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Fluid Balance and Shock
Outline
Fluid Balance
A. Fluid Compartments

1. osmolarity of all three fluid compartments is always the same,
normally 280 -295mosm. (it may be more or less, but will always
equilibrate until it is the same in all three compartments
2. each compartment is separated from each other by a
semipermeable membrane

For example in the diagram above, the cell membrane of the red
blood cells separates intravascular from intracellular, the capillary
membrane separates intravascular from interstitial, the cell membrane
of cells located in the tissue separates intracellular from interstitial
B. Principles (Factors) Governing Movement of Fluid Between Compartments
1. Osmosis ( definition of osmosis- movement of water across a
semipermeable membrane from an area of lesser concentration to an
area of greater concentration)a..Role of Na+
1. volume of ECF depends chiefly upon concentration of this ion
(about 1/2 of osmotic pressure of ECF due to concentration of
this ion)2. if Na+ increases in intravascular then (because of osmosis) fluid will be pulled from interstitial and intracellular. If this continues the shift of fluid may cause
a. hypervolemia of intravascular compartment
b. dehydration of the interstitial and intracellular3. if Na+ decreases in intravascular then (because of osmosis)
fluid will shift from intravascular into interstitial and
intracellular. If this is significant enough it will cause
a. hypovolemia of intravascular compartment
b. edema of interstitial and intracellular4. the kidneys play an important role in regulating the
concentration of Na+ via the renin angiotensin mechanism (see diagram in HTN leture)
b.Role of Colloids
1. colloids are large proteins
2. albumin, synthesized by liver, mostly responsible for
maintaining colloidal osmotic pressure in intravascular fluid
compartment.
c. Role of glucose
2. Balance between hydrostatic and colloidal osmotic pressure (cop)
a. hydrostatic pressure is a mechanical force. It is greatest closest to
the heart and then drops off as distance from heart increases,
hence the proximal ends of capillaries have a higher hydrostatic
pressure then do the distal ends .Hydrostatic pressure works
within the intravascular compartment to push fluid out into the
interstitialb. as blood enters capillary fluid is pushed out into interstitial tissue
(because hydrostatic pressure is greater than cop at this point.)
at the end of the capillary, most of the fluid is pulled back in
(because hydrostatic pressure has dropped and cop is now
greater)3. Role of Lymph system
4. Altered Capillary Permeability.
Shock
A.Def. a pathologic syndrome characterized by abnormal cell metabolism that results from inadequate perfusion and oxygenation or cellulardysfunction
B. Cardiogenic
1. more than 80% of pts who develop cardiogenic shock after an MI
will die
2. due to extensive loss of ventricular myocardium (usually 40% or
more), cardiac output drops.
3. a vicious cycle ensues - because of decreased C.O. and decreased
BP get increase in SNS activity causing peripheral vasoconstriction
(increases afterload) and renin angiotensin system activated causing
increase in preload. Increased afterload and preload just further
aggravate situation
C. Circulatory Shock (actual or relative loss of intravascular volume)
1. Hypovolemic
a. signs of shock occur when vascular volume depleted 15 -25%
b. may be due to hemorrhage or shift of fluid out of intravascular
fluid compartment (third spacing)
c. signs and symptoms
1. mild
a. minimal tachycardia
b. slight decrease in BP
c. mild peripheral vasoconstriction (cool hands and feet)
2. moderate
a. HR= 100 -120 bpm
b. decrease in pulse pressure
c.systolic pressure = 90 -100 mm Hg
d. restlessness
e. sweating, pallor
f. oliguria
3. severe
a. HR > 120 bpm
b. BP < 60 mm Hg systolic
c. mental stupor
d. anuria
e. acidosis
2. Obstructive
a. inability of heart to fill properly (e.g. cardiac tamponade) or
b. obstruction to outflow from the heart (e.g. pneumothorax)
3. Distributive (also called normovolemic shock since although
decreased C.O., not decreased total blood volume as occurs in
hypovolemic)
a. Neurogenic
1. caused by decreased sympathetic control of blood vessel tone
