CARDIOLOGY - ACS and 12-LEAD ECG (Week 11) Flashcards
1
Q
What % blood supply to the heart comes from the LCA?
How about the RCA?
A
85% blood supply to the heart from LCA
15% from RCA
2
Q
Can MI affect any area of the heart?
A
yes of course
3
Q
Label the coronary arteries in the diagram below.
A
4
Q
List the three layers of coronary arteries.
A
1) Tunica intima - innermost layer
2) Tunica media - middle layer
3) Tunica adventitia - outermost layer
5
Q
Describe characteristics of the tunica intima
A
- 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
6
Q
Describe characteristics of the tunica media
A
- 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
7
Q
Describe characteristics of the tunica adventitia
A
- outermost layer
- composed of flexible and connective tissue which helps hold the vessel open
8
Q
Ischemic heart disease is the _____ cause of death worldwide and ______ cause of death in Canada
A
leading cause of death worldwide
2nd leading cause in Canada
9
Q
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?
A
Chest pain
15% diagnosed with ACS
10
Q
In Ontario, approximately ______ patients per year experience a STEMI (out of a population of 15 million people)
A
8000
11
Q
Define Acute Coronary Syndrome (ACS)
A
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)
12
Q
The 3 I’s of ACS
A
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)
13
Q
Treatment of ACS
A
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)
14
Q
ASA (A 5A’s)
A
- acetylsalicyclic acid
- anti-inflammatory
- anti-pyretic
- anti-platelet aggregator
- analgesic
15
Q
What are the 3 types of ACS?
A
1) unstable angina
2) ST segment elevation MI (STEMI)
3) Non ST segment elevation MI (Non-STEMI)
16
Q
What is the most common cause of ACS?
A
Rupture of atherosclerotic plaque
17
Q
Define atherosclerosis
A
- “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
18
Q
What happens when cardiac muscle does not receive enough oxygen? What is this called?
A
chest discomfort may ensue, known as angina pectoralis (aka angina)
ischemia may lead to cellular injury and ultimately infarction
19
Q
What are the two main types of angina? Describe the symptoms and characteristics.
A
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
20
Q
Which demographics may cardiac disease/ischemia present atypically?
What would these symptoms be?
A
women, older adults, diabetics
Symptoms: mental status changes, abdominal symptoms (including persistent heartburn), vague complaints of being ill
21
Q
What characteristics of plaques would help you differentiate them?
A
makeup
vulnerability to rupture
tendency to make blood clots
22
Q
What are the two types of plaques?
A
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
23
Q
What happens if the fibrous cap of a plaque tears/ruptures, and how would the body respond to this insult?
A
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
24
Q
Thromboxane A2
A
- 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
25
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
26
Define myocardial infarction
occurs when the blood flow to the heart muscle stops or is suddenly decreased long enough to cause cellular death
27
Acute MI usually results from what
thrombus
less commonly results from coronary spasm (as in cocaine abuse) or coronary embolism
28
Signs and Symptoms of MI include
* chest pain (possibly same as unstable angina)
* usually last longer than 20-30 minute and no relief with regular tx
* anxiety
* denial
* ashen skin (pale/grayish colour)
* fatigue
* confusion
* loss of consciousness
29
Is it possible to distinguish between patients experiencing unstable angina and acute MI during initial presentation?
NO. may be impossible during initial presentation
the diagnosis of an infarction is made based on: **incident history, signs and symptoms, ECG findings, and blood test results** that confirm presence of an infarction
in blood tests, you're looking for troponin (elevated by 20-fold or more) - it's an enzyme that gets released from damaged myocardial tissue
30
OPQRST
**O - Onset/origin**
* have you experienced this before? compare
* sudden vs gradual onset
* when did it start and what were you doing when it started?
**P - Provocation** - take a deep breath, better or wose?
**Q - Quality** - open ended questions or give opposite characteristics
**R - Radiation** - generalized vs localized; point to where it hurts
**S - Severity** - scale 1-10
**T - time** - how long ago, time of onset
31
On an ECG, recognition of an MI relies on indicative morphological ECG changes of:
QRS complex
T wave
ST Segment
the changes occur in relation to certain events during infarction
32
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
33
Abnormal pathologic Q wave characteristics
* \>0.04 seconds in duration OR
* more than 1/3rd the height of the R wave in that lead
34
The keystone to prompt STEMI recognition is
12 lead ECG
35
According to the ALS PCS, what clinical situations would warrant a 12-lead ECG?
