Cardiology Flashcards

Question

What are the risk factors for aortic aneurysm:

Answer 1

The precise aetiology of AAA is complex and multifactorial, typically involving a combination of genetic, environmental, and lifestyle factors. Risk factors include: Being male Age 65 or over Smoking Hypertension Hypercholesterolaemia Family history of AAA Personal history of peripheral arterial disease or myocardial infarction COPD Connective tissue disorders (i.e. Marfan's)

Answer 2

Most AAAs remain asymptomatic for a long time and are often detected incidentally during radiological investigations for other abdominal or pelvic conditions. When symptomatic, the clinical presentation can vary: Pulsatile abdominal mass: The most classical finding on physical examination is a pulsatile, expansile abdominal mass. This is typically non-tender unless rupture is imminent. Approximately 3 in 5 AAA over 3 cm are palpable. This may also be associated with abdominal bruit. Abdominal or back pain: Pain is usually a late manifestation, suggesting rapid expansion or impending rupture of the aneurysm. It is typically severe, constant, and localised in the abdomen or lower back, often radiating to the flank or groin. There can also be testicular pain if the blood supply to this area is compromised by rupture 90% of aortic aneurysms are infrarenal (originating below the renal arteries) In advanced cases, a large aneurysm may cause symptoms due to compression or displacement of adjacent structures, resulting in early satiety, nausea, weight loss, altered bowel habits, or deep venous thrombosis (due to compression of the inferior vena cava).

Answer 3

Offered to men at age 65 Consists of an abdominal ultrasound Follow-up screening depends on the size of the aneurysm: Small AAA (3-4.4cm): Yearly repeat ultrasound is offered. Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered. Large AAA (>5.5cm): Surgical intervention is generally recommended.

Answer 4

Once an abdominal aortic aneurysm has been detected, further investigations may be required, including: Computed Tomography (CT) Angiography: CT angiography is the imaging modality of choice for preoperative evaluation, determining the size, shape, and extent of the AAA, and planning the surgical approach. It provides detailed information about the aneurysm's relationship to branch arteries and the potential presence of thrombus or calcification within the aneurysm. It is also the preferred imaging modality in suspected rupture cases due to its rapid acquisition time and high sensitivity and specificity. Magnetic Resonance Angiography (MRA): MRA is an alternative to CT angiography for patients who cannot be exposed to ionizing radiation or iodinated contrast medium. MRA can provide high-resolution images of the AAA and surrounding structures but is less readily available and takes more time than CT. Blood tests: While there is no specific blood test to diagnose AAA, complete blood count, coagulation profile, renal function tests, and electrolyte levels are typically evaluated prior to surgery. Finally, regular surveillance of known AAAs is critical. The frequency of surveillance depends on the size of the aneurysm, with smaller aneurysms monitored less frequently and larger ones requiring closer observation.

Answer 5

Management of abdominal aortic aneurysms may be through conservative measures such as: Surveillance: This is typically offered for smaller aneurysms with a lower risk of rupture. It is very rare for smaller AAA to rupture. Small AAA (3-4.4cm): Yearly repeat ultrasound is offered. Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered. Large AAA (>5.5cm) require referral to vascular surgery to be seen within 2 weeks of diagnosis. Measures to reduce the risk of rupture: Referral to a stop-smoking service Management of hypertension

Answer 6

Elective repair of AAA may be considered for individuals with AAA who meet the following criteria: They are symptomatic Their AAA has grown by more than 1 cm in 1 year and is larger than 4 cm Their AAA is 5.5 cm or larger Two primary surgical options are available for managing AAA: Open surgical repair Typically best for men under age 70. However, it can be contraindicated by anaesthetic risks, medical comorbidities or anatomic difficulties (i.e. horseshoe kidney, stoma, numerous previous surgeries resulting in significant adhesions) Endovascular Aneurysm Repair (EVAR) A stent graft is inserted through the femoral arteries into the aorta, where it channels blood flow into the iliac arteries. The surrounding aneurysm then becomes thrombosed around the graft. EVAR has reduced perioperative deaths and is associated with shorter hospital stays. However, it has an overall higher long-term morbidity and mortality than open repair.

Answer 7

Rupture AAA rupture is a surgical emergency. Abdominal aortic aneurysms are more likely to rupture in women than men but are more common in men and such account for more presentations in men. AAA tend to enlarge over time and with increasing size, the risk of rupture increases. Embolization Rarely distal embolisation from mural thrombus can lead to symptoms related to ischemia, most commonly affecting the distal extremities, such as blue toe syndrome. Open Repair-Related Complications Those undergoing open surgical repair of an AAA have risks including: Spinal cord ischaemia Anastomotic pseudoaneurysm Graft infection Death (mortality during elective repair is reported to be 5% of men and 7% of women) EVAR-Related Complications Patients who have undergone EVAR may require surveillance for EVAR-related complications. Endoleak Defined as the presence of blood flow within the aneurysm sac but outside the EVAR graft Contrast-enhanced CT angiography, or contrast-enhanced ultrasound if CT is contraindicated, is used to assess for endoleak. They can be repaired using open, endovascular or percutaneous intervention for endoleak Post-implantation syndrome Cytokine release due to EVAR can cause fever, back pain and feeling generally unwell following EVAR.

Answer 8

Abdominal aortic aneurysms will continue to increase in diameter, with the ultimate outcome being rupture. However, many individuals with AAA do not rupture during their lifetimes. The rupture of AAA is fatal for many individuals. For those who have had their AAA electively repaired before rupture, those who have had an open surgical repair tend to fare better with reduced complications and overall improved survival.

Answer 9

Abdominal aortic aneurysms most frequently occur below the level of the renal arteries (infrarenal region).

Answer 10

Take an A to E approach and put out a medical emergency call; patients may require intubation due to reduced levels of consciousness Ensure patients where there is a strong suspicion of a ruptured AAA are urgently transferred to a specialist vascular centre In some cases this may not be appropriate and a palliative approach to management may be taken in conversation with the patient and their family (e.g. patients over the age of 85 with significant comorbidities) Ensure wide-bore IV access is obtained Keep patients nil by mouth Medical: Resuscitation with IV fluids and blood, targeting a systolic blood pressure of 90-120mmHg Inotropes may be required; these patients generally have a poor prognosis Ensure adequate analgesia is given for pain Surgical: Emergency surgery is required to repair the rupture - this may be with endovascular aneurysm repair (EVAR) or open surgery

Answer 11

Dissection occurs when a tear in the tunica intima of the aorta creates a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta.

Answer 12

Hypertension Connective tissue disease e.g. Marfan's syndrome Valvular heart disease Cocaine/amphetamine use

Answer 13

Stanford Type A: Involves the ascending aorta, arch of the aorta Stanford Type B: Involves the descending aorta.

Answer 14

Usually presents in men over the age of 50 Sudden onset 'tearing' chest pain or interscapular pain radiating to the back. It can also present with (depending on how far the dissection extends): Bowel/limb ischaemia Renal failure Syncope

Answer 15

Radio-radial delay Radio-femoral delay Blood pressure differential between arms of >20mmHg

Answer 16

CT angiogram is used to diagnose dissection but other investigations can suggest the diagnosis and/or its complications: ECG - May show ischaemia in specific territories if dissection extends into coronary arteries. Echocardiogram - May demonstrate pericardial effusion and aortic valve involvement. Chest x-ray - May show a widened mediastinum Bloods: Troponin may be raised D-dimer may be positive

Answer 17

Prompt diagnosis and treatment is required as rupture carries an 80% mortality rate.

Answer 18

Resuscitation if necessary Cardiac monitoring Strict blood pressure control (e.g. IV metoprolol infusion)

Answer 19

Depends on the type of dissection Type A: Usually requires surgical management (e.g. aortic graft) Type B: Normally managed conservatively with blood pressure control. If there is evidence of end organ damage then endovascular/open repair may be performed. In haemodynamically stable patients with confirmed Stanford type B aortic dissection initial management is with intravenous beta blockers (to prevent propagation of the dissection) and opioid analgesia

Answer 20

Death due to internal haemorrhage Rupture End organ damage (renal or cardiac failure) Cardiac tamponade Stroke Limb ischaemia Mesenteric ischaemia

Answer 21

A deep vein thrombosis (DVT) is a blood clot or thrombus that blocks a deep vein, commonly in the legs or pelvis.

Answer 22

Thrombophilia Hormonal (COCP, pregnancy and the postpartum period, HRT) Relatives (family history of VTE) Older age (>60) Malignancy Bone fractures Obesity Smoking Immobilisation (long-distance travel, recent surgery or trauma) Sickness (e.g. acute infection, dehydration)

Answer 23

Unilateral erythema, warmth, swelling and pain in the affected area Pain on palpation of deep veins Distention of superficial veins Difference in calf circumference if the leg is affected This should be measured 10cm below the tibial tuberosity 3cm difference between the legs is significant

Answer 24

The two-level DVT Wells score is used to risk-stratify patients into patients likely or unlikely to have a DVT as follows: Add one point for each of: Active cancer (treatment within the last 6 months or palliative) Paralysis, paresis, or recent plaster immobilisation of the legs Recently bedridden for 3 days or more, or major surgery within the last 12 weeks Localised tenderness along the distribution of the deep venous system Entire leg is swollen. Calf swelling by more than 3 cm compared with the other leg Pitting oedema confined to the symptomatic leg Collateral superficial veins Personal history of DVT Minus 2 points if an alternative cause is considered at least as likely as a DVT. If the score is 2 or more: DVT is likely and an ultrasound doppler of the proximal leg veins should be done within 4 hours If this isn't possible within 4 hours, do a D-dimer test, start interim anticoagulation and arrange the doppler to happen within 24 hours If the score is 1 or less: DVT is unlikely and a D-dimer should be sent If the results cannot be obtained within 4 hours, offer interim anticoagulation whilst awaiting results If the D-dimer is positive, do an ultrasound doppler of the proximal leg veins If it is negative, anticoagulation should be stopped if it was started and an alternative diagnosis considered Baseline blood tests should be taken when anticoagulation is started, including a FBC, U&Es, LFTs and a coagulation screen.

Answer 25

First-line anticoagulant medications are DOACs (e.g. apixaban, rivaroxaban) If these are not suitable, second-line options include low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban, or LMWH bridging with warfarin (with a target INR of 2.5) Treatment duration should be at least 3 months for all patients, and 3-6 months for people with active cancer At this point the risk of VTE recurrence should be weighed against the risks of continuing anticoagulation to make a decision about whether to continue In cases of provoked DVTs (where a major transient risk factor is identifiable e.g. surgery), anticoagulation would usually be stopped at 3 months In cases of unprovoked DVTs, consider testing for thrombophilia with antiphospholipid antibodies in patients who are stopping anticoagulation Patients with unprovoked DVTs should be reviewed with baseline blood tests and an examination to investigate the possibility of an undiagnosed cancer - further investigations should be guided by the patient's signs or symptoms

Answer 26

Pulmonary embolism Post-thrombotic syndrome (chronic venous hypertension post-DVT that may cause significant morbidity) Complications of anticoagulation e.g. gastrointestinal bleeding

Answer 27

Generally speaking surgical patients should receive both mechanical and pharmacological VTE prophylaxis after surgery. Mechanical prophylaxis can start immediately after surgery (assuming the surgery is not on the leg) and pharmacological prophylaxis should start 12 hours later to reduce the risk of bleeding. Please note that although this is what is suggested by guidance, many surgeons have personal preferences when it comes to VTE prophylaxis.

Answer 28

A 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg.

Answer 29

Primary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation. Although the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.

Answer 30

Hypertension can be classified according to how high a patient's blood pressure is. Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg

Answer 31

Hypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension.

Answer 32

Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. 1st line: ABPM or home blood pressure monitoring if ABPM is not tolerated or declined. Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). Urine dip and albumin:creatinine level Blood glucose, lipids and renal function Fundoscopy for evidence of hypertensive retinopathy ECG: look for evidence of LV hypertrophy N.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). N.B. Referral for same-day specialist assessment should be arranged for people with: Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI).

Answer 33

Step 1: ACE-inhibitor (e.g. Ramipril) if <=55 years old DHP-Calcium Channel Blocker (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan) Step 2: (If maximal dose of Step 1 has failed or not tolerated) Combine CCB and ACE-I/ARB Step 3: (If maximal doses of Step 2 has failed or not tolerated) Add thiazide-like diuretic (e.g. Indapamide) Step 4: Resistant Hypertension If blood potassium <4.5mmol/L then add spironolactone If >4.5mmol/L increase thiazide-like diuretic dose Other options at this point if the potassium is >4.5mmol/L include: Alpha blocker (e.g. Doxazosin) Beta blocker (e.g. Atenolol) Referral to cardiology for further advice

Answer 34

Weight loss Healthy diet (reduce salt and saturated fats) Reduce alcohol and caffeine Reduce stress Stop smoking

Answer 35

Age <80 ABPM target <135/85 Age >80 ABPM target <145/85 (due to risk of postural drop and falls) T1DM with end-organ damage <130/80

Answer 36

Increased risk of morbidity and mortality from all causes Coronary artery disease Heart failure Renal failure Stroke Peripheral vascular disease

Answer 37

ACE inhibitors such as ramipril can sometimes cause angioedema as they lead to a build-up of bradykinin. This can present as swelling of the lips and the throat and, in severe cases, difficulty breathing.

Answer 38

Secondary hypertension is the persistent elevation of blood pressure due to an identifiable cause.

