Monitoring and Management of Ventilatory Support

Monitoring and Management of Ventilatory Support

Educational Objectives

• List the reasons for monitoring the patient receiving ventilatory

support

• List and describe the methods of evaluating patient oxygenation

• List and describe the methods of evaluating patient ventilation

• List and describe the ventilator parameters monitored

• List the normal hemodynamic values

• Describe the effects that mechanical ventilation may have upon

the hemodynamic parameters

Reasons for Monitoring the Patient

1. Establish baseline measurements

2. Allow trending to be observed in order to

document progress or lack of progress

3. Determine efficacy of treatment in order to

modify as needed

4. Determine limits of alarm parameters

Evaluation of Oxygenation – is There a Problem?

• Physical Findings

– Heart rate

– Respiratory rate

– Work of breathing

• Use of accessory muscles

• Retractions


Physical Findings

– Cyanosis

• Peripheral

• Central or circumoral (surrounding the mouth)

– Level of consciousness/mental status

• Confusion

• Drowsiness

• Anxiety


Laboratory Findings– Arterial blood gases

• PaO2

• SaO2 (measured or calculated?)

• Hemoglobin (Hb)/Hematocrit (Hct)

• Total oxygen content (CaO2)

– Level of consciousness/mental status

• Confusion

• Drowsiness

• Anxiety– Pulse oximetry– Lactic acid levels

Determine Cause of Hypoxemia

CO-Oximetry Results

– Oxyhemoglobin (HbO2)

– Carboxyhemoglobin (HbCO)

– Methemoglobin (MetHb)

– Hemoglobin (Hb)/Hematocrit (Hct)


Laboratory Findings

– Oxygen consumption (O2)

• Normal value – 250 mL/min

• Determined by Fick Equation

Where is cardiac output, CaO2 and are arterial

and mixed venous O2 content

• Increase in oxygen consumption necessitates increase in

oxygen delivered


– Alveolar-arterial Gradient [P(A-a)O2]

• Normal value – 5 to 15 mm Hg while breathing room air;

increases to 100 to 150 mm Hg while breathing 100%

oxygen

• Determined by subtracting arterial value from arterial

blood gas result from alveolar value using alveolar air

equation


– Arterial to Alveolar Oxygen Ratio (PaO2/FIO2)

• Normal Value – 400 to 500 mm Hg while breathing

room air

• Used to define acute lung injury (ALI) and acute

respiratory distress syndrome (ARDS)

– PaO2/FIO2 < 300 mm Hg in ALI

– PaO2/FIO2 < 200 mm Hg in ARDS


Radiologic Findings

– Consolidation

– Fluid

– Free air

Management Options – FIO2

• If FIO2 < 0.6, increase oxygen concentration;

if no PEEP is employed, may add 5 cmH2O of

PEEP first

• If FIO2 > 0.6, consider reducing as soon as

patient’s condition permits to avoid

complications


Titration of Oxygen Level

– If the patient’s oxygenation status is unknown or critical, always start ventilatory support with an FIO2 of 1.0

– General goal – maintain PaO2 between 60 and 80 mmHg or SpO2 greater than 90%

– Determination of desired PaO2

Desired PaO2 = Desired FIO2 x Actual PaO2

FIO2 (Actual)


– General guideline for reduction of FIO2

• Decrease in increments of 5 to 10%

• Follow each reduction by drawing arterial

blood gases or oximetry; allow at least

fifteen minutes after the change for

equilibration of blood

Management Options – PEEP

Positive End Expiratory Pressure (PEEP)

Maintenance of baseline pressure above atmospheric level

• Minimum PEEP

– Least amount of PEEP necessary to achieve and

maintain a PaO2 of at least 60 mmHg


• Optimal PEEP

– The level of PEEP at which oxygen delivery is

maximized while minimizing hemodynamic side

effects

– Generally only employed on patients requiring

> 10 cm H2O


Method for Determination of Optimal PEEP– Determine baseline values of blood pressure,

mixed venous oxygen level, arteriovenous oxygen content difference, PaO2, static compliance, and cardiac output

– Increase level of PEEP in increments of 2 cmH2O, measuring values at each increment

– When a decline in oxygen delivery is observed, the optimal PEEP has been exceeded

