cardiology Flashcards

Question

how to interpret ECG steps

Answer 1

look at patient - unwell? well? take pulse and BP - what are you expecting to see immediately look for any clear scary abnormalities and get help if necessary 'RRPWQST' R - rate - for speed if <3 large squares between each QRS complex is >100bpm and >6 = <50bpm R - rhythm - reg or irreg P - p wave - always present? = sinus rhythm. if cant see p wave always then atria not activated normally, if more than 1 p wave before every QRS then ventricles are not activated normally = heart block W - width - QRS <3 small squares, if not its slow Q - any deep Q waves present? if so shows old myocardial infarction S - ST segment - depressed (ischaemia) or elevated? (infarction) T - T wave - any abnormal or inverted T waves? NORMALLY INVERTED IN AVR, V1. if inverted in any other then could be ischaemia or ventricular hypertrophy.

Answer 2

narrow complex - electrical activation starts in sinoatrial node, atrial muscle or AV node. rate usually >120bpm, p waves may or may not be visible broad complex - electric starts from ventricles at a rate faster than from sa node, no p waves, >120bpm complete heart block - atria and ventricles not synchronized and work independently, but both are beating reg due to intrinsic activity. p and QRS completely independent sinus arrhythmia - normal ECG except affected by resps - this is normal, distance between QRS is shorter during insp extrasystoles - aka ectopic beats which may originate from atria, AV node or ventricles and basically just come early making it look irregular - if from supraventricular (atria or AV node) then = narrow QRS, if from ventricles = wide QRS af = totally disorganised atrial electric, no p waves, irregularly irregular, QRS can be narrow vf = totally chaotic ventricular activity without efficient pump = death without resus - squiggle on sheet

Answer 3

>120bpm <45bpm = ischaemia, hypotension, sepsis af = valve disease, alcoholism, ischaemia, infection complete heart block = any heart disease ST elevation or depression = infarction or ischaemia abnormal t wave inversion = infarction, ischaemia, PE wide QRS = any heart disease

Answer 4

pulmonary arteries systolic pressure - on ECHO based on the velocity of the ejection of the pulmonary valve, we can work out how hard the pressure is there - if >40mmhg then there is high pressure there

Answer 5

arrhythmia (tachy, brady, sudden death)

Answer 6

angina | MI

Answer 7

when coronary art disease becomes obstructive, this can cause angina these plaques are stable - strong fibrous cap protects the blood from exposure to the lipid core of the lesion - preventing thrombosis

Answer 8

STEMI angina/unstable NSTEMI, awaiting trop confirmation other - PE, aortic dissection, reflux, MSK pain

Answer 9

causes anything that causes atrial stretch - HTN, HF, valve disease, lung disease, obesity, age, hyperthyroid, alc patho rapid chaotic atrial firing causes stagnation of blood in atria leads to thrombus formation and risk of embolism - > high risk of stroke reduction of cardiac output may lead to HF types paroxysmal - spont term within 7 days normally <48 hours recurrent - 2+ episodes persistent - last longer than 7 days, can degen to permanent permanent - long standing > 1 year, not successfully terminated by cardioversion ``` RF age HTN HF CAD valvular DM CKD ``` symps none or tiredness/dizziness/ breathlessness, palps. chest discomfort or just generally 'off' assoc SVT ``` ECG absent p oscillating baseline atrial rate - 350-600 vent rate 100-180 irreg irreg ``` ``` ix ECG +/- 24 hour ambulatory ECG for paroxysmal TFT FBC UE renal func LFT/coag for warfarin imaging - transthoracic echocardiogram ``` mx main priority is thromboproph, then sympt improvement with rate or rhythm control if needed then: RATE - first line BB or limiting CCB (diltiazem, verapamil), dual therapy + digoxin or two of: BB, diltiazem, dig RHYTHM >48hrs OF AF anticoag with warfarin 3w or NOAC if high stroke risk (calculate CHADS2-VASc score) before cardioversion alternative = transoesophageal echo to exclude left atrial appendage thrombus- then can be heparinised and cardioverted immediately. electrical > pharma for this. if high risk of cardioversion failure then 4w amiodarone or sotalol prior post cardioversion - 4 weeks anticoag <48hrs OF AF heparinise if risk of ischaemia - lifelong anticoag offer transoesophageal electrical cardioversion - consider amiodarone if structural heart disease. if unsuccessful BB or dronedarone or amiodarone (if no HF or LV dysfunction), dont use fleicanide if ischaemic or structural if drug rx fails - left atrial catheter ablation (if paroxysmal) or pace and ablate (if perm) at AV node - will need anticoag 4 weeks before + during procedure lifestyle factors - weight loss, diet, reduction of alc comp stroke HF cardiomyopathy

Answer 10

def HR >100bpm narrow QRS <0.12s unless related to BBB ``` types atria or SA node: - sinus tachy - AFib - AFlutter - Atrial tachy AV node - junctional: - AV re-entrant tachy AVRT - AV nodal re-entrant tachy AVNRT - sino-atrial re-entrant tachy - lown-ganong-levine syndrome - mahaim-type pre-excitation - also has LBBB morph with right accessory pathway ``` ``` causes drugs conduction disease (age) surgery aortic endocarditis ``` patho circus movement tachycardias with reentry circuit set up in diastole coronary blood flow increases. As HR increases diastole shortens. Decreased flow to heart with increased ventricular rate course onset is sudden initiated by prem beat stop abruptly but may recur - hence paroxysmal ``` symps usually intermittent palps syncope/presyncope fatigue light headed ``` MANAGEMENT most dont need mgmt but if symptomatic or need to prevent comps: ABCDE o2 + IV access whack on monitoring - ECG, BP, sats, record 12 lead YES adverse features? aka shock, syncope, MI, HF -> DC cardiovert up to 3 times -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours NO ADVERSE FEATURES: 1. REGULAR vagal manoeuvres IV adenosine - 6mg -> 12mg -> 12mg with ECG monitoring (CI in asthmatics, use verapamil instead) if rhythm restored -> probs re-entry paroxysmal SVT, do another 12 lead in sinus, if recurs give adenosine again if rhythm not restored -> A flutter - get expert help + BB IRREG ? AF IVBB or diltiazem, consider IVDig or amiodarone if evidence of HF, if <48 hrs IV amiodarone regular attacks reduced by secondary prevention - anti-arrythmic drugs (BB, flecainide, amiodarone etc) usually cured by invasive ablation - requires electrophysiological study

Answer 11

def usually reg, broad >0.12 QRS >3 PVCs in a row at >100bpm may be sustained >30s or non-sustained patho Re-entry, increased myocardial automaticity. Re-entrant circuits often occur in zone of fibrosis or ischaemia surrounding damaged myocardium e.g. post MI morphological classification monomorphic - uniform morphology polymorphic - varying torsades-de-pointes - variant type of polymorphic VT with cyclic variation of complexes and associated with long QT syndromes - can degen to VF ``` ECG features AV dissoc fusion + capture beats QRS concordance in chest leads - +VE indicates origin on post ventricular wall (wave moves towards chest leads) bizarre QRS axis RSR complexes in V1 (bad rabbit ear) if starts in left = RBBB if in right = LBBB ``` ``` causes drugs conduction disease (age) - re-entry commonest surgery aortic endocarditis ``` ``` symps tiredness dizziness breathlessness sudden death - supraventricular syncope normally haemodynamically unstable requiring immediate help - supra ``` mx ABCDE, access + 02 + monitoring (ECG, BP, sats) immediate DC cardioversion recurrence - up to 3 shocks amiodarone 300mg IV over 10-20mins and repeat shock then 900mg over 24 hours if refractory if irreg/stable - AF with BBB rx as narrow complex, polymorphic VT = magnesium 2g over 10 mins if reg/stable - VT amiodarone as above, if prev SVT consider adenosine as this is usually due to damage prevention is needed by regular anti-arrythmic drugs: BB/CBB, common to require implantable cardioverter defib unless having an acute MI if drug therapy fails -> electrophysiological study comps may degen to VF

Answer 12

``` previous MI HBP genetic causes drugs (chemo, alc) idiopathic ```

Answer 13

HF with reduced ejection fraction | preserved Ejection fraction

Answer 14

transthoracic echocardiogram (USS)

Answer 15

mainstay is transthoracic echocardiography to detect ventricular impairment newer test for elevated serum B-type Natriuretic peptide cardiac MR

Answer 16

single chamber pacemaker - in RA or RV dual chamber pacemaker - bradyarrhythmia, IN RA/V implantable cardioverter/defib - treat VT or VF. can also pace bradycardias cardiac resynchronisaton therapy - mx HF. can also pace bradycardia (CRT-P). has leads into RA + V, AND LV

Answer 17

``` degen RF congenital endocarditis papillary muscle rupture after MI ```

Answer 18

diagnosis - transthoracic echo | transoesophageal better images particularly of mitral

Answer 19

metallic prothesis - requires lifelong warfarin, which can only be stopped if bridged with heparin. NOACs not used. biological (tissue from donor or animal)

Answer 20

spinal canal stenosis or Intermittent Claudication - can be differentiated by asking if its worse going downhill = spinal canal stenosis uphill = intermittent claudication (working harder)

Answer 21

``` def Narrowing of arteries distal to AoAr most often due to atherosclerosis ``` ``` classification Fontaine: 1) asymptomatic, 2) intermittent claudication, 3) ischaemic rest pain, 4) critical limb ischaemia (*ischaemic rest pain + ulceration/gangrene) + acute limb ischaemia (sudden decrease in perfusion due to thromboembolism) ``` rutherford I - Ischaemic but not threatened - no neuro or muscle tenderness, but delayed cap refill, doppler monophasic IIa - Ischaemic and threatened but not immediate - +mild sensory and rest pain IIb - Ischaemic and immediately threatened - severe rest pain, sensorimotor deficit, muscle tenderness, no cap refil, no doppler signals III - Irreversible ischaemia (Not salvageable) - severe rest pain, profound sensorimotor, profound pallor with fixed cyanotic skin, no doppler, raised CK, lactate and met acid pres Intermittent claudication Cramping pain in calf, thigh, buttock on walking. Symptoms worse uphill. Relieved by rest. Rest time, claudication distance. Ischaemic rest pain Severe unremitting pain in foot, stops from sleeping, relieved by dangling or foot on cold floor O/E Absent/reduced femoral pulse (+ popliteal, posterior tibial and dorsalis pedis) Trophic changes: pale, cold, hairless, skin change Ulcers, poorly healing wounds, gangrene if diabetes review in 24 hours (amputation) Buerger’s angle 20 degrees, cap refill prolonged ddx Sciatica, spinal stenosis, DVT, entrapment ix BP, FBC (anaemia aggravates), ESR (giant cell arteritis), thrombophilia screen, BG, lipids, ECG (CAD), renal function, urine dip *Doppler ultrasonography (dublex) to calculate ABPI: SBP ankle/SBP arm Normal = 1 <0.9 = mild PAD, <0.8 = mod, <0.5 = ischaemic rest pain mgmt CV RF: smoking, ex (2hrs/week for 3 months), weight, statins, ACEI (*but beware renal artery stenosis), manage DM, manage HTN Antiplatelet therapy: *clopidogrel +... best medical treatment targets - <140 systolic, total chol <4, LDL <2, HBa1c <59 Supervised exercise (2hrs/week) Vasodilator therapy - e.g. naftidrofuryl oxalate Imaging if considering revascularisation: Duplex USS ± CT angiography Revascularisation if suitable and attempted CVRF - angioplasty and stenting CI Assess by vascular MDT Manage pain: paracetamol + weak/strong opioid Imaging: Duplex USS ± contrast enhanced CT angiography Revascularisation with angioplasty and stenting (percutaneous transluminal angioplasty) - aorto-bifemoral bypass graft, femoro-popliteal bypass graft ?Amputation comp *Acute limb ischaemia due to thrombus or embolism *6 Ps: pale, pulseless, pain, perishingly cold, parasthesia, paralysed *mottling -> irreversible Urgent hand-held doppler + urgent angiography: Requires re-vasc in 4-6 hours with *immediate heparinisation If embolism = surgical embelectomy (Fogarty balloon emolectomy catheter) If thrombotic = thrombolysis, angioplasty or bypass *Find the source of the emboli: ECG, echo, aortic USS Infection and poor healing Gangrene

Answer 22

