Shock

Shock

¨ Shock is a cardiovascular collapse and is defined as: systemic hypotension owing to reduction either in cardiac output or in effective circulating blood volume.

¨ It is the consequence of a number of potentially lethal clinical events e.g. severe hemorrhage, extensive trauma or burns, large myocardial infract, massive lung embolism and sepsis.

¨ It is the end result of hypotension followed by tissue hypo perfusion and cellular hypoxia.

¨ Although the hypoxia and the metabolic effects cause, initially, reversible cell injury, persistence of the shock causes irreversible cell injury and can culminate in the death of the individual.

Shock can be classified into 3 general categories:

1. Cardiac: results from heart pump failure cause by intrinsic myocardial damage, ventricular arrhythmias, cardiac tamponate or outflow obstruction (e.g. lung embolism)

2. Hypovolumoic: results from hemorrhage or fluid loss e.g. trauma, burns.

3. Septic : systemic microbial infection usually caused by gram negative bacteria and sometimes by G + and fungal infection.

Pathogenesis of shock

¨ The septic shock is mostly due to G- bacteria which produce endotoxin (endtoxic shock) which are bacterial wall lipopolysaccharide (LPS) released when the wall is degraded by inflammation. The LPS consist of toxic fatty acids core and a complexed polysaccharide coat (like Ag O) unique to every bacterial specie. Injecting LPS along can produce septic shock

¨ G+ have analogous molecules.

¨ The LPS complexed with blood proteins bind with CD14 on monocytes system, endothelial cells and other cells activating them. It also activates the complement system (this is intended to help bacterial eradication)

¨ Monocytes respond by producing TNF which in turn induce IL-1 synthesis. Both these cytokines act on endoth, to produce other cytokines (IL6-8) and induce also adhesive molecules. This cascade of cytokines enhance a local acute inflammation response and improve clearance of the infection.

The cascade: TNF—IL-1---IL-6,8—PAF AND NO-----stimulate increased permeability, vasodilatation and coagulation cascade.





Higher doses of LPS produce higher level of cytokines and other mediators which result in:

1. Systemic vasodilatation (hypotension)

2. Diminished myocardial contractility

3. Wide spread of endoth, injury and activation causing systemic leukocyte adhesion and lung capillary damage with ARDS.

4. Activation of the coagulation system culminating in DIC.

¨ The hypotension is due to widespread vasodilatation and heart pump failure. The DIC results in multiorgan system failure in which kidneys, brain and liver are the most important resented organs.

¨ Septic shock can be called systemic inflammation syndrome. The pharmacological use of anti-inflammatory drugs like steroids and antibiotics is of a great use to control the septic shock.

¨ Super antigens (bacterial proteins) like that of staphylococcus can produce a shock similar to that of septic one.



Stages of shock

Shock is a progressive disorder that, if not corrected leads to death. It evolves into 3 general stages:
Initial non progressive phase in which compensatory mechanism are activated and perfusion of vital organs are maintained.


Progressive phase with tissue hypoxia and worsening circulatory and metabolic imbalance like acidosis.
Irreversible stage which sets in after the body has incurred cellular and tissue injury so severe that if corrected the hypovolumia survival is not possible.

I.In the first phase, neuro-ormonal mechanism maintain cardiac output and blood pressure. These include the bar receptor reflex, increase sympathetic tone, release of catecholamine, ADH, renin-angiotensine reflex.

¨ All these produce tachycardia, peripheral vasoconstriction (responsible for the pallor and coolness of the skin.) In the septic shock there is vasodilatation and hence warm flushed skin.

¨ Coronary and cerebral circulation is less sensitive to these compensatory sympathetic responses and have normal blood flow.

II.If the underlying cause is not corrected the shock passes to the progressive phase in which there are widespread hypoxia of the tissue. With the oxygen deficit the aerobic respiration is replaced by anaerobic glycolysis and consequent lactic acid formation, metabolic acidosis that culminate in PH reduction and blunting of the vasomotor responses. The latter induce arteriolar vasodilatation and pooling of blood to the microcirculation. The peripheral pooling not only worsen the cardiac output but also puts endoth, at risk for developing anoxic injury with subsequent DIC.

¨ The widespread tissue anoxia does not spare the vital organs which begin to fail. The patient is confused and urinary output decline.

III.Unless intervened, the shock enters in an irreversible stage.

The widespread cell injury is reflected by lysosomal enzyme leakage, further aggravating the shock:

1) Myocardial contractile worsens due to NO synthesis

2) If the ischemic bowel allows intestinal flora to enter the circulation and endotoxic shock superimposes.

¨ Complete renal shutdown due top tubular necrosis.

¨ Thereafter, despite heroic measures death ensues.

Management and prognosis.

¨ Hypovolumic shock in young health individual has good prognosis in 80% to 90% of the cases if properly managed.

¨ Large myocardial infract and gram negative septic shock carry mortality rate up to 75% of the cases, even with the best care currently available.