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Year 3 - Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What conditions might cause a raised troponin level (not associated with an ACS)

A

Mainly:
- Large pulmonary embolism
- Advanced renal failure

Also:
- Severe congestive heart failure
- Myocarditis
- Aortic dissection
- Aortic stenosis
- Malignancy
- Stroke
- Severe sepsis

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2
Q

What 4 conditions may mimic ST elevation on ECG

A
  1. Early repolarisation
    - especially in leads V1 and V2
  2. Pericarditis
  3. Brugada syndrome
    - ion channel mutation predisposing to ventricular tachycardia (misdiagnosed as anterior STEMI)
  4. Takotsubo cardiomyopathy
    - stress reaction in middle-aged females
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3
Q

STEMI (ACS) - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management steps (immediate and longer term)

A

Pathophysiology:
- Myocardial infarction which is full thickness
- Caused by complete coronary vessel obstruction, usually by a thrombus

Presentation:
- Dull, crushing, central chest pain which can radiate to shoulder tip, neck or jaw
- Sympathetic response e.g. sweating
- SOB
- Nausea / vomiting

ECG changes:
- ST elevation in 2 or more leads in the same zone
- OR LBBB

Investigations:
- Full blood count including troponin I and creatine kinase levels
- ECG

Management:
Immediate
- Cannulation (IV access)
- Pain relief (Morphine and anti-emetics)
- Dual anti-platelet therapy:
1. Aspirin 300mg loading dose (75mg lifelong)
2. Prasugrel 60mg loading dose
- Primary percutaneous coronary intervention (PPCI) without thrombolysis if within 2 hrs of presentation, thrombolysis if PCI not available

Longer term
- Medications: beta-blocker, ACEi and statin
- Manage risk factors (smoking cessation, hypertension, hyperlipidaemia, diabetic control)

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4
Q

N-STEMI (ACS) - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management steps (immediate and longer term)

A

Pathophysiology:
- Myocardial infarction which is partial thickness
- Caused by partial coronary vessel obstruction, usually by a thrombus

Presentation:
- Dull, crushing, central chest pain which can radiate to shoulder tip, neck or jaw
- Sympathetic response e.g. sweating
- SOB
- Nausea / vomiting

ECG changes:
- ST depression
- T wave inversion
- Pathological Q waves

Investigations:
- Full blood count including troponin I and creatine kinase levels
- ECG

Management:
Immediate
- Pain relief (Morphine and anti-emetics)
- Aspirin 300mg loading dose (75mg lifelong)
- LMWH (Enoxaparin)
- Repeat ECG
- May give Ticagrelor
- Nitrates (for coronary artery spasm)

Longer term
- Manage risk factors (smoking cessation, hypertension, hyperlipidaemia, diabetic control)

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5
Q

Explain the procedures of Primary percutaneous coronary intervention (PPCI) and thrombolysis with respect to STEMI and time period when they can be used post-MI

A

Primary percutaneous coronary intervention (PCI):
- Angiography used to visualise blockages in coronary arteries
- Balloon used to open vessel back up, stent used to keep open long term
- Doesn’t involve thrombolysis
- Used within 2 hours of presentation

Thrombolysis:
- Fibrinolytic medication to dissolve thrombi
- Examples: Streptokinase, Alteplase, Tenecteplase
- However significant risk of bleeding
- Used if PPCI isn’t available within 2 hours of presentation

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6
Q

Outline the use of the GRACE score in NSTEMI treatment (what the scores mean)

A

GRACE score:
- Predicts the risk of the patient having another MI or death in the next 6 months
- Used to assess for the need to carry out PCI with a patient with NSTEMI

< 5% = low risk
5-10% = medium risk
> 10% = high risk

If medium or high risk (5%+), then consider for PCI within next 4 days

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7
Q

Outline how the management of STEMI and NSTEMI differs

A

Main management for STEMI (MOAN + PCI/thrombolysis)
- Morphine (IV)
- Oxygen (controlled)
- Aspirin (300mg stat)
- Nitrates (GTN)
Then cardiac team carry out PCI within 2 hours, if not then thrombolysis