Answer 39

Primary intrinsic renal disease: most common cause of secondary hypertension. Chronic kidney disease: complex pathophysiology as hypertension itself is a leading risk factor for CKD. Glomerulonephritis Diabetic nephropathy Polycystic kidney disease Chronic pyelonephritis Vascular disease: Renal artery stenosis: unilateral or bilateral stenosis of renal arteries. Older patients this can be attributed to atherosclerosis, younger female patients this may be due to fibromuscular hyperplasia. Aortic coarctation: narrowing of the aortic arch near the remnants of the ligament arteriosum forces the left ventricle to pump harder leading to hypertension. More common in children or adolescents. Vasculitides including Takaysau arteritis. Endocrine disease: Conn's disease: primary hyperaldosteronism due to the overproduction of aldosterone by the adrenal glands. Blood tests reveal a hypokalaemia and hypernatraemia. Patients may present with tetany, muscle weakness, oliguria or nocturia. Cushing's syndrome: may be primary or secondary and is due to the excess of cortisol. Increase cortisol leads to increased absorption of sodium and increases vascular sensitivity to catecholamines and angiotensin II driving hypertension. Phaeochromocytoma: rare, primary adrenal tumour producing catecholamines that drives hypertension. Presents with a classical triad of sweating, headaches and tachycardia. It is diagnosed with 24 hour urinary or plasma metanephrines. Drugs: many drugs are indicated in secondary hypertension including NSAIDs, corticosteroids (Cushing's syndrome), mineralocorticoids, immunosuppressants (e.g. ciclosporin), atypical antipsychotics (clozapine or olanzapine) or recreational drugs (cocaine, amphetamines etc.).

Answer 40

Occipital pulsatile headache +/- visual disturbance Bilateral retinal haemmorhages +/- exudates and papilloedema on fundoscopy Chest pain +/- signs of heart failure Acute-onset confusion

Answer 41

Intrinsic renal disease: ballotable kidneys, fingerpricks for glucose testing, signs and symptoms of renal failure. Coarctation of the aorta: systolic murmur loudest over scapulae, radio-femoral delay or radio-radial delay (depends on site of coarctation). Cushing's syndrome: moon facies, abdominal striae, buffalow hump, thin skin etc. Conn's syndrome: weakness, tetany, cramps, or oliguria. Phaechromocytoma: classical triad of episodic headaches, sweating and tachycardial.

Answer 42

A few clinical clues may suggest secondary hypertension including: Younger patients (<40 years old) with few comorbidities Severe hypertension or hypertension resistant to treatment New hypertension in patients with previously stable or low readings Hypertension with associated symptoms or electrolyte disturbances It is important to refer patients who you think have secondary hypertension. Specialist centres often prefer that these patients are not started on antihypertensives as this may interfere with further investigation.

Answer 43

Bedside 24h ABPM: for the definitive diagnosis of hypertension. Urine dipstick: evidence of glomerulonephritis, diabetic nephropathy or CKD. Urinary metanephrines: diagnosis of phaeochromocytoma. ECG: look for evidence of LVH. Bloods Dyselectrolytaemia: hypokalaemic and hypernatraemic suggests Conn's. Renal function: may suggest CKD or other primary renal pathology. Raised urea and creatinine if acute kidney injury. Endocrinological: Early morning cortisol, 24h urinary cortisole or dexamethasone suppression testing: Cushing's syndrome. Plasma or urinary metanephrines: phaeochromocytoma. Aldosterone:renin ratio: Conn's disease. Imaging Renal USS: shrunken kidneys (CKD), large, cystic kidneys (PCKD), or narrowing of renal arteries (renal artery stenosis). Renal biopsy: intrinsic kidney disease. Further imaging including CT CAP, MRI brain, or MR aortogram if looking for the weirder and wonderful causes of secondary hypertension.

Answer 44

Complications of secondary hypertension include all the same complications of primary hypertension (including stroke, aneurysm formation, heart failure, renal failure) alongside complications of the underlying disease. Secondary hypertension often leads to resistant hypertension unless the underlying disease is treated.

Answer 45

Gangrene occurs when a tissue receives insufficient perfusion and dies. It can be considered to be wet or dry.

Answer 46

Wet gangrene is also referred to as infectious gangrene. It includes necrotising fasciitis (infection of the subcutaneous fascia and fat), gas gangrene (caused by Clostridium), and gangrenous cellulitis (typically found in immunocompromised individuals).

Answer 47

Dry gangrene is an ischaemic type of gangrene that occurs secondary to chronically reduced blood flow. It causes tissues to become cold, dry and die.

Answer 48

The exact incidence is unknown, but wet gangrene is less common than dry gangrene. It is often seen in immunocompromised patients, those with diabetes mellitus, and individuals with peripheral vascular disease.

Answer 49

The incidence is higher in the elderly, smokers, and individuals with peripheral arterial disease or diabetes mellitus. It's estimated that about 10% of people with diabetes will have some form of gangrene during their lifetime.

Answer 50

This condition is commonly caused by an infectious agent. Necrotising fasciitis is typically due to Streptococcus pyogenes or other bacteria. Gas gangrene is most commonly caused by Clostridium perfringens. These bacteria release exotoxins, which cause clotting of blood vessels, death of muscle and enable the proliferation of bacteria. The gas produced causes the spreading of muscular fibres. Necrotising fasciitis can be subdivided into: Type I: Polymicrobial Polymicrobial meaning it may involve gram-positive cocci, gram-negative rods and/or anaerobes Most common form. Risk factors include peripheral vascular disease and diabetes mellitus. Type II: Group A beta haemolytic streptococci Type III: Marine Fibrio vulnificus Type IV: Fungal

Answer 51

Immunocompromise Diabetes mellitus Older age Trauma to the skin (which enables entry of the microbial into the tissue)

Answer 52

This type of gangrene is often secondary to chronically reduced blood flow. Causes include: Peripheral arterial disease (i.e. atherosclerosis) Risk factors are the same as other cardiovascular risk factors (i.e. smoking, diabetes mellitus, Thrombosis, often related to vasculitis and hypercoagulable states Vasospasm, often linked to cocaine use or Raynaud's phenomenon. Extreme cold injury (frostbite) Embolism (i.e. cardiogenic or septic) Venous insufficiency Prolonged venous insufficiency can result in high pressure and occlusion within the veins

Answer 53

Patients typically present with symptoms of fever and sepsis. Starts as swelling and erythema, but can progress to discharge and the area may darken/become black. There may be bullae formation. The necrotic area is poorly demarcated from the surrounding tissue. There may be a foul-smelling odour. In gas gangrene, there is subcutaneous crepitus and anaesthesia.

Answer 54

Dry gangrene shows a well-demarcated necrotic area without signs of infection. The area is often cold and pale. Auto-amputation often occurs in these cases.

Answer 55

Laboratory Investigations: Full blood count, inflammatory markers (CRP, ESR), blood cultures to identify the causative organism, and lactic acid levels to assess the severity. Imaging: X-ray, ultrasound, or CT scan to assess the extent of the disease and look for gas within the tissue. Tissue Biopsy: To confirm diagnosis and identify the causative organism.

Answer 56

Doppler ultrasound: This can be used to determine ABI and degree of peripheral arterial disease. Laboratory Investigations: Full blood count, inflammatory markers (CRP, ESR) to rule out wet gangrene, glucose level to evaluate for diabetes, and coagulation profile in case of suspected hypercoagulability. Imaging: Doppler ultrasound or angiography to assess blood flow and locate the site of blockage. Tissue Biopsy: Not typically needed but can confirm diagnosis if uncertain.

Answer 57

Management requires: Analgesia Broad-spectrum intravenous antibiotics Surgical debridement: Excision of removals of necrotic tissue. Amputation may be done in severe cases

Answer 58

Surgical debridement and restoration of blood supply to the affected area Restoration of perfusion may be achieved through embolectomy, thrombectomy, thrombolysis or bypass surgery. Amputation may be required depending on the severity and extent of the necrosis. Hyperbaric oxygen is sometimes used This delivers above-normal levels of oxygen to the patient. This oxygen is then delivered to the affected area and encourages more rapid healing.

Answer 59

Antiplatelet agents for those with peripheral arterial disease Lipid-lowering therapy (i.e. statins) Smoking cessation Diet and exercise advice

Answer 60

Gangrene can result in: Conversion to wet gangrene Dry gangrene can convert to wet gangrene if the tissue becomes infected. Sepsis Risk of sepsis is higher in wet gangrene due to the underlying infectious aetiology Amputation

Answer 61

Aortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body.

Answer 62

Normally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.

Answer 63

Senile calcification: most common cause in those >65y/o. Congenital bicuspid valve: most common cause in those <65y/o. Rheumatic heart disease William's syndrome: supravalvular stenosis

Answer 64

The symptoms of severe AS can be remembered by the mnemonic 'SAD'. Syncope Angina Dyspnoea Other symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death.

Answer 65

Slow-rising carotid pulse Narrow pulse pressure Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy) Ejection systolic murmur Heard best at the second intercostal space on the right Can be described as "harsh" Radiates to the carotids Soft S2 heart sound: absent S2 corresponds with severity Ejection click may be heard in some cases (early systolic)

Answer 66

Bedside ECG: LVH, left axis deviation, and poor R wave progreesion. Imaging CXR: cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible. Echocardiogram: definitive diagnosis. Definitive diagnosis of aortic stenosis. Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters: Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring) Valve area < 1.0cm x2 Aortic jet velocity >4 m/s Exercise testing: may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS. Cardiac MRI: can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification.

Answer 67

Aortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body.

Answer 68

Normally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.

Answer 69

Senile calcification: most common cause in those >65y/o. Congenital bicuspid valve: most common cause in those <65y/o. Rheumatic heart disease William's syndrome: supravalvular stenosis

Answer 70

The symptoms of severe AS can be remembered by the mnemonic 'SAD'. Syncope Angina Dyspnoea Other symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death.

Answer 71

Slow-rising carotid pulse Narrow pulse pressure Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy) crescendo-decrescendo Ejection systolic murmur Heard best at the second intercostal space on the right Can be described as "harsh" Radiates to the carotids Soft S2 heart sound: absent S2 corresponds with severity Ejection click may be heard in some cases (early systolic)

Answer 72

Bedside ECG: LVH, left axis deviation, and poor R wave progreesion. Imaging CXR: cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible. Echocardiogram: definitive diagnosis. Definitive diagnosis of aortic stenosis. Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters: Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring) Valve area < 1.0cm x2 Aortic jet velocity >4 m/s Exercise testing: may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS. Cardiac MRI: can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification.

Answer 73

Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all. Patients who do not meet the criteria for intervention should have regular echocardiography follow-up, with severe AS being monitored every 6 months, mild-to-moderate AS monitored yearly, and younger patients can be monitored every two to three years.

Answer 74

Medical management of AS involves symptom management of left ventricular failure with diuretics and optimising heart failure medications with beta-blockers and ACE-I etc. Isolated medical therapy should only be used in those who are not suitable for intervention.

Answer 75

Intervention in AS is indicated in the following patients: All patients with symptomatic aortic stenosis Asymptomatic patients with a left ventricular ejection fraction (LVEF) < 55% Asymptomatic patients with an LVEF > 50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing Asymptomatic patients with an LVEF > 50% who have the following risk factors Aortic valve peak velocity > 5m/s x2 Severe calcification and peak velocity progression >= 0.3m/s x2 Markedly elevated BNP levels (more than twice upper limit) without other explanation Severe pulmonary hypertension (pulmonary artery systolic pressure > 60mmHg) Aortic valve area less than 0.6 cm2 Choices of intervention are transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR). TAVI is favoured with patients with severe comorbidities, previous heart surgery, frailty, restricted mobility, and those older than 80 years of age. SAVR is favoured for patients who are low risk and younger.

Answer 76

Aortic stenosis if left untreated can lead to LV failure. It is also implicated in sudden cardiac death.

Answer 77

It can be defined as an irregular aortic leaflet thickening and focal increased echogenicity, but is distinguished from aortic stenosis because there is no impairment of valve leaflet excursion, and peak doppler velocities are normal or only minimally elevated (markedly elevated in stenosis) Aortic sclerosis is an asymptomatic condition that can be incidentally revealed through physical examination or via echocardiogram. It is caused by age-related senile degeneration of the valve.

Answer 78

Classic findings are an ejection systolic murmur that does not radiate to the carotids, there is normal S2, pulse character and volume.

Answer 79

A loud fourth heart sound is due to a rigid ventricle. In the above case, stenosis of the aortic valve has resulted in left ventricular hypertrophy and likely failure. This is secondary to increased afterload.

Answer 80

Aortic regurgitation (AR), or aortic insufficiency (AI), occurs when the aortic valve fails to prevent blood from leaking back across the valve during diastole.

Answer 81

Older populations M>F congenital aortic valve/root defects (bicuspid aortic valve, Marfan's syndrome)

Answer 82

Normally, the aortic valve closes tightly at the end of systole (S2) and prevents blood from flowing back into the left ventricle. In aortic regurgitation, the valve leaflets fail to close tightly due to valve disease or the aorta around the valve has dilated which allows the backflow of blood across the valve and into the left ventricle.

Answer 83

Infective endocarditis: infective process leads to valve destruction and leaflet perforation. Most common acute cause of acute AR. Aortic dissection: primarily causes regurgitation due to dilatation of aortic root (functional AR). Traumatic rupture of valve leaflets: blunt chest trauma or deceleration injury can disrupt valve leaflets leading to valve incompetence. Iatrogenic causes: balloon valvotomy or TAVI. Non-native aortic valve regurgitation: valve replacements can be complicated by acute AR. Tissue prosthetic valves may degenerated and mechanical valves may thrombose causing incomplete closure of the valve or paravalvular leak.

