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Respiratory Insufficiency

and Failure

Presenter: Dr Frank John

Facilitator: Dr B. L. Mtinangi

Physiology Group 1
Layout
Introduction
Classification/types of respiratory
insufficiency and failure
Pathophysiology
Some lung diseases which lead to resp.
failure
Clinical presentation
Diagnosis & management
References
Introduction
The aim of breathing is to supply the blood
with adequate amount of oxygen needed for
tissue metabolism and clear the blood
carbondioxide from tissues.
Therefore the level of O2 and CO2 in the
blood must be maintained within normal
ranges.
Failure of the respiratory system to maintain
those gases within normal range leads to
respiratory insufficiency/failure.
Types/classification of RF
RF can be classified in various ways:
According to duration; acute/chronic.
According to blood gas analysis;
Hypoxemia- O2 level below 60 mmHg
Hypercapnea- CO2 level above 45 mmHg
According to functional classification
Controller RF Resp centres in brain and
medulla.
System RF lungs, spinal cord
According to ventilatory pump
partial or global
According to origin obstructive or restrictive
Transfer of oxygen of inhaled air into
the blood and
of waste carbon dioxide of blood into
the lungs
Ventilation

Gas Exchange Hypercapnic respiratory failu

Hypoxemic respiratory failure


Respiratory Failure
inadequate blood oxygenation or CO2 removal
A syndrome rather than a disease
PaO2 < 60 mmHg or PaCO2 > 50 mmHg

Hypoxemic Hypercapnic
PaO2 < 55~60 mmHg or SaO2 < 90%
PaCO2 > 45~50 mmHg
with FiO2 >= 60%

This two types of respiratory failure always coexist

Acute: develops in minutes to hours, pH < 7.30


Chronic: develops over several days or longer
Ventilation
CNS PNS Respiratory Muscles Airways
Efferents Chest Wall

Dysfunction of any component


CNS
Afferents/
of the ventilation system may Alveoli
Intergration result in ventilatory failure

Chemoreceptors PaO2 Alveolar Minute


PaCO2 Ventilation Ventilation
Respiratory drive
O2 demand Motor neuron/nerve function
CO2 production Muscle strength
Dead space Respiratory mechanics

VE MSV
Minute Ventilation Maximal Sustainable Ventilation

MSV = MVV/2
PaCO2 = K VCO2 / VA
VA= VE (1- VD/VT) MVV = 40 FEV1
MVV: Maximal voluntary ventilation

Ventilatory Demand Ventilatory Suppl

Ventilaroty Demand > Ventilatory Supply Ventilator


Respiratory Failure
in a patient with Asthma

Ventilatory Demand Ventilatory Supp


Dead Space Ratio

CO2 Production
VA= VE (1-
VD/VT)

PaCO2 = K VCO2 /Minute


VA Ventilation

CO2 Hypercapnic
Production
Dead Space Respiratory Failu
Ratio
Minute
Ventilation
Hypercapnic Respiratory Failure

Increase carbon dioxide production


Fever, sepsis, seizure, obesity, anxiety
Increase work of breath (Asthma, COPD)
high carbohydrate diet with underlying lung
disease
Hypercapnic Respiratory Failure

Decrease minute ventilation (hypovent.)


CNS disorders
stroke, brain tumor, spinal cord lesions, drug overdose
Peripheral nerve disease
Guillain-Barre syndrome, botulism, myasthenia gravis
Muscle disorders
muscular dystrophy, respiratory muscles fatigue
Chest wall abnormalities
scoliosis, kyphosis, obesity
Metabolic abnormalities
myxedema, hypokalemia
Airway obstruction
Upper airway obstruction, Asthma, COPD
Hypercapnic Respiratory Failure

Increase dead space


Airway obstruction
Upper airway obstruction
Asthma, COPD
Foreign body aspiration

ARDS, Pulmonary embolism


Chest wall disorder
Response well to oxygen therap
PAO2 = PiO2 PACO2/R
A-a gradient = PAO2 PaO2

PaO2 = [ FiO2(PATM-PH2O) PaCO2/R ]


[ A-a gradient]

Low Inspired Oxygen


Alveolar Hypoventilation
Shunt
V-Q mismatch
Diffusion impairmen

Hypoxemic Respiratory Fail


Hypoxic Respiratory Failure

1. Low inspired oxygen


High altitudes

2. Hypoventilation
Conditions described in hypercapnic
respiratory failure
Oxygen therapy improve hypoxemia but may
worsen the hypoventilation
Hypoxic Respiratory Failure