Main management NSTEMI (BATMAN + GRACE score):
- Base the decision about angiography / PCI on GRACE score
- Aspirin 300mg stat dose
- Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
- Morphine titrated to control pain
- Antithrombin therapy with Fondaparinux
- Nitrates (GTN)

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8
Q

List the complications of an MI (DARTH VADER)

A

Death
Aneurysm
Ruptures (ventricular wall, septum, papillary muscles)
Tamponade
Heart failure

Valvular disease (papillary muscle rupture or septal rupture)
Arrhythmia
Dressler’s syndrome (pericarditis)
Embolism
Recurrence

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9
Q

Describe Dressler’s syndrome and how it presents, including ECG changes

A

Post-MI syndrome
- Pericarditis that typically occurs 2-3 weeks post-MI
- Caused by a localised immune response

Presentation:
- Pleuritic chest pain, worse on lying flat and better on sitting up
- Pericardial rub on auscultation
- Pericardial effusion
- Low grade fever
- Rarely: cardiac tamponade

ECG changes:
Labile ECG changes (change over time)
- Low QRS complex
- Alternating QRS complex height (electrical alternans)
- Global ST elevation

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10
Q

Stable angina - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management

A

Pathophysiology:
- Atherosclerotic plaques cause narrowing of the coronary arteries leading to reduced blood supply to areas of heart muscle, felt as chest pain
- Occurs on exertion and emotion
- Relieves with rest (chest pain not present at rest)

Presentation:
- Dull, central aching chest pain
- If severe, may have autonomic symptoms e.g. sweating
- Key: present on exertion, relieved on rest
- May have cardiovascular risk factors present

ECG changes:
- None present unless previous ACS/MI

Investigations:
- Full blood count including troponin I and creatine kinase levels, full lipid profile
- ECG
- Calculate angina risk score
High risk: CT coronary angiogram
Medium risk: Echo or stress MRI
Low risk: CT calcium scoring (if high, CT angio)

Management:
- Aspirin 75mg OD
- Sublingual GTN spray
- Beta-blockers and calcium-channel blockers (symptom control)
- Manage cardiovascular risk factors

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11
Q

Hypertension - state the following:
- Pathophysiology
- 3 stages of hypertension
- Management

A

Pathophysiology:
- Increased blood pressure
- Can be primary, or secondary to another condition

3 stages of hypertension:
Stage 1 = BP > 140/90
Stage 2 = BP > 160/100
Stage 3 (severe) = BP > 180 OR diastolic > 110
(home readings 5mmHg less on top and bottom)

Management:
Conservative:
- Weight loss / increase exercise
- Moderate their salt intake
- Smoking cessation
- Limit alcohol

Medical:
Under 55:
1) ACEi
2) Add CCB
3) Add diuretic
Over 55 or afro caribbean:
1) CCB
2) Add ACEi
3) Add diuretic

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12
Q

List some causes of hypertension

A

Essential/primary hypertension (95%)

Others (ROPE):
- Renal stenosis
- Obesity
- Pregnancy
- Endocrine = Conn’s syndrome (hyperaldosteronism) / Cushing’s syndrome (high cortisol) / pheochromocytoma

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13
Q

Explain the difference between emergency hypertension and urgent hypertension

Explain how the differences in how you aim to manage the 2 situations (LEGS)

A

Emergency hypertension:
- High BP associated with a critical event
- e.g. MI, AKI, encephalopathy, pulmonary oedema
Aim of treatment: reduce diastolic BP to < 110 in 3-12 hrs
Give (LEGS):
- IV Labetalol
- IV Esmolol
- IV GTN
- IV Sodium Nitroprusside

