Clinical Science Session

MECHANICAL VENTILATION

Oleh :

Mala Azitha 1310311088

Mira Mustika 1210312008

Rinaldi Syahputra 1010313100

Preseptor :

dr. Liliriawati Ananta Kahar, SpAn, KIC

BAGIAN ANESETESIOLOGI DAN TERAPI INTENSIF

FAKULTAS KEDOKTERAN UNIVERSITAS ANDALAS

RSUP Dr. M. DJAMIL

PADANG

2017
 CHAPTER I

INTRODUCTION

1.1 BACKGROUND

Mechanical ventilation is an attempt to help or replace a persons spontaneous

breathing.Providing management in patients with mechanical ventilation among the critical

care unit, general surgical medicine, even at home. This mechanical ventilation can be

channeled through a ventilator, or assisted by an assistant by compressing a bag or set of

bellows. Mechanical ventilation is a life-saving technology, but when used improperly, this

technology can increase morbidity and mortality rates. For that, a good understanding of

mechanical ventilation is required.

This paper will discuss the definition, classification, indication, setting, mode,

objective, and complication of mechanical ventilation.

 CHAPTER 2

DISCUSSION

2.1 Definition

Mechanical ventilation is a life support treatment1,8. Mechanical ventilator is a

machine that helps people breathe when they are not able to breathe enough on their own1,9.

Mechanical ventilation process gases moved into the lungs by means of a mechanical device.

With continuous mechanical ventilation a patient is intubated or receives a tracheostomy and

receives variable degrees of assistance to meet respiratory requirements in an uninterrupted

fashion.2,8,9

The mechanical ventilator is also called a ventilator, respirator, or breathing machine.

Most patients who need support from a ventilator because of a severe illness. And most of

them are cared for in a hospitals intensive care unit (ICU).1

2.2 Aim of mechanical ventilation

To get oxygen into the lungs and body

To help the body get rid of carbon dioxide through the lungs

To ease the work of breathingSome people can breath on their own, but it is very

hard. They feel short of breath and uncomfortable.

To breathe for a person who is not breathing because of injury to the nervous system,

like the brain or spinal cord, or who has very weak muscles.

2.3 Physiologic of mechanical ventilation

To support or manipulate pulmonary gas exchange

 The objective applications of mechanical ventilator is to normalize alveolar

ventilation. In certain specific clinical circumtances, the application is to achieve an

alveolar ventilation greater than normal. Besides, using of mechanical ventilation is to

achieve and maintain a level of arterial blood oxygenation. In ventilatory system its

means an SaO2 >90%.3

To increase lung volume

To achieve sufficient lung expansion in order to prevent atelectasis.3

To reduce or manipulate the work of breathing

Teh reduce teh patients work of breathing when it is increased by elevated airmay

resistance or reduce compliance and the patients spontaneouss efforts are oneffective

or incapable of being sustained. In this situations, ventilatory support will be use until

the specifics therapies reverse the condition.3

To prevent hypoxemia

To increase PaO2 trough increasing alveolar ventilation, increaseing lung volume,

decreasing O2 consumption to relieve hypoxia.3

To prevent acute respiratoty acidosis

Mechanical ventilation is to corret an immediately acidemia, rather than necessarily to

achieve a normal arterial PaO2.3

To relieve respiratory distress

To relieve intolerable patient discomfort while the primary disease process reverses

or improves.3

2.4 Indication

The objectives of the MV are the maintenance of exchange gas, correction of

hypoxemia and acidosis respiratory associated with hypercapnia, work relief respiratory

muscles, reverse or avoid fatigue of the respiratory muscles, reduce the consumption of
oxygen and allow the application of specific therapies. The main indications for starting

support ventilatory are: resuscitation due to cardiac arrest, hypoventilation and apnea,

respiratory failure and hypoxemia due to intrinsic pulmonary disease, mechanical failure of

the respiratory system, prevention of respiratory complications, reduced respiratory muscle

work and muscle fatigue. The table 1shows the parameters that can indicate the need for

ventilation support.5

Normal and abnormal parameters that may indicate the need for ventilatory support

and the laboratory criteria for MV and the initial settings are shown in Table 1.6
2.5 Mechanical ventilator principles

a. Ventilator settings

Volume

In volume-targeted ventilation, a machine-delivered Vt is set to be consistent with

adequate gas exchange and patient comfort.3 In adult normally Vt varies between 5-15

