At the level of L5, the common iliac veins join together to form the inferior vena cava (IVC).

Anatomy of the Inferior Vena Cava

The inferior vena cava (IVC) originates from the fifth lumbar vertebrae and is formed by the merging of the left and right common iliac veins. It passes to the right of the midline and receives drainage from paired segmental lumbar veins throughout its length. The right gonadal vein empties directly into the cava, while the left gonadal vein usually empties into the left renal vein. The renal veins and hepatic veins are the next major veins that drain into the IVC. The IVC pierces the central tendon of the diaphragm at the level of T8 and empties into the right atrium of the heart.

The IVC is related anteriorly to the small bowel, the first and third parts of the duodenum, the head of the pancreas, the liver and bile duct, the right common iliac artery, and the right gonadal artery. Posteriorly, it is related to the right renal artery, the right psoas muscle, the right sympathetic chain, and the coeliac ganglion.

The IVC is divided into different levels based on the veins that drain into it. At the level of T8, it receives drainage from the hepatic vein and inferior phrenic vein before piercing the diaphragm. At the level of L1, it receives drainage from the suprarenal veins and renal vein. At the level of L2, it receives drainage from the gonadal vein, and at the level of L1-5, it receives drainage from the lumbar veins. Finally, at the level of L5, the common iliac vein merges to form the IVC.

There are four factors that impact stroke volume: cardiac size, contractility, preload, and afterload. When someone has heart failure, their stroke volume decreases. If there is an increase in parasympathetic activation, it would lead to a reduction in contractility. Hypertension would increase afterload, which means the ventricle would have to work harder to pump blood into the aorta. If there is an increase in central venous pressure, it would lead to an increase in preload due to an increase in venous return.

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.

Aschoff bodies, which are granulomatous nodules consisting of giant cells around areas of fibrinoid necrosis, are pathognomonic for rheumatic heart disease. This condition is often a sequela of acute rheumatic heart fever, which occurs due to molecular mimicry where antibodies to the bacteria causing a pharyngeal infection react with the cardiac myocyte antigen resulting in valve destruction. The bacterial organism responsible for the pharyngeal infection leading to rheumatic heart disease is the group A β-hemolytic Streptococcus pyogenes.

In contrast, Staphylococcus aureus is a gram-positive, coagulase-positive bacteria that often causes acute bacterial endocarditis with large vegetations on previously normal cardiac valves. Bacterial endocarditis typically presents with a fever and new-onset murmur, and may be associated with other signs such as Roth spots, Osler nodes, Janeway lesions, and splinter hemorrhages. Staphylococcus epidermidis, on the other hand, is a gram-positive, coagulase-negative bacteria that often causes bacterial endocarditis on prosthetic valves. Streptococcus viridans, a gram-positive, α-hemolytic bacteria, typically causes subacute bacterial endocarditis in individuals with a diseased or previously abnormal valve, with smaller vegetations compared to acute bacterial endocarditis.

Rheumatic fever is a condition that occurs as a result of an immune response to a recent Streptococcus pyogenes infection, typically occurring 2-4 weeks after the initial infection. The pathogenesis of rheumatic fever involves the activation of the innate immune system, leading to antigen presentation to T cells. B and T cells then produce IgG and IgM antibodies, and CD4+ T cells are activated. This immune response is thought to be cross-reactive, mediated by molecular mimicry, where antibodies against M protein cross-react with myosin and the smooth muscle of arteries. This response leads to the clinical features of rheumatic fever, including Aschoff bodies, which are granulomatous nodules found in rheumatic heart fever.

To diagnose rheumatic fever, evidence of recent streptococcal infection must be present, along with 2 major criteria or 1 major criterion and 2 minor criteria. Major criteria include erythema marginatum, Sydenham’s chorea, polyarthritis, carditis and valvulitis, and subcutaneous nodules. Minor criteria include raised ESR or CRP, pyrexia, arthralgia, and prolonged PR interval.

Management of rheumatic fever involves antibiotics, typically oral penicillin V, as well as anti-inflammatories such as NSAIDs as first-line treatment. Any complications that develop, such as heart failure, should also be treated. It is important to diagnose and treat rheumatic fever promptly to prevent long-term complications such as rheumatic heart disease.

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 facial artery is the primary source of blood supply to the face, originating from the external carotid artery after the lingual artery. It follows a winding path and terminates as the angular artery at the inner corner of the eye.

