PHYSIOLOGY
ELECTROCARDIOGRAPHY
PAMANTASAN NG LUNGSOD NG MAYNILA2.02
COLLEGE OF MEDICINE 2020
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
JEREMIAS T. BALGUA JR., MD | SEPTEMBER 20, 2016
OUTLINE
I. Electrocardiogram
a. Clinical Utility of ECG
II. Anatomy/physiology of the conducting system a. ECG and membrane potential of ventricular cell
b. Mechanism of sinus nodal rhythmicity c. Normal cardiac depolarization and repolarization
d. Normal cardiac conduction steps III. The normal ECG
a. Components of an ECG tracing b. Segments and Intervals IV. ECG leads
a. Limb leads
i. Standard bipolar limb leads ii. Einthoven’s triangle/ law iii. Augmented unipolar limb leads b. Precordial/chest leads
c. Additional types of ECG leads
V. Flow of current around the heart during the cardiac cycle
VI. Currents of Injury
VII. ECG interpretation and associated abnormalities a. Rhythm
b. Rate c. Axis
i. Axis Deviations
d. P wave morphology and duration e. P-R interval
i. AV blocks (1st, 2nd, 3rd degree) f. QRS morphology and duration
i. Bundle Blocks (Left and right) ii. Abnormal Voltages of the QRS
Complex
iii. Prolonged and Bizarre Patterns of the QRS Complex
g. ST segment (depression and elevation) h. T wave, U wave and QT interval
i. Premature contractions i. Premature atrial contractions ii. Premature ventricular contractions j. Paroxysmal tachycardia
i. Atrial paroxysmal tachycardia / A-V Nodal Paroxysmal Tachycardia / supraventricular tachycardia iii. AV nodal re-entrant tachycardia
(AVNRT)/ atrioventricular nodal re-entrant tachycardia
iv. Ventricular Paroxysmal Tachycardia
k. Atrial fibrillation l. Atrial flutter
m. Ventricular Tachycardia n. Ventricular fibrillation
o. Agonal rhythm to asystole/Cardiac arrest VIII. Anti-arrhythmic drugs
I. ELECTROCARDIOGRAM (ECG/EKG)
Is a test that records the electrical activity of the heart as detected by electrodes attached to the outer
surface of the skin and recorded by a device external to the body.
Info about: pattern of depolarization, mass of
electrically active cardiac muscles, rate and rhythm.
The waves produced by myocardial depolarization and repolarization have three chief characteristics: o Duration- measured in fractions of a second
o Amplitude- measured in millivolts (mV)
o Configuration- referring to the shape and
appearance of the wave
CLINICAL UTILITY OF ECG
Baseline or initial evaluation of all patients especially 40 years old and above
Patients on drug therapy (anti-arrhythmic drugs)
Patients on pacemaker, with heart failure, and with myocardial ischemia (and other coronary artery disease)
Patients who will undergo surgery
o Most of the time, any major or minor surgery is accompanied by arrhythmia
II. ANATOMY / PHYSIOLOGY OF THE CONDUCTING SYSTEM
Figure 1. Anatomy of the heart showing the pacemakers.F
Lifted from 2019 1D trans:
SA node AV node AV bundle AV bundle branches Purkinje fibers
Pacemakers of the heart: 1. Sinoatrial Node (SA node)
located lateral to the sulcus terminalis of the right atrium
composed of specialized spindle shaped cells with almost no contractile muscle filaments
has an intrinsic automaticity (fires inherently: self-excitation)
o faster discharge rate o diastolic depolarization
RMP nearer to threshold
Leakiness to Na and Ca
the only one with IF channel (funny current)
Discharges at a rate of 60-100 beats per minute
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
*Why is the SA node the dominant pacemaker?
Because of its action potential
o Has the fastest rhythmical discharge rate among the AV node and Purkinje Fibers
Has less negative RMP than ventricular muscle fibers (faster to reach threshold)
o SA node RMP: -55 to -60 mV o AV node RMP: -60 to -70 mV
2. Atrioventricular Node (A-V node)
receives impulse from SA node from intermodal pathways (found in the atrium)
Discharges at a rate of 40-60 bpm
Also exhibits rhythmical excitation
3. Purkinje Fibers
Discharges at a rate of 30-40 bpm
Also exhibits rhythmical excitation
A. ECG AND MEMBRANE POTENTIAL OF A VENTRICULAR CELL
Figure 2. Recordings of ECG with intracellular membrane potential (red curve) and contraction (blue curve) of one heart cycle in a ventricular fibre.
Across the ventricular cell membrane there is a steady potential difference of almost the same size as the equilibrium potential for K+ (-94 mV), that is -90 mV. This negative potential is referred to as the resting membrane potential (RMP), because it represents the potential difference across the cell membrane (inside negative) at rest between successive action potentials.
Any process that reduce the absolute size of the RMP (ie, depolarize the membrane) tends to activate (open) fast Na+-channels. These channels contain fast opening and fast closing gates (inactivation gates). Electrochemical forces favor the abrupt influx of Na+ from neighboring regions. Hereby, the potential is further diminished and more and more Na+-channels are activated or opened. The threshold potential for release of an action potential is a rise of 25 mV from -90 mV. The cardiac action potential is an all-or-none response, which can be divided into five phases:
Phase 0
o Fast depolarization o Abrupt upstroke
o Rapid entry of Na+ into the cell through the fast Na+-channels.
o The fast Na+-influx causes phase 0 of atrial, ventricular and Purkinje action potentials
o The fast Na+-channels are both voltage- and time-dependent.
o Stops at about +30 mV, because the fast Na+-channels become voltage-inactivated by closure of inactivation gates. The potential difference approaches the equilibrium potential for Na+ (+ 60 mV), but only reaches +30 mV. The conduction velocity along the fast response fiber increases with the AP-amplitude and especially with the slope of phase 0.
