Pathophysiology of left-to-right shunts
- Grace C Kung, MD
Grace C Kung, MD
- Associate Professor of Pediatrics
- University of Southern California Keck School of Medicine
- John K Triedman, MD
John K Triedman, MD
- Section Editor — Pediatric Cardiology
- Professor of Pediatrics
- Harvard Medical School
In conditions with left-to-right shunt, blood from the systemic arterial circulation mixes with systemic venous blood. Multiple factors influence the extent of flow through the shunt and its physiologic effects.
The pathophysiology of left-to-right shunts is reviewed here. The evaluation and management of specific cardiac lesions are discussed separately. (See appropriate topic reviews).
FETAL AND TRANSITIONAL CIRCULATION
In the fetus, oxygenated blood is delivered from the placenta via the umbilical vein, which traverses through the liver via the ductus venosus to join the inferior vena cava (IVC) (figure 1). Approximately 45 percent of the umbilical venous blood enters the portal venous system and perfuses the liver en route to the right atrium, while the remainder enters the right atrium directly. This oxygenated umbilical venous blood, which enters the right atrium from the IVC, is preferentially directed across the patent foramen ovale to the left atrium and ventricle. This provides the coronary circulation and arteries supplying the head and neck with relatively well-oxygenated blood.
Blood returning through the superior vena cava is more likely to cross the tricuspid valve, and is ejected via the main pulmonary artery to the lungs or through the ductus arteriosus into the descending aorta. Overall, most of the blood exiting the right ventricle passes right-to-left across the ductus, with only 8 to 10 percent of the fetal cardiac output perfusing the lungs. This distribution of flow is favored by the constriction of the pulmonary arterial bed, resulting in a high pulmonary vascular resistance (PVR), and by the low vascular resistance in the placenta, which results in low systemic vascular resistance (SVR).
With the onset of respiration after delivery, the lungs expand and systemic oxygenation rises. This results in pulmonary vasodilatation and a drop in PVR [1,2]. At the same time, ligation of the umbilical cord removes the placenta from the circulation, with a subsequent increase in SVR. The net impact of these changes is a sudden reversal of blood flow in the ductus from the aorta to the pulmonary artery. In general, increased arterial oxygenation at the ductus results in its constriction and subsequent permanent closure. In addition, the increased pulmonary blood flow, associated with increased pulmonary venous return to the left atrium, usually results in simultaneous functional closure of the foramen ovale. (See "Physiologic transition from intrauterine to extrauterine life".)
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- FETAL AND TRANSITIONAL CIRCULATION
- Shunt size
- Pulmonary effects
- Neurohumoral activation
- Metabolic effects
- Pulmonary hypertension
- CLINICAL MANIFESTATIONS
- Respiratory effects
- Pulmonary infections
- Poor growth
- Time of presentation
- CAUSES OF SHUNTING
- Atrial level shunts
- - Newborns
- Ventricular level shunts
- - Small VSDs
- - Moderate VSDs
- - Large VSDs
- Associated lesions
- Changes during cardiac cycle
- Arterial level shunts
- OTHER INFLUENCES ON SHUNTING
- Other cardiac lesions
- Increased PVR