Respiratory failure and respiratory support

Primary purpose of mechanical ventilation:

-To reduce the work of breathing
-To support the gas exchanges
-To buy time for other interventions to revers or treat the cause of respiratory distress
-To permit pharmaceutic depression of the respiratory center during anesthesia or disease state of
depressed consciousness

Respiratory failure is when respiratory system fails in one/ both of its gas exchange function:
Oxygenation and CO2 elimination

4 types of Respiratory failure:

*Type 1 Respiratory Failure- Hypoxemic respiratory failure
-impairment of O2 transfer in the lungs
-Causes:
# V/Q mismatch (ventilation/ perfusion)
# Shunt
# Hypoventilation
# Impaired diffusion
# Reduce O2 supply (Low inspired O2 fraction)

*Type 2 Respiratory Failure- Hypercapnic respiratory failure

-due to absolute or relative hypoventilation
-Causes:
# Increased CO2 production (fever, sepsis, burns, overfeeding)
# Reduced CO2 elimination by alveolar ventilation:
-decreased CNS drive (anaesthesia, overdose, CNS lesion)
-neuromuscular disease (MG, ALS, GBS, myopathies, etc)
-increased work of breathing (WOB) -> respiratory muscle fatigue, inadequate ventilation
-Asthma/ COPD
-Pulmonary fibrosis
-Kyphoscoliosis
-Increased physiologic dead space (hypovolemia, poor cardiac outut, alveolar over distension)

*Type 3 Respiratory failure (Peri operative)

-Causes:
# Atelectasis due to low FRC (functional residual capacity) in abnormal abdomen wall mechanics.
Often results in type 1 or type II respiratory failure.

*Type 4 Respiratory failure (Shock)

-Causes:
# Secondary to cardiovascular instability, who are intubated and ventilated in the process of
resuscitation for shock, and the goal of ventilation is to stabilize gas exchange

**ARDS diagnosis based on Berlin criteria:

Timing: Within 1 week of a known clinical insult or new/worsening respiratory symptoms.
Chest imaging: Bilateral opacities not fully explained by effusion. Lobar/ Lung collapse or nodules
Origin of edema: Respiratory failure not fully explained by cardiac failure or fluid overload. Needs
objective assessment (eg. ECHO) to exclude hydrostatic edema if no risk factor present.
Oxygenation: Mild, moderate, severe based on PaO2/ FiO2 ratio
The PaO2/FiO2 ratio, also known as the P/F ratio, is a clinical tool used to assess the degree of
hypoxemia (low blood oxygen levels) in patients, particularly those with respiratory issues. Here’s
the rationale behind it:

1. **PaO2 (Partial Pressure of Oxygen in Arterial Blood):**

- PaO2 measures the amount of oxygen gas in arterial blood and indicates how well oxygen is
able to move from the lungs to the blood.
- It is obtained through an arterial blood gas (ABG) test.

2. **FiO2 (Fraction of Inspired Oxygen):**

- FiO2 represents the concentration of oxygen in the air mixture that is inhaled by the patient.
Room air has an FiO2 of approximately 21% (or 0.21). When supplemental oxygen is provided,
FiO2 increases.
- It is expressed as a decimal (e.g., 100% oxygen = 1.0, 50% oxygen = 0.5).

3. **P/F Ratio:**
- The PaO2/FiO2 ratio is calculated by dividing the PaO2 by the FiO2. This standardized ratio
allows clinicians to account for the varying levels of supplemental oxygen patients might receive.
- For example, if a patient has a PaO2 of 80 mmHg while breathing 50% oxygen (FiO2 of 0.5), the
P/F ratio would be 160 (80 / 0.5).

4. **Clinical Significance:**
- The P/F ratio helps in assessing the severity of hypoxemia.
- **Normal Values:** A P/F ratio above 300 is generally considered normal.
- **Mild Hypoxemia:** A P/F ratio between 200-300 suggests mild respiratory impairment.
- **Moderate Hypoxemia:** A P/F ratio between 100-200 suggests moderate impairment often
associated with acute respiratory distress syndrome (ARDS).
- **Severe Hypoxemia:** A P/F ratio below 100 suggests severe hypoxemia, also commonly
related to severe ARDS.

