These guidelines are updated once every five years, and reflect the latest scientific research on CPR and ECC (Emergency Cardiac Care). There are 10 minor things that people often miss or neglect during CPR. CPR means life. So here are 11 tips that must be kept in mind during CPR.

High Quality CPR: Top Ten Tips

1. Call 9-1-1.

2. Send someone for the Automated External Defibrillator (AED).

3. Immediately begin CPR if an adult victim is unresponsive and not breathing normally.

4. “C-A-B” (Compressions – Airway – Breathing). The AHA emphasizes the importance of early,

uninterrupted chest compressions.

5. Untrained rescuers should perform hands-only compressions: “Push hard and fast” on the

center of the victim’s chest or follow the directions of EMS dispatchers.

6. Trained rescuers should provide 30 compressions and 2 rescue breaths (if they are willing and

able) in order to improve outcomes, especially for pediatric victims.

7. Depth: Compress the chest at least 2 inches/5 cm (adults) or 1/3 depth of chest (children and

infants).

8. Rate: Provide 100 compressions per minute, to the beat of the Bee Gee’s song “Stayin’ Alive.”

9. Recoil: Allow the chest to recoil fully between compressions.

10. Minimize interruptions: Do not delay or interrupt chest compressions to check pulse or rhythm.

When more than one rescuer responds, one rescuer should ready the AED (automated external

defibrillator) while the other rescuer performs chest compressions.

11th tip: get trained! Skills deteriorate. Refresh your CPR training at least once every two years

Source: cardiacscience.com

Opioid overdose can be lethal

Clinical Features Of Opiod Intake in body are-

• Rapid, intensely presurable experience
• Heightened sexual arousal
• Increase dose required for same experience within weeks

Withdrawl Symptoms include-

• Intense craving
• Rhinorrhea, Lacrimation
• Yawning
• Perspiration, Shivering, Piloerection
• Vomiting and diarrhea, abdominal cramps.
• Tachycardia, hypertension, mydriasis ( dilation of Pupil )
• Facial flushing.

Hallmark Of Opioid Poisoning are- 

• Respiratory depression – may lead to death
• Pin-point Pupil
• CNS depression- decresed level of consciousness.
• Signs of IV drug misuse like needle tract marks, tattoo.

 

Severe –

• Respiratory depression
• Hypotension
• Non-cardiogenic pulmonary edema
• Hypothermia
• Death due to Respiratory arrest and Gastric aspiration
• Others- Ventricular Arrhythmia, Conduction defects and heart blocks

Lab Diagnosis Criteria ( CDC)

• Biologic: A case in which opioids are detected in urine, as determined by hospital or commercial laboratory tests. Fentanyl derivatives and certain other synthetic opioids (e.g., oxycodone) might not be detected by routine toxicologic screens.

- OR-

• Environmental: Detection of opioids in environmental samples, as determined by FDA

Management-
1. Clear Airway and provide Respiratory support

2. Supplement increase flow Oxygen administration
- Severe cases Endotrachel intubation may be required.

3. Antidote- Naloxone is the anti-dote for Opioids. Naloxone is given in dose of 0.8-2 mg bolus IV and repeated every 2 minutes until pupil dilates. Opioid overdose is a challenging condition that requires a difficult balancing act between over and under treatment with naloxone. Nalorphine is an alternative.

Naloxone is a pure opioid antagonist that prevents or reverses the effects of opioids by direct competition at mu, kappa, and sigma opioid receptor binding sites. It reverses both exogenous and endogenous opioids (endorphins, enkephalins, and dynorphins).

More reading: BMJ Naloxone in Opioid overdose

4. O2 saturation must be monitored .

5. Management of Hypotension.

6. CPAP/ PEEP for ventilator support.

SAY NO TO DRUGS- Medchrome Against Drug Abuse

Methanol (methyl alcohol, wood alcohol, wood spirit, CH3OH) is widely used for industrial and automotive purposes but is unfit for consumption by humans and animals. It is common to find methanol in products like anti-freeze, canned heating sources like Sterno, varnish, windshield wiper fluid, paint thinner, and fuel additives. Poisonings occur from accidental ingestion of methanol-containing products or when it is misguidedly ingested as an ethanol substitute. A blood level of >50 mg/dl methanol is associated with severe poisoning.

Mechanism of Action

Methanol can be adsorbed through the skin or from the respiratory or gastrointestinal tract upon ingestion and is metabolized in liver. Various steps of reaction are:

1. Alcohol dehydrogenase (ADH) catalyzes the conversion of methanol to formaldehyde.
2. Aldehyde dehydrogenase converts formaldehyde to formic acid.
3. Formic acid undergoes folate-dependent pathway (in the presence of tetrahydrofolate enzyme) and produce carbondioxide (CO2) and water.

Methanol itself has relatively low toxicity but the accumulation of formate (metabolism is very slow) in the body leads to metabolic acidosis.

