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Pulmonary Flashcards

1
Q

What is the primary control of ventilation?

A

Central control from the brainstem. Senses blood pH & decrease in pH stimulates ventilation (increase in rate &/or depth of breathing).

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2
Q

What is the secondary control of ventilation?

A

Peripheral control from PaO2 sensors in the aortic arch. Decrease in PaO2 (hypoxemia) results in increase rate &/or depth of breathing.
*This is why chronic CO2 retainers rely on mild hypoxemia.

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3
Q

What is the clinical indicator of ventilation?

A

PaCO2 (Not PaO2)

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4
Q
  • Tidal volume (Vt) x respiratory rate.
  • Normal is 4L/min
  • Increase = increase work of breathing
A

Minute ventilation

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5
Q

What is the primary muscle of ventilation?

A

The diaphragm

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6
Q

What is the optimal position for ventilation?

A

Upright sitting position. The worst is flat on their back.

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7
Q

Volume of air that does not participate in gas exchange.

A

Dead space ventilation

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8
Q

~ 2ml/kg of Vt

Everyone has this, it is normal. No gas exchange at level of nose down to alveoli.

A

Anatomic dead space

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9
Q

Pathologic, non-perfused alveoli, PE.

A

Alveolar dead space

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10
Q

Anatomic dead space + alveolar dead space

A

Physiological dead space

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11
Q

Results in increase alveolar dead space! A clot in the pulmonary circulation.

A

Pulmonary embolism

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12
Q

Movement of blood past alveoli

A

Pulmonary perfusion

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13
Q

What is normal ventilation/perfusion ratio?

A

4L ventilation/min (V) / 5L ventilation/min (Q)

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14
Q

Ideal lung unit?

A

0.8 ratio

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15
Q

What lung do you want down?

A

The GOOD one

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16
Q

What is the treatment for VQ mismatch?

A

Give oxygen & treat underlying problem

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17
Q

An extreme V/Q mismatch that even 100% FiO2 will not correct.
-Example: ARDS.

A

Shunt

Treatment: Give 100 FiO2 & increase PEEP

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18
Q

Thebesian veins of the heart empty into the left atrium. This is why the normal oxygen saturation on room air is 95% to 99% & cannot be over 100% on RA.

A

Normal physiological shunt

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19
Q

What type of shunt is ventricular or atrial septal defects?

A

Anatomic shunt

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20
Q

Blood goes through lungs but does not get oxygenated resulting in ____?

A

Refractory hypoxemia.

*This is what happens in ARDS & is a pathologic shunt

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21
Q

Extends time of gas transfer, increases driving pressure, decreases surface tension of alveoli (preventing atelectasis)

A

PEEP

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22
Q

Delivery of O2 at meet tissue demands at the cellular level.

A

Adequate oxygenation

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23
Q

Normal arterial oxygen (PaO2)?

A

80-100 mmHg on RA

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24
Q

Normal mixed venous (SvO2)?

A

60-75%

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25
Q

What is the most sensitive indicator of oxygenation at the cellular level?

A

Mixed venous oxygen saturation

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26
Q

Normal oxygen content (CaO2)?

A

15-20 ml/100 ml blood

*Important when addressing anemia

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27
Q

Normal oxygen delivery (DO2)?

A

900-1100 ml/min

*Seen with pump problems

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28
Q

Normal oxygen consumption utilization (VO2)?

A

250-350 ml/min

*Low with septic shock

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29
Q

Normal alveolar-arterial (A-a) gradient?

A

<10 mmHg

*Indicates if gas transfer is normal and if not, how bad the V/Q mismatch or shunt is.

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30
Q

When do cells begin to have difficulty maintaining aerobic metabolism?

A

When PaO2 is less than 60

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31
Q

When SpO2 is at 90%, what is PaO2?

A

60%

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32
Q

What way does the oxyhemoglobin dissociative curve shift when hemoglobin holds onto oxygen?

A

Shifts to the left

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33
Q

What way does the oxyhemoglobin dissociative curve shift when hemoglobin releases oxygen?

A

Shifts to the right

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34
Q

What causes the oxyhemoglobin dissociative curve to shift left?

A

Alkalosis (low H+), low PaCO2, hypothermia, low 2,3-DPG. Bad for patients even though SaO2 high because it’s stuck to hemoglobin.

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35
Q

What causes the oxyhemoglobin dissociative curve to shift right?

