BASIC ECG, CARDIAC ARRYTHMIAS
Ranulfo Javelosa, Jr., M.D.
November 09, 2010
LEGEND
Normal text : lecture ppt, 2011B trans, Guyton and ECG Made Easy
Italicized: AUDIO
INTRODUCTION
Augustus Waller – introduced the concept that the heart has
electrical potential
The ECG provides information for:

Rhythm

Rate

Enlargement

Injury/infarction
REVIEW
Phase 0
is the upstroke of the action potential (depolarization)
If upstroke is due only to ICa, it will be slow
If the upstroke is due to both ICa and INa, it will be fast.
Corresponds to the onset of QRS
Factors that decrease the slope of phase 0 by impairing the
influx of Na+ (e.g., hyperkalemia, or drugs such as flecainide)
tend to increase QRS duration
Phase 1
The rapid repolarization component of the action potential
(when it exists)
due to almost total inactivation of INa or ICa, and may also
+
depend on the activation of a minor K current not listed
previously, called Ito (for transient outward current).
Phase 2
plateau phase of the action potential, which is prominent in
ventricular muscle
2+
+
depends on the continued entry of Ca or Na ions through
their major channels, and on a minor membrane current due to
the Na-Ca exchanger
corresponds to the isoelectric ST segment
conditions that prolong phase 2 (use of amiodarone,
hypocalcemia) increase the QT interval
shortening of this phase, as by digitalis administration or
hypercalcemia, abbreviates the ST segment
Phase 3
repolarization component of the action potential
It depends on IK
Corresponds to the inscription of the T wave
Phase 4
constitutes the electrical diastolic phase of the action potential
In SA and AV nodal cells, changes in IK, ICa, and If produce
pacemaker activity during phase 4
Purkinje fibers also exhibit pacemaker activity, but use only I f
Atrial and ventricular muscle have no time-dependent currents
during phase 4
Transmembrane potential (Ventricular Muscle). (What goes in, what
goes out of membrane potential)
Underlying cardiac potentials are 4 major time-dependent and
voltage-gated membrane currents:
+
1. The Na current (INa) is responsible for the rapid depolarizing
phase of the action potential in atrial and ventricular muscle and
in Purkinje fibers. It is also the largest current in the heart.
2. The Ca2+ current (ICa) is responsible for the rapid depolarizing
phase of the action potential in the SA node and AV node; it also
triggers contraction in all cardiomyocytes. It passes primarily
through L-type Ca2+ channels.
+
3. The K current (IK) is responsible for the repolarizing phase of
the action potential in all cardiomyocytes.
4. The "pacemaker current" (If) is responsible, in part, for
pacemaker activity in SA nodal cells, AV nodal cells, and Purkinje
fibers. It is mediated by a nonselective cation channel.
Sinoatrial (SA) node / Sinus node
Located in the R atrium
Primary pacemaker
Cells fire spontaneously; i.e., they exhibit automaticity
Atrioventricular (AV) node
Located near the atrioventricular groove and the tricuspid valve
Secondary pacemaker
Purkinje fibers
For rapid conduction of action potentials
Tertiary pacemaker
Any pathologies in the tricuspid, R atrium, septum, would
affect this part of the conducting system
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Page 1 of 16
The bundle branches would be running along the surface
of the interventricular septum. Therefore, congenital heart
diseases like VSD, ASD, could affect this flow of electricity.
When AV valves (tricuspid and mitral) close, you have the S1, and
this is at the same time as QRS also. Rapid ejection phase and then
the depolarization. The T wave, you have the repeat of the cycle
during diastole.
Atrial excitation – p-wave
Atrial systole at the beginning of the Q
Ventricular excitation – QRS
Ventricular systole after T wave
Ventricular diastole – U wave
