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4th Year Medicine 2 > Cardiology Part 1 > Flashcards

Cardiology Part 1 Flashcards

1
Q

Describe S1 and S2 heart sounds?

A
  • S1 (normal) – closing of the atrioventricular valves (mitral and tricuspid) – start of systole
  • S2 (normal) – closing of semilunar valves (pulmonary and aortic) – end of systole beginning of diastole
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2
Q

Describe S3 and S4 heart sounds?

A
  • S3 (normal or pathological)- 0.1 secs after S2, caused by rapid ventricular filling (twanging of chordae tendinae), normal in young patients, in older patients can be due to heart failure
  • S4 (always pathological) – directly before S1, always abnormal and is relatively rare. It is due to a stiff/ hypertrophic ventricle. Turbulent flow from atria trying to put blood into a stiff ventricle
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3
Q

What heart sound is always pathological?

A

S4

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4
Q

Two special manuovres to hear heart murmurs better on examination?

A
  • Turn patient to left hand side to hear mitral stenosis better
  • Get patient to lean forwards breathe in out and hold it to hear aortic regurgitation better
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5
Q

What is aortic stenosis and what are common causes?

A

Narrowing of aortic valve means it doesn’t open properly in systole
* The most common cause is aortic stenosis is calcific aortic valvular disease which is essentially degenerative and happens in old age
* Some people have a congenital bicuspid valve – these can undergo calcific changes more quickly than the normal tricuspid valves
* Rheumatic fever can also cause aortic stenosis although this is less common now

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6
Q

Presentation of aortic stenosis?

A
  • There are usually no symptoms until it is moderately severe
  • Symptoms: exercise induced syncope, angina, dyspnoea
  • Auscultation: aortic stenosis causes an ejection systolic murmur that radiates to the carotids and is described as a diamond shaped crescendo decrescendo murmur
  • ECG may show signs of left ventricular hypertrophy
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7
Q

Aortic stenosis murmur?

A
  • Auscultation: aortic stenosis causes an ejection systolic murmur that radiates to the carotids and is described as a diamond shaped crescendo decrescendo murmur
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8
Q

Ejection systolic crescendo decrescendo murmur that radiates to the carotids?

A

aortic stenosis

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9
Q

Management of aortic stenosis?

A
  • All symptomatic patients should get an aortic valve replacement
  • You can either get a valve replaced with a mechanical valve or a tissue valve
  • Mechanical valves last longer so are a better option for younger patients however you need to take warfarin with them
  • Tissue valves don’t last as long but are a better option for elderly as don’t require warfarin
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10
Q

What is aortic regurgitation and causes?

A

valve becomes leaky and there is backflow of blood
* Leaflet damage due to infective endocarditis
* Annulus damage caused by Marfan’s or aortic dissection
* Rheumatic fever was also a cause but this is now less common

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11
Q

Presentation of aortic regurgitation?

A
  • Significant symptoms tend to occur late and not until there is left ventricular failure
  • Symptoms: dyspnoea, pounding of heart, angina pain
  • Exam: collapsing pulse, wide pulse pressure, displaced apex beat (because left ventricle has increased in size)
  • Auscultation: early diastolic murmur heard best by listening over the left sternal edge with the patient leaning forwards
  • CXR may show cardiomegaly
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12
Q

Murmur for aortic regurgitation?

A

early diastolic murmur heard best by listening over the left sternal edge with the patient leaning forwards

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13
Q

early diastolic murmur heard best by listening over the left sternal edge with the patient leaning forwards

A

aortic regurgitation

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14
Q

Management of aortic regurgitation?

A
  • May need to treat underlying cause e.g. if they have an infection treat it
  • ACE inhibitors or beta blockers can help
  • Because symptoms are caused by heart failure, unfortunately if not picked up until this point then surgery will not recover the heart damage that has already occurred
  • Valve replacement could be performed before significant symptoms occur
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15
Q

What is mitral stenosis and causes?

A

Narrowing of the mitral valve means it doesn’t open properly in diastole

Causes
* The most common cause is rheumatic heart disease caused by rheumatic fever which is a result of infection with group A beta haemolytic strep
* Rheumatic fever is less common now meaning so is mitral stenosis

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16
Q

Presentation of mitral stenosis?

