Cardiology Flashcards

Question

BNP / NT-pro BNP cut off

Answer 1

* Increased inotropy/contractility (high pressures) * Higher systolic blood pressure (higher peak) * Increased stroke volume (wider loop)

Answer 2

- Vasopressor - SBP and DBP have increased but SV is lower - ESV is higher as aortic valve closes earlier due to higher afterload which results in EDV increasing as more blood left in ventricle after systole. No change in inotropy

Answer 3

* Decreased preload/EDV (shifted left) * Decreased stroke volume (narrower loop) * Reduced systolic blood pressure (lower peak)

Answer 4

* Negative inotropy * SBP, SV and LVESP have decreased * ESV has increased (less blood pumped) (shifted right) * EDV has increased (because more time to fill) (shifted right) EF has decreased (SV lower and EDV higher)

Answer 5

1. Activity limiting symptoms despite OMT 2. Active patients who prefer PCI over OMT for QoL 3. Anatomy for which revascularisation has a proven survival benefit (e.g. proximal LAD lesion with LVEF <30% or evidence of a large area of potentially ischaemic myocardium)

Answer 6

Timing of angiography depends on RISK: (1) Very high risk criteria - immediate invasive strategy within 2 hours (2) High risk criteria - early invasive strategy within 24 hours (3) Intermediate risk criteria => angio within 72 hours of admission (4) Low risk

Answer 7

1. BP >180/110mmHg 2. Recent trauma / surgery 3. GI or GU bleeding within last 2-4 weeks 4. Stroke / TIA in last 12 months 5. Prior ICH at any time 6. Current anticoagulation or coagulopathy (relative contraindication with Warfarin)

Answer 8

Phases - Phase 4 spontaneous depolarisation (pacemaker potential) - Phase 0 depolarisation - Phase 3 repolarisation 1. When membrane potential is very negative (about -60mV) => depolarisation of pacemaker cells is initiated by slow inward Na current = funny current Phase 4 (spontaneous depolarisation) 2. As the membrane potential reaches -50mV => transient or T-type calcium channels open Phase 4 3. As membrane depolarises to -40mV => long-lasting L-type calcium channels open Phase 0 depolarisation 4. With further influx of Ca ions, action potential threshold is reached (between -30mV and -40mV) 5. During phase 0 - funny Na channels and T-type calcium channels close 6. Repolarisation occurs due to opening of K channels => K efflux ; concurrently L-type Ca channels close Phase 3

Answer 9

1. Resting membrane potential is very negative (approx. -90mV) due to efflux of potassium ions (fast sodium channels and L-type slow calcium channels are closed) Phase 4 2. Threshold voltage for depolarisation is -70mV => triggers opening of fast sodium channels 3. Rapid depolarisation due to Na influx through fast sodium channels ; at the same time potassium channels close (so outward directed K conductance ceases) Phase 0 (rapid early depolarisation) 4. Brief repolarisation due to transient outward K current Phase 1 (early depolarisation) 5. L-type calcium channels open up when membrane potential depolarised to approx. -40mV => plateau phase that prolongs the action potential Phase 2 (plateau) 6. Repolarisation occurs when L-type calcium channels become inactivated and K efflux increases Phase 3 (repolarisation) Effective refractory period occurs because sodium channels remain inactivated after they close till membrane is repolarised

Answer 10

ECG: associated with AF, AV conduction disease, low QRS voltages in limb leads TTE: non-dilated, marked wall thickening, "granular sparking" of myocardium, bi-atrial enlargement, normal systolic function, impaired longitudinal contraction with apical sparing CMR - global subendocardial / transmural LGE

Answer 11

Clinical screening for 1st degree relatives of patient with HCM (clinical exam, ECG, TTE) - LVH typically occurs during adolescence (hence screen annually in 1st degree relatives between 12-18 yrs.) - BUT there is a possibility for delayed-onset hypertrophy - therefore screen every 5 years for >18 yrs.