– Return PEEP level to previous increment


General Guidelines for Reduction of PEEP

– Decrease in increments of 2 cm H2O

– Follow each reduction by drawing blood gases or

oximetry; allow at least fifteen minutes after the

change for equilibration of blood

– Reduction of PEEP to zero prior to extubation

may be neither necessary nor advantageous

Management Options – Tidal Volume

Increasing Tidal Volume (VT) may be used for

recruitment of alveoli if hypoventilation

contributes to hypoxemia

Normal Value – 6 to 12 mL/kg IBW

Management Options – Inspiratory Time

Prolongation of inspiratory time to a point

where inspiratory time exceeds expiratory

time

Normal I:E ratio – 1:1.5 to 1:2

Management Options – Inspiratory Time

Principle of Use

– Increase in inspiratory time (TI) causes increase

in

– Increase in aids in maintaining integrity of

alveoli and recruiting atelectatic alveoli

– Associated with improvement in

– Associated with improvement of PaO2 in patients

with ARDS

Management Options – Bronchial Hygiene

• Postural drainage

• Percussion

• Adequate humidification

• Ambulation, sitting up, turning patient

Management Options – Patient Positioning

• Ambulation, sitting up helpful in improving

oxygenation

• Turning patient from side to side aids in

bronchial hygiene

Management Options – Patient Positioning

Prone Positioning

– May result in dramatic improvement in

oxygenation in patients with ARDS and ALI

– Care must be taken to ensure tubes and lines are

not displaced during turning

– May improve and reduce shunting by

removing pressure of the heart on the dorsal

regions

Evaluation of Ventilation – Physical Findings

Breathing Patterns

– Apnea

– Tachypnea

– Bradypnea

– Abnormal breathing patterns

Work of Breathing

– Use of accessory muscles

– Retractions

Evaluation of Ventilation – Physical Findings

Heart Rhythms

– Abnormal rhythms

– Tachycardia

– Bradycardia

Chest excursion

Altered Mental State

– Anxiety

– Confusion

– Combativeness

– Somnolence

Evaluation of Ventilation – Diagnostic Findings

Arterial Blood Gases

– Increased PaCO2

– Decreased pH

– Decreased PaCO2

Bedside Spirometry Results

– Negative inspiratory force (NIF) – < -20 cmH2O

– Spontaneous tidal volume – < 5 mL/kg IBW

– Vital capacity – < 10 mL/kg IBW

Evaluation of Ventilation – Determine Cause of Problem

Hypoventilation

– Inadequate alveolar ventilation –

A = (VT – VDS) (f)

– Increase in physiologic dead space –

VD/VT = (PaCO2 – PECO2)/PaCO2


Increase in Carbon Dioxide Production

– Stress

– Shivering

– Pain

– Asynchrony with ventilator

– High carbohydrate diet


Change in Lung and Chest Mechanics– Compliance – C = ∆V/∆P

• ∆V = VT Corrected for Tubing Compliance

• ∆P = Pplat – PEEP

Causes of decreased lung compliance– Atelectasis– Pulmonary edema– ALI/ARDS– Pneumothorax– Fibrosis


Causes of decreased thoracic compliance

–Obesity

–Pleural effusion

–Ascites

–Chest wall deformity

–Pregnancy


Cause of increased lung compliance

• COPD


Causes of increased thoracic compliance

–Flail chest

–Loss of chest wall integrity

–Change in patient position


Change in Lung and Chest Mechanics

– Airway Resistance – RAW = ∆P/∆

• ∆P = (Ppeak – Pplat)

• ∆ = flow


Causes of increased resistance

– Bronchospasm

– Mucosal edema

– Secretions

– Excessively high rate of gas flow

– Small endotracheal tube

– Obstruction of endotracheal tube

– Obstruction of the airway


Causes of decreased resistance

– Bronchodilator administration

– Decrease in flow of gas

– Administration of bronchial hygiene


• Loss of Muscle Strength/Neurological Input

– Rapid Shallow Breathing Index (RSBI)

• Indication of whether patients have the

ability to breathe without ventilatory

support


Loss of Muscle Strength/Neurological Input

– Rapid Shallow Breathing Index (RSBI)

