Cardio Flashcards

Question

How do you control cardiogenic shock in AHF?

Answer 1

Some ‘COLD’ patients whose AHF has led to a potentially reversible cardiogenic shock may present with haemodynamic instability (systolic blood pressure <90mmHg). These patients require early expert help. Specialists may consider inotropes (e.g. dobutamine) to increase cardiac output and peripheral perfusion, and vasopressors (e.g. adrenaline) to increase blood pressure and vital organ perfusion. The use of these drugs is associated with poorer outcomes.

Answer 2

Increase CO by optimising preload and contractility whilst decreasing afterload.

Answer 3

Before discharge, consider offering patients with reduced ejection fraction (LVEF <40%) heart failure a selection of treatments: - Diuretics - ACE inhibitors / ARBs - Beta Blockers - Aldosterone antagonist

Answer 4

ACEi/ARBs decrease activation of the renin-angiotensin-aldosterone system (RAAS). Contraindications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.

Answer 5

Begin therapy once established on a diuretic and ACEi/ARB, and when BP and congestion are controlled. Beta-blockers decrease heart rate, myocardium oxygen demand and RAAS activation. Contraindications include asthma, 2nd or 3rd-degree atrioventricular block, sick sinus syndrome and sinus bradycardia. ‘Start low and go slow’

Answer 6

Antagonise aldosterone increasing sodium excretion causing diuresis and decreased afterload.

Answer 7

Ivabradine

Answer 8

Sacubitril valsartan

Answer 9

Hydralazine and nitrate:

Answer 10

About 40% of people admitted to hospital with heart failure die or are readmitted within 1 year.9 AHF may cause arrhythmias, particularly atrial fibrillation. There is an increased risk of stroke and other thromboembolic diseases following an episode of AHF.

Answer 11

Chronic heart failure (CHF) is a clinical syndrome involving reduced cardiac output because of impaired cardiac contraction. Typical clinical symptoms of CHF include shortness of breath, fatigue and ankle swelling

Answer 12

The most common causes of heart failure in the UK are coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension. Other causes of heart failure include: Endocrine disease: hypothyroidism, hyperthyroidism, diabetes, adrenal insufficiency, Cushing’s syndrome Medications: calcium antagonists, anti-arrhythmics, cytotoxic medication, beta-blockers. High-output cardiac failure occurs in states where demand exceeds normal cardiac output such as pregnancy, anaemia and sepsis.

Answer 13

The acronym HIGH-VIS is useful to remember some of the causes of CHF: Hypertension (common cause) Infection/immune: viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis) Genetic: hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM) Heart attack: ischaemic heart disease (common cause) Volume overload: renal failure, nephrotic syndrome, hepatic failure Infiltration: sarcoidosis, amyloidosis, haemochromatosis Structural: valvular heart disease, septal defects

Answer 14

Dyspnoea on exertion Fatigue limiting exercise tolerance Orthopnoea: the patient may be using several pillows to reduce this symptom. Paroxysmal nocturnal dyspnoea (PND): attacks of severe shortness of breath in the night that are relieved by sitting up (pathognomonic for CHF). Nocturnal cough with or without the characteristic ‘pink frothy sputum’. Pre-syncope/syncope Reduced appetite

Answer 15

Paroxysmal nocturnal dyspnoea (PND) describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze. They may describe having to sit on the side of the bed or walk around the room, gasping for breath. They may feel suffocated and want to open a window to get fresh air. Symptoms improve over several minutes. There are a few proposed mechanisms to explain paroxysmal nocturnal dyspnoea. Firstly, fluid settles across a large surface area of the lungs as they lie flat to sleep, causing breathlessness. As they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively. Secondly, during sleep, the respiratory centre in the brain becomes less responsive, so the respiratory rate and effort do not increase in response to reduced oxygen saturation like they would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before they wake up feeling very unwell. Thirdly, there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed, reducing cardiac output.

