Rheumatic Fever and its Effects on Cardiac Valves

Rheumatic fever is a condition caused by group A β-haemolytic streptococcal infection. To diagnose it, the revised Duckett-Jones criteria are used, which require evidence of streptococcal infection and the presence of certain criteria. While all four cardiac valves may be damaged as a result of rheumatic fever, the mitral valve is the most commonly affected, with major criteria including carditis, subcutaneous nodule, migratory polyarthritis, erythema marginatum, and Sydenham’s chorea. Minor criteria include arthralgia, fever, raised CRP or ESR, raised WCC, heart block, and previous rheumatic fever. Mitral stenosis is the most common result of rheumatic fever, but it is becoming less frequently seen in clinical practice. Pulmonary regurgitation, aortic sclerosis, and tricuspid regurgitation are also possible effects, but they are less common than mitral valve damage. Ventricular septal defect is not commonly associated with rheumatic fever.

Understanding Dressler Syndrome

Dressler syndrome is a condition that occurs several weeks after a myocardial infarction (MI) and results in fibrinous pericarditis with fever and pleuropericardial chest pain. It is believed to be an autoimmune phenomenon, rather than a result of viral, bacterial, or fungal infections. While these types of infections can cause pericarditis, they are less likely in the context of a recent MI. Chlamydial infection, in particular, does not cause pericarditis. Understanding the underlying cause of pericarditis is important for proper diagnosis and treatment of Dressler syndrome.

Understanding the Electrocardiogram: Key Components and Timing

As a junior doctor, interpreting electrocardiograms (ECGs) is a crucial skill. One important aspect to understand is the timing of key components. The QT interval, which measures ventricular depolarization and repolarization, gives an indication of the duration of ventricular systole. However, this measurement is dependent on heart rate and is corrected using Bazett’s formula. The P wave results from atrial depolarization, while the QRS complex is caused by ventricular depolarization. The first heart sound, which coincides with the QRS complex, results from closure of the AV valves as the ventricles contract. The second heart sound, occurring at about the same time as the T wave, is caused by closure of the aortic and pulmonary valves. Understanding the timing of these components is essential for accurate ECG interpretation.

Systolic Valvular Murmurs

A systolic valvular murmur can be caused by aortic/pulmonary stenosis or mitral/tricuspid regurgitation. It is important to note that the location where the murmur is heard loudest can be misleading. For instance, if it is aortic stenosis, the murmur is expected to radiate to the carotids. However, the significant factor to consider is that the murmur is heard loudest on inspiration. During inspiration, venous return to the heart increases, which exacerbates right-sided murmurs. Conversely, expiration reduces venous return and exacerbates left-sided murmurs. To remember this useful fact, the mnemonic RILE (Right on Inspiration, Left on Expiration) can be used.

If a systolic murmur is enhanced on inspiration, it must be a right-sided murmur, which could be pulmonary stenosis or tricuspid regurgitation. However, in this case, only pulmonary stenosis is an option. systolic valvular murmurs and their characteristics is crucial in making an accurate diagnosis and providing appropriate treatment.

Choosing the Right Statin Dose for Secondary Prevention of Coronary Events

All patients who have had a myocardial infarction should be started on an angiotensin-converting enzyme (ACE) inhibitor, a beta-blocker, a high-intensity statin, and antiplatelet therapy. Before starting a statin, liver function tests should be checked. The recommended statin dose for secondary prevention, as per NICE guidelines, is atorvastatin 80 mg od. Simvastatin 40 mg od is not the most appropriate drug of choice for secondary prevention, and atorvastatin is preferred due to its reduced incidence of myopathy. While simvastatin 80 mg od is an appropriate high-intensity statin therapy, atorvastatin is still preferred. Atorvastatin 20 mg od and 40 mg od are too low a dose to start with, and the dose may need to be increased to 80 mg in the future.

For the management of heart failure, first line options include ACE inhibitors, beta-blockers, and aldosterone antagonists. In this case, the patient was already on a beta-blocker and an ACE inhibitor which had been effective. The addition of an aldosterone antagonist such as spironolactone would be the best option as it prevents fluid retention and reduces pressure on the heart. Ivabradine is a specialist intervention that should only be considered after trying all other recommended options. Addition of furosemide would only provide symptomatic relief. Insertion of an implantable cardiac defibrillator device is a late-stage intervention. Encouraging regular exercise and a healthy diet is important but does not directly address the patient’s clinical deterioration.

