Respiratory Distress Flashcards
(47 cards)
cardinal signs of resp distress
2 or more of:
Tachypnoea (RR>60)
Recession: sternal, rib, subcostal
Grunting
Central cyanosis
pathophysiology of tachypnea
Definition: Respiratory rate sustained above 60 breath/min.
Pathophysiology: Infant requires a faster respiratory rate to maintain normal gas exchange because of pulmonary pathology.
pathophysiology of recessions
Definition: Indrawing between the ribs during inspiration is intercostal recession. Indrawing at the costal margin is sub-costal recession.
Pathophysiology: Stiff lungs require a greater negative intrapleural pressure to maintain inflation = intercostal recession.
Flattened diaphragms due to hyperinflation increase the vector of the force perpendicular to the chest wall at the site of insertion of the diaphragm = subcostal recession.
pathophysiology of grunting
Definition: A grunting or groaning sound made during each exhalation.
Pathophysiology: Exhalation against a closed glottis produces the sound. This provides positive airway pressure, reduces atelectasis and improves gas exchange. Inhalation tends to be short while exhalation is prolonged.
pathophysiology if cyanosis
Definition: A clinically apparent blue colour which may be peripheral (hands and feet) or central (tongue, mucous membranes) due to increased concentration of deoxygenated haemoglobin >4,5g/dL.
Pathophysiology: Impaired gas exchange increases circulating deoxygenated haemoglobin concentration > about 4,5g/dl produces clinically apparent cyanosis. Central cyanosis is a clinical indication of hypoxaemia. Oxygenated haemoglobin is pink. Deoxygenated haemoglobin is blue.
most common causes of RD
Hyaline membrane disease
Wet Lung Syndrome
Meconium aspiration syndrome
Pneumonia
CCAM
congenital cystic adenomatoid malformation, now called CPAM: congenital pulmonary airway malformation: condition where an entire lobe of lung is replaced by non-working/non-functional cystic piece of abnormal lung tissue
non-resp causes of RD
Hypothermia
Hypoglycaemia
Congenital heart disease
Metabolic acidosis
who is at risk of HMD
Preterm <35 weeks gestation
Infant of diabetic mother
pathophysiology of HMD
Surfactant deficiency- only produced after 34 weeks gestation.
Surfactant = complex lipoprotein comprised of 6 phospholipids and 4 apoproteins. Functionally, lecithin is the principle phospholipid.
synthesized in the Golgi apparatus of the endoplasmic reticulum of the type II pneumocytes.
Surfactant lowers alveolar surface tension allowing alveolar expansion with minimal effort and prevents alveolar collapse during expiration.
Synthesis of surfactant is inhibited by hypoxia, hypothermia, acidosis.
natural hx of HMD
soon after birth –> Progressively worse for 72 hours then improves as baby begins to produce surfactant.
clinical presentation of HMD
- resp distress
- inactive
- poor tone
- oedematous
- premature
HMD CXR features
Under-expanded lungs
Bilateral disease
Fine reticular-granular “ground-glass” infiltrates
Extend from the hilum to lung peripheries
Air-bronchograms
normal lung expansion
8 posterior ribs; therefore under-expansion would be less than 8 posterior ribs
complications of HMD
Respiratory failure
Pneumothorax
Peri-and intraventricular hemorrhage
PDA leading to heart failure
Secondary pneumonia
Chronic lung disease
mx for HMD
> Prevention
- antenatal steroids to mom if preterm delivery before 34 weeks expected.
> Respiratory support to relieve hypoxia
- Generally will require CPAP
- Aim to maintain sats 90-94% to prevent the complications of oxygen toxicity
> Surfactant replacement therapy:
- Preferably by LISA method, other way is via InSurE
general support for HMD
Transfer to ICU/ high care
Monitoring: Sats, RR, BP, HR, temp, glucose
Temperature control
Nutrition: IV fluids, milk feeds, TPN if unable to initiate feeds
Optimise blood pressure: inotropes if necessary
Optimise haemaglobin: blood transfusion of necessary
Antibiotics for suspected infection
LISA vs InSurE
LISA: less invasive surfactant administration
InSurE: intubation, surfactant, extubation
who is at risk for meconium aspiration?
Term or post-term babies who have been stressed in utero.
More at risk if wasted or UGA
pathophysiology of MAS
Stressed baby passes meconium before delivery
–> Meconium is then inhaled into the lungs when first breaths are taken - Gasping may take place in utero in a stressed baby.
> Meconium is irritant to the lungs causing chemical pneumonitis
> Particulate matter can block bronchi and bronchioles resulting in areas of emphysema and atelectasis
4 injury mechanisms in MAS
- Chemical pneumonitis
- VQ mismatch
- Emphysema
- Surfactant deficiency/washout
clinical findings in MAS
- meconium liquor, nails, skin, chord or placenta
- RD
- hyper inflated chest
MAS CXR features
- Hyperinflated
- Patchy areas of collapse and over-distension.
- Complications such as pneumothorax or pneumomediastinum.
complications of MAS
Respiratory failure
Pneumothorax
Pneumomediastinum
Persistent pulmonary hypertension of the newborn
HIE
Secondary bacterial infection
Chronic lung disease
