Currently, there are three beta-blockers that have been approved for the treatment of chronic heart failure. These medications include bisoprolol, carvedilol, and nebivolol.

Chronic HF is a common clinical syndrome resulting from coronary artery disease (CAD), HTN, valvular heart disease, and/or primary cardiomyopathy. There is now conclusive evidence that β-blockers, when added to ACE inhibitors, substantially reduce mortality, decrease sudden death, and improve symptoms in patients with HF. Despite the overwhelming evidence and guidelines that mandate the use of β-blockers in all HF patients without contraindications, many patients do not receive this treatment.

Patients who have a STEMI caused by a blockage in the left circumflex artery (LCX) will usually show ST elevation in leads I and AVL. These leads correspond to the high lateral area of the heart, which is supplied by the LCX artery.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Pericarditis refers to the inflammation of the pericardium, which can be caused by various factors such as infections (typically viral, like coxsackie virus), drug-induced reactions (e.g. isoniazid, cyclosporine), trauma, autoimmune conditions (e.g. SLE), paraneoplastic syndromes, uraemia, post myocardial infarction (known as Dressler’s syndrome), post radiotherapy, and post cardiac surgery.

The clinical presentation of pericarditis often includes retrosternal chest pain that is pleuritic in nature. This pain is typically relieved by sitting forwards and worsened when lying flat. It may also radiate to the shoulders. Other symptoms may include shortness of breath, tachycardia, and the presence of a pericardial friction rub.

The pericardium receives sensory supply from the phrenic nerve, which also provides sensory innervation to the diaphragm, various mediastinal structures, and certain abdominal structures such as the superior peritoneum, liver, and gallbladder. Since the phrenic nerve originates from the 4th cervical nerve, which also provides cutaneous innervation to the front of the shoulder girdle, pain from pericarditis can also radiate to the shoulders.

According to NICE guidelines, amiodarone is recommended as the initial choice for pharmacological cardioversion of atrial fibrillation (AF) in individuals who have evidence of structural heart disease.

Further Reading:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

Adenosine is given through a rapid IV bolus, followed by a flush of saline solution. In adults, the starting dose is 6 mg, and if needed, an additional dose of 12 mg is given. If necessary, another dose of either 12 mg or 18 mg can be administered at intervals of 1-2 minutes until the desired effect is observed.

It is important to note that the latest ALS guidelines recommend an 18 mg dose for the third administration, while the BNF/NICE guidelines suggest a 12 mg dose.

However, patients who have undergone a heart transplant are particularly sensitive to the effects of adenosine. Therefore, their initial dose should be reduced to 3 mg, followed by 6 mg, and then 12 mg.

This particular patient has a high risk of experiencing an acute coronary syndrome. Therefore, it is recommended to administer aspirin at a dosage of 300 mg and clopidogrel at a dosage ranging from 300-600 mg.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Adenosine is a type of purine nucleoside that is primarily utilized in the diagnosis and treatment of paroxysmal supraventricular tachycardia. Its main mechanism of action involves stimulating A1-adenosine receptors and opening acetylcholine-sensitive potassium channels. This leads to hyperpolarization of the cell membrane in the atrioventricular (AV) node and slows down conduction in the AV node by inhibiting calcium channels.

When administering adenosine, it is given rapidly through an intravenous bolus, followed by a saline flush. The initial dose for adults is 6 mg, and if necessary, additional doses of 12 mg or 18 mg can be given at 1-2 minute intervals until the desired effect is observed. It is important to note that the latest ALS guidelines recommend 18 mg for the third dose, while the BNF/NICE guidelines suggest 12 mg.

One of the advantages of adenosine is its very short half-life, which is less than 10 seconds. This means that its effects are rapid, typically occurring within 10 seconds. However, the duration of action is also short, lasting only 10-20 seconds. Due to its short half-life, any side effects experienced are usually brief. These side effects may include a sense of impending doom, facial flushing, dyspnea, chest discomfort, and a metallic taste.

There are certain contraindications to the use of adenosine. These include 2nd or 3rd degree AV block, sick sinus syndrome, long QT syndrome, severe hypotension, decompensated heart failure, chronic obstructive lung disease, and asthma. It is important to exercise caution when administering adenosine to patients with a heart transplant, as they are particularly sensitive to its effects. In these cases, a reduced initial dose of 3 mg is recommended, followed by 6 mg and then 12 mg.

It is worth noting that the effects of adenosine can be potentiated by dipyridamole, a medication commonly used in combination with adenosine. Therefore, the dose of adenosine should be adjusted and reduced in patients who are also taking dipyridamole.

Tricuspid regurgitation is characterized by a continuous murmur that spans the entire systolic phase of the cardiac cycle. This murmur is best audible at the lower left sternal edge and has a low frequency. Interestingly, the intensity of the murmur increases during inspiration and decreases during expiration, a phenomenon referred to as Carvallo’s sign.

Further Reading:

Tricuspid regurgitation (TR) is a condition where blood flows backwards through the tricuspid valve in the heart. It is classified as either primary or secondary, with primary TR being caused by abnormalities in the tricuspid valve itself and secondary TR being the result of other conditions outside of the valve. Mild TR is common, especially in young adults, and often does not cause symptoms. However, severe TR can lead to right-sided heart failure and the development of symptoms such as ascites, peripheral edema, and hepatomegaly.

