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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
108 T. Jones, R. McIntyre and E. Peltz
surrogate for adequate oxygen delivery an ScVO2 goal of ≥70% was chosen.
After CVP, MAP and HCT (≥30) were optimized then dopamine was started
and titrated to improve oxygen delivery and achieve this ScvOs goal. Overall,
28 and 60 day mortality and overall length of stay were significantly lower in
the early goal directed therapy patients as compared with patients receiving
standard therapy. Indicators of perfusion including base deficit, lactate and
pH were also significantly improved with goal directed therapy. With goal
directed resuscitation to improve oxygen delivery including preload, afterload, contractility, and inotropic support to achieve a goal ScvOs ≥70%
patient outcomes were improved. (N Engl J Med 2001; 345: 1368–1377).
• In a multicenter, randomized controlled trial of 300 patients in septic shock,
Jones et al. found there was no difference in mortality between patients who
were resuscitated based on improving lactate clearance vs SvO2. Both goals
were achieved by a combination of transfusion and inotropes, however no
difference between patient groups was achieved after reaching an initial goal
MAP and CVP (JAMA 2010; 303(8): 739–746).
• In addition to sepsis, early mitochondrial oxidative dysfunction occurs in
trauma patients. By measuring decoupling of tissue oxyhemoglobin and
cytochorome a,a3 redox, Cairns et al. found that trauma patients in multiorgan
failure displayed early evidence of mitochondrial oxidative dysfunction
(J Trauma 1997; 42(3): 532–536) In both trauma and septic patients, despite
resuscitation to goal, it is difficult to correct O2 utilization deficits at the
cellular level.
Chapter 5-(ii)
Recognition and Characterization of Shock
Anna Kristina Melvin, PA-C* and Walter L. Biffl, MD
* Physician Assistant, Boulder Community Hospital
†
Associate Director of Surgery, Denver Health Medical Center,
Professor of Surgery, University of Colorado School of Medicine
†
Take Home Points
• Shock represents inadequate perfusion of tissues with oxygenated blood.
• The characterization of shock is of practical importance in that it impacts
definitive treatment.
• Characterization of the type of shock is based on history and physical
examination along with a few basic diagnostic maneuvers.
Background
• Shock represents inadequate perfusion of tissues with oxygenated blood,
resulting in cellular hypoxia.
• Shock may be manifested by alterations in physiology (hypotension,
tachycardia, tachypnea), alterations in physical exam (decreased level of
Contact information: (Anna Kristina Melvin) Boulder Community Hospital, 1100 Balsam
Ave, Boulder, CO 80304; (Walter L. Biffl ) Dept. of Surgery, DHMC, 777 Bannock St.,
MC 0206, Denver, CO 80204; Tel.: 303-602-1861, email: walter.biffl @dhha.org; Anna.
kristina@bch.org
109
110 A. K. Melvin and W. L. Biffl
consciousness, delayed capillary refill, cool or mottled extremities), or
alterations in laboratory values/organ function (metabolic acidosis, oliguria,
azotemia).
• The etiology of shock is of practical importance in that it impacts the overall
treatment plan.
• There are seven fundamental types of shock which differ in both patho-
physiology and treatment:
{ Obstructive
{ Cardiac compressive
{ Cardiogenic
{ Neurogenic
{ Septic
{ Hypovolemic
Hemorrhagic
{ Anaphylactic
Main Body
Recognition of shock
• Shock may be recognized based on manifestations of the shock state, or the
response to the shock state.
• Manifestations of shock result from hypoperfusion, and include alterations
in physiology (hypotension), alterations in physical exam (decreased level
of consciousness, delayed capillary refill, cool or mottled extremities), or
alterations in laboratory values/organ function (metabolic acidosis, oliguria,
azotemia).
• The compensatory response to hypoperfusion may include alterations in
physiology (tachycardia, tachypnea), or alterations in physical exam (delayed
capillary refill, cool extremities).
Characterization of shock (Fig. 1)
• Obstructive shock, generally due to tension pneumothorax or other cause of
mediastinal shift, narrows the vena cavae and obstructs venous return to the
point of cardiovascular collapse. Evaluation of physical exam for jugular venous
distension, tracheal deviation, and breath sounds should make the diagnosis;
ultrasound can reveal a pneumothorax. Chest X-ray should not be necessary.
