Lesson 3 - Diagnostic Tests and Treatments Flashcards

1
Q

CARDIAC ENZYMES and TROPONINS

A
  • several enzymes and markers are normally present in myocardial cells - following cardiac injury, these enzymes are released into the bloodstream - so, following myocardial damage, elevation of these enzymes is expected - results determine the extent of damage as well as the progress in healing - different enzymes elevate, peak and return to normal at various times - for this reason, blood work is drawn on a serial basis - blood is drawn every 6-12 hours (depending on hospital policy) - normal values often vary slightly from institution to institution, depending on the lab’s calibration parameters - cardiac enzymes can also be released into the bloodstream with most other muscle damage as well (ie. IM injections, skeletal muscle damage, CVA) - for this reason, IM injections are avoided until all serial blood work is completed
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2
Q

CK (creatine kinase)

A
  • sometimes called CPK (creatine phosphokinase) - the CK is the first enzyme to elevate following myocardial damage - elevating levels can be detected within 4-6 hours of injury - the level peaks in about 24 hours, and return to normal in 2-3 days - CK is found in cardiac muscle, as well as the brain and skeletal muscle
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3
Q
  • so, how do we know if the CK elevates because of cardiac injury or because of damage to other muscle tissue?…
A
  • the MB subfraction (isoenzyme CK-MB) is specific to cardiac tissue - the CK is fractionated (divided) into isoenzymes to determine how much of this CK elevation is related to cardiac tissue damage - so, elevated CK-MB can safely indicate cardiac damage (ie. MI) - the CK-MB elevates as early as 2-6 hours following cardiac injury - the level peaks in about 24 hours, and returns to normal in 2-3 days
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4
Q

AST (aspartate transaminase)

A
  • also called SGOT (serum glutamic-oxaloacetic transaminase) - the AST rises slower than the CK, and not as high - elevation can be detected in 6-12 hours - the AST peaks in about 36 hours - it returns to normal in 3-4 days - the AST can also elevate with hepatic disease
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5
Q

LDH (lactate dehydrogenase)

A
  • the LDH begins to elevate within 8-10 hours following injury - the level peaks by day 2-3, and returns to normal in 1-2 weeks - because of its slow elevation, often this enzyme is not ordered in the first 24 hrs - LDH appears in almost all body tissues
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6
Q

, how do we know that cardiac damage is what caused the LDH to elevate?…

A
  • LDH has five isoenzymes (LD1 to LD5) - isoenzymes LD1 and LD2 appear primarily in cardiac tissue - a ‘flipped’ LD pattern of LD1 greater than LD2 indicates cardiac damage
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7
Q

PROTEINS (CARDIAC MARKERS)

A

Troponins Myoglobin

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8
Q

Troponins

A
  • troponins are muscle proteins bound to the filaments of contractile muscle - these sensitive markers exist in muscle that contracts (skeletal and cardiac) - there are 3 troponin isotopes (troponin I, T and C) - troponin I: found only in cardiac muscle - troponin T: found in cardiac and skeletal muscle - troponin C: found in the brain - troponin I is the only cardiac specific marker - troponin I has a 100% sensitivity for diagnosing cardiac damage - troponin I is released into the bloodstream within 3-6 hours - it peaks in about 14-20 hours, and returns to normal in 10-15 days - because troponin I is specific to cardiac tissue and since it stays elevated for so long, a late diagnosis of MI is possible
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9
Q

Myoglobin

A
  • this is an oxygen binding muscle protein found in skeletal and muscle protein - it releases into the bloodstream with any muscle damage (skeletal and cardiac) - myoglobin may be the first marker to elevate after cardiac injury - levels rise in 1-4 hours - the level peaks at 6-8 hours, and returns to normal in 24 hours - myoglobin cannot be fractionated and as such cannot be truly diagnostic of cardiac damage
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10
Q

LIPID STUDIES

A
  • the lipid profile provides an indication of pre-existing hyperlipidemia - studies can include total cholesterol, triglycerides and lipoprotein fractionation - cholesterol and triglycerides vary independently of each other - patients must be fasting for 12 hours prior to a lipid profile
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11
Q