The Best Vein for Measuring Central Venous Pressure

Pericardial tamponade can lead to compression of the heart by the pericardium, resulting in decreased intracardiac diastolic pressure and reduced blood flow to the right atrium. This can cause distension of the jugular veins, making the right internal jugular vein the best vein for measuring central venous pressure (CVP). Unlike the right external vein, which joins the right internal vein at an oblique angle, the right internal vein has a straight continuation with the right brachiocephalic vein and the superior vena cava, making CVP measurement more accurate. On the other hand, the left internal jugular vein makes an oblique union with the left brachiocephalic vein and the external jugular veins, making it a less reliable indicator of CVP. Similarly, the left external vein also joins the left internal vein at an oblique angle, making CVP reading less reliable.

Virchow’s Triad and Its Three Categories of Thrombosis Factors

Virchow’s triad is a concept that explains the three main categories of factors that contribute to thrombosis. These categories include stasis, injuries or trauma to the endothelium, and blood hypercoagulability. Stasis refers to abnormal blood flow, which can be caused by various factors such as turbulence, varicose veins, and stasis. Injuries or trauma to the endothelium can be caused by hypertension or shear stress, which can damage veins or arteries. Blood hypercoagulability is associated with several conditions such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, disseminated malignancy, late pregnancy, and smoking.

It is important to note that current thrombosis or past history of thrombosis and malignancy are not included in the triad. Malignancy is a specific procoagulant state, so it is covered under hypercoagulability. Virchow’s triad and its three categories of thrombosis factors can help healthcare professionals identify and manage patients who are at risk of developing thrombosis. By addressing these factors, healthcare professionals can help prevent thrombosis and its associated complications.

The Pathological Progression of Myocardial Infarction: A Timeline of Changes

Myocardial infarction, commonly known as a heart attack, is a serious medical condition that occurs when blood flow to the heart is blocked, leading to tissue damage and potentially life-threatening complications. The pathological progression of myocardial infarction follows a predictable sequence of events, with macroscopic and microscopic changes occurring over time.

Immediately after the infarct occurs, there are usually no visible changes to the myocardium. However, within 3-6 hours, maximal inflammatory changes occur, with the most prominent changes occurring between 24-72 hours. During this time, coagulative necrosis and acute inflammatory responses are visible, with marked infiltration by neutrophils.

Between 3-10 days, the infarcted area begins to develop a hyperaemic border, and the process of organisation and repair begins. Granulation tissue replaces dead muscle, and dying neutrophils are replaced by macrophages. Disintegration and phagocytosis of dead myofibres occur during this time.

If a patient survives an acute infarction, the infarct heals through the formation of scar tissue. However, scar tissue does not possess the usual contractile properties of normal cardiac muscle, leading to contractile dysfunction or congestive cardiac failure. The entire process from coagulative necrosis to the formation of well-formed scar tissue takes 6-8 weeks.

In summary, understanding the timeline of changes that occur during myocardial infarction is crucial for early diagnosis and effective treatment. By recognising the macroscopic and microscopic changes that occur over time, healthcare professionals can provide appropriate interventions to improve patient outcomes.

Electrocardiogram (ECG) Changes Associated with Hypo- and Hyperkalaemia

Hypo- and hyperkalaemia can cause significant changes in the ECG. Hypokalaemia is associated with increased amplitude and width of the P wave, T wave flattening and inversion, ST-segment depression, and prominent U-waves. As hypokalaemia worsens, it can lead to frequent supraventricular ectopics and tachyarrhythmias, eventually resulting in life-threatening ventricular arrhythmias. On the other hand, hyperkalaemia is associated with peaked T waves, widening of the QRS complex, decreased amplitude of the P wave, prolongation of the PR interval, and eventually ventricular tachycardia/ventricular fibrillation. Both hypo- and hyperkalaemia can cause prolongation of the PR interval, but only hyperkalaemia is associated with flattening of the P-wave. In hyperkalaemia, eventually ventricular tachycardia/ventricular fibrillation is seen, while AF can occur in hypokalaemia.

Management of Suspected Myocardial Infarction

Explanation:

When a patient presents with symptoms suggestive of myocardial infarction (MI), a troponin level should be checked. If the level is only slightly raised, it does not confirm a diagnosis of MI, but neither does it rule it out. Therefore, a repeat troponin level should be performed at least 3 hours after the first level and sent as urgent.

