Cardiology

Question 1

What is the cut off blood pressure value for further investigation

Answer 1

Age < 80 years
Clinic 140/90 mmHg ABPM 135/85 mmHg
Age > 80 years
Clinic150/90 mmHg ABPM 145/85 mmHg

Question 2

What is offered if BP is found to be over 140/90

Answer 2

Ambulatory BP monitoring or home BP monitoring

Question 3

What is done if on ABPM or HBPM BP remains below 135/85

Answer 3

nothing

Question 4

What is stage 1 hypertension? When is this treated?

Answer 4

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Treat if <80 years and any of the following
-target organ damage
-established cardiovascular disease
-renal disease
-diabetes
-10 yr cardiovascular risk greater than or equal to 10%

Question 5

What is stage 2 hypertension? when is this treated?

Answer 5

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
-treat all

Question 6

What is severe hypertension?

Answer 6

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

Question 7

When would you admit for specialist assessment of severe hypertension?

Answer 7

admit for specialist assessment if:

signs of retinal haemorrhage or papilloedema (accelerated hypertension) or
life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)

Question 8

What is done for severe hypertension that doesn’t warrant admission?

Answer 8

if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)

if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM.
if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days

Question 9

What is ABPM? and what is offered if this isnt tolerated or declined?

Answer 9

Ambulatory blood pressure monitoring (ABPM)

at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements

If ABPM is not tolerated or declined HBPM should be offered

Question 10

What is HBPM?

Answer 10

Home blood pressure monitoring (HBPM)

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
BP should be recorded twice daily, ideally in the morning and evening
BP should be recorded for at least 4 days, ideally for 7 days
discard the measurements taken on the first day and use the average value of all the remaining measurements

Question 11

Describe lifestyle modifications that should be advised for patients to lower BP

Answer 11

a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
caffeine intake should be reduced
the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight

Question 12

Descrbe stage 1 management of hypertension

Answer 12

patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A)
angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
patients >= 55-years-old or of black African or African–Caribbean origin: Calcium channel blocker (C)
ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line

Question 13

Describe stage 2 management of hypertension

Answer 13

if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic
if already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide-like Diuretic
for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
(A + C) or (A + D) or (C + A) or (C + D)

Question 14

Describe stage 3 treatment of hypertension

Answer 14

add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)

Question 15

Describe stage 4 treatment of hypertension

Answer 15

NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
confirm elevated clinic BP with ABPM or HBPM
assess for postural hypotension.
discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker

Question 16

What is the most common cause of secondary hypertension?

Answer 16

primary hyperaldosteronism, including Conn’s syndrome. This makes it the single most common cause of secondary hypertension.

Question 17

What are 4 renal causes of secondary hypertension?

Answer 17

Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include:

glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis

Question 18

What are 5 endocrine causes of secondary hypertension?

Answer 18

Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood pressure:

phaeochromocytoma
Cushing's syndrome
Liddle's syndrome
congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
acromegaly

Question 19

What are 5 drug causes of hypertension?

Answer 19

Drug causes:

steroids
monoamine oxidase inhibitors
the combined oral contraceptive pill
NSAIDs
leflunomide

Question 20

What are the blood pressure targets for patients with T1DM? What drug is first line? what drug should be avoided?

Answer 20

Intervention levels for recommending blood pressure management should be 135/85 mmHg unless the adult with type 1 diabetes has albuminuria or 2 or more features of metabolic syndrome, in which case it should be 130/80 mmHg

Because ACE inhibitors/or angiotensin-II receptor antagonist (A2RBs) have a renoprotective effect in diabetes they are the first-line antihypertensive regardless of age.

The routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides, as they may cause insulin resistance, impair insulin secretion and alter the autonomic response to hypoglycaemia.

Question 21

What is BNP? What are 3 causes of raised BNP? What are 3 causes of reduced BNP?

Answer 21

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.

Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.

Question 22

What are three effects of BNP?

Answer 22

Effects of BNP

vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

Question 23

What are four clinical uses of BNP?

Answer 23

Diagnosing patients with acute dyspnoea
-a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
-NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure

Prognosis in patients with chronic heart failure
-initial evidence suggests BNP is an extremely useful marker of prognosis

Guiding treatment in patients with chronic heart failure
-effective treatment lowers BNP levels

Screening for cardiac dysfunction
-not currently recommended for population screening

Question 24

What is the mechanism of action of ACE inhibitors?

Answer 24

inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys

renoprotective mechanism
angiotensin II constricts the efferent glomerular arterioles
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli
this is particularly important in diabetic nephropathy

ACE inhibitors are activated by phase 1 metabolism in the liver

Question 25

What are the 4 common side effects of ACEI?

Answer 25

Cough occurs in around 15% of patients and may occur up to a year after starting treatment thought to be due to increased bradykinin levels angioedema: may occur up to a year after starting treatment hyperkalaemia first-dose hypotension: more common in patients taking diuretics

Question 26

What are the 5 cautions/contraindications of ACEI

Answer 26

-pregnancy and breastfeeding - avoid -renovascular disease - may result in renal impairment -aortic stenosis - may result in hypotension -hereditary of idiopathic angioedema -specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

Question 27

What is the interaction between diuretics and ACEI?

Answer 27

patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) significantly increases the risk of hypotension

Question 28

Describe the monitoring of ACEI

Answer 28

urea and electrolytes should be checked before treatment is initiated and after increasing the dose a rise in the creatinine and potassium may be expected after starting ACE inhibitors acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis

Question 29

When are ARBs used? who should you exercise caution in? what is the mechanism?

Answer 29

Given to patients who can't tolerate ACEI (usually due to cough) Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-effects include hypotension and hyperkalaemia. Mechanism - block effects of angiotensin II at the AT1 receptor

Question 30

What is the treatment of all patients who present with an ACS?

Answer 30

aspirin 300mg oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines morphine should only be given for patients with severe pain previously IV morphine was given routinely evidence, however, suggests that this may be associated with adverse outcomes nitrates can be given either sublingually or intravenously useful if the patient has ongoing chest pain or hypertension should be used in caution if patient hypotensive

Question 31

What are the ECG criteria for patients with STEMI?

Answer 31

STEMI criteria clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of: 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years 1.5 mm ST elevation in V2-3 in women 1 mm ST elevation in other leads new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 32

When is PCI offered? what kind of stents are used? what access is preferred?

Answer 32

percutaneous coronary intervention should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI) if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis radial access is preferred to femoral access

Question 33

When is fibrinolysis offered?

