Cardiology Flashcards
1
Q
What are the sensitivity, specificity, PPV and NPV for CTCA?
A
High sensitivity = low false negatives
High specificity = low false positives
High NPV = rules out CAD
Low PPV = presence of CAD and degree of stenosis does not always correlate to obstructive plaque on invasive coronary angio
2
Q
What are the indications for CTCA?
A
- Evaluation of chest pain syndrome with uniterpretable or equivocal stress test (ETT, stress echo)
- Evaluation of chest pain syndrome with intermediate pre test probability of CAD, uninterpretable ECG or unable to exercise
- Acute chest pain with intermediate pre test probability of CAD, no ECG changes and negative serial enzymes
3
Q
How should stable ischaemic chest pain be investigated?
A
Non invasively:
-exercise or stress ECG
- exercise or dobutamine stress echo
- dipyridamole/adenosine nuclear perfusion
- cardiac CT or MRI (non stress)
4
Q
What are the risks of invasive coronary angiography?
A
1 in 1000 risk:
-stroke
-MI
- contrast anaphylaxis
- major surgery at puncture site
- emergency angioplasty or surgery
- death
1 in 100 risk of
- arrhythmia
- surgical repair at puncture site
- minor contrast reaction
- AKI
1 in 20 risk of major bruising
1 in 10 lose pulse at radial puncture site
5
Q
What is the gold standard for anatomical assessment in coronary artery disease?
A
Invasive coronary angiography
6
Q
What is the gold standard for assessing coronary ischaemia?
A
Invasive coronary angiogram (specifically through measurement of FFR)
7
Q
What is involved in stress echo?
A
- Pre stress echo: evaluates LVEF, diastology, valves, wall motion
- Stress applied (exercise or drug) and assess ECG, symptoms, haemodynamics, exercise capacity
- Post stress echo: wall motion, diastology, RVSP
8
Q
How is myocardial ischaemia defined in stress echo?
A
Exercise induced ST changes or exercise induced RWMAs
9
Q
How is myocardial ischaemia defined in ETT?
A
ST segment abnormality
10
Q
Why is a stress echo more sensitive and specific than ETT?
A
Able to assess RWMAs - degree of wall thickening (should increase > 50%) which precedes ECG changes on ischaemic cascade
Less false negatives
Less False positives with stress echo for women
11
Q
What is LVH criteria?
A
S in V1orV2 + R in V6 >35
OR
S in V3 + R in aVL > 22
12
Q
Describe rheumatic AS
A
Fusion of commisures
13
Q
How is severe AS defined?
A
AS jet velocity > 4 m/s
OR
Mean gradient >40 mmHg
OR AVA >1 cm2
14
Q
What is a key feature of low flow severe AS?
A
Reduced stroke volume < 35 mL/m2
15
Q
What is the only treatment that improves patient outcomes for severe AS?
A
Valve replacement
- low surgical risk = AVR
- intermediate risk = AVR or TAVR
- high risk = TAVR
16
Q
What is the most common cause of Aortic Regurgitation?
A
Congenital abnormality such as bicuspid valve
17
Q
Describe AR murmur
A
Early diastolic decrescendo murmur loudest left sternal edge
- increased on full expiration
- increased with handgrip or squat due to increased afterload
May also hear low pitched mid diastolic rumbling of austin flint murmur (where AR jet impinges AVML)
18
Q
How is severe AR defined?
A
-Flail leaflet or wide coaptation defect
- large jets
- steep decceleration
- holodiastolic flow reversal in aorta
- dialted LV
19
Q
What are the indications for AVR for AR?
A
Severe AS with symptoms or have impaired LVEF
Moderate or severe and if otherwise having cardiac surgery
20
Q
What are causes of acute severe AR?
A
Aortic dissection or endocarditis or trauma
Short diastolic murmur
21
Q
What are the two types of MR?
A
Primary: degenerative caused by leaflet prolapse, chordae rupture, endocarditis, RHD
Secondary: functional, normal valve in presence of LV dysfunction
22
Q
Describe MR murmur
A
holosystolic murmur +/- diasotlic murmur
23
Q
What LVEF indicates reduced LV function in severe MR?
A
LVEF < 60% indicates reduced contractility as MR reduces work of LV
24
Q
How is primary severe MR managed?
A
symptoms or LV dysfunction and low surgical risk = MVR
high surgical risk = mitraClip (transcatheter edge to edge MV repair
25
How is secondary MR managed?
Managed medically as for HF +/- CRT as first line
If refractory:
- LVEF > 50% = MVR
- LVEF < 50% = MitraClip
Concurrent CABG = MVR
Surgical management 1st line does not reduce hospitalisations or death
26
Which valve is most commonly involved in RHD?
