Introduction to Synthetic Aperture

Radar: Concepts and Practice E. David

Jansing
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About the Author

E. David Jansing, Ph.D., is a chief engineer at the Johns Hopkins

University Applied Physics Laboratory and a lecturer in the Johns
Hopkins University Whiting School of Engineering’s Engineering for
Professionals program. He has been studying synthetic aperture
radar for more than 20 years and has been teaching a graduate-level
course on SAR for nearly 10 years. Dr. Jansing has more than 20
years’ experience in remote sensing, especially in imaging,
exploitation, analysis, and data collection/planning for SAR, hyper-
spectral imaging, and infrared imaging. Machine learning,
particularly deep learning, has been the focus of his exploitation
efforts and he has a patent for a novel maritime vessel detection
using synthetic aperture radar. A graduate of the University of
Louisville, Dr. Jansing has spent time working the research,
development, and operational sides of military, intelligence, and
commercial remote sensing. He currently lives in Cathedral City, CA.
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 Contents

Preface
Acknowledgments

1 Introduction to Synthetic Aperture Radar

1.1 Introduction
1.2 Origins of SAR
1.3 Examples of Synthetic Aperture Radar Systems
1.3.1 Magellan
1.3.2 TerraSAR-X
1.3.3 ImSAR
1.3.4 ICEYE
1.3.5 Capella Space Systems
1.4 Timing and Geometry
1.4.1 Imaging Modes
1.4.2 Geometry
1.4.3 Timing
1.5 The Synthetic Aperture

2 Ranging
2.1 Range via Echoing
2.2 The Linear Frequency-Modulated Chirp
2.3 Detecting the Received LFM Chirps
2.3.1 Quadrature Demodulation
2.3.2 Dechirping

3 Imaging
 3.1 Mathematical Model
3.1.1 The Doppler Effect
3.1.2 Pulse Repetition Frequency and Doppler Chirp Rate
3.1.3 Synthetic Aperture and Exposure Time
3.1.4 Azimuth Resolution
3.2 Simulated Point Scatterers Using Quadrature Demodulation
3.3 Simulated Point Scatterers Using Dechirp

4 Image Formation
4.1 The Image Formation Chain
4.2 Motion Compensation
4.3 Processing Tools
4.3.1 Fourier Transforms
4.3.2 Interpolation

5 Image Formation Algorithms for Quadrature

Demodulated Data
5.1 Range-Doppler Algorithm
5.1.1 Algorithm Overview
5.1.2 Raw Radar Data
5.1.3 Step 1: Range Compression
5.1.4 Step 2: Azimuth FFT
5.1.5 Step 3: Range Cell Migration Compensation
5.1.6 Step 4: Azimuth Compression
5.1.7 Step 5: Azimuth IFFT
5.2 Omega-K or Range Migration Algorithm
5.3 Quadrature Demodulation versus Dechirp

6 Image Formation Algorithms for Dechirped Data

6.1 Polar Formatting
6.1.1 Steps 1 and 2: Create Polar Grid and Project Polar-to-
Cartesian
6.1.2 Step 3: Define Inscribed or Circumscribed Grid
6.1.3 Steps 4 and 5: Interpolate and 2D FFT
 6.2 The Backprojection Algorithm
6.2.1 Computer-Aided Tomography
6.2.2 Synthetic Aperture Radar Tomographic Model
6.2.3 Reconstruction Using the Backprojection Algorithm

7 Autofocus
7.1 Sources of Phase Error
7.1.1 Phase Error within a Pulse
7.1.2 Phase Error across the Aperture
7.2 Map Drift
7.3 Phase Gradient Autofocus
7.3.1 Center Shift at Each Range Bin
7.3.2 Windowing
7.3.3 Fourier Transform to Range-Compressed Domain
7.3.4 Phase Error Estimation Using the Maximum Likelihood
Estimator
7.3.5 Removal of Phase Error

8 Image Quality
8.1 Speckle
8.2 Multilook
8.2.1 Subaperturing
8.2.2 Multilook for Speckle Reduction
8.3 Other Speckle Reduction Techniques
8.4 Aperture Weighting
8.5 Image Quality Metrics

9 Linear Frequency-Modulated Continuous Wave Systems

9.1 LFMCW Systems
9.2 LFMCW Transmitter-Receiver Model
9.3 LFMCW Mathematical Model
9.4 Motion Compensation for LFMCW

10 Remote Sensing with Synthetic Aperture Radar

 10.1 Polarimetry
10.2 Ocean Remote Sensing
10.2.1 Wakes
10.2.2 Ice Monitoring
10.2.3 Oil Spills
10.3 Deep Learning

11 Interferometry
11.1 The Basics
11.2 Terrain Estimation
11.3 Coherent Change Detection
11.4 Earthquakes

12 Moving Objects in Synthetic Aperture Radar

12.1 Mathematical Model
12.2 Challenges with Moving Object Estimation and Single-
Channel SAR
12.3 Other Types of Moving Objects

