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Step 2 Secrets > Acid-Base & Electrolytes > Flashcards

Acid-Base & Electrolytes Flashcards

1
Q

How do you analyze ABG values?

A

Three basic points:
1. pH –> acidosis vs. alkalosis as the primary event.
2. Look at Carbon Dioxide (CO2) value.
If high:
— Respiratory Acidosis (pH 7.4)
If Low:
— Respiratory Alkalosis (pH > 7.4) –OR–
— Compensating for Metabolic Acidosis (pH 7.4) –OR–
— Compensating for Respiratory Acidosis (pH 7.4)

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2
Q

T/F: the body does not compensate beyond a normal pH.

A

True. the pH will never correct greater than 7.4. Overcorrection does not occur.

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3
Q

List the common causes of acidosis

A
    • (+) AG Metabolic Acidosis: MUD PILERS **
  • Methanol
  • Uremia
  • DKA
  • Polyethylene Glycol
  • Isonizaid, Iron Overdose
  • Lactic Acidosis
  • Ethylene Glycol
  • Rhabdomyolysis
  • Salicylate Overdose
    • Non - AG Metabolic Acidosis: HARD UPS **
  • Hyperalimentation (Refeeding syndrome…)
  • Acetazolamide (all of the “-zolamides” )
  • RTA type II (Proximal Tubule dysfx)
  • Diarrhea
  • Ureteroenteric fistula
  • Pancreaticoduodenal fistula
  • Spironolactone
    • Respiratory Acidosis: AC/DC’s **
  • Asthma
  • COPD
  • Drugs (Opioids, barbiturates, BZDs, EtOH: resp. depression)
  • Chest wall problems (paralysis, pain, GBS, MG crisis)
  • Sleep apnea
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4
Q

List the common causes of alkalosis.

A
    • Metabolic Alkalosis **
  • Diuretics (except carbonic anyhydrases)
  • Vomiting
  • Volume Contraction
  • Antacid Abuse/ Milk - Alkali Syndrome
  • Hyperaldosteronism
    • Respiratory Alkalosis **
  • Anxiety/Hyperventilation
  • ASA/Salicylate Overdose
  • PE ****
  • Compensation for DKA
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5
Q

What type of acid-base disturbance does ASA overdose cause?

A 
Respiratory alkalosis with metabolic acidosis (+AG)
Have to look for co-existing S/Sx:
- tinnitus
- hypoglycemia
- vomiting
- h/o of "swallowing pills"

Treatment: Alkalization of urine speeds excretion

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6
Q

What happens to the blood gas of patients with chronic lung conditions?

A

pH may be alkaline during the day because they breath better when awake.

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7
Q

Should you give bicarbonate to a patient with acidosis?

A

Step 1: IVF
Step 2: Correction of underlying disorder
Step 3: If all other measures fail and the pH remains

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8
Q

The blood gas of a patient with asthma has changed from alkalotic to normal, and the patient seems to be sleeping. Is the patient ready to go home?

A

NO - this means that the patient is crashing!!! they have tired themselves out and are no longer blowing off CO2.

pH in an asthma pt is initially high because they are trying to eliminate CO2. When this stops, then they retain CO2 (remember COPD) and the pH normalizes. At this point they can become acidotic and will require emergency intubation.

Appropriate treatment protocol:

  1. PREPARE for elective intubation
  2. Continue aggressive medical management with β-2 agonists (Albuterol Nebs), steroids, O2.
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9
Q

asthmatic + acidosis = really bad or just bad?

A

Really bad situation!!! need emergency intubation because the patient has reached the point of respiratory muscle fatigue 2/2 increased WOB.

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10
Q

List the signs and symptoms of hyponatremia.

A
  • Lethargy
  • Seizures
  • Mental status changes / confusion
  • Cramps
  • Anorexia
  • Coma
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11
Q

How do you determine the cause of hyponatremia?

A

Step 1: determine volume status

HYPOVOLEMIC Hyponatremia: DADA

  • Dehydration
  • Addison’s Disease
  • Diuretics
  • hypoAldosteronism (High K+)

EUVOLEMIC Hyponatremia: OPS

  • Oxytocin use
  • Psychogenic polydipsia
  • SIADH

HYPERVOLEMIC Hyponatremia: CNTHR

  • Cirrhosis
  • Nephrotic Syndrome
  • Toxemia
  • Heart Failure
  • Renal Failure
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12
Q

Hypo is hyponatremia treated?

A

Hypovolemic Hyponatremia: IVF with NS

Euvolemic & Hypervolemic Hyponatremia: Water/ Fluid restriction

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13
Q

What medication is used to treated SIADH if water restriction fails?

