Cardiology Flashcards

1
Q

ACS
- Presentation
- ECG changes, including territories + arteries affected
- Differentials for ST elevation and depression on ECG

A

Presentation
- Central crushing chest pain w/ radiation to both, left or right arm/jaw
- Sweating, n+v, SOB, syncope
- Rise in troponin (STEMI + NSTEMI) or no rise (unstable angina)

ECG changes
- STEMI. ST elevation in 2 contiguous leads:
- >1mm (small square) in most leads
- in V2-3: >1.5 in women; >2.0 in men >40 or >2.5 in men <40

NSTEMI
- >0.5mm in 2 continguous leads

New LBBB (most likley anterior/anteroseptal)

Territories
II, III, aVF = inferior = right coronary artery
V1-2 = septal = LAD
V3-4 = anterior = LAD
I, aVL, V5-6 = lateral = Left circumflex
V4-6, aVL = anterolateral = left circumflex + LAD

Posterior MI = flat ST depression, upright t waves + tall R waves in V1-3 (confirm w/ posterior leads V7-9)

Differentials for ST segment changes

ST Elevation
- STEMI
- Pericarditis/myocarditis
-High take-off (normal variant)
- Left ventricular aneurysm (if persisting after MI)
- Prinzmetal’s angina (coronary artery spasm)
- Takotsubo cardiomyopathy
- Rare: subarachnoid haemorrhage

ST Depression
- Secondary to abnormal QRS (LBBB, RBBB, LVH)
- Ischaemia
- Digoxin
- Hypokalaemia
- Syndrome X (anginal chest pain w/ no angio abnormalities. Type of IHD, more common in post- and perimenopausal women)

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2
Q

Describe the immediate and long-term management of ACS

A

Immediate in all
- MONA
- Morphine, oxygen (only if needed)
- Nitrates (subling or IV) (caution in hypotension)
- Aspirin 300mg (in all)

  • Then depends on ECG changes:

STEMI
- If PCI available within 120mins -> PCI
Give Prasugrel prior to PCI

  • If PCI not available within 120mins -> thrombolysis
    Give an antithrombin: fondaparinux (if low bleeding risk + angio not happening immediately) or unfrac heparin (if higher bleeding risk or immediate angio)

Give *ticagrelor *post-procedure

If ECG changes persist post-thrombolysis then PCI

N.B. Antiplatelets - switch to clopidogrel in all cases if high bleecing risk or patient already on anticoagulant

NSTEMI/Unstable Angina
If unstable e.g. hypotension -> immediate angio + PCI

Otherwise stratify risk using GRACE
- If high risk (3 or more%) - angio/PCI within 72h
Give unfractionated heparin and dual antiplatelts w/ prasugrel, ticagrelor or clopi (clopi if on anticoag already)

  • If low risk (<3%) - conservative management - Dual antiplatelet therapy: Aspirin + ticgrelor (if low bleeding risk) or clopi (if high bleed risk)

Long-term/Secondary Prevention
ABCs
- ACEi
- B- blocker
- C - clopidogrel/Dual antiplatelet therapy
- S - statin

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3
Q

Give possible post-MI complications and how they present

A

Early Complications
Cardiac Arrest - most secondary to VF
Cardiogenic Shock
Tachycarrhytmia - e.g. VF
Bradyarrhythmia - AV block - esp w/ inferior MI
Pericarditis - common within first 48h -> pain worse lying down, pericardial rub, pericardial effusion on echo

Later Complications
Chronic Heart Failure = ACE + B-blockers improve long-term prog; loop diuretics for symptoms
Dressler’s Syndrome - 2-6/52 post-MI - autoimmune reaction -> fever, pleuritic pain, pericardial effusion + raised ESR.
Treat w/ NSAIDs
Left Ventricular Aneurysm - persistent STE + LV failure. Thrombus can form within the aneurysm, increasing stroke risk.
Left Ventricular Free Wall Rupture - - 1-2/52 post-MI -> acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, dimished heart sounds) - needs urgent pericardiocentesis + thoracotomy
Ventricular Septal Defect -
- Rupture of septum in 1st week -> acute HF, pan-systolic murmur
- Echo to exclude acute mitral regurg (presents v similar)
- Urgent surgical correction needed
Acute Mitral Regurgitation
- More common in infero-posterio MI -> ischaemia/rupture of pappilary muscle
- -> acute hypotension, pulmonary oedema, systolic murmur
- Vasodilators + emergency surgical repair

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4
Q

Stable Angina
- Presentation (+ how this is different to unstable)
- Investigation
- Management

A

Presentation
- Chest pain on exertion + relieved by rest
- Unstable: on minimal exertion/at rest and not relieved by rest/nitrates

Investigation
- ECG - often normal but can be changes
- Stress test - ECG, cardiact CT, stress echo/angio

