Week 1/2 - A(3) - Yr 4 ECG Module - (Section 4-7) - Ischaemia/Infarction, Pericarditis, Ventricular hypertrophy, B.B.B, ECG Workshop Qs COPY Flashcards
ISCHAEMIA / INFARCTION It is important to be able to determine whether ECG changes affect a particular vasciular territory Which leads match which vascular territory and which artery supplies this territory of the heart?
V1-V4 - anterior heart supplied by left anterior descending artery V5,6, I and AVL - lateral heart supplied by left circumflex artery (CAP TEST STATES –> Anterior - V2-V5 Anteroseptal - V1-V3 Anterolateral V4-6, I, aVL) II,II avF - inferior heart supplied by right coronary artery
Myocardial ischaemia causes changes to the ECG appearance * T wave changes and ST changes What are the different changes in Twaves than can be seen in the ECG as markers of ischaemia?
T wave changes Tall T wave acutely Can also be biphasic Can also be inverted Flattened Twaves sometimes after a long period of time after MI
What are the different changes in ST segment in mycordial ischaemia? What ST changes are bad prognostic factors?
ST segment changes * ST depression can occur (>/= 0.5mm (half a small box) depression in >/=2 contiguous leads) * Widespread and deep depression are generally bad prognostic factors of the ischaemia
What is the difference between tall t waves in myocardial ischaemia vs in hyperkaelmia?
Myocardial ischaemia - the t waves are broad based and not pointed Hyperkaelaemia - tall tented t waves - narrow based and pointed
ECG changes in myocardial infarction - there can be many What is a STEMI? When can Q waves in some MI patients and what does this suggest?
ST-elevation occurs in ST-elevated myocardial infarctions - early identification and treatment improves prognosis The developent of pathological Q waves can occur usually between 2-24 hours after infarction and may suggest necrosis and loss of viable myocardium
How are pathological q waves defined? * Ie how many leads must the Q waves be present in and what depth for a patholoigcal Q wave diagnosis? * What are the criteria for pathological Qwave diagnosis in the diffeent leads?
Pathological Q waves must be present in any two contiguous leads, & be >1mm in depth (1 small box) * Any Q waves in leads V1-V3 * Q waves >0.03 (1.5 small boxes) seconds in leads I, II, aVL, aVF or V4, V5 or V6
Remember there are other causes for ST segment elevation Name one other cause? eased by sitting forward
Pericarditis is another cause of ST elevation - saddle shaped ST segment elevation
There are criteria that need to be followed when carrying out coronary reperfusion therapy (be it using a PCI or thrombolysis) You must look for typical symptoms of MI plus ECG criteria What is the ECG criteria?
ECG criteria for coronary reperfusion ST elevation * >1mm in two contiguous limb leads (I,aVL or II, III and aVF) * >2mm in two contiguous chest cleads Posterior myocardial infarction Left bundle branch block
What is the re-perfusion therapy offered in a patient presenting with a STEMI? What is the presentation time for these treatments to be carried out?
PCI is the preferred reperfusion management if * presentation is within 12 hours of onset of symptoms and * primary PCI can be delivered within 120 minutes of STEMI diagnosis * (angiographic identification of the thombosis and revascularise with stent) Offer fibrinolysis to people with acute STEMI presenting within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of STEMI diagnosis
ECG criteria for coronary reperfusion ST elevation >1mm in two contiguous limb leads (I,aVL or II, III and aVF) >2mm in two contiguous chest cleads Posterior myocardial infarction Left bundle branch block What can ST depression in V1-V3 also mean?
Posterior myocardial infarction - would see ST segment depression V1-V3 Remember - posterior heart supplied by posterior interventricular artery - a branch of right coronary artery
A 46 year old man presents to the ED with chest pain. This is his ECG. What is this trace consistent with? * Anterior STEMI * Lateral STEMI * LBBB * RBBB * Infero-posterior STEMI
Can see marked ST depression in leads V1, V2 and V3 - points to possibly ischaemia or posterior MI ST elevation in leads II, III and aVF Infero-posterior STEMI is the answer
A 64 year old man presents to the ED with chest pain. This is his ECG. What is this trace consistent with? Lateral STEMI Anterior STEMI RBBB LBBB Infero-posterior STEMI
Unsure about this one Correct answer was LBBB - looking closely can see the WiLLiaM for LBBB (W in V1 and M in V6)
PERICARDITIS Pericarditis is an important cause of ST elevation and it is important to be able to recognise it What is it usually secondary to and what are the symptoms?
Pericardial inflammation is usually secondary to MI or Viral Infection Symptoms are usually a * Pleuritic chest pain (worse on inspiration or lying flat) and relieved by sitting forward, * Fever, and * Pericardial friction rub on auscultation
What ECG changes are seen in pericarditis?
