1. Initiating Ventilatory Support

2. Objectives List the indications for ventilatory support
List the factors analyzed to determine initial ventilator modes and settings
Define the current modes of ventilation, listing The advantages and disadvantages of each
Basic intro to settings

3. First a Review of Ventilation formulas…
Ve, VA, Compliance

4. Indications for Ventilatory Support
Respiratory failure (type I or II)
Exacerbation of COPD
Neuromuscular disease
Coma

5. The volume of carbon dioxide eliminated per minute (which in a steady state is equal to that produced by the body (V'CO2) is dependent on the concentration of carbon dioxide in alveolar gas and οn V'A.
V'CO2=V'A× alveolar CO2 concentration or alveolar CO2 concentration=V'CO2/V'A.

6. Hypoxemia
The condition of hypoxemia refers to the low partial pressure of oxygen in the arterial blood. Hypoxemia is often confused with either anoxia, asphyxia, hypoxia or anemia. Although, these are in some way related to reduction in the levels of oxygen in the body, these are distinct medical conditions.
Anoxia is the absence of oxygen supply in the body. This implies extremely low levels of oxygen in the body.
Asphyxia is the absence of oxygen along with the accumulation of carbon dioxide.
Hypoxia is the deficiency of oxygen in some specific part of the body.
Anemia refers to a condition when oxygen content in the arterial blood is low and the partial pressures in the arterial blood are high.
Hypoxemia refers to refers to a condition when oxygen content in the arterial blood is low as also the partial pressures in the arterial blood.

7. Arterial Oxygen Content (CaO2)
The arterial oxygen content can be given by the following equation:
Arterial Oxygen Content = (Hgb x 1.34 x SaO2) + ( x PaO2) where,
Hgb is the hemoglobin SaO2 is the percentage of hemoglobin saturated with oxygen PaO2 is the partial pressure of arterial oxygen

8. Clinical Manifestations of Type I Respiratory Failure
Clinical signs of hypoxemia
Dyspnea
Tachycardia
Tachypnea
Use of accessory muscles of ventilation
Nasal flaring
Cyanosis – peripheral and central
Central nervous system dysfunction – irritability, confusion, coma

9. Symptoms of Hypoxemia Symptoms of mild hypoxemia: Restlessness Anxiety
(The symptoms of hypoxemia depend on the severity i.e. the amount by which the partial pressure has reduced.)
Symptoms of mild hypoxemia:
Restlessness
Anxiety
Disorientation, confusion, lassitude and listlessness
Headaches

10. Symptoms of Hypoxemia Symptoms of acute hypoxemia:
Cyanosis (Skin appearing bluish due to insufficient oxygen)
Cheyne-Stokes respiration (irregular pattern of breathing)
Increased blood pressure
Apnea (temporary cessation of breathing)
Tachycardia (increased rate of heartbeats, more than 100 per min)
Hypotension (abnormally low blood pressure, below 100 diastolic and 40 systolic. Here, as an effect of an initial increase in cardiac output and rapid decrease later.)
Ventricular fibrillation (irregular and uncoordinated contractions of the ventricles)
Asystole (severe form of cardiac arrest, heart stops beating)
Polycythemia (abnormal increase in RBCs. The bone marrow may be stimulated to produce excessive RBCs in case of patients suffering from chronic hypoxemia)
Coma

11. Clinical Manifestations of Acute Ventilatory Failure

12. Clinical Manifestations of Type I Respiratory Failure
Auscultation
Wheezing indicates bronchospasm (asthma?)
Diminished (COPD?)
Unilateral wheezing – endobronchial lesion, FBAO
Unilaterally diminished or absent – atelectasis, infection, effusion

14. Clinical Manifestations of Type I Respiratory Failure
Radiologic Findings
“Black” radiograph
Hyperinflated lungs (COPD) – V/Q mismatch
“White” radiograph
Occlusion of alveoli – shunt

17. Clinical Manifestations of Type II Respiratory Failure
Decreased respiratory drive
Bradypnea leading to apnea
Clinical signs of decrease in respiratory drive
Respiratory rate < 12 bpm
Altered state of consciousness (increase CO2, amonia, blood sugar, ICB…)
Rapid, shallow breathing pattern (obesity, neuromuscular)
Evidence of trauma (brain injury)
Fatigue (hypothyroidism, sleep apnea)
Radiologic findings – atelectasis secondary to hypoventilation

18. Clinical Manifestations of Type II Respiratory Failure
Neurological disease
Drooling, dysarthria (unable to speak), weak cough (ALS)
Unable to swallow (Dysphagia)
Muscle wasting
Diaphragmatic weakness
Supine paradoxical breathing (ALS)
Lower extremity weakness, progressing superiorly (Guillain-Barre)
Ocular muscle weakness (myasthenia gravis)

