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Hypertension prelims 16/10/08 16:25 Página iii

An Atlas of Investigation and Management

HYPERTENSION
Edward D Frohlich
Alton Ochsner Medical Foundation
New Orleans, USA

Hector O Ventura
Alton Ochsner Medical Foundation
New Orleans, USA

CLINICAL PUBLISHING
OXFORD
Hypertension prelims 16/10/08 16:25 Página iv

Clinical Publishing
an imprint of Atlas Medical Publishing Ltd
Oxford Centre for Innovation
Mill Street, Oxford OX2 0JX, UK

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© Atlas Medical Publishing Ltd 2009

First published 2009

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted,
in any form or by any means, without the prior permission in writing of Clinical Publishing or Atlas Medical
Publishing Ltd

Although every effort has been made to ensure that all owners of copyright material have been acknowledged
in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought
to our attention

A catalogue record for this book is available from the British Library

ISBN-13 978 1 904392 15 6

ISBN-10 1 904392 15 6
ISBN e-book 978 1 84692 524 5

The publisher makes no representation, express or implied, that the dosages in this book are correct.
Readers must therefore always check the product information and clinical procedures with the most
up-to-date published product information and data sheets provided by the manufacturers and the most
recent codes of conduct and safety regulations. The authors and the publisher do not accept any
liability for any errors in the text or for the misuse or misapplication of material in this work

Project managed by Prepress Projects Ltd, Perth, UK

Typeset by Initial Typesetting Services, Edinburgh, UK
Printed by T G Hostench, s.a.
Hypertension prelims 16/10/08 16:25 Página v

Contents

Preface and a brief apologia vi

Abbreviations vii

Dedication viii

Introduction ix

1. Pathophysiology: disease mechanisms 1

2. Evaluation of the patient 15

3. Clinical pharmacology of antihypertensive agents 37

4. Uncomplicated essential hypertension 55

5. The heart in hypertension 73

6. The kidney in hypertension 89

7. Renal arterial disease 113

8. Concluding comments 123

Epilogue 125

Index 127
Hypertension prelims 16/10/08 16:25 Página vi

vi

Preface and a brief apologia

In a textbook of this nature, it is in order to provide the Another concern (as a past Editor-in-Chief of two major
prospective reader and potential reviewer with a brief journals and the author of several textbooks and many
overview of the goals, limits and editorial guidelines that we papers) was related to our selection of reference material.
set for ourselves in preparing the material for this atlas. In The purpose of this text was to present neither a literature
the Introduction we provide some personal remarks related review nor a current state of the art. We therefore chose to
to our agreement to organize and present our repertoire of provide ‘suggested reading’ so that the reader can consult in
visual material, but, perhaps, a few words might be in order the peer-reviewed literature the primary references for the
here to explain our selection. clinical and experimental material we use to support our
First, a number of friends and colleagues encouraged us to pictorial, tabular and diagrammatic material.
publish the material for many of our lectures over the years. With these comments, we sincerely hope that the atlas
Our publisher further supported these comments although material, the accompanying discussion and suggested
he raised the concern that some material and references reading are of value to the reader. We hope that this book
might seem to be dated. We agreed and exerted particular will be of value to readers who are clinicians and students of
effort to select only that pictorial and diagrammatic material hypertension and who are interested in the pathophysiology
which we strongly believed was currently pertinent for of hypertensive disease.
presentation and for pedagogic purposes.
Hypertension prelims 16/10/08 16:25 Página vii

vii

Abbreviations

ACE angiotensin-converting enzyme LV left ventricle

ACEI angiotensin-converting enzyme inhibitor LVH left ventricular hypertrophy
ARB angiotensin receptor blocker LVS left ventricular strain
AT angiotensinogen MAP mean arterial pressure
AV arteriolar–venular MI myocardial infarction
BB beta blocker L-NAME nitro-L-arginine methyl ester hydrochloride
CBC complete blood count NSAID non-steroidal anti-inflammatory drug
CCB calcium channel blocker PKD polycystic kidney disease
CHD coronary heart disease PRA plasma renin activity
CHF congestive heart failure PSA prostate-specific antigen
COPD chronic obstructive pulmonary disease PV plasma volume
CPV cardiopulmonary volume PWT pulmonary wall thickness
DBP diastolic blood pressure RA renal afferent
ECG electrocardiogram RE renal efferent
ERBF estimated renal blood flow RHD rheumatic heart disease
ESRD end-stage renal disease SHR spontaneously hypertensive rat
FF filtration fraction SBP systolic blood pressure
GFR glomerular filtration rate SNFF single-nephron filtration fraction
HCTZ hydrochlorothiazide SNGFR single-nephron glomerular filtration rate
HCVD hypertensive cardiovascular disease SNPF single-nephron plasma flow
HHD hypertensive heart disease SMA smooth muscle actin
IP3 inositol triphosphate TPR total peripheral resistance
ISA intrinsic sympathomimetic activity TSH thyroid-stimulating hormone
IVU intravenous urography UPE urinary protein excretion
WKY Wistar–Kyoto rat
Hypertension prelims 16/10/08 16:25 Página viii

viii

Dedication

We dedicate this textbook to our wives, Sherry Frohlich and added dimension to nurture family as well as our pro-
Laurie Ventura, and to our children, who share with us the fessional colleagues. This is the long-standing commitment
very honest and warm thirst for knowledge, whether in the of the well-rounded physician, and it is the obligation of all
medical or in other academic environments. It is this teachers and professionals to impart a better life to man
understanding of the need to impart one’s personal or within our professional careers.
professional knowledge and experience which provides an
Hypertension prelims 16/10/08 16:25 Página ix

ix

Introduction

Producing an atlas on hypertension was not at the forefront hypertensive patient; an elucidation of the mechanisms of
of my thinking until I was approached by Jonathan Gregory, action of the varied modes of therapy including non-drug as
commissioning editor at Clinical Publishing, who was well as pharmacological entities; and my personal overview
interested in publishing such a textbook. Indeed, in recent and investigative and clinical experience with two vital areas,
years, I have questioned the importance of hypertension as the heart and kidney in hypertension.
a discipline. Institutions such as mine no longer maintain a Most national and international guidelines present a
separate hospital service for admitting patients with the straightforward concept for the evaluation and treatment of
diagnosis of hypertension; and the numbers of patients with patients with hypertension; and they presently suggest a
primary problems relating to hypertension have diminished clear-cut course of action with respect to treatment unless
considerably. This is in striking contrast to the early days of there are complicating considerations. For the most part, we
my academic career, when a large majority of hospitalized agree with this presentation; but, of course, as is the case
patients were admitted with hypertensive emergencies or with most consultants, consideration must be focused on the
hypertension associated with myocardial infarction, patient in whom complicating factors suggest specific
congestive heart failure, angina pectoris, stroke or renal problems. To my way of thinking, the major areas that
involvement. Today, a patient with hypertension who is require more specific attention relate to the hypertensive
hospitalized because of myocardial infarction, acute patient with cardiac or renal involvement. Indeed, cardiac
coronary syndrome or renal failure is immediately sent to a and renal failure continue to increase in frequency despite
specialized unit. Yes, we have certainly come a long way over the reduction in deaths from stroke or coronary heart
the past five decades. disease and the fact that hypertensive emergencies are today
On the other hand, the number of patients with rather rare. Patients with hypertension who are hospitalized
hypertension continues to increase all over the world. with myocardial infarction or with end-stage renal disease,
Clearly, this is partly the result of what I have termed the as well as patients with an acute stroke, require very
‘numbers game’ of disease. That is to say, the limits of specialized hospital services. And so we are left with the
normal – whether of blood pressure, blood sugar need to consider in detail the heart in hypertension and the
concentration or body weight – continue to converge, and so kidney in hypertension. Both deserve very specific
the number of potential patients with hypertension or discussions in a textbook for the primary care physician or
diabetes mellitus or obesity continues to rise. And as a internist, cardiologist or nephrologist, all of whom deal with
consequence, the increasing attention demanded by these a large number of such patients who are not covered
diseases falls on the shoulders of the primary care physician, adequately by current clinical guidelines. Moreover, over the
and with this responsibility comes a greater need for a clear past few years I have on several occasions been invited to
understanding of the pathophysiology of these diseases and present my thoughts on this matter to such physicians, and
their management. Related to the increased attention these so I was convinced that now might be an appropriate time
diseases receive, and the increase in the number of such to share my personal thoughts in an ‘atlas’ format. It became
patients seen in any physician’s day-to-day practice, are apparent to me that in such a book I would be able to impart
remarkable innovations in diagnosis and management. And not only my personal clinical experience, but also the
so the subject arose of yet another textbook about hyper- ongoing work in my laboratories, which focuses primarily on
tension. I was won over by the need to confine the text to the heart and kidney. At this point in my thinking about the
just these subjects: classification of the disease; a clear subject, I discussed the merits of the task with my long-time
insight into the pathophysiology and initial evaluation of the friend and colleague, Hector Ventura. Hector convinced me
Hypertension prelims 16/10/08 16:25 Página x

x Introduction

of the potential ‘need’ for such an undertaking, and when he To complete our task we want to express our appreciation
‘volunteered’ to assist me I readily agreed. Thus, the to Jonathan Gregory for stimulating our thinking about how
concept and the format for this atlas of hypertension to present the very common problem of hypertension in the
developed and we thereupon began this job. practice setting. We also want to express our warm and
Not infrequently, we are invited to write a book review. heartfelt appreciation to our wives and children, first and
Often, one of the major pitfalls for an author is to clearly foremost, for their abiding understanding of our need to
identify what the book is trying to achieve; and so we were spend more time away from home and family in order to
very careful to ensure that we express our thinking clearly. meet yet another deeply personal commitment. It is to them,
We did not want to write a textbook that deals with the our dear families, that we dedicate this endeavour. In
hypertensive patient who presents with problems that con- addition, we want to express our appreciation to our office
stitute an emergency or those who require hospitalization in staff (Lillian Buffa, Caramia Fairchild and Pamella
a special care unit. Nor did we want to discuss the patient Tadesco), whose continuous support of our daily
whose demographic characteristics are such that specific professional activities permitted us to pursue yet another
chapters need be dedicated to a discussion of the role of the job.
patient’s age, race or gender, or the patient who suffers from It would be totally remiss of me not to mention a few
a new popular syndrome. In the final analysis, when the stumbling blocks that I encountered along the way during
physician is confronted by a particular patient, the relation- the preparation of this book: the sudden striking of
ship is one-on-one, and the decision about diagnosis and Hurricanes Katrina and Rita; the associated flooding and
therapy for that person is very specific and unique for that loss of my home and long-to-be remembered library
clinical situation. (including ‘saved’ copies of completed chapters on hard
Thus, we accepted Jonathan Gregory’s invitation and drives and disks), records and recollections; an enforced
presented to him our revised thinking. We proposed a evacuation from New Orleans to our daughter’s home in
textbook that would present our personal opinions about Chicago; and conversation and support from my son in New
hypertensive disease and its cardiac and renal complications Jersey whereby personal refocusing was made possible. And,
as it relates to everyday pathophysiological assessment and finally, I want to express my (our) appreciation to our
about the choice of therapy not only for the relatively colleagues and institution, who continue to provide the
uncomplicated patient but also for the frequently ambience and culture required to pursue an academic
encountered patient with complications affecting the heart dimension to the overall healthcare effort (especially in the
and kidneys. This material would, we believe, best be past difficult times).
presented as tables or figures that would hopefully clarify
our thinking on patient management as suggested by our Edward D. Frohlich, MD
clinical as well as laboratory experience. New Orleans, LA
May 2008
Hypertension ch1 16/10/08 14:51 Página 1

Chapter 1 1

Pathophysiology:
disease mechanisms

Introduction

Systemic arterial hypertension is one of the most common Moreover, hypertension is a key determinant risk for
cardiovascular diseases of industrialized populations. It premature cardiovascular morbidity and mortality end-
affects approximately 20% of adults in these societies, and a points (Table 1.2). It is, therefore, necessary to understand
much higher proportion in certain demographic groups (e.g. the nature of the disease pathophysiologically; by doing so,
blacks, the elderly). The disease is the major treatable risk it is then possible to conceive, develop, and select. This,
factor underlying coronary heart disease (Table 1.1), and then, is the mission of this atlas.
exacerbates and accelerates the atherosclerotic process.

Table 1.2 Complications and end-points promoted

Table 1.1 Risk factors underlying coronary heart
by hypertension that result in premature
disease
cardiovascular morbidity and mortality

Brain
Not treatable
• Haemorrhagic stroke
• Advancing age
• Thrombotic stroke
• Male gender
• Embolic stroke
• Black race
• Positive family history
Heart
• Angina pectoris involving coronary arterioles
Treatable
• Occlusive epicardial coronary arterial diseases
• Hypertension
• Congestive heart failure
• Hyperlipidaemia
• Left ventricular diastolic dysfunction
• Tobacco consumption
• Obesity
Kidney
• Diabetes mellitus
• Renal arterial disease
• End-stage renal disease
Unresolved (as to whether treatment reverses risk)
• Embolic renal disease
• Left ventricular hypertrophy
• Exacerbation of diabetic renal disease
• Hyperinsulinism
• Hyperuricaemia
Other hypertensive emergencies
• Indices of inflammation (e.g. C-reactive protein)
• Dissecting aortic aneurysm
• Accelerated and malignant hypertension
• Crisis from phaeochromocytoma
• Eclampsia
• Other pressor emergencies
Hypertension ch1 16/10/08 14:51 Página 2

2 Pathophysiology: disease mechanisms

The mosaic Altered haemodynamics

It was approximately 60 years ago that Irvine H. Page To understand the pathophysiological alterations associated
described his concept of the mosaic of hypertension (see with the systemic arterial hypertensive diseases, there must
Further reading). Inherent in his thesis was the belief that first be a clear-cut understanding of the haemodynamic
hypertension is multifactorial in causation. This is because alterations associated with a persistent elevation of arterial
all of the mechanisms that serve to control arterial pressure pressure. By definition, hypertension is a haemodynamic
in normal individuals as well as in those patients with disorder in which the elevated arterial pressure may be
hypertensive disease relate to each other in a kaleidoscopic associated with an increased cardiac output and/or total
fashion, each with the others. Thus, all mechanisms are peripheral resistance (11.2).
critical for maintaining homeostasis, physiologically or In most patients with essential hypertension, the elevated
pathophysiologically (1 1.1A, B ). arterial pressure is associated with an increased total
The factors depicted in Page’s mosaic clearly are not all- peripheral resistance. In some patients, however, an elevated
inclusive but serve to satisfy the underlying model cardiac output may also participate. The relationship
suggesting that many (if not most) diseases are multif- between arterial pressure, cardiac output, and total
actorial in causation. In the case of hypertension, the funda- peripheral resistance is discussed more extensively in
mental driving physiological purpose is to maintain normal subsequent chapters. However, when one considers the
tissue perfusion. In hypertension, this is accomplished at the magnitude of the elevated pressure, changes in blood
expense of an increased vascular resistance and, hence, the viscosity do not have major importance. Nevertheless,
elevated arterial pressure which is the primary clinical intravascular rheological changes may alter local tissue
characteristic of hypertensive disease. blood flow dynamics in the major target organs. Thus, it is
possible that some degree of increased viscosity promotes
changes in blood rheological characteristics which could

A B
Chemical Chemical
Racial Aging
Elasticity Reactivity Elasticity factors factors Reactivity

Hormonal Reno-
pressor
Tissue Tissue
Cardiac perfusion Vascular perfusion
(pressure/ Neural (pressure/ Volume
output calibre resistance)
resistance)

Sodium Excess

Neural Volume Cardiac Vascular

output Associated Sexual
diseases factors calibre
Viscosity Viscosity

1.1 Page’s mosaic theory of hypertension. A: the original theory; B: including additional factors as modified by the author.
Each of these (and other) factors interrelate with one another in order to maintain normal tissue perfusion in response to
an increasing vascular resistance and at the expense of the abnormally elevated arterial pressure. (Modified from Frohlich
ED: Clinical classifications of hypertensive diseases. In: Atherosclerosis and Coronary Artery Disease. V Fuster, R Ross,
E Topol (eds.). Lippincott-Raven, Philadelphia, 1996.)
Hypertension ch1 16/10/08 14:51 Página 3

Pathophysiology: disease mechanisms 3

exacerbate the haemodynamic alterations in the coronary, distributed throughout the various organ circulations. The
renal, and brain circulations. mechanism responsible for this resistance increase is an
For the most part, however, the increased total peripheral augmented vascular smooth muscle tone, primarily in the
resistance (or, in organ circulations, their corresponding precapillary arterioles, and accounts for the state of increased
vascular resistances) is the established haemodynamic arteriolar tone (i.e. arteriolar constriction) that is implicit in
hallmark of the hypertension and is more or less uniformly the multifactorial nature of the disease (Table 1.3).

