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TCAD - Multi-lead ECG
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- 2. Goals ▪ Improve patientoutcomes by reducing time from first medical contact to PCI. ▪ Improve protocol compliance. ▪ Improve ECG interpretation skills of ALS providers.
- 3. Objectives ▪ Describe thedifference between monitoring and assessing. ▪ Describe the importance of early ECG acquisition and transmission. ▪ Demonstrate proper lead placement for a 12- and 15-lead ECG. ▪ Describe a systematic approach of 12-lead interpretation.
- 4. Monitoring vs Assessing Monitoring ▪The purpose of “monitoring” is to identify any changes in the patient’s heart rhythm. ▪ Does not diagnose! ▪ Lead placement doesn’t matter. ▪ Stick one on the nose and one on the toes…. V-Fib and asystole will look the same. Assessing ▪ Evaluating electrical changes in a multi-lead ECG. ▪ Identifying useful and potentially life-saving information. ▪ Utilizing this information to prepare your treatment plan ▪ Proper lead placement is absolutely crucial!
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- 6. Obtaining quality tracings ▪Prepare the skin ▪ Clean and dry the skin ▪ Shave any excessive hair ▪ Gently scrape skin to remove surface layer of dead cells ▪ Position the patient ▪ Supine is best. Fowler’s or semi-fowlers is acceptable. ▪ Serial ECG’s should be in same position. ▪ Place limbs on supportive surfaces ▪ Patient should be comfortable and relaxed.
- 7. Obtaining quality tracingscont… ▪ Stop the vehicle ▪ Secure the trunk cable to the patient’s clothing ▪ Position cables and/or lead wires to prevent pulling away from the patient ▪ Ensure the electrodes are not dried out Most poor tracings are the result of poor electrode- skin contact and can be resolved with proper skin preparation.
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- 9. Lead Placement ▪ Limbleads ▪ RA/LA on forearm proximal to wrist ▪ RL/LL on lower leg proximal to ankle ▪ Avoid boney prominences and major muscle groups ▪ Precordial leads ▪ V1 – 4th intercostal space right of the sternum ▪ V2 – 4th intercostal space left of the sternum ▪ V3 – Directly between V2/V4 ▪ V4 – 5th intercostal space at midclavicular line ▪ V5 – Level with V4 at left anterior axillary line ▪ V6 – Level with V5 at left midaxillary line (V4, V5, and V6 should be in a straight line)
- 10. Locating V1 ▪ Placeyour finger at the notch in the top of the sternum. ▪ Move your finger slowly downward about 1.5 inches to the Angle of Louis. ▪ Move lateral and just below the Angle of Louis to the 2nd intercostal space. ▪ Move your finger down two more intercostal spaces to the 4th intercostal space.
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- 12. P Waves ▪ PWave: ▪ The first positive deflection from the isoelectric line ▪ Represents Atrial depolarization ▪ Normal P wave morphology: ▪ Smooth contour ▪ Monophasic in lead II ▪ Biphasic in V1 ▪ Normal P wave axis is between 0° and +75° ▪ P waves should be upright in leads I and II, inverted in aVR ▪ < 120 ms (duration) ▪ < 2.5 mm in the limb leads (amplitude) ▪ < 1.5 mm in the precordial leads (amplitude)
- 13. Q Waves ▪ QWave: ▪ The first negative deflection from the isoelectric line ▪ Represents the normal left-to-right depolarization of the interventricular septum ▪ Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6) ▪ Small Q waves are normal in most leads ▪ Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant ▪ Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3) ▪ Considered pathological if: ▪ > 40 ms (1 mm) wide ▪ > 2 mm deep ▪ > 25% of depth of QRS complex ▪ Seen in leads V1-3
- 14. Other Waves ▪ RWave: ▪ The first positive deflection from the isoelectric line ▪ S Wave: ▪ The first negative deflection from the isoelectric line after the R wave ▪ R Prime Wave: ▪ The second positive deflection in a QRS complex ▪ QS Wave: ▪ The entire complex is negative (there is no R wave to help identify the Q or S wave) ▪ Delta Wave: ▪ A slurred upstroke in the QRS complex
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- 16. Systematic Approach To 12-Lead ECGInterpretation
- 17. Systematic Approach ▪ Identifythe underlying Rhythm (Lead II) ▪ In wide-complex tachycardia use the VT criteria ▪ Evaluate the Axis for deviation and hemiblocks ▪ Determine the presence of a Bundle Branch Block (BBB) ▪ Using ISAL, determine infract location. ▪ Secondary Survey
- 18. Identifying VT ▪ 12-leadECG is 96% diagnostic for VT identification. ▪ Lead II is only 34% accurate for diagnosing VT. ▪ A-fib with WPW and SVT with BBB are often misdiagnosed as VT.
