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Medical conditions > Cardiovascular > Flashcards

Cardiovascular Flashcards

MLA - aortic and mitral valve diseases

1
Q

Describe the murmur heard in a patient with aortic stenosis

A
  • Ejection systolic.
  • Crescendo-decrescendo (‘diamond-shaped’), meaning it gets louder and then goes quiet.
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2
Q

Describe the murmur heard in aortic regurgitation.

A
  • Early diastolic,
  • High-pitched and blowing in nature (decrescendo)
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3
Q

Describe the murmur heard in mitral stenosis.

A
  • Mid diastolic murmur.
  • Low-pitched and rumbling.
  • Opening snap.
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4
Q

Describe the murmur heard in mitral regurgitation.

A

Pansystolic (a.k.a. holosystolic). High-pitched and blowing.

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5
Q

What can a collapsing (Corrigan’s) pulse indicate?

A

Aortic regurgitation or PDA.

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6
Q

2 clincal signs of aortic regurgitation.

A
  • Early diastolic murmur
  • Wide pulse pressure/ collapsing pulse
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7
Q

Clinical signs of mitral stenosis

A
  • Flushed face (due to reduced cardiac output) and weak pulse
  • Irregular pulse (atrial fibrillation)
  • Signs of pulmonary hypertension
  • RV heave (right ventricular hypertrophy)
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8
Q

Which valve abnormality increases the risk of atrial fibrillation?

A

Mitral stenosis.

Atrial enlargement causes AF

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9
Q

Radiation into carotids is suggestive of ____________.

A

Aortic stenosis.

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10
Q

What might a radio-radial delay indicate?

A

Aortic coarctation
Subclavian stenosis
Aortic dissection
Aneurysm

Mechanism: the narrowing of one of the vessels affects blood flow to one arm more than the other.

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11
Q

S1 sound signifies….

A

Mitral and tricuspid valve closure.

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12
Q

Are left-sided murmurs easier to hear on expiration or inspiration?

A

Expiration.

‘RILE’ = Right -inspiration, Left - expiration.

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13
Q

How does aortic stenosis affect blood pressure and pulse character?

A

Slow-rising pulse (usually carotids - diminshed and delayed upstroke) and Narrowed pulse pressure, often defined as less than 25-30 mmHg.

Occurs due to reduced stroke volume and increased afterload from the narrowed aortic valve, resulting in low systolic and relatively higher diastolic blood pressures.

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14
Q

Mitral stenosis murmur accentuation manoeuvre.

A

Left lateral decubitus position. Expiration.

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15
Q

What is usually the first symptom of aortic stenosis?

A

Exertional dyspnoea.

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16
Q

Classical triad of aortic stenosis symptoms.

A

‘SAD’: syncope, angina, and dyspnoea (exertional)

Other symptoms: palpitations, fatigue, heart failure symptoms.

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17
Q

How does dyspnoea present in aortic regurgitation and mitral valve disease?

Think positional and timing

A
  • SOB
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea (PND)

Due to pulmonary congestion

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18
Q

Most important RFs for valve disease

A
  1. Age
  2. History of rheumatic fever
  3. History of infective endocarditis
  4. Congenital heart defects / valve atresia
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19
Q

Causes of mitral stenosis.

A
  • Rheumatic fever. (most common) —can also cause tricuspid stenosis
  • Mitral annular calcification.
  • Autoimmune conditions (e.g., SLE).
  • Congenital mitral valve dysfunction.
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20
Q

Causes of mitral regurgitation. (List 2 specifc ones)

A
  • Mitral valve prolapse.
  • Papillary muscle dysfunction or rupture (post-MI).
  • Rheumatic fever.
  • Calcification
  • Infective endocarditis.
  • Cardiomyopathy.
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21
Q

Important/emergency cause to rule out in mitral regurgitation

A

MI

Rupture/dysfunction of chordae tendinae or papillary muscles

https://els-jbs-prod-cdn.jbs.elsevierhealth.com/cms/attachment/a13f471d-1d14-4a74-baeb-d1f1d800a888/gr2_lrg.jpg image link

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22
Q

Causes of aortic stenosis.

