Manual of Pediatric Cardiac Intensive Care [PDF]

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Manual of



Pediatric Cardiac Intensive Care



Manual of



Pediatric Cardiac Intensive Care Pre- and Postoperative Guidelines



Manoj Luthra MS, DNB, MCh (Cardiothoracic Surgery), FIACS Professor of Cardiothoracic Surgery and Dean Armed Forces Medical College Pune, Maharashtra, India



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ELSEVIER A division of Reed Elsevier India Private Limited



Manual of Pediatric Cardiac Intensive Care Luthra ELSEVIER A division of Reed Elsevier India Private Limited Mosby, Saunders, Churchill Livingstone, Butterworth-Heinemann and Hanley & Belfus are the Health Science imprints of Elsevier. © 2012 Elsevier All rights are reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the publisher. ISBN: 978-81-312-3050-3 Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The authors, editors, contributors and the publisher have, as far as it is possible, taken care to ensure that the information given in this text is accurate and up-to-date. However, readers are strongly advised to confirm that the information, especially with regard to drug dose/usage, complies with current legislation and standards of practice. Please consult full prescribing information before issuing prescriptions for any product mentioned in this publication.



Published by Elsevier, a division of Reed Elsevier India Private Limited. Registered Office: 305, Rohit House, 3, Tolstoy Marg, New Delhi – 110 001. Corporate Office: 14th Floor, Building No. 10B, DLF Cyber City, Phase-II, Gurgaon, Haryana – 122 002. Senior Commissioning Editor: Shukti Mukherjee Bhattacharya Managing Editor (Development): Shabina Nasim Development Editor: Shravan Kumar Manager – Publishing Operations: Sunil Kumar Manager – Production: NC Pant Typeset by Olympus Premedia Pvt. Ltd. ( formerly Olympus Infotech Pvt. Ltd.), Chennai, India. www.olympus.co.in Printed and bound at Shree Maitrey Printech Pvt. Ltd., Noida



“While it is human to err, it is inhuman not to try, if possible, to protect those who entrust their lives into our hands from avoidable failures and danger” —Max Thorek (1880–1960)



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Foreword



The ability to escort the cardiac patient through the pre- and postinterventional or operative period in the intensive cardiac care unit successfully is the most important part of a clinician’s commitment. A pediatric cardiac patient requires to be handled by an integrated group of specialists that may include not only the surgeon, cardiologist and intensivist but a host of other related specialities. Given this complexity, there is a need for guidelines and protocols to be laid down and a common approach to be followed at any institution. There is an exhaustive amount written on cardiac intensive care as the subject is vast and varied, but not always readily accessible. This book is a practical reference guide with a balanced perspective that can be consulted when faced with a challenging pediatric cardiac case or read otherwise. It is never easy to remember pediatric doses of even common drugs and this manual would serve as a useful aid. Newer techniques and consensus statements have been incorporated. A number of related aspects and complications have been covered which of course is highly relevant as we are dealing with situations where in a large number of drugs are being used on a sick child often in a background of altered ‘milieu interior’. Writing a foreword for this book has brought to the forefront, my own involvement of over three decades, in the surgical treatment of children with heart disease. There have been exciting new developments occurring in the field of intensive care all the time, however, the fundamental issues in management have not changed greatly. Often variations in management amongst the treating specialists are more variations in style rather than substance, and accepted institutional norms of treatment will be of immense benefit to our junior colleagues. Despite the explosive growth of digital technologies, residents and fellows still need that “manual” which is a concise and readable summary of established clinical methods and protocols. I believe this book can stand as one of those cornerstones of intensive care therapy of a child. Graham Nunn FRACS Consultant Pediatric Cardiothoracic Surgeon Formerly, Director of Pediatric Cardiac Surgery, Mater Children’s Hospital, Brisbane, Australia



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Preface



The ability to manage a pediatric cardiac surgical patient in the pre- and postoperative period is as important as the surgery itself. Undoubtedly, the continued improvement in monitors, ventilators, and analyzers has made the task easier, and the results today are better than ever before. Despite the advancement, the precision of a medical device can only compliment a clinician’s knowledge and his practical abilities, and is not going to prevent complications and errors in medical or surgical management. So much has been written about the prevention and management of complications and errors, yet there is no substitute for simple protocols, check lists, and guidelines. This book is an effort in that direction. It summarizes and reiterates the accepted pre- and postoperative guidelines in the intensive care of pediatric cardiac surgery patients. It has been my endeavor to prepare a practical sort of a book that can be easily read at leisure and referred to at the bedside and provide relevant information with drug doses and protocols. I have aimed to keep the chapters short and highly relevant thereby providing simple solutions and explanations to clinical problems rather than offering detailed physiological explanations. Drugs relevant to the system under consideration have been given in tables so that these can be easily referred to at the point of care. Drug doses have been quoted primarily from two sources, the online pharmaceutical reference drugs.com web site (http://www.drugs.com/) and “Martindale: The Complete Drug Reference” (Pharmaceautical Press, Great Britain). Wherever applicable, the current international guidelines on the topic under consideration have been quoted. In several of the chapters, I have taken the liberty of mentioning a relevant quotation at the beginning to provide the reader something to think about! Even though this book is specifically written for the perioperative management of the child undergoing cardiac surgery, it will be equally useful to physicians and nursing staff who are actively involved in the bedside management of any acutely ill child. This book targets cardiac surgery, pediatric and critical care residents working in cardiac intensive care units and junior cardiac surgery consultants. It will address the need of a reference



x



Preface



manual for general surgery and medicine residents too, while on rotation in the cardiac care unit. In the end, I do sincerely hope that I have been able to write something worthwhile for the new cardiac surgeon in the making, which will in some small way contribute to his ascent to the pinnacle of his profession. I am sanguine that this book will also prove adequate for others involved in the intensive care of children.



Acknowledgments In the preparation of this manual I owe a deep debt of gratitude to many of my colleagues from various departments at the college who spared their valuable time to review the chapters in their areas of specialization— Drs. JK Kairi and Sharmila Sinha from the Department of Pharmacology, Drs. Mukti Sharma and Daljit Singh from Pediatrics and Neonatogy, Drs. Ravi Chaturvedi and Vipul Sharma from Anesthesiology, Dr. Velu Nair from Medicine, Dr. Jyoti Kotwal from Hematology, Dr. Subroto Dutta from Cardiology, and Dr. Gaurav Kumar from my Department of Cardiothoracic Surgery. I am grateful to Dr. Prabel Deb for verifying the bibliography and sources. I had the opportunity to interact with some very fine people of the editorial staff of Elsevier, the publishers of this book, and in particular wish to express my gratitude to Mr. Shravan Kumar, Ms. Shabina Nasim, and Ms. Shukti Mukherjee for their professional attitude and support for this project. I would like to thank Mr. Benjamin Jacob who was involved with the initial conception of the book and provided the time and encouragement. The excellent line diagrams and ECGs were made by Mr. Nishant Shinde from the Medical Arts Department. I guess the maximum contribution to any medical text is none other than the patient himself. He provides us not only the purpose of the text but the practical experience to go with it. Even though I mention them last, I owe my wife and daughters so much more than patience, cheer, and sound judgment. Manoj Luthra



Contents



Foreword Preface Acknowledgments



vii ix x



1



Hemodynamic Monitoring



2



Low Cardiac Output



15



3



Inotropes and Other Vasoactive Drugs



24



4



Congestive Heart Failure



32



5



Cardiac Tachyarrhythmias



37



6



Bradyarrhythmias and Pacemakers



63



7



Hypertensive Emergencies



78



8



Pulmonary Hypertension



83



9



Cyanotic Spells



87



10



Pediatric Resuscitation



89



11



Fluid and Electrolytes



100



12



Arterial Blood Gas Analysis



112



13



Parenteral Nutrition



124



14



Enteral Feeding



130



15



Gastrointestinal Drugs



136



16



Postoperative Respiratory Complications



140



17



Acute Respiratory Distress Syndrome



146



1



xii



Contents



18



Postoperative Bronchospasm



150



19



Ventilation



156



20



Ventilator Associated Pneumonia



176



21



Antibiotics



182



22



Sepsis and Multiorgan Dysfunction



202



23



Systemic Antifungal Agents



211



24



Sedatives, Analgesics, and Muscle Relaxants



217



25



Seizures



227



26



Management of the Comatose Child



233



27



Acute Kidney Injury



241



28



Coagulation Disorders in the Postoperative Period



256



29



Antithrombotic Agents



267



30



Management of Anaphylaxis



273



Appendices A B C D E F G H I J K L M N O



International System of Units (SI Units) and Conversion Factors Vital Signs Anthropometric Measurements and Major Motor Milestones Hematological Parameters Normal Laboratory Values for Children Composition of Frequently Used Parenteral Fluids Size and Length of Pediatric Endotracheal Tubes and Suction Catheters Postoperative Checklist on Arrival in ICU Postoperative Instructions Fluid Prescription after Open Heart Surgery Calculations of Drug Infusions Preparation of Various Concentrations of Solutions Cries Pain Scale Drug Prescription in Renal Failure Pediatric Blood Levels of Commonly Used Drugs



Index



277 280 281 283 285 287 289 290 291 295 297 299 301 302 306 307



Hemodynamic Monitoring “Everything that can be counted does not necessarily count; everything that counts cannot necessarily be counted” — Albert Einstein (1879 –1955)



Isovolumic relaxation Isovolumic contraction



Pressure (mmHg)



Ejection Aortic valve opens 120 100 80 60 A-V valve closes 40 a 20 0 R P



Diastasis Rapid Atrial systole inflow Aortic valve closes



A-V valve opens c



Aortic pressure Atrial pressure



v Ventricular pressure ECG



T



Q S Fig. 1: Cardiac cycle.



Mean Arterial Pressure The mean arterial pressure (MAP) determines the volume of blood flow to various organs of the body. It is dependent upon the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP) based on the following relationship: MAP = (CO × SVR) + CVP At normal resting heart rates, MAP can be approximately calculated by adding one-third of the pulse pressure to the diastolic pressure: MAP = DBP + 1⁄ 3 (SBP − DBP) (SBP: systolic blood pressure, DBP: diastolic blood pressure)



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Manual of Pediatric Cardiac Intensive Care



However, at higher heart rates, because of the altered shape of the arterial pressure waveform, the MAP is approximated more closely by the arithmetic mean of systolic and diastolic pressures. The 5th percentile systolic and 5th and 50th percentile mean arterial pressure in normal children can be estimated by the following clinical formulae: SBP (5th percentile at 50th height percentile) = (2 × age in years) + 65 MAP (5th percentile at 50th height percentile) = (1.5 × age in years) + 40 MAP (50th percentile at 50th height percentile) = (1.5 × age in years) + 55. The 5th percentile SBP values have been used to define hypotension in various age groups.



Pulse Pressure Systolic pressure



Pulse pressure (mmHg)



120 Dicrotic notch



Diastolic pressure



80 Fig. 2: Normal arterial pressure waveform.



The pulse pressure is the difference between the systolic and diastolic pressures. An increase in stroke volume or vasodilatation causes widening of the pulse pressure; examples of causes include, anemia, fever, aortic regurgitation, and AV malformation. A decrease in stroke volume or vasoconstriction results in narrowing of the pulse pressure as in hypovolemia, congestive cardiac failure, aortic stenosis, and cardiac tamponade.



Analysis of the Arterial Pressure Waveform The arterial pressure waveform consists of an upstroke to the level of the peak systolic pressure, and then a decline to the level of the end diastolic pressure. The down slope is interrupted by the dicrotic notch, which is a



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3



mmHg



150



100 Normal 50



mmHg



150



100 Overshoot 50



mmHg



150



100 Damped trace 50 Fig. 3: Systolic overshoot and damped arterial waveforms.



reflection of the closure of the aortic valve. The characteristics of the pressure recordings depend upon various factors: Systolic overshoot is a false higher blood pressure reading than the actual pressure because of the dynamic response characteristics of the monitoring system. This may happen when there is a sudden rise in the pressure upstroke of the wave form, as in the pressure recordings in hypertension or rapid heart rates. Damping of the blood pressure tracing abnormally narrows the pulse pressure and should be suspected when the dicrotic notch is not visible on the recording. Damping can be caused by air bubbles or blood in the monitoring lines or kinking of the arterial cannula. The level of the transducer has an effect on the blood pressure recording. Transducer level above the actual level of the left atrium results in under-estimation of the blood pressure and vice versa. (1 cm difference in transducer level causes a 0.74 mmHg variation in the measured pressure, i.e., a level 10 cm below will result in an overestimation of 7.4 mmHg). Correct transducer level is more important for recording CVP and PA pressures, since these pressures are much lower with a smaller range of variation.



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Manual of Pediatric Cardiac Intensive Care



Ascending aorta



Abdominal aorta



Radial artery Fig. 4: Change in the arterial waveform as the arterial pulse travels peripherally.



Site of recording: The arterial pressure waveform also changes as it travels from the central aorta to the periphery, the systolic pressure rises and the diastolic pressure falls (i.e., the pulse pressure widens) and in addition the dicrotic notch appears later. The MAP in the aorta is slightly higher than in the radial artery. Cardiac lesions: Various pathological conditions of the heart also result in alteration of the morphology of the arterial pressure waveform: ■



Pulsus tardus et parvus occurs in aortic stenosis, the upstroke of the pulse rises slowly and peaks late (tardus), the pulse amplitude is small (parvus) with an anacrotic notch on the upstroke and an absent dicrotic notch.



■



In a collapsing pulse, a large stroke volume causes the arterial pulse to rise rapidly and an increased runoff results in a lower diastolic pressure with a wide pulse pressure, e.g., aortic regurgitation and patent ductus arteriosus.



■



In a bisferiens pulse, the arterial pressure pulse has two systolic peaks because of the large stroke volume and a wave of reflection. The bisferiens pulse may be present in aortic regurgitation, in patients with mixed aortic regurgitation and stenosis, and in hypertrophic cardiomyopathy.



■



Pulsus alternans is recognized by the presence of alternating large and small systolic peaks. It is a sign of severe left ventricular systolic dysfunction and may become evident during general anesthesia. Ventricular bigeminy also creates alternating pressure peaks in the arterial pressure waveform, but the ECG rhythm reveals bigeminy. In pulsus alternans, the ECG is regular with a normal QRS configuration.



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5



Normal pulse



Pulses tardus et parvus



Collapsing pulse



Bisferiens pulse



Pulsus alternans Fig. 5: Different arterial waveforms in diseased conditions of the heart.



Pulsus paradoxus is an exaggeration of the inspiratory fall in systolic arterial pressure (more than 10 mmHg) noted during spontaneous respiration. Some inspiratory reduction of blood pressure is normal, and pulsus paradoxus is an exaggeration of this normal phenomenon. It is found in cardiac tamponade, constrictive pericarditis, and in patients with airway obstruction or bronchospasm. Baseline pressure 110 mmHg



■



70 0 Inspiration



Expiration



Inspiration



Fig. 6: Pressure variation during intermittent positive pressure ventilation.



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Blood pressure variation during positive pressure ventilation: A phenomenon that is reverse of pulsus paradoxus is seen during positive pressure ventilation due to changes in systemic venous return. During inspiration, there is an augmentation of systolic pressure and a later decrease in pressure during expiration (in an adult patient, up to a 5 mm increase followed by a 5 mm fall below the baseline measured at end expiration). Hypovolemia results in an increase in this variation, especially downwards even if the systolic pressure is normal.