Urgent hypertension:
- High BP NOT associated with a critical event
- but is associated with hypertensive retinopathy (grade 3/4)
- e.g. MI, AKI, encephalopathy, pulmonary oedema
Aim of treatment: reduce diastolic BP to < 110 in 24 hrs
- IV Labetalol
- IV Esmolol
- IV GTN
- IV Sodium Nitroprusside

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14
Q

Explain hypertensive retinopathy and the changes seen on fundoscopy (acute and chronic)

A

Damage to eye resulting from hypertension (acute or chronic)

Acute hypertension:
- Vasoconstriction in retinal vessels
- Optic disc oedema
Severe acute hypertension:
- Flame-shaped hemorrhages
- Cotton-wool spots
- Yellow hard exudates

Chronic hypertension:
- Arteriovenous nicking
- Vessel wall changes

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15
Q

List the organs that are targets for organ damage in HTN

A
  • Eyes (retinopathy)
  • Brain
  • Vessels (TIA/stroke / aneurysm)
  • Heart (HF / MI / ischaemia)
  • Kidneys (nephrosclerosis/renal failure)
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16
Q

Outline some tests to assess for end-organ damage in hypertension

A

Kidneys = urine dip and albumin:creatinine level
Eyes = fundoscopy (retinopathy)
Heart = ECG (LV hypertrophy)

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17
Q

List 8 causes of heart failure (I HAV CCCH)

A

Ischaemic heart disease

Hypertension
Atrial fibrillation
Vascular heart disease

Chronic lung disease
Cardiomyopathy
Cancer drugs (previous)
HIV

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18
Q

List some factors indicating a very poor prognosis for someone with heart failure

A
  • Regular hospital admissions with HF
  • Increasing age
  • Severe fluid overload
  • Multiple co-morbidities
  • Very high NT-proBNP levels
  • Severe renal impairment
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19
Q

List some conditions that cause high NT-proBNP levels (other than HF)

A
  • HF
  • Atrial fibrillation
  • R ventricle strain
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20
Q

List some findings on a chest x-ray in heart failure

A
  • Cardiomegaly
  • Perihilar shadowing
  • Pleural effusions
  • Air bronchograms
  • Oedema in alveoli
  • Increased width of vascular pedicle
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21
Q

Heart failure - state the following:
- Pathophysiology (including types)
- Presentation
- ECG changes
- Investigations
- Management

A

Pathophysiology:
- Failure of the heart to supply the demands of the body
- HF with reduced EF OR HF with preserved EF
- Left OR right sided HF OR congestive

Presentation:
- SOB
- Lethargy/tiredness
Left HF
- Cough (white/pinky frothy sputum)
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
- Bibasal crackles
Right HF
- Peripheral pitting oedema
- Raised JVP

ECG changes:
- Evidence of ischaemic heart disease

Investigations:
- Echo = KEY
- Bloods = NT-proBNP
- ECG
- Chest x-ray (cardiomegaly)

Management:
Lifestyle modification
1. Diuretics (Furosemide)
2. ACEi / ARB
3. Sacubitril / Valsartan
4. Beta blocker
5. Other vasodilators
- If the above fails: CRT (cardiac resynchronisation pacemaker) or ICD (implantable cardiac defibrilators)

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22
Q

Outline the NYHF classification for heart failure (stage 1-4)

A

Stage 1:
- No limitations

Stage 2:
- Some limitation on physical activity
- No symptoms at rest

Stage 3:
- Significant limitation on physical activity
- No symptoms at rest

Stage 4:
- Unable to carry out physical activity without symptoms
- May have symptoms at rest

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23
Q

State where an aortic stenosis murmur is best heard and describe the murmur

A

Best heard: 2nd ICS on right

Murmur:
- High pitched ejection systolic murmur
- Crescendo-decrescendo
- Radiates to neck/carotids

