Archive for the ‘ L3-Circulatory Shock ’ Category

L3- Circulatory Shock

The Circulatory Shock

It is failure of the peripheral circulation.


Inadequate tissue perfusion with blood due to decreased cardiac output and arterial blood pressure.

Types of circulatory Shock

1- Hypovolemic Shock

2- Cardiogenic (obstructive) shock

3-Low resistance (distributive) shock


Hypovolemic Shock

-It is characterized by: hypotension, rapid pulse, cold pale skin, rapid respiration, intense thirst, and restlessness or mental dullness.

-The volume of the circulating plasma is decreased

The mean circulatory pressure falls

Venous return decreases

Cardiac output decreases

Arterial blood pressure drops.

Causes of hypovolemic shock

1- severe hemorrhage

2- severe trauma leading to damage of muscle and bone. There is extensive hemorrhage in the damaged tissues

3- severe burns. Large volumes of plasma are lost

4- loss of large volumes of extracellular fluid as in excessive vomiting, sweating and in severe diarrhea

Hemorrhage and hemorrhagic shock

-Hemorrhage is loss of blood from the circulatory system.

-It may be external or internal.  The latter is dangerous because death may occur before diagnosis

Effects of hemorrhage

This depends mainly upon two factors:

1-The rate with which the loss occurs:

-gradual small loss

-sudden large loss

2-The amount of blood lost:

-less than 30%

-more than 30%

Compensatory physiologic mechanisms

1-Immediate compensatory mechanisms

2-Delayed compensatory mechanisms

1- Immediate compensatory mechanisms

I. The drop of arterial blood pressure and central venous pressure

→ decrease the rate of discharge of impulses from the arterial and atrial mechanoreceptors

→ stimulation of the pressor area and inhibition of the depressor area.

This will lead to the following:

1-stimulation of VMC. There will be increased sympathetic discharges to:

a- arterioles except  that of brain and heart


→ Raise the ABP

2-Stimulation of the cardiostimulator center and inhibition of the cardioinhibitory center.

→ Increase of the heart rate

II-  The stress condition

→ Increased discharge of sympathetic impulses to the adrenal medulla leading to secretion of more catecholamines:

A-increase the effects of sympathetic nervous system on the cardiovascular system

B-Stimulate the reticular formation of the brain stem à increase the tone of skeletal muscles and the patient becomes restless

C-It also helps spleen contraction

Stress pathways


III. Stimulation of chemoreceptors in the aortic body and carotid body.

This leads to:

A-Stimulation of the pressor area and depression the depressor area à increase the heart rate and raise the ABP.

B-Stimulation of the respiratory center à respiration becomes raid

IV –Release of hormones:



-Angiotensin II

V- Increased blood coagulation mechanisms:

This aims at closing the blood vessel injury and prevention of further blood loss.

-Formation of the extrinsic thromboplastins from the injured tissues.

-Adrenaline secreted increases liver fibrinogen and prothrombin.

2- Delayed compensatory mechanisms

1-The aim is to correct the deficiency of the circulating plasma volume:

a-tissue fluid shift  →


c-liver reformed albumin

d-Increased secretion of aldosterone and ADH

2-Increased erythropoiesis

The circulating erythropoietin rises in response to low oxygen supply to the tissues. This stimulates the bone marrow erythropoiesis

Irreversible Shock

The severity of the state of shock depends upon the rate and volume of the blood lost by the patient.

* Some patients die rapidly after severe rapid hemorrhage.

* If the amount of blood lost is less than 30% of the total blood volume, the compensatory mechanisms raise the arterial blood pressure and the patient recovers

* If the amount of blood loss is more than 30%, the compensatory mechanisms are not sufficient to correct the ABP. The patient passes into a state of irreversible or terminal shock in spite of  intensive treatment. This condition ends with death of the patient (death cycle).

Causes of irreversible shock

1- Severe cerebral ischemia that results in failure of VMC and cardio accelerator centre. This leads to lowering of the ABP and slowing of the heart.

2- The drop of ABP leads to severe cardiac ischemia with further lowering of the ABP.

This is a vicious cycle or positive feedback cycle.

3-Relaxation of precapillary sphincters while the venules remain constricted. The blood stagnates in capillaries. The blood vessels undergoes necrosis. The blood escapes into tissue spaces.

Treatment of shock

1-Removal of the cause of shock

2- Helping the compensatory homeostatic mechanisms to raise the ABP to ensure adequate perfusion of the tissues:

-In hemorrhagic and traumatic shock, since blood loss is the cause of shock, treatment is based on rapid blood transfusion.

-In burn shock the shock is mainly due to loss of plasma. Treatment of this type of shock is based on giving plasma or plasma expanders.

Blood transfusion


Drugs used in the treatment  of shock

1-Glucocorticoids as they decrease the permeability of capillaries

2- Do not use excess vasoconstrictors as the blood vessels are already severely constricted.

3-Sedatives may be used in small doses as they inhibit the medullary centers (VMC)

General instructions for the patient

-The patient should be kept in supine position.

-The level of the feet raised few centimeters above the horizontal position to help the venous return.

-Do not over-warm the patient as this may dilate the arteriolar blood vessels