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AKT revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Name the 4 valves of the heart and their positions?

A

Tricuspid - between R atrium and R ventricle.
Pulmonary - between R ventricle and pulmonary artery
Mitral - between L atrium and L ventricle
Aortic - between L ventricle and aorta

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2
Q

Name the order of auscultation of the 4 heart valves? (from R to L side of body)

A

Aortic
Pulmonary
Tricuspid
Mitral

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3
Q

What two heart valve disorders are most common among the elderly?

A

aortic stenosis
mitral regurgitation

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4
Q

which murmur causes a crescendo-decrescendo ejection systolic murmur that radiates to the carotids?

A

aortic stenosis

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5
Q

what is the pathophysiology of aortic stenosis?

A

Atherosclerotic and calcium deposits on the aortic valve, causing the valve to harden and tighten.

This overall reduces the amount of blood which can flow through into the aorta from the left ventricle.

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6
Q

what are some common causes of aortic stenosis?

A

atherosclerotic disease (I.e CVD)
age
rheumatic fever

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7
Q

what are some clinical signs on examination of aortic stenosis?

A

ejection systolic murmur radiating to carotids
narrow pulse pressure
slow rising pulse
thrill

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8
Q

what are some symptoms of aortic stenosis?

A

dyspnoea
syncope/presyncope
chest pain

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9
Q

what are some of the physiological consequences of aortic stenosis?

A

leads to left ventricular hypertrophy, as the heart pumps harder in order to compensate for the stenosed valve, and this eventually can lead to congestive cardiac failure

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10
Q

what are some investigations to consider in patients presenting with dyspnoea, chest pain or syncope - and you are suspicious of aortic stenosis?

A

ECHO
BNP
ECG

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11
Q

What is the management of aortic stenosis?

A

surgical AVR is the treatment of choice for young, low/medium operative risk patients.

transcatheter AVR (TAVR) is used for patients with a high operative risk

balloon valvuloplasty

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12
Q

what medications must be avoided in aortic stenosis?

A

antihypertensives - they will reduce peripheral vascular resistance and preload, which overall reduces the hearts ability to maintain adequate output. Generally, surgical intervention is required for aortic stenosis rather than antihypertensives.

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13
Q

what valve disorder causes a pan systolic murmur, best heard at the apex and radiating to the axilla?

A

mitral regurgitation

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14
Q

how does mitral regurgitation lead to heart failure?

A

Mitral regurgitation causes heart failure primarily through chronic volume overload on the left ventricle, leading to ventricular dilation, reduced contractility, and subsequent left ventricular failure. The increased pressure in the left atrium and pulmonary circulation leads to pulmonary congestion and potentially pulmonary hypertension. As the disease progresses, these changes culminate in symptomatic heart failure, with both systolic and diastolic dysfunction, and eventually right-sided heart failure in severe cases.

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15
Q

what are the consequences of untreated mitral regurgitation?

A

heart failure - initially L sided heart failure, then R sided heart failure.
pulmonary hypertension
atrial fibrillation

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16
Q

what are some symptoms of mitral regurgitation?

A

fatigue
dyspnoea
nocturnal paroxsymal dyspnoea
orthopnea
palpitations

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17
Q

what are some risk factors for mitral regurgtitation?

A

Female sex
Lower body mass
Age
Renal dysfunction
Prior myocardial infarction
Prior mitral stenosis or valve prolapse
Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome

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18
Q

what is the management of mitral regurgitation?

A

if clinically stable and MR is chronic - trial of diuretics to reduce the preload, and vasodilators such as ACE-I and ARB’s.

if clinically unstable, or severe - surgical MR replacement or repair.

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19
Q

what are the clinical signs of left heart failure?

A

dyspnoea
PND
orthopnea
breathlessness on exertion
fatigue
chest pain

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20
Q

what are the clinical signs of right heart failure?

A

peripheral oedema
breathlessness
abdominal discomfort
hepatomegaly / splenomegaly due to overload
JVD
weight gain

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21
Q

what investigations would you arrange for a patient in which you suspected heart failure?

