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OS 213 Respiratory Exam 2 > ARF and ARDS > Flashcards

ARF and ARDS Flashcards

1
Q

Used when there is either hypoxemia or hyoercapnia or both

A

Acute respiratory Failure

- Laboratory diagnosis

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2
Q

ARF is a laboratory diagnosis

A

Needs ABG

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3
Q

Criteria for ARF

A

pO2 <60mmHg and pCO2 >45 mmHG at rest, on room air and at sea level

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4
Q

Criteria for ARF in patients with chronic hypercapnic respiratory failure or COPD

A

Sudden deviation of 5 mmHg or more from previously stable levels represent Acute Respiratory Failure superimposed on chronic RF

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5
Q

Types of ARF

A

Hypoxemic

Hypercapnic

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6
Q

Hypoxemic RF

A

Hypoxemia, usually with hypocapnia

Low oxygen stimulates tachypnea (higher RR) which leads to lower CO2 level in ABG

Usually present in the context of diffuse lung injury

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7
Q

Prototype of Hypoxemic Respiratory Failure

A

ARDS

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8
Q

Hypercapnic Respiratory failure

A

Hypercapnia and hypoxemia are present

“Alveolar hypoventilation”

PAtients are usually sleepy and are bradypneic causing lower level of oxygen and higher CO2 level

Lungs are okay, problem is in pumping effect

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9
Q

Hypercapnic Respiratory failure

A

Increased CO2

PaCO2 = K x (VCO2/Va)

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10
Q

Alveolar Ventilation (VA)

A

VE-VD

VE=minute ventilation (RR x TV) = 60ml/kg
VD= Dead space

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11
Q

Minute ventilation (VE)

A

RR x TV

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12
Q

Alveolar Ventilation in Emphysema

A

High VD, LOW VE

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13
Q

Central cause of hypercapnic respiratory failure;

A

Decrease in Va

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14
Q

Causes of Decrease VA

A

Decrease VE with normal VD

Increase in VD with normal VE

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15
Q

Decrease in VE with normal VD

A

Anything that decreases RR (central control)

Anything that decreases TV (Chest wall disorders)

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16
Q

Increases in VD with normal VE

A

Disorders of neuromuscular origin

Disorders of increased VD

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17
Q

Disorders of ventilation

A

Disorders of Central Respiratory Control
Disorders of the chest wall
Disorders of neuromuscular origin

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18
Q

Disorders of Central Respiratory Control

A

Idiopathic hypoventilation (Ondine’s curse)
Central sleep apnea
Narcotic/sedative overdose - MOST COMMON CAUSE
Diseases of the Medulla
Hypothyroidism
Metabolic Alkalosis
Rabies

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19
Q

Disorders of the Chest Wall

A

Affects the tidal volume, not RR

a. Primary kyphoscoliosis
b. obesity - most common cause of decrease TV
c. Thoracoplasty
d. Method of removing TB infection but causes lung destruction
e. Pleural thickening-fibrosis decreases the compliance of the chest wall

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20
Q

Disorders of Neuromuscular Origin

A

Affects Tidal volume

a. GBS
b. MG or Eaton lambert
c, ALS
d. Spinal Cord injuries - most common
e. Peripheral nerve disorders
f. Skeletal muscl disorders
g. polymyositis
h. electrolyte abnormalities
i. drugs

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21
Q

Electrolyte abnormalities - causes respiratory muscular weakness

A

Hypophastemia
Hypomagnesemia
Hypokalemia - MOST common cause of ICU admission

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22
Q

Disorders of Increased VD

A

intrinsic lung problem
(+) VQ mismatch -> increase VD
Primary prototypes:

Emphysema(sever COPD) -most common
Characterized in a lot of cases with Rapid shallow breathing

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23
Q

Consequences of hypercapnia

A

Hypoxemia
Acidosis
Increased PVR
Dilatation of cerebral blood vessels

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24
Q

Hypoxemic Respiratory Failure

A

Characterized by severe hypoxemia, not responsive to supplemental high flow Oxygen

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25
Q

Inability to transfer adequate oxygen from the alveolar space to the pulmonary capillary blood