Phase 1
o Early repolarization from the upstroke. o K+-efflux.
Phase 2
o Plateau of the action potential
o Slow Ca2+-Na+-channels remain open for a long period - up to 300 ms.
o The net influx of Ca2+ and Na+ is almost balanced by a net efflux of K+, so the balance is forming the plateau. Ca2+ activates the muscle contractile process. When the slow Ca2+-Na+-channels close at the end of the plateau, the voltage-gated K+-channels are activated, and the permeability for K+ increases rapidly.
Phase 3
o Terminal repolarization. With all the K+-channels open, large amounts of K+ diffuse out of the ventricular fiber. The equilibrium potential for K+ (-94 mV) and the RMP is rapidly approached.
Phase 4
o The RMP of - 90 mV
o The Na+-K+ pump restores ionic concentrations by exchanging Na+ for K+ in a ratio of 3:2.
Phase 5
o Relative refractory period (RR), and the T-wave in the ECG. The long absolute refractory period (AR) of the ventricular cells covers the whole shortening phase of the contraction (blue curve). In the absolute refractory period all fast Na+-channels are voltage-inactivated and closed, which prevents sustained tetanus. As a consequence, no stimulus is sufficient to trigger contraction regardless of size.
o In the relative refractory period, enough of the fast Na+-channels are recovered, so that a sufficiently large stimulus can break through and produce an action potential although smaller than normal. o The long absolute refractory period protects the
cardiac pump, as it is not possible to bring ventricles into smooth tetanus.
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
As described above, the cardiac muscle fiber has a horizontal plateau because of the slow Ca2+-Na+-channels (phase 2). Skeletal muscle fibers have no plateau, because they do not open slow Ca2+-Na+-channels for a long time.
B. MECHANISM OF SINUS NODAL RHYTHMICITY
Types of Membrane Ion Channels in the Cardiac Muscles
1. Fast Na channels 2. Slow Na-Ca channels 3. K channels
Figure 3. Membrane action potential.
Opening of fast channels influx of positive Na+ ions rapid upstroke spike AP in ventricular muscle fiber
Plateau in ventricular muscle fiber is due to the slower sodium calcium channels.
Opening of the K+ channels diffusion of many positive K+ ions in the outward direction membrane returns to the RMP.
In Sinus Nodal Fibers
Sinus node RMP is less negative than ventricular muscle fibercell membranes of sinus fibers are naturally leaky to Na+ and Ca++, and positive charges of the entering Na+ and Ca++ ions neutralize some of the intracellular activity.
At sinus fibers’ RMP, fast Na+ channels have already been inactivated (blocked). Only the slow Na+-Ca++ channels can open and cause action potential.
S-A node AP is slower to develop that in ventricular muscle.
After AP, the return of the potential to its negative state occurs slow compared to the abrupt return in the ventricular fibers.
Phase 4 –spontaneous depolarization (pacemaker
potential) triggers AP
Phase 0 – depolarization phase at AP Phase 3 – repolarization
End of repolarization, ion channels ["funny" currents ("If")] open that conduct slow, inward (depolarizing)
Na+ currents Membrane potential (MP) begins to spontaneously depolarize initiating Phase 4.
As the MP reaches about -50 mV, transient or T-type
Ca++ channel opens inward directed Ca++ currents
further depolarize the cellmembrane continues to depolarizeL-type Ca++ channels opensmore Ca++ to enter the cellfurther depolarize cell until AP threshold is reached.
Figure 4. Purkinje Fiber and SA Node Action Potential SA Node Action Potential
Phase 4= slow decline in the outward movement of K+
as the K+ channels responsible for Phase 3 continue to close.
Phase 0 = increased Ca++ conductance (gCa++) thru
the L-type Ca++ channels depolarization. Funny currents and Ca++ currents close.
Phase 3 = Repolarization occurs K+ channels open
(increased gK+)increasing the outward directed, hyperpolarizing K+ currents.
At the same time, the L-type Ca++ channels become inactivated and close, which decreases gCa++ and the inward depolarizing Ca++ currents.
C. NORMAL CARDIAC DEPOLARIZATION AND REPOLARIZATION
Firing of SA node is the atrial depolarization (P wave)
General direction of electric current o Base to apex
Polarity of the wave depends on the direction of the AP conduction with respect to the polarity of the lead o If impulse goes towards the electrode (same
polarity) positive deflection (R wave)
o If impulse goes away from the electrode (opposite polarity) negative deflection (Q or S wave)
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
D. NORMAL CARDIAC CONDUCTION STEPS
Figure 5. Normal sinus rhythm of the heart
1. Spread of Depolarization from SA node (P wave)
SA sending impulse - (P wave in Lead 1 and aVF lead)
2. Conduction from SA node to AV node
Isoelectric AV node
No depolarization or repolarization happening
3. Ventricular Depolarization (QRS complex)
Q wave – septal depolarization (from AV node) o Depolarization of septum Right
ventricle
o Away from the general direction
R wave – apical and early ventricular depolarization
o Completion of septal depolarization
S wave – late ventricular depolarization
o The last area of the heart to be depolarized is the posterior wall at the base of the heart
o Completes the ventricular depolarization (base to apex)
Analogy of Dr. Balgua:
Dapat papunta ka sa Alabang, pero nag side trip ka sa NAIA (away from the general direction = Q wave)
After NAIA, pupunta ka sa Paranaque, which is papunta pa rin sa Alabang (general direction = R wave)
Detour sa Asian Hospital (away from the general direction = S wave)
Bumalik na sa bahay (depolarization is complete)
4. Repolarization (T wave)
Septum initially has a positive outside, negative inside
Depolarized – creates a different electric potential - From the field of negativity goes to
positivity (base to apex) - Creates a positive inside
- Establishes direction of electric current
Repolarization- vector force of downward to L side upward T wave in both Lead I and aVF
- Current goes from electronegative apex to electropositive base
T wave – ventricular repolarization (ends to
epicardium) o Always upright
- Because the electric current goes to the electropositive potential
3
of
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
Is there an atrial repolarization? Where is it in the graph? Atrial repolarization occurs a little bit earlier than
ventricular depolarization. Since the electrical force of QRS is much higher than atrial repolarization, it is masked by the complex.
