Pediatric Cardiac Anesthesia Handbook (eBook)

James A. DiNardo, Viviane G. Nasr (Autoren)

eBook Download: EPUB

2024 | 1. Auflage
384 Seiten
Wiley (Verlag)
978-1-119-83541-7 (ISBN)

Infos

A concise yet comprehensive overview of the anesthetic management of pediatric patients with congenital heart disease

Designed for ease of use, The Pediatric Cardiac Anesthesia Handbook is divided into two parts: Part One covers the basic assessment of patients, including cardiovascular physiology, the pathophysiology of coronary heart disease, preoperative evaluation, intraoperative management, and interpretation of cardiac catheterization data. Part Two contains templated chapters that address a variety of disorders, allowing easy reference to anatomical and physiological features, surgical therapies, anesthetic approach, and postoperative management.

Now in its second edition, The Pediatric Cardiac Anesthesia Handbook contains new chapters on coagulation and blood management, echocardiography, risk scoring systems, and postoperative critical care management, as well as a completely revised chapter on mechanical circulatory support.

Providing clear and reliable, this easily referable pocket-sized resource:

• Addresses the additional complexities of pediatric patients and the anesthetic considerations for non-cardiac surgery after heart and heart-lung transplantation
• Provides guidelines on specific lesions for the pediatric anesthesiologist caring for cardiac patients presenting for non-cardiac surgery
• Contains templated chapters that allow easy reference by members of the multidisciplinary team, such as cardiologists, cardiac intensivists, perfusionists, and surgeons
• Features high-quality illustrative echocardiographic images in every chapter and bulleted content designed for rapid reference

Written by an expert author team at the world-renowned Boston Children's Hospital, The Pediatric Cardiac Anesthesia Handbook is a must-have guide and study aid for anesthesiology and cardiac critical care trainees and practitioners who manage patients with congenital heart disease.

VIVIANE G. NASR, M.D., MPH, FASA is Chief of the Division of Cardiac Anesthesia at Boston Children's Hospital, where he holds the Francis X. McGowan, Jr., MD Chair in Cardiac Anesthesia. Dr. Nasr is an Associate Professor of Anesthesia at Harvard Medical School.

JAMES A. DINARDO, M.D., FAAP, FASA is the past Chief of the Division of Cardiac Anesthesia at Boston Children's Hospital and previous holder of the Francis X. McGowan, Jr., MD Chair in Cardiac Anesthesia. Dr. DiNardo is a Professor of Anesthesia at Harvard Medical School.

Textauszug

1
Cardiovascular Development

The incidence of congenital heart disease (CHD) is approximately 7–10 per 1000 live births. Most congenital heart defects are the result of an interaction of genetic predisposition and environmental factors. Environmental factors such as drugs, viral infection, maternal diabetes, or maternal alcohol abuse may account for specific lesions. Knowledge of cardiac development is a must to understand congenital heart lesions. This chapter reviews the embryology and cardiovascular physiology at birth.

Embryology

It is essential to understand the basic embryology and origin of the cardiac structures in order to appreciate the specific lesions described in the next section of the Handbook. It is beyond the scope of this Handbook to discuss the details of cardiac development, including: (i) cardiac sidedness or asymmetry; (ii) cardiac looping; (iii) formation of outflow tracts; and (iv) septation. The embryologic structures and their corresponding adult structures are listed in Table 1.1.

Cardiovascular Physiology

Circulatory changes occur at birth and continue over the first few days and the first months of life, and are considerable. They need to be appreciated in order to understand their profound effects on neonatal cardiovascular physiology. It is not coincidental that 50% of neonates born with CHD will become ill enough during the first days or weeks of life to require medical or surgical intervention. Optimal perioperative and anesthetic management of the neonate with CHD must be based on a firm understanding of these developmental changes.

Fetal Circulation

Fetal circulatory channels shunt blood away from the lung such that both ventricles, in parallel, contribute to systemic oxygen delivery by pumping blood to the systemic arterial system. This parallel circulation permits normal fetal growth and development even in fetuses with cardiac malformations.

Oxygenated blood from the placenta returns to the fetus via the umbilical vein, which enters the portal venous system. The ductus venosus connects the left portal vein to the left hepatic vein at its junction with the inferior vena cava (IVC). This allows approximately 50% of umbilical venous blood to bypass the hepatic sinuses. The remainder of the umbilical venous flow passes through the liver and enters the IVC via the hepatic veins. Fetal IVC blood is a combination of blood from the lower fetal body, umbilical vein, and hepatic veins. The stream of blood from the ductus venosus has a higher velocity in the IVC than the stream from the lower body and hepatic veins. This higher velocity facilitates delivery of this higher‐oxygen content blood across the foramen ovale (FO) into the left atrium (LA) (Figure 1.1).

Table 1.1 Cardiovascular embryologic structure and the corresponding structures in adults.

