Cardiology Flashcards
What is heart failure?
Definition – the inability of the heart to supply the needs of the body despite adequate filling pressure
What is the New york heart association classification of heart failure?
Classification – New York Heart Association
1. NYHA Class I
• No symptoms
• No limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea, or palpitations
2. NYHA Class II
• Mild symptoms
• Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations, or dyspnoea
3. NYHA Class III
• Moderate symptoms
• Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
4. NYHA Class IV
• Severe symptoms
• Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
What is the difference between systolic and diastolic failure?
Systolic failure – inability of the ventricle to contract normally, resulting in reduced cardiac output. EF <40%. Caused by IHD, MI and cardiomyopathy
Diastolic failure – inability of the ventricle to relax and fill normally, causing increased filling pressure. Typically, EF>50% - HFpEF. Caused by ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity.
Which side of the heart is most often involved in heart failure?
Most commonly this occurs in the left ventricle however it can occur in the right.
RVF and LVF can occur independently or together as CCF.
What causes right heart failure?
Causes of RVF = LVF, pulmonary stenosis and lung disease (cor pulmonale).
What signs and symptoms might you find in someone with chronic heart failure?
Chronic
• Dyspnoea
• Cough that may be worse at night associated with pink/frothy sputum
• Orthopnoea – breathlessness when lying flat
• Paroxysmal nocturnal dyspnoea- severe attack of breathlessness and coughing at night
• Wheeze
• Weight loss (may be hidden by weight gained from oedema)
• Bi-basal crackles on examination
• Displaced apex beat
• Low BP with narrow pulse pressure
What signs and symptoms does right sided heart failure specifically cause?
Specific right sided HF Features = Raised JVP, hepatomegaly, peripheral oedema, ascites, nausea, facial enlargement, and epistaxis.
What is acute heart failure?
Life-threatening worsening of HF can be de novo or decompensated HF. Precipitated by ACS, hypertensive crisis, acute arrhythmia and valvular disease.
What symptoms might someone in acute heart failure present with?
- Breathlessness
- Reduced exercise tolerance
- Ankle swelling and general oedema
- Fatigue
- Elevated JVP
- Cyanosis
- Tachycardia
- Displaced apex beat
- Wheeze
- S3 heart sounds
- Pulmonary fine crackles
How should someone with heart failure be investigated?
N-terminal pro-B-type natriuretic peptide (NT-proBNP) – always first line
• If ‘high’ then arrange specialist assessment and transthoracic echo within 2w
• If ‘raised’ then arrange specialist assessment and transthoracic echo within 6w
BNP produced by LV in response to strain and associated with poor prognosis
Routine bloods especially looking at eGFR
Chest X-ray
ECG
Cardiac MRI helps if echo not easily interpreted
Angiogram if suspicion of new coronary artery disease
What can influence a BNP level to be higher or lower than normal other than heart failure?
BNP can however be influenced by other factors
Increased levels – LVH, ischaemia, tachycardia, RV overload, hypoxaemia, GFR <60ml/min, Sepsis, COPD, diabetes, Age > 70 and liver cirrhosis
Decreased levels – obesity, diuretics, ACEi, beta blockers, ARB and aldosterone antagonists
How should someone in acute heart failure be managed?
- Sit up and give high flow oxygen
- IV access and monitor ECG – treat any arrhythmias
- Investigations as above
- Opiates pain medication, IV diamorphine
- IV Loop diuretics (no change in mortality)
- GTN spray unless systolic BP < 90
- If Systolic > 100 start infusion of isosorbide dinitrate
Consider Inotropic agents, CPAP and discontinue beta blockers
Once stable and improving – daily weights, change to oral furosemide, consider adding thiazide if on high dose and reassess chronic management
How are patients with chronic heart failure with reduced ejection fraction managed, including general, pharmacological and surgical?