III. THE NORMAL ECG
Figure 6. Normal ECG tracing 1. P wave
upright in leads I, aVF and V3 - V6
normal duration of less than or equal to 0.11 seconds
polarity is positive in leads I, II, aVF and V4 - V6; diphasic in leads V1 and V3; negative in aVR
shape is generally smooth, not notched or peaked
* Representation of atrial depolarization 2. QRS wave
Duration less than or equal to 0.12 seconds, amplitude greater than 0.5 mV in at least one standard lead, and greater than 1.0 mV in at least one precordial lead. Upper limit of normal amplitude is 2.5 - 3.0 mV.
Small septal Q waves in I, aVL, V5 and V6 (duration less than or equal to 0.04 seconds; amplitude less than 1/3 of the amplitude of the R wave in the same lead).
Represented by a positive deflection with a large, upright R in leads I, II, V4 - V6 and a negative deflection with a large, deep S in aVR, V1 and V2
In general, proceeding from V1 to V6, the R waves get taller while the S waves get smaller. At V3 or V4, these waves are usually equal. This is called the transitional zone
* Representation of tubular depolarization
3. T wave
T wave deflection should be in the same direction as the QRS complex in at least 5 of the 6 limb leads
normally rounded and asymmetrical, with a more gradual ascent than descent
should be upright in leads V2 - V6, inverted in aVR
amplitude of at least 0.2 mV in leads V3 and V4 and at least 0.1 mV in leads V5 and V6
isolated T wave inversion in an asymptomatic adult is generally a normal variant
* Representation of ventricular repolarization
4. Equidistant r-r intervals 5. Regular
Rhythm is regular if it has a P wave) 6. Rate:
60-100 (rule of 300) 7. Axis
Look only at Lead I and aVF, if both upright, normal axis
8. PR interval: Normally between 0.12 and 0.20 seconds.
9. ST segment
isoelectric, slanting upwards to the T wave in the normal ECG
can be slightly elevated (up to 2.0 mm in some precordial leads)
never normally depressed greater than 0.5 mm in any lead
10. QT interval
Durations normally less than or equal to 0.40 seconds for males and 0.44 seconds for females.
Figure 6. Parts of ECG tracing
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
A. COMPONENTS OF AN ECG TRACING
Calibrations can be used to compute for the duration of the different intervals and determine certain abnormalities
Standard Calibration in ECG = 25 mm /second
1 second/ 50 mm = calibration used to better visualize very fast heart rates
a. Horizontal axis – measures time
o 1 small square = 1 mm = 0.04 sec
o 1 big square(5 small squares) = 5 mm = 0.2 sec
b. Vertical axis – measures voltage o 1 small square = 1 mm = 0.1 mV o 10 small squares = 1 mV o 1 big square = 5 mm = 0.5 mV o
NORMAL TIME INTERVAL
P waves - < 3 small squares (0.08-0.12s)
PR interval - < 5 small squares (0.12-0.2s)
QRS complex –1.5-2 squares tall (0.08-0.12 sec)
B. SEGMENTS AND INTERVALS
Segment - straight line connecting two waves
Interval - encompasses at least one wave plus the
connecting line \
PR interval (normal is about 0.16 sec) time from
START of atrial depolarization to the START of
ventricular repolarization
PR segment time from the END of atrial
depolarization to the
Start of ventricular repolarization
ST segment – end of ventricular depolarization to start of ventricular repolarization
QT interval (normal is about 0.35 sec) START of
Ventricular depolarization to the END of Ventricular
repolarization
0.36-0.46s (males); 0.36-0.48s (females)
QRS interval duration of Ventricular depolarization
T wave – depends on electrolyte; elevated in high K or may be inverted
Note:
PQ and ST segments- isoelectric (same amplitude)
IV. ECG LEADS
Standard ECG use of 12 leads, with each lead determined and placed by the placement and orientation of various electrodes on the body. Each lead views the heart at a unique angle, enhancing its sensitivity to a particular region of the heart. The more views, the more information
provided.
Standard Chest Lead ECG
Normal: Left-side lead Pediatrics: Right-side lead
12-lead ECG
Six limb leads - 3 standard; 3 augmented Six precordial leads
composed of limb leads and chest leads
15- lead ECG
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
paediatric patients are directed to the right (until
12 years old), so we need to get the right side v1, v3, v4, v5 and v6
Electrocardiographic Leads (12-Lead ECG)
1. Limb Leads
i. Standard Bipolar Limb Leads ii. Augemented Unipolar Limb Leads 2. Chest/Precordial Leads
A. LIMB LEADS
i. Standard Bipolar Limb leads
1. I - Right arm (-) -> Left arm (+);
0°
2. II - Right arm (-) -> Left leg (+);
60°
3. III - Left arm (-) -> Left leg (+);
120°
- Frontal plane activity
ii. Einthoven’s Triangle
Follows the direction of the three leads mentioned; forming a triangle
- Einthoven’s Law
o Voltage of I + III = Voltage of II
o Follows normal heart electrical courses o Obtain electric potentials of two leads,
third one can be solved
o Can be used to check if electrodes placed correctly
Flow:
o Apex is electropositive;
o Outside of heart is electropositive; o Inside is electronegative
o Electronegative would be attracted to the electropositive potentials going to the apex
o Flow of circuit is towards the apex and that is the normal impulse conduction of the heart.
iii. Augmented Unipolar Limb Leads
- Placing an electrode on the left arm, right arm, and left foot with a ground lead on the box, will produce an amplification of electrical potential. Augmented unipolar leads aVR was known to be
the ground lead, lahat ng wave forms naka-positive deflected upwards except aVR, aVR reflects the electrical force in the posterior form of the heart. So if aVR is upright, mali placement ng leads.
