Mechanical Ventilation Learning Package, Exams of Biomechanics

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Sharon-Ann Shunker, CNC, Liverpool ICU

SWSLHD

Mechanical Ventilation Learning

Package

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 Basic Airway Management  Management of the Obstructed Airway

• 1. Respiratory Anatomy & Physiology Page Contents List
• 2. Pulmonary Ventilation: Pleural pressure Page
• 3. Pulmonary Circulation Page
• 4. Relationship between Ventilation and Perfusion Page
• 5. Lung Volumes & Capacities Page
• 6. Dead Space Ventilation Page
• 7. Lung Mechanics: Compliance & Resistance Page
• 8. Oxygenation Page
• 9. Arterial Blood Gases Page
• 10. Airway Management Page
• 11. Oxygen Therapy Page  Use of Guedel & Nasopharyngeal Airways
• 12. Tracheal Intubation Page
• 13. Mechanical Ventilation Page
  •  Non Invasive Ventilation – CPAP & BiPAP Page
  •  Invasive Ventilation Principles Page
  •  Modes of Ventilation Page
  •  Ventilation Parameters Page
  •  Alarm Settings Page
  •  Ventilation Emergency Drill Page
  •  Troubleshooting Alarms Page
  •  Humidification Page
  •  Weaning from Mechanical Ventilation Page
  •  Nursing Care of the Mechanically Ventilated Patient Page
• 14. Legend for Sedation Score Page
• 15. Legend for Pain Score Page
• 16. Learning Activities Page
• 17. Reference List Page

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Functions of the respiratory system The major function of the respiratory system is to supply oxygen and eliminate carbon dioxide from the body. In addition to the vital function of gas exchange, the respiratory system fulfils the following functions^13

 Acid base regulation – Through the process of ventilation, the lung removes CO 2 and regulates the pH of the body. Regulation of pH is accomplished by removing volatile acid (ie acid converted into the gaseous state; in this case, carbonic acid converted to CO 2 ).

 Blood reservoir – The lung receives the venous blood from the right ventricle. Due to the capacity of the pulmonary circulation to receive blood, the lung acts as a reservoir from which the left side of the heart draws blood.

 Filtering mechanism – The lung also constantly filters the air we breathe and removes trapped particles through the mucocillary clearance mechanism and the lymphatic system. The lung also acts as a filtering mechanism for blood by removing particles such gas bubbles, small fibrin or blood clots, fat cells, aggregates of platelets or WBC, and other pieces of cellular debris.

 Metabolism – The lung produces some very important chemicals that serve physiological regulatory functions such as vascular dilatation, blood clotting, lung structural stability and neurotransmitters. Some chemicals passing through the lungs are converted into their more active form, such as angiotensin I, produced by the kidneys, which is converted to angiotensin II, a potent vasoconstrictor

Control of respiration7,

Breathing is usually involuntary but voluntary breathing is necessary when the person is doing other activities such as walking, talking, singing, etc. In these cases homeostatic changes in ventilatory rate and volume are adjusted automatically by the nervous system to maintain normal gas exchange.

The lung is innervated by the autonomic nervous system (ANS). Fibres of the sympathetic division in the lung branch from the upper thoracic and cervical ganglia of the spinal cord, while fibres of the parasympathetic division travel in the vagus nerve, which is important in the regulation of ventilation. The respiratory centers in the brain stem control involuntary ventilation by transmitting impulses to the respiratory muscles causing them to contract or relax.

The pneumotaxic center in the upper pons functions to maintain rhythmic respirations. It stimulates the expiratory center, which then sends inhibitory signals to the inspiratory center. Inspiration ends and expiration begins. Strong stimuli from the pneumotaxic center result in shorter inspiration, and mild stimuli results in a longer one. The apneustic center sends stimuli to the inspiratory center and prolongs inspiration. The pneumotaxic center usually overrides the apneustic center. Impulses are transmitted from lung receptors, which are receptors that respond to physical changes in the pulmonary system, and chemoreceptors, which are receptors that respond to changes in oxygen or carbon dioxide concentrations, through the sympathetic and parasympathetic divisions of the ANS and the respiratory centers in the brain stem.^25

