Conditions - ACS and Arrhythmias Flashcards
Points of auscultation
Aortic valve - right side second intercostal space, next to sternum
Pulmonary valve - left side second intercostal space, next to sternum
Tricuspid valve - Left side, 4th intercostal space, near the sternum
Mitral valve - Left side, 5th intercostal space, mid clavicular line
What is ACS
3 acute states of myocardial ischaemia which can lead to infarction and necrosis
Unstable Angina / STEMI / NSTEMI
Difference between unstable angina and angina
UA not relieved by GTN spray
UA occurs at rest / no specific triggers
UA lasts for 30 mins or longer whereas SA lasts for 15 mins only
UA due to rupture of atherosclerotic plaque whereas SA due to formation of atherosclerotic plaque narrowing the vessel
Difference between STEMI and NSTEMI
STEMI due to complete occlusion of blood vessel whereas NSTEMI is due to severe occlusion of blood vessel
STEMI causes ST elevation / new left bundle branch block on ECG whereas NSTEMI does not
What is the cause of ACS
Acute rupture of atherosclerotic plaque -> exposes collagen in the plaque to platelets -> blood clot forms and occludes the vessel
What are the reasons for rupture of atherosclerotic plaque
Young, fatty plaques are more likely to rupture
Bending and twisting of vessels during heart contraction
Change in intraluminal pressure
Injury
Which type of MI is due to acute coronary artery event
Type 1
What causes type 2 MI
oxygen supply / demand mismatch
Which type of MI are most NSTEMI and STEMI part of
Type 1
How can acute MI lead to heart failure
Myocardial ischaemia can lead to myocardial infarction hence necrosis
This causes the heart to lose muscle and eventually it may mean that the heart can no longer pump sufficient CO = heart failure
Symptoms of MI
Unstable angina
Sweating / clammy
Pale
May show heart failure symptoms
What are the symptoms of unstable angina
Severe pain
pain may radiate to neck and arms
Pain is 30 mins or longer
Occurs at rest
Not relieved by GTN spray
Diagnosis of MI
History
Urgent ECG
Measure troponin level
What may the results from ECG and troponin level be for NSTEMI and STEMI
STEMI - ST elevation and reciprocal ST depression or new LBBB + elevated troponin level
NSTEMI - non-ST elevation; T wave inversion and ST depression + elevated troponin level
Why isn’t troponin the definitive diagnosis of MI
Because other conditions can cause myocardial necrosis hence elevated troponin level
When should you start treatment for STEMI
Immediately after ECG diagnosis. Do not wait for troponin level results as ECG diagnosis is sufficient to indicate STEMI
Which troponin levels indicate myocardial necrosis
Troponin I and C
What is the management of STEMI
Immediate management - MONA
IV diamorphine
Oxygen
GTN
Aspirin + ticagrelor / clopidegrol
Anti-emetics
Immediate PCI within 120 mins of ECG diagnosis
Fibrinolysis if PCI not available promptly -> refer to PCI center -> angiography +/- PCI
What is the dosage of aspirin given to STEMI patients
300mg
Which antiplatelet should be used instead for STEMI patients going for immediate PCI
Prasugrel / clopidogrel (not ticagrelor)
What is the management of NSTEMI or UA
Calculate GRACE score
MONA
IV diamorphine
Oxygen
GTN
Aspirin + fondaparinux
What does GRACE score show
6 months mortality risk
What is the management for patients with very high GRACE risk score
immediate invasive angiography +/- PCI within 2 hours
What is the management for patients with high GRACE risk score
Early invasive angiography (<24 hour)
What is the management for patients with intermediate GRACE risk score
Invasive angiography (<72 hours)
What is the management for patients with low GRACE risk score
Non-invasive testing
If symptoms worsen -> invasive angiography
What are the non-invasive testing methods for NSTEMI
Cardiac MRI
Transthoracic echocardiogram
Stress echocardiogram
CT angiography
What antiplatelets should be given to patients with intermediate to very high GRACE risk score