``` def is a particular complication that may occur following fractures (or following ischaemia reperfusion injury in vascular patients). It is characterised by raised pressure within a closed anatomical space (fibro-osseous compartments). The raised pressure within the compartment will eventually compromise tissue perfusion resulting in necrosis. The two main fractures carrying this complication include supracondylar fractures and tibial shaft injuries ``` features Pain, especially on movement (even passive) excessive use of breakthrough analgesia should raise suspicion for compartment syndrome Parasthesiae Pallor may be present Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise Paralysis of the muscle group may occur diagnosis Is made by measurement of intracompartmental pressure measurements. Pressures in excess of 20mmHg are abnormal and >40mmHg is diagnostic mgmt This is essentially prompt and extensive fasciotomies In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when smaller incisions are performed Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients require aggressive IV fluids Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to be considered Death of muscle groups may occur within 4-6 hours

Answer 23

``` ddx graft occlusion compartment syndrome reperfussion DVT ```

Answer 24

normal diameter 2cm so AAA >3 growth 1-6mm/year with AAA types True aneurysms are an abnormal dilation of an artery due to a weakened vessel wall. By contrast, false aneurysms are external hematomas with a persistent communication to a leaking artery. causes atherosclerosis pres Mainly asymptomatic: often incidental finding Pain in back, abdomen, loin or groin *DDx for loin to groin Pulsatile abdominal swelling May rupture -> shock Distal trashing - dusky fingers from dislodged thrombus debris O/E Bimanual palpation supra-umbilical - detect 60%>3cm and 80>5cm Abdominal bruit Retroperitoneal haemorrhage - Grey Turner’s sign = flank bruising ix FBC, clotting, renal, liver, crossmatch, ESR/CRP ECG, CXR *USS for initial assessment CT for more anatomical detail, evidence of mural thrombus - *crescent sign - indicates blood within thrombus - imminent rupture MRI angiography mgmt Small = < 5.5cm, large = >5.5cm Regular USS monitoring 3-4.5cm = yearly, 4.5-5.5cm = 3 monthly, 5.5cm or larger - consider surgery Medical mgmt: smoking, HTN, statin, antipt, low dose aspirin Inform DVLA at *over 6cm Elective surgical repair if >5.5cm or rapid expansion >1cm/year or symptomatic: Open EndoVascularAR screening offer at 65 if USS neg - rules out AAA for life

Answer 25

patho virchows triad - stasis, hypercoagulability, endothelial damage ``` ix two-level wells score: active cancer <6m immobilisation of leg bedridden >3 days or maj surg<12w localised tenderness entire leg swollen calf swelling >3cm to other side pitting odema on just sympt leg collateral superficial veins prev DVT alt diag as least as likely - -2 ``` DVT likely = 2+ unlikely = 1 point or less mgmt DVT likely => proximal leg USS <4hrs - +ve anticoag -ve then d-dimer if not <4hrs then d-dimer and anticoag in meantime anticoag - apixaban (DOAC) for at least 3 months if provoked, if unprovoked 6 m

Answer 26

arterial signal ABPI venous reflux

Answer 27

acute ischaemia diabetic foot sepsis leaking AAA bleeding

Answer 28

``` pain hair loss nail atrophy ulcers gangrene ```

Answer 29

gold - clot activator and serum separating green - heparin purple - EDTA (anticoag)

Answer 30

150mmol/l intra | 4mmol/L extra

Answer 31

cell hyperpolarisation | increased duration of action potential or refractory period

Answer 32

Na/K-ATPase channel - active transport that requires energy for it to transport (because they move against their conc gradients)

Answer 33

causes hypokalaemia | by stimulation of Na-K-ATPase channels in tissues such as skeletal muscle

Answer 34

PCT | on the Na-HCO3 channel

Answer 35

late distal tubule + collecting duct at the Na-K-ATPase channels

Answer 36

thick ascending limb on loop of henle put back in via the Na-K-ATPase channel on the collecting duct

Answer 37

(exports as in out of tubule to body) carbonic anhydrase inhibitor - acetazolamide = PCT, inhibits exports of Na/HCO3 channel loop diuretics - furose, bumetanide, torsemide, ethacrynic acid = thick ascending limb of loop of henle, inhibits Na, 2Cl, K export channel thiazide diuretics - hydrochlorothiazide, chlorothiazide = DCT, inhibits Na, Cl exports ADH - increases H20 absorption at late DCT/collecting duct k+ sparing - spironolactone, eplerenone = late DCT/collecting duct, block the action of a hormone called aldosterone and this causes the kidney to pass out more fluid and keep potassium.

Answer 38

juxtaglomerular cells on the afferent arteriole that activates B2 receptors causing release of renin -> RAAS system

Answer 39

decrease BP = low renal perfusion - juxtaglomerular appartus releases renin - this increases conversion of angiotensinogen to angiotensin 1. this goes to lungs to find ACE and changes to angiotension 2. this goes to adrenals which converts steroid precursors to aldosterone. aldosterone = nacl reabsorption + k+ excretion and h20 retention.

Answer 40

increases sympathetic activity nacl reabsorption + k+ excretion and h20 retention. arteriolar vasoconstriction pit gland post lobe - ADH secretion - collecting duct - h20 absorption

Answer 41

insulin + catecholamines acidaemia - k+ + h+ are exchanged at tissues and result in hyperkalamia. hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.

Answer 42

Angiotensin receptor blockers (ARBs), also known as angiotensin II receptor antagonists, are used to treat high blood pressure and heart failure. They are also used for chronic kidney disease and prescribed following a heart attack. They include valsartan, losartan and candesartan.

Answer 43

tenting T waves flattening/loss of p waves broad QRS complex sine wave appearance - progressively widened QRS eventually merges with T wave, forming sine wave pattern - VF or asystole follows. can cause eventually heart blocks

Answer 44

severity mild - 5.5-5.9 mod 6-6.4 severe >6.5 ``` causes acute kidney injury drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin (through inhibition of aldosterone) metabolic acidosis eg DKA Addison's disease rhabdomyolysis, burns, trauma massive blood transfusion beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment digoxin ``` pseudohyperkalaemia tourniquet + clenched fist ``` pres non specific weakness fatigue flaccid paralysis depressed tendon reflexes palps chest pain ``` ``` ix U/E check for tox eg dig ABG - met acid ECG - no p wave, broad QRS, slurred s wave, peaked T wave ``` mgmt ABCDE + 12 lead ECG find cause - stop/treat emergency correction = 1. stabilise cardiac membrane - IV calcium gluconate (this does NOT lower pot) 10 10 10 - 10ml 10% every 10 min 2. short-term shift pot from extra to intra - insulin/dex infusion, neb salbutamol 3. removal of pot from body - calcium resonium (enema most effective), loop diuretics, dialysis (haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia)

Answer 45

reduction in T wave amplitude depression of ST segment U waves - small positive deflection after the T-wave in V2/3 prolong PR U have no Pot and no T, but a long PR and a long QT

Answer 46

classification mild 3.1-3.5 mod 3.5-3 severe <3 causes alkalosis - vomiting, thiazide + loop diuretics, cushings, conns acidosis - dirrhoea, renal tubular acidosis, acetazolamide, partially treated diabetic ketoacidosis inadequate intake - TPN, IV ``` features mild - asymp <3 = muscle weakness/pain, constipation <2.5 = neuromuscular probs, severe ascending paralysis and weakness -> resp failure, ileus + hypotonia, parasthesia + tetany ``` ``` ix u+e bicarc glucose serum mag ECG - to detect dig tox ``` mgmt pot replacement - mod/low risk = sandok, IV replacement NEVER BOLUS, NEVER >10MMOL/HR with cardiac monitoring + 1-3 hourly bloods magnesium deficiency - always treat mag deficiency first!! comp cardiac arrhythmia + sudden death dig Digoxin and K inhibit each others binding to Na/K ATPase Hyperkalaemia reduces digoxin activity, hypokalaemia increases activity

Answer 47

``` SN node atrium AV node bundle of His L and R bundle branches purkinje fibres ```

Answer 48

``` R-R interval large sq 1 = 300bpm 2 = 150 bpm 3 = 100bpm 4 = 75pm 5 = 60pm 6 = 50pm ```

Answer 49

ventricular contraction

Answer 50

ventricular tachycardia

Answer 51

1. depolarisation is moving towards that lead 2. depolarisation is moving away 3. depolarisation is perpendicular to that lead

Answer 52

strain on the R or L of the heart causing increase work and size of the muscle on that side that is causing a greater electrical effect on that side skewing the electrical axis.

Answer 53

v1/2 - RV V3/4 septum 5/6 - LV

Answer 54

1. rhythm 2. conduction intervals 3. cardiac axis 4. description of QRS complexes 5. description of ST segments and T waves followed by ur interpretation: normal or abnormal then the ?underlying pathology that would cause this

Answer 55

def bradycardia + AV block <60bpm sinus brady - every p wave followed by a QRS + <60bpm causes physiological - athletes, young due to high resting vagal tone patho - acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP ``` pres syncope fatigue dizziness ischaemic chest pain palps ``` mgmt if rate >40bpm but asymp dont treat, but look for cause and maybe change drugs if <40bpm or symp: IV atropine 500mcg (in emergency) - anticholinergic i.e muscarinic antagonist, reduces vagal tone not worked? give more up to 6 doses try noradenaline temp pacing wire - transcutaneous cardiac pacing long term - permanent implantable pacemaker - specialist review

Answer 56

``` def result of dysfunction of SA node with impairment of ability to generate impulse ``` causes idiopathic fibrosis of node - assoc with ischaemia + dig tox ECG sinus brady sinoatrial block - transient failure of impulse conduction to atrial myocardium, pause between p waves sinoatrial arrest - prolonged pause without p wave activity, unrelated to PP interval assoc escape rhythms - spont activity from subsidiary pacemaker located in atria, AV junc or ventricles (junct - normal QRS 40-60bpm, ventricular - broad complex slow 15-40bpm) mgmt tachy-brady syndrome or AF treat if symp - permanent atrial or dual chamber pacemaker if with tachy + dig or verapamil (anti-arrhythmic)

Answer 57

inhibits parasymp so pupil dilation urinary retention dry eyes constipation

Answer 58

AV conduction may be delayed, intermittently blocked or completely blocked. abnormal conduction of AV node or bundle of His ``` causes MI/ischaemia (inferior) infection - lyme disease immunological (SLE) myocarditis endocarditis degen of his-purkinje drugs - dig, BB, CCB ``` ``` types 1ST DEGREE BLOCK delay of atrial impulse to ventricles - PR >0.2s constant - every P followed by QRS pres - benign ``` 2ND DEGREE BLOCK intermittent failure of conduction from atria to ventricles. some P are not followed by QRS. MOBITZ TYPE 1 aka Wenkebach. failure at AV node level. PR progressively lengthens then is blocked. pres - usually asymp, mgmt if symptomatic or inferior MI cause MOBITZ TYPE 2 - intermittent failure of P wave conduction and loss of QRS. failure at bundle branch therefore wide QRS. PR constant but prolonged. 2:1 or 3:1 block. risk of asystole if symp pacing required atropine useless as past AV node 2:1 BLOCK - difficult to tell whether its mobitz 1 or 2. but can be caused by dig tox or ischaemia 3RD DEGREE BLOCK complete failure of conduction of atria to ventricles normally caused by myocardial fibrosis - independent P and QRS waves: AV dissociation. - if block in or above HIS (nodal) - QRS narrow rate id 45-60 - if block in or below - wide slow QRS <45 ``` mgmt stable - observe unstable or risk of asystole - mob type 2, complete HB or prev asystole: - atropine 500mcg IV repeat up to 6 times for response - try noradrenaline next - transcutaneous cardiac pacing ```

Answer 59