Table 1.3 Active and passive mechanisms that alter vascular resistance

I. Constriction II. Dilatation

Active Active
• Adrenergic stimulation (i.e. increased neural input or • Acetylcholine
increased vascular responsiveness to normal neural • Nitric oxide
input) • Kinins: bradykinin, kallidin
• Catecholamines: norepinephrine (noradrenaline), • Prostaglandins (some)
epinephrine (adrenaline), dopamine • Catecholamines: low-dose epinephrine (adrenaline),
• Renopressor: angiotensin II dopamine
• Cations: Ca2+, K+ (high concentration) • Histamines
• Other humoral substances: vasopressin, serotonin, • Peptides (atrial natriuretic peptide, insulin, secretin,
certain endothelins, certain prostaglandins vasoactive intestinal polypeptide, parathormone,
calcitonin gene-related peptide, substance P,
Passive endorphins, enkephalins)
• Oedema: extravascular compression • Renal medullary phospholipid substance (medullin)
• Vessel wall waterlogging • Cations: K+ (low concentration), Mg2+
• Increased blood or plasma viscosity • Vasoactive metabolites: adenosine, Krebs intermediate
• Obstruction (proximal): thrombosis, embolus, metabolites, acetate
rarefaction
• Hyposmolarity Passive
• Temperature: cold • Reduced blood or plasma viscosity
• Increased plasma tonicity
• Hyperosmolarity
• Temperature: heat

Arterial pressure

Total peripheral resistance Cardiac output Viscosity

Organ/vascular resistances Heart rate Stroke volume Vessels Blood

Oragan 1 + organ 2 + organ 3 etc.

1.2 The haemodynamic concept inherent in hypertension.

Hypertension ch1 16/10/08 14:51 Página 4

4 Pathophysiology: disease mechanisms

This book emphasizes those mechanisms that have been clinical forms of hypertension. Consideration of the pertinent
related to essential hypertension, since this primary form of underlying pressor mechanisms in those secondary forms of
hypertension occurs in approximately 95% of all patients with hypertension provides a basis for a more comprehensive
systemic arterial hypertension. Moreover, this pathophysio- insight into the overall mechanisms that could participate in
logical discussion is also relevant to other (i.e. secondary) patients with essential hypertension (Table 1.4).

Table 1.4 Classification of the various forms of systemic arterial hypertension

Primary (essential) hypertension Renal parenchymal disease Drugs, chemicals, and foods
(hypertension of undetermined cause) • Chronic pyelonephritis • Excessive alcohol intake
• Borderline (labile) or ‘high normal’ • Acute glomerulonephritis • Excessive dietary sodium intake
hypertension or prehypertension • Chronic glomerulonephritis • Exogenously administered adrenal
(essential hypertension) • Polycystic renal disease steroids
• Essential hypertension: systolic • Diabetic nephropathy • Birth control pills
pressures >139 mmHg and diastolic • Others: amyloidosis, ureteral • Adrenal steroids for asthma,
pressures >89 mmHg obstruction malignancies, anabolic steroids
• Isolated systolic hypertension: • Liquorice excess (imported primarily
systolic pressures >139 mmHg with Hormonal disease from the Netherlands not synthetic
diastolic pressures <89 mmHg • Thyroid in USA, UK)
• Hyperthyroidism • Cold preparations:
Secondary hypertension • Hypothyroidism phenylpropanolamine, nasal
• Aortic coarctation • Hashimoto's thyroiditis decongestants
• Snuff and tobacco
Central nervous system diseases Adrenal cortical hypertension • Street drugs (e.g. cocaine)
• Increased spinal fluid pressure • Cushing's disease or Cushing's
• Tumours syndrome Complications from specific therapies
• Diencephalic syndrome • Primary hyperaldosteronism • Antidepressant therapy (tricyclic
• Bilateral hyperplasia antidepressants, MAO inhibitors)
Renal arterial disease (renovascular • Adrenal enzymatic deficiencies • Chronic steroid administration
hypertension) • Cyclosporine (transplantation and
• Non-atherosclerotic (fibrosing): Adrenal medullary hypertension (i.e. certain disease immunosuppressive
intimal fibroplasia, medial phaeochromocytoma) therapy)
fibroplasia, fibromuscular • Beta-adrenergic receptor agonists
hyperplasia, subadventitial Other endocrine (e.g. for asthma)
fibroplasia • Ectopic production of hormones • Radiation nephritis and arthritis
• Atherosclerotic (tumours) • Lithotripsy therapy for renal calculi
• Aneurysm(s) of renal artery • Growth hormone excess (e.g.
• Embolic acromegaly, gigantism) MAO, monoamine oxidase.
• Extravascular compression (of renal • Hypercalcaemic diseases (e.g.
artery): tumour, fibrosis hyperparathyroidism, milk-alkali
• Perinephric hull (Page kidney) syndrome, hypervitaminosis D,
• Exacerbation of diabetic renal metastatic bone disease, idiopathic
disease hypercalcaemia)
• Oral contraceptive-exacerbated
hypertension
Hypertension ch1 16/10/08 14:51 Página 5

Pathophysiology: disease mechanisms 5

Arteriolar constriction results in enhanced phosphorylation of myosin light chains.

Arteriolar (and, for that matter, venular) smooth muscle This increased calcium ionic milieu may be achieved either
tone is increased in hypertension, although all of the through an inflow of calcium ions through calcium- or
mechanism(s) responsible are not entirely known. No other receptor-activated membrane channels or by a release
doubt, this relates to the many pressor and depressor factors of calcium ions from intracellular organelles, although
that normally participate in regulating vessel tone and calcium may be released from the mitochondria or from
calibre and, hence, arterial pressure (Table 1.3). It follows binding with protein substrates through secondarily
that these factors also participate in the increased vascular activated biochemical processes. The net increase in
resistance in most patients with essential hypertension. intracytoplasmic calcium ion concentration promotes the
Lessons concerning regulation of increased vascular formation of inositol triphosphate (IP3) and diacylglycerol.
resistance have been learned from the variety of secondary IP3 serves as the second messenger, mediating the calcium
forms of hypertension in which specific pressor and ion release and the resulting mechanical coupling that
depressor mechanisms are involved (Table 1.4). permits an enhanced state of contractility of vascular
It is likely that the increased vascular resistance in most smooth muscle.
patients with essential hypertension may be mediated
through more than one pressor mechanism. Some of these Arteriolar structure
mechanisms are predetermined by inborn genetic factors, Another factor participating in the increased vascular
since it has become increasingly apparent that the resistance of hypertension is an increased wall-to-lumen
pathophysiological alterations in essential hypertension are ratio of the arteries and arterioles. This structural alteration
polygenetic in origin. Furthermore, many of the pressor and in hypertension serves to amplify the arteriolar responsive-
depressor mechanisms that seem to be operative have been ness to constrictor stimuli that maintains the hypertensive
well documented to increase actively vascular smooth disease process. Recent investigations have suggested that
muscle tone. Many new mechanisms are elucidated with the haemodynamic stress of vessel stretch may be an
each passing year. Thus, vascular smooth muscle tone is important additional mechanism responsible for the vessel
abnormally increased as a result of one or more of those wall thickening, or even of myocytic hypertrophy of the left
factors that participate in the underlying disease process and ventricle. Several reports have indicated that upon stretch of
are then expressed in the clinical manifestations of that the ventricular or arteriolar (e.g. renal, coronary) myocyte,
patient’s disease. As a consequence of the increased total one or more of a vast array of ‘early genes’ or proto-
peripheral resistance, arterial pressure rises in order to oncogenes participate in initiating DNA-directed myocytic
maintain tissue perfusion; this occurs at the expense of the and collagen (and likely other) growth. Some of these
vascular and cardiac systems, and the specific indices of growth factors are themselves vasoconstrictors (e.g.
organ damage and functional impairment that secondarily angiotensin II, norepinephrine [noradrenaline], endothelin),
result. and they may even be generated within the arteriolar or
As suggested in Tables 1.2 and 1.3, the increased tone of ventricular endothelium or wall itself. Intriguingly, they may
the arteriolar or venular smooth muscle occurs no matter also participate in the separate but related process of
what mechanism(s) participate. Thus, for example, the atherogenesis. Hence, this may explain the close relationship
vascular myocyte is constricted by enhanced adrenergic of these two common and comorbid diseases (i.e.
input or elevated circulating levels of catecholamines; hypertensive vascular disease and atherosclerosis).
alterations in circulating or local autocrine/paracrine effects
of humoral substances; local or systemic participation of Pre- and postcapillary constriction
vasoactive peptides (e.g. angiotensin II, endothelin); ions; For the most part, all patients with hypertension have an
and growth factors. Alternatively, increased vascular increased arterial pressure that is associated with an
resistance may also be produced by reduced local or increased contractile state of vascular smooth muscle in
systemic amounts of vasodilating agents, local vasoactive both the arterioles and venules. The movement of plasma or
peptides or ions, and vasoactive metabolites (Table 1.3). interstitial fluid across the capillaries follows Starling
Whatever the myocytic stimulus, there is a resultant rise in mechanics, and depends upon the hydrostatic and colloid
cytoplasmic free calcium ions from their resting state that osmotic pressures in the intravascular and interstitial
Hypertension ch1 16/10/08 14:51 Página 6

6 Pathophysiology: disease mechanisms

compartments, respectively (1 1.3). Additionally, the wall-to- 1.4). This intravascular volume redistribution phenomenon
(1
lumen ratio of the arterioles, which is increased in has been demonstrated clinically in patients with essential
hypertension, further increases vascular resistance and hypertension as well as in naturally occurring or other
arterial pressure (i.e. the Folköwian hypothesis). The experimental forms of hypertension. Thus, early in the
increased tone of the smooth muscle in the arteriolar wall is development of hypertension, systemic venoconstriction
responsible for the increased arteriolar constriction. As a may not be associated with intravascular volume contraction
result of the constriction and, consequently, the increased 1.4). However, as arteriolar and venular constriction
(1
total peripheral resistance and arterial pressure, left progresses, capillary hydrostatic pressure increases and
ventricular afterload increases pari passu, providing the circulating intravascular volume diminishes. This is
major haemodynamic determinant for the structural probably the consequence of two factors: movement of
ventricular adaptation of left ventricular hypertrophy and plasma from the circulation into the extravascular
the associated events of hypertensive heart disease. These compartment and renal excretion of some of the circulating
precapillary changes are associated with generalized volume as arterial pressure increases (i.e. the Guytonian
constriction of the postcapillary venules, which reduces total phenomenon of pressure natriuresis). The intravascular (i.e.
body venous capacity. The simultaneous events of arteriolar plasma) volume contraction results in other recognizable
and venular constriction relate to several pathophysiological factors (Table 1.5). Thus, as diastolic and mean arterial
phenomena and consequences of hypertensive disease (1 1.4). pressures or total peripheral resistance increase in
hypertensive patients with essential hypertension or with
Venoconstriction 1.5A , B , C)
renal arterial disease, plasma volume contracts (1
The reduced venous capacity resulting from postcapillary and renal parenchymal disease.
venular constriction diminishes the overall venular capacity In contrast, patients with parenchymal disease of the
of the peripheral circulation. As a result, the circulating kidney demonstrate an increased plasma volume as diastolic
intravascular volume is redistributed from the periphery to pressure increases (11.6) due to renal mechanisms subserving
the central circulation to increase venous return to the heart volume expansion.
(i.e. cardiopulmonary volume) and, hence, cardiac output

Colloid
Hydrostatic osmotic
pressure pressure
TPR CPV

Precapillary Postcapillary
arterioles venules
Interstitial fluid Capillary
PV

1.3. The four pressure determinants of transcapillary fluid 1.4. The role of pre- and postcapillary tone in regulating
migration elucidated by Starling. plasma volume. TPR, total peripheral resistance; PV,
plasma volume; CPV, cardiopulmonary volume.
Hypertension ch1 16/10/08 14:51 Página 7

Pathophysiology: disease mechanisms 7

32 25

Plasma volume (ml/cm)

22
21
20
20
Plasma volume (ml/cm)

19
15
18
17
16
90 100 110 120 130 140 150 160 170 180
15 Mean arterial pressure* (mmHg)
14
*MAP – diastolic BP + 1/3 pulse pressure
13 B
r = –0.468
12 P = <0.001
80

Total peripheral resistance (units)

80 90 100 110 120 130
Systolic arterial pressure (mmHg) 70
A
corrected for BSA
60
1.5 Relationship between plasma volume and arterial
pressure. Contraction of plasma volume in men with
50
essential hypertension as diastolic (A) or mean arterial
(B) pressures increase or as total peripheral resistance
40
increases in male hypertensive patients with essential
hyprtension or renal arterial disease (C).
30

20
–30 –25 –20 –15 –10 –5 0 5 10 15 20
Total blood volume (% normal)
C

Table 1.5 Clinically recognizable correlates of contracted

intravascular (plasma) volume

• Elevated haemoglobin concentration and haematocrit

• Increased plasma protein concentration (e.g. albumin, fibrinogen)
• Increased blood (and plasma) viscosity
• Hyperuricaemia
Hypertension ch1 16/10/08 14:51 Página 8

8 Pathophysiology: disease mechanisms

High haematocrit and haemoglobin Table 1.6 Forms of hypertension associated with
The higher haematocrit and haemoglobin levels in essential alterations of intravascular (plasma) volume
hypertension explain the clinical term ‘reactive’ or ‘relative’
polycythaemia. This entity is frequently detected in patients
with essential hypertension and was first described by Contracted plasma volume
Gaisböck at the turn of the twentieth century. Unlike • Increasing severity of essential hypertension
polycythaemia rubra vera, there is neither a leucocytosis or • 'High-renin' essential hypertension
thrombocytosis, nor is there associated splenomegaly. The • Renal arterial disease
elevated haemoglobin and haematocrit in Gaisböck
• Phaeochromocytoma
syndrome is classically described in the ‘ruddy’ patient with
essential hypertension with contracted plasma volume. This
relative increase in red cell mass with a reduced plasma Expanded plasma volume
volume has been measured in a large number of patients • Volume-dependent essential hypertension
with essential hypertension. In contrast, some patients have – Low plasma renin activity
a volume-dependent essential hypertension in whom the
– Hypertension in black patients
magnitude of plasma volume is directly related to the height
of arterial pressure (Table 1.6). • Steroid-dependent hypertension
This, then, provides an explanation why those patients – Primary hyperaldosteronism
with essential hypertension have plasma volume contraction – Cushing’s disease or syndrome
may lose effective control of arterial pressure when they are • Renal parenchymal disease (including end-stage
treated only with an adrenergic inhibitor or a direct acting, renal disease)
smooth muscle relaxing vasodilators (e.g. sodium
• Left ventricular failure
nitroprusside in the intensive care situation). Thus, plasma
volume expands as pressure is reduced with treatment and, • Patients with prior contracted plasma volume treated
under these conditions, blood pressure control can then be with smooth muscle vasodilators and alpha-
restored with diuretic administration. Indeed, this explains adrenergic receptor blocking agents
the phenomenon of ‘pseudotolerance’ (1 1.6).

