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3rd year medicine > cardiology > Flashcards

cardiology Flashcards

1
Q
  • autosomal dominant - exertional dyspnoea - angina - syncope - following exercise - sudden death (due to ventricular arrhythmias) - jerky pulse - ejection systolic murmur diagnosis
A

hypertrophic obstructive cardiomyopathy

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2
Q

Hypertrophic obstructive cardiomyopathy + ………… –> sudden death in young athletes

A

ventricular arrhythmia

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3
Q

infancy: heart failure adult: hypertension radio-femoral delay mid systolic murmur - max over back apical click from aortic valve associated with bicuspid aortic valve

A

Coarctation of the aorta - a congenital narrowing of the descending aorta.

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4
Q

ECG changes in hypotrophic obstructive cardiomyopathy

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep narrow (dagger-like) Q waves
atrial fibrillation may occasionally be seen

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5
Q

70yrs

HTN 170/106

no symptoms

what does the ECG show

A

RBBB + left axis deviation = bifascicular block

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6
Q

what does the ECG show

A

bifascicular block (RBBB + left axis deviation) + first degree heart block (PR interval >5 small sqrs)

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7
Q

34yrs

unwell

fever

no PMH

IV drug user

alcoholic

smoker

pansystolic murmer in left lower sternal edge and enlarged cervical lymph nodes

most helpful investigation to make a diagnosis?

diagnosis?

A

infective endocarditis (fever + murmur + IV drug user)

blood cultures - 3 sets

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8
Q

most common bacteria cause of infective endocarditis

A
  1. staphylococcus aureus

other:

streptococcus viridans

coagulase-negative staph (staph. epidermidis) - after prosthetic valve surgery

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9
Q

non-infective causes of endocarditis

A

systemic lupus erythematosus

malignancy: marantic endocarditis

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10
Q

culture negative causes of endocarditis

A

prior abx therapy

coxiella burnetii

bartonella

brucella

HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

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11
Q

35yrs

bouts of palpitations

SOB on exertion

ejection systolic murmur

asymmetric hypertrophy in septal region on echo

cardiovascular MR - systolic anterior movement of anterior leaflet of mitral valve

diagnosis?

A

hypertrophic obstructive cardiomyopathy

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12
Q

45yrs

palpitations - for 40mins - no obvious trigger

no chest pain or dyspnoea

ECG: regular tachycarida (180bpm) with QRS 0.10s

BP: 106/70

O2 sats: 98%

valsava manoeuvre: no effect

next appropriate course of action (treatment)?

diagnosis?

A

diagnosis: supraventricular tachycardia

acute management:

  1. valsava manoeuvre
  2. IV adenosine (contraindicated in asthmatics - verapamil instead)
  3. electrical cardioversion
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13
Q

treatments to prevent episodes of supraventricular tachycardia

A

beta-blockers

radio-frequency ablation

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14
Q

65yrs

type 2 diabetes - started on insulin

PMH: heart attack- on beta-blocker, calcium channel blocker, ace-inhibitor, statin, GTN

which medication can lead to reduced awareness of symptoms of hypoglycemic event following his insulin use?

A

beta blocker

eg. atenolol

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15
Q

side effects of beta blockers

A

bronchospasm

cold peripheries

fatigue

sleep disturbances, including nightmares

erectile dysfunction

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16
Q

contraindications of beta blockers

A

uncontrolled heart failure

asthma

sick sinus syndrome

concurrent verapamil use: may precipitate severe bradycardia

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17
Q

61yrs

central crushing chest pain

ECG: ST elevation in leads II, III and aVF

PMH: HTN : ramapril, aspirin, simvastatin

what is the optimum manamgement?

A

primary percutaneous coronary intervention - gold standard for ST-elevation MI

aspirin

P2Y12-receptor antagnoist - clopidogrel/ ticagrelor

unfractionated heparin / LMWH (for PCI)

where PCI is not available, use thrombolysis + alteplase + ECG after 90mins - if no resolution then PCI

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18
Q

management for hyperglycaemia in acute coronary syndromes

A

dose-adjusted insulin with regular monitoring of blood glucose levels to glucose <11

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19
Q

82yrs

lives in care home

off feet for last week - now unresponsive

temp 28 degrees

what changes would you expect to see on ECG?

A

hypothermia:

  • J-waves - small hump at the end of the QRS complex
  • bradycardia
  • first degree heart block
  • long QT interval
  • atrial and ventricular arrhythmias
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20
Q

what are Q waves on ECG associated with?

A

previous MI

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21
Q

what are delta waves on ECG associated with?

A

Wolff-Parkinson-white syndrome

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22
Q

what are saddle ST elevation on ECG associated with?

A

pericarditis

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23
Q

what ECG changes are considered as normal variants in an athlete

A
  • sinus bradycardia
  • junctional rhythm
  • first degree heart block
  • wenckebach phenomenon
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24
Q

causes of peaked T waves on ECG

A

hyperkalaemia

myocardial ischaemia

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25
Q

what are the causes of inverted T waves on ECG

A

myocardial ischaemia

digoxin toxicity

subarachnoid haemorrhage

arrhythmogenic right ventricular cardiomyopathy

pulmonary embolism (S1Q3T3)

brugada syndrome

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26
Q

what is increased P wave amplitude on ECG a sign of

A

cor pulmonale

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27
Q

causes of ST depression on ECG

A
  • secondary to abnormal QRS (LVH, LBBB, RBBB)
  • ischaemia
  • digoxin
  • hypokalaemia
  • syndrome X
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28
Q

causes of prolonged PR interval on ECG

A

idiopathic

ischaemic heart disease

digoxin toxicitiy

hypokalaemia

rheumatic fever

aortic root pathology (eg abscess 2ndry to endocarditis)

lyme disease

sarcoidosis

myotonic dystrophy

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29
Q

what condition is a short PR interval seen in

A

wolf parkinson white syndrome

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30
Q

causes of left axis deviation

/\

= left

\/

A

let anterior hemiblock

LBBB

inferior MI

wolff-parkinson-white syndrome - right sided accessory pathway

hyperkalamia

congenital: ostium primum ASD, tricuspid atresia

minor LAD in obese people

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31
Q

causes of right axis deviation

\/

= right

/\

A

right ventricular hypertrophy

left posterior hemiblock

lateral myocardial infarction

chronic lung disease –> cor pulmonale

pulmonary embolism

ostium secundum ASD

wolff-parkinson-white syndrome - left sided accessory pathway

normal in infant <1yrs

minor RAD in tall people

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32
Q

how to remember the difference between RBBB and LBBB

A

WiLLiaM MaRRoW

in LBBB there is a W in V1 and an M in V6

in RBBB there is a M in V1 and a W in V6

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33
Q

what is this ECG showing

A

right bundle branch block (RBBB)

diagnostic criteria:

  • broad QRS >120ms
  • M shaped QRS in V1-3

wide, slurred S wave in lateral leads

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34
Q
A
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35
Q

causes of RBBB

A
  • normal variant - more common with increasing age
  • right ventricular hypertrophy
  • chronically increased right ventricular pressure - eg cor pulmonale
  • pulmonary embolism
  • myocardial infarction
  • atrial septal defect (ostium secundum)
  • cardiomyopathy or myocarditis
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36
Q

causes of ST elevation on ECG

A

MI

pericarditis/ myocarditis

normal variant

left ventricular aneurysm

Prinzmetal’s angina (coronary artery spasm)

takotsubo cardiomyopathy

rare: subarachnoid haemorrhage

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37
Q

what does this ECG show

A

hyperkalaemia:

  • peaked T waves
  • prolonged PR segment
  • loss of P waves
  • broad bizarre QRS complexes
  • sine wave (severe hyperkalaemia)

suspect hyperkalamia in patients with new bradyarrhythmia or AV block or newly on haemodyalysis or taking any combo of:

ACEi, potassium-sparing diuretics or potassium supplements

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38
Q

what does this ECG show

A

LBBB

W in V1 and M in V6

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39
Q

causes of LBBB

A
  • ischaemic heart disease
  • HTN
  • aortic stenosis
  • cardiomyopathy
  • hyperkalaemia
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40
Q

PE investigations

A

if PE is suspected:

  1. wells score:

PE likely: >4 points

PE unlikely: 4 points or less

if PE likely: immediate CTPA (if delayed, give DOAC e.g. apixaban, rivaroxaban)

if -ve no further investigations

if PE unlikely: D-dimer

if +ve: immediate CTPA

if -ve: consider alternative diagnosis

if allergy to contrast media or renal impairment do V/Q scan instead of CTPA

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41
Q

what does this ECG show

A

pulmonary embolism

S1Q3T3:

  • large s wave in lead 1
  • large Q wave in lead III
  • inverted T wave in lead III

sinus tachycardia - most common abnormality seen

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42
Q

what does this ECG show?

features of the condition on ECG

A

wolff parkinson white syndrome

  • short PR interval
  • wide QRS complexes with slurred upstroke (delta wave)
  • left axis deviation if right sided accessory pathway (majority)

type A: left sided accessory pathway:

