A summary of the vessels involved in different types of myocardial infarction, along with the corresponding ECG leads and the location of the infarction.

For instance, an anteroseptal infarction involving the left anterior descending artery is indicated by ECG leads V1-V3. Similarly, an anterior infarction involving the left anterior descending artery is indicated by leads V3-V4.

In cases of anterolateral infarctions, both the left anterior descending artery and the left circumflex artery are involved, and this is reflected in ECG leads V5-V6. An extensive anterior infarction involving the left anterior descending artery is indicated by leads V1-V6.

Lateral infarcts involving the left circumflex artery are indicated by leads I, II, aVL, and V6. Inferior infarctions, on the other hand, involve either the right coronary artery (in 80% of cases) or the left circumflex artery (in 20% of cases), and this is shown by leads II, III, and aVF.

In the case of a right ventricular infarction, the right coronary artery is involved, and this is indicated by leads V1 and V4R. Lastly, a posterior infarction involving the right coronary artery is shown by leads V7-V9.

Prinzmetal angina is a rare form of angina that typically occurs during periods of rest, specifically between midnight and early morning. The attacks can be severe and happen in clusters. This condition is caused by spasms in the coronary arteries, even though patients may have normal arteries. The main treatment options for controlling these spasms are calcium-channel blockers and nitrates. The spasms often follow a cyclical pattern and may disappear after a few months, only to reappear later on.

Unstable angina may present similarly to Prinzmetal angina, but it does not exclusively occur at night and the exercise tolerance test results are typically abnormal.

Decubitus angina, on the other hand, is angina that occurs when lying down. It is often a result of cardiac failure caused by increased intravascular volume, which puts extra strain on the heart.

Takotsubo cardiomyopathy, also known as acute stress cardiomyopathy, can present in a manner similar to an acute myocardial infarction. The cause of this condition is unknown, but it tends to occur in individuals who have recently experienced significant emotional or physical stress. The term Takotsubo refers to the shape the left ventricle takes on, resembling an octopus pot with a narrow neck and round bottom. ECGs often show characteristic changes, such as ST-elevation, but subsequent angiograms reveal normal coronary arteries. The diagnosis is confirmed when the angiogram shows the distinctive octopus pot shape of the left ventricle.

There is no indication of a psychogenic cause in this particular case.

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.

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.

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.

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.

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.

Carvallo’s sign is a term used to describe the phenomenon where the systolic murmur of tricuspid regurgitation becomes louder when taking a deep breath in. Tricuspid regurgitation is characterized by a continuous murmur that starts in systole and continues throughout the entire cardiac cycle. This murmur is best heard at the lower left sternal edge and has a low frequency. In addition to Carvallo’s sign, other features of tricuspid regurgitation include the presence of an S3 heart sound, the possibility of atrial arrhythmias such as flutter or fibrillation, the presence of giant C-V waves in the jugular pulse, hepatomegaly (often with a pulsatile nature), and the development of edema, which may be accompanied by lung crepitations or pleural effusions.

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.

The clinical symptoms of mitral stenosis include shortness of breath, which tends to worsen during exercise and when lying flat. Tiredness, palpitations, ankle swelling, cough, and haemoptysis are also common symptoms. Chest discomfort is rarely reported.

The clinical signs of mitral stenosis can include a malar flush, an irregular pulse if atrial fibrillation is present, a tapping apex beat that can be felt as the first heart sound, and a left parasternal heave if there is pulmonary hypertension. The first heart sound is often loud, and a mid-diastolic murmur can be heard.

The mid-diastolic murmur of mitral stenosis is a rumbling sound that is best heard at the apex, in the left lateral position during expiration, using the bell of the stethoscope.

Mitral stenosis is typically caused by rheumatic heart disease, and it is more common in females, with about two-thirds of patients being female.

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.

Mitral regurgitation is characterized by a continuous murmur throughout systole that is often heard loudest at the apex and can be heard radiating to the left axilla.

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.

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.

