Cardiology Flashcards
What conditions might cause a raised troponin level (not associated with an ACS)
Mainly:
- Large pulmonary embolism
- Advanced renal failure
Also:
- Severe congestive heart failure
- Myocarditis / pericarditis
- Aortic dissection
- Aortic stenosis
- Malignancy
- Stroke
- Severe sepsis
What 4 conditions may mimic ST elevation on ECG
- Early repolarisation
- especially in leads V1 and V2 - Pericarditis
- Brugada syndrome
- ion channel mutation predisposing to ventricular tachycardia (misdiagnosed as anterior STEMI) - Takotsubo cardiomyopathy
- stress reaction in middle-aged females
STEMI (ACS) - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management steps (immediate and longer term)
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)
N-STEMI (ACS) - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management steps (immediate and longer term)
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)
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
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
Outline the use of the GRACE score in NSTEMI treatment (what the scores mean)
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
Outline how the management of STEMI and NSTEMI differs
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)
List the complications of an MI (DARTH VADER)
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
Describe Dressler’s syndrome and how it presents, including ECG changes
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
Stable angina - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management
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
Hypertension - state the following:
- Pathophysiology
- 3 stages of hypertension
- Management
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
List some causes of hypertension
Essential/primary hypertension (95%)
Others (ROPE):
- Renal stenosis
- Obesity
- Pregnancy
- Endocrine = Conn’s syndrome (hyperaldosteronism) / Cushing’s syndrome (high cortisol) / pheochromocytoma
Explain the difference between emergency hypertension and urgent hypertension
Explain how the differences in how you aim to manage the 2 situations (LEGS)
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
Explain hypertensive retinopathy and the changes seen on fundoscopy (acute and chronic)
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
List the organs that are targets for organ damage in HTN
- Eyes (retinopathy)
- Brain
- Vessels (TIA/stroke / aneurysm)
- Heart (HF / MI / ischaemia)
- Kidneys (nephrosclerosis/renal failure)
Outline some tests to assess for end-organ damage in hypertension
Kidneys = urine dip and albumin:creatinine level
Eyes = fundoscopy (retinopathy)
Heart = ECG (LV hypertrophy)
List 8 causes of heart failure (I HAV CCCH)
Ischaemic heart disease
Hypertension
Atrial fibrillation
Vascular heart disease
Chronic lung disease
Cardiomyopathy
Cancer drugs (previous)
HIV
List some factors indicating a very poor prognosis for someone with heart failure
- Regular hospital admissions with HF
- Increasing age
- Severe fluid overload
- Multiple co-morbidities
- Very high NT-proBNP levels
- Severe renal impairment
List some conditions that cause high NT-proBNP levels (other than HF)
- HF
- Atrial fibrillation
- R ventricle strain
List some findings on a chest x-ray in heart failure
- Cardiomegaly
- Perihilar shadowing
- Pleural effusions
- Air bronchograms
- Oedema in alveoli
- Increased width of vascular pedicle
Heart failure - state the following:
- Pathophysiology (including types)
- Presentation
- ECG changes
- Investigations
- Management
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)
Outline the NYHF classification for heart failure (stage 1-4)
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
State where an aortic stenosis murmur is best heard and describe the murmur
Best heard: 2nd ICS on right
Murmur:
- High pitched ejection systolic murmur
- Crescendo-decrescendo
- Radiates to neck/carotids
State where an aortic regurgitation murmur is best heard and describe the murmur
Best heard: sternal edge on left
Murmur:
- Soft pitched early diastolic murmur
- Blowing
- Doesn’t radiate
- Associated with collapsing pulse and head bobbing
State where an mitral regurgitation murmur is best heard and describe the murmur
Best heard: 5nd ICS on right, midclavicular line
Murmur:
- High pitched pan-systolic murmur
- Blowing
- Radiates to axilla
Outline common causes of aortic stenosis
- Age-related calcification
- Rheumatic fever
- Congenital bicuspid valve
- Chronic kidney disease
Outline common causes of aortic regurgitation
- Age-related calcification
- Rheumatic fever
- Idiopathic dilation of aorta
- CT diseases e.g. Marfan’s syndrome
Outline common causes of mitral regurgitation
- Rheumatic fever
- Infective endocarditis
- CT diseases e.g. Marfan’s syndrome
- Pectus excavatum
- Ischaemic heart disease
- Drugs
- Left ventricle dilation
Outline the presentation of someone with aortic stenosis
- Dyspnoea on exertion
- Reduced exercise tolerance
Will do on to develop triad of:
- Heart failure
- Angina
- Syncope
Outline the presentation of someone with aortic regurgitation
May be asymptomatic for many years
- Palpitations
- Dyspnoea on exertion
- Reduced exercise tolerance
- Collapsing pulse
- Head bobbing
Murmur: early diastolic murmur, loudest at left sternal edge
Outline the presentation of someone with mitral regurgitation
May be asymptomatic for MANY years (up to 16 yrs)
- Dyspnoea on exertion
- Reduced exercise tolerance
Outline the investigation and management for aortic stenosis
Echo - assess severity of stenosis and rest of heart
- Surgery (depending on asymptomatic/symptomatic or LVSD)
- TAVI (transcatheter aortic valve implantation)
Outline the investigation and management for aortic regurgitation
Echo - assess severity of regurgitation and rest of heart
- Surgery