Cholesterol

A
  • cholesterol is not freely transported in the blood - it is transported on ‘lipoproteins’ - there are two fractions of cholesterol (HDL-C and LDL-C) - lipoprotein fractionation isolates and measures the two types of cholesterol: - HDL-C - cholesterol carried on high density lipoproteins (HDL) - these are transported out and metabolized by the liver - a beneficial lipoprotein - LDL-C - cholesterol carried on low density lipoproteins (LDL) - these are absorbed into blood vessels and muscle walls - a concentration of LDL-C in arteries contributes to atherosclerosis - a harmful lipoprotein - high LDLs (‘bad’ lipoprotein) is a risk factor for coronary artery disease (CAD) - high concentrations of HDLs (the ‘good’ lipoprotein) decreases the CAD risk - the balance of HDL-LDL is more significant than the total concentration of serum cholesterol - therefore, lipoprotein fractionation is a more valuable tool (HDL-LDL ratio)
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12
Q

Triglycerides

A
  • a third type of lipoprotein is the very low density lipoprotein (VLDL) - triglycerides are predominant in the harmful VLDLs
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13
Q

COAGULATION TESTS

A
  • coagulation studies are performed to screen for clotting disorders, and to determine the effectiveness of treatment or drug therapy - dissolving the clot can be promoted by inhibiting thrombin, antiplatelet drugs, or fibrinolytic therapy - usually, one of the 3 main studies are conducted (PTT, PT, INR)
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14
Q

PTT (partial thromboplastin time)

A
  • the actual time it takes for blood to clot can be determined by adding specific chemicals to the blood sample - this time frame is the PTT - normally, after adding these specific chemicals, blood clots in 21-35 seconds - longer times are required when anticoagulating a patient - the PTT is used to monitor IV heparin therapy - blood is drawn serially according to a heparin nomogram (as per hospital policy) - the PTT result determines the dosing and titration of heparin therapy - PTT times can vary between institutions, based on lab machine calibrations
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15
Q

PT (prothrombin time)

A
  • commonly called a pro-time - again, specific chemicals are combined with the blood sample to determine how long it takes a clot to form - normally, it takes blood 10-14 seconds to clot, after adding these chemicals - longer times are required when anticoagulating a patient - used to assess and monitor oral anticoagulation therapy (ie. warfarin) - several medical conditions, medications, and diet can affect the PT result - some examples are: - increased PT: fever, heart failure, aspirin, diuretics, alcohol - decreased PT: diabetes, antacids, Vit K, and vegetables high in Vit K - PT times can vary between institutions, based on lab machine calibrations
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16
Q

INR (international normalized ratio)

A
  • this is a measurement of the PT that is standardized across all laboratories - INR is considered the test of choice to monitor oral anticoagulation therapy - there are specific INR targets for cardiovascular disorders - atrial fibrillation: 2.0-3.0 - pulmonary embolism, deep vein thrombosis: 2.0-3.0 - mechanical prosthetic heart valve: 2.5-3.5 - there is a marked risk for thromboembolism for those with mechanical heart valves, if the INR falls to below 2.5
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17
Q

CONTINUOUS CARDIAC MONITORING

A
  • cardiac monitoring assesses the heart’s electrical activity - there are two common ways to assess cardiac electrical activity: 1) continuous bedside monitoring and telemetry 2) 12 lead ECG (to be studied in Coronary Care 2) - this course explores continuous cardiac monitoring/telemetry
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18
Q

Polarization

A
  • polarization is the cardiac cell’s resting state - the cardiac cell is inactive
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19
Q

Depolarization

A
  • this is an electrical process that occurs when myocardial cells are stimulated and discharge their stored electrical forces - it is a state of excitability that results from electrical (ionic) stimulation
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20
Q

