Chapter 9 Flashcards
What are some indications a 12 lead ECG is needed?
- Abdominal or epigastric pain
- Assisting in dysrhythmia interpretation
- Chest pain or discomfort
- Diabetic ketoacidosis
- Dizziness
- Dyspnea
- Electrical injuries
- Known or suspected electrolyte imbalances
- Known or suspected medication overdoses
- Right or left ventricular failure
- Status before and after electrical therapy
- Stroke
- Syncope or near-syncope
- Unstable patient, unknown etiology
What leads view the lateral part of the heart?
D1, aVL, V5, V6
What leads view the inferior part of the heart?
aVF, DII, DIII
Which leads view the anterior part of the heart?
V3, V4
Which leads view the septum (part of heart)?
V1, V2
What happens when there is a lack of oxygen in the tissue due to low circulation?
- Ischemia
- Acute myocardial injury
- Myocardial infraction
Layout of the 12 lead ECG
Lateral - V5, V6, aVL, DI
Inferior - aVF, DII, DIII
Anterior - V3, V4
Septum - V1, V2
aVR - none
Vectors
Mean vector identifies the average of depolarization waves in one portion of the heart
Mean P vector — represents the average magnitude and direction of both right and left atrial depolarization
Mean QRS vector — represents the average magnitude and direction of both right and left ventricular depolarization
Axis
Mean axis — average direction of a mean vector — only identified on frontal plane
Axis of a lead — an imaginary line joining the positive and negative electrodes of a lead
Electrical axis — refers to determining the direction (or angle in degrees) in which the main vector of depolarization is pointed
Hexaxial reference system
The hexaxial reference system represents all of the frontal plane (limb) leads with the heart in the center
Forms a 360 degree circle around the heart
Normal axis of the heart is between -30 degrees and +90 degrees
Quadrant method = aVF +90 degrees
DI 0 degrees
Determine electrical axis
Look for the longest QRS in leads DI, DII, DIII, aVR, aVL, aVF
Look at longest S wave
- Calculate # of squares there are from isoelectric line up the R wave (in mmV)
- Calculate # of squares there are from isoelectric line down S wave (in mmV)
- Subtract
Estimate if they would look + or -
Determination of QRS quadrant deviation
DI (+) & aVF (+) = normal
DI (+) & aVF (-) = left axis deviation
DI (-) & aVF (+) = right axis deviation
DI (-) & aVF (-) = northwest extreme axis deviation or undetermined
Steps to analyze 12 lead ECG
- aVR - is it flipped? If it is, EKG was done correctly
- Move to most useful (most viewed lead) lead II (lateral) then continuous leads (DIII, aVF) — are they normal? Is there deviation?
- Followed in whatever order of sections (anterior, inferior, etc) you want to follow. Are they normal? Is there deviation
Acute coronary syndrome
Unstable angina (UA)
Non ST-segment elevation myocardial infarction (NSTEMI)
ST-segment elevation MI (STEMI) — sign of acute myocardial infarction
Indicative and reciprocal changes - what does each change mean (elevation, inverted waves, etc)
Inverted T waves - ischemia
ST elevation - acute myocardial infarction
Pathological Q wave (deep Q wave - more than 1/3 of QRS) - old scar of a myocardial infarction — abnormal
What do changes in 2 contiguous leads mean?
Indicative changes are significant when they are seen in at least two contiguous leads (two leads in the same heart area)
Two leads are contiguous if they look at the same or adjacent areas of the heart or if they are numerically consecutive chest leads
How do you assess the extent of infarction using leads?
Evaluate how many leads are showing indicative changes — changes in only a few leads suggests a smaller infarction
The more proximal the vessel blockage — the larger the infarction. The greater the number of leads showing indicative changes
Anterior infarction
Left main coronary artery supplies — left anterior descending artery (LAD) and circumflex artery (Cx)
Anterior myocardial infarction occurs when the blood supply to the LAD artery is disrupted
Evidence of anterior myocardial infarction can be seen in leads V3 and V4.
