APPROACH TO REFRACTORY HYPOXEMIA (1).pptx

This ppt helps in understanding the types of hypoxia and need of accurate interventions and management at a particular point.

1. APPROACH TO REFRACTORY HYPOXEMIA - DR ISHA CHHEDA

2. DEFINITION HYPOXIA : is defined as deficiency in either the delivery or the utilization of oxygen at the tissue level, which can lead to changes in function, metabolism and even structure of the body. ARTERIAL HYPOXEMIA : is defined as partial pressure of oxygen in arterial blood (PaO2) less than 80 mmHg while breathing in room air .

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4. CAUSES OF HYPOXEMIA The mechanisms that can cause hypoxemia can be divided into those that increase P(A-a)O2 and those where P(A-a)O2 is preserved. 1) HYPOVENTILATION 2) LOW INSPIRED OXYGEN 3) RIGHT TO LEFT SHUNT 4) VENTILATION PERFUSION INEQUALITY 5) DIFFUSION IMPAIRMENT A – stands for ALVEOLAR a – stands for arterial blood

5. HYPOVENTILATION Hypoventilation refers to condition in which alveolar ventilation is abnormally low in relation to oxygen uptake or carbon dioxide output. Alveolar ventilation is the volume of fresh inspired gas going to the alveoli (i.e. non dead space ventilation). Hypoventilation occurs when the alveolar ventilation in reduced and the alveolar PO2 therefore settles out at a lower level than normal. For the same reason, the alveolar PCO2 and thus arterial PCO2 are raised. P(A-a)O2 is normal. PaCO2 is elevated (hypercapnia) Increasing the fraction of oxygen (FiO2) can alleviate the hypoxemia and the hypercapnia can be corrected by mechanically ventilating the patient to eliminate CO2.

6. CAUSES OF HYPOVENTILATION 1 . D epression of the respiratory center by drugs, such as morphine derivatives and barbiturates . 2. Diseases of the brain stem, such as encephalitis . 3. Abnormalities of the spinal cord conducting pathways, such as high cervical dislocation ; anterior horn cell diseases, including poliomyelitis . 4. Affecting the phrenic nerves or supplying the intercostal muscles. 5 . D iseases of the myoneural junction, such as myasthenia gravis . 6 . D iseases of the respiratory muscles themselves, such as progressive muscular dystrophy ; thoracic cage abnormalities (e.g., crushed chest ). 7. Diseases of nerves to respiratory muscles (e.g., Guillain Barre syndrome ). 8 . Upper airway obstruction (e.g . thymoma ). 9. Hypoventilation associated with extreme obesity ( pickwickian syndrome ) 10. Miscellaneous causes, such as metabolic alkalosis and idiopathic states.

7. LOW INSPIRED OXYGEN [ PI O2 ] Examples- 1) A decrease in barometric pressure [e.g. breathing at high altitude ]. 2) A decrease in FIO2 – accidental [e.g. anesthetist does not supply enough oxygen or improper installation of oxygen supply lines or a leak in the breathing circuit ]. Here P(A-a)O2 normal PaCO2 is decreased . This reduction in PaCO2 ( hypocapnia ) is due to hyperventilation in response to hypoxemia . Peripheral chemoreceptors sense the low arterial PO2 and initiate an increase in ventilation through their input to the medullary respiratory centre

8. RIGHT TO LEFT SHUNT Shunt refers to the entry of blood into the systemic arterial system without going through ventilated areas of lung. Shunt may be anatomical or physiological . P(A-a)O2 is elevated. PaCO2 is normal . Anatomic shunt : when a portion of blood bypasses the lungs through an anatomic channel. • In healthy individuals : i ) A portion of the bronchial circulation’s (blood supply to the conducting zone of the airways) venous blood drains into the pulmonary vein. ii) A portion of the coronary circulation’s venous blood drains through the thebesian veins into the left ventricle. Note : i & ii represent about 2% of the cardiac output and account for 1/3 of the normal P(A-a)O2 observed in health . Congenital abnormalities : i ) intra-cardiac shunt [e.g. Tetralogy of Fallot : ventricular septal defect + pulmonary artery stenosis] • ii) intra-pulmonary fistulas [direct communication between a branch of the pulmonary artery and a pulmonary vein].

9. Physiologic shunt: In disease states, a portion of the cardiac output goes through the regular pulmonary vasculature but does not come into contact with alveolar air due to filling of the alveolar spaces with fluid [e.g. pneumonia, drowning, pulmonary edema ] An important diagnostic feature of a shunt is that the arterial PO2 does not rise to the normal level when the patient is given 100% oxygen to breathe . Examples of intrapulmonary shunt- (a) Collapsed and fluid filled alveoli are examples of intrapulmonary shunt . (b) Anomalous blood return of mixed venous blood bypasses the alveolus and thereby contributes to the development of intrapulmonary shunt.

