CARDIOVASCULAR S C I E N C E S F O R U M

Transcrição

CARDIOVASCULAR
S C I E N C E S
F O R U M
CARDIOVASC SCI FORUM Jan. / Mar. 2007 Vol. 2 / NUMBER 1
EDITORIAL COORDINATION
Otoni M. Gomes (Brazil),
Pascal Dohmen (Germany),
Alfredo I. Fiorelli (Brazil),
José Carlos Dorsa V. Pontes (Brazil).
ASSOCIATED EDITORS
Antônio S. Martins (Brazil),
Carlos Henrique Marques Santos (Brazil),
Danton R. Rocha - Loures (Brasil),
Domingo M. Braile (Brazil),
Domingos Sávio Souza (Sweden),
Elias Kallás (Brazil),
Michael Dashwood (England),
Ricardo Gelpi (Argentina),
Tomas A. Salerno (USA).
Sponsored by: Fundação Cardiovascular São Francisco de Assis - ServCor (MG - Brazil)
Fundação Cardiovascular S. Francisco de Assis / ServCor - Truth is Jesus . St John 14.6
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Prof. Dr. Cristina Kallás Hueb
Prof. Dr. Elias Kallás,
Prof. Dr. Eduardo S. Bastos
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Prof. Dr. Fábio B. Jatene
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Prof. Dr. José Carlos D. V. Pontes
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Prof. Dr. Tofy Mussivand (Canadá)
Prof. Dr. Tomas A. Salerno (USA)
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of Cardiorespiratory Physiology and Experimental Cardiology of the Brazilian Society of Cardiology, Department of
Experimental Research of the Brazilian Society of Cardiovascular Surgery (DEPEX - SBCCV), SBCCV Department of
Extracorporeal Circulation and Mechanical Assisted Circulation (DECAM - SBCCV), SBCCV Departament of Cardiology
(SBCCV - DECARDIO, SBCEC - Brazilian Society of Extracorporeal Circulation.
CARDIOVASCULAR
S C I E N C E S
F O R U M
CARDIOVASC SCI FORUM Jan. / Mar. 2007 Vol. 2 / NUMBER 1
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CARDIOVASCULAR
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Cardiovasc Sci Forum
Jan. / Mar. 2007
Vol. 2 / Number 1
Page 05
CONTENTS
EDITORIAL
The Evolution of Heart’s Morphology Metaphors (Portuguese text)
Gomes OM
Page 08
ORIGINAL REPORTS
Caracterización Regional de la Biomecanica Venosa:Rol de la Complacencia y Viscosidad em el Retorno Venoso
(Spanish text)
Zócalo Y, Lluberas S, Bia D, Armentano R
Page 16
Utilization of the iodine etanolic solution for red-faced heart stimulating complex study in vertebrates
animals (Portuguese text)
Abreu RA, Ferreira E, Souza CM
Page 20
UPDATING ARTICLES
Pulmonary Embolism (English text)
Carvalho Jr, Ildevaldo J; Carvalho MBL; Bicalho RC; Bicalho; Carvalho JI
Page 31
Updade in Diagnosis and Treatment of the Aneurisms of Mesenteric Arteries
Santos CHM, Pontes JCDV
Page 35
INSTRUCTION FOR AUTHORS
Page 37
UPCOMING MEETINGS SESSION
Page 38
PEER REVIEW
(English text)
EDITORIAL
Cardiovasc Sci Forum Jan. / Mar. 2007
Vol. 2 / Number 1
A Evolução das Metáforas da Morfologia Cardíaca
Otoni Moreira Gomes*
A morfologia estrutural e histológica do coração apresenta bem definidos o epicárdio, miocárdio e
endocárdio.
Na evolução deste conhecimento, dois equívocos resistiram durante muitos anos: o do sincício
miocárdico e o dos sinusóides na microcirculação
coronária. O primeiro, porque a histologia óptica exibe
de maneira incontestável a fusão entre os cardiomiócitos, possibilitando como óbvia a conclusão de que o
miocárdio era um sincício, portanto, sem individualidade celular(1, 2).
A partir de 1950, com o progresso da microscopia eletrônica, definiu-se a individualidade celular miocárdica com a identificação dos discos intercalares na transição celular(3,4).
Na microcirculação, os estudos de Wearn
e Col(5), em 1933, interpretando o extravasamento
de solução injetada sob pressão no miocárdio como
definição morfológica de sinusóides foram confirmados por Hammond e Austen(6), em 1967, e por Hammond e Moggio(7), em 1971. Contudo, o principal fator
na aceitação contundente da existência dos sinusóides
na microcirculação miocárdica foram os resultados da
técnica de implante intramiocárdico da artéria torácica
interna, realizada e estudada por Vineberg(8), a partir
de 1946 e por Vineberg e Lewin(9), em 1972. Porém,
em nenhum momento os sinusóides foram histologicamente encontrados como vasos visíveis, pela presença siquer de endotélio contínuo e anastomosado,
sendo que Tsang e Chiu(10) explicam o equívoco nessas
investigações pelo uso necessário, na época, de técnicas de corrosão que destruindo o endotélio impediam
sua visualização histológica após a injeção de substancias no miocárdio.
* Fundação Cardiovascular São Francisco de Assis / ServCor
Departamento de Cirurgia da Faculdade de Medicina da UFMG
Coube a Chiu e Scott(11), a primeira investigação com técnica compatível com o estudo histológico real dos fenômenos envolvidos na preservação
da perviedade dos implantes de artéria mamária no
miocárdio. Esses autores empregaram a injeção intramiocárdica, sob pressão fisiológica, de hemácias
nucleadas de sangue de ave: puderam então observar
na histologia que as hemácias nucleadas, diferentes
das hemácias anucleadas dos cães estudados, estavam
no espaço intersticial e não dentro de microvasos de
sistema sinusóide.
Interessante, que os sinusóides existem na circulação miocárdica embrionária e persistem em anfíbios e cobras mas vão sendo substituidos pela microcirculação arterial dependente na medida em que
a complexidade cardíaca vai aparecendo. Assim, nas
aves, podem ser vistos pequenos nichos residuais intramiocárdicos de sistema sinusoidal, porém, mesmo
nas aves, já insuficientes para a demanda funcional(11).
Elementos residuais do sistema sinusóide podem escassamente ser localizados em algumas espécies como
em cães, ratos, coelhos e gatos(12). Já, em corações humanos, a persistência de focos de sinusóides pode ser
observada em cardiopatias congênitas graves, como a
atresia tricúspide e na atresia pulmonar que cursam
com pressões endocavitárias elevadas forçando fluxo
retrógrado pelas veias de Thebésio, o que dificulta a
involução embriogenética dos sinusóides(10).
Hodiernamente, sinusóides vasculares são definidos
como lagos microvasculares, de parede endotelial,
interligados, sem a membrana basal contínua como
nos ca-pilares e normalmente existindo no fígado,
baço, medula óssea e algumas glândulas endócrinas.
Entretanto, nenhum livro moderno de histologia descreve sua presença no miocárdio(13).
A “Lâmina miocárdica” (Myocardial band)
com a metáfora da “corda enrolada” como aparece
em livro de anatomia(14) foi introduzida mais recente-
mente, com os estudos avançados de anatomia e fisiologia desenvolvidos por Torrent-Guasp, Kocica e
col.(15-22) deduzindo que massa ventricular única tenha,
literalmente enrolado em torno de si mesma formando o ventrículo esquerdo, o septo interventricular e
progredindo em segunda volta para formar o ventrículo direito. Ou seja, a mesma lâmina muscular que se
enrolou para formar o ventrículo esquerdo completo
com o septo interventricular é que vai, em segunda
volta, externa, sobre a parede lateral do VE, passar
para o lado direito e forma o VD. Contudo, alguns autores têm já questionado e discordado desse conceito
e das implicações clínicas resultantes(23, 24) e as considerações aqui expostas possivelmente contribuem para
análise do problema.
O conceito da “corda enrolada” parece assemelhar-se com o equívoco do sincício miocárdico,
que, proposto como definição histológica, após esclarecido pela microscopia eletrônica, continuou como
definição apenas da velocidade de difusão da corrente
elétrica de ativação do miocárdio, ou seja, como “sincício elétrico”.
Torrent-Guasp verificou e descreveu a fisiologia espetacular da propagação da corrente de estímulo
desse “sincício elétrico” como a “circulação elétrica”
do coração, título de um de seus importantes livros(25).
Contudo, evidèncias embriogenéticas, anatomo-patológicas e funcionais contrariam o conceito morfológico base da metáfora da “corda enrolada”.
Assim, é clássica a constatação de que todo
o corpo cardíaco é formado simultaneamente, compondo o Tubo Cardíaco, primeiro órgão contrátil,
com atividade iniciada cerca do 18º ao 21º dia na embriogênese(26). De fato, no Tubo Cardíaco já estão as
paredes dos futuros ventrículos direito e esquerdo, isto,
porque o septo interventricular origina-se, em sentido
craneal, de brotos musculares do ápice ventricular, e,
no sentido caudal, dos coxins endocárdicos, que junto
com o septo membranáceo forma as válvulas cardíacas. Outro centro embrio-nário compõe a parte septal
que separa as vias de saídas ventriculares(27).
Do ponto de vista funcional, é fato comprovado que a substituição de segmentos amplos ventriculares não impede a contração da musculatura normal
preservada.
Evidência anatomopatológica marcante contra a lâmina única enrolada, temos nos corações com
ventrículo único e nas grandes comunicações interventriculares, porque sem esse pedaço correspondente também não poderia haver progressão muscular ao
redor do VE para ir compor o VD e as hipoplasias
isoladas e acentuadas de VD ou VE não impedem a
REFERÊNCIAS BIBLIOGRÁFICAS
1. Testut L, Latarjet A. Tratado de Anatomia Humana, Barcelona
- Madrid, Salvat Editores S.A., 195.
2. Guyton AC, Hall JD. Tratado de Fisiologia Médica, 9ª Ed., Rio
de Janeiro, Guanabara Koogan, 1997.
3. Junqueira LC, Carneiro J. Histologia Básica, 8ª Ed., Rio de Janeiro, Editora Guanabara Koogan, 1995.
4. http://www.afh.bio.br/sustenta/Sustenta5.asp
5. Wearn JT, Mettier SR, Klumpp TG, Zscthesche LJ. The Nature
of the Vascular Communications Between the Coronary Arteries
and the Chambers of the Heart. Am Heart J, 1933; 9:143-164.
6. Hammond GL, Austen WG. Drainage Patterns of Coronary
Arterial Flow as Determined from the Isolated Heart. Am J
Physiol, 1967; 212:1435-40.
7. Hammond GL, Moggio RA. Function of Microvascular Pathways in Coronary Circulation. Am J Physiol, 1971; 220:1463-7.
8. Vineberg AM. Development of Anastomosis between the
Coronary Vessels and a Transplanted Internal Mammary Artery.
Can Med Assoc J, 1946; 55:117-9.
9. Vineberg AM, Lewin MM. Revascularization of Both Cardiac
Ventricles by Right Ventricular Implants. Can Med Assoc J, 1972;
106:763-9.
10. Tsang JC-C, Chiu RC-J. The Phantom of “Myocardial Sinusoids”: A Historical Reappraisal. Ann Thorac Surg, 1995;
60:1831-5
11. Chiu RC-J, Scott HJ. The Nature of Early Run-off in Myocardial Arterial Implants. J Thorac Cardiovasc Surg, 1973; 65:76877
12. Lukenheimer A, Merker J, Lukenheimer PP. Functional Anatomy of the Coronary Sinusoids. In Mohl W, Wolner E, Glogar D.
Eds. The Coronary Sinus. New York, Springer, 1984.
13. Blood W, Fawcett DW. Textbook of Histology, 10th Ed.,
Philadelphia, Saunders, 1986.
14. Di Dio LJA. Tratado de Anatomia Sistêmica Aplicada. São
Paulo, Atheneu, 2002.
15. Torrent-Guasp F. La Estructura de la pared ventricular izquierda. Comunicación I. Rev Esp Cardiol, 1972; 25: 68-81.
16. Torrent-Guasp F. La Estructura de la pared ventricular izquierda. Comunicación II. Rev Esp Cardiol, 1972; 25: 109-118.
17. Torrent-Guasp F. La estructura de la pared ventricular y su
proyección quirúrgica. Cir Cardiovasc, 1972; 1: 93-108.
18. Torrent-Guasp F, Ballester M, Buckberg GD, Carreras F, Flotats A, Carrió I, Ferreira A, Samuels LE, Narula J. Spatial orientation of the ventricular muscle band. Physiologic contribution and
surgical implications. J Thorac Cardiovasc Surg, 2001;122:389-
92.
