Fluid and Hemodynamic Disorders Flashcards
(13 cards)
What are the fluid compartments in body?
2/3 = intracellular fluid (ICF)
1/3 extracellular fluid (ECF)
80% interstitial fluid
20% blood plasma
What is capillary oncotic pressure based off of?
proteins like albumin, globulins and fibrinogen that do not leave the capillary and draw water
What is the major cation in the extracellular fluid?
Sodium
- total body sodium is the principal determinant of extracellular fluid volume because it is the major cation in the extracellular fluid
Extracellular fluid volume depends on the regulation of renal sodium excretion, How?
- Atrial natriuretic factor
🔹 What is it?
A hormone released by the atria of the heart in response to high blood volume/pressure (atrial stretch).
🔹 Effect on sodium excretion:
- Increases sodium excretion (natriuresis)
🔹 Mechanisms:
- Dilates afferent arteriole, increasing glomerular filtration rate (GFR)
- Inhibits renin release → suppresses RAAS
- Inhibits sodium reabsorption in the collecting ducts
- Suppresses aldosterone secretion
📌 Bottom line: Promotes loss of sodium and water due to hypervolemia → lowers blood pressure
- RAAS
- sympathetic nervous system
🔹 What is it?
The “fight or flight” system activated by stress or low perfusion pressure (e.g., blood loss).
🔹 Effect on sodium excretion:
- Decreases sodium excretion
🔹 Mechanisms:
- Vasoconstriction of afferent arteriole → ↓ GFR → ↓ filtration of sodium
- Stimulates renin release → activates RAAS
- Directly increases sodium reabsorption in proximal tubule
📌 Bottom line: Conserves sodium and water in emergencies
How does congestive heart failure lead to edema?
- In left-sided HF → blood backs up into the lungs → pulmonary edema (fluid in lungs)
- In right-sided HF → blood backs up into veins of the body → peripheral edema (legs, ankles)
- Backup increases venous & capillary hydrostatic pressure
- Imagine squeezing a garden hose: pressure builds up inside
- This increased hydrostatic pressure in the capillaries pushes more fluid out into the surrounding tissue - Fluid leaks out → edema
- Normally, some fluid leaves capillaries and is drained by the lymphatic system
- But in CHF, too much fluid leaks out, and the lymphatics can’t keep up
- So fluid builds up in the interstitial space = edema
🔁 Bonus: Why the body makes it worse
CHF also activates:
- RAAS (renin-angiotensin-aldosterone system) → retains sodium and water
- SNS (sympathetic nervous system) → vasoconstriction and more fluid retention
✅ These systems try to help, but they just add more fluid → worsening the edema
Why does CHF stimulate RAAS?
🔴 In congestive heart failure (CHF):
- The heart isn’t pumping effectively.
- so less blood reaches the kidneys (↓ perfusion).
- The kidneys think there’s low blood volume or low blood pressure, even if the body is full of fluid.
🧠 The kidneys respond by activating RAAS through releasing renin enzyme from juxtaglomerular cells — because they think the body is dehydrated or losing blood.
Angiotensin II: Constricts blood vessels (↑ BP), stimulates aldosterone
Aldosterone (from adrenal glands, specifically adrenal cortex) Tells kidneys to retain sodium and water
😬 Why this makes CHF worse:
In CHF:
- The heart is already weak.
- Adding more fluid and pressure makes it harder for the heart to pump.
- This leads to worsening edema and congestion.
Explain how Liver cirrhosis leads to obstruction of portal blood flow and leads to ascites
🩸 Step-by-step: How cirrhosis → ascites
- Cirrhosis scars the liver
- The liver becomes fibrotic (scarred and stiff)
- Blood has a hard time flowing through it - This causes portal hypertension
- The portal vein brings blood from the intestines → liver
- When blood can’t pass easily through the liver, it backs up
- This increases pressure in the portal vein = portal hypertension - High pressure → fluid leaks out
- The increased pressure in portal circulation causes:
- Capillaries in the gut and mesentery to leak fluid
- Fluid enters the peritoneal cavity → ascites - Hypoalbuminemia makes it worse
- The liver makes albumin, which keeps fluid in the vessels (oncotic pressure)
- In cirrhosis, albumin production drops → ↓ oncotic pressure
- So even more fluid leaks out - RAAS and ADH activation (trying to help but worsens things)
- Low blood volume in vessels (even though there’s fluid in belly!) → triggers RAAS & ADH
- This causes the kidneys to retain more sodium and water
- Which leads to even more ascites
What is Nephrotic Syndrome?
