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Non Invasive Ventilation for Respiratory Failure

Self-Directed Learning Package

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Author(s): Ruth Payne,

Clinical Nurse, Critical Care Unit.

Editor(s): Lisa Gatzonis, Education & Research Unit Manager, Lisa Self Staff Development Nurse, Critical Care , Maggie Mutters RN, Nurse Specials Unit.

Released: February 2010

Reviewed: August 2017, V. Sozos A/SDN

When producing learning modules we endeavour to maintain a high level of accuracy and completion. However, no responsibility is taken for any consequential problems as a result of using this learning module. The contents of this module may be revised without prior notice.

This learning module is intended for the use of Joondalup Health Campus employees in the course of their employment only. This module may not be reproduced or reprinted for any other purpose without prior permission.

©

Joondalup Health Campus 2013

For more information, please contact:

Training & Development Joondalup Health Campus PO Box 242

JOONDALUP WA 6919

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Table of Contents

INTRODUCTION ... 5

CONTEXT ... 5

PURPOSE ... 5

LEARNING OUTCOMES ... 5

MODULE ICONS ... 6

MECHANISMS OF RESPIRATORY FAILURE ... 7

TYPE I AND TYPE II RESPIRATORY FAILURE ... 8

SIGNS AND SYMPTOMS OF RESPIRATORY FAILURE ... 9

MANAGEMENT OF RESPIRATORY FAILURE... 10

INDICATIONS FOR NIV ... 11

CONTRA INDICATION FOR NIV ... 11

MODES OF VENTILATION ... 12

CPAP (CONTINUOUS POSITIVE AIRWAY PRESSURE)... 12

BIPAP (BI-LEVEL POSITIVE AIRWAY PRESSURE). ... 12

PRESSURE SUPPORT (PS)... 13

NURSING MANAGEMENT ... 17

PATIENT APPLICATION AND EDUCATION ... 18

ONGOING PATIENT MONITORING ... 18

TROUBLE SHOOTING ... 19

SELF ASSESSMENT ... 21

REFERENCES ... 23

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Introduction

Context

Non-invasive ventilation (NIV) is a common method of treatment for respiratory failure to improve oxygenation and decrease work of breathing. It refers to the provision of ventilatory support through the use of a mask and positive airway pressure.

Purpose

This self-directed learning package (SDLP) has been designed for Registered & Enrolled Nurses who care for patients working within the critical care setting. The nurse is required to understand the implications of initiating the treatment of Non-Invasive Ventilation (NIV) and the medical conditions for which it may be implemented and the ongoing nursing care.

It is an essential part of this learning package that all noted work practices and health record forms are accessed and read by the learner.

Along with this package, read the following SDLPs & Policies:

 Arterial Blood Gases SDLP

 Respiratory: Oxygen therapy C18.20

 Non-invasive positive pressure mechanical ventilation guidelines C14.44

Learning Outcomes

After completion of this SDLP the nurse should be able to:

 Describe the physiology of Type 1 and Type 2 respiratory failure

 Understand symptoms that require NIV

 Understand the principles of continuous positive airway pressure (CPAP)

 Understand the principles of biphasic positive airway pressure. (BIPAP)

 Demonstrate set up and ongoing use of NIV equipment

 Describe the nursing care of patients undergoing NIV treatment

NIV Competency to be assessed on completion of the NIV SDLP by an SDN.

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Module Icons

KEY POINT TO REMEMBER

A significant item/statement that you may find useful for future reference

REFERENCES

Direction to policy, page, book, Intranet etc where further information can be found

ACTIVITIES

An individual or group exercise that facilitates the reinforcement of learning outcomes

ASSESSMENTS

An individual or group exercise that provides an indication of competency achieved for specified learning outcomes

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Mechanisms of respiratory failure

The function of the respiratory system is gas exchange. Respiratory failure is defined as inadequate gas exchange whereby the normal levels of oxygen and carbon dioxide cannot be maintained.(4) Further definition is expanded to include arterial oxygen tension measurement of a PaO2 of less than 60mmHg (8kpa) and/or a carbon dioxide tension (PCO2) of greater than 50mmHg (6kpa).(3)

The act of respiration uses 3 processes in the normal functioning lung.

