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.

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.

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.

Mitral stenosis is a condition characterized by a narrowing of the mitral valve in the heart. One of the key features of this condition is a loud first heart sound, which is often described as having an opening snap. This sound is typically heard during mid-late diastole and is best heard during expiration. Other signs of mitral stenosis include a low volume pulse, a flushed appearance of the cheeks (known as malar flush), and the presence of atrial fibrillation. Additionally, patients with mitral stenosis may exhibit signs of pulmonary edema, such as crepitations (crackling sounds) in the lungs and the production of white or pink frothy sputum. It is important to note that a water hammer pulse is associated with a different condition called aortic regurgitation.

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.

Severe aortic stenosis is characterized by several distinct features. These include a narrow pulse pressure, which refers to the difference between the systolic and diastolic blood pressure readings. Additionally, individuals with severe aortic stenosis may exhibit a slow rising pulse, meaning that the pulse wave takes longer to reach its peak. Another common feature is a delayed ejection systolic murmur, which is a heart sound that occurs during the ejection phase of the cardiac cycle. The second heart sound (S2) may also be soft or absent in individuals with severe aortic stenosis. Another potential finding is the presence of an S4 heart sound, which occurs during the filling phase of the cardiac cycle. A thrill, which is a palpable vibration, may also be felt in severe cases. The duration of the murmur, as well as the presence of left ventricular hypertrophy or failure, are additional features that may be observed in individuals with severe aortic stenosis.

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.

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.

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.

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.

Hypertrophic obstructive cardiomyopathy (HOCM) is a primary heart disease characterized by the enlargement of the myocardium in the left and right ventricles. It is the most common reason for sudden cardiac death in young individuals and athletes. HOCM can be inherited in an autosomal dominant manner, and a family history of unexplained sudden death is often present.

Symptoms that may be experienced in HOCM include palpitations, breathlessness, chest pain, and syncope. Clinical signs that can be observed in HOCM include a jerky pulse character, a double apical impulse (where both atrial and ventricular contractions can be felt), a thrill at the left sternal edge, and an ejection systolic murmur at the left sternal edge that radiates throughout the praecordium. Additionally, a 4th heart sound may be present due to blood hitting a stiff and enlarged left ventricle during atrial systole.

On the other hand, Brugada syndrome is another cause of sudden cardiac death, but patients with this condition are typically asymptomatic and have a normal clinical examination.

Supraventricular tachycardia (SVT) is the most common arrhythmia that occurs in children and infants, causing cardiovascular instability. According to the current APLS guidelines, if a patient with SVT shows no signs of shock and remains stable, initial attempts should be made to use vagal maneuvers. If these maneuvers are unsuccessful, the following steps are recommended:

– Administer an initial dose of 100 mcg/kg of adenosine.
– After two minutes, if the child is still in stable SVT, administer another dose of 200 mcg/kg of adenosine.
– After an additional two minutes, if the child remains in stable SVT, administer another dose of 300 mcg/kg of adenosine.

If these measures do not resolve the SVT, the guidelines suggest considering the following options:

– Administer adenosine at a dose of 400-500 mcg/kg.
– Perform a synchronous DC shock.
– Administer amiodarone.

When using amiodarone, the initial dose should be 5-10 mg/kg given over a period of 20 minutes to 2 hours. This should be followed by a continuous infusion of 300 mcg/kg/hour, with adjustments made based on the response, increasing by 1.5 mg/kg/hour. The total infusion rate should not exceed 1.2 g in a 24-hour period.

If defibrillation is necessary for the treatment of SVT in children, it should be performed as a DC synchronous shock at a dosage of 1-2 J/kg.

