Hemodynamic consequences of respiratory interventions in preterm infants

Abstract

Advances in perinatal management have led to improvements in survival rates for premature infants. It is known that the transitional period soon after birth, and the subsequent weeks, remain periods of rapid circulatory changes. Preterm infants, especially those born at the limits of viability, are susceptible to hemodynamic effects of routine respiratory care practices. In particular, the immature myocardium and cardiovascular system is developmentally vulnerable. Standard of care (but essential) respiratory interventions, administered as part of neonatal care, may negatively impact heart function and/or pulmonary or systemic hemodynamics. The available evidence regarding the hemodynamic impact of these respiratory practices is not well elucidated. Enhanced diagnostic precision and therapeutic judiciousness are warranted. In this narrative, we outline (1) the vulnerability of preterm infants to hemodynamic disturbances (2) the hemodynamic effects of common respiratory practices; including positive pressure ventilation and surfactant therapy, and (3) identify tools to assess cardiopulmonary interactions and guide management.

Fig. 1. Differences in extremely preterm infants influencing cardiopulmonary transition at birth during mask ventilation.

Mask leaks, intermittent glottic closure, fluid filled and surfactant deficient canalicular lung reduce alveolar PAO2 for a given FiO2. Vasodilator response of pulmonary arterial smooth muscle cells (PASMC) from preterm to PO2 is impaired resulting in persistently elevated pulmonary vascular resistance leading to right-to-left (R-L) shunts at patent ductus arteriosus (PDA) and patent foramen ovale (PFO). Persistent hypoxemia and trigeminal cardiac reflex due to mask pressure on the face can lead to bradycardia and respiratory depression. Copyright Satyan Lakshminrusimha.

Fig. 2. Anatomic and physiologic pulmonary differences in extremely preterm infants.

The canalicular stage lung with surfactant deficiency, reduced elastin and fewer pores of Kohn and canals of Lambert increases tendency to collapse. Hypoxemia and brain pathology such as intraventricular hemorrhage (IVH) lead to respiratory depression. A relatively large, floppy epiglottis and laryngotracheobronchomalacia contribute to airway obstruction. Soft, compliant chest wall, stiff lungs, horizontal rib alignment and a flat diaphragm with fewer type I muscle fibers prevent achieving and sustaining functional residual capacity (FRC). Respiratory depression, failure to sustain FRC and presence of right-to-left atrial and ductal shunts contribute to hypoxemia. Copyright Satyan Lakshminrusimha.

Fig. 3. Cardiopulmonary interactions during spontaneous breathing and positive pressure ventilation (PPV).

A Spontaneous inspiration is associated with negative alveolar and intrathoracic pressure enhancing systemic venous return, increasing right ventricular (RV) preload and pulmonary blood flow (Qp). B During PPV, inflation increases alveolar, intrathoracic, right and left atrial (RA and LA) pressure impeding systemic venous return and reducing RV preload. Increasing alveolar pressure influences Qp. Low alveolar pressure increases extraalveolar pulmonary vascular resistance (PVR) while reducing alveolar PVR (inset in figure B). High alveolar pressure reduces extraalveolar PVR and increases alveolar PVR. The net total PVR is lowest at functional residual capacity (FRC). High intrathoracic pressure enhances systemic blood flow by increasing the intrathoracic to extrathoracic gradient. Copyright Satyan Lakshminrusimha (with permission).