Regulation of BF-Rao Flashcards by Lew George

What is the importance of ECFV regulation? (i.e. how does it affect CO?)

ECFV determines PV, which in turn determines mean circulatory filling pressure; therefore, cardiac output?

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What directly determines ECFV?

Na+ balance: ECFV is directly proportional to TBNa+.

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What proportion determines ECFV?

ECFV = ECF[Na] / P[Na]

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Is ECFV independent of P[Na]? Why?

Yes, bc under normal conditions P[Na] is kept constant by AVP-mediated water excretion thru kidney

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When are the only times that P[Na] would change?

Only when gain or loss of Na+ exceeds thirst mechanism and kidney’s ability to correct the situation

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How do you determine P[Na]?

P[Na] = (Amt of ECF Na)/ECFV

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What has to be balanced to maintain Na balance?

Na intake and output
Na Intake→ Dietary intake (150 mmol/d), Iatrogenic (meds, 150mmol/l of saline)
Na Output: A. Skin (0-20%) sweat→half isotonic, insensible (50mEq/L) B. GI (0.5-10%)→ diarrhea (HCO3 excretion); vomiting (isotonic) C. Renal (80-90%)→regulated by homeostatic mechanisms

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What are three causes of Na+ imbalance?

Diarrhea 2. Excessive sweating 3. Diuretics

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What is the consequence of Na retention (150meq/d)?

Retention (150meq/d)→retention of 1 L of water to maintain isotonicity→ increase BW by 1 kg (per L of water)

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What is an indicator of Na+ balance/imbalance?

Change in BW over a short period

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What type of patients require daily monitoring of BW? What can their BW’s be used for?

renal failure on dialysis; can use their BW to calculate how much dialysis may be required

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If you retain more Na+, what happens to ECFV?

It increases

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How much Na is filtered at the glomerulus? (P[Na]=139 mEq/L)

How much of the filtered Na is reabsorbed?

FL=180L/d (GFR) x 139 (P[Na]) = 25000meq/d

95-99.9% is reabsorbed

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Where does Na reabsorption occur? What percent of filtered load of Na in each location?

a. Isotonic reabsorption in PT (most Na, ~64%)
b. L of H (tALH & TALH): ~28% reabsorbed
c. DT and CD: ~7% reabsorbed

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What are signs of ECFV deficit (Decrease in ECFV)? (3)

Hypotension (decrease in systemic BP)→ evident when standing, only when PV is significantly reduced)
Decrease in both systolic and diastolic pressure accompanied by increase in pulse
Orthostatic hypotension→esp this one

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Sign of moderate to severe ECFV expansion?

Edema (lower extremities)→ requires an increase in ECFV by 2.3-3L; seen in CRF and HF (due to excessive salt and water retention)

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Sign of a more severe increase in ECFV?

Pulmonary edema

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Other signs of ECFV expansion? (2)

Heart sounds → S3 gallop due to increase in venous congestion
Distension of large veins (neck veins) due to increase in central venous pressure

What is a cause of edema with normal or low ECFV? What causes this?

Hypo-albuminemia due to either liver disease or nephrotic syndrome
Also Burn patients (increased endothelial permeability)

What determines the fluid distribution between ISF and Plasma?

Starling forces

How fast does the body respond to changes in plasma osmolarity? For instance, how and how fast would it respond to drinking 1 L of water?

The kidneys will respond within minutes via thirst and AVP mechanisms causing diuresis→increased urine flow and osmolarity. Plasma osmolarity is only slightly reduced and water balance is restored in 1-2 hours.

Why is it that daily Na+ intake determines ECFV? How does it influence ECFV?

Renal Na excretory system responds relatively slowly to changes in Na+ input (2-4 days to restore balance); Increase NaCl intake, increase ECFV and vice versa

Does high or low salt intake cause elevated BP? How should hypertensive patients change their diet?

High salt intake→increased ECFV→ increased PV→ increased BP

They should reduce their salt intake

What is a salt-sensitive hypertensive patient?

A patient with hypertension who wont respond to reduced salt intake, but instead require reduced salt intake and diuretics

How is ECFV monitored in the body?

Stretch receptors and baroreceptors located large veins, atria, arteries

What are the three types of stretch/baroreceptors that monitor ECFV? How do they respond to stretch/increased BP?

