The Infographic Guide to Medicine

Neeral L. Shah
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The Infographic Guide to
MEDICINE
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NEERAL SHAH
A good infographic is worth a thousand words
Preface
As a medical student I always struggled reading numerous pages of text to try and pick
out details of diseases and therapies. Trained as an engineer, I found images flowcharts
and algorithms easier to understand. More recently, as a medical educator, I took notice
that many of my students also favored visually based materials to help provide a basis
for their learning. They often seek out these resources to provide them with quick
snapshots and commit high yield details to memory. At the same time, I had
encountered infographics that were being used to explain complex topics for the
purpose of patient education. I was surprised to learn that while infographics were being
used to convey information to patients, this modality was not being used in medical
education.

With my specialty training in gastroenterology and transplant hepatology, I set out to

develop a set of infographics for this field. With the help of two other physicians (Joseph
Mort and Joanna Odenthal), who were medical students at the time, we developed an
initial set of 29 infographics that covered major topics in gastroenterology and
hepatology. We studied the literature in graphic design for optimal layouts, space to text
ratios, and white space use. Keeping these guidelines in mind, we created and edited
an initial set of infographics. The weeks after we released this initial set of infographics,
many learners asked about their origin, inquired about access, and provided valuable
feedback. Word of mouth spread quickly and learners beyond our institution and in
other parts of the world were downloading our infographics. We surveyed some of the
initial users and found that 93% of survey participants reported the infographics being
useful. The top three reasons learners identified that they would use infographics were
knowledge reinforcement prior to patient care (55%), exam preparation outside of
patient care (26%), and knowledge reinforcement after patient care (10%). It seemed a
graphical summary of high yield clinical pearls could be used for exams, but more
importantly, to help improve patient care. The graphical nature allowed quick review of a
topic, and provided cues to recall previously learned material.

From this initial concept, and a partnership with McGraw Hill, I decided to expand the
topic areas beyond gastroenterology and hepatology. We enlisted the help of content
experts from many different fields in medicine and many technologically savvy medical
students (many from my own institution, the University of Virginia). With everyone’s
help, we were able to create this first edition, “The Infographic Guide to Medicine” that
covers over 600 topics. Coordinating the work of more than 13 associate editors and
over 75 students was challenging, but it was also rewarding to bring multiple viewpoints
to the final design. Each card we know has been reviewed by at least 4-5 people
looking to optimize the design and distill difficult concepts.

I am proud to say, to my knowledge, this is the first book dedicated to infographics for
medical education. These clear and concise infographics provide a great overview as
an adjunct to a learner’s foundational learning, and helps to solidify concepts in their
busy schedules. The culmination of this book would not have been possible without the
innumerable hours dedicated by medical students and associate editors from around
the United States. I also could not have completed this without the endless support of
my wife. I hope you are able to use these infographics as you create your own culture
and community of learning to ultimately provide better care to your patients.

Neeral L. Shah, M.D.

Copyright
The Infographic Guide to Medicine

Copyright © 2021 by McGraw Hill. All rights reserved. Except as permitted under the
United States Copyright Act of 1976, no part of this publication may be reproduced or
distributed in any form or by any means, or stored in a data base or retrieval system,
without the prior written permission of the publisher.

Book ISBN 978-1-260-45398-0

Book MHID 1-260-45398-7

This book was set in Minion Pro by KnowledgeWorks Global Ltd.

The editors were Amanda Fielding, Julie Grishaw and Christina M. Thomas.

The production supervisor was Richard Ruzycka.

Project management was provided by Harleen Chopra, KnowledgeWorks Global Ltd.

The cover designer was W2 Design.

 Acid and Alkali Ingestion
Most injuries
occur at a pH
under 3 or over
11

Clinical Presentation
Eschar Stridor Children:
Drooling Vocal hoarseness Vomiting
Odynophagia/dysphagia Chest pain Refusing oral intake

Respiratory distress may be caused by edema of the upper airway, aspiration

Conditioning ofsubstance
of the caustic Training intoTasks
the tracheobronchial tree, or inhalation of fumes
Absence of oral burns does NOT exclude esophageal injury

