Cardio

Question 1

Normal axis

Answer 1

-30 - +90 degrees

Question 2

PR interval

Answer 2

From atrial depolarisation to ventricular depolarisation *120-200ms
Prolonged = AV block
Shortened = atrial impulse to ventricles quicker i.e. accessory pathway associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White

Question 3

QRS

Answer 3

Width, height, shape. Normal = 80-120ms.
Narrow = <120ms, impulse down His and Purkinje
Broad = >120ms, abnormal depolarisation, e.g. ectopic
Height: small = <5mm in limb and <10mm in chest, tall = ventricular hypertrophy
Delta = WPW
Pathological Q: >2mm or >40ms
R and S: normally have R wave progression (small in V1 and large in V6) transition S>R to R>S is normally in V3 or V4

Question 4

ST segment

Answer 4

End of S to start of T: elevation significant if >1mm in 2 or more limb leads or >2mm in 2 or more chest leads, depression significant if >0.5mm in 2 contiguous leads

Question 5

T wave

Answer 5

Ventricular repolarisation:
tall if >5mm in limb AND >10mm in chest associated hyperacute STEMI and hyperkalaemia
Inverted: *normal in V1 and lead III, associated ischaemia, PE, BBB

Question 6

U wave

Answer 6

A small deflection after T wave, 0.5mm, best seen in V2 and V3
Seen in electrolyte disturbances, hypothermia, antiarrhythmics e.g. digoxin, more pronounced with slower

Question 7

Sinus bradycardia
Definition 
Causes 
Symptoms
Treatment

Answer 7

<60bpm where every P wave is followed by a QRS

Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)

Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP

Syncope, fatigue, dizziness, ischaemic chest pain, palpitations depending on cause

Treatment is Rate < 40 or symptomatic - IV atropine -
Temporary pacing wire

Question 8

Sick sinus syndrome

Answer 8

Dysfunction of SA node with impairment of ability to generate impulse

Normally idiopathic fibrosis of node, also associated with ischaemia and digoxin toxicity (fibrosis may be amyloid or sarcoid)

Causing - Sinus bradycardia, sinoatrial block (Pause length of 2 or more PP intervals), sinoatrial arrest

Treatment - Pacing

Question 9

Heart block
Causes
Types
Managment

Answer 9

MI/ischaemia (inferior), infection (Lyme disease), immunological (SLE), myocarditis, endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB)

Delay of atrial impulse to ventricles
1st = PR > 0.2s, PR constant, every P followed by QRS
Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS
Mobitz type I (Wenckebach) failure at level of AV node. PR interval progressively lengthens and is then blocked.
Mobitz type II intermittent failure of P wave conduction. Fixed PR interval, dropped QRS waves (2:1 block or 3:1 block)

Unstable - Atropine & Trans cutaneous pacing
Stable - Usually a organic cause & Dual chamber pacing

Question 10

Sinus tachy
Causes
Ix
Treatment

Answer 10

Every P followed by QRS, rate 100 - 270

Physiological: exertion, anxiety, pain
Pathological: fever, anaemia, hypovolaemia
Endocrine: thyrotoxicosis, phaeo
Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol

Ix - 12 lead ECG, cardiac enzymes, FBC (anaemia), TFT

Treatment
Acute: Hemodynamically stable - Vagal manoeuvres
BB or non-dihydropyridine CCB (diltiazem, verapamil)

Question 11

Atrial SVT
Causes
ECG findings
Types

Answer 11

Typically from ectopic source in atrial muscle
150-250 bpm (slower than flutter)

Abnormal p-wave morphology
Atrial rate 150-250
Variable ventricular rate but regular

Benign (80-140bpm elderly)
Incessant ectopic (rare)
Multifocal (COPD, varying p-wave morphology)
Atrial tachycardia with block (digoxin toxicity) basically a fast heart block

Question 12

AVNRT SVT
Common?
Symptoms
ECG
Treatment

Answer 12

• Most common cause of paroxysmal narrow complex tachycardia
• Late teens or early 20s

Sudden onset palpitations ± CP, SOB ± syncope
*Neck pulsation

Regular rhythm, narrow QRS, rate 130-250
Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)
Atrial and ventricular depolarisation together - P waves buried in QRS

Haemodynamically unstable - DC cardioversion
First line: Vagal maneuvers may stop as transiently block AV node
Second line: *Adenosine
Prophylaxis - Drugs affecting AV node: digoxin, diltiazem, verapamil, fleicanide or a B blocker
Curative: radiofrequency ablation