Septal infarction
Changes in leads V1 and V2 will show septal infarction
If an infarction involve anterior wall AND septum, there will be changes in V1, V2, V3, V4
R wave progression
R wave becomes taller and S wave becomes smaller as the chest electrode is moved from right to left
V3 and V4 normally record an equiphasic RS complex — transitional zone
Transition zone is where the R wave amplitude begins to exceed the amplitude of the S wave
Early transition is when change is seen in V2
Late transition describes a delay in transition until leads V4 and V5
Poor R wave progression
Phrase used to describe R waves that decrease in size from V1 to V4
Lateral infarction
Seen in DI, aVL, V5 and V6
May be associated with an anterior, inferior, or posterior infarction
Inferior infarction
Seen in leads DII, DIII, aVF
Increased parasympathetic nervous system activity is common with inferior MIs, resulting in bradydysrhythmias
Conduction delays (first degree AV block, second degree AV block type 1) are common and are usually transient
Inferobasal infarction
Occur in conjunction with an inferior or lateral infarction
None of the 12 leads view posterior wall, additional leads (V7 to V9) may be used to view the posterior surface
Changes include STE in these leads
Mirror test may be helpful in recognizing the ECG changes suggesting an inferobasal MI
Right ventricular infarction
RVI is usually the result of a right coronary artery (RCA) occlusion.
Right side chest leads are used in this situation
Intraventricular conduction system — bundle of his
Normally the only electrical connection between atria and ventricles
Connects AV node with the bundle branches
Conducts impulse to right and left bundle branches
Intraventricular conduction system — right bundle branch
Travels down right side of inter ventricular septum
Conducts impulse to right ventricle
Long, thin, and more fragile than the left
Intraventricular conduction system — left bundle branch
Begins as a single structure that is short and thick (left common bundle branch or mainsterm)
Divides into subdivisions called fascicles
Bundle branch activation
Normally, left side of the interventricular septum is stimulated first
Electrical impulse then crosses the septum to stimulate the right side
Left and right ventricles are then depolarized at the same time
If the delay or block occurs in one of the bundle branches, the ventricles will not be depolarized at the same time — impulse travels first down the unblocked branch, stimulates that ventricle, impulse must then ravel from cell to cell through the myocardium to stimulate the other ventricle
Bundle branch block (BBB) - how to recognize it?
Measure the QRS complex duration
Select the widest QRS complex with a discernible beginning and end
Lead V1 is probably the single best lead to use when differentiating between forms of bundle branch block
How to recognize complete or incomplete BBB? Intraventricular conduction delay?
If a BBB pattern is discernible and the QRS measure 0.12 sec or more in an adult, it is called complete right or left bundle branch block
If a BBB pattern is discernible and the QRS duration is between 0.11 and 0.119 sec in adults, it is called an incomplete right or left BBB
If the QRS is wide but there is no BBB pattern, the term wide QRS or intraventricular conduction delay is used to describe the QRS
Easy way to figure out if its a right bundle branch block (RBBB) or a left bundle branch block (LBBB)
View lead V1
Move from the J point back into the QRS complex
Determine if the terminal portion (last 0.04sec) of the QRS complex is positive or negative
Positive — RBBB
Negative — LBBB
Causes of right BBB
Can occur in individuals with no underlying heart disease, but occurs more commonly in the presence of organic heart disease
May occur secondary to a right ventricular infarction
Causes of left BBB
May occur secondary to —
Anteroseptal (more common) or inferior MI
Conduction system degeneration
Acute heart failure
Acute pericarditis or myocarditis