Answer 16

Clinical findings on cardiovascular examination may include: Tachycardia at rest Hypotension Narrow pulse pressure Raised jugular venous pressure Displaced apex beat (due to left ventricular dilatation) Right ventricular heave Gallop rhythm on auscultation (pathognomic for CHF) Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis) Pedal and ankle oedema Clinical findings on respiratory examination may include: Tachypnoea Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields Reduced air entry on auscultation with stony dullness on percussion (pleural effusion) Clinical findings on abdominal examination may include: Hepatomegaly Ascites

Answer 17

ECG + urinalysis + Bloods + Echo + CXR + Cardiac MRI

Answer 18

should be performed on all patients with suspected heart failure. An ECG may identify evidence of previous myocardial infarction (e.g. ‘Q’ waves) or arrhythmias (AV block or atrial fibrillation). A normal ECG makes heart failure unlikely

Answer 19

may show glycosuria (diabetes) or proteinuria (renal disease)

Answer 20

Tachycardia Atrial fibrillation (due to enlarged atria) Left-axis deviation (due to left ventricular hypertrophy) P wave abnormalities (e.g. P.mitrale/P.pulmonale due to atrial enlargement) Prolonged PR interval (due to AV block) Wide QRS complexes (due to ventricular dyssynchrony)

Answer 21

FBC: anaemia U&Es: renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia) LFTs: hepatic congestion Troponin: if considering recent myocardial infarction Lipids/HbA1c: ischaemic risk profile TFTs: hyperthyroidism/hypothyroidism Cardiomyopathy screen N-terminal pro-B-type natriuretic peptide

Answer 22

Serum iron and copper studies (to rule out haemochromatosis and Wilson’s disease) Rheumatoid factor, ANCA/ANA, ENA, dsDNA (to rule out autoimmune disease) Serum ACE (to rule out sarcoidosis) Serum-free light chains (to rule out amyloidosis)

Answer 23

N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured in all patients presenting with symptoms and clinical signs of heart failure to inform the type and urgency of further investigations such as echocardiography: NT-proBNP level >2000 ng/L – refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks NT-proBNP level 400-2000ng/L – refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks NT-proBNP level <400 ng/L – heart failure unlikely

Answer 24

Left ventricular hypertrophy Tachycardia Liver cirrhosis Diabetes Acute or chronic renal disease

Answer 25

Cardiac MRI is the gold standard investigation for assessing ventricular mass, volume and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views

Answer 26

Chronic heart failure can be classified structurally based on left ventricular ejection fraction (LVEF). LVEF is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole. LVEF is usually measured using transthoracic echocardiography, however, MRI, nuclear medicine scans and transoesophageal echocardiography can also be used

Answer 27

The New York Heart Association’s (NYHA) classification system relies on patient symptoms and level of function:3 Class I: no symptoms during ordinary physical activity Class II: slight limitation of physical activity by symptoms Class III: less than ordinary activity leads to symptoms Class IV: inability to carry out any activity without symptoms

Answer 28

Fluid and salt restriction Regular exercise Smoking cessation Reduced alcohol intake

Answer 29

Calcium channel blockers (e.g. verapamil, diltiazem) Tricyclic antidepressants Lithium NSAIDs and COX-2 inhibitors Corticosteroids QT-prolonging medications

Answer 30

Functional capacity, fluid status, cardiac rhythm, cognitive status and nutritional status Renal function The frequency of monitoring depends on the patient’s clinical condition.

Answer 31

A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) L – Loop diuretics (e.g., furosemide or bumetanide)

Answer 32

Diuretics ACEi Beta Blockers ARBs Mineralocorticoid/aldosterone receptor antagonists (MRAs) Sodium-glucose cotransporter-2 (SGLT2) inhibitors

Answer 33

Diuretics should be prescribed to relieve symptoms of fluid overload (e.g. shortness of breath, peripheral oedema). Diuretics (e.g. furosemide) work by increasing sodium excretion via diuresis, ultimately reducing cardiac afterload. Doses should be titrated according to clinical response and renal function should be closely monitored.

Answer 34

All patients with CHF and a reduced ejection fraction (≤40%) should be commenced on an ACE inhibitor unless contraindicated. ACE inhibitors have been shown to improve ventricular function and reduce mortality. U&Es should be checked prior to starting treatment and then after 1-2 weeks of treatment.

Answer 35

include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.

Answer 36

Beta-blockers (e.g. bisoprolol) should be prescribed for all patients with symptomatic heart failure and reduced LVEF (≤40%) unless contraindicated. Beta-blockers decrease heart rate, myocardial oxygen demand and RAAS activation. Blood pressure and heart rate need to be monitored carefully when adjusting doses.

