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Respiratory Y3 > Respiratory Failure > Flashcards

Respiratory Failure Flashcards

1
Q

What is respiratory failure?

A

Acute or chronic impairment of gas exchange between the lungs and the blood causing hypoxia with or without hypercapnia (e.g., caused by acute decompensation of chronic pulmonary disease).

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2
Q

What is hypoxic vs hypercapnic respiratory failure?

A
  • Hypoxic respiratory failure (type 1 respiratory failure) is hypoxia without hypercapnia.
  • Hypercapnic respiratory failure (type 2 respiratory failure) is hypoxia with an arterial partial pressure of carbon dioxide.
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3
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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4
Q

What is meant by “pulmonary transit time” and when can this change?

A

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

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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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

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22
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

23
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
24
Q

What are some examples of chronic respiratory failure?

A
  1. Pulmonary/Airways:
    - COPD
    - Lung fibrosis
    - CF
    - lobectomy
  2. Musculoskeletal:
    - Muscular dystrophy
25
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

26
Q

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

A
  1. Infective exacerbation
    - COPD
    - CF
    - Myasthenic crises
  2. Post operative
27
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

28
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

29
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

30
Q

What is type IV resp failure?

A

Type 4 respiratory failure results from hypoperfusion of respiratory muscles as patients are 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)

31
Q

What are the risk factors for acute resp failure?

A
  • Infection
  • Viral
  • Bacterial
  • Aspiration
  • Trauma
  • Pancreatitis
  • Transfusion
  • Cigarette smoking
  • chronic lung disease
  • upper/ lower airway obstruction
    -alveolar abnormalities
  • perfusion abnormalities
  • cardiac failure
  • peripheral nerve abnormalities
  • muscle system abnormalities
  • opioid and sedative medicines
  • toxic fumes and gases
  • CNS disorders
  • acute vascular occlusion
  • pneumothorax
  • hypercoagulable states
32
Q

What are the risk factors for chronic resp failure?

A
  • COPD
  • Pollution
  • Recurrent pneumonia
  • Cystic fibrosis
  • Pulmonary fibrosis
  • Neuro-muscular diseases
33
Q

What presenting symptoms of Resp failure can be found in the history?

A

(COMMON):
1. Presence of risk factors - tobacco use, young age, old age, respiratory system illness, injury or infection, cardiac failure, and hypercoagulable states.
2. Direct trauma to the thorax and neck
3. Dyspnoea
4. Confusion
5. Stridor - noisy breathing that occurs due to obstructed air flow through a narrowed airway
6. Inability to speak
7. Headache
8. Hypoventilation
9. Cardiac rhythm disturbances

(UNCOMMON):
1. loss of airway/gag reflex, underlying neuromuscular disorder, drug use, seizure, coma, asterixis, papilledema

34
Q

What signs of resp failure can be found on physical examination?

A
  • Tachypnoea
  • Accessory breathing muscle use
  • Retraction of intercostal spaces
  • Cyanosis
35
Q

What investigations are used to monitor resp failure?

A

1st investigations to order:
- Pulse oximetry - Acute drops in SpO₂ <80% are associated with respiratory failure. 
- ABG
Investigations to consider:
- FBC (An elevated or low white blood cell count can indicate the presence of infection.)
- D- dimer (rule out PE)
- Serum bicarbonate (HCO3)- Chronic respiratory acidosis, commonly seen with COPD, is associated with raised HCO₃, which slowly develops over time.
- ECG
- CXR
- Pulmonary function tests
- Urine or serum toxicology
- Chest CT
- CT pulmonary angiography (CTPA)
- Ventilation/perfusion lung scan
- Capnometry
- Cardiothoracic ultrasound

36
Q

How is respiratory failure managed?

A
  1. Airway obstruction:
    - 1st line - airway clearance plus supplemental oxygen
    - Adjunct- treatment of underlying causes
  2. No acute upper airway obstruction: stable
    - Supplemental oxygen, treatment of underlying causes
    - 2nd line - non-invasive positive pressure ventilation
  3. Unconscious:
    - Supplemental oxygen, treatment of underlying causes
    - 2nd line - endotracheal intubation and mechanical ventilation
    - Adjunct: rapid sequence induction (RSI) and treatment of underlying causes
37
Q

What are some complications that may be associated with respiratory failure?

