Cardiac Poisons – An Overview

Poison is a substance or chemical that causes damage to living tissues and has an injurious or fatal effect on the body. It can be taken through various modes through ingested, inhaled or absorbed.

Cardiac poisons mainly act on the heart, either directly on the muscle or through its nerve supply. These types of poisons generally produce a deleterious effect due to poisoning of the cardiac muscle. Most cases of cardiac poisons are accidental poisoning by plants containing certain compounds (glycosides or alkaloids) which are poisonous in nature and effect.

There are certain drugs that are although taken for the treatment of Cardiac dysfunction, but may affect adversely which could be lethal.

Cardiac poison can be classified into four types. In this article, we will discuss all types of cardiac poisons in detail.

Classification of Cardiac Poison 

1. Cardiotoxic Plant Poisons 
2. Diuretics 
3. Antihypertensives 
4. Antiarrhythmics

1. Cardiotoxic Plant Poisons

a) Nicotine

Nicotine is a colorless, liquid alkaloid found in several species of tobacco plants. It is an extremely fast-acting poison. All parts of the plants are poisonous except the ripe seed. The dried leaves of the plant contain 1-8% nicotine and are smoked, chewed and snuffed. Nicotine is rapidly absorbed from all mucous membranes, skin and lungs.

1 cigarette = 15-20 mg nicotine of which 1-2 mg is absorbed by smoking.

Mode of Action: Nicotine acts on the autonomic ganglia which initially stimulates but in later stages is depressed and blocked. It also acts on somatic Neuromuscular Junction and afferent fibers from sensory receptors. It also suppresses appetite while increasing basal energy expenditure, leading to weight loss. 

Signs & Symptoms of Acute Nicotine Poisoning: Burning sensation in stomach and abdominal pain, nausea, hypersalivation, muscle weakness, low blood pressure, meiosis, coma, paralysis and death due to respiratory failure.

Signs & Symptoms of Chronic Nicotine Poisoning: Cough, wheezing, anorexia, vomiting, diarrhea, anemia, tremors, and irregularity of heart with extrasystoles.

Fatal Dose: 50-100 mg of nicotine and 15-30 gm of crude tobacco

Fatal Period: 5 to 15 mins

Treatment: Solution of tannic acid, bowel evacuation and activated charcoal.

Post mortem Appearances of Nicotine Poisoning: Asphyxia, brownish froth at mouth and nostrils.

b) Aconite

Aconite is commonly known as monk’s hood, blue rocket, bish, bikh, sweet poison, or Devil’s helmet. Its common varieties are Aconitum napellus and Aconitum ferox. The plant Aconite is grown in garden and its flowers are grown in the Himalayan ranges in India. It has no odour, but is sweetish in taste hence the name Mitha Bish.

All varieties and all parts of the Aconite are poisonous.

Mode of Action: It disrupts the normal ion balance in heart muscle cells, which can cause potentially fatal arrhythmias, including ventricular tachycardia, the principle cause of death. 

Signs and Symptoms: The initial signs are gastrointestinal nausea, vomiting, diarrhoea and burning in the abdomen. Pupils are dilated and contracted. Hypotension, bradycardia, sinus tachycardia and ventricular arrhythmias. Death is due to paralysis of heart, respiratory centre or both. 

• Fatal Dose of root is 1 gm and aconitine is 2 to 5 mg.
• Fatal Period is 2 to 6 hrs.

Treatment is done by close monitoring of blood pressure and cardiac rhythm. Gastric lavage with lukewarm water and weak solution of iodine in tannic acid. The major physiological antidote is atropine which is used to treat bradycardia.

Postmortem Appearances: Asphyxia, stomach and duodenal mucosa shows congestion.

Medico legal importance:- Commonly found in accidental poison, cattle poison. Its root are used in criminal abortion cases. 

c) Quinine

Bark of numerous species of Cinchona plant contains quinine and cinchonidine. The medicinal use of quinine is the treatment of malaria.

Mode of Action: It has strong protoplasmic poison with anaesthetic effect. Its severe cardiovascular toxicity results from their sodium channel blocking effects with hypotension and cardiac arrest. It stimulates and then lowers the central nervous system.

Sign and Symptoms: Headache, ringing in the ears, pupils dilated and fixed, mental confusion, abdominal pain, vomiting, diarrhea, hypotension, cyanosis, coma and convulsions.

Fatal Dose: 8 – 15 gm

Fatal Period: 6 hrs

Treatment: Wash the stomach with concentrated solution of magnesium sulphate which is left in stomach for rapid elimination of poison.

Postmortem Appearances: Congestion of visceral tissues, haemolysis of RBCs and renal tubules may be choked by Hb.

Medico legal importance: They are commonly used in accidental cases and self-poisoning cases are rare.

