Cardiology Flashcards
How should arrhythmias be investigated?
- bloods: (TFTs, U&Es, glucose, FBC)
- baseline ECG without symptoms
- Echo (not diagnostic)
- 24 hr ECG
- implantable loop recorders
When do you worry about ectopic beats on a 24hr ecg?
when they occur >20% of the time, it may lead to heart failure
Describe how regular narrow complex (SVT) regular tacharrhythmias are treated if the pt is haemodynamicaly stable? (4 steps)
1st: Valsalver maneouvre
2nd: carotid sinus massage
3rd: adenosine 6mg IV then 12mg x2
4th: IV verapamil or betablockers(last resort// in asthma)
5th: electrocardioversion (do this 1st if haemodynamically unstable)
How should narrow complex irregular tachycardias be treated initially?
(if haemodynamically unstable, if new onset within 48hrs, if been present for >48hrs and if infrequent episodes)
Treat as AF- by far most likely diagnosis
DC if haemodynamically unstable
If presents acutely (within 48hrs)-> chemical rhythm control with amiodarone or 300mg PO flecainide then DC and if urgent rate control needed use CSM, VSM, bisoprolol then verapamil
If old: anticoagulate and offer bisoprolol for rate control/ digoxin in HF. Then bring back in two weeks for cardioversion. Flecainide PRN can be used in infrequent symptomatic AF.
What are the criteria on the CHA2DS2 VASc score?
Congestive heart failure/ LVSD Hypertension Age >75 Diabetes Stroke/ TIA/ VTE Vascular disease Age 65-75 Sex -female
What are the criteria on the HAS BLED score?
Hypertension Abnormal liver or renal function Stroke Bleeding Labile INR Elderly (>65) Drugs or alcohol abuse
What can be done in AF if anticoagulants are not tolerated or contraindicated?
left atrial appendage occlusion
Give 5 causes of AF
- hypertension
- valvular disease
- heart failure
- IHD
- chest infection
- PE
- lung cancer
- alcohol
- hyperthyroid
- electrolyte disturbance
- infections
- diabetes
- age
How are unstable bradycardia treated?
- 500micrograms atropine IV every 3-5 mins (upto 6 times)
- Then give Iv adrenaline 2-20 micrograms/ min IVI while you try to get someone todo transcutaneous pacing
- find and treat cause (eg electrolyte disturbance)
How should pulseless VT and V fib be treated?
defibrillation +/- lidocaine
adrenaline every 3-5 mins and amiodarone after 3 shocks
How should unstable and stable sustained VT with a pulse be treated?
unstable: sedate and do DC cardioversion x 3 then amiodarone 300mg over 20 mins whilst doing more DC shocks, check and correct electrolytes
stable: amiodarone, then flecainide then lidocaine then cardioverision or pacing
How can non sustained VT be treated?
beta blockers- may also need implantable defibrillator
What is torsade de pointes
A very regular broad complex tachy with pointed QRS complexes.
Associated with long QT.
How is torsade de pointes treated?
IV magnesium sulphate 2mg- if unsucessful then sedate for DC cardioversion
Look for cause of long QT (drugs, hypokalaemia, bradycardia, genetics)
Other anti arrhythmics cant be used as they prolong QT
How would you calculate the heart rate from an ECG strip?
Each strip is 10 seconds long
Count the amount of QRS and then multiply by 6
Bradycardia can be caused by SA or AV node dysfunction. Give 4 causes of SA node dysfunction
Hypothyroidism
Hypothermia
Rheumatic Fever
Haemachromatosis
What is Sick Sinus?
Sinus Node Fibrosis
Presents as Tachy Brady
Complete HB occurs when there is no relationship between P and QRS. How does the ECG change depending on where the block is?
Occurring at Bundle of His - Narrow Escape Complex
Occurring below Bundle of His - Broad Escape Complex
Give 3 causes of Complete HB
Digoxin toxicity
Inferior STEMI
Severe Hyperkalaemia
What is a Junctional Rhythm
Abnormal rhythm arising from AV node
How would you manage ACUTE AF (<48hrs ago)? What do you need to consider?