A
  • Age-related calcification
  • Congenital unicuspid/bicuspid aortic valve
  • Rheumatic fever

+ any processes that might cause inflammatory changes in valve e.g. hypertension, infective endocarditis, dyslipidaemia

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23
Q

Systemic conditions that can cause aortic regurgitation

In addition to valve disease

A
  • Connective tissue disorders (Marfan’s etc.),
  • spondyloarthropathies (ankylosing spondylitis and psoriatic arthritis),
  • chronic HTN, tertiary syphillis.

Aortic root dilatation

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24
Q

3 complications of aortic root dilatation

A

Risk of aortic dissection, rupture, and regurgitation.

e.g. in Marfan’s syndrome

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25
Q

What aortic valve change usually precedes stenosis?

What clinical sign might help you differentiate this?

A

Aortic sclerosis. (senile degenerative change)

Ejection systolic murmur but no carotid radiation, and normal pulse character/volume.

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26
Q

Which right-sided valve condition is usually only affected by a congenital defect?

A

Pulmonary stenosis

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27
Q

Pulmonary and tricuspid regurgitation is often secondary to…?

A

Left-sided heart failure, pulmonary hypertension

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28
Q

Cardiac changes as a result of mitral regurgitation.

May be visualised in CXR.

A

Dilation of the left ventricle and atrium.

May result in ‘S3’ in advanced disease due to rapid filling of a dilated ventricle

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29
Q

3 standard investigations for valve disease.

A

ECG, CXR, echocardiogram

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30
Q

Possible ECG findings in aortic valve disease.

A

Left ventricular hypertrophy (increased effort to pump blood)

e.g. Increased QRS voltage, absent Q waves, left axis deviation

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31
Q

Definition of mean pressure gradient.
e.g. in aortic stenosis

Measured in echocardiogram

A

The average pressure difference between the left ventricle and aorta during systole; higher gradients signify more severe AS (>40mmHg)

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32
Q

Imaging method used to investigate a regurgitation murmur.

In addition to ECG, CXR, echo.

A

Colour flow doppler: sensitive and specific.

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33
Q

TAVI is only indicated in _______ .

A

Aortic stenosis.

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34
Q

Definitive treatment options for aortic stenosis.

For patients who are symptomatic or have severe disease

A
  • Valve replacement (open heart) - needs to be surgically fit
  • Transcatheter aortic valve implantation (TAVI) :)

Balloon valvuloplasty is a less invasive procedure that improves blood flow, but is usually temporary.

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35
Q

Definitive treatment of aortic regurgitation.

A

Valve replacement

only for symptomatic and severe disease

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36
Q

Medical management in aortic valve disease

A

ACEi/ ARBs

Aim to reduce systolic BP and reduce strain on heart.

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37
Q

Why are patients with symptomatic aortic stenosis usually advised to receive prompt replacement surgery?

A

Poor prognosis of survival without surgery:

2-3 years with angina/syncope,
1 year with heart failure

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38
Q

Which anticoagulant is used in atrial fibrillation caused by mitral stenosis?

A

Warfarin.

Additionally, in AF, rate control is crucial

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39
Q

What type of surgical treatment is preferred for mitral valve diseases?

A

Valve repair

not valve replacement due to higher risks of mortality

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40
Q

First-line definitive treatment of mitral stenosis.

A

Transcatheter Balloon Valvotomy (opens valve up)

Second-line: valve replacement

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41
Q

Role of diuretics in mitral stenosis.

A

Management of fluid overload/ pulmonary congestion.

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42
Q

Definitive treatment of mitral regurgitation.

A

Mitral valve repair

(More beneficial than replacement with lower mortality)

43
Q

Why might valve regurgitations present as emergencies?

A

Due to triggers e.g. infective endocarditis, trauma (e.g. post-MI), aortic dissection

causing acute deterioration of valve function and poor cardiac output. No adaptive remodelling could occur.

https://academic.oup.com/ehjacc/article/11/8/653/6652667#368371754

44
Q

Complications of valvulopathies.

A
  • Congestive heart failure
  • Arrythmias e.g. AF especially due to mitral valve diseases
  • Injuries from falls/syncope
  • Stroke
  • Cardiac arrest
45
Q

What is the definition of an abdominal aortic aneurysm (AAA)?

