Cardiology Flashcards
(140 cards)
1
Q
Define an arterial aneurysm
A
When an artery has enlarged greater than 1.5x its expected diameter
2
Q
How big does an aortic aneurysm need to be before a driver’s licence needs to be suspended in Australia?
A
> 5.5cm unless a vascular surgeon has approved them to have a driver’s licence.
3
Q
How big does an aneurysm need to be to require surgical repair?
A
In men >5.5cm. In women, >5.0cm. Risk of rupture is related to diameter in an exponential relationship.
4
Q
How often should a AAA be reviewed with ultrasound if it is 5.0cm?
A
Every 6 months. Between 5 and 5.5cm, and it needs to be reviewed every 3 months. Between 4.0 and 4.5 is every 12 months, and between 3.0-3.9cm is every 24 months.
5
Q
Are S3 and S4 heard in systole or diastole?
A
Diastole. S3 is heard just after S2, and S4 just before S1, but both aer diastolic heart sounds.
6
Q
What causes S1?
A
The near simltaneous closing of the mitral and tricuspid valves at the beginning of simultaneous R and L ventricular isometric contraction. There is a physiologically normal 0.04s split between the mitral and triscupid valves (mitral closes slightly faster), but this cannot be percieved via auscultation.
7
Q
What causes S2?
A
The closure of the aoritc pulmonic valves at the begining of R and L ventricular relaxation. Physiologically, S2 is split because the aortic valve closes faster than the pulmonic valve.
8
Q
What is meant by splitting of the S2?
A
Normally S2 is split because the aortic valve closes faster than than the pulmonic valve - but the duration of the split should vary with the respiratory cycle. When breathing, there is increased venous return to the right atrium and ventricle. This increases the RV pressures, which increases the duration of systole on the right side - further increasing the split between right P2 and A2.
9
Q
What causes S3?
A
Early diastolic sound. Often heard and normal in children - possibly originating from the tensing of the cordae tendinae. In adults, it is caused by blood rushing into dilated ventricles.
10
Q
What causes S4?
A
It’s caused by the vibration of the ventricular wall during atrial contraction (late diastole). It is heard due to a stiffened (non-compliant) ventricle being hit by blood from the atrial kick. This is always pathogenic and heard in ventricular hypertrophy, mycocardial ischaemia or the olds.
11
Q
What pathologies are are assocaited with splitting of the first heart sound?
A
Right bundle branch block. Delay in closing of the tricuspid valve due to delayed contraction of the right ventricle.
Ebstein’s anaomly (congential heart disease where the septal and posterior tricuspid valve leaflets are displaced towards the apex) can also cause a split S1
12
Q
What pathologies are associated with increased splitting, but still variable, second heart sound?
A
Anything that further delays emptying of the right ventricle during systole. So, reduced pulmonary pressure will do this, or increased venous return, or right bundle branch block (first and second heart sound splitting possible due to RBBB). Pulmonary stenosis will do this (delayed RV ejection), so too will a VSD due to increased pressure in the right ventricle.
The other thing that can increase the S2 split is the faster closure of the aortic valve secondary to mitral regurgitation - the left ventricle empties rapidly through the aorta and the left atria, allowing the aortic valve to close faster than usual.
13
Q
What leads to fixed splitting of the second heart sound?
A
Atrial septal defect. An ASD creates a two signs - 1) it causes a left to right shunt that leads to increased filling of the right ventricle. This leads to increased pressure when the right ventricle goes through systole, and an ejection systolic murmur through the pulmonary valve due to the increased flow 2) It also causes a permanent high RV pressure state (like during inspiration) which causes delayed closing of the pulmonary valve and fixed splitting of P2 from A2.
14
Q
What causes a loud S1?
A
Either tachycardia due rapid closure of the mitral valve at the ende of brief diastole, or mitral stenosis due to the lack of gradual closure of the leaflets, and instead a sharp sudden closure.
15
Q
What is Ebstein anomoly?
A
It’s a congential defect of the right heart involving displacement of the tricuspid valve. Severity of symptoms depends on the severity of abnormal anatomy. The tricsupid valve leaflets are variable still stuck to the myocardium and displaced. The hinge points of the septal and posterior leaflet are resultantly shifted towards the apex.
16
Q
What dynamic echocardiographic heart problems are seen in patient’s with an Ebstein anomoly?
A
Various degrees of tricuspid regurgitation. Small remaining RV and usually dysfunctional.
17
Q
What other heart defects are often seen in patients with Ebstein anomaly?
A
Patent foramen ovale or ASD is in up 80% of Ebstein pts. Ventricular septic defects. Patent ductus arteriosus.
Pulmonary outflow obstruction is rare.
