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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Foreword
- •Contents of Volume I
- •Contents of Volume II
- •Contributors
- •1.1 Introduction
- •1.4.3 Acute Stroke
- •1.4.4 CNS Infection
- •1.4.1 Sepsis
- •1.4.2 Acute Encephalopathy
- •1.4.5 Severe Community-Acquired Pneumonia
- •1.4.6 Nosocomial Pneumonia
- •1.4.7 Pulmonary Edema
- •1.4.8 Fever
- •References
- •2.1 Introduction
- •2.4 ECG Nomenclature
- •2.4.1 P Wave
- •2.4.2 PR Interval
- •2.4.3 QRS Complex
- •2.4.4 J Point
- •2.4.5 ST Segment
- •2.4.6 T Wave
- •2.4.7 QT Interval
- •2.4.8 U Wave
- •2.4.9 RR Interval
- •2.5.1 P Wave
- •2.5.1.1 Atrial Arrhythmias
- •Atrial Fibrillation
- •Atrial Flutter
- •Atrial Tachycardia
- •Multifocal Atrial Tachycardia
- •2.5.1.2 Interatrial Blocks
- •Intermittent Interatrial Block (I-IAB)
- •Advanced Interatrial Block (A-IAB)
- •2.5.2 P-QRS Ratio
- •2.5.2.1 Shortened P-QRS Ratio
- •Wolff-Parkinson-White Syndrome (WPW)
- •Junctional Rhythm
- •Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
- •2.5.2.3 Prolonged P-QRS Ratio
- •2.5.3 PR Interval
- •2.5.3.1 Shortened PR Interval
- •2.5.3.2 Prolonged PR Interval
- •2.5.3.3 Second-Degree AV Block
- •Advanced AV Block
- •Third-Degree AV Block (Complete Heart Block)
- •2.5.4 PR Segment
- •2.5.4.1 PR-Segment Elevation
- •2.5.4.2 PR-Segment Depression
- •Acute Pericarditis
- •Acute Myocardial Ischemia
- •2.5.5 Q Waves
- •2.5.6 QRS Complex
- •2.5.6.1 Heart Rate
- •2.5.7 QT Interval
- •2.5.8 ST Segment
- •2.5.8.1 ST-Segment Depression
- •2.5.8.2 ST-Segment Elevation
- •2.5.9 T Waves
- •2.5.9.1 Inverted T Wave
- •2.5.9.2 Flattened T Wave
- •2.5.9.3 Peaked T Wave
- •References
- •Further Reading
- •3.1 Introduction
- •3.2.2 Nasogastric Tube
- •3.2.3 Central Venous Catheters
- •3.2.4 Cardiac Devices
- •3.2.5 Arterial Catheters
- •3.3 Cardiopulmonary Abnormalities
- •3.3.1 Pulmonary Edema
- •3.3.2 Acute Respiratory Distress Syndrome
- •3.3.3 Atelectasis
- •3.3.4 Aspiration
- •3.3.5 Pneumonia
- •References
- •4.1 Introduction
- •4.5 Modes of Mechanical Ventilation
- •4.5.1 Volume Control Ventilation
- •4.5.2 Pressure Control Ventilation
- •4.5.3 Pressure Support Ventilation
- •4.6 Patient-Ventilator Interactions
- •4.6.1 Trigger Dyssynchrony
- •4.6.2 Flow Dyssynchrony
- •4.6.3 Cycle Dyssynchrony
- •4.9.1 Acute Respiratory Distress Syndrome
- •4.9.2 Severe Asthma Exacerbation
- •4.11 Summary
- •5.10 Neuromuscular Blockade
- •References
- •5.1 Introduction
- •5.3 Pathobiology
- •5.4 ARDS Phenotypes
- •5.5 Lung-Protective Ventilation
- •5.6 Positive End-Expiratory Pressure
- •5.7 Conservative Fluid Management
- •5.8 Moderate-to-Severe ARDS
- •5.9 Prone Positioning
- •5.11 Corticosteroids
- •5.12 Inhaled Pulmonary Vasodilators
- •5.13 Veno-Venous Extracorporeal Membrane Oxygenation
- •5.14 Survivorship
- •References
- •6.1 Introduction/Epidemiology
- •6.2 Physiology
- •6.2.2 Physiology During COPD Exacerbation
- •6.4 Pharmacologic Treatment
- •6.4.1 Bronchodilators
- •6.4.1.1 Mechanism
- •6.4.2 Glucocorticoid Therapy
- •6.4.2.1 Mechanism
- •6.4.2.4 Duration
- •6.4.3 Antimicrobials
- •6.4.3.1 Antibiotic Patient Selection
- •6.4.4.1 Nonpharmacologic Interventions
- •6.4.4.2 Opioids
- •6.4.4.3 Benzodiazepines
