Class 3 (01|25|22) Pulmonary alterations: Acute respiratory failure and Acute respiratory distress syndrome Flashcards

1
Q

What is respiratory failure?

A

Respiratory failure is a state in which one or both gas exchange functions are inadequate. Either the amount of oxygen travelling in the blood is insufficient or the amount of carbon dioxide being exhaled from the lungs are inadequate.

When there is inadequate carbon dioxide being eliminated, it results in elevated C02 levels in the body. This leads to HYPERCAPNIA (also called hypercarbia).

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2
Q

What are the two causes of resp failure?

A

Hypoxemic: There is an issue with oxygenation.
Hypercapnic: Often referred to as ventilatory failure. There is an imbalance between supply and demand.

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3
Q

Describe Hypoxemic respiratory failure.

A

Hypoxemic: There is an issue with oxygenation.
The primary problem is an inadequate transfer of oxygen between the alveoli and pulmonary capillary bed.
The lungs may be receiving enough oxygen, but the main issue is the inability to transfer the oxygen into the blood.
Usually a result of a combination of reasons

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4
Q

What are the 4 primary reasons for hypoxemic respiratory failure

A

Ventilation-Perfusion Mismatch
Shunting
Diffusion Limitations/dead space
Alveolar Hypoventilation

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5
Q

Describe Ventilation-Perfusion Mismatch in Hypoxemic resp failure.
What can cause it (3)?
What is the primary intervention/treatment?

A

There are alterations in the body that can result in a mismatch of this ratio of blood perfusing the lungs and the amount of fresh gas that reaches the alveoli. (normal ratio 1:1)

pneumonia: the alveoli are often collapsed and filled with pus and fluid. So, the amount of blood attempting to perfuse the lungs is going to be greater than the amount of fresh gas that can reach the alveoli.
COPD
Atelectasis or pain: If a patient is post-op and is not breathing deeply due to pain, then hypoventilation can actually cause atelectasis.

Primary intervention/treatment: administration of oxygen/determine the cause of the mismatch

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6
Q

Describe shunting in Hypoxemic resp failure

What can cause it? (2)

A

Shunting: This is when the blood exits the heart without having participated in gas exchange.

Can be caused by:
Anatomical shunt: hole in between the atria or ventricles of the heart

Intrapulmonary shunt: The blood flows through the capillaries in the lungs but gas exchange is not taking place. Commonly the alveoli being filled with fluid. Examples could be pneumonia, pulmonary edema, acute respiratory distress syndrome.

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7
Q

Describe Diffusion Limitations/dead space Hypoxemic resp failure.
What can cause it? (2)

A

decrease in gas exchange which takes place on the alveolar capillary membrane, typically happens due to the damage or thickening of the membrane.

Can be caused by
pulmonary fibrosis: condition in which the lungs become scarred over time

emphysema: linings of the tiny air sacs in your lungs become damaged

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8
Q

Describe Alveolar Hypoventilation in Hypoxemic resp failure

What can cause it? (3)

A

Alveolar Hypoventilation: decrease in the respiratory rate or in the depth of breathing. This causes an increase in carbon dioxide retention and a decrease in Pa02.

Can be caused by:
CNS dysfunction - i.e. CNS depressants, head injury.
chest wall dysfunction, such as having fractured ribs.
neuromuscular disease

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9
Q

Alterations that affect the respiratory system causing hypoxemic respiratory failure. (5)

A

Acute respiratory distress syndrome
Pneumonia
Toxic inhalation (smoke)
Hepatopulmonary syndrome: low-resistance flow state, ventilation-perfusion mismatch
Massive pulmonary embolism (thrombus emboli, fat emboli)

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10
Q

Alterations that affect the cardiac system casuing hypoxemic respiratory failure.
(3)

A

Anatomical shunt
Cardiogenic pulmonary edema
Shock (decreased blood flow through pulmonary vasculature)

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11
Q

Describe Hypercapnic respiratory failure.

