Module 2: Invasive Respiratory Support Flashcards
Ventilation
movement of gases in and out of the pulmonary system
Ventilation is comprised of both pulmonary and alveolar ventilation.
- Pulmonary ventilation is the volume of air exchanged between the environment and the lungs.
- Alveolar ventilation is the volume of air entering the alveoli that takes part in gas exchange per minute.
Respiration
involves the exchange of oxygen and carbon dioxide at the alveolar-capillary level and at the capillary-cellular level.
Ventilation occurs unconsciously and is maintained by various bodily functions. These include:
The Central Nervous System:
The respiratory centre is located in the medulla oblongata, located in the brain stem. Here, breathing patterns are adjusted in response to various levels of pCO2 and pO2 in the blood.
Stretch Reflexes:
These are located in the chest wall and airways and serve to alter the breathing pattern to maintain adequate minute ventilation (Minute Ventilation is the product of Rate X Volume).
Chemoreceptors:
Located in the aorta and the common carotid artery, chemoreceptors respond to increases and decreases in Pa02, PCO2 and pH, particularly in the presence of hypoxemia and acidocis. Examples:
↑pCO2 will lead to increased minute ventilation.
↓pCO2 will lead to decreased minute ventilation.
↓pO2 leads to increased minute ventilation.
Normal alveolar ventilation occurs
when an infant has a sufficient respiratory drive and sufficient energy to inflate and deflate the lungs, maintaining some volume at the end of every breath known as the functional residual capacity (FRC).
functional residual capacity (FRC)
FRC is maintained when sufficient surfactant minimizes surface tension (tendency for alveoli to collapse) and the alveoli remain slightly open at the end of each exhalation. Some gas remains, making the next inhalation significantly easier, decreasing the work of breathing (WOB).
Recall that the younger the gestational age, the more likely they are to have the following:
↓ surfactant ↓ alveoli ↓ capillaries ↑ distance between alveoli and capillaries Small airways Underdeveloped, weak muscles Underdeveloped pulmonary vasculature Cartilaginous rib cage
Respiration
is the act of inhalation and exhalation for the purpose of gas exchange within the lungs and at a cellular level. It allows the exchange of gas, (primarily oxygen and carbon dioxide) between an individual and his or her environment. Respiration is more than ventilation. It is dependent on:
Sufficient alveolar ventilation Alveolar/capillary diffusion Pulmonary perfusion Hemoglobin Peripheral perfusion
Gas is exchanged in two places:
in the lungs and at the cellular level. Alveolar respiration occurs in the lungs; cellular respiration occurs in the tissues.
The cardiovascular system acts as a conduit between these two sites of gas exchange. The brain acts as a central controller. The whole process looks something like this:
see picture on desktop
The entire process of respiration occurs in all body cells. The three main systems responsible for gas exchange are:
pulmonary system
circulatory system
nervous system.
The pulmonary system plays a key role in gas exchange or respiration. Alveolar respiration (gas exchange that occurs between the alveoli and the pulmonary capillaries in the lungs) is a result of three interdependent processes:
alveolar ventilation
pulmonary perfusion
diffusion across the alveolar-capillary membrane to allow for pulmonary perfusion.
Pulmonary perfusion
is also an important requirement for gas exchange. Pulmonary perfusion refers to the flow of blood through the portion of the circulatory system that supplies the lungs. De-oxygenated blood travels from the right side of the heart through the pulmonary arteries to the lungs where oxygen will be picked up and returned to the left heart through the pulmonary veins. The oxygenated blood can then travel out the aorta and to the rest of the body. At the same time, the blood transported to the lungs by the pulmonary artery will deliver CO2 picked up from the tissues and carry it to the lungs for elimination.
Pulmonary perfusion is dependent on oxygen and pH. In response to hypoxia and acidosis, pulmonary vasoconstriction leads to diminished pulmonary perfusion and pulmonary hypertension.
Diffusion
across the alveolar-capillary membrane occurs because of the pressure gradients for oxygen and carbon dioxide. These gases move from areas of high pressure toward areas of low pressure. Oxygen moves from the alveoli to the capillaries and carbon dioxide moves from the capillaries to the alveoli.
Oxygen and CO2 diffuse across the alveolar-capillary membrane differently.
CO2 is much more diffusible than O2. Even with diminished perfusion, CO2 diffuses readily from pulmonary venous and capillary blood to the alveoli. Once in the alveoli, CO2 is dependent on adequate alveolar or minute ventilation for elimination.
CO2 is a primary indicator of adequate alveolar ventilation. Changes in carbon dioxide levels are primarily due to changes in minute ventilation. Specifically, elevated CO2 indicates hypoventilation; CO2 depletion indicates hyperventilation.
Hypoventilation is the term used to describe a breathing pattern that results in decreased minute ventilation. The pattern may be one of:
diminished tidal volume
decreased rate
both
The circulatory system
The circulatory system acts as a courier, transporting gases between tissues and the lungs. It is responsible for delivering oxygen from the lungs to the cells and carbon dioxide from the cells to the lungs. The heart is the pump and the vasculature is the conduit.
Cardiac output is a reflection of the heart’s ability to perform this important function. Cardiac output is the volume of blood pumped by the heart in one minute, (mls/min). Cardiac output is a product of heart rate × stroke volume. Stroke volume is the volume of blood pumped with each beat (Litres/beat).
Stroke volume is a product of three factors:
preload
afterload
contractility.
Together these three factors determine stroke volume. Combined with heart rate, these factors determine cardiac output.
Preload
refers to the volume of blood in the ventricles prior to contraction (systole).
Afterload
refers to the pressure or resistance against which the ventricles are pumping (diastolic blood pressure).
Contractility
refers to the strength of contraction of the heart muscle.
CO2 is transported in three ways:
dissolved in plasma
attached to hemoglobin
combined with H20 to form H2CO3 (carbonic acid)
Most CO2 is dissolved in plasma or as carbonic acid; very little is carried by hemoglobin.
Oxygen is transported in two ways:
dissolved in plasma
attached to hemoglobin
Most oxygen is carried attached to hemoglobin (98%) and a very small amound is dissolved in plasma (2%).
Once arterial blood (containing oxygen and CO2) reaches capillary beds in the tissues, the process of cellular respiration occurs.
Central Nervous System
Chemoreceptors in the aorta and carotid arteries as well as in the cerebrospinal fluid (CSF) detect changes in blood gas composition. Nerves relay the information to the brain, and necessary adjustments in ventilation are made. Respiration is controlled by two types of chemoreceoptors:
Central Chemoreceptors
Peripheral Chemoreceptors
Central Chemoreceptors
located in the brain stem and respond to the acidity of the CSF
involved in control of respiratory rate and depth of breath
Example: acidic CSF results in hyperventilation, alkalotic CSF results in hypoventilation.
