Cardiology Flashcards
Define an arterial aneurysm
When an artery has enlarged greater than 1.5x its expected diameter
How big does an aortic aneurysm need to be before a driver’s licence needs to be suspended in Australia?
> 5.5cm unless a vascular surgeon has approved them to have a driver’s licence.
How big does an aneurysm need to be to require surgical repair?
In men >5.5cm. In women, >5.0cm. Risk of rupture is related to diameter in an exponential relationship.
How often should a AAA be reviewed with ultrasound if it is 5.0cm?
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.
Are S3 and S4 heard in systole or diastole?
Diastole. S3 is heard just after S2, and S4 just before S1, but both aer diastolic heart sounds.
What causes S1?
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.
What causes S2?
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.
What is meant by splitting of the S2?
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.
What causes S3?
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.
What causes S4?
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.
What pathologies are are assocaited with splitting of the first heart sound?
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
What pathologies are associated with increased splitting, but still variable, second heart sound?
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.
What leads to fixed splitting of the second heart sound?
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.
What causes a loud S1?
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.
What is Ebstein anomoly?
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.
What dynamic echocardiographic heart problems are seen in patient’s with an Ebstein anomoly?
Various degrees of tricuspid regurgitation. Small remaining RV and usually dysfunctional.
What other heart defects are often seen in patients with Ebstein anomaly?
Patent foramen ovale or ASD is in up 80% of Ebstein pts. Ventricular septic defects. Patent ductus arteriosus.
Pulmonary outflow obstruction is rare.
What conduction issues are seen in patient’s wth Ebstein anomaly?
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.
How does anthracycline induced cardiotoxicity work, and what makes it more likely?
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.
What is Dexrazoxane?
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.
What are the three TTE measurements that relate tot he aortic valve that are used in clinical decision making for aortic stenosis?
- Maximum aortic velocity 2. Mean pressure gradient, and 3. Valve area
What medication post TAVI have been shown to reduce all cause mortality?
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.
At what stage of aortic stenosis should patients receive an aortic valve replacement?
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.
What defines stage D1 aortic stenosis (a stage requiring AVR)?
On dabutamine stress testing: maximum velocity >4.0m/s with a valve area of <1.0cm^2, mean pressure gradient > or = 40mmHg.
In patients with heart failure, is RBBB or LBBB associated with increased mortality risk?
LBBB
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.
What does CRT improve when implanted in patients in whom it is indicated?
Restores ventricular synchrony which improves LVEF, reduces HF symptoms, increases survival.
What age is generally considered the cut off, after which patients are considered to be unlikely to benefit from surgical AVR?
75 years old
What are the contraindications for TAVI?
Severe COPD, debilitating stroke, active malignancy, and dementia with less than 12 months survival likely.
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.
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).
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.
What are the classic ECG findings in type 2 Brugada syndrome?
> 2mm saddle shaped ST elevation in a lead of V1-V3
What are the classic ECG findings in Type 3 Brugada syndrome?
Coved or saddle ST elevation of less than 2mm in leads V1-3.
How is Brugada syndrome inherited?
Autosomal dominant with variable penetrence. It’s more common in men for some reason.
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.
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.
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).
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.
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.
What medications are known Brugada syndrome triggers?
Sodium channel blockers, beta blockers, antipsychotics, alcohol, cocaine. Extensive additional list, but these are the main groups.
What is the most common type of cardiac amyloidosis?
Transthyretin amyloidosis - hereditary and wild type. Light chain amyloidsosis is next most common.
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.
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.
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.
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.
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.
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.
Where can you biopsy to try to diagnose amyloidosis?
Abdominal fat pad, bone marrow, a clinically involved organ (e.g. kidney, heart), rectum
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.
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.
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.
Do you anticoagulate people with cholesterola emboli?
No, this makes it worse. Statins can be used and may improve outcomes.
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.
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.
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.
