The pediatric cardiology inpatient nurse’s communication challenge
The pediatric cardiology inpatient nurse works in a specialty where a child’s heart condition is frequently visible to the family through symptoms they can observe — the bluish tinge of chronic cyanosis, the labored breathing of pulmonary congestion, the pallor and cool skin of low cardiac output — while the mechanisms behind the treatment decisions are entirely invisible and often seem to contradict the diagnosis they have been given.
Three recurring communication failures define the challenge in the pediatric cardiology inpatient unit with particular frequency.
The first is the cardiorenal paradox in heart failure. A child admitted for acute decompensated dilated cardiomyopathy is diagnosed with a heart problem. The treatment includes intravenous furosemide — a drug the family knows acts on the kidneys to increase urine output. The family cannot reconcile these two facts. If the problem is the heart, why is the doctor treating the kidneys? The nurse must explain that the failing heart, by backing up fluid into the venous system, creates elevated renal venous pressure that impairs the kidneys’ ability to filter — and that furosemide addresses the mechanism by which the heart failure compounds itself through the kidney, while simultaneously reducing the fluid overload that is drowning the lungs.
The second is the Tet spell intervention paradox. A mother watching a nurse respond to her infant’s hypercyanotic episode by pressing the baby’s knees firmly to her chest cannot understand why a physical maneuver is the treatment for what is clearly a cardiac emergency. The nurse must explain the anatomy of tetralogy of Fallot, the mechanism of infundibular spasm, and how increasing systemic vascular resistance through limb compression can reverse the pressure gradient across a ventricular septal defect to redirect blood toward the lungs.
The third is the milrinone paradox after cardiac surgery. A father who has been told that the congenital heart defect repair was successful comes to the pediatric cardiac ICU to find his infant being started on a medication described as making the heart beat faster and harder. He cannot understand how a heart that just underwent open surgery should be made to work harder. The nurse must explain that milrinone increases contractility through a mechanism that simultaneously reduces the resistance the heart must pump against — producing more cardiac output with less wall stress per beat, not more — and that the need for this support does not mean the surgical repair failed.
Three conversations from the pediatric cardiology inpatient unit:
Scenario 1: Mateo Reyes-Gómez — 8 years old, Houston, Texas
Mateo Reyes-Gómez had been brought to the emergency department six days earlier after his mother noticed that he had been unusually tired for three weeks, had been falling asleep during homework, and had complained of shortness of breath walking up the stairs to their apartment. At the pediatrician’s office, his heart rate was 118 and his SpO2 was 92 percent on room air. The pediatrician heard a soft systolic murmur and bilateral basal crackles and sent him to the children’s hospital emergency department by direct referral.
Chest X-ray showed cardiomegaly with a cardiothoracic ratio of 0.68 and bilateral perihilar infiltrates consistent with pulmonary edema. Echocardiogram confirmed severely dilated left ventricle with diffusely reduced wall motion, ejection fraction 15 percent by biplane Simpson’s method, and functional mitral regurgitation grade 2+ from annular dilatation. BNP was 1,840 pg/mL. He had 3+ pitting edema to the knees. His weight was 4.2 kg above his weight at his last well-child visit three months earlier — retained fluid. His creatinine had risen from a baseline of 0.8 mg/dL to 1.1 mg/dL.
He was admitted to the pediatric cardiology inpatient unit. IV furosemide was started at 1 mg/kg every six hours. He had diuresed 1.4 liters in the first 24 hours and already looked more comfortable. His creatinine, rather than continuing to rise as the team had explained it might, had fallen back to 0.9 mg/dL.
Carlos Reyes worked the overnight shift at a large regional warehouse, supervising a crew of thirty. He had arrived at the hospital directly from his shift, still in his company polo shirt, and had not slept. He sat across from pediatric cardiology inpatient nurse Daniela Fuentes-Morales with the morning labs printout in his hand, looking at the creatinine trend.
“Quiero entender algo que no me cuadra,” he said. “Me dijeron que el problema de Mateo es el corazón. El corazón está débil. Eso lo entiendo. Pero el tratamiento principal que le están dando — el furosemide — es un diurético. Actúa sobre los riñones para sacar líquido. ¿Por qué están tratando los riñones si el problema es el corazón? ¿Y por qué la creatinina, que empezó a subir, ahora bajó después del diurético? Eso tampoco lo entiendo.” (I want to understand something that does not add up to me. They told me Mateo’s problem is the heart. The heart is weak. That I understand. But the main treatment they are giving him — furosemide — is a diuretic. It acts on the kidneys to remove fluid. Why are they treating the kidneys if the problem is the heart? And why did the creatinine, which had started to rise, fall back down after the diuretic? That I also do not understand.)
