Indomethacin is a medication that hinders the production of prostaglandins in infants with patent ductus arteriosus by inhibiting the activity of COX enzymes. On the other hand, bosentan, an endothelin receptor antagonist, is utilized to treat pulmonary hypertension by blocking the vasoconstricting effect of endothelin, leading to vasodilation. Although endothelin causes vasoconstriction by acting on endothelin receptors, it is not employed in managing PDA. Adenosine receptor antagonists like theophylline and caffeine are also not utilized in PDA management.

Understanding Patent Ductus Arteriosus

Patent ductus arteriosus is a type of congenital heart defect that is generally classified as ‘acyanotic’. However, if left uncorrected, it can eventually result in late cyanosis in the lower extremities, which is termed differential cyanosis. This condition is caused by a connection between the pulmonary trunk and descending aorta. Normally, the ductus arteriosus closes with the first breaths due to increased pulmonary flow, which enhances prostaglandins clearance. However, in some cases, this connection remains open, leading to patent ductus arteriosus.

This condition is more common in premature babies, those born at high altitude, or those whose mothers had rubella infection in the first trimester. The features of patent ductus arteriosus include a left subclavicular thrill, continuous ‘machinery’ murmur, large volume, bounding, collapsing pulse, wide pulse pressure, and heaving apex beat.

The management of patent ductus arteriosus involves the use of indomethacin or ibuprofen, which are given to the neonate. These medications inhibit prostaglandin synthesis and close the connection in the majority of cases. If patent ductus arteriosus is associated with another congenital heart defect amenable to surgery, then prostaglandin E1 is useful to keep the duct open until after surgical repair. Understanding patent ductus arteriosus is important for early diagnosis and management of this condition.

Infective endocarditis is the likely diagnosis, which can be suspected if there is a fever and a murmur. The presence of vegetations on echo and positive blood cultures that meet Duke criteria can confirm the diagnosis. Of the given options, the only known risk factor for infective endocarditis is getting a new piercing. Alcohol binging can increase the risk of alcoholic liver disease and dilated cardiomyopathy, while asbestos exposure can lead to asbestosis and mesothelioma. Marijuana smoking may be associated with psychosis and paranoia.

Aetiology of Infective Endocarditis

Infective endocarditis is a condition that affects patients with previously normal valves, rheumatic valve disease, prosthetic valves, congenital heart defects, intravenous drug users, and those who have recently undergone piercings. The strongest risk factor for developing infective endocarditis is a previous episode of the condition. The mitral valve is the most commonly affected valve.

The most common cause of infective endocarditis is Staphylococcus aureus, particularly in acute presentations and intravenous drug users. Historically, Streptococcus viridans was the most common cause, but this is no longer the case except in developing countries. Coagulase-negative Staphylococci such as Staphylococcus epidermidis are commonly found in indwelling lines and are the most common cause of endocarditis in patients following prosthetic valve surgery. Streptococcus bovis is associated with colorectal cancer, with the subtype Streptococcus gallolyticus being most linked to the condition.

Culture negative causes of infective endocarditis include prior antibiotic therapy, Coxiella burnetii, Bartonella, Brucella, and HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella). It is important to note that systemic lupus erythematosus and malignancy, specifically marantic endocarditis, can also cause non-infective endocarditis.

The Coeliac Axis and its Branches

The coeliac axis is a major artery that supplies blood to the upper abdominal organs. It has three main branches: the left gastric, hepatic, and splenic arteries. The hepatic artery further branches into the right gastric, gastroduodenal, right gastroepiploic, superior pancreaticoduodenal, and cystic arteries. Meanwhile, the splenic artery gives off the pancreatic, short gastric, and left gastroepiploic arteries. Occasionally, the coeliac axis also gives off one of the inferior phrenic arteries.

The coeliac axis is located anteriorly to the lesser omentum and is related to the right and left coeliac ganglia, as well as the caudate process of the liver and the gastric cardia. Inferiorly, it is in close proximity to the upper border of the pancreas and the renal vein.

Understanding the anatomy and branches of the coeliac axis is important in diagnosing and treating conditions that affect the upper abdominal organs, such as pancreatic cancer or gastric ulcers.

The patient’s examination findings suggest aortic regurgitation, which is characterized by an early diastolic, high-pitched, blowing murmur that is louder when the patient sits forward and at the left sternal edge. Aortic regurgitation can also cause a collapsing pulse, dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, and visible pulsing red colouration of the nails (quincke’s sign).

