Physiology of Shock

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Shock may be defined as generalized inadequacy of blood flow throughout the body that causes tissue damage due to very little supply of nutrients and ineffective removal of waste products.

It is a state of widespread hypoperfusion of cells and tissues due to inadequate effective circulatory blood volume that results in ineffective delivery of oxygen and nutrients to cells and tissues and inadequate clearance of metabolites, which may lead to tissue damage.
Effects-of-inadequate-perfusion-on-cell-function

Types of Shock

1. Hypovolemic Shock

Hypovolemic shock or “cold shock” is due to inadequate fluid in vascular system. It may be due to hemorrhage, trauma, surgery, burns or dehydration (vomiting, diarrhea, sweating, etc.)

Effects of hemorrhage depend on the amount of blood loss and its speed. Rapid loss of 30% of blood may produce death while loss of 40-50% slowly in 24 hours may not produce shock even.

Hemorrhage is classified as moderate if blood loss is less than one litre (less than 20%) while it is termed severe if blood loss is greater than one litre (greater than 20%).

2. Distributive Shock

Distributive shock is caused by marked vasodilatation and venous pooling. It may be:

Neurogenic or vasogenic (fainting)
Anaphylaxis (Histamine shock)
Sepsis (Endotoxic shock) also known as “warm shock”

3. Cardiogenic Shock

Cardiogenic shock is due to inadequate pumping action of the heart. It may occur due to myocardial infarction, congestive cardiac failure, arrhythmias or severe valvular disease.

4. Obstructive Shock

Obstruction to blood flow in lungs or heart causes congested shock or obstructive shock. It may occur as a result of tension pneumothorax, pulmonary embolism, cardiac tumor or cardiac temponade.

Fundamental Features of Shock

The common feature to all entities of shock is inadequate tissue perfusion as a result of inadequate cardiac output.

Sympathetic reflexes play a vital role in shock. A person may die within 30 minutes on removal of 15-20% of blood without sympathetic reflexes. Whereas he may sustain 30-40% of blood loss with intact sympathetic reflexes. These reflexes maintain blood flow through brain and heart till the arterial blood pressure falls below 70mmHg.

General Features of Shock

Hypotension (systemic blood pressure less than 100 mmHg)
Tachycardia (pulse rate greater than 100/minute), low volume pulse
Cold, clammy skin, cyanosis at peripheries
Rapid, shallow respiration
Drowsiness, confusion, irritability, restlessness
Sweating
Oliguria (urine output less than 30 ml/hour)
Central venous pressure or jugular venous pressure is decreased in hypovolemia and anaphylaxis while increased in cardiogenic or obstructive shock. They may be low, normal or high in septic shock.

Stages of Shock

There are three major stages of shock:

1. Non progressive or compensated stage

The normal circulatory compensatory mechanisms eventually cause full recovery without help from outside therapy.

The circulatory system can recover as long as the degree of hemorrhage is not greater than a critical level. The sympathetic reflexes and other mechanisms compensate enough to prevent deterioration of circulation, which are all negative feedback control mechanisms of circulation, that attempt to return the cardiac output and blood pressure back to normal.

Baroreceptor reflexes and CNS ischemic response occurs within 30 seconds. Reverse stress relaxation of circulatory system, formation of angiotensin by kidneys and formation of vasopressin by posterior pituitary takes 10 minutes to an hour. Miscellaneous compensatory mechanisms that return the blood volume to normal take one to 48 hours to develop and include:

increased absorption of fluid from intestines
fluid shift
conservation of salt and water by kidneys
increases appetite for salt and water (thirst mechanism)

2. Progressive stage

Shock becomes steadily worse until death. In this type hemorrhage occurs beyond the critical amount. Even a few milliliters of blood loss make a difference between life and death.

Then shock becomes progressive if the shock itself causes still more shock through vicious cycle of cardiovascular deterioration by positive feedback mechanisms, leading thereby to progressive reduction in cardiac output. Events include:

cardiac depression
vesomotor failure
thrombosis of microcirculation (sludging of blood)
release of endotoxins
generalized cellular deterioration
lactic acidosis
increased capillary permeability
renal failure

3. Irreversible/Refractory stage

Shock has progressed to an extent that all forms of known therapeutic measures are inadequate to save the person’s life, even though, for the moment, the person is alive (due to extensive tissue damage).

Irreversible shock is characterized by progressive cardiovascular deterioration and patient no longer responds to therapeutic measures even if blood volume is returned to normal, cardiac output remains depressed.

Hypoxic tissue damage occurs due to profound vasoconstriction of precapillary sphincters and venules (in splanchnic area). After 3-5 hours pre-capillary sphincters relax but venules remain constricted leading to stagnation of blood. Adherence of granulocytes to injured vessels releases oxygen leading to tissue damage. Entry of bacteria into circulation from GIT occurs as well.

Events include:

severe cerebral ischemia
severe myocardial ischemia
vasomotor cortex depression
acidosis
acute respiratory distress syndrome
depletion of cellular energy
release of myocardial toxic factor from ischemic pancreas
Death

Sequence of Events after Acute Hemorrhage

This constitutes non progressive or compensated shock. Three phases are present:

1. Nervous mechanisms

These are mostly concerned with compensation and recovery. In the first few hours, hemoglobin and hematocrit remains normal. Hemorrhage causes decreased blood volume leading to decreased venous return and decreased cardiac output and blood pressure.

Decreased blood pressure activates baroreceptor and chemoreceptor reflexes, which act on vasomotor cortex causing tachycardia, increased respiratory rate. Adrenal glands produce epinephrine and norepinephrine causing vascular spasm.

2. Restoration of Blood Volume

Restoration of blood volume occurs over 1-2 days. This includes fluid shift, fluid absorption in intestines and kidneys and antidiuretic hormone-renin-angiotensin-aldosterone system.

Hemodilution causes decreased hemoglobin and hematocrit.

3. Replacement of RBCs

Increased reticulocyte count up to 10-15% occurs in 4-7 days, and return to normal within 2 weeks. RBC/hemoglobin concentration is restored in 6-8 weeks.