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24
Q

State where an aortic regurgitation murmur is best heard and describe the murmur

A

Best heard: sternal edge on left

Murmur:
- Soft pitched early diastolic murmur
- Blowing
- Doesn’t radiate
- Associated with collapsing pulse and head bobbing

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25
Q

State where an mitral regurgitation murmur is best heard and describe the murmur

A

Best heard: 5nd ICS on right, midclavicular line

Murmur:
- High pitched pan-systolic murmur
- Blowing
- Radiates to axilla

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26
Q

Outline common causes of aortic stenosis

A
  • Age-related calcification
  • Rheumatic fever
  • Congenital bicuspid valve
  • Chronic kidney disease
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27
Q

Outline common causes of aortic regurgitation

A
  • Age-related calcification
  • Rheumatic fever
  • Idiopathic dilation of aorta
  • CT diseases e.g. Marfan’s syndrome
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28
Q

Outline common causes of mitral regurgitation

A
  • Rheumatic fever
  • Infective endocarditis
  • CT diseases e.g. Marfan’s syndrome
  • Pectus excavatum
  • Ischaemic heart disease
  • Drugs
  • Left ventricle dilation
29
Q

Outline the presentation of someone with aortic stenosis

A
  • Dyspnoea on exertion
  • Reduced exercise tolerance

Will do on to develop triad of:
- Heart failure
- Angina
- Syncope

30
Q

Outline the presentation of someone with aortic regurgitation

A

May be asymptomatic for many years
- Dyspnoea on exertion
- Reduced exercise tolerance

  • Collapsing pulse
  • Head bobbing
31
Q

Outline the presentation of someone with mitral regurgitation

A

May be asymptomatic for MANY years (up to 16 yrs)
- Dyspnoea on exertion
- Reduced exercise tolerance

32
Q

Outline the investigation and management for aortic stenosis

A

Echo - assess severity of stenosis and rest of heart

  • Surgery (depending on asymptomatic/symptomatic or LVSD)
  • TAVI (transcatheter aortic valve implantation)
33
Q

Outline the investigation and management for aortic regurgitation

A

Echo - assess severity of regurgitation and rest of heart

  • Surgery
  • May use ACEi to reduce afterload, if severe or if LVSD
34
Q

Outline the investigation and management for mitral regurgitation

A

Echo - assess severity of regurgitation and rest of heart (particularly LV function)

  • Surgery (repair or replace)
  • Diuretics (may use ACEi or B-blockers if LVSD)
35
Q

Infective endocarditis - state the most common organisms in:
- Valves (not been replaced)
- Within 1 yr post-valve replacement
- More than 1 yr post-valve replacement
- IV drug users
- Immunocompromised

A

Valves (not been replaced):
- Viridans streptococci
- Staph aureus

Within 1 yr post-valve replacement:
- Coag negative staphylococci

More than 1 yr post-valve replacement:
- Viridans streptococci
- Staph aureus
- Enterococcus faecalis

IV drug users:
- Staph aureus

Immunocompromised:
- Fungal

36
Q

State 2 key investigations for diagnosis of infective endocarditis

A
  • Blood cultures, at least 3 over a few hours, from different sites
  • Echocardiogram for presence of vegetations, TOE is better than TTE
37
Q

Outline antibiotic therapy for infective endocarditis depending on causative organism:
- Viridans streptococci
- Staph aureus
- Enterococci

A

Viridans streptococci:
- Benzylpenicillin (IV)
- Low dose Gentamicin (IV)

Staph aureus:
- Flucloxacillin (IV)
- Gentamicin (IV)

Enterococci:
- Amoxicillin (IV)
- Low dose Gentamicin

38
Q

State some tests to monitor the progression of infective endocarditis in response to treatment

A

Echos (weekly)
- Monitor vegatation size
- Look for complications

ECGs (twice weekly)
- Look for conduction disturbances

Blood tests (twice weekly)