Answer 12

Two most commonly associated genes: (1) Beta myosin heavy chain (MYH7) (2) Myosin binding protein C (MYBPC) Only 50% patients have an identifiable mutation Absence of an identified sarcomeric mutation does not exclude diagnosis of HCM Perform genetic testing if: - suspicion of a genetic condition known to cause LVH (Fabry's disease, lysosomal storage diseases) - 1st degree relatives of patient with HCM where a specific mutation has been identified

Answer 13

1. Ejection systolic murmur (harsh, crescendo-descrescendo) - caused by LVOT obstruction (due to a combination of LV septal hypertrophy and SAM of the MV) - radiates to axilla and base (BUT not to neck) - becomes more intense with Valsalva (AS murmur either does not change or becomes less intense) & sitting upright - as both of these manouevres worsen LVOT obstruction - becomes less intense with squatting/sitting, with handgrip and passive leg elevation 2. Mid-late systolic murmur at apex - due to MR with posteriorly directed jet 3. JVP with prominent A wave 4. S4 heart sound (in late diastole due to blood entering a hypertrophied ventricle) 5. Paradoxical splitting of S2 (occurs during expiration, disappears during inspiration) Caused by delayed closure of AV 6. Double carotid pulse - brisk upstroke and bifid (due to sudden deceleration of blood due to mid-systolic obstruction) 7. Laterally displaced and forceful apex beat 8. Systolic thrill at apex or left lower sternal border 9. Parasternal lift suggests significant MR or pulm HTN

Answer 14

Syncope during exertion or immediately after exertion occurs in 15% patients with HCM - risk factors including NSVT on ambulatory ECG monitor, small LV cavity size, age <30

Answer 15

Resuscitated cardiac arrest Age <30 yrs. Early age at symptom onset Family history of SCD NSVT Syncope Exertional ischaemia or hypotension Septal thickness >30mm LVOT LA enlargement CMR - LGE

Answer 16

Clinical signs of chronic severe AR - widened pulse pressure - collapsing pulse (water hammer pulse) - long descrescendo high-pitched diastolic murmur - S3 (early diastolic filling from AR) - Low-pitched mid-diastolic rumble - as aortic regurgitant jet impinges on anterior mitral valve leaflet (Austin Flint murmur) - heard at apex TTE signs of chronic severe AR - abnormal aortic valve leaflets - large jets of flow on doppler - steep jet deceleration rate <200msec - LV dilatation - prominent reversal of diastolic flow in the descending aorta (AKA prominent holodiastolic reversal)

Answer 17

surgical aortic valve replacement is the main treatment option If not fit for surgery -ACEi and dihydropyridine CCBs may help with symptoms in symptomatic chronic severe AR, but do NOT delay progression to surgery

Answer 18

- affects metal / bioprosthetic, aortic and mitral valves equally - early PVE more common (within 1st year) - caused by Staph, gram negative, fungi; typically affects junction between sewing ring and annulus with perivalvular abscess, dehiscence, pseudoaneurysm and fistulae - late PVE - after 1st year, similar organisms to NVE - staph, strep viridans, strep gallolyticus, enterococcus, typically affects the leaflets -staph PVE - most severe form of endocarditis, mortality > 48% - TTE less sensitive for PVE than NVE. New periprosthetic leak or valve dehiscence on TTE, perivalvular abscess on CT and abnormal uptake on PET are major criteria for PVE - staph PVE and complicated PVE have worse prognosis if do not have surgery Need at least 6 weeks Abx for staph PVE For MRSA: fluclox + rifampicin + 2 weeks gent For MSSA: vanc + rifampicin + 2 weeks gent - uncomplicated and non-staph PVE can be managed conservatively

Answer 19

- most common organism is coagulase negative Staph (60-80%) 50% methicillin resisatnt for empiric Rx is vancomycin - remove hardware in all cases - noting risk of PE when pulling lead - reconsider need for new device - only insert new device if blood cultures negative for 72 hrs, should implant on contralateral side

