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5 life-threatening causes of syncope

7/28/2023

https://youtu.be/u3lPowU4_bY

Life-threatening syncope:

Cardiogenic syncope refers to the loss of consciousness caused by a transient disruption of cerebral blood flow resulting from cardiac dysfunction. This condition is of great importance as it can indicate an underlying cardiac problem that needs urgent attention. Studies suggest that up to 20% of patients experiencing syncope have an underlying cardiac cause, highlighting the significance of recognizing and addressing cardiogenic syncope. Electrocardiography (ECG) and point-of-care ultrasound (POCUS) are valuable tools for identifying the causes of cardiogenic syncope.

Brugada Syndrome:

Brugada syndrome is a genetic disorder that affects the sodium channels in the heart, resulting in characteristic ECG patterns. However, Brugada patterns can be transient, appearing and disappearing, which makes diagnosis challenging. Patients with a history of syncope and suspected Brugada pattern on their ECG require referral to an electrophysiologist for further evaluation. In some cases, these patients may need the implantation of an automatic implantable cardioverter-defibrillator (AICD) to manage the risk of sudden cardiac arrest.

Wolff-Parkinson-White (WPW) syndrome:

ECG findings indicative of WPW syndrome include a short PR interval and Delta waves. WPW syndrome involves an abnormal accessory pathway in the heart that can lead to rapid atrial fibrillation and ventricular tachycardia, potentially causing syncope. Patients with suspected WPW syndrome should be admitted to the hospital and referred to an electrophysiologist for potential ablation therapy.

Torsades de Pointes:

Prolonged QT interval can lead to Torsades de Pointes, which is a life-threatening arrhythmia that can cause sudden cardiac death in patients with structurally normal hearts. When the QTc interval exceeds 500 milliseconds, it requires attention and management of the underlying cause. Common causes include electrolyte imbalances, medications, or congenital. Torsades de Pointes can be treated with magnesium sulfate or electrical cardioversion.

Aortic dissection:

Aortic dissection can also be a cause of syncope in adults. It results from a tear in the aortic wall, which can lead to blood leaking into the aortic wall, causing the inner and outer layers of the artery to separate. This can lead to the obstruction of blood flow to the brain, resulting in syncope. It is important to note that after regaining consciousness, the patient may not complain of severe chest pain. As aortic dissection can rapidly worsen and lead to death, it is critical to obtain a prompt diagnosis and initiate appropriate treatment, which may include surgical intervention. Early recognition of aortic dissection as a cause of syncope is essential to prevent further complications.

Pulmonary embolism:

Pulmonary embolism occurs when a blood clot travels from the lower extremities to the lungs, blocking blood flow and causing hypoxemia. After regaining consciousness, the patient may not complain of chest pain or have a swollen leg, making it crucial to consider pulmonary embolism in the differential diagnosis of syncope. Diagnostic tests, such as a D-dimer test and an antero-septal and inferior T wave inversion on ECG, can be valuable in identifying pulmonary embolism as the cause of syncope. Early recognition and prompt treatment, such as anticoagulation therapy, can prevent further complications and reduce the risk of recurrence. It is essential to consider this diagnosis in patients with syncope, particularly those with risk factors such as recent surgery, immobility, or cancer.

Take Home Message:

In summary, when evaluating a patient with syncope, always consider cardiogenic causes. Conduct a thorough ECG evaluation, looking for signs of myocardial ischemia, arrhythmias, Brugada patterns, short PR intervals, Delta waves, and prolonged QT intervals. These findings can provide important clues for identifying the underlying cardiac condition. Prompt referral to an electrophysiologist is crucial for further evaluation and management, which may include medications, implantable devices, or ablation therapy, depending on the specific diagnosis. Work-up for any underlying causes, such as electrolyte imbalances or medications, is essential for preventing further episodes of cardiogenic syncope. Finally, it is important to always keep in mind the two catastrophic causes of syncope: aortic dissection and pulmonary embolism.

5-step ECG analysis

7/28/2023

https://youtu.be/Vldnx9zitIY

The 5-step ECG analysis (the must-have ACLS Skill):

Step 1: Determine the rate of the rhythm.

Method 1: The 6 Second Method. Count number of R waves on the 6 second strip and multiply by 10.
Method 2: The Big Box Method. Divide 300 by the number of big boxes in between two consecutive R waves. This is only used for regular rhythms.

Step 2: Determine the regularity of the rhythm.

Regular rhythm means constant R to R interval.
Regularly irregular rhythm means variable R to R interval with a pattern.
Irregularly irregular rhythm means variable R to R interval with no pattern.

Step 3: Determine the QRS duration.

The QRS complex represents ventricular depolarization.
To measure the QRS complex, count the number of small boxes from the beginning to the end of the QRS complex, then multiply by 0.04 seconds.
The normal range of QRS is 0.06 to 0.12 seconds.

Step 4: Determine the presence of P waves.

In lead II , the P wave is typically a small positive deflection from the isoelectric baseline that occurs just before the QRS complex.

Step 5: Determine AV conduction.