Answer 33

fibrinolysis should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) that does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI

Question 34

what antiplatelets are given prior to PCI?

Answer 34

Further antiplatelet prior to PCI this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug if the patient is not taking an oral anticoagulant: prasugrel if taking an oral anticoagulant: clopidogrel

Question 35

What drug therapy is given during PCI?

Answer 35

patients undergoing PCI with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus patients undergoing PCI with femoral access: bivalirudin with bailout GPI

Question 36

What procedures other than stenting can be done during PCI?

Answer 36

Other procedures during PCI thrombus aspiration, but not mechanical thrombus extraction, should be considered complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock

Question 37

Describe the management of patients with NSTEMI/unstable angina

Answer 37

1. Aspirin 300mg and fondaparinux (if PCI not planned immediately) 2. Estimate a 6 month mortality (GRACE) - if low risk <=3% give ticagrelor -If high risk >3% do PCI, offer immediately or within 72hrs. Add prasugrel or ticagrelor, give unfractionated heparin, use drug-eluting stents

Question 38

How does the management of patients with NSTEMI/unstable angina change if they are at high risk of bleeding?

Answer 38

Consider swapping fondaparinux to a different antithrombin/dose, swapping prasugrel for ticagrelor or ticagrelor for clopidogrel If patients on anitcoagulations use clopidogrel

Question 39

What is the grace score? -what 6 factors are taken into consideration?

Answer 39

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors: age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels

Question 40

Describe the risk stratification of the GRACE score

Answer 40

Predicted 6mth mortality, risk of future adverse cardiac events 1.5% or below Lowest > 1.5% to 3.0% Low > 3.0% to 6.0% Intermediate > 6.0% to 9.0% High over 9.0% Highest

Question 41

Describe the further durg therapy given to patients going for PCI with unstable angina/NSTEMI

Answer 41

Further drug therapy unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor if taking an oral anticoagulant: clopidogrel

Question 42

Describe the further drug therapy for patients who are medically managed with NSTEMI/Unstable angina

Answer 42

Further drug therapy further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) if the patient is not at a high risk of bleeding: ticagrelor if the patient is at a high risk of bleeding: clopidogrel

Question 43

What is the mechanism of action of clopidogrel? What is an important interaction?

Answer 43

Mechanism antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets Change omeprazole to lansoprazole

Question 44

Describe chest pain in MI

Answer 44

Cardiac-sounding pain heavy, central chest pain they may radiate to the neck and left arm nausea, sweating elderly patients and diabetics may experience no pain Risk factors for cardiovascular disease

Question 45

What is the diagnosis? History of asthma, Marfan's etc Sudden dyspnoea and pleuritic chest pain

Answer 45

Pneumothorax

Question 46

Describe the features and risk factors of PE

Answer 46

Sudden dyspnoea and pleuritic chest pain Calf pain/swelling Current combined pill user, malignancy

Question 47

What is the diagnosis? Sharp pain relieved by sitting forwards May be pleuritic in nature

Answer 47

Pericarditis

Question 48

What is pericarditis?

Answer 48

Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks.

Question 49

What are 9 causes of pericarditis?

Answer 49

viral infections (Coxsackie) tuberculosis uraemia post-myocardial infarction early (1-3 days): fibrinous pericarditis late (weeks to months): autoimmune pericarditis (Dressler's syndrome) radiotherapy connective tissue disease systemic lupus erythematosus rheumatoid arthritis hypothyroidism malignancy lung cancer breast cancer trauma

Question 50

What are the clinical features of pericarditis?

Answer 50

chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include a non-productive cough, dyspnoea and flu-like symptoms pericardial rub

Question 51

Describe 3 investigations for pericarditis

Answer 51

ECG changes the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis all patients with suspected acute pericarditis should have transthoracic echocardiography bloods inflammatory markers troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

Question 52

What is found if coronary / spinal arteries are involved in an aortic dissection? what if the distal aorta is involved?

Answer 52

coronary arteries → angina spinal arteries → paraplegia distal aorta → limb ischaemia

Question 53

Can patients with pericarditis be managed as outpatients?

Answer 53

the majority of patients can be managed as outpatients patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient

Question 54

What is the treatment of pericarditis? 3

Answer 54

treat any underlying cause, most patients however will have pericarditis secondary to viral infection, meaning no specific treatment is indicated strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over

Question 55

what is the chest pain type and findings in aortic dissection?

Answer 55

'Tearing' chest pain radiating through to the back Unequal upper limb blood pressure

Question 56

Shingles - does pain come first or rash?

Answer 56

Pain often precedes the rash

Question 57

When does aortic dissection occur? where in the aorta is this found? who is this most common in?

Answer 57

This occurs when there is a flap or filling defect within the aortic intima. Blood tracks into the medial layer and splits the tissues with the subsequent creation of a false lumen. It most commonly occurs in the ascending aorta or just distal to the left subclavian artery (less common). The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered. It is most common in Afro-carribean males aged 50-70 years.

Question 58

What are 7 associations with aortic dissection?

Answer 58

hypertension: the most important risk factor trauma bicuspid aortic valve collagens: Marfan's syndrome, Ehlers-Danlos syndrome Turner's and Noonan's syndrome pregnancy syphilis

Question 59

Describe the pulse found in aortic dissection

Answer 59

weak or absent carotid, brachial, or femoral pulse variation (>20 mmHg) in systolic blood pressure between the arms

Question 60

what is found when examining heart sounds of patients with aortic dissection? what happens to their blood pressure?

Answer 60

aortic regurgitation hypertension

Question 61

What is found on ECG of aortic dissection?

Answer 61

the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

Question 62

Describe the classification system for aortic dissection? how are they treated?

Answer 62

In the Stanford classification system the disease is classified into lesions with a proximal origin (Type A) and those that commence distal to the left subclavian (Type B). Proximal (Type A) lesions are usually treated surgically, type B lesions are usually managed non operatively. type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases

Question 63

What are the ECG findings of PE?

Answer 63

Diagnosis may be suggested by various ECG findings including S waves in lead I, Q waves in lead III and inverted T waves in lead III. Confirmation of the diagnosis is usually made through use of CT pulmonary angiography.

Question 64

What is the typical history of a peptic ulcer?

Answer 64

Patients usually develop sudden onset of epigastric abdominal pain, it may be soon followed by generalised abdominal pain. There may be features of antecendant abdominal discomfort, the pain of gastric ulcer is typically worse immediately after eating whereas eating may improve pain of duodenal ulcer

Question 65

what is the diagnosis of peptic ulcer? how is this managed?

