2. What is ACS?
⢠ACS is coronary disease that is causing an
acute illness, inclusive of:
â Ischemia/unstable angina (UA or USA)
â Non-ST Elevation MI (NSTEMI)
â ST Elevation MI (STEMI)
⢠STEMI and NSTEMI are relatively new
terms; âNQMIâ and similar terms are no
longer used
⢠The term âAMIâ is still used and is usually
synonymous with STEMI
3. Epidemiology of ACS
⢠AMI most common 6am to noon due to
elevated bp, catacholamines and platelet
aggregability
⢠AMI more common in winter
⢠>1 million infarcts/500k US deaths per year
⢠Leading cause of mortality in US
⢠Annual cost >$120 billion per year
4. STEMI
⢠Acute phase is <6 hrs from onset
⢠Immediate transfer to interventional
cardiac cath lab is most effective
treatment!
⢠Fibrinolytics is also definitive treatment
7. Layers of the Heart
⢠1. Endocardium-inner
⢠2. Myocardium-
middle
⢠3. Epicardium-outer
⢠4. Pericardium-sac
around heart
8. Blood Flow through Heart
⢠Blood flows from VC
to the R atria.
⢠It crosses the
tricuspid valve into
the R ventricle.
⢠It goes past the
pulmonic valve into
the pulmonary artery
and the lungs.
9. Blood Flow cont.
⢠Blood comes from the
lungs via the pulm.
veins into the L atria.
⢠It crosses the mitral
valve into the L vent.
⢠It goes past the aortic
valve into the aorta
and the systemic and
coronary circulation.
10. Heart Valves
**Valve order T-P-M-A**
⢠Two types: atrioventricular and semilunar.
⢠AV: Open as the result of lower ventricular
pressure
â Tricuspid and Mitral valves
⢠Semilunar: Located between the ventricles
and great arteries
â Pulmonic and Aortic
11. Coronary Circulation
⢠Right and Left coronary arteries originating
at the coronary ostia at the base of the
aorta.
â Left Coronary Artery
⢠Left Anterior Descending
â Anterior, 2/3 of the septum, partial lateral
wall
⢠Left Circumflex
â Primary Lateral Wall circulation
â Right Coronary Artery
⢠Right atrium, right ventricle, inferior &
posterior wall of left ventricle.
15. ⢠Polarization: No electrical activity. Inside
of cell negative.
⢠Depolarization: Na+ rapidly rushes in and
causes inside to become positive.
⢠Repolarization: Na+ stops and K+ leaks
out as cell returns to resting levels.
18. SA Node
⢠Initiates electrical
impulses at a rate of 60-
100 bpm.
⢠Reaches threshold and
depolarizes more rapidly
than other cardiac cell.
⢠Blood supply from SA
node artery (from RCA in
55% of hearts).
20. Atrioventricular Junction
⢠AV node and Bundle
of His
⢠Electrical link
between atria and
ventricle
21. AV Node
⢠Supplied by RCA in 90% of hearts and
LCx in 10%.
⢠Delays conduction to allow atria to empty
22. Bundle of His
⢠Dual blood supply from LAD and PDA
⢠Intrinsic pacemaker rate of 40-60 bpm
⢠Normally is the only electrical connection
between the atria and the ventricles.
23. Right and Left Bundle Branch
⢠RBB innervates RV
⢠LBB innervates the
septum and LV
⢠LBB has 3 divisions:
â Anterior fascicle
â Posterior fascicle
â Septal fascicle
24. Purkinje Fibers
⢠Spread from the septum into the papillary
muscles and downward into the apex of
the heart
⢠Penetrates 1/3 of the way into the ventricle
muscle mass
⢠Intrinsic rate of 20-40 bpm
25. Electrophysiology
⢠Depolarization
â Complete depolarization normally results in
muscle contraction
⢠Threshold
â minimal stimulus required to produce excitation of
myocardial cells
26. Electrophysiology
⢠Repolarization
â Process of returning to resting potential state
⢠Sodium influx stops and potassium leaves cell
⢠Sodium pumped to outside the cell
â Relative refractory period
⢠cell will respond to a second action potential but the
action potential must be stronger than usual
â Absolute refractory period
⢠cell will not respond to a repeated action potential
regardless of how strong it is
27. Electrophysiology
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
K+ K+ K+
K+ K+
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
Myocardial cells are POLARIZED. They have more positive charges
outside than inside.