Mitral valve - more commonly stenosis
27
Describe appearance of rheumatic MS
Fusion of commisures = fish mouth
Thickened + restricted AVML = hockey stick
28
Which rheumatic valve disease should you give anticoagulation for A Fib regardless of CHADSVASc?
Mitral stenosis
29
In which rheumatic valve disease should you give a B-blocker for tachycardia with pulmonary oedema?
Mitral stenosis
30
Describe MS murmur
Low pitch diastolic rumble
(bell in left lateral with full expiration)
31
How is severe MR defined?
Valve area < 1.5 cm2
OR Mean gradient > 10 mmHg
Or PAP > 50 mmHg
32
When is intervention for rheumatic Mitral Stenosis indicated?
Balloon valvuloplasty for pliable valves with thrombus in severe or progressive MS
MVR for severe MS with severe symptoms and low surgical risk
33
What is the most common cause of tricuspid regurgitation?
80% are functional
34
Should isolated TR be managed surgically?
No - poor outcomes especially if RV dysfunction and pulmonary hypertension
35
What is different about mixed valve disease?
Often does not progress to severe grade but associated with higher morbidity and mortality
Requires specialist team input to guide appropriate management
36
What is normal global longitudinal strain on TTE?
More than 20%
37
What information os gained from GLS on TTE?
- Can indicate RWMAs
- Early detection of cardiotoxicity in cancer therapies (earlier detection than LVEF)
38
What is pre capillary pulmonary hypertension?
Where arterial tree is obstructed, PAP is greater than LA pressure
39
What is post capillary pulmonary hypertension?
Normal lung circulation but raised LA pressure causes high PAP
40
How is pulmonary hypertension measured on ECHO?
Doppler gradient across tricuspid valve + bernoulli equation to estimate RVSP
41
How is pulmonary hypertension defined?
PAP (equal to RVSP) > 20-25 mmHg
42
What is the significance of pre and post capillary hypertension with regard to management?
- post capillary hypertension should be managed with diuresis
- pre capillary should be treated with pulmonary vasodilator drugs
43
When is it safe to do DCCV for AFib?
- presentation with < 48 hours onset symptoms
- stabled on anticoagulation at least 4 weeks
- TOE rules out LAA thrombus
Same risk of stroke between these groups
44
What are the four best known causes of congenital heart disease?
1. Trisomy 21 - VSD/AVSD
2. 22q11 deletion (Digeorge syndrome)- great artery malformation (tetralogy of Fallot)
3. Lithium - Ebsetin anomaly, TV anomaly
4. Rubella - peripheral PA stenosis
45
What is the complication of patent ductus arteriosus?
Failure to close causes left to right shunt (aorta -> pulmonary artery) which can cause LV failure
46
Why is location of pulmonary valve stenosis significant?
If valvular is amenable to balloon valvuloplasty
Otherwise sub-valvular and spravalvular may require stenting
47
What is Noonan syndrome?
Autosomal Dominant syndrome associated with RAAS/MAPK gene mutation
Wide set eyes
Low set ears
Short stature
Pulmonary stenosis
48
What is Williams Syndrome?
Autosomal Dominant syndrome resulting from deletion of WBSCR of 7q11.23
-Developmental Delay and cognitive impairment
-Overfriendly and anxious
-Elastin arteriopathy: pulmonary stenosis and and supravalvular aortic stenosis
-Specific facies
- Poor growth
- Connective tissue abnormalities
- Endocrinopathies: early puberty, hypercalcaemia, hypercalciuria, hypothyroidism, diabetes
49
What are the co-morbidities associated with Coarctation of the aorta?
- biscuspid aortic valve
- hypertension (even after repair)
- Arch hypoplasia
- cerebral aneurysms
- aortic dissection
- repair site aneurysms
50
What are the 4 lesions of tetralogy of fallot?
- VSD
- RV hypertrophy
- Over-riding aorta (shifted right)
- Pulmonary stenosis
51
What are complications seen post repair of tetrology of fallot?
- pulmonary regurgitation (esp if transannular patch used in repair)
- pulmonary stenosis
- arrhythmias (atrial > ventricular)
- RV/LV dysfunction
- Aortic root dilatation (needs screening)
52
What is Ebstein's anomaly?
- ASD
- Accessory pathways; 20% have WPW
- Arrhythmia
- TR
- Abnormal RV (smaller than RA)
53
What is truncus arteriosus?
Failure of aorta and pulmonary artery to separate during embryonic development resulting in single outflow track to both aorta and lungs
54
What are non-cardiac complications of congenital heart disease?
- psycho-scoial issues (depression, anxiety)
- substance abuse
- needle phobia
- non-adherence with medications and follow up
55
What is cyanotic heart disease?
Presence of right to left shunt resulting in deoxygenated blood entering systemic circulation. This results in chronic hypoxia
Causes include large ASD, large VSD, anomalous pulmonary vein drainage
56
What are complications of cyanotic heart disease?