Management
- In all:
Aspirin
Statin
GTN (2x 5 mins apart, then 999)
Lifestyle modification

1st line: B-blocker OR rate limiting CCB (eg. verapamil or diltiazem) (NEVER both together –> heart block)

2nd line: B-blocker PLUS non-rate limiting CCB (e.g. amlodipine or nifedipine)

3rd line - if above not tolerated: Long-acting nitrate (isosorbride mononitrate - if standard release need to give asymmetrical dosing to allow drug free period each day to reduce risk of resistance); Ivabradine, Nicorandinal, Ranalozine

(don’t add third drug alongside CCB/B-blocker unless awaiting PCI/CABG)

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5
Q

Aortic Dissection
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology
- Tear between tunica intima + media
- RFs: connective tissue disease, male, age 50-70, HTN, atherosclerosis

Stanford Classification
- Type A - involves ascending aorta. Can be confined to ascending aorta (DeBakey II) or propogate to aortic arch (DeBakey I)
- Type B - does not involve ascending aorta (DeBakey 3)

Presentation
- Tearing chest pain radiating to back
- Tachycardia, hypotension, new aortic regurg, end-organ hypoperfusion
- Backward tear -> aortic regurg/incompetence, inferior MI due to RCA involvement
- Forward tear -> unequal arm pulse/BP, stroke, renal failure

Investigation
Type A: surgical. Control BP between 100-120 systolic.
Type B - conservative, bed rest, reduce BP w/ IV labetolol to prevent progression

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6
Q

Tachycardia Algorithm

A

Are adverse features present?
- Yes –> synchronised DC shock (up to 3x, then help)
-Shock, Syncope, Myocardial Ischaemia, HF

If no adverse features:

Narrow QRS
Regular (SVT (AVNRT or AVRT))
- Vagal manoeuvres
- Adenosine IV (6mg, then 12mg, then 18mg)
- Verapamil or B-blocker

Irregular (probs AF)
- B-blocker
- Consider digoxin/amiodarone if evidence of HF

Broad Complex
Irregular - seek help, could be:
- AF w/ bundle branch block (treat as per irregular narrow)
- OR polymorphic VT (torsades) - 2g Mg IV over 10 mins (N.B. torsade is caused by long QT)

Regular
- VT - Amiodarone 300mg IV
- OR if previous certain SVT w/ BBB or aberrant conduction treat as SVT

For the regular rhythms (both broad + narrow) if above ineffecitve -> synchronised DC shock up to 3 attempts

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7
Q

Bradycardia Algorithm

A

A-E approach + treat reversible causes

Adverse features? (shock, syncope, myocardia ischaemia, HF)

If Yes –>
1. Atropine 500mcg IV (can repeat up to max of 3mcg)
2. Isoprenaline/ Adrenaline infusion OR transcutaneous pacing (+ seek help)

If No –>
Is there a risk of aystole? (recent asystole, mobitz II or complete heart block, ventricular pause >3s) –> treat as per adverse features

If No risk of asystole -> observe

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8
Q

How is HTN diagnosed?
What is the target BP aim?

A

Diagnosis
Stage 1 HTN
Clinic BP >140/90 AND ABPM/HBPM average >135/85

Stage 2 HTN
Clinic BP >160/100 AND ABPM/HBPM >150/95

Stage 3 HTN (Severe)
Clinical BP >180 OR Diastolic > 110

Basically:
Clinic Reading >180 = treat now
Same day specialist ref if: Malignant/Accelerated HTN (papilloedema or retinal haemorrhages) OR life-threatening Sx (new confusion, chest pain, HF or AKI) OR if suspecting phaeochromocytoma (labile/posutral hypotension, palps, pallor, diaphoresis, abdo pain)
Clinic reading >140 but <180 - ABPM/HBPM
ABPM/HBPM
<135/85 - not hypertensive
>135/85 = stage 1
>150/95 = Stage 2

Who to treat?
All Stage 2 or 3
Some stage 1:
- >80
- <80 PLUS one of: target end organ damage, establised CVS disease, renal disease, DM, QRISK 10% or more.

Blood Pressure Target
- <80yo
Clinic: 140/90
Home: 135/85
- >80yo
Clinic: 150/90
Home: 145/85

N.B. pts <40yo w/ stage 1 HTN should be referred - ? secondary cause

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9
Q

Give possible causes and features of secondary hypertension

A

Renal
- Nephritic syndrome (haematuria, HTN, drop in renal function)
- Pyelonephritis
- Adult polycystic kidney disease (HTN, abdo pain, haematuria, UTIs, stones)
- Renal artery stenosis (worsening kidney function w/ ACEi)

Endocrine
- Phaeochromocytoma (headache, sweating, flushing, tachy, postural hypotension)
- Hyperaldosteronism (e.g. conn’s) - raised Na, low K+
- Cushing’s (buffallo hump, moon face etc.)
- Liddle’s syndrome (rare genetic disorder caused by abnormal renal function)
- Congenital adrenal hyperplasia
- Acromegaly (too much GH)

Drugs
- Steroids
- MAOI
- COCP
- NSAIDs
- Leflunomide (DMARD)

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10
Q

What is involved in management of HTN?

