PHYSIOLOGY

FLUID DISTRIBUTION
The body in divided in two compartment, and extracelular and intracelular
compartment separeted by the membranes
Membrane = Barrier
About 60% of the body mass is water
Relationship ICF/ECF: 2/3:1/3
Na+ stay ousite the extracellular compartment can cross the cell membrane
ECF is divided in ISF and vascular membrane separeted by capillary
membrane
ISF: Interstitial FLUID
Vascular Volumen: Proteins (Albumin cant cross the capillary membrane
OSMOSIS
mOsm/kg: concentration of particles per Kg of solvent
Osmolarity = Osmolality
Glucose effective osmole
Effective osmole: Solute which cant cross the membrane is effective
causing the movement of water
In DM glucose cant cross
GLUT 1 is a receptor for glucose in Red blood cells (RBC)
GLUT 4 in adipose tissue and muscle
Effecitve osmole for the vascular compartment: Albumbin
OSMOSIS
EXTRACELLULAR SOLUTES
Na+: 140
K+: 4
Cl: 104
HCO3- : 24
Measured in mEq/L; mmol/L; mM

BUN: 15
Cr: 1
Glucose: 80
Measured in mg/dl and mg%
Osmolar GAP

= 2 + + +
18 2.8
15
= 2 + + +
20 3
80 30
= 2 140 + + +
20 3

Estimated osmolality: 280 + 4 + 5= 289

OSMOLAR GAP
Osmolar Gap: Difference in stimated and measured osmolarity.
Measure should be more than 15 above stimated

Result of Clinical vignette

100 30
= 2 150 + + = 315
20 3

Plasma osmolarity of paciente: 320

Osmolarity measured of the paciente: 315
Osmolar gap: 320 315 = 15
Darrow Yannet Diagram
Excersice are in the book (pag 8)

Two big player for volumen regulation are:

Aldosterone
Anti-Diuretic Hormone (ADH; also called AVP
 Primary factors regulating Renin PP Renin
1. Perfusion pressure to the kidney (PP) PP Renin
2. Sympathetic stimulation (Beta-1 receptor) Renin [+ ] Renin
3. Na+ delivery to the macula densa (Nephron) [+ ] Renin
Primary factors regulating Aldostenore RAAS
1. Plasma (angiotensin II) stimulates release (RAAS)
NEGATIVE FEEDBACK SYSTEM
2. Plasma K+ stimulates release
Primary factors regulating ADH (AVP)
1. Plasma osmolarity stimulates Oms - AVP
Oms - AVP
2. Blood volumen/pressure (inversely related)
BD AVP
BD AVP
Examples
Volumen Distribution Regulation Clinical
ECF BP Loss of hypotonic fluid
ICF RAAS Dehydration
Sweating and respiration)
Hypotonic urine (diabetes inspida)
OSM AVP ADH could be cause
Volumen Distribution Regulation Explaination Clinical
ECF BP
Add more osmole Excessive salt intake
ICF RAAS which stay in Hypertonic saline
Extracellular Hypertonci manitol
OSM AVP // volumen Initial effect of hyperglycemia
Volumen Distribution Regulation Explaination Clinical
ECF BP Primary polidipsia hypotonic
saline
ICF RAAS Add more wter so
SIADH
it drops osmolarity
Increased ADH could be the
OSM AVP cause
Volumen Distribution Regulation Explaination Clinical
ECF BP Infusion of isotonic fluid such as saline (entire ECF
expands)
No change ICF RAAS Add more equal solute Infusion of solution with colloids (dextran, plasma
(osmole) and water with proteins) expands plasma portion of ECF
No change OSM AVP Pathology: Increased Aldosterone, Primary
aldosteronism (Conn's sndrome)
Volumen Distribution Regulation Explaination Clinical
ECF BP
ICF RAAS
Loss more osmoles
Decreased of Aldosterone
Addison's disease
OSM AVP //
 Flow
Venous Pressure
Blood Volumen
Fluid Flux
Hydrostatic Pressure (P)
Filtration (+)
Osmotic forces in the intersticial

Osmoles = Plasma protein

c Any solute that doesnt croos the
membrane is gonna pull wter
Osmotic/Oncotic pressure ()
Absorption (-)
Hydrostatic pressure in the
interstitial

