5.03 Approach to Common Water and Electrolytes Flashcards

1
Q

In diarrhea, a common accompaniment is loss of which electrolyte?

A

K+ so expect possible hypokalemia

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2
Q

Water vs Volume balance

A

Volume/Saline Balance - that means px is either vol deficit or volume excess.
When we talk abt vol, it is synonymous to talking about saline bc the total body Na determines the amount of volume in your body so you can also use saline balance or vol balance

Water balance - only talking abt osmolality or whether pxโ€™s plasma is diluted or concentrated. Talking abt water deficit or xs.

THERE IS A DIFFERENCE BETWEEN VOL BALANCE AND WATER BALANCE!! Easiest analogy for this: vol balance - talking about analogy to coffee: small cup or big mug of coffee of the same size but diff volume. For water balance, two cups of coffee of the same size but one is v concentrated (like espresso) and one is cafe americano (w/c is more or less a little diluted) so talking abt osmolality or conc not how much volume there is.

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3
Q

Percentage of water in body weight

Body Fluid Compartments

A

55-60% of body weight is water

Fluid compartments
40% Intracellular Fluid
20% Extracellular fluid
>5% Intravascular (Plasma)
>15% Interstitial
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4
Q

Major cation in the ECF? ICF

A

PISO
Potassium In, Sodium Out

ECF: Na+

ICF: K+

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5
Q

Daily water losses/Daily water output

A

Total output: 2.5 L

Urine: 1 - 1.5 L
Skin: 0.7 L
Feces: 0.15
Sweat: 0.15

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6
Q

Example you have 70 kg male so body water what is the water composition?

If you add 1.5 L of D5W I, how will water be distributed?

A

60% of body weight (70 kg) = 42 L
>ICF: โ…” = 28 L
>ECF: โ…“ = 14 L

The 1.5 L D5W will be distributed across all compartments of the body. Because freely permeable, water given in the intravascular space is eventually distributed all throughout so osmolality becomes lower because you added.

1.5 divided by โ…” for ICF and โ…“ for ECF. Remember EC is further divided into intravasc and interstitial. 125 mL remaining in intravascular space. Showing you that you cannot expand effectively your intravascular space if youโ€™ll just give D5Water or water.

Thus, we do NOT use D5W or water in to expand intravasc space in px.

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7
Q

After receiving 1.5 L of plain NSS IV, the ECF compartment of a person is expected to expand by how many mL?

How many mL will remain in the intravascular space?

A

1500 mL.

Inject 1.5 L NSS IV, inject in EC, and itโ€™ll be distributed in the extracellular space only.

Why?
Na+ although can pass through PM and go into the cell, will just be pumped out again by your Na/K pump so itโ€™ll go out again, and effectively remain in the extracellular space.

For the intravascular space, 375 mL (ยผ of 1.5 L) will remain there and the rest goes into the interstitial space.

SO BETTER FLUID CHOICE TO EXPAND INTRAVASCULAR VOLUME rather than D5W or water.

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8
Q

Control of ECF

  • Afferent limb
  • Efferent limb
A

-Afferent limb:
HOW BODY DETECTS:
Remember, the priority of your body to maintain an effective circulating volume that means the intravascular space is the one most affected by the body so there are several sensors for your body to know how much is in the intravascular space. The sensors are found in the heart - in the atrium, ventricles; lungs, big arteries, big arteries (carotid, aortic arch baroreceptorsZ), kidneys brain, and even in the liver so there are many sensors that will tell your body whatโ€™s happening to the intravascular volume and they usually sense if there is a decrease in intravasc volume or effective circulating volume.

-Efferent limb:
HOW IS THE CONTROL AFFECTED: All of the main way that the body corrects fluid volume is through the kidneys. It will adjust your GFR (so that means if you have to reduce intravasc volume, the renal blood flow will go down and the filtration rate will go down so that you will not be losing fluid into your kidneys). It will also adjust the absorption factors that will allow greater absorption of your fluids and solutes into the tubules. And thereโ€™s activation of your hormones - your RAAS, ADH, PG, Natriuretic. Your renal nerves are also involved. But all of them basically ctrl your fluid retention in the kidneys.

