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.

According to NICE guidelines, the usual threshold score for initiating anticoagulation in this case is 2.

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.

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

Further Reading:

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

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

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

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

This patient is displaying symptoms consistent with a diagnosis of an acute myocardial infarction. It is important to provide pain relief as soon as possible. One option for pain relief is GTN, which can be taken sublingually or buccally. However, if there is suspicion of an acute myocardial infarction, it is recommended to offer intravenous opioids such as morphine.

Aspirin should be offered to all patients with unstable angina or NSTEMI as soon as possible and should be continued indefinitely, unless there are contraindications such as a bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered promptly after presentation.

For patients without a high bleeding risk who do not have coronary angiography planned within 24 hours of admission, fondaparinux should be administered. However, for patients who are likely to undergo coronary angiography within 24 hours, unfractionated heparin can be offered as an alternative to fondaparinux. In cases of significant renal impairment (creatinine above 265 micromoles per litre), unfractionated heparin with dose adjustment guided by clotting function monitoring can also be considered as an alternative to fondaparinux.

Routine administration of oxygen is no longer recommended, but it is important to monitor oxygen saturation using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with an oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, with a target SpO2 range of 94-98%. For individuals with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, a target SpO2 range of 88-92% should be aimed for until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI who are undergoing percutaneous coronary intervention.

For more information, please refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.

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.

The characteristic with the highest likelihood ratio for AMI is the radiation of chest pain to the right arm or both arms. Additionally, the history characteristics of cardiac pain also have a high likelihood ratio for AMI.

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.

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.

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.

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

Further Reading:

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

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

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

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

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

Patients with mitral regurgitation can go for extended periods without experiencing any symptoms. They may have a normal exercise tolerance and show no signs of congestive cardiac failure. However, when cardiac failure does occur, patients often complain of breathlessness, especially during physical exertion. They may also experience fatigue, difficulty breathing while lying flat (orthopnoea), and sudden episodes of difficulty breathing at night (paroxysmal nocturnal dyspnoea).

In terms of clinical signs, mitral regurgitation can be identified through various indicators. These include a displaced and volume loaded apex beat, which can be felt during a physical examination. A palpable thrill may also be detected at the apex. Additionally, a pansystolic murmur, which is loudest at the apex and radiates to the axilla, can be heard. This murmur is typically most pronounced when the patient holds their breath during expiration. Furthermore, a soft first heart sound and signs of left ventricular failure may be present.

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.

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

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

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

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

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

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

The most appropriate initial treatment for this patient would be intravenous labetalol. Labetalol is a non-selective beta blocker with alpha-blocking properties. It is the preferred initial treatment for aortic dissection because it helps to reduce blood pressure and heart rate, which can help to decrease the shear forces acting on the aortic wall and prevent further dissection. Intravenous administration of labetalol allows for rapid and effective control of blood pressure.

Other treatment options, such as intravenous magnesium sulphate, intravenous verapamil, GTN sublingual spray, and oral nifedipine, are not appropriate for the management of aortic dissection. Magnesium sulphate is used for the treatment of certain arrhythmias and pre-eclampsia, but it does not address the underlying issue of aortic dissection. Verapamil and nifedipine are calcium channel blockers that can lower blood pressure, but they can also cause reflex tachycardia, which can worsen the condition. GTN sublingual spray is used for the treatment of angina, but it does not address the underlying issue 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.

Post myocardial infarction ventricular septal defect (VSD) is a rare but serious complication that occurs when the cardiac wall ruptures. It typically develops 2-3 days after a heart attack, and if left untreated, 85% of patients will die within two months. The murmur associated with VSD is a continuous sound throughout systole, and it is loudest at the lower left sternal edge. A palpable vibration, known as a thrill, is often felt along with the murmur.

Dressler’s syndrome, on the other hand, is a type of pericarditis that occurs 2-10 weeks after a heart attack or cardiac surgery. It is characterized by sharp chest pain that is relieved by sitting forwards. Other signs of Dressler’s syndrome include a rubbing sound heard when listening to the heart, pulsus paradoxus (an abnormal drop in blood pressure during inspiration), and signs of right ventricular failure.

Mitral regurgitation also causes a continuous murmur throughout systole, but it is best heard at the apex of the heart and may radiate to the axilla (armpit).

Tricuspid stenosis, on the other hand, causes an early diastolic murmur that is best heard at the lower left sternal edge during inspiration.

Lastly, mitral stenosis causes a rumbling mid-diastolic murmur that is best heard at the apex of the heart. To listen for this murmur, the patient should be in the left lateral position, and the stethoscope bell should be used during expiration.

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

Further Reading:

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

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

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

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

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.

For patients suspected of having acute coronary syndromes (ACS), it is recommended that they receive 300 mg of aspirin and pain relief in the form of glyceryl trinitrate (GTN) with the option of intravenous opioids such as morphine. However, if the patient is pain-free after taking GTN, there is no need to administer morphine. The next steps in medical management or intervention will be determined once the diagnosis is confirmed.

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.

One of the signs of digoxin toxicity is yellow-green vision. Other clinical features include feeling generally unwell, lethargy, nausea and vomiting, loss of appetite, confusion, and the development of arrhythmias such as AV block and bradycardia.

Further Reading:

Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia.

ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem.

Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

Cardiac enzymes do not increase in unstable angina. However, if cardiac markers do rise, it is classified as a non-ST elevation myocardial infarction (NSTEMI). Both unstable angina and NSTEMI can have a normal ECG. An extended ventricular activation time indicates damage to the heart muscle. This occurs because infarcting myocardium conducts electrical impulses at a slower pace, resulting in a prolonged interval between the start of the QRS complex and the apex of the R wave. A positive troponin test indicates the presence of necrosis in cardiac myocytes.

Summary:
Marker | Initial Rise | Peak | Normal at
Creatine kinase | 4-8 hours | 18 hours 2-3 days | CK-MB = main cardiac isoenzyme
Myoglobin | 1-4 hours | 6-7 hours | 24 hours | Low specificity due to skeletal muscle damage
Troponin I | 3-12 hours | 24 hours | 3-10 days | Appears to be the most sensitive and specific
HFABP | 1-2 hours | 5-10 hours | 24 hours | HFABP = heart fatty acid binding protein
LDH | 10 hours | 24-48 hours | 14 days | Cardiac muscle mainly contains LDH

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.

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

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

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

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

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

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

Unstable angina is characterized by the presence of one or more of the following symptoms: angina of effort occurring over a few days with increasing frequency, episodes of angina occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. The electrocardiogram (ECG) may appear normal or show T-wave/ST-segment changes, and cardiac enzymes are typically within normal range.

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

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

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

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

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.

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.

There is no known connection between the use of cannabis and aortic dissection. Some factors that are recognized as increasing the risk of aortic dissection include hypertension, atherosclerosis, aortic coarctation, the use of sympathomimetic drugs like cocaine, Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, tertiary syphilis, and pre-existing aortic aneurysm.

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.

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

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

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

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.