Resp - Ventilation

Question 1

How can non-invasive ventilation be delivered?

Answer 1

• Using dedicated non-invasive ventilators.
• Using NIV modes on conventional ICU ventilators.
• Delivered via nasal masks (either covering the nose, or nasal cushions placed into the nostrils), full-face masks which may cover the nose or mouth or may literally cover the whole face.
• Helmets: similar to but stiffer than CPAP helmets
• Non-invasive ventilation can also be delivered via a cuirasse or iron lung

Question 2

In what situations may non-invasive ventilation be beneficial?

Answer 2

• NIV reduces the need for tracheal intubation and invasive ventilation in acute exacerbations of COPD, cardiogenic pulmonary oedema and ventilatory failure in the immunocompromised patient.
• Intervention to avoid of re-intubation in patients who have recently been extubated after a period of mechanical ventilation.
• Elective weaning strategy in patients who are difficult to wean from invasive ventilation.
• Prophylactic use to reduce post-operative atelectasis.
• Palliation: breathlessness and symptoms of CO2 retention in patients with MND with a max
  inspect mouth pressure worse than 40cmH2O and without severe bulbar involvement or
  MND.

Question 3

Where is NIV contraindicated?

Answer 3

• Impaired level of consciousness: inability to protect airway. May be used if due to high CO2 which may recover.
• Severe confusion,
• Copious secretions,
• Patients with facial injuries or burns.
• High risk vomiting/bowel obstruction.
• Unstable head and neck: may lose airway if head topples to one side. Try soft collar in this situation.
• Upper GI surgery: controversial.

Question 4

What settings are effective?

Answer 4

• Normally initially set in terms of IPAP or EPAP at pressures of 10 and 5 respectively.
• Can be increased to 20 IPAP, above which point leakage is common
• Adjustment of face mask straps to achieve a better seal may involve slackening straps to
  avoid distortion

Question 5

When is NIV more likely to fail?

Answer 5

• Hypoxia.
• Unilateral white out from consolidation.
• Persistent metabolic acidosis.
• Poor mask fit: may cause facial ulceration and high delivery pressures.
• Failure to improve @ 4 hours: plan B, review options for invasive ventilation.

Question 6

What are the main variables that we can control in mechanical ventilation?

Answer 6

-Flow
-Volume
-Pressure

Question 7

What are the four phases of each breath? What are the phase variables

Answer 7

Each breath has four phases: the initiation phase, inspiratory phase, plateau phase and the expiratory phase.

Each phase has a variable which controls how it starts, how it proceeds, and how it finishes.

-TRIGGER:
The variable controlling the initiation phase; controls how and by whom the breath is initiated

• LIMIT:
  The variable controlling the inspiration phase
• CYCLING:
  The variable controlling when the breath changes from an inspiration to an expiration.
• PEEP:
  The variable controlling what pressure is applied at the end of expiration: Positive End-Expiratory Pressure.

Question 8

What is Plateau Pressure

Answer 8

PLATEAU PRESSURE is the relationship between volume and compliance. It is the pressure measured on an inspiratory hold. It is the pressure at the end of inspiration, which in the absence of flow, and removal of airway resistance, is essential alveolar pressure.

Airway pressure = (resistance of airways) + (alveolar pressure)

The alveolar pressure should not get above 30 cmH2O.

Question 9

What is Alveolar Pressure?

Answer 9

Volume/compliance + PEEP

Question 10

What is Airway pressure?

Answer 10

Flow x Resistance + Vol/Compliance + PEEP

Question 11

How does PEEP improve oxygenation?

Answer 11

• Increasing lung volume by recruiting collapsed alveoli (thereby reducing the intrapulmonary shunt)
• Pushes alveolar oedema fluid out of the alveoli and into the interstitium

Question 12

How does PEEP reduce the work of breathing?

Answer 12

Supplies the pressure required to overcome airway obstruction
- Supplies the pressure required to overcome Intrinsic PEEP

Question 13

What is a shunt?

Answer 13

Shunt is the percentage of blood passing through the lungs which doesnt get oxygenated.

Question 14

What is the effect of PEEP on preload?

Answer 14

Increased intrathoracic pressure, thus
o Decreased venous return,
o Thus reduced left ventricular stroke volume
o Thus reduced left ventricular contractility
o Thus reduced left ventricular oxygen demand
o If the left ventricle is decompensating because it is overfilled and overstretched ( “congestive” heart failure) the decreased preload will push it back into the more efficient area of the Frank Starling curve.

Question 15

What are the effects on RV afterload?

Answer 15

Increased intrathoracic pressure = increased pulmonary artery pressure, thus
o Increased right ventricular afterload
o Thus, increased right ventricular work and thus oxygen demand
o With a crappy right ventricle, this could really impair the left ventricular function- the left ventricle depends on the right for filling.

Question 16

What are the effects of LV afterload?