18
Q
What conduction issues are seen in patient’s wth Ebstein anomaly?
A
Accessory conduction pathways are seen in 6-36% of patients leading to SVT. The addition of pre-excitation and Wolff-Parkinson-White syndrome is the most concerning. These patients also develop right bundle branch block. AF/Aflut may be seen in older patients.
19
Q
How does anthracycline induced cardiotoxicity work, and what makes it more likely?
A
The anthracyclines cause cardiac toxicity in a total lifetime dose dependent manner. The cardiotoxicity is not fully understood, but is likley to do with off target binding to topoisomerase 2 beta which is highly prevalent in cardiomyocytes (topo 2 alpha is intended target for cancer treatment), but has some known things likely to make it worse - 1. high iron availability 2. age less than 18 or over 65 years old 3. female gender 4. renal failure 5. previous radiotherapy involving the heart 6. pre-existing heart disease 7. carbonyl reductase gene polymorphisms 8. patients with haemochromatosis associated gene varients.
20
Q
What is Dexrazoxane?
A
Drug that competes with the anthrcyclines to bind the offtarget topoisomerase 2beta (anthracyclines have their anticancer effect by binding topoisomerase 2 alpha) in order to protect the topoisomerase 2 beta cardiomyocytes.
21
Q
What are the three TTE measurements that relate tot he aortic valve that are used in clinical decision making for aortic stenosis?
A
- Maximum aortic velocity 2. Mean pressure gradient, and 3. Valve area
22
Q
What medication post TAVI have been shown to reduce all cause mortality?
A
RAS inhibtion (ACEi or ARB) if the patient is hypertensive, and antiplatelet (SAPT) for life OR anticoagulant for life if there is another indication for it (e.g. AF). Note SAPT is not added to anticoagulant if patient is already on an anticoagulant.
23
Q
At what stage of aortic stenosis should patients receive an aortic valve replacement?
A
Stage D (TAVI or SAVR) or stage C (TAVI or SAVR for those also with other cardiac surgery OR LVEF < 50% OR SAVR only for those with exercise test with reduce in exercise capacity or BP drop OR Vmax >5 OR BNP > 3x normal OR rapid disease progression). Stages A-C are all asymptomatic and split on the basis of valve funciton. Note that if patients have Stage C disease, they should undergo exercise stress testing with TTE to see if symptoms can be elicited and to observe for a fixed valve area.
24
Q
What defines stage D1 aortic stenosis (a stage requiring AVR)?
A
On dabutamine stress testing: maximum velocity >4.0m/s with a valve area of <1.0cm^2, mean pressure gradient > or = 40mmHg.
25
In patients with heart failure, is RBBB or LBBB associated with increased mortality risk?
LBBB
26
What are the indications for Cardiac Resynchronisation Therapy?
1) HFrEF with ejection fraction of less than 35% after maximal medical therapy and at least three months after the initial diagnosis:
-For a QRS 130 -149ms with LBBB and NYHA symptoms II-IV ->CRT. If non-LBBB and severe symptoms, CRT will be considered.
-For QRS >149ms and LBBB for NYHA I AND ischaemic cardiomyopahty -> CRT.
-For QRS >149ms with LBBB and NYHA II-VI -> CRT.
-For QRS >150 without LBBB, patients should be considered for CRT with NYHA II-IV.
2) Pts with HFrEF with LVEF 35-50% who require ventricular pacing for another reason >40% of the time, or who have a QRS >150ms with LBBB and HF symptoms.
27
What does CRT improve when implanted in patients in whom it is indicated?
Restores ventricular synchrony which improves LVEF, reduces HF symptoms, increases survival.
28
What age is generally considered the cut off, after which patients are considered to be unlikely to benefit from surgical AVR?
75 years old
29
What are the contraindications for TAVI?
Severe COPD, debilitating stroke, active malignancy, and dementia with less than 12 months survival likely.
30
In the presence of cardiac stent requiring antiplatelet treatment, if a new diagnosis of AF is made with CHADSVASC score of > 3, what is the right anticoagulation plan for stroke prophylaxis?
Big study in Japan in NEJM 2019 looed at this - rivaroxaban alone is not inferior to antiplatelet plus rivaroxaban and carries a lower risk of bleeding. It probably extends to all doacs, but the study was on rivaroxaban.
31
What are the antianginal medications?
-Rate control to reduce myocardial O2 demand- beta blockers (first line), ivabradine, non-dihydrophyridine calcium antagonists (e.g. verapamil, diltiazem).
-Coronary artery and peripheral arterial and venous relaxants (nitrates, nicorandil (potassium channel activitor), dihydropyridine calcium channel blockers.
