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ACLS Megacode

1/17/2024

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ACLS Megacode:

Initial Assessment:
- Check for responsiveness, breathing, and pulse.
- If unresponsive, call for help and initiate CPR.
- Attach defibrillator pads and monitor.

CPR:
- Perform chest compressions at a rate of 100-120/min, allowing full chest recoil.
- Provide rescue breaths at a ratio of 30:2.
- Continue CPR until ROSC is achieved or until medical help arrives.

Defibrillation:
- If VF/VT is present, deliver a defibrillation shock of 360 joules biphasic or 360 joules monophasic.
- If unsuccessful, increase the energy level to 400 joules biphasic or 400 joules monophasic and repeat.
- Continue defibrillation attempts until ROSC is achieved or until medical help arrives.

Emergency Medications:
- Epinephrine: 1 mg IV/IO every 3-5 minutes.
- Vasopressin: 40 units IV/IO every 3-5 minutes (if refractory to epinephrine).
- Amiodarone: 300 mg IV/IO over 20 minutes (if refractory to defibrillation).
- Lidocaine: 1 mg/kg IV/IO (if refractory to defibrillation).
- Sodium bicarbonate: 1 mEq/kg IV/IO (if metabolic acidosis).
- Calcium chloride: 10 mg/kg IV/IO (if hyperkalemia or calcium channel blocker overdose).

Advanced Airway Management:
- Intubate the patient if CPR is ineffective or if the patient is unable to maintain a patent airway.
- Consider cricothyrotomy if intubation is unsuccessful.

Post-ROSC Care:
- Monitor vital signs closely.
- Provide supportive care, including oxygen therapy, fluid resuscitation, and antibiotics.
- Address any underlying medical conditions that may have contributed to the arrest.

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Brugada Syndrome

1/14/2024

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Brugada syndrome

Brugada syndrome is a rare but potentially life-threatening inherited disease that predisposes patients to fatal cardiac arrhythmias.
The syndrome is characterized by the ECG findings of a right bundle branch block and ST-segment elevations in the right precordial leads (V1 to V3).
Genetically, Brugada syndrome is primarily linked to mutations in the SCN5A gene, accounting for 15 to 30% of cases.
However, its inheritance follows an autosomal dominant pattern with variable expressivity and reduced penetrance.
Environmental factors, such as temperature, certain medications, electrolyte imbalances, and cocaine use, can influence its presentation.
The prevalence of Brugada Syndrome is approximately 3 to 5 per 10,000 people. Brugada syndrome is approximately 8 to 10 times more common in males than females.
Brugada syndrome is also more prevalent in those who are of Southeast Asian descent.
The mean affected age is 41 years old.
Brugada syndrome accounts for 4% of all sudden cardiac deaths.

Clinical manifestations

Symptoms of Brugada syndrome vary widely, with many individuals remaining asymptomatic.
Those who do experience symptoms might encounter blackouts, seizures, palpitations, chest discomfort, breathlessness, or dizziness.
Sudden cardiac death, often during sleep, is a potential outcome.
Brugada syndrome is usually diagnosed between 22 and 65 years of age It is rarely diagnosed in children.
Interestingly, symptoms might emerge due to triggers like high temperatures, alcohol intake, or dehydration.

Diagnostic Tools of Brugada Syndrome

The primary diagnostic tool is an ECG conducted in a hospital setting.
The use of high-lead positions is thought to increase the diagnostic yield by upto 1.5 times compared with standard lead positions.
When ECG findings remain equivocal or when spontaneous type 2 or type 3 Brugada pattern is observed, a drug challenge using sodium channel blockers is performed to evoke the type 1 Brugada ECG pattern.
Additionally, genetic testing for causative mutations should be considered in specific scenarios.

ECG Patterns of Brugada Syndrome

Three ECG pattern types were described in patients with Brugada syndrome, although only type 1 changes are considered diagnostic.
A type 1 Brugada ECG consists of coved ST-segment elevation greater than or equal to 2 mm with a negative T-wave in the right precordial leads, which are thought to be representative of pathophysiological changes in the RVOT.
Type 1 pattern consists of coved ST-segment elevation with T-wave inversion.
Type 2 and type 3 patterns consist of saddleback ST-segment configuration with variable levels of ST-segment elevation.
The ST-segment elevation is greater than 1mm in type 2 and less than 1 mm in type 3.
Pragmatically, only a type 1 pattern is diagnostic for Brugada syndrome, whereas patients with type 2 and type 3 patterns should undergo sodium channel blocker provocation testing.
Type 1 pattern consists of coved ST-segment elevation with T-wave inversion.
Type 2 and type 3 patterns consist of saddleback ST-segment configuration with variable levels of ST-segment elevation.
The ST-segment elevation is greater than 1mm in type 2 and less than 1 mm in type 3.

Diagnosis of Brugada Syndrome
Brugada syndrome is diagnosed when type 1 Brugada ECG pattern is associated with one of the following clinical criteria:

Documented VF or polymorphic VT,
Family history of sudden cardiac death at age younger than 45,
Coved-type ECGs in family members,
Inducibility of VT with programmed electrical stimulation,
Syncope.
Nocturnal agonal respiration.

