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

18. INVESTIGATIONS

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

22. TREATMENT

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

26. VENTILATION
MECHANICAL

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

29. INDICATIONS FOR TRACHEAL INTUBATION AND MECHANICAL VENTILATION
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

45. CONDITIONS REQUIRING MECHANICAL VENTILATION
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

46. TERMS USED IN MECHANICAL VENTILATORY SUPPORT
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