A

First line - BNP blood test

Additional investigations to consider -
ECG
ECHO
24 hour BP monitoring
24 ECG - if suspecting AF

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22
Q

what actions should be carried out based on the BNP level?

A

BNP > 2000 -> urgent referral to cardiology in 2 weeks

BNP 400- 2000 -> referral to cardiology in 6 weeks, and ECHO

BNP < 400 -> watch and wait

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23
Q

what factors can affect the BNP level?

A

chronic kidney disease - reduced exertion of BNP
pregnancy
liver disease
diabetes
COPD
sepsis

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24
Q

what is the first line management of heart failure?

A

ACE-I

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25
Q

what is BNP?

A

a hormone produced mostly by the cardiac tissue in response to L heart strain

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26
Q

what drugs reduce BNP?

A

ACE-I
ARB
diuretics

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27
Q

what raises the BNP?

A

CKD
liver disease
diabetes
COPD
heart failure
MI

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28
Q

what classification is used for severity of heart failure?

A

New York Heart Association Classification (NYHA)

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29
Q

NYHA I

A

No symptoms, no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

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30
Q

NYHA II

A

mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

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31
Q

NYHA III

A

moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

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32
Q

NYHA IV

A

severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

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33
Q

First line medical management of heart failure?

A

ACE-I and Beta Blocker

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34
Q

How does an ACE-I work?

A

Reduce afterload, decrease blood pressure, and prevent remodeling of the heart.

By inhibiting the production of ACE which converts angiotensin I to angiotensin II. The role of angiotensin II is to vasoconstrict, and so ACE inhibitors reduce vasoconstriction, overall reducing the blood pressure and after load.

Additionally, angiotensin II is responsible for causing the release of aldosterone. Aldosterone causes retention of sodium and water vi the kidneys, increasing the overall blood volume and causing hypertension. ACE-I inhibit this, leading to overall reduction in preload, and hypertension.

ACE-I also prevent harmful cardiac remodeling, and reduce the workload on the heart.

35
Q

What are some examples of ACE-I?

A

Ramipril
Lisinopril

36
Q

What are contraindications to the use of ACE-I?

A

If there is confirmed valvulopathy that is causing haemodynamic instability
angio-oedema
renal artery stenosis
pregnancy
hyperkalaemia
hyponatraemia

37
Q

how does a beta blocker work in heart failure?

A

Reduced Heart Rate: Slowing the heart rate reduces the heart’s workload and allows more time for the heart to fill with blood during each beat, improving cardiac output.

Decreased Myocardial Oxygen Demand: By reducing the force of the heart’s contractions and lowering blood pressure, beta blockers decrease the heart’s oxygen demand, which is beneficial in heart failure.

Inhibition of Harmful Remodeling: Chronic activation of the sympathetic nervous system can lead to harmful changes in the heart’s structure (remodeling).
Beta blockers help prevent or reverse this remodeling, improving heart function over time.

38
Q

what are some contraindications to beta blockers?

A

Uncontrolled heart failure
Asthma/severe COPD
Sick sinus syndrome
Concurrent verapamil use - can cause severe bradycardia

39
Q

what is second line treatment for heart failure?

A

add in an aldosterone receptor antagonist (also known as mineralocorticoid receptor antagonists)

40
Q

what are some examples of aldosterone receptor antagonists?

A

spironolactone
eplernone

41
Q

how do aldosterone receptor antagonists work in heart failure?

A

Reduction of Fluid Retention: By inhibiting aldosterone, ARAs reduce sodium and water reabsorption in the kidneys, decreasing fluid buildup and relieving symptoms like edema and pulmonary congestion.

Decreased Blood Pressure: Lowering fluid volume helps reduce blood pressure, which can decrease the heart’s workload.

Prevention of Cardiac Remodeling: ARAs help prevent harmful changes in the heart’s structure and function, such as fibrosis and hypertrophy, improving overall heart function and symptoms.

42
Q

what are some contraindications to the use of aldosterone receptor antagonists?

