Cardio Flashcards

1
Q

What is angina?

A

Angina is symptomatic reversible myocardial ischaemia

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2
Q

Features of angina

A

1 Constricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms.

2 Symptoms brought on by exertion.

3 Symptoms relieved within 5min by rest or GTN.

All 3 features = typical angina; 2 features = atypical angina; 0–1 features = non-anginal chest pain.

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3
Q

Precipitants of angina

A

Exertion, emotion, cold weather, and heavy meals.

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4
Q

Most common cause of angina

A

Atheroma

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5
Q

Stable angina

A

Induced by effort, relieved by rest. Good prognosis.

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6
Q

Unstable angina

A

Angina of increasing frequency or severity; occurs on minimal exertion or at rest; associated with increased risk of MI.

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7
Q

Basic tests to consider with angina

A
  • ECG
  • Blood tests:
    • FBC, U&E, TFTs, lipids, HbA1c
  • Echo
  • Chest X-ray
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8
Q

Investigations for ischaemic heart disease (IHD) include:

A
  • Exercise ECG - assess for ischaemic ECG changes.
  • Angiography - either using cardiac CT with contrast, or transcatheter angiography (more invasive but can be combined with stenting)
  • Functional imaging - stress echo (echo whilst undergoing exercise or receiving dobutamine), cardiac MRI.
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9
Q

Management of angina

A
  • Address exacerbating factors
  • Secondary prevention of cardiovascular disease:
    • 75mg aspirin daily if not contraindicated.
  • PRN Symptom pain relief
    • Glyceryl trinitrate (GTN) spray or sublingual tabs.
  • Anti-anginal medication
    • First line: beta blocker and/or calcium channel blocker
  • Revascularization
    • Percutaneous coronary intervention (PCI)
    • CABG
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10
Q

Acute coronary syndromes

A

ACS includes unstable angina and myocardial infarctions (MIs)

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11
Q

What is the common underlying pathology of acute coronary syndromes?

A

plaque rupture, thrombosis, and inflammation

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12
Q

How could you differentiate between MI and unstable angina?

A

MIs have raised troponin, unstable angina does not.

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13
Q

Risk factors for acute coronary syndromes

A
  • Non-modifiable:
    • age,
    • male gender,
    • family history of IHD (MI in 1st-degree relative <55yrs).
  • Modifiable:
    • smoking,
    • hypertension,
    • DM,
    • hyperlipidaemia,
    • obesity,
    • sedentary lifestyle,
    • cocaine use
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14
Q

Classical presentation of MI

A

Acute central chest pain, lasting >20min, associated with nausea, sweatiness, dyspnoea, palpitations.

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15
Q

Revascularistaion of STEMI patients and very high-risk NSTEMI patients

A

should receive immediate angiography ± PCI

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16
Q

Medications for MI

A
  • Antiplatelets
    • Aspirin (75mg OD) and a second anti-platelet agent (eg clopidogrel)
  • Anticoagulant
  • Beta-blockade reduces myocardial oxygen demand
  • ACE-i in patients with LV dysfunction, hypertension, or diabetes unless not tolerated
    (consider ARB). Titrate up slowly, monitoring renal function.
  • High-dose statin, eg atorvastatin 80mg.
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17
Q

PCI or CABG

A

Patients with single-vessel coronary artery disease and normal LV function usually undergo PCI, and those with triple-vessel disease and abnormal LV function more often undergo CABG.

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18
Q

Definition of heart failure

A

Cardiac output is inadequate for the body’s requirements.

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19
Q

Symptoms of left ventricular failure (LVF)

A
  • dyspnoea,
  • poor exercise tolerance,
  • fatigue,
  • orthopnoea,
  • paroxysmal nocturnal dyspnoea (PND),
  • nocturnal cough (±pink frothy sputum),
  • wheeze (cardiac ‘asthma’),
  • nocturia,
  • cold peripheries,
  • weight loss.
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20
Q

Causes of left ventricular failure

A
  • IHD
  • MI
  • cardiomyopathy
  • ventricular hypertrophy
  • constrictive pericarditis
  • tamponade
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21
Q

Causes of right ventricular failure

A
  • LVF,
  • pulmonary stenosis,
  • cor pulmonale
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22
Q

