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312 Cards in this Set

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A 52-year-old man presents to the acute medical unit with cellulitis of the right leg. A diagnosis of sepsis secondary to cellulitis is made. He is initially treated with IV flucloxacillin and 1 litre of 0.9% saline. He initially responds well however after 20 minutes he develops nausea and vomiting. On examination there is a widespread urticarial rash. Nursing observations reveal a sudden drop in blood pressure and a rise in heart rate. You suspect a diagnosis of anaphylaxis. You immediately remove the cannula to stop further administration of flucloxacillin and ask one of your colleagues to bring the crash trolley. You administer 500 micrograms of intramuscular adrenaline and 200 mg of intramuscular hydrocortisone. You also give a fluid challenge test with further 0.9% saline. What other treatment should he receive?

10 mg of chlorphenamine




As per the Resuscitation council prophylaxis guidelines, this patient should also receive 10 mg of chlorphenamine (intramuscular or slow IV).

A 23-year-old woman is on the combined oral contraceptive pill and has just returned from holiday in Japan. She reports that she is feeling very short of breath. You suspect a pulmonary embolism and perform an ECG.Which one of the following is the most common ECG finding in pulmonary embolism?

Sinus tachycardia

The most common ECG finding in patients with pulmonary embolism is

sinus tachycardia




The S1, Q3, T3 pattern is often quoted in textbooks but is rarely seen.

A 50-year-old man presents to the emergency department with heart palpitations. He is not experiencing chest pain. He has a long history of alcohol abuse. On examination there is no signs of shock, heart failure or syncope. He appears malnourished. An ECG shows an irregular tachycardia of 165 beats per minute with a QRS duration of 155ms. Laboratory results reveal a potassium of 2.1 mmol/l. What should be the next step in management?

Administration of 2g of magnesium

The irregular tachycardia with a broad QRS complex is suggestive of either

polymorphic ventricular tachycardia (VT), pre-excited atrial fibrillation, or atrial fibrillation with bundle branch block.

Ventricular tachycardia: management

Whilst a broad complex tachycardia may result from a supraventricular rhythm with aberrant conduction, the European Resuscitation Council advise that in a peri-arrest situation it is assumed to be ventricular in origin




If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure, syncope) then immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks

Ventricular tachycardia: management




Drug therapy

amiodarone: ideally administered through a central line




lidocaine: use with caution in severe left ventricular impairment




procainamide

Ventricular tachycardia: management




If drug therapy fails

electrophysiological study (EPS)




implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

Verapamil should NOT be used in VT

true

You are working in the general medical clinic where a 42-year-old woman comes for review following a recent, short admission to hospital where she was treated for a paracetamol overdose. She has a past history of depression but denies any other previous problems. During the review, she is found to have a manual blood pressure reading of 165/85 mmHg. Clinical examination of cardiovascular and respiratory systems are normal, as is urine dip and fundoscopy. What should be your next course of management in relation to her blood pressure?

Offer ambulatory blood pressure monitoring




In 2011 the National Institute for Clinical Excellence updated its 2006 guideline for the management of hypertension (see the link below for the quick reference guide). Within this guideline, the first line use of ambulatory blood pressure monitoring (ABPM) to confirm hypertension in those found to have an elevated clinic reading (> 140/90 mmHg) is emphasised. When using ABPM to confirm a diagnosis of hypertension, two measurements per hour are taken during the persons waking hours. The average value of at least 14 measurements are then used to confirm a diagnosis of hypertension.Generally speaking, secondary causes of hypertension should be sought in; patients under 40 who lack traditional risk factors for essential hypertension, patients with other sings and/or symptoms of secondary causes, and patients with resistant hypertension. Although in reality the most common cause of secondary hypertension is hyperaldosteroneism, and as such a trial of an aldosterone antagonist such as spironolactone is often employed as both a therapeutic and diagnostic measure.

Drug treatment of essential hypertension can be summarised as follows, but for a more detailed explanation see the link below;

Step 1; Age <55 - ACE inhibitor. Age >55 or of black African or Caribbean origin - calcium channel blocker




Step 2; ACE inhibitor + calcium channel blocker




Step 3; ACE inhibitor + calcium channel blocker + thiazide-like diuretic




Step 4; consider further diuretic or beta-blockade or alpha blocker and seeking expert advice

Hypertension: diagnosis

NICE published updated guidelines for the management of hypertension in 2011. Some of the key changes include:




classifying hypertension into stages




recommending the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM)

dx

dx

Flow chart showing simplified schematic for diagnosis hypertension following NICE guidelines

Hypertension: diagnosis




Why were these guidelines needed?

It has long been recognised by doctors that there is a subgroup of patients whose blood pressure climbs 20 mmHg whenever they enter a clinical setting, so called 'white coat hypertension'. If we just rely on clinic readings then such patients may be diagnosed as having hypertension when the vast majority of time there blood pressure is normal.This has led to the use of both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) to confirm the diagnosis of hypertension. These techniques allow a more accurate assessment of a patients' overall blood pressure. Not only does this help prevent overdiagnosis of hypertension - ABPM has been shown to be a more accurate predictor of cardiovascular events than clinic readings.Blood pressure classificationThis becomes relevant later in some of the management decisions that NICE advocate.StageCriteriaStage 1 hypertensionClinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHgStage 2 hypertensionClinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHgSevere hypertensionClinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHgDiagnosing hypertensionFirstly, NICE recommend measuring blood pressure in both arms when considering a diagnosis of hypertension. If the difference in readings between arms is more than 20 mmHg then the measurements should be repeated. If the difference remains > 20 mmHg then subsequent blood pressures should be recorded from the arm with the higher reading.It should of course be remember that there are pathological causes of unequal blood pressure readings from the arms, such as supravalvular aortic stenosis. It is therefore prudent to listen to the heart sounds if a difference exists and further investigation if a very large difference is noted.NICE also recommend taking a second reading during the consultation, if the first reading is > 140/90 mmHg. The lower reading of the two should determine further management.NICE suggest offering ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg.If however the blood pressure is >= 180/110 mmHg:immediate treatment should be consideredif there are signs of papilloedema or retinal haemorrhages NICE recommend same day assessment by a specialistNICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)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 measurementsIf ABPM is not tolerated or declined HBPM should be offered.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 seatedBP should be recorded twice daily, ideally in the morning and eveningBP should be recorded for at least 4 days, ideally for 7 daysdiscard the measurements taken on the first day and use the average value of all the remaining measurementsInterpreting the resultsABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greaterABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)offer drug treatment regardless of ageNext question

A 65-year-old patient with a known history of stable angina is presented to his GP with poor control of his symptoms. He is taking atenolol for the angina. The patient's allergy notes indicate that he had developed ankle oedema when tried on nifedipine in the past for hypertension. According to NICE guidelines, which of the following drugs can be added to help control his symptoms?

Ivabradine




The combination of a non-dihydropyridine (E.g verapamil and diltiazem) and a beta blocker is contraindicated due to the risk of marked bradycardia. NICE guidelines recommend the addition of a long-acting nitrate, ivabradine, nicorandil or ranolazine if a dihydropyridine calcium channel blocker is not tolerated.

Angina pectoris: drug management




The management of stable angina comprises lifestyle changes, medication, percutaneous coronary intervention and surgery. NICE produced guidelines in 2011 covering the management of stable angina

all patients should receive aspirin and a statin in the absence of any contraindication




sublingual glyceryl trinitrate to abort angina attacks




NICE recommend using either a beta-blocker or a calicum 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. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)




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




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 or ranolazine




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

Nitrate tolerance

many patients who take nitrates develop tolerance and experience reduced efficacy




the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness




this effect is not seen in patients who take modified release isosorbide mononitrate

Ivabradine

a new class of anti-anginal drug which works by reducing the heart rate




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. Bradycardia, due to the mechanism of action, may also be seen




there is no evidence currently of superiority over existing treatments of stable angina

A 23-year-old woman presents to the emergency department with heart palpitations. She is not experiencing chest pain. On examination there is no signs of shock, heart failure or syncope. A 12 lead ECG demonstrates a regular narrow complex tachycardia with a rate of 168 bpm. There are no obvious P waves visible. Vagal manoeuvres fail to terminate the arrhythmia. What should be the next step in management?

Administration of 6mg of intravenous adenosine




The regular narrow complex tachycardia with absence of P waves is suggestive of a supraventricular tachycardia. Since vagal manoeuvres have failed to terminate the rhythm it would be appropriate to administer 6mg of intravenous adenosine.