19. Clinical Manifestations of Type II Respiratory Failure
Increased work of breathing
Increasingly rapid, but shallow breathing (exacerbation of COPD)
Diminished breath sounds
Irritability, confusion

20. Chronic Respiratory Failure
Development of respiratory failure in patients with chronic respiratory conditions over an extended period of time, as much as years
Allows compensatory mechanisms to adapt to the disease state
Most commonly Type II failure with compensatory metabolic alkalosis (COPD)
Compensation for Type I is polycythemia (Fibrosis/COPD)
May be complicated by superimposed acute respiratory failure

21. Chronic Respiratory Failure With Superimposed Acute RF
Precipitating factors
Bacterial or viral infections
Congestive heart failure
Pulmonary embolism
Chest wall dysfunction
Non-compliance with medical orders
“Normal” blood gases for these patients may be outside normal limits

22. Chronic Respiratory Failure With Superimposed Acute RF
Goals of therapy
Normalization of pH
Elevation of SaO2
Improvement of airflow
Treatment of infections
Maintain fluid status

23. Indications for Ventilatory Support
Acute respiratory failure
Post-Operative respiratory failure (over sedation, complications)
Sepsis (sudden increase in VO2 and CO2 production)
Cardiac failure (MI, CHF…)

24. Indications for Ventilatory Support
Acute respiratory failure
ARDS (from PN, Sepsis…)
Trauma (blood loss, head trauma…)
Pneumonia (causing plugs…)

25. Indications for Ventilatory Support
Apnea (sedation, drug OD…)
Impending respiratory failure
Inability to oxygenate

26. Clinical Manifestations of Acute Ventilatory Failure
Rapid, shallow respiratory pattern frequently have pleural space disease (pleural effusion, hemothorax, pneumothorax).

27. Clinical Manifestations of Acute Ventilatory Failure
Patients with end-expiratory effort and wheezes on chest auscultation frequently have small airway obstructive disease (asthma).
Patients with deep, labored chest movements frequently have pulmonary parenchymal disease (pulmonary edema, pulmonary contusions, space-occupying masses).
Patients with obvious stridor, minimal air movement at the nares or mouth, and marked inspiratory effort typically have upper airway obstruction (laryngeal edema or paralysis, foreign body aspiration).
These patterns are hardly exclusive: Often patients have multiple problems, and some patients may have serious underlying respiratory problems and yet clinically appear normal.

28. What nonrespiratory conditions can mimic acute respiratory distress?
Numerous disorders cause tachypnea, orthopnea, and other signs referable to the respiratory system in the absence of true respiratory disease. These disorders can confuse the clinician. Disorders such as hyperthermia, shock, metabolic acidosis and alkalosis, hyperthyroidism, fear or anxiety, pericardial tamponade, anemia, abdominal organ enlargement or ascites, and abnormalities with central control of respiration from drugs and metabolic or organic central nervous system disease are all causes of signs that may mimic true respiratory distress.

29. Clinical Manifestations of Acute Ventilatory Failure
Cardiovascular symptoms
Tachycardia; when severe bradycardia
Hypertension; when severe, hypotension
Vasodilation

30. Clinical Manifestations of Acute Ventilatory Failure
Neurologic symptoms
Headache
Drowsiness; when severe non-responsiveness
Convulsions
Biots/Cheyne stokes breathing

31. Clinical Manifestations of Acute Ventilatory Failure
Other signs
Sweating
Redness of the skin

32. Goals of Ventilatory Support
Maintenance of adequate alveolar ventilation and oxygen delivery
Restore acid-base balance

33. Goals of Ventilatory Support
Reduce the work of breathing
Reduce myocardial work secondary to hypoxemia And increased work of breathing

34. Considerations When Initiating Ventilatory Support
Type of airway: endotracheal tube vs. tracheostomy tube
Pressure-controlled vs. volume-controlled ventilation- depends on if patient has pre-existing congestion, loss of compliance, known lung problems

35. Pressure-Controlled Ventilation
Pressure support ventilation (PSV)
Designed to augment spontaneous ventilation (increases Spontaneous tidal volume)
Patient-triggered, pressure- limited, flow-cycled ventilation
Used to overcome RAW imposed by ETT
May be stand-alone mode or used with SIMV/CPAP

36. Pressure-Controlled Ventilation
Pressure control ventilation (PCV)
Delivery of mandatory support breaths at a set inspiratory pressure (pressure limited/time cycled)
May be used in assist-control mode or with SIMV
Set pressure limit (PIP) and Inspiratory time
Volume and flow vary

