Severepoisoning may lead to haemodynamic instability or collapse, which is also associatedwith deterioration of other organ functions such as respiratory arrest or depression,gas exchange abnormalities, convulsions, and electrolyte and acid-base disorders. These metabolic factors furtherdeteriorate the cardiac function and may potentiate the toxicity. The immediatefocus on managing severely poisoned patient is to follow the resuscitationprotocols—a prompt assessment and maintenance of compromised airway, supportingthe breathing, and optimization of circulation. Poor respiratory efforts or inadequateventilation may require short term mechanical ventilatory support, till thetoxin is reversed or metabolized.

(19)Optimization of blood pressure should be achieved initially withintravenous (IV) fluids boluses. Specific antidote administration may help tooptimize blood pressure.   Hypotension unresponsive to adequate fluidresuscitation may indicate the need of administration of vasopressor &inotropic agents depending on clinical presentation. (20) Theinotropic agents are proarrhythmic and may further enhance the cardiovasculartoxicity. Antiarrhytmic administration for management of arrhythmias associatedwith poisoning should be avoided due to proarrhythmic potential and negativeinotropic effect of these drugs. It is prudent to correct the acidosis,hypokalaemia, hypomagnesaemia, and hypoxia, which reduces the chance ofarrhythmia.

(20) There is significant advancement inmanagement and improved outcome of toxin induced cardiovascular shock in last 3decades. This is contributed by improvement in bedside haemodynamic monitoring,better understanding of shock, and aggressive supportive therapy forhaemodynamic optimization. (21, 22) Still the incidence ofcardiovascular collapse in patients with acute intoxication is as high as 17% (23)Sudden cardiac death in a younger and otherwise healthy population is mostlikely due to poisoning. (24)  The onset of cardiovascular effects afterpoison ingestion is short and depends not only on ingested quantity but on severityof toxic profile, type of toxin as well.

   TOXIC SUBSTANCES WITH CARDIOTOXIC POTENTIALA.    Drugs: The pathophysiology of drug induced cardiotoxicity and hypotensioninclude hypovolemia, depressed myocardial function, arrhythmias, and systemicvasodilatation. Mainly the acute toxic heart failure is due to systolicdysfunction secondary to reduced myocardial contractility.(25)  Cardiotoxic potential is not restricted to cardiovascular drugsonly, the mortality remains higher in compounds having membrane stabilizingactivity. (26)a.      WITHMEMBRANE STABILIZING ACTIVITY                                                             i.     Anti-arrhythmics(Vaughan Williams class I)                                                           ii.

     BetaBlockers (Propranolol, acebutolol, nadoxolol, pindolol etc)                                                         iii.     Dopamineand norepinephrine uptake inhibitors (bupropion)                                                          iv.     Anti-epileptics(Phenytoin and Carbamazepine)                                                            v.     Antimalarialagents (Qunine and Chloroquin)                                                          vi.     Polycyclicantidepressants (Imipramine, Desipramine, Amitritptyline and Doxepin)                                                        vii.     Opiods(dextropropoxyphene)                                                      viii.

     RecreationalAgent (Cocain)                                                          ix.     Amphetamine-likesubstancesb.     OTHER DRUGS                                                             i.     Calcium channel blockers (Nifedipine,Nicardipine, Verapamil, Diltiazem etc)                                                           ii.     Meprobamate                                                         iii.     Colchicine                                                          iv.

     Cardiac glycosides (digoxin)                                                            v.     H1 Antihistaminic                                                          vi.     Beta Blockers (without membranestabilizing activity)B.     PESTICIDESa.     INSECTICIDES (27)                                                             i.

     Organophosphate, Carbamatesb.     HERBICIDES                                                             i.     Paraquetc.      RODENTICIDES (28, 29)                                                             i.

     Aluminium phosphide                                                           ii.     Yellow Phosphorus                                                         iii.     Zinc Phosphide C.    PLANTTOXINS(30,31) The most severe form of plant toxins mayproduce complete heart block, Bradyarrhythmia, tachyarrhythmia or ventriculararrhythmia.                                                              i.     Aconite                                                           ii.     TaxusD.    OTHERSa.

     CARBON MONOXIDE (32)b.     CYANIDE HOW ECMO SUPPORT IS BENIFICIAL IN POISONING?The standard indication of usingECMO is acute severe heart or lung failure unresponsive to optimal conventionaltherapy with high mortality risk. ECMO should be considered if the mortalityrisk is 50% and ECMO should be started in most circumstances at 80% mortalityrisk (33) is similar for poisoned patients. Moreover these patientsare relatively young and otherwise healthy. One can expect a better outcome oncethe toxin is either metabolized or completely eliminated from the body.

ECMOmay be useful in providing adequate cardiac output and maintain tissue perfusionwhich helps in redistribution from central circulation and facilitate themetabolism and excretion of poison by improving hepatic and renal blood flow. (8) ECMO supports both cardio respiratoryfunction (VA ECMO) and respiratory function alone (VV ECMO) for a longerduration depending on indication. It is primarily indicated in patients withsuch severe cardiovascular dysfunction or severe ventilation and/or oxygenationproblems that they are unlikely to survive conventional therapies and mechanicalventilation.(34) Toxins such as organic hydrocarbon (paint remover,thinner) which on aspiration damages the lungs and leads to ARDSwithout circulatory compromise. There are no guidelines for the appropriatetime for ECMO initiation in severely poisoned patients.

The decision aboutinitiation primarily depends on the clinical judgment. However it is importantto understand that ECMO should be initiated before irreversible end organdamage occurs.(8)The available scoring system for classifying thepoisoning patients has its own limitations due to its subjective nature howeverit may help to identify the most severe form of patients (Grade 3 & 4) (35) Bridge to recovery Toxic substances having potential for cardiotoxicity, whereantidote is not available may be fatal even with conventional support.   VA ECMO can support the cardiac function inpoisoned patients with severe cardiotoxicity who are having severe left or rightventricular dysfunction, persistent life threatening arrhythmias or evencardiac arrest unresponsive to conventional management. As cardiovascularfunction starts recovering once the toxic substance is either metabolized orexcreted from the body.

The duration of ECMO support depends on several factorssuch as severity of toxicity and recovery cardiac dysfunction, half life oftoxin, and organ dysfunction at the time of initiation of ECMO etc. (36,37)   Venoarterial(VA) ECMO reduced cardiac oxygen consumption and provided both hemodynamic andrespiratory support as a bridge to recovery. (38) Patients who have toxin induced ARDS whilestable haemodynamically who are unresponsive to high ventilatory support can bemanaged with VV ECMO till the recovery of gas exchange function of lungs.

(39)Even in cases of multiple drug intoxication or unknown poisoning withcardiogenic shock ECMO support can be beneficial. (40)

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