2. aVR (Right)
- Positive (+) terminal: Right Arm - Negative deflection
- -150° normal
- Electrode positioning opposite the flow of depolarization from R atrium to R ventricle
3. aVL (Left)
- Positive terminal: Left arm - No deflection
- Electrode position perpendicular to flow of depolarization
- -30° normal
4. aVF (Foot)
- Positive terminal: Left leg - Positive Deflection
- Electrode parallel to depolarization flow from L atrium to L ventricle
- 90° normal
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
B. CHEST/PRECORDIAL LEADS
- Electrical activity at horizontal plane
- records mainly the electrical potential of the cardiac musculature immediately beneath the electrode.
C. ADDITIONAL LEADS
a. Posterior Lead ECG
- Lungs and muscle barriers prevent anterior ECG to detect posterior heart damage
- Used to record myocardial damage on the posterior part of the heart
b. Right-sided 12-Lead ECG
- Maybe used to detect right-side heart damage - Mirror of the standard
- “R”version of V3 to V6
V. FLOW OF CURRENT AROUND THE HEART DURING CARDIAC CYCLE
Electrical current flows from depol area to polarized area
First areas to be depol in left ventricular area: o Anterior preseptal wall
o Posterior preseptal wall o Center of Left septum
o These are the sites of insertions of the 3 branches of the Left Bundle Branch
Last area to be depol: Posterobasal areas of Left
ventricle
Septal activation: starts @ mid 3rd of left side, then
spreads across interventricular septum: left to right and apex to base
Right ventricle depol:
o Starts at insertion of Right Bundle
Branch close to anterior papillary
muscle > free wall > pulmonary conus -> posterobasal areas
o Sept Septal surface to anterior free walls to the posterior and basal regions in an apex to base direction
THUS,
o Leads I, II, III, aVL, and aVF – upward (positive) o aVR – downward (downward)
o V3, V4- isoelectric o V1, V2- small R, peak S
o V3-V6 – increasing R wave; decreasing S wave o V5, V6- well developed R wave
1st pic: Impulse from SA node to atrial walls
2nd pic: Impulse reach AV node, delay .1second
3rd pic: Bundle branches (R and L) carry impulses from
AV node to Apex
4th pic: Signal spread through the ventricles
VI. CURRENTS OF INJURY
When part of the heart remains partially or completely depol
Current flows between pathologically depol and normally depol even between heartbeat
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
Injured part = negative since it is depolarized and sends negative charges to surrounding muscles fibers
Causes:
o Trauma = inc. memb permeability = no full
repol
o Infection = damage muscle membranes
o Ischemia
*Current of injury effect on QRS complex
In the figure above, a small area in the base of the left ventricle is newly infarcted (loss of coronary blood flow).
During the T-P interval (polarization) abnormal
negative current (125o) still flows from the infarcted
area at the base of the left ventricle and spreads toward the rest of the ventricles. With the base of the vector, the negative end, toward the injured muscle.
As shown in the lower portions of the figure, even before the QRS complex begins, this vector causes an
initial record in lead I below the zero potential line,
because the projected vector of the current of injury in lead I points toward the negative end of the lead I axis.
Lead II - the record is above the line because the projected vector points more toward the positive
terminal of the lead.
Lead III - the projected vector points in the same direction as the positive terminal of lead III so that the record is positive. Furthermore, because the vector lies almost exactly in the direction of the axis of lead III, the voltage of the current of injury in lead III is much greater than in either lead I or lead II.
By vectorial analysis, the successive stages of electrocardiogram generation by the depolarization wave traveling through the ventricles can be constructed graphically, as demonstrated in the lower part.
When the heart becomes totally depolarized, at the end of the depolarization process (as noted by the next-to-last stag), all the ventricular muscle is in a negative state. Therefore, at this instant in the electrocardiogram, no current flows from the ventricles to the electrocardiographic electrodes because now both the injured heart muscle and the contracting muscle are depolarized. Next, as repolarization takes place, all of the heart finally repolarizes, except the area of permanent depolarization in the injured base of
the left ventricle. Thus, repolarization causes a return of the current of injury in each lead, as noted at the far right.
VII. ECG INTERPRETATION AND ASSOCIATED ABNORMALITIES
Guide: 1. Rhythm
2. Rate: atrial and ventricular 3. Axis
4. P wave morphology and duration 5. P-R interval
6. QRS morphology and duration 7. ST segment
8. T wave, U wave and QT interval
A. RHYTHM
Check for P-waves on LeadII, V1, V2
The P waves must be upright in leads II, III and aVF. The P waves are upright because the direction of the impulse is going toward the inferior wall away from the SA node
Check for regularity of R-R interval (normal sinus rhythm)
II, V1, and V2 since it is on the side of the atrium
B. RATE
ECG grid:
o 1mm block (small) = 1/25 of a sec (.04)
o 5mm block (large) = 1/5 of a sec (.20)
Measure R-R interval
Rule of 300
For regular rhythms: Rate = 300 / number of large squares in between each consecutive R wave.
For very fast rhythms: Rate = 1500 / number of small squares in between each consecutive R wave.
For slow or irregular rhythms: Rate = number of complexes on the rhythm strip x 6 (this gives the average rate over a ten-second period).
