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Cardiology Flashcards

1
Q

Describe hypertrophic obstructive cardiomyopathy (HoCM)

A

AD disorder causing cardiac hypertrophy, usually septal

clinical features
- asymptomatic
- exertional dyspnoea
- syncope
- angina
- jerky pulse
- bisferiens pulse (2 separate systolic beats)

murmur: ejection systolic
> louder on Valsalva, quieter on squatting

  • sudden cardiac death is mainly caused by ventricular arrhythmias (males > females)
  • can happen at rest or exercising
  • S4 heart sound
  • associated with Freidreich’s ataxia and Wolff Parkinson White

Echo: MR SAM ASH
- mitral regurgitation
- systolic anterior motion (SAM) of anterior mitral valve leaflet
- asymmetric septal hypertrophy

ECG
- Non-specific ST segment and T wave abnormalities, progressive T wave inversion
- Deep Q waves

management
> beta-blockers first-line
> ICD
> surgical myectomy, alcohol septal ablation, heart transplant

  • avoid ACEi
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2
Q

Name scores used to determine risk of stroke in AF

A

CHA2DS2VASc
> CHF
> Hypertension
> Age >75 (2)
> Diabetes
> Stroke / TIA / VTE (2)
> Vascular disease
> Age 65-74
> Female

If >=2 in females or >=1 males, consider anticoagulation

prescribe DOAC even if single episode of paroxysmal AF

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3
Q

Describe the management of SVT

A

Regular narrow complex tachycardia

Acute management

vagal manoeuvres:
> Valsalva manoeuvre
> carotid sinus massage

intravenous adenosine
> rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
> contraindicated in asthmatics - verapamil is a preferable option

DC electrical cardioversion

Prevention of episodes
beta-blockers
radio-frequency ablation

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4
Q

Describe Eisenmenger’s syndrome

A

Reversal of a left-to-right shunt in a cogenital heart defect due to pulmonary hypertension

Uncorrected left-to-right results in remodelling of the pulmonary microvasculature leading to pulmonary hypertension

associated with
- ventricular septal defect
- atrial septal defect
- patent ductus arteriosus

Features
- original murmur may disappear
- cyanosis
- clubbing
- right ventricular failure
- haemoptysis, embolism

CXR: cardiomegaly and pulmonary engorgement

Management: heart-lung transplant

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5
Q

describe the murmur associated with a VSD

A

Blowing pansystolic murmur

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6
Q

Describe the causes of infective endocarditis

A

IVDU (typically causing tricuspid lesion)
- staph aureus (most common)
> tricuspid regurgitation: pansystolic murmur heard loudest over left lower sternal edge, louder during inspiration

Post-valvular surgery (first 2 months post-surgery)
- staphylococcus epidermis (coagulase negative staph or CoNS)

Streptococcus bovis is associated with colon cancer

Streptococcus viridans is the most common cause in developing countries (streptococcus mitis, streptococcus sanguinis) - mouth and dental plaques, caused by poor dental hygiene or following dental procedures

Non-infective
- Systemic lupus erythematosus (Libman-Sacks)
- Malignancy: marantic endocarditis

Culture negative causes:
- prior antibiotics
- Coxiella burnetii
- HACEK: Haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

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7
Q

Describe the management of NSTEMI

A

Aspirin + ticagrelor + fondaparinux
> give unfractionated heparin if patient is undergoing PCI

Clopidogrel instead of ticagrelor if patient at high risk of bleeding

Consider PCI
> coronary angiography within 72h if GRACE score >3%
> immediate PCI if unstable

Nitrates can be given if no hypotension present

Cannot drive for 4 weeks post-MI

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8
Q

describe the initial management of ACS

A
  • Aspirin 300mg
  • Oxygen if sats <94
  • Morphine if severe pain
  • Nitrates if not hypotensive
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9
Q

Describe the management of a STEMI

A

Coronary reperfusion therapy

  • Percutaneous coronary intervention (PCI)

> If presentation is within 12h of onset of symptoms and PCI can be delivered within 120 minutes
dual antiplatelet i.e. aspirin and one of the options below

> if patient not on anticoagulant: prasugrel
if patient on anticoagulant: clopidogrel