The internal carotid artery provides blood to the front and middle parts of the brain, while the vertebral artery, a branch of the subclavian artery, supplies the spinal cord, cerebellum, and back part of the brain. The brachiocephalic artery supplies the right side of the head and arm, giving rise to the subclavian and common carotid arteries on the right side.

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.

Thiazides and thiazide-like drugs, such as indapamide, work by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule, which inhibits sodium reabsorption. Bendroflumethiazide is a thiazide diuretic that prevents the absorption of sodium and chloride by inhibiting the sodium-chloride transporter, resulting in water remaining in the tubule through osmosis. Mannitol is an osmotic diuretic that is used to reduce intracranial pressure after a head injury. Spironolactone is an aldosterone antagonist, while furosemide acts on the thick ascending loop of Henle to prevent the reabsorption of potassium, sodium, and chloride. Acetazolamide is a carbonic anhydrase inhibitor that is used to treat acute angle closure glaucoma.

Thiazide diuretics are medications that work by blocking the thiazide-sensitive Na+-Cl− symporter, which inhibits sodium reabsorption at the beginning of the distal convoluted tubule (DCT). This results in the loss of potassium as more sodium reaches the collecting ducts. While thiazide diuretics are useful in treating mild heart failure, loop diuretics are more effective in reducing overload. Bendroflumethiazide was previously used to manage hypertension, but recent NICE guidelines recommend other thiazide-like diuretics such as indapamide and chlorthalidone.

Common side effects of thiazide diuretics include dehydration, postural hypotension, and electrolyte imbalances such as hyponatremia, hypokalemia, and hypercalcemia. Other potential adverse effects include gout, impaired glucose tolerance, and impotence. Rare side effects may include thrombocytopenia, agranulocytosis, photosensitivity rash, and pancreatitis.

It is worth noting that while thiazide diuretics may cause hypercalcemia, they can also reduce the incidence of renal stones by decreasing urinary calcium excretion. According to current NICE guidelines, the management of hypertension involves the use of thiazide-like diuretics, along with other medications and lifestyle changes, to achieve optimal blood pressure control and reduce the risk of cardiovascular disease.

Troponin I is a cardiac biomarker that binds to actin, which holds the troponin-tropomyosin complex in place and regulates muscle contraction. It is the standard biomarker used in conjunction with ECGs and clinical findings to diagnose non-ST elevation myocardial infarction (NSTEMI). Troponin I is highly sensitive and specific for myocardial damage compared to other cardiac biomarkers. Troponin C, another subunit of troponin, plays a role in Ca2+-dependent regulation of muscle contraction and can also be used in the diagnosis of myocardial infarction, but it is less specific as it is found in both cardiac and skeletal muscle. Copeptin, an amino acid peptide, is released earlier than troponin during acute myocardial infarction but is not widely used in clinical practice and has no interaction with troponin. Myoglobin, an iron- and oxygen-binding protein found in both cardiac and skeletal muscle, has poor specificity for cardiac injury and is not involved in the troponin-tropomyosin complex.

Understanding Troponin: The Proteins Involved in Muscle Contraction

Troponin is a group of three proteins that play a crucial role in the contraction of skeletal and cardiac muscles. These proteins work together to regulate the interaction between actin and myosin, which is essential for muscle contraction. The three subunits of troponin are troponin C, troponin T, and troponin I.

Troponin C is responsible for binding to calcium ions, which triggers the contraction of muscle fibers. Troponin T binds to tropomyosin, forming a complex that helps regulate the interaction between actin and myosin. Finally, troponin I binds to actin, holding the troponin-tropomyosin complex in place and preventing muscle contraction when it is not needed.

Understanding the role of troponin is essential for understanding how muscles work and how they can be affected by various diseases and conditions. By regulating the interaction between actin and myosin, troponin plays a critical role in muscle contraction and is a key target for drugs used to treat conditions such as heart failure and skeletal muscle disorders.

The basilar artery is formed by the union of the vertebral arteries at the base of the pons, which is the most appropriate answer. If a patient has stenosis in their vertebral artery, it can increase the risk of a posterior circulation stroke by reducing perfusion to the brain or causing an arterial embolus.

The anterior aspect of the spinal cord is not the most appropriate answer as it is supplied by the anterior spinal arteries, which branch off the vertebral arteries and descend past the anterior aspect of the brainstem to supply the spinal cord’s anterior aspects.

