Hall qs Flashcards

1
Q

What is compression volume and how to calculate it?

A

Its the voulme of TV that isabsorbed by the breathing circuit.

(V delivered - V measured) / RR and then divided by peak airway pressure.

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2
Q

How differentiate the side effects of nitroprusside causing methemoglobinemia, cynaide toxicity, or thiocynate toxicity?

A
  • Methemoglbinemia; cause pulse ox to read 85%.
  • Cyanide: Metabolic ascidosis & resistent to hypotensive meds, confirmed with elevated mixed venous PO2
  • Thiocynate: in RF patients develop nausea, mental confusion, skeletal ms weakness.
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3
Q

To prevent postop pulm complications, which lung parameter should be maximized?

A

FRC

The goal to ensure it will be greater than closing volume (small airway closure volume).
Achived by ambulation, IS, deep breathing, positive pressure breathing.

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4
Q

Formula to calculate pulmonary vascular resistance?

A

(PAP mean - PAOP)/ CO then multiplied to 80

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5
Q

When is the time risk for second MI for patients with h/o MI undergoing surgery?

A

3rd postop for unknown reasons.

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6
Q

Whats the anesthetic concern in obesity patients?

A
  • Hypertensive, cardiomegaly & L sided HF (because CO must increase ~ 0.1 L/min for each kg of adipose tissue.
  • Reduced FRC
  • Airway often difficult.
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7
Q

classification of FEV/FVC in obstructive disease?

A

70% mild
60% moderate
50% sever

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8
Q

Which arrhythmia is ineffective by DC and cant be a choice in unstable patients?

A

Multifocal atrial tachycardia.

because it is a non-re-entrant mechanism (its ectopic rhythm) and therefore DC cant terminate it.

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9
Q

how much increase of PaCO2 in apnea period?

A

for the first minute it increase ~ 6 mm Hg then 3-4 mmHg each minute thereafter.

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10
Q

TPN complications?

A
  • Hyperglycemia
  • Hypoglycemia (if TPN stopped sudden)
  • Low Mg, PO4, Ca, K
  • Volume overload
  • catheter sepsis
  • Renal/hepatic dysfunciton
  • Thrombisis of central veins
  • Nonketotic hyperosmolar coma
  • increase work of breath due to increased CO2 production 2/2 overfeeding
  • Hyperchoremic metabolic ascidosis
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11
Q

O2 requirements in adults vs neonates?

A

Adults -> 3-4 mL/kg/min

Neonates -> 7-9 mL/kg/min (thats why alveolar ventilation doubles to meet increased O2 requirement)

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12
Q

Normal adult FRC volume?

A

2,4 L (1,2 L RV + 1,2 L ERV)

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13
Q

Formula to calculate O2 content in blood?

A

1.39 x Hgb x SaO2 + (0.003 x PaO2)

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14
Q

How much increase in minute ventilation with inhaled CO2?

A

2-3 L/min/mm Hg increase in PaCO2

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15
Q

What is the P50 of PaO2 that is required to produce 50% saturation of Hgb?

A

26 mmHg

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16
Q

What are the 2 factors that work of breathing related too?

A

1) work required to overcome the elastic force of the lung
2) the work required to overcome airflow or frictional resistances of the airway.

in other words its the product of transpulmonary pressure (the pressure differences between alveolar wall pressure and intrapulmonaty pressure)

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17
Q

Factors affecting mixed venous O2 sat? and what decreases it? (normal Svo2 is 75%)

A

1) Hgb % -> Anemia, decreases it
2) arterial PO2 -> Hypoxia, decreases it.
3) CO -> low CO decreases SvO2
4) O2 consumption -> increased consumption, decreases SvO2

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18
Q

Normal vital capacity is?

A

4.5 L in 60-70 ml/kg adult

its the total lung volume 6L - RV 1.2 = 5L)

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19
Q

If respiratory drive (minute ventilation) responds to low PaO2 through carotid bodies, how would you explain the increase in minute ventilation in CO poising since PaO2 will be normal?

A

by increased lactic acidosis produced by tissue hypoxia.

20
Q

An acute increase in PaCo2 of 10 mmHg will result in decrease in pH of …?

A

0.08 pH units

21
Q

How dose acidosis stimulate ventilation? whats the volatile effect on it?

A

1) via Carotid bodies mediated ventilator response to arterial acidosis.
2) The acidosis of CSF will stimulate ventilation via medullary chemoreceptors in forth cerebral ventricle.

Voltaile will greatly attenuate the carotid & aortic body mediated ventilator response to arterial acidosis but has little effect on medullary chemoresptors-mediated ventilator response to CSF acidosis.

22
Q

Formula to calculate HCO3 deficit? used treatment with NaHCO3 in metabolic acidosis

A

TBW x (24-HCO3) x 0.3

23
Q

What are the compnsatory mechanisim for respiratory alklosis?

A

1) shift in the equlibrium of HCO3 buffer system to increase production of CO2
2) alkilosis stimulates phosphofructokinase which increase glycolysis and production of pyruvate & lactic acidosis.
3) Decrease in HCO3 absorption by kidney.