19. Torrent-Guasp F, Buckberg GD, Clemente C, Cox JL, Coghlan HC, Gharib M. The structure and function of the helical heart
and its buttress wrapping. I. The normal macroscopic structure
of the heart. Semin Thorac Cardiovasc Surg, 2001; 13:301-19.
20. Torrent-Guasp F, Kocica MJ, Corno AF, Carreras-Costa F,
Flotats A, Cosin Aguillar J, Wen H. Towards new understanding
of the heart structure and function. Eur J Cardiothorac Surg,
2005; 27:191-201.
21. http://www.revespcardiol.org/Images/25v58n06/grande/
25v5
8n06-1307642fig02jpg.
22. Kocica MJ, Corno AF, Carreras-Costa F, Ballester-Rodes M,
Moghbel MC, Cueve CNC, Lackovic V, Kanjuh VI, TorrentGuasp F. The helical ventricular myocardial band: global, threedimensional, functional architecture of the ventricular myocardium. Eur. J. Cardiothorac. Surg., 2006; 29 (suppl. 1):S21-S40.
23. Von Segesser LK. The Myocardial band: fiction or fact?. Eur.
J. Cardiothorac Surg, 2005; 27:181-182.
24. Lunkenheimer PP, Redmann K, Anderson RH. Further discursions concerning the unique myocardial band. Eur J Cardiothorac Surg, 2005; 28:779-80.
25. Torrent-Guasp F. The electrical circulation. Denia: Imp. Fermar, 1970.
26. Langman J. Embriologia Médica - Desarrollo humano normal
y anormal. México, Editorial Interamericana, 1964.
27. Moore LK. Embriologia Clínica, 4ª Ed. Rio de Janeiro, Editora Guanabara-Koogan S/A, 1990.
28. Macruz R, Snitcowsky R. Cardiologia Pediátrica. São Paulo,
Sarvier, 1984.
ORIGINAL
REPORTS
CARACTERIZACIÓN REGIONAL DE LA BIOMECÁNICA VENOSA: ROL DE LA COMPLACENCIA Y VISCOSIDAD EN EL RETORNO VENOSO
(*) Yanina Zócalo, Sebastián Lluberas
(*, **) Daniel Bia
(*, ***) Ricardo Armentano
RESUMEN
Introducción: Diferentes características del sistema venoso (Ej. Existencia de válvulas, vasoconstricción refleja), se han relacionado con el control del
retorno venoso hacia el corazón, ante cambios abruptos en la posición corporal. El rol de las propiedades
biomecánicas venosas en la función de control hemodinámico, no ha sido aclarado.
Objetivo: Caracterizar las propiedades biomecánicas de la pared venosa, y analizar el rol que podrían de-sempeñar en el control del retorno venoso.
Métodos: En un simulador circulatorio, se midió
presión y diámetro de cuatro segmentos venosos, procedentes de siete ovinos: yugular (cuello), cava anterior
(tórax), cava posterior (abdomen) y femoral (miembro
posterior), durante cambios cíclicos en presión entre
0 y 50 mmHg. Se construyó la relación diámetro-presión, que presentó histéresis, y se calculó la complacencia venosa a bajas (<10 mmHg) y elevadas presiones
(>25 mmHg), en la fase de carga y descarga, mediante
*. Departamento de Fisiología, Facultad de Medicina.
Universidad de la República, General Flores 2125 (CP: 11800)
Montevideo, Uruguay. [email protected]
**. ESFUNO, Facultad de Enfermería, Universidad de la República, Hospital de Clínicas “Dr. Manuel Quintela” (3er piso)
Av. Italia s/n (CP: 11600), Montevideo, Uruguay.
[email protected]
***. Facultad de Ingeniería, Ciencias Exactas y Naturales, Universidad Favaloro. Solís 453
C1078AAI, Buenos Aires, Argentina. [email protected]
Autor para correspondencia: Dra. Yanina Zócalo. Departamento
de Fisiología. Facultad de Medicina. Universidad de la República
General Flores 2125. CP: 11800 Montevideo.
Republica Oriental del Uruguay
Teléfono: 0598 2 9243414 extensión: 3313 - Fax: 0598 2 9240395
E-mail: [email protected]
Vol. 2 / Number 1
el cálculo de pendientes de la relación. La viscosidad
parietal se evalúo como la diferencia entre las complacencias obtenida a altas y a bajas presiones, y utilizando un Kelvin-Voigt mediante el índice viscoso.
Resultados: Todos los segmentos presentaron
comportamiento viscoelástico. Independientemente
del segmento y la fase analizada, la complacencia fue
menor a altas presiones (p<0.05). La complacencia
disminuyó hacia la periferia. La viscosidad fue mayor
en las venas periféricas (p<0.05).
Conclusión: Las venas presentaron diferencias
biomecánicas región-dependientes. La viscosidad y
complacencia, y las diferencias regionales en las mismas, podrían considerarse como mecanismo de compensación pasivo, inmediato, importante en el rol de
las venas en la determinación del retorno venoso.
Palabras Clave: Complacencia
Fisiología
Venas
Viscosidad
ABSTRACT
Introduction: Different characteristics of the venous system (i.e. Venous valves, reflex venoconstriction) have been related to the control of the venous
return towards the heart, during sudden changes in the
body position. The role of the veins’ wall biomechanical properties in the haemodynamic control remains
to be elucidated.
Objective: To characterize the veins’ wall biomechanical properties, and to analyse the role that they
would have in the control of the venous return.
Methods: In a circulation mock, pressure and
diameter were measured in venous segments from
seven sheep: jugular (neck), anterior cava (thorax),
posterior cava (abdomen) and femoral (posterior
limb), during cyclic changes in pressure, between 0
and 50 mmHg. From the diameter-pressure relationship, which showed hysteresis, the venous compliance
was calculated at low (<10 mmHg) and high pressure
(>25 mmHg) levels, during the charge and discharge,
through pendents of the relationship. The wall vis-
cosity was evaluated using the difference between the
compliance at high and low pressure levels, and as the
viscous index (Kelvin-Voigt model).
Results: The venous segments showed viscoelastic behaviour. For all the segments, during both
phases (charge and discharge), the compliance was
lower at high pressure (p<0.05). The compliance was
lower towards the periphery. The viscosity was higher
in the peripheral segments (p<0.05).
Conclusion: The veins showed region-dependent
biomechanical differences. The viscosity and compliance, and their regional differences among veins, could
be considered as a passive, immediate mechanism of
compensation, important in the determination of the
venous return.
Key words: Compliance
Physiology
Veins
Viscosity
INTRODUCCIÓN
El sistema venoso desempeña un rol fundamental en el control hemodinámico. En condiciones
fisiológicas, el sistema asegura un retorno sanguíneo
al corazón, adecuado y ajustado, en magnitud y tasa,
a las diferentes condiciones hemodinámicas. Distintas
características del sistema venoso (Ej. existencia de
válvulas, vasoconstricción venosa refleja) se han relacionado con el control del retorno venoso hacia el
corazón ante cambios abruptos en la posición corporal(1). Sin embargo, la importancia de las propiedades
biomecánicas de la pared venosa en la función de control hemodinámico de las venas aún no esta claramente
definida. Lo que es más, el estudio de las propiedades
biomecánicas vasculares ha tenido un interés y crecimiento dispar, siendo la biomecánica arterial muy estudiada, en comparación con la biomecánica de la pared
venosa. Teniendo en cuenta, que la capacidad funcional de los vasos sanguíneos depende de las propiedades viscoelásticas de la pared vascular, determinadas
a su vez por las cantidades absolutas y relativas, y por
la organización de los constituyentes parietales(2, 3, 4,
5), comprender el funcionamiento normal y patológico
del sistema venoso, requiere conocer el comportamiento elástico y viscoso de la pared venosa.
Con relación al comportamiento biomecánico
venoso, existen numerosas interrogantes, y algunos
aspectos deben ser destacados. Primero, si las diferentes venas presentan un comportamiento biomecánico
similar o si existen diferencias región-dependiente
perma-nece controversial. Segundo, la elasticidad y/o
complacencia venosa ha sido estudiada por varios au-
tores, en estudios estáticos(6, 7), pero pocos estudios
analizan el comportamiento dinámico de las paredes
venosas, y consecuentemente se conoce poco acerca
de las propiedades viscosas (frecuencia-dependientes) de las venas en condiciones hemodinámicas fisiológicas. Tercero, diversos trabajos analizan el comportamiento biomecánico de venas en condiciones
hemodinámicas arteriales, como forma de valorar
su utilidad como prótesis vasculares(5, 8), pero pocos
estudios se han desarrollado con el fin de analizar la
respuesta biomecánica venosa en condiciones habituales (fisiológicas) de presión y distensión.
En este contexto, este trabajo tuvo como objetivo caracterizar las propiedades biomecánicas de
la pared venosa, y analizar el rol que podrían desempeñar en el control del retorno venoso. Para ello se
caracterizó el comportamiento biomecánico dinámico
de la pared venosa, sometida a variaciones agudas en
la presión intra vascular. Considerando que podrían
existir diferencias región-dependientes entre diferentes venas del organismo (al igual que en el sistema arterial), se estudiaron venas del cuello (yugular), tórax
(cava anterior), abdomen (cava posterior) y miembro
posterior (femoral).
MATERIAL Y MÉTODOS
Preparación quirúrgica
Siete ovejas raza Merino con pesos corporales entre 35 y 42 Kg., se anestesiaron mediante administración intravenosa de pentobarbital sódico (35
mg/Kg.). La ventilación se mantuvo a través de una
sonda orotraqueal, con ventilación con presión positiva (Dragger SIMV Polyred 201, España).
La disección del paquete vascular del cuello,
de la pata trasera del hemicuerpo derecho y una toracotomía y laparotomía permitieron abordar y disecar
las venas: yugular, femoral, cava anterior y cava posterior (Fig. 1).
Figura 1. Esquema de los segmentos venosos estudiados, y su
localización en el organismo ovino.
Segmentos de 5-6 centímetros de longitud de
cada vena se marcaron mediante puntos de sutura en
sus extremos. Seguidamente, el animal se sacrificó mediante administración de pentobarbital sódico y cloruro de potasio, y los segmentos se escindieron. Los segmentos se conservaron en solución Tyrode oxigenada
a 37ºC y con pH=7,4. Similar procedimiento de obtención de segmentos vasculares, fueron realizados en
trabajos previos(4, 5, 9).
Todos los procedimientos descritos se desarrollaron en acuerdo con la Guía para el cuidado y uso
de animales de laboratorio publicada por el Instituto
Nacional de Salud de Estados Unidos de América
(NIH publicación No. 85-23, revisada 1996).
Estudios biomecánicos
Para el análisis biomecánico, los segmentos
vasculares escindidos se montaron en un simulador
circulatorio, constituido por tubuladuras de polietileno, una cámara de complacencia, un regulador de resistencia tubular, un reservorio con solución Tyrode,
y un corazón artificial (Jarvik Modelo 5, Kolff Medical Inc., Salt Lake City, Utah, USA), alimentado por
una bomba neumática eléctrica. En un sitio donde la
continuidad de las tubuladuras se interrumpe, los segmentos fueron interpuestos, ligando sus extremos sobre las tubuladuras, cerrando así el sistema por el cual
circula solución Tyrode oxigenada, a 37º C y pH=7,40.
Para asegurar un adecuado análisis biomecánico, los
segmentos se estudiaron a la misma longitud de in
vivo(4).
La manipulación de los controles de la bomba,
la cámara de complacencia, las resistencias, y la altura
del reservorio, permitió determinar cambios cíclicos
(1,8 Hz) de presión en el rango de presiones seleccionado (0 y 50 mmHg). Una vez montado cada segmento, se dejó transcurrir 10 minutos en condiciones
de presión y frecuencia de bombeo estables, antes de
comenzar los registros.
La presión intra vascular se midió mediante
un micro transductor de presión (Rango dinámico de
1200 Hz.; Konigsberg Instruments, Inc., Pasadena,
CA), previamente calibrado a 37º C, utilizando un
manómetro de mercurio. Para el registro del diámetro
vascular dos cristales de ultrasonido (5 MHz, 2 mm de
diámetro) fueron suturados a la adventicia vascular, en
sitios diametralmente opuestos. La correcta posición
de los cristales se comprobó mediante la visualización
de las señales en la pantalla de un osciloscopio (Tektronix modelo 465B). Utilizando un sonomicrómetro
(Respuesta en frecuencia 1000 Hz.; Triton Technology
Inc. San Diego, CA) y considerando una velocidad de
ultrasonido de 1580 m/s, se calculó el diámetro a partir del tiempo de tránsito de la señal ultrasónica entre
10
cristales. Previo a los registros, la señal de diámetro
se calibró utilizando el sistema de calibración del sonomicrómetro. Mayor información sobre el simulador
circulatorio y sobre la metodología de estudio puede
encontrarse en trabajos previos de nuestro grupo(4, 5, 9,
10).
