Cardiology 3 Flashcards

Question

Features of Catecholaminergic polymorphic ventricular tachycardia?

Answer 1

Features exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope sudden cardiac death symptoms generally develop before the age of 20 years

Answer 2

beta-blockers implantable cardioverter-defibrillator

Answer 3

a microvascular angina Features angina-like chest pain on exertion ST depression on exercise stress test (down sloaping) but normal coronary arteries on angiography Management nitrates may be beneficial

Answer 4

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

Answer 5

Chest/back pain (typically severe and sharp, tearing in nature) pulse deficit Aortic regurgitation HTN ## Footnote other features may result from the involvement of specific arteries. For example: coronary arteries → angina spinal arteries → paraplegia distal aorta → limb ischaemia 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

Answer 6

Stanford classification type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases DeBakey classification type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally type II - originates in and is confined to the ascending aorta type III - originates in descending aorta, rarely extends proximally but will extend distally ## Footnote classically chest pain is more common in type A dissection and upper back pain is more common in type B dissection. However, there is considerable overlap and both chest and back pain are present in many patients

Answer 7

Mechanism of action inhibits phosphodiesterase, elevating platelet cAMP levels which in turn reduce intracellular calcium levels other actions include reducing cellular uptake of adenosine and inhibition of thromboxane synthase

Answer 8

S1 closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis S2 closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

ejection systolic murmur louder on inspiration

Answer 13

Aspirin and statin BB or CCB Increase to the max tolerated dose If ongoing angina - can add: a long-acting nitrate ivabradine nicorandil ranolazine ## Footnote if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used 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)

Answer 14

1972 (10, 9, 7, 2)

Answer 15

hypertension: systemic (loud A2) or pulmonary (loud P2) hyperdynamic states atrial septal defect without pulmonary hypertension

Answer 16

Aortic stenosis

Answer 17

atrial septal defect

Answer 18

deep inspiration RBBB pulmonary stenosis severe mitral regurgitation

Answer 19

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2) LBBB severe aortic stenosis right ventricular pacing WPW type B (causes early P2) patent ductus arteriosus

Answer 20

Reversed split s2

Answer 21

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

Answer 22

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

Answer 23

**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

Answer 24

Step 3 treatment 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) Step 4 treatment 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**

Answer 25

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

Answer 26

Aspirin P2Y12 receptor antagonist (clopi or ticagrelor) Unfractionated herparin in those who are going to have PCI (alternative =LMWH) PCI Thrombolysis is PCI is not available ## Footnote An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Answer 27

amyloidosis (e.g. secondary to myeloma) - most common cause in UK haemochromatosis post-radiation fibrosis Loffler's syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children sarcoidosis scleroderma

Answer 28

primarily characterized by decreased compliance of the ventricular endomyocardium causes predominately diastolic dysfunction

Answer 29

Features similar to constrictive pericarditis low-voltage ECG Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis prominent apical pulse absence of pericardial calcification on CXR the heart may be enlarged ECG abnormalities e.g. bundle branch block, Q waves

Answer 30

echo cardiac MRI

Answer 31

Pulsus alternans is a physical finding characterised by alternating strong and weak pulses despite a regular heart rhythm. It is highly specific for severe left ventricular systolic dysfunction, particularly in the setting of acute decompensated heart failure. Pulsus alternans occurs due to beat-to-beat variation in stroke volume, reflecting the heart's inability to maintain consistent contractile force when severely compromised ## Footnote Its presence indicates significant cardiac decompensation and correlates with elevated left ventricular filling pressures, making it the most specific finding for this clinical scenario.

Answer 32

Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.

Answer 33

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

Answer 34

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

Answer 35

HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD

Answer 36

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 ## Footnote In patients with accessory pathways, such as those with Wolff-Parkinson-White syndrome, AV nodal blocking drugs should be avoided in atrial fibrillation. This is because blocking the AV node may enhance the rate of conduction through the accessory pathway, causing atrial fibrillation to degenerate into ventricular fibrillation (VF).

Answer 37

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.

Answer 38

visual effects, particular luminous phenomena, are common headache bradycardia, heart block

Answer 39

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 live

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

causes transient heart block in the AV node agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux adenosine has a very short half-life of about 8-10 seconds ## Footnote Adenosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.

Answer 44

chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

Answer 45

Clopidogrel Prasugrel Ticagrelor Ticlopidine

Answer 46

Adenosine diphosphate (ADP) is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12. The main target of ADP receptor inhibition is the P2Y12 receptor, as it is the one which leads to sustained platelet aggregation and stabilisation of the platelet plaque.