- •6.4.4.4 Dexmedetomidine
- •6.4.4.5 Ketamine
- •6.4.5 Adjunctive Therapies
- •6.4.5.1 Magnesium
- •6.4.5.3 Vitamin D
- •6.4.5.4 Venous Thromboembolism Prophylaxis
- •6.4.5.5 Smoking Cessation
- •6.4.5.6 Bowel Regimen
- •6.4.5.7 Mucolytics
- •6.4.5.8 Nutrition
- •6.4.5.9 Post-Discharge Adjuncts
- •6.5 ICU-Level Interventions
- •6.5.1 Noninvasive Positive-Pressure Ventilation
- •6.5.2 High-Flow Nasal Canula
- •6.5.3 Invasive Mechanical Ventilation
- •6.6 Conclusion
- •References
- •7.1 Introduction
- •7.1.1 What Is Asthma?
- •7.2 Diagnosis
- •7.2.1 Physical Examination
- •7.2.2 Laboratory Data
- •7.2.3 Radiographic Findings
- •7.3.1 Standard-of-Care Therapy
- •7.3.3 Potential Adjunctive Therapies
- •7.3.3.1 Inhaled Corticosteroids (ICSs)
- •7.3.3.4 Intravenous (IV) Aminophylline
- •7.3.3.5 Intravenous (IV) Beta2-Agonists
- •7.3.3.6 Leukotriene Antagonists (LTRAs)
- •7.3.3.7 Intramuscular (IM) or IV Epinephrine
- •7.3.3.8 Inhaled Anesthetics
- •7.3.3.9 Inhaled Helium-Oxygen (Heliox)
- •7.3.3.10 Intravenous Ketamine
- •7.3.4.1 Subcutaneous (SC) Biologics
- •7.4.1 Noninvasive Ventilation (NIV)
- •7.4.2 Invasive Mechanical Ventilation (IMV)
- •7.6.1 Outpatient Follow-Up
- •7.7 Summary
- •References
- •8.1 Introduction
- •8.1.3.2 Anatomic Location
- •8.1.3.3 Chronicity
- •8.1.4 Clinical Presentation
- •8.1.4.1 Symptoms
- •8.1.4.2 Physician Examination
- •8.1.4.3 Cardiopulmonary Compromise
- •8.2.1.1 Clinical Pretest/Scores
- •8.2.1.2 D-Dimer-Level Interpretations
- •8.2.2 Computed Tomography Pulmonary Angiography (CTPA)
- •8.2.3 Mortality Risk Assessment
- •8.2.3.1 PE Severity Index Score
- •8.2.3.2 Prognostic Indicators
- •8.3.2 High-Risk PE
- •8.4 Systemic Thrombolytic Therapy
- •8.4.1.1 High-Risk PE
- •8.4.1.2 Intermediate-Risk PE
- •8.4.1.3 Cardiac Arrest
- •8.5.2 Percutaneous Mechanical Interventions
- •8.5.2.2 Catheter-Directed Thrombolysis
- •8.5.3 Surgical Embolectomy
- •8.5.4 Mechanical Circulatory Support
- •8.6.1 PE Response Team (PERT)
- •8.6.3.1 Renal Dysfunction
- •8.6.3.4 Cancer
- •8.6.3.5 Treatment Failure
- •8.7 Conclusion
- •References
- •9.1.2 ECMO Outcomes
- •9.2 ECMO During Cardiopulmonary Resuscitation (eCPR)
- •9.2.1 Extracorporeal Carbon Dioxide Removal
- •9.3 ECMO Management
- •9.3.3 Fluid Management
- •9.4.1 Coagulation Changes
- •9.4.2 Transfusion Thresholds
- •9.4.3.1 Heparin
- •9.4.3.2 Direct Thrombin Inhibitors
- •9.4.4 Monitoring Anticoagulation
- •9.6.2.1 Opioids
- •9.6.2.2 Ketamine
- •9.6.2.3 Propofol
- •9.6.2.4 Benzodiazepines
- •9.6.2.5 Dexmedetomidine
- •9.7.1 Aminoglycosides
- •9.7.2 Beta-Lactams
- •9.7.4 Antifungals
- •9.9 Other Complications
- •9.9.1 Bleeding
- •9.9.2 Thrombosis
- •9.9.3 Neurologic
- •9.10 Conclusion
- •References
- •10.1 Type 1–5 Myocardial Infarctions
- •10.2 Acute Coronary Syndrome (Type 1 MI)
- •10.3 Clinical Presentation/Evaluation
- •10.4 Non-pharmacologic Therapy
- •10.5 Pharmacologic Therapy
- •10.5.1 Fibrinolytics
- •10.5.2 Anticoagulants
- •10.5.2.1 Heparins
- •10.5.2.2 Direct Thrombin Inhibitors
- •10.5.3 Antiplatelets
- •10.5.3.1 Aspirin
- •10.5.3.2 P2Y12 Inhibitors
- •Clopidogrel
- •Prasugrel
- •Ticagrelor
- •10.5.3.3 Glycoprotein IIb/IIIa Receptor Inhibitors
- •10.5.3.4 Cangrelor
- •10.7 Long-Term Management
