ELECTROCARDIOGRAM (ECG)

Prepared by: Leonardo P. De Guzman III, RN,MAN ELECTROCARDIOGRAM (ECG or EKG) Is non invasive diagnostic procedure that measures the electrical activity of your heart. The heart generates electrical signal which flows out from your heart through your body. Small electrical sensors called electrodes that are put on your skin can sense the electricity that began in your heart. The electrical activity is then turned into a graph. This can give doctors an idea of whether your heart is beating normally. An ECG is used to: Diagnose heart attacks and rhythm problems Offer clues about other heart conditions and conditions not primarily related to the heart Detect conditions that alter the bodys balance of electrolytes (eg, potassium and calcium) Detect other problems, such as overdoses of certain drugs ASSESSMENT Chest pain - need to note the TIMING, QUALITY, QUANTITY, LOCATION, PRECIPITATING OR AGGRAVATING FACTORS, RELIEVING FATORS, ASSOCIATED MANIFESTATIONS ELECTROLYTE IMBALNCE EX: Potassium (K) Calcium (Ca) Patients previous cardiac history

Components of ECG Tracing P-WAVE - First component of a normal ECG ; & always precedes the QRS waves.

- Represents that Atrial Depolarization (stimulation) has occurred & the impulse originated in the SA node at the atria. - Time duration- between 0.6 to 0.11 seconds. -Configuration- usually rounded & upright. - Variance of P Wave: Peaked P-wave- signify right atrial hypertrophy Broad or Notched P wave- associated with left atrial hypertrophy. Inverted P wave- indicate impulse not coming from SA node meaning not from the pacemaker but from AV or junctional areas. Varying P waves- if the shapes & sizes of P wave very, the impulse may be originating at various sites, at times caused by irritability in the atrial tissue or damage near the SA node. Missing P wave- if a P wave doesnt precede each QRS complex, a third degree AV block is suspected. P-R INTERVAL - Represents the activity from the beginning of atrial depolarization to the beginning of ventricular depolarization; or it is the time it takes an impulse to travel from the SA node through the atria & to AV node down to the bundle branches. - Time duration about 0.12 to 0.20 seconds ( 3-5 small squares) SIGNIFICANCE The PR interval can provide some evidence of an impulse formation or conduction delay disturbance such as AV Blocks. The PR interval varies with the HR shortens with Tachycardia & lengthen with Bradycardia. VARIANCE: a. Short PR interval- indicates that the impulse originated in other areas like the AV junction but not the SA Node. b. Prolonged PR interval- indicates impulse is delayed as it passes through the AV node but there are blocks such as 1st degree heart block. Or cardiac toxicity. QRS COMPLEX: Represents ventricular depolarization that follows the PR interval. Configuration differs in all 12 leads Time duration: 0.06 to 0.10 seconds adult.

Q- having negative deflection; R-positive deflection & S-negative deflection VARIANCE: 1. If QRS longer than 0.10 sec & P-wave not apparent- signify the impulse probably originated in the ventricle indicating a Ventricular Arrhythmia 2. If QRS longer than 0.10 second but P wave apparent- signify impulse most likely is of supra ventricular in origin & is delayed in the ventricle due to a conduction defect such as BBB. And with BBB- QRS configuration show an extra notch in RS wave. 3. QRS complex does not appear or is missing after each P wave- we suspect a condition in which the impulse conduction to the ventricle is being interrupted such as AVB or Ventricular Standstill. T-WAVE : Represent ventricular repolarization; where the hearty cells can regain (-) charge; here the cells are readying to be depolarized again; cells here are vulnerable to another strong stimuli Configuration- round & symmetrical. VARIATIONS: 1. Inverted T-wave to some lead is normal; however, but for L1,L2,L3 & V6 indicative of myocardial ischemia. 2. Peaked T wave- indicative of Hyperkalemia ( Tented P wave) 3. Notched T wave- indicative of Pericarditis in adult but is normal for children. 4. Varied T wave- indicative of electrolyte imbalance (may be large & small ). QT INTERVAL Represent ventricular depolarization & repolarization ; this extends from the beginning of the QRS complex to the end of the T wave. Time duration- between 0.36 to 0.44 seconds RULE OF THUMB: QT interval should not be greater than the distance between consecutive R wave ( called the R-R interval) within a regular rhythm. VARIANCE: 1. Shortened QT interval indicative of Hypercalcemia 2. Prolonged QT interval indicative of: a.)Congenital anomaly

b.)Due to some medication (anti-arrhythmias) c.) Normal for some trained adult athletes d.) Lead to other life-threatening condition ST SEGMENT Represent the end of ventricular depolarization & beginning of ventricular repolarization. SIGNIFICANCE: Any changes in ST segment such as an elevation may indicate MI. VARIANCE: 1. ST segment elevation- indicative of myocardial injury 2. ST depression- indicative of Ischemia 3. ST changes- indicative of inflammatory heart conditions, LVH, PE, Electrolyte imbalance.