``` ASSOC conds mainly pathological Rheumatic heart disease RVH - could be due to cor pulmonale IHD - aka MI myocarditis cardiomyopathy degen disease of conduction system PE ``` patho depolarisation of RV delayed LV depol normal therefore first part of QRS normal spread depol from L to R through non-specialised tissue ``` ECG MarroW - M in V1 and W in V6 QRS >0.12s secondary R wave in V1/2/3 RSR deep wide slurred S wave in 1, V5/6 T wave inversion in V1/2 ```

Answer 60

``` assoc conds coronary art disease HTN heart disease dilated cardiomyopathy anterior infarction ``` blood supply LAD + right coronary art therefore if LBBB - extensive disease ``` ECG WilliaM - wide QRS >0.12s absent Q in V5/6 broad R in I, V5/6 deep S in V1,2 assoc LAD ```

Answer 61

ix 12 lead ECG Ix for electrolyte imbalance UE, glucose, Ca, Mg, TFT, toxicology mgmt If symptomatic (syncope, hypotension, heart failure) or rate <40: Resus, IV access FBC, UE, glucose, Ca, Cr, cardiac enzymes, TFT, digoxin level Treat cause: correct electrolytes, stop negative chronotropes Treat bradycardia: IV atropine 0.5mg (may repeat up to 3mg) Poor response - transcutaneous pacing May also try glycopyrrolate (antimuscarinic), glucagon (if due to BB or CCB) Temporary or permanent pacing (esp @heart block, sick sinus)

Answer 62

ventricular tachy regular - monomorphic, right venticular outflow tract, fascicular irreg - torsades de points, polymorphic ventricular tachy supraventricular with aberrant conduction or ventricular pre-excitation any SVT may present as broad aberrant conduction - usually manifests as LBBB or RBBB WPW AF with AV re-entrance patient >35, hist of IHD or CHF signs AV dissociation: cannon waves in JVP, variable intensity first heart sound

Answer 63

``` def every P followed by QRS, >100bpm ``` ``` causes physiological - exertion, anxiety, pain patho - fever, anaemia, hypovolaemia endocrine - thyrotoxicosis, phaemochromocytosis pharma - adrenaline, albs, alc, caffeine ``` ECG every P followed by QRS rate 100-200 ``` ix 12 lead ECG cardiac enzymes RBC TFT ``` mgmt acute - haem stable (ie not hypotensive) - vagal manoeuvres: carotid massage, vasalva, facial immersion in cold water ongoing - exlude BB or non-dihydropyridine CCB (diltiazem, verapamil)

Answer 64

source ectopic in atrial muscle rate - 150-250bpm ECG ectopic unifocal p waves usually precede normal looking QRS complexes, unless aberration present usually <250bpm abnormal p wave morphology - inverted p waves in inferior leads rate 150-250 variable ventricular rate but reg may have varying degrees of AV block ``` types benign - elderly 80-140bpm incessant ectopic multifocal - COPD, varying p wave morph atrial tachycardia with block - dig tox (baso a fast heart block) ``` ectopic atrial rhythm is similar but rate <100 bpm

Answer 65

``` def/types classified according to duration: - first ep - recurrent (>2 eps) - paroxysmal (lasting <7days) - persistent (>7 days) - long standing persistent (>1 year) - permanent (>1 year if rhythm control not successful or attempted) ``` ``` asssocs most forms of heart disease: - CAD - HTN - valvular - congenital - cardiomyopathy some metabolic - thyrotoxicosis and toxins eg alc ``` patho mechanism unknown disorganised atrial electrical and contractile activity ECG absence of P-waves irregularly irregular activation of ventricles fine fibrillatory waves visible in ECG baseline 'ashman phenomenon' - aberrantly conducted ventricular beats usually with RBBB morphology mx high risk of thromboembolism -> CHA2DS2-VASc score to figure out if to anticoag rate vs rhythm control with drugs DC cardioversion +/or ablation therapy

Answer 66

what is it regular narrow complex tachycardia caused by re-entry circuit in RA ``` classification TYPICAL (type 1) - involving the IVC and tricuspid isthmus with anti-clockwise re-entry producing inverted/neg flutter waves in leads I, II, aVF and positive waves in V1. ATYPICAL (type 2) - atrial rate is higher and rhythm more unstable. less amenable to ablation than type 1. ``` causes similar to AF most common - CAD, HTN, hyperthryoid, obesity, alc, COPD ECG saw tooth flutter waves visible on ECG rate of 300bpm atria (200-400). ventricular rate determined by degree of AV block, 2:1 the commonest + 4:1. if 1:1 can happen via accessory pathway (WPW), progresses to VF and is medical emergency. no p waves therefore 2:1 atrial flutter should always be suspected with someone who presents with 150bpm + narrow complex tachy ``` ix ECG +/- 24 hour ambulatory ECG for paroxysmal TFT FBC UE renal funct LFT/coag for warf imaging - echo for underlying cardiac function ``` mgmt similar to fibrillation but more sensitive to cardioversion ventricular rate slowed with digoxin, BB or CBB DC cardioversion to convert to SR definitive therapy - radiofrequency ablation to tricuspif isthmus anticoag

Answer 67

def extra beats that originate outside the sinus node from ectopic atrial pacemaker appear interspersed throughout an underlying rhythm can be single or repetitive ECG ectopic premature P wave always incomplete pause after a PAC, owing to reset the sinus node the ectopic p wave normally generates a QRS complex

Answer 68

LONG SHORT WEIRD long R-R interval followed by short R-R interval then a disrupted QRS with RBBB morphology (M)

Answer 69

def simiar to PAC but less frequent ectopic beat that originates in atrio-ventricular node + His bundle p wave is negative compensatory interval is shorter than PAC simultaneous capture of the atria (retrograde) and ventricles (anterograde) ECG retrograde P wave before or after QRS (often hidden) in inferior leads usually short PR interval

Answer 70

discrete multifocal p waves with differing morphologies several ectopics happening in atria firing off currents 100-250bpm varying PR intervals followed by normal QRS complexes unless aberration present ventricular response is irregularly irregular can be confused with AF - but you do have p waves so cant be AF if rate <100bpm its called multifocal atrial rhythm

Answer 71

EPI most common onset late teens or early 20s abrupt + offset following PAC patho - Two functionally and anatomically different pathways in AV node with common path in lower AV node and bundle of His. One path fast with long refractory, one slow with quick refractory. - In sinus, travels down fast and depolarises ventricles, also travels down slow but common path is still refractory - Slow pathway recovers first, AVNRT initiated if premature atrial beat at critical moment when fast pathway refractory. Impulse travels down slow then retrogradely up fast creating re-entry circus motion ``` pres sudden onset palps SOB syncope neck pulsation ``` ``` ECG hr 150-250bpm reg rhythm narrow QRS p wave is retrograde but may not be visible in II, III, AVF (inferior leads) ``` mgmt terminated by vagal manoeuvres and AV nodal blocking drugs eg adenosine (short acting and works on AV node) , proph - BB/CCB + adeno curative - radiofrequency ablation FULL MANAGEMENT most dont need mgmt but if symptomatic or need to prevent comps: ABCDE o2 + IV access whack on monitoring - ECG, BP, sats, record 12 lead YES adverse features? aka shock, syncope, MI, HF -> DC cardiovert up to 3 times -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours NO ADVERSE FEATURES: 1. REGULAR vagal manoeuvres IV adenosine - 6mg -> 12mg -> 12mg with ECG monitoring (CI in asthmatics, use verapamil instead) regular attacks reduced by secondary prevention - anti-arrythmic drugs (BB, flecainide, amiodarone etc) usually cured by invasive ablation - requires electrophysiological study

Answer 72

``` def re-entry circuit involves AV node and an extra-nodal bypass pathway ``` most common extra-nodal conduction pathway is the accessory pathway known as Bundle of Kent in the WPW syndrome - this is a congenital atrio-ventricular bypass tract which can exist in a variety of locations and in some patients there are multiple pathways. can conduct in both directions but rare this can cause early activation of ventricles = pre-excitation WPW = risk of sudden death classification - Type A - less common, accessory pathway in left = positive delta-wave in all precordial leads, dominant R wave in V1 Type B = much more common, pathway in right side of heart. neg delta wave in leads V1/2, no dom R wave in V1 assoc with LAD ``` ECG short PR interval <0.12 delta-wave with slurring of R wave wide QRS >0.11 repolarisation is abnormal causing inverted T wave ``` ``` types of conduction ORTHODROMIC - common, antegrade conduction via normal pathway, retrograde conduction via accessory pathway QRS can be normal p-waves buried in QRS or retrograde ST depression + T dep common 200-300bpm ANTIDROMIC - less common, antegrade conduction via accessory pathway, features of pre-excitation, wise QRS . p waves buried or retrograde HR 200-300bpm ``` worries AF can occur in WPW and sometimes flutter - the accessory pahway can allow for rapid conduction, bypassing AV node = high ventricular rates -> VT or VF wide QRS complex owing to abnormal ventricular depolarisation via accessory pathway irregular rhythm potentially lifethreatening mgmt definitive = radiofrequency ablation of accessory pathway med = - sotalol (should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation) - amiodarone - flecainide

Answer 73

junctional escape beats - av node takes over from SA node as pacemaker if a problem, creating a 40-60bpm junctional escape rhythms - defined as 3 or more junctional escape beats in succession. AV dissociaton or retrograde atrial capture. can occur normally in athletes or in sinus node disease or BB accelerated junctional rhythms - active junctional pacemaker firing at rate of 60-99bpm - result of ischaemia, inflam, drugs and some electrolyte disturbances. retrograde p waves in ST segment. QRS appears normal. non-paroxysmal junctional tachycardia accelerated junctional rhythm but with a rate of >/=100bpm

Answer 74

def arise as ectopic impulses from ventricular myocardium both RV + LV can be one off or more if frequent = >10 per hour on 24 hr ECG monitoring ECG wide QRS t wave in opposite direction to the R wave with a full compensatory pause if from RV = LBBB QRS pattern, LV = RBBB pattern causes common in fit healthy indi but can be assoc with: - underlying heart disease (HTN, CAD, valvular, CM, congenital) - drugs - antidep, aminophylline, dig, amphetamines, anaesthetic agents, cocaine, caffeine, alc - infection -stress - electrolyte disturbances ``` pres can be asymp palps sensation of missed beats heart thumps dizziness dyspnoea chest pain syncope - rare ``` differentiating from PAC - this one has same space between two R waves around etopic as before when in sinus = complete rest. in PAC these distances will be different

Answer 75

temp alteration of QRS morphology under conditions where a normal QRS would be expected. can occur with sinus beats or ectopics and sustained arrhythmias. causes ashman phenomenon is one cause as well as tachy/brady or cos of an accessory pathway ECG QRS complex = RBBB morphology

Answer 76

def ectopic ventricular pacemaker exceeds sinus rate leading to independent ventricular rhythm AV dissociation is present but fusion and sinus capture beats are often present ECG reg broad QRS complexes >120ms rate 50-99bpm = 3 beats in a row qualifies as this ``` causes common after reperfusion by thrombolysis or PPCI in STEM, dog tox electrolyte disturbance high vagal tone in athletes ``` course usually benign + self-limiting

Answer 77

def in normal heart there is a hierachy of pacemaker tissues with different intrinsic depolarisation rates. usually subsidary pacemakers are suppressed from above ie by the SA node in NSR if sequence interrupted a lower pacemaker takes over in idioventricular escape the block occurs above the ventricles usually in the AVN but mybe higher ECG broad QRS >0.12 rate 20-50bpm ``` causes 3rd degree AV block sinus arrest SA block hyperkalaemia AV nodal blocking drugs eg BB, CCB, dig ```