A
  • In developed countries symptoms of mitral stenosis will generally not appear until decades after the first attack of rheumatic fever (hence important to take a detailed history)
  • Mitral stenosis causes progressively severe dyspnoea because there is an elevation in left atrial pressure causing back pressure to the lungs and then interstitial pulmonary oedema, might then develop pulmonary hypertension and heart failure
  • Symptoms: dyspnoea, fatigue, palpitations, malar flush (bilateral, cyanotic or dusky pink discoloration over the upper cheeks, to do with the lower cardiac output and different bits of vasoconstriction and vasodilation as a result)
  • Auscultation: mid-diastolic rumbling murmur localised to the apex
    • tapping apex beat and loud S1
  • Those with mitral stenosis are predisposed to AF as they have enlargement of their left atrium
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17
Q

Mitral stenosis murmur?

A

mid-diastolic rumbling murmur localised to the apex

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18
Q

mid-diastolic rumbling murmur localised to the apex

A

mitral stenosis

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19
Q

What type of valve disease are you prone to AF?

A

mitral stenosis as there is enlargement of the left atrium

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20
Q

Management of mitral stenosis?

A
  • Treatment depends on how severe the disease is
  • Need to treat any AF
  • May do valve replacement
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21
Q

What type of valve disease is associated with malar flush?

A

mitral stenosis

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22
Q

What is mitral regurgitation? Causes?

A

The mitral valve does not close properly in systole

Causes
* One of the most common causes is degenerative myxomatous disease which causes valve prolapse (this can occur primary (generally in older people) or secondary to conditions such as Marfans or Ehlers Danlos syndrome)
* Another cause is papillary muscle rupture due to MI
* Infective endocarditis can also cause damage to valve and mitral regurgitation
* Again, rheumatic heart disease is an important cause but less common now due to better treatments

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23
Q

Presentation of mitral regurgitation?

A
  • May not get symptoms for many years
  • Symptoms: palpitations, dyspnoea and orthopnoea, fatigue
  • Auscultation: pansystolic murmur which may radiate to the axilla
  • Exam: displaced apex beat
  • ECG may show left ventricular hypertrophy
  • CXR may show cardiomegaly
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24
Q

Murmur for mitral regurgitation?

A

pansystolic murmur which may radiate to the axilla

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25
Q

Management of mitral regurgitation?

A
  • It can be managed conservatively if mild and monitored
  • If there is heart enlargement surgical valve replacement is generally done and also if patients are symptomatic surgery will be done
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26
Q

pansystolic murmur that may radiate to the axilla?

A

mitral regurgitation

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27
Q

Describe the 6 grades of murmurs?

A

1 - difficult to hear
2- quiet
3- easy to hear
4- easy to hear with a palpable thrill
5- easy to hear with stethoscope barely touching chest
6- can hear with stethoscope basically off the chest

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28
Q

Stenosis causes
Regurgitation causes

A

stenosis causes hypertrophy because the atria or ventricles are pushing really hard to get blood through
regurgitation causes dilatation as back flow of blood stretches the muscle

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29
Q

Tapping apex beat and loud S1?

A

mitral stenosis

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30
Q

Investigation to diagnose valvular problems?

A

echocardiography

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31
Q

Explain what AF is?

A
  • Arrhythmia where there is contraction of the atria that is uncoordinated, rapid and irregular
  • This results in irregularly irregular ventricular contractions, tachycardia, heart failure due to poor filling of the ventricles during diastole, risk of stroke
  • There is a tendency for the blood to collect in the atria and form blood clots which can embolise to the brain and cause a stroke
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32
Q

Who gets AF?

A
  • Mitral stenosis can cause AF
  • Ischaemic heart disease
  • Sepsis
  • Hyperthyroidism
  • Hypertension
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33
Q

Define paroxysmal AF?

A
  • Paroxysmal AF – when a patient has 2 or more episodes of AF that terminate spontaneously, such episodes last less than 7 days (typically < 24 hours)
34
Q

Define persistent AF?

A
  • If the arrythmia is not self-terminating the term persistent AF is used
35
Q

Define permanent AF?