Question 13

AF
Risk factors
Causes
Precipitants 
Symptoms

Answer 13

Age, HTN, heart failure, CAD, valvular disease, DM, CKD

CAD, HTN, valvular disease, hyperthyroidism, alcohol

Alcohol, caffeine

SOB, palp, syncope, chest discomfort, stroke/TIA

Question 14

Chronic AF Management

Answer 14

Rate control
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)

Rhythm control
Cardiovesion with flecanide (Treat with amiodarone for 4w preceding CV)
B Blocker/ AV node ablation

Question 15

Acute AF treatment

Answer 15

If hemodynamically unstable:
DC cardioversion is preferred + continue thrombophylaxis for 4 weeks

If pharmacological cardioversion - Amiodarone IV
Offer heparin immediately then introduce warfarin

Question 16

CHADsVasc
HAS BLED
Targert INR

Answer 16

CHF (1), HTN >140/90 (1), >75 (2), DM (1), prior stroke/TIA (2), vasc dis: MI, PVD (1), 65-75 (1), female (1)
Consider male > 1 or anyone > 2, warfarin or NOAC

HASBLED - HTN (>160), abnormal liver or renal 1/2, stroke, bleeding Hx or predisp e.g. anaemia, labile INR, elderly >65, drugs (alcohol, NSAIDs, antipt) 1/2

INR 2-3 (non valvular) (n.b. Prosthetic valves, post MI = 2.5-3.5)

Question 17

Atrial flutter managment

Answer 17

Rhythm control: cardioversion or medications
DC cardioversion (if >48hours ensure adequate anticoag)
Or IV amiodarone, sotalol, fleicanide
Recurrence: *radiofrequency catheter ablation (90-95% success)

Question 18

Broad Complex tachycardia types

Answer 18

Ventricular tachycardia
Regular: Monomorphic ventricular tachycardia, right ventricular outflow tract tachycardia, fascicular tachycardia
Irregular: Torsades de Points, polymorphic ventricular tachycardia

Supraventricular with aberrant conduction or ventricular-pre excitation
Aberrant conduction - usually manifests as LBBB or RBBB (Suspect if has prev BBB)
WPW
AF with atrioventricular re-entrance

Nb always treat as VT are more likely and more dangerous

Question 19

VT ecg changes

Answer 19

ECG normally monomorphic QRS complex (unless disturbed by capture or fusion beats)
Needs 3 in a row
Bizarre QRS morphology as impulse does not follow normal intraventricular conduction
If starts in left vent gives RBBB, if starts in right vent gives LBBB
Ventricular rate 120-300

Question 20

VT management
Unstable
Stable

Answer 20

Support ABC, O2 and venous access
Monitor ECG, BP, sats
Identify and treat reversible cause e.g. electrolyte abnormalities potassium

Unstable (chest pain, reduced consciousness, heart failure) *reduced CO
Synchronised DC shock (up to 3 attempts)
Amiodarone 300mg IV over 10-20 minutes and repeat shock then 900mg over 24 hours if refractory

If regular/stable (VT) - Amiodarone as above.

VT is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB) or consider ICD implantable cardioversion defibrillator

Nb If stable but irregular = TdP

Question 21

Torsades de points
Risk
Treatment
Causes

Answer 21

Type of polymorphic ventricular tachycardia in which cardiac axis rotates over a sequence of 5-20 points. QRS amplitude varies similarly giving twisting appearance.
In sinus may be seen as prolonged QTc.

May deteriorate to Ventricular fibrillation
IV magnesium sulphate (2g magnesium for other broad irregular i.e. polymorphic)

Drugs: anti-arrhythmics class III (amiodarone), antibacterials (erythromycin, trimethoprim), TCAs
*Electrolyte: hypokalaemia/hypomagnaesaemia

Question 22

VF
Causes
ECG changes
Treatment

Answer 22

Antiarrhythmic drugs, AF, hypoxia, ischaemia, fast VT, previous heart disease

*Shockable: VF and pulseless VT
Non-shockable: asystole and PEA (pulseless electrical activity)
Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500
Amplitude decreases with duration: coarse to fine.

