well-maintained
cardiogram may show low voltage, the CVP is often ele- mean arterial blood pressure from increased systemic
vated, and a chest x-ray may show an enlarging heart. vascular resistance.
With severe hypovolemia, the CVP may be normal Abdominal pressure is increased by a variety of mech-
despite tamponade, and may become elevated onIy anisms (see Table 6-4). It is most easily measured with a
after fluid resuscitation. An echocardiogram shows bladder catheter: 50 to 100 mL flujd is inserted into the
fluid surrounding the heart, with diminished ventricu- bladder through the fluid sampling port on a Foley
lar volumes. catheter; the catheter is damped distal to the sampling
It is important to distinguish this etiology of hypo- port; and pressure is measured by connecting the needle
perfusion from congestive heart failure (CHF) or car- in the sampling port to standard hemodynamic monitor-
diogenic shock because reducing fluid intake and ing tubing, using the pubis as the zero pressure level.
administering a diuretic would reduce venous return Physical examination often shows evidence of
further in tamponade. As stated, CHF usually results in hypoperfusion along with a tensely distended abdomen
normal or elevated blood pressure. Severe tamponadE' and possibly distended neck veins. The most effective
results in hypotension. Therefore, tamponade simulates treatment is to relieve the pressure. However, aggres-
cardiogenic shock more dosely than CHF. Because car- sive fluid management to increase MSP may be the only
diogenic shock requires a major insult to myocardial option in some cases where, for instance, exploration of
function (see later), hypotension with elevated CVP the abdomen is considered prohibitively risky. When
should increase suspicion of tamponade or a tension hemodynamics and respiratory function are severely
pneumothorax unless obvious evidence of severe myo- impaired by increased abdominal pressure, then open-
cardial malfunction is found. ing the abdomen and dosing it with a prosthesis or
The incidence of cardiac tamponade in surgical leaving it packed open may be the best alternative.
patients is low, and it is most often seen in patients with
chest trauma or in those undergoing cardiac surgery. Cardiogenic Hypoperfusion
Removal of the fluid surrounding the heart (pericardio- and Cardiogenic Shock
centesis) is the most effective therapy, and it can result in To cause cardiogenic shock, or hypotension, on a car-
a dramatic improvement in cardiac output. However, diac basis, cardiac function must be severely disrupted
venous return also improves as a result of increasing (cardiac index < 2.2 L/min/m2) from etiologies such as
MSP with intravenous fluid. Therefore, vigorous fluid those listed in Table 6-16.Hypoperfusion of this magni-
administration should be provided despite elevated CVP.
tude, especially when it is secondary to myocardial
Decreased Venous Return: infarction, is associated with a high mortality rate. Car-
Tension Pneumothorax diogenic shock is a dinical entity distinct from CHF. In
CHF, arterial blood pressure is characteristically well
Tension pneumothorax reduces venous return by maintained or increases. This characteristic distin-
producing an extracavitary increase in CVP and by guishes cardiogenic shock (the term applied to signifi-
increasing venous resistance in the chest. Tensionpneu- cant reductions in systolic pressure) from CHF.
mothorax may occur spontaneously from rupture of a In general, the diseases listed in Table 6-16 are not
bleb or, more commonly, after penetrating or blunt subtle and do not cause gradual alterations in cardiac
trauma. Physical examination shows evidence of
decreased perfusion, along with decreased breath Table 6-16. Etiologies of Cardiogenic Shock
sounds over the affected thorax, tracheal deviation
away from the affected thorax, and distended neck Acute ischemia
veins. A chest x-ray may be the first due to a tension Ventricular wall intarct
pneumothorax, but most often, the diagnosis is made at Papillary muscle infarct
the beside without radiologic assistance. Ventricular septal detect
Treabnent consists of emergentIy releasing the ten- Acute valvular disease; mitral. tricuspid. or aortic regurgitation
sion (e.g.,placing a 14-gauge needle into the chest, plac- Arrhythmias
ing a finger in a large penetrating injury), followed by Rapid supraventricular
dosed thoracostomy. Administration of intravenous Bradycardia
fluid to increase MSP is also beneficial, and neck vein Ventricular tachycardia
distension may not be evident with severe hypovolemia. Miscellaneous
End-stage cardiomyopathy
Decreased Venous Return: Increased Severe myocardial contusion
Abdominal Pressure Severe myocarditis
Severe left ventricular outflow obstruction
Increased abdominal pressure (> 20 mm Hg) dimin- Severe left ventricular inflow obstruction
ishes venous return by increasing intrathoracic preE--
~ ,.

6: Shock 101

lunction. Hypotension is more often a disease of hypo- Table 6-17. Treatment 01 Cardlogenic Shock
volemia than a disease of severe impairment of cardiac
(unction. When a c1inician decides not to administer Reversal 01 underlying disease
fluid to a hypotensive patient, he or she is actually mak- Coronary artery bypas~
ing a diagnosis of cardiogenic shock. Cardiogenic shock Valve replacement
is the only major circulatory deficit that can be wors- Rx myopathy
Repair ventricular septal delect
~ned by the administration of fluid. Becausecardiogenic
shock is secondarY to severe, usuallv obvious, cardiac Reduce preload
Decrease water intake
disease, the clinician should be able to document the Diuretics
occurrence of a marked insult to cardiac function. With- Venous dilation
out such documentation and the associated recognition Nitroglycerin
of a disease that requires aggressive monitoring and Calcium channel blocker~
management in a critical care setting, the c1inician Narcotics
should consider the hypotensive patient to be hypo- Reduce afterload
volemic and not in cardiogenic shock. Nitroprusside
Physical Examination Diuretics
Physical examination shows hypotension, tachycar-
dia, tachypnea, peripheral vasoconstriction, distended Increase contractility
Intravenous inotrope~
neck veins, agitation, and confusion. An S~gallop may
be apparent, and when valvular dysfunction is present, Increase arterial oxygen
associated murmurs may be auscultated. Supplemental O.
Mechanical ventilation

Laboratory Aids
Cardiogenic shock is assodated with chest x-ray evi-
dence of pulmonary edema, metabolic acidosis (lactic Table 6-18. Hemodynamic Effects of Inotropic Drugs
acidosis), increased CVP and PAOP, and increased BUN and Vasodilator~
and creatinine. A cardiogram often shows evidence of
acute ischemia, infarct, or arrhythmias. An echocardio- Hemodynamic Parameters
gram can provide information about ventricular waU
m060n and valve function. The cardiac index is low Heart Rate Contractility Preload Afterload
« 2.2 L/min/m2), and both systemic and pulmonary
vascular resistance are high. Dopamine i i i i or NC
Dobutamine , ii J NCorJ
Treatment Isoproterenol i1 ii J J
As always, treatment is based on the etiology.Arrhyth- Nitroprusside - NC J J.J
mias are usually the most readily treated etiology of
severe cardiac impairment. Arrhythmias are diagnosed
Nitroglycerin NC J.J. J

and treated as described in textbooksthat cover advanced NC. no chanpf:.