- Drugs that induce cellular tolerance to ischaemia - piperazine derivatvies including trimetazidine (big RCT in 2020 shows this probably doesn't work) and ranolazine (works).
32
What are the classic ECG findings in type 1 Brugada syndrome?
ECG findings of a 'coved' ST segment with elevation >2mm in at least 2 of leads V1-V3 AND clinical symptoms.
33
What are the classic ECG findings in type 2 Brugada syndrome?
>2mm saddle shaped ST elevation in a lead of V1-V3
34
What are the classic ECG findings in Type 3 Brugada syndrome?
Coved or saddle ST elevation of less than 2mm in leads V1-3.
35
How is Brugada syndrome inherited?
Autosomal dominant with variable penetrence. It's more common in men for some reason.
36
What is the most common gene implicated in Brugada syndrome?
SCN5A. Others include SCN10A, L-type calcium channel genes KCNE2/3. SCN5A is a cardiac sodium channel. Worth noting that factors other than genes contribute to patients having the syndrome and not just the ECG pattern - this includes differently shaped right ventricles, preceding aggrevating factors like psychotropic drug use, cocaine, fevers, changes changes to autonomic tone.
37
How do you diagnose Brugada syndrome?
Classic Type 1 ECG changes (coving ST-elevations in V1 and 2 of greater than 2mm) spontaneously or following a drug (e.g. flecainide) challenge AND clinical features: sudden cardiac arrest, VF, polymorphic VT, syncope, nocturnal agonal respiration.
38
What patients classically have Brugada syndrome, and how do they usually present ?
With sudden cardiac arrest in 1/3 of patients. Pts are normally 22 to 65. In south asian male population Brugada appears to be more common. It occurs more often at night than during the day, and usually when the patient is asleep. Classically, this is secondary to VF or polymorphic VT. Syncope is the presentation in another 1/3 of patients. Brugada pts sometimes present with AF (increased risk compared to background population).
39
Who should undergo a Brugada drug challenge?
Contraindicated in patients with a type 1 rhythm spontaneously. If a patient has type 2 Brugada pattern and symptoms, or asymptamtic Brugada 2 pattern with family history of cardiac death under 45. Can use flecainide, procainamide, ajmaline or pilsicainide.
40
How is Brugada syndrome treated?
Insertion of ICD and avoidance of triggers (fever, drugs known to be implciated). If pts keep getting ICD shocks, they may also need an antiarrhythmic.
41
What medications are known Brugada syndrome triggers?
Sodium channel blockers, beta blockers, antipsychotics, alcohol, cocaine. Extensive additional list, but these are the main groups.
42
What is the most common type of cardiac amyloidosis?
Transthyretin amyloidosis - hereditary and wild type. Light chain amyloidsosis is next most common.
43
What is transthyretin?
Protein made in the liver that normally trasnports thryoid hormone and retinol. In tranthyretin amyloidosis (so called ATTR) - misfolded proteins accumulate, deposite in tissue, and cause organ dysfunction.
44
What gene is involved in hereditary amyloidosis and how is it inherited?
The gene is the TTR gene. It shows autosomal dominant inheritence with variable penetrence.
45
What age do symptoms of cardiac amyloidosis typically present? What are the non-cardaic manifestations
For AL amyloid, usually present with multisystem disease over the age of 40. For patients with ATTR amyloidosis however, the age of onset is typically >60 and usually >70. Rarely, some hereditary forms of ATTR have an early onset. ATTR is associated with preceding peripheral neuropathy, spinal canal stenosis and spontaneous tendon rupture.
46
How do patients with cardiac amyloidosis present?
Patient's with cardiac amyloidosis usually present with symptoms of heart failure. Often they present with syncope, likely due to bradyarrhythmias or advanced AV block. Alternatively, they may have sinus node disease. ATTR cardiac amyloid can also present as severe AS.
47
What are the classic echocardiogram and ECG findings of cardiac amyloidsosis? What other tests can be done?
-There is often a thick LV wall with a discordantly low voltage QRS (low sensitivity feature).
- Apical sparing of longitudinal strain (highly sensitive and specific for amyloidosis and good for early detection)
-Bi-atrial dilatation, diastolic dysfunction
-70% have a pseudoinfarction pattern on ECG.
-Bone tracer scintigraphy NM scan that looks for uptake in amyloid --specifically ATTR - affected tissue. Cf with AL amyloid which has limited tracer uptake. If all systemic paraprotein screening is negative, bone tracer scintigraphy can be used to diagnose ATTR cardiac amyloidosis.
-cardiac mri with gadolinium enhancement has distinct diagnostic pattern - native myocardial T1 elevation is an early disease marker with high diagnostic accuracy.
48
What are the treatment options available for ATTR cardiac amyloidsois?