- 19. VT using axiscriteria ▪ ERAD w/positive deflection in V1 = VT ▪ Upright V1 is one of three criteria ▪ Big mountain, little mountain ▪ Steep peek (“steeple”) ▪ Slurred downstroke (fireman’s hat) ▪ RAD w/negative deflection in V1 = VT ▪ Fat R wave (>40ms) ▪ Notched or slurred downstroke ▪ Pathological LAD w/positive V1 ▪ In patients with previous MI
- 20. Other VT indicators/criteria ▪Concordance in precordial leads. ▪ Negative concordance suggests VT. Be sure to determine if the rhythm is atrial in origin. A LBBB can be negative concordance. ▪ Positive concordance may indicate either VT or WPW. Must rule out WPW before determining VT. ▪ AV dissociation ▪ Cannon A waves ▪ P waves out of place ▪ Different S1 heart sound
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- 23. Axis and Hemiblocks ▪The Axis is the direction of flow of the electrical impulses.
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- 25. Axis Deviation Causes ▪Left Axis Deviation ▪ Normal variation ▪ Mechanical shifts from expiration, ascites, abdominal tumors, high diaphragm from pregnancy, obesity, etc. ▪ Left anterior hemiblock ▪ LBBB ▪ WPW syndrome ▪ Hyperkalemia ▪ Right Axis Deviation ▪ Mechanical shifts from inspiration, emphysema ▪ RVH ▪ RBBB ▪ Left posterior hemiblock ▪ WPW syndrome ▪ Pulmonary embolism ▪ Arrhythmias
- 26. Axis and HemibockChart Axis Lead I Lead II Lead III Notes Normal Axis 0° to 90° Physiological Left Axis 0° to -40° Pathological Left Axis -40° to -90° Anterior Hemiblock Right Axis 90° to 180° Posterior Hemiblock Extreme Right Axis >180° Ventricular in origin
- 27. Bundle Branch Blocks ▪Two types ▪ LBBB ▪ RBBB ▪ Diagnosed in lead V1 ▪ QRS complex width >120 ms (0.12 sec) ▪ Use the Turn signal approach
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- 30. Bifascicular blocks ▪ Abifascicular block is a blockage of two of the three pathways to contract the ventricles in an organized fashion. ▪ A LBBB is always a bifascicular block. ▪ An anterior or posterior hemiblock with a RBBB is also a bifascicular block
- 31. Trifascicular blocks Combination RBBLAD LPD ECG 1 C C C Complete AVB 2 C C I RBBB + LAH + AVB 3 C I C RBBB + LPH + AVB 4 I C C LBBB + AVB 5 C I I Various combinations depending upon relative degrees of incomplete fascicular block 6 I C I 7 I I C 8 I I I ** C = completely blocked, I = incompletely blocked, and AVB = manifestations of first or second degree A-V block
- 32. I See AllLeads
- 33. ST Changes ▪ Measurefor ST changes 1 mm past the J-point (40 ms) ▪ Must be >1 mm to be significant ▪ Must occur in two or more contiguous or continuous leads
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- 35. Ischemia, Injury, andInfarction ▪ Ischemia – lack of oxygen ▪ Represented by T-wave inversion ▪ Increased T-wave amplitude ▪ ST-segment depression ▪ Injury – “Acute MI” ▪ Represented by ST-segment elevation ▪ Infarction – Necrosis/dead ▪ Represented by pathological Q-waves ▪ Q-wave is wider than .04 sec ▪ Q-wave is greater than 1/3 the entire QRS complex
- 36. AMI Locator • Inferior= RCA • Leads II, III, aVF • Reciprical I, aVL • Septal = LAD • Leads V1, V2 • Anterior = LAD
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- 38. What to expect ▪Anterior MI – LAD ▪ Most lethal, highest mortality. “Widow Maker” ▪ Can develop Complete Heart Block, VF, or VT ▪ If presents with hemiblocks or BBB; apply combo pads and prepare for the worst ▪ Can extend into the septum and/or lateral walls ▪ Nitrates are great! ▪ Spare the fluids
- 39. What to expect ▪Inferior MI - RCA ▪ Most common seen ▪ Can be very lethal ▪ 50% have posterior and/or right ventricle involvement and hypotension ▪ Could also have 1st degree AV block or 2nd degree type 1 AV block ▪ Nausea is common ▪ Look for RVI with V4R ▪ Nitrates with caution ▪ Fluids may be needed to support BP
- 40. 15-lead ECG ▪ Canlocate isolated posterior MI ▪ ST segment depression in V1 is good indicator (reciprocal changes) ▪ Use V8 and V9 and V4R ▪ Should be done on all Inferior MI to look for Right Ventricular infarction. ▪ 50% of Inferior MI have posterior and/or right ventricle involvement ▪ RVI is a preload problem and could cause dramatic hypotension with nitrates. ▪ Clinical signs of RVI include JVD, dry lungs, and hypotension
- 41. 15-Lead ECG • V4R– 5th intercostal space midclavicular line (same as V4 but on the other side) • V8 – On the back, 5th intercostal space midscapular line. • V9 – On the back, 5th intercostal space between V8 and the spine. • Move V4 to V4R • Move V5 to V8 • Move V6 to V9 • Run a second ECG • Label the different leads.
