Physiological Stages In Shock Clinical Features And Complications Notes

Shock

Shock is a clinical syndrome of cardiovascular collapse characterised by an acute reduction of effective circulating blood volume (hypotension) and an inadequate perfusion of cells and tissues (hypoperfusion).

There are 3 major forms of shock: hypovolaemic, cardiogenic and septic.

Read And Learn More: General Pathology Notes

All forms of shock involve basic mechanisms as:

1. Reduced effective circulating blood volume
2. Impaired tissue oxygenation, and
3. Release of proinflammatory mediators.

Shock is divided into 3 stages: 

1. Initial reversible stage (compensated shock),
2. Progressive decompensated shock, and
3. Finally the stage of irreversible decompensated shock.

Shock causes morphologic changes in different organ systems, notably in the brain (hypoxic encephalopathy), heart (haemorrhage and necrosis), lungs (ARDS), kidneys (tubular necrosis), adrenals (haemorrhage and necrosis), liv er (focal necrosis), gut (haemorrhagic gastro enteropathy) and other organs.

Clinically, shock is characterised by low blood pressure, low body temperature, feeble pulse, shallow respiration, pale face and cold clammy skin. When left untreated, shock results in multiple organ dysfunction syndrome.

Obstructive Circulatory Disturbances:

This group of disturbances includes thrombosis, embolism and infarction.

Thrombosis Definition and Effects:

Thrombosis is the process of the formation of solid mass in circulation from the constituents of flowing blood; the mass itself is called a thrombus.

A term commonly used incorrectly as synonymous with thrombosis is blood clotting—while thrombosis is characterised by events that essentially involve activation of platelets, the process of clotting involves only conversion of soluble fibrinogen to insoluble polymerised fibrin. Besides, clotting is also used to denote coagulation of blood in vitro for example In a test tube. ‘

Haematoma is the extravascular accumulation of blood for example Into the tissues. Haemostatic plugs are the blood clots formed in healthy individuals at the site of bleeding for example In injury to the blood vessel. In other words, haemostatic plug at the cut end of a blood vessel may be considered the simplest form of thrombosis.

Haemostatic plugs are useful as they stop escape of blood and plasma, whereas thrombi developing in the unruptured cardiovascular system may be life-threatening by causing

One of the following harmful effects:

•  Ischaemic injury: Thrombi may decrease or stop the blood supply to part of an organ or tissue and cause ischaemia which may subsequently result in infarction.
•  Thromboembolism: Thrombus or its part may get dislodged and be carried along in the bloodstream as embolus to lodge in a distant vessel.

Pathophysiology (Stages of Shock)

Although deterioration of the circulation in shock is a progressive and continuous phenomenon and compensatory mechanisms become progressively less effective, shock is divided arbitrarily into 3 stages

1. Compensated (non-progressive, initial, reversible) shock
2. Progressive decompensated shock
3. Irreversible decompensated shock

1. Compensated (Non-Progressive, Initial, Reversible):

Shock In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood so that the vital organs (brain and heart) are adequately perfused and oxygenated.

This is achieved by activation of various neurohormonal mechanisms causing widespread vasoconstriction, and by fluid conservation by the kidney. If the condition that caused the shock is adequately treated, the compensatory mechanism may be able to bring about recovery and re-establish the normal circulation; this is called compensated or reversible shock.

These compensatory mechanisms are as under:

• Widespread vasoconstriction: In response to reduced blood flow (hypotension) and tissue anoxia, the neural and humoral factors (for example Aroreceptors, chemoreceptors, catecholamines, renin, and angiotensin- are activated.
  • All these bring about vasoconstriction, particularly in the vessels of the skin and abdominal viscera.
  • Widespread vasoconstriction is a protective mechanism as it causes increased peripheral resistance, increased heart rate (tachycardia) and increased blood pressure.
  • However, in septic shock, there is initial vasodilatation followed by vasoconstriction.
  • Besides, in severe septic shock, there is elevated level of thromboxane A₂ which is a potent vasoconstrictor and may augment the cardiac output along with other sympathetic mechanisms.
  • Clinically, cutaneous vasoconstriction is responsible for cool and pale skin in initial stage of shock.
• Fluid conservation by the kidney:  In order to compensate the actual loss of blood volume in hypovolaemic shock, the following factors may assist in restoring the blood volume and improve venous return to the heart:
  • Release of aldosterone from the hypoxic kidney by activation of renin-angiotensin-aldosterone mechanism.
  • Release of ADH due to decreased effective circulating blood volume.
  • Reduced glomerular filtration rate (GFR) due to arteriolar constriction.
  • Shifting of tissue fluids into the plasma due to lowered capillary hydrostatic pressure (hypotension).
• Stimulation of adrenal medulla: In response to low cardiac output, adrenal medulla is stimulated to release excess of catecholamines (epinephrine and nor-epinephrine) which increase heart rate and try to increase cardiac output.

