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Unit 2 > Hemodynamics & Fluid Disorders (10/23c) [Biomedical] > Flashcards

Hemodynamics & Fluid Disorders (10/23c) [Biomedical] Flashcards

1
Q

Fluid in the Body

A

Total body water = 50-70% of body weight

⅔ intracellular, ⅓ extracellular (contains plasma and interstitial fluid)

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2
Q

Extracellular and intracellular differ in ___ concentration

A

ion

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3
Q

Plasma and interstitial fluid differ in ___ concentration

A

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

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4
Q

Exchange occurs in the microcirculation

A

Gasses, solutes, and fluids exchanged between vasculature and tissue

Microcirculation involves arterioles, capillaries, venules, arteries, veins, and lymphatic network

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5
Q

How are gasses and solutes exchanged?

A

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

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6
Q

Gasses and solutes exchange by diffusion

A

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

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7
Q

Fluid flow is determined by

A

Resistance to flow

Pressure gradient between capillary and interstitium

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8
Q

Resistance to flow

A

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

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9
Q

Pressure gradient between capillary and interstitium

A

Determined by Starling Forces

  • hydrostatic pressure
  • oncotic pressure
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10
Q

Starling Forces - Hydrostatic Pressure

A

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

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11
Q

Starling Forces - Oncotic Pressure

A

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

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12
Q

Osmosis

A

flow of fluid due to differences in solute concentration across a membrane

Fluid goes from low → high solute concentration

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13
Q

Osmotic Pressure

A

amount of pressure we would have to apply to stop the flow of fluid

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14
Q

Fluid Exchange Along the Capillary - Arterial End

A

ΔP > Δ𝜋

Net filtration, or movement of fluid out of the vasculature (out of capillary, into interstitium)

Generally 3 mL/min

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15
Q

Fluid Exchange Along the Capillary - Venous End

A

ΔP < Δ𝜋

Net absorption, or movement of fluid into the vasculature (out of interstitium, into capillary)

Generally 2.7 mL/min

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16
Q

Filtration vs Absorption

A

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

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17
Q

Edema

A

results when fluid remaining after absorption exceeds capacity of lymph vessels to collect and return

accumulation of fluid in the interstitial space

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18
Q

Edema - Causes

A

Disruption of lymphatic system

Altered Starling Forces

  • increased hydrostatic pressure
  • decreased oncotic pressure

Increased capillary permeability

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19
Q

Edema - Disruption of Lymphatic System

A

Lymphedema — edema causes by dysfunction of or damage to lymph system

Primary = congenital

Secondary = resulting from trauma or surgery

20
Q

Edema - Altered Starling Forces, Increased Hydrostatic Pressure

A

Increased venous resistance

Increased capillary hydrostatic pressure

  • increased filtration
  • increased fluid accumulation → edema
21
Q

Causes of increased venous resistance in edema - DVT

A

Usually unilateral

Swollen limb due to increased filtration

Tenderness along venous distribution, erythema and heat due to inflammation of vein (phlebitis)

22
Q

Causes of increased venous resistance in edema - Heart Failure

A

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)
23
Q

Edema - Altered Starling Forces, Decreased Oncotic Pressure

A

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
24
Q

Hypoalbumenia

A

low albumin concentration in plasma

Causes

  • liver disease
  • nephrotic tissue
  • burns
  • protein calorie malnutrition
25
Q

Edema - Increased Capillary Permeability

A

Histamine release causes:

Contraction of endothelial cells opens pores

Fluid, proteins, and WBCs leak out of capillary

Fluid accumulation → edema

26
Q

Noninflammatory Edema

A

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)
27
Q

Inflammatory Edema

A

CAUSE
- increased capillary permeability

FLUID
- exudate (high protein content)

CLINICALLY

  • nonpitting
  • signs of inflammation
28
Q

Edema Terms - Dependent

A

edema in lowermost region

29
Q

Edema Terms - Anasarca

A

generalized edema

30
Q

Edema Terms - Effusion

A

accumulation of fluid in enclosed space

In the joint, pleural space

31
Q

Edema Terms - Ascites

A

accumulation of fluid in peritoneal cavity, causing abdominal swelling

32
Q

Edema Terms - Compartment Syndrome

A

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
33
Q

Immediate Effect of Hemorrhage on CV System

A 
Decreased blood volume → 
decreased venous return → 
decreased stroke volume → 
decreased cardiac output → 
decreased blood pressure
34
Q

Hemorrhage and Baroreceptor Reflex

A 
Increased SNS activity → 
increased HR → 
increased contractility → 
increased TPR → 
increased BP
35
Q

Hemorrhage and Renin-Angiotensin-Aldosterone System

A

Increased fluid volume →
increased Na+ and H2O reabsorption →
decreased urine output

36
Q

What causes cool, pale skin?

A

Increased TPR →
peripheral vasoconstriction →
decreased blood flow to skin →
cool pale skin

37
Q

Circulatory Shock

A

Results from hypoperfusion of tissues

Cellular hypoxia →
anaerobic metabolism →
metabolic acidosis →
cell injury or death

38
Q

Signs of shock

A

Weak, rapid pulse

Hypotension

Low urine output

Altered mental status
- anxiety → confusion → unconscious

39
Q

Stages of Shock

A

Initial
Compensatory
Progressive
Refractory

40
Q

Stages of Shock - Initial

A

Cellular hypoxia → reliance of anaerobic metabolism

41
Q

Stages of Shock - Compensatory

A

Hypercapnia and acidosis → hyperventilation

Activation of baroreceptor reflex and RAA system to increase BP

42
Q

Stages of Shock - Progressive

A

If compensatory mechanism fails, increase metabolic acidosis

General vasodilation → decrease peripheral resistance

Histamine release → fluid leakage, edema

43
Q

Stages of Shock - Refractory

A

Irreversible damage to cells → organ failure → death

44
Q

Types/Causes of Shock - Hypovolemic

A

fluid loss due to hemorrhage, burns, vomiting/diarrhea

45
Q

Types/Causes of Shock - Cardiogenic

A

failure of cardiac pump

46
Q

Types/Causes of Shock - Obstructive

A

obstruction of blood flow due to tamponade, aortic stenosis, or pulmonary embolism

47
Q

Types/Causes of Shock - Distributive

A

septic, anaphylactic, neurogenic

Unit 2 (27 decks)

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