cardiac life support. When the etiology is not an arrhyth-

mia, the same sequence of interventions used to increase
cardiac output in CHF may be used for cardiogenicshock Table 6-19. Complications 01the Intraaortic Balloon Pump
(Tables6-17and 6-18).However, hypotension (often < 90
nun Hg systolic) makes the use of vasodilators alone less Injury to lemoral vessel~
attractive. Therefore, a combination of inotropic drug Ischemic extremity
support and vasodilation is frequently used. Mechanical Hemolysis or thrombocytopenia
support of the heart with an intraaortic baJloon pump Inlection
(IABP)increases cardiac output while reducing preload
and afterload. lABP may be more successful than high-
dose dobutamine in supporting patients during severe
cardiac impairment. lABPmay be adequate to support a tory deficit, the underlying state of the patient's circula-
patient until cardiac function improves, or may be tion, and the magnitude of ceUular and organ malfunc-
required until surgery (e.g., replacement of the aortic tion recognized during the hypoperfusion insult. How-
valve, coronary revascularization)is performed. Compli- ever, for most c1inicalconditions, bedside recognition of
cations of IABPare listed in Table6-19. normal circulation is adequate for assessing the outcome
of resuscitation. Such variables as normal (the designa-
Endpoints for Resuscitation tion of normal depends on knowledge of the patient's
of the Circulation premorbid blood pressure) or increasing blood pressure,
Endpoints for resuscitation of the circulation depend pulse rate of less than 100/min, normal or improved
on such variables as the primary etiology of the circula- mental status, urine output greater than 0.5 mL/kg/hr,

- - --
102 Essentialsof General Surgery

warm extremities, and resolution of metabolic acidosis temic inflammation). This inflammation may cause cel-
usually suffice. lular malfunction and death in remote organs. In the
However, patients who have had a severe ce]]ular systemic inflammatory response syndrome (SIRS),
insult may require more complicated hemodynamic mon- many disease states cause systemic inflammation, prob-
itoring and adjustment of the circulation. Certainly, ably as a result of the activation of ceHular mediators of
patients who are in cardiogenic shock require precise inflammation at remote sites.
hemodynamic monitoring (i.e., pulmonary artery To meet the definition of SIRS, a patient must have
catheterization, echocardiogram, cardiac catheterization) two or more of the fo]]owing conditions: (1)tempera-
to make the proper diagnosis and adjust therapy. In ture greater than ~8.5°C or less than 36°C; (2)heart rate
such cases, return of the cardiac index from low greater than 90 beats/min; (3) respiratory rate greater
« 2.2 L/rnin/m2) to normal (2.5-3.5 L/rnin/m2), along than 20 breaths/rnin or Paco2 less than 32 torr; and
with normal amounts of oxygen delivery (400mL/rnin/m2) (4) total leukocyte count greater than 12,000cells/mm,
and consumption (130 mL/rnin/m2), may allow cellular less than 4000ce]]s/mm3, or greater than 10%immature
and organ function to recover. A normal cardiac index forms. Many patients with systemic inflammation, but
may also be adequate in patients with underlying heart without evidence of significant cellular and organ mal-
disease who have a further reduction in cardiac function function (i.e., not in shock) may meet .the definition of
from noncardiac causes and then undergo resuscitation of SIRS.The SIRSvariables of hypothermIa « 36° C) and
their circulation dose to baseline. Unfortunately, despite leukopenia « 4000 cells/mm3) are associated with more
the achievement of normal cardiac index and oxygen severe inflammation, as are systolic hypotension and
parameters, patients with or without severe acute or evidence of organ malfunction (e.g., elevated BUN and
chronic heart disease commonly continue to have cellular creatinine, oliguria, altered mental status, decreased
malfunction that progresses to organ failure and death arterial oxygenation, increased bilirubin, decreased
after a severe hypoperfusion insult. platelets). These patients are in shock, even if infection
The recognition that normal circulation, oxygen is not present and the term sepsis cannot strictly be
delivery, and oxygen consumption may be inadequate applied. Therefore, the traditional concept of septic
for ceHular and organ recovery after severe hypoperfu- shock is too narrow. Patients with severe systemic
sion was inferred from epidemiologic data that associ- inflammation are in shock. When infection is the cause
ated an. increase in these parameters (cardiac index> of severe systemic inflammation, then septic shock can
4.5 L/min/m2; oxygen delivery> 600 mL/min/m2; oxy- be considered thejdiagnosis.
gen consumption> 170 mL/rnin/m2) with eventual
survival. In patients who achieve these endpoints, Effects of Severe Inflammation
metabolic acidosis usually resolves. This situation also on the Circulation
portends a favorable outcome. Therefore, several inves- Severe systemic inflammation is associated with
tigators champion the use of fluids, inotropes, and alterations in both total body and regional perfusion.
sometimes vasodilators to push for these hemodynamic Mechanisms that reduce cardiac output during systemic
endpoints in every criticaHy ill patient. The resuJts of inflammation are listed in Table 6-21.
such management remain controversial, with some The most common etiology of inadequate cardiac out-
studies supporting these endeavors and others finding put during inflammation is decreased venous return,
an increase in mortality rates. which results from both loss of intravascular fluid and
vasodilation. Intravascular volume decreases as plasma
Severe Inflammatory States exudes into the primary focus of inflammation (area of

Inflammation is a normal response to tissue injuJ)', Table 6-21. Circulatory Disorders in Severe Inflammation: Reduced
and it is necessary for tissue repair and wound healing. Cardiac Output
However, although localized inflammation in response
to an insult is usuaHy beneficial, severe tissue injury Hypovolemia
from a variety of causes (Table 6-20) can result in Peripheral vasodilation
inflammation distant from the original disease (sys- Increased capillary permeability, local or total body
Intracellular migration of fluid
Sequestration in gastrointestinal tract lumen
Table6-20. Etiologies of Systemic Inflammation (Partial List) Myocardial depression
Increased pulmonary vascular resistance
Infection (meets definition of sepsis) Hypoxia
Trauma Platelet emboli
Thromboxane release
Serotonin release
Ischemia or reperfusion: regional or total body
White blood cell aggregation
Deficits in the microcirculation
Drug reactions Gastrointestinal tract
Hemolytic transfusion reactions Renal

--- -~-
-- --- - -- . ~ . - - ~-- _.- -.