Acronyms

Variables

Glossary

Index
 Preface

If you are new to synthetic aperture radar (SAR), you should be

warned: SAR is just complicated. There is no other way to put it. A
friend of mine put it this way: “SAR theory is fractured.” And it is.
There is little to no standardization in vocabulary, variables, or
techniques.
There are so many different ways to look at SAR: systems
engineering, radar engineering, signal processing, algorithm
development, automatic target recognition, statistical processing. I
doubt there is a text that sufficiently covers all of these areas
simultaneously and certainly this book doesn’t try. This book
approaches SAR from a signal processing perspective, as many SAR
books do. However, this book is unique in the sense that it explicitly
commingles imaging geometries and breaks out the mathematical
models by demodulation type (quadrature demodulation versus
dechirp processing). It is the demodulation type that typically drives
image formation processing, with the image geometry (such as
stripmap versus spotlight) playing a secondary role (or no role at all,
in some cases). (A notable exception to this is wide-aperture SAR,
where the need to fully compensate range cell migration for image
formation is likely the driving factor.)
This book evolved from years of working in and teaching
synthetic aperture radar. There are several excellent texts that
examine SAR from a specific vantage point, often geometry or
system driven. When teaching, it’s difficult to ask students to
purchase multiple books for a single course. For the practitioner, it is
more convenient to have a single reference for an overview, rather
than have five or six SAR theory books on your shelf. This work pulls
together all of the materials needed for a graduate-level course in
synthetic aperture radar, and presents the material in a fashion that
will be useful for the seasoned practitioner as well.
The reader should come to this topic with a solid background in
digital signal processing. If terms such as Nyquist sampling rates,
Fast Fourier Transforms, and windowing are foreign to you, you
might consider building a foundation in signal processing first before
tackling this topic. The reader should also have at least a basic
understanding of radar before approaching this topic. While there is
some discussion of the radar range equation and antenna beam
patterns, this work idealizes most of the radar engineering portion of
SAR. It is assumed that the power levels, analog-to-digital
conversion, and local oscillators are perfect (or at least very well
behaved). There are plenty of sources of error, but for an
introductory text, it seemed like overkill to identify them all.
The reader should approach this book in the order it was written,
which is from foundation to application. For the novice, the first few
chapters that cover the geometric and signal models are essential
and cannot be skimmed. Full understanding of later chapters,
including image formation, SAR applications, and image quality
techniques, requires that mathematical foundation. Novices must
read and understand the first four chapters before moving to more
advanced topics. Practitioners looking for an easy reference to
advanced topics (autofocus, for example) are welcome to skip
ahead, realizing that the lack of standardization within the SAR
communities may cause some confusion. A variables list and
glossary are included at the end of the book for easy reference. A
conscious effort was made to standardize variables within the text
itself, so the variables presented here may not match the variables
as they were originally published in their respective journal or
conference articles, or as they appear in other texts.
Finally, there was a conscious decision made to not include full
blocks of code in this book. Programming languages evolve rapidly
and it isn’t clear to anyone what development language will be in
popular use in 10 years’ time. At the time of this writing, MATLAB
from MathWorks and open-source Python with data analysis
packages are two popular development and data analysis languages
in use among SAR practitioners. R, however, is gaining traction as a
well-rounded statistical and algorithm platform. Including all of these
choices in entire blocks of code is a daunting (and perhaps
impossible) task. So, if there is any code at all, it is small snippets of
code in MATLAB and Python that hint to implementation of specific
steps (such as the proper way to instantiate a Fast Fourier
Transform), not entire blocks of code that accomplish a specific
algorithmic task, such as the Polar Formatting Algorithm (PFA). It is
my considered opinion, having wrestled with SAR and taught SAR to
others for decades, that the best way to understand a specific
concept in SAR is to code it up yourself. There are open-source
toolboxes available for various development language flavors,
including MATLAB and Python. Notable contributions in this area are
the National Geospatial-Intelligence Agency’s MATLAB SAR Toolbox1
and Python SAR Toolbox, SARPy,2 and RITSAR,3 a Python tool set
developed by a student from the Rochester Institute of Technology.
If algorithm development is not your strong suit, you might consider
one of these toolboxes for implementation and understanding of
various topics covered in this book.

E. David Jansing, Ph.D.

1 https://github.com/ngageoint/MATLAB_SAR
2 https://github.com/ngageoint/sarpy
3 https://github.com/dm6718/RITSAR
 Acknowledgments

