MKSAP Questions Flashcards
S3: Describe and indicates?
Ventricular gallop, caused by the rush of blood in early diastole into a distended ventricle, occurs just after S2. Sign of systolic heart failure
S4: Describe and indicates?
Late diastolic sound, heard as the atria forces blood into a stiffened ventricle.
When is the most likely time for cardiac transplantation failure and what is the investigation ? When is this investigation usually performed ?
Graft failure most likely within the first 6 months, then after 12 months. Signs of heart failure occur occasionally. However, often there are no clinical signs of failure - routine endomyocardial biopsy is performed within 12 months.
How common is coronary artery disease in transplant?
Vasculopathy is present in 50% of patients by the 5 year mark.
Name risk stratification scores for ACS (STEMI/NSTEMI/UA)
TIMI score, HEART score but Australia we are now using the GRACE score - High >140 points, intermediate 100-140 points and <100 low risk.
Stratifies 3 - 6 month mortality
Name the 10 high risk features of chest pain and what does ‘high risk’ mean?
High risk is >10% risk of death/MI within 6 months: ACRONYM - HANDSOME EP Haemodynamic instability (killip class) Arrythmia (VT) New ECG changes (TWI, ST >2mm) Diaphoresis Syncope Ongoing Chest pain New Mitral Regurg EF <40% Elevated Trop Prior MI, CABG, PCI
Management of Low, intermediate and high risk ACS
LOW: Early discharge, medical therapy and cardiac review
INTER: Observe, further risk stratification ?OP investigation with provocation, reclassify
HIGH: Aggressive medical therapy, early coronary revascularisation and angiography
What is Myxomatous valve disease?
Non-inflammatory progressive disarray of the valve structure caused by a defect in the mechanical integrity of the leaflet due to the altered synthesis and/or remodeling by type VI collagen. Often leaflets can not meet due to thickening and regurgitation eventuates
When is it indicated to repair a regurgitant Mitral Valve compared with observation?
- Symptomatic patients with LVEF >30%
- Asymptomatic patients with EF 30-60% or end diastolic diameter >40mm
- Patients already undergoing another cardiac procedure.
Reasonable to consider in New AF with MR and pulm. HTN (>50 mmHg)
Serial investigations would be indicated if none of the above but ongoing MR (6-12 monthly review)
If surgery poses a prohibitive risk then a catheter based device may be considered.
Inhibition of what ‘factor’ greater increases hypertensive risk in chemotherapy agents? How does this occur (mechanism)?
VEGF inhibition (e.g. Bevacizumab) used in met. gynaecological and GI cancers can cause HTN through several mechanisms; altered nitric oxide production, increased endothelin 1 and alterations in the pressure natruesis relationship. Very common occurence - may even be related to therapeutic response. Typically 60 days post, but as early as a week.
What does cisplatin increase risk of?
Increased risk of VTE, SVT, myocardial ischemia and cardiomyopathy
Common cardiotoxicities of Paclitxel. Cardiomyopathy increases with the addition of which other medication?
Bradycardia and heart block can cause hypotension.
Doxorubicin in combination with paclitaxel can cause cardiomyopathy.
Posterior inferior rib notching is an indication of what
Collateral blood flow - potentially caused by coarctation of the aorta
What is associated in 50% of patients with coarctation of the aorta?
Bicuspid aortic valve
What is the CHADS2VASC score
Risk of stroke in patients with AF: Congestive heart failure HTN Age 65-74 = 1 pt, 75 + 2 pts Diabetes Sex - female 1 Stroke hx Vascular history (MI, peripheral disease, aortic plaque) Greater than 2 = should anticoag`
When is Warfarin indicated rather than a DOAC?
Valvular AF, metallic prosthetic valve
Signs of LVH on ECG
General ECG features include: ≥ QRS amplitude (voltage criteria; i.e., tall R-waves in LV leads, deep S-waves in RV leads) Delayed R wave peak in V6 (i.e., time from QRS onset to peak R is ≥ 0.05 sec- non voltage criteria ). Repolarisation abnormalities of ST depression.
Can add V1 S wave to taller R wave in V5 or 6 if >35mm then LVH
R wave in I and S wave in III = >25 mmHg also diagnostic
“If 1 + 6 = 7 you’ve got LVH” i.e. if V1 + V6 = 7 squares or 35 mm then LVH
Name findings that limit an ECGs interpretation
Left BBB, LVH, Pre-exitation, Ventricular pacing, digitalis effect, (PLEVL)
What is Coronary artery calcium scoring?
A number that is obtained non-invasively through CT imaging to help to stratify cardiovascular risk. A number between 100-300 indicates a moderate risk within a 5 year period. 300+ helps to stratify as higher risk.
Name the three causes of pericarditis (global groups)
Idiopathic, radiation, infectious
Interferon gamma assay helps to measure what?
Tuberculosis
Measurement of what fluid is 100% sensitive for TB in pericardial fluid?
Adenosine deaminase
How do you determine the difference between true anatomical aortic stenosis and pseudostenosis?
Dobutamine stress echocardiogram: i.e. this will help to evaluate if the low flow/cardiac output is dependant on the valve, or combination of valve and cardiac function.
In patients with heart failure and subsequent cardiogenic shock what is the most appropriate initial treatment ?
Inotropic agents and intensive care - e.g. dobutamine or milrinone. Milrinone is renally excreted so beware in AKI
Beta blockers ionotropic activity ?
Negative ionotrope and should be withheld in acute settings of shock. Even in the setting of tachycardia.
Treatment for Atrial Flutter 1st and refractory
1st line Cardioversion, anti-arrythmic agents and catheter ablation
Amiodarone toxicity concerns/features
End organ toxicity, neurological side effects such as tremor, liver dysfunction and pulmonary toxicity.
PDA (patent ductus arteriosis) murmur characterisation including progression signs/features.
L clavicle position, Envelops S2, ‘continuous’.
May have bounding pulse and wide pulse pressures.
Large PDA could have Pulm. HTN and eisenmengers
What is Cardiac X Syndrome?