6: Shock 103

'"llIfV or infection). When svstemic inflammation devel- tract and kidneys appear to be particularly prone to
. 'I i'n response to the primary focus of inflammation, such alterations.
I,I.,...mamav' also exude into some or a11of the other tis-
.II"S. Such' exudation causes an increase in interstitial Effects of Severe Inflammation
"lIid, , hich becomes protein-rich compared with nor- on CeJ]u]ar Function
111.11. In general, interstitial fluid is maintained in the Severe inflammation can result in alterations of ceHu-
.., Iface])ular space by active ce])ular processes that lar metabolism that are independent of inflammation-
11I..intain ceH membrane integrity and perform such induced reductions in oxygen delivery, but simi1ar to
IlInctions as sodium-potassium exchange, which keeps
abnormalities recognized with hypoperfusion. In fact,
"\ 'Iassium in the ceH and sodium out of the cel]' Severe the neuroendocrine response to severe inflammation is
Illflammation may interfere with active ceH membrane
simi1arto that described for severe hypoperfusion, and
IlInction, decrease ion-exchange capabiJities, and aHov.' can result in such common alterations as elevated levels
I II II re interstitial water and solutes to enter ceHs.Deple- of blood glucose and lactic acid. However, the elevation
111111 of interstitial fluid is another mechanism that in lactic acid level that is associated with severe inflam-
.Ig~ravates plasma volume loss. mation is not necessarily secondary to ce])ular anaero-
Ileus is common during severe inflammation, regard-
bic metabolism. Increased lactic add production can
"'ss of the location of the primary focus. Ileus can cause
also develop secondary to alterations in glucose metab-
IllIid to accumulate in the lumen of the gastrointestinal
olism that are associated with increased pyruvate pro-
lfilct, which can be as voluminous as that sequestered duction or decreased pyruvate metabolism without
,luring bowel obstruction. mitochondrial malfunction (i.e., aerobic glycolysis).
Co11ectively, the exudation of plasma volume into Therefore, an elevated lactic acid level does not neces-
inflammatory fod, the accumulation of fluid in the gas- sarily support the conclusion that a patient has inade-
Irointestinal tract, and the migration of fluid into ceHs is
known as the third space, to distinguish it from normal
quate oxygen delivery. In addition, the same ce])-
depolarizing molecule that appears in the circulation
plasma and interstitial fluid spaces. The magnitude of after hypovolemic hypoperfusion is present after inflam-
the third space effect is roughly proportional to the
matory insults. Further, a decrease in serum ionized cal-
magnitude of tissue injury or infection that is present. cium is common in both hypoperfusion and inflamma-
The primary.effect of third-space fluid accumulation is tory states. This decrease, shown experimentally to be
to deplete intravascular volume and impair venous associated with increased intracellular calcium, is also
Vasodi1ation of the systemic veins and arterioles is
likely a marker ior cell/membrane malfunction.
characteristic of severe inflammation, and several
inflammatory mediators are implicated as causative
(e.g., histamine, kin ins, prostacydin, nitric oxide).
Diagnosis and Mana~ement
of Severe Inflammation
Increasing the capacitance of veins decreases MSP and
may decrease venous return, especiaHy if CVP (dis-
cussed previously and in the section on venous return) The dinical manifestations of severe systemic inflam-
does not decrease proportionaHy because of increased mation (Table 6-22) are as potentially varied as the
pulmonary vascular resistance. many organs that may manifest malfunction. Most
Severe inflammation may directly depress the func- patients have hemodynamic alterations, but sometimes
tion of previously normal myocardial ce11s.Less severe abnormal lung, central nervous system, hematologic, or
inflammation may result in augmented malfunction of other organ iunction is the primary evidence of inflam-
previously abnormal cardiac tissue. Therefore, cardiac
mation, rather than hemodynamic changes. Therefore, a
output may be impaired and result in a physiology that high index of suspicion of the patient at risk, aug-
is consistent with an excess, rather than a deficit, of
intravascular volume (i.e., CHF, cardiogenic shock
physiology). Recognition of such cardiogenk states of .
1able 6-22. Common Clinical Manifestations
of Severe Inflammation
hypoperfusion during inflammation is important for
proper therapeutic intervention (see later).
Severe inflammation is associated with increased Vital signs
pulmonary vascular resistance. This increase in right Temperature elevation. hypothermia
ventricular aiterload may cause dilation of the right Tachycardia
ventride, decreased right ventricular ejection, and Tachypnea
impaired iming of the leit ventride. Right atria] pres- Hypotension with warm or cold extremities
sure may increase and impair venous return. Change in mental status
In addition to the recognized effects on cardiac func- Respiratory insufficiency
tion and cardiac output, which can reduce total body Ileus
perfusion, severe inflammation may cause deficits in Oliguria. increased urine protein
the microcirculation, which in turn can result in regional Elevated hemoglobin. thrombocytopenia, leukocytosis, leukopenia
ischemia to organs or within organs. This ischemia wiJ) Increased serum glucose. decreased ionized calcium
accentuate ceH and organ injury. The gastrointestinal

- .
104 Essentialsof General Surgery

mented by evidence gathered during physical examina- Cardiovascular Examination

tion and with selected laboratory tests, supports the Hypotension and tachycardia are usually present,
diagnosis of significant inflammation. along with crisp heart tones. After intravascular volume
is restored, the extremities are warm, demonstrating
The Patient at Risk good capillary refill. Hypotension with warm hands
The first category of risk is a patient who recently and feet usually represents the response to inflamma-
acquired a disease (e.g., severe pancreatitis) or had an tion, although anaphylaxis and a high spinal cord injury
injury (e.g., unstable pelvic fracture with ruptured can produce similar findings. Jugular venous pressure
is low by clinical examination.
spleen) that is characterized by severe inflammation. As a result of plasma exudation and the other cau~
The second category of risk is a patient who has an
underlying condition (e.g., immunosuppression after of plasma volume Joss, the patient usually is sequester-
liver transplantation) or who recently underwent a pro- ing fluid. This sequestration can be sudden or, if the
cedure (e.g., elective colon resection for carcinoma) that patient has been monitored in a hospital setting, the
makes systemic inflammation, particularly from infec- positive fluid balance and an increase in weight may
tion, more likely.Any patient who has had a significant have been documented for several days before acute
deterioration is noted.
episode of hypoperfusion (e.g., cardiogenic shock after
an acute myocardial infarction, upper gastrointestinal Myocardial depression from inflammation might
.hemorrhage sufficient to result in hypotension) is also at cause elevated jugular venous pressure, hypertension,
risk for systemic inflammation, either at the time of the and an 53gallop. Myocardial depression that is severe
hypoperfusion or days later. enough to result in hypotension and a clinical picture
identical to cardiogenic shock is possible. However,
such myocardial malfunction is much less common
Physical Examination than are circulatory deficiencies secondary to hypo-
Outward Manifestations vo]emia. The clinician must be careful to distinguish the
The patient is usually restless and may have alter- fluid sequestration and positive fluid balance associated
ations in mental status ranging from delirium to coma. with severe inflammation (which is universal) from the
In fact, mental status changes may precede obvious same phenomena seen with cardiogenic states. Treating
hemodynamic or respiratory findings. These alterations hypovolemia with fluid restriction and diuretics causes
sometimes lead the clinician to a misdirected evaluation further circulatory embarrassment.
(i.e., computed tomography of the brain). Such alter- Fluid administration is directed at restoring and
ations in central nervous system function are rarely maintaining the plasma and blood volume that is
focal and are most consistent with a metabolic threatened by the fluid sequestration associated with
encephalopathy. severe inflammation. Thus, the primary reason for fluid
If intravascular volume is decreased, the skin is cool administration is to support the circulation. Often the
and possibly mottled, with vasoconstriction most often circulation is assessed with urine output. Decreased
evident in both the upper and lower extremWes. Capil- urine output secondary to severe inflammation is most
lary refill time is also decreased. often caused by inadequate cardiac output. Therefore, it
is a marker of inadequate circulation.
VHal Signs .
Usually, severe systemic inflammation is seen as a
Laboratory Studies
decrease in blood pressure, an increase in heart rate, an Hematologic Studies
increase in respiratory rate, and elevated temperature. An increase in total white blood cell count, particu-
Patients who have underlying cardiac disease may have ]arly young PMNs, is most common. Leukopenia
hemodynamics that are more consistent with congestivE' denotes more severe disease and consists mostly of
heart failure (i.e., elevated blood pressure, tachycardia). immature PMNs. The platelet count usually falls, and
Hypothermia may be present in the most severe cases. evidence of consumption of coagulation proteins, with
breakdown of fibrinogen (increased prothrombin time,
Lung Examination increased partial thromboplastin time, and increased
At lung examination, the lungs may be clear, even fibrin split products or D-dimer), denotes more severe
when acute respiratory distress syndrome (ARDS) is disease. Hemoglobin may increase as plasma exudes
present. However, rales, rhonchi, and bronchospasm into inflammatory sites. This increase indicates hemo-
may be found. Examination findings consistent with concentration, and may be a useful tool in assessing
consolidation (e.g., tubular or tubulovesicular breath intravascular volume resuscitation because plasma vol-
sounds, egophony) may assist in locating an inflamma- ume is likely to be inadequate until the hemoglobin
tory process, but they are clearly not specific to systemic returns to the patient's baseline value.
inflammation. The lung examination is not sufficiently
specWc to permit a diagnosis of systemic inflammation Lung Studies
or other etiology of diffuse pulmonary malfunction. A decrease in arterial Po. and Pco. is characteristic of
severe systemic inflammation as well as many other
n . .- .. -....