A 185 B

175
Systolic blood pressure (mmHg)

Diastolic blood pressure (mmHg)

165 120

110
155
100
145
90
135
80

125 70

115
70 80 90 100 110 120 PV (% normal)
PV (% normal)

1.6 Expansion of plasma volume in patients with essential hypertension as systolic and diastolic pressures increase when
adrenergic inhibitors or direct-acting smooth muscle relax vasodilators are used.
Hypertension ch1 16/10/08 14:51 Página 9

Pathophysiology: disease mechanisms 9

Oedema hydrostatic pressure in patients with hypertensive

A second clinical example of coincident pre- and nephrosclerosis (i.e. the Brenner hypothesis). Thus, both
postcapillary vasoconstriction may be demonstrated in those afferent and efferent glomerular arteriolar constriction
patients with severe hypertensive retinopathy. It provides an occurs in patients with prolonged systemic arterial hyper-
explanation for the transudation of protein through the tension, with renal parenchymal involvement favouring
retinal capillary bed in patients with accelerated elevated glomerular hydrostatic capillary pressure,
hypertension as well as those with papilloedema associated glomerular ultrafiltration of protein, and consequent
with malignant hypertension (see Chapter 2). A third hyalinosis and glomerulosclerosis. With therapeutic
example relates to development of oedema in patients reduction of afferent and efferent arteriolar resistance (with
receiving calcium antagonists. This oedema is the angiotensin-converting enzyme inhibitors or angiotensin II
consequence not of renal-mediated fluid retention but, receptor blockade), glomerular hydrostatic pressure will also
rather, of the potent drug-induced precapillary arteriolar diminish in association with reduced filtered protein and
dilatation associated with reflex postcapillary constriction. reversal or inhibition of further progression of glomerular
This is particularly experienced with prolonged standing or sclerosis (see Chapter 6). These findings provide credibility
when seated for a long time with the legs dependent. to the concept that angiotensin II participates in the
progression of nephrosclerosis in essential hypertension as
High cardiac output hypertension well as in diabetic renal disease; they also strongly suggest
A fourth example of the phenomenon of pre- and post- that inhibition of angiotensin II confers significant benefit to
capillary constriction provides, in part, a pathophysiological these patients.
explanation for the increased cardiac output and hyper-
dynamic circulation observed during development of Fluid volume partitions
essential hypertension. Thus, early in the elaboration of As originally postulated by Starling, local haemodynamic
hypertension (i.e. patients with borderline or ‘labile’ and other pressure alterations are responsible for the
hypertension), when blood pressure is elevated only at times movement of water across the major body fluid
but is normal at other times, cardiac output is increased. compartments (1 1.3 ). These factors include the local
This increased output is related to the translocation of the capillary hydrostatic and local tissue pressures as well as the
circulating intravascular volume from the periphery to the protein oncotic pressures, intravascularly and extra-
central circulation as a result of the postcapillary (i.e. vascularly. In general, total body water is normal in essential
venular) constriction. Although the total peripheral hypertension and seems to be normally distributed between
resistance at this stage is said to be ‘normal’, it has been the extracellular and intracellular fluid compartments.
suggested that it is ‘inappropriately so’, since, should cardiac However, although there is much epidemiological evidence
output become elevated to the same extent in normotensive suggesting deranged sodium handling in patients with
individuals, their total peripheral resistance would be slightly hypertension, there is little evidence supporting the concept
reduced. With progression of the hypertensive vascular that total body sodium is increased in hypertensive disease
disease and, as the pre- and postcapillary vasoconstriction or that it is associated with expanded total body water or,
increase further, the intravascular (i.e. plasma) volume even, increased blood pressure sensitivity. In contrast,
progressively contracts as described above. This contraction emerging data suggest other effects of sodium excess on
in circulating intravascular volume proportionally heart, aorta, kidney, and vessels. In addition, there is good
diminishes the cardiopulmonary volume, decreases right clinical investigative evidence that the extracellular fluid
atrial venous return and, thus, the cardiac output is reduced volume may be maldistributed in hypertension. Thus, as
to a more normal level than the output observed earlier in intravascular (i.e. plasma) volume becomes contracted in
the disease. patients with essential hypertension, it may be associated
with greater interstitial fluid volume. This movement of
Nephrosclerosis fluid from the intravascular to the extravascular (including
A fifth example, which has more recently become appreci- interstitial) fluid compartments has specific pathophysiological
ated clinically, relates to the increased intraglomerular implications (1 1.7).
Hypertension ch1 16/10/08 14:51 Página 10

10 Pathophysiology: disease mechanisms

(i.e. salt) loading. The major problem lies in the elusive

Body fluid compartments
ability to define just which patients with essential hyper-
Extracellular Intracellular
tension are sodium sensitive and those which are not. The
Plasma best proof in the individual patient is to restrict sodium
RBC Interstitial
intake to see if blood pressure becomes reduced. The sub-
ject currently remains one of great controversy. As we
59Fe describe later, salt excess is associated with structural and
functional derangements of the target organs of the disease.
51Cr

T1824 Hormonal alterations

Because of the controversial role of sodium in essential
131I
hypertension, many studies have focused upon the role of
Inulin adrenal corticosteroids and their regulatory genes in the
Substances used

SO4 pathogenesis of hypertension in at least some patients.

82Br There have been very few patients with essential
42K
hypertension who have demonstrated an abnormality of
24Na
steroidal mechanisms underlying the hypertension disease
D 2O process. In general, aldosterone seems to be synthesized,
THO released, and excreted in proportion to the levels of
Antipyrine stimulation of the renin–angiotensin system in patients with
essential hypertension; there does not seem to be any clear-
cut derangement in adrenal steroid biosynthesis in such
patients. In those patients with abnormalities in steroidal
biosynthesis and release, the derangements are due to
1.7 Extracellular and intracellular body fluid compartments specific adrenal diseases (Cushing’s syndrome and disease,
and the various labels used to determine them primary hyperaldosteronism, hydroxylase and other enzyme
quantitatively. deficiencies). Recent studies in many of these secondary
hypertensions have demonstrated specific genetic enzymatic
abnormalities that account for the steroidal defect.
Hormonal alterations have been demonstrated in other
Sodium metabolism patients with hypertension (Table 1.4).
As suggested above, many epidemiological studies have
demonstrated a direct correlation between the magnitude of Neural mechanisms
dietary sodium intake and the prevalence of hypertension in The autonomic nervous system normally participates in the
many populations. Other studies have shown that in those control of arterial pressure; this role may be altered in
societies with daily sodium dietary intakes of <60 mmol patients with essential hypertension. One would normally
(mEq), hypertension is practically non-existent and these expect that, as arterial pressure increases, heart rate should
populations fail to show a rise in arterial pressure with slow. However, most patients with essential hypertension
ageing. Furthermore, still other epidemiological studies demonstrate a faster resting heart rate than normal. This is
have demonstrated that there may be genetically determined but one manifestation of the phenomenon of the ‘resetting’
alterations in sodium transport across cell membranes in or altered baroreceptor sensitivity in hypertension. In
different populations of patients with essential hypertension. addition, increased release, sensitivity, and excretion of
Notwithstanding the abundance of the above epidemi- norepinephrine (noradrenaline) has been repeatedly
ological data supporting an important role for the sodium demonstrated in patients with essential hypertension and,
ion in essential hypertension, there is a relative paucity of more frequently, in patients with borderline or earlier stages
pathophysiological data confirming this thesis clinically. of the disease. These findings have been supported by the
Indeed, only about one-third of patients with hypertension demonstration of increased serum catecholamine con-
demonstrate increased pressure responsiveness to sodium centration in proportion to the altered haemodynamics in
Hypertension ch1 16/10/08 14:51 Página 11

Pathophysiology: disease mechanisms 11

these patients. The elevation of serum catecholamine normal levels in patients with essential hypertension but not
concentration in these patients, however, is not nearly as in those with phaeochromocytoma.
high as in patients with phaeochromocytoma.
It is of interest that in patients with less severe essential Renopressor system
hypertension, particularly those with a hyperdynamic beta-
adrenergic circulatory state (with or without idiopathic The enzyme renin is released from the juxtaglomerular
mitral valve prolapse syndrome), serum norepinephrine apparatus of the kidney through several mechanisms (Table
(noradrenaline) concentration is frequently elevated. This 1.7). Renin acts on its circulating peptide substrate
finding provides one explanation for the altered haemo- angiotensinogen, produced in the liver, resulting in the
dynamic findings as well as the augmented myocardial generation of the pressor octapeptide angiotensin II (1 1.8). The
contractility, the idiopathic mitral valve prolapse, and the octapeptide apparently generates other peptides whose actions
associated cardiac dysrhythmias. In general, there have been are under active investigation. Angiotensin II has a number of
no alterations reported in catecholamine biosynthesis or in sites of action, most notably in blood vessels and adrenal
release or reuptake of these substances, although increased cortex, to produce vasoconstriction and aldosterone release,
responsiveness of beta-adrenergic receptor sites has been respectively. In addition, angiotensin is also generated locally
reported (see Chapter 5). Furthermore, the reported altered in heart, vessels, kidneys, and other organs with specific local
responses to upright tilting, Valsalva manoeuvres, and actions (Table 1.8). The precise roles for these local systems are
tyramine stimulation of norepinephrine (noradrenaline) not yet clearly known but intracellular generation of
release from nerve endings may provide a useful indication angiotensin II affects muscle protein synthesis, with inherent
of adrenergic neural participation in certain patients with implications relating to the development or reversal of vascular
essential hypertension. and ventricular hypertrophy. Local generation of angiotensin
Several years ago, the clonidine suppression test was II may be of particular importance in: (a) the function of the
introduced to differentiate patients with phaeochromo- cardiac or arteriolar myocyte which produces the peptide (an
cytoma from those patients with essential hypertension (who intracrine function); (b) the effect on neighbouring cells (an
demonstrate smaller elevations of plasma catecholamines). autocrine function); or (c) association with other hormones
Clonidine (a centrally acting adrenergic inhibitor) admini- (e.g. kinins, catecholamines, atrial natriuretic peptide,
stration will suppress elevated catecholamine levels to endothelin) within that organ (a paracrine function) (1 1.9).

Table 1.7 Mechanisms of increased Table 1.8 Sites of action of angiotensin II

renin release from the kidney

Site Action
• Reduced renal blood flow and/or Vascular smooth muscle Vasoconstriction
perfusion pressure Adrenal medulla Release of catecholamines
Adrenal cortex Aldosterone
• Contracted intravascular volume
Medulla of brain Thirst
• Dietary sodium restriction (<100 mmol Medullary centres Augment adrenergic outflow
[mEq]/day) Paravertebral ganglia Augment norepinephrine
• Increased beta-adrenergically mediated (noradrenaline) release
neural input Local synthesis of angiotensin II in:
• Reduced aldosterone levels in blood Heart Myocytic hypertrophy, fibrosis,
• Upright posture apoptosis
Brain Adrenergic outflow
• Hormones or humoral agents (e.g.
Arteries Myocytic hypertrophy, fibrosis
catecholamines)
Other organs (uterus, liver, To be resolved
• Drugs (e.g. diuretics) salivary glands)
Hypertension ch1 16/10/08 14:51 Página 12

12 Pathophysiology: disease mechanisms

Liver

Angiotensinogen Kidney

Renin

ACE2
Angiotensinogen I Angiotensinogen 1–9

Angiotensin-
Bradykinin ACE1 converting
enzyme (ACE1) ACE ACE1

Inactive fragments
ACE2
Angiotensinogen II Angiotensinogen 1–7

AT1 AT2 AT4

Receptors

Local systems

Vascular
smooth
muscle Heart
Brain
Adrenal
medulla

Other
organs

1.8 Generation of angiotensin II: the classical endocrine renin–angiotensin system.

Measurement of plasma renin activity (PRA) has hypertensive diseases including renal arterial disease and
important clinical implications not only in the classification steroidal forms of hypertension (see Chapters 2, 6 and 7).
of patients with essential hypertension, but in other Much interest has been engendered in recent years about
Hypertension ch1 16/10/08 14:51 Página 13

Pathophysiology: disease mechanisms 13

10
9
8
7
Endocrine Endocrine 6
5

Intracrine 3

PRA (ng/ml)
1
9
8
7
6
5
Paracrine/autocrine 4

1.9 Systemic and local renin–angiotensin systems.

2

the role of the renin–angiotensin system in patients with 1

essential hypertension. Laragh and his colleagues have 70 75 80 85 90 95 100 105 110 115 120
Blood volume (% normal)
suggested that patients with essential hypertension may be
classified (or ‘profiled’) according to the levels of PRA,
expressed with respect to 24-hour sodium excretion. PRA 1.10 Plasma renin vs. blood volume in normal men and
can be increased in those patients with reduced dietary men with essential hypertension.
sodium intake (<100 mmol [mEq]) and, conversely, PRA
will be reduced in those patients with excessive dietary organs, but also may modify the actions of other blood- or
sodium intake. This categorization has been used not only neurally borne or local substances. In this fashion, certain
conceptually with respect to the pathophysiological agents may exert their physiological actions most subtly by
alterations, but also for selecting antihypertensive therapy acting in concert with other substances. It is well known, for
on a physiological basis. Thus, those patients with high PRA example, that angiotensin II can augment or amplify
may be at increased risk of premature cardiovascular events, adrenergic function by its interaction with norepinephrine
stroke, other morbidity, and death. In contrast, those (noradrenaline) at certain brain centres, as well as at
patients with low PRA may be at less risk. No precise peripheral ganglionic or postganglionic sites. Angiotensin
physiological mechanism has been offered to explain this may also interact with kinins and prostaglandins in kidney,
association. However, it is known that the higher the arterial with atrial peptides at nerve endings, on the cardiac myocyte
pressure and the more severe the vascular disease, the at the vascular smooth muscle membrane, and with other
greater will be the total peripheral resistance. Consequently, peptides (e.g. endothelin, neuropeptide Y, substance P) at
a more contracted intravascular volume will result, and the the vascular smooth muscle membrane or intracellularly.
more contracted the intravascular volume, the greater will Another possible example of this modulatory cardiovascular
be the PRA (1 1.10). With contraction of intravascular action occurs with L-arginine, nitric oxide, and bradykinin at
volume, blood and plasma viscosities also increase; this the endothelial level to alter local haemodynamic functions.
could be expressed on a microcirculatory level in the Endothelial dysfunction (i.e. impaired nitric oxide synthesis)
coronary or cerebral circulation by augmented protein occurs in hypertension, cardiac failure, atherosclerosis,
concentration (including fibrinogen levels) and, hence, obesity, diabetes mellitus, ageing, cigarette smoking,
greater predisposition for thrombosis. hyperlipidaemia, and in postmenopausal women not
It is particularly pertinent at this point to consider that receiving oestrogen replacement therapy. These dysfunctions
hormones, vasoactive substances, and other chemicals and may be modified by agents that are used to manage these
growth factors not only act at their own ‘classical’ target conditions and, hence, may reverse endothelial dysfunction.
Hypertension ch1 16/10/08 14:51 Página 14