A

Lifestyle advice
- Reduce salt, caffeine + alcohol
- Stop smoking
- Exercise/Weight loss
- Balanced diet

Medication
- <55 OR T2DM
1st: ACEi or ARB
2nd: add CCB or Thiazide-like diuretic
3rd: All 3
4th: If K+ <4.5 = spironolactone; if K+ >4.5 B-blocker or A-blocker
5th: specialist review

  • > 55 and no T2DM OR Black ethnicity
    1st: CCB
    2: add ACEi/ARB or Thiazide-like diuretic (if black consider ARB rather than ACEi
    3rd: All 3
    4th: As above
    5th: specialist
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11
Q

ACE Inhibitors
- Examples
- Side effects
- Cautions and contraindications
- Interactions
- Monitoring

A

Examples
Ramipril, enalapril

Side effects
- Dry cough
- Angioedema (can occur up to a year after starting)
- Hyperkalaemia
- 1st dose hypotension (esp if also taking diuretics)

Cautions + CI
- pregnancy/breastfeeding, renovascular disease (can worsen renal impairment), aortic stenosis (-> hypotension), hyperkalaemia

Interactions
- Hypotension (esp w/ diuretic use)

Monitoring
- U&Es before treatement + after any dose increase
- Increase in serum creat up to 30% from baseline + increase in K+ up to 5.5 is acceptable
- (N.B. significant renal impairment can occur in undiagnosed B/L renal artery stenosis)

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12
Q

ALS
- Give possible reversible causes of cardiac arrest
- Describe the ALS algorithm

A

Reversible causes
- 4 Ts: Thrombus, Tamponade, Tension pneumothorax, Toxins
- 5 Hs: Hypokalaemia (electrolyte imbalance), Hypoglycaemia, Hypothermia, Haemorrhage

ALS Algorithm
- Chest compressions: 30:2
- Every 2 mins check rhythm + shock as needed:
‘Shockable’ - VF, pulseless VT
‘Non-Shockable’ - Asystole, PEA

  • Drugs
    IV or IO

Adrenaline 1mg (1:10,000) ASAP for non-shockable OR after 3rd shock in shockable. Repeat every 2 cycles (4 mins)

Amiodarone 300mg after 3rd shock

Other
- Consider thrombolytic drugs if PE is suspected as cause
- If witnessed cardiac arrest whilst on monitor - give up to 3 successive shocks prior to CPR (f shockable rhythm)

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13
Q

Chronic Heart Failure

  • Pathophysiology
  • Presentation
  • Investigation
  • Management
A

Pathophysiology
Causes: dilated cardiomyopathy, AF, ischaemia, HTN, valve abnormalities, myocarditis

Presentation
- SOBOE
NYHA
I - no limitation/symptoms
II - mild sx, ok at rest, ordinary activity leads to fatigue, SOB or palps
III - moderate - less than ordinary activity leads to symptoms
IV - severe, symptoms at rest

  • PND, orthopnoea, wheeze, pink frothy sputum

Investigations
- BNP
>400 or >2000 NTproBNP = high = r/v within 2/52
>100-400 or >400-2000 - raised - r/v within 6/52

  • Echo (if raised BNP)

Management
- Medications
- 1st: ACEi and B-blocker (start one at a time. Improve mortality in those w/ reduced EF)
- 2nd: aldosterone antagonist e.g. spironolactone or eplerenone (monitor K+ as both these + ACEi can increase it)
3rd: Specialist (eg. ivarbradine, Sacubitril-valsartan (NOT with ACEi/ARB), hydralazine, nitrate, digoxin)
(dig good w/ co-existant AF, Hydralazine + nitrate good for black ethnicity)

Other
- Cardiac Resynchronisation therapy - if wide QRS complex and EF <35%
- Annual influenza + one-off pneumococcal vaccine
- Exercise training

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14
Q

Describe the management of acute heart failure

A

1st: IV loop diuretics e.g. furosemide or bumetanide

Possible additional:
- O2
- Resp failure –> CPAP
- Hypotension (<85) –> inotropic agents, vasopressors, mechanical circulatory assistance
- Severe HTN, ischaemia or mitral/aortic regurg -> vasodilatros (nitrates)

N.B. continue normal reg HF meds alongisde. Only stop B-blockers if HR <50 or 2nd/3rd AV block

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15
Q

Atrial Fibrillation
- Presentation
- Investigation
- Management

A

Presentation
- Palpitations +/- SOB, tired, lightheaded, chest pain
- paroxysmal (self-terminating)
- Persistent (>7 days OR needs intervention to convert to sinus)
- Long-standing persistent - >1yr
- Permanent - patient/physician stop deciding to convert (acceptance)