Supraventricular tachycardia

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.Acute managementvagal manoeuvres: e.g. Valsalva manoeuvreintravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable optionelectrical cardioversionPrevention of episodesbeta-blockersradio-frequency ablation

Supraventricular tachycardia acute management

vagal manoeuvres: e.g. Valsalva manoeuvre




intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option




electrical cardioversion

Supraventricular tachycardia




Prevention of episodes

beta-blockers




radio-frequency ablation

A 57 year old gentleman has a known history of aortic stenosis. During a routine cardiology clinic appointment he states he has had worsening shortness of breath over the past few months and has had a few fainting episodes. A recent ECHO shows aortic stenosis with a mean gradient of 45mmHg and mild associated aortic regurgitation. An ECG in clinic shows left ventricular hypertrophy, left bundle branch block and a prolonged PR interval.Which of the following is most likely to indicate the need for valve replacement surgery?

Presence of symptoms



In general, aortic valve replacement is indicated in symptomatic patients with severe aortic stenosis. The presence of symptoms is associated with a mortality of 2-3 years. The triad of symptoms is dyspnoea, chest pain and syncope. Valve replacement in asymptomatic patients is more controversial.

Aortic stenosis




Features of severe aortic stenosis

narrow pulse pressures




low rising pulse




delayed ESM




soft/absent S2




S4




thrill




duration of murmur




left ventricular hypertrophy or failure

Causes of aortic stenosis

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

Management of AS

if asymptomatic then observe the patient is general rule




if symptomatic then valve replacement




if asymptomatic but valvular gradient > 50 mmHg and with features such as left ventricular systolic dysfunction then consider surgery




balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

A 78-year-old man presents to the emergency department with shortness of breath. He is not experiencing chest pain. He has a past medical history of angina and two myocardial infarctions. On examination there is bibasal crepitations of the lungs and bilateral pitting oedema of the lower extremities. An ECG shows a sinus bradycardia of 35 beats per minute. What should be the next step in management?

Administration of 500 micrograms of intravenous atropine




This patient has a sinus bradycardia. As per the Resuscitation Council bradycardia guidelines, since this patient has adverse features, he should receive 500 micrograms of intravenous atropine.

Peri-arrest rhythms: bradycardia

Adverse signs




The following factors indicate haemodynamic compromise and hence the need for treatment:


-shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating,cold, clammy extremities, confusion or impaired consciousness


-syncope


-myocardial ischaemia


-heart failure




Atropine is the first line treatment in this situation. If this fails to work, or there is the potential risk of asystole then transvenous pacing is indicated




Potential risk of asystole


The following indicate a potential risk of asystole and hence the need for treatment with transvenous pacing:


-complete heart block with broad complex QRS


-recent asystole


-Mobitz type II AV block


-ventricular pause > 3 seconds




If there is a delay in the provision of transvenous pacing the following interventions may be used:


-atropine, up to maximum of 3mg


-transcutaneous pacing


-adrenaline infusion titrated to responseNext question

A middle-aged man presents with central chest pain. This has been since present this morning and is described as 'severe' and 'burning'. Examination of the cardiovascular system is unremarkable with a heart rate of 84/min, blood pressure of 148/9...

A middle-aged man presents with central chest pain. This has been since present this morning and is described as 'severe' and 'burning'. Examination of the cardiovascular system is unremarkable with a heart rate of 84/min, blood pressure of 148/92 mmHg and oxygen saturations of 98% on room air. You obtain an ECG:




What does the ECG show?

Normal ECG

The following ECG changes are considered normal variants in an athlete:

sinus bradycardia




junctional rhythm




first degree heart block




Wenckebach phenomenon

A 68-year-old male is admitted to the surgical ward for assessment of severe epigastric pain. His abdomen is soft and non tender. However the Nurse forces you to look at the ECG. It looks abnormal. Which of the following features is an indication for urgent coronary thrombolysis or percutaneous intervention?

ST elevation of 1mm in leads II, III and aVF

ECG changes for thrombolysis or percutaneous intervention:

ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR




ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR




New Left bundle branch block

ST elevation of 1mm in leads II, III and aVF reflects significant cardiac ischaemia due to the

right coronary artery occlusion.





right coronary artery occlusions puts the patient at risk of cardiac arrhythmias (due to blood supply to the sino atrial node).

true

Thrombolysis or percutaneous intervention in myocardial infarction

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply.

Thrombolysis




examples

alteplase




tenecteplase




streptokinase

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




pregnancy




severe hypertension

Side-effects

haemorrhage




hypotension - more common with streptokinase




allergic reactions may occur with streptokinase

A 65-year-old man with no significant past medical history is admitted to the Emergency Department. His ECG is consistent with an anterior myocardial infarction. Unfortunately he develops cardiac arrest shortly after arriving in the department. What is the most common cause of death in patients following a myocardial infarction?

Ventricular fibrillation

Myocardial infarction: complications




Patients are at risk of a number of immediate, early and late complications following a myocardial infarction (MI).

Cardiac arrest




Cardiogenic shock




Chronic heart failure




Tachyarrhythmias




Bradyarrhythmias




Pericarditis




Left ventricular aneurysm




Left ventricular free wall rupture




Ventricular septal defect




Acute mitral regurgitation

Myocardial infarction: complications




Cardiac arrest

This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

Myocardial infarction: complications




Cardiogenic shock

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump

Myocardial infarction: complications




Chronic heart failure

As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.

Myocardial infarction: complications




Tachyarrhythmias

Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.

Myocardial infarction: complications




Bradyarrhythmias

Atrioventricular block is more common following inferior myocardial infarctions.

Myocardial infarction: complications




Pericarditis

Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.




Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Myocardial infarction: complications




Left ventricular aneurysm

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Myocardial infarction: complications




Left ventricular free wall rupture

This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Myocardial infarction: complications




Ventricular septal defect

Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.

Myocardial infarction: complications




Acute mitral regurgitation

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

One day following a thrombolysed inferior myocardial infarction a 72-year-old man develops signs of left ventricular failure. His blood pressure drops to 100/70mmHg. On examination he has a new early-to-mid systolic murmur.

Papillary muscle rupture




This patient has developed acute mitral regurgitation secondary to papillary muscle rupture.




The differential diagnosis is ventricular septal rupture.

Four weeks after an anterior myocardial infarction a 69-year-old presents with pulmonary oedema. The ECG shows persistent ST elevation in the anterior leads.

Left ventricular aneurysm

A 65-year-old man has a cardiac arrest two days after being admitted to hospital following a myocardial infarction

Ventricular fibrillation




Whilst any of the above could be theoretically life-threatening the question asks for the most likely cause. Ventricular fibrillation is the most common cause of death following a myocardial infarction.

A 62-year-old man is reviewed. His blood pressure is poorly controlled at 152/90 mmHg despite treatment with ramipril 10mg od, bendroflumethiazide 2.5mg od and amlodipine 10mg od. In addition to the antihypertensives he also takes aspirin and simvastatin. His most recent blood tests show the following:Na+139 mmol/lK+4.2 mmol/lUrea5.5 mmol/lCreatinine98 µmol/lWhat is the most appropriate change to his medication?

Add spironolactone

Which one of the following ECG changes is most consistent with a tricyclic overdose?

QRS widening

Tricyclic overdose

Overdose of tricyclic antidepressants is a common presentation to emergency departments. Amitriptyline and dosulepin (dothiepin) are particularly dangerous in overdose.

Tricyclic overdose Early features relate to

anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

Tricyclic overdose




ECG changes include:

sinus tachycardia




widening of QRS




prolongation of QT interval




Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

Tricyclic overdose mgmt

IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity




arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias




intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity




dialysis is ineffective in removing tricyclics

The new (and much more complicated) Joint European Society of Cardiology/American College of Cardiology definition of a pathologic Q wave is:

any Q-wave in leads V2 - V3 >= 0.02 s or QS complex in leads V2 and V3




Q-wave >= 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4 - V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4 - V6; II, III, and aVF)




R-wave >= 0.04 s in V1 - V2 and R/S >= 1 with a concordant positive T-wave in the absence of a conduction defect

ECG: coronary territories




ECG changes and coronary artery affected

Anteroseptal


V1-V4


Left anterior descending




Inferior


II, III, aVF


Right coronary




Anterolateral


V4-6, I, aVL


Left anterior descending or left circumflex




Lateral


I, aVL +/- V5-6


Left circumflex




Posterior


Tall R waves V1-2


Usually left circumflex, also right coronary

Diagram showing the correlation between ECG changes and coronary territories in acute coronary syndrome

An 83-year-old male presents with recurrent episodes of collapse with associated loss of consciousness lasting a few minutes. These episodes occur at rest and on exertion. He has no previous cardiac history and takes no regular medications. Resting 12-lead ECG shows normal sinus rhythm. Observations on admission are within normal limits. No significant deficit between lying and standing blood pressure.What would be the most helpful investigation to determine the underlying cause of the recurrent collapse?