A

A localised enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal. Most commonly fusiform.

46
Q

Where are AAAs most commonly located? Below which landmark?

A

Most commonly infrarenal, with about one-third extending into the iliac arteries.

47
Q

What is the prevalence of AAAs in the NHS UK AAA screening programme for men over 65?

A

The prevalence is 1.34%, meaning 1 in 70 men over 65 has an AAA.

48
Q

What are the typical clinical features of a non-ruptured AAA?

A

Most AAAs are asymptomatic and detected incidentally.

If symptoms are present, they may include deep, gnawing abdominal/back pain, a pulsatile abdominal mass, fever (if infectious)

49
Q

Symptoms of AAA rupture

Onset?

A

Sudden, severe abdominal or back pain, with pallour, SOB/tachycardia, syncope and vomiting.

50
Q

What is the first-line imaging modality for screening and diagnosing an AAA?

A

Aortic ultrasound (USS)

51
Q

What is the recommended definitive imaging for a ruptured AAA?

A

Thin slice Computed Tomography Angiography (CTA) is recommended for ruptured AAA.

52
Q

Immediate management of a suspected ruptured AAA.

e.g. patient presenting with abdo pain, SOB and hypotension.

A

Immediate resuscitation with O2, IV fluids (large-bore cannulae) and blood transfusions, and emergency surgery (either open repair or EVAR) by vascular surgeons.

53
Q

What are the surgical options for AAA repair?

A

The options include Endovascular Aneurysm Repair (EVAR) and Open Surgical Repair.

EVAR is preferred for ruptured infrarenal AAAs in men over 70 and women of any age, while open repair is typically preferred for men under 70.

54
Q

What are some complications associated with AAA repair?

A
  • abdominal compartment syndrome,
  • endoleak,
  • rupture,
  • thromboembolism,
  • infection, and
  • aortoenteric fistula.
55
Q

Due to non-specific abdominal/back pain, what other conditions might AAA mimic?

A

Renal colic, acute pancreatitis, diverticulitis, mesenteric ischaemia, GI perforation

Must rule out AAA if it is a differential

56
Q

3 Indications of a non-ruptured AAA that require elective surgery?

What diameter –> urgent 2-week referral to vascular surgeons?

A
  1. > 5.5 cm,
  2. Getting larger rapidly (expanding <1cm/year),
  3. Symptomatic i.e. painful.
57
Q

What is the ‘classic triad’ of ruptured AAA?

A
  • Flank/back pain
  • hypotension
  • pulsatile abdominal mass + tenderness

Only seen in about 50% of patients

58
Q

Most important sign of a ruptured AAA

A

Hypotension/shock

Others: tachycardia, abdominal distension, pallor, syncope

Suspect rAAA in patients > 50 years presenting with abdominal/back pain and hypotension

59
Q

First-line management for small AAA.

List non-pharmacological and pharmacological

A

Managing risk factors for vascular damage and rupture: smoking cessation, diet, exercise, anti-hypertensives and statins.

60
Q

2nd most common aortic region to be affected by an aneurysm.

1st = abdominal

A

Thoracic aorta

(T4 up to T12 vertabrae)

61
Q

What is aortic dissection?

A

A tear in the intimal layer of the aorta, creating a false lumen through which blood can flow.

This can lead to life-threatening complications, including rupture and organ ischemia. Prompt diagnosis and management are crucial to improve outcomes.

62
Q

What are the layers of the aortic wall?

A

The aortic wall consists of three layers: Intima, Media, and Adventitia.

63
Q

What does a tear in the aortic intima cause?

A

Dissection, false lumen.

64
Q

What are the primary causes of aortic dissection?

A

Aortic dissection is primarily caused by conditions that weaken the aortic wall or increase aortic pressure. e.g. Hypertension, atheroscelrosis, and heavy lifting

65
Q

Why does aortic dissection lead to organ ischaemia?

A

The false lumen can compress the true lumen and branch vessels. It can also cause thrombi and embolise arteries.

66
Q

How are Type A and Type B dissections distinguished?