1. Neural Stretch Receptors: in large veins, respond to venous distention, signals pituitary gland to regulate AVP/ADH→regulate NK2C in tALH 2. Atrial Stretch Receptors: A. end central signal via parasymp fibers in vagus nerve to centers involved with AVP secretion, B. symp signals to kidney and CV centers C. Secrete ANP (Na excr regulation) 3. Arterial Baroreceptors: signals to pituitary gland to secrete AVP→reg's Na excretion

What are the body's mechanisms for regulating Na+ excretion by the kidney?

1. Changes in GFR (Na excre is proportional to GFR) 2. Aldosterone (increases Na reabs in DT/CD) 3. Natriuretic hormone (ANP) (reduced Na reabs) 4. Renin-Ang system (increases Na reabs in response to reduced ECFV) 5. Others: symp nerves, PG's, etc.

How do changes in GFR affect Na excretion?

Changes in GFR result in proportional changes in filtered load of Na, and therefore changes in Na excretion

While small changes in GFR are undetectable, they can result in what?

Marked change in Na excretion and a proportional increase in L of H load of Na+ and therefore more Na in CD and DCT

What is pressure natriuresis?

A situation where GFR and therefore Na+ is regulated by arterial BP. 50% increase in systolic BP→3-5 fold increase in urine flow and urinary Na+ excretion. It's is only slightly compensated for by reducing GFR.

If BP increases, what happens to urinary Na+ excretion?

it increases

How does pressure natriuresis (arterial BP regulation) affect an isolated kidney (w/out symp or hormonal regulation) vs an intact system?

A. There is an acute effect on the isolated kidneyy; 2-3 fold increase in Na output for every 30-50 mmHg change in arterial BP. B. The intact system is very effective at preventing increase in BP by increasing Na+ excretion. This pressure natriuresis is synergized with reduced renin, Ang-II and aldosterone.

Where is aldosterone made/secreted? What stimulates it release? What inhibits it release?

Adrenal cortex, stimulated by plasma K and angiotensin, inhibited by plasma Na

What is the action of aldosterone and where does it act?

It acts exclusively on DCT and CD, where it increases reabs of Na.(for specific mechanism look at slide bc already been posted in another set of note cards)

Is aldosterone likely to play a role in the rapid regulation of Na+ excretion (hemorrhage)? Why?

No; bc aldosterone has a relatively slow effect on Na reabsorption in DT and CD

Where is ANP produced? What stimulates its secretion? What are the targets of its action?

Made in cardiac atria cells; It's secretion is increased when P[Na] increases, but the actual direct stimulant is atrial distention; target is several renal tubular segments and renal blood vessels

What are the three actions of ANP? Net effect of these actions?

1. Tubule→inhibits Na reabsorption 2. Renal vessel→increases GFR (dilate aff, constrict eff) and Na excretion 3. Adrenal cortex→ inhibits aldosterone secretion Net effect: Decrease Na reabsorption, increase Na excretion and therefore, reduce ECFV

In the RAAS, what stimulates JG cells to secrete renin?

1. Reduced systemic BP/tissue perfusion 2. Reduced ECFV 3. Increased Symp NS firing 4. Decreased Renal Arterial pressure

What two ways does Ang-II increase Na reabs?

1. It directly stimulate Na-H exchanger in the PT | 2. (Indirect) It stimulates release of aldosterone which stimulates Na reabs in DCT and CD.

What are some additional factors that affect renal absorption?

1. Sympathetic Nerves reduce GFR and increase proximal Na reabs 2. PGs, Bradykinin, and Dopamine are produced in the kidney and cause diuresis and natriuresis 3. Ouabain-like Factor (inhibits Na reabs) is produced in atrium and causes diuresis and natriuresis

What three regulatory mechanisms are activated by hypovolemia (volume depletion)? Look at flow chart on slide

1. AVP 2. RAAS 3. Norepinephrine

What three regulatory mechanisms are activated in response to volume expansion? What is the net effect of these mechanisms?

1. Suppression of hypovolemic hormones 2.Release of Natriuretic hormones 3.Peritubular factors Net effect: increased Na+ excretion

What two changes stimulates release of AVP/ADH? To what extent do these changes have to be?

1. 1% decrease in osmolarity or 2. 10% decrease in ECFV will both stimulate AVP release

What happens if ECFV increases by ~4-5L? What if ECFV decreases by 4-5L?

edema; death