Tafamidis. This drug stabilises the ATTR tetramer and may thus reduce formation of TTR amyloid. The other option is liver transplant which then gives the patient TTR that isn't misfolded. Workup for liver transplant should commence as soon as cardiac ATTR is diagnosed.
49
Where can you biopsy to try to diagnose amyloidosis?
Abdominal fat pad, bone marrow, a clinically involved organ (e.g. kidney, heart), rectum
50
How does atropine work?
It competes for acetylcholine to bind to muscurinic and nictotinic Ach receptors. This antagnoises the parasympathetic 'breaks' on the heart and allows for sympathetic drive to increase the heart rate. Atropine is also used, therefore, to decrease other effects of Ach overload - to treat siallorhoea, to treat organophosphate poinsoning and so on.
51
What increases the risk of cholesterol embolism?
It can occur spontaneoulsy, however it is often proceded by an iatrogenic event. The most common are invasive vascular procedure (angiography or vascular surgery) or after commencing anticoagulant therapy.
52
What is the classic presentation of cholesterol emboli?
Usualy 2 to 4 weeks after an inciting event - peripheral emboli and AKI. However patients can be asymptomatic, or have a full blown vasculitis picture. Eosinophilia is common in up to 80% of acases.
53
Do you anticoagulate people with cholesterola emboli?
No, this makes it worse. Statins can be used and may improve outcomes.
54
When is CTCA indicated?
In symptomatic patients with pre-test probablity for CAD too low to prompt angiography. Can also be used to evaluate graft patency in previous CABG patients. Can't be used to see stent in stent stenosis. Should not be used in patients with acute MIs. Note, the patient needs to be able to hold their breath for 10s, hold their arms above their heads, and tolerate beta-blockers and nitrates to prepare for the procedure.
55
What are the indications for surgery in infective endocarditis?
CCF refractory to medical therapy
Fungal infective endocarditis
Persistent sepsis after 72hrs of abx
Recurrent septic emboli after 2 weeks of abx
Rupture of aneurysm fo the sinus of valsalva
Conduction disturbances caused by septal abscess
Kissing infection of the anterior mitral leaflet in patients with IE of the aortic valve.
56
What are the contraindications for SGLT2 inhibitors?
Recurrent urinary infections, CrCl <30ml/min, threatened limbs. No that they act as a diuretic, so patient needs to not be hyopvolaemic. Will reduce BGL, so inuslin and sulfonylureas (e.g. gliclazide) are then free to cause hypoglycaemia.
57
What features on TTE are classic of HFpEF?
LVEF > 50%, LV end diastoilic volume of < 97ml/m^2 and raised LV filling pressures indicated by an E/e' of > 15.
58
What is the only medication to show reduced rates of hospitalisation in patients with HFpEF?
Spironolactone
59
What causes hypertrophic cardiomyopathy?
Genetic disease. 60-70% of cases are related to sarcomere gene mutations.
60
What are the defining cardiac anomalies in patients with hypertrophic cardiomyopathy?
LV outflow obstruction, diastolic dysfunction, mycocardial ischaemia, mitral regurgitation
61
What are the clinical featuers of HoCM?
Heart failure, chest apin or arrythmias including those leading to syncope or to sudden cardiac death.
62
Does the risk of Brugada syndrome-related sudden cardiac death increase with exercise?
No
63
What murmur is likely to be heard in patient's with HoCM? What can be done to make this murmur more obvious?
Harsh crescendo/decrescendo systolic murmur heard loudest at the apex due LVOT obstruction and mitral regurgitation. The LVOT component radiates to the base of the heart, so is often confused with AS. If there isn't significant LVOT obstruction, you might instead hear a mid-late systolic murmur at the apex which radiates to the axillar and is associated with the MR alone.
The LVOT obstruction murmur can be increased in intensity with maneouvers that enhance the obstruction - going upright after swautting, sitting or being supine OR the valsalva maneuver.
3rd and 4th heart sounds are also often heard
64
What non-auscultatory exam findings might be present in a patient with HoCM?
Apical heave, brisk, bifid, upstroking carotid pulse, prominant a wave, systolic thril at apex or lower left sternal edge
65
What are the typical ECG findings in HoCM?
Down sloping ST segments and T-wave inversion, most prominent in I, aVL and V4-6. Prominent abnormal Q waves. P wave abnormalities consistent with LA or biatrial enlargement. Prominent voltages.
66
After TTE and ECG, what investigations should be done in patients with HoCM?
Holter monitor due to high risk of ventricular arrhythmias. Exercise stress testing with TTE to establish degree of LVOT obstruction and ischaemia under exercise stress. Cardiac MRI is performed to most accurately describe cardiac morphology and measure LVOT at rest.