- •10.7.1 High Bleed Risk (HBR)
- •10.7.2 Statins
- •10.7.3 Beta-Blockers
- •10.7.5 Mineralocorticoid Receptor Antagonists
- •References
- •11.1 Introduction
- •11.2.2 What is Ejection Fraction?
- •11.4 Understanding Blood Pressure
- •11.5 Preload vs. Afterload
- •11.6 Acute Decompensated Heart Failure
- •11.6.2 Etiology
- •11.8 Treating Volume Overload
- •11.8.1 Loop Diuretics
- •11.9 Intravenous Vasodilators
- •11.10 Cardiogenic Shock
- •11.10.1 Inotrope Clinical Pearl
- •11.12 Digoxin
- •11.12.3 Loading Dose
- •11.12.4 Maintenance Dosing
- •11.12.5 Monitoring
- •11.12.7 Distribution
- •11.12.8 Drug-Drug Interactions
- •11.12.9 Digoxin Toxicity
- •11.13 ADHF Clinical Pearls
- •11.13.3 Avoid Phenylephrine
- •11.13.4 Use Mean Arterial Pressure (MAP)
- •11.14 Guideline-Directed Medical Therapy
- •11.15 Venous Thromboembolism (VTE) Prophylaxis
- •11.16 Conclusion
- •References
- •12.1 Introduction
- •12.3 Diagnostic Findings
- •12.4.1 Oxygen Therapy
- •12.4.2 Pharmacological Management
- •12.4.3 Mechanical Circulatory Support (MCS)
- •12.5 Pulmonary Hypertension
- •12.6 The Pharmacist’s Role
- •12.7 Conclusion
- •References
- •13.1 Introduction
- •13.2 Atrial Arrhythmias
- •13.2.2 Atrioventricular Blocks
- •13.2.3 Atrial Fibrillation
- •13.2.3.2 Anticoagulation
- •13.2.3.3 Rate vs. Rhythm Control
- •13.2.4 Atrial Flutter
- •13.2.5 Supraventricular Tachycardia (SVT)
- •13.3 Ventricular Arrhythmias
- •13.3.1 Premature Ventricular Complexes
- •13.3.2 Ventricular Tachycardia
- •13.3.2.1 Torsades de Pointes
- •13.3.3 Ventricular Fibrillation
- •13.3.4 Ventricular Arrhythmia Treatment Strategies
- •13.3.4.1 ICD Implantation
- •13.3.4.2 Pharmacologic Treatments
- •13.3.4.3 Catheter Ablation
- •13.4 Conclusion
- •References
- •14.1 Introduction
- •14.3.2 Laboratory Assessment
- •14.3.3 Imaging
- •14.3.4 Invasive Hemodynamic Monitoring
- •14.4.1 Distributive
- •14.4.2 Cardiogenic
- •14.4.3 Hypovolemic
- •14.4.4 Obstructive
- •14.5 Management
- •14.6 Conclusion
- •References
- •15.1 Background
- •15.2 Diagnosis
- •15.3 Management
- •References
- •16.1 Introduction
- •16.3 Hemodynamics
- •16.5 Pharmacological Management
- •16.5.1 Hyperosmolar Therapy
- •16.5.3 Barbiturate Coma
- •16.6 Nonpharmacological Treatments
- •16.6.2 Temperature Management
- •16.6.3 Prophylactic Hypothermia
- •16.7 Adjunct Therapies
- •16.7.2 Venous Thromboembolism (VTE) Prophylaxis
- •16.7.3 Antibiotic Prophylaxis
- •16.7.4 Stress Ulcer Prophylaxis (SUP)
- •16.7.5 Tranexamic Acid
- •16.7.6 Glucose Targets
- •16.7.7 Steroids
- •16.8 Complications
- •16.8.1 Paroxysmal Sympathetic Hyperactivity
- •16.8.3 Central Fever
- •16.8.4.1 Diabetes Insipidus
- •16.8.4.3 Cerebral Salt Wasting Syndrome
- •16.9 Conclusion
- •References
- •17.1 Introductory Case
- •17.2 Introduction
- •17.4 Pathophysiology
- •17.5 Acute Therapies
- •17.5.1 Thrombolytic Therapy
- •17.5.2 Thrombectomy
- •17.5.3 Blood Pressure Management
- •17.5.4 Acute Anticoagulation
- •17.5.5 Antiplatelet Therapy
- •17.6 Early Complications
- •17.6.1 Hemorrhagic Conversion
- •17.6.2 Angioedema
- •17.6.3 Malignant Cerebral Edema
- •17.7 Secondary Prevention
- •References
- •18.1 Introduction
- •18.4 Therapeutic Drug Monitoring
- •18.5 Adverse Drug Effects