Answer 84

Rheumatic heart disease - most common in developing countries. Age-related calcification Congenital bicuspid aortic valve Connective tissue disorders: Marfan's syndrome, Ehler's Danlos Infective endocarditits Rheumatological conditions: rheumatoid arthritis, ankylosing spondylitis, APLS, giant cell arteritis,

Answer 85

Sudden cardiovascular collapse Acute pulmonary oedema - shortness of breath, sweating, pallor, peripherally vasoconstricted

Answer 86

More insidious, slower onset Exertional dyspnoea, orthopnoea, PND Stable angina even in absence of coronary artery disease (due to reduction in diastolic coronary perfusion)

Answer 87

De Quincke's sign - nail bed pulsation Waterhammer pulse De Musset's sign - head hobbing Corrigan's sign - dancing carotids Muller's sign - pulsation of the uvula Traube's sign - pistol shot (bruit heard on auscultation of femoral pulse) Auscultation: *Early diastolic murmur - heard best at the aortic region, leaning forward and on expiration. Soft S1 and occasional ejection flow murmur.

Answer 88

Observations: widened pulse pressure. Throat swab for group A strep. ECG: LVH and p mitrale in chronic AR. Bloods Inflammatory markers and blood cultures - infective endocarditis. Auto-antibody screen - rheumatological causes. Imaging: Transthoracic echocardiogram - definitive diagnosis. Cardiac MRI - indicated in those with moderate-to-severe AR with suboptimal TTE findings. Invasive cardiac catheterisation - detailed information on AR severity, LV function and size, pressures and valve gradient, and dimensions of aortic root.

Answer 89

Used to slow the rate of aortic root dilatation in high risk patients (e.g. Marfan's or bicuspid aortic valve). Beta blockers +/- losartan are used to lower systolic blood pressure. Patients with severe asymptomatic AR should be seen and monitored annually. If LV diameters or systolic function change significantly, follow-up should be 3-6 monthly.

Answer 90

Surgical intervention is indicated in: Symptomatic AR. Asymptomatic AR with: poor LVEF (<=50%), LV and diastolic diameter >70mm or LV end-systolic diameter >50mm. Infective endocarditits refractory to medical therapy. Significant enlargement of ascending aorta.

Answer 91

Acute AR can lead to cardiovascular collapse and de novo acute heart failure. Chronic AR that is not treated will lead to chronic heart failure with predominantly left ventricular symptoms (pulmonary oedema).

Answer 92

In aortic regurgitation, blood flows back into the left ventricle (LV) during diastole, leading to volume overload. This results in an elevated LVEDP, which causes the mitral valve to close earlier and less forcefully during the start of systole. The early closure of the mitral valve diminishes the intensity of the S1 sound.

Answer 93

Arterial thrombosis refers to the formation of a blood clot (thrombus) in an artery, which can lead to serious health complications.

Answer 94

It is primarily categorised into two types: coronary thrombosis, affecting the arteries that supply the heart, and cerebral thrombosis, impacting those supplying the brain.

Answer 95

Pathogenesis involves endothelial injury, stasis or turbulence of blood flow, and hypercoagulability - collectively known as Virchow's triad.

Answer 96

The clinical presentation varies depending on the affected site. Coronary thrombosis may manifest as myocardial infarction, while cerebral thrombosis can lead to stroke symptoms.

Answer 97

Diagnosis typically involves imaging techniques such as angiography or ultrasound alongside laboratory tests for coagulation parameters.

Answer 98

Management strategies encompass anticoagulant and antiplatelet therapy to prevent further clot formation and propagation. In some cases, surgical interventions like thrombectomy or angioplasty may be necessary. Secondary prevention includes addressing modifiable risk factors such as hypertension, hyperlipidaemia, smoking cessation and diabetes control. - Thrombolysis- what’s this? dissolve blood clot - Embolectomy- what’s this? operation to remove clot - Angioplasty- what’s this? operation to widen the affected artery - CABG- what’s this? surgery to divert blood around the blocked artery

Answer 99

Atherosclerosis - Atrial fibrillation - Antiphospholipid syndrome

Answer 100

Any break in the skin that is located beneath the knee and has lasted longer than 2 weeks without healing is defined as an ulcer by NICE. Arterial ulcers, also known as ischaemic ulcers, are open sores that develop due to insufficient blood supply, commonly associated with peripheral arterial disease.

Answer 101

Arterial ulcers are believed to account for 10% of ulcers in the UK, whilst venous ulcers account for 80%. The majority of the remaining 10% are mixed (i.e. both arterial and venous in aetiology) and other more rare causes of ulcers. These ulcers are particularly common among elderly populations and are more common in men.

Answer 102

Arterial ulcers are primarily caused by peripheral arterial disease, typically due to atherosclerosis, leading to inadequate blood supply to the distal extremities. When a minor injury occurs to the limb, there is poor perfusion, and the injury is unable to heal, resulting in the formation of an ulcer. For individuals with more advanced arterial disease, the perfusion may be sufficiently poor to cause cellular death and ulcer formation without a preceding trauma to the leg. This may also occur as a result of rupture of an atherosclerotic plaque, which produces an embolism and occlusion of a downstream artery, ischaemia to the portion of tissue and the formation of an ulcer.

Answer 103

Smoking Hypertension Coronary artery disease Personal history of stroke or TIA Diabetes mellitus Peripheral arterial disease Obesity Being male

Answer 104

Occur distally (e.g. at the heel or toe tips) Are small and deep Have a well-defined, 'punched out' margin Limited exudate Granulated base, which does not bleed much on debridement They are typically painful with pain at rest The pain is often worse at night and relieved by dangling legs out of the bed Associated with other features of peripheral arterial disease: Weak distal pulses and cool temperature of extremities The surrounding skin may be shiny and pale, with prolonged capillary refill time. Hair atrophy Nail dystrophy Claudication pain: Pain in buttocks and calves occurring on exertion, and resolving with rest. This progresses to rest pain with increasing severity of peripheral arterial disease.

Answer 105

Physical examination Capillary refill time will be prolonged Buerger test: With the patient lying supine, their leg is raised 45 degrees for 1 minute and then lowered. The test is considered to be positive if the leg appears white on elevation and then hyperaemic when lowered. Ankle-brachial pressure index (ABPI) Calculated by measuring ankle blood pressure using a hand-held Doppler and dividing this by the brachial blood pressure < 0.8: indicates peripheral arterial disease 0.5-0.8: indicates significant peripheral vascular disease <0.5: indicates severe arterial disease 1.3: may indicate stiff arteries due to calcification. ABPI may be falsely high in diabetics. Doppler ultrasound: To assess the patency of the arteries and veins. In some cases, angiography might be needed to evaluate the extent of arterial blockage. Skin swabs are done when there are associated skins of infection, and should not be done routinely.

Answer 106

Lifestyle modification Smoking cessation advice should be provided. Wound care: The ulcer should be cleaned and properly dressed regularly. Management of comorbidities (i.e. diabetes and blood pressure management) Medications Antiplatelet drugs (such as aspirin or clopidogrel) Statins to reduce cholesterol levels Surgical interventions: Skin grafting to repair the damaged skin Angioplasty: Re-opening of the stenosed vessels to reperfuse the tissue to enable the ulcer to heal. Bypass grafting: The stenosed vessel is bypassed using a graft to enable re-perfusion of the ischaemic tissue.

Answer 107

Non-healing Recurrence Amputation Severe, non-healing ulcers may require amputation.

Answer 108

Intermittent claudication - cramping pain, discomfort, or fatigue in the muscles of the legs (most commonly the calves), that occurs during exercise or walking and is relieved by rest

Answer 109

hair loss and shiny appearance of the skin

Answer 110

Cardiac arrest is a severe medical emergency characterised by the cessation of functional circulation due to failure in the heart's pumping action

Answer 111

The condition can be categorised as asystole, pulseless electrical activity (PEA), ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT).

Answer 112

Recognition of cardiac arrest often relies on the absence of pulse, consciousness, and normal breathing. Resuscitation efforts should commence immediately with cardiopulmonary resuscitation (CPR) and early defibrillation if VF or pVT is identified.

Answer 113

Hypoxia Hypovolaemia Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders Hypothermia

Answer 114

Thrombosis (coronary or pulmonary) Tension pneumothorax Tamponade - cardiac Toxins

Answer 115

into those with: 'shockable' rhythms: ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT) 'non-shockable' rhythms: asystole/pulseless-electrical activity (asystole/PEA)

Answer 116

Major points include: chest compressions the ratio of chest compressions to ventilation is 30:2 chest compressions are now continued while a defibrillator is charged defibrillation a single shock for VF/pulseless VT followed by 2 minutes of CPR if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend 'up to three quick successive (stacked) shocks', rather than 1 shock followed by CPR drug delivery IV access should be attempted and is first-line if IV access cannot be achieved then drugs should be given via the intraosseous route (IO) delivery of drugs via a tracheal tube is no longer recommended adrenaline adrenaline 1 mg as soon as possible for non-shockable rhythms during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock repeat adrenaline 1mg every 3-5 minutes whilst ALS continues amiodarone amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered. a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead thrombolytic drugs should be considered if a pulmonary embolus is suspected if given, CPR should be continued for an extended period of 60-90 minutes

Answer 117

- Ventricular fibrillation (VF) → shockable rhythm - Pulseless ventricular tachycardia (VT) → shockable rhythm - what is this? Absence of carotid pulse in the presence of sinus tachycardia - Pulseless electrical activity (PEA)- non-shockable rhythm - what is this? Absence of carotid pulse in the presence of sinus rhythm - Asystole- non shockable rhythm - What are the most common causes of VT and VF? **(2)** IHD and acute MI

Answer 118

Heart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.

Answer 119

HF is common: the prevalence in the UK is estimated at 1-2%. HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population. In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease. Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.

Answer 120

HF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features).

Answer 121

Low-output HF vs. High-output HF Low-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet.

Answer 122

The common causes of low-output HF will be further discussed below. Common causes of high-output HF include: Anaemia Arteriovenous malformation Paget's disease Pregnancy Thyrotoxicosis Thiamine deficiency (wet Beri-Beri) These can be remembered with the AAPPTT mnemonic.

Answer 123

Systolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis). In comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis.

Answer 124

HF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop.

Answer 125

The NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest). Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea. Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea. Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary). Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.

Answer 126

Clinical features of left heart failure (LHF) LHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion. Symptoms Shortness of breath on exertion Orthopnoea Paroxysmal nocturnal dyspnoea Nocturnal cough (± pink frothy sputum) Fatigue Signs Tachypnoea Bibasal fine crackles on auscultation of the lungs Cyanosis Prolonged capillary refill time Hypotension Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation.

Answer 127

Clinical features of right heart failure Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output). Symptoms Ankle swelling Weight gain Abdominal swelling and discomfort Anorexia and nausea Signs Raised JVP Pitting peripheral oedema (ankle to thighs to sacrum) Tender smooth hepatomegaly Ascites Transudative pleural effusions (typically bilaterally)

Answer 128

NT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value. Interpret NT-pro-BNP results as follows: 2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks. 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks. If <400ng/L: diagnosis of heart failure is less likely.

Answer 129

Arrange a 12-lead ECG in all patients ECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). Transthoracic echocardiogram (TTE) An echocardiogram will confirm the presence and degree of ventricular dysfunction. Bloods: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors) Chest Xray

Answer 130

EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction). EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction). EF 50-70% with normal BNP = normal.

Answer 131

CXR: CXR findings in heart HF can be remembered by the ABCDEF mnemonic: A: Alveolar oedema (with 'batwing' perihilar shadowing) B: Kerley B lines (caused by interstitial oedema) C: Cardiomegaly (cardiothoracic ratio >0.5) D: upper lobe blood diversion E: Pleural effusions (typically bilateral transudates) F: Fluid in the horizontal fissure

Answer 132

Weight loss if BMI >30. Smoking cessation Salt and fluid restriction - improves mortality Supervised exercise-based group rehabilitation programme for people with heart failure. Offer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure.

Answer 133

Medical management Symptom management: For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure. Management which improves mortality: 1st line = ACE-I and beta-blocker Consider ARB if intolerant to ACE-I. Consider hydralazine if intolerant to ACE-I/ARB. If symptoms persist and NYHA Class 3 or 4 consider adding: Aldosterone antagonists = spironolactone or eplerenone. Hydralazine and a nitrate for Afro-Caribbean patients. Ivabradine if in sinus rhythm and impaired EF. Digoxin = useful in those with AF. This worsens mortality but improves morbidity. NICE also advices seeking specialist guidance for prescribing SGLT2 inhibitors (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.

Answer 134

Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine.

Answer 135

Cardiac resynchronisation therapy Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled: QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III QRS interval 120-149ms without LBBB, NYHA class I-III QRS interval 120-149ms with LBBB, NYHA class I

Answer 136

Bradycardia, hypotension, fatigue, dizziness ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema tiredness, peripheral coldness and bronchospasm.

Answer 137

Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido

Answer 138

Hypotension, hyponatraemia/kalaemia, The BNF reports high doses or rapid intravenous administration of loop diuretics can cause tinnitus and deafness.