ml/kg of body wieght. When selecting volume, thorax compliance, ventilation, and

barotrauma should be considered.3

Respiratory rate

Set mandatory rate of adult normally varies between 4 and 20/min. Gas delivery rate

depend on the mode of ventilation selected, the delivered Vt, dead space to tidal

volume ratio, metabolic rate, targeted PaCO2 level and the level of spontaneous

ventilation.3

Flow rate

The selection of flow rate is primarily determined by the level of spontaneous

inspiratory effort. Peak of inspiratory flows ahould ideally match patient peak

inspiratory demands. This normally to be set at 40 to 100L/min.3

Inspiratory time / I:E ratio

Spesific Ti and I:E ratio is generally based on hemodynamic response to ventilation,

oxygenation status and level of spontaneous breathing. In spontaneous breathing gas

delivery should be coordinated with patient inspiratoty effort to ensure synchrony

which is requires about 0.8 to 1.2 and I:E about 1:2 to 1:1.5.3
 Flow rate

Selection of flow profile is available onlu in volume-targeted approaches to

ventilation.3

This is often overlooked in volume-targeted modes. This flow rate is particularly

important for patient comfort as it affects respiratory work, dynamic hyperinflation,

and auto-PEEP. In most ventilators, the flow rate is regulated directly. In other

ventilators, eg Siemen 900cc, the flow rate is determined indirectly from the

respiratory rate and I: E ratio.4,6

Example:

Respiratory rate = 10

Respiratory cycle time= 6s

I:E ratio = 1:2

Inspiration time = 2s

Expiration time = 4s

Tidal volume = 500 ml

Flow rate = volume/inspirasi time

= 500 ml per 2 s

Sensitivity

Ventilator-trigger sensitivity should be set at the most sensistive level that prevent

self-cycling because mechanical ventilators and astificial airways impose a resistive

load on spontaeously beathing ventilator-assisted patient.3

 FIO2

Regarding the effect of highh FiO2s on lung ijunry, the selection of FiO2 should

depend on the target PaO2, PEEP level, MAP and hemodynamic status. So the lowest

acceptable FiO2 should be selected.3 In most cases, FiO2 should be 100% when the

patient is intubated and connected to the ventilator for the first time. When placement

of the endotracheal tube has been established and the patient stabilized, FiO2 should

be lowered to the lowest concentration that can still sustain oxygen saturation of

hemoglobin, because high oxygen concentrations can cause pulmonary toxicity. The

main purpose of ventilation is to maintain the saturation value on 90% or more.

Sometimes the value may change, for example in conditions requiring a protection

against the lungs from tidal volume, pressure, and oxygen concentration that too

large. In this situation, the oxygen saturation target can be lowered to 85% when the

factors contributing to oxygen delivery are being optimized.4

PEEP (positive end-expiratory pressure)

PEEP is applied to recruit lung volume, elevate MAP, and improve oxygenation.

PEEP also decrease venous return and preload of LV. The optimal level of PEEP

depends on the desired physiologic response.3 As the name implies, PEEP serves to

maintain the positive pressure in airway at some level during the expiratory phase.

PEEP is distinguished from continuous positive airway pressure (CPAP) based on

when used. PEEP is only used in the expiratory phase, while CPAP takes place during

the whole respiration cycle.4

The use of PEEP during mechanical ventilation has potential benefits. In acute

hypoxemia respiratory failure, PEEP increases the average alveolar pressure,

 increases the area of atelectasis reexpansion, and can expel fluid from the alveolar

space to the interstitial thus allowing alveoli previously covered or submerged by

fluid, to participate in gas exchange. In cardiopulmonary edema, PEEP can reduce left

ventricular preload and afterload, thus improving cardiac performance.4

In hypercapneal respiratory failure caused by airway obstruction, patients often

experience lack of time for expiration resulting in dynamic hyperinflation. This leads

to the auto-PEEP, ie, the end of alveolar expiratory pressure is higher than

atmospheric pressure. When auto-PEEP is obtained, it is necessary to trigger a

ventilator in the form of a higher airway negative pressure than the triggering

sensitivity or auto-PEEP. If the patient is unable to achieve it, then the inspirational

effort becomes futile and can increase the work of breathing. Using PEEP can

overcome this because it can reduce auto-PEEP from the total negative pressure

required to trigger the ventilator. In general, PEEP is stepped up gradually until the

patient's breathing effort can trigger the ventilator constantly to 85% of predicted

auto-PEEP.4

Tidal Volume

In some cases, tidal volume should be lower especially in acute respiratory distress

syndrome. When adjusting tidal volume in certain modes, the approximate roughly

ranges from 5 to 8 ml / kg of body weight. In patients with normal lungs, but

intubated for some reason, tidal volume is used up to 12 ml / kg of body weight. The

tidal volume must be adjusted to each individual to maintain plateau pressure below

35 cm H2O. Plateau pressure is determined by a breath-holding maneuver during

inspiration called the late alveolar inspiratory pressure in patients who are relaxed.4
 Increased plateau pressure does not always followed by increased risk of barotrauma.