Answer 65

Diagnosis may be made by erect chest x-ray which may show a small amount of free intra-abdominal air (very large amounts of air are more typically associated with colonic perforation). Treatment is usually with a laparotomy, small defects may be excised and overlaid with an omental patch, larger defects are best managed with a partial gastrectomy.

Question 66

What is boerhaaves syndrome? where is this found? what is the history? what is a complication

Answer 66

Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting. The rupture is usually distally sited and on the left side. Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting. Severe sepsis occurs secondary to mediastinitis.

Question 67

What is the diagnosis of boerhaaves syndrome? how is this treated?

Answer 67

Diagnosis is CT contrast swallow. Treatment is with thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin. Delays beyond 24 hours are associated with a very high mortality rate.

Question 68

When does chest pain warrant referral?

Answer 68

Referral current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission chest pain 12-72 hours ago: refer to hospital the same-day for assessment chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

Question 69

What are the three features of anginal pain? what constitutes typical angina vs atypical angina vs non-anginal chest pain?

Answer 69

NICE define anginal pain as the following: 1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms 2. precipitated by physical exertion 3. relieved by rest or GTN in about 5 minutes patients with all 3 features have typical angina patients with 2 of the above features have atypical angina patients with 1 or none of the above features have non-anginal chest pain

Question 70

What are the investigations for angina?

Answer 70

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes): 1st line: CT coronary angiography 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) 3rd line: invasive coronary angiography

Question 71

Give examples of non-invasive functional imaging?

Answer 71

Examples of non-invasive functional imaging: myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or stress echocardiography or first-pass contrast-enhanced magnetic resonance (MR) perfusion or MR imaging for stress-induced wall motion abnormalities

Question 72

What should all patients be offered who have angina?

Answer 72

all patients should receive aspirin and a statin in the absence of any contraindication sublingual glyceryl trinitrate to abort angina attacks

Question 73

What are 3 adverse effects of statins?

Answer 73

-myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin) -liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range -there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who've previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage

Question 74

what are 2 contraindications to statins?

Answer 74

Contraindications macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course pregnancy

Question 75

What 4 patient groups should be offered a statin?

Answer 75

Who should receive a statin? all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease) following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10% patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy

Question 76

What are the first line medications for angina?

Answer 76

NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on 'comorbidities, contraindications and the person's preference' if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used

Question 77

What to do if there is a poor response to initial treatment of angina?

Answer 77

if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od) if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa

Question 78

What calcium channel blockers should be used if in combination with a beta blockern to treat angina?

Answer 78

if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine) remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)

Question 79

What to do if a patient can't tolerate the addition of a beta blocker/calcium channel blocker and they are on monotherapy for angina?

Answer 79

if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate ivabradine nicorandil ranolazine

Question 80

What is nicorandil?

Answer 80

Nicorandil is a vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

Question 81

What are 3 adverse effects of nicorandil? what is the contraindication to nicorandil;?

Answer 81

Adverse effects headache flushing skin, mucosal and eye ulceration gastrointestinal ulcers including anal ulceration Contraindications left ventricular failure

Question 82

When can a third drug be added in angina care?

Answer 82

if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

Question 83

What is the mechanism of action of nitrates?

Answer 83

Mechanism of action nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

Question 84

What are 4 side effects of nitrates?

Answer 84

ide-effects hypotension tachycardia headaches flushing

Question 85

what to do if patients get nitrate tolerance?

Answer 85

many patients who take nitrates develop tolerance and experience reduced efficacy NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

Question 86

Describe the use of adrenaline in ALS

Answer 86

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

Question 87

Describe the use of amiodarone in ALS

Answer 87

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

Question 88

What are th 4 'h's reversible causes of cardiac arrest?

Answer 88

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

Question 89

What are th 4 'T's reversible causes of cardiac arrest?

Answer 89

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

Question 90

What are the classical features of tamponade? what other features are seen? 6

Answer 90

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure. Classical features - Beck's triad: hypotension raised JVP muffled heart sounds Other features: dyspnoea tachycardia an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: electrical alternans

Question 91

What is kussmauls sign?

Answer 91

Kussmaul's sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis.

Question 92

What is the difference between tamponade and constrictive pericarditis: JVP Pulsus paradoxus Kussmaul's sign Characteristic features

Answer 92

JVP Absent Y descent /X + Y present Pulsus paradoxus Present /Absent Kussmaul's sign Rare / Present Characteristic features - /Pericardial calcification on CXR

Question 93

How common is AF?

Answer 93

It is very common, being present in around 5% of patients over aged 70-75 years and 10% of patients aged 80-85 years

Question 94

Describe the classification of AF

Answer 94

AF may by classified as either first detected episode, paroxysmal, persistent or permanent. first detected episode (irrespective of whether it is symptomatic or self-terminating) recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rated control and anticoagulation if appropriate

Question 95

What is used in rate controlling AF?

Answer 95

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF. If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following: a betablocker diltiazem (calcium channel blocker) digoxin

Question 96

What is CHA2DS2-VASc score?

Answer 96

C Congestive heart failure 1 H Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2 Age 65-74 years 1 D Diabetes 1 S2 Prior Stroke, TIA or thromboembolism 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1 S Sex (female)

Question 97

What CHA2DS2-VASc score suggests anticoagulation?

Answer 97

0 No treatment 1 Males: Consider anticoagulation Females: No treatment (this is because their score of 1 is only reached due to their gender) 2 or more Offer anticoagulation

Question 98

What is the orbit score?

Answer 98

Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2 Age > 74 years 1 Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2 Renal impairment (GFR < 60 mL/min/1.73m2) 1 Treatment with antiplatelet agents 1

Question 99

What does the orbit score mean?

Answer 99

ORBIT score Risk group Bleeds per 100 patient-years 0-2 Low 2.4 3 Medium 4.7 4-7 High 8.1

Question 100

How to cardiovert patients who's AF has been less than 48hrs onset?

Answer 100

If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either: electrical - 'DC cardioversion' pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary

Question 101

Describe the cardioversion process for patients with AF who have had this for longer than 48hrs

Answer 101

If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately. NICE recommend electrical cardioversion in this scenario, rather than pharmacological. If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

Question 102

What is the management of AF following a stroke or TIA?

Answer 102

Management following a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy for longer-term stroke prevention, NICE Clinical Knowledge Summaries recommend warfarin or a direct thrombin or factor Xa inhibitor the timing of when to start depends on whether it is a TIA or stroke following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

Question 103

Who shouldn't be offered rate control as a first line strategy in AF?