  • right axis deviation
  • dominant R wave in V1

type B: right sided accessory pathway: (majority of cases)

  • left axis deviation

no dominant R wave in V1

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43
Q

associations of WPW syndrome

A

HOCM (hypertrophic obstructive cardiomyopathy)

mitral valve prolapse

Ebsteins anomaly

thyrotoxicosis

secundum ASD

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44
Q

management for Wolff Parkinson White syndrome

A

definitive treatment:

radiofrequency ablation of the accessory pathway

medical therapy:

sotalol (not when atrial fibrillation- can lead to ventricular fibrillation),

amiodarone,

flecainide

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45
Q

what does this ECG show?

features

A

digoxin toxicity:

  • down-sloping ST depression (‘reverse tick’ ‘scooped out’)
  • flattened/ inverted T waves
  • short QT interval
  • arrythmias e.g. AV block, bradycardia
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46
Q

what does this ECG show

features

A

hypokalaemia:

  • U waves
  • small/absent T waves (usually inversion)
  • prolonged PR interval
  • ST depression
  • long QT

rhyme:

in Hypokalaemia, U have no Pot and no T, but you have a long PR and a long QT

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47
Q

a new LBBB points towards what diagnosis

A

ACS

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48
Q

coronary artery territories on ECG

A

I, V5-6: left circumflex (lateral)

II, III, aVF: right coronary artery (inferior)

V1-V4: left anterior descending (anterior)

I, aVL, V4-6: left anterior descending or left circumflex

Tall R waves V1-2: usually left circumflex, also right coronary

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49
Q

ECG changes of an acute MI - chronologically

A
  • hyperacute T waves - first sign (only persist a few mins)
  • ST elevation develops
  • T waves become inverted within first 24hrs (can last days/months)
  • pathological Q waves - develop after several hrs to days. persist indefinitely
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50
Q

heart appears morphologically and histologically normal

autosomal dominant

most common in middle aged men

FHx sudden cardiac death (<45yrs)

nocturnal agonal respiration (gasping breaths) during sleep

events usually occur at rest or during sleep

ECG attached

diagnosis?

A

Brugada syndrome

pseudo-RBBB and persistent ST elevations in V1-V2

type 1:

ST elevations

downsloping ST segment

inverted T wave

type 2:

ST elevation

saddle back ST-T wave

upright or biphasic T wave

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51
Q

what can brugada syndrome ECG changes be accentuated by

A

fever

drugs (e.g. beta blockers, TCA)

toxins (e.g. alcohol, cocaine)

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52
Q

modifiable risk factors for ACS

A

smoking

diabetes mellitus

hypertension

hypercholesterolaemia

obesity

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53
Q

chest pain - central/ left sided

may radiate to jaw or left arm

heavy - ‘elephant on chest’

dyspnoea

sweating

nausea and vomiting

pale and clammy

diagnosis?

A

ACS

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54
Q

investigations for ACS

A

ECG

cardiac markers - troponin

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55
Q

what does this ECG show

A

ST- elevation MI (STEMI)

  • ST elevation in leads II, III, AVF = right coronary artery blockage
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56
Q

what does this ECG show

A

STEMI

in leads:

II, III, aVF

aVR

V1, V3-6

right coronary artery

left anterior descending

left circumflex?

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57
Q

management of ACS (angina + NSTEMI)

A

MONA:

M: morphine + metoclopramide

O: O2 if sats <94%

N: nitrates: GTN

A: aspirin + ticagrelor

+

heparin/ LMWH

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58
Q

management for ACS (STEMI)

A

PCI

MONA BASH:

M: morphine + metoclopramide

O: O2 if sats <94%

N: nitrates: GTN (acutely and indefinitely)

A: aspirin + clopidogrel (acutely and indefinitely) 300mg then 75mg each

B: beta-blocker - indefinitely

A: ACEi - if contraindicated use angiotensin-II receptor antagonist

S: statin 80mg

H: heparin/ LMWH

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59
Q

what does this ECG show

A

Torsades de pointes

polymorphic ventricular tachycardia associated with a long QT interval

it may deteriorate into ventricular fibrillation and lead to sudden death

clue: psychiatric patient - as can be caused by antipsychotics, tricyclic antidepressants

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60
Q

causes of long QT interval

A

congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs

tricyclic antidepressants

antipsychotics

chloroquine

terfenadine

erythromycin

electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia

myocarditis

hypothermia

subarachnoid haemorrhage

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61
Q

management of Torsades de pointes

A

IV magnesium sulphate

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62
Q

side effects of nitrates (GTN)

A

have vasodilating effects - angina and heart failure management

hypotension

tachycardia

headache

flushing

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63
Q

staging of HTN

A

stage 1:

clinic BP >= 140/90

ABPM/HBPM>= 135/85

stage 2:

clinic BP>= 160/100

ABPM/HBPM>= 150/95

severe HTN

clinic systolic BP>= 180

or clinic diastolic BP>= 110

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64
Q

lifstyle advice for HTN

A

low salt diet

caffeine intake reduced

stop smoking

drink less alcohol

eat a balanced diet

exercise more

lose weight

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65
Q

what stage of HTN do you treat regardless of age

A

stage 2 (clinic BP >= 160/100, ABPM>= 150/95)

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66
Q

ABPM>= 135/85 (stage 1) when to treat

A

treat if <80yrs AND any of the following:

target organ damage

established cardiovascular disease

renal disease

diabetes

10 year Qrisk >10%

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67
Q

treatment for HTN

A

Step 1 treatment

patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotension receptor blocker (ACE-i or ARB): (A)

angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)

patients >= 55-years-old or of Afro-Caribbean origin: Calcium channel blocker (C)

ACE inhibitors have reduced efficacy in patients of Afro-Caribbean origin are therefore not used first-line

Step 2 treatment

if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic

if already taking a Calcium channel blocker add an ACE-i or ARB

for patients of Afro-Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor

(A + C) or (A + D)

Step 3 treatment

add a third drug to make, i.e.:

if already taking an (A + C) then add a D

if already (A + D) then add a C

(A + C + D)

Step 4 treatment

NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice

first, check for:

confirm elevated clinic BP with ABPM or HBPM

assess for postural hypotension.

discuss adherence

if potassium < 4.5 mmol/l add low-dose spironolactone

if potassium > 4.5 mmol/l add an alpha- or beta-blocker

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68
Q

a patient of Afro-Caribbean origin is taking a calcium channel blocker for hypertension, if they require a second agent what should this be?

A

ARB (losartan, candesartan) in preference to ACEi

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69
Q

if a patient of any age with HTN also has diabetes, which medication should they be started on

A

ACEi (ramipril) or ARB

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70
Q

step 4 HTN management with reference to K+

A

K+ <4.5 = spironolactone

K+ > 4.5 = apha (doxazosin) or beta blocker (atenolol)

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71
Q

what is a target INR for patients suffering from recurrent pulmonary embolisms and recurrent deep-vein thrombosis receiving anticoagulation

A

INR 3.5

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72
Q

what is the target INR for treatment of DVT or PE, AF, cardioversion, mitral stenosis, bioprosthetic heart valves, MI

A

INR 2.5

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73
Q

is long term warfarin required in bioprosthetic valves in the absence of AF

A

no

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74
Q

which anticoagulant should be used first line for PE and for how long

A

DOAC (apixaban, rivaroxaban) once diagnosis is suspected - continued if diagnosis confirmed

(including in active cancer)

if contraindicated use LMWH followed by dabigatran/ edoxaban or LMWH followed by vitamin K antagonist (warfarin)

if renal impairment severe: LMWH

if antiphospholipid syndrome: LMWH then warfarin

all patients have anticoagulation for at least 3 months

after that:

provoked - stopped after 3 months

unprovoked - further 3 months (6 in total)

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75
Q

treatment for PE with haemodynamic instability

A

thrombolysis - first line for massive PE with circulatory failure (eg hypotension)

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76
Q

what does a high INR mean

A

the higher the INR the longer time your blood takes to clot

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77
Q

what is the management for a patient on warfarin with recurrent PEs that is below their target INR

A

target INR = 3.5

increase dose of warfarin

may be considered for IVC filters - stop clots from the legs moving into the pulmonary arteries

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78
Q

what happens to the ST segment of the ECG in a posterior STEMI

A

in leads V1-V3:

ST depression

tall, broad R-waves

upright T waves

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79
Q

NSTEMI ECG signs

A

no ST elevation

T wave inversion

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80
Q

side effects of loop diuretics

A

eg furosemide

ototoxicity - hearing loss, tinnitus

hypotension

hyponatraemia, hypokalaemia, hypomagnesaemia, hypocalcaemia

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81
Q

anteroseptal: ECG leads and coronary artery?

A

V1-V4

left anterior descending

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82
Q

inferior leads and coronary artery?

A

II, III, AVF

right coronary

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83
Q

anterolateral leads and coronary artery?

A

V4-6, I, aVL

left anterior descending or left circumflex

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84
Q

lateral leads and coronary artery?

A

I, aVL +/- V5-6

left circumflex

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85
Q

posterior leads and coronary artery?

