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Clinical > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the physiology behind VF?

A

Rapid, uncoordinated contraction of ventricles causing QRS to become irregular.

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2
Q

How is VF managed?

A

Desynchronised cardioversion and CPR in between shocks.

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3
Q

What is pharmacological intervention can be used after 3 unsuccessful shocks to manage VF (refractory VF)?

A

IV adrenaline (1mg 1:10000) and amiodarone (300 mg).

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4
Q

What is the physiology behind VT? What is seen on ECG?

A

Rapid contraction of ventricles means body isn’t perfused correctly. Causes a monomorphic broad complex tachycardia.

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5
Q

How do we manage a haemodynamically stable patient in VT?

A

300 mg amiodarone over 20 minutes then 900 mg over 24 hours.

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6
Q

How do we manage a haemodynamically unstable patient in VT?

A

chest compressions at a rate of 100-120/minute (30:2 ratio) and delivery of DC cardioversion.

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7
Q

What is seen on ECG for Torsades?

A

Polymorphic broad complex tachycardia.

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8
Q

How is Torsade’s managed?

A

2g IV magnesium sulphate

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9
Q

What ECG abnormalities are associated with hypomagnesaemia?

A

Prolonged QT interval which can convert into Torsade’s.

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10
Q

How do we manage a sinus bradycardia with haemodynamic compromise?

A

IV atropine 500 micrograms every 3-5 minutes up to 3mg total.
If this fails, convert to transcutaneous pacing.

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11
Q

What medication can be used to manage bradycardia once 3mg of atropine has been used but transcutaneous pacing is not available?

A

IV isoprenaline

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12
Q

What is the biggest SE of atropine 6-12 hours after administration?

A

Agitation.

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13
Q

What are the ECG signs of AF?

A

Irregularly irregular rhythm and lack of p waves.

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14
Q

If someone presents in AF with haemodynamic compromise how is it managed?

A

Synchronised cardioversion.

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15
Q

Can you cardiovert someone who presents, haemodynamically stable, in AF whose symptoms started 3 days ago?

A

No - 48 hours is the cut off for cardioversion due to risk of clot. These patients need to be anticoagulated before they can be cardioverted.

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16
Q

What medications can be used for rate control of AF?

A

1st line is beta blockers (diltiazem if CI),
Can also use digoxin if these are unsuccessful (250mg loading dose followed by 250 mg 6 hours later and then oral OD doses).

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17
Q

What medications can be used to rhythm control someone in AF?

A

Amiodarone (dangerous long-term SEs),
Class 1c antiarrhythmics - flecainide/propafenone - which are used as ‘pill in pocket’ to take when patients become symptomatic (can only be used in someone with a structurally normal heart).

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18
Q

If someone in AF has a regular HR what is the other pathology occurring?

A

3rd degree (complete) heart block. Ventricle isn’t receiving atrial signals so irregular rhythm isn’t transmitted so there is a normally ventricular rate.

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19
Q

What is Brugada Syndrome? What are the signs on ECG?

A

tachyarrhythmias caused by Na channel pathology, often familial.
ECG: concavity and elevation of ST segment in V1-3 and T waves inversion.

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20
Q

Which of the following is associated with life-threatening arrhythmias in someone with Brugada syndrome?
a) Hypotension
b) Hyponatraemia
c) Fevers

A

C- fevers, accentuating the ECG signs and causing ventricular arrhythmias.

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21
Q

SVT can be categorised into 3 different types, what are these?

A
  • AVNRT (atria-ventricular node re-entry tachycardia)
  • Atrial flutter
  • Accessory pathways (WPW)
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22
Q

What is seen on ECG for AVNRT? How is it managed?

A

Narrow complex tachycardia with no P waves.
Management:
1) vagal manoeuvres
2) Adenosine (6, 12, 18)
3) If unsuccessful try synchronised cardioversion (or if haemodynamically compromised)

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23
Q

Why can we not prescribe adenosine for atrial flutter? How do we manage it?

A

DOES NOT respond to adenosine as it is independent to the ventricle and adenosine blocks AV node (so if you gave it the atria would continue to fire).
Managed with beta blockers and if this is unsuccessful may need synchronised cardioversion.

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24
Q

What is seen on ECG for atrial flutter? What is the rate?

A

Sawtooth baseline.
Atrial rate around 300bpm, ventricular rate around 150bpm (every other beat transmitted).

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25
Q

What is the signs of an accessory pathway on ECG? How is it managed?

A

Preexcitation (delta waves), shortened PR.
Manage the same as AF.

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26
Q

What is sick sinus syndrome? What are the symptoms?

A

Bradycardia, prolonged heart beats, and arrhythmias, disfunction of SA node.
Dizziness, syncope, SOB, fatigue

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27
Q

What is classed as a prolonged QT interval for men and women?

