Respiratory Flashcards
Explain the stages of lung development
EMBRYONIC
- 0-6 weeks
- trachea and bronchi formed
PSEUDOGLANDULAR
- 7-16 weeks
- brochioles, terminal bronchioles, pulmonary circulation established
- breathing movements by week 10
CANALICULAR
- 17-24 weeks
- respiratory bronchioles, primitive alveoli formed
- primitive type 1 and 2 pneumocytes form
SACCULAR
- 25-36 weeks
- alveolar ducts, thin-walled alveolar sacs,
- primitive type 1 and 2 pneumocytes continue forming
- surge in production of surfactant from 32-36 weeks
ALVEOLAR
- >37 weeks
- definitive alveoli and mature type 2 cells formed
- maturation across next 5 years - this is protective when infants require ventilation or resp support which may cause some level of damage
Identify the common respiratory diseases in the newborn period
Respiratory distress syndrome
Meconium aspiration syndrome
Transient tachypnoea of the newborn
Apnoea
Apnoea of prematurity
Bronchopulmonary dysplasia
Pneumonia
Persistent pulmonary hypertension of the newborn
What is the role of surfactant
Surfactant reduces surface tension in the alveoli to prevent alveolar collapse and form a functional residual capacity
- the air remaining in the lungs at the end of expiration
- produced by type I and II pneumocutes in large quantities from 32 weeks
- infants <26 weeks there is not enough surfactant to sustain ventilation
What are the 5 cardinal signs/s+s/clinical manifestations of respiratory distress
Grunting - the infant is attempting to close or partially close the glottis during expiration to create their own functional residual capacity and avoid atelactasis
Cyanosis - in the first 24 hours peripheral is normal, central indicates L-R shunting. After 24hrs none is normal
Nasal flaring - compensatory to increase airway diameter to increase volume of air
Tachypnoea - >60 is an attempt to increase O2 intake
Rib retractions - indicates poor lung compliance, use of accessory muscles to increase airway resistance and bring in more air
Secondary consequences of apnoea is bradycardia
Differentiate between respiratory distress and RDS
Resp distress - the presentation of two or more of the cardinal signs
RDS - the clinical diagnosis of a surfactant deficiency or dysfunction
Outline the pathophysiology and risk factors for RDS
Pathophysiology: disorder of the preterm lung due to surfactant deficiency
- lung has not matured to a stage where pneumocytes are porducing significant nlevels of surfactant to maintain FRC, leading to resp distress
Risk factors:
- preterm
- MAS - denatures surfactant
- poorly controlled GDM - denatures surfactant
- asphysxia - denatures surfactant
- cold stress - denatures surfactant
- male
Midwifery management:
- temperature control
- minimal handling
- blood cultures and antibiotics
- nasal CPAP
Outline the pathophysiology and risk factors for TTN
Pathophysiology: Pulmonary oedema resulting from a delay in the reabsorption and clearance of amniotic fluid from fetal lungs
- typically still clears within 2-3 days
Risk factors:
- term
- caesar
- precip
- exposure to methamphetamines
- LGA
- maternal diabetes
Midwifery management:
- CPAP
- fluid restrictions and fluid balance
- BGL
- antis and cultures - exclude pneumonia and spesis
- monitor for S+S of respiratory distress and obs
Outline the pathophysiology and risk factors for MAS
Pathophysiology: An infant experiences a hypoxic event in utero which leads them to pass meconium. The infant then gasps at or around birth leading to the aspiration of meconium which causes airway obstruction, stimulates an inflammatory response in the lungs, denatures surfactant,
Risk factors:
- post term
- asphyxiation/ non-reassuring CTG
- PET and other conditions of HTN which decrease fetal reserves
- smoking and substsance use
Midwifery management:
- increased monitoring - mec obs
- temp control
- CPAP or HFNC
- cultures and antis
- minimal handling
- potential intubation
Outline the pathophysiology and risk factors for apnoea of prematurity
Pathophysiology: premature infants, especially below 34 weeks, have an immature cerebral cortex and brainstem. This menas they have a decreased respiratory drive and a decreased sensitivity to changes in O2 and CO2, which causes periods of apnoea (cessation of breathing >20 seconds)
- also a condition of exclusion - rule out sepsis
- proportional to decreasing gestational age
- resolves before or at term (takes till term for infants <28 weeks)
Risk factors:
- prematurity
Midwifery management:
- caffeine citrate - stimulant which stimulates all immature respiratory responses which cause apnoea
- monitoring of vital signs - cardiorespiratory monitoring etc.