• f/VT

– If < 100 breaths/min/L, patient has ability to breathe without ventilator

– If > 100 breaths/min/L, patient will likely not be able to sustain spontaneous breathing

– Maximal inspiratory pressure

– Maximum voluntary ventilation

Evaluation of Ventilation – Management Options

Increase Alveolar Ventilation

– Increase in Mechanical Tidal Volume

• Normal Volume – 6 to 12 mL/kg IBW

• Most direct way to change alveolar ventilation

• Should normally not exceed 12 to 15 mL/kg IBW

• Associated with increase in peak inspiratory pressure

which has increased risk of trauma to lung


– Increase in spontaneous ventilation

• More advantageous to patient than increasing

mechanical tidal volume

• Augmentation by pressure support mode helps

overcome resistance of ventilator circuit and

artificial airway


Increase Alveolar Ventilation

– Increase in Mechanical Rate

• Normal Value – 12 to 18 Breaths per Minute

• Should Normally not Exceed 20 Breaths per Minute

• Prediction of Desired Rate

New rate =


Decrease Carbon Dioxide Output (Production)

– Medicate patient to relieve pain, stress, and prevent

asynchrony, decreasing work of breathing

– Maintain patient’s temperature within normal range

– Provide appropriate nutrition


Treat Underlying Pulmonary Pathophysiology

Maintain airway in patent state

– Prevent accumulation of secretions in airway

– Use properly sized artificial airway

– Prevent occlusion of airway by patient; use

bite block

Considerations in Management – Permissive Hypercapnea

Allowing PaCO2 level to remain elevated above

45 mmHg

• Purpose

– Maintain plateau pressure at an acceptable level (<

30 cm H2O) by decreasing tidal volume to less than

6 mL/kg and increasing respiratory rate, thereby

minimizing trauma and cardiovascular side effects


Method

– Decrease tidal volume and increase respiratory rate, while maintaining minute volume

– If PaCO2 increases and pH decreases, either permit normal metabolic compensation or administer medications to maintain level at 7.25 to 7.35

– Institute gradually to allow PaCO2 to increase gradually over hours or days


Relative Contraindications or Cautions

– Presence of cardiac ischemia– Presence of pulmonary hypertension– Compromised left ventricular function– Right heart failure– Head trauma– Intracranial disease– Metabolic acidosis


Absolute Contraindication

– Intracranial lesions

Considerations in Management – Creation of Intrinsic PEEP

Intrinsic PEEP

– Alveolar pressure above the applied PEEP at the

end of exhalation


Contributing factors• Pressure support ventilation

• Airway obstruction

• Rapid respiratory rate

• Insufficient flow rate

• Relatively equal I:E ratio

• High minute volume

• History of air trapping


Problems associated with intrinsic PEEP

– Increase in work of breathing – patient must

overcome PEEP in order to trigger breaths

– Underestimation of mean airway pressure

– Increase in hemodynamic side effects

– Increase in volutrauma


Determination of Intrinsic PEEP

– Esophageal balloon

– End-expiratory hold by ventilator


Correction or Reduction of Intrinsic PEEP

– Improve ventilation and reduce air trapping

by use of bronchodilators

– Prolong expiratory time by increasing flow or

reducing tidal volume or frequency

Considerations in Management – Inverse Ratio Ventilation (IRV)

IRV - Mode of ventilation in which the

inspiratory time is longer than the expiratory

time

Purpose

– Treatment of patients with refractory

hypoxemia not responsive to conventional

modes of mechanical ventilation


Physiology

– Overcome non-compliant lung tissue

– Recruitment of collapsed alveoli

– Increase in time for diffusion of oxygen across

the alveolar-capillary membrane

– Increase in mean airway pressure


Method

– Decrease inspiratory flow

– Increase in inflation hold time

– In APRV mode, can be created when

pressure release rate is less than 20/minute


Because of the increase in mean airway pressure,

there is an increased potential for hemodynamic

side effects; these are usually limited during acute

administration because the pressure is not

communicated to the cardiovascular system

Considerations in Management – Extracorporeal Membrane Oxygenation (ECMO)