Answer 37

include asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.

Answer 38

If a patient is unable to tolerate an ACE inhibitor (usually due to persistent cough) an ARB (e.g. candesartan) should be prescribed as an alternative. Patients must have normal serum potassium and adequate renal function to commence an ARB.

Answer 39

A low-dose aldosterone antagonist (e.g. spironolactone or eplerenone) should also be prescribed if a patient continues to have symptoms of heart failure despite diuretics, ACE inhibitors and beta-blockers. MRAs antagonise aldosterone, increasing sodium excretion via diuresis, ultimately decreasing cardiac afterload.

Answer 40

SGLT2 inhibitors (e.g. dapagliflozin) can be used as add-on therapy in patients with a reduced LVEF (<40%). Dapagliflozin has been shown to reduce the risk of cardiovascular events and hospital admission. This benefit occurs regardless of the patient’s glycaemic control.

Answer 41

Ivabradine inhibits the sinoatrial node, slowing the heart rate of patients in sinus rhythm, increasing stroke volume whilst preserving myocardial contractility. It has been shown to reduce cardiovascular death or hospitalisation for heart failure by 18%.

Answer 42

Surgical procedures may be used to treat underlying valvular heart disease. Implantable cardioverter defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus rhythm if they identify a shockable arrhythmia. These are used in patients who previously had ventricular tachycardia or ventricular fibrillation. Cardiac resynchronisation therapy (CRT) may be used in severe heart failure, with an ejection fraction of less than 35%. CRT involves biventricular (triple chamber) pacemakers, with leads in the right atrium, right ventricle and left ventricle. The objective is to synchronise the contractions in these chambers to optimise heart function. A heart transplant may be considered in suitable patients with severe disease.

Answer 43

Arrhythmias: atrial fibrillation and ventricular arrhythmias Depression and impaired quality of life Loss of muscle mass Sudden cardiac death Prognosis is poor overall, with approximately 50% of people with heart failure dying within five years of diagnosis.7

Answer 44

HF-rEF and HF-pEF typically develop left-sided heart failure. This may be due to increased left ventricular afterload (e.g. arterial hypertension or aortic stenosis) or increased left ventricular preload (e.g. aortic regurgitation resulting in backflow to the left ventricle).

Answer 45

Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).

Answer 46

pulmonary oedema dyspnoea orthopnoea paroxysmal nocturnal dyspnoea bibasal fine crackles

Answer 47

peripheral oedema ankle/sacral oedema raised jugular venous pressure hepatomegaly weight gain due to fluid retention anorexia ('cardiac cachexia')

Answer 48

Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis

Answer 49

Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists

Answer 50

Arrhythmias are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle.

Answer 51

Ventricular tachycardia Ventricular fibrillation

Answer 52

Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse) Asystole (no significant electrical activity)

Answer 53

refers to a fast heart rate with a QRS complex duration < 0.12 seconds (3 small squares)

Answer 54

Sinus tachycardia (treatment focuses on the underlying cause) Supraventricular tachycardia (treated with vagal manoeuvres and adenosine) Atrial fibrillation (treated with rate control or rhythm control) Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)

Answer 55

Sinus tachycardia will take the normal P wave, QRS complex and T wave pattern. Sinus tachycardia is not an arrhythmia and is usually a response to an underlying cause, such as sepsis or pain.

Answer 56

looks like a QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, and so on. There are P waves, but they are often buried in the T waves, so you cannot see them. It can be distinguished from atrial fibrillation by the regular rhythm and atrial flutter by the absence of a saw-tooth pattern.

Answer 57

It can be tricky to distinguish SVT from sinus tachycardia. SVT has an abrupt onset and a very regular pattern without variability. Sinus tachycardia has a more gradual onset and more variability in the rate. The history is also important, where sinus tachycardia usually has an explanation (e.g., pain or fever), while SVT can appear at rest with no apparent cause.

Answer 58

absent P waves and an irregularly irregular ventricular rhythm.