Repolarization

A
  • this is a recovery period that follows depolarization, as the cells begin to restore their electrical energy - repolarization is the cell’s return to a state of rest
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21
Q
  • previously, we learned that the SA node normally initiates all impulses….
A
  • previously, we learned that the SA node normally initiates all impulses - under normal circumstances, the SA node does not generate another impulse until repolarization of the previous impulse is complete - once the previous impulse is completely repolarized and cells are resting again, SA node depolarization will occur again - the combined periods of stimulation (depolarization) and recovery (repolarization) constitute a cardiac cycle (one heart beat) - the cardiac cycle is a chemical process involving the exchange of ions across the semi-permeable cardiac cell membrane - these positive and negative ions create electricity - the heart’s electrical activity (depolarization and repolarization) can be detected, recorded and measured using the cardiac monitor - electrical forces within the heart transmit outward to the body’s skin surface - so, electrodes placed on the body surface will detect these electrical forces - as changes in electrical activity occur, the flow of these forces causes upward and downward deflections to be recorded - the deflections are then magnified through the bedside monitor or ECG machine (galvanometer) for greater visibility - they can then be recorded on a moving piece of paper to obtain a continuous print-out or “picture” of the heart’s electrical activity
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22
Q

ECG LEADS

A
  • electrical forces within the heart travel in multiple directions simultaneously - therefore, to obtain a comprehensive view of the heart’s electrical activity, it is necessary to record the flow of current from different angles - the placement of 3 electrodes (LA, RA, LL) allows us to view electrical activity in the frontal plane (a longitudinal surface view) - to obtain accurate recordings, proper electrode placement is important - each electrode is marked with one of the following combination of letters: RA (Right Arm) white electrode LA (Left Arm) black electrode LL (Left Leg) red electrode - with bedside and telemetry monitoring, the red electrode (LL) is placed on the lower left torso to allow for patient comfort, movement and ambulation - if 4 electrodes are used with bedside monitoring, the green electrode (RL) is placed on the lower R torso. This electrode does not record any electrical activity. It only serves as a “grounding” electrode - 5 lead bedside monitoring also includes a brown electrode, strategically placed on the precordium, to monitor a vector lead (discussed in Coronary Care 2) - the frontal plane/surface provides 3 of the major views (leads I, II, III) - the cardiac monitor determines electrodes to be positive (+) or negative (-) in lead I RA electrode (-) LA electrode (+) in lead II RA electrode (-) LL electrode (+) in lead III LA electrode (-) LL electrode (+) - a hypothetical line can be drawn between any of two of the three recording electrodes - this hypothetical line is called a ‘lead’ - (remember the RL electrode does not record electrical activity) - from an electrical standpoint, a hypothetical triangle (Einthoven’s triangle) is formed by these three leads, with the heart at the center - each lead is considered to be electrically equidistant from the heart - when 2 poles/electrodes have different polarities (–ve and +ve), the heart’s electrical current flowing between the 2 areas can be examined - lead II is the hypothetical line joining the electrodes placed on the RA and LL
23
Q
  • usually, lead II is the view used for bedside/telemetry monitoring. Here’s why…
A
  • the electrode placement for lead II is as follows: an electrode is placed on the RA or R upper chest (- pole) an electrode is placed on the LL or L lower torso (+pole) - between these 2 areas, a hypothetical line can be drawn - this hypothetical line is lead II (picture a line drawn between your RA & LL) - normally, the majority of impulses and electrical current transmit through the conduction pathways along this ‘down-and-to-the-left’ hypothetical line (reviewing the conduction system in Lesson 1 might help to visualize this) - the LV is the largest and hardest-working chamber - therefore, it requires the most electrical stimulation and energy to depolarize - so the majority of the heart’s electrical activity is aimed ‘down-and-to-the-left’ toward the LV. This is parallel to the same hypothetical line as lead II
24
Q

impulse traveling toward a (+) pole …

A

is recorded as an upward/positive deflection

25
Q

impulse traveling away from a (+) pole …

A

is recorded as a downward/negative wave

26
Q

the heart depolarizes …

A
  • the heart depolarizes the same way with each lead (normally, down toward the LV) - various leads view the same electrical activity, but from different angles, so they produce different looking ‘pictures’ - the analogy of a child eating an ice cream cone might help to visualize… - a picture taken from the front shows the child’s face and the ice cream cone - a picture taken from the side shows the child’s profile - a picture taken from the back shows the back of his head, and no ice cream - all 3 pictures are taken when the child is doing the same activity, but all three pictures look different
27
Q