Young patients with typical angina picture, abnormal stress testing but angiographically normal coronary arteries. Hypothesised to be a microvascular dysfunction that causes the same angina like symptoms. Vasodialators can be trialled
Most appropriate management of intermittent claudication first line
First line supervised exercise program with a Phosphodiesterase III inhibitor (Cilostazol - Pletal) inhibs platelet aggregation and vasodialates - if no improvement within 3 months then inhib can be stopped. This is despite there being meta-analysis showing no improvement in community walking at 3 months.
Single anti-platelet can also be used - not indicated for DAPT.
Size of AAA considered for repair
> 5.5 cm or greater than 0.5 cm per year expansion or patients with symptoms likely related to the AAA.
Open vs. endovascular AAA repair
Patients operative risk and life span need to be factored in and ability to adhere to monitoring with EVAR. Involvement of mesenteric or renal arteries is also of consideration (usually Open).
What is the highest risk factor for CVD
Untreated lipid profile. i.e. Low HDL, high triglycerides and LDL
Yearly stable heart failure review - details
EUC/renal function, functional capacity assessment and history, volume status and medication. Repeat echo only recommended if clinical change or alteration of mediation
Name two markers of myocardial fibrosis
Soluable ST2 and Galectin 3
Management of WPW outpatient
Eletrophysiology study as first line, Echo should also be obtained to ensure structurally normal heart. This would likely lead to an ablation
Marfan Syndrome aortic root size classifications pregnancy
4.5 cm recommended operation prior preg due to risk of aortic disection. 4-4.5 may require 6 months of observation and observed stability. Smaller than 4 cm considered safe.
Features of a cardiac fibroelastoma
small (12mm x 9mm average), mobile, attached to endocardium by a stalk. More common left sided.
Atrial myxoma features
large and often associated with obstructive features (10-15%). 75% of cases the tumour arises from the fosa ovalis of the left atrium.
Features of non-bacterial thrombotic endocarditis
caused by endothelial injury in the presence of hypercoagulable state. Vegetations are typically wart like, irregular, flat and most commonly associated with advanced malignancy.
Common association with eisenmenger syndrome that may improve quality of life
iron deficiency
Outline the PCI pathway in ACS
First question of ?Is PCI available within 120 mins of presentation? if yes–> PCI. If not, then a pharmacoinvasive treatment approach is taken to deliver pharmacological thrombolysis prior to rescue PCI in an available centre.
What is the score used to assess PVD and what scores are significant ?
Ankle - brachial index: i.e. ankle pressure/brachial. If >1.4 then signifies a calcified, un-interpretable result. Toe - brachial index then indicated. Toe pressure below 40 mmHg is diagnostic or ratio <0.7.
Otherwise with the ABI: 1 -1.4 normal, .9-1 borderline .4-.9 mild/moderate, 0-0.4 severe.
When would you use exercise ABI (ankle-Brachial index) ?
Exercise ABI if patients have borderline ABI 0.9-1 with high risk of PAD. Post exercise decrease of more than 20% in pressure is diagnostic.
Modified Duke criteria use and list score
For endocarditis diagnosis: need 2 major, 1 major and 3 minor or 5 minor
2 major and 5 minor are :
1. BC postitive for IE organisms
2. Evidence of endocardial involvement (echo showing vegetations, mass, new valvular regurgitation, abscess)
Minor:
Predisposition (IVDU, heart condition etc. )
Fever
Valvular phenomena (emboli, infarcts)
Immunologica phenomena (GN, oslers nodes, rheumatoid factor)
Microbiological evidence: positive BCs that dont meet major criteria
List Endocarditis organisms
HACEKES + C Hemophillus spp. Acitinobacter actinomycemcometanis Cardiobacterium hominis Eikenella spp. Kingella kingae Staph. aureus enterococci spp. \+ Coxiella Burnetti with IgG titre >1:800
Cultures must be 12 hours apart or 3/4 cultures drawn within an hour.
Surgical indications for Endocarditis surgery
- symptomatic heart failure and valvular dysfunction
- left sided IE with fungal infection and resistant organisms
- Complications such as abscess
- Heart block
- Bacteraemia persisting beyond 5-7 days despite abx.
How to risk stratify patients with CV risk
Pooled cohort equations are available to stratify common risk factors. A result of less than 5% ASCVD (atherosclerotic cardiovascular disease) is considered low risk, 5 -7.5 intermediate and 7.5 or higher is hgih risk.
However there are non typical risk factors that are not included in the scoring system eg. HIV 1.5 -2 x higher risk of ASCVD.
Investigation of choice for intermediate risk patient with stable angina.
Exercise ECG - functional testing
Three beta-blockers that have been shown to be effective in treatment of HFrEF
Metoprolol succinate, carvedilol and bisoprolol.
If maximal dose Beta blocker given to patient with HFrEF- what else can be added to reduce HR (assuming otherwise maximal medical therapy)
ivabradine: phosphodiesterase inhibitor
Given if HR >77 at rest
Criteria for Cardiac resynchronisation therapy in heart failure?
LVEF <35%, class II-IV symptoms, guideline directed medical therapy failure (90 days), sinus rhythm, LBBB and QRS>150 ms
Cornerstone features of restrictive CM
elevated BNP (>400 typically), pulmonary HTN, DGE on CMRI and simultaneous rise and fall or R and L ventricular pressures with respiration (lack of ventricular interdependance).
Fabry’s disease define and cardiac features
lysosomal storage disorder: manifestations begin in childhood.
FABRY C
Fever, foam cells
Alpha galactosidase A deficiency and Angiokeratomas
Boys and Burning pain (neuropathic pain)
Renal failure
YX (X linked recessive)
Ceramide trihexoside accumulation and CVD
Two types of Aortic dissection and their management
Type A: ascending aortic dissection/involving aortic root
Type B: distal to left subclavian artery
If any type A, haemodynamic compromise, intramural haematoma or ulceration then immediate surgery is warranted.
Type B : manage HTN with IV Beta blockers and second line sodium nitropusside if not resolving to beta blockers.
Which two medications increase risk of pericardial effusion?
Minoxidil and hydralazine
Which medication commonly started post STEMI has a common side effect of dyspnoea?
Ticagralor. P2Y12 inhibitor . expected in 15 -20% of patients.
Typical presentation of an ischemic VSD
Post ischemic event involving septum, 3-5 days post - pan systolic murmur . Heart failure and shock.