Prasugrel or ticagrelor
What should be given to NSTEMI patients that are going to have invasive angiography
LWMH
What is the post MI management
Beta Blockers - bisnoprolol
ACEi - ramipril
Aspirin + clopidogrel or ticagrelor
Statin
Cardiac rehabilitation
ECHO
What are the complications of MI
Ventricular fibrillation
HF
Left ventricular free wall rupture
Mitral regurgitation
Cardiogenic shock
Ventricular septal defects
Acute pericarditis
Aneurysm
Which type of infarct most commonly causes heart block
Inferior infarct
What is supraventricular tachycardia
Tachycardia originating above ventricles; including atrial flutter, atrial fibrillation, ectopic atrial tachycardia, AVNRT, AVRT
What does ectopic atrial tachycardia mean
Abnormal electrical signal started from within the atrium and takes over the SA node
What are Junctional rhythms
AV node takes over SA node and propagates impulses to atria and ventricles at the same time so atria and ventricles contract simultaneously
What are the ECG findings for junctional rhythms
Narrow QRS complex
Absent P wave, masked by QRS complex
What does re-entrant circuit mean
A continuous wave of depolarisation in a circular path; as the depolarisation travels to its site of origin, it reactivates that site
Which arrhythmias uses reentrant circuit
Atrial Flutter
Atrial Fibrillation
AVNRT
AVRT
What are the requirements for re-entrant circuits to occur
1) require 2 conduction pathways
2) 1 pathway is slow but short refractory period ; the other pathway is fast but long refractory period
What is an accessory pathway
Abnormal connection between atria and ventricles, faster conduction than through AV node
What are the common symptoms of arrhythmia
Palpitations
Dizziness
Syncope / pre syncope
dyspnea
Mechanism of atrial flutter
Normal impulse from SA node passes to the circular circuit in atria and AV node at the same time
This causes the atria to contract rapidly
The reentrant circuit also stimulates the AV node every time it passes but not all impulses will be conducted to the ventricles
Not all impulses generated in reentrant circuit in atria passes into ventricles. Why is that
Due to AV node block - normal AV node has a delay in conducting impulse from atria to ventricles
Depends on the degree of AV node block
What is the common ratio between atrial flutter waves and QRS complex
2:1
2 flutter waves to 1 QRS complex due to AV node delay
Where does atrial flutter occur
Common in right atrium but can spread in left atrium
Which type of reentrant circuit does atrial flutter use
Macro-re entrant circuit
What are the ECG findings for atrial flutter
Narrow QRS complex
2:1 (but can be 3:1 / 4:1 as well)
saw-tooth baseline
Regularly irregular
Regularly irregular vs irregularly regular
Regularly irregular - recurrent pattern of irregularity
Irregularly irregular - completely disordered
Which type of arrhythmia increases risk of stroke
Atrial fibrillation
Mechanism of atrial fibrillation
- multiple spontaneous waves of excitation leading to atrial muscles contracting independently and ineffectively
- the abnormal electrical impulses are intermittently passed down to the ventricles through AVN
Ventricular rate in AF is variable between people. Why is that
Due to variable AVN conduction speed
This means that young patients with fast AVN are very symptomatic
What can be caused by chaotic contractions of the atria
Blood stasis, increasing risk for blood clots to form
Risk factors for AF
Mitral regurgitation
Atrial / ventricular dilation
Atrial / ventricular hypertrophy
Wolff-Parkinson syndrome
Hypertension
Obesity
Thyroid dysfunction
Infections
Where does the arrhythmia of AF often originate from
left atrial myocytes
Why is it important to measure all apical, radial and carotid pulses
Because sometimes the abnormal ventricular contractions may not be strong enough to transfer fast pulses to the radial artery.