Daniela recognized that both questions — the furosemide paradox and the creatinine improvement — had the same answer, and that explaining it well would give Carlos a framework for understanding almost everything else they were doing for Mateo.
“Las dos preguntas tienen la misma respuesta, y se la voy a explicar porque creo que va a cambiar cómo entiende todo lo que está pasando. El corazón y los riñones de Mateo están conectados de una manera que hace que lo que le pasa al corazón afecte directamente cómo funcionan los riñones.” (Both questions have the same answer, and I am going to explain it because I think it will change how you understand everything that is happening. Mateo’s heart and kidneys are connected in a way that makes what happens to the heart directly affect how the kidneys work.)
Carlos put down the printout. “Adiélante.” (Go ahead.)
“El corazón de Mateo no puede bombear con la fuerza suficiente. Con la fracción de eyección al 15 por ciento — cuando lo normal es más del 55 — cada vez que el corazón se contrae, solo saca una fraccion pequeña de la sangre que tiene dentro. Eso significa que la sangre se acumula dentro del corazón y detrás de él. El cuerpo interpreta eso como una emergencia — como si Mateo estuviera perdiendo sangre o muy deshidratado. Activa dos sistemas de emergencia. Uno de ellos — el sistema renina-angiotensina-aldosterona — llega a los riñones y les dice que retengan sal y agua para aumentar el volumen en la sangre. El otro — el sistema nervioso simpático — produce vasoconstricción y retención adicional de sodio. Los dos sistemas están tratando de ayudar, pero en realidad están empeorando la situación. El problema de Mateo no es que le falta volumen — es que el corazón no puede mover el volumen que ya tiene. Retener más agua empeora la congestin.” (Mateo’s heart cannot pump with enough force. With ejection fraction at 15 percent — when normal is above 55 — every time the heart contracts it only ejects a small fraction of the blood inside it. That means blood accumulates inside the heart and behind it. The body interprets that as an emergency — as if Mateo were losing blood or severely dehydrated. It activates two emergency systems. One of them — the renin-angiotensin-aldosterone system — reaches the kidneys and tells them to retain salt and water to increase blood volume. The other — the sympathetic nervous system — produces vasoconstriction and additional sodium retention. Both systems are trying to help, but they are actually making the situation worse. Mateo’s problem is not that he lacks volume — it is that the heart cannot move the volume it already has. Retaining more water worsens the congestion.)
Carlos was following closely. “¿Y los riñones?” (And the kidneys?)
“Ahí está la segunda parte. La sangre que se acumula detrás del corazón sube la presión en todas las venas del cuerpo — la presión venosa central. Las venas del cuerpo drenan a la vena cava inferior, que entra al corazón derecho. Cuando la presión venosa central sube, esa presión se transmite hacia atrás por la vena cava inferior. Las venas renales — las venas que salen de los riñones y drenan a la vena cava — también sienten esa presión elevada.” (There is the second part. The blood that accumulates behind the heart raises the pressure in all the veins of the body — the central venous pressure. The veins of the body drain into the inferior vena cava, which enters the right heart. When central venous pressure rises, that pressure transmits backward through the inferior vena cava. The renal veins — the veins that exit the kidneys and drain into the vena cava — also feel that elevated pressure.)
“¿Y eso cómo afecta la filtración?” (And how does that affect filtration?)
“El riñón filtra la sangre en estructuras pequeñísimas llamadas glómerulos. El glómerulo funciona como un filtro de presión: la sangre entra a alta presión por la arteria aferente, y el líquido se filtra hacia una cápsula — la cápsula de Bowman — que tiene una presión menor. La diferencia de presión entre la arteria y la cápsula es lo que genera la filtración. Cuando la presión venosa renal sube — porque la vena cava está congestionada — esa presión se transmite hasta la cápsula de Bowman y la presión dentro de la cápsula sube. Cuando la presión en la cápsula sube, la diferencia con la arteria se reduce. El glómerulo filtra menos. La TFG baja. La creatinina sube.” (The kidney filters blood in tiny structures called glomeruli. The glomerulus works like a pressure filter: blood enters at high pressure through the afferent arteriole, and fluid filters into a capsule — Bowman’s capsule — that has a lower pressure. The pressure difference between the artery and the capsule is what generates filtration. When renal venous pressure rises — because the vena cava is congested — that pressure transmits back to Bowman’s capsule and the pressure inside the capsule rises. When the pressure in the capsule rises, the difference with the artery decreases. The glomerulus filters less. GFR falls. Creatinine rises.)