Diagnosis and Workup

Acid or Alkali?
Detailed history to determine substance pH,
concentration, volume, and patient intent
Acids = superficial coagulation necrosis
Alkaline = deeper liquefactive necrosis
Check for coingestants in suicidal patients
Early endoscopy(within 12-24 hours
of ingestion) for severe ingestions or
persistent symptoms
Ingestion of lye in pediatric patient

omplications
Early: perforations leading to hemodynamic
instability/mediastinitis/subcutaneous emphysema
Late: scarring of pylorus and esophageal strictures 
Reproduced with permission from Knoop KJ,

Increased risk of squamous cell esophageal cancer Stack LB, Storrow AB, et al: The Atlas of Emergency
Medicine, 4th ed. New York, NY: McGraw Hill 2016.
Photo contributor: Philip E. Stack, MD.

Management
Establish large-bore IV access and resuscitate with crystalloids
Manage airway and monitor for hemodynamic instability
Cricothyrotomy due to oropharyngeal
Oral intubation with direct visualization OR
edema, tissue friability, and bleeding

Contraindicated:
Activated charcoal/induced emesis (if caustic agent is only known ingestant)
Blind nasotracheal intubation Dilution/neutralization therapy

Copyright © 2022 by McGraw Hill. 107

03_Emergency Medicine_p105-190.indd 107 01/09/21 4:52 PM

 Acute Abdomen
New-Onset, Severe Abdominal Pain Tenderness Often Requiring Surgical Intervention

Inflammation Perforation
Appendicitis Cholecystitis Bowel Perforation PUD, Diverticulitis,
IBD
age >55

Periumbilical to RLQ Pain Ruptured AAA

RUQ Pain
Rebound Tenderness “Four Fs” Young Female with
Ruptured Ectopic
+ β-hCG

Obstruction Ischemic
Bowel Obstruction Volvulus Mesenteric Ischemia Elderly
Atrial Fibrillation
Strangulated Hernia Bulging
Vomiting, Constipated Abdominal Mass
Secondary to Adhesions, Intermittent Pelvic
Ovarian Torsion
Hernia, or Malignancy Extremes of Age Pain; Young Female

Intra-abdominal Nonsurgical Extra-abdominal

PID MIMICS
Myocardial Infarction
Pancreatitis
Pulmonary Embolism
Nephrolithiasis
Pneumonia
UTI/Pyelonephritis

Management
Stabilize Patient
Reproduced with permssion
from Papadakis MA, McPhee SJ,
Obtain Diagnostic Imaging
Rabow MW: Current Medical
Diagnosis & Treatment 2019. Consider Antibiotics to Cover
Intra-abdominal Pathogens
New York, NY:
McGraw Hill; 2019.

Cholecystitis, Screens for Appendicitis, Consult with Surgical Subspecialty as

Screens for Perforation Obstruction,
Free Fluid (Free Air), Ruptured AAA, Appropriate for Definitive Therapy
(Ectopic, SBO (Air and Ischemic Pain Management
Trauma) Fluid Levels) Bowel

Copyright © 2022 by McGraw Hill. 108

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 #1 Acute
Cause of acute
liver failure in
the United
Acetaminophen
States
Toxicity
Clinical Presentation Workup

Serum acetaminophen
Most patients are...
level
asymptomatic
Liver function tests, coagulation
But some may present with... tests
The above labs may initially be
normal
anorexia,
nausea, vomiting,
right upper quadrant pain,
liver failure,
hepatic encephalopathy,
renal failure, Helpful adjuncts:
metabolic acidosis, complete metabolic panel, drug
death screen, electrocardiogram

Management

Consider activated charcoal if If acetaminophen level = Possibly toxic per

presentation <1 hour status post- Rumack–Matthew nomogram...
ingestion

If single, acute ingestion, use...

N-Acetylcysteine (NAC)
Rumack–Matthew Nomogram
Repletes antioxidant
Treatment
Line glutathione

Serum If chronic ingestion, consider...