Answer 20

Cultures should be negative within 48 hrs of starting empiric therapy

Answer 21

- Complicated and staph PVE always need surgery - Generally do not do surgery for R) sided IE unless - (1) RV dysfunction 2ndary to severe TR not responding to diuresis (2) large residual tricuspid vegetations >20mm after recurrent septic emboli (3) persistent vegetation with respiratory insufficiency requiring ventilatory support after recurrent pulmonary emboli Indications for surgery in pts with L) sided NVE (1) Heart failure - refractory or causing haemodynamic instability; secondary to severe valvular regurgitation or stenosis (2) Uncontrolled infection -growing vegetation, perivalvular abscess, fistulae, false aneurysm, new AV block, abscess - fungal or multi-resistant organism - Staph PVE or PVE caused by non-HACEK gram negatives - persistently positive BCs or sepsis > 1 week despite abx (3) Prevention of embolic phenomenon - persistent vegetations 10mm or larger despite 1 or more embolic phenomenon, despite appropriate Abx

Answer 22

· When to suspect FH? 1. CHD in <55 yrs, males OR <60 yrs. females 2. Family members with premature CVD 3. Family members with tendon xanthomas 4. Severely elevated LDL - > 5mmol/L in adults, >4 mmol/L in children 5. First degree relatives of patient's with FH · When to suspect homozygous FH? 1. Extensive xanthomas 2. Marked premature and progressive CVD 3. Total cholesterol > 13 mmol/L 4. Most patients develop CAD and aortic stenosis <20 yrs. and die before 30 yrs.

Answer 23

· Loss of function mutation in LDLR or apoB genes, or gain of function mutation in PCSK9 · 95% cases of FH are caused by mutations in LDLR (>1000 identified mutations) Mutations can be associated with reduced function or loss of function of LDLR -> loss of function mutations result in more severe hypercholesterolaemia and CVD

Answer 24

Statins- competitive inhibition of HMG-CoA reductase -> involved in the rate limiting step of intra-hepatic cholesterol synthesis (conversion of HMG-CoA -> mevalonate) Reduction in intra-hepatic cholesterol synthesis => upregulated expression of LDLR gene via sterol regulatory element binding protein (SREBP) => reduced LDL, trigs levels, increased HDL level Pleitropic effects - anti-inflammatory and anti-oxidant -> reduction in CRP, plaque stabilisation, anti-inflammatory effects. Every 1mmol/L reduction in LDL -> reduces major vascular events by 20%, major coronary events by 20%, CAD death by 20%, total stroke by 17%, total mortality by 10% over 5 years

Answer 25

Clinical features · High pitched holosystolic murmur * Radiates to axilla (anterior leaflet) * Radiates to sternum (posterior leaflet) * Increases with handgrip · Can also sometimes have a diastolic flow murmur · Sharp upstroke pulse Parasternal impulse - in second half of systole, suggestive of left atrial enlargement Clinical signs of chronic severe MR · Small volume pulse · Enlarged LV with displaced apex beat · Apical thrill · Soft S1, early A2, loud S3, diastolic rumble · Signs of pulm HTN · No S4 - either has AF or poorly contractile dilated LA Acute severe MR S4 heart sound

Answer 26

· Biatrial enlargement · Severe diastolic dysfunction · Increased wall thickness · Relatively preserved LV cavity size and systolic function · Tissue imaging parameters indicate sick tissue Disease specific features on TTE · Amyloidosis - RV mildly thickened, 'granular' myocardium · Sarcoidosis - myocardial thinning · Radiation - calcified valves, locally thickened pericardium or FWMA in the same region Hypereosinophilic syndrome - thrombi

Answer 27

In non-valvular AF - 2/3 stroke is cardioembolic, of which 90% is due to LAA thrombus LAA closure may be indicated in patients with high stroke risk (CHADSVASC >2) but contraindication to lifelong anticoagulation (e.g. high bleeding risk) Early trials did not show advantage over Warfarin - however, NOACs now SOC- new trials underway

