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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Order for presenting ECGs (11 steps)

A
  1. Pt details, time of ECG, presenting complaint
  2. Paper speed
  3. Rate
  4. Rhythm
  5. Axis
  6. P waves
  7. PR interval
  8. QRS complex
  9. ST segment
  10. T waves
  11. QT interval
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2
Q

ECG paper speed

A

25 mm/s

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3
Q

Rate on ECG

A

300/big squares

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4
Q

Causes of L axis deviation

A

LBBB, LVH

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5
Q

Causes of R axis deviation

A

RBBB, RVH/ cor pulmonale

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6
Q

How big should a P wave be?

A

2 squares tall, 3 squares wide

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7
Q

Tall P wave

A

Large RA

P pulmonale

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8
Q

Broad or bifid P wave

A

Large LA

P mitrale

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9
Q

What does the PR interval represent? How big should it be?

A

AV node to bundle of His

5 small squares or fewer

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10
Q

How big should the QRS complex be?

A

3 small squares across - wider is bundle block

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11
Q

What are you looking for in the ST segment?

A

STEMI/ NSTEMI

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12
Q

In which leads should T waves be negative?

A

AVR and V1

+V2-V3 in blacks

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13
Q

Describe the position of ECG leads on the paper

Anterior
Inferior
Lateral
High lateral
Septal
A

I avR V1 V4
II avL V2 V5
III avF V3 V6

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14
Q

Which vessels are affected in the following infarctions?

Anterior
Inferior
Lateral
High lateral
Posterior
A 
Anterior: RCA
Inferior: LAD
Lateral: circumflex
High lateral: circumflex
Posterior: RCA or circumflex
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15
Q

Rate if 1 large square

A

300

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16
Q

Rate if 2 large squares

A

150

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17
Q

Rate if 3 large squares

A

100

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18
Q

Rate if 4 large squares

A

75

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19
Q

Rate if 5 large squares

A

60

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20
Q

Rate if 6 large squares

A

50

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21
Q

Describe atrial flutter ECG

A

Saw-tooth (f waves)
ventricular rate usually 2:1 or 3:1
narrow QRS

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22
Q

Causes of ST elevation

A

STEMI
Prinzmetal’s angina
Pericarditis (saddle-shaped)
Ventricular aneurysm

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23
Q

Causes of ST depression

A

Ischaemia (flat)

Digoxin (down-sloping)

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24
Q

Definition of ST elevation

A

> 1 mm in limbs

> 2 mm in chest

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25
Q

Definition of ST depression

A

> 0.5 mm

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26
Q

Causes of inverted T waves

A 
Strain
Ischaemia
Ventricular hypertrophy
BBB
Digoxin
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27
Q

How does hyperkalaemia present on ECG?

A

Peaked T waves

flattened T waves in hypo

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28
Q

Definition of angina

A

Pain on exertion that is relieved in 5 minutes by GTN

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29
Q

Which pain is resolved by nitrates?

A

angina and oesophageal pain

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30
Q

What causes a sudden increase in exertional angina?

A

rupture of atheromatous plaque - may progress to MI

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31
Q

causes of angina

A

usually atheroma

also: thrombosis, spasm (Prinzmetal), inflammation (arteritis)

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32
Q

Investigations for angina

A

ECG: t wave flattening/ inversion, ST depression, partial/ complete LBBB

Bloods: FBC, TFTs, glucose, lipids, U&Es, LFTs (before starting statins)

Exercise ECG: ST depression > 1 mm

Stress echo (exercise or dobutamine)

Gold standard: coronary angiography

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33
Q

Mx angina

A

Conservative: Lifestyle/ manage risk factors
Aspirin (75 mg)
Statin

First-line: GTN spray, beta-blocker OR rate-reducing CCB (eg verapamil)

Second-line: beta-blocker AND CCB (non rate-limiting, eg nifedipine)

third-line other nitrates, KCBs (eg nicorandil), new anti-anginals (ivabridine, ranolazine)

Revascularisation

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34
Q

What are the options for revascularisation?