A

Type A dissection involves the ascending aorta and is more dangerous, requiring immediate surgical intervention.

Type B dissection involves the descending aorta and is generally less immediately life-threatening, with initial management focusing on blood pressure control.

Type A: severe anterior chest pain, radiation to jaw/arms or stroke-like symptoms, syncope, and hypotension;

Type B: severe interscapular/back pain, abdominal pain, and hypertension.

67
Q

What are common clinical features of aortic dissection?

A

Common features include sudden onset of severe chest or back pain, often ‘tearing’ or ‘ripping’, unequal pulses, pulse deficit, variation in blood pressure, and possible aortic regurgitation.

68
Q

List 2 possible features on a chest X-ray in aortic dissection.

A

The chest X-ray may show a widened mediastinum, dilated aortic arch.

69
Q

What is the gold-standard imaging modality for aortic dissection?

A

CT angiography is the gold-standard imaging modality for definitive diagnosis of aortic dissection.

70
Q

Which one is the false lumen?

A

The left one. Imagine it engulfing the true lumen and has horns.

71
Q

Management of all type A aortic dissections.

A

Immediate surgical repair (of aortic root).

72
Q

Medical management in all aortic dissections to control blood pressure.

A

IV labetalol 50 mg

Second line: verapamil or diltiazem.

73
Q

Management of stable type B dissections.

A

Conservative : labetalol and anti-hypertensives.

If unstable: endocascular repair.

74
Q

Define SVT.

A

Group of tachyarrhythmias originating above the ventricles, typically characterised by rapid heart rates (usually >100 bpm) and regular narrow QRS complexes.

75
Q

Types of SVT.

A

Common types of SVT include:

  1. Atrioventricular nodal re-entrant tachycardia (AVNRT).
  2. Atrioventricular re-entrant tachycardia (AVRT).
  3. Atrial tachycardia.
  4. Atrial flutter.
76
Q

Most common type of SVT.

A

AVNRT.

77
Q

First-line medication for termination of AVNRT/AVRT.

A

Adenosine. Rapid IV push with saline flush.

Temporarily blocks AV node conduction to terminate AVNRT or AVRT.

After vagal maneuovres have failed.

78
Q

Definitive treatment for recurrent symptomatic SVT (success rate >95% for AVNRT and AVRT).

A

Catheter ablation.

79
Q

In a tachycardic patient (HR~150):

A Narrow QRS suggests the electrical impulse originated ______________________________ ?

A Wide QRS suggests the electrical impulse originated ______________________________ ?

A

Narrow QRS: atrium
Wide QRS: ventricles

80
Q

When might you suspect HOCM?

In who? Symptomatology?

A

Typically onset of chest pain in an adolescent during strenous exercise , but can also happen at rest.

Associated with dizziness, dyspnoea, palpitations etc.

81
Q

What is Mavacamten and how does it work?

A

Treatment of HOCM in adults by binding to (inhibiting) cardiac myosin.

It reduces the number of myosin-actin cross-bridges, decreasing the excessive contractility of the heart muscle and allowing it to relax more effectively. This relaxation reduces the obstruction in the LVOT, improves cardiac filling pressures, and enhances overall cardiac function.

82
Q

What are the characteristic ECG findings in HOCM?

A
  • LV hypertrophy: increased praecordial voltages, often meeting the criteria for LVH.
  • Dagger-like Q waves.
  • P-mitrale, arrhtymias, Giant T-wave inversions: particularly in the apical variant of HOCM (Yamaguchi syndrome), where the apex is thickened.
83
Q

Does HOCM cause primarily systolic or diastolic dysfunction?

A

Diastolic dysfunction.

84
Q

Pattern of inheritance in HOCM?

A

Often AD inheritance.

85
Q

How is genetic testing done for HCM? What are the steps?

A

1) Genetic counselling.

2) Sample collection: blood or saliva sample.

3) Lab analysis:
DNA sequencing.
Gene panels.

4) Interpretation of results:
Variant classification: the identified genetic variants are classified based on their potential to cause disease (e.g., pathogenic, likely pathogenic, variant of uncertain significance, likely benign, benign).