This patient has developed a non-ST elevation myocardial infarction (NSTEMI). The electrocardiogram (ECG) reveals widespread ST depression, indicating widespread subendocardial ischemia. Additionally, the troponin test results are positive, indicating myocyte necrosis.

The acute coronary syndromes consist of unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

Unstable angina is characterized by one or more of the following: angina of effort occurring over a few days with increasing frequency, angina episodes occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. The ECG may show T-wave/ST-segment changes, similar to this case. Cardiac enzymes are typically normal, and the troponin test is negative in unstable angina.

Non-ST elevation myocardial infarction (NSTEMI) typically presents with sustained cardiac chest pain lasting more than 20 minutes. The ECG often shows abnormalities in T-waves or ST-segments. Cardiac enzymes are elevated, and the troponin test is positive.

ST-elevation myocardial infarction (STEMI) usually presents with typical cardiac chest pain suggestive of an acute myocardial infarction. The ECG reveals ST-segment elevation and the development of Q waves. Cardiac enzymes are elevated, and the troponin test is positive.

The clinical symptoms of mitral stenosis include shortness of breath, which tends to worsen during exercise and when lying flat. Tiredness, palpitations, ankle swelling, cough, and haemoptysis are also common symptoms. Chest discomfort is rarely reported.

The clinical signs of mitral stenosis can include a malar flush, an irregular pulse if atrial fibrillation is present, a tapping apex beat that can be felt as the first heart sound, and a left parasternal heave if there is pulmonary hypertension. The first heart sound is often loud, and a mid-diastolic murmur can be heard best at the apex in the left lateral position during expiration using the bell of the stethoscope.

Mitral stenosis is typically caused by rheumatic heart disease, with about two-thirds of patients being female. During pregnancy, the increase in plasma volume can lead to elevated left atrial and pulmonary venous pressures. This can exacerbate any symptoms related to mitral stenosis and potentially result in pulmonary edema, as seen in this case.

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.

Beta blockers are the primary treatment for long QT syndrome (LQTS). This patient probably has an undiagnosed congenital LQTS because there is no obvious cause. If there is a known cause of LQTS that can be removed, removing it may be the only necessary treatment. However, in all other cases, beta blockers are usually needed to prevent ventricular arrhythmias. Ventricular arrhythmias happen because of increased adrenergic activity. Beta blockers reduce the effects of adrenergic stimulation.

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.

The diagnosis in this particular case is malignant (accelerated) hypertension. The patient’s blood pressure is greater than 220/110, and they also have retinal haemorrhages and papilloedema. During the examination, it is important to look for other features such as the presence of a 3rd heart sound, ankle oedema, bilateral basal crepitations, and any focal neurological deficit.

Given the patient’s symptoms and physical findings, the most appropriate initial treatment would be to administer Furosemide 40 mg intravenously. Furosemide is a loop diuretic that helps remove excess fluid from the body, which can alleviate symptoms of fluid overload such as shortness of breath and edema. By reducing fluid volume, Furosemide can help improve the patient’s breathing and relieve the strain on the heart.

Further Reading:

Cardiac failure, also known as heart failure, is a clinical syndrome characterized by symptoms and signs resulting from abnormalities in the structure or function of the heart. This can lead to reduced cardiac output or high filling pressures at rest or with stress. Heart failure can be caused by various problems such as myocardial, valvular, pericardial, endocardial, or arrhythmic issues.

The most common causes of heart failure in the UK are coronary heart disease and hypertension. However, there are many other possible causes, including valvular heart disease, structural heart disease, cardiomyopathies, certain drugs or toxins, endocrine disorders, nutritional deficiencies, infiltrative diseases, infections, and arrhythmias. Conditions that increase peripheral demand on the heart, such as anemia, pregnancy, sepsis, hyperthyroidism, Paget’s disease of bone, arteriovenous malformations, and beriberi, can also lead to high-output cardiac failure.

Signs and symptoms of heart failure include edema, lung crepitations, tachycardia, tachypnea, hypotension, displaced apex beat, right ventricular heave, elevated jugular venous pressure, cyanosis, hepatomegaly, ascites, pleural effusions, breathlessness, fatigue, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough or wheeze, and Presyncope.