The causes of TR can vary. Primary TR can be caused by conditions such as rheumatic heart disease, myxomatous valve disease, or Ebstein anomaly. Secondary TR is often the result of right ventricular dilatation due to left heart failure or pulmonary hypertension. Other causes include endocarditis, traumatic chest injury, left ventricular systolic dysfunction, chronic lung disease, pulmonary thromboembolism, myocardial disease, left to right shunts, and carcinoid heart disease. In some cases, TR can occur as a result of infective endocarditis in IV drug abusers.

Clinical features of TR can include a pansystolic murmur that is best heard at the lower left sternal edge, Carvallo’s sign (murmur increases with inspiration and decreases with expiration), an S3 heart sound, and the presence of atrial arrhythmias such as flutter or fibrillation. Other signs can include giant C-V waves in the jugular pulse, hepatomegaly (often pulsatile), and edema with lung crepitations or pleural effusions.

The management of TR depends on the underlying cause and the severity of the condition. In severe cases, valve repair or replacement surgery may be necessary. Treatment may also involve addressing the underlying conditions contributing to TR, such as managing left heart failure or pulmonary hypertension.

Patients who have bradycardia and show ventricular pauses longer than 3 seconds on an electrocardiogram (ECG) are at a high risk of developing asystole. The following characteristics are indicators of a high risk for asystole: recent episodes of asystole, Mobitz II AV block, third-degree AV block (also known as complete heart block) with a broad QRS complex, and ventricular pauses longer than 3 seconds.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

Aortic sclerosis is a condition that occurs when the aortic valve undergoes senile degeneration. Unlike aortic stenosis, it does not result in any obstruction of the left ventricular outflow tract. To differentiate between aortic stenosis and aortic sclerosis, the following can be used:

Feature: Aortic stenosis
– Symptoms: Can be asymptomatic, but may cause angina, breathlessness, and syncope if severe.
– Pulse: Slow rising, low volume pulse.
– Apex beat: Sustained, heaving apex beat.
– Thrill: Palpable thrill in the aortic area can be felt.
– Murmur: Ejection systolic murmur loudest in the aortic area.
– Radiation: Radiates to carotids.

Feature: Aortic sclerosis
– Symptoms: Always asymptomatic.
– Pulse: Normal pulse character.
– Apex beat: Normal apex beat.
– Thrill: No thrill.
– Murmur: Ejection systolic murmur loudest in the aortic area.
– Radiation: No radiation.

Aortic stenosis leads to the presence of a murmur during the ejection phase of the cardiac cycle. This murmur is most audible at the right second intercostal space and can be heard extending into the right neck.

Mitral regurgitation, on the other hand, produces a high-pitched murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is best heard at the apex of the heart and can be heard radiating into the axilla.

Tricuspid regurgitation is characterized by a blowing murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is most clearly heard at the lower left sternal edge.

Ventricular septal defect results in a harsh murmur that occurs throughout the entire systolic phase of the cardiac cycle. This murmur is best heard at the third or fourth left intercostal space and can be heard radiating throughout the praecordium.

Aortopulmonary shunts are an extremely rare cause of a murmur that occurs throughout the entire systolic phase of the cardiac cycle.

Mitral regurgitation is characterized by several clinical features. One of the main signs is a pansystolic murmur that can be heard throughout the entire systolic phase of the cardiac cycle. This murmur often radiates to the left axilla. Another notable feature is a soft S1 heart sound, which is the first heart sound heard during the cardiac cycle. Additionally, a 3rd heart sound, also known as an added sound, can be detected in patients with mitral regurgitation. As the condition progresses to moderate to severe levels, signs such as a laterally displaced apex beat with a heave may become apparent.

Further Reading:

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Tricuspid regurgitation is commonly caused by right ventricular dilatation, often as a result of heart failure. Other factors that can contribute to this condition include right ventricular infarction and cor pulmonale. The clinical signs of right-sided heart failure are frequently observed, such as an elevated jugular venous pressure, peripheral edema, hepatomegaly, and ascites.

The murmur associated with tricuspid regurgitation is a pansystolic murmur that is most audible at the tricuspid area during inspiration. A thrill may also be felt at the left sternal edge. Reverse splitting of the second heart sound can occur due to the early closure of the pulmonary valve. Additionally, a third heart sound may be present due to rapid filling of the right ventricle.

An abnormal QTc, which is the measurement of the time it takes for the heart to recharge between beats, is generally considered to be greater than 450 ms in males. However, some sources may use a cutoff of greater than 440 ms as abnormal in males. To further categorize the QTc, a measurement of 430ms or less is considered normal, 431-450 ms is borderline, and 450 ms or more is considered abnormal in males. Females typically have a longer QTc, so the categories for them are often quoted as less than 450 ms being normal, 451-470 ms being borderline, and greater than 470ms being abnormal.

Further Reading:

Long QT syndrome (LQTS) is a condition characterized by a prolonged QT interval on an electrocardiogram (ECG), which represents abnormal repolarization of the heart. LQTS can be either acquired or congenital. Congenital LQTS is typically caused by gene abnormalities that affect ion channels responsible for potassium or sodium flow in the heart. There are 15 identified genes associated with congenital LQTS, with three genes accounting for the majority of cases. Acquired LQTS can be caused by various factors such as certain medications, electrolyte imbalances, hypothermia, hypothyroidism, and bradycardia from other causes.

The normal QTc values, which represent the corrected QT interval for heart rate, are typically less than 450 ms for men and less than 460ms for women. Prolonged QTc intervals are considered to be greater than these values. It is important to be aware of drugs that can cause QT prolongation, as this can lead to potentially fatal arrhythmias. Some commonly used drugs that can cause QT prolongation include antimicrobials, antiarrhythmics, antipsychotics, antidepressants, antiemetics, and others.