A

Oxygenation Failure

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26
Q

Measures the lungs ability to transfer oxygen to the capillary blood

A

Alveolar-aterial Oxygen Gradient

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27
Q

A-a gradient computation

A

PAO2 - PaO2

PAO2 = FiO2 x (Pb-PH2O) - PaCO2/RQ

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28
Q

How many percent of the atmosphere is oxygen

A

21%

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29
Q

Atmosphereic barometric pressure

A

760 mmHg at sea level

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30
Q

Water vapor pressure (inspired air is maximally saturated with water vapor at the alveolar level)

A

47 mmHg

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31
Q

Amount of carbon dioxide produced per mole of oxygen comsumed

A

Respiratory quotient

0.8 - regular diet
1.1 - pure CHO
0.7 - pure fat
4-6 if you consume 5000kcal meal

COPD is a CO2 problem - limit CHO

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32
Q

Normal A-a gradient

A

<20mmHg

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33
Q

Hypoxemic RF suggestive of intrinsic lung disease has a gradient of??

A

<20mmHg

34
Q

Syndrome of severe, acute respiratory failure characterized by respiratory distress, severe impairment of oxygenation, and non-cardiogenic pulmonary edema

A

ARDS

35
Q

Pathologic injury specific to ARDS

A

Diffuse alveolar damage

36
Q

ARDS definition by AECC

A

Acute onset(24hours). less than 7 days, never chronic

Bilateral infiltrates on CXR -look white

Pulmonary wedge pressure <18 mmHg or absence of clinical evidence of left atrial hypertension

Acute lung injury (PaO2: FiO2 <300)

ARDS: PaO2: FiO2 <200

37
Q

Berlin definition of ARDS

A

within 1 week of clinical insult

Bilateral opacities

Oxygenation:
MILD: 200-300 mmHg
MODERATE : 100-200 mmHg
SEVERE: <100mmHg

38
Q

if your PaO2 is >80, FiO2 is ____

A

21%

39
Q

Initial symptoms of ARDS

A

Tachypnea

40
Q

Most common ABG manifestation of ARDS

A

Hypocapnia

41
Q

Direct Lung Injury

A 
Aspiration of gastric contents
Severe thoracic trauma
Diffuse pulmonary infection
Toxic gas
Near Drowning
42
Q

Indirect Lung injury

A 
Severe sepsis
Sever enon thoracic trauma; multiple long bone frature
Hypovolemic shock
Hypertransfusion
Acute pancreatitis
Reperfusion injury
43
Q

Clinical Manifestation of ARDS

A

Rapid, 12-48 hours of the predisposing event but may be up to 5 days

44
Q

Pathophysiology of ARDS

A

Systemic inflammation

Failure of hypoxic vasoconstriction - > shunt and severe hypoxemia

45
Q

Temporal features for DAD

A 
Exudative phase (1-7 days)
Proliferative phase (7-21 days)
Fibrotic phase (>21 days)
46
Q

Exudative phase

A 
Interstitial and alveolar edema
Hemorrhage
Leukoagglutination
Necrosis: Type II pneumocytes, epithelial cells
Hyaline membrane
platelet fibrin thrombi
  • STill reversible
47
Q

proliferative phase

A 
Interstitial myofibroblast reaction
Luminal organizing fibrosis
Chronic inflammation
Parenchymal necrosis
Type 2 hyperplasia macrothrombi

*Phase acted on by steroids

48
Q

Fibrotic phase

A

Collagenous fibrosis
Macrocytic honeycombing
Mural fibrosis
Medial hypertrophy

49
Q

Radiologic findings in ARDS (CXR)

A
  • hard to diff from CHF
    Diffuse bilateral infiltrates
    Focal infiltrates
50
Q

CT SCAN findings of ARDS

A

Early phase: Ground glass opacities and homogenous consolidation distributed peripherally

Reversal of lung opacification when patients are placed in the prone position

51
Q

ABG TEst of ARDS

A

early phase : respiratory alkalosis (CO2 goes down at the start) with severe hypoxemia (comes later)

Clearance of CO2 is compromised giving way to respiratory acidosis

52
Q

What happens when your lungs becomes fibrotic?

A

TV becomes smaller which will increase your CO2

53
Q

Protective ventilation

A

Dont overstretch the lung

54
Q

Death in ARDS is due to?

A

Multiple organ failure and sepsis

55
Q

Only way you can prevent ARDS in patients is???

