1. 12 Lead EKG 101
A Basic Overview of How to Interpret 12 Lead EKGs and Treat a Cardiac Patient
Region IV Pre-Hospital Systems Coordination Committee

2. Purpose:
The purpose of this course is to provide pre-hospital clinicians with the tools necessary to identify the basic A&P of the heart, interpret 12 Lead EKGs, localize and treat AMIs as well as recognize imposters and potential complications.

3. Basic Cardiac Anatomy & Physiology
Muscular pump about the size of your fist
primary function is to pump oxygenated blood to the rest of the body.
Made up of four chambers,
right and left atria
right and left ventricles
The septum is a thin muscular wall that separates the right and left sides of the heart.
Each contraction of the heart occurs in response to an electrical impulse that starts in the upper portion of the heart.
Blood is moved in a closed circuit through the body by the pumping of the heart.

4. Basic Cardiac Anatomy & Physiology
The heart contracts and pumps blood out to the body (systole) and relaxes to fill with more blood (diastole).
The heart muscle itself is like all other organs in the body and requires oxygen to function.
The oxygen-rich blood is circulated to the heart muscle through the coronary arteries.
There are two main arteries:
Right coronary artery
Left main coronary artery
both start at the aorta
These vessels then branch off into smaller and smaller vessels along the surface of the heart.

5. In order to perform work, the heart needs oxygen and nutrients.
There are two main arteries:
Right coronary artery (RCA)
Left coronary artery (LCA).
The left coronary artery divides into:
Left anterior descending (LAD) branch
Left circumflex branch(LCX)
The right coronary artery and the branches of the left coronary artery provide numerous smaller branches which penetrate the heart muscle, supplying it with blood.
Both coronary arteries originate from the aorta and run along the surface of the heart.
In the majority of human hearts, coronary circulation follows a predictable pattern.

6. Left Main Coronary Artery
Branches quickly into the LAD & LCX. Involves almost 2/3 of the heart muscle
Right Coronary Artery (RCA) The RCA supplies blood to the bottom (inferior) portion and part of the back (posterior) portion of the left ventricle. The posterior portion of the septum is also supplied with blood from the RCA.
SA Node 55%
AV Node 90%
AV Blocks
Left Anterior Descending Branch (LAD) The LAD supplies blood to the front (anterior) portion of the left ventricle, apical including most of the anterior portion of the septum separating the ventricles.
Bundle Branch Block, AMI, CHF
Left Circumflux Branch (LCX) The LCX supplies blood to the left side (lateral) portion and the back (posterior) portion of the left ventricle.
SA Node 45%
AV Node 10%
Lateral & posterior MI

7. Sino-Atrial (SA) Node: natural cardiac pacemaker
Sino-Atrial (SA) Node: natural cardiac pacemaker. The heartbeat starts here and spreads throughout the network of conduction fibers in the two atria causing them to contract.
Normally, the heartbeat can only reach the ventricles (the two lower chambers), after it has passed through the atrioventricular (AV) node.
Atrioventricular (AV) Node: slows down the electrical signal so that the atrial contractions can finish filling the ventricles completely. The AV node also prevents the lower chambers from beating too fast if the atria develops a fast rhythm (tachyarrhythmia).
His Bundle, bundle branches, and the Purkinje system : The electrical signal finally passes to the ventricles causing the ventricles to contract

8. Anatomy of an EKG
The EKG, or a measure of this electrical activity of the heart, is comprised of 3 primary parts...
1. P wave---electrical depolarization of the atria...contraction follows...
2. QRS COMPLEX---electrical depolarization of the ventricles...contraction follows...
3. T wave---electrical repolarization of the ventricles...and thus, relaxation...