Management of long QT syndrome involves addressing any underlying causes and using beta blockers. In some cases, an implantable cardiac defibrillator (ICD) may be recommended for patients who have experienced recurrent arrhythmic syncope, documented torsades de pointes, previous ventricular tachyarrhythmias or torsades de pointes, previous cardiac arrest, or persistent syncope. Permanent pacing may be used in patients with bradycardia or atrioventricular nodal block and prolonged QT. Mexiletine is a treatment option for those with LQT3. Cervicothoracic sympathetic denervation may be considered in patients with recurrent syncope despite beta-blockade or in those who are not ideal candidates for an ICD. The specific treatment options for LQTS depend on the type and severity of the condition.

Mitral stenosis is a condition characterized by a narrowing of the mitral valve, which can lead to various symptoms. One common symptom is a mid-late diastolic murmur, which can be heard during a physical examination. This murmur may also be described as mid-diastolic, late-diastolic, or mid-late diastolic. Additionally, patients with chronic mitral stenosis may not experience any symptoms, and the murmur may only be detected incidentally.

A significant risk associated with mitral stenosis is the development of atrial fibrillation (AF). When AF occurs in patients with mitral stenosis, it can trigger acute pulmonary edema. This happens because the left atrium, which is responsible for pumping blood across the narrowed mitral valve into the left ventricle, needs to generate higher pressure. However, when AF occurs, the atrial contraction becomes inefficient, leading to impaired emptying of the left atrium. This, in turn, causes increased back pressure in the pulmonary circulation.

The elevated pressure in the left atrium and pulmonary circulation can result in the rupture of bronchial veins, leading to the production of pink frothy sputum. This symptom is often observed in patients with mitral stenosis who develop acute pulmonary edema.

Further Reading:

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Adrenaline should be administered promptly once access to the circulatory system has been established in cases of non-shockable cardiac arrests such as PEA or asystole. The recommended dose is 1 mg, which can be given either as 10 mL of a 1:10,000 solution or as 1 mL of a 1:1000 solution through the intravenous (IV) or intraosseous (IO) routes.

In cases of shockable cardiac arrests like ventricular fibrillation (Vf) or pulseless ventricular tachycardia (pVT), adrenaline should be administered after the third shock has been delivered and chest compressions have been resumed. The same dose of 1 mg can be given using the same concentration options as mentioned earlier.

Subsequently, adrenaline should be administered every 3-5 minutes, alternating with chest compressions, without interrupting the compressions. The alpha-adrenergic effects of adrenaline cause constriction of blood vessels throughout the body, leading to increased pressures in the coronary and cerebral circulation.

The beta-adrenergic effects of adrenaline have positive effects on the heart, increasing its contractility (inotropic) and heart rate (chronotropic), which may also enhance blood flow to the coronary and cerebral arteries. However, it is important to note that these benefits may be counteracted by increased oxygen consumption by the heart, the potential for abnormal heart rhythms, temporary decrease in oxygen levels due to abnormal blood flow in the lungs, impaired microcirculation, and increased dysfunction of the heart after the cardiac arrest.

While there is no evidence supporting the long-term benefits of adrenaline use in cardiac arrest cases, some studies have shown improved short-term survival rates, which justifies its continued use.

Adrenaline and isoprenaline are considered as second-line medications for the treatment of bradycardia. If atropine fails to improve the condition, transcutaneous pacing is recommended. However, if pacing is not available, the administration of second-line drugs becomes necessary. Adrenaline is typically given intravenously at a dosage of 2-10 mcg/minute, while isoprenaline is given at a dosage of 5 mcg/minute. It is important to note that glucagon is not mentioned as a treatment option for this patient’s bradycardia, as the cause of the condition is not specified as a beta-blocker overdose.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

Aortic stenosis is a common condition where the valve in the heart becomes narrowed due to the progressive calcification that occurs with age. This typically occurs around the age of 70. Other causes of aortic stenosis include calcification of a congenital bicuspid aortic valve and rheumatic fever.

The symptoms of aortic stenosis can vary but commonly include difficulty breathing during physical activity, fainting, dizziness, chest pain (angina), and in severe cases, sudden death. However, it is also possible for aortic stenosis to be asymptomatic, meaning that there are no noticeable symptoms.

When examining a patient with aortic stenosis, there are several signs that may be present. These include a slow-rising and low-volume pulse, a narrow pulse pressure, a sustained apex beat, a thrill (a vibrating sensation) in the area of the aorta, and an ejection click if the valve is pliable. Additionally, there is typically an ejection systolic murmur, which is a specific type of heart murmur, that can be heard loudest in the aortic area (located at the right sternal edge, 2nd intercostal space) and may radiate to the carotid arteries.

It is important to differentiate aortic stenosis from aortic sclerosis, which is a degeneration of the aortic valve but does not cause obstruction of the left ventricular outflow tract. Aortic sclerosis can be distinguished by the presence of a normal pulse character and the absence of radiation of the murmur.

Amiodarone is a medication that is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while chest compressions are being performed. The prescribed dose is 300 mg, given as an intravenous bolus that is diluted in 5% dextrose to a volume of 20 mL. It is important to note that amiodarone is not suitable for treating PEA or asystole.

In cases where VF/pVT persists after five defibrillation attempts, an additional dose of 150 mg of amiodarone should be given. However, if amiodarone is not available, lidocaine can be used as an alternative. The recommended dose of lidocaine is 1 mg/kg. It is crucial to avoid administering lidocaine if amiodarone has already been given.