C. AXIS
a. Hexaxial Reference System (plot method)
Normal: -30° to 110°
Right Axis Dev: 120° to 180°
Left Axis Dev: -90° to -20°
Indeterminate Dev: 180° to -90°
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
b. Axis Isoelectric Method
Identify the lead where R and Q is most isoelectric. (Isoelectric QRS has equal positive and negative deflections)
Check the lead perpendicular to it (consult axis graph below)
Check the perpendicular lead if the QRS is deflecting positively or negatively; if negative, reference point will be 180° from it
Example:
o Say, the lead with the most isoelectric QRS (same R and Q height in ECG trace; none shown here) is Lead III (120° as shown in axis graph below)
o Select the perpendicular lead, which is aVR
o Check if aVR’s QRS is deflecting positively or negatively (in ECG trace; none shown here)
o If positively deflecting = extreme RAD (-150°); if Negatively deflecting = normal axis(30°)
c. Axis by Lead I and Lead II
if both (+) = Normal
if lead II upward = RAD
if lead II downward = LAD
if both downward = Extreme RAD
d. Axis by Thumb Rule
Check QRS Complexes in lead I and AVF Then Check intersection
1. Left thumb = lead I 2. Right thumb = avR 3. If both are up, normal
4. If right thumb up, right axis deviation 5. If left thumb up, left axis deviation 6. If both down, extreme right axis deviation
Causes of Axis Deviations
(with “*” = additional info) 1. Left shift axis
- Expiration (flattens heart horizontally) - Lying down
- Obese, sedentary (Fats push heart upwards) 2. Right shift axis
- Inspiration - Standing up
- Tall lanky party people -
3. *Hypertrophy
axis shifts on the same ventricle
the bigger would be the electrical force supinating over the other ventricles
left ventricle create more electrical force overpowering the right ventricle -> axis shifts to left
When one ventricle greatly hypertrophies, the axis of the heart shifts toward the
hypertrophied ventricle for two reasons.
First, a far greater quantity of muscle exists on the hypertrophied side of the heart than on the other side, and this allows generation of
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
greater electrical potential on that side. Second, more time is required for the depolarization wave to travel through the hypertrophied ventricle than through the normal ventricle. Consequently, the normal ventricle becomes depolarized considerably in advance of the hypertrophied ventricle, and this causes a strong vector from the normal side of the heart toward the hypertrophied side, which remains strongly positively charged. Thus, the axis deviates toward the hypertrophied ventricle.
4. *Bundle Blocks
Ordinarily, the lateral walls of the two ventricles depolarize at almost the same instant (both the left and the right bundle branches of the Purkinje system transmit the impulse almost the same instant). Potentials generated by the two ventricles almost neutralize each other. If only one of the major bundle branches is blocked, the cardiac impulse spreads through the normal ventricle long before it spreads through the other. Therefore, depolarization of the two ventricles does not occur even nearly simultaneously, and the depolarization potentials do not neutralize each other. As a result, axis deviation occurs.
a. RBBB (Right Bundle Branch Block)
When the right bundle branch is blocked, the left ventricle depolarizes far more rapidly than the right ventricle, so the left side of the ventricles becomes electronegative as long as 0.1 second before the right. Therefore, a strong vector develops, with its negative end toward the left ventricle and its positive end toward the right ventricle. In other words, intense right axis deviation occurs. In the figure below, an axis of about 105 degrees is shown instead of the normal 59 degrees and a prolonged QRS complex because of slow conduction.
b. CLBBB (Complete Left Bundle Branch Block)
When the left bundle branch is blocked, cardiac depolarization spreads through the right ventricle two to three times as rapidly as through the left ventricle. Consequently, much of the left ventricle remains polarized for as long as 0.1 second after the right ventricle has become totally depolarized. Thus, the right ventricle becomes electronegative, whereas the left ventricle remains electropositive during most of the depolarization process, and a strong vector projects from the right ventricle toward the left ventricle. In other words, there is intense left axis deviation of about -50 degrees because the positive end of the vector points toward the left ventricle. This is demonstrated in figure below, which shows typical left axis deviation resulting from left bundle branch block.
The duration of the QRS complex is greatly prolonged because of extreme slowness of depolarization in the affected side of the heart. This extremely prolonged QRS complex differentiates bundle branch block from axis deviation caused by hypertrophy.
D. P WAVE MORPHOLOGY AND DURATION
E. P-R INTERVAL
Conduction time from SA node to AV node
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
AV blocks
o 1st Degree – prolonged conduction time; prolonged PR interval
o 2nd Degree
Type 1 – Progressive
prolonged time leading to drop beat; can be a precursor for a pacemaker implantation Type 2 – can lead to block at
bundle of His (type 3) o 3rd Degree
- Complete heart block - Block bundle of His onwards - No impulse to ventricles - AV dissociation
F. QRS MORPHOLOGY AND DURATION
Only lasts for .1sec
Abnormalities (blocks) o Right Bundle Branch Block
V1 – batman(?)
V6 – Inverted T wave; Wide S terminal
o Left Bundle Brach Block
V1 – Wide QRS complex; inverted T wave
V6 – Twin R-wave peaks Signals acute MI
Abnormalities (voltage)
1. Increased Voltage
- Hypertrophy (increase in muscle quantity) causes generation of increased quantity of electricity conducted
2. Decreased Voltage
MI
- Decreased muscle mass - Slower depol wave propagation - Prolonged QRS and lower voltage Pulmonary Effusion
- Pleural effusion (extracellular fluid),
to a lesser extent, also can "short-circuit" the electricity around the heart so that the voltages at the surface of the body and in the electrocardiograms are decreased. Emphysema
- conduction of electrical current through the lungs is depressed considerably because of excessive quantity of air in the lungs.
