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3rd Year Conditions > Cardio > Flashcards

Cardio Flashcards

1
Q

What is acute coronary syndrome?

A
  • thrombus from an atherosclerotic plaque blocking a coronary artery
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2
Q

What are the main coronary arteries and what do they supply?

A
  1. RCA - right atrium, right ventricle, inferior aspect of left ventricle, posterior septal area
  2. LCx - left atrium, posterior aspect of left ventricle
  3. LAD - anterior aspect of left ventricle, anterior aspect of spetum
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3
Q

What are the 3 types of acute coronary syndrome?

A
  • unstable angina
  • STEMI
  • NSTEMI
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4
Q

How is acute coronary syndrome diagnosed?

A
  • patient presents with symptoms
  • perform ECG
  • ST elevation or new left bundle branch block = STEMI
  • No elevation then perform a troponin blood tes
  • raised troponin and/or other ECG changes (ST depression, T wave inversion) = NSTEMI
  • normal troponin and normal ECG = unstable angina or another MSK cause
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5
Q

Symptoms of acute coronary syndrome

A
  • nausea and vomiting
  • sweating
  • feeling of impending doom
  • SOB
  • palpitations
  • pain radiating to jaw or arms
  • if goes away with rest then consider angina
  • be aware that diabetics don’t present with normal chest pain
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6
Q

What would ECG changes would you expect to see in STEMIs and NSTEMIs?

A
  1. STEMI: ST elevation or new left bundle branch block

2. NSTEMI: ST depression, T wave inversion, Q waves

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7
Q

Match the ECG leads with the corresponding arteries

A
  • I, aVL, V3-6 = left coronary
  • V1-4 = Left anterior descending
  • I, aVL, V5-6 = left circumflex
  • II, III, aVF = right coronary
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8
Q

What can cause raised troponins?

A
  • MI
  • chronic renal failure
  • myocarditis
  • aortic dissection
  • PE
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9
Q

Investigations for Acute coronary syndrome?

A
  • ECG
  • troponins
  • physical exam
  • Bloods
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10
Q

How is acute coronary syndrome managed?

A
  1. Acute STEMI: PCI (if available within 2 hours) if not then thrombolysis (significant risk of bleeding, streptokinase, alteplase, tenecteplase)
  2. NSTEMI: BATMAN (beta blockers, aspirin 300mg, ticagrelor 180mg, morphine, anticoagulant fondaparinux, nitrates to relieve spasm)
    - to prevent ACS: aspirin 75mg, clopidogrel or ticagrelor, atorvostatin 80mg, ACE inhibitor, atenolol, aldosterone (if you have heart failure)
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11
Q

What are the 4 different types of MI?

A
  1. Due to acute coronary event
  2. Secondary to increased demand/reduced supply of O2
  3. Sudden cardiac death suggestive of ischaemic event
  4. MI associated with PCI/stunting/CABG
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12
Q

How does heart failure present?

A
  • SOB
  • looking and feeling unwell
  • cough with frothy white/pink sputum)
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • peripheral oedema
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13
Q

How is heart failure diagnosed?

A
  • clinical presentation
  • N-terminal pro-B type natriuretic peptide
  • echocardiogram
  • ECG
  • listen to lung bases for crackles
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14
Q

What can cause heart failure?

A
  • ischaemic heart disease
  • valvular heart disease (aortic stenosis)
  • hypertension
  • arrhythmias (AF)
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15
Q

How is heart failure managed?

A
  • refer to specialist
  • surgical treatment for severe aortic stenosis or mitral regurgitation
  • stop smoking
  • exercise at tolerated
  • treat co-morbidities
  • ACE inhibitor
  • Beta blocker
  • Aldoesterone
  • loop diuretics
  • if acute then sit patient up, give O2 if sats are low, give furosemide and monitor fluid balance
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16
Q

Signs of heart failure on examination

A

Left: tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles

Right: raised JVP, hepatomegaly, ascites, ankle/sacral oedema

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17
Q

Signs of heart failure on a CXR

A
  • alveolar shadowing
  • kerley B lines
  • cardiomegaly
  • upper lobe diversion
  • pleural effusion
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18
Q

Causes of atrial fibrillation

A
  • thyrotoxicosis
  • hypertension
  • pneumonia
  • alcohol
  • hypertension
  • mitral valve disease
  • ischaemic heart disease
  • rheumatic heart disease
  • cardiomyopathy
  • pericarditis
  • sick sinus syndrome
  • atrial myxoma
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19
Q

Presenting symptoms of atrial fibrillation

A
  • often asymptomatic
  • palpitations
  • SOB
  • syncope
  • symptoms of cause of AF
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20
Q

Signs of atrial fibrillation

A
  • irregularly irregular pulse

- difference in apical beat and radial pulse

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21
Q

Main differential of AF

A
  • ventricular ectopics

- this will disappear when the heart rate goes over a certain threshold

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22
Q

AF on an ECG

A
  • absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular rhythm
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23
Q

Valvular vs non-valvular AF

A
  • valvular = mitral stenosis

- non-valvular = anything else (incl. mitral regurg)

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24
Q

How can AF be treated?