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2. PULMONARY VENTILATION: PLEURAL PRESSURES

The lungs and chest wall are separated by the parietal and visceral pleura. Between the parietal and visceral pleura is the interpleural space. The pressure within the interpleural space is usually negative due to the natural tendency of the lungs to collapse and the chest wall to expand. It is this negative interpleural pressure that keeps the alveoli open and through the interaction of the lungs and chest wall interpleural pressure is altered, enabling the movement of gas into and out of the lungs (ventilation). In the intact chest, the lungs move as the chest wall and diaphragm moves because of the maintenance of a pressure in the interpleural space that is negative with respect to the alveolar pressure. As the thoracic dimensions increase, pleural pressure is reduced which causes the lungs to increase in volume (inspiration). As the thoracic dimensions decrease, pleural pressure and alveolar pressure is increased, causing gas to flow out of the lungs (expiration).45,

Interpleural pressure (quiet breathing with normal lungs)

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(Source: pulmonary circulation, web.cateret.edu)

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4. RELATIONSHIP BETWEEN VENTILATION AND PERFUSION

Gas exchange is the key function of the lungs. It is affected by the anatomy of the capillaries and alveoli. Due to a number of physiological factors, ventilation (V) to perfusion (Q) ratio is not matched in a 1:1 relationship. Normal alveolar ventilation is about 4L/min and pulmonary capillary perfusion is about 5L/min, hence normal ventilation to perfusion ratio (V/Q) is 0.8. Perfusion to the pulmonary circulation, like ventilation, is not evenly distributed and is dependent on hydrostatic pressures.

In the upright position the lung apices receive less perfusion compared with the bases.

In the supine position apical and basal perfusion is almost equivalent, but the posterior portion of the lung receives more perfusion than the anterior lung.

Throughout the lung the bases receive more ventilation per unit volume than the apices.

Blood flow in the pulmonary capillary network (perfusion) is affected by pressure within the surrounding alveoli. The pressure gradient between the arterial and venous end of the pulmonary circulation effects blood flow, but as alveolar pressure can be greater than venous or arterial pressure, this affects blood flow and gas exchange.

In the upright posture, the three zones are:

Zone 1: (upper area of lungs) Alveolar air pressure greater than either pulmonary arterial and venous pressures, so blood flow is reduced and there is alveolar deadspace. This is more evident in the patient on positive pressure ventilation.

Zone 2: (middle area of lungs) Alveolar air pressure less than pulmonary arterial pressure but greater than pulmonary venous pressure, there is a normal V/Q ratio.

Zone 3: Alveolar air pressure is less than both pulmonary arterial and venous pressures, so ventilation is reduced, leading to shunting. Alveoli are perfused but not adequately ventilated.

Optimal ventilation and perfusion happens in both zone 2 & 3.^10

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5. LUNG VOLUMES AND CAPACITIES

Respiratory volumes and capacities

Source: Marieb 1992, pages 742–

As noted above, interpleural pressures result from the relationship between forces generated by the chest wall and lung. This relationship also determines the resting volume of the lungs (at end of normal expiration). This volume is called the functional residual capacity (FRC). This is the point where chest wall forces and lung forces are in balance. The following concepts are very important to appreciate.

IRV

3100

TV

500

ERV

1200

RV

1200

IC

3600

FRC

2400

TLC

5800 Closing Volume

Airway ClosureBegins

Closing Capacity

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Inspiration and expiration

50

Inspiration and expiration refer to changes in lung volume. Change in lung volume requires the generation of a pressure difference. The pressure difference (for spontaneous breathing) is generated by the respiratory muscles. The pressure change required to produce a given change in lung volume (compliance) varies depending upon how full the lungs are. Recording the volume change for particular pressure change produces what is called the lung pressure–volume curve (or the static pressure – volume relationship). This relationship is sigmoidal; that is, the pressure required to produce volume change at low and high lung volumes is much greater than that needed to produce volume change in the middle section. This middle section corresponds to normal tidal breathing in the healthy lung.

Pressure / Volume Curve

Where tidal breathing occurs in a lung already approaching total lung capacity (eg very small vital capacity, or as a result of hyperinflation) the pressure (negative pressure) that the respiratory muscles must generate will be much higher than that required for normal tidal breathing at normal FRC. Where tidal breathing occurs in a lung with reduced FRC (near residual volume) the same consideration applies (eg obesity/abdominal distension, atelectasis). This means that at these two extremes (TLC/FRC) the work of breathing will be increased.

Reduction in lung volume^50

Reduction in lung volume below a certain level results in airway closure (small airways such as respiratory bronchioles). The lung volume at which this occurs is known as the closing capacity (CC). In older people and those with chronic lung disease, some of the lungs’ elastic recoil is lost, with a resulting decrease in intrapleural pressure. Thus the volume at which airway closure occurs is higher (closer to FRC).