Answer 59

the atrial rate is usually around 300 beats per minute and gives a saw-tooth pattern on the ECG. A QRS complex occurs at regular intervals depending on how often there is conduction from the atria. This often results in two atrial contractions for every one ventricular contraction, giving a ventricular rate of 150 beats per minute. Atrial flutter gives a sawtooth appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia. There may be 3:1, 4:1 or variable conduction ratios.

Answer 60

loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure

Answer 61

synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.

Answer 62

refers to a fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.

Answer 63

Ventricular tachycardia or unclear cause (treated with IV amiodarone) Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium) Atrial fibrillation with bundle branch block (treated as AF) Supraventricular tachycardia with bundle branch block (treated as SVT)

Answer 64

Normally the electrical signal passes through the atria once, stimulating a contraction, then disappears through the atrioventricular node into the ventricles. Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. The atrial rate is usually around 300 beats per minute. The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute.

Answer 65

Treatment is similar to atrial fibrillation, including anticoagulation based on the CHA2DS2-VASc score. Radiofrequency ablation of the re-entrant rhythm can be a permanent solution.

Answer 66

from the start of the QRS complex to the end of the T wave.

Answer 67

More than 440 milliseconds in men More than 460 milliseconds in women

Answer 68

A prolonged QT interval represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraction. Depolarisation is the electrical process that leads to heart contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.

Answer 69

Torsades de pointes is a type of polymorphic ventricular tachycardia. It translates from French as “twisting of the spikes”, describing the ECG characteristics. On an ECG, it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes gets progressively smaller, then larger, then smaller, and so on. Torsades de pointes will terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac arrest.

Answer 70

Long QT syndrome (an inherited condition) Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia

Answer 71

Stopping and avoiding medications that prolong the QT interval Correcting electrolyte disturbances Beta blockers (not sotalol) Pacemakers or implantable cardioverter defibrillators

Answer 72

Correcting the underlying cause (e.g., electrolyte disturbances or medications) Magnesium infusion (even if they have normal serum magnesium) Defibrillation if ventricular tachycardia occurs

Answer 73

premature ventricular beats caused by random electrical discharges outside the atria. Patients often present complaining of random extra or missed beats. They are relatively common at all ages and in healthy patients. However, they are more common in patients with pre-existing heart conditions (e.g., ischaemic heart disease or heart failure).

Answer 74

appear as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.

Answer 75

Bigeminy refers to when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on.

Answer 76

Reassurance and no treatment in otherwise healthy people with infrequent ectopics Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death Beta blockers are sometimes used to manage symptoms

Answer 77

First-degree heart block occurs where there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex. On an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square).

Answer 78

Second-degree heart block is where some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block: Mobitz type 1 (Wenckebach phenomenon) Mobitz type 2 There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block). A 2:1 block is where there are two P waves for each QRS complex. Every other P wave does not stimulate a QRS complex. It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.

Answer 79

Mobitz type 1 (Wenckebach phenomenon) is where the conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.

Answer 80

Mobitz type 2 is where there is intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves. The PR interval remains normal. There is a risk of asystole with Mobitz type 2.

Answer 81

Third-degree heart block is also called complete heart block. There is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.

Answer 82

Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. A heart rate under 60 can be normal in healthy fit patients without causing any symptoms.

Answer 83

Medications (e.g., beta blockers) Heart block Sick sinus syndrome

Answer 84

Sick sinus syndrome encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.

Answer 85

refers to the absence of electrical activity in the heart (resulting in cardiac arrest).

Answer 86

Mobitz type 2 Third-degree heart block (complete heart block) Previous asystole Ventricular pauses longer than 3 seconds

Answer 87

Intravenous atropine (first line) Inotropes (e.g., isoprenaline or adrenaline) Temporary cardiac pacing Permanent implantable pacemaker, when available

Answer 88

Transcutaneous pacing, using pads on the patient’s chest Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly

Answer 89

antimuscarinic medication and works by inhibiting the parasympathetic nervous system.

Answer 90

Inhibiting the parasympathetic nervous system leads to side effects of pupil dilation, dry mouth, urinary retention and constipation.

Answer 91

The NICE guidelines on hypertension (updated 2022) suggest a diagnosis of hypertension with a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.

Answer 92

also known as primary hypertension. It means a high blood pressure has developed on its own and does not have a secondary cause.