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- 43. LBBB…now what? ThinkQRS ▪ Q waves seen in at least two lateral leads (I, aVL, V5, V6) ▪ R wave regression seen from leads V1-V4 ▪ Late notching of the S wave in at least 2 of leads V3-V5 I aVL V5 V6 V1 V2 V3 V4
- 44. AMI in LBBB ▪Gusto-1 trial ▪ Look for three things ▪ Is there ST-segment elevation >=1mm and is concordant with QRS axis? ▪ Is there ST-segment depression >=1mm in V1, V2, or V3?
- 45. AMI in LBBBcont… ▪ Is there ST-segment elevation >=5mm discordant from the QRS axis? ▪ Yes to two or more of these questions shows a greater than 90% chance the patient is having an AMI.
- 46. Atrial Abnormalities ▪ RightAtrial Enlargement (RAE) ▪ Tall, Pointed P waves in Inferior leads >2.5mm ▪ Think 3 P’s… Pointed, Prominent, Pulmonary ▪ Causes of RAE ▪ Congenital heart disease ▪ Tricuspid or pulmonary valve disease ▪ Pulmonary hypertension ▪ Implications: ▪ Generally not an acute problem ▪ Frequently seen with Right Ventricular Hypertophy ▪ Can be seen with other criteria indicating more severe problems, i.e. pulmonary embolism
- 47. Atrial Abnormalities ▪ LeftAtrial Enlargement (LAE) ▪ Lead II: widened P wave with a notched or “m” shaped appearance ▪ Lead V1: broad, terminal negative P deflection of more than 1 mm. ▪ Causes of LAE ▪ Hypertension ▪ Pulmonary edema ▪ LVH ▪ AMI ▪ Mitral or aortic valve stenosis ▪ Implications ▪ See causes… no treatment of the specific problem.
- 48. Ventricular Hypertrophy ▪ RightVentricular Hypertophy ▪ Caused by increased pressure in the right ventricle ▪ ECG findings: ▪ RAE ▪ Narrow QRS ▪ Right Axis Deviation ▪ R wave height in V1 >7mm ▪ Asymmetrical downsloping ST segment in inferior leads. “Strain” ▪ Implications: ▪ Not an acute problem ▪ Similar causes as RAE
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- 50. Ventricular Hypertrophy ▪ LeftVentricular Hypertrophy (LVH) ▪ Caused by increased pressure or volume in the left ventricle. ▪ Often found in: ▪ HTN ▪ AMI ▪ Ischemic heart disease ▪ Cardiomyopathy ▪ ECG Criteria: ▪ LAE (this plus any other QRS voltage criteria is diagnostic) ▪ QRS is generally narrow or slightly widened with “strain” ▪ Axis is usually normal
- 51. Ventricular Hypertrophy ▪ LeftVentricular Hypertrophy (LVH) cont… ▪ Voltage Criteria: ▪ Rule of 35 ▪ Measure the deepest S wave from either V1 or V2; add this number to the tallest R wave of lead V5 or V6. If this number is greater than 35, and the patient is at least 35 years old, then criteria is met. ▪ R wave in Lead aVL is >11mm ▪ R wave >20 mm in inferior leads ▪ R wave >20 mm in V6 ▪ R wave >25 mm in V5 ▪ S wave > 25 mm in V1 or V2 ▪ If complexes look large, assume hypertrophy. Look for evidence of “strain”
- 52. “Strain” ▪ Strain isthe hallmark presentation of hypertrophy. ▪ A strain pattern is to hypertrophy what reciprocal changes are to ST elevation; they clinch the diagnosis. ▪ Strain is evidenced by asymmetrical ST depression and T wave inversion that almost looks biphasic. ▪ Best seen in lateral or inferior leads. (II, III, aVF, V5, or V6)
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- 54. Ventricular Hypertrophy ▪ Concernswith LVH ▪ Patients with LVH have a higher incidence of sudden death and ischemic arrhythmias ▪ It can mimic the ST depression or elevation seen with myocardial ischemia ▪ It may be caused by AMI ▪ In the presence of LBBB, LVH criteria are not determined ▪ May be a useful clue as to hemodynamic condition
