Coma patients always died before IVs

Cardiac arrest under special circumstances: electrolyte imbalances, poisoning, drowning, hypothermia, heat sickness, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrical accidents

8a Life-threatening electrolyte imbalances


Electrolyte imbalances can cause cardiac arrhythmias and cardiac arrest. Life-threatening cardiac arrhythmias are usually associated with disturbances of the potassium balance, particularly hypercalemia, and less frequently with imbalances in serum calcium and serum magnesium levels. In some situations, therapy for a life-threatening electrolyte disorder should be initiated before the laboratory values ​​are received.

The electrolyte limit values ​​given here are merely indicative for the clinical therapy decision. The exact values ​​that make therapeutic intervention necessary depend on the clinical condition of the patient and the extent of the electrolyte changes. There is little or no evidence-based information on the treatment of electrolyte disorders during cardiac arrest, so that treatment strategies for patients without cardiac arrest are used.

The treatment guidelines for these disorders have not changed significantly since the international guidelines in 2005 [1].


Identify and treat life-threatening electrolyte imbalances before cardiac arrest occurs. Eliminate all triggering factors (e.g. medication) after the initial treatment. Monitor electrolyte levels to prevent the disorder from recurring. Monitor kidney function in patients at increased risk of electrolyte imbalances (e.g. chronic kidney disease, heart failure). Regularly review dialysis therapy for dialysis patients to avoid inappropriate electrolyte shifts during therapy.

Potassium disorders

Potassium Homeostasis

The extracellular potassium levels are regulated in a narrow range between 3.5-5.0 mmol / l. Usually there is a large concentration gradient between the intracellular and extracellular fluid compartments. This potassium gradient across the cell membrane contributes to the excitability of nerve and muscle cells, including heart muscle cells.

When assessing serum potassium levels, the influence of changes in serum pH must be taken into account. When the serum pH drops (acidosis), the serum potassium level rises because potassium is moved from intracellularly into the vasculature. With increasing serum pH (alkalosis), the serum potassium concentration falls because potassium is shifted intracellularly. Consider the influence of pH changes on potassium levels when treating hyper- or hypocalemia.


This is the most common electrolyte disorder associated with cardiac arrest. Usually it is caused by an increased release of potassium from the cells or by an excretion disorder of the kidneys or an accidental administration of potassium chloride.


There is no uniform definition of hyperkalemia. The authors defined hyperkalemia as a serum potassium value greater than 5.5 mmol / l; indeed, the hyperkalemia is to be regarded as a continuum. As potassium levels rise above this limit, the risk of undesirable effects increases and thus the need for rapid therapeutic intervention. Serum potassium levels above 6.5 mmol / L are defined as severe hyperkalaemia.


There are numerous potential causes of hyperkalemia such as kidney failure, drugs [angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), β-receptor blockers, trimethoprim], cell and / or Tissue destruction (rhabdomyolysis, tumor disintegration, hemolysis), metabolic acidosis, endocrine disorders (Addison's disease), periodic hyperkalemic paralysis or a diet that may be the sole cause of manifest chronic renal insufficiency. Pathologically changed erythrocytes or thrombocytosis can simulate increased potassium concentrations [2].

The risk of hyperkalemia is even increased when several risk factors such as the use of ACE inhibitors and NSAIDs or potassium-sparing diuretics are combined.

Recognizing hyperkalemia

Rule out hyperkalemia in patients with arrhythmia or cardiac arrest [3]. Patients may experience symptoms such as increasing muscle weakness to flaccid paresis, paresthesia, or weakened deep tendon reflexes. On the other hand, the clinical picture can be overlaid by the underlying disease that triggered the hyperkalemia. The first signs of hyperkalemia can also be abnormal ECG changes, arrhythmias, cardiac arrest or sudden cardiac death. Changes in the ECG occur depending on the absolute serum potassium concentration and the rate at which the serum level rises. With serum potassium levels above 6.7 mmol / l, ECG changes are found in most patients [4]. Using a blood gas analyzer that allows the determination of potassium can prevent delaying the diagnosis.