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9
Q

Which of the ff laboratory results is compatible with volume depletion?

A. Low serum albumin
B. Hemoconcentration
C. BUN/Creatinine ratio of 10:1
d. Urine sodium > 40 meq/L

A

B. Hemoconcentration

Low serum albumin
-Increases because you have dec volume = concentration of plasma solutes

BUN/Creatinine ratio normal is 10-20:1.
-When you have vol depletion, both of them will go up bc you have dec RBF, dec GFR so both of them will go up. But you will notice that your urea (BUN), goes higher than crea making the ratio greater than 20:1 in px w/ vol depletion and explanation. When you have reduced blood flow to the kidneys due to vol depletion, you will also have reduced urine flow in the tubules and that will trigger the reabsorption of urea from the tubules back to the blood so your urea in the blood goes up, higher, since it is reabsorbed in states of deficit. But your crea is not reabsorbed so crea does not go up as high as urea.

Urine sodium

  • Reflection of how kidneys are expanding to the volume status
  • How kidneys are expanding to the vol status
  • If low, px has dec RBF = tubules will reabsorb as much as it can to the sodium filtered. Thus, urine sodium is expected to go down and the cut off is 20. Urine sodium of less than 20 meq/L is whatโ€™s expected in a px w/ volume depletion and w/ a fxning kidney tubules.
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10
Q

Best way to assess volume status?

A

Physical Examination

-Most importantly: Body Weight

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11
Q

Every 1 kg change in body weight = how much fluid change?

A

1L of saline either retained or lost

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12
Q

T or F. If px does not eat anything, she may lose more than 0.5 kg in a day.

A

F F F!!!

If px did not eat anything, the weight will not change by more than 1โ„2 a kilo a day. If the change is greater than that, then that means those changes are due to fluid retention or fluid losses so body wt is very impt.

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13
Q

Clinical Dx for Volume Status

  1. Weight
  2. BP
  3. Pulse
  4. CVP
  5. Skin turgor
  6. Buccal mucosa
  7. Hands, axillary region
  8. Edema
  9. Hgb/Hct
A

Clinical Dx for Volume Status

  1. Weight
    - Deficit: Dec
    - Excess: Inc
  2. BP
    - Deficit: Dec or orthostatic drop depending on severity
    - Excess: Inc
  3. Pulse
    - Deficit: Inc
    - Excess: Normal or Inc(?)
  4. CVP
    - Deficit: Dec
    - Excess: Inc
    - Measured via jugular venous distension; not all the time correlated

Other parameters that arenโ€™t as helpful but may give a clue:

  1. Skin turgor
    - Deficit: Poor
    - Excess: Normal
  2. Buccal mucosa
    - Deficit: Dry
    - Excess: Moist
  3. Hands, axillary region
    - Deficit: Dry
    - Excess: Moist
  4. Edema
    - Deficit: (-)
    - Excess: (+)
  5. Hgb/Hct
    - Deficit: Inc (concentrated)
    - Excess: Dec
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14
Q

How to determine severity of the deficit

A

Mild
BP: Normal BP
Estimated amount of fluid deficit: 3% of BW (1.5 - 2 L)

Moderate
BP: with postural hypotension
Estimated amount of fluid deficit: 6% (3-4 L)

Severe
BP: with frank hypotension
Estimated amount of fluid deficit: 9% (x > 5 L)

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15
Q

How do you replace fluids?

A

Replace only half of the estimated fluid deficit, then re-evaluate. Reason for this: we donโ€™t want to create iatrogenic problems. We donโ€™t want to immediately give back the amt that is lost and then cause volume overload on the px because estimate is wrong. So better to correct only half then re-eval then give again half until youโ€™ve corrected everything. Then the initial fluid deficit is suggested to be corrected w/in 1st 6 hrs.

โ—‹ So in px w/ mild - probably give abt a liter in the 1st 6-8 hrs, going to give half of estimated (2L).

