CARDIOLOGY Flashcards

1
Q

What is the investigation of choice for ?PE when a pt has renal impairment?

A

V/Q scan - safer as does not use iodine-based contrast

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2
Q

ECG findings in posterior MI?

A

Changes in V1-V3 - Horizontal ST depression, broad R waves, upright T waves and dominant R wave in V2

Confirmed by ST elevation and Q waves in posterior leads

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3
Q

What can be used to treat bradycardia and shock?

A

Atropine is first line

Otherwise - transcutaneous pacing or an isoprenaline/adrenaline infusion

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4
Q

What are the 8 reversible causes of cardiac arrest?

A

Hypothermia
Hypoxia
Hypovolaemia
Hypokalaemia / hyperkalaemia / hypoglycaemia
Tension pneumothorax
Toxins
Tamponade
Thrombosis

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5
Q

How do you manage a PE with haemodynamic instability?

A

Thrombolysis

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6
Q

What are the 2 classification systems for aortic dissection?

A

Stanford classification
DeBakey classification

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7
Q

Outline the Stanford classification of aortic dissection

A

type A - ascending aorta
type B - descending aorta, distal to left subclavian origin

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8
Q

Outline the DeBakey classification of aortic dissection

A

type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

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9
Q

Investigations for ?aortic dissection?

A

CXR for widened mediastinum
CT angiography of CAP
(TOE for unstable pts who can’t have a CT)

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10
Q

Whats the triad for cardiac tampnated?

A

Elevated JVP
Hypotension
Muffled heart sounds

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11
Q

What Can be given to PAEDS pt when they have coarctation of the aorta?

A

Prostaglandins to maintain a patent ductus arteriosus
Corrective surgery

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12
Q

What is eisenmengers syndrome?

A

The reversal of a left-to-right shunt associated with ventricular and atrial septal defects and PDA

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13
Q

Contraindications for statins?

A

Pregnancy and breastfeeding - discontinue 3 months before attempting to conceive due to risk of congenital anomalies
Liver disease

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14
Q

Interactions with statins?

A

Macrolide antibiotics
Warfarin
Ciclosporin
Dihydropyridine CCB
Amiodarone
Fibrates
Grapefruit juice
HIV protease inhibitors

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15
Q

ECG changes on a posterior MI?

A

Changes in V1-3:
Horizontal ST depression
Tall, broad R waves
Upright T waves
Dominant R wave in V2

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16
Q

What is the most common cause of death following an MI?

A

Cardiac arrest caused by V fib

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17
Q

Which MIs have the highest risk of AV block as a complication?

A

Inferior MIs as supplied by RCA which also supplies SAN

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18
Q

When does pericarditis typically occur after an MI?

A

In the first 48 hours or it can occur at 2-6 weeks known as Dressler’s syndrome

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19
Q

How does Dressler’s syndrome present?

A

Fever
Pleuritic pain
Pericardial effusion
Raised ESR

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20
Q

How do you identify a left ventricular aneurysm present post-MI?

A

ST elevation remains >2 weeks following the MI

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21
Q

What is the clinical significance of a left ventricular aneurysm post-MI?

A

Can predispose to ventricular arrhythmias, sudden cardiac death, congestive cardiac failure and mural thrombus (=stroke risk)

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22
Q

When does left ventricualr free wall rupture present?

A

1-2 weeks after the MI

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23
Q

How do left ventricular free wall ruptures present?

A

Acute HF secondary to cardiac tamponde = raised JVP, pulsus paradoxes, diminished heart sounds

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24
Q

When do ventricualr septal defects tend to occur post-MI?

A

Within the first week after MI

25
Q

Features of ventricular septal defect post-MI?

A

Acute HF
Pan-systolic murmur
(Echocardiogram will exclude acute MR)

26
Q

Which coronary territory myocardial infarct is most likely to cause acute mitral regurgitation?

A

Infero-posterior infarction = RCA

27
Q

How does acute mitral regurgitation present post-MI?

A

Acute hypotension
Pulmonary oedema
Early-to-mid systolic murmur

28
Q

Who does takayasu’s arteritis typically affect?

A

Young Asian females

29
Q

Presentation of takaysu’s arteritis?

A

Unequal bp in upper limbs
Carotid bruit and tenderness
Absent or weak peripheral pulses
Upper or lower limb claudication on exertion
Aortic regurgitation in 20%

30
Q

What is Takayasu’s arteritis?

A

A large vessel vasculitis that can commonly cause occlusion of the aorta

31
Q

ECG features of hypokalaemia?

A

U waves
Small or absent T waves
Prolonged PR
ST depression
Long QT

32
Q

Normal QT interval?

A

350-440ms men
350-460mg women
9-11 small squares
(Should be less than half the preceding RR interval)

33
Q

Which diuretics cause hypokalaemia and which cause hyperkalaemia?

A

Thiazide and loop diuretics cause hypokalaemia due to increased Na+ reabsorption in exchange for K+ and H+
Potassium sparing diuretics like amiloride or aldosterone antagonists can cause hyperkalaemia

34
Q

Signs of right heart strain on ECG?

