Cardiology Flashcards

Question

Infective Endocarditis: TYPICAL ORGANISMS

Answer 1

- strep viridans - staph aureus - strep bovis - Coxiella Burnetti

Answer 2

HACEK GROUP - Haemophilus parainfluenzae / aphrophilus / paraphrophilus - Actinobacillus actinomycetemcomitans - Cardiobacterium Hominis - Eikinella Corrodens - Kingella spp

Answer 3

``` Domains: 1 - Disease activity 2 - Diagnostic certainty 3 - Valve involved or IVDU 4 - Right or Left heart 5 - Culture report 6 - Demographic ``` Disease activity a) Active = currently positive IE cultures b) Healed = past IE now biologically sterile c) Persistent = IE not eradicated after appropriate Abx d) Recurrent = Recurrence post definitive cure - difficult to differentiate from persistent - POOR PROGNOSIS Diagnostic Certainty a) Established = Dukes Criteria Confirmation b) Suspected = IE infection suspected without evidence of endocardial involvement c) Possible but other causes also exist Valve involvement a) native b) prosthetic c) Endocarditis ``` Right or Left ?IVDU ?Dental work ?VSD / ASD Bubble echo ``` ``` Culture: Organisms in keeping with BE 1.strep viridans 2.coxiella burnetty 3.staph aureus ``` HACEK - haemophilus parainfluenza / actinobacillus / cardiobacterum hominis / eikinella corrodens/ kingella

Answer 4

The Renin Angiotensin and Aldosterone system is a feedback mechanism which drives sodium retention and therefore water retention to maintain blood pressure by increasing circulating volume, increase preload and increase CO It is therefore activated chronically in heart failure and drives its pathogenesis low BP / hypovolaemia / low CO renin release from kidneys JM apparatus -angiontensinogen (liver) --renin-->angiotensin 1 -increase vascular tone angiotensin 1 -Converted by ACE pleura--> angiotensin 2 angiotensin 2 - Increase Na asborption PCT - Na in / H+ out - aldosterone release from adrenal cortex - DCT Na reabsorption / CL and K+ excretion - increased vascular tone - Stimulates ADH release from post pituitary

Answer 5

There are 3 natriuretic peptides ANP - atria - endocrine BNP - ventricular - endocrine CNP - arterial sheer stress - pararcrine role - inhibitor of vascular and glomerular proliferation and interstitial matrix production Released in response to plasma volume expansion (STRETCH) Released in response to rising Ang II as an autofeedback mechanism They stimulate natriuresis - dilate afferent arteriole and constrict efferent arteriole - increased GFR - increased delivery of sodium to DCT / LoH / PCT for excretion Arterial dilatation -ANP and BNP Vasodilation and VEGF inhibition - CNP Inhibit ADH release -DCT Aquaporin II channels then close THEREFORE IDEAL WOULD BE TO INCREASE ANP/BNP/CNP half life. Trials were promising re: Neprilysin inhibitor BUT combined ACEi + Neprilysin - angioedema More evidence for combined single agent therapies Uncontrolled cardiac failure on ACEi Switch to ARB + NEP = valsartan + SACUBITRIL PARADIGM-HF trial REDUCED MORTALITY BY 20%

Answer 6

Neprilysin inhibitor | prolong ANP / BNP / CNP halflife

Answer 7

Also known as primary ciliary dyskinesia - Bronchiectasis - Dextrocardia - faint heart sounds - ECG = reverse R wave progression from v1-v6

Answer 8

Right ventricular MI in 30% cases - reduced RV compliance and stroke volume - reduced LV filling and therefore reduced CO - activation of RAAS Tricuspid regurg --->pansystolic murmur Raised JVP - giant C wave and shallow V trough

Answer 9

Thiazide like diuretic - missing benzothiadiazine group Act to block DCT Na+ reabsoprtion via NA+/CL- channel Thought to have greater efficacy to reduce diastolic and systolic BP No increased incidence of DM2 / hyponatraemia / hypokalaemia

Answer 10

Adenosine is a very short acting agent which causes a transient AV block and is useful in slowing or chemically cardioverting a supra-ventricular tacchyarhythmia

Answer 11

Ivabridine is a sodium funny channel blocker used in ANGINA / HEART FAILURE =If Particularly present in SAN and AVN. Slows cardiac conduction without negagively impacting on force of contraction i.e. improves diastolic filling and therfore increase stroke volume and CO Adjunctive medication in heart failure but must be in sinus rhythm. Reduces hospital admission and mortality when ready on maximal therapy

Answer 12

CHA2DS2VASC2 risk stratification for stroke risk in AF HASBLED score must be done alongside to also apply risk of bleeding Vs risk of stroke ``` CHA2DS2VASC2 Congestive heart failure (or Left ventricular systolic dysfunction) 1 Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1 Age ≥75 years 2 Diabetes Mellitus 1 Prior Stroke or TIA or thromboembolism 2 Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1 Age 65–74 years 1 Sex Category (i.e. female sex) 2 score =0 - no anticoagulation score >1 CHA2DS2VASC2 = low moderate risk as for >2 score >2 moderate to high risk consider warfarin /apixaban / rivaroxaban / dabigatran ``` note renal dose / increased bleeding profile with dabigatran also consider risk of UGIB

Answer 13

Hypertension: (uncontrolled, >160 mmHg systolic) 1 Abnormal renal function: Dialysis, transplant, Cr >2.26 mg/dL or >200 µmol/L 1 Abnormal liver function: Cirrhosis or Bilirubin >2x Normal or AST/ALT/AP >3x Normal 1 Stroke: Prior history of stroke 1 Bleeding: Prior Major Bleeding or Predisposition 1 Labile INR: (Unstable/high INR), Time in Therapeutic Range 65 years 1 Prior Alcohol or Drug Usage History (≥ 8 drinks/week) 1 Medication Usage Predisposing to Bleeding: (Antiplatelet agents, NSAIDs) 1 score of ≥3 indicates "high risk" and some caution and regular review of the patient is needed >5 = >10per 100

Answer 14

Describes relationship between stroke volume and end diastolic volume This relies on the constant that ventricular output = atrial input 1. stroke volume of the heart increases with ventricular filling 2. increased volume = increased stretch = increased contraction force 3. The limit of ventricular filling is reached and this results in a plateau of contraction force and ventricular dilatation.

Answer 15

P mitrale | end diastolic murmur

Answer 16

1st line for atrial tacchyarythmias - slow sinus rhythm - increase diastolic filling time - greater filling = greater stretch = greater recruitment and contractile force = greater CO Resistance = Amiodarone Digoxin not good for PAF - does not reduce frequency and does may prolong paroxysm

Answer 17

X linked recessive mutation in Dystrophin Similar to DMD but later onset and milder Present 5-15 years of age or later - dilated cardiomyopathy - early onset - Calf hypertrophy - proximal weakness

Answer 18

Critical congenital heart defect of tricuspid valve <1% of heart defects 1/200,000 live births 1. Annulus of tricuspid in normal position 2. valve leaflests face into the right ventricle and may be attached to the walls o the septum 3. RV becomes atrialised 4. RA therefore very enlarged and the RV small in size Associated tricuspid regurg - pansystolic murmur - right sternal edge Associated with WPW -Transient Supraventricular tacchyarhythmia

Answer 19