SINUS RHYTHM- is a term which is applied when ALL the following criteria are met. This rhythm is consistent with an intact conduction pathway from the SINUS NODE to the VENTRICULAR SONDUCTION SYSTEM. P wave- present, configuration normal, before the QRS Rhythm regular / ( irregular) Rate- 60 100 / minute PR INTERVAL- 0.12-0.20 seconds QRS width- 0.06-0.10 seconds QT INTERVAL- 0.35-0.44 ST Segment- Normal

SINUS TACHYCARDIA: Occurs when sinus node creates an impulse at a faster than normal rate around 100-160 beats/min. ( Rate 160/min-indicate Ectopic Focus) ; but QRS shape/configuration normal. ST is almost same as NSR except for the rate. ETIOLOGY: Sinus Tachycardia (ST) occurs sometimes in a healthy person without seriousness ; but when ST persist or is prolonged needs medical attention. ST persist too long, may be caused by acute blood loss, anemia, shock, hypovolemia, Congestive heart failure, extreme pain, Hypermetabolic states, high fever, too strenuous exercise, too much anxiety. CLINICAL MANIFESTATION: 1. Patient will have a peripheral pulse rate greater than 100 beats/min, but with a regular rhythm. 2. Usually, Pt. will be asymptomatic. However, if Pt.s cardiac output falls & compensatory mechanisms fall, Pt. may experience hypotension, syncope & blurring of vision. INTERVENTION: 1.Unless Pt. shows signs & symptoms of decrease cardiac output or hemodynamic instability, treatment usually isnt required. 2. A symptomatic Pt. may be given drugs such as Propanolol to regulate the HR. But treatment would focus on finding the cause of Sinus Tachycardia.

SINUS BRADYCARDIA Sinus node creates an impulse at a slower than normal rate below 60/min. ECG tracing shows the P,QRST complexes to be normal in size & configuration, except for the lowered rate. SIGNIFICANCE: Many athletes develops sinus bradycardia because their heart are well- conditioned & thus maintain stroke volume with reduced effort.

ETIOLOGY: 1. SB may be seen when Pt. may be in a slower metabolic needs- sleep, hypothermia, hypothyroidism, vagal stimulation activities such as vomiting, suctioning, severe pain ,extreme emotion. 2. In MI Pt. involving the Inferior wall, has a tendency to increase vagal tone & may eventually cause SB. 3. Certain drugs such as anti-cholinesterase, beta blockers, digitalis & Morphine may also cause SB. CLINICAL MANIFESTATION: The Pt. will have a peripheral rate of 60/min and below but have regular rhythm. If Pt. unable to compensate for the decrease in cardiac output- S/S like hypotension, syncope & blurring of vision & palpitation will be manifested. INTERVENTION: If Pt. asymptomatic, treatment isnt necessary, but if symptomatic, treatment should be aimed to identify & correct the underlying cause. Atropine may be given by IV push to regulate the HR. If medical management not effective may have to start Temporary Pacemaker.

PREMATURE VENTRICULAR CONTRACTION- (PVC) In PVC, ventricles are stimulated by an ectopic focus in their walls. They contract too early giving an extra heart beat & because the focus of stimulation is outside the normal pathway, the impulse will travel around the ventricle at a slower rate, resulting in wide & bizarre QRS complex. PVC Ventricular Dysrythmia can cause a decrease in cardiac output which in turn will make the heart work harder to eject the additional blood on the next sinus beat. A PVC may be caused by certain drugs cardiac glycosides & sympathoimmetic drugs such as Epinephrine. Conditions such as electrolyte imbalance, Hypokalemia, hypocalcemia can trigger PVCs. Exercise, ingestion of caffeine, tobacco & alcohol can trigger PVCs . CLINICAL MANIFESTATION:

PR may be normal 60-100/min but it is the rhythm that may be irregular.. When palpating the peripheral pulse, one may feel a longer than normal pause immediately after the PVC. Palpitation, signs of decrease cardiac output- hypotension,syncope & blurring of vision. INTERVENTION: Treatment will depend on the cause of the problem. If PVC results from a cardiac problem- DOC is Lidocaine ( Xylocaine) 50-100mg given by IV Bolus followed by a constant infusion of 1-4mg/min IV drip. If PVC is caused by SB where myocardial irritation triggers its manifestation DOC is Atropine to increase the HR- treating the SB you eliminate the PVC.

VENTRICULAR TACHYCARDIA-( VT ) When 3 or more PVCs occurs in a row & the rate exceeds 100/min this is called VT ; it may be Paroxysmal ( lasting for a few beats) or sustained (longer time). PATHOLOGY: There is no association between the atrial rhythm & ventricular rhythm ; hence, VT develops & ends suddenly. It is a major Arrhythmia, which can reduce cardiac output & lower BP. Here the Pt. may not be able to withstand the increase Myocardial irritability & consequently, V Fib will develop. The rapid ventricular rate of PVCs will lower down the effective ventricular filling time Atrial & vent. Activity are dissociated decrease cardiac output abruptly increase risk for CV collapse lead to V. Fibrillation (Fatal) ECG INTERPRETATION: ECG show series of wide, slightly irregular QRS complexes. Rate: Atrial ( P wave) cannot be determined or looks absent; but is actually obscured by QRS. : Ventricular ( QRS complex) rapid 100-200/min & are very wide. - PR Interval & Q - not measurable ETIOLOGY: VT usually results from Myocardial irritability.

