215a
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
First a Review of Ventilation
formulas…
 http://www.youtube.com/watch?v=mF4OvuzlfXc&fea
ture=related
 Ve, VA, Compliance
Indications for Ventilatory Support
 Respiratory failure (type I or II)
 Exacerbation of COPD
 Neuromuscular disease
 Coma
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.
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.
 http://www.youtube.com/watch?v=f8zIVc9yTMg
Arterial Oxygen Content
(CaO2)
 The arterial oxygen content can be given by the following equation:
Arterial Oxygen Content = (Hgb x 1.34 x SaO2) + (0.0031 x PaO2)
where,
Hgb is the hemoglobin
SaO2 is the percentage of hemoglobin saturated with oxygen
PaO2 is the partial pressure of arterial oxygen
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
Symptoms of Hypoxemia
(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
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,


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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
Clinical Manifestations of Acute
Ventilatory Failure
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
Clinical Manifestations of
Type I Respiratory Failure
 Radiologic Findings
 “Black” radiograph

Hyperinflated lungs (COPD) – V/Q mismatch
 “White” radiograph

Occlusion of alveoli – shunt
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
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)
Clinical Manifestations of
Type II Respiratory Failure
 Increased work of breathing
 Increasingly rapid, but shallow breathing (exacerbation
of COPD)
 Diminished breath sounds
 Irritability, confusion
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
Chronic Respiratory Failure With
Superimposed Acute RF
 Precipitating factors
 Bacterial or viral infections
 Congestive heart failure
http://www.youtube.com/watch?v=JJAMYHAwCMs&feature=related
 Pulmonary embolism
 Chest wall dysfunction
 Non-compliance with medical orders
 “Normal”
blood gases for these patients may be outside
normal limits
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
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…)
Indications for Ventilatory Support
 Acute respiratory failure
 ARDS (from PN, Sepsis…)
 Trauma (blood loss, head trauma…)
 Pneumonia (causing plugs…)
Indications for Ventilatory Support
 Apnea (sedation, drug OD…)
 Impending respiratory failure
 Inability to oxygenate
Clinical Manifestations of Acute
Ventilatory Failure
Rapid, shallow respiratory pattern frequently have
pleural space disease (pleural effusion,
hemothorax, pneumothorax).
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.
 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.
Clinical Manifestations of Acute
Ventilatory Failure
 Cardiovascular symptoms
 Tachycardia; when severe bradycardia
 Hypertension; when severe, hypotension
 Vasodilation
Clinical Manifestations of Acute
Ventilatory Failure
 Neurologic symptoms
 Headache
 Drowsiness; when severe non-responsiveness
 Convulsions
 Biots/Cheyne stokes breathing
Clinical Manifestations of Acute
Ventilatory Failure
 Other signs
 Sweating
 Redness of the skin
Goals of Ventilatory Support
 Maintenance of adequate alveolar ventilation and
oxygen delivery
 Restore acid-base balance
Goals of Ventilatory Support
 Reduce the work of breathing
 Reduce myocardial work secondary to hypoxemia
And increased work of breathing
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
 http://www.youtube.com/watch?v=4O4vGPqM2RM
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
 http://www.youtube.com/watch?v=oLZ0fcJ9Rhw&NR=1
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
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
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 106 + 6 lbs for every inch over 60 inches
 IBW=woman 105 + 5 lbs for ever inch over 60 inches
 For restrictive disease 5-7 ml/kg
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
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
Non-Invasive (NPPV) vs. Invasive PPV
 Advantages of NPPV
 Avoidance of intubation
 Preservation of natural airway defenses
 Patient comfort
Non-Invasive (NPPV) vs. Invasive PPV
 Advantages of NPPV
 Maintenance of speech and swallowing
 Intermittent use
Non-Invasive (NPPV) vs. Invasive PPV
 Disadvantages of NPPV
 Patient cooperation essential
 Limited access to airway during ventilation
 Discomfort from mask
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
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
Partial vs. Full Ventilatory Support
 Partial ventilatory support
 Use of ventilator settings requiring patient to provide
portion of the ventilation
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
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
Full Ventilatory Support
 Ventilator provides the full minute ventilation; no
patient contribution
 Assist-control mode
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
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
Initial Ventilator Settings
 Trigger sensitivity
 Flow triggering may have slightly less work than
pressure triggering
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
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
Decelerating – set in VC, automatic
in PC
Constant Flow – VC only
Increases MAP, decreased I-time
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
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
Initial Ventilator Settings
 Pressure limit
 Start at 50 cmH2O
 Adjust to 10 to 20 cmH2O above peak pressure when
patient is stable