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PHTY3250 Cardiorespiratory > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Describe the steps of normal respiration.

A
  1. respiratory controller (voluntary or involuntary)
  2. respiratory muscles (rib cage and abdomen) create a pressure gradient to draw air in
  3. movement of air
  4. alveolar ventilation
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2
Q

What drives involuntary respiratory control?

A

increased carbon dioxide in the blood

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3
Q

What reduces respiratory drive from the respiratory centre or cortical control?

A

medications i.e. anesthetic, head injuries, tumours, CVA’s

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4
Q

Which muscles are involved in respiration?

A

diaphragm, intercostals, SCM, scalenes

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5
Q

What can reduce muscle activation during respiration?

A

reduced nerve conduction (i.e. GBS, spinal cord injury, poliomyelitis)

myopathies, muscle dystophy, fatigue, surgical incisions (reduced muscle function as well as pain inhibition)

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6
Q

What can reduce rib movement during respiration?

A

rib fractures (pain inhibition), kyphoscoliosis, pneumothorax/haemothorax/pleural effusion, abnormal chest wall compliance

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7
Q

What can reduce alveolar ventilation?

A

secretions or tumour/s within bronchi, bronchitis, asthma

decreased surfactant, pulmonary oedema, inflammation (i.e. in pneumonia), or emphysema in the alveolus

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8
Q

What is the functional residual capacity (FRC)?

A

the volume of gas in the lungs after a normal inspiration- this participates in gas exchange during inspiration and expiration

we always want to increase FRC to maintain fresh air in the lungs

supine position= reduced FRC
sitting and standing upright= increased FRC

the abdominal contents move down with gravity, allowing the diaphragm to expand more which increases the FRC

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9
Q

What is the closing capacity (CC)?

A

the volume of air in the lungs when small airways start to collapse during expiration, trapping air inside

in a healthy individual, this is at the residual volume i.e. CC=RV, and does not encroach on FRV i.e. CC<FRC

in abnormal respiration, CC>FRC resulting in early collapse of airways resulting reduced ventilation

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10
Q

How does the relationship between CC and FRC change with age?

A

by 45 years the CC encroaches on the FRC in supine and by 65 years the CC encroaches on the FRC upright

the weaker the respiratory muscles and the more obese, the more difficult the respiration (adipose tissue presses on lungs)

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11
Q

What is hypoxaemic pulmonary vasoconstriction?

A

a protective response that will constrict the pulmonary vessels if there is a reduction of oxygen in a particular area of the lungs

this diverts blood to areas with greater ventilation therefore increasing oxygen in the blood

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12
Q

What is atelectasis?

A

‘imperfect expansion’ or collapsed alveoli due to inadequate ventilation

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13
Q

What are the different types and causes of atelectasis?

A

micro atelectasis (patchy areas seen in post-op patients due to anaesthesia affecting surfactant)

plate atelectasis (small areas of collapse due to pulmonary oedema or pneumonia)

compression atelectasis (structural reason for collapse i.e. tumour or cardiomegaly)

absorption atelectasis (physical blockage of a bronchiole by mucous plug)

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14
Q

What are the effects of atelactasis?

A

there is a ventilation-perfusion mismatch resulting in hypoxemia and in some cases hypercapnia (high levels of CO2)

this results in reduced FRC and lung compliance and therefore work of breathing increases and more oxygen will be consumed

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15
Q

What are the clinical signs of atelectasis?

A

Palpation:
decreased chest wall movement
+/- increased temperature

Auscultation:
decreased or absent breath sounds
+/- fine end-inspiratory crackles (as the alveoli reinflate at the end of inspiration)

Special tests:
decreased SPO2, Pa)2 and chest xray

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16
Q

What are some risk factors for atelectasis?

A

surgical incision
previous respiratory condition
smoking history
obestiy
age
impaired cognitive function
monotonous pattern of mechanical ventilation (absence of normal sigh/changes in breathing pattern)
body position (supine, slouched)

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17
Q

How can we reverse ateletasis?

A

maintain air in the lungs at all times to overcome the critical opening pressure

encourage ‘slow laminar flow’ inspiration acknowledging the Newtonian Law of Viscosity

use inspiratory holds to:
-overcome different time constants
-encourage collateral ventilation
-use alveolar interdependence to open up alveoli
-stimulate surfactant release

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18
Q

What is critical opening pressure?