Takotsubos CM: describe typical case
older female, stressful or emotional event. Typically apical ballooning of the heart. Typically normal or near normal coronaries. Causes reversible systolic dysfunction.
Favourable features for intervention in Pulmonary stenosis and name intervention
balloon valvuloplasty. Favourable features of peak gradient greater than 50mmHg or mean gradient greater than 30 mmHg. If there is co-existing regurgitation then likely to need replacement. Also may need surgery with small annulus, severe subvalvular or supravalvular stenosis or another cardiac lesions requiring surgery.
What should be avoided in cardiac testing in patients with reactive airways disease? and when is it useful?
Adenosine, Dipyridamole - useful in the setting of stress testing with LBBB
Safest BP agents in pregnancy
methyldopa and labetalol
Indications for mitral valve replacement
- symptomatic patients with a LVEF >30%
- asymptomatic patients with a LVEF 30-60% and/or a LV end diastolic diameter >40mm
- patient undergoing another cardiac surgical procedure
Most common cause of sudden cardiac death in athletes
HCM (hypertrophic)
Risk factors for SCD and hence an indication to implant ICD in HCM patients
- massive myocardial hypertrophy
- previous cardiac arrest due to ventricular arrythmia
- blunted blood pressure response or hypotension during exercise
- unexplained syncope
- Nonsustained VT
- Family hx of SCD + HCM
Diagnosis of patient with PEA 3 days post anterior STEMI
Left ventricular free wall rupture
Right sided heart failure + fever + elevated inflammatory markers + ventricular interdependence + recent surgery/intervention + low BNP (around 100)
Constrictive pericarditis
Medical treatment of constrictive pericarditis
NSAID + colchicine
Cornerstone of HFpEF therapy
Maintaining euvolaemia – i.e. diuretics, fluid restrictions if required
Indication for ivabradine
HR >70, HFrEF, already on beta blocker
Elevated central pressure + right heart failure + pAF + mid systolic murmur
ASD
Most common ASD
Ostium Secundum
‘fixed splitting of the S2’
ASD
Fixed splitting of S2 + mitral regurgitation + LAD on ECG
Ostium priumium ASD all other ASDs are unlikely to cause mitral issues, they usually cause 1st deg HB and typically a Right bundle
Score used to help dictate statin therapy in middle aged patients
Pooled cohort equation for 10 year risk ASCVD (atherosclerotic cardiovascular disease) used in patients 40-75
Anticoagulation requirement for patient with new mechanical heart valve
Warfarin + aspirin for at least 3 months as long as 6, then warfarin lifelong
Antithrombotic for bioprosthetic valve
Aspirin life long
Target INR for aortic vs. mitral mechanical valve
2.5 aortic and 3 mitral
Split S2 and its correlation with ECG
Typically with a RBBB
Pattern with aberrant conduction AF and appropriate treatment if stable
Irregularly irregular pattern with wide complex tachycardia and RBBB. Treatment with beta blocker and anticoagulation
CABG indications
Significant Left main or bifurcation disease, Triple vessel disease
Common complication of LVAD
Stroke – 20 %
Which kind of murmurs decrease on standing?
Benign flow murmurs
Paradoxical splitting of the S2 (what does it mean and what does it indicate)
Splitting of S2 during expiration, delay in LV emptying, aortic stenosis
Duration of DAPT for DES post stable angina
6 months – aspirin plus a P2Y12 inhibitor
BMS duration of DAPT for stable angina
1 month
Duration of DAPT following intervention for acute coronary syndrome
12 months
Treatment of atrial myxoma
Surgical removal
Atrial myxomas produce what in order to generate constitutional symptoms (fatigue etc. )
Interleukin 6
Inheritance of Noonans syndrome and association
Autosomal dominant associate with congential cardiac lesions – primarily pulmonary stenosis and HCM. Low set ears, deep philtrum and webbed neck. Heterogenous inheritance – predominant PTPN11 (Protein tyrosine phosphatase)
Downs syndrome – Inheritance and cardiac predisposition
Trisomy 21 caused by a non-disjunction. Predominantly it is inherited from the mother (88%). AVSD is common and congenital cardiac disease of some form in 40%. Ostium Primuim is also common (ASD)
Marfan syndrome – inheritance and cardiac predisposition
Autosomal dominant, mutations on the FBN1 gene on Chromosome 15 which enodes fibrin 1 (i.e. marfan syndrome is a connective tissue genetic disorder). Common is aortic sinus dilatation with a propensity to dissection. Left sided heart valves also are prone to early degredation and prolapse.
Turners syndrome – inheritance and cardiac predisposition
Absence of X chromosome (only affects women) Low hair line, webbed neck. Aortic valve abnormalities/bicuspidvalve, aortic aneurysm and coarctation of the aorta are the classic cardiac manifestations.
Cardiomyopathy (NYHA II-III) + HFrEF + syncope = what intervention
ICD to decrease risk of SCD
Severity on echocardiogram of AS by measurements of pressure gradient and valve area
Mild (<25 mmHG mean gradient and >1.5 cm2) Moderate (25-40 and 1-1.5) Severe >40 and <1) Very severe (>70 and <0.6) normal valve area of 3cm2
Mital stenosis severity by size and pressure
Progressive (<5 mmHg mean gradient and mitral area >1.5) Severe (5-10 mmHg and 1-1.5) Very severe (>10 and <1) normal valve area of 5cm2
Mitral regurgitation fraction and classification
<20% mild, 20-40 moderate, 40-60 moderate to severe, greater than 60 severe with regurg. Orifice >0.4
Medical therapy for mitral stenosis
Diuretics and long acting nitrites. Beta blockers and CCBs (non-dihydropyridine) can help slow heart rate and improve left ventricular diastolic filling time.
Indications with withhold beta blocker during STEMI
Cardiogenic shock
Indications to withhold nitroglycerin in STEMI
shock (BP<90), bradycardia or tachycardia, RV infarction, or use of a phosphodiesterase inhibitor such as sildenafil in the past 24 to 48 hours.
Indications for aortic root replacement in bicuspid aortic valve
Root >5.5 cms or >5cm but increased by 0.5 or more in a year. Annual surveillance required for smaller 4.5 and 4.5 – 5.5 6 monthly.
