Fluid and hemodynamics disorders I Flashcards
total volume of water in the body
36 liters
- 24 within cells
- 12 extracellular
intracellular fluid % body weight
40%
extracellular fluid % body weight
16%
blood serum % body weight
4%
approximate blood volume
5 liters
- 3 liters in plasma
- 2 liters in cells (hematocrit 40%)
what is hematocrit represent?
% volume of cells to total volume
what influences water movement between compartments
changes in molecular components in the different compartments
what is osmolarity is approximately equal to
between the compartments (intracellular a little higher)
what determines water flow from intravascular space to extravascular space?
protein concentrations within the vascular space
where is sodium excluded from?
intracellular
changes in sodium equilibrates
between the vascular and interstitial spaces, but cases net flux of water into or out of cells
osmole gap
calculated 172
measured 198
-something in plasma adding to osmolality don’t know: ketones, ethyleneglycol, methyl-alcohol
percent of serum proteins thats albumin
60%
-influenced by degree of hydration, synthesis by liver
protein content: IG’s
16%
albumin:immunoglobulin ratio
A:G is 3:4:1
in serum electrophoresis: albumin peak
tallest widest peak
what does decrease in serum protein?
influences the shift of water from blood to the interstitium (edema)
main intracellular ion
potassium
changes in sodium concentrations act primarily to?
change the volume of cells, NOT shift water into or out of the intersitial space (both water and sodium are freely exchanged)
NO EDEMA
in renal failure edema results from?
increased hydrostatic pressure NOT changes in sodium concentrations
what does acidosis do to fluid?
shift hydrogen ions from outside the cell and replaced potassium which leaves the cell-> resulting in hyperkalemia
edema
accumulation of excessive fluid within intercellular tissue spaces or body cavities
two types of edema
- inflammatory (exudate)
2. non-inflammatory (transudate)
difference between the two types edema
increase in vasodilation
anasarca
generalized edema
pitting edema
occurs where fluid collects-> usually LE
ascites
hydroperitoneum
-peritenium
effusions
collection of fluid within potential space
-can be transudate or exudate
pleural effusions
congestive heart failure, infections, neoplasms
examples of effusions
pleural effusions
pericardial effusions
hemorrhagic effusion-> bloody fluid within a cavity (TB)
edema and effusion
what can cause edema can cause effusion
some causes of effusions
hemorrhages
tumors
infections
how is it determined what caused an effusion
aspirated to determine composition
edema: two ways to increase in interstitial fluid
- increased delivery of fluid to interstitial space
2. decreased efflux of fluid from interstitial space
edema mechanism
- increased vascular permeability
- increased hydrostatic pressure (decreased venous outflow)
- decreased protein in the blood
- decreased lymphatic flow
four components hydrostatic pressure
- hydrostatic pressure
- Plasmoid colloid: bring fluid into vasculature
- Lymphatics
- Venous statsis
Hydrostatic pressure change
can mean hypertension
plasma colloid changes
scerosis
lymphatics changes can mean
surgical obstruction
venous stasis can mean
no flow on venous side-> increase pressure-> edema
-pulmonary edema with heart failure, thrombosis, cirrhosis of liver
increased hydrostatic pressure
- obstruction of normal blood flow on venous side of capillaries
- localized: venous thrombosis in extremities, pulmonary edema
- generalized: increased vascular volume due to fluid retention, can effect subcutaneous tissues, visceral tissues (pulmonary edema, pleural effusion, etc)
congestive heart failure
can be left sided or right
left sided heart failure
results in increased pressures in venous pulmonary system, leading to edema within alveoli
-pulmonary
right sided heart failure
results from in increased pressures in vena cava, mainly liver, from liver congestion and peripheral edema
-peripheral edema is increased in lower limbs
thrombosis of hepatic vein
Bud-chiaria syndrome
what can cause sodium and water retention
acute reduction of renal function
-inadequate perfusion of kidneys resulting in activation of renin/angiotensin
mechanism of water/sodium retention
retained Na + water—-> increased intravascular volume—-> increased hydrostatic pressure—->edema
decreased oncotic pressure can be caused by
- loss of albumin: nephrotic syndrome, protein-losing enteropathies
- decreased synthesis of albumin: hepatic cirrhosis, liver failure
- malnutrition: kwashiokor-> protein caloric undernutrition
lymphatic obstruction
normal net flow of fluid from capillaries to lymphatics
-obstruction results in collection of fluid in extravascular space-> subcutaneous edema or ascites (obst. of liver lymphatics)
causes of obstruction to lymphatics
filariasis
neoplasma
scarring
pathological features of edema
enlarged, swollen tissues
- spaces separating cells within tissues
- fluid filling spaces
clinical syndromes
pulmonary edema cerebral edema nephrotic syndrome-> anscarca right sided heart failure-> -peripheral edema "dependent edema" -liver congestion: nutmeg liver
hyperemia characteristics
arteriole congestion
- red in color
- active or reactive
- inflammatory
congestion characteristics
passive
involves veins
blue in color
left heart
hyperemia
increased blood flow into capillary beds
-DUE TO arterial or arteriolar dilation
causes of hyperemia
- sympathetic neurogenic mechanisms
2. release of vasoactive substances-> histamine, serotonin
redness associated with
heat dissipation (fever, exercise)
blushing
inflammation
congestions
accumulation of blood within capillaries
- DUE TO impaired venous drainage
- increased deoxygenated hemoglobin in blood (cyanosis)
- chronic congestion can lead to ischemia, necrosis
nutmeg liver
right heart failure
-obstruction of vena cava or hepatic vein
gross features of nutmeg liver
Alternating areas of light (pale hepatocytes) and dark (distended sinusiods) in a pattern resembling a nutmeg
microscopic features nutmeg liver
congestion of central vein with increased blood in sinusoids
+/- atrophy or necrosis centrilobular hepatocytes
+/- fatty change in perilobular hepatocytes (chronic ischemia)
pulmonary edema->CHF
left heart failure
gross features pulmonary edema
wet, heavy, boggy lungs
microscopic features of pulmonary edema
congestion of pulmonary veins
- transudate and red cells within alveoli
- “heart failure cells”-> alveolar macrophages containing hemoglobin
hemorrhage
blood outside of cardiovascular system -vascular disruption -diapedesis petechia, purpura, ecchymosis hematoma hemopericardium, hemothorax, hemoperitoneum, hemarthrosis, hematosalpinx
consequences of hemorrhage
shock-> severe blood loss
-if results in decreased intravascular volume, then tachycardia, pale, cool skin
hematoma: benign-> skin bruise, lethal-> brain
cardiac tamponade: decreased venous return due to increased fluid volume in pericardium
anemia