Answer 139

Headache, palpitations, flushing

Answer 140

Dizziness, blurred vision, GI disturbances

Answer 141

Thrush, UTIs, DKA in patients with pre-existing diabetes

Answer 142

Pulsus alternans is an arterial pulse which alternates between strong and weak beats due to variations in systolic pressures. The variation of systolic pressure is secondary to poor ejection fraction, resulting in raised end-systolic volume. This raised end-systolic volume causes raised diastolic volume, resulting in stretching of the myocardial muscle and a stronger subsequent contraction of the heart. It is an indicator of dysfunction of the left ventricle and is a poor prognostic indicator of heart failure.

Answer 143

Digoxin is no longer considered first-line management in atrial fibrillation, however, it is useful in patients with co-existent heart failure with a reduced ejection fraction and those who do very little exercise and is therefore the correct answer.

Answer 144

The patient presents with features consistent with cor pulmonale (right heart failure caused by chronic lung disease). Signs of right heart failure include ankle/sacral pitting oedema, ascites, tender smooth hepatomegaly, and a raised JVP

Answer 145

Chronic lung diseases, including COPD, can cause cor pulmonale, leading to right ventricular dysfunction and manifesting as signs such as raised JVP, hepatomegaly, pitting oedema, and a cough with white sputum.

Answer 146

Infective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves.

Answer 147

Age >60 years Male sex IVDU: predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis. Poor dentition and dental infections Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects. Prosthetic valves Previous history of infective endocarditis Intravascular devices: central catheters and shunts. Haemodialysis HIV infection

Answer 148

A damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis.

Answer 149

IE can be considered according to duration of symptoms. Acute IE: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to S.aureus infection. Subacute IE: patients has signs or symptoms for 6 weeks up to 3 months. Chronic IE: patients has signs or symptoms that persist for longer than 3 months.

Answer 150

Native-valve endocarditis: patient without prosthetic valve implant. Prosthetic-valve endocarditis: Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections.

Answer 151

**MATP** - Mitral valve - Aortic valve - Tricuspid valve - Pulmonary valve - Which valve is most likely affected in IV drug use? Tricuspid

Answer 152

Staphylococcus epidermidis

Answer 153

Staph. aureus: now the most common cause of IE. Coagulase positive. Strep. viridans: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. Enterococci Coagulase negative staphylococci e.g. staph. epidermidis: common culprit of prosthetic valve endocarditis. Strep. bovis: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients. Fungal HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE).

Answer 154

Common presenting symptoms: Fever: most common symptom. Night sweats Anorexia Weight loss Myalgia Others: Headache Arthalgia Abdominal Pain Cough Pleuritic pain

Answer 155

Febrile Cachectic Clubbing Splenomegaly

Answer 156

Cardiac: Murmur: fever + new murmur is infective endocarditis until proven otherwise. Bradycardia: aortic root abscess tracks down to the AVN causing heart block. Vascular phenomena: Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. Immunological phenomena: due to immune-complex deposition. Splinter haemorrhages Osler's nodes: painful pulp infarcts on end of fingers. Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. Glomerulonephritis: identified on urine dip.

Answer 157

Duke Criteria

Answer 158

useful mnemonic to remember the criteria is 'BE FIVE PM': Major Criteria: Blood Cultures Evidence of Endocardial Involvement: Echo Minor Criteria: Fever Immunological phenomena Vascular phenomena Echocardiogram minor criteria Predisposing features Microbiological evidence that does not meet major criteria. For a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present.

Answer 159

2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). Single positive blood culture for Coxiella burnetti or positive antibody titre

Answer 160

Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. Abnormal activity around site of prosthetic valve implantation on PET-CT Paravalvular lesions on cardiac CT

Answer 161

Fever: >38.0 degrees celsius. Immunological phenomena: Roth spots, splinter haemorrhages or Olser's nodes. Vascular phenomena: evidence of septic embolis (splenic infarct/abscess), Janeway lesions. Echocardiogram minor criteria: not meeting above criteria. Predisposing features: known valvular disease, IVDU, prosthetic valves etc. Microbiological evidence that does not meet major criteria: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE

Answer 162

increasing prolongation of PR interval suggests development and worsening of aortic root abscess.

Answer 163

look for haematuria which may suggest development of glomerulonephritis.

Answer 164

Mainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term.

Answer 165

Native valve: amoxicillin (+/- gentamicin) Pen-allergy/MRSA: vancomycin (+/- gentamicin) Prosthetic valve: vancomycin + rifampicin + gentamicin

Answer 166

1st line: flucloxacillin 2nd line: vancomycin + rifampicin

Answer 167

1st line: flucloxacillin + rifampicin + gentamicin

Answer 168

1st line: benzylpenicillin 2nd line: vancomycin + gentamicin

Answer 169

1st line: ceftriaxone

Answer 170

Despite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: Haemodynamic instability Severe heart failure Severe sepsis despite antibiotics/failed medical therapy Valvular obstruction Infected prosthetic valve Persistent bacteraemia Repeated emboli Aortic root abscess Common exam question: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess

Answer 171

Acute valvular insufficiency causing heart failure Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm) Embolic complications causing infarction of kidneys, spleen or lung Infection e.g. osteomyelitis, septic arthritis

Answer 172

Antibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. Evidence has shown that there is no consistent association between having an interventional procedure and the development of infective endocarditis. In fact, regular brushing of teeth causes much greater, repetitive bacteraemia compared to a single interventional procedure. Further to this, the clinical effectiveness of antibiotic prophylaxis has never been proven. NICE (CG94), on balance of the evidence, suggests that antibiotic prophylaxis against infective endocarditis results in a greater risk of anaphylaxis than any potential benefit, and is also not cost effective. Prophylaxis is therefore not recommended.

Answer 173

Staphylococcus aureus is considered the most common cause of infective endocarditis, particularly in acute presentations. It is a coagulase-positive organism frequently associated with intravenous drug use or healthcare-associated infections. However, this patient’s subacute presentation and negative blood cultures should raise suspicion of HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) infective endocarditis.

Answer 174

This typically causes a subacute presentation of infective endocarditis in patients with existing cardiac disease. It is one of the alpha haemolytic Streptococci and causes partial haemolysis on agar

Answer 175

This patient has subacute infective endocarditis, with acute mesenteric ischaemia due to septic emboli as a complication. CT angiography is the definitive diagnostic method for acute mesenteric ischaemia

Answer 176

Acute mesenteric ischemia (AMI) is a life-threatening surgical emergency characterized by the abrupt onset of blood flow restriction (hypoperfusion) to a portion of the small intestine. This disruption may be either occlusive or non-occlusive, affecting primarily the superior mesenteric artery.

Answer 177

Arterial Embolism: The most common cause, often resulting from atrial fibrillation or other embolic sources such as infective endocarditis or aortic aneurysm. Arterial Thrombosis: Usually associated with atherosclerosis, especially in patients with a history of ischemic heart disease or peripheral vascular disease. Venous Thrombosis: Occurs less commonly and is often linked to hypercoagulable states. Non-Occlusive Mesenteric Ischemia: Typically associated with low-flow states such as heart failure, shock, or during major surgery.

Answer 178

Sudden severe abdominal pain and guarding, often out of proportion to the physical examination Nausea and vomiting Signs of shock, such as hypotension, tachycardia, altered mental status Metabolic acidosis on arterial blood gas (ABG) analysis Rectal bleeding can occasionally be seen in advanced ischemia The embolic nature of a mesenteric infarction causes a sudden evacuation of the bowels that may contain blood, as the infarction leads to bleeding into the gut wall, lumen and peritoneal cavity new onset atrial fibrillation

Answer 179

Blood tests: Full blood count, liver function tests, renal function, coagulation profile, and lactate levels Arterial blood gas (ABG): To identify metabolic acidosis Imaging: CT angiography is the diagnostic modality of choice due to its ability to visualize the occlusion and surrounding bowel.

Answer 180

The primary objectives in managing AMI are rapid diagnosis, stabilization of the patient, and restoration of bowel perfusion. This can be achieved through: Resuscitation: Including fluid management and correction of metabolic abnormalities Anticoagulation: Typically with intravenous heparin to limit progression of thrombosis or embolism Surgical intervention: Including embolectomy, arterial bypass, or bowel resection if necrosis is present Non-surgical intervention: Such as intra-arterial vasodilators or thrombolytic therapy Supportive care: Including analgesia, antibiotics if needed, and nutritional support.

Answer 181

Chronic mesenteric ischaemia is a pathological condition typically presenting in elderly patients, characterized by insufficient blood supply to the intestines, usually due to gradual blockage or narrowing of the mesenteric arteries.

Answer 182

Chronic mesenteric ischaemia (CMI) is a relatively uncommon condition primarily affecting the elderly population. The overall incidence and prevalence are difficult to establish due to underdiagnosis and the coexistence of other diseases with similar presentations. Typically, CMI is most frequently observed in patients aged 60 years and above. It is estimated that significant stenosis or occlusion of the celiac and mesenteric arteries, which leads to CMI, may be present in up to 7% of individuals over the age of 65. The condition appears to be slightly more prevalent in women compared to men, with a ratio of approximately 3:2. The underlying risk factors for CMI, including smoking, hypertension, hyperlipidemia, diabetes, and a history of cardiovascular disease, align with those of the general atherosclerotic disease. Consequently, the prevalence of CMI is expected to rise alongside the increasing prevalence of these risk factors in the aging population. CMI is a serious condition, with untreated symptomatic disease associated with high mortality rates, often due to the development of acute mesenteric ischaemia. However, with prompt diagnosis and appropriate management, the prognosis can be significantly improved.

Answer 183

Patients often have risk factors for arterial disease, such as smoking, diabetes, hypercholesterolemia, and a history of myocardial infarction. They may also have risk factors for embolic disease, notably atrial fibrillation.

Answer 184

Diffuse, colicky abdominal pain, which worsens after eating Significant weight loss, as patients avoid eating due to the pain Diarrhoea Gastrointestinal bleeding, presenting as melaena or haematochezia (secondary to mucosal sloughing) Physical examination often reveals abdominal tenderness. An epigastric bruit may be present, indicative of turbulent flow in the narrowed vessels.

Answer 185

Bedside investigations - VBG to check for raised lactate Duplex ultrasound: A non-invasive method to detect blood flow and identify blockages in the mesenteric arteries. Gold standard: Computed Tomography (CT) angiography: Helps to visualize the anatomy of the mesenteric arteries and the presence of any blockages. Mesenteric angiography: An invasive procedure that provides detailed images of the blood vessels supplying the intestines, typically used when other investigations are inconclusive or prior to intervention.

Answer 186

Risk factor modification: Smoking cessation, control of diabetes and hypercholesterolemia. Symptom relief: Medications like vasodilators may be used to increase blood flow to the intestines. Revascularization: Percutaneous transluminal angioplasty (PTA) with or without stenting or surgical revascularization procedures are typically used for patients with severe symptoms or when conservative management fails.

Answer 187

Hypoperfusion of the large bowel

Answer 188

Inferior mesenteric artery

Answer 189

- Area near splenic flexure - 2/3 transverse colon is at high risk due to being watershed areas

Answer 190

- Age - AF - Smoking - Hypertension - Diabetes

Answer 191

Ischaemic heart disease (IHD), also known as coronary artery disease, is a condition characterised by reduced blood supply to the myocardium due to stenosis or occlusion of the coronary arteries.

Answer 192

The primary aetiological factor is atherosclerosis, which leads to progressive narrowing and hardening of the arteries.

Answer 193

Clinical presentations can vary from asymptomatic disease to angina pectoris, myocardial infarction or sudden cardiac death.

Answer 194

Diagnosis usually involves clinical assessment, electrocardiogram (ECG), exercise stress testing, and imaging techniques like echocardiography or coronary angiography. Biomarkers such as troponins can also be used to identify acute ischaemia.

Answer 195

- Beta blocker- Bisoprolol/atenolol OR - Rate limiting CCB- Verapamil/diltiazem - When would you need to prescribe both? If only 1 isn’t working - Overall medical management? **(4)** **BAGS** - Beta blocker (or CCB) - Aspirin (75mg) - GTN - Statin (20mg) - What can you do if symptoms are not controlled medically? May have PCI or CABG

Answer 196

- What do we use if we prescribe both? - Nifedipine/amlodipine (non-cardioselective CCB) as CCB can’t be used alongside beta blocker - Causes severe bradycardia and heart block - In what condition are BB’s contraindicated? Asthma

Answer 197

Mitral stenosis refers to the narrowing of the mitral valve which reduces blood flow to the left ventricle.

Answer 198

Normally, the mitral valve opens during diastole to allow left ventricular filling. In mitral stenosis, the thickened and calcified mitral valve reduces the amount of blood that can flow through the valve into the left ventricle during diastole. This leads to a reduction in the end-diastolic volume in the left ventricle and increases the volume of blood in the left atrium. The increased volume of blood in the left atrium leads to atrial dilatation (predisposes to atrial fibrillation), pulmonary congestion and ultimately right heart failure.

Answer 199

The commonest cause of mitral stenosis is rheumatic heart disease. Pathophysiology: the body produces antibodies to target the streptococcal antigens that occur in rheumatic fever. These antibodies also attack valvular tissue (autoimmune molecular mimicry) leading to valvular disease.

Answer 200

Mitral annular calcification (age-related) Congenital mitral stenosis (rare) Mucopolysaccharidosis (metabolic disorder affecting connective tissue) Carcinoid syndrome, causing valve disease Systemic disease, including systemic lupus erythematosus (SLE) and rheumatoid arthritis. Atrial outflow obstruction due to other conditions, such as atrial myxoma, may cause symptoms similar to MS.