Lifestyle factors – better diet such as less salt, fat, and sugars
Annual flu vaccine and one-off pneumococcal vaccine
Treat cause if possible and exacerbating factors such as anaemia, thyroid and infections
Avoid NSAIDS and verapamil which worsen HF
Heart failure with reduced ejection fraction
1st line – ACE-I and/or beta blockers
2nd line – Aldosterone antagonists – spironolactone (be aware this and ACEi can cause hyperkalaemia)
3rd line – Ivabradine (inhibits the SAN) – criteria = sinus rhythm > 75 and LVEF < 35%
– Digoxin – does not improve mortality only symptoms, but useful if coexistent AF
– Hydralazine in combination with nitrate – useful in afro-Caribbean patients
– Cardiac resynchronization therapy – criteria = widened QRS
Defibrillator or ICD – due to tendency for VT and VF
Cardiac Transplant if suitable
What is different about the management of heart failure with preserved ejection fraction?
Heart failure with preserved ejection fraction
Diuretics and treatment of hypertension, diabetes, AF and coronary artery disease
Cardiac Transplant if suitable
What is acute coronary syndrome?
Umbrella term covering presentations of ischaemic heart disease (also known as coronary artery disease and coronary heart disease). This occurs as a result of build up of fatty plaques within the walls of the coronary arteries leading to gradual narrowing and the risk of rupture and clot formation.
How is ACS classified into 3 types?
• Unstable Angina - no troponin release and no myocardial infarction
- Crescendo angina where increasing severity of symptoms over a few days provoked by decreasing exertion
- Angina that presents recurrently and unpredictably both at rest and at exertion
- Unprovoked and prolonged episodes of angina
- NSTEMI – troponin positive without ST elevation, caused by incomplete block/complete block with collateral supply but troponin rise
- STEMI – complete block without collateral supple troponin rise
What are the risk factors for ACS?
Increasing age Male gender Family History Smoking Diabetes Hypertension Hypercholesterolaemia Obesity
What are the clinical features of someone with ACS?
Tight/crushing/heavy/constricting, central/left-sided chest pain that can radiate up to the jaw or down to the arms (can be no pain in female patients, elderly or diabetics) Sweating, pale and clammy Tachycardia Nausea and Vomiting Shortness of breath (dyspnoea) Palpitations Cardiac failure Mitral regurgitation if papillary muscles affected
How should someone with suspected ACS be investigated?
ECG and Cardiac enzymes (Troponin I and T and creatinine kinase)
In the ECG you should look for evidence of ischaemia
• New ST segment elevation (can only assess if in sinus rhythm and no BBB)
• New LBBB with broadened QRS
• Pathological Q waves
Echocardiogram evidence of new loss of viable myocardium
Coronary angiogram showing new intracoronary thrombus
LAD syndrome ECG shows deep T-wave inversion and biphasic T-waves (start positive then go negative)
How does the location of ST elevation in an ECG suggest the location of a narrowing or occlusion?
Left anterior descending infarct = anterior territory = V1- V4
Left circumflex artery infarct = lateral territory = 1, aVL V5 and V6
Right coronary artery = inferior territory = 2, 3 and aVF
Note posterior MI may present with reciprocal ST depression and tall R waves in V1-2
How is ACS managed acutely?
First line treatment follows the acronym MONAC:
Morphine 1-10 mg titrate to pain
Oxygen (if <94% sats)
Nitrates – Glyceryl Trinitrate (GTN given IV)
Aspirin 300mg and one of
• Clopidogrel 600mg if already on an anticoagulant
• Ticagrelor 180mg if undergoing fibrinolysis
• Prasugrel 60mg if undergoing PCI
Reperfusion therapy
PCI (percutaneous coronary intervention) = angioplasty followed by a stent
Thrombolysis with a fibrinolytic drug as well as antithrombin therapy to prevent further thrombus formation, for this use LMWH or fondaparinux unless angioplasty likely in the next 24 hours or creatinine >265umol/l then give unfractionated heparin.
Once identified how are STEMIs managed?
PCI is gold standard if <12hrs since onset and available within 2hrs
If less than 12 hours from presentation and PCI not available within 2 hours, then thrombolysis followed by maintenance in hospital medications. After 90 minutes repeat ECG looking for 50% resolution in ST elevation. If inadequate resolution, then rescue PCI is superior to repeat thrombolysis. If successfully treated a follow up PCI is still beneficial.
Once identified how are NSTEMIs and UA managed?
All patients should receive Aspirin
If unstable then immediately start MONA and proceed to PCI and high risk management
Add fondaparinux if no IMMEDIATE PCI planned, if creatinine > 265 or immediate PCI planned then give unfractionated heparin instead. Following this calculate the 6-month mortality GRACE score.
