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WFH > Cardiology 3/8/20 > Flashcards

Cardiology 3/8/20 Flashcards

1
Q

anatomical groups of ECG leads which leads are lateral?

A

precordial: V5 and V6 (low lateral) limb: I and aVL (high lateral)

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2
Q

anatomical groups of ECG leads which leads are inferior?

A

II, III and aVF

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3
Q

PR interval should be between…

A

120-200ms (3-5 small squares)

  • long PR interval = 1st degree AV block
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4
Q

QRS complex should be…

A
  • ≤120ms duration (<3 small squares)
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5
Q

RA enlargement shown on ECG by…

A

tall (>2.5mm), pointed P waves (P pulmonale)

  • typically in chronic lung disease (eg. COPD)
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6
Q

LA enlargement shown on ECG by…

A

bifid/notched P wave (M shape - P mitrale) in limb leads

  • mitral regurg/stenosis
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7
Q

causes of short PR interval

A

Wolff-Parkinson-White syndrome (delta wave)

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8
Q

causes of prolonged PR interval (1st degree heart block)

A
  • idiopathic
  • ischaemic heart disease
  • hypokalaemia (hyperkalaemia rarely can cause prolonged PR)
  • digoxin toxicity
  • infection

> rheumatic fever

> endocarditis

> Lyme disease

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9
Q

normal cardiac axis

A

-30 to +90 degrees (shown by both leads I and II being positive)

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10
Q

left axis deviation

A

-30 to -90 degrees (shown by leads I and aVF/III LEAVING)

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11
Q

right axis deviation

A

+90 to +180 degrees (shown by lead I and aVF/III RETURNING)

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12
Q

north west axis

A

-90 to -180 degrees (lead I negative and aVF negative - very rare)

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13
Q

tachycardia with broad QRS can be…?

A
  • atrial (supraventricular) tachycardia with BBB
  • ventricular tachycardia
  • in atrial tachycardia with BBB, each QRS complex is preceded by a P wave at a constant distance
  • in ventricular tachycardia, atria and ventricles are beating independently of one another so QRS complexes are not preceded by P waves at a constant distance
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14
Q

acute inferior MI

A
  • ST elevation in the inferior leads II, III and aVF
  • reciprocal ST depression in the anterior leads
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15
Q

acute anterior MI

A
  • ST elevation in the anterior leads V1 - 6, I and aVL (V3/V4 more pronounced)
  • reciprocal ST depression in the inferior leads II, III, aVF
  • hyperacute (tall) t waves
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16
Q

old MI shown by…

A
  • pathological Q waves in anatomical distribution (eg. II, III and aVF for an inferior lesion)
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17
Q

broad QRS caused by:

A
  • ventricular origin (eg VT)
  • BBB
  • hyperkalaemia
  • pacemaker
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18
Q

causes of ST depression

A
  • myocardial ischaemia
  • digoxin toxicity
  • hypokalaemia
  • ventricular hypertrophy
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19
Q

QT interval should be….

A
  • <440 for men
  • <460 for women
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20
Q

ECG signs of LBBB

A
  • broad QRS
  • WiLLiaM (W in QRS of V1/2, M in V6)
  • left axis deviation
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21
Q

ECG signs of RBBB

A
  • broad QRS
  • MaRRoW (M in QRS of V1/2, W in V6)
  • wide S wave in lead I
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22
Q

first degree heart block

A

lengthened PR interval (>200ms)

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23
Q

second degree heart block

A

type 1 (Mobitz I)

  • progressive prolongation of the PR interval until a dropped beat occurs

type 2 (Mobitz II)

  • PR interval is constant but the P wave is often not followed by a QRS complex (intermittent dropped beats)
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24
Q

third (complete) degree heart block

A
  • no association between the P waves and QRS complexes
  • can be fatal and usually symptomatic
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25
Q

electrolyte responsible for cardiac myocyte depolarisation

A

Na+

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26
Q

electrolyte responsible for cardiac myocyte repolarisation

A

K+ (Ca2+ causes partial plateau)

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27
Q

causes of LVH

A
  • hypertension
  • valvular disease (AS)
  • hypertrophic cardiomyopathy
  • athletes
  • congenital HD
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28
Q

causes of RVH

A
  • pulmonary hypertension
  • valvular disease (pul. regurg)
  • lung disease
  • congenital HD
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29
Q

features of arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

autosomal dominant inheritance

  • RV myocardium replaced by fibrofatty tissue
  • palpitations
  • syncope
  • sudden cardiac death
  • ECG changes
  • enlarged hypokinetic RV with a thin wall may be seen on echo
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30
Q