5. **Practical Application:**
- The P/F ratio is particularly useful in critical care settings to guide decisions about oxygen
therapy and mechanical ventilation.
- It also helps track the progress and response to treatment in patients with acute lung injury,
pneumonia, sepsis, or ARDS.

By using the P/F ratio, healthcare providers can better understand and manage the oxygenation
status of patients, making it a valuable component in the toolbox for respiratory therapy and
critical care management.

(From GPT-4)

Normal peak inspiratory flow is 20-30L/min

O2 supplemental devices divided into low flow system and high flow system.
Low flow system O2 is therapeutic gas mixture of inspired O2 and ambient air at peak inspiration,
and thus, FiO2 is variable and not easily calculable.
High flow system O2 deliver flow higher than peak inspiratory flow and thus no mixture of O2 with
ambient air and FiO2 is set and fixed

Low flow systems:

Nasal cannula (1-6L/min) (FiO2 24% - 40%)
Face mask (5L-10L/min) (FiO2 35% - 55%)
Non-rebreathing mask (15L/min) (FiO2 80% - 95%)

High flow systems:

Rebreathing mask
Venturi mask (Precise FiO2 24% - 50%)
HFNC (contraindication in nose injury, base of skull injury) (PEEP Effect ~1cmH2O/ 10L/min)
(typical indication in Type 1 respi failure, although it reduces the dead spaces, however first choice
in hypercapnic respi failure is NIV)

NIV (Non-invasive ventilation), mechanical ventilation that doesn’t need an artificial airway (ETT,
tracheostomy)- typically used in hypercapnic COPD, cardiogenic pulmonary edema.

2 Common NIV settings: CPAP and BIPAP

CPAP (Continuous Positive Airway Pressure), works by simply increase the circuit pressure above
atmospheric pressure. Providing positive pressure to keep airway open in obstructive airway,
usually in OSA. In hospital, for hypoxemic respiratory failure in cardiogenic pulmonary edema,
positive intrathoracic pressure reduces LV afterload. Additional support can be provided if pt’s
inspiratory effort was registered, thus CPAP became PSV (Pressure support ventilation)

BIPAP (Bilevel positive airway pressure), cyclical switches between 2 levels of pressure, which in
apneic patient would cause inspiration and expiration, allow patient breath spontaneously. It
increases intrathoracic pressure and also reduce the WOB. Preferred mode in hypercapnic COPD
patients.

When to start NIV:

-Respiratory distress
-Respiratory failure (not corrected by O2 therapy alone)
-PO2/FiO2 <300mmHg [40 kPa] ; 1kPa= 7.5mmHg
-PCO2>45
-pH < 7.35
-disease in which NIV has proven to be effective are AECOPD, hypercapnic acidosis, pulmonary
edema, postoperative respiratory failure
-absence of contraindications

When to terminate NIV and proceed to intubation:

-hemodynamic instability
-decrease level of consciousness
-worsening PH and PaCO2
-worsening PaO2
-tachypnea >30/min
-intense dyspnea
-signs of increased WOB
-inability to clear secretions
-agitation with or intolerance of NIV with progressive respiratory failure

Contraindications of NIV:
-cardiac or respiratory arrest
-inability to keep a patent airway (coma or obtunded metnal status) and/ or to manage secretions
-anatomical abnormalities which prevent interface fitting (facial or upper airway trauma, surgery)
-intractable emesis or GI bleeding
-severe hemodynamic instability

Positive intrathoracic pressure (such as that generated by positive pressure ventilation) can affect
cardiac function, including reducing left ventricular afterload. Here's how this occurs:

1. **Increased Intrathoracic Pressure:**

- When positive pressure is applied to the lungs, either through mechanical ventilation or
positive end-expiratory pressure (PEEP), the pressure within the thoracic cavity increases.

2. **Reduced Venous Return:**

- Higher intrathoracic pressure can compress the great veins (e.g., superior and inferior vena
cava), which reduces venous return to the right heart. Although this might at first seem
counterproductive, it can have a downstream effect that benefits the left heart.

