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MRCP > Clinical cardiology + vascular > Flashcards

Clinical cardiology + vascular Flashcards

1
Q

Inotropes

A

Increase cardiac contractility in order to increase cardiac output (CO) e.g. in cardiac arrest, cardiogenic shock.

Adrenaline
- beta-1 = increases contractility and HR
- 0.05mcg/kg/min.
- At higher doses alpha-1 activity predominates -> vasoconstriction -> end-organ ischaemia

Dobutamine
- in doses of 5- 10mcg/kg/min
- higher doses have more vasopressor effect

Isoprenaline

Milrinone
- Purely inotropic
- Phosphodiesterase inhibitor
- Does not cause tachycardia

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2
Q

Vasopressors

A

Induce vasoconstriction in order to increase PVR
- e.g. sepsis, hypovolaemia
- Increases the heart’s oxygen demand so risk of angina/ischaemia

Noradrenaline
- alpha-1 = vasoconstriction
- Can combine with dobutamine, milrinone etc.
- Risk of reflex bradycardia and peripheral ischaemia
- 0.05mcg/kg/min

Vasopressin
- VR1 = vasoconstriction.

Phenylephrine

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3
Q

Mean arterial pressure

A

Aim 65 mmHg

If older, more likely to have atherosclerosis and HTN with chronic adaptation so aim higher e.g. 75-85 mmHg

Too low = hypoperfusion
Too high = ischaemic injury

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4
Q

HFrEF - management

A

1st line
- Symptomatic
- Loop diuretic

  • Prognostic
    • ACEi/ARB
    • Aldosterone antagnist
    • SGLT2 inhibitor
  • Other
    • Lifestyle advice
    • Pneumococcal + influenza vaccines

2nd line with LVEF < 35%
- Switch to sacubitril/valsartan
- If QRS > 120ms, CRT-P/D
- If HR > 75 but sinus, ivabradine
- African-American, hydralazine

3rd line:
- LVAD
- Heart transplant
- Palliative support

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5
Q

Cardiac resynchronisation therapy (CRT)

A

Indications:
- Heart failure with broad QRS
- Evidence of dyssynchronous activity of the
ventricles
- May signify a level of BBB
- Dyssynchrony impairs the ventricular function

Technique:
- RA + RV + LV leads
- Paces almost all the time for maximum LV function
- Set at a higher than normal rate + patient beta-
blocked

CRT-P
- Biventricular pacemaker to synchronise the ventricles

CRT-D
- Biventricular pacemaker with added defibrillation activity

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6
Q

NYHA functional classification

A

Class I
- No limitation in physical activity
- No symptoms with ordinary physical activity

Class II
- Slight limitation in physical activity
- Symptomatic with ordinary physical activity
- Asymptomatic at rest

Class III
- Marked limitation in physical activity
- Asymptomatic at rest
- Symptomatic with less than ordinary physical activity

Class IV
- Symptomatic at rest
- Unable to complete personal care without severe symptoms

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7
Q

HFpEF - management

A

Control BP, heart rate, arrhythmias

Symptomatic support with loop diuretics

ACEi/ARB/ARNI
MRA
SGLT2 inhibitor

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8
Q

Pulsus alternans

A

When an arterial pulse alternates between strong and weak beats

L-sided = heart failure, AS, cardiomyopathy

R-sided = PE, pulmonary HTN

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9
Q

Acute heart failure aetiology

A

ACS
Hypertensive crisis
Arrhythmia
PE
Infection/inflammation
Tamponade

Mechanical
- Free wall rupture
- Acute MR
- Chest trauma
- Infective endocarditis
- Aortic dissection

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10
Q

Acute heart failure - the four presentations and management

A
  1. Acute decompensation/congestion
    - Onset over days
    - IV loop diuretics +/- metolozone
  2. Acute pulmonary oedema
    - IV loop diuretics
    - High-flow oxygen +/- CPAP
  3. Isolated RV failure
    - More gentle diuresis + I/O monitoring possible
  4. Cardiogenic shock
    - Inotropes
    - If not responding, consider vasopressors and acute RRT
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11
Q

HFrEF - causes

A

Defined as LVEF < 40%

MI
Dilated cardiomyopathy
Myocarditis
Valvular heart disease

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12
Q

HFpEF - causes

A

Clinical heart failures with LVEF > 40%

HTN
LVH
HOCM
Amyloidosis/sarcoidosis
Valvular heart disease

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13
Q

Hypertrophic cardiomyopathy - causes

A

HOCM
Friederich’s ataxia
Fabry disease

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14
Q

Dilated cardiomyopathy - causes

A

Alcohol
Myocardial damage e.g. post-MI or post-myocarditis
Pregnancy
Chagas disease
TB
Infiltrative disease e.g. amyloidosis
Thiamine deficiency
Genetic

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15
Q

Restrictive cardiomyopathy

A

Genetic
Amyloid
Sarcoid
Scleroderma
Hereditary haemochromatosis

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16
Q

Takotsubo cardiomyopathy

A

Stress-induced, ?SNS overdrive

ECG changes + trop rise with normal angiogram

Echo - apical hypokinesis
CT angio - no lesions

Mx - diuretics, ACEi, beta-blockers

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17
Q

Peripartum cardiomyopathy

A

Defined as new clinical heart failure occurring towards the ends of, or up to 5 months after, pregnancy.

Usually presents as reduced LVEF with no other cause found

Stable - vaginal delivery
Unstable - emergency C-section

Variable recovery, up to 70% within 6 months

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18
Q

Pacemarker-induced cardiomyopathy

A

Defined as a reduction in LVEF > 10% following PPM placement

Develops in 1/8 of people receiving a PPM for complete heart block with normal LVEF.