If low risk GRACE (= 3%) then conservative management, add in ticagrelor if not at high risk of bleeding or clopidogrel if they are
If high risk (>3%) then offer PCI within 72 hours (or immediately if unstable). Give unfractionated heparin regardless of whether they had fondaparinux or not. Add in prasugrel or ticagrelor if not taking an oral anticoagulant or clopidogrel if they are
How should blood glucose levels be managed during ACS?
Hyperglycaemia should be managed with sliding scale insulin infusion with regular CBG monitoring to levels <11.1mmol/l.
What are the rules regarding driving in the following heart conditions and procedures?
ACS ACS successfully treated by PCI Elective angioplasty Angina CABG Pacemaker insertion ICD Catheter ablation Heart transplant
- No driving for 4 weeks unless successfully treated by angioplasty then it is 1 week
- Elective angioplasty – 1 week off driving
- Angina – cease driving if symptoms occur at rest/at the wheel
- CABG – 4 weeks off driving
- Pacemaker insertion – no driving for 1 week
- ICD – if for sustained Ventricular arrhythmia then stop driving for 6 months. If prophylactically then stop for 1 month. Group 2 driving not allowed with ICD.
- Catheter ablation – 2 days off driving
- Heart transplant – do not drive for 6 weeks
How do we prevent further ACS events in the future?
Aspirin (75mg) indefinitely and another antiplatelet for 12 months either Ticagrelor for if medically managed or Ticagrelor or Prasugrel if PCI
Anticoagulation until discharge
Beta blocker (If contraindicated Ca+ channel blocker such as verapamil or diltiazem)
ACEi if LV dysfunction, HTN or diabetes
Statin
Cardiac Rehabilitation
What is stable angina?
Constricting discomfort in the chest, neck, shoulders, jaw or arms precipitated by physical exertion and relieved by rest or GTN spray within 5 minutes. All 3 features = typical, 2 features = atypical.
How should suspected stable angina be investigated?
If diagnosis cannot be excluded by clinical assessment then 1st, 2nd and 3rd line investigations should be:
- CT coronary angiography
- Non-invasive functional imaging (e.g. myocardial perfusion scintigraphy/single photon emission computed tomography MPS/SPECT, stress echocardiography, contrast enhanced MRI or MRI imaging for stress-induced wall motion abnormalities
- Invasive coronary angiography
What lifestyle modifications should patients make to managed stable angina?
Lifestyle modifications Reduce weight Reduce saturated fats and healthy diet Stop smoking and drinking alcohol Control diabetes, hypertension and cholesterol levels Exercise regularly
How is stable angina managed pharmacologically?
Pharmacology
- Aspirin
- Statin
- Sublingual GTN (tolerance often generated)
- Beta blockers OR calcium channel blocker and increase to max dose as required
- If no control gained, then use dual therapy.
For Ca+ blocker if used alone then use negative ionotropic and rate limiting such as verapamil or diltiazem, if used in combination with beta blocker then use long acting dihydropyridine such as MR nifedipine, amlodipine and felodipine DO NOT prescribe verapamil AND beta-blocker due to risk of complete heart block.
- Long acting nitrate, ivabradine (reduced HR), nicorandil (vasodilator) or ranolazine.
Only add in 3rd drug with dual therapy whilst awaiting PCI or CABG
What side effects can patients expect from Ca+ blockers, beta blockers, nitrates, Ivabradine and Nicorandil?
Calcium channel blockers – headaches, flushing, ankle oedema and verapamil = constipation
Beta blockers – bronchospasm, fatigue, cold peripheries, sleep disturbance and dizziness
Nitrates – headache, postural hypotension and tachycardia
Ivabradine – visual effects, headache, bradycardia, and heart block
Nicorandil – headache, flushing and anal ulceration (CI in left ventricular failure)
What surgery can be used to managed stable angina?
Percutaneous coronary intervention
What is hypertension?
Definition – blood pressure above 140/90 that stays persistently high across multiple readings or a 24-hour average blood pressure reading > 135/85 measured by ABPM or HBPM
How are ambulatory and home blood pressure monitoring done?