A

> 460 in women, >440 in men

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28
Q

Is an Ejection fraction <50% associated with systolic or diastolic heart failure?

A

Reduced ejection fraction heart failure is Systolic dysfunction (LV can’t contract properly to squeeze out blood).

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29
Q

Preserved ejection fraction heart failure is an EF over what %? What is this also known as?

A

EF >50%, aka diastolic heart failure (LV unable to fill properly).

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30
Q

How do we improve mortality for heart failure patients with a reduced EF?

A

BASH: betablocker, ACEi, spironolactone, hydralazine.

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31
Q

Can medications improve mortality for pts with HFpEF (diastolic failure)?

A

No - manage comorbidities.

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32
Q

Is a 4th heart sound pathological?Why?

A

YES - forceful atrial contraction against a stiff hypertrophic LV.

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33
Q

What is cor Pulmonale? Signs on ECG?

A

Right heart failure secondary to COPD.
P pulmonary waves (pulmonary HeTN causing right atrial enlargement)

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34
Q

Thyrotoxicosis and anaemia are examples of what type of heart failure?

A

High output cardiac failure (increased CO to compensate for higher demand)

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35
Q

What is first line management of stable angina?

A

GTN and beta blockers

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36
Q

ACS management?

A
  • 300 mg aspirin
  • morphine (pain)
  • nitrates
  • oxygen (only if not saturating)
  • metoclopramide (if feeling nauseous)
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37
Q

MI of what artery puts the pt at an increased risk for rupture of their interventricular septum?
What are the complications of this?
What murmur is heard?

A

LAD - interruption of septal supply.
cardiogenic shock, haemodynamic compromise, biventricular failure. A harsh holosystolic murmur may be heard.

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38
Q

How do you manage a pt with an interventricular septal rupture?

A

Aim is to reduce afterload.
Medical: Nitroprusside (decreased HeTN in acute heart failure).
Surgical: (intra-aortic balloon pump)

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39
Q

What artery is taken for use in bypass graft on LAD?

A

Internal mammary.

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40
Q

Aortic regurgitation is associated with which murmur? What other signs may be seen?

A

Diastolic decrescendo murmur at the left sternal border.
Quincke’s sign (pulsating of nail beds), collapsing pulse (radial pulse disappears when raising arm due to incompetence and backflow of blood across valve).

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41
Q

Aortic Stenosis is associated with what murmur?

A

Ejection systolic murmur at the second intercostal space.

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42
Q

What less typical murmur can aortic stenosis cause?

A

Can also cause a musical pansystolic murmur at the apex (Gallavardin phenomenom).
This is due to vibrations that travel from the calcified valve.
This murmur DOES NOT radiate to the axilla.

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43
Q

What clinical signs are associated with aortic stenosis?

A

Exertional breathlessness, low-volume pulse, narrow pulse pressure, quiet S2.

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44
Q

What makes aortic stenosis severe?

A

Valvular area <1cm, elevated pressure gradient >40mmHg.

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45
Q

Mitral stenosis is associated with what murmur? What is it exagerated by?

A

Mid-end diastolic murmur with an opening snap.
It is exaggerated by expiration and is heard best with the bell of the stethoscope.

46
Q

Left atrial enlargement is associated with with valvular disorder? What does this look like on an ECG?

A

Mitral stenosis: force that the atria must pump against causes hypertrophy.
Seen as M mitral waves (notched p waves) on ECG.

47
Q

Mitral regurgitation is associated with what murmur?

A

Blowing pan-systolic murmur heard loudest at the apex. Exaggerated by expiration, radiates to the axilla.

48
Q

What makes mitral regurgitation severe?

A

Regurgitant volume >60mls/beat.

49
Q

How might acute mitral regurgitation present? What is it caused by?

A

Sudden-onset pulmonary oedema, hypotension and cardiogenic shock.
Ischaemic (e.g., post MI), or non-ischaemic (infection, trauma, etc).

50
Q

What murmur is tricuspid regurg associated with?

A

Holosystolic murmur at left sternal border.

51
Q

Which prosthetic valve is associated with schistocytes?

A

Mechanical valves - causes haemolysis of RBCs causing these fragments to be present in blood.

52
Q

What is Beck’s Tryad?

A

Raised JVP, muffles heart sounds and HoTN = cardiac tamponade.

53
Q

What is pulsus paradoxus?

A

Exaggerated drop in systolic BP during inspiration, associates with cardiac tamponade.

54
Q

What are the 2 types of Aortic Dissection? How are they managed?

A

Type A: ascending aorta - surgical repair
Type B: descending aorta - surgical repair if evidence of end organ damage, otherwise managed medically with IV labetalol to control BP.

