respiratory failure: an introduction ramadan m bakr mbbch, msc, dm, dc, dha, dis, md maccp, mers,...
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Respiratory Failure:an introduction
Ramadan M BakrMBBch, MSc, DM, DC, DHA, DIS, MD
MACCP, MERS, MESC.
Professor of Chest Diseases,Menoufiya University
فمْن َي�رد الله� أْن َي�هِد�َي�ه ”ه لإلسالِم� ومْن ِدَر� ْح َص� ر� َي�ْشه� ِدَر� عْل َص� ل�ه� َي�ْج َي�رد أْن َي�ِض�
عِد فى ا* َك�أَن�ما َي�َص� ر�َج� ضيقا* َح�السماء“
125)َصِدق الله العظيم ) األَنعاِم
Respiratory Failure
• Definition Respiratory failure is a syndrome in
which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination.
• Clinically
Respiratory failure is defined as PaO2 <60 mmHg while breathing air at sea level, with normal or PaCO2 >49 mmHg.
Classification
• hypoxaemic respiratory failure:– PaO2 60 mm Hg when breathing
room air• hypercapnic respiratory failure:
– PaCO2 50 mm Hg.
Respiratory system anatomy
1-CNS (cortex & medulla) 2-Peripheral nervous system (spinal cord, AHCs, phrenic & intercostal nerves )
3- Respiratory muscles ( intercostal ms & diaphragm) with their motor endplates
4- Pleura & chest wall ( ribs, vertebrae & sternum)
5- Lungs, including;
a- Upper airways
b- Lower airways = bronchial tree
c- Alveoli & interstitium
d- Pulmonary vasculature
Basic respiratory physiology
O2CO2
Oxygen in
• Depends on– PAO2
– Diffusing capacity– Perfusion– Ventilation-perfusion matching
Carbon dioxide
Water vapour
Oxygen
Nitrogen
2A2A2A2A NPOHPCOPOPpressure Alveolar
Oxygen in
• Depends on– PAO2
• FIO2
• PACO2
• Alveolar pressure• Ventilation
– Diffusing capacity– Perfusion– Ventilation-perfusion matching
Carbon dioxide out
• Largely dependent on alveolar ventilation
• Anatomical dead space constant but physiological dead space depends on ventilation-perfusion matching
)V-( V xR R nv e n t i l a t i o A l v e o l a r DT
Carbon dioxide out
• Respiratory rate• Tidal volume• Ventilation-perfusion matching
Pathophysiology
1. Hypoventilation = dead space ventilation (VD/VT)
2. Ventilation/ perfusion (V/Q)
mismatch
3. Intrapulmonary shunt ( Qs/QT )
4. Diffusion limitation ?
Pathophysiologic mechanisms
underlying RF
Metabolic activity of the tissues leads to CO2 production (VCO2). If there is a ↓ in alveolar ventilation (VA) or ↑ in dead space ventilation ( VD/VT), CO2 will accumulate in tissues, increasing the arterial CO2 tension (PaCO2) & hence alveolar CO2 tension (PACO2) { this is called hypoventilation }, thus;
PACO2 (PaCO2) = VCO2 × K VA
Hypoventilation:
The hypoventilation (↑PA CO2 i.e. PaCO2) will lead ultimately to decrease of alveolar oxygen tension (PAO2) & hence the arterial oxygen tension (PaO2) according to the alveolar gas equation:
PAO2 = ( PB – PH2O ) FIO2 – PaCO2/R
= (760 – 47 )0.21 – (40/0.8)=100 mmHg
= (760 – 47 )0.21 – (80/0.8)= 50 mmHg
The proper matching between ventilation (V) & blood flow (Q) within the lungs is necessary for adequate O2 uptake & CO2 elimination. Thus, each lung zone receives an amount of V matched with an amount of Q. As lung disease develops, V/Q mismatch occurs with some units having low V/Q ratio, adding less O2 to the pulmonary capillary blood than normal units & units having high V/Q ratio, adding no more O2.
V/Q mismatch
75% 75%
100% 75%
87.5%
PaO2 (kPa)
Hb
satu
rati
on (
%)
8
90
Pulse oximetry
When Qs/ Qt exceeds 5% (of the total cardiac output), it is considered pathological which is seen in lung diseases associated with collapsed, or fluid filled alveoli e.g. pneumonia, pulmonary edema …etc. or in intrapulmonary A/V fistulas &/or intracardiac Rt to Lt shunts. ↑ Qs/ Qt is one extreme of V/Q mismatch, where the alveoli receive no ventilation but blood continues to flow.