Carlos sat back. “¿Entonces la creatinina de Mateo no subió porque los riñones están enfermos?” (So Mateo’s creatinine did not rise because the kidneys are sick?)
“Correcto. Los riñones de Mateo están estructuralmente sanos. La creatinina subió porque la presión venosa elevada les está impidiendo filtrar correctamente. Es lo que llamamos síndrome cardiorrenal de tipo 1 — el corazón está dañando la función renal a través de la presión venosa, no porque los riñones estén enfermos.” (Correct. Mateo’s kidneys are structurally healthy. The creatinine rose because elevated venous pressure is preventing them from filtering correctly. It is what we call cardiorenal syndrome type 1 — the heart is impairing renal function through venous pressure, not because the kidneys are diseased.)
“¿Entonces el furosemide...?” (So the furosemide...?)
“El furosemide bloquea un transportador en la parte del riñón que reabsorbe sodio — el asa de Henle. Al bloquear ese transportador, el riñón excreta más sodio y agua en la orina. Mateo pierde el exceso de líquido que retuvo — los 4 kilos de más, el edema en las piernas, el líquido en los pulmones. Al reducir el líquido en el sistema venoso, baja la presión venosa central. La vena cava se descomprime. Las venas renales se descomprimen. La presión dentro de la cápsula de Bowman baja. El gradiente de filtración se restaura. Por eso la creatinina bajó después del furosemide — no porque tratamos los riñones, sino porque quitamos la presión que les estaba impidiendo filtrar. Al mismo tiempo, al reducir el líquido venoso, le quitamos carga al corazón. El ventrículo izquierdo de Mateo, que está ya muy dilatado y trabajando al mínimo de su capacidad, tiene menos volumen que manejar. Eso se llama reducir la precarga — y es parte del tratamiento de la insuficiencia cardiaca.” (Furosemide blocks a transporter in the part of the kidney that reabsorbs sodium — the loop of Henle. By blocking that transporter, the kidney excretes more sodium and water in the urine. Mateo loses the excess fluid he retained — the 4 extra kilograms, the edema in the legs, the fluid in the lungs. By reducing fluid in the venous system, central venous pressure falls. The vena cava decompresses. The renal veins decompress. Pressure inside Bowman’s capsule falls. The filtration gradient is restored. That is why creatinine fell after the furosemide — not because we treated the kidneys, but because we removed the pressure that was preventing them from filtering. At the same time, by reducing venous fluid, we reduce the load on the heart. Mateo’s left ventricle, which is severely dilated and working at the minimum of its capacity, has less volume to manage. That is called reducing preload — and it is part of the treatment for heart failure.)
Carlos was quiet for a moment. He picked up the creatinine printout again and looked at it. “Entonces el furosemide no está tratando los riñones como si estuvieran enfermos,” he said slowly. “Está interrumpiendo el mecanismo por el cual el corazón débil hace que los riñones empeoren la congestión. Y al reducir la congestión venosa, también ayuda a los riñones a filtrar mejor.” (So the furosemide is not treating the kidneys as if they were sick. It is interrupting the mechanism by which the weak heart causes the kidneys to worsen the congestion. And by reducing venous congestion, it also helps the kidneys filter better.)
“Exactamente eso,” Daniela said. (Exactly that.)
Carlos looked out the window. The morning shift was already under way on the ward, carts moving, nurses passing. “¿El corazón de Mateo se puede recuperar?” (Can Mateo’s heart recover?)
“Esa es la pregunta correcta. La miocardiopatía dilatada en niños tiene mejores tasas de recuperación que en adultos. Un porcentaje significativo de niños con miocardiopatía dilatada idiopatica — que es el tipo más probable de Mateo hasta que encontremos una causa — recupera la función ventricular normal con tratamiento médico en los primeros uno a dos años. El tratamiento que estamos empezando — el furosemide para la congestión, más otros medicamentos para el sistema renina-angiotensina que vienen después — es el camino para darle al corazón de Mateo las mejores condiciones para recuperarse.” (That is the right question. Dilated cardiomyopathy in children has better recovery rates than in adults. A significant percentage of children with idiopathic dilated cardiomyopathy — which is the most likely type for Mateo until we find a cause — recover normal ventricular function with medical treatment in the first one to two years. The treatment we are starting — furosemide for the congestion, plus other medications for the renin-angiotensin system that come next — is the path to giving Mateo’s heart the best conditions to recover.)