Analysis of the Central Venous Pressure R P



T Q S



a



ECG v



c x



y



Normal JVP



a c



v x



y



Cannon ‘a’ wave



v a



Giant ‘v’ wave Fig. 7: CVP waveforms and its correlation with the ECG.



The central venous pressure (CVP) is a measure of the mean right atrial pressure, and the waveform reflects the events of cardiac contraction. There are three positive waves (a, c, and v) and two negative descents (x and y), and these correlate with different phases of the cardiac cycle and ECG. ■



‘a’ wave: This wave is a reflection of right atrial contraction and immediately follows P wave on ECG.



■



‘c’ wave: During early ventricular contraction, there is a slight elevation of the tricuspid valve into the right atrium resulting in the c wave. It therefore correlates with the end of the QRS segment on ECG.



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7



■



‘x’ descent: The x descent is caused by the downward movement of the ventricle during systole.



■



‘v’ wave: Right atrial filling results in the v wave.



■



‘y’ descent: The y descent is produced by blood flow into the right ventricle in diastole. It therefore precedes P wave on ECG.



Central venous pressure falls slightly with spontaneous inspiration, and increases marginally with positive pressure inspiration and forced exhalation. Addition of positive end expiratory pressure (PEEP) further increases the CVP, though this may not be significant. (A PEEP of 10 cm H2O is likely to increase the CVP by less than 3 mmHg). The CVP falls because of hypovolemia, shock, and vasodilatation. It is elevated in case of hypervolemia, increased pulmonary vascular resistance, or right ventricular failure.



Abnormal CVP Waveforms Trace



Lesion



Cannon ‘a’ waves



Complete heart block, tricuspid stenosis, pulmonary hypertension, pulmonary stenosis



Absent ‘a’ waves



Atrial fibrillation



Giant ‘v’ waves



Tricuspid regurgitation



Canon ‘a’ waves are produced in AV dissociation because of contraction of the atrium against a closed tricuspid valve. These may also be seen in tricuspid stenosis, pulmonary hypertension, and pulmonary stenosis due to resistance to RV filling. In tricuspid regurgitation, the c wave and x descent are replaced by giant ‘v’ waves because of the regurgitation of blood into the right atrium during ventricular contraction. This can cause a false elevation in the mean CVP. In cardiac tamponade, the CVP is elevated and the y descent is absent.



Normal Pressures and Saturations in Pediatric Heart Chamber



Pressure (mmHg)



O2 saturation (%)



Right atrium (mean)



2–6



60–80



Right ventricle



30/3



60–80



Pulmonary artery (systolic)



15–25



Pulmonary artery (diastolic)



6–12



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Manual of Pediatric Cardiac Intensive Care



Chamber



Pressure (mmHg)



Pulmonary artery (mean) Left atrium (mean)



O2 saturation (%)



15 6–12



97–100



Left ventricle



100/6



97–100



Aorta



100/60



97–100



Left ventricular end diastolic pressure (LVEDP) is a reflection of LV function, and in the absence of mitral valve disease the LVEDP is equal to the left atrial pressure (LAP). Further, if there is no obstruction in the pulmonary venous or capillary blood circulation, the LAP will equal the pulmonary capillary wedge pressure (PCWP). Therefore, the LAP or PCWP is used to monitor left heart function in addition to the volume status of the patient. The LAP can be measured by a direct LA line placed at surgery, and the PCWP can be measured by a pediatric Swan Ganz catheter (4-5 F). Right ventricle



Pulmonary artery



25 mmHg



20 15



Wedge



10 Right atrium 5 0 Fig. 8: Pressure trace in various locations on the right side of the heart.



Central venous pressure is equal to the right atrial pressure and right ventricular end diastolic pressure (RVEDP) provided there is no obstruction to central venous return (e.g., SVC syndrome, IPPV with high airway pressures) or tricuspid valve disease and is a reflection of the RV function and the volume status of the patient. Pulmonary artery pressure provides objective evaluation of pulmonary hypertension and can be measured by a thermistor PA catheter or a Swan Ganz placed via a large vein or by a direct PA catheter placed at surgery. A continuous postoperative recording is useful in the management of children with pulmonary artery hypertension.



Systemic Arterial Oxygen Saturations In normal individuals, systemic arterial oxygen saturation (SpO2) is 97–100% and systemic venous oxygen saturation (SvO2) is 60–80%. The



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100



100



98 97



90



91 90



9



80



SpO2 (%)



70 60 50 40 30 20 10 27



0 0



10



20



30



40 50 60 PaO2 (mmHg)



70



80



90



100



Fig. 9: Normal oxygen dissociation curve (Centre graph) with shift to the left and right.



SpO2 varies with the partial pressure of oxygen, but the relationship is not linear and is described by the oxygen dissociation curve. The implication of the sigmoid shape of the oxygen dissociation curve is that at the lower and upper end of the curve, i.e., at PaO2 of less than 20 mmHg and more than 60 mmHg, a significantly large change in PaO2 results in little change in SpO2. At PaO2 range of 20–60 mmHg, a small change in PaO2 results in a marked change in SpO2. Provided the patient’s pH is normal, one can approximately estimate the PaO2 from the recorded SpO2 by the rule of 4-5-6, 7-8-9. 1. SpO2 of 90% : 60 mmHg PaO2 2. SpO2 of 80% : 50 mmHg PaO2 3. SpO2 of 70% : 40 mmHg PaO2 However, with a shift of the oxygen dissociation curve to the left (↑ pH, ↓ temperature, ↓ PaCO2) there is an increased affinity of hemoglobin for oxygen and the same O2 saturation implies a lower PaO2. With a shift of the curve to the right (↓ pH, ↑ temperature, ↑ PaCO2), there is a decreased affinity for oxygen and with the same O2 saturation, the PaO2 is higher.



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Manual of Pediatric Cardiac Intensive Care



Systemic Venous Oxygen Saturation



Decreased SvO2



Causes



Remark



Decreased oxygen supply



Hypoventilation, pulmonary edema, atelectasis, anemia, residual intracardiac R–L shunt.



Increased oxygen demand



Fever, pain, shivering, arrhythmia, cardiac failure.



Decreased cardiac output Increased SvO2



Increased oxygen supply Decreased oxygen demand



Mechanical ventilation, PEEP, sedation, anesthesia. Inotropic support, tachycardia.



Increased cardiac output



Systemic venous oxygen saturation (SvO2, normal range: 60–80%) can be monitored continuously with a specialized PA catheter or in vitro, with blood samples obtained from the right atrium or superior vena cava. SvO2 monitoring provides assessment of tissue oxygenation. It shows whether the oxygen supply is adequate to meet the tissue demands and is thus a non-specific indicator of the cardiac output.



Hemodynamic Calculations Calculation



Child normal values



Adult normal values



Cardiac output (CO)



CO = Stroke volume × heart rate



At birth: 300–400 mL/kg/min



5–6 L/min



Cardiac index (CI)



CI =



3.0–4.5 L/min/m2



2.7–4.3 L/min/m2



Systemic vascular resistance (SVR: dynes-sec-cm−5)



SVR =



MAP − CVP × 80 CO



1200–2800 dynes-sec-cm−5



1000–1300 dynes-sec-cm−5



Pulmonary vascular resistance (PVR: dynes-sec-cm−5)



PVR =



MPA − PCWP × 80 CO



40–320 dynes-sec-cm−5



150–250 dynes-sec-cm−5



Cardiac output BSA



MAP: mean arterial pressure, CVP: central venous pressure, MPA: mean pulmonary artery pressure, PCWP: pulmonary capillary wedge pressure, BSA: body surface area.



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Cardiac Output Cardiac output (liters/minute) is defined as the amount of blood ejected from the left ventricle in 1 minute. Stroke volume (SV) is the amount of blood ejected from the left ventricle with each beat. CO = Stroke volume (SV) × Heart rate (HR) Stroke volume = End diastolic volume (EDV) – End systolic volume (ESV) Ejection fraction (EF) = (SV/EDV) × 100% The average cardiac output for an adult is about 5–6 liters per minute at rest and the stroke volume 50–80 mL per beat. Cardiac output can be measured by a number of clinical methods ranging from intracardiac catheterization to non-invasive assessment of the arterial pulse. The standard method of measuring CO used in the laboratory is by the Fick’s oxygen consumption method, which requires measurement of: 1. ‘O2 consumption per minute’ using a spirometer, 2. ‘The arterial O2 content’ of peripheral arterial blood, 3. The ‘mixed venous O2 content’ from a sample of blood taken from the pulmonary artery. Then, CO =



O2 consumption (Arterial O2 content − Venous O2 content)



“Arterial O2 content − Venous O2 content” is also known as the arterio-venous oxygen difference. The arterial and venous oxygen content of the blood can be calculated from the fact that the oxygen in the blood is bound to hemoglobin and that one gram of hemoglobin can carry 1.34 mL of O2 and a small amount of oxygen is in a dissolved state. O2 content of blood = [Hb (g/dL) × 1.34 × % saturation of blood] + [0.0032 × Partial pressure of O2 (mmHg)] At the bedside, the cardiac output can be calculated by the thermodilution technique, using a cardiac output computer after placing a thermistor PA catheter or a pediatric Swan Ganz catheter (4-5 F).



Systemic Vascular Resistance An abnormally high SVR indicates peripheral vasoconstriction (e.g., in response to hypovolemia or inotropes). An abnormally low SVR reflects



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Manual of Pediatric Cardiac Intensive Care



peripheral vasodilation (e.g., in septic shock or as a result of administration of vasodilator drugs).



Pulmonary Vascular Resistance Normal PVR is approximately one-sixth of the SVR. PVR may be abnormally high in cardiac disease associated with pulmonary hypertension, in lung disease, pulmonary embolism, acidosis or hypoxia.



Calculation of Shunts BODY



BODY



AO



SVC/IVC



LV LA



RA RV



PV



PA



AO



LV LA



SVC/IVC



L–R



PV



RA RV



PA



LUNGS



LUNGS



Fig. 10: Line diagram of normal circulation (L); Circulation in L–R shunt (R). AO: aorta, SVC: superior vena cava, IVC: inferior vena cava, RA: right atrium, RV: right ventricle, PA: pulmonary artery, PV: pulmonary veins, LA: left atrium, LV: left ventricle.



Qp (SpO2 − MVO2 ) = Qs (PVO2 − PAO2 ) Qp: pulmonary blood flow, Qs: systemic blood flow, SpO2: systemic arterial O2 saturation, MVO2: mixed venous O2 saturation (MVO2 is the average of SVC, IVC, and RA saturation and the average of SVC and IVC saturations, in case of VSD), PVO2: pulmonary venous O2 saturation (assumed 98% if not measured), PAO2: pulmonary artery O2 saturation.



The ratio of pulmonary to systemic blood flow (Qp/Qs) is used to quantify the shunt. Oxygen saturation of blood samples obtained from various cardiac chambers are used to calculate pulmonary and systemic blood flow as noted in the formula above. The shunt can also be calculated



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13



more accurately by obtaining systemic and pulmonary blood flows by the Fick’s method. Qp/Qs > 1.5:1.0 is a significant shunt. In the normal circulation, the systemic and the pulmonary circulation are in series. The blood which is ejected into the aorta, returns to the right heart via the SVC/IVC and then is pumped into the pulmonary circulation. Thus, the pulmonary blood flow is equal to the systemic blood flow. In L–R shunt, part of the systemic blood flow bypasses the systemic circulation and flows directly into the pulmonary part of the circulation with every cycle, so that the systemic circulation is depleted of this blood and the pulmonary circulation has this additional amount of blood flow. Therefore, the effective pulmonary blood flow in: ■



Left-to-right shunt = Systemic blood flow + Shunt flow



■



Right-to-left shunt = Systemic blood flow − Shunt flow.



Bibliography 1. Beerbaum P, Körperich H, Barth P, et al. Noninvasive quantification of left-to-right shunt in pediatric patients. Phase-contrast cine magnetic resonance imaging compared with invasive oximetry. Circulation 2001;103:2476–82. 2. Bell DR. Cardiac muscle mechanics and the cardiac pump. In: Rhodes RA, Bell DR eds. Medical Physiology. Principles for Clinical Medicine 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 2009:243–62. 3. Grap MJ. Pulse oximetry. Crit Care Nurse 2002;22:69–74. 4. Gupta R, Yoxall CW, Subedhar N, Shaw NJ. Individualised pulse oximetry limits in neonatal intensive care. Arch Dis Child Fetal Neonatal Ed 1999;81:F194–6. 5. Haque IU, Zaritsky AL. Analysis of the evidence for the lower limit of systolic and mean arterial pressure in children. Pediatr Crit Care Med 2007;8(2):138–44. 6. Heitmiller ES, Nyhan D. Perioperative monitoring. In: Nichols DG, Cameron DE, Greeley WJ, Lappe DG, Ungerleider RM, Wetzel RC eds. Critical Heart Disease in Infants and Children St Louis: Mosby; 1995:467–96. 7. Joao PRD, Faria F Jr. Immediate post operative care following surgery. J Pediatr (Rio J) 2003;79(Suppl 2):S213–22. 8. Klabunde RE. Central venous pressure waveforms. University of Virginia, School of Medicine. [Updated: 2005 Apr 21; cited: 2011 Oct 15] Available at: http://www.healthsystem.virginia. edu/internet/anesthesiology-elective/cardiac/cvpwave.cfm. 9. López-Herce J, Bustinza A, Sancho L, et al. Cardiac output and blood volume parameters using femoral arterial thermodilution. Pediatr Int 2009;51:59–65. 10. Mark JB, Slaughter TF, Reeves JG. Cardiovascular monitoring. Practice Guidelines for Perioperative Transesophageal Echocardiography and Practice Guidelines for Pulmonary Artery Catheterization. Churchill Livingstoine. © 1979 [Updated: 2000; cited: 2011 Feb 22] Available at: http://web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v03/ 030267r00.HTM 11. McGhee BH, Bridges EJ. Monitoring arterial blood pressure: what you may not know. Crit Care Nurse 2002;22:60–4, 66–70, 73 passim. 12. O’Rourke RA, Silverman ME, Shaver JA. The history, physical examination & cardiac auscultation. In: Fuster V, Alexander RW, O’Rourke RA eds. Hurst’s The Heart Vol 1. The McGraw-Hill Companies Inc; 2004:217–94.



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13. Powell FL Jr. Oxygen and carbon dioxide transport in the blood. In: Johnson LR ed. Essential Medical Physiology 3rd ed. California, USA: Academic Press. An Imprint of Elsevier; 2003:289–98. 14. Salyer JW. Neonatal and pediatric pulse oximetry. Respir Care 2003;48(4):386–96. 15. Schlame M, Blanck TJJ. Cardiovascular system. In: Gabrielli A, Layen AJ, Yu M eds. Civetta, Taylor & Kirby’s Critical Care 4th ed. Philadelphia: Lippincott Williams and Wilkins; 2009:682–99. 16. Tamer DM, Watson DD, Kenny PP, et al. Noninvasive detection and quantification of left-toright shunts in children using oxygen-15 labeled carbon dioxide. Circulation 1977;56:626–31.