Hx for peripartum CM and treatment
LV systolic dysfunction with onset toward the end of pregnancy or post delivery. Beta blockers, digoxin, hydralazine, nitrates or diuretics depending on symptoms. AVOID ACE, ARBs, aldosterone agonists (teratogenic) unless post partum.
Ix for presyncope and palpitations that occur every one to two weeks
event recorder – i.e. to map symptom/rhythm correlation
Ix for patient with symptoms occurring every month to two monthly
Implantable loop recorders to evaluate infrequent arrhythmias
BNP general range for heart failure
Less than 100 nearly excludes diagnosis, greater than 400 typically supports the diagnosis
Why is it important to differentiate mobitz I to mobitz 2 and what are they
Mobitz 1- progressive lengthening on PR interval before dopping QRS – reverse whatever may be causing it and no need for PPM. Mobitz 2 – fixed PR interval with occasional unconducted P waves. This has a high propencity to continue to complete heart block
Indications for valve replacement in severe aortic regurgitation
Presence of symptoms attributable to regurgitation, LVEF <50% or another indication for cardiac surgery (e.g. CABG) also can be beneficial in patients with ventricular dilatation (end systolic dimension >50mm or indexed end systolic dilatation >25 mm/m2)
If severe symptoms without these criteria surveillance every 6-12 months is required.
Post STEMI with heart failure complicating – first choice medical therapy
ACE or ARB
Beta blockers should also be implemented within first 24 hours unless evidence of cardiogenic shock. Calcium channel blockers, like beta blockers, are negative chronotropic and inotropic agents.
How to risk stratify a patient with HCM + AF and what is best management?
Warfarin anticoagulation (2-3) is required given the large risk of thromboembolic events. DOACs haven’t been tested. CHADS2VASC does not take HCM into account – therefore, can not be used as a risk stratifier
What investigation aids in the diagnosis of valvular heart disease and guides surgical management? When would it be used instead of echo?
Echo is always first line. However, cardiac catheterization would be used to help guide surgical management, in particular, when symptoms do not marry up with echo reports. I.e. exertional dyspnoea, murmur, carotid tardis and ‘moderate stenosis’ it is valuable to perform a cath.
Management of small VSD
Surveillance 3-5 years with echocardiogram
Most common type of VSD
Perimembranous (80%)
What type of cardiac abnormality would be imaged with a CMRI?
Membranous VSD
Duration of endocarditis prophylaxis in patients with repaired cyanotic heart condition (prosthetic material)
6 months post procedure
Common cardiac manifestation seen in patients with SLE
Pericardits (40%) and occasionally associated with neutrophilic pericardiac effusion
Next most appropriate investigation in a patient at intermediate risk of cardiac disease and risk factors who is asymptomatic
Coronary artery calcium scoring
CAC score >300 meaning and other factors that may result in the same result
stratifies as high risk. LCL >4.14, genetic hyperlipidaemias, premature CAD, ABI <0.9
HFrEF calcium channel blockers – when to use and which to use
Only for use for control of hypertension despite use of ACE, B blocker and aldosterone agonist. Amlodipine and felodipine are able to be used but non-dihydropyridine CCBs are associated with worse outcomes.
Cut off for use of spironolactone
reatinine of less than 220 in men and 175 in women due to risk of hyperkalaemia
First line revascularization therapy for Multivessel disease and diabetes
CABG
Indications for CABG
Multivessel disease and left ventricular dysfunction, diabetes and MVD
Thersehold for intervention for PVCs
Premature ventricular contractions >10,000 per day or >10% of beats if monomorphic.
Common outcome for patients with frequent PVCs, investigation, management
1/3rd of patients will go on to develop PVC induced cardiomyopathy. Important to investigate with Echo or CMRI to evaluate contractility and structural heart disease. Managemtn 1st line is Beta blockers and CCBs. If refractory, young or progressive LV failure catheter ablation
Acute infarct + 3 days down the tract developing new pulmonary oedema
Mitral regurgitation from papillary muscle rupture post inferior MI
Indications for commencing secondary prevention for ASCVD
Atherosclerotic cardiac disease includes: Peripheral artery disease, acute coronary syndrome, angina, previous revascularization, stroke including TIA
Indication and class of Evolocumab
PCSK9 (proprotein convertase) – decrease LDL levels in patinets on max station, with familial hyperchol or established ASCVD
Treatment of end stage heart failure and crtiteria for transplantation
LV assist devices can be used to increase survival, however are also associated with complications (GI bleeding, infection etc. ). For cardiac transplantation, patient must be of good compliance, suitable age ?<70, no end-organ dysfunction from diabetes, no active malignancy for 5 years, no kidney dysfunction and low burden of chronic disaease
Most common disorder post TOF repair
Pulmonary regurgitation
Clinical findings of right heart volume overload
parasternal lift/heave, soft systolic outflow murmur, split S2 (unless regurgitant pulmonary valve)
AAA less than 4 cm chance of rupture per year and surveillance plan
2%, 24-36 month
AAA 4-5cm chance of rupture per year and surveillance plan
3-12 %6-12 monthly USS
Indication for AAA repair
> 5.5 cm, symptoms resulting from AAA, AAA increasing by >0.5 cm per year
New AV block or 1st degree heart block in the setting of IE ?cause and most appropriate investigation
potential aortic root abscess/ periaortic abscess. Requires TOE
Indications for PCI with stable angina
refractory angina symptoms while receiving optimal medical therapy, unable to tolerate medical therapy due to contraindications, or high risk features on non-invasive testing
Most appropriate anticoagulant during pregnancy with mechanical valve
Warfarin when dose does not exceed 5 mg. In patients who prefer to not take during the 1st trimester, IV dose adjusted unfractionated heparin, dose-adjusted low molecular weight heparin subcut is also appropriate.
