CARDIOLOGY - ACS and 12-LEAD ECG (Week 11) Flashcards
What % blood supply to the heart comes from the LCA?
How about the RCA?
85% blood supply to the heart from LCA
15% from RCA
Can MI affect any area of the heart?
yes of course
Label the coronary arteries in the diagram below.
List the three layers of coronary arteries.
1) Tunica intima - innermost layer
2) Tunica media - middle layer
3) Tunica adventitia - outermost layer
Describe characteristics of the tunica intima
- the innermost layer
- composed of a single layer of endothelium cells which lines the vascular system
- makes direct contact with arterial blood
- poses risk for damage from conditions like smoking
Describe characteristics of the tunica media
- middle layer
- composed of smooth muscle tissue/cells
- functions to maintain tone and regulate blood flow
- innervated by fibers of the ANS which allows constriction and dilation of the vessel
Describe characteristics of the tunica adventitia
- outermost layer
- composed of flexible and connective tissue which helps hold the vessel open
Ischemic heart disease is the _____ cause of death worldwide and ______ cause of death in Canada
leading cause of death worldwide
2nd leading cause in Canada
What is one of the most common symptoms of ischemic heart disease, prompting paitents to seek medical care?
Of those that do go seek medical care (ED), what % is diagnosed with ACS?
Chest pain
15% diagnosed with ACS
In Ontario, approximately ______ patients per year experience a STEMI (out of a population of 15 million people)
8000
Define Acute Coronary Syndrome (ACS)
conditions caused by a sequence of pathological events - a temporary or permanent blockage of a coronary artery
the sequence of events range from the 3 I’s (ischemia, injury, infarction)
The 3 I’s of ACS
1) Ischemia - a decreased supply of oxygenated blood to a body part or organ (i.e. blood supply to the myocardium is impaired) - may or may not see an inverted T wave
- as seen by flattening of ST segment, ST segment depression, and/or T wave inversion
2) Injury - prolonged ischemia (ST elevation)
3) Infarction - necrosis; tissue death (may or may not show Q wave; or significant/pathological Q waves)
- formation of pathological Q wave in 50% of cases
- presence of pathological Q wave is suggestive of prior MI (but not always)
Treatment of ACS
REPERFUSION THERAPY
Two ways:
1) Mechanical
- PCI (percutaneous coronary intervention) aka angioplasty
- an intervention that mechanically opens the artery using a balloon
- may include the placement of a stent in blocked arteries
- CABG - treatment for narrow/blocked arteries by creating bypass tracts
2) Pharmalogical
- fibrinolytics
- administration of thrombolytics that breakdown the clot (fibrinolytics & thrombolytics are interchangeable)
ASA (A 5A’s)
- acetylsalicyclic acid
- anti-inflammatory
- anti-pyretic
- anti-platelet aggregator
- analgesic
What are the 3 types of ACS?
1) unstable angina
2) ST segment elevation MI (STEMI)
3) Non ST segment elevation MI (Non-STEMI)
What is the most common cause of ACS?
Rupture of atherosclerotic plaque
Define atherosclerosis
- “athero” meaning gruel, “sclerosis” meaning hardness
- a form of arteriosclerosis
- thickening/hardening of vessel walls caused by a buildup of fatty deposits in the lining of large and middle sized arteries
- as the fatty deposit build up, opening of the artery narrows and blood flow decreases
- blockage may lead to cardiac muscle becoming ischemic
- formation of atherosclerotic plaque in the tunica media
What happens when cardiac muscle does not receive enough oxygen? What is this called?
chest discomfort may ensue, known as angina pectoralis (aka angina)
ischemia may lead to cellular injury and ultimately infarction
What are the two main types of angina? Describe the symptoms and characteristics.
1) Stable angina
- S/S: chest pain or “discomfort”, which may be centered or radiate to neck/jaw, upper back, L shoulder, either arm; SOB
- May occur after the 4 E’s
- Exertion
- Eating
- Emotional distress
- Extreme temperatures
- often relieved by rest; meds like nitro
2) Unstable angina (preinfarction angina)
- S/S: possibly same as stable angina AND N/V and diaphoresis; may be more painful than usual
- Characterized by 1 or more of the following:
- symptoms occur at rest (or with minimal exertion) and usually last more than 20 minutes
- symptoms that are severe and/or of new onset
- symptoms that are more severe, prolonged or frequent in a patient with a history of stable angina
- not relieved by rest
Which demographics may cardiac disease/ischemia present atypically?
What would these symptoms be?
women, older adults, diabetics
Symptoms: mental status changes, abdominal symptoms (including persistent heartburn), vague complaints of being ill
What characteristics of plaques would help you differentiate them?
makeup
vulnerability to rupture
tendency to make blood clots
What are the two types of plaques?