In an MI, cardiac enzymes are released from dead myocytes into the blood, causing enzyme levels to rise and eventually fall as they are cleared from blood. If the patient has had an MI, the repeat troponin level should either be further raised or further reduced. If the level remains roughly constant, then an alternative cause should be sought, such as pulmonary embolism, chronic kidney disease, acute kidney injury, pericarditis, heart failure, or sepsis/systemic infection.

Admission to the Coronary Care Unit (CCU) is not warranted yet. Further investigations should be performed to ascertain whether an admission is needed or whether alternative diagnoses should be explored.

Safety-netting and return to the GP should include a repeat troponin level to see if the level is stable (arguing against an MI) or is rising/falling. A repeat electrocardiogram (ECG) should be performed, and a thorough history and examination should be obtained to identify any urgent diagnoses that need to be explored before the patient is discharged.

Thrombolysis carries a risk for bleeding, so it requires a clear indication, which has not yet been obtained. Therefore, it should not be administered without proper evaluation.

The alanine transaminase (ALT) level has been used as a marker of MI in the past, but it has been since superseded as it is not specific for myocardial damage. In fact, it is now used as a component of liver function tests.

Treatment Options for Hyperkalaemia: Understanding the Role of Calcium Gluconate, Insulin and Dextrose, Calcium Resonium, Nebulised Salbutamol, and Dexamethasone

Hyperkalaemia is a condition characterized by high levels of potassium in the blood, which can lead to serious complications such as arrhythmias. When a patient presents with hyperkalaemia and ECG changes, the initial treatment is calcium gluconate. This medication stabilizes the myocardial membranes by reducing the excitability of cardiomyocytes. However, it does not reduce potassium levels, so insulin and dextrose are needed to correct the underlying hyperkalaemia. Insulin shifts potassium intracellularly, reducing serum potassium levels by 0.6-1.0 mmol/l every 15 minutes. Nebulised salbutamol can also drive potassium intracellularly, but insulin and dextrose are preferred due to their increased effectiveness and decreased side-effects. Calcium Resonium is a slow-acting treatment that removes potassium from the body by binding it and preventing its absorption in the gastrointestinal tract. While it can help reduce potassium levels in the long term, it is not effective in protecting the patient from arrhythmias acutely. Dexamethasone, a steroid, is not useful in the treatment of hyperkalaemia. Understanding the role of these treatment options is crucial in managing hyperkalaemia and preventing serious complications.

Understanding the Ejection Systolic Murmur in Hypertrophic Cardiomyopathy: Decreased by Squatting

Hypertrophic cardiomyopathy (HCM) is a condition characterized by asymmetrical hypertrophy of both ventricles, with the septum hypertrophying and causing an outflow obstruction of the left ventricle. This obstruction leads to an ejection systolic murmur and reduced cardiac output. However, interestingly, this murmur can be decreased by squatting, which is not typical for most heart murmurs.

Squatting affects murmurs by increasing afterload and preload, which usually makes heart murmurs louder. However, in HCM, the murmur intensity is decreased due to increased left ventricular size and reduced outflow obstruction. Other findings on examination may include a jerky pulse and a double apex beat.

While HCM is often asymptomatic, it can present with dyspnea, angina, and syncope. Patients are also at risk of sudden cardiac death, most commonly due to ventricular arrhythmias. Poor prognostic factors include syncope, family history of sudden death, onset of symptoms at a young age, ventricular tachycardia on Holter monitoring, abnormal blood pressure response during exercise, and septal thickness greater than 3 cm on echocardiogram.

In summary, understanding the ejection systolic murmur in HCM and its unique response to squatting can aid in the diagnosis and management of this condition.

Verapamil and Beta Blockers: A Dangerous Combination

Verapamil is a type of medication that blocks calcium channels in the heart, leading to a decrease in cardiac output and a slower heart rate. However, it also has negative effects on the heart’s ability to contract, making it a highly negatively inotropic drug. Additionally, it may impair the conduction of electrical signals between the atria and ventricles of the heart.

According to the British National Formulary (BNF), verapamil should not be given to patients who are already taking beta blockers. This is because the combination of these two drugs can lead to dangerously low blood pressure and even asystole, a condition where the heart stops beating altogether.