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Low Cardiac Output “The heart is the chief mansion of the soul, the organ of vital capacity, the beginning of life, the foundation of the vital spirits… the first to live, the last to die” —Ambroise Paré (1510–1590)*



Clinical Evaluation of Low Cardiac Output Parameter



Normal perfusion



Low cardiac output



Skin



Warm, brisk capillary fill



Sluggish capillary refill (>3–4 sec), mottled appearance, peripheral cyanosis



Color of mucous membranes



Pink



Pallor



Temperature



Normal



Cool periphery, core temperature >39°C



Heart rate



As per age



Tachycardia



Blood pressure



As per age



↓ BP, narrow pulse pressure ↑ respiratory variation of BP in hypovolemia



Urine output



Normal



Oliguria, anuria



Neurological status



Age appropriate activity



Irritable, lethargic



Feeding



Eats well/strong sucking reflex



Weak sucking reflex, tires during feeding



GIT



Normal



↑ gastric tube aspirate, abdominal distension, later jaundice, ↑ liver enzymes



Hydration



Normal



Sunken fontanelle, poor skin turgor, dry mucous membranes in prolonged hypovolemia



CVP/LAP



2–6 mmHg/6–12 mmHg



↓ in hypovolemia, CVP ↑ in RV failure



Mixed venous saturation



60–80%



3–4 sec). Absent pulses, mottling of the skin, and peripheral cyanosis are late signs.



Blood Pressure In the initial phases of low cardiac output, the blood pressure may be well maintained by vasoconstriction. In hypovolemia, even though the blood pressure is normal, a narrow arterial pulse pressure (0.5 mg/kg/h. Cyanide toxicity is more likely if hepatic dysfunction is present; thiocyanate is cleared by the kidney and toxicity is more likely if there is renal dysfunction or with prolonged infusion. An early sign of cyanide toxicity is increasing resistance to doses of nitroprusside (tachyphylaxis). Subsequent clinical features include metabolic acidosis, tachycardia, hypertension, cardiac arrhythmias, CNS dysfunction, metabolic acidosis, and increased mixed oxygen saturation (as a result of the inability to utilize oxygen). Treatment consists of mechanical ventilation with 100% oxygen and administration of sodium thiosulfate (150 mg/kg over 15 min) or 3% sodium nitrite (5 mg/kg over 5 min). Manifestations of thiocyanate toxicity include abdominal pain, vomiting, weakness, tinnitus, tremor, agitation, progressing to lethargy, seizures and coma. Treatment requires clearance of excess thiocyanate by dialysis. NTG causes venodilatation more than arteriolar dilatation. This results in a decrease in LV filling pressure (preload) relatively more than systemic vascular resistance (afterload). As low-dose infusions are titrated upward, the earliest response is a decrease in cardiac filling pressures (i.e., CVP and LAP) with little or no change in cardiac output. As the dose rate is increased further, the cardiac output begins to rise as a result of progressive arterial vasodilatation. Further increases in the dose rate will eventually produce a drop in blood pressure.



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Milrinone is an inodilator and has an inotropic effect on the heart, and a dilator effect on the circulation, which significantly decreases the SVR and PVR. It increases the CO with little effect on HR and myocardial oxygen demand. Milrinone has a longer half-life than dobutamine and is very useful in pulmonary HTN. It is administered with a loading dose followed by a continuous infusion. Reductions in infusion rate may be necessary in patients with renal impairment and should not be used in patients with a creatinine >2.5. It has a long half-life and if not excreted by the kidneys can cause severe hypotension and right sided heart failure. Milrinone in combination with adrenaline or dopamine is advocated in the management of low cardiac output in the postoperative cardiac patient with pulmonary hypertension. Vasopressin is a potent vasopressor that may be used in several forms of shock, notably septic shock. The vasoconstrictive action of vasopressin is mediated through V1 receptors in the vessels of the skin, skeletal muscle, and small intestines. In recommended doses, blood flow to the coronaries, cerebral, pulmonary, and renal vascular beds, is preserved. It leads to increase in blood pressure, decrease in heart rate, and reduction in the dose requirements of other catecholamines. It has an antidiuretic effect, which is mediated through V2 receptors in the capillaries at the renal distal tubules and collecting ducts, which causes increased reabsorption of water to augment systemic blood volume. High doses of vasopressin cause intense vasoconstriction, which can result in gangrene of the tips of fingers and toes, and ischemia of other organs, including the gastrointestinal tract and kidneys. Extravasation may result in tissue necrosis. Other complications include arrhythmias, hyponatremia, thrombocytopenia and bronchial constriction. The halflife of vasopressin is 10–35 minutes, and its vasoconstrictive effect can be counteracted by vasodilators, such as nitroglycerin or nitroprusside. Alprostadil (PgE1) is indicated in infants with congenital heart defects and a duct dependant pulmonary or systemic circulation to keep the ductus temporarily open. Infants with decreased pulmonary blood flow will respond with an increase in PaO2, and infants with diminished systemic blood flow will show an improvement in the blood pressure and a decrease in the acidosis. Alprostadil injection should be infused for the shortest time and at the lowest dose that produces the desired result. Apnea has been reported in about 12% of the neonates on alprostadil infusion. Other adverse reactions include fever, irritability, seizures, hypotension, thrombocytopenia, cerebral bleeding, and gastric outlet obstruction when the duration of infusion has exceeded 120 hours. Infusion is started at 0.05–0.1 mcg/kg/min. It may be necessary to increase the dose to obtain a therapeutic response. After an adequate response, the infusion rate is reduced to provide the lowest possible dosage (0.01–0.025 mcg/kg/min) to maintain the response. (500 mcg of alprostadil is added to 50 mL saline/dextrose for infusion).



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Inotropes and Other Vasoactive Drugs



29



Epoprostenol (PgI2, prostacyclin) is a prostaglandin that causes vasodilatation of the vascular beds, including the pulmonary and cerebral circulation, and is a potent inhibitor of platelet aggregation. There is a fall in the mean systemic and pulmonary artery pressures and a decrease in the SVR and PVR. Indications for its use include long-term intravenous treatment of primary pulmonary hypertension and for the management of pulmonary hypertension secondary to congenital heart diseases and congenital diaphragmatic hernia. It is initiated at the rate of 0.5–2 ng/kg/min and increased by 0.5–1 ng/kg/min every 30–60 min until dose limiting clinical effects are noted or to a maximum of 16 ng/kg/min. Symptoms of overdose include flushing, headache, hypotension, tachycardia, nausea, vomiting, and diarrhea, which require the dose to be reduced. Epoprostenol enhances the hypotensive effects of other vasodilators and increases risk of bleeding with anticoagulants and other antiplatelet agents.



Method of Preparation of Infusion and Dose Calculation Two alternative methods of drug formulation that allow for ease of calculations are described below. Various formulas for dose calculation are given in Appendix K. Method 1 Drug



Formulation



Method of dose calculation



Dopamine/dobutamine



3 mg/kg in 50 mL 15 mg/kg in 50 mL



1 mL/h = 1 mcg/kg/min 1 mL/h = 5 mcg/kg/min



Adrenaline/noradrenaline/ isoprenaline



0.3 mg/kg in 50 mL



1 mL/h = 0.1 mcg/kg/min



NTG/sodium nitroprusside



3 mg/kg in 50 mL



1 mL/h = 1 mcg/kg/min



Milrinone



0.75 mg/kg in 50 mL



1 mL/h = 0.25 mcg/kg/min



Method 2 Drug



Formulation



Method of dose calculation



Dopamine/dobutamine



50 mg in 50 mL (1000 mcg/mL)



0.3 × body wt (mL/h) = 5 mcg/kg/min



Sodium nitroprusside/NTG/ milrinone



5 mg in 50 mL (100 mcg/mL)



0.3 × body wt (mL/h) = 0.5 mcg/kg/min



Adrenaline/isoprenaline/ noradrenaline



0.5 mg in 50 mL (10 mcg/mL)



0.3 × body wt (mL/h) = 0.05 mcg/kg/min



Vasopressin



5 units in 50 mL (0.1 unit/mL)



0.3 × body wt (mL/h) = 0.0005 unit/kg/min



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Manual of Pediatric Cardiac Intensive Care



In children, to decrease the fluid intake, usually 2 × the above strength of solutions are prepared (dopamine/dobutamine: 100 mg in 50 mL; milrinone/NTG/ sodium nitroprusside: 10 mg in 50 mL; adrenaline/noradrenaline/isoprenaline: 1 mg in 50 mL and vasopressin 10 units in 50 mL), so that “0.3 × body wt ÷ 2” in mL/h would then provide the doses noted in the Method 2 table above. In a 12 kg child, dopamine prepared in a concentration of 100 mg in 50 mL of 5% dextrose administered at a rate of 1.8 mL will give a dose of 5 mcg/kg/min (0.3 × 12 ÷ 2 in mL/h = 5 mcg/kg/min). Similarly, in adults 4 × strength may be prepared, then “0.3 × body wt ÷ 4” in mL/h would give the above doses, e.g., for dopamine, 200 mg in 50 mL in a 50 kg adult, 3.75 mL/h would give 5 mcg/kg/min (0.3 × 50 ÷ 4 in mL/h = 5 mcg/kg/min). Diluents: Diluents may be 5% dextrose in water, 5% dextrose in halfnormal saline, normal saline, or Ringer’s lactate. SNP and NTG are prepared in dextrose only.



Bibliography 1. Alprostadil injection. Available at: dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=14726 2. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med 2005;165(1):17–24. 3. Bellomo R, Giantomasso DD. Noradrenaline and the kidney: friends or foes? Crit Care 2001;5:294–8. 4. Biaggioni I, Robertson D. Adrenoceptor agonists & sympathomimetic drugs. In: Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology 11th ed. USA: McGraw Hill Inc.; 2009:127–48. 5. Buck ML. Low-dose vasopressin infusions for vasodilatory shock: adverse effects. Pediatr Pharm 2003;9(9) [Updated: 2003 Sep 10; cited: 2011 Sep 28]. Available at: http://www.medscape.com/viewarticle/462394. 6. Choudhury M, Saxena N. Inotropic agents in pediatric cardiac surgery patients: current practice, concerns, and controversies. Indian J Anaesth 2003;47:246. 7. Esoprostenol. Available at: http://nursing.ucsfmedicalcenter.org/NursingDept/AdultProcedures/ PDFsafter12-29-2003/FlolanInfusionforPulmonaryHypertensionAdult.pdf 8. Epoprostenol. Package insert: information for healthcare professionals flolan 1.5. Available at: www.medicines.ie/pdfviewer.aspx?isattachment=true...9841. 9. Gilmore K. Pharmacology of vasopressors and inotropes. Pharmacology 1999;10:4. [Cited: 2011 Dec 17] Available at: http://www.nda.ox.ac.uk/wfsa/html/u10/u1004_01.htm. 10. Gomersall C. Nitroprusside. The Chinese University of Hong Kong. [Updated: 1999 Dec; cited: 2011 Sep 28]. Available at: http://www.aic.cuhk.edu.hk/web8/sodium_nitroprusside.htm. 11. Helfaer MA, Wilson MD, Nichols DG. Pharmacology of cardiovascular drugs. In: Nichols DG, Cameron DE, Greeley WJ, Lappe DG, Ungerleider RM, Wetzel RC, eds. Critical Heart Disease in Infants and Children. St Louis: Mosby; 1995:185–213. 12. Hill NS, Antman EM, Green LH, Alpert JS. Intravenous nitroglycerin. A review of pharmacology, indications, therapeutic effects and complications. Chest 1981;79(1):69–76.



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31



13. Ilbawi MN, Idriss FS, DeLeon SY, Berry TE, Duffy CE, Paul MH. Hemodynamic effects of intravenous nitroglycerin in pediatric patients after heart surgery. Circulation 1985;72(3 Pt 2): II101–7. 14. Infusions. In: Alder Hey Book of Children’s Doses 6th ed. Liverpool: Royal Liverpool Children’s Hospital (Alder Hey); 1994:254–5. 15. McAuley DF. What are the current recommendations regarding the use of vasopressin in the treatment of shock? [Cited: 2011 Apr 14]. Available at: http://www.globalrph.com/vasopressin_shock.htm. 16. Milrinone. South Thames retrieval service. 2008 Jan [Cited: 2011 Sep 28]. Available at: http:// www.strs.nhs.uk/resources/pdf/guidelines/milrinone.pdf. 17. Nitroprusside toxicity treatment. Available at: www.openanesthesia.org/index.php?title= Nitroprusside_toxicity. 18. Patel BM, Chittock DR, Russell JA, Walley KR. Beneficial effects of short-term vasopressin infusion during severe septic shock. Anesthesiology 2002;96:576–82. 19. Sodium nitroprusside. In: Sweetman SC, ed. In Martindale The Complete Drug Reference 36th ed. IL, USA: Pharmaceutical Press 2009:1397–8. 20. Vasopressin. In: USP Drug Dispensing Information Vol I. Massachusetts: Drug Information of the Health Care Professional. Thompson Micromedex; 2004:2816–7. 21. Westfall TC, Westfall DP. Neurotransmission: the autonomic and somatic motor nervous systems. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basic of Therapeutics 12th ed. USA: McGraw Hill Inc.; 2011:171–218.



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Congestive Heart Failure “For suddenly a grievous sickness took him, that makes him gasp and stare and catch the air” —King Henry VI; Part II - William Shakespeare (1564–1616)



Clinical Manifestations Low cardiac output ● ● ● ● ●



Failure to thrive Sweating during feeding Tachycardia Cool periphery Oliguria



Left heart failure ●



● ●



Respiratory distress (tachypnea, chest retractions) Rales/crepitations Pulmonary edema



Right heart failure ● ● ● ● ●



Raised jugular venous pulse Hepatomegaly Edema Pleural effusion Ascites



In general, heart failure results either from an excessive volume overload (left-to-right shunts, regurgitant lesions), pressure overload (aortic stenosis, coarctation), or from a primary myocardial abnormality (myocarditis, cardiomyopathy). Other lesions that can result in congestive heart failure (CHF) are arrhythmias, pericardial diseases, and a combination of various factors. Clinical manifestations of CHF are a combination of features of low cardiac output, left heart failure, and right heart failure. The decrease in cardiac output because of CHF triggers a compensatory sympathetic response resulting in tachycardia, vasoconstriction, and renin–angiotensin mediated fluid retention. Fluid retention initially increases the cardiac output by increasing the end diastolic volume (preload) but eventually results in renal and other organ dysfunction. Left-sided heart failure is associated with signs of pulmonary venous congestion (tachypnea, chest retractions, rales, pulmonary edema), whereas right-sided heart failure is associated with signs of systemic venous congestion (raised jugular venous hepatomegaly, edema, ascites, pleural effusion). In pediatric patients, failure of one ventricle invariably affects the other ventricle and children usually present with signs of biventricular failure. CHF with normal cardiac output is called compensated CHF, and CHF with inadequate cardiac output is called decompensated failure.



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Congestive Heart Failure



33



Signs of CHF vary with the age of the child. Infants have sweating during feeding, inability to complete feeding (taking 40 min/feed), and failure to thrive. Pulsus alternans (alternate strong and weak pulse) or pulsus paradoxus (an inspiratory fall in systolic pressure of >10 mmHg) are observed in infants with severe CHF. A gallop rhythm may be present. Signs of pulmonary venous congestion include tachypnea (sleeping respiratory rate of >50/min) and chest retractions. Right-sided venous congestion is characterized by hepatosplenomegaly and, less frequently, edema, ascites, and a distended jugular venous pulse. In severe cases, persistent low cardiac output may result in signs of renal and hepatic failure. Chest X-ray shows cardiac enlargement, i.e., a cardiothoracic ratio of >60% in the newborn and >55% in older infants. However, it is well to note that an expiratory film can often be misinterpreted as showing cardiac enlargement. Older children may have fatigue or sometimes syncopy. Clinical findings include hypotension, cool extremities with poor peripheral perfusion, a low volume pulse, and decreased urine output. Left-sided venous congestion causes tachypnea and wheezing. Right-sided congestion results in hepatosplenomegaly, raised jugular venous pulse, edema, ascites, and pleural effusion. Renal and liver function tests may be deranged.