Carlos nodded. He folded the printout carefully and put it in his shirt pocket. “Voy a llamar a su mamá y le explico,” he said. (I am going to call his mother and explain.)
Scenario 2: Lucía Martínez-Herrera — 7 months old, San Antonio, Texas
Lucía Martínez-Herrera had been diagnosed with tetralogy of Fallot at three days of life when her newborn pulse oximetry screen returned a value of 87 percent and a subsequent echocardiogram confirmed: malaligned outlet ventricular septal defect with posterior deviation of the outlet septum, an overriding aorta receiving approximately 40 percent of its outflow from the right ventricle, moderately severe subpulmonary infundibular stenosis with peak gradient 48 mmHg, and right ventricular hypertrophy. She had been followed in the pediatric cardiology clinic every six weeks. Her oxygen saturations had been acceptably stable at 85 to 90 percent on room air. The surgical team had planned for elective complete repair at six to eight months of age once her weight reached 6 kilograms. She had been admitted to the pediatric cardiology inpatient unit three days earlier for pre-operative monitoring and weight optimization.
At 9 AM on her fourth inpatient day, the nursing assistant went to check on Lucía during a routine vital sign check. She found Lucía crying forcefully from a blood draw attempt that had been made thirty seconds earlier by the phlebotomist, who had left the room. The nursing assistant noticed the crying was intensifying, Lucía’s lips were darkening to deep violet, and her SpO2 monitor was reading 72 and declining.
Pediatric cardiology inpatient nurse Sofía Ríos-Castellanos responded to the bedside in under ninety seconds. She found SpO2 at 59 percent and declining. The systolic murmur — which had been clearly audible at every previous exam, a harsh grade 3/6 ejection murmur in the left upper sternal border from the infundibular stenosis — was inaudible. Lucía was hyperpneic, deeply cyanotic, and inconsolable.
Sofía took Lucía from the crib, placed her in the knee-chest position with the infant’s hips and knees flexed fully to the chest, held firmly with both arms, and began administering blow-by oxygen from the wall outlet. She called out to the nursing assistant: “Necesito morfina 0.1 mg/kg IV ahora. Avisa al equipo.” (I need morphine 0.1 mg/kg IV now. Alert the team.)
Gabriela Martínez had been in the room, sitting in the chair beside the crib, when the spell started. She had jumped to her feet at the first sign of Lucía’s darkening lips. She watched Sofía press her daughter’s knees hard against her chest and hold them there. Within two minutes, the SpO2 monitor read 68. Then 74. The crying had softened. The deep gasping respirations were easing.
“¿Qué está haciendo?” Gabriela asked, her voice controlled but urgent. “¿Por qué le está apretando las piernas? Si el problema es el corazón, ¿no hay que hacer algo con el corazón?” (What are you doing? Why are you squeezing her legs? If the problem is the heart, shouldn’t you do something with the heart?)
Sofía spoke clearly without taking her eyes off the monitor. “Lo que estoy haciendo le está ayudando al corazón. Le voy a explicar exactamente cómo. Primero, Lucía está mejorando — el oxímetro ya va subiendo. Esté tranquila y cuénteme si le cambia algo en la cara.” (What I am doing is helping her heart. I will explain exactly how. First, Lucía is improving — the oximeter is already rising. Stay calm and tell me if anything changes in her face.)
SpO2 was now 79. Lucía’s crying had reduced to intermittent whimpers. The morphine arrived and was administered. SpO2: 83.
Gabriela was watching both the monitor and her daughter’s face. The violet color was fading. “¿Por qué la posición?” she asked again, quieter now. (Why the position?)
“Para entender eso necesito explicarle cómo funciona el corazón de Lucía,” Sofía said, adjusting her hold slightly as SpO2 reached 87. “El corazón de Lucía tiene una pared incompleta entre los dos ventrículos — el tabique. Hay un agujero grande — la comunicación interventricular. A través de ese agujero, la sangre puede pasar en cualquier dirección. La dirección en que pasa depende de las presiones en cada lado. Normalmente, la presión del lado izquierdo es mayor que la del derecho, así que una parte de la sangre va de izquierda a derecha, hacia los pulmones. Eso le da a Lucía una saturación de alrededor del 85 por ciento — no normal, pero suficiente para mantenerla estable.” (To understand that I need to explain how Lucía’s heart works. Lucía’s heart has an incomplete wall between the two ventricles — the septum. There is a large hole — the ventricular septal defect. Through that hole, blood can flow in either direction. The direction it flows depends on the pressures on each side. Normally, the pressure on the left side is higher than on the right, so some blood flows from left to right, toward the lungs. That gives Lucía a saturation of around 85 percent — not normal, but enough to keep her stable.)
