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Respiratory Failure and Role of ABGs in ICU (Presenter: Dr Hasheela T. U. N)

Respiratory failure role of abg's in icu

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Respiratory Failureand Role of ABGs in ICU

(Presenter: Dr Hasheela T. U. N)

Components of the respiratory system

Gas-exchange (Interface)organ• Lungs (parenchyma)

• Blood vessels (pulmonary and

bronchial)

Ventilatory pump• Thoracic wall• Respiratory muscles• Brainstem and cortex• Anterior horn cells (S.C.)• Phrenic nerves and other

nerves

Definition

:- a syndrome in which the respiratory system fails in one or both of its gas exchange functions i.e. oxygenation and/or carbon dioxide elimination, such that the levels of arterial oxygen (PaO₂) and carbon dioxide (PaCO₂) partial pressures cannot be maintained within their normal ranges.

Normal value HYPOXEMIA

PaO₂ 80 - 100mmHg ( 11 - ... kPa) < 60mmHg (< 8 kPa) on R.A.

< 80mmHg (<11 kPa) on FiO² > 40%

Normal value HYPERCAPNIA

PaCO₂ 35 - 45mmHg ( … - 6.0 kPa) > 50mmHg (> 6.7 kPa)

CLASSIFICATION

HYPOXAEMIC (TYPE I)• Failure of oxygenation

HYPOXEMIA without HYPERCAPNIA

VENTILATORY (TYPE II)• Respiratory “PUMP” FAILURE

↓HYPOXEMIA and HYPERCAPNIA

CLASSIFICATION

HYPOXAEMIC TYPE IABG CHANGES:• PaO₂ ↓(< 60 mmHg / 8.0 kPa)

• PaCO₂ normal or ↓ (<50 mmHg /6.7 kPa)

• PA-aO₂ ↑

VENTILATORY TYPE IIABG CHANGES:• PaO₂ ↓(< 60 mmHg / 8.0 kPa)

• PaCO₂ ↑(> 50 mmHg /6.7 kPa)

• PA-aO₂ normal• pH↓ (Acidosis)

Causes

Hypoxaemic (Type I) • Pneumonia• ARDS• Pulmonary fibrosis• Asthma• COPD• Pnemothorax• PE• Obesity• Pulmonary Hypertension

Hypercapnic (Type II)• COPD / Severe Asthma• Drug Overdose (Opiates

benzodiazepines,)• CNS Injury (SCI, CVA)• Primary muscle disorders

(Duchenne muscular dystrophy)• Neuromuscular junction disorders

(eg. Myasthenia gravis)• Anatomical chest deformities (eg. Kyphoscoliosis, Flail chest)• Obesity Hypo-ventilatory

(Pickwickian) syndrome

Pathophysiology

HYPOXAEMIC TYPE I• 1. (V/Q) mismatch

• 2. True Shunt

• 3. Diffusion Impairment

• 4. Reduced Inspired Oxygen Concentration

↓↑ A-a PO₂ gradient

↓HYPOXAEMIA

VENTILATORY TYPE II1. Respiratory “PUMP”

FAILURE↓

Inadequate alveolar ventilation↓

CO₂ Accumulation↓

HYPERCAPNIA

Pathophysiology• Alveolar-arterial PO₂ gradient (‘A–aDO₂’):

PA-aO₂ = PAO₂ - PaO₂[Normal range: (< 15-20 mmHg)]

(Also, “A–aDO₂” < [age in years/4] + 4)

NB: ↑ “A–aDO₂” → ↑ “Dead Space”

Alveolar gas equation:

• Useful in differentiating btw Hypoxia due to Lung pathology vs external factors

Alveolar gas equation variables definitions

Quantity Description Sample value

pAO2The alveolar partial pressure of oxygen (pO2)

107 mmHg (14.2 kPa)

FIO2

The fraction of inspired gas that is oxygen (expressed as a decimal).

0.21

PATMThe prevailing atmospheric pressure 760 mmHg (101 kPa)

pH2O

The saturated vapour pressure of water at body temperature and the prevailing atmospheric pressure

47 mmHg (6.25 kPa)

paCO2

The arterial partial pressure of carbon dioxide (pCO2)

40 mmHg (4.79 kPa)

RER The respiratory exchange ratio 0.8

CLINICAL PRESENTATIONRF may be preceded by signs of respiratory distress:

• Tachypnoea (>25/min)• Breathlessness• Gasping or pursed lip

breathing• Tight chest • Sweating, clamminess• Agitation• Sitting or hunched

posture

• Sense of impending doom

• Inability to complete a sentences

• Cyanosis• HYPOXAEMIA Sats<92%• HYPERCAPNEA

Pre-terminal Signs

• Bradycardia, dysrhythmias, hypotension• Bradypnoea or silent chest• Decreased L.O.C

DIAGNOSTICS

1) VITAL SIGNS AND INSPECTION(BP, O₂ Sat, RR, T°C, LOC, airway patency)