A
  • Pneumothorax
  • Endotracheal tube misplacement or dislodgement
  • Nosocomial infection
  • Throat pain, dental injury, soft tissue damage, tracheal inflammation and stenosis from intubation
  • Infection from CPAP or BiPAP
  • Skin necrosis from CPAP and BiPAP
  • Nasal mucosa damage
38
Q

Describe the prognosis for respiratory failure?

A

Mortality associated with acute respiratory failure is often related to a person’s overall health and the potential development of systemic organ dysfunction that can occur with acute illness

39
Q

What is ARDS?

A

“Acute Respiratory Distress Syndrome” is a form of severe hypoxemic respiratory failure

when there is inflammatory injury to the alveolar capillary barrier due to infection or injury. The inflammation causes fluid from nearby blood vessels (oedema) to leak into the alveoli, making breathing increasingly difficult.

The lungs can become inflamed after: pneumonia or severe flu

40
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

41
Q

What changes are seen in alveolar during acute lung injury?

A
  • The alveolar epithelium (lining of the vascular supply) inflamed/ injured
  • Macrophages brought to site of injury and produce IL-6, IL-8 (cytokine that recruit neutrophils)
  • Increased neutrophils release:
    1. Proteases (digest proteins; breaking down walls of alveoli)
    2. Reactive oxygen species (free radical damage)
    3. More cytokines (increasing inflammation)
42
Q

What are effect does increased inflammation have on gas exchange in ARDS?

A
  1. More blood clots
  2. Endothelium becomes leaky
    (pulmonary oedema)
  3. Pneumocytes get injured & die:
    - Type 1: less gas exchange
    - Type 2: less surfactant (alveoli collapse)
  4. Dead cells & protein- rich fluid build up and form Hyaline membranes (huge sign of ARDS on imaging)
    - makes gas exchange more difficult
43
Q

What are the different types of pneumocytes?

A

Pneumoncytes are alveolar cells:
Type 1: thin cells that line the alveoli, increase surface area for gas exchange
Type 2: Make surfactant, keeps the alveoli open
Dust cells (alveolar macrophages): consume dust & dangerous particles

44
Q

What is meant by Ventilation Perfusion Mismatch?

A

This is when the lungs continue to have good perfusion, but can not ventilate properly, like in ARDS, due to the edema, infiltrates and alveolar collapse. Therefore there is deoxygenated blood passing the lungs that does not pick up oxygen (Hypoxia)

45
Q

How can ARDS lead to restrictive lung disease?

A
  • In ARDS there is an increased inflammatory response, leading to an increase in macrophages.
  • These macrophages attract & activate fibroblasts
  • Fibroblasts eventually lead to scar tissue formation in the lung which causes restrictive lung disease
46
Q

What are the symptoms of ARDS?

A
  • Severe & life threatening
  • Begins with shortness of breath a few hours after initial injury
  • Rapidly worsens to resp failure
  • Hypoxemia- cyanosis (bluish skin)
  • Edema- Crackling sound (rales: collapsed alveoli popping open)
47
Q

how does pulmonary transit time change with ARDS

A
  • Gas exchange & pulmonary transit time is much less efficient/ larger following damage
48
Q

What investigations are used to monitor 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

49
Q

What criteria needs to be met for diagnosis of ARDS?

A

4 criteria:
1. Acute: < 1 week
2. X- Ray or CT scan: white out
3. PF ratio < 300 mmHg
(this is the partial pressure of O2 in arterial blood divided by % O2 in inspired air)
4. Ensure resp distress is NOT caused by heart failure:
- In heart failure pulmonary edema is cause by increased bp
- In ARDS bp is normal
- Bp can be measured with a catheter wedged in the pulmonary artery
- Heart failure can be assessed with cardial US

50
Q

What pharmacological interventions are used to treat ARDS?

A
  • Steroids
  • Salbutamol
  • Surfactant
  • N-Acetylcysteine
  • Neutrophil esterase inhibtitor
  • GM-CSF
  • Statins
51
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
52
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 End Expiratory Pressure (PEEP) to help the airways open & low tidal vol to prevent over-inflation of the alevoli
53
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
54
Q

What imaging is used to view the lungs?

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

Respiratory Y3 (20 decks)

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