ARF and ARDS Flashcards
Used when there is either hypoxemia or hyoercapnia or both
Acute respiratory Failure
- Laboratory diagnosis
ARF is a laboratory diagnosis
Needs ABG
Criteria for ARF
pO2 <60mmHg and pCO2 >45 mmHG at rest, on room air and at sea level
Criteria for ARF in patients with chronic hypercapnic respiratory failure or COPD
Sudden deviation of 5 mmHg or more from previously stable levels represent Acute Respiratory Failure superimposed on chronic RF
Types of ARF
Hypoxemic
Hypercapnic
Hypoxemic RF
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
Prototype of Hypoxemic Respiratory Failure
ARDS
Hypercapnic Respiratory failure
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
Hypercapnic Respiratory failure
Increased CO2
PaCO2 = K x (VCO2/Va)
Alveolar Ventilation (VA)
VE-VD
VE=minute ventilation (RR x TV) = 60ml/kg
VD= Dead space
Minute ventilation (VE)
RR x TV
Alveolar Ventilation in Emphysema
High VD, LOW VE
Central cause of hypercapnic respiratory failure;
Decrease in Va
Causes of Decrease VA
Decrease VE with normal VD
Increase in VD with normal VE
Decrease in VE with normal VD
Anything that decreases RR (central control)
Anything that decreases TV (Chest wall disorders)
Increases in VD with normal VE
Disorders of neuromuscular origin
Disorders of increased VD
Disorders of ventilation
Disorders of Central Respiratory Control
Disorders of the chest wall
Disorders of neuromuscular origin
Disorders of Central Respiratory Control
Idiopathic hypoventilation (Ondine’s curse)
Central sleep apnea
Narcotic/sedative overdose - MOST COMMON CAUSE
Diseases of the Medulla
Hypothyroidism
Metabolic Alkalosis
Rabies
Disorders of the Chest Wall
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
Disorders of Neuromuscular Origin
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
Electrolyte abnormalities - causes respiratory muscular weakness
Hypophastemia
Hypomagnesemia
Hypokalemia - MOST common cause of ICU admission
Disorders of Increased VD
intrinsic lung problem
(+) VQ mismatch -> increase VD
Primary prototypes:
Emphysema(sever COPD) -most common
Characterized in a lot of cases with Rapid shallow breathing
Consequences of hypercapnia
Hypoxemia
Acidosis
Increased PVR
Dilatation of cerebral blood vessels
Hypoxemic Respiratory Failure
Characterized by severe hypoxemia, not responsive to supplemental high flow Oxygen
Inability to transfer adequate oxygen from the alveolar space to the pulmonary capillary blood
Oxygenation Failure
Measures the lungs ability to transfer oxygen to the capillary blood
Alveolar-aterial Oxygen Gradient
A-a gradient computation
PAO2 - PaO2
PAO2 = FiO2 x (Pb-PH2O) - PaCO2/RQ
How many percent of the atmosphere is oxygen
21%
Atmosphereic barometric pressure
760 mmHg at sea level
Water vapor pressure (inspired air is maximally saturated with water vapor at the alveolar level)
47 mmHg
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
Normal A-a gradient
<20mmHg
Hypoxemic RF suggestive of intrinsic lung disease has a gradient of??
<20mmHg
Syndrome of severe, acute respiratory failure characterized by respiratory distress, severe impairment of oxygenation, and non-cardiogenic pulmonary edema
ARDS
Pathologic injury specific to ARDS
Diffuse alveolar damage
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
Berlin definition of ARDS
within 1 week of clinical insult
Bilateral opacities
Oxygenation:
MILD: 200-300 mmHg
MODERATE : 100-200 mmHg
SEVERE: <100mmHg
if your PaO2 is >80, FiO2 is ____
21%
Initial symptoms of ARDS
Tachypnea
Most common ABG manifestation of ARDS
Hypocapnia
Direct Lung Injury
Aspiration of gastric contents Severe thoracic trauma Diffuse pulmonary infection Toxic gas Near Drowning
Indirect Lung injury
Severe sepsis Sever enon thoracic trauma; multiple long bone frature Hypovolemic shock Hypertransfusion Acute pancreatitis Reperfusion injury
Clinical Manifestation of ARDS
Rapid, 12-48 hours of the predisposing event but may be up to 5 days
Pathophysiology of ARDS
Systemic inflammation
Failure of hypoxic vasoconstriction - > shunt and severe hypoxemia
Temporal features for DAD
Exudative phase (1-7 days) Proliferative phase (7-21 days) Fibrotic phase (>21 days)
Exudative phase
Interstitial and alveolar edema Hemorrhage Leukoagglutination Necrosis: Type II pneumocytes, epithelial cells Hyaline membrane platelet fibrin thrombi
- STill reversible
proliferative phase
Interstitial myofibroblast reaction Luminal organizing fibrosis Chronic inflammation Parenchymal necrosis Type 2 hyperplasia macrothrombi
*Phase acted on by steroids
Fibrotic phase
Collagenous fibrosis
Macrocytic honeycombing
Mural fibrosis
Medial hypertrophy
Radiologic findings in ARDS (CXR)
- hard to diff from CHF
Diffuse bilateral infiltrates
Focal infiltrates
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
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
What happens when your lungs becomes fibrotic?
TV becomes smaller which will increase your CO2
Protective ventilation
Dont overstretch the lung
Death in ARDS is due to?
Multiple organ failure and sepsis
Only way you can prevent ARDS in patients is???
Restrictive Transfusion Therapy
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
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
Patient is already hypoxemic but O2 saturation is still normal - what type of poisoning
CO poisoning - pulse oxymetry cannot differentiate carboxyhemoglobin from oxyhemoglobin
Oxygen supplementation and goals
keep Hb at least 88-90% saturated (-60mmHg)
Oxygen supplementation in on-going myocardial or cerebral ischemia
70mmHg (92-94%)
Formula for oxygen Delivery
CO x CaO2
CaO2 = arterial oxygen content
1.39 x SaO2 x Hb) + (0.0031 x PaO2
Methods of Oxygen Delivery
Nasal prongs Simple Face Mask Partial Rebreather masks Non Rebreather Masks Venturi MAsks
Advantage of nasal prongs
Allow Patients to eat, drink, and speak during O2 administration
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
FiO2
inspiratory flow and pattern
RR, exhalation time
O2 flow rate
Mouth Breathing
Limitations of Nasal prongs
limited to less than 5L/min
Simple Face Masks
No valve or reservoirs
Advantage of Simple Face masks
at 6-10 L/min, FiO2 ranges from 0.35-0.6
rebreathing is minimized
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
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
Highest FiO2 achieved may reach almost ____
0.85
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
Masks usually for COPD
Venturi Masks
More precise control of FiO2
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
Who are candidates for NPPV
alert, cooperative paients hemodynamic stability No need for ET intubation No acute facial trauma Properly fitted mask
Indications for mechanical Ventilation
Presence of apnea; tachypnea (>40/min)
BP <80mmHg
RF cannot be corrected by any other means
Ventilation that allows small tidal volumes using high respiratory rates
high frequency oscillatory Ventilation
use of perfluorocarbons
Partial Liquid ventilation
Characteristics of perfluorocarbons
High solubility for oxygen
High solubility for CO2
immiscibility with surfactant
Low surface tension
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
OPTIMAL MANAGEMENT OF ARDS
Ventilate with lung protective strategy
USE PEEP
Conservative fluid measurement
Steroids have no role for early ARDS
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%