What are the ECG findings of atrial fibrillation
Irregularly irregular
Narrow QRS complex
Absence of discrete P waves
Long RR interval -> short RR interval
What are the complications of AF
Ischaemic stroke
HF
Cardiogenic shock
What causes AVNRT
Micro re-entry circuit within the AV node
Mechanism of AVNRT
1) A normal impulse from SA node passes into AV node where there are 2 anatomical conduction pathways
2) The impulse travels to both slow and fast pathways but only the impulse from fast pathway travels down to ventricles
3) Another impulse (pre ectopic beat) travels down to slow pathway bc fast pathway is still in refractory period
4) This causes the ventricles to be excited again. The impulse then travels back up to fast pathway to re-excite atria
What are the ECG findings of AVNRT
Rapid, narrow QRS complex
regular tachycardia (>/ 100bpm)
Absent P waves
What causes AVRT
macro re-entry circuit - uses accessory pathway
Mechanism of AVRT
Impulses travel retrograde (ventricles -> atria) or antegrade (atria -> ventricles)
Types of AVRT
Antidromic
Orthodromic
What is antidromic AVRT and its ECG findings
Anterograde AVRT
Wide QRS complex
Shortened PR interval
Absent P waves
What is antidromic AVRT and its ECG findings
Induced by premature atrial beat, the premature impulse travels down to the accessory pathway
broad QRS complex
Retrograde P wave after QRS complex
What is ventricular tachycardia
Rapid recurrent ventricular depolarisation from a focus within the ventricles
What can ventricular tachycardia cause
Syncope
Cardiac arrest
Decrease / loss of cardiac output
What are the ECG findings of VT
Regular tachycardia
Rapid, broad QRS
Absent P waves
What is Torsades de point
A type of VT due to depolarisation from multiple foci in ventricles
What are the ECG findings of Torsades de Point
variable QRS complex
Prolonged QT
What is ventricular fibrillation
When the ventricles start contracting independently and no longer meaningfully
Pulseless is a common feature of which type of arrhythmia
Ventricular fibrillation
Why is ventricular fibrillation so serious
Because the heart loses its ability to pump hence there is no cardiac output, leading to cardiogenic shock / cardiac arrest
What are the classes of anti-arrhythmics
Class I - blocks Na+ channels
Class II - Beta blockers
Class III - blocks K+ channels
Class IV - CCB
Which classes are rate controlling anti-arrhythmics
Class II and Class IV
Class I anti-arrhythmic subtypes
Ia - disopyramide; intermediate rate
Ib - lignocaine; fast rate
Ic - flecainide; slow rate
Example of class III drug
Amiodarone
Mechanism of action of amiodarone
Blocks K+ channels to prolong action potential duration
Why isn’t amiodarone used for long term rhythm control
Long term use has high risk of
pulmonary fibrosis
thyroid disorders
photosensitivity
peripheral neuropathy
Why may a diabetic not experience chest pain when he has STEMI
Due to diabetic neuropathy
What CCB are used as anti-arrhythmic drugs
dilitiazem
Verapamil
What treatment is required to prevent blood clots in patients with atrial fibrillation
Anti-coagulants
What anti coagulants are used to reduce risk of stroke in A fib patients
DOAC
Vitamin K antagonist such as Warfarin
Examples of DOAC
Apixaban
Rivaroxaban
What assessment tool is used to measure how likely it is for a A fib patient to get a stroke
CHA2DS2VASc tool
What is the guideline for haemodynamically stable patient w acute Afib
If new onset -> rate or rhythm control
If not new onset -> rate control -> rhythm control
What is considered as new onset atrial fibrillation
less than 48hrs
What is the treatment for haemodynamically unstable patient w acute Afib
emergency synchronized DC cardioversion
What is considered as haemodynamically unstable
Symptoms of shock
Syncope
signs of heart failure
Chest pain
Pulmonary oedema
When should rate control not be used
If the patient
- has atrial flutter appropriate for ablation
- HF primarily caused by AF
- AF with a reversible cause
What are the rate controlling drugs used for Afib
First line - Beta blockers except sotalol / CCB
Digoxin - for patients with heart faillure
What are the rhythm controlling drugs used for AFib
flecainide or propafenone if no structural / ischaemic heart disease
Amiodarone if there is structural disease
Beta blockers for long term rhythm control
What is the treatment guideline for haemodynamically unstable patient with atrial flutter
Emergency synchronized DC cardioversion
What is the treatment guideline for haemodynamically stable atrial flutter
rate control
When is ablation strategy used
recurrent atrial flutter despite drug treatment
What is the guideline for ventricular fibrillation
1) ABCDE
2) defibrillation
3) chest compressions
4) inject adrenaline and amiodarone after 3rd shock
5) inject adrenaline every 3-5 mins (every alternate shock)
What is the management for pulseless ventricular tachycardia
1) ABCDE
2) defibrillation
3) chest compressions
4) inject adrenaline and amiodarone after 3rd shock
5) inject adrenaline every 3-5 mins (every alternate shock)
What is the management for VT with pulse
If haemodynamically stable -> amiodarone
If haemodynamically unstable -> synchronized DC cardioversion
Is defibrillation synchronized or unsynchronized
Unsynchronized
How to manage haemodynamically stable patient w torsades de point