* cardiac ischemica
* acute cardiogenic pulmonary edema
* tachycardia
* bradycardia
* SOB
* upon ROSC
36
Precordial lead placement
V1 – 4th intercostal space to the right of the sternum
V2 – 4th intercostal space to the left of the sternum
V3 – Directly between V2 and V4
V4 – 5th intercostal space at left midclavicular line
V5 – Level with V4 at the left anterior axillary line
V6 – Level with V5 at left midaxillary line
Leads view LV from position of +ve electrodes; do not use nipples as landmarks for chest electrode placement (because their location varies)
37
Identify the views of the heart in a 12 lead
38
High lateral leads
I, aVL
39
low lateral leads
V5, V6
40
Leads that view the lateral wall
I, aVL, V5, V6
41
Leads viewing inferior wall
II, III, and aVF
42
Leads viewing septal wall
V1 and V2 (remember, looking on tranverse plane)
43
Leads looking at anterior wall
V3, V4
44
ECG changes are significant when seen in _______ and \_\_\_\_\_\_\_\_\_\_\_\_leads
contiguous & reciprocal
45
True or False. ECG changes suspected as myocardial ischemia, injury and infarction are not found in every lead
True
46
What are continguous leads?
**two or more** leads that look at the same part of the heart (I and aVL)
OR
**numerically consecutive** chest leads (V1 and V2)
47
What are reciprocal leads?
leads opposite to the affected area
aka reciprocal changes and/or "mirror image" changes
48
The most indicative change that provides the strongest evidence of an early MI is
ST segment elevation
49
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)
50
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
51
If you suspect an inferior infarction, what would be your next steps?
perform a 15 lead ECG to try and discover an RVI or posterior MI
52
Right ventricular infarctions
* views the posterior wall of the RV
* 50% of patients with inferior infarctions have some involvement of the RV
* RV is responsible for the heart's preload and is supplied by the marginal artery of the RCA
* occlusion of this artery is referred to as **RVI**
* RVI should always be suspected when ECG changes suggesting an inferior infarct are seen
* DO A 15-LEAD
* Additional S/S that provide further evidence of an RVI
* **JVD**
* **Hypotension -** LV can only pump as much as it receives so when the RV loses some of its ability to pump blood into the pulmonary circuit and then the LA and LV, it will be less volume leading to hypotension
* **Clear lung sounds**
53
Posterior wall infarctions
* views the posterior wall of the LV
* occurs in 50% of all inferior MIs
* posterior wall is supplied by circumflex artery in most patients however in some patients it is supplied by the RCA
* i.e. a posterior wall MI can occur with an occlulsion to the PDA of the RCA
* however, the posterior wall DOES NOT create extraordinary hemodynamic effects that an RVI does
* **INDICATIVE CHANGES: V8 and V9**
* **RECIPROCAL CHANGES: V1, V2, (and V3)**
54
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
55
After doing a 15-lead ECG, what would suggest inferior and RVI?
ST equal or greater than 1mm in **V4R AND inferior leads**
56
15-Lead ECG Indications
**1) Any inferior AMI (especially accompanied by ST depression in V1-V3** - i.e. the reciprocal changes)
**2) Tall R waves and ST depression in V1-V3 on its own in symptomatic ACS patient** - you always want V1 and V2, and to a lesser extent you'll see it in V3
57
Indications of posterior MI after viewing 15-lead?
ST elevation equal or greater than 1mm in **V8 and V9**
58
Indications of Inferior/Posterior MI after viewing 15 lead?
ST elevation equal or greater than 1mm in **inferior leads AND V8 and V9**
59
Indications of Inferior/Posterior with RVI after viewing a 15-lead
ST elevation of equal or greater than 1mm in **inferior leads _AND_ V4R _AND_ V8 and V9**
60
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**
61
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**
62
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**
63
Anteroseptal infarctions
* affects both anterior and septal walls of the LV
* **INDICATIVE CHANGES: V1, V2, V3, V4**
* **RECIPROCAL CHANGES: V8 and V9**
64
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**
65
Possible complications of MIs
* lethal dysrhythmias and death
* heart failure
* ventricular aneurysms
* nonlethal dysrhythmias (such as a-fib)
* septal rupture (tear) that may occur anywhere in the setpum
* "cardiac cripple" - a condition seen when a patient has severe fear of any physical activity believe it may cause another MI
