RESPIRATORY FAILURE-EVALUATION AND MANAGEMENT
Dr Binila Chacko
Associate Professor
Medical ICU, CMC Vellore
DR THOMAS COGAN
DR WILLIAM HOWES
RESPIRATION
CELLULAR
RESPIRATION
TRANSPORT OF
GASES
VENTILATION
DEFINITION
Failure of the lung to maintain adequate gas exchange
Abnormalities of arterial blood gas tensions.
PaO2 < 60 mmHg with or without hypercarbia PaCO2 > 46
mmHg
Onset usually acute or sub-acute
WHY IS THIS TOPIC IMPORTANT
•
•
Common problem
360,000 cases per year United States
• 36% die during hospitalization
• Estimated that respiratory failure will become more common as
the population ages, increasing by as much as 80 percent in the
next 20 years
PHYSIOLOGY
PACEAMAKER
PUMP
Increased airway resistance
Decreased lung compliance
Resistance
REDUCECompliance
PUMP EFFICIENCY
INCREASE WORK OF
BREATHING
GAS EXCHANGER
FACTORS AFFECTING EFFICIENCY OF
GAS TRANSFER
Alveolar capillary interface
Transit time of blood in the pulmonary capillaries
0.7seconds
PaO2
PAO2 Alveolar partial pressure of oxygen
Diffusing capacity
Ventilation-perfusion matching
PAO2 determinants
Alveolar pressure
Alveolar gas equation
Alveolar
PAO2=(FiO2 x713)-PACO2/R
pressure=PAO2+PACO2+PA(H20)+PA
N2
FiO2
PACO2
PaO2
PAO2
Diffusing capacity
Transit time in the pulmonary capillaries-0.7seconds
Alveolar capillary interface
Increase in thickness
Since CO2 diffusion 20 times that of oxygen
usually hypoxemia unless there is ventilatory failure
PaO2
PAO2
Diffusing capacity
Ventilation-perfusion matching
Normal alveolar ventilation (V) about 4 to 6 L, Perfusion (cardiac
output, Q) about 5 L
Normal V/Q=0.8-1.2
V/Q matching
Intracardiac/intr
apulmonary
Anatomical/
physiological
Predominant
hypoxemia
Predominant
hypercarbia
PaO2 quick recap
PAO2
Alveolar pressure, FiO2 and the PaCO2
Diffusing capacity
Alveolar capillary membrane and time across pulmonary capillaries
Ventilation-perfusion matching
Dead space and shunt effect
Carbon dioxide outflow
Dependent on alveolar ventilation
Resp rate x (VT-VD)
Respiratory rate
Tidal volume
Ventilation-perfusion matching
VT=Tidal volume
VD=Dead space
Again shows the importance of V/Q
matching in carbon dioxide regulation
TYPES
Physiological approach
Type 1 and 2
Pathophysiological approach
Types 1 to 4
TYPES
SHUNT
Hypoxemic/type
I respiratory
failure
Hypercapnic/typ
e II respiratory
failure
IN AN UNWELL PATIENT
CLINICAL EXAMINATION
HAPPEN IN
PARALLEL
MANAGEMENT
Clinical assessment
TO ASSESS SEVERITY
TO DETERMINE THE CAUSE
Clinical assessment
RESPIRATORY COMPENSATION
RESPIRATORY
COMPENSATION
SYMPATHETIC STIMULATION
RESPIRATORY
COMPENSATION
RESPIRATORY
SYMPATHETIC
TACHYPNEA
WORRY
COMPENSATION
STIMULATION
IF
TACHYCARDIA
SYMPATHETIC
STIMULATION
USE
SYMPATHETIC
OFTISSUE
ACCESSORY
RR
>30/MIN
HYPOXIA
STIMULATION
MUSCLES
HYPERTENSION
TISSUE
HYPOXIA
CAN’T
SYMPATHETIC
ALTERED
SPEAK
TISSUE
MENTAL
IN
HYPOXIA
FULL
STIMULATION
STATUS
SENTENCES
SWEATING
HEMOGLOBIN
DESATURATION
SHOCK-DECREASED
HEMOGLOBIN
AGITATED/CONFUSED
TISSUE
DESATURATION
HYPOXIA
ORGAN
PERFUSION
TISSUE HYPOXIA
DETERIORATING
HEMOGLOBIN
CYANOSIS
DESATURATION
DESPITE
THERAPY
HEMOGLOBIN DESATURATION
To determine the cause…
APPLYING PHYSIOLOGY TO PATHOLOGY
Approach to Type I respiratory failure
Hypoxemia
reduction in oxygen in the blood-low PaO2
Hypoxia
reduction in oxygen in the tissues
LOW PaO2 =HYPOXEMIA
Low PAO2
Overdistended
alveoli(Intrinsic/extrinsic-PEEP)
Decreased blood supply-Pulmonary
Alveolar capillary
embolism/Shock
Alveolar disease
(fluid/pus/protein/bloo
d)
Intra-pulmonary shunting collapsed lung (atelectasis)
MUST REMEMBER
More than one pathophysiological process may co-exist.