The ECG changes in pericarditis are usually widespread changes involving >1 vascular territory * There is an upward concave ST elevation (saddle shaped ST segment) * PR depressions * ECG changes do not evolve
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Statements 1,2,3 and 4 are false Statement 5 is correct - patient should be given analgesia with NSAIDs if not contra-indicated Add colchicine for 3 months (colcichine affects the way in which white blood cells work)
VENTRICULAR HYPERTROPHY Ventricular hypertrophy is the thickening of the ventricular walls When can it be physiological?
Healthy cardiac hypertrophy (physiological hypertrophy or athlete’s heart) is normal response to healthy exercise or pregnancy, which results in an increase in the heart’s muscle mass.
Unhealthy cardiac hypertrophy (pathological hypertrophy) is the response to disease such as hypertension, heart muscle injury (MI) , heart failure etc How does right ventricular hypertrophy look on ECG? * What happens to the r waves and s waves in right ventricular hypertrophy and explain why? * What happens to the axis? R waves - depolarisation of main ventricular mass S waves - depolarisation of ventricles at the base
High amplitude QRS complexes suggest ventricular hypertrophy Suspect Right ventricular hypertrophy if dominant R wave in V1 and deep Swave in V6, also right axis deviation Normally V1 and 2 have a very small R wave because the right ventricle does not have a lot of mass. In hypertrophy there is more muscle mass so large R-wave.
How does left ventricular hypertrophy look on ECG? * What happens to the r waves and s waves in left ventricular hypertrophy and explain why? R waves - depolarisation of main ventricular mass S waves - depolarisation of ventricles at the base
High amplitude QRS complexes suggest ventricular hypertrophy Suspect Left ventricular hypertrophy if dominant S wave in V1 and dominant R wave in V6 Left ventricle already has muscle mass but in hypertrophy , alot more so R waves in V5/6 are large
BUNDLE BRANCH BLOCK Describe the electrical conduction through the heart?
Normally rate is controlled by the SA node - cells with the highest rate of automaticity Electrical activity then flows through the AV node, the bundle of His which separates in left and right bundle blocks before reaching the purkinje fibres at the base of the ventricular myocardium
In patients in whom there is a disruption of the electrical conducting system eg in complete heart block or bundle branch block, what can occur and at what rate?
A escape rhythm can occur which is usually regular and occurs at approximately 40bpm This is where a different part of the heart has automaticity and causes contraction - if in the ventricles (ventricular escape rhythm), it will cause broad regular QRS complexes
What does the left bundle branch block divide into?
The left bundle branch blokc splits into the * anterior hemi bundle (left anterior hemi bundle (LAHB)) and * posterior hemi bundle (left posterior hemi bundle (LPHB)
What are phases of activation in the bundle branches? * Ie what direction is septal depolarisation and what waves does this cause * when does the depolarisation of the ventricles occur
Phase 1 -Septal depolarisation occurs from left to right Phases 2 and 3 Depolarisation of the free wall of the left and right ventricles then occurs together
How do the phases of activation appear on leads V1 to V6 on an ECG?
Phase 1 - depolarisation of the septum - causes a small Q wave in leads V4,5,6 as it is away from these electrodes (left to right) Phase 2 - depolarisation of the left &right ventricles - small r wave in V1,2,3 because ventricular mass smaller here r wave progression means R>3 in V4,5,6 as left ventricular mass large
What is a bundle branch block and what leads are best to look at to determine which bundle is blocked? What happens to the QRS?
A bundle branch block is a delay of conduction in either of the bundle branches Best to look at leads V1 and V6 to determine the type In BBB the QRS complex is >0.12seconds
What is a partial / incomplete bundle branch block?
A partial / incomplete bundle branch block is where the pattern of a RBBB or LBBB is present however the QRS complexes are <0,12 seconds
What stimulates the right ventricle in RBBB? What pattern is seen on ECG?
In RBBB the right ventricle is stimulated by impulses form the left ventricle Best seen in V1 * M shaped QRS in V1 (rSR pattern) * W shaped QRS in VQ6 * (MoRRoW)
Obviously there is the MoRRoW pattern in RBBB Now name all the ECG criteria Ie QRS duration S wave changes What is seen in the different leads
ECG criteria for RBBB * QRS >0.12 seconds * RSR pattern in V1 (M) * W pattern V6 * Prolonged (slurred ) S wave in V6
What changes in the phases of activation of the fasicles of the heart in RBBB?