RVF symptoms

A
  • peripheral oedema (up to thighs, sacrum, abdomi- nal wall),
  • ascites,
  • nausea,
  • anorexia,
  • facial engorgement,
  • epistaxis.
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23
Q

Causes of low output cardiac failure

A
  • Excessive preload: eg mitral regurgitation or fluid overload (eg renal failure or too
    rapid IV infusions, particularly in the elderly and those with established HF).
  • Pump failure: systolic and/or diastolic HF, decreased heart rate (eg beta blockers, heart block, post MI), negatively inotropic drugs (eg most antiarrhythmic agents).
  • Chronic excessive afterload: eg aortic stenosis, hypertension.
24
Q

High output heart failure

A
  • This is rare. Here, output is normal or increased in the face of increased needs.
  • Causes: anaemia, pregnancy, hyperthyroidism
25
Q

How is a diagnosis of heart failure made?

A

Requires symptoms of failure and objective evidence of car- diac dysfunction at rest

26
Q

What criteria is used for congestive cardiac failure?

A

Framingham criteria

27
Q

Signs of heart failure

A
  • cyanosis,
  • decreased BP,
  • narrow pulse pressure,
  • pulsus al- ternans,
  • displaced apex (LV dilatation),
  • RV heave (pulmonary hypertension),
  • signs of valve diseases.
  • Severity can be graded using the New York classification
28
Q

Investigations for heart failure

A
  • ECG and B-type natriuretic peptide
  • If either is abnormal, then echocardiography is required.
29
Q

Drugs used to manage heart failure

A
  • Loop diuretics to relieve symptoms, eg furosemide 40mg/24h
  • ACE-inihibitor - Consider in all those with left ventricular systolic dysfunction (LVSD); improves symptoms and prolongs life. If cough is a problem, an angiotensin receptor blocker (ARB) may be substituted
  • Beta-blockers decrease mortality in heart failure
  • Mineralocorticoid receptor antagonists: Spironolactone (25mg/24h PO) decreases mortality by 30% when added to conventional therapy
  • Digoxin helps symptoms
30
Q

How is a diagnosis of hypertension diagnosed?

A

Confirm with 24hr ambulatory BP monitoring (ABPM); or a week of home readings.

NB: the diagnostic threshold is lower ~135/85mmHg.

31
Q

Essential Hypertension

A

Cause unknown

~95% of cases

32
Q

Causes of secondary hypertension

A
  • Renal disease
    • glomerulonephritis, chronic pyelonephritis, or polycystic kidneys
  • Endocrine disease
    • Cushing’s, pheochromocytoma, acromegaly, hyperparathyroidism
  • Other
    • Coarctation, pregnancy
    • Drugs: steroids, MAOIs, oral contraceptive pill, cocaine, amphetamines
33
Q

Lifestyle changes to treat hypertension

A
  • stop smoking;
  • low-fat diet.
  • Reduce alcohol and salt intake;
  • increase exercise;
  • reduce weight if obese.
34
Q

Hypertension drug treatment if ≥55yrs, and in black patients of any age

A

1st choice is a Ca2+ channel antagonist or thiazide

35
Q

Hypertension drug treatment if <55

A

ACE inhibitor or ARB

Consider beta blockers in younger people

36
Q

Mitral regurgitation (MR)

A

Backflow through the mitral valve during systole.

37
Q

Causes of mitral regurgitation

A
  • Functional (LV dilatation);
  • annular calcification (elderly);
  • rheumatic fever;
  • infective endocarditis;
  • mitral valve prolapse;
  • ruptured chordae tendinae;
  • papillary muscle dysfunction/rupture (eg post-MI)
38
Q

Symptoms of mitral regurgitation

A
  • Dyspnoea;
  • fatigue;
  • palpitations;
  • symptoms of causative factor (eg fever).
39
Q

Signs of mitral regurgitation

A
  • AF;
  • displaced, hyperdynamic apex;
  • pansystolic murmur at apex radiating to axilla;
40
Q

Mitral regurgitation investigations

A
  • ECG:
    • AF; LVH.
  • CXR:
    • big LA & LV; mitral valve calcification; pulmonary oedema.
41
Q

Mitral regurgitation management

A
  • Control rate if fast AF.
  • Diuretics improve symptoms.
  • Surgery for deteriorating symptoms; aim to repair or replace the valve before LV is irreversibly impaired.
42
Q

