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7 Human Organ Systems
Cardiology**
An Integrated Approach
Adel Elmoselhi
I:. LANGE
Cardiology: An Integrated
Approach
Elmoselhi_FMxx_p00i-xvi.indd 1 08/09/17 11:55 am

Cardiology: An Integrated
Approach
ADEL ELMOSELHI, MD, PHD

Associate Professor
Basic Medical Sciences Department
College of Medicine
University of Sharjah
Sharjah, United Arab Emirates and
Adjunct Associate Professor
Physiology Department
Michigan State University
East Lansing, Michigan
New York Chicago San Francisco Athens London Madrid Mexico City
Milan New Delhi Singapore Sydney Toronto

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To my late parents, for unconditional love that
has shaped my life; to my wife, Melody, for
her love and support throughout our journey
together; and to my children, Sarah and Noah,
for bringing joy to my heart and sacrificing our
time together while I worked on this book.

Contents
Contributors ix
Preface xi
Abbreviations xii
SECTION I
| EMORPHOLOGY
MBRYOLOGY AND
OF THE HEART
9 Arrhythmias and Antiarrhythmic Drugs / 131
SANDEEP BANGA AND NAGIB T. CHALFOUN
AND VESSELS 10 Valvular Heart Diseases / 151

SAQIB AHMED AND GREGORY A. BERNATH
1 Development of the Heart and 11 Congestive Heart Failure and Management
Blood Vessels / 3 Drugs / 169
MOHAMED A. ELADL MOHSIN K. KHAN AND AMAURY SANCHEZ
2 Anatomical Structure of the Heart / 19 12 Congenital Heart Diseases / 183
AKRAM JAFFAR HARIKRISHNAN K. N. AND JOSEPH J. VETTUKATTIL
13 Systemic Arterial Hypertension and
| HFUNCTIONS
SECTION II EART AND VASCULAR Antihypertensive Drugs / 201
HUSSAIN IBRAHIM AND PRERANA MANOHAR
14 Myocardial Diseases / 215
3 Cardiovascular Circuitry and SANDEEP BANGA, PREETI BANGA, AND SUDHIR MUNGEE
Hemodynamics / 35 15 Pericardial Diseases / 227
ADEL ELMOSELHI SHAHEER ZULFIQAR AND MANIVANNAN VEERASAMY
4 Electrophysiology of the Heart / 51 16 Diseases of the Peripheral Vessels / 239
ADEL ELMOSELHI AND MOHAMED SEIF SANDEEP BANGA, PREETI BANGA, AND SUDHIR MUNGEE
5 Cardiac Output and the Pressure-Volume 17 Cardiovascular Drugs / 255
Relationship / 71 MAHA M. SABER-AYAD
KRISTEN MILLADO, MARGARET CHI, AND ADEL ELMOSELHI
6 The Cardiac Cycle / 83 Answers to Case Studies / 283
KATHRYN LARUSSO AND ADEL ELMOSELHI
7 Regulation of Arterial Blood Pressure and
Microcirculation / 93
ADEL ELMOSELHI
SECTION III
| CPROCESSES:
ARDIOVASCULAR DISEASE
DIAGNOSTIC
AND MANAGEMENT
APPROACHES
8 Ischemic Heart Disease and
Management Drugs / 111
ANTHONY PAGANINI, DEBORAH E. BLUE, AND ADEL
ELMOSELHI
vii

Contributors
Saqib Ahmed, MD, MRCP(UK) Clinical Assistant Professor of Medicine

Internal Medicine Resident Michigan State College of Human Medicine
Grand Rapids Medical Education Partners Grand Rapids, Michigan
Grand Rapids, Michigan Chapter 9
Chapter 10
Margaret Chi, MD, MPH
Preeti Banga, MD(Radiology) Internal Medicine Residency
CIRA (Central Illinois Radiology Associates) Kaiser Permanente
OSF St. Francis Medical Center Los Angeles, California
Peoria, Illinois Chapter 5
Chapters 14 and 16
Mohamed A. Eladl, MD, MSC, PhD
Sandeep Banga, MBBS, MD, DNB Assistant Professor
Cardiology Research Fellow Department of Basic Medical Sciences
Division of Electrophysiology–Cardiology College of Medicine
Frederik Meijer Heart and Vascular Institute University of Sharjah
Spectrum Health College of Human Medicine Sharjah, United Arab Emirates
Michigan State University Chapter 1
Grand Rapids, Michigan
Chapters 9, 14, 16 Adel Elmoselhi, MD, PhD
Associate Professor
Gregory A. Bernath, MD Basic Medical Sciences Department
Interventional Cardiologist College of Medicine
Spectrum Health Medical Group University of Sharjah
Cardiovascular Services Sharjah, United Arab Emirates and
Grand Rapids, Michigan Adjunct Associate Professor
Chapter 10 Physiology Department
Deborah E. Blue, MD, MT(ASCP)
Chapters 3–8
Technical Director, Microbiology
Technical Director, Blood Bank
Spectrum Health Regional Laboratory/Michigan
Harikrishnan K. N., MBBS, MD
Pathology Specialists, PC Cardiology Fellow
Grand Rapids, Michigan Congenital Heart Center
Chapter 8 Helen DeVos Children’s Hospital of Spectrum Health
Chapter 12
Nagib T. Chalfoun, MD
Electrophysiologist
Division of Electrophysiology–Cardiology
Hussain Ibrahim, MD
Frederik Meijer Heart and Vascular Institute Cardiology Fellow
Spectrum Health and University of Texas Medical Branch, Division
of Cardiology
Galveston, Texas
Chapter 13
ix

x Contributors
Akram Jaffar, MD, PhD Maha M. Saber-Ayad, MD(Pharm),

Senior Instructor MRCP(UK), FRCP(Edin.)
Department of Medical Neuroscience Associate Professor of Pharmacology
Dalhousie University College of Medicine
Halifax, NS, Canada University of Sharjah
Chapter 2 Sharjah, United Arab Emirates
Chapter 17
Mohsin K. Khan, MD
Clinical Assistant Professor of Medicine Amaury Sanchez, MD
Internal Medicine Hospitalist Internal Medicine Residency
Spectrum Health Medical Group Grand Rapids Medical Education Partners
Michigan State University Michigan State University
Grand Rapids, Michigan Grand Rapids, Michigan
Chapter 11 Chapter 11
Kathryn LaRusso, MD, MPH Mohamed Seif, MD, FRCP(Edin. UK), CBCCT
General Surgery Resident MSc Leadership in Health Profession Education
UT Health Science Center San Antonio RCSI Head
San Antonio, Texas Internal Medicine and Family Medicine Departments and
Chapter 6 Senior Consultant Cardiologist
University Hospital of Sharjah
Prerana Manohar, MD, FRCPC Sharjah, United Arab Emirates
Medical Director Chapter 4
The Heart and Wellness Institute and
Associate Professor Manivannan Veerasamy, MD
College of Human Medicine SHMG Hospitalist
Michigan State University Core Faculty, Internal Medicine Residency
Grand Rapids, Michigan Grand Rapids Medical Education Partners
Chapter 13 Michigan State University
Kristen Millado, MD Chapter 15
Internal Medicine Residency
George Washington University Joseph J. Vettukattil, MBBS, MD, DNB, CCST,
Washington, DC FRCPCH, FRSM, FRCP
Chapter 5 Pediatric Interventional Cardiologist
Congenital Heart Center
Sudhir Mungee, MD Helen DeVos Children’s Hospital of Spectrum Health
Director, Cardiology Fellowship Program Grand Rapids, Michigan
Division of Cardiology Chapter 12
University of Illinois College of Medicine at Peoria
Peoria, Illinois Shaheer Zulfiqar, MBBS, MD
Chapters 14 and 16 Hospitalist, Internal Medicine
Parkview Medical Center
Anthony Paganini, PhD Pueblo, Colorado
Associate Professor Chapter 15
Director of Professional Educational Affairs
Departments of Physiology and Radiology
College of Human Medicine
Chapter 8

Preface
The aim of this work is to integrate the basic and clinical keys, annotated with brief explanations. A short list of Sug-
science topics of the cardiovascular system in a deliberately gested Readings is also included at the end of each chapter.
clinically oriented review book. Approximately half of the As the scope of the material is enormous, the book focuses
medical schools in the United States have already imple- on the most common medical problems in the cardiovascular
mented an integrated curriculum in their pre-clinical programs, system and the high-yield areas directed toward medical pro-
a trend which is growing both nationally and internationally. grams and residency training programs. This review book is
This trend is due in part to the proven benefits of the evidence- intended to be used as a supplement to university-prepared
based practice of medicine as well as the increasing number course materials and can serve as an aggregate study guide,
of integrative clinical vignette questions in the medical and especially for the clinically oriented healthcare professional
healthcare professional license examinations. Thus, this book programs.
was created to provide a comprehensive review that includes A particular strength of this book is that it brings together
almost all pre-clinical and clinical subjects of the cardiovas- the collective efforts of more than 20 faculty and clinicians
cular system in a compact volume, replacing the individual from diverse academic specialties. It has been an extraordi-
subject-specific books, which are now of limited relevance nary experience collaborating on this project with such an
to current curriculum implementation and clinical practice, impressive ensemble of colleagues who represent an interna-
and providing an instructional resource that is more closely tional range of institutions, from the College of Human Medi-
aligned with an integrative approach to the teaching and prac- cine, Michigan State University and other teaching hospitals
tice of medicine. in Grand Rapids, Michigan; Dalhousie University, Halifax,
The book consists of three sections and 17 chapters. The NS, Canada; and the College of Medicine, University of Shar-
first section has 2 chapters that cover the embryological devel- jah and University Hospital in the United Arab Emirates.
opment and anatomical structure of the cardiovascular sys- In an interesting coincidence, on a personal note, I am
tem; the second section consists of 5 chapters that explore the writing this preface on the campus of the Harvard T.H. Chan
basic physiological and biochemical functions of the heart and School of Public Health, where I am participating in a Global
bloods vessels. The last section, which is the most substantial, Health Delivery Program and reflecting on the interconnec-
has 10 chapters that address the most common cardiovascu- tivity and impact of the global setting on determining best
lar diseases in terms of their causes, risk factors, pathophysi- evidence-based practices and veritas (truth) with regard to
ological processes, clinical manifestations, diagnoses, and knowledge and the delivery of healthcare. Certainly, this
treatment. The final chapter focuses on the most commonly review volume is a testament to the strength of inclusion of
used cardiovascular pharmacological drugs, their mechanisms a diverse range of experts in a field of cardiovascular health
of actions, clinical uses, and adverse effects. Embedded in professionals. May this volume serve to support the educa-
almost all chapters are Clinical Correlation boxes which high- tion and training of medical students, residents, and all other
light valuable practical applications, and each chapter con- healthcare professional trainees.
cludes with clinical Case Study questions resembling those
found on licensing examinations, along with their answer Adel Elmoselhi, MD, PhD
xi