6: Shock 105

'",;: di~ease states. The increase in physiologic shunt, ated with inflammation in the presence of normal oxy-
IIId1 resuJts in a decrease in arterial P02' is associated gen concentrations. Therefore, like ionized calcium,
01II slimuli that increase minute ventilation and the~e abnormalities do not distinguish severe inflam-
I," n'il~e arterial PCO:. A chest x-ray may be clear or mation from a decrease in either regional or global per-
III.I\' demonstrate loss of lung volume as well as evi- fusion. Persistent metabolic lacidosis could mean that
.1.'lh'l' of pulmonary fluid accumulation, most often either di~ease is present and should prompt further
""111 a noncardiogenic pathophysiology (i.e., ARDS). diagnostic and, possibly, therapeutic efforts.
III,' clinician should recognize that respiratory signs
.11111 symptoms and laboratory data during severe Treatment
IlIlIammation (shortness of breath, tachypnea, crackles,
Treating the Underlying Cause
\\ III'czing, decreased arterial P02' chest x-ray showing
"hTeased lung water) may be indistinguishable from
Once severe inflammation is recognized, the first
IlIlIse seen with CHF. In addition, he or she should rec- principle of treatment is to determine the underlying
.';~Ilizethe dangers of misdiagnosing the effects of cause and initiate appropriate therapy (Table 6-23).
',,'verelung inflammationas CHF. Infection and infection-like processes (i.e., infusion of
endotoxin) are the most commonly considered etiolo-
I 'ri ne Studies gies of severe inflammation. However, reactions to
drugs or transfusions and tissue injury without infec-
Oliguria is common during severe inflammation, and tion (i.e.,early severe pancreatitis) can also cause severe
'" most often secondarv to low intravascular volume
systemic inflammation that is indistinguishable from
,llld inadequate circulation. Jt causes laboratory test that seen with the invasion of microorganisms.
sults that are consistent with a prerenal state (e.g., ele- While the search for the primary disease is underway
,'aled urine specific gravity, low urine sodium, and therapy is initiated, vital organ function must be
II1creased urine osmolality, elevated BUN:creatinine supported until the primary process is under control.
ratio). Unfortunately, systemic inflammation may continue
~erum Chemistries
despite adequate resolution of the initiating insult. In
some patients, inflammation appears to become self-
An elevated blood glucose level is common during sustaining, as though a positive feedback system
inflammation from su'ch alterations as increased gluco- developed in one or more of the organs with systemic
neogenesis, glycogen lysis, and relative insulin resistance. inflammation. For instance, ARDS initiated by an
For many years, decreased total serum calcium has inflammatory process in the abdomen causes inflamma-
been recognized as associated with one particular tory cells to accumulate in the lungs. The inflammation
severe inflammatory disease, pancreatitis. The amount caused by these pulmonary cells usually, but not
of decrease correlates with the severity of disease. Ion- always, subsides when the underlying illness is effec-
ized calcium is the calcium that is not bound to albu- tively treated. Sometimes the lung inflammation
min. Therefore, it is not affected by albumin concentra- becomes chronic despite resolution of the first inflam-
tions, which can change significantly during critical matory focus. .

iJIness. Ionized calcium is also better correlated with -

As discussed later, novel therapies that focus on
parathyroid hormone release compared with total interrupting various steps in the inflammatory process
calcium. are being studied to determine whether they can ame-
Ionized calcium decreases with any disease that liorate the adverse effects of severe inflammation and
causes either severe hypoperfusion or inflammation. improve clinical outcome. In addition, therapies
This decrease is not secondary to inadequate para thor- designed to enhance immunologic function may pre-
mone secretion. Several recent studies showed an vent subsequent inflammatory insults from infection or
increase in intracellular calcium during or after hypo- microbiologic by-products.
perfusion or inflammatory states. In addition, the mag-
nitude of the decrease correlates with the severity of di~- Supporting Organ Function: Cardiovascular
ease. Although it is not specific for inflammation, and Pulmonary
ongoing severe inflammation must be considered in any Support of the circulation usually starts with treat-
patient who has decreased ionized calcium. In contrast, ment of hypovolemia. The result is usually an increase
a normal ionized calcium level is unusual during severe
inflammation or hypoperfusion. Therefore, a norma]
value suggests that a severe acute systemic insult is not Table 6.23. Treatment of Severe Inflammation
The combination of electrolyte or arterial blood gas
]evels that are consistent with metabolic acidosis and an Control etiology
Drug or transfusion reaction
elevated lactic acid level is often seen in severe inflam-
Tissue injury
mation. An elevated lactic add level may develop sec- Infection
ondary to anaerobic metabolism, suggesting hypoper- Support organ function
fusion as the cause. However, an elevated lactic acid
level can also result from metabolic alterations associ- Antagonize inflammatoryand metabolic mediators