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16
Q

Limitation of using PE to assess volume depletion

A

โ—‹ As said earlier, in assessing the vol status, use PE. V useful esp in the presence of mod to severe vol depletion. However in cases of mild vol depletion or mild vol excess, the PE would have significant limitation so much so that in some studies, clinicians can only correctly predict vol status 50% of the time using PE technique.

โ—‹ Even your CVP measurement and your PAWP measurement are not really that accurate as found out by newer studies so current recommendations or parameters we could use to assess vol status actually is recommending the use of dynamic variables such as measuring CO before and after volume challenge or doing leg racing test and measuring CO.

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17
Q

Treatment of Volume Deficit

A
  1. Quantify total deficit
  2. Quantify volume losses
  3. Estimate basic daily maintenance requirement
  4. Identify concomitant electrolyte and water imbalance
  5. Formulate replacement plan w/c should include the ff:
    a. Quantify replacement = deficit + active losses + basic daily requirement
    b. Replacement fluid = plain NSS or LR or balanced crystalloids; modify accdgly to concomitant electrolyte imbalance
    c. Rate of replacement = dependent on severity and rate of onset of the deficit
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18
Q

Basic daily requirement (Maintenance) of:

a. Water
b. Sodium
c. Potassium

A

a. Water: 2000 - 2500 mL
b. Sodium: 50 - 150 meq
c. Potassium: 40 - 80 meq

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19
Q

Q: Why do we have to give D5 together with water and not just plain or sterile water IV?

A

If you give a hypotonic fluid anything below the osmolality of the plasma, you will have intravascular hemolysis bc your RBC will burst in the presence of hypotonic fluid that you are infusing into the veins so D5 there will make fluid isoosmotic to plasma.

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20
Q

What will happen if you give a lot of NSS?

A

Cl lvls go up

Then we have your plain NSS or D5 NSS (normal saline soln) and that is 0.9% NaCl or 0.9 g NaCl per 100 mL = 154 meq/L Na and 154 meq/L Cl, you remember your serum Cl has an upper limit of abt 150 so giving a lot of NSS would make the Cl lvls in the blood higher.

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21
Q

What is your โ€œbalanced crystalloidsโ€ soln?

A

Lactated Ringerโ€™s

-come also in D5 LR of just plain LR, it has 130 meq/L Na and 4 meq/L K and some other small amts of other electrolytes. You can see this is more balanced hence called balanced crystalloids. Lvl of Na and K is v similar to blood.

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22
Q

What do you give in very severe or acute hyponatremic px?

A

Hypertonic solution like 3% NaCl IV

23
Q

Current recommendation in giving crystalloids

A

3 - 4 L of NSS then shift to LR

  • Avoids hyperchloremic metabolic acidosis in giving too much isotonic saline solution
  • Now, weโ€™ve mentioned earlier that normal plasma Cl is only abt up to 105 or in some labs 115 so it is v far from 154 meq Cl present in normal saline so the px may develop hyperchloremic metabolic acidosis if you give a lot of isotonic saline. So the recommendation now is if you have given abt 3-4L of normal saline and the px still needs crystalloids then maybe you can shift to LR.
24
Q

Adverse effects of resuscitation fluids

  1. Albumin
  2. Hydroxyethyl starch (HES)
  3. Dextrans
  4. Crystalloids
  5. NSS
A
  1. Albumin
    - colloid w/c expands intravascular volume easily but very expensive and is associated w/ increased mortality in traumatic brain injury
  2. HES
    - associated w/ increased AKI and renal-replacement therapy
    - No longer recommended as a volume expander
  3. Dextrans
    - Impaired coagulation and allergic rxn
  4. Crystalloids
    -Clinically significant interstitial edema
    -Remember for every L you give this via IV, 3โ„4 or 750 mL would be
    retained in the interstitial space and therefore may easily cause
    interstitial edema.
  5. NSS
    - Hyperchloremic metabolic acidosis and AKI
25
Q

Recommendation staet for shock

A

Give IV resuscitation w/ crystalloid or colloid, depending on w/c is available, at 20 mL/kg as a bolus (meaning 1 - 1.5 L fast drip) over 15-30 mins to bring px out of shock as quickly as possible.

