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Outline of Lecture


Clinical Case

A 22 years old young man met road traffice accident resulting in profuse bleeding from deep cut in left thigh, fracture neck of left femur resulting in haematoma formation. O/E pulse 110/min, Weak, Skin is cold, BP 80/50 mm Hg

Q-1: What is your diagnosis?

Q-2: What is pathophysiology of this condition?



Profound hemodyamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs


“Transition between life and death”


Failure to oxygenate & nourish the body adequately


Mortality > 20%




Shock affects mitochondria first


Without oxygen mitochondria convert fuels to lactate → lactic acid


Failure of the krebs cycle

Oxygen is the final electron accepter to form water

Lactic Acid

Early shock

Skeletal muscle and splanchnic organs 1st affected

Lactic acid production



Pyruvate delivery from glycolysis can overwhelm krebs cycle

Systemic Response

Decreased vascular wall tension increases sympathetic stimulation (blocked in sepsis)

Increased epi, norepi, corticosteroids, renin, and glucagon

Increased glycogenolysis and lipolysis


Increased glucose and FFA’s to TCA can overwhelm it

Immune Response

Neutrophil and macrophage activation due to hypoxia

Enzymatic organ damage

Capillary plugs causing microischemia

TNF and Interleukins released

Types of Shock

Cardiogenic (intracardiac vs extracardiac)




neurogenic (spinal shock)

adrenal insufficiency



Cardiogenic Shock, intracardiac

Myocardial Injury or Obstruction to Flow


valvular lesions


Severe CHF


Hypertrophic Cardiomyopathy


Presentation of Cardiogenic Shock

Pulmonary Edema



weak pulses



Cardiogenic Shock, extracardiac

Pulmonary Embolism

Cardiac Tamponade

Tension Pneumothorax

Presentation will be according to underlying disease process.

Hypovolemic Shock

Reduced circulating blood volume with secondary decreased cardiac output

Acute hemorrhage





Presentation of Hypovolemic Shock


flat neck veins

clear lungs

cool, cyanotic extremities

evidence of bleeding?

Anticoagulant use

trauma, bruising


Distributive Shock

Peripheral Vasodilation secondary to disruption of cellular metabolism by the effects of inflammatory mediators.

Gram negative or other overwhelming infection.

Results in decreased Peripheral Vascular Resistance.

Distributive Shock:  Presentation



clear lungs, evidence of pneumonia

warm extremities

flat neck veins


Diagnosing Shock

Response to fluids



Evidence of infection

Swan-Ganz Catheter?

Swan-Ganz Catheter

Utilized to differentiate types of shock and assist in treatment response.


Probably overused by physicians.  Studies documenting increased mortality in patients with catheters versus no catheters, although somewhat swayed by selection bias.

Swan-Ganz Interpretation


Correct underlying disorder if possible and then direct efforts at increasing the blood pressure to increase oxygen delivery to the tissues.

Maintain a mean arterial pressure of 60   (1/3 systolic + 2/3 diastolic)

Keep O2 sats >92%, intubate if neccesary


Correction of hypotension

Normal Saline should be administered anytime a patient is hypotensive.  If hypotension exists give more NS. ***

If possible give blood as it replaces colloid.


Inotropic agents for cardiogenic shock

Intra-aortic Balloon Pump for cardiogenic

Autonomic Drugs in Shock

Management of Cardiogenic Shock

Attempt to correct problem and increase cardiac output by diuresing and providing inotropic support.  IABP is utilized if medical therapy is ineffective.  Catheterization if ongoing ischemia

Cardiogenic shock is the exception to the rule that NS is always given for hypotension  NS will exacerbate cardiac shock.

Management of Septic Shock

Early goal directed therapy

Identification of source of infection

Broad Spectrum Antibiotics

IV fluids


Steroids ??

Recombinant human activated protein C ( Xygris)

Bicarbonate if pH < 7.1

Management of Hypovolemic Shock

Correct bleeding abnormality

If PT or PTT elevated then FFP

Aggressive Fluid replacement with 2 large bore IV’s or central line.

Pressors are last line, but commonly required.


Addison’s Disease

Deficiency of cortisol and aldosterone production in the adrenal glands

This is suspected when patient is non-responsive to fluids and antibiotics.

Electrolytes may reveal hyponatremia and hyperkalemia

Hydrocortisone 100 mg IV immediately then taper appropriately




Septic shock – 35-40% (1 month mortality)

Cardiogenic shock – 60-90%

Hypovolemic shock – variable/mechanism

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