Causes of mitral stenosis

A
  • Rheumatic fever
  • Congenital
  • Prosthetic valve
43
Q

Mitral stenosis presentation

A
  • Normal mitral valve orifice area is ~4–6cm2. Symptoms usually begin when the orifice becomes <2cm2.
  • Pulmonary hypertension causes dyspnoea, haemoptysis, chronic bronchitis-like picture;
  • pressure from large left atrium on local structures causes hoarseness (recurrent laryngeal nerve), dysphagia (oesophagus), bronchial obstruction;
  • also fatigue, palpitations, chest pain, systemic emboli, infective endocarditis (rare).
44
Q

Signs of mitral stenosis

A
  • Malar flush on cheeks (due to decreased cardiac output);
  • low-volume pulse;
  • AF common (due to enlarged LA);
  • tapping, non-displaced, apex beat (palpable S1);
  • RV heave.
  • On auscultation: rumbling mid-diastolic murmur (heard best in expiration, with patient on left side)
45
Q

Mitral stenosis investigations

A
  • ECG: AF; RVH;
  • CXR: left atrial enlargement (double shadow in right cardiac silhouette); pulmonary oedema; mitral valve calcification.
  • Echo is diagnostic
46
Q

Mitral stenosis investigations

A
  • If in AF, rate control is crucial; anticoagulate with warfarin
  • Diuretics decrease preload and pulmonary venous congestion.
  • If this fails to control symptoms, balloon valvuloplasty (if pliable, non-calcified valve), open mitral valvotomy, or valve replacement.
47
Q

Aortic stenosis causes

A
  • Senile calcification is the commonest
  • Others:
    • congenital (bicuspid valve, Williams syndrome)
    • rheumatic heart disease.
48
Q

Presentation of aortic stenosis

A
  • The classic triad includes angina, syncope, and heart failure.
  • Also: dyspnoea; dizziness; faints; systemic emboli if infective endocarditis; sudden death.
49
Q

Aortic stenois signs

A
  • Slow rising pulse with narrow pulse pressure;
  • heaving, non-displaced apex beat;
  • LV heave;
  • aortic thrill;
  • ejection systolic murmur
50
Q

Aortic stenosis investigations

A
  • ECG
  • CXR: LVH; calcified aortic valve; post- stenotic dilatation of ascending aorta
  • Echo: diagnostic
51
Q

Managemenet of aortic stenosis

A
  • If symptomatic, prognosis is poor without surgery: 2-3yr survival if
    angina/syncope; 1-2yr if cardiac failure.
  • Prompt valve replacment
  • If the patient is not medically fit for surgery, transcatheter aortic valve implantation may be attempted
52
Q

Causes of aortic regurgitation

A
  • Acute:
    • Infective endocarditis,
    • ascending aortic dissection,
    • chest trauma.
  • Chronic:
    • Congenital,
    • connective tissue disorders (Marfan’s syndrome, Ehlers–Danlos),
    • rheumatic fever,
    • rheumatoid arthritis,
    • SLE,
    • hypertension,
    • osteogenesis imperfecta.
53
Q

Aortic regurgitation symptoms

A
  • Exertional dyspnoea,
  • orthopnoea,
  • paroxysmal nocturnal dyspnoea
54
Q

Signs of aortic regurgitation

A
  • Collapsing pulse;
  • wide pulse pressure;
  • displaced, hyperdynamic apex beat;
  • high-pitched early diastolic murmur (heard best in expiration, with patient sat forward)
55
Q

Investigations for aortic regurgitation

A
  • ECG: LVH.
  • CXR: cardiomegaly; dilated ascending aorta; pulmonary oedema.
  • Echo is diagnostic.
  • Cardiac catheterisation to assess: severity of lesion; anatomy of aortic root; LV function; coronary artery disease; other valve disease.
56
Q

Management of aortic regurgitation

A
  • The main goal of medical therapy is to reduce systolic hypertension; ACE-i are helpful.
  • Echo every 6–12 months to monitor.
  • Indications for surgery: severe AR with enlarged ascending aorta, increasing symptoms, enlarging LV or deteriorating LV function on echo; or infective endocarditis refractory to medical therapy.