Drugs Used in the Treatment of Heart Failure Drug



Dosage



Remarks and side effects



Digoxin



Children Digitalizing dose Preterm: PO 20 mcg/kg/day, IV 15 mcg/kg/day Term: PO 30 mcg/kg/day, IV 20 mcg/kg/day < 2 yr: PO 40–50 mcg/kg/day, IV 30–40 mcg/kg/day 2–10 yr: PO 30–40 mcg/kg/day, IV 20–30 mcg/kg/day >10 yr: PO 10–15 mcg/kg/day, IV 8–12 mcg/kg/day 50% dose is given initially, 25% at 8 h, and 25% at 16 h. Maintenance dose is started 24 h after loading. Maintenance dose Preterm: PO 2.5 mcg/kg q12h Neonate–10 yr: PO 5 mcg/kg q12h >10 yr: PO 2.5 mcg/kg q12h IV: 75% of oral dose is given.



Approx time to steady state is 5–10 days and the therapeutic range is 0.8–1.2 ng/mL (sample is taken 6 h after oral/IV dose). The bioavailability of the tablet is 70%, and syrup 80% of the IV dose.



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Digoxin is potentiated by amiodarone, diltiazem, verapamil, and quinidine; the maintenance dose should be halved if any of these are also given.



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Manual of Pediatric Cardiac Intensive Care



Adults Digitalizing dose IV 0.5–1 mg PO 0.75–1.5 mg 50% of total dose is given initially, then 25% dose in each of 2 subsequent doses at 8–12 h intervals. Maintenance dose IV 0.1–0.4 mg q24h PO 0.125–0.5 mg q24h Renal failure Crcl 10–15 mL/min—reduce dose by 50%; Crcl 220 bpm



Child HR 180 bpm



Child HR >180 bpm



PR interval normal, PR < RP



P absent or PR >RP



Normal (PR < RP) or 1°/2° block



Antiarrhythmic Drugs Drug



IV dose



Oral dose



Adenosine



Children 100 mcg/kg rapid IV bolus (max 6 mg) followed by a 5 mL saline flush. If required, repeat 200 mcg/kg IV (max 12 mg). This dose can be repeated twice.



Effective in reentrant SVT (AVRT, AVNRT) and rarely in some forms of VT. May transiently decrease the rate but does not convert other types of SVT.



Adults Initial dose: 6 mg rapid IV bolus (administered in 1–2 seconds), followed by a 5 mL saline flush.



May cause bronchospasm and a feeling of chest constriction as an adverse effect.



If required a12 mg IV dose can be repeated twice.



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Indication



Cardiac Tachyarrhythmias



Drug



IV dose



Oral dose



Indication



Amiodarone



Children Loading 5 mg/kg IV infusion over 30–60 minutes. Maintenance 5–10 mcg/kg/ min IV infusion (max total dose 15 mg/day).



Children Calculate doses for children 1 year age) 0.1–0.3 mg/kg/dose (max 5 mg) IV over 10 minutes. Repeat dose after 30 minutes if required (max 10 mg). Adults 2.5–5 mg IV. Repeat 5–10 mg every 15–30 minutes if required to a max 20 mg.



3–6 mg/kg/day in divided doses q8h.



Adults 500 mg q6h



Adults 240–320 mg/day in divided doses q6–8h (digitalized patient); 240–480 mg/day (nondigitalized patient).



Indicated in stable, regular VT. Contraindicated in torsades. 2nd line therapy in atrial fibrillation, atrial flutter, and reentrant SVTs.



Adverse effects include AV block and asystole, which requires reversal with 10% Inj. calcium gluconate 0.2–0.3 mL/kg IV (alternatively administer calcium gluconate IV prophylactically prior to verapamil).



IV: intravenous, IO: intra osseous, ET: via endotracheal tube. Drug requires to be flushed with 5 mL normal saline, followed by 5 ventilations.



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56



Manual of Pediatric Cardiac Intensive Care Flowchart for the Management of Tachyarrhythmias Evaluate patient Monitor blood pressure Monitor rhythm



Stable



Unstable



12 lead ECG



Narrow complex



Wide complex



• Synchronized DC shock (1–4 J/kg) • IV analgesia



Regular



Irregular



Monomorphic recurrent VT Sustained monomorphic VT • Amiodarone • Lignocaine • Procainamide • Cardioversion (sustained VT)



SVT with aberrant conduction • Adenosine • Diltiazem • β-blocker • Amiodarone



Polymorphic recurrent VT Sustained polymorphic VT • Cardioversion (sustained VT) • Follow-up with amiodarone or β-blocker • Magnesium sulfate for torsades



Regular Irregular



• Vagal maneuvers • Adenosine



Rhythm converted



Rhythm not converted



Re-entry SVT • Prevent recurrence with diltiazem or β-blocker



AET Atrial flutter JET Re-entry SVT • Diltiazem/β-blocker/ amiodarone



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Atrial fibrillation Atrial flutter with variable block MAT • Diltiazem/β-blocker/ amiodarone



Cardiac Tachyarrhythmias



57



Management of Narrow QRS Complex Tachycardias DC Cardioversion Cardioversion is used as the first line of therapy in the hemodynamically unstable patient with an atrial arrhythmia or VT. The dose of the initial shock for cardioversion in children is 0.5–1 J/kg, which is increased to 2 J/kg if there is no response to this shock. (In the adult, the shock sequence is an initial shock of 120 J followed by 200 J when a biphasic defibrillator is used. With a monophasic waveform, an initial shock of 200 J is followed by 360 J.) For cardioversion (atrial or ventricular), the DC shock must be synchronized to the QRS complex because a shock that falls on the T wave can induce VF. The initial dose for defibrillation in children in VF or pulseless VT is 2 J/kg, which is increased to 4 J/kg in subsequent shocks. (The default initial energy dose with a biphasic defibrillator recommended for defibrillation in adults is 120 or 200 J. If a monophasic defibrillator is used, the recommended initial dose is 360 J.) Defibrillation does not require synchronization. IV analgesia and sedation is necessary prior to cardioversion in all awake patients, e.g., fentanyl 1 mcg/kg + midazolam 0.05–0.1 mg/kg IV can be given. Midazolam may be repeated 0.05 mg/kg at 2–3 minutes intervals up to a total of 0.2 mg/kg. Alternatively, ketamine 1–2 mg/kg IV provides 5–10 minutes of surgical anesthesia.



Vagal Maneuvers In a hemodynamically stable patient with a regular rhythm, first vagotonic maneuvers can be tried. These vagotonic maneuvers include the Valsalva maneuver, unilateral carotid sinus massage, or application of an ice pack to the face. One method of Valsalva maneuver is to have the child blow through an obstructed straw. This may terminate the arrhythmia (AVRT, AVNRT) or transiently slow the ventricular rate so that the relationship of the P waves with the QRS complexes becomes evident and it becomes possible to diagnose the rhythm disorder. Normal P waves are present in sinus tachycardia and retrograde P waves (negative in lead II, positive in aVR.) may be apparent in reentrant tachycardias. P waves outnumber the QRS complexes in atrial flutter or AET with a block. Vagal maneuvers and adenosine are ineffective in atrial fibrillation.



Adenosine The action of adenosine is similar to vagotonic maneuvers and acts by slowing AV nodal conduction. It may terminate reentrant tachycardias or



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Manual of Pediatric Cardiac Intensive Care



cause transient slowing of the ventricular rate. It acts in 10–20 seconds and causes a brief (2–3 seconds) period of cardiac standstill, which is followed by return of normal sinus rhythm or a recurrence of the arrhythmia. Its advantages are the short half-life (160 msec. (VT from the conduction system has QRS −30°. (Not valid in presence of left bundle branch block)



Right axis (posterolateral accessory pathway will have left axis deviation).



Occasionally concordant pattern in precordial leads. (Entirely +ve or –ve QRS complexes in all precordial leads)



Concordant pattern is absent in precordial leads. (Left posterolateral AP has concordant pattern)



Wide complex tachycardia has several potential causes, which include (i) VT; (ii) SVT with aberrant interventricular conduction (bundle branch



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Cardiac Tachyarrhythmias



61



blocks) or atrioventricular conduction over an accessory pathway (WolffParkinson-White); and (iii) QRS widening due to drugs, electrolyte abnormalities, or ventricular pacing.



Management of Broad QRS Complex Tachycardia (>0.09 Second) 1. Drugs In patients with VT, even though DC cardioversion is the most effective treatment, it requires systemic analgesia and sedation, thus monomorphic VT with adequate vital end-organ perfusion and no signs of hemodynamic compromise can initially be treated with intravenous amiodarone, lignocaine, or procainamide. As hypomagnesemia is a cause of VT, especially torsades, a stat dose magnesium sulfate (50 mg/kg over 20 minutes) can also be given. Any electrolyte abnormalities are corrected. 2. Cardioversion If medical therapy fails to correct the rhythm or the patient is unstable, synchronized cardioversion is given in increments (children 0.5–2 J/kg, adults 120 J initially, then 200 J if unsuccessful). Amiodarone is also indicated after electric cardioversion to prevent further episodes of VT. 3. Adenosine When it is not possible to differentiate VT from a supraventricular arrhythmia with aberrant conduction,the options available are: (i) Inj. adenosine (0.1 mg/kg IV) may be considered in a hemodynamically stable patient in regular rhythm with a monomorphic QRS. It may convert the supraventricular arrhythmia to sinus rhythm. (ii) IV amiodarone. (iii) Alternatively, synchronized cardioversion (0.5–2 J/kg in children, 120–200 J in adults) may be attempted in the first place.



Cardiac Arrest Cardiac arrest is classified into (i) shockable rhythm and (ii) non-shockable rhythm, based upon whether the particular arrhythmia responds to defibrillation or not. The two shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia, while the two non-shockable rhythms are



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asystole and pulseless electrical activity. These patients require emergency management as per the PALS protocols (see chapter on Pediatric Resuscitation).



Bibliography 1. Cardiac arrhythmias. South Thames Retrieval Service. 2009 Jan [Cited: 2011 Sep 21]. Available at: http://www.strs.nhs.uk/resources/pdf/guidelines/arrythmias.pdf 2. DeSouza IS, Ward CD. Ventricular tachycardia. [Updated: 2011 Jan 19; cited: 2011 Sep 21]. Available at: http://emedicine.medscape.com/article/760963. 3. Gillette PC, Case CL, Kastor JA. Junctional ectopic tachycardia. In: Kastor JA, ed. Arrhythmias Philadelphia: WB Saunders Company; 1994:218–23. 4. Iyer RV. Drug therapy considerations in arrhythmias in children. Indian Pacing Electrophysiol J 2008;8:202–10. 5. Kantoch MJ. Supraventricular tachycardia in children. Indian J Pediatr 2005;72:609–19. 6. Lawrence III JH, Kanter RJ, Wetzel RC. Pediatric arrhythmias. In: Nichols DG, Cameron DE, Greeley WJ, Lappe DG, Ungerleider RM, Wetzel RC. Critical Heart Disease in Infants and Children St Louis: Mosby; 1995:17–253. 7. Mennuni M, Bianconi L. Management of tachyarrhythmias in the emergency room. © 1998. [Cited: 2011 Sep 21]. Available at: http://www.xagena.it/einthoven/eint0137.htm 8. Myeburg RJ, Kessler KM. Ventricular fibrillation. In: Kastor JA, ed. Arrhythmias Philadelphia: WB Saunders Company; 1994:395–450. 9. Overview of Arrhythmias. The Merck Manuals: online medical library. [Updated: 2010 Jan; cited: 2011 Sep 21] Available at: http://www.merckmanuals.com/professional/cardiovascular_disorders/arrhythmias_and_conduction_disorders/overview_of_arrhythmias.html 10. Penny-Peterson ED, Naccarelli GV. Supraventricular tachycardia. In: Yusuf S, Cairns JA, Camm AJ, Fallen EL, Gersh BJ, ed. Evidence Based Cardiology 3rd ed. Blackwell Publishing; 2010:606–18. 11. Prescription Drug Information, Interactions & Side Effects. [Cited: July 2012] Available at: http://www.drugs.com/ 12. Reentrant Supraventricular Tachycardias (SVT, PSVT). The Merck Manuals: online medical library. [Updated: 2010 Jan; cited: 2011 Sep 21] Available at: http://www.merckmanuals.com/ professional/cardiovascular_disorders/arrhythmias_and_conduction_disorders/reentrant_ supraventricular_tachycardias_svt_psvt.html 13. Robida A. Early arrhythmias in children after cardiac surgery. Heart Views 1999;1:223–8. Available at: http://www.hmc.org.qa/heartviews/VOL1NO6/07CONGENITAL_HEART_DISEASE. htm 14. Rosenthal L, McManus DD. Atrial Fibrillation. [Updated: 2010 Jun 1; cited: 2011 Sep 21]. Available at: http://emedicine.medscape.com/article/151066-overview. 15. Sanatani S, Hamilton RM. Supraventricular Tachycardia, Atrial Ectopic Tachycardia. [Updated: 2011 Sep 12; cited: 2011 Sep 21]. Available at: http://emedicine.medscape.com/ article/898784. 16. Saxena A, Juneja R, Ramakrishnan S. Working Group on Management of Congenital Heart Diseases in India. Drug therapy of cardiac diseases in children. Indian Pediatr 2009;46:310–38. 17. Schlechte EA, Boramanand N, Funk M. Supraventricular tachycardia in the primary care setting: age-related presentation, diagnosis, and management. J Pediatr Health Care 2008; 22:289–99. 18. Valsangiacomo E, Schmid ER, Schüpbach RW, et al. Early postoperative arrhythmias after cardiac operation in children. Ann Thorac Surg 2002;74:792–6.



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Bradyarrhythmias and Pacemakers “I seriously doubt if anything I ever do will ever give me the elation I felt that day when my own two cubic inch piece of electronic design controlled a living heart” —Wilson Greatbatch (1919–2011)*



Heart Blocks



Fig. 1: First-degree heart block.



Fig. 2: Mobitz type 1 second-degree heart block.



Fig. 3: Mobitz type 2 second-degree heart block. *Wilson Greatbatch was the inventor of implantable cardiac pacemaker. He is credited with 320 inventions and more than 150 patents.



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Fig. 4: Complete heart block.



Types of Heart Block Type



ECG findings



Comments



First-degree AV block



PR interval is prolonged above the upper limit of normal for age. All QRS complexes are preceded by a P wave.



PR prolongation may be caused by drugs such as digoxin, β-blockers, or calcium channel blockers and also occurs in a variety of cardiac diseases.



Second-degree AV block Mobitz type 1 (also called Wenckebach block) Mobitz type 2



In Mobitz type 1, second-degree AV block, the PR interval is progressively prolonged with each beat, until a P wave is not followed by a QRS complex. The cycle is constantly repeated. In Mobitz type 2, second-degree AV block, after a number of normal beats a QRS complex is blocked (2:1 block, 3:1 block). The PR interval does not lengthen before a dropped beat. More than one dropped beat may occur in succession.