Following cardiac procedures
Other causes of BBB
Aortic valve disease
Congenital, hypertensive, and rheumatic heart disease
Trauma (cardiac surgery)
Rate related BBB
Nonischemic diseases
What to do about BBB
BBB in an asymptomatic patient requires non specific treatment
RBBB generally requires no specific treatment — RBBB in the setting of an acute MI requires close ECG monitoring
LBBB can produce STE and wide Q waves that mimic infarction — close ECG monitoring and frequent patient reassessment are essential
Chamber abnormalities
Cardiomyopathy — heart disease involving the heart muscle and resulting in abnormal enlargement
Cardiac enlargement — refers to either
dilation of a heart chamber — cavity getting bigger, but muscle staying the same. Heart struggles to pump the larger amount of blood gathered in chambers
Hypertrophy of the heart muscle — increasing the thickness of the myocardial wall — muscle gets thicker leaving less space for blood in chambers
Cardiac hypertrophy — thickening of the heart muscle, with resultant enlargement of a heart chamber. Hypertrophy is commonly accompanied by dilation
Ventricular hypertrophy
Hypertrophy increases the QRS amplitude and is often associated with ST segment depression and asymmetrical T wave inversion
Left ventricular hypertrophy
Find the tallest R wave (calculate voltage) and deepest S wave (calculate voltage)
For LVH
S (from V1 or V2) + R (from V5 or V6) >= 35mm
Right ventricular hypertrophy
Find the tallest R wave (calculate voltage) and deepest S wave (calculate voltage)
For RVH
R (from V1 or V2) + S (from V5 or V6) >= 13mm
Electrolyte disturbances
Electrolyte imbalances may increase cardiac irritability and cause cardiac dysrhythmias
ECG can be evaluated for evidence of electrolyte disturbances
Electrolyte disturbances — sodium
Important in maintaining water balance. Most abundant electrolyte in the body.
Necessary for the normal conduction of impulses in nerve and muscle fibers
Plays an important role in the voltage of action potentials
Hypernatremia (sodium excess)
May result from the retention of relatively more sodium than water or it may be caused by a loss of relatively more water than sodium
Possible signs and symptoms:
1. Restlessness, irritability
2. Thirst
3. Dry and flushed skin
4. Dry mucous membranes
5. Decreased urine output
6. Seizures
7. Coma
Does not cause any significant ECG changes
Hyponatremia (sodium deficit)
May result in the following:
1. Inadequate sodium intake
2. Prolonged diuretic therapy
3. Excessive diaphoresis
4. Excessive loss of sodium from trauma (burns)
5. Adrenal insufficiency
6. Renal disease
7. Severe gastrointestinal (GI) fluid losses
8. Some medications (may impair water excretion and contribute to hyponatremia)
Possible signs and symptoms:
1. Irritability
2. Fatigue
3. Headache
4. Nausea and vomiting
5. Abdominal cramps
6. Muscle weakness
Does not cause any significant ECG changes
Potassium
Primary intracellular fluid cation
Essential for many cell functions including the following:
1. Cardiac and neuromuscular activity
2. Resting membrane potential
3. Growth
4. Enzyme function
5. Regulation of fluid volume and pH
Hyperkalemia (potassium excess)
Possible causes:
1. Acute or chronic renal failure
2. Excessive administration of intravenous potassium
3. Metabolic acidosis
4. Ingestion of excessive amounts of salt substitutes
5. Medications
6. Widespread cell damage (crush injuries, burns)
Electrocardiographic signs of hyperkalemia
1. Tall, peaked (tented), narrow, symmetric T waves
2. P waves decrease in amplitude as potassium levels increase
3. PR interval and QRS duration increases as potassium level increases
Hypokalemia (potassium deficit)
Possible causes:
1. Prolonged diuretic therapy with thiazide diuretics or furosemide
2. Inadequate dietary intake of potassium
3. Administration of potassium deficient parenteral fluids
4. Starvation
5. Severe gastrointestinal fluid losses
6. Laxative use without replacement of potassium
*Electrocardiographic signs of hypokalemia:
1. ST segment depression
2. Decrease in T wave amplitude
3. Prominent U wave
4. P wave amplitude and duration are usually increased
5. Slight prolongation of PR interval
6. Increased QRS duration with severe hypokalemia
Hypokalemia (potassium deficit)
Possible causes:
1. Prolonged diuretic therapy with thiazide diuretics or furosemide
2. Inadequate dietary intake of potassium
3. Administration of potassium deficient parenteral fluids
4. Starvation
5. Severe gastrointestinal fluid losses
6. Laxative use without replacement of potassium
*Electrocardiographic signs of hypokalemia:
1. ST segment depression
2. Decrease in T wave amplitude
3. Prominent U wave
4. P wave amplitude and duration are usually increased
5. Slight prolongation of PR interval
6. Increased QRS duration with severe hypokalemia
Calcium
Important in bone formation, in nerve and muscle function and in blood clotting
Hypercalcemia (calcium excess)
Possible causes:
1. Hyperparathyrodism
2. Chronic and acute renal failure
3. Excessive vitamin D or vitamin A intake
4. Hyperthyroidism
5. Adrenal insufficiency
6. Cancer (breast, lung, multiple myeloma)
7. Excessive use of calcium containing antacids
8. Excessive intake of calcium supplements
Electrocardiographic changes associated with hypercalcemia
1. Shortening of the ST segment
2. Decreased QT interval duration
Hypocalcemia (calcium deficit)
Possible causes:
1. Renal disease
2. Dietary deficiency of calcium and vitamin D
3. Pancreatic disease
4. Malabsorption because of small bowel disease
5. Hypoparathyroidism
6. Certain medications
Electrocardiographic changes associated with hypocalcemia:
1. Lengthening of ST segment
2. Increased QT interval duration
Magnesium
Essential role in the following:
Membrane stability
Skeletal muscle concentration
Respiratory smooth muscle function
Hypermagnesemia (magnesium excess)
Possible causes:
1. Hypothyroidism
2. Addison disease
3. Excessive parenteral magnesium (eclampsia)
4. Excessive use of magnesium containing antacids, laxatives, or enemas in patients with impaired renal function
Depresses AV and intraventricular conduction
-increases potential for bradycardia and AV blocks
Hypomagnesemia (magnesium deficit)
Possible causes:
1. Prolonged or excessive diuretic therapy
2. Excessive calcium or vitamin D intake
3. Administration of intravenous fluids or total parenteral nutrition without magnesium replacement
4. Hypercalcemia
5. Malabsorption associated with disease of the small intestine, malnutrition, and alcohol use disorder
Although hypomagnesia does not produce significant ECG changes, it has been implicate as a possible cause of torsades de pointes
Analyzing the 12 lead Electrocardiographic (Book)
- Identify the rate and underlying rhythm. Identify any premature beats and pauses.
- Estimate the QRS axis using leads DI and aVF
- Analyze waveforms, segments, and intervals. Before examining waveforms, quickly look at the calibration marker and determine if it is standard, half standard, or twice the standard. Next, examin each lead, selecting one good representative waveform or complex in each lead. Inspect each waveform, noting any changes in orientation, shape, size, and duration.
- Examine for evidence of ischemia, injury, and infarction. Look for the presence of ST segment displacement (STE or ST segment depression)
- Look for evidence of other conditions. Is there evidence of chamber enlargement, electrolyte imbalances, or conditions that mimic MI (LVH, LBBB, ventricular rhythm, ventricular paced rhythm)?
- Interpret your findings
Analyzing 12 lead ECG (slides)
- Identify the rate and underlying rhythm. Identify any premature beats and pauses
- Determine the QRS axis using leads DI and aVF
- Analyze waveforms, segments and intervals
- Examine for evidence of ischemia, injury and infarction. Look for the presence of ST segment displacement
- Look for evidence of other conditions. Is there evidence of chamber enlargement, electrolyte imbalances, or conditions that mimic MI?