67
What LV wall thickness is considered abnormal in the TTE evaluation for hypertrophic cardiomyopathy?
LV wall thickness greater than 14mm.
68
What are the non-hypertrophic cardiomyopathy causes of increased LV wall thickness?
Hypertension, AS, Fabry disease
69
How is hypertrophic cardiomyopathy inherited?
Autosomal dominant with very high penetrence.
70
What should be done for first degree relatives of patients with HoCM?
Gene testing, physicial exam, ECG, TTE.
71
What is the most common extracardiac complication o infective endocarditis?
Embolic cerebral events
72
What dichotomy is established to guide treatment after a diagnosis of hypertrophic cardiomyopathy with NYHA II-IV heart failure is made?
LVOT obstruction with > 30mmhg at rest or with exercise provocation Vs no LVOT obstruction
73
How are patients with HCM, heart failure and LVOT obstruction of >30mmHg treated?
Monotherapy with beta-blockers is first line. Second line is BB and dispyramide OR a nondihdropyridine calcium channel blocker (e.g. verapamil) and disopyramide. If this fails, then options include a surgical septal myectomy or alcohol septal ablation.
74
How are patietns with HCM and heart failure with LVOT obstruction <30mmHg treated?
If LVEF is greater than 50%, manage with BB or caclicum channel blocker monotherapy +/- symptomatic management with diuretics if overloaded. For LVEF < 50% then manage as for HFrEF. No role for myectomy or alcohol ablation in either case if no LVOT, so if symptoms of heart failure worsen, then consider heart transplant.
75
In patients with hypertrophic cardiomyopathy, what are the factors that are associated with an increased risk of sudden cardiac death? What do you do if someone has one of these risk factors?
1. Prior cardiac arrest or sustained ventricular arrhythmias
2. Family history of first degree or close relative <50 years of age with SCD judged definitely or likely due to HCM.
3. Recent syncope suspected to arrhthymic in origin
4. Massive LV hypertrophy (>30mm anywhere in LV wall)
5. LV apical aneurysm of any size
6. End-stage HCM with LV ejection fraction < 50%.
If one or more of these factors is present, the patient should have an ICD placed reduce the risk of sudden cardiac death. Favorable CMR imaging, age (>60), and small or no NSVT episodes may alter this decision.
76
What is the most common adverse effect following alcohol ablation for the treatment of hypertrophic cardiomyopathy with heart failure?
Complete heart block requiring a pace maker.
77
What is commotio cordis?
VF after being hit in the heart with a forceful, usually round, object.
78
What percentage of patients with HOCM have LVOT obstruction?
About 70%
79
What is the Keith-Wagener grading system used for? What is meant by each grade?
Hypertensive retinopathy grading. Grade 1 = isolated narrowing of retinal arterioles. Grade 2: moderate to marked narrowing of arterioles associated with a copper wire appearance or arteriovenous nicking. Grade 3 Hypertensive retinal haemorrhage or exudates are present. Grade 4: papilloedema is present.
80
What is evlocumab?
Evolocumab and alirocumab are monoclonal antibodies that inhibit Proproetin Convertase Sublitisn/Kexin Type 9 (PCSK9). PCSK9 normally inhibits LDL receptor recyling, which in turn limits the ability for tissue to sequester LDL from the extracellular space. Inhibting PCSK9 therefore allows for increased LDL receptor recycling and greater sequestering of LDL from blood plasma. PCSK9 inhibitors are administered subcut.
81
How do statins work?
They inhibit HMG-CoA reductase, thereby increasing the LDL receptor synthesis.
82
How does ezetemibe work?
Binds to gut NPC1L1 preventing LDL absorption.
83
What is mipomersen?
Inhibitor of apoB-100 synthesis and LDL synthesis. Used in refracory hyperlipidaemia
84
What is the normal QT interval duration for males and females?
Males < 470ms. Females <480ms.
85
Nearly all drugs that cause QT prolongation do so by blocking what channel?
The IKr potassium channel. Encoded by the KCNH2 gene - often implicated in congenital QT prolongation.
86
Regarding the onset of torsades de pointe in patient's with QT prolongation, what rhythm is likely to be seen prior to torsades onset in acquire vs congenital QT prolongation?
In patients with acquired QT prolongation, typically bradycardia with sinus pauses preceded torsade de pointe. In congenital QT prolongation, bradycardia with pauses, or adrenergic surges (emotional/physical) can preced torsades. The latter is particularly true of type 1 and to a lesser degree type 2 inherited long QT syndrome.