A
  1. Rate or rhythm control
  2. Anticoagulation
  • Rate control is first-line UNLESS: reversible cause, new onset (within 48 hrs), causing heart failure, symptomatic despite being effectively rate controlled
  • Go for beta blocker, calcium channel blocker or digoxin
  • Rhythm control if reversible cause, new onset, casing heart failure, symptomatic despite effective rate control
  • Cardioversion is used
  • Immediate if less than 48 hours or unstable
  • Delayed if more than 48 hours and stable
  • anticoagulate for 3 weeks before delayed cardioversion
  • cardioversion is achieved using flecanide or amiodarone (if structural heart disease)
  • or use electrical cardioversion
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25
Q

What is the CHADSVASc score?

A
  • risk of stroke
  • used for AF patients, to determine best anticoagulation policy
  • Congestive heart failure, hypertension, age, diabetes, prior stroke, vascular disease, female
  • 1 = consider
  • 2 or more = offer anticoagulation
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26
Q

What is the HAS-BLED score?

A
  • patients on anticoagulation
  • risk of serious bleed each year
  • hypertension, abnormal renal and liver function, stroke, bleeding, labile INRs, elderly, drugs or alcohol
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27
Q

What is aortic dissection?

A

tear in the inner layer of the aorta, allowing blood to flow between the layers of the wall of the aorta (between intima and media)

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28
Q

Which part of the aorta is usually affected by dissection?

A
  • ascending aorta and arch

- right lateral area of ascending aorta is under most stress from blood leaving the heart

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29
Q

What is the Stanford system of classifying aortic dissection?

A
  • Type A = ascending aorta before brachiocephalic artery

- Type B = descending aorta, after subclavian artery

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30
Q

What is the DeBakey system of classifying aortic dissection?

A
  • Type I begins in the ascending aorta and involves at least the aortic arch
  • Type II is isolated to the ascending aorta
  • Type IIIa begins in the descending aorta and involves only the section above the diaphragm
  • Type IIIb begins in the descending aorta and involves the aorta below the diaphragm
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31
Q

Risk factors for developing aortic dissection

A
  • age
  • male
  • smoking
  • hypertension (main one)
  • poor diet
  • reduced physical activity
  • raised cholesterol
  • bicuspid aortic valve
  • coarction of aorta
  • aortic valve replacement
  • CABG
  • connective tissue disorders
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32
Q

Presentation of aortic dissection

A
  • difficult to spot
  • sudden onset, severe ripping or tearing chest pain
  • anterior chest when ascending is affected
  • back is descending is affected
  • some don’t have chest pain
  • hypertension
  • differences in BP between arms
  • radial pulse deficit
  • diastolic murmur
  • focal neurological deficit
  • chest and abdominal pain
  • collapse
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33
Q

How is aortic dissection diagnosed?

A

ECG and CXR to exclude MI

CT angiogram to confirm the diagnosis

MRI angiogram has more detail but takes longer

34
Q

How is aortic dissection treated?

A
  • surgery
  • analgesia
  • BP and HR control using beta blockers
  • type A = midline sternotomy
  • type B = thoracic endovascular aortic repair
35
Q

Complications of aortic dissection

A
  • MI
  • stroke
  • cardiac tamponade
  • aortic valve regurgitation
  • death
36
Q

Define AAA

A
  • dilation of the abdominal aorta with a diameter of more than 3cm
37
Q

Risk factors for developing an AAA

A
  • male
  • age
  • smoking
  • hypertension
  • family history
  • existing cardiovascular disease
38
Q

How can we screen for AAA

A
  • US scan for men at age 65

- if above 3cm then referred to a vascular team

39
Q

How do AAAs present?

A
  • usually asymptomatic
  • non-specific abdominal pain
  • pulsatile and expansile mass when palpated
  • as an incidental finding on xray, US or CT
40
Q

How can we diagnose an AAA?

A

US is initial investigation

CT angiogram to give a detailed picture of the aneurysm and helps guide elective surgery to repair the aneurysm

41
Q

How can we classify AAAs?

A
  • Normal = less than 3cm
  • Small = 3 - 4.4cm
  • Medium = 4.5 - 5.4cm
  • Large = above 5.5cm
42
Q

How should we manage AAAs?