A

Hypercapnic: Often referred to as ventilatory failure. There is an imbalance between supply and demand.

The ventilatory supply: is the max ventilation. This is what a patient can do without their respiratory muscles becoming fatigued.
The ventilatory demand: is the amount of ventilation that an individual needs in order to keep the carbon dioxide level within normal range.
In most cases, the supply exceeds the demand. Our bodies are able to adapt to that.

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12
Q

What are the four primary reasons for hypercapnic resp failure? (4)

A

Dysfunction of the Airway or Alveoli
CNS Depression
Abnormalities of the Chest Wall:
Neuromuscular Conditions:

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13
Q

Describe CNS depression in Hypercapnic respiratory failure.

What can cause it? (4)

A

CNS Depression: not breathing deeply or quickly enough, then it can suppress the respiratory drive. As a result, that carbon dioxide level is going to increase.

Can be caused by 
High spinal cord injury 
Brainstem infarction 
Sever head injury 
Overdoes
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14
Q

Describe Abnormalities of the Chest Wall in Hypercapnic respiratory failure.
What can cause it? (2)

A

Abnormalities of the Chest Wall: Conditions that limit the amount of lung expansion

Can be caused by:
Flail chest: Flail chest is a life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall.

Change in spinal cord alterations: scoliosis which effect the lungs ability to take full breaths

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15
Q

Describe Neuromuscular Conditions Hypercapnic respiratory failure.
What can cause it? (3)

A

Neuromuscular Conditions: muscle dysfunction/paralysis/weakness inhibiting breathing

  • Can be caused by:
    Multiple sclerosis: common demyelinating disease, in which the insulating covers of nerve cells in the brain and spinal cord are damaged.

Muscular dystrophy: progressive weakness and breakdown of skeletal muscles over time.

Guillain-Barre syndrome: rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system.

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16
Q

Describe Dysfunction of the Airway or Alveoli Hypercapnic respiratory failure.
What can cause it? (3)

A

Dysfunction of the Airway or Alveoli: air trapping or any obstruction to air flow.

Can be caused by:
Cystic fibrosis: Long-term issues include difficulty breathing and coughing up mucus as a result of frequent lung infections

Asthma

Emphysema: linings of the tiny air sacs in your lungs become damaged

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17
Q

Alterations that affect the CNS causing hypercapnic respiratory failure. (4)

A

Brainstem infarction
sedative and opioid overdose
Spinal Cord injury
severe head injury

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18
Q

Alterations that affect the chest wall causing hypercapnic respiratory failure. (4)

A

Thoracic trauma (eg; flail chest)
Kyphoscoliosis
Pain
Morbid obesity

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19
Q

Alterations that affect the Neuro-muscular system causing hypercapnic respiratory failure. (9)

A
Myasthenia gravis
Critical illness polyneuropathy 
acute myopathy 
toxic ingestion 
amyotrophic lateral sclerosis 
phrenic nerve injury 
Guillain-Barré syndrome 
poliomyelitis 
muscular dystrophy 
multiple sclerosis
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20
Q

Alterations that affect the respiratory system causing hypercapnic respiratory failure. (3)

A

Asthma
COPD
Cystic fibrosis

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21
Q

What is Kyphoscoliosis?

A

Kyphoscoliosis is an abnormal curve of the spine on two planes: the coronal plane, or side to side, and the sagittal plane, or back to front. It’s a combined spinal abnormality of two other conditions: kyphosis and scoliosis.

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22
Q

What is Myasthenia gravis?

A

Myasthenia gravis (MG) is a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles.

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23
Q

What are the early signs of resp failure

A

change in mental status: restlessness, agitation, confusion, combative
Tachycardia; tachypnea; as body realized no enough O2 or too much CO2 — use of accessory muscles
Mild hypertension in the
patient position - laying flat and sings of resp distress and more comfortable sitting up
dyspnea
respiratory alkalosis: tachy

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24
Q

What are the late signs of resp failure?

