Fluid Compartment and Edema Flashcards

1
Q

Edema is abnormally large amounts of fluid int he ___ space

A

interstitial space

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2
Q

outline the difference in body compartments; the intracellular, interstitial and extracellular spaces

A

intracellular: inside the body’s cells

Extracellular compartments; outside the body’s cells. can be broken down into :

  1. intravascular space; space inside the blood vessels
  2. interstitial space; space outside the blood vessels and outside the cells. Specifically, edema is caused by buildup in this space.
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3
Q

4 elements that regular interstitial fluid

A
  1. hydrostatic pressure
  2. oncotic pressure (balances out hydrostatic pressure)
  3. porosity and
  4. lymphatic drainage.

starling forces; disruption in these forces leads to fldui leaving the vessels and into the interstitial.

disruption in lymphatics prevents adequate drainage, keeping fluid back into the interstitial.

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4
Q

Hydrostatic pressure; causes fluid to flow into the __– raised by __ retention.

A

Hydrostatic pressure; causes fluid to flow into the intersitium– raised by salt retention.

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5
Q

main protein that creates oncotic pressure in the vessels

A

albumin.

Oncotic pressure; created by proteins that attract fluid– albumin– holds fluid in the vessels. Pulls fluid from interstitial to the vessels. Counteracts the hydrostatic pressure.
◦ Hydrostatic pressure is always higher, but if oncotic pressure decreases significantly, there is not enough oncotic pressure to offset the hydrostatic pressure, causing fluid to flow from the vessels back into the interstitial space.

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6
Q

___ continuously monitores extracellular compartment pressure. monitors the overall strethc in the arterial system, and are located in the __ __, ___ __, __ and __

A

Baroreceptors: continuously monitors pressure. Monitors stretch of arterial system
• Located in the carotid sinus, afferent arterioles, aorta and heart.

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7
Q

Effective partial blood volume (EABV):

A

blood volume that perfuses the body’s organs. The pressure that perfuses the baroreceptors in the glomeruli or carotid sinus. Not directly measurable.
• Like the filling of water balloons– either too full, just right, or too squishy (depending on brand– even with the same volume)
• If the skin is tightly stretched, the balloon can “burst in your hand”– over filled arterial system. The baroreceptors are highly stressed and perceives increased pressure which shuts off RAAS system
• Under gilled system increased RAAS system, increasing the salt and water retention to increase fluid.
• Overall, the EABV is he effective pressure filling our arterial system. An overfilled or underfilled EABV will either suppress or activate the RAAS system.
• We can’t measure baroreceptor stretch directly (thus can’t measure eabv directly)– must assess vital signs, physical exam and urine sodium which can show the state or organ perfusion

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8
Q

vital signs that can indicate organ perfusion or EABV

A

◦ Blood pressure– important to have baseline blood pressures for interpretation. Postural changes are useful.
◦ JVP
◦ Capillary revel
◦ Measurement of IVC via U’S
◦ Urine sodium <20 mol or FENa<1%– signs of undefiled EABV

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9
Q

two main types of edema

A
  • pitting vs non-pitting
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10
Q

pitting edema can be broken down into

A

general vs localized edema

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11
Q

two main causes of localized edema

A

1. increased hydrostatic pressure

◦ increased hydrostatic pressure causes fluid extravasation
◦ Usually due to venous obstruction– moves fluid to interstitium
◦ DVT, mass effect from cancer, venous insufficiency, central venous stenosis (narrowing of superior or inferior vena cava, in the case of SVC obstruction– swelling of both arms and the face. In IVC obstruction, this presents with bilateral leg edema). Sometimes can be hard to tell compared to generalized edema.
‣ In dvt, the vein is blocked due to blood clot, which causes back up of pressure. Causes edema in the leg

2. incresaed porosity.

‣ Localized inflammation can lead to leaky blood vessels in the specific site of injury
‣ Ex/ burns and infection (cellulitis)
• Most patients present with other cardinal symptoms like fever, pain or rash.

