Introduction: Nasal continuous positive airways pressure (n-CPAP)
is an effective treatment in premature infants with respiratory distress.
The cardio-pulmonary interactions secondary to n-CPAP
are well studied in adults, but less well described in premature
infants. We postulated that there could be important interactions
with regard to the patent ductus arteriosus (PDA).
Methods: Prospective study, approved by the local ethic committee.
Premature infants less than 32 weeks gestation, _7 days-old,
needing n-CPAP for respiratory distress, but without the need of
additional oxygen were included in the study. Every patient had a
first echocardiography with n-CPAP and then n-CPAP was
retrieved. 3 hours later the echocardiography was repeated by the
same investigator and then the patient replaced on n-CPAP.
Results: 14 premature newborn were included, mean gestational age
of 28 _ 2 weeks, mean weight 1.1 _ 0.3 Kg and height 39 _ 3 cm.
Echocardiographic measurements are depicted in Table 1.
Significant finding were observed between measurement on n-
CPAP or without n-CPAP: on end diastolic left ventricular diameter
(12.8 _ 1.6 mm vs. 13.5 _ 2 mm), on end systolic left
ventricular diameter (8.4 _ 1.3 mm vs. 9.1 _ 1.5 mm), left
atrium diameter (8.9 _ 2.2 mm vs. 10.4 _ 2.5 mm), maximal
velocity on tricuspid valve (46 _ 10 cm/s vs. 51 _ 9 cm/s), calculated
Qp (3.7 _ 0.8 L/min/m2 vs. 4.3 _ 0.8 L/min/m2). Only
three patients have demonstrated a PDA during the study.
Conclusion: Positive end expiratory pressure (Peep) has hemodynamic
effects which are: reduction of systemic and pulmonary
venous return as shown by the changes on tricuspid valve inflow,on
the calculated Qp and finally on the diameter of the left atrium and
left ventricle.We found in premature infants the same hemodynamic
effects than those described in adults but with lower Peep values.
This could be due to the particular elasticity and weakness of the
thoracic wall of premature infants. Interestingly the flow through
a PDA seems also to be diminished with Peep, but the number of
patients is insufficient to conclude. Further investigation will be
needed to better understand these interactions.
Table 1. Echocardiographic measurement (mean (SD)).
With n-CPAP Without n-CPAP p value
RV ED diameter (mm) 6.3 (1.7) 6.04 (1.1) NS
LV ED diameter (mm) 12.8 (1.6) 13.5 (2.0) _0.05
LV ES diameter (mm) 8.4 (1.3) 9.1 (1.5) _0.05
SF (%) 34 (5) 33 (6) NS
Ao valve diameter (mm) 7.4 (1.3) 7.4 (1.2) NS
LA diameter (mm) 8.9 (2.2) 10.4 (2.5) _0.05
Vmax Ao (cm/s) 70 (16) 71 (18) NS
Vmax PV (cm/s) 69 (15) 72 (16) NS
Vmax TV (cm/s) 46 (10) 51 (9) _0.05
Vmax MV (cm/s) 53 (17) 54 (18) NS
Qp (L/min/m2) 3.7 (0.8) 4.3 (0.8) _0.05
Qs (L/min/m2) 4.0 (0.8) 4.0 (0.7) NS
Qp/Qs 0.92 (0.14) 1.09 (0.23) _0.05
RV: right ventricle, LV: left ventricle, ED: end diastolic, ES: end systolic, SF:
shortening fraction,Ao: aortic valve, LA: left atrium,Vmax: maximum Doppler
Velocity, Qp: pulmonary output, Qs: systemic output, NS: non significant.