Abbreviations
ABI ankle-brachial index

ACC American College of Cardiology
ACE angiotensin-converting enzyme (ACE) inhibitors
ACh acetylcholine
ACTH adrenocorticotropic hormone
ADH antidiuretic hormone
AFib or AF atrial fibrillation
AFl atrial flutter
AHA American Heart Association
AICD automated implantable cardioverter defibrillator
AL amyloidosis
ANA antinuclear antibody (ANA) test
ANP atrial natriuretic peptide
APD action potential duration
APTT Activated Partial Thromboplastin Time
AR aortic regurgitation
ARBs angiotensin II receptor blockers
ARP absolute refractory period
ART antidromic reentrant tachycardia
ARVC arrhythmogenic right ventricular cardiomyopathy
ARVD arrhythmogenic right ventricular dysplasia
AS aortic stenosis
ASDs atrial septal defects
AV atrioventricular
aVF augmented voltage left foot
aVL augmented voltage left arm
AVP arginine vasopressin
aVR augmented voltage right arm
AVR aortic valve replacement
AVNRTs atrioventricular nodal reentrant tachycardias
AVRTs atrioventricular reentrant tachycardias
BAT baroreflex activation therapy

BNP B-type natriuretic peptide
bpm beats per minute
BSA body surface area
BVH biventricular hypertrophy
CABG coronary artery bypass graft (CABG) surgery

CADs cardiovascular diseases
cAMP cyclic adenosine monophosphate
xii

Abbreviations xiii
CARDIA Coronary Artery Risk Development in Young Adults

CCBs calcium channel blockers
CCF congestive cardiac failure
cGMP cyclic guanosine monophosphate
CHB complete heart block
CHD congenital heart disease
CHF congestive heart failure
CICR calcium-induced calcium release
CKD chronic kidney disease
CMR cardiovascular magnetic resonance (CMR) imaging
CO cardiac output
CoA coarctation of the aorta
CPA conventional peripheral angiography
CPVT catecholaminergic polymorphic ventricular tachycardia
CTA computed tomography angiography
CVA cerebrovascular accident
CVDs chronic venous disorders
CVI cavotricuspid isthmus
Cx circumflex (branch)
DADs delayed afterdepolarizations

DCM dilated cardiomyopathy
DESs drug-eluting stents
DHPs dihydropyridines
DORV double outlet right ventricle
DP diastolic pressure
DVT deep vein thrombosis
ECG electrocardiography/electrocardiogram
EDP end-diastolic pressure
EDV end-diastolic volume
EF ejection fraction
ERP effective refractory period
ESC European Society of Cardiology
ESV end-systolic volume
ERP effective refractory period
GFR glomerular filtration rate

GSV great saphenous vein
HCM hypertrophic cardiomyopathy

HLHS hypoplastic left heart syndrome
HR heart rate
5HT 5-hydroxytryptamine
HTN hypertension
ICD implantable cardioverter defibrillator

IHD ischemic heart disease
ICS intercostal space
IHD ischemic heart disease
INR international normalized ratio

xiv Abbreviations
IVC inferior vena cava

IVS interventricular septum
JET junctional ectopic tachycardia

JVD jugular vein distention
JVP jugular venous pressure
LA left atrium
LAA left atrial appendage
LAD left anterior descending (branch)
LAP left atrial pressure
LBBB left bundle branch block
LDL low-density lipoprotein
LMWHs low molecular weight heparins
LTRI lower respiratory tract infection
LV left ventricle
LVAD left ventricular assist device
LVEDP left ventricular end-diastolic pressure
LVES left ventricular end-systolic
LVH left ventricular hypertrophy
LVOT left ventricular outflow tract
MAHA microangiopathic hemolytic anemia

MAP mean arterial pressure
MAT multifocal atrial tachycardia
MI myocardial infarction
MIP maximum intensity projection
MMVD mixed mitral valve disease
MR mitral regurgitation
MRA magnetic resonance angiogram
MV mitral valve
MVP mitral valve prolapse
MYBPC3C myosin-binding protein C
MYH7 myosin heavy chain 7
NCX sodium-calcium exchanger

NDF net driving force
NDHPs non-dihydropyridines
NPY neuropeptide Y
NSAIDs nonsteroidal anti-inflammatory drugs
NSTEMI non-ST elevation myocardial infarction
ORT orthodromic reentrant tachycardia
PACs premature atrial contractions

PAH pulmonary arterial hypertension
PCI percutaneous coronary intervention
PDA patent ductus arteriosus
PDE-3 phosphodiesterase isozyme 3
PE pulmonary thromboembolism
PET positron emission tomography
PETN pentaerythritol tetranitrate

Abbreviations xv
PFO patent foramen ovale

PND paroxysmal nocturnal dyspnea
PRU peripheral resistance unit
PS pulmonary stenosis
PSV peak systolic velocity
PSVT paroxysmal supraventricular tachycardia
PTA percutaneous transluminal angioplasty
PTRA percutaneous transluminal renal angioplasty
PVCs premature ventricular contractions
PVE prosthetic valve endocarditis
PVR pulmonary vascular resistance
RA right atrium
RAAS renin-angiotensin-aldosterone system
RCA right coronary artery
RCM restrictive cardiomyopathy
RFA radiofrequency ablation
RHC right heart catheterization
RPLS reversible posterior leukoencephalopathy syndrome
RRP relative refractory period
RV right ventricle
RVH right ventricular hypertrophy
RVOT right ventricular outflow tract
SA sinoatrial
SACT sinoatrial conduction time
SAM systolic anterior motion
SBP systolic blood pressure
SCD sudden cardiac death
SERCA sarcoplasmic reticulum Ca2+-ATPase
SJS Stevens-Johnson syndrome
SLE systemic lupus erythematosus
SNP supranormal period
SNS sympathetic nervous system
SOB shortness of breath
SP systolic pressure
SR sarcoplasmic reticulum
STEMI ST segment elevation myocardial infarction
SV stroke volume
SVC superior vena cava
SVR systemic vascular resistance
SVTs supraventricular tachycardias
TA tricuspid atresia
TAPVC total anomalous pulmonary venous connection
TAPVR/D total anomalous pulmonary venous return/drainage
TAVR transcatheter aortic valve replacement
TCPC total cavopulmonary connection
TEE transesophageal echocardiogram
TEN toxic epidermal necrolysis
TIMI Thrombolysis in Myocardial Infarction
TnC troponin C

xvi Abbreviations
TnI troponin I
TnT troponin T
TNNT2 cardiac troponin T
ToF tetralogy of Fallot
TPR total peripheral resistance
TR tricuspid regurgitation
TTE transthoracic echocardiograms
TV tricuspid valve
TXA2 thromboxane
UFH unfractionated heparin
V1A vasopressin type 1A (V1A) receptor

V2 vasopressin type 2 (V2) receptor
VFib or VF ventricular fibrillation
VSDs ventricular septal defects
VT ventricular tachycardia
VTE venous thromboembolism
VVs varicose veins
vWF von Willebrand factor
WPW Wolff-Parkinson-White (WPW) syndrome

SECTION
I
EMBRYOLOGY AND
MORPHOLOGY OF THE HEART
AND VESSELS
Elmoselhi_CH01_p001-018.indd 1 08/09/17 12:20 pm

Chapter 1
Development of Learning Objectives
the Heart and Blood By the end of this chapter the student will be able to:
• Discuss the development of the heart tube.
Vessels • Describe heart tube looping, chamber formation,

and the series of septation that occur for the
MOHAMED A. ELADL development of atria, ventricles, and great vessels.
• Recognize the relationship of heart tubes to the
pericardial cavity.
Introduction • Indicate the development of valves and conducting
Unlike most other organ systems, the function of the car- system of the heart.
diovascular system is critical for embryonic survival. Thus,
• Distinguish the development of the aortic arches and
development of the heart and vascular system begins very
list its derivatives.
early, originating from both the embryonic and extra embry-
onic mesoderm of the embryo. The heart is the first organ to • Indicate the major changes that happened in
form during embryogenesis. development of the sinus venosus.
Before the age of 3 weeks, the nutrient materials reach • List and provide a brief anatomical description of the
the fetus by simple diffusion. After that age, the embryo is congenital anomalies of the heart and major blood
no longer able to satisfy its nutritional requirements by diffu- vessels.
sion alone, thus the blood vessels begin to develop and nour-
• Diagram the fetal circulation and recall the changes
ish the embryo. Blood cells and blood vessels arise from the that occur after birth.
mesoderm. Blood vessels form in two ways: vasculogenesis,
whereby vessels arise from blood islands, and angiogenesis,
which entails sprouting from existing vessels (Fig. 1.1).
and a caudal inflow part, which represents the primitive atrium
(Fig. 1.3B). Two additional constrictions appear in the cra-
Development of the Heart Tube nial outflow part differentiating it into 3 chambers from the
The first sign of the development of the heart is the formation caudal to cranial ends; the primitive ventricle, bulbus cordis,
of cardiogenic cords. These are canalized to form 2 endocar- and truncus arteriosus, which are distally continuous with the
dial tubes (day 19). These tubes develop from condensation aortic sac (Fig. 1.3C). The caudal inflow part dilates and forms
of splanchnopleuric mesoderm in the cardiogenic region of the sinus venosus and the heart tube then divides into 5 cham-
the trilaminar germ disc. The cardiogenic region is cranial to bers: sinus venosus, primitive atrium, primitive ventricle, bul-
the neural plate (Fig. 1.2A). bus cordis, and truncus arteriosus (Fig. 1.3D).
On day 20, lateral and cephalic folding of the trilaminar With further growth and elongation, the linear heart tube
germ disc over the course of several days brings the endo- undergoes an asymmetric looping process (days 23-28). The
cardial tubes together and tucks them ventrally in the tho- caudal inflow region of the heart tube adopts a more cranial
racic region at the base of the yolk sac. This process also final position due to bending of the heart tube as a U-shaped
brings the septum transversum into its adult position inferior loop (Fig. 1.3E); and then the poles of the heart converge and
to the heart. the heart now appears as an S-shape; with the first bend in
On day 21, medial migration and midline fusion of the the S between the bulbus cordis and ventricle, and the sec-
endocardial tubes form the primary heart tube through ond bend between the atrium and sinus venosus. The bulbus
which blood eventually flows in a cranial direction (Fig. 1.2B cordis and truncus arteriosus move ventrally to the atrium to
and Fig. 1.3A). The mesenchyme surrounding the tube con- form the outflow tract and the atrium now lies superior to the
denses to form the myoepicardial mantle (the future myo- ventricle. Blood begins to circulate through the embryo by
cardium). Gelatinous connective tissue called cardiac jelly day 24. The looping process brings the primitive areas of the
separates this mantle from the endothelial heart tube (the heart into the proper spatial relationship for development of
future endocardium). the adult heart (Fig. 1.4).
A constriction appears in the heart tube and divides it into While the heart is growing, it pushes into the dorsal wall
the cranial outflow part representing the primitive ventricle, of the empty pericardial sac during development and becomes

