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Clinical Modules > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Atherosclerosis definition

A

Combination of fatty deposits in artery walls (atheromas) and hardening/ stiffening of vessel walls (sclerosis)

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2
Q

Consequences of atherosclerosis

A
  • stiffening of artery walls -> extra resistance against blood flow -> high blood pressure -> inc strain on the heart
  • stenosis -> reduced blood flow (eg angina)
  • plaque rupture -> thrombus -> vessel blocked -> ACS
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3
Q

CVD non-modifiable risk factors

A
  • Older age
  • Family history
  • Male
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4
Q

CVD modifiable risk factors

A
  • Raised cholesterol
  • Smoking
  • Alcohol consumption
  • Poor diet
  • Lack of exercise
  • Obesity
  • Poor sleep
  • Stress
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5
Q

End results of atherosclerosis

A
  • Angina
  • Myocardial infarction
  • Transient ischaemic attacks
  • Strokes
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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6
Q

What does QRISK3 calculate

A

percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years

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7
Q

QRISK3: what threshold for what intervention?

A

10% or above - should be offered statin

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8
Q

How soon should lipids be checked after starting a statin?

A
  • check 3 months after starting
  • increase dose to aim for a greater than 40% reduction in non-HDL cholesterol
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9
Q

When should LFT’s be checked after starting a statin

A
  • check within 3 months of starting and again at 12 months
  • Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use - only need to be stopped if rise is <3 times the upper limit of normal
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10
Q

Statin side effects

A
  • Myopathy (causing muscle weakness and pain)
  • Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
  • Type 2 diabetes
  • Haemorrhagic strokes (very rarely)
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11
Q

Statins should be stopped when taking which medication?

A

macrolide abx (clarithromycin/ erythromycin)

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12
Q

4 methods of secondary prevention of CVD

A

4 A’s (depends on condition):
* Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
* Atorvastatin 80mg
* Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
* ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

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13
Q

Clinical diagnosis of familial hypercholesterolaemia

A

* Family history of premature cardiovascular disease (e.g., myocardial infarction under 60 in a first-degree relative)
* **Very high cholesterol **(e.g., above 7.5 mmol/L in an adult)
* **Tendon xanthomata **(hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)

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14
Q

At what threshold of sclerosis do exertional symptoms show?

A

70-80% sclerosed

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15
Q

Cause of angina

A
  • atherosclerosis of coronary arteries -> reduced blood flow to the heart
  • high oxygen demand (eg exercise) -> insufficient blood supply -> chest pain
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16
Q

Stable vs unstable angina

A
  • “stable” = symptoms only come on with exertion, always relieved by rest or GTN spray
  • “unstable” = symptoms appear randomly at rest -> ACS, requires immediate management
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17
Q

Angina investigations

A
  • Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
  • ECG (a normal ECG does not exclude stable angina)
  • FBC (anaemia)
  • U&Es (required before starting an ACE inhibitor and other medications)
  • LFTs (required before starting statins)
  • Lipid profile
  • Thyroid function tests (hypothyroidism or hyperthyroidism)
  • HbA1C and fasting glucose (diabetes)
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18
Q

What does cardiac stress testing involve?

A
  • assesses heart function during exertion
  • stress the heart with exercise (eg treadmill) or medication (eg dobutamine)
  • cardiac function assessed via ECG, echocardiogram, MRI or a myocardial perfusion scan (nuclear medicine scan)
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19
Q

2 types of coronary angiography

A
  • CT coronary angiography - inject contrast and take CT images
  • Invasive coronary angiography - insert catheter into radial/ femoral artery, direct through to coronary arteris, inject contrast and take X-ray images (gold standard)
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20
Q

Stable angina management

A
  • R – Refer to cardiology
  • A – Advise them about the diagnosis, management and when to call an ambulance
  • M – Medical treatment
  • P – Procedural or surgical interventions
  • S – Secondary prevention
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21
Q

3 aims of medical management of stable angina

A
  • Immediate symptomatic relief during episodes of angina - GTN spray
  • Long-term symptomatic relief - beta blocker +/- CCB, specialist drugs (isosorbide mononitrate, Ivabradine, Nicorandil, Ranolazine)
  • Secondary prevention of cardiovascular disease (4A’s)
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22
Q

How does GTN work

A
  • GTN causes vasodilation by relaxing vascular smooth muscle
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23
Q

How to use GTN spray

A
  • Take the GTN when the symptoms start
  • Take a second dose after 5 minutes if the symptoms remain
  • Take a third dose after a further 5 minutes if the symptoms remain
  • Call an ambulance after a further 5 minutes if the symptoms remain
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24
Q

What does percutaneous coronary intervention involve?