Drugs or disease processes that affect the AV node produce this type of block, e.g., digoxin or an inferior infarction. Mobitz type 2 block is usually caused by an organic lesion in the conduction pathway and is not the effect of drugs. It may progress to complete heart block and is an indication for a pacemaker implantation.



Third-degree AV block (complete heart block)



No conduction between the atria and Complete heart block can ventricles takes place and both function be congenital and also independently at different rates. caused by injury to the Normal P waves may be present or there conduction pathway during may be an atrial arrhythmia. Alternatively, surgery or as a side effect of drug toxicity. there may be no atrial activity. With associated junctional escape rhythm, the QRS complexes have a normal configuration; while with ventricular escape rhythm, the QRS has a wide abnormal configuration.



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NASPE/BPEG Generic Code for Pacemakers 1. Chamber(s) paced



2. Chamber(s) sensed



3. Response to sensing



4. Rate modulation



5. Multisite pacing



O None



O None



O None



O None



O None



A Atrium



T Triggered



R Rate modulation



A Atrium



V Ventricle



V Ventricle



I Inhibited



V Ventricle



D Dual (A + V)



D Dual (A + V)



D Dual (T + I)



D Dual (A + V)



The North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG) have devised a generic letter code to describe the types and functions of pacemakers. The first three letters are used to describe pacing functions in bradycardia and heart blocks. 1. The letter in the first position identifies the chamber paced (O, none; A, atrium; V, ventricle; D, dual chamber [A + V]). 2. The second is the chamber sensed (O, none; A, atrium; V, ventricle; D, dual). 3. The third letter corresponds to the response of the pacemaker to an intrinsic cardiac event (O, none; I, inhibited; T, triggered; D, dual [I + T]). 4. The fourth letter indicates both programmability and rate modulation. 5. The fifth position of the code is used to indicate whether multisite pacing is present.



Pacing Modes Parameters to be set in various modes Parameters



AAI



VVI



DVI



VDD



DDD



Rate



+



+



+



+



+



+



+



+



+



Upper rate A sense



+



A output



+



+



+



V sense



+



+



+



+



V output



+



+



+



+



+



+



+



+



PVARP AV interval



+



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External (or temporary) pacemakers may be single chamber or dual chamber pacemakers. Single chamber pacemakers are capable of pacing only the atria or ventricle at one time and can be programmed in the VVI, VOO, AAI, or AOO mode. Dual chamber pacemakers are capable of synchronously pacing the atria and the ventricle. Demand pacemakers are pacemakers with single and double chamber pacing modes with a sensing function, which causes triggering or inhibition of a paced event (AAI, VVI, DVI, VDD, DDD). 1. In AOO mode, the atria is paced at a fixed rate with no atrial or ventricular sensing. AOO pacing may be used for overdrive pacing in atrial arrhythmias. 2. In VOO pacing, the ventricles are paced at a fixed rate with no atrial or ventricular sensing. This type of pacing can be used in an emergency and also during surgery when electrocautery causes interference with demand pacing. 3. In AAI mode, the atria are paced and sensed. Intrinsic atrial activity inhibits the paced atrial impulse, otherwise the atria is paced at a set rate. This type of pacing is commonly used in sinus node dysfunction with intact AV conduction. 4. In VVI pacing, the ventricle is paced and sensed. If an intrinsic ventricular beat is sensed the paced impulse is inhibited, otherwise, the ventricle is paced at the set rate. In VVI pacing, there is no AV synchrony. This type of pacing may be used for episodic AV block or bradycardia in small infants. 5. In DVI pacing, both the atrium and ventricle are paced but only the ventricle is sensed. It allows AV sequential pacing, if after an atrial stimulus, AV conduction takes place, ventricular pacing is inhibited; otherwise, ventricular pacing occurs. Competing atrial rhythm may precipitate atrial flutter or fibrillation, since atria is not sensed. 6. In VDD mode, the ventricle is paced but both atrium and ventricle are sensed. Provided the intrinsic atrial rate is higher than the set atrial rate, sequential pacing will occur. In other circumstances when there is no atrial activity or the intrinsic atrial rate is slow, VDD mode functions like VVI. 7. A DDD device is a dual-chamber pacemaker, which is capable of sensing both atria and ventricles, and then triggering or inhibiting the paced output in either chamber. A sensed atrial impulse will inhibit the atrial pacing impulse and after the programmed AV delay, it will initiate a ventricular paced event. In case it senses an intrinsic ventricular impulse, ventricular pacing is inhibited.



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Access Sites for Pacing Site



Indication



Epicardial



Postoperatively



Transcutaneous



In an emergency till another method of pacing can be initiated



Transvenous



Used in the absence of epicardial pacing wires



Esophageal



Management of atrial arrhythmias by overdrive pacing



Epicardial pacing is used postoperatively after cardiac surgery. In the bipolar system of wire placement, two wires each are sutured to the right atrium and right ventricle, while in the unipolar system one negative electrode is attached to the RA and one to the RV and the two positive electrodes are attached to the subcutaneous tissue. The advantage of the bipolar system for temporary postoperative pacing is that lower pacing outputs and sensing thresholds are needed for pacing. Single or double chamber pacing is instituted by the appropriate set of wires. By convention, atrial wires are made to exit on the right of the sternum and the ventricular wires to the left of the sternum. Transcutaneous asynchronous ventricular pacing can be initiated in an emergency by an external pacing device or pacing capable defibrillator unit through skin electrodes. This method of pacing requires high energy for capture and is used only as a bridge for a couple of hours till pacing can be established by another method. Transvenous pacing is instituted via a lead inserted under fluoroscopic guidance to pace the RV (VVI/VOO). Transesophageal pacing can only be used to pace the atria so it is not useful in AV dissociation. Its main use is in the treatment of atrial arrhythmias for overdrive pacing using a specialized generator. High pacing output over a long period can cause esophageal perforation.



Pacemaker Parameters Pacemaker Output The lowest output (defined in mV or mA) that will result in contraction of atrium or ventricle is called the capture threshold. The duration of the pacing impulse (defined in milliseconds) is known as the pulse width. In temporary pacemakers, the pacing output can be set but the pulse width is a fixed parameter. To establish the pacemaker output required for capture of the atria, the following method is used. The pacing rate is set to 10 beats/min above the



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patient’s intrinsic heart rate and if the AV conduction is intact, the AV interval is kept less than the intrinsic AV interval. Starting with an atrial output of 5 mV, the output is decreased till capture is lost or increased till capture occurs. Capture is indicated by the presence of an atrial pacing spike followed by a P wave. For safety reasons, the pacing output is kept at twice the value which was required for capture. The output required for pacing the ventricle is similarly determined (start with 5 mV). Capture is indicated by the presence of a ventricular pacing spike followed by a wide pacing complex. The pacing output is again kept at twice the value determined for capture. If the AV conduction is intact, increasing the AV interval to more than the patients AV interval will allow conducted ventricular beats.



Sensing The sensing threshold is the highest voltage set on the pacemaker at which the pacemaker can still detect the intrinsic atrial or ventricular electrical impulse. Setting the threshold too high will cause failure of sensing (undersensing) leading to fixed-rate pacing (AOO/VOO), and setting it too low will result in sensing of other activity (oversensing) and loss of pacing. The optimal atrial sensing threshold is established by keeping the pacing rate to 10 beats/min below the patient’s intrinsic atrial rate and the pacing output set to a minimum. Starting with the maximum atrial sensing threshold, which results in fixed rate pacing, the sensing threshold is slowly reduced till the pacemaker starts to sense. The sensing threshold is set to half this value, but if muscle activity is sensed, this setting is increased. This is repeated for ventricular threshold.



Pacing Rate Single chamber pacing modes require a single rate setting. In AAI and VVI modes, the pacemaker will pace at the set rate unless exceeded by the intrinsic rate. Dual chamber pacing modes require a lower rate setting and an upper tracking rate setting. The upper rate is the maximum rate at which the pacemaker will pace the ventricle even if the sensed intrinsic atrial rate becomes higher than this set rate. At intrinsic atrial rates above the upper tracking rate, the ventricular response results in a second-degree AV block (Wenckebach response). This is a safety measure, which prevents pacemaker mediated tachycardia resulting from tracking of high atrial rates.



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Refractory Periods P



P



AVI



PVARP Fig. 5: Refractory periods. AVI: atrioventricular interval, PVARP: post ventricular atrial refractory period.



Total atrial refractory period (TARP) is the combination of the atrioventricular interval (AVI) (which is analogous to the PR interval) and the post ventricular atrial refractory period (PVARP) (which is the period beyond the ventricular sensed or paced impulse during which also the atria are refractory). The purpose of the refractory period is to prevent the atrial channel of the pacemaker from sensing the output impulse of the ventricular lead (cross talk), retrograde P waves, or the QRS complex (far field R waves) as atrial signals. Ventricular refractory period (VRP) follows the ventricular paced or sensed impulse and prevents the ventricular channel of the pacemaker from sensing of the pacing stimulus and the R waves. VRP is not programmable on temporary pacemakers (typical values for VRP are 200–350 msec). DDD pacemakers have settings for upper tracking rates, AVI, and PVARP. Higher tracking rates in children require shorter PVARP or/and AVI. Too short an AV interval may not allow adequate ventricular filling (generally set between 100–140 msec for children and 150–200 msec in adults when paced at 80–110/min) and too short a PVARP may result in oversensing or pacemaker-mediated tachycardia.



Initial Pacemaker Settings Atrial and ventricular output



Typical atrial: 5 mA/mV Typical ventricular: 8–10 mA/mV



AV interval (same as PR interval) In children 100–140 msec. Sets automatically with the set rate Atrial and ventricular sensing threshold



Typical atrial: 0.4 mV (6 years): 2.5–5 mg q24h or in divided doses q12h.



A 12 hours dose may provide better efficacy in children. It has a gradual onset of action and may take 5–7 days for full effect thus dose adjustments should be made only after this period.



Adults: 5–10 mg q24h. Atenolol Children: 1–1.2 mg/kg q24h; increase to a max 2 mg/kg q24 h. Adults: 25–100 mg/kg q24h; increase to a max 200 mg q24h.



Cardio-selective β-blocker. Contraindicated in pulmonary edema and cardiogenic shock. May cause bradycardia, hypotension, second or third degree AV block. Exercise caution in diabetes and asthma.



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Drug



Remarks



Captopril Children: 0.3–6 mg/kg/day in divided doses q8h. Adults: 6.25–12.5 mg q8–12h; increase to a max 50 mg q8h.



Onset of action in 15–30 minutes and duration of action 8–12 hours. Starting with a lower dose, the dose is increased over 1–2 weeks.



Diltiazem Children: 1.5–2 mg/kg/day in divided doses q6–8h; increase to a max 3.5 mg/kg/day. Adults: 30–60 mg q6–8h; increased to a maintenance of 180–360 mg/day in divided doses q6–8h. (Diltiazem SR 60–120 mg q12h; increased to a maintenance of 180–360 mg/day in divided doses q12h)



Maximum antihypertensive effect is seen within 2 weeks.



Enalapril Children: 0.1–0.5 mg/kg/day divided q12–24h. Adults: PO 2.5–5 mg/day divided q12–24h; increase to a max 20 mg/day.



Starting with a lower dose, the dose is gradually increased over a period of 2 weeks. Cough is a common reported side effect.



Hydralazine Children: 0.75–1 mg/kg/day in divided doses q6h; increase to a max 8 mg/kg/day. Adults: 10–50 mg q6h.



Directly acting arteriolar vasodilator. May induce reflex tachycardia and increased cardiac output, which can blunt its hypotensive effect. After an oral dose, it has an effect in 20–30 minutes that lasts 2–4 h (less than IV).



Labetalol Children: 1–3 mg/kg/day in divided doses q12h PO; increase to a max 10 mg/kg/day. Adults: 100–400 mg q12h.



Predominant β-blocker with some α-blocking action. Peak plasma levels occur 1–2 hours after oral administration with a half life of 6–8h. Steady state is achieved on the third day of dosing.



Metoprolol Children (1–17 yr): 1–2 mg/kg/day in divided doses q12h; increase to a max 6 mg/kg/day. Adults: 100 mg/day in divided doses q12–24h; increase to a max 450 mg/day.



Modest β1 selectivity. Bronchospasm, bradycardia, heart block may take place.



Nifedipine Children: Hypertensive urgency: 0.25–0.5 mg/kg q4–6h PRN (max 10 mg/dose or 3 mg/kg/day). Hypertension: SR tablets 0.25–0.5 mg/kg/day in divided doses q12–24h; increase to a max 3 mg/kg/day.



Calcium channel blocker that reduces blood pressure within 5–20 minutes, with maximum effects in 60–90 minutes. Available for oral/sublingual use and is recommended only for children with hypertensive urgency.



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Hypertensive Emergencies



Drug



81



Remarks



Adults: Hypertension: 10 mg q8h; increase to max 180 mg/day in divided doses q6–8h. SR tablet 30–60 mg q24h; increase to max 120 mg q24h. Propranolol Children: 0.5–1 mg/kg/day in divided doses q6–12h; increase to a max 8 mg/kg/day. Adults: 40 mg/dose q12h; increase to a max 640 mg/day.



Non-selective β-blocker. Contraindicated in bronchial asthma, heart failure, and heart block. Starting with a lower dose, the dose is increased every 3–5 days till the desired effect.



A hypertensive crisis is an extreme elevation of blood pressure that may be life-threatening or likely to result in significant morbidity if untreated. It occurs infrequently in children but may be associated with renovascular hypertension, head injury, in the postoperative period following cardiopulmonary bypass, repair of coarctation of the aorta and supra-aortic stenosis. Hypertensive crisis is classified as either a hypertensive emergency or a hypertensive urgency. Hypertensive emergency is said to be present when the blood pressure is extremely high (1.3–1.5 times 95th percentile) and end-organ damage (cardiac, CNS, renal, lung, or eye) is evident. Hypertensive encephalopathy is an example of a hypertensive emergency and is suggested by the presence of vomiting, fever, ataxia, stupor, and seizures. Hypertensive urgency is present when the blood pressure is significantly high, but end-organ damage is not present. In response to a hypertensive crisis, it is important to select an agent with a rapid and controlled action and to carefully monitor the reduction of blood pressure. In hypertensive emergencies, the aim is to lower the mean arterial pressure by a maximum of 25% in a period of minutes by the use of IV antihypertensives and then gradually to normal over the next 48 hours. In hypertensive urgencies, the blood pressure is gradually reduced to normal in 48 hours with either IV or oral medication. There is a risk of cerebral and renal hypoperfusion if reduction of blood pressure is done at a rate faster than this. Vasodilators (sodium nitroprusside or nicardipine) may first be given to control the hypertension. In case optimum control of hypertension is not achieved by IV vasodilators, a β-blocker (esmolol or labetalol) can be added to the vasodilator or used in its place. Intravenous labetalol is the drug of choice in a hypertensive encephalopathy, where vasodilators may increase the cerebral blood flow and increase brain damage. Labetalol blocks both α- and β-adrenergic receptors and a controlled reduction of blood pressure can be achieved.



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IV/IM diazoxide, hydralazine, or oral nifedipine are other alternative drugs, especially in hypertensive urgencies. Sublingual administration of nifedipine is no longer recommended. Hypertensive crises may be associated with sodium and volume depletion, and volume expansion with isotonic sodium chloride must also be considered. Urine output requires diligent monitoring. A number of drugs, used alone or in combination, are available for the subsequent management of persistent hypertension. These include (i) calcium channel blockers—nifedipine, diltiazem, amlodipine; (ii) ACE inhibitors— captopril, enalapril; (iii) diuretics—furosemide, thiazides, K+ sparing diuretics; and (iv) β-blockers—propranolol, nadolol, metoprolol, atenolol.