Answer 78

``` def arise from protected ventricular ectopic focus that fires at a fixed rate independent of the basic rhythm, usually sinus = parallel rhythm with varying coupling intervals with an underlying rhythm ``` assoc structural heart disease super rare

Answer 79

chest leads

Answer 80

all the waves go up from the base line | neg all go down from baseline

Answer 81

Capture beats — occur when the sinoatrial node transiently 'captures' the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration. Fusion beats — occur when a sinus and ventricular beat coincides to produce a hybrid complex.

Answer 82

``` accquired heart disease eg CAD congential long QT Brugada syndrome Hypertrophic cardiomyopathy dilated cardiomyopathy catecholamine polymorphic ventricular tachycardia syndrome drug tox - tricyclic antidep, antiarrhythmics electrolyte disturbance espesh K + ```

Answer 83

def disorganised and chaotic heart rhythm in which effective pumping action of the ventricles ceases causing 'cardiac arrest' fatal rf CAD acute MI chronic infarction scar ``` causes VT AF antiarrhythmic drugs can be idiopathic sudden arrhythmic death syndrome - affects 500 people p.a in uk electrocution drowning ``` ``` ECG chaotic - varying amplitudes no identifiable P, QRS, T rate 150-500 amplitude decreases with duration: coarse AF to fine AF ``` mgmt acute: immediate CPR rapid electrical defib ideally with biphasic modality long term - BB and implantable cardioverter defibrillator survival out of hosp <10% in hosp 24%

Answer 84

patho sinus node has two types of cells, a core of pacemaker (P) cells which generate the impulse and an outer layer of transitional (T) cells which transmit the impulses to the RA. In S-A Exit Block the P cells continue to fire but there is malfunction/failure of transmission by the T cells types 1st 2nd - types I + II (only one that can be reliably diagnosed from ECG) 2 TYPE I - has wenckebach phenomenon of progressive worsening conduction - shortening of PP interval until P wave dropped. irreg rhythm. the P-P pause < sum of two preceding P-P before pause. P-P after pause is greater than before. 2 TYPE II - dropped p waves at reg intervals. pause is approx 2x basic p-p, assuming reg rhythm 3rd - complete absence of p waves. rhythm maintained by junctional escape - if not complete pause which may be difficult to distinguish or progress to sinus arrest -> asystole

Answer 85

``` if the patient had coexistent heart failure first onset AF or obvious reversible cause younger than 65 symptomatic ```

Answer 86

decide whether to anticoag in AF ``` congestive heart failure +1 HTN (or rx) +1 age >/= 75 +2, 65-74 +1 diabetes +1 prior stroke or TIA +2 vascular disease - including ischaemic heart disease + peripheral +1 sex - f +1 ``` ``` 0 = no treatment 1 = males consider anticoag, female no treatment 2+ = anticoag ``` if chads vasc says no anticoag ensure a transthoracic echo has been done to exclude valvular heart disease which with AF is abso indication for anticoag offer choice of warfarin or NOAC - always do a HASBLED risk assessment for warfarin before prescribing

Answer 87

risks of starting someone on warfarin or not HTN - uncontrolled systolic >160 +1 Abnormal renal function (dialysis or cr >200) OR abnormal liver function (cirrhosis, bilirubin >2 times normal, AST/ALT/ALP >3 x normal) +1 each for liver or renal Stroke hist Bleeding hist Liable INR (time in therapeutic range <60%) elderly >65 years Drugs predisposing to bleeding (antiplatelets, NSAIDs) or alc use (>8 drinks/week) +1 for each >/= 3 indicates high risk of bleeding

Answer 88

history of falls old age alc excess hist of bleeds

Answer 89

2-3 (non-valv) prosthetic valves, post MI - 2.5-3.5 switch to NOAC

Answer 90

congen - jervell-lange nielsen (abnormal pot channel) romano-ward syndrome drugs - amiodarone, sotalol, class 1a antiarrhythmic drugs, tricyclic antidepressants, fluoxetine, chloroquine, terfenadine, erythromycin other - electrolyte (hypo cal/kal/magn), acute MI, myocarditis, hypothermia, subarac haem

Answer 91

patho ventricular + broad origin = posterior fascicle. produces relatively short QRS (0.12-0.14) ECG QRS = RBBB + LAD

Answer 92

patho ventricular + broad spreads inferiorly ECG LBBB + RAD mx BB or CBB

Answer 93

types atrial tachy with abberant conduction - broad complex tachy with L or R BBB WPW if antidromic (travels the opposite way up nerve) antidromic AV re-entrant tachy AF with accessory pathway differentiating If RBBB ventricular origin if QRS > 0.14s, axis deviation, concordance all deflections positive If LBBB ventricular origin if QRS > 0.16s, axis deviation, concordance all deflections negative CHECK PREV ECG, if pre-existing BBB suspect SVT danger of misdiagnosis - safest to treat broad complex as ventricular tachycardia - giving verapamil to pt with VT may cause hypotension, acceleration and death - could use adenosine to temp block conduction through AV node to find out origin

Answer 94

shockable - VF, pulseless VT nonshockable - asystole, PEA (pulseless electrical activity)

Answer 95

what is it Genetically inherited condition characterised by abnormal ECG and increased risk of sudden death. Autosomal dominant. Sodium channels ``` ECG Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T (Brugada sign) + Documented VF or PVT Fam Hx sudden death <45 Coved ECG ``` mgmt ICD implantable cardioverter defibrillator

Answer 96

*Sinus tachycardia - main finding S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10% Assoc RBBB

Answer 97

Late delta wave, positive deflection at junction of QRS and ST segment, associated with hypothemia

Answer 98

``` class 1 - acts on section 0 of action potential Na channel blocker 1a = moderate: quinidine, procainamide 1b = weak: lidocaine, phenytoin 1c = strong: flecainide, proafenone ``` ``` class 2 - acts on section 4 BB - propanolol, metoprolol ``` ``` class 3 - acts on section 3 K+ channel blocker amiodarone, sotalol ``` ``` class 4 - acts on section 2 ca2+ channel blocker verapamil + diltiazem ```

Answer 99

``` adenosine dig diltiazem verapamil fleicanide ```

Answer 100

``` indication For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work ``` action Blockade Na/K/Ca channels, antagonist alpha and beta adrenergic receptors which reduces automaticity, slows conduction and increases refractory period including in AV node (therefore reduces vent rate in AF and AFl) adverse effects Hypotension during IV infusion. Chronic use lungs (pneumonitis), heart (AV block), liver (hepatitis), skin (grey discolouration), *thyroid (long half life) Amiodarone iodine rich and very similar levothyroxine. Can cause hypothyroidism CI Severe hypotension, heart block, thyroid disease interactions Increases plasma conc of NDHP-CCB and digoxin therefore these should be halved prescribing Always requires senior unless in cardiac arrest (after third shock) - give 300mg bolus

Answer 101

indication First line diagnostic and therapeutic in SVT (inc junc) action Adenosine receptor agonist on cell surface. In heart reduces automaticity and increases refractoriness -> slows sinus rate, slows conduction and increases AV node refractoriness (breaks re-entry circuit) only works if circuit involves AV node. Blocks conduction to ventricles allowing closer inspection of atrial rhythm Very short duration - half life 10s important Blocks SA and AV node - causes bradycardia and asystole - doom feeling May induce bronchospasm in asthma or COPD prescribing Always IV, must be in once-only 6mg, if ineffective may give 12mg, must always monitor with continuous ECG

Answer 102

aka cardiac glycoside indication Reduce ventricular rate (AF, AFl) - after CCB or BB Severe heart failure - 3rd line ``` action Negatively chronotropic (HR), positively inotropic (contractility). In AF indirect path increases vagal tone (PSNS - lost in exercise). Reduces conduction at AV node. In HF has direct effect on myocytes - inhibits Na/K pumps causing increased intracellular Na. This means Ca accumulates in cell increasing contractile force (Na/Ca exchange) ``` important SE Digoxin toxicity - arrhythmias, low therapeutic index (margin therapeutic to toxic) Bradycardia, GI upset, visual disturbance (blurred/yellow), headache, nausea *Gynaecomastia warnings CI at second degree heart block. Reduced dose in renal failure. Increased risk of toxicity in *hypokalaemia, hypomagnaesaemia, hypercalcaemia Digoxin competes potassium at Na/K pump. When serum K low competition is reduced and effect increased important interactions Loop + thiazide diuretics cause hypokalaemia - toxicity Amiodarone, CCB, spironolactone all increase plasma digoxin - toxicity prescribing Loading dose in AF/Afl - 15mcg/kg lean body mass orally once daily In elderly give in divided dose If no effect give additional 5mcg/kg Calculating maintenance Fraction of loading dose adjusted for renal function 100=⅓, 50 = ¼, 25 = ⅕, 10 = ⅙, 0 = 1/7 HF - no loading dose - give 62.5-125mcg PO OD Can give IV - only if slowly ``` monitoring Monitor symptoms (or vent rate) + ECG + renal dysfunction + hypokalaemia ``` tox symps Nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision levels Plasma concentration digoxin Target 1.0-1.5nmol/l Above 2.0nmol/l suggests toxicity ECG ST-segment depression - reverse tick sign

Answer 103

eg + usefulness Verapamil (most cardio-selective) + diltiazem (non-dihydropyridine) + amlodipine (dihydropyridine) action Rate control in SVT inc AF +AFl Decrease Ca entry to vascular and cardiac cells induces relaxation + vasodilation in arterial smooth muscle + myocardial contraction in heart. Suppress cardiac conduction particularly over AV node Reduced rate, contractility and afterload decreases oxygen demand preventing angina SE Ankle swelling, flushing, headache - dihydropyridine e.g. amlodipine Verapamil - constipation, bradycardia, heart block Diltiazem (mixed) CI Don’t prescribe with BB - both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole prescribing HF, bradycardia + asystole For acute SVT verapamil may be given IV *the only one IV