Answer 16

Left ventricular afterload = sum of systemic arterial resistance and left ventricular
transmural pressure.
- Increased intrathoracic pressure = increased transmural pressure i.e. the pressure generated by the left ventricle = (pressure generated by LV muscle ) +(pressure added to it by the PEEP)
- In normal people, that contribution is tiny.
o Remember, PEEP of, say, 10cmH2O is equal to 7.35 mmHg
o In normal people, the left ventricle generates a systolic ejection pressure of about 80mmHg – and that’s just to open the aortic valve. If your left ventricle is diseased, it cant pump effectively against the afterload, and
pulmonary oedema ensues.
o If pulmonary oedema ensues, the lung volume and lung compliance drop.
o If the lung volume and compliance drop, the respiratory effort must generate lower pressures to suck more air in
o The lower pressures decrease the transmural pressure, and thus increase the relative afterload.
o The increased afterload causes more pulmonary oedema. Thus, by reducing the afterload-increasing effects of increased respiratory effort, PEEP it cant pump effectively against the afterload, and pulmonary oedema ensues.

Question 17

How can PEEP affect other organs?

Answer 17

• reduced urine output due to decreased cardiac output, if your patient is already volume depleted
• decreased splanchnic blood flow due to decreased cardiac output, etc etc
• increased hepatic venous congestion due to decreased venous return to the heart
• increased INTRACRANIAL PRESSURE due to decreased venous return to the heart
• Decreased peribronchial lymphatic flow could actually decrease the rate of oedema removal, not to mention clearance of necrotic debris in pneumonia.

Question 18

What are some of the contraindications to PEEP?

Answer 18

o Tension Pneumothorax - it will get worse
o Hypovolemic shock – cardiac output will decrease
o Bronchopleural fistula - it wont heal
o High intracranial pressure - it will get higher

Question 19

What is dead space?

Answer 19

Dead space can be defined as a volume of gas which does not take part in gas exchange.

Dead space can be classified into 3 types

Anatomical dead space
This includes any breathing system or airway plus mouth, trachea and the airways up until the start of the respiratory zone. The typical volume in an adult is about 150mls (See section 1)

Alveolar dead space
This occurs when areas of the lung are being ventilated but not being perfused and this leads to what is known as V/Q mismatch.
Large increases in alveolar dead space commonly occur in the following conditions: pneumonia, pulmonary oedema, pulmonary embolism

Physiological dead space
This is a combination of alveolar and anatomical dead space added together.
Dead space is usually 30% of VT

Question 20

How is breathing controlled?

Answer 20

Central control

The mechanism by which respiration is controlled is complex. There is a group of respiratory centres located in the brainstem producing automatic breathing activity. This is then regulated mainly by input from chemoreceptors. This control can be overridden by voluntary control from the cortex. Breath-holding, panting or sighing at will are examples of this voluntary control.

The main respiratory centre is in the floor of the 4th ventricle, with inspiratory (dorsal) and expiratory (ventral) neurone groups. The inspiratory neurones fire automatically, but the expiratory ones are used only during forced expiration. The two other main centres are the apneustic centre, which enhances inspiration, and the pneumotaxic centre, which terminates inspiration by inhibition of the dorsal neurone group above.

The chemoreceptors that regulate respiration are located both centrally and peripherally. Normally, control is exercised by the central receptors located in the medulla, which respond to the CSF hydrogen ion concentration, in turn determined by CO2
, which diffuses freely across the blood-brain barrier from the arterial blood. The response is both quick and sensitive to small changes in arterial pCO2 (PaCO2). In addition, there are peripheral chemoreceptors located in the carotid and aortic bodies most of which respond to a fall in O2 , but some also to a rise in arterial CO2.

The degree of hypoxia required to produce significant activation of the O2 receptors is such that they are not influential under normal circumstances, but will do so if profound hypoxia (PaO2 < 8kPa) occurs, for example at high altitude when breathing air (see later in Special circumstances).

Question 21

What are the benefits of prone ventilation?

Answer 21

Optimisation of V/Q matching

Increase in FRC

Decreased atelectasis

Facilitates secretion drainage

Heart sits against the sternum (rather than left lung), therefore the lung is less compressed

Decreased transpleural pressure gradient between dependent and non-dependent lung in the prone position

Plateau pressure is more uniformly distributed when prone -> more uniform alveolar ventilation

Recruitment manoeuvres have been shown to be more effective in the prone position

Alterations in chest wall mechanics -> allowing lungs to inflate at lower pressures

Dorsoventral orientation of large airways

Question 22

What are some of the Absolute CI to ECMO

Answer 22

Progressive non-recoverable cardiac disease (not transplant candidate)

Progressive and non-recoverable respiratory disease (irrespective of transplant status)

Chronic severe pulmonary hypertension

Advanced malignancy

Graft versus Host disease

Weight >120kg

Unwitnessed cardiac arrest

Question 23

What are some of the Relative CI for ECMO?

Answer 23

Age > 75 years

Multi-trauma with multiple bleeding sites

CPR > 60 minutes

Multiple organ failure

CNS injury