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DaO CO CaO
22
=
aggregation
Coronary
microcirculatory damage
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9.
INTRODUCTION TOSHOCK
Babar Fiza and VivekMoitra
CASE
A 54- year- old woman with a history of coronary artery disease and congestive heart failure is in the operating room for
exploratory laparotomy due to toxic megacolon. Her mental status is altered, urine output is low, and kidney injury is
acute. Hemoglobin level is 7.4 g/ dL. Blood pressure is 84/
Decreased cardiac output
↓ Venous
return
Decreased tissue perfusion
Metabolic
acidosis
Intracellular
fluid loss
Cellular
hypoxia
↓
perfusion
36mmHg and respiratory rate is 30 breaths per minute.
INTRODUCTION AND DEFINITION
Shock, a clinical syndrome of circulatory failure, occurs when
inadequate tissue perfusion causes cellular dysfunction and
injur y.1 e multiple inammatory mediators released impair
Figure9.1 Decreased tissue perfusion and shock results in a feed- forward loop
that can exacerbate cellular injury and tissue dysfunction. SOURCE:Adapted from
Zuckerbraun, Brian S., etal. “Shock.” Schwartz’s Principles of Surgery, 10e. Eds. F.Char les
Brunicardi, etal. NewYork, NY:McGraw- Hill, 2014 with permission from McGraw- Hill.
Parenchymal cell injury
Endothelial activation/
Cellular
the cell’s use of oxygen, causing more cellular injury, microcirculatory damage, and poor tissue perfusion from maldistribution of blood ow (Figure 9.1).2 Cellular dysoxia, or loss of
interdependence in oxygen delivery and metabolism, produces
and obstructive shock, less than 2% of all cases.5 Mortality
from cardiogenic shock is greater than 50%; mortality from
septic shock ranges from 20% to 40%.
6– 8
lactate through oxygen- limited ATP production.3 If tissue perfusion is not restored, the result is multiple organ dysfunction
syndrome (MODS) or evendeath.
PATHOPHYSIOLOGY
CLASSIFICATION AND EPIDEMIOLOGY
Shock can be categorized according to four pathophysiological mechanisms: hypovolemia (from loss of blood or
uid), cardiogenic origin (poor pump function), extracardiac obstruction (obstructed ow in the cardiovascular circuit), and distributive factors (vasodilation) (Figure 9.2).4
ese distinct underlying mechanisms are not mutually
exclusive. For example, patients with distributive factors
causing septic shock also can have cardiomyopathy.
Although the exact incidence of shock perioperatively is
unknown, it is estimated that one- third of adult patients in
the intensive care unit are in shock.5 Septic shock accounts
for 62% of cases; cardiogenic shock, 17% of cases; hypovolemic shock, 16% of cases; distributive shock, 4% of cases;
Shock, irrespective of underlying pathology, damages cells
via an impaired balance between delivery of oxygen/ nutrients to the tissues and oxygen metabolism. Global oxygen
delivery (DaO2), the amount of oxygen delivered to the tissue from the lungs, is a product of cardiac output (CO) and
the oxygen content of arterial blood (CaO2):
Cardiac output is determined by ventricular stroke volume (SV) and heart rate (HR) and can be represented by
the equation CO=HR × SV. Stroke volume is the dierence between end diastolic volume (EDV) and end systolic volume (ESV). e EDV is the ventricular volume
before systolic contraction. e ESV is the residual blood
le in the ventricle aer emptying during systole. e EDV
67

68
CaO Hgb1.34SaO (PaO 0.003)
222
=+
Cardiogenic Shock Distributive Shock
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SVR and
venousreturn
Sepsis
Anaphylaxis
Neurogenic
Contractility
Myocardial Infarct
Valvular abormalities
Hypovolemic Shock Obstructive Shock
Circulating Volume
and venous return
Hemorrhage
Dehydration
is determined by preload volume, and ESV is determined
by cardiac contractility and aerload. us, stroke volume is inuenced by preload, aerload, and contractility.
Conditions such as hypovolemia from hemorrhage and
dehydration from diabetic ketoacidosis reduce preload.