It all started with a single image. While working on my dissertation

at the University of Louisville, my advisor and friend Dr. Darrell
Chenoweth handed me a single synthetic aperture radar to study.
That image and research led me to Naval Air Weapons Station, China
Lake (NAWS/China Lake), in Ridgecrest, CA, where I spent a
fascinating and educational summer in 1996 studying SAR and
various ways to use it. Mr. John Knecht served as my mentor there
and I’m extremely grateful to him and Dr. Chenoweth for my
introduction to the world of SAR.
My introduction to the elegant and challenging details of SAR
processing came from the late Dr. Stuart Melzer while I worked at
The Aerospace Corporation. Stu was a patient teacher who, despite
my struggles in understanding, took his time to show me the way.
His influence over me in this topic was powerful and I will be forever
in his debt. I’m also thankful for the interactions and technical
discussions I had with my Aerospace colleagues, particularly in my
development of short courses in SAR. The genesis of this material
started there.
My work in SAR was further refined when I moved to the Johns
Hopkins University Applied Physics Laboratory. It was there that I
was invited to produce a full-semester, graduate-level course in the
Johns Hopkins University Engineering for Professionals program,
which is part of the Whiting School of Engineering. I am eternally
grateful to Dr. Brian Jennison, the chair of the Electrical and
Computer Engineering Department where the SAR course lives, for
his gentle and patient encouragement in the development of the
course and this text. I’m thankful to the Janney 2.0 program within
the Applied Physics Laboratory, which partially funded the writing of
this book, giving me a good deal of freedom to work on this text
during my work day. Their financial contribution to this book cannot
be understated; without it, I fear that the text would never have
been written.
I am also extremely grateful to my APL colleagues Mr. Chad
Hawes, Mr. Howard Schoeberlein, Dr. Chung-Fu Chang, Dr. Mark
Baker, Mr. Chris Watkins, Dr. Rick Chapman, Dr. Steve Scorpio, Dr.
Greg Avicola, Dr. Michael Nord, Dr. Eric Ericson, Dr. David Porter, Mr.
Eric Larsen, Dr. Chris Gifford, Dr. Rich Gasparovich, Dr. Christopher
Boswell, and Dr. Bob Henrick for their time, patience, and
understanding in helping me refine my knowledge of SAR through
discussion and application. I’m the sort of person who relishes
discussion and conversation among a large number of folks. It is, in
essence, how I learn. It typically involves a whiteboard (in the office)
and sometimes a bourbon (outside the office). Thanks to all of you
for providing such a supportive and educational working
environment. And thanks to my previous and current supervisors,
Ms. Cyndi Utterback and Ms. Anna Slowikowski. Their
encouragement and support played a significant role in the creation
of this book.
And to my editor, Ms. Lara Zoble at McGraw Hill, thank you for
your patience through this process. Without your guidance and
support, this text would not be possible. I want to extend my thanks
to my students who helped edit the text before it was sent to the
publisher, as well as to my intern, Ms. Danielle Hardy, who provided
valuable comments during the writing phase of the book.
I am indebted to both Riley Hansen and Larry Moore at ImSAR.
They provided system specifications for their airborne SAR platforms,
called NanoSAR Pods (NSPs), as well as example imagery from those
pods that they kindly granted me permission to reprint. Their fine
imagery is displayed on the front cover of this book. I’ve had the
pleasure of working with Riley and Larry performing data collections
“in the field.” Their willingness to help, to advocate, and to provide
cannot be understated. I am also grateful for imagery and support
provided by ICEYE. Their beautiful imagery also adorns this text. I
would also like to thank Capella Space Systems for their
contributions of imagery and system specifications to this book.
They are new to the SAR world and their recent successes produce
marvelous, beautiful, and useful imagery.
I am compelled to thank my family for their patience, support,
encouragement, and drive. My parents, Barbara and Bob, planted
the idea in my head that I could do anything, if I just tried hard
enough. I have worked hard not to prove them wrong and I am
eternally in their debt for encouraging that philosophy. In 1981, they
purchased my first computer, a Commodore 64. It started a love
affair with computers and algorithm development that burns hot in
me to this day. My sister, Rebecca, is an educator of fine young
women and men in the sciences. Her undying devotion to her
students is a shining light and a source of enlightenment and
encouragement to me. I thank her and her husband, Andrew, who
suffered through engineering school with me at the University of
Louisville, he as a civil engineering student and I as an electrical and
computer engineering student. And to their adult children, Ian and
Elaine, thanks for letting me be the cool yet nerdy uncle. To the
Walters—Granny, Grumpy, Ed, Erin, Cassie, Patrick, Tyler, Ronan,
Kira, and Megan—thank you for all of the support, encouragement,
and shared meals where the deeply dangerous question was asked,
“So what is it that you do, exactly?”
To Larry and John, thank you from the bottom of my heart. Your
support and encouragement were sometimes the only things
keeping me going.
Finally, to my grandparents, Edna, Robert Sr., Angela, and
Michael, thank you. No words could fully describe the positive and
loving impact you had on my life and my work. May all of you rest in
peace. This work is fully dedicated to your memory.

E. D. J.
 CHAPTER 1

Introduction to Synthetic
Aperture Radar

In this chapter, the very basics of radar will be presented, along with
the advantages to radar imaging over passive optical imaging and
some examples of existing synthetic aperture radar (SAR) sensors.
Additionally, the basic geometry model will be presented, along with
some of the terminology that is unique to SAR. Finally, the term
“synthetic aperture” will be defined, as well as why it is needed to
produce high-resolution radar images.

1.1 Introduction
Synthetic aperture radar1—typically abbreviated SAR, which can
cause confusion with the acronym for “search and rescue”—is a
strange beast. Few understand it’s value. To most, it’s a poor
substitution for an optical image.
Figure 1.1 shows a comparison of an optical image, shown at the
top of the figure, with a SAR image, shown on the bottom of the
figure.2 The SAR image appears “grainy” or noisy as compared to
the optical image. The SAR image is from TerraSAR-X, a German SAR
satellite. Both images have a ground sample spacing of 1.25 meters.
The concept of resolution in SAR is somewhat different than that of
optical imaging; this will be covered later in the book.
FIGURE 1.1 A comparison between an optical image (top) and a SAR image
(bottom). [Image credit: Merkle, Luo, Auer, Müller, and Urtasun (2017). Reprinted
under CC BY-SA 3.0.]