Definition of sustained VT
> 30 secs or requires termination due to haemodynamic collapse
Common QT prolonging antibiotics
Macrolides and fluroquinolones
Indication for aortic r valve replacement in asymptomatic patient
severe regurgitation with dilatation of LV or systolic dysfunction (high risk of SCD). End systolic diameter of 50mm or greater, less than 50% EF
Inheritability of HCM
Autosomal dominant – all first degree relatives of patients with gene mutation require testing and assessment regardless of symptoms
How to best evaluate CVD in patient with baseline LBBB
Adenosine or vasodialator CT : the ST segments are unreliable due to LBBB, therefor exercise echo or dobutamine can not be relied upon. Instead, with dilatation, hyperaemia will show a clinically relevant stenosis (i.e. will not be able to dilate)
Antiplatelet management post NSTEMI without PCI
12 months of aspirin and P2Y12 inhibitor
PLATO trial showing ticagralor to be superior to clopidogrel
Prasugrel is recommended if the patient undergoes PCI but is no more effective than clopidogrel in the setting of medically managed ACS.
Pericardial thickening, fibrosis, R heart failure post virus or chest irradiation
Constrictive pericarditis
Best test for outpatient evaluation of cryptogenic stroke
30 day non-invasive ECG monitoring has a 5 fold increase on detecting AF than 24-48 hour monitoring.
Emergent management of acute exacerbation of heart failure
Intravenous diuretic
Medication given for symptomatic PAD to improve symptoms and walking distance. When are these medications contraindicated?
Phosphodiesterase inhibitors (cilostazol, milrinone) when combined with a vasodialator and anti-platelet agents. Black box warning on their use with heart failure.
Treatment for patient with narrow complex tachycardia and clinically stable e.g. WPW with orthodromic AVRT
Adenosine - Patient with SVT. Very short half life (6 seconds). It is contraindicated in patients with AF with antidromic tachycardia - this will present with a widened QRS duration >120 ms due to an accessory pathway conduction
Elevated right heart pressure, concentric wall thickening, preserved systolic function and pulmonary HTN. Low voltage QRS
Cardiac amyloid. Occasionally caused by mutation in transthyretin. Monoclonal gamopathy is occasionally seen in immunoglobulin light chain amyloid. Endomyocardial biopsy is more sensitive than abdominal fat biopsy.
Association between bicuspid aortic valve and coarctation
50% of patients with coarctation of the aorta will also have a bicuspid aortic valve.
Titration guide to beta blockers in heart failure
maximal dose beta blocker has been shown to decrease mortality in heart failure. Important to consider volume status before up-titrating. Goal is 2-4 weekly up-titration and only when euvolaemic. Target HR 60
CYP3A4 interactions in patient with angina
non-dihydropyridine CCB and ranolozine (decresaes late sodium current and wall tension) -
Ketoconazole, clarithromycin and ritinovir are strong inhibitors and CCBs are mild -
likewise CCBs and atorvastatin may also result in increased levels (i.e. atorvastatin is a substrate of CYP3A4)
How to identify fascicular blocks in LBBB
L posterior: Negative QRS lead 1, postitive in aVF. L anterior positive QRS in lead 1 and negative in aVF with LBBB pattern.
Indications for ASD closure
R heart enlargement and symptoms. Platypnea-orthodexia and befotre pacemaker are also reasonable due to the risk of systemic thromboembolism
Types of AF
Paroxysmal: spontaneous onset duration <7 days before returning to sinus
Persistant 7 days to 12 months
Long standing >12 months
Permanent - decision at this stage to rate control rather than rhythm control.
Percentage risk of stroke per year in AF
4-5%, this is higher in valvular AF and those with mechanical valves
RELY trial: findings?
Dabigatran 150mg BD was more effective than Warfarin and 110mg BD was equivalent in the prevention of stroke. Dabigatran 110mg had lower rates of bleeding - 150mg was equivalent.
Dabigatran 150mg had a higher rate of GI bleedin
Warfarin had a higher rate of intracranial bleed
Rocket trail findings
Rivaroxaban was non-inferior to warfarin and there was no difference in terms of major bleeding
ARISTOTLE trial
Apixaban vs. warfarin: Apixaban was non-inferior and lowered rates of bleeding. Lower all cause mortality compared with warfarin
Cardioversion rules in AF
Less than 48 hours can proceed direct to DC cardioversion, if stable and >48 hours - anticoagulate for 3 weeks, cardiovert then 4 weeks post anticoag too. If haemodynamic compromise then TOE to exclude thrombus, cardiovert and anticoag for 4 weeks post.
If drastically unstable with heart failure, hypotension, angina) then DC cardioversion can be performed
Flecanide method of action
Class 1C antiarrythmic acting on sodium channels. Good for acute onset AF 2mg/kg over 10 mins - do not use in structural heart disease.
Amiodarone method of action and half life
Class I, II, III and IV properties cardioversion occurs slowly over the course of hours. Half life of 58 days.
Significant amount of side effects: nausea, vomiting, heart block, thyroid, hepatic, pneumonitis, fibrosis, optic neuritis, tremor, ataxia
Sotalol method of action
Class II and III - beta blocker and potassium channel blocker (phase 3 rapid K channels) not used for acute cardioversion. Highly useful in the setting of ventricular based tachycardias and reduced ejection fraction where an ICD is contraindicated due to surgical risk.
Choice of DCR agent in severe structural heart disease
Amiodarone
Most effective medication in sustaining sinus rhythm post DCR
amiodarone - but significant side effects
Vagally mediated AF treatment (i.e. fit male with night time AF)
Disopyramide
Adrenergically based AF i.e. during exercise
Beta blocker, 2nd sotalol and third amidarone
Pharmacological DCR in structurally abnoraml hearts or HFrEF
dofetilide or lesser degree amidarone
AFFIRM STUDY
no difference between rate of rhythm control in patients with AF.
If symptomatic –> rhythm
If long term –> go rate
short term young –> rhythm
Most common mechanism of flutter
macro re-entry circuit around the tricuspid annulus
General guide to stroke risk despite anticoag with CHADSVASC
2 or lower <1%
4/5 = 2%
7 = 4%
8-9 = 6%
HASBLED score
HTN Abnormal renal or hepatic function Stroke Bleeding hx. labile INRS Elderly Drugs
Unconscious patient, long QRS, dilated pupils –> dx.
?Tricyclic overdose (amitryptyline) - anticholinergic effects . Blocks pre-synaptic neurotransmitter i.e. affecting sodium channels in Phase 0 of cardiac cycle.