4 Section I Embryology and Morphology of the Heart and Vessels
Angioblast Vasculogenesis Angiogenesis 2. Situs inversus: As with dextrocardia, this condition

is caused by transposition of the abdominal viscera
Mother (Fig. 1.5B).
vessel 3. Ectopia cordis: Due to failure of the lateral folds to fuse
and failure of the thoracic wall to form, the heart is partly
or completely exposed on the surface of the thorax. This
condition is marked by widely separated halves of the
sternum with an open pericardial sac.
Sprouting Bridging Intussusception Development of the

Atrioventricular Canal
Dorsal and ventral atrioventricular endocardial cushions
appear at the dorsal and ventral wall of the atrioventricular
canal (Fig. 1.6A). The 2 endocardial cushions grow toward
Daughter vessels
each other and fuse together to form the septum intermedium.
This septum divides the atrioventricular canal into right and
FIGURE 1.1 Schematic illustration showing angioblasts in the embryo,
which assemble in a primitive network (vasculogenesis) that expands and left halves (Fig. 1.6B, C).
remodels (angiogenesis). Smooth muscle cells cover the endothelial cells
during vascular myogenesis and stabilize vessels during arteriogenesis.
Fate of the Atrioventricular Canal
surrounded to such a degree that 2 layers of the dorsal tissue 1. The upper part of the atrioventricular canals is
become opposed. This is referred to as the dorsal mesocar- absorbed into the corresponding atria (right and left).
dium. The dorsal mesocardium suspends the heart for a time 2. The lower part of the atrioventricular canals is
but soon breaks down during looping, leaving the heart sus- absorbed into the corresponding ventricles (right and left).
pended at its cranial and caudal surfaces but not at the back. 3. The septum intermedium shares in the formation of
The gap, which persists where the dorsal mesocardium once the interatrial septum and the membranous part of the
was, is called the transverse sinus (a point of communication interventricular septum.
across the pericardial coelom) (Fig. 1.3E).
After looping and chamber formation, a series of septa-
tion events divide the left and right sides of the heart, separate Anomalies of the Atrioventricular Canal
the atria from the ventricles, and form the aorta and pulmo-
nary artery from the truncus arteriosus. Cardiac valves form 1. Persistent atrioventricular canal: A common channel
between the atria and the ventricles and between the ventricles between the 2 atria and 2 ventricles that is formed when
and the outflow vessels. the septum intermedium fails to form.
2. Unequal division of the atrioventricular canal: This
leads to mitral stenosis and/or tricuspid regurgitation,
Anomalies in the Position of the Heart when deviation of the septum intermedium to the left
1. Dextrocardia with situs solitus: The heart tube bends side or tricuspid stenosis and/or mitral regurgitation,
to the opposite direction and therefore is displaced to the when deviation of the septum intermedium occurs to the
right and its chambers and its vessels are reversed as in a right side.
mirror image (Fig.1.5A).
Early heart-forming Neural folds Pericardial Foregut Forming heart

regions coelom
A B
FIGURE 1.2 Schematic depiction of a transverse section through an early embryo. A. Depicts the bilateral region where early heart tubes form.
B. Shows the bilateral heart tubes subsequently migrating to the midline and fusing to form the linear heart tube. (Reproduced, with permission, from
Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011.)

Chapter 1 Development of the Heart and Blood Vessels 5
TA
TA
BC
BC
PV TA SV
PV PV
PA
PA
PA BC PV
SV
A B C D E
FIGURE 1.3 Schematic depiction of changes in an early heart tube in a human. A. The 2 heart tubes fuse to form a single heart tube. B. A constriction
appears dividing the heart tube into the primitive ventricle (PV) cranially and the primitive atrium (PA) caudally. C. Two additional constrictions appear in
the PV forming the bulbus cordis (BC) and truncus arteriosus (TA). D. The area where the veins enter the heart tube enlarges and forms the sinus venosus
(SV). E. Bending of the heart tube as a U-shaped loop, breaking the dorsal mesocardium and forming the transverse sinus (arrow).
3. Mitral atresia: Complete fusion of the cusps of the separated from the septum intermedium by an opening
mitral orifice. called the ostium primum (Fig. 1.7A).
4. Tricuspid atresia: Complete fusion of the cusps of the •• Before complete closure of the ostium primum, the upper
tricuspid. part of the septum primum will break down to form the
ostium secundum (between the upper margin of the septum
primum and the roof of the primitive atrium), allowing free
Development of the Interatrial passage of blood flow from the right to left side (Fig. 1.7B).
Septum •• A crescent fold from the cephalic wall of the primi-
The primitive atrium is divided into a right and left atrium due tive atrium (septum secundum) grows downward to
to the following changes: the right side of the septum primum toward the septum
intermedium, but does not with it. Its free concave edge
•• A sickle-shaped septum (septum primum) grows from begins to overlap the foramen secundum and the new
the roof of the primitive atrium toward the septum passage formed between the right and left atria is called
intermedium. The lower rim of the septum primum is the foramen ovale. This foramen is not a simple orifice,
but an oblique passage for the blood to pass from the
right atrium to the left atrium, between the lower edge of
the septum secundum and the septum intermedium, then,
Arterial pole
in-between the septum primum and foramen secundum
(Fig. 1.7C).
•• Before birth, the pressure in the right atrium is higher
OFT because the lungs are not functioning and more oxygen-
ated blood reaches the right atrium from the placenta
via the inferior vena cava. This allows the blood to
pass from the right atrium to the left atrium through the
foramen ovale. After birth, the pressure inside the left
AVC atrium increases and exceeds that of the right atrium
because of stoppage of the placental circulation and
exposure to cold, which stimulates the respiration and
Venous pole lung functions, therefore more blood reaches the left
atrium (from the lungs).
FIGURE 1.4 The heart appears as an S-shape, with the first bend in the •• The difference in the pressure between the 2 atria presses
S between the bulbus cordis and ventricle, and the second bend between the septum primum against the septum secundum and the
the atrium and sinus venosus (blue). The atrioventricular canal (AVC) 2 septa fuse together, and as a result, the lower edge
is between the primitive common atrium and the primitive ventricle;
and the outflow tract (OFT) is continuous cranially. (Reproduced, with
of the septum secundum will form the a nnulus ovalis
permission, from Pahlm O, Wagner GS, eds. Multimodal Cardiovascular and the septum primum will form the fossa ovalis (the
Imaging: Principles and Clinical Applications. New York: McGraw-Hill; 2011.) depression below the annulus ovalis) (Fig. 1.7D).

A B
FIGURE 1.5 A. Posteroanterior view of a patient with dextrocardia and situs solitus. Note that the aortic arch and the stomach air bubble are both on
the left (situs solitus), and the apex of the ventricles is pointing to the right inferiorly. B. Situs inversus chest x-ray. A 26-year-old female complains of chest
pain. Her evaluation was negative except for situs inversus. A chest x-ray (CXR) shows a right-sided cardiac apex, aortic knob, gastric bubble. The angles of
the mainstem bronchi suggest situs inversus. (Part A: Reproduced, with permission, from Fuster V, Harrington RA, Narula J, Eapen ZJ, eds. Hurst’s The Heart.
14th ed. New York: McGraw-Hill; 2017. Part B: Reproduced, with permission, from Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of Emergency
Medicine. 3rd ed. New York: McGraw-Hill; 2010. Photo contributor: Katie Johnson, MD.)
Anomalies of the Interatrial Septum develop or by excessive destruction of the cephalic part
of the septum primum.
1. Trilocular heart: This condition is caused by the failure 4. Premature closure of foramen ovale: This leads to
of the interatrial septum (septum primum and septum intrauterine death of the fetus since the blood does not
secundum) to develop and thus the heart consists of only reach the aorta to be distributed to different tissues of
3 chambers (2 ventricles and 1 atrium). the fetus.
2. Persistent ostium primum (Fig. 1.8A): This is the most 5. Patent foramen ovale (Fig. 1.8C): Failure of fusion
common form of atrial septal defects (ASDs), due to the between the septum primum and septum secundum
failure of the septum primum to fuse with the septum causes this condition. There is an orifice between the
intermedium, which prevents the ostium primum from right and left atria that allows a passage of blood from the
closing. right to the left when the pressure inside the right atrium
3. Persistent ostium secundum (Fig. 1.8B): This condition is increased, as it would be during crying and exercise.
is caused by the failure of the septum secundum to Therefore, it is potentially cyanotic heart disease.
6. Septal aneurysm (Fig. 1.8D): This is caused by a
redundancy in the septum primum, and may move back
and forth across the foramen ovale.
PA PA
Development of the
SI
SI Interventricular Septum
Anatomically, the interventricular septum consists of a large
PV PV PV muscular part and a small membranous part. The muscular
part develops as a crescent ridge and arises from the endocar-
dium of the floor of the primitive ventricle. The ridge increases
A B C in depth due to the force of the bloodstream on both of its
sides. An interventricular foramen persists at the upper edge
FIGURE 1.6 Schematic depiction of the process of development of the of the muscular part. The membranous part develops from
atrioventricular canal. A. Formation of the ventral and dorsal endocardial
cushions (arrows). B. The septum intermedium (SI) in the atrioventricular
the septum intermedium as well as the right and left bulbar
canal between the primitive atrium (PA) and the primitive ventricle (PV). ridges. This membranous part will close the interventricular
C. The atrioventricular canal is divided into two halves. foramen (Figs. 1.9A, B).