Usually, hyperkalemia is progressive ECG changes such as:

  • 1st degree AV block (extended PQ interval> 0.2 s),

  • flattened or absent P-waves,

  • high, pointed (tent-shaped) T-waves that are larger than the R-wave in more than one lead,

  • ST segment depression,

  • ST merging wave (sine waveform),

  • widened QRS complexes (> 0.12 s),

  • ventricular tachycardia,

  • Bradycardia,

  • Cardiac arrest [pulseless electrical activity (PEA), pulseless ventricular tachcardia (pulseless VT) / ventricular fibrillation (VF), asystole].

Principles of hypercalemia treatment

The 3 crucial steps in the treatment of hyperkalaemia are [5]:

  1. 1.

    Protection of the heart,

  2. 2.

    Moving potassium into the cells,

  3. 3.

    Removing potassium from the body.

IV calcium administration is not generally indicated without ECG changes. The effectiveness of treatment should be monitored, watch for recurrence of hyperkalaemia, and recurrence prevented. If z. If, for example, there is an urgent suspicion of hyperkalemia due to changes in the ECG, life-saving treatment should be initiated before laboratory results are received. The treatment of hypercalemia is the subject of a Cochrane review [6].

Patients without cardiac arrest

Check "Airway, breathing, circulation, disability, exposure" (ABCDE) and correct any disturbance. Establish intravenous access, measure the serum potassium concentration, and record an ECG. Treatment depends on the severity of the hyperkalemia.

The following values ​​are guidelines for treatment.

  • Slight increase (5.5-5.9 mmol / l):

    • Removal of potassium from the body: potassium-exchanging resins (calcium resonium 15–30 g or sodium polystyrene sulfonate (Kayexalate®) 15–30 g in 50–100 ml of 20% sorbitol, either orally or as a retention enema (onset of action after 1–3 h, maximum effect after 6 h),

  • Finding out the cause of the hyperkalemia in order to eliminate it and to prevent subsequent increases in potassium (e.g. pharmaceuticals, diet).

  • Moderate increase (6–6.4 mmol / l) without changes in the ECG:

    • Move potassium intracellularly with glucose / insulin: 10 I.U. fast-acting insulin and 25 g glucose i.v. over 15–30 min (onset of action after 15–30 min, maximum effect after 30–60 min, monitor blood sugar level).

    • Removal of potassium from the body as described above.

    • Hemodialysis: consider if patient is oliguric. Hemodialysis is more effective at removing potassium than peritoneal dialysis.

  • Severe hyperkalemia (≥6.5 mmol / l) with no ECG changes. Get expert advice and:

    • Use several methods to move potassium intracellularly:

    • Glucose / insulin (see above)

    • Salbutamol 5 mg by inhalation; several doses (10–20 mg may be necessary; onset of action after 15–30 min).

    • Sodium bicarbonate, 50 mmol over 5 min IV, in the presence of metabolic acidosis (onset of action after 15-30 min). Bicarbonate alone is less effective than glucose and insulin or inhaled salbutamol; it is best combined with other medications [7, 8].

    • Use the methods of removal from the body listed above.

  • Severe hyperkalemia (≥6.5 mmol / l) with toxic ECG changes. Get expert advice and:

    • Primarily protect the heart with calcium chloride: 10 ml 10% calcium chloride IV over 2–5 min to antagonize the toxic effects of hyperkalaemia on the myocardial cell membrane. This protects the heart by reducing the risk of pulseless VT / VF without lowering the serum potassium level (onset of action after 1–3 min).

    • Shift potassium intracellularly with several methods (see above).

    • Use methods of elimination from the body.

    • Immediate consultation with a specialist is essential.

Cardiac arrest patients

  • Modification of the basic measures ("basic life support", BLS)

    • There are no modifications to the basic measures associated with electrolyte imbalances.

  • Modification of the extended measures ("advanced life support", ALS)

    • Stick to the universal algorithm. Hyperkalemia can be quickly confirmed if a blood gas machine is available. Protect the heart primarily: 10 ml of 10% calcium chloride as a rapid IV injection.

    • Moving potassium intracellularly:

      • Glucose / Insulin: 10 IU fast acting insulin and 25 g glucose fast IV give.

      • Sodium bicarbonate, 50 mmol, as a rapid IV injection (for severe acidosis or kidney failure).

      • Removal of potassium from the body: Dialysis: consider in cardiac arrest due to treatment-resistant hyperkalemia. Various dialysis procedures have been used safely and effectively for cardiac arrest; however, this will be reserved for specialized centers.