9. P wave: Represents positive and negative deflections of atrial contraction and relaxation
PR Interval: Distance between the P wave and the R wave. Should be consistent
QRS Complex
Q wave: First negative deflection
Normal in I, aVL, V1, V6
Significant or pathologic is one box wide and/or 1/3 the height of the R wave
R Wave: First positive deflection
S Wave: Next negative deflection

10. ST Segment: Essentially isoelectric, slopes gentely upward
J point: the point at which the ST Segment takes off from the QRS complex
T Wave: Upright always in leads I, II, V2-V6. aVR is always negative. Leads III, aVL, aVF, and V1 can be positive or negative
U Wave: Seen best in V3, same polarity as T wave, sign of hypokalemia
QT Interval: One complete ventricular cycle. None are > ½ the preceding R-R

11. Putting the A&P with the EKG

12. Einthoven’s Triangle Lead I - + Lead III Lead II
extends from the right to the left arm
Lead III
extends from the left arm to the left foot
Lead II
extends from the right arm to the left foot

13. This is an example a 12-lead EKG.
Anatomy of a 12-Lead EKG
This is an example a 12-lead EKG.

14. Anatomy of a 12-Lead EKG (cont.)
At the bottom of this 12-lead are rhythm strips (highlighted).
Any of the 12-leads can be shown as rhythm strips.
You can configure the device to show you any of the six limb leads on the rhythm strip (I, II, III, aVR, aVL or aVF).

15. Anatomy of a 12 Lead EKG (cont.)
The format of the 12-lead EKG is very standard. While there are a few exceptions, the format you see here is typical of what you will see in most 12-lead EKGs done in North America.

16. Anatomy of a 12-Lead EKG (cont.)
The 12-lead can provide a computer generated interpretation.
When you see “ACUTE MI SUSPECTED” the machine is right about 98% of the time.
In order to attain specificity, if the computer isn’t absolutely sure that an AMI is present, it will not say anything about it.
In other words YOU are the primary interpreter, the computer is your backup.

17. Anatomy of a 12-Lead EKG (cont.)
The 12-Lead is very good at measuring intervals and durations.
It is better at measuring the PR-interval and the QRS width.
We express these intervals and durations in seconds
12-lead expresses them in milliseconds. It is simple to convert milliseconds to seconds.

18. Anatomy of a 12-Lead EKG (cont.)
When you use an EKG to determine the cardiac rate and rhythm, certain sampling time is required.
12-lead interpretation: Only one beat from each lead is needed to make an interpretation.

19. Anatomy of a 12-Lead EKG (cont.)
There are six positive electrodes on the chest, yielding six leads.
There are four electrodes on the limbs from which the EKG machine makes another six leads.
Each lead has one positive electrode.
Positive electrode is a camera.
view is from the positive electrode toward the negative electrode.
The portion of the left ventricle that each leads “sees” is determined by the location of that positive electrode.
Different placements of the electrodes will yield different viewpoints.

20. Anatomy of a 12-Lead EKG (cont.)
Types of Leads
Limb Leads
Chest Leads
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6

21. Anatomy of a 12-Lead EKG (cont.)
View of Posterior Heart Wall
Leads V1 & V2
Tall R
ST Depression
Upright T-Wave
Tall R Wave and ST Depression are hallmarks of Posterior Wall MI

22. Anatomy of a 12-Lead EKG (cont.)
View of Inferior Heart Wall
Leads II, III, aVF
Looks at inferior heart wall
Looks from the left leg up

23. Anatomy of a 12-Lead EKG (cont.)
View of Lateral Heart Wall
Leads I and aVL
Looks at lateral heart wall
Looks from the left arm toward heart
*Sometimes known as High Lateral*

24. Anatomy of a 12-Lead EKG (cont.)
View of Lateral Heart Wall
Leads V5 & V6
Looks at lateral heart wall
Looks from the left lateral chest toward heart
*Sometimes referred to as Low Lateral or Apical view*

25. Anatomy of a 12-Lead EKG (cont.)
View of Entire Lateral Heart Wall
Leads I, aVL, V5, V6
- Looks at the lateral wall of the heart from two different perspectives
Lateral Wall

26. Anatomy of a 12-Lead EKG (cont.)
View of Anterior Heart Wall
Leads V3, V4
Looks at anterior heart wall
Looks from the left anterior chest