• Fever, tachycardia, tachypnea → Infection• Fever, lethargy → CNS infection /septic encephalopathy• ↑Pulsus paradoxus (>10 mmHg) → Asthma or COPD• Ethanol odour → Intoxication

DIAGNOSTICS

2) NEUROLOGICAL EXAMINATION

• Depressed mental status (lethargy or coma) → Central drive failure• Pupillary constriction (miosis) “pinpoint pupils” → Opiate overdose(Severe hypercarbia causes miosis as well)• Sensory deficits → Polyneuropathy (e.g. GBS)• Muscle fasciculations → Motor neuron diseases (e.g. ALS)

DIAGNOSTICS3) Head and Neck

• Stridor, drooling → upper airway obstruction

4) Chest• Pattern of respiratory muscle contraction, chest diameter and

intergrity (Flail chest), presence of abnormal breath sounds

5) Abdomen• Normal abdominal wall movement during inspiration is

outward, inward movement with inspiration is paradoxical and suggests diaphragmatic fatigue.

DIAGNOSTICSLaboratory Testing

1. Arterial Blood Gas (ABG)ABGs are required very early and should be obtained as soon as possible after C-A-B has been assessed.

DIAGNOSTICS

Normal values of arterial blood gases (at R.A., sea level, 37°C)

DIAGNOSTICSInterpretative remarks:

• PaO₂ < 60mmHg(8kPa) →HYPOXEMIA• PaCO₂ > 50 mmHg(6.7 kPa) →HYPERCAPNIA

• pH < 7.35 → ACIDOSIS• pH >7.45 → ALKALOSIS

DIAGNOSTICSInterpretative remarks:

• ↓PaO₂ → TYPE I (Hypoxemic) RF

• ↑PaCO₂, ↓pH →Acute TYPE II (Hypercapnic) RF

• ↑PaCO₂, slightly↓pH, ↑HCO₃⁻ → Chronic TYPE II (Hypercapnic) RF

DIAGNOSTICSInterpretative remarks:

• The "50–50 rule" of intubating is OUTDATED!• Respiratory acidosis (pH<7.20–7.25) is an indication

ventilatory support.• Interpretation of an inadvertent venous blood

gas (VBG) must be avoided.• Elevated HCO⁻₃ is evidence of chronic

respiratory acidosis.

DIAGNOSTICS

2. Complete Blood Count (CBC)• Leukocytosis → infection• Anemia (dyspnea,↓O₂ transport to tissues, but in isolation

will not cause ventilatory failure.

3. Lumbar Puncture (LP) • (essential in cases of suspected CNS infection or GBS)

4. Serum Chemistries• (↓Ca,Mg,PO⁻ may contribute to respiratory muscle fatigue)

5. Toxicology Tests6. Pulmonary Function Tests

DIAGNOSTICSImaging and Other Tests

• CXR • (Pneumonia, atelectasis, pulmonary oedema, evidence of chronic

lung disease, tumours, chest wall and pleural abnormalities)

• CT Scan • (tumours, parenchymal lung disease, pleural and chest wall

disease)

• MRI• (encephalitis, brain stem pathology, and spinal cord injury)

• ECG• (evidence of chronic lung disease, left ventricular failure or valve

disease)

Principles of treatment

• Emergency treatment should follow principles of cardiopulmonary resuscitation (C-A-B);

• Ensure patent airway• Administer oxygen to maintain sats >90%• Correct hypoperfusion/anaemia

followed by treatment of underlying (reversible) causes:• Acidosis/Alkalosis• Hypovolemia• Hypoxia• Pneumothorax• Pulmonary embolism

Principles of treatment (Cont…)

• All patients with acute VF not responding to simple measures in an emergency room, clinic, or hospital ward setting should be monitored in an intensive/intermediate care unit.

• Inhaled bronchodilators should be administered to all patients with bronchospasm.

• Fever reduction with acetaminophen will decrease CO₂ production.

• Avoid excessive caloric intake (which increases CO₂ production)

Principles of treatment (Cont…)

• Consider non-invasive ventilatory support:• CPAP: continous positive airway pressure• BiPAP: Biphasic positive airway pressure

• Evaluate patient for the need of Endotracheal intubation and mechanical ventilation (e.g. in cases of severe respiratory failure with PaO2 less than 50 mmHg).

Principles of treatment (Cont…)

• DRUGS:• Respiratory stimulants (eg. Doxapram) (rarely used)

• Antidote for sedative overdose» Opioids → naloxone» Benzodiazepines → flumazenil

• Physiotherapy to mobilise secretions.

***************The End***************

THANK YOU!!!

References1. Hanley M. E., Welsh. H., Current Diagnosis & Treatment in Pulmonary

Medicine,1st ed. Denver, Colorado, September 2003.2. Kim E. Barrett, Susan M. Barman, Scott Boitano, and Heddwen L. Brooks,

Ganong's Review of Medical Physiology, 24th ed., Singapore,2012. 3. BMJ Publishing Group Limited, BMJ Best Practice, 2015

http://bestpractice.bmj.com (accessed 13-04-2015).