> Offer unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor + dual antiplatelet therapy if undergoing primary PCI with radial access

  • Fibrinolysis if primary PCI cannot be given within 120 mins
    > alteplase + fondaparinux
    > repeat ECG in 60-90 mins and transfer for urgent PCI if ST elevation has not resolved
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10
Q

describe Brugada syndrome

A

Sodium channelopathy causing a high incidence of sudden death in patients with structurally normal hearts

Features
- ECG abnormality
> coved ST elevation in >1 of V1-V3 followed by a negative t wave

  • and one of the following criteria:
  • documented VF
  • polymorphic VT
  • family history of sudden cardiac death <45 yrs old
  • coved type ECGs in family members
  • syncope
  • nocturnal agonal respiration
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11
Q

describe mitral stenosis

A

main cause is rheumatic fever

features
- dyspnoea
- haemoptysis
- mid-late diastolic murmur
- loud S1
- opening snap (indicates mitral valve leaflets are still mobile)
- low volume pulse

CXR - left atrial enlargement, associated with AF

management
- if associated with AF, anticoagulate with warfarin / DOAC
- asymptomatic: monitor
- symptomatic: percutaneous mitral commissurotomy

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12
Q

which medication used in the treatment of angina can be associated with tolerance?

A

isosorbide mononitrate

may need changes in dosing regimes

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13
Q

list coronary arteries responsible for MI and the leads they are associated with

A

anteroseptal
> V1-V4
> LAD

inferior
> II, III, aVF
> RCA
> AV block can occur following inferior MI

anterolateral
> V1-6, aVL
> proximal LAD

lateral
> I, aVL +/- V5, V6
> left circumflex

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14
Q

describe the ECG features in posterior MI

A

ECG features
- tall R waves in V1 and V2
- confirmed by ST elevation and Q waves in posterior leads

affected vessel: left circumflex, right coronary

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15
Q

what kind of infarct can cause bradycardia or arrythmias?

A

right coronary infarct as this supplies AV node

> leads II, III and aVF

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16
Q

describe the management of acute heart failure

A

SODIUM
- Sit up
- Oxygen aiming for 94-98%
- Diuretics: IV furosemide
- IV fluids should be STOPPED
- Underlying causes treated
- Monitor fluid balance

Nitrates if concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease
> contraindication - hypotension

If still hypoxic: CPAP

If hypotensive
> dobutamine
> norepinephrine
> mechanical circulatory assistance: intra-aortic balloon counterpulsation, ventricular assist devices

Regular medications for heart failure like beta-blockers or ACEi should be continued unless shock, <50 bpm, 2nd or 3rd degree heart block

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17
Q

describe arrhythmogenic right ventricular dysplasia (ARVD)

A

AD inherited cardiac disorder that is the second most common cause of sudden cardiac death after HOCM

pathophysiology - right ventricular myocardium is replaced by fatty and fibrofatty tissue

features
- palpitations
- syncope during exertion
- family history of sudden cardiac death in relative <40 years old

ECG findings
> epsilon wave: small positive deflection at the end of QRS
> T wave inversion in leads V1-3

Echocardiogram
> enlarged hypokinetic right ventricle with a thin free wall

management
- sotalol as antiarrhythmic
- catheter ablation to prevent VT
- implantable cardioverter defibrillator (ICD)

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18
Q

describe Naxos disease

A

AR variant of ARVD

triad of ARVD, palmoplantar keratosis and woolly hair

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19
Q

describe aortic stenosis and its management

A

clinical features of symptomatic disease (worse on exertion)
- chest pain
- dyspnoea
- syncope
- heart failure
- pulsus tardus et parvus (weak and late)

  • murmur: ejection systolic murmur radiating to carotids
    > fixed splitting of heart sounds
    > Gallavardin phenomenon: auscultation at cardiac apex reveals a holosystolic murmur that sounds like mitral regurgitation

features of severe aortic stenosis
- collapsing pulse
- thrill during systole
- narrow pulse pressure
- S4
- left ventricular hypertrophy or failure

causes
- degenerative calcification
- bicuspid aortic valve
> click heard start of systole
- post-rheumatic disease
- subvalvular: HOCM
- William’s syndrome: supravalvular aortic stenosis

investigations
- echocardiogram: assess pressure gradient and surface area of valve
> elevated aortic pressure gradient, reduced valve area, reduced left ventricular ejection fraction, LVH

management
- asymptomatic: observe
> consider surgery if valvular pressure gradient >40 mmHg and LVSD