ECG PAPER MEASUREMENTS

A
  • internationally, cardiac monitoring paper is standardized, with 2 basic elements Amplitude Duration
28
Q

Amplitude

A
  • this element measures voltage - amplitude is reflected by a series of horizontal lines 1mm apart - each mm represents 1/10 of a milliVolt (the basic unit of electrical intensity) - amplitude shows direction of electrical forces (positive and negative deflections)
29
Q

Duration

A
  • this element is more important in rhythm analysis than amplitude - it is used to calculate actual time frames for various electrical activities to occur - duration is measured using a series of vertical lines,1mm apart - the time interval between each vertical line is 0.04 seconds - every 5th line on ECG monitor paper is boldly inscribed (every 5th line is darker) - so, the time frame between each bold line is 0.20 secs (0.04 sec x 5 = 0.20 sec)
30
Q

CHARACTERISTICS OF A NORMAL CARDIAC COMPLEX

A
  • PQRSTU are arbitrarily selected letters, and have no additional meaning
31
Q

P wave

A
  • this wave reflects the electrical activity associated with the impulse originatingfrom the SA node, passage through the atria and subsequent atrial contraction
  • therefore, it represents atrial depolarization after the SA node ‘fired’
  • normally, in lead II, the P wave is positively deflected (the waveform is upright)because the impulse travels from the - RA area (SA node) toward the + LL area
  • the P wave duration is no longer than 0.16 secs (the atria require < 0.16 secs tocontract)
  • if a P wave is present with each beat and each P wave is normal in shape andsize, it can be correctly assumed that each stimulus originated in the SA nodeand depolarized the atria normally
  • when examining P waves, there are 3 questions to consider:
  • 1) is there a P wave before each QRS?.. Answer should be Yes…
             because the atria should depolarize before the ventricles
  • 2) do all the P waves look the same?.. Answer should be Yes…because the
             SA node should initiate every impulse the same way and transmit
    
             each impulse through the atria the same way
  • 3) are there any extra P waves?.. Answer should be No…because the atria
             should only depolarize once with each ventricular contraction
  • if a P wave is absent or abnormal, the atria did not contract or contractedabnormally, indicating that the impulse originated from somewhere other thanthe SA node with abnormal conduction through the atria
32
Q

QRS complex

A
  • the QRS complex represents ventricular depolarization
  • the QRS should be narrow with a duration of < 0.10 secs (2½ small boxes)
  • it is measured from the beginning of Q wave to the end of the S wave (fromwhere the complex leaves the baseline to the time it returns to the baseline)
  • not every ventricular complex has a Q, an R, and an S, but they are still referredto as QRS complexes
  • variations can be: QR, RS, or only a Q wave or an R wave
  • the Q wave is the first negative deflection below the baseline
  • the R wave is the first positive deflection above the baseline
  • the S wave is a negative deflection, that follows the R wave
33
Q

T wave

A
  • represents the major portion of the ventricular recovery phase, after contraction
  • therefore, it represents ventricular repolarization
  • normally, in lead II, the T wave is upright (a positive deflection)
  • it should deflect in the same direction as the majority of the QRS complex
  • it should not exceed 5mm amplitude
34
Q

U wave

A
  • this is a small wave of low voltage that sometimes follows the T wave
  • the U wave is not always present, with each patient
  • when present, the U wave deflects in the same direction as the T wave
  • it is no greater than ¼ the height of the T wave
  • the cause and clinical significance is not well understood
  • may possibly represent repolarization of the purkinje fibers
  • clinically, U waves are often seen in hypokalemic states
35
Q