24-hour Holter monitor

Ventricular tachycardia

Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

There are two main types of VT:

monomorphic VT: most commonly caused by myocardial infarction




polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interval are listed below

Causes of a prolonged QT interval

Congenital


Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)


Romano-Ward syndrome (no deafness)




Drugs


amiodarone, sotalol, class 1a antiarrhythmic drugs


tricyclic antidepressants, fluoxetine


chloroquine


terfenadine


erythromycin




Other


electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia


acute myocardial infarction


myocarditis


hypothermia


subarachnoid haemorrhage

Ventricular tachycardia management

If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure or rate > 150 beats/min) then immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks

A 59-year-old man with ischaemic heart disease experiences chest pain whilst walking up a hill. He uses his sublingual glyceryl trinitrate (GTN) spray.




Which one of the following side-effect profiles best describes the likely consequences of taking the GTN spray?

Hypotension + tachycardia + headache

Nitrates

Nitrates are a group of drugs which have vasodilating effects. The main indications for their use is in the management of angina and the acute treatment of heart failure. Sublingual glyceryl trinitrate is the most common drug used in patients with ischaemic heart disease to relieve angina attacks.

Nitrates Mechanism of action

cause release of nitric oxide in smooth muscle, increasing cGMP which 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

Nitrates

hypotension




tachycardia




headaches




flushing

Nitrate tolerance

many patients who take nitrates develop tolerance and experience reduced efficacy




the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness




this effect is not seen in patients who take modified release isosorbide mononitrate

An 83-year-old male presents with ischaemic sounding chest pain that has persisted for the past one hour. A 12-lead ECG is performed and shows deep T wave inversion in leads V1 and V2. Which is the most likely implicated coronary artery?

Proximal left anterior descending artery




Wellens' syndrome is an ECG manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in patients with unstable angina. It is characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads.

A 72-year-old female with known coronary artery disease presents with acute onset central chest pain at rest radiating to the jaw. The pain was initially controlled with GTN spray however is currently not resolving. The 12-lead ECG shows ST depression in the anterior leads with associated T wave inversion. Her drug history includes: aspirin 75mg OD, ramipril 10mg OD, bisoprolol 5mg OD, atorvastatin 80mg OD, ivabradine 2.5mg BD, allopurinol 100mg OD, gliclazide 80mg BD, metformin 500mg BD. She is loaded with aspirin and clopidogrel and anti-coagulated with enoxaparin. Troponin-T levels come back at 60ng/L (6 hours) and 280ng/L (12 hours). During her stay she experiences ongoing chest pain and the decision is made for primary PCI. What drug should be commenced to prevent early myocardial infarction?

Glycoprotein IIb/IIIa inhibitor infusion

Acute coronary syndrome: management of NSTEMI

All patients should receive


aspirin 300mg


nitrates or morphine to relieve chest pain if required




Antithrombin treatment. Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given.




Clopidogrel 300mg should be given to all patients and continued for 12 months.Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.




Coronary angiography should be considered within 96 hours of first admissionto hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.

The table below summaries the mechanism of action of drugs commonly used in the management of acute coronary syndrome:

Aspirin


Antiplatelet - inhibits the production of thromboxane A2




Clopidogrel


Antiplatelet - inhibits ADP binding to its platelet receptor




Enoxaparin


Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa




Fondaparinux


Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa




Bivalirudin


Reversible direct thrombin inhibitor

You are a F2 doctor working in the Emergency Department. A 61-year-old woman is admitted to the department after being brought in by her husband. For the past hour she has experienced severe central chest pain. On arrival she is haemodynamically ...

You are a F2 doctor working in the Emergency Department. A 61-year-old woman is admitted to the department after being brought in by her husband. For the past hour she has experienced severe central chest pain. On arrival she is haemodynamically stable with no signs of heart failure. Her oxygen saturations are 98% on room air. Her past medical history includes hypothyroidism and having a duodenal ulcer 20 years ago. Her only current medication is thyroxine 75mcg od. The ECG is shown below:




What is the most appropriate management for you to initiate within the first few minutes prior to senior review?

Aspirin + clopidogrel + glyceryl trinitrate + titrate morphine as required




On the ECG there is deep ST depression in I-III, aVF, and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main origin.

A 74-year-old man presents to his GP for a medication review. Blood pressure is recorded as 184/72. This is confirmed on two further occasions. What is the most appropriate first line therapy?

Amlodipine




The 2011 NICE guidelines recommended treating isolated systolic hypertension the same way as standard hypertension. In this age group calcium channel blockers would be first-line.

Isolated systolic hypertension

Isolated systolic hypertension (ISH) is common in the elderly, affecting around 50% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH reduced both strokes and ischaemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is contradicated by the 2011 NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension.

dx

dx

Aortic dissection




An intraluminal tear has formed a 'flap' that can be clearly seen in the ascending aorta. This is a Stanford type A dissection.

Aortic dissection:




Stanford classification

type A - ascending aorta, 2/3 of cases




type B - descending aorta, distal to left subclavian origin, 1/3 of cases

Aortic dissection:




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

what are the 2 different classifications for aortic dissection

Stanford




DeBakey

Aortic dissection: management




Stanford Type A

surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Aortic dissection: management




Stanford Type B*

conservative management




bed rest




reduce blood pressure IV labetalol to prevent progression

aortic arch

A 53-year-old man is reviewed in clinic. Two months ago he was started on ramipril after being diagnosed with stage 2 hypertension following ambulatory blood pressure monitoring. His clinic readings had decreased from 164/96 mmHg to 142/84 mmHg. Unfortunately he has developed a troublesome, dry cough over the past 4 weeks. What is the most appropriate course of action?

Stop ramipril and start losartan

Angiotensin-receptor blockers should be used where ACE inhibitors are not tolerated

true



What is the shown on the ECG?

What is the shown on the ECG?

Atrial flutter with variable block




Whilst 'sawtooth' waves are seen the rhythm is irregular suggesting a diagnosis of atrial flutter with variable block.

Atrial flutter

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

Atrial flutter




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

Atrial flutter Management

is similar to that of atrial fibrillation although mediction 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



What course of action are they likely to recommend?

What course of action are they likely to recommend?

Transfer the patient to the coronary care unit

If you suspect acute coronary syndrome then obviously the first step is to work through the basics:

oxygen (if appropriate), aspirin, nitrates and morphine.

IF ECG shows severe myocardial ischaemia with ST depression in V2-V6. There is also ST elevation in aVR which is highly suggestive of

either three vessel disease or left main stem disease.




This actual patient went on to have a PCI which showed 100% RCA (probably chronic), 99% LAD, and 95% Circumflex disease. He underwent an urgent CABG resulting in a very satisfactory outcome.

Acute myocardial infarction (MI) on ECG

hyperacute T waves are often the first sign of MI but often only persists for a few minutes




ST elevation may then develop




the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months




pathological Q waves develop after several hours to days. This change usually persists indefinitely

Definition of ST elevation*

new ST elevation at the J-point in two contiguous leads with the cut-off points:




>=0.2 mV in men or >= 0.15 mV in women in leads V2-V3




and/or >= 0.1 mV in other leads

Acute myocardial infarction (MI) on ECG




what features do you see

hyperacute T waves




STEMI




T waves inversion




pathological Q waves



pathological Q wave

Which one of the following statements regarding coarctation of the aorta is true?

It is associated with having a bicuspid aortic valve

Coarctation of the aorta definition

Coarctation of the aorta describes a congenital narrowing of the descending aorta.

Coarctation of the aorta is more common in

males (despite association with Turner's syndrome)

Coarctation of the aorta features

infancy: heart failure




adult:


hypertension


radio-femoral delay


mid systolic murmur,


maximal over 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

Coarctation of the aorta is associated with

Turner's syndrome




bicuspid aortic valve




berry aneurysms




neurofibromatosis

A 68-year-old man is admitted with severe community acquired pneumonia. A diagnosis of sepsis secondary to pneumonia is made. The sepsis 6 protocol is initiated however the patient unfortunately goes into cardiac arrest. Prompt CPR is initiated. An ECG shows pulseless electrical activity. What should be the next step in management?

Administration of 1mg of intravenous adrenaline



What is the most likely diagnosis?

What is the most likely diagnosis?

Acute pericarditis




The ECG shows widespread ST elevation but the most diagnosis feature of the ECG is the depression - this is very specific for pericarditis and makes the diagnosis clear.

Acute pericarditis

Pericarditis is one of the differentials of any patient presenting with chest pain.