- positioning head and neck in neutralposition
- temp control
- O2 supplementation
- nasal CPAP >32 weeks
Goals of care and interventions for an infant presenting with respiratory distress
Warm:
Nursed naked in temp controlled incubator
- to maintain NTE and avoid cold stress
- naked to observe S+S of resp distress
Septic workup
- FBE, CRP, U+E, Cultures - esp with temp instability to rule out sepsis
Sweet:
Hydration and nutrition via TPN and lipids
- to ensure adequate nutrition for resp demands
- NBM as a full tummy pushes up on diaphragm into already compromised lungs
Monitor BGLS
- to assess for hypoglycaemia which may be increasing O2 demands and worsening resp distress
Pink:
Nurse in prone position supervised
- reduces pressure of diaphragm
- enables maximum expansion of lungs with least amount of effort
Maintain clear airway
- avoid obstruction which can cause hypoxia and resp distress
Apply supplementary O2 or resp support as required
- to maintain oxygen within therapeutic levels
- increase ease of respiration and use positive pressure to maintain airway patency and push out fluid
Oxygen and cardirespiratory monitoring
- ensure consistent monitoring in case of brady or apnoea or hypoxic episode
Monitor blood gases
- assess for hypoxia and hypercarbia to titrate O2
Correct any low BP
- admit BP and with cares
Calm:
Developmental care practices
Family centred care practices
Pain management
Outline the pathophysiology and risk factors for chronic lung disease (BPD)
Pathophysiology: damage to lungs resulting from volutrauma and barotrauma caused by mechanical ventilation, or long term use of oxygen, when required in RDS or other conditions
Risk factors:
- prematurity
- any condition requiring ventilation eg. RDS, patent ductus arteriosis
Midwifery management:
- minimise lung damage - use safe pressures when ventilation
- support growth and development to reduce respiratory distress so O2 can be weaned effectively
- adequate nutrition - support lung development and energy to respire independently
- temp control
- fluid restriction - not placing any more strain on lungs
Outline the pathophysiology and risk factors for pneumonia
Pathophysiology: consolidation at the base of the lung due to infection
- can manifest early - typically due to GBS, viruses or bacterial infections acquired in utero (syphillis, rubella)
- can manifest late - coag neg staphylococci, e. coli etc.
- candidia (oral thrush) especially in preterm infants can transcend into pneumonia
- tachy, febrile, fast resp rate
Risk factors:
- prolonged ROM and labour
- GBS/infected amniotic fluid
- HAI pneumonia from parents, nurses or visitors
Midwifery management:
- bloods and cultures
- antibiotics
- Oxygen or CPAP if required
- mantain nutrition
- maintain temp
- parenteral nutrition and lipid if oral intolerance
- monitoring obs
Outline the pathophysiology and risk factors for pneumothorax
Pathophysiology: air leaks into the pleural cavity, applying pressure on the affected lung causing it to collapse.
- can be spontaneous - in prem babies where lung tissue is more fragile
- can be due to mechanical ventilation - high pressures within the lung cause the alveoli to rupture, and for air to leak through to the pleural space
- can be due to MAS - the thick mec causes areas of air trapping in alveoli, which causes them to be overdistended and rupture (ball valve effect)
- can be due to RDS - as surfactant replacement therapy is occuring, lungs suddenty start functioning more independently, but ventilator remains at same pressure. this overaerates and bursts alveoli, however this is less common now.
Risk factors:
- prem
- MAS
- RDS
Midwifery management:
- O2 therapy
- chest tube insertion
- needle aspiration
- mechanical ventilation adjustments to reduce further air leaks
- obs
Outline the pathophysiology and risk factors for PPHN
Pathophysiology:
Risk factors:
Midwifery management:
Transition to breathing
At birth infants transition from in utero circulation to extrauterine circulation in order to take their first breath
Triggered by
- change in temperature
- change in balance of O2 and CO2
- tactile stimulation and pressure
- fluid filled spaces fill with air which allows fluid to be absorbed into bloodstream, allowing gas exchange (squeezing supports this)
- fetal shunts close and bloodflow is redirected to fetal lungs
initiation and sustainence of regular respirations
fetal catecholamines released in labour stimulates release of surfactant which mobilises lung fluid