It is important to note that aortic stenosis does not cause a diastolic murmur or collapsing pulse. Instead, it typically produces an ejection systolic murmur that is louder on expiration and may cause a slow rising pulse.

Similarly, mitral regurgitation does not cause a diastolic murmur or collapsing pulse. It typically produces a pansystolic murmur.

Mitral stenosis causes a mid-late diastolic murmur but does not commonly cause a collapsing pulse.

Pulmonary stenosis causes an ejection systolic murmur but does not commonly cause a collapsing pulse or diastolic murmur.

Aortic regurgitation is a condition where the aortic valve of the heart leaks, causing blood to flow in the opposite direction during ventricular diastole. This can be caused by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta. The most common causes of AR due to valve disease include rheumatic fever, calcific valve disease, and infective endocarditis. On the other hand, AR due to aortic root disease can be caused by conditions such as aortic dissection, hypertension, and connective tissue diseases like Marfan’s and Ehler-Danlos syndrome.

The features of AR include an early diastolic murmur, a collapsing pulse, wide pulse pressure, Quincke’s sign, and De Musset’s sign. In severe cases, a mid-diastolic Austin-Flint murmur may also be present. Suspected AR should be investigated with echocardiography.

Management of AR involves medical management of any associated heart failure and surgery in symptomatic patients with severe AR or asymptomatic patients with severe AR who have LV systolic dysfunction.

The cephalic vein is a superficial vein in the upper limb that runs over the fascial planes and terminates in the axillary vein after piercing the coracoid membrane. It is located anterolaterally to the biceps.

The Cephalic Vein: Path and Connections

The cephalic vein is a major blood vessel that runs along the lateral side of the arm. It begins at the dorsal venous arch, which drains blood from the hand and wrist, and travels up the arm, crossing the anatomical snuffbox. At the antecubital fossa, the cephalic vein is connected to the basilic vein by the median cubital vein. This connection is commonly used for blood draws and IV insertions.

After passing through the antecubital fossa, the cephalic vein continues up the arm and pierces the deep fascia of the deltopectoral groove to join the axillary vein. This junction is located near the shoulder and marks the end of the cephalic vein’s path.

Overall, the cephalic vein plays an important role in the circulation of blood in the upper limb. Its connections to other major veins in the arm make it a valuable site for medical procedures, while its path through the deltopectoral groove allows it to contribute to the larger network of veins that drain blood from the upper body.

In the treatment of heart failure, medications are used to improve the heart’s ability to pump blood effectively. Beta blockers, such as bisoprolol, are commonly prescribed to slow the heart rate and improve filling. The first-line drugs for heart failure are beta blockers and ACE inhibitors. Therefore, the patient in question will be prescribed an ACE inhibitor, such as ramipril, as the second drug. Ramipril works by reducing venous resistance, making it easier for the heart to pump blood out, and lowering arterial pressures, which increases the heart’s pre-load.

Carvedilol is not the correct choice for this patient. Although it can be used in heart failure, the patient is already taking a beta blocker, and adding another drug from the same class could cause symptomatic bradycardia or hypotension.

Digoxin is not the appropriate choice either. While it can be used in heart failure, it should only be initiated by a specialist.

Sacubitril-valsartan is also not the right choice for this patient. Although it is becoming more commonly used in heart failure patients, it should only be prescribed by a specialist after first and second-line treatment options have been exhausted.

Chronic heart failure can be managed through drug treatment, according to updated guidelines issued by NICE in 2018. While loop diuretics are useful in managing fluid overload, they do not reduce mortality in the long term. The first-line treatment for all patients is a combination of an ACE-inhibitor and a beta-blocker, with clinical judgement used to determine which one to start first. Aldosterone antagonists are recommended as second-line treatment, but potassium levels should be monitored as both ACE inhibitors and aldosterone antagonists can cause hyperkalaemia. Third-line treatment should be initiated by a specialist and may include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin, and cardiac resynchronisation therapy. Other treatments include annual influenzae and one-off pneumococcal vaccines. Those with asplenia, splenic dysfunction, or chronic kidney disease may require a booster every 5 years.