- 55. Electrolyte Disturbances ▪ Potassium(K+) ▪ Hypokalemia ▪ Serum levels below 3.5-5 mEq/L ▪ Common causes include vomiting, diarrhea, and diuretics ▪ Common signs and symptoms include ▪ Muscle weakness ▪ Polyuria ▪ Atrial flutter, heart blocks and bradycardia ▪ ECG findings ▪ ST segment depression ▪ T waves flattened or joined with U waves ▪ U waves get larger than T wave as potassium drops ▪ QT interval appears to lengthen ▪ PR interval increases
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- 57. Electrolyte Disturbances ▪ Potassium(K+) ▪ Hypokalemia treatment ▪ Monitor ECG ▪ Increase dietary intake of potassium ▪ In severe cases, IV KCL
- 58. Electrolyte Disturbances ▪ Potassium(K+) ▪ Hyperkalemia ▪ Serum levels above the normal range (3.5 – 5.0 mEq/L) ▪ Most commonly caused by renal failure ▪ SA node can quit at 7.5 mEq/L ▪ VF or asystole at 10-12 mEq/L
- 59. Electrolyte Disturbances ▪ Potassium(K+) ▪ Hyperkalemia ECG findings ▪ Mild cases (<6.5 mEq/L) ▪ Tall tented “peaked” T waves with narrow base ▪ Normal P waves ▪ Best seen in leads II, III, V2 and V4 ▪ Moderate cases (<8 mEq/L) ▪ QRS widens ▪ Broad S waves in V leads ▪ LAD ▪ ST segment is gone, contiguous with the peaked T waves ▪ P waves start to go away ▪ Severe cases (>8 mEq/L) ▪ P waves disappear ▪ Sine waves
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- 61. Electrolyte Disturbances ▪ Potassium(K+) ▪ Hyperkalemia Treatment ▪ Sodium Bicarb 100-150 mEq added to 1 Liter bag of NS ▪ Consider IV Calcium Gluconate 10% 10-30 ml IV over 1-5 minutes ▪ Consider Glucose 10% 200-500 ml in 30 minutes and 500-1000 ml over the next several hours
- 62. QT Interval ▪ QTinterval represents the time from start of depolarization of the ventricles to the end of repolarization. ▪ Measured from the start of the QRS complex to the end of the T wave. ▪ Causes of Prolonged QT interval include: ▪ Hypokalemia, Hypocalcemia ▪ Drugs: quinidine, amiodarone, tricyclics, disopyramide, phenothiazines ▪ Liquid protein diets, myocarditis, AMI, LVH, hypothermia ▪ Causes of Shortened QT interval include; ▪ Hypercalcemia, Digitalis therapy
- 63. QT interval QT IntervalTable Heart Rate R-R Interval QTc and Range 40 1500 460 (410-510) 50 1200 420 (380-460) 60 1000 390 (350-430) 70 860 370 (330-410) 80 750 350 (320-390) 90 670 330 (300-360) 100 600 310 (280-340) 120 500 290 (260-320) 150 400 250 (230-280) 180 330 230 (210-250) 200 300 220 (200-240)
- 64. Pericarditis ▪ S/S ofPericarditis ▪ Chest pain, dyspnea, tachycardia, FEVER, weakness ▪ CP can be sharp and severe ▪ Made worse by LYING Flat, better by SITTING UP ▪ Pain for hours or days ▪ 90% have ECG evidence ▪ ECG findings include: ▪ ST segment elevation ▪ Concave (curved up) in all leads except V1 and aVR ▪ T wave elevation (starts above the isoelectric line) ▪ ST segment depression or T wave inversion ▪ Almost all leads down (later stage)
- 65. Pericarditis ▪ Pericarditis diagnosis ▪Chest pain, pleuritic, relieving factors ▪ No response to NTG ▪ Pericardial rub ▪ ECG changes do not localize an artery (everything up)
- 66. Putting it alltogether Prep the patient (shave, dry, position, calm) Place leads in proper places Analyze ECG Identify rhythm If wide complex use VT criteria Evaluate Axis and Hemiblocks Evaluate QRS width in V1 for BBB LBBB and AMI criteria Evaluate for acute MI ST segment changes I see all leads 15 lead if necessary Treat for Acute MI if present Comprehensive assessment Chamber enlargement Electrolyte changes QT interval Other conditions
- 67. Transmitting ▪ Two typesof transmitting ▪ From Archives ▪ From Home screen ▪ Two types of connections ▪ Direct Connect ▪ Bluetooth ▪ Two types of destinations ▪ To a receiving facility ▪ To a PCR