Intervals and Segments

A

PR interval

ST segment

QT Interval

36
Q

PR interval

A
  • this interval represents the period of time for depolarization to spread from theSA node, through the atria, AV node, the AV junction and reach the ventricles
  • it is measured from the beginning of the P wave to the beginning of the QRS
  • the normal PR interval is 0.12 to 0.20 seconds (3 to 5 small boxes)
  • if the PR interval is prolonged, there is an abnormality in conduction betweenthe atria and the ventricles (it took too long for the impulse to get from the SAnode through to the ventricles)
  • measure the length of each PR interval, and assess for consistency:
  • PRs are all the same length (constant PR interval)
  • PRs are not all the same length (variable PR interval)
37
Q

ST segment

A
38
Q

QT Interval

A
  • represents the time frame for the total ventricular depolarization andrepolarization process
  • so, the QT is measured from the beginning of the QRS to the end of T wave
  • a normal QT interval is < 0.44 seconds
  • a standard rule of thumb: the QT should never be > than ½ the RR interval
  • QT lengthening can be the result of:
  • medications (ie: procainamide, quinidine)
  • bradycardia (slow heart rates)
  • hypokalemia
  • hypomagnesia
  • a long QT interval can lead to life-threatening arrhythmias, such as a form of VTcalled ‘torsade-de-pointes’ (discussed in Lesson 4)
39
Q

Why do arrhythmias occur?

A

Arrhythmias occur for 2 main reasons:

1) Disturbances in impulse formation
- an abnormal site of impulse origin
ie. ) impulses originate somewhere other than the SA node
- an abnormal mechanism of impulse formation
ie. ) too fast, too slow or irregular impulse formation
2) Disturbances in conduction
- when the SA node initiates impulses normally, but there is an abnormal delay or

block in their conduction from the SA node through to the ventricles

40
Q

STEPS TO RHYTHM INTERPRETATION

A

Each rhythm strip should be studied systematically and in an orderly fashion

The order in which a rhythm strip is analyzed is not as important as ensuring all the steps are included

It is important to analyze the entire strip, not just one or two beats

41
Q

1) Calculate Heart Rates

A

The following data explains the principles behind rate calculations:

  • standard ECG and rhythm strip paper is graphed as follows:
  • 1 small box represents 0.04 seconds
  • 1 large box = 5 small boxes (where the lines are bolded)
  • so, 1 large box represents 0.20 seconds (0.04 sec x 5 = 0.20 seconds)
  • therefore, 5 large boxes represent 1 second (0.20 sec x 5 = 1 second)
  • if 5 large boxes = 1 second, then 15 large boxes = 3 seconds (on the ECGpaper, there is a small marking on the paper, at every 3 second interval)
  • if 15 large boxes = 3 seconds, then 30 large boxes = 6 seconds
  • when calculating the radial pulse, we often count for 30 seconds, and multiplyby 2 to equal 60 seconds (1 minute)
  • this same principle is used when calculating heart rates on the cardiac monitor’sprintout (the rhythm strip)
42
Q
  • to calculate the AR (atrial rate)…
A
  • P waves indicate that the atria have contracted
  • count the number of P waves in a 6 second strip (30 large boxes) and multiplyby 10 to determine the rate per 60 sec (1minute)
43
Q
  • to calculate the VR (ventricular rate)…
A
  • QRS complexes represent contraction of the ventricles
  • count the number of QRS complexes in a 6 second strip (30 large boxes) andmultiply by 10 (counting the tops of the R waves is the easiest)
44
Q
  • with any regular rhythm, the following 2 methods may also be used:
A
  • atrial rate:
  • divide the number of large boxes between 2 P waves, into 300
  • divide the number of small boxes between 2 P waves, into 1500
    - ventricular rate:
  • divide the number of large boxes between 2 QRSs, into 300
  • divide the number of small boxes between 2 QRSs, into 1500
  • dividing the number of P waves into the numbers of boxes between the P wavesis not accurate with irregular rhythms, because of the variations in PP intervals
  • dividing the number of R waves into the numbers of boxes between the R wavesis not accurate with irregular rhythms, because of the variations in RR intervals
45
Q