Answer 103

Rate control should be offered as the first‑line treatment strategy for atrial fibrillation except in people: whose atrial fibrillation has a reversible cause who have heart failure thought to be primarily caused by atrial fibrillation with new‑onset atrial fibrillation (< 48 hours) with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm for whom a rhythm‑control strategy would be more suitable based on clinical judgement

Question 104

What agents are used to maintain SR in patients with a history of AF?

Answer 104

Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation beta-blockers dronedarone: second-line in patients following cardioversion amiodarone: particularly if coexisting heart failure

Question 105

Describe the anticoagulation in catheter ablation for AF -prior to procedure -post procedure

Answer 105

Anticoagulation should be used 4 weeks before and during the procedure it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per their CHA2DS2-VASc score if score = 0: 2 months anticoagulation recommended if score > 1: longterm anticoagulation recommended

Question 106

What are three complications of catheter ablation for AF?

Answer 106

cardiac tamponade stroke pulmonary vein stenosis

Question 107

What is the success rate of catheter ablation for AF?

Answer 107

around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patients who've undergone multiple procedures around 80% are in sinus rhythm

Question 108

Describe the ECG findings of atrial flutter

Answer 108

ECG findings 'sawtooth' appearance as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min flutter waves may be visible following carotid sinus massage or adenosine

Question 109

Describe the management of atrial flutter

Answer 109

Management is similar to that of atrial fibrillation although medication may be less effective atrial flutter is more sensitive to cardioversion however so lower energy levels may be used radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

Question 110

What is the mechanism of action of amiodarone?

Answer 110

Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

Question 111

What are 4 disadvantages of amiodarone?

Answer 111

The use of amiodarone is limited by a number of factors very long half-life (20-100 days). For this reason, loading doses are frequently used should ideally be given into central veins (causes thrombophlebitis) has proarrhythmic effects due to lengthening of the QT interval interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin numerous long-term adverse effects (see below)

Question 112

Describe the monitoring of patients taking amiodarone

Answer 112

Monitoring of patients taking amiodarone TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months

Question 113

What are the adverse effects of amiodarone? 10

Answer 113

thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval

Question 114

what is the acute management of SVT? what is used to prevent SVT?

Answer 114

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

Question 115

What is the mechanism of action of warfarin?

Answer 115

Mechanism of action inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

Question 116

What are the two indications for warfarin?

Answer 116

mechanical heart valves target INR depends on the valve type and location mitral valves generally require a higher INR than aortic valves. second-line after DOACs: venous thromboembolism: target INR = 2.5, if recurrent 3.5 atrial fibrillation, target INR = 2.5

Question 117

what are 5 factors that can potentiate warfarin?

Answer 117

Factors that may potentiate warfarin liver disease P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin cranberry juice drugs which displace warfarin from plasma albumin, e.g. NSAIDs inhibit platelet function: NSAIDs

Question 118

How do you manage high INR with major bleeding

Answer 118

Stop warfarin Give intravenous vitamin K 5mg Prothrombin complex concentrate - if not available then FFP*

Question 119

How do you manage INR >8 and mild bleeding?

Answer 119

Stop warfarin Give intravenous vitamin K 1-3mg Repeat dose of vitamin K if INR still too high after 24 hours Restart warfarin when INR < 5.0

Question 120

How do you managed INR >8 and no bleeding?

Answer 120

Stop warfarin Give vitamin K 1-5mg by mouth, using the intravenous preparation orally Repeat dose of vitamin K if INR still too high after 24 hours Restart when INR < 5.0

Question 121

HOw do you manage INR 5-8 with mild bleeding?

Answer 121

Stop warfarin Give intravenous vitamin K 1-3mg Restart when INR < 5.0

Question 122

How do you manage INR 5-8 with no bleeding?

Answer 122

Withhold 1 or 2 doses of warfarin Reduce subsequent maintenance dose

Question 123

Name 7 inducers of P450 enzyme? what happens to INR?

Answer 123

INR decreases antiepileptics: phenytoin, carbamazepine barbiturates: phenobarbitone rifampicin St John's Wort chronic alcohol intake griseofulvin smoking (affects CYP1A2, reason why smokers require more aminophylline)

Question 124

Name 11 P450 enxyme inhibitors |(INR increases)

Answer 124

antibiotics: ciprofloxacin, clarithromycine/erythromycin isoniazid cimetidine,omeprazole amiodarone allopurinol imidazoles: ketoconazole, fluconazole SSRIs: fluoxetine, sertraline ritonavir sodium valproate acute alcohol intake quinupristin

Question 125

What are 4 side effects of warfarin?

Answer 125

haemorrhage teratogenic, although can be used in breastfeeding mothers skin necrosis when warfarin is first started biosynthesis of protein C is reduced this results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration thrombosis may occur in venules leading to skin necrosis purple toes

Question 126

What are 3 indications of DOAC?

Answer 126

prevention of stroke in non-valvular AF. NICE stipulate that certain other risk factors should be present. These are complicated and differ between the DOACs but generally require one of the following to be present: prior stroke or transient ischaemic attack age 75 years or older hypertension diabetes mellitus heart failure prevention of VTE following hip/knee surgery treatment of DVT and PE

Question 127

What is aortic regurgitation and what can cause this?

Answer 127

Aortic regurgitation (AR) is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole. It can be caused either by disease of the aortic valve or by distortion or dilation of the aortic root and ascending aorta.

Question 128

What are the 5 causes of aortic valve disease that present chronically as aortic regurgitation

Answer 128

rheumatic fever: the most common cause in the developing world calcific valve disease connective tissue diseases e.g. rheumatoid arthritis/SLE bicuspid aortic valve (affects both the valves and the aortic root

Question 129

What is the cause of aortic valve disease that presents acutely as aortic regurgitation?

Answer 129

infective endocarditis

Question 130

What is the cause of aortic root disease that presents acutely as aortic regurgitation?

Answer 130

aortic dissection

Question 131

What are the 5 causes of aortic root disease that present chronically as aortic regurgitation?

Answer 131

bicuspid aortic valve (affects both the valves and the aortic root) spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome

Question 132

What are 6 features of aortic regurgitation?

Answer 132

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre collapsing pulse wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

Question 133

What is the investigation and management of aortic regurgitation?

Answer 133

Suspected AR should be investigated with echocardiography. Management medical management of any associated heart failure surgery: aortic valve indications include symptomatic patients with severe AR asymptomatic patients with severe AR who have LV systolic dysfunction

Question 134

What are four features of symptomatic aortic stenosis?