More common with isolated R-sided pacing due to dyssynchronous contraction

Mx - upgrade to CRT

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19
Q

Clubbing - aetiology

A

Lung:
- Cancer - esp. NSCLC, mesothelioma
- ILD
- Complicated TB
- Suppurative lung disease e.g. abscess, empyema, bronchiectasis, cystic fibrosis
- Sarcoidosis

Heart:
- Congenital cyanotic heart disease
- Subacute infective endocarditis
- Atrial myxoma

GI:
- Malabsorption
- IBD
- Cirrhosis incl. PBC

Other:
- Grave’s disease

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20
Q

Aortic stenosis - causes and presentation

A

Occurs in 2% of over-65s

Causes
- Age-related calcification
- Rheumatic fever
- Paget’s disease of the bone
- Bicuspid aortic valve (1-2% of live births)

Signs:
- Slow-rising pulse
- Narrow pulse pressure
- Ejection systolic murmur with radiation
- +/- clinical heart failure

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21
Q

Aortic stenosis - management

A

Medical
- Beta-blockers
- Diuresis

Surgical
- TAVI
- Surgical valve replacement

Uses metallic valve if age < 65 or biologic if > 65
- Metallic valves must be anticoagulated with warfarin but have a longer life-time

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22
Q

Aortic stenosis surgical criteria

A

Symptomatic low-flow AS

Asymptomatic severe
- Vmax (peak aortic jet velocity) more than 5 m/s
- Aortic valve area less than 0.6 cm2
- LVEF (left ventricular ejection fraction) less than 60% y
- BNP/NT-proBNP level more than twice the upper limit of normal
- symptoms unmasked on exercise testing.

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23
Q

Mitral regurgitation - causes and presentation

A

Causes:
- Acute - MI, trauma, endocarditis
- Chronic - age-related, rheumatic fever

Signs:
- Irregularly irregular pulse
- Systolic thrill at apex
- Pansystolic murmur with radiation to axilla

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24
Q

Mitral regurgitation - management

A

Medical - anticoagulation if concurrent AF

Surgical = valve repair
- LVEF < 60%
- ESDI more than 2.2 cm/m2
- Increase of systolic pulmonary artery pressure to more than 60 mgHg on exercise testing

33% survival at 8 years without surgery

Death usually due to heart failure but can be sudden secondary to arrhythmia

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25
Q

Infective endocarditis - causes

A

Native valve
- Staph. aureus
- viridans Strep. - post-dental
- Enterococcal
(HACEK, Strep. bovis)

Prosthetic valve
- Staph. epidermidis
- Staph. aureus
- viridans Strep.
(Pseudomonas, HACEK, fungal)

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26
Q

Duke’s criteria

A

Major
- Positive blood cultures - at least 2 taken more than 12hr apart
- Imaging evidence on TOE

Minor
- Predisposing condition
- Fevers > 38
- Embolic phenomena e.g. Janeway lesions, septic emboli
- Immunological phenomena e.g. Osler’s nodes, Roth spots
- Microbiological findings

Definitive diagnosis requires:
2 major
1 major + 3 minor
5 minor

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27
Q

Infective endocarditis - management

A

Native valve:
- Min 2-6 weeks of therapy
e.g. vancomycin + gentamicin

Prosthetic valve:
- May require lifelong suppressive therapy
e.g. vancomycin + gentamicin + rifampicin

Surgery
- High mortality and morbidity
- May be required if there is acute severe valve dysfunction or aortic root abscess

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28
Q

Postural hypotension - causes

A

Neurogenic
- T2DM
- Parkinson’s
- SCLC
- MGUS

Cardiac
- Arrhythmias
- Aortic stenosis

Endocrine
- Dehydration
- Adrenal insufficiency

Medications:
- Diuretics - esp. thiazides
- Alpha-blockers
- Antihypertensives
- Insulin
- Levodopa

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29
Q

Postural hypotension - diagnosis and management

A

Diagnosis:
- SBP drop by 20 mmHg
- SBP drop to <90 mmHg
- DBP drop by 10 mmHg with symptoms

Management:
- Fludrocortisone - MRA
- Midodrine - alpha-1 agonist

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30
Q

Aortic root dilatation

A

A form of juxta-cardiac AAA which can cause aortic regurgitation and can acutely dissect

Aetiology:
- Age-related
- CTDs e.g. Marfans, vasculitis
- HTN

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31
Q

S1 abnormalities

A

Quiet = low CO
- Reduced LV function
- Rheumatic MR
- Long PR interval (1st degree HB)

Loud = high CO
- Large stroke volume
- Mitral stenosis
- Short PR interval

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32
Q

S2 abnormalities

A

Physiological splitting
- AV closes slightly before PV because left contracts before right
- Increases with inspiration, decreases with expiration

Wide splitting
- Delayed RV emptying e.g. RBBB, pulmonary HTN

Reverse splitting
- Delayed LV emptying e.g. LBBB, LV outflow obstruction

Quiet S2
- Aortic stenosis

Loud S2
- Systemic or pulmonary HTN

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33
Q

S3

A

Occurs just after S2
‘Lub-dub-ta’

Normal if pregnant, febrile, <30 y.o.
Otherwise HF, MR.

When combined with tachycardia is called a gallop rhythm

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34
Q

S4

A

The sound of blood being forced into a stiff non-compliant ventricle

Just before S1

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35
Q

ECG parameters

A

Rate
- R waves x 6
- 300 / no. large squares in R-R interval

Rhythm

Axis
- aVF and I
- normal = both positive
- left = I +ve, aVF -ve
- right = I -ve, aVF +ve

Morphology
- QRS < 120ms aka 3 small
- PR 120-220ms aka 3-5 small
- QT < 450ms

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36
Q

Prolonged PR interval

A

aka 1st degree heart block

PR > 5 sq or 200ms

AVN fibrosis
Medication e.g. digoxin, amiodarone, CCBs
Hypo or hyperkalaemia

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37
Q

Bundle-branch and fascicular blocks

A

LBBB
- Always pathological e.g. posterior STEMI
- WiLLiaM
- May have TWI in lateral leads

RBBB
- May be benign
- MaRRoW

Bifascicular block
- RBBB + axis deviation (usually LAD)
- LAD = L anterior fascicle
- RAD = L posterior fascicle

((((Trifascicular block
- RBBB + axis deviation + 1st degree heart block - OLD, TRUE WOULD BE COMPLETE HEART BLOCK))))

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38
Q

Posterior STEMI ECG

A

Usually occurs alongside inferior ± lateral infarction

Obstruction of LCX is most common

ST depression V1-V4
Dominant R in V1-V2
ST elevation in V7-V9
New LBBB

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39
Q

Anterior STEMI ECG

A

Poorest prognosis

Obstruction of LAD

ST elevation V1-V4
ST depression II, aVF
Preceding hyperacute T waves

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40
Q

Inferior STEMI ECG

A

Obstruction of RCA (80%) or LCX (20%) depending on dominance

ST elevation II, III, aVF
ST depression aVL
Preceding hyperacute T waves
Later develop deep Q waves