A

Demeclocycline –> Induces nephrogenic DI

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14
Q

What happens if hyponatremia is corrected too quickly?

What fluids should be used to correct hyponatremia and at what rate?

A

Central Pontine Myelinolysis (CPM)

Correct hyponatremia with:

If (+) Seizures –> Hypertonic Saline –> Briefly and cautiously

All other situations use NS (99% of the time this is the best choice).

Rate of correction: 0.5 - 1.0 mEq/L/hr. MAX!

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15
Q

What causes FALSE Hyponatremia?

A
  1. Hyperglycemia (When s[Glc] > 200mg/dL, correct sodium by adding 1.6mEq/L for each rise in 100mg/dL of s[Glc].
  2. Hyperproteinemia
  3. Hyperlipidemia

for #2, 3: TB[Na+] is normal, measured is low. Do NOT give supplemental Na+

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16
Q

What is the s[Na+] correction for s[Glc] > 200mg/dL?

A

add 1.6mEq/L to s[Na+] for every 100mg/dL above 200 mg/dL s[Glc]

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17
Q

What causes hyponatremia in post-op patients?

A

MCC: combo of pain + narcotics –> SIADH with overaggressive IVF administration

Rare cause that is often tested: Adrenal Insufficiency (s[K+] is high and BP is ↓ –> RAAS + Aldosterone system is defective)

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18
Q

What is the classic cause of hyponatremia in PREGNANT patents about to deliver?

A

Oxytocin - has an ADH-like effect

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19
Q

What are the S/Sx of hypernatremia?

A
  • AMS/ Confusion
  • SZs
  • Hyperreflexia
  • Coma
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20
Q

What causes hypernatremia?

A 
MCC: dehydration
Watch for:
- diuretic use
- Diabetes Insipidus
- Diarrhea
- Renal Dx 
- Iatrogenic causes (i.e. Excessive IVF admin.)

Rare causes:
SCDx –> Renal disease
Isosthenuria –> Inability to [urine]
Hypokalemia and Hypercalcemia –> impairs kidney’s ability to [urine]

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21
Q

How is hypernatremia treated?

A

Water replacement protocol is dependent on whether patient is hypovolemic +/- Sx:

Euvolemic Hypernatremia: Free Water Supplementation

Hypovolemic, ASx Hypernatremia: 5% Dextrose NS.

Hypovolemic, (+) Sx Hypernatremia: 0.9% Saline until euvolemic, then add 5% Dextrose. Once HD Stable, switch to 1/2 NS

Note: 5% Dextrose is NOT D5W and D5W should NOT be used in the tx of hypernatremia.

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22
Q

What are the S/Sx of Hypokalemia?

A

Skeletal Muscle: Weakness, Ventilatory Failure
If Smooth Muscle is affected: Paralytic Ileus, Hypotension
Cardiac Muscle: U waves, PVCs, PACs, Ventricular/Atrial Tachyarrhythmias

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23
Q

What is the effect of serum pH on s[K+]?

A

Δ pH = Δ s[K+] via cellular shift

Alkalosis –> Hypokalemia
Acidosis –> Hyperkalemia

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24
Q

Treatment for hyperkalemic patients

A

CBIGK:

  1. Calcium Gluconate
  2. Bicarbonate (Severely Hyperkalemic patients)
  3. Insulin
  4. Glucose
  5. Kayexalate

If the pH is deranged, fixing the pH will likely correct the s[K+]

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25
Q

What is the interaction between Digoxin and K+?

A

The heart is very sensitive to ↓ s[K+] when on Digoxin.

s[K+] should be monitored closely, ESPECIALLY in patients taking diuretics (think CHF patients!!)

26
Q

How should s[K+] be corrected?

A

Hypokalemia → corrected slowly!
PO replacement is preferred
IV replacement for NPO or severe derangements

DO NOT exceed > 20mEq/hr. K+ and always use Telemetry to track ECG when using IV K+ to trace any arrhythmias.

27
Q

When hypokalemia persists even after significant K+ repletion, what should you do?

A

Check the magnesium level.

When s[Mg2+] is ↓, the body cannot retain K+ effectively.

Correction of s[Mg2+] allows correction of s[K+]

28
Q

What are the S/Sx of Hyperkalemia?

A
  • Weakness
  • Paralysis

Most important: ECG Δs → Peaked T-waves, Widening of QRS, PR Prolongation, loss of P-waves → Sine Waves (when s[K+] > 5) → Asystole, V. Fib (when s[K+] > 7)

29
Q

What are the indications for emergent dialysis?

