Respiratory Disorders Flashcards

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1
Q

Changes in pregnancy of the respiratory system?

A
  • Enhanced respiratory efficiency is required to meet the increased metabolic demands of the woman, fetus and placenta
  • Yet compared to exercise, pregnancy makes little demand on respiratory reserve function
  • 20% ↑in oxygen consumption and this is met by 20-50% increase in resting ventilation which is apparent in the end of the first trimester
  • ↑ metabolic demand for oxygen by maternal and fetoplacental unit
  • Position of the diaphragm rises by about 4cm due to enlarging uterus
  • ↑ transverse diameter of chest
  • Capillary engorgement of respiratory tract with increased friability of mucus membranes
  • 40-50% ↑ in resting minute ventilation mainly from a rise in tidal volume: breathe in more and hold in more
  • Changes in Pa02 and PaC02 occur as there is less air remaining in the lungs after expiration to be mixed with air after the next inspiration.
  • Mild respiratory alkalosis is normal in pregnancy with arterial pH increasing slightly from 7.4 to 7.45.
  • Resp rate remains unchanged at 12-15 at rest
  • Subjective feelings of breathlessness are common.
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2
Q

Tidal volume and changes in pregnancy?

A

Definition: Amount of air passing in and out of the lungs during a single breath.

Changes in pregnancy:

  • Increased in 40%
  • From 500ml to 700ml
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3
Q

Inspiratory capacity and changes in pregnancy?

A

Definition: The total amount of air that can be inspired with maximal effort.

Changes in pregnancy:
- Increased by 200-300 ml by late pregnancy.

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4
Q

Functional residual capacity and changes in pregnancy?

A

Definition: The volume of air in the lungs at the end of normal passive expiration.

Changes in pregnancy:
- Decreased by about 500mls.

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5
Q

Blood gases and changes in pregnancy?

A

Definition: Normal pH 7.38-7.45.

Changes in pregnancy:
- Mild respiratory alkalosis as reduced CO2 in arterial blood and consequent reduction in serum bicarbonate due to enhanced ventilation. Balance favours optimal O2/CO2 exchange.

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6
Q

Respiratory rate and changes in pregnancy?

A

12-15 at rest

Changes in pregnancy:
- No change, breaths more deeply rather than frequency

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7
Q

Labour changes to the respiratory system?

A
  • Strong contractions of the uterus increases metabolism = ↑ demand for 02+ Pain and anxiety= hyperventilation common
  • Contractions decrease blood supply in intervillous space
  • Changes in acid-base status due to this hyperventilation and ↑02 consumption potentially hazardous to both mother and fetus.
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8
Q

What happens postnatally to the respiratory system?

A
  • Rapid reversal of changes
  • Reduction in progesterone and decrease in intra-abdominal pressure
  • Blood gases return to pre-pregnant levels within 24hrs
  • Anatomical and ventilatory changes return to normal within 1-3 weeks
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9
Q

Assessment of respiratory function?

A
  • Clinical – respiration rate, depth, pattern, noting presence of cough wheeze or production of sputum, accessory muscles being used- stomach.
  • Listening to breath sounds with stethoscope
  • Peak Expiratory flow rate (PEFR)
    o Maximum ability of exhalation during forced expiration
    o Measured by a peak flow meter
    o In normal pregnancy peak flow unaffected
    o Probably due to balance between broncho dilating forces and broncho constricting
    o Results can guide medication prescription
  • Forced expiratory volume in one second (FEV1)
    o Amount of air that can be forcibly expired after maximal expiration in one second
    o Gives a more accurate indication of lung volume
    o Measured by a spirometer
    o Normal values unaffected by pregnancy
  • Pulse oximeter
    o Used to measure pulse rate along with level of oxygen saturation in the peripheral blood (SA02)
  • Chest X-ray
    o Will show the lungs, heart and major blood vessels and reveal any abnormality.
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10
Q

Management

A
Oxygen therapy
Oxygen delivery methods:
All systems require:
1. Oxygen supply.
2. Flow meter.
3. Oxygen tubing.
4. Delivery device.
5. (Humidifier)- the higher the concentration of oxygen the more dry it can get 

Delivery devices:
- Non-rebreathing mask
o Allows the delivery of high concentrations of oxygen (85% at 15 litres/min).
o Has a reservoir bag to entrain oxygen.
o One way valves prevent room and expired air from diluting the oxygen concentration.
o A tight seal is essential.
o Reservoir bag must be seen to expand freely.