14 Pathophysiology: disease mechanisms

Further reading

Ross RC, Bowen-Pope DP, Raines EW: Platelets, Dunn FG, Chandraratna P, de Carvalho JGR, Basta LL,
macrophages, endothelium, and growth factors. Their Frohlich ED: Pathophysiologic assessment of
effects upon cells and their possible roles in atherogenesis. hypertensive heart disease with echocardiography. Am. J.
In: Atherosclerosis. KT Lee (ed). Annals N.Y. Acad. Sci. Cardiol. 1977;3 39:789–795. These three references are clinical
1985;4 454:254–260. The first report demonstrating that the pathophysiological studies describing the development of labile
initial functional derangement of the ventricle (myocytic and essential hypertension. The third reference provides that
stretch) initiates the process of hypertrophy through stimulating first support to the former discussions on the clinical, structural,
DNA-mediated protein synthesis. It provides a model for and functional progression of hypertensive heart disease.
many subsequent studies. Tarazi RC, Dustan HP, Frohlich ED, Gifford RW Jr,
Libby P, Warner SJC, Salomon RN, Birinyi LK: Production Hoffman GC: Plasma volume and chronic hypertension.
of platelet-derived growth factor-like mitogen by smooth Relationship to arterial pressure levels in different hyper-
muscle cells from human atheroma. N. Engl. J. Med. tensive diseases. Arch. Intern. Med. 1970;1 125:835–842.
1988;3 318:1493–1498. Tarazi RC: Haemodynamic role of extracellular fluid
Sarzani R, Arnaldi G, Takasaki 1, Brecher P, Chobanian volume. Circ. Res. 1976; 38(Suppl 11):73–83.
AV: Effects of hypertension and aging on platelet-derived Dustan HP, Tarazi RC, Frohlich ED: Functional correlates
growth factor and platelet-derived growth factor receptor of plasma renin activity in hypertensive patients.
expression in rat aorta and heart. Hypertension Circulation 1970;4 41:555–567. These three references are
1991;1 18(Suppl. 111):93–99. studies that develop the concept of fluid volume alterations in
These two references provide excellent discussions on how local clinical hypertensionand the functional correlates of PRA in
vascular growth factors participate in atherogenesis. Most patients with essential hypertension.
interestingly, these mitogenic factors in atherosclerosis may be Sealeyj E, Laragh JH: The renin–angiotensin–aldosterone
the same factors that participate in hypertension, thereby system for normal regulation of blood pressure and
offering a conceptual explanation as to how one disease sodium and potassium homeostasis. In: Hypertension:
exacerbates the other. Pathophysiology, Diagnosis, and Management. JH Laragh,
Page IH: Hypertension Mechanisms. Grune and Stratton, BM Brenner (eds). Raven Press, New York, 1990,
Orlando, FL; 1987. pp.1287–1317.
Page IH: Pathogenesis of arterial hypertension. ].A.M.A. Bühler FR, Laragh JH, Baer L, Vaughan ED Jr, Brunner
1949;1 140:451–458. HR: Propranolol inhibition of renin secretion: a specific
Frohlich ED: (State of the Art): The first Irvine H. Page approach to diagnosis and treatment of renin-
lecture: The mosaic of hypertension: past, present, and dependent hypertensive diseases. N. Engl. J. Med.
future. J. Hypertension 1988;6 6(Suppl. 4):S2–S11. These 1972;2 287:1209–1214. These references introduce the concept
three references provide discussions on the mosaic concept of and therapeutic rationale for the profiling of PRA in
Page relating to the multifactorial nature of hypertension and hypertension.
left ventricular hypertrophy. Alderman MH, Madhavan S, Ooi WL, Cohan H, Sealey JE,
Frohlich ED, Apstein C, Chobanian AV, et al.: The heart in Laragh JH: Association of the renin sodium profile with
hypertension. N. Engl. J. Med. 1992;3 327:998–1008. the risk of myocardial infarction in patients with
Summary of the heart in hypertension by working group of the hypertension. N. Engl. J. Med. l991;3 324:1098–1104. This
National Heart, Lung, and Blood Institute. reference and Bohler et al. (1972) profile PRA to hypertensive
Frohlich ED, Kozul Vj, Tarazi RC, Dustan HP: outcomes.
Physiological comparison of labile and essential
hypertension. Circ. Res. 1970;2 27(l):55–69.
Frohlich ED, Tarazi RC, Dustan HP: Clinical-physiological
correlations in the development of hypertensive heart
disease. Circulation 1971;4 44:446–455.
Hypertension ch2 16/10/08 14:56 Página 15

Chapter 2 15

Evaluation of the patient

Introduction Family history

As with all clinical problems, it is essential to evaluate the One striking feature of the concept of hypertension as a
patient thoroughly before considering management and multifactorial disease is the presence of a strong family
treatment. If therapy is initiated before overall clinical history of hypertension in some patients. When there is a
evaluation has been performed, important clues may be family history of hypertension or of premature
obscured. Consider, for example, the patient with systemic cardiovascular death, the likelihood of secondary forms of
arterial hypertension currently taking as simple a treatment hypertension may be less (Table 2.2). However, should any
as a thiazide diuretic. Associated metabolic changes may of the secondary forms of hypertension be established, it is
distort the clinical picture, including biochemical and possible that the patient may also have essential
cardiovascular risk factors (Table 2.1). This chapter hypertension, since the latter is present in about 20% of the
considers important clues that may be obtained from a overall population. Hence, it is important to search for and
careful personal and family history, physical examination, control other important cardiovascular risk factors,
and basic laboratory evaluation. particularly in patients with a family history of premature
death (Table 2.3). Should hypertension occur in both
Table 2.1 Biochemical and other risk factors parents, there are additional considerations; since
affecting patient evaluation when receiving a hypertension is a polygenetic disease, there is a greater
thiazide diuretic likelihood that the disease may be more complex and severe.

Biochemical
• Increased serum concentration of:
– Creatinine
– Glucose
– Cholesterol Table 2.2 Clues suggesting a diagnosis of
– Uric acid secondary hypertension
– Calcium
• Decrease serum concentration of: • Absence of a family history of hypertension
– Potassium • Sudden onset of hypertension in a child or older adult
– Magnesium
• Sudden appearance of an elevated pressure when
pressure had been well controlled previously
Other risk factors
• Diabetes mellitus • Appearance of refractoriness to previous effective
• Hyperlipidaemia antihypertensive therapy
• Hyperuricaemia • Physical examination findings or abnormal laboratory
• Hypertension, curable causes findings suggestive of a secondary cause of
• Elevated serum C-reactive protein hypertension
Hypertension ch2 16/10/08 14:56 Página 16

16 Evaluation of the patient

Table 2.3 Important factors in the family history Table 2.4 Symptoms of hypertension related to
target organ involvement

Family history of premature death from

Brain
• Myocardial infarction
• Transitory episode(s) of sensory or motor deficit
• Heart failure
• Dizziness, fainting, vertigo
• Stroke
• Sudden loss of vision (total or part of visual field)
• Kidney failure
• Sudden lancinating vertical headache (ruptured
aneurysm)
Coexistent risk factors with hypertension
• Transient sensory motor or speech defects
• Atherosclerosis
• Obesity
Cardiovascular
• Diabetes mellitus
• Diminished exercise tolerance
• Hypercholesterolaemia or other hyperlipidaemias
• Easily fatigued
• Gout
• Palpitations
• Smoking
• Feeling of 'skipped heartbeats'
• Physical inactivity
• Faster heart rate that persists after exercise ceases
• Microalbuminuria
• Chest pain, even in the absence of occlusive coronary
• Age (male ≥55 years; female ≥65 years)
disease
• Black race
• Shortness of breath
• Peripheral oedema
• Heat intolerance or facial or upper chest flushing
• Florid complexion (Gainsböck’s syndrome) associated
with increased haemoglobin, haematocrit
• Slow to heal skin ulcerations

Kidney
• Nocturia – diminished renal concentrating ability
• Flank pain – suggests renal arterial disease, stones,
cystic disease
Clinical history • Haematuria – arterial disease, glomerulonephritis,
cysts, stones
In most patients with systemic hypertension there are • Appearance of 'foamy' urine
generally no clinical manifestations other than elevated • Sudden flank pain with or without haematuria
systolic and/or diastolic pressures. Therefore, unless blood
pressure is measured in all patients, hypertension will
remain unrecognized and untreated, and there will be no
further improvement in the control rates of hypertensive Physical examination
disease in any given population.
The most common symptoms traditionally related to Blood pressure measurement
hypertension have been fatigue, headache and epistaxis, but Hypertension cannot be controlled and its complications
these symptoms are among the most common complaints cannot be prevented if blood pressure is not routinely
offered by any patient seeking medical attention. However, measured and properly obtained during every physical
when other symptoms are present, they are more likely to be examination. This should be done by all primary care
related to the ‘target organ’ (i.e. heart, kidneys, brain) of the physicians, specialists, dentists and other health care
disease (Table 2.4). In this regard, it is important to question professionals. However, it is important to emphasize that the
the more subtle signs so that the correct diagnosis can be diagnosis should not be made on the basis of any single
made for those patients with earlier stage 1 hypertension. measurement. Repeated measurements should be obtained
Hypertension ch2 16/10/08 14:56 Página 17

Evaluation of the patient 17

Table 2.5 Procedure for the indirect measurement part of the physical examination on which the diagnosis of
of blood pressure hypertension is more dependent than the precise and repeated
measurement of blood pressure.

• Patients should be seated with the arm bared, Ophthalmoscopy

supported, and at heart level. The patient should not The small vessels of the optic fundus provide an excellent
have smoked or ingested caffeine within 30 minutes means for assessing the degree of systemic vasoconstriction
before measurement 2.1A–F). This examination should be performed routinely.
(2
• Measurement should begin after at least 5 minutes of The earliest stage (group 1) of hypertensive vascular disease
rest. The appropriate cuff size must be used to ensure is recognized by increased tortuosity and mild constriction
an accurate measurement. The cuff bladder should of the vessels. Coexisting sclerotic changes are manifested
nearly (at least 80%) or completely encircle the arm by the discontinuity of the vessels at the arteriovenous (AV)
• Measurements should be taken with a mercury crossings (i.e. AV nicking (group 2)(22.1B). The appearance
sphygmomanometer, a recently calibrated aneroid of exudates and haemorrhages (group 3) signals accelerated
manometer or a calibrated electronic device hypertension; and with the appearance of papilloedema
• Both the systolic and diastolic pressure should be (group 4), malignant hypertension is established (2 2 .1C–F).
recorded. Disappearance of sound (phase V) should The American Ophthalmological Association has offered
be used for the diastolic reading a more detailed classification based upon the degree of nar-
• Two or more readings separated by 2 minutes must rowing of both the retinal arterioles and venules (Table 2.6).
be taken and an average reading obtained. If the
first two readings differ by >5 mmHg, additional Peripheral pulses
readings must be obtained The femoral and brachial arterial pulsations in all patients
• In addition, blood pressure must be measured in with hypertension must be compared in order to search for
both arms on the initial physical examination and any delay in the propagation of the aortic pulse wave,
periodically thereafter. It is not unusual that the suggesting the presence of aortic coarctation (particularly in
measured pressure will be reduced over several younger patients). Although this diagnosis should be
years from the initial examination in those elderly considered in all patients, including adults, it may also
patients with occlusive brachial arterial disease suggest an atherosclerotic occlusive process in the elderly,
• During the procedure the patient and examiner particularly if there are asymmetrical brachial arterial
should refrain from talking pressures or if, on long-term follow-up, there is an un-
explained reduction in pressure taken in one arm, or a
reduction or loss of peripheral pulsations. If that occurs,
pressure should be measured in the contralateral arm, and
during each individual examination, and the diagnosis is further evaluation can be done for occlusive vascular
established if these blood pressure measurements are made disease.
two or three times, and were elevated on three successive Auscultation of the carotid arteries for systolic bruits may
office visits (including the first). The American Heart provide signs of preventable strokes and transient ischaemic
Association, the Joint National Committee and the World attacks (especially if associated with neurological signs and
Health Organization have all recommended similar follow- symptoms). It is important to dissociate bruits heard over
up procedures for repeated measurements based upon the the carotid arteries from transmission of aortic systolic
initial measurements. ejection-type murmurs. This usually can be clarified by
These recommendations advise use of a systematic listening carefully for the timing and character of the bruits.
technique (Table 2.5) and additionally advise on the purpose Furthermore, funduscopy may reveal cholesterol emboli in
and meaning of blood pressure measurements, with specific the retinal arterioles. Renal arterial bruits on examination of
recommendations on follow-up. Furthermore, should the the abdomen, flanks and back provide an important sign of
patient assist in follow-up with home blood pressure renovascular hypertension. Systolic bruits are more
measurements, the instrument must be calibrated and commonly detected, especially in older patients, and may
validated periodically (at least once annually). There is no not be associated solely with occlusive renal arterial disease.
Hypertension ch2 16/10/08 14:56 Página 18

18 Evaluation of the patient

A B

Superior temporal
artery and vein

Superior nasal
artery and vein

Optic disc Macula

lutea

Central retinal
artery and vein

Inferior nasal
artery and vein

Inferior temporal
artery and vein

C D

E F
Hypertension ch2 16/10/08 14:56 Página 19

Evaluation of the patient 19

2.1 Fundoscopy in hypertension. A: normal funduscopic examination demonstrating vessels and the optic nerve head;
B: severe arteriolar constriction; C: marked arteriolar tortuosity; D: marked arteriolar constriction and flame-shaped
haemorrhages; E: accelerated hypertension with severe arteriolar constriction, haemorrhages and exudates; F: malignant
hypertension with severe arteriolar constriction and tortuosity, haemorrhages, exudates and papilloedema.

Table 2.6 Classification of hypertensive retinopathy

Keith–Wagener–Barker classification Generalized sclerosis

• Group I – tortuosity, minimal constriction • Grade 1 – increased light-striping; mild AV nicking
• Group II – as above + arteriovenous nicking • Grade 2 – coppery arteriolar colour; moderate AV
• Group III – as above + haemorrhages and exudates nicking; veins almost completely invisible below
• Group IV – papilloedema arteriolar crossing
• Grade 3 – silver arteriolar colour; severe AV nicking
American Ophthalmological Society Committee • Grade 4 – arterioles visible only as fibrous cords
Classification (Wagener–Clay–Gipner) without bloodstreams
Generalized arteriolar constriction:
• Grade 1 – arterioles 3/4 of normal calibre; AV ratio of 1:2 Haemorrhage and exudates
• Grade 2 – arterioles 1/2 of normal calibre; AV ratio of 1:3 Grades 1 to 4 (based on the number of affected
• Grade 3 – arterioles 1/3 of normal calibre; AV ratio of 1:4 quadrants divided by 2)
• Grade 4 – arterioles thread-like or invisible
Papilloedema
Focal arteriolar constriction or sclerosis Grades 1 to 4 (based on dioptres of elevation)
• Grade 1 – localized arteriolar narrowing to 2/ calibre of
3
proximal segment
• Grade 2 – localized arteriolar narrowing to 1/ calibre of
2
proximal segment
• Grade 3 – localized arteriolar narrowing to 1/ calibre of
3
proximal segment
• Grade 4 – arterioles invisible beyond focal constriction,
arteriolar–venular.