Dialysis indication

Hemodialysis is the most effective method of eliminating potassium from the body. The basic principle is the diffusion of potassium ions over a transmembrane potassium ion gradient. Typically, the serum potassium decreases by 1 mmol / l in the first 60 min with a subsequent decrease of 1 mmol / l in the following 2 h. The effectiveness of hemodialysis for potassium elimination can be improved by dialysis with a low potassium concentration in the dialysate [9], a high blood flow [10] or a high bicarbonate concentration [11] in the dialysate. Consider hemodialysis at an early stage in the event of hyperkalemia caused by manifest renal insufficiency, oliguric acute kidney failure (urine production <400 ml / day) or by major tissue destruction. If hyperkalemia does not respond to drug therapy, hemodialysis is also indicated. After the initial treatment, the serum potassium levels often rise again. In hemodynamically unstable patients, continuous veno-venous hemofiltration (CVVH) does not affect cardiac output as much as intermittent hemodialysis. CVVH is available in many intensive care units today.

Cardiac arrest in hemodialysis patients

Cardiac arrest is the leading cause of death in hemodialysis patients [12]. Specific events that occur during hemodialysis require several new considerations.

Initial measures

Call the resuscitation team and seek expert advice immediately. While BLS is being performed, an experienced dialysis nurse is supposed to look after the dialysis machine. Usually the patient's blood is transfused back and the patient is then disconnected from the device, although this is not the fastest method [13].


A shockable heart rhythm (VF / VT) is more common in patients on hemodialysis [14, 15] than in the general population [16, 17].

Further studies are needed to find the safest defibrillation technique on dialysis. Most dialysis machine manufacturers recommend disconnecting the patient from the machine before defibrillation [18]. An alternative fast technique of locking the dialysis machine has been published. Disconnection is not necessary with CVVH [13]. The use of automated external defibrillators (AED) in dialysis centers can facilitate early defibrillation [19].

Vascular access

In life-threatening situations and in cardiac arrest, dialysis access can be used for pharmacotherapy [13].

Potentially reversible causes

All the usual reversible causes (4 Hs and HITS; see Section 4 "Extended resuscitation measures for adults") also apply to dialysis patients. Electrolyte imbalances, especially hyperkalemia and fluid overload (e.g. pulmonary edema) are the most common.


Hypokalaemia is common in hospitalized patients [20]. Hypokalemia increases the incidence of cardiac arrhythmias, especially in patients with pre-existing heart disease and in patients treated with digitalis.


Hypokalaemia is defined as a serum potassium concentration <3.5 mmol / l. Serum potassium concentrations <2.5 mmol / l are defined as severe hypokalaemia and can be symptomatic.


Hypokalaemia can include through potassium losses through the gastrointestinal tract (diarrhea), drugs (diuretics, laxatives, steroids), losses through the kidneys (renal tubular disorders, diabetes insipidus, dialysis), endocrine disorders (Cushing's syndrome, hyperaldosteronism), metabolic alkalosis, magnesium losses and one too low intake. Treatment for hyperkalaemia can also cause hypokalaemia.

Detecting hypokalaemia

Rule out hypokalaemia in any patient with arrhythmia or cardiac arrest. In dialysis patients, hypokalemia usually occurs at the end of dialysis or during continuous ambulatory peritoneal dialysis (CAPD).

As the potassium concentration decreases, the nerves and muscles are primarily affected, causing fatigue, weakness, leg cramps and constipation. In severe cases (K+ <2.5 mmol / l), rhabdomyolysis, ascending paralysis and breathing problems can occur.

EKG changes in hypokalaemia include:

  • U-waves,

  • flattened T-waves,

  • ST segment changes

  • Arrhythmias, especially in patients receiving digital therapy,

  • Cardiac arrest (PEA, pulseless VT / VF, asystole).


Treatment will depend on the severity of hypokalemia, the appearance of symptoms, and the EKG changes. Potassium should preferably be replaced slowly, but IV administration is necessary in emergencies. The maximum recommended dose for IV administered potassium is 20 mmol / h, however, in the case of cardiac arrhythmias that affect the circulation or impending cardiac arrest, a faster dose, e.g. B. indicated 2 mmol / min over 10 min with subsequent administration of a further 10 mmol over 5-10 min. Continuous ECG monitoring is essential when infusing potassium. The potassium doses must be adjusted to the closely monitored serum potassium concentrations.

