Table of content1- Definition 2- Causes and Types of Shocks 3- Clinical Features of Shock 4- Systemic Changes in Shock 5- Stages of Shock 5- Outcome of Shock |
Definition:
Shock is a clinical state of systemic hypoperfusion, in which there is progressive cardiovascular collapse associated with acute reduction in cardiac output and effective circulating blood volume, resulting in hypotension, and organs insuffincy.
Adequate organ perfusion depends on arterial blood pressure (BP), which in turn depends on: Cardiac output (CO), peripheral vascular resistance (PVR).
(CO) = Stroke Volume x Heart rate.
In turn, stroke volume depends on: Preload (i.e., blood volume), and after-load (i.e. Arterial resistance, & myocardial contractility). Any defect in any of these factors might result in shock.
Causes and Types of Shocks:
Shock can be classified into: hypovolemic shock, cardiogenic shock, distributive shock.
Hypovolemic Shock:
This type is caused by reduced blood volume,
reduction in circulating blood volume results in a reduction of the
preload which leads to inadequate left ventricular filling, reflected as
decreased left right ventricular end diastolic volume and pressure.
The reduced preload culminates in decreased cardiac output which leads to widespread tissue hypoperfusion .
Causes of Hypovolemia:
Haemorrhage, dehydration in cases of vomiting or diarrhoea. The effect of haemorrhage depends on the rate and amount of blood loss.
Hypovolemic shock is the most common type of shock in clinical practice. A normal healthy adult can lose half a liter (10%of blood volume) without significant symptoms, but loss of 25% or more of the blood volume results in significant hypovolemia.
cardiogenic Shock:
This is a shock that results from severe depression of cardiac performance, primarily resulting from pump failure of the right or left ventricle.
The most common cause :
Most common Cause is left ventricular MI,
shock occurs when > 40% of ventricular mass is damaged, and
mortality rate may reach 80% of affected individuals. 
Causes of Cardiogenic Shock:
- Acute MI occurs if ≥ 40% of ventricular mass are involved,-Ventricle outflow obstruction, e.g., aortic stenosis, hypertrophic cardiomyopathy
-Reduction in cardiac output, e.g. Aortic or mitral regurgitation
- Arrhythmia
-Cardiac tamponade (gross fluid accumulation in the pericardial space)
-Tension pneumothorax (gas accumulation in pleural space)
-Massive pulmonary embolism
-Severe pulmonary hypertension
Distributive Shock:
Refers to subtypes of shock caused by profound
peripheral vasodilatation despite normal or high cardiac output and
characterized by, inadequate perfusion of tissues due to mis-distribution
of blood flow, and the blood is not reaching the tissues adequatly.
Causes of Distributive Shock:
Septic shock, anaphylactic shock, neurogenic shock
Septic Shock:
Serious bacterial infections caused by Gram-negative organisms, e.g., E. Coli and gram positive bacteria (Bacteroides), or fungi. Pathogenesis:
Cell walls of microorganisms contain endotoxins which are activate inflammatory mediators, that induce vasodilatation & increase capillary permeability resulting in reduced cardiac output and presenting with shock.
Anaphylactic Shock:
Defined as a wide spread vasodilatation and
vascular permeability, that results from the widespread allergic reaction
to an antigen. This hypersensitivity reaction is life threatening. 
The pathophysiology is due to re-exposure to antigen, resulting in degradation of IgE bound mast cells and basophils. The released contents of granule lead to vasodilatation, Increased vascular permeability, broncho-constriction and increased mucus production.
Neurogenic Shock:
Shock that results from the loss or suppression of
sympathetic tone causing massive vasodilatation in the venous
vasculature, venous return to the heart, cardiac output, and the most
common aetiology include: spinal cord injury above T6 level, and
severe pain. 
Clinical Features of Shock:
Low blood pressure, rapid, weak pulse, low urine output, confusion and CNS disturbance, cold extremities, cyanosis and loss of skin elasticity.
Systemic Changes in Shock:
All systems are affected, in a trial of adaptation, but the net results are:
Lungs:
Changes in the rate and depth of breathing, metabolic acidosis which stimulates respiratory centre resulting in hyperventilation and adult respiratory distress syndrome (ARDS).
Kidneys:
The secretary function of the kidneys is always disturbed in shock. This is due to the circulatory collapse and hypotension but it may be aggravated by the secretion of renin by the kidney itself, aldosterone by the adrenal and antidiuretic hormone by the posterior pituitary gland. These hormones are secreted in an attempt to retain fluid and restore the blood volume as a compensatory mechanism.
Adrenal Gland:
In addition to the release of aldosterone in response to changes in kidney function and fluid electrolyte disorders, adrenal gland also secretes gluococorticoids hormones.
GIT:
Acute ulceration of the stomach and duodenum may complicate shock, the mechanism is not known. This is called Curling's or stress ulcers and may be due to increased stress hormones.
CNS:
During the compensated phase of shock, cerebral ischemia is associated with changes in the state of consciousness (confusion), and when the blood pressure falls to levels below 50-60 mHg, the brain suffers serious ischaemic damage.
Stages of Shock:
Initial Stage:
In this stage tissues are under-perfused and associated with decreased cardiac output, increased anaerobic metabolism and lactic acid.
Compensatory Stage:
Reversible condition in which sympathetic system is activated, in an attempt to compensate the hypoperfusion state.
Progressive Stage:
State of progress in the compensatory with lactic acid production and development of metabolic acidosis. Irreversible or Refractory Stage: In this stage, there is cellular necrosis and multiple organ dysfunction syndromes may occur (death is expected).
Theoretically, at some point in its evolution shock becomes irreversible due to the severity of vascular impairment and tissue damage. No certain indications are available to say when this point is reached.
Measurements of blood pressure and central venous pressure indicate the severity of the vascular disturbance, but may respond to treatment, unfortunately, when reaching this point death is highly sexpected.
Outcome of Shock:
There are three possible outcomes :complete recovery after convalescence, survival with permanent damage, and death.