A

hyperkalaemia
severe renal impairment
Addisons disease
hypersensitivity to ARA

43
Q

what is the third line management of heart failure?

A

Third-line treatment should be initiated by a specialist.

Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy.

44
Q

how does ivabradine work?

A

Ivabradine is typically used in heart failure patients with a resting heart rate of ≥70 beats per minute despite optimal treatment with other heart failure medications, particularly when beta-blockers are contraindicated or not tolerated.

It acts on the funny channels in the SA, to reduce heart rate thus reducing the strain on the heart.

45
Q

what are some side effects of ACE-I?

A

dry cough
fatigue
dizziness
headaches

46
Q

what are some side effects of beta blockers?

A

fatigue
dizziness
nausea
constipation
cool peripheries

47
Q

MOA of digoxin?

A

Increases myocardial contractility

Decreases conduction within the AV node

48
Q

Indications of digoxin?

A

Atrial flutter
AF
Heart failure

49
Q

Side effects of digoxin?

A

GI upset
Arrhythmia
Confusion
Dizziness
Blurred vision

50
Q

how does heart failure cause hypertension?

A

The heart’s reduced ability to pump blood effectively leads to decreased renal perfusion. This stimulates the kidneys to retain sodium and water to compensate for the reduced blood volume, increasing blood volume and contributing to higher blood pressure. This also activates the RAAS, which leads to vasoconstriction, and further elevates blood pressure.
Heart failure also stimulates the sympathetic nervous system, leading to further vasoconstriction.

51
Q

HTN stage 1

A

clinic BP > 140/90
ABPM > 135/80

52
Q

HTN stage 2

A

clinic BP > 160/100
ABPM > 150/95

53
Q

HTN stage 3 / severe

A

clinic BP > 180/110

54
Q

when to offer treatment in stage 1 HTN?

A

if < 80 years and has -

Target organ damage
Established cardiovasular disease
Established renal disease
Diabetes
10 year risk >10%

55
Q

when should you admit in severe hypertension?

A

Signs of retinal haemorrhage or papilloedema (accelerated hypertension)

New onset confusion, chest pain, acute kidney injury, heart failure

56
Q

what are some causes of HTN in younger patients? (i.e. <40 years)

A

essential HTN (likely genetic)

endocrine:
- phaechromocytoma
- primary hyperaldosteronism (conn’s)
- cushings disease (excessive cortisol causes HTN)
- renal disease (i.e. renal artery stenosis, polycystic kidney disease)
- thyroid (both hyperthyroidism and hypothyroidism)

Cardiac:
- coarctation of the aorta
- congenital cardiac disease (HOCM)

Meds:
- COCP
- stimulants

Lifestyle:
- severe obesity
- high salt intake

57
Q

patient < 40 years with HTN?

A

Refer to secondary care to consider underlying causes

58
Q

BP targets in T1DM?

A

<135/85

Unless have albuminuria or 2 features of metabolic syndrome, then it is <130/80

59
Q

Step 1 HTN management: <55 years or T2DM

A

ACE-I/ARB

60
Q

Step 1 HTN management: > 55 years or black/carribean?

A

CCB

61
Q

Step 2 HTN management: <55 years or T2DM

A

ACE-I/ARB plus CCB OR thiazide like diuretic

62
Q

Step 2 HTN management: >55 years or black/caribbean

A

CCB plus ACE-I/ARB OR thiazide like diuretic

63
Q

Step 3 HTN management

A

ACE-I/ARB + CCB + thiazide like diuretic

64
Q

Step 4 HTN management

A

K <4.5: low dose spironolactone

K >4.5: alpha or beta blocker

65
Q

Name some examples of ARB

A

Losartan
Candesartan
Irbesartan

66
Q

MOA of spironolactone?

A

Potassium sparing mineralcorticoid receptor antagonist - antaognises the effects of aldosterone, meaning Na and water are not retained in the kidney, and so causing diuresis.