Sgarbossas criteria
Identifying infarct in patients with LBBB or pacing:
- Greater than 5 mm disconcordant rise in ST segment with LBBB
- Or Greater than 1 mm concordant rise in ST segment
- Or greater than 1 mm of concordance in the negative direction in right sided leads i.e. V1-3.
Mainstay of therapy for LQTc
Beta blockers, cardiac pacing and implantable defib.
Treatment of hyperkalaemia with life threatening cardiac arrythmia
calcium gluconate 10% in 10ml IV over 2-3 mins or calcium chloride IV
Metabolic acidosis with hyperkalaemia and volume depletion
8.4% sodium bicarb. 50 ml IV over 5-10 mins
+ IV insulin 10 units bolus + glucose 10% 250ml over 15 mins or glucose 50% 50ml over 10 mins
BRUGADA algorithm
In order of decreasing specificity but increasing sensitivity
Absence of RS complex in precordial leads –> yes? suggests VT
R-S interval >100 ms in one precordial lead?
AV dissociation
Morphology criteria for VT present both in precordial leads and V6
Indications for ICD
- Patients with prior AMI (at least 40 days ago) and LVEF <30%
- Patients with cardiomyopathy NYHA II-III and LVEF <35%. (note patients with non-ischaemic cardiomyopathy require a trial of optimal medical therapy for at least 3 months)
- Patients as above with QRS >150 would also be candidates for biventricular pacing
- Patients with syncope who have structural heart disease and inducible sustained VT or VT going on VF on EP study
- Select patients with underlying disorders who are deemed at high risk for life threatening VT/VF (congenital long CT, Brugada, ARVC)
Wellens Syndromes
Biphasic T wave in V2, Deeply inverted T wave in V1-4,
Stable WPW patient with runs of tachyarrythmia
flecanide
Brugadas sign
RBBB pattern, downsloping ST elevation (J wave) followed by a negative T wave
Classes of antiarrythmics and how they act
Class 1 = sodium channel blockade Class 2 = Beta sympathetic activity Class 3 = Potassium channel blockage Class 4 = Calcium channel blockage Class 5 are miscellaneous
Dx when PR <0.12seconds but no delta wave
Lown-gangong-levin syndrome
Drugs to avoid in Torsades
Class Ia, Ic and III(Quinidine, flecanide, amiodarone, sotalol)
When does Ischemic heart disease become highest possibility of sudden cardiac death compared with congenital causes?
40
Features of Arrythmogenic right ventricular dysplasia ECG
Epsilon wave V1-3, TWI V2-3, prolonged QRS in V1-3, incomplete or complete RBBB.
Normal myocardium is replaced with fibro-fatty tissue. Caused by genetically defective desmosomes i.e. cell cell adhesive structures.
Catecholeminergic Polymorphic ventricular tachycardias
Classic feature is bidirectional VT, there is no structural change to the heart. Rest ECG normal. Typically appears with issues during sport. Autosomal dominant
Dextrocardia vs. limb lead reversal on ECG
Pericordial leads will be normal in limb lead reversal.
OTherwise very similar. Right axis, +ve aVR and negative lead 1.
Hydralazine method of action
arteriolar vasodilatation
Nifedipine method of action
Calcium channel blocker (voltage gated) leading to reduced contractility
Nitroglycerine method of action
Exogenous nitric oxide which leads to muscle relaxation predominantly veins –> leads to pooling and decreased pre-load
Prazocin method of action
Alpha blocker leads to vasoconstriction of smooth muscle
Clopidogrel method of action
inhibits binding of ADP to P2Y12 receptor and subsequent activation of the glycoprotein complex.
Three absolute contraindications to anticoagulation
active bleeding, severe bleeding diathesis or platelet count <20,000 m3 (i.e. 20 on australian testing) , neurosurg, occular bleeding or intracranial bleeding in past 10 days.
Mechanism of action dihydropyridine CCBs and BONUS which is selective for cerebral vasculature
reduction in vascular smooth muscle tone via L type calcium channels (peripheral rather than myocardial)
Nimodipine for SAH
Mechanism of action non-dihydropyridine CCBs
Act on Cardiac and arteriolar smooth muscle reducing contractility and heart rate. Contraindicated in Heart Failure
Mechanism of action of digoxin
Blocks the Sodium-potassium ATPase increasing intracellular sodium and calcium which in turn increases contractility (positive ionotropic effect) - subsequent negative chronotropic effect as there is increased extracellular K i.e. lowers the resting membrane potential
Age and renal function determine the half life–> anephric 3.5 -5 days otherwise around 24 hours.
Measurement of digoxin in acute toxicity and ECG finding
on presentation - at 6 hours, then 2-4 hourly until <6.4 in acute- chronic every 6-12 hours
DIG LEVELS DO NOT NECESSARILY CORRELATE WITH TOXICITY
Classically a atrial tachycardia with AV block. Digitalis i.e. reverse tick is only seen in chronic dig toxicity.
Management of symptomatic bradycardia
IV atropine - antimuscarinic i.e. inhibits the parasympathetic nervous system
Antidote to digoxin
digibind aka FAB fragments
Once administered the Digoxin level become UNRELIABLE due to it measuring bound and unbound dig.
NSAID of choice in cardiac disease
non-selective NSAID –> Naproxen (Naprosyn)
Drugs which increase plasma renin levels
Diuretics (spiranolactone), dihydropyridine CCBS, ACE/ARBs
Drugs which decresae plasma renin levels
Beta-blockers, Clonidine, methydopa, NSAIDs
Flecanide monitoring requirement
Post commencement (i.e. first two weeks) need to monitor UECs due to accumulation in renal disease and also hyponatraemia especially with thiazides
Dosing of nitrates specifically long acting
Important to have a nitrate free period due to the risk of tachyphylaxis. Half life of 4-5 hours, therefor normally dosed in morning and afternoon
Carvidolol MOA
Beta1-2 and alpha 1 antagonist
Anti-dote in beta blocker overdose
Glucagon: receptors within the heart which have been found to have postitive ionotropic and choronotropic effects
No-ACS but intervention with DES in patient with AF- post op anticoagulation
NOAC + Clopidogrel or warfarin + clopidogrel. PIONEER and WOEST studys showing triple therapy to have significantly higher rates of bleeding
PCSK9 inhibition and use
Used in patients with known history of stroke of IHD. Reduction in MI and Stroke but no change to all cause mortality.