Answer 134

chest pain dyspnoea syncope / presyncope (e.g. exertional dizziness) murmur an ejection systolic murmur (ESM) is classically seen in aortic stenosis classically radiates to the carotids this is decreased following the Valsalva manoeuvre

Question 135

What are 8 features of severe aortic stenosis?

Answer 135

narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure

Question 136

What are 5 causes of aortic stenosis, which is most common?

Answer 136

degenerative calcification (most common cause in older patients > 65 years) bicuspid aortic valve (most common cause in younger patients < 65 years) William's syndrome (supravalvular aortic stenosis) post-rheumatic disease subvalvular: HOCM

Question 137

Describe the management of aortic stenosis?

Answer 137

if asymptomatic then observe the patient is a general rule if symptomatic then valve replacement if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery

Question 138

Describe the options for aortic valve replacement in aortic stenosis

Answer 138

options for aortic valve replacement (AVR) include: surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined transcatheter AVR (TAVR) is used for patients with a high operative risk

Question 139

Mitral regurgitation -What is this? -Is this common? -What is the result of this if not treated?

Answer 139

Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the mitral valve on systole. It is the second most common valve disease after aortic stenosis. The mitral valve is located between the left atrium and ventricle, and regurgitation leads to a less efficient heart as less blood is pumped through the body with each contraction. This said, MR is common in otherwise healthy patients to a trivial degree and does not need treatment. As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myocardium becomes less efficient, and eventually go into irreversible heart failure.

Question 140

What are 7 risk factors of mitral regurgitation?

Answer 140

Risk factors Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome

Question 141

What are 5 causes of mitral regurgiation?

Answer 141

-Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting structures. -Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does not close properly and allows for backflow. Most patients with this have a trivial degree of mitral regurgitation. - Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to develop endocarditis as opposed to their peers. -Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves and therefore result in mitral regurgitation. - Congenital

Question 142

What are the signs and symptoms of MR?

Answer 142

Symptoms Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema. Signs The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2

Question 143

What may be seen on CXR/ECG/Echo with MR?

Answer 143

Investigations ECG may show a broad P wave, indicative of atrial enlargement Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle Echocardiography is crucial to diagnosis and to assess severity

Question 144

What are the treatment options for MR?

Answer 144

Treatment options Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone In acute, severe regurgitation, surgery is indicated The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates When this is not possible, valve replacement with either an artificial valve or a pig valve is considered

Question 145

What is mitral stenosis? what are the 4 causes?

Answer 145

Mitral stenosis describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle. This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart. It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever. Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

Question 146

What is rheumatic fever? what is the pathogenesis?

Answer 146

Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection. Pathogenesis Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries this response leads to the clinical features of rheumatic fever Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Question 147

How is rheumatic fever diagnosed?

Answer 147

Diagnosis is based on evidence of recent streptococcal infection accompanied by: 2 major criteria 1 major with 2 minor criteria

Question 148

What indicates recent strep. infection in the diagnosis of rheumatic fever?

Answer 148

Evidence of recent streptococcal infection raised or rising streptococci antibodies, positive throat swab positive rapid group A streptococcal antigen test

Question 149

What are 5 major criteria in the diagnosis of rheumatic fever?

Answer 149

Major criteria erythema marginatum Sydenham's chorea: this is often a late feature polyarthritis carditis and valvulitis (eg, pancarditis) The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur) subcutaneous nodules

Question 150

What are 4 minor criteria in the diagnosis of rheumatic fever?

Answer 150

Minor criteria raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interva

Question 151

What is the management of rheumatic fever?

Answer 151

Outline of management antibiotics: oral penicillin V anti-inflammatories: NSAIDs are first-line treatment of any complications that develop e.g. heart failure

Question 152

what are 8 clinical features of MS?

Answer 152

dyspnoea ↑ left atrial pressure → pulmonary venous hypertension haemoptysis due to pulmonary pressures and vascular congestion may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins mid-late diastolic murmur (best heard in expiration) loud S1 opening snap indicates mitral valve leaflets are still mobile low volume pulse malar flush atrial fibrillation secondary to ↑ left atrial pressure → left atrial enlargement

Question 153

What features would indicate severe MS?

Answer 153

Features of severe MS length of murmur increases opening snap becomes closer to S2

Question 154

What is seen on CXR and echo in MS?

Answer 154

Chest x-ray left atrial enlargement may be seen Echocardiography the normal cross-sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross-sectional area of < 1 sq cm

Question 155

What is the management of mitral stenosis in -patients with AF -Asymptomatic patients -symptomatic patients

Answer 155

patients with associated atrial fibrillation require anticoagulation currently warfarin is still recommended for patients with moderate/severe MS there is an emerging consensus that direct-acting anticoagulants (DOACs) may be suitable for patients with mild MS who develop atrial fibrillation asymptomatic patients monitored with regular echocardiograms percutaneous/surgical management is generally not recommended symptomatic patients percutaneous mitral balloon valvotomy mitral valve surgery (commissurotomy, or valve replacement)

Question 156

biological / bio-prosthetic valves -What is the origin? -What is a major disadvantage? -is long term coag needed?

Answer 156

Usually bovine or porcine in origin Major disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term

Question 157

Mechanical heart valves -What is the most common type? -What is the advantage? -What is the major disadvantage? -Is anti-coag needed?

Answer 157

he most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays Mechanical valves have a low failure rate Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed.

Question 158

What are the INR targets for mechanical heart valves?

Answer 158

Warfarin is still used in preference to DOACs for patients with mechanical heart valves Following the 2017 European Society of Cardiology guidelines, aspirin is only normally given in addition if there is an additional indication, e.g. ischaemic heart disease. Target INR aortic: 3.0 mitral: 3.5

Question 159

What is balloon valvuloplasty?

Answer 159

balloon valvuloplasty may be used in children with no aortic valve calcification in adults limited to patients with critical aortic stenosis who are not fit for valve replacement

Question 160

What is the first line investigation for heart failure?

Answer 160

NICE issued updated guidelines on diagnosis and management in 2018. Previously the first-line investigation was determined by whether the patient has previously had a myocardial infarction or not this is no longer the case - all patients should have an N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test first-line. Interpreting the test if levels are 'high' arrange specialist assessment (including transthoracic echocardiography) within 2 weeks if levels are 'raised' arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

Question 161

What are normal/high/raised levels of BNP vs NTproBNP

Answer 161

BNP NTproBNP High levels > 400 pg/ml (116 pmol/litre) > 2000 pg/ml (236 pmol/litre) Raised levels 100-400 pg/ml (29-116 pmol/litre) 400-2000 pg/ml (47-236 pmol/litre) Normal levels < 100 pg/ml (29 pmol/litre) < 400 pg/ml (47 pmol/litre)

Question 162

What 11 things can increase BNP

Answer 162

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

Question 163

What 6 things can decrease BNP

Answer 163

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

Question 164

What is the first line treatment for heart failure?