Answer 104

``` indication First line IHD reduce angina CHF improve prognosis AF reduce rate and maintain sinus rhythm SVT to restore sinus rhythm ``` action B1 in heart, B2 in smooth muscle blood vessels and airways Via B1 reduce force and speed of conduction in heart - reduces cardiac work and oxygen demand and increase myocardial perfusion Prolong refractory period of AV node Lower BP by reducing renin secretion SE fatigue, cold extremities, headache, impotence CI Asthma - B2 blockade causes bronchospasm, usually safe in COPD Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol) Don’t use with NDHPCCB

Answer 105

sympathetic only

Answer 106

para + symp components

Answer 107

volume of blood ejected from LV per min preload, contractility, HR, afterload SV X HR

Answer 108

systemic vascular resistance x CO

Answer 109

Preload or degree of stretch is critical factor for stroke volume. Increased EDV (end-diastolic volume) leads to increased myocardial stretch Increased myocardial stretch leads to increased contractility and increased stroke volume decreasing end systolic volume This implies in blood loss - reduce EDV = reduced CO *preload is EDV, afterload is ventricular pressure at end of systole

Answer 110

APTM - all prostitutes take money A - aortic rse 2nd P - pulmonary lse 2nd T - tricuspid - rse 4th M - mitral midclav 5th

Answer 111

levines scale Grade 1 Heard by an expert in optimum conditions Grade 2 Heard by a non-expert in optimum conditions Grade 3 Easily heard, no thrill Grade 4 Loud murmur, palpable thrill Grade 5 Very loud murmur, often heard over a wide area, palpable thrill Grade 6 Extremely loud, heard without a stethoscope

Answer 112

S1 - closure mitral and tricuspid (M1 + T1) S2 - closure aortic and pulmonary (A2 + P2) - might split on deep inspiration - delayed P2

Answer 113

pulm HTN/ Pulm stenosis

Answer 114

HF - sounds like galloping horse

Answer 115

systolic - between S1 + 2 (may be innocent in children and preg) diastole - always patho, between S2+1

Answer 116

@apex + radiate to axilla, heard best in left lateral position MR Pansystolic - burrrr MS Loud opening snap S1 and mid-diastolic murmur - lub de-durrrr

Answer 117

where Uncommon, timing is as for mitral murmurs @lower right sternal TS Pre systolic May occur in RVH, marked wave on JVP TR Pansystolic Does not radiate to axilla

Answer 118

L2IS PS Crescendo-decrescendo systolic (louder then softer).disappear on inspiration ``` PR Early diastolic (Graham Steel due to pul HTN due to MS) ```

Answer 119

Transmitted to carotid, R2IS, best held on breath hold AS Crescendo-decrescendo systolic. In stenosis A2 is soft. AoScl not transmitted carotids. lub whoosh dub AR Early diastolic best heard leaning forward on breath hold (pulmonary diappears) lub tarrrr

Answer 120

PRESSURE OVERLOAD valve anatomy three thin cusps epi most freq due to senile calc ``` assoc CAD bicuspid valve RF williams syndrome ``` pres Classic triad: chest pain (predisposes to chest pain), heart failure (obstruction -> LV hypertrophy -> LV failure), syncope (insufficient blood) SOBOE O/E Slow rising pulse Narrow pulse pressure (diff between syst and dia) LV hypertrophy -> apex thrill Ejection systolic murmur that radiates to carotids Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids ix ECG: LVH (*S wave V1 depth + R wave height V5/V6 > 35mm) or strain (ST depression and T wave inversion in lateral leads) CXR: calcification of aortic ring, cardiac enlargement, post stenotic dilatation *Echo (transthoracic): confirms presence + degree, + left ventricular function + thickness Doppler echo for severity - pressure gradient > 50, area <1cm2 - reassess 6 monthly mgmt Avoid heavy exertion, modify RF for CAD If symptomatic - prompt valve replacement - first line If not fit for surgery Second line - balloon valvuloplasty - risk of re-stenosis TAVI - transcatheter aortic valve replacement ``` comp Predisposition to infective endocarditis Antibiotic prophylaxis Small emboli Decompensation - increased pressure in pulmonary - CHF Anticoagulate mechanical heart valves Target INR 2.5-3.5 for aortic Target 2-3 for others if no other risk factors (AF, previous stroke then 2.5-3.5) ```

Answer 121

VOLUME OVERLOAD causes Bicuspid aortic valve (congenital), rheumatic fever (@developing), infective endocarditis, collagen vascular disease, degenerative (@developed) connective tissue disease RA/SLE age 40-60 - degen assoc SLE, Marfan’s, Ehler-danlos, Turner’s, aortic dilatation with anky spon, acute AR in IE or aortic dissection (severe chest/back pain) syphilis HTN pres Acute - cardiovascular collapse SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea) O/E Early diastolic murmur as R2IS sitting forward in expiration not well transmitted to carotids Collapsing water hammer pulse Wide pulse pressure Austin Flint soft rumbling low pitched late diastolic murmur heard at apex Quinckes sign - nailbed pulsation de musset sign - head bobbing ix ECG - LVH (RV1 + SV5/6 >35mm) CXR - ?signs of heart failure due to volume overload TTE + colour doppler mgmt medical - LVH = diuretic, ACE i Valve replacement screening Screen family members of patiens with Marfan’s Mild - mod - review yearly + 2 yearly echo, severe i.e. left ventricular diameter/ejection fraction monitor 6 monthly

Answer 122

patho Structural abnormality of valve -> increased LA pressure + pulmonary artery pressure Pulmonary HTN -> RV dilatation and tricuspid regurg + RV failure RV failure: raised JVP, liver congestion, ascites, peripheral oedema static blood in LA = thromboembolism causes Congenital, rheumatic fever (most common), degenerative calcification (elderly) (SLE, RA, IE, amyloid) pres Asymptomatic for years then deteriorate Progressive breathlessness (SOBOE, orth, PND), palpitations due to AF, systemic emboli Symptoms due to enlarged LA - hoarseness, dysphagia O/E Malar flush (CO2 retention), raised JVP, RVH - laterally displaced apex/RV heave (4th intercostal tricusp), signs of RHF (hepatomegaly, ascites, peripheral oedema) Mid-late diastolic murmur best heard in left lateral Loud S1 with opening snap low volume pulse AF ix ECG: AF, large LA P-mitrale (bifid), RVH (dominant R wave in V1 >7mm tall, dominant S wave in V5/V6 >7mm deep) CXR: LA enlargement, interstitial oedema (Kerley A/B lines), prominent pulmonary vessels Echo -the normal cross sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross sectional area of < 1 sq cm mgmt If AF: anticoagulant therapy indicated For dyspnoea: diuretics (reduce preload) or nitrates For exercise tolerance: BB or NDHPCCB If symptomatic: Valve balloon: PMC percutaneous mitral commisurotomy follow up yearly comp AF, pulmonary HTN, thromboembolism, RHF, rheumatic fever, IE prevention Prophylaxis for rheumatic fever and infective endocarditis (penicillin>)

Answer 123

``` def Mitral valve does not close properly causing leaking of blood from left ventricle back to LA ``` how it causes HF? As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myometrium becomes less efficient, and eventually go into irreversible heart failure. epi Second most common, assoc females, low BMI, advanced age cause Now less rheumatic fever so most common cause is degenerative MI, CAD, IE, post mitral valve surgery, Ehler-Danlos, SLE, rheumatic fever ``` RF Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome ``` pres most asymp Acute leads to rapid pulmonary oedema (papillary muscle rupture/IE) -> surgery Chronic MR eventually causes heart failure and breathlessness, fatigue, oedema O/E Pansystolic blowing murmur at apex radiating to axilla Laterally displaced apex beat S3 gallop ix ECG: enlarged LA: broad P wave, AF CXR: enlarged left atrium and left ventricle (cardiomeg) Echo: confirm Dx and severity (based on jet into atrium) mgmt If signs of LV dysfunction or AF - surgery med acute - Nitrates, diuretics, positive inotropes + intra-aortic balloon pump to increase CO HF? ACEI, + BB + spiro monitor 6 monthly surg - If acute and severe *Valve repair ``` comp pulm HTN LV dysfunction AF thromboembolism due to AF ```

Answer 124

reaction to an infection patho Group A beta haemolytic streptococci (pyogenes) Antigen mimicry - antibody to cell wall of strep cross reacts with valvular glycoproteins and cardiac myocytes -> inflammation and scarring type 2 hypersensitivity when? 2-4 weeks post streptococcal pharyngitis or skin infection ``` what affected? joints skin heart nervous system ``` which valve 90-95% mitral RF overcrowding poor hygiene skin infection pres + criteria 3w post sore throat JONES CRITERIA Evidence of recent strep infection (e.g. scarlett fever, positive throat swab, increased/rising antistreptolysin O titre or DNase B titre) Plus 2 major or 1 major + 2 minor JONES PEACE major: Joints - large joint arthritis - NSAID (red, hot, swollen) O (heart 40%) - carditis - pancarditis pericardium, myocardium, endocardium (valv), tachycardia, murmur, pericardial rub Nodules (10%) painless and subcutaneous on extensors Erythema marginatum (5%) - pale red macules/papules 1-3cm Sydenham’s chorea (20%) jerking of upper limbs - purposeless ``` minor: PR interval prolongation (not if carditis major) ESR very raised Arthralgia (not if arthritis) CRP very raised Elevated temp (>90% are over 39 degrees) ``` ix Evidence of streptococcal: throat culture, antistreptococcal antibodies (ASO, *anti-DNase B) rise during first month. Check 2 weeks apart for a rise ECG: PR, ST elevation (saddle shape) suggests pericarditis CXR - ?heart failure FBC (WCC), ESR, CRP Doppler echo for carditis mgmt Enforce bed rest till inflam markers normal Eradicate strep - single IV benzylpenicillin + oral penicillin Treat HF: diuretics, ACEI and digoxin Suppress inflammation: NSAIDs For chorea: self-limiting, may suppress with haloperidol (beware EPSE) comp carditis mitral stenosis congestive HF secondary prev abx proph - 5 yrs or till 21, 10 if carditis

Answer 125

suspect when fever new murmur = endocarditis until proven otherwise why affects vavles Valves have a poor blood supply therefore it is hard for WBC and drugs to reach them organism Staphylococci (aureus) invasive procedures/drug users, streptococcus viridans (subacute) (dental procedures) staph epidermidis - most common cause following valve replacement non-infective - SLE ``` rf Valve: rheumatic disease, replacement Congenital structural heart Previous IE Hypertrophic cardiomyopathy IVDU - tricusp ``` pathogenesis All have non-bacterial thrombotic endocarditis (sterile fibrin-platelet vegetation) for adhesion and invasion Invading organism clump and form thrombus and produce agglutinating antibodies Organism destroys valve leaflets Immune system activates forming immune complexes - cutaneous, kidney or arthritis course Acute - thrombus by invading org or valve trauma (wires) Subacute - sufficient bacteria for invasion of thrombus Non-bacterial - SLE, CKD, neoplasia which valve mitral > atrial > both pres Subacute: fatigue, low grade fever, polymyalgia, loss of appetite, wt loss Acute: rapidly progressing infection *Majority are fever + chills + poor appetite + wt loss FROM JANE Fever > 38 + tachycardia Roth’s spots - eyes, retinal haemorrhage with pale centre Osler’s nodes - painful red blisters @ terminal phalanges and toes Murmur - Tricuspid with s.aureus Janeway lesions - painless red maculae on thenar eminence Anaemia/Arthritis: subacute = asymmetic > 3 jts, acute = septic monoarticular Nail haemorrhage - splinter - red and linear Embolic phenomena e.g. stroke Subacute: clubbing diagnosis MODIFIED DUKES CLASSIFICATION pathological criteria +ve 2 maj 1 maj + 3 minor 5 minor PATHO +ve histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content) MAJOR: 1. Blood culture: 2 separate +ve blood cultures 2. Echo: evidence of endocardial involvement: vegetation/abscess MINOR 1. Blood culture 1 +ve blood culture 2. Fever >38 3. Vascular phenomena: major arterial emboli, janeway lesions, IC haem 4. Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, RF 5. Predisposition - IVDU, heart condition ``` ix FBC - wcc, anaemia ESR/CRP RF transthoracic echo within 24 hours blood cultures (subacute or chronic = 3 sets from peripheral sites within 6 hours between them, acute = start abx then take 2 within 1 hour) CXR ECG ``` mgmt Start ABX empirical (IV) General: amoxicillin + gentamicin for native valve Severe sepsis: vancomycin + gentamicin Prosthetic valve - vanco + rifampicin + low-dose gent Confirm staph: 4W IV flucloxacillin (or vancomycin +rifampicin if MRSA) Confirm strep 4W IV benzylpenicillin + low dose gent indications for surg: - severe valvular incompetence - aortic abscess (often indicated by a lengthening PR interval) - infections resistant to antibiotics/fungal infections - cardiac failure refractory to standard medical treatment - recurrent emboli after antibiotic therapy ``` comps MI percarditis glomerulonephritis stroke + otehr embolic phenomena s.aureus most common - tricuspid murmur ``` proph abx for those at high risk undergoing dental procedures