67
Q

what are the contraindications to spironolactone

A

Addison’s disease
Hyperkalaemia
Acute renal insufficiency, significant renal compromise, anuria (means it will be ineffective as no aldosterone produced)

68
Q

what are the 3 different categories of angina?

A

stable angina

unstable angina

non-cardiac chest pain

69
Q

what is the diagnostic criteria for stable angina?

A

Three of the features:

Precipitated by physical exertion.

Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.

Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.

70
Q

what is the diagnostic criteria for unstable angina?

A

Two of the features:

Precipitated by physical exertion

Constricting discomfort in the front of the chest, in the neck, shoulders, jaw or arms.

Relieved by rest of GTN within about 5 minutes.

In addition, atypical symptoms include gastrointestinal discomfort, and/or breathlessness, and/or nausea.

71
Q

Risk factors for angina?

A

Increasing age.

Male sex.

The presence of cardiovascular risk factors (i.e. CKD, HTN, T2DM, obesity, cholesterol, and chronic inflammatory conditions such as RA)

A history of established coronary artery disease (for example previous myocardial infarction, coronary revascularization).

Family history of early MI

72
Q

Management of first presentation of stable typical angina?

A

Referral to rapid access chest pain clinic
Commence GTN sublingual spray
ECG

73
Q

what advice should you give a patient with stable typical angina - whilst they are awaiting rapid access chest pain clinic?

A

Instruct the person that if they experience chest pain they should:

Stop what they are doing and rest.

Use their glyceryl trinitrate spray or tablets as instructed.

Take a second dose after 5 minutes if the pain has not eased.

Call 999 for an ambulance if the pain has not eased 5 minutes after the second dose, or earlier if the pain is intensifying or the person is unwell.

74
Q

what is the pharmacological first line treatment of angina?

A

Prescribe a beta-blocker or a calcium-channel blocker (CCB) as first-line regular treatment to reduce the symptoms of stable angina, depending on the person’s comorbidities, contraindications, and preference

beta blocker - better if HR > 70
CCB - better if HR <70, or if has HTN

75
Q

what is the pharmacological second line treatment of angina?

A

beta blocker + CCB together

76
Q

what is the third line treatment of angina?

A

If both beta-blockers and CCBs are contraindicated or not tolerated, consider monotherapy with one of the following drugs.:

A long-acting nitrate (such as isosorbide mononitrate).
Nicorandil.
Ivabradine.
Ranolazine.

77
Q

what drug treatment should be offered for secondary prevention of further CVD in angina?

A

Consider low dose antiplatelet therapy - i.e. aspirin 75mg OD

Consider ACE-I - especially in patients who have T2DM, HF, CKD and HTN.

Consider statin.

78
Q

in which patients with angina should you consider early referral to cardiologist ?

A

Previous myocardial infarction, coronary artery bypass graft, or percutaneous transluminal coronary angioplasty and development of angina.

ECG (electrocardiographic) evidence of previous myocardial infarction or other significant abnormality.

Newly diagnosed atrial fibrillation and angina.

Heart failure and angina.

An ejection systolic murmur suggesting aortic stenosis.

Any suggestion of hypertrophic cardiomyopathy (for example by family history, physical examination, or ECG).

79
Q

what are some causes of angina?

A

cardiac causes:
- atherosclerotic disease in the blood vessels supplying the heart
- left ventricular hypertrophy (this can happen in cardiomyopathies, HTN, aortic stenosis, AF)

non-cardiac causes:
- anaemia
- blood loss

80
Q

how should a patient with angina who is considered high risk for CVD be managed?

A

optimise management of comorbidities i.e. heart failure, CKD, T2DM, HTN

advice to stop smoking

encourage eating a cardioprotective diet

encourage increase in physical activity - within the limits of what is comfortable for the patient

limit alcohol consumption

81
Q

how often should patients with angina have a routine review with the GP?

A

Review the person every 6 months to 1 year depending on the stability of their angina and their comorbidities.

82
Q

what should be covered during a routine angina review?

A

review symptoms - severity, frequency etc.

review CVD risk and any new modifiable risk factors

83
Q
A

AKT revision (10 decks)

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