Report generation: detailed report is produced, summarising the findings and implications for patient and family health.

5) Post-test counselling:
Result discussion: the genetic counsellor will discuss the results with the patient.

Family screening.

86
Q

Does dilated cardiomyopathy cause predominantly diastolic or systolic dysfunction?

A

Systolic

Pathophysiology: increased heart strain causes dilation and impaired contraction of the heart’s ventricles, leading to systolic dysfunction. This can result in heart failure and other complications, such as RAAS activation, further worsening cardiac functioning.

87
Q

What is the most common cause of dilated cardiomyopathy?

A

Ischaemic heart disease (50-60% of cases).

Other causes (increased strain):
1. Chronic hypertension.
1. Infections: viral myocarditis, HIV, Lyme disease e.t.c.
1. Toxins: alcohol abuse, cocaine, meth, and chemotherapeutic agents (e.g., doxorubicin, daunorubicin). Heavy metals like cobalt can also cause DCM.
1. Metabolic disorders: thyroid, diabetes
1. Peripartum cardiomyopathy: pregnancy-related DCM can develop in women during the last month of pregnancy or within five months postpartum.

88
Q

Does restrictive cardiomyopathy cause predominantly diastolic or systolic dysfunction?

A

Diastolic — doesn’t fill as much.

89
Q

Symptoms/signs of restrictive cardiomyopathy (RCM).

A

Similar to those of heart failure:

> Dyspnoea
Fatigue
Oedema
Palpitations
Chest pain
Ascites

90
Q

Restrictive cardiac myopathies are usually caused by ________ conditions?

A

Largely auto-immune damage to the cardiac muscle itself.

Such as:
2. Amyloidosis
2. Haemochromatosis
3. Sarcoidosis
4. Connective tissue disease (e.g., scleroderma).
5. Cancer treatments: e.g., chemotherapy and radiotherapy.
6. Other: e.g., endomyocardial fibrosis and Loeffler syndrome.

91
Q

What are the three types of cardiomyopathies?

A
  1. Hypertrophic (obstructive)
  2. Dilated,
  3. Restrictive

Cardiomyopathy is a disease of the heart muscle that affects its size, shape, and ability to pump blood.

92
Q

Which type of cardiomyopathy is characterized by an enlarged heart and decreased pumping ability?

A

Dilated cardiomyopathy.

93
Q

Fill in the blank: Hypertrophic cardiomyopathy is often associated with __________.

A

Genetic mutations.

94
Q

What is the primary management strategy for patients with dilated cardiomyopathy?

A

Use of heart failure medications such as ACE inhibitors, beta-blockers, mineralocorticoids, and diuretics.

Advances: ICD etc.

according to UK NICE guidelines

95
Q

What is the main risk factor for developing hypertrophic cardiomyopathy?

A

Family history of the condition.

96
Q

True or False: Restrictive cardiomyopathy is characterized by stiff heart walls that restrict filling.

A

True.

97
Q

What is the recommended first-line treatment for symptomatic patients with hypertrophic cardiomyopathy?

A

Beta-blockers.

Second-line drugs: Verapamil/diltiazem, Disopyramide,
New: Mavacamten

Invasive procedures:
Septal myectomy, Alcohol septal ablation
ICD

98
Q

What diagnostic test is commonly used to assess cardiomyopathies?

A

Echocardiogram.

99
Q

What is the key feature of restrictive cardiomyopathy on echocardiogram?

A

Abnormal diastolic filling with preserved systolic function.

100
Q

In terms of prognosis, which type of cardiomyopathy generally has the worst outcomes?

A

Dilated cardiomyopathy.

101
Q

Fill in the blank: The primary cause of dilated cardiomyopathy in the UK is __________.

A

Ischemic heart disease.

102
Q

What is the recommended treatment approach for advanced heart failure due to cardiomyopathy?

A

Consideration for heart transplantation.

103
Q

What is a common symptom of cardiomyopathy that patients may report?

A

Shortness of breath during exertion.

104
Q

Investigations for cardiomyopathies.

A

ECG
Echocardiogram
Cardiac MRI

+genetic testing for HOCM.

Medical conditions (25 decks)

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