However, when the abdominal bruit is associated with a development of left ventricular hypertrophy (LVH),
diastolic component in the upper quadrants of the abdomen increased ventricular mass may be suspected by a sustained
or flanks, the possibility of renal arterial disease becomes apical lift although it may not be detectable by the chest
much more likely and should be focused on. roentgenogram. The electrocardiogram and echocardio-
graphic assessment are more sensitive. Nevertheless, the
Cardiac examination earliest clinical index of cardiac involvement in hypertension
Even before cardiac structure is altered (particularly in is left atrial enlargement, which may be suspected by an
young patients), precordial palpation may reveal evidence atrial diastolic gallop (fourth heart sound or the bruit de
of functional hyperdynamic cardiac changes, namely gallop). This finding is highly concordant with at least two of
hyperdynamic apical impulse and a faster heart rate. As the four electrocardiographic criteria of left atrial abnormality
heart adapts structurally to the increasing afterload by (Table 2.7, 2.2).
Hypertension ch2 16/10/08 14:56 Página 20

20 Evaluation of the patient

Table 2.7 Abnormal diagnostic

electrocardiographic criteria Terminal P wave forces in
V1 ≤0.04 mm-s

Left atrial abnormality – two of four of the following

criteria
• P wave in lead II ≥ 0.3 mV and ≥0.12 s
• Bipeak interval in notched P wave ≥ 0.04 s Bipeak interval >0.04 s in Bipeak >0.04 s
• Ratio of P wave duration to PR segment ≥1.6 (lead II) notched P waves
• Terminal atrial forces (in V1) ≥0.04 s

Left ventricular hypertrophy P wave/PR segment ratio >1.6 P PRs

• Ungerleider index +15% on chest X-ray alone P/PRs >1.6
• Ungerleider index +10% on chest X-ray + two of the
following ECG criteria: 2.2 Electrocardiographic criteria for left atrial abnormality.
– Sum of tallest R and deepest S waves ≥4.5 mV
(precordial)
– LV 'strain' – i.e. QRS and T wave vectors 180° apart
– QRS frontal axis <0°
– All three of ECG criteria above

Haemodynamic and echocardiographic studies have

demonstrated that when electrocardiographic evidence of
left atrial abnormality is present (even without other
indications of LVH), there is adequate evidence of impaired
left ventricular (LV) systolic function. As LVH becomes
more evident clinically, as indicated above, there is palpable
evidence of a sustained LV lift (or ‘heave’) and further
impairment of contractile function. In patients with severe 2.3 Buffalo hump.
LVH, the presence of a third heart sound (ventricular
diastolic gallop) eventually connotes the presence of early associated with abdominal striae and girdle obesity.
LV failure. In those patients with a very high arterial Neurofibromatosis or café-au-lait skin spots can suggest
pressure, an aortic diastolic ‘blowing’ murmur may occur as possible coexistent phaeochromocytoma (2 2.4A–C). In the
the result of a functional eversion of the aortic cusp by days prior to effective antihypertensive therapy, cutaneous
elevated pressure and total peripheral resistance. The more ulcerations were seen as manifestations of severely impaired
frequently heard precordial or vascular systolic ejection cutaneous blood flow (2 2.5). Appearance of anaemia on
murmur suggests either outflow tract obstruction from physical examination in the black patient should suggest
(absolute or relative) aortic stenosis (associated with coexistent haemoglobinopathy or anaemia secondary to
ageing), or a haemic murmur related to a hyperkinetic chronic renal disease. Careful abdominal examination is
circulation or coexistent anaemia. necessary for the auscultation of bruits, as well as for the
presence of the palpable kidneys of polycystic kidney disease
Other physical findings (PKD). When the latter occurs, hepatic cysts, secondary
The so-called ‘buffalo hump,’ seen on the back below the polycythaemia and cerebral aneurysmal disease of the circle
2.3). This may also be
neck, suggests Cushing’s syndrome (2 of Willis should also be considered.
Hypertension ch2 16/10/08 14:56 Página 21

Evaluation of the patient 21

A B

C
Phentolamine
230
220
210
200
190
Blood pressure (mmHg)

180
170
160
2.4 Neurofibromatosis. A, B: skin lesions; C: patients may 150
also have a phaeochromocytoma. When the angiotensin II 140
130
anatagonist saralasin is infused it stimulates the release 120
of catecholamines from the phaeochromocytoma. 110
Medullary blood pressure is reduced with administration of 100
90
the adrenergic antagonist phentolamine. The 80
phaeochromocytoma was subsequently surgically 70
removed. 60
50

110
(beats/min)
Heart rate

100
90
80
70
60
0 10 20 30 40 50 60 70 80 90 100
▲ Saralasin ▲
1.3 mg/min

2.5 Hypertension-related cutaneous skin ulceration.

The lesion was slow healing but improved with blood
pressure control.
Exploring the Variety of Random
Documents with Different Content
qauiafalido="" envutfiro="" .y="" chr="" ahax.="" oeflauaya=""
ubre="" s.i="" califa="" eferipto.="" arrib="" chcb.y="" lu=""
bicron="" fice="" focorro="" bolui="" egypto.="" ytornar=""
combatir="" efta="" toraarlah="" meterlah="" fuego.="" enga=""
vueftras="" animas="" chaid="" fehan="" ydo="" :="" yr=""
vofotros="" hirie="" todo="" pelean="" quedaffen="" deellos=""
hombres="" alanceados="" cada="" vno="" leuantar="" ti=""
pondr="" ciudad.="" yaconteci="" como="" delerufal="" caufadel=""
pharaon="" fefali="" atierra="" beniarain="" apartarle="" alli=""
pueblo.="" yquando="" debcn-iamin="" cftauaallivn="" prepofito=""
llamaua="" ieriashijo="" deselemias="" dehananiasiefte=""
prendi="" te="" acueftas="" chaldeos.="" mentira="" acuefto=""
nolo="" efeuch="" antes="" lenas="" truxolo="" delante=""
principes.="" ayraron="" contra="" acot="" puficronlo=""
delonath="" efcriba="" aquella="" hecho="" siendo="" pues=""
entrado="" mazmorra="" camarillas="" lapnfion="" auiendo=""
eftado="" all="" muchos="" fac="" pregunt="" efeondidamente=""
es.y="" mano="" bjbylonia="" entrenado.="" sedechias:=""
peque="" contrati="" tus="" ef="" pu="" carcek="" donde=""
eftan="" vueftros="" prophetaj="" prophetizauan="" diziendo=""
vedr="" vofoti="" oye="" ruego="" mi="" se="" cayga="" dcti=""
hagas="" bolueren="" dclonathan="" muera="" mand=""
depofitaron="" patio="" haziendole="" dar="" vna="" torra=""
placea="" panaderos="" haftacj="" gaftalle.="" qued=""
ieren.ias="" cnel="" guaida..="" cap.="" gheb.yendofe="" yra=""
b="" heb.="" caei="" foflb.="" ii.="" t="" s.="" arr.="" v.9=""
cfuua="" rey.=""/>
 C A P I T. I E XXXVIII. R E *Arr/. 2t-9 a Hcb. fu alma. q.d.
ganará fu rida. b El bien. cO.enel foflb. 1L á Familiar criado del Rey.
e Heb. en ni mano. IEremiru es echado en vn/i mazmorra cenagofa
¡torios principes con confattimteto del Key, porque perfuadta ál
Vtteblo que fe diejje a los Chaldeos. 1 1. Abdemelech ¿thiope criado
del Key ruc^a por el, y lo faca deaüi. III. íl Key le habla enfeaeto.y el
le perfuade aque fe de' co tiempo .i los Cbaldcos,fi quiere cuitar ftt
extrema calamtdadyy la de la ciudad y de todo fu?ueLlo, Y oyó
Saphacias hijo de Machá,y Gedelias hijo de Phalfur, y Iuchal hijo
deSelemias, yPhaíTur hijodeMelchias , las palabras que íeremias
hablaua á todo el Pueblo,diziendo. . i Anfi dixo Iehoua : * El que fe
quedare enerta ciudad morirá á cuchillo, á hambre, y á peílilencia :
mas el que fe faliére á los Chaldeos, biuirá,ya fu vidaleferá por
defpojo,y biuirá. 3 AiifT dixo IehouájEntregádo ferá entregada erta
ciudad en mano del exercito de Babylonia, y tomarlahá. 4 Y dixeron
los Principes ál Rey : Muera aora efte hombre : porque deefta
manera defmaya las manos de los varones de guerra, que han
quedado enefta ciudad , y las manos de todo el Pueblo , hablandoles
tales palabras: porque eñe hombre no bufca h la paz deefte Pueblo,
mas el mal. y Y dixo elReySedechias,Helo ay:en vuef tras manos
eftá, que el Rey no podrá contra, vofotros nada. 6* Y ellos tomaron
á Ieremias,y hizieronlo echar c en la mazmorra de Melchias hijo de
Amelech , que eflaua en el patio de la guardary metieron á Ieremias
coníbgas. Y en la mazmorra no auia agua, fino cieno : y hundiófe
Ieremias en el cieno. 7 ^[ Yoyendo Abde-melcch Ethiope hóbre^E
unucho que eftaua en cafa del Rey, que aman puerto á Ieremias en
la mazmorra , y eftando fentado el Rey á la puerta de Ben-iamin, 8
Abdemelech falió de cafa del Rey, y habló álRey,diziendo: 9 Mi Señor
el Rey,Mal hizieron e/tos varones entodo loq han hecho con Ieremias
Propheta,ál qual hizieron echar en la mazmorrarporque alli fe morirá
de hábre: porque noay mas pan en la ciudad. 10 YmádóelRcyál
mifmo Abdemelech Ethiope,diziendo,Toma e entu poder treynta
hombres de aqui , y haz facar á Ieremias Propheta déla mazmorra
antes que muera. n Y tomó Abde-melech en fu poder hóbres.y entró
á la cafa del Rey ál lugar debaxo de la theforer¡a,y tomó de alli
trapos vieMIAS. 17.0 jos,traydos,y viejos, rotos.y echólos á Ieremias
con logas en Ij -nazmorra: u Y dixo Abdc- melcch Ethiope á
Ieremias,Pon aora cjjos trapes viejos, traydos,y rotos, debaxo de los
Ibbacos de tus bracos debazo de lasfogas.Y hizolo aníi Ieremias. 1}
Y facaron á Ieremias con fogas,y fubieronlo déla mazmorra.y quedó
íeremias en el patio déla guarda. 14 q¡ Y embió el Rey Sedechias , y
hizo traerá íi 2 Ieremias Propheta á la tercera entrada que eftaua en
la Cafa de Iehoua : y dixo el Rey á Ieremias:Preguntote vna
palabra,no me encubras ninguna coíá. iy Y Ieremias dixo á
Sedechias: Si telo denunciare/ no me matarás i y fi te diere có- f Hcb
mafejo,no me efeucharás. tando no 16 Y juró el Rey Sedechias
enfecreto ale- me™ra:' remias,diziendo,BiueIehoua^ que nos hi- a"s'
zo efta anima , 11 que no te matare, ni te en- ¿a v¡ja> tregaré en
mano de eftos varones' que buf- h Hcb. fi te can tu anima. matare, y
17 Y dixo Ieremias á Sedechias , An(í di- f» te xo IehouaDios délos
exercios,Dios delf- 1 te rael : Si faliendo faheres á los Principes del
f/^""™ Rey de BabyIonia,f tu anima biuirá, y efta ¿¡¡uirás, ciudad
noferá metida á fuego, y biuirás tu y tu cafa: 18 Mas fino falieres á
los Principes del Rey de Babylonia , efta ciudad íerá entregada en
mano délos Chaldeos, y meterlahá á fuego , y tu no efeaparás defus
manos. 19 Y dixo el Rey Sedechias á Ieremias: Temóme á caufa de
los ludios q fe acortaron á los Chaldeos,que por ventura no me
entreguen en fus manos,y me efearnezei. ro Y dixo Ieremias,No
entregarán. Oye aora la boz de Iehoua que yo te hablo , y aurás
bien,y biuirá tu anima. 21 Y fino quifieres falir , ' efta es la pala- 1 r.0
dicho bra que me ha moftrado Iehoua: ver.18. 2i m Y heaqui que
todas las mugeres que m Yaliéde han quedado en cafa del Rey de
luda , fon ^ facadasálos Principesdel Rey de Babylonia : y ellas
mifmas dirán: Engañáronte, y pudieron mas que tu n tusamigos:0
atolla- n Heb.Ios ron enel cieno tus pies, boluieronfe atrás, varones
de 2í Y á todas tus mugeres y tus hijos fa- tu.D.az.' ,, < x, 5 i • ' r
oAludeála carana!os(_haldeos,y tu también no elca- pena^aei parás
defus manos, mas por mano del Rey ie dieron de Babylonia ferás
prefo , y P áefta ciudad v.6. quemarás á fuego. pS.contu 24 Y dixo
Sedechias á Ieremias , Nadie obftinació. fepa eftas palabras, ynó
morirás. 2? Y fi los Principes oyeren,quejo he hablado cótigo,y
viniere áti,y te dixeré,Declaranos aora q hablarte conel Reyuno nos
lo encubras,y no te mataremos:y que te di xo el Rey: F F iü
The text on this page is estimated to be only 25.08%
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17' I E R E luego de Unte del rey. bHeb.y íHeb.lnzc i6

