DOCSLIB.ORG

Cardiac Emergencies in Neonates

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cardiac Emergencies in Neonates ACTA SCIENTIFIC MEDICAL SCIENCES Volume 3 Issue 6 June 2019 Review Article Cardiac Emergencies in Neonates Samah Alasrawi* Pediatric Cardiologist, AlJalila Children Heart Center, Dubai UAE *Corresponding Author: Samah Alasrawi, Pediatric Cardiologist, AlJalila Children Heart center, Dubai, UAE Received: May 14, 2019; Published: May 24, 2019 Abstract Introduction: The diagnosis of cardiac disease in the neonates is not always straight forward because physical examination, ECG, and CXR are often difficult to interpret in the newborn period compared to older infant or child. The most important factors in narrowing down the diagnostic possibilities are: Although echocardiography is required to precisely define the anatomical abnormality, it is usually possible to define. The clinical presentation • Shock (ductal dependent systemic circ.) (Grey baby) • Cyanosis (ductal dependent pulmonary circ.) (Blue Baby) including severe Ebstein’s anomaly • CHF congestive heart failure (shunt lesions) (Pink Baby) • Arrhythmia The timing of the presentation (age) Associated non cardiac or genetic anomalies Objective: To Concentrates on few points which make the diagnosis and managements of cardiac emergencies in neonates easier. Keywords: Neonates; Cardiac; Emergencies Introduction The most important factors in narrowing down the diagnostic The diagnosis of cardiac disease in the neonates is not always possibilities are straight forward because physical examination, ECG, and CXR are • The clinical presentation - • Shock (ductal dependent systemic circ.) (Grey der infant or child. baby) often difficult to interpret in the newborn period compared to ol • Cyanosis (ductal dependent pulmonary circ.) (Blue Baby) including severe Ebstein’s anomaly an - Although echocardiography is required to precisely define the • GHF congestive heart failure (shunt lesions) - atomical abnormality, it is usually possible to define the functi (Pink Baby) dings. onal abnormality on the basis of the clinical and radiographic fin • The timing of the presentation (age) • Associated non cardiac or genetic anomalies The timing of presentation and severity depends on • Nature and severity of defect So the vital signs and clinical examination in newborns are very • The alteration in cardiovascular physiology secondary to important And lead to the right diagnosis: (Right sided obstructive the effect of the transitional circulation as lesions(cyanosis), Left sided obstructive lesions (Collapse), Mixing • Closure of ductus/restriction of patent foramen ovale lesions (cyanosis with CHF), ASD dependent lesions (cyanosis with (PFO) CHF) And give a chance to start PGE1 when there is any suspicion • Fall in pulmonary vascular resistance (PVR) of PDA dependent lesion (systemic or pulmonary) before the Echo. Citation: Samah Alasrawi. “Cardiac Emergencies in Neonates”. Acta Scientific Medical Sciences 3.6 (2019): 109-113. Cardiac Emergencies in Neonates 110 Neonatal Presentations PDA dependent pulmonary circulation 1. Cyanosis 2. Shock 3. CHF 4. Arrhythmias 1. Pulmonary Atresia, Intact Ventricular Septum 2. Pulmonary Atresia, VSD and PDA Septicemia, respiratory disorders, persistent pulmonary hyper- tension of newborn (PPHN), inborn errors of metabolism and so 3. Pulmonary Atresia with Single Ventricle on. 4. Severe forms of Epstein's anomaly Neonatal Presentations What is common to all these lesions 1. Cyanosis 2. Shock 3. CHF 4. Arrhythmias Oligemic lung fields on CXR Admixture lesions Septicemia, respiratory disorders, persistent pulmonary hyper- tension of newborn (PPHN), inborn errors of metabolism and so • Transposition of Great Arteries, intact Interventricular septum on. • Total Anomalous Pulmonary venous connection Cyanosis • Truncus Arteriosus Cardiac causes • Double Outlet Right Ventricle with VSD • PDA dependent pulmonary circulation • Single ventricle anomalies with or without Pulmonary ste- • Admixture lesions nosis • intracardiac shunt Critical Right ventricular outflow tract obstruction with intra Critical Right ventricular outflow tract obstruction with cardiac shunt Case 1 • Critical Pulmonary Stenosis with interatrial communicati- Asymptomatic neonate was discharged on breast feeds on • Suddenly presents at 3 days of life with bluish discolor- • Tetralogy of Fallot with Critical Pulmonary Stenosis ation Pulmonary causes • Sats 70, mild tachypnea and minimal distress, soft ESM, No response to oxygen Primary lung disease • Ventilation –mild increase in saturations (75%) • Respiratory distress syndrome • Meconium aspiration Plan: Start Prostaglandin E1 and get Echo CXR: Oligemic lung fields and no cardiomegaly Figure 1 PPHN Why PGE1 started, can we do it without echo, what is the probable • Pneumonia DD. • Pulmonary atresia with VSD Airway Tracheo-obstruction esophageal fistula • Choanal atresia, laryngotracheomalacia, laryngeal web, vocal cord paralysis • Extrinsic compression of the lungs • Pneumothorax • Chylothorax, Hemothorax • Diaphragmatic Hernia, Space occupying lesions Neurologic causes • Drug-induced depression of respiratory drive, • Intracranial hemorrhage, • Post asphyxia cerebral dysfunction, Figure 1 • Central apnea • Respiratory neuromuscular dysfunction Citation: Samah Alasrawi. “Cardiac Emergencies in Neonates”. Acta Scientific Medical Sciences 3.6 (2019): 109-113. Cardiac Emergencies in Neonates 111 • Spinal muscular atrophy, Hematologic causes • Infant botulism, Methemoglobinemia or polycythemia cyanotic with normal Pao2 • Neonatal myasthenia gravis How to identify cardiac vs respiratory causes of cyanosis (Table 1) Parameters Respiratory pattern Saturation difference PC02 Response to 100 % between right upper limb oxygen (Rt)and lower Limb (LL) Cardiac disease Increased respiratory rate Usually no difference unless Normal or low No with minimal distress Primary pulmonary Increased respiratory No difference High Increased saturations specific lesions significant change disease rate with distress PPHN Increased respiratory rate >10% Normal or high May or may not with distress Rt >LL change Table 1 Hyperoxia Test Limitations of hyperoxia test Differentiate mainly cardiac from respiratory cyanosis (Table 2) • False positive TAPVC and HLHS may respond to oxygenation If resting saturations are less than 95%. • False negative At Fio2 = At Fio2 = PaCo2 Pulmonary disease with a massive intrapulmonary shunt may 0.21 1.00 not respond to oxygenation. Pao2 Pao2 (Saturation (Saturation Differential cyanosis %) %) Preductal saturation > Post-ductal saturation Normal >70 (>95) >300 (100) Normal • Persistent Pulmonary Hypertension of the newborn Pulmonary disease 50 (85) >150 (100) 111211 (PPHN) Neurological disease 50 (85) >150 (100) High • Interrupted aortic arch (Figure 2), critical coarctation Methemoglobinemia >70 (<85) >200 (<85) Normal of the aorta and critical aortic stenosis. Cardiac disease 40-60 (75- <ISO (<93) Normal 93) Lower limb blue, Rt upper limb pink PPHN Preductal 40- Variable Nomal/ 70 (75-95) high Post ductal Variable <40 (75) Table 2: Hyperoxia test. Interpretation of hyperoxia test • PaO2 more than 250 mmHg excludes cyanotic congenital heart disease • PaO2 is more than 150, cyanotic CHD unlikely • Pao2 less than 150, Cyanotic CHD Figure 2 Citation: Samah Alasrawi. “Cardiac Emergencies in Neonates”. Acta Scientific Medical Sciences 3.6 (2019): 109-113. Cardiac Emergencies in Neonates 112 Reverse differential cyanosis • A healthy newborn who presents after 48-72 hrs of life with Pink Lower limb, blue upper limb - culty. The post ductal saturation higher than the preductal saturation. sudden onset of pallor, grey appearance and breathing diffi • Not passing urine