Shock is the most common and important cause of the death among the surgical patients Death occurs rapidly as result of the 1- Profound state of the shock 2- Consequence of the organ ischemia 3- Reperfusion injury
Shock is the systemic state of the low tissue perfusion, which is inadequate for the normal cellular respiration. With insufficient delivery of the oxygen and glucose cells switch from aerobic to inaerobic metabolism.
Pathophysiology of the shock is divided in to three categories 1- Cellular 2- Microvascular 3- Systemic
Reduced tissues perfusion dec. cellular O2 switch from aerobic to anaerobic metabolism accumulation of the lactic acid in the blood “Systemic Metabolic Acidosis”. As glucose within cells exhausted stop respiration failure of Na+/K+ pump of cellular membranes lysosomal enzymes become released lyses of the cells Potassium released into the blood stream.
As tissues ischemia progress change in the internal environment of the body activation of the immune and coagulation systems. Hypoxia and acidosis activate compliment and the prime neutrophils generation of the O2 free radicals and release of the cytokines. Above two mechanism leads to injury to endothelials cells of the capillaries damage endothelial cells become leaky tissues edema exacerbating tissues hypoxia
Systemic pathophysiology involves 1- Cardiovascular system 2- Respiratory system 3- Renal System 4- Endocrine System
Due to tissues edema pre-load & after – load decrease Compensatory baro receptor response increase sympathetic activity release of the catecholamine tachycardia and systemic vasoconstriction Above mechanism not associated with the shock result from the sepsis.
Metabolic acidosis and increase sympathetic response increase respiratory rate and minuet ventilation increase the excretion of the CO2 Compensatory respiratory alkalosis.
Due to dec. preload and afterload dec. perfusion pressure in the kidneys reduce filtration at glomerulus dec. urine output activation of renin – angiotensin – aldosterone system further vasoconstri – -on increase water and sodium reabsorbtion from kidneys further edema exacerbating further ischemia.
In addition to adrenal and renin-angiotensin system, vasopressin release from the hypothalamus in response to decrease preload vasoconstriction and reabsorbtion of the sodium and water
During period of the systemic hypoperfusion cellular and organ damage progress just because of the direct effects of tissues hypoxia and local activation of the inflammation. Further injury is also occurs once restoration of the normal circulation acid and K+ load that has build up myocardial depression, vascular dilatation and hypotension. The cellular and humoral elements activated by the hypoxia flushed back into circulation further endothelial injury Acute lung injury, acute renal injury, multiple organs failure and death. Reperfusion injury only attenuated by reducing extent and duration of the tissue hypoxia.
Clinically shock is divided on the basis of the initiating mechanism 1- Hypovolemic Shock 2- Cardiogenic Shock 3- Obstructive Shock 4- Distributive Shock 5- Endocrine Shock
Hypovolemic shock is caused by the reduce circulating volume. It may be due to following causes 1- Hemorrhage 2- Non – Hemorrhagic Non-hemorrhagic causes includes following 1- Poor Fluid intake (dehydration) 2- Excessive loss of fluid in vomiting, diarrhea, urinary loss as in diabetes and “third spacing” in which fluid loss in GIT & interstitial space E.g. bowl obstruction and pancreatitis. Hopovolaemia is most common cause of the shock and in some degree also component of the all other shock.
Cardiogenic shock result from primary failure of the heart to pump the blood to the tissues and causes of that shock include followings 1- Myocardial Infarction 2- Cardiac Dysrhthemia 3- Valvular Heart Disease 4- Blunt myocardial Injury 5- Cardiomyopathy Cardiac insufficiency may also be caused by myocardial depression resulting from 1- Endogenous factors (Bacterial and humoral agents as in sepsis) 2- Exogenous factors (pharmaceutical and drug abuse) Evidence of the systemic hypertension with pulmonary or systemic edema may co – exist with the classic signs of the shock.
There is reduction in preload because of the mechanical obstruction of the cardiac filling. Common causes of the obstructive causes are followings 1- Cardiac Temponade 2- Tension Pneumothorax 3- Massive Pulmonary Embolus In each of the above situation there is dec. filling of the left or right ventricles leading to reduce preload Fall In Cardiac Output.
That describe the cardiovascular response in variety of the conditions such as 1- Septic Shock 2- Anaphylaxis 3- Spinal Cord Injury Inadequate organs perfusion accompanied by the 1- Vascular dilatation 2- Hypotension 3- Low systemic vascular resistance 4- Inadequate afterload
There is vasodilatation is caused by the release of the histamine in the systemic circulation. That occurs mostly in allergic reaction.
In high spinal cord injury there is failure of the sympathetic outflow and that leads to inadequate vascular tone.
There is release of the bacterial products such as endotoxin and activation of the cellular and humoral components of immune system. There is maldistribution of blood flow at microvascular level with arteriovenous shunting and dysfunction of cellular utilization of the oxygen. Mostly in the late phase of the septic shock hypovolaemia result from fluid loss into interstitial space and there may be myocardial depression which complicate the clinical picture.
Endocrine shock may present as complication of 1- Hypovolemic Shock 2- Cardiogenic Shock 3- Distributive Shock Causes Of Endocrine Shock 1- Hypo or Hyperthyroidism 2- Adrenal Insufficiency