Protocolo experimental y
recolección de datos
Los diámetros y presiones de los segmentos
venosos fueron registrados y almacenados durante
un único estado estable. En todos los experimentos
se registró a niveles de baja (<10 mmHg) y alta presión (>25 mmHg), de manera de analizar el comportamiento biomecánico por encima y por debajo del nivel
de presión de quiebre(11).
Las señales temporales fueron visualizadas
en tiempo real, y digitalizadas con una frecuencia de
muestreo de 200 Hz. Entre 20 y 30 ciclos consecutivos
de cada segmento se digitalizaron para posterior análisis.
Análisis de Datos
A partir de las señales de diámetro y presión
de cada segmento se construyó, para cada latido, la
relación diámetro-presión (D-P). Dicha relación presentó en todos los casos un área de histéresis, encerrada por una rama ascendente (de ascenso de presión
o de carga) y una descendente (de descenso de presión
o de descarga) (Fig. 2).
Figura 2. Esquema de la relación diámetro-presión de un
segmento venoso, y de los sitios donde se calculó la complacencia vascular. Para cada uno de los niveles de presión, bajos
(<10 mmHg) y altos (> 25 mmHg) la complacencia vascular
se calculó en la fase ascendente o de carga (círculos blancos) y
descendente o de descarga (círculos negros), como la pendiente
de la relación.
Teniendo en cuenta esto, la complacencia vascular se cuantificó como la pendiente de la relación
D-P en 4 sitios distintos: en la rama de carga y en la
rama de descarga, la complacencia se calculó a “bajas
presiones” (presiones <10 mmHg) y altas presiones
(presiones >25 mmHg). Para el cálculo de la complacencia, se ajustaron relaciones lineales, teniendo en
cuenta entre 5 y 7 puntos de la curva diámetro-presión, en forma análoga a lo descrito en la literatura(6, 12)
(Figura 2). En todos los casos los ajustes lineales para
cálculos de pendiente tuvieron un R2>0,9.
La existencia de una relación D-P con una
rama ascendente y una rama descendente separadas,
de manera que encierran un área, se debe al comportamiento viscoso de la pared venosa(2, 3, 6). Consecuentemente, para un mismo nivel de presión y/o diámetro
vascular, la diferencia entre las pendientes de ascenso
y de descenso de las curvas diámetro-presión se consideró indicadora del nivel de viscosidad parietal. Teniendo en cuenta lo anterior, para cada nivel de presión - alto y bajo - se calculó la diferencia entre las
pendientes de la fase de ascenso (carga) y de descenso
(descarga) de la relación D-P vascular. De esta manera,
se obtuvieron dos indicadores de histéresis del bucle
D-P: para bajas presiones (ΔCBP) y para altas presiones (ΔCAP). Adicionalmente, la viscosidad de la pared
venosa se calculó mediante la metodología de eliminación del área de histéresis de la relación D-P, utilizada previamente en diversos trabajos(2,3,4,9). Para ello
el comportamiento viscoelástico de la pared venosa
fue modelado mediante un Kelvin-Voigt(2, 3, 4, 9).
Análisis Estadístico
Los valores de presión y diámetro, y de los
parámetros biomecánicos fueron expresados como
valor medio ± desvío estándar (VM ± DE). Los valores fueron comparados usando un ANOVA seguido de Test de Bonferroni. Se adoptó un umbral de
p<0,05.
RESULTADOS
La Tabla 1 presenta los valores de presión y
diámetro obtenidos en cada grupo de segmentos. Nótese que todos los segmentos se sometieron a similar
varia-ción de presión. Nótese las diferencias en los
diámetros entre las venas, con disminución de los mismos hacia la periferia.
Tabla 1: Parámetros hemodinámicos
V. Yugular
V. Cava Anterior
V. Cava Posterior
V. Femoral
P. Máxima (mmhg)
52 ± 5
53 ± 5
51 ± 6
55 ± 7
P. Mínima (mmhg)
2±1
2±1
1±1
2±1
a
a,
b
D. Máximo (mm)
10.4 ± 3.1
13.5 ± 1.6
20.3 ± 2.1
6.1 ± 0.6 a, b, c
D. Mínimo (mm)
9.2 ± 3.1
10.9 ± 1.6 a
18.6 ± 2.4 a, b
5.4 ± 0.4 a, b, c
Valores medios ± desvío estándar. P: presión. D: diámetro. V: vena. Estadística: ANOVA seguido de Test de Bonferroni.
Significancia: a, b, c p<0.05 respecto de V. Yugular, V. Cava Anterior, y V. Cava Posterior, respectivamente.
La Fig. 3 presenta los valores de complacencia obtenidos durante la rama ascendente o de carga, y descendente
o de descarga de la pared venosa, para cada uno de los cuatro grupos de venas.
Figura 3. Complacencia venosa para cada grupo de segmentos venosos estudiado, durante las maniobra de carga y descarga, para
bajas y altas presiones. Valores medios ± desvío estándar. Estadística: ANOVA seguido de Test de Bonferroni. Significancia: a, b, c
p<0.05 respecto de V. Yugular, V. Cava Anterior, y V. Cava Posterior, respectivamente.
11
Para cada segmento venoso, la complacencia fue menor a elevadas presiones (p<0,05). Adicionalmente,
para un mismo nivel de presión la complacencia venosa fue mayor en las venas centrales respecto de las periféricas (p<0,05), salvo al comparar la cava posterior y la femoral durante la carga y a altas presiones (p= NS).
La Tabla 2 presenta los parámetros utilizados para caracterizar la viscosidad parietal. Nótese que independientemente del indicador utilizado, la viscosidad fue mayor a medida que las venas se hicieron más periféricas. Adicionalmente, nótese que las venas centrales - cava anterior y posterior - no mostraron diferencias en los
niveles de viscosidad, independientemente del indicador utilizado.
Tabla 1: Parámetros hemodinámicos
ΔCBP (mm/mmHg)
ΔCAP (mm/mmHg)
V. Yugular
V. Cava Anterior
V. Cava Posterior
V. Femoral
11.2 ± 2.1
5.2 ± 1.9 a
5.5 ± 1.8 a
11.3 ± 2.0 b, c
307.4 ± 57.7
148.1± 24.6 a
157.9 ± 27.9 a
340.8 ± 60.5 b, c
0.89 ± 0.13
0.35 ± 0.09 a
0.43 ± 0.17 a
1.53 ± 0.23 a, b, c
Valores medios ± desvío estándar. V: vena. ΔCBP y ΔCAP: diferencia absoluta entre la complacencia venosa de la curva de carga y
descarga, a bajas y altas presiones, respectivamente. η: índice de viscosidad parietal. Estadística: ANOVA seguido de Test de Bonferroni.
Significancia: a, b, c p<0.05 respecto de V. Yugular, V. Cava Anterior, y V. Cava Posterior, respectivamente.
η (mmHg.s/mm)
DISCUSIÓN
Consideraciones metodológicas
A continuación, discutiremos algunos aspectos del diseño metodológico, por considerarse claves
para cumplir con el objetivo propuesto e interpretar
en forma adecuada los resultados del presente trabajo.
Se estudiaron segmentos vasculares ovinos
debido a la similitud del sistema cardiovascular ovino
con el humano(13). Optamos por utilizar segmentos
venosos en lugar de anillos vasculares, frecuentemente
utilizados, ya que los segmentos son mejores para reproducir las condiciones hemodinámicas de in vivo, y
para preservar la forma e integridad de la pared vascular(6, 12). La técnica utilizada para el registro de diámetro y presión in vitro ha sido previamente validada
y utilizada por nuestro grupo(2, 3, 4, 5, 9, 10).
Debido a la dependencia de la respuesta biomecánica respecto de los niveles de presión, para comparar en forma adecuada los diferentes segmentos
venosos, se realizó un análisis isobárico(3,4,5,9,10). Los
niveles de presión en los que se evaluó la respuesta
parietal se escogieron considerando valores pasibles
de ser encontrados en condiciones fisiológicas, por
ejemplo ante cambios posturales. De esta manera, teniendo en cuenta que la presión en venas ovinas puede
encontrarse en un rango de 0-50 mmHg, se caracterizó el comportamiento biomecánico parietal, a niveles
de presión comprendidos en dicho rango. Finalmente,
dado que la relación diámetro-presión presentó histéresis, y que cada fase (ascendente y descendente)
presenta un comportamiento que podría considerarse
bifásico, se caracterizó la complacencia venosa, tanto
en la fase ascendente como en la descendente, y en
cada una de ellas en dos niveles de presión distintos:
bajas (por debajo del punto de quiebre) y altas presio-
12
nes (por encima del punto de quiebre)(11,14).
El comportamiento biomecánico parietal depende no solo del nivel de presión o distensión parietal, sino también de la velocidad y/o frecuencia de
estimulación(2,3). Por esta razón, realizamos un análisis
dinámico de la respuesta biomecánica parietal que nos
permitió evaluar las propiedades velocidad o frecuencia-dependientes, a través de la obtención de indicadores de la histéresis (ΔCBP y ΔCAP) y del comportamiento viscoso (η) parietal.
Caracterización biomecánica
La complacencia vascular relaciona los cambios de volúmenes asociados con cambios en los niveles
de presión de distensión(15). Vasos sanguíneos con
elevados niveles de complacencia presentan grandes
cambios de volumen sanguíneo ante cambios de presión(15). La evaluación de la complacencia es útil en la
caracte-rización biomecánica vascular, particularmente
en los vasos sanguíneos venosos, dado que los mismos
tienen, dentro de las principales funciones el controlar, la distribución corporal del volumen sanguíneo y
el retorno venoso, determinante del gasto cardíaco;
funciones en las que la capacidad de almacenamiento
sanguíneo venoso es fundamental. Al respecto, en la
actualidad numerosas metodologías de valoración biomecánica de segmentos venosos humanos, se basan en
el cálculo de la complacencia vascular(11, 16, 17).
Los resultados obtenidos para cada segmento
venoso muestran que la complacencia fue menor a
altas presiones que a bajas presiones (Figura 3). Este
hallazgo evidencia la reconocida dependencia de la
complacencia respecto de los niveles de presión, y los
resultado son coincidentes con los datos de la bibliografía disponible(11, 14). Asimismo, los resultados obtenidos evidenciaron que la complacencia presenta
diferencias entre segmentos venosos del organismo.
Consecuentemente la capacidad de almacenar sangre
a partir de un determinado cambio en la presión intravascular presenta diferencias regionales (Figura 3).
Al respecto, en términos generales las venas centrales
(cava anterior y posterior) presentaron mayor complacencia que las venas periféricas, tanto en condiciones
de carga (ascenso de presión) como de descarga (descenso de presión). La complacencia parietal depende
de la cantidad absoluta y relativa, y de la organización
de los diferentes componentes parietales, fundamentalmente elastina, colágeno y músculo liso. En relación
con lo anterior se han descrito diferencias regionales
en la estructura venosa, e incluso diferencias en distintos sectores de una misma vena(18). Estas diferencias podrían estar relacionas con las diferencias en
complacencia halladas en nuestro trabajo. Asimismo,
las mismas podrían interpretase como adaptaciones a
las distintas condiciones de trabajo (condiciones hemodinámicas) de las venas de diferentes regiones del
organismo, tal como se analizará más adelante(11).
La viscosidad parietal es la propiedad por la
que los constituyentes de la pared vascular se resisten
a ser deformados, de una manera velocidad o frecuencia-dependiente. El músculo liso parietal ha sido identificado como el principal determinante del comportamiento viscoso de la pared vascular. Dicha viscosidad
esta relacionada con la energía disipada y en el caso
venoso es mayor en las venas periféricas. Existen dos
teorías principales que intentan explicar la génesis de
la viscosidad de las paredes vasculares. La teoría pasiva propone que la viscosidad es una propiedad de
los componentes parietales, reconociendo al músculo
liso como principal determinante(2, 3). Por otra parte,
la teoría activa considera a los mecanismos de generación de tensión activa muscular en la determinación
de la viscosidad de la pared vascular(2, 3). Considerando
los resultados experimentales que sustentan una y otra
teoría, y que las mismas no se excluyen mutuamente,
la viscosidad parietal podría explicarse por la conjunción de ambas. Recientemente Silver y colaboradores
evidenciaron que el colágeno tipo III (presente en las
paredes vasculares) presenta importantes niveles de
viscosidad, por lo que el colágeno podría tener mayor
importancia en la determinación de la viscosidad parietal, que la reconocida hasta el momento(6).
