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Department of Medicine Manipal College of Medical Sciences

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1 Department of Medicine Manipal College of Medical Sciences
RESPIRATORY FAILURE AND MECHANICAL VENTILATION ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

2 Inability of the lungs to perform the function of gas exchange- the transfer of oxygen from inhaled air into the blood and the transfer of carbon dioxide from the blood into exhaled air Defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg

3 Classification Type 1 hypoxemic respiratory failure Type 2
hypercapnic respiratory failure Acute Chronic

4 1. failure to oxygenate 2. failure to ventilate
Respiratory failure is caused by: 1. failure to oxygenate characterized by decreased PaO2 2. failure to ventilate characterized by increased PCO2

5 1. Failure to oxygenate: due to ventilation perfusion mismatch
decreased inspired O2 tension increased CO2 tension ventilation perfusion mismatch Pneumonia Oedema P E reduced O2 diffusion capacity due to interstitial edema fibrosis thickened alveolar wall Deoxygenated blood from pulmonary artery

6 V – Q Mismatch V/Q incresed = physiological dead space
Pulmonary embolism Obliteration of blood vessels emphysema V/Q reduced = physiological shunt Collapse of alveoli – atelectasis Loss of surfactant Airway obst. - COPD Fluid filling Anatomical shunt increased – anastomosis between pulmonary & systemic vessels

7 2. Failure to ventilate Causes: Airway Chest wall Respiratory muscles
Respiratory centers Airway Chest wall Respiratory muscles

8 C.O.P.D. Pneumonia Pulmonary edema Pulmonary fibrosis Asthma
Hypoxemic (type I) PaO2 <60 mm Hg CO2 level may be normal or low associated with virtually all acute diseases of lung with V/Q mismatch Common causes C.O.P.D. Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Hypercapnic (type II) PaCO2 of >50 mm Hg pH depends on the level of bicarbonate, dependent on the duration of hypercapnia caused by- Alveolar hypoventilation C.O.P.D. Neuromuscular disorders Guillain-Barré syndrome Diaphragm paralysis Amyotrophic lateral sclerosis Muscular dystrophy Myasthenia gravis severe obstruction with a FEV1 of less than 1 L or 35% of normal

9 Pulmonary arterial hypertension Pneumoconiosis
Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Granulomatous lung diseases Cyanotic congenital heart disease Bronchiectasis Adult respiratory distress syndrome Fat embolism syndrome Chest wall deformities Kyphoscoliosis Ankylosing spondylitis Central respiratory drive depression Drugs - Narcotics, benzodiazepines, barbiturates Neurologic disorders - Encephalitis, brainstem disease, trauma Primary alveolar hypoventilation Obesity hypoventilation syndrome (Pickwickian Syn)

10 Carol Yager (1960 – 1994) 730 KG BMI 252

11 Acute and chronic respiratory failure
Acute respiratory failure develops over minutes to Hours No time for renal compen. pH is less than 7.3. clinical markers of chronic Hypoxemia- polycythemia cor pulmonale Are absent Chronic respiratory failure develops over several days allowing time for renal compensation an increase in bicarbonat conc. pH -only slightly decreased. clinical markers of chronic hypoxemia polycythemia cor pulmonale Are present

12 Alveolar-to-arterial PaO2 difference (A-a Gradient)
Determines the efficiency of lungs at carrying out of respiration Aa Gradient = ( /4(PCO2)) - PaO2 Normal < 10mm increase in alveolar-to-arterial PO2 above 15- 20 mm Hg indicates pulmonary disease as the cause of hypoxemia Normal in Hypoventilation

13 Signs Symptoms &

14 Underlying disease process
(pneumonia, pulmonary edema, asthma, COPD) associated hypoxemia hypercapnia

15 Hypoxemia Symptoms coma Signs shortness of breath
confusion & restlessness Seizures coma Signs Cyanosis variety of arrhythmias from hypoxemia & acidosis Polycythemia – in long-standing hypoxemia

16 Hypercapnia Vasodilation leading to Extrasystoles & other arrythmias
Morning headache flushed skin & warm moist palms full & bounding pulse Extrasystoles & other arrythmias muscle twitches flapping tremors - asterixis drowsiness Asterix

17 Now answer this question-
If you are forced to choose one of these, which one you will like to have ? Hypoxia Hypercapnia


19 A.B.G. (arterial blood gases) complete blood count
anemia contribute to tissue hypoxia polycythemia indicate chronic hypoxemic respiratory failure Associated organ involvement R.F.T. L.F.T. .

