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Hypovolemic Shock

Shock is a physiologic state characterized by a significant reduction of


systemic tissue perfusion, resulting in decreased oxygen delivery to the
tissues. Prolonged oxygen deprivation may lead to sequential cell death, endorgan damage, multi-system organ failure, and death.
Types of shock: hypovolemic, cardiogenic and distributive
o Hypovolemic shock is a consequence of decreased preload due to
intravascular volume loss. During hypovolemic shock, the diminished
preload decreases the CO and the SVR increases in an effort to
compensate for the diminished CO and maintain perfusion to the vital
organs
A few cardinal signs of shock, across all three types include hypotension,
oliguria, altered mental status, cool clammy skin and metabolic acidosis.
Postural hypotension is a suggestive finding of hypovolemic shock
3 stages to shock
o Preshock- It is characterized by rapid compensation for diminished
tissue perfusion by various homeostatic mechanisms. Ex tachycardia,
peripheral vasoconstriction
o Shock-the compensatory mechanisms are overwhelmed and signs of
organ dysfunction appear. At this stage physiological disturbance is
significant, for example 25% loss of effective circulating volume in
hypovolemic shock
o End-organ failure- irreversible organ and tissue damage leading to
patient death (urine output may decrease even further).
Mortality rate is varied for hypovolemic shock but quite high for distributive
(35-60% septic shock) and cardiogenic (60-90%)
IV Solutions/Treatment for hypovolemic shock
To treat hypovolemic shock, the following need to be considered: the rate of
fluid replacement; the type of fluid infused; and the role for buffer therapy in
patients with concurrent lactic acidosis
In general, at least one to two liters of isotonic saline are initially given as
rapidly as possible in an attempt to restore tissue perfusion and prevent
irreversible damage. This should be given as long as blood pressure remains
low
3 major classes of replacement fluids
o Crystalloid solutions saline solutions, buffered solutions(bicarbonate
buffered solution)
o Colloid containing solutions- albumin solutions, dextran, hyperoncotic
starch
o Blood products
Crystalloids, usually saline solutions, are generally preferred for the
management of patients with severe volume depletion not due to bleeding.

However more must be given in comparison to colloid solutions since there is


extravascular distribution

IV Solutions
o

Volume expanders
o Colloid solutions- contain large molecular weight molecules and
preserve colloid pressure
o Crystalloid solutions- most common is isotonic saline (.9%
concentration) or ringers lactate solution (usually used for burns or
blood loss)
o Blood products such as fresh frozen plasma

Hydrochlorothiazide vs Lisinopril
Hydrochlorothiazide MoA it acts on the distal convoluted tubule to decrease
sodium and concomitant water resorption. Specifically it acts on the Na-Cl
cotransporter by competing for the chlorine site on the transporter. Also, in
an unrelated mechanism it also promotes calcium resorption
Lisinopril
o Used for decreasing blood pressure and it patients with MI and heart
failure.
o MoA- it competitively inhibits angiotensin converting enzyme (ACE),
preventing the conversion of Angiotensin I to Angiotensin II. It raises
plasma renin levels (due to a negative feedback mechanism). ACE
inhibitors in turn decrease activity in the RAAS system. CNS
mechanism may also be involved since angiotensin increases
adrenergic outflow from CNS

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