Peripheral Chemoreceptors
located in the aortic arch and carotid arteries
respond to changes in oxygen concentrations, carbon dioxide and pH
regulate breathing breath to breath
What happens if CNS is damaged?
Central nervous system depression or damage can lead to respiratory problems such as bradypnea, bradycardia, apnea, hypoventilation, hyperventilation, and hypotension. When using mechanical ventilation, these central nervous system responses are bypassed, thereby implicating an external control that is subject to error and ongoing adjusting.
key point
Mechanical ventilation is largely aimed at improving alveolar ventilation, but alveolar ventilation is only one part of what happens in the lungs and only one part of the whole process of respiration. When working with mechanical ventilation, look at the case in the context of factors that can influence respiration such as pulmonary hypoperfusion, anemia, poor peripheral perfusion, and hypovolemia (too name a few).
Which parameters of the blood gas are used to assess ventilation? Acid-base balance? Oxygenation?
Ventilation is assessed by looking at the pCO2. Acid-base balance is assessed by looking at the pH, pCO2, and
HCO3. Oxygenation is assessed by looking at the pO2 and the O2 saturation.
Which parameter is used to determine the respiratory component of acid-base abnormalities? Which one determines the metabolic component?
The pCO2 determines the ventilatory component. An increase in pCO2 creates a decrease in pH which is called “respiratory acidosis” (or ventilatory acidosis). It is due to hypoventilation.
The HCO3 determines the metabolic component. A net decrease in HCO3 causes a decrease in pH and is called metabolic acidosis. It is due to many etiologies, such as anaerobic metabolism producing lactic acid, a loss of HCO3 from the kidney or failure of the kidney to eliminate excess H+.
Why is the amount of carbon dioxide in the blood a direct measure of ventilation?
Because the amount of carbon dioxide in the blood is a reflection of the amount produced by metabolism and the amount exhaled through ventilation, or breathing. As metabolism does not change greatly, pCO2 is an indication of ventilation.
Explain “compensation” using compensated respiratory acidosis as an example.
When hypoventilation leads to respiratory acidosis (↓ pH, ↑ pCO2, and HCO3), the body will compensate by creating a compensated metabolic alkalosis. The kidneys will retain HCO3 and when the levels elevate, it looks like this: Normal pH, ↑pCO2, and ↑ HCO3.
Whereas elimination of CO2 is only dependent on adequate ventilation, tissue oxygenation is dependent on several processes. What are they?
Tissue oxygenation is dependent on adequate ventilation. In addition, tissue oxygenation is dependent on: oxygen delivery to the tissues (cold, hypovolemia, cardiac failure can lead to tissue hypoxia) and presence of anemia (reduced oxygen carrying capacity resulting in reduced oxygen content of the blood). When hypoventilation leads to respiratory acidosis (↓ pH, ↑ pCO2, and HCO3), the body will attempt to bring the pH back to nomal by retaining bicarbonate.
it is important to note the primary goal of mechanical respiration: to improve minute ventilation. The desired outcomes of mechanical ventilation include:
to achieve and maintain adequate pulmonary gas exchange
to minimize the risk of lung injury
to reduce patient work of breathing (WOB)
to optimize patient comfort
Positive Pressure Ventilation
Positive pressure ventilation occurs when we try to move air into the patient’s lungs by way of an endotracheal tube or non-invasive mask to create a positive pressure there by creating a forceful delivery of gas to inflate the lungs. Mechanical Ventilation in the neonatal population will be dependent not only on the airway anatomy and pulmonary pathophysiology of this particular population, but also on how various diseases will impact them. Thus, there is no one way to ventilate the neonatal patient but a variety of ventilators, modes of ventilation, and methods of ventilation that will be chosen based on the airway anatomy, pathophysiology, and disease process specific to each individual.
Achieving and Maintaining Adequate Pulmonary Gas Exchange
Mechanical ventilation is the application of positive inspiratory pressure to inflate the lungs. Remember that mechanical ventilation is aimed primarily at improving gas exchange by increasing minute ventilation. Minute ventilation is improved by increasing either the tidal volume or the rate. When minute ventilation increases, oxygen supply and carbon dioxide elimination increase.
Key point
The lungs have an inherent ability to match ventilation and perfusion (by increasing perfusion to well-ventilated areas). Therefore, re-inflation of atelectatic alveoli, through mechanical ventilation, will help to increase pulmonary perfusion. As well, the increased oxygen levels associated with improved alveolar ventilation and supplemental oxygen will further improve pulmonary perfusion. Finally, alkalinization through hyperventilation (by increasing respiratory rates and tidal volumes to decrease CO2 and pH) is thought to increase pulmonary perfusion by reducing pulmonary vasoconstriction caused by acidosis and hypoxia.
Diffusion is improved by increased mean airway pressure. An increased mean airway pressure allow for recruitment of collapsed alveoli and/or reistribution of lung fluid to decrease deadspace ventilation (an area of ventilation in absense of perfusion), and shunting (an area of normal perfusion but absent of ventilation). In particular, oxygen diffusion is enhanced when mean airway pressure is increased. This will allow for better exchange of gases across the alveolar-capillary membrane, assisting with alveolar ventilation.
Minimizing the Risk of Lung Injury
As gas is delivered under pressure to the newborn lung, the airway expands in proportion to its compliance; therefore, the more compliant the airway, the greater the change in airway diameter with mechanical ventilation (Greenspan & Shaffer, 2006). These authors go on to explain that the newborn airway is much like a balloon:
Once a balloon has been inflated, it is generally easier to inflate it again because of the structural changes to the balloon wall. Similarly, once the structure of the airway wall is compromised by mechanical ventilation, it will behave differently when subsequent pressure is applied. Although the airway may recoil to its original shape after the exhalation of each breath, some elasticity will be lost over time and the airway will become larger than normal.
Reducing WOB
Some infants will be born with immature or compromised respiratory, circulatory, or central nervous systems. This may lead to increased work of breathing which may present as tachpnea, tachycardia, indrawing, nasal flaring, grunting or decreased or absent respiratory drive. Mechanical ventilation is aimed at decreasing the work of breathing. This is accomplished by setting the appropriate tidal volume, respiratory rate with the option of pressure support to achieve required alveolar ventilation and also by using positive end-expiratory pressure to maintain FRC and thereby improve compliance.
Optimizing Patient Comfort
Imagine struggling to breathe – what an upsetting and stressful sensation. Supporting the infant to breathe is of utmost importance; not only for their survival, but as a comfort measure as well. These vulnerable infants need to be utilizing their reserves for growth – not using their energy to breath. Strategies to optimize infant comfort will ideally reduce their WOB and minimize “fighting the ventilator.”Interventions may include:
Ensuring the best mode of ventilation is being utilized Non-pharmacologic measures Facilitated tucking Skin-to-skin Nesting Noise reduction Pharmacologic sedation/pain control
Using Positive Pressure Ventilation
Positive pressure ventilation is when air is moved into the patient’s lungs via and endotracheal or tracheostomy tube to create a positive pressure to inflate the lungs. Mechanical ventilation in the neonatal population will be dependent on the airway anatomy, pulmonary pathophysiology and disease process. There is no one way to ventilate a baby, but options in terms of ventilators, modes and methods by which to ventilate that meet their individual needs. Most ventilators use positive pressure inflation of the lungs.
