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Rounds - Board study > AcidBase > Flashcards

AcidBase Flashcards

1
Q

Write the Starling Equation

A

J= net filtration

J = LpS (Hydrostatic P cap) – (hydrostatic P int) - ó (oncotic P plasma – oncotic P int)

J = LpS (P cap – P int) – ó

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2
Q

In the Starling equation, what favors filtration versus reabsorption/retention?

A

FAVORS FILTRATION:

Capillary hydrostatic pressure

Interstitial oncotic pressure

FAVORS RESORPTION/RETENTION

Capillary oncotic pressure

Interstitial hydrostatic pressure

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3
Q

Where is the anatomical location of the endothelial glycocalyx?

A

On the endothelial surface (luminal)

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4
Q

List 4 functions of the endothelial glycocalyx

A

Maintain vascular permeability
Antithrombotic / anti-inflammatory surface (decreases interaction of procoagulant and proinflammatory molecules with endothelium)
Mechanotransduction - Nitric oxide “a potent vasodilator)

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5
Q

What damages the glycocalyx?

A

Trauma
Inflammation
Toxins (ie bacterial endotoxin LPS)
ANP release - rapid large volume crystalloid therapy
Hyperglycemia - marker of proinflammatory disease or causative? both?

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6
Q

What are 4 core proteins of the glycocalyx?

A

Syndecan-1
Heparan sulfate
Chondroitin sulfate
Hyaluronan

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7
Q

According to the modified Starling hypothesis, the development of interstitial edema is predominantly dependent on the:

A

Microvascular hydrostatic pressure

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8
Q

In acute hypervolemia induced by crystalloid and/or colloid fluid resuscitation, what mediator causes deterioration of the endothelial surface?

A

Atrial natriuretic peptide

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9
Q

According to the modified Starling equation, the oncotic pressure gradient determines fluid movement between which two spaces?

A

Intravascular and subglycocalyx

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10
Q

What whole blood colloid osmotic pressure maintenance target may reduce the risk of edema formation and secondary organ dysfunction in dogs and cats?

A

15 mmHg

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11
Q

What capillary wall has the highest reflection coefficient: liver, kidney, heart or brain?

A

Brain or kidney

REFLECTION Coefficient – 0 = all leak, 1 = no leakage

J= net filtration

J = LpS (Hydrostatic P cap) – (hydrostatic P int) - ó (oncotic P plasma – oncotic P int)

J = LpS (P cap – P int) – ó

LEAKY reflection coefficient = Hepatic sinusoids (0)

Midrange reflection coefficient = lungs (0.5)

TIGHT reflection coefficient = brain (1), Kidneys (1)

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12
Q

Label the disease states suggested by the picture below:
Hypernatremia due to paintball ingestion
SIADH
Hypernatremia due to hypotonic loss
CHF on furosemide and pimobendan
Normal

A
  1. Normal
  2. Hypotonic loss
  3. Paintballs
  4. SIAD
  5. CHF
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13
Q

Which electrolyte disturbances are commonly associated with metabolic alkalosis?

A

Hypokalemia
Hypochloremia

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14
Q

T/F: metabolic alkalosis generally leads to an extracellular and intracellular alkalosis

A

False: Hydrogen lost from the GIT tract leads to the generation of plasma bicarbonate. Metabolic alkalosis can be due to Hydrogen lost (GIT or renal), sodium bicarb administration, volume contraction, hypokalemia (as potassium moves out of the cells, hydrogen or Na moves into cells to maintain electroneutrality) and leads to MORE hydrogen inside cells (intracellular acidosis).

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15
Q

List 2 ways the kidneys can perpetuate a metabolic alkalosis?

A
  1. Decreased GFR (volume depletion and renal failure)
  2. Increased tubular reabsorption (in PT, loop of henle, collecting tubules) also predisposed by hypokalemia, hyperaldosteronism, hypochloremia
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16
Q

Explain how decreased effective circulating volume enhances bicarbonate reabsorption.

A

a. Angiotensin II increases activity of Na-H exchanger, aldosterone leads to Na reabsorption and generation of lumen negative that promotes hydrogen excretion in collecting tubules intercalate cells (typeA). The decrease in bicarbonate excretion in metabolic alkalosis is associated with volume depletion due to enhanced net bicarbonate reabsorption in the distal nephron.

b. With concurrent hypochloremia, to the degree that Na is reabsorbed without Cl following will create a relative negative lumen that leads to a greater stimulus to hydrogen secretion. The net effect of the almost complete reabsorption of filtered bicarbonate is the paradoxical finding of an acid urine despite the presence of extracellular alkalemia.

17
Q

What effect does hypochloremia have on the following parts of the kidney?