28. Electrophysiology
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
K+ K+ K+ K+ K+
Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+
Stimulation of cell opens âfastâ channels in cell membrane. Na+ rapidly
enters cell. Now there are more positive charges inside than outside.
The cell is DEPOLARIZED.
29. Electrophysiology
⢠Depolarization causes Ca2+ to be released
from storage sites in cell.
⢠Ca2+ release causes contraction.
Calcium couples the
electrical event of
depolarization to the
mechanical event of
30. Electrophysiology
Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+
Na+
K+ K+
Na+ Na+
K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+
Cell then REPOLARIZES by pumping out K+ then Na+ to restore
normal charge balance.
31. Electrophysiology
Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+
Na+
K+ K+
Na+ Na+
K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+
Finally, the Na+-K+ pump in the cell membrane restores the proper
balance of sodium and potassiuim.
32. Cardiac Conduction Cycle
Phase 0 = rapid Na influx
Phase 1 = stop Na influx, K efflux, Cl influx
Phase 2 = Ca influx, K influx Sarcomere:
Phase 3 = stop Ca influx, minimal K efflux, Na Fast Sodium
efflux Channels
Phase 4 = resting membrane potential state
34. What is an electrocardiogram?
⢠Picture of the electrical activity of the heart
⢠Used to evaluate/monitor heart rate, effects of
disease, meds, or injury, pacemaker function,
electrolytes, conduction disturbances, mass of
muscle, orientation of heart in chest or presence
of ischemic damage.
35. Leads
⢠Record of electrical activity between two
electrodes.
⢠Averages the current flow at a specific
time in a portion of the heart.
⢠3 types: standard limb leads, augmented
leads and precordial (chest) leads.
⢠Each has positive and negative pole.
⢠The positive electrode is like an âeyeâ.
36. Leads (cont.)
⢠If the impulse is moving toward the
positive electrode the waveform goes up.
⢠If away, the waveform goes down.
⢠If perpendicular, it will either be biphasic or
a straight line.
⢠No electrical activity is called the baseline
or isoelectric line.
37. Standard Limb Leads
⢠Leads I, II, III
⢠Einthovenâs triangle
⢠The voltage of I + III =
II
38. Lead I
⢠Shows lateral surface
of the left ventricle
⢠Normally is upright
because the impulse
is moving toward the
positive electrode.
39. Lead II
⢠Views inferior surface
of the left ventricle
⢠Normally positive
⢠Commonly used for
monitoring
40. Lead III
⢠Views inferior surface
of the left ventricle
⢠Usually the QRS is
positive but the P may
be +, - or biphasic
41. Augmented Limb Leads
⢠Letters stand for
âaugmented voltage
___â
⢠Only consist of one
electrode on the body
surface
⢠Negative point is the
center
42. aVR
⢠Views heart from right
shoulder
⢠Does not view the
walls of the heart,
only the base and
great vessels
⢠Normally negative
43. aVL
⢠Views heart from the
left shoulder
⢠Views high lateral wall
of the left ventricle
⢠Usually biphasic
because
depolarization is
perpendicular to the
electrode
44. aVF
⢠Views the heart from
the left leg
⢠Views the inferior wall
of the left ventricle
⢠Should be positive
55. 12 Lead EKG Technique
⢠Effective contact between electrode and
skin is essential
⢠Try to exclude artifact
â Internal (larger patients)
â External (60hz noise)
⢠Precise placement of precordial
electrodes
⢠Correct patient position
56. Technically Accurate EKG Tracing
⢠Remember Einthovenâs triangle
⢠Lead I + Lead III = Lead II
⢠P waves positive in lead II and negative in aVR
⢠R waves in V1-V6 should gradually progress
from negative to upright
⢠Check standardization box before interpreting
the EKG tracing
57. Interpretation of the 12-Lead ECG
⢠In the limb leads
â P wave is typically upright in leads I, II, aVL
and aVF
â P wave is often biphasic in lead III and is
negatively deflected in lead aVR
⢠In precordial leads
â P wave is typically upright in leads V5 and V6
â Lead V1 is biphasic, and leads V2 and V4 are
variable
58. Interpretation of the 12-Lead ECG
⢠Septal depolarization is not always seen
on the ECG. When it is, there will be a
small Q wave in leads I, aVL, V5, and V6.