Defibrillation
BB and ICD (implantable cardioverter defibrillators)

Question 23

Brugada syndrome

Brugada sign

Answer 23

Autosomal dominant gentic condition affecting sodium channels causing sudden death <45yrs

Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T (Brugada sign)
+ Documented VF or PVT

ICD implantable cardioverter defibrillator

Question 24

PE ECG changes

Answer 24

*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
Assoc RBBB
R heart strain = T wave inversion in V1-V4

Question 25

``` Amiodarone Indications Pharmacology Side effects CIs ```

Answer 25

For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work Blockade Na/K/Ca channels, antagonist alpha and beta adrenergic receptors which reduces automaticity. Hypotension during IV infusion. Chronic use lungs (pneumonitis), prolonged QT (AV block), liver (hepatitis), skin (grey discolouration), hypothyroid (Iodine rich) Severe hypotension, heart block, thyroid disease

Question 26

Adenosine Indications Pharmacology Side effects

Answer 26

First line diagnostic and therapeutic in SVT (inc junc) Adenosine receptor agonist on cell surface. Very short duration - half life 10s Blocks SA and AV node - causes bradycardia and asystole - doom feeling May induce bronchospasm in asthma or COPD

Question 27

``` CCB Indiactions Pharmacology Side effects CIs ```

Answer 27

Verapamil (most cardio-selective) + diltiazem (non-dihydropyridine) + amlodipine (dihydropyridine) 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. Reducing rate, contractility and afterload decreases oxygen. Ankle swelling, flushing, headache - dihydropyridine e.g. amlodipine Verapamil - constipation, bradycardia, heart block Diltiazem (mixed) Don’t prescribe with BB - both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole

Question 28

``` B Blockers Indications Pharmacology Side effects CIs ```

Answer 28

``` First line in IHD reduce angina CHF improve prognosis AF reduce rate and maintain sinus rhythm SVT to restore sinus rhythm ``` 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 via prolonging AV refractory. Lower BP by reducing renin secretion Fatigue, cold extremities, headache, impotence Asthma - B2 blockade causes bronchospasm, usually safe in COPD Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)