A

a. Macula densa: decreased Cl delivery to the macula densa will result in lesss NaCl reabsorption and promote renin release that leads to secondary hyperaldosteronism and increased distal hydrogen secretion. The activity of Na-K-2Cl carrier in the luminal membrane of the macular densa is determined by the availability of the Cl.
b. Intercalated cells in the collecting tubules: luminal H-ATPase pump is associated with the passive cosecretion of the Cl to maintain electroneutrality. A decline in the tubular fluid Cl concentration will facilitate this process by maximizing the transtubular gradient for Cl secretion.
c. Type B intercalated cells: H-ATPase along basolateral membrane leads to H reabsorption with HCO3 excretion (C/o of chloride/bicarbonate exchanger)

18
Q

In which scenario would contraction alkalosis occur?
Hemoabdomen
Small bowel diarrhea
Vomiting
Type II RTA

A

Vomiting

Hypovolemia will produce an alkalosis only when the fluid lost contains an excess of hydrogen ions or an excess of chloride in relation to bicarbonate

19
Q

Hypokalemia tends to lead to a metabolic alkalosis due to?

A

Increased luminal negativity in distal nephron secondary to decreased Cl reabsorption leading to subsequent distal hydrogen excretion.

20
Q

Which scenario(s) would perpetuate a metabolic alkalosis?
Hypoadrenocorticism
Hypokalemia
Increased Na reabsorption
Decreased chloride reabsorption

A

Hypokalemia
Increased Na reabsorption
Decreased chloride reabsorption

21
Q

Your patient has a pH of 7.45 with a [HCO3] of 45. What would be a complete respiratory compensatory response of the pCO2?

A

pCO2 55

22
Q

What effect would an SpO2 of 90% have on the above compensatory response?

A

No effect; hypoxemic stimulation to respiratory in alkalemic patients does not become prominent until the PO2 is below 50mmHg.

23
Q

A one year old MN pitbull presents with a history of vomiting and radiographs consistent with a pyloric outflow tract obstruction. Anticipate the blood gas findings and explain their occurrence.

A

a. Under normal conditions, each mEq of hydrogen secreted generates a transient 1mEq increase in bicarbonate, but under normal conditions, the increase in the plasma bicarbonate is transient since the entry of the acid into the duodenum stimulates an equal amount of bicarbon secretion from the pancreas. However, if the vomiting or NG suction, there is no stimulus for bicarbonate secretion of the gastric juice is removed so there is an alkalosis, which is enhanced with hypokalemia and hypovolemia
b. Blood gas: metabolic alkalosis with hypochloremia, hypokalemia, increased plasma bicarbonate

24
Q

Diuretic use can lead to metabolic alkalosis secondary to (select as many as appropriate):
Decreased bicarbonate reabsorption
Hypokalemia
Increased aldosterone from volume depletion
Increased NaCl delivery in distal nephron leading to enhanced hydrogen secretion with concomitant chloride secretion

A

Hypokalemia
Increased aldosterone from volume depletion
Increased NaCl delivery in distal nephron leading to enhanced hydrogen secretion with concomitant chloride secretion

25
Q

What is the anticipated rise in HCO2 in a patient with chronic respiratory acidosis with PCO2 of 60?

A

HCO3 30

26
Q

How would the anticipated rise of HCO3 in a patient with acute respiratory acidosis with a PCO2 of 60 change from a chronic respiratory acidosis?

A

Hypercapnia-induced stimulation of HCO3 reabsorption persists even though the PCO2 has been returned toward normal. The original increment in H secretion takes 3-5 days to reach is maximum level and reversal may be equally slow. Chronic respiratory acidosis with rapid correction may lead to a cerebral alkalosis and is also associated with hypoxemia (that can cause renal vasoconstriction) and Cl loss through the urine through H excretion in collecting tubules.

27
Q

What are 3 main reasons why hypokalemia is associated with metabolic alkalosis?

A

Transcellular shift- potassium leaks out and hydrogen leaks in so the intracellular acidosis results in an increase in hydrogen excretino in PT (via Na-H exchanger)

Common causes of metabolic alkalosis include vomiting, diuretics, mineralocorticoid excess that induce both H and K loss

28
Q

Why is sodium bicarbonate administration controversial in the setting of organic anion acidosis?

A

Because the organic anion can be metabolized back to bicarbonate once the underlying abnormality is corrected

29
Q

T/F: In general, neurologic signs are more common with respiratory than with metabolic alkalosis

A

True

30
Q

Metabolic alkalosis WITH hypovolemia and hypochloremia is common with: (select all that apply)
a. Vomiting
b. diuretic use
c. hyperaldosteronism

A

Vomiting
Diuretic use

31
Q

Metabolic alkalosis WITH euvolemia is common with:
Vomiting
Diuretic use
Hyperaldosteronism

A

Hyperaldosteronism

32
Q

List three therapies you’d recommend for a patient with a history of vomiting that has a concurrent metabolic alkalosis, hypotension, and hypokalemia

A

NaCl to restore ECF volume and remove stimulus for Na retention (and thereby increased bicarbonate reabsorption) and increased Cl delivery which will promote bicarbonate secretion in the cortical collecting tubule (if Cl concentration is high this will drive more Cl inside cell and promote bicarb excretion through type B intercalated cells) as well as increase activity of NaK2Cl in macula densa thereby resulting in increased NaCl reabsorption and less renin and thereby aldsterone release)
Give KCl
Give antacids
Monitor changes in pH

Rounds - Board study (2 decks)

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