Supplies nodal arteries so risk of new significant heart block

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41
Q

Lateral STEMI ECG

A

Usually occurs in conjunction with anterior infarction due to involvement of the main LAD

Obstruction of small branches of LAD or LCX

ST elevation V5-V6, I, aVL
ST depression II, aVF

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42
Q

Occlusion myocardial infarction (OMI)

A

Defined as ECG patterns which do not fully meet the criteria for STEMI but nevertheless suggest coronary occlusion requiring urgent PCI

  • Elevation in 2 contiguous inferior leads + depression in aVL
  • New RBBB + LAFB
  • T waves out of proportion to R waves
  • ST depression maximal in V1-V4 with progression to V5-V6
  • Multilead ST depression + ST elevation in aVR
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43
Q

Spontaneous coronary artery dissection (SCAD)

A

A rare cause of MI most commonly presenting in young healthy women

Causes:
- Connective tissue disorders
- Hormonal changes associated with pregnancy
- No association with atherosclerosis or trauma

Presentation very similar to NSTEMI/STEMI
- Chest pain
- Elevated troponin
- ST changes

Coronary angiogram is key for investigation and treatment

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44
Q

T wave morphologies

A

Normal:
- Mostly upright
- Possible TWI in aVR and V1
- Amplitude <5mm in limb, <10mm in precordial

Peaked
- Tall, narrow, symmetrical peaked

Hyperacute
- Broad
- Asymmetrically peaked

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45
Q

T wave inversion (TWI)

A

Can be normal to have TWI in I and aVR.

More widespread TWI is normal in childhood due to right-sided predominance

Other causes:
- BBB - left = I/aVL/V5-6, right = V1-V3
- Hypertrophy
- HTN
- Heart strain/PE
- Ischaemia/infarction - dynamic during, fixed afterwards
- HOCM

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46
Q

Biphasic T waves

A

In which the T wave has two phases, one going up and the other down
- MI = up - down
- Hypokalaemia = down - up

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47
Q

Wellen syndrome

A

A pattern of inverted or biphasic T waves in V2-3 which, when accompanied with chest pain, is high suggestive of critical stenosis of the LAD

Type 1 (25%)
- Biphasic T wave - up then down

Type 2 (75%)
- Deep, symmetrical TWI

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48
Q

Wolff-Parkinson-White synrome

A

Presence of an accessory conducting pathway (the Bundle of Kent) which allows some electricity to bypass the AVN
- Short PR interval
- Delta wave

Causes two types of SVT
- Orthodromic
- Narrow QRS
- Treat as SVT
- Antidromic
- Delta wave + broad QRS
- Treat with procainamide, cardioversion.

Management:
- Medical
- e.g. flecainide, sotalol, amiodarone
- Pathway ablation
- If symptomatic, FHx of sudden death, or high-
risk professions

49
Q

Palpitations

A

An increased awareness of the heartbeat - usually because it is strong, fast, or irregular

Causes
- Substances - caffeine, alcohol, tobacco, salbutamol
- Ectopic beats
- Narrow complex tachycardia
- Panic attack
- Thyrotoxicosis

High-risk features:
- Previous MI
- Previous cardiac surgery
- Associated syncope or cardiac chest pain
- FHx of sudden death

50
Q

Premature ventricular complexes (PVCs)

A

Ventricular ectopics which are significant because they can lead to VT/VF by setting up circuits
- Associated with sudden cardiac death post-MI
- More = worse prognosis
- In healthy patients can be substance-induced (e.g. caffeine), thyrotoxicosis, iatrogenic (e.g. digoxin)

Treatment:
- Correct electrolytes - K+ > 4.0, Mg > 1.0
- Improve respiratory state
- Avoid triggers

51
Q

Antiarrhythmics (Vaughan-Williams classification)

A

Class I
- Block fast sodium channels which cause phase 0 (aka rapid depolarisation)
- Slows upstroke, no effect on duration/refractoriness
- IA and IC bind both activated and inactivated states so are useful during tachyarrhythmia
- IB bind during the inactivated state and are most useful when there is myocardial ischaemia
- IA = procainamide, IB = lidocaine, IC = flecainide.

Class II
- Beta-blockers - esp. action at beta-1-adrenoceptors
- Beta-1 = increased SAN firing, increased
conduction velocity
- e.g. atenolol, bisoprolol etc.

Class III
- Mechanism variable but lead to prolongation of the cardiac action potential, mainly by inhibition of repolarizing K+ currents and increasing QTc
- Esp. potent in suppressing arrhythmias caused by reentrant signs
- e.g. amiodarone, sotalol

Class IV
- Calcium channel blockers
- Suppress ectopic pacemaker action, decrease conduction velocity, prolong repolarisation at the AVN
- e.g. diltiazem, verapamil

Class V
- Increase vagal tone at SAN/AVN
- e.g. digoxin

52
Q

Pacemakers - implantation

A

Technique:
- Implanted in subclavian region on opposite side to dominant hand
- Done under local anaesthetic
- Up to three leads - right atrial, right ventricular, left ventricular

Complications:
- Site infection
- Pneumothorax - if leads placed via subclavian vein

53
Q

Dual chamber pacing

A

Right atrial + right ventricular leads
- On-demand pacing

Lead selection:
- Atrial fibrillation = RV only
- Paroxysmal AF = RA + RV
- Young sick sinus = RA only. Older = RA + RV

Pacing cycle:
- Intrinsic P wave sensed in RA = A SENSED
- If no ventricular contraction in a given time, ventricle is paced = V PACED
- After this there is no atrial activity so the atria are paced = A PACED
- If ventricular activity is sensed, the RV leads are inhibited = V SENSED

54
Q

Implantable cardioverter defibrillator (ICD)

A

Indications
- Primary prevention - high risk of severe ventricular arrhythmia
- Inherited e.g. HOCM, Brugada, long QT
- Prev. surgical repair of congenital heart
disease
- Previous MI with LVEF < 35% and symptomatic
heart failure
- Secondary prevention - known severe ventricular arrhythmia without treatable cause
- Spontaneous sustained VT with syncope or
instability
- Spontaneous sustained VT with LVEF < 35%
and NHYA III symptoms or better