Amiodarone is classified as a membrane-stabilizing antiarrhythmic drug. It works by prolonging the duration of the action potential and the refractory period in both the atrial and ventricular myocardium. This medication also slows down atrioventricular conduction and has a similar effect on accessory pathways.

Additionally, amiodarone has a mild negative inotropic action, meaning it weakens the force of heart contractions. It also causes peripheral vasodilation through non-competitive alpha-blocking effects.

It is important to note that while there is no evidence of long-term benefits from using amiodarone, it may improve short-term survival rates, which justifies its continued use.

Anaphylaxis, also known as anaphylactic shock, is characterized by certain symptoms similar to other types of shock. These symptoms include low blood pressure (hypotension), rapid heart rate (tachycardia), irregular heart rhythm (arrhythmia), changes in the electrocardiogram (ECG) indicating reduced blood flow to the heart (myocardial ischemia), such as ST elevation, and in severe cases, cardiac arrest.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

The classic ECG features of atrial fibrillation include an irregularly irregular rhythm, the absence of p-waves, an irregular ventricular rate, and the presence of fibrillation waves. This irregular rhythm occurs because the atrial impulses are filtered out by the AV node.

In addition, Ashman beats may be observed in atrial fibrillation. These beats are characterized by wide complex QRS complexes, often with a morphology resembling right bundle branch block. They occur after a short R-R interval that is preceded by a prolonged R-R interval. Fortunately, Ashman beats are generally considered harmless.

The disorganized electrical activity in atrial fibrillation typically originates at the root of the pulmonary veins.

In stable patients with SVT, it is recommended to first try vagal manoeuvres before resorting to drug treatment. This approach is particularly applicable to patients who do not exhibit any adverse features, as mentioned in the case above.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

Adrenaline is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) once chest compressions have been resumed. The recommended dose is 1 mg, which can be administered as either 10 mL of 1:10,000 or 1 mL of 1:1000 concentration. Subsequently, adrenaline should be given every 3-5 minutes, alternating with chest compressions, and it should be administered without interrupting the compressions. While there is no evidence of long-term benefit from the use of adrenaline in cardiac arrest, some studies have shown improved short-term survival, which justifies its continued use.

Aortic stenosis can be identified through various clinical signs. These signs include a slow rising and low-volume pulse, as well as a narrow pulse pressure. The ejection systolic murmur, which is loudest in the aortic area (2nd intercostal space, close to the sternum), is another indicator. Additionally, a sustained apex beat and a thrill in the aortic area can be felt when the patient is sitting forward at the end of expiration. In some cases, a 4th heart sound may also be present. It is important to note that in severe cases of aortic stenosis, there may be reverse splitting of the second heart sound. However, fixed splitting of the 2nd heart sound is typically associated with ASD and VSD. Lastly, the presence of an ejection click can help exclude supra- or subaortic stenosis, especially if the valve is pliable.

Wolff-Parkinson-White (WPW) syndrome is a condition that affects the electrical system of the heart. It occurs when there is an abnormal pathway, known as the bundle of Kent, between the atria and the ventricles. This pathway can cause premature contractions of the ventricles, leading to a type of rapid heartbeat called atrioventricular re-entrant tachycardia (AVRT).

In a normal heart rhythm, the electrical signals travel through the bundle of Kent and stimulate the ventricles. However, in WPW syndrome, these signals can cause the ventricles to contract prematurely. This can be seen on an electrocardiogram (ECG) as a shortened PR interval, a slurring of the initial rise in the QRS complex (known as a delta wave), and a widening of the QRS complex.

There are two distinct types of WPW syndrome that can be identified on an ECG. Type A is characterized by predominantly positive delta waves and QRS complexes in the praecordial leads, with a dominant R wave in V1. This can sometimes be mistaken for right bundle branch block (RBBB). Type B, on the other hand, shows predominantly negative delta waves and QRS complexes in leads V1 and V2, and positive in the other praecordial leads, resembling left bundle branch block (LBBB).

Overall, WPW syndrome is a condition that affects the electrical conduction system of the heart, leading to abnormal heart rhythms. It can be identified on an ECG by specific features such as shortened PR interval, delta waves, and widened QRS complex.

Hypothermia can cause various changes in an electrocardiogram (ECG). These changes include a slower heart rate (bradycardia), the presence of Osborn waves (also known as J waves), a prolonged PR interval, a widened QRS complex, and a prolonged QT interval. Additionally, shivering artifact, ventricular ectopics (abnormal heartbeats originating from the ventricles), and even cardiac arrest (ventricular tachycardia, ventricular fibrillation, or asystole) may occur.

Further Reading:

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.

Pericarditis refers to the inflammation of the pericardium, which can be caused by various factors such as infections (typically viral, like coxsackie virus), drug-induced reactions (e.g. isoniazid, cyclosporine), trauma, autoimmune conditions (e.g. SLE), paraneoplastic syndromes, uremia, post myocardial infarction (known as Dressler’s syndrome), post radiotherapy, and post cardiac surgery.

The clinical presentation of pericarditis often includes retrosternal chest pain that worsens with lying flat and improves when sitting forwards, along with shortness of breath, rapid heartbeat, and the presence of a pericardial friction rub.

Characteristic electrocardiogram (ECG) changes associated with pericarditis typically show widespread concave or ‘saddle-shaped’ ST elevation, widespread PR depression, reciprocal ST depression and PR elevation in aVR (and sometimes V1), and sinus tachycardia is commonly observed.