Modified form of cardiopulmonary bypass

used to provide relatively long-term support

for the function of oxygenation of the tissue

using an extracorporeal machine capable of

gas exchange


Purpose

– Intrinsic recovery of the lungs

– Support gas exchange

– Provide adequate tissue perfusion

– Support cardiac function


Indications

– Failure of advanced ventilator strategies

– Oxygen Index (OI) greater than 40 –

OI = (Mean Airway Pressure x FIO2 x100)/PaO2

– Acute deterioration


Technique

– A cannula is inserted into the right atrium via the right jugular vein

– Blood is withdrawn through the cannula

– The blood passes through a membrane oxygenator where oxygen and carbon dioxide are exchanged

– The blood is then warmed and reinfused into the right common carotid artery

Considerations in Management – High Frequency Ventilation (HFV)

High Frequency Positive Pressure Ventilation (HFPPV)

– Mode of ventilation in which a conventional ventilator delivers a rapid rate at a low tidal volume

Technique:

• Respiratory rate is set at minimum of 60 breaths per minute

• Tidal volume is set at less than 5 mL/kg IBW


High Frequency Jet Ventilation (HFJV)

– Mode of ventilation in which a pulse of high velocity blended gas is introduced through a side port of the endotracheal tube

– Conventional ventilator provides PEEP and intermittent breaths

– Rate of jet pulses set between 60 and 600 breaths per minute

– Inspiratory time of jet is 20 to 40 milliseconds


High Frequency Oscillatory Ventilation (HFOV)

– Mode of ventilation in which 180 to 3000 pulses per minute are delivered to the airway

Technique

• Ventilator frequency is set usually between 5 and 6 Hz; the lower the hertz (Frequency), the higher the tidal volume

• Flow is continuous at 15 to 20 Lpm

• Inspiratory time is set at 33%


High Frequency Oscillatory Ventilation

• Lung volume is determined by observing chest “wiggle” (visible vibration from shoulder to mid-thigh area)

• Mean airway pressure should start at 5 cm H2O above the mean airway pressure observed during conventional ventilation

• Chest X-ray should be done within four hours of initiation of HFOV to evaluate lung volume

• No breaths are delivered at conventional volumes


Comparison of High Frequency Techniques

HFPPV HFJV HFOV

Expiration Passive Passive Active

Pressure Waveform

Variable Triangular Sine

Tidal Volume

> Dead Space Ventilation

< Dead Space Ventilation

< Dead Space Ventilation

Frequency 60 – 150/min 60 – 600/min 180 – 3000/min


Advantages of HFV

– Lung protection – limits overdistention of alveoli by means of smaller volumes and lower peak inspiratory pressures; decrease in barotrauma

– Decrease in complications including compromised cardiac output and increased intracranial pressure

– Increases mean airway pressure; improves alveolar recruitment with PEEP, both set and intrinsic

– Improved gas exchange; improvement in ventilation/perfusion matching from rapid flow pattern


Contraindications and Hazards– No absolute contraindications– Relative contraindication or caution

• Chronic obstructive lung disease• Non-homogenous

Hazards• Air trapping• Inadequate humidification• Tracheal injury from high flow velocity• Inadequate monitoring• lung disease

Hemodynamic Monitoring – Arterial Blood Pressure Monitoring

Assessment of overall cardiovascular tone and dependability of oxygen delivery

Normal Value

– Systolic – 100 to 140 mmHg

– Diastolic – 60 to 95 mmHg; many cardiologists are now stating that the diastolic should be maintained no higher than 80 mmHg

Hemodynamic Monitoring – Catheterization

Arterial Catheter– Site of Insertion

• Radial artery (preferred)• Brachial• Femoral • Dorsalis pedis

– Site of Placement • In systemic artery in proximity of insertion site

– Purpose• Measurement of systemic arterial pressure• Source of sample for arterial blood gases


Central Venous Catheter

– Site of insertion

• Subclavian

• Internal jugular vein

– Site of placement

• Superior vena cava or in or near right atrium

– Purpose

• Measurement of central venous pressure

• Administration of fluid and/or medication


Pulmonary Artery Catheter (Swan-Ganz or Flow-Directed Catheter)– Site of insertion

• Subclavian • Internal jugular vein

– Site of Placement • Branch of pulmonary artery

– Purpose• Measurement of CVP, PAP, and PCWP• Collection of mixed venous blood gas samples• Monitoring of mixed venous oxygen saturation• Measurement of cardiac output• Provision of cardiac pacing