Give Heparin and aim to DC cardiovert
Generally cardiovert young patients due to stroke risk (always listen for carotid bruits first)
AVRTs are Narrow Complex Tachycardias, describe their pathway
Impulse starts in AV node, travels to ventricles and then back up into atria via accessory pathway (ORTHODROMIC)
AVNRTs are Narrow Complex Tachycardias, describe their pathway
Re-entrant loops form within the AV node itself
What is diagnostic on an ECG about AVRT/AVNRTs?
No P Waves
Describe the managements of AVRT/AVNRT
Aim to transiently block the AVN (also helps differentiate it from AF)
1 - Vagal Manouvres
2 - IV Adenosine (6mg, then 12g, then 12mg with long flush)
Describe 3 side effects of Adenosine
Chest Discomfort
Transient Hypotension
Flushing
Describe the 2 types of VT
Monomorphic - Appearance of all beats match eachother, common post MI scarring
Polymorphic - Beat to beat variation, includes Torsades de Pointes
Ventricular Tachycardia can be managed medically (lidocaine), but when would you cardiovert?
If haemodynamically compromised
What are fusion beats?
Sinus and ventricular beats fuse
What are capture beats?
Normal conduction of SVT beats
Appears normal
What is SVT with Aberrancy?
Aberrancy is a functional BBB with increased HR
Won’t be able to tell the different between SVT with BBB until back in sinus rhythm
What is Antidromic WPW?
AVRT that conducts the opposite way
Conducts down through accessory pathway and up through AV node
Delta waves form as the impulse passes through accessory pathway
Treated the same as NCT
what are some cardiac and non cardiac causes of arrhythmias
Cardiac
- ischaemic heart disease (IHD)
- structural changes eg left atrial dilation secondary to mitral regurgitation
- cardiomyopathy
- pericarditis, myo-carditis
- aberrant conduction pathways
Non cardiac-
- caffeine, smoking, alcohol
- pneumonia
drugs (B2 agonists, digoxin, L-dopa, tricyclics, doxorubicin)
- metabolic imbalance (K, Ca, Mg, hypoxia, hypercapnia, metabolic acidosis, thyroid disease)
- phaeochromocytoma.
how do arrhythmias generally present
Palpitations, chest pain, syncope/pre syncope, hypotension or pulmonary oedema. Some arrhythmias may be asymptomatic incidental findings eg AF.
what are the different types of continuous egg monitoring and describe them and their uses
- Telemetry- an inpt wears ECG leads and the signals are shown on screens being watched by staff thus if a dangerous arrhythmia occurs, help is immediately available. Reserved for those at high risk of dangerous arrhythmias eg immediately post-STEMI.
- Excersise ECGs- the pt excersises, the BP and ECG are monitored, looking for ischameic changes, arrhythmias and features suggestive of arrhythmia risks such as delta waves
- Holter monitors- the pt wears an ECG monitor which records their rhythm for 24h-7d, this is later analysed. These can also be used to pick up ST changes of suggestive ischaemia.
- Loop recorders- These record only when activated by the pt and they record a small amount of ECG data before the event. Useful of the arrhythmia causes loss of consciousness/ infrequent epidoseed
- Pacemakers and ICDs- these record details of cardiac electrical activity and device activity. This information can be useful for establishing an arrhythmic origin for symptoms
what is the definition of bradycardia
Heart rates of less than 60bpm are considered to be bradycardia.
However, it is more helpful to classify a bradycardia as absolute (<40bpm) or relative when the heart is innapropriately slow for the haemodynamic state of the pt.
what are the signs of haemodynamic instability
- Systolic bp<90mmHg
- HR<40bpm
- Poor perfusion and urine output
- Ventricular arrhythmias requiring suppression
- Heart failure
what are some causes of sinus node disease? when is pacing required as the treatment?
- sinus bradycardia may be due to medications
- Hypothyroidism, hypothermia and sleep apnoea should be considered
- Less commonly sinus bradycardia can be the result of rheumatic fever, viral myocarditis, amyloidosis, haemochromatosis and pericarditis.
- common in the elderly as it is fibrosis of the sinus node
Pacing is rarely required in an acute setting. not all pt will be symptomatic, in pt with symptomatic sinus node disease a pacemaker is indicated.
how may a sick sinus syndrome patient present and how would you treat?