Monitor BP v well.

If px has not improved, can continue to give another dose of that. If px improves, taper IV fluid to 10 mL/kg/hr (~500-700 mL/hr) then go down further up to 2-3 mL/kg/hr (100 - 150 mL/hr) maintaining that for at least 48 hrs while monitoring pxโ€™s hemodynamic status.

26
Q

In sepsis-induced tissue hypoperfusion, what do you give?

A

Initial fluid challenge meaning a minimum of 30 mL/kg (~ 2L) and if the px will not improve with this dose, can proceed to giving other agents (e.g. vasopressors).

27
Q

How to treat volume xs?

A

> Determine if thereโ€™s xs via PE<

  1. Quantify excess
    - Rough estimate
    - Best quantified via weight measurement
  2. Limit fluid and salt intake
    - First strategy to not make the vol xs worse
  3. Diuretics
    - Loop vs. distally acting
    - Depending on the severity and renal fxn
  4. Monitor body wt, input, and output
  5. Dialysis or Ultrafiltration
    - If retention and renal fxn is really very poor and px does not respond to diuretics
28
Q

What is the serum osmolality for a 35 year old male with the ff:

Serum Na = 140 meq/L
Blood sugar = 5 mmol/L
BUN = 4 mmol/L?

A

Answer: 289

Osmolality = 2 (serum Na) + Glucose + Urea

Shortcut: 2 x Serum Na

Shortcut bc in a normal situation wherein the glucose and urea lvls are normal that means no renal failure, no uncontrolled DM then amt of glucose and urea in a normal indiv is less than 5% of serum osmolality so negligible

โ—‹ Reason for multiplying by 2: serum Na is the most common cation in the ECF and we know that when you have cation, you have accompanying anion and therefore since osmolality refers to total solutes divided by the vol of water therefore need to consider both cation and anion and you can simply multiply serum Na by 2.

29
Q

What does a high serum sodium imply? How about a low serum sodium?

A

High serum sodium = water deficit

Low serum sodium = water excess
*If your serum sodium is low, that plasma is diluted, you have water excess

30
Q

Regulation of body water

A
  1. ADH release
    - Many things that stimulate it but on a minute to minute basis, stimulus: SERUM OSMOLALITY.
    - If serum osmolality goes up or serum Na goes up, it is quickly sensed by your brain in the hypothalamic area โ€”> Release ADH telling tubules to reabsorb all the water โ€”> correct the elevated osmolality in the serum

-MORE IMPT SENSOR/STIMULUS IN ADH RELEASE: ECV
Brain is v sensitive to effective circulating volume.
-If eff circ vol is low (e.g. dec CO, BP) -> stim ADH release -> kidneys retain a lot of water + vasoconstrictor effect

  1. Thirst mechanism
31
Q

Clinical manifestations of hyponatremia?

A

Hyponatremia = water xs

โ—‹ Main feature: Neurologic
-Bc it causes swelling of your cells and we know that your brain cells are the most sensitive for swelling or shrinkage thus, sx of water balance is mainly neurological so lethargy, headache, confusion, apprehension, depressed reflexes, seizures, coma

โ—‹ Ofc there could also be ms sx and GI sx

32
Q

A 21 y/o male diabetic px complains of dizziness, generalized weakness, and a BP of 80/50 mmHg. He has uncontrolled hyperglycemia, with serum Na = 125, serum osmolality = 270, urine Na = 100 meq/L, and urine sugar of +3. The px most likely has:

A. Pseudohyponatremia
B. Hypervolemic hyponatremia due to AKI
C. Euvolemic hyponatremia due to SIADH
D. Hypovolemic hyponatremia due to osmotic diuresis

A

Ans. D. Hypovolemic hyponatremia due to osmotic diuresis

Actually this q is easy to answer bc you are given a px who is obviously hypovolemic w/ BP below (on the shock lvl) so eliminates the top 3 bc only hypovol is D