Acute myocardial infarction, acute valvular failure, and
dysfunction aer cardiac surgery impair myocardial contractility. Sepsis, spinal cord injury, and anaphylaxis cause
vasodilation and reduce systemic vascular resistance.
Oxygen bound to hemoglobin and oxygen dissolved in
blood determine arterial oxygen content (CaO2):
approximately 25% of the oxygen bound to hemoglobin.
When oxygen delivery is insucient to meet the tissue’s
oxygen demand, the amount of oxygen extracted from
hemoglobin increases (SvO2 decreases), and cellular oxygen
consumption remains independent of delivery. In a state of
maximal oxygen extraction, oxygen consumption will eventually begin to fall linearly with decreasing oxygen delivery. At this critical point of oxygen delivery (DaO
oxygen consumption becomes directly proportional to
oxygen delivery, and cells produce lactate in response to
anaerobic metabolic metabolism. An elevated lactate level
is oen associated with decreased SvO2, but elevated lac-
Venous Return &
Outflow Obstruction
Tamponade
Tension Pneumothora
Pulmonary Embolism
Figure9.2 Underlying cardiovascular
derangements in each type
ofshock.
2critical
),
tate levels with normal SvO2 are possible in septic shock.
Dysfunctional extraction and use of oxygen by tissues dur-
Most of the oxygen in blood is bound to hemoglobin and
ing sepsis mediates production of lacticacid.
9
is the major determinant of arterial oxygen content. e
amount of dissolved oxygen is smaller and contributes minimally to the arterial oxygen content.
CLINICAL PRESENTATION
Disease processes that decrease hemoglobin concentration or the oxygen saturation of hemoglobin can impair
oxygen delivery. Compared to normal hemoglobin, carboxyhemoglobin and methemoglobin have dierent
oxygen- carrying capacities that reduce oxygen delivery and
utilization even if cardiac output is normal.
Under normal conditions, venous blood returning
to the right heart is approximately 75% saturated (mixed
venous oxygen saturation, SvO2) because tissues consume
Physical examination ndings, physiological perturbations,
and biochemical testing identify shock (Figure 9.3). In the
early phase of shock and reduced cardiac output, systemic
vascular resistance may increase to maintain blood pressure.10 Hypotension alone is not a pre- requisite for shock
because in patients with chronic hypertension, blood pressure may decrease moderately. Preserved blood pressure
can be associated with inadequate tissue perfusion and
68 PART III.SHOCK

T
Cold, clammy skin
Physical Examination Findings in Shock
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69
Altered Mental Status,
delirium, agitation
achycardia
Tachypnea,
Dyspnea
Figure9.3 Common physical examinations
ndings observed in patients with
shock. Physical examination ndings in
combination with data from physiological
measures and biochemical test results
can assist the clinician in the diagnosis
ofshock.
hyperlactemia.11 If blood pressure is preserved by excessive
sympathetic tone, anesthetics can unmask hypotension.
Tissue perfusion can be assessed by observing the body’s
response through “three organ windows” (peripheral, renal, and
neurologic). Peripheral vasoconstriction from hypoperfusion
causes cold, clammy, or discolored skin. Adecline in higher cortical function, disorientation, and obtundation suggest diminished
brain perfusion. Reduced cardiac output to renal parenchyma
decreases glomerular ltration rate and urine output. ese
changes can be dicult to assess in patients who already suer
from chronic renal failure or cognitive impairment.
Oliguria
Ileus,
abdominal pain
increase adrenergic output, stimulate adrenal secretion of
epinephrine, and reduce vagal activity.
13,14
Reductions in
le and right atrial pressures and decreased renal perfusion stimulate the renin- angiotensin system. Renin release
increases angiotensin II, a powerful vasoconstrictor, and
stimulates the adrenal cortex to release aldosterone to maintain intravascular volume via renal tubular reabsorption of
sodium (Figure9.4).
e venous system contains 70% of the total blood volume, the arteries 18%, and terminal arteries and arterioles 3%.