Answer 93

can be remembered with the “ROPED” mnemonic: R – Renal disease O – Obesity P – Pregnancy-induced hypertension or pre-eclampsia E – Endocrine D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)

Answer 94

Renal disease ; When the blood pressure is very high or does not respond to treatment, consider renal artery stenosis. Renal artery stenosis can be diagnosed with duplex ultrasound or an MR or CT angiogram.

Answer 95

Most endocrine conditions can cause hypertension. Hyperaldosteronism (Conn’s syndrome) is an important cause and may be present in 5-10% of patients with hypertension.

Answer 96

Glomerulonephritis Chronic pyelonephritis Diabetic nephropathy Renal cell carcinoma Polycystic kidney disease Obstructive uropathy

Answer 97

Renal artery stenosis Coarctation of the aorta

Answer 98

Primary hyperaldosteronism Phaeochromocytoma Cushing’s syndrome Acromegaly Hypothyroidism Hyperthyroidism

Answer 99

Combined oral contraceptive pill Corticosteroids Non-steroidal anti-inflammatories (NSAIDs) Venlafaxine Alcohol Illicit drugs (e.g. cocaine)

Answer 100

Sex: up to 65 years women tend to have lower blood pressures than men, however, between the ages of 65-74 years women tend to have higher blood pressures. Ethnicity: people of Black African and Black Caribbean origin are at a higher risk of developing HTN. Age: blood pressure rises with increasing age. Lifestyle factors: cigarette smoking, excess alcohol consumption, excess dietary salt intake, obesity and lack of physical activity.

Answer 101

Headache Visual disturbances Seizures Nausea and vomiting Chest pain

Answer 102

Haematuria ‘Frothy’ urine suggestive of proteinuria Dyspnoea (pulmonary oedema) Lower limb swelling (peripheral oedema) Flank tenderness and pain Weight loss is suggestive of renal cell carcinoma

Answer 103

Headache Epistaxis Intermittent claudication Lower limb weakness Cold legs and feet

Answer 104

Muscle weakness, muscle spasms and paraesthesia are suggestive of hyperaldosteronism. Severe headache, palpitations and sweating are suggestive of phaeochromocytoma. Weight gain particularly abdominal, facial and on the back of the neck and shoulders is suggestive of Cushing’s syndrome. Tall statures, swelling of the hands and feet and deepening of the voice are suggestive of acromegaly. Weight gain, cold intolerance and low mood are suggestive of hypothyroidism. Weight loss, heat intolerance and palpitations are suggestive of hyperthyroidism.

Answer 105

Autosomal dominant polycystic kidney disease: enlarged palpable kidneys when balloting the kidneys. Renal artery stenosis: renal bruits heard when auscultating over the area of the renal arteries. Coarctation of the aorta: systolic murmur in the left infraclavicular region under the left scapula and radio-femoral delay. Cushing’s syndrome: moon facies, abdominal purple striae and bruising. Hypothyroidism: brittle nails, dry skin and thin hair. Hyperthyroidism: fine tremor, palmar erythema and a neck goitre.

Answer 106

Ischaemic heart disease (angina and acute coronary syndrome) Cerebrovascular accident (stroke or intracranial haemorrhage) Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms) Hypertensive retinopathy Hypertensive nephropathy Vascular dementia Left ventricular hypertrophy Heart failure

Answer 107

Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24-hour ambulatory blood pressure or home readings to confirm the diagnosis. Having blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect involves more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

Answer 108

NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.

Answer 109

Clinic Reading : > 140/90 Ambulatory/Home Reading : > 135/85

Answer 110

Clinic Reading : > 160/100 Ambulatory/Home Reading : > 150/95

Answer 111

Clinic Reading : > 180/120

Answer 112

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage Bloods for HbA1c, renal function and lipids Fundus examination for hypertensive retinopathy ECG for cardiac abnormalities, including left ventricular hypertrophy

Answer 113

NICE recommend calculating the QRISK score, which estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. When the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

Answer 114

healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.

Answer 115

A – ACE inhibitor (e.g., ramipril) B – Beta blocker (e.g., bisoprolol) C – Calcium channel blocker (e.g., amlodipine) D – Thiazide-like diuretic (e.g., indapamide) ARB – Angiotensin II receptor blocker (e.g., candesartan)

Answer 116

Angiotensin receptor blockers (ARBs) are recommended by NICE instead of ACE inhibitors in patients of Black African or African-Caribbean family origin. (Can replace ACEi) ARBs are an alternative if the person does not tolerate ACE inhibitors (commonly due to a dry cough). ACE inhibitors and ARBs are not used together.

