Shock is the failure of the circulatory system for nutrition and tissue oxygenation. It is a state of inadequate tissue perfusion. This poor perfusion tissue leads to cell dysfunction and eventually death.


Septic shock

Depends essentially on the balance between its basic components: cardiac pump efficiency, adequate blood volume and vascular tone right. A flaw in any of them leads to imbalance that leads to circulatory shock.

A good circulatory status depends on the balance between cardiac sufficiency, blood volume and vascular tone. Rupture of the above can lead to shock.

Major deficiencies


alterations in vascular tone.

deficiencies in cardiac sufficiency.

Hypovolemic Shock

It installs as a consequence of reduced blood volume, evidence of which is the emergence of a heightened adrenergic activity as a clearing attempt in front of the decrease in cardiac output and decreased cardiac output and blood pressure caused by those sharp reduction. The loss of 30% of total blood volume triggers a hypovolemic shock. The blood shortage is the main cause of hypovolemic shock.

The internal or external bleeding provided the largest contingent of this variety of hypovolemic shock, called hemorrhagic shock. Plasma losses, internal or external, are also an important factor causing hypovolemic shock.

You lose so evident in the large burns, severe expediencies in the cavity exudates, etc.. Extracellular fluid losses to the outside, resulting from uncontrollable vomiting or severe diarrhea, and those to the third space in bowel obstruction, are another cause of hypovolemic shock due to dehydration.

Neurogenic shock

It is the result of a disturbance in the systemic capillary vasomotor failure. In this type of shock the heart and blood volume remain normal, but there is circulatory failure by the lack of an adequate vascular tone involves mainly the capillary circulation.



In Vaso-plegia the cause of circulatory failure is the disparity between an increased capacity of the vascular bed and blood volume, a sudden and intense vasodilation installed by direct influence of the agent acting via neurogenic or humoral (vasodilator substances) producing fall perifornical arteriolar resistance and decreased precapillary sphincter (which is flooded with blood the capillary bed) and blood stasis alters tissue nutrition. This type of shock seen in anaphylactic reactions, in vasodilation produced by the release of vasoactive substances of the type histamine, bradykinin; in psychotropic poisoning (barbiturates), ganglioplegics or anesthetics, pain.

Persistent and excessive vasoconstriction is installed first and metarterioles arterioles, precapillary sphincters and venules, and blocks the blood supply by decreasing the supply circulation to the tissues, causing severe hypoxic ischemic cell injury.

After ischemia, there is the release of local mediators vasotropics vasodilator, which causes total deterioration vasomotion microcirculation, relaxing and precapillary sphincters metarterioles with consequent flooding of the capillary bed and hypoxic stasis.

It is seen in severe infections, the action of vasoconstrictor drugs, and use of vasopressors in the treatment of shock.

Cardiogenic Shock

In this type of shock is circulatory failure triggered or maintained by an acute failure in the heart pumping, dropping the debt in less than half the normal value.

It is the heart pump failure, which is associated with arterial vasoconstriction induced by baroreceptor front of the small injection volume and a marked dilatation of the disability sector cardiac venous blood return pump. The cardiac pump failure may be primary in origin, organic or functional injury of the heart itself, or secondary to myocardial functional impairment, caused by diseases of other systems.

The main causes of cardiogenic shock include myocardial infarction (in this case, the gravity and intensity of the shock depends on the extent of the injury) acute heart failure, arrhythmias that trigger to turn the systoles Shock inefficient (eg. The If tachycardia or fibrillation); myocarditis by altering myocardial fiber and hence its contractile capacity.

It is a state of impaired production of cellular energy by the action of bacterial toxins on the cell membrane, mainly injures and destroys the mitochondria, which cut the cycle of oxidative phosphorylation. Injure lysosomal membranes, thereby, releasing hydrolytic enzymes in the cell that destroy it.

Endotoxins activate the complement system. C5a interacts with the membrane of neutrophil leukocytes altering enough to cause disruption of the lysosomal membrane.

The head of irreversible cell damage and abnormalities of the microcirculation that are observed in septic shock, it would be the massive release of lysosomal enzymes into the circulation by the action of endotoxins. The septic is an acquired disorder of cellular metabolism by different infectious agents.

The main trigger injury process occurs at the mitochondrial level. It disrupts the energy cycle and cell installed multiorgan dysfunction.

General Pathophysiology

But the ultimate consequences are almost same for all: decreased cardiac output and cell injury, a result is reached by three mechanisms: a) reduction of venous return (bleeding), b) decreased myocardial contractility (heart failure), c) combination of both (sepsis).

Reduced venous return to active bleeding, rapid dehydration, plasmapheresis and acute cardiac tamponade. Decreased myocardial contractility occurs in heart failure acute heart attack in parodistic tachycardia, extreme bradycardia in the terminal phase of chronic heart failure.

Slowing of the stimulation of vagal cardioinhibitory center and reduced the inhibition of sympathetic cardioaccelerator and vasoconstrictor centers. The result of this is the cardiac acceleration, increased myocardial contractile power and arteriolar vasoconstriction that occasionally happen in the skin, muscles and viscera, except the brain and myocardium.

It makes stimulating the adrenal medulla thus increases the secretion of adrenaline and noradrenaline which further contributes to vasoconstriction

Causes of shock:



Heart failure.