A
  • In permanent AF there is continuous atrial fibrillation which cannot be cardioverted or attempts to do so are deemed inappropriate
36
Q

Presentation of AF?

A
  • May be asymptomatic and picked up incidentally
  • Palpitations
  • SOB
  • Syncope
  • Chest pain
  • Signs: irregularly irregular pulse, signs of other conditions e.g. mitral stenosis murmur, signs of thyroid disease etc.
37
Q

Investigations for AF?

A
  • ECG (allows you to differentiate between AF and ventricular ectopics which can also cause an irregularly irregular pulse)
  • May need to look for underlying cause in some cases e.g. TFTs
38
Q

Aspects of AF management?

A

rate and rhythm control
anticoagulation to reduce stroke risk

39
Q

Rate control should be offered as first line in AF except in

A
  • Whose AF has a reversible cause
  • Who have heart failure thought to be primarily caused by AF
  • With new onset AF
  • With atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
  • For whom a rhythm control strategy would be more suitable based on clinical judgement

(explanation: rhythm control may effectively reduce irreversible AF remodelling and prevent AF deaths, heart failure and strokes in high risk patients, so if the AF is reversible, new or they have heart failure rhythm control will be better)

40
Q

Rate control drugs in AF?

A
  1. Beta blocker
  2. Diltiazem (CCB)
  3. Digoxin
41
Q

Describe rhythm control in AF?

A
  • This involves cardioversion (single event used to convert to sinus rhythm) and/ or long term medical control to keep the heart at a constant rhythm
  • Cardioversion can be electrical or pharmacological
  • Pharmacological cardioversion may involve flecanide or amiodarone (if structural heart disease present)
  • Long term rhythm control can be done with a beta blocker, dronedarone or amiodarone
42
Q

Describe long term anticoagulation to reduce stroke risk in AF?

A

• For most people the benefit of anticoagulation outweighs the risk of bleeding
• Offer anticoagulation with a DOAC to people with AF and CHADVASc score of 2 or above e.g. apixaban, rivaroxaban, edoxaban
• HAS BLED score can be used to assess risk of haemorrhage

43
Q

Radiofrequency ablation is good for arrhythmias caused by _______

A

re-entrant pathways
(as you ablate the pathway causing the arrhythmia)

44
Q

A normal PR interval is?

A

0.12 to 0.2 seconds (3-5 small boxes)

45
Q

Risk factors for primary hypertension?

A
  • Increasing age
  • Family history
  • Physical inactivity
  • Male
  • Obesity
  • Diet high in fats and salts
  • Excessive alcohol intake
  • African American Descent
46
Q

Definitions of hypertension and stages?

A
  • Simply, hypertension is BP > 140/90
  • Generally, for a diagnosis patients would need to do either ambulatory BP monitoring or home BP monitoring with an average taken
  • More than 140/90 = stage 1
  • More than 160/100 = stage 2
  • More than 180/120 = stage 3
47
Q

Initial diagnosis of hypertension?

A

All patients diagnosed with hypertension should have their cardiovascular risk assessed using an appropriate calculator (NICE recommend QRISK)
In all patients with hypertension offer to:
1. Send a urine sample to test for albumin: creatinine ratio and test for haematuria using a reagent strip
2. Take a blood sample to measure HbA1c, electrolytes, creatinine, eGFR, total cholesterol and HDL cholesterol
3. Examine fundi for evidence of hypertensive retinopathy
4. Arrange for 12 lead ECG to be performed

48
Q

Management of hypertension, who gets pharmacological treatment?

A

All patients should be given lifestyle advice

Who should start anti-hypertensive treatment?
- Adults of any age with persistent stage 2 hypertension
- Consider it in those under 80 with stage 1 who have target organ damage, established CVS disease, renal disease, diabetes or an estimated 10 year cardiovascular disease risk of 10% or more
- There are further guidelines on other situations to start anti-hypertensive therapy found here: https://www.nice.org.uk/guidance/ng136/chapter/recommendations#stage-2-hypertension

49
Q

Step wise pharmacological treatment of hypertension?