- risk of embolism: DVT arises to arterial clots causing stroke or limb ischaemia, cerebral abscess
- secondary erythrocytosis (distinct from polycythaemia does not require venesection)
57
What is fontan circuit?
Surgical procedure for single chamber or right heart hypoplasia that connects IVC/SVC directly to pulmonary circulation
Palliative procedure where complete repair is not possible
58
What is the best imaging modality to image the aorta?
CT chest (3D reconstructed)
59
What are the key principles of medical management of aortic aneurysm?
Blood pressure control
-> 1st line is B-blocker, often poorly tolerated in young patients
-> ARB in Marfans as block TGFB1 signalling
Restrictions on weight lifting and exercise
Close monitoring in pregnancy/pre pregnancy repair
60
What are the inherited causes of thoracic aortic anuerysms?
- bicuspid aortic valve
- Turner syndrome (also associated with bicuspid AV)
- Ehler's danlos
- Familial thoracic aortic anuerysm (fast growth rate)
- Loey's Dietz (faster growth and higher dissection risk)
- Marfan syndrome (fast growth rate)
- Non specific connective tissue disorder
- Cono-truncal anomalies (TOF, truncus arteriosus as have dilated aortic root)
61
What are the indications for surgical repair of ascending aortic aneurysm?
-Any aortic anuerysm > 55 mm
-Biscuspid AV with risk factors (coarctation, FHx, growth >3-5 mm/year) > 50 mm
-Marfan > 50 mm
Loeys Dietz > 42 mm
Turner syndrome > 27 mm/m2
62
What ECG findings suggest a cardiac cause for syncope?
Bifasicular block (RBBB + LAFB)
QRS > 120 ms
Mobitz II type 2 AV block
Sinus bradycardia (< 50 bpm, pauses > 3secs or >5secs with AFib)
NSVT
Pre-excitation
Features of channelopathy or cardiomyoptahy
Pathological Q waves
63
What medications have evidence for the use in vasovagal syncope?
Midodrine (a1 receptor agonist)
Fludrocortisone (synthetic steroid with high mineralocorticoid receptor activity)
Paroxetine (SSRIs)
Not beta blockers
64
How do you assess an SVT (narrow complex tachycardia, QRS < 120 ms)?
1. Irregular = Afib, Atach with variable conduction, MAT
2. Regular without p-waves = AVNRT or other
3. Regular with non- conducted p-waves = AFib or AFlutter
4. Regular with conducted p-waves and RP interval < 90 ms = AVNRT
5. Regular with conducted p-waves and RP < PR interval but greater than > 90 ms = AVRT, atypical AVNRT or Atach
6. Regular with conducted p-waves and RP > PR interval = Atach, PJRT or atypical AVNRT
65
How should SVT be treated?
- unstable = DCCV
- Stable = vagal manoeuvres, IV adenosine (not in severe asthma as causes bronchoconstriction), IV CCB or B-blocker (CCB never in broad complex or WPW)
66
How are SVTs managed in the long term?
- Vagal manoeuvres if infrequent
- catheter ablation for AVNRT, WPW, unifocal Atach, CTI-dependent flutter
-pill in pocket flecainide 200-300 mg stat (need B-blocker cover)
- medications: b-blocker, CCB, digoxin, Flecainide (need b-blocker), sotalol, amiodarone
67
What are management strategies for AFlutter?
- Anticoagulation
- rate control with AV nodal blockade
- Pharmacological cardioversion
- DCCV
- ablation
68
What is the CHA2DSVASc2 score and when is anticoagulation indicated?
Score > 1
Congestive heart failure
Hypertension
Age: 1 if 65-74, 2 if >75
Diabetes
Stroke or TIA or previous arterial thromboembolism
Vascular disease (prior MI or PAD
Sc is for women
69
What is the HAS-BLED score?
Yearly risk of bleeding
Hypertension
Alcohol, antiplatelets and anti-inflammatories
Stroke
Bleeding: major bleeding labile INR
Liver disease
Elderly: age > 65
Dialysis/end stage renal disease
70
What anticoagulation should be used for AFib?
- NOACs in non-valvular AFib, no benefit when switching over from warfarin in frail adults over 75 as per FRAIL-AF trial
- warfarin in metallic heart valves and moderate to severe mitral stenosis (valvular AF)
71
When should DOACs be held and restarted around surgery?
Low risk = 1 day before
High risk = 2 days before
EXCEPT dabigatran in CrCl < 50 when should be held 4 days before high risk and 2 days before low risk surgery
All can be restarted on days 2-3
72
How is AFib managed?