A
  • treat reversible risk factors
  • smoking
  • healthy diet and exercise
  • optimise management of hypertension, diabetes and hyperlipidaemia
  • yearly screens for 3-4.4cm
  • 3 monthly for 4.5-5.4cm
  • elective repair for patients with any of: symptomatic aneurysm, diameter growing more than 1cm per year, diameter above 5.5cm
  • elective repair involves inserting an artificial graft into the section of the aorta affected by the aneurysm
  • open repair via a laparotomy
  • endovascular aneurysm repair via femoral arteries
  • inform DVLA if above 6cm
  • stop driving if above 6.5cm
43
Q

What are the most common causes of infective endocarditis?

A
  • streptococci
  • staphylococci
  • enterococci
44
Q

What are the risk factors for infective endocarditis?

A
  • prior history
  • presence of prosthetic heart valve
  • abnormal valves
  • congenital heart disease
  • post-heart transplant
  • recent dental work/poor dental hygiene
  • IV drug use
45
Q

How does infective endocarditis present?

A
  • fever with sweats/chills/rigors
  • malaise
  • arthralgia
  • myalgia
  • confusion
  • skin lesions
46
Q

Signs of infective endocarditis on examination

A
  • pyrexia
  • tachycardia
  • signs of anaemia
  • clubbing
  • janeway lesions and osler’s nodes
  • splinter haemorrhages
47
Q

Investigations for infective endocarditis

A
  • Bloods (rheumatoid factor positive is common)
  • Urinalysis (microscopic haematuria, proteinuria)
  • Blood culture
  • Echocardiogram
  • Duke’s classification
48
Q

Management of infective endocarditis

A
  • Antibiotics, benzylpenicillin or gentamicin
  • Strep = flucloxacillin/vancomycin/gentamicin
  • Enterococci = ampicillin/gentamicin
  • Culture -ve = vancomycin or gentamicin
  • Surgery if urgent valve replacement needed
49
Q

Complications of infective endocarditis

A
  • valve incompetence
  • fistulae or abscesses
  • aneurysm
  • heart failure
  • renal failure
  • glomerulonephritis
50
Q

How should ventricular tachycardia be treated?

A
  • amiodarone infusion
51
Q

What is atrial flutter, what are the associated conditions and how is it treated?

A
  • when electrical signal keeps looping around the atria to keep atrial contractions at 300bpm, enters ventricle every second so 150bpm ventricular contraction
  • sawtooth appearance on ECG with p wave after p wave
  • hypertension, IHD, cardiomyopathy, thyrotoxicosis
  • rate/rhythm control with beta blockers or cardioversion
  • treat underlying cause
  • anticoagulation based on CHA2DS2VASc score
52
Q

What is supraventricular tachycardia?

A
  • electrical signal re-entering the atria from the ventricles and back through the AV node causing another ventricular contraction
  • results in self-perpetuating electrical loop without an end-point
  • QRS followed immediately by a T wave and so on
53
Q

What are the 3 different types of SVT?

A
  1. Atrioventricular nodal re-entrant tachycardia - re-entry point is back through the AV node
  2. Atrioventricular re-entrant tachycardia (WPWS)
  3. Atrial tachycardia - electrical signal originates in the atria somewhere other than the SAN
54
Q

How should stable patients with SVT be managed? How should it be managed in the long-term?

A
  • continuous ECG
  • Valsalva manoeuvre (blow hard against resistance)
  • Carotid sinus massage
  • Adenosine
  • Direct current cardioversion if all else fails
  • beta blockers, calcium channel blockers or amiodarone
55
Q

Contraindications to adenosine

A
  • asthma
  • COPD
  • heart failure
  • heart block
  • severe hypotension
56
Q

Causes of prolonged QT

A
  • long QT syndrome
  • medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide, antibiotics)
  • electrolyte disturbance (hypokalaemia, hypomagnesia, hypocalcaemia)
57
Q

How should torsades de pointes be managed?

A

correct the cause, magnesium infusion, defibrillation if VT occurs

  • avoid medications that cause QT interval prolongation, correct electrolytes, beta blockers (not solatol) and pacemaker/implantable defibrillator
58
Q

Describe the different types of heart block

A
  1. First degree = delayed atrioventricular conduction through the AV node (PR interval longer than normal)
  2. Second degree Mobitz 1 = atrial impulses get weaker and then a missed conduction (increasing PR and then absent QRS)
  3. Second degree mobitz 2 = intermittent failure or interruption of AV conduction resulting in missing QRS complexes (normal PR interval but regular missing QRS ,2:1, 3:1)
  4. Third degree = complete heart block, no relationship between P waves and QRS complexes. Significant risk of asystole
59
Q

How are unstable heart blocks treated?

