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MRCP I > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Pulsus parodoxus

A

Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or
absent pulse in inspiration
* Severe asthma, cardiac tamponade

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2
Q

Slow-rising/plateau

A
  • Aortic stenosis
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3
Q

Collapsing

A

Aortic regurgitation
* Patent ductus arteriosus
* Hyperkinetic (anemia, thyrotoxic, fever, exercise/pregnancy)

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4
Q

Pulsus alternans

A

Regular alternation of the force of the arterial pulse
* Severe LVF

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5
Q

Bisferiens pulse

A

‘Double pulse’ - two systolic peaks
* Mixed aortic valve disease

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6
Q

Jerky’ pulse

A

Hypertrophic obstructive cardiomyopathy*

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7
Q

S1 heart sound

A

Closure of mitral and tricuspid valves
* Soft if long PR or mitral regurgitation
* Loud in mitral stenosis
* Variable intensity in complete heart block

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8
Q

Causes of a loud S2

A

Hypertension: systemic (loud A2) or pulmonary (loud P2)
* Hyperdynamic states
* Atrial septal defect without pulmonary hypertension

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9
Q

Causes of a soft S2

A

Aortic stenosis

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10
Q

Causes of fixed split S2

A

Atrial septal defect

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11
Q

Causes of a widely split S2

A

Deep inspiration
* RBBB
* Pulmonary stenosis
* Severe mitral regurgitation

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12
Q

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)

A

LBBB
* Severe aortic stenosis
* Right ventricular pacing
* WPW type B (causes early P2)
* Patent ductus arteriosus

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13
Q

S3 heart sound

A

Caused by diastolic filling of the ventricle
* Considered normal if < 30 years old (may persist in women up to 50 years old)
* Heard in left ventricular failure, constrictive pericarditis
* Gallop rhythm (S3) is an early sign of LVF

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14
Q

s4 sound

A

may be heard in aortic stenosis, HOCM, hypertension
* caused by atrial contraction against a stiff ventricle
* in HOCM a double apical impulse may be felt as a result of a palpable S4

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15
Q

Kussmaul’s sign

A

paradoxical rise in JVP during inspiration seen in constrictive pericarditis. Kussmaul’s sign → constrictive pericarditis

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16
Q

JVP ‘a’ wave

A

a’ wave = atrial contraction
* Large if atrial pressure e.g. Tricuspid stenosis, pulmonary stenosis, pulmonary
hypertension
* Absent if in atrial fibrillation

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17
Q

Cannon ‘a’ waves

A

caused by atrial contractions against a closed tricuspid valve
* Are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm,
single chamber ventricular pacing

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18
Q

Regular cannon waves

A
  • Ventricular tachycardia (with 1:1 ventricular-atrial conduction)
  • Atrio-ventricular nodal re-entry tachycardia (AVNRT)
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19
Q

Irregular cannon waves

A

Complete heart block

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20
Q

c wave JVP

A

‘c’ wave
* Closure of tricuspid valve
* Not normally visible

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21
Q

‘v’ wave JVP

A

Giant v waves in tricuspid regurgitation

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22
Q

‘x’ descen

A

Fall in atrial pressure during ventricular systole

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23
Q

y’ descent

A

Opening of tricuspid valve

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24
Q

Left ventricular ejection fraction

A

stroke volume / end diastolic LV volume) * 100%

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25
Q

Stroke volume

A

end diastolic LV volume - end systolic LV volume

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26
Q

ECG normal variants:

A
  • Junctional rhythm
  • First degree heart block
  • Wenckebach phenomenon

LBBB is always pathological

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27
Q

ECG changes may be seen in hypothermia:

A

Bradycardia
* ‘J’ wave - small hump at the end of the QRS complex
* First degree heart block
* Long QT interval
* Atrial and ventricular arrhythmias

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28
Q

Digoxin ECG features:

A

Down-sloping ST depression (‘reverse tick’)
* Flattened/inverted T waves
* Short QT interval
* Arrhythmias e.g. AV block, bradycardia

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29
Q

Causes of ST depression:

A

Normal if upward sloping
* Ischemia
* Digoxin
* Hypokalemia
* Syndrome X

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30
Q

LBBB

A

Diagnosis: criteria to diagnose a left bundle branch block on ECG:
* Rhythm must be supraventricular in origin (P wave present)
* QRS duration ≥ 120 ms (3 small squares)
* QS or rS complex in lead V1(note: r is small-not capital = small-not tall r in ECG)
* RsR wave in lead V6.

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31
Q

Prolonged PR interval causes

A

Causes:
* Idiopathic
* Ischemic heart disease
* Digoxin toxicity
* Hypokalemia*
* Rheumatic fever
* Aortic root pathology e.g. Abscess secondary to endocarditis
* Lyme disease
* Sarcoidosis
* Myotonic dystrophy

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32
Q

causes of left axis deviation

A
  • Left anterior hemiblock
  • Left bundle branch block
  • Wolff-parkinson-white syndrome* - right-
    sided accessory pathway
  • Hyperkalemia
  • Congenital: ostium PRIMUM ASD,
    tricuspid atresia
  • Minor LAD in obese people
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33
Q

Causes of right axis deviation (RAD)

A

Right ventricular hypertrophy
* Left posterior hemiblock
* Chronic lung disease
* Pulmonary embolism
* Ostium SECUNDUM ASD
* Wolff-parkinson-white syndrome* - left-
sided accessory pathway
* Normal in infant < 1 years old
* Minor RAD in tall people

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34
Q

Isolated systolic hypertension (ISH)

A

common in the elderly, affecting around 10% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH ↓ both strokes and ischemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is not contraindicated by the 2006 NICE guidelines which recommend treating ISH in the same stepwise fashion as standard hypertension

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35
Q

Hypertension: initial treatment

A

Patients < 55-years-old: ACE inhibitor
* Patients > 55-years-old or of Afro-Caribbean origin: calcium channel blocker or thiazide
diuretic

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36
Q

The target blood pressure

A

140/90 mmHg

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37
Q

Causes of secondary HTN

A

Renal - accounts for 80% of secondary hypertension o Glomerulonephritis
o Pyelonephritis
o Adultpolycystickidneydisease o Renal artery stenosis

Endocrine disorders
o Cushing’s syndrome
* Others
New drugs
o Primary hyperaldosteronism including Conn’s syndrome
o Liddle’s syndrome
o Congenital adrenal hyperplasia (11-β hydroxylase deficiency) o Pheochromocytoma
o Acromegaly

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38
Q

Direct renin inhibitors

A

Aliskiren (branded as Rasilez)
* By inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
* No trials have looked at mortality data yet. Trials have only investigated fall in blood pressure.
Initial trials suggest aliskiren ↓ blood pressure to a similar extent as angiotensin converting
enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
* Adverse effects were uncommon in trials although diarrhea was occasionally seen
* Only current role would seem to be in patients who are intolerant of more established
antihypertensive drugs

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39
Q

Examples of centrally acting antihypertensives include:

A

Methyldopa: used in the management of hypertension during pregnancy
* Moxonidine: used in the management of essential hypertension when conventional
antihypertensives have failed to control blood pressure
* Clonidine: the antihypertensive effect is mediated through stimulating α-2 adrenoceptors in the
vasomotor center.

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40
Q

The blood pressure target

A

140/90 mmHg (normal and diabetes)
If there is end-organ damage the target
is 130/80 mmHg

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41
Q

HTN and diabetes

A

ACE inhibitors are first-line*. Otherwise managed according to standard NICE hypertension
guidelines
* BNF advises to avoid the routine use of beta-blockers in uncomplicated hypertension,

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42
Q

Pericarditis Features

A

Features
* Chest pain: may be pleuritic. Is often relieved by sitting forwards
* Other symptoms include non-productive cough, dyspnea and flu-like symptoms
* Pericardial rub
* Tachypnea
* Tachycardia

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43
Q

Pericarditis causes

A

Causes
* Viral infections (Coxsackie)
* TB
* Uremia (causes ‘fibrinous’ pericarditis)
* Trauma
* Post MI, Dressler’s syndrome
* Connective tissue disease
* Hypothyroidism

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44
Q

Pericarditis ECG changes

A

Widespread ‘saddle-shaped’ ST elevation
* PR depression (most sensitive)

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45
Q

Myocarditis: causes

A
  • Viral: coxsackie, HIV
  • Bacteria: diphtheria, clostridia
  • Spirochetes: Lyme disease
  • Protozoa: Chagas’ disease, toxoplasmosis
  • Autoimmune
  • Drugs
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46
Q

strongest risk factor for developing infective endocarditis

A

is a previous episode of endocarditis.