  • Simple facemask
    o Easy to use.
    o Allows administration of variable concentration dependant on flow of fresh gas up to 40%.
    o Requires a good fit.
  • Nasal cannulae (nasal prongs/speculae)
    o Easy to use.
    o Well tolerated.
    o Comfortable for long periods.
    o Patient can eat and talk easily.
    o Possible to deliver oxygen concentrations of 24-40% at flow rates of 1-6 litres/min.
    o Flow rates in excess of 4 litres/min might cause discomfort and drying of mucous membranes and are best avoided.
  • Venturi mask
    o Mixes a specific volume of air and oxygen.
    o Useful for accurately delivering low concentrations of oxygen.
    o Valves are colour coded and flow rate required to deliver a fixed concentration is shown on each valve.
    o Can deliver oxygen concentrations between 24-60%.
  • Humidification
    o Is recommended if more than 4 litres/min is delivered.
    o Helps prevent drying of mucous membranes.
    o Helps prevent the formation of tenacious sputum.
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11
Q

Asthma

Definition

A
  • Chronic inflammatory condition of the airways, defined as a reversible airway obstruction.
  • “an intermittent disorder, characterised by temporary bouts of inflammation (associated with swelling and excessive production of mucus) of the airways which leads to wheezing, coughing and breathlessness”.
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12
Q

Pathophysiology of asthma

A
  • Exposure to known triggers results in an exaggerated inflammatory response
  • Release of:
    o mast cells, eosinophils, macrophages, T-lymphocytes and neutrophils (all types of WBC)
    o vasoconstrictor substances (histamine and leukotriene)
  • Narrowing of airways due to contraction of smooth muscle and oedema of the bronchial endothelium
  • terminal bronchioles, respiratory bronchioles, alveoli
  • increase of mucus production; difficulty in breathing.
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13
Q

Triggers of asthma

A
  • Upper respiratory tract viral infections: cold and coughs
  • House dust mites, pollens, animal dander
  • Exercise
  • Reduction or omission of regular medications
  • Cold air
  • Hyperventilation
  • Drugs such as aspirin and non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen and diclofenac- talk to the anaesthesits
  • Food and drinks such as nuts, milk and egg allergies, preservatives or colouring agents
  • Gastro-oesohageal reflux
  • Environmental pollutants such as cigarette smoke and traffic fumes
  • Stress and psychological factors.
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14
Q

Signs and symptoms in asthma

A
  • Cough
  • Dyspnoea
  • Tachypnoea
  • Thick sputum
  • Increased respiration
  • Breathlessness
  • Tachycardia
  • Wheezy breathing
  • Use of accessory muscles- as the body wants the most oxygen
  • Chest tightness
  • Inability to complete sentence
  • Worse at night and early morning.
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15
Q

Step 1- Mild intermittent asthma

A
  • Symptoms infrequent and mild
  • Inhaler containing a medicine called a short-acting beta2-agonist
  • Relieve asthma symptoms for three to six hours, start working within five minutes
  • Work by relaxing the muscles of the airways and decreasing the amount of mucus and by preventing the muscles around airways tightening.
  • Known as reliever inhalers
  • i.e. salbutamol, atrovent.
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16
Q

Step 2- Regular preventer therapy

A
  • Asthma symptoms more frequent, i.e more than twice a week, woken at least once a week due asthma symptoms, an asthma attack in the last two years, or use of short-acting beta2-agonist inhaler more than twice a week.
  • Corticosteroids inhaler usually bd
  • Still use short-acting beta2-agonist inhaler if symptomatic
  • Mode of action not entirely clear, but they are known to reduce the amount of inflammation in the airways and prevent asthma attacks occurring.
  • i.e Becotide (becloforte), Budesonide, Flixotide.
17
Q