27. Anatomy of a 12-Lead EKG (cont.)
View of Septal Heart Wall
Leads V1, V2
Looks at septal heart wall
Looks along sternal borders

28. Anatomy of a 12-Lead EKG (cont.)
I Lateral
II Inferior
III Inferior
aVR
aVL Lateral
V1 Septal
aVF Inferior
V2 Septal
V3 Anterior
V4 Anterior
V5 Lateral
V6 Lateral

29. Anatomy of a 12-Lead EKG - ST Segment
The ST segment is normally iso-electric (baseline) neither elevated or depressed.
May slope upward toward a relatively tall T wave
The ST segment is probably the single most important element to identify on the ECG when looking for evidence of AMI.

30. The Three I’s Ischemia Injury Infarct lack of oxygenation
ST depression or T inversion
Injury
prolonged ischemia
ST elevation
Infarct
death of tissue
may or may not show in Q wave
This information will aid in understanding the ECG subsets in the next section.
Define ischemia, injury and infarct.
Note that the definitions are correlated with specific ECG criteria.
Note that “injury” is also ischemia and does not imply any permanent damage or death to tissue. The term injury simply means ischemia identified by ST segment elevation.

31. CARDIAC ISCHEMIA
( Myocardial ischemia, Ischemic heart disease, Ischemia, Myocardium ischemia, Silent ischemia )
Cardiac ischemia is a situation in which the blood flow within a coronary artery is limited to the point where the oxygen needs of the heart muscle cannot be met (hypoxia).

32. CARDIAC ISCHEMIA
Minor episodes of cardiac ischemia tend to cause little long-term damage to the heart, but these episodes can sometimes cause serious effects in some patients:
They can cause arrhythmias, which can lead to either syncope or cardiac arrest and sudden cardiac death.
Severe or lengthy episodes can trigger a result in myocardial infarction.
The collective effects of minor episodes of cardiac ischemia can potentially lead to cardiomyopathy.

33. Symptoms of Cardiac Ischemia
May be painful symptoms of cardiac ischemia,
Pain, pressure or discomfort from cardiac ischemia is angina. Angina may feel like a squeezing vise or crushing pressure deep in the chest behind the sternum. May also be felt in the shoulders, arms, back, neck or jaw.

34. EKG in Acute Ischemia
Tracing taken during an episode of anginal pain that occurred while the patient was at rest. Marked ST elevation in leads V2‑5 with some ST depression in aVF.

35. EKG after Acute Ischemia
This tracing was taken 30 minutes after the initial. The patient was pain‑free and asymptomatic. The ST segments are isoelectric, and the ECG is normal

36. Evaluation after Acute Ischemia
Subsequent clinical evaluation
serial ECGs
enzyme determinations,
revealed no evidence of acute myocardial infarction. Disappearance of the ST elevation and the absence of clinical and electrocardiographic evidence of infarction on subsequent examinations indicate that initial ECG is representative of severe, acute, and reversible ischemia.

37. Well Perfused Myocardium
Epicardial Coronary Artery
Lateral Wall of LV
Septum
Left
Ventricular
Cavity
Point out the epicardial artery and it’s branches reaching toward the endocardium.
The endocardium is less well perfused and has higher oxygen demand than epicardial tissue. Illustrate higher demand with glass of water.
When the myocardium is well perfused, the ST segments are isoelectric (equal to the T-P segment).
Positive Electrode
Interior Wall of LV

38. Normal ECG
ST segments are iso-electric.

39. Ischemia Epicardial Coronary Artery Lateral Wall of LV Septum Left
Ventricular
Cavity
The vessel lumen is now narrowed by a clot. If the clot is incomplete or collateral circulation is good, only the hardworking, poorly perfused sub-endocardial tissue will become ischemic.
This is represented on the ECG by ST depression or T wave inversion.
Positive Electrode
Interior Wall of LV

40. Ischemia Inadequate oxygen to tissue Subendocardial
Represented by ST depression or T inversion
May or may not result in infarct
Define ischemia.
Inadequate oxygen to tissue.
Represented by ST depression or T inversion.
May or may not result in infarct (duration of clot and demand).
If infarct develops, may or may not display Q wave.
The direction of ST deviation is a poor predictor of Q wave development.