“¿Y hoy?” (And today?)
“El corazón derecho de Lucía tiene otro problema: la salida del ventrículo derecho hacia los pulmones está parcialmente bloqueada por un músculo — el infundíbulo. Ese músculo está engrosado y estrecha el paso. Cuando Lucía lloraba con fuerza hace unos minutos, ese músculo entró en espasmo — se contrajo completamente y bloqueó casi toda la salida del ventrículo derecho hacia los pulmones. La sangre desoxigenada del ventrículo derecho no podía salir hacia los pulmones — así que salió por el agujero del tabique hacia el ventrículo izquierdo, y de ahí al resto del cuerpo. Sangre sin oxígeno llegando al cuerpo. La saturación bajó a 52 por ciento.” (Lucía’s right heart has another problem: the outlet of the right ventricle toward the lungs is partially blocked by a muscle — the infundibulum. That muscle is thickened and narrows the passage. When Lucía was crying forcefully a few minutes ago, that muscle went into spasm — it contracted completely and blocked almost all of the right ventricle’s outlet toward the lungs. Deoxygenated blood from the right ventricle could not exit toward the lungs — so it exited through the hole in the septum toward the left ventricle, and from there to the rest of the body. Blood without oxygen reaching the body. Saturation fell to 52 percent.)
Gabriela had both hands pressed to her mouth. “¿Y el soplo que desapareció?” (And the murmur that disappeared?)
“Muy buena observación. Ese soplo que hemos escuchado desde que Lucía nació es el sonido de la sangre pasando a través del paso estrecho del infundíbulo hacia los pulmones. Cuando el músculo se contraje completamente y ya no pasa sangre por ahí, no hay turbulencia, no hay soplo. La desaparición del soplo durante el episodio es una señal de que el bloqueo es completo. Por eso actué inmediatamente.” (Very good observation. That murmur that we have heard since Lucía was born is the sound of blood passing through the narrow passage of the infundibulum toward the lungs. When the muscle contracts completely and no blood passes through there, there is no turbulence, no murmur. The disappearance of the murmur during the episode is a sign that the blockage is complete. That is why I acted immediately.)
“¿Y la posición?” Gabriela asked again, her voice steady now. Lucía’s SpO2 was 89 and her crying had stopped. (And the position?)
“Para cambiar lo que está pasando en el agujero del tabique, necesito cambiar la diferencia de presión entre los dos ventrículos. Si subo la presión en el ventrículo izquierdo más que en el derecho, la sangre vuelve a preferir ir de izquierda a derecha — hacia los pulmones — en lugar de de derecha a izquierda. ¿Cómo subo la presión en el ventrículo izquierdo? Aumentando la resistencia en las arterias del cuerpo — la resistencia vascular sistémica. Cuando el cuerpo tiene que bombear contra más resistencia, la presión dentro del ventrículo izquierdo sube. La posición de rodillas al pecho comprime las arterias grandes de las piernas — la femoral, la ilíaca. La sangre tiene más resistencia para llegar a las piernas. Esa resistencia se transmite hacia atrás y sube la presión en el ventrículo izquierdo. Cuando la presión del lado izquierdo es mayor que la del derecho, la sangre a través del agujero vuelve a ir de izquierda a derecha, hacia los pulmones. Lucía empieza a oxigenar.” (To change what is happening at the hole in the septum, I need to change the pressure difference between the two ventricles. If I raise the pressure in the left ventricle more than in the right, blood will again prefer to go from left to right — toward the lungs — instead of from right to left. How do I raise pressure in the left ventricle? By increasing resistance in the body’s arteries — systemic vascular resistance. When the body has to pump against more resistance, the pressure inside the left ventricle rises. The knee-chest position compresses the large arteries of the legs — the femoral, the iliac. Blood has more resistance to reach the legs. That resistance transmits backward and raises pressure in the left ventricle. When the pressure on the left side is greater than on the right, blood through the hole goes left to right again, toward the lungs. Lucía starts oxygenating.)
Gabriela lowered her hands from her face. She was looking at her daughter, whose color had returned and who was now regarding Sofía with the calm, unsettling focus of a seven-month-old who has no sense of what had just happened.