Answer 164

The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol. ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction

Question 165

What is the second line treatment for heart failure?

Answer 165

The standard second-line treatment is an aldosterone antagonist these are sometimes referred to as mineralocorticoid receptor antagonists. Examples include spironolactone and eplerenone it should be remembered that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored

Question 166

What other drug can be used as an add on treatment for heart failure?

Answer 166

There is an increasing role for SGLT-2 inhibitors in the management of heart failure with a reduced ejection fraction these drugs reduce glucose reabsorption and increase urinary glucose excretion examples include canagliflozin, dapagliflozin and empagliflozin the evidence base shows SGLT-2 inhibitors reduced hospitalisation secondary to heart failure and cardiovascular death international guidelines widely recommend their usage. In terms of NICE, a technology appraisal from 2021 support the use of dapagliflozin as an add-on to optimised standard care

Question 167

What are 5 third line therapies for heart failure?

Answer 167

Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy

Question 168

What is ivabradine? what are 3 adverse effects?

Answer 168

Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity. Adverse effects visual effects, particular luminous phenomena, are common headache bradycardia, heart block

Question 169

when is ivabradine used for heart failure?

Answer 169

ivabradine criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%

Question 170

when is sacubitril-valsartan used for heart failure? (entresto)

Answer 170

sacubitril-valsartan criteria: left ventricular fraction < 35% is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs should be initiated following ACEi or ARB wash-out period

Question 171

When is digoxin used for heart failure?

Answer 171

digoxin digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties it is strongly indicated if there is coexistent atrial fibrillation

Question 172

when is hydralazine in combination with nitrate used for heart failure?

Answer 172

hydralazine in combination with nitrate this may be particularly indicated in Afro-Caribbean patients or if unable to tolerate ACEI/ARB

Question 173

When is cardiac resynchronisation therapy used for heart failure?

Answer 173

cardiac resynchronisation therapy indications include a widened QRS (e.g. left bundle branch block) complex on ECG

Question 174

What vaccines are used in heart failure?

Answer 174

offer annual influenza vaccine offer one-off pneumococcal vaccine adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years

Question 175

What is used to classify severity of heart failure and describe the 4 classes?

Answer 175

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class I no symptoms no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations NYHA Class II mild symptoms slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea NYHA Class III moderate symptoms marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms NYHA Class IV severe symptoms unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Question 176

What is a loop diuretic?

Answer 176

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl. There are two variants of NKCC; loop diuretics act on NKCC2, which is more prevalent in the kidneys. As loop diuretics work on the apical membrane they must first be filtered into the tubules by the glomerulus before they can have an effect. Therefore patients with poor renal function may require escalating doses to ensure a sufficient concentration is achieved within the tubules

Question 177

What are two indications for loop diuretics?

Answer 177

Indications heart failure: both acute (usually intravenously) and chronic (usually orally) resistant hypertension, particularly in patients with renal impairment

Question 178

What are 9 adverse effects of loop diuretics?

Answer 178

hypotension hyponatraemia hypokalaemia, hypomagnesaemia hypochloraemic alkalosis ototoxicity hypocalcaemia renal impairment (from dehydration + direct toxic effect) hyperglycaemia (less common than with thiazides) gout

Question 179

How do thiazide diuretics work?

Answer 179

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.

Question 180

What are 8 common adverse effects of thiazide like diuretics?

Answer 180

Common adverse effects dehydration postural hypotension hypokalaemia due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions hyponatraemia hypercalcaemia the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones gout impaired glucose tolerance impotence

Question 181

What are 4 rare adverse effects of thiazide diuretics

Answer 181

thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis

Question 182

What are 5 side effects of beta blockers?

Answer 182

bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction

Question 183

What are 4 contraindications of beta blockers?

Answer 183

uncontrolled heart failure asthma sick sinus syndrome concurrent verapamil use: may precipitate severe bradycardia

Question 184

What is first-degree heart block?

Answer 184

First-degree heart block PR interval > 0.2 seconds asymptomatic first-degree heart block is relatively common and does not need treatment

Question 185

What is second-degree heart block?

Answer 185

Second-degree heart block type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Question 186

What is third-degree heart block?

Answer 186

Third-degree (complete) heart block there is no association between the P waves and QRS complexes

Question 187

What is brugada? how is it inherited? who is this more common in?

Answer 187

Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5,000-10,000. Brugada syndrome is more common in Asians.

Question 188

What is found on ECG with WPW? 4

Answer 188

short PR interval wide QRS complexes with a slurred upstroke - 'delta wave' left axis deviation if right-sided accessory pathway in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation right axis deviation if left-sided accessory pathway

Question 189

How do you distinguish between type a and type b wpw?

Answer 189

Differentiating between type A and type B type A (left-sided pathway): dominant R wave in V1 type B (right-sided pathway): no dominant R wave in V1

Question 190

What are 5 associations of WPW

Answer 190

Associations of WPW HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD

Question 191

What is the treatment of WPW?

Answer 191

definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

Question 192

Describe the pathophysiology of brugada?

Answer 192

Pathophysiology a large number of variants exist around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

Question 193

What is the most common form of cardiomyopathy?

Answer 193

Dilated cardiomyopathy

Question 194

Describe the ECG changes found in brugada

Answer 194

ECG changes convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave partial right bundle branch block the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome

Question 195

What is the management of brugada?

Answer 195

Management implantable cardioverter-defibrillator

Question 196

What are primary cardiomyopathies?

Answer 196

Primary cardiomyopathies - predominately involving the heart

Question 197

HOCM - Is this common? what causes this? what are the echo findings?

Answer 197

Leading cause of sudden cardiac death in young athletes Usually due to a mutation in the gene encoding β-myosin heavy chain protein Common cause of sudden death Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy Autosomal dominant

Question 198

Arrhythmogenic right ventricular dysplasia - What is this? what is the gene mutation? what is found on ECG? Is this autosomal dominant?

Answer 198

Right ventricular myocardium is replaced by fatty and fibrofatty tissue Around 50% of patients have a mutation of one of the several genes which encode components of desmosome ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex Autosomal dominant

Question 199

HOCM and ARVD - what is the treatment?