The region anterior to the cavernous sinus is not the most appropriate answer. The internal carotid arteries pass anterior to the cavernous sinus before branching off to anastomose with the circle of Willis, mainly contributing to the anterior circulation of the brain.

The pontomesencephalic junction is not the most appropriate answer. The superior cerebellar arteries branch off from the distal basilar artery at the pontomesencephalic junction.

The Circle of Willis is an anastomosis formed by the internal carotid arteries and vertebral arteries on the bottom surface of the brain. It is divided into two halves and is made up of various arteries, including the anterior communicating artery, anterior cerebral artery, internal carotid artery, posterior communicating artery, and posterior cerebral arteries. The circle and its branches supply blood to important areas of the brain, such as the corpus striatum, internal capsule, diencephalon, and midbrain.

The vertebral arteries enter the cranial cavity through the foramen magnum and lie in the subarachnoid space. They then ascend on the anterior surface of the medulla oblongata and unite to form the basilar artery at the base of the pons. The basilar artery has several branches, including the anterior inferior cerebellar artery, labyrinthine artery, pontine arteries, superior cerebellar artery, and posterior cerebral artery.

The internal carotid arteries also have several branches, such as the posterior communicating artery, anterior cerebral artery, middle cerebral artery, and anterior choroid artery. These arteries supply blood to different parts of the brain, including the frontal, temporal, and parietal lobes. Overall, the Circle of Willis and its branches play a crucial role in providing oxygen and nutrients to the brain.

Severe hyponatraemia can occur when PPIs and thiazide diuretics are used together. The patient in question has recently experienced hyponatraemia, which is most likely caused by the combination of indapamide and omeprazole. It is probable that omeprazole was prescribed for his indigestion, while he is likely taking indapamide due to his history of congestive heart failure. It is important to note that the other options listed can cause hypernatraemia, not hyponatraemia.

Thiazide diuretics are medications that work by blocking the thiazide-sensitive Na+-Cl− symporter, which inhibits sodium reabsorption at the beginning of the distal convoluted tubule (DCT). This results in the loss of potassium as more sodium reaches the collecting ducts. While thiazide diuretics are useful in treating mild heart failure, loop diuretics are more effective in reducing overload. Bendroflumethiazide was previously used to manage hypertension, but recent NICE guidelines recommend other thiazide-like diuretics such as indapamide and chlorthalidone.

Common side effects of thiazide diuretics include dehydration, postural hypotension, and electrolyte imbalances such as hyponatremia, hypokalemia, and hypercalcemia. Other potential adverse effects include gout, impaired glucose tolerance, and impotence. Rare side effects may include thrombocytopenia, agranulocytosis, photosensitivity rash, and pancreatitis.

It is worth noting that while thiazide diuretics may cause hypercalcemia, they can also reduce the incidence of renal stones by decreasing urinary calcium excretion. According to current NICE guidelines, the management of hypertension involves the use of thiazide-like diuretics, along with other medications and lifestyle changes, to achieve optimal blood pressure control and reduce the risk of cardiovascular disease.

The Na+/K+ ATPase restores the resting potential.

The cardiac action potential does not involve slow sodium influx.

Phase 3 of repolarisation involves rapid potassium influx.

Phase 2 involves slow calcium influx.

Understanding the Cardiac Action Potential and Conduction Velocity

The cardiac action potential is a series of electrical events that occur in the heart during each heartbeat. It is responsible for the contraction of the heart muscle and the pumping of blood throughout the body. The action potential is divided into five phases, each with a specific mechanism. The first phase is rapid depolarization, which is caused by the influx of sodium ions. The second phase is early repolarization, which is caused by the efflux of potassium ions. The third phase is the plateau phase, which is caused by the slow influx of calcium ions. The fourth phase is final repolarization, which is caused by the efflux of potassium ions. The final phase is the restoration of ionic concentrations, which is achieved by the Na+/K+ ATPase pump.

Conduction velocity is the speed at which the electrical signal travels through the heart. The speed varies depending on the location of the signal. Atrial conduction spreads along ordinary atrial myocardial fibers at a speed of 1 m/sec. AV node conduction is much slower, at 0.05 m/sec. Ventricular conduction is the fastest in the heart, achieved by the large diameter of the Purkinje fibers, which can achieve velocities of 2-4 m/sec. This allows for a rapid and coordinated contraction of the ventricles, which is essential for the proper functioning of the heart. Understanding the cardiac action potential and conduction velocity is crucial for diagnosing and treating heart conditions.