Patients with a potassium deficiency are often also magnesium deficient. Magnesium plays an important role in potassium uptake and, particularly in the myocardium, in maintaining intracellular potassium levels. Filling up the magnesium stores supports the faster correction of hypokalaemia and is recommended in severe cases of hypokalaemia [21].

Disorders of the calcium and magnesium balance

Measures for the detection of the treatment of calcium and magnesium disorders are summarized in Tab. 1


Electrolyte imbalances are one of the most common causes of cardiac arrhythmias. Of all electrolyte imbalances, hyperkalemia is the fastest fatal. If there is an urgent clinical suspicion of an electrolyte disorder, prompt treatment can save many patients from developing cardiac arrest.

8b poisoning

General considerations

Poisoning is rarely the cause of cardiac arrest, but remains a major cause in victims under 40 years of age [22]. The evidence for the therapy is essentially based on small case series, animal studies and case reports. Medication or recreational drug poisoning and household product poisoning are the main drivers of hospital admission and demand from poison control centers.

Incorrect dosage, interaction, and other medication errors can also cause harm. Accidental poisoning is most common in children. Poisoning murder is rare. The population can also be exposed to pollutants through industrial accidents, wars or terrorist attacks.

Preventing cardiac arrest

Check airway, breathing, circulation, disability, exposure (ABCDE). Obstruction of the airways and respiratory arrest as a result of impaired consciousness are a common cause of death after suicidal poisoning [23].Aspiration of gastric juice can occur as a result of poisoning with centrally acting sedatives. The early endotracheal intubation of unconscious patients by a trained helper reduces the risk of aspiration. Pharmaceutical and drug-induced hypotension usually responds to fluid intake, but occasionally vasopressors (e.g. norepinephrine infusion) are necessary. Remaining comatose for long periods of time in an unchanged position can cause pressure sores and rhabdomyolysis. Electrolyte values ​​(especially potassium), blood glucose value and an arterial blood gas analysis should be determined, as well as the body temperature, since the thermoregulation is disturbed. Hypothermia and hyperthermia (hyperpyrexia) can occur with some pharmaceuticals and drugs. Blood and urine samples for analysis are necessary. Severe intoxication patients should be treated in an intensive care unit. Decontamination, forced elimination and antidotes may be indicated; they are mostly of minor importance [24]. Excessive alcohol consumption is often associated with poisoning.

Modifications of basic and extended measures

  • You should attach great importance to your own safety if the cardiac arrest has a suspicious cause or is unexpected. This is v. a. if more than one patient is affected.

  • If chemicals such as cyanides, hydrogen sulfide, corrosive substances or organophosphates are involved, mouth-to-mouth resuscitation should be avoided.

  • Life-threatening tacharrhythmias should be treated by cardioversion according to the guidelines on “Peri-arrest” arrhythmias ”(see Section 4). This includes the compensation of electrolyte and acid-base disorders.

  • The toxins should be identified as possible. Relatives, friends and ambulance personnel can provide useful information. The physical examination of the patient can provide diagnostic information such as odor, puncture sites, changes in the pupil and traces of burns in the mouth.

  • Medication overdose or drugs can trigger hypothemia (see section 8d) or hyperthermia (see section 8e), so the body temperature must be measured.

  • Long resuscitation may be necessary, especially in young patients, as the toxin can be metabolized or excreted during prolonged resuscitation.

  • Alternative therapeutic approaches that can be promising in severely poisoned patients are: higher drug doses than in standard protocols, “off label use” of drugs, prolonged resuscitation measures.

  • Regional or national poisoning centers provide information on the treatment of the poisoned. The International Program on Chemical Safety (IPCS) also lists Poison Control Centers on its website:

  • Online databases for information on toxicology and hazardous chemicals:

Specific therapeutic measures

In the case of poisoning, there are only a few therapeutic measures that are immediately effective and improve the outcome [25, 26, 27, 28, 29]. These are decontamination, repeated administration of activated charcoal, forced elimination and the use of specific antidotes. Most of these measures should only be used on the recommendation of experts. Advice from poison control centers is necessary for current therapy recommendations for severe and rare cases of poisoning.