Other factors include:
* Previously normal valves (50%, typically acute presentation)
* Rheumatic valve disease (30%)
* Prosthetic valves
* Congenital heart defects
* Intravenous drug users (IVDUS, e.g. Typically causing tricuspid lesion)

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47
Q

Most common cause of endocarditis

A

Streptococcus viridans
* Staphylococcus epidermidis if < 2 months post valve surger

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48
Q

streptococcus viridans - endocarditis

A

most common cause - 40-50%) → has good prognosis

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49
Q

Staphylococcus epidermidis - endocarditis

A

ass/w prosthetic valves

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50
Q

Staphylococcus aureus - endocarditis

A

especially acute presentation, IVDUS)

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51
Q

Streptococcus bovis endocarditis

A

associated with colorectal cancer

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52
Q

Bacteroides fragilis endocardtis

A

endocarditis is very rare complication of colonic resection, bacteria reaches
heart via venous return, this is why it affects right > left side → Treat with Metronidazole

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53
Q

Culture negative causes (BP-CHB) endocarditis

A

Brucella
* Prior antibiotic therapy
* Coxiella burnetii
* HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
* Bartonella

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54
Q

Poor prognostic factors endocarditis

A
  • Staph aureus infection
  • Prosthetic valve (especially ‘early’, acquired during surgery)
  • Culture negative endocarditis
  • Low complement levels
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55
Q

Diagnosis endocarditis

A

Pathological criteria positive, or
* 2 major criteria, or
* 1 major and 3 minor criteria, or
* 5 minor criteria

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56
Q

Major criteria endocarditis

A
  1. Positive blood cultures
    * Two positive blood cultures showing typical organisms consistent with infective endocarditis,
    such as Streptococcus viridans and the HACEK group.
    * Persistent bacteremia from two blood cultures taken > 12 hours apart or three or more positive
    blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis.
    * Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci.
    * Positive molecular assays for specific gene targets
  2. Evidence of endocardial involvement
    * Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation
    or dehiscence of prosthetic valves), or
    * New valvular regurgitation
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57
Q

Minor criteria endocarditis

A

Predisposing heart disease
* Microbiological evidence does not meet major criteria
* Fever > 38oc
* Vascular phenomena: major emboli, splenomegaly, clubbing, splinter hemorrhages, petechiae
or purpura
* Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots (boat shaped
hemorrhages in retina)
* Elevated CRP or ESR

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58
Q

Current management guidelines endocarditis

A

Initial blind therapy - flucloxacillin + gentamicin (benzylpenicillin + gentamicin if symptoms
less severe)
* Initial blind therapy if prosthetic valve is present or patient is penicillin allergic - vancomycin
+ rifampicin + gentamicin
* Endocarditis caused by staphylococci - flucloxacillin (vancomycin + rifampicin if penicillin
allergic or MRSA)
* Endocarditis caused by streptococci → benzylpenicillin + gentamicin (vancomycin +
gentamicin if penicillin allergic)

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59
Q

Initial blind therapy - endocardtisis

A

Initial blind therapy - flucloxacillin + gentamicin (benzylpenicillin + gentamicin if symptoms
less severe)

Initial blind therapy if prosthetic valve is present or patient is penicillin allergic - vancomycin
+ rifampicin + gentamicin

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60
Q

endocarditis treatment when caused by staphylococc

A
  • flucloxacillin (vancomycin + rifampicin if penicillin
    allergic or MRSA)
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61
Q

endocarditis treatment when caused by streptococci

A

benzylpenicillin + gentamicin (vancomycin +
gentamicin if penicillin allergic)

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62
Q

Heart Failure: treatments

A

ACE inhibitors (SAVE, SOLVD, CONSENSUS)
* Spironolactone (RALES) (improved prognosis not mortality)
* β-blockers (CIBIS)
* Hydralazine with nitrates (VHEFT-1)

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63
Q

Digoxin in HF

A

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

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64
Q

Left ventricular ejection fraction =

A

(stroke volume / end diastolic LV volume ) * 100%

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65
Q

Stroke volume =

A

end diastolic LV volume - end systolic LV volume

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66
Q

Cardiac output =

A

stroke volume x heart rate

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67
Q

Pulse pressure =

A

Systolic Pressure - Diastolic Pressure

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68
Q

Systemic vascular resistance =

A

mean arterial pressure / cardiac output

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69
Q

Donepezil adverse effects

A

is relatively contraindicated in patients with bradycardia
adverse effects include insomnia

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70
Q

Diastolic Heart Failure:

A

Basics:
* 1/3 of heart failure is diastolic (normal Left Ventricular Systolic Function-LVSF)
* Mortality in Diastolic HF is 5-8% (lower than Systolic HF: 10-15%)

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71
Q

Diastolic Heart Failure: Management:

A

Initially, reduction of pulmonary venous pressure (PVP) and congestion, using diuretics
* ARBs are superior to ACE inhibitors

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72
Q

Cardiac Tamponade: Features

A
  • Raised JVP, with an absent Y descent - this is due to the limited right ventricular filling
  • Tachycardia
  • Hypotension
  • Muffled heart sounds
  • Pulsus paradoxus (which occurs also in Asthma)
  • Kussmaul’s sign (much debate about this) (more in constrictive pericarditis)
  • ECG: electrical alternans
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73
Q

key differences between constrictive pericarditis and cardiac tamponade are:

A

Cardiac tamponade
Absent Y descent
Pulsus paradoxu
Kussmaul’s sign

pericarditis
X + Y present
AbsentPericardial calcification on CXR

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74
Q

MUGA

A

Multi Gated Acquisition Scan, also known as radionuclide angiography
* Radionuclide (technetium-99m) is injected intravenously
* The patient is placed under a gamma camera
* May be performed as a stress test
* Can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are used

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75
Q

Cardiac Computed Tomography (CT)

A

useful for assessing suspected IHD, using two main methods:
* Calcium score: there is known to be a correlation between the amount of atherosclerotic plaque calcium and the risk of future ischemic events. Cardiac CT can quantify the amount of calcium
producing a ‘calcium score’
* Contrast enhanced CT: allows visualization of the coronary artery lumen

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76
Q

Cardiac MRI:

A

gold standard for providing structural images of the heart. It is particularly useful when assessing congenital heart disease, determining right and left ventricular mass and differentiating forms of cardiomyopathy. Myocardial perfusion can also be assessed following the administration of gadolinium. Currently CMR provides limited data on the extent of coronary artery disease.