The septum depolarises from left to right as normal and the left ventricle is depolarised as normal However the right ventricle is depolarised late causing a wide QRS due to slow conduction through the myocardial cells
How does RBBB affect the interpretation of an MI?
RBBB does not affect the interpration of an MI THere is no alteration of the intial part of the complex in V1 (RS still normal, just the additional R at the end of the complex) and abnormal Q waves an usually still be seen in V1-V3
What are the causes of RBBB?
Causes of RBBB include normal variant Pulmonary embolism Cor pulmonale (Right sided heart failure due to pulmonary hypertension- can lead to RVH)
What activates the LV in left bundle branch block? What is the typical pattern seen on ECG?
LV is activated by the right ventricle in LBBB and results from injury to BOTH left anterior and posterior hemi bundles Can see W shaped QRS in V1 due to notching of the S wave (notched QS complexes) M shaped QRS complexes in V6 Prolonged QRS complexes >0.12 seconds
How does LBBB affect MI interpretation?
LBBB makes interpretation of the ECG very difficult and ST segment and T wave changes should not be diagnosed y the inexperienced
RBBB could be a normal variant or caused by different things eg pulmonary embolism or cor pulmonale What are causes of left bundle branch block?
Usually indicative of heart disease IHD MI Hypertension NEW LBBB may represent a STEMI
A hemiblock is a defect in conducton along one of the two hemifascicles of the left bundle branch Which is the most common? How does it present onECG?
Left anterior hemiblock is by far the most common type Causes left axis deviation (cardiac axis -30 to -90 degrees) Initial r wvaes in the inferior leads (II, III, aVF)
Why is left posterior hemiblock rare?
Left posterior hemiblock is rare as Left posterior hemibundle has a dual blood supply from left anterior descending artery and posterior interventricular artery - from RCA
What are the signs of left posterior hemiblock on ECG?
Left posterior hemiblock Right axis deviation (cardiac axis +90 to +180 degrees) an S1 Q3 pattern (s waves in lead 1, Q eaves in lead III)
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Left bundle branch Can’t see the W in V1 but can see the M pattern in lead V5
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Right bundle branch block QRS >0.12 seconds RSR pattern in V1 (M) W pattern V6 Prolonged (slurred ) S wave in V6
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Left bundle branch block
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Left anterior hemiblock Causes left axis deviation (cardiac axis -30 to -90 degrees) Initial r wvaes in the inferior leads (II, III, aVF)
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Left posterior hemiblock Right axis deviation (cardiac axis +90 to +180 degrees) an S1 Q3 pattern (s waves in lead 1, Q eaves in lead III)
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* Rate = 300 / approx 3.5 = 86 * or count the number of complexes (10 second strip ) and x6 = 13x6 = 88bpm * Rhythm is regular * Every QRS preceded by a pwave and every pwave followed by a QRS * PR interval ECG diagnosis - normal sinus rhythm
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* Rate = 300 / approx 5 = 60bpm * Rhythm is regular * Every QRS preceded by a pwave and every pwave followed by a QRS * PR interval ECG diagnosis - normal sinus rhythm
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* Rate = 8 QRS complexes in 30 squares, x 10 and we get 80bpm * Rhythm is irregular * Every QRS preceded by a pwave and every pwave followed by a QRS * PR interval ECG diagnosis - sinus rhythm with sinus arrythmia - due to phsyiological changes cardiac timing due to changes in vagal tone during respiration
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* Rate = 10 QRS complexes in 30 large squares (6 seconds) x 10 - 100bpm * Rhythm is irregular * No clear pwaves * PR interval not measurable * ST segment normal * T wave normal * Ragged baseline * Tall QRS complexes, tall rwaves in V4,5,6 * ECG diagnosis - atrial fibrillation and LVH
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Rate = 17/18 QRS complexes in 30 large squares = 17/180bpm Rhythm is irregular Pwaves not discernible PR interval unclear ST segment normal T wave normal ECG diagnosis - fast Afib (pulse >100bpm)
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* Rate = 300 / approx 4.5 = 67bpm * Rhythm is regular * Every QRS preceded by a pwave and every pwave followed by a QRS * PR interval * ECG diagnosis - anterolateral STEMI - MI fits with history
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R ate = 300 / approx 5 = 60bpm Rhythm is regular Every QRS preceded by a pwave and every pwave followed by a QRS PR interval ST segment elevetaion in leads II, III and aVF - almost looks saddle shaped but there is no widespread ST elevation for pericarditis ECG diagnosis - INferior STEMI
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* Rate = 300 / 2.5 = 120bpm * Rhythm is regular * Every QRS preceded by a pwave and every pwave followed by a QRS * PR interval ECG diagnosis - anterolateral ischaemia with sinus tachycardia