A collapsing pulse, also known as a water hammer pulse, is a common clinical feature associated with aortic regurgitation (AR). In AR, the pulse rises rapidly and forcefully before quickly collapsing. This pulsation pattern may also be referred to as Watson’s water hammer pulse or Corrigan’s pulse. Heart sounds in AR are typically quiet, and the second heart sound (S2) may even be absent if the valve fails to fully close. A characteristic early to mid diastolic murmur is often present. Other typical features of AR include a wide pulse pressure, a mid-diastolic Austin-Flint murmur in severe cases, a soft S1 and S2 (with S2 potentially being absent), a hyperdynamic apical pulse, and signs of heart failure such as lung creases, raised jugular venous pressure (JVP), and tachypnea.

Further Reading:

Valvular heart disease refers to conditions that affect the valves of the heart. In the case of aortic valve disease, there are two main conditions: aortic regurgitation and aortic stenosis.

Aortic regurgitation is characterized by an early diastolic murmur, a collapsing pulse (also known as a water hammer pulse), and a wide pulse pressure. In severe cases, there may be a mid-diastolic Austin-Flint murmur due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams. The first and second heart sounds (S1 and S2) may be soft, and S2 may even be absent. Additionally, there may be a hyperdynamic apical pulse. Causes of aortic regurgitation include rheumatic fever, infective endocarditis, connective tissue diseases like rheumatoid arthritis and systemic lupus erythematosus, and a bicuspid aortic valve. Aortic root diseases such as aortic dissection, spondyloarthropathies like ankylosing spondylitis, hypertension, syphilis, and genetic conditions like Marfan’s syndrome and Ehler-Danlos syndrome can also lead to aortic regurgitation.

Aortic stenosis, on the other hand, is characterized by a narrow pulse pressure, a slow rising pulse, and a delayed ESM (ejection systolic murmur). The second heart sound (S2) may be soft or absent, and there may be an S4 (atrial gallop) that occurs just before S1. A thrill may also be felt. The duration of the murmur is an important factor in determining the severity of aortic stenosis. Causes of aortic stenosis include degenerative calcification (most common in older patients), a bicuspid aortic valve (most common in younger patients), William’s syndrome (supravalvular aortic stenosis), post-rheumatic disease, and subvalvular conditions like hypertrophic obstructive cardiomyopathy (HOCM).

Management of aortic valve disease depends on the severity of symptoms. Asymptomatic patients are generally observed, while symptomatic patients may require valve replacement. Surgery may also be considered for asymptomatic patients with a valvular gradient greater than 40 mmHg and features such as left ventricular systolic dysfunction. Balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement.

Atropine is a medication that slows down the movement of the digestive system and is not recommended for use in individuals with intestinal blockage. It works by blocking the effects of a neurotransmitter called acetylcholine, which is responsible for promoting gastrointestinal motility and the emptying of the stomach. Therefore, atropine should not be given to patients with gastrointestinal obstruction as it can further hinder the movement of the intestines.

Further Reading:

Types of Heart Block:

1. Atrioventricular (AV) Blocks:
– Disrupt electrical conduction between the atria and ventricles at the AV node.
– Three degrees of AV block: first degree, second degree (type 1 and type 2), and third degree (complete) AV block.

– First degree AV block: PR interval > 0.2 seconds.
– Second degree AV block:
– Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs.
– Type 2 (Mobitz II): PR interval is constant, but the P wave is often not followed by a QRS complex.
– Third degree (complete) AV block: no association between the P waves and QRS complexes.

Features of complete heart block: syncope, heart failure, regular bradycardia (30-50 bpm), wide pulse pressure, JVP (jugular venous pressure) cannon waves in neck, variable intensity of S1.

2. Bundle Branch Blocks:
– Electrical conduction travels from the bundle of His to the left and right bundle branches.
– Diagnosed when the duration of the QRS complex on the ECG exceeds 120 ms.

– Right bundle branch block (RBBB).
– Left bundle branch block (LBBB).
– Left anterior fascicular block (LAFB).
– Left posterior fascicular block (LPFB).
– Bifascicular block.
– Trifascicular block.

ECG features of bundle branch blocks:
– RBBB: QRS duration > 120 ms, RSR’ pattern in V1-3 (M-shaped QRS complex), wide S wave in lateral leads (I, aVL, V5-6).
– LBBB: QRS duration > 120 ms, dominant S wave in V1, broad, notched (‘M’-shaped) R wave in V6, broad monophasic R wave in lateral leads (I, aVL, V5-6), absence of Q waves in lateral leads, prolonged R wave peak time > 60 ms in leads V5-6.

WiLLiaM MaRROW is a useful mnemonic for remembering the morphology of the QRS in leads V1 and V6 for LBBB.

The second heart sound (S2) is created by vibrations produced when the aortic and pulmonary valves close. It marks the end of systole. It is normal to hear a split in the sound during inspiration.

A loud S2 can be associated with certain conditions such as systemic hypertension (resulting in a loud A2), pulmonary hypertension (resulting in a loud P2), hyperdynamic states (like tachycardia, fever, or thyrotoxicosis), and atrial septal defect (which causes a loud P2).

On the other hand, a soft S2 can be linked to decreased aortic diastolic pressure (as seen in aortic regurgitation), poorly mobile cusps (such as calcification of the aortic valve), aortic root dilatation, and pulmonary stenosis (which causes a soft P2).