- chest cavity enlarges, and the lungs tend to envelop the heart to a greater extent than normally. Therefore, the lungs act as an insulator to prevent spread of electrical voltage from the heart to the surface of the body, and these results in decreased
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
electrocardiographic potentials in the various leads.
Prolonged and Bizarre Patterns of QRS Complex
1. Prolonged QRS: Cardiac Hypertrophy, Prolonged Conduction
o Hypertrophy -> longer pathway of impulse to travel
o QRS lasts as long as depol spreads through ventricles
o Prolonged up to .09 to .12 second
2. Prolonged QRS: Purkinje System Block
o Blocked Purkinje fibers -> Impulse conducted by Ventricular Muscles instead -> velocity decreased up to 1/3 of original
o Prolonged up to .14or greater
*block below bundle of His requires
pacemakers since the ventricular muscles will be dominant pacemaker by then, and will only produce slow heart rates.
3. Bizarre QRS
a. Destruction of cardiac muscles
b. Multiple small local blocks in Purkinje system -> irregular cardiac impulse -> rapid voltage shift and axis deviation -> double or triple peaks in ECG
G. ST SEGMENT
ST Segment depression in myocardial ischemia
Downslope = 0.5mV is a significant depression
ST segment elevation->Myocardial infarction
Upslope=chair-like pattern
H. T wave, U wave and QT interval
• Hyperkalemia- peak T waves; ventricular arrhythmia
• Hypercalcemia-short QT
• Hypocalcemia- slow contraction; prolonged QT • Hypokalemia- flattened T wave
• Hypokalemia- U wave appear in severe hypokalemia with flattened T and prominent U • PVC - Prolonged QT
I. PREMATURE CONTRACTION
also called extrasystole/premature beat/ectopic beat.
most result from ectopic foci in the heart
Causes:
1. Local areas of ischemia
2. Small calcified plaques at different points in the heart , which press against the adjacent cardiac muscle so that some of the fibers are irritated;
3. Toxic irritation of the A-V node, Purkinje System, or myocardium caused by drugs, nicotine or caffeine 4. Mechanical initiation of premature contractions is also
frequent during cardiac catheterization; large numbers of premature contractions often occur when the catheter enters the right ventricle and presses against the endocardium
PREMATURE ATRIAL CONTRACTIONS
“palpitations kapag nakikita niyo si crush”
P wave of this beat occurred early
• P-R interval shortened (ectopic origin of the beat is in the atria near the A-V node)
• causes: ischemia vs. calcified plaques vs. toxic irritation of the AV node, Purkinje system, or myocardium, drugs
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
nicotine, caffeine
• compensatory pause
• interval between the premature contraction and the next succeeding contraction is slightly prolonged
o Cause: premature contraction originated in the atrium some distance from the sinus node, and the impulse had to travel through a considerable amount of atrial muscle before it discharged the sinus node. Consequently, the sinus node discharged late in the premature cycle, and this made the succeeding sinus node discharge also late in appearing.
• other causes: healthy people can have it; smoking, puyat, sobrang starbucks, redbull, alcohol, milk tea • pulse deficit
o a deficit in the number of radial pulses occurs when compared with the actual number of contractions of the heart
o heart contracts early ventricles will not have filled with blood normally stroke volume output depressed/ almost absent pulse wave passing to the peripheral arteries is
weak
PREMATURE VENTRICULAR CONTRACTIONS
• “Bizarre QRS”
• Sunod sunod na PVCS Vtac!!!
• wide QRS: impulse conduction thru ventricle not through Purkinje fibers
• QRS high voltage: impulse travel only one direction (no neutralization effect of depolarization waves): with one entire single ventricle(common in left ventricle) is depolarized ahead of the other large electrical potentials
• T is opposite in direction: slow conduction of impulse (causes the muscle fibers that depolarize first also to repolarize first)
j PAROXYSMAL TACHYCARDIA
• Some abnormalities in different portions of the heart ( such as atria, the Purkinje system, or the ventricles) can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart.
• caused most frequently by re-entrant circus movement feedback pathways that set up local repeated self-reexcitation. Because of the rapid rhythm in the irritable focus, this focus becomes the pacemaker of the heart. • "paroxysmal" - heart rate becomes rapid in paroxysms,
with the paroxysm beginning suddenly and lasting for a
few seconds, a few minutes, a few hours, or much longer. Then the paroxysm usually ends as suddenly as it began, with the pacemaker of the heart instantly shifting back to the sinus node.
• can be stopped by eliciting a vagal reflex (pressing on the neck in the regions of the carotid sinuses)
• quinidine and lidocaine can used
ATRIAL PAROXYSMAL TACHYCARDIA/ A-V NODAL PAROXYSMAL
TACHYCARDIA/SUPRAVENTRICULAR TACHYCARDIA
Atrial or A-V nodal paroxysmal tachycardia, both of which are called supraventricular
demonstrates in the middle of the record a sudden increase in the heart rate from about 95 to about 150 beats per minute.
inverted P wave is seen before each QRS-T complex, and this P wave is partially superimposed onto the normal T wave of the preceding beat. This indicates that the origin of this paroxysmal tachycardia is in the atrium, but because the P wave is
abnormal in shape, the origin is not near the sinus node.
PACs SVTs VTAC
Paroxysmal tachycardia often results from an aberrant rhythm that involves the A-V node. This usually causes almost normal QRS-T complexes but totally missing or obscured P waves.
tachycardias,
usually occurs in young, otherwise healthy people, and they generally grow out of the predisposition to tachycardia after adolescence.
In general, supraventricular tachycardia frightens a person tremendously and may cause weakness during the paroxysm, but only seldom does permanent harm come from the attack.
AV NODAL RE-ENTRANCT TACHYCARDIA/ ATRIOVENTRAL NODAL RE-ENTRANT TACHYCARDIA
• most common regular supraventricular tachycardia
• Originates from a location within the heart above the bundle of His.