Answer 117

Thiazide-like diuretics are used as an alternative if the patient does not tolerate calcium channel blockers (commonly due to ankle oedema).

Answer 118

ACEi e.g. Ramipril or ARB e.g. Losartan

Answer 119

Calcium Channel Blocker e.g. amlodipine

Answer 120

ACEi/ARB + CCB

Answer 121

ACEi/ARBs + thiazide-like Diuretics e.g Indapamide

Answer 122

CCBs + thiazide-like Diuretics or ACEi/ARBs

Answer 123

ACEi/ ARBs + CCBs + thiazide-like Diuretics

Answer 124

ACEi/ ARBs + CCBs + thiazide-like Diuretics + Spironolactone

Answer 125

ACEi/ ARBs + CCBs + thiazide-like Diuretics + Doxazocin/ Atenolol

Answer 126

Step 4 depends on the serum potassium level: Less than or equal to 4.5 mmol/L consider a potassium-sparing diuretic, such as spironolactone More than 4.5 mmol/L consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)

Answer 127

Spironolactone is a potassium-sparing diuretic. It works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption. It can be helpful when thiazide diuretics are causing hypokalaemia.

Answer 128

Systolic : <140 Diastolic : < 90

Answer 129

Systolic : < 150 Diastolic : > 90

Answer 130

refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema.

Answer 131

The NICE guidelines recommend a same-day referral for patients with accelerated hypertension. Therefore, patients with a blood pressure above 180/120 require a fundoscopy examination to look for these key findings. Additional complications also warrant same-day assessment, such as confusion, heart failure, suspected acute coronary syndrome or acute kidney injury. Patients admitted with a hypertensive emergency are assessed for secondary causes and end-organ damage. Their blood pressure is closely monitored while medications bring it under control.

Answer 132

Sodium nitroprusside Labetalol Glyceryl trinitrate Nicardipine

Answer 133

Inhibit the conversion angiotensin I to angiotensin II

Answer 134

Cough Angioedema Hyperkalaemia

Answer 135

Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction

Answer 136

Flushing Ankle swelling Headache

Answer 137

Inhibit sodium absorption at the beginning of the distal convoluted tubule

Answer 138

Hyponatraemia Hypokalaemia Dehydration

Answer 139

Block effects of angiotensin II at the AT1 receptor

Answer 140

Hyperkalaemia

Answer 141

Peripheral arterial disease (PAD) refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication.

Answer 142

Intermittent claudication is a symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.

Answer 143

Chronic limb-threatening ischaemia (previously critical limb ischaemia) is the end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. There is a significant risk of losing the limb.. The features are pain at rest, non-healing ulcers and gangrene. Critical limb ischaemia typically causes burning pain that is worse at night when the leg is raised, as gravity no longer helps pull blood into the foot.

Answer 144

Acute limb ischaemia refers to a rapid onset of ischaemia in a limb. Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.

Answer 145

Ischaemia refers to an inadequate oxygen supply to the tissues due to reduced blood supply.

Answer 146

Necrosis refers to the death of tissue.

Answer 147

Gangrene refers to the death of the tissue, specifically due to an inadequate blood supply.

Answer 148

Athero- refers to soft or porridge-like and -sclerosis refers to hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls). Atherosclerosis affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. Lipids are deposited in the artery wall, followed by the development of fibrous atheromatous plaques.