Ambulatory blood pressure monitoring (2 measurement per hour whilst awake) or home blood pressure monitoring (BP measured morning and evening with 3 readings each time, repeat for 4-7 days, discard first measurement then use average of the rest).
What causes hypertension?
Primary – cause unknown (95% of cases)
Secondary
• Renal diseases e.g. glomerulonephritis, chronic pyelonephritis, PCKD and renovascular disease
• Endocrine disorders such as: primary hyperaldosteronism Conn’s syndrome (5-10%), Cushing’s, pheochromocytoma, acromegaly and congenital adrenal hyperplasia , Liddle’s syndrome and hyperthyroidism.
• Others e.g. coarctation of the aorta, pregnancy, NSAIDs, glucocorticoids, and drugs such as the COCP
How does hypertension present?
Asymptomatic unless >200/120 in which case headache, visual disturbance, and seizures
Hypertensive retinopathy, CKD, IHD
What investigations should be done on someone with hypertension?
U&E, Ca+ and urine dipstick looking for proteinuria and potassium levels
Fasting blood glucose or HbA1c and lipid levels to gauge overall risk
ECG, echo and renal US
Fundoscopy
When should patients be managed based on their stage of hypertension?
Stage 1 = ABPM/HBPM >/= 135/85 – treat <80yrs only if end organ damage, CVD, renal disease, diabetes, or 10-year cardiovascular risk >/= 10%. Consider treating all under 60yrs with stage 1 as Q risk may underestimate at this age group.
Stage 2 = ABPM/HBPM >/=150/95 – treat all patient regardless of age
Severe hypertension – clinical systolic >/= 180 or diastolic >/= 120 – admit to hospital if signs of retinal haemorrhage, papilloedema or life-threatening symptoms such as confusion, chest pain, heart failure or AKI. Also consider phaeochromocytoma. If none of these then arrange urgent investigations for end organ damage, if found start management immediately otherwise repeat BP measurement in 7 days
What lifestyle modifications should patients with hypertension be advised for?
Lifestyle Changes – eating more healthy foods, less salt, less caffeine, more exercise, stop smoking and drinking, less cholesterol and lose weight.
How is hypertension managed pharmacologically?
Pharmacological
- Ace inhibitor or Angiotensin II receptor blockers (i.e. candesartan or losartan)
- Add in a calcium channel blocker or a thiazide diuretic
- Use all 3 (ACEi/A2RB, Ca+ blockers, and thiazide diuretic)
- If K+ < 4.5 add in spironolactone if K+ > 4.5. add an alpha or beta blocker
If over 55 or Afro-Caribbean, then start on with calcium channel blocker and add A2RB later.
What are the common side effects of the 3 main drug classes used in hypertension?
Side effects
ACEi – cough, hyperkalaemia, and angioedema
Calcium channel blockers – flushing, ankle swelling and headache
Thiazide diuretics – hyponatraemia, hypokalaemia, hypercalcaemia, gout, impaired GTT, impotence and dehydration
A2RB – hyperkalaemia
What treatment target should we aim for in patients with hypertension?
Blood pressure targets
Age<80yrs = <140/90 or ABPM/HBPM < 135/85
Age > 80yrs = <150/90 or ABPM/HBPM < 145/85
What is Aliskiren?
Note new drug Aliskiren – direct renin inhibitor preventing conversion of angiotensin to angiotensin I. Similar affect on BP as ACEi but fewer SE, no mortality data yet.
What is malignant hypertension?
Rapid increase in blood pressure resulting in vascular damage. Typically seen with bilateral retinal haemorrhages and papilloedema. Very high mortality rate if not treated. Patients present with severe headaches, visual disturbances, BP over 200/130.
What complications can malignant hypertension lead to if left untreated?
This can precipitate AKI, heart failure, cerebral infarction, MI and encephalopathy. This is much more common in younger people and black people.
How should malignant hypertension be managed?
Patients should be treated immediately with IV labetalol or sodium nitroprusside with the aim of reducing their blood pressure by 15-20% within minutes to an hour and have a target BP of 160/120
What are the common cardiac and non-cardiac causes of arrhythmias?
Cardiac – IHD, structural changes, cardiomyopathy, pericarditis, and myocarditis
Non-cardiac – caffeine, smoking, alcohol, pneumonia, drugs and metabolic disturbance
How can arrhythmias present?
