Shock Syndromes

7/27/2019 Shock Syndromes

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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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Cardiogenic Shock

Blunt cardiac injury

Cardiac tamponade

Air embolus

Myocardial infarction


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Tension Pneumothorax

Acute respiratory distress

Subcutaneous emphysema Absent breath sounds

Hyperresonance to percussion

Tracheal shift


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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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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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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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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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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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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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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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Calcium Administration

Most patients receiving blood transfusion

do not need calcium supplementation

Excessive calcium supplementation may be

harmful

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Shock Syndromes

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