55
Q

How is hypercalcaemia seen on ECG?

A

J waves (positive deflection at the junction between QRS and ST) and short QT.

56
Q

How is hypocalcaemia seen on ECG?

A

QT prolongation.

57
Q

Signs of hyperkalaemia on ECG?

A

1) tall tented T waves
2) flattened p waves
3) widening of PR and QRS
4) loss of p waves (sinusoidal wave)

58
Q

How do we manage acute pulmonary oedema secondary to heart failure?

A

maintain sats (oxygen if required), start IV diuretics

59
Q

What are the most common causes of infective endocarditis? What are the risk factors for each?

A

Staph aureus: IVDU, prosthetic valves,
Streptococcus viridans: poor dental hygiene,
Streptococcus epidermis: prosthetic valves, indwelling catheters.

60
Q

What is included in the minor dukes criteria for IE?

A
  • Fever
  • Vascular phenomena
  • Immunological phenomena
  • +ve culture
61
Q

How is IE managed in pts with a) native b) prosthetic valves? How long is the treatment?

A

a) amoxicillin +/- gentamicin
b) vancomycin +/- rifampicin
6 weeks of IVs.

62
Q

At what point would IE need surgical intervention?

A

Prolonged PR on ECG (suggesting aortic root abscess)

63
Q

What valves is most commonly affected in IVDUs with IE?

A

Tricuspid (right sided receives blood from circulation first where the bacteria comes from)

64
Q

How is pericarditis seen in ECG? How is it managed?

A

Saddle shape deformity.
First line is colchicine/NSAIDs (ibuprofen 600 mg 8 hourly or 750-100 mg aspirin 8 hourly then taper down over 4 weeks).

65
Q

What is rheumatic heart disease? What are the long-term complications?

A

Pancarditis (inflammation of entire heart).
Fibrosis, stenosis, and regurgitation of heart valves.

66
Q

What is the most common cause of myocarditis? How is it investigated and mx? What is a possible complication?

A
  • Coxsackie B virus
  • Endomyocardial biopsy (gold standard)
  • Supportive +/- corticosteroids
  • Dilated cardiomyopathy
67
Q

How do you differentiate pericarditis from myocarditis?

A

Peri is more pleuritic chest pain which is often positional.
Myo is much more diffuse and not position dependent.

68
Q

A pansytolic murmur at the left sternal edge is indicative of what?

A

VSD.

69
Q

Mutation of beta-myosin heavy chains occurs in what heart condition?

A

HOCM.

70
Q

An ejection systolic murmur heard loudest between the shoulder blades is associated with which pathology? What other sign is associated? What genetic condition is associated?

A

Coarctation of the aorta.
Radio-femoral delay.
Turners syndrome.

71
Q

An infant who presents with peripheral and central cyanosis, respiratory distress, and a single and loud S2 is what? What sign is seen on XR? How is it diagnosed?

A

Transposition of the great vessels.
Egg on a string sign on CXR.
Echo showing the aorta originating from the RV.

72
Q

What structural changes can compensate for transposition of the great vessels?

A

PDA or VSD to allowing mixing of the circulations.

73
Q

What group of mums are at an increased risk of transposition of the great vessels in their babies?

A

Diabetics.

74
Q

What is Ebstein’s abnormality? What is it caused by?

A

Tricuspid valve incompetence (low insertion of valve), RA hypertrophy, small RV.
Maternal lithium use.

75
Q

What isthe inheritance patterm of HOCM? What does it cause?

A

Hypertrophic obstructive cardiomyopathy - autosomal dominant condition leading to hypertrophic LV without an apparent cause.

76
Q

What murmurs (2 of them) might be heard in auscultation of someone with HOCM? Why is this?

A

Ejection systolic murmur - between lower left sternal edge and apex, due to LVOTO (LV outflow tract obstruction).
Pansystolic murmur - at the apex radiating to axila, due to SAM (systolic anterior motion) of mitral valve.

77
Q

What is Eisenmenger syndrome? How is it managed?

A

Untreated congenital cardiac defects lead to clubbing, RV failure, cyanosis. These complcations occur when a left to right shunt reverses due to HeTN.
Needs heart-lung transplant.

78
Q

Digoxin OD causes what sign on ECG? How is it managed?

A

Reverse tick sign after QRS, can also cause a first degree heart block.
Give IV digibind.

79
Q

Should ACEIs be stopped prior to surgery?

A

YES - they hold a great risk of severe HoTN.

80
Q

What should be measured 2 weeks after starting ACEIs?

A

Creatinine, if increased by >30% then stop.

81
Q

What criteria are included in the CHADVASC score?

A
  • stroke/thromboembolic disease, >75 y/o (2 points each)
  • CHF/LVEF <40%, , vascular disease, 65-74 y/o, HeTN, diabetes, (1 point each).