 Transfer of oxygen across the alveolus

 Transport of oxygen to the tissues

 Removal of carbon dioxide from blood into the alveolus

Acute respiratory failure is a medical emergency, which involves a disorder of respiratory function that results in abnormal gas exchange. This could be due to impairment of the lungs, their ability to act as a pump or a combination of the two. It may be obstructive as in CAL and Asthma, restrictive e.g. pneumonia, chest wall deformity or neuromuscular disorders, or cardiogenic as in pulmonary oedema.

Four mechanisms may contribute to respiratory failure.

Hypoventilation = this is when there is a decrease in tidal or minute volume, which can give the characteristic rise in PCO2, as in conditions causing respiratory depression such as neuromuscular dysfunction, airway obstruction and exhaustion. Tidal volume is the volume, in mls, of each breath taken. Minute volume, being the total respiratory volume taken over one minute. Calculated as number of breaths x tidal volume = minute volume.

Diffusion impairment = this occurs due to an increased thickening of the alveolar-capilliary membrane which results in an imbalance of gas exchange between the alveolar and blood interfaces. In health this barrier is very thin. The most common acute cause is pulmonary oedema; the most common cause for chronic diffusion deficit is pulmonary fibrosis.

Shunts = these occur when the venous blood supply reaches the arterial circulation without passing an area of ventilated lung, for example when the alveolar are filled with pus, oedema, blood or tumour (called intra-pulmonary shunt). Extra pulmonary shunt is cardiac in origin, more readily seen in children when the blood is shunted from right to left of heart bypassing the lungs.

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Ventilation Perfusion Mismatch VQ mismatch is an imbalance between alveolar ventilation and pulmonary capillary blood flow. This is the most common mechanism involved in respiratory failure and commonest cause of hypoxaemia. This mismatch involves the presence of a degree of shunt and dead space in the same lung. In other words the alveolar may be adequately oxygenated but the ability for transfer of O2 and CO2 is restricted due to the alveolar having no perfusion or vice versa. Common causes are pneumonia, pulmonary oedema, severe asthma, Pulmonary Oedema and Chronic Obstructive Airways Disorders.

Type I and Type II Respiratory failure

Respiratory failure is either Type I (oxygen failure) or Type II (ventilation failure). Type I affecting one gas and Type II affecting 2 gases.(3)

Hypoxaemia (Type I) and Hypercapnia (Type II).

Hypoxaemic Type I Respiratory Failure

Type I respiratory failure is caused by a fall in the alveolar and arterial oxygen levels and is often caused by an acute reversible condition. Blood gas analysis would show a low PaO2 with a normal or low PaCO2. High levels of oxygen are required to prevent hypoxic tissue damage.

This is the most common form of respiratory failure and is characterised with filling of the alveolar units with fluid or collapse as in pneumonia and pulmonary oedema.

↑PH ↓PCO2 and ↓PO2 = Hypoxaemic gas analysis

Type II Respiratory Failure

Type II failure also known as HYPERCAPNIC respiratory failure is characterised with a PaCO2 of more than 50mmHg. This type of failure is more difficult to detect in the ward patient as a rising PC02 will not be detected by saturation monitoring. Hypoxaemia is common in this type of patient as carbon dioxide rises, oxygen levels will fall. Clinical signs include vasodilation, headache, bounding pulses, tremor and or falling conscious level. Common causes are COPD, asthma and drug overdose. There is evidence that the prompt use of Non Invasive Ventilation for COPD patients will decrease mortality, decrease length of stay and prevent the complications associated with invasive ventilation.(NICE 2010).