โ—‹ How do we know itโ€™s due to osmotic diuresis? The urine sugar of +3 tells us that it is due to osmotic diuresis bc the sugar in the lumen of the tubules will draw the Na and water into the lumen and then go out in the urine so urine Na is still elevated despite the px being hypovolemic w/ BP on shock lvl. Kidneys still do not conserve Na bc thereโ€™s another mechanism drawing the sodium out into the lumen of the tubules and into the urine. This is not A bc A means the px has hyponatremia (loss of Na) but serum osmolality is normal. However in this case serum osmolality is low (normal: 290 - 300) so true hyponatremia.

33
Q

True hyponatremia vs. Pseudohyponatremia

Common causes?

A

We mentioned true hyponatremia or hypotonic hyponatremia meaning to say you have low serum osmolality w/ low serum Na. Then the other side we have pseudohyponatremia. So to distinguish these two, the best way is to measure serum osmolality.

Common causes of pseudohyponatremia (rare) would be:

  • presence of a lot of osmotic substances like mannitol
  • v high cholesterol and TG lvl
  • v high globulin albumin lvl

โ—‹ Now after you have determined that px indeed has true hyponatremia w/c is most often the case clinically, then assess volume status - whether the px is vol depleted or vol deficit, vol xs, or normal volume/euvolemia. So as you can see there really is a difference bet water balance (hyponat) and volume balance down here (doc pointed at assess ECF vol part) that the kidney is the reason why you are losing Na, there are renal losses of Na whether from the tubules malfxning or you have diuretics on board or other substances causing the diuresis. However, if urine sodium is low meaning to say the losses are not from your kidneys, you have extra renal losses and your kidneys are responding v well by conserving the sodium, so you may have GI losses. These are the common reasons for this so burns.

In the situation that you have hyponat and euvol, that means no evidence of vol depletion or vol xs meaning to say you have a normal body sodium content but your body is retaining water. You have an xs of body water. In these situations you expect your urine sodium not to be v low bc if v low, it means you are conserving the Na. In this situation your causes would be - you probably have endocrine d/o slide such as GC def, Hypothy, stress, drugs causing ADH release, or SIADH.

The third classification if you have hyponat and hypervol (so retain Na and water) and your water retention is more than your retention of Na thus you have relative water xs. In this situation if you see urine Na is low, meaning to say your kidneys are trying to conserve that means probably your ECBVol is low and you can see this in px w/ CHF, liver cirrhosis, some forms of GN presenting as nephrotic syndrome w/ v low serum albumin lvl. If your urine Na is high, then probably your kidneys cannot respond to whatโ€™s happening and that is a reflection of renal failure. Thatโ€™s also the reason why you have hypervolemia.

Hyponat
Hyper/hypovol + Urine Na > 20 = renal; if x < 20 = extra renal
Euvol + U Na

34
Q

Which of the ff is NOT associated with SIADH?

A. Narcotic drugs
B. Bronchogenic Carcinoma
C. Meningioma
D. CHF

A

D. CHF

โ—‹ Why? Bc in px w/ CHF, you have a dec ECBV remember your heart is failing, you have dec CO. So dec ECBV is a v strong stimulus for ADH release so therefore this is not inappropriate bc if the I in SIADH refers to inappropriate. In CHF you have elev ADH lvl but is appropriate for the condition.

โ—‹ In the other options, these are situations where you donโ€™t really need the ADH to go up but bc they are exogenously produced or effected by drugs, your ADH lvls go up.

35
Q

Diagnostic Criteria for SIADH

A

โ—‹ Clinical Euvolemia

โ—‹ Hypotonic hyponatremia - meaning serum osmolality is really low

โ—‹ Normal hepatic, renal, and cardiac fxn

โ—‹ Normal thyroid and adrenal fxn - can also cause hyponat

โ—‹ Urine osmolality > 100 mOsm/kg despite low serum osmolality - reflecting that kidney is trying to conserve water by making urine concentrated

โ—‹ Urine sodium > 20 meq/L - meaning kidneyss are not trying to conserve Na reflecting that px is not volume depleted

36
Q

Major guidelines for the management of hyponatremia?