- May use ACEi to reduce afterload, if severe or if LVSD
Outline the investigation and management for mitral regurgitation
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)
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
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
State 2 key investigations for diagnosis of infective endocarditis
- Blood cultures, at least 3 over a few hours, from different sites
- Echocardiogram for presence of vegetations, TOE is better than TTE
Outline antibiotic therapy for infective endocarditis depending on causative organism:
- Viridans streptococci
- Staph aureus
- Enterococci
Viridans streptococci:
- Benzylpenicillin (IV)
- Low dose Gentamicin (IV)
Staph aureus:
- Flucloxacillin (IV)
- Gentamicin (IV)
Enterococci:
- Amoxicillin (IV)
- Low dose Gentamicin
State some tests to monitor the progression of infective endocarditis in response to treatment
Echos (weekly)
- Monitor vegatation size
- Look for complications
ECGs (twice weekly)
- Look for conduction disturbances
Blood tests (twice weekly)
Outline the most common causes of AF (affects mrs SMITH)
Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension
+ excess alcohol
Atrial fibrillation - state the following:
- Pathophysiology
- Presentation
- Investigations
- ECG findings
- Key principles in management
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)
Outline the CHADSVAS and HAS-BLED scores, what they are used for
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)
List some reversible factors that can be targeted that reduce someone’s bleeding risk
- Alter other bleeding medications e.g. Aspirin, NSAIDs
- Reduce hypertension
- Improve INR
- Reduce alcohol consumption
List some benefits of DOACs (over Warfarin)
- 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)
List some cardiovascular risk factors (modifiable)
- Hypertension
- Hypercholesterolaemia
- Smoking
- Excessive alcohol intake
- Lack of exercise
- Poor diet
Cardiac tamponade - state the following:
- Pathophysiology
- Common causes
- Presentation
- ECG changes
- Investigations
- Management
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
Hyperlipidaemia - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Investigations
- Management
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
Explain the 3 branches of peripheral arterial disease
- Acute limb ischaemia
- Chronic peripheral arterial disease
- Critical limb ischaemia
Acute limb ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Chronic peripheral arterial disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Critical limb ischaemia - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline the 2 shockable rhythms and the 2 un-shockable rhythms
Shockable:
- Ventricular tachycardia
- Ventricular fibrilation
Unshockable:
- Asystole
- Pulseless electrical activity
Outline the treatment of an unstable patient with tachycardia
Up to 3 x DC cardioversion
Outline the treatment of stable patients with tachycardia
1. Stable with narrow complex tachycardia
2. Stable with broad complex tachycardia
- 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 - Stable with broad complex tachycardia:
- Amiodarone infusion
Atrial flutter - state the following:
- Pathophysiology
- Associated conditions
- Presentation
- ECG changes
- Management
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
Supraventricular tachycardias (SVTs) - state the following:
- Pathophysiology
- 3 main types of SVT
- Presentation
- Management
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
Outline the 4 types of narrow complex tachycardias (tachycardias that are not broad)
- Sinus tachycardia
- SVT (supraventricular tachycardias)
- Atrial fibrillation
- Atrial flutter
Outline how Adenosine works in the treatment of supraventricular tachycardias (SVTs) and how it is given
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
Outline Wolff-Parkinson-White syndrome, the ECG changes and the definitive treatment
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
List some arrhythmias that are cured with radiofrequency ablation
SVTs incl. Wolff-Parkinson-White syndrome
Atrial fibrillation
Atrial flutter
List some contraindications for giving Adenosine in SVTs
- Heart block
- Heart failure
- Asthma / COPD
- Severe hypotension
Torsades de Pointes - state the following:
- Pathophysiology
- Common causes
- ECG changes
- Management
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
Outline 1st degree heart block and management
Constant prolonged PR interval (>0.12-0.2s)
No dropped QRS complexes
Management:
No management required, reassure
Outline 2nd degree Mobitz T1 heart block and management
Increasing prolonged PR interval (>0.12-0.2s), until QRS complex is dropped
Management:
No management required, reassure
Outline 2nd degree Mobitz T2 heart block and management
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
Outline 3rd degree heart block and management
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
Hypertrophic cardiomyopathy - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management
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
Pericarditis - state the following:
- Pathophysiology
- Presentation
- ECG changes
- Investigations
- Management
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
Outline some indications for pacemakers
- Heart block (2nd degree Mobitz type 2 and 3rd degree)
- Sick sinus syndrome
- Heart failure
- Symptomatic bradycardia
- Drug resistant tachyarrhythmias
List some potential causes of left axis deviation
- Left ventricular hypertrophy
- Left bundle branch block
- Inferior MI
- Wolff-Parkinson White syndrome
List some potential causes of right axis deviation
- Right ventricular hypertrophy
- Lateral myocardial infarction
- Acute / chronic lung disease e.g. PE or COPD
- Hyperkalaemia
- Wolff-Parkinson White syndrome
