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.

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.

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.

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.

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

Distinguishing between unstable angina and other acute coronary syndromes can be determined by normal troponin results. Unstable angina is characterized by new onset angina or a sudden worsening of previously stable angina, often occurring at rest. This condition typically requires hospital admission. On the other hand, stable angina is predictable and occurs during physical exertion or emotional stress, lasting for a short duration of no more than 10 minutes and relieved within minutes of rest or sublingual nitrates.

To diagnose unstable angina, it is crucial to consider the nature of the chest pain and negative cardiac enzyme testing. The presence or absence of chest pain at rest and the response to rest and treatment with GTN are the most useful descriptors in distinguishing between stable and unstable angina. It is important to note that patients with unstable angina may not exhibit any changes on an electrocardiogram (ECG).

If troponin results are abnormal, it indicates a myocardial infarction rather than unstable angina.

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.

Marfan’s syndrome is a condition that greatly increases the risk of aortic dissection. This patient exhibits several characteristics commonly seen in individuals with Marfan syndrome, such as tall stature, low BMI, and pectoral abnormalities like pectus carinatum and excavatum. Additionally, their long limbs and fingers are also indicative of Marfan’s syndrome. It is important to note that aortic dissection tends to occur at a much younger age in individuals with Marfan syndrome compared to those without connective tissue diseases. The median age for type A dissection in Marfan’s patients is 36.7 years, while for type B dissection it is 40 years. In contrast, individuals without Marfan’s syndrome typically experience dissection at the ages of 63 and 62 years for type A and type B dissections, respectively.

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.

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

Further Reading:

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

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

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

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

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

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

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.

To manage aortic dissection, it is important to lower the systolic blood pressure to a range of 100-120 mmHg. This helps decrease the strain on the damaged artery and minimizes the chances of the dissection spreading further. In this patient, symptoms such as tearing chest pain and a widened mediastinum on the chest X-ray are consistent with 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.

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.

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

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

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

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

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

Atropine should not be given to patients with certain conditions, including heart transplant, angle-closure glaucoma, gastrointestinal motility disorders, myasthenia gravis, severe ulcerative colitis, toxic megacolon, bladder outflow obstruction, and urinary retention. In heart transplant patients, atropine will not have the desired effect as the denervated hearts do not respond to vagal blockade. Giving atropine in these patients may even lead to paradoxical sinus arrest or high-grade AV block.

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

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

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

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

Further Reading:

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

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

Severe aortic stenosis (AS) is characterized by several distinct features. These include a slow rising pulse, an ejection systolic murmur that is heard loudest in the aortic area and may radiate to the carotids, and a soft or absent S2 heart sound. Additionally, patients with severe AS often have a narrow pulse pressure and may exhibit an S4 heart sound.

AS is commonly caused by hypertension, although blood pressure findings can vary. In severe cases, patients may actually be hypotensive due to impaired cardiac output. Symptoms of severe AS typically include Presyncope or syncope, exertional chest pain, and shortness of breath. These symptoms can be remembered using the acronym SAD (Syncope, Angina, Dyspnoea).

It is important to note that aortic stenosis primarily affects older individuals, as it is a result of scarring and calcium buildup in the valve. Age-related AS typically begins after the age of 60, but symptoms may not appear until patients are in their 70s or 80s.

Diastolic murmurs, on the other hand, are associated with conditions such as aortic regurgitation, pulmonary regurgitation, and mitral 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.

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 a 1:10,000 solution or 1 mL of a 1:1000 solution.

Subsequently, adrenaline should be given every 3-5 minutes, alternating with chest compressions. It is important to administer adrenaline without interrupting chest compressions to ensure continuous circulation and maximize the chances of successful resuscitation.

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.

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.

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.

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

Further Reading:

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

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

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

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

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

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

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.

The mortality rate associated with pulmonary edema as a result of acute heart failure secondary to cardiogenic shock during hospitalization is 50%.

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.

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.

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

Further Reading:

Types of Heart Block:

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

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

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

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

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

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

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

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.

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.

Lidocaine is commonly used as both an anti-arrhythmic medication and a local anesthetic. However, it is important to note that it should not be used as an anti-arrhythmic therapy in patients with Local Anesthetic Systemic Toxicity (LAST). This is because lidocaine can potentially worsen the toxicity symptoms in these patients.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

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.

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

Further Reading:

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

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

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

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

Pericardial friction rub is a common finding in pericarditis and is often described as a sound similar to squeaking leather. This patient exhibits symptoms that are consistent with acute pericarditis, including flu-like illness with muscle pain and fatigue, chest pain that worsens when lying down and improves when sitting up or leaning forward, and the presence of a pleural rub. The gradual onset of symptoms rules out conditions like pulmonary embolism or acute myocardial ischemia. It is important to note that while the pericardial rub is often considered part of the classic triad of clinical features, it is only present in about one-third of patients. Additionally, the rub may come and go, so repeated examinations may increase the chances of detecting this sign.

Further Reading:

Pericarditis is an inflammation of the pericardium, which is the protective sac around the heart. It can be acute, lasting less than 6 weeks, and may present with chest pain, cough, dyspnea, flu-like symptoms, and a pericardial rub. The most common causes of pericarditis include viral infections, tuberculosis, bacterial infections, uremia, trauma, and autoimmune diseases. However, in many cases, the cause remains unknown. Diagnosis is based on clinical features, such as chest pain, pericardial friction rub, and electrocardiographic changes. Treatment involves symptom relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and patients should avoid strenuous activity until symptoms improve. Complicated cases may require treatment for the underlying cause, and large pericardial effusions may need urgent drainage. In cases of purulent effusions, antibiotic therapy is necessary, and steroid therapy may be considered for pericarditis related to autoimmune disorders or if NSAIDs alone are ineffective.