Cardiovascular physiology involves the study of the functions and processes of the heart and blood vessels. One important measure of heart function is the left ventricular ejection fraction, which is calculated by dividing the stroke volume (the amount of blood pumped out of the left ventricle with each heartbeat) by the end diastolic LV volume (the amount of blood in the left ventricle at the end of diastole) and multiplying by 100%. Another key measure is cardiac output, which is the amount of blood pumped by the heart per minute and is calculated by multiplying stroke volume by heart rate.

Pulse pressure is another important measure of cardiovascular function, which is the difference between systolic pressure (the highest pressure in the arteries during a heartbeat) and diastolic pressure (the lowest pressure in the arteries between heartbeats). Factors that can increase pulse pressure include a less compliant aorta (which can occur with age) and increased stroke volume.

Finally, systemic vascular resistance is a measure of the resistance to blood flow in the systemic circulation and is calculated by dividing mean arterial pressure (the average pressure in the arteries during a heartbeat) by cardiac output. Understanding these measures of cardiovascular function is important for diagnosing and treating cardiovascular diseases.

The posterior triangle of the neck is an area that is bound by the sternocleidomastoid and trapezius muscles, the occipital bone, and the middle third of the clavicle. Within this triangle, there are various nerves, vessels, muscles, and lymph nodes. The nerves present include the accessory nerve, phrenic nerve, and three trunks of the brachial plexus, as well as branches of the cervical plexus such as the supraclavicular nerve, transverse cervical nerve, great auricular nerve, and lesser occipital nerve. The vessels found in this area are the external jugular vein and subclavian artery. Additionally, there are muscles such as the inferior belly of omohyoid and scalene, as well as lymph nodes including the supraclavicular and occipital nodes.

Possible Diagnosis for a Young Man with Night Sweats and Clubbing of Fingers

This young man has been experiencing night sweats and has clubbing of the fingers, which suggests a long history of illness. These symptoms, along with the presence of a murmur, point towards a possible diagnosis of infective endocarditis. Other symptoms that may be present in such cases include splinter haemorrhages in the nails, Roth spots in the eyes, and Osler’s nodes and Janeway lesions in the palms and fingers of the hands.

In summary, the combination of night sweats, clubbing of fingers, and a murmur in a young man may indicate infective endocarditis. It is important to look for other symptoms such as splinter haemorrhages, Roth spots, Osler’s nodes, and Janeway lesions to confirm the diagnosis.

The range of stroke volumes is between 55 and 100 milliliters.

The stroke volume refers to the amount of blood that is pumped out of the ventricle during each cycle of cardiac contraction. This volume is usually the same for both ventricles and is approximately 70ml for a man weighing 70Kg. To calculate the stroke volume, the end systolic volume is subtracted from the end diastolic volume. Several factors can affect the stroke volume, including the size of the heart, its contractility, preload, and afterload.

Here is a mnemonic to remember the order in which the branches of the external carotid artery originate: Some Attendings Like Freaking Out Potential Medical Students. The first branch is the superior thyroid artery, followed by the ascending pharyngeal, lingual, facial, occipital, post auricular, and finally the maxillary and superficial temporal arteries.

Anatomy of the External Carotid Artery

The external carotid artery begins on the side of the pharynx and runs in front of the internal carotid artery, behind the posterior belly of digastric and stylohyoid muscles. It is covered by sternocleidomastoid muscle and passed by hypoglossal nerves, lingual and facial veins. The artery then enters the parotid gland and divides into its terminal branches within the gland.

To locate the external carotid artery, an imaginary line can be drawn from the bifurcation of the common carotid artery behind the angle of the jaw to a point in front of the tragus of the ear.

The external carotid artery has six branches, with three in front, two behind, and one deep. The three branches in front are the superior thyroid, lingual, and facial arteries. The two branches behind are the occipital and posterior auricular arteries. The deep branch is the ascending pharyngeal artery. The external carotid artery terminates by dividing into the superficial temporal and maxillary arteries within the parotid gland.

Dig Toxicity and its Treatment

Dig Toxicity can occur as a result of taking antibiotics that inhibit enzymes, especially if the prescribing physician does not take this into account. One of the most common signs of dig toxicity is the reverse tick abnormality, which can be detected through an electrocardiogram (ECG).

To treat dig toxicity, it is important to first address any electrolyte imbalances that may be present. In more severe cases, a monoclonal antibody called digibind may be administered to help alleviate symptoms. Overall, it is important for healthcare providers to be aware of the potential for dig toxicity and to take appropriate measures to prevent and treat it.