Investigation
- ECG - irregularly irregular, no p waves

Management
Rhythm Control
- Emergency electrical cardioversion (if unstable)
- Elective pharm or electrical cardioversion:

Onset <48h –> heparinise PLUS electrical or pharm (amiodarone if structural heart disease OR flecainide) cardioversion

Onset >48h -> anticoag for 3/52 prior to electrical cardioversion. (or TOE to exclude left atrial appendage thrombus)
Then anticoag at least 4/52 (ongoing duration depends on risk of recurrence)

maintenance of rhythm control: B-blockers, dronedarone or amiodarone

**Rate Control **

Rate control is 1st line except: AF w/ reversible cause, HF primarily due to AF, new onset (<48h), flutter (ablation instead)

Can use:
B-blocker (CI in asthma)
CCB (verapamil or diltiazem)
DIgoxin (if person does little exercise or coexistent HF)

Catheter Ablation
- If AF doesn’t respond or who which to avoid antiarrhythmic meds
- Give Anticoags for 4/52 prior + continue after based on stroke risk (ablation controls rhythm but doesn’t alter stroke risk)

**Anticoagulation **- consider w/ any hx of AF (not just current AF)
- CHADVASC >/=1 in men or >/=2 in women
- Balance w/ bleeding risk: ORBIT score

  • 1st: DOAC (apixaban, dabigatran, edoxaban, rivaroxaban)
  • 2nd: warfarin (if DOAC CI or not tolerated)

N.B. Anticoagulation w/ DOAC should be started 2/52 after an ischaemic stroke

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16
Q

Aortic Stenosis - causes, presentation, management

Aortic Regurgitation - causes, presentation, management

A

Aortic Stenosis
Causes
- <65yo- bicuspid valve
- >65yo - degenerative calcification
- Other: William’s syndrome, post-rheumatic, HOCM

Presentation
- chest pain, SOB, syncope, extertional dizziness, ejection systolic murmur
- Narrow pulse pressure, slow rising pulse

Management
- asymptomatic - observe (UNLESS valv gradient >40 w/ LVSD)
- Symptomatic -> valve replacement or balloon valvuloplasty (if unfit for replacement)

Aortic Regurgitation
Causes
- Valve disease: rheumatic fever, calcification, IE, connective tissue disease
- Aortic root disease: aortid dissection, HTN, syphilis, Marfarn’s, Ehler Danlos

Presentation
- Early diastolic murmur, collapsing pulse, wide pulse pressure, quincke’s (nailbed pulsation), Dr Musset (head bobbing)

Echo to diagnose

Mangement
- Medical mx of associated HF
- Surgery if symptomatic severe AR OR asymptomatic w/ severe AR + LVSD

17
Q

Hyperlipidaemia

  • Lifestyle measures
  • Primary Prevention
  • Secondary Prevention
A

Lifestyle measures
- Cardioprotectice diet
- Physical activity
- Weight management
- Smoking cessation

**Primary Prevention **
Who to give it to?

-40-84yo w/ QRISK > 10%
-anyone >85

  • Don’t use QRISK in T1DM OR CKD:
  • T1DM - give primary prevention if: >40yo, DM for more than 10yrs, established nephropathy, other CVS risk factors (eg. HTN or obesity)
  • CKD - atorvastatin 20 to all patients

(QRISK may underestimate risk in: HIV, serious mental health, meds causing dyslipidaemia eg. antipyschotic, steroids; or autoimmun disorders)

Primary prevention: Atorvastatin 20mg OD (if non HDL hasn’t falled by 40% then consider increasing to 80mg)

Secondary Prevention
- All patients w/ known IHD OR cerebrovascular disease OR peripherl arterial disease
- Atorvastatin 80mg

Measuring lipids
- results feed into QRISK score BUT if v high then need to conisder familial hypercholesterolaemia + Ix further if:
- Total cholesterol >7.5mmol/l and/or
- personal/fam hx of premature coronary heart disease (event before 60)

18
Q

Statins
- Adverse Effects
- Contraindications
- Follow up/Monitoring

A

Adverse Effects
- Myopathy (myalgia, myositis, rhabdomyolysis, asymptomatic rise in CK)
- Liver Impairment - check LFTs at baseline, 3/12 and 12 months. Discontinue if transaminase conc 3x upper limit.
- Increased risk intracerebral haemorrhage in patient w/ prev stroke

Contraindications
- Macrolides (e.g. erythromycin, clarithromycin)
- Pregnancy (for all lipid lowering drugs - women w/ familial hypercholesterolaemia should stop meds 3/12 prior to trying to conceive)

Follow up
- At 3/13 should:
- repeat full lipid profile and LFTs
- If non-HDL cholesterol not dropped by at least 40% consider increasing dose to 80mg

19
Q

What is Buerger’s Disease?