A

tall R waves V1-2

usually left circumflex, also right coronary

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86
Q

what diagnosis does a NEW LBBB point towards

A

ACS

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87
Q

what cardiac conditions are hypertrophic obstructive cardiomyopathy associated with

A

wolff parkinson white syndrome

Friedrich’s ataxia

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88
Q

short PR interval

wide QRS

upsloping delta wave

condition?

A

wolff parkinson white syndrome

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89
Q

ECG changes in hypertrophic obstructive cardiomyopathy

A

left ventricular hypertrophy (increased amplitude of QRS)

non specific ST and T wave abnormalities

progressive T wave inversion

deep Q waves

AF

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90
Q

saw tooth pattern on ECG

A

atrial flutter

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91
Q

first degree heart block

A

increased PR interval >200ms

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92
Q

increasingly prolonged PR interval until there is a dropped beat before restarting the pattern

A

second degree type 1 heart block - Wenckebach’s

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93
Q

no association between the atria and ventricles on ECG

long term management

A

third degree heart block

pacemaker

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94
Q

features of Hypertrophic obstructive cardiomyopathy

A

often asymptomatic

exertional dysponoea

angina

syncope - typically following exercise

sudden death

jerky pulse, double apex beat

ejection systolic murmur - increases with valsalva manoeuvre and decreases on squatting

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95
Q

ECHO findings of Hypertrophic obstructive cardiomyopathy

A

mneumonic - MR SAM ASH:

MR mitral regurg

SAM systolic anterior motion (of the anterior mitral valve leaflet)

ASH asymmetic hypertrophy

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96
Q

presentation of stable angina

A

chest pain on exertion <20mins

radiates to left arm/jaw

sweating

relieved by GTN

ECG: normal/ST depression

Troponin: normal

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97
Q

management of stable angina

A

GTN

Aspirin 75mg OD

Bisoprolol

ACEi

statin

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98
Q

difference in presentation (signs and symptoms and investigations) between unstable angina and NSTEMI

A

unstable angina:

exertional chest pain relieved by GTN

Troponin: no elevation

NSTEMI:

chest pain > 20mins

not relieved by GTN

troponin: raised

both have ST depression +/- T wave inversion

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99
Q

STEMI presentation

A

chest pain > 20mins

sweating

not relieved by GTN

ECG: ST elevation, new LBBB

troponin: raised

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100
Q

immediate management for STEMI

A

PCI (if available within 2hrs - if not thrombolysis)

morphine + metoclopramide

O2 if <90%, SOB or pulmonary oedema

nitrates: GTN if not effective –> iV nitrate

Aspirin 300mg + clopidogrel 300mg

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101
Q

long term management for STEMI

A

aspirin 75mg (lifelong) + clopidogrel 75mg (12months)

Beta blocker - bisoprolol (if no CI - asthma, COPD)

ACEi - within 24hrs

Statin - atorvastatin 80mg

Heparin - LMWH SC or fondaparinux SC

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102
Q

60yr male

3day hx

sharp, tearing pain in center of chest

radiating straight through to back between shoulder blades

most likely diagnosis?

A

aortic dissection

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103
Q

56yr man

2hr hx central chest pain radiating to left arm

sweaty

ECG: ST elevation in leads II, III and aVF

troponin significantly raised

which is the most likely coronary vessel to be occluded

A

right coronary artery

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104
Q

what are the coronary territories

A

II, III AVF: inferior (right coronary artery)

prominant R in V1 V2: posterior MI (posterior descending artery)

V1-V4: anterior/septal (left anterior descending)

I, aVL, V5, V6: lateral (left circumflex)

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105
Q

44yr M

sudden onset chest pain radiating to jaw

sweating and nausea

ECG: ST elevation in V1-V6, I, aVL

what is the single most likely occluded coronary artery

A

left main coronary artery

V1-V4: left anterior descening

V5-V6, I, aVL: left circumflex

as both are affected the left main coronary artery is most likely to be affected

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106
Q

65yr M

central chest pain radiating to left arm 2hrs

increasingly regular chest pain over last 2 weeks

type 2 diabetes- metformin

ECG

single most likely occluded coronary artery (look at ECG)

A

right coronary artery

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107
Q

76yr W

SOB on minimal exertion 5 days

walking upstairs - central chest tightness

pain free since being diagnosed with CAD 10yrs ago

troponin (36hrs after onset of pain): 1.45 (0-0.4)

ECG: T wave inversion in inferolateral leads

single most appropriate immediate step in management

A

previous IHD hx + ischaemic ECG + raised troponin –> treat as per protocol for ACS (NSTEMI)

aspirin 300mg PO + clopidrogrel 300mg PO

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108
Q

52 yr M

sudden central chest pain whilst watching TV

suffocating sensation rose up to neck and made it difficult to breath

arrived at ED within 2hrs of onset of pain

ECG: ST depression, T wave inversion

troponin: 0.09 (normal <0.10) taken after 1hr of onset of pain

following morning looks pale, clammy

single most appropriate course of action

A

repeat troponin level

first troponin taken 1hr after onset- may not have risen yet - needs to be repeated - 12hrs after onset of pain

also needs cardiac monitoring

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109
Q

causes of low cardiac output (leading to heart failure)

A

pump failure:

  • systolic failure: impaired contraction –> MI, dilated cardiomyopathy, HTN, myocarditis
  • diastolic failure –> impaired filling –> pericardial effusion/ tamponade (fluid in pericardium –> constriction)/ constriction
  • arrhythmias: AF, bradycardia, hyeart block, tachycardia –> antiarrhythmics (beta-blockers, CCB)

excessive preload:

aortic, mitral regurgitation

fluid overload

excessive afterload:

  • aortic stenosis
  • HTN

hypertrophic obstructive cardiac myopathy

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110
Q

causes of high cardiac output (leading to heart failure)

A

increased needs –> RVF initially –> left ventricular failure

Anaemia

Thyrotoxicosis

Pregnancy, Pagets

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111
Q

cor pulmonale

A

abnormal enlargement of right side of heart due to lung disease or disease of pulmonary lblood vessels

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112
Q

right sided heart failure symptoms and signs

A

fluid retention in legs

ascites

anorexia and nausea

signs:

increased JVP + jugular venous distension

hepatomegaly

cant go through right side of heart so backlog of fluid. therefore excess fluid in jugular –> raised JVP

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113
Q

causes of right sided heart failure

A

LVF

cor pulmonale

tricuspid and pulmonary valve disease

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114
Q

left sided heart failure symptoms and signs

A

body not getting oxygenated blood properly from left side of heart, backlog of fluid into lungs

symptoms:

exertional dispnoea, fatigue

orthopnoea, PND

nocturnal cough (+- pink frothy sputum)

wheeze

improves 15-30mins after getting up

signs:

tachypnoea

S3 gallop on heart sounds (after S2)

tachycardia

cardiomegaly with displaced apex

bi-basal inspiratory pulmonary crepitations (sign of fluid)

cold peripheries +- cyanosis

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115
Q

causes of left sided heart failure

A

IHD

idiopathic dilated cardiomyopathy

systemic HTN

mitral and aortic valve stenosis

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116
Q

what is congestive cardiac failure

A

long term LVF leading to RVF or disorders affecting entire myocardium

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117
Q

what criteria is used to determine the diagnosis of congestive heart failure

explain it

A

Framingham criteria for CCF

diagnosis: presence of at least 2 major criteria

or 1 major criteria and 2 minor

major:

  • PND
  • raised JVP
  • basal crepitations
  • cardiomegaly
  • acute pulmonary oedema

increased venous pressure (>16)

weight loss >4.5kg in 5d

minor:

bilateral ankle oedema

nocturnal cough

dyspnoea on ordinary exertion

hepatomaly

pleural effusion

30% in vital capacity

tachycardia

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118
Q

investigations for chronic heart failure

A

bloods:

  • FBC, U&Es, BNP, TFTs, glucose, lipids

CXR: ABCDEF

Alveolar shadowing

Kerley B lines

Cardiomegaly (cardiothoracic ratio >50%)

Dilated prominent upper lobe vessels

Effusions

Fluid in fissures

ECG - LVH, Q-waves

Echocardiogram - key investigation

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119
Q
A
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120
Q

what does left ventricular hypertrophy look like on ECG - what criteria can you use

A

tall QRS complexes

Sokolow Lyon criteria: add height of R wave in V5 or V6 and S wave in V1

if its over 35mm you have left ventricular hypertrophy

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121
Q

classification to determine severity of Chronic CCF

A

NYHA criteria

I: no limitation of activity (>2 flights of stairs with ease)

II: comfortable at rest, dysnpnoea on ordinary activity (2 flights of stairs with difficulty)

III: marked limitation on ordinary activity (can climb < 1 flight of stairs)

IV: dyspnoea at rest, all activity –> discomfort

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122
Q

management for chronic CCF

A

1st line:

ACEi/ARB + BB + loop diuretic (furosemide) (ABD)

monitor K+ levels

2nd line:

potassium sparing diuretics (spironolactone)

vasodilators: hydralazine + isosorbide dinitrate

sacubitril valsartan

3rd line:

digoxin or

ivabradine

invasive therapies:

cardiac resynchronisation +- implantable cardioverter defib (ICD)

coronary revascularisation

partial left ventriculectomy

heart transplantation

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123
Q

side effect of loop diuretic

A

decreases K+

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124
Q

side effect of ARB

A

increases K+

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125
Q

acute presentation of HF

A

new onset or decompensation of chronic HF

peripheral/pulmonary oedema

+- peripheral hypoperfusion (cold extremities)

symptoms:

dyspnoea

orthopnea, PND

pink frothy sputum

signs:

distresses, pale, sweaty

tachycardia, tachypnoea

pulsus alternans (alternating strong and weak pulse - indicative of left ventricular systolic impairment - poor prognosis)

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126
Q

management of acute HF/ pulmonary oedema

A

sit patient upright

O2 - 15L/ min via reservoir mask - target SpO2: 94-98%

IV access: bloods: FBC, U&Es, Troponin, BNP, ABG

diamorphine 1.25-5mg IV - pain

furosemide 40-80mg IV slowly

GTN 2 puffs

give positive inotropes (e.g dobutamine IV) (strengthen force of heart beat)

increase renal perfusion by low-dose dopamine

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127
Q

36yr F

lethargic

increasingly dizzy over last 2 months

usually well but reports long and very heavy periods, especially in last 6 months

T:36.6.

HR: 110bpm

BP: 95/65

JVP raised

bilateral ankle oedema pitting to mid calf

bibasal find end inspiratory crepitations

single most appropriate next step

A

symptomatic anaemia (Hb usually <50g/L) causing heart failure

management: packed red cells 2U IV slowly + diuretic e.g furosemide IV (alternate between units)

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128
Q

78yr F

admitted with HF

underlying cause determined to be aortic stenosis

which sign is most likely to be present

A

bibasal crepitations

left sided heart failure –> respiratory symptoms

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129
Q

stages of HTN

A

stage 1: 140/90

stage 2: 160/100

severe: 180/110
malignant: 180/110 + organ damage

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130
Q

causes of HTN

A

renal: renal artery stenosis, glumerulonephritis, polycycstic kideny disease
endocrine: increased T4 (hyperthyroidism), cushings, pheochromocytoma, acromegaly, Conns
drugs: steroids, NSAIDs, cocaine, COCP

pre-eclampsia

coarctation of aorta - consider if young

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131
Q

HTN end organ damage

A

CANCER

Cardiac:

  • IHD, LVH –> CCF
  • AR, MR

Aortic:

  • aneurysm
  • dissection

Neuro:

  • CVA (cerebrovascular accident): ischaemic, haemorrhagic
  • encephalopathy (malignant HTN)

Eyes: hypertensive retinopathy

Renal:

  • proteinuria
  • CRF
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132
Q

investigations of HTN

A

bedside: urinalysis: haematuria, Alb:Cr ratio
bloods: FBC, U&Es, glucose, fasting lipids
imaging: 12 lead ECG: LVH, old infarct

calculate 10yr CV risk: QRISK2

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133
Q

diagnosis of HTN

A

clinic BP > 140/90:

offer ABPM

calculate CV risk & look for organ damage

ABPM <135/85: normotensive –> no treatment

ABPM >135/85: stage HTN –> treat if QRISK > 20%/10yrs or end organ damage

ABPM >150/95: stage 2 HTN –> treat

Clinic BP >180/110 –> consider treatment immediately, consider referral

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134
Q

<55. >55/afrocaribbean

A C

A+ C (or D)

A+ C + D

resistant HTN:

A+C+D+ consider further diuretic (spironolactone) or alpha blocker/ beta blocker

seek expert opinion

A: ACEi or ARB (ARB with CCB if afrocaribbean for second line)

C: CCB: nifedipine, amlodipine

D: thiazide like diuretic: furosemide, indapamide

A
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135
Q

causes of aortic stenosis

A

calcification

congenital

136
Q

symptoms and signs of aortic stenosis

A

symptoms:

angina

syncope

HF: SOB, orthopnoea, PND

signs:

early systolic click (if young valve)

ejection systolic murmur (right 2nd ICS - sit forward to enhance)

  • parvus tardus: slow rising pulse
  • narrow pulse pressure

aortic thrill

137
Q

causes of aortic regurgitation

A

infective endocarditis

ascending aortic dissection

rheumatic fever

connective tissue

138
Q

symptoms and signs of aortic regurgitation

A

aortic regurg mimics LVF:

symptoms:

exertional dyspnoea

PND

orthopnoea

signs:

collapsing pulse

early diastolic/ mid diastolic murmur - heard at Erb’s point (left 3rd ICS)

wide pulse pressure

Quincke’s (capillary pulsations with light pressure on finger nail bed)

Corrigan’s (abrupt distension and collapse of carotid arteries)

De Musset’s (head bobbing in synchronisation with heart beat)

139
Q
A
140
Q

causes of mitral stenosis

A

rheumatic fever

congenital

mitral calcification

141
Q

symptoms and signs of mitral stenosis

A

symptoms:

dyspnoea

fatigue

haemoptysis

signs:

mid-diastolic murmur (with a snap) (Bell) - at apex

malar flush

low-volume pulse

increased JVP later on

AF

tapping apex beat

142
Q

causes of mitral regurgitation

A

mitral valve prolapse

LV dilatation

post-MI

rheumatic fever

connective tissue

143
Q

symptoms and signs of mitral regurgitation

A

symptoms:

dyspnoea

fatigue

pulmonary congestion

signs:

pansystolic murmur - radiates to axilla (S3)

AF

left parasternal haeve

displaced apex beat

144
Q

57yr F

worsening SOB

decreased exercise tolerance

rhuematic fever in adolescence

essential HTN

mitral stenosis

which of the following is not a sign of mitral stenosis?

A.Malar flush

B.Atrial fibrillation

C.Pan-systolic murmur which radiates to axilla

D.Tapping, undisplaced apex beat

E.Right ventricular heave

A

pan-systolic murmur which radiates to axilla

145
Q

76yr M

collapsing at home

recovered within minutes - fully alert and orientated

first episode of this

increasing SOB - last 6 months

episodes of central chest pain

BP: 115/88

crackles at both bases

ECG: borderline LVH

which murmur and where would you expect to find on auscultation

A

crescendo systolic murmur best heard at right sternal edge (ejection systolic murmur)

aortic stenosis:

  • syncope
  • angina
  • HF
146
Q

49yr F

increasing SOB - last 3 months

no chest pain or cough

no ankle swelling

BP: 158/61

pulse collapsing

pulse:88bpm

crackles at both lung bases

decrescendo diastolic murmur at left sternal edge

most likely diagnosis?

A

aortic regurgitation

147
Q

Hyperlipidaemia presentation

A

CVD

xanthomata

pancreatitis (increased triglycerides)

148
Q

investigations for hyperlipidaemia

A

non-fasting lipids

non-HDL cholesterol

149
Q

management for hyperlipidaemia

A

lifestyle advice:

  • lose weight
  • increase fibre, fresh fruit, veg
  • increase exercise

treat those with known CVD and DM and with QRISK > 20%

1st line:

  • statins - e.g atorvastatin (10mg OD)

2nd line:

  • fibrates - bezafibrate
  • cholesterol absorption inhibitors - ezetimibe

niacin/ nicotinic acid

PCSK9 inhibitors: high risk & homozygous FH patients

150
Q

presentation of arrhythmias

A

palpitation

chest pain

syncope

hypotension

asymptomatic

151
Q

classifications of bradycardias

A

sinus bradycardia

1st degree heart block

2nd degree heart block:

  • wenkebach/ Mobitz type I
  • Mobitz type II

complete heart block:

  • junctional
  • ventricular
152
Q

causes of heart block

A

DIVISIONS

most important: drugs, ischaemia, vagal hypertonia, hypothyroidism, hypokalaemia

Drugs

Ischaemia/ infarction

Vagal hypertonia

Infection

Sick sinus syndrome

Infiltration: restrictive/ dilated cardiomyopathies

O:

hypOthyroidism

hypOkalaemia

hypOthermia

Neuro: increased ICP

Septal defect: ASD

Surgery or catheterisation

153
Q

what does this ECG show

A

first degree heart block

prolongation of PR interval to >0.2s (>5 small squares)

(normal PR 3-5ss)

154
Q

what does the ECG show

A

2nd degree heart block - Mobitz type 1 (Wenckebach)

progressive PR prolongation and then drops beat

155
Q

what is the ECG?

A

this ECG shows 3:1 Mobitz II block

intermittent non-conducted P waves without progressive PR interval prolongation

usually fixed amount on non conducted P waves for every successfully conducted QRS complex

e.g. Mobitz II where there are two P waves for every one QRS = 2:1 Mobitz II

three P waves for every one QRS 3:1 Mobitz II block

156
Q

what does this ECG show?

