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Wednesday, February 17, 2021

Mechanical Ventilation: Indications. Ventilator mode, Settings, Trouble shooting by nurses note

 MECHANICAL VENTILATION 



Although it is a life-saving intervention, mechanical ventilation or intermittent positive pressure ventilation (IPPV) exposes the patient to a large number  of potential risk and complications. These include the effects of positive intra-thoracic and intra-pulmonary pressure (barotrauma, decreased venous return ) and the increased risks associated with endotracheal intubation. Nurses must be fully aware of these risks and understand how to reduce them in order to protect the patient. 

Indications for mechanical ventilation 

  • To support acute ventilatory failure. 
  • To reverse life-threatening hypoxaemia. 
  • To decrease the work of breathing. 
Causes of acute ventilatory failure 

  • Respiratory centre depression- decreased conscious level, intra-cerebral events, sedative or opiate drugs.
  • Mechanical disruption- flail chest (multiple rib fractures resulting in a free segment of chest wall), diaphragmatic trauma, pneumothorax, pleural effusion. 
  • Neuromuscular disorders - acute polyneuropathy, myasthenia gravis, spinal cord trauma or pathology, Guillain Barr'e syndrome, critical illness. 
  • Reduced alveolar ventilation-airway obstruction (foreign body, bronchoconstriction, inflammation, tumour), atelectasis, pneumonia, pulmonary oedema ( cardiac failure and ARDS) , obesity, fibrotic lung disease. 
  • Pulmonary vascular disruption-pulmonary embolus, ARDS,  cardiac failure. 
Causes of hypoxaemia 

  • V/Q mismatch-pulmonary embolus, obstruction of the pulmonary microcirculation, ARDS.
  • Shunt-pulmonary oedema, pneumonia, atelectasis, consolidation. 
  • Diffusion (gas exchange ) limitation - pulmonary fibrosis, ARDS, Pulmonary oedema. 
Causes of increased work of breathing 

  • Airway obstruction.
  • Reduced respiratory compliance. 
  • High CO2 production (e.g. due to burns, sepsis, overfeeding ).
  • Obesity. 
Physiological effect of mechanical ventilation. 

IPPV has significant effects the respiratory, cardiac, and renal systems, These are principally related to increased intra-thoracic pressure and its effect on normal physiological responses.

Decreased cardiac output and venous return 

Increased intra-thoracic pressure reduce venous return (the passive flow of blood from central veins to the right atrium) and increases right ventricular afterload (the resistance to blood flow out of the ventricle by the pulmonary circulation ). This reduce right ventricular output and consequently ventricular filling and ultimately output. The use of PEEP means that this occurs throughout the respiratory cycle. 

Effects - hypotension, tachycardia, hypovolemia, decreased urine output. 

Management - fluid loading to optimize stroke volume and cardiac  output. Inotropes may be necessary if cardiac function is compromised. 

Increased incidence of barotrauma

The pressure required to deliver gas to the alveoli through airways which may be resistant to gas flow can cause damage to more compliant areas through over-distension. Greater damage is caused at higher tidal volumes, causing gas to escape into the pleura and interstitial tissues. Up to 15% of patients develop barotrauma. The risk is particularly high in conditions with increased airway resistance due to bronchoconstriction, such as asthma. 

  • Effects-pneumthorax, pneumomediastinum, subcutaneous emphysema. 
  • Management-tidal volume that are close to physiological values (e.g. 6-8 mL/kg ). Avoid high airway pressures, if necessary by manipulating the inspiratory:expiratory (I:E) ratio. Chest drain management of pneumothorax is required. 
Ventilator associated pneumonia 

Ventilator-associated pneumonia (VAP) develops 48 h or later after commencement of mechanical ventilation via endotracheal tube or tracheostomy. It develops as a result of colonization of the lower respiratory tract and lung tissue by pathogens. Intubation compromises the integrity of the oropharynx and trachea, allowing oral and gastric secretions to enter the airways. 

VAP is the most frequent post-admission infection in critical care patients, and significantly increases the number of mechanical ventilation days, the length of critical care stay, and the length of hospital stay overall. Patients at increased risk include those who are immunocompromised, the elderly, and those with chronic illnesses (e.g. lung disease, malnutrition, obesity ).

Diagnosis of VAP is difficult due to the number of differential diagnosis that present with the same signs and symptoms (e.g. sepsis, ARDS, Cardiac failure, lung atelectasis). Radiological changes include consolidation and new or progressive infiltrate. Clinical signs include pyrexia >38°c, raised or reduced white blood cell (WBC) count, new-onset purulent sputum, increased respiratory secretions / suctioning requirements, and worsening gas exchange. Microbiology criteria include a positive blood culture growth not related to any other source, and positive cultures from bronchoalveolar lavage. 

Use of care bundle approach has been demonstrated to be an effective preventive strategy. The department of Health has established a care bundle with six elements for the prevention of ventilator-associated pneumonia, which should be reviewed daily. 