A

Buerger’s Disease (aka thromboangiitis obliterans) is a small/medium vessel vasculitis strongly associated w/ smoking
–> Extremity ischaemia (intermittent claudication + ischaemic ulcers)
–> Superficial thrombophlebitis
—> Raynaud’s phenomenom

Suspect in young smoking patients w/ symptoms similar to limb ischaemia

20
Q

Wolff-Parkinson White

Pathophysiology
Presentation + ECG findings
Management

A

Pathophysiology
- congenital accessory conducting pathway (-> AVRT)
- Accessory pathway does not slow conduction so risk of AF –> VF

Presentation
- Asymptomatic
- Exertional dizziness, palpitations, SOB, chest pain, syncope
- arrest

ECG Findings
- Short PR interval
- Wide QRS complex w/ slurred upstroke (delta wave)
- LAD (if right sided pathway)
- RAD + dominant R wave in V1 (if left sided pathway)

Management
- Definitive: ablation of accessory pathway
- Medical: Sotalol (unless coexistent AF), amiodarone, flecainide

Dont give AV node blockers as risk of VF

21
Q

DVLA Guidance. What are the rules in the following situations?
- Hypertension
- Elective Angioplasty
- CABG
- ACS
- Angina
- Pacemaker insertion
- ICD
- Successful catheter ablation for arrhythmia
- Aortic aneurysm >6cm
- Heart transplant

Also for the acute MI how long till return to sexual intercourse? How long till return to work?

A

Hypertension
- drive as normal BUT if bus/lorry no driving if BP consistently >180 syt or 100 diastolic

Angioplasty (elective)
- 1/52 off

CABG
- 4/52 off

ACS
4/52 off OR 1/52 if successfully treated w/ angioplasty

Angina - stop if symptoms at rest/at wheel

Pacemaker - 1/52 off

ICD - if done for sustained ventricular arrhythmia no driving for 6/12. If done prophylactically no driving for one month.

Successful catheter ablation - 2 days off

Aortic aneurysm >6cm - notify DVLA. Annual review. If >6.5cm no driving.

Heart transplant - no driving for 6/52

MI - return to SI after 1/12. Return to work (most jobs) after 2/12.

22
Q

Prolonged QT interval
- Presentation, ECG findings + complications
- Causes
- Management

A

Causes
Congenital
- Long QT Syndrome. 3 subtypes: QT1, 2, 3.
- Jervell-Lange-Nielsen syndrome
- Romano - ward syndrome

Drugs
Amiodarone
Sotalol
TCAs, SSRIs (esp citalopram)
Methadone
Erythryomycin
Haloperidol
Ondansetron

Other
Hypocalcaemia, hypokalaemia, hypomagnesaemia
Acute MI
Myocarditis
Hypothermia
Subarachnoid

Presentation
Long QT syndrome:
QT1 - exertional syncope, often swimming
QT2 - syncope following emotional stress, auditory stimuli or exercise
QT3 - events often at night or at rest
Sudden cardiac death

Management
- Avoid drugs which prolong QT interval + other precipitants if appropriate
- B-Blockers
- ICDs in high risk cases

23
Q

Prolonged QT interval
- Presentation, ECG findings + complications
- Causes
- Management

A

Causes
Congenital
- Long QT Syndrome. 3 subtypes: QT1, 2, 3.
- Jervell-Lange-Nielsen syndrome
- Romano - ward syndrome

Drugs
Amiodarone
Sotalol
TCAs, SSRIs (esp citalopram)
Methadone
Erythryomycin
Haloperidol
Ondansetron

Other
Hypocalcaemia, hypokalaemia, hypomagnesaemia
Acute MI
Myocarditis
Hypothermia
Subarachnoid

Presentation
Long QT syndrome:
QT1 - exertional syncope, often swimming
QT2 - syncope following emotional stress, auditory stimuli or exercise
QT3 - events often at night or at rest
Sudden cardiac death

Management
- Avoid drugs which prolong QT interval + other precipitants if appropriate
- B-Blockers
- ICDs in high risk cases

24
Q

Cardiac Tamponade

Causes
Presentation
Management

A

Causes
- Left ventricular free wall rupture (post-MI)
- Dissecting aortic aneurysm
- Post-surgery
- Pericarditis
- Trauma

Presentation
Beck’s Triad: Raised JVP, muffled heart sounds, hypotension
Other: SOB, tachy, pulsus paradoxus (drop in BP in inspiration)
ECG: electrical alternans (alternating amplitude of QRS between beats)

25
Q

Infective Endocarditis

Pathophysiology (cause, valves affected, causative organisms)
Presentation
Investigation
Management