A

the pressure needed to overcome surface tension and achieve initial reinflation of collapsed regions

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19
Q

What is the Newtonian Law of Viscosity?

A

sticky surfaces peel apart more easily when the action is done slowly

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20
Q

What is collateral ventilation?

A

relying on neighboring alveoli to inflate blocked-off alveoli via collateral channels

different names of channels:
inter bronchiolar channels of Martin
bronchiolar-alveolar channels of Lambert
alveolar pores of Kohn

21
Q

What is alveolar interdependence?

A

if one alveolus starts to collapse, it will exert a stretching force on a neighbouring alveoli and force the reopening of the collapsed alveoli

this is increased at vital capacity vs tidal volume hence why we use deep breaths to make use of this concept

22
Q

What are time constants?

A

refers to the timing of ventilation of the alveolar (time constant= compliance x resistance)

in a healthy lung, alveoli are relatively uniform so it takes the same rate and pressure to inflate them

in an unhealthy lung, there may be increased resistance and increased or decreased compliance resulting in varying time to fill

inspiratory holds can overcome this by allowing for different time constants

23
Q

What occurs during increased work of breathing (WOB)?

A

increase accessory muscle use, increased respiratory rate and decreased energy available for other organs

24
Q

How do we manage increased work of breathing (WOB)?

A

through positioning and breathing control

position:
-recovery/supported positions i.e. forward lean sitting/standing (reverse origin/insertion of pectorial muscles to assist with expanding the thorax)
-breathe control encourages gentle tidal breathing through nose and focusing on the lower chest expanding

25
Q

Compare and contrast hypoxemia and hypoxia.

A

hypoxaemia refers to acute or chronic inadequate oxygen in the blood (less than 80 mmHg, severe is below 60mmHg)

most commonly due to a V/Q mismatch but could also be due to hypoventilation or reduced oxygen available i.e. due to altitude

hypoxia refers to inadequate oxygen at the tissues

results from hypoxaemia, reduced cardiac output, reduced haemoglobin or increase metabolic demands i.e. due to burns

26
Q

What is hypercapnia?

A

increased carbon dioxide levels (>50mmHg, normal being 35-45mmHg) in the blood due to hypoventilation, increased metabolism i.e. burns/trauma/fever

27
Q

What are some clinical signs of respiratory distress?

A

early: restlessness, anxiety, tachycardia/tachypnea (RAT)

late: bradycardia, extreme restlessness, dyspnea (BED)

long term: end-organ hypoxia (confusion, aggression, reduced awareness, cyanosis/blue fingertips, reduced HR, reduced BP)

28
Q

What is respiratory failure? What types are there?

A

when the respiratory system is unable to provide adequate gas exchange for metabolic requirements

type 1: hypoxaemia

type 2: hypoxaemia + hypercapnia

29
Q

What is the oxyhaemoglobin dissociation curve?

A

refers to the haemoglobin saturation levels and how these relate to our oxygen requirements

we require our oxygen saturation to be above 96% (after this is plateaus and no further saturation is useful)

below 90% there is a steep decline in oxygen saturation

30
Q

How do the clinical signs vary between type 1 and type 2 respiratory distress?

A

type 1 restlessness, pale skin and ‘plucking’ movements

type 2 drowsiness, flushed skin and coma

31
Q

How do we manage type 1 respiratory failure?

A

improve ventilation:
-breathing exercises (thoracic expansion)
-non-invasive ventilation

mobilise & remove secretions
- airway clearing techniques
-suction

32
Q

How do we manage type 2 respiratory failure?

A

oxygen therapy
non-invasive ventilation

or

intubation

33
Q

How does pulse oximetry work and how can it be helpful to us?

A

it measures the percentage of oxygen carried by haemoglobin (blood oxygen levels)

normal SpO2= >96% (according to the oxyhaemoglobin dissociation curve)

inaccurate with low perfusion (cold finger), hypotension, movement, skin pigmentation, nail polish

34
Q

How does oxygen therapy work?

A

works to correct hypoxaemia and therefore aim to reduce tissue hypoxia

reduces WOB, how hard the heart has to work and cerebral vasodilation

can be delivered continuously, intermittently or nocturnal

35
Q

What are some dangers to using oxygen therapy?