Answer 28

**FOR DABIGATARAN (AS PER ETG) If <75 YRS and CrCl 30-50mL/min OR incr. risk of major bleeding => 110mg BD If >75 yrs. and CrCl > 30mL/min => 110mg B

Answer 29

For CKD stage 4-5 -> apixaban preferred, because less dependent on kidney function for clearance compared with other DOACs in US High percentage of Dabigatran is renally cleared - Do not use Dabigatran if CrCl <30 mL/min - Do not use Apixaban if CrCl <25 mL/min Do not use Rivaroxaban if CrCl <15 mL/min ; data for use of Rivaroxaban in CrCl 15-29mL/min is limited

Answer 30

Risk of intracranial bleeding and haemorrhagic stroke is higher with Warfarin Risk of major bleeding overall - similar with dabigatran and rivaroxaban compared to warfarin Rate of major bleeding with apixaban was significant lower than Warfarin In high risk of GI bleeding -> apixaban and dabigatran preferred over Warfarin and rivaroxaban

Answer 31

- Overall, no different in mortality & morbidity - Early rhythm control in newly diagnosed AF (< 12 months) - is associated with lower risk of adverse CV outcomes, lower risk of death from stroke or CV causes, compared to usual therapy - in heart failure with LVEF <35%, catheter ablation reduces death and HF hospital

Answer 32

- Cather ablation associated with better QoL outcomes - reduced recurrence of symptomatic AF, improved healthcare usage, improved QoL - In terms of mortality, thromboembolism, bleeding => similar outcomes - Reduction in death and HF hospitalisation in CASTLE-AF study with catheter ablation in LVEF <35%

Answer 33

○ Older age ○ Longstanding, persistent AF (vs paroxysmal) ○ Increased LA size ○ Female ○ Valvular or structural heart disease Untreated risk factors for AF e.g. obesity Risks - Pulmonary vein stenosis - Atrial perforation causing atrio-oesophageal fistulas

Answer 34

Typical flutter - caused by a macro re-entrant circuit involving the cavo-tricuspid isthmus (RA). Characterised by upright p waves / flutter waves in V1 and negative saw-tooth flutter waves in leads II and III. Atypical flutter - caused by macro re-entrant circuit involving another part of the atrium. Characterised by upright p waves in all leads. Ablation more challenging in atypical flutter

Answer 35

- if patient with accessory pathway / WPW is given an AV nodal blocking agent - patient with AF on flecainide -> atrial flutter with 1:1 conduction (therefore should pair flecainide with AV nodal blocking agent - sympathetic stimulation

Answer 36

Non-selective beta 1 and beta 2 agonist Primarily a chronotropic & inotropic agent, not a vasopressor Beta 1 stimulation -> predominantly chronotropic effects (increases automaticity, increases AV nodal conduction), also inotropic effects Beta 2 stimulation -> vasodilation, reduction in peripheral vascular resistance, specifically decreases in DBP Usually improves coronary blood flow Indications: heart block, bradycardia with haemodynamic compromise Contraindications: - tachycardias / tachy-arrhythmias - recent MI - may increase infarct size & incr. ventricular ectopic activity - IHD / angina - may exacerbate symptoms - HTN - may increase SBP - Heart block due to digoxin toxicity -> isoprenaline increases risk of ventricular arrhythmias

Answer 37

○ Consider catheter ablation for symptomatic AF in select patients with HFrEF CASTLE-AF study - catheter ablation led to reduced death and HF hospitalisation in patients with LVEF <35%; compared to medical therapy (rate or rhythm control)