3. Shunt (blood flow dont exposed to


alveolar)
Can be anatomical or physiological
Anatomical eg rt to lt shunts-ASD, pulmonary arterial-
venous shunts, blood flow through collapsed lung.
Physiological shunts-reduced ventilation to a well perfused
lung.
In both PaO2 is reduced and PaCO2 may be normal or
reduced.
O2 therapy may or may not improve the condition in phys
shunt.
Hypoxic Respiratory Failure

4. Ventilation-Perfusion Imbalance
Pulmonary emboli- produce alveolar dead
space
Pulmonary edema, pneumonia, abscess-
impair regional ventilation produce reduced
PaO2 and Hb saturation
COPD-increase resistive work of breathing
affecting both V & P
Hypoxic Respiratory Failure

5. Diffusion Impairment
Interstitial lung disease
Pulmonary fibrosis, Connective tissue
disease, Interstitial pneumonia, interstitial
pulmonary TB
Atelectasis due obstruction or lack of
surfactant -RDS
Obstructive lung disease
Emphysema, Asthma
Some dses which lead to
resp. failure
Chronic Pulmonary Emphysema:
Excess air in the lung due to complex
obstructive and destructive process of the
lungs from long term smoking.
Bronchial obstruction cause increase in
airway resistance, work of breathing and
difficult in expiration
Loss of alveolar walls decrease diffusing
capacity of the lung
Loss of alveolar capillaries lead to increase
vasc. resistance then pulm HT then rt heart
failure
Abnormal V/Q ratio with either:
Low V/Q physiological shunt (poor aeration)
High V/Q physiological dead space (wasted
ventilation)
Progress over years and lead to hypoxia and
hypercapnea then death
Pneumonia:
Is any inflammatory condition of the lung, commonest
being bacterial pneumonia
Infection begins in the alveoli and progress in the
membrane where it bcom inflammed and porous. This
cause fluids and blood cells to leak out
The alveoli become filled with blood cells and fluid

.
mm
Pneumonia ct..
The major pulmonary abnormalities are:
Reduction in the total surface area of the
respiratory membrane
Decrease V/Q ratio
Both these effects cause hypoxemia and
hypercapnea
Atelectasis
Means collapse of the alveoli
It can occur in a localized areas or in the
entire lung
Can be caused by total obstruction of the
airway or due to surfactant deficiency
Both expiratory volume and rate are reduced
leading to severe dyspnoea
History & Physical Examination

Acute or Chronic
Underlying ( heart / lung ) diseases
Drugs history

Wheezing? Rhonchi? Crackes?


Diminish breath sound?
Air-space consolidation?
S/S of heart failure
Clubbing finger
Clinical Presentations of
Acute Respiratory Failure
Breath pattern:
rapid-deep rapid-shallow slow-shallow
Accessory respiratory muscles used:

Paradoxical respiration:

Hypoxemia
dizziness, irritable, conscious change, tachycardia,
cyanosis, peripheral vasodilatation, pulmonary
vasoconstrition.
Hypercapnia
Headache, somnolence, conscious change
Workup
LAB:
Arterial blood gas; Pulse oxymeter
CBC,
Cardiac enzyme
Electrolytes: K, Pi, Mg Ca, Na.
Biochemistry data,

ECG (cardiac echo)


Chest X-ray (chest CT, lung scan)
Lung function test
PA catherter
Neurological exam (Brain CT, EEG)
Management
Establish Airway
Establish Ventilation
Oxygen Therapy
Treat the circulatory failure
NOTE: Oxygen therapy is beneficial in hypoxia
due to: hypoventilation, high altitude, impaired
alveolar membrane diffusion.
The other forms of hypoxia are resistant bcoz
the problem might be in the transport mech.
and O2 is already available
Airway Management

Head tilt-chin lift / Jaw-thrust maneuver


Artificial airway (Oral or Nasal airway)
Laryngeal Mask Airway
Endo-Tracheal intubation
Tracheostomy
Artificial respiration:
Resuscitator
Tank Respirator:+/- pressure
References
Guyton and Hall Physiology textbook
Ganong Medical Physiology
Essentials of respiration
Postgraduate lecture notes 2008 by Dr B. L.
Mtinangi
Internet