10. VENTILATION PERFUSION INEQUALITY PaCO2 is normal P(A-a)O2 is elevated VA/Q inequality is the most common cause of hypoxemia in disease states In patients with obstructive or restrictive ventilatory diseases , decreased ventilation may result from structural or functional abnormalities of the airway and can lead to decreased VA/Q units On the other hand , lung units with increased VA/ Q ratios can develop disorders that lead to over ventilation of lung units, conditions such as emphysema , for example, in which patients have airspace enlargement as a result of the destruction of the alveolar sac distal to the terminal bronchiole . Moreover, the development of impaired perfusion through the pulmonary vasculature, as observed in cases of pulmonary embolism or pulmonary vasospasm , may cause high VA/ Q ratios

11. VENTILATION PERFUSION INEQUALITY Reflex mechanisms are present in the lung to minimize the effect of VA/Q inequality, thus avoiding or minimizing the detrimental effects of impaired gas exchange One mechanism is hypoxic pulmonary vasoconstriction (HPV), whereby a fall in VA/Q leads to the development of alveolar hypoxia which in turn causes vasoconstriction of the perfusing arteriole. This effect is beneficial for pulmonary gas exchange because it decreases the denominator of the VA/Q relationship, thereby partially correcting regional VA/Q imbalance and improving arterial hypoxemia HPV appears to operate over a range of alveolar PO2 values between 30 and 150 mmHg . The mechanism by which alveolar hypoxia sends the message to trigger regional vasoconstriction is unclear, but may involve the release of humoral messengers. Many factors, however, can significantly interfere with HPV certain drugs such as calcium channel blockers, beta-agonists, and inhalational anesthetic agents. Lower respiratory tract infections or disease processes that cause elevations in left atrial pressure can also interfere with HPV. In addition, although HPV may be helpful in improving arterial hypoxemia, a progression in vasoconstrictor effect can lead to the development of secondary pulmonary hypertension and, eventually, right heart failure

12. DIFFUSION LIMITATION • It is now generally believed that oxygen, carbon dioxide, and indeed all gases cross the blood-gas barrier by simple passive diffusion Fick's law of diffusion states that the rate of transfer of a gas through a sheet of tissue is proportional to the tissue area (A) and the difference in partial pressure (P1-P2) between the two sides , and is inversely proportional to the thickness (T) The rate of diffusion is also proportional to a constant, D, which depends on the properties of the tissue and the particular gas. The constant is proportional to the solubility (Sol) of the gas , and inversely proportional to the square root of the molecular weight (MW)

13. DIFFUSION LIMITATION CONT.. PaCO2 is normal. P(A-a)O2 is normal at rest but may be elevated during exercise . Diffusing capacity is reduced by diseases in which the thickness is increased , including diffuse interstitial pulmonary fibrosis, asbestosis, and sarcoidosis . It is also reduced when the area is decreased , for example, by pneumonectomy . The fall in diffusing capacity that occurs in emphysema may be caused by the loss of alveolar walls and capillaries

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15. DIAGNOSIS OF RESPIRATORY FAILURE History Physical examination Laboratory investigations

16. SYMPTOMS Neurologic symptoms: Headache Visual disturbances Anxiety Confusion Memory loss Hallucinations Loss of consciousness Asterixis (hypercapnia ) Weakness Decreased functional performance

17. Specific organ symptoms: Pulmonary Cough Chest pains Sputum production Stridor Dyspnea (resting vs. exertional) Cardiac Orthopnea Peripheral edema Chest pain Other Fever Abdominal pain Anemia Bleeding

18. PHYSICAL EXAMINATION P hysical examination of patients with hypoxemia begins with a quick, but thorough, general assessment. T he initial priority is to triage patients who present with severe forms of respiratory failure from those with less severe form 1)General findings: Mental alertness Ability to speak in complete sentences Respiratory rate > 35 breaths/min Heart rate > or < 20 beats from normal Pulsus paradoxus present? Elevated work of breathing? Using accessory muscles Rib cage or abdominal paradox 2) Specific organ dysfunction: Pulmonary: Stridor Wheezes Rhonchi Crackles . Cardiac: • Tachycardia, bradycardia • Hypertension, hypotension • Crackles • New murmur Renal • Anuria Gastrointestinal • Distended • Pain to palpation • Decreased bowel sounds