39
Q

Outline the most common causes of AF (affects mrs SMITH)

A

Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension

+ excess alcohol

40
Q

Atrial fibrillation - state the following:
- Pathophysiology
- Presentation
- Investigations
- ECG findings
- Key principles in management

A

Pathophysiology:
- Abnormal electrical conduction causes uncontrolled, uncoordinated, irregular and rapid contraction of the atria
- This leads to irregular conduction through to the ventricles resulting:
- Irregularly irregular contraction of ventricles
- Tachycardia
- Heart failure
- Increased risk of stroke

Presentation:
- Mostly asymptomatic
- Irregularly irregular pulse
- Palpitations
- SOB
- Syncope
- Chest discomfort
- Recent stroke/TIA

Investigations:
- ECG
- 24 hr cardiac monitoring if intermittent AF suspected
- Echo (if structural heart disease, need to control rhythm soon or as a baseline for long term treatment)

ECG findings:
- Absent P waves
- Irregularly irregular ventricular rhythm
- Narrow QRS complex

Key principles in management:
- Rate/rhythm control
Rate: beta blockers
Rhythm: cardioversion (immediate / elective or pharmacological) or long term medication control (Amiodarone / Flecainide)
- Anticoagulation with DOACs (over Warfarin)

41
Q

Outline the CHADSVAS and HAS-BLED scores, what they are used for

A

CHADSVASC - used to guide whether someone should have anticoagulation based on amount of risk factors

CHD / LVEF < 40%
Hypertension
Age (2) > 75
Diabetes
Stroke / TIA / thromboembolism (2)
Vascular disease
Age 65-74
Sex (female)

HAS-BLED - used to determine bleeding risk and guide non-pharmacological methods of reducing coagulation risk

Hypertension
Abnormal liver / renal function (1 each)
Stroke
Bleeding
Labiile INR
Elderly >65
Drugs / alcohol (1 each)

42
Q

List some reversible factors that can be targeted that reduce someone’s bleeding risk

A
  • Alter other bleeding medications e.g. Aspirin, NSAIDs
  • Reduce hypertension
  • Improve INR
  • Reduce alcohol consumption
43
Q

List some benefits of DOACs (over Warfarin)

A
  • Don’t require regular INR monitoring
  • Much fewer interactions with other CYP450 enzyme drugs and foods (leafy green veggies)
  • Slightly better at preventing strokes (compared to Warfarin)
  • Slightly reduced bleeding risk (compared to Warfarin)
44
Q

List some cardiovascular risk factors (modifiable)

A
  • Hypertension
  • Hypercholesterolaemia
  • Smoking
  • Excessive alcohol intake
  • Lack of exercise
  • Poor diet
45
Q

Cardiac tamponade - state the following:
- Pathophysiology
- Common causes
- Presentation
- ECG changes
- Investigations
- Management

A

Pathophysiology:
- Accumulation of fluid in the pericardial lining (between visceral and pleural layers)
- Constricts the filling/expansion of the heart, leading to reduced cardiac output
- Can be sudden or chronic

Common causes:
- Infective e.g. viral / bacterial / TB
- Autoimmune e.g. Dressler’s syndrome (post-MI), RA, SL
- Pericarditis
- Chronic renal failure
- Chest trauma
- Post surgery e.g. valve replacement
- Malignancy / radiotherapy-induced
- Idiopathic

Presentation:
Beck’s TRIAD of:
1. Hypotension
2. Distant heart sounds
3. Elevated jugular venous pressure
- Central, dull chest pain
- Symptoms of reduced cardiac output e.g. syncope or dizziness / SOB / peripheral cyanosis / lethargy
- Raised troponins
- Symptoms related to underlying cause e.g. fever, cough

ECG changes:
- Labile ECG changes
- Low QRS height
- Electrical alternans (alternating heights of QRS)
- Tachycardia