A

STEP 1:

Offer an ACE inhibitor (or ARB) to:
Adults who have T2DM of any family origin (including black African/ african-carribbean)
Any adults under 55
If an ACE inhibitor is not tolerated due to a cough then offer an ARB
consider ARBs may be better in those who are black african/ african Caribbean

Offer a CCB to:
Adults over age 55 who do not have T2DM
Adults who are black African/ African-caribbean, of any age (unless they have T2DM)
If a CCB is not tolerate because of oedema offer a thiazide like diuretic

STEP 2:
Offer the opposite drug e.g. those on ACEi offer CCB and vice versa

STEP 3:
Offer combination of ACEi, or ARB, CCB and/ or thiazide diuretic

STEP 4:
This is considered as resistance hypertension
Consider spironolactone for those with blood potassium 4.5 mmol/l or less
Consider an alpha or beta blocker if potassium more than 4.5 mmol/l

50
Q

Diagnosis of hypertension with T2DM any age?

A

ACEi

51
Q

Caucasian adult under 55 diagnosis of hypertension?

A

ACEi

52
Q

ACEi not tolerated due to cough?

A

offer ARB

53
Q

Diagnosis of hypertension in a caucasian adult over 55 who does not have T2DM?

A

CCB

54
Q

Black african who has hypertension but also T2DM?

A

ACEi/ ARB

55
Q

Black african who has hypertension and is 45?

A

CCB - they get CCB at any age

56
Q

If CCB is not tolerated?

A

(often due to oedema)
offer a thiazide diuretic

57
Q

Resistant hypertension, potassium 4.5mmol/l or less?

A

offer spironolactone

58
Q

Resistant hypertension, potassium over 4.5mmol/l?

A

alpha blocker or beta blocker

59
Q

Define malignant/ accelerated hypertension?

A
  • This is a medical emergency
  • Need a same day referral if: clinic BP 180/120 or higher, with signs of retinal haemorrhage or papilloedema of life-threatening symptoms such as new onset confusion, chest pains, signs or heart failure or AKI
60
Q

Management of malignant hypertension?

A
  • Treatment of malignant hypertension involves sodium nitroprusside, labetalol, GTN and nicardipine
  • Need to be careful not to drop the BP too quickly as this may result in inadequate perfusion
61
Q

Describe secondary hypertension and causes?

A

High blood pressure caused by another condition – to treat this you need to treat the underlying cause

More common causes of secondary hypertension:
- Renal parenchymal disease
- Renal artery stenosis
- Primary aldosteronism
- Pregnancy induced hypertension

Less common causes:
- Phaeochromocytoma
- Cushings syndrome

62
Q

Explain what acute left ventricular failure is?

A
  • This occurs when an acute event results in the left ventricle being unable to move blood efficiently through the left side of the heart
  • When blood cannot flow efficiently through the left side of the heart there is a backlog of blood in the left atrium, pulmonary veins and the lungs causing pulmonary oedema
63
Q

Triggers of acute left ventricular failure?

A

Acute left ventricular failure is often the result of decompensated chronic heart failure (i.e. one of these triggers occurs in someone already with chronic heart failure pushing them into acute failure)
- Iatrogenic – aggressive IV fluids in a frail elderly patient with chronic heart failure
- Myocardial infarction
- Arrythmias
- Sepsis
- Hypertensive emergencies

64
Q

Presentation of acute left ventricular failure?

A
  • Acute shortness of breath on lying flat
  • Cough with frothy white or pink sputum
  • Look and feel unwell
  • Tachypnoeic and tachycardiac
  • Sometimes S3
  • Low oxygen sats
  • Bilateral basal crackles on auscultation
65
Q

CXR of pulmonary oedema?

A
  • Alveolar oedema (bat wings)
  • Kerley B lings (interstitial oedema)
  • Cardiomegaly
  • Dilated upper zone vessels
  • Pleural effusions
66
Q

Cardiomegaly on CXR can be defined as?

A

diameter of the heart is greater than or equal to 50% of the transverse diameter of the chest

67
Q

Management of acute left ventricular failure and pulmonary oedema?