Step 3- Add-on therapy

A
  • Symptoms still not under control,
  • Second preventer inhaler to take along with the first, long-acting beta2-agonist.
  • Work in the same way as short-acting beta2-agonists, but take longer to take effect and can last up to 12 hours.
  • Still no response = increase corticosteroids and long-acting beta2-agonists
  • Should only use long-acting beta2-agonist inhaler in combination with inhaled corticosteroids inhaler, and not by itself as studies have shown that using only long-acting beta2-agonists can increase the risk of an asthma attack occurring
  • i.e Serevent, Foradil (usually powders).
18
Q

Step 4- Persistent poor control

A
  • If treatment still not successful, the amount of inhaled corticosteroids may be increased to its maximum safe dose, and additional preventer medicines will be tried. Some possible alternatives are outlined below.
  • Leukotriene receptor antagonists - oral medication (tablet) that works by blocking a chemical reaction that can lead to inflammation of the airways.
  • Theophyllines - oral medication helps to widen the airways by relaxing the muscles around them. In some people, theophyllines have been known to cause a number of side effects, including headaches, nausea, insomnia, vomiting, irritability and stomach upsets.
  • Slow release beta2-agonist tablets - these work in the same way as long-acting beta2-agonists, but they are particularly good at preventing night-time symptoms i.e. albuterol.
19
Q

Step 5- Continuous or frequent use of oral steroids

A
  • Long term use of oral steroids carries possibly serious side effects, so they will only be used once all other treatment options have been tried and all trigger factors have been eliminated as far as possible.
  • Oral steroids carry a risk if they are taken for more than three months, or if they are taken frequently (three or four course of steroids a year).
  • Side effects can include: Osteoporosis, Hypertension, Diabetes, Weight gain, Cataracts and glaucoma, Thinning of the skin, Easy bruising, Muscle weakness
  • Most common drug used = prednisolone.
20
Q

How might the course of asthma change during pregnancy?

A
  • In 1/3 of cases, asthma improves, while 1/3 will remain the same and 1/3 will worsen
  • Physiological changes in pregnancy which have opposing effects are that progesterone and cortisol are bronchodilators while prostaglandins are bronchoconstriction.
21
Q

The course of asthma in pregnancy depends on various factors, including?

A
  • Existing asthma state and its severity
  • Presence of respiratory infection – bacterial, viral
  • Presence of known triggers, e.g. dust mites, animal dander, cigarette smoke, pollen/moulds/spores
  • Smoking habit
  • Exercise habit; exposure to emotional stress
  • More likely if the fetus is male
  • Unsupervised reduction in medication due to concern about possible teratogenic effects of the fetus- inhalational rather than oral preparations are used as these reduce systematic effects including placental transfer.
  • Severity of asthma tends to peak at 29-36 weeks, coinciding with peak progesterone levels
    o Progesterone inhibits glucocorticoid (cortisol, cortisone)- GLUCOCORTICOIDS = corticosteroids predominantly involved in CHO metabolism, and in fat/protein metabolism; also involved in many other activities, e.g. alteration in connective tissue response to injury; inhibition of inflammatory and allergic reactions; most important ones are CORTISOL (hydrocortisone) and CORTISONE receptor sites, thus affecting the clinical course of asthma and its responsiveness to drug therapy
  • Rise in free cortisol levels at 1-10 weeks and 37- 40 weeks dampens down asthma symptoms
  • Oesophageal reflux in late pregnancy can stimulate the release of histamines from the gastric mucosa, triggering an asthma attack.
  • Most women experience few or no adverse effects on maternal or fetal wellbeing
  • Poor symptomatic control and frequent exacerbations during pregnancy may cause chronic maternal hypoxia, with resultant decreased fetal oxygenation
  • Left uncontrolled, asthma has been associated with increased incidence of maternal and fetal/neonatal morbidity and mortality
    o Intrauterine growth restriction (IUGR), preterm birth, low birthweight, Caesarean section birth.
22
Q