  • symptomatic: valve replacement
    > surgical AVR if young
    » TAVI (transcatheter aortic valve replacement) if high risk
    » balloon valvuloplasty in children or adults not fit for valve replacement

nitrates are contraindicated, give furosemide for symptomatic relief

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20
Q

Describe ventricular septal defect and its management

A

most common cause of congenital heart disease

aetiology
- associated with chromosomal disorders e.g. Down’s syndrome, Edward’s syndrome, Patau syndrome, cri-du-chat syndrome
- congenital infections
- acquired causes e.g. post-MI

Post-natal presentation
- failure to thrive
- features of HF
> hepatomegaly
> tachypnoea
> tachycardia
> pallor

murmur: pan-systolic murmur heard at the lower left sternal border
> louder in small defects

Management
- small VSDs often close spontaneously - monitor

  • large VSDs:
    > medication for HF e.g. diuretics
    > pulmonary artery banding
    > surgical closure: transvenous catheter closure, open heart surgery

Complications
- aortic regurgitation
- infective endocarditis
- Eisenmenger’s syndrome
- right heart failure
> associated with firm, smooth, tender and pulsatile liver edge
- pulmonary hypertension

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21
Q

list complications following MI

A
  • left ventricular free wall rupture
  • left ventricular aneurysm
  • ventricular septal defect
    > pansystolic murmur
    > acute pulmonary oedema
  • mitral valve prolapse
    > 2-7 days post-MI
    > sudden pulmonary oedema
    > sinus tachycardia
    > late systolic murmur accompanied by mid-systolic click
  • Dressler’s syndrome
  • heart failure
  • re-infarction
    > test with creatine kinase MB (CK-MB)
  • death
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22
Q

describe an atrial septal defect (ASD)

A

asymptomatic in childhood

only progress to give symptoms if they remain untreated to adulthood

murmur: mid-systolic, crescendo-descrescendo murmur heard loudest at upper left sternal border
> murmur radiates to the back
> fixed S2 splitting

if left-to-right shunt exists, paradoxical embolisation can occur
> Stroke in young patients with DVT (embolus bypasses lungs)

management:
> small: monitor
> large: catheter-based closure / open heart surgery

complications: stroke, pulmonary hypertension, right-heart failure, Eisenmenger syndrome

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23
Q

Describe the management of chronic heart failure

A

First-line for all patients:
- ACEi + beta-blocker
> start one drug at a time

Second-line
- aldosterone antagonist aka mineralocorticoid receptor antagonist e.g. spironolactone, eplerenone

  • SGLT2i

Third-line
- ivabradine: contraindicated in HR <70bpm
- sacubitril valsartan (ARNI)
- hydralazine + nitrate: more effective in Afro-Caribbean patients
- digoxin
- cardiac resynchronisation therapy (CRT)

offer annual influenza vaccine + one-off pneumococcal vaccine
> those with asplenia, splenic dysfunction of CKD need a booster every 5 years

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24
Q

describe ECG changes associated with mitral stenosis

A

P mitrale
- left atrial hypertrophy/strain e.g. in mitral stenosis
- broad, notched (bifid) P waves
> most pronounced in lead II