DezirlesHas,9 Suppliqué al Rey que caer mi HO me hizieífe tornar en
cafa de Ionathan, porque no me muricíTe allí. 27 Y vinieron todos los
Principesa leremias,y preguntaronle:y el les refpondió conforme a
todo loque el Rey le auia mandado,y » dexarófe deel, porque no fue
oy.«allarÓdel. do el negocio. 28 Y Iercmtas quedó enel patio déla
guarda harta el dia que fue tomada lerufalem: y allí eftaua quando
fue tomada lerufalem. C A P I T. XXXIX. IUrufalemes tomada de
UsChaldcosy pueffd a fuego: y huyédofi el Rey cñ los fuyos es
tomado y tray*lo delante del rey de ñabylonia , el c¡ual dejpues de
¿uer degolladole/kí hijos y fui printipesdelante deel, le faca los ojos,y
lo embia aprtfionado a iiabylonia. I 1. leremias es facado déla
carceby fuello en líbertadpor mandado del R.ey de Rabyloma- i 1 1.
Dios efeafta del peligro a Abdemclech Etbiope por fu piedad. *z.
Rryei 25,1. Aba. fj,4. 1" Dezienibre. clunio. dHcb.fiablá tonel juyzios.
t HA.eeENel * noueno año de Sedechias Rey deluda f enel mes
Décimo, vino Nabuchodonofor Rey de Babylonia contodo fu exercito
contra Ierufalé,y cercáronla. 2 Yenel vndecimo año de Sedechias c
enel mes Quarto, álos nueue del mes, fue rota la ciudad: 3 Y entraré
todos los Principes del Rey de Babylonia, y agentaron ala puerta del
medio, Nergal Sarezer,Samgar-nebó,Sarfechirrij Rab-faris , Nergal-
Sarezer, Rabmagj y todos los demás Principes del Rey de Babylonia.
4 Y fuc,que viéndolos Sedechias Rey de luda, y todos los varones de
guerra, huyeron : y falieronfe de noche déla ciudad por el camino
déla huerta del Rey, por la puerta de entre los dos muros:y falló por
el camino del deílcrto. y Mas el exercito de los Chaldeos los íiguió , y
alcanzaron á Sedechias en los llanos de lericó: y tomaró!o,y
hizieronlo fubiraNabuchodonoforRey de Babylonia en Reblatha en
tierra de limath , y fentenciolo. 6 Y degolló el Rey de Babylonia los
hijos de Sedechias en fu prefencia en Reblan thá,y a todos los
nobles deluda degolló el Rey de Babylonia. 7 Ycfacó los ojos al Rey
Sedech¡ai,y aprilionólo en grillos para licuarlo enBsbylonia. 8 Y los
Chaldeos puíieron a fuego la cafa del Rey y las cafas del Pueblo.y
derribaron los muros de lerufalem: y Y la reda del Pueblo que auia
quedado i Fue libre. III. MIA S. 772 en la ciudad, v ^ los queíeauian
acoflado 1 HA.fo» ael , y todo el refto del Pueblo q auia que- "ydo(
S1* dado .trafpalió Nabuzardan capitán de la guarda en Babylonia.
jo Y del v ulgo de los pobres que no teman nada , hizo quedar
Nabuzardan capitán déla guarda entierra de luda : y dioles entonces
viñas y heredades. 11 qr Y Nabuchodouoíór auia mandado ||. acerca
de leremias & por Nabuzardan ca- g Heb.en pitan de la
guarda,diziendo, mano de N. ti Tómalo y h mira por el , y tío le
haqas hHcb. pon mal ninguno : antes harás conel como el te fobre el
cus dixere. °'ÜJ' 13 Y embió Nibuzardá capitán de la guarda,)'
NabufezbaZjRab-Sarcs, y Neregel, y Serefer, y Reb-Mag, y todos los
Principes del Rey de Babylonia. 14 Y embiaron.y lomarorrá leremias
del patio de la guarda, y entregarólo á Godolias hijo de Ah¡cam,hijo
de Saphan , paraq lo íacalle á cafa, y 1 biuio entre el Pueblo. 15:
^[Yauia (ido palabra de Iehoua a leremias citando prefo enel patio
de la guarda» diziendo, 16 Vé,y habla a AbdemelcchEthiope,diziendo
, Anírdixo Iehoua de los exercitos, Dios de lfrael , Heaqui queyo t
traygo mis t Cumplo. palabras fobre eíla ciudad para mal y no pa ra
bien, y 1 ferán en tu prefencia aquel dia, 1 EflFecluar17 Y en aquel
diajyo te libraré, dixoleho- ^enan en ua,y no ferás entregado en
mano de aquelíos de quien tu tienes temor:porque efeapando te
efcaparc,y no caerás á cuchiHo,y m tu vida te ferá por
defpojorporque tuuif- m Ganarás te confianza en mi}dixo Iehoua. tu
v'da, co* r a p 1 t vr mofilaroC* V,\ T- ,X L; . . , ba'ras.notá I
Uremias es puesto en libertad por el Capitán de la ja rlTI¿¿¿ guarda
delrey de ñabylonia: y le da dones y hbtr- ^e ios (("¿j. tad que vaya
donde l 1 7 haíidoá deluda, que yuan captiuos cnBabyloiua: vofotroJ
2 Y el capitán de la guarda tomó á lere- cfta p3|A. mias , y dixole ,
Iehoua tu Dios habló eñe bra. mal contra eíle lugar, P HA. fi 3 Y
truxolo, y hizo Iehoua fegun que auia lu,fn.° cn dicho, porq pcccañcs
contra lchouá, y no tus 0'0, . oyítes fu boz,° por tato os ha venido
edo. Pf" vcnir 4 Yaorayo te hcfoltado ov délas cfpo- q Hcb.PAfas
que/e'»*» en tus manos ; ^ íi te eíiá b;cn dró mil
oveuircóniigoenBabylonia,vcn,yyo ^mi- ¡o» fobrcii. rarc.
The text on this page is estimated to be only 29.94%
accurate

17J I E R E raré por tí.Y Sino tceítá bien venir conmigo en

Babylonia, dexalo. Mira, toda ia tierra eftá delante de ti , á loque
mejor y mas cómodo te pareciere yr,ve. iTercm. y Y aun 3 el no auia
reftondidoejuefe boluccEl capitl ria,quando celledixo, Buelueteá
Godolias hijo de Ahicam , hijo de Saphan , al qual el Rev de
Babylonia ha puerto íbbre todas e Libre. 'as ciudades de luda, y biuc
conel c en mef hcb.á to- dio del pueblo.ó ^adonde re pareciere mas
do Ioq de- cómodo de yr,ve.Y diole el Capitán de la recho en gUarcja
prefentes y dones, y embiólo. ^araTndar 6 Y vino Ieremias á
Godolias hijo de Aanda*" hicam en Mafphath,y moró có el en medio
del Pueblo que auia quedado en la tierra. 7 Y todos los Principes del
exercito que olauan por el campo , ellos y fus hombres, oyeron como
el Rey de Babylonia auia puerto á Godolias hijo de Ahicam fobre la
tierra, y que le auia encomédado los homgHeb.dela brcs,y las
mugeres,y los niños: y » los popobreu bres de la tierra, los que no
fueron trafpafdelatie- fados en Babylonia: rra' 8 Y vinieron á
Godolias en Mafphath, es a faber Ifm3el hijo de Nathanias, y Iohaná,
y Ionathan hijos de Careé,y Sareas hijo de Thanehumeth, y los hijos
de Ophi, Nethophathita,y lezonias hijo de Maachathi, ellos y fus
hombres. 9 Y juróles Godolias hijo de Ahicam hijo de Saphan áellos
yáfus hombres, dizié*i.Ríy. íf, do,*No tégays temor de feruir á los
Chal24. déos: habitad en la tierra , y feruid al Rey de Babylonia,y
aureys bien. 10 Y veysaqui que yo habito en Mafh Para re phath h
para eftar delante de los Chaldeos cebirá los qUe vendrán á
nofotros: y vofotros coged frl'eb el ^ Vino Y ' el Pan,y el azeyte, y
poneldo en verano, vueftros almazenes, y quedaos en vuertras q. d.
hazed ciudades que aucys tomado. vueftro 11 Y aníimifmo todos los
ludios que eftaAgofto. ua en Moab,y entre los hijos de Ammon,y en
Edom,y losque eftauan en todas las tierras,oyeron dezircomo el Rey
deBabylotQiic que- nia auia concedido t rerto de íudá,y q auia daten
al- pueft0 (bbre ellos á Godolias hijo de AhifudT.SC" cam>hi>° de
Saphan: IComo la Ytornaronfe todos los ludios detovcr.io.q.d. das las
partes adondeauian íído echados: hiiicron y vinieron en tierra deluda
á Godolias en grande A- Mafphath , y cogeron vino y muy mucho
gofio. 1 pan J 1$ YIohanan hijo de Caree,y todos los mHcb.No
Principes de los exercitos queetiauan enel fabes fabie-
camp0jVinieron á Godolias en Mafpbath. nHcb. pa- x4 ^ Ydixeróle,™
No fabes decierto cora herirte 010 Baalis Rey de los hijos de Ammon
ha alma. embiadoalfroael hijo de Nathanias "para MIAS. 774
matarte?Mas Godolias hijo de Ahicam no los creyó. ir YIohanan hijo
de Caree habló á Godolias en fecreto en Mafphath, diziédo, yo yré
aora,y heriré á Ifmael hijo de Nathanias,y hombre no lo fabrá. porq
te ha de matar, y todos los ludios q fehá recogido á ti fe derramarán,
y perecerá la rerta de Iudaí 16 Y Godolias hijo de Ahicam dixo á
Iohanan hijo de Caree, No hagas efto , porq falfo es loque tu dizes
de Ifmael. C A P I T. XLI. ISmael mata atrajeion á'Godolia* ,y
haxfotrai infígnes crueldades, y toma confino a loscjue auian
quedado para licuarla ala tterradelos Kmmonitat. I I . \ohanan
le(igue,y le quita lagentefy el fe le efeapa. Y Aconteció enel mes
Séptimo que vino Ifmael hijo de Nathanias , hijo de Eliíama de la
fimiente real, y algunos Principes del Rey, y diez hóbres conel, á
Godolias hijo de Ahicam en Mafphath, y 0 comieron ay pan juntos en
Mafphath. o Tuuíe1 Ylcuancofe Ifmael hijo de Nathanias, róvanqte. y
los diez hombres que conel , y hineró á cuchillo á Godolias hijo de
Ahica, hijo de Saphan, al qual auia puerto el Rey de Babylonia fobre
la tierra, y matólo, j Anliniifno hirió Ifmael á todos los ludios que
eftauan conel , con Godolias, en Mafphath , v á los foldados
Chaldeos que fe hallaron allí. 4 Y fue quevn diadeípues que mató i
GodoIias,y no lo fupo hombre, y Vinieron hombres de Sichem, v de
Silo, y de Samaría, ochenta hombres , rayda la barua , y rotas las
ropas, y arañados , y trayá en fus manos Prefente y perfume para
licuar en la Cafa de lehoua. 6 Y fallóles al encuctrode Mafphath
Ifmael hijo de Nathanias p llorado ; yacóte- p Heb.yéció q como los
encótró,dixoles,Veni á Go do andáJo dolías hijo de Ahicam: yllorádo.
7 Y fue que quando vinieron en medio de la ciudad , Ifmael hijo de
Nathanias los degolló al medio del algibe,el y los varones que
eTlauan conel. 8 Y fueron hallados diez hóbres entreellosq dixeró á
Ifmael, No nosmates, porq tenemos enel cápo^theforos de trigos,y
q Silos efceuadas, y azeyte, y miel.y dexólos, y no conc^os» los
mató enrre fus hermanos. 9 Y el algibe en q echó Ifmael todos los
cuerpos délos varones q hirió por caufa de Godolias,era el mifmo q
auia hecho el rey Afsá por caufa de BaafaRey delfrael :efte hinchió
de muertos Ifmael hijo de Natha nías. FF .íiij
 II. a I os criados del Rey. bHefe. allegáronte. cSea acepto.
d Heb. vn poca de mucho. 17? I E R E 10 Y lleuó captiuo Ifmael á
todo el reílo del pueblo que eflaua* en Mafphach, las hijas del Rey,y
á todo el Pueblo que auia qdado en Mafphathj queNabuzardan
capitán de la guarda auia encargado á Godolias hijo de Ahicam,y
lleuolos captiuos Ifmael hijo de Nathanias, y fuefe para paíTar fe á
los hijos de Ammon. ir m Y oyó Iohanan hijo de Caree,y todos los
Principes de los exercitos que cslauan conel,todo el mal que hizo
Ifmael hijo de Nathanias. 11 Y tomaron todos los varones, y fuero
para pelear con Ifmael hijo deNathanias,y halláronlo junto á Aguas
muchas que es en Gabaon. 15 Yaconteció que como todo el Pueblo
que eftaua có Ifmael oyó á Iohananhijo de Caree,y a todos los
Principes de los exercitos que nenian conel, alegrarorífe: 14 Y todo
el Pueblo que Ifmael auia traydo captiuo de Mafphath,tornarófe ,y
boluieron, y fueronfe á Iohaná hijo de Caree, iy Mas Ifmael hijo de
Nathanias fe efeapó delante de Iohanan con ocho varones, y fuefe a
los hijos de Ammon. 16 YIohanan hijo de Caree,y todos los Principes
de los exercitos que conel eTiauant tomaron todo el reílo del Pueblo
que auian tornado de Ifmael hijo de Nathanias de Mafphathjdcfpues
que hirió á Godolias hijo de Ahicam , hombres de guerra y
mugercs,y niños, y 3 los cunuchos queel auia tornado de Gabaon. 17
Y fueió,y habitaró en Geruth-Chimlum,quc es cerca de Beth-
lehcm,para partirfe,y roeterfe en Fgypto: 18 Por caufa délos
Chaldeos: porque temiáácaufadeellos,porauerh crido Ifmael hijo de
Nathanias a Godolias hijo de A hicam,ál qual el Rey de Babylonia
auia puefto fobrela tierra. C A P I T. X L I f. EL Vuebloy los principes
requieren a Ieremias que ore por ellos á Dios, y le confulte para
faber loque harán :y el les refponde que la -voluntad de Dios es que
fe queden en la Herraj no [epaten aEgypto,como lopenfauan
bazerjino quieren morir alia mala mucrte,incumendo enyra de Dios
de tmeuo,porno ha^er fu yoluntad. Y b Vinieron todos los principes
de los exercitos, y Iohanan hijo de Caree^ Iezonias Hijo deOfaias,y
todo el pueblo dcfde el menor hada el mayor, t Y dixeróá lercmias
propheta , c cayga aora nucílro ruege delate de ti, y ruega por
nofotros á Iehouá tu Dios por todo cite rcfto.porque auemos
quedado d vnos poli Fácil, 6 trabaj o fo. MIAS. t76 eos de muchos,
como tus ojos nos veen. 3 ParaquelehouatuDios nos enfeñecamino
por donde vamos , y eloque hemos cHcb. padehazer. labra qha4
YleremiasProphetales dixo:Yaheoy- gamosdo . Heaqui oro á Iehoua
vueftro Dios como aueys dicho : y íerá que f todo loq le- ^eb. t0'
houaosreípondiere,os enfeñaré:no os de- " xaré palabra. y Y ellos
dixeron á Ieremias , Iehoua fea entre nofotros teftigo déla verdadf y
de la f Heb.del* lealtad, fino hizieremos conforme ^ ¿todo ^ ^ >t0
aquello para loqual Iehoua tu Dios te em- japaiábra. biáre a
nofotros. 6 Ora/éa h bueno,ora ma!o,ala boz d"e Iehoua nueftro
Dios,ál qual te embiamos,obedeceremos, porque obedeciédo ala boz
de Iehoua nueftro Di o s,ay amos bien. 7 Yaconteció que a cabo de
diez dias fue palabra de Iehoua á Ieremias, 8 Y llamó á Iohaná hijo
de Caree,yá todos los principes de los exercitos que^rfnan conel , y
a todo el pueblo defde el menorhaftael mayor. 0 Y dixoles,Án(i dixo
Iehoua Dios delfraelálqual meembiaftes paraque 1 hiziefle 1 °ra
 »77 I E R E au ergotizados, c Heb. bicndo fa bcd. ra
peregrinar alia, morirán a cuchillo, a hambre, y á peílilencia : ni aurá
deellos quien quede biuo,n¡ quien efeape delante del mal que yo t ra
ygo fobre ellos. 18 Porque aníi dixo Ichoua de los exercitos Dios de
Ifrael , Como fe derramó mi enojoymiyraíbbrelos moradores
delerufalé j aníi le derramará mi yra fobre vofotros,quando entrardes
en Egypto': y fca Formula reys a por juramento, y por efpanto,y por
y cxemplo maldición, y ^porarfrentajy no vereys de juramé.) mas
efte lugar. to á las gen ,9 khoua habló fobre vofotros , órelib^Biuíre
s 1u'as
 '79 IEREMIAS. :2o eftán el diadeoyafloladas, niay enellas
morador. $ A caufa déla maldad decllos que hizieron,haziendome
enojar,yendoa orTVecer fahumerios, honrrando diofes ágenos, que
ellos no conocieró , volbtros ni vueftros padres. 4 Y embié á vofotros
á rodos mis fieruos prophetas madrugando.y embiando,y difabra
del?- 2iendiófe en las ciudades de luda, y en las placas de Ierufalem,
b y tornáronle en foledad y en deftruycion,como parece o y. 7 Aora
pues, Anfi dixo lehoua de los exer c V dás c'tos J^'°$de Ifrael :
Porque hazeys tan S;rande mal contra vueftras c animas para er
talados varón y muger,niño y mamante de en medio de
Iuda,paraque no os dexeys reliquias? tco$°[dolos ^ Haziendome
enojar ¿ por las obras de vueftras manos , ofreciendo fahumerios á
diofes ágenos en la tierra deEgypto, adondeaueys entrado para
morar , paraq os acabeys , yfeays por maldición y por vergüenza á
todas las gentes de la tierra? p Aueysos oluidado délas maldades de
vueftros padres, ydelasmaldadesdelos Reyes deluda , y de las
maldades de íiis mugeres, y de vuellras maldadesproprias, y de las
maldades de vuefttas mugeres q hizieron en tierra de Iudá , y en las
placas t No os a- de Ierufalem? ueysarrc- io c No fehan quebrantado
hafta el dia ponido . de oy,ni han auido temor , ni han caminanmt.
de cío en mi Ley , ni en ipis derechos q di de P"^ Jante de
vofocros,y delante de vueftros pa dres. ii Portáto anfi dixo lehoua de
los exer•* Am. 9,4. citos Dios de Ifrael:*Heaqui que yo pongo mi
roftro en vofotros para mal, y para acabar á todo Iudá . 11 Y tomare
ál refto de luda q pulieron fus roftros para entrar en tierra de Hgypto
para morar allá,y todos ferán coníumidos en tierra de Egypto :
caerán á cuchillo, ferán confumidos de hambre, delde el mas
pequeño halla el mayoría cuchillo y a há» f Arr-4«, tr. bre morirán, y
^ferán por jurameto, y por efpa»to,y por maldición, y poraffrenta. if
Y vilitarc á los que moran en tierra de Egypto, como vifíté á
Ierufalem, con cují hillo y. con hambre,y conpcftilencia. 14 Y no aurá
quien e/cape, ni quien quede biuo del refto de lucia, que entraron en
tierra de Egypto para inorar allá, para boluer á la tierra de luda & ,
por laqual ellos £ Heb.que fofpiran por boluer para habitar allátpor-
elloslcuanque no bolueran, (1 no los que efeapá- t3n fu an'* iy
Yrefpondieronálmifmoleremias todos los que fabian que fus mugeres
auiá offrecido fahumerios á diofes ágenos, y todas las mugeres q
eftauan preientes, vna grande compaña, y todo el Pueblo q habitaua
en tierra de Egypto en Pathures, diziendo: 16 La palabraq nos has
hablado en nóbre de lehoua , h no oymos de ti : 5c«mí 6* 17 Antes '
haremos de hecho toda pala- ¡mpUcj¿c¡*a bra que há falido de
nueftra boca para of- notable, frecer fahumerios f álaReyna del cielo,
¡ Hcb. lure y derramándole derramaduras 1 como aue mos haxiémos
hecho nofotros ,ynueftros padres, do (] dnueftros Reyes , y nueftros
Principes , en ^'^^jg las ciudades de Iudá, y en las placas dele-
voto ¿jaue. rufalem.y fuemos hartos depan,y fuemos mosprome
alegres, y nunca vimos mal. ti do para 18 Mas defde que ceífamos
de offrecer fahumerios á la Reyna del cielo, y de der- J^^jJ^*
ramarle derramaduras , nos falta todo, y . • *0ffá, á cuchillo,)' á
hambre lomos confumidos. jjrei 19 * Y quando nofbtras offrecimos
fa- *J^rr,y)Iy> humerios a la Reyna del cielo, y le derramamos
derramaduras, por ventura hezimos le m fin nueftros maridos tortas
pa- m Sin el cora alegrarla , y derramárnosle derrama fentimiéto
duras? de nueftros 10 Y habló Ieremias á todo el Pueblo, *V*!Í* \ , •
, -i 1 1 1CS q Citólo a los liombres,y alas mugeres, y a todo el 1q
p0fj¡a a. común que le aujan rcfpondido efto,di- curarlaley. ziendo:
Num. 50, ? 11 Por ventura no fe há acordado lehoua, y no há venido
á fu memoria el fahume rio que ofTreciftes en las ciudades deluda, y
en las placas de Ieruíálc vofotros,y vueftros padres , vueftros Reyes ,
y vueftros Principes.y el Pueblo de la tierra? 21 Y no pudo fuffrir mas
lehoua á caufa de la maldad de vueftras obras , á caufa de las
abominaciones que aurades hechorpor tanto vueftra tierra fué en
aífolamiento , y en efpanto,y en maldición , halla no qdar
morador,como/Mr?rf oy. ij Porque offreciftes fahumerios, y peccaftes
contra lehoua , y no oyfteslaboz de lehoua , ni anduuiftes en fu
Ley,nien fus derechos, ni en fus teftimonios: portáto há venido fobre
vofotros efte mal com o parece oy. 14 Y dixo Iereraias á todo el
Pueblo , y ato 
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*8i I E R E M I A S. ■ ffl a Arr.v.t7. b Elfos a la vcnl.id Ion

