Hemodynamics & Fluid Disorders (10/23c) [Biomedical] Flashcards
Fluid in the Body
Total body water = 50-70% of body weight
⅔ intracellular, ⅓ extracellular (contains plasma and interstitial fluid)
Extracellular and intracellular differ in ___ concentration
ion
Plasma and interstitial fluid differ in ___ concentration
protein
Plasma contains a lot more soluble proteins with negative charge (EX: albumin)
not much in interstitial bc too big to diffuse across capillary membrane
Exchange occurs in the microcirculation
Gasses, solutes, and fluids exchanged between vasculature and tissue
Microcirculation involves arterioles, capillaries, venules, arteries, veins, and lymphatic network
How are gasses and solutes exchanged?
Capillary cell walls are only 1 endothelial cell thick
At cell junctions, the pores can increase as cells pull away and cause leakage
Gasses and solutes exchange by diffusion
Vesicular transport is minimal
Gasses and solutes exchange by diffusion
Lipid soluble substances (O2, CO2) diffuse through the endothelial cells
Water solubles (ions, glucose, amino acids) diffuse through pores
Plasma proteins are too large to diffuse
Fluid flow is determined by
Resistance to flow
Pressure gradient between capillary and interstitium
Resistance to flow
Determined by permeability of the capillary wall (K)
Cerebral capillary K is very low → not leaky
- mechanism behind blood-brain barrier
Muscle capillary K is intermediate
Glomerular capillary K in kidney is very high → is leaky
Pressure gradient between capillary and interstitium
Determined by Starling Forces
- hydrostatic pressure
- oncotic pressure
Starling Forces - Hydrostatic Pressure
the mechanical pressure of blood on vessel walls
tends to push fluid out of the capillary
Pc = capillary hydrostatic pressure
Pi = interstitial hydrostatic pressure
- much lower than Pc
Starling Forces - Oncotic Pressure
pressure due to negatively charged proteins that are too big to leave capillary
tends to pull fluid into the capillary
𝜋c = capillary oncotic pressure
𝜋i = interstitial oncotic pressure
- nearly 0 since few proteins outside
Osmosis
flow of fluid due to differences in solute concentration across a membrane
Fluid goes from low → high solute concentration
Osmotic Pressure
amount of pressure we would have to apply to stop the flow of fluid
Fluid Exchange Along the Capillary - Arterial End
ΔP > Δ𝜋
Net filtration, or movement of fluid out of the vasculature (out of capillary, into interstitium)
Generally 3 mL/min
Fluid Exchange Along the Capillary - Venous End
ΔP < Δ𝜋
Net absorption, or movement of fluid into the vasculature (out of interstitium, into capillary)
Generally 2.7 mL/min
Filtration vs Absorption
90% of what we filter is reabsorbed
The lymph vessels pick up the remaining 10% (0.3 mL/min) and return it to the blood via the vena cava
Edema
results when fluid remaining after absorption exceeds capacity of lymph vessels to collect and return
accumulation of fluid in the interstitial space
Edema - Causes
Disruption of lymphatic system
Altered Starling Forces
- increased hydrostatic pressure
- decreased oncotic pressure
Increased capillary permeability
Edema - Disruption of Lymphatic System
Lymphedema — edema causes by dysfunction of or damage to lymph system
Primary = congenital
Secondary = resulting from trauma or surgery
Edema - Altered Starling Forces, Increased Hydrostatic Pressure
Increased venous resistance
Increased capillary hydrostatic pressure
- increased filtration
- increased fluid accumulation → edema
Causes of increased venous resistance in edema - DVT
Usually unilateral
Swollen limb due to increased filtration
Tenderness along venous distribution, erythema and heat due to inflammation of vein (phlebitis)
Causes of increased venous resistance in edema - Heart Failure
Pulmonary Edema (left sided failure)
- right ventricular output exceeds left
- pressure backs up
- fluid accumulation in pulmonary tissue
Peripheral Edema (right sided failure)
- left ventricular output exceeds right
- pressure backs up
- fluid accumulation peripherally (bilateral LE)
Edema - Altered Starling Forces, Decreased Oncotic Pressure
Albumin accounts for 50-60% of plasma protein
- normally 3.5-5.5 g/dL
- oncotic pressure ~ 25 mmHg
Decreased protein in plasma leads to decreased oncotic pressure
- decreased absorption
- fluid accumulation → edema
Hypoalbumenia
low albumin concentration in plasma
Causes
- liver disease
- nephrotic tissue
- burns
- protein calorie malnutrition
Edema - Increased Capillary Permeability
Histamine release causes:
Contraction of endothelial cells opens pores
Fluid, proteins, and WBCs leak out of capillary
Fluid accumulation → edema
Noninflammatory Edema
CAUSE
- altered Starling forces
- disruptions of lymphatic system
FLUID
- transudate (low protein content)
CLINICALLY
- pitting
- generally dependent region
- no signs of inflammation (except w/ DVT or phlebitis)
Inflammatory Edema
CAUSE
- increased capillary permeability
FLUID
- exudate (high protein content)
CLINICALLY
- nonpitting
- signs of inflammation
Edema Terms - Dependent
edema in lowermost region
Edema Terms - Anasarca
generalized edema
Edema Terms - Effusion
accumulation of fluid in enclosed space
In the joint, pleural space
Edema Terms - Ascites
accumulation of fluid in peritoneal cavity, causing abdominal swelling
Edema Terms - Compartment Syndrome
limb-threatening increase in pressure in fascial compartment due to bleeding or swelling of tissue in that compartment
EARLY SIGNS
- numbness, paresthesias along dermatomes in that compartment
- severe progressive pain, worse with stretch or squeezing of affected muscles
- taut, shiny skin
LATE SIGNS
- paralysis
- diminished pulses
Immediate Effect of Hemorrhage on CV System
Decreased blood volume → decreased venous return → decreased stroke volume → decreased cardiac output → decreased blood pressure
Hemorrhage and Baroreceptor Reflex
Increased SNS activity → increased HR → increased contractility → increased TPR → increased BP
Hemorrhage and Renin-Angiotensin-Aldosterone System
Increased fluid volume →
increased Na+ and H2O reabsorption →
decreased urine output
What causes cool, pale skin?
Increased TPR →
peripheral vasoconstriction →
decreased blood flow to skin →
cool pale skin
Circulatory Shock
Results from hypoperfusion of tissues
Cellular hypoxia →
anaerobic metabolism →
metabolic acidosis →
cell injury or death
Signs of shock
Weak, rapid pulse
Hypotension
Low urine output
Altered mental status
- anxiety → confusion → unconscious
Stages of Shock
Initial
Compensatory
Progressive
Refractory
Stages of Shock - Initial
Cellular hypoxia → reliance of anaerobic metabolism
Stages of Shock - Compensatory
Hypercapnia and acidosis → hyperventilation
Activation of baroreceptor reflex and RAA system to increase BP
Stages of Shock - Progressive
If compensatory mechanism fails, increase metabolic acidosis
General vasodilation → decrease peripheral resistance
Histamine release → fluid leakage, edema
Stages of Shock - Refractory
Irreversible damage to cells → organ failure → death
Types/Causes of Shock - Hypovolemic
fluid loss due to hemorrhage, burns, vomiting/diarrhea
Types/Causes of Shock - Cardiogenic
failure of cardiac pump
Types/Causes of Shock - Obstructive
obstruction of blood flow due to tamponade, aortic stenosis, or pulmonary embolism
Types/Causes of Shock - Distributive
septic, anaphylactic, neurogenic