A

Pathophysiology
- Risk Factors/valve:
Prev healthy valve (50%) (-> mitral)
IVDU (–> Tricuspid)
Rheumatic Valve Disease (30%)
Prosthetic valve
Congenital heart defects
Recent piercings

(N.B. no prophylaxis given for dental shit)

Causative organisms:
- most common: Staph Aureus
- Dental hygeine + developing countries: Strep viridans
- Prosthetic valve surgery: Staph epidermidis (2 months post-surgery organisms go back to normal)
- Colorectal cancer - strep bovis
- Non-infective: SLE, malignancy

Culture negative:
- Prior abx
- HACEK: Haemophilis Actinobacillius, Cardiobacterium, Eikenella, Kingella
- Coxiella, Bartonella, Brucella

Presentation
- Septic signs: fever, rigors, night sweat, weight loss, anaemia, splenomeg, clubbing
- Cardiac: new murmur, long PR/AV block (aortic root abscess)
- Immune complex deposition: haematuria, renal failure, roth spots (eyes), osler’s nodes (painful)
- Embolic: janeway lesions, splinter haemorrhages

Presentation can be acute or subacute
Acute –> HF (likley staph aureus/IVDU + more likley to cause septic emboli)
Abnormal valves more likely -> subacute
Investigation
Diagnosis based on modified Duke’s Criteria, pathological criteria OR 2 major OR 1 major + 3 minor OR 5 minor
- Patho - +ve histology on autopsy
- Major:
- 1. - +ve cultures (3 taken 12h apart w/ 2 +ve w/ typical organisms)
- 2.Evidence of endocardial involvement (++ve echo or new valve regurg)
Minor
1. predisposing heart condition or IVDU
2. micro not meeting major
3. Fever >38
4. vasc phenomena
5. Immunological

Management
- Staph –> fluclox or vanc (+rifampicin for prosthetic valve)
- Strep –> benpen +/- gent
- Enterococci -> amox + gent
- HACEK - ceftriaxone
(altho depends on local guidelines/sensitivities0

26
Q

Pericarditis
Causes
Presentation
Investigation
Management

A

Causes
- Viral (coxsackie), TB, uraemia, trauma, post-MI (acute or dressler syndrome), connective tissue disease, hypothyroi, malig

Presentation
- Chest pain: pleuritic, relieved sitting forward,worse lying down
- Other: dry cough, SOB, flu-like sx, pericardial rub (heard best in expiration w/ pt sat up + learning forward), tachycardia

Investigation
ECG - global saddle-shaped ST elevation and PR depression (this is most specific for pericarditis)
Echo

Management
- Underlying cause
- NSAIDs + colchicine (if idiopathic or viral)

27
Q

Give possible causes of genetic cardiomyopathies, including key features, investigation results and management

A

*Hypertrophic obstructive (HOCM)
- Inheritance: autosomal dominant
- Symptoms: asymptomatic, exertional SOB, angina, post-exercise syncope, sudden death in young (ventricular arrhythmia)
- Signs: jerky pulse, double apex beat, ejection systolic murmur (due to outflow obstruction or mitral regurg)
- Echo: MR SAM ASH
MR (mitral regurg); SAM (systolic anterior motion of mitral valve), ASH (asymmetric hypertrophy)
- ECG: LVH, non-specific ST + T wave abnormalities, deep Q, AF
- Mx: ABCDE (Amiodarone, B-block or verapamil, Cardioverter defib, Dual chamber PPM, Endocarditis prophylaxis)
- Avoid: nitrates, ACEi, inotropes

Arrhythmogenic right ventricular dysplasia
- Inheritance: Autosomal dominant. 2nd most common cause of sudden cardiac death in young. R ventricular myocardium replced by fatty tissue -> ventricular arrhythmias
- Presentation: sudden cardiac death, exertional palps or syncope, HF
- ECG- V1-3 t inversion + epsilon wave (terminal notch in QRS complex)
- Echo: dilated, hypokinetic right ventricle
- Tx: anti-arrhythmics (e.g. B-block or amiodarone or sotalol), warfarin to prevent thrombus, ablation, defib

28
Q

Cardiomyopathy can be classed as:
- Primary (primarily involving the heart), secondary (part of generalised systemic disorder).
- Primary can be: genetic (HOCM or righ ventricular arrhythmogenic), acquired or mixed (genetic predisposition triggered by secondary process)
- Within this it can be dilated (can’t pump) or restricted (can’t fill/relax) or hypertrophic (less effective pumping)

Give examples of primary and secondary cardiomyopathies

A

**Primary **
- Genetic: HOCM + arrhythmogenic right ventricular dysplasia
- Acquied:

Peripartum - between last month of pregnancy + 5/12 post-partum. More common in older women, greater parity, multiple gestations

Takotsubo - stress induced; transient apical ballooning of myocardium. Supportive tx.