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77
Q

Exercise ECG:

A

USELESS in patients with:
* Conduction abnormalities
* resting (ECG) abnormalities like ST segment depression of >1mm
* WPW
* Digoxin
* Ventricular paced rhythm

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78
Q

mmediate management of suspected acute coronary syndrome (ACS)

A

Glyceryl trinitrate
* Aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel)
outside of hospital
* Do not routinely give oxygen, only give if sats < 94%*
* Perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does
not exclude ACS

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79
Q

refer chest pain

A

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

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80
Q

in chest pain NICE suggest the following in terms of oxygen therapy:

A

Do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
* People with oxygen saturation (SpO2) < 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
* People with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

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81
Q

NICE define anginal pain as the following:

A

Constricting discomfort in the front of the chest, neck, shoulders, jaw or arms o Precipitated by physical exertion
o Relieved by rest or GTN in about 5 minutes
* Patients with all 3 features have typical angina
* Patients with 2 of the above features have atypical angina
* Patients with 1 or none of the above features have non-anginal chest pain

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82
Q

Stable Angina: management

A

In good exercise tolerance, consider medical therapy before angiography (β-
blocker is the most important)
* If pain is worsening, no need for exercise test, directly do angiography (Cath)

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83
Q

Medication stable angina

A

All patients should receive aspirin and a statin in the absence of any contraindication
* Sublingual glyceryl trinitrate to abort angina attacks
* β-blocker is the preferred initial treatment. For patients unable to take a β-blocker there is no
clear guidelines on the best alternative. Options include a rate-limiting calcium-channel blocker (verapamil or diltiazem); a long-acting dihydropyridine calcium-channel blocker (e.g. modified- release nifedipine); a nitrate; or a potassium-channel activator

If there is a poor response to initial treatment then the β-blocker should be ↑ to the maximum tolerated dose (e.g. atenolol 100mg od)
* Again, there are no clear guidelines on the next step treatment. CKS advise adding a long-acting dihydropyridine (e.g. nifedipine, amlodepine, felodipine) although other options include isosorbide mononitrate and nicoran

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84
Q

Prinzmetal angina

A

dihydropyridine calcium channel blocker (depine family; amlodepine)

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85
Q

Nitrate tolerance stable

A

Many patients who take nitrates develop tolerance and experience ↓ efficacy
* 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 mononitra

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86
Q

Ivabradine (Procoralan)

A

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

NICE 2011 Guidelines:
* In good exercise tolerance, consider medical therapy before angiography (β-
blocker is the most important)
* If pain is worsening, no need for exercise test, directly do angiography (Cath)

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87
Q

Acute Coronary Syndrome: all its should get

A

All patients should receive
- Aspirin 300mg
- Nitrates or morphine to relieve chest pain if required

Clopidogrel 300mg and low molecular weight heparin (principally enoxaparin) should also be added to higher risk patients

lopidogrel 300mg should be given to patients with a predicted 6 month mortality of more than 1.5% or patients who may undergo percutaneous coronary intervention within 24 hours of admission to hospital. Clopidogrel should be continued for 12 months.

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88
Q

Acute Coronary Syndrome: Antithrombin treatment.

A

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 patient’s creatinine is > 265 μmol/l unfractionated heparin should be given.

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89
Q

Clopidogrel (Plavix®) Interactions

A

Concurrent use of proton pump inhibitors (PPIs) may make clopidogrel less effective (MHRA July 2009)
* This advice was updated by the MHRA in April 2010, evidence seems inconsistent but omeprazole and esomeprazole still cause for concern. Other PPIs such as lansoprazole should be OK

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90
Q

Intravenous glycoprotein IIb/IIIa receptor antagonists ACS

A

(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.

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91
Q

Coronary angiography

A

should be considered within 96 hours of first admission to 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.

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92
Q

Aspirin moa

A

Antiplatelet - inhibits the production of thromboxane A2

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93
Q

Clopidogrel moa

A

Antiplatelet - inhibits ADP binding to its platelet receptor

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94
Q

Enoxaparin moa

A

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

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95
Q

Fondaparinux

A

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

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96
Q

Bivalirudin

A

Reversible direct thrombin inhibitor

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97
Q

Poor prognostic factors: ACS

A

Age
* Development (or history) of heart failure,
Killip class*
* Peripheral vascular disease
* ↓ systolic blood pressure
* Initial serum creatinine concentration
* Elevated initial cardiac markers
* Cardiac arrest on admission
* ST segment deviation

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98
Q

Anteroseptal MI

A

V1-V4
Left anterior descending

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99
Q

Inferior MI

A

II, III, aVF
Right coronary

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100
Q

Anterolateral MI

A

V4-6, I, aVL
Left anterior descending or left circumflex

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101
Q

Lateral MI

A

I, aVL +/- V5-6
Left circumflex

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102
Q

Posterior MI

A

Tall R waves V1-2 Usually left circumflex, also right coronary

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103
Q

Posterior aortic or coronary sinus ->

A

left coronary artery (LCA)

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104
Q

Anterior aortic or coronary sinus _>

A

right coronary artery (RCA)

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105
Q
  • LCA (Left Main, LM) →
A

LAD + circumflex

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106
Q

RCA →

A

posterior descending

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107
Q

RCA supplies

A

SA node in 60%, AV node in 90%

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108
Q

MI ll patients should be offered the following drugs

A
  • ACE inhibitor
  • β-blocker
  • Aspirin
  • Statin
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109
Q

Clopidogrel post MI

A

After an ST-segment-elevation MI, patients treated with a combination of aspirin and clopidogrel during the first 24 hours after the MI should continue this treatment for at least 4 wk
* (NSTEMI): following the 2010 NICE unstable angina and NSTEMI guidelines clopidogrel
should be given for the first 12 months if the 6 month mortality risk is > 1.5%
* Improves prognosis post MI
* Side effect: < 1% TTP usually 2 weeks after commencing the drug.

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110
Q

contraindications to Thrombolysis

A
  • Active internal bleeding
  • Recent hemorrhage, trauma or surgery (including dental extraction)
  • Coagulation and bleeding disorders
  • Intracranial neoplasm
  • Stroke < 2 months
  • Aortic dissection
  • Recent head injury
  • Pregnancy
  • Severe hypertension
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111
Q

Dressler’s Syndrome:

A

This usually occurs 1 to 8 weeks after MI.
Presentation:
* Malaise, fever, pericardial pain
* Elevated erythrocyte count
* Sometimes may also have pleuritis and pneumonitis.

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112
Q

dressers syndrome

A

Treatment involves aspirin and analgesics. Corticosteroids and non-steroidal anti-inflammatory agents are best avoided in the first 4 weeks after MI as they delay myocardial healing. Aspirin in large doses is effective. Recurrences can occur, and in such cases colchicine is helpful.

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113
Q

ST Elevation Myocardial Infarction (STEMI) - In the absence of contraindications, all patients should be given

A
  • Aspirin
  • Clopidogrel: the two major studies (clarity and commit) both confirmed benefit but used different loading doses (300mg and 75mg respectively)
  • Low molecular weight heparin

PCI
. Thrombolysis if not

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114
Q

Thrombolysis MI

A

Tissue plasminogen activator (TPA) has been shown to offer clear mortality benefits over
streptokinase
* Tenecteplase is easier to administer and has been shown to have non-inferior efficacy to
alteplase with a similar adverse effect profile

n ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation
* If there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis

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115
Q

Coronary Angiography (CAG) complications:

A

Vascular complications: the most common complication overall is hemorrhage from access (right femoral artery mostly then right radial artery), much less common is rupture of coronary artery during revascularization or rupture of any artery from access to target artery
* Contrast Induced Nephropathy (CIN), higher incidence in diabetic patients and patients known to have renal dysfunction (prevented by good hydration)
* Cholesterol embolisation
* Arrhythmias (include arrest, ventricular and supraventricular) especially in primary intervention
(in case of acute MI)
* Reaction to contrast

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116
Q

Two main complications may occur due to stenting:

A

Stent thrombosis: due to platelet aggregation as above. Occurs in 1-2% of patients, most commonly in the first month. Usually presents with acute myocardial infarction
* Restenosis: due to excessive tissue proliferation around stent. Occurs in around 5-20% of patients, most commonly in the first 3-6 months. Usually presents with the recurrence of angina symptoms. Risk factors include diabetes, renal impairment and stents in venous bypass grafts

117
Q

Types of stent

A

Bare-metal stent (BMS)
* Drug-eluting stents (DES): stent coated with paclitaxel or rapamycin which inhibit local tissue
growth. Whilst this ↓ restenosis rates the stent thrombosis rates are ↑ as the process of stent endothelisation is slowed

BMS in T2DM: restenosis risk in 6 months is 40-50%

118
Q

most important factor in preventing stent thrombosis

A

antiplatelet therapy. Aspirin should be continued indefinitely. The length of clopidogrel treatment depends on the type of stent, reason for insertion and consultant preference.