↓PH ↑pCO2 ↓PO2 = Hypercapnic gas analysis

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Signs and symptoms of Respiratory Failure

The main Symptom of respiratory failure is shortness of breath.

Signs of failure are

:

Overall look The patient is usually pale, sweaty, clammy and looks frightened, exhausted or obtunded.

Most patients with respiratory failure tend to sit up unless the cause is CNS related

Respiratory rate

Arterial Blood Gases

≤8 or more than 30 min. Slow resp rate in conjunction with fatigue is an ominous sign. (below 8 and above 36 is MET call for JHC)

Interrupted speech. Unable to finish sentences PH ≤ 7.30 & or PaCO2 ≥ 55mmHg

Pulse rate Tachycardia is usually associated with respiratory failure

Bradycardia is usually a late and sinister sign

SpO2 ≤ 88% This roughly corresponds to a PaO2 of 60mmHg

(less than 90% = MET at JHC)

Confusion, agitation or convulsions Usually caused by hypoxia and can put the patient and staff at risk of injury.

Reduction in level of consciousness Usually associated with hypercapnia or severe hypoxia

Chest signs Prolonged expiratory phase (wheeze)

Use of accessory muscles

In drawing of suprasternal notch (airway obstruction) See-saw respiration pattern (obstruction or exhaustion)

Cardiovascular system Examine the cardiovascular system as heart failure is a common cause of respiratory failure.

(taken from Scottish Intensive care Society © with additional inclusions)

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Management of Respiratory Failure

Non-Invasive ventilation is aimed at reversing the acute phase of respiratory failure whilst supporting ventilation and preventing any other organ dysfunction through the use of a face mask

NIV is now frequently used as a first line treatment in a selected group of patients, for example, those likely to respond rapidly to NIV such as cardiogenic pulmonary oedema or an acute exacerbation of Chronic Obstructive Pulmonary Disease (COPD). (2) It assists respiration by providing a constant low flow pressure to hold open the airways, 2creating a positive inspiratory and expiratory pressure through the use of a tight fitting mask. This makes the work of

breathing easier, increases tidal and minute volume and decreases respiratory rate. Examples of medical conditions whereby NIV may be commenced are: Sleep apnoea/ obesity

hypoventilation disorder, neuromuscular disorders, bronchiectasis to name a few. (4)

It may be the treatment of choice due to the following benefits:

 Decreased mortality

 Decreased need for intubation

 Reduction in treatment time

 Rapid improvement in pH and respiratory rate within the first hour. Relieves symptoms of respiratory distress and work of breathing.

 Decreased complication associated with treatment, e.g less risk of pneumonia

 Decreased length of hospital stay.

 Patients able to remain in control of their treatment and are able to communicate with the health care team

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The decision to commence NIV treatment is a medical one based on patient history and disease process.

Review the work practice Non Invasive Positive Pressure mechanical ventilation guideline. C14.44

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Indications for NIV

 Hypercapnia PaCO2 ≥ 55mmHg

 Hypoxaemia

 Increased respiratory rate ≥ 30bpm

 Respiratory distress and increased work of breathing

 Intensivist, Respiratory Physician &/or senior medical staff prescribed.

Contra indication for NIV

 Un-cooperative patient – co-operation of the patient influences the success and outcome of NIV. Confused patients may not be able to tolerate this intervention

 Imminent cardiac arrest

 Undrained pneumothorax

 Vomiting

 Inability to protect their own airway

 High risk of aspiration due to copious airway secretions . Also the frequent removal of the mask that would be required would out way any benefits

 Orofacial abnormalities which interfere with the mask-face interface

 Recent oesophageal or gastric surgery – pressure in the upper airways may cause pressure on an anastomosis.