To diagnose heart failure, NICE recommends three key tests: N-terminal pro-B-type natriuretic peptide (NT‑proBNP), transthoracic echocardiography, and ECG. Additional tests may include chest X-ray, blood tests (U&Es, thyroid function, LFT’s, lipid profile, HbA1C, FBC), urinalysis, and peak flow or spirometry.

Management of cardiogenic pulmonary edema, a complication of heart failure, involves ensuring a patent airway, optimizing breathing with supplemental oxygen and non-invasive ventilation if necessary, and addressing circulation with loop diuretics to reduce preload, vasodilators to reduce preload and afterload, and inotropes if hypotension or signs of end organ hypoperfusion persist.

In summary, cardiac failure is a clinical syndrome resulting from abnormalities in cardiac function. It can have various causes and is characterized by specific signs and symptoms. Diagnosis involves specific tests, and management focuses on addressing

Having Mobitz II AV block increases the risk of developing asystole. Other risk factors for asystole include recent asystole, third degree AV block (complete heart block) with a broad QRS complex, and a ventricular pause lasting 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

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.

Narrow QRS complex tachycardia is a term used to describe a fast heart rhythm with a pulse rate over 100 bpm and a QRS duration shorter than 120 ms.

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.

The primary location for aortic dissection, which is being considered in this case, is the ascending aorta.

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.

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.

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.

Aortic regurgitation is a condition where the aortic valve fails to close tightly, resulting in the backflow of blood from the aorta into the left ventricle during ventricular diastole. This valvular lesion presents with various clinical symptoms and signs.

The clinical symptoms of aortic regurgitation include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. These symptoms are experienced by patients during physical activity, while lying flat, and during episodes of sudden nighttime breathlessness, respectively.

On the other hand, the clinical signs of aortic regurgitation can be observed during physical examination. These signs include a collapsing pulse, widened pulse pressure, hyperkinetic laterally displaced apex beat, and a thrill in the aortic area. Additionally, an early diastolic murmur can be heard, which is loudest at the lower left sternal edge when the patient is sitting forward and exhaling.

Aortic regurgitation is also associated with several eponymous signs, which are named after the physicians who first described them. These signs include Corrigan’s sign, which is characterized by visible and forceful neck pulsation. De Musset’s sign refers to head nodding in time with the heartbeat. Quincke’s sign is the observation of visible nail bed capillary pulsation. Duroziez’s sign is the presence of a diastolic murmur heard proximal to femoral artery compression. Traube’s sign is the perception of a pistol shot sound over the femoral arteries. The Lighthouse sign is the blanching and flushing of the forehead. Becker’s sign is the pulsation seen in retinal vessels. Rosenbach’s sign is the presence of a pulsatile liver. Lastly, Muller’s sign refers to pulsations of the uvula.

In summary, aortic regurgitation is a valvular lesion that leads to the incomplete closure of the aortic valve. It manifests with various clinical symptoms, signs, and eponymous findings, which can be identified through careful examination and observation.

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.

Unstable angina is characterized by the presence of one or more of the following symptoms: 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. The electrocardiogram (ECG) may appear normal or show T-wave/ST-segment changes, and cardiac enzymes are typically within normal range.

On the other hand, stable angina is defined by central chest pain that is triggered by activities such as exercise and emotional stress. This pain may radiate to the jaw or left arm and is relieved by resting for a few minutes. It is usually brought on by a predictable amount of exertion.

Prinzmetal angina, although rare, is a variant of angina that primarily occurs at rest between midnight and early morning. The attacks can be severe and tend to happen in clusters. This type of angina is caused by coronary artery spasm, and patients may have normal coronary arteries.

Decubitus angina, on the other hand, is angina that occurs when lying down. It often develops as a result of cardiac failure due to an increased volume of blood within the blood vessels, which places additional strain on the heart.

Lastly, Ludwig’s angina is an extremely serious and potentially life-threatening cellulitis that affects the submandibular area. It most commonly arises from an infection in the floor of the mouth, which then spreads to the submandibular space.

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.

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.