⢠The T wave will usually be recorded in a
positive deflection in the same leads that
record a positive deflection in the R wave.
59. Systematic Approaches
⢠Use the same method of analysis each
time to ensure consistent interpretation.
⢠Questions to consider when looking for
arrhythmias
â Is the rhythm fast or slow?
â Is the rhythm regular or irregular?
â Are there any P waves?
â Are all P waves the same?
60. Systematic Approaches
⢠Questions to consider (continued)
â Does each QRS complex have a P wave?
â Is the PR interval constant?
â Are the P waves and QRS complexes
associated with each other?
â Are the QRS complexes narrow or wide?
â Are the QRS complexes grouped or not?
â Are there any dropped beats?
62. Hemiblock
⢠Block of one of
the two fascicles
of the left bundle
branch system
⢠Marked axis
deviation often
indicates
hemiblock
63. Trifascicular System
⢠Part of the electrical conduction system
â Right bundle branch
â Left bundle branch
⢠Branches into two separate fascicles
⢠Left anterior hemifascicle (fascicle)
⢠Left posterior hemifascicle (fascicle)
65. Trifascicular System
⢠Electrical impulse can travel to the
ventricles in three ways:
â Right bundle branch
â Left anterior hemifascicle
⢠Blood supply from LAD
â Left posterior hemifascicle
â Blood supply from RCA and circumflex
66. Left Anterior Hemiblock
⢠Anterior hemifascicle of left bundle branch
blocked
â Ischemia, necrosis
⢠ECG finds:
â Pathological left-axis deviation
â Small Q wave in LI
â Small R wave in LIII
â Narrow QRS possible
68. Left Posterior Hemiblock
⢠Posterior fascicle of left bundle branch
blocked
⢠ECG finds:
â Pathological right-axis deviation
â Small R waves in LI
â Small Q waves in LIII
â Right ventricular hypertrophy
⢠Clinically more significant than left anterior
block
70. Clinical Significance of
Hemiblock
⢠Mortality rate for patients with AMIs with
hemiblocks four times greater than those
without
⢠Risk factor for complete heart block
â Patient considered high risk if AV block
presents with hemiblock
⢠In AMI setting, can indicate proximal artery
occlusion
71. Axis
⢠Definition: axis is the average vector
(direction) of the cardiac electrical impulse
in the vertical plane.
⢠We are concerned with the QRS axis,
which is the direction of the ventricular
depolarization impulse.
72. Axis
⢠What does this mean?
â The electrical impulse that depolarizes the
heart travels a certain route thru the heart
â The vertical plane is the one that runs head to
toe when the patient is facing forward
â The average direction the impulse travels in
this plane is the axis
â Simple, right?!
73. Axis
⢠Measured in degrees
â 0° is at 3 oâclock
â 180° is at 9 oâclock
â Degrees are positive
from 3 oâclock to
9 oâclock in clockwise
direction
â Degrees are negative
from 3 oâclock to
9 oâclock in
counterclockwise
direction
74. Axis Quadrants
⢠The axis circle is divided into four
quadrants
â Normal= 0° to +90°
â RAD= +90° to Âą180°
â LAD= 0° to -90°
â Indeterminate axis= -90° to Âą180°
⢠This makes sense as the normal impulse travels
from SA node to ventricles in a SW direction!
⢠All quadrants besides normal are âdeviatedâ
75. Rapid Axis and
Hemiblock Determination
⢠See âRapid Axis and Hemiblock Chartâ on the
next slide.