2. Progressive Decompensated Shock:

This is a stage when the patient suffers from some other stress or risk factors (for example ,Pre-existing cardiovascular and lung disease) besides persistence of the shock condition, that causes progressive deterioration.

The effects of resultant tissue hypoperfusion in progressive decompensated shock are as under:

• Pulmonary hypoperfusion:  Decompensated shock worsens pulmonary perfusion and increases vascular permeability resulting in tachypnoea and adult respiratory distress syndrome
  (ARDS).
• Tissue ischaemia:  Impaired tissue perfusion causes a switch from aerobic to anaerobic glycolysis resulting in metabolic lactic acidosis. Lactic acidosis lowers the tissue pH which, in turn, makes the vasomotor response ineffective.

This results in vasodilatation and peripheral pooling of blood. Clinically, at this stage, the patient develops confusion and worsening of renal function.

3. Irreversible Decompensated Shock:

When the shock is so severe that in spite of compensatory mechanisms and despite therapy and control of etiologic agent which caused the shock, no recovery takes place, it is called decompensated or irreversible shock.

Its effects due to widespread cell injury are as follows:

• Progressive vasodilatation: During later stages of shock, anoxia damages the capillary and venular wall while arterioles become unresponsive to vasoconstrictors listed above and begin to dilate.
• Vasodilatation results in peripheral pooling of blood which further deteriorates the effective circulating blood volume.
• Increased vascular permeability:  Anoxic damage to tissues releases proinflammatory mediators which cause increased vascular permeability. This results in escape of fluid from circulation into the interstitial tissues thus deteriorating effective circulating blood volume.
• Myocardial depressant factor (MDF):  Progressive fall in the blood pressure and persistently reduced blood flow to myocardium causes coronary insufficiency and myocardial ischaemia due to release of myocardial depressant factor (MDF). This results in further depression of cardiac function, reduced cardiac output and decreased blood flow.
• Worsening pulmonary hypoperfusion:  Further pulmonary hypoperfusion causes respiratory distress due to pulmonary oedema, tachypnoea and adult respiratory distress syndrome (ARDS).
• Anoxic damage to heart, kidney and brain:  Progressive tissue anoxia causes severe metabolic acidosis due to anaerobic glycolysis. There is release of proinflammatory cytokines and other inflammatory mediators and the generation of free radicals.
• Since highly specialised cells of the myocardium, proximal tubular cells of the kidney, and neurons of the CNS are dependent solely on aerobic respiration for ATP generation, there is ischaemic cell death in these tissues.
• Hypercoagulability of blood:  Tissue damage in shock activates coagulation cascade with release of clot promoting factor, thromboplastin and release of platelet aggregator, ADP, which contributes to the slowing of blood-stream and vascular thrombosis.

In this way, hypercoagulability of blood with consequent microthrombi impairs the blood flow and cause further tissue necrosis. Clinically, at this stage the patient has features of coma, worsened heart function and progressive renal failure due to acute tubular necrosis.

Morphologic Features:

Eventually, shock is characterised by multisystem failure. The morphologic changes in shock are due to hypoxia resulting in degeneration and necrosis in various organs. The major organs affected are the brain, heart, lungs and kidneys. Morphologic changes are also noted in the adrenals, gastrointestinal tract, liver and other organs.