This comparison is a bit misleading. Optical sensors measure

incoming radiation in either the solar or thermal regions, making
them passive. SAR sensors measure incoming radiation in the radio
wave region; the incoming radiation is provided by either the SAR
sensor or another (sometimes noncooperative) radiation source,
making SAR an active sensing modality. This makes SAR a “24/7”
Another random document with
no related content on Scribd:
in the anterior vena cava, under the influence of the expiratory effort;
sometimes to emphysema, tuberculosis, etc.; in other cases to the
return of blood towards the vena cava and jugulars at the moment of
auricular systole, as a result of lesions of the tricuspid or auriculo-
ventricular orifices.
By palpation of the veins their permeability can be estimated, also
the degree of distension or obstruction, and the condition of their
contents.
Capillary system. Among methods of arriving at the state of the
circulatory system must be included an examination of the vascular
condition of the accessible mucous membranes, such as those of the
eye, mouth, nostril, vulva, etc. This examination is easy to carry out,
and is of value in diagnosing congestive states, pneumonia, and local
inflammation.
Blood. Examination of the blood is sometimes necessary for the
exact diagnosis of certain diseases, and therefore should be carried
out whenever occasion requires. The physical state, coloration, and
rapidity of coagulation afford valuable data in certain diseased
conditions, and indicate the approximate richness in hæmoglobin,
the normal or abnormal composition of the plasma, and the richness
of the blood in white corpuscles.
Microscopic examination is still more valuable, whether carried
out by the moist method, in which a drop of blood is compressed
under a cover glass, or the dry method with or without staining. In
the latter case the specimen is fixed with a mixture of equal parts of
alcohol and ether or by immersing it in a 1 per cent. solution of osmic
acid.
By this means it is possible to detect the condition of the red and
white blood corpuscles and hæmatoblasts; the existence or non-
existence of leucocytosis and its degree, as well as the existence, for
instance, of leucocythæmia.
The blood corpuscles may also be counted.
Histological examination, supplemented by suitable staining,
reveals the presence of normal or abnormal blood corpuscles,
parasites such as piroplasma, or microbes such as bacteria.
Such examination necessarily presupposes a knowledge of what
should be looked for in the normal state.
 In normal blood the red blood corpuscles predominate. They are
all similar in form and, with few exceptions, of the same size. They
stain strongly with acid solutions such as eosine. In pathological
conditions, large or giant corpuscles may be found (macrocytes), as
well as those of medium size (normal) and small size (microcytes).
Some are vigorous and stain deeply; others, on the contrary, are
degenerating or dead, and have no greater affinity for one
constituent than for another of the double or triple stains commonly
employed.
In pathological conditions the hæmatoblasts occur in very varying
numbers.
The white blood corpuscles found in health may be classified as
follows:—
Large and small lymphocytes, each of which has a round
voluminous nucleus and a narrow border, and contains a non-
granular protoplasm; their proportion varies between 22 per cent.
and 25 per cent.:
Polynuclear leucocytes or polymorphous leucocytes with a single
nucleus, which originate in bone marrow, stain best with neutral
colours, and are present in the proportion of 70 per cent. to 72 per
cent.:
Mononuclear leucocytes with an ovoid eccentric nucleus stain best
with basic colours, and form about 1 per cent.:
Polynuclear leucocytes stain best with eosine or acid colours, and
form about 1 per cent. to 2 per cent.
When these white blood corpuscles are in larger number the
condition is known as leucocytosis, and when one or other variety is
in very great excess the condition is known as leucæmia.
 CHAPTER I.
CARDIAC ANOMALIES.

ECTOPIA OF THE HEART.

Ectopia of the heart, i.e., congenital malformation in which the

heart is displaced from its normal position and thrust sometimes
completely beyond the thoracic cavity, is not very rare. The heart
may be well developed, but it is not enclosed by the thoracic walls
when the thoracic cavity closes during the first stages of embryonic
life. The sternum, which is cartilaginous and becomes ossified only at
a later period, remains fissured along the median line, and the
fissure, usually of oval form and with rounded margins, surrounds
the auricles and the vessels at the base of the heart. The ventricles
form a hernia projecting beyond the thorax, which then only contains
the two pleural sacs and a complete mediastinal partition. The
pericardium remains undeveloped.
Despite this malformation, the embryo develops. The fœtus may in
due season be brought forth living, but as a rule death occurs in a few
hours.
The diagnosis is easy, but this malformation cannot be treated.
All that can be done is to protect the ectopiated organ against
external violence in cases where the young creature is born alive.
 CHAPTER II.
PERICARDITIS.

Pericarditis consists in inflammation of the pericardial sac. It is

attributable to different causes, varying in importance and in
causation.
Specific pericarditis may be produced by the tubercle bacillus,
or it may develop during an attack of contagious peripneumonia.
Tuberculous or peripneumonic forms of pericarditis as a rule form
only complications of chronic pulmonary tuberculosis or
peripneumonia. They are very rarely primary in character, and, like
the allied forms of pleurisy, assume a vegetative and adhesive form
in tuberculous cases.
Moussu has never seen the true exudative form either in acute or
chronic tuberculosis, but only vegetative and caseous forms.
Simple acute pericarditis. Cases of simple acute exudative
pericarditis have been described, and have been referred to chills,
wounds, or injuries in the region of the heart, and in a few cases to
the rheumatic diathesis.
Such forms of pericarditis may occur, but probably are very rare,
for Moussu has seen but two cases. As the symptoms correspond
exactly to those of exudative pericarditis produced by a foreign body,
it is unnecessary to describe them specially.
The only important detail to bear in mind with this disease is the
possibility of cure by suitable treatment, such as the application of
stimulants or vesicants to the cardiac zone, the administration of
salicylate of soda or diuretics, and complete rest.
The diagnosis, moreover, should be confirmed by making an
aseptic exploratory puncture with the capillary trocar. The nature of
the liquid withdrawn will indicate whether the case is one of simple
acute pericarditis or pericarditis due to a foreign body.
Cancerous pericarditis is generally secondary, and is caused by
development of tumours on the pericardial serous membrane, and in
the myocardium. Moussu, however, has seen one case of primary
cancerous pericarditis, the tumours being found only on the
periphery of the myocardium. The growth assumes a vegetative form
with moderate exudation. The symptoms, however, so closely
approach to those of exudative pericarditis due to foreign bodies that
only the latter variety, which is by far the most frequent in animals of
the bovine species, need be described.

EXUDATIVE PERICARDITIS DUE TO FOREIGN BODIES.