A

PCI (will need long-term aspirin + clopi)

CABG (preferred if 3 vessel disease, LAD, diabetic, PVD)
MICABG (uses mammary)

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35
Q

Definition unstable angina

A

Angina at rest

or

Exertional angina that does not respond to max meds

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36
Q

Histological definition of STEMI/ NSTEMI

A

MI: cell death secondary to ischaemia

NSTEMI: confined to endocardium

STEMI: full-thickness

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37
Q

How may elderly present with MI?

A

maybe little pain, present with sudden LVF (profound SOB/ syncope)

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38
Q

How does STEMI present on ECG?

A

ST > 1 mm in 2 consecutive chest leads

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39
Q

How does a STEMI ECG change over 24h?

A

ST elevation begins to resolve
T waves begin to invert
pathological Q waves (deflect)

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40
Q

What should be considered if ST elevation persists after 1 week?

A

reinfarction

LV aneurysm

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41
Q

Investigations in MI

A

Bloods:
FBC: often leucocytosis, anaemia can precipitate
U&Es: monitor K+, renal function can worsen with hypoperfusion
Blood glucose
Lipids
Troponin

ECG
CXR: 
     widening mediastinum = aortic dissection (X thrombolysis)
     HF: pulm oedema, cardiomyopathy 
Echo: not first-line, but helpful
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42
Q

Rise and fall of troponin

A

Rises within 6-14hrs, falls after 2 weeks

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43
Q

Non-acute management of MI

A

3-5 days in hospital, examined daily by cardiologist

all have statin
all have 75 mg aspirin indefinitely
clopi 300 mg for 4 weeks (long, eg year if stents)

if large MI/ HF, ACEi after 3 days
if EF poor, spiro
nitrates

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44
Q

Early complications of MI (0-48h)

A 
arrhythmias: VT, VF, SVT, heart block
cardiogenic shock (from LVF, RVF)
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45
Q

Medium complications of MI (2-7 days)

A

arrhythmias
PE
rupture of papillary muscles*
rupture of IV septum/ free wall rupture

*usually present as acute failure/ death

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46
Q

Late complications of MI (7 days+)

A

Sudden death on PRAED Street

arrhythmias
cardiac failure
Dressler syndrome (secondary pericarditis)
LV aneurysm
mural thrombosis + systemic embolisation
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47
Q

What does a cardiologist examine for following MI?

A

Chest pain: ? further MI - urgent coronary angio
Signs of cardiac failure/ new murmurs: ?mitral regurg secondary to papillary musc rupture - diuretics + urgent echo
Pericarditis
Hypotension: ?drug-induced or cardiogenic shock
Bradycardia: ?heart block after inferior MI/ or v large anterior MI with septal necrosis

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48
Q

What follow-up should occur after MI?

A

Cardiac rehab

exercise tolerance test after 6 weeks

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49
Q

DVLA rules about MI

A

no driving for 1 week (4 weeks if not had surgery)

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50
Q

Managing cardiogenic shock

A

If reversible, eg MI, can treat with IABP (intra-aortic balloon pump) - using ECG for timing, inflates during diastole –> forcing blood back to coronary arteries and forward to renal arteries

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51
Q

Causes of sinus tachy

A 
Physiological
Fever
Thyrotoxicosis
Hypotension
Hypoxia
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52
Q

Causes of atrial tachy

A

structural abnormality, CAD, digitalis toxicity

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53
Q

Atrial rate in atrial tachy

A

150 - 200 bpm (origin not SA node)

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54
Q

What might be needed to view atrial tachy on ECG?

A

Adenosine

Carotid sinus massage

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55
Q

How may atrial tachy appear on ECG?