``` pre-excitation syndrome Supraventricular tachycardia due to accessory pathway delta waves short pr rbbb ``` ``` Also associated with Ebsteins anomally rbbb TR Tricuspid valve leaflets inverted intro RV Atrialisation of RA Small RV Large C waves Deep V wave -large RA reduced CO ``` DC cardioversion for short term control RF ablation definitive avoid digoxin and verapamil may precipitate greater conduction via accessory pathway

Answer 20

``` pre-excitation complex accessory pathway short PR no delta wave no rbbb ```

Answer 21

positive qrs v1 - rSr pattern = M negative deflection V6 = W pattern Diagnostic: Broad QRS > 120 ms RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) Wide, slurred S wave in the lateral leads (I, aVL, V5-6) Associated Features - ST depression and T wave inversion in the right precordial leads (V1-3) - Sometimes rather than an rSr’ pattern in V1, there may be a broad monophasic R wave or a qR complex. 1 - RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle. 2 - The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged. 3 - The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads. 4 - Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, - ST depression - T wave inversion in the right precordial leads. - Cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.

Answer 22

Inferior MI Core pulmonale / pulm HTN / CF / COPD / bronchiectasis PE Rheumatic heart disease Degenerative disease of conduction system

Answer 23

Factor Xa inhibitor

Answer 24

Congenital disorder genetic mutations in ion channels 2 forms: ROMANO WARD SYNDROME JERVELL AND LANG-NIELSON ``` =QT prolongation on ECG 0 >450ms . Associated with ventricular tachyarrhythmia -syncope -arrest -sudden death ``` Treatment: B-blockade Reduces rate and increases ventricular diastole Reduces risk of life threatening VT

Answer 25

One of two recognised sydromes of congenital long QT syndrome ``` Associated with : VT syncope arrest sudden death ``` treatment: B blockade - reduce risk of VT / VF Implantable defibrillator

Answer 26

One of two recognised sydromes of congenital long QT syndrome ``` Associated with : VT syncope arrest sudden death ``` treatment: B blockade - reduce risk of VT / VF Implantable defibrillator

Answer 27

1. IV beta blockade to reduce BP 2. CT aorta angio 3. Discussion with cardiothoracics Mortality untreated is 25-30% at 24 hours and up to 75% at 2 weeks AD confined to descending aorta (80%) has a better prognosis

Answer 28

1. Inferior ST elevation - aortic dissection may compress and occlude the RCA ostium 2. Aortic regurgitation Corrigans sign in the neck Quinke's signs in the nails Collpasing radial pulse Early diastolic murmur radiating to axilla Ventricular heave due to higher end diastic vol Displaced apex asassociated with dilatation 3. Pericardial rub 4. Retrosternal CP + interscapular tearing pain ``` RF Marfinoid - dilated Aortic root Ehlers Danos Rheumatic heart disease Trauma ```

Answer 29

AS with syncope = median survival of 4 months without surgery 1. Aortic stenosis Vs sclerosis due to slow rising pulse 2. ECHO shows severe AS an since symptomatic all more reason for urgent valve replacement 3. inpatient angio + admission ``` Criteria for AS: grading MILD >1.5cm sq pressure <20mmHg MOD 0.5-1.5cm sq pressure gradient 20-40mmHg SEVERE <0.5cm sq. pressure >40mmHg ``` Valve area better as the gradient may change with any evidence of LV impairment / past MI etc VALVE AREA SHOULD BE NORMALISED TO BODY SURFACE AREA - severe AS <0.6cm sq/metre sq STRESS ECHO: good to use to decide if AS is causing LV impairment and therefore may benefit from surgery. -?BP drop -?pre-syncope If AS is not connected to LV impairment then there is no point in doing surgery Cardiac Catheterisation: Catheterisation of stenosed Aortic valve is associated with MRI evidence of stroke in 22% of cases and neurological defect in 3% HOWEVER CORONARY ANGIO USEFUL TO PLAN IF CABG SHOULD BE DONE ALONGSIDE TAVI ``` Management: 6-12 month follow-up if asymptomatic Surgery if symptomatic / stenosis severe recommended OR >40mmHg or <1cm sq / 0.6cm sq / m sq (in LV imp) EJF< 45% LVH>15mm BP drop during exercise VT on tape ```