Answer 126

``` def Myocardial disorder in which heart muscle is structurally and functionally abnormal without CAD, valvular disease, HTN, congenital ``` classification 1 PRIMARY SECONDARY from: Impaired LV function: CKD, cirrhosis, stress Multisystem disease: sarcoid, amyloid, SLE Endocrine: diabetes, thyroid Drugs: alcohol, cocaine abuse classification 2 1. Dilated - *most common, left or both ventricles dilated with impaired contraction Ischaemic, alcoholic, thiamine def (Beri-beri), coxsackie, chagas, SLE 2. Hypertrophic - 2nd common, left/right ventricular hypertrophy, usually familial (AD) - beta myosin 3. Restrictive - rare, reduced diastolic filling with near normal systolic function e.g. amyloid, fibrosis, sarcoidosis, radiation, haemochromatosis, Loefflers epi Can occur at younger age *suspect this at a young person presenting with heart failure, arrhythmia or thromboembolism gen ix Bloods: FBC, ESR, U+E, LFT, cardiac enzyme, TFT CXR ECG: usually abnormal Transthoracic doppler echocardiography: can confirm Dx of hypertrophy and exclude valvular MRI: to distinguish constrictive and restrictive disease gen mgmt Often symptomatic: treat heart failure and prevent thromboembolism and sudden death If high risk arrhythmia consider implantable cardioverter defibrillator All require thorough assessment of functional capacity and cardiac function

Answer 127

more than likely AF 1. ABCDE 2. 02 + IV access 3. monitoring on - ECG, BP ,02 + record 12 lead ECG 4. identify + treat reversible causes eg electrolytes ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours NO ADVERSE FEATURES -> control rate with BB or diltiazem, consider dig or amiodarone if evidence of HF

Answer 128

GET EXPERT HELP ASAP 1. ABCDE 2. 02 + IV access 3. monitoring on - ECG, BP ,02 + record 12 lead ECG 4. identify + treat reversible causes eg electrolytes ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours ``` NO ADVERSE FEATURES -> potential causes: AF with BBB - > as for narrow complex pre-excited AF -> consider amiodarone polymorphic VT (TDP) -> magnesium 2g over 10 mins ```

Answer 129

1. ABCDE 2. 02 + IV access 3. monitoring on - ECG, BP ,02 + record 12 lead ECG 4. identify + treat reversible causes eg electrolytes ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours NO ADVERSE FEATURES -> VT or uncertain -> amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours prev confirmed SVT with BBB -> give adenosine as for reg narrow tachy

Answer 130

``` what is it all 4 chambers dilated Ventricular chamber enlargement + contractile dysfunction with normal LV wall thickness due to biochemical abnormality of cardiac muscle. causes systolic dysfunction MOST COMMON - 90% ``` ``` causes idiopathic Ischaemia, HTN doxorubicin - drug genetic (AD) - duchenne musclar dystrophy *alcoholism, thyrotoxicosis, SLE/RA, coxsackie, thiamine -Beri beri *cocaine abuse ``` ``` pres Symptomless to sudden death *Heart failure - congestive: L (dyspnoea, fatigue, orthopnoea, PND) R (oedema, JVP, ascites) + 3rd/4th heart sound + cardiomegaly (displaced apex) Arrhythmia - AF or *VT Thromboembolism - by stasis ``` ix CXR: CHF: ABCDE (alveolar oedema - bat wing, kerley B - interstitial, cardiomegaly (balloon like heart), dilated upper lobe vessels, pleural effusion) ECG: sinus tachycardia, LBBB or non-specific T or ST change, or *AF Echo: marked dilatation LV, reduced systolic/diastolic function, MR or TR, mural thrombus Bloods: BNP: for heart failure Potential biopsy for amyloid, sarcoid ``` mgmt aim = improve cardiac function furosemide ACEi/ARB + BB - reduce LV EF treat AF further - biventricular pacing of class 3/4 HF, ICD if high risk VT ``` comp progressive HF sudden death from ventricular arrhythmia

Answer 131

what is it LVH, mitral valve abnormalities, impaired diastolic filling, disorganised cardiac myocytes (disarray) and fibrosis on biopsy predom diastolic dysfunction causes AD genetic inheritance, mutation in gene coding for beta-myosin or troponin assoc Mitral regurgitation, AF in 20% friedreichs ataxia WPW leads to Dynamic obstruction of LV outflow tract, myocardial ischaemia, SV/V tachyarrhythmia epi *Most common cause of sudden cardiac death in young people and athletes due to arrhythmia or obstruction of LV outflow tract ``` pres 20-30s mainly asympt Dyspnoea, chest pain, palpitations, syncope typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis (from arrhythmia and outflow tract obstruction) sudden death - vent arrhythmias ``` O/E Forceful apex beat, *double impulse if LVOTO Harsh ejection systolic murmur *augmented by standing or Valsalva LVOTO @left sternal edge radiating to mitral and aortic area ± mitral regurgitation murmur jerky pulse ix ECG: LVH: *S wave V1 depth + R wave height V5/V6 > 35mm Ischaemic changes: ST segment changes, T wave inversion deep Q Left axis deviation AF (20%) Most common arrhythmias are premature ventricular complexes (above) ``` Echo: *Diagnostic: Transthoracic echo: LV thickening (<20mm = low risk) mnemonic - MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH) ``` CXR - atrial enlargement if mitral regurgitation, variable cardiomegaly Genetic testing Endocardial biopsy for amyloid causing thickening mgmt - ABCDE + others Amiodarone or catheter ablation BB or CCB - verapamil or diltiazem for reduce ventricular contractility which decreases LVOT gradient Cardioverter defib - if risk of sudden death Dual chamber pacemaker Endocarditis proph ``` rx AF if LVOT high - septal myectomy genetic counselling avoid competitive sport avoid nitrates, ACE-i, inotropes ```

Answer 132

what is it Normal LV cavity size and systolic function but increased myocardial stiffness therefore mainly fills in early diastole (reduced) leading to increased atrial pressure epi old assoc AF ddx constrictive pericarditis ``` causes Endomyocardial fibrosis (Lofflers), *amyloid (worst), sarcoid, haemochromatosis, rad ``` pres - Usually present with HF but normal systolic i.e. dyspnoea, fatigue, loud S3, pulmonary oedema, murmur - Features of RVF predominate: raised JVP, hepatomegaly, oedema, ascites - *v. similar to constrictive pericarditis: Kussmaul’s sign (increased JVP with inspiration), pulsus paradoxus (decreased pulse + BP at inspire) ``` ix CXR: ABCDE ECG: low voltage complexes Echo: non-dilated, non-hypertrophied ventricles, atrial enlargement, sparkling@amyl *Cardiac catheterisation for pressures ``` mgmt Manage heart failure, amiodarone for ventricular arrhythmia, anticoagulate (AF), BB and CCB for rate control AF, transplantation sometimes indicate

Answer 133

what is it acute or chronic inflam of myocardium ``` pres MI + FEVER usually young patient fatigue chest pain arrhythmias ``` causes *Viral infection fever, malaise, lethargy, fatigue Coxsackie B virus, HIV diphtheria Immune mediated: SLE, sarcoidosis, scleroderma Toxic: alcohol, heavy metals Electric shock ix FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT, BNP raised +ve Viral serology *Gold standard - endomyocardial biopsy Cardiac MRI may differentiate transient and permanent tissue damage therefore good to diff from infarction ECG: ST elev/dep + T wave inversion, tachycardia CXR: normal cardiac silhouette but other signs of heart failure mgmt Treat cause: viral = supportive + bed rest If acute: i.e. fever, flu-like, WCC + haemodynamic compromise to ITU Symptomatic hypotension: +ve inotropes i.e. phosphodiesterase inhibitors or dopamine Anticoag if AF comp CHF, pulmonary oedema, cardiogenic shock

Answer 134

``` flecainide CCB lithium NSAIDs drugs prolonging QT - erythromycin ```

Answer 135

what is it life-threatening emergency AHF without a past history of heart failure is called de-novo AHF. Decompensated AHF is more common (66-75%) and presents with a background history of HF. AHF is usually caused by a reduced cardiac output that results from a functional or structural abnormality. ``` causes - CHAMP coronary syndrome hypertensive emergency arrhythmia mechanical - acute valve leak, VSD, LV aneurysm P.E ``` PRES patient looks acutely unwell - pale and grey cold clammy peripheries ?cyanotic frothy blood stained sputum in a pot - 'pink' orthopnoeic using accessory muscles cardiac asthma - wheeze O/E sinus tachy or AF systolic hypotensive signs of cardiomegaly - displaced apex, signs of valve disease third and fourth heart sounds right sided or bilateral pleural effusions ix FBC - anaemia as cause U+E, creatinine - for diuretics blood glucose B-type natriuretic peptide - raised level confirms diagnosis ABG - hypoxic? resp acidosis? trop - rule out infarction ECG - arrhythmia, heart block, ischaemia, ventricular hypertrophy ECHO - within 48 hour for evidence of reduced ejection fraction and valvular heart disease CXR - Aveolar effusion, B- kerley B lines (fluid in septal lines)/bats wings (prominent hilar shadows), cardiomegaly, diversion of upper lobes/diffuse mottling of lung fields, Effusion in interlobar fissures ``` mgmt Pour SOD Pour away their IV fluids aka STOP Sit up Oxygen Diuretics - IV furosemide 40mg stat ``` other thing to consider - IV pain killer (opiates are vasodilators so be careful), NIV or CPAP, inotropes (dobutamine) if systolic <90. might need vasodilators if systolic <90 = GTN or isosorbide mononitrate

Answer 136

This occurs when the left ventricle is unable to adequately move blood through the left side of the heart and out into the body. This causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.

Answer 137

``` sepsis tachycardia pulmonary embolism renal impairment COPD ```

Answer 138

what is it It is caused by either impaired left ventricular contraction (“systolic heart failure”) or left ventricular relaxation (“diastolic heart failure”). This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart causes Ischaemic Heart Disease Valvular Heart Disease (commonly aortic stenosis) Hypertension Arrhythmias (commonly atrial fibrillation) pres RHF: peripheral oedema, abdo distension (ascites), facial engorgement, pulsing in neck and face (tricuspid regurg) LHF: dyspnoea, fatigue, cold peripheries, muscle wasting, orthopnoea, PND, nocturnal cough - pink frothy sputum O/E - Tachypnoea, tachycardia, cool peripheries, cyanosis, displaced apex (LV dilatation), RV heave (pulmonary HTN), raised JVP Cardiac asthma: bilateral basal end-inspiratory crackles ± wheeze Peripheral oedema, tender hepatomegaly (pulsatile at TR) Gallop rhythm due to S3 or murmur of mitral or aortic valve diseas ix first line blood test - N-terminal pro-B-type natriuretic peptide: - if levels are 'high' >2000pg/ml arrange specialist assessment (including transthoracic echocardiography) within 2 weeks - if levels are 'raised' 400-2000pg/ml arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks ECHO - function - reduced ejection fraction or valvular disease 12 lead ECG - CXR FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes mgmt ACE-i lisinopril 2.5mg daily + BB bis 1.25mg daily intolerant of ACE -> ARB - candesartan 4mg daily intolerant of ARB -> hydralazine or nitrate increases doses for clinical effect if @ max and no effect + aldosterone receptor antagonist eg spiro 25mg daily refer for consideration of sacubitril valsartan, dig, ivabridine, resynch therapy Lifestyle (ex, smoking, alc, diet), patient education, depression Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic Inform DVLA, air travel likely ok Manage comorbities: HTN, prevention MI, diabetes prognosis 50% die within 4 years, worse prognosis if reduced ejection fraction

Answer 139

NEW YORK HEART ASSOCIATION STAGING SYSTEM Class I asymptomatic on normal physical Class II slight limitation no restriction flying Class III less than ordinary activity - symptoms oxygen may be required Class IV inability to carry out any activity - symptoms oxygen recommended

Answer 140

this is the percent of blood that is pumped out of the left ventricle after each contraction An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat normal = 50-70 too high = >75 - hypertrophic cardiomyopathy too low <40 = HF or cardiomyopathy 40-50 = borderline