Acute pericarditis features

chest pain: may be pleuritic. Is often relieved by sitting forwards




other symptoms include non-productive cough, dyspnoea and flu-like symptoms




pericardial rub




tachypnoea




tachycardia

Acute pericarditis Causes

viral infections (Coxsackie)




tuberculosis




uraemia (causes 'fibrinous' pericarditis)




trauma




post-myocardial infarction, Dressler's syndrome




connective tissue disease - Marfans




hypothyroidism

ECG changes for acute pericarditis

widespread 'saddle-shaped' ST elevation




PR depression: most specific ECG marker for pericarditis

Should be offered annually for all patients with heart failure

Influenza vaccine

Should be introduced first-line in patients with stable impaired left ventricular function

ACE inhibitor + beta-blocker

Has only been demonstrated to improve mortality in patients with NYHA class III or IV heart failure who are already taking an ACE inhibitor

Spironolactone

A 73 year old woman presents to the Emergency Department with progressive shortness of breath. On examination the patient has an S3 gallop rhythm, bibasal crepitations and pitting oedema up to both knees. An ECG shows signs of left ventricular hypertrophy and a chest X-ray shows small bilateral pleural effusions, cardiomegaly and upper lobe diversion.Given the likely diagnosis, which of the following drugs has been shown to improve long-term survival?

Ramipril

A 62-year-old man comes for review. In the past month he has had two episodes of 'passing out'. The first occurred whilst going upstairs. The second occurred last week whilst he was getting out of a swimming pool. There were no warning signs prior to these episodes. He was told by people who witnessed the episode last week that he was only 'out' for around 15 seconds. He reports feeling 'groggy' for only a few seconds after the episode. On examination pulse is 90 / minute, blood pressure 110/86 mmHg, his lungs are clear and there is a systolic murmur which radiates to the carotid area. Which one of the following investigations should be arranged first?

Echocardiogram




The systolic murmur may be a pointer to aortic stenosis (AS). Syncope is a late sign and typically occurs on exertion in patients with AS. It is therefore important to exclude this condition as a priority.

An exercise tolerance test would be contraindicated in a patient with suspected aortic stenosis.

true

Features of severe aortic stenosis

narrow pulse pressure




slow rising pulse




delayed ESM




soft/absent S2




S4




thrill




duration of murmur




left ventricular hypertrophy or failure

Causes of aortic stenosis

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

Aortic stenosis management

if asymptomatic then observe the patient is general rule




if symptomatic then valve replacement




if asymptomatic but valvular gradient > 50 mmHg and with features such as left ventricular systolic dysfunction then consider surgery




balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

when would you consider balloon valvuloplasty over valve replacement for aortic stenosis

patients with critical aortic stenosis who are not fit for valve replacement

A 70 year-old man presents with a history of chest pain on exertion. He is known to have hypertension, currently treated with amlodipine, and he is also on simvastatin for primary prevention. The chest pain is dull in nature and is relieved within a few minutes of rest. His symptoms have been relieved by the use of his wife's GTN. Which additional medication would be indicated here?

Atenolol




This man presents with classic features of angina. He is already taking a calcium channel blocker for hypertension, so the next most appropriate treatment would be a beta blocker. Verapamil would be an alternative if he wasn't taking any other medications.

Doxazosin is an alpha blocker used in

in refractory hypertension

Angina pectoris: drug management




NICE produced guidelines in 2011 covering the management of stable angina

all patients should receive aspirin and a statin if no CI




sublingual glyceryl trinitrate to abort angina attacks




beta-blocker or a calicum channel blocker first-line




increase to maximum dose tolerated




combine BB + CCB/nitrate, ivabradine, nicorandil or ranolazine




add third drug to BB + CCB if awating PCI/CABG





The management of stable angina comprises

lifestyle changes, medication, percutaneous coronary intervention and surgery.

when using calcium channel blockers and beta blockers for managment of angina what should you remember

CCB if used as a monotherapy then rate limiting drugs used e.g. verapamil or diltiazem




if CCB + BB used then use long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine)

What should you do if a patient develops tolerance to nitrate tolerance

take next dose earlier

Ivabradine features

a new class of anti-anginal drug which works by reducing the heart rate




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. Bradycardia, due to the mechanism of action, may also be seen




there is no evidence currently of superiority over existing treatments of stable angina



Which one of the following would explain the changes seen on the ECG?

Which one of the following would explain the changes seen on the ECG?

Hypokalaemia

U waves which are pathognomonic of

hypokalaemia.



ECG features of hypokalaemia



(U waves in the pic)

ECG features of hypokalaemia




(U waves in the pic)

U waves




small or absent T waves (occasionally inversion)




prolong PR interval




ST depression




long QT

A 42-year-old overweight man presents with a two day history of anterior chest pain that is worse on deep inspiration and lying down

Pericarditis

A 67-year-old female with a history of chronic lymphocytic leukaemia presents with a 3 day history of burning pain in the right lower chest wall. Clinical examination is unremarkable

Shingles




Pain and paraesthesia often proceeds the rash

A 25-year-old man with a history of Marfan's disease presents with sudden onset shortness of breath and pleuritic chest pain

Pneumothorax

Musculoskeletal chest pain

One of the most common diagnoses made in the Emergency Department.




The pain is often worse on movement or palpation.




May be precipitated by trauma or coughing

Shingles

Pain often precedes the rash

Pulmonary embolism

Sudden dyspnoea and pleuritic chest pain




Calf pain/swelling




Current combined pill user, malignancy

Pneumothorax

History of asthma, Marfan's etc




Sudden dyspnoea and pleuritic chest pain

Myocardial infarction

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

You are doing the discharge summary for a 56-year-old man who is being discharged following a ST-elevation myocardial infarction (MI) for which he was treated with a percutaneous coronary intervention. He has no past medical history of note. Following NICE guidance, which of the following best describes the medications which he should be taking?

Dual antiplatelet therapy + beta-blocker + ACE-inhibitor + statin

Myocardial infarction: secondary prevention




All patients should be offered the following drugs:

dual antiplatelet therapy (aspirin plus a second antiplatelet agent)




ACE inhibitor




beta-blocker




statin

A 24-year-old woman is found to have a blood pressure of 170/100 mmHg during a routine medical check. She is well and clinical examination is unremarkable. Blood tests show:Na+140 mmol/lK+2.6 mmol/lBicarbonate31 mmol/lUrea3.4 mmol/lCreatinine77 µmol/lWhich one of the following investigations is most likely to be diagnostic?

Renin:aldosterone ratio

Which one of the following investigations is most likely to be diagnostic of Conn's syndrome?

Renin:aldosterone ratio

A 60-year-old man is admitted with severe central chest pain to the resus department. The admission ECG shows ST elevation in leads V1-V4 with reciprocal changes in the inferior leads. Which one of the following is most likely to account for these findings?

100% occlusion of the left anterior descending artery

The admission ECG shows ST elevation in leads V1-V4 with reciprocal changes in the inferior leads. Which one of the following is most likely to account for these findings?

100% occlusion of the left anterior descending artery

Causes of ST elevation

myocardial infarction




pericarditis




normal variant - 'high take-off




'left ventricular aneurysm




Prinzmetal's angina (coronary artery spasm)




A 71-year-old man who is known to have atrial fibrillation comes for review. He had a transient ischaemic attack two weeks ago and takes bendroflumethiazide for hypertension but is otherwise well. His latest blood pressure is 124/76 mmHg. You are discussing management options to try and reduce his future risk of having a stroke. What is his CHA2DS2-VASc score?rare: subarachnoid haemorrhage, part of spectrum of changes in hyperkalaemia

A 71-year-old man who is known to have atrial fibrillation comes for review. He had a transient ischaemic attack two weeks ago and takes bendroflumethiazide for hypertension but is otherwise well. His latest blood pressure is 124/76 mmHg. You are discussing management options to try and reduce his future risk of having a stroke. What is his CHA2DS2-VASc score?

4

HASBLED scoring system.

H = Hypertension, uncontrolled, systolic BP > 160 mmHg


= 1




A = Abnormal renal function (dialysis or creatinine > 200) Or Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal


= 1 for any renal abnormalities


= 1 for any liver abnormalities




S = Stroke, history of = 1




B = Bleeding, history of bleeding or tendency to bleed


= 1




L = Labile INRs (unstable/high INRs, time in therapeutic range < 60%) = 1




E = Elderly (> 65 years)


= 1




D = Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs)OrAlcohol Use (>8 drinks/week)


= 1 for drugs


= 1 for alcohol

A baby is delivered on the ward and on the neonatal examination a systolic heart murmur is heard. An echocardiogram shows right atrial hypertrophy and the septal and posterior leaflet of the tricuspid valve attached to the right ventricle. What is this condition most commonly known as?