A

AEIOU

A: severe Acidosis (pH

30
Q

What causes hyperkalemia?

A
  • Renal Failure (AKI or CKD)
  • Severe tissue destruction (2/2 release of ↑IC[K+], i.e. rhabdo)
  • RTA Type IV ( 1° Renin or Aldosterone Df. or 2° Hypoaldosteronism 2/2 Addison Dx, SCDx, interstitial Dx, or DM!!!) (DM is a biggie!!)
  • Medications (stop K+ - sparing diuretics, βBs, NSAIDs, ACE-I, ARBs)
  • Adrenal Insufficiency (↓ s[Na+] + ↓ BP)
31
Q

What should you suspect if an ASx patient has Hyperkalemia?

A

1st consideration if patient is ASx + Nml ECG = blood sample is hemolyzed. Hemolysis = false ↑[K+].
Repeat test.

32
Q

ASx hyperkalemic patient, sample NOT hemolyzed. What is the treatment protocol?

A
  1. ECG to determine cardiotoxicity
    IF s[K+] 6.5 -and/or- (+) ECG Δs → Immediate IV Tx.
    Protocol:
  2. Calcium Gluconate → cardioprotective
  3. Bicarbonate (Severely Hyperkalemic patients) → alkalosis → EC → IC K+ shift
  4. Insulin → helps K+ shift
  5. Glucose → prevents hypoglycemia
33
Q

If Insulin and Bicarbonate are not listed on the exam, what can be administered to help shift K+ from EC → IC compartment?

A

β-2-agonists

34
Q

If a Sx or severely hyperkalemic patient has renal failure or initial Tx is ineffective, what should be done?

A

Emergent Hemodialysis + transfer to ICU

35
Q

What are the S/Sx of hypocalcemia?

A
  1. Neurologic Findings (MC: Tetany → (+) Chovstek & Trousseau Sign)
  2. Depression
  3. AMS (Encephalopathy)
  4. Dementia
  5. Laryngospasm
  6. Convulsions/ SZs
  7. ISOLATED QT-PROLONGATION
36
Q

Treatment of hypocalcemia

A

Step one: Determine if it is “True” Hypocalcemia by….

  1. Check s[Albumin]
  2. Check ionized or free s[Ca2+]
37
Q

Correction for s[Ca2+] in hypoalbuminemia

A

For every 1g/dL ↓ s[albumin] for s[albumin]

38
Q

Causes of hypocalcemia

A
  1. DiGeorge Syndrome (Tetany 24-48hrs s/p birth, absent thymic shadow on CXR)
  2. Renal Failure (2/2 dysfx of Vit. D metabolism)
  3. Hypoparathyroidism (MCC: s/p parathyroidectomy where all 4 parathyroid glands are accidentally removed)
  4. Vitamin D Df.
  5. Pseudohypoparathyroidism (Albright Hereditary Osteodystrophy)
  6. Pancreatitis
  7. RTA type I (Distal)
39
Q

What is Albright Hereditary Osteodystrophy

A

ADDx; mΔ GNSA-1 gene;
conferred via maternal imprinting
If mom gives it to you: full phenotype (AAIO + hypocalcemia)
If dad gives it to you: partial phenotype (Pseudo pseudo, no hypocalcemia)

Presentation: Child with...
S/Sx of chronic low calcium:
    - mental retardation
    - spastic movements
    - dry hair & skin
    - dental abnormalities

AND
tetany, SZ, myopathy, psych ds.

Presentation in adults: dementia, Tetany, SZs, myopathy, psych ds

40
Q

Cause of hypocalcemia in children?

A
  1. Hypoparathyroidism
  2. Pseudohypoparathyroidism
  3. Albright Hereditary Osteodystrophy
  4. Hypomagnesemia
  5. Vitamin D Deficiency
41
Q

What is the relationship between ↓s[Ca2+] and ↓s[Mg2+]?

A

It is difficult to correct the calcium until the magnesium is corrected

42
Q

How does the pH affect s[Ca2+]? When is this consideration most important?

A

Alkalosis due to → EC → IC Ca2+ shift

Clinically this scenario is MC in hyperventilation / anxiety syndromes where the patient eliminates too much CO2, becomes alkalotic, and then develops perioral and extremity tingling

Treat by correcting pH

43
Q

What is the relationship between Calcium and Phosphorous?

When is this relationship important to really look at?