Answer 38

- cardiac glycoside - positive inotrope (weak) and negative chronotrope -inhibits Na/K ATPase in heart Increases intracellular Na concentration -> decr. influx of Na and efflux of Ca via the Na/Ca pump p Increases intracellular Ca which is stored in SR -> more Ca is released with each action potential -> increased inotropy - increases central vagal activity -> decreases HR, decreases AV conduction. LESS effective at reducing HR during exercise or states of increased sympathetic tone Common mild side effects - N&V, anoerexia, GI disturbance, bradycardia, rash, headache, drowsiness, dizziness Serious adverse effects - thrombocytopenia, seizures, confusion, psychosis, ventricular arrhythmias

Answer 39

- hypokalaemia is associated with increased risk of digoxin toxicity at lower concentrations (cautious use of thiazide and loop diuretics - preference K sparing diuretics) - hypothyroidism may increase dig levels - renal impairment

Answer 40

In digoxin toxicity -> hyperkalaemia reflects the degree of digoxin toxicity and the risk of death Hypokalaemia also increases risk of digoxin toxicity at a lower serum digoxin concentration

Answer 41

Main clinical manifestations (1) Cardiac - most dangerous, any type of arrhythmia (except rapidly conducting atrial arrhythmias) (2) GI disturbance (3) Neurological changes - including visual disturbance, confusion Yellow eyes Downsloping ST depression Management of dig toxicity (1) Supportive care A-E (2) GI contamination - if presents <2 hours of acute intoxication (3) Digoxin specific antibody fragments (Fab) IF: -> Life-threatening arrhythmia (e.g. CHB, Mobitz II, VF, VT) -> End-organ dysfunction (e.g. renal failure, altered mental status) -> Hyperkalaemia (K>5) HyperK reflects severity of toxicity and risk of death - but aggressive Rx of hyperK is NOT warranted, as it does NOT reduce mortality, and incr. risk of hypoK after Rx with Fab Do not measure serum dig concentration after giving dig specific Abs because measures both unbound and bound (inactive) drug. Monitor clinically, if concentration monitoring needed - only free serum dig concentration can be interpreted

Answer 42

> 90% TR is secondary / functional - primarily in association with L) heart disease Causes of primary TR: - Infective endocarditis - Rheumatic heart disease - Carcinoid syndrome - Myxomas - Endomyocardial fibrosis - Congenital valve dysplasia (Ebstein's anomaly) - Thoracic trauma - Iatrogenic trauma- 30% PPM/ICD leads

Answer 43

In severe TR, pulmonary pressure are likely to be underestimated

Answer 44

* Preferred intervention if surgical TV repair or replacement * TV surgery usually occurs in conjunction with left sided valve surgery * If severe primary or secondary TR OR * Tricuspid annulus dilatation * Isolated TV surgery outcomes are not ideal * Severe primary or secondary TR with: ○ Symptoms OR assoc. RV dilation ○ Otherwise, for medical therapy * If severe secondary TR is associated with severe RV or LV dysfunction or severe pulm HTN -> would be for medical management In these cases, need to be cautious of pulmonary HTN and RV dysfunction

Answer 45

20% dilated cardiomyopathy is genetic - most commonly due to mutations in genes encoding sarcomere and desmosomal proteins - most common mutation is in Titin gene - lamin A/C (LMNA) and desmin mutations also common - X-linked mutation in dystrophin uncommon 80% dilated cardiomyopathy acquired

Answer 46

Causes of death in DCM - progressive HF OR SCD due to ventricular arrhythmias (or more uncommonly - bradyarrhythmias) Predictors of SCD - LGE on MRI - QRS fragmentation and T wave alternans on ECG LGE on MRI predicts risks of all-cause mortality, heart failure hospitalisation and SCD

Answer 47

- aborted cardiac arrest - sustained ventricular arrhythmia - nocturnal agonal respiration OR arrhythmic syncope with a positive sodium channel blocker test

Answer 48

- fever > 38C - failure to respond to therapy by 1 week - subacute onset - large pericardial effusion - cardiac tamponade