Bibliography 1. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiology Clin 2006;24:135–46. 2. Flanigan JS, Vitberg D. Hypertensive emergency and severe hypertension: what to treat, who to treat, how to treat. Med Clin North Am 2006;90:439–51. 3. Hari P, Sinha A. Hypertensive emergencies in children. Indian J Pediatr 2011;78(5):569–75. 4. Houtman P. Management of hypertensive emergencies in children. Paediatr Perinat Drug Ther 2003;5(3):107–10. 5. Hypertension in Children and Adolescents. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. U.S. Department Of Health And Human Services. National Institutes of Health National Heart, Lung, and Blood Institute. National High Blood Pressure Education Program NIH Publication No. 04-5230. August 2004. 6. Perez MI, Musini VM, Wright JM. Pharmacological interventions for hypertensive emergencies. Cochrane Database of Systematic Reviews 2008;1: CD003653. DOI: 10.1002/14651858. CD003653.pub3. 7. Prescription Drug Information, Interactions & Side Effects. [Cited: July 2012] Available at: http://www.drugs.com/ 8. Robertson J, Shilkofski N. Drug doses. The Harriet Lane Handbook 17 ed. Philadelphia: Mosby; 2005:1053–68. 9. Temple ME, Nahata MC. Treatment of pediatric hypertension. Pharmacotherapy 2000;20(2): 140–50. 10. Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest 2000;118: 214–27.



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Pulmonary Hypertension “All we know is still infinitely less than all that remains unknown” —William Harvey (1578–1657)*



Factors Controlling Pulmonary Circulation Parameter



Pulmonary vasoconstrictors



Pulmonary vasodilators



pH



Acidosis



Alkalosis



Oxygenation



Hypoxia



Oxygen



Temperature



Hypothermia



Normothermia



Stimulation



Pain, agitation



Sedation, analgesia



Ventilation



Hypoventilation, alveolar hyperinflation



Mild hyperventilation



The parameters for pulmonary arterial hypertension in children are the same as for adult patients. It is defined as a mean pulmonary artery (PA) pressure of more than 25 mmHg at rest (or more than 30 mmHg during exercise), with a pulmonary vascular resistance of more than 3 Woods units/m2 in the presence of a normal left atrial pressure (i.e., 2



4 + (age ÷ 4)



3.5 + (age ÷ 4)



A patent airway is established with endotracheal (ET) intubation. This facilitates mechanical ventilation with 100% oxygen, minimizes pulmonary aspiration, and enables suctioning of the trachea. The position of the ET tube is confirmed clinically by bilateral chest movement and breath sounds and the absence of gastric insufflation sounds over the stomach. The position is subsequently assessed radiologically. Endtidal CO2 and pulse oximetry are additional monitoring aids.



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Cuffed ET tubes decrease the risk of aspiration and may be preferable. When a cuffed tube is used, an optimal cuff pressure is needed to be maintained (20–30 cm H2O). Laryngeal mask airway is an alternative to bag-mask ventilation when endotracheal intubation is not feasible.



Routes of Drug Administration IV access is secured with a peripheral venous, external jugular, or femoral vein cannulation. If cannulation is not immediately successful (>90 seconds), the intraosseous (IO) route or ET tube is utilized in an emergency for drug administration and later an IV cannula is placed. All drugs and resuscitative fluids may be given via the IO route, but only lignocaine, adrenaline, atropine, and naloxone (mnemonic LEAN) can be given via the ET tube. When drugs need to be administered via the ET tube, chest compressions are stopped briefly, medications are given into the ET tube and followed with a flush of at least 5 mL of normal saline and 5 consecutive positivepressure ventilations. Optimal endotracheal doses of medications are in general double or triple the IV doses for lidocaine, atropine, and naloxone.



Defibrillation The doses of drugs and DC shock are based on the patient’s body weight, which may be estimated from the age if the weight is unknown: Age



Estimated body weight



Newborn



3.5 kg



1 year



10 kg



1–10 years



(age in years + 4) × 2



Defibrillation is equally effective with manual or self adhesive pads. Adult size (8–10 cm) paddles or adhesive pads are used for children more than 10 kg weight and infant size (4.5 cm) for children under 10 kg. One paddle is firmly placed over the right side of the upper chest and the second on the left of the nipple over the lower ribs (cardiac apex), with preferably at least a 3 cm gap between the paddles. In infants and small children, paddles or pads may alternately be applied to the front and back of the chest. The initial dose in ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) is 2 or 4 J/kg, but the subsequent shocks recommended are 4 J/kg. Higher energy levels may be considered, not exceeding 10 J/kg in refractory cases. No synchronization with the ECG is required, and IV sedation or analgesia are not indicated.



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The initial adult dose (with a biphasic defibrillator) for VF is 120–200 J and subsequent shocks 200–360 J, depending upon the manufacturers recommendations.



Monitoring Arterial Pressure Line If the patient has an arterial monitoring line in place, the amplitude of the arterial pressure trace on the monitor can be used to evaluate the efficacy of the chest compressions and the return of spontaneous circulation (ROSC). End Tidal Carbon Dioxide Monitoring (ETCO2) ETCO2 monitoring (capnography or colorimetry) is recommended to confirm tracheal tube position and to help guide therapy, especially the effectiveness of chest compressions during CPR. Pulse Oximetry The systemic arterial oxygen saturation can only be recorded once a perfusing rhythm is present.



Drugs Adrenaline Adrenaline is a potent α, β1, and β2 agent and causes vasoconstriction in the dose recommended in CPR. It enhances the coronary perfusion pressure, stimulates spontaneous contractions, and increases the intensity of VF so increasing the likelihood of successful defibrillation. Amiodarone Amiodarone is a membrane stabilizing antiarrhythmic drug. It causes bradycardia and also has a mild negative inotropic effect. Hypotension is related to the rate of administration of the drug and is because of an α-blocking effect as well as a consequence of the histamine released by the solvent used (polysorbate 80 and benzyl alcohol). Amiodarone is preferably administered in a central line as it can cause thrombophlebitis when injected into a peripheral vein. Atropine Atropine is not a routine part of ALS algorithms as it has not shown improvement in the outcome of cardiac arrest. Atropine may increase myocardial oxygen demand and have its associated side effects. It is indicated when bradycardia is unresponsive to improved ventilation and circulatory support.



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The dose of atropine is 0.02 mg/kg, however, a minimum dose of 0.1 mg is given to avoid paradoxical bradycardia because of its central effect at low doses.



Calcium Calcium administration is not recommended for administration during CPR and should only be given when specifically indicated, e.g., for hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or hyperkalemia. Sodium Bicarbonate Acidosis during cardiac arrest is best corrected by effective CPR. Administration of sodium bicarbonate increases CO2 production and intracellular acidosis. It has a negative inotropic effect, increases the sodium load and shifts the oxygen dissociation curve to the left impairing oxygen release to the tissues. Sodium bicarbonate administration may however be considered in special circumstances such as hyperkalemic cardiac arrest or in prolonged arrest. Catecholamines and sodium bicarbonate should not be administered through the same IV line simultaneously because alkaline solutions inactivate catecholamines. Magnesium Administration of magnesium is indicated in children only if there is known hypomagnesemia or for treatment of torsades de pointes. Lignocaine Lignocaine may be given in the acute management of ventricular tachycardia (including torsades) and multiple ventricular ectopics but is a less effective alternative to amiodarone. Toxic effects of lignocaine include myocardial depression, drowsiness, and seizures.



PALS Protocols Abnormal cardiac rhythms, which do not produce a cardiac output (i.e., cardiac arrest), can be categorized into (i) shockable rhythms (ii) nonshockable rhythms based upon whether the particular arrhythmia responds to defibrillation or not. The two shockable rhythms are ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT), while the two nonshockable rhythms are asystole and pulseless electrical activity (PEA).



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Protocol for shockable rhythm Cardiac arrest • Bag-mask ventilation (15:2; compressions:breaths) • Chest compression rate 100–120/min • Monitor cardiac rhythm (rhythm–shockable) • Tracheal intubation (ventilation rate 8–10/min) • Monitor ETCO2 • Establish vascular access (IV/IO) DC shock 2 J/kg • CPR × 2 minutes • Check rhythm DC shock 4 J/kg • Resume CPR • Amiodarone 5 mg/kg (after 3rd & 5th shock only) • CPR × 2 minutes



• Resume CPR • Adrenaline 10 mcg/kg, IV/IO • CPR × 2 minutes • Check rhythm DC shock 4 J/kg



During CPR • Adrenaline is administered after every alternate DC shock. • Reversible causes are corrected. • At any stage, if on rhythm check there is asystole, non shockable protocol is commenced instead. • At any stage, when there is ROSC, post resuscitation care is instituted.



Ventricular Fibrillation and Pulseless Ventricular Tachycardia The only effective treatment of VF or pulseless VT is DC shock: 1. CPR ECC is started at a rate of 100–120/min and with bag-mask ventilation, 2 breaths are given after every 15 chest compressions. The child is intubated as soon as feasible with minimal interruption to CPR, and chest compressions are then given continuously at a rate of 100–120/min and ventilation at 8–10 breaths/min. On return of spontaneous circulation, chest compressions are stopped and the ventilation rate is adjusted to 12–20/min (depending on the age of the patient).



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2. Defibrillation ●



As soon as the defibrillator is ready and it is confirmed that the rhythm is shockable, an initial DC shock of 2 J/kg is given and the CPR is resumed without reassessing the rhythm.



●



After every 2 minutes of CPR, the rhythm is assessed and if it remains shockable, a DC shock of 4 J/kg is repeated.



3. Adrenaline ●



Inj. adrenaline 10 mcg/kg IV (0.1 mL of 1:10,000 solution) is administered after the 2nd shock and repeated after the 4th and 6th shocks (i.e., after every 2 shocks).



●



In the Resuscitation Council, UK guidelines 2010, adrenaline is given first after 3 shocks and then after every 2 shocks.



4. Amiodarone ●



Refractory VF or VT is treated with amiodarone 5 mg/kg (or lignocaine 1 mg/kg IV, if amiodarone is NA) after the 3rd shock and if required after the 5th shock.



5. Asystole/PEA If asystole or PEA is noted anytime on rhythm assessment prior to giving a shock, non-shockable protocol is instituted. 6. Return of spontaneous circulation ●



If there is ROSC, CPR is discontinued and post-resuscitation care is commenced.



●



If VF/VT recurs after successful defibrillation, resumption of CPR sequence and defibrillation is indicated. Amiodarone bolus is given (unless 2 doses have previously been administered) and a continuous infusion is started.



Asystole and Pulseless Electrical Activity PEA (formerly known as electromechanical dissociation) is recognized by slow, wide QRS complexes, but there is no cardiac output; at times, the ECG is relatively normal but the pulses are absent. 1. CPR ECC is initiated at a rate of 100–120/min, and a compression:ventilation ratio of 15:2 is provided with bag-mask ventilation. The child is intubated with minimal interruption to CPR and then continuous chest compressions are given at a rate of 100–120/min and ventilation at 8–10 breaths/min. The chest compressions are discontinued only on ROSC and the ventilation rate is adjusted to 12–20/min (depending on the age of the patient).



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Protocol for non-shockable rhythm Cardiac arrest • Bag-mask ventilation (15:2; compressions:breaths) • Chest compression rate 100–120/min • Monitor cardiac rhythm (rhythm non-shockable) • Tracheal intubation (ventilation rate 8–10/min) • Monitor ETCO2 • Establish vascular access (IV/IO) Adrenaline 10 mcg/kg IV



• CPR × 2 minutes • Check rhythm • CPR × 2 minutes • Check rhythm During CPR • Adrenaline is administered after every alternate loop of CPR (i.e., every 3–5 minutes). • Reversible causes are corrected. • At any stage, if on rhythm check the rhythm becomes shockable, shockable protocol is commenced instead. • At any stage, when there is ROSC, post resuscitation care is instituted.



2. Adrenaline Inj. adrenaline 10 mcg/kg IV (0.1 mL/kg of 1:10,000 solution) is administered as soon as it is confirmed that the rhythm is nonshockable and CPR is continued. The rhythm is checked after every 2 minutes of CPR. Adrenaline is repeated after every two such cycles of CPR and cardiac rhythm check (i.e., every 3–5 minutes). 3. DC shock Whenever the rhythm converts to VF, a DC shock of 4 J/kg is administered and the shockable rhythm protocol followed. 4. Correct reversible causes Any evident cause of arrhythmia or associated metabolic disorder is treated. Hypovolemia is corrected with a bolus of 20 mL/kg of crystalloid. 5. Discontinuing CPR CPR is discontinued only when there is ROSC or it is decided to terminate the effort.



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Torsades de Pointes Torsades is a variant of polymorphic VT and deteriorates rapidly to VF or pulseless VT, so CPR is initiated as soon as possible. An IV infusion of magnesium sulfate (25–50 mg/kg; maximum single dose 2 g) is administered over several minutes and the heart is defibrillated.



Bradycardia If the heart rate is less than 60/min and is associated with signs of poor peripheral perfusion, CPR is urgently needed. 1. CPR All inotrope lines, stopcocks, and infusion pumps are checked to confirm these are functioning, and adequate oxygenation and ventilation is ensured. If bradycardia with signs of poor perfusion persists, CPR with ECC at the rate of 100–120/min is instituted. 2. Adrenaline Adrenaline 10 mcg/kg (0.1 mL/kg of 1:10,000 solution) IV bolus can be given to increase the HR. If IV/IO access not available, it may be administered via the ET tube in a dose of 100 mcg/kg (0.1 mL/kg of 1:1000 solution). 3. Atropine In bradycardia due to increased vagal tone or primary AV conduction block, atropine 0.02 mg/kg IV/IO bolus or an endotracheal dose of 0.04–0.06 mg/kg may be effective. 4. Cardiac pacing In complete heart block or sinus node dysfunction unresponsive to ventilation, chest compressions, or medications, some form of cardiac pacing will be needed.



Management After Resuscitation 1. Oxygen 100% oxygen is used for initial resuscitation. After ROSC, the FiO2 is reduced to achieve an oxygen saturation of 94–98%. However, in the single ventricle patient, who has undergone a bidirectional superior cavopulmonary shunt or a systemic to pulmonary artery shunt, following resuscitation from cardiac arrest, FiO2 should be adjusted



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to optimize the systemic and pulmonary blood flow and the arterial oxygen saturation maintained at around 80%. 2. Hypothermia Mild hypothermia may improve neurological outcomes, whereas fever may be detrimental following ROSC. A child who remains in coma following successful resuscitation may benefit from core cooling to 32–34°C for at least 24 hours. Following a period of hypothermia, the child is rewarmed slowly (0.25–0.50°C/h). 3. Blood glucose control Hypo- and hyperglycemia are avoided following resuscitation. Moderate glucose control (as against tight glucose control) has been advocated.