Palpitations Chest pain Syncope or pre-syncope Hypotension Pulmonary oedema SOB Asymptomatic Exercise induced symptoms are concerning
What investigations should you order in someone you think has an arrhythmia?
12-lead ECG -stand alone
24-hour Holter monitor plus patient diary of when they feel palpitations. Can step up to external loop recorder or implantable loop recorder if still find nothing
Blood tests U&Es including Mg+ and Ca+, TFTs and FBC
Echocardiogram
Provocation tests
What are tachyarrhythmias?
These are arrhythmias (i.e. not sinus) that occur with a HR >100bpm.
How are tachyarrhythmias assessed and managed acutely?
Assess patient using ABCDE Are adverse features present? • Shock • Syncope • Myocardial infarction • Heart failure If yes, then unstable and require up to 3 Synchronised DC shocks If this fails seek expert help. Give amiodarone 300mg IV over 10-20minutes then repeat a shock following this give Amiodarone 900mg over 24 hours.
If adverse features are not present, then must assess whether QRS complex is narrow (<0.12s) or broad (>0.12s).
How are regular narrow complex tachyarrhythmias managed?
In these the ventricles are being depolarised via the normal conduction pathway.
Attempt vagal manoeuvres such as:
• Carotid sinus massage whilst lying patient with head below their legs
• The Valsalva manoeuvre (blowing out against a closed airway i.e. shut mouth, pinch nose and attempt to expel air)
• Forced cough (pressure in chest stimulates vagus nerve)
• Push knees against the chest
• Stimulate the gag reflex
• Cold water treatment on the face
Failing this Adenosine is used to help visualize the underlying rhythm. Monitor ECG constantly and give rapid IV bolus followed by flush, start with 6mg, followed by 12mg and if still nothing can attempt with 12mg again.
If any of the above resolves the tachyarrhythmia, then it was likely a re-entry paroxysmal SVT such as Atrioventricular re-entry tachycardias AVNT like Wolf Parkinson White or Atrioventricular nodal re-entry tachycardia (AVRNT) which are circuits from within the AVN. A 12 lead should be recorded whilst they are in sinus rhythm, if they return back to the SVT then consider prophylactic anti-arrhythmic drugs
If sinus rhythm is not achieved, then seek expert help as this I likely Atrial flutter and needs rate controlling.
How are irregular narrow complex tachycardias managed?
This indicates it is probably AF in which case rate control should be achieved with a beta-blocker or diltiazem. If in heart failure consider digoxin or amiodarone. Assess risk of stroke and anticoagulate appropriately.
How are broad complex tachyarrhythmias managed?
In these the ventricles are being depolarised via the an abnormal conduction pathway.
Regular
If VT or the rhythm us unclear, then give amiodarone300mg IV over 20-60 minutes following by 900mg over 24 hours. If patient known to be SVT with a bundle branch block treat as for regular narrow complex tachycardia.
Irregular
Seek expert help and opinion. Possibilities include AF with bundle branch block in which case treat as for irregular narrow complex. If pre-excited AF then consider amiodarone. If Torsade’s de pointes (VT with a varying axis) long QT is a predisposing factor so give IV magnesium.
What are ventricular ectopics and when should they be investigated?
Define: bigeminy, trigeminy , couplet and triplet
Ventricular ectopics – common and can be symptomatic, pulse may feel irregular If frequently missing beats. On ECG the ectopic will appear as a broad complex QRS. Occasional ventricular ectopic very common in healthy individuals, if >60/hr require further investigation
- Bigeminy – ectopic every other beat
- Trigeminy – every third beat
- Couplet – two ectopic together
- Triplet – three ectopics together
What is atrial fibrillation?
Atria are beating in non-synchronous random way meaning there is a lack of P-waves and the ventricles only respond randomly when a signal gets through causing an irregular pulse. Cardiac output will decrease by 10-20% as ventricles are not primed by the atria.
What causes atrial fibrillation?
Cardiac: Ischaemic Heart Disease, hypertension, heart failure, and mitral valve disease
Other: PE, pneumonia, hyperthyroidism, caffeine, alcohol and post-op.
What are the clincial features of atrial fibrillation?