A

ST depression and T wave inversion in V1-3, II, III, aVF
Right axis deviation
Dominant R wave in V1
Dominant S wave in V5 or V6

35
Q

Signs of left heart strain on ECG?

A

ST depression and T wave inversion in I, aVL and V5-6
Increased R wave

36
Q

Outline the CHA2DS2-VASc score?

A

Congestive HF - 1
Hyptn - 1
Age >=75 - 2
Age 65-74 - 1
Diabetes - 1
Prior stroke, TIA, thromboembolism - 2
Vascular disease - 1
Sex female - 1

37
Q

How do we interpret the CHA2DS2-VASc score?

A

0 no treatment
1 - consider anticoagulant in males only
2 or more - offer anticoagulation to all

38
Q

First line Antihypertensive in any person with diabetes?

A

ACEi

39
Q

What organism causes rheumatic fever?

A

Strep pyogenes

40
Q

Symptoms of rheumatic fever?

A

Erythema marginatum
Sydenham’s chorea - often a late feature
Polyarthritis
Carditis and valvulitis
Subcutaneous nodules
Pyrexia

41
Q

What usually causes HOCM?

A

Autosomal dominant mutation in the gene encoding beta-myosin heavy chain protein or myosin-binding protein C = left ventricle hypertrophy -> decreased compliance -> decreased cardiac output

42
Q

What usually cases Arrhythmogenic right ventricular dysplasia?

A

50% have a mutation of one of the several genes which encode the components of the desmosone = right ventricualr myocardium is replaced by fatty and fibrofatty tissue

43
Q

ECG findings in arrhythmogenic right ventricular dysplasia?

A

T wave inversion in V1-3
Epsilon wave may be found in 50% - terminal notch in QRS complex

44
Q

What causes dilated cardiomyopathy?

A

Idiopathic most commonly
alcohol or cocaine
Myocarditis - coxsackie B virus, HIV etc
Ischaemic heart disease
Peripartum
wet beri beri
doxorubicin
Inherited e.g. duchenne muscular dystrophy
Haemochromatosis or sarcoidosis

45
Q

What causes restrictive cardiomyopathy?

A

amyloidosis
post-radiotherapy
Loeffler’s endocarditis

46
Q

Biopsy findings in HOCM?

A

myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy

47
Q

Symptoms of HOCM?

A

Often asymptomatic
Exertional dyspnoea
Angina
Syncope - typically following exercise
Sudden death
Jerky pulse, double apex beat
Systolic murmurs

48
Q

Echo findings in HOCM?

A

MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

49
Q

ECG findings in HOCM?

A

Left ventricular hypertrophy -> progressive T wave inversion, non-specific ST changes, deep Q waves

50
Q

What is the most common form of cardiomyopathy?

A

Dilated - 90%

51
Q

Features of dilated cardiomyopathy?

A

HF symptoms
Systolic murmur from MR or TR
S3
Balloon appearance of heart on CXR

52
Q

What causes atrial flutter?

A

Re-entrant rhythm in one of the atriums causing the signal to go around the atrium without interruption giving an atrial rate of ~300bpm
The signal does not usually enter the ventricles on every lap due to the long refractory period of thr AVN so you often get 2 atrial contractions for 1 ventricular contraction giving a ventricular rate of 150bpm

53
Q

Outline the pathophysiology behind torsades de pointes?

A

Prolonged QT represents prolonged repolarisation which gives rise to early after-depolarisations which spread throughout the ventricles causing a contraction before proper repolarisation

54
Q

What are ventricualr ectopics? who do they occur in?

A

Premature ventricular beats caused by random electrical discharges outside the atria
Relatively common in all ages and healthy pts but more common in pts with heart conditions e.g. IHD or HF

55
Q

What is sick sinus syndrome?

A

Dysfunction of the SAN which leads to atrial rates that are inappropriate for normal requirements - can cause Brady or tachyarrhythmias

56
Q

What can cause sick sinus syndrome?

A

Idiopathic fibrosis - age related degeneration of SAN - this is most common
Heart disorder: IHD, Myocarditis, pericarditis, rheumatic heart disease, infiltration diseases
Congenital abnormalities
Iatrogenic e.g. damage to SAN during heart surgery
Drugs: digoxin, BB, CCB, anti-arrhythmias
Hypothermia, hypothyroidism, hypoxia
Hyperkalaemia, hyperthyroidism

57
Q

What is Long QT sundrome? Why is it important to recognise?

A

An inherited condition associated with delayed repolarisation of the ventricles
It can lead to VT or torsades de pointes which can cause collapse and sudden death

58
Q

Causes of long QT syndrome?

A

Jervell-Lange-Nielsen syndrome (causes deafness)
Romano-ward syndrome
Drugs: amiodarone, Sotalol, class 1a antiarrhtjmics, TCA, SSRIs, methadone, chloroquine, erythromycin, haloperidol, ondansetron
Electrolytes: low calcium, phosphate or magnesium
Acute MI
Myocarditis
Hypothermia
SAH

59
Q

How does long QT syndrome present?

A

May be picked up on routine ECG or following family screening
Can cause syncope following exertion, emotional stress or auditory stimuli