Therefore, it is important for healthcare professionals to carefully consider a patient’s medication history before prescribing verapamil. If a patient is already taking beta blockers, alternative treatments should be considered to avoid the potentially life-threatening consequences of combining these two drugs.

Coarctation of the Aorta: Symptoms and Diagnosis

Coarctation of the aorta is a condition that can present with various symptoms. These may include headaches, nosebleeds, cold extremities, and claudication. However, hypertension is the most typical symptom. A mid-systolic murmur may also be present over the anterior part of the chest, back, spinous process, and a continuous murmur may also be heard.

One important radiographic finding in coarctation of the aorta is notching of the ribs. This is due to erosion by collaterals. It is important to diagnose coarctation of the aorta early on, as it can lead to serious complications such as heart failure, stroke, and aortic rupture.

Common Heart Murmurs and their Association with Rheumatic Heart Disease

Rheumatic heart disease (RHD) is a condition resulting from untreated pharyngitis caused by group A beta-haemolytic streptococcal infection. RHD can lead to heart valve dysfunction, most commonly the mitral valve, resulting in mitral stenosis. The characteristic murmur of mitral stenosis is a mid-diastolic rumbling murmur that follows an opening snap after S2. Aortic stenosis can also be present in RHD but is less prevalent. Other heart murmurs associated with RHD include a high-pitched blowing diastolic decrescendo murmur, which is associated with aortic regurgitation, and a continuous machine-like murmur that is loudest at S2, consistent with patent ductus arteriosus. A late systolic crescendo murmur with a mid-systolic click is seen in mitral valve prolapse. A crescendo-decrescendo systolic ejection murmur following an ejection click describes the murmur heard in aortic stenosis. It is important to recognize these murmurs and their association with RHD for proper diagnosis and management.

Auscultation of Heart Valves: Locations and Sounds

The human heart has four valves that regulate blood flow. These valves can be heard through auscultation, a medical technique that involves listening to the sounds produced by the heart using a stethoscope. Here are the locations and sounds of each valve:

Tricuspid Valve: This valve is located on the right side of the heart and can be heard at the left sternal border in the fourth intercostal space. The sound produced by this valve is a low-pitched, rumbling noise.

Aortic Valve: The aortic valve is located on the left side of the heart and can be heard over the right sternal border at the second intercostal space. The sound produced by this valve is a high-pitched, clicking noise.

Pulmonary Valve: This valve is located on the right side of the heart and can be heard over the left sternal border at the second intercostal space. The sound produced by this valve is a high-pitched, clicking noise.

Thebesian Valve: The Thebesian valve is located in the coronary sinus and its closure cannot be auscultated.

Mitral Valve: This valve is located on the left side of the heart and can be heard by listening at the apex, in the left mid-clavicular line in the fifth intercostal space. The sound produced by this valve is a low-pitched, rumbling noise.

In summary, auscultation of heart valves is an important diagnostic tool that can help healthcare professionals identify potential heart problems. By knowing the locations and sounds of each valve, healthcare professionals can accurately diagnose and treat heart conditions.

Medications for Acute Coronary Syndrome: Indications and Uses

Acute coronary syndrome (ACS) is a medical emergency that requires prompt and appropriate treatment to prevent further damage to the heart muscle. The management of ACS involves a combination of medications and interventions, depending on the type and severity of the condition. Here are some commonly used medications for ACS and their indications:

1. Fondaparinux: This medication is a factor Xa inhibitor that is used for anticoagulation in ACS without ST-segment elevation. It is usually given along with other drugs such as aspirin, clopidogrel, and nitrates to prevent blood clots and reduce the risk of future cardiovascular events.

2. Warfarin: This medication is used for the treatment and prevention of venous thrombosis and thromboembolism. It is not indicated for the immediate management of ACS.

3. Furosemide: This medication is a diuretic that is used to treat pulmonary edema in patients with heart failure. It is not indicated for ACS as it may cause dehydration.

4. Paracetamol: This medication is not effective as an analgesic option for ACS. Morphine is commonly used for pain relief in ACS.

5. Simvastatin: This medication is a statin that is used for the long-term management of high cholesterol levels. It is not indicated for the initial management of ACS.

In summary, the management of ACS involves a combination of medications and interventions that are tailored to the individual patient’s needs. Prompt and appropriate treatment can help improve outcomes and reduce the risk of future cardiovascular events.