87
What are the risk factor for torsades in patients with drug induced prolonged QT? (apart from drugs and their additive and dose dependent impact)
Being female is the greatest risk factors. Up to 70% are female. Other risk factors include having family members with prolonged QT intervals, or having underlying structural heart disease. Hypokalaemia, hypomagnesaemia and hypocalcaemia are all risk factors.
88
What genes are implicated in congential long QT syndrome? (there are 3 types)
LQTS 1 - KCNQ1, LQTS 2 - KCNH2, and LQTS3 - SCN5A (recall that this is the gene also most commonly associated with Brugada syndrome). These 3 genes account for 80% of all congenital LQT syndrome.
89
What inheritence patterns are seen with LQTS?
Cardiac only disease is typically autosomal dominance with low penetrence. However, there are syndromic versions (Jervella and Lange-Nielsen syndrome) of LQTS that include QT prolongation and sensoroneural hearing loss.
90
How do LQTS patients present?
Most people will go their lives asymmptomatic and be diagnosed on an incidental ECG. However, a smaller portion will present with syncope, or syncope followed by a generalised seizure. Rarely, the presentation is sudden cardiac death.
91
How does pregnancy influence patients with LQTS?
The first 6-9months postpartum sees a greater risk of cardiac events. Almost exclusively an issue for women with LQT2.
92
How does menopause influence cardiac event risk in patients with LQTS?
In patients with LQT2, there is a marked increase in risk of cardiac events during menopause transition and post menopause. In contrast, patients with LQT1 have a reduced risk of events after menopause.
93
How does isoprenaline work?
Beta 1 adrenergic receptor agonist. Inotropic and chronictropic agent. Leads to increased systolic and decreased diastolic pressure. Leads to increased coronary blood flow.
94
What are the most important triggers for ventricular arrhythmias in patients with LQTS?
Exercise, and particularly swimming and diving, are associated with ventricular arrhyhtmias in patients with LQTS, particularly LQT1. Emotional triggers, loud noises, sudden wakening by an alarm clock or loud noise are all associated with ventricular arrhythmias in patients particularly with LQT2.
95
What is the most common LQTS subtype?
LQT1 (35%). then LQT2 (25-35%), then LQT3 (5-10%).
96
Which subtypes of LQTS are most likely to have experience a life threatening ventricular arrhythmia whilst asleep?
LQT2 and LQ3. Much rarer in LQT1.
97
Which subtypes of LQTS are most likely to have experience a life threatening ventricular arrhythmia whilst asleep?
LQT2 and LQ3. Much rarer in LQT1.
98
Which leads should be used to measure a QT interval?
Reference ranges are based on Leads II and V.
99
What's are U wave? What are it's normal characteristics? What can cause an abnormal U wave?
U wave is caused by delayed purkinje fibre repolarisation. Normal U wave becomes more obvious as heart rate slows down. It should go in the same direction as the T wave. The U wave voltage should be no more than 25% the size of the T-wave, and it's maximum amplitute should be 1-2mm.
Abonormal U waves are those that fall outside the above criteria (prominent) or are inverted.
Prominent U waves are seen in bradycardia, severe hypokalaemia. Sometimes hypocalcaemia, hypomagnesaemia, hypothermia, raised ICP, LVH and HoCM and some antiarrhythmics.
Inverted U waves are seen with CAD, HTN, valvular heart disease, congenital heart disease, cardiomyopathy, hyperthyroidism. If a patient has chest pain, inverted U waves are very sensitive to mycoardial ischaemia.
100
What additional testing should be done for patients after LQTS is suspected on the basis of ECG findings and history?
Exercise stress test to look for changes in T wave morphology to stratify risk of exercise associated ventricular arrythmias. Genetic testing is now standard of care as the gene involved will help define the risk of sudden cardiac death/arrest/ventricular arrhymia for the patient.
101
At a minimum, what testing needs to be done to tell a congenital LQTS patient's family member they don't have LQTS?
An ECG AND genetic testing. A normal ECG alone does not exclude LGTS.
102
What is first line treatment in patients with long QT syndrome and a history of syncope?
Beta-blocker. Specificall propanolol or nadolol - more efficacious than atenolol or metoprolol. Beta-blockers have been shown to reduce the risk of syncope and sudden cardiac death.
103
What treatment, in addition to beta-blockers should be offered to patients with LQT3?
Mexiletine. CYP2D6 genotype should be obtained along with drug levels as this drug is metabolised in a highly variable way from patient to patient based on their CYP2D6 variant.
104
What treatments should be offered to patients with LQTS and recurrent sycnope despite beta-blockade or patients with resuscitated cardiac arrest? Or assymptomatic patients with QT interval >550ms?
Left cardiac sympathic denervation and an ICD with built in single lead pacing. Sometimes LCSD is kept is a back-up after ICD insertion if ongoing ICD shocks are occuring.