3. **Decreased Transmural Pressure on the Left Ventricle:**

- Transmural pressure is the pressure difference across the wall of the heart chambers. It is
defined as the difference between the internal ventricular pressure and the intrathoracic pressure.
- With positive intrathoracic pressure, the pressure around the heart increases. Since afterload
refers to the pressure the heart must work against to eject blood, an increased external pressure
(intrathoracic pressure) reduces the pressure gradient the ventricle has to overcome. This
effectively decreases left ventricular transmural pressure.

4. **Decreased Left Ventricular Afterload:**

- Left ventricular afterload is the resistance the left ventricle must overcome to circulate blood.
By decreasing the transmural pressure, positive intrathoracic pressure reduces the effective
afterload.
- Lower afterload reduces the workload on the left ventricle, potentially enhancing cardiac
output and reducing the oxygen demand of the myocardium.

5. **Improved Cardiac Performance:**

- With reduced afterload, the left ventricle can eject blood more efficiently. This can be
particularly beneficial in conditions like heart failure, where decreased afterload can aid in better
cardiac performance and reduced myocardial stress.
- Additionally, in patients with compromised left ventricular function, reducing afterload may
prevent further deterioration and support the circulation more effectively.

These physiological changes illustrate why positive pressure ventilation can be a valuable
therapeutic tool in managing patients with certain cardiac conditions. However, it’s important to
balance these effects with the potential downsides, such as reduced venous return leading to
decreased cardiac output in patients with certain vulnerabilities. Close monitoring and adjustment
by healthcare providers are crucial.

Certainly! Let's work through an example calculation of transmural pressure to illustrate how
positive intrathoracic pressure affects the left ventricular afterload.

### Example Calculation

#### Given Data:

1. **Internal Ventricular Pressure (P_internal):**
- Assume during systole (when the left ventricle is contracting) the internal ventricular pressure
is 120 mmHg.

2. **Intrathoracic Pressure (P_intrathoracic):**

- In spontaneous breathing, the intrathoracic pressure is typically negative, around -5 cmH2O
(approximately -4 mmHg when converted to mmHg).

However, let's consider a scenario with positive intrathoracic pressure, such as during
mechanical ventilation, where intrathoracic pressure is elevated, say, +10 cmH2O (approximately
+7.4 mmHg when converted to mmHg).

### Step-by-Step Calculation:

1. **Transmural Pressure (P_transmural):**

- Transmural pressure is defined as the difference between the internal ventricular pressure
(P_internal) and the intrathoracic pressure (P_intrathoracic).

\[
P_{transmural} = P_{internal} - P_{intrathoracic}
\]

2. **Calculate Transmural Pressure in Normal Breathing:**

If P_internal = 120 mmHg and P_intrathoracic = -4 mmHg,

\[
P_{transmural} = 120 \, \text{mmHg} - (-4 \, \text{mmHg}) = 120 \, \text{mmHg} + 4 \, \
text{mmHg} = 124 \, \text{mmHg}
\]

So, the transmural pressure is 124 mmHg.

3. **Calculate Transmural Pressure with Positive Intrathoracic Pressure:**

If P_internal = 120 mmHg and P_intrathoracic = +7.4 mmHg,

\[
P_{transmural} = 120 \, \text{mmHg} - 7.4 \, \text{mmHg} = 120 \, \text{mmHg} - 7.4 \, \
text{mmHg} = 112.6 \, \text{mmHg}
\]

So, the transmural pressure is 112.6 mmHg in this scenario.

### Interpretation:

- **Normal Breathing (Negative Intrathoracic Pressure):**

- Transmural Pressure: 124 mmHg

- **Positive Pressure Ventilation (Positive Intrathoracic Pressure):**

- Transmural Pressure: 112.6 mmHg

In this example, when a positive intrathoracic pressure of +7.4 mmHg is applied, the transmural
pressure decreases from 124 mmHg to 112.6 mmHg. This reduction in transmural pressure
signifies a decrease in the effective afterload that the left ventricle has to overcome to eject blood.
Consequently, this can facilitate the left ventricle's job, potentially improving cardiac output and
efficiency in conditions where the heart might otherwise be struggling. This illustrates how
positive intrathoracic pressure can positively affect cardiac function by decreasing left ventricular
afterload.

(From GPT-4)