SP SP
FO
PV PV PV
A B C D
FIGURE 1.7 Schematic depiction of the process of development of the interatrial septum. A. The septum primum (blue) is separated from the septum
intermedium by the ostium primum (arrow). B. At the superior edge of the septum primum, clefts begin to form that provide a second opening, the
ostium secundum (arrow). The ostium secundum provides an alternate right-to-left shunt, and the ostium primum closes. C. The septum secundum
(green), begins to grow down from the roof of the right atrium, just lateral to the septum primum. The septum secundum permits the right-to-left shunt
of blood through a space called the foramen ovale (arrow). D. After birth, when pulmonary circulation increases blood pressure in the left atrium, the
membranous septum primum is pressed against the septum secundum. The 2 septa eventually fuse and block the right-to-left shunt of blood, and the
lower edge of the septum secundum will form the annulus ovalis (green), and the septum primum will form the fossa ovalis (FO) (the depression below
the annulus ovalis).
Ostium Septum Ostium Small cavities appear in the myocardium; they unite
primum primum secundum
together to form larger cavities, separated from each other by
ridges variable in size that project into the interior of the ven-
tricle. These ridges will differentiate into trabecullae carnae,
papillary muscles, and chorda tendineae.
RA LA RA LA
Endocardial
A cusion B
Septum
secundum Septal
Foramen aneurysm
ovale
RA LA RA LA
C D
FIGURE 1.8 The formation of the atrial septum and its abnormalities. MS
A. Migration of the septum primum with the ostium primum in the lead. MS
If the septum primum does not fuse with the endocardial cushions, a
primum atrial septal defect (ASD) results. B. Once the septum primum A B
fuses with the endocardial cushions, a hole or fenestration appears in the
middle of the septum, the ostium secundum. C. The septum secundum FIGURE 1.9 Schematic depiction of the process of development of the
then migrates along the right atrial (RA) side of the septum primum, interventricular septum. A. Muscular interventricular septum (MS) begins
normally covering the ostium secundum. If the septum secundum does to grow superiorly from the ventricular floor between the primitive right
not cover the hole, a secundum ASD results. The septum secundum and left ventricles. This septum stops short of the atrioventricular canal,
generally completes its migration to the endocardial cushion, leaving leaving a space called the interventricular foramen (white arrow), which
a large ovale hole, the foramen ovale persisting. If the septi do not permits blood from both ventricles to exit via the bulbus cordis. B. The
fuse after birth, a pathway referred to as a patent foramen ovale (PFO) membranous part (white arrow) develops from septum intermedium
persists between the RA and left atrium (LA). D. In some patients, there as well as the right and left bulbar ridges. The yellow arrows show the
is redundancy in the septum primum, and it may move back and forth appearance of the papillary muscles as a result of the multiple small
across the foramen ovale. This is referred to as an atrial septal aneurysm. cavities that develop within the myocardium.

subarterial), perimembranous (the inlet portion of

the membranous septum), and malalignment (found
in tetralogy of Fallot [TOF] with an overriding aorta)
defects.
b. Muscular VSDs, often multiple, may be located in the
inlet or outlet regions or within the trabecular portion
Supracristal of the septum.
Membranous
Development of Truncus Arteriosus
AV canal type and Bulbus Cordis (Outflow Tract)
Pairs of opposing ridges appear in the region of the truncus
Muscular
arteriosus (truncal swelling) and conus cordis region (bulbar
swelling) (Fig. 1.11). Neural crest cells also contribute to form
these swellings. Two truncal swellings grow in opposite direc-
tions (the right superior one grows distally and to the left,
and the left inferior one grows distally and to the right side),
creating a spiral septum dividing the truncus arteriosus into
aortic and pulmonary channels. Two bulbar swellings (right
FIGURE 1.10 Anatomic location of ventricular septal defects (VSDs). dorsal and left ventral) meet each other and form the bulbar
septum, which divide the bulbus cordis into an outflow tract
Anomalies of the Interventricular for the right ventricle (infundibulum) and the left ventricle
(vestibule). They are also attached to the spiral septum and
Septum the membranous part of the IV septum.
1. Complete absence of the interventricular septum: This
condition is caused by the failure of both the muscular
and membranous part of the interventricular septum to
Anomalies of Truncus Arteriosus
develop. The heart consists of only 3 chambers; 3 atria and Bulbus Cordis
and 1 ventricle. 1. Transposition of the Great Arteries
2. Ventricular septal defect (VSD) (Fig. 1.10): This is Transposition of the great arteries (TGA) occurs when the
classified anatomically according to the defects of both aortopulmonary septum fails to form a spiral course during
the membranous and muscular portions of the ventricular partitioning of truncus arteriosus. The aorta arises from the
septum. right ventricle and the pulmonary artery originates from the
a. Membranous VSDs can be subdivided into left ventricle (Fig. 1.12). The TGA is divided into dextro-
supracristal (also known as doubly committed looped (d-TGA) and levo-looped (l-TGA). The looping
Ao PT
APS
AoS APS
SLV
TS
CTS
CC
CS
Co Myo
A B C
FIGURE 1.11 Schematic diagram of some of the developmental events involved in the septation of the outflow tract. A. The stage at which the
endocardial cushion tissues in the outflow tract (conal cushions and truncal swellings) and the aorticopulmonary septum have not yet fused. B. The
truncal swellings contribute to the formation of the semilunar valves of the aorta (Ao) and pulmonary trunk (PT), whereas the fusing conal cushions
(CCs) form the mesenchymal outlet septum. At this stage, the conal myocardium starts to myocardialize the outlet septum. C. One of the final stages.
The aorticopulmonary septum (APS) has now completely separated the Ao and PT above the level of the semilunar valves, whereas below the valves,
the outlet septum divides the outlet segment of the heart in a subaortic and subpulmonary outlet. AoS, aortic sac; CS, conal septum; CTS, conotruncal
segment; Myo, myocardialization; SLV, semilunar valve; TS, truncal swelling. (Reproduced, with permission, from Fuster V, Walsh RA, Harrington RA, eds.
Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011.)

refers to the right or left looping of the primitive heart tube

Posterior during fetal development, which determines whether the
Anterior atria and ventricles are concordant (the right atrium attaches
to the right ventricle and the left atrium attaches to the left
Aortic Pulmonary ventricle), or discordant. L-transposition of the great arter-
valve valve
ies is associated with atrioventricular discordance (the
right atrium attaches to the left ventricle and the left atrium
Aorta attaches to the right ventricle), and is also termed congeni-
Pulmonary
artery
tally corrected TGA. L-transposition of the great arteries
is a rare variant of TGA. The d-TGA can be subdivided
into d-TGA with an intact ventricular septum (55%-60%)
and d-TGA with VSD (40%-45%), one-third of which are
Left
hemodynamically insignificant. Pulmonic stenosis, causing
ventricle significant left ventricular outflow tract obstruction, rarely
occurs with an IVS and in approximately 10% of d-TGA/
VSDs.
2. Aortopulmonary Window
Aortopulmonary window (APW) is a rare congenital lesion,
Ventricular occurring in about 0.2% of patients, characterized by incom-
septum plete development of the aortopulmonary septum. In the
majority of cases, APW occurs as a single defect of minimal
length, which begins a few millimeters above the semilunar
Patent
ductus valves on the left lateral wall of the aorta (Fig. 1.13). Coronary
Septal artery anomalies, such as an aberrant origin of the right or
defect Pulmonary left coronary artery from the main primitive atrium (PA), are
artery occasionally present.
Left
ventricle
3. Persistent Truncus Arteriosus
This is a rare anomaly, comprising between 1% and 4% of
Aorta Right
ventricle
all cases of congenital heart diseases. It is the result of failed
development of the aortopulmonary septum and subpulmo-
FIGURE 1.12 Typical transposition of the great arteries. The aorta nary infundibulum (conal septum). Normal septation leads
arises from the morphologic right ventricle and is anterior to and to the development of both pulmonary and systemic outflow
slightly to the right of the pulmonary artery, which originates from the tracts, division of the semilunar valves, and formation of the
morphologic left ventricle. Inset at the bottom illustrates the independent
aorta and pulmonary arteries. Failure of septation results in a
systemic and pulmonary circulations, which may be connected by a
patent ductus arteriosus or atrial septal defect. Inset at the top illustrates VSD (absence of the infundibular septum), a single semilunar
a common relationship of the 2 great arteries in typical transposition. valve, and a single arterial trunk. It is characterized by a single
(Reproduced, with permission, from Doherty GM, ed. CURRENT: Diagnosis great artery that arises from the heart, overrides the ventricular
& Treatment: Surgery. 14th ed. New York: McGraw-Hill; 2015.)
A B C
FIGURE 1.13 A-C. Classification of aortopulmonary window.