The risk is determined by the transalveolar pressure which is the result of a reduction

between alveolar pressure and pleural pressure. In patients with chest wall edema,

abdominal distension or ascites, chest wall compliance decreases. This causes

increased pleural pressure during lung expansion. Increased transalveolar pressure is

rare occurs in patients who have normal lung compliance.4

b. Pressure measurements

Peak

Peka pressure is the maximun pressure obtainable during active gas delivery. In

vom=lume targeted ventilation, peak pressure is depend on both cmpliance and

airways resistance. With preassure-trageted ventilation, th epeak inspiratory pressure

is approximately equal to the target pressure. However, the initial system pressure mat

axceed the pressure target by about 1 to 3 cm H2O.3

Plateau

Plateau is the end-inspiratory pressure during a period of at least 0.5 s of zero gas

flow. It should be measured on the forst breath after the setting of an inflation hold

and requires passive ventilation.3

Mean

Teh system pressure average over the entire ventilatory period is defines as MAP.

MAP as displayed on monitoring devices almost always underestimates mean alveolar

pressure. So, mean alveolar pressure counted in othe formula.3

 End-Expiratory

This is the airway pressure at the termination of expiratory phase, normally equal to

atmospheric or applied PEEP level.3

2.6 Ventilator modes7

a. Volume-cycled mode

Inhalation proceeds until a set tidal volume (TV) is delivered and is followed by

passive exhalation. A feature of this mode is that gas is delivered with a constant inspiratory

flow pattern, resulting in peak pressures applied to the airways higher than that required for

lung distension (plateau pressure). Since the volume delivered is constant, applied airway

pressures vary with changing pulmonary compliance (plateau pressure) and airway resistance

(peak pressure).

A major disadvantage is that high airway pressures may be generated, potentially

resulting in barotrauma. Close monitoring and use of pressure limits are helpful in avoiding

this problem. Note that ventilators set to volume-cycled mode function well as monitors of

patients' pulmonary compliance, which will be decreased in physiological states such as

worsening ARDS, pneumothorax, right mainstem intubation, chest-wall rigidity, increased

intra-abdominal pressure, and psychomotor agitation ("fighting the vent"). These

pathophysiological states increase peak pressure and should be considered whenever pressure

alarms are sounded.

In pressure-cycled settings, by contrast, such states result only in reduced delivered

volumes and may not trigger alarms. Given that the airway resistance and pulmonary

compliance of the critical emergency department(ED) patient is unknown,the volume-cycled

mode is recommended for initial ventilation of most patients.

b. Pressure-cycled mode
 A set peak inspiratory pressure (PIP) is applied, and the pressure difference between

the ventilator and the lungs results in inflation until the peak pressure is attained and passive

exhalation follows. The delivered volume with each respiration is dependent on the

pulmonary and thoracic compliance.

A theoretical advantage of pressure-cycled modes is a decelerating inspiratory flow

pattern, in which inspiratory flow tapers off as the lung inflates. This usually results in a more

homogeneous gas distribution throughout the lungs. However, no definite evidence exists that

this results in a reduction of the rate of ventilator-induced lung injury or overall mortality.

Nevertheless, pressure-cycled ventilation has achieved considerable popularity in the

intensive care setting for management of patients with ARDS, whose lungs are most likely to

be characterized by a broad range of alveolar dysfunction and are also most vulnerable to the

effects of barotrauma and volutrauma.

A major disadvantage is that dynamic changes in pulmonary mechanics may result in

varying tidal volumes. This necessitates close monitoring of minute ventilation and limits the

usefulness of this mode in many emergency department patients. However, newer ventilators

can provide volume-assured pressure-cycled ventilation, which increase peak pressures as

needed to deliver a preset minimum tidal volume.

c. High-frequency oscillatory support

In this ventilatory strategy, ultra-high respiratory rates (180-900 breaths per minute)

are coupled with tiny tidal volumes (1-4 mL/kg) and high airway pressures (25-30 mm

water). This is a commonly accepted ventilatory setting for premature infants and has now

also been used in small critical care unit studies on patients with ARDS, with reports of

improving oxygenation and lung recruitment.