â Designed to help clinicians quickly determine
presence of axis deviation and hemiblock
⢠Two ways to use chart
â When cardiac monitor does not provide axis angle:
⢠Assess LI, II, and III on ECG
⢠Determine if QRS complex is deflected more positively or
negatively in each lead
⢠Compare finds to âRapid Axis and Hemiblock Chartâ
â When cardiac monistor provides axis angle:
⢠Compare monitor readout (donât trust machine)
82. Significance of Axis Deviation
⢠Shifts away from infarcted tissue
⢠Left Deviation â Left Hypertrophy, WPW,
Septal defects, Hyperkalemia
⢠Right Deviation â Right Hypertrophy, Left
Posterior Hemiblock, PE, Atrial defects,
Chronic lung disease
⢠Extreme Right â V-Tach, Paced,
Anterolateral Infarct
83. Bundle Branch Blocks
⢠Definition
â Block to the left or right bundle branch system
⢠Left bundle branch block more clinically significant
â Higher mortality
â Results in wide QRS
â >120 ms
⢠Etiology
â Myocardial ischemia, infarction
â Congenital defects
86. Bundle Branch Blocks
âTurn Signal Criteriaâ
⢠MCL-1, any of the precordial leads can be
used
⢠QRS must be >120 ms
87. Bundle Branch Blocks
âTurn Signal Criteriaâ
⢠Technique
⢠View the QRS of V1 (or MCL-1)
⢠Lies immediately over the right ventricle and provides the best
view of the superior aspect of the interventricular septum
⢠Identify the J point of the QRS
⢠Draw a horizontal line from the J point either to an
intersecting line of the QRS or to the beginning of the
QRS
⢠Will produce a triangle pointing upward or downward
⢠When pointing upward, triangle indicates a right bundle branch block
⢠When you push a vehicleâs turn signal upward, the signal lights
indicate a right turn
⢠When pointing downward, triangle indicates left bundle branch block
⢠When you pull a vehicleâs turn signal downward, the signal lights
indicate a left turn
90. Rate-Dependent Bundle
Branch Blocks
⢠Easy to misidentify as VT
â VT therapy could result in rapid hemodynamic
compromise
⢠MCL-1 useful for differentiating
tachycardia with BBB from VT
â RSRâ complex >120 ms = RBBB, not VT
â QRS >120 ms = LBBB, not VT
92. Coronary Plaques
⢠Have the consistency
of toothpaste
⢠Cells within plaque
synthesize and
secrete proteins that
promote clot
formation
⢠Prone to rupture if
they are large and
have a soft lipid core
93. Coronary Artery Obstruction
⢠If the clot partially occludes the artery:
â Acute coronary syndrome or unstable angina
⢠If the clot fully occludes the artery:
â Myocardial infarction
94. Angina
⢠Stable
â Onset with physical exertion or stress. Lasts 1 â 5
minutes and is relieved by stress.
⢠Unstable
â Change in Stable angina frequency, quality, duration, or
intensity. Lasts >10 minutes despite rest and/or NTG.
⢠Variable
â Spontaneous noted at rest (sleeping); relieved by NTG
⢠Silent
â Asymptomatic with evidence of ischemia
⢠Mixed
â Combination of the above
95. Types of Infarctions
⢠Divided into Transmural and non-transmural
MIs.
⢠Transmural: Extends through full thickness of
the myocardium and includes the endocardium
and epicardium.
⢠Subendocardial: Damage is limited to the
subendocardial surface.
96.
97.
98. Ischemia, Injury and Infarction â
12 Leads
⢠Changes usually begin early and progress
⢠May take more than an hour for changes
to show
⢠20-30% of infarcts do not change the
12-lead EKG
-must base diagnosis on labs and
clinical presentation
99. Hyperacute T Waves
⢠The T wave can become tall and narrow
because of ischemia.
⢠The first change that might appear is an
upward slanting of the ST segment and a
subtle enlargement of the T wave.
⢠The hyperacute T waves are localized to
the area of ischemia and infarction.
100. ST-Segment Elevation
⢠Caused by changes that affect ventricular
depolarization and repolarization
⢠Non-MI changes can also cause this
condition
â Left BBB
â Ventricular rhythms
â LVH
â Pericarditis
â Early repolarization
101. ST-Segment Elevation
⢠A persistent ST-segment elevation may
indicate a ventricular aneurysm.
⢠In benign J-point elevation, the T wave is
clearly distinguished as a separate wave.
⢠With myocardial disease, the elevated J
point bows upward and merges with the T
wave.