106 Essentialsof General Surgery

in cardiac output such that hypotension is alleviated, if insertion should be used when the potential advantage,
nof completely reversed. The temperature of the as described earHer,is considered worth the risk.
extremities also changes from cool to warm. For most During severe inflammation, myocardial depression
patients, the combination of restoration of intravascular may be a manifestation of decreased function of the
volume, peripheral vasodiJation, and the neurohumoral myocardial catecholamine receptors. Phosphodiesterase
response to inflammation produces a hyperdynamic inhibitor drugs (e.g., amrinone), which do not require
(cardiac index> normal) circulatory state. Urine output this receptor function for action, may be particularly
and mental status usually improve. Unfortunately, pul- useful inotropic agents during severe inflammation.
monary function does not characteristically improve In a patient who is hyperdynamic, has elevated car-
dramaticany with treatment of hypovolemia alone. Ion- diac output, and has low systemic resistance states, the
ized cakium aJterations and metaboHc acidosis mayor use of an alpha agent (e.g., norepinephrine, neo-
may not improve as a resuJt of simple improvement in synephrine) may be indicated, especially when certain
the circulation. vessels with fixed stenoses (e.g., atherosclerotic plaques
Red blood cen transfusion is reserved for patients in renal, carotid, or coronary arteries) are likely to
who have ongoing hemorrhage or hemoglobin levels of require higher mean arterial pressure for adequate per-
less than 10 g/100 mL and who have abnormalitjes that fusion. Under these circumstances,. the use of such
are consistent with inadequate oxygen deHvery. For vasoconstrictors (with simultaneous documentation of
patients with hemoglobin levels of more than 10 g/1oo no significant reduction in cardiac output) may increase
mL, simply increasing hemoglobin does not appear to mean arterial pressure and provide evidence of better
significantly improve oxygen consumption. organ perfusion (e.g., increased urine output).
Dopamine, usuany in low, or "renal," concentrations, Endpoints for resuscitation of the circulation during
is commonly administered during severe inflammation. severe inflammation are as controversial as those
Because dopamine, even at these low doses, tends to described in the hypoperfusion section. Because severe
increase left ventricular end-diastolic pressure as car- inflammation commonly increases cardiac index, one
diac output increases, this drug has a physiologic effect indicator that inflammation is resolving may be a
that is similar to fluid infusion, and is most useful when decrease in cardiac index (e.g., from 5.0 to
hypovolemia is the primary abnormaHty. 3.5 L/min/m2) and an increase in systemic resistance
The diagnosis and treatment of a cardiogenic state usu- (e.g., from 350 to 900 dynes-see/emS).
ally requires more complicated monitoring than simply Support Ofl pulmonary function often requires
recording blood pressure, pulse, skin color, mental status, mechanical ventiJation and various associated teeh-
urine output, and electrolyte concentrations. Insertion of a niques of ventilator management. Such management is
pulmonary artery catheter (PAC) allows more precise sufficient when arterial oxygen saturation is greater
measurement of cardiac filling pressures and the response than 90%.
to inotropic and vasodilator manipuJations. .

The primary advantage of PAC insertion is the ability

to acquire hemodynamic data to assist in hemodynamic Achieving a Balance in the Effects of JnflammaHon
diagnostic and therapeutic decision-making. Given the Much experimental and clinical research has' evalu-
evidence that achieving excenent circu]ahon is associ- ated the antagonism of inflammatory and metabolic
ated with improved outcome in patients who have mediators in severe inflammatory states (Table 6-24).
severe hypoperfusion or inflammation, using techno- Many studies show promise, but none has become stan-
logic devices (which might indude echocardiography) dard therapy.
to evaluate the circulation and possibly avoid continu- As previously stated, inflammation has beneficial
ing hypoperfusion dearly appears beneficial. This argu- effects (e.g., wound healing, defense against invasive
ment is not supported by data accrued during routine organisms) that are important for survival during crit-
use of PACs, however, because critical assessment of the ical iJJness. Therefore, a successful outcome depends
circulation is not Hkely to be crucial for any common iJ)- significantly on a balance between the beneficial and
ness or surgical intervention (e.g., major vascular sur- the detrimental effects of inflammation. Therapy that
gery). Likewise, it may be difficult to discern a survival aggressively suppresses inflammation (i.e., pharma-
advantage to using such equipment in large groups of cologic doses of anti-inflammatory steroids) may pro-
patients in the intensive care unit. However, an individ- vide short-term benefits (e.g., improvement in hemo-
ual patient may achieve a distinct advantage, especiany dynamic and pulmonary function), but the loss of the
when a therapeutic intervention that reverses hypoper- beneficial effects of inflammation may result in death
fusion is documented. secondary to recurrent infecHon or wound break-
The disadvantages of PAC insertion indude compli- down.
cations related to central venous access (e.g., pneumo- For an of the therapies listed in Table 6-24, this bal-
thorax, central venous thrombosis) as wen as those ance must be considered. The benefits of inflamma-
associated with the cardiac location (e.g., ventricular tion are primariJy local (i.e., at the focus of tissue
arrhythmias, damage to the tricuspid or pulmonic injury or infection). The detrimental effects are pri-
valves, rupture of the pulmonary artery). Ventricular marily systemic (e.g., alterations in circulation or pul-
arrhythmias are usuany not sustained, and anatomic monary function). Therapies that a]]ow local inflam-
injuiies are rare. Despite the relatively low risk, PAC mation to continue while the systemic inflammation

6 : Shock 107

IS suppressed may a]]ow the proper inflammatory A Practical Guide to the Patient
b.llance. .
in Shock
In general, these therapies are most helpful in
patients ,...'ho appear to have severe systemic inflam-
Once a patient is recognized to be in shock, the guid-
IIliltion despite usua]]y adequate therapy for the
ing principles are to: (1)provide an exce]]ent circulation
Irnderlying mness. For instance, consider a 65-year-old and (2) treat severe inflammation.
previously heaJthy woman who has perforated diver-
IkuHtis and undergoes a sigmoid resection with end-
sigmoid colostomy. OrdinariJy, fluid resuscitation, sur- Recognize the Patient in Shock
gery, and antibiotics are sufficient to reverse the Clearly, the first step in the evaluation and manage-
detrimental effects of this severe inflammatory j)Jness ment of the patient who is in shock is to recognize that
.1I1dsupport the proper balance between the beneficial a deficit in t.ota]body ce]]ular function is present. The
and detrimental effects of inflammation. However, if history is the first due to the patient who is at risk
IIrgan maHunction (e.g., ARDS, hyperdynamic circu]a- (Table 6-25). Next, bedside examination can provide
Iion, impaired renal function) consistent with ongoing dues, but severe hypotension and marked tachycardia
severe inflammation is stiU present 3 to 4 davs later, may not always accompany other evidence of shock
Ihen one possible explanation is that the inflammation (Table6-26).Next come common laboratory,data, which
stimulated in other organs by the perforated divertic- are frequently abnormal during shock (Table6-27).
ulitis is responsible for the lack of resolution, despite
therapy that is often sufficient. In other words, the Provide an Excellent Circulation
detrimental and beneficial effects of severe inflamma- An accurate diagnosis of the state of the circulation is
tion are out of balance. Under such circumstances, critical (see the section on hypoperfusion states).
therapy directed at the systemic inflammation may be The patient. who is in cardiogenic shock requires
warranted. aggressive hemodynamic monitoring as well as

Table6.25. Characteristics of the PatienfWho Is at Risk for Shock

Table 6-24. Antagonism of Inflammatory

and Metabolic Mediator~ Trauma or burn
Vascular catastrophE
Interference with eHeets of endotoxin Acute cardiac disease
Clear endotoxin trom the circulation Acute abdominal diseaSE
Antiendotoxin antibody Severe extraabdominal infection
Bind toxin to membrane
Drug exposure
Filter toxin out
Interfere with binding of endotoxin to effector cells (i.e.. bactericidal
or permeability-increasing protein)
Interference with the activation of proinflammatory cytoklne~ Table 6-26. Bedside Examination Indicators of Shock
Nonsteroidal anti-inflammatory agents
Inhibition of IL,'-converting enzyme Hypotension

Interference with the activity of increased pro-inflammatory cytokines Tachycardia

Anti-TNF. anti.IL., antibodies Tachypnea
Binding of TNF and IL-' with excess receptor~ Hyperthermia or hypothermia
Blocking of effector cell receptors (i.e.. administration of IL-' Peripheral vasoconstriction and cool extremities
receptor antagonist)
Hypotension with warm extremities
Continuous blood filtration
Agitation and altered mental status
Administration of anti-inflammatory cytokine~
Interference with superoxide activity
Decrease production
Increase scavenging
Interference with secondary mediators Table 6.27. Common Laboratory Abnormalities With Shock
Cyclooxygenase system
Nitric oxide system Metabolic acidosis
Histamine. serotonin, kinin system Elevated blood urea nitrogen and creatinine
Coagulation system Leukocytosis or leukopenia
Interference with inflammatory cell activation by blocking activation Elevated blood glucose
receptors (I.e., inhibition of leukocyte integrin and selectin) Decreased platelet count
Decreased ionized calcium
IL. inlerleukin. TNF. tumor necrosis factor.