and not taking feeds over last 4-6 hrs We notice it in many cases like: • Metabolic acidosis • TGA with (critical coarctation of the aorta, interrupted • Start prostaglandin E1 suspecting duct dependent systemic aortic arch, critical aortic stenosis) circulation?? • TGA with PPHN. • Other measures to stabilize including ventilation and inotro- pes (unless echo rules out cardiac lesion). Classification of Cyanotic CHD Decreased PBF Cardiac causes of shock: • TOF/TGA, VSD, PS/DORV, VSD, PS/TA, VSD, PS/SV, PS/ • Duct dependent systemic circulation and Left ventricular Pulmonary atresia • Critical Aortic stenosis and coarctation, Inter- Increased PBF outflow Tract obstructions rupted aortic arch TGA, VSD/Truncus/TAPVC (admixture)/SV without PS/TA, VSD • Hypoplastic Left Heart Syndrome (HLHS) without PS • Obstructive TAPVC Chest X ray • Rhythm disturbances: Tachyarrhythmias and Brady ar- rhythmias (e.g. complete heart block) (figure 3) Prostaglandin E1 How do we start Prostaglandin? • Dose - 0.001-0.4 microgram/kg/min infusion • Higher doses 0.1 mic/kg/min should be used to reopen the closed PDA (or if there is sudden onset of severe cya- nosis or shock). • Once the duct has opened, dose can be reduced to a mini- mum Figure 3: High PBF (left) and low PBF (right). If no Response to prostaglandin Infusion (Table 3). • Rule out respiratory issues Diagnosis Management • - Transposition of Great Arteries Needs emergency megaly with Intact Ventricular Septum and Balloon Atrial Septostomy Assess pulmonary blood flow and presence of Cardio a restrictive interatrial Increased PBF features on CXR communication • Cardiomegaly Obstructed TAPVC Emergency surgery • Increased vascularity Non Cardiac Diagnosis Treatment of etiology Shock Table 3 Case 2 Congestive heart failure D3 old baby –suddenly sick Cyanotic heart disease with high pulmonary flow • Poor feeding, Not passing urine • Truncus Arteriosus
Load more

Recommended publications
  • Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality Without Pulmonary Hypertension Or Intracardiac Shunt Karam Obeid1*, Subeer K
    Original Scientific Article Journal of Structural Heart Disease, June 2018, Received: September 13, 2017 Volume 4, Issue 3:79-84 Accepted: September 27, 2017 Published online: June 2018 DOI: https://doi.org/10.12945/j.jshd.2018.040.18 Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality without Pulmonary Hypertension or Intracardiac Shunt Karam Obeid1*, Subeer K. Wadia, MD2, Gentian Lluri, MD, PhD2, Cherise Meyerson, MD3, Gregory A. Fishbein, MD3, Leigh C. Reardon, MD2, Jamil Aboulhosn, MD2 1 Department of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA 2 Department of Internal Medicine, Ahmanson/UCLA Adult Congenital Heart Disease Center, Los Angeles, California, USA 3 Department of Pathology, Ronald Reagan/UCLA Medical Center, Los Angeles, California, USA Abstract benign course without episodes of dissection or rup- Background: The natural history of pulmonary artery ture despite 6/11 patients with PAA ≥ 5 cm. PA dilation aneurysms (PAA) without pulmonary hypertension, progresses slowly over time and does not appear to intracardiac shunt or significant pulmonary valvular cause secondary events. Echocardiography correlates disease has not been well studied. This study looks to well with magnetic resonance imaging and computed describe the outcome of a cohort of adults with PAA tomography and is useful in measuring PAA over time. without significant pulmonic regurgitation and steno- Copyright © 2018 Science International Corp. sis. Imaging modalities utilized to evaluate pulmonary artery (PA) size and valvular pathology are reviewed. Key Words Methods: Patients with PAA followed at the Ahmanson/ Pulmonary artery aneurysm • Pulmonary stenosis • UCLA Adult Congenital Heart Disease Center were in- Pulmonary hypertension • Aortic aneurysm cluded in this retrospective analysis.