Symptoms: syncope and pre-syncope, light headedness, palpitations, breathlessness
Management: thromboembolism prophylaxis if episodes of AF are detected, permanent pacemakers for pt with symptomatic bradycardia or sinus pauses
• Some pt develop a ‘tachy Brady syndrome’ suffering from alternating tachycardia and bradycardic rhythms. This can prove difficult to treat medically as treating one circumstance (eg tachycardia) increases the risk from the other
• Pacing for bradycardic episodes in combination with rate slowing medications for tachycardia episodes may be required if the pt is symptomatic or usntable.
what is first degree heart block and how would you treat
- characterised by a PR interval>0.2secs. Every atrial depolarisation is followed by conduction to the ventricles but with delay
- no specific treatment is indicated.
- For pt on digoxin, check for toxicity.
- Also take care with other rate limiting drugs. If there are symptoms of dizziness or syncope cardiac monitoring should be considered to identify higher degrees of block.
what is 2nd degree type 1 heart block and how would you treat
- this is characterised by progressive lengthening of the PR interval, followed by failure of the atrial impulse to conduct to the ventricles giving P wave conduction failiure (dropped QRS).
- Progressive fatigue of AV nodal cells- due to functional suppression of AV conduction (eg drugs, reversible ischaemia).
- It can occur in fit young pt with high vagal tone so can be seen during the night if monitored. It can occur quite frequently following inferior MI and rarely proceeds to complete heart block.
- No specific therapy is indicated. Higher degrees of AV block should be looked for if pt present with syncope or dizziness. Does not require pacing unless poorly tolerated.
what is 2nd degree type 2 heart block and how would you treat
- characterised by a constant PR interval followed by a sudden failure of a P wave to be conducted to the ventricles, this is less common, but indicates more serious involvement of the conduction system.
- Much more likely to have haemodynacmic compromise, severe bradycardia and progression to third degree heart block
- In the absence of a recent acute coronary event, permanent pacing should be arranged (if drugs have been excluded).
what is 3rd degree (complete) heart block and how would you treat
- characterised by no conduction from the atria to the ventricles and thus AV dissociation.
- There is no relationship between the P waves and QRS completes.
- This block can occur above the AV node at the His region (narrow complex escape and usually well tolerated such as congenital complete heart block) or beneath the AVN with broad complex escape (not well tolerated).
- Causes include various anti-arrhythmic drugs but more notably digoxin toxicity. It can occur following inferior STEMI (<10% cases) and in this context can resolve in hours to days. It is a more ominous finding following anterior MI (infranodal). Another important cause is severe hyperkalaemia ( can be treated with IV calcium chloride- 10ml of 10% solution over 3-5 mins). In the haemodynamically unstable pt, atropine can be administered (600μg to a maximum of 3mg). Isoprenaline is administered ar a rate of 5μg/min and can be tried.
- Urgent permanent pacing is indicated and should be considered within 24hr is all pt except those with a reasonable likelihood of recovery of conduction- such as in pt w a recent coronary event.
what is the commenest cardiac arrhythmia
Atrial fibrillation
what are some signs and symptoms of AF? what is the main risk of AF
Symtoms: may be asymptomatic or cause chest pain, palpitations, dyspnoea, or faintness.
Signs: irregularly irregular pulse, the apical pulse rate is greater than the radial rate, and the first heart sound is of variable intensity; signs of LVF. Remember to examine the pt as AF is often associated with non cardiac disease
main risk is embolic stroke. Warfarin reduces this
what are the principles of AF management
There are two key parts of managing pt with AF:
1. Rate/ rhythm control
2. Reducing stroke risk
NICE advocate using a rate control strategy except in a number of specific situations such as coexistent heart failure, younger than 65, first onset AF or where there is an obvious reversible cause
• <48hr rate or rhythm, >48/ time unclear then usually rate control but if rhythm anticoagulant for 3wks!
what is the rate control management of AF
- 1st Bisoptolol or CCB eg verapamil
- 2nd Digoxin (preferred if concurrent heart failiure) then amiodarone
- If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following: a b blocker, diltiazem or digoxin.