La existencia de propiedades de la pared venosa velocidad o frecuencia-dependientes ha sido
referida tempranamente en la bibliografía(18), pero en
nuestro conocimiento, no existen trabajos que analicen la viscosidad venosa en forma independiente,
mediante el cálculo de índices de viscosidad, como se
propone en este trabajo. Nuestros resultados evidenciaron primeramente que la pared venosa presenta
comportamiento viscoso. Adicionalmente, se encontró, que independientemente del índice utilizado para
caracterizarla, la viscosidad parietal fue mayor en las
venas más alejadas del corazón.
Consideraciones fisiológicas
Como es reconocido, y como fue mencionado previamente, uno de los principales objetivos del
sistema venoso es asegurar un adecuado retorno de
la sangre al corazón. El retorno sanguíneo es el resultado de la acción de fuerzas contrapuestas. Por un
lado, existen factores que se oponen al retorno, favoreciendo el flujo venoso centrífugo (Ej. la presión hidrostática, aumentos de presión abdominal), mientras
que otros factores favorecen el retorno, generando
un flujo venoso centrípeto (Ej. Vis a tergo, aspiración
torácica, pulsación de las arterias, compresión de la
plantilla venosa plantar al caminar, bombeo muscular)(1, 19). Cambios en las posiciones corporales determinan modificaciones en los factores que condicionan
el retorno venoso. En estas situaciones, numerosos
mecanismos se ponen en marcha para asegurar el
mante-nimiento del retorno venoso, a pesar del rápido
disbalance que se genera en el equilibrio de fuerzas(19).
Particularmente durante la adopción del ortostatismo
o durante el descenso del hemicuerpo anterior en un
cuadrúpedo, los mecanismos tienden principalmente a
impedir que el incremento en presión hidrostática determine grandes flujos retrógrados de sangre hacia los
lechos periféricos, y la consecuente reducción del retorno venoso al corazón en los latidos siguientes. Entre otros factores, la acción de las válvulas venosas y el
baroreflejo venoso se han descrito como mecanismos
de compensación(1, 19). Al respecto, ante un cambio de
posición que moviliza grandes volúmenes de sangre
hacia los lechos distales, el cierre de las válvulas de las
venas profundas y la venoconstricción periférica, evitan el flujo retrógrado masivo hacia sectores distales, y
el consecuente vaciado y reducción de la presión en las
venas centrales, al fragmentar la columna hidrostática,
y al aumentar la impedancia al flujo retrógrado, respectivamente. De hecho, alteraciones en los mecanismos
de cierre valvulares y/o del sistema baroreflejo se han
relacionado con la hipotensión ortostática en algunas
situaciones clínicas(1, 19, 20).
En este contexto, los resultados obtenidos
en este trabajo permiten postular la existencia de
un mecanismo fisiológico de determinación del retorno venoso y llenado de las venas centrales, y de
compensación ante cambios posturales, dependiente
13
de las propiedades biomecánicas pasivas de los segmentos venosos, y de las diferencias biomecánicas
región-dependientes (gradientes) entre los segmentos
centrales y distales. Al respecto, la menor complacencia venosa, una vez superado un punto de inflexión o
quiebre, situado en niveles de bajas presiones (aproximadamente 10-15 mmHg), y la existencia de viscosidad parietal, podrían considerarse mecanismos para
limitar los niveles y las tasas de distensión parietal ante
cambios de posición. Más aún, este mecanismo, por
ser fundamentalmente pasivo (no requiere activación
muscular ni del sistema nervioso), y a la vez intrínseco
de la pared vascular (no requiere de otros elementos
más que la propia pared vascular) podría ser el primer
mecanismo de compensación que actuaría limitando
los efectos de los cambios de posición corporal.
Adicionalmente, la mayor viscosidad de las venas más alejadas del corazón, respecto de las centrales,
permitiría postular que el mecanismo de compensación
propuesto cobraría mayor relevancia en las venas periféricas. De esta manera, ante un cambio abrupto de
posición, serían mayoritariamente las venas periféricas, seguidas de las venas centrales, las que resistirían
la sobre distensión, determinando el escurrimiento de
la sangre hacia las venas centrales, favoreciendo así el
retorno venoso.
Por otra parte, los elevados niveles de complacencia de las venas centrales y sus bajos niveles de viscosidad permitirían que inversamente a lo mencionado, ante cambios de posición tendientes a aumentar el
retorno venoso (Ej. al elevar los miembros inferiores)
las grandes venas centrales puedan “acomodar o almacenar” grandes volúmenes de sangre, sin importantes
aumentos de la presión venosa, y consecuentemente
sin mayor sobrecarga auricular. Adicionalmente, la elevada complacencia de las venas centrales permitiría
que se minimizara la transmisión centrífuga de las
ondas de presión y flujo generadas por la contracción
auricular. De esta manera, al igual que su contraparte
arterial, las venas con mayores niveles de complacencia al encontrarse cercanas al corazón, permitirían reducir la generación y transmisión de ondas retrógradas (centrífugas) y consecuentemente para minimizar
la carga externa que soportarían las aurículas en cada
eyección.
mentos venosos presentaron un comportamiento viscoelástico, es decir poseen complacencia e histéresis.
Independientemente del segmento analizado y de la
fase de carga o de descarga analizada, la complacencia
venosa fue significativamente menor a altas presiones.
El comportamiento biomecánico presentó diferencias
regionales, con aumento de la complacencia y reducción de la viscosidad parietal hacia las venas centrales.
Dichos gradientes biomecánicos jugarían un rol protagónico en asegurar un adecuado retorno venoso.
CONCLUSIÓN
En el presente trabajo se caracterizó el comportamiento biomecánico de segmentos venosos
ovinos, analizando la relación instantánea diámetro-presión vascular, en función de la complacencia
(inclinación) y la histéresis (área) del bucle. Los seg-
9. Cabrera Fischer EI, Bia Santana D, Cassanello GL, Zocalo Y,
Crawford EV, Casas RF, Armentano RL. Reduced elastic mismatch achieved by interposing vein cuff in expanded polytetrafluoroethylene femoral bypass decreases intimal hyperplasia. Artif Organs. 2005; 29(2): 122-30.
14
AGRADECIMIENTOS
Al Sr. Elbio Agote por su importante contribución durante el desarrollo de las experiencias.
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H15-21.
8. Berceli SA, Showalter DP, Sheppeck RA, Mandarino WA, Borovetz HS. Biomechanics of the venous wall under simulated arterial conditions. J Biomech. 1990; 23(10): 985-9.
10. Bia D, Zocalo Y, Pessana F, Armentano R, Perez-Campos
H, Saldias M, Alvarez I. Femoral arteries energy dissipation and
filtering function remain unchanged after cryopreservation procedure. Transpl Int. 2005; 18(12): 1346-55.
11. Risk MR, Lirofonis V, Armentano RL, Freeman R. A biphasic
model of limb venous compliance: a comparison with linear and
exponential models. J Appl Physiol. 2003; 95(3): 1207-15.
12. Mavrilas D, Tsapikouni T. Dynamic mechanical properties of
arterial and venous grafts used in coronary bypass surgery. Journal of Mechanics in Medicine and Biology. 2002; 2(3-4): 1-9.
13. Kohler TR, Kirkman TR. Dialysis access failure: A sheep
model of rapid stenosis. J Vasc Surg. 1999; 30(4): 744-51.
14. Molas MC, Bia D, Zócalo Y, Craiem D, Risk M, Armentano
R. Validación Experimental del Modelo Bifásico de la Relación
Compliance-Presión en Venas. Tercer Congreso Virtual de Cardiología por Internet. Federación Argentina de Cardiología. 1º de
setiembre-30 de noviembre, 2003. Páginas:1-6. http://www.fac.
org.ar/tcvc/llave/c410/molas.
15. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries. Theoretical, Experimental and Clinical Principles. London,
UK: Edward Arnold, 1998.
16. de Groot PC, Bleeker MW, Hopman MT. Ultrasound: a reproducible method to measure conduit vein compliance. J Appl
Physiol. 2005; 98(5): 1878-83.
17. Neglen P, Raju S. The pressure/volume relationship of the
calf: a measurement of vein compliance? J Cardiovasc Surg (Torino). 1995; 36(3): 219-24.
18. Alexander RS. Chapter 31: The peripheral venous system.
Handbook of physiology. Section 2: Circulation. Volume II.
American Physiological society. Waverly Press, Inc., Baltimore,
Maryland. 1963.
19. Guyton AC, Hall JE. Texbook of Medical Physiology. W.B.
Saunders Company; 11th edition 2005, ISBN 0-721-60240-1.
20. Freeman R, Lirofonis V, Farquhar WB, Risk M. Limb venous
compliance in patients with idiopathic orthostatic intolerance and
postural tachycardia. J Appl Physiol. 2002; 93(2): 636-44.
15
ORIGINAL
ARTICLES
Vol. 2 / Number 1
UTILIZAÇÃO DA COLORAÇÃO COM SOLUÇÃO
ETANÓLICA DE IODO NO ESTUDO MACRO E MICROSCÓPICO DO COMPLEXO ESTIMULANTE DO
CORAÇÃO EM VERTEBRADOS
Ronaldo Araújo Abreu1, Enio Ferreira2
Cristina Maria de Souza3
Abstract:
The structure nodal can be characterized as being mass of heart muscular fibers specialized, involved
by woven abundant fibroelastic tissue, predominantly
woven collagen. In this work five anatomical molds of
heart of vertebrates were produced, with the purpose
of contributing with the characterization of the study
of the stimulating complex in different species: fish,
amphibians, reptiles, birds and mammals.
The hearts were red-faced with solution iodine
etanolic, dissected in stereoscopic microscope and collected fragments for the histomorfological analysis, in
order to evidence the anatomical pattern presented by
the stimulating complex. With base in the morphology of the studied pieces was possible to observe that
the solution iodine etanolic was shown effective in the
identification of the stimulating complex of different
species.
Key Words: Stimulating complex
Vertebrates
Solution iodine etanolic
1, 2 Msc Faculdade
Itabirana de Saúde – FISA/FUNCESI, Itabira, MG, Brazil
1 MscMD Departamento de Morfologia, Faculdade de Medicina
da UNINCOR, Belo Horizonte, MG, Brazil
2 MscMV Departamento de Patologia Geral, Laboratório de
Pato-logia Comparada da Universidade Federal de Minas
Gerais (UFMG), Belo Horizonte, MG, Brazil
3 Bio Faculdade Itabirana de Saúde – FISA/FUNCESI, Itabira, MG, Brazil
16
INTRODUÇÃO:
Estudos sobre o complexo estimulante no coração do homem e de mamíferos domésticos relatam
que suas primeiras descrições datam de 1893 realizadas
por His Jr. (1), o qual foi intitulado mais tarde de feixe
de His (fascículo atrioventricular). O conhecimento da
anatomia do sistema de condução foi marco para pesquisas subseqüentes (2).
O coração é um órgão muscular que contrai
ritmicamente e possui complexo próprio para gerar estímulos e transmitir a excitação produzida. No
miocárdio, uma camada média e espessa, contém células musculares cardíacas arrumadas em espirais complexos ao redor de orifícios das câmaras. Estes nós são
estruturas especializadas na geração ou condução dos
impulsos elétricos do coração (3).
Podemos descrever histomorfologicamente a
estrutura nodal como sendo uma massa de fibras musculares cardíacas especializadas, envolvidas por abundante tecido fibroelástico, predominantemente tecido
colágeno e irrigação sanguínea própria, caracterizada
pela presença de artéria e veia nodal (4). O glicogênio
é um polímero de cadeia ramificada α-D-glicose, encontrado nas células animais em forma de grânulos,
presentes em células do fígado e de músculos bem alimentados. Esse composto pode ser facilmente identificado nos tecidos através de uma reação especifica
com o iodo, formando um complexo azul chamado
adsorbato azul (5). Assim, essa estrutura pode ser caracterizada por meio de colorações especiais (Tricrômio de Masson ou Gomori).
Apesar de o complexo estimulante ser bem
caracterizado estudos sobre sua morfologia, nos vertebrados, são escassos e pouco conclusivos.