vueftnos vo tos°n alas riré la tierra,deftruyré la ciudad y los que
fy^i"^5 en ella moran? ^ ¿°¿tMi o Subid cauallos.y " alborotaos
carros, exercitos. y falgan los valientes : los Ethiopes , y los nHeb.
en de Lybia que toman efeudo , y los de Lyr loqueced. día que
tomany encefan arco. 10 Mas eife día fer'a á Iehoua Dios de los
exercitos día de vegada , para végarfe de fus enemigos:y el
cuchillotragará,y fe hartará y fe embriagará de lafangre deeüos :
porq ra a
 ^aron. $>t, l E R E matanza ferá álehoua Dios de los
exercitos en tierra del Aquilón al rio Euphrates. n Subeá Galaad, y t-
omabalfamo Virgé hija de Egypto: por demás multiplicarás
medicinas, no a y cura paran. 12 Las Gentes oyeron tu verguen^a.y
tu aHcb.fuer clamor hinchió la tierra: porque a fuerte fe te en fuer-
encontró con fuerte , y cayeron ambos jútc trompe- jos. ij Palabra
que habló Iehoua áleremias Propheta acerca de la venidade
Nabuchodonofor Rey de Babylonia para herir la tierra deEgypto. 14
Denunciad en Egypto, y hazed faber en Magdalo;hazed faber
también en Merophis,y en Thaphncs, dezid , Eftá quedo, y
aparejaterporque cuchillo ha de tragar ^cu comarca. if Porque ha
rehuydo tu fuerte?no fe pudo tener,porque Iehoua lo rempuxó. 16
Multiplico c los caydos: cada vno tábien cayó (obre fu compañero, y
dixeron, Leuantate yboluamosnos a nueftro pueblo^ á la tierra de
nueltro natural de delante del cuchillo e vencedor. 17 Clamaron alli,
Pharaon Rey de Egypto,Re? de f rebuelta: ^ dexó pallar el tiempo
feúalado. g Perdió la >8 Biuo yo, dize el Rey, Iehoua de los eoccaílon
xercitos es funóbre, que'1 como Thabor de vencer, entre los montes
, y como Charmelo en la Heb.hiio mar,aníi ' vendrá. 19 Haztetvafos
de tranfmigracion moradora hija deEgypto, porq Memphis ferá por
yermo, y ferá aífoladahafta no quedar morador. 20 Bezerrahermofa
Egypto, deftruyció del Aquilón viene,viene. 21 Sus foldados también
en medio deella como bezerros engordados ; que también ellos fe
boluieron, huyeron todos íín parar fe.-porque el dia de fu
quebrantamiento vino fobre ellos, el tiempo de fu vifitacion. 22 1
Subozyrácomodcferpientej porq con exercito vendrán , y con hachas
viene m á ella como cortadores de leña. 23 "Cortarófu monte.dize
Iehoua,porq no podran fer °contados:porq ferán mas q langoftas.ni
tendrá numero. 24 Aucrgonc_ofe la hija deEgypto : ferá entregada
en mano del Pueblo del Aquilón. 2y Dixo Iehoua de los exercitos
Dios de Ifrael , Hcaqui que yo viííto al Pueblo de Alcxandria, y á
Pharaó, y á Egypto,y á fus diofes,y á fus Reycs,y á Pharaon , y á losq
enel confian, ifí Y entregarloshc en mano de losq bufb Heb.tu
alderredor. c Hcb. el caydo. d Heb." nacimiento, c O, violeto. fO,
reboltofo. partir, h Podcrofo. i S. Nabuchodonofor. t Malas, líos ,
baúles &C. 1 Délos Babylonios m A Egypto. nOt. Cortad, o S. los
enemigos, Ot. hallados. MIAS. 184 can fu anima, y en mano de
Nabuchodonofor Rey de Babylonia, y en manó de fus fieruos : y
defpues ferá habitadacomo en los dias paíTados,dixo Iehoua. 27 m *
Y tu no temas íieruo mió Iacob, ynodefmayes Ifrael , porque heaqui
q yo p te faluo de lexos,y á tu fimiente déla tierra de fu captiuidad.Y
boluerá Iacob y defcanfará,y ferá profperado,y no aurá quien lo
efpante. 28 Tu mi fíeruo Iacob,no temas,dize Iehoua , porque
conúgofoy yo : porque haré confumacion en todas las gentes á Jas
quales te echare: mas en ti no haré cófumació: mas caftigartehe*3
con juyzio,y talando no te talaré. CAPIT. XLVII. PKophctixa la
dcTlruyciún de los TaleTtinos por los Chaldeos. PAlabrarde Iehoua
que fue á Ieremias propheta acerca de los Paleftinos antes que
Pharaon hiriefle á Gaza. 2 Anfi dixo Iehoua;Heaqui que fuben aguas
delatarte del Aquilon,y s tornarfehan en arroyo, y alagarán la tierra y
1 fu plenitud , ciudades y moradores deellas : y los hóbres
clamaran,)- todo morador déla tierra aullará, 3 Por el fonido de las
vñas de fus fuertes c4H.ccncli^.y 16.de \fasas dedonde
 aS.los enemigos.los Chald. cHeb.dc gente, q.d. de fer
pueblo poríí. *Arr. 17,5. d Sed como &c. q.d. amontaos, huyd al
defícrto. e El ¡dolo de Moab. i.Rcy. 11,7. f Habla co los deftruydores
de Moab. h Mcth.del vino viejo. */, Rey. 12, 29*Ifa.i6,7. íS.Dios. t El
fceptro. el reyno fuertey florido; 1 Heb.fed q.d. en lugar fin nin gun
luftrc de gloria. 185 I E R E DF Moab. Anfi dixo Iehoua de los
ejércitos Dios de Ifrael: Ay, de Nebó que fue deftruyda, fue
auergonc^da.Canathaim fue tomada: fue confufa Mifgab,y dcfmayó.
2 No fe alabará ya mas Moab de Hesbon 3 penfaron mal , Venid y
quitémosla c de entre las gentes. También tu Madmen ferás
cortada,cuchillo yrá tras ti. 3 Boz de clamor de Oronaim , dertruycion
y gran quebrantamiento. 4 Moab fue quebrantada^ hizieron que
feoyeíTeelclamordefus pequeños. c Porque á la fubida de Luith con
lloro fubirá el que llora: porque á la decédida de Oronaim los
enemigos oyeron clamor de quebranto. 6 * Huyd.efcapad vueftra
vida,ydfean como retama enel defierto. 7 Porque porquanto
confiarte en tus haziendas,y en tus theíoros,tu también ferás tomada
: y e Chamos fáldrá en captiuerio; fus facerdotes y fus principes
juntamente. 8 Y vendrá deftruydor á cada vna de las ciudades, y
ninguna ciudad efeapará 5 y perderlehá el valle, y deftruyrfehá la
camp aña, como dixo Iehoua. 9 Dad alas áMoab.paraqueboládo
buele:yfus ciudades ferán deíiertas harta no tjuedar enellas morador.
10 * Maldito elque hiziere engaííofamétela obra de Iehoua:y maldito
elque detuuiere fu cuchillo de la fangre. ir Quieto eftuuo Moab defde
fu mocedad,y el ha ertado repofado h fobre fus hezes.ni fue
traíTegado de vafo en vafo,ni nú. ca fue en captiuidad.portanto
quedó fu labor enel, y fu olor nolehá trocado. 12 Portanto heaqui
que vienen dias , dixo Iehoua, en que yo le embiaré tra fraudadores
que lo harán fraíportar : y vaziarán fus vaíbs, y romperán fus odres.
13 Y Moab fe auergonc;ará de Chamos, * de la manera que la Cafa
de Ifrael fe auergon^ó de Bethelfu confianza. 14 Como direys,*
Valientes fomos,y roburtos hombres para la guerra? i? Deftruydo fue
Moab, y fus ciudades * afloló:y fus efeogidos mácebos decindieron al
degolladero, dixo el Rey,Iehoua de los exercitos es fu Nombre. 16
Cercano eíia'el qbrantamiéto de Moab para vcnir:y fu mal fe
appreífura mucho. 17 Compadeceos deel todos Iosquee¡f¿arredor
deehy todos losq fabeys fu nóbre,dezid,Como fe qbró la vara de
fortaleza^ el báculo de hermofura? 18 Deciendede la gloria, fientate
en 1 feMIAS. co moradora hija de Dibonrporque el deftruydor de
Moab fubió contra ti,difsipó tus fortalezas. 19 Párate enel camíno,y
mira, ó moradora de Aroer:pregunta á la que vá huyendo y á la que
efcapó,Di le, Que ha acótecido? 10 Auergon^ófe Moab,porque fue
quebrantado. Aullad, y clamad.Denunciad en Arnon que Moab es
dertruydo: 21 Y que vino juyzio fobre la tierra de la campaña;fobre
Helon,y fobie Iafá,y fobre Mephaath. (Beth-diblathaim, 22 Y fobre
Dibon,y fobre Nabo, y fobre 23 Y fobre Cariathaim , y
fobieBethgamul,y fobre Beth- maon. 24 Y fobre Carioth , y fobre
Boírá, y fobre todas las ciudades de tierra deMoab, las de lexos,y las
de cerca. 2f Cortado es ni el cuerno de Moab, y fu braceo
quebrantado, dixo Iehoua. 26 Embriagaldo , porque contra Iehouá fe
engrandeció:y rebuelquefe Moab fobre fu vomito,y Isa por efearnio
también el. 27 Y no te fue á ti Ifrael por efcarmo,como íi lo tomaran
entre ladrones?porcj defde que n hablarte deel,te has mouido. 28
Defamparad las ciudades, y habitad en peñafeos, ó moradores de
Moab : y fed como la paloma que haze nido de tras déla boca de la
cauerna. 29 Oydo hemos la foberuta de Moab , q es muy foberuio:fu
hinchazón, y fu foberuia,y fu altiuez,Ia altura de fu coraron. 30 Yo
conozco, dize Iehoua, fu yra,° y fin verdad, p fus mentiras, no harán
aníí. 31 Portanto yo aullaré fobre Moab, y fobre todo Moab haré
clamor,y fobre los va roñes de Cirherés gemiré. 3a r Con lloro de
Iazer lloraré por ti ó vid de Sabamá: tus ramos paífaron la mar, harta
la mar de Iazer llegaron; fobre s tu agorto yfobretuvédimia vino
deflruydor. 33 * Yferá cortada la alegria y el regozijo de los campos
labrados, y de la tierra de Moab; y haré ceflar el vino de los lagares,
no pifarán con canción : la canción, aoferá canción. 34 t El
clamor,defde Hefebon harta Eleá le; hartalafa u dieron fu boz :
Defde Scgor harta Oronaim bezerra de tres años ; porq tábié las
aguas de Nérim ferá dertruydas. 3f Yharéceífar deMoab , dize
Iehoua, quien facrifiq en altar, y quié ofFrezcafahu merio á fus
diofes. 35 Portáto mi coracó , por caufa de Moab,refonará como
flautas: y mi coracó, por caufa de los varones de Cirherés, refonará
como flautas: porq las riqzas q hizo, perecieron.- 37 * Por-m El
reyno. y fu fu n Defde 4 burlarte del, incarrifte cnefta pena, de fer tu
tambiétras puerto de tu tierra. o Sin fuerces iguales a fu foberuia. es
loque dize Ifa.16,6. p Sus fanfarronerías fus fieros fe eos. q
Heb.gemirá. r Como lloré á Iazer. s Heb.tu verano. *Ifa. 26,10. t S.fe
oyó*, u S. fe oye?. tí>.i5,y.
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1*7 I E R E M 1 A & i?8 *\pd. iy, 8. 37 * Porque en toda