Collett and Edwards Van Praagh •• Type III: The right and left pulmonary arteries arise from
more widely separated orifices on the posterior truncal wall.
•• Type IV: The branch pulmonary arteries are absent. Pulmo-
nary blood flow is derived from aortopulmonary collaterals.
I A1 4. Tetralogy of Fallot
Tetralogy of Fallot (TOF) is caused by an unequal division
of truncus arteriosus due to anterior displacement of the spi-
ral septum (conal septum) toward the pulmonary trunk. This
results in pulmonary stenosis with right ventricular hyper-
trophy, which results in widening of the aorta and originates
from both the right and left ventricles and patent interventricu-
II lar foramen (Fig. 1.15).
A2
Development of the Conductive
System of the Heart
The specialized conduction system of the human heart is most
III likely derived from specialized cardiomyocytes of the primary
heart field along the 4 intersegmental zones of the primitive
heart tube: the sinoatrial (SA) ring between the sinus venosus
and primitive atrium (which gives rise to the sinus node and
part of the atrioventricular [AV] node), the AV ring between
the primitive atrium and primitive left ventricle (which con-
A3
tributes to the AV node), the primary ring between the primi-
tive left ventricle and the bulbus cordis (which gives rise to
the His bundle and bundle branches), and the ventriculoarte-
rial ring between the bulbus cordis and the truncus arteriosus.
During cardiac looping, these rings come together at the inner
curvature of the heart tube, and portions of these rings lose
IV A4
their specialized character (Fig. 1.16). There are also contri-
butions from neural crest cells to both the venous and arterial
FIGURE 1.14 There are similarities between the Collett and Edwards poles and from epicardium-derived cells (second heart field),
and the Van Praagh classifications of truncus arteriosus. Type I is the same especially for peripheral Purkinje fiber development and
as A1. Types II and III are grouped as a single type, A2, because they are annulus fibrosis formation.
not significantly distinct embryologically or therapeutically. Type A3
denotes the unilateral pulmonary artery with collateral supply to the
contralateral lung (hemitruncus). Type A4 is the truncus associated with
the interrupted aortic arch (13% of all cases of truncus arteriosus). Development of the Aortic Arches
Aortic arch development involves the sequential development
septum, and supplies the pulmonary, systemic, and coronary and then involution of 6 arch pairs, which arise from paired
circulations. The two major classification systems are those dorsal aortae that fuse distally (Fig. 1.17A, B). In mammals,
of Van Praagh, described in 1965 and Collett and Edwards, the fifth aortic arch is rudimentary. By the 10-mm embryonic
described in 1949 (Fig. 1.14). The Van Praagh system is based stage, the first 2 aortic arches have regressed; the third, fourth,
on the presence or absence of a VSD, the degree of formation and sixth are present; and the truncoaortic sac has been
of the aorticopulmonary septum, and the status of the aortic divided by the formation of the aorticopulmonary septum, so
arch; whereas the Collett and Edwards classification mainly that the sixth arches are now continuous with the pulmonary
focuses on the origin of the pulmonary arteries from the com- trunk (Fig. 1.17C). In the 14-mm embryo, the dorsal aortae,
mon arterial trunk, as follows: between the third and fourth arches, have disappeared, and the
third arches begin to elongate (Fig. 1.17D). The right sixth
•• Type I: A common arterial trunk gives rise to a main arch has disappeared, but the left sixth arch persists as the
pulmonary artery and the aorta. ductus arteriosus (DA). The recurrent laryngeal nerves hook
•• Type II: The right and left pulmonary arteries arise around the sixth aortic arches on their way to the develop-
directly from and in close proximity to the posterior wall ing larynx and so on the right it hooks around the proximal
of the truncus. part of the right subclavian artery (fourth arch) and around

Normal heart Tetralogy of Fallot
Conal septum
A B
FIGURE 1.15 Anatomy of tetralogy of Fallot (TOF). Note that in TOF, the conal septum is displaced anteriorly and to the right, resulting in a smaller
pulmonary artery orifice and subpulmonic obstruction.
DA formed by the distal part of the sixth aortic arch on the form the ligamentum arteriosum. The derivatives of the aortic
left side. arches are summarized in (Table 1.1).
Finally, by the 17-mm embryo stage, the right dorsal aorta
•• The aortic arch develops from the following:
has become atrophic between its junction with the left dorsal
aorta; the origin of the right seventh intersegmental artery •• The truncoaortic sac, which will form the proximal
has now become attenuated and later disappears (Fig. 1.17E). part of the arch to the origin of the brachiocephalic
The remaining components of the right dorsal aorta and right artery.
fourth aortic arch form the proximal subclavian artery. The •• The left horn of the truncoaortic sac, which gives rise
distal part of the left sixth aortic arch, the ductus arteriosus, to the proximal part of the arch between the origin of
normally closes within the first few hours following birth to brachiocephalic and left common carotid arteries.
SAR
AS
PA
VAR SV AVR
VOS
VIS
PR
FIGURE 1.16 Development of the specialized conduction system. Left. After initiation of normal rightward (“dextro”) looping of the early heart tube,
rings at the transitional zones appear. Middle. During later development and early septation, these rings appear at the putative junctions between
chambers—the sinoatrial ring (SAR; teal), atrioventricular ring (AVR; blue), primary ring at the bulboventricular foramen (PR; yellow), and ventriculoarterial
ring (VAR; green). Right. Position of the rings in the developed heart. AS, aortic sac; PA, primitive atrium; SV, sinus venosus; VIS, ventricular inlet segment;
VOS, ventricular outlet segment. (Adapted with permission from Jongbloed MR, Mahtab EA, Blom NA, et al. Development of the cardiac conduction
system and the possible relation to predilection sites of arrhythmogenesis. Scientific World Journal. 2008;8:239-269.)

III
Rt. aortic
arch I
IV
II
VI
III Primitive
Rt. aortic
pulmonary
arch I
IV arteries
Rt. aortic VI Primitive
arch II pulmonary
Rt. dorsal arteries Rt. 7th
aorta Dorsal intersegmental
aortae art.
A B C
External
Internal carotid art.
Common carotid
carotid arteries Internal
arteries carotid
External arteries
Rt. subclavian Brachiocephalic
carotid
artery trunk
arteries
Rt. carotid Lt. carotid Aortic Rt. subclavian
duct duct arch artery Ductus
IV Lt. vertebral Rt. pulmonary arteriosus
III
art. art.
VI Ductus
arteriosus Lt. subclavian art.
Rt. pulmonary Lt. 7th interseg- Pulmonary

artery mental artery trunk
Pulmonary trunk
D E F
FIGURE 1.17 Aortic arch development. In the 20-day human embryo (E8 in the mouse), the first pair of pharyngeal arteries (I) have formed and
connect the arterial pole of the heart with the paired dorsal aortae (DA). In the 30-day human embryo (~E10 in the mouse), the first arch artery has
degenerated, and II, III, and IV are present and connected to the dorsal aortae and to the arterial pole of the heart (not shown) through the aortic sac
(AS). The paired dorsal aortae have fused caudally to the heart. By 40 days (~E11 in the mouse), the arteries of the first 2 arches have regressed and
those of arches III to VI are present. The pulmonary arteries (PAs) start sprouting out from the VI arch arteries, which are the precursors of the pulmonary
trunk. In the 6-week embryo (E12.5 in the mouse), the right VI pharyngeal artery and the right dorsal aorta are in regression, and the left VI pharyngeal
artery degenerates. The left VI pharyngeal arch artery splits from the aortic trunk to form the pulmonary trunk, which remains connected as the ductus
arteriosus to the left dorsal aorta. By 7 weeks, the definitive aortic arch has formed with derivatives of the pharyngeal artery III forming the left and right
common carotids (LCC and RCC) and those of the IV pharyngeal arteries make small contributions to the right subclavian artery and aortic arch. The left
and right subclavian arteries (LSA and RSA) have remodeled their position to become connected, respectively, to the aortic arch and the brachycephalic
artery (BCA; derived from the aortic sac). The right dorsal aorta has degenerated at this stage. (Reproduced, with permission, from Fuster V, Harrington RA,
Narula J, Eapen ZJ, eds. Hurst’s The Heart. 14th ed. New York, NY: McGraw-Hill; 2017.)
•• The left fourth aortic arch, which gives rise to the part •• The left subclavian artery develops from the left sev-
of the arch between the origin of left common carotid enth intersegmental artery and left dorsal aorta opposite
and left subclavian artery. the left seventh intersegmental artery.
•• The left dorsal aorta between the fourth and sixth aor- •• The right subclavian artery develops from the right
tic arches, which will give rise to the distal part of the fourth aortic arch, right seventh intersegmental artery,
arch of the aorta. and right dorsal aorta opposite the right seventh interseg-
•• The brachiocephalic artery develops from the right mental artery.
horn of the truncoaortic sac.
•• The right and left internal carotid arteries develop Anomalies of the Aortic Arch Arteries
from the distal portion of the third aortic arch and the Most aortic arch anomalies are secondary to abnormal reten-
dorsal aorta cranial to the third aortic arch. tion or disappearance of various embryonic vascular segments.

Table 1.1 Derivatives of aortic arch vessels

Part Derivatives
First aortic arch In both sides: disappear and the remaining part forms the maxillary artery
Second aortic arch In both sides: disappear and the remaining part forms the stapedial artery
Third aortic arch In both sides:
Proximal part—common carotid artery
Distal part—internal carotid artery
Fourth aortic arch Right artery: right subclavian artery
Left artery: arch of the aorta
Fifth aortic arch In both sides: disappear
Sixth aortic arch Right artery/Proximal part: right pulmonary artery
Distal part: disappear
Left artery/Proximal part: left pulmonary artery
Distal part: ductus arteriosus
Truncoaortic sac and left horn Arch of the aorta
Right horn Brachiocephalic artery
Dorsal aorta Right: internal carotid artery cranial to the third arch
The rest: disappear
Left: internal carotid artery cranial to the third arch
Arch of aorta between the fourth and sixth arch
Descending aorta distal to the sixth arch
1. Patent ductus arteriosus (PDA): This is one of the aortic arch and the proximal part of the right dorsal aorta
most frequently seen abnormalities of the great vessels in have been obliterated. The right subclavian artery is
which there is a patent duct between the left pulmonary formed from the right seventh intersegmental artery and
artery and the arch of the aorta distal to its branches. the distal part of the right dorsal aorta.
It is potentially cyanotic heart disease, more common The branches of the arch of aorta from right to left
in females than in males and may be accompanied are the brachiocephalic artery, which is continuous as the
by other congenital heart disease, such as aortic right common carotid artery, left common carotid, left
stenosis, pulmonary stenosis, and Fallot’s tetralogy. subclavian artery, and right subclavian artery.
An anatomic variant of the PDA is the aortopulmonary
window (Fig. 1.18), which is usually a relatively large
communication between the ascending aorta and the
Patent ductus Type III Type II
main pulmonary artery. arteriosus
2. Double aortic arch: This develops when there is a
Type I
failure of the distal part of the right dorsal aorta to
disappear. A vascular ring around the trachea and
esophagus with varying degrees of compression of
these structures may occur (Fig. 1.19). The left arch of
the aorta will give origin to the brachiocephalic artery,
which is continuous as the right common carotid, left
common carotid artery, and left subclavian artery.
A B
The right arch of the aorta will give origin to the right
subclavian artery. FIGURE 1.18 Anatomic locations of patent ductus arteriosus (A) and
3. Abnormal origin of the right subclavian artery aortopulmonary window (B), with multiple distinct anatomic locations
(aberrant right subclavian artery): The right fourth possible.