Rememeber that the goals of mechanical ventilation are to:
achieve and maintain adequate pulmonary gas excahnge
minimize the risk of lung injury
to reduce work of breathing
to optimize patient comfort
While we initiate mechanical ventilation to mitigate problems of hypercapnia, hypoxia, apnea and WOB, the possible complications associated with this treatment can have life-long consequences.
mechanical ventilation is NOT like normal breathing. Specifically, it differs from normal breathing in two important ways:
- The pressure needed to inflate the lungs with mechanical ventilation is much greater than the pressure needed with normal breathing.
- Mechanical ventilation bypasses the normal internal biochemical feedback mechanism that controls breathing.
Normal Ventilation
Normally, when we inhale, our lungs expand as a result of negative intrathoracic and intrapleural pressure. This negative pressure actually pulls the lungs open from the outside — much the way a vacuum bag is expanded inside the vacuum chamber of a vacuum cleaner. As a result, the pressure within the lungs does not increase significantly as the lungs inflate.
Positive Pressure Ventilation
Mechanical ventilation does not work in this way. Rather, mechanical ventilation uses high positive pressure exerted on the inside of the lungs to push them open from the inside — much like blowing up a balloon. As a result, the pressure within the lungs increases significantly as the lungs inflate. In fact, without this significant increase in pressure, the lungs would not inflate.
What is the problem using mechanical ventilation?
The problem with using positive pressure to inflate an infant’s lungs is that this pressure causes damage to fragile and developing lung tissue. Edema, inflammation, scarring, over-inflation, and loss of elasticity are a few of the more common and more serious problems that result from the barotrauma, (damage due to pressure) caused by positive pressure ventilation, and volutrauma, (damage due to over-distension of the lung).
Pressure
refers to force. For example, in mechanical ventilation, pressure refers to the force being applied to the inside of the alveoli as they are being inflated. Think about blowing up a balloon. Pressure is the force you use to inflate the balloon.
Volume
refers to the space something occupies. For example, in ventilation, volume refers to the amount of gas inside the alveoli. Think about the balloon you have just used force to inflate. Volume refers to the amount of gas inside the balloon after it is inflated.
Generally pressure and volume are directly related. The greater pressure you apply to inflate the lung, the greater the volume you will achieve. However, the relationship between volume and pressure is mediated by how easy the lung is to inflate. Normally two types of forces impose the inflation of the lungs. These forces are compliance and resistance:
These forces are compliance and resistance:
Compliance: (Litres/cmH20)
How compliant a baby’s lungs are affects how much volume moves into a lung at a given pressure. It affects how much pressure is required to achieve a given end-inflation volume within a lung. Think about two balloons. One is slightly inflated and the other is collapsed. It takes less pressure to inflate the first balloon because it is more compliant. It would take more pressure to achieve the same volume in the collapsed balloon because it requires more pressure to inflate, and is therefore less compliant.
Resistance (cmH20/Litre/second)
Resistance is the measurement of the frictional forces that must be overcome during breathing. An increase in force can be a result of anatomical structures of the airways, decrease diameter of the endotracheal tube size, increase in secretions, bronchospasm, mucosal edema (to name a few). An increase in resistance will require more pressure to achieve the same end-inflation volume within a lung.
Types of Mechanical Ventilation
There are three basic methods that have been developed to replace the mechanisms of normal breathing in mechanical ventilation. They are negative-pressure ventilation, positive-pressure ventilation, and high frequency ventilation.
Negative-pressure ventilation
Attempts to mimic the normal function of the respiratory muscles (for example, the iron lung). As outlined already in this module, this type of ventilatory strategy was widely used because it imitated natural breathing by exerting negative pressure on the chest as the diaphragm does. Technical advances in positive pressure ventilation have led to rapid development of the modern day positive pressure ventilators, and various modes of ventilation. This type of ventilation is rarely seen in NICUs.
Positive Pressure Ventilation
Occurs when a ventilator is used to force air into the patient’s lungs by means of an endotracheal tube or tracheostomy tube.
High Frequency ventilation
Uses above normal ventilating rates with below normal ventilating volumes. You will explore HFV in more detail in NSNE 7920.
We’ll now take a closer look at Volume ventilation and Pressure Ventilation – two primary controlled variables of ventilation. Again, choosing which method will depend on the individual baby – how they respond, what their pathology is - all the while optimizing ventilation while minimizing lung injury.
Volume Ventilation
Volume ventilation is designed to deliver tidal volumes most appropriate for adequate gas exchange. Recall that tidal volume is the volume of gas inhaled or exhaled during a normal breath. Volume ventilators have a control dial that permits selection of a specific tidal volume. When the tidal volume and/or the inspiration time for that breath have been reached, inspiration ends.
Do volume ventilators limit pressure in any way? Yes. Here is an example.
Recall that normal tidal volume for an infant is 3–7 ml/kg. A 2 kg infant would likely require a tidal volume of 5 ml/kg = 10 ml. What amount of pressure is required to deliver this tidal volume? That would depend on the compliance and resistance of the infant’s lung. If the infant’s lungs are very compliant, low pressures would be required. If they are stiff and noncompliant, higher pressures would be required. If however, this infant’s lungs are so stiff that very high pressures would be needed to reach 10 ml of volume; there is a safety feature that prevents this from happening. This safety feature is called a pressure limit. Recall that high inspiratory pressures contribute to the barotrauma that infant’s lungs experience as a result of mechanical ventilation.
Key point
In addition to lung compliance, increased resistance would also lead to increased pressures necessary for reaching preset tidal volumes. Again, causes for increased resistance would be kinked ventilator tubing, a blocked ET tube, or an increase in secretions to mention a few. In these cases, the pressure limits would be reached before the tidal volume was reached.
To review, volume ventilation provides target tidal volumes with each breath. Volume ventilation does this using the pressures needed based on compliance and resistance. Pressure limits prevent the infant from receiving extremely high pressures. With volume ventilation, inspiration ends when the tidal volume and/or inspiratory time have been reached.
Pressure Ventilation
Pressure ventilation is a time cycled and pressure limited mode that provides a constant pressure at the airways and allowing the respiratory therapist to set a desired pressure limit, inspiratory time and rate. On inspiration the desired pressure will be achieved and a volume will be delivered until the set inspiratory time is reached. Normal inspiratory times for infants range from 0.2 seconds to 0.4 seconds. In pressure control ventilation, tidal volume will be variable depending on lung compliance and resistance.
Normal pressures used to mechanically ventilate infants using pressure ventilators range from 12 cm H2O to 40 cm H2O. What kinds of tidal volumes are delivered with these pressures?