Recognition and Characterization of Shock 111
• Cardiac compressive shock is generally due to pericardial tamponade, in which
fluid accumulates in the nondistensable pericardium and restricts cardiac
diastolic filling. Evaluation of physical exam for jugular venous distension
and heart tones; electrocardiogram for low voltage; and echocardiogram for
pericardial effusion and cardiac contractility, will aid in characterization.
• Cardiogenic shock represents inadequate cardiac output due to heart failure,
dysrhythmia, or acute coronary syndrome. Evaluation of physical exam for
jugular venous distension and heart tones; electrocardiogram for rhythm and
ischemic changes; and echocardiogram for cardiac contractility, will aid in
characterization.
• Neurogenic shock is caused by disruption of sympathetic pathways causing
loss of vasomotor tone. Tachycardia is often absent, and skin is often pink and
warm. The clinical context of a spinal cord injury and loss of distal sensorimotor function will aid in characterization.
• Septic shock is a severe systemic inflammatory response to infection. In the
context of a source of infection, leukocytosis or leukopenia, and fever or
hypothermia will aid in characterization.
• Hypovolemic shock is the most common type in the surgical patient.
Hypovolemia may result from hemorrhage (traumatic, gastrointestinal, postoperative, etc.), fluid sequestration (due to infectious or inflammatory
processes, bowel obstruction, etc.) or dehydration (due to insensible/wound
losses, lack of intravenous or enteral intake). Evaluation of hydration status
(by physical exam, ultrasonography, or central venous pressure monitoring)
and measurement of hemoglobin concentration, in the appropriate clinical
context, will aid in characterization. The amount of intravascular fluid loss
corresponds to the clinical manifestations (Table 1).
• Anaphylactic shock must be considered if there is no other explanation. It
may be due to drug or blood transfusion reaction, or allergic reaction to food,
latex or other substance.
112 A. K. Melvin and W. L. Biffl
Practical Algorithm(s)/Diagrams
Fig. 1. Algorithm for characterization of shock.
Recognition and Characterization of Shock 113
Table 1. Physiologic manifestations of fluid loss by categories.
Class I Class II Class III Class IV
Blood Loss, % <15 15–30 30–40 >40
Blood Loss, mL <750 750–1500 1500–2000 >2000
Heart Rate, bpm <100 >100 >120 >140
Systolic Blood Pressure Normal Normal Decreased Decreased
Respiratory Rate/min <20 20–25 25–35 >35
Mental Status Normal/Anxious Anxious Agitated/Confused Lethargic
Urine Output mL/hr >30 20–30 <20 Nil
Review of Current Literature with References
• Advanced Trauma Life Support for Doctors student Manual, 8th Ed. Chicago,
IL: American College of Surgeons, 2008.
{ This represents the gold standard for trauma evaluation and resuscitation.
• Boffard KD (ed): Manual of Definitive Surgical Trauma Care, 3
London, UK: Hodder Arnold, 2011.
{ Developed for International Association for Trauma Surgery and Intensive
Care, this course emphasizes rapid diagnosis and intereventions.
• Ferrada P, Anand RJ, Whelan J, et al. Limited transthoracic echocardiogram:
So easy any trauma attending can do it. J Trauma 2011; 71: 1327–1332.
{ Outlines the utility of echocardiography to assess cardiac contractility,
pericardial fluid, and overall fluid status.
• Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign:
International guidelines for management of severe sepsis and septic shock:
2012. Crit Care Med 2013; 41: 580–637.
{ The latest evidence-based guidelines for identification and management
of septic shock.
rd
Ed.
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Chapter 5-(iii)
Resuscitation Strategies
Fredric M. Pieracci, MD, MPH*
* Acute Care Surgeon, Denver Health Medical Center
Take Home Points
• Obey the four main principals of resuscitation:
(1) Only resuscitate patients in shock.
(2) Resuscitate based on shock etiology; multiple etiologies frequently co-exist.
(3) Re-evaluate frequently with pre-determined markers.
(4) Stop resuscitation once pre-determined markers are reached.
• There is no consensus on the benefit of volume expansion with crystalloid vs.
colloid. Colloid is more expensive.
• Hypotensive resuscitation should be reserved for highly selected trauma
patients in hemorrhagic shock in the field. There is no place for it in the ICU.
• Volume expansion with hypertonic saline may be beneficial in two very
specific clinical scenarios: (1) remote locations and (2) severe traumatic brain
injury.