- 68. Transmitting ▪ To aReceiving Facility ▪ All 12-leads should be transmitted ▪ Generally done from the home screen ▪ Uses the Titan Gateway ▪ Procedure ▪ Obtain a quality ECG ▪ Ensure the Titan Gateway is plugged in ▪ Press Transmit button ▪ Select Report (ie. 12-Lead 1) ▪ Select Site (ie. SRMC Branson) ▪ Send
- 69. Titan Gateway ▪ TitanII Wireless Gateway ▪ Transmits data from the LP15 to the LifeNet system ▪ Connects to the TCADMobile wifi ▪ Only works when plugged in ▪ Only works when in range of the ambulance ▪ Is not a modem ▪ LifeNet system
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- 81. References ▪ Conover, M.B. (1992). Understanding Electrocardiography Arrhythmias and the 12-lead ECG. St. Louis: Mosby Year Book. ▪ Marriott, H. J. (1988). Practical Electrocardiography. Baltimore: Williams & Wilkins. ▪ Page, R. (2005). 12-lead ECG for Acute and Critical Care Providers. Upper Saddle River: Pearson Education, Inc. ▪ Wellens, H. J., & Conover, M. B. (1992). The ECG in Emergency Decision Making. Philadelphia: W.B. Saunders Company.
Editor's Notes
- #3 The STEMI committee at CMCB has worked hard to develop and implement the Code Stemi protocol which is designed to reduce the door to PCI time of patients having an acute MI. Part of the algorithm allows for the ED physician to activate the Cath lab based on the report of the paramedic providing pre-hospital care. It is vital, for two reasons, that we are able to accurately interpret the ECG’s we are running. First, we do not want to misdiagnose a patient and provide inappropriate care, and second we want to limit false activations of the cath lab. Through call review and CQI, it has also been determined that as a general rule, we do a poor job of obtaining quality ECG’s. Poor ECG’s are difficult if not impossible to diagnose and cause delays in patient care. For these reasons, we are going to spend some time learning how to obtain quality ECG’s through proper lead placement and patient prep. We will also review the basics of ECG interpretation and dive into some non-acute ECG findings that could benefit you and the patient in proper diagnosing and treatment plans.
- #11 The Angle of Louis is where the manubrium joins the body of the sternum. (Manubrium is in green and the Body of the sternum is in blue) When moving your finger down the manubrium from the sternal notch, you should feel a slight horizontal ridge or elevation. This is the Angle of Louis. Just below and lateral is the 2nd intercostal space.
- #17 When we evaluate an ECG, it is important that we utilize a systematic approach. This way we evaluate the same aspects of the ECG each time and nothing is overlooked. If you stopped an just one of the leads and don’t look at the big picture you will misdiagnose the findings.
- #18 These 4 steps will provide you with the important information for the acute management of the cardiac patient. We will spend a little time on each of these items. Then we will address the non-acute aspects of the 12-lead in the secondary survey
- #19 2000 AHA Guidelines put an end to “unknown origin wide complex tachycardia.” They now call for a 12-lead ECG to attempt to diagnose the specific rhythm. This is to discourage the “give a drug and see what happens approach.” Dr. Marriott had a compelling study that demonstrated that Lead II’s diagnostic accuracy for VT as being 34%. That means when faced with a decision about a wide complex rhythm in Lead II, you would guess wrong 66% of the time.
