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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
Inability to transfer adequate oxygen from the alveolar space to the pulmonary capillary blood
Oxygenation Failure
26
Measures the lungs ability to transfer oxygen to the capillary blood
Alveolar-aterial Oxygen Gradient
27
A-a gradient computation
PAO2 - PaO2 PAO2 = FiO2 x (Pb-PH2O) - PaCO2/RQ
28
How many percent of the atmosphere is oxygen
21%
29
Atmosphereic barometric pressure
760 mmHg at sea level
30
Water vapor pressure (inspired air is maximally saturated with water vapor at the alveolar level)
47 mmHg
31
Amount of carbon dioxide produced per mole of oxygen comsumed
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
32
Normal A-a gradient
<20mmHg
33
Hypoxemic RF suggestive of intrinsic lung disease has a gradient of??
<20mmHg
34
Syndrome of severe, acute respiratory failure characterized by respiratory distress, severe impairment of oxygenation, and non-cardiogenic pulmonary edema
ARDS
35
Pathologic injury specific to ARDS
Diffuse alveolar damage
36
ARDS definition by AECC
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
Berlin definition of ARDS
within 1 week of clinical insult Bilateral opacities Oxygenation: MILD: 200-300 mmHg MODERATE : 100-200 mmHg SEVERE: <100mmHg
38
if your PaO2 is >80, FiO2 is ____
21%
39
Initial symptoms of ARDS
Tachypnea
40
Most common ABG manifestation of ARDS
Hypocapnia
41
Direct Lung Injury
``` Aspiration of gastric contents Severe thoracic trauma Diffuse pulmonary infection Toxic gas Near Drowning ```
42
Indirect Lung injury
``` Severe sepsis Sever enon thoracic trauma; multiple long bone frature Hypovolemic shock Hypertransfusion Acute pancreatitis Reperfusion injury ```
43
Clinical Manifestation of ARDS
Rapid, 12-48 hours of the predisposing event but may be up to 5 days
44
Pathophysiology of ARDS
Systemic inflammation | Failure of hypoxic vasoconstriction - > shunt and severe hypoxemia
45
Temporal features for DAD
``` Exudative phase (1-7 days) Proliferative phase (7-21 days) Fibrotic phase (>21 days) ```
46
Exudative phase
``` Interstitial and alveolar edema Hemorrhage Leukoagglutination Necrosis: Type II pneumocytes, epithelial cells Hyaline membrane platelet fibrin thrombi ``` * STill reversible
47
proliferative phase
``` Interstitial myofibroblast reaction Luminal organizing fibrosis Chronic inflammation Parenchymal necrosis Type 2 hyperplasia macrothrombi ``` *Phase acted on by steroids
48
Fibrotic phase
Collagenous fibrosis Macrocytic honeycombing Mural fibrosis Medial hypertrophy
49
Radiologic findings in ARDS (CXR)
* hard to diff from CHF Diffuse bilateral infiltrates Focal infiltrates
50
CT SCAN findings of ARDS
Early phase: Ground glass opacities and homogenous consolidation distributed peripherally Reversal of lung opacification when patients are placed in the prone position
51
ABG TEst of ARDS
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
What happens when your lungs becomes fibrotic?
TV becomes smaller which will increase your CO2
53
Protective ventilation
Dont overstretch the lung
54
Death in ARDS is due to?
Multiple organ failure and sepsis
55
Only way you can prevent ARDS in patients is???
Restrictive Transfusion Therapy
56
TIP off points Hypercapnic RF
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
Tip off points Hypoxemic RF
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
Patient is already hypoxemic but O2 saturation is still normal - what type of poisoning
CO poisoning - pulse oxymetry cannot differentiate carboxyhemoglobin from oxyhemoglobin
59
Oxygen supplementation and goals
keep Hb at least 88-90% saturated (-60mmHg)
60
Oxygen supplementation in on-going myocardial or cerebral ischemia
70mmHg (92-94%)
61
Formula for oxygen Delivery
CO x CaO2 | CaO2 = arterial oxygen content 1.39 x SaO2 x Hb) + (0.0031 x PaO2
62
Methods of Oxygen Delivery
``` Nasal prongs Simple Face Mask Partial Rebreather masks Non Rebreather Masks Venturi MAsks ```
63
Advantage of nasal prongs
Allow Patients to eat, drink, and speak during O2 administration
64
Disadvantage of Nasal Prongs
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
FiO2
inspiratory flow and pattern RR, exhalation time O2 flow rate Mouth Breathing
66
Limitations of Nasal prongs
limited to less than 5L/min
67
Simple Face Masks
No valve or reservoirs
68
Advantage of Simple Face masks
at 6-10 L/min, FiO2 ranges from 0.35-0.6 | rebreathing is minimized
69
Disadvantages of Simple Face Masks
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
Partial Rebreather (Reservoir) masks
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
Highest FiO2 achieved may reach almost ____
0.85
72
Non rebreather Masks
Similar to rebreather masks except for two sets of one way valves: FiO2 up to 0.8 to 0.95 can be achieved
73
Masks usually for COPD
Venturi Masks More precise control of FiO2
74
Delivery of Positive pressure ventilation to the lungs without endotracheal intubation
NPPV ``` Bilevel Positive Airway Pressure IPAP and EPAP Biphasic positive airway pressure CPAP with inspiratory assist Pressure Support with assist ```
75
Who are candidates for NPPV
``` alert, cooperative paients hemodynamic stability No need for ET intubation No acute facial trauma Properly fitted mask ```
76
Indications for mechanical Ventilation
Presence of apnea; tachypnea (>40/min) BP <80mmHg RF cannot be corrected by any other means
77
Ventilation that allows small tidal volumes using high respiratory rates
high frequency oscillatory Ventilation
78
use of perfluorocarbons
Partial Liquid ventilation
79
Characteristics of perfluorocarbons
High solubility for oxygen High solubility for CO2 immiscibility with surfactant Low surface tension
80
Indications for ECMO
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
OPTIMAL MANAGEMENT OF ARDS
Ventilate with lung protective strategy USE PEEP Conservative fluid measurement Steroids have no role for early ARDS
82
Lung protective strategy:
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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