Answer 149

Stiffening of the artery walls, leading to hypertension (raised blood pressure) and strain on the heart (whilst trying to pump blood against increased resistance) Stenosis, leading to reduced blood flow (e.g., in angina) Plaque rupture, resulting in a thrombus that can block a distal vessel and cause ischaemia (e.g., in acute coronary syndrome)

Answer 150

Older age Family history Male

Answer 151

Smoking Alcohol consumption Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s) Low exercise / sedentary lifestyle Obesity Poor sleep Stress

Answer 152

Diabetes Hypertension Chronic kidney disease Inflammatory conditions such as rheumatoid arthritis Atypical antipsychotic medications

Answer 153

Angina Myocardial infarction Transient ischaemic attack Stroke Peripheral arterial disease Chronic mesenteric ischaemia

Answer 154

Pain Pallor Pulseless Paralysis Paraesthesia (abnormal sensation or “pins and needles”) Perishing cold

Answer 155

Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of: Thigh/buttock claudication Absent femoral pulses Male impotence

Answer 156

Skin pallor Cyanosis Dependent rubor (a deep red colour when the limb is lower than the rest of the body) Muscle wasting Hair loss Ulcers Poor wound healing Gangrene (breakdown of skin and a dark red/black change in colouration)

Answer 157

Reduced skin temperature Reduce sensation Prolonged capillary refill time (more than 2 seconds) Changes during Buerger’s test

Answer 158

Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test. The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees. The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go: Blue initially, as the ischaemic tissue deoxygenates the blood Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration The dark red colour is referred to as rubor.

Answer 159

Arterial ulcers are caused by ischaemia secondary to an inadequate blood supply

Answer 160

Are smaller than venous ulcers Are deeper than venous ulcers Have well defined borders Have a “punched-out” appearance Occur peripherally (e.g., on the toes) Have reduced bleeding Are painful

Answer 161

Venous ulcers are caused by impaired drainage and pooling of blood in the legs.

Answer 162

Occur after a minor injury to the leg Are larger than arterial ulcers Are more superficial than arterial ulcers Have irregular, gently sloping borders Affect the gaiter area of the leg (from the mid-calf down to the ankle) Are less painful than arterial ulcers Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)

Answer 163

Ankle-brachial pressure index (ABPI) Duplex ultrasound – ultrasound that shows the speed and volume of blood flow Angiography (CT or MRI) – using contrast to highlight the arterial circulation

Answer 164

Ankle-brachial pressure index (ABPI) is the ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm. These readings are taken manually using a Doppler probe. For example, an ankle SBP of 80 and an arm SBP of 100 gives a ratio of 0.8 (80/100). Interpretation (as per NICE CKS 2024): 1.0 – 1.4: normal 0.9 – 0.99: possible peripheral arterial disease Less than 0.9: suggests peripheral arterial disease Less than 0.5: suggests severe and limb-threatening ischaemic

Answer 165

Lifestyle changes are required to manage modifiable risk factors (e.g., stop smoking). Optimise medical treatment of co-morbidities (such as hypertension and diabetes). Exercise training, involving a structured and supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating.

Answer 166

Atorvastatin 80mg Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable) Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)

Answer 167

Endovascular angioplasty and stenting Endarterectomy – cutting the vessel open and removing the atheromatous plaque Bypass surgery – using a graft to bypass the blockage Endovascular angioplasty and stenting involve inserting a catheter through the arterial system under x-ray guidance. At the site of the stenosis, a balloon is inflated to create space in the lumen. A stent is inserted to keep the artery open. Endovascular treatments have lower risks but might not be suitable for more extensive disease.

Answer 168

Patients with critical limb ischaemia require urgent referral to the vascular team. They require analgesia to manage the pain. Urgent revascularisation can be achieved by: Endovascular angioplasty and stenting Endarterectomy Bypass surgery Amputation of the limb if it is not possible to restore the blood supply

Answer 169

Patients with acute limb ischaemia need an urgent referral to the on-call vascular team for assessment. Management options include: Endovascular thrombolysis – inserting a catheter through the arterial system to apply thrombolysis directly into the clot Endovascular thrombectomy – inserting a catheter through the arterial system and removing the thrombus by aspiration or mechanical devices Surgical thrombectomy – cutting open the vessel and removing the thrombus Endarterectomy Bypass surgery Amputation of the limb if it is not possible to restore the blood supply

Answer 170

Varicose veins are distended superficial veins measuring more than 3mm in diameter, usually affecting the legs.

Answer 171

Reticular veins are dilated blood vessels in the skin measuring less than 1-3mm in diameter.

Answer 172

Telangiectasia refers to dilated blood vessels in the skin measuring less than 1mm in diameter. They are also known as spider veins or thread veins.