Reduces LDL levels and receptors
Metraminol and Noradrenaline MOA
Alpha agonism with vasoconstriction
Ivabridine MOA
Blocks HCN4 channel pore inhibiting inward cation movement at the SA node.
• inhibits hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels (f-channels) within SA node
o Results in disruption of ion current flow prolongs depolarisation, slows firing in SA node and reduced HR
Antithrombotic therapy with AF after ACS with medical management
Stratify in high or low risk of bleeding
Low risk: triple therapy 6 months, dual therapy 12 months life long OAC
High risk: triple therapy one month follwed by additional 11 months of antiplatelet + warfarin
This is also the regime for low risk bleeders in patients who received PCI
High risk patients post PCI Triple one month, then Dual up to 6 months, then OAC long term
PRAMI trial and the CvLPRIT trial
Treatment of non-culprit lesions during index admission or STEMI PCI reduces cardiac death, refractory angina and cardiac death. Greatest benefit in people with diabetes, multi-vessel disease and left main disease
Thromboaspiration in STEMI
Doesn’t change outcome, doesn’t decrease infarct size
ORBITA trial
No difference in exercise tollerance between Stable angina patients undergoing PCI vs. those who are medically managed.
Was under powered and also much different baseline exercise.
The wash up –> Must have physilogical proof of ischemia prior to intervention in patients with stable angina
GRACE score and mortality following ACS depending on early or delayed intervention
No difference in treatment of ACS early or delayed, except those with high GRACE score
Most common coronary artery involved in aortic disection
Right coronary
Risk stratification of invasive surgery post PCI
BARE METAL: Less than 6 weeks post PCI--> high risk Greater than 6 weeks -->Lower risk DRUG ELUDING: >1year with no risk factors --> lower risk >1 year with RF --> high risk <1 year --> high risk RISK FACTORS: Clinical and anatomical: prev. thrombosis of stent, old, ACS previously, diabetes, heart failure, renal disease. Small stent (3mm), long stent (18mm), multiple stents, bifurcation stent, left main stent, ostial stent
TRANSFER AMI
transfer to PCI center within 6 hours of commencing thrombolysis
Kussmal’s sign
paradoxical rise in JVP on inspiration may be present in pericarditis or RV infarction
Management of STEMI depending on time of onset
Symptoms <1hr prior to arrival and PCI within 1 hour available –> PCI, if no –> fibronolysis
Symptom onset 1-3 hours prior –> PCI available within 90 mins, PCI, not–> lysis
Symptoms 3-12 hours –> PCI within 90 mins onsite or offsite within 120 mins –> PCI if not, lysis
Lipid goals in patients
Community: LDL,2 mmol/l and HDL >1
High risk patients: LDL <1.8 and HDL >1
ECG features for arrythmogenic right ventricular dysplasia
Autosomal dominant, epsilon waves, prolonged QRS in V1-3, prolonged S wave up-stroke and TWI in V1-3
Atrial flutter
Originates from the right atrium as a macro-re-entry circuit
WOEST/PIONEER trials re. AF
If significant bleeding >6 months post PCI then can have de-escalated anti-coag. Aspirin ceased in preference to clopidogrel.
Patients who are very high risk of bleeding with DES can have dual therapy with non-inferior outcomes
Most common valvular pathology in RHD
mitral stenosis
Prophylaxis in RHD
Minimum 10 years or until 21, whichever is longer. If moderate disease then to continue to 35, if severe then to 40.
Criteria for acutre rheumatic fever
2 major or 1 + 1
FEAR CRECN
Minor= FEAR fever, elevated inflam. markers, arthralgia and pR prolongation, CNS involvement (sydenham chorea), nodules (subcutaenous)
Major = Carditis, Rthritis (arthritis), erythema marginatum
adit. mimicry of strep M protein, glucosamine and myosin is thought to cause the carditis
Most common genetic pre-disposition for DCM
Titin-trancating variants within the TTN gene
Medical management of HCM
Beta blockers: improve symptoms, reduce LVOT gradient and preserve LV function. Non-dihydropyridine CCBs likewise Disopyramide - class 1a anti-arrythmic, negative inotrope, but improves symptoms in HOCM
Surgical management of HCM
Septal myomectomy –> NYHA III or IV, resting or provoked LVOT gradient >50mmHg, recurrent syncope
BiV pacing is only ever indicated if invasive procedures are contraindicated
Indications for AICD
o Survived cardiac arrest due to VT or VF
o Spontaneous sustained VT causing syncope or haemodynamic compromise (life expectancy greater than 1 year)
o Estimated 5-year risk of sudden cardiac death >6% and a life expectancy >1 year
♣ Age
♣ Non-sustained VT
♣ Maximum LV wall thickness >30mm
♣ Family history of sudden cardiac death at a young age
♣ Syncope
♣ Left atrial size
♣ LVOTO
♣ Exercise blood pressure response
o Not recommended for insertion <40 days post-MI
• LV wall thickness >30mm greatest indication for ICD insertion in HCM
• Indications for biventricular pacemaker-defibrillator
o NYHA class III or IV heart failure
o EF <35%
o QRS width >130msec +/- LBBB
Valvular manifestation in HCM
MR
Mutation responsible for autosomal dominant HCM
cardiac myosin binding protein c
JVP rising with inspiration + R wave progression + increased ratio of early diastolic filling-to-atrial filling
restrictive cardiomyopathy
Features suggestive of heart failure on echocardiogram
o Diastolic heart failure E/A ratio of <1
♣ E/A ratio refers to velocity of flow across MV. Decreases with increased resistance (reduced relaxation of ventricle)
o Systolic heart failure decreased fractional shortening : fractional shortening refers to the decrease in size of the ventricle after systole i.e. end systolic volume vs end diastolic volume.
