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Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What’s the main molecule type responsible for carrying cholesterol into the intima?

A

LDL (low-density lipoprotein).

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2
Q

What happens during phase 1 of the cardiac cycle?

A

Potassium efflux.

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3
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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4
Q

Describe the murmur heard in aortic regurgitation.

A

Early diastolic,
High-pitched and blowing in nature (decrescendo).

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5
Q

Describe the murmur heard in mitral stenosis.

A

Mid diastolic murmur.
Low-pitched and rumbling.
Opening snap.

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6
Q

Describe the murmur heard in mitral regurgitation.

A

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

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7
Q

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

A

Aortic regurgitation or PDA.

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8
Q

At which positions should you auscultate for heart murmurs?

A

2nd intercostal space, right sternal edge: aortic.

2nd intercostal space, left sternal edge: pulmonic

3rd intercostal, left sternal edge: Erb’s Point.

4th intercostal space, left sternal edge: tricuspid.

5th intercostal space, midclavicular line: mitral.

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9
Q

Accentuation maneouvres for heart murmurs.

A

1) Valsalva:
Phase 1 (strain): decreases venous return, reducing left ventricular volume and intensity of most murmurs (e.g., aortic stenosis and mitral regurgitation).

Phase 2 (release): increases venous return, augmenting murmurs of aortic regurgitation, mitral regurgitation, and HOCM.

2) Respiration:
>Inspiration: increases right ventricular preload, augmenting right-sided murmurs (e.g., tricuspid stenosis, tricuspid regurgitation).

> Expiration: increased left ventricular preload, augmenting left-sided murmurs (e.g., mitral stenosis and mitral regurgitation).

3) Squatting:
>Increases venous return and afterload, augmenting murmurs of aortic regurgitation, aortic stenosis, mitral regurgitation, and diastolic murmur of mitral stenosis.

4) Standing:
Decreases venous return, reducing left ventricular volume and intensity of most murmurs (e.g., aortic stenosis, mitral regurgitation).

5) Handgrip:
>Increases afterload and peripheral arterial resistance, reducing murmurs of aortic stenosis, HOCM, mitral valve prolapse, and papillary muscle dysfunction.

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10
Q

When should you suspect ACS based on chest pain duration?

A

When the pain in the chest or other areas (e.g., arms, back, or jaw) lasts longer than 15 minutes.

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11
Q

What are the characteristics of chest pain that may indicate ACS?

A

Dull, central, and/or crushing pain; associated with nausea/vomiting, sweating, or dyspnoea; associated with haemodynamic instability (e.g., systolic blood pressure less than 90 mm/Hg); new-onset pain or abrupt deterioration of stable angina, occurring frequently with little or no exertion, and often lasting longer than 15 minutes.

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12
Q

Should the response to GTN be used to confirm or exclude a diagnosis of ACS?

A

No, the person’s response to GTN should not be used to confirm or exclude a diagnosis of ACS.

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13
Q

What is the general approach to diagnosing ACS?

A

Most people require referral or admission to hospital to confirm the diagnosis of ACS.

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14
Q

What initial tests should be offered to people suspected of having ACS?

A

A resting 12-lead ECG and a blood sample for high-sensitivity troponin I or T measurement.

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15
Q

Should high-sensitivity troponin tests be used for people in whom ACS is not suspected?

A

No, high-sensitivity troponin tests should not be used for people in whom ACS is not suspected.

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16
Q

What should be considered if the person’s pain was more than 72 hours ago and they have no complications?

A

Consider diagnosing ACS in primary care.

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17
Q

What ECG changes may indicate ischaemia or previous myocardial infarction?

A

Pathological Q waves, LBBB, ST-segment and T-wave abnormalities (e.g., T-wave flattening or elevation, or T-wave inversion).

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18
Q

Does a normal ECG confirm or exclude a diagnosis of ACS?

A

No, a normal ECG alone does not confirm or exclude a diagnosis of ACS. The ECG findings must be considered in conjunction with other findings.

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19
Q

What does a detectable troponin level indicate?

A

It indicates damage to the myocardium, such as in myocardial infarction.

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20
Q

How soon after a myocardial infarction is serum troponin detectable using high-sensitivity testing?

A

Within 3-6 hours following a myocardial infarction.

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21
Q

How long can serum troponin remain elevated after a myocardial infarction?

A

It can remain elevated for a variable time, usually several days, but it can be up to 2 weeks.