Activation of the sympathetic nervous system increases ventricular lling via venoconstriction, which expels blood from
ORGAN RESPONSE AND SIGNS OFSHOCK
Based upon the general discussion above concerning shock
as a disease state of tissue hypoperfusion, we now will present the specic responses to shock for each organ system.
the venous capacitance system into the systemic circulation to
increase ventricular lling.15 Although sympathoadrenal activation increases heart rate, some cases of severe hemorrhage
result in a vagally mediated paradoxical bradycardia.
16
In most forms of shock, adrenergic stimulation also
constricts arteries to maintain mean arterial pressure. In
neurogenic, endocrine, and the early stages of septic shock,
CENTRAL NERVOUS SYSTEM RESPONSES
In most patients without chronic hypertension, the brain
does not compensate for decreased perfusion via cerebral
autoregulation when the mean arterial pressure is less than
60mmHg.12 When cerebral perfusion decreases, a decline
in cortical function can cause agitation, confusion, lethargy,
altered mental status, and delirium.
however, systemic vascular resistance is depressed, aerload
is reduced, and cardiac output is normal or high. Circulating
myocardial depressant factors contribute to myocardial dysfunction in hemorrhagic and late septic shock.
Approximately 40% of patients with septic shock develop
myocardial dysfunction from impaired systolic contractility. Diastolic dysfunction when ventricular relaxation is
impaired in septic shock can worsen with tachycardia.
17
CARDIOVASCULAR RESPONSES
If arterial baroreceptors and central chemoreceptors sense
hypotension, hypovolemia, and hypoxia, these receptors
INTRODUCTION TOSHOCK 69
RESPIRATORY RESPONSES
Hypoxia and hypoperfusion activate central medullary
respiratory centers and peripheral chemoreceptors to

70
Cardiogenic
Hypovolemic
Anaphylactic,
Neurogenic
Direct effects of primary disturbance (uncompensated)Compensatory responses
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shock
Myocardial
failure
↓↓ Cardiac contractility
↓↓ Activity of arterial baroreceptors
↓↓ Parasympathetic activity
Heart
↑↑ Heart rate ↑↑ Contractility ↑↑ Arteriolar tone↑↑ Venous tone
shock
Fluid
loss
↓↓ Mean circulatory filling pressure
↓↓ Central venous pressure
↓↓ Cardiac output
↓↓ Mean arterial pressure
Medullary cardiovascular centers
Septic shock
Vasodilator
↓↓ Venous tone
↓↓ Cardiac filling
release
↓↓ Total peripheral resistance
Below = 60 mm Hg
Cerebral ischemic response
↑↑ Sympathetic activity
shock
↓↓ Sympathetic
nerve activity
↓↓ Arteriolar tone
Systemic organs
Figure9.4 Cardiovascular alterations in shock. SOURCE:Adapted from Mohrman, David E., and Lois Jane Heller. “Chapter11. Cardiovascular Function in Pathological Situations.”
Cardiovascular Physiology, 8e. Eds. David E.Mohrman, and Lois Jane Heller. NewYork, NY:McGraw- Hill, 2014 with permission from McGraw- Hill.
increase minute ventilation and respiratory rate, decrease
tidal volumes, and cause respiratory alkalosis. Dead space
ventilation is increased from ventilation perfusion mismatching when minute ventilation increases and cardiac
output decreases. e additional work of breathing combined with an impaired diaphragmatic muscle from hypoperfusion causes respiratory failure. Shock- induced acute
respiratory distress syndrome is mediated by lung injury
from resuscitation- induced oxidant radicals, inammatory
damage to the alveolocapillary endothelium, and release of
proteinaceous uids into the alveoli.
RENAL RESPONSES
↓ Capillary pressure
Fluid absorption
↑ Cardiac output ↑↑ Total peripheral resistance
↑ Mean arterial pressure
↓↓ Organ blood Flow
in shock are mediated by alterations in macro- and microcirculation, activation of the renal sympathetic nervous
system, inammatory cytokine- mediated cell death, and
apoptosis.