Acetaminophen
Time Status Post
Level
Ingestion NAC if serum acetaminophen level
or liver function tests elevated

Nomogram cannot be used for Liver transplant may be needed

levels <4 hours status post ingestion for severe cases (ie, fulminant
liver failure)

Acetaminophen level >150 mcg/mL at Survivors of acetaminophen toxicity

4 hours status post ingestion = Possibly toxic rarely have sequelae

Copyright © 2022 by McGraw Hill. 109

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 Acute Appendicitis
Obstruction and subsequent inflammation and bacterial overgrowth of the vermis
appendix

Etiology

Fecalith (most common)

Lymphoid tissue
Tumors
Helminthic infection

Clinical Presentation

Generalized abdominal pain that

moves to RLQ (McBurney’s point)
Reproduced with permission from Brunicardi FC, Andersen DK,
May be associated with nausea, Billiar TR, et al: Schwartz's Principles of Surgery, 11th ed.
vomiting, fever, anorexia New York, NY: McGraw Hill; 2019.

McBurney’s Point Diagnosis

Clinical diagnosis: Imaging for

surgical planning
CT for most. US or MRI for pregnant
or pediatric patients
Labs are frequently nonspecific but
may aid in excluding other diagnosis

Treatment

Most patients require urgent

appendectomy to prevent perforation
Pre-op patients should be given
antibiotics: cefoxitin,
piperacillin/tazobactam, or ceftriaxone
and metronidazole

Copyright © 2022 by McGraw Hill. 110

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 Acute Isoniazid Toxicity

Active and latent Clinical diagnosis based on

tuberculosis treatment history of tuberculosis
treatment and seizure
Decreases mycolic acid
synthesis
One of World Health Helpful adjuncts: fingerstick
Organization's essential glucose, complete metabolic
medicines panel, toxicology screen,
electrocardiogram
May also decrease
γ-aminobutyric acid
(GABA) synthesis

Clinical
Presentation
Management

Clinical Use
Workup

Altered mental status, Vitamin B6 (ie, pyridoxine)

seizure, metabolic acidosis, facilitates GABA synthesis
coma, death

Benzodiazepines may also be

given to potentiate GABA
activity

Recurrent, refractory Supportive (ie, airway

seizures are management by assisting
pathognomonic oxygenation, ventilation, etc.)

Copyright © 2022 by McGraw Hill. 111

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 Alcohol
Intoxication
Ethanol (CH3CH2OH)
Epidemiology
Significant global impact
30-40% of all medical or surgical
patients have an alcohol-related health
problem
Alcohol use disorder estimated to affect
3-5% of the population
Mechanism
Increased GABA activity and decreased
NMDA activity
Dopamine release contributes to its
addictive potential
Euphoria and disinhibition at lower
doses
At higher doses, respiratory depression
and coma can occur
Copyright © 2022 by McGraw Hill.
03_Emergency Medicine_p105-190.indd 112
Metabolism
Ethanol absorbed in the stomach within
30-45 minutes
Oxidation through alcohol
dehydrogenase to acetaldehyde
Reduction of NAD to NADH
Elimination
Oxidation follows zero-order kinetics
Concentration of alcohol in tissues has
negligible effects on the rate of
oxidation
In healthy individuals, metabolized at a
rate of approximately 150 mg of alcohol
per kilo of body weight per hour or one
drink per hour
112
01/09/21 4:53 PM
 Alcohol
Withdrawal
A life-threatening condition
Mild Withdrawal
Initial tremor
High blood pressure
Tachycardia
Anxiety/agitation
3-36 hours (after last drink)
Delirium Tremens
Most severe form of withdrawal
Visual hallucinations
Severe autonomic hyperactivity
with vital sign abnormalities
Seizures
Can lead to death
2-7 days
Copyright © 2022 by McGraw Hill.
03_Emergency Medicine_p105-190.indd 113
Alcoholic Hallucinations
Visual hallucinations without
delirium present after more
prolonged abstinence
Withdrawal seizures also
possible
12-48 hours
Management
First line: Benzodiazepines
Consider thiamine and folate
replacement for nutritional
deficiencies
EtOH & benzos activate GABA receptors
113
01/09/21 4:53 PM
 Anaphylactic Shock

Causes
Hymenoptera (eg, bee) stings
Food (eg, nuts)
Drug (eg, penicillin)
Plasma proteins in transfusion (patients
with IgA deficiency)
Echinococcus granulosus cyst rupture

Cascade
IgE degranulates mast cells
Histamine and tryptase released
Sudden drop in SVR & PCWP
Compensatory increase in cardiac output
Distributive shock (warm and dry)
Chemokines and cytokines cause tissue
damage