A

Paradoxical breathing - abdomen and chest are moving in the opposite manner (maximal use of accessory)
Bradypnea: For patients who have tachypnea, we might see bradypnea now. This is because they are so tired because of breathing so fast.
respiratory acidosis: Bradypnea causing an accumulation CO2
Dyspnea — worsening — speaking 1-2 words
Cyanosis — unreliable (LATER)
Worsening mental status — unresponsive (LATER)

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25
Q

What is the purpose of ventilatory support?

A

oxygen and removal of carbon dioxide

26
Q

What are two non-invasive ventilatory support?

A

CPAP

BiPAP

27
Q

Describe CPAP

A

continuous positive airway pressure (inward flow
of air against exhalation, which can be uncomfortable for patients)

28
Q

Describe BiPAP

A

bi-level positive airway pressure (difference in pressure on inhalation and exhalation)
Aid in patients with atelectasis and are having trouble taking deep breaths

29
Q

What are two invasive ventilatory support?

A

ETT

tracheostomy

30
Q

Describe ETT

A

balloon inserted throat VIA oral or nasal cavity

31
Q

Describe tracheostomy

A

incision on the anterior aspect of the neck and opening a direct airway through an incision in the trachea

32
Q

Who/why would someone need an invasive airway for ventilation support? (9)

A
obstructions 
significant facial edema 
General anesthésia 
Unstable airway
developed respiratory failure and they need support for a longer amount of time 
Immature lungs 
COMA score less then 8 
Protect against aspiration 
Loss of airway reflexes or protection
33
Q

Describe intubation.

A

procedure where HCP use a laryngoscope though mouth/nose past the larynx into the trachea where the tube keeps the airway open VIA balloon
They cannot talk
Once EET tube is inserted, osculate chest to ensure air entry OR chest Xray

34
Q

What does mechanical ventilation do?

What are the two main typer historically?

A

Machine the enhances pulmonary gas exchange

  1. Negative Pressure ventilation
  2. Positive pressure ventilation:
35
Q

Describe Negative Pressure ventilation

A

Negative Pressure ventilation: iron lung - chest wall was sucked out and air moved into the lungs

36
Q

Describe Positive pressure ventilation

A

much safer where air is pushed into the lungs (VIA volume, pressure fluctuations OR pressure needs to be reached in lung where the volume fluctuates)

37
Q

What does FiO2 values indicate?

A

Fraction of inspired oxygen (FiO2) is the percentage of O2 delivered to the patient. The FiO2 ranges from 0.21 (room air) to
1 (100% O2)

38
Q

What dose PEEP stand for? Why is PEEP important?

A

PEEP — “Positive end-expiratory pressure”

Receive this: the pressure in the pulmonary system at the end of expirations - prevents alveoli from collapsing with a residual volume
When incubated: there epiglottis is left open so mechanical ventilation give PEEP

39
Q

What does Mechanical Ventilation impact on for the patient?

A
  • cannot communicate Placed past vocal cords
  • discomfort
  • potential complication
40
Q

What are 5 potential complications in Mechanical Ventilation?

A

air being pushed into airway where its increased further because it need to be above PEEP - decrease venous returns from head

cause injury to lungs (leading to teach)
prolonged: infection, VAP

Decreased venous return: decrease retune from kidneys and other non vital organs causing damage

Decreased gastric mobility

41
Q

What are 5 ways to prevent complications in Mechanical Ventilation?

A

Damage to upper airway, teeth, trachea: Secure tube to prevent movements
Sinusitis: sinuses cannot drain
mucosal lesions: breakdown of much membranes
Ventilator induced lung injury
Ventilator associated pneumoni

42
Q

What is VAP?

A

Ventilator Associated Pneumonia

43
Q

Why are intubated patients susceptible to the development os VAP?

A

immune system: not functioning

Unable to expel secretions

44
Q

What other contributing factors might exist in the critically ill patient when on ventilation? (3)

A

decrease ciliary activity
Plaque can go down trachea and into lungs
Patients being fed enterally increase risk of aspiration

45
Q

What are the 5 components of the adult VAP ‘bundle’?