This condition has been

erroneously described as
traumatic pericarditis, but
the latter term would
suggest that the disease was
due to an injury acting from
without. It may be defined
as a disease produced by the
discharge into the
pericardial cavity of some
foreign body from the
gastric compartments.
Boizy in 1858 described
several cases of this kind of
pericarditis. Hamon in 1866
gave an excellent table of
symptoms. Roy in 1875
supplemented this with
numerous observations
showing clearly the
possibility of recognising the
disease by clinical
Fig. 174.—Tumours of the surface of examination. Pericarditis
the heart. Primary cancerous due to foreign bodies is to-
pericarditis and myocarditis. day one of the best
characterised diseases of the
ox, and it is easy to diagnose.
Before approaching the etiological side of the question, it is
necessary to recall in a few words the anatomical arrangement of the
pericardium and its relations to neighbouring organs.
 In the ox the diaphragm presents a marked concavity directed
towards the abdomen. The pericardium, situated exactly in the
median plane, is fixed by its point to the sternum. A fold of adipose
tissue directly connects it with the anterior surface of the diaphragm.
On the abdominal side the conical right compartment of the rumen is
in free communication with the reticulum, which is closely applied to
the posterior surface of the diaphragm on the median line opposite
the spot occupied by the pericardium on the anterior surface (Fig.
176). As a result of this arrangement any object passing through the
reticulum and diaphragm in the median plane would enter the
pericardial cavity. These particulars indicate clearly how this form of
pericarditis is produced.
Causation. One of the chief causes of pericarditis by a foreign
body is connected with the way in which oxen feed. They rapidly
swallow their food and any foreign bodies that may be concealed in
it, submitting it later on to a second mastication in the course of
rumination. This method of feeding results in bolting the food almost
without mastication, hence the possibility of swallowing foreign
bodies.
The proximity of the reticulum to the pericardium is also an
important factor, because the foreign bodies fall into the reticulum as
soon as the bolus of food begins to break up. It is important to notice,
moreover, that pericarditis is commonest on farms where the oxen
are attended by women, or in regions where sharp objects are to be
found on roads or pastures frequented by the animals, such as the
vicinity of needle, nail, and rivet factories.
The sole cause is the penetration of a foreign body into the
pericardial sac.
Pathogeny. All kinds of foreign bodies are swallowed by oxen, as
is abundantly shown by post-mortem examinations. These
indigestible bodies pass with the food into the rumen, and
accumulate in the deepest portions of that receptacle. Owing to
physiological contractions the lower wall of the rumen rises to the
level of the orifice of communication with the reticulum, and so
passes much of the material accumulated within it into this organ.
Soft foreign bodies fall towards the lower parts of the reticulum,
but sharp objects may lodge in its walls. Very often the bodies
penetrate in this way without causing reticulitis or grave
inflammation. The functions of the reticulum are not impeded. The
commonest of such objects are needles, pins, nails, or fragments of
iron wire. On account of their form, needles are the most dangerous.
The sharpness of one extremity ensures its passing readily through
the tissues, and as the point is the part that offers least resistance,
the needle continues gradually to penetrate.
If the foreign body becomes implanted vertically in the lower wall
of the rumen or reticulum it may be expelled directly through the
medium of an abscess. This is a favourable termination, though it
usually results in permanent gastric fistula.
More often the objects penetrate the anterior wall of the reticulum
and gradually work their way towards the diaphragm, impelled by
the movements of the reticulum and the other digestive
compartments. They perforate the muscle and pass into the thoracic
cavity, either in the direction of the pericardium or of the pleural
sacs.
First as to the penetration of the pericardium. The foreign body,
whatever it may be, produces by its presence alone very marked
irritation, and as in addition it is always infected in consequence of
its having passed through the digestive compartments, inflammation
is set up to a degree proportionate to the pathogenic qualities of the
infective agent.
Symptoms. The early symptoms are those of indigestion, and not
of pericardial disease, a fact which is easy to understand, because at
first the whole mischief is in the abdominal cavity. The patients are
dull, restless, and seem to be suffering from an obscure ailment.
They remain standing more than usual, show more than ordinary
deliberation in lying down, lose appetite, cease to ruminate regularly,
and exhibit intermittent tympanites.
The cause of these symptoms is as follows: At first the reticulum is
partly immobilised by the local inflammation, and at a later stage
movement of the diaphragm is checked by reflex action when the
sharp body has progressed far enough to touch it. The rhythmic
movements of the reticulum and the diaphragm are interfered with,
rumination is disturbed, eructation ceases, and tympanites appears.
The patient often utters slight groans, particularly when forced to
move; but as this is a sign common to all grave diseases it can only
give rise to a suspicion as to what has occurred. In ten to fifteen days
this primary phase may have terminated; but it is impossible to say
how long it lasts, for it varies with each animal as with each variety of
foreign body, and it may be prolonged for months.
From the moment it reaches the thoracic cavity the foreign object
makes its way towards the channel formed on either side by the ribs
and below by the sternum, and therefore towards the point of the
heart. This is the second phase of development.
The passage of the foreign body through the diaphragm occupies a
more or less considerable time, depending on its length; the
beginning of this second phase is characterised by relative
immobility of the circle of the hypochondrium during respiration.