- #24 After identifying the rhythm, we look at the axis. So what is an axis? Axis can be defined as the general direction of electrical impulses as they travel through the heart. Normally this electrical path is from upper right to lower left. The axis may be “normal” or may have a left or right “axis deviation”. The QRS axis is calculated by taking the sum of all the currents generated within the ventricles during electrical systole. These measurements are the positive or negative amperage generated by the electrical impulse of the heart as measured by each limb lead. As the impulse move toward the positive electrode it makes a positive deflection on the ECG, and a negative or downward deflection as it moves away. Assessing the direction, or axis, of these impulses provides clues about the severity of a patient’s condition.
- #25 To calculate the numerical axis, one must know the “hexaxial reference system.” By taking the three sides of Einthoven’s triangle each of which represents one of the standard limb leads and rearranging them so that they bisect each other, we obtain a “triaxial reference system.” If we add to this three further lines to represent the unipolar limb leads (avl, avr, avf), the final figure consists of six bisecting lines, each representing one of the six limb leads. As an electrical impulse travels through the heart, it will write the largest deflection (positive or upward) on the lead whose line of derivation is parallel to the impulse’s path, and it writes the smallest deflection on the lead perpendicular to it. Remember that we are evaluating the QRS complex, which represents the electrical impulses in the ventricals.
- #28 Now that we know the rhythm, the axis, and whether or not there is a hemiblock, let’s evaluate to see if there is a Bundle Branch Block A BBB is an electrical phenomenon characterized by a widened QRS complex of at least 0.12 seconds (120 ms). A BBB is diagnosed from an ECG and differential diagnosis is most easily made in V1. The bundle branch system is an important part of the ventricular depolarization syncytium, the feature of the ventricles (or atrium) that produces simultaneous depolarization. The result being an organized contraction. The bundle branch system is made up of two branches. The right bundle branch and the left bundle branch. The right bundle branch is a single branch, while the left bundle branch divides into anterior and posterior hemifascicles. Blood supply for the bundle branches usually comes from the Left Anterior Descending artery, but can also be from the AV nodal artery of the right coronary artery. Compromised oxygenated blood supply to the cardiac conduction system can slow or even stop the conduction of impulses.
- #33 This is what is often referred to as the secondary survey of a 12-lead. Accomplished by using the phrase “I See All Leads.” The first letter of each word representing the order of the lead groups. Inferior, Septal, Anterior, Lateral. Looking for the ST changes related to acute MI. This also reminds us to look at ALL leads, and not stop at the first sign of trouble.
- #38 The Right Coronary Artery (RCA) supplies the inferior wall of the left ventricle. Supplies oxygenated blood to the SA node in 50% of people, the AV node in 90% of people and the Right ventricle. The Posterior Descending Artery (a branch of the RCA) supplies the posterior fascicle of the left bundle branch, and the posterior wall of the left ventricle. The Left Anterior Descending Artery (LAD) known as the “Widow Maker” supplies the anterior wall of the left ventricle, the intraventricular septum, the Right bundle branch, and the Left bundle branch. The Left Circumflex Artery (LCA) supplies the lateral wall of the left ventricel, the SA node in 50% of patients, the AV node in 10% of patients, and the posterior wall of the left ventricle.
- #70 What happens after you hit send? The LP is connected to the Titan II Gateway via a serial cable. The Titan is connected to the ambulance router via wifi (specifically TCAMobile). The router is connected to the modem (airlink) via LAN network cable. Modem connects to the internet via cell signal. Data is transmitted from the LP through these connections over the internet to the LifeNet system, basically a cloud server, that then directs the data to a receiving target (site). The target then directs the data to where it wants it to go. For example: If you select SRMC Branson (Cox Branson), once the data hits the receiving target, it is directed to the ward clerk, the charge nurse, and the cath lab (depending on criteria set). This is also how the data is received by Clinical Department through the LifeNet Connect.
- #72 Sinus Rhythm Normal Axis No BBB ST elevation II, III, aVF ST depression V2, V3, V4, Inferior MI Do a 15-lead
- #73 VT
- #76 Sinus rhythm with bigeminy unifocal pvc’s Normal Axis LBBB No Q waves in lateral leads No R wave regression No S wave notching in V3-5 No indication of acute MI
- #77 Sinus rhythm with 1st degree AV block Right axis deviation (posterior hemiblock) LBBB No indication of Acute MI
- #80 Sinus rhythm Normal axis No BBB ST elevation V2, V3, V4, V5
- #81 Sinus rhythm Physiologic LAD (no hemiblock) No BBB T wave elevation, with U shaped st-segments in V2, V3, V4, V5, V6, I, II, aVL Pericarditis