Answer 201

Mitral stenosis typically remains asymptomatic until the degree of stenosis is advanced. Symptoms tend to begin when the valve area falls <1.5cm^2. Common symptoms include: Gradual exertional dyspnoea and reduced exercise tolerance. Dyspnoea secondary to pulmonary venous congestion. Haemoptysis: increased pulmonary pressures and vascular congestion, which can manifest as pink/blood stained sputum, or frank haemoptysis. Palpitations: atrial fibrillation (AF) is common in patients with MS due to elevated left atrial pressures and subsequent left atrial enlargement Chest pain: can occur as a result of pulmonary hypertension and right ventricular hypertrophy, or due to AF with fast ventricular response. Thromboembolism (cerebral or systemic): secondary to AF. Hoarseness: enlarged L atrium can compress the recurrent laryngeal nerve (Ortner's syndrome). Peripheral oedema / abdominal discomfort (hepatomegaly) - due to right heart failure.

Answer 202

Mitral facies (malar flush): cutaneous vasodilation due to carbon dioxide retention. Low volume pulse Irregularly irregular pulse: AF. Elevated JVP (prominent 'a' wave due to raised right atrial pressure, or absent 'a' wave in AF). Tapping, non-displaced apex beat (palpable S1). Right ventricular heave (suggestive of pulmonary hypertension). Inspiratory crepitations (pulmonary oedema) and other signs of right heart failure.

Answer 203

Loud S1 (becomes softer with increasing calcification) Loud P2 with pulmonary hypertension (later stages S2 splits) Opening snap heard at apex (only with pliable valves) Mid-to-late diastolic murmur Low pitched rumble, most prominent at apex Loudest in expiration Heard best with patient lying on left side Heard best using stethoscope bell (low frequency) Graham-Steell murmur (early diastolic murmur - only if pulmonary regurgitation present secondary to pulmonary hypertension)

Answer 204

ECG may show: P-mitrale (a broad notched P wave due to left atrial enlargement) Right ventricular hypertrophy Right axis deviation Atrial fibrillation: caused by left atrial enlargement CXR may show evidence of pulmonary oedema and left atrial enlargement Echocardiogram: will show degree of stenosis and impairment of ventricular filling. Cardiac MRI may show valvular vegatations.

Answer 205

Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all. If a patient has asymptomatic MS they should undergo regular follow-up echocardiography to assess degree of stenosis and its progression.

Answer 206

Treatment of complications including atrial fibrillation with rate control and anticoagulation. Diuretics can provide symptomatic relief for pulmonary congestion and peripheral oedema. Medical management is not an alternative to definitive interventional treatment.

Answer 207

For symptomatic patients there are three treatment options: Balloon valvuloplasty: only appropriate if valve is pliable and non-calcified. Percutaneous mitral valvotomy: for patients with moderate disease. Open valve repair/replacement: for patients with severe disease who are not too high risk for surgery but are not candidates for percutaneous intervention. Valves are more likely to be metal than bioprosthetic. Treatment is difficult in patients who have severe disease or who have inadequate valve morphology and are high risk for open surgery.

Answer 208

t first, progression is slow but once the onset of symptoms occurs the progression happens more rapidly. Initial symptoms are related to the following complications: Atrial fibrillation (AF) and thromboembolism - palpitations, poor exercise tolerance and symptoms of cardioembolic stroke. Pulmonary hypertension - dyspnoea and haemoptysis. Dilated left atrium - can impinge on local structures, leading to hoarseness, dysphagia and bronchial obstruction. Patients may also present with symptoms of decompensated heart failure, either due to the valvular disease itself (along with a precipitant like infection) or can be secondary to non rate-controlled AF.

Answer 209

Mitral regurgitation (MR) is the backflow of blood into the left atrium during systole due to the incompetence of the mitral valve.

Answer 210

Normally, the mitral valve closes at the beginning of systole to prevent backflow of blood into the left atrium. In mitral regurgitation, the mitral valve fails to close sufficiently meaning there is a backflow of blood across the mitral valve into the left atrium. Over time, this leads to the enlargement of the left atrium and leads to volume overload in the left side of the heart ultimately leading to LV failure.

Answer 211

Acute MR is a cardiac emergency and may present with sudden-onset pulmonary oedema, hypotension and cardiogenic shock. See section on management of acute pulmonary oedema. Causes of Acute MR Ischaemic MR: primarily due to papillary muscle rupture secondary to a postero-inferior myocardial infarction. Non-ischaemic MR: ruptured chordae tendineae due to any of a number of causes. Myxomatous disease (mitral prolapse) Infective endocarditis Rheumatic heart disease - acute or chronic Trauma Spontaneous rupture Prosthetic valve MR: Tissue valvelet rupture due to endocarditis, degeneration or calcification. Paravalvular regurgitation due to infection or suture rupture. Valve thrombus or infection causing impaired closure.

Answer 212

Leaflet causes: Mitral valve prolapse (MVP) is a common cause of chronic MR (accounting for approximately 5% of cases). Please see separate section on MVP. Degenerative disease (causing prolapse) Rheumatic fever (presents typically in the younger patients <20, whereas MS is more common in older patients) Infective endocarditis Systemic inflammatory disorders e.g. SLE, scleroderma Connective tissue disorders e.g. Marfan's, Ehlers-Danlos syndromes Congenital causes e.g. mitral valve clefts Hypertrophic cardiomyopathy causing abnormal valve movements Drug related damage, e.g. ergotamine, bromocriptine, 'fen-phen' (fenfluramine - anorectic drug, now banned) Chordae related causes: Myxomatous valve disease (causing prolapse) Trauma Papillary muscle related causes:: Myocardial ischemia or infarction (regional wall motion abnormalities - RWMA - can cause inadequate systolic function and poor closure) Dilated cardiomyopathy Annular related causes: Calcification, either due to rheumatic fever or age-related Dilation due to dilated cardiomyopathy or connective tissue disorders Prosthesis related causes: Paravalvular leak Ring or strut fracture Leaflet deterioration in tissue valves Infective endocarditis Thrombus or pannus formation which can obstruct valve closure

Answer 213

Shortness of breath Exertional dyspnoea Fatigue Weakness and signs of overt pulmonary oedema, hypotension and cardiogenic shock.

Answer 214

Mild-to-moderate MR: asymptomatic until significant systolic dysfunction, pulmonary hypertension or symptomatic atrial fibrillation (AF). Fatigue and exertional dyspnoea are most common, a result of decreased cardiac output as well as increased pulmonary pressures due to increased left atrial pressures.

Answer 215

'Blowing' pansystolic murmur Loudest at the apex Radiates to the axilla Louder on expiration Louder on rolling to the left S1 may be quiet or absent If patients are in decompensated heart failure Bilateral lung crepitations Raised JVP S3/S4 Peripheral/sacral oedema oedema Acute MR can present with signs of acute pulmonary oedema, hypotension and cardiogenic shock.

Answer 216

Bedside ECG: p-mitrale (broad notched p wave due to left atrial enlargement), LVH and left axis deviation. Bloods NT pro-BNP: raised in heart failure reflects increased ventricular stress. Imaging CXR: evidence of pulmonary oedema and left atrial enlargement. Definitive diagnosis is made using echocardiogram which allows assessment of: Size and pressure of regurgitant jet Size of valve lesions Structural complications such as left atrial enlargement or systolic dysfunction

Answer 217

Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all. If a patient has asymptomatic MR they should undergo regular follow-up echocardiography.

Answer 218

Treatment of concurrent complications: AF with rate control and anticoagulation Heart failure with diuretics, ACE-Inhibitors, and beta-blockers. Acute MR is a medical emergency and should be treated according to acute pulmonary oedema guidelines (please see section).

Answer 219

The definitive management for symptomatic MR is surgery - there are two main options: Mitral valve repair (mitral valvuloplasty) - this is preferable as is preserves all components of the native valve and avoids use of prostheses. Mitral valve replacement - offers the choice between a mechanical valve (lifelong anticoagulation but long-lasting), and a bioprosthetic valve (limited durability but no need for anticoagulation)

Answer 220

Myocarditis, also known as an inflammatory cardiomyopathy, refers to inflammation of the myocardium (heart muscle). It often occurs alongside inflammation of the pericardium (sac that surrounds the heart) and it is then described as myopericarditis.

Answer 221

Heart failure Thromboembolism secondary to AF Haemoptysis secondary to pulmonary hypertension and symptoms of right heart failure are possible but less common than in mitral stenosis (MS). Infective endocarditis and associated symptoms can also complicate MR.

Answer 222

Myocarditis occurs due to the infiltration of inflammatory cells into heart tissue.

Answer 223

Classification of myocarditis can be considered according to cause. The most common cause in Europe and the UK are viruses, with Cocksackie B being the most common culprit. Worldwide, Chagas disease is the most common cause following infection from Trypanosoma cruzi.

Answer 224

Cocksackie B virus: most common cause of myocarditis in Europe and the UK. COVID-19 Adenovirus Epstein Barr Virus

Answer 225

Diphtheria Clostridia Neiseria gonorrhoea

Answer 226

Trypanosoma cruzi

Answer 227

Kawasaki disease Scleroderma, SLE, sarcoid and systemic vasculitides

Answer 228

Antipsychotics incl. clozapine Immune-checkpoint inhibitors Mesalazine

Answer 229

Chest pain: often described as sharp, stabbing. If pericardial involvement, chest pain may be worse on lying down. Shortness of breath Palpitations Lightheadedness Syncope Fever and viral prodrome Severe cases can present with sudden unexplained cardiac death.

Answer 230

Asymptomatic or non-specific signs may be present. Dull heart sounds If myopericarditis a pericardial rub may be heard. In fulminant myocarditis the patient may have signs of heart failure.

Answer 231

Bedside ECG: non-specific ST segment and T wave changes (may suggest location of myocardial involvement); arrhythmias; tachycardia; and ectopic beats. Bloods Raised Troponin and CK-MB: can be markedly elevated. Inflammatory markers: may also be elevated and may indicate cause. Consider viral serology to determine aetiology of the myocarditis. Imaging Echocardiogram: reveal ventricular dysfunction or regional wall motion abnormalities. Cardiac MRI: help confirm diagnosis of myocarditis and indicate extent of inflammation. Endomyocardial biopsy: gold-standard diagnostic tool. Histopathology shows infiltration of inflammatory cells into the myocardium and myocardial necrosis.

Answer 232

Hallmark of treatment is supportive and addressing the underlying cause. Patients with severe myocarditis may require ITU support and vasopressors. Patients with viral acute myocarditis may benefit from a course of corticosteroids. After recovery, patients should be advised to limit activity for a few months.

Answer 233

Complications of myocarditis may include heart failure, arrhythmias, or dilated cardiomyopathy.

Answer 234

A young adult presenting with acute chest pain, breathlessness, and a recent history of viral illness, alongside sinus tachycardia and T wave inversion on ECG, should raise suspicion for myocarditis.

Answer 235

Acute pericarditis is inflammation of the pericardium, the fibroelastic sac that surrounds the heart. Inflammation can also extend to the myocardium (heart muscle), in which case the condition is referred to as perimyocarditis or myopericarditis depending on which is predominant.

Answer 236

Idiopathic Infective causes Viruses - viruses which cause pericarditis are coxsackie B viruses, echovirus, CMV, herpesvirus, HIV among other rarer causes. Bacteria - staphylococcus, pneumococcus, streptococcus (rheumatic carditis), haemophilus and M. tuberculosis. Fungi and parasites (rare) Malignant causes Lung cancer Breast cancer Hodgkin's lymphoma Cardiac causes Heart failure may cause pericarditis Post-cardiac injury syndrome (Dressler's syndrome) including post-traumatic Radiation - often secondary to therapy for other malignancies Drugs and toxin causes Anthracycline chemotherapy (Doxorubicin) Hydralazine Isoniazid Methyldopa Phenytoin Penicillins (hypersensitivity) Rheumatological disease Systemic lupus erythematous (SLE) Rheumatoid arthritis Sarcoidosis Vasculitides (Takayasu's, Behcet's) Other causes Renal failure (uraemia) - indication for emergency dialysis. Hypothyroidism Inflammatory bowel disease Ovarian hyperstimulation

Answer 237

Pleuritic chest pain: central, worse on inspiration. Postural chest pain: worse on lying flat and relieved on leaning forward. Fever

Answer 238

Pericardial friction rub - high-pitched scratching noise, best heard over the left sternal border during expiration. Pathogonomonic of pericarditis. Pericarditis can lead to the development of a pericardial effusion and cardiac tamponade in which case signs such as hypotension, raised JVP and muffled heart sounds (Beck's Triad) may be present.

Answer 239

Bedside 1st line = ECG ECG features include: Widespread saddle ST elevation (not following vascular territories) and PR depression. ECG changes can sometimes evolve over weeks: 1-3 weeks: normalisation of ST changes, T wave flattening 3-8 weeks: flattened T waves become inverted 8+ weeks: ECG returns to normal

Answer 240

Bloods Serial troponins: tend not to peak as in an MI, but tend to stay consistently elevated in the acute phase. Inflammatory markers: raised inflammatory markers (WCC, CRP and ESR) are in keeping with an acute pericarditis. Viral serology: may help to identify cause of the acute pericarditis. Imaging Echocardiogram - used to assess for pericardial effusion and distinguish between pericarditis and MI (e.g. looking for the absence of regional wall motion abnormalities). Angiogram - shows normal coronary arteries (which excludes MI). Cardiac MRI - in atypical cases, cardiac MRI can be used to visualise inflammation of the pericardium.