    [Show full text]
  • Risk of Necrotizing Enterocolitis in Very-Low-Birth-Weight Infants with Isolated Atrial and Ventricular Septal Defects
    Journal of Perinatology (2014) 34, 319–321 & 2014 Nature America, Inc. All rights reserved 0743-8346/14 www.nature.com/jp ORIGINAL ARTICLE Risk of necrotizing enterocolitis in very-low-birth-weight infants with isolated atrial and ventricular septal defects J Bain1,2, DK Benjamin Jr1,2, CP Hornik1,2, DK Benjamin3, R Clark4 and PB Smith1,2 OBJECTIVE: Necrotizing enterocolitis (NEC) is associated with a significant morbidity and mortality in premature infants. We sought to identify the frequency of NEC in very-low-birth-weight infants with isolated ventricular septal defects (VSDs) or atrial septal defects (ASDs) using a large multicenter database. STUDY DESIGN: We identified a cohort of infants with birth weight o1500 g cared for in 312 neonatal intensive care units (NICUs) managed by the Pediatrix Medical Group between 1997 and 2010. We examined the association between the presence of an ASD or a VSD with development of NEC using logistic regression to control for small-for-gestational age status, antenatal steroid use, antenatal antibiotic use, gestational age, sex, race, Apgar score at 5 min and method of delivery. RESULT: Of the 98 523 infants who met inclusion criteria, 1904 (1.9%) had an ASD, 1943 (2.0%) had a VSD and 146 (0.1%) had both. The incidence of NEC was 6.2% in infants without septal defects, 9.3% in those with an ASD, 7.8% in those with a VSD, and 10.3% in infants with both an ASD and a VSD. Compared with infants without septal defects, the adjusted odds ratios for developing NEC for each group—ASD alone, VSD alone and ASD with VSD—were 1.26 (95% confidence interval 1.07 to 1.49), 1.27 (1.07 to 1.51) and 1.79 (1.03 to 3.12), respectively.
    [Show full text]
  • Vagal Tone Regulates Cardiac Shunts During Activity and at Low Temperatures in the South American Rattlesnake, Crotalus Durissus
    J Comp Physiol B (2016) 186:1059–1066 DOI 10.1007/s00360-016-1008-y ORIGINAL PAPER Vagal tone regulates cardiac shunts during activity and at low temperatures in the South American rattlesnake, Crotalus durissus Renato Filogonio1,2 · Tobias Wang2 · Edwin W. Taylor1,3 · Augusto S. Abe1 · Cléo A. C. Leite4 Received: 2 February 2016 / Revised: 18 May 2016 / Accepted: 3 June 2016 / Published online: 13 June 2016 © Springer-Verlag Berlin Heidelberg 2016 Abstract The undivided ventricle of non-crocodilian rep- pulmonary and systemic blood flow in both groups, but tiles allows for intracardiac admixture of oxygen-poor and net cardiac shunt was reversed in the vagotomized group oxygen-rich blood returning via the atria from the sys- at lower temperatures. We conclude that vagal control of temic circuit and the lungs. The distribution of blood flow pulmonary conductance is an active mechanism regulating between the systemic and pulmonary circuits may vary, cardiac shunts in C. durissus. based on differences between systemic and pulmonary vas- cular conductances. The South American rattlesnake, Cro- Keywords Reptiles · Snakes · Cardiac shunt · Vagus talus durissus, has a single pulmonary artery, innervated nerve · Arterial pressure · Blood flow · Vascular regulation by the left vagus. Activity in this nerve controls pulmonary conductance so that left vagotomy abolishes this control. Experimental left vagotomy to abolish cardiac shunting Introduction had no effect on long-term survival and failed to identify a functional role in determining metabolic rate, growth or The undivided ventricle of the non-crocodilian reptile resistance to food deprivation. Accordingly, the present heart enables variable proportions of cardiac output to investigation sought to evaluate the extent to which car- bypass the systemic or pulmonary circulations, resulting diac shunt patterns are actively controlled during changes in either left-to-right (L–R) or right-to-left (R–L) cardiac in body temperature and activity levels.