The abnormal sensibility and pain impede contraction of the
diaphragm.
Palpation of the region of the xiphoid cartilage then reveals
abnormal sensibility, and sometimes causes the animal to resent
being handled.
From this time the pericardial symptoms proper commence, the
foreign body having come in contact with the pericardium. This
phase, unlike those which precede it, presents well-defined
symptoms. The irritation of the heart and its ganglionic system by a
foreign body in the pericardium is shown by considerable
acceleration of the heart beats even before there is any exudation
into the pericardial sac. Instead of 60 to 70 beats, the normal
number, the pulse may rise to 80, 90, 100, or even 110 beats per
minute. The heart sounds are tumultuous, dull and ill-defined, while
the pulse appears bounding and strong.
But this period of cardiac excitement while persisting is soon
complicated by other symptoms. As soon as the foreign body
penetrates the pericardial sac, there is infection, which produces an
active form of inflammation and abundant exudation. From this time
the pulse becomes weaker and weaker, until, under the steadily
increasing pressure on the heart, it is almost imperceptible.
There is only moderate fever. As soon as the exudation becomes
considerable, the symptoms of pericarditis grow very marked: they
may be grouped in the following order, according to their
importance.
 A. Cardiac symptoms. On palpation of the cardiac zone on the
left the impulse of the heart is no longer felt. Percussion, which
under normal circumstances reveals only partial dulness, now seems
to give pain, and indicates abnormal dulness distributed in a vertical
plane. The pulmonary lobes between the pericardium and thoracic
walls are thrust upwards. The distended pericardial sac approaches
the parietal layer of the pleura and may adhere to it, hence the
dulness. This dulness extends as far back as the xiphoid appendix of
the sternum, and can be detected on both sides, marginated above by
a convex line.
In rare cases the dulness is absent, being partially replaced by
tympanitic resonance, due to the presence of gases in the distended
pericardial cavity, which gases originate in the digestive reservoirs or
result from putrid fermentation of the pericardial exudate.
Simple or double pleurisy, or even pneumonia of the cardiac lobes
resulting from infection by contiguity, may complicate cases of rapid
pericarditis. The dulness then appears modified, as do the signs
observed on auscultation.
Auscultation furnishes valuable indications. From the outset it
reveals acceleration of the heart. At a later stage, but only for a short
time, it permits of the detection of the pericardial rubbing sound
which precedes serous exudation, and which may persist for several
days when large quantities of false membrane are produced.
If exudate is present in considerable quantities a liquid sound is
heard at each heart beat. The heart appears to be beating in water,
but the liquid note varies considerably. It has been termed the
“claclaque” sound (Lecouturier, 1846), in allusion to the sound
produced by the meeting of water ripples; “clapotement” sound
(Boizy, 1858), with reference to the sound produced under the
influence of a light breeze on the borders of a stream; “glou-glou”
sound (Roy, 1875), suggested by the noise of liquid escaping from an
inverted bottle into a resonant vessel, etc. It is important, however,
to remember that cases occur (principally when the pericardium is
greatly distended and entirely filled with liquid) where, with the
animal at rest, these sounds are difficult to detect. To render them
noticeable the patient must be walked for a few yards.
Vernant, again, has described a sound as of dripping water, of
quite special character; he compared it to that resulting from the fall
of drops of liquid on to a marble table or into a half-filled vessel. So
far as can be ascertained this sound of dripping water greatly
resembles that heard in pneumo-thorax, but it is less resonant and
less prolonged.
It appears to be characteristic of the presence of air in the
pericardial cavity, and its special quality varies with the quantity
accumulated in the pericardium. Masked by these pericardial sounds
the beating of the heart seems dull, badly defined, distant and stifled.
B. Jugular
symptoms.
The “jugular”
symptoms are
secondary, and
result from the
accumulation of
liquid in the
pericardial
cavity. No intra-
pericardial
exudate can
exist without
exerting
pressure on the
heart, and as
the auricles
have very thin
walls and are
more
compressible
than the
ventricles, this Fig. 175.—Appearance of a patient suffering from
pressure fully-developed pericarditis.
immediately
causes difficulty
in the return circulation, whence venous stasis, varying in intensity,
but clearly visible and appreciable on account of the distension of the
jugulars.
 The venous stasis is general, for the pulmonary veins are as much
compressed as the posterior and anterior venæ cavæ, but it is only
apparent in the large superficial veins. This stasis is accompanied by
venous pulse, and particularly by peripheral or internal œdema,
œdema of the lung, intestine, mesentery, etc., of the submaxillary
space and of the dewlap and entrance to the chest. Œdema of the
submaxillary space is specially characteristic, for it appears almost
first amongst external signs. That of the dewlap follows at a later
stage, and extends backwards as far as the umbilicus, rising above
this point as high even as the entrance to the chest and the axillary
region.
C. Pulmonary symptoms. The pulmonary symptoms result
from difficulty in the return circulation and from the venous stasis.
They are due to passive congestion and œdema of the lung or to
hydro-thorax. At rest the respiration may appear fairly regular, but at
the least movement it is accelerated, and may rise to 40 or even 60
per minute.
Percussion reveals lessened resonance of the parts, and in the case
of hydro-thorax dulness marginated by a horizontal line, as in
pleurisy.
On auscultation the vesicular murmur may sometimes have
diminished or even disappeared, while the respiration may be
blowing, as in active congestion, and in exceptional cases a tubal
souffle may be observed. In most cases the animal has a paroxysmal,