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25
describe acute mitral regurgitation
More common infero-posterior infarction causes: ischaemia or rupture of papillary muscle features - Acute hypotension - pulmonary oedema - early-to-mid systolic murmur management - vasodilator therapy - emergency surgical repair.
26
describe - left ventricular aneurysm - left ventricular free wall rupture
left ventricular aneurysm - ischaemic damage weakens myocardium resulting in aneurysm formation - S3, S4 heart sounds - ECG: persistent ST elevation and left ventricular failure - thrombus may form within aneurysm increasing risk of stroke - gradual onset pulmonary oedema, no chest pain - management: anticoagulation left ventricular free wall rupture - occurs around 1-2 weeks after MI - presents with acute heart failure secondary to cardiac tamponade > raised JVP, pulsus paradoxus, diminished heart sounds - ECG: widespread ST elevation - management: urgent pericardiocentesis and thoracotomy
27
describe a patent ductus arteriosus
acyanotic congenital heart defect > connection between pulmonary trunk and descending aorta murmur - normal S1 with a CONTINUOUS crescendo-decrescendo "MACHINERY" murmur that continues during S2 - BELOW left clavicle risk factors: maternal rubella infection, prematurity features - shortness of breath - difficulty feeding - poor weight gain - LRTIs - bounding collapsing pulses - large pulse pressure diagnosis: echocardiogram shows left-to-right shunt, hypertrophy complications: pulmonary hypertension, right ventricular hypertrophy, left ventricular hypertrophy management - give neonate indomethacin (or ibuprofen) if echo shows PDA 1 week postnatally: inhibits prostaglandin synthesis - monitor until 1 year with echos - after 1 year: transcatheter or surgical closure (earlier if symptomatic)
28
describe Tetralogy of Fallot
4 coexisting pathologies lead to right-left shunt - ventricular septal defect (VSD) - overriding aorta - pulmonary valve stenosis - right ventricular hypertrophy > severity of right ventricular outflow tract obstruction (pulmonary stenosis) determines degree of cyanosis and clinical severity risk factors: rubella, diabetic older mother, DiGeorge syndrome murmur due to pulmonary stenosis: ejection systolic murmur loudest at pulmonary area (upper left sternal area), louder on inspiration diagnosis: echocardiogram > CXR: boot-shaped heart features - cyanosis - clubbing - poor feeding - ejection systolic murmur - tet spells: cyanotic episode precipitated by waking, physical exertion or crying management - total surgical repair by open heart surgery
29
describe coarctation of the aorta
congenital narrowing of descending aorta associations - turner's syndrome - bicuspid aortic valve - berry aneurysms - neurofibromatosis features - infancy: duct-dependent CHD > may present with sudden collapse as ductus arteriosus closes > tachypnoea, increased WOB > weak femoral pulses > poor feeding, grey and floppy baby > underdevelopment of left arm (reduced flow to subclavian artery) and legs > swollen extremities - adult: > hypertension > left ventricular heave (left ventricular hypertrophy) > radio-femoral delay - murmur: ejection systolic murmur, radiates to back management - critical coarctation: prostaglandin E1 (alprostadil) to keep ductus arteriosus open while awaiting surgery > surgery will ligate ductus arteriosus and correct coarctation - mild: asymptomatic until adulthood may not require surgical input
30
describe congenital pulmonary valve stenosis
associations - tetralogy of fallot - william syndrome - noonan syndrome - congenital rubella syndrome features - fatigue on exertion - shortness of breath - dizziness, fainting - murmur: ejection systolic murmur heard loudest at pulmonary area (second intercostal space, left sternal border) - palpable thrill in pulmonary area - right ventricular heave due to right ventricular hypertrophy - raised JVP diagnosis: echocardiogram management - mild: monitor - symptomatic or more significant stenosis: balloon valvuloplasty via venous catheter; open heart surgery
31
describe Ebstein's anomaly
congenital condition where tricuspid valve is lower in right side of heart leading to bigger right atrium and smaller right ventricle associated with > right-to-left shunt across atria via ASD leading to cyanosis > Wolff-Parkinson-White syndrome presentation - heart failure - gallop rhythm (addition of S3 and S4) - cyanosis - SOB, tachypnoea - poor feeding - collapse or cardiac arrest diagnosis - echocardiogram management - treat arrhythmias and heart failure - definitive is surgical correction