    [Show full text]
  • Prevalence of Migraine Headaches in Patients with Congenital Heart Disease
    Prevalence of Migraine Headaches in Patients With Congenital Heart Disease Tam Truong, MD, Leo Slavin, MD, Ramin Kashani, BA, James Higgins, MD, Aarti Puri, BS, Malika Chowdhry, BS, Philip Cheung, BS, Adam Tanious, BA, John S. Child, MD, FAHA, Joseph K. Perloff, MD, and Jonathan M. Tobis, MD* The prevalence of migraine headaches (MH) is 12% in the general population and increases to 40% in patients with patent foramen ovale. This study evaluated the prevalence of MH in patients with congenital heart disease (CHD). Of 466 patients contacted from the UCLA Adult Congenital Heart Disease Center, 395 (85%) completed a questionnaire to determine the prevalence of MH. Patients were stratified by diagnosis of right-to-left, left-to-right, or no shunt. A group of 252 sex-matched patients with acquired cardiovascular disease served as controls. The prevalence of MH was 45% in adults with CHD compared to 11% in the controls (p <0.001). Of the 179 patients with MH, 143 (80%) had migraines with aura and 36 (20%) had migraines without aura versus 36% and 64% observed in the controls (p <0.001). The frequency of MH was 52% in the right-to-left shunt group, 44% in the left-to-right, and 38% in the no ,NS). In patients with a right-to-left shunt who underwent surgical repair ؍ shunt group (p 47% had complete resolution of MH, whereas 76% experienced >50% reduction in headache days per month. In conclusion, the prevalence of MH in all groups of adults with CHD is 3 to 4 times more than a sex-matched control population, with increasing prevalence of MH in patients with no shunt, left-to-right, and right-to-left shunt.
    [Show full text]
  • Grown up Congenital Heart Disease Patient Presenting for Non Cardiac Surgery: Anaesthetic Implications Mohammad Hamid Aga Khan University
    eCommons@AKU Department of Anaesthesia Medical College, Pakistan November 2010 Grown up congenital heart disease patient presenting for non cardiac surgery: anaesthetic implications Mohammad Hamid Aga Khan University Mansoor Ahmed Khan Aga Khan University Mohammad Irfan Akhtar Aga Khan University Hameedullah Aga Khan University Saleemullah Aga Khan University See next page for additional authors Follow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_anaesth Part of the Anesthesiology Commons, and the Surgery Commons Recommended Citation Hamid, M., Khan, M., Akhtar, M., Hameedullah, ., Saleemullah, ., Samad, K., Khan, F. (2010). Grown up congenital heart disease patient presenting for non cardiac surgery: anaesthetic implications. Journal of the Pakistan Medical Association, 60(11), 955-9. Available at: http://ecommons.aku.edu/pakistan_fhs_mc_anaesth/19 Authors Mohammad Hamid, Mansoor Ahmed Khan, Mohammad Irfan Akhtar, Hameedullah, Saleemullah, Khalid Samad, and Fazal Hameed Khan This article is available at eCommons@AKU: http://ecommons.aku.edu/pakistan_fhs_mc_anaesth/19 Review Article Grown up Congenital Heart Disease patient presenting for non cardiac surgery: Anaesthetic implications Mohammad Hamid, Mansoor Ahmed Khan, Mohammad Irfan Akhtar, Hameedullah, Saleemullah, Khalid Samad, Fazal Hameed Khan Department of Anaesthesia, Aga Khan University Hospital, Karachi. Abstract chances of survival6 and reduces complications associated with heart defects. Congenital heart disease patients surviving to adulthood have
