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Cardiovascular & Respiratory Medicine > Respiratory failure > Flashcards

Respiratory failure Flashcards

1
Q

What is respiratory failure?

A

Syndrome of inadequate gas exchange due to dysfunction of one or more components of the respiratory system

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2
Q

Describe the process of oxygen loading in the lungs

A
  1. Blood flows through the alveolar capillary (lining the alveolar)
  2. Oxygenation occurs through the alveolar- capillary membrane barrier (v. thin)
  3. Oxygen is taken up by the erythrocytes (RBCs)
  4. CO2 also will flow from a higher conc in your blood across into the alveolous to be excreted (down the conc gradient)
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3
Q

What is meant by “pulmonary transit time”?

A

“time taken for oxygenation to occur”
- in some disease (e..g lung infection)
- the barrier is wider;
- Diffusion is less efficient
- transit time increases

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4
Q

compare the “pulmonary transit time” with the “gas exchange time”

A

Gas exchange time is less (occurs faster);
- Exchange of CO2 happens much faster
- goes down much larger conc gradient
- CO2 excreted more rapidly

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5
Q

Describe the ventilation/ perfusion ratio at the top of the lungs

A

The apex (zone 1) of the lung has a higher V/Q ratio
- Very low perfusion (wasted ventilation)
= less ventilation (less perfusion than ventilation)

  1. GRAVITY:
    - reduced blood flow to the apex
    = wasted ventilation; not enough blood for gas exchange
  2. ALVEOLI SIZE:
    - Alveoli larger (but less compliant; don’t expand)
    - less blood flow
    - decreased pulmonary intravascular pressure
    = less perfusion
    - less ventilation
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6
Q

Describe the ventilation/ perfusion ratio at the base of the lungs?

A

The base (zone 3) of the lung has a lower V/Q ratio
- more ventilation
- much more perfusion (not enough air to match the O2 from the blood= wasted perfusion)

  1. GRAVITY:
    - increased blood flow
    - increased perfusion
  2. ALVEOLI SIZE:
    - smaller alveoli (more compliant; expand)
    - increased blood flow
    - higher intravascular pressure
    = more perfusion
    - more ventilation
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7
Q

describe the change in alveolar and arterial pressure in zones 1,2 and 3

A

Zone 1:
- PA>Pa>Pv
(pressure in the alveolar A is higher than the arterial pressure a)
- poor perfusion= poor ventilation
- if pulmonary pressure drops no gas exchange takes place= dead space

Zone 2:
Pa>PA>Pv
- ventilation and perfusion fairly well matched (both good)

Zone 3:
Pa>Pv>PA
-(pressure in the arterial is higher than the alveolar pressure)
- increased perfusion

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8
Q

What is meant by “tidal volume”?

A

Tidal volume is the amount of air breathed in with each normal breath

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9
Q

What is “inspiratory reserve volume”?

A

Inspiratory reserve volume is the maximum amount of ADDITIONAL air that can be taken into the lungs after a normal breath. (additional air; does not include tidal volume)

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10
Q

What is meant by “inspiratory capacity”?

A

The maximum volume of air that can be inspired after reaching the end of a normal, quiet expiration
(IC= IRV + TV)
usually= 3600 ml

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11
Q

What is meant by “Expiratory reserve volume”?

A

Expiratory reserve volume is the maximum amount of ADDITIONAL air that can be forced out of the lungs after a normal breath. (additional; does not include tidal volume)

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12
Q

What is meant by “residual volume”?

A

Residual volume is the amount of air that remains in a person’s lungs after fully exhaling.
- Lungs don’t completely empty
- that would cause them to collapse

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13
Q

What is meant by “vital capacity”?

A

Vital capacity (VC) refers to the maximal volume of air that can be expired following maximum inspiration
VC= IRV + TV + ERV

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14
Q

What is meant by “functional residual capacity”?

A

Functional residual capacity (FRC), is the volume remaining in the lungs after a normal, passive exhalation
FRC= ERV + RV

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15
Q

What is “total lung capacity”?

A

The total lung capacity (TLC) is the maximal volume of gas in the lungs after a maximal inhalation:
TLC= IRV + TV +ERV +RV

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16
Q

What is “minute ventilation”? how is it worked out?

A

“Gas entering and leaving the lungs”
Minute ventilation (L/min)=
Tidal volume (L) x breathing frequency (breaths/ min)
usually= 6L/min

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17
Q

What is “alveolar ventilation” how is it worked out?

A

“Gas entering and leaving the alveoli”
Alveolar ventilation (L/min)=
[Tidal volume (L) - Dead space (L)] x breathing frequency (breaths/ min)
usually= 4.2 L/ min

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18
Q

What is meant by dead space?

A

the volume of ventilated air that does not participate in gas exchange- just oscillating to keep the airway open

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19
Q

What is meant by “compliance”? how is it worked out?