A

Acidosis (high H+), high PaCO2, fever, high 2,3-DPG. Good for tissues even though SaO2 low.

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36
Q

An organic phosphate found in RBCs that has the ability to alter the affinity of hgb for oxygen.

A

2,3-DPG
*Decreased = hgb holding on to O2
Increased = hgb releases O2

37
Q

What causes decreased 2,3-DPG?

A

Multiple blood transfusions of banked blood, hypophosphatemia, hypothyroidism.

38
Q

What causes increased 2,3-DPG?

A

Chronic hypoxemia (high altitudes, chronic HF), anemia, hyperthyroidism.

39
Q

Do you use the pulse oximeter to monitor oxygenation status for the patient with CO poisoning.

A

NO because it cannot differentiate between CO & O2.

40
Q

What are normal carboxyhemoglobin levels?

A 
0-5% Normal
<15% Often seen in smokers
15-40% Headache & some confusion
40-60% Loss of consciousness, cheyne-stokes respirations
50-70% Mortality >50%
41
Q

What is the treatment for CO poisoning?

A

100% FiO2 until symptoms resolve & carboxyhemoglobin levels <10%. Hyperbaric oxygen chamber is available, generally within 30 min.

42
Q
  • Measurement of the elastic properties of the LUNG.
  • Tidal volume / plateau pressure (minus PEEP)
  • Increase in plateau pressure will decrease compliance
  • Affects (decreases) people with mainly airway problems (asthma) = increase work of breathing
  • Normal is ~45-50 ml/cm H2O
A

Static compliance

43
Q
  • Measurement of the elastic properties of the AIRWAY.
  • Tidal volume / peak inspiratory pressure (minus PEEP)
  • Increase in peak inspiratory pressure will decrease compliance
  • Affects (decreases) with pulmonary problems that involve the lungs (pneumonia, ARDS) = work of breathing
  • Normal is ~45-50 ml/cm H2O
A

Dynamic compliance

44
Q

When the H+ concentration is increased, the pH decreases & when the H+ concentration is decreased, the pH increases.

A

Henderson-Hasselbalch

*Inverse relationship between H+ & pH

45
Q

What is PaCO2 controlled by?

A

The lungs.

*It is a respiratory parameter & the lungs can change it in minutes

46
Q

What is HCO3 controlled by?

A

The kidneys.

*It is a metabolic parameter & is a slow change

47
Q

The difference between positive & negative anions.

A

Anion gap

*Will be increased in metabolic acidosis (DKA).

48
Q

What is normal anion gap?

A

5-15 mEq/L

49
Q

Problems with increase anion gap?

A

Ketoacidosis, uremia, salicylate intoxication, methanol, alcoholic ketosis, unmeasured osmoles (ethylene glycol, paraldehyde), lactic acidosis (shock, hypoxemia)

50
Q

A rapidly occuring inability of the lungs to maintain adequate oxygenation of the blood with or without impairment of carbon dioxide elimination.
*PaO2 <60, with or without PaCO2 >50 or more with pH <7.30.

A

Acute respiratory failure

51
Q

Examples of hypoxemic acute respiratory failure?

A

Pneumonia, ARDS, atelectasis, pulmonary edema, PE, interstitial fibrosis, asthma

52
Q

Examples of hypercapneic acute respiratory failure?

A

CNS depression (opiates), increase ICP, COPD, flail chest, ALS, Guillain-Barre syndrome, MS, MG, spinal cord injury, ARDS, asthma, COPD.

53
Q

Intended for patients with hypoxemia respiratory failure who have increased work of breathing. Includes FiO2 and 1 pressure setting in cm H2O pressure.

54
Q

Intended for patient with hypoxemia and/or hypercapneic respiratory failure. Includes FiO2 and 2 pressure settings (inspiratory & expiratory pressure).

55
Q

How does non-invasive ventilation affect preload and afterload?

A

It decreases it

56
Q

What sign is significant for fat emboli?

57
Q

Treatment for PE?

A
  • Fluids
  • Anticoagulation (Coumadin on 1st day if able)
  • Fibrinolytic therapy (for patients with hemodynamic compromise with low risk for bleeding)
58
Q

Mean PA pressure greater than 25 mmHg at rest & wedge pressure less than 16 mmHg at rest with secondary right heart failure.

A

Pulmonary HTN

59
Q

What is normal mean PA pressure?