Diante da dificuldade na obtenção de infor-
mações pormenorizadas, sobre detalhes da técnica de
estudo com moldes vasculares aplicáveis as diferentes dimensões e texturas observadas na escala animal,
seria de grande contribuição, a realização de estudos
sobre a anatomia comparada do complexo estimulante
nos vertebrados, a partir da técnica de coloração com
solução etanólica de iodo.
MATERIAL E METODOS
Foram utilizados corações de peixe (Tilapia
rendalli), anfíbio (Bufo paracnemis), réptil (Crotalus
catalinensis), ave (Gallus gallus) e mamífero (Oryctolagus cuniculus), constituindo um exemplar de cada
classe, num total de 5 peças. Os animais foram obtidos
no Mercado Municipal de Itabira/MG e de um sistema de criação doméstico localizado na mesma cidade.
Técnica de Injeção de Solução
Etanólica de Iodo
Utilizou-se uma seringa de 10mL, duas sondas de no 4
e um recipiente do tipo béquer, com solução etanólica
de iodo. Para peças pequenas procedeu-se da seguinte
maneira: 1) secção transversal no ápice do coração; 2)
imersão do coração em solução etanólica de iodo. Para
peça grande procedeu-se da seguinte maneira: 1) separação e identificação dos vasos da base do coração; 2)
canulização dos vasos com sonda no 4; 3) injeção da
solução etanólica de iodo.
Em seguida, todos os corações foram lavados
em água corrente e dissecados na região de estudo. Para
tanto foi utilizados instrumentos cirúrgicos adequados,
um campo visual de uma lupa frontal (aumento 3 dioptrias) e microscópio esterioscópico. Após esta análise
foram retirados os seguintes fragmentos do coração
de cada animal: Seio venoso, margem atrioventricular
direita, margem anterior direita da parede atrial, septo
interventricular, trigono de Koch (nó atrioventricular) e junção cava superior-átrio direito (nó sinoatrial).
Após o procedimento estes fragmentos foram fixados
e enviados para análise histológica.
Técnica Histológica
Os tecidos foram fixados em formol neutro,
tamponado a 10% e processados pela técnica rotineira de inclusão em parafina (6). Secções histológicas
de 4 µm foram coradas pelas técnicas da hematoxilinaeosina (6) e tricrômio de Gomori para avaliação morfológica e evidenciação de tecido fibroconectivo (7).
As colorações especiais compreendem um
conjunto de tinturações utilizadas para ressaltar determinados tipos de estruturas no tecido. A coloração especial tricrômio de Gomori é utilizada principalmente
para evidenciação de tecido fibroconectivo, onde
podemos observar fibras colágenas com coloração
verde-azulácea (7, 8).
RESULTADOS
A técnica de coloração com utilização da
solução etanólica de iodo como marcador do complexo estimulante, identificadas em microscópio esterioscópico, foram confirmadas por meio do estudo
histomorfológico do tecido cardíaco.
No peixe (Tilapia rendalli), o estudo macroscópico da anatomia cardíaca revelou a presença de
átrio e ventrículo único. Após a utilização da solução
etanólica de iodo não foi possível a definição da anatomia de uma estrutura nodal. Estes achados foram
confirmados a histologia, onde foi possível observar
apenas a presença discreta e não delimitada de tecido
fibroelástico, esboçando sugestivamente um primitivo
seio coronário (Fig.1).
Fig.1- (Tilapia rendali) – Corte transversal da parede atrial- nó
atrioventricular (Tricrômio de Gomori – 50x). Observa-se músculo atrial em coloração avermelhada, e feixes discretos de fibras
nodais em coloração esverdeada.
No anfíbio (Bufo paracnemis), a anatomia
cardíaca definiu-se pela presença de átrio direito e esquerdo septados completamente e ausência de ramos
arteriais coronários. Após utilizar a solução etanólica
de iodo neste coração, não foi identificada nenhuma
estrutura nodal formada. Esses achados foram confirmados no estudo histomorfológico, que identificou
a presença de fibras colágenas dispersas pelo tecido
cardíaco e uma suposta “primitiva estruturação” nodal
na região atrioventricular (Fig.2).
17
Fig.2- (Bufo paracnemis) – Corte transversal da parede atrial nó sinoatrial (Tricrômio de Gomori – 50x). Observa-se tecido
muscular em coloração avermelhada e uma fraca dispersão feixes
de fibras nodais em coloração esverdeada. Entre as fibras nodais
nota-se ausência de formações vasculares.
No réptil (Crotalus catalinensis), o coração
apresenta completa separação da câmara atrial direita
e esquerda, com preservação do seio coronário. Similar ao observado nos espécimes anteriores, após utilização da solução etanólica de iodo, não foi possível
identificar nenhuma estrutura nodal na parede atrial,
nem mesmo na região do septo interventricular, o que
também foi confirmado à histologia (Fig.3).
Fig.4- (Gallus gallus ) – Corte transversal da parede atrial- nó
sinoatrial (Tricrômio de Gomori – 50 x). Observa-se feixes de
fibras nodais em coloração esverdeada. Entre as fibras nodais
nota-se a presença de formações vasculares representadas pela
artéria e veia nodal (setas).
O coração do mamífero foi muito bem caracterizado macroscopicamente e histomorfologicamente,
sendo possível observar a estrutura do nó sinoatrial na
margem superior da parede atrial, o nó atrioventricular
na região septal ventricular, feixes internodais e artéria
nodal (Fig.5).
Fig.4- (Oryctolagus cuniculus) – Corte transversal da parede do
septo interventricular - nó atrioventricular (Tricrômio de Gomori – 50 x). Observa-se a presença de tecido do miocárdio em
coloração avermelhada e feixes de fibras nodais em coloração esverdeada. Entre as fibras nodais nota-se a presença de formações
vasculares representadas pela artéria nodal (seta).
Fig.3- (Crotalus catalinensis) – Corte transversal da parede atrial
e septo interventricular (Tricrômio de Gomori – 50 x). Observase músculo atrial em coloração avermelhada, e feixes de fibras
nodais em coloração esverdeada. Entre as fibras nodais não há
presença de formações vasculares.
No coração da ave (Gallus gallus), a anatomia
cardíaca apresentou-se composta por duas câmaras
atriais e duas ventriculares com septação completa.
A coloração com solução etanólica de iodo permitiu
identificar nitidamente a anatomia do complexo estimulante. A presença desse complexo foi inteiramente
confirmada à histologia, caracterizado pela presença
de feixes nodais e a estruturação de ambos os nós sinoatrial e atrioventricular no tecido cardíaco, e formações vasculares representadas pela veia e artéria nodal
(Fig.4).
18
DISCUSSÃO
Sabendo que nos tecidos cardíacos, em especial
na região do complexo estimulante, encontra-se uma
maior quantidade de glicogênio, utilizamos a solução
etanólica de iodo, como um marcador da estruturas do
complexo estimulante, facilitando assim o seu estudo
(8, 9, 10).
A técnica de coloração anatômica com a
solução etanólica de iodo utilizada, nesta investigação,
apresentou resultados satisfatórios para a evidenciação
da estrutura nodal, com a coloração esperada do tecido cardíaco. O uso deste material trouxe maior nitidez,
destacando os componentes anatômicos macroscópicos estudados.
Rodrigues (11) demonstrou a partir de moldagem em acetato de vinil, ausência de circulação coronária nos moldes de peixes (Peixe arabaiana, Elagatis
bipinnulatus).
O coração do peixe (Tilapia rendalli) constituise de um sistema cardíaco simples, com apenas duas
câmaras cardíacas, sem vasos sangüíneos coronários.
Ramsay (12) afirmou que os vertebrados inferiores na
escala zoológica não possuem vasos sangüíneos, sendo
a difusão seu modo de nutrir o coração. A coloração
do tecido cardíaco, por meio da solução etanólica de
iodo mostrou-se eficaz, pois a análise macroscópica
das estruturas estudadas apresentadas aqui foi comprovada na histologia.
O coração do anfíbio (Bufo paracnemis) apresentou maior complexidade e diferenciação na morfologia de suas câmaras cardíacas apresentando septação
interatrial completa (10). Também neste trabalho, as
identificações histomorfológicas corresponderam aos
achados macroscópicos.
Grasse (4) relatou que a irrigação do coração de
anfíbios ocorre pelo sangue circulante nas cavidades
cardíacas devido à ausência de artérias coronária a partir do bulbo aórtico como demonstrou Mooré (4).
No réptil, de acordo com o observado no coração da serpente (Crotalus catalinensis), foi possível
observar uma evolução cardíaca em relação aos animais anteriores, o ventrículo é parcialmente dividido
por uma estrutura septal e há presença de uma discreta
nutrição (4). Os achados histomorfológicos corresponderam às análises macroscópicas, o que validou a coloração com solução etanólica de iodo.
Getty (13), a trabalhar com galinhas relatou a
presença de novos vasos sangüíneos no miocárdio e
septo interventricular.
Na ave (Gallus gallus),a morfologia cardíaca,
definiu-se pela formação de quatro câmaras cardíacas,
com presença de fibras nodais que confirmaram à histologia. Com a nítida estruturação dos nós, sinoatrial
e atrioventricular, presentes neste coração permite-se
inferir que a presença de vasos sangüíneos e principalmente de artérias com ramificações, ao longo do
tecido cardíaco tenha permitido a caracterização de
um sistema próprio de nutrição e condução do coração das aves (13).
O modelo produzido da espécie Gallus gallus
confirmam dados da literatura, o que valida mais uma
vez a ação da solução etanólica de iodo como identificador do sistema de condução.
No mamífero (Oryctolagus cuniculus), a presença de estruturas bem definidas é justificado pelo
completo sistema circulatório; composto por estruturas nodais independentes, na qual predominam fibras
colágenas, fibroblastos e inúmeros nervos (9). Ocorreu correspondência da análise macroscópica com a
histologia, na qual foram encontradas células alonga-
das em forma de feixes similares aos encontrados por
Mazoon (4), ditas células P (4). Mais uma vez a solução
etanólica de iodo para a coloração do tecido cardíaco
fica validada.
Este estudo deixa a proposta de realizações de
novas pesquisas cientificas, com o aprimoramento da
técnica utilizada, o que abre uma possibilidade de sua
utilização sob a forma de compostos não tóxicos que
possam ser usados nas câmaras cardíacas humanas em
cirurgias, para a evidenciação do complexo estimulante
e principalmente das estruturas nodais e seus ramos.
REFERÊNCIAS
1. Grassé, PP. Traité de zoologie. Paris: Masson Editeurs; 1954.
p.1145.
2. Cardoso JR, Severino RS, Mota FCD, Martins AK, Silva FOC.
Aspectos da Irrigação do Nó Atrioventricular e Tronco do Fascículo Atrioventricular em Bovinos Mestiços Girolando. Brazilian
Journal al of Veterinary 2003; 40:6:314-20
3. Gartner LP, Hiatt JL. Tratado de Histologia. Rio de Janeiro:
Ganabara Koogan; 1997.
4. Williams PL, Warwick R, Dyson M, Bannister LH. Gray
Anatomia. 30a ed.Vol.l . Rio de Janeiro: Guanabara Koogan.
2004. p.648-74.
5. Campbell MC. Bioquímica. Porto Alegre : Artemed; 2000.
p.430-32. Grassé, PP. Traité de zoologie. Paris: Masson Editeurs;
1954. p.1145.
6. Luna LG. Manual of Histologic Staining Methods of the
Armed Forces Institute of Pathology. 3a ed. New York: Mac
Graw Hill; 1968; p.258.
7. Ham A W. Histologia. 8a ed. Rio de Janeiro: Ed. Guanabara
Koogan; 1983.
8. Prophet EBM, Arrington JB, et al. AFIP Laboratory Methods in Histotechnology. Washington Am. Registry of Pathology;
1992. p278.
9. Melo SR, Lacerda CAM, Souza RR. Características Ultra-estruturais do nó sinoatrial de rato Wister. Acta Scientiarum Maringá, 2002; 24:3:681-685.
10. Moore JA. Physiology of the Amphibia. New York: Academic Press; 1964. p540.
11. Rodrigues TMA, Palmeira JAO, Mendonça JT, Gomes OM.
Estudo Evolutivo da Anatomia das Artérias Coronária em Espécies de Vertebrados com Técnicas de Moldagem em Acetato de
Vinil (Vinilite). Rev Bras Cir.Cardiovasc 1999; 14:4:331-339.
12. Ramsay, JA. Introdução à Fisiologia Animal. São Paulo:
EDUSP e Polígona. 1968. p173.
13. Getty R. Anatomia dos Animais Domésticos. Rio de Janeiro:
Interamericana; 1981. p.1350.