104. Ischemia
⢠Lack of blood may be due to a decreased
supply or an increased demand
â Causes a delay in repolarization
⢠ST segment is depressed if it is more than
1 mm below the isoelectric line at .04 sec
past the J-point
⢠Inverted T waves are always normal in
aVR and may be normal in III and V1
105. Injury
⢠Injured tissue does not depolarize
completely and remains more positive
than other tissue
⢠ST segment is elevated more than 1mm
above the baseline at 0.04 sec after the
J-point in 2 or more related leads
106. Infarction
⢠Q waves must be wider the 0.04 sec &/or
greater than 25% of the height of the R
wave
⢠Q waves may be normal in III and aVR
⢠Small Q waves in I, aVL, V5 and V6 are not
infarction but are septal depolarization
⢠Q waves in the V leads is also known as
poor R wave progression
107. Reciprocal Changes
⢠Mirror image that occurs when two
electrodes view the AMI from opposite
angles
â Tall, upright T waves
â ST seg depression
â Taller R waves
⢠May or may not be present and may
indicate more severe damage
110. Inferior Wall MI
⢠May involve RV and/or LV
⢠Usually RCA and sometimes LCx
⢠Indicative changes: II, III, aVF
⢠Reciprocal changes: I, aVL
â Sometimes anterior precordial leads
114. Inferior MI
⢠Bradycardia
⢠Atrial fib
⢠AV Blocks:
â 1st degree, 2nd degree type I, 3rd degree with junctional
escape mechanism
⢠Hypotension (treat with fluids)
⢠Possible NTG, Morphine intolerance
⢠Hiccoughs, Vomiting, JVD
⢠Will Have clear lungs
⢠Possible RV failure (RCA involved)
115. Anterior MI
⢠Left ventricle
⢠Involves the LAD
⢠Indicative changes: V1-4
118. Anterior MI
⢠Sinus tachycardia
⢠AV blocks
â 2nd degree II, 3rd degree with ventricular escape
mechanism
⢠Bundle Branch Blocks
â Beware if RBBB b/c septal arteries are high in LAD
and a lot of muscle has probable been damaged
⢠LV failure
⢠Pulmonary edema
⢠Hypotension is bad sign
119. Lateral Wall MI
⢠Left Ventricle
⢠Involves the LCx
⢠Indicative changes: I, aVL, V5-6
⢠Reciprocal changes: II, III, aVF
121. Lateral Wall
⢠Bradycardia
⢠Possible junctional rhythms
⢠Possibly AV Blocks
â 1st degree
â 2nd degree, type I
â 3rd degree, junctional escape mechanism
122. Posterior Wall
⢠Back of LV
⢠Generally involves the
LCx but may be PDA
coming off RCA
⢠Indicative changes: V7-9 (if
you do posterior leads)
⢠Reciprocal changes: (look
for these as your best
clues)
â Tall R waves in V1-2
â ST depression in V1-2
⢠Frequently paired with
inferior MI
124. Non-Q wave MI
⢠Subendocardial MI
⢠30% of all MIâs
⢠Non-specific ST-T wave changes without
Q wave formation
⢠Usually hemodynamically stable
⢠Risk of âextensionâ is significant
125. Serum Cardiac Markers
⢠CK-MB subfomes for Dx within 6 hrs of MI onset
⢠cTnI and cTnT efficient for late Dx of MI
⢠CK-MB subform plus cardiac-specific Troponin
best combination
⢠Do not rely solely on Troponins because they
remain elevated for 7-14 days and compromise
ability to diagnose recurrent infarction
126. MI Management and Treatment
⢠Nitrates to improve coronary blood flow;
venous pooling reduces cardiac output, O2
use, and decreased preload.
⢠Morphine vasodilates and decreases
preload and afterload. Decreases
sympathetic tone causing a decreased HR
and O2 consumption.
⢠Beta-blockers decrease HR and contractility
and increase diastolic filling time.
⢠Calcium Channel Blockers produce dilation
of the coronary arteries and collateral
vessels, decreasing contractility and
conduction.
128. Thrombolytics
⢠Indications
â New onset ST segment elevation MI
⢠Contraindications
â Relative: HTN, recent trauma, pregnancy
â Absolute: Active internal bleeding,
suspected aortic dissection, intracranial
neoplasm, prior hemorrhagic CVA or any
CVA <1 yr old.
129. Angioplasty
⢠Best outcome if <90 minutes from onset
⢠Treat chest pain
⢠Inhibit clotting
⢠Watch for bleeding and reocclusion post
procedure.
â Leg kept straight
â Head of bed < 30 degrees elevation
131. Pericarditis
⢠Inflammation of the pericardium, the
membrane that surrounds the heart
â May cause ST-segment elevation and T-wave
flattening or inversion
â ST-segment and T-wave changes tend to be
throughout all leads of the ECG.
â The T wave usually does not invert until the
ST segment has returned to baseline.
