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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

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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:    

Extensive anterior wall myocardial infarction Right ventricular infarction Arrhythmia Commotio cordis

CARDIOGENIC SHOCK Defined by:  

Systolic blood pressure 20 mmHg

Or 

Cardiac index 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: 

 

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 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 160 bpm

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Pre-school >140 bpm

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School-puberty >120 bpm

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Puberty-adult >100 bpm

Shock Signs Tachycardia-age Influenced by:   

Age Pacemaker Medications

SHOCK Summary:    

 

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