108 Essentialsof General Surgery

pharmacologic and possibly mechanical assistance of Treat Severe Inflammation

the circulation (see earlier sections). This level of care
Treating severe inflammation requires recognition
clearly requires a critical care environment and physi- that an inflammatory disease is present (see discussion
cian expertise. The decision may be made to per/orm of severe inflammatory states). Next, the focus of severe
emergency cardiac catheterization or cardiac surgery. inflammation must be localized and treated (e.g., antibi-
The hypotensive supine adult who does not have a otics for pneumonia, colon resection for perforated
cardiogenic process most often has lost at least 30% of diverticulitis). Usually, these interventions suffice.
intravascular volume (approximately 1500 mL in a Occasionally, the other methods described in the section
70-kg person). Rep]acement with crystalloid requires a on severe inflammatory states are used to diminish the
3:1 ratio as the crystalloid distributes throughout the effects of severe inflammation.
extracellular space. Therefore, 4500mL crystalloid solu- Hypoperfusion can cause inflammation or aggravate
tion is required to begin plasma volume restitution in established inflammation. Therefore, providing an
this patient. Because there is no organ in the body that excellent circulation is as much a treatment of inflam-
is improved by hypoperfusion, and because prolonged mation as is the use of antibiotics or surgery. As a corol-
hypoperfusion induces or aggravates tissue inflamma- ]ary, because inflammation can induce both total body
tion, restitution of an adequate circulation should be and regional hypoperfusion, treating inflammation
accomplished rapidly (within minutes, if possible, with improves the circulation.
two large-bore intravenous lines wide open).
When decreased venous return (most often as a result
of hypovolemia) is the cause of hypoperfusion, a diag- Conclusion
nostic evaluation of the etiology of impaired venous
return must occur simultaneously with restoration of the Total body cellular malfunction (i.e., shock) can result
circulation. Venous return can unprove with fluid infu- from various insults that may be broadly categorized as
sion, regardless of the' underlying etiology of the severe hypoperfusion or severe inflammatory distur.
decrease (e.g., hypovolemia vs pericardial tamponade). bances. Almost invariably, hypoperfusion and inflam-
As described in previous sections, the circulatory mation coexist in patients who have shock. Restoring an
parameters that indicate an excellent circulation may excellent circulation and treating severe inflammation
vary from patient'to patient, but general bedside guide- are the keys to preserving cellular and organ function
lines are listed in Tab]e 6-28.More sophisticated indica. and preventing death from shock.
tors of an excellent circulation have been proposed, and
may be of particular value when evidence of organ mal-
function is present, despite bedside indicators that the Multiple-Choice Questions
circulation is adequate (i.e., BUN and creatinine levels
are increasing when the blood pressure and pulse are 1. The most common cause of severe hypovolemic
normal; Table 6-29). hypoperfusion is:
A. Peritonitis
B. Burns
Table 6-28. Bed~ide Indicators of an Excellent Circulation C. Hemorrhage
D. Sepsis
E. Spinal cord injury
Normal blood pressure and pulse for the individual
Normal mental status
2. The major component of a decrease in cardiac output
Warm extremities
in hypovolemia is:
Urine output ~ 0.5 mUkglhr A. Increased systemic vascular resistance
Resolution of metabolic acidosis B. Decreased venous return
C. Myocardial ischemia
D. Increased pulmonary vascular resistance
E. low hemoglobin
Table 6-29. Monitors of Circulation Status
3. In a 70-kg man who has a 20% loss of intravascular
Cardiac index > 4.5 Uminlm2 volume, the volume of isotonic electrolyte solution
Mixed venous O2 saturation ~75% required to return the vascular volume to normal is:
Oxygen delivery > 600 mUminlm2 A. 500 ml
Oxygen consumption .> 170 mUminlm2 B. 1500 ml
Gastric mucosal pH
C. 3000 ml
(tonometer measurement) > 7.35 D. 4500 ml
E. 6000 ml
Right ventricular end diastolic
volume index > 100 mUlTi
4. A 45-year-old man is admitted to the hospital with
Ideal values indicate a good prognosis. hematemesis. His blood pressure is 90/60 mm Hg,
6: Shock 109

his pulse rate is 120/min, and he is diaphoretic and 11. Match the following phrase with the best single
restless.The best therapy for his restlessness is: response. Response to catecholamine elevation:
A. Intravenous diazepam A. Elevatedarterial lactate
B. Rapid intravenous fluid administration B. Elevatedblood sugar
C. Intramuscular chlordiazepoxide (librium) admin- C. Both
istration D. Neither
D. Nasal oxygen
E. Restraints 12. Match the following phrase with the best single
response. Necessary to make the diagnosis of severe
5. The most practical, objective bedside monitor of the hypovolemic hypoperfusion:
adequacy of volume resuscitation in states of severe A. Elevatedarterial lactate
hypovolemic hypoperfusion is determination of: . B. Elevatedblood sugar
A. Serial lactate levels C. Both .
B. Mental status D. Neither
C. Urinary output
D. Blood pressure
E. Arterial blood gases 13. After intravascular volume restitution, the hyperdy-
namic response to severe inflammation is character-
6. As severe inflammation progresses to cardiogenic ized by:
hypoperfusion: A. Decreased oxygen consumption
A. Cardiac output increases B. Decreased intrapulmonary shunt
B. Pulmonary artery occlusion pressure decreases C. Increased peripheral vascular resistance
C. Arterial lactate level decreases D. Increasedcardiac output
D. Oxygen delivery decreases E. The universally beneficial application of the
E. Respiratoryrate decreases . vasoactivedrugs norepinephrine and epinephrine

7. The first therapeutic measure to improve blood pres- 14. The hormones that affect hemodynamic parameters
sure and cardiac output in severe inflammation is: the most during severe hypovolemic hypoperfusion
A. Dopamine administration are:
B. Dobutamine administration A. Epinephrineal1ldnorepinephrine
C. Nitroprussideadministration B. Insulinand glucagon
D. Steroid administration C. Glucocorticoids
E. Intravenousfluid administration D. Mineralocorticoids
E. Antidiuretichormones
8. Which of the following hemodynamic variables is
within the normal range~
A. Systemic vascular resistance of 2500 dynes- 15. The biochemical effects of severe hypovolemic
sedcm-~ hypoperfusion and severe inflammation are charac-
B. Cardiac index of 3.3 Umin/m2 terized by: .