A

SODIUM
S – sit up
O- oxygen
D- diuretics (IV furosemide)
I - intravenous fluids should be stopped
U- underlying causes identified/ treated
M- monitor fluid balance

If still struggling could give CPAP

68
Q

What is heart failure?

A
  • The state in which the heart is unable to pump blood at a rate commensurate with the requirements of tissues or only at a high pressure
  • Can be due to impaired contraction (systolic) or impaired relaxation (diastolic)
69
Q

Symptoms and signs of heart failure?

A

Symptoms:
* Shortness of breath
* Paroxysmal nocturnal dyspnoea (waking up suddenly short of breath- improves on sitting up and walking around)
* Orthopnoea
* Reduced exercise tolerance and fatigue
* Ankle swelling
* Tenderness in abdomen (due to hepatosplenomegaly)
* Complaints of swollen abdomen

Signs:
* Ankle swelling
* Elevated JVP
* Crackles at lung bases on auscultation
* 3rd and 4th heart sounds
* Pleural effusions
* Tender hepatosplenomegaly

70
Q

Investigations for heart failure?

A
  • BNP testing is very sensitive for heart failure
  • ECG should be performed
  • Blood tests and urinalysis (renal function, liver function, thyroid, lipids, HBA1c, FBC)
  • Patients should generally be referred for specialist assessment and ECHO to confirm diagnosis
71
Q

Management of heart failure?

A

Lifestyle advice:
* Diet
* Discuss fluid and salt intake and potential restrictions
* Stop smoking
* Regular exercise
* Make sure vaccinations are up to date and annual pneumococcal and flu

Pharmacological Management:
* Diuretics should be given to improve symptoms of fluid overload (usually a loop and usually furosemide)
* Digoxin can help improve symptoms by increasing cardiac contractility (this is a really toxic drug though and has a narrow therapeutic window)
* Beta blockers help improve survival
* ACE inhibitors help improve survival
* Aldosterone antagonists e.g. spironolactone help improve survival
* Vasodilators e.g. nitrates help improve survival
* Ivabradine helps improve survival

In general: ACEi, beta blocker and aldosterone antagonist to improve survival plus digoxin and furosemide to improve symptoms

Other options:
* Revascularization
* Cardiac resynchronization therapy
* Transplant

72
Q

3 drugs that improve survival in heart failure?

A

ACEi, beta blocker and aldosterone antagonist

73
Q

If indication for both antiplatelet and anticoagulant?

A

just give the anticoagulant - reduces risk of bleeding

74
Q

When should a patient who has an arryhthmia be cardioverted?

A

when they are haemodynamically unstable

75
Q

Explain the difference between sychronised and unsynchronised shocks and when you use them?

A

synchronised shocks involve timing the shock with the ECG pattern so it is delivered in the right place - this should be done in all supraventricular tachycardias and VT with a pulse (ie usually situations when the patient is awake)

Defibrillation refers to unsychronised shocking. Unsynchronised shocks should be used in pulseless VT and VF.

76
Q

Explain what external pacing is and when it is used?

A

AKA transcutaneous pacing
it is a machine which you can deliver controlled pulses of electric current
it is used for symptomatic bradycardia if atropine fails

77
Q

Aspirin dose for prevention vs acute situations?

A

75mg for prevention, 300mg for acute situation

78
Q

Explain what bundle branch block is and normal conduction in heart?

A

normal conduction = SA node - atria - AV node- Bundle of his - left and right bundle branches - purkinje fibres - ventricles

if there is a block in one of the bundle branches there will be a delay in that ventricle contracting as the electrical signal will go around all the other ventricle first before travelling to that ventricle

79
Q

Causes of BBB?

A

most BBB is caused by fibrosis or scarring of the BBB

80
Q

In lead 2 BBB will cause?

A

widened QRS complex as there is a delay in the second ventricle contracting

81
Q

How to tell BBB on ECG?

A

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

82
Q

Define ST elevation?

A

 More than 1mm ST elevation in 2 adjacent limb leads, or > 2mm ST elevation in at least 2 contiguous precordial leads (e.g. v1, v2 etc)
 New onset bundle branch block

 1 little box = 1mm
 Big box = 5mm
 On the calibration – that should be 10mm – 1cm

4th Year Medicine 2 (14 decks)

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