Answer 241

1st line: exercise restriction and NSAIDS (+ PPI) for 1-2 weeks. 2nd line: colchicine (SE: diarrhoea, use in caution in those with renal or hepatic impairment). 3rd line: corticosteroids (for those who cannot tolerate or refractory to NSAIDS).

Answer 242

1st line: IV antibiotics +/- pericardiocentesis if purulent exudate present. Rare cases - pericardectomy may be performed if adhesions or recurrent tamponade occurs.

Answer 243

1st line: corticosteroids (due to the risk of reactivation and if infection has been ruled out).

Answer 244

Complications are rare but include cardiac tamponade and pericardial effusion requiring pericardiocentesis. In the long term patients occasionally develop constrictive pericarditis.

Answer 245

Dressler's syndrome is acute pericarditis occuring several weeks after a myocardial infarction, where an ECG shows widespread ST elevation, PR depression, and a downward sloping T-P segment (Spodick's sign The most specific ECG finding in Dressler's syndrome is PR depression which may be seen in addition to concave ST-segment elevation.

Answer 246

A raised jugular venous pulse that increases with inspiration is indicative of increased right atrial pressure, suggesting restricted heart chamber filling in conditions such as constrictive pericarditis.

Answer 247

Constrictive pericarditis is the result of scarring and loss of elasticity of the pericardial sac. The scarred pericardium prevents normal cardiac filling which leads to the restriction of ventricular volume, stroke volume, and ultimately cardiac output.

Answer 248

Patients present with symptoms of heart failure: Fatigue Reduced exercise tolerance Exertional dyspnoea Peripheral oedema

Answer 249

Raised JVP Kussmaul's sign: paradoxical rise in JVP with inspiration. Pulsus paradoxus: more commonly seen in cardiac tamponade. It results due to the drop in cardiac output on inspiration. Heart sounds may be quiet (if pericardial effusion also present) Pericardial knock: high-pitched, early diastolic sound that occurs when stiff pericardium results in sudden arrest of ventricular filling.

Answer 250

CXR: small heart +/- pericardial calcification Echocardiogram: demonstrates ventricular filling defect and heart failure with preserved ejection fraction (HFpEF). Cardiac MRI: helps differentiate from restrictive cardiomyopathy.

Answer 251

Hallmark of management of constrictive pericarditis is surgical excision of the fibrosed pericardium (pericardiectomy).

Answer 252

Constrictive pericarditis is the result of a fibrosed and scarred pericardium. Restrictive cardiomyopathy is when there is increased myocardial stiffness. Causes of restrictive cardiomyopathy include amyloidosis and post-radiotherapy. These two conditions are very difficult to distinguish clinically. Clues that suggest constrictive pericarditis over restrictive cardiomyopathy: Paradoxical pulse CXR shows pericardial calcification Cardiac MRI shows a thickened pericardium Endomyocardial biopsy shows an absence of amyloid or other infiltrative diseases.

Answer 253

A pulmonary embolism (PE) is when one or more blood clots lodge in and obstruct the pulmonary arterial vasculature. Typically these emboli arise from a thrombus in the deep veins of the lower limb (a DVT).

Answer 254

Once a PE is diagnosed, severity can be determined using the PE Severity Index (PESI) score - This looks at 11 factors (e.g. presence of tachycardia, hypotension, confusion) to give an overall score which can be used to classify patients as very low risk/low risk/intermediate risk/high risk/very high risk - These correspond to estimated 30 day mortality rates which range from 0.7% in very low risk patients to 25% in very high risk patients - This can be used to stratify appropriateness for outpatient care versus admission Patients who are clearly haemodynamically unstable are high-risk and all require admission Another important marker of high-risk patients is right ventricular strain - All patients should have a troponin; if this is elevated or there are features of right heart strain on the CTPA then an echocardiogram should be done

Answer 255

The ""typical triad"" of symptoms is as follows, although all three features are rarely present simultaneously: Sudden-onset shortness of breath (the commonest symptom, present in around half of patients) Pleuritic chest pain Haemoptysis Cough may also be present without haemoptysis Syncope or pre-syncope are concerning symptoms indicating massive PE Right ventricular ischemia can lead to retrosternal chest pain Symptoms of a DVT such as leg pain or swelling may be present Small PEs may be asymptomatic and detected incidentally on imaging

Answer 256

Tachypnoea Crackles on auscultation Tachycardia Hypoxia Low-grade pyrexia in some In massive PE: - Hypotension - Cyanosis - Signs of right heart strain (e.g. a raised JVP, parasternal heave and loud P2)

Answer 257

Well's score:

Answer 258

3 points clinical signs and symptoms of a DVT PE is the most likely diagnosis 1.5 points tachycardia (heart rate >100 beats/minute) immobility > 3 days or major surgery within 1 month previous PE or DVT 1 point haemoptysis current malignancy Wells score 4 or less - PE unlikely, do a D-dimer a low D-dimer excludes a PE a raised D-dimer should be further investigated (e.g. with a CTPA) Wells score more than 4 - PE likely - Further investigate with a CTPA or V/Q scan

Answer 259

Bedside tests ECG may be normal or show sinus tachycardia In a massive PE, there may be evidence of right-heart strain (P pulmonale, right axis deviation, right bundle branch block, nonspecific ST/T wave changes) The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III and inverted T waves in lead III) is seen in less than 20% of patients ABG may be normal or show type 1 respiratory failure and/or a respiratory alkalosis due to hyperventilation Bloods D-dimer - not a specific test but has a 95% negative predictive value (i.e. it is useful to help rule out a PE if negative) FBC may show anaemia or thrombocytosis in underlying malignancy CRP may be raised in malignancy or intercurrent infection U&Es are needed to assess renal function prior to a CTPA LFTs as a baseline e.g. to assess suitability for anticoagulation Coagulation screen as a baseline before starting anticoagulation Troponin to assess for myocardial damage Imaging Chest X-ray - typically normal in PE but helpful in ruling out differentials (e.g. pneumonia, pneumothorax), may show: Fleischner sign - an enlarged pulmonary artery Hampton's hump - a peripheral wedge shaped opacity Westermark sign - regional oligaemia CT pulmonary angiogram (CTPA) - the diagnostic test of choice for a PE, will show filling defect(s) in the pulmonary vasculature V/Q scan - preferred in severe renal impairment or contrast allergy Ultrasound doppler of the lower limbs - to investigate for an underlying DVT Transthoracic echocardiogram - to investigate for right heart strain

Answer 260

Oxygen if hypoxic Fluid resuscitation if hypotensive Analgesia for chest pain Patient education - if starting anticoagulation ensure patient has an alert card Low-risk patients may be suitable for discharge with anticoagulation and outpatient follow up - The simplified PESI (Pulmonary Embolism Severity Index) may be used to help risk stratify - Patients get 1 point for each of age > 80, history of cancer, chronic cardiopulmonary disease, heart rate > 110, systolic blood pressure < 100, oxygen saturations < 90%) - Outpatient management can be considered in patients scoring zero

Answer 261

Anticoagulation with low molecular weight heparin (LMWH) or a direct oral anticoagulant (DOAC such as rivaroxaban) should be administered immediately if there is high clinical suspicion of a PE This can be stopped if a PE is ruled out Once a PE is confirmed, most patients will continue on a DOAC as these tend to be more convenient for patients If a DOAC is unsuitable, warfarin or LMWH may be considered In cases of massive PE (hypotension for over 15 minutes), patients should be treated with thrombolysis (an IV bolus of Alteplase) There is an associated risk of haemorrhage but this is lower than the risk of death from a massive PE High risk PEs should also be considered for thrombolysis on a case-by-case basis

Answer 262

The duration of anticoagulation treatment depends on the aetiology of the PE A provoked PE should be treated for 3 months (3-6 months if active cancer) Consider continuing treatment for unprovoked PEs beyond 3-6 months In some cases (e.g. certain thrombophilias), patients should be anticoagulated for life - however this needs to be balanced with bleeding risk

Answer 263

Interventional: Embolectomy may be considered in patients with a massive PE when thrombolysis is contraindicated Catheter-directed thrombolysis can be used in specialist centres for patients with a high bleeding risk (ie. postoperative patients)

Answer 264

Disease characterised by narrowing and occlusion of the peripheral arteries due to atherosclerotic plaques

Answer 265

- Smoking- main one - Diabetes - Hypertension - Hyperlipidaemia

Answer 266

Pain on exertion due to inadequate blood flow during exercise, causing fatigue, discomfort, or pain

Answer 267

Compromise of blood flow to an extremity, causing chronic limb pain at rest (worse at night) for at least 2 weeks - What can patients develop? **(2)** - Arterial ulcers - Gangrene

Answer 268

Sudden decrease in limb perfusion that threatens limb viability

Answer 269

- Pain - Paralysis - Paraesthesia - Pulseless - Pallor - Perishingly cold

Answer 270

Atrial fibrillation

Answer 271

Happens in young male smokers with symptoms similar to limb ischaemia - List symptoms of Buerger’s disease **(2)** - Paraesthesia/cold sensation in fingers or limbs - Raynaud’s phenomenon

Answer 272

- Buttock claudication - Impotence - Absent/weak distal pulses

Answer 273

- Most patients are asymptomatic - Intermittent claudication- Cramping pain of leg which is worse upon exertion, relieved by rest - Diminished or absent pulse - ED (impotence) - Thigh or buttock pain when walking - What artery is affected in calf pain? Femoral artery - What artery is affected in buttock pain? Iliac artery - What are red flags? **(2)** - Resting pain - Skin changes- Ulcers or Gangrene - What is this indicative of? Critical limb ischaemia

Answer 274

- What is 1st line? Ankle-brachial pressure index - What is ABPI? Ratio of systolic ankle BP to systolic brachial BP - What ABPI indicates PAD? <0.8 - What ABPI indicates critical limb ischaemia? <0.5 - What is 1st line for intermittent claudication? Duplex ultrasound scan - What do we determine? Can determine site, severity and length of stenosis - What is 1st line for acute limb ischaemia? Bedside handheld arterial doppler scan - What do you do after & why? Lower limb CT angiography to quantify extent of occlusion

Answer 275

- Lie patient flat on bed and lift leg to 45° - Limb developing pallor indicates arterial insufficiency - What does <20° Buerger’s angle indicate? Severe limb ischaemia - What happens when patient swings leg over bed? Reactive hyperaemia is seen

Answer 276

- What is lifestyle management for intermittent claudication? **(2)** - Smoking cessation - Exercise training - What is medical therapy for intermittent claudication? **(3)** - Antiplatelet therapy (Clopidogrel or Aspirin) - Statins - Anti-hypertensives - What’s the overall prescription then for intermittent claudication? **(3)** - Lifestyle measures (exercise) - Clopidogrel 75mg once daily - Atorvastatin 80mg once daily (as secondary prevention) - What can you prescribe if exercise is ineffective and patient doesn’t want to be referred for angioplasty or bypass surgery? Naftidrofuryl oxalate- vasodilator that can alleviate pain in PVD - What do we do if risk factor modification and exercise hasn’t improved symptoms? Refer for surgical revascularisation

Answer 277

- IV heparin initially - Analgesia + fluids + oxygen - Then refer to vascular surgery- what different options are there? **(3)** - Embolectomy - Bypass - Amputation

Answer 278

Normal mean pulmonary arterial pressure is 11-20mmHg. Pulmonary hypertension is characterised by an increase in this to above 25mmHg at rest. There are a variety of causes, all of which involve an increase in pulmonary vascular resistance which ultimately leads to right heart failure due to increased backpressure on the right ventricle.