32
describe transposition of the great arteries
attachments of aorta and pulmonary trunk are swapped > right ventricle pumps blood into aorta and left ventricle pumps blood into pulmonary vessels associated with: VSD, coarctation of aorta, pulmonary stenosis diagnosis > loud single S2, no murmur, no respiratory distress > antenatal US > if undetected during pregnancy, presents with cyanosis soon after birth management - prostaglandin infusion - maintain ductus arteriosus - balloon septostomy to create an atrial septal defect - open heart surgery: arterial switch - definitive management
33
describe Wellen's syndrome
ECG pattern caused by high-grade stenosis in left anterior descending coronary artery features - may or may not be pain free - cardiac enzymes may be normal/minimally elevated. ECG features - biphasic or deep T wave inversion in V2-3 - minimal ST elevation - no Q waves
34
describe aortic regurgitation
causes - chronic due to valve disease > rheumatic fever > calcific valve disease > connective tissue diseases e.g. RA - chronic due to aortic root disease > bicuspid aortic valve > spondyloarthropathy e.g. ankylosing spondylitis > hypertension > syphilis > Marfan's, Ehlers-Danlos - acute due to valve disease: infective endocarditis - acute due to aortic root disease: aortic dissection features - early diastolic murmur - collapsing pulse > bisferiens pulse in mixed aortic valve disease (stenosis + regurgitation) - wide pulse pressure - Quincke's sign - nailbed pulsation - De Musset's sign - head bobbing - mid-diastolic Austin-Flint murmur in severe AR investigation - echocardiography management - surgery (TAVI) - if symptomatic with severe AR or asymptomatic with severe AR and LVSD
35
state the first-line investigation for stable chest pain of suspected coronary aetiology
Contrast-enhanced CT coronary angiogram
36
list acyanotic and cyanotic congenital heart conditions
acyanotic - ventricular septal defect (VSD) - atrial septal defect (ASD) - patent ductus arteriosus (PDA) - coarctation of the aorta - aortic valve stenosis cyanotic - tetralogy of Fallot (more common overall) - transposition of the great arteries (TGA) (more common lesion presenting at birth) - tricuspid atresia
37
describe an atrioventricular septal defect (AVSD)
defect associated with trisomy 21 features - poor feeding - breathlessness - poor weight gain - puffiness - tachycardia murmur: systolic murmur heard loudest at upper left sternal edge management - surgical repair
38
describe an innocent murmur
aka physiological / functional murmurs common in children, do not require treatment unless causing symptoms features - systolic - short, soft and often vibratory/musical or "buzzing" - best heard at left upper sternal border (pulmonary area) - varies with posture - no thrill - localised with no radiation - no added sounds e.g. clicks venous hum: continuous blowing noise heard just below clavicles Still's murmur: low pitched sound heard at lower left sternal edge
39
describe the different types of MI
- Type I: primary coronary event - Type II: ischaemia due to increased oxygen demand / decreased supply - Type III: sudden cardiac death - Type IV: related to PCI (4a) or stent thrombosis (4b) - Type V: related to CABG
40
Describe the clinical features and treatment of cardiac tamponade
clinical features - Beck's triad: elevated venous pressure (CVP), reduced arterial pressure, reduced heart sounds - Pulsus paradoxus - electrical alternans on ECG > different heights of consecutive QRS complexes May occur with as little as 100ml blood Definitive management > emergency thoracotomy > if they still have a cardiac output, this should occur in theatre with clam shell approach > If there is a significant delay, consider a pericardiocentesis
41
describe constrictive pericarditis
caused by any cause of pericarditis, particularly TB features - dyspnoea - right heart failure: elevated JVP, ascites, oedema, hepatomegaly - pericardial knock: loud S3 - Kussmaul's sign is positive: JVP rising on inspiration - pulsus paradoxus is absent, unlike cardiac tamponade CXR - pericardial calcification
42
Describe normal ECG variants in an athlete
- first degree heart block - sinus Bradycardia - Mobitz type 1 (Wenckebach) phenomenon - junctional rhythm
43
Describe the classical features of aortic dissection and its management