A widely split S2 can occur during deep inspiration, right bundle branch block, prolonged right ventricular systole (seen in conditions like pulmonary stenosis or pulmonary embolism), and severe mitral regurgitation. However, in the case of atrial septal defect, the splitting is fixed and does not vary with respiration.

Reversed splitting of S2, where P2 occurs before A2 (paradoxical splitting), can occur during deep expiration, left bundle branch block, prolonged left ventricular systole (as seen in hypertrophic cardiomyopathy), severe aortic stenosis, and right ventricular pacing.

Stable angina is characterized by chest pain in the center of the chest that is triggered by activities such as exercise and emotional stress. The pain may spread to the jaw or left arm and can be relieved by resting for a few minutes. Typically, the pain is brought on by a predictable amount of exertion.

On the other hand, unstable angina is defined by the presence of one or more of the following: angina of effort occurring over a few days with increasing frequency, episodes of angina occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. In unstable angina, the ECG may appear normal or show T wave / ST segment changes, and cardiac enzymes are usually normal.

Prinzmetal angina is a rare form of angina that typically occurs at rest between midnight and early morning. These attacks can be severe and happen in clusters. It is caused by spasms in the coronary arteries, and patients with this condition often have normal coronary arteries.

It is important to note that gastro-esophageal reflux (GORD) is not relevant to this question and is included in the patient’s history to distract the candidate. Typical symptoms of GORD include heartburn and acid regurgitation, and it can also present with non-cardiac chest pain, dyspepsia, and difficulty swallowing.

Lastly, Ludwig’s angina is a serious and potentially life-threatening infection in the submandibular area. It most commonly occurs due to an infection in the floor of the mouth that spreads into the submandibular space.

In cases of myocarditis, levels of cardiac muscle enzymes (CK-MB, Troponin I, and Troponin T) and B-type natriuretic peptide (BNP) are usually elevated. It is important to note that CK-MB is a subtype of CK, so an increase in CK-MB will also result in an increase in total CK levels. This poses a challenge in differentiating myocarditis from coronary artery disease in the emergency department. Typically, a definitive diagnosis is not made until the patient undergoes additional tests such as angiography and possibly endomyocardial biopsy (EMB).

Further Reading:

Myocarditis is inflammation of the myocardium, the middle layer of the heart wall, that is not caused by a blockage in the coronary arteries. It can be caused by various factors, including infections (such as viruses, bacteria, parasites, and fungi), immune reactions, toxins, physical injury, and certain medications or vaccines. Coxsackie virus is the most common cause of myocarditis in Europe and the USA, while globally, Trypanosoma cruzi, which causes Chagas disease, is the most common cause.

The symptoms of myocarditis can vary widely and often resemble those of heart failure or coronary heart disease. Common symptoms include chest pain, palpitations, breathlessness, fatigue, and swelling. The clinical presentation can also be influenced by the underlying cause of the inflammation. Diagnosis of myocarditis is challenging as there is no specific clinical presentation, and the gold standard test, endomyocardial biopsy, is not readily available in emergency departments.

Various tests can be performed to aid in the diagnosis of myocarditis, including electrocardiogram (ECG), chest X-ray, cardiac enzymes (such as troponin or CK-MB), brain natriuretic peptide (BNP) levels, and echocardiogram. These tests may show non-specific abnormalities, such as ST-segment and T-wave abnormalities on ECG, bilateral pulmonary infiltrates on chest X-ray, elevated cardiac enzymes and BNP levels, and left ventricular motion abnormalities on echocardiogram.

Management of myocarditis is primarily supportive, focusing on treating cardiac failure and addressing the underlying cause. Supportive care and conventional heart failure therapy, such as ACE inhibitors or angiotensin II receptor blockers, vasodilators, beta-blockers, and diuretics, may be used to improve cardiac function and reduce symptoms. Treatment of the underlying cause, such as antiparasitic agents for Chagas disease or antibiotics for bacterial infections, may also be necessary. In severe cases leading to cardiogenic shock, more aggressive treatment with invasive monitoring, inotropes, vasopressors, and potentially heart transplantation may be required.

In summary, myocarditis is inflammation of the myocardium that can be caused by various factors. It presents with a wide range of symptoms and can be challenging to diagnose. Management involves supportive care, treatment of cardiac failure, and addressing the underlying cause. Severe cases may require more aggressive treatment and potentially heart transplantation.

When treating adults with bradycardia, a maximum of 6 doses of atropine 500 mcg can be administered. Each dose is given intravenously every 3-5 minutes. The total dose should not exceed 3mg.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

Lown-Ganong-Levine (LGL) syndrome is a condition that affects the electrical conducting system of the heart. It is classified as a pre-excitation syndrome, similar to the more well-known Wolff-Parkinson-White (WPW) syndrome. However, unlike WPW syndrome, LGL syndrome does not involve an accessory pathway for conduction. Instead, it is believed that there may be accessory fibers present that bypass all or part of the atrioventricular node.

When looking at an electrocardiogram (ECG) of a patient with LGL syndrome in sinus rhythm, there are several characteristic features to observe. The PR interval, which represents the time it takes for the electrical signal to travel from the atria to the ventricles, is typically shortened and measures less than 120 milliseconds. The QRS duration, which represents the time it takes for the ventricles to contract, is normal. The P wave, which represents the electrical activity of the atria, may be normal or inverted. However, what distinguishes LGL syndrome from other pre-excitation syndromes is the absence of a delta wave, which is a slurring of the initial rise in the QRS complex.