Question 29

Preload

Answer 29

Volume of blood in the ventricles at the end of diastole

Question 30

Afterload

Answer 30

Resistance LV must overcome to circulate blood

Question 31

``` AS Causes Symptoms Signs Imaging ```

Answer 31

Three thin cusps (bicuspid valve predisposes) Most frequent valvular heart disease (10% >80) due to senile calcification CAD - see CAD RF, bicuspid valve (common cause in young), rheumatic fever Classic triad: chest pain (predisposes to chest pain), heart failure (obstruction -> LV hypertrophy -> LV failure), syncope (insufficient blood) SOBOE Slow rising pulse Narrow pulse pressure (diff between syst and dia) LV hypertrophy -> apex heave Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids 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

Question 32

AS Management Complications

Answer 32

If symptomatic - prompt valve replacement - first line If not fit for surgery Antibiotic prophylaxis Second line - balloon valvuloplasty - risk of re-stenosis TAVI - transcatheter aortic valve replacement Predisposition to infective endocarditis 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)

Question 33

AR Causes Symptoms Signs

Answer 33

Bicuspid aortic valve (congenital), rheumatic fever (@developing), infective endocarditis, collagen vascular disease, degenerative (@developed) 40-60 - from degenerative SLE, Marfan’s, Ehler-danlos, Turner’s, aortic dilatation with anky spon, acute AR in IE or aortic dissection (severe chest/back pain) Acute - cardiovascular collapse SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea) 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 ECG - LVH (RV1 + SV5/6 >35mm)

Question 34

MS Causes Symptoms Signs

Answer 34

Congenital, rheumatic fever (most common), degenerative calcification (elderly) (SLE, RA, IE, amyloid) Asymptomatic for years then deteriorate Progressive breathlessness (SOBOE, orth, PND), palpitations due to AF, systemic emboli Symptoms due to enlarged LA - hoarseness, dysphagia ``` 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 ``` 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

Question 35

MR Causes Symptoms Signs

Answer 35

Second most common, assoc females, low BMI, advanced age Now less rheumatic fever so most common cause is degenerative MI, CAD, IE, post mitral valve surgery, Ehler-Danlos, SLE, rheumatic fever, Chronic MR eventually causes heart failure and breathlessness Pansystolic blowing murmur at apex radiating to axilla Laterally displaced apex beat S3 gallop ECG: enlarged LA: P-mitrale, AF CXR: enlarged left atrium and left ventricle Echo: confirm Dx and severity (based on jet into atrium)

Question 36

Jones Peace criteria What for? Stand for?

Answer 36

Rheumatic fever - Strep pyogenes 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 PR interval prolongation (not if carditis major) ESR very raised Arthralgia (not if arthritis) CRP very raised Elevated temp (>90% are over 39 degrees)

Question 37

Infective endocarditis Organisms Risk factors Which valve commonest?

Answer 37

Fever + new murmur = endocarditis until proven otherwise Staphylococci (aureus) invasive procedures/drug users, streptococcus viridans (subacute) (dental procedures), enterococcus or strep pyogenes ``` Valve disease/ replacement Congenital structural heart Previous IE Hypertrophic cardiomyopathy IVDU ``` Mitral

Question 38

IE Diagnosis Treatment

Answer 38

Duke’s classification BE|BEFVIP 2 major, 1 major + 3 minor, 5 minor Blood culture: 2 separate +ve blood cultures Echo: evidence of endocardial involvement: vegetation/abscess Blood culture 1 +ve blood culture Fever >38 Vascular phenomena: major arterial emboli, janeway lesions, IC haem Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, RF Predisposition - e.g. IVDU, heart condition Start ABX empirical (IV) General: amoxicillin + gentamicin for native valve Severe sepsis: vancomycin + gentamicin Confirm staph: 4W IV flucloxacillin (or vancomycin if MRSA) Confirm strep 4W IV benzylpenicillin Nb. Blood cultures (subacute or chronic = 3 sets from peripheral sites with 6hrs between them, acute = start

Question 39

Cardiomyopathy

Answer 39

Myocardial disorder in which heart muscle is structurally and functionally abnormal without CAD, valvular disease, HTN, congenital Dilated - *most common, left or both ventricles dilated with impaired contraction Ischaemic, alcoholic, thiamine def (Beri-beri), coxsackie, chagas, SLE. + 3rd/4th heart sound + cardiomegaly (displaced apex) Hypertrophic - 2nd common, left/right ventricular hypertrophy, usually familial (AD) - beta myosin. Strong association with Mitral regurg. Forceful apex beat, & Harsh ejection systolic murmur Restrictive - rare, reduced diastolic filling with near normal systolic function e.g. amyloid, fibrosis, sarcoidosis, radiation, haemochromatosis, Loefflers

Question 40

Myocarditis What? Causes? Ix?

Answer 40

Acute or chronic inflammation of myocardium Similar to myocardial infarction with fever *Viral infection fever, malaise, lethargy, fatigue Coxsackie virus Immune mediated: SLE, sarcoidosis, scleroderma Toxic: alcohol, heavy metals Electric shock FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT +ve Viral serology *Gold standard - endomyocardial biopsy ECG: ST elev/dep + T wave inversion

Question 41

RHF vs LHF symptoms 4x each

Answer 41

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

Question 42

Signs of HF (5)

Answer 42

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 disease

Question 43

Ix for HF

Answer 43

If previous MI -> 2 week wait for specialist and doppler echo (LV func, diastolic func, LV thickness, valvular disease) No previous MI -> BNP measurement (B-type natriuretic hormone) - released into blood when myocardium stretched. >400 pg/ml - 2 week wait for specialist and doppler. 100-400 - 6 week. <100 - heart failure unlikely 12 lead ECG for aetiology, and treatment: rate control in AF, pacing for bradycardia FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes CXR: for other causes of breathlessness. HF ABCDE (alveolar - bat wing, kerley B - interstitial, cardiomegaly >50% cardiothoracic ratio, dilated upper lobe, effusion)

Question 44

Acute HF treatment

Answer 44

Oxygen + IV diuretics (furosemide) ± NIV (only if severe dyspnoea + acidaemia) or IV (if resp failure or reduced conc) When stable: BB (bisoprolol or metoprolol) + ACEI (or ARB) + aldosterone antagonist (spironolactone) *monitor renal function, electrolytes, HR and BP for diuretics and BB Follow up in 2 weeks

Question 45

Chronic HF treatment

Answer 45

Lifestyle (ex, smoking, alc, diet), patient education, depression Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic Inform DVLA, air travel likely ok Medical for LV systolic dysfunction 1st: ACEI + BB - monitor with U+E, Cr, eGFR for ACEI (start low and increase dose) 2nd: Aldosterone antagonist (spironolactone), ARB or hydralazine with nitrate - monitor K+ 3rd: digoxin or ivabradine or cardiac resynchronisation 4th: Implantable cardioverter defibrillator if previous ventricular arrhythmia

Question 46

Statins When? Side effects? Need to monitor

Answer 46