Coarctation occurs in about 10% of congenital heart

diseases. There are 2 types of coarctation:
a. Preductal (Fig. 1.22A): Where the coarctation is
proximal to the entrance of ductus arteriosus. The
ductus arteriosus is persistently open, if closed, it is
incompatible with life.
b. Postductal (Fig. 1.22B): Where the coarctation of
the aorta is distal to the entrance of the ductus
arteriosus. This permits development of collateral
circulation during the fetal period and the ductus
arteriosus is usually obliterated.
6. Persistent ductus caroticus: The ductus caroticus is
the portion of the embryonic dorsal aorta between third
and fourth arch arteries that normally disappears early
in development. Its persistence results when the internal
FIGURE 1.19 Anterior (left) and posterior (right) views of the double carotid arteries develop from the distal part of the third
aortic arch constricting the trachea and esophagus. (Reproduced, with aortic arch artery and the dorsal aorta between the third
permission, from Doherty GM, ed. CURRENT: Diagnosis & Treatment: and fourth aortic arch arteries. Thus, the left internal
Surgery. 14th ed. New York: McGraw-Hill; 2015.) carotid artery originates directly from the arch of aorta
and the right internal carotid artery originates from the
right subclavian artery.
The right subclavian artery crosses the middle 7. Right arch of the aorta: The entire right dorsal aorta
line (Fig. 1.20) to reach the right upper limb anterior to persists and the distal part of the left dorsal aorta
the esophagus and trachea, and compresses them. The involutes. So the right arch of the aorta is developed
right recurrent laryngeal nerve does not hook around the from the aortic sac, the right horn of the aortic sac, and
right subclavian artery, but passes directly to the larynx the right fourth aortic arch artery. The brachiocephalic
and supplies it. A transverse compression band in the artery, right common carotid artery, and right subclavian
esophagram suggests the diagnosis. artery are the branches of the right arch of aorta left to
4. Interrupted aortic arch (IAA): It is a rare defect, right. It may pass anterior to the trachea and esophagus
comprising approximately 1% of all cases of congenital causing dyspnea and dysphagia, respectively.
heart disease results from obliteration of the fourth aortic
arch on both sides. There is absence of luminal continuity
between the ascending and descending aortae. It does not
occur as an isolated defect in most cases, as a VSD or Development of Veins
PDA is usually present. The IAA is classified based on In the fifth week, 3 systems of veins can be recognized: the
the location of the interruption (Fig. 1.21). umbilical venous system, which disappears after birth; the
5. Coarctation of the aorta: It is a constriction of the vitelline system, which develops into the portal system; and
aorta distal to the origin of the left subclavian artery. the cardinal system, which forms the caval system.
Right common Left common

carotid artery carotid artery
Right vertebral Left vertebral

artery artery
Left subclavian
Right subclavian
artery
artery
Aberrant right
subclavian
artery
Aorta
Trachea Esophagus
FIGURE. 1.20 Aberrant right subclavian artery. The right subclavian artery arises in the descending aorta, distal to the origin of the left subclavian
artery. It crosses the midline either behind the esophagus, between the esophagus and the trachea, or anterior to the trachea.

IA LC
LS
IA LC
IA PDA Fate of Sinus Venosus
PDA
LS LC LS
1. The right horn is enlarged and absorbed into the right
RPA atrium to form the smooth posterior part of the right
LPA
atrium.
Ao MPA 2. The left horn is reduced in size to form the oblique vein
of left atrium.
A B C 3. The body becomes reduced in size to form the coronary
sinus.
FIGURE 1.21 Anatomic types of an interrupted aortic arch.
A. Interruption distal to the left subclavian artery. B. Interruption
4. The sinoatrial valves (Fig. 1.23C):
between the left subclavian and left carotid arteries. C. Interruption a. The upper ends of right and left venous valves unite
between the left carotid and innominate arteries. Ao, aorta; IA,
innominate artery; LPA, MPA, RPA, left, main, and right pulmonary
to form the septum spurium.
arteries; LC, left carotid artery; LS, left subclavian artery; PDA, patent b. The left sinoatrial venous valve will be absorbed
ductus arteriosus. (Reproduced, with permission, from Jonas RA. into the interatrial septum.
Interrupted aortic arch. In: Mavroudis C, Backer CL, eds. Pediatric Cardiac c. The right sinoatrial venous valve derivatives:
Surgery. 2nd ed. St. Louis, MO: Mosby; 1994:184.) i. The upper one-third with septum spurium
gives rise to crista terminalis.
ii. The middle one-third gives rise to the valve of
IVC.
Developmental Changes iii. The lower one-third gives rise to the valve of
in the Sinus Venosus coronary sinus.
Sinus venosus is a dilatation of the primitive atrium, which
receives the veins of the body, intestine, and placenta. At
an early stage (Fig. 1.23A), the sinus venosus is composed
Fetal Circulation (Fig. 1.24)
of the body (the central part) and right and left horns. Each During fetal life, the oxygenated blood coming from the pla-
horn receives a vitelline vein that carries unoxygenated blood centa is carried via the left umbilical vein to the left branch
from the yolk sac, the umbilical vein that carries oxygenated of the portal vein. Part of this blood is carried via the ductus
blood from the placenta, and the common cardinal vein that venosus to the inferior vena cava while the other part enters
is formed by the union of the anterior and posterior cardinal the liver by means of the portal vein and leaves it by means of
veins and carries unoxygenated blood from the body wall. the hepatic veins to the inferior vena cava. The blood passes
As a result of development of the liver on the right side from the inferior vena cava to the right atrium.
and the presence of transverse anastomoses between the The greater part of this blood passes through the foramen
left and right cardinal veins, the blood is shifted to the right ovale, the left atrium, where it is mixed with a small amount
side and so the blood that reaches the right horn becomes of venous blood coming from the lungs through the pulmo-
more than that of left horn. This leads to an increase in the nary veins. This mixture, still of high oxygen content, passes
size of the right horn, while the left horn becomes reduced in to the left ventricle and then to the aorta. Most of the blood
size and the sinoatrial orifice, at first, lies transversely, then supplies the heart itself, the head and neck, the brain, and the
becomes vertical and guarded by 2 valves (the right and left upper limbs.
venous valves) (Fig. 1.23B). The smaller portion of the blood reaches the right atrium
via the inferior vena cava together with the deoxygenated
blood returning from the upper part of the body via the supe-
rior vena cava, entering the right ventricle and then into the
Preductal Postductal pulmonary trunk. Since the lungs of the fetus are not function-
coarctation coarctation ing, a small amount of this blood enters the pulmonary vas-
cular bed while most of the blood passes through the ductus
arteriosus into the descending aorta to join the blood coming
to this part of the aorta from the left ventricle. It supplies the
lower limbs, the trunk, and the viscera. Most of the blood is
returned back to the placenta by means of 2 umbilical arteries.
Changes in Fetal Circulation at Birth

A B
The placental circulation stops and as a result, the left
FIGURE 1.22 Anatomic features of aortic coarctation. A. Preductal umbilical vein becomes obliterated and forms the ligamentum
coarctation, in which differential cyanosis may occur. B. Postductal teres of the liver, the ductus venosus becomes obliterated and
coarctation. forms the ligamentum venosum of the liver and the umbilical

Anterior Anterior
cardinal vein cardinal vein

cardinal vein Sinus venosus cardinal vein
Right S.A.O. Left

horn horn
Body
Posterior Right vetilline Left vetilline Posterior

cardinal vein vein vein cardinal vein
Right umbilical Left umbilical
vein vein
A
Anterior Anterior i ii

Sinus venous a
Right Left c
S.A.O. Body
horn horn
C
Posterior Right vetilline Left vetilline Posterior

cardinal vein vein vein cardinal vein
Right umbilical Left umbilical
vein vein
B
FIGURE 1.23 Schematic illustration of the process of development of sinus venosus. A. The sinus venosus is formed of central part (body), right horn
and left horns. Each horn receives 2 vitelline veins, 2 umbilical veins, and 2 common cardinal veins which are formed by the union of the anterior and
posterior cardinal veins. The sino atrial orifice (SAO) is lying horizontally. B. The enlargement of the right horn at the expense of left horn and central part.
The sinoatrial orifice, becomes vertical. C. Derivatives of the valves guarding the sinoatrial orifice. The upper ends of the right and left venous valves unite to
form the septum spurium. The left sinoatrial venous valve will be absorbed into the interatrial septum. The upper third of the right sinoatrial venous valve
with septum derivatives gives rise to crista terminalis. The middle one-third gives rise to the valve of IVC, and the lower one-third gives rise to valve of the
coronary sinus.
arteries become obliterated and form the lateral umbilical 3 months after birth. As a result, the ductus arteriosus becomes
ligaments. obliterated and forms the ligamentum arteriosum, the foramen
Pulmonary circulation starts due to the immediate ovale becomes obliterated forming the fossa ovalis from the
functional closure of the ductus arteriosus and the foramen septum primum and the annulus ovalis from the edge of the
ovale. Their anatomical closure is usually not complete until septum secundum.

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Then said his granny:
“I will make a drum of a bit of old skin. Do you get inside and roll
past the lion and the vulture and the tiger.”
So granny made a drum of a bit of skin, and Lambikin jumped
inside the drum, and off he rolled toward home.
But before he had gone very far he met the lion, who was waiting
for him, and the lion said:
“Drummikin, have you seen Lambikin?”
But Lambikin called out from inside the drum:
“Fallen into the fire, and so will you.

On, little Drummikin, tum, tum, too.”
Then the lion thought the woods must be on fire, so he ran off as
fast as he could.
But Lambikin had not gone very far when the vulture flew down for
his dinner.
“Drummikin, have you seen Lambikin?” asked the vulture.

On, little Drummikin, tum, tum, too,”
said Lambikin in a gruff voice from the inside of the drum.

Then the vulture thought that the woods must surely be on fire, so
he flew far above the treetops.
The tiger caught his tail and was not able to move.
Lambikin rolled merrily along a little way farther, but soon he met
the striped tiger, who was waiting for his dinner.
“Drummikin, have you seen Lambikin?” asked the striped tiger.