Differential Diagnosis for a Patient with Vasovagal Syncope

Vasovagal syncope is a common cause of transient loss of consciousness. The hallmark of this condition is the three Ps – pallor, palpitations, and sweating. In patients with a history of vasovagal syncope, the ECG is typically normal. A prolonged PR interval may be seen in young athletes, but first-degree heart block rarely causes cardiac syncope. Ischemic heart disease is not a significant factor in this condition, and a family history of myocardial infarction is not relevant.

If there are no features suggesting a more serious cause of transient loss of consciousness or a significant personal or family cardiac history, the patient can be discharged from the Emergency Department. However, they should be advised to seek medical attention if they experience any further episodes.

Other conditions that may cause transient loss of consciousness include complete heart block, hypertrophic cardiomyopathy, substance misuse, and long QT syndrome. However, in this case, the patient’s history and ECG are not suggestive of these conditions.

Complications Following Myocardial Infarction

One of the complications that can occur 2-6 weeks after a myocardial infarction (MI) is Dressler’s syndrome. This autoimmune reaction happens as the myocardium heals and can present with pyrexia, pleuritic chest pain, and an elevated ESR. Pulmonary embolism is not suggested by this presentation. Another complication is myomalacia cordis, which occurs 3-14 days post-MI and involves the softening of dead muscles leading to rupture and death. Ventricular aneurysm may also form due to weakened myocardium, resulting in persistent ST elevation and left ventricular failure. Anticoagulation is necessary to prevent thrombus formation within the aneurysm and reduce the risk of stroke. Heart failure is unlikely to cause the above presentation and blood test results.

Characteristics of Patent Ductus Arteriosus

Patent ductus arteriosus is a condition that is characterized by an unusual increase in oxygen saturation between the right ventricle and pulmonary artery. This is often accompanied by elevated pulmonary artery pressures and a high wedge pressure. These data are typical of this condition and can be used to diagnose it. It is important to note that patent ductus arteriosus can lead to serious complications if left untreated, including heart failure and pulmonary hypertension. Therefore, early detection and treatment are crucial for improving outcomes and preventing long-term complications.

Differentiating Pulmonary Oedema from Other Cardiac and Respiratory Conditions

Pulmonary oedema is a condition characterized by the accumulation of fluid in the lungs due to left ventricular failure. It presents with symptoms such as shortness of breath, raised jugular venous pressure, and a third heart sound. Bi-basal crackles are also a hallmark of pulmonary oedema. However, it is important to differentiate pulmonary oedema from other cardiac and respiratory conditions that may present with similar symptoms.

Tricuspid regurgitation is another cardiac condition that may present with a raised JVP and a third heart sound. However, it is characterized by additional symptoms such as ascites, a pulsatile liver, peripheral oedema, and a pansystolic murmur. Pneumonia, on the other hand, is a respiratory infection that presents with a productive cough of yellow or green sputum and shortness of breath. Bronchial breath sounds may also be heard upon auscultation.

Pulmonary embolus is a condition that presents with chest pain, shortness of breath, and signs of an underlying deep vein thrombosis. Pericardial effusion, on the other hand, is characterized by the accumulation of fluid in the pericardial sac surrounding the heart. It may eventually lead to cardiac tamponade, which presents with hypotension, shortness of breath, and distant heart sounds. However, bi-basal crackles are not a feature of pericardial effusion.

In summary, it is important to consider the specific symptoms and characteristics of each condition in order to accurately diagnose and differentiate pulmonary oedema from other cardiac and respiratory conditions.

Post-Myocardial Infarction (MI) Precautions: Guidelines for Alcohol, Machinery, Driving, Sex, and Exercise

After experiencing a myocardial infarction (MI), also known as a heart attack, it is crucial to take precautions to prevent further complications. Here are some guidelines to follow:

Alcohol Consumption: Patients should be advised to keep their alcohol consumption within recommended limits, which is now 14 units per week for both men and women.

Operating Heavy Machinery: Patients should avoid operating heavy machinery for four weeks post MI.

Bus Driving: Patients should refrain from driving a bus or lorry for six weeks post MI. If the patient had angioplasty, driving is not allowed for one week if successful and four weeks if unsuccessful or not performed.

Sexual Intercourse: Patients should avoid sexual intercourse for four weeks post MI.

Vigorous Exercise: Patients should refrain from vigorous exercise for four weeks post MI.