Men = 1, women = 2 then Anticoagulate.

82
Q

What ECG abnormality can clarithromycin cause?

A

Prolonged QT - can precipitate into torsades.

83
Q

What are the classes of antiarrhythmics?

A

I) block fast Na channels to prolong phase 0 (flecainide)
II) decrease conduction through AV node (beta blockers)
III) voltage gated Na channel antagonists (amiodarone)
IV) voltage gated Ca channel antagonists (verapamil)

84
Q

What are absent A waves on JVP waveform a sign of?

A

AF, sinus tachycardia

85
Q

What are flutter waves on JVP waveform a sign of?

A

Atrial flutter

86
Q

Prominent A waves on JVP waveform are a sign of what?

A

1st degree AV block

87
Q

Cannon A waves on a JVP waveform may be a sign of what 2 pathologies?

A

AV dissociation, VT

88
Q

What are large A waves a sign of on JVP waveform?

A

Tricuspid stenosis, R atrial myxoma, pulmonary HeTN, pulmonary stenosis

89
Q

Absent X waves on JVP waveform are a sign of what?

A

Tricuspid regurg

90
Q

Large CV waves are a sign of what on JVP waveform?

A

Tricuspid regurg, constrictive pericarditis

91
Q

Slow Y waves are a sign of what on JVP waveform?

A

Tricuspid stenosis and R atrial myxoma

92
Q

Rapid Y descent is JVP waveform is a sign of what?

A

Constrictive pericarditis, severe R heart failure, tricuspid regurg, ASD.

93
Q

Absent Y descent is a sign of what on JVP waveform?

A

Cardiac Tamponade

94
Q

Is Pulseless VT a shockable rhythm?

A

YES

95
Q

What is Dressler’s Syndrome? How is it managed?

A

Post MI pericarditis: pleuritic chest pain, pericardial friction rub, pericardial effusion, fever, malaise, leucocytosis, etc.
NSAIDs and 2 weeks of dual antiplatelet therapy (high dose aspirin and something like clopidogrel).

96
Q

What valvular pathology is most commonly associated with rheumatic heart disease?

A

Mitral stenosis, but can be any.

97
Q

What could be happening if someone presents with a NEW onset mitral regurgitation?

A

Papillary muscle rupture and rupture of chorda tendinea.

98
Q

Why can flecanide be used to manage WPW?

A

Blocks transmission across accessory pathway and reduce tachycardia.
Can be used for acute and chronic control.

99
Q

What is Chaga’s Disease?

A

Infection with parasite trypanosoma cruzi, chronic infection leads to dilated cardiomyopathy and mega-oesopahgus.

100
Q

What are the risk factors for a PDA?

A

Female sex, prematurity, neonatal respiratory distress syndrome, maternal rubella, and family hx.

101
Q

How might a baby with a PDA present?
How is this managed?

A

Non-specific respiratory distress, irritability, difficulty feeding, murmur heard at the 2nd ICS on the left sternal edge.
Mx: oral indomethacin or ibuprofen (inhibit prostaglandins to encourage closure)

102
Q

What is pulsus alternans?

A

Alternating strong and weak pulses, marker of heart failure. Caused by changes in systolic pressure caused by reduced ejection fraction.

103
Q

What is the recommended INR for someone with a metallic heart valve?

A

2.5-3.5 (ideal of 3 but higher for mitral valve as there is physiologically more stasis around here)

104
Q

If a thrill is felt what grade does this make the murmur? What does this mean?

A

at least grade 4/6, meaning it is always pathological.

105
Q

Heart failure can lead to pulmonary hypertension, what are the symptoms/signs? How is it investigated? What value is the diagnosed at?

A

SOB, fatigue, exertional syncope, pansystolic murmur, loud S2.
Echo followed by right heart catheterisation.
>20mmHg.

106
Q

What is Takotsubo cardiomyopathy? What are the investigation results?

A

Stress induced cardiomyopathy.
- ECG: ST elevation in V1-6
- Raised cereal troponins (but not increasing)
- No blockage on angiogram
- Echo: hypokinesis and apical ballooning

107
Q

What is the best lipid panel for predicting risk of cardiac disease?

A

Total cholesterol/HDL ratio.
(The lower the ratio the better).

108
Q

What is the NYHA classification?

A

Classifying heart failure by symptoms.
Class I (no symptoms) to IV (unable to do any physical activities, sx at rest)

109
Q

What is the most common arrhythmia to result from an acute MI?

A

VF

110
Q

What complication of an MI, which usually occurs within 24 hours, causes cardiac tamponade and haemodynamic collapse?

A

Left ventricular free wall rupture

111
Q
A

Clinical (27 decks)

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