1. Rate control: 1st line is B-blockers, CCBs except in CHF, 2nd line is digoxin, 3rd line is rhythm control
2. Rhythm control:
in structural heart disease flecainide or sotalol is first line and amiodarone second line
in structurally normal heart amioadrone is first line, 2nd line is sotalol or B-clocker
3rd line is ablation
73
What are indications for ablation in atrial fibrillation and what is the most common site ablated?
- symptomatic pAF or refractory permanent AF
- AFib in HFrEF
Pulmonary veins
73
Does ablation for Afib improve mortality?
No
Reduces symptom burden and QoL
Evidence that reduces hospitalisation and death in HFrEF (CASTLE-AF trial)
74
What are features of pathological AV block (Mobitz II type 2)
- wide QRS
- short PR
- block worse on exertion
- associated with anterior MI
- associated with syncope
75
What is sinus node dysfunction and indications for treatment?
< 50 bpm with sinus pauses > 3 seconds
Treatment indicated for chronotropic incompetence (failure to reach 80% predicted HR)
NB OSA common treatable cause of sinus node dysfunction
76
What are the indications for PPM for bradycardia?
Absence of reversible cause in Mobitz II type or complete heart block
Symptomatic patients without reversible cause in patients with:
-sinus node dysfunction
- Afib with bradycardia
- bradycardia due to goal directed medical therapy e.g b-blocker in HF
- Mobitz I or 1st degree HB with clear correlation to symptoms
77
When is CRT indicated?
In patients with symptomatic heart failure on medical therapy with LVEF < 35% and QRS > 150 ms
Shown to improve mortality in patients without AFib
78
Who should be considered for PFO closure?
Stoke patients with high RoPE score
79
When should Left atrial appendage occlusion be considered?
In patients with non-valvular AFib with contraindications to lifelong anticoagulation
80
What are absolute contraindications to TOE?
Oesophageal tumour, stricture, fistula or perforation
Active upper GI bleed
Perforated bowel or bowel obstruction
Unstable C-spine
Uncooperative patient
81
What are the indications for TOE?
Infective endocarditis
Pre DCCV or ablation
To exclude cardiac source of embolus
Aortic dissection
Non diagnostic TTE
Cardiac surgery/structural procedures
82
What features on TOE support a diagnosis of infective endocarditis?
Vegetations (lobulated, echogenic, indepedently mobile)
Abscess (echolucent space)
New partial dehiscence of prosthetic valve8
83
What two features are required to diagnose SVT with aberrancy?
SVT + evidence of BBB (typically in V1 and V6)
84
How is scar mediated VT managed?
-VT controlled with anti-arrhythmic or ablated
-Needs work up for structural heart disease: ECHO, MRI, angiogram
- ICD if indicated
84
How is idiopathic VT managed?
VT suppression with medication
Can consider ablation if recurrent
(note will have structurally normal heart)
84
What is the diagnostic criteria of heart failure?
Symptoms and/or signs of heart failure caused by a structural or functional cardiac abnormality and corroborated by at least one of:
- elevated BNP
- objective evidence of cardiogenic pulmonary congestion
85
What are the subclassifications of HF?
HFrEF = LVEF < 40%
HFmrEF = LVEF 41-49%
HFpEF = LVEF > 50%
HFimpEF = improvement in LVEF with HFrEF
86
Which investigations are indicated for the diagnosis of heart failure?
12 lead ECG
CXR
BNP
TTE
87
What maintenance therapies should be used in heart failure?
HFrEF:
- ACEi/ARB/ARNi + Beta blocker + MRA + SGLT2i
- consider ivabradine if HR > 70 and LVEF <35%
- hydralazine in African patients
- IV iron if ferritin < 100 or if 100-300 with Tsat
< 20%
HFmrEF: ACEi/ARB + Beta blocker + MRA
HFpEF: low dose MRA, SGLT2i
88
What is the NYHA HF classification?
Class I - No symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
Class II - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
Class III - Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20—100 m).Comfortable only at rest.
Class IV - Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
89
How is goal directed medical therapy initiated in congested vs euvolaemic patients with HF?
- Congested: ARNi/ACEi/ARB and SGLT2i, then add MRA, then B-blocker once euvolaemic
-euvolaemic: ARNi/ACEi and B-clocker, then add MRA and SGLT2i
90
What is the goal for LDL in high risk individuals?
< 1.8 or > 50% reduction in LDL
91
When should Lp(a) be measured and how should it be managed?
Measured in people with premature CVD or stroke
Aggressive LDL reduction (<1.5)
ACEi if proteinuric
Nicotinic acid
92
What is the pathological basis of familial hypercholesterolaemia?
AD inherited
Increases LDL resulting in increased cholesterol deposit
93
What is the treatment of hypercholesterolaemia?
1st line: statin
2nd line: statin + ezetimibe
3rd line = PCSK9i if high risk and LDL > 2.6 despite statin and ezetimibe