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7. LUNG MECHANICS: COMPLIANCE AND RESISTANCE

The mechanical characteristics of the lung greatly influence both normal lung function and pulmonary

disability. The two major factors involved in lung mechanics are compliance and resistance, as

outlined below.^50

Compliance

Normally inspiration is an active process, accomplished through the expansion of the lungs and the

thorax. The ease with which the lungs and thorax can be expanded, or distended, is referred to as

compliance. Total compliance therefore depends not only on the elasticity of the lung tissue, but also

on that of the thoracic cage.

Compliance determines the change in volume for a given change in pressure. For example, if a

patient is able to sustain a large increase in tidal volume with a small fall in pleural pressure then their

lungs are compliant. If a patient requires a large fall in pleural pressure for a relatively small increase

in tidal volume then their lung tissue is non-compliant.

Compliance is reduced by any factor that:

Reduces the natural elasticity of the lungs, eg fibrosis, or interstitial oedema.

Reduces the total number of functional alveoli, eg atelectasis or airway obstruction.

Increases the stiffness of the chest wall, eg splinting because of pain.

Decreases the stiffness of the chest wall, eg post-sternotomy, resulting in decreased FRC.

Checks the ability of the thorax to increase in volume, eg abdominal distension.

Compliance is therefore a relationship between volume and pressure and can be estimated by

dividing the change in volume by the change in pressure as follows:

Compliance = change in volume change in pressure

For example, your patient is receiving the following ventilator parameters:

PEEP – 10 cm H 2 O

Tidal volume – 1000 mL

End inspiratory hold or plateau pressure – 35 cm H 2 O

In this case, the change in volume is 1000 mL and the change in pressure is 25 cm H 2 O. The change in

pressure is determined by subtracting the level of PEEP (10 cm) from the end inspiratory hold pressure (

cm). Remember, we are interested in the change in pressure and in this case the pressure is rising from a

baseline of 10 cm to a total pressure of 35 cm of water, the resultant change in pressure is therefore 25 cm.

The total lung compliance (lung and chest wall) for this patient is:

1000 35-

= 1000 = 40mL /cmH 2 O 25

You will note that the estimated value for compliance is stated in mL/cm H 2 O. In the above example,

this means that for a 1 cm increase in pressure the patient would experience a 40 mL rise in volume.

The normal value for adult compliance is a combination of lung and thoracic wall compliance and is

70–100 mL/cm H 2 O.^50

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Clinically, there are two types of compliance measurements that can be determined These are

dynamic compliance and static compliance.

Dynamic compliance is calculated by the following formula:

Dynamic compliance = Tidal volume

Peak inspiratory pressure - PEEP

Static compliance is calculated by the following formula:

Static compliance = Tidal volume

Plateau pressure - PEEP

To obtain the static compliance, an inspiratory pause must be initiated. This pause will result in a

period of no gas flow and allow the pressure in the alveoli to equilibrate with the ventilator circuit

pressure. The measurement of static compliance may be useful in eliminating the following variables

that may influence compliance readings: resistance to flow, distribution of gases and recruitment time

of closed lung units.

Compliance alters during phases of a maximal inspiration. At lung volumes near RV and TLC, the

lung tissue is less compliant (ie not as distensible). This results in an ‘S’ shaped curve (see following

figure). Conceptually, this is similar to blowing up a balloon. It is more difficult to inflate a balloon at

the beginning of inflation. Once the balloon starts to inflate, less pressure (or work) is required to

inflate the balloon. As the balloon reaches its total capacity and draws near to bursting, a greater

pressure is required to achieve a unit volume increase. Thus the lung, like a balloon, requires greater

pressures at the beginning (near functional residual capacity) and end of inspiration (near total lung

capacity) for relatively small increments in tidal volume; this is a state of decreased lung compliance.

In the middle of inspiration, little pressure is required for increases in volume – ie the lungs are more

compliant.

High Resistance

Low Compliance

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Resistance^50

Resistance refers to impedance to flow. For gas to flow, a pressure difference must exist between the two ends of a tube. The relationship between the driving pressure and the resultant flow is termed the resistance. Airway resistance is the pressure difference between the alveoli and mouth divided by flow rate.

Resistance to flow may be inspiratory or expiratory. Factors that may increase both inspiratory and expiratory resistance include:

 Bronchial tone.  Sputum.  Oedema.  External breathing circuits (eg ETT / tracheostomy tube and other circuit components).

Airflow obstruction can lead to gas trapping, which results in dynamic hyperinflation (auto PEEP, intrinsic PEEP, inadvertent PEEP). The possible effects of auto PEEP are:

 Tidal volume may cycle close to total lung capacity (TLC), ie reduced lung compliance (increased risk of barotrauma).  Increased effort required for ventilator triggering or initiation of gas flow.  Increased work of breathing.  Decreased preload and cardiac output.