Technique:
- Similar implantation to PPM
- Ventricular leads contain additional defibrillation coil

55
Q

Brugada syndrome

A

Aetiology:
- Autosomal dominant channelopathy
- 25% have FHx
- Usually mutation of SCN5 which encodes cardiac voltage-gated sodium channels

Presentation:
- Asymptomatic
- Syncope
- VT/VF
- Sudden death

ECG when in arrhythmia:
- Type 1
- coved ST elevation >2mm in more than one of
V1-V3, followed by TWI.
- Type 2
- Saddle ST elevation >2mm V1-V3
- Type 3
- Either of the above but ST elevation < 2mm

Increased risk of arrhythmia with alcohol, fever, periods of high vagal tone like sleep, rest, or after a meal

Definitive management = ICD

56
Q

HOCM - ECG

A

LVH with giant QRS in lateral leads and deep dagger Q waves
± arrythymias e.g. AF, SVT, VT, VF

57
Q

HOCM - echo

A

Mnemonic - MR SAM ASH

Mitral regurgitation (MR)
Systolic anterior motion (SAM) of the anterior mitral valve leaflet
Asymmetric hypertrophy (ASH)

Evidence of LVOTO - left ventricular outflow tract obstruction
- Septal hypertrophy + narrowing of LVOT causes abberrant blood flow which displaces mitral valve leaflets anteriorly.
- Mitral valve also anatomically more susceptible to this displacement
- Loss of leaflet coaptation -> LVOTO, MR

LVOTO may need to be elicited e.g. Valsalva, exercise, strain.

58
Q

HOCM - clinical

A

Aetiology:
- Unexplained LVH
- 1/500 people
- Often FHx but not always
- 40% due to mutations in beta-myosin heavy
chain

Signs:
- Either ESM (due to LVOTO) or pansystolic (MR)

Investigations:
- Ambulatory ECG
- ECHO - gold-standard
- cMRI if echo suboptimal
- add late gadolinium enhancement (LGE) to
detect secondary myocardial fibrosis
- Genetic testing

Management:
- General:
- Mild-to-moderate exercise
- Pregnancy safe if condition is stable
- Lifestyle changes
- Obstructive symptoms:
- 1st line - beta-blockers
- 2nd line - add diltiazem
- 3rd line - surgical e.g. septal ablation,
myomectomy
- ICD
- Known to have had ventricular arrhythmias
- FHx of sudden death
- Episodes of syncope
- Massive LVH
- LVEF < 50%
- Children with runs of SVT
- End-stage:
- Consider heart transplant if having ventricular
arrhythmias or NYHA III+ symptoms
- LVAD if unavailable
- CRT if develop LBBB

59
Q

Atrial fibrillation - types

A

First detected episode

Paroxysmal AF
- At least 2 recurrent self-terminating episodes lasting < 7 days

Persistent AF
- AF which is not self-terminating and has persisted for > 7 days

Permanent AF
- AF which cannot be cardioverted

60
Q

Atrial fibrillation - investigation and management

A

Investigations:
- Ambulatory ECG
- TTE - AF + valve pathology is absolute indication for anticoagulation

Rhythm control
- If first episode, co-existent HF, reversible cause
- Electrical cardioversion - synchronised
- Must either have been in AF for < 48h,
anticoagulated for 21-28 days, or no evidence
of clot on TOE
- Will need to stay on anticoagulation for at least
28 days afterwards
- Chemical cardioversion
- Flecainide - no structural disease, pill in pocket
if well with AF and no CKD (dose = 200mg)
- Amiodarone - if IP, more unwell, structural
disease
(- AF ablation)

Rate control
- Beta-blocker e.g. bisoprolol
- Rate-limited CCB e.g. diltiazem, verapamil
- Combination therapy - 2/3rds dose of BB +
CCB/digoxin
- Digoxin used mainly if limited exercise and unable
to tolerate other medications

61
Q

Digoxin ECGs

A

Digoxin effect
- normal when taking digoxin
- ‘Reverse tick’ - downsloping ST depression
- Flattened, inverted, or biphasic T waves
- Short QT

Digoxin toxicity
- Frequent PVCs e.g. bigeminy, trigeminy
- Sinus bradycardia
- Slow AF
- AV block
- VT

62
Q

Digoxin toxicity

A

Precipitants:
- Overdose
- Renal failure
- Concurrent infection
- Hypokalaemia

Features:
- GI - nausea/vomiting, anorexia, diarrhoea
- Visual - blurred vision, yellow/green, haloes
- CVS - palpitations, pre-/syncope, SOB
- CNS - confusion, fatigue, delirium

ECG - can be a number of arrhythmias
- Frequent PVCs e.g. bigeminy, trigeminy
- Sinus bradycardia
- Slow AF
- AV block
- VT

Diagnosis = digoxin levels

Management = Digibind, correct electrolytes

63
Q

Tachyarrhythmia - emergency management

A

Unstable features? e.g. syncope, hypotension, MI, heart failure, shock
- DCCV

Narrow complex regular
- Likely AVNRT or AVRT e.g. SVT
- 1st line - vagal manoeuvres
- 2nd line - IV adenosine 6mg - 12mg - 18mg or
verapamil if asthmatic
- 3rd line - cardioversion

Narrow complex irregular
- Most likely fast AF

Broad complex regular
- Likely VT unless known BBB
- Loading amiodarone (300mg IV over 30 mins)
then maintenance infusion (900mg over 24h)
- oral loading (10-15g total needed to load, 200mg
TDS for 7 days then BD for 7 then OD as long as
needed)
- NB avoid amiodarone if known long QT

Broad complex irregular
- Seek expert advice
- Most commonly AF + BBB but possibility of
torsades de pointes
- Do not give amiodarone until confirmed

64
Q

VT - ECG appearance

A

Monomorphic
- Uniform complexes
- Originates from a single complex in the ventricles

Polymorphic
- Complexes of variable amplitude
- Sign of more unstable electrical activity

65
Q

VT - classification of duration

A

Salvo
- 3-5 beats

Non-sustained
- VT lasting more than 6 beats but less than 30s

Sustained
- VT lasting >30s or with haemodynamic instability

66
Q

Atrial fibrillation with rapid ventricular response (RVR)