Ebstein's anomaly

Ebstein's anomaly

is a congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle. It is sometimes referred to as 'atrialisation' of the right ventricle.

Ebstein's anomaly is associated with

tricuspid incompetence (pan-systolic murmur, giant V waves in JVP)




Wolff-Parkinson White syndrome

Ebstein's anomaly may be caused by exposure to lithium in-utero

true

A 21-year-old man collapses whilst playing football with his friends at the weekend. By the time he is brought into the emergency department he is pronounced dead following cardiac arrest despite adequate life support being given. His family cannot understand how this has happened saying that he has always been fit and healthy and was a keen sportsman, they do however note that two other family members have died young in similar circumstances.




Which of the following methods of inheritance is correct for this condition?

Autosomal dominant

A 68-year-old man with a past history of aortic stenosis is reviewed in clinic. Which one of the following features would most guide the timing of surgery?

Symptomatology of patient

Aortic stenosis management: AVR if symptomatic, otherwise cut-off is gradient of 50 mmHg

true

A 72-year-old man is admitted to the Emergency Department with chest pain. On initial assessment he is noted to be pale, have a heart rate of 40/min and a blood pressure of 90/60 mmHg. Which one of the coronary arteries is most likely to be affected?

Right coronary

Complete heart block following a MI? -

right coronary artery lesion




The atrioventricular node is supplied by the posterior interventricular artery, which in the majority of patients is a branch of the right coronary artery. In the remainder of patients the posterior interventricular artery is supplied by the left circumflex artery.

Complete heart block features

syncope




heart failure




regular bradycardia (30-50 bpm)




wide pulse pressure




JVP: cannon waves in neck




variable intensity of S1

Types of heart block

First degree heart block




Second degree heart block


- type 1


- type 2




Third degree (complete) heart block

First degree heart block

PR interval > 0.2 seconds

Second degree heart block: type 1

aka Mobitz I or Wenckebach:




progressive prolongation of the PR interval until a dropped beat occurs

Second degree heart block: type 2

aka Mobitz II: PR interval is constant but the P wave is often not followed by a QRS complex

Third degree (complete) heart block

An 82-year-old man is reviewed. He is known to have ischaemic heart disease and is still getting regular attacks of angina despite taking atenolol 100mg od. Examination of his cardiovascular system is unremarkable with a pulse of 72 bpm and a blood pressure of 158/96 mmHg. What is the most appropriate next step in management?

Add nifedipine




NICE guidelines recommend adding a calcium channel blocker for angina which is not adequately controlled with beta-blocker monotherapy. Verapamil is contraindicated whilst taking a beta-blocker and diltiazem should be used with caution due to the risk of bradycardia.

A 72-year-old man is admitted with chest pain. He has associated nausea and vomiting. On examination he is pale and sweaty. An ECG shows ST elevation in V3-V6. A diagnosis of ST elevation myocardial infarction is made. The patient unfortunately deteriorates and goes into cardiac arrest. Prompt CPR is initiated. One cycle of CPR is completed before a heart tracing is obtained. The ECG shows monomorphic ventricular tachycardia. The patient still has no pulse. What should be the next step in management?

Defibrillation

A 59-year-old female is admitted to the Emergency Department with a 30 minute history of central chest pain radiating to her left arm. An ECG shows ST elevation in leads II, III, aVF. Which coronary artery is most likely to be affected?

Right coronary

Inferior MI

right coronary artery lesion



coronary territories

You are reviewing a 56-year-old man who has recently been successfully cardioverted following an episode of ventricular tachycardia. He had recently been treated with a course of erythromycin. You are interested to see if he has an underlying prolonged QT interval. What is the most appropriate way to measure the QT interval on the ECG?

Time between the start of the Q wave and the end of the T wave

QT interval: Time between the start of the Q wave and the end of the T wave

true

You are called to the coronary care unit. A patient who has been admitted following a myocardial infarction has developed a broad complex tachycardia. You suspect a diagnosis of polymorphic ventricular tachycardia. Which one of the following factors may have precipitated this?

Hypokalaemia

management for VT

Drug therapy


-amiodarone: ideally administered through a central line


-lidocaine: use with caution in severe left ventricular impairment


-procainamide




If drug therapy fails


-electrophysiological study (EPS)


-implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

The following ECG changes are considered normal variants in an athlete:

sinus bradycardia




junctional rhythm




first degree heart block




Wenckebach phenomenon

A 64-year-old man with a history of ischaemic heart disease and poor left ventricular function presents with a broad complex tachycardia of 140 bpm. On examination blood pressure is 110/74 mmHg. Fusion and capture beats are seen on the 12 lead ECG. What is the first line drug management?

Amiodarone

A 72-year-old man is started on amlodipine 5mg od for hypertension. He has no other past medical history of note and routine bloods (including fasting glucose) and ECG were normal. What should his target blood pressure (based on clinic readings) be once on treatment?

140/90 mmHg

Blood pressure target (based on clinic readings) for patients < 80 years - 140/90 mmHg

true for HTN

A 71-year-old woman comes for review. She was diagnosed with angina pectoris recently and is currently taking aspirin 75mg od, simvastatin 40mg on and atenolol 100mg od. If her anginal symptoms are not controlled on this medication, what is the most appropriate next step?

Add a long-acting dihydropyridine calcium-channel blocker

A 23-year-old woman presents to the Emergency Department with a friend from work. Around 30 minutes ago she developed a 'fluttering' in her chest. She reports feeling 'a bit faint' but denies any chest pain or shortness of breath. An ECG shows a regular tachycardia of 166 bpm with a QRS duration of 0.11ms. Blood pressure is 102/68 mmHg and oxygen saturations are 99% on room air. What is the most appropriate management?

Carotid sinus massage

Supraventricular tachycardia

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

Supraventricular tachycardia




Acute management

vagal manoeuvres: e.g. Valsalva manoeuvre




intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option




electrical cardioversion

Prevention of Supraventricular tachycardia episodes

beta-blockers




radio-frequency ablation

Wendy, 48, presents to the Emergency Department after feeling faint earlier that day. She is found to be in atrial fibrillation. She is known to have structural heart disease as a result of an ill-functioning mitral valve, but is otherwise fit and healthy. What is the most appropriate treatment if pharmacological cardioversion is agreed upon?

Amiodarone

If pharmacological cardioversion (i.e. give drug for AF) has been agreed on clinical and resource grounds for new-onset atrial fibrillation, offer:

flecainide or amiodarone if there is no evidence of structural or ischaemic heart disease or




amiodarone if there is evidence of structural heart disease.'

Digoxin therapy is only recommended in patients presenting with non-paroxysmal atrial fibrillation only if they are sedentary.

true

Atenolol and diltiazem are both methods of rate control for AF as opposed to pharmacological cardioversion.

true

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

amiodarone




flecainide (if no structural heart disease)




others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

if you dx new onset AF and patient has structural heart disease what drug should you give

amiodarone

if you dx new onset AF and patient has NO structural heart disease what drug should you give

flecainide or amiodarone

What is the most appropriate management?

What is the most appropriate management?

Admit the patient to hospital

A 71-year-old patient presents to the Emergency Department with a 30 minute history of crushing central chest pain. ECG shows tall R waves in V1-2. Which coronary territory is likely to be affected?

Posterior

Which of the following features is not associated with patent ductus arteriosus?

Bisferiens pulse




PDA is associated with a collapsing pulse

PDA is associated with a collapsing pulse

true




acyanotic congenital heart defect




connection between the pulmonary trunk and descending aorta




more common in premature babies, born at high altitude or maternal rubella infection in the first trimester

Patent ductus arteriosus management

indomethacin closes the connection in the majority of cases




if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

Which one of the following statements regarding adult advanced life support is correct?

Chest compressions should continue whilst the defibrillator is charging

Each one of the following may cause left bundle branch block, except:

Atrial septal defect

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

Causes of LBBB

ischaemic heart disease




hypertension




aortic stenosis




cardiomyopathy




rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

An 84-year-old man comes for review. Four weeks ago an opportunistic blood pressure reading was taken and recorded as 150/92 mmHg. You therefore arranged ambulatory blood pressure monitoring (ABPM) along with a standard hypertension work-up. You did not calculate his 10-year cardiovascular risk on account of his age. The following results were obtained:Na+141 mmol/lK+4.2 mmol/lUrea6.5 mmol/lCreatinine101 µmol/lTotal cholesterol4.9 mmol/lHDL cholesterol1.2 mmol/lFasting glucose5.5 mmol/lUrine dipstick was normal. The ECG showed sinus rhythm, 72 bpm and first degree heart block.The daytime average blood pressure reading was 145/80 mmHg. What is the most appropriate course of action?