``` QRISK2 > 10% (10 year risk) - primary prevention (20mg) if <84 History of CVD Familial hypercholesterolaemia Anyone over 85 80mg for secondary prevention ``` Myalgia, stiffness, weakness, cramping (usually at around 6 months) Liver function test

Question 47

Secondary causes of hypertension

Answer 47

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 (liable and postural hypotension), acromegaly, hyperparathyroid Coarctation aorta Pre-eclampsia and pregnancy Drugs - decongestants, COCP, steroids

Question 48

Malignant hypertension

Answer 48

``` 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 ```

Question 49

End organ damage

Answer 49

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

Question 50

TLD used in HTN

Answer 50

Indapamamide

Question 51

Lead areas & vessels on ECG

Answer 51

V3, V4 - Anterior - LAD I, V5, V6 - Lateral - circumflex II, III, aVF - Inferior - RCA V1, V2 - Septal - LAD

Question 52

Symptoms of angina (3)

Answer 52

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

Question 53

Angina Ix

Answer 53

12 lead ECG: ischaemic changes @exercise stress test ST/T wave flattening or inversion FBC (anaemia), FBG (diabetes), FBChol/triglycerides, LFT (baseline before statin) U+E (renal func), TFT (increased work, hypo assoc cholesterol) Refer all with suspected angina to Rapid Access Chest Pain Clinic for confirmation of Dx and severity assessment- Urgently - within 2 weeks

Question 54

Angina management

Answer 54

Stop activity: use GTN (spray/tablets), if pain doesn’t ease 2nd dose @ 5 minutes, 3rd dose @ 5 minutes, wait 5 minutes then 999 (i.e. after 15 mins total) Short acting nitrate: GTN (with explanation as above) to prevent 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 Amlodipine) CCB + BB If intolerant or CI: consider long acting nitrate or nicorandil or ivabradine Reduce cardiac RF Aspirin 75mg or clopidogrel- antiplatelet (establish bleeding tisk), statin if indicated, ACE-I for HTN/diabetes Review at 2-4 weeks

Question 55

ACS Types In young In old/diabetic

Answer 55

STEMI (ST elevation and acute CP > 20 mins) NSTE-ACS - acute CP + transient/persistent ST depression or T wave inversion/flattening -NSTEMI - with a rise in troponin levels -Unstable angina - without Consider non-atherosclerotic -> coronary emboli (infected valve), vasculitis, coronary artery spasm, cocaine, increased O2 requirement (hyperthyroidism), decreases O2 delivery (anaemia) Elderly or DM may not have CP

Question 56

ACS ix

Answer 56

12 lead ECG ST elevation - transient = angina, fixed = acute infarction ST depression or T wave inversion = unstable angina or NSTEMI Pre-existing CAD = LVH, Q waves Cardiac enzymes: troponin T, troponin I, CK-MB (creatinine kinase) Within 6 hours - troponins most sensitive (3-6 hours post infarct - max at 12-24 hours) *test troponins at 6 and 12 hours If unstable angina minor elevations in trop may suggest future risk CK is cardiac specific, troponins are a marker for cardiac necrosis but also marker for skeletal muscle injury Bloods: FBC (anaemia and baseline for anticoagulants), blood glucose (hyperglycaemia is common = poor prog), renal function, electrolytes, lipids, TFT Imaging: CXR (complications of ischaemia i.e. pulmonary oedema etc. , or PE, pneumothorax, TAA), TTE wall motion abnormalities

Question 57

ACS immediate management

Answer 57

Resuscitation: ABCDE (IV fluids) Pain: GTN + intravenous opioid with antiemetic (morphine + metoclopramide) Dual antiplatelet: loading dose *300mg aspirin + ticagrelor 180mg Assess O2 sats: give high flow O2 if <94% Monitor with 12 lead ECG

Question 58

NSTEMI mamangement

Answer 58

GTN + Morphine + Metaloclopramide O2 Loading does of Aspirin and Ticagrelor - Both go down long term Fondaparinux (antithrombotic) if angiography planned > 24 hours, hep if < 24 hours) Assess future risk with TIMI Revascularisation (PCI or CABG) if appropriate if medium to high -discontinue ATP 5 days pre CABG

Question 59

STEMI mamangement

Answer 59

GTN + Morphine + Metaloclopramide O2 Loading does of Aspirin and Ticagrelor - Both go down long term ECG *Immediately assess suitability for reperfusion: PCI or fibrinolysis Offer coronary angiography + PCI if can be given within 120mins and within 12 hours of onset) For PCI must use an injectable anticoagulant unfractionated heparin + ticagrelor If beyond 12 hours offer coronary angiography + if evidence of continuing ischaemia Offer fibrinolysis (2nd choice) if PCI cannot be given within 120 mins - alteplase (tissue plasminogen activator), streptokinase CABG - for multiple artery infarction Drugs for secondary prevention, cardiac rehabilitation, lifestyle changes

Question 60

Drugs post MI (5)

Answer 60

ACEI, Dual antiplatelet (aspirin + clopidogrel) BB Statin, Monitor BP, monitor renal function, assessment of LV function

Question 61

Acute complications of MI

Answer 61

Acute MI (5-10%), cardiogenic shock, ischaemic mitral regurgitation, arrhythmia Early pericarditis (10%) - 24-96 hours, generally asymptomatic Dressler’s syndrome: late pericarditis, inflammatory reaction in response to necrotic tissue, occurs at *2-8 weeks - severe chest pain, worse supine

Question 62

Cardiac arrest management

Answer 62

ABC call 999 999 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

Question 63

Pericarditis Symptoms Causes

Answer 63

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 ``` Viral: *coxsackie, EBV + staphylococcal/haemophilus... Rheum: *SLE, sarcoid + …. Post MI: *Dressler’s 24-72 hours Drugs: hydralazine Other: *uraemia ```

Question 64

Pericarditis ECG changes

Answer 64

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

Question 65

Pericarditis managment

Answer 65

Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis) Admit if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs *falling blood pressure and shock - suspect cardiac tamponade - immediate peircardiocentesis with echo

Question 66