Care
Airway management
IM epinephrine (1:1000)
Anti-H1 and anti-H2
Steroids

MIMIC
Scombroid poisoning

Copyright © 2022 by McGraw Hill. 114

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 Antiarrhythmic Toxicity
Class Ia
Sodium Channel Blockers
Disopyramide, Procainamide,
Quinidine
Clinical presentation:
Dysrhythmia, hypotension,
anticholinergic effects, SLE-like
reaction (procainamide, chronic),
cinchonism (quinidine, chronic)
EKG: Wide QRS and prolonged
QTc
Treatment *:
Lidocaine
Sodium bicarbonate for
hypotension
Class II
β-Blockers
Clinical presentation:
Bradycardia, hypotension, AMS
Labs: HYPOglycemia
EKG: QRS widening
(propranolol), heart block
Treatment *:
Calcium
Glucagon
High-dose insulin
Consider lipid emulsion therapy
for refractory toxicity
General presentation:
Antiarrhythmic toxicity may cause
hypotension, dysrhythmias, and AMS
Copyright © 2022 by McGraw Hill.
03_Emergency Medicine_p105-190.indd 115
and Overdose
Class Ib
Sodium Channel Blockers
Lidocaine
Clinical presentation:
Neuro: Circumoral numbness,
tongue paresthesia -> anxiety ->
seizure -> coma
Cardio: Hypotension,
bradycardia, dysrhythmia
Heme: Methemoglobinemia
EKG: Normal QRS and short
QTc
Treatment *:
Seizure precautions
Lipid emulsion therapy
Class III
Potassium Channel Blockers
Amiodarone
Clinical presentation:
Acute toxicity: Hypotension,
ventricular dysrhythmia,
bradycardia
Chronic toxicity: Pulmonary
fibrosis, thyroid dysfunction,
corneal, hepatic, and cutaneous
toxicity (blue-gray discoloration)
EKG: Prolonged QTc
Treatment *:
Magnesium to treat torsades
Treatments:
QRS widening: Sodium bicarbonate
QTc prolongation: Magnesium
115
Class Ic
Sodium Channel Blockers
Flecainide
Clinical presentation:
Dysrhythmia, hypotension
Labs: Hyponatremia
EKG: Prolongation of PR,
QRS, and QTc. Ventricular
tachyarrhythmia and
bradycardia
Treatment *:
Mainly supportive care
Consider lipid emulsion
therapy for refractory
toxicity
Class IV
Calcium Channel
Blockers
Clinical presentation:
Bradycardia, hypotension,
AMS
Labs: HYPERglycemia
EKG: Heart block
Treatment *:
Calcium
Glucagon
High-dose insulin
Consider lipid emulsion
therapy for refractory toxicity
*Supportive care (required by all):
Airway management
Breathing assistance
Circulation support
01/09/21 4:53 PM
 Anticholinergic Toxicity
Causes of Toxicity:

Medications (ie, antihistamines, atropine); Mushrooms; Plants

(ie, Jimsonweed)

Clinical Presentation

Tachycardia "Red as a beet" "Dry as a bone"

- Earliest & most reliable - Cutaneous vasodilation to - Sweat glands are innervated by muscarinic
sign!!!! compensate for loss of sweat production receptors, and thus anticholinergics produce dry skin

"Hot as a hare" "Blind as a bat" "Mad as a hatter" "Full as a flask"

- Interference with normal - Dilation and ineffective - Delirium; hallucinations - Reduced detrusor muscle
heat dissipation (sweating) accommodation that contraction and inhibited sphincter
leading to hyperthermia manifests as blurry vision relaxation leads to urinary retention

Evaluation & Management

1 Understand the clinical features of overdose

Tachycardia

Flushing, anhidrosis, hyperthermia, blurry vision (mydriasis),

agitated delirium, and diminished bowel sounds

2 Perform basic screening tests Diagnosis is based on clinical findings

Fingerstick glucose—to rule out hypoglycemia

Acetaminophen and salicylate levels—to rule out common coingestions
ECG—to rule out conduction system poisoning 
Pregnancy test of all women of childbearing age

3 Manage anticholinergic toxicity

Stabilization of airway, breathing, and circulation
IV access, supplemental O2, cardiac monitoring, and continuous pulse oximetry
Antidotal therapy with physostigmine in the case of both peripheral
and moderate central toxicity
Symptomatic treatment as needed including sodium bicarbonate
(prolonged QRS or arrhythmias), benzodiazepines (agitation and
seizures), and possibly activated charcoal