    [Show full text]
  • Norman H. Silverman, M.D., D. Sc. (Med.), FACC, FAHA, FASE
    Norman H. Silverman, M.D., D. Sc. (Med.), FACC, FAHA, FASE IDENTIFYING DATA Date of Birth Sept. 29, 1942 Citizenship: U.S.A. Ethnicity: Caucasian California Medical License #: A25867 ACADEMIC HISTORY Education Date Institution and Location Degree or Title Major 1960–1967 University of the Witwatersrand M.B., B.Ch. Medicine Johannesburg, South Africa Post-doctoral and Residency Training 1967–1968 Johannesburg General Hospital Surgery Intern Medical Intern 1969 Johannesburg Children’s Hospital Senior House Officer Pediatrics 1969–1972 University of the Witwatersrand Residency Pediatrics Hospitals 1970 South African College Fellow Pediatrics of Medicine, F.C.P. (S.A.) 1972–1974 University of California, Fellow Cardiology San Francisco 1985 University of the Witwatersrand, D.Sc.Med. Medicine Johannesburg, South Africa Thesis title: Two-dimensional Echocardiography in Congenital Heart Disease Licenses and Boards 1972 ECFMG # 080-243-9 1973 Diplomate of the American Board of Pediatrics 1975 Certified, Sub-board of Pediatric Cardiology 1994 BNDD #AS6050215 1994 Radiation operator license #RHD-121449 Other Study and Research Opportunities 1977–1979 Granting Agency: National Foundation of March of Dimes Title: Echocardiographic Evaluation of Pulmonary Hypertension in Children with Congenital Heart Disease Role: PI 1978–1980 Granting Agency: California Heart Association Title: Two-dimensional Echo Volume Analysis in Congenital Heart Disease Role: PI 1987 Granting Agency: Academic Senate of the University of California, San Francisco Title: Fetal
    [Show full text]
  • Quantification of Left-To-Right Cardiac Shunt
    QUANTIFICATION OF LEFT-TO-RIGHT CARDIAC SHUNT Quantification of Left-to-Right Cardiac Shunt VJR Schelfhout, Rijnstate, Arnhem 1. Introduction In conditions with a left-to-right (L-R) shunt, blood from the systemic arterial circulation mixes with systemic venous blood. This results in oxygenated blood flowing into the right side of the heart and back to the lungs. To maintain an adequate amount of blood circulating throughout the body, cardiac output from the left side of the heart must increase to maintain normal forward flow through the aorta in the setting of abnormal flow being shunted to the right side of the heart. Output from the right side of the heart is also increased, as it must eject both the normal volume of blood returning from the body plus the volume being shunted from the left side of the heart. These effects can lead to elevated pulmonary pressure and heart failure. Nuclear medicine assessment of an L-R shunt uses a first pass analysis technique, in which an intravenous bolus of a radiopharmaceutical is tracked using rapid dynamic imaging through the heart and lungs. The study is predicated on demonstrating early return of activity to the lungs after the initial flow. 2. Methodology This guideline is based on available scientific literature on the subject, the previous guideline (Aanbevelingen Nucleaire Geneeskunde 2007), international guidelines from EANM and/or SNMMI if available and applicable to the Dutch situation. 3. Indications a. Quantification of an intracardiac shunt diagnosed by echographic Doppler b. Follow-up examination after treatment c. Assessment for further angiographic analysis 4.