“Entonces la posición no es para el corazón directamente,” Gabriela said. “Es para las arterias de las piernas, porque al aumentar la resistencia ahí, el ventrículo izquierdo puede mandar más sangre a los pulmones en lugar de que la sangre desoxigenada llegue al resto del cuerpo.” (So the position is not for the heart directly. It is for the arteries of the legs, because by increasing resistance there, the left ventricle can send more blood to the lungs instead of deoxygenated blood reaching the rest of the body.)
“Exactamente eso,” Sofía said. SpO2 was 91. “Y la morfina que le dimos relaja el músculo del infundíbulo que entró en espasmo — reduce la señal del sistema nervioso simpático que lo estaba contrayendo. Los dos juntos — la posición y la morfina — interrumpen el ciclo.” (Exactly that. And the morphine we gave relaxes the infundibular muscle that went into spasm — reduces the sympathetic nervous system signal that was contracting it. Both together — the position and the morphine — break the cycle.)
“¿Esto va a volver a pasar antes de la cirugía?” (Is this going to happen again before surgery?)
“Es posible. Los episodios tienden a ocurrir más al levantarse por la mañana, durante el llanto intenso, o durante la defecación — situaciones que aumentan el tono simpático o cambian las presiones del pecho. Ahora que el equipo sabe que Lucía tuvo un episodio, vamos a hablar con el cirujano sobre acelerar la fecha de la operación. Los episodios hipercianóticos frecuentes son una indicación para avanzar la cirugía antes de lo planeado.” (It is possible. Episodes tend to occur most often in the morning on waking, during intense crying, or during defecation — situations that increase sympathetic tone or change chest pressures. Now that the team knows Lucía had an episode, we are going to speak with the surgeon about advancing the date of the operation. Frequent hypercyanotic episodes are an indication to advance surgery earlier than planned.)
Gabriela sat down beside her daughter’s crib. She reached in and touched Lucía’s hand. Lucía closed her fingers around her mother’s index finger and held it.
Scenario 3: Diego Espinoza-Morales — 5 months old, Dallas, Texas
Diego Espinoza-Morales had been diagnosed with complete atrioventricular septal defect and trisomy 21 at his fetal anatomy ultrasound at 20 weeks gestation. A fetal echocardiogram had confirmed: complete common AV valve with primum ASD and large inlet VSD, balanced ventricles, no other anomalies. He was delivered at a center with pediatric cardiac surgery capability and followed in the pediatric cardiology clinic from birth. His weight gain had been adequate with caloric fortification of breast milk. At five months, weighing 5.8 kilograms, he underwent complete surgical repair: reconstruction of the divided common AV valve into a competent left and right AV valve, closure of the primum ASD with a pericardial patch, and closure of the inlet VSD with a dacron patch. Cardiopulmonary bypass time was 112 minutes. Cross-clamp time was 74 minutes. Surgeon’s note: good biventricular function on separation from CPB with pressors; defects fully closed on transesophageal echo; no residual shunting.
On post-operative day one, the nursing assessment at 6 AM showed: heart rate 184, blood pressure 62/40, extremities cool and mottled to the elbows and knees, capillary refill time 5 seconds, urine output 0.4 mL per kilogram per hour over the preceding 4 hours (oliguria threshold is 1 mL per kilogram per hour), mixed venous oxygen saturation from the central venous line 54 percent (normal >65%), and point-of-care lactate 3.1 mmol/L (normal <2.0). The bedside nurse called the fellow. Pediatric cardiac intensive care attending Dr. Marcos Villanueva-Herrera reviewed the data and ordered milrinone infusion at 0.5 mcg per kilogram per minute to be started immediately, in addition to increasing the existing dobutamine infusion from 5 to 7.5 mcg per kilogram per minute.
Roberto Espinoza drove a long-haul delivery route five days a week. He had taken the week off for Diego’s surgery and had barely slept since the operation. He arrived at the pediatric cardiac ICU at 6:45 AM just as the milrinone was being prepared. He read the medication bag label.
“Espere,” he said to the nurse setting up the infusion. “Ya me dijeron que este medicamento hace que el corazón lata más rápido y más fuerte. ¿Es ese el medicamento correcto para un corazón que acaba de ser operado? Tengo miedo de que si hacemos trabajar al corazón más, se va a cansar. Le acaban de abrir el pecho. Le estuvieron en el corazón por más de una hora.” (Wait. They already told me this medication makes the heart beat faster and harder. Is that the right medication for a heart that just had surgery? I am afraid that if we make the heart work harder, it will get tired. They just opened his chest. They were inside his heart for more than an hour.)