105
What are the echocardiographic features of severe mitral stenosis?
Transmitral mean gradietn >10mmHg, enlarged left atrium, mitral valvular area <1.5cm, evidence of pulmonary hypertension.
106
In mixed mitral disease with symptoms and pulmonary hypertension, what is the best option for treatment?
Valve replacement. If there was just stenosis you you could to percutaneous valuloplasty with a balloon. If it was just regurg, you could do a repair.
107
For treatment resistent hypertension in patients already taking an ACEi/ARB + HCT + peripheral calcium channel blocker, what agent should be added next?
Mineralcorticoid receptor antagonist (e.g. spironolactone)
108
In what conditions is endocarditis abx prophylaxis recommended?
1) Prothetic cardiac vavles, including TAVIs. 2) Prosthetic material used for cardiac valve repair such as annuloplasty rings and chords. 3) Previous infective endocarditis. 4) Congenital heart disease if it a) involved unrepaired cyanotic defects or b) repaired defects with redisdual defects at or adjacent to the site of a prosthetic pathc or device. 5) Rheumatic heart disease.
109
For what surgical procedures should antibiotic infective endocarditis prophylaxis be considered in patients at risk of IE?
1) Dental procedures, 2) skin os MSK procedures involving infected tissue, 3) respiratory tract or ENT procedures involving infected tissue, 4) GI or GU procedures where surgical prophylaxis would be required or if there is an active infection.
110
What are the latest Jones criteria for an acute rheumatic fever diagnosis?
To make a diagnosis of acute rheumatic fever (ARF), patients must have 2 major manifestations AND evidence of a precding Strep A infection OR Sydenham chorea alone with other causes of chorea excluded OR 1 major AND 2 minor manifestations AND evidence of previous Strep A infection.
Major criteria for high risk groups:
- carditis, polyarthritis or aseptic monoarthrisis or polyarthralgia, sydenham chorea, erythema marginatum, subcutaneous nodules.
Major criteria for non-high risk groups:
-carditis, polyarthritis, sydenham chorea, erythema marginatum, subcutaneous nodules
Minor criteria for high risk groups
- fever over 38 degrees, monoarthralgia, ESR >30mm/hr or CRP >30, prolonged PR interval on ECG
Minor criteria for non-high risk groups:
- Fever over 38.5 degrees
- Polyarthralgia or aseptic monoarthritis
ESR >60mm/hr or CRP over 30
- Prolonged PR interval on ECG
To detect intercurrent or prior Strep A infection: throat swab and culture, throat strep A antigen, throat swab strep A pcr or antistreptolysin O ab or another strep A ab in serology.
111
What age group is most likley to experience acute rheumatic fever compared with rheumatic heart disease?
ARF is most common in 5-14yo children, whereas RHD is most common in adults aged 35-39.
112
What is the treament for acute rheumatic fever?
Benzathine penicillin G every 4 weeks, or every 3 weeks for high risk patients for a minimum of 10 years after the last ARF episode or until age 21 if no evidence of RHD OR til age 35-45 if moderate to severe RHD.
113
What conditions are included within the rheuamtic fever term 'carditis'?
Pericarditis, myocarditis and valvulitis.
114
What proportion of patients with ARF will go on to develop RHD?
Onc estudy in 2013 in Australia showed that within 10 years of ARF, 60% of patients had developed rheumatic heart disease.
115
Which coronary artery most often supplies the posterior descending artery?
In about 90% of patients, this it the right coronary artery. The remaineder are said to be left coronary artery dominant and the PDA branches from the LCA.
116
What complications can occur post RCA MI?
SA node involved, RA dysfunction, RV dysfunction, LV dysfunction (PDA branch).
117
What is the most common cause of sinus node dysfunction?
Age related progressive fibrosis of the sinus node and surrounding atrial myocardium.
118
How do you distinguish between takatsubo cardiomyopathy and ACS?
History will help, but no that in ~15% of patients with takutsubo, there is concurrent ACS on angiography. TTE is helpful - if there is wall motion abnormality that crosses coronary artery boundries this is suggestive of takatusubo. It is necessary to do coronary artery angiography to exlcude plaque formation. Once ACS has been exluded, diagnosis can be made on the basis of ECG abnormalities, elevated troponin levels, abscence of pheochromocytoma and absence of myocarditis (they often get an MRI if CRP/ESR are elevated).
119
What drug improves long-term survival in patients who have had takatsubo cardiomyopathy?
ACE inhibitors or ARBs
120
What are the echocardiographic subtypes of takatsubo?
Apical type (most common), midventricular type, basal type and focal type. The area mentioned in each type appears stunned on TTE and doesn't respect coronary artery territories.
