shock syndromes
TRANSCRIPT
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Shock
Mazen Kherallah, MD, FCCP
Internal Medicine, Infectious Disease
and Critical Care Medicine
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First StepRecognize its Presence
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No Laboratory Test Diagnoses
Shock
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Shock Syndromes
Cardiogenic Hypovolemic Distributive Obstructive
LVF
Arrhythmias
Hemorrhagic
Non-
hemorrhagic
Septic
Neurogenic
Adrenal
P. Embolism
Pneumothorax
Aortic Stenosis
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Clinical Appreciation of the Presence of
Inadequate Organ Perfusion
and Tissue Oxygenation
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Second StepIdentify the Probable
Causes
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Traumatized and Shocked
Patients
Hypovolemic shock
Cardiogenic shock
Neurogenic shock
Septic shock
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Treatment should be initiated
simultaneously with theidentification of probable cause of
the shock state
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Hemorrhage is the most common
cause of shock in the injured
patient
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I. Initial Patient Assessment
Recognition of Shock
Tachycardia and cutaneous vasoconstriction
are the usual and early physiologic response
to volume loss
Tachypnea
Narrowed pulse pressure
Hypotension when patients blood volume
loss is more than 30%
Hematocrit or hemoglobin concentration are
not reliable
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I. Initial Patient AssessmentRecognition of Shock
Tachycardia
Greater than 160 in infant
Greater than 140 in preschool age child
Greater than 120 in school age child
Greater than 100 in an adult
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I. Initial Patient AssessmentRecognition of Shock
Unable to produce Tachycardia
Limited cardiac response to catecholamine
stimulation: elderly Concurrent use of beta-adrenergic blocking
agents
The presence of a pacemaker
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I. Initial Patient AssessmentClinical Differentiation of Etiology of Shock
Hemorrhagic Shock
The most common cause of shock after injury
All patients with multiple injuries have an elementof hypovolemia
Most patients with nonhemorrhagic shock state
respond partially or briefly to volume resuscitation All patients with shock should initially be treated
with volume replacement
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I. Initial Patient AssessmentClinical Differentiation of Etiology of Shock
Nonhemorrhagic Shock
Cardiogenic shock
Tension pneumothorax
Neurogenic shock
Septic shock
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Nonhemorrhagic Shock
Cardiogenic Shock
Blunt cardiac injury
Cardiac tamponade
Air embolus
Myocardial infarction
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Nonhemorrhagic Shock
Tension Pneumothorax
Acute respiratory distress
Subcutaneous emphysema Absent breath sounds
Hyperresonance to percussion
Tracheal shift
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Nonhemorrhagic Shock
Neurogenic Shock
Isolated intracranial injuries do not cause
shock Spinal cord injury may produce hypotension
due to loss of sympathetic tone
Hypotension without tachycardia orcutaneous vasoconstriction
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Nonhemorrhagic ShockSeptic Shock
Uncommon after injury
May occur if patients arrival to ER is delayed
several hours
Penetrating abdominal injuries and
contamination of the peritoneal cavity with
intestinal contents
Normal circulating volume, modest tachycardia,
warm and pink skin, and a wide pulse pressure
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II. Hemorrhagic Shock in the Injured
Patient
Definition of Hemorrhage
Acute loss of circulating blood volume
Normal adult blood volume is 7% of bodyweight
Normal pediatric blood volume is 8-9% of
the body weight Calculation is based on ideal body weight
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II. Hemorrhagic Shock in the Injured
Patient
Direct Effect of Hemorrhage
The distinction between classes may not be
apparent in an individual patient
Volume replacement should be directed bythe response to initial therapy rather than by
relying solely on the initial classification
Several confounding factors profoundlyalter the classic hemodynamic response
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Confounding Factors that alter the Classic
Hemodynamic Response
The patients age
Severity of the injury
Type and anatomical location of the injury
Time lapse between injury and initiation of
treatment
Prehospital therapy
Medication used for chronic conditions
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Classification of Hemorrhagic Shock
Class I Class II Class III Class IV
Blood loss (ml) Up to 750 750-1500 1500-2000 >2000
Blood loss (%) Up to 15% 15-30% 30-40% >40%
Pulse rate 100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure Normal Decreased Decreased Decreased
Respiratory
rate