ECG abnormalities of arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

in V1-3:

  • T wave inversion
  • epsilon wave (in 50%) - ε = M shaped terminal notch in QRS complex
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31
Q

management of arrhythmogenic right ventricular cardiomyopathy (ARVC)

A
  • sotalol
  • catheter ablation to prevent ventricular tachycardia
  • implantable cardioverter-defibrillator
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32
Q

ECG change with severe hypothermia

A
  • J waves (Osborne waves)
  • atrial or ventricular arrhythmias
  • bradycardia
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33
Q

features of Brugada syndrome

A

autosomal dominant inheritance

  • more common in asian populations
  • around 30% have a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
  • sudden cardiac death
  • ECG changes
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34
Q

ECG changes of Brugada syndrome

A
  • ST elevation followed by a negative T wave in > 1 of V1-V3
  • right bundle branch block
  • ECG changes may be more apparent following the administration of flecainide or ajmaline (the investigation of choice in suspected cases of Brugada syndrome)
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35
Q

management of Brugada syndrome

A

implantable cardioverter-defibrillator

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36
Q

features of hypertrophic obstructive cardiomyopathy

A

autosomal dominant inheritance

  • common cause of sudden death (leading cause of sudden cardiac death in young athletes - Muamba)
  • echo findings include:

> mitral regurgitation (MR)

> asymmetric septal hypertrophy

> systolic anterior motion (SAM) of the anterior mitral valve

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37
Q

features of dilated cardiomyopathy

A

genetic predisposition, worsened by environmental factors

  • most common cardiomyopathy
  • classic findings of heart failure
  • systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
  • balloon appearance of the heart on the chest x-ray
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38
Q

causes of dilated cardiomyopathy

A

genetic predisposition combined with:

  • alcohol
  • IHD
  • coxsackie B virus
  • wet beri beri
  • doxorubicin

MOST COMMONLY it is idiopathic

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39
Q

features of restrictive cardiomyopathy

A

autosomal dominant

  • least common cardiomyopathy
  • rigid heart walls prevent efficient pumping of blood
  • may be asymptomatic
  • heart failure symptoms
40
Q

causes of restrictive cardiomyopathy

A

genetic predisposition combined with:

  • amyloidosis/sarcoidosis/haemochromatosis
  • post-radiotherapy
  • Loeffler’s endocarditis
41
Q

management of restrictive cardiomyopathy

A

treat symptoms of heart failure

42
Q

features of peripartum cardiomyopathy

A

develops between last month of pregnancy and 5 months post-partum

  • more common in

> older women

> greater parity

> multiple gestations

  • symptoms of heart failure
43
Q

features of Takotsubo cardiomyopathy

A
  • stress-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
  • transient, apical ballooning of the LV
  • treatment is supportive
44
Q

which artery and which leads - LAD

A

V1-V4 (anterior)

45
Q

which artery and which leads - right coronary

A

II, III, aVF (inferior)

46
Q

which artery and which leads - circumflex

A

I, V5-V6 (lateral)

47
Q

immediate management of acute coronary syndrome (STEMI/NSTEMI/unstable angina)

A

no longer MONA

  • morphine only in severe pain
  • nitrates
  • aspirin 300mg
  • ticagrelor (or clopidogrel)
  • unfractionated heparin (especially prior to PCI)
  • PCI if eligible ASAP
  • monitor O2 sats, only offer O2 to:

> those with sats <94% who are not at risk of hypercapnic resp failure (aim for 94-98%)

> those with COPD who are at risk of hypercapnic resp failure (aim for 88-92%) further management and secondary prevention once stable

48
Q

secondary prevention of ACS (STEMI/NSTEMI/unstable angina)

A
  • ACE inhibitor (indefinitely)
  • dual antiplatelet therapy (aspirin plus a second antiplatelet) for up to 12 months
  • beta-blocker (indefinitely if reduced left ventricular ejection fraction)
  • statin
49
Q

ECG findings of hypokalaemia

A
  • ST depression
  • prominent U wave
  • shallow T wave
  • prolonged PR
50
Q

ECG finding of hyperkalaemia

A
  • tall, tented T waves
  • loss of P wave
  • broad QRS complex
  • ST elevation
51
Q

ECG features of digoxin

A
  • down-sloping, ‘scooped out’ ST depression
  • flattened/inverted T waves
52
Q

ECG changes in PE

A
  • classic ECG changes seen in PE are:

(‘S1Q3T3’)