A

aka fast AF

Triggers - PIRATES
Pulmonary embolism
Ischaemia
Respiratory disease
Atrial enlargement or myxoma
Thyrotoxicosis
Ethanol
Sepsis/sleep apnea

Unstable - cardioversion

Stable
- Optimise electrolytes
- K+ > 4.0, Mg = 1.0
- Rate control
- Beta-blockers
- Digoxin loading
- Oral - 500mcg, then after 6hr 500mcg,
maintenance at 125mcg
- IV - 500-1000mcg split over 2 doses and 6hr
- Rhythm control
- Consider anticoagulation

67
Q

Tachy-brady syndrome

A

Alternating bradycardia and paroxysmal tachycardia
- Usually supraventricular
- After tachy may have delayed sinus recovery
causing a sinus pause or exit block
- If prolonged can cause syncope

Causes
- Idiopathic fibrosis (most common, sick sinus syndrome)
- Ischaemia
- Infiltration
- Cardiomyopathy
- Congenital
- Autonomic dysfunction
- Hypothyroidism
- Hyperkalaemia
- Medications e.g. digoxin, BB, CCBs

Management
- Treat reversible causes
- PPM insertion

68
Q

Heart block

A

Most commonly due to age-related fibrosis but can be secondary to many cardiac conditions e.g. ischaemia, infiltration, SLE, lyme disease

Types:
- 1st degree
- PR > 200ms
- 2nd degree
- Type I
- Progressive PR lengthening until dropped
complex
- Usually due to reversible conduction block
at the level of the AV node - increased
fatiguability
- Type II
- Intermittent dropped beats
- Due to failure of the Purkinje fibres, often
irreversible damage
- 3rd degree/complete
- Dissociation between P and QRS

Management:
- Unstable
- Atropine 500mcg IV - up to 3mg total
- Transcutaneous pacing
- Aim for transvenous pacing + PPM insertion as
soon as possible
- Stable
- 1st degree/2nd degree type 1
- nothing if asymptomatic, else atropine
- 2nd degree type 2 + complete
- Monitoring, temporary pacing, aim for PPM

69
Q

CHA2DS2-VASc

A

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

70
Q

Orbit score

A

Replacement for HAS-BLED

  • Haemoglobin (males < 130, female < 120) or haematocrit (males < 4-0%, female < 36%) = (2)
  • Age > 74 = (1)
  • Bleeding hx (GI, intracranial, stroke) = (2)
  • Renal impairment (eGFR < 60) = (1)
  • Treatment with antiplatelets = (1)

Low risk - 0-2
Medium risk - 3
High risk - 4-7

71
Q

Chest pain - causes

A

Cardiovascular
- ACS and angina
- Myo/pericarditis
- Aortic dissection

Respiratory
- Pneumothorax
- Pulmonary embolism
- Pneumonia

Gastrointestinal
- Oesophageal spasm
- GORD
- Peptic ulcer
- Pancreatitis

Other
- MSK
- Radiculopathy
- Anxiety
- Shingles

72
Q

Myocarditis

A

Myocarditis is an inflammatory cardiac disorder which can lead to acute heart failure
- Fulminant = hours-to-days
- Non-fulminant = days-to-weeks

Causes:
- Viral - coxsackie B, adenoviruses
- Eosinophilic - Chagas, parasites hypersensitivity
- Granulomatous - TB, sarcoid
- Drug-induced - vaccines, chemo, ETOH

Features:
- Sharp stabbing chest pain
- Fever
- New heart failure - SOB, orthopnea, dizziness
- Palpitations
- Recent infectious prodrome - coryza, diarrhoea

Investigations:
- Bloods incl. viral serology, serial trops
- Imaging e.g. cMRI
- Myocardial biopsy is gold-standard

Management:
- Symptomatic relief from acute heart failure
- Colchicine for pain, up to 2-3 months after resolution

73
Q

Long QTc

A

QTc = An estimate of QT at a standardised heart rate of 60bpm

Long if :
Men > 440ms
Women > 460ms

Aetiology:
- Hypokalaemia
- Hypomagnesaemia
- Hypocalacaemia
- Hypothermia
- Raised ICP
- Medications
- Ischaemia
- Congenital

74
Q

T wave alternans

A

Beat-to-beat variation in T wave amplitude or polarity

Associated with long QT

Often secondary to ischaemia, increases risk of re-entrant arrhythmias

75
Q

Aortic dissection

A

Classification:
- Type A
- 2/3
- ascending aorta
- Type B
- 1/3
- descending aorta

Aetiology:
- HTN
- Trauma
- CTDs
- Bicuspid aortic valve, Turner’s, Noonan’s syndrome

Features:
- Severe, ‘tearing’ pain radiating to back
- > 20mmHg discrepancy in BP
- New AR
- Angina, paraplegia, limb ischaemia

Imaging:
- CT angiograhpy - look for false lumen
- TOE - in unstable patients

Management:
- Type A - surgical repair
- Type B - strict BP control (SBP 100-120)

76
Q

Abnormal JVP x 9

A

Heart failure: elevated

PE: elevated

Pericardial effusion: elevated, prominent y descent

Pericardial constriction: elevated w kussmauls sign (inc on insp)

SVCO: elevated w loss o pulsation

Afib: absent a waves

Tricuspid stenosis: giant a waves

Tricuspid regurg: giant V waves

Complete heart block: cannon waves

77
Q

Ventricular septal defects (VSDs)

A

Most common congenital abnormality in children and second most common in adults

Predominantly create pathology through formation of a shunt, with risk of Eisenmenger syndrome

Features:
- Pansystolic murmur
- Heard best at L sternal edge
- CHF
- Fluid overload, raised JVP etc.
- Eisenmenger
- Cyanosis
- Syncope
- Dyspnea
- Clubbing

Management:
- Small = observation
- Isolated medium/large = percutaneous closure
- Large, complex or haemodynamic compromise = surgical closure

78
Q

Right heart catheterisation

A

Insertion of Swan-Ganz catheter into the right side of the heart via a large peripheral vein

RA
< 5 mmHg

RV
- 15-30 / 3-8

Pulmonary artery
- Systolic = RV
- 15-25 / 4-12

PCWP
- Indirect estimate of LA pressure
- Helps to quantify LVF and mitral stenosis
- < 12mmHg