Secondary
Infective - coxsackie, chagas disease (D)
Infiltrative - amyloidosis (R)
Storage - haemochromatosis (R)
Toxicity- doxorubicin (D), alcoholic (D)
Inflammatory - sarcoidosis (R initially)
Endocrine - DM, thyrotoxicosis, acromegaly (D)
Neuromusc - Freidreich’s ataxia, duchenne-becker muscular dystrophy, myotonic drystrophy
Nutritional - wet beriberi (thiamine) (D)
Autoimmune - SLE (D)
Loeffler’s endocarditis (R) - rare, abnormal endomyocardial infiltration w/ eosinophils

29
Q

Syncope
- Causes
- Investigation
- Management

A

Causes
Reflex syncope (neurally mediated):
- Vasovagal (trigger -emotion, pain, stress)
- Situational (cough, micturition, GI)
- Carotid sinus syncope

Orthostatic syncope
- Primary autonomic failure: Parkinson’s, lewy body dementia
-Secondary autonomic failure: Diabetic neuropathy, amyloidosis, uraemia
- Drug induced: diuretics, alchohol, vasodilators
- Vol depletion: haemorrhage, diarrhoea

Cardiac syncope
- Arrhythmia: bradycardia (AV block) or tachy
- Structural: Aortic stenosis, MI, HOCM
- Other: PE

Investigation
- CVS exam
- Postural BP: >20 systolic or >10 diastolic drop OR drop in systolic <90 = diagnostic
- ECG
- Carotid sinus massage
- tilt table test
- 24h ECG

Management
- Depends on cause
- Vasovagal: avoid triggers, fluids, avoid precipitating meds e.g. anti-HTN, diuretic
- Orthostatic: meds r/v, compression stockings, fluids, increase salt, fludrocortisone
- Aortic stenosis: valve replacement
- HOCM: amiodarone, b-blocker, cardiac defib, dual chamber PPI

30
Q

ECG changes in electrolyte disturbances

  • Hypercalcaemia
  • Hypocalcaemia
  • Hyperkalaemia
  • Hypokalaemia
A

Hypercalcaemia - Short QT
Hypocalcaemia - Long QT

Hyperkalaemia - T ‘tented’ t waves, loss of p waves, broad QRS, sinusoidal, VF
Hypokalaemia - absent t waves, long pr, ST depression, long QT, u waves

31
Q

ECG changes in the following conditions:

  • Hypothermia
  • Brugada syndrome
  • Digoxin Toxicity
A

Hypothermia - bradycardic, long QT, J (osborne) wave (hump at end of QRS complex), 1st degree heart block, arrhythmia

Brugada Syndrome - autosomal dominant. Can -> sudden cardiac death.
ECG - convex ST elevation in V1-3 w/ negative t wave; partial RBBB (changes more obvious after flecainide - Ix of choice)
Mx - implantable cardioverter-defibrillator

Digoxin Toxicity
- Down-sloping ST dep (‘reverse tick’), flattened/inverted t waves, short QT, AV block/bradycardia

32
Q

What are the different types of heart block? How are they managed?

A

First Degree - PR >0.2s (5 small squares). Normally asymptomatic. No treatment needed.

Type 1 Second Degree (mobitz 1, wenkebach) - progressive PR prolongation until dropped beat. PPM.

Type 2 Second Degree (Mobitz II) - PR interval constant then sudden drop of QRS (2:1 block = 2 p waves but only one QRS; 3:1 3 p waves one qrs) etc. PPM.

3rd degree (complete) heart block - no relationship between p + QRS - PPM
Features: syncope, HF, regular brady (30-50bpm), wide pulse pressure

Causes of heart block: MI, cardiomyopathy, sarcoidosis, hypokalaemia, digoxin toxicity, aortic root pathology, rheumatic fever

33
Q

Give causes of the following:

  • Increased p wave amplitude
  • Broad, notched p waves
  • Peaked t waves
  • Inverted t waves
  • Increased QRS amplitude
A

Increased p wave amplitude - cor pulmonale

Broad, notched p waves - left atrial enlargment e.g. due to mitral stenosis

Tall peaked t waves - hyperkalaemia, MI (part of evolving STEMI changes)

Inverted t waves - MI, hypokalaemia, digoxin tox, subarachnoid, PE (S1Q3T3), brugada, arrhythmogenic right ventricular cardiomyopathy

Increased QRS amplitude :
1. increased distance from lead to heart - COPD, obesity, pleural/pericardial effusion, constrictive pericarditis
2. Infiltration of heart: amyloidosis, scleroderma, haemachromatosis
3. Metabolic: hypothyroid

34
Q

What are the following types of pulse associated with?
- Pulsus paradoxus
- Slow-rising pulse
- Collapsing Pulse
- Pulsus alternans
- Bisferiens pulse
- Jerky pulse

A

Pulsus paradoxus (fall in BP during inspiration -> faint/absent pulse in inspiration) - cardiac tamponade, severe asthma

