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Year 5 Medicine for Finals > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What causes the first heart sound, S1?

A

Closing of the AV valves - mitral/tricuspid

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2
Q

What is happening in the heart after the first heart sound?

A

Systole - contraction of the ventricles pumping the blood to the lungs and body

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3
Q

What causes the second heart sound?

A

Closure of the aortic/pulmonary valves

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4
Q

What sometimes causes a third heart sound?

A

The 3rd heart sound is during the rapid filling phase in the the atria

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5
Q

What is the 4th heart sound sometimes heard?

A

That is atrial systole

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6
Q

Why is a 4th heart sound of atrial systole sometimes heard and can it be a non-pathological sign?

A

Atrial contraction into a non-compliant or hypertrophied ventricle. It is low pitched, and always abnormal.

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7
Q

What are the causes of a 4th heart sound? (4)

A
  1. Heart failure
  2. MI
  3. Cardiomyopathy
  4. Hypertension (pressure overload)
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8
Q

What is the 3rd heart sound, is it always pathological?

A

It is a ventricular sound - blood rushing in during the rapid filling phase of early diastole. Stiff or dilated ventricles suddenly reaches its elastic limit and decelerates the incoming rush of blood. It can be normal in children and young adults up to age 30.

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9
Q

What are the causes of a 3rd heart sound other than young age? (6)

A
  1. Heart failure
  2. MI
  3. Cardiomyopathy
  4. Hypertension (pressure overload)
  5. Mitral and aortic regurgitation (volume overload) - leaky valves - common!
  6. Constrictive pericarditis - uncommon - but causes restriction so not allowing diastole due to fibrotic membrane
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10
Q

In a CV examination, what do you look for on inspection?

A
  1. Anaemia
  2. Cyanosis
  3. Breathlessness
  4. Is the patient unwell looking?
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11
Q

What are the 5 signs of endocarditis? + 3 rarities

A

2 in the hands: clubbing & splinter haemorrhages
1 in the heart: changing murmur
2 in the abdomen: splenomegaly, microscopic haematuria
(plus all the rare ones - Oslers nodes, Janeway lesions, Roth spots)

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12
Q

What are the 4 stages of clubbing?

A
  1. Increased fluctuancy of the nail bed
  2. Loss of angle
  3. Increased curvature of the nail
  4. Expansion of the terminal phalanx
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13
Q

Before reaching the praecordium, what needs to be done in a CV examination? (7)

A

Check for:

  1. Anaemia, cyanosis, breathlessness
  2. Hands for clubbing/splinter haemorrhages
  3. Pulse - rate, rhythm, character, volume
  4. Collapsing pulse test
  5. Ask for or measure blood pressure
  6. Neck for collapsing pulse
  7. JVP
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14
Q

If there is a collapsing pulse in the neck, what is this sign called and what does it suggest?

A

Corrigan’s sign/pulse - aortic regurgitation

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15
Q

After the peripheral examination, what needs to be done for a CV examination of the praecordium? (7)

A
  1. Look for scars (midline sternotomy scar for example)
  2. Apex beat: position and character
  3. Left parasternal area (for right ventricular impulses)
  4. Check for thrills
  5. Auscultation - bell and diaphragm from apex to neck
  6. Patient on left side with bell for mitral stenosis
  7. Patient sitting forward, at end of expiration, using the diaphragm - for aortic regurgitation
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16
Q

What are the causes of AF? (5)

A
  1. Ischaemic heart disease
  2. Rheumatic heart disease
  3. Thyrotoxicosis
  4. Alcohol
  5. Hypertension
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17
Q

What are the two main possible explanations for an irregularly irregular pulse and how would you distinguish them without an ECG?

A
  1. AF
  2. Multiple ectopics
    - exercise reduces ectopics but in AF the heart rate will increase but remain irregular
    (another cause of an irregular pulse is heart block, but they will have bradycardia)
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18
Q

How do you assess to see if AF is well controlled?

A

Listen with your stethoscope to the apical beat and it should be less than 80 if it is well controlled

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19
Q

Why is there sometimes a difference between the pulse rate taken at the wrist and the heart rate timed at the apex?