19– 21
Acute tubular necrosis from hypoperfusion
is the most common pathology in shock- induced kidney
injury. When renal blood ow decreases and aerent arterial vasoconstriction increases from sympathetic stimulation, glomerular ltration rate (GFR) slows. Aer aerent
arterial vasoconstriction maximizes, the renal cortex and
eventually the medulla are injured. Clinically, a reduction
18
in GFR decreases urine output.
GASTROINTESTINAL RESPONSES
Acute kidney injury from circulatory shock increases the
risk of mortality. e many causes of acute kidney injury
70 PART III.SHOCK
e splanchnic circulation system receives about 25% of a
person’s cardiac output and contains approximately 20%

Pyruvate NADH HLactate NAD+++↔ ++
[]
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71
of the body’s total blood volume. is circulatory system
is a large reserve that supports the systemic circulation during hypovolemia or cardiac failure.15 When cardiac output
decreases, a simultaneous decrease in ow through the
splanchnic arteries shis blood volume from the splanchnic
veins to the heart. Active constriction of venioles accounts
through immune- mediated mechanisms. In critically ill surgical patients, blood loss and subsequent volume replacement with crystalloids, when severe, can signicantly
decrease the platelet count. Additional risk factors for
thrombocytopenia include fresh frozen plasma and blood
cell transfusion.
26
for approximately 25%– 30% of the total volume transferred back to theheart.
With decreased cardiac output in shock, there is a
disproportionate vasoconstriction of the aerent mesenteric arterioles mediated by the renin- angiotensin axis.
Vasconstriction sustains total systemic vascular resistance,
or aerload, to maintain systemic arterial pressure and
perfusion of nonmesenteric organs at the expense of perfusion of the mesenteric organs. Septic shock can decrease
or increase mesenteric perfusion, but oxygen consumption
increases to exceed the capacity of mesenteric oxygen deliver y.22 Clinically, gut hypoperfusion may be manifested as
ileus, nonocclusive mesenteric ischemia, gastritis, acalculous cholycystitis, or colonic submucosal injury. If gut ischemia damages the gut mucosal barrier, enteric bacteria and
antigens are transferred to the systemic circulation.
23
e liver is also at risk for ischemic injury in shock.
Hepatic injury is associated with mild elevations in transaminases and lactate dehydrogenase. ese values peak in
1– 3 days and then normalize. “Shock liver” and serious
hepatic dysfunction happen with a severe and prolonged
METABOLIC AND NEUROENDOCRINE RESPONSES
Hyperglycemia, glucose intolerance, and insulin resistance
are common in shock. Stress releases adrenocorticotropic
hormone (ACTH), which stimulates cortisol secretion.
Cortisol maintains vascular reactivity to circulating catecholamines through up- regulating adrenergic receptors
and inhibiting the action of proinammatory cytokines.
Cortisol decreases peripheral uptake of glucose, enhances
lipolysis, and increases gluconeogenesis.27 e adrenal
medulla releases epinephrine, which makes skeletal muscle
resist insulin, decreases insulin secretion by the pancreas,
and increases glycogenolysis and gluconeogenesis. ese
alterations increase glucose levels for glucose- dependent
organs such as the brain and heart.28 Metabolic alterations
that decrease clearance of triglycerides or increase triglyceride synthesis via increased hepatic lipogenesis cause
hypertriglyceridemia.29 Nitrogen balance is negative when
protein is catabolized as an energy substrate. If the process
of protein catabolism continues, muscle wasting is severe.
insult (hemorrhage, sepsis, surgery), especially in patients
with underlying hepatic disease. Lactate clearance, protein
synthesis, gluconeogenesis, and glycogenolysis are reduced,
and transaminase levels rise.
24
IMMUNOLOGICAL RESPONSES
Immune dysfunction in shock arises from disruption of
mucosal barriers, especially of the gut, leading to transloca-
HEMATOLOGICAL RESPONSES
Shock causes disseminated intravascular coagulation (DIC)
by activating systemic coagulation and through derange-
tion of bacteria; parenchymal tissue injury from trauma or
surgery; free radical injury; or dysfunction of the cellular
and humoral immune systems through direct ischemic or
mediator- induced mechanisms.