Asthma attacks in pregnancy

A
  • Mild asthma
    o Unlikely to deteriorate during pregnancy/labour
  • Severe asthma
    o Higher risk of worsening in pregnancy/puerperium
  • Acute attacks are unlikely during labour because of increased endogenous steroids and cortisol which cause bronchodilation
  • Exacerbations or more frequent ‘attacks’ may be related to changes in compliance with medication regimes
    o Directed by medical advice
    o Client’s own decision (fear, anxiety, misinformation).
23
Q

Acute severe asthma

A
  • Midwives have an important role in helping prevent severe asthma attacks through providing education and support about continuation of triggers, early recognition of chest infection and the importance of early admission in the event of deterioration because of the rapidity of the deteriorating events.
  • Extremely dangerous condition requiring care in ICU and respiratory physician.
  • May require short courses of oral steroids if asthma symptoms not controlled with inhalers
  • Status asthmaticus is a medical emergency
  • Can get rapid deterioration of maternal condition, requiring immediate intervention
  • Signs & symptoms
    o Peak expiratory flow rate less than 50% of normal
    o Oxygen saturation falls to 90% or less
    o Blood gases outside normal range ( decrease of pO2; ↑pCO2)
    o Tachypnoea (over 25 breaths/minute)
    o Tachycardia (heart rate over 110 bpm)
    o Acute distress, inability to speak, cyanosis, collapse
  • First-line management of this condition:
    o Transfer urgently to hospital
    o Hydration
    o Oxygen therapy (high flow rate)
    - Aim to maintain oxygen saturation above 95%
    o Antibiotics for suspected infection
    o Bronchodilators delivered via nebuliser/O2
    o Systemic corticosteroids
    o Respiratory stimulants
    o Reassurance, information, support
    o Doctors may request chest X-ray
    o Ensure A&E staff know not to avoid steroids in the pregnant client with acute exacerbation of asthma.
24
Q

Antenatal care of women with asthma

A
  • Initial advice and ongoing monitoring of respiratory function
  • Appropriate involvement of obstetrician and physician (and family G.P.)
  • Assessment and documentation of the woman’s asthma triggers
  • Education measures, including smoking cessation information
  • Encourage compliance with drug therapy
  • For women who are in-patients in hospital, ensure ready access to medication and equipment (e.g. salbutamol inhalers, mouthpieces for peak flow devices, nebuliser devices).
25
Q

Intrapartum care of women with asthma

A
  • Advising them what to expect
  • Acute asthma is rare in labour
  • Monitor maternal condition
    o Close liaison with obstetrician and respiratory physician (may also involve anaesthetist)
  • Ensure fetal wellbeing
    o Continuous fetal monitoring may be indicated in severe asthma
  • Maintain adequate hydration in labour
  • Appropriate pain relief; support coping mechanisms. Careful of pethidine – bronchospasm.
  • If anaesthesia is required – regional blockage to general anaesthetics due to the risk of chest infection.
  • Continue normal asthma medication in labour
    o If currently taking oral steroids (prednisolone) at a dose exceeding 7.5mg daily to control asthma, will require IV steroids (hydrocortisone, 100mg 6-8 hourly) in labour
  • Prostaglandins
    o (induction of labour; treating PPH)
    o PGE2 (dinoprostone) - bronchodilator effects
    o PGF2a (hemabate) - can cause bronchospasm -> vasoconstricts
    o ? Mifepristone and misoprostol but not usually the case with E series
  • Analgesia
    o Epidural blockade safe
    o ‘Entonox’ safe, but remember – not humidified, so can dry airways and exacerbate wheezing
    o Opiates can cause respiratory depression
  • Cautious use of uterotonic drugs
    o Ergometrine alone can cause bronchospasm, especially if client exposed to- vasoconstriction- G.A.
    o Syntometrine not apparently cause for concern.
26
Q

Postpartum care for women with asthma

A
  • Monitoring for haemorrhage
  • Encouragement of breastfeeding, particularly where there is a strong family history of allergic conditions. The big 5- asthma, eczema, hayfever, migrane,
  • Women return to their pre-pregnancy asthma status within 3 months postpartum
  • Avoiding use of non-steroidal anti-inflammatory drugs, e.g. diclofenac.