A

This is a pulse deficit - loss of diastolic filling time with fast ventricular rates. This is why rate control is important in AF, as if it is less than 80 then there should be no pulse deficit and every beat counts, but if there is tachycardia there is insufficient diastolic filling time to create a cardiac output - so there is no palpable pulse for that beat, but just enough blood flow to move the valves, so heart sounds are heard

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20
Q

What is a pulse deficit - just for revision?

A

When the ventricular rate is so fast, there is not enough time for diastolic filling, so enough blood is in to create a heart sound for the blood passing the valves, but not enough cardiac output to supply peripherals - so no peripheral pulse. If the heart is slowed down, then it gives enough time for diastole, and filling of the ventricles. Hence why rate control is vital in AF.

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21
Q

What is the first line medication for AF in terms of rate control?

A

Beta blocker e.g. bisoprolol

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22
Q

If the first line medication for AF is contraindicated, what is second line?

A

Diltiazem - if the patient is active, digoxin if they are sedentary

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23
Q

What is the third line treatment for rate control of AF?

A

Dual therapy e.g. bisoprolol + digoxin

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24
Q

What are the indications for rhythm control of AF?

A
  1. New onset within the last 48 hours
  2. LVF primarily due to AF
  3. Reversible causes e.g. thyrotoxicosis
  4. Clinically indicated e.g. young person
  5. Symptoms despite attempted rate control
  6. Acutely unwell
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25
Q

What is the rhythm control treatment for AF?

A

Electrical or chemical cardioversion e.g. flecainide

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26
Q

After cardioversion, what is the rhythm control prophylaxis give to some people e.g. those with paroxysmal AF? (what is first line)

A

First line: bisoprolol

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27
Q

What is the second line rhythm control prophylaxis given to people who had cardioversion or paroxysmal AF? (3 drugs dependent on LV dysfunction)

A
  1. Amiodarone if LV dysfunction
  2. Dropedarone if no LV dysfunction
  3. Flecainide if no CHD or LV dysfunction
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28
Q

When is flecainide 50mg BD prescribed to someone who has experienced AF?

A

“pill in pocket” - if no other heart disease and infrequent episodes, with a normal pulse and BP.

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29
Q

In addition to rhythm and/or rate control, what other medication needs to be prescribed to pretty much everyone with AF?

A

Anti-coagulation

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30
Q

What are the indications for use of warfarin rather than a DOAC? (2)

A
  1. Mitral stenosis

2. Metal valve

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31
Q

In a patient with AF on warfarin, what is the level of INR looking to achieve?

A

2-3 - target 2.5

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32
Q

In a patient with a prosthetic mitral valve, what is the aim for INR?

A

3-4

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33
Q

What are the causes of aortic stenosis?

A
  • Degenerative calcification*
  • it is always this, but happens quicker if you have:
    1. Congenital bicuspid valve with degenerative changes
    2. Rheumatic heart disease
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34
Q

What are the signs of aortic stenosis?

A
  1. Slow rising pulse
  2. Low volume pulse with low pulse pressure
  3. Apex beat forceful but not displaced (pressure overload)
  4. Ejection systolic murmur
  5. High pitched in the carotids
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35
Q

What happens to the left ventricle with aortic stenosis?

A

It becomes hypertrophied due to the pressure overload

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36
Q

In addition to aortic stenosis, what are the other causes of left ventricular hypertrophy (or pressure overload to the left ventricle)?

A
  1. Hypertension
  2. Coarctation of the aorta
  3. Hypertrophic cardiomyopathy
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37
Q

What is the definitive treatment for aortic stenosis?

A

Valve replacement

38
Q

How is the severity of aortic stenosis judged?

A

Level of exercise induced; syncope, angina and breathlessness

39
Q

What is the difference between aortic sclerosis and aortic stenosis?

A

Aortic stenosis is fusion of the commisures - valve leaflets fuse and you get the signs associated e.g. rising pulse, ejection systolic murmur radiating to the neck, powerful apex beat, whereas aortic sclerosis is thickening of the valve leaflets, this doesn’t cause a murmur that radiates to the carotids and there is no evidence of left ventricular hypertrophy on ECG.