Bibliography 1. Biarent D, Bingham R, Eich C, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 6. Paediatric life support. Resuscitation 2010;81:1364–88. 2. Kleinman ME, Chameides L, Schexnayder SM, et al. American Heart Association. Pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics 2010;126:e1361–99. 3. Kleinman ME, de Caen AR, Chameides L, et al. Pediatric Basic and Advanced Life Support Chapter Collaborators. Pediatric basic and advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Pediatrics 2010;126:e1261–318. 4. Kotur PF. An update on pediatric resuscitation. Indian J Anaesth 2004;48:330. 5. Part 12: Pediatric Advanced Life Support. Circulation 2005;112:IV-167–IV-187. Resuscitation Council (UK). [Updated: 2010 Dec; cited: 2011 Feb 22] Available at: http://www.resus.org.uk/ pages/pals.pdf 6. Burke DP, Bowden BF. Modified paediatric resuscitation chart. BMJ 1993;306:1096–8. 7. Pediatric Drug Lookup. CPR Pediatric Drug Dosages. Pediatriccareonline. [Updated: 2011 Mar 21; cited: 2011 Apr 29] Available at: http://www.pediatriccareonline.org/pco/ub/view/ Pediatric-Drug-Lookup/153899/all/cpr_pediatric_drug_dosages 8. Madden SCV. Paediatric drug doses. University Hospitals Coventry and Warwickshire N.H.S. Trust. [Updated: 2011 Mar 21; cited: 2011 Apr 29] Available at: http://www.esculape.com/ pediatrie/medicament_dose.html#index.



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Fluid and Electrolytes “A good heart and kidneys can survive all but the most willfully incompetent fluid regimen” —Mark M Ravitich (1910–1989)*



Fluid and electrolyte management can be divided into two components: (i) maintenance therapy and (ii) deficit therapy. Maintenance therapy comprises of replacement of the ongoing physiological losses of water and electrolytes, which occur in urine, sweat, respiration, and stool. Maintenance fluid requirements need to be increased if there are additional losses, as with fever, surgical drainage or ongoing gastrointestinal losses. The requirements are decreased in oliguric renal failure, edematous states and in the syndrome of inappropriate ADH secretion. Deficit therapy comprises of existing water and electrolyte deficits, which may be present as a result of gastrointestinal, urinary, skin or blood loss and third-space sequestration.



Maintenance Therapy Daily electrolyte requirements in children Electrolytes



Daily requirement (mmol/kg)



Normal blood levels



Sodium (Na)



2–4 mmol/kg



136–145 mmol/L



Potassium (K)



2–3 mmol/kg



3.5–5.0 mmol/L



Calcium (Ca)



0.2–0.4 mmol/kg



Total Ca: 2.2–2.8 mmol/L (8.8–11.2 mg/dL) Ionized Ca: 1.1–1.4 mmol/L (4.4–5.4 mg/dL)



Magnesium (Mg)



0.15–0.25 mmol/kg



1.8–3.0 mg/dL (1.5–2.5 meq/L or 0.75–1.25 mmol/L)



Chloride (Cl)



3 mmol/kg



95–105 mmol/L



*Mark M Ravitich was a renowned pediatric surgeon, teacher, author of medical textbooks, and editor of several medical journals.



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Daily maintenance fluid requirements in a newborn Age (days)



Daily requirement (mL/kg/day)



Hourly requirement (mL/kg/h)



Type of fluid



1



20–40



2–3



10% Dextrose



2



40–60



3–4



1/5



Saline + 10% dextrose



3



60–80



4–6



1/5



Saline + 10% dextrose



4



80–100



6–8



1/5



Saline + 10% dextrose



Daily maintenance fluid requirements in infants and children Weight (kg)



Daily requirement



Hourly requirement



Type of fluid



0–10



100 mL/kg



4 mL/kg



¼ Saline in 10% dextrose



11–20



1000 mL (for 10 kg) + 50 mL/kg (for wt >10 kg)



40 mL (for 10 kg) + 2 mL/kg (for wt >10 kg)



¼ Saline in 5% dextrose



21–30



1500 mL (for 20 kg) + 20 mL/kg (for wt >20 kg)



60 mL (for 20 kg) + 1 mL/kg (for wt > 20 kg)



½ Saline in 5% dextrose



Maintenance Fluid Requirement Maintenance fluid requirements in infants and children can be calculated based on body weight or surface area. By the body weight method, 100 mL/kg is the requirement for the first 10 kg, 50 mL/kg for the next 10 kg, and 20 mL/kg for the remaining weight. By the surface area method (applicable to children >10 kg), the requirement is 1500–2000 mL/m2/day.



Type of Fluid The type of IV fluid required to be given is dependent on the electrolyte requirement of the child. One liter of normal saline (NS) contains 154 mmol of Na and an equal concentration of chloride. One liter of ¼ NS will contain about 38 mmol of sodium, which will meet the daily sodium requirement of children up to 20 kg. The maintenance regimen is changed to a more concentrated saline solution (e.g., ½ NS instead of ¼ NS) if the serum sodium drops, or to a more dilute solution if the serum sodium starts to rise. The daily potassium requirement calculated as per body weight is added to the days IV fluid unless the patient is hyperkalemic or in renal failure. 2 mmol of potassium added to every 100 mL of maintenance fluid will approximately provide the daily potassium requirement of 2 mmol/kg/day. The calcium requirement can be given as 1–2 mL/kg/day of 10% calcium gluconate by continuous IV infusion.



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Daily maintenance requirements of adult patients with normal renal function are met with two liters of half isotonic (½ N) saline, to which 20 mmol of potassium chloride (KCl) is added per liter. Patients with ongoing gastrointestinal or third-space losses may require a higher rate of saline (or blood) administration to maintain volume balance. Gastric aspiration fluids are replaced by N/2 saline and intestinal losses by NS. Guidelines for fluid therapy in postoperative open heart patients Post Op day



Hourly fluid maintenance requirement



Day of operation



1 mL/kg/h (for first 10 kg) + 0.5 mL/kg (for next 10 kg) + 0.25 mL (for remaining weight)



Day 1 Post Op



2 mL/kg/h (for first 10 kg) + 1 mL/kg/h (for next 10 kg) + 0.5 mL/kg/h (for remaining weight)



Day 2 Post Op



3 mL/kg/h (first 10 kg) + 1.5 mL/kg/h (for next 10 kg) + 0.75 mL/kg/h (for remaining weight)



Day 3 Post Op



Normal maintenance, i.e., 4 mL/kg/h (first 10 kg) + 2 mL/kg/h (for next 10 kg) + 1 mL/kg/h (for remaining weight)



In the immediate postoperative period following cardiac surgery, there is a need for fluid restriction because of cardiac dysfunction and fluid retention caused by cardiopulmonary bypass. The general guidelines for fluid administration following open heart surgery are enumerated in the table. The total fluid intake is restricted to 25–50% of normal maintenance on the day of surgery and increased each morning by 20–25% (provided systemic or pulmonary edema is not present) until normal requirement is reached. (Based on these guidelines, the calculated daily requirement in the immediate postoperative period for an open heart surgery patient is given in Appendix J.) After closed heart surgery one can commence with a higher intake, 50% of the normal daily requirement is given on the day of surgery and normal requirements can be given the following day or on day 2.



Deficit Therapy Analysis of the severity of dehydration by physical signs Clinical sign



Mild



Moderate



Severe



Pre-illness body wt



10% loss



Skin color



Pale



Ashen



Mottled



Skin turgor



↓



Tented



Tented



Dryness of mucous membranes



+



++



++



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Fluid and Electrolytes



Clinical sign



Mild



Moderate



Heart rate



Normal/↑



↑



↑↑



Blood pressure



Normal



Normal/↓



Shock



Urine output



↓



↓↓



Azotemic



103



Severe



Fontanelle (12 yr: 20–40 mg/day in divided doses q12–24h PO.



Reduce dose in severe liver disease.



Sucralfate suspension (1 g in 5 mL)



0–1 yr: 6 mL/day in divided doses q4h PO. 2–6 yr: 12 mL/day in divided doses q4h PO. 7–12 yr: 18 mL/day in divided doses q4h PO. >12 yr: 30 mL/day in divided doses q4h PO.



Contraindicated in severe renal impairment.



Stress Ulceration and Upper GI Bleeding Stress ulceration and upper gastrointestinal bleeding are well-known complications in the postoperative period in children operated for heart disease. Some of the factors which increase the risk of stress ulceration are as follows: ■ ■



Children on ventilator for >48 hours Coagulopathy



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Unstable hemodynamic condition requiring high doses of intravenous catecholamines Re-thoracotomy Multiorgan dysfunction or sepsis Steroids



Various available prophylactic agents include H2-receptor blocking agents, proton pump inhibitors (PPIs), sucralfate, and antacids. H2-receptor antagonists (ranitidine, famotidine) decrease the acid secretion in the stomach and lower the incidence of stress ulceration and the occurrence of GI bleeding. PPIs however, provide a higher level of stomach pH control and are therefore more effective therapy for prophylaxis. At the same time, this elevation in the level of gastric pH has been implicated in an increase in bacterial colonization of the gut promoting bacterial translocation and an increased incidence of blood-borne sepsis and also an increased incidence of aspiration and ventilator-associated pneumonias. H2 blocking agents and PPIs are therefore not generally used for routine postoperative prophylaxis but in patients who are at a higher risk for GI bleeding and in the treatment of GI bleeding. Sucralfate has not been shown to be as effective as H2 blockers and PPIs in the control of stress ulceration but since it does not increase the gastric pH, it may be safer and has been recommended for routine use in postoperative protocols. It may also be used in combination with H2-receptor blocking agents, and PPIs in the treatment of GI bleeding. Antacids are associated with diarrhea and electrolyte disturbances and have not proven to be of any benefit in GI prophylaxis.



Bibliography 1. Allen ME, Kopp BJ, Erstad BL. Stress ulcer prophylaxis in the postoperative period. American Journal of Health-System Pharmacy 2004;61(6). Medscape. [Updated: 2004 Apr 16; cited: 2011 Apr 26] Available at: http://www.medscape.com/viewarticle/472701. 2. Araujo TE, Vieira SM, Carvalho PR. Stress ulcer prophylaxis in pediatric intensive care units. J Pediatr (Rio J) 2010;86(6):525–30. 3. Arora NK, Ganguly S, Mathur P, Ahuja A, Patwari A. Upper gastrointestinal bleeding: etiology and management. Indian J Pediatr 2002;69(2):155–68. 4. Behrens R, Hofbeck M, Singer H, Scharf J, Rupprecht T. Frequency of stress lesions of the upper gastrointestinal tract in paediatric patients after cardiac surgery: effects of prophylaxis. Br Heart J 1994;72:186–9. 5. Cook D, Guyatt G, Marshall J, et al. A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Canadian Critical Care Trials Group. N Engl J Med 1998;338(12):791–7. 6. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N Engl J Med 1994;330:377–81. 7. Deorari AK. Rational drug therapy. In: Ghai OP, Paul VK, Bagga A, ed. Essential Paediatrics 7th ed. New Delhi: CBS Publishers & Distributors Pvt Ltd; 2009:729–30.



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8. Elliot MJ, Delius RE. Renal issues. In: Chang AC, Hanley FI, Wernovsky GU, Wessei DL, ed. Pediatric Cardiac Intensive Care Pennsylvania: Williams and Wilkins; 1998:388. 9. Ephgrave KS, Kleiman-Wexler R, Pfaller M, et al. Effects of sucralfate vs antacids on gastric pathogens: results of a double-blind clinical trial. Arch Surg 1998;133(3):251–7. 10. Fennerty MB. Pathophysiology of the upper gastrointestinal tract in the critically ill patient: rationale for the therapeutic benefits of acid suppression. Crit Care Med 2002;30:S351–5. 11. Prescription Drug Information, Interactions & Side Effects. [Cited: July 2012] Available at: http://www.drugs.com/ 12. Reveiz L, Guerrero-Lozano R, Camacho A, Yara L, Mosquera PA. Stress ulcer, gastritis, and gastrointestinal bleeding prophylaxis in critically ill pediatric patients: a systematic review. Pediatr Crit Care Med 2010;11:124–32. 13. Sean C. Sweetman. Gastrointestinal drugs. Martindale: The Complete Drug Reference 36th ed. 2009:1693–778.



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Postoperative Respiratory Complications “It is unsettling to find how little it takes to defeat success in medicine” —Atul Gawande* (In: Better: A Surgeon’s Notes on Performance)



Pulmonary Dysfunction Postoperative pulmonary dysfunction (PPD) refers to an impairment of blood gases and alteration of lung mechanics in the immediate post surgical period. The cause of the dysfunction is primarily because of the inflammatory response and microatelectasis initiated by cardiopulmonary bypass (CPB) resulting in abnormalities of oxygen and carbon dioxide transfer across the alveolar membrane. The AaDO2 is significantly higher, and there is a decrease in the vital capacity, functional residual capacity, and lung compliance following CPB. In the extubated patient, this may be clinically evident by tachypnea, respiratory distress, and tachycardia. The severity of dysfunction may range from hypoxemia (which is present to a variable degree in all patients following CPB) to acute respiratory distress syndrome (ARDS) (0.4–2%). Recovery from PPD requires a variable period of postoperative mechanical ventilation. Appropriate mode of ventilation, moderate PEEP, and repeated endotracheal suctioning gradually improves the oxygenation and increases the functional residual capacity permitting extubation. Thereafter, positioning, pain management, and chest physiotherapy further improves alveolar recruitment. Postoperative pain is certainly an important consideration in patient recovery, and failure to control postoperative pain may itself result in inadequate tidal volume with increasing areas of lung collapse and poor blood gases.



Pleural Effusion Causes of pleural effusion in the postoperative period include right heart failure, fluid overload, pulmonary edema, and extravasation from extracardiac *Atul Gawande is a practicing general surgeon and author of three best sellers, Complications, Better and The Checklist Manifesto which are based on his personal experience of surgical triumphs, errors, and controversies.



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shunts. The inflammatory response to CPB may also itself result in small, transient effusions. Small effusions will resolve with treatment of the cause, however, large effusions will require chest tube drainage. The most appropriate position for chest drains for fluid collections is the 5th or 6th intercostal space in the posterior axillary line.



Chylothorax Chylothorax may occur after injury to the thoracic duct or its tributaries either within the pericardium or more often after extrapericardial operations, e.g., Blalock–Taussig shunt or coarctation repair. It may also be seen after open heart procedures associated with high systemic venous pressure, especially the Fontan operation. Often, a chylothorax becomes evident only after 2–7 days of surgery. The reason for this is that lymph initially accumulates in the posterior mediastinum until the mediastinal pleura gives way, usually into the right pleural cavity.



Diagnosis Presence of a milky white effusion, which increases with the intake of dietary fat, is an indication of a chylothorax. Chyle is sterile and can be distinguished from other opalescent collections by the presence of chylomicrons, which are stained with Sudan III and estimation of the triglyceride content (>110 mg/dL). Chyle has a protein concentration of 2.2–6 g/dL and has a white blood cell count >1000/mL with a lymphocyte fraction >80%.



Management As a first step, conservative management is initiated with chest tube drainage and a fat-free formula consisting of only proteins and starch or a dietary intake of medium chain triglycerides instead of normal fats. Medium chain triglycerides are absorbed directly into the portal venous system and allow healing of the injured duct. Alternatively, the child is placed on IV hyperalimentation at the time of diagnosis or later after a trial of the above management. Inj. somatostatin (or its synthetic analog octreotide) has been effectively used to treat chylothorax in various dosing schedules. One recommended dose is 80–100 mcg/kg/day, which can be given in divided doses 8 hourly either IM or IV. An alternative dose protocol is 1–4 mcg/kg/h as a continuous infusion. It is tapered after cure and may need to be given up to 3 weeks. If the drainage persists, recommendations about the length of conservative management vary considerably. One opinion is to continue aggressive



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nonoperative management for 4 weeks before surgical intervention. Other authors have advocated surgical intervention at 1–2 weeks if there is no significant improvement in the drainage. Operative procedures include surgical ligation of the injured duct at the site of operation or above the right diaphragm. Alternatively, a pleurodesis or a pleuroperitoneal shunt may be performed.