Answer 47

A drug interaction exists between clopidogrel and proton pump inhibitors, particularly omeprazole and esomeprazole, leading to reducing antiplatelet effects. Patients with prior stroke or transient ischaemic attack, high risk of bleeding, and prasugrel hypersensitivity are absolute contraindications to prasugrel use. Ticagrelor is contraindicated in patients with a high risk of bleeding, those with a history of intracranial haemorrhage, and those with severe hepatic dysfunction. It is also to be used with caution in those with acute asthma or COPD, as ticagrelor-treated patients experience higher rates of dyspnoea.1

Answer 48

Examples candesartan losartan irbesartan 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

Answer 49

concurrent use of proton pump inhibitors (PPIs) may make clopidogrel less effective PPIs such as lansoprazole should be OK

Answer 50

Clopidogrel belongs to a class of drugs known as thienopyridines which have a similar mechanism of action. Other examples include: prasugrel ticagrelor ticlopidine

Answer 51

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

Answer 52

during diastole

Answer 53

vasodilator: can decrease cardiac afterload diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

Answer 54

Atrial myxoma 75% occur in the keft atrium - most commonly attaches to the fossa ovalis

Answer 55

systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin, clubbing emboli atrial fibrillation mid-diastolic murmur, 'tumour plop' echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum

Answer 56

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 pai

Answer 57

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

Answer 58

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

Answer 59

Opening snap

Answer 60

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.

Answer 61

left ventricular failure

Answer 62

headache flushing skin, mucosal and eye ulceration gastrointestinal ulcers including anal ulceration

Answer 63

The most common cause of death in patients following a myocardial infarction is ventricular fibrillation.

Answer 64

viral: coxsackie B, HIV bacteria: diphtheria, clostridia spirochaetes: Lyme disease protozoa: Chagas' disease, toxoplasmosis autoimmune drugs: doxorubicin

Answer 65

usually young patient with an acute history chest pain dyspnoea arrhythmias

Answer 66

bloods ↑ inflammatory markers in 99% ↑ cardiac enzymes ↑ BNP ECG tachycardia arrhythmias ST/T wave changes including ST-segment elevation and T wave inversion

Answer 67

treatment of underlying cause e.g. antibiotics if bacterial cause supportive treatment e.g. of heart failure or arrhythmias

Answer 68

heart failure arrhythmia, possibly leading to sudden death dilated cardiomyopathy: usually a late complication

Answer 69

all the criteria must be absent to have negative PERC result, i.e. rule-out PE this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn't the diagnosis this low probability is defined as < 15%, although it is clearly difficult to quantify such judgements a negative PERC reduces the probability of PE to < 2% if your suspicion of PE is greater than this then you should move straight to the 2-level PE Wells score, without doing a PERC

Answer 70

the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However, this change is seen in no more than 20% of patients right bundle branch block and right axis deviation are also associated with PE sinus tachycardia may also be seen

Answer 71

Atrial fibrillation - cardioversion: amiodarone + flecainide ## Footnote others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone Less effective agents beta-blockers (including sotalol) calcium channel blockers digoxin disopyramide procainamide

Answer 72

AV dissociation fusion or capture beats positive QRS concordance in chest leads marked left axis deviation history of IHD lack of response to adenosine or carotid sinus massage QRS > 160 ms

Answer 73

mixed aortic valve disease In Bisferiens pulse you would see two systolic peaks to their pulse

Answer 74

Variable intensity of S1 ## Footnote variation in PR interval seen in CHB causes variation in S1 intensity.

Answer 75

a form of congenital heart defect generally classed as 'acyanotic'. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis connection between the pulmonary trunk and descending aorta usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance more common in premature babies, born at high altitude or maternal rubella infection in the first trimester

Answer 76

left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat

Answer 77

most centres now recommend initial expectant supportive care rather than early pharmacologic therapy as spontaneous closure often occurs if hemodynamically significant ΡDA remains or the infant remains ventilator dependent after one week of age then pharmacological closure is generally recommended: ibuprofen, indomethacin or paracetamol inhibits prostaglandin synthesis given to the infant, not to the mother in the antenatal period closes the connection in the majority of cases indomethacin use is declining due to increased side-effect profile compared to other drugs

Answer 78

indications for closure moderate or large ΡDA prior episode of endocarditis small audible PDΑ technique: transcatheter ΡDA closure rather than pharmacological therapy (ibuprofen/indomethacin) which is not effective in term infants

Answer 79

Infective endocarditis diagnosed if pathological criteria positive, or 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria Pathological criteria Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content) Major criteria Positive blood cultures two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or positive molecular assays for specific gene targets Evidence of endocardial involvement positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or new valvular regurgitation Minor criteria predisposing heart condition or intravenous drug use microbiological evidence does not meet major criteria fever > 38ºC vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Answer 80

Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis*

Answer 81

nitrates ACE-inhibitors inotropes

Answer 82

The persistent dry cough experienced by the patient after starting treatment with lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is a well-known side effect due to the accumulation of bradykinin. ACE inhibitors block the conversion of angiotensin I to angiotensin II, which results in vasodilation and reduced blood pressure. However, ACE also degrades bradykinin, a potent vasodilator peptide. When ACE is inhibited by lisinopril, bradykinin accumulates and can cause a persistent dry cough. ## Footnote occurs in around 15% of patients and may occur up to a year after starting treatment thought to be due to increased bradykinin levels