A

Abnormal P waves

1:1 or slower

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56
Q

Atrial rate in atrial flutter

A

250 - 350 bpm

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57
Q

Causes of atrial flutter

A

alcohol, caffeine, structural abnormality, pulmonary disease (PE, infection, pneumothorax)

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58
Q

Presentation of atrial flutter

A

palpitations, dizziness, HF

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59
Q

Atrial rate in AF

A

300 - 600 bpm

variable ventricular response

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60
Q

Classifications of AF

A

Transient (paroxysmal)
Persistent (> 1 week)
Chronic (permanent)

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61
Q

Causes of AF

A

heart: IHD, atrial septal defect, mitral stenosis, rheumatic heart disease
lungs: lung disease, hypercapnia, hypoxia
hypertension, thyrotoxicosis, metabolic abnormalities, alcohol, sepsis

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62
Q

Clinical features of AF

A

palpitations, dizziness, SOB –> HF

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63
Q

Signs of AF

A

irreg irreg pulse (+/- haemodynamic compromise), no a waves (JVP)

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64
Q

Investigations for AF

A

ECG

Bloods: FBC, TFTs, U&Es, LFTs, coagulation screen (pre-warfarin)

CXR: cardiac structural causes
consider echo

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65
Q

ECG findings for AF

A

no p waves, variable R-R interval

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66
Q

Management AF

A

Treat underlying cause, if poss

RATE CONTROL: beta-blockers or CCBs, consider digoxin monotherapy if sedentary
RHYTHM CONTROL (if rate control doesnt work): cardioversion (or meds, eg flecanide) 
ANTICOAGULATION: Chadvasc score will advise warfarin or apixiban/ rivaroxaban/ others
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67
Q

Complications of AF

A

increased risk of stroke/ embolic disease
premature death
may be DVLA precautions

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68
Q

What is Wolff-Parkinson-White Syndrome?

A

Atrial re-entry tachycardia: accessory excitatory pathway (Bundle of Kent) linking atrium to ventricle

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69
Q

Signs of WPW syndrome

A

Tachycardia

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70
Q

Symptoms of WPW syndrome

A

palpitations, dizziness, collapse, sudden death (tachyarrhythmia)

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71
Q

How does WPW show on ECG?

A

Short PR interval, delta wave (slurred upstroke to QRS)

NB normal when impulse not via Bundle of Kent

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72
Q

Management of WPW

A

Needs ablation.

Meds complicated: some don’t affect accessory pathway

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73
Q

How many people experience ventricular ectopics?

A

About 50%

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74
Q

How do ventricular ectopics present?

A

Asymptomatic or ‘heavy thump’ followed by compensatory pause

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75
Q

Management of ventricular ectopics

A

Beta-blockers if symptomatic

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76
Q

Causes of ventricular ectopics

A

Idiopathic, increased caffeine, hypokalaemia, fever, underlying cardiac abnormality

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77
Q

How do ventricular ectopics appear on ECG

A

not preceded by p wave, weird shape, compensatory pause

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78
Q

Definition of ventricular tachy

A

Lasts over 30 secs or causes haemodynamic compromise - >120 bpm

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79
Q

Causes of ventricular tachy

A

IHD (+/- MI) - cardiomyopathy - metabolic abnormalities - drug toxicity - long QT syndrome

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80
Q

Symptoms of ventricular tachy

A

palpitations, chest pain, syncope

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81
Q

Signs of ventricular tachy

A

tachycardia with hypotension, varying 1st HS, occasional cannon waves (giant a waves)

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82
Q

ECG apperance of ventricular tachy

A

Graves
wide QRS, > 120 bpm
monomorphic or polymorphic

83
Q

Complications of ventricular tachy

84
Q

Management of anti-arrhythmics

A

amiodarone, DC cardioversion, implantable cardiac defib

85
Q

What can be confused with VT?

A

SVT with BBB (use carotid sinus massage/ adenosine - these have no effect on VT)

both are fatal

86
Q

What is torsades de pointes?

A

specific type of polymorphic VT

ECG: irreg + rapid, twisting around axis

87
Q

Complications of torsades?