A

HOB 45 degrees (decease risk for aspiration and helps lung expansions)

Sedation vacation daily (does the patient still need to ventilated)

ETT with port for continuous sub-glottic suction (allows for continuous suction)

Oral care / decontamination (oral flora changes 48 hours later as well plaque where bacteria can grow - brushing teeth, suctioning, chlorhexidine swabs)

Avoidance of scheduled ventilator circuit changes (do not want to open up circuit if it doesn’t need to be opened NOT 48 HOURS)

46
Q

What is different for the pediatric recommendations for VAP prevention compare to those for adults?

A

more cautious because of less research

Oral Hygiene different - stage of development (no teeth, baby teeth?)

47
Q

What is ARDS?

A

ACUTE RESPIRATORY DISTRESS SYNDROME

It is a progressive disorder that prevents appropriate gas exchange.
Some sort of inflammatory or immune response occurs within the lungs and initiates a cascade of events and result with respiratory failure

48
Q

What is the pathophysiology of ARDS?

A

The capillaries around the alveoli have increased permeability. This means they are letting more fluid in than they normally would

Leads to fluid filling the alveoli and capillaries lose their ability to hold the fluid and it leaks out to the alveoli. This causes the release of the inflammatory cytokines.

49
Q

What are cytokines?

A

Cytokines: damage the lung tissue, which in turn, produces more fluid in the alveoli. The damage to the lungs causes scarring which leads to a decrease in lung compliance (not bale to fully expand).

50
Q

What can cause ARDS?

A

Examples: sepsis, burn injuries, trauma, or near drownings.

51
Q

Describe the diagnostics of ARDS?

A

No specific biomarker or lab test we can do.

Evidence of an underlying condition - i.e. pneumonia.

Chest x-ray will show diffuse bilateral infiltrates. Commonly known as “white outs”.

The ABG will show refractory hypoxemia

52
Q

What are the values for Pa02 and Fi02 ratio (mild, moderate and sever) in ARDS?

A

< 300 = mild
< 200 = moderate
< 100 = severe

53
Q

What is ‘normal’ FiO2?

A

NORMAL: ~ 400-500 mmHg

54
Q

What is a s/s that the ARDS is worsening?

A

The progression of ARDS is shown when Patient will be requiring more and more oxygen to remain at the same saturation. Not responding to the same amount of oxygen as before

55
Q

Describe the management of ARDS?

A

No proven drug to be effective.
treat the underlying cause
position the patient to be lying prone for better expansion of the lungs.
If ventilated: We can increase PEEP to increase the amount of air in the alveoli after expiration. Helps to ensure the alveoli won’t collapse.

56
Q

What are the three factors that determine gas exchange in the lungs?

A

Ventilations (V): breath size
Perfusion (Q): pulmonary blood flow
Diffusion: movement of gases across the tissue between pulmonary blood and alveolar air

57
Q

What are the ventilators setting?

A

Ventilators will use respiratory rate (RR) and tidal volume (Vt) to work out a set minute volume.

58
Q

What are the four nursing goals for ARDS?

A

to restore

  1. ABG values
  2. Breath sounds
  3. Breathing patterns
  4. Ability to clear secretions
59
Q

What can be implemented for respiratory support in ARDS?

A
Oxygen Administration 
Mobilization of Secretions. 
Hydration and Humidification 
Chest Physiotherapy 
Airway Suctioning 
Positive-Pressure Ventilation
60
Q

What can be implemented for drug/medication support in ARDS? (5)

A
Relief of Bronchospasm 
Reduction of Airway Inflammation. 
Reduction of Pulmonary Congestion 
Treatment of Pulmonary Infections 
Reduction of Severe Anxiety, Pain, and Agitation
61
Q

What can be implemented for medical support in ARDS?

A

Treating the Underlying Cause
Maintaining Adequate Cardiac Output
Maintaining Adequate Hemoglobin Concentration