Slow-rising pulse - aortic stenosis

Collapsing pulse - aortic regurgitation, patent ductus arteriosus, hyperkinetic state (anaemia, thyrotoxic, fever, exercise, pregnancy)

Pulsus alternans - severe LVF

Bisferiens pulse - mixed aortic valve disease (double pulse w/ two systolic peaks)

Jerky Pulse - HOCM

35
Q

What are the following scoring systems used for?
- ABCD2
- NYHA
- DAS28
- Child-Pugh Classification
- HAD
- PHQ-9
- GAD - 7
- SCOFF
- FAST
- IPSS
- Gleason
- APGAR
- Bishop
- Ranson Criteria

A
  • ABCD2 - risk stratification post-TIA
  • NYHA - HF severity scale
  • DAS28 - Disease activity in RA
  • Child-Pugh Classification - Severity of liver cirrhosis
  • HAD- Hospital Anxiety + depression scale (assesses severity of symptoms)
  • PHQ-9 - Patient health questionnaire - assesses severity of depression symptoms
  • GAD - 7 - generalised anxiety disorder
  • SCOFF - used to detect eating disorders + guide treatment
  • FAST - Alcohol screening tool
  • IPSS - International prostate symptom score
  • Gleason - indicates prognosis in prostate Ca
  • APGAR - Assesses health of newborn immediately after birth
  • Bishop - Assesses whether induction of labour is needed
  • Ranson Criteria - Acute pancreatitis mortality
36
Q

Palpitations
Causes
Investigation

A

Causes
- Irregular, fast - AF, flutter w/ variable block
- Regular, fast - SVT, VT
- Dropped/missed beat - Atrial/Ventricular ectopic
- Regular pounding - anxiety
- Slow - B-block, antiarrhythmics

Investigation
- 12 lead ECG
- TFTs - hyper can precipitate AF/other arrhythmia
- U&Es
- FBC

  • Then to capture the episode
  • Holter monitoring - continuous 24h + patient keeps symptom diary
  • External loop recorder
  • Implantable loop recorder
37
Q

Mitral Stenosis
Mitral Regurgitation

Causes, presentation, investigation, management

A

Mitral Stenosis
- Causes: rheumatic fever (others exist but rare)
- Present: SOB, haemoptysis, mid-late diastolic murmur, loud S1 w/ opening snap, low volume pulse, malar flush, AF
- CXR: left atrial enlargement
- Ix: echo to diagnose
- Mx:
- Associated AF - warfarin (rather than doac)
- Asymptomatic: monitor w/ echo
- Symptomatic - mitral balloon valvotomy or valve replacement

Mitral Regurgitation (2nd most common valve disease after AS)
Causes: MI (papillary muscle rupture); mitral valve prolapse; IE, Rheumatic fever, congenital
Presentation - most asymp but can -> left ventricular failure -> fatigue, SOB, oedema
Pansystolic blowing murmur
ECG - broad p wave (atrial enlargement)
Cardiomegaly
Echo
Mx -
Acute cases: nitrates, diuretics, inotropes, intra-aortic balloon pump
HF - ACEi + B-blockers + spironolactone
Severe -> surgery (repair >replacement)

38
Q
  • How are patients presenting with acute chest pain managed in primary care?
  • How are patients with stable chest pain investigated?
A

Acute Chest Pain
- Current chest pain OR pain within past 12h and abormal ECG –> A&E
- Chest pain 12-72h ago: same-day hosp assessment
- Chest pain >72h ago - ECG + trop then decide

Stable Chest Pain
Anginal pain, 3 features:
1. Constricting discomfort in chest, neck, shoulder, jaw or arm
2. precipitated by exertion
3. relieved by rest or GTN within 5 mins
All 3 = typical angina
2 = atypical angina
1 = non-anginal chest pain

Further Ix:
1st: CT coronary angiography
2nd: non-invasive functional imaging (myocardial perfusion scintigraphy; stress echo; MR perfusion + to look for wall motion abnormalities)
3rd: invasive coronary angiography

39
Q

Causes of:
- LBBB
- RBBB
- Axis Deviation
- What are bifascular and trifascicular block?

A

LBBB = always pathological
Causes: MI (if pre-existing LBBB then Sgarbossa criteria used to diagnose MI); HTN, AS, cardiomyopathy, dig tox, hyperkalaemia

RBBB - normal variant, RVH, cor pulmone, PE, MI, atrial septum defect, cardiomyopathy/myocarditis

Axis Deviation
- Left: LBBB, inferior MI, WPW, hyperkalaemia, obesity, atrial septal defect, left anterior hemiblock
- Right: RVH, left posterior hemiblock, lateral MI, cor pulmonale, PE, WPW, tall people

Bifasicular block - RBBB w/ left or right axis deviation
Trifasicular block - complete heart block + RBBB + left or right axis deviation