40
Q

What are the causes of mitral regurgitation? (3 groups with causes)

A
  1. Leaflet: congenital, endocarditis, degenerative
  2. Papillary muscle and chordae: mitral valve prolapse, ACS (infarcts papillary muscle), Marfan’s syndrome
  3. Annular dilatation: cardiomyopathy, ischaemic heart disease with heart failure (valve ring increases with size, and therefore can’t close properly)
41
Q

What are the signs of mitral regurgitation?

A
  1. Apex beat usually displaced
  2. Quiet first heart sound
  3. Pansystolic murmur radiates loudly to axilla
  4. Second heart sound not heart
    sound: BURRRRRRRR
42
Q

What is the treatment for mitral regurgitation? - for mild/moderate and then severe

A

Mild and moderate: ACE inhibitors (reduces total peripheral resistance), diuretics +/- anticoagulants
Severe: valve repair

43
Q

What are the differences between an aortic stenosis murmur and a mitral regurgitation murmur?

A

Both are systolic but…
AS: ejection systolic with radiates to the carotids, with a powerful non-displaced apex
MR: pansystolic murmur at the apex which radiates to the axilla, with a displaced apex.

44
Q

What are the causes of mitral stenosis? (5)

A
  1. Rheumatic fever
  2. SLE
  3. Rheumatoid arthritis
  4. Carcinoid syndrome
  5. Infective endocarditis
45
Q

What are the signs of mitral stenosis?

A
  1. Malar flush - due to pulmonary hypertension
  2. AF - atrium bears the brunt of the stenosis
  3. Apex beat tapping in quality - loud first heart sound
46
Q

Why is there a loud first heart sound in mitral stenosis?

A

There is a high left atrial pressure keeping the valve open until late in diastole - then systole slams it shut

47
Q

What is the sound heard in mitral stenosis?

A

LUB (loud first heart sound) De Derrrrrr (diastolic rumbling, low pitched murmur)

48
Q

What can be seen on a CXR in someone with mital stenosis?

A

Aortic appendage - on the left side (left side of patient) - there should be a concave area which is protruding, more prominent left atrium. This is sometimes operated on and a plastic watchmen device placed into the appendage to occlude it

49
Q

Why does the atrium enlarge with mitral stenosis?

A

As the pressures increase in the atrium, and the atrium is very thin walled, so blows up like a balloon

50
Q

What happens in the progress of mitral stenosis, once pulmonary hypertension occurs?

A

You get cor pulmonale –> pulmonary arerial hypertension –> right ventricular hypertrophy –> tricuspid regurgitation –> right heart failure

51
Q

Why would someone with severe mitral stenosis get a raised JVP, oedema and ascites?

A

Due to right heart failure - increased pressure from the mitral stenosis leads to pressure on the pulmonary arteries, leading to right ventricular hypertrophy and tricuspid regurgitation

52
Q

What is the treatment for mitral stenosis?

A

Mild - medical treatment; anticoagulants, diuretics, rate control of AF
Moderate - trans-septal valvuloplasty or valve replacement
Severe (valve area reduced to 1.5cm) - valve replacement

53
Q

What is a potential problem with repairing mitral stenosis with valvuloplasty?

A

Causing mitral regurgitation

54
Q

What are the signs of aortic regurgitation? (5)

A
  1. Collapsing pulse - Corrigans pulse
  2. Collapsing pulse at neck - Corrigan’s sign
  3. De Mussets sign - head bobbing
  4. Diastolic murmur ‘lub taaaaarr’
  5. Apex beat displaced
55
Q

What are the causes of aortic regurgitation? (5)

A
  1. Rheumatic heart disease
  2. Endocarditis
  3. Ank spond
  4. Tertiary syphilis
  5. Marfans syndrome
56
Q

How can you increase the volume of a murmur?

A

Get the patient to exercise

57
Q

What type of murmur do mechanical prosthetic heart valves cause?

A

Ejection systolic due to turbulent flow over the ping pong ball in systole.
There is a loud opening click as the ball hits the cage, then the turbulent flow, and then the closing sound as ball engages with the valve rim

58
Q

What is the mnemonic for complications of valve replacement?

A 
POSH valve
P - paravalvular leak 
O - obstruction 
S - subacute bacterial endocarditis
H - haemolysis due to turbulence 
Valve failure - e.g. rupture of the commisures with regurgitation or calcification with stenosis
59
Q

If someone with ACS has positive troponins, what are the two potential diagnoses?