A

3rd degree heart block (complete heart block)

all atrial activity fails to conduct to ventricles

no relation between atria and ventricles contracting so P waves and QRS complexes are unrelated (no pattern between them)

157
Q

treatment for bradycardias (including heart blocks)

A

if asymptomatic + rate >40bpm - no treatment needed

if symptomatic or rate <40bpm –> urgent

  • rx underlying cause: MI, drugs, thyroid, electrolytes
  • IV atropine 0.6-1.2g
  • temporary pacing wire

elective –> permanent pacing

  • Mobitz II

complete heart block

sick sinus

AF

158
Q

how to differentiate between narrow and broad complex tachycardias?

A

both have rate >100bpm

narrow complex: supraventricular tachycardia

tachy originating from above/within AV node

QRS <3ss

broad complex: ventricular tachycardia

QRS >3ss

tachy originating within ventricles

159
Q

what are the causes of narrow complex (supraventricular) tachycardias that have a regular rhythm/ irregular rhythm

A

narrow QRS + regular rhythm:

sinus tachycardia

atrial flutter

SVT

narrow QRS + irregular rhythm

AF (no P waves)

MAT (multifocal atrial tachycardia)

160
Q

what are the causes of broad complex (ventricular) tachycardias with regular rhythm/ irregular rhythm

A

broad QRS + regular rhythm:

ventricular tachycardia

sinus tachycardia

AF with BBB/WPW

broad QRS + irregular rhythm:

VF

AF with BBB

AF with pre-excitation

161
Q

what does sinus tachycardia look like and how would you control it

A

normal P wave followed by normal QRS

>100bpm

162
Q

what does the ECG show

A

AF

absent P waves

irregualr QRS complexes (rhythm)

163
Q

what does this ECG show

A

atrial flutter

sawtooth appearance

atrial rate ~260-340bpm

due to re-entrant circuit usually in RA

ventricular rate often 150bpm (2:1 block)

164
Q

types of junctional tachycardias

A

AV nodal re-entry tachycardia

Wolf parkinson White syndrome

165
Q

what is the ECG?

A

AV nodal re-entry tachycardia

P waves absent or immediately before/after QRS

normal QRS

typical: no P wave or P wave inverted after QRS complex
atypical: P wave inverted before QRS

166
Q

what does the ECG show

A

Wolf-Parkinson-White syndrome

short PR interval

slurred upstroke of QRS - delta wave

167
Q

narrow complex tachycardia management

A
  1. carotid sinus massage (1 side only) or blow the plunger out a syringe
  2. IV adenosine 6mg rapid bolus - if no response 12mg, if no response another 12mg after 1-2 mins

(amiodarone if adenosine CI or not successful)

  1. if pt compromised –> DC cardioversion
    - hypotension: BP <90
    - heart failure

impaired consciousness

HR >200bpm

  1. maintenance therapy: beta blockers or verapamil
168
Q

20yr F

palpitations 6hrs

similar episodes before - never lasted this long

ECG - regular rhythm 160bpm with inverted P waves in leads II, III and aVF and narrow complexes.

vagal manoeuvres do not work

after adenosine 6mg IV - normal sinus rhythm 90bpm restored

single most likely origin of her tachycardia

A

AV node

av nodal re-entry tachycardia

169
Q

21yrs M

sudden onset rapid palpitations

uncomfortable but not SOB, no chest pain

SVT rate 170bpm

carotid sinus transient reversion to sinus rhythm

tachycardia resumed

next step in management?

A

IV adenosine

DC cardioversion if bpm >200

170
Q

signs symptoms and causes of AF

A

irregular QRS rhythm, no p waves

symptoms: palpitations, SOB, faintness, angina, fatigue
signs: irregularly irregular pulse, signs of LVF

causes:

anything leading to: raised atrial pressure, increased atrial muscle mass, atrial fibrosis

common:

IHD
rheumatic heart disease

thyroxicosis

hypertension

171
Q

investigations for AF

A

ECG - absent p waves + irregular QRS

bloods: troponin, U&Es, TFTs, Mg2+, Ca2+, FBC

echo:

LV function

valve lesions

to exclude intracardiac thrombus prior to conversion

172
Q

causes of slow AF

A

hypothermia

digoxin toxicity

medications

sinus node dysfunction

173
Q

management of AF

A

rate control:

1st line: BB (bisoprolol) or CCB (verapamil)

2nd line: digoxin/ amiodarone

rhythm control:

cardioversion if <48hrs -electrical/pharmacological

1st line: IV flecainide

2nd: amiodarone - antiarrhythmic

anticoagulants:

LMWH until full risk of emboli assessed

if risk of emboli high (>2) DOAC

check with CHADSVASC score

174
Q

what is paroxysmal AF

management?

A

self-limiting <7days, recurs

prevention: BB, amiodarone, sotalol

Rx “pill in pocket”: flecainide

anticoagulate: use CHA2DS2 VASc score

175
Q

what is the CHA2DS2 VASc score

A

Coronary heart disease

HTN

age >75 - 2 points

Diabetes

Stroke, TIA - 2 points

Vascular disease

Age 65-74

Sexual category (female)

if > or = 2 - change warfarin to DOAC

176
Q

62yr M

palpitations

AF on ECG

ventricular rate 130/min

mild chest discomfort but not acutely distressed

noticed 3hrs before coming to hospital

first episode

best first-line therapy

A

attempt DC cardioversion

177
Q

hyperkalaemia causes and signs (including ECG signs)

A

hyperkalaemia: serum K+ >5.5

causes:

  • inability of kidney to excrete K+
  • impaired absorption of K+ by cells

clinical signs:

often non specific

generalised muscle weakness

chest pain, palpitations

ECG signs:

peaked T waves

flattened P wave

increased PR interval

widened QRS

178
Q

what does this ECG show

A

hyperkalaemia

  • Peaked T waves
  • Flattened P wave
  • ↑ PR interval
  • Widened QRS
179
Q

diagnosis

A

pericarditis

saddle shape

180
Q

psych patient

recent cardiac arrest

diagnosis?

A

long QT syndrome

181
Q

three types of supraventricular tachycardia

A

AV nodal re-entrant tachycardia: re-entrant point is back through AV node

AV re-entrant tachycardia: re-entry point is an accessory pathway (wolff-Parkinson-White syndrome)

atrial tachycardia: orginates in atria but not at SAN (abnormally generated activity in atria)

182
Q

SVT on ECG

A

narrow complex tachycardia (QRS <0.12)

183
Q

acute mangement of SVT in stable patient

A

continuous ECG monitoring

first line: valsalva manoeuvre: blow hard against resistance

  1. carotid sinus massage
  2. adenosine - rapid bolus antecubital fossa 6, 12, 12 (brief asystole or brady on administration)
    - alternative is verapamil (CCB)
  3. direct current cardioversion if others fail
184
Q

contraindications for adenosine

A

asthma

COPD

cardiac failure

heart block

severe hypotension

185
Q

long term management for paroxysmal (recurring) SVT

A

drugs: beta blocker, CBB, or amiodarone

radiofrequency ablation

186
Q

treatment for wolf parkinson white syndrome

A

definitive treatment is radiofrequency ablation of accessory pathway

187
Q

what does the ECG show

what ECG signs

A

wolf parkinson white syndrome

short PR interval (<0.12 / < 5 small squares)

wide QRS (>0.12)

delta wave - slurred upstroke on QRS

188
Q

when are antiarrythmic medications contraindicated in the management of WPW syndrome

A

when they develop atrial fibrillation or atrial flutter at the same time as WPW

can lead to promotion of the accessory pathway

189
Q

which conditions can radiofrequency ablation be used on

A

atrial fibrillation

atrial flutter

supraventricular tachycardias

WPW syndrome

190
Q

diagnosis of ECG

acute mangement

A

Torsades de pointes

  • ventricular tachycardia
  • height of QRS progressively get smaller, then larger, then smaller etc
  • occurs in patients with prolonged QT interval

acute management:

  • correct cause

- magnesium IV

defib if VT occurs

191
Q

causes of prolonged QT

A

long QT syndrome (inherited)

meds: antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide abx

electrolyte disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

192
Q

long term management of prolonged QT syndrome

A

avoid meds that prolong QT interval

correct electrolyte disturbances

beta blockers (not sotalol)

pacemaker or implantable defib

193
Q

random brief palpitations

diagnosis + management

A

ventricular ectopic

  • random abnrmal broad QRS on background of normal ECG

Management:

  • check bloods for aneamia, electrolyte disturbance, TFTs

no treatment in healthy

specialist in patients with background of heard conditions or other concerning features

194
Q

treatment for unstable or risk of asystole bradycardias/ AV node blocks (mobitz type 2, complete heart block or previous asystole)

A

first line: atropine 500mcg IV

no improvement: atropine 500mcg repeated (up to 6 doses for total to 3mg)

other inotropes (noradrenaline)

transcutaneous cardiac pacing (defib)

195
Q

treatment for high risk asystole (mobitz type 2, complete heart blcok or previous asystole)

A

temporary transvenous cardiac pacing (electrode in wire into vein to stimulate heart directly)

permanent implantable pacemaker

196
Q

tachycardia treatment summary

narrow complex:

atrial fibrillation

atrial flutter

SVT

broad complex:

ventricular tachycardia

if known SVT with bundle branch block

A

atrial fibrillation: rate control with beta blocker or diltiazem (CCB)