121
Should TAVI or SAVR be offered to patients with asymmptomatic severe aortic stenosis?
No. No evidence for this.
122
For patients with diabetes, and left main or triple vessel disease, what is the best option for revasculation? (PCI vs CABG)
CABG
123
What are the 4 types of NSTEMI?
Type 1: secondary to acute coronary artery thrombosis with incomplete mural thickening infarction. Type 2: hypoperfusion in the setting of systemic illness leading to mismatch of cardiomyocyte O2 demand and supply. Type 3: MI resulting in death when biomarkers were not available. Type 4a: MI related to PI. Type 4b: MI related to stent thrombosis. Type 5 MI related to CABG.
124
What is the life threatening issue that occurs with Wolff-Parkinson-White patients?
If they go into to AF via their accessory pathway, it is completely unrestricted by their AV node (unlike AF in patients without WPW). This rhythm can evolve into VF and sudden death. Paroxysmal AF rates are high in WPW patients - 10-38%.
125
What is the treatment for WPW related AF with haemodynamic instability?
DC cardioversion
126
What is the treatment for WPW related AF without haemodynamic instability?
Flecainide or amiodarone would also be useful. Note that adenosine, beta-blockers and non-dihydropyridine calcium channel blockers all exert AV nodal blockade and are contraindicated in WPW related AF as they will likely make it worse by forcing current over the accessory pathway and increase the risk of VF and death.
127
Minoxidil is used to manage blood pressure. How does it work?
Smooth muscle relaxation in of arterioles by antagnosing the effect of ATP on ATP dependent potassium channels. This leaves smooth muscle cells hyperpolarised, which impairs the function of voltage-gated calcium channels and reduces intracellular calcium. Adverse effects are hirsutism, salt retention. Because of this, minoxidil is usually administerd with a loop diuretic to counter fluid/salt retention.
128
How does moxonidine work to lower blood pressure?
Impairs central control of vasoconstriction by stimulating the imidazoline recepotr in the brainstem, which in turn decreases central catecholamine synthesis. Moxonidine also has, to a lesser extent, alpha 2 receptor inhibition peripherally.
129
There are TWO ways that beta 1 blockers reduce blood pressure. How do they do this?
Slowing heart rate yes, but also they bind to beta-1 receptors in the kidney that results in decreased renin secretion!
130
How does hydralazine work to reduce blood pressure?
Interferes with inositol triphosphate's effects on the sarcoplasmic reticulum in vascular smooth muscle, decreases calcium release, causes relaxation.
131
What is Eisenmenger's syndrome?
In patients with concurrent atrial septal defects and progressive pulmonary hypertension, the gradually increasing pulmonary vasculer resistance leads to a right to left shunt forming through the ASD.
132
What are the clinical signs of Eisenmenger's syndrome?
It's all the features of right heart failure and chronic pulmonary hypertension: cyanosis, clubbing, polycythaemia, elevated JVP with dominant a wave, right ventricular heave, forth heart sound, loud P2, pulmonary ejection click, pulmonary regurgitation.
133
What are the components of the tetrology of fallot?
VSD, right ventricular outflow obstruction, overriding aorta, right ventricular hypertrophy.
134
What are the clinical features of repaired tetrology of fallot?
Cyanosis, clubbing, polycythaemia, right ventricular heave, a thril at the left sternal edge, a single seconda heart sound (A2), and short pulmonary ejection murmur on auscutlation, a A BOOT SHAPED HEART, right ventricular enlargement, decreased vascularity of lung vessels on CXR.
135
What is coarctation of the aorta?
Congenital abnormality. Associated with turner syndrome. It's basically a narrowing of the descenting aorta, it is typically located at the insertion of the ductus arteriorsis just distal to the left subclavian artery.
136
What are the typical clinical findings of coarctation of the aorta in an adult?
A better developed upper than lower body, radiofemoral delay, hypertension in the upper limbs only, mid-diastolic murmur over the precordium, hypertensive fundi changes, a small aortic knucle and rib notching on CXR. Coarctation of the aorta is associated with Turner Syndrome and with intracranial aneurysms.
137
What is the most common type of ASD?
Ostium secundum. Next is ostium primum. Note that a patent PFO doesn't count as an ASD.
138
What pulmonary condition is a contraindication to ASD closure?
PAH
139
What additional clinical signs are seen in patients who have an ostium primum ASD rather than an ostium secondum ASD?
Often have an associated mitral valve defect leading to regurgitation, and/or tricuspid valve defect leading to regurgitation, or an assocaited VSD. Ostium primum defects are often associated with Down syndrome.
140
What murmur is heard with a patent ductus arteriosus?
A continuous murmur along the left stenal border. ECG would normally show LVH.