somewhat frequent cough, due to reflex irritability of the pneumo-
gastric.
Cruzel in addition mentions a double respiratory movement like
that produced in the horse by broken wind. This is really the result of
hydro-thorax, and is not a constant symptom.
D. General symptoms. When the disease has lasted a certain
time the patients show certain well-marked general symptoms: they
remain standing in one position for long periods, with the head and
neck extended, the front legs thrust outwards from the trunk and the
body rigid, as though the least movement caused them pain. The
general attitude expresses anxiety, the animals lie down with great
care and seldom remain long in this position, which interferes with
the functions of the heart and lung. In the last stages the animals
remain constantly standing, appetite is almost entirely lost, and they
waste rapidly.
The course of pericarditis due to foreign bodies is very variable.
Sometimes death occurs in eight or ten days. In other cases the
animal may survive for weeks, provided it is well tended. Everything
depends on the rapidity with which the foreign body moves and on
the character of the infectious organisms which it introduces into the
pericardium. Death is the inevitable termination, and occurs as a
consequence of cardiac and respiratory syncope. It may follow
suddenly as the result of a simple forced movement, even when the
animal still seems to retain some amount of strength. When the
organisms introduced into the pericardium are of marked virulence,
complications such as septic pleurisy and pneumonia may be
observed, and death soon takes place.
It has been suggested that recovery might follow a return of the
foreign body towards the reticulum. This view can only have been
advanced as a consequence of errors in diagnosis, either as to the
existence of pericarditis or as to its nature. Pericarditis due to cold or
rheumatism sometimes becomes cured spontaneously.
Death, again, may suddenly occur by syncope when the foreign
body penetrates the myocardium, passes through it, and enters the
ventricular cavities.
The return of the foreign body is not conceivable, at all events after
it arrives in the pericardial cavity. Up to that time the only
disturbance is of a digestive character; no pericarditis exists. But
when for example the disturbance is due to long fragments of iron
wire which may extend from the reticulum as far as the pericardium,
it is clear that the pericarditis is of a kind which cannot be cured
without leaving traces. In our opinion, natural recovery is
impossible.
Diagnosis. The diagnosis of pericarditis cannot be made until
such pericarditis actually exists, i.e., until the disease has arrived at
the third stage of development mentioned above.
As long as the symptoms point only to the first or second stage, the
logical diagnosis is reticulitis produced by a foreign body. At this
time the development of pericarditis, although possible, is not
inevitable.
 When, on the other hand, one knows how the digestive
disturbance has originated and developed and thereafter notes signs
of cardiac irritation, disappearance of the cardiac impulse, dulness of
the heart sounds, venous stasis, etc., the diagnosis is easy even thus
early.
Mistakes are not very likely. Only in some cases are they liable to
occur, as in acute peripneumonia of the anterior pulmonary lobes,
causing compression of the pericardium of the anterior vena cava
and producing secondarily venous stasis and œdema of the dewlap.
Cases of specific pericarditis due to peripneumonia also occur, and
under such circumstances a mistake would be even more excusable.
Nevertheless, the temperature curve in itself is a sure indication, for
whilst in peripneumonia the fever is always very marked, it is
scarcely noticeable in pericarditis due to a foreign body.
When the diagnosis of pericarditis has been arrived at it is
desirable to determine the exact nature of the disease, for whilst
cases of pericarditis due to foreign bodies are incurable and in the
interest of the owner the animals should be slaughtered, pericarditis
due to cold or rheumatism may be successfully treated. Rheumatism
generally affects the synovial membranes even before it produces
pericarditis, and this indication, supplemented by the history of the
case usually ensures one against mistakes regarding the initial cause.
It is much more difficult to distinguish pericarditis due to a foreign
body from pericarditis due to carcinoma and from the forms of
pseudo-pericarditis produced by lesions in the neighbourhood of the
heart. When considering the latter we shall deal with this particular
point.
Prognosis. The prognosis is always fatal.
Lesions. When the foreign body is very thin and sharp, the
reticulum may not become attached to the diaphragm. In such cases
its passage has been rapid and the tissues have healed.
Usually the reticulum, diaphragm and pericardium are united by a
mass of fibrous tissue as thick as a man’s arm. It resembles a fibrous
sleeve surrounded by an œdematous zone, usually of slight extent.
This mass of new fibrous tissue is traversed by a sinuous tract
resulting from the irritant action of the foreign body on the
surrounding tissues. All writers describe this fibrous sleeve, which,
however, only occurs in cases where a very long foreign body has
occupied a considerable time in passing from the reticulum to the
cavity of the chest.
In very exceptional cases the sinuous tract is ramified, possibly as
a result of displacements of the foreign body.
The orifices of the tract are to be found, one in the reticulum, the
other in the pericardium. On the side of the reticulum there is never
more than one opening, and in many instances the tract is already
closed on that side, either by exuberant granulations or by a cicatrix.
On the contrary, the fistula is more frequently open in the
pericardial cavity. Its walls are of very varying appearance,
depending on their age: they may be red, greyish, soft or hard, and
when the lesion is of old standing they may have been converted into
a sclerotic tissue.
 Fig. 176.—Appearance of the lesions in a case of fatal pericarditis. P, inflamed
pericardium, distended with exudate and adherent to the neighbouring
pulmonary lobes; 1, posterior lobe; 2, cardiac lobe; 3, anterior lobe; Fp, pleural
false membranes.