20 Chest radiograph Echocardiography
frequently reveals the cause of respiratory failure distinguishes between cardiogenic noncardiogenic pulmonary edema Echocardiography when cardiac cause of acute respiratory failure is suspected left ventricular dilatation regional or global wall motion abnormalities severe mitral regurgitation provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure

21 Other Tests PFT in the evaluation of chronic respiratory failure ECG
to evaluate the possibility of a cardiovascular cause of respiratory failure dysrhythmias resulting from severe hypoxemia and/or acidosis


23 Hypoxemia major immediate threat to organ function
oxygen supplementation and/or ventilatory assist devices The goal is to assure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mm Hg or more SaO2 of greater than 92%

24 Supplemental oxygen administered via
nasal prongs face mask in severe hypoxemia, intubation and mechanical ventilation often are required Airway management Adequate airway vital in a patient with acute respiratory distress The most common indication for endotracheal intubation (ETT) is respiratory failure What is the role of tracheostomy??

25 Hypercapnia without hypoxemia
generally well tolerated not a threat to organ function hypercapnia should be tolerated until the arterial blood pH falls below 7.2 hypercapnia and respiratory acidosis managed by correcting the underlying cause providing ventilatory assistance Treatment of coexisting condition with approptiate drugs


27 Mechanical ventilation is a method to
mechanically assist or replace spontaneous breathing

28 Mechanical Ventilatior What is it?
Machine that generates a controlled flow of gas into a patient’s airways Oxygen and air are received from cylinders or wall outlets blended according to the prescribed inspired oxygen tension (FiO2) Delivered to the patient using one of many available modes of ventilation.The magnitude of rate and duration of flow are determined by the operator

Protection of airway Removal of secretions Hypoxaemia PaO2 < 60 mmHg SpO2 < 90% despite CPAP with FIO2 > 0.6 Hypercapnia if conscious level impaired or risk of raised intracranial pressure Increased Alveolar-arterial gradient of oxygen tension (A-a DO2) with 100% oxygenation Vital capacity falling below 1.2 litres in patients with neuromuscular disease Removing the work of breathing in exhausted patients Body_ID: B008019

30 Ventilatory workload is increased by loss of lung compliance
inspiration/ventilation is usually supported to reduce O2 requirements and increase patient comfort

31 Respiratory failure is caused by 1. Failure to ventilate
characterized by increased PCO2 2. Failure to oxygenate characterized by decreased PaO2

32 Failure to ventilate Increase the patient’s alveolar ventilation
rate depth of breathing by using mechanical ventilation

33 Failure to oxygenate Restoration and maintenance of lung volumes by using recruitment maneuvers Recruitment maneuvers are used to reinflate collapsed alveoli: due to pressure generated by ventilator during inspiration alveoli are inflated PEEP is used to prevent derecruitment

34 What do we mean by PEEP ? Girl’s changing room

35 PEEP amount of pressure above atmospheric pressure present in the airway at the end of the expiratory cycle PEEP improves gas exchange by preventing alveolar collapse recruiting more lung units increasing functional residual capacity redistributing fluid in the alveoli

36 Dangers of PEEP Overdistension of lungs – Barotrauma
Will increase intracranial tension Reduce venous return to right side of heart leading to reduced cardiac out put & hypotension The ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension


38 Air flow continues until
Modes of ventilation: Air flow continues until a predetermined volume has been delivered – volume controlled airway pressure generated – pressure controlled

39 Flow reverses, when the machine cycles into the expiratory phase, the message to do this is
either at a preset time preset tidal volume preset percentage of peak flow

40 Mechanical breaths may be
Controlled (Controlled mandatory ventilation -CMV) ventilator is active patient passive assisted (Synchronised intermittent mandatory ventilation - SIMV) patient initiates and may or may not participate in the breath

41 Controlled mandatory ventilation (CMV)
Most basic classic form of ventilation Pre-set rate and tidal volume Does not allow spontaneous breaths Appropriate for initial control of patients with little respiratory drive severe lung injury circulatory instability

42 Synchronized Intermittent Mandatory Ventilation (SIMV)
method of partial ventilatory support to facilitate liberation from mechanical ventilation patient could breathe spontaneously while also receiving mandatory breaths As the patient’s respiratory function improved, the number of assisted is decreased, until the patient breaths unassisted


44 Iron Lung

Post-operative • After major abdominal or cardiac surgery Respiratory failure ARDS Pneumonia COPD Acute severe asthma Aspiration Smoke inhalation, burns Circulatory failure Following cardiac arrest Pulmonary oedema •Low cardiac output-cardiogenic shock Neurological disease Coma of any cause Status epilepticus Drug overdose Respiratory muscle failure (e.g. Guillain-Barré, poliomyelitis, myasthenia gravis) Head injury-to avoid hypoxaemia and hypercapnia, and to reduce intracranial pressure Bulbar abnormalities causing risk of aspiration (CVA, myasthenia gravis) Multiple trauma