On, little Drummikin, tum, tum, too,”
said Lambikin; but the striped tiger had very sharp ears.
“Lambikin is inside Drummikin,” he said, and he started after the
drum as fast as he could go. He nearly caught it, for he went so very
fast, but they came to a bramble bush. The tiger caught his tail and
was not able to move, and out of the drum jumped Lambikin.
Then off he frolicked home again as frisky and happy as ever a
lamb could be.
BROTHER WOLF
AND THE ROCK.
Once upon a time Brother Wolf dressed himself up very finely, just
like an Indian. He put feathers on his head, and moccasins on his
feet, and beads around his neck. Then he bought a very gay blanket,
just like a chief’s blanket. He wrapped it all around him, and then he
started on a journey.
As he traveled, he came to a big Rock. Brother Wolf thought that
he had never seen such a nice Rock, such a smooth, round, shining
Rock. But Brother Wolf thought that the Rock looked cold. So he
took off his blanket and wrapped it around the Rock to keep the old
Rock warm.
Then Brother Wolf started traveling again, but he had not gone
very far when he heard a loud noise—that was the thunder; and he
saw a bright light—that was the lightning; and he felt something wet
on his nose—that was the rain. So Brother Wolf ran back in great
haste to the Rock.
“Oh, Rock,” cried Brother Wolf, “it is storming, and I shall be wet.
Give me back my blanket to keep off the rain.”
But, no, Rock would not. Old Rock said he would just keep Brother
Wolf’s blanket a little longer.
Then Brother Wolf hid under a tree, and, by and by, along came
Brother Fox.
“Oh, Brother Fox,” said Brother Wolf, “go to Rock and bring back
my blanket.”
So Brother Fox went to old Rock and told him that Brother Wolf
wanted back his blanket to keep the rain off his nose. But, no, old
Rock would not give up the blanket.
Then Brother Fox went back and told Brother Wolf, and Brother
Wolf cried because he knew his feathers would be spoiled. They sat
under a tree, and the rain poured and poured, the lightning flashed,
and the thunder roared. Brother Wolf asked Brother Fox to please go
again to old Rock and ask for the blanket, but Brother Fox said, “No.”
After a while they heard a great noise, and a loud roaring. The
stones in the road began to come skipping by. Brother Wolf peeped
out from under the tree. There was old Rock rolling down the road.
The rain had started him, and he was coming so hard that he tore
great furrows of earth, and uprooted the trees. He came so fast that
he could not stop himself.
Brother Fox scampered into a hole to hide, but he left the tip end
of his tail sticking out. Old Rock just grazed it as he went by, and that
is why the tip of Brother Fox’s tail is pointed.
On and on went old Rock until he came to a river. Splash, in he
went, and that was the last that anybody saw of Rock, for he went
straight to the bottom.
When the rain was over, Brother Wolf and Brother Fox went down
to the river bank to look for old Rock, but they could not find him
anywhere. On the top of the water floated Brother Wolf’s gay
blanket, so they waited until it came ashore, and they dried it in the
sun.
Then Brother Wolf said “Good-by” to Brother Fox, and put on his
blanket again, and traveled.
LITTLE BEAR.
Once upon a time, there was an Indian boy and he had a little
sister. Now the little sister was not like an Indian child, for she was a
bear.
Early one morning the boy started out to seek his fortune, but Little
Bear wished to go too.
“No, no, Little Bear, you cannot go. You must stay at home and
watch the fire,” said her brother. Then he tied Little Bear to the door
posts that she might not run away.
He had not gone very far on his journey when he heard TRAMP,
TRAMP, TRAMP, in the path behind him. There was Little Bear
following with the door posts on her back.
“Oh, Little Bear, I told you to stay at home and watch the fire,” said
the boy.
He led Little Bear back, and this time he tied her to a pine tree.
He had not gone very far when he heard once more, TRAMP,
TRAMP, TRAMP, in the path behind him. There was Little Bear
following with the pine tree on her back.
“Oh, Little Bear, you must stay at home and watch the fire,” said
the boy.
He led Little Bear back, and this time he tied her to a rock.
He started on his journey again, but he had not gone a stone’s
throw, when he heard THUMP, THUMP, THUMP, in the path behind
him. There was Little Bear following him with the rock on her back.
“What shall I do with you, Little Bear?” said the boy. But just then
they came to a wide brook with no bridge to span it.
“How shall I cross?” said the little boy.
Little Bear pushed the rock into the water. She laid the pine tree
across the rock for a bridge. They both walked across the brook in
safety.
“Well, you may come with me, Little Bear,” said the boy.
They journeyed for many days until they came, at last, to some
very dark woods. In the woods they met Brother Wolf carrying a
candle to light him on his way.
“The sun is lost from the sky,” said Brother Wolf; “the old squaw
pulled it down.”
“Oho, I can find the sun,” said Little Bear, “but you must first give
me two lumps of maple sugar.”
Brother Wolf gave Little Bear two lumps of maple sugar and she
hurried along until she came to the old squaw’s wigwam. The old
squaw was stirring a kettle of rice over her fire. Little Bear crept up
behind her. Little Bear dropped the two lumps of maple sugar into
the kettle. As the old squaw stirred, she tasted her rice.
“It is too sweet,” she said; “I must go to the field for more.”
While she was gone, Little Bear found the sun, which the old
squaw had hid in her wigwam. Little Bear tossed it back to the sky
again.
When the old squaw came back from the rice fields and missed
her sun, she was very angry. She looked for it many, many days, but
the clouds hid it from her. Then, one night, she pulled the moon
down, and hid that away in her wigwam.
So there was no light in the evening. Brother Wolf lighted his
candle again, and he hurried after the boy and Little Bear, who had
started on their journey again.
“The moon is gone from the sky,” said Brother Wolf, “the old
squaw has pulled it down.”
“Oho, I can find the moon,” said Little Bear; “give me two pinches
of salt, Brother Wolf.”
Brother Wolf gave Little Bear two pinches of salt, and Little Bear
crept up to the old squaw again, and threw the salt in her kettle of
rice.
“The rice is too salty,” said the old squaw, tasting as she stirred; “I
must go to the field for more.”
While she was gone, Little Bear snatched the moon from the
wigwam, where the old squaw had hid it, and tossed it up to the sky
again.
Brother Wolf snuffed his candle, for he did not need it any more,
but the old squaw was very angry. The old squaw ran after Little
Bear. She caught her, and she put her in a bag, and tied the bag to a
tree. Then she went for her spoon with which to beat Little Bear.
But while she was gone, Little Bear bit a hole in the bag with her
teeth. She slipped out. Then she filled the bag with the old squaw’s
pots and pans. When the old squaw came back, and began beating
the bag, she broke all her dishes.
Then the boy and Little Bear picked up enough sun gold and moon
silver which had fallen by the road to make them rich for always. And
Little Bear traveled with her brother wherever he went after that. Was
she not a clever Little Bear?
HOW THE PIGS CAN
SEE THE WIND.
Once upon a time, Mrs. Pig lived in a fine house of her own with
her five little pigs. Four of the little pigs were black, but the smallest
pig was white and he was as the apple of his mother’s eye.
Around the hill from Mrs. Pig’s house lived Brother Wolf, and
Brother Wolf had a mighty good mouth for pig meat. Every night Mr.
Wolf came through the garden gate, and he walked round and round
Mrs. Pig’s house, sniffing and snuffing, and calling in a soft voice:
“Mrs. Pig, Mrs. Pig, let me come in,

The corn is ripe, and the frosts begin.”
But Mrs. Pig always locked her door fast, and Brother Wolf had to
go home without any pig meat.
One night Brother Wolf thought of a trick. He put a very high hat
on his head. He put shoes on his feet. He tied a necktie around his
neck, and he looked just like Mr. Man.
Then he put a bag of corn over his shoulder, and he walked,
TRAMP, TRAMP, up the brick walk that led to Mrs. Pig’s house, and
he rapped loudly on Mrs. Pig’s door.

The corn is ripe, and the frosts begin,”
he said.
“Who knocks?” asked Mrs. Pig, peeping through the window, the
little white pig under her arm.
“Mr. Man, come to put a mark on your little pigs,” said Brother
Wolf.
Then Mrs. Pig opened the door, and she turned out the four little
black pigs. But the little white pig was as the apple of her eye, and
she hid him in the cupboard.
So Brother Wolf emptied all the corn out of his bag, and he put in
the four little pigs, and he carried them home with him.
By and by, Brother Wolf was hungry for more pig meat, so he
dressed himself in his clothes again. He put his bag of corn over his
shoulder, and he rapped loudly at Mrs. Pig’s door, calling:

“Who knocks?” asked Mrs. Pig.

“Mr. Man, come to put a mark on your little white pig,” said Brother
Wolf.
But Mrs. Pig barred the door, and locked the window, and hid the
little white pig in the dresser, for he was as the apple of her eye.
Then Brother Wolf was very angry, and he took off his hat and his
shoes and his necktie. He hurried up and down the roads until he
met Mr. Wind, who wore a red cloak, and was sweeping the fields.
Brother Wolf told Mr. Wind how he had a mighty good mouth for
pig meat. Mr. Wind said he would help Brother Wolf, for he always
liked a romp.
So Mr. Wind and Brother Wolf went to Mrs. Pig’s house and they
rapped loudly on the door, and Brother Wolf called out:

But never a word did Mrs. Pig say.
“Who knocks?” asked Mrs. Pig.
“Blow, Mr. Wind,” said Brother Wolf.