Aortic stenosis grading: Velocity, mean gradient and valve size
velocity: Normal 2, mild <3, moderate 3-4, severe >4
Mean gradient: Normal <5,mild <25, moderate 25-40 severe >40
Valve size Normal 3-4, mild >1.5, moderate 1-1.5, severe <1
When is TAVI contraindicated
bicuspid aortic valves
Contraindications to balloon mitral valvulotomy
o Mitral valve area >1.5cm2
o Left atrial thrombus
o Moderate/severe MR
o Severe or bicommisural calcification
o Absence of commissural fusion
o Severe concomitant aortic valve disease or severe combined TS/TR
o Concomitant CAD requiring bypass surgery
Raised JVP that falls with respiration, and has blunted y-descent
Cardiac Tamponade
Canon-a waves
complete heart block
Cardiac myocyte in heart failure in the elderly
increased sarcoplasmic reticulum cyclic AMP
JVP wave forms
o A wave atrial contraction
♣ Elevated if atrial pressure elevated (e.g. TS, PS, pulmonary hypertension)
♣ Absent in AF
♣ Cannon ‘a’ waves caused by atrial contractions against closed tricuspid valve (complete heart block, VT, ventricular ectopics, nodal rhythm, single chamber ventricular pacing)
o C wave closure of tricuspid valve (nor normally visible)
o X descent fall in atrial pressure during ventricular systole
o V wave due to passive filling of blood into the atrium against a closed tricuspid valve
♣ Giant v waves in tricuspid regurgitation
o Y descent opening of tricuspid valve
What physiologcally occurs during muscle contraction
• Muscle contraction is associated with release of calcium by sarcoplasmic reticulum
Hepatic proprotein convertase subtilisin/kexin type 9
• increases circulating LDL levels by inducing destruction of LDL receptors
The major components involved in relaxation of cardiac muscle
Actin and troponin
Mechanism of ezetimibe
inhibits gut absorption of cholesterol from food and bile
When and why should GTN tablets be replaced
Every 3 months due to degredation and decreased potency
MOA aspirin
irreversibly inhibits COX1 and COX2, suppressing production of prostaglandins and thromboxanes
Effects of cholestyramine, gemfibrozil and omega fatty acids on lipids
Cholestyramine: Increases triglycerides and decreases LDL
Gemfibrozil Increase HDLs reduces LDL and triglycerides
Omega fatty acids reduced triglycerides
Carvidolol MOA
non-selective beta-blocker with 1-adrenoreceptor blocking activity
Perhexaline uses
• used in the treatment of congestive heart failure and refractory angina
o Improves exercise tolerance and increases workload needed to induce ischemia
o No evidence of mortality benefit
o Major side effects hepatotoxicity, peripheral neuropathy and hypoglycaemia
Metabolised by cytochrome P4502D6
Dobutamine MOA
Dobutamine • increases cardiac output by stimulating beta-1 and alpha-1 adrenoceptors in the myocardium
Adenosine MOA and contraindications
• depression of SA and AV nodal activity and agonises cAMP-mediated catecholamine stimulation of ventricular muscle
o Has negative chronotropic and dromotropic effects
o Also a direct agonist against A1 (gAMP-coupled K+ channel)
o Adverse effects bronchospasm, flushing, SOB, chest pain
o Contraindications second and third degree AV block, allergy, asthma and COPD (relative)
Recommended dietary intake of sodium to reduced cardiac events
3-6 g
AR Features on exam and eponymous names
- Corrigan pulse/”water hammer” – on palpation of radial or brachial arteries, exaggerated when arm is raised. Inc SV causes distension of peripheral arteries and inc systolic pressure. Regurgitation back into LV then causes quick drop in pressure with collapse of peripheral arteries and low diastolic pressure. Results in a wide pulse pressure, leading to water hammer pulse.
- Other signs associated with hyperdynamic pulse: pistol shot pulse heard over femoral arteries (Traube’s sign), pulsation in fingertips or lips (Quinke’s pulses), head bob with each heart beat (DeMusset’s sign), systolic pulsations of liver (Rosenbach’s sign) and spleen (Gerhard’s sign).
Nifidipine MOA
CCB, Induces coronary vasodilation, improves cardiac oxygen delivery and reduces peripheral vascular resistance, this in turn reduces afterload
Hydralazine MOA
Arteriolar vasodilation –> reflex sympathetic stimulation –> tachycardia and fluid retention . Contraindicated in heart failure with high cardiac output such as in hyperthyroidism, and also HF due to obstruction. But otherwise is often used with nitrate in HF.
Nitroglycerine MOA
Exogenous nitric oxide. predominately venodilates predominantly acting to reduce preload
Prazocin MOA
Selective alpha blocker, blocks alpha 1, predominantly acting to relax smooth muscle in the bladder
Also act on post synaptic alpha receptors leading to arterial and venodilation (reduces afterload and pre-load)
Captopril MOA
ACEi
Reduces sodium retention, reduces vasoconstriction and reduces water resorption. This reduces afterload
Management of Acute orthodromic WPW with SVT (give stable and unstable answer)
Unstable: Cardioversion Stable 1st line: Vagal manoeuvres (blow into a syringe) 2nd line: Adenosine IV 3rd line IV verapamil or diltiazem
IV adenosine: 6mg given bolus followed by a flush 20mls. After 2 minutes if tolerated but nil effect –> 12mg stat. If after 2 minutes still SVT –> 18mg adenosine with flush (pads on) - half life of drug 6 seconds.
The initial Adenosine dose should be reduced to 3 mg in patients taking
dipyridamole or carbamazepine, those with a transplanted heart or if given
by central venous access.
Management of Acute antidromic SVT or AF with VT
Broad complex - AV blockade will put patients into VF or asystole –> if in doubt always treat as VT
Unstable: DCR
Stable 1. Amiodarone or Flecanide
Definitive therapy with Ablation
ABCD (L) - drugs are contraindicated: Adenosine, beta blockers, calcium channel blockers, digoxin, lignocaine
Five groups of Pulmonary hypertension and some treatment options
ABCDE
Group 1: Pulmonary arterial hypertension (arterial)
Group 2: PH related to cardiac disease (Beating heart)
Group 3: PH related to lung disease (Can’t be cardiac, already had it, lungs)
Group 4: PH related to blockD vessels - PEs
Group 5: Else: PH related to miscellaneous causes, medications, etc.