60
Q

Pulmonary HTN that is sporadic & hereditary due to localized small pulmonary muscular arterioles (collagen vascular disease, drug/toxin induced).

A

Group 1 defined by WHO

61
Q

Pulmonary HTN due to left HF, valvular heart disease.

A

Group 2 defined by WHO

62
Q

Pulmonary HTN due to lung diseases or hypoxemia.

A

Group 3 defined by WHO

63
Q

Pulmonary HTN due to chronic thromboembolic problems.

A

Group 4 defined by WHO

64
Q

Pulmonary HTN due to unclear or multifactorial (sarcoidosis).

A

Group 5 defined by WHO

65
Q

Cough, hoarseness, hemoptysis. Often seen in pulmonary HTN.

A

Ortner’s syndrome

66
Q

What kind of murmur do you hear with pulmonary HTN?

A

Systolic ejection murmur with increased intensity of pulmonic component of S2, diastolic pulmonic regurgitation murmur, right sided murmurs, & gallops are heard with inspiration.

67
Q

How long after admission to qualify for HAP?

68
Q

What is diagnostic of pneumonia on WBC differential?

A

Increase bands (>10%)

69
Q

Goal of antibiotic therapy with pneumonia?

A

Give 1st dose within 4 hours. Given organism specific as soon at C&S available.

70
Q

Who should get pneumonia vaccine?

A

Patient 65 & older

71
Q

What is the most common aspiration?

A

Oropharyngeal

72
Q

What side do aspirations occur most?

A

The RIGHT bronchus because its shorter, wider, & with less of an angle.

73
Q

What does BP do with aspiration?

A

HoTN due to big fluid shifts

74
Q

If you witness aspiration, what should you do?

A
  • Place patient in slight Trendelenburg, on right side to aid drainage.
  • Suction mouth & pharyngeal areas.
  • Bronchoscopy for large particles
75
Q

Acute condition that triggers an inflammatory response resulting in an increase in permeability of the pulmonary capillary membrane that allows a transudation of proteinaceous fluid into the interstitial and alveolar space.
*This causes damage to Type 2 alveolar cells. These cells are responsible for surfactant production, which is why atelectasis occurs.

A

ARDS or ALI or non-cardiac pulmonary edema

76
Q

What is the criteria for ARDS/ALI?

A
  • Acute onset
  • Not due to HF
  • REFRACTORY hypoxemia, meaning present even with FiO2 at 100%
  • P/F ratio = 200 for ARDS & 201-300 for ALI
  • Wedge = 18 mmHg
77
Q

Stabilizes alveoli (“keeps them open”), increases lung compliance, eases work of breathing.

A

Surfactant

78
Q

What do you want to limit plateau pressure to in ARDS/ALI?

A

30 cm H2O or less.

79
Q

What do you want to limit Vt to in ARDS/ALI?

A

4-6 ml/kg. Low Vt will cause a raise in the PaCO2 (permissive hypercapnea) and a drop in pH.

80
Q

Type of pneumothorax due to therapeutic or diagnostic procedures.

A

Iatrogenic pneumothorax

81
Q

When air is unable to exit pleural space and causes mediastinal shift.

  • Outside air enters because of disruption of chest wall and parietal pleura.
  • Lung air enters because of disruption of visceral pleura.
A

Tension pneumothorax

82
Q

Signs & symptoms of spontaneous and traumatic pneumothorax?

A

Dyspnea, tachycardia, CP, unequal chest excursion, tracheal deviation TOWARD affected side, hypoxemia, decreased or absent breath sounds on affect side.

83
Q

Signs & symptoms of tension pneumothorax?

A

Tracheal deviation AWAY from affected side, tachycardia, distended neck veins, hypotension.

84
Q

How far above carina should the ETT be?

85
Q

What has a greater degree of dead space ventilation ETT or trach?

86
Q

What is the difference between AC & SIMV mode?

A

The patients spontaneous breaths in SIMV mode are at the patient spontaneous Vt, whereas in AC mode the patient’s spontaneous breaths will give them the set Vt.

87
Q

Ideal Vt outside of ARDS?

A

8-10 ml/kg

88
Q

Ideal vent settings for someone with asthma?

A
  • Provide short inspiratory time & long expiratory time
  • Low rate
  • Low Vt
  • High peak flow rate
  • Monitor for auto PEEP

CCRN (8 decks)

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