Following these guidelines can help prevent further complications and aid in the recovery process after a myocardial infarction.

Echocardiographic Findings in Hypertrophic Obstructive Cardiomyopathy

Hypertrophic obstructive cardiomyopathy (HOCM) is a condition characterized by thickening of the heart muscle, particularly the septum, which can lead to obstruction of blood flow out of the heart. Echocardiography is a useful tool for diagnosing and monitoring HOCM. Here are some echocardiographic findings commonly seen in HOCM:

Reduced left ventricular cavity size: Patients with HOCM often have a banana-shaped left ventricular cavity, with reduced size due to septal hypertrophy.

Increased left ventricular outflow tract gradients: HOCM can cause obstruction of blood flow out of the heart, leading to increased pressure gradients in the left ventricular outflow tract.

Systolic anterior motion of the mitral leaflet: This is a characteristic finding in HOCM, where the mitral valve moves forward during systole and can contribute to obstruction of blood flow.

Asymmetrical septal hypertrophy: While some patients with HOCM may have symmetrically hypertrophied ventricles, the more common presentation is asymmetrical hypertrophy, with thickening of the septum.

Mitral regurgitation: HOCM can cause dysfunction of the mitral valve, leading to mild to moderate regurgitation of blood back into the left atrium.

Overall, echocardiography plays an important role in the diagnosis and management of HOCM, allowing for visualization of the structural and functional abnormalities associated with this condition.

Differentiating Arterial Conditions: Understanding the Symptoms and Causes

When it comes to arterial conditions, it is important to understand the symptoms and causes in order to make an accurate diagnosis. Here, we will explore several potential conditions and how they may present in a patient.

Stenotic Arteries:
Coarctation of the aorta is a potential condition to consider in younger adults with poorly controlled hypertension. Symptoms may include weak or absent femoral pulses, heart failure, and left-ventricular hypertrophy. Angiography may reveal stenosis in the middle and proximal segments of the left anterior descending artery, as well as in the left circumflex artery.

Thickened Arteries:
Atherosclerosis, or the build-up of plaque in the arteries, is a risk factor for heart attacks and stroke. However, it is unlikely to explain persistently high blood pressure or an absent femoral pulse.

Aortic Aneurysm:
While chronic high blood pressure can increase the risk of an aortic aneurysm, sudden, intense chest or back pain is a more common symptom. Additionally, a patient with an aneurysm would likely have low blood pressure and an elevated heart rate, which is inconsistent with the vitals seen in this presentation.

Calcified Arteries:
Calcification of arteries is caused by elevated lipid content and increases with age. While it can increase the risk of heart attack and stroke, it would not explain the absence of a femoral pulse or extremely high blood pressure.

Patent Foramen Ovale:
This condition, which predisposes patients to paradoxical emboli, is typically diagnosed on an echocardiogram and is unlikely to cause hypertension. It should be considered in patients who have had a stroke before the age of 50.

In summary, understanding the symptoms and causes of arterial conditions is crucial for accurate diagnosis and treatment.

The patient is experiencing cardiac tamponade, which is caused by fluid in the pericardial sac compressing the heart and reducing ventricular filling. This is likely due to pericarditis caused by recent radiotherapy. Beck’s triad of low blood pressure, raised JVP, and muffled heart sounds are indicative of tamponade. Urgent pericardiocentesis is necessary to aspirate the pericardial fluid, preferably under echocardiographic guidance. A fluid challenge with sodium chloride is not recommended as it may worsen the pericardial fluid. Ibuprofen is not effective in severe cases of pericardial effusion. GTN spray, morphine, clopidogrel, and aspirin are useful in managing myocardial infarction, which is a differential diagnosis to rule out. LMWH is not appropriate for tamponade and may worsen the condition if caused by haemopericardium.

Investigating Cardiac Chest Pain: Recommended Tests

When a patient presents with cardiac chest pain, it is important to conduct appropriate investigations to determine the underlying cause. The following tests are recommended:

Computed Tomography (CT) Coronary Angiogram: This non-invasive test uses CT scanning to detect any evidence of coronary artery disease and determine its extent. It is considered the gold standard test for investigating cardiac chest pain.

Angiogram: Before undergoing an angiogram, the patient should first have an exercise tolerance test (ETT) to assess real-time cardiac function during exertion. If the patient experiences ischaemic changes and reduced exercise tolerance, an angiogram may be necessary.