Copyright © 2022 by McGraw Hill. 116

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 Anticoagulant Toxicity and
Overdose

Classes: Vitamin K antagonists (warfarins), direct thrombin inhibitors,

factor Xa inhibitors, and heparins

Clinical Presentation
Hemoptysis Widespread bruising

Bloody stools Fatigue

Lightheadedness Intracranial hemorrhage

Gross hematuria

Diagnosis and Workup

For warfarins: Increased PT For heparins: Increased activated PTT (aPTT) is
within 24-72 hours is diagnostic diagnostic

For Xa inhibitors and direct thrombin inhibitors:

Specific labs are not available
Warfarins are also found in rodenticides!
Increased PT or PTT is suggestive but nonspecific

Other useful labs:

BUN, creatinine, CBC, blood
type, and cross-match

Management
For warfarins, use PO/IV vitamin K Idarucizumab reverses dabigatran (direct thrombin inhibitor)
(delayed effect) or FFP (immediate effect)
Andexanet reverses factor Xa inhibitors
Protamine reverses heparins
Vitamin K not indicated!

Support for serious bleeding:

FFP, prothrombin complex concentrate, blood product
replacement, or activated factor VII as needed

Copyright © 2022 by McGraw Hill. 117

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 Anticonvulsant Overdose
Mechanism of Action
Enhanced GABA Calcium Channel Sodium Channel NMDA SV2A
Transmission Inhibition Inhibition Inhibition Stimulation

Benzodiazepines Lamotrigine Lamotrigine Lamotrigine Levetiracetam

Barbiturates Topiramate Topiramate Topiramate
Tiagabine Carbamazepine Carbamazepine Carbamazepine
Vigabatrin Valproic acid Valproic acid
Ethosuximide Phenytoin
Gabapentin Oxcarbazepine

Clinical Presentation

Cardiac
Confusion Ataxia Nystagmus Seizure Hypotension
Arrhythmias

Workup and Management

Obtain drug history Activated charcoal

Electrocardiogram
Benzodiazepines for seizures
Basic metabolic panel
Sodium bicarbonate for QRS
Serum anticonvulsant concentrations prolongation

Ammonia level for suspected L-carnitine or hemodialysis for

valproic acid toxicity valproic acid overdose

Copyright © 2022 by McGraw Hill. 118

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 Antipsychotic Overdose
Clinical Presentation
Lethargy Hypotension Agitated Neuroleptic
Extrapyramidal
and and delirium and malignant Presentation
symptoms depends on the
sedation tachycardia confusion syndrome
specific
antipsychotic
ingested as well
as the patient's
age, tolerance,
and co-
intoxicants.

QTc Prolongation and Torsades des Pointes

Diagnosis and Workup

Fingerstick EKG to rule out Acetaminophen
Serum
glucose to rule conduction system and salicylate concentrations of
the ingested
out hypoglycemia abnormality levels antipsychotic can
be obtained, but
these tests are not
readily available
or useful in the
acute setting.

Evaluation mainly consists of excluding other more harmful agents as the

cause of the patient's presentation.

Management
Activated charcoal if Treatment is
no contraindications primarily supportive Antipsychotic
overdose
generally has a
good prognosis.
The mainstay of
treatment is
supportive care.

Copyright © 2022 by McGraw Hill. 119

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 Barbiturate Overdose
Duration Cl– channel open GABA CNS Activity

Clinical Presentation Diagnosis

Lethargy Mild - - - - - - - - - - - - - - - - Moderate - - - - - - - - - - - - - - - - Severe Specific Findings:

Patient history of barbiturate
ingestion
Slurred speech Urine drug screen

Nonspecific Findings:
Nystagmus
Skin bullae
Altered electrolytes, glucose, BUN,

Ataxia creatinine, arterial blood gas

Abnormal pulse oximetry, chest
radiograph
Bradycardia

Management
Hypotension

Supportive:
Protect airway and assist
Hypothermia
ventilation
Increase blood pressure
Diminished pupillary
Treat hypothermia
reflex/pinpoint pupils

Decontamination &
Respiratory arrest Elimination:
Activated charcoal
(if mental status allows)
Coma
Hemodialysis in severe cases
WARNING: Brainstem reflexes Urine alkalinization
may be suppressed and patient
may appear neurologically dead (phenobarbital only!)