- Interpret your findings
A 66 year old man presents with persistent chest pain that has been present for 1 hour. His 12 lead ECG reveals STE in leads V2, V3, and V4 and his cardiac biomarkers are elevated. You suspect __________
A. Stable angina
B. Unstable angina
C. ST elevation myocardial infarction (STEMI)
D. Non ST elevation myocardial infarction (NSTEMI)
C
An acute coronary syndrome diagnosis is based on the patient’s clinical presentation , history, ECG findings, and cardiac biomarker results. If ST segments are elevated in two contiguous leads, and elevated cardiac biomarkers are present, the diagnosis is STEMI. If ST elevation is not present, but biomarker levels are elevated. The diagnosis is NSTEMI. If the ST segments are not elevated and cardiac biomarkers are not elevated, the diagnosis is unstable angina
Which of the following is probably the single best lead to use when differentiating between right and left bundle branch blocks?
A. Lead II
B. Lead V1
C. Lead V4
D. Lead aVR
B
The criteria for bundle branch block recognition may be found in any lead of the ECG. However, went differentiating right bundle branch block from left bundle branch block, pay attention to the QRS morphology (shape) in specific leads. Lead V1 is probably the single best lead to use when differentiating between right bundle branch block and left bundle branch block
When leads I and aVF are used to determine the electrical axis, left axis deviation is present if the QRS is _______
A. Positive in lead I and positive in lead aVF
B. Positive in lead I and negative in lead aVF
C. Negative in lead I and negative in lead aVF
D. Negative in lead I and positive in lead aVF
B
Current flow to the left of normal is called left access deviation (between -30 and -90 degrees). If the QRS complex is predominantly positive in I and negative in aVF, left access deviation as present
When evaluating the ECG for the presence of chamber enlargement, an ECG machines sensitivity must be calibrated so that a 1 millivolt electrical signal will produce a deflection measuring exactly _______ mm tall.
A. 0.5
B. 1
C. 5
D. 10
D
When evaluating the ECG for chamber enlargement, it is essential to check the calibration marker to ensure that it is 10mm (1mV) tall
Which of the following ECG changes is one of the earliest to occur during a STEMI but may have resolved by the time the patient speaks medical assistance?
A. Pathological Q wave
B. Hyper acute T waves
C. Horizontal ST segments
D. Lengthening of the QT interval
B
Hyperacute (tall) T waves are sometimes called “ tombstone” T waves, and typically measure more than 50% of the preceding R wave. In addition to an increase in height, the T wave becomes more symmetric and may become pointed. These changes are often not recorded on the ECG because they have typically resolved by the time the patient seeks medical assistance.
Although a right ventricular infarction may occur by itself, it is more commonly associated with a(n) ______ wall myocardial infarction.
A. Septal
B. Lateral
C. Inferior
D. Anterior
C
The right ventricle is supplied by the right ventricular marginal branch of the RCA. Occlusion of the right ventricular marginal branch results in an isolated right ventricular infarction (RVI). Occlusion of the RCA proximal to the right ventricular marginal branch results in an inferior and right ventricular infarction. RVI should be suspected when ECG changes suggesting an inferior infarction are seen.
Which of the following are possible ECG signs of hyperkalemia?
A. Peaked P waves
B. Prominent U waves
C. Tall, peaked T waves
D. Elevated ST segments
E. Shortened PR intervals
F. Increased QRS duration
C, F
ECG signs of hyperkalemia may include: tall, peaked (tented), narrow, symmetric T waves QRS duration increases as potassium level increases P wave decreases in amplitude as potassium level increases. PR interval duration increases as potassium level increases.
Which of the following are possible ECG signs of sodium disturbances?
A. Prominent U waves
B. Low P wave amplitude
C. Prolonged PR intervals
D. ST segment depression
E. Sodium disturbances do not cause any significant changes on the ECG
E
Sodium disturbances do not cause any significant changes on the ECG
Patients experiencing _______ and _______ infarctions are most likely to develop bundle branch blocks
A. Septal
B. Lateral
C. Inferior
D. Anterior
E. Inferobasal
F. Anteroseptal
A, F
The septum, which contains the bundle of his and bundle branches, is usually supplied by the left interior descending coronary artery. ECG changes, infarction or seen leads V1 and V2 the site of infarction is limited to the septum. The entire anterior wall is involved, ECG changes will be visible in V1, V2, V3, V4. A blockage in this area may result in both right and left bundle branch blocks. Second degree atrioventricular (AV) block type II, and the third-degree AV block
Normal electrical axis lies between ______ in the frontal plane.