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22
Q

What other conditions can cause an increase in serum troponin?

A

Conditions such as arrhythmias, pericarditis, pulmonary emboli, and myocarditis.

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23
Q

What factors should be taken into account when interpreting high-sensitivity troponin measurements?

A

Clinical presentation, time from onset of symptoms, resting 12-lead ECG findings, pre-test probability of NSTEMI, length of time since the suspected ACS, probability of chronically elevated troponin levels in some people, and the fact that 99th percentile thresholds for troponin I and T may differ between males and females.

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24
Q

What should you check first when assessing a person for ACS?

A

Check whether the person currently has chest pain.

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25
Q

If a patient with possible ACS is pain-free, what should you ask next?

A

Ask when their last episode of pain was, and in particular if it was within the last 12 hours.

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26
Q

What aspects of chest pain should you ask about if you suspect a patient has ACS?

A

Nature, onset, duration, site, and radiation of chest pain.

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27
Q

What type of chest pain is strongly suggestive of cardiac chest pain?

A

An acute onset, with central or band-like chest pain which radiates to the person’s jaw, arms, or back.

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28
Q

What type of chest pain is more suggestive of a pulmonary or MSK cause?

A

Persistent, localised chest pain.

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29
Q

What type of chest pain is typical of angina?

A

Exertional chest pain.

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30
Q

What does pleuritic chest pain suggest?

A

MSK or pulmonary cause.

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31
Q

What associated sign/symptom can be seen with cardiac or pulmonary causes of chest pain?

A

Breathlessness/dyspnoea.

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32
Q

What associated symptoms make angina less likely?

A

Chest pain associated with palpitations, dizziness, or difficulty swallowing.

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33
Q

What should you ask about regarding the person’s history of chest pain?

A

Ask about chest pain and previous investigations (e.g., ECG or chest X-ray).

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34
Q

Can a normal resting 12-lead ECG rule out stable angina?

A

No.

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35
Q

What does an abnormal ECG indicate?

A

It makes the diagnosis of coronary artery disease more likely, but does not confirm that the chest pain is stable angina.

36
Q

What is the significance of a recent normal coronary angiogram?

A

It is helpful to exclude coronary artery disease as a cause of chest pain.

37
Q

What cardiovascular risk factors should be assessed in a patient with potential ACS?

A

> Older age.
Smoking status.
Male sex.
Hypertension.
Diabetes mellitus.
Hyperlipidaemia.
Family history.

38
Q

What other conditions should be considered as causes of chest pain?

A

Respiratory (e.g., PE) and gastroenterological disease (e.g., GORD), MSK problems (e.g., costochondritis, precordial catch syndrome), and previous trauma.

39
Q

What psychological conditions should be considered if there are clinical features suggesting the diagnosis?

A

Anxiety and depression, as psychogenic or non-specific chest pain is a common cause of chest pain in primary care.

40
Q

Which people with chest pain should be admitted to hospital?

A

Most people with a serious cause of chest pain require hospital admission and will need initial pre-hospital management prior to transfer.

41
Q

What clinical features suggest a serious cause of chest pain?

A

Respiratory rate of more than 30 breaths per minute, tachycardia greater than 130 beats per minute, systolic blood pressure less than 90 mmHg or diastolic blood pressure less than 60 mmHg (unless this is normal for them), oxygen saturation less than 92% or central cyanosis (if no history of chronic hypoxia), altered level of consciousness, and raised temperature (especially if higher than 38.5°C).

42
Q

When should people with suspected acute coronary syndrome (ACS) be admitted?

A

If they have current chest pain, signs of complications (such as pulmonary oedema), are pain-free but had chest pain in the last 12 hours with an abnormal ECG or no ECG available, or have a recent history of ACS with further chest pain.

43
Q

When should you consider admitting people with suspected ACS if pain has resolved?

A

If there are signs of complications, using clinical judgement to decide whether emergency or urgent referral is appropriate.

44
Q

How should you position a person with chest pain while waiting for admission?

A

Sit the person up.

45
Q

When should you offer supplemental oxygen to a person with chest pain?

A

Only if their oxygen saturation (SpO2) is less than 94% and they are not at risk of hypercapnic respiratory failure, or if they have chronic obstructive pulmonary disease and are at risk of hypercapnic respiratory failure.

46
Q

What is the target SpO2 for people not at risk of hypercapnic respiratory failure?

A

94–98%, using a simple face mask with a flow rate of 5–10 L/min.