``` Cardiac tamponade What Commonly associated with? Symptoms/Signs? ECG Management ```

Answer 66

Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise *Pericarditis*, malignancy (breast/lung), Dressler’s, infective (HIV, TB), connective tissue (SLE, RA, dermatomyositis, systemic sclerosis), trauma 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) Low voltage QRS complex. Electrical alternans. Amplitude increases and decreases beat to beat QRS O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis

Question 67

Acute limb ischaemia

Answer 67

* 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

Question 68

ACE inhib CI in

Answer 68

Bilateral renal artery stenosis

Question 69

Peripheral vascular disease Ix Mangement

Answer 69

ABPI Clopidogrel Risk factor management Assess for stenting/angioplasty Vasodilator therapy

Question 70

Aortic dissection What? Where? Presentation?

Answer 70

Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen ``` Type A (70%) - aortic arch and ascending aorta proximal to *L subclavian Type B (30%) - descending aorta distal to L subclavian CV RF + aortic disease + cocaine/amfetamines + M/ED + bicuspid valve ``` 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

Question 71

Aortic dissection managment

Answer 71

Manage HTN aggressively - aim 100-120SBP IV beta blockers (labetalol) to reduce ventricular contraction IV nitroprusside (emergency vasodilator) Surgical repair

Question 72

Thoracic aortic aneurysm presentation

Answer 72

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

Question 73

Marfans and Aortic aneurysm

Answer 73

Require lifelong BB, regular imaging of aorta and restriction physical activity

Question 74

AAA

Answer 74

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

Question 75

Rupture of AAA Presentation Management

Answer 75

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 FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E CXR, AXR (75% are calcified) ECG for MI Large bore IV access Group and crossmatch, order 4-6 units blood, FFP, Pt Immediate theatre

Question 76

Hypovolaemic shock Cause Presentation Management

Answer 76

Blood loss - haemorrhage, fluid loss - dehydration/burns/pancreatitis Cold, unwell, anxious, faint, SOB, pain (from bleeding) Pale, sweaty, tachypnoea, cold peripheries, increased CRT, hypotension, tachycardia 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 resus

Question 77

Cardiogenic shock Cause Presentation & Signs Management

Answer 77

Most often caused by acute MI (affecting anterior wall) - or pericardial tamponade/severe constrictive pericarditis or obstructive PE or tension pneumothorax CP, N+V, dyspnoea, sweat, confusion/disorientation, palpitations O/E: pale, mottled, slow CR, hypotension, tachy/brady, JVP, oedema, 3rd/4th HS, quiet HS A+B - intubation ± mechanical ventilation, O2 C - gain venous access often require central venous access as peripherally shut down - send bloods (FBC, U&E, BNP, Trop,) IV fluid if depleted volume 250ml bolus (cardiac dysfunction) Monitor - cardiac monitoring, BP - art line, venous pressure - CVC, urinary catheter Pain relief *IV morphine and cardiac inotropes *dopamine or dobutamine Revascularisation