Step I. Rapid filling of ventricles
Ventricular pressure drops below atrial pressure
AV valves are open, semilunar valves are closed
Rapid ventricular filling occurs
70-90% of the ventricles fill with blood
CARDIAC CYCLE
Aortic valve closure
Aortic valve opening
↑ in ventricular pressure
Step II. Atrial systole
P wave occurs
Atrial contraction – lateral 1/3 of diastole
Pushed 10-30% more blood into ventricle
*timing of complexes to the clinical events (heart sounds)
S4 – atrial contraction  after p-wave
P-wave – atrial depolarization
After atrial excitation, atrial contraction follows
After ventricular excitation ventricular contraction 
tricuspid and mitral valve closure  S1
S2 and S3 comes after the p-wave
P to beginning of R-wave – diastole
QRST – systole
Step III. Isovolumetric contraction
QRS just occurred
Contraction of the ventricles causes ventricular pressure to rise
above atrial pressure
AV valves close
Ventricular pressure is still less than aortic pressure
Semilunar valves are closed
Volume of blood in the ventricle is EDV
Step IV. Ejection
Contraction of the ventricles causes ventricular pressure to rise
above aortic pressure,
Semilunar valves open
Ventricular pressure is greater than atrial pressure
AV valves are still closed
Volume of blood ejected by the ventricles: stroke volume (SV)
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of that lead, and a negative deflection if the wave spreads toward
the negative pole.
If the mean orientation of the depolarization vector is at right
angels to a given lead axis, a biphasic (equally positive & negative)
deflection will be recorded
Step V.
T-wave occurs
Ventricular pressure drops below aortic pressure
Back pressure causes semilunar valves to close
Step VI. Isovolumetric relaxation
AV valves are still closed
Semilunar valves are still closed
Volume of blood in ventricles: ESV
Ventricular pressure drops
P
Q
R
Limb Leads
Record potentials transmitted onto the frontal plane
3 standard “bipolar” leads (I, II, III) and 3 augmented “unipolar”
leads (aVR, aVL, aVF)
S
T
U
ECG
ECG Leads
Configured so that a positive (upright) deflection is recorded in a
lead if a wave of depolarization spreads toward the positive pole
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Atrial repolarization is usually too low in amplitude to be
detected, but it may become apparent in such conditions as
acute pericarditis or atrial infarction
PR interval – should not be >1 big square
From the start of the P to the start of the Q or R wave
Prolongation is used in assessing AV blocks or conduction
defects
Normally 120-200msec
Measures the time bet. atrial and ventricular depolarization,
w/c includes the physiologic delay imposed by stimulation of
cells in the AV junction area.
Chest / Precordial Leads (6)
Surround the heart to pick up activity of different chambers
Record potentials transmitted onto the horizontal plane
V1 – 4th ICS, R parasternal border
Near to R ventricle
th
V2 – 4 ICS, L parasternal border
V3 – b/w V2 & V4
Closest to L ventricle
th
V4 – 5 ICS, LMCL
th
V5 – 5 ICS, LAAL
Nearest the septum
V6 – 5th ICS, LMAL
 Inferior leads (for inferior wall infarction): II, III, aVF
 Lateral leads (lateral wall problems): I, aVL, V5, V6
 Anterior leads (ant. wall infarction): V1 to V4
V1 and V2 – for RV hypertrophy, infarction
V5 and V6 – for LV infarction, enlargement, hypertrophy
QRS interval – should not be >3 small squares (~2.5small squares)
Normally 100-110 ms or less
Prolongation could mean a delay of propagation of impulse in
the ventricles
Reflects the duration of ventricular depolarization
QT interval
Includes both ventricular depolarization & repolarization times
and varies inversely with the heart rate
R-R interval – interbeat interval
SEQUENCE OF ECG INTERPRETATION
THE NORMAL ECG