Some cardiac condition can bring about VT such as : AMI, CAD, RHD, Mitral Valve proloapse, Heart Failure & Cardiomyopathy. Non-cardiac conditions- Pulmonary Embolism, electrolyte imbalance, & drug toxicity-digitalis, Quinidine, epinephrine. CLINICAL MANIFESTATION: 1.Pts peripheral pulses is not palpable anymore because rate is too fast- due to low perfusion. S/S of low cardiac output and eventually became unresponsive. INTERVENTION: When you detect VT, immediately check yourpt for responsiveness & LOC. Give immediate treatment. If pt. alert-give lidocaine bolus ; if after medication still not effective may recommend to proceed to Synchronized cardioversion. If pt. suffers CV collapse-loss of consciousness, prepare instead to defibrillate. If you are at pts bedside immediately deliver a single precordial thump, while CPR team are preparing the paddles & awaiting for electrical charge.

VENTRICULAR FIBRILLATION Rapid disorganized & quivering of the ventricles developed because of rapid impulse formation & irregular impulse transmission. The focus of impulse is in the Ventricles but all fire together so there is no organized conduction &no organized contraction. The Ventricles displays those quivering motion & are unable to fill or expel blood with any rhythmic pattern. V. FIB CLINICAL MANIFESTATION: There are no audible heart sounds, no palpable pulses, no response THIS IS A MAJOR ARRYTHMIA may be fatal. This is a MEDICAL EMERGENCY-immediate intervention is necessary or death could occur within minutes. TYPES OF VENTRICULAR FIBRILLATION:

Coarse Fibrillation- indicates more electrical activity in the ventricles than the fine fibrillation. Fine Fibrillation- fibrillatory waves become finer as acidosis & hypoxemia develop. ECG INTERPRETATION: Atrial rate & rhythm cannot be determined. Ventricular rate & rhythm cannot be determine. P wave is indiscernible ; PR interval is also indiscernible. QRS complex duration is indiscernible. T- wave is indiscernible. SIGNIFICANCE: With Ventricular Fibrillation, the ventricles quiver rather than contract. As a result, they fail to pump blood & cardiac output falls to zero. If fibrillation continues, it eventually leads to ventricular asystole or standstill. ETIOLOGY: AMI Cardiomyopathy Drug induced digitalis, quinidine toxicity Irritation from pacemaker electrode Acidosis and Electrolyte Inbalance During Cardiac Cath/ cardiac surgery Immediately following electrocution CLINICAL MANIFESTATION: The pt. will be in cardiopulmonary arrest, so pt will be unresponsive & have no palpable pulse. To verify the absence of a pulse, try to palpate the carotid or femoral pulse. If pt. is responsive & pulse is palpable, check to see if pt is shivering. Because in some cases, excessive muscle movement can create an ECG pattern like that of ventricular fibrillation. Sometimes also, electrical interference such as one coming from the most common electric razor so Nurses always evaluate the pt. first when you see this ECG pattern.

INTERVENTION The only effective treatment for ventricular fibrillation is Defibrillation. To increase its effectiveness at the same time give \epinephrine & anti-arrythmic drugs such as lidocaine or procainamide give IV push because time is critical. CPR & other life-support measures should be started while you are waiting for the defibrillator

VENTRICULAR ASYSTOLE- CARIAC STANDSTILL -With VS, electrical activity in the ventricles stops. What will be seen on an ECG Strip is almost flat line. Some activity may be evident in the atria, but the atrial impulse isnt conducted to the ventricles. P waves may continue for a time, but the QRS complexes have disappeared. ECG INTERPRETATION: Atrial rate & rhythm is indiscernible Ventricular rate & rhythm doesnt even exist. P wave is absent. PR interval not measurable; QRS complex is absent; T wave absent. Because of these findings, one would interpret the ECG as showing Asystole. SIGNIFICANCE: Asystole is life threatening. Without ventricular activity, ventricular contraction does not occur. Consequently, there is no cardiac output or perfusion. ETIOLOGY: 1. Any condition that causes inadequate blood flow can lead to Asystole. 2. Non-cardiac causs include pulmonary embolism, air embolism & hemorrhage. 3. Cardiac causes include ineffective cardiac contractility stemming from heart failure, heart rupture, MI or cardiac tamponade & insufficient conduction, AVB, & Cocaine overdose.

CLINICAL MANIFESTATION: The pt. will be in CP arrest; so pt will be unresponsive & will not be able to palpate a pulse. - Nurse, please verify the absence the absence of a pulse, try to palpate the carotid or femoral pulse. Same ECG pattern may appear if the pts electrodes fall off or the monitor probably is not turned ON. Nurses evaluate the patient before you try to perform any emergency measures.

INTERVENTION: A pt. with Asystole needs immediate treatment including CPT & other life-support measures. If pt has a temporary demand pacemaker, turn it on & check the electrodes as well.