2) Determine Rhythm Regularity

A
  • if the SA node generates impulses on a regular basis, the heart contractsregularly, and the rhythm should be regular
  • both atrial regularity and ventricular regularity can be determined
  • the rhythms are deemed regular if the waveforms occur at regular intervals, orat intervals with slight variances of < 0.12 seconds
  • both the atrial and ventricular rhythms should occur at regular intervals
  • to assess regularity of the atrial rhythm, measure the distances between everyP wave (the PP intervals)
  • if they occur at regular intervals with a variance of < 0.12 seconds, the atrialrhythm is considered regular
  • to determine the ventricular rhythm, measure the distances between each QRScomplex (the RR intervals)
  • if the RR intervals occur regularly with a variance of < 0.12 seconds, theventricular rhythm is regular
  • when using calipers to assess regularity, rotate the calipers from leg to legrather than lifting the calipers off the rhythm strip
46
Q

2) Determine Rhythm Regularity (cont’d)

A
  • another option is with the use of a scrap piece of paper…
  • place the paper along the rhythm strip with the ECG waveforms still visible
  • on the scrap paper, draw lines to indicate where 3 consecutive P waves arelocated, to determine atrial regularity
  • move your paper back and forth along the entire rhythm strip
  • if the atrial rhythm is regular, the marks you drew on your scrap paper will‘line up’ with all the other P waves on the rhythm strip
  • repeat this same procedure, this time using the QRS complexes to assessventricular regularity
  • using the tops of the R waves is the easiest way to measure the distancesbetween the QRS complexes, hence the term RR intervals
47
Q

3) Examine the P Waves

A
48
Q

4) Examine the PR Intervals

A
49
Q

5) Examine the QRS complexes

A
  • examine each QRS complex and assess for normal characteristics and criteriaas previously noted
  • do all the QRS complexes look the same
  • are they all narrow (less than 0.10 seconds)
  • is there a QRS complex after each P wave
50
Q

6) Examine the Remaining Waves, Segments, Intervals

A
  • examine T waves, U waves (if present), ST segments, and QT intervals
  • assess for criteria and normal characteristics as previously noted
51
Q

NORMAL SINUS RHYHM (NSR)

A
  • it is important to understand NSR, as this is the yardstick against which all otherrhythms are analyzed
  • NSR is used to describe a rhythm that “fits” all the normal rate, rhythm, waveform,and interval criteria and characteristics:

1) the HR is 60-100: the SA node is initiating impulses at a normal rate of

60-100 times per minute

2) regular rhythm: the SA node initiates impulses at regular intervals, at a

               regular pace

3) normal P waves: the atria depolarize normally
4) constant PR intervals of 0.12 sec to 0.20 sec: the time required for the

impulse to transmit from the SA node to the ventricles is normal

5) narrow QRS complexes of < 0.10 seconds: the ventricles are

depolarizing normally, taking < 0.10 seconds to contract

52
Q

General Rules for Arrhythmia Treatment

A
53
Q

Other Important Points

A
54
Q

Lesson Summary:

A

The most common cardiac enzymes assessed are the CK, AST and LDH.

Troponin I is specific to cardiac tissue, and its elevation indicates cardiac muscle damage.

Lipoproteins are usually fractionated. This is done by analysis of HDL (good lipoprotein) and LDL (bad lipoprotein).

Coagulation tests are performed as a baseline prior to fibrinolytic therapy, and to assess the effectiveness of anticoagulation therapy.

PTT helps ensure effective Heparin therapy.

PT and INR monitor the effects of oral anticoagulation (Warfarin/Coumadin).

Depolarization is the cardiac cell’s state of excitability.

Repolarization is the cell’s state of returning to rest.

Each small square on the ECG paper represents 0.04 seconds.

The P wave represents atrial depolarization, and the QRS complex indicates that the ventricles are depolarizing.

The T wave reflects ventricular repolarization.

The U wave possibly represents repolarization of the purkinje fibers and may not be present.

The PR interval represents the length of time required for an impulse to travel from the SA node until it reaches the ventricles.

The QT interval represents the time frame for the total ventricular depolarization and repolarization processes to occur