- •18.7 Anti-seizure Medications
- •18.7.1 Available Parenteral Preparations
- •18.7.1.1 Benzodiazepines: GABAA Receptor Activation
- •18.7.1.2 Other GABAergic Therapies
- •Barbiturates: GABAergic
- •Phenobarbital
- •Pentobarbital Infusion
- •Propofol Infusion: GABAergic
- •18.7.1.3 Second-Line Non-anesthetic ASMs
- •Levetiracetam: Synaptic Vesicle Protein 2A Binding

354
G. J. Hu and C. O’Kane
cardiac ablation if they continue to have recurrent sustained monomorphic VT that
is refractory to antiarrhythmic therapy, as epicardial ablations were found to be
independent predictors for complete short-term success [44, 68]. However, longterm outcomes such as VT-free survival and recurrence were not as prevalent as
compared to patients with ischemic cardiomyopathy. Although rare, complications
associated with catheter ablation procedures include heart block, thrombosis, newonset arrhythmias, and even death.
13.4 Conclusion
Early and/or urgent recognition and diagnosis of cardiac arrhythmias are crucial as
these may have serious and fatal implications if not treated promptly. Depending on
the type of arrhythmia that patients present with, treatments provided will vary.
However, the overarching goal remains the same: correct the abnormal rhythm and
address any reversible causes. Medication selection is often based on patientspecic factors and may sometimes require hospital admission for therapy initiation. A thorough evaluation of patients’ previous interventions can guide appropriate
initiation of therapies if they present with persistent or refractory arrhythmias. There
is an opportunity for pharmacists to have a signicant impact on arrhythmia management for patients. Pharmacists can aid in obtaining prior medication histories,
appropriately recommending and dosing medications, and assessing for drug interactions with other concurrent medication use. Especially in emergent situations,
pharmacists can advocate for appropriate dosing and timing of medications as well
as correct preparations of the medication product. These actions are of tremendous
benet to the medical team and ultimately promote patient safety and efcacy.
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G. J. Hu and C. O’Kane

Chapter 14
Shock
LucasR.Goss, AnnetteEsper, andSeemaS.Tekwani
14.1 Introduction
Shock is a life-threatening condition that requires prompt recognition and treatment, as it is often the nal common pathway for which illnesses lead to death.
Shock is a state in which the supply of oxygen is inadequate to meet the demand for
oxygen by the body’s tissues. This results in cellular hypoxia, which subsequently
results in cell membrane dysfunction, intracellular edema, leakage of intracellular
contents into the extracellular space, and inadequate regulation of intracellular
pH.If left untreated, this will result in cell death, organ dysfunction, lactic acidosis,
inammatory cascades, and potentially death. Although shock may be reversible,
the longer the shock is present, the more the tissue hypoxia and organ dysfunction
occur. This may potentially result in irreversible organ dysfunction and ultimately
death [1–4]. This is why identication of shock as well as diagnosing and treating
the underlying cause is crucial.
