People with chronic mitral regurgitation often experience atrial fibrillation.

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

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

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

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

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

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

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

Further Reading:

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

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

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

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

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

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

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

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

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

Further Reading:

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

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

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

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

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.

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.

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

Cardiac tamponade is characterized by several classical signs, including distended neck veins, muffled heart sounds, and hypotension. When neck veins are distended, it suggests that the right ventricle is not filling properly. In cases of trauma, this is often caused by the compression of air (tension pneumothorax) or fluid (blood in the pericardial space). One important distinguishing feature is the deviation of the trachea.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

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

Further Reading:

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

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

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

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

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

Further Reading:

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

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

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

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

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

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.

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

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

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

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

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

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.

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

Further Reading:

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

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

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

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

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

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

Fibrinolysis is a treatment option for patients with ST-elevation myocardial infarction (STEMI) if they are unable to receive primary percutaneous coronary intervention (PCI) within 120 minutes, but fibrinolysis can be administered within that time frame. Primary PCI is the preferred treatment for STEMI patients who present within 12 hours of symptom onset. However, if primary PCI cannot be performed within 120 minutes of the time when fibrinolysis could have been given, fibrinolysis should be considered. Along with fibrinolysis, an antithrombin medication such as unfractionated heparin (UFH), low molecular weight heparin (LMWH), fondaparinux, or bivalirudin is typically administered.

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.

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.

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

Further Reading:

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

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

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

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

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

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

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

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

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.

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.

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

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

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

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.

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.

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

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

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

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

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

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.

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.