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Electrocardiogram 1
Electrocardiogram lab
| Question | Answer |
|---|---|
| 12 lead ecg may show: | changes or damage to heart, i.e.: ischemia, infarction, enlargement. |
| p wave represents | atrial depolarization |
| qrs wave | electrical depolarization of the ventricles (ventricular contraction) |
| t wave | ventricular depolarization, gets ready for next impulse/contraction. |
| pr interval | represents time from atrial depolarization to the begging of ventricular depolarization (0.12-0.20 seconds) |
| qrs interval | amount of time for ventricular depolarization (less than 0.12 seconds) |
| qt interval | time measurement of ventricular activity (0.34-0.43 seconds). this can be prolonged due to effects of medications. (can cause serious heart rhythm disturbances) |
| medications the change the qt intervals | lidocaine, pronestyle, amiodaroe. |
| u wave | repolarization of purkinje fibgers. |
| normals sinus rhythem | 60-100 bpm heart rate and intervals all normal. (shorter intervals = decreased cardiac output) |
| Common heart rates: | normal sinus rhthym: 60-100 bpm sinus bradycardia: <60 bpm sinus tachycardia: 101-200 bpm paroxysmal supraventricular tachycardia extra beat in atrium): 150-200 bpm atrial fibrillation:350-600 beats junctional rhythm: 40-180 bpm (decreased cardiac ou |
| common heart rates continued: | ventricular tachycardia: 150-250 bpm (w/ or w/o pulse, cardiac output is decreased) ventricular fibrillation: can not measure rate. |
| Sinus bradycardia: | HR is less than 60 bpm. Don't let the pt. sit for long period of time. Give atropine (Increases heart contraction), pacemaker, or if cause by drugs, hold them. |
| S & S of sinus bradycardia | pale, hypotension, angina, syncope, all intervals normal, decreased coronary perfusion, decreased bp --> mi and CHF, decreased cardiac output, dizziness. |
| sinus tachycardia: | HR 101-200 bpm. decreased CO (because of decreased fill time) & coronary artery filling, increased O2 demand and workload of heart. give beta blockers (decrease force of contractions and rate), lopressor. |
| S & S of sinus tachycardia: | dizziness, dyspnea, hypotension. |
| Paroxysmal supraventricular tachycardia (atrial) | orgin: anywhere above the bundle of his. HR: 150-220 bpm. causes: CAD, digitalis toxicity. |
| S&S of paroxysmal supraventricular tachycardia | hypotension, angina, dyspnea,. |
| treatment of paroxysmal supraventricular tachycardia | adenosine, cardizem (slows down heart to see is there's a "p" wave), beta blockers, calcium channel blockers, amiodarone, vagal stimulation (valsalva maneuver and coughing) |
| Atrial flutter: | Atrial rate: 200-350bpm. No measurable PR or QT intervals, caused by: CAD, HTN, mitral valve disease, pulmonary embolus, cardiomyopathy, high risk of CVA and CHF. |
| treatment for atrial flutter: | calcium channel blockers, beta blockers, cardioversion, amiodarone, radio frequency ablation. |
| Atrial fibrillation: | multiple impulses from the atria outside av node. irregular regular rhythm. HR 350-600 bpm. no p wave and no pr interval. Causes: CAD, rheumatic heart disease, heart failure, pericarditis, |
| treatment for atrial fibrillation: | cardioversion, digoxin, cardizem, beta blockers, coumadin. |
| junctional dysrhythmias: | oringinate in area of SA node due to failed AV node firing, junction becomes pacemaker. caused by: CAD, CHF, IWMI, cardiomyopathy. HR 40-60 bpm. |
| treatment for junctional dysrhythmias: | if symptomatic, treat with atropine, beta and calcium channel blockers, amiodarone, and pacemaker. |
| Atrioventricular heart block 1st degree: | prolonged PR intervals (SA node takes too long to fire to P wave) >.20 seconds. caused by: MI, CAD, digoxin toxicity, rheumatic fever, drugs (beta blockers, calcium channel blockers) |
| AV heart block 2nd degree: mobitz type 1- wenchebach | . Not every P wave creates a qrs. P wave belong longer until QRS is dropped. caused by: impending complete heart block, MI, rheumatic fever, digoxin toxicity. |
| treatment of AV block 2nd degree: | cardiac monitor and oxygen, atropine, temporary pacemaker if symptomatic bradycardia, temporary pacemaker, |
| av heart block 2nd degrreL mobitz type 2: | conduction block in the av node or below the bundle of his. some qrs dropped, pr normal. can lead to 2rd degree HB. caused by: CAD, MI, Rheumatic heart disease, HR: 40-60 bpm. |
| treatment of 2nd degree/mobitz type 2: | epinephrine or vasopressin IVP, hold digoxin, temporary pacemaker, |
| Av heart block 3rd degree | complete heart block between the atria and ventricles. No relation between p waes and qrs complexes. independent pacemakers within atria and ventricles. HR: 30-40 bpm. caused by: severe heart disease, i.e: CAD, MI, cardiomyopathy, drug overdose. |
| S&S of 3rd block: | CHEST PAIN, SHOCK FROM DECREASED MYOCARDIAL PERFUSION, DECREASED HEART RATE, BP, AND CO. |
| treatment of 3rd block: | oxygen, atropine, ephinephrine, dopamine, isuprel, temporary PM, permanent PM. |
| PVC's | -doesn't produce pulse early qrs complex with no p wave. (ventricular tachycardia: 3 or more consecutive beats of PVC) worry that pt will go into v-tach or v-fib. |
| ventricular bigeminy: | PVC occur with every other beat |
| ventricular trigeminy | PRVC occur with every third beat |
| causes of PVC | MI, CAD, CHF, Drugs (digoxin, epinephrine, hypoxia, fever, stress, hypokalemia, caffine, alcohol. |
| treatment of PVC: | if greater than 10/min, start lidocaine or amiodarone IV drip, give oxygen, check potassium levels and replace if low. |
| ventricular tachycardia (continued PVC with no break) | pulse or pulseless. rapid irregular rate with no p wave and wide bizarre beats from the ventricle. HR: 150-250 bpm. brief: with pulse, patien can tolerate. long: no pulse, immediate treatment. |
| Cause of ventricular tachycardia: | MI, CAD, Respiratory failure, frequent PVCs. |
| treatment for ventricular tachycardia: always check for pulse first!!! | with pulse: amiodarone, lidocaine, procainamide, cardioversion. without pulse: treat like v-fib, CPR, defibrillation, epinephrine, amiodarone, IV drip. |
| ventricular fibrillations | No p, qrs, or t waves, no bp, no hr, no respirations, chaotic waves can lead to brain damage. caused by: MI, CHF, cardiomyopathy, electric shock, hypoxemia, acidosis, drug toxicity. |
| treatment for ventricular fibrillations: | immediate CPR, defibrillation and advanced cardiac life support protocol, epinephrine, lidocaine, amiodarone, magnesium sulfate, procainemide follows ACLS protocol. |
| Ventricular asystole or cardiac standstill | total absence of ventricular electrical activity. No pr or qrs complexes. No pulses, no bp, patient is unresponsive, pulseless, no respirations. (pretty much dead) |
| causes for ventricular asystole: | acidosis, HF, hyperkalemia |
| treatment for ventricular asystole: | CPR, O2, epinephrine, atropine, vasopressin, intubation, pacemaker, IV push drugs. |
Created by:
Lindsay515
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