Paper speed: 25mm/sec
Vertical Axis
1 small square = 1mm (0.1mV)
1 large square = 5mm (0.5mV)
2 large squares = 1mV
Horizontal Axis
1 small square = 0.04sec
1 large square = 0.2sec
2 large squares = 1sec
ECG Waveforms & Intervals
P wave = atrial depolarization
Normal atrial depolarization vector is oriented downward &
toward the subject’s left, reflecting the spread of depolarization
from the sinus node
Since this vector points toward the positive pole of lead II &
toward the negative pole of lead aVR, the normal P wave will
be positive in lead II & negative in lead aVR.
QRS complex = ventricular depolarization
Normal ventricular depolarization proceeds as a rapid,
continuous spread of activation wavefronts
ST-T-U complex (ST segment, T wave, and U wave) = ventricular
repolarization
1.
2.
3.
4.
5.
6.
7.
Rate
Rhythm
Axis
Hypertrophy
Infarction
Injury
Ischemia
Interpretation Sequence
 Check the patient details—is the ECG correctly labelled?
o Are the electrodes correctly placed?
o Interchanged electrodes  reversed polarity
 What is the rate?
 Is this sinus rhythm? If not, what is going on?
 What is the mean frontal plane QRS axis? (You may wish at this
stage to glance at the P and T wave axes, too.)
 Are the P waves normal (Good places to look at are II and V1)
 What is the PR interval?
 Are the QRS complexes normal? Specifically, are there:
o Significant Q waves
o Voltage criteria for LV hypertrophy
o Predominant R waves in V1
o Widened QRS complexes
 Are the ST segments normal, depressed, or elevated? Quantify
the abnormalities.
 Are the T waves normal? What is the QT interval?
 Are there abnormal U waves?
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Step 1: RATE
Identify an R wave that falls on the marker of a ‘big block’
Each large square (5mm) represents 0.2 seconds, so there are
five large squares per second, and 300 per minute.
Count the number of the big blocks to the next R wave
300 ÷ # of big squares
1500 ÷ # of small squares
Relationship Between the Number of Large Squares Covered by the
R-R Interval and the Heart Rate
R-R Interval (Large Squares)
Heart Rate (beats/minute)
1
300
2
150
3
100
4
75
5
60
6
50
What is the Rate?
18 small squares: 1500/18 = 83bpm
The normal pacemaker is the SA node; the signal then
propagates through the AV node, and activates the ventricles.
When the heart follows this pathway at a normal rate and in
this sequence, the rhythm is called a "normal sinus rhythm."
SA Node: 60-100bpm
AV Node: 40-60bpm
Ventricular: no p-wave, <40bpm
Normal Sinus Rhythm
Sinus rhythm: when depolarization begins in the sinoatrial (SA) node
Normal Sinus Rhythm elements:
R-R measurement
Should be the same
P-P measurement
P-P to R-R measurement
Should have a constant PR interval
QRS interval should be <0.12s
P should always be followed by QRS
P wave should be identical, upright, uniform and
occurring regularly
P always followed by a QRS
3 big squares: 300/3 = ~100bpm
4 big squares: 300/4 = ~75bpm
19 small squares: 1500/19 = 79bpm
Junctional Rhythm
originate at AV node with retrograde and anterograde direction
Normal/narrow QRS
P-wave may be absent or may show after QRS
HR is slow (40-60bpm)
can be due to β-blocker, digitalis toxicity, myocarditis, dengue
fever, R Coronary branch occlusion
Step 2: RHYTHM
Sinus?
Junctional (AV node)?
Ventricular?
Pacemaker?
Atrial fibrillation?
Ventricular Fibrillation?
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7 big squares: 300/7 = 42bpm
Nodal Escape: if region around the AV node takes over as the focus
of depolarization
Rate is 100/minute
No P waves in junctional beats (indicates either no atrial
contraction or P wave lost in QRS complex)
Normal QRS complexes
Ventricular Rhythm
originate from purkinje fibers
Wide QRS
Impulse originates from one side of the ventricle