> large S wave in lead I

> large Q wave in lead III

> inverted T wave in lead III

  • only seen in 20% patients
  • also commonly:

> RBBB

> right axis deviation

53
Q

causes of RBBB

A
  • increasing age
  • right heart overload (ventricular hypertrophy/cor pulmonale/PE/atrial septal defect/RV strain)
  • myocardial infarction
  • cardiomyopathy or myocarditis
54
Q

causes of LBBB

A
  • ischaemic heart disease
  • hypertension
  • aortic stenosis
  • cardiomyopathy
    rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
55
Q

ECG features of multifocal atrial tachycardia

A
  • at least 3 different P wave morphologies
  • rate = 100-180bpm
  • irregular rhythm
56
Q

CHA2DS2VASc

A

C = CHF

H = hypertension

A = age

> 75+ = 2

> 65-74 = 1

D = diabetes

S = prior stroke or TIA (2 points)

V = vascular disease (eg. IHD/PAD)

S = sex (female = 1 point)

0 = no treatment (check transthoracic echo for valvular disease)

1 = consider anticoagulation in males, no treatment in females

>1 = offer anticoagulation

57
Q

HASBLED2

A

score to assess bleeding risk

H = hypertension (uncontrolled - sys >160)

A = abnormal:

> renal function = dialysis or creatinine > 200

> liver function = cirrhosis or bilirubin > 2x normal or ALT/AST/ALP > 3x normal

S = previous stroke

B = history of major bleed/tendency to bleed

L = labile/high INRs

E = elderly (>65 yrs)

D = drugs, drink

> medication predisposing to bleeding = 1 point

> drinks > 8 alcoholic drinks/week = 1 point

3+ points = high risk of bleed so anticoag should be avoided where possible

58
Q

true abdo aortic aneurysm (AAA)

A

involves all 3 layers of arterial wall

  • most common in elderly men
59
Q

false abdo aortic aneurysm (AAA)

A

only involves 1 layer of arterial wall

60
Q

indications for surgical management of AAA

A
  • symptomatic aneurysms (80% annual mortality if untreated)
  • increasing size above 5.5cm if asymptomatic
  • rupture (100% mortality without surgery)
61
Q

S3 heart sound (gallop)

A
  • caused by diastolic filling of the ventricle
  • considered normal if < 30 years old and athletes
  • heard in:

> left ventricular failure (e.g. dilated cardiomyopathy)

> constrictive pericarditis (called a pericardial knock)

> mitral regurgitation

62
Q

S4 heart sound

A
  • may be heard in:

> aortic stenosis

> HOCM

> hypertension

  • caused by atrial contraction against a stiff ventricle therefore coincides with the P wave on ECG
  • in HOCM a double apical impulse may be felt as a result of a palpable S4
63
Q

split S2 vs S3

A
  • S3 is a low-pitched sound (better heard with bell)
  • split S2 is high pitched (better with diaphragm)
  • S3 sound is heard best at the cardiac apex
  • split S2 is best heard at the left upper sternal border
64
Q

cause of waterhammer/collapsing pulse

A

aortic regurgitation

65
Q

indications for digoxin use

A
  • atrial fibrillation (rate control)
  • has use for symptom relief in heart failure
66
Q

effects of digoxin

A
  • reduced conduction through AV node, leads to reduced ventricular rate AF and AFlutter
  • increases strength of cardiac contaction (+ inotropic)
  • slows heart rate via vagus nerve stimulation
67
Q

features of digoxin toxicity

A

not defined by plasma concentration

  • arrhythmias (e.g. AV block, bradycardia)
  • generally unwell (lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision)
  • gynaecomastia
68
Q

causes of digoxin toxicity

A

narrow therapeutic range so digoxin toxicity more likely to occur in:

  • hypokalaemia (classically)
  • iatrogenic

> amiodarone

> verapamil

> diltiazem

> spironolactone

> PPI (increases digoxin effect, while antacids decrease effect)

  • elderly
  • renal failure
  • myocardial ischaemia
69
Q

management of digoxin toxicity

A
  • digibind
  • correct arrhythmias
  • monitor potassium
  • remove cause if poss (eg. medication)
70
Q

features of aortic dissection

A
  • chest pain: typically severe, radiates through to the back and ‘tearing’ in nature
  • aortic regurgitation
  • hypertension
  • other features may result from the involvement of specific arteries, eg. coronary arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischaemia
71
Q

management of aortic dissection

A

Type A (ascending aorta, 2/3rds cases)

  • BP control
  • surgical management

Type B (descending aorta)