Then Mr. Wind began to puff himself out bigger and bigger. He
huffed and he puffed and he blew a mighty gale. He blew round the
garden, and he pulled up the corn and threw it down on the ground.
He slammed the gate and he rattled the window. He shook the door,
and he cried, “WHE-EE, WHE-EE,” in the keyhole, did Mr. Wind.
Brother Wolf was so frightened that his hair stood up straight on
his back. Out of the garden he ran, and around the hill. He never
stopped, nor looked behind him, and no one ever saw him in Mrs.
Pig’s garden again.
“WHE-EE, WHE-EE, let me in,” called Mr. Wind.
Mrs. Pig opened her door a crack, and peeped out with the little
white pig under her arm, for he was the apple of her eye.
HUFF, PUFF, the door blew open wide. When Mrs. Pig saw Mr.
Wind in his red cloak running around the garden, she hurried off to
the woods with her little white pig, and she never came home for a
day and a night.
And that is how the pigs first came to see the wind. If you do not
believe it, just watch them run when Mr. Wind comes huffing and
puffing through the garden.
THE TALKING
GRASS.
Once upon a time when there were only Indians and animals in
our land, there was a green hill covered with long talking grass. The
four winds of heaven brought the grasses news of what was going
on in the world, and of the coming of hunters. Then the grasses
whispered this news to their friends, the little red Fox, the Hare, the
Deer, and the Wolf. If the animals were too far away to hear the soft
voices of the grasses, they gave the messages to the Butterflies.
The hill was the refuge of these animals, and the talking grasses
were their friends.
One day a great band of hunters came from their camp in the
valley, up the hill. They were armed with bows and arrows. They
planned to kill enough game to give them food for a long time. But
the grasses knew that the hunters were on their way. They warned
the animals, who hid at once. When the hunters reached the hill,
they saw nothing but green grass waving in the wind. Many bright
butterflies flew above it.
The hunters listened and heard the grasses talking to one another.
They saw, too, the trails of the animals as they had passed through
it. They guessed at once what had happened.
“The grasses have told the animals to flee and hide from us,” they
said. “We must kill them. To-night we will rest and sleep among
them, for we are tired with our long journey. But to-morrow we will
tear every blade of grass up by its roots.”
At these cruel words the grasses became still. They loved their life
on the hill, with their roots in the earth and their green blades
reaching up to the sunshine. Now they knew that they were going to
die in the morning. They could neither sing nor talk any more. But
the Butterflies knew the grasses’ peril. They flew away, one by one,
so that the hunters would suspect nothing, until they came to the
Fox’s den. They told him of the great danger of the talking grasses.
They begged him to do anything that he could to save them.
The Fox set off at once. He did not stop until he came to a dark
cave on the side of a mountain. Here the Fire Manito lived. Few
dared speak to him, for he was a very mighty Manito. He was able to
destroy man or beast at his will. But when he saw the eager,
trembling little Fox, waiting outside, the Fire Manito asked him his
errand. The Fox told him that the grasses were to be killed in the
morning, unless something was done to save them.
The Manito went to the back of his cave and brought out a heap of
black stones. There was no light in them. He told the Fox about
them.
“They came from the depths of the earth,” he said. “The Great
Spirit mixed a million sunbeams in each. Then he hid them in the
earth until they should be needed to give heat and light to man. Now
we will use the black stones to save the grasses.”
The Manito heated the stones in his wood fire and they glowed like
red rubies. He sent the Fox ahead to tell the grasses to be brave.
He, himself, followed with his arms full of the glowing stones which
did not burn him because he was the Fire Manito.
The hunters had arisen early and waited at the foot of the hill,
ready to rush up and tear up the grasses. But the Manito laid the
brightly burning stones in a circle about the hill. The hunters were not
able to get through. It was a ring of fire and it frightened them. They
had never seen burning coals before. They went back to their camp
and the grasses were safe, for the coals burned to ashes without
touching them.
The grasses soon found their voices again, and they have been
talking to their friends, the animals, ever since. In the summer they
tell the Field Mouse and the Hare where to hide safely. In the spring
they tell the Deer that they are fresh and green for his food. When it
is winter, a few of the grasses stand up, stiff and tall, above the snow
as the lone gray Wolf runs by. They guide him to food. In the fall the
whispering of the dry grasses helps the Fox to double his trail so that
no one may catch him.
Who of you have heard the voices of the grasses?
HOW THE FOX
PLAYED HERDSMAN.
Once upon a time there was a little old woman who had a farm of
her very own with sheep, and cows, and swine. But the little old
woman was so busy making butter and minding the dairy that she
had no time to look after the herds.
One fine morning she started out to hire a herdsman. Now she
had not gone very far when she met a bear.
“Whither away, Goody?” asked Bruin of the little old woman.
“Oh, I am off to engage a herdsman for my farm,” said Goody in
reply.
“Why not hire me, Goody?” asked Bruin.
“Can you call the flocks at evening?” asked the little old woman.
“You should just hear me,” said Bruin, and he called in a very loud
and gruff voice, “OW, OW.”
“No, no, I won’t have you,” said the little old woman as soon as
she heard his gruff voice, and off she went on her way.
She had not gone a day’s journey farther when she met a wolf.
“Whither away, Goody?” asked the wolf of the little old woman.
“Oh, I am off to engage a herdsman for my farm,” said Goody.
“Why not hire me, Goody?” asked the wolf.
“You should just hear me,” said the wolf, and he called in a shrill
voice, “UH, UH.”
“No, no,” said the little old woman as soon as she heard that, and
off she went on her way.
But before the end of another day’s journey, whom should the little
old woman meet but Brother Fox, sitting beside a blackberry bush,
and sunning himself.
“Whither away, Goody?” asked Brother Fox.
“Oh, I am off to engage a herdsman for my farm,” said Goody in
reply.
“Why not hire me, Goody?” said Brother Fox.
“Ah, you should hear me,” said Brother Fox. He opened his mouth
very wide, and sang in a sweet voice:
“Tum-ti-ti, tum-ti-ti-tra-la-la.”
“You will do very well,” said the little old woman, quite carried away
with the fox’s sweet singing. “You shall come home with me, and be
my herdsman.”
Things went very well for a little while at the farm. Early each
morning Brother Fox led the sheep and the cows and the swine to
pasture, and at night he led them home again, and locked the barn,
and bolted the pigpen.
But, somehow, after a week, the flocks and the herds seemed
smaller each night when the little old woman went out to make the
rounds of the farm.
“Where is the small black pig?” she asked of Brother Fox.
“Loitering in the meadow,” said Brother Fox, wiping his mouth with
his paw.
“Where is the old ram?” asked the little old woman.
“He stops behind at the brook,” said Brother Fox, turning his head
away that Goody might not see him laughing.
So Goody went back to the dairy, and she wondered and
wondered what made the flocks grow smaller.
At last she had churned enough butter to make a fine cake and
she went out to the poultry roost for eggs with which to enrich it.
Alas, such a hubbub, and cackling, and fussing did she find.
The cock stood on the pump, crying loudly, “Cock-a-doodle-do.”
The hens ran about cackling, and out of their midst walked Brother
Fox with a chicken over his back, and his hat full of eggs.
And as he went along he sang to all the poultry yard:
“Tum-ti-ti, Tum-ti-ti,
Tum, tum, ti,
Old Goody’s herdsman,
Sly Reynard, am I.”
“Well, it’s certainly a very poor herdsman you are,” cried the little
old woman. “Where is the small black pig? Where is the old ram?”
She ran after Brother Fox, who dropped his eggs and broke every
one, and tipped over the churn as he passed the dairy. The little old
woman picked up the dasher, and would have beaten Brother Fox,
but he was too quick for her, and reached the woods, with a drop of
cream on the tip end of his tail.
So the little old woman learned what had become of her herds,
and Brother Fox was never able to get that cream from off his tail,
The tip end has been white ever since he played at being a
herdsman.
MR. ELEPHANT
AND MR. FROG.
Once upon a time, when Mr. Elephant and Mr. Frog lived together
in the same wood with Mr. Fox and Mr. Tiger and Mr. Hare and Mr.
Lion, the animals were all very good friends.
Mr. Elephant was very, very big, and Mr. Frog was very, very little,
but every day they went walking together, Mr. Elephant going in
front, tramp, tramp, tramp; and Mr. Frog going on behind, hop, hop,
hop.
One night when they came home, Mr. Hare, who was a saucy little
fellow, ran to meet them, and he said:
“Oho, Mr. Frog says Mr. Elephant is his horse.”
Then Mr. Fox and Mr. Tiger and Mr. Lion all followed after Mr.
Hare, crying:
“Oho, oho, Mr. Elephant is Mr. Frog’s horse.”
Mr. Elephant turned around, and he said in a very gruff voice to
Mr. Frog:
“Did you tell them, grandson, that I was your horse?”
And Mr. Frog said in a high, squeaky voice:
“No, no, grandfather.”
But all the time Mr. Frog was thinking of a trick to play on Mr.
Elephant.
The next day, Mr. Elephant and Mr. Frog started off for a long walk.
Mr. Frog had heard of a place where the swamps were deep and

Cardiology An Integrated Approach Human Organ Systems Dec 29 2017 - 007179154X - Mcgraw Hill 1St Edition Elmoselhi Full Chapter

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Cardiology An Integrated Approach Human Organ Systems Dec 29 2017 - 007179154X - Mcgraw Hill 1St Edition Elmoselhi Full Chapter

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Cardiology-An Integrated Approach

(Human Organ Systems) (Dec 29,

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ADEL ELMOSELHI, MD, PHD

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AND VESSELS 10 Valvular Heart Diseases / 151

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Saqib Ahmed, MD, MRCP(UK) Clinical Assistant Professor of Medicine

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Akram Jaffar, MD, PhD Maha M. Saber-Ayad, MD(Pharm),

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ABI ankle-brachial index

BAT baroreflex activation therapy

CABG coronary artery bypass graft (CABG) surgery

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CARDIA Coronary Artery Risk Development in Young Adults

DADs delayed afterdepolarizations

GFR glomerular filtration rate

HCM hypertrophic cardiomyopathy

ICD implantable cardioverter defibrillator

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IVC inferior vena cava

JET junctional ectopic tachycardia

MAHA microangiopathic hemolytic anemia

NCX sodium-calcium exchanger

ORT orthodromic reentrant tachycardia

PACs premature atrial contractions

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PFO patent foramen ovale

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UFH unfractionated heparin

V1A vasopressin type 1A (V1A) receptor

WPW Wolff-Parkinson-White (WPW) syndrome

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Vessels • Describe heart tube looping, chamber formation,

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Angioblast Vasculogenesis Angiogenesis 2. Situs inversus: As with dextrocardia, this condition

Sprouting Bridging Intussusception Development of the

Early heart-forming Neural folds Pericardial Foregut Forming heart

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subarterial), perimembranous (the inlet portion of

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refers to the right or left looping of the primitive heart tube

FIGURE 1.13 A-C. Classification of aortopulmonary window.

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Normal heart Tetralogy of Fallot

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Rt. pulmonary Lt. 7th interseg- Pulmonary

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Table 1.1 Derivatives of aortic arch vessels

Third aortic arch In both sides:

Proximal part—common carotid artery

Distal part—internal carotid artery

Fourth aortic arch Right artery: right subclavian artery

Left artery: arch of the aorta