119
Q

Cholestrol Embolism:

A

Overview
* Cholesterol emboli may break off causing renal disease
* Seen more commonly in arteriopaths, abdominal aortic aneurysms
Features
* Eosinophilia
* Purpura
* Renal failure
* Livedo reticularis

120
Q

Clopidogrel pathway of activation

A

pro-drug whose action may be related to adenosine diphosphate (ADP) receptor on platelet cell membranes.

clopidogrel irreversibly inhibits is P2Y12

blockade of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway.

IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor

121
Q

Supraventricular tachycardia (SVT)

A

haracterized 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.

122
Q

Supraventricular tachycardia (SVT) -acute management

A

cute management
* Vagal maneuvers: e.g. Valsalva maneuver
* Adenosine 6mg then 12mg then 12mg - contraindicated in asthmatics - verapamil is a preferable
option (if no control) then
* Electrical cardioversion

123
Q

SVT Prevention of episodes

A

β-blockers (Sotalal)
* Flecainide.
* Radio-frequency ablation

124
Q

Premature Ventricular Contractions (PVCs):

A
  • Occurring frequently ( ≥6 beats/min )
  • Bigeminal rhythm
  • Short runs of ventricular tachycardia (V. Tach)
  • R-on-T phenomenon
  • Associated with serious organic heart disease
  • Left ventricular decompensation (Decompensated Heart Failure)
125
Q

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillatio

A
  • Amiodarone
  • Flecainide (if no structural heart disease)
  • Others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone
126
Q

Less effective agents in cardio version in AF

A
  • Calcium channel blockers
  • Digoxin
  • Disopyramide
  • Procainamide
127
Q

AF Onset < 48 hours

A

if atrial fibrillation (AF) is of less than 48 hours onset patients should be heparinised and a transthoracic echocardiogram performed to exclude a thrombus. Following this, patient may be cardioverted, either:
* Electrical - ‘DC cardioversion’
* Pharmacology - amiodarone if structural heart disease, flecainide in those without structural
heart disease

128
Q

AF Onset > 48 hours

A

f AF is of greater than 48 hours then patients should have therapeutic anticoagulation for at least 3 weeks. If there is a high risk of cardioversion failure (e.g. previous failure or AF recurrence) then it is recommended to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion. If there was very acute history on presentation and the patient was in significant heart failure then DC cardioversion would be appropriate, as per Advanced Life Support guidelines.
Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence.

129
Q

gents used to control rate in patients with atrial fibrillation

A

β-blockers
* Calcium channel blockers
* Digoxin

130
Q

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

A
  • Sotalol
  • Amiodarone
  • Flecainide
  • Others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone,
    quinidine
131
Q

af Factors favoring rate control

A

Older than 65 years
* History of ischemic heart disease

132
Q

Factors favoring rhythm control

A

Younger than 65 years
* Symptomatic
* First presentation
* Lone AF or 2nd° AF (e.g. alcohol) * Congestive heart failure

133
Q

It is recommended that AF be classified into 3 patterns:

A

First detected episode (irrespective of whether it is symptomatic or self-terminating)
* Recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate
spontaneously then the term paroxysmal AF is used (the most AF that benefit from β blocker). Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self- terminating then the term persistent AF is used. Such episodes usually last greater than 7 days
* In permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation if appropriate

134
Q

CHADVASC

A

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A Age > 75 years 1
D Diabetes 1
S2 Prior Stroke or TIA 2

135
Q

Ventricular Tachycardia:
Monomorphic VT:

A

Monomorphic VT: most commonly caused by myocardial infarction

136
Q

Polymorphic VT:

A

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 later.

137
Q

Features suggesting VT rather than SVT with aberrant conduction

A
  • A V dissociation
  • Fusion or capture beats
  • Positive QRS concordance in chest leads
  • Marked left axis deviation
  • History of IHD
  • Lack of response to adenosine or carotid sinus massage
  • QRS>160ms
138
Q

VT Drug therapy

A
  • Amiodarone: ideally administered through a central line
  • Lidocaine: use with caution in severe left ventricular impairment
  • Procainamide
139
Q

VERAP
MIL SHOULD NOT BE USED IN VT

A

Verapamil should never be given t
a patient with a broad complex tachycardia as it may precipitate
ventricular fibrillation in patients
ith ventricular tachycardia. Adenosine is sometimes given in this
situation as a ‘trial’ if there is a stro
g suspicion the underlying rhythm is a supraventricular tachycardia
with aberrant conducti

140
Q

V Tach in Digoxin Toxicity:

A

If drug
* *
Treat with lidocaine and phenytoin
Avoid Amiodarone and Procainamide (↑ Toxicity)
D/C shock when all measures fail (but usually unsuccessful)
therapy fails Electrophysiological study (EPS)
Implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

141
Q

Torsades De Pointes RF

A

Risk factors:
*♀
* ↓HR
* CHF
* Digoxin
* Prolonged QT and Subclinical long QT syndrome
* Severe alkalosis
* Recent conversion from A

142
Q

Causes of long QT interval

A
  • Congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
  • Antiarrhythmics: amiodarone, sotalol, class I-a antiarrhythmic drugs
  • Tricyclic antidepressants
  • Antipsychotics
  • Chloroquine
  • Terfenadine
  • Erythromycin
  • Electrolyte: Hypocalcemia, Hypokalemia, Hypomagnesemia
  • Myocarditis
  • Hypothermia
143
Q

TdP management

A
  • IV magnesium sulphate
  • Correct K+ if hypo
  • Override pacing (set pacemaker to be faster than patient rate then decrease the rate)
  • D/C shock
144
Q

Multifocal Atrial Tachycardia (MAT)

A

may be defined as irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease (e.g COPD)

anagement
* Correction of hypoxia and electrolyte disturbances
* Rate-limiting calcium channel blockers are often used first-line
* Cardioversion and digoxin are not useful in the management of MAT

145
Q

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

A
  • Systolic BP < 90 mmHg
  • ↓ conscious level
  • Chest pain
  • Heart failure
    If any of the above adverse signs are present then synchronised DC shocks should be given
146
Q

Broad-complex tachycardia

A

Regular
* Assume ventricular tachycardia (unless
previously confirmed SVT with bundle
branch block)
* Loading dose of amiodarone followed by
24 hour infusion

Irregular
* AF with bundle branch block - treat as
for narrow complex tachycardia
* Polymorphic VT (e.g. torsade de
pointes) - IV magnesium

147
Q

Narrow-complex tachycardia

A

Regular
* Vagal manoeuvres followed by IV
adenosine
* If above unsuccessful consider diagnosis
of atrial flutter and control rate (e.g. β- blockers)

Irregular
* Probable atrial fibrillation
* If onset < 48 hr: consider electrical or
chemical cardioversion
* >48 HR: Rate control (e.g. β-blocker or
digoxin) and anticoagulation

148
Q

Bradycardiaa adverse signs

A

The following factors indicate hemodynamic compromise and hence the need for treatment:
* Heart rate < 40 bpm
* Systolic blood pressure < 100 mmHg
* Heart failure
* Ventricular arrhythmias requiring suppression

149
Q

Potential risk of asystole

A

The following indicate a potential risk of asystole and hence the need for treatment with transvenous pacing:
* Complete ♥ block
* Recent asystole
* Mobitz type II ♥ block
* Symptomatic 2nd degree
* Ventricular pause > 3 seconds

150
Q

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

A
  • Atropine, up to maximum of 3mg
  • Transcutaneous pacing
  • Adrenaline infusion titrated to response
151
Q

Complete heart block

A

Features
* Syncope
* Heart failure
* Regular bradycardia (30-50 bpm)
* Wide pulse pressure
* JVP: cannon waves in neck
* Variable intensity of S1.

152
Q

Trifasicular Block:

A

The combination of RBBB, LAHB and long PR interval has been called trifasicular block.