47
Q

What is the target SpO2 for people with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure?

A

88–92%, using a 28% venturi mask with a flow rate of 4 L/min.

48
Q

How should you manage suspected acute coronary syndrome (ACS) while awaiting admission?

A

Treat pain with glyceryl trinitrate (GTN) and/or an opioid (e.g., intravenous diamorphine 2.5 mg to 5.0 mg, given slowly over 5 minutes), give aspirin 300 mg, take a resting 12-lead ECG and send the recording with the person to the hospital.

49
Q

How should you manage acute pulmonary oedema while awaiting admission?

A

Give an intravenous diuretic (e.g., furosemide 40 mg to 80 mg, given slowly), an intravenous opioid (e.g., diamorphine 2.5 mg to 5.0 mg, given slowly over 5 minutes), an intravenous anti-emetic (e.g., metoclopramide 10 mg), and a nitrate (e.g., GTN spray, two puffs).

50
Q

How should you manage a life-threatening tension pneumothorax while awaiting admission?

A

Consider inserting a large-bore cannula through the second intercostal space in the mid-clavicular line on the side of the pneumothorax.

51
Q

What should you monitor while a person with chest pain is awaiting admission?

A

Exacerbations of pain and other symptoms, pulse, blood pressure, heart rhythm, oxygen saturation (using pulse oximetry), resting 12-lead ECG (repeat if necessary), and pain relief (and review for efficacy).

52
Q

When should you refer a person with chest pain for an urgent same-day assessment?

A

If they have suspected ACS and are pain-free with chest pain in the last 12 hours and a normal ECG with no complications, or chest pain in the last 12–72 hours with no complications.

53
Q

When should you refer a person with chest pain within 2 weeks?

A

If they have suspected ACS and are pain-free with chest pain more than 72 hours ago and no complications, suspected underlying malignancy (e.g., lung cancer), or a lung or lobar collapse or pleural effusion (if admission is not required).

54
Q

When should you refer a person with chest pain routinely?

A

Answer: If they have suspected stable angina where the diagnosis cannot be excluded in primary care, chest pain where the cause is unclear, or a clear diagnosis for chest pain but symptoms persist despite management in primary care.

55
Q

How should you manage a person with chest pain who does not require hospital admission?

A

Arrange appropriate investigations if the cause of chest pain cannot be confidently established by clinical features alone, manage the underlying cause (e.g., prescribe analgesia for musculoskeletal chest pain, arrange blood tests for stable angina, reassure and manage anxiety for non-specific or psychogenic chest pain), and provide specific treatments for conditions like dyspepsia, community-acquired pneumonia, acute exacerbation of asthma or COPD, chronic pancreatitis, shingles, and Bornholm’s disease.

56
Q

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

A

An AAA is a localised dilation of the abdominal aorta, typically defined as an aortic diameter of 3.0 cm or greater.

57
Q

Why is an AAA considered a significant condition?

A

It is significant due to the risk of rupture, which can lead to life-threatening internal bleeding.

58
Q

Describe the pathophysiology of AAA development.

A

The development of an AAA involves the weakening of the aortic wall due to chronic inflammation, causing degradation of structural proteins like elastin and collagen, leading to dilation and potential rupture of the aorta. Mechanical factors such as high blood pressure also play a key role.

59
Q

Where are AAAs most commonly located?

A

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

60
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.

61
Q

List the major risk factors for developing an AAA.

A

Major risk factors include age (particularly over 65), male sex, smoking, hypertension, family history, diabetes, COPD, and connective tissue disorders such as Marfan syndrome and Ehlers-Danlos syndrome.

62
Q

What are the typical clinical features of an AAA?

A

Most AAAs are asymptomatic and detected incidentally. If symptoms are present, they may include deep, gnawing abdominal pain, a pulsatile abdominal mass, hypotension, syncope, pallor, abdominal distension, fever (if infectious), and signs of rupture such as tachycardia and shock.

63
Q

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

A

Aortic ultrasound (USS) is the first-line imaging modality.

64
Q

What is the recommended definitive imaging for a ruptured AAA?

A

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

65
Q

How is the management of a suspected ruptured AAA typically handled?

A

It is a surgical emergency requiring immediate referral to a regional vascular service, immediate resuscitation with IV fluids and blood transfusions, and emergency surgery (either open repair or EVAR).

66
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.

67
Q

What are some complications associated with AAA repair?