Q waves in V2 and V3 are typically abnormal and indicate a pathological condition. Q waves are negative deflections that occur before an R wave. They can be either normal or abnormal. Small normal Q waves, which are less than 1mm deep, may be present in most leads. Deeper normal Q waves are commonly seen in lead III, as long as they are not present in the adjacent leads II and AVF. On the other hand, pathological Q waves are usually deeper and wider. In particular, Q waves should not be observed in V2 and V3. The specific criteria for identifying pathological Q waves are as follows: any Q wave in leads V2-V3 that is greater than 0.02s in duration or a QS complex in leads V2-V3; a Q wave that is greater than 0.03s in duration and deeper than 1mm, or a QS complex, in leads I, II, aVL, aVF, or V4-V6 in any two leads of a contiguous lead grouping; an R wave that is greater than 0.04s in duration in V1-V2 and has an R/S ratio greater than 1, along with a concordant positive T wave, in the absence of a conduction defect. In healthy individuals, the T-wave is normally inverted in aVR and inverted or flat in V1. T-wave inversion in III is also considered a normal variation. If there is ST elevation in lead V1, it would suggest a ST-elevation myocardial infarction (STEMI) rather than a non-ST-elevation myocardial infarction (NSTEMI).

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.

This ECG indicates changes that are consistent with an acute inferoposterior myocardial infarction (MI). There is ST elevation in leads I, II, aVF, and V6, along with reciprocal ST depression in leads V1-V4 and aVR. Additionally, there are tall dominant R waves in leads V2-V3 and upright T waves in leads V2-V3. Based on these findings, the most likely vessel involved in this case is the right coronary artery.

To summarize the vessels involved in different types of myocardial infarction see below:
ECG Leads – Location of MI | Vessel involved
V1-V3 – Anteroseptal | Left anterior descending
V3-V4 – Anterior | Left anterior descending
V5-V6 – Anterolateral | Left anterior descending / left circumflex artery
V1-V6 – Extensive anterior | Left anterior descending
I, II, aVL, V6 – Lateral | Left circumflex artery
II, III, aVF – Inferior | Right coronary artery (80%), Left circumflex artery (20%)
V1, V4R – Right ventricle | Right coronary artery
V7-V9 – Posterior | Right coronary artery

Distinguishing between unstable angina and other acute coronary syndromes can be done by looking at normal troponin results. If serial troponin tests come back negative, it can rule out a diagnosis of myocardial infarction. Unstable angina is characterized by myocardial ischemia occurring at rest or with minimal exertion, without any acute damage or death of heart muscle cells. The patient in question shows ECG and biochemical features that align with this definition. Vincent’s angina, on the other hand, refers to an infection in the throat accompanied by ulcerative gingivitis.

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.

The septum, which is a part of the heart, can be best identified by examining leads V1 and V2. The septum receives its blood supply from the proximal left anterior descending artery (LAD). The LAD is responsible for supplying blood to the anterior myocardium and also contributes to the blood supply of the lateral myocardium. If the LAD becomes blocked, it can result in ST elevation in all the chest leads.

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.

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.

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, the ECG may show artifacts caused by shivering, as well as the presence of ventricular ectopics. In severe cases, hypothermia can lead to cardiac arrest, which may manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

Further Reading:

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, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

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.

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.

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.

Decubitus angina typically occurs in individuals who have congestive heart failure and significant coronary artery disease. When the patient assumes a lying position, the heightened volume of blood within the blood vessels puts stress on the heart, leading to episodes of chest pain.

Orthostatic hypotension is a condition where patients feel lightheaded and may experience tunnel vision when they stand up from a lying down position. These symptoms are often worse in the morning. The patient’s history of recurrent episodes after being in a supine position for a long time strongly suggests orthostatic hypotension. There are no signs of epilepsy, such as deja-vu or jambs vu prodrome, tongue biting, loss of bladder or bowel control, or postictal confusion. The normal ECG and consistent timing of symptoms make postural orthostatic tachycardia syndrome (PAF) less likely. There are no neurological deficits to suggest a transient ischemic attack (TIA). The prodromal symptoms, such as tunnel vision and lightheadedness, align more with orthostatic hypotension rather than vasovagal syncope, which typically occurs after long periods of standing and is characterized by feeling hot and sweaty. Although carotid sinus syndrome could be considered as a differential diagnosis, as the patient’s head turning on getting out of bed may trigger symptoms, it is not one of the options.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

The patient is currently taking 20 mg of Atorvastatin once daily. They do not have a history of heart disease, vascular disease, or stroke. Their blood pressure is 148/92 mmHg, pulse rate is 86 bpm, and respiration rate is 1.