That depends on lung compliance, and resistance. For example, at a pressure of 15 cm H20, a very compliant lung might receive a normal tidal volume of 3–7 ml/kg. At the same pressure of 15 cm H20, a very stiff and noncompliant lung likely only receives a tidal volume of 1–2 ml/kg. Similarly, increased resistance in the airway from secretions will decrease the tidal volume entering the lungs. Pressure ventilation does not control tidal volume. The physicians, nurses, and respiratory therapists caring for an infant select peak inspiratory pressures which are most likely going to deliver adequate tidal volumes.
How do health care providers decide what pressures will achieve normal tidal volumes for a particular infant? They do this by selecting peak inspiratory pressures which:
- produce normal chest movements,
- normalize pCO2 and pH, and
- are within the 12–40 cm H2O range.
Gas Delivery
The major difference between pressure and volume breaths is the way in which inspiratory gas flow is delivered to the infant. “In both time-cycled pressure-limited ventilation and pressure-control ventilation there is a rapid acceleration of gas flow at the onset of inspiration, resulting in rapid pressurization of the circuit and the achievement of peak pressure and volume delivery early in inspiration” (Donn & Boon, 2009, p. 1237). Flow then decreases. This creates a peaked flow waveform and rapidly rising and falling pressure waveform (Figure 1). Therefore, breaths may be considered as being “front-end loaded.”
Modes of Ventilation
The mode of ventilation is determined by the breath type and the pattern in which the breath is delivered. It is made up of three factors: the targeted control variable, (pressure vs. volume), whether the breath is mandatory, spontaneous, or assisted, and the timing of the delivered breath (for instance, is it continuous, intermittent or spontaneous).
Controlled Ventilation
In this mode of ventilation, breaths (pressure or volume) are delivered by the ventilator at preset intervals based on respiratory rate, tidal volume, and inspiratory flow rate. In between these controlled breaths, the infant cannot take any of his/her own breaths. The ventilator is in complete control of every breath. For example, if the ventilator is set to deliver 20 breaths per minute (bpm), it would initiate inspiration every 3 seconds (60 sec/min ÷ 20 breath/min = 3 sec/breath). No other breaths are possible. In other words, the infant cannot “over breathe” the ventilator. Controlled Mandatory ventilation is often used with paralyzed patients or patients with no drive to breath. This mode of ventilation is common in patients with ARDS, or in patients with a poor respiratory drive to breath such as apnea of prematurity, neuromuscular disorders, or sedated patients.
Assist Ventilation
In this mode, the client can initiate a pressure or volume breath by making some inspiratory effort. The ventilator then responds by delivering a breath at the same parameters as a mandatory breath. This method works well for clients who are alert with a normal respiratory drive, but who are not able to ventilate effectively because of lung disease.
Assist-Control Ventilation
Assist-control ventilation is a combination of the first two modes – control and assist. In this mode initiation of the breath can either be patient triggered or time triggered. A breath rate, sensitivity to patient effort, and type of breath (volume or pressure) are set. The patient can breathe faster than the preset breath rate but the set volume or pressure will be delivered with each breath. As you read in Snow & Brandon’s article (2007), “this allows the infants to self-regulate by reducing their rate as their ventilatory status improves; this subsequently reduces barotrauma” (p. 13). This mode works well in infants who have a strong respiratory drive and are not heavily sedated.
Assist Control-Volume Guarantee
Assist-Control, Volume Guarantee (AC-VG) is a type of assist-control ventilation on the Dräger Babylog 8000 plus ventilator. It delivers a guaranteed tidal volume with each breath using the least amount of pressure, based on a breath to breath analysis. The patient is able to trigger the ventilator to deliver the breath, which will deliver a mandatory breath. The mandatory breath delivered will be based on the set tidal volume, the set inspiratory time, using a constant set flow, to deliver the volume with the least amount of pressure. Should the patient not trigger the ventilator, the ventilator will deliver a breath based on the set respiratory rate to maintain the desired minute ventilation.
Intermittent Mandatory Ventilation (IMV)
Intermittent Mandatory Ventilation is similar to the control ventilation, with one important difference. Between the ventilator controlled breaths the infant is free to breathe on his/her own. This is often referred to as over breathing the ventilator. For example, a predetermined rate of 30 could be set and the ventilator would deliver 30 evenly spaced breaths per minute, initiating inspiration every 2 seconds. Recall that inspiratory times range from 0.2 to 0.4 sec. This means that at a rate of 30 and an I time of 0.3, every IMV breath leaves 1.7 seconds during which the infant can exhale and then take additional breaths from the ventilator circuit. However, if the baby does not want a breath every 0.3 seconds (perhaps they just took their own breath), they will receive a breath regardless. You can imagine how uncomfortable this mode may be for the infant with a strong respiratory drive. As Snow and Brandon (2007) outline in their article, this discomfort “occurs when a mandatory or forced breath is given out of synchrony with the infant’s own respiratory effort” (p.11). The authors go on to say that, “Synchronized intermittent mandatory ventilation (SIMV) was created to limit these adverse effects” (p. 11).
Synchronized Intermittent Mandatory Ventilation (SIMV)
Synchronized Intermittent Mandatory Ventilation (SIMV) is similar to IMV in that a predetermined rate is selected and in between these breaths the infant can take additional breaths. What is different is that rather than the ventilator breaths being evenly spaced over a minute, they are synchronized to the infant’s own rate of breathing.
That is, for each breath the ventilator waits for the patient’s next inspiratory effort, and when the effort is sensed the ventilator assists the patient by delivering a mandatory breath there by attempting to synchronize the ventilator breaths with the infant’s own breaths. If no breath is sensed within the preset window of time a mandatory breath will be given.
SIMV avoids one of the problems associated with mechanical ventilation, that is, asynchrony between the infant and the ventilator. In the past this has been referred to as the infant “fighting” the ventilator. It has been managed in the past in a variety of ways, including increasing the IMV rate so that the infant can no longer over breathe the ventilator, sedating the infant, and even using pharmacological paralysis to eliminate the infant’s ability to breathe on his/her own. All of these approaches to management of asynchrony have drawbacks. Increasing the IMV rate eliminates the possibility of weaning the infant from the ventilator. Sedating and/or paralyzing the infant results in a range of neurologic, feeding, muscular, and circulatory problems. SIMV is an approach to management of mechanical ventilation that overcomes many of the problems (discomfort, fighting the ventilator etc.) associated with traditional IMV.
Pressure Support Ventilation (PSV)
Pressure Support Ventilation (PSV) is a method of ventilation where the patient controls the breathing rate. The patient must be able to trigger each breath. The ventilator “supports” spontaneous breathing up to a preset pressure. Pressure support can be given in adjunct with another mode, such as SIMV/PS. Pressure support ventilation is a common weaning mode of ventilation.