A

patients with COPD (reduces the drive to breathe as these patients main driver is reduced oxygen – as opposed to increased carbon dioxide in healthy people)

oxygen toxicity (high oxygen levels in the air can lead to changes in the lungs resulting in reduced pulmonary compliance)

depression of the ciliary function (drying out leading to thickening secretions)

absorption atelectasis (increasing oxygen leads to moving out of nitrogen which is vital for maintaining alveoli open)

36
Q

How can we minimise the dangers of oxygen therapy?

A

ensure correct flow and oxygen level
ensure correct fit of device
monitor improvements/deterioration
minimise supplemental oxygen amount and duration
humidification

37
Q

What are the two types of oxygen therapy devices?

A

variable: i.e. nasal prongs, face mask, rebreather

rate of oxygen varies with the patients breathe rate, depth and peak inspiratory flow (PIF) demands

fixed: i.e. multivent, venturi, puritan

rate of oxygen is fixed as total flow usually exceeds patient’s peak inspiratory flow demands

38
Q

What are the benefits of using nasal prongs and what settings are typically used? Are nasal prongs variable or fixed?

A

inexpensive & comfortable for the patient, they can eat/drink as normal while wearing them, however can cause pressure areas around nose/mouth

typically 1-4L/min at FiO2 0.24-0.36 (0.4 incremements of oxygen per 1L/minute flow rate)

variable device

39
Q

What are the benefits of using an Inspiron or Hudson mask and what settings are typically used? Are these masks variable or fixed devices?

A

Inexpensive and able to deliver higher levels of oxygen due to the higher flow rate used (this is to prevent rebreathing of exhaled gases that get trapped inside the mask, even though there are holes for that CO2 to escape)

typically 5-10L/min with FiO2 at 0.4-0.6

variable devices

40
Q

What are the benefits of using a partial rebreather mask and what settings are typically used? Are these masks variable or fixed devices?

A

can deliver higher O2 concentrations due to the bag attached to mask which holds O2 (a non-rebreather mask has the bag but also has valves to allow expired air to escape)

typically 6-10L/min FiO2 0.44-0.6

variable devices

41
Q

What are the benefits of using a non-rebreather mask and what settings are typically used? Are these masks variable or fixed devices?

A

can deliver highest O2 concentrations due to bag attached to mask which holds O2 (same as partial rebreather masks), however has a valve to reduce rebreathing of expired air so less likely to retain CO2

typically 10-15Lmin FiO2 0.6-0.8

variable devices

42
Q

What are the benefits to using a multivent, venturi or puritan oxygen device? What settings are typically used? Are these variable or fixed devices?

A

delivers high oxygen flow rates at a fixed amount so we know exactly how much the patient is getting, they are more expensive however

typically flow rate of 3-15L/min FiO2 0.24-0.6, depending on how much O2 the patient needs

fixed devices

43
Q

How do fixed oxygen therapy devices ensure that the patient is recieving the amount of O2 prescribed?

A

they deliver the O2 at a flow rate that exceeds the patient’s peak inspiratory flow demands, so the patient has no choice but to inhale the prescribed % of oxygen

44
Q

How can we protect ciliary function from being affected by oxygen therapy?

A

hydration: IV fluids, oral fluids

humidification: warms the air

nebulisation: adds moisture to the air (needs a high flow rate to cause a ‘baffle’ effect [drive molecules into the lungs] >6L per minute)

45
Q

At what FiO2 is humidification indicated?

A

> 0.35 FiO2

46
Q

Why would we use medical air instead of oxygen when using nebulisation with COPD patients?

A

nebulisation requires high flow rates of >6L per minute to create the baffle effect (forcing the molecules into the lungs in the air)

if high flow rates and therefore high levels of FiO2 are used in COPD patients, we may decrease their drive to breath (as it is typically a hypoxic drive to breath)

47
Q

What is aerosol therapy?

A

suspension of fine liquid or solid particles in air to deliver medication directly to the lungs through a breathing action

particles need to be small enough that they make it deep into the lungs but not so small that they do not deliver an adequate dose of medication

48
Q

Name three different inhalers.

A

metered dose inhaler (puffer) +/- spacer
turbuhaler
handihaler

49
Q

What is the advantage of using an aerobika or PEP mouthpiece device over an acapella or flutter device?

A

aerobika & PEP mouthpieces can be used with a nebuliser at the same time, this is helpful for patients who have multiple medications to take and multiple airway clearance treatments needed per day

PHTY3250 Cardiorespiratory (12 decks)

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