Gastrointestinal decontamination

Activated charcoal absorbs most pharmaceuticals and drugs. The therapeutic benefit of the administration of activated charcoal decreases with increasing time since the ingestion of the poison. The administration of activated charcoal could not prove any improvement in the clinical outcome. A single dose of activated charcoal in patients who have been ingested with a potentially toxic amount of a poison (known to be adsorbed by activated charcoal) should be considered if it was not more than 1 hour ago [30]. Administer activated charcoal only to patients with preserved protective reflexes or secured airways.

Multiple doses of activated charcoal significantly increase drug / drug elimination, but no controlled study has shown a reduction in morbidity or mortality. These should therefore only be used on expert advice.

The benefit of gastric lavage is poorly documented. It should only be considered within the first hour after oral ingestion of a potentially life-threatening dose. Even under these conditions, no clinical benefit could be proven in controlled studies. Gastric lavage is contraindicated if the airway is not secured or if a solvent with a high risk of aspiration or a corrosive substance has been swallowed [27, 28].

In studies on volunteers, an intestinal irrigation led to a significantly reduced bioavailability of the drugs taken, but there is no controlled clinical study that proves an improved outcome in the intoxicated patient. Based on studies on volunteers, colonic irrigation can theoretically be helpful in cases of ingestion of a potentially toxic depot preparation or enteric-coated medication, in removing iron, lead, zinc or ingesting packets of illegal drugs. Colon irrigation is contraindicated in patients with intestinal obstruction, perforation, ileus and circulatory instability [31]

Laxatives or emetics (e.g. ipecacuanha syrup) play no role in the treatment of acute poisoning and are not recommended [26, 32, 33].

Accelerated elimination

Urinary alkalization (urine pH value> 7.5) by IV administration of sodium bicarbonate is the method of choice for moderate or severe salicylate poisoning in patients who do not require dialysis [25]. Urinary alkalization with high diuresis (about 600 ml / h) should also be considered in patients with severe herbicide poisoning (2,4-dichlorophenoxyacetic acid and methylchlorophenoxypropionic acid, mecoprop). Hypokalaemia is the most common complication of alkalosis.

Hemodialysis or hemoperfusion can only be useful in eliminating certain life-threatening toxins. Hemodialysis can remove substances or metabolites that are water-soluble and have a small volume of distribution and low protein binding. Hemoperfusion can eliminate substances that are highly protein-bound.

Special poisonings

Only some of the causes of acute poisoning cardiac arrest are addressed in these guidelines.


Patients at risk for cardiac arrest

Benzodiazepine overdose can cause loss of consciousness, respiratory depression and hypotension. Flumazenil, a competitive antagonist of benzodiazepines, should only be used to antagonize sedation with a single dose of a benzodiazepine and only if there is no risk of seizures or if there is no history of convulsions. Antagonizing benzodiazepine intoxication with flumazenil can cause considerable side effects (seizures, arrhythmia, hypotension and withdrawal syndromes; [34, 35, 36]) in patients with benzodiazepine addiction or co-medication with proconvulsive substances such as tricyclic antidepressants. The routine use of flumazenil in the comatose patient with benzodiazepine overdose is not recommended.

Modifications of basic and extended measures

Specific modifications in cardiac arrest with benzdiazepines are not necessary [36, 37, 38, 39, 40].


Opioid intoxication usually leads to suppression of the respiratory drive, followed by respiratory failure or respiratory failure. The respiratory effects of opioids can be quickly reversed by the opioid antagonist naloxone.

Patients at risk of cardiac arrest

In severe opioid-induced respiratory depression, it has been shown that there are fewer adverse effects if the airways are cleared, oxygen is administered and the patient is ventilated prior to administration of naloxone [41, 42, 43, 44, 45, 46, 47]; however, naloxone administration can eliminate the need for intubation.

The preferred route of administration for naloxone depends on the experience of the helper: IV, intramuscular (IM), subcutaneous (SC) and intranasal (IM) administration are possible. It may be quicker to use a route other than IV because it saves the time it takes to create venous access, which can be extremely difficult for IV drug addicts.

The initial dosage for naloxone is 400 μg IV [43], 800 μg IM, 800 μg s.c. [43]. or 2 mg i.n. [48, 49]. Massive opioid intoxication can make the titrated administration of 6–10 mg naloxone necessary. The duration of action of naloxone is 45–70 minutes, but respiratory depression after opioid overdose can persist for 4–5 hours. Accordingly, the clinical duration of action of naloxone may be less than that of severe opioid intoxication. Titrate the dose until the patient is breathing adequately again and showing the protective reflexes.