37. Pressure-Controlled Ventilation
Pressure control ventilation (PCV)
Useful in limiting airway pressure and providing a decreasing flow, which may improve gas distribution and synchrony
Can be set in any patient, however most often used for patients with low compliant lungs, especially if high PEEP levels will be used

38. Volume-Controlled Ventilation
Used primarily to maintain constant tidal volume
Useful when lung mechanics are changing due to pathophysiology
Set Tidal volume based on patient’s IBW in a range of 8-12 ml/kg and flow rate
IBW= men lbs for every inch over 60 inches
IBW=woman lbs for ever inch over 60 inches
For restrictive disease 5-7 ml/kg

39. Volume-Controlled Ventilation
Volume control is volume limited and flow cycled
Can be set in AC or SIMV modes
Direct control over Ve
I-time and pressure vary depending on patients lung compliance

40. Pressure-Regulated Volume Control (PRVC) Ventilation
Offers pressure-controlled ventilation while guaranteeing a volume
Pressure and flow fluctuate to maintain a constant minimum TV
May not work well with restrictive lungs

41. Non-Invasive (NPPV) vs. Invasive PPV
Advantages of NPPV
Avoidance of intubation
Preservation of natural airway defenses
Patient comfort

42. Non-Invasive (NPPV) vs. Invasive PPV
Advantages of NPPV
Maintenance of speech and swallowing
Intermittent use

43. Non-Invasive (NPPV) vs. Invasive PPV
Disadvantages of NPPV
Patient cooperation essential
Limited access to airway during ventilation
Discomfort from mask

44. Non-Invasive (NPPV) vs. Invasive PPV
Disadvantages of NPPV
Ulceration, face sores, eye irritation, rhinitis, dry nose
Stomach pain from gastric inflation
Leak from improper fit
Aspiration risk

45. Non-Invasive (NPPV) vs. Invasive PPV
Disadvantages of NPPV
Transient hypoxemia from mask disconnection
BiPAP limited to maximum of 30 cmH2O
Time consuming procedure
Drying of secretions/plugs

46. Partial vs. Full Ventilatory Support
Partial ventilatory support
Use of ventilator settings requiring patient to provide portion of the ventilation

47. Modes of Partial Ventilation
Synchronized intermittent mandatory ventilation (SIMV)
Pressure support ventilation (PSV)
Volume support ventilation (VSV), PSV will fluctuate depending on set minimum VT

48. Modes of Partial Ventilation
Adaptive pressure ventilation (APV)
Adaptive support ventilation (ASV)
Mandatory minute volume ventilation (MMV)
WE WILL TALK ABOUT THE ADAPTIVE MODES IN A SEPARATE LECTURE

49. Full Ventilatory Support
Ventilator provides the full minute ventilation; no patient contribution
Assist-control mode

50. Initial Ventilator Settings
Choice of mode (AC, IMV/SIMV, PCV, PRVC, APRV)
Tidal volume (VT) – 8 to 12 ml/kg IBW
Rate (f) – typically backup rate of 8-12 breaths /min

51. Initial Ventilator Settings
Trigger sensitivity (either flow or pressure)
Typically -0.5 to -2.o cmH2O to minimize effort
May need to be adjusted to avoid auto-cycling on some ventilators
Applies only to patient triggered breaths

52. Initial Ventilator Settings
Trigger sensitivity
Flow triggering may have slightly less work than pressure triggering

53. Initial Ventilator Settings
Inspiratory flow
60 to 80 L/min. to achieve an inspiratory time of 1 second and an I:E ratio of 1:2 or better
May require higher flows in patients with COPD to lengthen expiratory time, allowing improved gas exchange

54. Initial Ventilator Settings
Flow waveform
Decelerating or decreasing flow waveform generally delivered in pressure ventilation
Decelerating waveforms generally decrease peak inspiratory pressure, but increase mean airway pressure

55. Decelerating – set in VC, automatic in PC

56. Constant Flow – VC only
Increases MAP, decreased I-time

57. Initial Ventilator Settings
Oxygen percentage (FIO2)
If little is known concerning patient, begin with FIO2 of 1.0, decreasing to 0.4 to 0.5 as quickly as possible
Patients with known blood gas results should be given FIO2 consistent with the known data

58. Initial Ventilator Settings
Positive end-expiratory pressure (PEEP)
PEEP of 5 cmH2O is advocated by some as “physiologic PEEP”
Should be adjusted as necessary to allow FIO2 to be reduced to 0.4 as quickly as possible

59. Initial Ventilator Settings
Pressure limit
Start at 50 cmH2O
Adjust to 10 to 20 cmH2O above peak pressure when patient is stable