Investigations:
- Routine bloods including troponins, BNP, ESR, CRP
- ECG
- Transthoracic echocardiogram
- Chest x-ray

Management:
- Analgesia
- Colchicine and NSAIDs (anti-inflammatories), may resolve and regular observations and echos
- If haemodynamically unstable - pericardiocentesis

46
Q

Hyperlipidaemia - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Elevated levels of total cholesterol, LDL cholesterol or non-HDL cholesterol
- Associated with cardiovascular disease

Risk factors:
- Abdominal obesity
- Type 2 diabetes
- Hypothyroidism
- Cholestatic liver disease
- Sedentary lifestyle
- Diet high in: saturated fat, trans-fatty acids, and cholesterol.
- Nephrotic syndrome
- Smoking
- Significant family history (e.g. early onset coronary heart disease) suggesting primary hypercholesterolaemia

Presentation:
- Usually asymptomatic until significant atherosclerosis has developed
- Corneal arcus
- Tendon xanthoma
- Xanthelasma
- History of coronary events

Investigations:
- Lipid profile
- Lipoprotein(a)
- Serum TSH (links with hypothyroidism)
- Consider genetic testing if familial suspected

Management:
- Dietary modifications (reduce saturation fats and add plant stanols/sterols to diet)
- Exercise plan
- Statins

47
Q

Explain the 3 branches of peripheral arterial disease

A
  1. Acute limb ischaemia
  2. Chronic peripheral arterial disease
  3. Critical limb ischaemia
48
Q

Acute limb ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Sudden occlusion of a limb artery, most commonly by a thrombus or trauma
- Leads to ischaemia distal to the obstruction

Presentation:
6 P’s
- Pallor
- Painful
- Paralysis
- Pulseless
- Paraesthesia
- Perishing with cold
- PLUS absent peripheral pulses

Investigations:
- Doppler ultrasound
- Immediate referral to vascular surgeons

Management:
- Analgesia
- Immediate referral to vascular surgeons: angioplasty / thrombectomy / thrombolysis / amputation

49
Q

Chronic peripheral arterial disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Narrowing of arteries (mostly due to atherosclerosis), leading to arterial insufficiency and claudication
- Pain on increased activity, due to increased supply, but no pain at rest

Presentation:
- Intermittent claudication
- Chronic skin changes

Investigations:
- ABPI (ankle/brachial < 0.9 = peripheral artery disease)
- Doppler ultrasound

Management:
- Lifestyle modifications e.g. exercise, smoking cessation
- Statins
- Antiplatelets
- Angioplasty / bypass graft if symptomatic

50
Q

Critical limb ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Acute worsening of chronic peripheral arterial disease, leading to pain at rest as well as during increased activity

Presentation:
- 6 P’s
- Pain at rest

Investigations:
- Doppler ultrasound
- None needed, immediate referral to vascular surgeons

Management:
- Analgesia
- Immediate referral to vascular surgeons: angioplasty / thrombectomy / thrombolysis / amputation

51
Q

Outline the 2 shockable rhythms and the 2 un-shockable rhythms

A

Shockable:
- Ventricular tachycardia
- Ventricular fibrilation

Unshockable:
- Asystole
- Pulseless electrical activity

52
Q

Outline the treatment of an unstable patient with tachycardia

A

Up to 3 x DC cardioversion

53
Q

Outline the treatment of stable patients with tachycardia
1. Stable with narrow complex tachycardia
2. Stable with broad complex tachycardia

A
  1. Stable with narrow complex tachycardia
    Need to determine whether it’s regular or irregular:
    Regular:
    - Look to treat underlying cause e.g. pain, sepsis
    - Vagal manoeuvres e.g. carotid sinus massage or valsalva manoeuvre
    - Adenosine (6mg IV bolus, then 12mg then 18mg)
    Irregular (most likely AF):
    - AF less than 48 hrs = rhythm control with Flecainide plus anticoagulation
    - AF more than 48 hrs = rate control with beta blockers plus anticoagulation
  2. Stable with broad complex tachycardia:
    - Amiodarone infusion
54
Q