- With rate control you have to accept that the pulse will be irregular but slow the rate down to avoid the negative effects on cardiac function
what are some contraindications of Bisoprolol and verapamil in AF patients
Bisoptolol (CI: asthma, COPD, heart block)
CCB eg verapamil (CI: heart block, hypotension, pulmonary oedema)
when should immediate vs delayed cardioversion be used in an AF patient
- There are a subgroup of pt for whom a rhythm control strategy should be tried first (coexistent heart failure, younger than 65, first onset AF or where there is an obvious reversible cause, <48hr rate)
- other pt may have had a rate control strategy initially but switch to rhythm control if symtoms/ HR fails to settle
- There is a choice between immediate cardioversion or delayed cardioversion:
- Immediate- if the AF has been present for less than 48hr or they are severely haemodynamically unstable.
- Delayed- if the AF has been present for more than 48 hrs and they are stable. If delayed cardioversion is chosen the pt must be anti coagulated for >3wks first. This is due to the fact that the moment a pt switches from AF to sinus rhythm presents the highest risk for embolism leading to stoke
what is atrial flutter and how do you treat
a regular atrial rhythm of approximately 300bpm. It conducts to the ventricles at a a rate of 2:1 (thus 150 ventricular bpm). It is characterised by a ‘saw tooth’ like baseline.
Anti AF drugs may not work but try anyway
- Cardioversion (anticoagulate first)
- IV amiodarone to restore sinus rhythm
- Amiodarone or sotalol to maintain it
- Aim to control rate as above (bisoprolol or verapamil)
- Cavotricuspid isthmus ablation (rarely)
what criteria may help differentiate SVT from VT
The Brugada criteria
What investigations are needed for angina
- ECG: pathological q waves, LBBB, ST segment changes, T flattening or inversion
- Bloods: (FBC (anaemia), U&E (renal function), glucose and cholesterol (RFs), LFTs (statins), Troponin if ECG changes or unstable
- Echo to asses function or if HCM or valve disease is suspected
How should stable angina be treated
- all need referral to cardio via rapid access chest pain clinic
- GTN spray for symptom relief
- aspirin (75-300mg) or clopidogrel for anticoagulant taking into account bleeding risk
- statins and other CVS risk reduction (HTN treatment, stop smoking etc)
- BB or CCB for hypertension to reduce risk factors
- ACEi if also got diabetes
- cardiac rehab (exercise)
- coronary revascularisation if high risk or medical therapy fails
How is an MI investigated?
- ECG
- Bloods: FBC, U&E, glucose, lipids, crp, troponin T and I and cardiac enzymes
- CXR
- pulse oxymetry
- cardiac catheterisation and angiography
- Echo
- MI perfusion scan / CTCA
How should a STEMI be treated? short and long term (inc drug doses)
- Aspirin (300mg) and ticagrelor (180mg) (or clopidogrel)
- Morphine (5-10mg)
- metaclopamide (anti emetic) 10mg
- GTN sublingual or IV (50mg in 50 ml NS at 2-10ml/hr)
- Oxygen if sats are low
- call cathlab for primary PCI or CABG if multi vessel disease, if no PCI available then thrombolysis
- long term continue dual antiplatelet for 12 months (add PPI for stomach protection)
- B blockers or CCB
- ACEi
- high dose statin
- Echo also needed to asses for HF
- long term treatment is for NSTEMI
What do you need to think about when assessing NSTEMI risk and need for angiography/ PCI?
- rise in troponin
- dynamic st or t wave changes
- diabetes
- CKD
- LVF
- recent PCI or prior CABG
What lead is normally the most positive? What would be the most positive in LBBB and RBBB respectively?
Lead II is normally the most positive
LBBB - aVL
RBBB- Lead III
State the normal parameters for the PR interval, the QRS interval and the QT interval
PR - 120-200ms
QRS - <120ms
QT - 2 large squares
RBBB can be present without heart disease, however name three common causes of LBBB
Anterior MI
CHF
Left Ventricular Hypertrophy
Describe the diagnostic features of a STEMI
Cardiac Chest Pain
ECG changes (persistent ST elevation or new LBBB)
Raised Troponin I (greater than 100 nanograms)