causing prolonged/delayed activation of the ventricles
No P-wave
HR is slower (40-60bpm)
Ventricular Escape
most commonly seen when conduction between the atria and
ventricles is interrupted by a complete heart block
After three sinus beats, the SA node fails to discharge. No atrial
or nodal escape occurs. After a pause, there is a single wide and
abnormal QRS complex with an abnormal T wave
8 small squares: 1500/8= 188bpm
Pacemaker Rhythm
Impulses originate at transvenous pacemaker
Wide QRS
Pacemaker spikes
Ventricular rhythm with faster HR
No p-wave
8.5 big squares: 300/8.5 = 35bpm
8.5 big
squares
HR: 150bpm (for figure below)
MI, metamphetamine, drugs
Patient can collapse
Can be tolerated in younger individuals
If with pulse and normal BP, give anti-arrhytmics
If no pulse is detected, start CPR and defibrillate
Spike
R
S
T
Ventricular Tachycardia
No P waves
Regular QRS complexes, rate 200/minute
Broad QRS complexes, duration 240 milliseconds with a very
abnormal shape
No identifiable T waves
Atrial Fibrillation (AF)
ECG has many but not identical P waves
RR interval is not constant
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Usually 5-10 P: 1 QRS
Irregularly irregular rhythm
HR variable
Causes: drugs, alcohol, ischemia, metabolic disturbances, heart
failure, dilatation, HTN
Aka “Holiday Heart Syndrome”
Step 3: QRS AXIS
The subtotal of the direction of the electrical activity of the
heart; normally, downward and to the left
Frontal QRS Axis
Course vs. Fine Fibrillation
Baseline coarsely or finely irregular; P waves are absent. Ventricular
(QRS) irregular, slow or rapid
Atrial Flutter
4P : 1 QRS
Saw-toothed configuration of the p-waves
Regular RR intervals
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Wolff-Parkinson-White syndrome – right-sided accessory
pathway
Tricuspid atresia
Ostium primum - OSD
Northwest territory – both lead I and aVF (-)
Causes:
Emphysema
Hyperkalemia
Lead transposition
Artificial cardiac pacing
Ventricular tacchycardia
Normal
Using leads I and aVF, the axis can be calculated to within one of the
four quadrants at a glance.
Shortcut:
1. You normally look at leads I and aVF.
2. Hold the results of lead I of the ECG with your left hand and
that of the aVF with your right.
3. With the index finger and middle finger of each hand, follow
the deflection of the waves (upward = +, downward = -) found
in the corresponding leads.
4. If both point upward, then it is normal. If both point downward,
then it is NW axis deviated.
5. If one is positive and the other is negative, then the opposite of
the hand holding the negative is the side where the deviation is
(in short, the one holding the upward deflection is the side of
the deviation)
Right Axis Deviation
Another way (for the mathematically gifted):
1. Plot the heights of the deflection of waves
-
+
+
2.
Get the vector
-
+
+
3.
Report in degrees of deviation
Left Axis Deviation
The QRS Axis
Normal Axis – both I and aVF (+)
Right axis deviation – lead I (-) and aVF (+)
Causes:
Normal finding in children and tall thin adults
Right ventricular hypertrophy
Chronic lung disease even without pulmonary HTN
Anterolateral myocardial infarction
Left posterior hemiblock
Pulmonary embolism
Wolff-Parkinson-White syndrome – left-sided accessory
pathway
Atrial septal defect
Ventricular septal defect
Left axis deviation – lead I (+) and aVF (-)
Causes:
Left ventricular hypertrophy
Inferior myocardial infarction
Artificial cardiac pacing
Emphysema
Hyperkalemia
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Step 4: P-R INTERVALS FOR AV BLOCK
A-V Block First-Degree
AV conduction lengthened
May be seen in normal individuals
Usually caused by drugs such as -blockers (metoprolol,
atenolol, propanolol), Ca2+ channel blockers (verapamil,
diltiazem) that can prolong the AV conduction
Associated with the ff:

coronary artery disease

acute rheumatic carditis

Beta blockers

digitalis

cardiomyopathy

normal sinus rhythm

prolonged PR interval (>1 big square or 0.2s)
o delay from SA node firing and spread of impulses
to AV node
Mobitz type I (Wenckebach)
P-R intervals become progressively longer until one P wave is
totally blocked and produces no QRS. After a pause, during
which the AV node recovers, this cycle is repeated.
Rate: depends on rate of underlying rhythm
Rhythm: irregular
P waves: normal (upright and uniform)
PR interval: progressively longer until one P wave is blocked
and a QRS is dropped
QRS: normal (0.06-0.10 sec)
A-V Block Second Degree
sudden dropped QRS
absence of QRS after 1 P-wave
Mobitz type II
no gradual prolongation (PR-PR-PR-dropped QRS)
more dangerous and indicates excessive damage to AV node
AV Block Third Degree
When there is complete dissociation between P wave and QRS
(Atrioventricular dissociation)
QRS occurs independently whenever it wants to
Atrial rate and ventricular rate are not the same
Indication for pacemaker
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Hyperkalemia
Hypothyroidism
Hypermagnesemia
Adrenal insufficiency
Drug-related
Beta blockers
Adenosine
Ca channel blockers
Anti-arrythmics (class I & III)
Digitalis
Lithium
Infectious
Endocarditis
Tuberculosis
Lyme disease
Diphtheria
Chagas disease
Toxoplasmosis
Syphilis
Dengue fever
Heritable/congenital
Congenital heart disease
Maternal SLE
Kearns-Sayre syndrome
Emery-Dreiffus MD
Myotonic dystrophy
Progressive familial heart block
Inflammatory
SLE
MCTD
Rheumatoid arthritis
Scleroderma
Infiltrative
Amyloidosis
Hemochromatosis
Sarcoidosis
Coronary artery disease
Acute MI (esp. inferior wall MI or R Coronary a.
involvement)
Neoplastic/traumatic
Lymphoma
Radiation
Mesothelioma
Catheter ablation
Melanoma
Degenerative
Lev disease
Lenegre disease
Step 5: ECTOPIC BEATS
Atrial vs. Ventricular Ectopy
Causes of AV blocks
Autonomic
Carotid sinus hypersensitivity
Metabolic/endocrine
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Step 6: CHAMBER ENLARGEMENT
Premature Atrial Contraction (PAC)
Originates from the atria; an independent focus decided to fire
a few msec ahead of the expected beat and override or insert
into the sequence of the P-wave firing
Not coming from the SA node
The following QRS is narrow
With P-wave
Left Atrial Enlargement
P wave duration equal or more than 0.12 sec.
Notched, slurred P wave in lead I and II (P mitrale).
Biphasic P wave in lead V1 with a wide, deep and negative
terminal component.
Premature Ventricular Contraction (PVC)
No P wave
Wide QRS
With gap
Right Atrial Enlargement
P wave duration equal or less than 0.11 sec.
Tall, peaked, narrow T wave equal or more than 2.5 mm in
amplitude in lead II,III or aVF (P pulmonale).
Mean P wave axis shifted to the right (more than +70 degrees).
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Ventricular Hypertrophy
Sinus tachycardia, Left Axis deviation, LVH, No PR prolongation, No
AV blocks (pic below)
Left Ventricular Hypertrophy
"Voltage criteria":
R or S wave in limb lead equal or more than 20mm
S wave in V1, V2 or V3 equal or more than 30mm
R wave in V4, V5 or V6 equal or more than 30mm.
Depressed ST segment with inverted T waves in lateral leads
(strain pattern; more reliable in the absence of digitalis therapy.
Left axis of -30 degree or more.
QRS duration equal or more than 0.09 sec.
Time of onset of the intrinsicoid deflection (time from the
beginning of the QRS to the peak of the R wave) equal or more
than 0.05 sec in lead V5 or V6.
Tall Rs in V5 and V6
Deep S in V1 and V2
Right Ventricular Hypertrophy
Tall R waves over the right precordium and deep S waves over
the left precordium ( R:S ratio in lead V1 > 1.0)
Normal QRS duration (if no bundle branch block)
Right axis deviation.
ST-T "strain" pattern over the right precordium.
Late intrinsicoid deflection in lead V1 or V2.
Tall Rs in V1 and V2
Deep S in V5 and V6
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Below: normal sinus rhythm (NSR), HR = 88, RA deviation (RAD), R
atrial enlargement (RAE), RVH
Step 7: QRS DURATION
NSR, 80bpm, RAD, PR interval normal, RAE, RVH
Sinus tachycardia, RAD, LAE, RVH
Left Bundle Branch Block
QRS duration equal or more than 0.12 sec.
Broad , notched or slurred R wave in lateral leads(I, aVL , V5,V6)
QS or rS pattern in the anterior precordium.
Secondary ST-T wave changes (ST and T wave vectors are
opposite to the terminal QRS vectors).
Late intrinsicoid deflection in lead V5 and V6.
Wide QRS due to prolonged ventricular depolarization (>0.12;
N: 0.08-0.1)
V5 and V6 – wide, notched R wave
V1 and V2 – deep S wave
With P-wave
o If w/o P-wave – sinus tachycardia
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Right Bundle Branch Block
QRS duration equal or more than 0.12 sec.
Large R' wave in lead V1 (rsR').
Deep terminal S wave in lead V6.
Normal septal Q wave.