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.

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

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.

The primary treatment option for hypertensive encephalopathy, a condition characterized by sudden confusion, severe headache, and coordination problems due to significantly elevated blood pressure, is labetalol.

Further Reading:

A hypertensive emergency is characterized by a significant increase in blood pressure accompanied by acute or progressive damage to organs. While there is no specific blood pressure value that defines a hypertensive emergency, systolic blood pressure is typically above 180 mmHg and/or diastolic blood pressure is above 120 mmHg. The most common presentations of hypertensive emergencies include cerebral infarction, pulmonary edema, encephalopathy, and congestive cardiac failure. Less common presentations include intracranial hemorrhage, aortic dissection, and pre-eclampsia/eclampsia.

The signs and symptoms of hypertensive emergencies can vary widely due to the potential dysfunction of every physiological system. Some common signs and symptoms include headache, nausea and/or vomiting, chest pain, arrhythmia, proteinuria, signs of acute kidney failure, epistaxis, dyspnea, dizziness, anxiety, confusion, paraesthesia or anesthesia, and blurred vision. Clinical assessment focuses on detecting acute or progressive damage to the cardiovascular, renal, and central nervous systems.

Investigations that are essential in evaluating hypertensive emergencies include U&Es (electrolyte levels), urinalysis, ECG, and CXR. Additional investigations may be considered depending on the suspected underlying cause, such as a CT head for encephalopathy or new onset confusion, CT thorax for suspected aortic dissection, and CT abdomen for suspected phaeochromocytoma. Plasma free metanephrines, urine total catecholamines, vanillylmandelic acid (VMA), and metanephrine may be tested if phaeochromocytoma is suspected. Urine screening for cocaine and/or amphetamines may be appropriate in certain cases, as well as an endocrine screen for Cushing’s syndrome.

The management of hypertensive emergencies involves cautious reduction of blood pressure to avoid precipitating renal, cerebral, or coronary ischemia. Staged blood pressure reduction is typically the goal, with an initial reduction in mean arterial pressure (MAP) by no more than 25% in the first hour. Further gradual reduction to a systolic blood pressure of 160 mmHg and diastolic blood pressure of 100 mmHg over the next 2 to 6 hours is recommended. Initial management involves treatment with intravenous antihypertensive agents in an intensive care setting with appropriate monitoring.

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.

Tietze’s syndrome is an uncommon condition that leads to localized pain and tenderness in one or more of the upper four ribs, with the second and third ribs being the most commonly affected. The exact cause of this syndrome is still unknown, although it has been suggested that it may be linked to repeated small injuries to the chest wall.

The pain experienced in Tietze’s syndrome is typically aggravated by movement, sneezing, and coughing, and it can also extend to the neck or shoulder on the affected side. In some cases, a firm swelling can be felt over the cartilage of the affected rib. While the pain usually diminishes after a few weeks or months, the swelling may persist.

Treatment for Tietze’s syndrome involves the use of pain-relieving medications, such as NSAIDs. In more severe or persistent cases, local steroid injections may be beneficial.

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.

This patient’s ECG shows signs consistent with hyperkalemia, including broad QRS complexes, tall-peaked T waves, and bizarre p waves. It is estimated that around 10% of patients with SLE have hyperkalemia, which is believed to be caused by hyporeninemic hypoaldosteronism. Additionally, the patient has been taking a high dose of ibuprofen, which can also contribute to the development of hyperkalemia. NSAIDs are thought to induce hyperkalemia by reducing renin secretion, leading to decreased potassium excretion.

Tenecteplase is a medication known as a tissue plasminogen activator (tPA). Its main mechanism of action involves binding specifically to fibrin and converting plasminogen into plasmin. This process leads to the breakdown of the fibrin matrix and promotes reperfusion at the affected site. Among the options provided, Tenecteplase is the sole drug that primarily acts by facilitating reperfusion.