153
Q

Indications for a Temporary Pacemaker

A

Symptomatic/hemodynamically unstable bradycardia, not responding to atropine
* Post-ANTERIOR MI: type 2 or complete heart block*
* Trifascicular block prior to surgery

154
Q

ndications of Implantable Cardiac Defibrillators (IDC):

A

Long QT syndrome
* Hypertrophic obstructive cardiomyopathy (HOCM)
* Previous cardiac arrest due to VT/VF
* Previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on
electrophysiology testing and ejection fraction < 35%
* Brugada syndrome

155
Q

Long QT Syndrome (LQTS)

A

inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in α subunit of the slow delayed rectifier potassium channel. A normal corrected QT is less than 440 ms in ♂s and 450 ms in ♀s.

156
Q

he most common variants of LQTS (LQT1 & LQT2) are caused by

A

efects in α subunit of the slow delayed rectifier potassium channel. A normal corrected QT is less than 440 ms in ♂s and 450 ms in ♀s.

157
Q

Coronary Angiography (CAG) complications

A

Vascular complications: the most common complication overall is hemorrhage from access (right femoral artery mostly then right radial artery), much less common is rupture of coronary artery during revascularization or rupture of any artery from access to target artery
* Contrast Induced Nephropathy (CIN), higher incidence in diabetic patients and patients known to have renal dysfunction (prevented by good hydration)
* Cholesterol embolisation
* Arrhythmias (include arrest, ventricular and supraventricular) especially in primary intervention
(in case of acute MI)
* Reaction to contras

158
Q

Two main complications may occur due to stenting:

A

Stent thrombosis: due to platelet aggregation as above. Occurs in 1-2% of patients, most commonly in the first month. Usually presents with acute myocardial infarction
* Restenosis: due to excessive tissue proliferation around stent. Occurs in around 5-20% of patients, most commonly in the first 3-6 months. Usually presents with the recurrence of angina symptoms. Risk factors include diabetes, renal impairment and stents in venous bypass grafts

159
Q

Bare-metal stent (BMS) in diabetic

A

BMS in T2DM: restenosis risk in 6 months is 40-50%

160
Q

Supraventricular tachycardia (SVT): acute management

A

Acute management
* Vagal maneuvers: e.g. Valsalva maneuver
* Adenosine 6mg then 12mg then 12mg - contraindicated in asthmatics - verapamil is a preferable
option (if no control) then
* Electrical cardioversion

161
Q

SVT management // prevention

A

Prevention of episodes
* β-blockers (Sotalal)
* Flecainide.
* Radio-frequency ablation

162
Q

Premature Ventricular Contractions (PVCs):

A

Occurring frequently ( ≥6 beats/min )
* Bigeminal rhythm
* Short runs of ventricular tachycardia (V. Tach)
* R-on-T phenomenon
* Associated with serious organic heart disease
* Left ventricular decompensation (Decompensated Heart Failure)

163
Q

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

A

Amiodarone
* Flecainide (if no structural heart disease)
* Others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

164
Q

If atrial fibrillation (AF) is of less than 48 hour

A

patients should be heparinised and a transthoracic echocardiogram performed to exclude a thrombus. Following this, patient may be cardioverted, either:
* Electrical - ‘DC cardioversion’
* Pharmacology - amiodarone if structural heart disease, flecainide in those without structural
heart disease

165
Q

If AF is of greater than 48 hours then

A

If there is a high risk of cardioversion failure (e.g. previous failure or AF recurrence) then it is recommended to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion. If there was very acute history on presentation and the patient was in significant heart failure then DC cardioversion would be appropriate, as per Advanced Life Support guidelines.
Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence.

166
Q

Agents used to control rate in patients with atrial fibrillation

A
  • β-blockers
  • Calcium channel blockers
  • Digoxin
167
Q

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

A
  • Sotalol
  • Amiodarone
  • Flecainide
  • Others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone,
    quinidine
168
Q

Factors favoring rate control

A

Factors favoring rhythm control
* Older than 65 years
* History of ischemic heart disea

169
Q

Factors favoring rhythm control

A

young (under 65)
Symptomatic
* First presentation
* Lone AF or 2nd° AF (e.g. alcohol) * Congestive heart failure

170
Q

It is recommended that AF be classified into 3 patterns:

A

First detected episode (irrespective of whether it is symptomatic or self-terminating)
* Recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate
spontaneously then the term paroxysmal AF is used (the most AF that benefit from β blocker). Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self- terminating then the term persistent AF is used. Such episodes usually last greater than 7 days
* In permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation if appropriate

171
Q

CHADS2

A

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A Age > 75 years 1
D Diabetes 1
S2 Prior Stroke or TIA 2

172
Q

The Royal College of Physicians and NICE are due to publish joint guidelines on the management of atrial fibrillation (AF) in 2006:

A

Following a stroke or transient-ischemic attack (TIA) warfarin should be given as the
anticoagulant of choice. Aspirin/dipyridamole should only be given if needed for the treatment
of other comorbidities
* In acute stroke patients, in the absence of hemorrhage, anticoagulation therapy should be
commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

173
Q

VERAP
MIL SHOULD NOT BE USED IN VT

A

Verapamil should never be given t
a patient with a broad complex tachycardia as it may precipitate
ventricular fibrillation in patients
ith ventricular tachycardia. Adenosine is sometimes given in this
situation as a ‘trial’ if there is a stro
g suspicion the underlying rhythm is a supraventricular tachycardia
with aberrant conduction

174
Q

V Tach in Digoxin Toxicity:

A

treat with lidocaine and phenytoin
Avoid Amiodarone and Procainamide (↑ Toxicity)
D/C shock when all measures fail (but usually unsuccessful)

175
Q

Torsades De Pointes

A

Risk factors:
*♀
* ↓HR
* CHF
* Digoxin
* Prolonged QT and Subclinical long QT syndrome
* Severe alkalosis
* Recent conversion from AF

176
Q

Causes of long QT interval

A
  • Congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
  • Antiarrhythmics: amiodarone, sotalol, class I-a antiarrhythmic drugs
  • Tricyclic antidepressants
  • Antipsychotics
  • Chloroquine
  • Terfenadine
  • Erythromycin
  • Electrolyte: Hypocalcemia, Hypokalemia, Hypomagnesemia
  • Myocarditis
  • Hypothermia
  • Subarachnoid hemorrhage
177
Q

tpd Management

A

IV magnesium sulphate
* Correct K+ if hypo
* Override pacing (set pacemaker to be faster than patient rate then decrease the rate)
* D/C shock

178
Q

VT regular

A

Regular
* Assume ventricular tachycardia (unless
previously confirmed SVT with bundle
branch block)
* Loading dose of amiodarone followed by
24 hour infusion

179
Q

Vt irregular

A

AF with bundle branch block - treat as
for narrow complex tachycardia
* Polymorphic VT (e.g. torsade de
pointes) - IV magnesium

180
Q

Narrow-complex tachycardia regular

A

Regular
* Vagal manoeuvres followed by IV
adenosine
* If above unsuccessful consider diagnosis
of atrial flutter and control rate (e.g. β- blockers)

181
Q

Narrow-complex tachycardia irregular

A

rregular
* Probable atrial fibrillation
* If onset < 48 hr: consider electrical or
chemical cardioversion
* >48 HR: Rate control (e.g. β-blocker or
digoxin) and anticoagulation

182
Q

Adverse signs bradycardia

A
  • Heart rate < 40 bpm
  • Systolic blood pressure < 100 mmHg
  • Heart failure
  • Ventricular arrhythmias requiring suppression

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

183
Q

Potential risk of asystole

A

Complete ♥ block
* Recent asystole
* Mobitz type II ♥ block
* Symptomatic 2nd degree
* Ventricular pause > 3 second

184
Q

Complete heart block

A

Syncope
* Heart failure
* Regular bradycardia (30-50 bpm)
* Wide pulse pressure
* JVP: cannon waves in neck
* Variable intensity of S1.

