Electrocardiograma y drogas
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IMPORTANCIA DEL ECGENTOXICOLOGIA
TOXICOLOGIA CLÍNICA
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HISTORIA
• En 1903, Guillermo Einthoven registra laactividad electrica del corazón y da su
respectivo nombre a las diferentesondas
• PREMIO NOBEL DE MEDICINA EN 1924
• “Elektrokardiogramme” : EKG • Electrocardiograma: ECG
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GENERALIDADES
• Segmento
• Intervalo
• Complejo
• Ondas
RR
Segmento PR
Intervalo PR
Segmento ST
Complejo QRSIntervalo QT
P
Punto J
T
U
Q
S
R
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GENERALIDADES
POSDESPOLARIZACIÓNTEMPRANA
POSDESPOLARIZACIÓN
TARDIA
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GENERALIDADES
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GENERALIDADES
• Método rápido
• Facilmente disponible• Barato
• Mejora el enfoque del paciente
• Desconocimiento
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COCAINA
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COCAINA
• Inhibición de los canales de sodio
• Aumento del tono simpático
• Arterioesclerosis acelerada y/ofenómenos proagregantes
• Vasoconstricción coronaria eisquemia
• Miocardiopatia
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COCAINA
• Prolongación del PR, QRS, QT
• Taquicardia supraventricular, TVP,FV
• Cambios en la onda T, elevación ST
• Infarto Q y no – Q• Bloqueo cardiaco
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COCAINA
• Patrón de Brugada
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ALCOHOLETÍLICO
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ALCOHOL• Edad media de la vida
• Sin enfermedad cardiaca subyacente
• Sin historia familiar o personal depalpitaciones o dolor toráxico
• No consumidores o consumo ocasional
• 135 gr de alcohol• Alteraciones electrolíticas como
hipomagnesemia, hipokalemia
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ALCOHOL
• Aparición varias horas post-ingesta
• El tipo de arritmia más frecuente es la
fibrilación auricular• Cede sin terapia farmacológica
• Seguimiento a 3 años sin tratamientono mostró nuevos episodios, mientrashaya abstinencia
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• Idiopáticas• Estimulo a la secresión de adrenalina y
noradrenalina por la médula suprarrenal• El aumento en los niveles de acidosgrasos etil – ester son arritmogénicos enpresencia de niveles aumentados de
catecolaminas• El acetaldehido es arritmogénico porliberación miocardica de NE
ALCOHOL
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“HOLIDAY HEART”
Disturbio agudo del ritmo o la
conducción cardiaca, asociado con unconsumo alto de alcohol, en una
persona sin otra evidencia clínica de
enfermedad cardiaca y que desaparecesin secuelas, con la abstinencia
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ALCOHOL
TIPO DE ARRITMIA No
Contraccion auricular prematura
Fibrilación atrial
Flutter auricularTaquicardia atrial paroxistica
Taquicardia de la unión
Contracción ventricular prematuraTaquicardia ventricular
4
12
63
4
61
Ettinger et al. Am Heart J 1978;
95:555
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ECG HOLIDAY
HEART
(n = 17)
CONTROLES
(n = 10)
P
PR
QRS
QTcFC
179 +/- 7
98 +/- 3
430 +/- 982 +/- 3
153 +/- 6
80 +/- 2
377 +/- 663 +/- 3
< 0.01
< 0.001
< 0.001< 0.001
Ettinger et al. Am Heart J 1978; 95:555
ELECTROCARDIOGRAMA
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OTRAS DROGAS DE ABUSO
• Marihuana
• MDMA
• LSD
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DIGOXINA
• QTc corto, “abombamiento” del ST,onda T invertida
• Prolongación del PR y bloqueo AVde grados variables
• CVP, flutter y fibrilación ventricular
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DIGOXINA
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ADT
• Bloqueo a los canales rápidos desodio
• Taquicardia sinusal (>120)
• QRS (>100mseg)
• R de aVR >3mm• QTc > 480mseg
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ADT
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ADT
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LITIO
• Aplanamiento o inversión de la onda T
• Depresión del segmento ST en
precordiales• QTc prolongado
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PICADURA DE INSECTOS
•
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PICADURA DE INSECTOS
J VENOM ANIM TOXINS 2000; 6 (1)
• Miocarditis
• Hipocalcemia e hiperpotasemia
• Contracciones ventriculares prematuras• Taquicardia y bradicardia sinusal
• QTc prolongado
• Elevación y depresión del ST, onda Q• Bloqueos de rama y bloqueo AV de primer y
segundo grado
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AMERICAN JOURNAL OF EMERGENCY MEDICINE Volume 18, Number 6 October 2000
PICADURA DE INSECTOS
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AMERICAN JOURNAL OF EMERGENCY MEDICINE Volume 18, Number 6 October 2000
PICADURA DE INSECTOS1
2
3
R
L
F
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CALCIOANTAGONISTAS Y
BETABLOQUEADORES• Bradicardia sinusal
• Bloqueo AV de diversos grados• Prolongación del PR
• Ritmos idioventriculares y de launión
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HIPERKALEMIA
• 5.5 – 6.5 mEq/L: ondas T altas de baseestrecha
• 6.5 – 7.5 mEq/L: ondas P bajas, punto Jdeprimido, moderado ensanchamientodel QRS
• 7.5 – 8.5 mEq/L: onda P plana y ancha,alargamiento del PR bloqueos de rama
• >8.5 mEq/L: ausencia de onda P, TV, FV • espironolactona, IECAS, heparina,
betabloqueadores, AINES, digoxina
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HIPERKALEMIA
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HIPOKALEMIA
• Depresión del ST
• Disminución progresiva del voltaje de laonda T
• Aparición de onda U
• Fusión de la T y la U
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HIPOKALEMIA
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HIPERCALCEMIA
• QTc corto• Segmento ST estrecho o ausente
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HIPOCALCEMIA
• Prolongación del QTc• Fluoracetato de sodio, aminoglucósidos,
etanol, furosemida, fenitoina,fenobarbital, fenitoina, teofilina
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QT PROLONGADO
• Duración sístole ventricular
• Derivaciones DI, aVR, V2 ypromediar
• Prolongar la onda T hasta la basal
• Voltaje onda U, mayor del 25% delvoltaje de la onda T
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QT PROLONGADO
491
536
440
600
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QT PROLONGADO
• Fórmula de Bazett
• Valor normal:
– 390 mseg en hombres – 440 mseg en mujeres
QTc = QT/
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QT PROLONGADO
• Edad
• Género
• Hora del dia• Diabetes mellitus
• Hipertensión arterial
• Infecciones SNC• LQTS
• Obesidad
• Alcoholismo
• Tabaquismo• Nefropatia
• Hepatopatia
• Enfermedadcoronaria
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QT PROLONGADO
• Incidencia del 1 al 8%
• Marcador de la predisposición a TdP
– Cardiomiopatias – Enfermedad coronaria – Medicamento implicado
– Interacciones medicamentosas – Suceptibilidad induvidual
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QT PROLONGADO
• Eritromicina
• Claritromicina
• TMSX• Quinolonas
– Esparfloxacina
– Grepafloxacina
• Cloroquina
• Ketoconazol
• Astemizol
• Hidroxicina
• Difenhidramina• Terfenadina
• Organofosforados
• Cisaprida• Metoclopramida
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QT PROLONGADO
• Amitriptilina
• Hidrato de cloral
• Clorpromazina• Haloperidol
• Imipramina
• Litio• Nortriptilina
• Amiodarona
• Bretilio
• Procainamida• Quinidina
• Propafenona
•
Sotalol • Dofetilide
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QT PROLONGADO