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SHOCK 2007
SHOCK
2007
Ariel G. Bentancur, MD
Emergency Department, Sheba Medical Center, Israel
“Dry” Definition of Shock
A circulatory situation where
inadequate tissue/end organ oxygenation and
perfusion is present.
End Organ?
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Brain
Heart
Kidneys
Gut
Expanded definition:
A generalized circulatory derangement causing
multiple organ hypoperfusion and strong
sympathetic activation, and when intense or
sustained enough ( minutes to hours) irreversible
metabolic, inflammatory, and clotting disorders
leading to the patient’s permanent function
deficit or death.
So how we recognize shock?
Grossly by:
Signs of strong sympathetic activation:
 Tachycardia
 Pallor
 Extremity coldness
 Sweating
 Tachypnea
Signs of hemodynamic instability:
 Inappropriate low blood pressure values
Signs of organ dysfunction:
 Altered consciousness
 Oliguria
BUT…
Depends on:

CATEGORY of shock

DEGREE of shock severity
SHOCK CATEGORIES
1.
2.
3.
4.
5.
6.
7.
HYPOVOLEMIC
CARDIOGENIC
NEUROGENIC
SEPTIC
ANAPHILACTIC
OBSTRUCTIVE
OVERDOSE/TOXIN RELATED
HYPOVOLEMIC SHOCK
The initial insult is a loss of circulatory fluid volume, by:
 Bleeding
 Burns
 Vomiting
 Diarrhea
 Sweating
 “Stomas”
 Third space fluid sequestration
CARDIOGENIC SHOCK
Severe myocardial pump failure due to:
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Extensive anterior wall myocardial infarction
Right ventricular infarction
Arrhythmia
Commotio cordis
CARDIOGENIC SHOCK
Defined by:
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Systolic blood pressure <90 mmHg
and
Wedge pressure of >20 mmHg
Or

Cardiac index <1.8 L/min
Or

Inotropics or intra-aortic balloon couterpulsation used to achieve
Systolic blood pressure >90 mmHg.
CARDIOGENIC SHOCK
Recognized by:
History: Acute Cardiac Syndrome or chest trauma.
ECG changes: arrhythmia or ST segment changes.
Echocardiographic demonstration of ventricular
hypokinesia.
NEUROGENIC SHOCK
Caused by severe injury to the CNS
Mechanism: A distribution Shock
 loss of nervous control of the vascular tone and subsequent fall
of peripheral vascular resistance.
 loss of vascular regulation.
 pooling of blood in the splanchnic bed
Clinical characteristics:
 Despite of shock presence the skin is warm and pink.
 Pulse is normal or slow due to unmatched parasympathetic tone.
SEPTIC SHOCK
It is also a distribution shock caused by severe
systemic infection.
Mechanism:
 Increased circulatory demand.
 A loss of the vascular tone with a subsequent
decrease of the peripheral vascular resistance.
 Circulatory volume unchanged but splachnic
bed volume sequestration is present.
SEPTIC SHOCK
Recognized by:
 History: present or recent febrile disease.
Physical examination:
 Hypotension
 Warm, dry skin.
 Tachycardia.
ANAPHYLACTIC SHOCK
Caused by exposure to allergen.
Mechanism:
 Distribution shock
 IgE/Mastocyte mediated acute reaction.
 Histamine/bradichinine/cytokine(ILC4)/PAF/
PGD2 mediated vasodilatation and blood
volume sequestration in the splanchnic bed.
ANAPHYLACTIC SHOCK
Recognized by:

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History of exposure.
History of past anaphylactic reaction.
Coexistence of: skin rush, angioedema,
bronchospasm.
OBSTRUCTIVE SHOCK
A restriction to blood flow or diastolic heart filling
like in:
Pericardiac Tamponade
Tension Pneumothorax
Stacked cardiac prosthetic valve
Massive Pulmonary Emboli
OBSTRUCTIVE SHOCK
Mechanism:
Blood Volume is normal
Cardiac pump function is normal
Vascular tone is normal
Increased resistance to blood flow or
ventricular diastolic function cause a low
cardiac output!
OVERDOSE/TOXIN RELATED
SHOCK
Caused by:
 Medications:
Drugs used for the treatment of hypertension:
Ca++ channel blockers
β-blockers
or
Digoxin
Tryciclic antidepressants

Toxins
Digested- scombroid fish poisoning
Snake bite
OVERDOSE/TOXIN RELATED
SHOCK
May develop through mixed mechanisms:


Vasodilatation and a decrease of peripheral
vascular resistance.
Decreased ventricular systolic function.
SHOCK SEVERITY DEGREE
Best understood by the severity classification of hemorrhagic shock:
Degree of
Hemorrhage
Estimated volume
of blood loss
Class 1
Very Mild
<15%
<750 ml
Class 2
Mild
15-25%
750-1500 ml
Class 3
Moderate
26-39%
1500-2000 ml
Class 4
Severe
≤40%
>2000 ml
Cardiovascular
signs
HR <100
Normal b.p.
HR >100
Normal b.p.
HR >120
Hypotension
HR >140
Deep hypotension
Respiratory signs
Normal RR
14-20
Mild tachypnea
20-30
Moderate tachypnea
30-35
Severe tachypnea
>35
CNS signs
Anxious
Irritable/confused/
combative
Lethargic/low pain
response
Lethargic/coma
Skin signs
Warm/pink/normal
capillary refill
Cool extremities/
Delayed capillary fill
Cool extremities/
Delayed capillary fill
Cool extremities/
Delayed capillary fill
Kidney/metabolic
Normal urine output
Normal serum PH
Oliguria 20-30ml/m
Normal serum PH
Oliguria<15ml/m/↑
urea/Metabolic
acidosis
Anuria
Severe acidosis
signs
Shock Signs
Tachycardia-age

Infant > 160 bpm

Pre-school >140 bpm
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School-puberty >120 bpm

Puberty-adult >100 bpm
Shock Signs
Tachycardia-age
Influenced by:
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
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Age
Pacemaker
Medications
SHOCK
Summary:
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Should be early recognized.
Sole reliance on SBP results in delayed recognition.
Treat shock and the causes early.
Hypovolemic versus cardiogenic versus distribution
versus obstructive versus mixed shock.
The clinical picture depends on type and severity.
If treated partially or late it becomes almost irreversible
resulting in MOF and death.
DISCUSSION
COMMON SENSE-MECHANISM
YES, SHOCK PRESENT
NO SHOCK PRESENT