A

STEMI or NSTEMI

60
Q

What ECG changes can be seen suggestive of ACS? (5)

A
  1. T wave inversion
  2. ST depression
  3. ST elevation
  4. Q waves
  5. New LBBB
61
Q

What are the independent risk factors for ACS/MI? (6)

A
  1. Smoking
  2. Hypertension
  3. Diabetes
  4. Hyperlipidaemia
  5. Family history
  6. CKD
62
Q

When should you suspect ACS? (8)

A
  1. If the pain occurs at rest
  2. Lasts more than 15 minutes
  3. Increases in frequency
  4. Severe
  5. Associated with nausea, vomiting, sweating
  6. Non-resolving with nitrates
  7. Central, retrosternal, band-like constriction
  8. Radiation to the jaw, neck, shoulder, arm
63
Q

What initial investigations are performed in someone with suspected ACS? (7)

A
  1. FBC (anaemia can cause cardiac ischaemia)
  2. U&Es (impaired renal function can cause false positive elevated troponin, also electrolytes causing arrhythmias)
  3. Glucose - diabetic?
  4. LFTs - (hepatic impairment relative contraindication for ticagrelor)
  5. Lipids
  6. Serial troponins
  7. ECG to assess ichaemic changes
64
Q

What does a Q wave on an ECG indicate - and what can this increase the risk of?

A

A Q wave implies a full thickness transmural infarct - which increases the risk of acute pericarditis

65
Q

What is the treatment for a STEMI? (4)

A
  1. Oxygen (if sats <94% or acutely unwell)
  2. Morphine & metoclopramide
  3. Aspirin 300mg
  4. Nitrates sublingually (not if aortic stenosis/severely hypotensive)
66
Q

What is the long-term medical treatment for STEMI?

A 
A - ACE inhibitors
B - beta blockers
C - cholesterol lowering (statins)
D - dual antiplatelet therapy 
E - ECHO to assess left ventricle
67
Q

In terms of antiplatelet therapy and STEMI, what is the order of events including PCI? (4)

A
  1. Aspirin 300mg
  2. Clopidogrel 300mg OR ticagrelor 180mg
  3. PCI
  4. Maintenance - aspirin 75mg daily indefinitely AND clopidogrel 75mg or ticagrelor 90mg for at least one year
68
Q

In new LBBB on an ECG, where has the thrombosis often occured?

A

In the septal branch of the right coronary artery (ST segments cannot be meaningfully assessed if LBBB present)

69
Q

For all other ACS - unstable angina and NSTEMI, what is the management? (6)

A
  1. Oxygen is desaturating
  2. Morphine & metoclopramide
  3. Aspirin 300mg
  4. GTN
    - then risk stratify - if intermediate/higher risk -
  5. Fonaparinux 2.5mg s/c daily
  6. Ticagrelor or clopidogrel and consider PCI within 72 hours of admission
70
Q

What is the mnemonic/sentence to remember complications of an MI?

A

Sudden death on PRAED street
- sudden death
P - pump failure (cardiogenic shock)
R - rupture of papillary muscle or septum
A - aneurysm and arrhythmias
E - embolism
D - dressler’s syndrome (and much more commonly - early acute pericarditis)

71
Q

What question is important to ask if there is a chance of acute pericarditis post MI?

A

Has your pain changed?

- often morphine won’t work for pericarditis and ibuprofen is more effective

72
Q

What are the qualities of pericardial pain? (3)

A
  1. Sharp and worse on inspiration
  2. Retrosternal and radiates to the left shoulder
  3. Worse lying flat and eased by sitting up
73
Q

In someone with acute LV failure or pulmonary oedema, how do they appear on inspection? (5)

A
  1. Unwell - pale and grey
  2. Cold, clammy peripheries - cyanosed
  3. Frothy blood stained sputum in pot
  4. Orthopnoeic using accessory muscles
  5. May have wheeze
74
Q

What are the signs of acute pulmonary oedema? (5)

A
  1. Sinus tachycardia or AF
  2. Hypotensive
  3. Cardiomegaly signs - displaced apex beat
  4. Third or fourth heart sounds
  5. Right sided or bilateral pleural effusions
75
Q

On a CXR of someone with LVF or pulmonary oedema, what will be seen? (4)