Diagnose stage 1 hypertension and advise about lifestyle changes

A 34-year-old man presents with a two day history of chest pain. The pain is worse on coughing and taking a deep breath in. Since this morning it has been constant and is present when you review him. He feels slightly short-of-breath. His oxygen saturations are 99% on room air, pulse is 72/min, blood pressure is 130/84 mmHg and ausculatation of the cardiorespiratory system is unremarkable. You obtain an ECG:© Image used on license from Dr Smith, University of MinnesotaWhat is the most likely diagnosis?



Myocardial infarction

Myocardial infarction

Which one of the following features is not part of the modified Duke criteria used in the diagnosis of infective endocarditis?

Prolonged PR interval

Infective endocarditis: Modified Duke criteria




Infective endocarditis diagnosed if

pathological criteria positive, or




2 major criteria, or




1 major and 3 minor criteria, or




5 minor criteria

Infective endocarditis: Modified Duke 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)

Infective endocarditis: Modified Duke criteriaMajor criteria

Positive blood cultures




Evidence of endocardial involvement

Infective endocarditis: Modified Duke criteriaMinor 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

Gap (1) = ACE-inhibitor + beta-blocker




Gap (2) = Hydralazine + nitrate




Gap (3) = Digoxin

A 41-year-old man presents with recurrent headaches. These typically occur 2-3 times a day and are associated with sweating and palpitations. As he was concerned that it may be due to blood pressure he borrowed his fathers home monitor. During these episodes his blood pressure is around 210/110 mmHg. Given the likely diagnosis, what is the most appropriate next test?

24 hour urinary collection of metanephrines




Phaeochromocytoma: do 24 hr urinary metanephrines, not catecholamines




Three 24 hour collections are needed as some patients have intermittently raised levels

Phaeochromocytoma

Phaeochromocytoma is a rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndromeBasicsbilateral in 10%malignant in 10%extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)Features are typically episodichypertension (around 90% of cases, may be sustained)headachespalpitationssweatinganxietyTests24 hr urinary collection of metanephrines (sensitivity 97%*)this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)Surgery is the definitive management. The patient must first however be stabilized with medical management:alpha-blocker (e.g. phenoxybenzamine), given before abeta-blocker (e.g. propranolol)

Phaeochromocytoma Tests

24 hr urinary collection of metanephrines (sensitivity 97%*)




this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

Phaeochromocytoma




Surgery is the definitive management. The patient must first however be stabilized with medical management:

alpha-blocker (e.g. phenoxybenzamine), given before a




beta-blocker (e.g. propranolol)

A 78 year old lady attends surgery with worsening shortness of breath over the past four months. She also complains of left sided chest pain and light-headedness on exertion, which resolve with rest. On examining her you find she has an ejection systolic murmur radiating to the carotids. Which of the following findings could you also expect to find on examination?

Narrow pulse pressure

A 60-year-old man is admitted with palpitations to the Emergency Department. An ECG on admission shows a broad complex tachycardia at a rate of 150 bpm. His blood pressure is 124/82 mmHg and there is no evidence of heart failure. Which one of the following is contraindicated in this situation?

Verapamil

Ventricular tachycardia - verapamil is contraindicated

true

A 66-year-old man presents with shortness-of-breath on exertion. On examination his blood pressure is 128/76 mmHg, pulse 78 / min and regular. Auscultation of his chest reveals an early diastolic murmur. Which one of the following conditions is most associated with this kind of murmur?

Aortic regurgitation

Ejection systolic murmurs

aortic stenosis




pulmonary stenosis, HOCM




ASD, Fallot's

Holosystolic (pansystolic) murmurs

mitral/tricuspid regurgitation (high-pitched and 'blowing' in character)




VSD ('harsh' in character)

Late systolic murmurs

mitral valve prolapse




coarctation of aorta

Early diastolic murmurs

aortic regurgitation (high-pitched and 'blowing' in character)




Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)

Mid-late diastolic murmurs

mitral stenosis ('rumbling' in character)




Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)

Continuous machine-like mumur

patent ductus arteriosus



murmurs

A cardiologist has asked you to start oral amiodarone for a patient who has previously been admitted with ventricular tachycardia. What tests is it important to ensure the patient has had prior to starting treatment?

TFT + LFT + U&E + chest x-ray

baseline tests before starting amiodarone

TFT + LFT + U&E + chest x-ray

Amiodarone

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)The use of amiodarone is limited by a number of factorslong half-life (20-100 days)should ideally be given into central veins (causes thrombophlebitis)has proarrhythmic effects due to lengthening of the QT intervalinteracts with drugs commonly used concurrently e.g. Decreases metabolism of warfarinnumerous long-term adverse effects (see below)Monitoring of patients taking amiodaroneTFT, LFT, U&E, CXR prior to treatmentTFT, LFT every 6 monthsAdverse effects of amiodarone usethyroid dysfunctioncorneal depositspulmonary fibrosis/pneumonitisliver fibrosis/hepatitisperipheral neuropathy, myopathyphotosensitivity'slate-grey' appearancethrombophlebitis and injection site reactionsbradycardia

A 50-year-old man complains of central, pleuritic chest pain 24 hours after being admitted with an anterior myocardial infarction. The pain is eased when he sits upright.

Pericarditis




This is early pericarditis. Dressler's syndrome is a seperate clinical phenomenon and is not generally seen in the first two weeks following a myocardial infarction.

After being admitted to the coronary care unit a middle aged man develops a regular, broad complex tachycardia. His blood pressure drops to 88/50 mmHg. He was admitted 6 hours previously following an anterolateral myocardial infarction.

Ventricular tachycardia




Broad complex tachycardia following a myocardial infarction is almost always due to ventricular tachycardia.

A 66-year-old woman suddenly develops dyspnoea 10 days after having an anterior myocardial infarction. Her blood pressure is 78/50 mmHg, JVP is elevated and the heart sounds are muffled. There are widespread crackles on her chest and the oxygen saturations are 84% on room air.

Left ventricular free wall rupture




The prognosis from such a catastrophic event is clearly poor unless this patient has immediate surgery.

Which one of the following treatments is not appropriate in the management of Wolff-Parkinson White?

Verapamil

Verapamil and digoxin should be avoided in patients with

Wolff-Parkinson White as they may precipitate VT or VF

Wolff-Parkinson White

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

Wolff-Parkinson White Possible ECG features include:

short PR intervalwide QRS complexes with a slurred upstroke - 'delta wave'




left axis deviation if right-sided accessory pathway*




right axis deviation if left-sided accessory pathway*

Wolff-Parkinson White




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



Management of WPW

Management of WPW

definitive treatment: radiofrequency ablation of the accessory pathway




medical therapy: sotalol***, amiodarone, flecainide

A 76-year-old man is reviewed. He was recently admitted after being found to be in atrial fibrillation. This was his second episode of atrial fibrillation. He also takes ramipril for hypertension but has no other history of note. During admission he was warfarinised and discharged with planned follow-up in the cardiology clinic. However, on review today he is found to be in sinus rhythm. What should happen regarding anticoagulation?

Continue lifelong warfarin



What is shown on the ECG?

What is shown on the ECG?

Ventricular fibrillation

tirofiban. What is the mechanism of action of this drug?

Glycoprotein IIb/IIIa receptor antagonist

A 75-year-old woman is brought to the Emergency Department by her family. She has been getting more short-of-breath over the last 6 weeks and says her energy levels are low. An ECG on arrival shows atrial fibrillation at a rate of 114 / min. Blood pressure is 128/80 mmHg and a chest x-ray is unremarkable. What is the appropriate drug to control the heart rate?

Bisoprolol

Atrial fibrillation

rate control - beta blockers preferable to digoxin




nb This question reiterates an important point which frequently comes up in exams - digoxin is no longer first-line for rate control in atrial fibrillation.

Agents used to control rate in patients with atrial fibrillation

beta-blockers




calcium channel blockers




digoxin (not considered first-line anymore as they are less effective at controlling the heart rate during exercise. However, they are the preferred choice if the patient has coexistent heart failure)

Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation

sotalol




amiodarone




flecainide




others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine

Factors favouring rate control in AF

Older than 65 years




History of ischaemic heart disease

Factors favouring rhythm control in AF

Younger than 65 years




Symptomatic




First presentation




Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol)




Congestive heart failure

Agents used FOR RATE CONTROL in patients with atrial fibrillation

BB (preferred over digoxin)




CCB




digoxin

Agents used FOR RHYTHM CONTROL in patients with a history of atrial fibrillation

sotalol




amiodarone




flecainide




OTHERS: disopyramide, dofetilide, procainamide, propafenone, quinidine



Which one of the following is most likely to explain the ECG changes?