Answer 30

NO CONTRAINDICATED BP modulation is a balance in AS - dropping BP may cause a drop in coronary perfusion pressure and further worsen symptoms of heart failure

Answer 31

- could be cardiac or pulmonary - signs of pulm HTN Diff: PE = expect nipping of pulmonary arteries are normal or pruned ASD - RV heave due to left to right shunt - development of Eisenmenger syndrome = RVH overcomes LV = right to left shunt - pulmonary artery engorgment due to higher CO state - RBBB Mx: TOE - ASD visualisation / quantify jet and PA pressure / valve gradient / direction of shunting Right heart catheter - suitability for closure Book CTPA if concerned re: PE

Answer 32

Heart failure - 0.5-2 | AF - 1.5-2.5

Answer 33

Therapeutic levels 0.5-2.5 depending on whether HF or AF / flutter Toxicity effects seen >10 and definitiely >13 >10mg in adults >4mg in children 1. complete heart block 2. bradycardia 3. unstable bradycardia - HS instability 4. VT - avoid adrenalin Management: Digoxin level If <6 hours - 75g activated charcoal via NG to bind and block further absoprtion ECG + continuous cardiac monitoring Atropine 500mcg for symptomatic bradycardia Repeat atropine 500mcg for recurrence Further recurrence A) FAB specific digoxin FAB fragment works as an opsoniser and is specific to digoxin epitope - binds and excludes B) Isoprenaline infusion ``` FAB indications: VT HD instability failed response to atropine hyperkalaemia digoxin level >13 or ingestion >10mg adult or 4mg child Recurrent bradycardia ```

Answer 34

1. negatively chronotropic - MYOCARDIAL + AVN - increases refractory period at phase 4 and 0 due to increased intracellular calcium due to inhibition of the Na/K /Ca pump - AVN parasympathetic effects 2. increases contractile force without increasing cardiac workload - Digoxin exerts a PNS effect on AVN - Digoxin inihibits Na/K/Ca exchanger in MYOCARDIUM - Results in higher INTRACELLULAR CALCIUM - Higher intracellular calcium prolongs phase 4 and phase 0 of cardiac AP - This results in slower repolarisation - This results in a decrease in heart rate - Increased Ca is stored within the sarcoplasmic reticulum and therefore more is available to act as a myosin cofactor and so contractile force is increased without increasing work DIGOXIN DOES NOT ALTER THE UNDERLIEING RHYTHM DIGOXIN SLOWS VENTRICULAR RATE AND IMPROVED DIASTOLIC FILLING REDUCING OXYGEN DEMAND THEREFORE DOES NOT REDUCE FREQUENCY OF ATTACKS OF PAF

Answer 35

Absolute contraindications for fibrinolytic use in STEMI include the following: [16] - Prior intracranial hemorrhage (ICH) - Known structural cerebral vascular lesion - Known malignant intracranial neoplasm - Ischemic stroke within 3 months - Suspected aortic dissection - Active bleeding or bleeding diathesis (excluding menses) - Significant closed head trauma or facial trauma within 3 months - Intracranial or intraspinal surgery within 2 months - Severe uncontrolled hypertension (unresponsive to emergency therapy) - For streptokinase, prior treatment within the previous 6 month

Answer 36

phenoxybenzamine gives alpha blockade preventing arterial vasoconstrction and hypertensive crisis - doxazocin DO NOT B BLOCKADE IN FIRST INSTANCE - Results in unopposed alpha stimulation and hypertensive crisis

Answer 37