To maintain homeostasis:

Fall in cardiac output.



A complex hyperactivity hypothalamus - pituitary as a result of impulses coming from the cortex and the periphery: produces a hypersecretion of ACTH that stimulates the adrenal cortex, resulting hypersecretion of glucocorticoids leads to higher blood glucose on the roads: gluconeogenesis and insulin resistance, the hypersecretion of mineralocorticoids produces water retention and sodium and potassium excretion at the kidney.

The mineralocorticoids and glucocorticoids increase the sensitivity of arterioles to catecholamines. The anterior pituitary thyrotropin secretion increases with increased production of thyroid hormone that tends to intensify the use of oxygen to the tissues. At the level of the posterior pituitary gland increases the secretion of antidiuretic hormone, which stimulates water reabsorption in the kidney.

At the fall of the renal capillary perfusion occurs via the baroreceptors and renin secretion juxtaglomerulars thereby generates angiotensin. Your arteriolar vasoconstrictor effect is in addition to catecholamines, also stimulates the production of angiotensin and mineralocorticoid aldosterone. The purpose of these changes is to maintain homeostasis face the new situation, which is achieved by three facts:

Rehabilitation of the continent to a reduced vascular, to which is reached by vasoconstriction.

Decreased normal loss of fluid and electrolytes that is expressed by oliguria due to renal vasoconstriction, the action of antidiuretic hormone and aldosterone.

Increased frequency and of the heart in an attempt to keep the minute volume.

The survival of aerobic cells depends on the availability of substrates and oxygen by the mitochondria which supplies the phosphate for energy needs and uses much of the oxygen supplied.

Cell death in the Shock come through inhibition of electron transport system caused by hypoxia and ischemia or direct injury of the cell due to endogenous or bacterial toxins.

Is swelling of the cell associated with increased intracellular sodium then appears edema of the endoplasmic reticulum and nuclear chromatin clustering. Mitochondria are beginning to provide expansion and clusters of electron dense material and calcium deposition.

In contrast to hypoxia, in endotoxic shock engagement of the mitochondrial membrane is much more severe and earlier, altering the membrane calcium transport, and inhibiting the synthesis of ATP and mitochondrial ATPase.

In septic shock, the commitment of the mitochondrion is the first change in the cell.

The injury of lysosomes with release of hydrolytic enzymes leading to irreversible shock state.

The cardiac depression observed in the shock could be an indirect manifestation of the effects of lysosomal hydrolases, fall in cardiac output and maintenance of the vicious circle of "Shock and described.

Stages of Shock

Stage I: Hypotension compensated.

Hypotension may be due to decreased cardiac output or vasodilation. The initial event in the great majority of cases of Shock is a fall in cardiac output rather than vasodilation.

The fall in minute volume and hypotension set in motion compensatory mechanisms, which improve the low blood pressure and maintain traffic flow of vital organs like the heart and brain.

Stage II: Decreased perfusion tissue.

Compensatory mechanisms to maintain perfusion of vital organs are functioning at its peak, but still insufficient.

The renal hypoperfusion reduces urine output volume, and subjects with coronary diseases signs of ischemia. The external condition of the patient shows marked sympathetic activity, with excess production of catechols skin with cyanosis, cold sweats and clammy, and poor skin perfusion.

Stage III: failure of the microcirculation with cellular injury.

The excessive and prolonged reduction of tissue perfusion produces a significant alteration in the function of cell membranes, aggregation of blood cells with marked circulatory disturbance in capillary flow, marked decrease in blood flow induce cell damage. Blood pressure gradually falls to critical levels at which they assume at perfución renal organ leads to the installation of an acute tubular necrosis.

The gastrointestinal tract ischemia produces necrosis of the intestinal epithelium to absorb bacteria and toxic products that damage the other vascular endothelium causing a syndrome of disseminated intravascular coagulation.

Severe metabolic acidosis resulting from anaerobic metabolism, further worsening the state of hypotension, this hypotension reduces coronary artery perfusion, especially in those patients with coronary artery disease.

This hyperfusion tissue cause cellular damage sustained.

The capillary endothelial injury leads to loss of fluids and proteins into the extravascular behavior exacerbating hypovolemia and hypotension. The cell membrane injury by ischemia and acidosis occurs with disruption of lysosomes loss of enzymes, alteration of the sodium pump with ionic imbalance, reduction and then loss of energy reserves - dependent, thus reaching to cell death.

Consequences of shock

- Alterations in the cell metabolism.

- Cell death from lack of oxygen and nutrients.

Etiopathogenesis - the causes.

Blood loss and intravascular volume decrease.

Acute bleeding: gastrointestinal, vascular lesions.

Hypovolemic Shock

Loss of liquids:





Relative hypovolemia:

neurogenic vasodilatation, spinal anesthesia.

Metabolic toxic Gram-negative sepsis.

Neurogenic Shock


Myocardial infarction

Myocarditis, heart failure: hypoxia, sepsis, drugs.

Allergic Shock

Microcirculatory dysfunction:


Septic Shock

Failure tissue perfusion.

Suffering and cell death.

Disseminated intravascular coagulation.

Cellular injury.


Four main types of shock, all of which lead to a common end point is the perfusion tissue, pain and cell death.

Pathophysiological Rating

Hypovolemic Shock

Cardiogenic shock.

Neurogenic shock.

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