Medications Associated with Gynaecomastia

Gynaecomastia, the enlargement of male breast tissue, can be caused by various medications. Spironolactone, ciclosporin, cimetidine, and omeprazole are some of the drugs that have been associated with this condition. Ramipril has also been linked to gynaecomastia, but it is a rare occurrence.

Aside from these medications, other drugs that can cause gynaecomastia include digoxin, LHRH analogues, cimetidine, and finasteride. It is important to note that not all individuals who take these medications will develop gynaecomastia, and the risk may vary depending on the dosage and duration of treatment.

Torsades to pointes, a type of polymorphic ventricular tachycardia, can be a fatal arrhythmia that is often characterized by a shifting sinusoidal waveform on an ECG. This condition is associated with hypocalcemia, which can lead to QT interval prolongation. On the other hand, hypercalcemia is associated with QT interval shortening and may also cause a prolonged QRS interval.

Hyponatremia and hypernatremia typically do not result in ECG changes, but can cause various symptoms such as confusion, weakness, and seizures. Hyperkalemia, another life-threatening electrolyte imbalance, often causes tall tented T waves, small p waves, and a wide QRS interval on an ECG. Hypokalemia, on the other hand, can lead to QT interval prolongation and increase the risk of Torsades to pointes.

Physicians should be aware that hypercalcemia may indicate the presence of primary hyperparathyroidism or malignancy, and should investigate further for any signs of cancer in affected patients.

Long QT syndrome (LQTS) is a genetic condition that causes a delay in the ventricles’ repolarization. This delay can lead to ventricular tachycardia/torsade de pointes, which can cause sudden death or collapse. The most common types of LQTS are LQT1 and LQT2, which are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.

There are various causes of a prolonged QT interval, including congenital factors, drugs, and other conditions. Congenital factors include Jervell-Lange-Nielsen syndrome and Romano-Ward syndrome. Drugs that can cause a prolonged QT interval include amiodarone, sotalol, tricyclic antidepressants, and selective serotonin reuptake inhibitors. Other factors that can cause a prolonged QT interval include electrolyte imbalances, acute myocardial infarction, myocarditis, hypothermia, and subarachnoid hemorrhage.

LQTS may be detected on a routine ECG or through family screening. Long QT1 is usually associated with exertional syncope, while Long QT2 is often associated with syncope following emotional stress, exercise, or auditory stimuli. Long QT3 events often occur at night or at rest and can lead to sudden cardiac death.

Management of LQTS involves avoiding drugs that prolong the QT interval and other precipitants if appropriate. Beta-blockers are often used, and implantable cardioverter defibrillators may be necessary in high-risk cases. It is important to note that sotalol may exacerbate LQTS.

Localisation of Myocardial Infarction

Myocardial infarction (MI) is a medical emergency that occurs when there is a blockage in the blood flow to the heart muscle. The location of the blockage determines the type of MI and the treatment required. An inferior MI is caused by the occlusion of the right coronary artery, which supplies blood to the bottom of the heart. This type of MI can cause symptoms such as chest pain, shortness of breath, and nausea. It is important to identify the location of the MI quickly to provide appropriate treatment and prevent further damage to the heart muscle. Proper diagnosis and management can improve the patient’s chances of survival and reduce the risk of complications.

The inheritance pattern of HOCM is autosomal dominant, which means that it can be passed down from generation to generation. Symptoms of HOCM may include exertional dyspnoea, angina, syncope, and an ejection systolic murmur. It is important to note that there may be a family history of similar cardiac problems or sudden death due to ventricular arrhythmias. Autosomal recessive, mitochondrial inheritance, and X-linked dominant inheritance are not applicable to HOCM.

Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic disorder that affects muscle tissue and is inherited in an autosomal dominant manner. It is caused by mutations in genes that encode contractile proteins, with the most common defects involving the β-myosin heavy chain protein or myosin-binding protein C. HOCM is characterized by left ventricle hypertrophy, which leads to decreased compliance and cardiac output, resulting in predominantly diastolic dysfunction. Biopsy findings show myofibrillar hypertrophy with disorganized myocytes and fibrosis. HOCM is often asymptomatic, but exertional dyspnea, angina, syncope, and sudden death can occur. Jerky pulse, systolic murmurs, and double apex beat are also common features. HOCM is associated with Friedreich’s ataxia and Wolff-Parkinson White. ECG findings include left ventricular hypertrophy, non-specific ST segment and T-wave abnormalities, and deep Q waves. Atrial fibrillation may occasionally be seen.