30
ments of the brinolytic pathway. Disseminated intravascular coagulation can be subdivided into two phenotypes:the
brinolytic (hemorrhagic) phenotype and the antibrinol-
LABORATORY STUDIES
ytic (thrombotic) phenotype. e predominant phenotype
depends on the etiology of shock. Sepsis- induced DIC
is the thrombotic phenotype; DIC in the early phase of
trauma is the brinolytic phenotype, which can cause massive bleeding. Disseminated intravascular coagulation during the later phases of trauma has a thrombotic phenotype
and is associated with MODS.
25
e stress response in circulatory shock can cause a reac-
tive thrombocytosis, which can progress to thrombocyto-
Laboratory data dierentiate the underlying etiology of
shock. In early shock, white blood cell count is elevated
due to demargination from the lining of blood vessels with
le shi and bands. Leukopenia results from sepsis and late
shock. Abnormalities are found in hemoglobin levels, plate-
let count, creatinine or liver functiontests.
Lactate levels greater than 2 mEq/ L suggest abnormal
metabolism.
penia in sepsis. Factors contributing to thrombocytopenia
in sepsis include platelet sequestration and destruction
INTRODUCTION TOSHOCK 71

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is represents the pathway in production of lactate.
Lactate serves as marker for global hypoperfusion and
anaerobic metabolism. Lactate levels rise if its production
exceeds its elimination. During anaerobic glycolysis, lactic
acid is formed from pyruvate by lactate dehydrogenase.
During this process, hydrogen ions are released as ADP
converts to ATP and acidosis begins to overwhelm the cell’s
buering capability. It is formed typically in tissues with
high rates of glycolysis, such as gut (responsible for over
50% of lactate production), skeletal muscle, brain, skin, and
erythrocytes. Normally, lactate levels remain low (1 mEq/
L) because of metabolism of lactate principally by the liver
through gluconeogenesis or oxidation via the Krebs cycle.
e kidneys metabolize about 30% of lactate.
Elevated levels are associated with impaired oxygen utilization and oxidative phosphorylation or inadequate tissue
oxygenation. Type Alactic acidosis results from insucient
oxygen delivery that decreases mitochondrial metabolism.
Pyruvate is converted to lactate. Type B lactic acidosis is
not related to oxygen delivery or poor lactate metabolism.
In Type B lactic acidosis, renal or hepatic disease reduces
clearance, or clearance is aected by drugs or inborn errors
of metabolism. Compared to a normal ratio of lactate to
pyruvate, a higher ratio supports a hypoxic mechanism of
lactate production associated with increased risk of mortality in septic shock.31 e amount of lactate produced may
correlate with total oxygen debt, the magnitude of hypoperfusion, and the severity ofshock.
factors can inuence CVP value, and a normal value at
times can be misleading. For example, loss of 10%– 20%
of total blood volume may not decrease CVP, because the
body mobilizes uids from the splanchnic circulation into
the systemic circulation. Anormal CVP, in contrast, can
also reect a compensated hypervolemia when an excessive
infusion of uid is compensated for by an accumulation of
blood in the splanchnic veins.15 us, CVP values should be
interpreted with caution.
Intracardiac pressures, mixed venous oxygen saturation
(SvO2), and cardiac output can be measured with a pulmonary artery catheter (PAC). Although a PAC maybe useful
in situations such as cardiogenic shock (especially right ventricular failure), its usefulness in management of most other
shock states remains controversial. Data obtained from a
PAC should be correlated with other available clinical data.
For example, a high mixed venous oxygen saturation and
high concentrations of lactate in blood are associated with
poor survival rates.
34
Echocardiography assesses le ventricular and right
ventricular function, pericardial eusions, tamponade, and
ventricular lling. Repeated bedside examination can help
detect changes in cardiac function over time. Stroke volume is assessed through calculation of velocity time integral (VTI) of the subaortic blood ow. Changes in stroke
volume aer a uid challenge can be identied by detecting
changes in VTI both through transesophageal and transthoracic echocardiography (Figure 9.5).