Answer 279

There are a variety of causes of pulmonary hypertension (with the main ones given below). An important differentiation should be made between pulmonary hypertension (the umbrella term for multiple causes) and pulmonary arterial hypertension which is one specific subtype. Pulmonary arterial hypertension - may be idiopathic, familial, associated with other diseases (e.g. HIV, connective tissue disorders or portal hypertension) or secondary to drugs or toxins (e.g. amphetamines, fenfluramine) Chronic pulmonary disease e.g. COPD, interstitial lung disease, bronchiectasis and obstructive sleep apnoea Chronic thromboembolic disease e.g. persistent or recurrent pulmonary emboli Chronic hypoventilation e.g. kyphosis or scoliosis, neuromuscular disorders Left heart disease e.g. chronic left heart failure or mitral stenosis Unclear or multifactorial mechanisms e.g. sarcoidosis, myelofibrosis, glycogen storage diseases

Answer 280

Group 1: pulmonary arterial hypertension Group 2: secondary to left heart diseases Group 3: secondary to chronic pulmonary diseases and/or hypoxia Group 4: due to chronic thrombotic or embolic disease Group 5: other causes including metabolic disorders, systemic disorders and haematological disease

Answer 281

Progressive shortness of breath Fatigue Syncope Fluid overload with ascites and peripheral oedema (late sign) Raised JVP Parasternal heave Loud P2 Presence of an S3 sound Pansystolic murmur indicative of tricuspid regurgitation (occurs due to the right ventricle becoming pressure and volume overloaded) End-diastolic murmur indicative of pulmonary regurgitation (due to high pulmonary pressures)

Answer 282

Bedside: ECG: may be normal or show signs of right heart strain such as P pulmonale, right ventricular hypertrophy and right axis deviation Bloods: LFTs: to investigate for liver disease (as portal hypertension may contribute to pulmonary hypertension) TFTs: as hyperthyroidism (or more rarely hypothyroidism) may cause pulmonary hypertension Autoimmune screen: e.g. ANA, ENA, scl-70 if an underlying connective tissue disorder is suspected Imaging: Chest X-ray: not diagnostic of pulmonary hypertension but abnormalities include an enlarged right atrium and ventricle, enlarged pulmonary arteries High resolution CT chest: to further investigate for underlying causes e.g. if interstitial lung disease is suspected CT or MR pulmonary angiography: to investigate for chronic thromboembolic disease Transthoracic echocardiogram: to assess right ventricular function, can be used to estimate pulmonary arterial pressures; may also show signs of left heart disease Special tests: Right heart catheterisation: the gold standard for diagnosing pulmonary hypertension as it allows direct measurement of pulmonary arterial pressure

Answer 283

As with any chronic disease, patient counselling and education Early involvement of palliative care especially in deteriorating patients or those with troubling symptoms In women of childbearing age with pulmonary arterial hypertension, counselling regarding the risks of pregnancy and provide contraceptive advice

Answer 284

Medical: Supportive treatment with supplementary oxygen for hypoxia Diuretics for fluid overload secondary to right heart failure Medical optimisation of the underlying condition (e.g. anticoagulation for chronic pulmonary emboli) Medications that reduce pulmonary vascular resistance: Calcium channel blockers e.g. nifedipine PDE-5 inhibitors e.g. sildenafil Prostacyclin analogues e.g. iloprost Endothelin receptor antagonists e.g. bosentan, ambrisentan Soluble guanylate cyclase stimulators e.g. riociguat Surgical: Thrombo-arterectomy or pulmonary balloon angioplasty may be considered for chronic thromboembolic disease Atrial septostomy is a palliative treatment where a hole is made between the atria to reduce right sided pressures A heart-lung transplant may be considered in severe cases

Answer 285

Right heart failure leading to peripheral oedema and congestive hepatopathy Exertional syncope which may lead to injuries Alveolar haemorrhage Pulmonary artery dissection (can be spontaneous or due to iatrogenic injury during cardiac catheterisation) Pericardial effusions High risk of death during pregnancy (25-50%) due to increased right ventricular stress

Answer 286

Cor pulmonale refers to right ventricular failure as a result of lung disease. Longstanding lung disease leads to pulmonary hypertension which puts increased stress on the right ventricle.

Answer 287

In a patient with a chronic lung condition, like severe COPD, chronic pulmonary arterial vasoconstriction occurs due to hypoxia. In order to overcome the increased pressures in the pulmonary circulation, the right side of the heart has to work harder. Initially, this leads to right ventricular hypertrophy but at a certain point the right ventricular can no longer compensate and this leads to right heart failure.

Answer 288

Symptoms: Fatigue Peripheral oedema Ascites Significant symptoms associated with the chronic lung conditions e.g. dyspnoea

Answer 289

Cyanotic Raised JVP with prominent a and v waves RV heave Loud P2 Pansystolic murmur with tricuspid regurgitation Graham-Steel murmur: functional pulmonary regurgitation as the valve itself is not diseases but chronic pulmonary arterial hypertension stretches the valvular attachments. Peripheral oedema Render, pulsatile hepatomegaly.

Answer 290

Bedside ECG: p pulmonale, RVH and R axis deviation. Bloods Routine bloods: chronic hypoxia in severe COPD may lead to a secondary polycythaemia. Imaging CXR: enlarged R atrium and ventricle with prominent pulmonary arteries. Echocardiogram: diagnostic to view impaired right ventricular function.

Answer 291

There are no specific cardiac treatments for right ventricular failure apart from diuretics to aid symptom relief (bumetanide and furosemide). The mainstay of treatment is to optimise the underlying respiratory pathology. Giving long-term oxygen therapy can help reduce pulmonary hypertension which can reduce the stress on the right ventricle. Rarely, heart-lung transplantation can be considered in young people.

Answer 292

Rheumatic fever, which almost always occurs with mitral or aortic valve disease

Answer 293

- Fatigue - Ascites - Oedema - Early diastolic murmur

Answer 294

- Diuretics - Surgical repair

Answer 295

Tricuspid regurgitation (TR) occurs when the tricuspid valve fails to prevent blood from leaking back into the right atrium during systole.

Answer 296

Normally, the tricuspid valve closes tightly at the beginning of systole (S1) and prevents blood from leaking back into the right atrium. In tricuspid regurgitation, the valve fails to seal tightly and blood leaks back into the right atrium thus increasing pressures in the right atrium and forcing the right ventricle to pump harder. Severe TR causes right-sided HF.

Answer 297

Infective endocarditis: consider in IVDU who present with fevers and a new murmur. Rheumatic heart disease Chronic lung disease Pulmonary embolism Secondary to pulmonary stenosis

Answer 298

Asymptomatic Fatigue Ankle swelling Abdominal swelling

Answer 299

Signs of right-sided heart failure: Raised JVP: prominent systolic 'V' waves. Ascites Peripheral oedema Pulsatile hepatomegaly Heart sounds Pansystolic murmur: loudest in the left parasternal region and on inspiration.

Answer 300

Bedside ECG: non-specific or p pulmonale (peaked p waves) or incomplete right bundle branch block. Bloods Inflammatory markers and blood cultures if infective endocarditits suspected. Imaging Transthoracic echocardiogram (TTE): to detect and quantify TR alongside assessing ventricular function. Cardiac MR: to further evaluate right ventricular size and function. Cardiac catheterisation (angiography): may be required prior to surgery to assess for coronary artery disease.

Answer 301

Conservative If asymptomatic and non-severe, tricuspid regurgitation may be monitored with sequential TTEs. Medical Treat underlying causes: e.g. IV antibiotics for infective endocarditits. Treat the right-sided heart failure and treat for fluid overload (loop diuretics). Surgical Consider surgery if severe, symptomatic and refractory to medical management. Surgical options include: Ring annuloplasty Valve replacement

Answer 302

If left untreated, severe TR will cause right-sided heart failure.

Answer 303

- Right sided murmurs louder on inspiration - Left sided murmurs louder on expiration

Answer 304

Pulmonary stenosis (PS) obstructs the blood flow from the right ventricle (RV) into the pulmonary bed, resulting in a pressure gradient greater than 10 mmHg across the pulmonary valve during systole.

Answer 305

Pulmonary stenosis is usually congenital is associated with the following syndromes: Tetralogy of Fallot (valvular) Noonan syndrome (valvular) Williams syndrome (supravalvular) It can also be as a result of congenital rubella infection. Very rarely, pulmonary stenosis can be acquired due to carcinoid syndrome.

Answer 306

Pulmonary stenosis typically causes right heart failure and may present with the following symptoms: Dyspnoea Fatigue Peripheral oedema Ascites

Answer 307

Dysmorphic facies if it occurs with a congenital syndrome such as Noonan syndrome or Williams syndrome. Raised JVP Right ventricular heave Ejection systolic murmur that radiates to the left shoulder and is best heard on expiration. Widely split S2 with a delayed P2.

Answer 308

ECG: p pulmonale, right axis deviation, and right ventricular hypertrophy. CXR: prominent pulmonary arteries and post-stenotic dilatation. Echocardiogram: degree of stenosis and ventricular function.

Answer 309

Like with all valve disease, mild asymptomatic valve disease rarely requires intervention. Surgical options for severe pulmonary stenosis include valvotomy (for valvular lesions) and balloon angioplasty (for supravalvular lesions). Treatment is considered in those with transvalvular pressure gradients >50mmHg.

Answer 310

The main complication of pulmonary stenosis is right heart failure. These patients are also at increased risk of infective endocarditis.

Answer 311

Any cause of pulmonary hypertension

Answer 312

Decrescendo murmur in early diastole

Answer 313

Loss of consciousness due to transient drop in blood flow to the brain caused by excessive vagal discharge

Answer 314

Most common cause of fainting in young people

Answer 315

- Emotions- such as? **(3)** - Fear - Severe pain - Blood phobia - Orthostatic stress- caused by? **(2)** - Prolonged standing - Hot weather

Answer 316

- What are they? **(4)** - Loss of consciousness lasting a short time - Patients may experience vagal symptoms before passing out - Dizziness - Sweating - Light-headedness - Twitching of limbs during blackout - Short post-ictal phase

Answer 317

- ECG- why? Check for arrhythmia - When would you do a 24hr ECG? Should be requested in those with multiple episodes of loss of consciousness with quick recovery times - Echocardiogram- why? Check for outflow obstruction - Lying/standing BP- why? Check for orthostatic hypotension - Fasting blood glucose- why? Check for DM/hypoglycaemia

Answer 318

- Patient education & avoiding triggers - Volume expansion- how? **(2)** - Increased dietary salts - Electrolyte rich sports drinks - Fludrocortisone

Answer 319

- Recurrences are common but often occur in clusters - In the long term, the mortality risk is very low, but injury is a concern due to recurrent falls, especially in older people - List complication of falls **(2)** - Injuries and fractures - Extradural or cerebral haemorrhages

Answer 320

Any break in the skin that is located beneath the knee and has lasted longer than 2 weeks without healing is defined as an ulcer by NICE. Venous ulcers, or stasis ulcers, on the other hand, arise due to inefficient blood return from the lower limbs, often associated with chronic venous insufficiency.

Answer 321

Venous ulcers are more common than arterial, accounting for up to 80% of leg ulcers, with the remaining 20% being mainly arterial or mixed venous/arterial. Approximately 1% of individuals will develop a venous ulcer during their lifetime. Venous ulcers are more frequent in middle-aged women.

Answer 322

Venous return in the lower limb relies on the action of the calf muscle pump to return blood up the leg. When the leg muscles relax, valves throughout the venous system prevent the blood from flowing backwards down the venous system. Venous ulcers result when this system fails, in what is referred to as chronic venous insufficiency. Through malfunction of venous valves and reduced calf muscle pump, venous return is impaired and results in venous hypertension in the lower limbs. Venous hypertension then causes dilation of the veins and oedema and venous skin change as fluid and pigment pass through the walls of the vein to deposit within the tissues.

Answer 323

Older age High BMI Reduced calf muscle pump action (i.e. immobility, sedentary lifestyle, limited range of motion of the ankle, prolonged standing) Being female History of deep vein thrombosis, leg fracture, or varicose veins Family history of leg ulcers Pregnancy

Answer 324

Occur in the gaiter area (the distal half of the leg) They are more often on the medial side of the leg Have sloping edges Bleed or ooze Associated with features of chronic venous insufficiency Haemosiderin deposition: brown-red discolouration of the skin Lipodermatosclerosis: an "inverted champagne bottle" appearance of the leg is produced due to hardening and tightening of the skin Atrophy blanche: Depressed white atrophic scars which form slight indentations on the surrounding pigmented skin. They are the result of venous hypertension causing dilatation of capillaries which then atrophy. Venous eczema: flaky, itchy and erythematous skin changes Venous oedema: Pitting oedema which improves on elevation of the lower limbs.

Answer 325

Physical examination An ankle brachial pressure index is calculated to assess for peripheral arterial insufficiency prior to application of compression bandaging. Bloods: FBC, Albumin, U+Es, and HbA1c to investigate for anaemia, poor nutrition, dehydration and diabetes, which all may slow healing ESR/CRP may be done to assess for inflammation and infection of the ulcers Doppler ultrasound: To assess the patency of the arteries and veins. This can be used to assess for deep venous incompetency. Skin swabs are done when there are associated skins of infection, and should not be done routinely.

Answer 326

Wound care: Ideally done by a district nurse or tissue viability nurse They should be debrided as appropriate and then cleaned with tap water. This is followed by appropriate dressing before the application of compression bandaging Patients may require simple analgesia prior to cleaning to reduce pain. Compression therapy to reduce venous hypertension Ankle-brachial pressure index (ABPI) must be done prior to the start of compression therapy. Individuals should be offered the strongest compression they can tolerate. Pentoxifylline This medication is sometimes used to enhance wound healing Individuals should be referred to secondary care if there is diagnostic uncertainty or if the ulcer has features of alternative diagnosis (i.e. rapidly developing) If an ulcer is rapidly developing, a referral to dermatology may be required for a biopsy to rule out malignancy. Surgical intervention for severe or refractory cases, where a skin graft may be used. Hyperbaric oxygen therapy has previously been used, but there is limited evidence to support its use. Measure to prevent venous ulcer recurrence include: Encourage patients to mobilise Elevation of legs Use of emollients and well-fitting footwear Compression hosiery Weight loss if BMI > 30

Answer 327

Infection Cellulitis Suggested by erythema, pain, warmth and swelling surrounding the ulcer, and may be associated with increased exudate Typically treated with oral antibiotics (i.e. flucloxacillin) Compression bandaging should continue during infection if possible. Osteomyelitis of underlying bone Sepsis Pain Typically managed with elevation of the affected limb and simple analgesia. Marjolin's ulcer A rare complication in which a malignancy develops in the base of the ulcer Reduced quality of life (i.e. pain limiting mobility, loss of independence) Eczematous skin changes Topical emollients can be used Recurrence It is common for venous ulcers to recur. It is advised that individuals use compression stockings to prevent recurrence.

Answer 328

It is estimated that approximately 50% of venous ulcers will heal within 6 months, but recurrence rates are reported to be as high as 70%. It is common for individuals to develop multiple venous ulcers which can then recur. Ulcers are less likely to heal and more likely to recur in individuals with: Wounds that are large or have been present for more than 12 months Impaired calf muscle pump Lower socioeconomic status Poor compliance with treatment Low ankle brachial pressure index (ABPI<0.8)

Answer 329

Atrial fibrillation (AF) is characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute. Delay at the AVN means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.

