Download RIGHT ATRIAL PRESSURE AS A MEASURE OF VENTRICULAR

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Hypertrophic cardiomyopathy wikipedia , lookup

Jatene procedure wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Atrial septal defect wikipedia , lookup

Ventricular fibrillation wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Transcript
A228
RIGHT ATRIAL PRESSURE AS A MEASURE OF VENTRICULAR CONSTRAINT IN THE
NEWBORN LAMB
Fauchère J-C, Skuza EM, Walker AM, Ramsden AR*, Grant DA
Centre for Baby Health Research, Institute of Reproduction and Development, Monash University, and
*
Neonatal Intensive Care Unit, Monash Medical Centre, 246 Clayton Road, Clayton, Melbourne, Victoria,
3168.
Due to their close apposition to the heart, the chestwall, the lungs and the pericardium constrain the heart, limit
diastolic filling, and thus limit cardiac output. Experimentally, ventricular constraint can be quantified by
measuring pericardial pressure using a balloon transducer but, as yet, no means of clinical assessment of
ventricular constraint in the sick newborn exists. Nor is there a method for assessing the impact of mechanical
ventilation on ventricular constraint. Aim: To determine if right atrial pressure is a useful estimate of
ventricular constraint in newborn lambs. Methods: We measured right atrial pressure (Pra) and thoracic
inferior vena cava pressure (Pivc) with fluid-filled catheters in 4 week old anaesthetised, ventilated lambs
(n=12). Pericardial pressure (Pper) was measured with a flat, liquid-containing balloon positioned over either
the left ventricle (n=6), or over the right ventricle (n=6). Initially, the relationships between mean Pra, Pper, and
Pivc were assessed while changing intravascular volume (Fig. 1). Pra, Pper and Pivc were subsequently
measured while airway pressure was briefly reduced from various levels of CPAP (2.5, 5, 7.5 and 15 cmH 2O) to
atmospheric pressure (Fig. 2). Changes in Pra, Pper, and Pivc (Pper, Pra and Pivc) were calculated
following the reduction of airway pressure to evaluate the effects of mechanical ventilation on ventricular
constraint (Fig. 3). Results: A strong linear relationship existed between Pra and Pper (Pra = 0.9 Pper + 0.3, r
= 0.9; p < 0.0001). A strong linear relationship also existed between Pra and Pivc (Pra = 1.0 Pivc - 0.1, r = 1.0;
p < 0.0001). Changes in Pper induced by altering airway pressure were reliably reflected by Pra (Fig. 3);
Pra = 0.8 Pper + 0.1, r = 0.97, p < 0.0001).
Figure 1
Figure 2
Figure 3
Airway
(cmH2O)
20
5
y = 0.99x - 0.74
2
R = 0.99
0
0
5
10
Pper (mmHg)
15
0
10
-10
10
-10
 Pra (mmHg)
Pericardial
(mmHg)
10
6
Right Atrial
(mmHg)
Pra (mmHg)
15
4
2
y = 0.80x + 0.05
2
R = 0.94
0
0
2
4
 Pper (mmHg)
6
Conclusions: Our study reveals that right atrial pressure and inferior vena cava pressure are accurate measures
of pericardial pressure and thus of ventricular constraint. Moreover, by briefly interrupting mechanical
ventilation, changes in right atrial pressure can be used to quantify the magnitude of ventricular constraint
arising from mechanical ventilation. Applications of our findings to the clinical setting may allow ventilation
to be manipulated with the aim of minimising ventricular constraint while optimising gas exchange.