Contact information: Denver Health Medical Center, 777 Bannock Street, MC 0206, A388,
Denver, CO 80206; Email: Fredric.pieracci@dhha.org
115
116 F. M. Pieracci
• Patients in hemorrhagic shock should be transfused until (1) the bleeding
is stopped and (2) end organ perfusion is restored. Avoid using arbitrary
hemoglobin transfusion triggers.
• Resuscitation to supra-normal tissue perfusion does not improve outcomes
and leads to massive volume expansion and its complications, most notably
cerebral edema and abdominal compartment syndrome [Chapter 8-(vi)].
• The use of pulmonary artery (PA) catheters in guiding resuscitation has fallen
out of favor because (1) several large series have failed to document an
outcome benefit and (2) less invasive, dynamic measurements of preload
responsiveness are now available [Chapter 5-(iv)].
Background
• Resuscitation is defined as the reversal of shock. Resuscitation is commonly
equated with volume expansion, which is only true if the etiology of shock is
hypovolemia. Rather, vasopressors for vasodilatory shock, inotropic support for cardiogenic shock, and decompressive laparotomy for abdominal
compartment syndrome (obstructive shock) are all considered “resuscitation.”
• Shock is defined as inadequate energy production to meet metabolic needs.
Most cases of shock are secondary to impaired oxygen delivery.
• Oxygen delivery is dependent upon six fundamental variables (listed below).
Derangement of one or more of these variables leads to the six types of shock
[Chapter 5-(ii)]. Resuscitation involves assessing and optimizing these six
variables (in order).
{ Hemoglobin concentration
{ Arterial hemoglobin oxygen saturation
{ Heart rate
{ Preload
{ Contractility
{ Afterload
• Oxygen supply-demand mismatch manifests by either organ specific or
global markers of tissue hypoperfusion.
• Organ-specific markers include altered mental status (central nervous system)
and oliguria (renal system). These markers are not specific for shock.
• Global markers are more specific for shock and include (1) venous hemo-
globin oxygen saturation, (2) serum lactate concentration and (3) serum
hydrogen concentration (or its surrogates, pH, serum bicarbonate concentration,
and base deficit).
Resuscitation Strategies 117
Main Body
Resuscitation strategies
• Timing of resuscitation: Animal models of hemorrhagic shock have
concluded that tissue damage becomes irreversible beyond a critical period
of hypoperfusion, after which restoration of tissue perfusion is superfluous.
This period is termed the “resuscitation window” and appears to be on the
order of 2 hours. Begin resuscitation immediately after recognizing shock.
• Resuscitation by protocol: This strategy refers generally to a standardized,
algorithm-based approach, which uses specific endpoints of resuscitation and
guides interventions until a prespecified endpoint is reached. Such algorithms
consist usually of a series of binary steps (e.g., transfuse for hemoglobin
concentration < 7 g/dL) that simplify the resuscitative process. Strict
adherence to resuscitation protocols has been criticized for resulting in
oversimplification of the complex, evolving the nature of shock. A standardized resuscitation protocol that limits variability in care yet allows room for
individualized interpretation of clinical circumstances represents a practical
compromise.
• Crystalloid vs. Colloid: The ideal fluid for volume expansion during resusci-
tation remains debated. There are no convincing data to support one over the
other. However, because colloid as compared to crystalloid involves increased
cost in the absence of a survival benefit, it is not recommended preferentially
for volume resuscitation.
• Hypertonic Saline: There are many potential benefits of using hypertonic
saline as a resuscitative fluid. Due to an increase in oncotic pressure, administration of hypertonic saline acts as a transient ‘‘auto transfusion’’ of fluid
from the interstitium to the vascular space. Similar to colloid, endpoints of
resuscitation may thus be achieved using less volume relative to crystalloid.
This benefit may be particularly important for patients with head injury, for
which cellular dehydration results in decreased intracranial pressure. The
relatively lower weight and volume. Clinical trials of hypertonic saline, with
or without the addition of dextran, have not substantiated the aforementioned
theoretical benefits, and the routine use of hypertonic saline as a resuscitative
fluid is not currently advocated.
• Blood product transfusion: See Chapter 9-(i).
• Blood substitutes: Hemoglobin-based oxygen carriers are currently not
approved for use in either North America or Europe.
• Resucitation to Supranormal tissue perfusion: Survivors of shock demonstrate
increases in oxygen delivery to “supranormal” levels (> 600 mL/min/m
2
).