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8. OXYGENATION

Tissue oxygenation depends on oxygen delivery and consumption. Three processes involved in oxygenation are:^17

 Intake of Oxygen (Pulmonary Gas Exchange or Pulmonary Ventilation).  Delivery of oxygen to the cells (Arterial Oxygenation) – DO 2  Oxygen consumption -use of oxygen by the cells for metabolism (Cellular Oxygenation) – VO 2.

The components of oxygenation (Source: Kidd & Wagner, 1997, pg:159)

Pulmonary gas exchange:17, Pulmonary gas exchange involves breathing O 2 in so it can be exchanged at an alveolar level with CO2. The O 2 is then attached to haemoglobin in the pulmonary capillaries.

Pulmonary gas exchange is dependent on three processes:  Ventilation  Diffusion – determined by:  Surface Area  Thickness  Length of exposure  Perfusion- determined by:  Haemoglobin  Affinity of O 2 to haemoglobin  Blood flow /Cardiac output

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The oxyhaemoglobin curve shows the relationship between, percent of haemoglobin saturation

(SaO 2 ) and partial pressure of arterial oxygen (PaO 2 ). A normal oxyhaemoglobin curve assumes

certain parameters. These being a pH of 7.4; temperature of 37oC and PaCO 2 of 40mmHg. At the

arterial end of the curve the slope is gentle; this reflects the alveolar - capillary O 2 transfer site. PaO 2

drops markedly with little change in SaO 2 at this point. At the steeper portion of the curve, venous

disassociation occurs as O 2 leave the haemoglobin and is transferred to the cells. At this site SaO 2

drops dramatically with little change in PaO 2.

Oxygenation at the cellular level depends on the ability of O 2 to bind with and be released from the Hb in the blood. Pa represents the partial pressure at which haemoglobin is 50% saturated

A shift to the left increases the affinity of Hb for O 2 with decreased tissue oxygenation and Pa. Causes of a shift to the left :  Alkalosis  Hypothermia  Decrease 2, 3 DPG - Massive blood transfusion and carbon monoxide poisoning  Hypocapnia

A shift to the right decreases the affinity of Hb for O 2 with increased tissue oxygenation and Pa. Causes of a shift to the right :

 Hyperthermia  Acidosis  Increased 2, 3 DPG - A by product of metabolism, hyperthyroidism and hypoxia  Hypercapnia

Oxyhaemoglobin – dissociation curve (Source:http://en.wikipedia.org/wiki/File:Oxyhaemoglobin_dissociation_curve.png)

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Oxygen Consumption VO 2 – Cellular Oxygenation13, Once oxygen is delivered to the cells it has to be utilised. It is essential for aerobic respiration.

Aerobic metabolism : Oxygen combines with food (Kreb Cycle) to form CO2, H 2 O and ATP.

Anaerobic metabolism : Glucose in the absence of O 2 is broken down to form ATP, pyruvate and lactic acid.

In normal conditions DO 2 is well matched to metabolic requirements. The oxygen consumption (VO 2 ) is about 25% of DO 2 , which results in an extraction ratio of 0.25. This leaves a reserve and when DO 2 decreases the extraction ratio increases allowing the VO 2 to remain constant. When oxygen extraction is maximum, further decrease in DO 2 will result in a fall in VO 2. This is because tissue extraction cannot compensate for decrease in delivery of oxygen. When this oxygen debt occurs, anaerobic metabolism produces lactic acid. If this is not corrected tissue hypoxia will result leading to cell damage and death (Hillman & Bishop, 1996)

The use of supplemental oxygen is necessary to relieve hypoxaemia. This is combined with measures to:

 Reduce oxygen requirements – cooling, mechanical ventilation, sedation, paralysis  Increase DO 2 - correct anaemia, low cardiac output and factors which shift the oxyhaemoglobin curve to the left.

(Source: Hillman & Bishop, 1996)

Oxygen Failure^17 Oxygen failure is a respiratory crisis in which the primary problem is hypoxemia, PaO 2 ≤ 60mmHg.

Hypoxemia (PaO 2 ) is defined as inadequate oxygen in arterial blood. Hypoxia i s defined as decreased oxygen supply to the cells or tissues.

PaO 2 , SaO 2 & SvO 2 are used to measure adequate oxygenation of the body. PaO 2 & SaO 2 can be measured by arterial blood gas, SvO 2 is mixed venous oxygen measured from a venous sample – true