  • Elevation of the head of the bed- the head of the bed is elevated to 30-45° (unless contraindicated)
  • Sedation level assessment- unless the patient is awake and comfortable, sedation is reduced or held for assessment at least daily (unless contraindicated ).
  • Oral hygiene- the mouth is cleaned with chlorhexidine gluconate (≥ 1-2% gel or liquids ) 6-hourly. Teeth are brushed 12 hourly with standard toothpaste. 
  • Peptic Ulcer prophylaxis 
  • Proper Hand hygiene 
  • DVT prophylaxis 
Modes of mechanical ventilation 

Controlled mechanical ventilation (CMV)

There is a set frequency of patient breaths delivered as either pressure controlled (with a set inspiratory pressure ) or volume controlled ( with a set tidal volume ).

Synchronized intermittent mandatory ventilation (SIMV) 

There is a set frequency of patient breath, but this mode of ventilation allows spontaneous breath to be taken in between. Ventilator breaths are synchronized to these spontaneous breath, and can be pressure controlled (SIMV-PC)  or volume  controlled (SIMV -VC). The current trend is for pressure-controlled ventilation in order to control pressure and limit potential barotrauma.

Volume controlled ventilation

The set tidal volume is delivered at a constant flow rate,resulting in changes to airway pressure through inspiration. The set tidal volume remains constant as lung compliance and resistance change. A high inspiratory flow rate delivers the set tidal volume more quickly. Therefore if ventilation is time cycled and the set tidal volume more quickly. Therefore if ventilation is time cycle and the set tidal volume has been reached before the end of inspiration, there will be a pause before expiration and the airway pressure will drop. High inspiratory flow rate will also elevate the peak airway pressure will drop. High inspiratory flow rates will also elevate the peak airway pressure. Therefore low inspiratory flow rates are recommended to keep the peak airway pressure as low as possible. Pressure-limited, volume controlled ventilation ensures that the tidal volume delivered is as close as possible to the set tidal volume for the pressure limit ( e.g. 30-35 cmH2O)

Pressure -controlled ventilation (PCV)

Set pressures throughout the inspiratory and expiratory cycle are delivered a decelerating flow rate, resulting in a tidal volume that varies with lung compliance and resistance. Common pressure controlled mode which also allow for pressure supported spontaneous breaths include BIPAP, PCV +, DuoPAP, BiLevel and Bi-vent  terms and abbreviations depend on the trademark name of the specific ventilator being used)

Pressure support ventilation (PSV)

A set level of inspiratory pressure support or tidal volume is delivered  when the patient triggers a breath. The tidal volume of each breath is dependent on ling compliance and respiratory rate. In addition, a back-up rate of breaths will occur if the patient does not initiate (trigger), breaths at the required rates. PSV ids used to provide ventilator support ( e.g when the patient's own respiratory efforts are diminished). This mode reduces the requirement for sedation, allows ongoing use of respiratory muscles, and provides the opportunity to gradually reduce the level of support to facilitate weaning. Pressure supported breaths can also be added into other modes which allow for spontaneous over and above the set mandatory controlled breaths (e.g. SIMV,BIPAP).

Mechanical ventilator settings

Respiratory rate (breath/min)

Typically respiratory rate is 10-15 breath/min. but it may be altered in order to optimize minute volume and /or PCO2

Tidal Volume (VT) (mL/kg)

Typically this is in range 6-8 mL/kg, but it may be altered to optimize minute volume and/or PCO2.

Minute Volume (MV or VE) (L/min)

Typically this is in the range 3-10 L/min. It is derived from tidal volume and respiratory rate.

Flow rate (V) (L/min)

Typically this is in the range 40-80 L/min, and adjusted to ensure that tidal volume is achived within inspiratory time. A decelerating flow pattern is always seen in pressure support modes.

Positive end expiratory pressure (PEEP) (cmH2O)

Typically this is in the range 5-10 cmH2O.

Airway pressure (cmH2o)

Typically plateau pressure is limited to < 30 cmH2O in order to reduce barotrauma.

Pressure support/assist (cmH2O)

Typically this is in the range 5-20 cmH2O, set according to patient requirements for assistance.

Inspiratory:expiratory (I:E) ratio

Typically this is 1;2 (i.e expiratory time is twice as long as inspiratory time). It may vary with extended or inverted ratios in order to increase time for inspiration in patients with severe airflow limitation (e.g. due to asthma), or to assist expiration by lengthening expiratory time and avoid trapping.

Trigger

This can be flow based, pressure based, volume based, or time based, and is vital for reducing the delay between the initiation of a breath and the ventilator response and thus the patients work of breathing.

  • Flow based triggers require the patient to produce a minimum flow rate of 1L/min to initiate  a breath.
  • Pressure-based triggers require the patient to generate a negative pressure of -1 to -10 cmH2O to initiate a breath.
  • Volume-based triggers requires the patient to inhale a certain volume of gas to initiate a breath.
  • Time-based triggers are independent of the patient effort, with preset frequency and delivered at regular intervals of time.
Pressure volume relationship

pressure-volume loops can be viewed graphically on most  modern ventilators, and the information obtained can be used to inform ventilators settings, such as PEEP and upper airway pressure limits.