41. ST depression
Note widespread ST depression and T waves inverted in several leads.

42. Injury Prolonged ischemia Transmural Represented by ST elevation
Usually results in infarct
Define injury. Ischemia affecting the epicardium represented by ST elevation.
Lack of oxygenation to tissue
Represented by ST elevation. Refereed to as the “injury pattern”.
Usually results in infarct (presumptive evidence of MI)
If infarct develops, may or may not develop Q wave
The direction of ST deviation is a poor predictor of Q wave development.

43. ST elevation Ask group to look for ST elevation.
The ST elevation implied epicardia ischemia (injury pattern).

44. Injury Thrombus Ischemia
If the clot is complete or the collateral circulation is poor, the ischemia will be transmural (through to wall). This is seen on the ECG as ST segment elevation.
Most often this occurs due to a complete and persistent clot. Spontaneous lysis at this point is rare and the tissue is expected to infarct unless acute reperfusion therapy can be rapidly initiated.
ST segment elevation is presumptive evidence of ACUTE MI.

45. Infarct Death of tissue Represented by Q wave
Not all infarcts develop Q waves
Death of tissue.
Traditionally represented by wide (equal to or greater than 40ms) Q wave.
Not all infarcts develop Q waves.
The direction of ST deviation (elevation or depression) is a poor predictor of Q wave development.

46. Infarction Many infarcts do not develop Q waves Infarcted Area
Electrically Silent
Death of myocardial tissue may result in the development of a pathologic Q wave.
Q wave development can not be predicted by the direction of ST segment deviation.
It does not occur with all infarcts.
Depolarization
Many infarcts do not develop Q waves

47. Q Waves
Pathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle.

48. Thrombus Infarcted Area Electrically Silent Ischemia Depolarization
During the evolution of an infarct, Q waves, ST elevation, and T inversion may occur together.
ST elevation is the most important finding to the emergency care provider. It is presumptive evidence of acute myocardial infarction.
Depolarization

49. Summary A normal ECG does NOT rule out ACS
ST segment depression represents ischemia
Possible infarct
ST segment elevation is evidence of AMI
Q wave MI may follow ST elevation or depression
A normal ECG does NOT rule out any Acute Coronary Syndrome.
ST segment depression represents ischemia, infarction is possible.
ST segment elevation represents epicardial ischemia, and is presumptive evidence of AMI.
Since necrosis may occur under all the these situations, a Q wave MI may follow ST elevation, ST depression or even a normal ECG.

50. Pathophysiology of the AMI
Chronic accumulation of atherosclerotic plaque in coronary vessels around the heart
Fibrous plaque prone to rupture, lead to thrombytic blockage
Clots form due to damaged tissue and platelets
Both release chemicals causing a clot to form
Forms a substance called fibren that traps cells and platelets eventually blocking and narrowing
Tissue damage in AMI results from rupture of plaque on vessel walls creating a chain reaction that forms a clot in the coronary artery.

51. Process of an AMI Impaired blood flow:
Produces varying degrees of myocardial injury
Damage dependent on flow reduction and duration
Tissue death progress quickly in a wave pattern
Begins with endocardium
Ends with epicardium
Infarction becomes larger toward the surface of the heart.
Ischemia – Shortage of oxygen at cellular level
Injury – Diminishing supply of oxygen
Infarct – cardiac cells die of anoxia.