    [Show full text]
  • Guidelines for Performing a Comprehensive Transesophageal
    ASE GUIDELINES AND STANDARDS Guidelines for Performing a Comprehensive Transesophageal Echocardiographic Examination in Children and All Patients with Congenital Heart Disease: Recommendations from the American Society of Echocardiography Michael D. Puchalski, (Chair), MD, FASE, George K. Lui, MD, FASE, Wanda C. Miller-Hance, MD, FASE, Michael M. Brook, MD, FASE, Luciana T. Young, MD, FASE, Aarti Bhat, MD, FASE, David A. Roberson, MD, FASE, Laura Mercer-Rosa, MD, MSCE, Owen I. Miller, BMed (Hons), FRACP, David A. Parra, MD, FASE, Thomas Burch, MD, Hollie D. Carron, AAS, RDCS, ACS, FASE, and Pierre C. Wong, MD, Salt Lake City, Utah; Stanford, San Francisco and Los Angeles, California; Houston, Texas; Seattle, Washington; Chicago, Illinois; Philadelphia, Pennsylvania; London, United Kingdom; Nashville, Tennessee; Boston, Massachusetts; and Kansas City, Missouri This document is endorsed by the following American Society of Echocardiography International Alliance Partners: Argentina Society of Cardiology, Asian-Pacific Association of Echocardiography, British Society of Echocardiography, Department of Cardiovascular Imaging of the Brazilian Society of Cardiology, Echocardiography Section of the Cuban Society of Cardiology, Indian Academy of Echocardiography, Indian Association of Cardiovascular Thoracic Anaesthesiologists, Indonesian Society of Echocardiography, Italian Association of Cardiothoracic Anesthesiologists, Japanese Society of Echocardiography, Korean Society of Echocardiography, National Society of Echocardiography of Mexico,
    [Show full text]
  • Resources When Caring for Women with Adult Congenital Heart Disease Or Other Forms of Cardiovascular Disease!!
    CARDIOVASCULAR DISEASE IN PREGNANCY AND POSTPARTUM TOOLKIT NOVEMBER 2017 Clinicians and Facilities: RESOURCES WHEN CARING FOR WOMEN WITH ADULT CONGENITAL HEART DISEASE OR OTHER FORMS OF CARDIOVASCULAR DISEASE!! Abha'Khandelwal,'MD,'MS'–'Stanford'University'School'of'Medicine' Julie'Arafeh,'MSN,'RN'–'Lucile'Packard'Children’s'Hospital,'Stanford'University' INTRODUCTION This chapter includes a summary of guidelines published by the American College of Cardiology and the American Heart Association in conjunction with other professional groups that manage adult cardiovascular disease.1,2 These guidelines are based on scientific evidence reviewed by experts in their field of practice. The purpose of the guidelines is to give clinicians the most current evidence upon which to base management of adults with specific cardiac disease. This synopsis is intended to provide information to clinicians who care for women with cardiac disease about current resources and management strategies. Key components of comprehensive, evidence- based care include resources consisting of diagnostic testing, imaging and experienced multidisciplinary staff. Recommendations for appropriate resources when providing care for adults with cardiac disease are also included.3 OB PROVIDERS: ADULT CONGENITAL HEART DISEASE (ACHD) GUIDELINES.1,2 •! Estrogen-containing oral contraceptives are not recommended for patients with Adult Congenital Heart Disease (ACHD) at risk of thromboembolism such as those with cyanosis, intra-cardiac shunt, severe pulmonary arterial hypertension (PAH) or Fontan repair. •! Patients with ACHD should consult with an ACHD expert before pregnancy to develop a plan for management of labor and the postpartum period. •! Preconception counseling is recommended for women receiving chronic anticoagulation with warfarin. •! Patients with intra-cardiac right to left shunt should have fastidious care of IV lines to avoid air embolus.
    [Show full text]
  • Balancing the Heart and the Lungs in Children with Large Cardiac Shunts Emergencies in Children with Large Cardiac Shunts
    Balancing the heart and the lungs in children with large cardiac shunts Emergencies in children with large cardiac shunts. B Rossouw, MB ChB, DTM, MMed (Paed), MSc (Sports Med), Certificate Critical Care (Paed) Consultant Paediatric Intensivist, Red Cross War Memorial Children’s Hospital, University of Cape Town Beyra Rossouw is a paediatric intensivist at Red Cross Children’s Hospital, with a special interest in cardiac critical care. Correspondence to: Beyra Rossouw ([email protected]) This article reviews the pathophysiology of low-pressure chamber. Therefore, in the is well preserved until end-stage disease, cardiorespiratory problems in children with normal heart shunt flow will be from the left usually only in late childhood or adulthood. cardiac shunt lesions. The close anatomical to the right heart. The larger the pressure When the LV myocardium contracts a large and physiological relationship of the heart difference between the chambers the more amount of the stroke volume (SV) is ejected and the lungs explains why disease in one blood will be shunted across the defect. through the shunt to the right heart and only system will affect the other. the remainder of the SV is ejected into the In newborns the pulmonary vascular aorta. The implication is that too little SV The pulmonary and cardiac circulations are resistance and the right heart pressures reaches the systemic circulation, giving rise inseparable. The cardiac system is a dual pump are high. Due to the low-pressure gradient to signs of poor perfusion and stimulation system (right and left ventricle) with the lungs between the left and right heart, there is of the neuroendocrine response.