A

atropine 500mcg IV

60
Q

Mitral stenosis causes, signs, complications

A
  • rheumatic heart disease or infective endocarditis
  • mid-diastolic, low pitched rumbling murmur
  • loud s1 then decrescendo-crescendo
  • malar flush due to CO2 retention
  • AF caused by left atrium strain
61
Q

Mitral regurgitation causes, signs, complications

A
  • idiopathic weakening of the valve, IHD, infective endocarditis, rheumatic heart disease, connective tissue disorders
  • pan-systolic, high-pitches whistling murmur, axilla
  • results in congestive cardiac failure due to reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart
62
Q

Aortic stenosis causes, signs, complications

A
  • most common
  • idiopathic age related calcification or rheumatic heart disease
  • ejection systolic, high pitched murmur with crescendo-decrescendo character
  • radiates to carotids
  • slow rising pulse
  • light headedness and fainting when exercising
63
Q

Aortic regurgitation causes, signs, complications

A
  • idiopathic age related weakness
  • connective tissue disorder
  • early diastolic, soft murmur
  • decrescendo at s2
64
Q

Risk factors for myocarditis

A
  • usually idiopathic
  • Viruses (coxsackie B, EBV, CMV, adenovirus, influenza)
  • Bacteria (streptococcal, TB, diphtheria)
  • Fungal (candidiasis)
  • Protozoal
  • Helminths
  • SLE, sarcoidosis, polymyositis
  • Drugs
65
Q

Presenting symptoms of myocarditis

A
  • fever, malaise, fatigue, lethargy
  • breathlessness
  • palpitations
  • sharp chest pain
66
Q

How should myocarditis be investigated?

A
  • 12 lead ECG
  • CXR
  • serum CK
  • serum CK-MB
67
Q

Risk factors for pericarditis

A
  • males
  • 20 to 50
  • transmural MI
  • cardiac surgery
68
Q

Features of pericarditis

A
  • sharp, severe retrosternal chest pain worse with inspiration and supine
  • relived when sitting forward
  • pericardial friction rub
  • Beck’s triad (raised JVP, low BP, muffled heart sounds)
69
Q

Types of peripheral vascular disease

A
  • intermittent claudication
  • limb ischaemia
  • arterial ulcers
  • gangrene
70
Q

Symptoms of PVD

A
  • intermittent claudication = cramping in calf, thigh or buttock after walking for a given distance
  • limb ischaemia = pain even on rest, ulcers, gangrene, night pain
71
Q

6 Ps of limb ischaemia

A

pain, pale, pulseless, paralysis, paraesthesia, perishingly cold

72
Q

Cause of venous ulcers, where do they usually form?

A

incompetent valves in the lower limbs leading to venous stasis and increased venous pressure

  • superior to medial malleoli
73
Q

Risk factors and features of venous ulcers

A
  • large, shallow
  • relatively painless
  • irregular margin
  • varicose veins, DVT, fracture, surgery
74
Q

What is classified as hypertension?

A

140/90 in clinic or 135/85 during ambulatory

75
Q

Causes of hypertension

A
  1. Essential = 95% of hypertension
  2. Secondary = ROPE
    - renal disease
    - obesity
  3. Pregnancy induced / pre-eclampsia
  4. Endocrine especially hyperaldosteronism
76
Q

Complications of hypertension

A
  • IHD
  • cerebrovascular accident
  • hypertensive retinopathy
  • hypertensive nephropathy
  • heart failure
77
Q

How often does NICE recommend we take blood pressure?

A
  • every 5 years if borderline for diagnosis but every year with T2DM
78
Q

Why might the blood pressure be more than 20/10mmHg higher in the clinic than at home?

A

white coat hypertension

79
Q

What are the different stages of hypertension?

A

Stage 1 = over 140/90 or 135/85

Stage 2 = over 160/110 or 150/95

Stage 3 = over 180/120

80
Q

What investigations should patients with a new diagnosis of hypertension have?

A
  • Urine albumin:creatinine ratio for proteinuria and dipstick for haematuria
  • Bloods for HbA1c, renal function and lipids
  • Fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities
81
Q

What medications for hypertension? How do we decide which to use?

A 
ACEi
Beta blocker
Calcium channel blocker
Thiazide-like diuretic
Angiotensin II receptor blocker

Angiotensin receptor blocker used instead of ACEi if not tolerant or black/African or Afro-Caribbean - don’t use them together

  • Medication for all with stage 2 or stage 1 and under 80 with Q-risk 10% or more, diabetes, renal disease, cardiovascular disease or end-organ damage
    1. Aged less than 55 and non-black = ACEi
    2. Aged over 55 or black or African or Afro-Caribbean = calcium channel blocker
    3. ACEi + Calcium channel blocker or ARB + calcium channel blocker
    4. ACEi/ARB + CCB + diuretic

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