A

Normal: ↑Ca2+ = ↓Phos. and vice versa (opposite directions)

In CKD this is important!! When you try to increase calcium with VD3 and calcium supplements you have to also reduce or restrict phosphorous intake.

44
Q

What are the S/Sx of hypercalcemia?

A

Hypercalcemia is most often ASx and discovered through routine lab tests.

When (+) Sx: “Bones, Stones, Groans, & Psychiatric Overtones”

Bones: Osteopenia, pathologic fractures
Stones: Nephrolithiasis, polyuria
Groans: Abdominal pain, anorexia, constipation, paralytic ileus, N/V
Psychiatric Overtones: Depression, psychosis, delirium/ confusion

Also = QT SHORTENING

45
Q

Hypercalcemia + Abdominal pain. What two conditions are often antecedent and associated with hypercalcemia?

A

PUD

Pancreatitis

46
Q

Causes of hypercalcemia

A

MCC: Hyperparathyroidism (MCC is a parathyroid adenoma, often associated with MEN IIa or IIb)

Other causes:

  • Vitamin A intoxication
  • Vitamin D intoxication
  • Sarcoidosis
  • Thiazide diuretics (Loops lose calcium, Thiazides retain calcium)
  • Familial hypocalciuric hypercalcemia (↓ U[Ca2+] + ↑s[Ca2+] which is an uncommon)
  • immobilization (2/2 increased osteoclastic bone resorption)
  • Malignancy
47
Q

What should be a follow up lab to an incidental finding of hypercalcemia?

A

PTH, U[Ca2+] 24 hr excretion

48
Q

Hypercalcemia that is aggravated by exposure to sunlight?

A

Sarcoidosis

49
Q

Why is hypercalcemia commonly seen in granulomatous diseases?

A

Granulomatous diseases: Sarcoidosis, tuberculosis, coccidiomycosis

The activated MØ (primarily M2) will release calcitriol in lung and lymph nodes, its release is independent of PTH.

50
Q

In immobilized patients, what intervention is helpful to prevent hypercalcemia?

A

Hypercalcemia in immobilized patients is 2/2 to ↑osteoclast activity. Bisphosphonates + hydration are effective interventions.

51
Q

How is ASx hypercalcemia treated?

A

Step 1: IVF
Step 2: Furosemide → Loops Lose Calcium
Step 3: PO Phosphorous (IV is contraindicated, dangerous)
Step 4: Calcitonin
Step 5: Bisphosphonates (osteoporosis: alendronate
Step 6: Prednisone (if Malignancy-induced Hypercalcemia)

52
Q

Bisphosphonate often used in Paget Dx?

A

Etidronate, it works like all other bisphosphonates in that it reduces osteoclastic activity.
UNLIKE the other bisphosphonates, it PREVENTS bone calcification.

for this reason etidronate is indicated for short term use only - 2 weeks to 3 months. If long term use is employed you run the risk of osteomalacia

53
Q

In what clinical scenario is hypomagnesemia usually seen?

A

Alcoholism → Mg2+ wasting through kidneys

54
Q

What are the S/Sx of Hypomagnesemia?

A

PROLONGED QT Interval on EC +/- Tetany

55
Q

In what clinical scenario is hypermagnesemia usually seen?

A

MCC: Iatrogenic in pregnant patients and treated for preeclampsia with Magnesium Sulfate.

56
Q

S/Sx of Hypermagnesemia

A
  • 1st sign: Decreased DTRs
  • Hypotension
  • Respiratory Failure

Sx are monitored closely as the are progressive!

57
Q

How is hypermagnesemia treated?

A
  1. STOP MAGNESIUM INFUSION!
  2. ABCs
  3. If Stable: IVFs
  4. Furosemide
  5. Last resort = Dialysis
58
Q

In what clinical scenarios is hypophosphatemia seen?

A
  • Uncontrolled DM (esp. in DKA)

- Alcoholic Patients

59
Q

S/Sx of hypophosphatemia?

A
  • NM distrubances: Encephalopathy, weakness
  • Rhabdomyolysis (esp. in Alcoholic patients)
  • Anemia
  • WBC & PLT dysfunction
60
Q

What is the IV fluid of choice in hypovolemic patients?

A

Normal Saline (0.9%NaCl) or Lactated Ringer (LRs) Solution - regardless of electrolyte problem.

61
Q

What is the maintenance fluid of choice for NPO patients?

A

1/2 NS with 5% Dextrose in Adults

1/4 NS with 5% Dextrose in Children 10 kg

62
Q

Should anything be added to IVF for NPO patients?

A

KCl: 10-20mEq/L to prevent hypokalemia (assuming nml baseline)

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