Shock

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• True hypovolemia
  • Bleeding i.e hemorrhagic shock
  • Fluid loss (e.g. diarrhoea, vomiting, bowel obstruction, ‘third’ spacing)
• Effective hypovolemia (distributive) where the vascular space increases but insufficient fluid is there to fill it.
  • Anaphylaxis
  • Neurogenic shock
  • Septic shock
• Pump problems
  • Cardiogenic shock (e.g. post-MI), cardiomyopathy
  • Mechanical (e.g. cardiac tamponade, tension pneumothorax), aortic stenosis
  • Electrical eg VT or AF or most fundamentally VF

In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses four types of shock: hypovolaemic, cardiogenic, distributive and obstructive shock:^[1]

• Hypovolemic shock – This is the most common type of shock and based on insufficient circulating volume. Its primary cause is loss of fluid from the circulation from either an internal or external source. An internal source may be hemorrhage. External causes may include extensive bleeding, high output fistulae or severe burns.
• Cardiogenic shock – This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include arrhythmias, cardiomyopathy, congestive heart failure (CHF), contusio cordis or cardiac valve problems.
• Distributive shock – As in hypovolemic shock there is an insufficient intravascular volume of blood. This form of “relative” hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance. Examples of this form of shock are:
  • Septic shock – This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative bacteria i.e. Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body. Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins produce a similar syndrome.
  • Anaphylactic shock – Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability.
  • Neurogenic shock – Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension.
• Obstructive shock – In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest. Several conditions result in this form of shock.
  • Cardiac tamponade in which blood in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
  • Tension pneumothorax. Through increased intrathoracic pressure, blood flow to the heart is prevented (venous return).
  • Massive pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs and hinders the return of blood to the heart.
  • Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

Recently a fifth form of shock has been introduced:

• Endocrine shock based on endocrine disturbances.
  • Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
  • Thyrotoxicosis may induce a reversible cardiomyopathy.
  • Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.
  • Relative adrenal insufficiency in critically ill patients where present hormone levels are insufficient to meet the higher demands

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Shock is a life-threatening condition and must be treated as such irrespective of the underlying cause.

• Cardiogenic shock

• Arrhythmic

• Sinoatrial block
• Atrioventricular block
• Ventricular tachycardia
• Supraventricular tachycardia

• Mechanical

• Hypertrophic cardiomyopathy
• Acute mitral regurgitation
• Ventricular septal defect

• Myopathic

• Cardiomyopathy
• Myocardial contusion
• Myocardial infarction
• Myocarditis
• Postischemic myocardial stunning
• Septic myocardial depression
• Hypothyroidism

• Pharmacologic

• Anthracyclines
• Calcium channel blockers

• Obstructive shock

• Decreased cardiac compliance

• Cardiac tamponade
• Constrictive pericarditis
• Idiopathic
• Postinfarction free wall rupture
• Trauma
• Tumor
• Uremia

• Decreased ventricular preload

• Intrathoracic tumor
• Mechanical ventilation with positive end-expiratory pressure (PEEP)
• Tension pneumothorax

• Increased ventricular afterload

• Aortic dissection
• Pulmonary embolism
• Acute pulmonary hypertension
• Saddle embolus

• Hypovolemic shock

• Fluid depletion

• Dehydration
• Diarrhea
• Extensive burns
• Polyuria
• Vomiting
• Third spacing (as in endometritis, pancreatitis, peritonitis, pleural effusions)

• Hemorrhage

• Ectopic pregnancy
• Gastrointestinal bleeding
• Perforated peptic ulcer
• Post-procedural or post-surgical
• Retroperitoneal hemorrhage
• Rupture ovarian cyst
• Trauma

• Distributive shock

• Sepsis
• Toxic shock syndrome
• Anaphylactic or anaphylactoid reaction
• Neurogenic shock
• Adrenal crisis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

There are four stages of shock, although shock is a complex and continuous condition and there is no sudden transition from one stage to the next.^[1]

Initial

During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.

Compensatory (Compensating)

This stage is characterized by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO₂). CO₂ indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin–angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.

Progressive (Decompensating)

Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body’s metabolic acidosis, the arteriolar and precapillary sphincters constrict such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.

Refractory

At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.

The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.

Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in re-infused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.