A
  • inserting catheter into radial/ femoral artery
  • guided to coronary arteries -> contrast injected to identify areas of stenosis -> dilate balloon to widen the lumen (angioplasty) and insert stent to keep it open
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25
Q

What does a coronary artery bypass graft involve?

A
  • offered in cases of severe stenosis
  • open chest with midline sternotomy incision
  • graft vessel attached to the affected coronary artery, bypassing the stenotic area
  • usually taken from saphenous vein/ internal mammary artery/ radial artery
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26
Q

PCI vs CABG

A
  • PCI has** faster recovery** and lower rate of strokes as a complication but** higher rate of requiring repeat revascularisation** (further procedures)
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27
Q

ACS Risk factors

A

Non modifiable
* Family history
* Age
* Ethnicity (S. Asian)

Modifiable
* Smoking
* Poor nutrition
* Sedentary lifestyle
* Alcohol
* Stress
* HTN
* Obesity
* DM

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28
Q

ACS presentation

A
  • central, constricting chest pain
  • radiates to jaw or arms
  • Sweating and clamminess
  • A feeling of impending doom
  • Shortness of breath
  • Palpitations
  • symtoms continue at rest for more than 15 minutes.
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29
Q

What does the RCA supply?

A

Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area

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30
Q

What does the circumflex artery supply?

A

Left atrium
Posterior aspect of the left ventricle

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31
Q

What does the LAD supply?

A

Anterior aspect of the left ventricle
Anterior aspect of the septum

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32
Q

Risk factor for silent MI

A

Diabetes

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33
Q

ECG changes in STEMI

A

ST-segment elevation
New left bundle branch block

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34
Q

ECG changes in NSTEMI

A

ST segment depression
T wave inversion

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35
Q

Which ECG leads correspond to the left coronary artery?

A

I, aVL, V3-6

anterolateral

36
Q

Which ECG leads correspond to the LAD?

A

V1-4

anterior

37
Q

Which ECG leads correspond to the circumflex?

A

I, aVL, V5-6

lateral

38
Q

Which ECG leads correspond to the RCA?

A

II, III, aVF

inferior

39
Q

What troponin result would indicate an NSTEMI?

A

a high or rising troponin on repeat tests in the context of suspected ACS

40
Q

non-ACS causes of raised troponin

A

Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

41
Q

Investigations for suspected/ confirmed ACS

A
  • ECG
  • troponin
  • Baseline bloods (FBC, U&E, LFT, lipids, glucose)
  • Chest x-ray
  • Echocardiogram (once stable)
42
Q

When to diagnose STEMI

A

ECG shows either:
ST elevation
New left bundle branch block

43
Q

When to diagnose NSTEMI

A

raised troponin, with either:
A normal ECG
Other ECG changes (ST depression or T wave inversion)

44
Q

When to diagnose unstable angina

A

sx suggestive of ACS with a normal troponin and either:
A normal ECG
Other ECG changes (ST depression or T wave inversion)

45
Q

Initial ACS management

A

C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)

46
Q

What to do if a pt is currently pain-free but has had ACS suggestive pain within the past 72 hours?