Continuous Positive Airway Pressure (CPAP)
CPAP provides a constant airway pressure that is maintained throughout the respiratory cycle. The patient is required to have a spontaneous drive to breath, and is not supported by a mandatory back-up breath. Its primary focus is to improve oxygenation by maintaining a healthy FRC. As you may know, CPAP is a very common mode of noninvasive ventilation in the spontaneous breathing infant population.
Airway Pressure Release Ventilation
Airway pressure release ventilation (APRV) has been described as continuous positive airway pressure (CPAP) with regular, brief, intermittent releases in airway pressure. APRV is designed to provide two levels of CPAP in which the patient will breathe spontaneously at both levels.
The upper level will be interrupted intermittently to drop to the lower level. Spontaneous breathing at the upper level helps with lung recruitment and improving the FRC while the intermittent drops to the lower level will aid in the alveolar emptying of gases and removal of CO2. This is also referred to as Bi-level Positive Pressure ventilation.
Advantages of APRV include lower airway pressures, lower minute ventilation, minimal adverse effects on cardio-circulatory function, ability to spontaneously breathe throughout the entire ventilatory cycle, decreased sedation use, and near elimination of neuromuscular blockade. Airway pressure release ventilation is consistent with lung protection strategies that strive to limit lung injury associated with mechanical ventilation.
Mandatory Minute Ventilation
Mandatory Minute Ventilation allows the clinician to set a minimum minute ventilation that the patient must achieve. The ventilator will increase either the breathing rate or the ventilating pressure to help the patient achieve the set minute ventilation if they are unable to achieve the set minute ventilation with their spontaneous effort. MMV is a common mode of ventilation used in children under sedation, or who may have a neuromuscular abnormality.
Guthrie et al. (2005) analyzed neonates receiving MMV versus SIMV and have this to add:
Mandatory minute ventilation (MMV) is a mode of ventilation that combines features of synchronized intermittent mandatory ventilation (SIMV) and pressure support ventilation (PSV). This mode of ventilation is theoretically a more intuitive approach to ventilator management. In MMV the mandatory ventilator rate is varied based upon the patient’s needs rather than delivering a constant preset rate. In MMV, the clinician chooses a minimum minute volume (the product of tidal volume and frequency) for the patient. If the patient’s spontaneous breathing, which is augmented with PSV, meets or exceeds this minute volume, no mandatory ventilator breaths are provided. If, however, the patient’s minute volume falls below the preselected minimum, the ventilator will provide ‘‘catch up’’ breaths at a fixed frequency to ensure that the patient receives this preselected minute ventilation.
What is the main difference between volume ventilation and pressure ventilation?
The main difference is this: volume ventilation delivers a set tidal volume.
Inspiration ends when a certain time has elapsed (I time) and a certain TV has been delivered.
Pressure ventilation delivers a set pressure. Inspiration ends when a certain time has elapsed (I time) and a certain pressure has been achieved.
What is the main limitation of pressure ventilation?
The main limitation of pressure ventilation is that when pressure is a constant, pre-set parameter, volume varies as compliance and resistance varies. Infants end up both over and underventilated.
What is the main advantage of volume ventilation?
The main advantage of volume ventilation is that it permits direct control of tidal volume. So that when compliance varies, pressure varies, but tidal volume is maintained. The lungs may be less damaged and there may be less BPD. Volume-targeted ventilation leads to small but clinically important improvements in short-term pulmonary outcomes, including BPD
What is the advantage of CPAP?
The advantage of CPAP is that a small amount of pressure is used to maintain alveolar inflation at end-expiration, without the potentially damaging effects of using positive pressure to fully inflate the lungs. The problem with CPAP is that it can decrease the work of breathing for some, and possibly many infants, but not all. Some infants will still tire out and need more positive pressure support. If not applied soon enough, CPAP may not successfully overcome the atelectasis that has already occurred. And, also if not applied early enough, the infant may be very tired by the time CPAP is started.
Upon admission to the NICU, Abby was placed in a pre-warmed incubator. She was pink, with expiratory grunting, nasal flaring, and intercostal and substernal retractions. Bilateral breath sounds were equal with crackles present. Her respiratory rate was 88 per minute. Initial laboratory data revealed a glucose of 4.3. The chest x-ray was consistent with RDS.
Her blood gas revealed the following: pH 7.18; PaO2, 40 mm Hg PaCO2, 55 mm Hg HCO3, 24 mEq/L B.E., –4 mEq/L. Because of Abby's prematurity, the respiratory acidosis, and the degree of respiratory distress present, she was intubated, begun on mechanical ventilation, and given exogenous surfactant therapy.
What are your primary goals for Abby?
- To maintain adequate oxygenation and ventilation
- To maintain a neutral thermal environment
- To provide fluids and nutrition sufficient to meet metabolic requirement and growth needs
- To maintain intact skin without breakdown
- To provide an environment free of noxious stimulation
- To foster positive parent-infant interaction
Take some time to think about what Abby’s family may find helpful when planning for home.
Did you mention things such as enabling and empowering this family throughout their NICU stay so that they felt more prepared to take Abby home? Things such as having them prepare and bath Abby, taking her temperature and changing her diapers are all steps that can prepare this family for home. Getting Denise to be involved in the plan for Abby – instead of telling Denise what Abby’s plan looks like…
It may be easier for us as nurses to do everything and feel that these babies are “ours” while in the NICU – however, enabling and empowering parents to take charge of their baby’s health as soon as possible will best prepare them for discharge and further enhance their experience and attachment to Abby. All so important for her development and parent-infant attachment!
Why was Abby, the infant in Case Study 2.1, ventilated?
Abby was ventilated because her respiratory disease was causing hypercapnia and hypoxia.
Although the hypoxia was being managed by providing 50% oxygen via an oxyhood, many nurseries, once an infant’s oxygen requirements reach 50–60%, will opt for mechanical ventilation as an approach to management. The hypercapnia can only be managed by mechanical ventilation.
There are two main differences between normal breathing and mechanical ventilation. These two differences put infants like Abby at risk for several problems. What are these problems?
The two main differences between normal breathing and mechanical ventilation are:
Normal breathing does not cause increased positive pressure within the lungs; mechanical ventilation does.
Normal breathing is regulated by internal biochemical feedback mechanisms; mechanical ventilation is regulated by the health care professionals manipulating the ventilator.
Regarding complications or problems, these differences give rise to several.
The high inspiratory pressures used with mechanical ventilation cause barotrauma to the lung tissue. This can result in edema, inflammation, scarring, overinflation, loss of elasticity, and, if these problems become chronic, this is called Bronchopulmonary Dysplasia.
The fact that an infant’s normal internal biochemical feedback mechanisms are being bypassed leads to the potential for the ventilator settings to be inappropriate for the infant’s needs. This can result in hypoxia, hypercapnia, and acidosis.
Abby was likely ventilated using a pressure controlled, volume guaranteed, time limited ventilator in the IMV mode. In your own words, explain what this means.