Treatment of Brugada Syndrome

Unfortunately, there's no definitive cure for Brugada syndrome, but management options exist.
For high-risk cases, implantable cardioverter-defibrillators (ICDs) serve as a crucial intervention.
Additionally, pharmacological treatments like quinidine or novel therapies like radiofrequency ablation offer promise, although their efficacy might vary.
Note that, the only proven therapy is an implantable cardioverter-defibrillator (ICD).
Quinidine has been proposed as an alternative in settings where ICD’s are unavailable or where they would be inappropriate (for example, neonates).
High temperature, excessive alcohol consumption, and specific medications, can exacerbate symptoms.
Lifestyle modifications is important in Brugada syndrome to avoid triggers that provoke the condition.

Conclusion

In summary, the pathophysiology of Brugada syndrome involves a mutation in cardiac sodium channels.
Typical ECG shows a pseudo-RBBB and ST elevations in leads V1 and V2. It is more prevalent in Asian males.
Treatment includes an implantable cardioverter-defibrillator to prevent sudden cardiac death.
Brugada syndrome is inherited in an autosomal dominant manner.

Brugada syndrome, though rare, demands careful management.
Personalized risk assessment, a multi-disciplinary approach, and regular follow-ups are pivotal.
While there's no cure, tailored interventions significantly reduce severe risks associated with this condition.

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Airway Management Tips

1/14/2024

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Airway Management Tips

Always have a nasopharyngeal airway and Yankauer suction ready.
Bag-valve-mask ventilation is a two-person procedure.
Proper bag-valve-mask ventilation include correct airway positioning and use of a nasopharyngeal airway.
Keep dentures in place during bag-valve-mask ventilation.
All unconscious patients are assumed to have a partial airway obstruction.
Usage of a tongue depressor before insertion of the LMA helps prevent the tongue from being pushed into the posterior pharynx by the LMA upon insertion.
Position the external auditory meatus on the same horizontal plane as the sternum and the patient’s face parallel to the ceiling.
Video laryngoscope improves success rate and glottic visualization compared with direct laryngoscope.
Use bedside ultrasound to confirm endotracheal tube position.
Patients undergoing rapid sequence intubation could have oxygen administered simultaneously via a nasal cannula (15 LPM) and non-rebreather masks or bag-valve-mask.
Impending respiratory failure is a clinical diagnosis, not based upon imaging or blood testing.
The LEMON assessment helps identify potential difficult airway.

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Modified Valsalva Maneuver for PSVT

1/14/2024

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Modified Valsalva Maneuver for PSVT

This modified Valsalva Maneuver is a simple yet effective technique used to treat stable PSVT.

Phase 1: Increasing Intrathoracic Pressure.

The first phase involves the patient performing a standardized "strain" by blowing into a 10mL syringe for approximately 15 seconds while sitting up or in a semirecumbent position.
This action contracts the thoracic and abdominal muscles, causing a drop in blood flow back to the heart (decreased preload) and the brain.
This drop stimulates the baroreceptor reflex, triggering the sympathetic nervous system (stress response) to raise blood pressure, cardiac output, and peripheral vascular resistance.

Phase 2: Sudden Drop in Intrathoracic Pressure.

After the 15-second strain, the patient stops blowing into the syringe just before being laid flat (or simultaneously).
This sudden decrease in intrathoracic pressure increases blood flow back to the heart, leading to an opposite effect of phase 1.
The body compensates by increasing parasympathetic (vagal) activity, decreasing heart rate, and promoting a relaxation response.

Phase 3: Laying Flat and Raising Legs to 45 Degrees.

The patient is then laid flat while raising their legs to 45 degrees.
This postural modification further increases blood flow back to the heart, boosting stroke volume and cardiac output.
This triggers even more vagal stimulation, causing a decrease in heart rate, potentially converting the patient back into sinus rhythm.

In conclusion, by manipulating the nervous system and leveraging physiology, this maneuver is a safe, simple, and cost-free treatment to treat PSVT.

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Morel-Lavallee Lesion

1/14/2024

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Morel-Lavallee Lesion

Background
Morel-Lavallee lesion (MLL) is a closed degloving injury resulting from blunt shearing or tangential forces. In this condition, hemolymph is collected in the closed space between the separated subcutaneous tissue and the underlying fascia. MLL is associated with a potential risk of skin necrosis and soft tissue infection. Its clinical manifestation varies from soft fluctuant swelling to skin necrosis or wound sepsis.

Physical examination
Physical examination findings that may help distinguish between closed degloving injuries and contusions include: skin mobility, subcutaneous fluctuation, decreased cutaneous sensation, tire marks, and friction burns.
Imaging studies for MLL include: Ultrasonography, CT scan, and MRI.
MRI is the imaging technique of choice due to its superior soft tissue resolution and ability to identify the presence or absence of a capsule surrounding the fluid collection, which guides treatment decisions.

Management
Management of Morel-Lavallee lesions depends on several factors, including the size, location, and presence of complications.
Nonoperative treatment with compression dressings, observation, and pain management is often sufficient for smaller lesions. However, larger or symptomatic lesions may require percutaneous aspiration or open surgical debridement to remove the fluid collection and prevent complications.

Take Home Message
Given their potential to mimic other conditions and contribute to surgical site infections, Morel-Lavallee lesions should be considered in the differential diagnosis for trauma patients presenting with soft tissue swelling, particularly in the prepatellar or hip regions. Early diagnosis and prompt initiation of appropriate management, including timely referral for definitive imaging and intervention, are crucial to prevent long-term complications and optimize patient outcomes.

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ACLS Megacode

Brugada Syndrome

Airway Management Tips

Modified Valsalva Maneuver for PSVT

Morel-Lavallee Lesion

AuthorTwitter: @jackcfchong[email protected]

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