Pathological shunt (↑ Qs/ Qt)
FIO2
Ventilation without
perfusion(deadspace ventilation)
Diffusion abnormality
Perfusion without
ventilation (shunting)
Hypoventilation
Normal
FIO2
Ventilation without
perfusion(deadspace ventilation)
Diffusion abnormality
Perfusion without
ventilation (shunting)
Hypoventilation
Normal
Perfusion without ventilation (Shunting)
• Intra-cardiac– Any cause of right to left shunt
• eg Fallot’s, Eisenmenger
• Intra-pulmonary– Pneumonia– Pulmonary oedema– Atelectasis– Collapse– Pulmonary haemorrhage or contusion
Perfusion without ventilation (shunting)
Intra-pulmonary• Small airways occluded ( e.g asthma, chronic
bronchitis)
• Alveoli are filled with fluid ( e.g pulm edema, pneumonia)
• Alveolar collapse ( e.g atelectasis)
FIO2
Ventilation without
perfusion(deadspace ventilation)
Diffusion abnormality
Perfusion without
ventilation (shunting)
Hypoventilation
Normal
V/Q mismatch:
Dead space ventilationAlveoli that are normally ventilated but
poorly perfused
Anatomic dead spaceGas in the large conducting airways that
does not come in contact with the capillaries e.g pharynx
V/Q mismatch:
Dead space ventilation
Physiologic dead space
Alveolar gas that does not equilibrate fully with capillary blood
Dead space ventilation
• DSV increase:• Alveolar-capillary interface destroyed
e.g emphysema• Blood flow is reduced e.g CHF, PE• Overdistended alveoli e.g positive-
pressure ventilation
FIO2
Ventilation without
perfusion(deadspace ventilation)
Diffusion abnormality
Perfusion without
ventilation (shunting)
Hypoventilation
Normal
Diffusion abnormality:
• Less common
• Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area
• Causes include:– Acute Respiratory Distress Syndrome– Fibrotic lung disease
FIO2
Ventilation without
perfusion(deadspace ventilation)
Diffusion abnormality
Perfusion without
ventilation (shunting)
Hypoventilation
Normal
V/Q =1 is “normal” or “ideal” V/Q =0 defines “shunt” V/Q =∞ defines “dead space” or “wasted ventilation”
V/Q possibilities : 0, 1, ∞
10 ∞
Causes of type I RF
– COPD ( early in disease)– Pneumonia – Pulmonary edema – Pulmonary fibrosis – Asthma – Pneumothorax – Pulmonary embolism – Pulmonary arterial hypertension
– Pneumoconiosis– Granulomatous lung diseases – Cyanotic congenital heart disease – Bronchiectasis – Adult respiratory distress syndrome
(ARDS)– Fat embolism syndrome– Pulmmonary A/V fistula– Lymphatic carcinomatosis
Causes of type II RF
• CVA, tumors , brain injuries.• Respiratory centre dysfunction, drug over-
dose, hypothyroidism, central hypoventilation, chr. metabolic alkalosis.
• Spinal injuries, Guillain-Barre, polio .• Neuromuscular diseases, myasthenia gravis,
muscular dystrophy, resp. m. fatigue, tetanus polymyositis, periodic paralysis & botulism.
• Chest wall/pleural diseases ; morbid obesity, kyphoscoliosis, pneumothorax, massive pleural effusion & flail chest, ankylosing spondylitis, thoracoplasty.
• Upper airways obstruction; tumor, foreign body, laryngeal edema
• Peripheral airway disorder & lung parenchyma; asthma, COPD, massive fibrosis.
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Brainstem
Spinal cordNerve rootAirway
Nerve
Neuromuscular junction
Respiratory muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
How to diagnose a case with RF?
This needs to follow these items: 1- High sense of clinical suspicion 2- Careful history taking & clinical exam., to elicit symptoms & signs of RF. 3- Confirmation of the diagnosis of RF with arterial blood gas (ABG) testing. 4- Other investigations to discover the underlying pathophysiology & other comorbideties.
Clinical manifestations of RF: These comprise two groups; 1- Those symptoms & signs that are related to the underlying disease e.g. pneumonia, COPD, neuromuscular disease, ARDS……etc. like cough, expectoration, hemoptysis, dyspnea, chest pain, wheezes…..etc. 2- 2nd group of symptoms & signs reflect hypoxemia &/or hypercapnea & acidosis ( all are nonspecific ).
Clinical manifestations related to hypoxemia & hypercapnea( all are non-specific and unreliable & are usually
related to cardiovascular, GIT & CNS )
• Cyanosis: bluish color of mucous membranes/ skin indicates hypoxemia & unoxygenated hemoglobin >5 g/DL ( not a sensitive indicator) .
• Respiratory; dyspnea: secondary to hypercapnia and hypoxemia, paradoxical breathing & respiratory alternans.
• CVS; tachycardia, hypertension, hypotension, pulmonary hypertension and cor-pulmonale or right ventricular failure.
• CNS; flapping tremors, muscle twitches headache, blurring of vision ( papilledema ) irritability, anxiety, convulsions, somnolence, confusion and coma .
• GIT; anorexia, nausea, vomiting, gastric dilatation, and paralytic ileus.
Patient’s assessment
• Careful history taking• Physical examination ( general & local )• Lab studies 1- ABG analysis → ↓O2, ↑CO2, ↓PH
2- CBC → anemia, polycythemia 3- Renal and hepatic functions 4- Electrolytes → potassium, magnesium, and phosphate
• Lung functions ( FEV1, FVC )→ obstructive & restrictive disorders• ECG → dysrhythmias • Echocardiography → ventricular dysfunction,
dilatation, valve diseases• Chest radiograph → pneumonia, COPD, pulmonary edema & ARDS……etc.• Right heart catheterization → pulmonary
capillary wedge pressure (PCWP), to correlate with plasma oncotic pressure (POP)
Management of respiratory failure: principles;
• Airway management • Primary objective is to reverse and prevent
hypoxemia with O2 therapy• Secondary objective is to control
hypercapnea and respiratory acidosis • Monitoring of the patient in the ICU• Treatment of the underlying disease
Thank you