Interpretation of Monitoring Flashcards

1
Q

Hypernatremia value

A

> 145

usually hypovolemic

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2
Q

CNS changes, mental status changes,
irritability, hyperreflexia, ataxia, seizures, hypotension
after induction.

A

signs and symptoms hypernatremia

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3
Q

Treatments for hypernatremia

A

volume
diuretics if hypervolemic
vasopressors, inotropes

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4
Q

Hyponatremia [more commom] value

A

Na <135, usually hypervolemic

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5
Q

CNS,lethargy, cramps, decreased reflexes, seizures.

A

hyponatremia s&s

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6
Q

Na+ <120 associated with

A

50% mortality rate

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7
Q

treatment hyponatremia

A
  • CHF inotropes
  • lasix
  • replete Na with 3% saline
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8
Q

Too rapid a correction with 3% saline (hypertonic saline) may lead to

A

demyelination of pontine neurons and a condition known as central pontine myelinolysis

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9
Q

Hyperkalemia value

A

> 5.5

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10
Q

f K+ > 6.0, what rhythm changes will you see?

A

prolonged PR, peaked T waves

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11
Q

significant S&S of high K?

A

conduction disturbances of the heart

[ESRD, HD, DKA, meds]

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12
Q

treatments of >K?

A

avoid acidosis, hypoventilation, >ETCO2
Calcium
lasix
glucose/insulin/D10

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13
Q

for every 10 mmHg change in EtCO2 the K+ changes

A

0.5 mEq

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14
Q

what med should you avoid with >K and why?

A

avoid succinylcholine, intubating dose ↑’s K+ 0.5 mEq

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15
Q

Hypokalemia value

A

<3.5

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16
Q

typical causes of

A

diuretics, N/V, GI losses

17
Q

muscle weakness, cramps, PVCs, high U waves,
flattened low or even inverted T waves, low ST
segment, worsens digoxin toxicity

A

S&S

18
Q

treatment

A

avoid hypoventilation, alkalosis
glucose
k replacement

19
Q

what does

A

prolongs

20
Q

causes of hypercalcemia

A

hyperparathyroid, cancer,

*breast cancer alone causes 25-50% of hypercalcemia.

21
Q

N/V, ↓ deep tendon reflexes, hypotonia,

confusion, lethargy

A

hypercalcemia S&S

22
Q

treatment hypercalcemia

A

Maintain hydration and UOP.
• Loop diuretics (avoid thiazide diuretics, they ↑Ca++
reabsorption)
• Monitor muscle relaxation using nerve stimulator.

23
Q

Hypocalcemia causes

A

↓’d PTH, ↓’d Mg+ (causes ↑’d end-organ resistance to PTH)
alkalosis (↑’d pH causes iCa++ bind to protein),
massive blood tx, (citrate binds Ca++),
pancreatitis,
hypoparathyroidism
removal of parathyroid

24
Q

tetany, twitching, laryngospasm, tingling lips &

fingers. Spontaneous action potentials are generated.

A

Hypocalcemia

25
Q

treatment hypocalcemia

A

Avoid hyperventilation
• Avoid alkalotic conditions, maintain normal to hypercarbic
state (↑EtCO2)
• IV replacement if severe symptomatology.

26
Q

Hypomagnesemia causes

A

Poor GI absorption, Dialysis, ETOH

27
Q

S&S hypomagnesemia

A

Dysrhythmias, Ventricular
–Muscle weakness/twitching/tetany
–Tetany

28
Q

Treatment

A

Supplemental Mg++
–Avoid diuretics Mg++ follows Na+
–Cautious with muscle relaxants
–Mg++ helps treat and correct refractory hypocalcemia and hypokalemia

29
Q

Hypermagnesemia causes

A

Rare, infusions for preeclampsia and pheo

30
Q

S&S hypermagnesemia?

A

–Lethargy, Loss of deep tendon reflexes, paralysis,
hypotension, heart block
–Acidosis worsens effects

31
Q

treatments hypermagnesemia?

A

temporary dialysis
–Loop diuretics
–Reduce muscle relaxants
–Adequate ventilation to prevent acidosis

32
Q

Measures the degree of systolic dysfunction

A

Ejection Fraction, normal 55 or greater

33
Q

Graded Systolic Dysfunction

A
  • Mild 45-54%
  • Moderate 30-44%
  • Severe less than 30%
34
Q

Indicator of balance between oxygen delivery &
consumption. Normal range 68-80%. Normal
extraction around 25%

A
Mixed Venous (SvO2) and Central 
Venous (ScvO2)
35
Q

Four primary factors impact SVO2

A

–Oxygen consumption (VO2)
–Hemoglobin level (hgb)
–Cardiac Output (CO)
–Arterial oxygen saturation (SaO2)

36
Q

Decreased svo2 causes

A
  • Increased VO2 (Fever, hyperthermia)
  • Decreased hgb (anemia, hemolysis)
  • Decreased SaO2
  • Decreased CO (ex: MI, CHF, hypovolemic states)
37
Q

increased svo2

A

• Decreased VO2 (cyanide toxicity, carbon monoxide poisoning, hypothermia, sepsis)
Increased hgb (volume depleted)
• Increased SaO2
•Increased CO (burns, inotropic drugs)