IMV means that inspiration is initiated by the ventilator for a set number of breaths and in between these ventilator breaths, Abby can breathe on her own. The breaths Abby takes on her own will be exactly what we have set on the ventilator in terms of volume. For example, she can trigger the ventilator to give her a breath as per the settings we have chosen.
Pressure controlled, time limited means that inspiration ends when a certain pressure has been reached within the lungs and a specific time has elapsed.
Volume guaranteed means that we select appropriate tidal volumes with which to ventilate Abby. The aim is to provide her with (on average) a much more stable assisted tidal ventilation from breath to breath.
The author of the vignette states that Abby required “high ventilatory support for several days.”
What do you think this means? Specifically, what rate and pressure do you think might have been used to ventilate Abby?
This likely means that in order to adequately ventilate Abby — that is, eliminate CO2 — high inspiratory pressures were required in order to achieve an adequate tidal volume. This suggests that her lungs were quite stiff or noncompliant. A lot of pressure was required to move a sufficient volume of gas in and out of her lungs. It may also mean that she required a high rate on the ventilator. This suggests that she may have been too ill to overbreathe the ventilator. Pressures as high as 30–40 may have been needed to inflate her lungs and achieve an adequate tidal volume. Ventilator rates as high as 60 may have been required to clear her CO2 if she was not breathing on her own. (Remember that infants normally breathe at a rate of 40–60 breaths per minute).
What disease does high ventilatory support put Abby at risk for?
As has already been mentioned, Bronchopulmonary Dysplasia (BPD) is a chronic lung disease that infants who have been ventilated are at risk for developing. Many of the infants you will see in the clinical area will have this disease.
Suppose that Abby is breathing out of synchrony with the ventilator. Imagine that she is being weaned and only needs a rate of 40 breaths per minute from the ventilator. She is over breathing on her own, but these breaths are not well synchronized with the ventilator breaths. For example, often when Abby is beginning exhalation of one of her own breaths, the ventilator delivers a mechanical breath. As a result, Abby is irritable, restless, and her blood gases are deteriorating. How might changing to SIMV assist Abby?
SIMV would permit both Abby and the ventilator to breathe without the concern that the ventilator breaths are interfering with Abby’s own breaths. With SIMV, the 40 ventilator breaths are not delivered in equal intervals. Rather, they are synchronized to be interspersed with Abby’s own breaths. This would enable Abby to over breathe the ventilator without becoming irritable and restless.
Rate
Every infant ventilator has a dial that permits selection of a range of rates, from as low as 10 breaths per minute to as high as 150 breaths per minute. The rate setting determines how many breaths will be delivered by the ventilator in a minute. Normally the rate is set between 10 and 60. The rationale for this range is that at less than 10 breaths per minute, the infant is likely ready to be off the ventilator. More than 60 breaths per minute is not physiologically normal. Most infants breathe at a rate of 40 to 60 breaths per minute.
This notion of physiologic normalcy is an important aspect of mechanical ventilation. Recall that at the beginning of this module we emphasized the idea that mechanical ventilation is not like normal breathing. However, wherever possible, it is preferable to use settings that are, in fact, physiologically normal. Rate is an example of a setting that can be manipulated within normal physiologic limits.
I Time
Inspiratory time is another example of a setting that can be manipulated within normal physiologic limits. Infants normally breathe with an inspiratory time of 0.2 to 0.4 seconds. Therefore, when using mechanical ventilation, this range is generally used to set I time.
I time controls when inspiration ends and expiration begins. It is important that expiratory time be longer than inspiratory time as this is how infants normally breathe. The relationship between inspiratory time and expiratory time is often referred to as the I:E ratio. It is always expressed with I as one, so it is always 1:?, depending on the length of I and E. It is not actually as complicated as it sounds and an example will likely help clarify the idea of I:E ratio.
Suppose that an infant is being mechanically ventilated at a rate of 60 breaths per minute. At this rate, each breath takes 1 second. Suppose the I time is 0.4 seconds. At a rate of 60 and an I time of 0.4, the E time is 0.6 seconds. The I:E ratio could be expressed as 0.4:0.6. However, it is easier to interpret the ratio when I is converted to 1 and the same conversion is done to E. In this case, in order to convert I to 1, we would have to multiply I by 2.5. Therefore, we do the same to E. That is, we multiply E by 2.5. The resulting I:E ratio is 1:1.5.
Peak Inspiratory Pressure
The peak inspiratory pressure (PIP) is the maximum pressure in the lungs during inspiration. The range of PIPs generally used to ventilate infants is 12 to 40 cm H2O. Higher pressures are used to ventilate stiffer lungs; lower pressures are used to ventilate more compliant lungs. The peak inspiratory pressure, in conjunction with compliance, and resistance determines the tidal volume that is delivered to the infant.
Volume
The volume set is the amount of gas in mls you wish the lungs to receive during a specific period of time, without exceeding a set PIP. A normal volume used in the neonatal population is 3-6 mls/kg (we are now excepting higher volumes as we have taken into consideration the deadspace of the flowsensors, which is about .8 ml. So often you will see 5or 5.5 mls/kg these days).
Positive End Expiratory Pressure
Another pressure that is manipulated on the ventilator that we have not yet discussed is positive end expiratory pressure, or PEEP. As the name suggests, PEEP is the pressure that is maintained within the lungs at the end of expiration. The normal range is 2 to 6 cm H2O. What this means is that at the end of expiration a small amount of pressure continues to be applied to the lungs. What might the purpose of this small amount of PEEP be?
The rationale for using PEEP with infants relates to the tendency of their alveoli to collapse at the end of every breath. Recall that because infants often lack adequate amounts of surfactant the surface tension within their alveoli is very high. This high surface tension causes their alveoli to collapse at the end of each breath. This means that with every inhalation, the alveoli are starting from a position of collapse.
This is a lot more work than if a small amount of air remains in the alveoli at the end of a breath. Remember the balloon analogy. It is easier to re-inflate a balloon if you don’t completely let the air out of it. Same thing with an infant’s alveoli. That’s what surfactant does. It decreases surface tension, decreasing the tendency to collapse, leaving a small amount of air in the alveoli, making the next breath easier to take.
PEEP does what surfactant would do, but in a different way. PEEP uses a small amount of pressure to maintain some air in the alveoli at the end of expiration - maintaining FRC. Using PEEP can reduce the amount of PIP needed for each breath.
Oxygen Concentration
A final ventilator setting we will discuss is oxygen concentration. All mechanical ventilators have air/oxygen blenders and can, therefore, deliver oxygen concentrations ranging from room air, 21%, to 100%. Infants who are ventilated generally require the same or slightly less oxygen than they required prior to being ventilated.
Alarms
ventilators have alarms that signal problems such as loss of oxygen, breathing circuit disconnection, or occlusion of the breathing circuit, as well as changes in the infant’s condition.