Copyright © 2022 by McGraw Hill. 120

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 Bee and
Wasp Stings
Uncomplicated
Local Reactions
Clinical Presentation Management
1-5 cm area of painful Remove stinger from wound if
redness/swelling present
Cold compresses
Develops within minutes, resolves
Oral antihistamine and topical
within a few hours/days
corticosteroids for pruritus

Large
Local Reactions
Clinical Presentation Management
Exaggerated redness and swelling at sting Cold compresses
site that ENLARGES over 1-2 days Oral prednisone for swelling
NSAIDs
Peaks at 48 hours, resolves in 5-10 days
Oral antihistamines and topical
corticosteroids for pruritus
IgE-mediated

Anaphylaxis
Acute, life-threateningˆIgE-mediated type I hypersensitivity reactionˆaffecting
2 or more organ systems, or sudden hypotension after allergen exposure

Clinical Presentation Management

Tachycardia IM epinephrine 1:1000

Vasodilation hypotension, edema Vasoconstriction

Bronchodilation
Upper airway edema stridor, hoarseness
Bronchospasm wheezing Airway management
Volume resuscitation
Urticaria, pruritus, flushing Adjunctive therapy
(antihistamines, H2-blockers,
Abdominal pain, nausea, vomiting glucocorticoids)
IgE-mediated

Copyright © 2022 by McGraw Hill. 121

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Another random document with
no related content on Scribd:
 LXXXI

NUIT EN LOCTUDY
12 novembre.

La nuit est noire comme un gouffre.

Le Noroit pousse une pluie épaisse et glacée. La rafale passe, rapide; et
le silence, entre-temps, s’établit sinistre, haineux, immense.
On devine la brume plus qu’on ne la voit, à l’éclat voilé des feux, dans le
lointain, aux points de l’horizon où l’on cherche les phares. Dans les
intervalles que laisse la rumeur du vent, on n’entend que le hurlement
rauque de la sirène, et le galop reculé de la terrible Torche. Le ciel et la
contrée se confondent en une masse d’encre, où court le reflet lugubre du
grand feu de Penmarc’h, semblable à un éclair louche sur un disque de
bitume.
Le vent jette contre les vitres les paquets d’eau qui s’y écrasent, et qui
dégouttent lentement. De temps en temps, l’eau roule du toit avec un
grincement qui ressemble à un cri étouffé de bête. Et la girouette crie,
comme une pie enrouée, sur son axe de rouille.
La mer roule sa plainte, là-bas, dans le gouffre de la nuit noire. Le
silence est bien plus émouvant de n’être troublé que par elle. Une tristesse
forte et large tombe sur tout le pays,—une tristesse qu’on aime comme un
hôte divin, inévitable et qui se fait craindre.
Et là-bas, partout, c’est l’Océan qui gronde, sur les bords de la Nuit. La
solitude est pleine de cette voix immense. Et celui qui l’écoute,—seul aussi,
—reste pensif, s’ennuie à l’idée d’entendre le son de la voix humaine, et
sent son cœur profond devenir taciturne...

C’est dans le même mois, nuit pour nuit, et par un temps semblable que
j’ai perdu ce que j’avais de plus cher au monde. La journée avait été
venteuse, livide et froide; le ciel était nuageux. Et le lendemain, je fus seul...
Et il plut à torrents... Et dans mon souvenir, je tremble encore à l’horreur où
me jetait l’idée de toute cette terre noire, glacée et humide... Hélas! sur cet
Amour si profond, que je n’en ai point été séparé sans être à jamais déchiré
de moi-même, que de soleils ont passé depuis, que de pluies sont tombées,
que de jours et de nuits...
La pensée ne peut fixer longtemps cet abîme, et refuse d’y croire. Ou, il
lui faudrait s’y précipiter...
Emporte, emporte-la donc, toi qui sais te répondre, solitaire Océan.
 L’ADIEU
19 novembre. Kenavo...