19
UPDATING
ARTICLES
Vol. 2 / Number 1
Pulmonary Embolism
Carvalho Jr, Ildevaldo J; Carvalho MBL;
Bicalho RC; Bicalho; Carvalho JI
Pulmonary embolism is a clinical syndrome
characterized by the obstruction of the lung artery or
of branches by thrombus. Calculatedly, 5 out of 10
000 patients shall have pulmonary embolism(1). The
mortality rate in the first hour is about 11%, which
accounts for 30% of those who were not diagnosed(2).
TEP (lung embolism) does not take place until clots
are formed and propagated. In several circumstances, other substances such as oil, amniotic liquid, gas,
greasy cells, talc, etc., can clot the lung. Over 90% of
REFERENCES
Modan et al, 1972
Rossman et al, 1974 (‘’)
Coon, 1976
Goldhaber et al, 1982 (‘’)
Goldman et al, 1983
Rubinstein et al, 1988 (‘’)
Landerfeld et al, 1988 (*)
Kaminski et al, 1989 (r)
Rao et al, 1990 (1)
Haunch et al, 1990 (‘’)
Mckelvie,1994
Morgenthaler et al, 1995
Stein et al, 1995 (1)
TOTAL
Table 1
Autopsy studies in TEP
n
Autopsy (+) n (%) Suspect (-) n (%)
2.107
353 (17)
235 (67)
250
16 (6)
8 (50)
4.600
267 (12)
514 (91)
1.455
54 (4)
38 (70)
300
24 (8)
15 (63)
1.276
44 (3)
30 (68)
233
15 (6)
11 (73)
21.529
67 (0,3)
59 (88)
231
18 (8)
11 (61)
131
16 (12)
13 (81)
132
16 (12)
13 (81)
2.427
92 (4)
63 (68)
404
20 (5)
14 (70)
35.075
1.302 (3,7%)
1.204 (78,6%)
These data can provide us with a notion of the
scope of the problem, whereas the presence of risk
factors and their evaluation comprise the initial step
for diagnostic suspicion. The main risk factors for vein
thrombosis are:
•
Surgical and non-surgical trauma
•
Immobilization
20
the cases of TEP have their origin in deep veins of the
inferior members, popliteal veins or even more proximal veins, as well as of prostate, uterine and renal areas and even of the interior of the heart chambers.
Virchow’s triad, which is characterized by stasis, intimal lesion and increased coagulation, constitutes the
main predisposing factor(3).
The table below shows that out of the TAP
cases confirmed by autopsy no diagnosis was performed in 78,6% of the cases.
•
•
•
•
•
•
•
Malign diseases such as multiple myeloma
Heart failure
Acute coronary syndrome
Obesity
Varicose veins
Estrogen
Childbirth
•
•
Chronic obstructive pulmonary disease
Thrombophilias
The following stand out among the thrombophilias:
•
Deficiency of the antithrombin
•
Deficiency of C, S proteins.
•
Resistance to C protein, or Leiden’s V factor.
•
Dysfibrinogenemia
•
Antiphospholipid syndrome
•
Mutations of the prothrombin
•
Disorders of the plaminogen
to the thrombus and to a decreased downstream blood
flow of the same. These conditions increase vascular
resistance and lead to higher lung blood pressure and
increased work of the right ventricle. The seriousness
depends on the size of the thrombus and whether or
not bacteria and previous lung diseases are present, in
addition to other possible comorbities. The endothelium ischemic lesion comprises a sequence of events
in which there is a decrease in surfactant within 2-3
hours, with total loss occurring within 15 to 16 hours,
followed by lung congestion, alveolar hemorrhage and
lung constriction within 24-48 hours. Lung infarction
can happen within 1 to 7 days with resolution of the
hemorrhage occurring within 7 to 10 days and resolution of the infarction in 2-3 weeks(5).
In addition to other comorbities:
•
Nephrosis
•
Pelvis and femur fractures
•
Paroxysmal nocturnal hemoglobinuria
The presence of previous vein thrombosis is Clinical manifestations
According to works such as UPET/USPET(6),
an important factor for recurrence. The relation between immobilization and thrombosis is a highly de- PIOPED(7), and Chest, 1991:100:598-603 the followfined factor(4). When the clot lodges in the lung arteries ing table shows the commemorative signs and sympor in one of their branches, immediate hemodynamic toms of this Syndrome.
consequences lead to an increased pressure proximal
Table 2
SIGNS AND SYMPTOMS UPETI USPET (%)
PIOPED (%)
Dyspnea
84
73
Pleural Pain
74
66
Cough
50
37
Pain MMII
39
26
Hemoptysis
28
13
RF > 20cpm
85
70
Rales
56
51
CF > 100 bpm
58
30
B2P > B2A
57
23
Pleural friction
18
03
Compatible clinical scenarios should be appraised in making the diagnosis as described in Table 3.
Table 3
CLINICAL SCENARIOS HIGHLY COMPATIBLE WITH TEP
Acute thoracic symptoms Syncope
Acute thoracic symptoms with conscious loss
Sudden failure or unclear heart failure or chronic pneumonia
Heart shock without AMI
Sudden tachycardia or cardiopulmonary arrest
Pleural pain and hemoptysis
Dyspnea and disproportionate hypoxia to the volume of pleural effusion
Physiopathology
This event leads to increased lung vascular resistance and higher pressure of the overloaded right
ventricle, resulting in microinfarcts of the right ventricle and increased shear stress, degradation of the
myofilaments, increased troponin levels, increased
messenger RNA le-vels and increased levels of both
brain and atrial natriuretic factor.
Table 4 below shows an algorithm diagnosis
to approach this pathology.
21
•
•
•
•
•
•
•
•
•
•
•
•
•
Table 4
Diagnostic approach
Pulmonary embolism: proposal of algorithm diagnosis
Suspicious: risk factors/clinical scenario
Chest X-rays
Blood count, plaques, prothrombin activity, TTPA.
Troponins
Atrial natriuretic factors
D-dimers
Blood gases: D(A-a)02
Electrocardiogram/echocardiogram
Scintilography V1Q
Duplex Scan MMII (Eco)
Helicoidal angiotomography
Lung arteriography
Chest X-rays
Chest X-rays are rather unspecific. The International Cooperative Pulmonary Embolism Registry
(ICOPER) conducted a consecutive study of 2454
patients diagnosed with lung clot, including patients
with both symptomatic and non symptomatic clot.
The table below shows the main findings(8) with chest
x-rays being normal in 25% of the patients with TEP.
Table 5
Abnormalities of Chest X-rays associated with pulmonary embolism
Patients whose
Percentage
abnormalities and/
Abnormalities
%
or radiographies
were interpreted
Heart growth
27
622/2315
Pleural effusion
23
523/ 319
Diaphragm elevation
20
457/2316
Increase of the heart area PA
19
443/2305
Atelectasy
18
410/2310
Infiltrated
17
400/2317
Lung congestion
14
330/2316
Oligemia
08
196/2315
Lung infarct
05
117/2312
Although some radiographic findings are less
frequent they can virtually become the determining
factor in diagnosis.
The radiograph below shows Westermark’s
sign due to decreased blood contribution to a segment
or to one lung. The presence of this sign should be
highly va-lued.
FIGURE 1
Note the increased transparency on the right lung in relation to
the left one. This sign is observed in 2% of the cases of TEP
22
Hampton’s hump is an image observed in the
Chest X-ray of a pleural-based shallow consolidation
in the form of a truncated cone with the base against
the pleural surface, which is a sign of TEP.
FIGURE 2
Hampton’s hump implicates in pulmonary infarction with occurrence around the seventh day.
FIGURE 3
Fleischner’s atelectasy - long lines (fibrous scars) arising out of the
invagination of the pleura at its base, resulting in pseudo-fissure.
Fleischener’s sign. With pleural effusion.
7 days. It may show no alteration in 30% of the cases
D - Dimer
The dimer D is the degradation product of fi- of TEP.
As the specificity of the test is low and the
brin under the action of plasmin. It is useful for the evaluation of deep vein thrombosis and pulmonary sensibility is high, it means that a negative value practiembolism. In patients like these the endogenous fi- cally excludes TEP and TVP. A positive result of the
brinolisis takes the formation of D-dimer. D-dimer test indicates that there is a high level of degradation
is detected one hour following the occurrence of the product of fibrin in the organism, and the anticoaguthrombus, the levels of which remaining elevated for lant therapy can lead to a false-negative test(9).
Table 6
D- Dimers - Stastistics
Sensibility
93%
(CI: 90 a 97 )
Specificity
25%
(CI: 90 a 97 )
Prevalence (Pretest probability)
26%
(CI:19 a 31)
Value positive predictive
30%
(Cl: 24 a 37 )
Value negative predictive
91%
(CI: 87 a 96)
Natriuretic factors and troponins
Brain natriuretic factor (BNP) is a small peptide secreted by cardiac myocytes for the control of
blood pressure and water balance. It is synthesized by
ventricular myocardial cells and stored as a pro-form.
Its secretion is in response to volume expansion or
pressure overload. BNP and NT-proBNP markers
23
are released following ventricular distension(10). The
usefulness of these factors has been demonstrated in
cases of ventricular dysfunction and acute coronary
artery syndromes and may pre-sent altered values in
cases of pulmonary embolism(11). The table below
shows comparative values, including alterations of
these markers, as well as of troponins, which are often
considered markers of acute coronary syndrome(12),
but can also present alterations in cases of TEP due to
the fragmentation of myocytes.
Blood gases
The alveolus-arterial gradient of oxygen is calculated by the following equation:
P (A-to) 02 = [FiO2 (PB - 47) - (PaCO2 I R) - PaO2]
Where
Fi:02 = inspired fraction of oxygen
PB = local barometric pressure
47 = pressure of steam of water in the aerial bronchus
R = breathing quotient often estimated at 0.8 under
breathing conditions
Fi02 greater than 0,6 = the correction by means of R
can be eliminated.
PaO2 and PaCO2 = arterial gases
There is substantial evidence that an alveolusarterial gradient of normal oxygen does not exclude
acute symptomatic pulmonary embolism. The combination of blood gases with the alveolus-arterial gradient of normal oxygen can be used to exclude pulmonary embolism. This is based on the observation that
patients who showed a clinical picture of pulmonary
embolism, with no history of previous heart and lung
disease, had hypoxemic res-piratory failure in 93% of
the cases and in 98% of the cases showed an increased
alveolus-arterial gradient of oxygen(13).
Electrocardiogram and pulmonary embolism
The electrocardiogram in acute pulmonary
embolism can show several configurations. The following findings, however, have proven to be most
common:
•
SI Q3T3 - prominent Sin DI waves and Q in
D3 wave with inverted T.
•
Total or partial right branch block that disappears following the acute phase
•
Deviation of the axis to the right.
•
Transition zone shifts from V4 to V5 and to
V6.
•
Elevation of ST in VI and AVR.
•
Low QRS amplitude.
•
Sinusal tachycardia, fibrillation atrial/flutter,
premature beats.
•
T-wave inversion from V1-4, often a late sign.
The SI Q3 T3 pattern refers to the clockwise
rotation of the heart as found in overloaded right ventricle, as observed in 10% of the cases with serious
pulmonary embolism. The right ventricle can grow
and the septum can shift to the right, leading to a
stretching that can generate alterations such as total or
partial right branch block. As a result the right atrium
volume can increase, thus contributing to the occurrence of arrhythmias(14).
Figure 4
Echocardiogram
Approximately 40% to 50% of the echocardiograms from patients with TEP show right ventricle
dysfunction. Acute vascular dysfunction and neurohormonal effects increase lung blood pressure leading to overload, dilation, dysfunction and ischemia
of the right ventricle, oftentimes with the intraventricular septum moving towards the left ventricle. In
1993 Goidhaber et al demonstrated the benefit of the
24
thrombolysis in the RV dysfunction(15). There is a correlation between the dysfunction of the right ventricle
and the evolution of patients with confirmed TEP.
Lung systolic pressure can be estimated measuring the top speed of the regurgitant tricuspid flow
obtained with the echocardiographic doppler. The
gradient through the tricuspid valve can be estimated
by the modified Bernoulli’s equation, P=4 V2, where
P stands for the difference between peak pressure of
right atrium and right ventricle, and V represents the
peak speed of the regurgitant jet, with the estimated
atrial pressure being added to the value of the gradient.
