Cardiovascular

toxicology
Nendyah Roestijawati
 Used : solvent
 Reacts wit amino- and thiol-  thiocarbamate 
inhibiting enzyme  metabolic abnormalities 
disturbances lipid metabolism and thyroid
function  hypercholesterolemia and
hypothyroidism  atherosclerosis
 Inhibition dopamine β-hydroxylase 
neuropsychiatric effect
 Inhibiton aldehyde dehydrogenase  disulfiram-
like reaction
 Depressed fibriolytic activity and hypertension

Carbondisulfide
 Symptoms and signs : encephalopathy,
polyneuropathy, fatigue, headache, dizziness,
disorientation, paresthesias, psychosis,
delirium. Chronic : hypertension, angina,
myocard infarc, presenil dementia, stroke,
sudden death. Chronic early sign : abnormal
ocular microcirculation  mycroaneurism,
hemorrhages (diabetic retinopathy)
 Lab : thyroxine ↓, cholesterol ↑, angiography,
ECG : ischemia, myocard infarc
Exercise testing

Clinical findings
 Vascular findings same as atherosclerotic
vascular disease
 Abnormal ocular microcirculation without
diabetes
 History exposure 5-10 years

Diagnostic
 Workplace 4 ppm (TWA)
 Periodic ocular fundi examination
 Removing worker from sources

Prevention & treatment

 CO  carboxyhemoglobin  reduce delivery
O2 to body tissues
 Syptoms and signs : headache, nausea,
dizziness, fatigue, dimmed vision, impaired
cognitive, vomiting, tachypnea, tachycardia,
hypertension, coma, convulsion,
cardiovascular and respiration depression
 Lab : HbCO ↑, gas analysis normal/slightly
reduced arterial oxygen tension, reduce PO2
and oxygen content.
 ECG : ischemic, myocardial infarction

Carbon monoxide
 Workplace 50 ppm  HbCO 5%
 100% O2 face mask  reduced to 80
minutes
 Hyperbaric O2 (3 atm) 25 minutes

Prevention & treatment

 Dilate blood vessels  stimulation of sympathetic
nervous system  RAA system  vasocontriction
 coronary vasoapasm with angina, myocarial
infarction, sudden death
 Monday morning angina
 Symptoms and signs : headache, hypotension,
tachycardia, warm and flushed skin  angina,
myocardial infarction (nausea, diaphoresis,
pallor, palpitations, severe chest pain)  sudden
death
 Lab : CKMB ↑, ECG : ST elevation/depression,
with or without T, Q pathologic

Organic nitrates
 Workplace 0,2 ppm nitroglycerin
 Monitoring decreasing blood pressure and
increasing HR
 Nitrat withdrawal : cardiac nitrates
(nitroglycerin, ISDN), ca blocker

Prevention & treatment

Hydrocarbon & CFC
 Dizziness, light-headedness, headaches,
nausea, drowsiness, lethargy,
palpitations, syncope
 Ataxia, nistagmus, slurred speech,
arrythmia, convusion, coma, cardiac
arrest
 Lab : hydrocarbon in expired air or blood

Clinical findings
 Proper handling of solvent and propellants
 Adequate ventilation
 Protective respiratory equipment
 Beta-adrenergic blocker
 Epinephrine and sympathomimetic drugs
should be avoided  precipitate further
arrhytmia

Prevention & treatment

 Inhibit acetylcholinesterase  accumulation
acetylcholine at cholinergic synapses and myoneural
junction
 Symptoms and signs : weakness, headache,
sweating, nausea, vomiting, abdominal cramps,
diarrhea, chest discomfort, dyspnea, inability to walk,
blurred vision. Cholinergic excess : small pupils,
diaphoresis, salivation, lacrimation, bronchial
secretion, muscle fasciculation, tachycardia and
hypertension  bradycardia and hypotension,
respiratory failure, convulsion, coma
 Lab : cholinesterase ↓, BGA : CO2 retention, hypoxia,
x-ray : pulmonary edema, ECG : QT prolongation,
ventricular tachycardia, non spesific ST-T changes

Organophosphate & carbamate

insecticides
 Use protective clothing and respirators
 Monitoring blood cell cholinesterase
 Decontaminations
 Support respiration and circulation
 Pralidoxime to reserve muscular paralysis
 Cardiac pacing
 Antiarrhytmic and ca blocker drugs should
be avoided  depress conduction

Prevention & treatment

 Antimony : parasitic infection  T wave changes, QT
prolongation  sudden death
 Arsenic : blackfoot disease  claucication and gangrene
extremities, ventricular arrythmia torsades de pointes
 Arsine : red blood cell hemolysis  hyperkalemia  cardiac
arrest, direct effect to myocardium
 Cadmium : hypertension
 Cobalt : myocardial necrosis with trombi, polycythemia,
pericardial effusion, thyroid hyperplasia  depress oxygen
uptake by mitochondria and interfere energy metabolism
similar to thiamine deficiency
 Lead : cronic renal disease, hypertension, cardiomyopathy,
direct toxic to myocardium

Heavy metals