A

usually self-limiting but can lead to VF

88
Q

Causes of VF

A

IHD, post-infection, torsades, prolonged QT, severe hypoxia

89
Q

Presentation of VF

A

syncope, cardiac arrest

90
Q

What does ECG show with VF?

A

wide QRS

squiggly mess

91
Q

Causes of bradyarrhythmias

A

Physiological (young athletes, sleep), sinus node disease (esp elderly), IHD affecting SA (RCA), drugs (beta-blockers, CCBs), sepsis, hypothyroidism, increased ICP, tumours (cervical, mediastinal), myocarditis, sarcoid

92
Q

How do bradyarrhythmias present?

A

usually asymptomatic

or: syncope, dyspnoea, hypotension

93
Q

How are bradyarrhythmias managed?

A

asymptomatic: no treatment
symptomatic: IV atropine, isoprenaline, pacing wire

94
Q

Two main classes of bradyarrhythmia

A

AV Block (first degree, second, third)

Bundle branch block

95
Q

Describe ECG for different degrees of AV block

A

First degree: slow, but all impulses are conducted - 40% will progress to other degrees

Second degree: not all impulses conducted between atria + ventricles

Mobitz I (Wenkebach): progressive prolongation of PR interval, dropped QRS
- can be benign (kids, athletes), or inferior MI

Mobitz II: P-R interval constant, QRS occasionally dropped
- risk of CHB, needs pacing

Third degree: P waves + QRS are independent

96
Q

Causes of BBB

A

ischaemia, infarction

97
Q

ECG findings for BBB

A

axis deviation
wide QRS
V1 and V6: WilliaM MarroW

98
Q

Which valves close: S1 and S2?

A

S1: AV valves (tricuspid and mitral)
S2: pulmonary + aortic

99
Q

What is rheumatic fever?

A

Group A strep pharyngeal infection

antibody-mediated immune response (type II hypersensitivity)

100
Q

Name of criteria for diagnosing rheumatic fever?

A

Duckett-Jones

1) evidence of beta-haemolytic strep infection (eg ASOT titre)
2) 1 major or 2 minor

MAJOR
carditis
arthritis
Sydenham’s chorea
erythema marginatum (red rash on trunk, clear centre)
nodules (pea-sized, extensor surfaces, painless)

MINOR
fever
high ESR/ CRP
long PR interval
arthralgia
101
Q

Describe the arthritis that usually accompanies rheumatic fever?

A

migrating polyarthritis affecting larger joints

102
Q

Management of rheumatic fever

A

High-dose benzylpenicillin
Anti-inflammatories for immune response
Abx (usually penicillin) ~5 years

103
Q

Main cause of mitral stenosis

A

Rheum fever

104
Q

Clinical features of mitral stenosis

A

Lungs: dyspnoea (pulm oedema), haemoptysis

Heart: AF (enlarged atria) + emboli

Compression due to large L atrium: hoarseness, dysphagia, L lung collapse (on L bronchus)

105
Q

Describe the murmur of mitral stenosis

A

Low-rumbling murmur at apex: hard to hear (reposition)

106
Q

What might you find on examination of someone with mitral stenosis or mitral regurg?

A 
Maybe AF
Raised JVP
Pulm oedema
Loud palpable murmur
Abdo: ascites, hepatomegaly
Peripheral oedema
107
Q

Causes of mitral regurgitation

A

PROBLEMS WITH MITRAL ANNULUS: senile calcification, LV dilatation (enlagement of annulus), abscess formation during IE

MITRAL VALVE LEAFLETS: IE, rheumatic fever, mitral valve prolapse

CHORDAE TENDINAE: idiopathic rupture, IE, CD tissue disorders

PAPILLARY MUSCLE: MI, infiltration, myocarditis

108
Q

Clinical presentation of mitral regurg

A

Acute: can be fatal - blood back to pulm veins

Chronic: heart has chance to decompensate - fatigue, dyspnoea

109
Q

Describe the murmur of mitral regurgitation

A

Loudest at apex, radiating to axilla
Murmur is pansystolic (high pitched blowing), soft first heart sound
Apex displaced (down+out) + thrusting

110
Q

Causes of aortic stenosis

A

Usually valvular:
senile calcification, severe atherosclerosis, congenital, rheum fever

Can be subvalvular, eg HOCM, or supravalvular

111
Q

Which test is absolutely contraindicated in AS?