  • beta blocker (IV labetalol)
  • bed rest
72
Q

complications of aortic dissection

A
  • cardiac tamponade
  • MI
  • renal failure
  • unequal arm pulses and BP
  • mediastinal bleed
73
Q

left anterior fascicular block

A
  • left axis deviation
  • qR complexes in lateral leads I and aVL
  • rS complexes in inferior leads II, III, aVF
  • QRS may be broad
74
Q

left posterior fascicular block

A
  • right axis deviation
  • qR complexes in inferior leads II, III, aVF
  • rS complexes in lateral leads I and aVL
  • QRS may be broad
75
Q

rate or rhythm control in AF

A

factors favouring rate control:

  • >65 years
  • history of ischaemic heart disease

factors favouring rhythm control:

  • <65 years
  • symptomatic
  • first presentation
  • lone AF or AF secondary to a corrected precipitant (e.g. alcohol)
  • congestive heart failure
76
Q

features of cardiac tamponade

A

life-threatening compression on heart (while pericardial effusion is less threatening)

Beck’s triad:

  • hypotension
  • raised JVP
  • muffled heart sounds

also can have:

  • dyspnoea
  • tachycardia
  • electrical alternans (differing QRS heights due to rocking of heart in pericardium)
77
Q

cardiac tamponade vs constrictive pericarditis

A
  • JVP

> tamonade = X only (TAMPaX)

> CP = X+Y (Coldplay X&Y)

  • pulsus paradoxus

> T = present

> CP = absent

  • Kussmaul’s sign (paradoxical rise in JVP on inspiration)

> T = rare

> CP = present

  • pericardial calcification on CXR

> T = absent

> CP = present

78
Q

management of cardiac tamponade

A
  • urgent pericardiocentesis
79
Q

features of acute pericarditis

A
  • chest pain: may be pleuritic, often relieved by sitting forwards
  • non-productive cough
  • dyspnoea/tachypnoea
  • tachycardia
  • pericardial rub
  • ECG changes
80
Q

ECG changes of acute pericarditis

A
  • changes in pericarditis are often global unlike by territories seen in ischaemic events
  • ‘saddle-shaped’ ST elevation
  • PR depression: most specific ECG marker for pericarditis anyone suspected of acute pericarditis should have an echocardiogram
81
Q

management of acute pericarditis

A
  • treat underlying cause
  • NSAIDs/colchicine for pain relief
  • supportive
  • corticosteroids if resistant and non-infective
  • reduce exercise for recurrent pericarditis, can add IVIg/azathioprine, then consider pericardiectomy if still unresponsive for pericardial effusion, pericardiocentesis may be required
82
Q

causes of cardiac tamponade

A
  • pericarditis
  • TB
  • iatrogenic (invasive procedure-related, post-cardiac surgery)
  • trauma
  • malignancy
  • connective tissue disease eg. SLE
83
Q

causes of pericarditis

A
  • viral infections (Coxsackie)
  • tuberculosis
  • uraemia (causes ‘fibrinous’ pericarditis)
  • trauma
  • post-myocardial infarction, Dressler’s syndrome
  • connective tissue disease
  • hypothyroidism
  • malignancy
84
Q

adverse effects of amiodarone

A

amiodarone is a class III antiarrhythmic

  • thyroid dysfunction
  • pulmonary fibrosis
  • liver fibrosis
  • photosensitivity
  • peripheral neuropathy
  • lengthened QT interval (proarrhythmic)
  • thrombophlebitis (so should be given at central veins ideally)
  • drug interactions (p450 inhibitor)
85
Q
A

VT

86
Q
A

V fib

87
Q
A

AF

88
Q
A

AFlutter

89
Q
A

Torsades de points

90
Q
A

STEMI anterolateral

91
Q
A

ischaemia

92
Q
A

bilateral PE

93
Q

consequences of long cQT interval

A

ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death

94
Q

drug causes of prolonged QT interval

A
  • amiodarone, sotalol
  • tricyclic antidepressants, SSRIs (especially citalopram)
  • methadone
  • erythromycin
  • haloperidol
  • ondanestron
95
Q

non-drug causes of prolonged QT interval

A
  • congenital
  • electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
  • myocardial infarction
  • myocarditis
96
Q

indications for surgery in infective endocarditis

A
  • haemodynamic instability
  • severe heart failure
  • severe sepsis despite antibiotics
  • valvular obstruction
  • infected prosthetic valve
  • persistent bacteraemia
  • repeated emboli
  • aortic root abscess

WFH (18 decks)

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