 Patients with a decreased conscious level

 Epistaxis

 Allergy to masks

(4,7)

Considerations for NIV

 Level of consciousness

 Able to maintain own airway

 Gag reflex present

 Breathing spontaneously

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Modes of ventilation

CPAP (Continuous Positive Airway Pressure)

This is the application of continuous positive pressure during the whole ventilation cycle, by

‘splinting’ the airways throughout inspiration and expiration. It improves work of breathing by counteracting the intrinsic Positive End Expiratory Pressure (PEEP) in those patients with chronic airway limiting disease and creates positive end expiratory pressure in others. The normal healthy individual is required to create a negative pressure to breathe in. Patients with severe lung disease are thought to not fully empty their alveoli resulting in a positive pressure in the airways at the end of expiration. Therefore to breathe in, these patients must first

overcome the positive pressure. Consequently the patient has to use accessory muscles to generate the required high negative pressure to allow inhalation, a process which further increases the work of breathing This is known as intrinsic PEEP and is often about 5cmH2O.

In addition CPAP redistributes lung water in cases of pulmonary oedema and acts as a splint to the upper airways for those patients suffering from obesity or sleep apnoea. Patients in

respiratory failure, who are becoming tired, will also benefit from the PEEP as it will decrease the work of breathing. In addition it helps to prevent the collapse of alveoli and aid in alveoli recruitment.

The application of CPAP increases intrathoracic pressure with a beneficial effect in decreasing left ventricular afterload.

This mode of NIV is most frequently commenced for patients in Type I respiratory failure to improve oxygenation starting at 10 cm H2O. It has been described as a similar experience to breathing with your head stuck out of a moving car.

BIPAP (Bi-level Positive Airway Pressure).

This mode delivers CPAP but also senses when an inspiratory effort is being made and delivers a higher pressure during inspiration. When the flow stops the pressure returns to the CPAP level. This positive pressure wave during inspiration unloads the diaphragm decreasing the work of breathing, allowing low levels of pressure support to facilitate gas exchange or to put another way …larger volumes are delivered for less respiratory effort! (2)

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This mode of NIV is useful for clearance of CO2 as in COPD

It is subdivided into the terminology IPAP = inspiratory positive airway pressure and EPAP = expiratory positive airway pressure (Also known as PEEP). This is the positive pressure remaining at the end of expiration.

IPAP aids inspirations to lower CO2 levels and EPAP aids in the recruitment of under ventilated lung and splints open the airways to increase O2 levels. (2,5,6)

PAP works in the same way as CPAP in that it improves oxygenation by raising the forced residual capacity & decreasing the work of breathing. However the key difference in this mode of ventilation is the IPAP.

Pressure support (PS)

Pressure support is the value of support calculated as the difference between IPAP and EPAP.

For example if IPAP is set at 15cmH2O and EPAP (or PEEP) is set at 5 cmH2O, the pressure support will be 10cmH2O. Pressure support decreases the work of breathing thereby averting muscle fatigue, increasing and improving tidal volumes, reduces tachypnoeic respiratory rates, reduces high CO2 levels and corrects acidosis.

With this mode the patient will determine rate, time and frequency of each breath with their respiratory effort triggering the supported breath. (6)

BIPAP terminology and its relationship to respiration.

The BIPAP machines at Joondalup Health Campus are the Vision or V60 and use single tubing. Exhalation is passive through the use of the exhalation port in conjunction with the EPAP.

IPAP = (Inspiratory positive airway pressure). Tidal volumes increase, ↑O2, ↓CO2, work of breathing is decreased as is respiratory rate.

EPAP = (expiratory positive airway pressure) this splints upper airways, ↑O2, ↑forced residual capacity, and counter balances intrinsic PEEP.

Rate = will assist in increasing minute volume hence decreasing PCO2

Inspiratory Flow = is driven by patient effort during spontaneous breathing.

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Rise Time = EPAP to IPAP flow rate transition. Supports inspiratory flow during spontaneous breathing.

Find the Vision BiPAP machine and follow the steps below to familiarise yourself with the equipment.