A
  • refer to hospital for same-day assessment
  • emergency admission if ECG changes or complications (eg signs of HF)
47
Q

STEMI management with reperfusion therapy

A
  1. offer PPCI if present within 12hrs of onset and can deliver PPCI in 120mins, otherwise fibrinolysis
  2. give DAPT post procedure
  3. cardiac rehab

https://www.nice.org.uk/guidance/ng185/resources/visual-summary-stemi-pdf-8900623405

48
Q

STEMI medical management

A
  • Offer ticagrelor with
    aspirin unless high
    bleeding risk
  • Consider clopidogrel
    with aspirin, or aspirin
    alone, for high bleeding
    risk
  • cardiology assessment
  • cardiac rehab

https://www.nice.org.uk/guidance/ng185/resources/visual-summary-stemi-pdf-8900623405

49
Q

NSTEMI/ unstable angina mx for low risk patients

A
  1. Consider conservative management without
    angiography
  2. Offer ticagrelor with aspirin unless high bleeding risk (clopidogrel instead)
  3. Consider ischaemia testing -> if positive consider angiography
  4. Cardiac rehab

(predicted 6-month mortality ≤ 3%)

https://www.nice.org.uk/guidance/ng185/resources/visual-summary-unstable-angina-nstemi-pdf-8900622109

50
Q

NSTEMI/ unstable angina mx for high risk patients

A
  1. Offer immediate angiography if clinically unstable, otherwise within 72 hours
  2. Offer prasugrel/ ticagrelor with aspirin if no CI
  3. Consider angiogram findings, discuss mx strategy
  4. Cardiac rehab

(predicted 6-month mortality > 3%)

https://www.nice.org.uk/guidance/ng185/resources/visual-summary-unstable-angina-nstemi-pdf-8900622109

51
Q
A
52
Q

What does the GRACE score predict

A
  • The GRACE score gives a 6-month probability of death after having an NSTEMI
  • 3% or less is considered low risk
  • Above 3% is considered medium to high risk
53
Q

Complications of MI

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

54
Q

What does the GRACE score predict

A
  • The GRACE score gives a 6-month probability of death after having an NSTEMI
  • 3% or less is considered low risk
  • Above 3% is considered medium to high risk
55
Q

Aetiology of Dressler’s syndrome

A
  • post-myocardial infarction syndrome
  • 2-3 weeks post MI
  • localised immune response that causes pericarditis
56
Q

What does the GRACE score predict

A
  • The GRACE score gives a 6-month probability of death after having an NSTEMI
  • 3% or less is considered low risk
  • Above 3% is considered medium to high risk
57
Q

Pericarditis causes

A
  • Idiopathic
  • Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses)
  • Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis)
  • Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma)
  • Uraemia (raised urea) secondary to renal impairment
  • Cancer
  • Medications (e.g., methotrexate)
58
Q

What is pericadial efffusion and what problems does it cause

A
  • the potential space of the pericardial cavity fills with fluid
  • inward pressure on the heart - harder for it expand during diastole
59
Q

What is pericardial tamponade and what problems does it cause

A
  • pericardial effusion is large enough to raide intra-pericardial pressure
  • reduces heart filling and cardiac output
  • emergency - requires drainage to relieve pressure
60
Q

Pericarditis presentation

A
  • low-grade fever
  • chest pain:
  • Sharp
  • Central/anterior
  • Worse with inspiration (pleuritic)
  • Worse on lying down
  • Better on sitting forward
  • Pericardial friction rub on auscultation
61
Q

Pericarditis investigations

A
  • bloods: inflammatory markers
  • ECG (saddle-shaped global ST-elevation, PR depression)
  • Echo
62
Q

Pericarditis mx

A
  • NSAIDs
  • Colchicine (longer-term, recurrence prophylaxis)
  • steriod 2nd line
  • treat underlying causes
  • pericardiocentesis if significant pericardial effusion/ tamponade
63
Q

Triggers of acute left ventricular failure

A
  • Iatrogenic (e.g., aggressive IV fluids in a frail elderly patient with impaired left ventricular function)
  • Myocardial infarction
  • Arrhythmias
  • Sepsis
  • Hypertensive emergency (acute, severe increase in blood pressure)
64
Q

Acute LVF presentation

A
  • acute SOB, worse lying down
  • looking and feeling unwell
  • cough - frothy white/ pink sputum
  • Signs: raised RR, reduced O2 sats, raised HR, 3rd HS, bibasal crackles, hypotension if severe
65
Q

