Fluid and Hemodynamics (trans 5) Flashcards
NORMAL DISTRIBUTION OF BODY WATER
Our body is composed of 60% water; and 40% comes from fat, mineral etc.
Water component (60% of BODY MASS)
- intracellular fluids (within the cell), comprising 60% of total body water
- extracellular fluids (outside the cell), comprising 40% of total body water
THE REMAINING 40%
- mineral (7%)
- Fat (15%)
- Protein (18%)
The extracellular fluids (40% of total body water)
o the intravascular/transcellular fluid (5% of total body weight), which is composed of the plasma and cellular components of blood
o the interstitial fluid (13% of total body weight), which bathes the tissues
The intracellular fluids = 2/3 of total body water
The extracellular fluids = 1/3 of total body of water
- Interstital = 95% of total extracellular fluid
- intravascular = 5% of total extracellular fluid
REMEMBER
- Fluid exchange, which occurs at the capillary level between the vascular and interstitial components, is very dynamic.
- Due to numerous junctional gaps found in capillaries, water is able to move freely between the two compartments.
- However, the volume lost at the arterial end is regained at the venous end of the capillaries
o At the arterial end, where the hydrostatic pressure is high, water tends to flow out to the interstitial space.
o As opposed to the venular end, where the osmotic pressure is high, water tends to flow back into the vascular compartment.
**Thus, in the normal hemodynamic state, there is no net gain or loss of fluid.
Homeostasis Maintenance
Normal fluid homeostasis is maintained within physiological ranges by the following:
o Endothelial/vessel wall integrity
o Intravascular pressure (primarily exerted by hydrostatic pressure)
o Plasma osmolarity (highly dependent on albumin concentration)
Two types of forces drive normal fluid exchange:
- Hydrostatic pressure (drives filtration)
2. Oncotic or osmotic pressure (drives reabsorbtion)
Homeostasis Maintenance:
Hydrostatic pressure
- Drives fluid out from the intravascular space to the interstitial space
Affected by:
- Cardiac output (eg. blood pressure)
- Vessel wall elasticity: if you have a blood vessel that is spastic or tonically contracted, you expect to see elevated blood pressure, and this will increase the hydrostatic pressure allowing water to move from the intravascular to the interstitial space
- Vascular tone
- Blood volume
Homeostasis Maintenance:
Oncotic or osmotic pressure
Pressure which drives fluid from the interstitium back into the intravascular space
Maintained by protein level in the blood especially that of serum albumin level
For instance, if albumin level is low, such as in malnutrition, osmotic pressure is reduced, thus, fluid reabsorption is decreased. This lead to edema, one of its most important clinical manifestations.
Normal Microcirculation Arterial Hydrostatic pressure: +36 oncotic pressure: -26 Net: +10 mmHg (leak-out)
Normal Microcirculation Venous Hydrostatic pressure: +16 oncotic pressure: -26 Net: - 9 mmHg (leak-out)
DERANGEMENTS: EDEMA
excessive accumulation of fluid in the interstitium and body cavities
an expansion of the interstitial fluid compartment
Abnormal manifestations in patients:
o the weight of the patient INCREASES => instead of being excreted, the water is retained in the extracellular space
o the skin is distended/bloated
o periorbital edema => water accumulates in tissues that are loose, i.e. under the eyes
DERANGEMENTS: EDEMA
Types of Edema
a. Inflammatory (Exudative) edema
o increased vascular permeability => water and other plasma components get out of the blood vessels
o e.g. thermal injury
b. Non-inflammatory (Transudative) edema
o changes in hemodynamic forces (hydrostatic and oncotic forces)
o e.g. malnutrition – problem of reduced oncotic pressure
c. Localized
Fluid accumulation tends to be regional, located in a particular organ system.
o Hydropericardium – fluid accumulates in pericardial sac
o Hydrothorax (pleural effusion) – edema is in thoracic cavity
o Hydroperitoneum (ascitis) – excessive fluid in peritoneal space
o Localized Sub-Epidermal Bullae – accumulation of water beneath the skin
d. Generalized (Anasarca)
o Congestive Heart Failure (CHF): the heart fails => cardiac output is reduced => back flowing of blood => blood retention in the lungs => increase in hydrostatic pressure => generalized edema
o Nephrotic Syndrome
o Malnutrition
o Hydrops Fetalis – fetus looks very big, shiny and swollen because of a congenital anomaly
Inflammatory Edema
Other term: Exudative
Protein content: HIGH => because of altered permeability of endothelial cells
Fibrin content: Fibrin-rich fluid
Cell content: Inflammatory cells typical (HIGH)
Specific gravity: > 1.020 (water contains proteins and cells)
Process: Usually a LOCALIZED process
Pathogenesis: Increase vascular permeability
Non-inflammatory Edema
Other term: Transudate
Protein content: LOW => no alteration in endothelial permeability
Fibrin content: No fibrin in fluid
Cell content: No inflammatory cells in fluid (or FEW)
Specific gravity:
Pathophysiologic Categories of Edema
a. Increased hydrostatic pressure
b. Reduced plasma osmotic pressure
c. Lymphatic obstruction
d. Sodium/Water retention
e. Inflammation
Pathophysiologic Categories of Edema:
Increased hydrostatic pressure
Clinical situations:
o Impaired venous return/increase venous pressure: CHF, constrictive pericarditis, liver cirrhosis, venous obstruction/compression
o Arteriolar dilatation: heat and neurohumoral regulation (i.e. in heat stroke patients, one of the clinical manifestations is general swelling)
Mechanism of Edema in Increased Hydrostatic Pressure. For example, in high blood pressure: the normal 36 mmHg at the arterial end is much higher => more water getting out => excessive accumulation of water in interstitial space.
Note: The lymphatic system attempts to compensate by increasing drainage
Pathophysiologic Categories of Edema:
Increased hydrostatic pressure - Pathogenesis of edema in CHF
o One of the prominent clinical manifestations of CHF is edema. In CHF, from whatever cause, the heart fails to function normally.
o Two types of heart failure: high-output and lowoutput cardiac failure. Whatever mechanism, the cardiac output is reduced. As a result, there is a reduction of Effective Arterial Blood Volume (EABV): the blood doesn’t come out, the volume is reduced, the circulating blood volume in the arterial side is decreased
o Secondary compensatory mechanisms come into play in order to maintain the EABV:
i. renin-angiotensin-aldosterone system – stimulates the kidney to reabsorb sodium and water into intravascular space => increased hydrostatic pressure
ii. vasopressin release –a peptide hormone released by the pituitary gland which promotes water retention by the kidneys
iii. sympathetic system
o These mechanisms will lead to sodium and water retention => increase plasma volume => transudation => EDEMA
Pathophysiologic Categories of Edema:
Increased hydrostatic pressure - Pathogenesis of edema in cirrhosis
o Cause: hepatitis (virus), metabolic disorders, alcohol (toxins)
o Produces scarring, which causes obstruction of the blood vessels in the liver and results in portal hypertension and splanchnic vasodilation => leads to localized accumulation of water in the abdominal cavity called ascites/hydroperitoneum
o Venous return is decreased which in turn causes decreased EABV => EDEMA