Answer 199

ICD

Question 200

What does mixed cardiomyopathy mean?

Answer 200

Mixed - rather confusingly most of the causes of dilated and restrictive cardiomyopathy are now listed separately in the 'secondary' causes. This category servers as a reminder that many patients will have a genetic predisposition to cardiomyopathy which is then triggered by the secondary process, hence the 'mixed' category

Question 201

What are 4 classic causes of dilated cardiomyopathy?

Answer 201

Classic causes include alcohol Coxsackie B virus wet beri beri doxorubicin

Question 202

What is the pathophysiology of dilated cardiomyopathy?

Answer 202

dilated heart leading to predominately systolic dysfunction all 4 chambers are dilated, but the left ventricle more so than right ventricle eccentric hypertrophy (sarcomeres added in series) is seen

Question 203

What are 4 features of dilated cardiomyopathy?

Answer 203

classic findings of heart failure systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation S3 'balloon' appearance of the heart on the chest x-ra

Question 204

What are classic causes of restrictive cardiomyopathy?

Answer 204

Classic causes include amyloidosis post-radiotherapy Loeffler's endocarditis

Question 205

What are two causes of acquired cardiomyopathy?

Answer 205

Peripartum cardiomyopathy and takutsubo

Question 206

When does peripartum cardiomyopathy occur? who is this most common in?

Answer 206

Typical develops between last month of pregnancy and 5 months post-partum More common in older women, greater parity and multiple gestations

Question 207

What is takutsubo cardiomyopathy? what is seen on echo? what is treatment?

Answer 207

'Stress'-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure Transient, apical ballooning of the myocardium Treatment is supportive

Question 208

What are infective causes of cardiomyopathy? 2

Answer 208

Coxsackie B virus Chagas disease

Question 209

What is an infiltrative cause of cardiomyopathy?

Answer 209

Amyloidosis

Question 210

What is a cause of storage cardiomyopthy?

Answer 210

Haemochromatosis

Question 211

What is a toxicity cause of cardiomyopathy? 2

Answer 211

Doxorubicin Alcoholic cardiomyopathy

Question 212

What is a granulomatous cause of cardiomyopathy?

Answer 212

Sarcoidosis

Question 213

What are endocrine causes of cardiomyopathy? 3

Answer 213

Diabetes mellitus Thyrotoxicosis Acromegaly

Question 214

what are neuromuscular causes of caridomyopthy? 3

Answer 214

Friedreich's ataxia Duchenne-Becker muscular dystrophy Myotonic dystrophy

Question 215

What nutritional deficiency can cause cardiomyopathy?

Answer 215

Beriberi (thiamine)

Question 216

What is an autoimmune cause of cardiomyopathy?

Answer 216

Systemic lupus erythematosis

Question 217

What is coarctation of aorta?

Answer 217

Coarctation of the aorta describes a congenital narrowing of the descending aorta. It is more common in males, despite an association with Turner's syndrome.

Question 218

What are four associations of co-arctation of aorta?

Answer 218

Associations Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis

Question 219

What are features of coarctation of aorta in infancy vs adults? What is found on examination? 3

Answer 219

Features infancy: heart failure adult: hypertension radio-femoral delay mid systolic murmur, maximal over the back apical click from the aortic valve notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Question 220

DVLA -What are the rules for hypertension?

Answer 220

Specific rules hypertension can drive unless treatment causes unacceptable side effects, no need to notify DVLA if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

Question 221

DVLA -What are the rules for ACS / angina?

Answer 221

angioplasty (elective) - 1 week off driving CABG - 4 weeks off driving acute coronary syndrome- 4 weeks off driving 1 week if successfully treated by angioplasty angina - driving must cease if symptoms occur at rest/at the wheel

Question 222

DVLA -What are the rules for pacemaker insertion?

Answer 222

pacemaker insertion - 1 week off driving

Question 223

DVLA -What are the rules for ICD?

Answer 223

mplantable cardioverter-defibrillator (ICD) if implanted for sustained ventricular arrhythmia: cease driving for 6 months if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers

Question 224

DVLA -What are the rules for successful catheter ablation for an arrythmia?

Answer 224

successful catheter ablation for an arrhythmia- 2 days off driving

Question 225

DVLA -What are the rules for aortic aneurysm?

Answer 225

aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review. an aortic diameter of 6.5 cm or more disqualifies patients from driving

Question 226

DVLA -What are the rules for heart transplant?

Answer 226

heart transplant: do not drive for 6 weeks, no need to notify DVLA

Question 227

Endocarditis prophylaxis -What should happen if patients at risk of endocarditis are undergoing gastro or GU investigations?

Answer 227

if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis

Question 228

What is buergers disease? What are the features 5

Answer 228

Buerger's disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking. Features extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon

Question 229

what is takayasus arteritis?

Answer 229

Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in younger females (e.g. 10-40 years) and Asian people.

Question 230

what are 6 features of takayasus arteritis? what is an association?

Answer 230

Features systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit and tenderness absent or weak peripheral pulses upper and lower limb claudication on exertion aortic regurgitation (around 20%) Associations renal artery stenosis

Question 231

What are the investigations and management for takayasu arteritis?

Answer 231

Investigations vascular imaging of the arterial tree is required to make a diagnosis of Takayasu's arteritis either magnetic resonance angiography (MRA) or CT angiography (CTA) Management steroids

Question 232

Anticoagulation with antiplatelet meds -What is done for patients who need Secondary prevention of stable cardiovascular disease with an indication for an anticoagulant

Answer 232

normally in this situation, all patients are recommended to be prescribed an antiplatelet if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated that anticoagulant monotherapy is given without the addition of antiplatelets

Question 233

Anticoagulation with antiplatelet meds -What is done for patients Post-acute coronary syndrome/percutaneous coronary intervention

Answer 233

in these patients, there is a much stronger indication for antiplatelet therapy generally patients are given triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months there is variation from patient to patient however given that the stroke risk in atrial fibrillation varies according to risk factors.

Question 234

Anticoagulation with antiplatelet meds -What if a patient develops a PE on antiplatelets?

Answer 234

if a patient on antiplatelets develops a VTE they are likely to be prescribed anticoagulants for 3-6 months an ORBIT score should be calculated. Those with a low risk of bleeding may continue antiplatelets. In patients with an intermediate or high risk of bleeding consideration should be given to stopping the antiplatelets

Question 235

What are the 2 indications for dabigatran?