Atrioventricular conduction is evaluated by assessing the relationship between the P waves and QRS complexes.
The P wave and QRS complex have a 1 to 1 relationship, meaning that for every P wave, a QRS complex is conducted.
The PR interval measures the time of depolarization of the atria to depolarization of the ventricles and reflects a physiological delay in AV conduction imposed by the AV node
To measure the PR interval, count the number of small boxes between the beginning of the P wave and the beginning of the QRS complex, then multiply by 0.04 seconds.

The normal PR interval is between 0.12 and 0.20 seconds.

ACLS ECG rhythms

7/28/2023

https://youtu.be/MJ4rY3Qa-yU

ACLS ECG Rhythms:

1. Ventricular fibrillation. Ventricular fibrillation is a chaotic electrical activity with no discernible QRS complex. Immediate defibrillation is necessary to restore normal rhythm.
2. Ventricular tachycardia (VT). VT can be classified as sustained or nonsustained, with a generally accepted cutoff of 30 seconds. The rhythm may arise from the ventricular myocardium, the distal conduction system, or both. Causes of VT include ischemic heart disease, cardiomyopathy or heart failure, myocarditis, heart valve disease, and idiopathic VTStable patients are treated with amiodarone; patients with unstable VT are treated with synchronized cardioversion; and patients with pulseless VT need immediate defibrillation.
3. Torsades de pointes. Torsades de pointes is a specific type of polymorphic ventricular tachycardia associated with QTc prolongation and characterized by a gradual change in amplitude and twisting of the QRS complexes around the isoelectric line on the ECG. The rhythm may terminate spontaneously or may degenerate into ventricular fibrillation, which can be deadly. The most common causes of acquired QT prolongation are drugs, such as antiarrhythmic agents, antibiotics, antipsychotics, and antidepressants. Other causes include electrolyte imbalances, such as hypokalemia and hypomagnesemia, and genetic mutations. Treatment of torsades de pointes include magnesium sulfate or electrical cardioversion.
4. Atrial fibrillation. Atrial fibrillation is characterized by no discernible P waves and an irregularly irregular heart beats. It has strong associations with heart failure, coronary artery disease, valvular heart disease, diabetes mellitus, and hypertension. Common medications for managing atrial fibrillation include diltiazem, verapamil, digoxin, and amiodarone. Anticoagulant therapy may be necessary to prevent the formation of blood clots in the atria, which can lead to stroke.
5. Atrial flutter. Atrial flutter is a supraventricular arrhythmia that is usually about 150 beats per minute. It is characterized by a "saw-toothed" flutter appearance on the ECG that represents multiple P waves for each QRS complex. Adenosine or calcium channel blockers are commonly used to treat atrial flutter.
6. Paroxysmal supraventricular tachycardia. PSVT is characterized by episodes of rapid, regular heart rate that begins suddenly and ends suddenly. Treatment options include vagal maneuvers, adenosine, calcium channel blockers, and beta blockers.
7. First degree AV block. First-degree AV block is characterized by a prolonged PR interval greater than 0.20 seconds. It usually requires no treatment. Atropine may be indicated when symptomatic.
8. Second degree AV block type I (Wenckebach). Second-degree AV block type I is characterized by a progressive lengthening of the PR interval until a beat is dropped. It usually requires no treatment. Atropine may be indicated when symptomatic.
9. Second degree AV block Type II. Second-degree AV block type II is characterized by intermittent dropped beats with a constant PR interval. Symptomatic patients may require a pacemaker, bridged with dopamine or epinephrine infusion.

10. Third degree AV block (complete AV block). Third-degree AV block is characterized by no conduction between the atria and ventricles. Symptomatic patients may require a pacemaker, bridged with dopamine or epinephrine infusion.

ACLS Medications

7/28/2023

https://youtu.be/zdiVUIu3OCM

ACLS Medications:

Adenosine. Adenosine is used to treat paroxysmal supraventricular tachycardia (PSVT). It can be given as a rapid I.V. push of 6 mg, followed by a 20 mL saline flush and then 12 mg if needed.
Amiodarone. Amiodarone is used to treat ventricular arrhythmias (VT or VF). It can be given as 150 mg I.V. drip over 10 minutes. Rapid I.V. push of 300 mg is indicated if the patient is pulseless.
Atropine. Atropine is used to treat symptomatic bradycardia. It can be given as 1 mg I.V. push, repeated every 3 to 5 minutes up to a maximum of 3 mg.
Diltiazem. Diltiazem is used to treat rapid atrial fibrillation or PSVT. It can be given as 15 to 20 mg I.V. over 2 minutes, followed by a second dose of 20 to 25 mg after 15 minutes if needed.
Dopamine. Dopamine is used to treat symptomatic bradycardia. It can be given as a continuous I.V. infusion starting at 5 to 10 microgram per kilogram per minute and titrated up to 20 to 50 microgram per kilogram per minute.
Epinephrine. Epinephrine is used to treat cardiac arrest, anaphylaxis, or symptomatic bradycardia. It can be given as a rapid I.V. push of 1mg every 3 to 5 minutes during cardiac arrest. Epinephrine is also used to treat anaphylaxis (0.5 mg IM) and symptomatic bradycardia (2 to 10 microgram per minute infusion).
Furosemide. Furosemide is used to treat heart failure and acute lung edema. It can be given as 20 to 40 mg I.V., you may double the dose if needed.
Magnesium sulfate. Magnesium sulfate is used to treat torsades de pointes or suspected hypomagnesemia. It can be given as 1 to 2 gram I.V. over 15 to 20 minutes.
Nitroglycerin. Nitroglycerin is used to treat acute coronary syndrome, acute myocardial infarction, heart failure or acute lung edema. It can be given as 12.5 to 25 microgram I.V. bolus, followed by 10 to 20 microgram per minute infusion. Nitroglycerin is contraindicated in patients with hypotension, RV infarction, or Viagra use.