1. Collect mask and tubing from store room. There are different size masks, so choose a mask that fits the patient create a good seal.

2. Plug in power cord

3. Connect white cord to oxygen outlet

4. Turn machine on pressing black button on back of machine – lift clear cover to access 5. The vision unit initiates a self test which takes 15 – 60 seconds.

6. After self test the unit will display the set up screen

7. The exhalation port test may be performed from this screen

8. Verify correct assembly of patient circuit and perform test. Ensure the circuit is completely occluded during the test sequence.

9. Press the test Exh port key on left of panel. This screen will provide instructions to perform test. Test takes approx 15 secs to complete.

10. To cancel the test at any time press the Cancel Test Soft Key.

11. Once complete press the Monitoring Hard Key at bottom left of the machine to begin system operation.

12. The system begins operation in the last mode and at the settings in use before the unit was powered down.

13. Familiarise yourself with all the key buttons, learning how to change modes, increase oxygen, reset alarms.

14. To turn off, the unit must be switched off first before disconnecting the main power source to prevent a system malfunction

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V60 BiPAP System

Procedure

Do or observe... Verify...

1. Connect ventilator to AC power and the oxygen supply. Assemble the patient breathing circuit.

Breathing circuit is assembled correctly.

2. Switch on power. You hear tones from both the backup alarm (high pitch) and the primary alarm (lower pitch).

3. Check active mask and exhalation port selection in Messages list.

Displayed mask and exhalation port match ones in use. If this needs to be altered go to Menu and select Mask/Port DEP (Respironics Disposable Exhalation Port).

Set the mode to S/T and make the following control settings: Rate: 4 BPM, IPAP: 10 cmH2O, EPAP: 6 cmH2O, I-Time: 1 sec, Rise: 1, Ramp: Off, O2:

21%. Make the following alarm settings:

Hi Rate: 90 BPM, Lo Rate: 1 BPM, Hi VT: 200 mL, Lo VT: OFF, HIP:

50 cmH2O, LIP: OFF, Lo VE: OFF

Test lung expands during inspiration and collapses during exhalation. There is a continuous

flow of gas from the exhalation port.

Disconnect the proximal airway pressure line from the ventilator connector.

Proximal Pressure Line Disconnect alarm is annunciated (audio, visual, and flashing Alarm LED) by the ventilator and remote alarm if connected

Reconnect the proximal airway pressure line, and manually reset alarm.

Proximal Pressure Line Disconnect alarm is reset

Set O2 to 40%. Wait for oxygen concentration to stabilize.

Oxygen analyzer reads between 35 and 45%

Disconnect the ventilator from AC power while the ventilator is running.

NOTE: If the ventilator has a backup battery, the battery must be

adequately charged to run this test. Recharge as necessary before running the test.

If the optional backup battery is installed:

• The ventilator switches over to battery

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power (battery symbol in right-hand corner of screen is displayed).

• The green LED above the ON/Shutdown key remains lit.

• The audible alarm sounds intermittently.

• Running on Internal Battery is shown.

• The Battery LED is off.

If the optional backup battery is not installed:

• An alternating backup alarm tone sounds and the Alarm LED flashes for a

minimum of 2 minutes.

9. If the backup battery is installed, reconnect the ventilator to AC power.

• The alarm resets.

• The ventilator is again running on AC (symbol displayed in right-hand corner of screen).

• The Battery LED flashes to indicate the battery is charging.

10.Return settings to hospital-standard values.

WARNING:To prevent possible patient injury, always return alarm settings to

hospital-standard values after the preoperational check.

NIV Evita XL

NIV can be delivered via the Evita XL Ventilators. If using the ventilator circuit with inspiratory and expiratory tubing, a mask without an exhalation valve and port must be used. Drager supply specific blue face masks,which differentiate them from the V60 and Vision Masks.

To initiate NIV follow the instructions below:

Mask NIV can only be changed in standby mode.