52. EKG Changes from Infarction
First Detectable Change in EKG
Tall T-waves
increase in height
more symmetric
may occur in the first few minutes
*Known as hyper acute phase*

53. EKG Changes from Infarction “The Acute Phase”
Signs of Myocardial Injury
ST Segment Elevation
Primary indication of injury
Occurs in first hour to hours
ST Segment Elevation in Leads
1mm or greater in limb leads
2 mm or greater in chest leads
Hallmark indication of AMI
*Known as Acute Phase*

54. EKG Changes of Infarction “Reciprocal Changes”
ST elevation in contiguous leads most often represents acute infarction
ST depression in contiguous leads may represent acute ischemia
In acute infarction, ST elevation in contiguous leads coupled with reciprocal ST depression in non-infarcting leads is added evidence of an AMI.

55. Reciprocal ST segment depression Acute ST segment elevation

56. EKG Changes from Infarction “T Wave Inversion”
Signs of Myocardial Injury
T wave inversion
presence of ischemia
May precede ST elevation
Prominent in precordial chest leads
Inversion in limb leads is pathologic
T wave inversion can be caused by other things than ischemia

57. EKG Changes from Infarction “The Indeterminate Phase”
Signs of Myocardial Infarction
Pathologic Q-wave
First indication of tissue death
First few to several hours
Q-wave ¼ size of QRS suggests infarct
Represent current or past events
Determine timing through ST elevation and T-wave inversion

58. Natural Progression of EKG in Infarction
Over time:
T-wave regains normal contour
ST-segment returns to isometric line
Q-wave remains as evidence of infarct
Indicates presence of previous MI
*ST segment elevation provides the strongest evidence of early recognition of AMI*

59. EKG Changes from Infarction (cont.)
All of the changes in the previous slides are: Indicative Changes
ST segment elevation is helpful in detecting an MI in its early stages
Hyperacute (Tall) T-waves alone are specific enough to diagnose an MI
T-wave inversion can occur with simple angina and is therefore not specific
Pathological Q-wave is the most accurate recognition of an MI
Not in the first few hours
ST segment elevation provides the strongest evidence for early recognition of an MI

60. ECG Variants Coronary Spasm: “Printzmetals angina”
Injury pattern that resolves w/ rest, NTG,O2 etc.
Early Repolarization: elevated “J” point seen best in V3,4. Key to Dx pt’s are usually young & asymptomatic
Pericarditis: ST elevation usually global associated w/ fever, pleuritic c/p.

61. ECG Variants due to Drugs or Electrolytes Imbalances
Hypokalemia: lg U waves ( usually taller than T) seen best in precordial leads. <2.7
Hyperkalemia:
Tall peaked T waves > 6.0
PR prolongs, QRS widens
P waves disappear > 8.0
Hypocalcemia:
Prolonged QT interval
Hypercalcemia:
Shortened QT interval
Digitalis effect:
ST depression- downsloping, curved ST segments.
“scooping”, “sagging”, flat or inverted T’s in lateral leads
PR prolonged
QT shortened

62. Bundle Branch Blocks “Turn Signal Rule”
This is a simple method for differentiating right bundle branch block from left bundle branch block. V1 will be the only lead you need to view
1. Locate the terminal (last) force of the QRS complex
2. Determine if it is pointing up or down.
3. Compare to the turn signal in your car:
Up is for a right turn & RBBB
Down is for a left turn and LBBB
Clinical significance:
Bundle branch is a significant complication of infarction. Since the left anterior descending artery is the primary supplier of the bundle branches, BBB is considered a complication of anterior septal infarcts.
When BBB is the result of MI, the incidence of pump failure is 65-70% and the in-hospital mortality rate is 40%-60%. The BBB itself is not dangerous, but the high mortality rate is due to the extensive amount of tissue death occurring when an infarct is serious enough to cause a BBB. Another manifestation of BBB is in the form of AV Block. This is why infranodal AV blocks are more serious and have wide QRS complexes.