magnesium sulfate
How to manage regular narrow QRS tachycardia
Vagal manouevres - ice / valsalva
if fail -> adenosine
Why shouldn’t adenosine be used in asthmatics
Because there is risk of bronchoscpasm
What can left ventricular thrombus cause
Episodes of vision loss
Why isn’t verapamil used with beta blockers
risk of complete heart block
Which vein is associated with atrial fibrillation
Pulmonary veins
Why is a loading dose of amiodarone needed
Because it has a long half life. A loading initial dose of amiodarone is needed to maintain the therapeutic concentration for a long half life
What is the treatment for Mobitz Type 1
Nothing, as they are mostly asymptomatic and will not cause complete heart block
Why is Mobitz Type II dangerous
patients are at risk of complete heart block
What is the management for Mobitz Type II
Permanent pacemaker
What is the management for third degree heart block (complete heart block)
Permanent pacemaker
Indications for permanent pacemakers
Type II heart block
Complete heart block
Sick sinus syndrome
Atrial fibrillation
Bradycardia
What does the P wave on ECG mean
Atrial depolarisation
Where is PR interval and what does it mean
Start of P wave to the beginning of Q
It represents the time taken for depolarisation to conduct through the AV node
What is not shown on ECG (depolarisation / repolarisation)
Atrial repolarisation
What is the normal length of PR interval
0.12 - 0.2 s
What is the normal length of P wave
0.08 - 0.1 s
What does T wave represent
Ventricular repolarisation
What does ST interval represent
Ventricular contraction
What does QRT represent
Ventricular depolarisation
What is the normal duration of QRT
Less than 0.1s
What does QT interval represent
The time taken for ventricles to depolarise and repolarise
What is the normal duration of QT interval
0.35 - 0.44 s at a heart rate of 60
depends on the heart rate
What does a small square on ECG represent
0.04s
What does a large square on ECG represent
0.2s
How to calculate heart rate from ECG (normal)
300 / number of large squares between 2 consecutive points (e.g. RR)
How to calculate heart rate if the person has irregular heartbeat
Calculate the number of QRS complexes on rhythm strip x 6
What are the colours for each limb electrode for ECG
Red - right wrist
Black - right limb
Yellow - left wrist
Green - left limb
Where should you place the upper limb electrodes
on ulnar styloid process (wrist)
Where should you place the lower limb leads
on medial or lateral malleolus
Where should you place V1 - V4
V1 - 4th intercostal space, right sternal edge
V2 - 4th intercostal space, left sternal edge
V3 - placed between V2 and V4
V4 - left 5th intercostal space in midclavicular line
Where should you place V5 and V6
V5 - left 5th intercostal space, anterior axillary line
V6 - left 5th intercostal space, mid axillary line
What are the lateral leads
I , aVL , V5-V6
What are the inferior leads
II , III , aVF.
What are the anterior/ septal leads
V1 - V4
What is the most common cause of death in the first hour of a patient having an acute MI
Ventricular fibrillation
Post MI complications
1) HF -> cardiogenic shock
2) Ventricular fibrillation -> cardiac arrest
3) ventricular septal wall defect
4) ventricular free wall rupture
5) mitral regurgitation
6) left ventricular aneurysm
7) pericarditis
8) Dressler’s syndrome
9) Mural thrombus
What are the complications that has a high risk of happening 0-24 hours post MI
Ventricular fibrillation -> cardiac arrest -> death
Heart failure -> cardiogenic shock
Why does heart failure occur post MI
Because ischaemia causes necrosis of muscle fibres -> too much fibrosis means that there will be decreased contractility of the heart
What are the histological findings of a heart 0-24hrs post MI
Early coagulative necrosis
Neutrophils
Wavy fibres
Hypercontracting myofibrils
What are the complications that have a high risk of developing 1-3 days post MI
Pericarditis
What are the signs and symptoms of pericarditis
Chest pain worsened by lying down and relieved by leaning forward
Pericardial rub
Pericardial effusion on CXR
What are the histological findings 1-3 days post MI
Extensive coagulative necrosis
Neutrophils
What are the complications that are at high risk of occurring 3 - 14 days post MI
Ventricular free wall rupture
Ventricular septal defect
What are the histological findings 3-14 days post MI
Granulation tissues
Macrophages
What causes acute mitral regurgitation post MI
Papillary muscle rupture
Signs of left ventricular free wall rupture
Diminished heart sounds
Raised JVP
pulsus alterans
What are the complications that are at high risk of developing 2weeks - months post MI
Dressler’s syndrome
What causes Dressler’s syndrome
autoimmune reaction against antigenic proteins formed as the myocardium recovers
Symptoms of Dressler’s syndrome
Signs of pericarditis
Fever
What type of murmur is produced by ventricular septal wall defect patients
Pan-systolic murmur
What conditions causes pan systolic murmur
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
What condition is associated to persistent ST elevation
Left ventricular aneurysm
Indications for permanent pacemakers
Type II heart block
Complete heart block
Sick sinus syndrome
Atrial fibrillation
Bradycardia