On the current patient window select Tube/Mask.

Select Mask (NIV) and press rotary knob to confirm.

Press Ventilator Settings soft key.

Select CPAP/PS and key in physician’s prescribed settings.

Touch Start and press rotary knob.

The Evita XL compensates leakages for an Adult up to 30 L/Min. (9)

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Nursing Management

Preparation

 A management plan should ideally be formulated for the first 4 hours of NIV to assist in the decision as to the need for escalation of therapy. (8)

 Choose the correct size of mask by using the sizing chart. Large air leaks will reduce effectiveness of treatment.

 Full-face masks are available in small and large sizes.

 Ventilator setting will be as per protocol and work practice, or as prescribed by the attending Doctor. As a guideline for BIPAP the inspiratory pressures should be commenced at 10 -15cmsH2O and the End expiratory pressure at 5cmH2O. Aim to provide a pressure support greater than 6 cmH2O. If you need to increase the EPAP then you must remember to change the IPAP setting at the same time by the same amount to keep the pressure support constant. Back up respiratory rate of 12 bpm. If inspiratory time needs to be set it should be 50%less than respiratory cycle.

 Oxygenation levels will be determined by target saturations as prescribed.

 It is important that the exhalation ports (either on the mask or at the mask end of the tubing) are fitted and functioning properly. Occlusion of the exhaust port can exacerbate hypercapnia through rebreathing.

 Humidification is not normally required during NIV.

 The incidence of gastric distension is low so the routine placement of a nasogastric tube is not required. However if patients do have distension then a nasogastric tube is indicated and ideally a fine bore placed to prevent excessive air leak.

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Patient Application and education

 It is important that the patient and family have been fully informed of the treatment. It can be quite claustrophobic for some patients. Explanations should also include that NIV supports their breathing to give the muscles a rest and allow them time to recover. The machine does not breathe for the patient but gently assists each breath that is taken. As the patient takes a breath in they will feel the flow of air from the machine, then as exhalation occurs there will be some resistance created to help keep the airways open.

Remember patient compliance is a major determinant of success.

 Patient should be sitting upright prior to commencement of treatment.

 Protect the nasal bridge with dressing such as duoderm or Mepitel to prevent pressure sores developing. This is a high risk area. Any existing facial skin condition may also be exacerbated. Check and document skin condition 2 hourly

 When beginning the therapy, the mask should initially be applied using handheld pressure and the pressure levels increased slowly. The use of the ramp setting can aid this by specifying a timeframe in which the pressures are increased. Instruct the patient to take slow deep breaths.

 The mask should be held in position using restraining straps to ensure a tight seal is obtained. If too loose air leaks will occur, if too tight there may be damage to facial tissue.

Ensure the system has quick release strap system and the patient knows how to use them if required.

 Stay with the patient until a regular breathing pattern in established

Ongoing patient monitoring

 To assess the initial effect of NIV, monitor response for decreasing heart rate, respiratory rate, blood pressure and decreasing work of breathing. Patient subjective responses should include feeling more comfortable and breathing easier. Observations should be recorded and monitored regularly as the patient’s condition warrants. At least hourly.

 Monitoring and recording of saturation levels to be done hourly. Remember these levels will show oxygenation but will not show improving/deteriorating CO2 levels.

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 Close attention must be made to oral, facial and eye hygiene. The high flow may cause conjunctivitis and damage to mucosa.

 Monitor arterial blood gases as prescribed

 If patient vomits roll onto side, remove mask immediately and suction patient’s mouth.

 Supplemental oxygen may need to be given during periods when the mask is removed.

 To give nebuliser place the T piece between the mask and the exhalation port. Activate the LEARN key when additional flow is commenced during nebuliser so that the machine is able to compensate

Trouble Shooting

This is a guide as to potential problems and solutions. These alterations must be undertaken in consultation with attending physician.