A

“The tendency to distort under pressure”
Compliance= change in vol in airway/ change in pressure needed to do so

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20
Q

What is meant by “elastance”? how is it worked out?

A

“The tendency to recoil to its original volume”
Elastance= change in pressure/ change in vol

21
Q

What is the difference between acute and chronic respiratory failure?

A

Acute respiratory failure is a short-term condition. It occurs suddenly and is typically treated as a medical emergency. Chronic respiratory failure is an ongoing condition. It develops gradually and requires long-term treatment

22
Q

What are some example of acute respiratory failure?

A
  1. Pulmonary:
    - Infection
    - aspiration
    - Pulmonary embolus
    - Haemoptysis
    - Primary graft dysfunction (Lung Tx)
  2. Extra-pulmonary:
    - Trauma
    - New medications
    - pancreatitis
    - sepsis
  3. Neuro-muscular:
    - Myasthenia/GBS
23
Q

What are some examples of chronic respiratory failure?

A
  1. Pulmonary/Airways:
    - COPD
    - Lung fibrosis
    - CF
    - lobectomy
  2. Musculoskeletal:
    - Muscular dystrophy
24
Q

What is meant but acute-on-chronic respiratory failure?

A

Acute-on-chronic respiratory failure (ACRF) occurs when relatively minor, although often multiple, insults cause acute deterioration in a patient with chronic respiratory insufficiency

25
Q

What are some examples of acute-on-chronic respiratory failure?

A
  1. Infective exacerbation
    - COPD
    - CF
    - Myasthenic crises
  2. Post operative
26
Q

What is Type 1 resp failure?

A

“type 1 or hypoxemic”
- failure of oxygen exchange
examples:
* Collapse
* Aspiration
* Pulmonary oedema
* Fibrosis
* Pulmonary embolism
* Pulmonary hypertension

27
Q

What is type II resp failure?

A

Type 2 respiratory failure occurs when the respiratory system cannot adequately remove carbon dioxide from the body, leading to hypercapnia
examples:
- issues in the Nervous system
- intramuscular issues
- muscle failure
- airway obstruction
- chest wall deformity

28
Q

What is type III resp failure?

A

Type 3 respiratory failure results from lung atelectasis. Because atelectasis (a complete or partial collapse of the lung) occurs so commonly in the perioperative period, this form is also called perioperative respiratory failure.
- Hypoxaemia or hypercapnoea
- PREVENTION:
* anesthetic or operative technique
* posture
* incentive spirometry
* analgesia
* attempts to lower intra- abdominal pressure

29
Q

What is type IV resp failure?

A

Type 4 respiratory failure results from hypoperfusion of respiratory muscles as in patients in shock.
(Septic/cardiogenic/neurologic)

Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic shock). Lactic acidosis and anemia can also result in type 4 respiratory failure
PREVENTION:
- Optimise ventilation improve gas exchange and to unload the respiratory muscles, lowering their oxygen consumption
- Ventilatory effects on right and left heart=
Reduced afterload (good for LV) Increased pre-load (bad for RV)

30
Q

What are the risk factors for acute resp failure?

A
  • Infection
  • Viral
  • Bacterial
  • Aspiration
  • Trauma
  • Pancreatitis
  • Transfusion
31
Q

What are the risk factors for chronic resp failure?

A
  • COPD
  • Pollution
  • Recurrent pneumonia
  • Cystic fibrosis
  • Pulmonary fibrosis
  • Neuro-muscular diseases
32
Q

What is ARDS?

A

ARDS happens when the lungs become severely inflamed from an infection or injury. The inflammation causes fluid from nearby blood vessels to leak into the tiny air sacs in your lungs, making breathing increasingly difficult. The lungs can become inflamed after: pneumonia or severe flu

33
Q

what are the causes of ARDS?

A

Pulmonary:
- Aspiration
- Trauma
- Burns: Inhalation
- Surgery
- Drug Toxicity

Extra- pulmonary:
- Trauma
- Pancreatitis
- Burns
- Transfusion
- Surgery
- BM transplant
- Drug Toxicity
MECHANISMS UNKNOWN

34
Q

What changes are seen in alveolar during acute lung injury?

A
  • The alveolar epithelium (lining of the vascular supply) inflamed/ injured
  • Increased neutrophils (secondary inflammation)
  • Macrophages produce IL-6, IL-8 (drive the secondary response)
35
Q

how does pulmonary transit time change with acute

A
  • Gas exchange & pulmonary transit time is much less efficient/ larger following damage
36
Q

How can you test for/ evidence of ARDS?