``` 1. CXR rule out PTX check lead placement RA + RV LV vai Coronary sinus and LV vein ``` 2. Pressure dressing for 24 hours 3. Wound review and discharge

Answer 38

40% of inferior MIs TWI in II / III / AVF - reciprocal depression ST in V5/V6 ECG: New complete heart block TWI in III / AVF - Raised JVP - peripheral oedema - Hypotension -reduce pulmonary flow - reduced preload - Very preload sensitive therefore nitrates can drop BP further

Answer 39

LAD supplies AV septum - EXPECT BBB anterior and lateral LV papillary muscle of mitral valve MOST COMMONLY OCCLUDED LAD stenosis / blockage - ANTERIOR MI ECG: ANT changes / INF reciprocal ST elevation V1 / V2 / and V4/V5 / AVL ST Depression in 2/3/avf MORE PROXIMAL OCCLUSION = GREATER DAMAGE - MORE WIDESPREAT ST ELEVATION

Answer 40

Circumflex branches off LAD or RCA majority of people = Right dominant gives rise to circumflex ECG = RCA dominant = post MI changes st depression v1/2 (anterior leads) ( just circ PDA spared ) IF left dominnant circumflex also supplies posterior descending after circumflex instead of RCA therefore inferior changes seen too (circ + PDA) St depression V1/v2 st elevation 2/3/avf ``` Supplies: SAN in 50% Left atrium Lateral LV wall anterior papillary of mitral valve posterior lateral wall LV (with right coronary) ```

Answer 41

Comes of aorta and runs in AV groove gives rise to posterior descending artery ``` supplies: SAN (50-73%) AVN (50-73%) - via right AV artery Right ventricle IV septum proximal encircling both BB ``` issue: infarction = BBB / bifascicular predispose to conduction abnormality RV infarction - hypotension / raised JVP / preload sensitive