Le dernier jour est venu: voici le matin, dont je ne verrai pas le soir, en
Bretagne. Je fais mes derniers pas le long de la mer entre les rocs et la
lande. Qui dira votre langueur, promenade de l’Adieu?—La terre que l’on
aime est comme une amie affligée, que l’on quitte pendant son sommeil.
J’ai laissé Pont-L’Abbé, et je revois l’Océan terrible. Les nuées de plomb
roulent lourdement dans le ciel pluvieux. Et les rocs impassibles, violents et
silencieux, comme les résolutions d’une âme volontaire, laissent écumer
contre leurs bases la colère des vagues. Le flot monte, noir comme les
violettes dans une prairie, par une journée d’orage. Au loin, sous un pan du
voile relevé où la lumière passe en éclaircie, le pré des vagues a la couleur
d’une sombre pensée, dont le cœur d’or pâle luit sur les pétales bleuâtres...
Adieu, donc.

Qu’aimerai-je, si je n’aime pas la tristesse, moi qui suis tout passionné et

tout triste. Et la tristesse de ce pays pensif est pour mon âme un berceau, où
m’endort une mère délicieuse. Celle qu’elle est se retrouve en celui que je
suis, et bien faite pour lui, bien fait pour elle.
Elle, qui est si douce, si dure, si frémissante dans ses rêves, et si
indifférente au reste de l’univers, connaît bien mon fiévreux ennui. Je vais
au bord le plus lointain de la terre, là où la Bretagne s’enfonce dans la mer,
maintenant que tous les hommes et ses propres fils se précipitent vers les
lieux de la foule; et je leur tourne, comme elle, un dos de granit.
Le tombeau de la mer est celui que j’envie,—la tombe très profonde, où
la colère est éternelle comme le mépris, et où la grâce suprême est solitaire.
Le tombeau de la mer orageuse est la demeure que j’envie,—celle où la
tempête est déserte, et où la paix elle-même est amère.
C’est vous que je préfère, ô vagues,—ou vous, landes muettes sous la
brume, entre les arbres pieux, qui baissent la tête, et les rocs indignés à la
nuque imployable qui ne cèdent jamais, et qui, tour à tour, pâlissent de
courroux, et s’assombrissent de noir dédain.
 Je veux mourir ici, où j’ai senti les linges tièdes de l’oubli envelopper
mes os brûlants de fièvre, et détendre mes muscles raidis. Je veux mourir
ici, où le rêve puissant de la vie s’endort dans une fraîche paix, qui le
délasse. Car, où ne se consume-t-il pas de son ardeur? Partout, il se dévore.
Taciturne et plein de chants, selon que l’une ou l’autre passion
l’emporte, ici j’ai la terre qui répond ou qui écoute, qui se tait quand il faut,
et qui parle. Émeraude au cœur profond, Bretagne, nous nous dirons nos
chants. Je veux mourir, roc sur ta roche, où le pâtre aux yeux purs chante
encore, tandis que la vierge aux cheveux de lin, pareille au soleil d’avril sur
les bouleaux, sourit tendrement de ses lèvres encore aussi virginales qu’elle.

Émeraude au cœur profond d’océan, tu es aussi violente et douce. Tes

vagues tuent; et tes prairies si vertes font un tapis où les pensers acerbes
s’endorment sur le gazon, au pied des chardons à la fleur cuisante.
Puissé-je épuiser ici une vie inépuisable, dont la sève coule dans mes
veines comme un fleuve d’or fondu et de puissance croupie. Puissé-je
endormir, sous les feuilles pluvieuses de Cornouailles, les bonds de la
domination et les humeurs de la volonté, qui se font vénéneuses de grandir
secrètes dans mon âme et de pousser sous des chaînes, ensevelies.
Puissé-je étendre à l’infini occidental des vagues le rêve de la grandeur,
que prétend insulter la vie. Et puissé-je endormir, sur les derniers bords des
solitudes atlantiques, la grandeur de mon désir dans une paix égale..