A

โ–  1 - If px is asymptomatic then that means do not rush to correct the hyponatremia. However if px is having seizures, comatose, then you have to urgently improve that serum Na lvl.
โ— Chronic hyponat = present for more than 48 hrs = less likely to have severe symptoms. Thus no need to correct urgently

โ–  2 - If you correct hyponat too fast in px w/ chronic hyponat - then at risk for osmotic demyelination syndrome w/c is a worst neurologic situation than what the px already has at that time bc ODS is permanent damage to brain. So current recom corr of plasma Na+ at speed less than 8 mEq/L/day so meaning close and frequent monitoring of Na is needed

Note: response to interventions can be highly unpredictable so frequent monitoring of plasma Na+ conc during corrective therapy is imperative!!!

37
Q

How do you manage the ff:

a. Hypovolemic hyponatremia
b. Normovolemic hyponatremia
c. Hypervolemic hyponatremia?

A

โ—‹ So how do you manage hypovolemic hyponatremia? Manage the vol status of the px. Correct the vol status, the vol deficit for this particular case bc hypovolemic. The priority is to correct vol deficit by giving isotonic saline/NSS and most of the time the water balance will be corrected by your kidneys on its own.

โ—‹ And if you have normovolemic hyponatremia, then your 1st strategy would just simply be to limit water intake and allow your regular water losses to take care of the xs water. Correct underlying endo abn like your thyroid and adrenal dysfxn. Remove offending drugs (causing ADH release)

โ—‹ If you have hypoervolemic hyponat, then correct the underlying state (HF or liver failure) and you can you use loop diuretics

38
Q

Acute Symptomatic Hyponatremia

A

Defn:
Na < 120 meq/L and duration of x < 48 hrs

Etiology: Post op, exercise w/ hypotonic fluid replacement, recreational drugs (ecstasy)
-One scenario that this can be seen is in a post-op px who received anesthesia, narcotic drugs for pain in a setting wherein the ADH lvls are v high so if you give these px a hypotonic fluid then they will retain the water and the Na will suddenly drop and cause seizure and a bad prognosis for px. So in post op px we avoid hypotonic fluids and we can only give isotonic fluids. In px who runs a marathon and give only water, then those px may develop acute symptomatic hyponat. In the same situation in px who are taking ecstasy who will have a lot of thirst and drink a lot of water may develop acute hyponat.

Tx: Aggressively using 3% saline +/- loop diuretics to raise the serum Na to x > 120 meq/L
*Vasopressin antagonist (Tolvaptan) - increases renal water excretion w/o significant Na excretion.

39
Q

65 y/o male complains of polyuria, dry mouth, headache, and blurred vision. He is clinically euvolemic, serum Na = 162, urine osmolality = 100 mOsm/L. The serum Na was corrected w/ D5W and vasopressin injection. The reason for the hypernatremia is:

A: Osmotic diuresis
B. Intake of diuretics
C. Nephrogenic diabetes insipidus
D. Central diabetes insipidus

A

D. Central Diabetes Insipidius

-Main reason for choosing this: If px responded to vasopressin injection bc that is the mech for central DI. You have dec prod and release of ADH. So if you provide it then you correct the hypernat.

โ—‹ If px did not respond to vasopressin then it may be due to nephrogenic DI bc tubules are resistant to effect of ADH or vasopressin.
โ—‹ Not due to diuresis bc px is clinically euvol. If you have osmotic diuresis or intake of diuresis than you would have some evidence of hypovolemia.

40
Q

How do we approach px w/ hypernatremia?

A

The important step is assessing fluid volume status of the px. Does the px have extracellular volume increase meaning px has volume xs and therefore, the hypernatremia is due to increase in salt ingestion = px has normal volume status but hypernatremic. This means, pure water deficit. If the osmolality is low, it means water is being lost through kidneys. If high, that means water is lost elsewhere (insensible losses).