Pure diffusion abnormalities are uncommon.
WHAT’S THE NEXT STEP?
Find out where the abnormalty is
Pa CO2
A-a gradient
A-a gradient
Low PaO2
Is the CO2 increased ?
Yes
No
A-a gradient
Is the A-a gradient increased ?
No
Yes
Response to oxygen therapy
Yes
V/Q mismatch
Alveolar disease
Interstitial disease
Diffusion problems
Pulmonary embolism
Low inspired FiO2
No
Shunt
Increased
Normal - pure
hypoventilation
Approach to hypercapnic respiratory
failure
Increased CO2 production
Increased CO2 production
Increased muscle activity (spasms, convulsions)
Reduced CO2 elimination
Hyper
metabolicCO
states
(fever,
sepsis)
Increased
production
2
CONTROLLER-BRAIN/SPINAL
CORD/NMJ
Carbohydrate rich feeds.
Reduced CO2 elimination
HYPERCAPNIA OCCURS ONLY IF CO2
ELIMINATION CANNOT KEEP PACE WITH
PUMP
PRODUCTION
ALVEOLOCAPILLARY
UNIT
Reduced CO2 elimination
Reduced elimination
High CO2
Increased production
Is the A-a gradient increased?
No
Yes
Pure hypoventilation
Response to oxygen therapy
PI Max
Yes
V/Q mismatch
Alveolar disease
Interstitial disease
Diffusion problems
Pulmonary embolism
No
Shunt
Low
Neuromuscular problem
Normal
Central hypoventilation
syndrome
Don’t forget to look at the pH
•
PaCO2 must always be considered in relation to the pH.
• Acute hypercapnic respiratory failure
• Shift in the pH,
• Compensatory mechanisms take time
•
Chronic hypercapnic respiratory failure
• pH is usually close to normal,
Management of hypoxemic respiratory
failure
• treatment of the underlying cause (specific
•
•
•
treatment)
improving oxygen delivery to the tissues
limiting potentially damaging therapies
reducing tissue oxygen demand.
Management of hypoxemic respiratory
failure
treatment of the underlying cause (specific treatment)
improving oxygen delivery to the tissues
DO2 = [1.39 x Hb x SaO + (0.003 x PaO )] x Q
Hb
SaO2
Increase FiO2
PaO2
PEEP
Cardiac index
2
2
Improving oxygen delivery
•
•
Target is to maintain cerebral oxygenation
Increase FiO2
• FiO2 start with 100% (unless COPD) and reduce FiO2 based on ABG (P/F
ratios)
•
Apply extrinsic PEEP - “Open lung ventilation” (can be done by invasive MV or
NIV)
• Physiological goal of preventing alveolar collapse
Oxygen delivery devices
Performance
Variable
Flow
Flow
Low the
flowoxygen concentration of the
air-oxygen mix reaching the
alveoli is not constant
deliver oxygen less than PIFR
Performance
Fixed
High flow
not influenced by respiratory rate,
deliver oxygen at flow rates
size of the reservoir or oxygen flow
higher than PIFR
rate
Oxygen delivery devices
Management of hypoxemic respiratory
failure
treatment of the underlying cause (specific treatment)
improving oxygen delivery to the tissues
limiting potentially damaging therapies
Lung protective ventilatory strategies
reducing tissue oxygen demand.
control of fever, sepsis or seizures
ventilatory support offloads the respiratory muscles
Alveolar recruitment
Increase tidal volumes (increase
distending pressures) - keep
alveoli open
Increase inspiratory time
Increase PEEP
How much tidal volume?