PERSISTING HYPERCAPNIA

Is chest expansion adequate? Listen to breath sounds and monitor chest expansion. Think of other causes e.g. Mucous plug, pneumothorax.

Reposition patient.

Increase IPAP, especially if the patient is obese or has a chest wall deformity.

Consider decreasing EPAP to increase tidal volume.

Mask/circuit leak? Check all connections secure Is the ventilator synchronous

with the patients breathing cycle?

If not, check circuit.

Increase trigger sensitivity

Increase back-up rate to just below spontaneous breathing rate If spontaneous breathing rate is rapid then decrease rise/ramp time if available

If patient has obstructive sleep apnoea then increase EPAP and consider nasopharyngeal airway

In chronic obstructive pulmonary disease there may be intrinsic PEEP so increase expiratory positive airway pressure

(20)

Rebreathing? Check the exhalation valve is not blocked.

Has the patient got the correct mask insitu.

Is medical therapy optimal?

Have any complications developed?

Refer to consulting physician

Constant Airway secretions? Requiring frequent removal of mask?

Nose mask with chin strap may allow more effective cough.

Anxiety? Sedation may be required but this usually rare.

Cause of anxiety may be due to hypoxia or hypercapnia.

Do they just need longer on NIV?

Continue monitoring and ensure regular medical assessments

PERSISTING HYPOXIA

Is chest expansion adequate? Ensure optimum ventilation as with persistent hypercapnia Consider increase in oxygen percentage.

Reposition patient.

Consider increasing EPAP to prolong ventilation perfusion time.

Urgent re-evaluation of treatment. ? need for escalation of treatment. CALL FOR HELP?

Constant Airway secretions? Requiring frequent removal of mask?

Nose mask with chin strap may allow more effective cough.

Anxiety? Sedation may be required but this usually rare.

Cause of anxiety may be due to hypoxia or hypercapnia.

Is medical therapy optimal? Refer to consulting physician Have any complications

developed?

Refer to consulting physician

Is the ventilator synchronous with the patients breathing cycle?

If not, check circuit.

Increase trigger sensitivity if available

Increase back-up rate to just below spontaneous breathing rate

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Self Assessment

1. Which conditions may require a patient to have BIPAP?

2. Name the 3 processes of respiration in the normal lung

3. Is pneumonia classified as a restrictive or an obstructive respiratory failure?

4. What difference would you expect in the gas results of a patient with Type I and Type II respiratory failure?

5. Give 6 signs of respiratory failure.

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6. Are all patients candidates for Non Invasive Ventilation?

7. List 6 contraindications to the use of Non Invasive Ventilation.

8. Describe EPAP.

9. Discuss six principles of nursing care that you need to undertake when caring for a patient with non invasive ventilation.

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References

1) Mas, A., & Masip, J. (2014). Noninvasive ventilation in acute respiratory failure.

International journal of chronic obstructive pulmonary disease, 9, 837-852.

2) Hess, D. R. (2013). Noninvasive ventilation for acute respiratory failure. Respiratory care, 58(6), 950-972.

3) Brill, S. E., & Wedzicha, J. A. (2014). Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease. International journal of chronic obstructive pulmonary disease, 9, 1241-1252.

4) New South Wales Agency for Clinical Innovation. (2013). Non-Invasive Ventilation for Adult Patients with Acute Respiratory Failure [Poster]. Retrieved from

https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0004/239755/NIV_11112013_A3.pdf

5) Credland, N. (2013, Sep). Non-invasive ventilation in COPD exacerbations. Nursing Times, 109, 16-9, 21. Retrieved from http://search.proquest.com/docview/1436063261 6) National institute of clinical excellence (2010) http://www.nice.org.uk/guidance/qs10 accessed November 2014

7) Respironics V60 users manual

8) British Thoracic Society Guidelines (2008)

9) Drager Instructions for use Evita XL/ Evita XL Neo SW 7.0n (2008)

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References

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