Answer 49

At least 2 of the following must be present: - pericarditic pain (sharp, pleuritic, relieved by sitting up & leaning forwards, worse when supine) - pericardial rub - new or worsening pericardial effusion - ECG changes - widespread STE or PR depression ECG pattern in acute pericarditis Stage 1 (first few hours to days) - widespread STE. STD in aVR and V1. PR elevation in aVR and PR depression in other leads. Stage 2 (within first week) - resolution of ECG changes Stage 3 - diffuse TWI (after ST changes normalise) Stage 4 - normal ECG

Answer 50

- Treat underlying cause (e.g. dialysis for uraemia, immunosuppression for CTD, antibiotics for purulent pericarditis) - Mainstay of therapy is - restriction of strenuous exercise + colchicine + NSAIDs; wean NSAIDs by 1 week, continue colchicine for 3 months Colchicine - improves remission rates and reduces recurrence rates, compared to NSAID therapy alone When should steroids be used in the treatment of pericarditis? - recurrent or chronic pericarditis - contraindications to NSAIDs (e.g. renal failure) - autoimmune pericarditis Role of pericardiotomy? - in recurrent pericarditis with persistent symptoms, after failure of medical therapy (colchicine, NSAIDs, steroids)

Answer 51

Rilonacept is an interleukin 1 alpha and interleukin 1 beta trap In patients with recurrent symptomatic pericarditis and elevated CRP - rilonacept led to rapid resolution and significantly lowered risk of recurrence

Answer 52

- LA thrombus - more than mild MR - significant AV disease or severe combined TS and TR - significant subvalvular involvement - absense of commissural fusion - severe calcification of the valve - MVA > 1.5cm2 - severe concomitant CAD

Answer 53

type 4a - PCI; type 4b - in-stent thrombosis

Answer 54

LM lesions with 50% or more stenosis are considered significant CAGS has a mortality benefit in LM disease In patients with low-intermediate complexity anatomy - PCI is a non-inferior option compared to CAGS when it comes to mortality, risk of stroke and MI at 3 years

Answer 55

The GRACE score predicts the risk of in-hospital, 6 month and 3 year mortality and AMI in patients presenting with acute coronary syndrome - SBP - HR - Age - Creatinine - Presence of heart failure - Cardiac arrest on presentation - STE - Elevated cardiac enzymes

Answer 56

Risk of intracranial bleeding and haemorrhagic stroke is higher with Warfarin Risk of major bleeding overall - similar with dabigatran and rivaroxaban compared to warfarin Rate of major bleeding with apixaban was significant lower than Warfarin In high risk of GI bleeding -> apixaban and dabigatran preferred over Warfarin and rivaroxaban

Answer 57

ANY patient with: - complete heart block - high grade AV block - Mobitz type II 2nd degree AV block ANY symptomatic patients with: - sinus node dysfunction - atrial fibrillation with bradycardia (tachy - brady syndrome) - bradycardia due to goal directed medical therapy - 2nd degree AV block Mobitz I or marked PR prolonged (1st degree AV block) with clear correlation with symptoms

Answer 58

SCN5A - cardiac sodium channel protein type 5 subunit alpha Autosomal dominant, loss of function mutation, with variable expression (M>F) 20-30% patients have mutations in SCN5A

Answer 59

Anti-arrhythmics - Procainamide - Fleicanide - Ajmaline Beta blockers Alpha agonists Nitrates Psychotropics - Lithium - TCA Anaesthetics - propofol - bupivacaine - procaine Other substances - ETOH - cocaine - Cannabis

Answer 60

Sodium channel blocker tests are NOT recommended in patients with spontaneous Brugada type 1 ECG pattern if there are ECG changes suspicious for Brugada BUT NOT type 1 pattern, consider a sodium channel blocker test in the following circumstances: - aborted cardiac arrest or sustained ventricular arrhythmia - arrhythmic syncope - history of nocturnal agonal respiration - family history of Brugada syndrome or family history of sudden arrhythmic death