14.2 Pathophysiology ofShock
Shock is a state of global tissue hypoperfusion, leading to an imbalance between
oxygen supply to the tissue and its demand. Oxygen delivery depends on the arterial
oxygen content of the blood and the cardiac output (Table14.1). The arterial oxygen
content is the sum of the oxygen bound to hemoglobin (product of hemoglobin
concentration (Hb) and the percentage of hemoglobin saturated with oxygen (sO2)
L. R. Goss · A. Esper · S. S. Tekwani (*)
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Emory University School
of Medicine, Atlanta, GA, USA
e-mail: seema.tekwani@emory.edu
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_14
359© The Author(s), under exclusive license to Springer Nature

360
Table 14.1 Relevant equations in shock physiology
Delivery of oxygen DO2=CO×{(1.39×Hb×sO2)+(PaO2×0.003)}
Fick CO=VO
Cardiac output CO=HR×SV
MAP CO×SVR
DO
delivery of oxygen, CO cardiac output , Hb hemoglobin, sO2 arterial oxygen saturation, PaO2
2
arterial partial pressure of oxygen; VO
tion, CVO
cular resistance, MAP mean arterial pressure
central venous oxygen saturation; HR heart rate, SV stroke volume, SVR systemic vas-
2
/1.34(Hb) (10) (CA O2%−CV O2%)
2
oxygen consumption, CAO2 central arterial oxygen satura-
2
L. R. Goss et al.
and the amount of dissolved oxygen in the blood (PaO2). Cardiac output is determined by the product of stroke volume (SV) and heart rate (HR). Stroke volume is
the amount pumped by the heart with each contraction, which further depends on
preload/end-diastolic volume, contractility of the heart, and afterload.
The abnormalities in each of these determinants of oxygen delivery can lead to
several types of shock (Flowchart 14.1).
Irrespective of the etiology of shock, when the delivery of oxygen (DO2)
decreases, more oxygen is extracted from the hemoglobin to a point of critical DO2,
beyond which the tissue starts producing energy by anaerobic metabolism. In sepsis, the cells may be unable to utilize oxygen despite normal to supranormal oxygen
delivery, thus leading to dysoxia and an anaerobic pathway for adenosine triphosphate (ATP) production.
When oxygen extraction is increased, this is seen as a drop in the oxygen saturation of the venous blood. This is often measured in the blood collected from the
superior vena cava via a central venous line and reported as central venous oxygen
saturation (ScVO2). Normal ScVO2 is 70–75%, and values <70% are indicative of
impaired oxygen delivery and increased extraction. In cases of dysoxia with
impaired tissue oxygen utilization, ScVO2 may be >80% and may indicate cell
death [5].
When anaerobic metabolism ensues, lactate is produced, leading to lactic acidosis. However, high lactate is nonspecic, and high lactate may also be seen in cases
of ischemia due to vascular causes like gut ischemia and gangrenous limb and in
cases of liver and kidney failure and many other causes like seizures, drug overdose,
cyanide poisoning, and thiamine deciency [6].

14 Sho ck
361
Heart Rate
output
Cardiac
Stroke
Volume
Determinants of oxygen delivery
blood
oxygen in
Dissolved
Afterload
Contractility
Decreased
Brady
/Tachy
arrhythmias
afterload
Decreased
Decreased
contractility
filling of
the heart
shock
Cardiogenic
shock
Neurogenic
shock
Distributive
Sepsis
Anaphylaxis
shock
Cardiogenic
shock
Obstructive
Arterial
Oxygen
content
O2
Arterial
Saturation
Hemoglobin
Preload
preload
Decreased
shock
Hemorrhagic
body fluid
Hypovolemic
shock / Loss of
Flowchart 14.1 Determinants of oxygen delivery and its abnormalities leading to several types of shock

362
L. R. Goss et al.
14.3 Diagnosis andEvaluation
Shock is a clinical diagnosis, made by incorporating history, physical examination,
and laboratory ndings. It is important to note that although these tools are used to
diagnose shock, shock is not dened by any single vital sign, physical examination
nding, or laboratory value. This understanding is crucial, as if misunderstood, it
may result in either more or less aggressive treatment than necessary. As an example, consider a patient who presents with symptoms of acute decompensated heart
failure, blood pressure of 90/70, heart rate of 112, elevated lactic acid, and cool
extremities. Although the mean arterial pressure (MAP) is above 65, it would be a
mistake to not diagnose this patient with cardiogenic shock, as it may result in
delayed, less aggressive, or inappropriate care. So, although shock is not dened by
any single vital sign, physical examination nding, or laboratory value, there are
common ndings seen in patients with shock.
