The Hypovolemic Shock                                                                               

You may be unfamiliar with terminology and mechanisms described in this section.  By the end of the course, you should be able to return to this section, read it over and understand it fairly comfortably!  You won't be given detailed quiz questions on shock!  This information is here to show the importance of fluids and the vast array of mechanisms available to monitor and protect fluid volumes and pressure.

A sufficiently low plasma volume (severe hypovolemia) will compromise cardiac output and blood pressure and may result in "hypovolemic shock" or "central ischemic response."  A central ischemic response means that the vasomotor centers (which reside in the brain stem and anterior hypothalamus and are part of the CNS) send a signal to the body via the sympathetic branch of the autonomic nervous system, in an attempt to quickly elevate blood pressure back up to normal levels.  Hypovolemic shock is due to decreased cardiac output, decreased blood pressure and, therefore, compromised capillary perfusion of tissues. You may be unfamiliar with some of the terminology below. Relax; we will cover these terms in more detail as we progress.

Nonprogressive hypovolemic shock (compensated shock)

Nonprogressive means that the victim of shock recovers.  Here, baroreceptor reflexes induce "sympathetic" vasoconstriction to increase b.p..  Baroreceptors are pressure receptors located in the carotid sinus, the aortic arch and in other major arteries of the neck and thorax.  Local hypoxic vasoconstriction also assists, a little bit, in elevating b.p.   The renin-angiotensin system is activated (we'll talk quite a bit about the renin-angiotensin system when we cover renal physiology, later) giving formation of angiotensin II (ANG-II).  ANG-II is a hormone which induces a whole host of effects intended to elevate blood pressure.  Among these are the fact that ANG-II causes peripheral vasoconstriction.  Vasoconstriction increases the resistance to bloodflow, resulting in an increase in b.p.  In addition, ANG-II stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary, to increase reabsorption of water in the distal tubules and collecting ducts of the kidney.  Thus, ADH will either increase b.p. or help to slow the decline in b.p.  Fluids will be absorbed from the gastrointestinal tract at a faster rate in an attempt to increase b.p.  We may also see a CNS ischemic response from the vasomotor center (cardiovascular center) if mean arterial pressure drops below 60 mmHg (mean arterial pressure in the systemic system is normally 90 to 95 mmHg.  The CNS ischemic response causes massive vasoconstriction via activation of the sympathetic nervous system in a last ditch effort to maintain b.p. and kidney and brain function. (Just a note of interest - the baroreceptors also function if the b.p. gets too high!)

Progressive hypovolemic shock (cardiovascular deterioration).  The term progressive shock means that, rather than recovering from shock, our victim gets worse!  Because of the lack of nutrients and oxygen arriving at the myocardium, cardiac activity is being depressed.  The heart is already hypoxic and sympathetic vasoconstriction of the coronary arteries makes the situation worse (even less oxygen to the myocardium).  The vasomotor center (cardiovascular center) eventually fails because it is not getting enough oxygen due to restricted central blood flow resulting from sympathetic vasoconstriction in early shock (in the first 10-15 min).   With reduced tissue perfusion and exchange, we begin to see thrombosis in small vessels (sludged blood) due to increased acid from the tissues.  This increase in acid (decrease in pH) causes circulating cells to agglutinate/clot.  Should prolonged hypoxia occur (hours), increased capillary fluid permeability ensues and fluid begins to transude from the capillaries.  As the gut attempts to increase fluid reabsorption we see enhanced endotoxin absorption in the gut.  As blood flow continues to decline, we see generalized cellular deterioration and tissue necrosis.  Despite all this, it is still possible to retrieve this patient from the brink!  They may suffer some permanent damage to the myocardium and other tissues.

Irreversible hypovolemic shock.  Here, we are talking about a "no win" situation.  We treat the victim for shock and we may even be able to normalize cardiac output and blood pressure with aggressive fluid therapy, but all to no avail.  With lack of myocardial nutrition and severe depletion of ATP, the deterioration of the myocardium is extensive and irreversible.  Due to acidosis, we see extensive and irreversible clotting in the capillary beds and widespread tissue necrosis.