A

Exercise test

112
Q

Clinical features of AS

A

may be asymptomatic

Dyspnoea (may lead to orthopnoea + paroxysmal nocturnal dyspnoea as LV fails)
Angina
Dizziness + syncope (esp exertional)
Sudden death
Emboli
113
Q

Examination findings in AS

A

Pulse: low volume
Carotid pulse: slow rising, small volume
BP: low with narrow pulse pressure
Lungs: bilateral basal creps (as LV fails)

114
Q

Describe the murmur of aortic stenosis

A

Radiates to carotids
Ejection systolic murmur
Palpable thrill + heave

115
Q

Causes of aortic regurg

A

VALVULR DISEASE: congenital, rheum fever, IE, RA, SLE, CD disease

AORTIC ROOT DISEASE: Marfan’s, osteogenesis imperfecta, ank spond

116
Q

Clinical features of aortic regurg

A

Asymptomatic

or dyspnoea

117
Q

Examination findings AR

A

Collapsing pulse, Quincke’s sign (visible capullary pulsation in nailbed)
Wide pulse pressure
De Musset sign (head bobbing), Corrigan sign (prominent neck veins)
Pistol shot femoral arteries

118
Q

Describe the murmur of AR

A

Early diastolic murmur

119
Q

Causes of tricuspid regurg

A

Mostly from dilatation of RV (RVF or pulmonary HTN)

Sometimes IE, congenital malformations

120
Q

Clinical presentation of TR

A

symptoms of RVF

121
Q

What is diff HF and CHF?

A

CHF = HF with fluid retention

122
Q

What is the key blood test for HF?

A

BNP (protective)

123
Q

Causes of HF

A

Heart disease: ischaemic, valvular, congenital, cardiomyopathy, myocarditis, endocarditis
Strain: PE, HTN

Precipitating factors: MI, infection, arrhythmia, anaemia, thyrotoxicosis, electrolyte disturbance, PE, pregnancy, vitamin deficiencies

KEY: NON-CONCORDANCE WITH MEDS

124
Q

What is diastolic HF?

A

Preserved systolic function
More common in old women
Due to impaired relaxation/ stiffening of myocardium

125
Q

Describe HF symptoms in terms of forward and backward effects

A

Forward: failure to pump to provide adequate perfusion

Backward: systemic + pulmonary oedema

126
Q

Clinical features of LVF

A

LUNGS

Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, lung creps, pleural effusions, pink frothy sputum, cyanosis
Cough: cardiac asthma (bronchoconstriction due to oedema) and bronchial oedema
Fatigue

127
Q

Clinical features of RVF

A

FLUID OVERLOAD

Peripheral oedema, ascites, tender pulsatile hepatomegaly, raised JVP

128
Q

Examination findings of severe CHF

A

cold peripheries, reduced pulse pressure, hypotension, gallop rhythm/ 3rd + 4th HS

cachexia

129
Q

Investigations for HF

A

FBC:
?anaemia
?leukocytosis in acute exacerbation

U&Es:
?low Na due to increased vasopressin (dilutional hyponatreaemia)
?low K common: diuretics
?high K common: K-sparing diuretics/ ACEi/ ARBS

BNP and cardiac enzymes

LFTs

TFTs

lipids

glucose

ABG: hypoxia, hypocapnia, metabolic acidosis

ECG: hypertensive changes, ischaemia, arrhythmias

Echo

CXR

Cardiac catheterisation: explore as mx may improve things!