    [Show full text]
  • Turning Crocodilian Hearts Into Bird Hearts: Growth Rates Are Similar for Alligators with and Without Right-To-Left Cardiac Shunt
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by DigitalCommons@CalPoly 2673 The Journal of Experimental Biology 213, 2673-2680 © 2010. Published by The Company of Biologists Ltd doi:10.1242/jeb.042051 Turning crocodilian hearts into bird hearts: growth rates are similar for alligators with and without right-to-left cardiac shunt John Eme1,*, June Gwalthney1, Tomasz Owerkowicz1, Jason M. Blank2 and James W. Hicks1 1University of California, Irvine, Ecology and Evolutionary Biology, 321 Steinhaus Hall, Irvine, CA 92697-2525, USA and 2California Polytechnic State University, San Luis Obispo, CA 93407-0401, USA *Author for correspondence ([email protected]) Accepted 4 May 2010 SUMMARY The functional and possible adaptive significance of non-avian reptiles’ dual aortic arch system and the ability of all non-avian reptiles to perform central vascular cardiac shunts have been of great interest to comparative physiologists. The unique cardiac anatomy of crocodilians – a four-chambered heart with the dual aortic arch system – allows for only right-to-left (R–L; pulmonary bypass) cardiac shunt and for surgical elimination of this shunt. Surgical removal of the R–L shunt, by occluding the left aorta (LAo) upstream and downstream of the foramen of Panizza, results in a crocodilian with an obligatory, avian/mammalian central circulation. In this study, R–L cardiac shunt was eliminated in age-matched, female American alligators (Alligator mississippiensis; 5–7 months of age). We tested the hypothesis that surgical elimination of R–L cardiac shunt would impair growth (a readily measured proxy for fitness) compared with sham-operated, age-matched controls, especially in animals subjected to exhaustive exercise.
    [Show full text]
  • Case 4 the Blue Baby
    Case 4 The blue baby Mrs Smith has brought her baby to A&E because she says Systems enquiry and past medical history ‘he has started turning blue’. • Does the child have any medical conditions? • Has the child had any breathing problems before? What are your immediate • Do the parents have any concerns about the child’s differential diagnoses? development? 1 Respiratory causes: • Are there any other signs of infection – poor feeding, • Congenital respiratory disorder. fever, sleepiness? • Acquired respiratory problem. • Congenital obstruction. Family history • Acquired obstruction. • Are there other family members with congenital heart 2 Congenital cyanotic heart disease: problems? • Tetralogy of Fallot. • Are the parents related? • Transposition of the great arteries. PART 2: CASES • Other rarer cyanotic defects. Obstetric history 3 Lack of respiratory drive: • Were there any problems at birth, e.g. meconium- • Seizure disorder. stained liquor? • Congenital CNS malformation. • Was the child born at term? • CNS infection. • Were there any problems with antenatal scans? • Drugs. What would you like to elicit from Baby Smith is only 3 days old. He was born at home, at the history? term, and everything had seemed fi ne until he started Demographics turning blue around the mouth a couple of hours ago. • Exactly how old is this baby? Congenital problems are Mrs Smith put this down to him crying at the time but it most likely to present in the fi rst month, cyanotic heart did not seem to improve when he calmed down. disease when the duct closes after 3–7 days. He was feeding well at the breast, but has not seemed interested today.
    [Show full text]