Atrial flutter: rate control with beta blocker

SVT: vagal manouvres and adenosine

VT: amiodarone + 3 synchronised shocks

SVT with bundle branch block: treat as normal SVT

197
Q

diagnosis + management

A

irregular complexes + no p waves = atrial fibrillation

Mx:

  • first line: rate control: BB or CCB

emergency cardioversion if haemodynamically unstable

  • 2nd line: rhythm control: amiodarone or flecainide or electrical cardioversion (if <48hrs since onset)

if patient needs rhythm control but been >48hrs delay electrical cardioversion for 3 weeks

  • anticoagulants: CHADVASC score (risk of clot) : heparin
198
Q

management for paroxysmal atrial fibrillation

A

paroxysmal AF terminates spontaneously within 7 days, usually within 48hrs

pill in pocket strategy: taking antiarrhythmic drugs only when an episode of atrial fibrillation starts

199
Q

diagnosis?

management

A

atrial flutter

- saw tooth appearance

- 150bpm

Mx:

rate/ rhythm control: BB or cardioversion

treat underlying cause

radiofrequency ablation

anticoagulation: CHADVASC score: heparin

200
Q

conditions associated with atrial flutter

A

HTN

ischaemic heart disease

cardiomyopathy

thyrotoxicosis

201
Q

what are the two shockable rhythms

A

ventricular tachycardia

ventricular fibrillation

202
Q

diagnosis + management

A

ventricular fibrillation

203
Q

management for ventricular fibrillation/ pulsless ventricular tachycardia

asystole/ pulseless electical activity (all electrical activity except ventricular tachycardia)

A

Mx:

  • ventricular fib/ pulseless tachy: CPR 2 mins + defib (cycle)

asystole/ PEA: CPR

during CPR:

  • adrenaline 1/10,000 every 3-5mins
  • sustained stable ventricular tachy/fib: amiodarone IV after 3 shocks
  • refer to specialist: implantable cardioverter defibrillator

if IV access not obtained use intraosseus route (bone marrow)

204
Q

indications for pacemaker

A

symptomatic bradycardias

mobitz type 2 AV block

third defree (complete) heart block

severe heart failure

(biventricular pacemakers)

hypertrophic obstructive cardiomyopathies

205
Q

types of pacemakers

A

single chamber: sit in right atria (problem with SAN)

dual chanber: right atria and right ventricle (to synchronise atria and ventricular contractions)

biventricular (triple chamber): right atria, right ventricle, left ventricle

  • patients with heart failure

also called cardiac resynchronisation therapy (CRT) pacemakers

implantable cardioverter defibrillators (ICDs):

  • continually monitor the heart and apply defib shock to cardiovert patient back to sinus rhythm if it identifies a shockable arrythmia
206
Q

diagnosis?

A

dual chamber pacing

  • spike before p wave (atrial pacing)
  • spike before QRS (ventricular pacing)
207
Q

investigations and management for carotid artery stenosis

A

can cause stroke or TIA

  • investigations of stroke/ TIA can pick it up

Ix: USS duplex

if narrowing showed on USS then:

CTA (using dye) or MRA

(CT angiography, MR angiography)

management:

  • first line: carotid endarterectomy - if stroke/TIA + moderate/severe stenosis (>50% narrowed) (carried out within 2wks of stroke/TIA)
    or: stenting - less invasive
208
Q

what is pericardiocentesis used to treat

A

removal of fluid from pericardium by needle aspiration

used to treat pericardial effusion & cardiac tamponade

209
Q

indications for CABG and how to investigate

A

Ix: coronary angiography

indications:

  1. left main coronary artery stenosis:
    - stenosis >50%
  2. left main equivalent:

> 70% stenosis in proximal LAD and proximal circumflex artery

  1. three vessel disease

especially in diabetes

  1. one or two vessel disease with extensive myocardium at risk and not suitable for PCI (eg balloons, stenting)
  2. coronary occulsive complications during PCI
  3. surgery for life-threatening complications
    e. g. after MI,
210
Q

techniques for CABG

A

on pump: arrested heart using cardiopulmonary bypass

off pump: with beating heart - no cardiopulmonary bypass

211
Q

vessels used for CABG

A
  1. left internal thoracic artery: gold standard for LAD

should always be used unless emergency with haemodynamic decompensation, or injury/stensois to artery

  1. reversed saphenous vein grafts - when many grafts needed (triple, quadruple bypass)
  2. right internal thoracic
  3. radial artery - prone to severe vasopasm
212
Q

palpable expansile pulsation in abdomen

Ix and management

A

AAA

Ix:

  • aortic USS to determine size

CT angiography for elective repair or suspected rupture being evaluated for repair

Mx:

monitoring size

treating peripheral artery disease

surgically:

  • symptomatic
  • asymptomatic >4cm and grown by >1cm in 1 yr
  • asymptomatic >5.5cm
  • open surgical repair: first choice of surgical intervention
  • endovascular stenting
  • laparoscopic repair
213
Q

pulsatile mass in abdo

severe abdo pain

hypotension

tachycardia

diagnosis + Ix + Mx

A

ruptured AAA

Ix: CT abdo in patients that are haemodynamically stable

if haemodynamically unstable: straight to surgery for repair - no imaging

214
Q

difference between a ruptured AAA and aortic dissection

A

aortic dissection: layers of the wall of the aorta separate allowing blood to flow between the layers causing further separation - increased risk of burst

ruptured AAA: the weakness in the wall due to the aneurysm lead to rupture

215
Q

screening for AAA

A

men >66: screening for AAA

especially with risk factors:

  • COPD
  • HTN
  • FHx
  • coronary, cerebrovascular or peripheral artery disease
  • hyperlipidaemia
  • smoker/ ex-smoker

aortic USS women > 70 with the following risk factors and not already excluded AAA:

  • same risk factors as above
216
Q

referral for AAA

A

aortic USS for diagnosis

AAA > 5.5cm = vascular referral within 2wks

AAA 3-5cm = vascular referral within 12 wks

217
Q

sudden onset pain

very severe

tearing or sharp pain

maximal at time of onset

diagnosis + Ix

A

aortic dissection

  • mainly in greater curvature of aorta or descending thoracic aorta

Ix: contrast CT angiography - not in haemodynamically unstable patients

echo can be used quickly at bed side

218
Q

initial management of thoracic aortic dissections and aneurysms

A

initial management:

  • fluid resus
  • BP control to reduce force of LV contraction: BB

target HR: 60-80

target systolic BP: 100-120

219
Q

management of type A aortic dissection

A

type A: ascending

Mx

  • intial management - fluid resus
  • urgent surgical management- replace ascending aorta with prosthetic graft
220
Q

management of acute type B aortic dissection

A

type B: descending

intial management: fluid resus

uncomplicated: no visceral or limb ischaemia, rupture uncontrollable HTN

  • medical management: BB first line or CCB (for COPD)

complicated:

  • open surgery or endovascular repair using stent graft (alternative)
221
Q

management of chronic type B dissection

A

conservative management

most develop complications which require surgical intervention

222
Q

management for thoracic aneurysms

A

ascending aorta: surgery for prosthetic graft on aorta

descending aorta: endovascular stent-graft placement

223
Q

what is Dressler’s syndrome

A

pericarditis that develops 2-10 wks after MI or heart surgery (acute post-MI pericarditis)

inflammatory response

224
Q

recent MI

low grade fever

chest pain

pericardial frictional rub

diagnosis

mangement

A

Dressler’s syndrome

(acute post MI pericarditis)

Mx:

NSAIDs eg aspirin

in severe symptoms or repeated drainage of effusion: steroids

225
Q

sharp chest pain

relieved on leaning forward

pain radiating to left shoulder or down arm

diagnosis

Ix

A

acute pericarditis

Ix:

  • ECG: saddle shape (ST elevation without reciprocal st depression)
  • CXR: globular cardiac enlargement
    echo: presence of effusion
226
Q

management of acute pericarditis

A

treating any underlying cause

analagesia - NSAIDs

large pericardial effusions complicated by hypotension: aspiration

may need aspiration for diagnostic purposes

227
Q

most common cause of pericardial effusion

A

coxsackie virus

other causes:

MI

pneumonia, septicaemia

renal failure

tuberculosis

hypothyroidism

trauma

cancer of breast or bronchus

228
Q

what can pericardial effusion cause

A

right and left heart failure

cardiac tamponade may occur

229
Q

diagnostic test for pericardial effusion

management

A

echo - diagnostic

Mx: diagnostic pericardiocentesis: cytology may show malignant cells etc

(pericardiocentesis: drainage)

+ treat underlying cause

230
Q

hypotension + shock

pulsus paradoxus

inaudible or distant (muffled) heart sounds

distension of neck veins

Kussmaul’s sign

confusion

diagnosis

A

cardiac tamponade

Beck’s triad of: hypotension, raised JVP, muffled heart sounds

pulsus paradoxus: large decrease in stroke volume, systolic BP and pulse during inspiration