19. REFRACTORY HYPOXEMIA There is no standard definition of refractory hypoxemia so far. However in patients on lung protective ventilation, majority of clinicians define refractory hypoxemia as: P/F < 100 or SaO2 < 88% or PaO2 < 60 mm Hg with FiO2 > 0.8 and Pplat > 30 cm H2O

20. Step 1 : Initiate Resuscitation and Identify the Reason for Deterioration Perform quick physical examination and initiate basic investigations such as arterial blood gas and the chest X-ray to arrive at probable cause for deterioration in respiratory status. • Prior to labelling patients as refractory hypoxemia, it is important to rule out reversible causes of hypoxemia

21. Step 2: Identifying the Therapies for Refractory Hypoxemia in a Given Setting Once reversible causes of refractory hypoxemia are ruled out, identify the availability of rescue therapies in the given resource setting and patient needs Broadly therapies for refractory hypoxemia (based on resource availability) can be classified into two categories: Therapies requiring minimal resources : Recruitment manoeuvres • Prone ventilation • Neuro-muscular blockade 2 . Therapies requiring high end gadgets: • Inhaled pulmonary vasodilators • HFOV • Extracorporeal membrane based techniques

22. Step 3: Understanding the Goals of Mechanical Ventilation in ARDS One has to be understand that irrespective of modalities used to improve oxygenation in refractory hypoxemia the goals of mechanical ventilation in ARDS stays the same. Oxygenation goal: PaO2 55–80 mm Hg or SaO2 88–95%. Plateau pressure ( Pplat ): <30 cm H2O. Driving Pressure < 14 cm H2O. pH goal: 7.20–7.45 (Permissive Hypercapnoea ).

23. Step 4: Consider Recruitment Manoeuvres Recruitment manoeuvre is application of a high level of sustained airway pressure to open up the collapsed alveoli and then apply appropriate PEEP to prevent the collapse of the recruited alveoli. There is still insufficient evidence to use recruitment manoeuvres routinely and electively in all patients of severe ARDS. Indications 1. As a temporary rescue therapy to improve oxygenation. Pre-requisites Patient should be well sedated/ paralysed . Patient should be hemodynamically stable. Patient should be well hydrated and not hypovolemic. Avoid in patients with chronic obstructive airway disease, intracranial hypertension and pregnancy. Patient with early diffuse ARDS are generally good recruiters, but patients with late ARDS (>1 week) and patients with focal ARDS generally do not respond well.

24. Step 5: Consider Prone Ventilation Physiology Prone ventilation reduces ventral-dorsal transpulmonary pressure difference. Reduces lung compression (gravitational readjustment of edema fluid). Improves ventilation perfusion mismatch. Improves bronchial drainage. Reversal of acute cor pulmonale Indications P/F < 150 with PEEP > 10 cm H2O. Within 36 h of onset of ARDS.

25. Step 6: Consider Adjunctive Neuromuscular Blockade Neuromuscular blockade has been postulated to facilitate lung protective low volume ventilation by improving patient ventilator synchrony . It limits the risk of asynchrony related alveolar collapse and regional alveolar pressure increase with overdistension of alveoli. It is also postulated to cause decrease in lung inflammation . Benefit with neuromuscular blockade have been documented in early ARDS with P/F < 150 (infusion for 48 h). This benefit has been shown with cisatracurium . It may also be used as an adjunct in patient having severe patient ventilator asynchrony despite heavy sedation . Neuromuscular blockade should be used judiciously considering that, its use is associated with critical illness neuromyopathy and is a confounder to neurological assessment.

26. STEP 7: Consider Extracorporeal Membrane Oxygenation (ECMO) ECMO is a technique where blood is removed from patient and passed through artificial biomembrane which functions to oxygenate blood and remove CO2 from blood and then return it back to patient. Thus essentially it is decoupling of mechanical ventilation and gas exchange. ECMO can be considered in severe ARDS especially in cases of refractory hypoxemia and in cases where adherence to lung protective ventilation leads to severe hypercapnic respiratory acidosis. ECMO thus provides an way to manage gas exchange well while managing mechanical ventilation with acceptable tidal volumes and plateau pressures. This decreases chances of VALI.

27. Other Rescue Therapies HFOV - HFOV is a type of ventilation which combines high respiratory rate (>180 breaths/min ) with tidal volumes as low as anatomical dead space. The oscillator delivers very low tidal volume. This prevents alveolar collapse and at the same time avoids high airway pressures. Risks with HOFV include hypotension and barotraumas. Inhaled Pulmonary Vasodilators – NITRIC OXIDE AND EPOPROSTENOL They promote pulmonary vasodilatation and improved blood flow to ventilated areas of lungs and divert blood away from poorly ventilated areas of lung. T his improves ventilation perfusion mismatch and thus improves oxygenation.

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