130
Q

Management of HF

A

Risk factors
HF nurse

ACEi (monitor renal failure/ hypotension)
Beta-blockers
Diuretics (furosemide + thiazides) - symptomatic only
Aldosterone antagonists (spiro potentiates ACEi, can cause K-retention)
Nitrates
Digoxin (AF + HF)
Hydralazine: potent vasodilator - better in blacks than ACEi - or additional therapy/ if ACEi/ARBS not tolerated

PACEMAKER

131
Q

Who does NICE recommend should get a pacemaker in HF?

A

Conduction problems

EF <35%

132
Q

Normal volume of pericardial fluid

133
Q

Causes of acute pericarditis

A

Viral (Coxsackie, EBV, HIV), bacterial, fungal, TB, rheum fever (when acute)
acute MI,
autoimmune disease (SLE, RA, sarcoid),
malignancy
uraemia [usually a haemorrhagic pericarditis, rapidly leading to tamponade - needs dialysis]

134
Q

Symptoms of acute pericarditis

A

Sharp retrosternal pain, relieved on leaning forward/ worse on lying, coughing, swallowing
Dyspnoea (pain on deep inspiration)

135
Q

Signs of acute pericarditis

A

Pericardial friction rub
Fever
Tachycardia

136
Q

Management of acute pericarditis

A

Treat underlying cause
Bed rest
NSAIDs

137
Q

Management of Dressler syndrome

A

NSAIDS + aspirin

Maybe CS

138
Q

Signs of Dressler Syndrome

A

Fever, pericarditis, pleurisy
1 week after MI
May have arthritis
tamponade not uncommon

139
Q

Pathophysiology of Dressler syndrome

A

Can only occur if pericardium exposed to blood - autoantibodies form - Type III

140
Q

What causes constrictive pericarditis?

A

Pericardium becomes fibrosed + thickening, restricting filling of heart during diastole

Any cause of acute pericarditis can persist

141
Q

How is constrictive pericarditis diagnosed?

A

Cardiac catheterisation is diagnostic (raised and equal end-diastole pressures)

142
Q

Causes of pericardial effusion

A

Acute pericarditis, MI with ventricular wall rupture, chest trauma, aortic dissection, cardiac surgery, neoplasia

143
Q

Symptoms of pericardial effusion

A

If acute, even small volumes can cause tamponade - HF signs

If gradual, even 2 L can be asymptomatic - may just be dull ache, dysphagia

144
Q

What is Light’s criteria? What measurements do you need?

A

For pericardial effusion

Need serum protein + LDH

145
Q

Causes of transudative pericardial effusions

A

CCF, hypoalbuminaemia

146
Q

Causes of exudative pericardial effusions

A

Infection, post-MI, malignancy, SLE, Dressler

147
Q

Causes of haemorrhagic pericardial effusions

A

Uraemia, aortic dissection, trauma, post-cardiac surgery

148
Q

Where to withdraw pericardial fluid?

A

Below xiphoid at 45 degrees towards shoulder

send fluid for cytology, microscopy, culture + biochemical analysis

149
Q

Where do infective vegetations usually occur?

A

usually valves but any area of turbulence (eg VSD)

150
Q

All cases of IE start with a sterile fibrin-platelet vegetation as a prerequisite for adhesion development. What does development depend upon?

A

Presence of anatomical abnormalities in heart’s surface
Haemodynamic abnormalities in heart
Host immune response
Virulence of pathogen
Presence of bacteraemia (transient bacteraemia is common: but healthy person should be ok)

151
Q

Causes of IE

A 
Rheum fever
Prosthetic valves
Pts with congenital heart disease surviving
Elderly
More IV drug use?
More abx resistance

at risk if invasive vasc procedures

152
Q

Most commonly affected valves in IE

A

mitral - aortic - others

153
Q

Common causative microbes in IE

A

Staph aureus: now most common
Strep viridans: prev most common (rheum fever)
Staph epidermidis: most common in pts with new prosthetic valves (under 2 months)

also enterococci, pseudamonas, fungi etc

154
Q

Usual classification of IE

A 
Acute IE (rapidly progressive)
Subacute IE (slowly progressive)
Non-bacterial thrombotic endocarditis: CKD, neoplasia, SLE, malnutrition
155
Q

Criteria for IE

A

Duke criteria

156
Q

How does IE present?