14.3.1 Vital Signs andPhysical Exam
Vital sign abnormalities are common in patients with shock. Most patients have hypotension, tachycardia, and tachypnea. Blood pressure, however, may be normal or rarely
elevated, due to sympathetic stimulation. Normotension in a patient that typically has
hypertension may be another clinical indication or shock. Tachycardia is commonly
present; however, patients on AV nodal blocking medications may not develop tachycardia. The metabolic derangements associated with shock as well as bradyarrhythmias that are the primary source of shock may cause bradycardia. Patients may have
tachypnea related to poor diaphragmatic perfusion, acidosis, pulmonary edema, pneumonia, or ARDS.As shock progresses and diaphragmatic weakness worsens, patients
may have a normal respiratory rate, bradypnea, or frank respiratory failure [7, 8].
Abnormal physical exam ndings in patients with shock are related to inadequate organ perfusion, cause of shock, and sympathetic stimulation. The occurrence
of these ndings is variable, and not all patients may have them. Table14.2 summarizes potential physical exam ndings one may see in patients with shock. These
ndings may support the diagnosis of shock and help to determine the shock’s
cause, but the lack of certain ndings does not rule out shock. It is worth noting that
decreased urine output is one of the rst signs of impaired organ perfusion in shock.
Urine output and capillary rell time are used at the bedside as surrogates for
organ perfusion. Decreased urine output reects renal hypoperfusion and is used as
a nonspecic marker of shock and is used to guide uid resuscitation in the absence
of advanced hemodynamic monitoring.
Capillary rell time (CRT) has been used as a sensitive marker of hypovolemia
in children and has been recently shown to be useful in adult shock as a prognostic
marker and as a guide to resuscitation [9]. Normal CRT is less than 3s, and more
than 5s is suggestive of impaired perfusion.

14 Sho ck
Table 14.2 Common physical exam ndings in patients with shock
General Ill appearing
Neuro Altered mental status
Cardiovascular Tachycardia
Respiratory Tachypnea
Renal Oliguria or low urine output
Skin Cool skin and extremities
Pale
Weak
Restlessness
Agitation
Somnolence
Bradycardia
Arrhythmias
Weak pulse
Jugular venous distension
Hypoxemia
Poor O
saturation waveform
2
Bradypnea
Anuria or no urine output
Dark urine
Warm skin and extremities
Diaphoresis
Delayed capillary rell
363
14.3.2 Laboratory Assessment
Lactic acid is commonly used to evaluate patients for shock and trend for therapy
response. The pathophysiology of lactic acidosis in shock is complex and occurs
through multiple mechanisms as described above. This includes a shift towards
anaerobic metabolism due to ischemia, catecholamine production, and decreased
clearance [10]. Unlike in other causes of shock, lactic acidosis in sepsis is mostly
due to catecholamine response, impaired cellular metabolism, and microcirculatory
dysfunction as opposed to tissue hypoxia [11, 12]. It is also important to note that
organ dysfunction in shock is related to elevated lactate due to impaired clearance.
This is because lactate clearance is primarily performed by the liver and kidney,
which are commonly affected in shock. Lactic acid may be used to aid in diagnosing
shock and evaluating response to treatment, particularly in cardiogenic and hemorrhagic shock [13, 14]. Elevated lactic acid has also been associated with increased
mortality in many causes of shock [15–17].
Central venous oxygen saturation (ScVO2) is another test used to aid in determining the cause of shock and monitoring response to therapy. Its pathophysiology
is described above and is based on the principles of delivery of oxygen (DO2) equation and Fick equation. By measuring a central venous oxygen saturation, one can
calculate the cardiac output; however, one may also presume that cardiac output is
low if the central venous oxygen saturation is low (<65%). Typically, a low ScVO2
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