Most important alterations found in echocardiograms can summarized as follows(16, 17):
•
Dilation of right cameras
•
Tricuspid regurgitation
•
Paradoxical movement of the septum
•
RVEDA/LVEDA> 0,6 *
Meaning:
Hypocinesia of the RV + TVP + symptoms of TEP
= TEP
Hypocinesia of the RV without hypotension: 40%50% of probability
Hypocinesia probability of the RV:
•
Has a mortality rate two times greater (14
days).
•
Larger recurrence of TEP
•
Greater risk of developing into pulmonary hypertension
Scintilography
The scintigraphic examination is made with
Tc99m Tecnesio-marked albumin particles which
are injected to impact the capillary arterioles of the
lung. The distribution of particles is proportional to
the blood flow. About 200 to 500 thousand particles
are injected. This exam is quite sensitive but it is not
specific as other conditions can determine defects of
lung perfusion. To improve specificity we also make
ventilation scintigraphic examinations with the use of
Xenon 133 doses. In Brazil, ventilation scintigraphic
examinations are made using DT-shovel-Tc-99m nebulization gas.
Essentially, a scintigraphic examination normal
result excludes recent lung clot. Scintigraphic examinations are used as an indirect diagnosis method since
it does not detect the clot itself. Other conditions such
as tumors, heart failure, pulmonary fibrosis and obstructive disease of the aerial branches can generate
defects. The result of the scintigraphic examination
is given in terms of high, intermediate and low prob-
ability, depending on the type of abnormality. A high
probability result means that there are large multiple
segmental perfusion defects and normal ventilation.
In this case the chances are that 85% of these patients
might have pulmonary clot. Furthermore, this implicates that 15% of these high probability patients do
not have lung clot. Most of the patients with suspected embolism are not classified as high probability patients because they have either a low, intermediate or
normal scintigraphic pattern probability, and in cases
like these the probability of clot is only of the order
of 25%. A clinical evaluation improves the accuracy
of this result provided that it conforms to the exams,
with only 1/3 of the patients being diagnosed. A low
probability scintilography does not exclude lung clot.
In face of a low probability scintigraphic examination
associated with low clinical probability the treatment
of pulmonary embolism is interrupted, which stands
in striking contrast with both scintigraphic and clinical
probability where the treatment is mandatory(18, 19).
The largest study to date on evaluating the role
of pulmonary ventilation/perfusion scintilography
for the diagnosis of TEP was the prospective investigation of pulmonary embolism diagnosis (PIOPED).
In a study of high probability ventilation/perfusion
for TEP, 40% sensibility and 98% specificity, as well
as an 87% predictive positive value were found. In patients with low or very low probability of TEP, as determined by scintigraphic studies, provided that there
is no risk factor, the prevalence of TEP was of 4,5%.
For patients with normal or low scintilography probability of TEP, as determined by scintigraphic studies,
showing either one or more risk factors for clot, the
prevalence of TEP was of the order of 12% and 21%
respectively. In the PIOPED study, however, most patients were classified as having an intermediate probability for TEP, based on either clinical or scintigraphic
criteria. For these patients, the combination of signs
and clinical symptoms with the sparkle-graphs findings was not enough for the definition of the picture,
and other investigations were deemed necessary for a
definite diagnosis(20, 21).
25
FIGURE 5
Algorithm for handling TEP(22) suspicious cases.
The frequency is estimated and the prevalence is associated for 1000 random patients.
FIGURE 6
26
Computerized helical tomogra- with sensibility of 90% and specificity of 96%. Its
phy
global accuracy drops when both central arteries and
The invasiveness of a spiral tomography exam- the outlying branches are evaluated altogether (sensiination is minimal. All it requires is a venous puncture bility of 63% and specificity of 89%).
The computerized spiral tomography has
and the administration of iodized outlying contrast. The resulting contrasted images of the arteries allow greater accuracy than ventilation and perfusion scintifor a direct visualization of the thrombus inside the lography in the diagnosis of pulmonary embolism(25).
artery. It also makes for good analysis of central arter- The yielding of helical TC in relation to central TEP
ies (that is, main branches, both lobar and segmental), can be evaluated with the data(23) provided in Table 7.
Table 7
Performance of helicoidal TC in central TEP
Sensibility
Specificity
nIN
(95% IC)
n’IN’
(95% IC)
617 (86)
(42-100)
12/13 (92)
(64-100)
7/7 (100)
(54-100)
3/3 (100)
(29-100)
15/15 (100)
(78-100)
36/36(100)
(90-100)
18/18 (100)
(74-100)
23/24 (96)
(79-100)
39/43 (91)
(78-97)
25/29 (86)
(68-96)
85/90 (94)
(86-98)
99/105(94)
(88-98)
VPP=93% - VPN= 95%
FIGURE 7
Helicoidal TC – TEP thrombus into pulmonary artery(24)
Pulmonary angiography
Lung angiogram is a definite invasive diagnosis
test, with low index of complications, using the technique of Seldinger for veined puncture, and a 6F to 8F
catheter, in addition to contrast injection of 20-35 ml/
second for two seconds, making it for an appropriate
visualization of the lung arterial tree. 1111 patients of
the PIOPED study were subjected to angiogram leading to the observation of the following complications:
death in 0.5%; non-fatal complications in 1%; minor
complications in 5%. Major complications are understood as comprising: death, acute respiratory failure,
kidney failure and hemorrhage that demanded more
than two units of blood transfusion. Minor complications comprise: sickness, vomits, hematomas, hypotension, urticaria, etc. In spite of the number of casualties
in this study, complications were classified as minor
25. Because of the aforementioned algorithm diagnosis this invasive procedure has been rarely used.
Angiography, however, is still considered a
gold standard for pulmonary thrombus in spite of
current trends favoring TC spiral multislices. The level
of concordance was 98% for lobar arteries, 90% for
segmental arteries, and only 66% for sub-segmental
arteries.
Treatment
The use of heparin in the initial phase is essential because it immediately inhibits the growth of
the thrombus and speeds up the resolution. Patients
under heparin therapy continue being at risk of embolism until the thrombus is dissolved by the process
27
of endogenous fibrinolysis or if organized.
with heparinization. Heparin can be used during preg
The initial dose of heparin should be from nancy as it does not cross the placentary barrier. Low5.000 to 10.000 units, and subsequent doses of 18 UI/ molecular-weight heparin has been proved beneficial
Kg/hour shall quickly result in a TTPa from 60 to 80s, with a similar performance to that of non-fractioned
which is necessary to maintain TTPa twice or three heparin. The TTPa value and weight-based protocol
times the control value. The activated partial throm- of heparin(26) shown below was implemented and has
boplastin time can be used for the control of heparin proven to be promising to best control coagulation in
doses and it should be maintained 11/2 to 2 1/2 times conformity with required parameters and with lesser
of it control value, or to maintain INR between 2 to hemorrhage.
3. Hemorrhage is the main complication associated
Table 8
Heparin venous protocol
TTPa below 35s: New dose of attack of 80u/Kg and increase of the continuous infusion by 4 u/Kg/h
TTPa between 35-44s: New dose of attack of 40 U/Kg and increase of the continuous infusion by 2 U/Kg/h
TTPa between 45 and 75s: Maintenance of the dose
TTPa among 76e 90s: Decrease of the infusion dose by 2 U/Kg/h
TTPa between 91 and 120s: Suspension of the infusion for 1 hour and, after this period, reduction of the dose
by 3 U/Kg/h
TTPa above 120s: Suspension of the infusion for 1 hour with subsequent reduction by half.
The anticoagulation treatment should be
maintained with an initial 5mg/day dose of warfarin
concomitantly at the start of heparin treatment. Doses
greater than 5 mg slightly reduced the time to obtain
an appropriate RNI, although hemorrhage cases increased significantly. On the average, five days should
be enough to ensure appropriate anticoagulation with
warfarin. During this period patients should be under
the concomitant use of heparin.
A six-month period treatment prevents most
cases of TEP recurrences(27), although it should be indefinitely administered in the case of recurrence and
in patients with thrombofilia.
Thrombolitics
Thrombolysis can save the life of patients with
pulmonary embolism, shock heart and hemodynamic
instability(28). There should be a fourteen-day time
lapse before a thrombolysis procedure becomes fully
effective, the effect of which is compared to heparin
around the seventh day. The premature use of thrombolytic drugs in selected cases can result in improved
clinical response, reducing right ventricle dysfunction
and the akinesia or hypokinesia area.
Patients with hemodynamic instability and RV
dysfunction, characterizing massive TEP, represent
the subgroup with worse prognosis and in this case a
thrombolytic therapy is recommended. Even though
it is considered the best therapeutic strategy for unstable patients, only one randomized study showed
significant difference in the mortality rate favoring the
group under streptokinase (1.500.000U in 1:00/hour),
if compared to the group under heparin(29, 30). There is
too much controversy in recommending thrombolytic
therapy for TEP in the case of patients showing no
dysfunction of the right ventricle, as these patients can
account for 40% to 50% of the cases. In this subgroup,
the use of thrombolysis improved the perfusion and
dysfunction of the right ventricle in echocardiograms
as well as the resolution of the thrombus in arteriographies, but did not reduce mortality rates if compared
to heparin(31), although it prevented the development
of chronic pulmonary hypertension, which is a fearsome lung complication of pulmonary embolism. The
table below shows a list a most used thrombolytic
agents in Brazil(32).
Table 9
Thrombolytic agents available in Brazil and approved by FDA for TEP
Agent
Mechanism of action
Therapeutic regime
Streptokinase
Indirect (compound formation Initial dose of 250 000 ui EV in 30
as the plaminogen for plasmin minutes, followed by continuos ingeneration). Direct (break of the fusion of 100 000 ui / hour for 24
plasminogen)
hours
RtPA
Direct (break of the plaminogen) 100 mg EV in 2 hours.
28
Surgery
The embolectomy is recommended in the case
of massive TEP, being counter-indicated for patients
under thrombolytic treatment or, more seldomly, for
those who in addition to showing no response to
thrombolysis still keep on being unstable in spite of
intensive care. The best surgery result is reserved for
the cases of subtotal obstruction of the pulmonary
artery trunk or of its main branches. Mortality rates
are high for patients undergoing embolectomy, mainly
when one considers the seriousness of this procedure.
On the other hand, in a later phase, one of
the most fearsome complications of embolism is pulmonary hypertension, the incidence of which being
around 0,5% of the cases.
Patients can experience meaning ful improvements with endarterectomy and with today’s more
straightforward criteria for surgery indication this
procedure has become less risky. Chronic pulmonary
hypertension major symptom is the progressive dyspnea that can be followed by dry cough. There can
be syncope and retrosternal chest pain in the case of
terminal patients(33).
Indications for thrombus endarterectomy
•
Class functional III or IV.
•
Pulmonary vascular resistance greater than
300 dina/cm-5.seg-1 or increased blood pressure under exercise.
•
Last episode of embolism over three months
ago.
•
Arteriography with thrombus with probable
surgery indication.
•
Absence of non-cardiac comorbities.
Vena cava filter
The first digging filters appeared at the clinic
late in the 60’. Improvements were made and today we
have more effective and safer models. Vena cava filters
are suitable for the prevention of TEP in patients with
anticoagulation contraindication and in those patients
with recurrent pulmonary embolism. This filter is indicted for patients with serious heart or lung dysfunction or high embolism risk. It is also recommended for
patients under the embolectomy subgroup.
There are several types of filters: net, cone,
basket, etc., which can be removable or not, depending on the material with which they are made.
The incidence of recurrence of pulmonary
embolism following the aforementioned procedures
can vary from 5% to 35%. Operative mortality rates
vary from 5% to 20%, and chronic vein insufficiency
may be a major or minor sequel in 2/3 of patients
undergoing this procedure’.
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Mosby, 1996.
29. Daniel LB, Parker Ja, Goldhaber SZ e cols. Relation of
duration of symptoms with response to thrombolytic therapy in
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15. Goldhaber SZ, Haire WD, Feldstein ML et al. Alteplase
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UPDATING
ARTICLES
Vol. 2 / Number 1
UPDATE IN DIAGNOSIS AND TREATMENT OF
THE ANEURISMS OF MESENTERIC ARTERIES
*Santos CHM, Gomes OM, Pontes JCDV
ABSTRACT
The aneurysms of the mesenteric arteries are
rare disease, corresponding at the most 8% of the visceral aneurysms and they attack 0,2% of the population, however, they have great rupture probability,
what checks them the great importance. The diagnosis
is usually made by the mesenteric arteriography, being able to be also used the methods diagnosis the
angio-CT and angio-MR. The treatment should be accomplished whenever diagnosed such disease, could
be goes conventional surgery or goes endovascular
therapy. The surgical treatment can consist of resection with reconstruction primary end-to-end, reserved
goes small aneurysms and that commit small arterial
segments; resection with interposition of synthetic
prostheses or veins; bondage arterial proximal to the
aneurysm and bypass; intestinal resection when there
are irreversible compromising of the vascularization
of the certain segment. The endovascular therapeutics
can be made by the injection of embolizant substances and goes transcatheter stent-graft placement. Recent studies check to the therapy endovascular larger
advantages in relation to the surgical treatment. The
main complications of the aneurysms of the mesenteric arteries are the intra-abdominal hemorrhage, digestive hemorrhage and dissection.