Some typical alarms include:
Low Tidal Volume Low Pressure Low PEEP/CPAP High Pressure High Inspiratory Rate Apnea Ventilator Inoperative High Frequency
If adequate temperature and humidity of inspired gases is not provided, the infant is at risk of airway damage due to loss of heat and moisture. This includes (but is not limited to):
Alteration of mucociliary transport Reduced airway defense Thickening of secretions Reduced airway patency and lung compliance Increased work of breathing, and Hypothermia
Factors that can challenge the delivery of optimal humidity include ambient conditions generated by an incubator and radiant warmer and endotracheal tube leakage (which can result in a loss of 15% or more of humidity content). To mitigate these factors:
- Remove the unheated extension from the circuit unless the incubator is set to 35 degrees or higher
- Remove the unheated extension if the infant is on a radiant warmer and cover the temperature probe with a reflective cover
- Ensure the temperature probe is snapped in all the way (even a mm out will make a difference)
- Monitor the endotracheal tube for leakage
- Utilize your respiratory therapist
Too Much Humidity
Too much humidity can literally instill infants from the condensation (especially small infants) and can occlude the inspiratory hose and interrupt ventilation. Excessive rainout (condensation) in the inspiratory hose can be drawn into the infant’s lungs if the inspiratory hose slants downward from the humidifier to infant. While the standard practice requires routing the hose so that rainout will drain away from the infant, moving the equipment may inadvertently dump collected rainout into the infant’s airways. Sometimes a water trap, a small container hanging beneath the lowest part of the hose, collects rainout. If no water trap is used, the breathing circuit should be quickly disconnected and drained at regular intervals. A heated inspiratory hose can prevent rainout if the device is properly used.
Another important consideration of rainout is that it can sometimes collect in the ventilator circuit. The ventilator can confuse the vibration of the water in the circuit as a triggered breath from the infant, and deliver extra breaths to the patient. The end result can be a very high respiratory rate being delivered. Rates as high as 100 can sometimes occur and result in a very low, and dangerous CO2 levels to in the infant. Please ensure your ventilator is not auto-triggering in this manner.
Too Little Humidity
Too little humidity can lead to the buildup of secretions that can block airways, decrease lung compliance, enable bacteria to invade mucosa, cause atelectasis (collapsed alveoli), and promote pneumonia.
Too Hot
A humidifier that produces excessively hot gases may burn an infant’s airways and cause general hyperthermia in small infants. Even though many units incorporate a nonelectric thermal fuse or backup thermostat that will immediately break the heater power circuit when an excessive temperature limit is reached, the humidifier and inspiratory tubing can act as a thermal well (especially if the humidifier holds a large volume of heated water) and produce inspiratory temperatures well above the power cutoff limit. Recall from NSNE 7200 the importance of maintaining a neutral thermal environment.
Infection
Reports of respiratory infection all seem to focus on the use of nonsterile water (often thought to be sterile) in humidifier reservoirs. During setup, the user may touch the inside of the humidification chamber and introduce bacteria. Reusable humidification chambers should be sterilized in accordance with manufacturer’s instructions and disposable reservoirs and chambers should be changed at the manufacturer’s specified interval. Infection will be discussed in more detail later in this module when we explore Ventilator Associated Pneumonia (VAP).
Heat and Moisture Exchanger
Providing humidification can be accomplished using either a heated humidifier (as the previous discussion suggests) or a heat and moisture exchanger (HME). HMEs are also known as hygroscopic condenser humidifiers or artificial noses. Whereas heated humidifiers operate to actively increase the heat and water vapor content of inspired gas, HMEs operate passively by storing heat and moisture from the infant’s exhaled gas and releasing it to the inhaled gas (Fassassi et al. 2007). Higher temperatures and humidity are obtained using a heated humidifier.
The drawbacks for using a HME include increased mechanical dead space plus increased flow resistance and thus increased work of breathing. The use of a HME could be a reliable and simple alternative for short- term invasive ventilation or during transport.
assessing and monitoring ventilated infants is a vital part of caring for infants receiving mechanical ventilation. This can be accomplished by:
clinical assessment of respiratory status, e.g., chest movement, color, peripheral perfusion.
blood gas analysis.
chest x-ray.
Noninvasive techniques to monitor blood gases
Increasingly, noninvasive techniques are being used to monitor blood gases. This is done via either a pulse oximeter or a transcutaneous CO2 monitor. CO2 can also be measured from the expiratory hose of the ventilator. Blood oxygen saturations and CO2 levels are valuable adjuncts in providing care to mechanically ventilated infants. They give continuous information about O2 saturation or pO2 and pCO2. They can, therefore, be used to assess an infant’s response to care (e.g., suctioning), ventilator setting changes, and handling. They can be used to detect trends over time. They can be used to wean an infant from the ventilator and assess their tolerance of CPAP. They can be used to plan care. They can be used to detect hypoxemia and hypercapnia early, allowing for early intervention, often before physical responses such as color change or bradycardia are apparent.
Explain, in your own words, respiratory acidosis.
Include in your explanation: the common causes and the resulting blood gas picture.
Respiratory acidosis is excess acid in the blood as a result of respiratory problems. The problems that can cause respiratory acidosis arise from ventilatory insufficiency and failure to eliminate CO2. For example, pneumonia, RDS, meconium aspiration, pulmonary hypoplasia, BPD — all of these conditions can be accompanied by insufficient ventilation and hypercapnia (↑ pCO2). The blood gas picture is characterized by ↑ pCO2, ↓ pH, and & HCO3−. For example: pCO2 50, pH 7.29, HCO3– 21
Explain, in your own words, compensated respiratory acidosis.
Why does it happen, how does it happen, and what is the resulting blood gas picture?
Compensated respiratory acidosis occurs when respiratory acidosis is not corrected. If left uncorrected,
the body will attempt to compensate for the ↓ pH. This is done by retaining HCO3−, a base which will increase the pH. Increasing an acidotic, low pH will normalize it. The blood gas picture changes from what was described above to one that is characterized by ↑ pCO2, ±, ↑ pH and ↑ HCO3−. For example, a typical compensated respiratory acidosis looks like: pCO2 50, pH 7.35, HCO3− 27.
This is such a common blood gas picture that the normal range of pH for infants with long-term respiratory problems is 7.30–7.45.
Explain, in your own words, respiratory alkalosis. Why is this generally an iatrogenic problem?
Respiratory alkalosis occurs because of too little CO2 and is generally the result of hyperventilation.
It is an usually iatrogenic problem among infants because hyperventilation rarely occurs naturally. Rather, hyperventilation often occurs as a result of too high a rate being set on the ventilator. The blood gas picture for respiratory alkalosis is characterized by: ↓ pCO2, ↑ pH, & HCO3−. For example, pCO2 28, pH 7.41, HCO3−22.
he relationship between blood gases and mechanical ventilation can be very broadly described as follows:
pO2 is affected by the Mean Airway Pressure (MAP) and the FiO2, while
pCO2 is affected by the Minute Ventilation.