AF can be paroxysmal only occurring periodically, but this eventually becomes constant.
Asymptomatic or painful, palpitations, dyspnoea, feeling faint and LV failure
ECG findings – Irregularly irregular beat, lack of P waves and Tachycardic (Fast AF)
How should atrial fibrillation be managed acutely?
Acute
If haemodynamically unstable then electrical cardioversion should be given as an emergency
If <48 hours anticoagulate with heparin
Rhythm control with DC cardioversion or pharmacologically with amiodarone/flecainide if successful further anticoagulation is unnecessary
If > 48hours rate control with bisoprolol or diltiazem. Rhythm control can only be used >48hours if patient has been anticoagulated for >3 weeks first or a transoesophageal echo has been performed to exclude thrombus, then patient can be treated as if <48 hours.
Following DC cardioversion in AF >48 hours patients must be anticoagulated for at least 4 weeks, and then a decision is made based on individual risk.
How should atrial fibrillation be managed chronically?
Chronic AF can be paroxysmal (self-terminating), persistent (not self-terminating), or permanent (cannot be cardioverted or attempts to do so are inappropriate). Rate control and anticoagulation are the main treatment options. Use rhythm control only if younger than 65, symptomatic, first presentation, congestive heart failure or AF from corrected precipitant
Rate control – beta-blocker or rate limiting calcium channel blocker (diltiazem) 1st choice. If this fails, then add digoxin and then consider amiodarone. Aim for resting heart rate of <90bpm. Digoxin first line if co existent heart failure.
Rhythm control – Elective DC cardioversion, must do echo first to check for clots or anticoagulate for 3 weeks prior. Can also use elective pharmacological cardioversion with flecainide or amiodarone.
Catheter Ablation – use in those where medication is not acceptable or has not worked. Performed percutaneously and aims to ablate faulty electrical pathways. Requires anticoagulation 4 weeks prior and at least 2 months after.
Who needs long-term anticoagulation in atrial fibrillation and how is this decided?
Decision based on score from CHA2DS2-VASc for stroke risk and HAS-BLAD for bleeding. If CHADS-VAS score is 2 or more then anticoagulate everyone, in males with a score of 1 consider anticoagulation. A score of 0 indicates low risk of stroke and no anticoagulation is required however a transthoracic echo should be done to rule out valvular disease – which in combination with AF is an absolute indication for anticoagulation. A HAS-BLAD score >3 indicates a high bleeding risk.
What is atrial flutter?
Underlying atrial rate is 300 so ventricular rate will be a factor of 300 dependant on the level of AV block.
How is atrial flutter treated?
Treated in similar way to fibrillation except that DC cardioversion preferred to pharmacological. Recurrence also high so ablation is recommended for long term control.
How should you assess someone for atrial flutter?
Important to assess after slowing ventricular rhythm down to visualise the atrial depolarisations either with carotid sinus massage or adenosine.
What are heart blocks?
In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles.
Describe first-degree heart blocks
First-degree heart block
PR interval > 0.2 seconds. Aasymptomatic first-degree heart block is relatively common and does not need treatment
Describe the two types of second-degree heart block
Second-degree heart block
- Mobitz I, Wenckebach: progressive prolongation of the PR interval until a dropped beat occurs
- Mobitz II: PR interval is constant, but the P wave is often not followed by a QRS complex
Describe the third-degree type of heart block or complete heart block
There is no association between the P waves and QRS complexes. The right coronary artery most commonly supplies AV node. Complete heart block is usually due to a degenerative disease in the elderly but can also be due to right coronary artery disease.
If SA node is not working, then a junctional rhythm from AV nodes takes over generally at about 30-50bpm in a regular bradycardia. You may not see a p wave as atria will contract at the same time as the ventricles.
How are heart blocks treated?
Heart blocks are treated using a dual lead pacemaker, one lead detects the atrial contraction the second stimulates the ventricles to contract as a result.
What is wolf parkinson white disorder?
Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF
What ECG features might you see in WPW disorder?
Possible ECG features include:
• Short PR interval
• Wide QRS complexes with a slurred upstroke - ‘delta wave’
• Left axis deviation if right-sided accessory pathway most common
• Right axis deviation if left-sided accessory pathway rare