Answer 235

Firstly it is an option in the prophylaxis of venous thromboembolism following hip or knee replacement surgery. Secondly, it is also licensed in the UK for prevention of stroke in patients with non-valvular atrial fibrillation who have one or more of the following risk factors present: previous stroke, transient ischaemic attack or systemic embolism left ventricular ejection fraction below 40% symptomatic heart failure of New York Heart Association (NYHA) class 2 or above age 75 years or older age 65 years or older with one of the following: diabetes mellitus, coronary artery disease or hypertension

Question 236

What is dabigatran?

Answer 236

Dabigatran is an oral anticoagulant that works by being a direct thrombin inhibitor. It is one of the drugs developed over the past 20 years as an alternative to warfarin, with the advantage that it does not require regular monitoring.

Question 237

What are 2 side effects of dabigatran?

Answer 237

Unsurprisingly haemorrhage is the major adverse effect. Doses should be reduced in chronic kidney disease and dabigatran should not be prescribed if the creatinine clearance is < 30 ml/min.

Question 238

What can be used to reverse dabigatran

Answer 238

Idarucizumab cab be used for rapid reversal of the anticoagulant effects of dabigatran

Question 239

What are 3 xanthomata types seen in hyperlipidaemia? what are these caused by?

Answer 239

Palmar xanthoma remnant hyperlipidaemia may less commonly be seen in familial hypercholesterolaemia Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees) Causes of eruptive xanthoma familial hypertriglyceridaemia lipoprotein lipase deficiency Tendon xanthoma, tuberous xanthoma, xanthelasma familial hypercholesterolaemia remnant hyperlipidaemia

Question 240

What is xantholasma? how is this managed? 4

Answer 240

Xanthelasma are yellowish papules and plaques caused by localized accumulation of lipid deposits commonly seen on the eyelid. They are also seen in patients without lipid abnormalities. Management of xanthelasma, options include: surgical excision topical trichloroacetic acid laser therapy electrodesiccation

Question 241

What is nictonic acid? what are the 3 adverse effects?

Answer 241

Nicotinic acid (niacin) is used in the treatment of patients with hyperlipidaemia, although its use is limited by side-effects. As well as lowering cholesterol and triglyceride concentrations it also raises HDL levels. Adverse effects flushing: mediated by prostaglandins impaired glucose tolerance myositis

Question 242

What are 4 first line investigations of palpitations?

Answer 242

First-line investigations include: -12-lead ECG: this will only capture the heart rhythm for a few seconds and hence is likely to miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (for example a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) may be seen. -thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias -urea and electrolytes: looking for disturbances such as a low potassium -full blood count

Question 243

If the first line investigations are normal in patients c/o palpitations, what is the next step?

Answer 243

The most common investigation is Holter monitoring portable battery operated device continuously records ECG from 2-3 leads usually done for 24 hours but may be used for longer if symptoms are less than daily patients are asked to keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptoms at the end of the monitoring a report is generated summarising a number of parameters including heart rate, arrhythmias and changes in ECG waveform

Question 244

If no abnormality is found on holter monitor in patients c/o palpitations, what is the next step?

Answer 244

If no abnormality is found on the Holter monitor, and symptoms continue, other options include: external loop recorder implantable loop recorder

Question 245

How do thrombolytic drugs work? give three examples

Answer 245

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. Examples alteplase tenecteplase streptokinas

Question 246

what are 8 contraindications to thrombolysis?

Answer 246

Contraindications to thrombolysis active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension

Question 247

What are three side effects of thrombolysis?

Answer 247

Side-effects haemorrhage hypotension - more common with streptokinase allergic reactions may occur with streptokinase

Question 248

ECG -What is seen in ventricular and atrial hypertrophy?

Answer 248

Left ventricular hypertrophy sum of S wave in V1 and R wave in V5 or V6 exceeds 40 mm Right ventricular hypertrophy: the R:S. ratio in V1 greater than 1 is suggestive of right ventricular hypertrophy. Left atrial enlargement bifid P wave in lead II with a duration > 120 ms in V1 the P wave has a negative terminal portion Right atrial enlargement tall P waves in both II and V1 which exceed 0.25 mV

Question 249

ECG changes with digoxin

Answer 249

down-sloping ST depression ('reverse tick', 'scooped out') flattened/inverted T waves short QT interval arrhythmias e.g. AV block, bradycardia

Question 250

What are the ECG changes with hypokalaemia?

Answer 250

ECG features of hypokalaemia U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

Question 251

What are the ECG changes in LBBB and RBBB

Answer 251

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW in LBBB there is a 'W' in V1 and a 'M' in V6 in RBBB there is a 'M' in V1 and a 'W' in V6

Question 252

What is long QT syndrome?

Answer 252

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females.

Question 253

What are two congenital causes of long QTS

Answer 253

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) Romano-Ward syndrome (no deafness)

Question 254

what are 7 drug causes of LQTS

Answer 254

-amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) -methadone -chloroquine -terfenadine** -erythromycin -haloperidol -ondanestron

Question 255

What are 6 non-drug and non-congenital causes of LQTS?

Answer 255

electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia acute myocardial infarction myocarditis hypothermia subarachnoid haemorrhage

Question 256

What are 4 features of LQTS?

Answer 256

may be picked up on routine ECG or following family screening Long QT1 - usually associated with exertional syncope, often swimming Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli Long QT3 - events often occur at night or at rest sudden cardiac death

Question 257

What is the management of LQTS? 3

Answer 257

Management avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise) beta-blockers*** implantable cardioverter defibrillators in high risk cases

Question 258

What causes the a wave in the JVP?

Answer 258

a' wave = atrial contraction large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension absent if in atrial fibrillation Cannon 'a' waves caused by atrial contractions against a closed tricuspid valve are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

Question 259

Describe the C / V / X descent / and Y descent of the JVP

Answer 259

'c' wave closure of tricuspid valve not normally visible 'v' wave due to passive filling of blood into the atrium against a closed tricuspid valve giant v waves in tricuspid regurgitation 'x' descent = fall in atrial pressure during ventricular systole 'y' descent = opening of tricuspid valve

Question 260

What happens during S1 heart sound

Answer 260

S1 closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis

Question 261

what happens during S2 heart sound?

Answer 261

S2 closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Question 262

What happens in S3 heart sound?

Answer 262

S3 (third heart sound) caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

Question 263

What happens in the S4 heart sounds

Answer 263

S4 (fourth heart sound) may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle therefore coincides with the P wave on ECG in HOCM a double apical impulse may be felt as a result of a palpable S4