132. Pericarditis
⢠Diagnostics
â Help determine etiology of pericarditis
â White blood cells
⢠Elevated in infection
â ESR
⢠Elevated in infection
â EKG
⢠Diffuse ST segment changes
⢠PR segment depression
⢠Inverted T waves
134. Pericardial Effusion
⢠Pathophysiology
â Abnormal buildup of fluid in the pericardial sac
â Secondary to:
⢠Pericarditis
⢠Trauma
â Places pressure on heart, decreases diastolic
filling pressures
135. Cardiomyopathies
⢠Cardiac disorders whose dominant feature is
pathologic change to the myocardium
⢠Include:
â Primary cardiomyopathies
⢠No underlying cause identified
â Secondary cardiomyopathies
⢠Have demonstrable underlying cause
⢠Three major categories
â Dilated cardiomyopathies
â Hypertrophic cardiomyopathies
â Restrictive cardiomyopathies
136. Dilated Cardiomyopathy
⢠Pathophysiology
â Myocardium enlarged, dilated
â All four chambers can be involved
â Often idiopathic
â Toxic, metabolic, infectious factors may be
involved
â Decreased SV, EF = Increased end systolic
volume
â Increased end systolic volume = Increased end
systolic pressure = Dilated chambers
137. Dilated Cardiomyopathy
⢠Clinical manifestations
â Fatigue, weakness
â Progressive signs and symptoms of CHF
â Right and left side
â S3, S4 summation gallop
â Mitral/tricuspid regurgitation murmurs
148. Aortic Stenosis
⢠Pathophysiology
â Opening of aortic valve is narrowed and obstructs
forward blood flow into aorta
â Left ventricle attempts to increase SV and CO
â Results in left ventricular hypertrophy
⢠Clinical manifestations
â Typically presents with triad of:
⢠Angina, Exertional syncope, Dyspnea on exertion
â Left Axis Deviation, Left Hypertrophy
⢠Treatment includes nitrates, diuretics, digitalis,
IABP as bridge to surgery
149. Aortic Regurgitation /
Insufficiency
⢠Pathophysiology
â Leaking aortic valve
â Rising left ventricular pressures result in:
⢠Left ventricular dilation, Left ventricular
hypertrophy, Left heart failure
⢠Presentation
â CHF, Hypotension, Angina, Wide Pulse
Pressure, Corriganâs Pulse
⢠Treatment â surgical repair
150. Mitral Stenosis
⢠Stenotic valve obstructs forward blood
flow from the left atrium into the left
ventricle
⢠Results in elevated left atrial pressure
⢠Pulmonary hypertension
â Right ventricle can fail
⢠Rheumatic fever most common cause
⢠Clinical presentation
â Exertional dyspnea, orthopnea, fatigue,
malaise, palpable diastolic thrill
151. Mitral Stenosis
⢠Management
â Treat symptoms of congestive heart failure
â Use diuretics
â Give nitrates
â Treat atrial fibrillation
â Conduct digitalis
â Complete anticoagulation for new-onset atrial
fibrillation
â Intervene surgically
153. Hypokalemia
⢠Decreased level of potassium
⢠Diagnostic criteria
â ST-segment depression
â Slightly decreased amplitude of the T waves
â Minimal prolongation of the QRS interval
â U wave is usually small and follows the T
wave.
154. Hypercalcemia
⢠Elevated levels of calcium
(normal 8.5 â 10.5 mg/dl)
⢠Diagnostic criteria
â Shortening of the ST-segment,
which, in turn, shortens the QT
interval
â PR interval may be prolonged
â QRS may lengthen
â T waves may become flat or invert
155. Hypocalcemia
⢠Reduced levels of calcium
⢠Diagnostic criteria
â A prolongation of the ST segment that
produces a lengthening of the QT interval
156. Coronary Artery Spasm
⢠Variant or Prinzmetalâs
angina
⢠May occur spontaneously
or:
â Exposure to cold
â Emotional stress
â Vasoconstricting meds
â Cocaine
â Smoking
⢠Mimics MI
Think of the EKG tracings for Lead I and III as someone looking at you, holding out their thumbs with their right thumb as Lead I and their left thumb as Lead III.
Lead I (Right) is upright. Lead III (left) is upright.
Lead I (Right) is upright. Lead III (left) is down. Consult Lead II, if it is also down, then it is an anterior hemiblock.
Lead I (Right) is down. Lead III (left) is up. Most likely a posterior hemiblock.
Lead I (Right) is down. Lead III (left) is down. This indicates a possible bifasicular block.