C. Pulmonary artery pressure of 70/50 mm Hg A. Decreased gluconeogenesis

D. Pulmonary vascular resistance of 480 dynes- B. Decreased glucocorticoid release
sedcm-~ C. Decreased muscle breakdown
E. Oxygen consumption of 80 to 100 mUmin D. Increased glycogen stores
E. Elevated blood glucose
9. Cardiogenic shock is distinguished from severe hypo-
volemic hypoperfusionby: 16. The normal usage of oxygen at rest is:
A. The depression in cardiac output in hypovolemic A. 250 mUmin
states B. 100 mUmin
B. The degree of vasoconstriction C. 500 mUmin
C. Oliguria . D. 2500 mUmin
D. Mental obtundation E. 1500 mUmin
E. Rightand leftventricularfilling pressure measure-
17. The most accurate predictor of oxygen consumption
10. Match the following phrase with the best single is:
response. Acute hemorrbage: A. Central venous pressure
A. Elevatedarterial lactate B. Mixed venous oxygen content
B. Elevatedblood sugar C. ArteriaJ oxygen saturation
C. Both D. Arteriovenous oxygen difference
D. Neither E. Pulmonary capillary wedge pressure

110 Essentialsof General Surgery

18. Of the following, the most important principle for resuscitation, and the probable need for packed
treating patients who have severe inflammation is to: red blood cells.
A. Maximize oxygen delivery and consumption B. The student initially estimates the amount of
B. Diagnose and treat the primary disease process blood loss in this patient, based on hypotension in
C. Maintain urine output the average-sized man. The student recognizes
D. Provide anti-inflammatory steroids that at least 30% of intravascular blood volume
E. Use vasconstricting drugs judiciously was lost.
19. Severe inflammation can produce all of the following C. The student recognizes the need for a bladder
alterations in the circulation EXCEPT: catheter to measure urine output and the need for
A. Decreased venous return from hypovolemia laboratory tests to assess the degree of circulatory
B. Myocardial depression deficit and inflammation. Laboratory tests should
C. Microcirculation deficits include: complete blood count with white cell dif-
D. Decreased venous return from increased intratho- ferential; arterial blood gases, especially to meas-
racic pressure ure arterial pH; serum electrolytes, blood urea
E. Increased pulmonary vascular resistance nitrogen, and creatinine; platelet count; coagula-
tion studies; and blood glucose.
20. Severe hypoperfusion begets inflammation primarily OBJECTIVE 3
as a result of:
A. Ischemiaand reperfusion pathophysiology After resuscitation begins, the student can describe
B. Translocation of organisms across the gastroin. the methods of evaluating where blood loss has
testinal tract occurred.
C. Lacticacid stimulation of inflammatorycells The student recommends further examination to
D. Activationof the c9agulation cascade evaluate the chest, abdomen, and extremities for evi-
E. Macrophage activation by ischemia dence of blood loss (e.g., fractures, abdominal tender-
ness, pelvic instability, displacement of the prostate).
Minimum Level of Achievement for Passing
Oral Examination Study Questions A. The student recognizes that hemorrhage is the
most likely etiology of the hypoperfusion.
B. The student knows the minimum requirements
CASE 1 for fluid resuscitation in a patient with hemor-
You arethe only attending physkian in a small com- rhagic shock.
munity emergency department. Paramedics arrive with
a 25-year-old man who, when leaving a tavern, stepped C. The student recognizes that performing the basic
off of the sidewalk and into the path of an oncoming clinkal examination will lead to the recognition of
motor vehicle. He is conscious and breathing sponta- suspicious areas for blood loss.
neously, and has a heavy odor of alcohol on his breath. Honors Level of Achievement
On arrival, his vital signs are: temperature 97.6°F,pulse A. The student can describe the possibility of tension
120/min, blood pressure 90/70 mm Hg, and respiratory pneumothorax or pericardial tamponade in the
rate 34 breaths/min. Pulse oximetry of his left ear patient with traumatic injury.
shows 95% saturation. There are no obvious areas of
B. The student can differentiate tension pneumotho-
ecchymosis over the upper abdomen or thorax. He is rax or pericardial tamponade from hemorrhagic
agitated and combative, and has cool, cyanotic extremi- shock.
ties. He has bilateral breath sounds and crisp heart
tones. There is no jugular venous distension. How C. The student can describe how much blood loss
would you assess and manage this patient's circulation? may occur in occult sites (e.g., abdomen, pelvis).
OBJECTIVE1 D. The student can describe the appropriate labora-
tory tests and the expected values, comparing
To evaluate the circulation in this patient, the student mild with severe circulatory alterations.
considers all diagnoses of severe hypoperfusion that are
related to trauma: severe hypovolemia from hemor-
rhage, tension pneumothorax, and perkardial tampon. CASE 2
ade. Based on the information given, the student hones You are a surgeon who is called to see a 60-year-old
in on the diagnosis of hemorrhagic hypoperfusion. man who arrived in the emergency room with severe
OBJECTIVE2 abdominal pain, fever, and chills of 4 days' duration.
His blood pressure is 60/40 mm Hg, pulse is 130/min,
The student outlines the treatment intervention for a
respiratory rate is 30 breaths/min, and temperature is
patient with hemorrhagic hypoperfusion. 102°F. He is agitated, his chest is clear, and findings at
A. The student recognizes the need for two large. cardiac examination are unremarkable. He has no jugu-
bore intravenous lines, the need for crystalloid lar venous distension. Abdominal examination shows
6 : Shock 111