2.7 Complication

Complication of airway intubation

The artificial airway allows potential pathogens to enter the trache from the external

enviroment, dramatically increasing the risk of nosocomial pneumonia. Moreover,

disruption of the coughing mechanism and mucociliary escalator encourages retention

of airway secretion.3

Tube misplacement and dislocation occur frequently. Although intubation of the right

or (less frequently) left main bronchus most commonly occurs at the time of

intubation, head movement may cause the tube orifice to migrate 2 cm in either

direction from its neutral position along the tube axis. Overdistention of the ventilated

lung and hypoventilation or atelectasis of the nonintubated lung.3

Glottic injury often occurs during unusually difficult or emergency intubation. Glottic

edema and minor erosive lesions of the vocal cords occur commonly during

prolonged intubation. Postextubation glottic dysfunction and lasting damage to the

vocal cords may occur, especially among women and among those patients in whom

large tubes are placed.3

Complication of PPV

-Barotrauma

There is little doubt that high ventilating pressures and excessive regional lung

volumes are damaging. All forms of barotraurna including interstitial and

subcutaneous emphysema, pneumomediastinum, pneumoperitoneuni,

pneunmopericardium. pneumothorax, tension cysts, systemic gas embolism, and

damage similar to bronchopulmonary dysplasia, have now been recognized in adult

patients.3
Strategies that prevent the exposure of the lung to high pressures (limiting

overdistention) and those that lower the VE requirement may be associated with less

ventilator induced tissue injury and improved outcome. Such ap proaches include

permissive hypercapnia, pressure-controlled ventilation and pressure-limited,

volume-cycled ventilation.3

-Oxygen Toxicity

High fractions ofinspired 02 (Flo,) are potentially injurious when applied over

extended periods. Because alveolar injury is an exponential function of inspired

oxygen concen tration (Flo,), even modest reductions in FIo, over the range of 0.6 to

1.0 may attenuate tissue damage.3

-Cardiovascular complication

Ventilatory support can help restore the balance between DO2, and O2 consumption

when it alleviates an intolerable breathing workload. Conversely, PPV often impairs

cardiac output by disturbing the loading conditions of the heart. 3

Mean lung volume or MalvP correlates best with the tendency of a given ventilatory

pattern to cause hemodynamic compromise. Under conditions of passive inflation,

MAP (as a clinically measurable reflection of MalvP) relates fundamentally to oxygen

exchange, cardiovascular perform ance, and fluid retention.3

Therefore, the hemodynamic effect of a given increment in MalvP will be accentuated

when the lungs are relatively compliant and/or the chest wall is stiff. Hemodynamic

consequences are predictably less when the patient makes spontaneous breathing

efforts. For these reasons, dynamic hyperinflation occurring in a passively ventilated

patient with severe airflow obstruction produces auto-PEEP that is particularly likely

to cause hemodynamic compromise. Maximizing 02 delivery may require expansion

 of intravascular volume, an intervention that has been associated with adverse

outcomes in patients with acute lung injury.3

Breathing effort and patient-ventilator asynchrony

The use of mechanical ventilation superimposes a clinician-selected pattern of

ventilation on the patient's natural breathing rhythm. Circuits that impose substantial

resistance and machines that respond poorly to the flow demands or cycling cadence

of the patient may result in dyspnea and an unnecessary breathing workload. Factor

that have been shown to increase the breathing workload during partial ventilatory

support include ET tube resistance, excessive triggering threshold or response delay,

insu.fficient flow capacity of the ventilator to meet peak patient demands, and the

development of dynamic hyperinflation.3

 CHAPTER 3
CONCLUTION

Mechanical ventilation is a life support treatment. Mechanical ventilator is a machine that

helps people breathe when they are not able to breathe enough on their own. The aim of this device

are To get oxygen into the lungs and body, to help the body get rid of carbon dioxide through

the lungs, to ease the work of breathingSome people can breath on their own, but it is very

hard. They feel short of breath and uncomfortable. And to breathe for a person who is not

breathing because of injury to the nervous system, like the brain or spinal cord, or who has

very weak muscles.

In using ventilation there also some complication such as complication in airway

intubation, complication of PPV and complication Breathing effort and patient-ventilator

asynchrony that may makes patient discomfort or brining up other new desease.
 LITERATURE

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