due to defect in vasomotor center of brain or sympathetic
outflow to blood vessels due to
a. brain injury
b. drugs
c. hypoxia
d. hypoglycemia
e. general anesthesia
2. loss of vascular tone causes pooling of blood in arterioles
and veins
b. Anaphylactic
1. caused by immunological reaction, release of histamine and other
vasodilator substances acting systemically
2. get pooling of blood
3. caused by allergic response, e.g. bee sting
4. accompanied by bronchospasm, contraction of GI and uterine
smooth muscle and urticaria or angioedema
c. Septic Shock
1. associated with infection and body's systemic response
to infection
2. most often caused by infection with bacteria
3. bacteria releases endotoxins which triggers off immune reactions
a. activates inflammatory reactions- side effect is
degranulation of mast cells, release of histamine, other
inflammatory substances, blockade of SNS induced
vasoconstriction in early stages- resulting in pooling
of blood and altered capillary permeability
b. interferes with coagulation
4. Two stages
a. Early ( (also called warm or pink or hyperdynamic)
1. total peripheral resistance decreased (because of SNS
blockade on peripheral blood vessels) (decreased
afterload)
2. blood pooling not returned to heart (decreased preload),
but heart maintains C.O. by increasing HR and
contractility
b. Late (also called cool, blue or hypodynamic)
1. C.O. drops, now resembles hypovolemic shock
D. Summary of Hemodynamic Pattern in Shock
| Type of Shock | Descriptiopn | Preload | Afterload |
| Cardiogenic | damage to myocardium of heart, decreased pumping | increased | increased |
| Hypovolemic | loss of blood volume, either intrinsic or extrinsic | decreased | increased |
| Early Septic | action of endotoxins, stimulation of inflammatory responses | decreased | decreased |
Discussion
Edema is an increase in fluid volume, mostly in the interstitial fluid compartment, but it may also occur in the intracellular fluid compartment. It is very important, clinically, to be able to describe edema as thoroughly and as detailed as possible. Therefore, many adjectives and terms can be used to describe differing conditions. Generalized edema means an expansion of both the interstitial and intracellular fluid compartments. Anasarca is a term used to mean a generalized massive edema involving all parts of the body, including the genitalia, chest wall and arms. Third spacing means a shift of large amounts of fluid from the intravascular to the interstitial. If edema in the interstitial space is caused because the lymphatic vessels, which normally drain the tissues, are blocked, then you have lymphedema. If the area of edema, after being palpated by an examiner, leaves a pit, then it is called pitting edema and can be scored on a scale of 1 - 4. Sometimes edema, upon palpation, does not produce a pit, then you have non pitting edema. If edema develops when an extremity is in one position but then disappears when placed in another position (for example, the ankle- edema appears when standing, disappears when the leg is elevated), then you have dependent edema. If the fluid in the interstitial space is being pushed out through the pores of the skin when pressed, then you have weeping edema. Edema occurring in the sacral area is called sacral edema, around the eyes it is periorbital edema. Large amounts of fluid accumulating in the peritoneal cavity (classic example of third spacing) is called ascites.
Clinically
Ascites is a frequent complication of liver disease. Three factors that occur in association with a damaged liver cause ascites: 1. the liver is unable to synthesize adequate amounts of albumin ( hence colloidal osmotic pressure drops, and fluid shifts into the interstitium), 2. the liver is congested, so blood returning to the liver is backed up, resulting in increased portal pressure, a type of hydrostatic pressure which pushes fluid out of blood vessels and 3. the liver is unable to metabolize aldosterone adequately, so the levels of aldosterone build up. Working at the kidney level this causes re absorption of sodium, pulling fluid from other tissues back into circulation where it is then shifted out into the peritoneal space.