185
Q

Trifasicular Block:

A

The combination of RBBB, LAHB and long PR interval has been called trifasicular block.

186
Q

Indications for a Temporary Pacemaker

A

Symptomatic/hemodynamically unstable bradycardia, not responding to atropine
* Post-ANTERIOR MI: type 2 or complete heart block*
* Trifascicular block prior to surgery

*post-Inferior MI complete heart block is common and can be managed conservatively if asymptomatic and hemodynamically stable

187
Q

Indications of Implantable Cardiac Defibrillators (IDC):

A

Long QT syndrome
* Hypertrophic obstructive cardiomyopathy (HOCM)
* Previous cardiac arrest due to VT/VF
* Previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on
electrophysiology testing and ejection fraction < 35%
* Brugada syndrome

188
Q

Long QT Syndrome (LQTS)

A

is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in α subunit of the slow delayed rectifier potassium channel. A normal corrected QT is less than 440 ms in ♂s and 450 ms in ♀s.

189
Q

Blockage of K+ channels causes

A

prolongation of QT

190
Q

Long QT Syndrome Causes:

A

Amiodarone
* Sotalol*
* Class I-a antiarrhythmic
* Tricyclic antidepressants * Chloroquine
* Terfenadine
* Macrolide (erythromycin) * Quinolones

191
Q

Long QT Syndrome Congenital

A

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

192
Q

Long QT1

A

usually associated with exertional syncope, often swimmin

193
Q

Long QT2

A
  • often associated with syncope occuring following emotional stress, exercise or
    auditory stimuli
194
Q

Long QT3 -

A

events often occur at night or at rest (associated with brady, so pacemaker may be
beneficial)

195
Q

Long QT4

A

associated with Parox. AF

196
Q

long qt Management

A
  • Avoid drugs which prolong QT and other precipitants if appropriate (e.g. Strenuous exercise)
  • 1st line pharmacological therapy is Mg+ IV (bolus then infusion)
  • β-blockers**
  • Implantable cardioverter defibrillators in high risk cases (if β-blockers fail)
  • Left stellate sympathectomy (if β-blockers fail or when there is multiple ICD shocks)
197
Q

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) - Pathophysiology

A

Pathophysiology
* Inherited in an autosomal dominant pattern with variable expression
* The right ventricular myocardium is replaced by fibrofatty tissue

198
Q

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

A

Presentation
* Palpitations
* Syncope
* Sudden cardiac death
Investigation
* ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
* Echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
* Magnetic resonance imaging is useful to show fibrofatty tissue

199
Q

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) - Management

A

Management
* Drugs: sotalol is the most widely used antiarrhythmic
* Catheter ablation to prevent ventricular tachycardia
* Implantable cardioverter-defibrillator

200
Q

Wolff-Parkinson White (WPW)

A

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

201
Q

Wolff-Parkinson White (WPW) - Possible ECG features include:

A

Possible ECG features include:
* Short PR interval
* Wide QRS complexes with a slurred upstroke - ‘delta wave’
* Left axis deviation if right-sided accessory pathway*
* Right axis deviation if left-sided accessory pathway*

202
Q

Wolff-Parkinson White (WPW) - Differentiating between type A and type B

A
  • Type A (left-sided pathway): dominant R wave in V1, seen in the above ECG.
  • Type B (right-sided pathway): no dominant R wave in V1
203
Q

Associations of WPW

A

HOCM
* Mitral valve prolapse
* Ebstein’s anomaly
* Thyrotoxicosis
* Secundum ASD

204
Q

wpw Management

A

Definitive treatment: radiofrequency ablation of the accessory pathway
* Medical therapy: sotalol**, amiodarone, flecainide
* For cardioversion: Flecainide is superior to Amiodarone

205
Q

Medications to avoid in wpw

A

sotalol should be avoided

Adenosine should be avoided as blocking the AV node can paradoxically ↑ ventricular rate resulting in fall in cardiac output. Verapamil and digoxin should also be avoided i

206
Q

Catecholaminergic polymorphic ventricular tachycardia (CPVT)

A

form of inherited cardiac disease associated with sudden cardiac death. It is inherited in an autosomal dominant fashion and has a prevalence of around 1:10,000.

Pathophysiology
* The most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum

207
Q

Catecholaminergic polymorphic ventricular tachycardia (CPVT) - Features

A

Features
* Exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
* Sudden cardiac death
* Symptoms generally develop before the age of 20 years

Management
* β-blockers
* Implantable cardioverter-defibrillator

208
Q

Brugada syndrome

A

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

209
Q

Brugada syndrome - Pathophysiology

A

Pathophysiology
* A large number of variants exist
* Around 20-40% of cases are caused by a mutation in the SCN5a gene which encodes the myocardial sodium ion
channel protein

210
Q

Brugada syndrome ecg

A

ECG changes
* Convex ST elevation V1-V3
* Partial right bundle branch block
* Changes may be more apparent following
flecainide

211
Q

Brugada syndrome management

A

management
* Implantable cardioverter-defibrillator
* Quinidine is useful in VF storm (indicated
by fast repeated ICD shocks)

212
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500. Mutations to various proteins including β-myosin, α-tropomyosin and troponin T have been identified. Septal hypertrophy causes left ventricular outflow obstruction. It is an important cause of sudden death in apparently healthy individuals.

213
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM)- Features

A

Often asymptomatic
* Dyspnea, angina, syncope
* Sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
* Jerky pulse, large ‘a’ waves, double apex beat
* Ejection systolic murmur: ↑ with valsalva manoeuvre and ↓ on squatting

214
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM)- Associations

A

Associations
* Friedreich’s ataxia
* Wolff-Parkinson White

215
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM) ECG

A

ECG
* Left ventricular hypertrophy (L VH)
* Atrial enlargement (abnormal P morphology)
* Progressive T wave inversion
* ST-T abnormalities
* Deep Q waves
* Axis deviation
* Prolonged PR or sinus bradycardia
* BBB (bundle brach block)
* Ectopic atrial rhythm
* Atrial fibrillation may occasionally be seen
Echo (Mr. Sam Ash):
* Mitral regurgitation (MR)
* Systolic anterior motion (SAM) of the anterior mitral valve leaflet
* Asymmetric hypertrophy (ASH)

216
Q

If LVOT gradient < 35 with signs of heart failure

A

responds well to β blockers

217
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM) Poor prognostic factors

A

Syncope
* Family history of sudden death
* Y oung age at presentation
* Non-sustained ventricular tachycardia on 24 or 48-hour holter monitoring

218
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM) Management

A

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

219
Q

Drugs to avoid Hypertrophic Obstructive Cardiomyopathy (HOCM)

A
  • Nitrates
  • ACE-inhibitors
  • Inotropes
  • Digoxin is contraindicated if there is significant LVOT gradient
220
Q

Dilated Cardiomyopathy (DCM)

A

Basics:
* Prevelance is 1% in adult – it ↑ to 10% at age of 80 yrs
* Annual mortality of cardiomyopathies and HF is 20%
* Dilated heart leading to systolic (+/- diastolic) dysfunction
* All 4 chambers affected but LV more than RV
* Features include arrhythmias, emboli, mitral regurgitation
* Absence of congenital, valvular or ischemic heart disease

221
Q

Dilated Cardiomyopathy (DCM) -

A

Other causes
* Inherited (see below)
* Infections e.g. Coxsackie A and B, HIV, diphtheria, parasitic
* Endocrine e.g. Hyperthyroidism
* Infiltrative* e.g. Hemochromatosis, sarcoidosis
* Neuromuscular e.g. Duchenne muscular dystrophy
* Nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency
* Drugs e.g. Doxorubicin

222
Q

Inherited dilated cardiomyopathy

A

Around a third of patients with DCM are thought to have a genetic predisposition
* A large number of heterogeneous defects have been identified
* The majority of defects are inherited in an autosomal dominant fashion although other patterns
of inheritance are seen