Controlled mandatory ventilation (CMV) Most basic classic form of ventilation Pre-set rate and tidal volume Does not allow spontaneous breaths Appropriate for initial control of patients with little respiratory drive, severe lung injury or circulatory instability Synchronised intermittent mandatory ventilation (SIMV) Pre-set rate of mandatory breaths with pre-set tidal volume Allows spontaneous breaths between mandatory breaths Spontaneous breaths may be pressure-supported (PS) Allows patient to settle on ventilator with less sedation Pressure controlled ventilation (PCV) Pre-set rate; pre-set inspiratory pressure Tidal volume depends on pre-set pressure, lung compliance and airways resistance Used in management of severe acute respiratory failure to avoid high airway pressure, often with prolonged inspiratory to expiratory ratio (pressure controlled inverse ratio ventilation, PCIRV) Pressure support ventilation (PSV) Breaths are triggered by patient Provides positive pressure to augment patient's breaths Useful for weaning Usually combined with CPAP; may be combined with SIMV Pressure support is titrated against tidal volume and respiratory rate

47 Continuous positive airways pressure (CPAP)
Positive airway pressure applied throughout the respiratory cycle, via either an endotracheal tube or a tight-fitting facemask Improves oxygenation by recruitment of atelectatic or oedematous lung Mask CPAP discourages coughing and clearance of lung secretions; may increase the risk of aspiration Bi-level positive airway pressure (BiPAP/BIPAP) Describes situation of two levels of positive airway pressure (higher level in inspiration) In fully ventilated patients, BiPAP is essentially the same as PCV with PEEP In partially ventilated patients, and especially if used non-invasively, BiPAP is essentially PSV with CPAP Non-invasive intermittent positive pressure ventilation (NIPPV) Most modes of ventilation may be applied via a facemask or nasal mask Usually PSV/BiPAP (typically cmH2O) often with back-up mandatory rate Indications include acute exacerbations of COPD

48 SCIENCE & ARTS Of mechanical ventilation

49 Large tidal volumes overstretch alveoli and injure the lungs
Small tidal volumes increase the contribution to dead space – wasted ventilation

50 Large PEEP overstretch alveoli and injure the lungs
Small PEEP does not correct V/Q mismatch & derecruitment

51 There is no ideal mode of ventilation for any particular patient
The science of mechanical ventilation is to optimize pulmonary gas exchange The art is to achieve this without damaging the lungs .

52 Complications


54 Major immediate complication
1. Hypotension due to vasodilatory effects of hypnotic drugs Treated with vasoconstrictors have an ampule of phenylephrine (a selective alpha adrenoceptor agonist) at hand to reverse vasodilatory hypotension Increase in intrathoracic pressure Treated with fluid boluses Always have an intravenous fluid drip running and be prepared to run in a liter or more of fluid quickly

55 Late complications 2. Barotrauma
Pneumothorax subcut emphysema 3. VALI (Ventilator Associated Lung Injury) 4. O2 toxicity 5. From prolonged immobility and inability to eat normally venous thromboembolic disease skin breakdown atelectasis Late complications

56 6. From endotracheal intubation
ventilator-associated pneumonia (VAP) tracheal stenosis vocal cord injury tracheal-esophageal or tracheal-vascular fistula

57 Measures to reduce complications
Elevating the head of the bed to > 30° decreases risk of ventilator-associated pneumonia routine turning of patient every 2 h decreases the risk of skin breakdown Keep the PEEP & TV in optimal range All patients receiving mechanical ventilation should receive deep venous thrombosis prophylaxis

58 Some special techniques
1. Inhaled nitric oxide very short-acting pulmonary vasodilator Delivered to the airway in concentrations of between 1 and 20 parts per million Improves blood flow to ventilated alveoli, thus improving V/Q mismatch, Oxygenation can be improved markedly benefit only lasts for 48 hours and outcome is not improved

59 2. techniques to reduce the high inflation pressures resulting from the stiff lungs (low compliance)
1. Low tidal volumes to reduce inflation pressures (6 ml/kg ideal body weight compared to 12 ml/kg) reduces mortality Minute ventilation reduced PaCO2 rises – permissive hypercapnia

60 3. Inverse ratio ventilation :
may improve oxygenation PCO2 may rise further 4. Prone positioning: improves oxygenation in ~70% of patients with ARDS

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