POISONING BY CARDIOVASCULAR DRUGS

Ayman Zaaqoq

Lecturer

Department of Forensic Medicine and Clinical Toxicology, ASU

2012-2013

CV TOXICITY

CV toxicity

Bradycardia

Digoxin

Beta-blockers

Calcium channel blockers

Tachycardia

Theophylline

CV TOXICITYINVESTIGATIONS

Investigation

Laboratory

S. drug level

Glucose

S.K+

KFTs

ABG

ECG

TOXICIT Y TREAT MEN TGENERAL GUID ELINES

Treatment

Stabilization Decontamination

GL

AC

Elimination

MDAC: dig., theo

Dialysis: theo

Antidote

Very high level

Serious C/P

Huge dose

Supportive

Bradycardia, AVB

Ventricular dysrhythmias

Hyperkalemia

MgSO4 IV

Overdrive pacing

Cardioversion

Phenytoin

TREATMENT OF SERIOUS DYSRHYTHMIAS

TdP V-tach

Cardioversion

NaHCO3 IV

Lignocaine

Phenytoin

Esmolol

DIGOXIN TOXICITY

Pharmaceutical

preparations: Lanoxin®,

Cardixin®

Plants: oleander

Animals: cane toad

DIGOXIN TOXICITYSOURCES

Accidental

Intentional

Therapeutic error

Decreased elimination

DIGOXIN TOXICITYFORMS

Acute Chronic

DIGOXIN TOXICITYMECHANISM

Digoxin

Θ Na+/K+-ATPase

↑ intracellular Na+

↑ extracellu

lar K+

Vagotonic Changes refractory period

↑ in AV node

↓ in atria and

ventricles

DIGOXIN TOXICITYACTIONS

Digoxin

↑ inotropy ↓ chronotropy ↑ automaticity ↑ potassium

DIGOXIN TOXICITYCLINICAL P ICTURE

C/P

CV GI Potassium imbalance Visual

DIGOXIN TOXICITYINVESTIGATIONS

Investigation

Laboratory

S.K+

SDC

KFTs

ABG

Glucose

ECG

ECG changes• Due to digoxin

intake• Due to digoxin

toxicity• Due to potassium

disturbances• Due to pre-existing

cardiac condition

DIGOXIN TOXICITYINVESTIGATIONS

DIGOXIN TOXICITYTREATMENT

Treatment

Stabilization (antidote)

Decontamination

GL (?)

AC

Elimination

MDAC

Antidote Supportive

Bradycardia, AVB

Ventricular

dysrhythmias

Hyperkalemi

a

DIGOXIN TOXICITYANTIDOTE: DIGIBIND

Indications

Laboratory

S.K+ SDC

High

Unavailable

Clinical History

BETA-BLOCKER TOXICITY

BETA-BLOCKER TOXICITYMECHANISM

BB

β-receptor blockade

Na channel blockade

Lipid solubility

BETA-BLOCKER TOXICITYACTIONS

BB

↓ inotropy ↓ chronotropy Wide QRS Θ CNS

BETA-BLOCKER TOXICITYCLINICAL P ICTURE

C/P

CVs CNS Metabolic

BETA-BLOCKER TOXICITYINVESTIGATIONS

Investigation

Laboratory

Glucose S.K+ KFTs

ECG

DIGOXIN TOXICITYTREATMENT

Treatment

Stabilization Decontamination

GL

AC

Antidote (Glucagon) Supportive

Bradycardia, hypotension

Wide QRS

Seizures

Hypoglycemia

CALCIUM CHANNEL BLOCKERS

CALCIUM CHANNEL BLOCKERS

They block slow Ca channels of vascular smooth muscles

and cardiac muscles.

Acute toxicity is similar to B-blockers

Treatment is as in B-blockers. In addition, CaCl2 10% 10ml

IV over 10 min for hypotension and myocardial depression.

THEOPHYLLINE TOXICITY

THEOPHYLLINE TOXICITYMODE

Mode of poisoning

Intentional Dosing errors

Parent error

Miscalculati

on

Change in the

frequency

Reduced clearanc

e

THEOPHYLLINE TOXICITYMECHANISM

Theophylline

↓cGMP & cAMP

Adenosine receptor block

↑catecholamines

THEOPHYLLINE TOXICITYC/P

GIT Nausea and vomiting Hematemesis Hypovolemic shock

CNS Anxiety Irritability, tremors Seizures, coma

CVS Sinus tachycardia Ventricular tachycardia Cardiogenic shock

Metabolic Hypokalemia Metabolic acidosis

THEOPHYLLINE TOXICITYINVESTIGATIONS

Investigation

Laboratory

S. Theophyllin

e

Glucose

S.K+

KFTs

ABG

ECG

THEOPHYLLINE TOXICITYTREATMENT

Treatment

Stabilization Decontamination

GL

Emesis (?)

Elimination

MDAC

Hemodialysis

Hemoperfusio

n

Antidote Supportive

THEOPHYLLINE TOXICITYTREATMENT

Supportive treatment

Tachycardia

Supraventriclua

r

Ventricular

Hypokalemia

Hypotension

Seizures

Vomiting

Thank you