• P wave comes after QRS
• Drug of choice: Adenosin, Beta blockers (Short acting beta blocker – esmolol), Calcium channel blockers (verapamil, diltiazem), Digoxin – but is not given in acute paroxysmal attacks because of its slow onset
• Pathogenesis - /dual mechanism proposed for re-entry From textbook of clinical electrocardiography, 3rd edition:
A dual concept mechanism consisting of fast and slow conducting pathways within the AV node is the proposed mechanism for its initiation. The prolonged P-R interval or prolonged A-H interval on bundle of His electrocardiography strengthens the concept of dual entry pathway within AV node. Therefore the present concept is that the AV node is
functionally split into two longitudinal pathways: 1. Beta pathway (fast pathway) : exhibits rapid
conductions and has a long refractory period
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
2. Alpha pathway (slow pathway) : conducts slowly and has a short refractory period Sir Balgua:
Functional block on fast pathway impulses conducted to slow pathway Before reaching ventricles, fast pathway would recover its refractoriness would attract slow impulses to retrogradely conduct to fast pathway impulses go up to activate atrium or travel to slow pathway re-entry
mechanism simultaneous action of atrium and ventricle walang P wave (P wave nasa loob ni QRS)
VENTRICULAR PAROXYSMAL TACHYCARDIA
• series of ventricular premature beats occurring one after another without any normal beats interspersed. • usually a serious condition o usually does
not occur unless considerable ischemic damage is present in the ventricles.
o ventricular tachycardia frequently initiates the lethal
condition of ventricular fibrillation because of
rapid repeated stimulation of the ventricular muscle.
• Causes: digitalis intoxication (causes irritable foci that lead to ventricular tachycardia
• Drug: quinidine (increases the refractory period and threshold for excitation of cardiac muscle blocking irritable foci)
k. ATRIAL FIBRILLATION
• Cause: atrial enlargement prevent the atria from emptying adequately into the ventricles, or from ventricular failure with excess damming of blood in the atria. The dilated atrial walls provide ideal conditions of a long conductive pathway, as well as slow conduction, both of which predispose to atrial fibrillation
• loss of atrial contraction • ECG: no P wave
• QRS-T complexes are normal, but their timing is irregular
• When the atria are fibrillating, impulses arrive from the atrial muscle at the A-V node rapidly but also irregularly. Because the A-V node will not pass a second impulse for about 0.35 second after a previous one, at least 0.35 second must elapse between one ventricular contraction and the next. Then an additional but variable interval of 0 to 0.6
second occurs before one of the irregular atrial fibrillatory impulses happens to arrive at the A-V node. Thus, the interval between successive ventricular contractions varies from a minimum of about 0.35 second to a maximum of about 0.95 second, causing a very irregular heartbeat.
• 125-160 beats (due rapid rate of the fibrillatory impulses in the atria)
• irregular ventricular rhythm: varied ventricular contractions 0.35-0.95 seconds
• The mechanism of atrial fibrillation is identical to that of ventricular fibrillation, except the location. Remember that the atrial muscle mass is separated from the ventricular muscle mass by fibrous tissue except for the conducting pathway through the A-V bundle. Therefore, ventricular fibrillation often occurs without atrial fibrillation.
• Not as lethal as ventricular fibrillation because blood still flows passively through the atria into the ventricles, and the efficiency ofventricular pumping is decreased only 20 to 30 %.
• Electroshock Treatment
l. ATRIAL FLUTTER
• “sawtooth” / flutter waves
• Different from atrial fibrillation in that impulse travels as a single large wave always in one direction around and around the atrial muscle mass
• 200-350 beats
• 2:1 or 3:2 AV conduction rhythm (2 flutter waves before it would be conducted to generate 1 QRS) o Because one side of the atria is contracting while the other side is relaxing, the amount of blood pumped by the atria is slight. Furthermore, the signals reach the A-V node too rapidly for all of them to be passed into the ventricles, because the refractory periods of the A-V node and A-V bundle are too long to pass more than a fraction of the atrial signals. Therefore, there are usually two to three beats of the atria for every single beat of the ventricles.
m. VENTRICULAR TACHYCARDIA
• cause: ischemia
• precedes ventricular fibrillation
• drugs: quinidine: Class IA anti-arrhythmic
• Anti-arrhythmic drugs can cause ventricular tachycardia
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
• Has dual edge – pro-arrhythmic and antiarrhythmic
n. VENTRICULAR FIBRILLATION
Choogs to Go! (machuchugi na!)
• Lethal emergency, most serious of all cardiac arrhythmias • Ventricular fibrillation results from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating portion after portion of ventricular mass and eventually feeding back onto itself to re-excite the same ventricular muscle over and over-never stopping. • When this happens, many small portions of the
ventricular muscle will be contracting at the same time, while equally as many other portions will be relaxing. The ventricular chambers remain in an indeterminate stage of partial contraction, pumping either no blood or negligible amounts.
• No repetitive electrocardiographic pattern can be ascribed to ventricular fibrillation.
• potentials change constantly and spasmodically because the electrical currents in the heart flow first in one direction and then in another and seldom repeat any specific cycle.
• The voltages of the waves: usually about 0.5 millivolt initially, but they decay rapidly so that after 20 to 30 seconds, they are usually only 0.2 to
0.3 millivolt. Minute voltages of 0.1 millivolt or less may be recorded for 10 minutes or longer after ventricular fibrillation begins.