Atrial flutter - state the following:
- Pathophysiology
- Associated conditions
- Presentation
- ECG changes
- Management

A

Pathophysiology:
- Large sections within the atria take part in re-entry circuit (re-entry arrythmia)
- Causes high volume of atrial contraction
- Approximately half of these make it through, resulting in a very high regular pulse

Associated conditions:
- Hyperthyroidism
- Hypertension
- Ischaemic heart disease
- Cardiomyopathy

Presentation:
- Palpitations
- Syncope / dizziness
- SOB
- Reduced exercise tolerance

ECG changes:
- Sawtooth appearance
- Usually 2 p waves to 1 QRS
- Regular tachycardia (equal but short distances between QRS complexes)
- Most prominent in leads: 2, 3 aVF, and V1

Management:
UNSTABLE
- Immediate direct current (DC) cardioversion (up to 3 shocks)
STABLE (similar to AFib)
- Rate control with beta blockers
- Start on anticoagulation e.g. LMWH
- Treat if underlying cause
- DC cardioversion IF not responding to drugs
- Consider radiofrequency ablation

55
Q

Supraventricular tachycardias (SVTs) - state the following:
- Pathophysiology
- 3 main types of SVT
- Presentation
- Management

A

Pathophysiology:
- Caused by re-entry circuit (re-entry arrhythmia)
- Electrical signal goes from the ventricles, back up to the atria

3 main types of SVT:
1. Atrial tachycardia - ectopic beats generated in atria
2. AV node re-entry tachycardia - re-entry goes through AV node
3. AV accessory re-entry tachycardia - re-entry goes through an accessory pathway e.g. Wolff-Parkinson-White syndrome

Presentation:
- Palpitations
- SOB
- Reduced exercise tolerance

Management:
Continuous ECG monitoring
1. Vasalva maneuver
2. Carotid sinus massage
3. Adenosine
If fail, may need electrical cardioversion
If paroxysmal (recurring) SVT, will either need radiofrequency ablation or medications e.g. b-blockers, CCB or Amiodarone

56
Q

Outline the 4 types of narrow complex tachycardias (tachycardias that are not broad)

A
  1. Sinus tachycardia
  2. SVT (supraventricular tachycardias)
  3. Atrial fibrillation
  4. Atrial flutter
57
Q

Outline how Adenosine works in the treatment of supraventricular tachycardias (SVTs) and how it is given

A

Adenosine slows cardiac conduction by blocking the AV node / accessory pathway and helps to reset back to sinus rhythm

  • Given as a rapid bolus
  • Brief period of asystole or bradycardia
58
Q

Outline Wolff-Parkinson-White syndrome, the ECG changes and the definitive treatment

A

Wolff-Parkinson-White syndrome:
- Atrioventricular reentry tachycardia, caused by a re-entry pathway between the ventricles and the atria
- Type of supraventricular tachycardia

ECG changes:
- Short PR interval
- Delta wave (slurred upstroke to QRS)
- Narrow QRS complex

Definitive treatment:
- Cardiac ablation, either heating therapy (radiofrequency ablation) or freezing therapy (cryoablation) on the affected area

59
Q

List some arrhythmias that cured with radiofrequency ablation

A

SVTs incl. Wolff-Parkinson-White syndrome
Atrial fibrillation
Atrial flutter

60
Q

List some contraindications for giving Adenosine in SVTs

A
  • Heart block
  • Heart failure
  • Asthma / COPD
  • Severe hypotension
61
Q

Torsades de Pointes - state the following:
- Pathophysiology
- Common causes
- ECG changes
- Management