Landmark NIH NHLBI ARDS network
Prospective, randomized, multi-center trial of 12 ml/kg vs 6 ml/kg
tidal volume positive pressure ventilation for treatment of acute
lung injury and acute respiratory distress syndrome
861 patients
The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional
tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000, 342:1301–
1308
OPTIMAL PEEP SETTING
Staircase recruitment manouvre
Defined as the lowest PEEP attainable
without causing a significant drop
(>10%) in PaO2
ARDSNet protocol
No agreed upon method of
determination
Thoracic tomography
•
Higher than the lower infection point on a pressurevolume loop
Oesophageal balloon directed estimation of pleural
pressures to calculate transpulmonary pressures and
guide PEEP titration
How do you set PEEP?
•
LIP is that point of the curve
where the slope of the line
changes significantly.
•
Believed to represent the
opening of majority of alveoli
How do you set PEEP?
Benefits of PEEP
Increases transpulmonary distending pressures
Displaces edema fluid into interstitium
Decreases atelectasis
Decrease in right to left shunt
Improved compliance
Improved oxygenation
Whom should I ventilate?
Decision to ventilate
Complex
Multifactorial
No simple rules
Severity
of
respiratory
failure
Cardiopulmonary
reserve
Adequacy
of
compensation
Ventilatory requirement
Underlying disease
Treatment already given
Risks of mechanical
ventilation
Always consider ..
Different clinical situations
Mild hypoxemia (PaO2 60 – 70 mmHg on room air)
a nasal cannula or a simple mask may be sufficient.
Moderate hypoxemia (PaO2 50-60 mmHg)
a partial re-breather mask or venturi device
latter preferred for COPD patients.
Severe hypoxemia (PaO2 <50 mmHg) not responding to simpler devices
non-rebreather systems (e.g. CPAP, non-invasive ventilation, Ambu-bag,
Bains)
Invasive mechanical ventilation
Specific to management of hypercapnic
respiratory failure
Reduce CO2 production
controlling fever and excess motor activity (convulsions)
Reducing carbohydrate intake. (R.Q Carbohydrates 1.0 and for
fat is 0.7)
Particularly important for COPD
To enhance CO2 elimination..
Respiratory drive can be increased
Reducing the use of sedation
Drugs that increase respiratory drive (COPD)
acetazolamide, medroxy-progesterone acetate
Benefit not proven in randomized trials
Ventilation-GOAL TO INCREASE ALVEOLAR
VENTILATION HYPERCARBIA DUE TO LOSS OF
PROGRESSIVE
Improve Lung mechanics
P ABCDE
HYPOXIA
KILLS!!
P- propping up
A-Analgesics to reduce chest pain
B-Bronchodilators
C-Compliance-ventilatory/non-ventilatory
strategies
D-Drugs such as xanthines
E-Electrolyte correction
IMPROVE LUNG
MECHANICS
HYPOXIC DRIVE IS RARE
Always consider ..
NIV COPD
The number needed to be treated for benefit
N=8 patients to save one life
N=5 to avoid one invasive mechanical ventilation
N=3 to avoid “a” complication of ventilation
Milder exacerbations
Evidence not clear
Post hoc analysis suggest benefit below pH of 7.37 and PaCO2 of > 55 mm Hg
NIV COPD
Failure rates in COPD exacerbations about 25%
Early failure predictors are
lack of improvement in pH
no change in the level of consciousness
no improvements in CO2 levels
worsening respiratory rate
NIV APO
CPAP appears to be superior to bi-level ventilation in terms of mortality (NNT
10 for CPAP)
Similar benefits of both CPAP and bilevel ventilation in reducing need for
mechanical ventilation (NNT 6 for CPAP and 7 for bilevel)
Failure of NIV
When do you say treatment has failed?
Complications have occurred
PaO2 continues to be low
PaCO2 continues to be elevated
is the patient on too much oxygen?
Is there excessive leakage in the circuit?
Are the ventilatory supports adequate (IPAP & EPAP)?
Is there patient-ventilator asynchrony?
Is re-breathing occurring
May need IMV
CASE
43 year old man
Community acquired pneumonia
Day 1 antibiotics
PaO2 60mmHg, Pa CO2 30mmHg, pH 7.15 on 15L/min oxygen
Respiratory rate 35/min
Agitated
RECAP
Investigations (clinical and lab) and management happen in parallel
PaO2 - PAO2, Alveolocapillary diffusion and V/Q abnormalities
PaCO2- Alveolar ventilation
Hypoxemia
PaCO2
A-a gradient
Response to increase in FiO2
Decide on therapy-Non invasive versus invasive mechanical ventilation
Lung protective ventilation