2. Diuretics

• Diuretics are the drugs that rise at the rate of urine formation. 
• The diuretics act directly on the kidney tubules to produce the scientific effects.
• They are used to control hypertension, to reduce oedema and in congestive heart failure.
• Most cases of toxicity are related to chronic use.
• Cardiovascular irregularities include bradycardia, conduction defects, sinus arrest, and hypotension.
• Cardiovascular symptoms have only been reported after chronic therapy and not from an acute ingestion.

3  Antihypertensives

Antihypertensives are a type of drugs that are used to treat hypertension or commonly known as high blood pressure.

a) Reserpine 

• Reserpine is an alkaloid present in the root of the Indian plant Rauwolfia serpentina. It has been used for treating hypertension for decades.
• Related alkaloids include alseroxylon, deserpidine, raubasine, and rescinnamine. 
• It is readily absorbed through oral and intramuscular dosing.
• It reduces catecholamines and serotonin superficially and centrally from nerve terminal fibers. The responses exhibit as CNS depression and peripheral sympatholysis.
• The adverse effects of reserpine include orthostatic hypotension, dizziness, blurred vision, bradycardia, nausea, vomiting and diarrhea. 
• It often induces depression. Overdose produces reflective CNS depression.

b) Methyldopa

• It acts centrally through an active metabolite, alphamethyl noradrenaline, to lower blood pressure. It is an antihypertensive.
• It may induce serious effects such as haemolytic anemia, hepatitis, pancreatitis, and myocarditis, and other lesser effects including headache, drowsiness, depression, edema, bradycardia, nightmares, disorders of sexual function, dryness of mouth, and nightmares. 
• Acute overdosage of methyldopa may result in severe hypothermia, dry mouth, nausea, vomiting, hypotension, dizziness, weakness and coma. 

c) Clonidine 

• Clonidine is a compound with active alpha-2 adrenergic agonist effects. 
• At high doses, it has been shown to act as a peripheral partial alpha-adrenergic receptor resulting in temporarily increasing blood pressure and pulse rate.
• It is also used in the treatment of attention deficit disorder, prophylaxis of migraine and management of ethanol, opiate, and nicotine withdrawal. 
• Its adverse effects include Dry mouth, drowsiness, hypotension, insomnia, arrhythmias and Gastro-intestinal distress. 
• Rebound hypertension is common in this case.

4. Antarrhythmics

The antiarrhythmic drugs are mainly used to treat cardiac arrhythmias. A cardiac arrhythmia is a disturbance or misdeed in the heart rate, rhythm or both, which requires management of one of the antiarrhythmic drugs. It may occur as a result of heart disease or from a disorder that disturbs cardiovascular function.

Conditions such as emotional stress, hypoxia, and electrolyte imbalance also may activate an arrhythmia. All antiarrhythmic drugs may cause new arrhythmias or worsen existing arrhythmias even though they are administered to resolve an existing arrhythmia. This phenomenon is called the proarrhythmic effect.

a) Procainamide 

• Procainamide is an antiarrhythmic agent with properties similar to that of quinidine.
• Its primary effects on the heart are to decrease electrical impulse conduction velocity through atrial and ventricular tissue.
• Overdose results in arrhythmias. 

b) Lignocaine 

• It is an aminoacyl amide. It is a artificial derivative of cocaine. 
• It is used as an anaesthetic agent as well as antiarrhythmic agent. It is effective in controlling ventricular arrhythmias.
• Adverse Effects includes vertigo, drowsiness, confusion, dysarthria, hearing loss, visual disturbances, agitation and coma.

c) Fenopraine

• It is an antiarrhythmic drug which blocks the fast sodium channel of the myocardial cell.
• It has some negative inotropic and beta-adrenoceptor blocking activity. It is structurally related to propranolol.
• It is administered orally for the treatment of serious ventricular arrhythmias. 
• Adverse Effects includes Bradycardia, cardiac conduction anomalies, hypotension, proarrhythmias, worsening of heart failure and headache.

Case of Cardiac Poisoning

in one of the interesting cases, a 21-year-old female was admitted in the emergency room with vomiting and light headedness, 15 hours after absorption of common oleander aqueous leaf extract.

She had been recommended to take the extract in order to conceive a baby. The patient was a non-smoker and non-alcoholic. On inspection, the blood pressure was 122/80 mmHg with irregular pulse of 46/min.

She was looking toxic due to excessive vomiting. Other general physical parameters were normal. Her chest and lungs were clear to auscultation and percussion. The patient was given 6 mg of venous atropine sulfate which did not resolve her bradycardia, but other symptoms were improved.

Next day, the patient was given venous atropine sulfate. 6 mg twice a day and tablet orciprenaline 10 mg three times a day. After three days, the patient was settled on request, with sinus node dysfunction and varying degree AV blocks but asymptomatic.

Conclusion 

It is remarkable that oleander poisoning can be fatal if small amount is ingested. The lethal oleander leaf dose of their patient to be nearly 4 gm.