And then another category would be you have hypernatremia and px is vol depleted or have vol deficit. Again check urine sodium and urine osmolality and if urine sod is elev meaning to say you are losing Na and water through the kidneys so diuresis. If urine Na is low, you are losing the Na and the water outside the kidneys meaning to say from GIT or skin

Note:

Urine osmolality cut off: x = 700 mOsm/L

41
Q

Clinical Manifestations of Hypernatremia?

A

Thirst, lethargy, neuro dysfxn due to brain cell dehydration, decreased vascular volume

42
Q

How to compute for water deficit?

A

Water deficit = 0.6 x BW in kg x [ (Serum Na - 140)/140]

43
Q

To have about 1 meq/L change in serum K, means you have ___ change in total body K+?

A

200 meq change in total body Na since 98% of K+ is intracellular

44
Q

ECG changes seen in hypokalemia and hyperkalemia?

A

1st thing to look at: T wave

  • Normally rounded and normal-sized
  • Hypokalemia: Shallow, flat, or inverted
  • Hyperkalemia: Tall, peaked

U wave
-Prominent in HYPOkalemia

QRS
-Widened in HYPERkalemia

45
Q

A 19 y/o male developed ms weakness and cramps. BP is 90/60, serum K = 3 meq/L, urine K = 10 meq/L, thyroid function is normal. Serum HCO3 = 18.

The hypokalemia is most likely due to:

A. Renal potassium wasting
B. Hyperaldosteronism
C. Extrarenal loss of K
D. Gitelman syndrome

A

Ans: C. Extrarenal loss of K
-Clue: Urine K is low. If kidney were the reason for loss of K then urine K would be high above 20 mEq/L. But here low, so losing K outside of kidney w/c is most likely GI losses.

โ—‹ All other options are K losing states and K lvl would be elevated

46
Q

Which of the ff can lead to movement of K out of the cells?

A. Metabolic Acidosis
B. Administration of insulin and glucagon
C. Inhalation of beta-agonists
D. IV Calcium Gluconate

A

A. Metabolic Acidosis

In presence of a lot of H+ in the extracellular space, some of the H+ will go into the cells and in exchange for that, another cation, your K+, will move out thus, hyperkalemia.

Calcium gluconate - does not move K+ in or out but stabilizes the membrane especially of cardiac muscle and thus, used as a tx for hyperkalemia.

47
Q

How to treat px w/ hypokalemia?

A

There is such a thing as spurious hypokal that means the K lvl is not really low. Itโ€™s a lab problem and usually this is seen if you do not immediately check or process the serum that was submitted to the lab. And if the K keeps on going into the cell esp if the px has v high WBC count then the serum K would turn out to be low when checked. This is not common.

โ—‹ Another scenario would be shifting of K into the cell that means there is really no change in the amt of total body K. It just moves from EC to IC and you can suspect it if the px is taking insulin, have thyroid d/o, or metab alkalosis.

โ—‹ So once youโ€™ve confirmed that px indeed has hypokal, then check BP. Bc in the presence of HPN and hypokal then you need to suspect a hyperaldosterone state so you need to check the plasma renin and plasma aldosterone to determine if you have high renin, high ald lvl OR low renin, high ald lvl causing both the hypertension bc of the hyperaldosteronism, Na+ is retained and K+ is lost thatโ€™s
why you have hypokal.

โ—‹ If the BP is normal, the next step would be to check urine K, to deter whether you are losing the K into the urine wherein your urine K is elev or losing K extrarenally wherein your using K is low. Another thing you have to check is your acid base status bc it can also help you distinguish the diff causes of hypokalemia.

48
Q

Things to remember about K+ replacement

A

Check renal function - px w/ renal failure, you have to be v careful abt K+ replacement. Do NOT want overcorrection -> hyperkalemia

Oral route safer

If IV:
Max rate of replacement: 40 meq/hr
Max conc in IVF: 40 meq/L
Cardiac monitoring advised if IV replacement if more than 10 meq/hr.
-Reason: Anything higher than this rate can cause fatal cardiac arrhythmias. Thus, anything greater than 10 meq/hr of replacement then you need to do it under cardiac monitoring.