35
Prognosis and adequacy of therapies is assessed by serial
lactate determinations. Elevated lactate levels in shock and
mortality have shown positive correlation. Lactate clear-
TREATMENTGOALS
ance indicates resolution of hypoperfusion and is used to
direct therapy and reduce mortality.
32
Regardless of the underlying cause of shock, the goal of
treatment is to restore circulatory perfusion and oxygen
MONITORING
delivery before organ dysfunction worsens. e treatment
of shock is initiated while investigating the underlying
cause. One treatment strategy, the VIP approach, highHemodynamic monitoring to recognize shock and guide
rapid therapy can be helpful in shock management. Patients
in shock should have an indwelling arterial line to measure
blood pressure and blood lactate levels. Fluid responsiveness is assessed from pulse pressure variation (PPV), systolic
pressure variation (SPV), or from inferior vena cava diameter and respiratory variability via echocardiography. ese
modalities require the patient to receive tidal volumes of at
least 8 mL/ kg and have normal sinus rhythm.
33
A central venous line may be necessary to administer
inotropes or vasopressors or volume for resuscitation. ere
is poor correlation between central venous pressure (CVP)
and preload for predicting volume responsiveness. Multiple
lights three areas for resuscitation: Ventilation (adequate
oxygenation), Infusion (blood, uid resuscitation), and
Pump/ pharmacological (restoration of cardiac competence
and administration of vasoactive medications).
36
Many patients in shock will require tracheal intubation
and mechanical ventilation. Apart from delivering oxygen
to the lungs, mechanical ventilation can also reduce oxygen
consumption by the respiratory muscles and decrease cardiac aerload in a failing heart. Decreased venous return,
however, may cause hypotension.
e goal of uid resuscitation is to improve stroke
volume and ventricular contractility indices. Although
no predened goals exist to guide the optimal amount of
72 PART III.SHOCK

Panel B
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73
pressure (MAP) and cardiac output (CO) to restore tissue
perfusion. In general, vasopressors should be titrated to
achieve a MAP of 65 to 70mmHg, but this goal is adjusted
based on the patient’s physiology and the clinician’s assessment of organ perfusion.38 Aer restoring mean circulating lling pressures and vascular tone, improving CO with
inotropes may improve systemic oxygen delivery and tissue
perfusion.
Panel A
CONCLUSION
Rapid identication and institution of therapy is paramount in reducing morbidity and the risk of mortality
from shock. Treatment includes hemodynamic stabilization, correction of the underlying cause, and reversal of a
hypoperfusedstate.
CASE- BASED LEARNING DISCUSSION
1. What is the dierential diagnosis for the patient’s
hypotension? How would you determine if she were in
shock? What are the organ- specic responses toshock?
Figure9.5 Left ventricular outow tract (LVOT) velocity time integral (VTI)
variation with respiration measured through bedside transthoracic
echocardiography. After obtaining an apical ve- chamber view, a pulse
wave Doppler sample volume is placed in the middle of the LVOT
adjacent to the aortic valve. Once the waveform is obtained over 3 or
4 respiratory cycles, a frozen image is obtained. The largest (usually at
end inspiration, if mechanically ventilated) and the smallest waveforms
over a single respiratory cycle are identied and traced. Using the aortic
continuity equation, and the calculation software of most ultrasound
machines, the VTI variation is calculated as the difference between the
maximum and the minimum VTI divided by the mean of the two values.
AVTI variation of more than 12% predicts uid responsiveness (dened
as an increase in cardiac output by at least 15% in response to a
standard uid bolus) with a sensitivity of 100% and a specicity of 89%.
Images courtesy of ICU Sonography http:// www.criticalecho.com.
2. Aer induction, a pulmonary artery catheter is placed.
Could you use a central venous or pulmonary diastolic
pressure to guide resuscitation? How can you measure
cardiac output in this patient? Can measuring velocity
time integral at the patient’s le ventricular outow
track be helpful?
3. What laboratory tests would you order in this patient
to guide her resuscitation? Assume her SvO2 is 90%.
What conditions could explain her elevated SvO2?