Tearing retrosternal chest pain radiating to back Difference in BP between left and right arms tear in ascending aorta may be indicated by new aortic murmur e.g. aortic regurgitation risk factor: pectus excavatum investigations - CXR: widened mediastinum - ECG: widespread ST depression with normal troponin - CT aortic angiogram (first-line if haemodynamically stable): false lumen > CT CAP if unavailable > transoesophageal echo (TOE) in clinically unstable patients Management type A - ascending aorta - control BP (IV labetalol) + surgery (aortic root replacement) type B - descending aorta - control BP(IV labetalol)
44
Describe the guidelines for statin treatment
QRISK score over 10% > atorvastatin first-line 20mg > Simvastatin if atorvastatin can't be tolerated > aim for reduction in non-HDL cholesterol >40% QRISK under 10% Dietary measures monitoring > LFTs at baseline, 3 months and 12 months
45
List adverse effects of amiodarone and describe monitoring requirements
- thyroid dysfunction: both hypothyroidism and hyper-thyroidism > in amiodarone-induced hypothyroidism, amiodarone can be continued with levothyroxine - corneal deposits - pulmonary fibrosis/pneumonitis - liver fibrosis/hepatitis - peripheral neuropathy, myopathy photosensitivity - 'slate-grey' appearance - thrombophlebitis and injection site reactions - bradycardia - lengthens QTc interval Monitor LFTs, TFTs every 6 months
46
describe the management of angina pectoris
All patients should receive aspirin and a statin > clopidogrel if previous stroke / PAD Sublingual GTN to abort angina attacks - first-line: beta-blocker e.g. atenolol > OR rate-limiting calcium channel blocker (verapamil, diltiazem) >> if using in combination with a beta-blocker use a longer-acting dihydropyridine CCB e.g. amlodipine, MR nifedipine If poor response increase to maximum tolerated dose If unsuccessful consider addition of - Long-acting nitrate e.g. isosorbide mononitrate - Ivabradine - Nicorandil - Ranolazine
47
describe Stokes-Adams syndrome
episodes of syncope due to intermittent complete heart block or other high-grade arrhythmia which compromise cerebral circulation bizarre, wide, inverted T-waves can be seen in Stokes-Adams attacks; do not necessarily imply new ischaemia
48
describe Wolff Parkinson White syndrome
pre-excitation syndrome where accessory pathway bypasses AV node leading to early depolarisation of ventricles this is an AV re-entry tachycardia (AVRT) - wide QRS with slurred upstroke - delta wave - short PR interval (<120ms) - left axis deviation if right-sided accessory pathway - right axis deviation if left-sided accessory pathway treatment - radiofrequency ablation of accessory pathway - medical therapy: sotalol, amiodarone, flecainide > echocardiogram must be done before use of flecainide to check for signs of structural heart disease
49
describe digoxin toxicity
digoxin mechanism of action: Na/K ATPase pump inhibition features > generally unwell, lethargy > nausea and vomiting, anorexia > confusion > yellow-green vision > gynaecomastia Arrhythmias > reverse tick sign: downsloping ST depression > premature ventricular complexes (PVCs) > ventricular tachycardia or ventricular fibrillation > sinus bradycardia predisposing factors - hypokalaemia, hypomagnesaemia - hypercalcaemia - hypernatraemia - acidosis - drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone, ciclosporin, bendroflumethiazide management > digibind > correct arrhythmias > monitor potassium
50
what is the target INR for the following mechanical valve replacements mitral aortic
aortic: 3.0 mitral: 3.5
51
Describe the management of atrial fibrillation
Rate control - beta-blockers - calcium channel blockers - digoxin > causes scooped ST depression rhythm control: patients who are young and symptomatic - beta-blockers - dronedarone (second-line following cardioversion) - amiodarone (co-existing HF) > anticoagulation for 3 weeks followed by cardioversion when AF >48h in duration catheter ablation if not responding to medication > patients should remain on anticoagulation (DOAC) as stroke risk is the same To determine the need for anticoagulation in AF: CHA2DS2VASc >=2
52
describe adverse effects and contraindications of statins
Adverse effects - myopathy - liver impairment contraindications - macrolides: clarithromycin / erythromycin - pregnancy
53
describe ECG changes seen in hypocalcaemia
QTc prolongation Severe: Osborn (J waves) Rare: AF or Torsades de Pointes if ECG changes present give urgent IV calcium gluconate
54
Describe bifascicular and trifascicular block
Bifascicular block: combination of RBBB with left anterior or posterior hemiblock e.g. RBBB with left axis deviation Trifascicular block features of bifascicular block as above + 1st-degree heart block
55
List causes of hypokalaemia and its ECG features