Which one of the following is most likely to explain the ECG changes?

Hyperkalaemia






This ECG has a number of features consistent with severe hyperkalaemia. There is a near sinusoidal pattern, with very wide QRS complexes, bizarre deep T-waves in V1 and V2 and peaked T-waves in V4 and V5.

You are considering prescribing an antibiotic to a 28-year-old man who tells you he has Long QT syndrome. Which antibiotic is it most important to avoid?

Erythromycin

A 70-year-old woman is brought to the Emergency Department by her relatives. For the past two hours she has experienced palpitations and 'tightness' in her chest. The ECG has a 'sawtooth' appearance with baseline atrial activity of around 300/min and a ventricular rate of 150/min. What is the most likely diagnosis?

Atrial flutter

Tachycardia with a rate of 150/min ?atrial flutter

TRUE

A 42-year-old man of Afro-Caribbean origin is diagnosed as having hypertension. Secondary causes of hypertension have been excluded. What is the most appropriate initial drug therapy?

Amlodipine

A 70-year-old woman with a history of type 2 diabetes mellitus and hypertension is reviewed in clinic. You can see from the records their is no evidence of diabetic retinopathy, chronic kidney disease or cardiovascular disease.Her current medication is as follows:simvastatin 40mg onramipril 10mg odamlodipine 5mg odmetformin 1g bdRecent blood results are shown below:Na+142 mmol/lK+4.4 mmol/lUrea7.2 mmol/lCreatinine86 µmol/lHbA1c45 mmol/mol (6.3%)Urine dipstick shows no proteinuria. Her blood pressure today in clinic is 134/76 mmHg.What is the most appropriate course of action?

No changes to medication required



A 70-year-old man has a routine ECG after being diagnosed with hypertension. Examination of his cardiovascular system is unremarkable other than a blood pressure of 170/106 mmHg.

What does the ECG show?

A 70-year-old man has a routine ECG after being diagnosed with hypertension. Examination of his cardiovascular system is unremarkable other than a blood pressure of 170/106 mmHg.




What does the ECG show?

Bifascicular block



What does the ECG show?

What does the ECG show?

The ECG shows both right bundle branch block and left axis deviation indicating bifascicular block.

ECG: bi/tri-fascicular block




Bifascicular block

Bifascicular block:




combination of RBBB with left anterior or posterior hemiblock


e.g. RBBB with left axis deviation

ECG: bi/tri-fascicular block




Trifascicular block

features of bifascicular block as above + 1st degree heart block

A 77-year-old woman is admitted to the Emergency Department with a three day history of lethargy and shortness-of-breath. She is confused and unable to give much useful history. On examination she is noted to be pale, pulse is around 160/min with a blood pressure of 80/56 mmHg. Her oxygen saturations are 96% on room air. An intravenous cannula is placed and bloods taken:Hb8.6 g/dlPlatelets411 * 109/lWBC5.2 * 109/lThe ECG is shown below:




A fluid bolus is given. What is the most appropriate management?




DC cardioversion 

DX Peri-arrest rhythms: tachycardia

DC cardioversion




DX Peri-arrest rhythms: tachycardia

The ECG shows an narrow complex tachycardia with an irregularly irregular pattern - fast atrial fibrillation

Peri-arrest rhythms: tachycardia

If any of the above adverse signs are present then synchronised DC shocks should be given




Treatment following this is given according to whether the QRS complex is narrow or broad and whether the rhythm is regular or irregular.

Broad-complex tachycardia MANAGMENT if regular or irregular rhythm

Regular rhythm (ASSUME ITS VT)


= give amiodarone




Irregular rhythm


1. AF with bundle branch block - treat as for narrow complex tachycardia


2. Polymorphic VT (e.g. Torsade de pointes) - IV magnesium

how do you treat Polymorphic VT (e.g. Torsade de pointes)

IV magnesium

Narrow-complex tachycardiaMANAGMENT if regular or irregular rhythm

Regular


- vagal manoeuvres then IV adenosine


- if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. Beta-blockers)




Irregular (prob AF)


- if onset < 48 hr consider electrical or chemical cardioversion


- rate control (e.g. Beta-blocker or digoxin) and anticoagulation

A 58-year-old man presents with breathlessness and chest discomfort. He has diet controlled diabetes, hypertension and hyperlipidaemia. He has a weak rapid, regular pulse of 160bpm, blood pressure is 80/50mmHg, he is cold peripherally and crepitations are heard bibasally on auscultation of the chest. An ECG shows a regular broad complex tachycardia.What is the best initial management of this arrhythmia?

Electrical cardioversion

Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs:

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating,cold, clammy extremities, confusion or impaired consciousness




syncope




myocardial ischaemia




heart failure

what should you do if any adverse signs associated with Peri-arrest rhythms: tachycardia

synchronised DC shocks should be given

A 41-year-old man is admitted with left-sided pleuritic chest pain. He has a dry cough and reports that the pain is relieved by sitting forward. For the past three days he has been experiencing flu-like symptoms. Given the likely diagnosis of acute pericarditis, what is the most likely finding on ECG?

Widespread ST elevation

A 75 year old gentleman with a past medical history of hypertension only, presents with a 3 month history of increasing breathlessness and swollen ankles. You decide to order a BNP test. Which of the following may give him a falsely low BNP result?

Being on ramipril for his blood pressure

B-type natriuretic peptide

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. Effects of BNPvasodilatordiuretic and natriureticsuppresses both sympathetic tone and the renin-angiotensin-aldosterone systemClinical uses of BNPDiagnosing patients with acute dyspnoeaa low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosisNICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failurePrognosis in patients with chronic heart failureinitial evidence suggests BNP is an extremely useful marker of prognosisGuiding treatment in patients with chronic heart failureeffective treatment lowers BNP levelsScreening for cardiac dysfunctionnot currently recommended for population screening



What is shown on the ECG?

What is shown on the ECG?

Inferior ST elevation MI + atrioventricular block






There is ST elevation in the II, III and aVF diagnostic of an inferior myocardial infarction. The PR interval is significantly prolonged (first degree heart block) suggestive that the AV node may have been affected by the infarction.

A 23-year-old woman is investigated after collapsing whilst jogging. She felt briefly unwell and dizzy prior to collapsing but quickly recovered. There has been no previous similar episodes. Routine blood tests are normal but the ECG shows a corrected QT interval of 480ms. What is the most appropriate management?

Propranolol

Each of the following are true regarding tricyclic overdose, except:

Dialysis is indicated in severe toxicity

Tricyclic overdose Management

IV bicarbonate




may reduce the risk of seizures and arrhythmias in severe toxicity

Tricyclic overdose

Overdose of tricyclic antidepressants is a common presentation to emergency departments. Amitriptyline and dosulepin (dothiepin) are particularly dangerous in overdose.Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.Features of severe poisoning include:arrhythmiasseizuresmetabolic acidosiscomaECG changes include:sinus tachycardiawidening of QRSprolongation of QT intervalWidening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmiasManagementIV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicityarrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmiasintravenous lipid emulsion is increasingly used to bind free drug and reduce toxicitydialysis is ineffective in removing tricyclics

A 34-year-old man who is known to have a congenital bicuspid aortic valve attends the dentist for polishing. What is the most appropriate management with regards to endocarditis prophylaxis?

No antibiotics needed

A 30-year-old woman is admitted to the Emergency Department following the acute onset of palpitations. Blood pressure is 124/84 mmHg and her pulse is 150/min. An ECG shows a narrow complex tachycardia. Intravenous access is gained and 6mg of adenosine is given with no effect. What is the most appropriate next step?

Intravenous adenosine 12 mg

Which one of the following calcium channel blockers is most likely to precipitate pulmonary oedema in a patient with known chronic heart failure?

Verapamil

Verapamil is the most highly negatively inotropic calcium channel blocker

true

Calcium channel blockers

Calcium channel blockers are primarily used in the management of cardiovascular disease. Voltage-gated calcium channels are present in myocardial cells, cells of the conduction system and those of the vascular smooth muscle. The various types of calcium channel blockers have varying effects on these three areas and it is therefore important to differentiate their uses and actions.

Calcium channel blockers

VerapamilAngina, hypertension, arrhythmias Highly negatively inotropicShould not be given with beta-blockers as may cause heart blockHeart failure, constipation, hypotension, bradycardia, flushingDiltiazemAngina, hypertension Less negatively inotropic than verapamil but caution should still be exercised when patients have heart failure or are taking beta-blockersHypotension, bradycardia, heart failure, ankle swellingNifedipine, amlodipine, felodipine (dihydropyridines)Hypertension, angina, Raynaud'sAffects the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of heart failureFlushing, headache, ankle swelling

A 40-year-old woman who is being treated for refractory hypertension undergoes a coronary angiogram after developing non-specific chest pains. The cardiologist takes a number of measurements during the procedure:Pressure (mmHg)Right femoral artery122/68Left ventricle202/104Aorta194/84The blood pressure in her left arm taking during the procedure was 188/74 mmHg. What is the most likely underlying diagnosis?