What conditions would cause the SvO2 to be low? Her
lactate is 6mmol/ L. What would you expect the lactate
level to be in sepsis?Why?
volume resuscitation in shock, in practice a uid challenge
assesses the patient’s actual response to uids. During a uid
challenge, 300– 500 mL of crystalloid solution is infused
over 20– 30 minutes.37 An increase in stroke volume or a
decrease in heart rate suggests uid responsiveness. e cli-
4. e patient’s pulse pressure variation is 18%, blood
pressure 104/ 42mmHg. Would you administer more
uids? Why? What would be the endpoint of uid
resuscitation?
nician halts further volume infusion in a patient who is a
nonresponder to prevent volume overload. e response to
uid therapy is assessed in the absence of any other change
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When shock is not reversed with uid therapy, vaso-
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10.
CARDIOGENICSHOCK
Martin Chen and MuoiTrinh
CLINICALCASE
experience major perioperative morbidities as non- heart-
failure patients.3 Even though the perioperative prevalence
A 56- year- old man with nonischemic dilated cardiomyopathy and a le ventricular ejection fraction of 10%– 15%
presents for urgent exploratory laparotomy due to a bowel
perforation, which occurred during screening colonoscopy
as part of a heart transplant evaluation. He has baseline
of HF is increasing, there is a paucity of published guide-
lines with regard to its management, as most pertain to the
management of patients with coronary artery disease, and
practitioners are oen le to make inferences with regard
to the care of this population.
4
symptoms of dyspnea on minimal exertion and he is maintained on carvedilol, lisinopril, simvastatin, spironolactone,
and furosemide. He had nothing by mouth for 8 hours prior
to the colonoscopy, and took all of his medications with a
sip of water this morning before the procedure. He has a
biventricular pacemaker with an implantable cardioverter
debrillator (BiV/ ICD). Plan is for preinduction arterial
line, general anesthesia with endotracheal intubation, and
PATHOPHYSIOLOGY OFDISEASESTATE
In order to understand the dierences in le and right heart
failure, and thus the appropriate treatment that should be
undertaken, an overview of the pathophysiology of each is
presentedbelow.
a central line aer induction.
INTRODUCTION
LEFT HEART FAILURE
Le heart failure, from either systolic or diastolic dysfunc-
tion (although the two oen coexist), decreases cardiac
Heart failure (HF) is a syndrome of inadequate systemic
perfusion caused by decreased myocardial pump function.
is can be due to right or le heart dysfunction, and can
be further subdivided into systolic or diastolic dysfunction,
although these entities oen coexist. e American Heart
Association estimates that there are nearly 6million adults
in the United States with HF, and that there are approximately 800,000 new cases diagnosed annually, predicting
that the prevalence of this disease will increase to greater
than 8million adults by 2030.1 As HF becomes more prevalent and the number of advanced therapies oered to this
patient population increases, it is clear that there will be an
increase in the number of planned and emergent surgical
procedures performed in patients with HF.2 ese patients
are at signicantly increased risk of major perioperative
complications and oen require specialized perioperative
care. One recent retrospective study found that patients
with worsening perioperative heart failure were almost
twice as likely to die and were 40%– 69% more likely to
output. In le ventricular systolic dysfunction, myocyte
injury— from ischemia, myocarditis, pressure or volume
overload, and/ or cardiomyopathy— decreases contractility.
e body attempts to maintain tissue perfusion through
activation of the sympathetic nervous system, the renin
angiotensin aldosterone system (RAAS), and later the
arginine vasopressin axis to retain water and increase vas-
oconstriction. e increase in preload and aerload ini-
tially preserves perfusion in the setting of reduced cardiac
output, but eventually causes volume overload and high
systemic vascular resistance, worsening the HF syndrome.
Additionally, chronic neurohumoral activation leads to
myocyte death, pathological myocardial remodeling, and
decreased myocardial performance.
4,5
Approximately 40% of patients with symptomatic
heart failure have a preserved left ventricular ejection
fraction (HFPEF) and diastolic heart failure.6 Diastole—
cardiac relaxation— is an active, energy- dependent process. Impaired relaxation can prevent accommodation to
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