The pericardium appears distended with a considerable quantity of

liquid of a special character—sometimes sero-sanguinolent,
sometimes almost or entirely purulent; sometimes yellowish, or
greenish-grey; sometimes frothy, inodorous, or very fœtid.
These characters depend on the nature and number of the germs
which have invaded the pericardial cavity. They also vary with the
gravity and number of the hæmorrhages produced by the action of
the foreign body on the myocardium.
The quantity of liquid also varies within very wide limits. There
may be scarcely any exudation. In that case the pericarditis is of a
partially adhesive character, with abundant false membranes. As a
rule the quantity of fluid exudation varies between seven and eight
quarts, but sometimes the quantity is much greater. Trasbot
described an instance in which the united weights of the heart and
pericardium exceeded 36 lbs. Hamon mentioned a case of
pericarditis in which the liquid exudate exceeded twenty quarts.
“When inflammation is first set up the liquid is serous, yellowish,
or reddish yellow. It contains fibrinous flocculi in suspension. Little
by little this exudate becomes purulent, whilst the internal layers of
the pericardial serous membrane undergo desquamation. These are
next covered with false membranes of varying appearance; the fibro-
albuminous exudation is wrinkled, villous and tufted. The two layers
of serous membrane are connected at certain points by this
exudation, the adhesions being sometimes very extensive. The
pericardial sac properly so called becomes the seat of marked
lardaceous thickening, due to inflammation. The heart appears
entirely covered with a layer of greyish or earthy-coloured
granulation tissue, which appears as though baked, and was
compared by Hamon to the back of a toad. It is atrophied as a
consequence of prolonged compression.
Under the influence of the eccentric pressure of the liquid the
pericardial sac is distended and comes in contact with the walls of
the chest, to which it may adhere. The foreign body, especially if
small, is not always easy to find.
The myocardium often displays interesting lesions. At first there is
thickening, or more commonly sclerous degeneration, of the
superficial layers covering the ventricles, and then appears a crop of
little miliary abscesses. Abscesses of considerable size have several
times been detected in the walls of the ventricles and in the
interventricular septum.
The foreign body, moreover, may not only injure the myocardium,
but may even perforate it completely and produce ulcerative
endocarditis (Cadéac). In this case infectious germs very rapidly
invade the circulation and all the tissues, and the animal dies of
pyæmia.
These essential lesions are accompanied by others of varying
importance. Thus the lung is congested throughout, and by
contiguity of tissue inflammation may extend from the pericardium
to the lower part of the pulmonary lobes and to the pleura.
 Interference with the return circulation induces lesions due to
venous stasis: dropsy of the chief serous membranes, œdema of the
connective tissue, pleural and peritoneal exudations, etc. If the hind
limbs never become swollen it is because the skin covering them is
very resistant and does not readily yield. The liver becomes
hypertrophied, congested and engorged with blood, and when the
animals live for some weeks, shows the appearances known as
cardiac or nutmeg liver.
Treatment. The treatment of pericarditis due to the presence of
foreign bodies is at present merely palliative. Often the only thing to
be done is to slaughter the animal.
We need not go back to the methods formerly recommended. All
are illusory or mischievous, such as the use of purgatives to arrest or
reverse the progress of the foreign body, removal of the foreign body
after opening the rumen, puncture of the pericardium, etc.
In 1878 Bastin successfully opened the pericardium and extracted
the foreign body through a window produced in the thoracic wall.
This operator recommends that after drawing the left limb forward
and incising the skin and muscles, the operator, with his hand bound
round with a cloth, should perforate the pleura, and then having
found the foreign body, proceed to extract it. By this method it seems
difficult to cause perforation of the pericardium, which would
certainly lead to the production of pneumo-thorax complicated with
fatal septic pleurisy.
It must be borne in mind that the two pleural sacs, right and left,
descend as far as the sternum (Fig. 173), and that it is not possible to
touch the pericardium directly without perforating the pleura.
Moussu has drained the pericardium through the pleura in the
hope of relieving the pressure on the heart and facilitating the
reabsorption of the œdema, in order to permit of the subsequent
slaughter of the animal, but has had unsatisfactory results. Lastly, he
has practised median trepanation of the sternum in the infra-
pericardiac region. Here again the operation is difficult, because of
the œdematous infiltration of all the substernal region, while it is so
dangerous to the patient, which must be cast and may suddenly
succumb, that it is of no use in ordinary practice.
 There is probably only one condition in which it would be possible
to attempt intervention with a fair chance of success, that is, when
there exists a fibrous connection between the pericardium, lung, and
wall of the chest on the right or left side.
In such cases aspiratory puncture or incision of the pericardium in
an intercostal space might prove of service, because it would not
expose the animal to the danger of pneumo-thorax.
The only difficulty lies in ascertaining beyond all question the
existence of such an adhesion before attempting operation, and this
is really very great, even having regard to the form of the dulness and
the absence of all respiratory sound in the lower third of the thoracic
cavity and cardiac zone. The pulmonary lobe between the heart and
chest wall may be thrust upwards and be partially adherent to the
pericardium and to the parietal pleura, and at the same time it may
be impossible to avoid producing operative pneumo-thorax when the
cartilages are resected to admit of incising the pericardium.
The only logical method seems to be puncture of the pericardium
through the xiphoid cartilage, as described below.
The topographical anatomy of the thoracic viscera shows that the
point of the pericardium extends along the sternum to a point close
to the lower insertion of the diaphragm, and that the pericardial sac
is only separated from the xiphoid region, or rather from the region
of the neck of the xiphoid appendix of the sternum, by the fatty
cushion at the point of the heart.
Fig. 177.—Lesions of exudative pericarditis produced by a foreign body. Relation of
the pericardium to the sternum and ensiform cartilage. Pericardium opened. D,
diaphragm; Œ, œdema of the dewlap, Ax, ensiform cartilage; F, liver; Vb, gall
bladder; 1, posterior lobe of the lung, drawn backwards; 2, cardiac lobe; 3, anterior
lobe; E, spot where the foreign body penetrated, towards the point of the
pericardium, between the neck of the ensiform cartilage and the circle of the
hypochondrium.

A glance at the annexed diagram (Fig. 177) will show this.

The diagram, carefully reproduced from an anatomical
preparation of an animal which succumbed to pericarditis, shows
that the distended pericardium extends close to the neck of the
xiphoid cartilage.
First stage. Identify the three following anatomical guiding
points:—
(1.) Xiphoid appendix and white line. (2.) Point at which the circle
of the hypochondrium becomes attached to the sternum. (3.) Point at
which the external mammary vein penetrates the abdominal wall
(Fig. 178).
Lines uniting these three points enclose a right-angled triangle,
which the operator must imagine to be bisected by a third line.
The incision, which should be about 8 inches in length, follows this
bisecting line at an equal distance between the white line and the
circle of the hypochondrium, to a point within about 8 inches of the
anterior margin of the mamma. All these points are readily
observable before the animal is cast.

Fig. 178.—Seat of operation for puncturing the pericardium by way of the ensiform
cartilage. L B, White line; H, line of the hypochondrium; V. M.a., anterior
mammary vein; P, point where the pericardium is punctured through the incision.

The cutaneous incision affords exit to large quantities of fluid, and

the pectoral muscles attached to the neck of the ensiform cartilage
can then be divided with the bistoury. The area of operation is thus
uncovered.
Second stage. The second phase comprises incision of the tissues
opposite the neck of the ensiform cartilage, about 8 inches in front of
the base of the triangle and at equal distances from the points Nos. 1
and 2; incision through the skin for a distance of 8 inches, and
dissection of the muscles of the ensiform region exposed at the neck
of the cartilage.