24
Q

In respiratory alkaloids, how much HCO3 decreased in response to decreased PCO2?

A

for every 10 mmHg PCO2, 5 mEq/L decrease in HCO3

25
Q

What mechanical ventilation mode choice is best to wean patients from ventilator?

A

Assist/controlled ventilation (positive pressure ventilation triggered by small breathing efforts produced by patient)

you need a mode to exercise their inspiration muscles and decrease mean thoracic pressure

26
Q

Assisted/controlled ventilation vs Synchronized Intermittent mandatory ventilation (SIMV)

A

ACV -> will deliver a set TV with patient trigger, and will continue to deliver TV at set rate if no trigger
SIMV -> will allow spontaneous breathing without giving the set TV, however it will continue giving the set TV at set rate (mandatory breath that is intermittent and synchronized).

27
Q

What is the normal P50 of hgb saturation?

A

The P50 is the oxygen tension at which hemoglobin is 50% saturated. The normal P50 is 26.7 mm Hg

28
Q

What causes low P50 (<26 mmHg) and causes leftward shift of oxyhemoglobin dissociation curve?

A

Leftward shift = increase affinity for O2

  • hypothermia (low Temp)
  • alkalosis (low H) + hypocarbia
  • fetal Hgb
  • hemoglobinopathy ; carboxyhemoglobin, methemoglobnemia, sulfhemoglobin
29
Q

What causes High P50 (>26 mmHg) and causes rightward shift of oxyhemoglobin dissociation curve?

A

Rightward shift = decrease affinity for O2

  • Hyperthermia (high temp)
  • Acidosis (high H) + hypercarbia
  • increased 2,3-DPG content
  • pregnancy
  • SCD, thalasemia
30
Q

What pulmonary mechanics decrease with age?

A

Due to progressive stiffining of cartilage and replacement of elastic tissue in thtercostal and intevertebral area will decrease the compliance of thoracic cage. (VC, TLC, FEV1, ventilator response to hypercapnia and hypoxemia also the dimished pulm capillary bed density will cause v/q mismatch which decreases PaO2).

however FRC, RV, and closing volume increased.

31
Q

Which acid-base disturbance is least well compensated?

A

Metabolic alkaloids

Hypoventilation is limited by maximum PaCO2 >55

32
Q

PaO2 calculation?

A

PaO2 = (Barometric pressure -47) x FiO2 - (Paco2/0.8)

33
Q

Which venous blood sample site closly correlate with arterial O2 & CO2 (PaO2 & PaCO2)?

A

Back of the hand

Because it has very little O2 extraction.

34
Q

Which portion of PFT has the least dependent on patient’s effort?

A

FEF 25-75%

because its obtained from the mid-expiratory portion of the flow volume loop.

35
Q

Would you see cynosis in CO poising?

A

No

36
Q

% of O2 consumption due to work of breathing?

A

2% needed to overcome the elastic recoil of the lung and thorax, along with airflow or frictional resistance of the airway.

37
Q

Anatomical dead space per kg

A

2 ml/kg

38
Q

Most important buffering system in body?

A

HCO3

39
Q

relationship of pH and potassium?

A

inversely related, every increase of 0.08 of pH there is a 0.5 mEq/L decrease of K

40
Q

Change in PaCO2 1 mmHg result in …. pH change

Change in PaCO2 1 mmHg result in …. HCO3 change

A

0.08 unit change in opposite direction

1 mEq/L change in same direction

41
Q

A change of 10 mEq/L in HCO3 result …. change in pH

A

0.15 units in same direction

42
Q

Right shift of oxyHgb curve

A

Pregnancy
Abnormal Hgb (Hgb S)
Volatile
Increased PaO2

43
Q

When treating a ptn with CO toxicity, what the half life of car carboxyhemoglobin if O2 treatment was 100%

A

It decreases the half life from 4 to 6 hours with room air to ~ 1 hour. (Hyperbaric chamber reduces it to 15-30 min)

44
Q

Positioning and ventilation associated with least risk for venous air embolism when removing the central line

A

goal is to have a positive pressure and greater then atmospheric at the site of removal

With trendelenburg (you keep the site below the level of the heart) which will keep the venous to atmospheric pressure positive

By mechanical ventilation or exhaling/valsalva in spontaneous breathing will make the venous-atmospheric pressure grater then spontaneous inhalation

45
Q

Adverse effects of acidosis

A
  • CNS depression
  • Increased ICP
  • CVS depression (partially offset by catecholamines secretion and elevated Ca)
  • cardiac dysthymia
  • vasodilation
  • hypovolemia
  • plum HTN (2/2 increase plum resistance)
  • hyperkalemia
46
Q

Extubation measurement criteria

VC 
PaO2 
A-a gradient 
pH 
Dead space/ TV ratio 
Max inspiration pressure at least
A
VC 15 mL/kg
PaO2 > 60 (FIO2 <0.5)
A-a gradient < 350
pH > 7.3
Dead space/ TV ratio <0.6
Max inspiration pressure at least -20
47
Q

Which lung zone has the highest V and Q?

A

Both ventilation and perfusion are greater near the base, but perfusion decreases quicker with each rib level. This leads to an increased V/Q ratio.