The predominant morphologic changes and their incidence are described below:

• Hypoxic Encephalopathy: Cerebral ischaemia in compensated shock may produce an altered state of consciousness. However, if the blood pressure falls below 50 mmHg as occurs in systemic hypotension in prolonged shock and cardiac arrest, brain suffers from serious ischaemic damage with loss of cortical functions, coma, and a vegetative state.
  • Grossly: The area supplied by the most distal branches of the cerebral arteries suffers from severe ischaemic necrosis which is usually the border zone between the anterior and middle cerebral arteries.
  • Microscopically: The changes are noticeable if ischaemia is prolonged for 12 to 24 hours. Neurons, particularly Purkinje cells, are more prone to develop the effects of ischaemia. The cytoplasm of the affected neurons is intensely eosinophilic and the nucleus is small pyknotic. Dead and dying nerve cells are replaced by gliosis.
• Heart In Shock: The heart is more vulnerable to the effects of hypoxia than any other organ. Heart is affected in cardiogenic as well as in other forms of shock. There are 2 types of morphologic changes in heart in all types of shock:

• • Haemorrhages and necrosis There may be small or large ischaemic areas or infarcts, particularly located in the subepicardial and subendocardial region.
  • Zonal lesions These are opaque transverse contraction bands in the myocytes near the intercalated disc.
• Shock Lung: Lungs due to dual blood supply are generally not affected by hypovolaemic shock but in septic shock, the morphologic changes in lungs are quite prominent termed ‘shock lung’.
  • Grossly: The lungs are heavy and wet.
  • Microscopically: Changes of adult respiratory distress syndrome (ARDS) are seen. Briefly, the changes include congestion, interstitial and alveolar oedema, interstitial lymphocytic infiltrate, alveolar hyaline membranes, thickening and fibrosis of alveolar septa, and fibrin and platelet thrombi in the pulmonary microvasculature.
• Shock Kidney: One of the important complications of shock is irreversible renal injury, first noted in persons who sustained crush injuries in building collapses in air raids in World War II. Renal ischaemia following systemic hypotension is considered responsible for renal changes in shock. The end-result is generally anuria and death.
  • Grossly: The kidneys are soft and swollen. The sectioned surface shows blurred architectural markings.
  • Microscopically: Tubular lesions are seen at all levels of the nephron and are referred to as acute tubular necrosis (ATN) which can occur following other causes besides shock . If extensive muscle injury or intravascular haemolysis is also associated, peculiar brown tubular casts are seen.

• Adrenals In Shock: The adrenals show stress response in shock. This includes release of aldosterone in response to hypoxic kidney, release of glucocorticoids from adrenal cortex and catecholamines like adrenaline from the adrenal medulla. In severe shock, acute adrenal haemorrhagic necrosis may occur.
• Haemorrhagic Gastroenteropathy: The hypoperfusion of the alimentary tract in conditions such as shock and cardiac failure may result in mucosal and mural infarction called haemorrhagic gastroenteropathy. This type of non-occlusive ischaemic injury of bowel must be distinguished from full-fledged infarction in which deeper layers of the gut (muscularis and serosa) are also damaged. In shock due to burns, acute stress ulcers of the stomach or duodenum may occur and are known as Curling’s ulcers.
  • Grossly: The lesions are multifocal and widely distributed throughout the bowel. The lesions are superficial ulcers, reddish purple in colour. The adjoining bowel mucosa is oedematous and haemorrhagic.
  • Microscopically: The involved surface of the bowel shows dilated and congested vessels and haemorrhagic necrosis of the mucosa and sometimes submucosa. Secondary infection may supervene and condition may progress into pseudomembranous enterocolitis.
• Liver In Shock:
  • Grossly: Faint nutmeg appearance is seen.
  • Microscopically: Depending upon the time gap between injury and cell death, ischaemic shrinkage, hydropic change, focal necrosis, or fatty change may be seen. Liver function may be impaired.

Other Organs: Other organs such as lymph nodes, spleen and pancreas may also show foci of necrosis in shock. In addition, patients who survive the acute phase of shock succumb to overwhelming infections due to altered immune status and impaired host defence mechanism

Clinical Features and Complications:

The classical features of decompensated shock are characterised by depression of four vital processes:

• Very low blood pressure
• Subnormal temperature
• Feeble and irregular pulse
• Shallow and sighing respiration

In addition, the patients in shock have pale face, sunken eyes, weakness, cold and clammy skin.

Life-threatening complications in shock are due to hypoxic cell injury resulting in immunoinflammatory responses and activation of various cascades (clotting, complement, kinin).

These include the following:

• Acute respiratory distress syndrome (ARDS)
• Disseminated intravascular coagulation (DIC)
• Acute renal failure (ARF)
• Multiple organ dysfunction syndrome (MODS)

With the progression of the condition, the patient may develop stupor, coma and death.