:Hydrostatic pressure in the capillary c :Oncotic pressure in the capillary

Oncotic pressure of the instertitial Hydrostatic pressure in the interstitial
 Filtration and Absortion Fluid Flux

Hydrosteatic pressure (P) Oncotic pressure ()

Pc promotes Filtration (+) means
pushing water out also means gradient
1. Hydrostatic pressure in the Capillary
Regulated by 3 things
1. FLOW (Regulated at arteiole)
2. VENOUS PRESSURE (directly related)
3. BLOOD VOLUMEN (Greater the volumen
greater thepressure
2. Oncotic pressure in the interstitial
Oncotic promotes Absorption (-)
Oulling water to the capillary
1. Oncotic pressure in the capillary
Osmoles in the capillary that pull water
out (Albumin)
2. Hydrostatic pressure in the intertitial
STARLING EQUATION Qf: filtration
k: filtration coeficiente
Relates to permeability
If the capillary is more permeable
increased the filtration
permaebility = Filtration

Lymphatics: Regulate
Oncotic pressure in the interstitial
(Hydrotastic pressure in the
intertitial)
Exercise
Calculate Net pressure
Calculate Net pressure
Pc: 25 mm Hg
PIF: 2 mm Hg (Pc + IF ) (c PIF)
c: 20 mm Hg (25+1) (20 + 2)
IF: 1 mm Hg
R: 4
Primary causes of edema
Increased Pc:
Flow: vasodilation
Venous pressure: Venous obstruction, heart failure
PITTING EDMA
Blood volumen: (Na+ retention) Heart failure

Increased IF : Hypothyroid Myxedema NO PITTING EDMA

Decreaed vascular oncotic pressure: Liver; Kidney

Increased Capillary permeability: Inflammatory response (TNF-Alpha;
histamine; bradykinin
Lymphedema: Filarial (W. Broncofti); bacterial lymphangitis (streptococci);
trauma, surgery, tumor
 CLINICAL VIGNETTE
If TNF (Tumor necrosis factor) and BK (Bradykinin) are
increased
Increased permeability
FLOW
PC (Hydrostatic Pressure in the capillary
FILTRATION
Which decreased PTC (precapillary arteriolar tone) and PNE
(Pre-capillary noepinephrine contration/release
 PURMONARY
PULMONARY EDEMA EDEMA

Most common form of pulmonary edema

Cardiogenic (elevated PC) Left atrial
In this condition the patient is not injecting blood pressure
(Right heart start to fail blood is going to back up)
Increased left atrial pressure
Increased venous pressure which in turn increased
capillary pressure Venous
Initially increased lymph Flow reduces interstitial pressure
proteins and is protective
First clinical sign is ORTHOPNEA (disnea when
supine), which can be relieved SITTING UPRIGHT Capillary
pressure
PULMONARY EDEMA Most common causes
Non-cardiogenic (increased
permeability)
Adult respiratory distress sndrome SEPSIS
(ARDS)
Most important

Due to direct injury of the alveolar Gastric Bacterial

epithelium or after a primary injury to aspitation pneumonia
the capillary endothelium

Clinical signs are severe disnea of Trauma

rapid onset, hipoxemia and diffuse
pulmonary inflitrates leading to
respiratory failure
PULMONARY EDEMA

Non-cardiogenic
Fluid accumulation as a result of the loss of epithelial
integrity
Presence of protein containing fluid in the alveoli
inactivates surfactant causing reduced lung
compliance
Pulmonary wegde pressure is normal or low
 VOLUMEN MEASUREMENTS
INDICATOR-DILUTION
Volumen of distrinution in
pharmacology
= albumin)
Properties of Tracer
Introduced into a vascular
compartment and distribute until
they reach a barrier they cant
pentrate.
Two major barrier are
Capillary membrane
Cell membrane
Plasma: Doesnt cross capillary (e.g
ECF: Cross capillary but not the cell
membrane (e.g., mannitor, sodium,
sucrose)
Total body water: Permeable to
capillary and cell membrane (water
and urea)
Volume measurement of compartments
Blood volumen: RBC volumen + plasma

Blood volumen =
1
Example
Ht:50mg (0.50) 3
= = 6
Plasma volumen = 3L 1 0.5