223
Q

Restrictive Cardiomyopathy

A

Features
* Similar to constrictive pericarditis
Restrictive cardiomyopathy vs Constrictive pericarditis, in restrictive:
* Prominent apical pulse
* Absence of pericardial calcification on CXR
* Heart may be enlarged
* ECG abnormalities e.g. Bundle branch block, Q waves

224
Q

Restrictive Cardiomyopathy causes

A
  • Amyloidosis (e.g. Secondary to myeloma) - most common cause in UK
  • Hemochromatosis
  • Loffler’s syndrome
  • Sarcoidosis
  • Scleroderma
225
Q

Atrial Myxoma:

A

Overview
* 75% occur in left atrium
* More common in ♀s
Features
* Systemic: weight loss, fever, clubbing
* Emboli
* Atrial fibrillation
* Mid-diastolic murmur, ‘tumour plop’

226
Q

Aortic Stenosis (AS):

A

Features of severe AS:
* Narrow pulse pressure
* Slow rising pulse
* Delayed ESM
* Soft/absent S2
* S4
* Thrill
* Duration of murmur
* Left ventricular hypertrophy or failure

Left ventricular systolic dysfunction will result in a ↓ flow-rate across the aortic valve and hence
a quieter murmur and low gradient on Echo

227
Q

Causes of AS

A

Degenerative calcification (most common cause in elderly patients)
* Bicuspid aortic valve (most common cause in younger patients)
* William’s syndrome (supravalvular aortic stenosis)
* Post-rheumatic disease
* Subvalvular: HOCM

228
Q

Aortic stenosis management:

A

AVR if symptomatic, otherwise cut-off is gradient of 50 mmHg

229
Q

Dobutamine echo

A
  • Dobutamine echo is used to assess the severity of AS in severe LVSF impairment
  • Patients with >20% increase in stroke volume after dobutamine means better prognosis
    post surgery compared to those with no LV contractile reserve.
230
Q

AS Management

A
  • 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
231
Q

Heyde’s syndrome:

A

well-known association between microcytic anemia and calcific AS. The treatment is to replace the valve, as the mechanism is thought to be due to destruction of von Willebrand’s factor as the platelets traverse the stenosed valve resulting in bleeding per rectum

232
Q

Aortic Regurgitation (AR)

A

Features
* Early diastolic murmur
* Collapsing pulse
* Wide pulse pressure
* Mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral
valve cusps caused by the regurgitation streams

233
Q

Aortic Regurgitation
Causes (due to valve disease)

A

Causes (due to valve disease)
* Rheumatic fever
* Infective endocarditis
* Connective tissue diseases e.g. RA/SLE
* Bicuspid aortic valve

Causes (due to aortic root disease)
* Aortic dissection
* Spondylarthropathies (e.g. Ankylosing spondylitis)
* Hypertension
* Syphilis
* Marfan’s, Ehler-Danlos syndrome

234
Q

Management: AR

A

Asymptomatic with LVSF <50% + dilated LV (EDD > 75mm – ESD>55mm)
↓
Consider AVR (Aortiv Valve Replacement)

235
Q

Mitral Valve Prolapse Associations

A

Associations
* Congenital heart disease: PDA, ASD
* Cardiomyopathy
* Turner’s syndrome
* Marfan’s syndrome, Fragile X
* Osteogenesis imperfecta
* Pseudoxanthoma elasticum
* Wolff-Parkinson White syndrome
* Long-QT syndrom

236
Q

Mitral Valve Prolapse Features

A

Patients may complain of atypical chest pain or palpitations
* Mid-systolic click (occurs later if patient squatting)
* Late systolic murmur (longer if patient standing)
* Complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

237
Q

Mitral Valve Prolapse Management:

A
  • Patients > 75 years who are in AF or with LVSF impairment, should be referred to surgical assessment as early as possible
  • TOE (transesophageal echo)can tell if the valve is for repair or replacement, can be done intra- operatily
  • Follow up is crucial as 15% of MVP patients develop the most serious complication after 15 years period of being prolapsed (TIA, Ischemic Stokes)
  • Mild to moderate MVP with normal LVSF → β blockers + echo follow up every 2-3 years
238
Q

Mitral Stenosis:

A

causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever. Rarer causes that may be seen in the MRCP include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

239
Q

Mitral Stenosis Features:

A

Features
* Mid-diastolic murmur (best heard in expiration)
* Loud S1, opening snap
* Low volume pulse
* Malar flush
* Atrial fibrillation
Features of severe MS
* Length of murmur ↑
* Opening snap becomes closer to S2

240
Q

Mitral Stenosis : Echocardiography

A
  • The normal cross sectional area of the mitral valve is 4-6 cm . A ‘tight’ mitral stenosis implies a
    2 cross sectional area of < 1 cm .
241
Q

Percutaneous Balloon Valvotomy:Mitral Stenosis

A

used to treat sever M.S. it is contraindicatin:
* Moderate to severe mitral regurgitation
* Left atrial thrombus
* Heavily calcified mitral valve
* Concomitant coronary artery or other valve disease requiring surgery.

242
Q

Lutembacher’s syndrome:

A

syndrome characterized by both MS & ASD. Both conditions may be congenital and occur concurrently, or the MS may occur as a result of rheumatic fever or other cause. Incidence of Lutembacher’s syndrome is higher in women due to the higher incidence of congenital ASD. Cardiac signs are mixed due to the two concurrent lesions. Presentation is typically in later life, with fatigue or atrial fibrillation. Ideally, surgery should be performed as early as possible due to the risks of Eisenmenger’s syndrome if untreated.

243
Q

Tricuspid Regurgitation:

A

Signs
* Pan-systolic murmur
* Giant v waves in JVP
* Pulsatile hepatomegaly
* Left parasternal heave

244
Q

Tricuspid Regurgitation:

A
  • Right ventricular dilation
  • Pulmonary hypertension e.g. COPD
  • Rheumatic heart disease
  • Infective endocarditis (especially intravenous drug users)
  • Ebstein’s anomaly
  • Carcinoid syndrome
245
Q

Prosthetic Valves: biological (bioprosthetic) valves

A

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

246
Q

Prosthetic Valves Mechanical valves

A

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
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.
Target INR
* Aortic: 2.0-3.0
* Mitral: 2.5-3.5

247
Q

Prosthetic Valve Thrombosis (PVT)

A

This complication occurs in 0.03 to 5.5% annually with equal frequency in bioprosthesis and mechanical valves. It is more common in mitral prosthesis and with subtherapeutic anticoagulation, this resulting in shock.

The best diagnostic modality is transoesophageal echocardiography
* Transthoracic echocardiography is the initial choice in sick patients, and if adequate
visualisation is not obtained TEE can be done.

248
Q

Prosthetic Valve Thrombosis (PVT)

A

Thrombolytic therapy should be given for patients in pulmonary edema or hypotension.
* In stable patients, surgery is a better option for left-sided PVT, while right-sided PVT should be
treated with thrombolytic agents.
* Serial echocardiography should be performed, and if the response is inadequate repeat
thrombolytic therapy can be given.

249
Q

Aortic Disection -

A

Aortic dissection
* Type A - ascending aorta - control BP(IV labetalol) + surgery
* Type B - descending aorta - control BP(IV labetalol)

250
Q

Aortic Dissection Type A

A

Ascending aorta (2/3 of cases)
Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention, by IV Labetalo

251
Q

Aortic Dissection Type B -

A

Descending aorta, distal to left subclavian origin
Conservative management
* Bed rest
* ↓ blood pressure IV labetalol to prevent
progression

252
Q

Aortic Dissection - Associations

A
  • Hypertension
  • Trauma
  • Bicuspid aortic valve
  • Collagens: marfan’s syndrome, ehlers-danlos syndrome
  • Turner’s and noonan’s syndrome
  • Pregnancy
  • Syphilis
253
Q

Aortic Dissection Complications of backward tear

A

Aortic incompetence/regurgitation
* MI: inferior pattern often seen due to right coronary involvement

254
Q

Primary Pulmonary Hypertension:

A

classification of pulmonary hypertension is currently changing with the term idiopathic pulmonary arterial hypertension (IPAH) becoming more widely used

255
Q

Secondary causes of pulmonary hypertension include

A

COPD, congenital heart disease
(Eisenmenger’s syndrome), recurrent pulmonary embolism, HIV and sarcoidosis.