63. Localizing the Area of Infarction
Indicative changes are not found in every lead
Only present in leads looking at the infarct
Indicative changes in two or more leads looking at the same portion of the heart are anatomically contiguous leads
Suspect AMI
ST segment elevation in two or more leads that are not contiguous
AMI not the suspected cause

64. Recognition & Localization
Recognizing infarct: Know which part of the heart each lead looks at
Localizing Infarct: Note which lead is displaying evidence and which portions of heart they are looking at
Leads Displaying Indicative Changes
II, III, aVF
V1 & V2
V3 & V4
V5, V6, I, and aVL
Location of Infarct Site
Inferior
Septal
Anterior
Lateral
*Simply knowing the changes to look for and which part of the heart each lead looks at*

65. Anterior Wall MI
Anterior Wall infarct: Occlusion of the Left Anterior Descending Artery (LAD)
2mm ST segment elevation in two or more of leads V1-V4
Reciprocal changes in leads II, III, aVF
Lethal due to large myocardium involvement
Possible conduction defects:
Bundle Branch Block
2nd Degree Block Type II
CHB

66. Anterior Wall MI

67. Inferior Wall MI
Inferior Wall MI: Occlusion of Right Coronary Artery (RCA)
At least 1mm ST segment elevation in leads II, III, aVF
Reciprocal ST depression in leads I & aVL or precordial leads
Conduction defects:
Sinus bradycardia
Sinus arrest
1st degree block
Accelerated Idoventricular rhythm
Complications:
Bradyarrhythmias – protective mechanism, 90% of blood supply for SA & AV nodes from the RCA
Hypotension – treated with fluids, consider right side involvement

68. Inferior Wall MI

69. Lateral Wall MI
Lateral Wall MI: results from occlusion of the Left Circumflex Artery
At least 1 mm ST segment elevation in leads I, aVL, V5 & V6 and /or 2 mm ST segment elevation in V5 & V6
Reciprocal ST depression in V1
Sometimes an extension of an Anterior or Inferior MI
Conduction defects are rare

70. Anterior/Lateral Wall MI

71. *Associated with dangerous conduction disturbances*
Posterior Wall MI
Posterior Wall MI: Occlusion of the Right Coronary Artery (RCA) or the Posterior Descending Artery
No leads that look at the posterior wall
Leads look at the infarct site from the opposite side(backwards)
ST depression in V1 & V2
Tall R waves in V1 and/or V2
Most often associated with Inferior MI
*Associated with dangerous conduction disturbances*

72. Posterior Wall MI

73. Right Ventricular MI
Right Ventricular MI: caused by proximal occlusion of the Right Coronary Artery (RCA)
Associated with Inferior Wall MI
Can happen independently
Standard 12-Lead does not assess right side of heart
Infarction is significant
Indicates large infarction
Indicates involvement of both ventricles
If the possibility of RVI exists a set of chest leads can be applied to the right side of the chest
V1-6R leads look at right ventricle
Lead V4R most accurate
Evidence of a Right Ventricular MI are present in Lead V4R only for the first four (4) hours of an MI

74. Right Ventricular MI

75. Septal Wall MI
Septal Wall MI: caused by septal perforation involving the LAD or the Posterior Descending
Most often in the setting of an Anterior MI
Loss of R-wave in leads V1, V2 or V3
May have ST segment elevation in V1 & V2
No reciprocal changes

76. Overview of Infarcts Location of Infarct Arterial Supply
Indicative Changes
Reciprocal Changes
Anterior
LAD
V1-V4
II, III, aVF
Inferior
RCA
I, aVL
Lateral
Circumflex
I, aVL, V5, V6 V1
Posterior
Posterior Descending (RCA)
None
V1, V2
Septal
Septal Perforating (LAD)
Posterior Descending (RCA
Loss of R wave in V1, V2, or V3
Maybe just some discussion of reciprocal changes? Debate of significance? Not all MI’s have reciprocal changes, that their presence may indicate a bigger infarct, more ischemic area. Sometimes reciprocal changes are more evident (stick out more) than ST elevation and help zero in on infarcted region.

