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Principles I > interpretation of monitoring data > Flashcards

interpretation of monitoring data Flashcards

1
Q

what usually causes hypernatremia?

A

Low total body water

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2
Q

what is considered hypernatremia?

A

Na+ > 145

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3
Q

what are signs and symptoms of hypernatremia?

A
  • CNS changes
  • mental status changes
  • irritability
  • hyperreflexia
  • ataxia
  • seizures
  • hypotension after induction
  • *think of AP, more Na+ available so it AP increases
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4
Q

what treatment and management are needed with hypernatremia?

A
  • delay surgery if signs and symptoms present
  • if volume depleted, may need CVP monitoring
  • replace free water
  • may need vasopressors and/or inotropic support with hypovolemia
  • VOD of drugs decrease, so may be more sensitive and need a decreased dose
  • if hypervolemic hypernatremia, give diuretics
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5
Q

what is considered hyponatremia?

A

Na+ < 135

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6
Q

what is commonly the cause of hyponatremia?

A

high total body water

  • more common than hypernatremia and usually more serious
  • seen often with CHF
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7
Q

what are signs and symptoms of hyponatremia?

A
  • CNS changes
  • lethargy
  • cramps
  • decreased reflexes
  • seizures
  • Na+ < 120 associated with 50% mortality rate
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8
Q

what treatment and management are needed with hyponatremia?

A
  • delay if possible and necessary to allow s/sx to resolve
  • if volume overloaded may need CVP monitoring
  • HF may need inotropic support
  • loop diuretics
  • acute symptomatic: tx with hypertonic saline
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9
Q

what should hypertonic saline be infused at?

A
  1. 5-2 mEq/hr
    * too rapid a correction with 3% saline may lead to demyelination of pontine neurons and a condition known as central pontine myelinolysis
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10
Q

what is considered hyperkalemia?

A

K+ > 5.5

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11
Q

when is hyperkalemia commonly seen?

A
  • ESRD
  • hemolysis (cell destruction releases K+)
  • DKA
  • drug therapy
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12
Q

what are signs and symptoms of hyperkalemia?

A
  • usually deal with electrical conduction system of the heart
  • K+ >6.0 can see prolonged PRI and peaked T waves
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13
Q

what is treatment and management of hyperkalemia?

A
  • delay if needed
  • avoid hypoventilation and high EtCO2 and acidosis
  • for every 10 mmHg change in EtCO2, K+ changes 0.5 mEq (may not want to do MAC d/t hypoventilation)
  • avoid Succs (increases K+ 0.5 mEq)
  • D10 plus insulin (glucose drives K+ into cell)
  • Ca++ (moves threshold higher away from rmp so wont see as many effects of hyperkalemia)
  • Lasix can help excrete
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14
Q

what is considered hypokalemia?

A

K+ < 3.5

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15
Q

what are common causes of hypokalemia?

A
  • diuretics
  • N/V
  • GI losses (NG suction)
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16
Q

what are signs and symptoms of hypokalemia?

A
  • muscle weakness
  • cramps
  • PVCs
  • U waves (right after T wave)
  • flattened T waves
  • low ST segment
  • digoxin toxicity
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17
Q

what are treatment and management of hypokalemia?

A
  • delay if needed
  • avoid hyperventilation and low EtCO2 and alkalosis
  • K+ replacement (20 mEq KCL over 30-45 min)
  • watch for prolonged muscle relaxation form NMBs
  • avoid glucose containing fluids
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18
Q

what are common causes of hypercalcemia?

A
  • hyperparathyroid (PTH)
  • cancer
  • breast cancer alone causes 25-50% of cases
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19
Q

what are signs and symptoms of hypercalcemia?

A
  • N/V
  • decreased deep tendon reflexes
  • hypotonia
  • confusion
  • lethargy
20
Q

what are treatment and management of hypercalcemia?

A
  • maintain hydration and UOP
  • loop diuretics
  • *avoid thiazide diuretics, they increase Ca++
  • monitor muscle relaxation w/ nerve stimulator (enhances NMB)
21
Q

what are common causes of hypocalcemia?

A
  • decreased PTH
  • decreased Mag (causes increased end-organ resistance to PTH)
  • alkalosis (increased pH causes Ca++ bind to protein)
  • massive blood transfusion (citrate binds Ca++)
  • pancreatitis
  • hypoparathyroidism
  • accidental removal of parathyroid
22
Q

what are signs and symptoms of hypocalcemia?

