Shock:
Introduction: shock is the most common and therefore the most important causes of death among surgical patients. Death may occur rapidly as a result of a profound state of shock or be delayed, resulting from the consequences of organ ischamia and reperfusion injury.
Shock : It is a systemic state of low tissue perfusion, which is inadequate for normal cellular respiration. With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism .If perfusion is not restored in a timely fashion, cell death ensues .
Classification of shock
based on the initiating mechanism .All states are characterized by tissue systemic hypoperfusion and different states may coexist within the same patient.
*hypovolaemic* cardiogenic *obstructive*distributive *endocrine
Hypovolaemic shock: it is caused a reduced circulating volume. It may be due to haemorrhagic or non-haemorrhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration)and excessive fluid loss because of vomiting, diarrhea, urinary loss(e.g.diabetes) , evaporation and third spacing, in which fluid is lost into the gastrointestinal tract and interstitial spaces, as for example bowel obstruction or pancreatitis. Hypovolaemia is probably the most common form of shock and is to some degree a component of all other forms of shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of cause.
Cardiogenic shock : Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues. Causes of cardiogenic shock include myocardial infarction, cardiac dysrhthmias, valvular heart disease, blunt myocardial injury and cardiomyopathy. Cardiac inssufficency may also be caused by myocardial depression resulting from endogenous factors (e.g. bacterial and humoral agents released sepsis) or exogenous factor such as pharmaceutical agents drug abuse. Evidence of venous hypertension with evidence of pulmonary or systemic oedema may coexist with the classic signs of shock.
Obstructive shock:
In obstructive shock there is a reduction in preload because of mechanical obstruction of cardiac filling. Common causes of obstructive shock include cardiac tamponade, tension pneumothrax, massive pulmonary embolus and air embolus. In each case there is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output.
Distributive shock
Distributive shock describes the pattern of cardiovascular responses characterizing a variety of conditions including septic shock, anaphylaxis and spinal cord injury. Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate Afterload and a resulting abnormally high cardiac output.
In anaphylaxis ,vasodilatation is caused by histamine release, where as in high spinal cord injury there is failure sympathetic outflow and adequate vascular tone(neurogenic shock). The cause in sepsis is less clear but is related to the release of bacterial products (endotoxins )and the activation of cellular and humoral components of the immune system. There is maldistribution of blood flow at a microvascular level with arteriovenous shunting and dysfunction of the cellular utilization of oxygen. In the later phases of septic shock there is hypovolaemia from Fluid loss into the interstitial spaces and there may be concomitant myocardial depression, which complicates the clinical picture \
Table1 cardiovascular and metabolic characteristics of shock
hypovolaemia cardiogenic obstructive distributive
Cardiac output low low low high
Vascular resistance high high high low
Venous pressure low high high low
Mixed venous saturation low low low high
Base deficit high high high high
Endocrine shock :it is may present as a combination of hypovolaemic, cardiogenic and distributive shock. Causes of endocrine shock include hypo and hyperthyroidism and adrenal insufficiency. Adrenal insufficiency 1eads to shock as a result of hypovolaemia and a poor response to circulating and exogenous catecholamines. Adrenal insufficiency may result from preexisting Addisons disease or it may be a relative insufficiency caused by a pathological disease state such as systemic sepsis.
Severity of shock :
Compensated shock There is adequate compensation to maintain the central blood volume and preserve flow to the kidneys ,lungs and brain . Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines )there may be no other physical signs of hypovolemia.There is a systemic metabolic acidosis and activation of humoral and cellular elements within the underperfused organs.
Decompesation Further loss of circulating volume overloads the bodys compensatory mechanisms and there is progressive renal ,respiratory and cardiovascular decompensation.Blood pressure is usually well maintained and only falls after 30-40% of the circulating volume is lost.
Mild shock: Initially there is tachycardia, tachypnoea and a mild reduction in urine output and the patient may exhibit mild anxiety. Blood pressure is maintained although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock ).
Moderate shock : As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5ml kg h . there is further tachycardia and now the blood pressure starts to fall. Patients become drowsy and mildly confused.
Severe shock : In severe shock there is profound tachycardia and hypotension. Urine output falls to zero and patients are unconscious with labored respiration.
Pitfalls : The classic cardiovascular responses described (Table 2) are not seen in every patient.
Capillary refill: Most patients in hypovolaemic shock will have cool, pale peripheries with prolonged capillary refill times; however, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a patient is shocked.
Tachycardia : it is may not always accompany shock. Patients who are on B-blockers or who have implanted pacemakers are unable to mount a tachycardia. when there is haemorrhage but little tissue damage , there may be a paradoxical bradycardia rather than tachycardia accompanying the shocked state.
Blood pressure : Hypotension is one of the last signs of shock. Children and fit young adults are able to maintain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure.
Table 2 Clinical features of shock
compensated mild moderate severe
OLactic acidosis + ++ ++ +++
Urine output normal normal reduced anuric
Level of consciousness normal Mild anxiety drowsy comatose
Respiratory rate normal increased increased laboured
Pulse rate Mild increase increased increased increased
Blood pressure normal normal Mild hypotension Severe hypotension