A

Injury= cell death
- TNF signalling (TNFR-1: TNFR1 plays a major role in maintaining immune homeostasis by promoting apoptosis)
- Macrophage activation: alveolar
- Neutrophil lung migration
- DAMP release: HMGB-1 and RAGE
- Cytokine release IL-6,8,IL-1B, IFN-y
- Necrosis in lung biopsies
- Apoptotic mediators: FAS, FAS-l, BCl-2

37
Q

What pharmacological interventions are used to treat ARDS?

A
  • Steroids
  • Salbutamol
  • Surfactant
  • N-Acetylcysteine
  • Neutrophil esterase inhibtitor
  • GM-CSF
  • Statins
38
Q

What therapeutic interventions are used to treat respiratory failure?

A

Treat underlying disease:
* Inhaled therapies
-Bronchodilators
- Pulmonary vasodilators
* Steroids
* Antibiotics
* Anti-virals
* Drugs
- Pyridostigmine
- Plasma exchange
- IViG
- Rituximab

Resp support:
- Physiotherapy
- Oxygen
- Nebulisers
- High flow oxygen
- Non invasive ventilation
- Mechanical ventilation
- Extra-corporeal support

Multiple organ support:
- Cardiovascular support
* Fluids
* Vasopressors
* Inotropes
* Pulmonary vasodilators
- Renal support
* Haemofiltration
* Haemodialysis
- Immune therapies
* Plasma exchange
* Convalescent plasma

39
Q

What options are considered to treat severe ARDS?

A
  • Increasing PEEP: A positive expiratory pressure (PEP) mask is a facial mask connected to a breathing valve which creates resistance on exhalation (breathing out) to help remove secretions (phlegm) from the lungs
  • Prone positioning
  • Inhaled pulmonary vasodilators & extracorporeal membrane oxygenation (as last resort)
40
Q

What specific interventions are used to treat ARDS?

A
  • Resp support
  • Intubation and ventilation
  • ARDS necessitates mechanical intervention
  • Types of ventilation:
  • Volume controlled (going in/ out of lungs)
  • Pressure controlled
  • Assisted breathing modes (patient triggers the breaths themself)
  • Advanced ventilatory modes
41
Q

How does the pressure volume loop of the lungs change with ARDS?

A
  • Compliance (= volume/pressure) is reduced in the injured lung compared to normal
  • lungs smaller/ more dense
  • increased work needed to open alveoli
  • increased stress on walls;
  • we use the positive inspiratory pressure peak to help the airways open
42
Q

Describe the mechanism for ventilator induced lung injury

A
  • Patients on ventilators are at risk of injury
  • if air takes a long time to leave their lungs= damage
  • you need to give them a long expiratory time on a ventilator
  • if not: air remains in the lungs
  • “gas trapping”
    = exhalation gets terminated
43
Q

What imaging is used to view the lungs?

A
  • CT scans (black areas= air, white= blood)
    Lung USS (ultrasounds)
44
Q

How do we test for lung injury in ARDS?

A

Murray score= average score of these 4 parameters:
PaO₂/FiO₂ ratio
CXR
PEEP
Compliance (ml/cm H₂O)

0 = normal
1-2.5 Mild
2.5 Severe
3 -> ECMO

45
Q

What is the national approach to ARDS?

A
  1. Telephone or online referral (if murray score > 3, pH < 7.2)
  2. Consultant case review
  3. Transfer of imaging
  4. Advice
  5. Retrieval
  6. Transfer
  7. Ongoing management
46
Q

What is the criteria for treatemnt of ARDS?

A

Inclusion Criteria:
* severe respiratory failure
non-cardiac cause (i.e. Murray Lung Injury score 3.0 or above)
* Positive pressure ventilation is not appropriate (e.g. significant tracheal injury).
* REVERSIBLE DISEASE PROCESS
UNLIKELY TO LEAD TO PROLONGED DISABILLITY

Exclusion Criteria:
* Contraindication to continuation of active treatment;
* Significant co-morbidity  dependency to ECMO support
* Significant life limiting co-morbidity

47
Q

What is ECMO?

A

In extracorporeal membrane oxygenation (ECMO), blood is pumped outside of your body to a heart-lung machine:
1. Drain blood from the IVC
2. goes out to a pump
3. Take blood out of IVC & put it through an artificial membrane which has O2 running along one side of it (blood through another)
4. GAS EXCHANGE OCCURS
5. We pump the blood back into the patient (now fully oxygenated)

48
Q

How effective is ECMO?

A

NOT V. EFFECTIVE:
- First major trial:
Stopped early for futility
Statistically no significant difference….
RBH survival 79%:
Best study mortality 24 to 31%
ISSUES:
Time to access
Referral system- Geographical inequity
Consideration of referral
TECHNICAL:
Obtaining access:
Internal jugular
Subclavian
Femoral
Circuit
Haemodynamics
Clotting/Bleeding
EXPENSIVE

Cardiovascular & Respiratory Medicine (14 decks)

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