Causes of Generalized Edema:

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12
Q

anasarca

A

massive swelling over the entire body. almost always due to salt and water retention (through separate pathways)

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13
Q

generalized edema is due to diseases that either ___ or ___ the arterial system

A

either unerfill (inadeuqate perfusion pressure) or overfilled arterial system

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14
Q

causes of undergilled EABV of generalized edema

A

◦ Low EABV leads to RAAS activation. Angiotensin 2 and aldosterone cause salt retention. This doesn’t fix the problem– continued salt and water retention leads to edema formation. Ex/ in CHF, salt and water retention will not help.

1. left ventricular heart failure: diseased heard leads to undefiled EABV, salt and water retention occurs, causing worsened contractility and thus more salt and water retentions.
◦ The retained salt and water pool in venous system, leading to increased hydrostatic pressure. Fluid build up in venous system, causing movement to interstitium–> edema
◦ Can also cause right heart failure

2. • Altered volume/increased capacitance ratio:
◦ Splanchnic circulation dilates (decompensated cirrhosisi)
◦ Decreases EABV and RAAS activation
◦ Salt and water retention. The retained salt and water pool in venous system, increaseing hydrostatic pressure and moving water to the interstitial.

3. Altered Starling Forces
• Increased hydrostatic pressure; direct transmission of pressure to the venue (ex in right heart failure which causes movement from venue to interstitial)
• Decreased oncotic pressure: decreased in albumin can result in movement of fluid out of vascular space into interstitium. EABV becomes underfilled and the body
◦ Neurotic syndrome; albumin leakage through glomerulus can cause the body to reabsorb salt despite nonactivateion of RAAS system
◦ kwashiokor
• Increased porosity: can lead to fluid extravasation out of the venules– sepsis, major burns and allergy.

Overall: generalized pitting edema due to an underfilled EABV is caused by left ventricular heart failure, altered volume or capacitance ratio, and altered starling forces. Overall the underfilling causes RAAS activation and salt and water retention.

  • • Pregnancy: vasodilation and thus RAAS activation and thus fluid accumulation and edema.
    • Non-dihydropyridine calcium channel blockers can also cause edema. The arterial system gets vasodilated which increases pressure in venous system and then again causes generalized edema due to under-filled EABV
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15
Q

mechanism of overfill pitting edema

A

RAAS system is shut down, but the kidney continue to reabsorb salt and water, causing an over-filled EABV, leading to increased hydrostatic pressure and edema. Unlike underfill edema, in overfill edema, the ktdney is reabsorbing salt despite the lack of signalling to do so with the RAS.

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16
Q

how does nephrotic syndrome cause edema?

A

Nephrotic syndrome can cause edema in two main mechanisms:

1) Underfill mechanism: the reduced intravascular oncotic pressure due to low albumin, which leads to fluid shift from the intravascular to interstitial compartment, resulting in underfill edema and secondary salt and water retention due to renin-angiotensin system activation.

2) Overfill mechanism: primary renal salt and water retention due to the intrinsic renal disease. Proteinuria itself causes primary salt and water retention in the kidney independent of the serum albumin, and the main site of this salt and water retention is at the principal cell. There is variable degree of contribution for both mechanisms in individual patients with nephrotic syndrome, depending on the clinical presentation. When there is elevated JVP, hypertension, and abnormal renal function, the main mechanism is Overfill edema such as in this case.

17
Q

main causes of non-pitting edema

A
  1. lymphedema
  2. thyroid dysorders.
18
Q

how does portal hypertension cause edema?

A

There are several mechanisms by which edema may occur in this case. First, patients with portal hypertension have splanchnic arterial vasodilatation, which shunts blood from the systemic circulation into the splanchnic circulation, leading to reduced EABV, reduced renal perfusion, and secondary salt and water retention. There is likely a second mechanism for edema in this case – hypoalbuminemia due to impaired hepatic synthetic function, which leads to a decreased oncotic pressure and subsequent leakage of fluid into the interstitial compartment. The mechanism for ascites also includes the two explanations above (secondary salt and water retention and reduced oncotic pressure), but also has an additional hemodynamic explanation. Patients with cirrhosis have arteriolar dilatation and sinusoidal hypertension, both of which increases hydrostatic pressure (at the arterial and venous end of the capillary, respectively). These four factors create a perfect storm for the movement of fluid from the intravascular to the interstitial compartment (in this case the peritoneal fluid cavity).