Answer 173

Veins contain valves that only allow blood to flow in one direction, towards the heart. In the legs, as the muscles contract, they squeeze blood upwards against gravity. The valves prevent gravity from pulling the blood back into the feet. When the valves become incompetent, the blood is drawn downwards by gravity and pools in the veins and feet. The deep and superficial veins are connected by vessels called the perforating veins (or perforators), which allow blood to flow from the superficial veins to the deep veins. When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them. This leads to dilatation and engorgement of the superficial veins, forming varicose veins.

Answer 174

When blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs. This gives a brown discolouration to the lower legs. Pooling of blood in the distal tissues results in inflammation. The skin becomes dry and inflamed, referred to as venous eczema.

Answer 175

The skin and soft tissues become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipodermatosclerosis.

Answer 176

Increasing age Family history Female Pregnancy Obesity Prolonged standing (e.g., occupations involving standing for long periods) Deep vein thrombosis (causing damage to the valves)

Answer 177

Varicose veins present with engorged and dilated superficial leg veins. They may be asymptomatic or have symptoms of: Heavy or dragging sensation in the legs Aching Itching Burning Oedema Muscle cramps Restless legs Patients may also have signs and symptoms of chronic venous insufficiency (e.g., skin changes and ulcers).

Answer 178

apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.

Answer 179

apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).

Answer 180

with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.

Answer 181

apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.

Answer 182

Duplex ultrasound can be used to assess the extent of varicose veins. It is an ultrasound that shows the speed and volume of blood flow.

Answer 183

Varicose veins in pregnancy often improve after delivery. Simple treatment measures include: Weight loss if appropriate Staying physically active Keeping the leg elevated when possible to help drainage Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)

Answer 184

Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein Stripping – the veins are ligated and pulled out of the leg

Answer 185

Prolonged and heavy bleeding after trauma Superficial thrombophlebitis (thrombosis and inflammation in the superficial veins) Deep vein thrombosis All the issues of chronic venous insufficiency (e.g., skin changes and ulcers)

Answer 186

Syncope is the term used to describe the event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall. Syncopal episodes are also known as vasovagal episodes, or simply fainting.

Answer 187

A vasovagal episode (or attack) is caused by a problem with the autonomic nervous system regulating blood flow to the brain. When the vagus nerve receives a strong stimulus, such as an emotional event, painful sensation or change in temperature it can stimulate the parasympathetic nervous system. Parasympathetic activation counteracts the sympathetic nervous system, which keeps the smooth muscles in blood vessels constricted. As the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”.

Answer 188

Patients often remember the event and can recall how they felt prior to fainting. This is called the prodrome, and involves feeling: Hot or clammy Sweaty Heavy Dizzy or lightheaded Vision going blurry or dark Headache

Answer 189

A collateral history from someone that witnessed the event is essential to get an accurate impression of what happened. During a vasovagal episode they may describe the person: Suddenly losing consciousness and falling to the ground Unconscious on the ground for a few seconds to a minute as blood returns to their brain There may be some twitching, shaking or convulsion activity, which can be confused with a seizure The patient may be a bit groggy following a faint, however this is different from the postictal period that follows a seizure. Postictal patients have a prolonged period of confusion, drowsiness, irritability and disorientation. There may be incontinence with both seizures and syncopal episodes.

Answer 190

Dehydration Missed meals Extended standing in a warm environment, such as a school assembly A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

Answer 191

Hypoglycaemia Dehydration Anaemia Infection Anaphylaxis Arrhythmias Valvular heart disease Hypertrophic obstructive cardiomyopathy

Answer 192

Prolonged upright position before the event Lightheaded before the event Sweating before the event Blurring or clouding of vision before the event Reduced tone during the episode Return of consciousness shortly after falling No prolonged post-ictal period

Answer 193

Epilepsy aura (smells. tastes or deja vu) before the event Head turning or abnormal limb positions Tonic clonic activity Tongue biting Cyanosis Lasts more than 5 minutes Prolonged post-ictal period

Answer 194

ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome 24 hour ECG if paroxysmal arrhythmias are suspected Echocardiogram if structural heart disease is suspected Bloods, including a full blood count (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)

Answer 195

Avoid dehydration Avoid missing meals Avoid standing still for long periods When experiencing prodromal symptoms such as sweating and dizziness, sit or lie down, have some water or something to eat and wait until feeling better

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