cabera bolara, y eftcndcráfus alas prefa. áMoab. 41 Tomadas fon las
ciudades , y tomadas fon las fortalezas : y fera á quel día el cS. de
par- cora^on de los valientes deMoab como el coraron demuger c en
anguftias . 41 YMoab ferá dertruydo para mas no fcr Pueblo porque
fe engrandeció contra d Alude a iehoua. ¡0*1 «"do 4? d Miedo>y
W°»y ,azo fobre li>ó mo ^os ca houá, enqueharéoyreaRabbath
délos i De los Amm. ua. 7 ^[ De Edom. Anfi dixo Iehoua de los * í#
exercitos : No aymas fabiduria en Theman ? Ha perecido el confejo
en los Tibios-corrompióle fu fabiduria? g Huyd, p bolueos ,
efeondeos en ííraas P Heb.bolparaeftar o moradores de Dedan:
porque uierf°n*f' el quebrantamiento de Efau traeré fobre j^nparah*
el, al tiempo que lo tengo de vifitár. Litar mora9 * Si vendimiadores
vinieran contra dores. &c, ti, no dexáran rebufeos ? Si ladrones de *
KbXitu. 3. noche, 1 tomaran loque ouieran- meneí- q Hcb.dcftcr>
truyeraruq. 10 Mas yo defnudaré á Efau , defeubriré ¿ó m^icrr» fus
efcondrijos : y no fe podra efeonder. tom^rjnpa Será dertruyda fu
íimiente , y fus herma- raílnos,y fus vtzinos : r y no ferá . r Hcb.y no
11 Dexa tus huérfanos, vo/oi' criaré: y eltus biudas fobre mi fe
confiarán. ¿"J**"11* 11 Porque aníi dixo Iehoua : Heaqui que t "^X.
que 1 los que no ertauan condenados á bcuer nojuyz,¡0j del cáliz , u
beuiendo bcuerán, y tu abfol- eno:. uiendo ferás abfuelto .''no ferás
abfuelto: u A buenos mas beuiendo beuerás • tragos. ij Porquepormi
juré, dixo Iehouaque en aflolamiento , en vergüenza, enfoledad,yen
maldición fera Bofrá : y todas fus ciudades ferán en aflólamiencos
perpetuos. 14 "Lafamaoy, c¡utdeparte de Iehoua * Hcb. II auia fido
embiado menfajero alas Gen- oydooyde tes,diziendo , juntaos y
venid contra ella, Ichy leuantaos ala batalla, ij Porque heaqui que
pequeño te he puerto entre las Gentes , menoípreciado entre los
hombres. 16 Tu
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necera. *Gr.i5),2). b S. elr^y de Rab. a Iudea,coino auf

nida del lordan. d Comov. 16. e S. enludf 1 . fVctiir corriendo de
ludca contra Edom. 16 Tu arrogancia te engaúó , y la foberuia do
tucorac^oo : que habitas en cauernas de pcñas:que tienes la altura
del monte : aunque alces, como águila tu nido, de a O, rfcar- ajj¿ te
|w¿ deceudir,dixo lehoua. 17 YferaEdom on aílolamieoro : todo a,
quel que pallare por ella 3 fe efpantará , y filuara fobre todas fus
plagas. 18 * Como en el tralioniamiento de Sodoma y de Gomorrha
y de fus cudaJ's Defíj" aya vezinas, /era ,dixo lehoua: no moraiá alli
deftruydo nadie,ni la habitará hijo de hombre. 19 Heaqui que como
león fubirácde la hinchazón del Iordan la morada fuerre: porque e
haré repofo,yhazerlohe ^ correr de fobre ella: y al que fuere
eícogido ^ la encargaré : porque quien e; femejante a mi-I o quien
me emplazará i o * quien lera aquel11 paftor 1 que me ofará refiftir?
zo Portanto oyd el confejo de lehoua, que ha acordado fobre Edom ;
y fus péfafSJludra. mientos que ha penfado fobre los mora*r\bb. 41,
1. dores deTheman.fCiertamente 'los mas hRey. no- pequeños del
hato los arraArarán , ydefJJ¿°ftj truyrán fus moradas con ellos,
ttrídelan. zl Del eftruendo de la cayda deellos la te de mi • tierra
tembló . y el grito de fu boz fe oyó t Heb. Si en el marBermejo. no
los ar- 22 Heaqui que m como águila fubirá , y nñríté los boIará:y
eftenderáfus alas fobre Bofra: 1 Los mas vi fij cor3ÍOn ¿e iQS
V3l,entcs ¿e £dom feles del exer > . ,. . . cito délos ra en aquel día
como el coraron de muger Chai: n en anguftias-. m Arr. 48, 23
^[DeDamafco.Auergoncofe Emath 4o- y Arphad, porque oyeron
malas nueuas: UL ro^f^eran l4 Defmayófe Damalco , boluióíe para
demente, huyr, y tomóle temblor : anguftia y doloHcb. derr. res le
tomaré, como de rouger que eftá de en la mar. parto . z
 II. tpi I E R E ynoloencubrays, dezid: Tomada es Baa
Sodi'ofes byloniajauergó^ado es a Bel, deshecho es délos Bab..
Merodach,auergó^adas fon fus efcujpturas, quebrados fon fus
ídolos, j Porque fubió contra ella Gente déla parte del Aquilón, laqual
pondrá fu tierra en aflolamiento , y no aurá quien en ella more ni
hombre ni animal :m ouieronfe,fueronfe. 4ff Enaquellos dias y en
aquel tiempo, dize Iehoua , vendrán ios hijos de Ifrael, ellos ylos
hijos deludá juntamente, yran andando y llorando , y bufcaran á
Iehoua fuDios. y Por el camino de Sion pregútarán, alli bArr 31 31
ew^erefjrd"fusr°ftros: Ver)id, y juntaos á y j2,4o.y 33 Iehouab con
Concierto cterno,que jamas 14.&C fepongaeloluido. cLos reyes, 6
Ouejas perdidas fueron mi Pueblo, losSaccrdo c fus paítores las
hizieron errar , por los tedios pro- montes las defcarriaron :
anduuieron de j ? ' * monteen collado, oluidaronfe de fus ma' jadas.
¿ S mal tra- 7 Todos los que los hallauan,Ios cornil: tan'dolos. ^fus
enemigos dezian,d No pecoaremos: cEncIqual porque ellos
peccaroná Iehoua c morada refldctoda de jufticia , y efperan^a de
fus padies Iejufticia. houa. 8 Huyd de en medio deBabylonia,y faf
Habla có lid de tierra de Chaldeos:y ffed como los 105 á'b T man^os
delante c'e' ganado : u"rlnll 9 Porque hcaqui que yo deípierto,y
Pueblo de nag° fubir contraBabylonia ayuntamjenIi captiui- to de
grádrs Gentes de la tierra del Aquidad. Eíd. 1. lon:y defde alli fe
aparejarán contra ella,y I- ferá tomada:fus flechas, como de valiente
no fe tornará en vano. 10 Y la tierra délos Chaldeos ferá por prefa :
todos los que la faqueáren, faldrán hartos,dixo Iehoua. 11 Porque os
alegraftes , porque os goh Heb. os zaftes deíbuyendo mi heredad ■
porq h os multiplicar héchiftes como bezerra de renucuos,y re5eí*
linchaftes ' como cauallos : ''o fuertes" 11 ^ Vueñra madre fe
auergon^ó mutBabvL * cho,aftVentofe laque os engendró . Veys
aqui las poftrimerias de las Gentes, defíer to,fequedad,y paramo. 11
Por la yra de Iehoua no fe habitará, I Heb.aíTa- mas fera 1 aífolada
toda ella : todo hombre lamiento. ¿ paífáxe por Babylonia , « fe
alfombrará, m O, efear- ^f, i r 1 v íiluaralobre todas lus plagas,
necera. / . ' ¿ , o . . n Paraccr- x4 Apercebios cotra Babylonia n
alderearla. redontodos los que entefays arcos tirad contra ella:no os
dudadlas factas, porque o Rendido peceó contra Iehoua. fclia. is*
Gritadcontra ella enderredor,°Dió fu mano, Caydo han fus
fundamétos, derM I A S. ribados fon fus muros:porque Vengan^a«
de Iehoua,Tomad végarc.a deella , Hazed con ella como ellahizo. 16"
Tabd deBabyloniafembrador,y el que tiene hoz en tiempo déla (lega t
delate de la efpada1* forjadora cada vno bol. P °» violeo ueráelroílro
hazia fu pueblo , cada vno u* huyrá hazia fu tierra. 17 Ganado
defcarriadoíw//í/olfrael,leo- ^ nes lo amontaré:*5 el rey de AíTyria lo
tra - y ^i'/* gó el primero, elle Nabuchodonofor rey ' ' ' de Bahylonia
lo defoífó el poflrero. 18 Portanto aníi dixolehoua de los exer citos
Dios de Ifrael: Heaqui que yo vifito al Rey de Babylonia y a fu tierra,
como vi ííté al rey de Aífyria: 19 Y tornare a traerá Ifrael á fu
morada, y pacerá al Carmelo,}' áBafan:y en el mote de Ephr3Ím y
de Galaad fe hartará fu anima. 20 En aquellos dias y en aquel
tiempo, dixo Iehoua , la maldad de Ifrael ferá huleada r y no
parecerá:y los peccados de Iu- r Heb.y no da , y no fe hallarán :
porque perdonaré á *1Ia' ^ic'1* los que ^oouiere dexado. 21 Sube
contra la tierra de contumaces, ^ rje|at'e contra ella, y contra los
moradores ' de la ni^yti j¿ viíitació.Deítruye,y mata en pos deellos,
fcrvifítada. dixo lehouary haz conforme á todo loque yo te he
mandado. 22 Eñruendo de guerra en la tierra, y qbrantamiento
grande. 2: Como fué cortado y quebrado x el 1 ^monar > r . cliude
Baa ? Como ic tor- , , byl. martillo de toda la tierra i nó Babylonia en
defierto entre las Gentes ? 24 Pufete lazos, y aun fuelle tomada ó
Babylonia,y tu nolo fupifte : fuerte hallada y aun prefa , porque
prouocafte áleho25/ Abrió Iehoua fu theíbro,y facó los va fos de fu
furor:porqueefta« obra de Iehoua, en la tierra de Chaldeos. 26 Venid
contra ella defde el cabo Je la tierra : abrid fus alholies : hollalda u
como ° *™> ' COm á parua , y deíhuylda : no le queden reli- tonej>
' quias . 27 Matad á todos fus nouillos , vayan al matadero: ay dellos
que venido es fu día, el tiempo de fu vifitacion . 28 Boz de los que
huyen , y efeapan de la tierra de Babylonia fe oy , paraque den las
nueuas en Sion déla venganza de Iehoua nueítro Dios, de la
venganza de fu Templo. 29 Hazed juntar fobre Babylonia fleche ros ,
á todos los que entefan arco : aíTentad capo fobre ella al derredor,
no efeape deella
 '9* I E R. E deella ninguno:pagalde fegun fu obra:có*
forme a todo loque ella hizo,hazed cone11a : porque cótra lehoua fe
enfoberueció, contrael SanÉro de Ifrael. jo Portanto fus mancebos
caerán en fus placas , y todos fus hombres deguerraferan talados en
aquel dia,dixo lehoua. 31 He aquí yo contrati,ó Soberuio,dixo el
Señor lehoua de los exercitos, porque tu dia es venido , el tiempo en
que te viGtaré. 31 Y el Soberuio trompezará y caerá , y no tendrá
quienlo leuáte: y encéderé fuego enfus ciudades,y quemará todos
fus al derredores. jj Aníí dixo Ieboua de los exercitos,Opprimidos
fueron los hijos de Ifrael y los hijos de luda juntamente:y todos los
que los tomaron captiuos ,fe los retuuieron: no los quifieron foltar:
tO.Ven- 34 El 3 Redemptor deellos es el Fuerte, gador.Tu- lehoua de
los exercitos es fuNóbre: pleytor* teádo pleyteará fu pley to
parahazer quietar la tierra,y turbar los moradores de Babylonia.
Cuchillo fobrelos Chaldeos,dixo lehoua , y fobre los moradores de
Babylonia, y fobrefus principes, y fobre fusfabios. bHeb.Ios 36
Cuchillo fobre ^ los adiuinos, y enlopictirofos. quecerán:cuchillo
fobre fus valiétes,y feran quebrantados. 37 Cuchillo fobre fus
cauallos y fobre fus carros , y fobre todo el vulgo que eftá c Sin fuer-
en medio deella: y feran c como mugeres: 9a ni cófcjo cuchillo fobre
fus theforos,y ferán faquea para cuitar dos_ dad! ami" ^ Sequedad
fobre fus aguas, y fecarfed De ido- han:porque tierra es d de
efculpturas,y en Vosyidola Ídolos enloquecen. »ras- 39 Portanto
morarán e beílias montefes f Heb'n'" C°n Satos : morar^n también
enella f po. * " líos de abeftruz , ni mas ferá poblada para gHeb. de
fiempre,ni fe habitará & para íiempre. generació 40 * h Como enel
traftornamiento de en genera- Dios á Sodoma y á Gomorrhayá
fasciueion. dades vezinas , dixo Iehouá, no morará alli *Ge».i$,
hombre,n¡ hijo de hombre la habitará. 41 Heaqui que yn Pueblo
viene de la parte del Aquilón, y rna gran Gente, y muchos reyes fe
leuátarán de los lados déla tierra: 41 Arco y lan^a tomarán, ferán
crueles, y no tendrán piedad. Su tropel fonará como la mar,y
caualgarán fobre cauallos : apercebirfe hán como hóbre á la pelea
contrati ó hija de Babylonia. 43 Oyó fu fama el Rey de Babylonia, y
fui manos fe defeoy untaré: anguíha le toar. 1/4.11,19. h Arri.49 18.
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