DESCRIPTORS: Aneurysm
Mesenteric arteries
*Federal University of South Mato Grosso - Department of Surgical Clinic
and Cardiovascular Foundation São Francisco de Assis.
Rua Aluízio de Azevedo, 606 - Jardim São Bento - Campo Grande
Mato Grosso do Sul - Brazil - CEP: 79004050
E-mail: [email protected]
Treatment
The first report of an aneurysm of splancnic
artery was described in 1770 by Beaussier when studying the visceral circulation of corpses. The aneurysms
of the visceral arteries are little frequent, however,
a vascular disease of great importance (1). The main
visceral arteries are originated from the celiac trunk,
which are, splenic, superior and inferior mesenteric,
gastric left, liverwort, gastroduodenal and pancreatic
duodenal. The aneurysm of the mesenteric superior
artery (MSA) it is rare, being present in one to each
12.000 autopsies. Only 5,5 to 8% of the cases of
visceral aneurysms and less than 0,5% of all of the
intra-abdominal aneurysms happen in MSA (2). Morrisey (3) told that among the visceral arteries, the ones
that more frequently present aneurysms are the splenics (60%), liverworts (20%) and mesenterics (5,5%).
Also Komori et al. (4) observed incidence of 8% of
aneurysms of mesenteric arteries (AMA) among the
aneurysms of the visceral arteries and, besides, they
identified larger propensity to rupture in AMA that us
too much.
The diagnosis of AMA frequently is made in
an exam discovery, once most of the aneurysms is asymptomatics (63%), although 23,9% come with rupture (5). Eventually the simple x-ray of abdomen can
take the suspicion of AMA when there is calcification
of their walls (6). Also the computerized tomography
of abdomen can be useful in diagnosis (5), however,
the selective mesenteric arteriography is now the “gold
standard” to diagnose such aneurysms (figure 1). Recently, other methods as the angio-CT (figure 2) and
angio-MR are winning space as methods diagnoses.
31
by deposition of embolic material in the vessels on either
side of the aneurysm or inside it (embolotherapy) and
for the stent-graft placement (figure 3).
Figure 1. Arteriography demonstrating a great aneurysm of superior mesenteric artery
Figure 3. Treatment of aneurysm of mesenteric artery for the
stent-graft placement.
A) Demonstration of the aneurysm; B) Stent-graft positioned
and absence of the aneurismatic image.
Figure 2. Abdominal CT angiography showing the typical finding of superior mesenteric artery aneurysm
The first appropriate handling of an aneurysm
of mesenteric artery happened in 1953 for DeBakey
and Cooley (7). Ever since the conventional surgical
treatment was adopted as therapeutics for such cases,
usually for aneurismatic resection and primary reconstruction or interposition of prostheses. However,
since 1991 when Parodi accomplished the treatment
endovascular of an aortic aneurysm, the enthusiasm
with this technique is increasing in the therapeutics of
the aneurysms, among them the one of the mesenteric
arteries.
Basically the treatment can be divided in surgical conventional or endovascular, besides the possibility of the patient’s simple attendance in some cases.
The surgical treatment can consist of resection with
primary reconstruction end-to-end, reserved for small
aneurysms and that commit small arterial segments;
resection with interposition of synthetic prostheses or
veins; bondage arterial proximal to the aneurysm and
bypass; and intestinal resection when there is irreversible compromising of the vascularization of a certain
segment. The endovascular therapeutics can be made
32
The classic treatment for such aneurysms has
been the surgical bondage or the resection, although
there is not a consensus as the best therapeutics, probably for being this rare disease, so that difficultly a service has great experience with such aneurysms to the
point of to determine the most appropriate treatment.
With the evolution of the interventionist radiology,
the embolization transcatheter has been presenting
good results.
According to Komori et al. (4) the best therapeutic option is the resection following by arterial reconstruction. Greek et al. (8) reports16 cases of splancnics artery aneurysms, of the three were located in the
superior mesenteric artery. All were treated by surgery
and just a patient (mesenteric superior artery) it presented long term recurrence.
Carr et al. (5) told 46 visceral artery aneurysms
in a period of 14 years, and of these five were only of
mesenteric arteries (four of the superior mesenteric
artery and one of the inferior). Twelve patients were
treated by transcatheter embolization, 17 by surgery
and the others were just observed. The authors concluded that the transcatheter embolization is an excellent option in selected cases.
Gabelmann et al. (9) with ten years of experience in endovascular embolization of visceral aneurysms, treated 25 patient with such aneurysms, of the
which 3 were mesenterics. They didn’t obtain success
in one of these cases of mesenteric aneurysm, but,
in a general way the results were excellent and the authors consider that this should be the choice treatment
because it offers important advantages in relation to
the conventional surgical treatment, including neces-
sary location of the aneurysm, access to the collateral
flow, and it is little invasive, as well as of easy access to
the aneurysms. Embolization can also be indicated as
temporary treatment for patient of high risk that need
immediate treatment of the hemorrhage.
Saltzberg et al. (10) demonstrated in a study
with 65 patient with aneurysms of visceral arteries, of
the which only three were of the superior mesenteric
artery,
that the endovascular embolization is a good therapeutic option, however, the traditional surgery with
bondage and bypass should still be indicated for selected cases.
Tulsyan et al. (11) told their results in the treatment of 48 patient with aneurysms of visceral arteries with approach endovascular, of the which just one
presented AMA. They concluded that this is an excellent treatment form for such disease.
Another recent therapeutic option is the stentsplacement. Rocek et al. (12) described a case of aneurysm of superior mesenteric artery treaty this way with
success. Nyman et al. (13) treated a single patient for
the stent placement in the superior mesenteric artery
complementing the therapeutics for the transcatheter
embolization, obtaining good result.
Sachdev et al. (14) made a comparison between
the surgical treatment and the endovascular therapy
in 59 patients with 61 aneurysms, between aneurysms
of celiac artery and mesenteric superior. Twenty-four
were treated by surgery and 35 by endovascular therapy. They observed similar therapeutic results, however,
with smaller morbidity and smaller time of hospitalization in the endovascular group.
In the medical literature we found other less
used forms of treatment, but with good results according to the authors. Richardson et al. (15) told their
experience with the bondage of the inferior mesenteric artery for laparoscopic approach in two patients
with aneurysms of this vase obtaining good results.
Another therapeutic option was used by Kemmter
et al. (16) to accomplish procedure described initially
by Cope and Zeit (17), the transcatheter injection of
trombine. Although the results have been favorable,
still few cases exist treated by this method so that can
recommend it.
An important doubt exists when we came
across with ourselves an AMA found in a routine exam
without the patient presents symptoms. Stone et al. (18)
made a study to analyze the need of same treatment
in the asymptomatic cases. They analyzed 21 patients
that had aneurysms exclusively of mesenteric arteries
(6,9% of the visceral aneurysms of the institution)
and they observed that 8 patients had rupture to the
presentation. Five were treated with beta-blocking and
of the remaining 16, eight had rupture. Of the total, 13 patients had aneurismatic calcifications, but, all
of the cases of rupture happened us that didn’t have
calcifications. Eleven patients were operated. The authors concluded that the aneurysms of mesenteric arteries are rare but they have great rupture probability,
mainly patient without aneurismatic calcifications and
they considered that the treatment should be indicated
for all of the cases.
Aneurysms of mesenteric arteries can present
as main complications the intra-abdominal hemorrhage, appealing digestive hemorrhage (19) or dissection. Rengstorff et al. (20) told a case of intra-abdominal hemorrhage due to the rupture of aneurysm of
inferior mesenteric artery, diagnosed by computerized
tomography of abdomen and angiography. The patient was treated by left hemicolectomia with success.
Also Salo et al. (21) told six cases of ruptured splancnic
aneurysms, of which one was in the superior mesenteric artery. This case was also treated by resection of
the aneurysm and of the affected intestinal segment
with good results. Maloney et al. (22) told a case of
high digestive hemorrhage for aneurysm of the superior mesenteric artery with fistula for the duodenum.
The accomplished treatment was the resection of the
aneurysm and end-to-end reconstruction with good
evolution. Also Moreira et al. (2) opted for the aneurismatic resection, however, with interposition of the
saphenous vein. According to these authors the bondage simple proximal and distal to the aneurysm with
intra-operative evaluation of the intestinal viability is
the choice treatment when there is no associated infection.
Sagiuchi et al. (23) told a rare case of dissection
of aneurysm of superior mesenteric artery, diagnosed
by computerized tomography of abdomen, and they
affirmed that most of the time the etiology is ignored,
could be due to arteriosclerosis, dysphasia, congenital
disorders of the connective tissue and trauma.
CONCLUSION
We can conclude that the aneurysms of the
mesenteric arteries are quite rare diseases, usually asymptomatics, but that can come in a significant number
of cases with rupture as first manifestation. They can
be treated by conventional surgery, although subsidies
exist for us to believe that the endovascular therapy is
so good or better than the conventional surgery, still
offering smaller morbidity and allowing a smaller hospitalization. Mesenteric artery aneurysms have larger
33
rupture probability that the other aneurysms of the
visceral arteries, so that the treatment should be indicated even in the asymptomatic cases.
DESCRIPTORS: Aneurism
Mesenteric arteries
Treatment
REFERENCES
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9. Gabelmann A, Gorich J, Merkle EM. Endovascular treatment
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PJ, Riles TS, Rockman CB. Is endovascular therapy the preferred
treatment for all visceral artery aneurysms?. Ann Vasc Surg 2005;
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Pierce G, Ouriel K. The Endovascular Management of Visceral
Artery Aneurysms. An Vasc Meeting 2006; 47: 118-24.
12. Rocek M, Peregrin JH, Dutka J, Ryska M, Belina F, Lastovickova J. Percutaneous treatment of a superior mesenteric artery
pseudoaneurysm using a stent-graft. AJR 2002; 178: 1459-61.
13. Nyman U, Svendesen P, Jivegard L, Klingenstierna H, Risberg
B. Multiple pancreaticoduodenal aneurysms: Treatment with superior mesenteric artery stent-graft placement and distal embolization. JVIR 2000; 11: 1201-1205.
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14. Sachdev U, Baril DT, Ellozy SH, Lookstein RA, Silverberg
D, Jacobs TS, Carroccio A, Teodoresco VJ, Marin ML. Management of aneurysms involving branches of the celiac and superior
mesenteric arteries: A comparison of surgical and endovascular
therapy. J Vasc Surg 2006; 44: 718-24.
15. Richardson WS, Sternbergh WC, Money SR. Laparoscopic
inferior mesenteric artery ligation: an alternative for the treatment of type II endoleaks. J Laparoendosc Adv Surg Tech 2003;
13:355-8.
16. Kemmeter P, Bonnell B, Wanderkolk W, Griggs T, Venerp
J. Percutaneous thrombin injection of splanchnic artery aneurysms: Two cases reports. JVIR 2000; 11:469-72.
17. Cope C, Zeit R. Coagulation of aneurysms by direct percutaneous thrombin injection. AJR 1986; 147: 383-7.
18. Ewm, Abbas M, Cherry KJ, Fowl RJ, Gloviczki P. Superior
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19. Wagner WH, Allins AD, Treiman RL, Cohen JL, Foran RF,
Levin PM, Cossman DV. Ruptured visceral artery aneurysms.
Ann Vasc Surg 1997; 11:342-7.
20. Rengstorff DS, Baker EL, Wack J, Yee LF. Intra-abdominal
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47: 769-72.
21. Salo JA, Salmenkivi K, Tenhunen A, Kivilaakso EO. Rupture
of splanchnic artery aneurysms. World J Surg 1986; 10: 123-7.
22. Maloney RD, Nealon Jr TF, Roberts EA. Massive bleeding
from a rupture superior mesenteric artery aneurysm duodenum.
Arch Surg 1976; 111: 286-8.
23. Sagiuchi T, Asano Y, Yanahiara H, Aoki Y, Woodhams R,
Hayakawa K. Three-Dimensional CT in isolated dissecting aneurysm of the superior mesenteric artery: a case report. Radiat
Med 2001; 19: 271-3.
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