A

Fever + systemic symptoms (maybe not in elderly)
New heart murmur in 50%

If subacute/ chronic, maybe non-specific symptoms like myalgia, flu-like symptoms

Presenting complaint may be CVA or other signs of microemboli, or splenectomy

157
Q

Investigations for IE

A 
Urine dip (microscopic haematuria - v sensitive)
Urinalysis for casts

Daily ECG: risk of heart block if affects aortic root

Blood cultures: 3 sets (ideally 1 before abx)

FBC: leucocytosis, thrombocytopenia (DIC), thrombophilia (acute phase response)
ESR/ CRP
U&amp;Es
LFTs
RhF + immune-complex titre

CXR: pulm oedema

Echo weekly (valve damage)

158
Q

Management of IE

A

Abx

Monitoring

159
Q

Complications of IE

A

Local destructive effects: valve incompetence, paravalvular abscess, prosthetic valve dehiscence, myocardial rupture
these can lead to (sometimes rapid) CCF and cardiogenic shock

Emboli/ non-infected fragments: stroke, cerebral abscess, ischaemic bowel, renal infarcts, digital infarcts, renal + hepatic abscesses (hepatic infarct rare: dual supply)

160
Q

Which are systolic and diastolic murmurs?

A

SYSTOLIC: stenosis of opp
DIASTOLIC: regurg of same

SYSTOLE:
AS, PS
MR, TR

DIASTOLE:
MS, TS
AR, PR

161
Q

Recommended daily calories

A

1800 men and women

162
Q

Recommended BMI

A

18.5 to 24.9

in S Asian, Chinese + Japanese: 18 to 23

163
Q

When sex after MI?

A

When comfortable to do so, usually 4 weeks

164
Q

Safety netting for cardiac pain

A

Red flags: refer to A&E by ambulance

Cardiac pain within last 12h: emergency referral

Cardiac chest pain within last 72h: same day referral

Cardiac chest pain stopped over 72h ago/ no complications: Rapid access chest clinic

165
Q

When should patient call ambulance after trying GTN spray?

A 
Dose
wait 5 mins
Dose
wait 5 mins
still pain: ambulance
166
Q

Contraindications of GTN

A

Phosphidoesterase inhibitors
24h between Viagra
48h for others

can cause severe hypotension/ death

167
Q

Cardio causes of clubbing

A

Cyanotic congenital heart disease

Infective endocarditis

168
Q

Closed foramen ovale

A

Fossa ovalis

169
Q

Major anatomical site for thrombus formation in AF

A

left atrial appendage

170
Q

Difference low-output and high-output HF

A

In low output the compensatory mechanisms fail, resulting in reduced cardiac output. Cool peripheries and weak pulses. Eg IHD, AS

In high-output the heart has normal/ increased cardiac output but cannot meet increased metabolic demands. Warm peripheries and normal pulses. Eg thyrotoxicosis, AV fistula, beriberi, pregnancy, severe anaemia

171
Q

General principle for introducing HF meds

A

One at a time until stable, use clinical judgement to decide which to start with

172
Q

Mx pericarditis

A

NSAIDs or aspirin until symptoms/ CRP resolves (usually 2 weeks)

Colchine usually used as adjunct to prevent recurrence

CS if connective-tissue or other rare cause (or others contra-indicated)

**NB post-MI pericarditis shouldnt be managed with NSAIDs as may intefere with healing of pericardium

173
Q

What should be investigated it IE caused by Strep gallolyticus (Strep bovis)

A

Colonoscopy for colorectal ca

174
Q

Empirical abx for IE

A

Native valves: vanc (or fluclox) with gentamicin (4-6 weeks)

Prosthetic valves: also rifampicin

175
Q

What causes Stokes-Adams attacks?