77. Overview of Infarcts
Suspect infarction when there are indicative changes in at least two anatomically contiguous leads
Indicative changes in many leads suggests larger infarct
With Inferior Wall MI suspect Right Ventricular Wall Infarct
Signs of possible Right Ventricular Wall Infarct:
Hypotension
JVD
Clear lung sounds
Causes of ST segment depression include digitalis, ischemia and reciprocal changes
Suspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3

78. Complications of Myocardial Infarction
Chest Pain: Most common complication
Treatment:
Oxygen and ASA (162 to 325)mg
NTG initially with Morphine if pain persists
Usually very effective
Right Ventricular Wall Infarct:
Reduces output of right ventricle decreasing left ventricular filling (decreased preload)
NTG and Morphine can worsen conditions
Decrease in blood pressure will worsen area of injury
Presence of Inferior Wall Infarction with no EKG or clinical evidence of right side infarct does not merit any extra caution when using NTG and Morphine
Should also stress that NTG should be given cautiously to patients with borderline blood pressure when evidence of RV Infarct exists.

79. Complications of Myocardial Infarction
AV Block Location: indicates electrical impulse from atrium is blocked from depolarizing the ventricles
Most common block is in the AV Node (nodal block)
Second most common block is in the Bundle Branches (infranodal)
Infarct frequently produces AV Block due to increase in parasympathetic tone
Local ischemia around node can produce the block
Less serious than block caused by tissue injury or death
Blocks in AV node produce narrow QRS complex
Bundle Branches produce wide complexes

80. Complications of Myocardial Infarction
Determining the type of QRS presented with is a useful tool in determining the location of the block
Nodal Block
Infranodal Block
Coronary Supply
Right Coronary Artery
Left Coronary Artery
QR Width
Narrow
Wide
Stability
Generally Stable
Often Unstable
Atropine Response
Usually improves
Often does not respond
Slide may be confusing. Better stated that if the QRS is narrow, then the block lies at the junction of the AV Node. If the QRS is wide, then the block lies below the level of the AV Node

81. Complications of Myocardial Infarction
Hypotension: A common treatment for hypotension which is secondary to the infarct is to administer fluid boluses and inotropic drugs (dopamine)
Hypotension in the setting of an inferior wall infarction is most likely secondary to right ventricular involvement.
Although RV Infarcts may require significant boluses to offset loss of preload, continuously monitor the patient for signs and symptoms of developing left sided failure.
Hypotension in the setting of an anterior wall infarction may not tolerate fluid boluses and may require a dopamine infusion.
Inferior Wall MI’s with RV involvement and hypotension may respond to fluid challenges of up to 2 liters. Boluses should be administered in 250 ml increments while assessing left ventricular function. Anterior Wall MI’s may not tolerate even small amounts of fluid and may require pressor intervention in the setting of hypotension.

82. Complications of Myocardial Infarction
Left Coronary Artery Occlusions
Right Coronary Artery Occlusions
Leads Showing Indicative Changes
V1-V6, I, aVL
II, III, aVF, V4R-V6R
Localization
Septal, Anterior, Lateral, Posterior
Inferior, Posterior, Right Ventricular
Pain Control
NTG & Morphine as appropriate
NTG & Morphine used with caution if RVI present
AV Block
Infrequent, usually wide ORS, often unstable, Atropine may be ineffective, use standby pacing
Frequent, usually narrow QRS, Generally stable, Atropine often effective, May not require treatment
Hypotension
cc fluid bolus, inotropic medications
Vigorous fluid therapy if RVI present, inotropic medications

83. Clinical Pearls
Suspect infarction when there are indicative changes in at least two anatomically contiguous leads
Indicative changes in a greater number of contiguous leads suggests a more extensive infarction
RV or Posterior infarcts should be considered in setting of Inferior Wall MI
RV: ST segment elevation in rV4
Posterior: ST depression +/or Tall Rwave in V1 & V2
Other clinical signs of RV Infarct may include:
Hypotension and JVD in the setting of clear lung sounds
Other causes of ST segment depression besides ischemia include digitalis effects and ventricular hypertrophy
Suspect Posterior Wall Infarctions when an Inferior Wall Infarction has ST depression in Leads V1-V3

84. Questions ?