14-20 20-30 30-40 >35
Urine output
(ml/h)
>30 20-30 5-15 Negligible
CNS/mental
status
Slightly
anxious
Mildly
anxious
Anxious/
confused
Confused/
lethargic
Fluid
replacement
Crystalloid Crystalloid Crystalloid/
blood
Crystalloid/
Blood
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III. Initial Management of Hemorrhagic
Shock
Physical Examination
Airway and breathing
Circulation: Hemorrhage control Disability: Neurologic examination
Exposure: Complete examination
Gastric dilatation: decompression
Urinary catheter insertion
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Contraindication to Insertion of Transurethral
catheter prior to Radiological confirmation of
an intact Urethra
Blood at the urethral meatus
High-riding, mobile, or nonpalpable prostate
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III. Initial Management of Hemorrhagic ShockVascular Access Lines
Must be obtained promptly
Two large-caliber (minimum of 16 gauge)
peripheral intravenous catheters
Large-caliber, central venous access
Central lines should be changed in more
controlled environment as soon as patients
condition permits
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III. Initial Management of Hemorrhagic ShockInitial Fluid Therapy
Ringers lactate solution is the initial fluid of
choice
Normal saline is the second choice
Normal saline has the potential of causing
hyperchloremic acidosis
Initial fluid bolus is given as rapidly as
possible, 1-2 liters for an adult and 20 mg/kg
for pediatric patient
3 for 1 rule: each mL of blood loss is
replaced with 3 mL of crystalloid fluid
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IV. Evaluation of Fluid Resuscitation and
Organ Perfusion
General
Blood pressure
Pulse pressure
Pulse rate
Central nervous system status
Skin circulation
Changes in central venous pressure line
Changes in PCWP and cardiac output
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IV. Evaluation of Fluid Resuscitation and
Organ Perfusion
Urinary Output
Adequate volume replacement should
produce a urinary output of approximately
0.5 mL/kg/hour in the adult
One mL/kg/hour is an adequate urinary
output for the pediatric patients
2 mL/kg/hour for children under 1 year of
age
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IV. Evaluation of Fluid Resuscitation and
Organ Perfusion
Acid/Base Balance
Respiratory alkalosis followed by metabolic
acidosis is seen in patients with earlyhypovolemic shock
Severe metabolic acidosis may develop
from long-standing shock
Persistent acidosis is due to inadequate
resuscitation or ongoing blood loss
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V. Response to Initial Fluid Resuscitation2000 mL Ringers lactate in adults or 20 mL/kg bolus in children
Rapid Response Transient
Response
No Response
Vital signs Return to normal Recurrence ofBP
and HR
Remain
abnormal
Estimated blood
loss
Minimal (10-
20%)
Moderate and
ongoing (20-40%)
Severe (>40%)
Need for more
crystalloid
Low High High
Need for blood Low Moderate to high Immediate
Bloodpreperation Type andcrossmatch Type-specific Emergencyblood release
Need for
operation
Possible Likely Highly likely
Early presence
of surgeon
Yes Yes Yes
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VI. Blood Replacement
Packed Red Blood Cells Versus Whole Blood Therapy
Restore the oxygen-carrying capacity of the
intravascular volume
Either whole blood or packed red cells can
be used.
Component therapy is used to maximizeblood product availability
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VI. Blood Replacement
Crossmatched, Type-specific, and Type O Blood
Crossmatched blood is preferable but itrequires approximately 1 hour to be
completed: should be used for patients whostabilize rapidly
Type-specific blood can be provided in 10minutes: this blood is compatible with ABO
an Rh blood types
Type O blood can be used in patients withexanguinating hemorrhage when type-
specific is not available
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VI. Blood Replacement
Warming Fluids-Plasma and Crystalloid
In patients receiving massive volume of
crystalloid, heat the fluid to 39 C beforeusing it to prevent hypothermia
Storage of crystalloids in a warmer with the
use of microwave oven
Blood products cannot be warmed in the
microwave ovenbut can be heated with the
passage through intravenous fluid warmer
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VI. Blood Replacement
Autotransfusion
Patients with a major hemothoarax
Sterile collection of blood through standardtube thoracotomy collection devices
Anticoagulation with sodium-citrate
solution, not heparin
Retransfusion of shed blood
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VI. Blood Replacement
Coagulopathy
Dilution of platelets and clotting factors
Averse effect of hypothermia on platelets
aggregation
Release of tissue thromboplastin by the
damaged neural tissue in patients with
closed head injury
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VI. Blood Replacement
Calcium Administration
Most patients receiving blood transfusion
do not need calcium supplementation
Excessive calcium supplementation may be
harmful