Respiratory Failure:an introduction

Ramadan M BakrMBBch, MSc, DM, DC, DHA, DIS, MD

MACCP, MERS, MESC.

Professor of Chest Diseases,Menoufiya University

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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