Pediatric cardiac ICU nurse Ana Castillo-Ramírez set the infusion aside for a moment. “La preocupación que tiene es muy lógica, y quiero explicarle exactamente por qué la milrinona es diferente a lo que imagina. No es un medicamento que hace al corazón trabajar más duro. Es un medicamento que hace al corazón trabajar más eficientemente.” (Your concern is very logical, and I want to explain exactly why milrinone is different from what you imagine. It is not a medication that makes the heart work harder. It is a medication that makes the heart work more efficiently.)
Roberto crossed his arms. His eyes moved from Ana to the medication bag and back. (He was asking her to convince him.)
“Primero: ¿por qué Diego necesita apoyo ahora, si la cirugía fue exitosa? La reparación del defecto fue exitosa — el ecocardiograma en quirófano mostró los parches cerrados y las válvulas funcionando. Pero durante la cirugía el corazón de Diego estuvo parado temporalmente con una solución de cardioplegía — una parada controlada para que el cirujano pudiera trabajar dentro de él sin que lata. Ese período de parada es isquemia controlada. Cuando el corazón vuelve a latir y la sangre regresa — la reperfusión — hay un período en que el músculo del corazón está aturdido. Las células del corazón están vivas y se van a recuperar, pero temporalmente no pueden contraerse con toda la fuerza. A eso lo llamamos aturdimiento miocárdico. Es esperado después de cualquier cirugía con circulación extracorporéa. La fracción de eyección real de Diego en este momento es menor que la que tendrá mañana o pasado mañana, cuando el músculo se recupere del aturdimiento.” (First: why does Diego need support now, if the surgery was successful? The defect repair was successful — the echocardiogram in the operating room showed the patches closed and the valves functioning. But during surgery Diego’s heart was temporarily stopped with a cardioplegia solution — a controlled stop so the surgeon could work inside it without it beating. That period of stopping is controlled ischemia. When the heart starts beating again and blood returns — reperfusion — there is a period in which the heart muscle is stunned. The heart cells are alive and will recover, but they temporarily cannot contract with full force. We call that myocardial stunning. It is expected after any surgery with cardiopulmonary bypass. Diego’s actual ejection fraction right now is lower than what it will be tomorrow or the day after, when the muscle recovers from the stunning.)
Roberto’s arms were still crossed but he was listening. “¿Y la milrinona?” (And milrinone?)
“La milrinona es un inhibidor de la fosfodiesterasa 3. La fosfodiesterasa 3 es una enzima que destruye una molécula llamada AMP cíclico dentro de las células del corazón. El AMP cíclico es una señal química dentro de la célula que le dice al corazón que se contraiga con más fuerza. Normalmente esa señal dura poco tiempo porque la fosfodiesterasa la destruye rápidamente. La milrinona bloquea esa destrucción — mantiene la señal activa más tiempo. El corazón de Diego se contrae con más fuerza por latido. Pero — y aquí está la diferencia — sin hacer latir el corazón más rápido. La misma señal química también relaja las paredes de las arterias — tanto las del cuerpo como las de los pulmones. La resistencia contra la que el corazón de Diego tiene que bombear disminuye.” (Milrinone is a phosphodiesterase 3 inhibitor. Phosphodiesterase 3 is an enzyme that destroys a molecule called cyclic AMP inside the heart cells. Cyclic AMP is a chemical signal inside the cell that tells the heart to contract with more force. Normally that signal lasts a short time because phosphodiesterase destroys it quickly. Milrinone blocks that destruction — keeps the signal active longer. Diego’s heart contracts with more force per beat. But — and here is the difference — without making the heart beat faster. The same chemical signal also relaxes the walls of the arteries — both those of the body and those of the lungs. The resistance against which Diego’s heart has to pump decreases.)
Roberto uncrossed his arms. “¿Menos resistencia es mejor?” (Less resistance is better?)
“Mucho mejor. Piense en esto: si un motor tiene que empujar una carga enorme, gasta más energía que si empuja la misma carga con menos resistencia. El corazón es lo mismo. Cuando el corazón bombea contra menos resistencia en las arterias — menos poscarga, lo llamamos — puede generar el mismo flujo de sangre con menos gasto de energía. Menos estrés en la pared del corazón por latido. Más gasto cardíaco con menos trabajo. La milrinona hace dos cosas al mismo tiempo: sube la fuerza de contracción y baja la resistencia que el corazón tiene que vencer. El resultado es que el corazón produce más flujo — y el cuerpo de Diego recibe más sangre oxigenada — con menos estrés por latido que con otros medicamentos que solo aumentan la fuerza sin reducir la resistencia.” (Much better. Think of it this way: if an engine has to push an enormous load, it uses more energy than if it pushes the same load with less resistance. The heart is the same. When the heart pumps against less resistance in the arteries — less afterload, we call it — it can generate the same blood flow with less energy expenditure. Less stress in the heart wall per beat. More cardiac output with less work. Milrinone does two things at the same time: it raises the force of contraction and lowers the resistance the heart has to overcome. The result is that the heart produces more flow — and Diego’s body receives more oxygenated blood — with less stress per beat than with other medications that only increase force without reducing resistance.)