256
Q

Primary pulmonary hypertension (PPH, now IPAH)

A
  • Pulmonary arterial pressure > 25 mmHg at rest, > 30mmHg with exercise
  • PPH is diagnosed when no underlying cause can be found
  • Around 10% of cases are familial: autosomal dominant
  • Endothelin thought to play a key role in pathogenesis
  • Associated with HIV, cocaine and anorexigens (e.g. Fenfluramine)
257
Q

Primary pulmonary hypertension Features

A

Features
* More common in ♀s, typically presents at 20-40 years old
* Progressive SOB
* Cyanosis
* Right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation

258
Q

Primary pulmonary hypertension - Management

A

Management
* Diuretics if right heart failure
* Anticoagulation
* Vasodilator therapy: calcium channel blocker, IV prostaglandins, bosentan: endothelin-1
receptor antagonist
* Heart-lung transplant

259
Q

Pulmonary Arterial Hypertension (PAH)

A

may be defined as a sustained elevation in mean pulmonary arterial pressure of greater than 25 mmHg at rest or 30 mmHg after exercise.
Features
* Exertional dyspnea is the most frequent symptom
* Chest pain and syncope may also occur
* Loud P2
* Left parasternal heave (due to right ventricular hypertrophy)

260
Q

PAH has recently been reclassified by the WHO:
Group 1: Pulmonary arterial hypertension (PAH)

A
  • Idiopathic*
  • Familial
  • Associated conditions: collagen vascular disease, congenital heart disease with systemic to
    pulmonary shunts, HIV**, drugs and toxins, sickle cell disease
  • Persistent pulmonary hypertension of the newborn
261
Q

Group 2 PAH has recently been reclassified by the WHO

A

Left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation

262
Q

Group 3: Pulmonary hypertension secondary to lung disease/hypoxia

A

COPD
* Interstitial lung disease * Sleep apnoea
* High altitude

263
Q

Group 4: Pulmonary hypertension due to thromboembolic disease

A

Sickle cell, Polycythemia ..etc

264
Q

Pulmonary hypertension Group 5: Miscellaneous conditions

A

Lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis

265
Q

Pulmonary hypertension most importance invest

A

Cardiac catheterisation is therefore the single most important investigation.

266
Q

Pulmonary hypertension treatment

A

acute vasodilator testing

If there is a positive response to acute vasodilator testing * Oral calcium channel blockers
If there is a negative response to acute vasodilator testing
* Prostacyclin analogues: treprostinil, ilioprost
* Endothelin receptor antagonists: bosentan
* Phosphodiesterase inhibitors: sildenafil

267
Q

Acyanotic - most common causes

A

Ventricular septal defects (VSD) - most common, accounts for 30%
* Atrial septal defect (ASD)
* Patent ductus arteriosus (PDA)
* Coarctation of the aorta
* Aortic valve stenosis

268
Q

common presenting cause of cyanotic congenital heart disease.

A

TGA most common at birth, Fallot’s most common overall

269
Q

cyanotic - most common causes

A
  • Tetralogy of Fallot
  • Transposition of the great arteries (TGA)
  • Tricuspid atresia
  • Pulmonary valve stenosis
270
Q

Patent Ductus Arteriosus (PDA)

A

Overview
* 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

271
Q

FPatent Ductus Arteriosus (PDA) features

A
  • Left subclavicular thrill
  • Continuous ‘machinery’ murmur
  • Large volume, collapsing pulse
  • Wide pulse pressure
  • Heaving apex beat
272
Q

Patent Ductus Arteriosus (PDA) Management

A
  • 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
273
Q

Ventricular Septal Defects (VSD)

A

re the most common cause of congenital heart disease. They close spontaneously in around 50% of cases. Non-congenital causes include post myocardial infarction
Features
* Classically a pan-systolic murmur which is louder in smaller defects

274
Q

Ventricular Septal Defects (VSD) Complications

A

Complications
* Aortic regurgitation*
* Infective endocarditis
* Eisenmenger’s complex * Right heart failure

275
Q

Atrial Septal Defects (ASDs)

A

are the most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years. Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common
Features

276
Q

Ostium secundum

A

Associated with Holt-Oram syndrome (tri-phalangeal thumbs)
* ECG: RBBB with RAD (secondum).

277
Q

Ostium primum

A

Present earlier than ostium secundum defects
* Associated with abnormal A V valves
* ECG: RBBB with LAD, prolonged PR interval

278
Q

asd features

A

Ejection systolic murmur, fixed splitting of S2
* Embolism may pass from venous system to left side of heart causing a stroke

279
Q

Patent foramen ovale (PFO)

A

is present in around 20% of the population. It may allow embolus (e.g. from DVT) to pass from right side of the heart to the left side leading to a stroke - ‘a paradoxical embolus’.
It’s the most common cause of stroke following DVT.

DO TOE (Transesophageal echocardiography)
There also appears to be an association between migraine and PFO. Some studies have reported improvement in migraine symptoms following closure of the PFO

280
Q

Coarctation of the Aorta

A

describes a congenital narrowing of the descending aorta, it is more common in ♂s (despite association with Turner’s syndrome). Surgical repair is the treatment, but even with repair sometimes recurrence happen.

281
Q

Coarctation of the Aorta features

A

eatures
* Infancy: heart failure
* Adult: hypertension
* Radio-femoral delay
* Mid or late 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

282
Q

Coarctation of the Aorta Associations

A

Associations
* Turner’s syndrome
* Bicuspid aortic valve
* Berry aneurysms
* Neurofibromatosis
* Accelerated Coronary Artesry Disease (CAD)
.

283
Q

Eisenmenger’s Syndrome

A

is characterized by the reversal of the left-right shunt due to pulmonary hypertension. The original murmur may disappear once Eisenmenger’s syndrome develops.

284
Q

Eisenmenger’s Syndrome Features

A

Associated with
* VSD * ASD * PDA
Features
* Original murmur may disappear
* Cyanosis
* Clubbing
* Right ventricular failure
* Hemoptysis, embolism Management
* Heart-lung transplantation is required

285
Q

Bicuspid Aortic Valve:

A

Overview
* Occurs in 1-2% of the population
* Usually asymptomatic in childhood
* The majority eventually develop aortic stenosis or regurgitation
* Associated with a left dominant coronary circulation (the posterior descending artery arises
from the circumflex instead of the right coronary artery) and turner’s syndrome
* Around 5% of patients also have coarctation of the aorta
Complications
* Aortic stenosis/regurgitation.
* Higher risk for aortic dissection and aneurysm formation of the ascending aorta

286
Q

Tetralogy of Fallot (TOF) - The four characteristic features are:

A
  • V entricular septal defect (VSD)
  • Right ventricular hypertrophy
  • Right ventricular outflow tract (RVOT) obstruction, pulmonary stenosis
  • Overriding aorta
    The severity of RVOT obstruction determines the degree of cyanosis and severity
287
Q

Tetralogy of Fallot (TOF)Other features

A
  • Cyanosis
  • Causes a right-to-left shunt
  • Ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
  • A right-sided aortic arch is seen in 25% of patients
  • Chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy

Management
* Surgical repair is often undertaken in two parts
* Cyanotic episodes may be helped by β-blockers to ↓ infundibular spasm

288
Q

Dextrocardia:

A

is a rare condition and occurs with in frequency in ♂:♀.
Classical ECG features:
* Inverted P in lead I
* Shift of the P axis (usually about +120 degrees) and reversed R wave progression.
* Reverse placement of the praecordial leads on the right chest at sites corresponding to the left
chest positions corrects this trend.

289
Q
A

MRCP I (21 decks)

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