A

Complications can include abdominal compartment syndrome, endoleak, rupture, thromboembolism, infection, and aortoenteric fistula.

68
Q

What is the long-term monitoring protocol after AAA repair?

A

Regular imaging to monitor for endoleaks and graft integrity, follow-up non-contrast CT every 5 years, managing cardiovascular risk factors, and prophylactic antibiotics for certain procedures.

69
Q

What is the prognosis for patients undergoing AAA repair?

A

Most patients undergoing open repair do not face graft-related complications, while those undergoing EVAR have higher chances of late complications and may require re-intervention. A major risk factor for poor morbidity is low skeletal muscle mass.

70
Q

List some complications of arterial ulcers.

A

> Infection
Gangrene
Chronic pain
Delayed healing

71
Q

How should an arterial ulcer be diagnosed?

A

> Clinical examination: appearance.
ABPI: Less than 0.9 suggests PAD.
Doppler ultrasound to assess blood flow and locate arterial blockages.
CT angiography or MR angiography may be used for detailed visualisation of the arterial system.

72
Q

Risk factors for arterial ulcers.

A

> Age
Smoking
Hypertension
Hyperlipidaemia
Diabetes

73
Q

Pathophysiology of arterial ulcers.

A

Reduced blood flow, leading to tissue ischaemia and necrosis.

Underlying cause is usually atherosclerosis.

74
Q

Management of arterial ulcer.

A

Medical Management:
>Risk factor modification (e.g., smoking cessation and diabetes control)

> Pharmacotherapy: antiplatelet agents (e.g., aspirin and clopidogrel), statins, and antihypertensive medications.

> Pain management: analgesics, including opioids if necessary to manage severe pain.

Wound care:
>Debridement
>Dressings
>Infection control

Revascularisation:
>Endovascular procedures: angioplasty and stenting to restore blood flow.
>Surgical options: bypass surgery for severe cases where endovascular procedures are not feasible.

Lifestyle modifications:
>Exercise: supervised exercise programmes to improve circulation.
>Diet: healthy diet to manage risk factors.

> Monitoring and follow-up.
Regular follow-up to monitor the ulcer and manage any complications.

> Ongoing assessment of vascular status and modification of treatment as needed.

75
Q

Outline the role of ANP, including its source, function, and mechanism.

A

Atrial natriuretic peptide is a hormone released by the atrial myocytes in response to atrial distension, hypertension, and fluid retention.

Its function is to increase renal excretion of sodium, to induce diuresis, and to reduce fluid retention.

It binds to specific receptors in the kidneys and blood vessels, leading to the production of cyclic guanosine monophosphate, which mediates its effects.

76
Q

What produces BNP?

A

Ventricular myocytes.

77
Q

What effect does BNP have on the RAAS system?

A

It inhibits the RAAS system.

78
Q

Aside from rheumatic fever, what can cause mitral stenosis?

A

Mitral annular calcification (MAC).
Infective endocarditis.
SLE.

79
Q

What is the definitive diagnostic test for mitral stenosis?

A

Transthoracic echocardiogram.
Transoesophageal echocardiogram can be used if the TTE was inconclusive, as it provides greater detail.

80
Q

Mitral stenosis facial signs.

A

Mitral flush due to chronic hypoxia.

81
Q

What type of arrhythmia does mitral stenosis commonly cause?

A

Atrial fibrillation. Increased thromboembolism risk.

82
Q

What is the thrombolytic drug of choice for treating patients with atrial fibrillation arising as a result of mitral stenosis?

A

Warfarin.

83
Q

First-line treatment for mitral stenosis.

A

Depends on the severity. Manage fluid retention with diuretics.

If symptomatic, perform surgery with a transcatheter balloon valvulotomy.

Beta-blockers.

84
Q

Mitral stenosis valve area.

A

Less than 1cm^2.

85
Q

Mitral annular calcification.

A

Degenerative calcification of the annulus of the mitral valve, leading to narrowing/thickening of the valve and potentially mitral valve dysfunction.

86
Q

Mitral stenosis signs/symptoms.

A

> Dyspnoea.
Orthopnoea.
Paroxysmal nocturnal dyspnoea.
Haemoptysis.
Chest pain.
Thromboembolism.
Fatigue (due to reduced cardiac output).
Mitral flush.
Mid-diastolic low-pitched rumbling murmur heard at the left sternal edge, 4th intercostal space. Opening snap.
Neck vein distension.
Palpitations.

Medicine (27 decks)

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