Diaphragmatic Paralysis Phrenic nerve injury can occur during surgery, along the course of the nerve in the mediastinal pleura either by cold cardioplegia solution, diathermy, or direct surgical trauma. It is a cause of failure to wean from the ventilator. It may be difficult to diagnose, and an abnormal abdominal breathing pattern in the extubated child may be the pointer. Respiratory distress and CO2 retention after extubation may require that the child be put back on the ventilator. X-ray chest after extubation reveals a raised dome of diaphragm with atelectasis, which was not evident during ventilation. Ultrasound examination or fluoroscopy confirms the paradoxical diaphragmatic movements (upward diaphragmatic movement during inspiration). Plication of the affected diaphragm may be needed before the child can eventually be extubated.



Pneumothorax Intermittent positive pressure ventilation (IPPV) or vigorous hand bagging may result in barotrauma and pneumothorax. Entry of air from around a loosely fitting chest drain can also be a cause. Pneumothorax is suspected in the ventilated patient, if there is an increase in the peak inspiratory pressure, a fall in the oxygen saturation, and a decrease of breath sounds on the affected side. In the extubated patient, there may be tachypnea, cyanosis, tracheal deviation away from the affected side, and reduced respiratory breath sounds. In tension pneumothorax, there is in addition, sudden hemodynamic decompensation manifested by hypotension and bradycardia or tachycardia. X-ray chest will show pneumothorax. In the unstable patient, rather than waiting for the X-ray, the diagnosis can be confirmed with a needle and syringe aspiration, and the pneumothorax relieved by the introduction of a 20 gauge needle. A chest tube is inserted subsequently. For a pneumothorax, the appropriate position for the chest tube is the third intercostal space in the anterior axillary line.



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Atelectasis Atelectasis produces tachypnea, tachycardia, and impairment of blood gases, depending upon the extent of collapse. In case of a large collapse, there is a decrease in chest expansion, a mediastinal shift towards the affected side, and diminished breath sounds over the corresponding area of the chest. The patient may have fever 48–72 hours after a persistent collapse lung. Radiological findings show infiltration of the collapsed segment or lobe. Typically, the right upper or middle lobe collapse obscures the right heart border, left upper lobe atelectasis may be evident by a triangular infiltrate extending to the upper mediastinum, and a left lower collapse causes an increased density of the cardiac silhouette.



Causes Collapse of the lung may be caused by obstruction of the endotracheal tube, or bronchial airway with blood clot or secretions. Vascular structures such as dilated pulmonary arteries or enlarged cardiac chambers, because of their close association with the respiratory tract, can cause extrinsic compression of the airways. The trachea, the left bronchus, and the origin of the right middle lobe bronchus are the more common sites of compression. Significant airway compression presents with pulmonary collapse or persistent wheezing or rarely it is a cause of failure of extubation of the ventilated patient.



Management Postoperative management involves measures to assist complete lung expansion and prevention of atelectasis. The ventilated child needs humidification of inspired gases, institution of adequate PEEP (or CPAP) and regular endotracheal suction. Minimal negative pressure (−80 to −120 mmHg) is utilized to aspirate endotracheal secretions so as not to cause epithelial damage. After the child is extubated, chest physiotherapy and adequate analgesia prevents pain and splinting of the chest. A collapse segment or lobe may re-expand with chest physiotherapy alone. More often it may require tracheal aspiration with a flexible bronchoscope. Alternatively, endotracheal intubation is done to allow tracheal suctioning. This is followed by short-term IPPV with PEEP before extubation. Atelectasis may be difficult to distinguish from pneumonia and nonresolving atelectasis may progress to pneumonia. Endotracheal secretions



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should be Gram stained and cultured, and appropriate prophylactic antibiotics should be started in non-resolving atelectasis.



Aspiration Pneumonitis Aspiration pneumonitis (Mendelson syndrome) is caused by an episode of vomiting or reflux, with aspiration of the gastric contents. This can possibly occur in a sedated or neurologically obtundated child or in a ventilated child in whom a non-cuffed endotracheal tube has been used. The aspiration causes a chemical pneumonitis, which may be followed subsequently by a bacterial infection. The extent of damage to the tracheobronchial tree depends upon the amount and acidity of the material aspirated, and the pathological lesions can vary from mild bronchiolitis to acute pulmonary edema.



Clinical Features The child usually presents with clinical features of mild to severe respiratory distress 2–5 hours after the episode of aspiration. Severe cases may progress to ARDS. Radiological findings vary from segmental or lobar consolidation to bilateral perihilar or multifocal opacities. In the recumbent child, the posterior segments of the upper lobes and the superior segments of the lower lobes are more likely to be involved.



Treatment Oropharyngeal and tracheal suctioning is urgently required in a child who has aspirated following vomiting. Pulse oximetry is monitored and supplemental oxygenation is provided. The need for intubation is assessed depending on the oxygenation and the patient’s neurological status. Antibiotics are indicated if aspiration pneumonitis fails to resolve within 48 hours; Pseudomonas aeruginosa, Klebsiella pneumoniae, and methicillin-resistant Staphylococcus aureus must be covered.



Bibliography 1. Apostolakis EE, Koletsis EN, Baikoussis NG, Siminelakis SN, Papadopoulos GS. Strategies to prevent intraoperative lung injury during cardiopulmonary bypass. J Cardiothorac Surg 2010; 5:1. [Cited: 2011 Oct 8] Available at: http://www.cardiothoracicsurgery.org/content/5/1/1. 2. Bandla HPR, Hopkins RL, Beckerman RC, Gozal D. Pulmonary risk factors compromising postoperative recovery after surgical repair for congenital heart disease. Chest 1999;116:740–7.



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3. Bennet NR. Paediatric intensive care. Br J Anaesth 1999;83:139–56. 4. Büttiker V, Fanconi S, Burger R. Chylothorax in children: guidelines for diagnosis and management. Chest 1999;116:682–7. 5. Chakrabarti B, Calverley PMA. Management of acute ventilatory failure. Postgrad Med J 2006;82:438–45. doi: 10.1136/pgmj.2005.043208. 6. Engelherdt T, Webster NR. Pulmonary aspiration of gastric contents in anaesthesia. Br J Anaesth 1999;83:453–60. 7. Helin RD, Angeles STV, Bhat R. Octreotide therapy for chylothorax in infants and children: a brief review. Paediatr Crit Care Med 2006;7(6):576–9. 8. Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Eur J Cardiothorac Surg 2007;32:362–9. 9. Ng CS, Wan S, Yim AP, Arifi AA. Pulmonary dysfunction after cardiac surgery. Chest 2002; 121:1269–77. 10. Oster JB, Sladen RN, Berkowitz DE. Cardiopulmonary bypass and the lung. In: Gravlee GP, Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2000:367. 11. Pratap U, Slavik Z, Ofoe VD, Onuzo O, Franklin RCG. Octreotide to treat postoperative chylothorax after cardiac operations in children. Ann Thorac Surg 2001;72:1740–2. 12. Sandora TJ, Harper MB. Pneumonia in hospitalized children. Pediatr Clin N Am 2005;52: 1059–81. 13. Wynne R, Botti M. Postoperative pulmonary dysfunction in adults after cardiac surgery with cardiopulmonary bypass: clinical significance and implications for practice. Am J Crit Care 2004;13:384–93.



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Acute Respiratory Distress Syndrome



Diagnosis Parameter



ARDS



Onset



Acute



Clinical setting



Predisposing condition exists



Gas exchange



PaO2/FiO2 10 g%.



Steroids



Steroids have no specific role.



Surfactant



Aerosolized surfactant may be of benefit in neonates.



Various ventilatory strategies in the management of ARDS have been advocated with debatable outcomes. One of the prevalent methods (ARDS network trial 2000) aims at ventilatory settings that prevent any further lung injury by achieving the lowest peak inspiratory pressures (PIP) and tidal volumes (TV) that will allow gas exchange. Some degree of CO2 retention (permissive hypercapnia) because of low TV is accepted. End expiratory atelectasis is prevented by appropriate levels of PEEP. Volume or pressure preset ventilation can be used. The following protocol is appropriate in volume assist control mode: 1. The initial TV is set at 5–7 mL/kg. 2. A plateau pressure of ≤30 cm H2O is maintained by reducing the TV to 5 or 4 mL/kg if necessary.



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3. The ventilator rate is set at 12–35 breaths/min to provide appropriate minute ventilation. Hypercapnea is accepted as a protective lung strategy and an increase in PCO2 (pH >7.10 and PCO2 40–90 mmHg) is allowed to the extent that it does not result in significant hemodynamic instability. 4. A moderate prolongation of inspiratory time (IT) is used to improve oxygenation (1:1 to 1:3). Excessive IT (which shortens the expiratory time) is avoided as this can cause intrinsic PEEP and lung injury. 5. One method recommended for setting the appropriate PEEP and FiO2 is to titrate levels of “PEEP and FiO2 combinations” against increasing oxygen saturations. The following combinations of FiO2/PEEP are stepped up to achieve an oxygenation goal of PaO2 55–80 mmHg (SaO2 88–95%): FiO2 PEEP (cm H2O)



0.3 0.4 5



8



0.5



0.6



0.7



0.8



8–10



10



10–14



14



0.9



1.0



14–18 18–22



6. Attempts to wean by pressure support are indicated when FiO2/PEEP ≤0.40/8.



Bibliography 1. Corne J, Carrol M, Brown I, Delany D, eds. Chest X-ray Made Easy 2nd ed. Churchill Livingston; 2002:56–63. 2. Christie JD, Lanken PN. Acute lung injury and acute respiratory distress syndrome. In: Hall JB, Schmidt GA, Wood LDH, eds. Principles of Critical Care 3rd ed. New Delhi: McGraw-Hill 2005:515–47. 3. Feng AK, Steele DW. Pediatrics, respiratory distress syndrome: treatment and medication. [Updated: 2009 Sep 18; cited; 2011 Feb 22]. Available at: http://emedicine.medscape.com/ article/803573. 4. Fiore ML, Lieh-Lai MW. Acute respiratory distress syndrome [Cited: 2011 Feb 22]. Available at: http://www.scribd.com/doc/24857688/ARDS-Lecture. 5. Hess D. Mechanical ventilation of patients with ARDS [Cited: 2011 Feb 22]. Available at: http://www.rcsw.org/Download/2004_RCSW_conf/ARDS%20Dean%20Hess.pdf 6. O’Croinin D, Chonghaile MN, Higgins B, Laffey JG. Bench-to-bedside review: permissive hypercapnia. Crit Care 2005;9(1):51–9. 7. Prodhan P, Noviski N. Pediatric acute hypoxemic respiratory failure: management of oxygenation. J Intensive Care Med 2004;19:140–53. 8. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301–8. 9. Varon J, Wenker OC. The acute respiratory distress syndrome: myths and controversies. The Internet Journal of Emergency and Intensive Care Medicine 1997;1(1). [Updated: 2009 Feb 13; cited: 2011 Feb 22]. Available at: http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ ijeicm/vol1n1/ards.xml.



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Postoperative Bronchospasm



Postoperative Causes Bronchospasm or respiratory wheeze in the immediate postoperative period is not uncommon and may be caused by a number of potential factors: 1. Primarily, it may be a manifestation of preexisting bronchial asthma or airway hypersensitivity. Bronchial irritation by the endotracheal tube, anesthetic gases, or secretions in predisposed individuals may precipitate an acute episode. 2. Hypersensitivity reactions to various drugs, in particular protamine, β-adrenergic blockers, and drugs that cause histamine release (e.g., morphine or atracurium), may induce bronchospasm. Activation of inflammatory factors by the CPB (e.g., C5a anaphylatoxin) may itself be the cause. 3. Bronchospasm may be a manifestation of pulmonary edema, possibly the result of over transfusion in a child with poor LV function. 4. Other postoperative respiratory complications (e.g., respiratory infection, pneumothorax, or atelectasis) may present with bronchospasm.



Assessment of Severity of Acute Bronchial Asthma Clinical feature



Mild



Moderate



Severe



Breathlessness



Only on activity, e.g., walking



Becomes breathless on talking. In infants, cry is softer and shorter; difficulty in feeding



Is breathless even on rest, inability to feed



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Clinical feature



Mild



Moderate



Severe



Ability to talk



Is able to talk in sentences



Talks in phrases or words



Drowsy/confused



Use of accessory muscles of respiration/ suprasternal retraction



Not in evidence



Evident



Evident. Breathing may be thoracoabdominal



Wheeze



Moderate, may be only end expiratory



Loud



Loud/may be inaudible



Pulsus paradoxus



Absent 60 mmHg



45 mmHg



SaO2%



>95%



91–95%



80%



60–80%



3 months



2 × Creat ↑ >3 × or Creat ↑ >4 mg/dL with an acute ↑ >0.5 mg/dL



12 yr*



55–85



12–18



110–135/65–85



th



Source: Kliegman RM, et al., eds. Nelson’s Textbook of Pediatrics 19 ed. Philadelphia: Saunders Elsevier; 2011:279–80. *From Dieckmann R, Brownstein D, Gausche-Hill M, eds. Pediatric Education for Prehospital Professionals. Sudbury, Mass, Jones & Bartlett, American Academy of Pediatrics; 2000:43–45. † From American Heart Association ECC Guidelines, 2000.



Hypotension* For purposes of resuscitation, hypotension has been defined as: ■



Age 16 yr



30–115 units/L



Aspartate aminotransferase (AST)(SGOT)



Infants



18–74 units/L



Children



15–46 units/L



Adults



5–35 units/L



Creatine kinase (CK)



Infants



20–200 units/L



Children



10–90 units/L



Adults



0–206 units/L (M), 0–175 units/L (F)



Lactate dehydrogenase (LDH)



Newborns



290–501 units/L



1 mo to 2 yr



110–144 units/L



>16 yr



60–170 units/L



Source: Pediatric Care Online; the American Academy of Pediatrics. Available at: www.pediatriccareonline.org.



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Crystalloids Fluid



Na K Ca Cl HCO3 Comments (mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L) (pH/tonicity [mOsm/L])



Plasma



140



4.5



2.3



100



26



pH 7.4, Osm 290



5% Dextrose



Dextrose 50 g/L Osm 277



10% Dextrose



Dextrose 100 g/L Osm 556



Normal saline (0.9% NaCl)



154



154



pH 5, Osm 308



½ Normal 77 saline (0.45 NaCl)



77



pH 5, Osm 154



Glucose 5% + saline 0.45%



77



77



Glucose 50 g/L Osm 431



Ringer lactate



130



4



Plasmalyte 148



140



5



1.5



109



28



Contains lactate 28 mmol/L; pH 6.5, Osm 273



98



29



Contains acetate 27 mmol/L, gluconate 23 mmol/L; pH 5, Osm 294



Colloids Fluid



Na K Ca Cl Other (g/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L)



Comments (pH/tonicity)



Haemaccel



145



5



6.25



145



Gelatin 35 g



7.4



Gelofusine



154