LV
- 100-140 / 3-12

Combination of PA + PCWP, via thermodilution technique, is used to measure pulmonary vascular resistance and therefore diagnose pulmonary HTN

79
Q

AF ablation

A

Indications:
- AF which has failed first-line medical treatment

Must take anticoagulation for 4-6 weeks prior
- Do not stop prior to the procedure

Stop beta-blockers, CCBs, and antihypertensives pre-procedure

Perform wide circumferential ablation around the pulmonary veins

80
Q

Secondary prevention of MI

A

Non-pharmacological:
- Stop smoking
- Weight loss

Pharmacological:
- ACEI (NNT = 22)
- Statin (NNT = 33)
- Aspirin (NNT = 42)
- Beta-blocker (NNT = 143)

81
Q

Pericarditis

A

Inflammation of the pericardium
- Can lead to involvement of the epicardium - ECG changes - or effusion - risk of tamponade

Causes:
- Infection (oft. viral)
- Uraemia
- Autoimmune
- Malignancy (esp. lung)

Features:
- Sharp stabbing central chest pain
- Better leaning forwards
- Worse coughing, lying back, moving
- May radiate to neck and arm
- Pericardial rub
- SOB

Investigations:
- ECG - saddle-shaped ST elevation
- Raised troponin
- Echo - diagnostic

Management:
- Treat underlying cause
- NSAIDS, colchicine

Complications:
- Myocarditis
- Tamponade

82
Q

Cardiac tamponade

A

Features:
- Beck’s triad:
- Hypotension
- Raised JVP
- Muffled heart sounds
- Tachycardia
- Pulsus paradoxus
- SOB with normal lung fields

Investigations:
- CXR = large globular heart
- Echo = diagnostic

Management:
- Emergency pericardiocentesis

83
Q

Constrictive pericarditis

A

Chronic inflammation leads the pericardium to become dense and fibrous

Aetiology:
- TB
- Trauma
- Purulent pericarditis

Features:
- Peripheral oedema
- Dyspnea
- Ascites
- Hepatomegaly

Investigations:
- CXR - normal sized heart
- Echo - restricted mitral filling, pericardial thickening

Management:
- Surgical excision

84
Q

Stable angina

A

Aetiology:
- Coronary atherosclerosis
- Tachycardia
- Anaemia
- Aortic stenosis
- LVH
- Coronary artery spasm

Features:
- Cardiac chest pain occurring on exertion
- Relieved with GTN
- Also fatigue, nausea, belching

Classification of severity:
- Class I - only with prolonged strenuous activity
- Class II - on climbing stairs or walking into wind
- Class III - on climbing 1 flight of stairs or going 50-100m on the flat
- Class IV - on any physical activity

Investigations:
- Stress testing - with ECG, echo, etc.
- Coronary angiography

Management:
- Lifestyle advice + secondary prevention meds
- Medical:
- GTN for breakthrough
- CCBs e.g. diltiazem, verapamil or beta-
blocker
- Consider ivabradine, nicorandil etc.
- If not managed with 4 agents, PCI/CABG

85
Q

Lown-Ganong-Levine syndrome (LGL)

A

Presence of an accessory pathway connecting the atria to the bundle of His, leading to bypass of the AVN
- vs WPW where it connects to the ventricular
myocardium

ECG - short PR, no delta waves

Management:
- Beta-blockers
- Pathway ablation

86
Q

Cardiac enzymes

A

Myoglobin:
- Released within 1hr of myocardial cell damage, elevated for 1-2 days afterwards

Troponins:
- Released within 4-6 hours of myocardial cell damage and remain elevated for up to 2 weeks
- TnI and Tnt are most sensitive

Creatinine kinase:
- Released c. 24h after myocardial cell damage and remain elevated for 3-4 days

87
Q

Thrombolysis contraindications

A

Relative:
- Prolonged traumatic CPR
- Recent surgery
- Bleeding disorders
- Pregnancy
- On anticoagulation and/or INR > 1.8

Absolute:
- BP > 180/110
- Head trauma within 2/52
- Known intracranial malignancy
- Active bleeding
- Stroke < 2/12 ago
- Suspected aortic dissection

88
Q

HTN - pharmaceuticals

A

ACEi
- Decrease circulating ATII -> decreased aldosterone -> decreased Na+ reabsorption
- Also increase bradykinin levels
- Dry cough
- Angioedema

ARBs:
- Blockade of AR2
- Useful in those who don’t tolerate ACEi

Thiazides:
- Inhibit the Na/Cl symporter in the DCT -> decreased Na+ reabsorption
- Takes 12 weeks to come into effect
- Early reduction in blood volume
- Slower vasodilation

CCBs:
- Predominantly blockade of L-type voltage-gated calcium channels
- Affects vascular tone + heart contractility
- Only amlodipine can be used in CHF patients

89
Q

Misc pharmaceuticals

A

Ivabradine
- Inhibition of If within the SAN - hyperpolarization-activated cyclic-nucleotide gated K+ channel

Hydralazine
- Direct-acting smooth muscle relaxant working primarily in resistance arterioles
- Inhibits inositol triphosphate-induced Ca2+
release from the sarcoplasmic reticulum

Nicorandil
- Nitrate + activates ATP-sensitive K+ channels -> induces hyperpolarization

Clopidogrel:
- Inhibitor of a P2YR, inhbiting ADP-mediated platelet aggregation
- Prodrug requiring activation by CYP2C19 which is active in only 2/3rds the population

90
Q

Coronary artery vasospasm (CAVS)

A

Presents on a spectrum from stable angina to ACS with potential to cause ischaemia

Most likely to occur at night due to increased activity of the PNS although SNS is also implicated in it’s pathophysiology

Investigations:
- Coronary angiography with provocative testing
- Need ECG changes, >50% luminal narrowing,
and symptoms

91
Q

Driving + PPMs

A

Pacemaker:
- Cannot drive car for 1 week
- Cannot drive group 2 vehicles for 6 weeks

ICD
- Car
- Primary prevention = 1 month
- Secondary prevention = 6 months
- Cannot drive for 6 months after any shock
- Cannot drive group 2

92
Q

Driving + ACS

A

Group 1
- Cannot drive for 1 week if had successful angioplasty
- Cannot drive for 4 weeks if either angioplasty was unsuccessful or didn’t happen.