Acute LVF investigations

A
  • Clinical assessment (history and examination, starting with an ABCDE approach in any acutely unwell patient)
  • ECG to look for ischaemia and arrhythmias
  • Bloods for anaemia, infection, kidney function, BNP, and consider troponin if suspecting myocardial infarction
  • Arterial blood gas
  • Chest x-ray
  • Echocardiogram
66
Q

Acute LVF management

A
  • hospital admission
  • ICU if severe pulmonary oedema/ cardiogenic shock
  • S – Sit up
  • O – Oxygen
  • D – Diuretics
  • I – Intravenous fluids should be stopped
  • U – Underlying causes need to be identified and treated (e.g., myocardial infarction)
  • M – Monitor fluid balance
67
Q

Causes of chronic heart failure

A
  • Ischaemic heart disease
  • Valvular heart disease (commonly aortic stenosis)
  • Hypertension
  • Arrhythmias (commonly atrial fibrillation)
  • Cardiomyopathy
68
Q

2 types of HF

A
  • Reduced ejection fraction (<50%) - systolic
  • Preserved ejection fraction (>50% with clinical features of HF) - diastolic
69
Q

HF presentation

A
  • Breathlessness, worsened by exertion
  • Cough, which may produce frothy white/pink sputum
  • Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
  • Fatigue
70
Q

Signs of HF

A
  • Tachycardia (raised heart rate)
  • Tachypnoea (raised respiratory rate)
  • Hypertension
  • Murmurs on auscultation indicating valvular heart disease
  • 3rd heart sound on auscultation
  • Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema
  • Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
  • Peripheral oedema of the ankles, legs and sacrum
71
Q

PND symptoms

A
  • waking up at night with severe SOB, cough and wheeze
  • having to sit up or walk around the room
  • sx improve over several minutes
72
Q

HF investigations

A
  • Clinical assessment (history and examination)
  • N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
  • ECG
  • Echocardiogram
  • Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
  • Chest x-ray and lung function tests to exclude lung pathology
73
Q

4 classes of NYHA

A

Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest

74
Q

5 principles of HF mx

A

R – Refer to cardiology
A – Advise them about the condition
M – Medical treatment
P – Procedural or surgical interventions
S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support

75
Q

NT-proBNP result cut-off for Echocardiogram

A
  • From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
  • Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
76
Q

4 drugs used for medical mx of HF

A
  • A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
  • B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
  • A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
  • L – Loop diuretics (e.g., furosemide or bumetanide)
77
Q

Threshold for HTN diagnosis

A
  • clinical reading > 140/90
  • ambulatory/ home readings > 135/85
78
Q

HTN causes

A
  • Essential (primary) HTN - 90%
  • Secondary:
    R – Renal disease
    O – Obesity
    P – Pregnancy-induced hypertension or pre-eclampsia
    E – Endocrine
    D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
79
Q

HTN complications

A
  • Ischaemic heart disease (angina and acute coronary syndrome)
  • Cerebrovascular accident (stroke or intracranial haemorrhage)
  • Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Vascular dementia
  • Left ventricular hypertrophy
  • Heart failure
80
Q

White coat syndrome

A

more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings

81
Q

HTN stages

A
  • Stage 1: clinc > 140/90, home > 135/80
  • Stage 2: clinic > 160/100, home > 150/ 95
  • Stage 3: > 180/120
82
Q

HTN investigations

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities, including left ventricular hypertrophy

83
Q

HTN mx

A

Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C.
Step 2: A + C. Alternatively, A + D or C + D.
Step 3: A + C + D
Step 4: A + C + D + fourth agent (potassium sparing diuretic/ alpha or beta blocker if K>4.5)

84
Q

HTN treatment targets

A

under 80yrs: <140/ <90
over 80yrs: <150/ <90

85
Q

malignant HTN definition

A
  • BP> 180/120 with retinal haemorrhages or papilloedema
86
Q

malignant HTN mx

A
  • same-day referral - hypertensive emergency
  • fundoscopy
  • assess for complications (confusion, HF, ACS, AKI)
  • assess for end-organ damage
  • monitor BP
  • IV meds:
  • Sodium nitroprusside
  • Labetalol
  • Glyceryl trinitrate
  • Nicardipine

Clinical Modules (11 decks)

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