Answer 141

``` def Complex inflammatory process characterised by accumulation of lipid, macrophages + smooth muscle cells within intimal plaques ``` steps 1. Fatty streak formation: Endothelial dysfunction -> increased permeability to fat and monocyte infiltration -> taken up by MP to make foam cells -> fatty streak Fatty streak progresses -> transitional plaque 2. Intimal hyperplasia: PDGF, TGF-B by macrophages, monocytes and damaged endothelium -> further accumulation of macrophage and smooth muscle cell proliferation 3. Fibrous cap: smooth muscle produces collagen 4. Plaque formation, or rupture may have fatty necrotic core The plaque may narrow the lumen or become unstable and rupture

Answer 142

mevalonate pathway HDL + LDL HDL - good cholesterol carries LDL away from arteries, LDL - bad cholesterol blocks arteries where Cholesterol -> liver (synthesis of bile salts) or endocrine glands (synthesis of steroids)

Answer 143

mechanism HMG-CoA reductase inhibitors ``` when do NICE recommend QRISK2 > 10% (10 year risk) - primary prevention if <84 History of CVD Familial hypercholesterolaemia Anyone over 85 ``` SE Myalgia, stiffness, weakness, cramping (usually at around 6 months) dose Atorvastatin 20mg for primary prevention, 80mg for secondary monitoring LFT

Answer 144

RF Modifiable: smoking, weight, alcohol, stress, exercise, dietary salt Non-modifiable: old, fam Hx, ethnicity, gender stages Stage 1: >140/90 or >135/85 on ABPM or HBPM (ambulatory) Stage 2: >160/100 or >150/95 Stage 3: >180/110 screening Often symptomless screen every 5 years for adults up to 80 then annually -10mmhg = Decreases risk heart disease risk of cardiovascular event 20% causes PRIMARY - essential SECONDARY - Renal disease: intrinsic (75%) i.e. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, or renovascular renal artery stenosis -> increased renin by decreased perfusion Endocrine: cushings, conns, thyroid, phaeo, acromegaly, hyperparathyroid, primary hyperaldosteronism Coarctation aorta Pre-eclampsia and pregnancy Drugs - decongestants, COCP, steroids calc BP = CO X TPR HTN crisis Malignant/accelerated hypertension (syst>200 or dia>130) + evidence of end-organ damage: *same-day assessment and immediate treatment (dec BP in hours) Hypertensive urgency (syst>180, dia>120) without end-organ damage, may dec BP over days suspect phaeo Labile or postural hypotension + headache, palpitations, pallor, sweating ``` end organ damage Brain - Encephalopathy: seizure, vomiting, nausea Dissection - delayed/weak femoral pulses Pulmonary oedema - heart failure Nephropathy - proteinuria ± loin bruit Eclampsia Papilledema Retinopathy (hypertensive) - Grade 1: tortuous retinal arteries + silver wiring - Grade 2: AV nipping - Grade 3: flame haemorrhages and cotton wool spots - Grade 4: papilloedema ``` ``` pres often asymp unless >200/120 headache visual disturbance seizure cushinoid conns - tetany, weak muscles, polyuria, hypokalaemia, thyroid, phaeo ``` ix 24 hour BP following diag: urea and electrolytes, creatinine: check for renal disease, either as a cause or consequence of hypertension HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease 12 lead ECG urine dipstick ?renal USS fundoscopy ``` mgmt lifestyle >135/85 rx with antihypertensive if >150/95 or >135/85 with: - age >80 with clinic >150/90 - age <80 with target organ damage, CV or renal disease, diabetes or 10yr CVD risk >10% MEDICAL MGMT T2DM <55 OR WHITE = 1. ACEi or ARB 2. +CBB or thiazide like diuretic 3. ACE-/ARB + CCB + thiazide like ``` 55+ OR BLACK = 1. CCB 2. +ACEi or ARB or thiazide like 3. all three PREGNANT = labetalol 100mg BD for mod HTN FINAL STEP FOR BOTH = confirm resitance + check for postural + discuss adherence seek expert advice add low dose spiro if k <4.5 alpha blocker or BB if k >4.5 monitoring use clinic BP measure sitting/standing in people with T2DM or postural hypo or >80

Answer 145

Multifactorial: genetic, lifestyle, environmental Modifiable: low SE status, smoking (60% higher), poor diet (high trans-fatty acid, low fibre, low fruit and veg), weight, low exercise, alcohol, stress and depression, *HTN (every 20/10 doubles risk of death), *cholesterol/hyperlipidaemia, *diabetes Unmodifiable: age, male, south asian, family Hx MI = x2, previous Hx, +ve family history <55 men or < 60 women, metabolic syndrome

Answer 146

``` def Chest pain or discomfort resulting from decreased blood supply to heart muscle, myocardium (ischaemia) without infarction ``` cause Usually due to narrowing of lumen of CAD due to atherosclerosis or thrombosis variants Decubitus (on lying down) Prinzmetal’s (at rest as a result of CA spasm) Stable - pain precipitated by predictable factor: exercise/emotion Unstable - angina occurs at any time, manage as ACS rf As before + cardiac abnormalities e.g. outflow obstruction (Aortic Stenosis) or hypertrophic obstructive cardiomyopathy pres 1 - constricting discomfort in front of check, neck, shoulders, jaw, arms 2 - precipitated by physical exertion 3 - relieved by rest or GTN in *5 minutes *typical if all, atypical if 2/3, non-anginal = 1 or 0 ddx Pain over 5 mins - MI Acute pericarditis - worse on inspiration, lying flat, swallowing MSK - worse on mvmt GORD Pleuritic pain - sharp pain on deep inspiration, ?pneumonia or PE ``` ix 12 lead ECG - ischaemic changes @ exercise stress test - ST/T wave flattening or inversion FBC glucose chol/triglycerides LFTs - baseline before starting statin U/E TFT estimate likelihood of CAD - all men >70 = 90%, w >70 = 60-90 unless high risk >90 = manage as angina 60-90 = invasive coronary angiography 30-60 = non-invasive functional imaging - stress echo 10-30 - CT calcium scoring <10 - reconsider Dx ``` mgmt REFER ALL ?ANGINA to rapid access chest pain clinic for confirmation of dx and severity assessment - within 2 weeks modify RF - patient edu advice on stopping activity and GTN spray, if pain doesn’t ease 2nd dose @ 5 minutes, 3rd dose @ 5 minutes, wait 5 minutes then 999 (i.e. after 15 mins total) PHARMA - Short acting nitrate: GTN First line anti-anginal: BB (atenolol, lower HR and BP, bradycardia, cold hands/feet, fatigue) or CCB (diltiazem/verpamil/amlodipine - ankle swelling, flushing) Second line: combination - *must be dihydropyridine CCB + BB If intolerant or CI: consider long acting nitrate or nicorandil or ivabradine Vasodilation - CCB and nitrates, cardiac depressants - BB and CCB Aspirin 75mg or clopidogrel- antiplatelet (establish bleeding tisk), statin if indicated, ACE-I for HTN/diabetes Review at 2-4 weeks if not controlled on medicine = CABG or PCI

Answer 147

trop neg = unstable angina trop posi = NSTEMI/STEMI

Answer 148

``` diagnosis two of three: 1. cardiac chest pain 2. positive trop 3. ECG changes - T wave inversion, ST elevation/dep, Q waves, new LBBB ``` ``` chest pain central restrosternal band-like constriction non-pleuritic radiates to left ``` ``` suspect ACS if: lasts longer than 15 mins occurs @ rest - unstable angina increasing in freq - cresendo angina severe - associated with n + v or sweating, non-resolving with nitrates ``` ``` rf smoking HTN DM hyperlipidaemia FH CKD ``` ix FBC - anaemia U and creat - impaired renal function can cause false posi elevation of trop, baseline levels required prior to ACE inhib electrolytes - hypokalaemia, hyperkalamia glucose LFT- baseline for statin, impaired = CI for ticagrelor lipids serial trops ECG - Q waves imply full thickness infarct, without = subendocardial mgmt STEMI with para - morphine + cyclizine, oxygen, nitrates ABCDE + o2 aspirin 300mg oral PPCI <12 hours since symps, <2hrs since arrival (if not poss then consider fibrinolytics eg altepase) - will be given loading dose of prasugrel prior follow up = ABCDE ACE-i BB Cholesterol lowering, high dose statin is also plaque stabilising Dual antiplatelet therpy - aspirin 75mg indef + prasugrel for at least one year Echo - to assess LV mgmt NSTEMI/unstable angina para give o2, GTN, morphine ABCDE aspirin 300mg stat risk stratify based on 6/12 mortality lowest risk <1.5 = aspirin, review as outpatient, ?exercise ECG, ?Angiogram low risk - 1.5-3% = fondaparinux, conservative - review as outpatinet ?exercise ECG, ?, Angiogram , aspirin + ticagrelor or clopidegrel intermediate >3% and high >6% = unfractionated heparin, early invasive mgmt PPCI -> aspirin + prasugrel if stented comps pump failure ruptureof papilary muscle or septum aneurysm and arrhythmias embolism -> mural thrombus -> stuck on wall dresslers syndrome (late 4-6 w later sharp pain = POST MI SYNDROME) - plus early acute pericarditis (doesnt respond to opioids

Answer 149

``` sharp, worse on insp retrosternal, radiates to left (shoulder) worse on lying flat eased by sitting up ```

Answer 150

current injury usually implying occlusion by ruptured plaque with in-situ thrombosis >1mm in limb or >2mm in 2 adjacent chest leads OR new LBBB

Answer 151

GRACE - global reg of acute cardiac events) Risk and Mortality Calculator ``` looks at age HR BP trop HF creat ```

Answer 152

*Post ACS = 4 weeks off driving, 1 week if treated by angioplasty

Answer 153

999 A+B (if breathing turn to recovery) C - CPR 30:2, when airway secured = uninterrupted compressions and ventilate at 10/min D defibrillator: AED automated external defibrillator Complete 2 minutes of CPR between debif attempts After 3rd shock give adrenaline + amiodarone 2 minutes CPR Adrenaline 2 minutes CPR Adrenaline

Answer 154

what is it Outer fibrous layer (parietal pericardium) and inner serous membrane (visceral pericardium) with 50ml fluid between Limits dilation, maintains ventricular compliance (Starling), fixes heart to sternum pathogen Inflammation of pericardium - pericardial vascularisation and infiltration with polymorphonuclear lymphocytes. Fibrinous reaction results in exudate and adhesions within pericardial sac and serous/haemorrhagic effusion develops ``` causes Viral: *coxsackie, EBV + staphylococcal/haemophilus... Rheum: *SLE, sarcoid + …. Post MI: *Dressler’s 24-72 hours Drugs: hydralazine Other: *uraemia ``` when granulomas TB, sarcoid, fungal, RA pres *Chest pain Dull, sharp, burning, pressing (up to severe) Felt substernal or precordial Radiates to neck or left trapezius *Aggravated by inspiration, cough, swallow, lying flat *Relieved by sitting up and lying forward O/E 60-85% pericardial friction rub - scratchy, louder in inspiration, heard at midline Tachypnoea, tachycardia, fever If *tamponade -> may exhibit Beck’s triad: Hypotension, elevated systemic venous pressure (JVP), muffled heart sounds If slow develop pulsus paradoxus - 10mmHg fall in SBP with insp ix Serial ECGs: Stage 1, diffuse concave ST segment elevation (saddle shape) with concordance of T waves, PR depression. Stage 2, return to normal and T wave flatten. Stage 3, T inversion. Stage 4, resolution of T wave. CXR: globular heart if > 250ml FBC (WCC), ESR/CRP (raised) U+E (uraemia?) cardiac enzymes (if MI) Echo - *if suspect effusion or tamponade (>20mm free fluid) *if suspect impending tamponade (RA or vent diastolic collapse on echo) - pericardiocentesis mgmt Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis) + colchine Admit if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs comps *falling blood pressure and shock - suspect cardiac tamponade - immediate peircardiocentesis with echo Chronic + symptomatic - pericardial resection Recurrent: colchicine in addition to NSAIDs