Inverted T wave in lead V1 (secondary T wave changes).
Late intinsicoid deflection in lead V1 and V2.
Step 8: ST SEGMENT ABNORMALITIES
ECG Changes in Acute Ischemia, Injury and Infarction.
Typically, three phenomena may occur on the ECG that are
characteristic of the evolution of a myocardial infarction (MI):
T wave inversion, indicating ischemia.
S-T segment elevation, indicating injury and the acuteness of
myocardial infarction (MI).
The presence of an abnormal Q wave, indicating tissue death
(necrosis).
The above abnormalities are usually seen in the ECG leads
representing the area of damage.
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Leads I, V5, V6 and AVL
ST elevation in I, V5-V6, AVL: acute lateral wall infarction
Localization of Infarction
Rare
V1: tall R
Localization of MI through ECG
Anterior wall
Anteroseptal
Inferior
Right ventricular
Posterior Wall
Leads I, V2, V3, V4
V1-V4: Q-wave and ST elevation (Anterior Wall infarction); T
inversion (Anterior wall ischemia)
V1-V6 involement: extensive anterior extending to the lateral
wall
V1 through V6
V1 through V3
II, III, aVF
V4R, V3R
V7 through V9
V1 through V3 ( ST depression)
Anterior wall
Anteroseptal
Inferior
Right ventricular
Posterior wall
Anterior wall infarct (V1-V4)
Leads V2, V3 and AVF
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Inferior Wall infarct (V2, V3, AVF)
Questions
The ECG rhythm is called:
a. Sinus bradycardia changing to ventricular tachycardia
b. Junctional rhythm with a run of ventricular tachycardia
c. Sinus rhythm terminating in ventricular fibrillation
d. Sinus bradycardia changing to junctional tachycardia
This ECG rhythm is called:
a. Sinus arrhythmias
b. Atrial fibrillation with ectopic atrial beats
c. Sinus tachycardia with ventricular couplets
d. Sinus rhythm, with ectopic atrial beats
***
Hello 2012! Hello 2nd sem!
As usual, hi sa mga Alphan brods and sisses ko—Taktak, Kenji, Tel,
Rors, Charm, Tristan and especially sa mga batchmates ko na sina
Faith, Jes, Vin, and Mel. Also, sa mga brods and sisses ko from 2013
and 2014, who’ll read this soon.
Hi rin sa PPG...so dilemma parin naten kung saan tayo kakain. Lapit
na Christmas!
Hi sa mga Med, Pedia, Surge, Psych (and ComMed?) groupmates
ko—tsismisan ulet lalo na si ‘Dencyo’ hahaha!
Happy aral! I hope this helps (though this looks like a photo album.
Sorry!) –hayzle
GRABE! Good luck sa topic na ito!
Isapuso natin ang pag-aaral nito. Magagamit natin ito next year.
Goodluck 2012! 
There are only two questions that human beings have ever fought
over, all through history: “How much do you love me?” and “Who’s
in charge?”
~Liz Gilbert in E.P.L.
Abby 
*hello to all the hardworking members of 2012 trans4med!!
especially to those i worked with in this trans: hayz, abby, and to our
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tweetmate charmy, melissa marie, sexy jessa, tellyteltel, faith,
POLARIS...and a special greeting to my mommy cyll who will be
This ECG rhythm is called:
a. Sinus rhythm with multifocal premature ventricular
complexes (PVCs)
b. Sinus bradycardia with ventricular paced beats
c. Sinus rhythm with paced ventricular beats
d. Junctional rhythm with unifocal PVCs
This ECG rhythm is called:
a. Junctional rhythm with a premature atrial complex (PAC)
b. Sinus bradycardia with a premature atrial complex (PAC)
c. Sinus arrhythmia
d. Sinus arrhythmia with a PVC
getting married next month
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*2012B, please support the vote for your Lantern Queen and escort
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* Regina Iustitiae Sorority, Ateneo Law, in cooperation with Phi
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--ANAtomy amphitheater (inspired by daisy duck
)
OMARISM (because you know this was coming...)
Alomar: “nung narinig ko na ang lec ay EKG for dummies, i almost left!"
This ECG rhythm is called:
a. Sinus tachycardia with a PVC
b. Atrial fibrillation with rapid ventricular response
c. Sinus tachycardia with a PAC
d. Sinus arryhtmia with a PVC
OMAR: I’m no escort. I’m either the host or the star. Armand has been
bugging me about wanting to be an escort again, he claims he is the key to
another victory.
DELOICIOUS: Ngeeeee... Can you believe this guy? Hahaha! wala na Omar.
You have escaped you're rightful throne as the escort of the lantern queen
for 2 years! pinoproject mo lang sa ibang lalake kaya kmi nlang ni Glen last 2
years. Pero ngayon, there is no escape my friend
CARLOTACIOUS: Sabi ni Omar he is either the host or the star. Pero diba it's
not a star. IT'S OMAR! :) kaya yun na ang theme the Lantern natin. Hahaha
DELOICIOUS: Tama carlo. At ung mas ok pa. Dba c lanter queen
magddescribe ng lantern? eh, what's more, C escort is the lantern!!!
wahahahahaha! It's not a star, it's freakin OMAR!!!
TRANSCRIBED BY: Hayzle Mallari, Abby Maralit, Ana Aurelia Santos, Carlo Benjamin Tañada
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