Coarctation of the aorta

What is the mechanism of action of bivalirudin in acute coronary syndrome?

Reversible direct thrombin inhibitor

A 57-year-old man with NYHA class III heart failure is currently treated with furosemide and ramipril. What is the most suitable beta-blocker to add to improve his long-term prognosis?

Bisoprolol

Both carvedilol and bisoprolol have been shown to reduce mortality in stable heart failure. The other beta-blockers have no evidence base to support their use

true

A 55-year-old man is admitted with central chest pain. His ECG shows ST depression in the inferior leads and the chest pain requires intravenous morphine to settle. Past medical history includes a thrombolysed myocardial infarction 2 years ago, asthma and type 2 diabetes mellitus. Treatment with aspirin, clopidogrel and unfractionated heparin is commenced. Which one of the following factors should determine if an intravenous glycoprotein Iib/IIIa receptor antagonist is to be given?

High GRACE (Global Registry of Acute Cardiac Events) risk score + whether a percutaneous coronary intervention is to be performed

A 74-year-old man with symptomatic aortic stenosis is reviewed in the cardiology clinic. He is otherwise fit and well and keen for intervention if possible. What type of intervention is he most likely to be offered?

Bioprosthetic aortic valve replacement

Prosthetic heart valves - mechanical valves last longer and tend to be given to younger patients

true

The most common valves which need replacing are the aortic and mitral valve. There are two main options for replacement:

biological (bioprosthetic) or mechanical.

Biological (bioprosthetic) valves

Usually bovine (cow) or porcine (pig) in origin

Biological (bioprosthetic) valves cons

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

Biological (bioprosthetic) valves




do these patients usually require long term anticoagulation

usually NOT




Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.

Mechanical valves

The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays

Mechanical valves have a low failure rate

true

Mechanical valves cons

Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed. Aspirin is normally given in addition unless there is a contraindication.

are patients with mechanical valves likely to require long term anticoagulation

yes




Aspirin is normally given in addition unless there is a contraindication.




also warfarin:


- Target INR


= aortic: 2.0-3.0


= mitral: 2.5-3.5

You are doing the annual review for a 67-year-old man who has type 2 diabetes. His glycaemic control is reasonable with metformin therapy; the latest HbA1c is 54 mmol/mol (7.1%). A few weeks ago he was noted to have a clinic blood pressure reading of 152/90 mmHg. A 24 hour blood pressure monitor was requested. The report shows his average blood pressure was 142/88 mmHg. What is the most appropriate course of action?

Start an ACE inhibitor

ACE inhibitors are first-line for

hypertension in diabetics, irrespective of the patients age

NICE recommend the following blood pressure targets for type 2 diabetics:

if end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg




Diabetes mellitus: hypertension managementotherwise < 140/80 mmHg

Diabetes mellitus: hypertension management

A 2013 Cochrane review casted doubt on the wisdom of lower blood pressure targets for patients with diabetes. It compared patients who had tight blood pressure control (targets < 130/85 mmHg) with more relaxed control (< 140-160/90-100 mmHg). Patients who were more tightly controlled had a slightly reduced rate of stroke but otherwise outcomes were not significantly different.Because ACE-inhibitors have a renoprotective effect in diabetes they are the first-line antihypertensives recommended for NICE. Patients of African or Caribbean family origin should be offered an ACE-inhibitor plus either a thiazide diuretic or calcium channel blocker. Further management then reverts to that of non-diabetic patients, as discussed earlier in the module.Remember than autonomic neuropathy may result in more postural symptoms in patients taking antihypertensive therapy.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.

Which one of the following ECG changes is associated with Wolff-Parkinson White syndrome?

Short PR interval

What is the target INR for a patient with a mechanical mitral valve?

2.5-3.5

Mechanical valves - target INR:

aortic: 2.0-3.0




mitral: 2.5-3.5

A 50-year-old man is found to have blood pressure measurements of 150/100mmHg, 148/95mmHg and 160/95mmHg on three consecutive visits to his GP surgery. He declines ambulatory blood pressure monitoring as it will interfere with his work as a window cleaner. Home blood pressure readings are consistently above 150/95mmHg. What is the best initial management?

Ramipril

A 31 year old man presents to the Emergency Department feeling very unwell. He states that he has recently been prescribed a course of antibiotics by his GP for a chest infection. An ECG shows polymorphic ventricular tachycardia (torsades de pointes).What medication is he most likely to be taking?

Clarithromycin

Torsades de pointes

Torsades de pointes ('twisting of the points') is a rare arrhythmia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death

Causes of long QT interval

congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome




antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs




tricyclic antidepressants




antipsychotics




chloroquine




terfenadine




erythromycin




electrolyte imbalance: hypocalcaemia, hypokalaemia, hypomagnesaemia




myocarditis




hypothermia




subarachnoid haemorrhage

Torsades de pointesis a rare arrhythmia associated with

long QT interval.




It may deteriorate into ventricular fibrillation and hence lead to sudden death

Torsades de pointes management

IV magnesium sulphate



What is shown on the ECG?

What is shown on the ECG?

Ongoing myocardial ischaemia

It's probably too much detail for finals but these changes are known as Wellens' syndrome - T waves changes seen due to proximal left anterior descending lesions which manifest clinically as unstable angina. The diagnostic criteria are:

progressive symmetrical deep T wave inversion in leads V2 and V3slope of inverted T waves generally at 60°-90°little or no cardiac marker elevationdiscrete or no ST segment elevationno loss of precordial R waves.pattern abnormal during chest-pain free periods

Which one of the following is not part of the major criteria for diagnosing rheumatic fever?

Prolonged PR interval

A 77 year old man presents with a 3 month history of worsening shortness of breath on exertion, orthopnoea and swelling of his ankles. He has a past medical history of NSTEMI, hypertension and benign prostatic hypertrophy. He takes ramipril, bisoprolol, aspirin, simvastatin and finasteride. According to NICE guidelines, which of the following options is most pertinent in the investigation of this mans symptoms?

Refer for transthoracic echocardiogram and specialist assessment within 2 weeks




The 2010 NICE guidelines on 'Chronic heart failure: diagnosis and management in primary and secondary care' have a very useful and clear algorithm for investigation of suspected heart failure. Having taken a detailed history and performed clinical examination, the pathway divides into two, depending on whether the patient has had a previous MI or not. We are told that this patient has had a NSTEMI in the past, thus it is not necessary to measure BNP level, as referral for specialist assessment and echocardiography is indicated regardless of natriuretic peptide levels.Starting furosemide would be a reasonable management option and would provide symptomatic relief (providing renal function and electrolytes were stable) but the question is specifically asking which of the options are 'pertinent in the investigation of heart failure.' It should be noted that whilst diuretics can improve symptoms of heart failure and improve exercise tolerance, they have no effect on overall mortality.ACE-Inhibitors are first line treatment in heart failure, and titrating ramipril up to the maximum tolerated dose over 2-4 weeks has been shown to improve prognosis in patients with left ventricular ejection fraction. However once again, the question is asking us about investigation of this mans symptoms and not management, and we are not told his current dose of ramipril - he may already be on the maximum dose!

Heart failure: diagnosis




The choice of investigation is determined by whether the patient has previously had a myocardial infarction or not.

Previous myocardial infarction


= arrange echocardiogram within 2 weeks




No previous myocardial infarction


= measure serum natriuretic peptides (BNP)


- if levels are 'high' arrange echocardiogram within 2 weeks


- if levels are 'raised' arrange echocardiogram within 6 weeks

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis.




BNPNT and proBNP

High levels> 400 pg/ml (116 pmol/litre)> 2000 pg/ml (236 pmol/litre)Raised levels100-400 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)

Factors which alter the BNP level:




Increase BNP levels

Left ventricular hypertrophyIschaemiaTachycardiaRight ventricular overloadHypoxaemia (including pulmonary embolism)GFR < 60 ml/minSepsisCOPDDiabetesAge > 70Liver cirrhosis

Decrease BNP levels

ObesityDiureticsACE inhibitorsBeta-blockersAngiotensin 2 receptor blockersAldosterone antagonists

A 72-year-old male is admitted to the Emergency Room following a collapse at church. ECG reveals dissociation between the P and QRS complexes with a rate of 40 / minute. Which one of the following clinical findings may also be found?

Variable intensity of S1