Answer 155

cardiac tamponade hypotension raised JVP muffled heart sounds

Answer 156

what is it Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise MEDICAL EMERGENCY pres Anxiety, fatigue, oedema, dyspnoea, tachyc, tachyp O/E: Beck’s triad if acute (muffled, JVP, hypotension) + distended neck veins, hepatomegaly, tachyc/p, pulsus paradoxus (*exaggeration of normal decrease in BP on inspiration, distinguish CT from pericardial effusion) patho On inspiration decrease ITP -> increased flow to RH -> pressure transmitted to septum which impairs LV filling ix ECG - Low voltage QRS complex. Electrical alternans. Amplitude increases and decreases beat to beat QRS CXR - Cardiomegaly, water-bottle shaped heart, calcification @ restrictive transthoracic echo - gold standard mgmt O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis

Answer 157

``` def Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen ``` course Acute < 14 days, subacute 15-90, chronic >90 ``` location Type A (70%) - aortic arch and ascending aorta proximal to *L subclavian Type B (30%) - descending aorta distal to L subclavian ``` RF CV RF + aortic disease + cocaine/amfetamines + M/ED + bicuspid valve pres Initial phase: Sudden tearing/sharp pain radiating to back, pulse loss Expansion phase: pressure increase causes rupture to pericardium (tamponade), or pleural space or mediastinum *Pain maximal at onset, migrates as dissection progresses To spinal arteries - paraplegia To distal aorta - limb ischaemia To carotids - neurological deficit To coronary - angina ``` ix BP in both arms differentiate from MI ECG CXR - widened mediastinum TTUS - site + extent MRI for diagnosis + identification of other vessels ``` worry about - rupture, multi-organ failure, cardiac tamponade, hypotension ``` mgmt IV access ABCDE analgesia ICU mgmt HTN aggressively - IV BB (labetalol) to reduce ventricular contraction, IV nitroprusside (emergency vasodilator) SURGERY - typeA to prevent rupture - graft type B - TEVAR ```

Answer 158

``` def Permanent and irreversible dilatation of bv by > 50% of normal diameter. True aneurysm involves all three layers ``` ``` types thoracic abdominal - the maj ruptured 26-28mm ``` ``` areas affected Acending aorta (51%), aortic arch, descending aorta (n.b. Aortic hiatus of diaphragm is at T12) ``` pathogen Complicated: inflammation, proteolysis and reduced survival of smooth muscle cells causes Genetic/familial (AD for TAA) Connective tissue: Marfan’s, Ehler Danlos Infection: HIV, syphilis Aortitis: GCA, RA, takyasu’s arteritis Trauma, weight lifting, cocaine, amfetamine (due to BP rise) RF Turner’s, COPD, CKD, HTN, age, smoking, atherosclerosis, bicuspid aortic valve pres Pain: chest, neck, upper back, mid back, epigastrium, acute - rupture imminent? dissection is sudden, tearing Symptoms due to local compression: hoarseness, cough, stridor, dyspnoea, SVC obstruction, dysphagia If rupture: acute pain + collapse/shock + aneurysm erosion into local structure: haematemesis (aorto-oesophageal fistula), haemoptysis (aorto-bronchial), haemothorax, cardiac tamponade ix Acute: FBC, clotting, renal/liver, cross-match, ECG, CT contrast, MR angiography Chronic: FBC, ESR/CRP, LFT/amylase, ECG, LuFT, USS, *TTE, *AUS (for AAA) CT angiography, MR angiography (for cause, infective, inflammatory, pancreas (DDx)) mgmt Surgery: *graft insertion or TEVAR (thoracic endovascular aneurysm repair) if symptomatic *regardless of size or Marfans Ascending > 5.5cm, descending >6cm comp - paraplegia due to spinal ischaemia, stroke, AKI Medical: smoking cessation, treat 2nd RF CVD if marfans - Require lifelong BB, regular imaging of aorta and restriction physical activity monitor 6 monthly MRI/CT and inform DVLA above certain size

Answer 159

pres Thoracic: chest pain indistinguishabe from MI + haemoptysis ± cardiac tamponade Abdominal: classic triad: flank/back pain, hypotension, pulsatile abdominal mass Pale + sweaty, weak thready pulse, hypotension ix FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E CXR, AXR (75% are calcified) ECG for MI mgmt Large bore IV access Group and crossmatch, order 4-6 units blood, FFP, Pt Immediate theatre Secure proximal aortic control Prosthetic graft repair and stem bleeding - EVAR prog only 1 in 3 reach hosp alive

Answer 160

types hypovolaemic - loss of blood/fluid cardiogenic - hf, heart cant pump to maintain CO distributive - anaphylaxis, sepsis, neurogenic obstructive - PE why it kills Triad of coagulopathy, hypothermia, metabolic acidosis -> leads to compensatory tachypnoea at risk organs Kidney (acute tubular necrosis), lung (ARDS), heart (MI), brain (confusion, irritability coma)

Answer 161

ix Hb, UE, LFT, group and crossmatch, ABG + lactate, monitor urine staging Class 1: 10-15% physiological compensation Class 2: 15-30% postural hypotension, urine to 20-30ml/Hr Class 3: 30-40%tachycardia >120, urine under 20, confused Class 4: 40% marked hypotension, tachycardia, tachypnoea, no urine, comatose Compensated baroreceptors result in increased myocardial contractility, tachycardia and vasoconstriction. Maintain BP. Release vasopressin, aldosterone, renin Progressive/uncompensated with myocardial depression, failure of vasomotor reflex, increased capillary permeability and lactic acidosis Irreversible: failure of vital organs mgmt Raise legs ABCDE Crossmatch + blood for Ix as previous + catheter + ABG Airway + high flow O2 + 2 large bore IV cannula Fluid resus saline or Hartmann’s 500ml over 15 mins *may give 2l total then escalate If haemorrhagic shock give blood as soon as possible O-ve Pain relief - pain increases metabolic rate and increases ischaemia IV opiates *vasopressors cause further tissue ischaemia Surgery to stem blood loss: e.g. REBOA after res

Answer 162

cause Most often caused by acute MI (affecting anterior wall) - or pericardial tamponade/severe constrictive pericarditis or obstructive PE or tension pneumothorax mgmt A+B - intubation ± mechanical ventilation, O2 C - gain venous accessl often require central venous access as peripherally shut down - send bloods IV fluid if depleted volume 250ml bolus (cardiac dysfunction) Monitor - cardiac monitoring, BP - art line, venous pressure - CVC, urinary catheter Ix: UE, preg, FBC, ABG, BNP, ECG, CTPA, CXR Pain relief *IV morphine and cardiac inotropes *dopamine or dobutamine Revascularisation

Answer 163

``` def Systemic hypersensitivity: sudden onset, rapidly progressing, life threatening ``` ``` pres Profound vasodilation (warm peripheries, low BP, tachycardia) Breathless/wheeze Urticaria/hives/angio-oedema *Oedema of face, pharynx, larynx ``` mgmt A (call for help if any signs of obstruction) B (treat resp distress) C (colour, pulse, BP) D (responsive?) E High flow O2 Lie flat and raise legs IM adrenaline *0.5mg adult, child: >12 = adult, 6-12 = 300mcg, <6 = 150mcg Expert intubation IV fluid challenge: large bore cannula: 500ml crystalloid in 5-10 mins, 250ml if known heart failure IV chlorphenamine + hydrocortisone Bronchodilators: salbutamol IV or nebulised, ipratropium inhaled, aminophylline IV

Answer 164

Life threatening organ dysfunction due to a dysregulated host response to infection Clinical criteria: organ dysfunction defined as an increase of 2 points or more on SOFA score - mortality rate 10%: qSOFA - HAT - Hypotension - < 100mmHg - Altered metal state - GCS < 15 - Tachypnoea - >=22 pres Bounding pulse, temperature, rigors, rapid capillary refill, vasodilation, warm peripheries ``` mgmt Blood cultures + septic screen, U+E Urine output - monitor hourly Fluid resuscitation Antibiotics - tazocin? gent? according to local guidelines Lactate, ABG/VBG Oxygen to correct hypoxia refer to ITU for inotropes ``` FBC, UE, urine dip, LFT, glucose, *clotting inc D-dimer and fibrinogen for DIC, CXR, AUSS - find the infection Complications DIC, renal failure, cardiorespiratory failure

Answer 165

chronic limb ischaemia - intermittent claudication (not progressive, ABPI >0.4, 1 year mortality 4% critical limb ischaemia - rest pain requiring opiates for >2/52 or evidence of tissue necrosis, ulceration or gangrene, ABPI <0.4, 1 year mort 12% acute limb ischaemia (thrombosis or embolus) - sudden decrease in limb perfusion that causes a threat to limb viability, 6Ps - pale, pulseless, painful, parasthesia, paralysed, perishingly cold, ABPI <0.1, 1 yr mort 20%

Answer 166

they have abnormally high ABPI's due to calcified vessels

Answer 167

small and painfull over pressure-points: back of heel, plantar aspect of big toe punched out margin at ankle, typically over lateral malleolus associated with cold foot, absent pulses and low ABPI ddx neuropathic ulcer - are painless and foot is warm with reduced sensation venous ulcers typically on medial calf or ankle with associated skin changes 10% of ulcers are mixed with venous and arterial components CI compression bandages contraindicated if arterial component - hence imp of checking ABPI prior to treating any ulcer

Answer 168

dry - ischaemic necrosis wet - infection plus ischaemia 50% of cases in diabetics surg options mid-tarsal amputation with femoro-distal graft below knee amputation

Answer 169

large and small vessel disease peripheral neuropathy leads to injury 'loss of protective sensation'

Answer 170

toxic factors - free radicals, histamine etc damage endothelial cells the caps leak protein rich fluid into the muscles, which then swell and increase pressure within compartment leads to vicious cycle as the swelling causes reduced venous return and cap perfusion leading to tissue hypoxia and further damage initially leg is warm and arterial pulses are retained similar events can occur with soft tissue trauma (crush unjury) and with fractures nerve necrosis = painful hyperasthesiae then loss of sensation, motor loss eg foot drop muscle necrosis = pain out of prop to injury, pain on passive movement of muscle, tense tender muscle on palp, rhado and AKI, later healing by fibrosis - volkmanns ischaemic contracture.

Answer 171

what is it dilated subcut vein with reversed blood flow 5% develop venous ulcer ``` rf FH preg obesity occupation ``` patho NORMAL 1. blood flows normally from distal to proximal, retrograde flow in superficial veins is prevented by valves 2. blood flows from superficial to deep, additional valves in perforating veins ensure one-way flow and protect superficial veins from high pressure 3. blood in deep veins returns to heart aided by pressure generated by calf muscle pump VARICOSE 1. primary valve prob in perfs = incompetent 2. high pressure from calf muscle pump transmitted outwards 3. superficial venous hypertension 4. varicose veins 5. progressive descending incompetence POST THROMBOTIC LIMB 1. add in to above prev DVT, damages deep vein valves + deep venous hypertension 2. more likely to develop - lipodermatoscelerosis, venous ulceration, 'post thrombotic limb' exam CEAP classification c1 = thread veins c2 = varicose c3 = oedema c4a = pigmentation and or eczema 4b = lipodermatosclerosis c5 = healed ulcer 'atrophie blanche' c6 = active ulcer inspect + palps assess level of perf vein incompetence: 1. sapheno-femoral junct - extensive varicose veins over medial calf/thigh, sometimes saphena varix 2. mid-thigh perf - hunters vein - varicose over medial calf 3. small sapheno-popliteal junction - varicose over lateral calf 4. medial calf perfs - cocketts veins - varicose over medial calf ix duplex uss tourniquet test - empty varicose by patient lying and raising leg, apply tourniquet high in thigh, ask patient to stand, veins below tourniquet fill and implies incomp perfs below that level, if remain empty then = above that level mgmt foam sclerotherapy endothermal ablation (laser or radiofreq) surgery - high tie and strip - trendelenberg procedure

Answer 172

damages subcut fat which become fibrotic = lipodermatosclerosis skin around ankle feels hard and is tethered to subcut tissue 'inverted champagne bottle' leg commonly assoc with deep vein reflux

Answer 173

IX, X, VII and prothrombin II | 9, 10, 12

Answer 174

AntiThrombinIII

cardiology Flashcards

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