A

Restrictive Transfusion Therapy

56
Q

TIP off points Hypercapnic RF

A

Initial rapid shallow breathing -> Bradypnea and Decreased sensorium

Skin is flushed

Muscle twitches may occur

O2 saturation will become lower as CO2 increases

Wheezing, poor air entry or even normal auscultatory findings

57
Q

Tip off points Hypoxemic RF

A

Dyspnea and tachypnea
Restlessness and anxiety/confusion and delirium
Tachycardia, Elevated BP, Neck vein distension
Cardiac arrhythmia
Cyanosis
Rales/crackles on ausculation or poor air entry

58
Q

Patient is already hypoxemic but O2 saturation is still normal - what type of poisoning

A

CO poisoning - pulse oxymetry cannot differentiate carboxyhemoglobin from oxyhemoglobin

59
Q

Oxygen supplementation and goals

A

keep Hb at least 88-90% saturated (-60mmHg)

60
Q

Oxygen supplementation in on-going myocardial or cerebral ischemia

A

70mmHg (92-94%)

61
Q

Formula for oxygen Delivery

A

CO x CaO2

CaO2 = arterial oxygen content
1.39 x SaO2 x Hb) + (0.0031 x PaO2

62
Q

Methods of Oxygen Delivery

A 
Nasal prongs
Simple Face Mask
Partial Rebreather masks
Non Rebreather Masks
Venturi MAsks
63
Q

Advantage of nasal prongs

A

Allow Patients to eat, drink, and speak during O2 administration

64
Q

Disadvantage of Nasal Prongs

A

Exact FiO2 delivered is not known
admixing of supplemented O2 with room air

Flows greater than 5L/min may cause tissue desiccation (Airway will dry up), pain

65
Q

FiO2

A

inspiratory flow and pattern
RR, exhalation time
O2 flow rate
Mouth Breathing

66
Q

Limitations of Nasal prongs

A

limited to less than 5L/min

67
Q

Simple Face Masks

A

No valve or reservoirs

68
Q

Advantage of Simple Face masks

A

at 6-10 L/min, FiO2 ranges from 0.35-0.6

rebreathing is minimized

69
Q

Disadvantages of Simple Face Masks

A

FiO2 is an estimate
It is dependent on O2 flow, inspiratory flow pattern and pt. tidal volume

*if the flow rate is 5L/min, Co2 accumulation can occur; rebreathing can occur

70
Q

Partial Rebreather (Reservoir) masks

A

Bag is reservoir of oxygen and must be pre-filled with oxygen

Higher FiO2 values possible (0.70-0.85)- allows for higher conc of oxygen

At >8L/min, the reservoir usually is kept full

71
Q

Highest FiO2 achieved may reach almost ____

A

0.85

72
Q

Non rebreather Masks

A

Similar to rebreather masks except for two sets of one way valves:

FiO2 up to 0.8 to 0.95 can be achieved

73
Q

Masks usually for COPD

A

Venturi Masks

More precise control of FiO2

74
Q

Delivery of Positive pressure ventilation to the lungs without endotracheal intubation

A

NPPV

Bilevel Positive Airway Pressure
IPAP and EPAP
Biphasic positive airway pressure
CPAP with inspiratory assist
Pressure Support with assist
75
Q

Who are candidates for NPPV

A 
alert, cooperative paients
hemodynamic stability
No need for ET intubation
No acute facial trauma
Properly fitted mask
76
Q

Indications for mechanical Ventilation

A

Presence of apnea; tachypnea (>40/min)
BP <80mmHg
RF cannot be corrected by any other means

77
Q

Ventilation that allows small tidal volumes using high respiratory rates

A

high frequency oscillatory Ventilation

78
Q

use of perfluorocarbons

A

Partial Liquid ventilation

79
Q

Characteristics of perfluorocarbons

A

High solubility for oxygen
High solubility for CO2
immiscibility with surfactant
Low surface tension

80
Q

Indications for ECMO

A

Static lung compliance of less than 0.5 ml/cm H2O/kg
Transpulmonary shunt of more than 30% on FiO2
Reversible RF
less than 10 days on MV

81
Q

OPTIMAL MANAGEMENT OF ARDS

A

Ventilate with lung protective strategy
USE PEEP
Conservative fluid measurement
Steroids have no role for early ARDS

82
Q

Lung protective strategy:

A

VT of 6ml/kg, Pplat target of <30 cm H20, non-toxic FiO2 with more modest PaO2 goal of pO2 of at least 55mmHg or SpO2 at least 88%

OS 213 Respiratory Exam 2 (15 decks)

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