“¿Por qué no simplemente dar más del otro medicamento — la dobutamina?” (Why not just give more of the other medication — dobutamine?)
“La dobutamina activa un receptor diferente — el receptor beta-adrenérgico — y también llega al AMP cíclico, pero por un camino diferente. El problema es que ese receptor también hace que el corazón lata más rápido. El corazón de Diego ya está en 184 latidos por minuto — ya latiendo muy rápido por la situación de bajo gasto. Aumentar la dobutamina sola seguiría subiendo la frecuencia y el consumo de oxígeno. La milrinona llega al mismo AMP cíclico por otro camino — sin activar el receptor beta — así que da la fuerza extra sin añadir más frecuencia. Los dos medicamentos juntos — dobutamina a dosis moderada y milrinona — son el estándar para el síndrome de bajo gasto después de cirujía de corazón congénito en niños porque se complementan exactamente de esa manera.” (Dobutamine activates a different receptor — the beta-adrenergic receptor — and also reaches cyclic AMP, but through a different pathway. The problem is that that receptor also makes the heart beat faster. Diego’s heart is already at 184 beats per minute — already beating very fast from the low output situation. Increasing dobutamine alone would keep raising the rate and oxygen consumption. Milrinone reaches the same cyclic AMP through another pathway — without activating the beta receptor — so it gives the extra force without adding more rate. Both medications together — dobutamine at moderate dose and milrinone — are the standard for low cardiac output syndrome after congenital heart surgery in children because they complement each other exactly in that way.)
Roberto was quiet for a long moment. He looked at Diego — the small face partially obscured by the ventilator tube, the leads on his chest, the multiple infusion lines, the saturation probe on his finger, the urinary catheter. He had been a large healthy baby; he was now a five-month-old in a CICU bed surrounded by more technology than Roberto had encountered in any other context.
“¿Cuándo va a mejorar?” Roberto asked. “No el monitor — él. Diego.” (When is he going to get better? Not the monitor — him. Diego.)
“El aturdimiento del músculo del corazón después de la cirugía con circulación extracorpórea típicamente mejora en 12 a 24 horas. Esperamos que para esta tarde o esta noche los números empiecen a mejorar — la saturación venosa mixta, el gasto urinario, el lactato. En las próximas 24 a 48 horas, si Diego responde bien a los medicamentos como esperamos, empezaremos a reducirlos gradualmente. El proceso de recuperación del corazón después de esta cirugía en un bebé de 5 meses es de una a dos semanas de hospitalización en total — tiempo en la UCIP y después en el piso de cardiología. El defecto está cerrado. Diego tiene las condiciones para recuperarse completamente.” (Myocardial stunning after surgery with cardiopulmonary bypass typically improves in 12 to 24 hours. We expect that by this afternoon or tonight the numbers will begin to improve — the mixed venous saturation, urinary output, lactate. In the next 24 to 48 hours, if Diego responds well to the medications as we expect, we will begin reducing them gradually. The recovery process for the heart after this surgery in a 5-month-old is one to two weeks of total hospitalization — time in the CICU and then on the cardiology floor. The defect is closed. Diego has the conditions to recover completely.)
Roberto put his hand very lightly on Diego’s forearm — the only part of his arm not covered by leads or lines — and left it there.
“Entonces la milrinona no está haciendo que el corazón de Diego trabaje más duro,” Roberto said. “Está haciendo que trabaje mejor — con más fuerza por latido y con menos resistencia en las arterias, sin el gasto extra de oxígeno que tienen los otros medicamentos.” (So milrinone is not making Diego’s heart work harder. It is making it work better — with more force per beat and less resistance in the arteries, without the extra oxygen expenditure of the other medications.)
“Exactamente,” Ana said. She restarted the milrinone setup. “Y mientras tanto, el músculo de Diego se está recuperando.” (Exactly. And meanwhile, Diego’s muscle is recovering.)