Group 2
- Cannot drive for 6 weeks

93
Q

Types of myocardial infarction

A

Type 1 - coronary artery-based

Type 2 - increased demand/reduced supply states with normal coronaries

Type 3 - sudden cardiac death from MI

Type 4 - due to PCI or stent thrombosis

Type 5 - due to cardiac surgery

94
Q

Type 2 MI

A

Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply
- e.g. vasospasm, hypovolaemia, sepsis, PE

Diagnosis:
- Elevated by changing troponin
- Clinical features inconsistent with type 1 MI
- Clinical conditions known to increase oxygen demand and/or decrease supply

Management:
- Treat underlying insult
- Screen for coronary artery lesions

95
Q

Post-CABG complications (10)

A

Specific:
- Atrial fibrillation
- Pulmonary HTN
- Pericardial effusion
- Pleural effusion (40%)
- Stroke
- Renal injury
- Haemodynamic instability

General:
- Sternal wound infections
- Graft failure
- Pneumonia
- VTE phenomena

96
Q

Congenital heart disease - radiological findings

A

L-> R shunt
- Enlarged heart
- Prominant pulmonary vasculature
- Fluid in lung fields

Aortic stenosis
- Prominent LV
- Aortic dilatation

Pulmonary stenosis
- Post-stenotic pulmonary artery dilatation

Coarctation of the aorta
- Prominent LV
- Rib notching

Tetralogy of Fallot
- Boot-shaped heart - apex above L hemidraphram + concave L heart border
- Small pulmonary arteries
- Oligaemic lung fields

Transposition of the Great Arteries
- Egg-on-side appearance

Total anomalous pulmonary venous drainage
- Small heart
- Pulmonary congestion - can be white-out

Ebstein’s anomaly
- Massively enlarged heart
- Pulmonary oligaemia

97
Q

Heart disease in congenital conditions

A

Friedrich ataxia - HOCM

Marfans - aortic dissection/aneurysm/regurg

Glycogen storage disease - type 2 cardiomyopathy

Noonan’s - pulmonary stenosis

William’s - supravalvular aortic stenosis, pulm sten

Romano-ward syndrome - long QT

Tuberous sclerosis - rhabdomyoma

Turners - bicuspid aortic valve

98
Q

Teratogens affecting the heart

A

Alcohol - ASD, TOF

Rubella - PDA, coarctation, TOF

Phenytoin - pulm stenosis

Lithium - ebstein anomaly

99
Q

Heart transplantation - rejection

A

Fever
Prolonging PR interval + reducing QRS voltages
Increasing heart size on CXR

100
Q

Acute mesenteric ischaemia

A

Aetiology:
- Embolic (50%)
- Arrhythmia
- Valve pathology
- Post-MI mural thrombus
- Aortic aneurysm
- Thrombotic (25%)
- Atherosclerosis
- Shock (20%)
- Mesenteric venous thrombosis (<10%)
- Dissection
- Vasculitis

Investigations:
- Blood gas
- Routine bloods
- CT angiography

Management:
- Urgent surgery
- Angioplasty/embolectomy
- Bowel resection if necrotic
- Usually requires relook laparotomy in 24-48hr

101
Q

Carotid artery stenosis

A

Plaque mostly found at the bifurcation of the CCA or within the proximal ICA

Can present with TIA/amaurosis fugax but then rapidly progresses to full stroke

Investigation:
- Duplex USS

Management:
- Lifestyle modification
- Medications e.g. statin, clopidogrel
- Surgery:
- If >50% stenosis on one side with sx or >70%
and asymptomatic
- Balance risk of future stroke with risk of stroke
due to intervention

102
Q

Leriche syndrome

A

aka aortoilliac occlusive disease

Due to severe atherosclerosis of the distal aorta or proximal common iliac

Classic triad:
- Thigh/buttock claudication
- Absent femoral pulses
- Male impotence

103
Q

ABPI

A

Used in the investigation of potential peripheral vascular disease

> 1.3 = arterial calcification

0.9 - 1.3 = normal

0.6 - 0.9 = mild PVD

0.3 - 0.6 = moderate-severe PVD

< 0. 3 = severe to critical PVD

104
Q

Peripheral vascular disease

A

Most commonly due to atherosclerosis of the peripheral arteries, with acute presentations due to thrombus formation

Intermittent claudication:
- Leg pain on exertion which is relieved by rest
- Investigations = ABPI
- Management:
- Lifestyle modification
- Supervised exercise training
- Statins, clopidogrel
- Revascularisation procedures

Critical (chronic) limb ischaemia
- Presence of claudication pain at rest, due to critical compromise of blood flow

Acute limb ischaemia
- A sudden decrease in limb blood flow which threatens viability, usually due to acute thrombus formation
- Features = 6 Ps
- Investigation = angiography
- Management:
- Medical - analgesia + unfractionated heparin
- IR - stenting, balloon
- Surgical - embolectomy, endarterectomy
- Limb amputation
- A key complication is compartment syndrome following limb reperfusion injury

105
Q

Thrombophlebitis

A

Aetiology:
- Trauma e.g. IV line insertion
- Lupus
- Cancer - migratory, due to hypercoagulable state
- Berger’s syndrome

Features:
- Low-grade fever
- Local redness or swelling along course of vein
- Symptoms worse when limb lowered

Management:
- Elevation + compression
- NSAIDs
- Abx if concurrent infection present

106
Q

Varicose veins

A

Common in older life.