Acute opioid withdrawal can lead to excessive sympathetic activity and complications such as pulmonary edema, ventricular arrhythmias, and severe agitation. Use naloxone with extreme caution to antagonize opioid intoxication in patients who you suspect opioid dependence.

Modifications of extended measures

There is no research showing the benefit of naloxone in opioid-associated cardiac arrest. Cardiac arrest is usually secondary to respiratory failure and is associated with severe central nervous system (CNS) hypoxia. The prognosis is therefore poor [42]. However, naloxone administration is unlikely to be harmful. If cardiac arrest has occurred, follow standard resuscitation protocol.

Tricyclic antidepressants

This section covers tricyclics and related drugs (e.g., amitriptyline, desipramine, imipramine, nortriptyline, doxepin, and clomipramine). Suicidal intoxication with tricyclic antidepressants is common and can lead to hypotension, seizures, and life-threatening arrhythmias. Cardiotoxicity from anticholinergic and sodium channel blocking effects can cause broad-complex tachycardia (VT).

Hypotension is given by α1- Receptor blockade intensified. Anticholinergic effects include mydriasis, fever, dry skin, delirium, tachycardia, ileus, and urinary retention.

Most life-threatening disorders occur within the first 6 hours after ingestion [50, 51, 52].

Patients at risk of cardiac arrest

A QRS widening (> 100 ms) and a right type are considered indicators of an increased risk of arrhythmias [53, 54, 55]. Sodium bicarbonate should be considered for the treatment of arrhythmias with tricyclic antidepressants [56, 57, 58, 59, 60, 61, 62, 63].

Even if the optimal arterial target pH value for sodium bicarbonate therapy has not yet been investigated in any study, an arterial pH value of 7.45–7.55 i. Generally accepted and makes sense.

There are experimental findings on the use of IV lipid infusions for the treatment of tricyclic toxicity, but only few data on use in humans [64, 65]. Antibodies against tricyclics have also proven to be advantageous in experimental models [66, 67, 68, 69, 70, 71]. A small human study demonstrated the safety of the therapy, but not its clinical benefit.

Modifications of basic and extended measures

There are no randomized clinical trials comparing conventional tricyclic cardiac arrest therapy with alternatives. Only a small series of cases showed an improvement through the administration of sodium bicarbonate [73].


Sympathetic overstimulation associated with cocaine intoxication can lead to agitation, tachycardia, hypertensive crisis, hyperthermia and coronary vasoconstriction and thus to myocardial ischemia with angina pectoris.

Patients at risk of cardiac arrest

In patients with severe cardiovascular toxicity, α-blockers (phentolamine; [74]), benzodiazepines (lorazepam, diazepam; [75, 76]), calcium channel blockers (verapamil; [77]), morphine [78] and sublingual (sl) can be administered Nitroglycerin [79, 80] can be used as needed to treat hypertension, tachycardia, mycoardial ischemia, and agitation. The evidence for or against the use of β-receptor blockers [81, 82, 83, 84], including those with α-blocking components (Carvedilol and Labetolol; [85, 86, 87]) is limited. It is unclear which antiarrhythmic drug is best for treating cocaine-induced tachyarrhythmias.

Modifications of basic and extended measures

The standard guidelines should be used in cardiac arrest [88].

Local anesthetics

The systemic toxicity of local anesthetics affects the CNS and the cardiovascular system. Severe agitation, loss of consciousness with or without tonic-clonic convulsions, sinus bradycardia, conduction blockages, asystole, and ventricular tachyarrhythmias can occur.

The following factors increase toxicity: pregnancy, extreme age group or hypoxemia. Typically, regional anesthesia-related intoxication occurs when the local anesthetic is accidentally administered intra-arterially or IV. is injected.

Patients at risk of cardiac arrest

Evidence for specific treatment methods is limited to case reports of cardiac arrest and severe cardiovascular intoxication as well as animal experiments. Patients with shock and cardiac arrest due to local anesthetic toxicity can benefit from IV therapy. 20% fat emulsion administered in addition to the standard resuscitation measures benefit [89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101