Chest X-ray: A chest X-ray is not a priority investigation for cardiac chest pain, as it does not aid in diagnosis unless there is evidence of associated heart failure or pleural effusions.

Full Blood Count: While anaemia could contribute to angina, a full blood count is not a first-line investigation for cardiac chest pain.

Troponin: Troponin levels may be raised in cases of myocardial damage, but are not necessary for managing angina. The recurring pain and relief with rest indicate angina, rather than a myocardial infarction (MI), which would present with crushing chest pain and dyspnoea that is not alleviated by rest.

Acute Mesenteric Ischaemia

Acute mesenteric ischaemia is a condition that occurs when there is a disruption in blood flow to the small intestine or right colon. This can be caused by arterial or venous disease, with arterial disease further classified as non-occlusive or occlusive. The classic triad of symptoms associated with acute mesenteric ischaemia includes gastrointestinal emptying, abdominal pain, and underlying cardiac disease.

The hallmark symptom of mesenteric ischaemia is severe abdominal pain, which may be accompanied by other symptoms such as nausea, vomiting, abdominal distention, ileus, peritonitis, blood in the stool, and shock. Advanced ischaemia is characterized by the presence of these symptoms.

There are several risk factors associated with acute mesenteric ischaemia, including congestive heart failure, cardiac arrhythmias (especially atrial fibrillation), recent myocardial infarction, atherosclerosis, hypercoagulable states, and hypovolaemia. It is important to be aware of these risk factors and to seek medical attention promptly if any symptoms of acute mesenteric ischaemia are present.

Cardiac Abnormalities and their Clinical Findings

Atrial Septal Defect:
Atrial septal defect is characterized by a prominent right ventricular cardiac impulse, a systolic ejection murmur heard best in the pulmonic area and along the left sternal border, and fixed splitting of the second heart sound. These findings are due to an abnormal left-to-right shunt through the defect, which creates a volume overload on the right side. Small atrial septal defects are usually asymptomatic.

Pulmonary Valve Stenosis:
Pulmonary valve stenosis causes an increased right ventricular pressure which results in right ventricular hypertrophy and pulmonary artery dilation. A crescendo–decrescendo murmur may be heard if there is a severe stenosis. Right atrial enlargement would not be present.

Mitral Regurgitation:
Mitral regurgitation would also present with a systolic murmur; however, left atrial enlargement would be seen before right ventricular enlargement.

Mitral Stenosis:
Mitral stenosis would present with an ‘opening snap’ and a diastolic murmur.

Aortic Stenosis:
Aortic stenosis is also associated with a systolic ejection murmur. However, the murmur is usually loudest at the right sternal border and radiates upwards to the jugular notch. Aortic stenosis is associated with left ventricular hypertrophy.

Clinical Findings of Common Cardiac Abnormalities

Common Cardiac Conditions and Their ECG Findings

Wolff-Parkinson-White syndrome is a condition that affects young people and is characterized by episodes of syncope and palpitations. It is caused by an accessory pathway from the atria to the ventricles that bypasses the normal atrioventricular node. The ECG shows a slurred upstroke to the QRS complex, known as a delta wave, which reflects ventricular pre-excitation. Re-entry circuits can form, leading to tachyarrhythmias and an increased risk of ventricular fibrillation.

Hypertrophic cardiomyopathy is an inherited condition that presents in young adulthood and is the most common cause of sudden cardiac death in the young. Symptoms include syncope, dyspnea, palpitations, and abnormal ECG findings, which may include conduction abnormalities, arrhythmias, left ventricular hypertrophy, and ST or T wave changes.

First-degree heart block is characterized by a prolonged PR interval and may be caused by medication, electrolyte imbalances, or post-myocardial infarction. It may also be a normal variant in young, healthy individuals.

Ebstein’s anomaly typically presents in childhood and young adulthood with fatigue, palpitations, cyanosis, and breathlessness on exertion. The ECG shows right bundle branch block and signs of atrial enlargement, such as tall, broad P waves.

Mobitz type II atrioventricular block is a type of second-degree heart block that is characterized by a stable PR interval with some non-conducted beats. It often progresses to complete heart block. Mobitz type I (Wenckebach) block, on the other hand, is characterized by a progressively lengthening PR interval, followed by a non-conducted beat and a reset of the PR interval back to a shorter value.