Can also occur in pregnancy, usually resolving upon delivery

Investigations:
- ABPI - to rule-out arterial pathology prior to compression stockins
- Duplex USS - prior to surgical referral

Management:
- Weight loss
- Leg elevation
- Compression stockings (incl. in pregnancy)
- Refer to vascular if symptomatic
- Pain, itchiness, heaviness, swelling, chronic
venous insufficiency
- Endothermal ablation, foam sclerotherapy,
ligation + stripping

107
Q

Phlegmasia

A

Uncommon condition resulting from acute, massive venous thromboembolism
- Mostly veins of the leg (iliofemoral), rarely arm
- Linked to hypercoagulable state - esp.
malignancy

Features:
- Phlegmasia alba dolens
- Initial phase
- Progresses over hours to days
- Severe pain + limb pallor + edema
- Phlegmasia cerulea dolens
- Second phase
- Severe pain + cyanosis -> bullae and necrosis

Management:
- Limb elevation
- Analgesia + fluids
- Thrombolysis
- Thrombectomy

108
Q

Lymphoedema

A

Aetiology:
- Post-surgical esp. for cancer
- Radiotherapy
- Infection - filariasis
- Psoriasis
- DVT/varicose veins

Investigation:
- Rarely required
- MRI or lymphoscintogram

Management:
- Exercise
- Limb elevation
- Limb massage
- Skin/nail care
- Liposuction or lipovascular anastomosis done in a minority of cases at speciality centres

109
Q

AAA screening

A

For men 65+ or women 70+ with risk-factors

< 3.0 - discharge
3.0 - 4.4 - repeat in 12 months
4.5 - 5.4 - repeat in 3 months

> 5.5 or growing > 1.0 in 1 year - vascular referral
Symptomatic - urgent vascular referral

110
Q

Long QT syndrome

A

A syndrome of channelopathies leading to prolonged QT with risk of arrhythmia and sudden death

Often present in unstable monomorphic VT

Aetiology:
- LQT1
- Most common
- KCNQ1 on Chr 11
- Slow delayed rectifier K+ channel
- LQT2
- KCNH2 on Chr 7
- Rapid delayed rectifier K+ channel
- LQT3
- SCN5A on Chr 3
- Slow Na+ channel

Management:
- Medical
- Beta-blockade
- ICD
- Mainly for LQT2/3 as higher risk of sudden
death

111
Q

S1

A

Produced by closure of the mitral and tricuspid valves
- Mitral closes just before tricuspid
- Wide splitting is always pathological

Associated with the ECG R-wave

Quiet S1 - rigid valve or delayed LV systole
- Mitral regurgitation
- Long PR interval
- Obesity
- 1st degree heart block
- LBBB

Loud S1 - long diastole, high volume
- Mitral stenosis
- Hyperdynamic states
- Tachycardia
- Low BMI
- Atrial myxoma

Widely split S1
- RBBB
- Ebstein’s anomaly
- Ventricular tachycardia

Variable intensity S1 - due to variable PR interval
- Complete heart block

112
Q

S2

A

Produced by closure of the aortic and pulmonary valves
- Some splitting is typical - aortic closes before
pulmonary due to high systemic pressures
- Splitting increases in inspiration

Loud
- HTN

Quiet/absent
- Severe aortic stenosis

Widely split
- Pathology which delays the end of right ventricular systole or slows exit of blood from the RV
e.g. RBBB, Pulmonary stenosis, VSD, Mitral
regurgitation

Fixed splitting
- aka no change with inspiration - because ASD allows equalisation of pressures between both side
e.g. ASD

Reversed splitting
- Closure of PV prior to AV
- Delayed LV systole - LBBB
- Slowed LV outflow - AS
- Additional supply of blood delaying closure -
PDA

113
Q

Cholesterol embolism

A

An uncommon complication of angiography

Features:
- Recent arterial instrumentation
- Marked eosinophilia
- AKI
- Livedo retricularis
- Acrocyanosis
- Limb ischaemia and other embolic phenomena

Management:
- Supportive
- No good evidence for thrombolysis, anticoagulation, or re-intervention

114
Q

Arrhthymogenic right ventricular cardiomyopathy

A

aka right ventricular dysplasia

2nd most common cause of sudden death in the young

Features:
- Palpitations
- Syncope
- Cardiac arrest
- Progressive RV failure

ECG:
- TWI in V1-3 without RBBB
- Epsilon potential - small deflection at end of QRS complex due to RV conduction delay

Echo:
- Dilated, hypokinetic RV with prominent apical trabeculae and dilated outflow tract

Histology:
- Fatty infiltration of RV myocytes with subsequent fibrosis

115
Q

Eisenmenger syndrome

A

A complication of congenital heart disease in which large anatomical shunts are present
e.g. VSD, ToF, large ASDs

Pathophysiology:
- Initial L -> R shunting
- Elevated RV and pulmonary pressures
- Eventual pulmonary arterial hypertension and
elevated venous resistance
- Then R -> L shunting

Features:
- Cyanosis
- Hypoxaemia despite maximal oxygen therapy (due to mixing)
- Other cardiac stress - oedema, chest pain, syncoep, SOBOE

Management:
- Only curative treatment is a heart transplant
- Vasodilators e.g. endothelin antagonists

116
Q

Heyde syndrome

A

Triad of aortic stenosis, GI bleeding, and acquired von Willebrand syndrome

Pathophysiology:
- Shear stresses + increased velocity across stenotic aortic valve cause unfolding and activation of vWF
- Uses up vWF and so less is available for normal clot formation, in particular predisposing to GI bleeding

Management:
- Aortic valve replacement

117
Q

Restrictive cardiomyopathy

A

A rare (5%) cause of cardiomyopathy, presenting in a similar way to constrictive pericarditis

Aetiology:
- Idiopathic
- Infiltrative disease - esp amyloidosis
- Radiation therapy
- Hypereosinophilia

Features:
- Right heart failure - raised JVP, peripheral oedema, hepatomegaly, cachexia
- SOB, PND, orthopnea

Investigations:
- ECG
- non-specific repolarisation disturbances,
small complexes
- Bloods
- Echo
- small ventricles, LVH, speckling
- Cardiac biopsy
- +ve Congo Red staining for amyloid

Management:
- Supportive - diuretics
- AF control

118
Q

Atrial myxoma

A

A cardiac tumour formed from the atrial muscle
- Most common cardiac tumour
- Mostly on L side
- Benign
- F > M

Features arise from embolisation, intra-atrial obstruction of cardiac output, and constitutional symptoms of malignancy

Features:
- Symptoms
- Fever
- Weight loss
- SOB
- Syncope
- Signs
- Transient mitral stenosis
- Early diastolic ‘plop’
- Distal embolisation
- Finger clubbing

Investigations:
- Bloods
- Raised WCC, low PLT, variable Hb
- Imaging:
- CXR - enlarged heart
- Echocardiogram

Management:
- Urgent surgical resection as high risk of growth and embolisation

MRCP (20 decks)

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