A

Paroxysmal arrhythmias, eg third-degree heart block

176
Q

What is holiday heart syndrome?

A

Binge-drinking causing self-limiting AF

177
Q

INR target in AF

A

2-3

2.5 to 3.5 if recurrent thromboembolic events on anticoag or metallic valves

178
Q

Murmur grades

A

Grade VI: audible without steth

Grade V: loud ++, audible with rim of steth, thrill

Grade IV: loud + thrill

Grade III: clearly audible (no thrill)

179
Q

Signs of constrictive pericarditis

A

KKK
Knock
Kussmaul Sign (paradoxical rise in JVP with inspiration)

180
Q

What is CHADSVasc for?

A

Assess risk of stroke (whether to start anticoag)

181
Q

What is HAS-BLED score for?

A

Assess risk of bleeding if on therapy

182
Q

What are the dysfunctions related to the different cardiomyopathies?

A

Dilated cardiomyopathy (systolic dysfunction - dad bods, can’t lift weights)

Hypertrophic cardiomyopathy (diastolic dysfunction - hulked up, can’t relax)

Restrictive cardiomyopathies (diastolic dysfunction - stiff, can’t relax)

183
Q

What is thought to cause Takotsubo cardiomyopathy?

A

‘broken heart syndrome’

ctecholamine-mediated response to severe stress events

184
Q

Symptoms of digoxin toxicity

A

Lethargy, N&V, delirium, xanthopsia (yellow flashes/ discolouration of vision)

185
Q

ECG changes in digitalis toxicity

A

Bradycardia, prolonged QT, AV block

Downsloping ST depression

186
Q

Mx digitalis toxicity

A

Typically hypokalaemia: so manage U&Es

Digibind (digoxin antibodies) available but seldom used

187
Q

How to differentiate L sided and R sided murmurs O/E

A

L sided loudest on exhalation

R sided loudest on inspiration

188
Q

Midline sternotomy + leg scar

A

CABG

+/- valve replacement

189
Q

Midline sternotomy without leg scar

A

valve replacement most likely

maybe CABG without vein graft, LIMA or radial artery graft

190
Q

Causes of raised JVP

A

RHF, volume overload, PE, constrictive pericarditis

191
Q

Causes of raised JVP with low BP

A

Tension pneumothorax, cardiac tamponade, massive PE, severe asthma

192
Q

Causes of elevated and fixed JVP

A

SVC obstruction

193
Q

Causes of cannon A waves

A

complete heart block, VEBs, VT

194
Q

Causes of giant V waves

A

TR (look for ear wiggling and pulsatile hepatomegaly)

195
Q

Causes of central cyanosis

A

Hypoxic lung disease
R-to-L cardiac shunt (cyanotic congenital heart disease, Eisenmenger’s)
Methaemoglobinaemia

if severe, can cause blue hands but usually warm

196
Q

Causes of peripheral cyanosis

A 
PVD
Raynaud's sx
Heart failure
Shock
(severe central cyanosis causes)
197
Q

Causes of irreg irreg pulse

A

AF
VEBs
Complete HB + variable ventricular escape

198
Q

Causes of absent radial pulse

A 
Congenital (usually bilateral)
Arterial embolism (eg due to AF)
Atheroma (usually subclavian)
Previous arterial line
Previous coronary angio
Cervical rib
Coarctation of the aorta
199
Q

Features of JVP (vs carotid)

A 
Double pulsation
Non-palpable
Obliterated when pressure applied at base of neck
Height changes with respiration
Height changes with angle of pt
Rises with hepatojugular reflux
200
Q

indication for adenosine

A

first-line to diagnose and treat SVT

201
Q

contra-indications of adenosine

A

hypotension, coronary ischaemia, asthma (bronchospasm)

careful in heart transplant + COPD

202
Q

Describe digoxin’s moa

A

reduces HR and increases force of contraction

203
Q

Abx associated with long QT

A

erythroMycin

204
Q

how does hypercalcaeMia present on ecg

Medicine (30 decks)

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