A

Pathophysiology:
- Occurs in patients with prolonged QT
- Type of ventricular tachycardia (polymorphic)
- Prolonged QT interval can cause random spontaneous depolarisations (afterdepolarisations)
- If ventricles continue to stimulate normal contractions without normal repolarisation = Torsades de Pointes
- TDP can either terminate spontaneously or progress to ventricular tachycardia and potentially cardiac arrest

Common causes:
- Mainly inherited (Long QT syndrome)
- Medications e.g. Amiodarone
- Electrolyte disturbances e.g. HYPOkalaemia, HYPOcalcaemia and HYPOmagnesemia

ECG changes:
- QTc prolongation
- Polymorphic QRS complex (height changes around the isoelectric line)

Management:
Acute
- Correct any underlying cause
- Magnesium infusion
- Defibrillation if VT occurs
Long term
- Beta-blockers
- Pacemaker/implantable defibrillator
- Avoid medications that prolong QT

62
Q

Outline 1st degree heart block and management

A

Constant prolonged PR interval (>0.12-0.2s)
No dropped QRS complexes

Management:
No management required, reassure

63
Q

Outline 2nd degree Mobitz T1 heart block and management

A

Increasing prolonged PR interval (>0.12-0.2s), until QRS complex is dropped

Management:
No management required, reassure

64
Q

Outline 2nd degree Mobitz T2 heart block and management

A

Stable PR interval, QRS complex is randomly dropped

Management:
IV Atropine 500mcg (repeat up to 6 times)
- May need other inotropes e.g. noradrenaline
- May require temporary transvenous cardiac pacing or permanent implantable pacemaker

65
Q

Outline 3rd degree heart block and management

A

Complete heart block
No synchronisation between P waves and QRS complexes

Management:
IV Atropine 500mcg (repeat up to 6 times)
- May need other inotropes e.g. noradrenaline
- May require temporary transvenous cardiac pacing or permanent implantable pacemaker

66
Q

Hypertrophic cardiomyopathy - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management

A

Pathophysiology:
- Autosomal dominant genetic heart condition
- Caused by abnormal proteins which cause septal hypertrophy, obstructing the left ventricular outflow and LV hypertrophy
- Often the cause of sudden cardiac death in young people and athletes

Presentation:
Many are asymptomatic
- Syncope on exertion
- SOB
- Chest pain
- Palpitations
- Ejection systolic murmur at the lower left sternal edge
- Family history of sudden cardiac death

ECG changes:
Left ventricular hypertrophy
- Increased QRS amplitude in V1-V4
- Non-specific t wave inversion

Investigations:
- ECG
- Echocardiogram
- MRI heart
- Genetic testing

Management:
Based on risk stratification and presence of symptoms
- High risk: ICD insertion for high risk sudden cardiac death patients
- Exercise restriction
- Reduce outflow obstruction e.g. with beta blockers, verapamil
- Surgical myectomy (removal of septum)
- Alcohol septal ablation
- Management of complications e.g. heart failure and arrhythmias

67
Q

Pericarditis - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management

A

Pathophysiology:
- Inflammation of the pericardium

Presentation:
- Chest pain, usually pleuritic and worse on lying flat
- Fever
- Pericardial friction rub

ECG changes
- Widespread saddle-shaped ST elevation
- PR depression
- Raised troponin

Investigations:
- ECG
- Troponin (tends not to peak like MIs but instead stays constantly elevated in the acute phase)
- Echo
- CT angiogram (rule out MI)

Management:
- Exercise restriction
- NSAIDs
- Colchicine (caution in renal / hepatic impairment)
- 2nd line treatment is corticosteroids
- IV antibiotics if bacterial cause
- Pericardiocentesis if purulent exudate

68
Q

Outline some indications for pacemakers

A
  • Heart block (2nd degree Mobitz type 2 and 3rd degree)
  • Sick sinus syndrome
  • Heart failure
  • Symptomatic bradycardia
  • Drug resistant tachyarrhythmias

Year 3 - Medicine (8 decks)

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