49
Q

Hyperkalemia

A
  • Serum K+ > 5.5 mEq/L
  • Check for renal dse (most common reason)
  • Massive cellular trauma
  • Addisonโ€™s disease (Dec Aldosterone)
  • K+ sparing diuretics
  • Insulin deficiency (K+ move out of cells)
  • Acidosis (K+ move out of cells)
  • Strenuous exercise (K+ move out of cells)
50
Q

Clinical manifestations of hyperkalemia

A
Early - hyperactive muscles, paresthesia
Late - ms weakness, flaccid paralysis
Change in ECG
Dysrhythmias
Bradycardia, heart block, cardiac arrest
51
Q

Treatment of hyperkalemia

A

Severe: Calcium gluconate IV

โ–  Ca gluconate is given if you have ECG changes to stabilize the cardiac membrane. This will only have transient effect.

โ–  Na bicarbonate IV is given if px is acidotic otherwise it is not going to have significant benefit

โ–  Glucose and insulin is given. Insulin will drive K into the cell transiently, the glucose there is to prevent hypoglycemia.

โ–  You can give px orally or via enema - K+ exchange resin to adsorb the K into the GIT and make it go out to the feces.

โ–  You can give diuretics esp loop to remove K into the urine

โ–  Can dialyse the px in severe hyperkal that is not responsive to the
measures above.

52
Q

Case: 65 y/o male w/ hx of CAD, admitted for DOB and decreasing UO.

BP = 140/80
Wt = 65 kg
Previous wt = 60 kg
PR = 110
Bilateral crackles
Grade 2 bipedal edema
RR = 30

Serum Na = 125 meq/L
Serum K = 6.0
Chloride = 90
Creatinine = 2 mg/dL

Identify the volume status, water balance, and K+ balance. Quantify then correct.

A

Volume Status: Excess
Quantify: 5 kg = 5 L excess
Correct: Loop diuretics IV (furosemide)
-Vol status - vol xs as evidence by edema, crackles, gain in weight
โ–  5kgwtgain=pxhasgained5Lofsaline
โ–  Management: IV loop diuretics (IV/fast bc px is already dyspneic and
pulmo congestion e.g. IV furosemide) AND restrict salt and water intake
of px

Water balance
Quantify: Hyponatremia; approx 4 L H2O
=0.6 x 65 x [(140-125)/140]
Correct: Loop diuretics and water/fluid restriction

K+ balance
Quantify: 6-4 = 2 meq/L; 2 x 200 mEq = 400 mEq total body K+ change
Correct: Loop diuretics (cause some K+ excretion), can also give while waiting for diuretic effect some glucose/insulin cocktail, K+ exchange resin

53
Q

General Principles in Fluid/Electrolyte Management

A

โ–  1. Do not completely rely on lab results, if it is NOT clinically compatible. Reason: It is frequent to see laboratory errors for electrolyte and acid base determination. They are v sensitive equipments. And therefore if they are not clinically compatible w/ the px, you may just have to repeat the laboratory test to be sure before you do any management. TREAT THE PX NOT THE LABORATORY RESULT.

โ–  2. Correct only half of the computed deficit. Although we gave you some formulas you can use to estimate amt of deficit, but they are just formulas and they are just estimates so rather than cause an iatrogenic problem by giving 100% of the estimate deficit right away, it is recommended to correct only half then reassess px and recompute if px really still has deficit.

โ–  3. Correct volume status as priority. Bc many times once you correct vol balance, the other electrolyte water balance would be corrected.

โ–  4. Rate of correction is proportional to the rate of development of the disorder. Meaning to say acute changes have to be corrected acutely. Chronic changes have to be corrected slowly corrected.

โ–  5. Re-evaluate frequently. You may sometimes even have to repeat your electrolyte blood accumulation every 4 hrs or 6 hrs so know exactly where you are in the management of the px.