It is important to note that LGL syndrome predisposes individuals to paroxysmal supraventricular tachycardia (SVT), a rapid heart rhythm that originates above the ventricles. However, it does not increase the risk of developing atrial fibrillation or flutter, which are other types of abnormal heart rhythms.

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

Tricuspid regurgitation leads to a pansystolic murmur that is most pronounced in the tricuspid area during inhalation. The primary cause of tricuspid regurgitation is right ventricular failure.

Other clinical signs that may be present in tricuspid regurgitation include a raised jugular venous pressure (JVP) and giant C-V waves. Additionally, features of increased right atrial pressure, such as ascites and dependent edema, may be observed. Pulsatile hepatomegaly and a thrill at the left sternal edge are also possible indicators. Reverse splitting of the second heart sound, due to early closure of the pulmonary valve, and a third heart sound, caused by rapid right ventricular filling, may be heard as well.

Aortic regurgitation, on the other hand, produces an early diastolic murmur that is most audible at the lower left sternal edge when the patient is sitting forward and exhaling.

In the case of mitral stenosis, a rumbling mid-diastolic murmur is best heard at the apex while the patient is in the left lateral position and exhaling, using the bell of the stethoscope.

Atrial myxomas are benign tumors that can develop in the heart. Most commonly found on the left side, they may obstruct the mitral valve, resulting in a mid-diastolic murmur similar to that of mitral stenosis.

Lastly, left anterior descending artery stenosis can cause an early diastolic murmur, also known as Dock’s murmur. This murmur is similar to that of aortic regurgitation and is best heard at the left 2nd or 3rd intercostal space.

Amiodarone is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while performing chest compressions. The prescribed dose is 300 mg, which should be given as an intravenous bolus. To ensure proper administration, the medication should be diluted in 20 mL of 5% dextrose solution.

In cases where VF/pVT continues after five defibrillation attempts, an additional dose of 150 mg of Amiodarone should be administered. It is important to note that Amiodarone is not suitable for treating PEA or asystole, and its use is specifically indicated for shockable cardiac arrest situations.

The ratio of chest compressions to ventilations is 15:2. This ratio has not been proven through experiments, but it has been validated through mathematical studies. When performing chest compressions on a child, it is recommended to make them at least 1/3 of the depth of the child’s chest. Additionally, the optimal compression rate is between 100 and 120 compressions per minute.
To protect the airway of an unconscious child, the oropharyngeal (Guedel) airway is the best option. However, it should not be used on awake patients as there is a risk of vomiting and aspiration.
In children, asystole is the most common arrest rhythm. This occurs when the young heart responds to prolonged hypoxia and acidosis by progressively slowing down, eventually resulting in asystole.

Brugada syndrome is a genetic disorder that is passed down from one generation to another in an autosomal dominant manner. It is characterized by abnormal findings on an electrocardiogram (ECG) and can lead to sudden cardiac death. The cause of death in individuals with Brugada syndrome is typically ventricular fibrillation, which occurs as a result of specific defects in ion channels that are determined by our genes. Interestingly, this syndrome is more commonly observed in South East Asia and is actually the leading cause of sudden unexplained cardiac death in Thailand.

One of the key features seen on an ECG that is consistent with Type 1 Brugada syndrome is a pattern known as right bundle branch block. Additionally, there is a distinct downward sloping coved ST elevation observed in leads V1-V3. These specific ECG findings help to identify individuals who may be at risk for developing Brugada syndrome and experiencing its potentially fatal consequences.

One way to assess for digoxin toxicity is by examining the patient’s electrocardiogram (ECG) for specific characteristics. In the case of digoxin toxicity, ECG findings may include downsloping ST depression, prolonged QT interval, tall tented T-waves, and possibly delta waves. However, a short PR interval (< 120ms) is not typically associated with digoxin toxicity. Further Reading: Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia. ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem. Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

Aortic dissection is a condition that occurs when the middle layer of the aorta, known as the tunica media, becomes weakened. This weakening leads to the development of cases of aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

Atropine acts as an antagonist to the parasympathetic neurotransmitter acetylcholine at muscarinic receptors. This means that it blocks the effects of the vagus nerve on both the SA node and the AV node, resulting in increased sinus automaticity and improved AV node conduction.

The side effects of atropine are dependent on the dosage and may include dry mouth, nausea and vomiting, blurred vision, urinary retention, and tachyarrhythmias. Elderly patients may also experience acute confusion and hallucinations.

Atropine is recommended for use in cases of sinus, atrial, or nodal bradycardia or AV block when the patient’s hemodynamic condition is unstable due to the bradycardia. According to the ALS bradycardia algorithm, an initial dose of 500 mcg IV is suggested if any adverse features such as shock, syncope, myocardial ischemia, or heart failure are present. If this initial dose is unsuccessful, additional 500 mcg doses can be administered at 3-5 minute intervals, with a maximum dose of 3 mg. It is important to avoid doses exceeding 3 mg as they can paradoxically slow the heart rate.

Asystole during cardiac arrest is typically caused by primary myocardial pathology rather than excessive vagal tone. Therefore, there is no evidence supporting the routine use of atropine in the treatment of asystole or PEA. Consequently, atropine is no longer included in the non-shockable part of the ALS algorithm.

Aside from its use in cardiac conditions, atropine also has other applications. It can be used topically in the eyes as a cycloplegic and mydriatic, to reduce secretions during anesthesia, and in the treatment of organophosphate poisoning.