difiuse abdominal tenderness with diffuse involuntarv Minimum Level of Ac11ieveJnentfor Passing
::lIarding. Rectal examination is negative. His extremi- A. The student recognizes that the patient requires
III'~are cool and vasoconstricted. An electrocardiogram resuscitation with large volumes of intravenous
...hows a sinus tachvcardia. fluid.
How would you' assess and manage this patient's cir-
. 'Illation deficit? B. The student recognizes trat hypoperfusion of thi~
magnitude from an intraabdominal inflammatory
OBjECTIVE] process commonly requires surgery.
Honors Level of Achievement
The student realizes that the patient requires rapid
rl'suscitation of the circulation. The student also real- A. The student can describe the various etiologies of
severe intra abdominal inflammation
lI'.es that this patient most likely has severe hypo-
,'olemic hypoperfusion, probably from severe inflam- B. The student can describe the systemic inflamma-
mation rather than cardiogenic shock. The student tory response syndrome (SIRS)and explain how
Ivcommends: this patient may fit this clinicalentity. .
A. Rapid administration of intravenous fluids. The C. The student can describe the fundamental princi-
student can describe the volume of crvstalloid ples of managing the patient with severe SIRS.
required to resuscitate a patient' who i~ These principles include achievement of an excel-
hypotensive. For a 70-kg man, it is the volume lent circulation and eradication of the severe
of crystalloid required to replace approximately inflammatory process.
30% of blood volume (1500 mL blood/4S00 mL
B. Insertion of nasogastric tube because of an acute ADDITIONAL QUESTIONS
abdominal process 1. What are the most common sites of infection that
C. Insertion of a bladder catheter to monitor resusci- cause SIRS and inflammation-induced hypoperfu-
tation sion? The student should consider, most commonly,
urinary tract infection, pneumonia, peritonitis, and
D. Blood tests, including complete blood count, elec- intra abdominal abscess.
trolytes, blood gases (to assess the degree of aci- 2. What are the etiologies of hypoperfusion from
dosis or respira\ory complications), and blood severe inflammation? The student should describe
cultures the causes of hypovolemia (vasodilation, exudation
E. No use of inotropes before aggressive fluid resus- of fluid into the area of inflammation as well as into
citation unless severe shock unresponsive to fluid other regions of the body, intracellular fluid migra-
resuscitation is present tion). In addition, the student should describe the
possibility of myocardial depression as well a~
OBJECTIVE 2 right-sided heart failure from increased pulmonary
vascular resistance.
The student attempts to make a diagnosis of the 3. How much fluid is usually required to correct the
cause of shock, including the following steps: hypovolemia that is seen with septic shock that is
A. Obtain a more detailed history, particularly a gas- caused by peritonitis? The student should recognize
trointestinal history related to such previous dis- that frequently 5 to 10 L crystalloid solution is
eases as uker disease, biliary tract disease, and. required to resuscitate hypovolemic patients who
diverticulosis. are in septic shock. .
B. If vital signs improve, obtain x-rays of the chest 4. Why is the central venous pressure (CVP) high in
and abdomen, some hypovolemic patients who have septic
shock? The student should recognize that increas.
OBJECTIVE 3 ing pulmonary vascular resistance in patients with
The student describes further management of the sepsis may be of a magnitude that will cause right
ventricular dvsfunction and elevation of venous
patient once resuscitation is complete, based on the var-
ious possible etiologies of severe inflammation from an 5. What should be done at the time of surgery for an
intraabdominal source.
intraabdominal process that produces septic shock?
A. The student describes the various potential etiolo- The student should describe the need to obtain
gies of this degree of inflammation from an smears and cultures of what appears to be infected
abdominal process (i.e., cholangitis, pancreatitis, fluid in the abdominal cavity and should recognize
perforated peptic ulcer, perforated diverticulitis, that correcting the primary underlying disease is
ischemic bowel). indicated (e.g., perform definitive ulcer surgery or
B. The student describes the processes that require sigmoid resection for perforated diverticulitis). The
emergency surgery for management: cholangiti~, student should also describe irrigation of thE'
perforated peptic ulcer, perforated diverticulitis, abdomen to remove as much contamination as
and ischemia. possible.

112 Essentials of General SurgeI')'

CASE 3 A. If hypovolemic shock is present, the student real-

You are the resident on the surgical intensive care izes that the patient has at least a 30%reduction in
unit. One of your patients is a 65-year-old man with intravascular volume.
known coronary artery disease. He recently underwent B. The student realizes that hypothermia con-
repair of a ruptured abdominal aortic aneurysm. Dur- tributed to the intense vasoconstriction and that,
ing the operation, the patient's blood pressure fell to if the patient is hypovolemic, he requires further
60 mm Hg systolic several times, for a total duration of repletion of vascular volume as the hypothermia
30 minutes. Urine output over the 3-hour operation was is corrected.
45 mL, despite administration of a diuretic and manni-
toJ. The last arterial blood pH obtained in the operating
C. The student can describe the therapeutic options
room, 15 minutes before the patient was transferred to
available for the patient who is in cardiogenic
the intensive care unit, was 7.3, with Po: of 120 mrn :Jig,
FI02 of 50%, Pco2 of 30 mrn Hg, and Tco2 of 20 mrn Hg. 1. Inotropic therapy: dobutamine
On arrival in the surgical intensive care unit, his blood 2. Vasodilator therapy: nitroglycerin or nitro-
pressure was 80/60 mrn Hg, pulse was 120 beats/min, prusside
respiration rate was 16 breaths/min, and temperature 3. Intraaortic balIoon pump inse~on
was 96° F. He received narcotic anesthesia and is stilI D. The student can describe the benefits and delete-
unconscious. His neck veins are not visible; he has a rious effects of each of the therapies provided for
central venous catheter in his right internal jugular vein, cardiogenic shock.
with marked edema above the clavicles; his chest is
clear; his heart sounds are distant; and his carotid, Minimum Level of Achievement fOTPassing
The student recognizes that the patient is in a state of
radial, and femoral pulses are palpable at 1+. No pulses
are palpated below the femoral arteries. He is severely
severe hypoperfusion, that hypovolemic hypoperfusion
vasoconstricted. is much more likely than cardiogenic shock, and that
vasoconstrictors are not used in the initial therapy for
OBJECTIVE 1 either hypovolemic or cardiogenic shock.
The student realizes that this patient requires rapid Honors Level of Achievement
evaluation of and resuscitation from the severe hypo- A. The student demonstrates a clear understanding of
perfusion state. The student also realizes that hypo- the volume of resuscitation needed for the
volemic shock is much more likely than cardiogenic hypotensive, vasoconstricted, nypothermic patient
shock, but is alert to the second possibility. The student who is in severe hypovolemic hypoperfusion.
begins evaluation and resuscitation with an algorithm B. The student can describe the effects of drugs and
similar to the following one: the intraaortic balIoon pump on myocardial oxy-
A. Obtain an electrocardiogram and compare it with gen consumption and the relation of this value to
previous cardiograms to evaluate the possibility the treatment of cardiogenic shock.
of a myocardial infarction. If the finding is nega-
tive, fluids are administered rapidly. C. The student can discuss the potential etiologies of
cardiogenic shock other than myocardial infarction.
B. Recognize that CVP monitoring alone wiJ] likely
D. The student demonstrates knowledge of the nor-
be inadequate because it does not provide infor-
mation about the left side of the heart or the car- mal pressures as measured with central venous
diac index. Therefore, insertion of a pulmonary
pressure or pulmonary'capilJary wedge pressures.
artery catheter is more helpful. SUGGESTED READINGS
C. Obtain other laboratory studies: hemoglobin, Baue AE, MOF/MODS, SIRS: an update. Shock1996;6:51-55.
electrolytes, and blood gases. Burchard KW. Gann OS, Wiles CE. 1M C/iniCQlHandbook for SurgiCQl
CritiCQlCare. New York, NY: Parthenon, 1999.
D. Avoid vasoconstricting drugs, even if clear evi- Califf RM, Bengtson JR. Cardiogenic shock (reviewl. N Engl J Med
dence of cardiac insult is present. 1994;330:1724-1730.
Eastridge B),Darlington DN, Evans }A, Gann OS.A circulating shock
E. If the electrocardiogram shows an acute myocar- protein depolarizes cells in hemorrhage and sepsis. Ann Surg
dial infarction, the student realizes that the man- 1994;219:298-305.
agement principles may be distinctly different if Livingston DH, Mosenthal AC. Deitch EA. Sepsis and multiple organ
the patient is in cardiogenic shock. The. student dysfunction syndrome: a clinical-mechanistic overview. N Horizons
can describe the hemodynamic parameters that Pricolo VE, Demaria E}, Burchard KW. Venous return: physiology,
are typical of cardiogenic shock. monitoring, and manipulation. ) and II. Surg Rounds 1993;
The student can describe the continuing efforts to
treat shock in patients with hypovolemia or cardiogenic