A. -30 and +90 degrees
B. -30 and -90 degrees
C. -90 and +/-180 degrees
D. +90 and +/- 180 degrees
A
In adults, the normal QRS axis is considered to be between -30 and +90° and the frontal plane. Current flow to the right of normal is called right access deviation (between +90 and +/-180°). Current flow in the direction opposite of normal is called indeterminate, “ no man’s land” northwest, or extreme right axis deviation (between -90 and +/-180 degrees). Current flow to the left of normal is called the left axis deviation (between -30 and -90°)
In a patient experiencing an acute coronary syndrome, T wave inversion suggests the presence of
A. Injury
B. Ischemia
C. Infarction
D. Cardiogenic shock
B
In a patient experiencing an acute coronary syndrome , T wave inversion suggest the presence of myocardial ischemia
Lead II is perpendicular to lead
A. II
B. III
C. aVF
D. aVL
D
In the hexaxial reference system, the axes of some leads are perpendicular to each other. For example, lead II is perpendicular to aVL, lead I perpendicular to lead aVF, and lead III is perpendicular to lead aVR
Which of the following statements is true regarding ventricular hypertrophy?
A. Hypertrophy increases the QRS amplitude
B. Hypertrophy increases the duration of the QRS complex
C. Leads I, V5, and V6 are the best leads to use when looking for ECG evidence of hypertrophy
D. ECG evidence of right ventricular hypertrophy is usually more readily evident than left ventricular hypertrophy
A, C
Ventricular muscle thickens (hyper trophies) when it’s sustain a persistent pressure overload. Dilation occurs because of persistent volume overload. The two often go hand-in-hand. Hypertrophy increases the QRS amplitude and is often associated with ST segment, depression and asymmetric T wave inversion. The right ventricle is normally considerably smaller than the left, it must become significantly enlarged before changes are visible on the ECG. Leads V1, V5, and V6 are used when looking for ECG evidence of hypertrophy
This can produce ST segment elevation and wide Q waves that look remarkably similar to infarction
Left bundle branch block
Term that refers to either dilation of a heart chamber or hypertrophy of the heart muscle
Cardiac enlargement
Leads commonly used to determine a six deviation
DI and aVF
Non ST elevation myocardial infarction and unstable angina
Non ST elevation acute coronary syndrome
Cardiac biomarkers and ST segments are elevated when this is present
STEMI
Leads that view the septum
V1 and V2
QRS pattern that is characteristic of right bundle branch block
rSR’
Most common form of cardiomyopathy
Dilated cardiomyopathy
Term used to describe a wide QRS that is not associated with a bundle branch block pattern
Intraventricular conduction delay
The P wave is tall, peaked, and usually of normal duration
Right atrial abnormality
Vessel that is usually blocked with an inferior myocardial infarction
Right coronary artery
Deflection of the terminal force of the QRS complex in V1 in the right bundle branch block
Positive
Vessel that is usually blocked with an anterior myocardial infarction
Left anterior descending artery
Characteristic ECG changes associated with right ventricular hypertrophy
Tall R waves in leads V1 through V3 and deeper than normal S waves in leads I, aVL, V5 and V6
Leads that view the lateral wall of the left ventricle
I, aVL, V5, V6
The final portion of the QRS complex
Terminal force
Characteristic ECG changes associated with left ventricular hypertrophy
Increased QRS amplitude and changes in the ST segment and T wave
QRS pattern that is characteristic of left bundle branch block
QS
Type of cardiomyopathy characterized by significant myocardial hypertrophy without ventricular dilation that results in a markedly reduced stroke volume because of impaired diastolic filing
Hypertrophic cardiomyopathy
Associated with prolongation of the middle and end of the P wave
Left atrial abnormality