The classic ECG features of atrial fibrillation include an irregularly irregular rhythm, the absence of p-waves, an irregular ventricular rate, and the presence of fibrillation waves. This irregular rhythm occurs because the atrial impulses are filtered out by the AV node.

In addition, Ashman beats may be observed in atrial fibrillation. These beats are characterized by wide complex QRS complexes, often with a morphology resembling right bundle branch block. They occur after a short R-R interval that is preceded by a prolonged R-R interval. Fortunately, Ashman beats are generally considered harmless.

The disorganized electrical activity in atrial fibrillation typically originates at the root of the pulmonary veins.

The majority of dissections happen in individuals between the ages of 40 and 70, with the highest occurrence observed in the age group of 50 to 65.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

Dressler’s syndrome is a form of pericarditis that occurs within 2 to 10 weeks following a heart attack or cardiac surgery. It is distinguished by intense chest pain that is usually alleviated by assuming an upright position. Additionally, individuals may experience a mild fever, a pericardial rub, pulsus paradoxus, and indications of right ventricular failure.

A significant proportion of the population experiences a difference of 10 mmHg or more in blood pressure between their upper limbs. Pericarditis can be identified by the presence of saddle-shaped ST elevation and pain in the trapezius ridge. Aortic dissection is characterized by a diastolic murmur with a decrescendo pattern, which indicates aortic incompetence.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

Wolff-Parkinson-White (WPW) syndrome is a condition that affects the electrical system of the heart. It occurs when there is an abnormal pathway, known as the bundle of Kent, between the atria and the ventricles. This pathway can cause premature contractions of the ventricles, leading to a type of rapid heartbeat called atrioventricular re-entrant tachycardia (AVRT).

In a normal heart rhythm, the electrical signals travel through the bundle of Kent and stimulate the ventricles. However, in WPW syndrome, these signals can cause the ventricles to contract prematurely. This can be seen on an electrocardiogram (ECG) as a shortened PR interval, a slurring of the initial rise in the QRS complex (known as a delta wave), and a widening of the QRS complex.

There are two distinct types of WPW syndrome that can be identified on an ECG. Type A is characterized by predominantly positive delta waves and QRS complexes in the praecordial leads, with a dominant R wave in V1. This can sometimes be mistaken for right bundle branch block (RBBB). Type B, on the other hand, shows predominantly negative delta waves and QRS complexes in leads V1 and V2, and positive in the other praecordial leads, resembling left bundle branch block (LBBB).

Overall, WPW syndrome is a condition that affects the electrical conduction system of the heart, leading to abnormal heart rhythms. It can be identified on an ECG by specific features such as shortened PR interval, delta waves, and widened QRS complex.

The timing of the initial rise, peak, and return to normality of various cardiac enzymes can serve as a helpful guide. Creatine kinase, the main cardiac isoenzyme, typically experiences an initial rise within 4-8 hours, reaches its peak at 18 hours, and returns to normal within 2-3 days. Myoglobin, which lacks specificity due to its association with skeletal muscle damage, shows an initial rise within 1-4 hours, peaks at 6-7 hours, and returns to normal within 24 hours. Troponin I, known for its sensitivity and specificity, exhibits an initial rise within 3-12 hours, reaches its peak at 24 hours, and returns to normal within 3-10 days. HFABP, or heart fatty acid binding protein, experiences an initial rise within 1.5 hours, peaks at 5-10 hours, and returns to normal within 24 hours. Lastly, LDH, predominantly found in cardiac muscle, shows an initial rise at 10 hours, peaks at 24-48 hours, and returns to normal within 14 days.

The leads V3 and V4 represent the anterior myocardial area.

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Torsades de pointes is a condition that is linked to low levels of potassium (hypokalaemia) and magnesium (hypomagnesaemia). When potassium and magnesium levels are low, it can cause the QT interval to become prolonged, which increases the risk of developing Torsades de pointes.

Further Reading:

Torsades de pointes is an irregular broad-complex tachycardia that can be life-threatening. It is a polymorphic ventricular tachycardia that can lead to sudden cardiac death. It is characterized by distinct features on the electrocardiogram (ECG).

The causes of irregular broad-complex tachycardia include atrial fibrillation with bundle branch block, atrial fibrillation with ventricular pre-excitation (in patients with Wolff-Parkinson-White syndrome), and polymorphic ventricular tachycardia such as torsades de pointes. However, sustained polymorphic ventricular tachycardia is unlikely to be present without adverse features, so it is important to seek expert help for the assessment and treatment of this condition.

Torsades de pointes can be caused by drug-induced QT prolongation, diarrhea, hypomagnesemia, hypokalemia, and congenital long QT syndrome. It may also be seen in malnourished individuals due to low potassium and/or low magnesium levels. Additionally, it can occur in individuals taking drugs that prolong the QT interval or inhibit their metabolism.

The management of torsades de pointes involves immediate action. All drugs known to prolong the QT interval should be stopped. Amiodarone should not be given for definite torsades de pointes. Electrolyte abnormalities, especially hypokalemia, should be corrected. Magnesium sulfate should be administered intravenously. If adverse features are present, immediate synchronized cardioversion should be arranged. sought, as other treatments such as overdrive pacing may be necessary to prevent relapse once the arrhythmia has been corrected. If the patient becomes pulseless, defibrillation should be attempted immediately.

In summary, torsades de pointes is a dangerous arrhythmia that requires prompt management. It is important to identify and address the underlying causes, correct electrolyte abnormalities, and seek expert help for appropriate treatment.