Infective endocarditis is most frequently caused by Streptococci viridans, which is commonly found in the oral cavity. This type of infection is often linked to patients with inadequate dental hygiene or those who have undergone dental procedures.

Aetiology of Infective Endocarditis

Infective endocarditis is a condition that affects patients with previously normal valves, rheumatic valve disease, prosthetic valves, congenital heart defects, intravenous drug users, and those who have recently undergone piercings. The strongest risk factor for developing infective endocarditis is a previous episode of the condition. The mitral valve is the most commonly affected valve.

The most common cause of infective endocarditis is Staphylococcus aureus, particularly in acute presentations and intravenous drug users. Historically, Streptococcus viridans was the most common cause, but this is no longer the case except in developing countries. Coagulase-negative Staphylococci such as Staphylococcus epidermidis are commonly found in indwelling lines and are the most common cause of endocarditis in patients following prosthetic valve surgery. Streptococcus bovis is associated with colorectal cancer, with the subtype Streptococcus gallolyticus being most linked to the condition.

Culture negative causes of infective endocarditis include prior antibiotic therapy, Coxiella burnetii, Bartonella, Brucella, and HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella). It is important to note that systemic lupus erythematosus and malignancy, specifically marantic endocarditis, can also cause non-infective endocarditis.

The anterior tibial artery is closely associated with the tibialis anterior muscle as it serves as one of the main arteries in the anterior compartment.

The anterior tibial artery starts opposite the lower border of the popliteus muscle and ends in front of the ankle, where it continues as the dorsalis pedis artery. As it descends, it runs along the interosseous membrane, the distal part of the tibia, and the front of the ankle joint. The artery passes between the tendons of the extensor digitorum and extensor hallucis longus muscles as it approaches the ankle. The deep peroneal nerve is closely related to the artery, lying anterior to the middle third of the vessel and lateral to it in the lower third.

Naftidrofuryl, a 5-HT2 receptor antagonist, can be used to treat peripheral vascular disease (PVD) and alleviate symptoms such as intermittent claudication. This medication works by causing vasodilation, which increases blood flow to areas of the body affected by PVD. On the other hand, drugs like doxazosin, an alpha 1 blocker, do not have a role in treating PVD. Beta blockers, which can worsen intermittent claudication by inducing vasoconstriction, are also not recommended for PVD treatment.

Managing Peripheral Arterial Disease

Peripheral arterial disease (PAD) is closely associated with smoking, and patients who still smoke should be provided with assistance to quit. Comorbidities such as hypertension, diabetes mellitus, and obesity should also be treated. All patients with established cardiovascular disease, including PAD, should be taking a statin, with atorvastatin 80 mg currently recommended. In 2010, NICE recommended clopidogrel as the first-line treatment for PAD patients over aspirin.

Exercise training has been shown to have significant benefits, and NICE recommends a supervised exercise program for all PAD patients before other interventions. Severe PAD or critical limb ischaemia may be treated with endovascular or surgical revascularization, with endovascular techniques typically used for short segment stenosis, aortic iliac disease, and high-risk patients. Surgical techniques are typically used for long segment lesions, multifocal lesions, lesions of the common femoral artery, and purely infrapopliteal disease. Amputation should be reserved for patients with critical limb ischaemia who are not suitable for other interventions such as angioplasty or bypass surgery.

Drugs licensed for use in PAD include naftidrofuryl oxalate, a vasodilator sometimes used for patients with a poor quality of life, and cilostazol, a phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects, which is not recommended by NICE.

As a result of the volume overload caused by heart failure, she will have a higher susceptibility to chest infections due to pulmonary edema and leg infections due to peripheral edema.

Chronic heart failure can be managed through drug treatment, according to updated guidelines issued by NICE in 2018. While loop diuretics are useful in managing fluid overload, they do not reduce mortality in the long term. The first-line treatment for all patients is a combination of an ACE-inhibitor and a beta-blocker, with clinical judgement used to determine which one to start first. Aldosterone antagonists are recommended as second-line treatment, but potassium levels should be monitored as both ACE inhibitors and aldosterone antagonists can cause hyperkalaemia. Third-line treatment should be initiated by a specialist and may include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin, and cardiac resynchronisation therapy. Other treatments include annual influenzae and one-off pneumococcal vaccines. Those with asplenia, splenic dysfunction, or chronic kidney disease may require a booster every 5 years.