1) Stable plaque
- unlikely to rupture
- hard
- thick fibrous cap over fatty center that separtes it from contact with the artery
2) Vulnerable plaque
- prone to rupture
- soft
- thin fibrous cap over fatty center that separates it from contact with the artery
- may rupture due to: exercise, emotional distress, erotic activity, exposure to illicit drugs (cocaine, marijuana, amphetamines), exposure to cold, acute infection
- Contributing factors: frictional force from blood flow, coronary spasm at teh site, internal plaque changes
What happens if the fibrous cap of a plaque tears/ruptures, and how would the body respond to this insult?
if cap tears/ruptures, its contents of plaque are exposed to the flowing blood
body responds by forming a plug with platelets that stick to the damaged lining of the vessel
Thromboxane A2
- secreted by platelets
- stimulates vasoconstriction which reduces blood flow at the site
- ASA prevents production of this chemical thus slowing the aggregation (clumping) of platelets
Describe the process of platelets clumping
1) once platelets are activated, receptors appear on the surface of the circulating platelets
2) fibrinogen molecules bind to these receptors to form bridges (links) between nearby platelets, allowing them to clump
3) as this process continues, fibrinogen molecules are converted into fibrin and a blood clot is formed
Define myocardial infarction
occurs when the blood flow to the heart muscle stops or is suddenly decreased long enough to cause cellular death
Describe the evolving pattern of STEMI
1st change: Development of the T wave (Hyperacute phase)
- increases in height, more symmetrical and pointed
- mar occur within the first few minutes of infarction
2nd change: ST Elevation (Early acute phase)
- primary indication of myocardial injury in progress
- may occur within the first few hours of infarction
3rd change: T wave inversion (later acute phase)
- T wave inversion suggests presence of ischemia (may preced the development of ST elevation; or happen simultaneously)
4th change: Development of Q wave (Fully evolve phase)
- 1st evidence that tissue death has occurred
- indicates presence of dead tissue and loss of electrical activity
- May appear hours to days of AMI S/S
Final change: Q wave remains (healed phase)
- in time, the T wave regains its normal contour and ST segment returns to isoelectric line but the Q waves remains as evidence an infarct has occurred
Identify the views of the heart in a 12 lead
Leads that view the lateral wall
I, aVL, V5, V6
Leads viewing inferior wall
II, III, and aVF
Leads viewing septal wall
V1 and V2 (remember, looking on tranverse plane)
Leads looking at anterior wall
V3, V4
What is considered “significant” ST segment elevation?
1) EQUAL or greater than 1mm in two or more contiguous limb leads (ex. II, III, aVF)
OR
2) EQUAL or greater than 2mm in two or more contiguous chest limbs (ex. V1 and V2)
Inferior wall infarctions
- views the inferior surface of the LV
- in most individuals, inferior wall is suppled by posterior descending branch of RCA
- eg. occlusions within PDA resulting in inferior wall infarction
- increased paramsympathetic activity is common with inferior wall MIs resulting in bradydysrhythmias
- as well, 1st and 2nd degree Type I are common and usually transient
- INDICATIVE CHANGES (leads facing the affected area): II, III, and aVF
- RECIPROCAL CHANGES (leads opposite the affected areas): I and aVL
15 lead ECG placement
1st step: Right chest lead placement
- after obtaining a standard 12-lead ECG printout, remove electrode wide attached to V4 and attach V4R
- V4R - 5th ICS at right midclavicular line (similar to V4 position but on other side of chest)
- so V4 becomes V4R (V4 Right)
2nd step: Posterior lead placement
- remove electrode wires attached to V5 and V6 and attach the following
- V8 - 5th ICS space at midscapular line
- V9 - 5th ICS space at left paravertebral line
- Leads V8 and V9 are on the same horizontal line as V5 and V6 of the chest
- V5 becomes V8
- V6 becomes V9
Lateral Wall Infarctions
- views the lateral surface of the LV
- lateral wall suppled by circumflex artery, LAD or a branch of RCA (so occlusions to proximal LAD or circumflex artery would be an example)
- INDICATIVE CHANGES: I, aVL, V5, and V6
- RECIPROCAL CHANGES: II, III, AVF
Septal wall infarctions
- views the septal area of the LV
- septum contains Bundle of His and bundle branches and is normally supplied by the LAD artery
- A blockage in the area may result in Right or left BBB, 2nd degree Type II, and 3rd degree AV blocks
- If anterior wall is also involved, ECG changes will be visible in V1, V2, V3, and V4
- INDICATIVE CHANGES: V1 and V2
- RECIPROCAL CHANGES: V8 and V9
Anterior Wall infarctions
- views the anterior wall of the LV
- left main coronary artery supplies both LAD and circumflex artery
- LAD supplies ~40% of blood to the LV (so a blockge in the LAD can therefore lead to complications)
- Increased sympathetic activity is common with anterior MIs resulting in tachydysrhythmias and high BP
- INDICATIVE CHANGES: V3 and V4
- RECIPROCAL CHANGES: V8 and V9
Anteroseptal infarctions
- affects both anterior and septal walls of the LV
- INDICATIVE CHANGES: V1, V2, V3, V4
- RECIPROCAL CHANGES: V8 and V9
Anteriolateral infarctions
- affects both anterior and lateral walls of the LV
- INDICATIVE CHANGES: I, aVL, V3, V4, V5 and V6
- RECIPROCAL CHANGES: II, III, aVF, V8 and V9