Embryologic structure	Adult structure

Truncus arteriosus

Aorta Pulmonary trunk

Bulbus cordis

Smooth part of right ventricle (conus arteriosus) Smooth part of left ventricle (aortic vestibule)

Primitive ventricle

Trabeculated part of right ventricle Trabeculated part of left ventricle

Primitive atrium

Trabeculated part of right atrium Trabeculated part of left atrium

Sinus venosus

Smooth part of right atrium (sinus venarum) Coronary sinus Oblique vein of left atrium

Aortic arches

1

*

2

*

3	Common carotid arteries Internal carotid arteries (proximal part)

4	Right subclavian artery (proximal part) Part of the aortic arch

5	Regresses in the human

6	Pulmonary arteries (proximal part) Ductus arteriosus

The IVC blood enters the right atrium (RA) and, due to the position of the Eustachian valve, Chiari network, and FO, enters the LA during 80% of the cardiac cycle. During the other 20% (atrial systole), IVC blood crosses the tricuspid valve and enters the right ventricle (RV). The overwhelming majority of superior vena cava (SVC) blood crosses the tricuspid valve and also enters the RV. Blood from the RV is ejected into the pulmonary artery (PA). Approximately 10–15% of blood from the PA passes through the lungs to reach the LA, and the rest is shunted to the distal aorta via the ductus arteriosus (DA). As a result, two‐thirds of the total fetal cardiac output is provided by the RV, with the remaining one‐third provided via the LV.

The dynamics of shunting at the level of the ductus venosus, FO, and DA result in a preferential delivery of the most highly oxygenated blood to the coronary and cerebral circulations. Obviously, this preferential delivery of oxygenated blood may be compromised in utero by cardiac lesions that prevent or reduce left ventricular output. At birth, a series circulation is established in which each ventricle pumps into a specific vascular bed (RV to pulmonary artery, LV to aorta). The removal of the placenta and the initiation of alveolar ventilation at birth have the immediate effect of establishing this series circulation. To maintain the adult series circulation, the fetal channels must be closed (Table 1.2). Complex neurochemical and hormonal influences affect the closing of these fetal shunts. Acidosis, sepsis, hypothermia, hypoxia, and hypercarbia may cause a reopening of the shunts and persistence of the fetal circulation (PFC). Most neonates who are critically ill from CHD have one or more of these inciting factors at the time of presentation. In some instances, the persistence of fetal circulatory channels may be beneficial or even mandatory for survival.

Figure 1.1 Course of the fetal circulation in late gestation. Note the selective blood flow patterns across the foramen ovale and the ductus arteriosus.

Source: Reproduced from Greeley et al. (2010)/with permission of Elsevier.

Closure of the Ductus Arteriosus

In the fetus, patency of the ductus arteriosus is maintained by high levels of prostaglandins (PGI2 and PGE1). There are two stages of ductal closure in the newborn: functional closure and permanent anatomic closure. Functional closure occurs by contraction of the smooth muscle of the ductal wall and usually occurs within the first day of life. An increase in PO2 and a decrease in prostaglandin levels contribute to functional closure. Oxygen is a dose‐dependent ductal constrictor that acts by increasing the rate of oxidative phosphorylation within smooth muscle cells. In addition, the response to oxygen may be age related; full‐term neonates have a more dramatic response to oxygen than immature newborns. Norepinephrine and epinephrine, by changing pulmonary and systemic vascular resistances, may secondarily contribute to ductal closure. Acetylcholine has a direct constrictor effect on ductal tissue. Permanent anatomic closure of the duct usually is accomplished by 2–3 weeks of life in the normal full‐term neonate. The lumen is sealed by fibrous connective tissue, leaving the vestigial structure, known as the ligamentum arteriosum.

Table 1.2 Fetal structures and their corresponding structure in adults.

Fetal structure	Adult structure

Foramen ovale

Fossa ovalis

Umbilical vein

Ligamentum teres

Ductus venosus

Ligamentum venosum

Umbilical arteries

Medial umbilical ligaments, superior vesicular artery

Ductus arteriosus

Ligamentum arteriosum

The survival of some neonates with congenital cardiac lesions is dependent on ductal patency. Because functional closure is a reversible event, the use of PGE1 infusions (0.01–0.05 μg kg–1 min–1) has been one of the major medical advances in the stabilization of neonates with ductal‐dependent heart lesions. Preterm neonates are at risk of delayed ductal closure. This may be due to a decreased degradation of PGE1, an increased production of PGE1, or a diminished sensitivity to the ductal‐constricting effects of oxygen. In instances in which delayed ductal closure is disadvantageous, prostaglandin inhibitors such as indomethacin (0.1–0.3 mg kg–1 PO or IV) have been used successfully to promote ductal closure and establish normal patterns of pulmonary blood flow.

Closure of the Foramen Ovale

In utero, the right atrial pressure is higher than the left atrial pressure. IVC blood flows in such a manner as to keep the FO open. The cessation of umbilical vein flow causes a significant decrease in venous return to the right heart, leading to a decrease in right atrial pressure. In addition, ventilation causes a marked increase in pulmonary arterial and venous blood...

Produkt-Details

• Erscheint lt. Verlag: 18.9.2024
• Sprache: englisch
• Themenwelt: Medizin / Pharmazie ► Gesundheitsfachberufe
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete ► Pädiatrie
• ISBN-10: 1-119-83541-0 / 1119835410
• ISBN-13: 978-1-119-83541-7 / 9781119835417