- occurs due to damage to the glomerulus, which is the filtering unit of the kidney
This results in:
1. proteinuria
- Why?
- In nephrotic syndrome, the glomeruli (filters in the kidneys) are damaged.
- Normally, they keep large proteins (like albumin) in the blood.
- But in nephrotic syndrome, the filter is too leaky, so protein spills into the urine.
- hypoalbuminemia
Why?
- Since albumin is lost in urine, the blood level of albumin drops.
- Albumin is important for oncotic pressure (keeps fluid inside vessels).
- So when albumin is low → fluid leaks out into tissues → edema. - hyperlipidemia
Why?
- The liver senses that blood protein levels are low, and tries to compensate.
- It ramps up protein production, but in doing so, it also makes more lipoproteins (fats).
- So you end up with high cholesterol and triglycerides in the blood. It’s kind of like the liver trying to “help” but overcompensates, creating excess fat too.
Edema secondary to lymphatic obstruction is called what?
Elephantiasis
Radical Mastectomy can also cause lymphedema and damage to lymph nodes - can wear elastic stockings to help due to compression decreasing filtration further
How does hypoproteinamia lead to edema?
🧪 What is hypoproteinemia?
- It means low protein in the blood, especially low albumin.
- Albumin is a protein made by the liver that helps hold water inside your blood vessels.
- It creates oncotic pressure (also called colloid osmotic pressure).
- Oncotic pressure is like a pulling force that keeps fluid inside the blood vessels instead of leaking out into tissues.
💧 So what happens when albumin is low?
1. ↓ Oncotic pressure
- There’s less pulling force to keep fluid in the capillaries.
- Fluid leaks out
- Water moves out of the blood into the interstitial space (tissues). - Edema forms
- This causes swelling in the legs, face, or belly (ascites).
Sodium retention and edema
What is sodium retention?
- Your kidneys usually filter sodium and then decide how much to keep (reabsorb) vs how much to pee out.
- When your body senses low blood volume or pressure, it tells the kidneys to keep more sodium.
- Water follows sodium → so keeping more sodium = keeping more water.
What is increased tubular reabsorption of sodium?
- This just means the kidney tubules (especially in the nephron) are reabsorbing more sodium back into the blood.
- Happens when signals like RAAS or the sympathetic nervous system are activated.
How does this cause edema?
1. Kidneys reabsorb more sodium
- Because of RAAS, low perfusion, heart failure, etc.
2.Water follows sodium
- So more water is kept in the blood, increasing blood volume.
3.↑ Hydrostatic pressure
- More volume = more pressure inside blood vessels.
- Fluid leaks out of capillaries
- If too much pressure builds up → fluid escapes into tissues. - ✅ Result = Edema (swelling)
🔁 Common conditions that do this:
1. Heart failure: poor kidney perfusion → activates RAAS
- Liver cirrhosis: less blood to kidneys → RAAS
- Kidney diseases: loss of protein → low oncotic pressure + RAAS activation
Inflammation and edema
- acute and chronic inflammation increases permeability
How do we prevent kidneys from stimulating RAAS when someone has CHF?
💡 In congestive heart failure (CHF):
- The heart pumps weakly → less blood reaches the kidneys
- Kidneys think there’s low blood volume → they activate RAAS
- RAAS causes:
1. Vasoconstriction (↑ afterload)
2. Sodium + water retention (↑ preload)
- Which makes CHF worse
So how do we stop the kidneys from over-activating RAAS?
We use medications that block RAAS and reduce its harmful effects.
- ACE inhibitors (e.g., enalapril, lisinopril)
- Block conversion of angiotensin I → angiotensin II
- ↓ Vasoconstriction
- ↓ Aldosterone release (→ less sodium & water retention)
- Net effect: lower BP and less fluid overload
- ARBs (e.g., losartan, valsartan)
- Block angiotensin II receptors
- Same effect as ACE inhibitors, but used if patients can’t tolerate ACEi (e.g., due to cough)
- Aldosterone antagonists (e.g., spironolactone, eplerenone)
- Block aldosterone’s action on the kidney
- Prevent sodium & water retention
- Help reduce edema and protect the heart