A
  1. Blunting of costophrenic borders
  2. Cardiomegaly
  3. Diffuse mottling of lung fields
  4. Pleural effusions/fluid in fissures
76
Q

What are the NICE guidelines for investigations for left ventricular heart failure? (8)

A
  1. FBC
  2. U&Es
  3. CBG to exclude underlying diabetes
  4. B-type natriuretic peptide
  5. ABG - acute respiratory acidosis
  6. Troponin
  7. ECG - evidence of arrhythmia/heart block/ischaemia
  8. ECHO
77
Q

To summarise NICE investigations for acute left ventricular heart failure, list them in groups?

A
  1. Bloods - FBC, U&Es, BNP, troponins, glucose, VBG or ABG
  2. ECG
  3. ECHO
78
Q

What is the mnemonic for the causes of acute left ventricular heart failure?

A 
CHAMP
C - coronary syndrome
H - hypertensive emergency
A - arrhythmia
M - mechanical e.g. acute valve leak, VSD, LV aneurysm 
P - pulmonary embolus
79
Q

What is the treatment for acute left ventricular heart failure AKA acute pulmonary oedema?

A 
OMFG
- sit the patient up 
- oxygen 15 L high floe
- morphine &amp; metoclopramide
- furosemide 40mg IV
- GTN spray 
...consider ionotropes e.g. dobutamine if systolic <90mmHg
...consider ITU care with CPAP if not improving
80
Q

What are the ECG changes for someone with hyperkalaemia? (4)

A
  1. Low flat P waves
  2. Broad bizarre QRS
  3. Slurring into ST segment
  4. Tall tented T waves
81
Q

What are the indications for a permanent pacemaker? (4)

A
  1. Sino-atrial disease e.g. sick sinus syndrome
  2. AV nodal disease - symptomatic second, and third degree heart block
  3. Atrial fibrillation with a slow ventricular rate
  4. Cardiac resynchronisation therapy for heart failure
    (mnemonic = SCAR)
    sick sinus syndrome
    complete heart block
    AV nodal ablation/AF
    Resynchronisation therapy
82
Q

What can be the complications of pacemaker insertion?

A
  1. Pulse generator - haematoma, infection, skin erosion, device failure
  2. Venous access - pneumothorax, air embolus
  3. Leads - lead displacement/fracture, venous thrombosis, endocarditis, cardiac perforation
83
Q

What investigations are performed if infective endocarditis is suspected? (5)

A
  1. FBC (raised WCC)
  2. CRP/ESR
  3. Urine dip and microscopy (microscopic haematuria)
  4. Blood cultures X3
  5. Transthoracic +/- transoesophageal ECHO
84
Q

Which organisms commonly cause endocarditis? (3)

A
  1. Strep viridans
  2. Staph aureus
  3. Enterococci
85
Q

What is the treatment for infective endocarditis if it is caused by strep viridans?

A

Penicillin and gentamicin IV for at least 2 weeks - then PO for a further month

86
Q

When would someone on antibiotic therapy for infective endocarditis, be required to have a longer course? (3)

A
  1. Non-strep cause
  2. Prosthetic valve
  3. Local complications e.g. abscess, fistula
87
Q

What criteria is used for the diagnosis of infective endocarditis?

A

Modified Dukes criteria - 2 major OR 1 major and 3 minor

Minor= predisposing factors, fever, vascular lesions, single blood culture, peripheral manifestations e.g. Oslers nodes, Roth spots, glomerulonephritis

Major = 2 positive blood cultures, positive ECHO, new valve regurgitation

88
Q

On CV examination, what are the reasons for being unable to palpate the apex beat? (4 DOPE)

A 
DOPE
dextrocardia
obesity
pericardial effusion
emphysema
89
Q

What are the finishing pieces to look for on a CV examination?

A

Sacral and peripheral oedema and auscultate the lung bases

90
Q

What is the New York Heart Association grading for heart failure - what does it assess?

A

Functional capacity

91
Q

What is the difference in sounds between the older Starr-Edwards valves and the newer bi-leaflet prosthesis?

A

The SE ones have both a loud first and a loud second heart sound, whereas the newer ones just have a loud second heart sound

Year 5 Medicine for Finals (4 decks)

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