Kussmaul’s sign: paradoxical rise in JVP on inspiration

231
Q

investigations and management for cardiac tamponade

A

Ix: echo - diagnostic

Mx: pericardiocentesis - can be diagnostic with cytology - send pericardial fluid for micro and cytology

232
Q

constrictive pericarditis

symptoms & signs

Ix

Mx

A

fatigue

SOB - on exertion

swelling of abdo (ascites) and ankes

pulsus paradoxus

kussmauls sign

pericardial knock (loud-high pitched S3)

Ix: echo - thickened pericardium with normally contracting ventricle

Mx: surgical: excision of pericardium

233
Q

investigation for new suspected heart failure

A

BNP (B-type natriuretic peptide) - used to rule out heart failure in values:

BNP <100

if BNP >100:

transthoracic doppler echo - cardiac abnormalities

234
Q

initial management for acute decompensation of heart failure

A

IV diuretic - higher dose to what they were admitted on

monitor U&Es, weight and urine output

NIV if low O2

treatment after stabilisation:

  • continue BB
  • stable for 48hrs before discharge
  • ACEi during hospital admission
  • spironolactone during hospital admission
  • surgical aortic valve replacement if due to severe aortic stenosis (or transcatheter aortic valve implantation for those unable to have surgery)
  • follow up with heart failure team within 2wks of discharge
235
Q

diagnosis of chronic heart failure

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP) in people with suspected heart failure

NT-proBNP > 2,000 = urgent specialist assessment + transthoracic echo within 2 wks

NT-proBNP 400-2000 = specialist assessment + transthoracic echo within 6 wks

NT-proBNP <400 = heart failure less likely

ECG

236
Q

management for chronic heart failure

A
237
Q

what is defined as hypertensive crisis

A

sudden increase in BP + acute end-organ damage (e.g. heart failure)

systolic BP >180

diastolic BP >120

238
Q

causes of hypertensive crisis

A
  • cerebral infarction
  • acute pulmonary oedema
  • hypertensive encephalopathy
  • acute aortic dissection
  • ACS
  • eclampsia
  • acute renal failure
  • phaeochromocytoma
239
Q

treatment for hypertensive crisis

A

gradual but prompt reduction in BP

within 1st hr: reduce BP no more than 25%

target BP within next 2-6hrs : 160/100

within next 24/48hrs: normal BP

phaeochromocytoma crisis and severe pre/eclampsia: systolic BP 140 within 1st hr

aortic dissection: 120 within 1st hr

BP control IV:

GTN

sodium nitroprusside

labetalol

specific cause treatments:

pulmonary oedema: GTN, sodium nitroprusside

ACS: GTN

aortic dissection: IV labetolol

eclampsia: labetalol + magnesium (seizure prevention)
phaeochromocytoma: IV phentolamine (a blocker)

240
Q

risk factors for infective endocarditis

A

dental procedures

surgery

infections

nonsterile injections

241
Q

most common bacteria to cause acute infective endocarditis

most common bacteria to cause subacute infective endocarditis

A

acute: staph aureus
subacute: viridens strep - usually affects people with pre-existing damage to heart valves

242
Q

fatigue

fever/ chills

malaise

new or changed heart murmur

comes on over hrs to days

may have damage to other organs eg glumerulonephritis

diagnosis

A

acute infective endocarditis

243
Q

what criteria is used to diagnose acute infective endocarditis

A

Dukes criteria

  • positive blood culutres
  • evidence of endocardial involvement in echo
244
Q

management of Infective endocarditis

A

empiric IV abx - then adapted to blood culture results - 4-6wks

native valves:

  • empiric abx: vancomycin

after blood cultures: penicillin G 4 wks

or gentamicin + penicillin G 2wks

prosthetic valves: same treatment 6 wks

IVDU:

empiric abx: vancomycin

after blood cultures:

IV nafcillin 2wks

PO cloxacillin 2wks

indications for surgery:

  • congestive heart failure
  • uncontrolled infection
  • systemic embolisation
  • prosthetic valve
  • fungal endocarditis
245
Q
A
246
Q

congenital heart disease in adults presentation

A

arrythmias

cyanosis

SOB- on exersion

high heart rate

peripheral oedema

247
Q

most common congenital heart disease in adults

A

tetralogy of fallot - most common cyanotic defect

then atrial septal defect - SOB, fatigue, palpitations - volume loaded right heart

ventricular sepatal defect: most common defect in children - loaded left side of heart

coarctation of aorta: presents with systolic HTN, murmur, absent or diminished femoral pulses (higher BP in arms than legs)

transposition of great arteries

248
Q

most important diagnostic tool for cardiomyopathies

A

echo

249
Q

what is dilated cardiomyopathy

A

most common type of cardiomyopathy

decreased ventricular contractility of the dilated left ventricle (LV) –> failure of the left and eventually right heart (decreased ventricular output)

Mx: manage congestive heart failure and treat underling cause

250
Q

what is restrictive cardiomyopathy

A

proliferation of connective tissue –> atrial enlargement (dilated)

causes right and left heart failure

diastolic filling reduced

ejection fraction normal

251
Q

most common cause of sudden heart failure in athletes and teenagers

A

hypertrophic cardiomyopathy

signs of left heart failure

sudden death

decreased LV cavity size

wall thickness significantly increased

252
Q

most common viral infections causing myocarditis

symptoms

A

parovirus B19

coxsackie virus

rheumatic fever - group A strep

non specific symptoms: (flu-like symptoms + new ECG changes) fever, fatigue, weakness, arrythmias, heart failure

253
Q

Ix and Mx of myocarditis

A

CXR: cardiac enlargement

elevated cardiac enzymes (CK, troponin)

further investigation: myocardial biopsy

Mx:

  • treat underling cause - e.g. abx
  • arrythmias - amiodarone

congestive heart failure - BB, ACEi, diuretics

254
Q

saddle ST elevation on ECG

diagnosis?

A

pericarditis

255
Q

diagnosis

A

hyperkalaemia

  • tall tented T waves
  • broad bizarre QRS complexes
256
Q

diagnosis

A

hypokalaemia

inverted T wave

prominant U wave (after T wave)

257
Q

diagnosis?

A

hypothermia

  • J waves (osborne waves)
  • most prominant in precordial/ chest leads (V1-V6)
  • height of peak equates to extent of hypothermia
258
Q

diagnosis

A

bifid (notched) p wave

sign of left atrial enlargement - most commonly due to:

mitral stenosis

259
Q

what drug is BB contraindicated with

A

BB contraindicated with rate limiting CCB (verapamil, diltiazem)

risk of heart block

can be used with normal CCB (amiodarone)

260
Q

diagnosis?

A

hypokalaemia

U waves

prolonged PR

absent/small T waves

long QT

in hypokalaemia U have no Pot and no T, but a long PR and a long QT

261
Q

hypotension

raised JVP (absent Y descent)

muffled heart sounds

diagnosis

A

cardiac tamponade

Becks triad

absent Y descent in cardiac tamponade

(TAMponade = TAMpaX)

262
Q

maangement of cardiac tamponade

A

urgent pericardiocentesis

263
Q

first three months following prosthetic valve surgery

which bacteria

A

staphylococcus epidermidis

264
Q

sudden onset endocarditis

IVDU

or

prosthetic valve replacement.

endocarditis after 3months

bacteria?

A

staph aureus

265
Q

endocarditis associated with colorectal cancer

A

strep bovis

266
Q

endocarditis associated with poor dental hygiene or dental procedure

bacteria?

A

strep viridans

267
Q

side effects of thiazide diuretics

A

hyponatraemia

hypokalaemia

hypercalcaemia

gout

dehydration

postural hypotension

268
Q

massive PE + hypotension

Mx

A

thrombolysis

269
Q

first line investigation for stable chest pain of ACS

A

first line: CT coronary angiography

2nd line: non-invasive functional imaging

3rd line: invasive coronary angiogrpahy

270
Q

new LBBB + ischaemia symptoms

A

MI

if someone has LBBB compare with old one to see if its new

271
Q

how should adenosine be administered for SVT

A

infused via large-calibre vein (e.g. right antecubital vein) or central route

large bore (16G) cannula used

272
Q

who should adenosine be avoided in

A

asthmatics

can cause bronchospasm

273
Q

Poorly controlled hypertension, already taking an ACE inhibitor, calcium channel blocker and a standard-dose thiazide diuretic (indapamide). K+ > 4.5mmol/l

next step

A

add alpha or beta blocker

274
Q

stages of HTN

A
275
Q

diagnosis

A

posterior MI

shows reciprocal changes therefore ST depression

ST depression and tall R waves in V1-3

276
Q

rheumatic fever from which infection

A

strep. pyogenes infection

277
Q

diagnosis of rheumatic fever major and minor criteria

A

diagnosis:

recent strep pyogenes infection plus:

  • 2 major criteria
  • 1 major with 2 minor criteria

major criteria:

  • erythema marginatum (pic)
  • sydenhams chorea (jerky, irregular movements)
  • polyarthritis
  • carditis and valvulitis
  • subcutaneous nodules

minor criteria:

  • raised ESR or CRP
  • pyrexia
  • arthralgia
  • prolonged PR interval
278
Q

for a person <80 with stage 1 HTN who do you treat

A

treat if:

diabetes

renal disease

QRISK >10 %

established coronary vascular disease

end organ damage

279
Q

what test is used to test reinfarction in window of 4-10 days after initial insult

A

creatinine kinase (lowers after 3-4 days)

troponin can be used 10 days after initial infarct (remains high for 10 days)

280
Q

what are the non-shockable rhythms

mx

A

pulseless electrical activity

asystole

give 1mg adrenaline IV + CPR

further adrenaline every 3-5 mins

281
Q

how many shocks can you give for VF/ pulseless VT

A

give 1 shock followed by 2 mins CPR rather than 3 shocks

282
Q

how many shocks can you give in a witnessed cardiac arrest in monitored patient

A
283
Q

VF/ VT cardiac arrest Mx

A

shock

CPR

adrenaline 1mg IV then every 3-5 mins on rotation with CPR

284
Q

type A vs type B aortic dissection

A

type B - distal to left subclavian origin

type A - ascending aorta - control BP (IV labetalol) + surgery

type B - descending aorta - control BP (IV labetalol)

285
Q

what can hypokalaemia lead to on ECG where it commonly presents in young people as cardiac syncope, tachyarrhythmias, palpitations or cardiac arrest

A

long QT syndrome

286
Q

MI leading to mitral regurg

cause?

A

rupture of papillary muscles

287
Q

major bleed whilst on warfarin?

A

stop warfarin

give IV vit K 5mg

prothrombin complex concentrate (or FFP if other unavailable)

288
Q

non pulsatile raised JVP

A

SVC obstruction

289
Q

blood pressure target > 80yrs

clinic reading

ABPM

A

clinic reading: 150/90

ABPM: 145/85

290
Q

blood pressure target <80yrs

clinic reading

ABPM

A

clinic: 140/90

ABPM: 135/85

291
Q

diagnosis

A

digoxin toxicity

downsloping ST depression

Inverted T wave

short QT interval

reverse tick, scooped out

292
Q

AF + acute stroke (non-haemorrhagic)

when should anticoag be started

A

two weeks after the event

due to risk of haemorrhagic transformation

293
Q

what is buergers disease associated with

A

smoking

294
Q

features of buergers disease

A

also called thromboangiitis obliterans

small and medium vessel vasculitis

associated with smoking

features:

  • extremity ischaemia:

intermittent claudication

ischaemic ulcers

  • superficial thrombophlebitis
  • raynauds phenomenon
295
Q

hypertension + notching of inferior border of ribs

A

coarctation of aorta

notching present in 70% of adults with coarctation

infants: hear failure
adults: HTN

radio-femoral delay

296
Q

monitoring of ACEi

A

monitor renal function and electrolytes before starting and if increasing

rise in creatinine and K+ may be expected after starting ACEi

acceptable changes:

  • creatinine up to 30% rise from baseline
  • increased K+ up to 5.5

significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis

297
Q

cardiac output low

pulmonary artery occulsion pressure low

what type of shock

A

hypovolaemic shock

cardiac output low in hypovolaemia due to decreased preload

298
Q

cardiac output low

pulmonary artery occulsion pressure high

what type of shock

A

cardiogenic shock

pulmonary pressure high in cardiogenic shock

299
Q

decreased systemic vascular resistance

high cardiac output

which type of shock

A

septic shock

decresed systemic vascular resistance - major feature

hyperdynamic circulation (increased circulatory volume)

300
Q

new onset AF presenting within 48hrs of presentation

mx

A

<48hrs: electrical cardioversion + anticoagulation (heparin, start prior)

if > 48hrs: start anticoag then electrical cardioversion after 3 weeks

or can perform transoesophageal echo to exclude thrombus to thrombolyse straight away wth anticoag

anticoag continued for at least 4 weeks after cardioversion

301
Q

contraindications to thrombolysis

A

active internal bleeding

recent haemorrhage, trauma or surgery (including dental extraction)

coagulation and bleeding disorders

intracranial neoplasm

stroke <3 months

aortic dissection

recent head injury

severe HTN

302
Q

heart failure mx

A

first line: ACEi + BB

2nd line: aldosterone antagonist (mineralocorticoid receptor antagonists) - spironolactone, eplerenone

3rd line: started by specialist. options:

  • ivabradine

sacubitril - valsartan

digoxin

hydralazine in combo with nitrate

cardiac resynchronisation therapy

annual influenza vaccine

one off pneumococcal vaccine

303
Q

which abx can cause torsades de pointes

A

macrolides - clarithromycin, erythromycin

304
Q

mx for torsades de pointes

A

IV magnesium sulphate

305
Q

breathing problems with clear chest

low sats

tachypnoeic and tachycardia

A

think PE

COPD - wheeze and crackles

asthma - wheeze

pneumothorax - absent breath sounds on one side

panick attack - wouldnt have low sats

306
Q

AF + acute stroke management

altready had aspirin and alterplase

A

aspirin daily (for stroke mx)

start anticoag in 2 wks (for AF)

307
Q

widespread ST elevation + PR depression

A

acute pericarditis

308
Q

pericarditis mx

A

NSAIDs + colchicine = first line

309
Q

mx of haemodynamically unstable AF

A

immediate electrical (DC) cardioversion followed by thromboprophylaxis

the cardioversion shouldnt be delayed for thromboprophylaxis

anticoag continued for 4 weeks

310
Q
A
311
Q

symptomatic bradycardia

(periarrest bradycardia

/haemodynamic instability)

mx

A

atropine 500mcg IV

features of bradycardia:

shock

myocardial ischaemia

heart failure

syncope

312
Q

which abx causes long QT syndrome

A

erythromycin

313
Q

suspected PE with a wells PE score of 4 or less

Ix

A

D-dimer

if 5 or above then do CTPA

314
Q

most common cause of mitral stenosis

A

rheumatic fever

315
Q

bacteria causing rheumatic fever

A

group A streptococcus (GAS)

indiginous population in central australia at risk

316
Q

features of mitral stenosis

A

mid-late diastolic murmur

loud S1 opening snap

malar flush

317
Q

pharmacological cardioversion for AF

A

if no evidence of structural or ischaemic heart disease:

flecainide or amiodarone

if evidence of structural heart disease:

amiodarone

318
Q

wolff parkinson white symptoms

A

palpitations

dizziness

high heart rate

asscociated with hypertrophic obstructive cardiomyopathy

319
Q

exertional dyspnoea

syncope following exercise

left ventricular hypertrophy

progressive T wave inversion

A

hypertropic obstructive cardiomyopathy

320
Q

AF with decompensation mx

A

synchronised DC cardioversion

can try pharmacological cardioversion (flecainide or amiodarone) if unsuccessful

321
Q

first line mx angina

A

BB or rate limiting CCB (verapamil) (cant be on both due to risk of heart block)

2nd line: BB + CCB

3rd line: PCI or CABG

isosorbide mononitrate given - 10-14hr gap inbetween doses to stop tolerance

322
Q

what valve problem is associated with Marfans syndrome

A

aortic regurg (wide pulse pressure + collapsing pulse)

323
Q

seondary prevention for MI

A

dual antiplatelet therapy (aspirin + ticagrelor)

ACE inhibitor

beta-blocker

statin

324
Q

bifascicular Vs trifascicular block

A

bifascicular block:

  • combination of RBBB + left antior or posterior hemiblock
    e. g. RBBB with left axis deviation

trifascicular block

  • features of bifascicular block + 1st degree heart block
325
Q

radio-femoral delay

A

co-arctation of aorta

326
Q

what congenital heart defect is turners syndrome associated with

A

coarctation of aorta

327
Q

COPD + pan systolic murmur

A

tricuspid regurgitation

caused by pulmonary HTN

328
Q

collapsing pulse

A

aortic regurgitation

329
Q

indications for transcutaneous pacing

A

complete heart block with broad complex QRS

Mobitz type II

recent asystole

ventricular pause >3s

330
Q

SVT on ECG

mx

A

narrow complex tachycardia

absent p waves

Mx:

acute:

  • vagal manoeuvres: valsalva, carotid sinus massage
  • IV adenosine 6, 12, 12 (contraindicated in asthmatics, verapamil is prefered)
  • electrical cardioversion

prevention of episodes:

  • BB
  • radio-frequency ablation
331
Q

most common cause of aortic stenosis by age

A

younger patients <65yrs: bicuspid aortic valve

older patients >65: calcification

332
Q

feel short of breath and adopt this position

A

tetralogy of fallot

overriding aorta, right ventricular hypertrophy, pulmonary stenosis, VSD

shows a tet spell - patient puts knees to chest

333
Q

caution of amiodarone

A

patient should keep out of direct sunlight

334
Q

drug contraindicated in renal artery stenosis

A

ACEi

335
Q

most common cause of mitral stenosis

A

rheumatic fever

previous fever

annular (ring-like) erythematous rash, commonly known as erythema marginatum

3rd year medicine (31 decks)

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