Answer 42

Comes off RCA supplies Right ventricle

Answer 43

RBBB + either left anterior fascicular or left posterior fascicular blockage Sign of extensive conductive disease Likely RCA infarct - supplies SAN / AVN and prox bundles Likely LAD - supplies AV septum housing bundles Hyperkalaemia ``` Causes: Ischaemic heart disease (40-60% cases) Hypertension (20-25%) Aortic stenosis Anterior MI (occurs in 5-7% of acute AMI) Primary degenerative disease of the conducting system (Lenegre’s / Lev’s disease) Congenital heart disease Hyperkalaemia (resolves with treatment) ``` ECG: RBBB + left axis or right axis deviation -MORROW -RSR V1-V3 -Wide QRS Conduction of RV delayed so propogation of RV contraction via myocyte junctions Majority conduction still via LV in isolated RBBB -Leads facing RV will see initially depol away as LV goes first then see large second R wave as RV delayed depol -Lateral leads see a slurred S wave due to Left V dominance but mistimed R V disrupting smooth isovolumetric contraction

Answer 44

- Erythromycin - lithium - amiodarone - sotolol - tacrolimus - quinine - fluoxetine / citalopram /

Answer 45

Atrial tachy SVT with at least 3 different P wave morphologies with variable PR and PP intervals Trigger: Hypoxia / hypercapnia Salbutamol nebs will worsen the SVT but are needed in the first instance to treat the airway In setting of COPD or asthma B-BLOCKADE is NOT APPROPRIATE - NO METOPROLOL / NO BISOPROLOL - bronchospasm - worsen obstruction Therefore second line = VERAPAMIL 5mg IV bolus load oral 40-120mg TDS Repat 72 hr ecg if reverts to SR to see if long term rate control is needed (unlikely) MOA Verapamil: block voltage-dependent calcium channels. calcium channel blockers are considered class-IV antiarrhythmic agents. Concentrated in the sinoatrial and atrioventricular nodes, Decrease impulse conduction through the AV node, thus protecting the ventricles from atrial tachyarrhythmias. Calcium channels are also present in the smooth muscle lining blood vessels. By relaxing the tone of this smooth muscle, calcium channel blockers dilate the blood vessels. - treating high blood pressure and angina pectoris. - increases the supply of blood and oxygen to the heart. -This controls chest pain, but only when used regularly.

Answer 46

Highly selective If blocker - funny channel blocker in SAN non inferior to atenolol and amlodipine in management of angina pectoris improves ET and reduces frequency of angina attacks Would therefore be good for b blocker contraindicated pathology

Answer 47

Spironolactone - reduced mortalitu by 30% at 25mg dose when added to conventional therapy Bisoprolol - reduced mortality and sudden cardiac death compared to pacebo Ramipril - reduced mortality by 15-30% in all stages of CHF inotlerance or ACEi or ARB USE HYDRALAZONE AND ISMN COMBO Data predates B blocker data

Answer 48

>1.4 = vascular hardeneing / claudication - VASC 0.9-1.4 = normal 0.8-0.9 - treat risk factors for claudication / BP / lipids / DM 0.5-0.8 = moderate stenosis = VASC - Int Claud <0.5 = critical claudication = VASC - rest pain

Answer 49

Microcytic anaemia + Calcific AS ``` Cause: Destruct of VwF as platelets (bound to VwF) cross calcific valve. This may cause PR blood loss. OR MICROANGIOPATHIC HAEMOLYSIS ``` management VALVE REPLACEMENT Mesenteric angiography to establish bleeding looking for ANGIODYSPLASIA

Answer 50

Aspirin Ticagrelor GTN Oxygen Fondaparinux Ticagrelor has been shown to be superior to Clopidogrel in the treatment of NSTEMI in reducing all cause mortality including stroke without an increase rate of bleeding (PLATO)