Hemodynamic Monitoring – Values Monitored

Value Normal Range Abnormal Value

Arterial Blood Pressure

90-140/60-90 mmHg

> 140/90 – Hypertension< 90/60 - Hypotension

MAP– Mean Arterial Blood Pressure 80 – 100 mmHg > 100 mmHg – Hypertension

< 80 mmHg - Hypotension

ECG – Electrocardiogram

Normal Heart Rate and Rhythm

PR interval > 0.2 sec., Tachycardia, Bradycardia, First-, Second- , and Third-Degree Heart Block, Premature Ventricular Contractions, Atrial Fibrillation, Atrial Flutter, Elevated S-T Segment, Inverted T Wave, Ventricular Tachycardia, Ventricular Fibrillation, Asystole


ValueNormal Range

Abnormal Value

CVP – Central Venous

Pressure2 – 6 mmHg

> 6 mmHg: Fluid Overload, Right Ventricular Failure, Pulmonary Hypertension, Valvular Stenosis, Pulmonary Embolism, Cardiac Tamponade, Pneumothorax, Positive Pressure Ventilation, PEEP, Left Ventricular Failure< 2 mmHg: Hypovolemia, Blood Loss, Shock, Peripheral Vasodilation, Cardiovascular Collapse

PAP – Pulmonary

Artery Pressure

20-35/5-15 mmHg

> 35/15 mmHg: Pulmonary Hypertension, Left Ventricular Failure, Fluid Overload< 20/5 mmHg: Pulmonary Hypotension, Hypovolemia, Cardiovascular Collapse


ValueNormal Range

Abnormal Value

– Mean Arterial

Pressure10 – 20 mmHg > 20 mmHg: Same as ↑ PAP

< 10 mmHg: Same as ↓ PAP

PCWP – Pulmonary Capillary Wedge Pressure

5 – 10 mmHg(< 18 mmHg)

> 18 mmHg: Left Ventricular Failure, Fluid Overload> 20 mmHg: Interstitial Edema> 25 mmHg: Alveolar Filling> 30 mmHg: Frank Pulmonary Edema



CO – Cardiac Output

4 – 8 L/min > 8 L/min: Elevated< 4 L/min: Decreased

CI – Cardiac Index 2.5 – 4 L/min/m2

> 4 L/min/m2: Elevated due to Stress, Sepsis, Shock, Fever, Hypervolemia, or Medications< 2.5 L/min/m2: Decreased due to Left Ventricular Failure, Myocardial Infarction, Pulmonary Embolus, High Levels of PPV, PEEP, Blood Loss, Pneumothorax, Hypovolemia



SVR – Systemic

Vascular Resistance

900 – 1400 Dynes-Sec/cm5

(11.25 – 17.5 mmHg/L/min

> 1400 Dynes-sec/cm5: Increased due to Vasoconstrictors, Late Septic Shock, Hypovolemia< 900 Dynes-sec/cm5: Decreased due to Vasodilators, Early Septic Shock

PVR – Pulmonary Vascular Resistance

110 – 250 Dynes-sec/cm5

1.38 – 3.13 mmHg/L/min

> 250 Dynes-sec/cm5: ↓pH, ↑PCO2, Vasopressors, Emboli, Hypoxemia, Emphysema, Interstitial Fibrosis, Pneumo- thorax< 110 Dynes-sec/cm5: Pulmonary Vasodilators, Nitric Oxide, Oxygen, Calcium Blockers

The End

Considerations in Management – Open Lung Ventilation

• Purpose - optimize lung mechanics and

minimize phasic damage by placing PEEP

above Pflex

• Pflex is the point on the pressure-volume

curve below which the alveoli begin to

collapse during exhalation


• Rationale

– Reinflation of atelectatic alveoli on a breath-by-

breath basis increases lung injury

– Determination of the Pflex on the pressure-volume

curve signifies the pressure at which alveolar

collapse occurs

– PEEP is applied just above the Pflex level


• Rationale

– This is a higher than conventional level of PEEP

allowing use of a lower tidal volume

– Respiratory rate is increased incrementally to

maintain an acceptable PaCO2, at times as high

as 35 breaths per minute

Documents

Monitoring and Management of Ventilatory Support