MAP and FiO2 → pO2
Blood oxygen levels, or pO2, are affected by ventilator FiO2 and MAP.
Hypoxemia is treated by:
↑ FiO2
↑ MAP
Mean Airway Pressure (MAP) refers to the average pressure in the lungs during one complete breath, including inspiration and expiration. MAP can be increased by:
↑ PIP
↑ PEEP
↑ flow
↑ I time
hypoxemia may be treated by:
↑ FiO2 ↑ PEEP ↑ PIP ↑ flow ↑ I time
Hyperoxia may be treated by:
↓ FiO2 ↓ PEEP ↓ PIP ↓ flow ↓ I time
key points
pO2 is affected by the FiO2 and the MAP.
pCO2 is affected by the Minute Ventilation.
Minute Ventilation → pCO2
Minute ventilation refers to the volume of gas moved in and out of the lungs in one minute. Minute ventilation = tidal volume × rate. Minute ventilation can be increased by increasing either the tidal volume or the rate or both.
Tidal volume is the volume of gas moved in and out of the lungs with each breath. On a time cycled, pressure limited ventilator (a typical infant ventilator) the tidal volume depends on the PIP and lung compliance. Lung compliance cannot necessarily be controlled by clinicians, however the PIP can. Therefore, tidal volume can be increased by increasing the PIP.
hypercapnia may be treated by:
↑ PIP
↑ rate
Hypocapnia may be treated by:
↓ PIP
↓ rate
Clinical Assessment with Mechanical Ventilation
Color
Respirations
Heart Sounds
Equipment Check
The following complications associated with mechanical ventilation
obstructed endotracheal tube self or accidental extubation right main stem intubation bronchopulmonary dysplasia sudden deterioration ventilator malfunction.
In particular, nurses are responsible for the infant’s safety, comfort and warmth during intubation.
Safety measures may include:
aspiration of stomach contents prior to intubation
premedication with anticholinergic (e.g., Atropine) and sedative (Morphine/Fentanyl)
increasing volume of QRS on the cardiorespiratory monitor to alert practitioners to infant’s heart rate
holding the infant still and midline during the procedure
providing oxygen and suctioning as needed
timing the duration of the procedure
monitoring an infant’s responses to the procedure (color, heart rate, tone)
documenting the procedure.
Comfort measures may include:
containment/bundling
warmth
medication for sedation and pain.
The American Association of Respiratory Care (AARC)(2010) suggests that successful suctioning of an intubated patient:
improves air exchange and breath sounds, decreases the peak inspiratory pressure (PIP), decreases airway resistance, increases dynamic compliance, increases tidal volume delivery when using pressure-limited ventilation, improves arterial blood gas values, improves oxygen saturation, and removes secretions.
Although ETT suctioning is a common procedure done in the NICU, it is not a benign procedure and thus should only be performed when necessary to maintain a patent airway and endotracheal tube. Risks of suctioning include:
Hypoxemia Bradycardia Atelactasis Bronchospasm Increased intracranial pressure Trauma to the airway’s mucosal lining and celia Bacterial colonization of the airway Ventilator associated pneumonia (VAP) Nosocomial sepsis Stress
Suctioning an ETT is done only when clinically indicated, based on an assessment of the infant. Clinical signs include:
oxygen desaturations visible and/or audible secretions course and/or decreased breath sounds on auscultation decreased chest expansion changes in respiratory rate and pattern bradycardia agitation decreased tidal volumes increased PIP changes in blood gas values.
Maintain sterile technique during this procedure.
There are two ETT suctioning systems:
open and closed
Open System Risks
Hypoxemia, atelectasis, pneumonia (VAP), trauma to the airway, sepsis, dislodgement of the ETT and changes in heart rate, blood pressure, and cerebral blood flow.
It has been shown that systolic BP increased significantly more during open suctioning (than closed) and a significant decrease in heart rate.
Closed System Benefits
Minimizes changes in oxygen saturation and decreases atelactasis.
Shorter length of time required for all physiologic parameters to return to baseline values seen with closed suctioning.
Decreased risk of VAP and associated bacterial infections.
The use of sterile normal saline (NS) instillations is controversial. However, best practice suggests that sterile NS should NOT be instilled during ETT suctioning. Though there is no recent evidence supporting benefits of instillation, documented risks include:
hypoxemia
bradycardia (vagal response)
barrier to gas exchange
bronchospasms
dislodgement of bacterial biofilm colonizing the ETT into the lower airway
increased risk of nosocomial pneumonia and infections
increased intracranial pressure.
Chest Physiotherapy
Once an infant has been ventilated for three or four days, it is a good idea to assess the need for physiotherapy.Physiotherapy may be helpful in infants with atelectasis in specific areas of their lungs, or to help mobilize thick, tenacious secretions that may lead to airway obstruction. Very sick infants may not tolerate chest physiotherapy and careful weighing of the benefits versus the risks must be done. Infants with metabolic bone disease, for example, may not be candidates for physiotherapy. Physiotherapy protocols differ from hospital to hospital.
Ventilator Associated Pneumonia
Ventilator Associated Pneumonia (VAP) is defined as pneumonia that develops 48 hours after a patient has been placed on mechanical ventilation. VAP can be of bacterial, viral, or even fungal etiology. Some of the causes linked to the onset of VAP during mechanical ventilation may include:
Aspiration of oropharyngeal secreations
Aspiration of esophageal/gastric contents
Inhalation of infectious material
Contamination of the ventilator circuit
Advancement of infectious material into the trachea/lungs during intubation, and suctioning.
Recently, several procedures have been added to the care of mechanically ventilated infants in order to help reduce the risk of acquiring VAP. These include:
Ensuring proper placement of the enteral feeding tube to prevent aspiration of esophageal/gastric contents
Elevating the head of the bed 34-45 degrees again to prevent aspiration
When suctioning, suction the mouth and nose first, before suctioning the endotracheal tube to prevent advancement of infectious materials into the trachea and lungs
Implementing the use of an in-line suction catheter and sterile suction techniques
Changing of ventilator circuits only when grossly contaminated to help maintain a closed system
Avoiding contamination of the ventilator circuit from condensate
Oral vs. nasal intubation
Positioning of the ventilator circuit so that the flow of condensation will be away from the patient.
The use of non-invasive ventilation when possible
DILIGENT HAND WASHING!!!
As soon as the respiratory disease process stabilizes and ventilatory needs decrease, weaning should begin. Weaning of the ventilated infant refers to decreasing the respiratory support by the ventilator and increasing the amount of respiratory support the infant provides themselves. This may include:
Decreasing the respiratory rate Decreasing the tidal volume Decreasing the PIP/PEEP Decreasing the FiO2 Changing the mode of ventilation from CMV to IMV/SIMV/PSV