A
  • tetany
  • twitching
  • laryngospasm
  • tingling lips and fingers
  • spontaneous APs are generated
23
Q

how does Ca++ and K+ affect rmp and threshold?

A
  • high K+ moves rmp up closer to threshold (more AP)
  • low K+ moves rmp down away from threshold (less AP)
  • high Ca++ moves threshold up away from rmp (less AP)
  • low Ca++ moves threshold down away from rmp (more AP)
24
Q

what are common causes of hypermagnesium?

A
  • infusions like for preeclampsia and pheochromocytoma

* rare

25
Q

what are signs and symptoms of hypermagnesium?

A
  • lethargy
  • loss of deep tendon reflexes
  • paralysis
  • hypotension
  • heart block
  • acidosis worsens
26
Q

what are treatment and management for hypermagnesium?

A
  • temporary dialysis
  • loop diuretics
  • reduce muscle relaxants
  • adequate ventilation to avoid acidosis
27
Q

what are common causes of hypomagnesium?

A
  • poor GI absorption
  • dialysis
  • ETOH
28
Q

what are signs and symptoms of hypomagnesium?

A
  • ventricular dysrhythmias
  • muscle weakness
  • twitching
  • tetany
29
Q

what are treatment and management for hypomagnesium?

A
  • supplemental Mag
  • avoid diuretics (Mag follows Na+)
  • caution with muscle relaxants
  • *Mg++ helps treat and correct refractory hypocalcemia and hypokalemia
30
Q

what is the FEV1 in pulmonary function tests?

A

volume forcefully exhaled in one second

31
Q

what is the FVC in pulmonary function tests?

A

total volume that can be forcefully exhaled

32
Q

how are FEV1 and FVC used in pulmonary function tests?

A

ration of FEV1/FVC used to distinguish between obstructive vs. restrictive pulmonary disease

33
Q

what is indicative of obstructive disease?

A
  • both FEV1 and FVC are low
  • ratio is < 0.7
  • mild = 0.6-0.7
  • moderate = 0.4- 0.6
  • severe = < 0.4
  • cant get as much of what is taken in out
34
Q

what is indicative of restrictive disease?

A
  • both FEV1 and FVC are low
  • ratio is > or equal to 0.7
  • cant get in much but can get most of it out in good timing
35
Q

what is mixed venous (SvO2) and central venous (ScvO2)monitoring?

A

indicator of balance between oxygen delivery and consumption

  • normal range 68-80%
  • normal extraction 25% (amount taken from blood to supply tissues, etc.)
36
Q

what are the four primary factors that impact SvO2?

A
  • oxygen consumption (VO2)
  • hemoglobin level (hgb)
  • cardiac output (CO)
  • arterial oxygen saturation (SaO2)
37
Q

how is O2 consumed?

A
  • consumption varies by organ
  • a lot taken up by coronary sinus
  • a lot used for myocardium and skeletal muscle
38
Q

when hgb, SaO2, and VO2 are stable, changes in SvO2 indicate what?

A

changes in CO

39
Q

SVO2 < 30% usually indicates what?

A

anaerobic metabolism

40
Q

how does the body compensate for increased VO2?

A

increasing CO

41
Q

what decreases SVO2?

A
  • increased VO2: fever, hyperthermia, stress, pain, shivering
  • decreased hgb: anemia, hemolysis
  • decreased SaO2
  • decreased CO: MI, CHF, hypovolemia
42
Q

what increases SVO2?

A
  • decreased VO2: cyanide toxicity, CO poisoning, hypothermia, sepsis, analgesia, sedation, ventilation
  • increased hgb: volume depleted
  • increased SaO2
  • increased CO: burns, inotropic drugs
43
Q

why is there an increase in SVO2 with sepsis?

A

in severe late stage sepsis, mitochondria are essentially poisoned by endotoxin leading to a defect in oxygen utilization

44
Q

what is the most reliable method of temperature monitoring?

A

bladder

45
Q

what is ejection fraction?

A
  • measures the degree of systolic dysfunction
  • stroke volume/ end-diastolic volume
  • typical SV approx. 70 ml, typical EDV approx. 120
  • typical EF approx. 58%
  • American society of echocardiology: normal EF 55% or >
46
Q

what are the different grades of systolic dysfunction?

A
  • mild = 45-54%
  • moderate = 30- 44%
  • severe = < 30%
47
Q

what happens with a poor EF?

A
  • drugs take longer to circulate, so pt. will take longer to induce
  • propofol not a good drug with poor EF patients

Principles I (18 decks)

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