Hypokalaemia with alkalosis > vomiting > thiazide and loop diuretics > Cushing's syndrome > Conn's syndrome (primary hyperaldosteronism) Hypokalaemia with acidosis > diarrhoea > renal tubular acidosis > acetazolamide > partially treated diabetic ketoacidosis Magnesium deficiency may also cause hypokalaemia. In such cases, normalizing the potassium level may be difficult until the magnesium deficiency has been corrected ECG features - U waves, small/absent T waves (or inversion), prolonged PR interval, ST depression, long QT
56
describe the management of hyperkalaemia
severe - sine wave pattern stabilisation of cardiac membrane: IV 10ml 10% calcium gluconate over 10 minutes IV insulin dextrose > 8 units of actrapid in 100ml of 10% dextrose over 30 mins nebulised salbutamol removal of potassium from body - calcium resonium - sodium zirconium - loop diuretics - haemodialysis
57
describe the causes and symptoms of acute left ventricular failure
often decompensated chronic heart failure triggers - iatrogenic (aggressive IV fluids in patient with LVSD) - MI, arrhythmia - sepsis - hypertensive emergency clinical features - shortness of breath - looking and feeling unwell - coughing up white/pink frothy sputum (pulmonary oedema) - tachycardia, tachypnoea - bilateral basal crackles on auscultation of lungs - hypotension if cardiogenic shock - if co-existing right heart failure > raised JVP > peripheral oedema investigations - CXR: cardiomegaly, pulmonary oedema - raised NT-pro-BNP - echocardiogram: left ventricular ejection fraction <50%
58
describe acute pericarditis and its causes
Aetiology > viral infections (Coxsackie) > tuberculosis > uraemia > post-myocardial infarction >> early (1-3 days): fibrinous pericarditis >> late (weeks to months): autoimmune pericarditis (Dressler's syndrome) Features > chest pain: may be pleuritic. Is often relieved by sitting forwards > other symptoms include a non-productive cough, dyspnoea and flu-like symptoms > pericardial rub Investigations > ECG changes >> widespread 'saddle-shaped' ST elevation >> PR depression: most specific ECG marker for pericarditis > all patients with suspected acute pericarditis should have transthoracic echocardiography > bloods >> inflammatory markers >> troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis Management > if high-risk features: fever > 38°C or elevated troponin: inpatient care > treat any underlying cause > avoid strenuous physical activity > NSAIDs + colchicine: first-line for patients with acute idiopathic or viral pericarditis
59
list QTc prolonging drugs
- SSRIs e.g. escitalopram/citalopram - tricyclic antidepressants - atypical antipsychotics - antiarrhythmics - amiodarone, sotalol - antiemetics - tetracyclines e.g. clarithromycin - quinines
60
describe Torsades de Pointes
polymorphic VT with long QTc may deteriorate into VFib causes - drugs: SSRIs, macrolides, TCAs, antipsychotics, antiemetics... - subarachnoid haemorrhage management - IV magnesium sulphate over 10 minutes
61
describe ECG changes for thrombolysis or percutaneous intervention
ECG changes for thrombolysis or percutaneous intervention: ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR New Left bundle branch block
62
when should beta-blockers be stopped in heart failure?
- heart rate < 50/min - second or third degree AV block - shock
63
describe atrial flutter and its management
features - supraventricular tachycardia - ECG findings > sawtooth appearance > flutter waves may be visible following carotid sinus massage or adenosine management - similar to AF but medication may be less effective - atrial flutter is more sensitive to cardioversion so lower energy levels may be used - radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
64
describe - air leak - chyle leak
air leak - persistent pneumothorax failing to drain despite chest drainage - when suction is applied, active and persistent bubbling may be seen chyle leak - damage to lymphatic duct - pale opalescent liquid may be draining from chest drain
65
state the mechanism of action of aspirin
inhibits the production of thromboxane A2
66
state the cause of long QT syndrome
loss of function or blockage of K+ channels
67
state anticoagulation of choice for mechanical and bioprosthetic valves
bioprosthetic: aspirin mechanical: warfarin + aspirin
68
describe cholesterol embolisation syndrome
spontaneous embolisation of cholesterol crystals from atherosclerotic plaque features - fever, malaise, myalgia - livedo reticularis - blue toe syndrome - AKI - deranged LFTs - raised cardiac enzymes - eosinophilia high mortality, supportive treatment

Phase 4 (14 decks)

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