Norepinephrine. Norepinephrine is used to treat cardiogenic or septic shock. It can be given as a continuous I.V. infusion starting at 0.5 to 1 microgram per minute and titrated up to 30 microgram per minute.

Cyanide poisoning

7/28/2023

https://youtu.be/1tYnVoQOl9k

Cyanide poisoning:

Cyanide intoxication occurs when the body is exposed to high levels of cyanide, a potent toxin that interferes with cellular respiration. Cyanide can be encountered through various routes, such as ingestion, inhalation, or dermal exposure. It is important to recognize the signs and symptoms early, as prompt diagnosis and treatment are crucial for favorable outcomes.

Clinical presentation
The clinical presentation of cyanide intoxication can vary depending on the route and amount of exposure. Common symptoms include:

1. Rapid onset of neurological manifestations: Patients may experience confusion, agitation, seizures, or loss of consciousness.
2. Cardiovascular instability: Cyanide can cause significant cardiovascular effects, including tachycardia, hypotension, and cardiac arrhythmias.
3. Respiratory distress: Cyanide interferes with cellular respiration, leading to rapid and labored breathing, and in severe cases, respiratory failure.

Diagnosis:

1. Arterial blood gas analysis may reveal metabolic acidosis and elevated lactate levels.
2. Measurement of cyanide levels in blood or body fluids can aid in confirming the diagnosis.

The management of cyanide intoxication:

1. Supportive measures: Ensure adequate oxygenation and ventilation to support respiratory function. Establish intravenous access for fluid resuscitation and maintain hemodynamic stability.
2. Antidotes: The administration of specific antidotes is critical to counteract the effects of cyanide. Hydroxocobalamin and sodium thiosulfate are commonly used antidotes that enhance cyanide detoxification and elimination.
3. Decontamination: If cyanide exposure is due to ingestion or dermal contact, decontamination measures such as gastric lavage or activated charcoal administration may be considered.
4. Adjunctive therapies: In severe cases, additional therapies such as hyperbaric oxygen therapy or hemodialysis may be necessary, especially when antidotes alone are insufficient. In severe cases of CN poisoning, if there is no response to supportive therapy, and there is no possibility for obtaining and administering hydroxocobalamin early in the course, hemodialysis might be considered as a method to remove free blood CN and thiocyanates and to remove toxic metabolic byproducts.

Antidotes of cyanide poisoning:
1. Hydroxocobalamin:

Hydroxocobalamin is a commonly used antidote for cyanide poisoning. It works by binding to cyanide to form cyanocobalamin, which is then excreted through the kidneys. Hydroxocobalamin has a high affinity for cyanide and rapidly scavenges free cyanide molecules in the body. It has the advantage of a wide therapeutic window and can be administered intravenously as a single dose.

2. Sodium Thiosulfate:

Sodium thiosulfate is another antidote used in the treatment of cyanide poisoning. It acts by enhancing the detoxification of cyanide through the conversion of cyanide to thiocyanate, which is less toxic and can be excreted in the urine. Sodium thiosulfate is often used in combination with hydroxocobalamin to enhance the efficacy of cyanide detoxification.

3. Methylene Blue:

Methylene blue is an alternative antidote that can lessen cyanide toxicity by re-establishing oxidation-reduction equilibrium and calcium channel activity. Methylene blue is administered intravenously and should be used cautiously in patients with G6PD deficiency, as it can induce hemolysis in these individuals.

4. Amyl Nitrite and Sodium Nitrite:

Amyl nitrite and sodium nitrite are inhalation and intravenous agents, respectively, that can be used in specific situations where hydroxocobalamin or sodium thiosulfate are not immediately available. These agents work by inducing methemoglobinemia, which sequesters cyanide and reduces its toxicity. However, their use is less common and may be associated with potential side effects and complications.

Summary:

It is important to note that the choice of antidote may depend on factors such as availability, patient characteristics, and the severity of cyanide poisoning. Prompt administration of these antidotes, as well as appropriate supportive care, is crucial in managing cyanide intoxication effectively.

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5 life-threatening causes of syncope

5-step ECG analysis

ACLS ECG rhythms

ACLS Medications

Cyanide poisoning

AuthorTwitter: @jackcfchong[email protected]

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Twitter: @jackcfchong
[email protected]