Symptoms

Initial Symptoms

Nervous system :

• CNS depression
• Headache
• Dizziness
• Prolonged coma
• Seizures
• Confusion
• Unconsciousness

Late symptoms (10-30 hours after exposure)

Eyes:

• Visual disturbances (like being in a snow storm)
• Blurring of vision (dilation of pupils)
• Congestion of optic disc
• Blindness

Respiratory:

• Dyspnoea
• Tachypnea

CVS:

• Bradycardia
• Hypotension

GIT:

• Severe epigastric pain
• Nausea and vomiting
• Diarrhea
• Pancreatitis
• Liver damage

Other Physical Findings:

• Bluish colored lips and finger nails
• Fatigue, leg cramps, weakness
• Odor of formaldehyde in breathe and urine

Diagnosis

1. Methanol concentration in blood higher than 50 mg/dl
2. Metabolic acidosis with an elevated anion gap and osmolar gap
3. Decrease in serum bicarbonate

Treatment and Management

There are 3 specific modalities of treatment for severe methanol poisoning:

• supression of metabolism by alcohol dehydrogenase to toxic products
• hemodialysis to enhance removal of methanol and its toxic products
• alkalinization to counteract metabolic acidosis

1. Keep the patient in a quiet, dark room; protect the eyes from light
2. Gastric lavage with sodium bicarbonate if the patient is brought within 2 hours of ingesting methanol. Supportive measures to maintain ventilation and BP should be instituted.
3. Combat acidosis by i.v. sodium bicarbonate infusion (prevents retinal damage)
4. Potassium chloride (KCl) infusion is needed only when hypokalemia occurs due to alkali therapy
5. Ethanol 100 mg/dl in blood saturates alcohol dehydrogenase and retards methanol metabolism. Ethanol (10% in water) is administered through a nasogastric tube; loading dose of 0.7 ml/kg is followed by 0.15 ml/kg/hour drip.
6. Nasogastric tube with activated charcoal may be inserted
7. Hemodialysis (clears methanol as well as formate and hastens recovery)
8. Fomepizole, an alcohol dehdrase inhibitor retards methanol metabolism. A loading dose of 15 mg/kg every 12 hours till serum methanol falls below 20 mg/dl, has been found effective and safe.
9. Administration of folic or folinic acid enhances metabolism of formate

Methanol intoxication in Nepal

There was an outbreak of methanol poisoning, leading to death of 10 people in Nepal in July-August,2008. “Sofi”, a locally brewed alcoholic drink, was adulterated with methanol. It was later banned. It occured due to illiteracy and ignorance of people in rural areas and lack of proper monitoring and control by government.

-OP compounds are widely used as pesticides, for eradication of vectors.

Malathion,Fenthion,Methamidophos,Diazinon,Chlorpyrifos,Parathion are the common insecticides.

Organophosphorus Poisoning

CLINICAL PRESENTATION

• Acute cholinergic syndrome:- occur within minutes of exposure.
• Pungent garlic like odour in breath, vomit and clothing; Muscarinic effects -miosis , bronchorrhoea, bronchospasm, salivation , lacrimation , abdominal pain , bradycardia
• Nicotinic effects- Muscle fasciculation, hyper-reflexia, flaccid muscle weakness with reduced tendon reflexes
• CNS effects- headache, dizziness, confusion, drowsiness, coma , fits , central respiratory depression
• The Intermediate Syndrome- begins 48hrs after poisoning but may be delayed for 72-96 hrs. Follows resolution of the acute phase , in some instances occurs while symptoms of acute phase are still present.
• Muscle weakness causing respiratory distress and failure; progression of muscle weakness from ocular muscles to the neck and proximal limbs to the respiratory muscles.

Organophosphate induced delayed polyneuropathy:-

Occurs 1-3 weeks after acute exposure due to degeneration of long myelinated nerve fibres. Cramping muscle pains in the legs , numbnesss and paraesthesiae in the distal upper and lower limbs, shuffling gait , wrist drop.

Muscle wasting and deformity, symmetrical flaccid weakness of distal limbs, tendon reflexes reduced or lost, absent ankle reflexes.

MANAGEMENT

-Removal from site of exposure and of contaminated clothing and contact lenses.

-airway cleared and high flow oxygen administered.

-skin washed with soap and water and eyes irrigated.

-gastric lavage within an hour of ingestion by KMNO4 via nasogastric tube after establishing intravenous access and airway protection.

-Atropine : 1.8-3mg bolus immediately.

Atropine vial 1 ml conating 0.6 mg

Double the dose every 5mins until atropinised- dilated pupil, clear lungs, dry tongue, normal heart rate and BP.

Heart rate maintain 110-120/min not<90.

Once patient is atropinised give 20-30% dose required for atropinisation as infusion/hr.

Eg: 15ml for atropinisation ( 1ml=0.6mg) then maintain at 20% dose of atropinisation at 1 hr i.e 3ml

Total dose = 3ml x 24 hr= 72ml

72ml/5 pint?15ml

In 1 pint put 15ml of atropine and as muscarinic effect decreases decrease dose i.e 8ml-6ml-4ml-2ml

-Oximes : Pralidoxime 1g bolus in 30 mins then infusion 0.5g/hr

Or

Pralidoxime 1g in 100ml NS drip in 30 mins stat then TDS for 5 days.

Or , Obidoxime 0.25mg bolus then infusion 0.75g/24hrs.

Convulsions are controlled with I.V. Diazepam.

Monitoring of ECG, blood gases, temperature, urea and electrolytes , amylase and glucose is mandatory.

OP poisoning cases should be always kept under observation in Intensive Care Unit for 5-6 days.

– Dr. Mahesh Shrestha