Answer 51

eGFR<20 --> switch to LMWH | active or concurrent bleeding or deranged INR

Answer 52

``` 1 LVF<35% and NYAC 3 or less 2 inducible arrhythmia 3 non sustained VT 4 familial long QT 5 HOCM 6 Brugada - V1-V3 ST elevation with RBBB 7 RV dysplasia 8 post tetralogy repair ``` ICD is superior to medication control of VT alone in LVF e.g. amiodarone alone reduces mortality by 20% vs 14% post MI almost totally due to a reduction in sudden cardiac death.

Answer 53

1. coag control - warf - APIX / RIVAROX 2, rhythm control - bisoprolol - amiodarone

Answer 54

Thallium contrast MRI of the heart = CAD evaulate Shows perfusion to tissue and gives more information than ECHO + angio and is less invasive than angiography Indications: >40 atypical CP + HTN Stress echo in the >40 htn group will have V1-V4 ST depression even without myocardial ischaemia Dobutamine or thallium labelled can be used for MI perfusion scan Thallium has greater sensitivity Dobutamine has greater specificity (stresses heart) Dobutamine good if patient cannot exercise e.g. stroke / injury / pain / bmi / pvd / arthritis AVOID IN WPW OR ROLAND LONG

Answer 55

DO NOT GIVE AMIODARONE - this may cause QT prolongation - Instead this needs IV MAGNESIUM which will reduce the availability of calcium and reduce the amplitude of the arrhythmia resulting in potential termination - DC CARDIOVERSION Drugs that cause QT prolongation or low MAG can cause TdP - erythromycin - ketoconazole - tricyclics esp in OD - sotalol

Answer 56

Competitive B blocker that causes QT prolongation and is useufl in management of VT / AF or flutter resistant to other medications AVOID in heart failure - increased risk of death likely due to QT prolongation

Answer 57

Slows AV conduction

Answer 58

Class III | refractory AF / Broad complex Tachys without HD compromise

Answer 59

Shockable rhythm - VF or VT | After 3 failed shocks

Answer 60

Shockable: VF or VT Every other cycle = Amiodarone alternate after 3rd cycle Unshockable : PEA / asystole every other cycle of CPR - no amiodarone

Answer 61

Stress ECHO Stress perfusion scans when patient cannot exercise Positive inotrope for low cardiac output states - MI - cardiomyopathy - sepsis

Answer 62

Assessment of LV output product of HR x SR normal range 2.5-4 <2.1 = cardiogenic shock

Answer 63

(Systolic + 2xdiastolic) / 3

Answer 64

B - blocker - cardio selective Bisoprolol aim to improve efficiency / contractility negatively chronotropic to reduce work Tolerated well even in COPD

Answer 65

Nitrates Diltiazem or ISMN do not alter MACE

Answer 66

Bisoprolol - improve mortality and remodelling ramipril - improve mortality candesartan / valsartan if not tolerating ramipril furosemide spironolactone - improve mortality Ivabridine - (BB subs - if HF + HR >75 / LVEF) - funny channel blocker - improve outcomes (LVEF severe / b blocker not tolerated / esacalted therapy Valsartan sacubitril - LVEF<35% - ARB + natrilutic peptidase inhibtor - reduce hyponatreamia - improves outcomes

Answer 67

Congenital or Acquired Acquired: Drug induced OD tricyclics / benzodiazepines avoid amiodarone / digoxin / any drug which prolonges AV depol Congenital LQT1 - higher risk for VT and SCD B blockade - blunt andrenergic tone as thought VT may be induced by high tone and depolarisations - propranolol bisoprolol nidolol Lifestyle mod avoid swimming and contact sports ICD pacemaker

Answer 68

3 Types Type 1: >2mm ST elevation in V1-V3 + TWI in V1-V3 Type 2: Saddle back ST elevation Type 3: mix of above but <2mm elevation ``` Plus collapse / syncopy VT/VF FMH SCD nocturnal agonal inspiration ```

Answer 69

liver / heart / mouth ``` Mouth ulcers flu like prodrome myocarditis pericarditis hepatitis ```

Answer 70

MYH7A - 40% HOCM | MYBPC3 - 40% HOCM

Answer 71

BOSENTAN - teratogenic Endothelin A receptor antagonists PROSTACYCLIN - pregnancy aim decerase pulmonary vascular resistance

Answer 72

Onset VF | This is due to asymmetrical septal hypertrophy increasing risk of aberrant ventricular rhythm.

Answer 73

More than 20 documented gene defects most commonly affecting a sodium channel Presentation with VF / VT and collapse incidental ECG finding ECG type 1 ST elevation and TWI V1-V3 >2mm type ST elevation saddleback - widespread Type 3 - <2mm type1 or type2 findings

Answer 74

Often lethal arrhythmia triggered by contusion to the chest during ventricular repolarisation which induces VT or VF

Answer 75

Target LDL <1.8 or a reduction by 50% if between 1.8-3.5 Peripheral AD is equivalent to CAD ad cerebrovascular disease risk