Ventilator parameters and initial settings

  • respiratory rate: 10-15 breaths/min
  • Tidal Volume; 6-8 mL/kg
  • Positive end expiratory pressure: 3-10 cmH2O
  • Peak airway pressure: ≤35 cmH2O
  • Inspiratory and Expiratory ratio: 1:2
  • Oxygen ( adjusted to blood gas results); 0.4-0.6 FiO2
The pressure-volume relationship in a ventilator breath consists of three stages

  • Initial increase in pressure with little change in volume
  • linear increase in volume as pressure increase
  • pressure increase with no further volume increase.
The inflection points represent the change between the different stages of the ventilator breath

Lower inflation point

This occurs between stages 1 and 2, and is the point at which airway resistance is overcome, allowing alveolar opening. In a patient who is fully ventilated and making little or no respiratory effort, the lower inflection point is the point at which lower airways would close on expiration. PEEP should therefore be set at this level to avoid gas trapping.

Upper inflection point

This occurs between stages 2 and 3, and is the point at which ling capacity for the breath has been reached. It can be used to adjust settings for maximum inspiratory pressure.

Protective lung ventilation

Protective lung ventilation is the current standard of care of mechanical ventilation for both ARDS and non-ARDS patients. Features include permissive hypercapnia, lower plateau pressures, and low tidal volume ventilation (4-8mL/kg) ( ideal body weight, not actual body weight).

Ideal body weight

  • Male patients: 50 kg + 2.3 kg for each inch over 5 feet.
  • Female patients: 45.5 kg + 2.3 kg for each inch over 5 feet.



Mechanical ventilation  trouble shooting 

The patient is highly vulnerable to number of problems while dependent on a mechanical ventilator. The critical care nurse is responsible for the patient"s safety, and it is his or her responsibility to ensure that any problems are recognized as soon as possible and dealt with in  an effective and timely manner.

Troubleshooting problems in the ventilate patient

High airway pressure: airway pressure alarm sounds, persistent rise in peak airway pressure, evidance of patient distress, haemodynamic instability.

Life threatening causes

  • Endotracheal tube (ETT) and / or ventilator tubing obstruction.
  • Peneumothorax
  • Severe bronchospasm.
Other causes

  • Build up of airway secretions
  • Asynchrony with mechanical ventilation ( tidal volume too high)
  • Patient coughing
  • ETT displacement
Interventions

  • Ascertain causes of high airway pressure and treat accordingly.
  • Consider manual ventilation if a patient is in respiratory distress
  • Emergency re-intubation
  • Review ventilator settings 
  • Check tubing and filter integrity
  • Auscultate lungs for abnormal breath sound.
  • Perform suction.
  • Check arterial; blood gas and treat accordingly
  • Review sedation if an increase with  or without paralysis is indicated.
Low airway pressure: pressure alarm sounds, audible air leak, decreased minute volume, evidence of patient distress, haemodynamic instability

Life threatening causes

ETT and /or ventilator tubing disconnection or leak.

Intervention
  • Ascertain cause of low airway pressure and treat accordingly.
  • Consider manual ventilation if patient is in respiratory distress.
  • Emergency re-intubation.
  • Check connections
  • Check tubing integrity.
  • Check cuff pressure.
  • Review ventilator settings.
  • Auscultate lungs for abnormal breath sounds.
  • Perform suction.
  • Check arterial blood gas and treat accordingly.
  • Review sedation if an increase with or without paralysis is indicated.
Low minute volume; Low MV alarm sounds, audible leak, evidence of patient distress, haemodynamic instability.

Life threatening causes
  • Disconnection from the ventilator.
  • Asynchrony with mechanical ventilation (i.e flow rate may be low to allow set volume in time allocated by set respiratory rate)
  • Air leak via chest drain.
intervention
  • Ascertain cause of low minute volume and treat accordingly.
  • Consider manual ventilation if patient is in respiratory distress
  • Emergency re-intubation
  • Check cuff pressure
  • Review ventilator settings (increase to compensate for chest drain)
  • Auscultate lungs for abnormal breath sounds.
  • Check arterial blood gas and treat accordingly.
  • Review sedation if an increase with or without paralysis is indicated.
High minute volume: high MV alarm sounds, evidence of patient making respiratory effort.

Effects
  • ventilator malfunction
  • Asychrony with mechanical ventilation ( patient making respiratory effort)
Interventions
  • Check causes of patient's tachypnoea ( e.g. pain hypoxia, hypercapnia)
  • Review ventilator settings.
Auto PEEP (intrinsic , air trapping); failure of alveolar pressure to return to zero at the end of exhalation, causing increased resistance to airflow and increased work of breathing.

Causes
  • Incomplete or impeded exhalation, as a result of either high MV ( > 10 L/min) or airway resistance(due to chronic pulmonary disease)
Interventions
  • Ensure low-compressible-volume ventilator tubing is used.
  • Review ventilator settings to reduce MV by decreasing respiratory rate or altering respiratory flow rate to decrease inspiratory time and increase expiratory time.
  • Reduce metabolic workload to reduce respiratory demand.







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