FIN
 TABLE

Dédicace III
I. — Vers l’Ouest 1
II. — De la Fenêtre 8
III. — La Paix de Kergoat 10
IV. — Le Fol et la Sœur blanche 13
V. — Naïk 17
VI. — Entrée à Benodet 23
VII. — Les Vieux 26
VIII. — Triomphe des Barbares 32
IX. — La Mer parle 36
X. — La Danse 40
XI. — Tugdual 43
XII. — Bucoliques de Septembre 47
XIII. — Fin de Fête 52
XIV. — La Belle du Mail 59
XV. — Une Hutte 62
XVI. — Fin du Jour 66
XVII. — Tempête 68
XVIII. — Visite au Phare 72
XIX. — Petits Bretons 75
XX. — Annonciation du Soir 79
XXI. — Brumaire 81
XXII. — Le Jour des Anges 84
XXIII. — Penmarc’h 92
XXIV. — Arcadie 95
XXV. — Calvaire 98
XXVI. — Seigneurs 101
 XXVII. — Le Pauvre Pêcheur 105
XXVIII. — Heures d’Automne 113
XXIX. — L’Ile 118
XXX. — Le Phare 121
XXXI. — En Fouesnant 124
XXXII. — Route au crépuscule 128
XXXIII. — Les Deux Mam-Gouz 131
XXXIV. — La Nuit des Fées 135
XXXV. — Glazik 138
XXXVI. — Le Jour des Morts 141
XXXVII. — Le Chant humilie les Bêtes 143
XXXVIII. — Dunes 146
XXXIX. — Matin en Mer 149
XL. — Soir d’Automne 152
XLI. — La «Douce» 155
XLII. — Spectacle 161
XLIII. — Fantômes 165
XLIV. — La Dame aux Oies 168
XLV. — Un Champ et le Chemin montant 173
XLVI. — Le Bain 176
XLVII. — Le Soir sur la Lande 180
XLVIII. — Le Vent 182
XLIX. — Estampe dans le goût du Japon 184
L. — L’Angelus 187
LI. — Le Fjord 189
LII. — Crépuscule d’Octobre 191
LIII. — Sainte Barbe 193
LIV. — Pontiques 200
LV. — Sur le Tertre 207
 LVI. — Combat des Dieux 211
LVII. — Pavois 214
LVIII. — L’Homme sans tête 216
LIX. — Pont-l’Abbé 228
LX. — Le Voyageur 233
LXI. — Foin de Rostillec 236
LXII. — Géorgiques 241
LXIII. — Port de guerre 248
LXIV. — La Foi 252
LXV. — La Lande d’Or 257
LXVI. — Les Fillettes 259
LXVII. — Feuilles Mortes 262
LXVIII. — Arcades Ambo 268
LXIX. — Les Phares 272
LXX. — Quête pour la bonne guérison 275
LXXI. — Fidèle 280
LXXII. — La Sainte 287
LXXIII. — L’Agneau 293
LXXIV. — La Jeune fille à la bague 296
LXXV. — Chant de la Nuit 298
LXXVI. — Un vieux Breton 300
LXXVII. — Lys et Pavots 303
LXXVIII. — Funérailles 306
LXXIX. — Le Manoir 309
LXXX. — Le petit Saint Jean 312
LXXXI. — Nuit en Loctudy 314
L’Adieu 316
Imprimerie Bussière
Saint-Amand (Cher).
 NOTES:
[A] Dans l’évêché de Cornouailles, au Bord de la mer bleue.
Cantique Breton.
[B]

Ar Vretoned
pennou kalled...

[C] Vent de Sud-Est: on prononce Suette.

[D] C’est le nom qu’on donne aux Bretons du pays de Pont-l’Abbé, où ils forment
sinon une race distincte, du moins un clan singulier par le costume, l’accent et les
mœurs particulières.
[E] Mon Dieu! mon Dieu!
[F] Bamm est le mot de Crozon pour dame! et, généralement, le condiment dont il
assaisonne tous ses discours.
[G] Mam-Goz,—grand’mère en breton: littéralement, vieille mère.
[H] C’est, pour le Breton, le nom de l’amie ou de la fiancée, de la bien aimée.
[I]

Petra gan
Al lapouzik war al lan?
..........
Gan hag gan hé vignonès...

[J] Jeu de mots. Fri, en breton, signifie: le nez.

[K] Comme on les nomme de la pièce caractéristique, qui termine la coiffe des
femmes.
[L]

Ann dud jentil nevez zo kri;

Gwel a oa re goz da vistri.

Cf. Barz-az-Breiz, 403.

[M] Mettre aux enchères.
[N] Cantique breton.
*** END OF THE PROJECT GUTENBERG EBOOK LE LIVRE DE
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