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DaO CO CaO
22
=
aggregation
Coronary
microcirculatory damage
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9.
INTRODUCTION TOSHOCK
Babar Fiza and VivekMoitra
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
36mmHg 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 inammatory mediators released impair
Figure9.1 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., etal. “Shock.” Schwartz’s Principles of Surgery, 10e. Eds. F.Char les
Brunicardi, etal. NewYork, 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 evendeath.
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 dier­ence 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 aer emptying during systole. e EDV
67
68
CaO Hgb1.34SaO (PaO 0.003)
222
=+
Cardiogenic Shock Distributive Shock
x
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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 aerload. us, stroke vol­ume is inuenced by preload, aerload, and contractility. Conditions such as hypovolemia from hemorrhage and dehydration from diabetic ketoacidosis reduce preload. Acute myocardial infarction, acute valvular failure, and dysfunction aer 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 insucient 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 oen associated with decreased SvO2, but elevated lac-
Venous Return & Outflow Obstruction
Tamponade Tension Pneumothora Pulmonary Embolism
Figure9.2 Underlying cardiovascular
derangements in each type ofshock.
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 lacticacid.
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 dierent 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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Altered Mental Status, delirium, agitation
achycardia
Tachypnea, Dyspnea
Figure9.3 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 ofshock.
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. Adecline 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 dicult to assess in patients who already suer 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 (Figure9.4).
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 OFSHOCK
Based upon the general discussion above concerning shock as a disease state of tissue hypoperfusion, we now will pres­ent the specic 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 60mmHg.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, aerload 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 TOSHOCK 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
Figure9.4 Cardiovascular alterations in shock. SOURCE:Adapted from Mohrman, David E., and Lois Jane Heller. “Chapter11. Cardiovascular Function in Pathological Situations.”
Cardiovascular Physiology, 8e. Eds. David E.Mohrman, and Lois Jane Heller. NewYork, 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, inammatory 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, inammatory 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 aerent arte­rial vasoconstriction increases from sympathetic stimula­tion, glomerular ltration rate (GFR) slows. Aer aerent 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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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 shis 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 signicantly 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 theheart.
With decreased cardiac output in shock, there is a disproportionate vasoconstriction of the aerent mesen­teric arterioles mediated by the renin- angiotensin axis. Vasconstriction sustains total systemic vascular resistance, or aerload, 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 proinammatory 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 antibrinol-
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 dierentiate 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 functiontests.
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 TOSHOCK 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 buering 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 Alactic acidosis results from insucient 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 aected 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 ofshock.
factors can inuence 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. Anormal CVP, in contrast, can also reect 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 eusions, 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 aer a uid challenge can be identied 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-
TREATMENTGOALS
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 aerload 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 predened goals exist to guide the optimal amount of
72 PART III.SHOCK
Panel B
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pressure (MAP) and cardiac output (CO) to restore tissue perfusion. In general, vasopressors should be titrated to achieve a MAP of 65 to 70mmHg, but this goal is adjusted based on the patient’s physiology and the clinician’s assess­ment of organ perfusion.38 Aer restoring mean circulat­ing lling pressures and vascular tone, improving CO with inotropes may improve systemic oxygen delivery and tissue perfusion.
Panel A
CONCLUSION
Rapid identication 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 hypoperfusedstate.
CASE- BASED LEARNING DISCUSSION
1. What is the dierential diagnosis for the patient’s hypotension? How would you determine if she were in shock? What are the organ- specic responses toshock?
Figure9.5 Left ventricular outow 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 identied 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. AVTI variation of more than 12% predicts uid responsiveness (dened as an increase in cardiac output by at least 15% in response to a standard uid bolus) with a sensitivity of 100% and a specicity of 89%. Images courtesy of ICU Sonography http:// www.criticalecho.com.
2. Aer 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 outow 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 6mmol/ 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/ 42mmHg. 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
REFERENCES
in therapy. In cases of hemorrhagic shock with rapid blood loss, rapid volume replacement may be needed to restore circulating volumes.
When shock is not reversed with uid therapy, vaso-
active agents may be necessary to increase mean arterial
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23. Rowlands BJ, Soong CV, Gardiner KR. e gastrointestinal tract as barrier in sepsis. Brit Med Bull. 1999;55:196– 211.
24. Strassbrug CP. Gastrointestinal disorders of the critically ill: shock liver. Baillieres Best Pract Res Clin Gastroenterol. 2003;17(3):369– 381.
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26. Shalansky SJ, Verma AK, Levine M, Spinelli JJ, Dodek PM. Risk markers for thrombocytopenia in critically ill patients:a prospective analysis. Pharmacotherapy. 2002; 22(7):803– 13.
27. Desborough JP. Stress response to trauma and surgery. Br J Anaesth. 2000;85:109– 17.
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29. Cetinkaya A, Erden A, Avci D, etal. Is hypertriglyceridemia a prog­nostic factor in sepsis? er Clin Risk Manag. 2014;10:147– 150.
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74 PART III.SHOCK
https://t.me/medicina_free
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10.
CARDIOGENICSHOCK
Martin Chen and MuoiTrinh
CLINICALCASE
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 oen 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 debrillator (BiV/ ICD). Plan is for preinduction arterial line, general anesthesia with endotracheal intubation, and
PATHOPHYSIOLOGY OFDISEASESTATE
In order to understand the dierences in le and right heart
failure, and thus the appropriate treatment that should be
undertaken, an overview of the pathophysiology of each is
presentedbelow. a central line aer induction.
INTRODUCTION
LEFT HEART FAILURE
Le heart failure, from either systolic or diastolic dysfunc-
tion (although the two oen 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 oen coexist. e American Heart Association estimates that there are nearly 6million 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 8million adults by 2030.1 As HF becomes more prev­alent and the number of advanced therapies oered 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 signicantly increased risk of major perioperative complications and oen 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 aerload 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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