Answer 330

The exact pathophysiology of AF is unclear, but factors that cause atrial dilatation through inflammation and fibrosis leads to disorganised electrical impulses (which originate near the pulmonary veins) that overwhelm the SAN. These disorganised electrical impulses are usually at a rate of 300-600 beats per minute and are intermittently conducted through the AVN leading to irregular activation of the ventricles.

Answer 331

Acute: lasts <48 hours Paroxysmal: lasts <7 days and is intermittent Persistent: lasts >7 days but is amenable to cardioversion Permanent: lasts >7 days and is not amenable to cardioversion Atrial fibrillation can also be classified as to whether it is 'fast' or 'slow'. Fast AF refers to AF that is at a rate of =>100bpm. Slow AF refers to AF that is at a rate of <=60bpm.

Answer 332

Ischaemic heart disease: most common cause in the UK. Hypertension Rheumatic heart disease (typically affecting the mitral valve): most common cause in less developed countries. Peri-/myocarditis

Answer 333

Dehydration Endocrine causes e.g. hyperthyroidism Infective causes e.g. sepsis Pulmonary causes e.g. pneumonia or pulmonary embolism Environmental toxins e.g. alcohol abuse Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia

Answer 334

Palpitations Chest pain Shortness of breath Lightheadedness Syncope

Answer 335

Irregularly irregular pulse rate with a variable volume pulse. A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction). An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles). On auscultation there may be a variable intensity first heart sound. Features suggestive of the underlying cause e.g. hyperthyroidism, alcohol excess, sepsis Features suggestive of complications resulting from the AF e.g. heart failure.

Answer 336

Definitive diagnosis: 12-lead ECG shows absence of p waves with an irregularly irregular rhythmn. If a person has a suspected diagnosis of paroxysmal AF which is not detected on standard ECG, arrange ambulatory electrocardiography or cardiology referral, depending on the frequency and duration of symptoms and local referral pathways Bloods Routine bloods: to look for reversible causes including infection (raised WCC or CRP), hyperthyroidism (raised T3/T4) or alcohol use (raised MCV and GGT). Imaging Echocardiogram: can be used to see if there is a cardiac cause of the AF e.g. left atrial dilatation secondary to mitral valve disease.

Answer 337

New-onset AF within 48 hours and haemodynamic instability Severe symptoms with ventricular rate >150 bpm or <40 bpm Acute decompensated heart failure AF complications (e.g., TIA/stroke) Acute reversible triggers (e.g., pneumonia, sepsis, thyrotoxicosis)

Answer 338

Synchronised DC cardioversion +/- amiodarone

Answer 339

Rate or rhythm control Rhythm control: DC cardioversion or anti-arrhythmics (e.g., flecainide, amiodarone) Anticoagulation with heparin if cardioversion is delayed

Answer 340

Rate control (beta-blockers, diltiazem, or digoxin) Anticoagulate for 3 weeks before attempting cardioversion, or perform TOE to exclude mural thrombus

Answer 341

Beta-blocker (e.g., bisoprolol) Rate-limiting calcium channel blocker (e.g., diltiazem)

Answer 342

AF due to a reversible cause Heart failure caused by AF New-onset AF When clinical judgment favors rhythm control

Answer 343

Electrical cardioversion Pharmacological cardioversion (e.g., flecainide, amiodarone, or sotalol)

Answer 344

To assess stroke risk for determining the need for anticoagulation.

Answer 345

Males: ≥1 Females: ≥2

Answer 346

To evaluate bleeding risk when considering anticoagulation.

Answer 347

Requires LMWH cover for 5 days when initiating INR monitoring is necessary Only oral anticoagulant licensed for valvular AF

Answer 348

Direct Oral Anticoagulants (DOACs): edoxaban, apixaban, rivaroxaban, dabigatran

Answer 349

Ablation of arrhythmogenic focus between pulmonary veins and left atrium High recurrence rate (50%); anticoagulation still required

Answer 350

Heart failure Systemic emboli: Ischaemic Stroke Mesenteric ischaemia Acute limb ischaemia Bleeding: GI Intracranial

Answer 351

Older age (>74) = 1 point R: Reduced hemoglobin (<13 mg/dL males, <12 mg/dL females) = 2 points B: Bleeding history = 2 points I: Insufficient renal function (eGFR <60) = 1 point T: Treatment with antiplatelets = 1 point

Answer 352

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

Answer 353

Acute management vagal manoeuvres: Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe carotid sinus massage intravenous adenosine rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg contraindicated in asthmatics - verapamil is a preferable option electrical cardioversion Prevention of episodes beta-blockers radio-frequency ablation

Answer 354

Local re-entry circuit within the AV node Re-entry circuit forms between atria and ventricles due to presence of accessory pathways (Bundle of Kent)

Answer 355

Normally, there is a co-ordinated electrical conduction system through the heart, starting at the sinoatrial node (SA node), the original pacemaker of the heart. This signal then travels down the surrounding atrial tissue to the atrioventricular node (AV node), which delays the signal to allow for atrial contraction first. After approximately 100 milliseconds of delay, the signal travels through the His-Purkinje system to send the signal to the left and right bundle branches, distributing the electrical signs to the ventricles and allowing for ventricular contraction. In general, SVT is caused by 1 of 3 mechanisms, either re-entry of signals, increased automaticity, or triggered activity. Re-entry This mechanism occurs most notably in AVRT, AVNRT and some forms of atrial tachycardia In this mechanism, there is normal electrical conduction from the atria to the ventricles in the normal pathway However, after this, retrograde conduction occurs via an accessory pathway from the ventricles back up to the atria This leads to repetitive impulse propagation and subsequent tachycardia Increased automaticity This mechanism is responsible for greater than 70% of cases of focal atrial tachycardia Normally, the SA node is responsible for generating the spontaneous action potentials to trigger myocardial contraction However, due to increased automaticity, a group of cardiac cells gain the ability to generate a spontaneous action potential which takes over from the normal SA node functioning The occurs due to pathological changes in the normal membrane resting potential of these cells This leads to rapid and spontaneous depolarisation of cells, which become the dominant rhythm and therefore result in episodes of tachycardia Alternatively, the SA node itself may exhibit enhanced automaticity and therefore trigger action potentials more frequently, leading to tachyarrhythmias Triggered activity This mechanism is largely responsible for atrial fibrillation and atrial flutter, as well as approximately 30% of focal atrial tachycardias SVT as a result of triggered activity occurs due to extra depolarisations which occur immediately after cell re-polarisation, termed 'after-depolarisations' If the after-depolarisations reach a sufficient amplitude to bring the membrane to the electrical threshold for depolarisation, a spontaneous action potential occurs These spontaneous action potentials, called a triggered response, lead to extra-systoles, which have the potential to trigger subsequent tachyarrhythmias

Answer 356

Atrio-ventricular nodal re-entrant tachycardia (AVNRT) Most common form of paroxysmal SVT Originates from a re-entrant retrograde electrical circuit involving the AV node, resulting in initiation and propagation of a cardiac tachyarrhythmia Atrio-ventricular re-entrant tachycardia (AVRT) The second most common form of paroxysmal SVT Similar to AVNRT, it originates via a re-entrant retrograde electrical circuit, however it involves an accessory pathway between the atria and the ventricles, rather than the AV node Some forms of AVRT may exhibit a Wolff-Parkinson-White pattern, whereby an accessory pathway capable of anterograde conduction leads to pre-excitation of the ventricles This accessory pathway is a bypass tract, therefore avoiding the AV node and therefore the normal delay which occurs at this point Leads to the characteristic 'delta wave' on ECG, whereby there is up-sloping at the start of the QRS complex due to the early ventricular excitation Atrial tachycardia May be either focal or multi-focal Focal: due to a single focus of atrial tissue generating more rapid action potentials, leading to a rapid tachyarrhythmia Multi-focal: this is synonymous with atrial flutter, whereby there is a re-entrant electrical circuit in the atria (usually around the tri-cuspid annulus and cavo-tricuspid isthmus) leading to rapid and recurrent de-polarisation without normal SA node functioning and conduction Atrial fibrillation The most common cardiac arrhythmia in general, which can sometimes be paroxysmal, however is more frequently persistent (lasting greater than seven days) Often present in older populations Usually due to long-term remodelling of the atrial tissue, leading to abnormalities in the normal SA node de-polarisation and conduction Instead, rapid and irregular firing from focuses in the atria other than the SA node lead to fibrillatory conduction throughout the atria, and this arrhythmia tends to be sustained due to the atrial tissue structural abnormalities

Answer 357

Clinical features Common symptoms for SVT include: Recurrent episodes of palpitations (95%) Dizziness or light-headedness (75%) Dyspnoea (45%) Chest pain or tightness Progressive fatigue Pounding in the head and/or neck SVT tends to present in discrete episodes which become more frequent and severe with time: Recurrent and paroxysmal Abrupt onset and offset Average duration of episode 10-15 minutes, but can last any period of time from seconds to hours Syncope Very uncommon When present, is a warning sign due to significant increase in risk of sudden cardiac death In adults, SVT episodes tend to present with a heart rate greater than 100 beats per minute

Answer 358

Ventricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.

Answer 359

Factors that increase the risk of VT include: Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia Structural heart disease including previous myocardial infarction and cardiomyopathies Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes) Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)

Answer 360

Pulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines: CPR will be in progress 120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock Adrenaline should be administered every 3-5 minutes thereafter A further dose of amiodarone 150 mg IV should be given after 5 shocks

Answer 361

If a patient has a pulse, management is determined by whether they have any of the following adverse features: Heart failure Myocardial ischaemia (chest pain) Shock Syncope If one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia. If this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).

Answer 362

First line treatment is amiodarone 300mg IV over 10-60 minutes. If this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.

Answer 363

This is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest). IV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).

Answer 364

An irregular broad complex tachycardia. This is always a pulseless rhythm. ECG features include: Tachycardia >100bpm QRS complexes are polymorphic and irregular (>120ms)

Answer 365

The patient should be managed according to the Advanced Life Support algorithm. VF is a shockable rhythm so a 200J bi-phasice unsynchronised shock should be administered. IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock. Adrenaline should be administered every 3-5 minutes thereafter.

Answer 366

Implantable cardioverter defibrillator (ICD)

Answer 367

Heart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. Sinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. Patients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death.

Answer 368

This is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.

Answer 369

High vagal tone: e.g. athletes Acute inferior MI Electrolyte abnormalities: e.g. hyperkalaemia Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors

Answer 370

First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.

Answer 371

Wenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.

Answer 372

MI (mainly inferior) Drugs such as beta/calcium channel blockers, digoxin Professional athletes due to high vagal tone Myocarditis Cardiac surgery

Answer 373

It is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.

Answer 374

Mobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The PR interval is constant (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system. In most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.

Answer 375

Infarction: particularly anterior MI which damages the bundle branches Surgery: mitral valve repair or septal ablation Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis Fibrosis: Lenegre's disease Infiltration: sarcoidosis, haemochromatosis, amyloidosis Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone

Answer 376

Definitive management is with a permanent pacemaker as these patients are at risk of complete heart block and at risk of becoming haemodynamically unstable.

Answer 377

Complete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm. ECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest.

Answer 378

Myocardial infarction: especially inferior Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine Idiopathic fibrosis

Answer 379

Management of complete (third degree) heart block is via the acute bradycardia guideline (see section). Permanent pacemaker requires insertion due to the risk of sudden death.

Answer 380

A bundle branch block (BBB) refers to when electrical impulses to the ventricles are slower than normal, leading to a widened QRS complex >120ms. It can be definied as a left bundle branch block (LBBB) or a right bundle branch block (RBBB). An incomplete BBB refers to when there is a partial delay in electrical conduction in the ventricles and the QRS complex is between 110 to 120ms.

Answer 381

The pneumonic WILLAM MARROW can be used to distinguish between LBBB and RBBB on ECG. In both, the QRS complex has a duration of >120ms. In V1 if the QRS complex has the appearance of a W (the rS' pattern) and in V6 the QRS has the appearance of M (due to a notched R wave) this is a left bundle branch block. WiLLaM. In V1 if there is an appearance of an M (due to the rSr'pattern) and in V6 the QRS complex usually looks normal (N). This is a right bundle branch block. MaRRoW.

Answer 382

Aortic stenosis Ischaemic heart disease Hyperkalaemia Digoxin toxicity Myocardial infarction - new LBBB can indicate STEMI.

Answer 383

Right ventricular hypertrophy Pulmonary embolism Ischaemic heart disease Congenital heart disease (ASD) Normal variant

Answer 384

Dehydration refers to a state of negative fluid balance, typically resulting from inadequate intake or excessive loss of body fluids. Clinically, it presents with symptoms such as dry mucous membranes, tachycardia, hypotension and reduced skin turgor. It can be categorised into isotonic, hypertonic or hypotonic dehydration based on alterations in serum osmolarity.

Answer 385

The most common etiologies include diarrhoea, vomiting, polyuria and fever. In certain patient groups such as the elderly or those with impaired cognition, inadequate fluid intake may also contribute significantly.

Answer 386

Investigation involves assessment of renal function and electrolytes. Elevated urea and creatinine levels suggest prerenal acute kidney injury due to volume depletion whereas disproportionate elevation of urea over creatinine is indicative of gastrointestinal losses.

Cardiology Flashcards

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