Causes:
1. PVC vs. ischemia
2. re-entry as a basis of VF: circus movement
o "circus movement – cause an impulse to continue to travel around circle, that is to cause “re-entry” of impulse into that muscle that has already been excited
o 3 conditions that can cause circus movement o First, if the pathway around the circle is too long, o Second, if the length of the pathway remains
constant but the velocity of conduction becomes
decreased enough
o Third, the refractory period of the muscle might
become greatly shortened. All these conditions occur
in different pathological states of the human heart, as follows:
1. A long pathway typically occurs in dilated hearts.
2. Decreased rate of conduction frequently results from
a. blockage of the Purkinje system, b. ischemia of the muscle,
c. high blood potassium levels, or many other factors.
3. A shortened refractory period commonly occurs in response to various drugs, such as
epinephrine, or after repetitive electrical stimulation. Thus, in many cardiac
disturbances, re-entry can cause abnormal patterns of cardiac contraction or abnormal cardiac rhythms that ignore the pace-setting effects of the sinus node.
o The re-entrant impulses in fibrillation are not simply a single impulse moving in a circle. Instead, they have degenerated into a series of multiple wave fronts that have the appearance of a "chain reaction."
3. long pathway of conduction (dilated hearts) vs. slow conduction
velocity (AV blocks/ischemia/hyperkalemia) vs. short refractory period(epinephrine)
4. fibrillation caused by 60 cycle AC: REENTRY unidirectional flow vs. slow conduction time vs.
short refractory period vs. division of impulses
• a 60-cycle electrical stimulus is applied through a stimulating electrode.
• Heart A
o The first cycle of the electrical stimulus causes a depolarization wave to spread in all directions, leaving all the muscle beneath the electrode in a refractory state. After about 0.25 second, part of this muscle begins to come out of the refractory state. Some portions come out of refractoriness before other portions.
o many lighter patches, which represent excitable cardiac muscle, and dark patches, which represent still refractory muscle.
o certain impulses travel for short distances, until they reach refractory areas of the heart, and then are blocked. But other impulses pass between the refractory areas and continue to travel in the excitable areas. Then, several events transpire in rapid succession, all occurring simultaneously and eventuating in a state of fibrillation.
State of fibrillation
1. Transmission of some of the depolarization waves around the heart in only some directions but not other directions (due to blockage).
2. the rapid stimulation of the heart causes two changes
in the cardiac muscle itself, both of which predispose to circus movement: (1) The velocity of conduction
through the heart muscle decreases, which allows a
longer time interval for the impulses to travel around
2.2 – ELECTROCARDIOGRAPHY
Physiology: ECG
[Condes, De Claro, Domingo, Fernandez, J.]
1D
the heart. (2) The refractory period of the muscle is
shortened, allowing re-entry of the impulse into
previously excited heart muscle within a much shorter time than normally.
3. Third, one of the most important features of fibrillation
is the division of impulses, as demonstrated in heart A. Progressive chain reactions many new wave fronts many small depolarization waves traveling in many directions at the same time.
4. Irregular pattern of impulse travel causes many circuitous routes for the impulses to travel, greatly lengthening the conductive pathway, which is one of the conditions that sustains the fibrillation. It also
results in a continual irregular pattern of patchy refractory areas in the heart.
5. One can readily see when a vicious circle has been
initiated: More and more impulses are formed, more and more patches of refractory muscle, more and more division of the impulses. Therefore, any time a single area of cardiac muscle comes out of refractoriness, an impulse is close at hand to re-enter the area.
o Heart B
o the final state that develops in fibrillation o many impulses traveling in all directions, o In fact, a single electric shock during this vulnerable period frequently can lead to an odd pattern of impulses spreading multi directionally around refractory areas of muscle, which will lead to fibrillation.
Treatment
Electroshock Defibrillation of the Ventricles • a strong high-voltage alternating electrical
current passed through the ventricles for a fraction of a second can stop fibrillation by throwing all the ventricular muscle into refractoriness simultaneously.
• However, the same re-entrant focus that had originally thrown the ventricles into fibrillation often is still present, in which case fibrillation may begin again immediately.
When electrodes are applied directly to the two sides of the heart, fibrillation can usually be stopped using 110 volts of 60-cycle alternating current applied for 0.1 second or 1000 volts of direct current applied for a few thousandths of a second. CPR
• Unless defibrillated within 1 minute after fibrillation begins, the heart is usually too weak to be revived by defibrillation because of the lack of nutrition from coronary blood flow. However, it is still possible to revive the heart by preliminarily pumping the heart by hand (intermittent hand squeezing) and then defibrillating the heart later.
Implanted cardioverter defibrillator ACLS
o. AGONAL RYTYHM TO ASYSTOLE/CARDIAC ARREST Ongoing choogs!
cessation of all electrical control signals in the heart. That is, no spontaneous rhythm remains.
Cardiac arrest may occur during deep anesthesia,
In some patients,severe myocardial disease can cause permanent or semi permanent cardiac arrest, which can causedeath.
To treat the condition, implanted electronic cardiac
pacemaker have been used successfully to keep
patients alive for months to years.
ANTI-ARRYTHMIC DRUGS
• can cause ventricular tachycardia
• Has dual edge – pro-arrhythmic and antiarrhythmic
Class I: Fast sodium (Na) channel blockers
• Ia - Quinidine, procainamide, disopyramide (depress phase 0, prolonging repolarization) – “Quezon Police District”
• Ib -phenytoin, Lidocaine, , mexiletine (depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization)
– “PLM”
• Ic -Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect on repolarization) –
“President Ferdinand Marcos” Class II: Beta blockers
• Propranolol , Esmolol Timolol , Metoprolol , Atenolol
Class III: Potassium (K) channel blockers
• Amiodarone, Sotalol, Ibutilide, Dofetilide
Class IV: Slow calcium (Ca) channel blockers
•
Verapamil, Diltiazem
Class V: Variable mechanism
• Digoxin, Adenosine, Magnesium sulfate,
wave and QT, U wave
and QT interval T wave, U wave and QT interval
