A/P Review and EKG Interpretation
A/P Review and EKG Interpretation NURS 479
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This 22 page Class Notes was uploaded by Lexi P on Friday September 23, 2016. The Class Notes belongs to NURS 479 at Catholic University of America taught by Connor-Ballard, P. in Fall 2016. Since its upload, it has received 37 views. For similar materials see Adults in Health and Illness in NURSING at Catholic University of America.
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Date Created: 09/23/16
Nurs 479 Adults in Health and Illness – Cardiac Nursing – A/P Review and EKG Interpretation Slide 1 – Title Slide 2 EKG’s have been around for about 50 years Slide 3 Coronary Care units were primarily for patients with AMI o Cardiac Care = Coronary Care 1962 – Bethany Hospital in Kansas City, KS – first CCU 1963 – Presbyterian Hospital in Philadelphia 1965 – NY Hospital-Cornell Medical Centre in NYC Holy Cross Hospital was the 4 in Silver Spring (1965) In just 4 years (1962-1966), the US went from 0 250 CCUs o This was made possible by technology EKG interpretation, mechanical ventilators, further advancement in cardiac drugs Slide 4 1964-1965 – CCU guidelines were published The 7 essentials for the ideal CCU o Cardiac arrest team o Quiet, peaceful environment o Adequate space for resuscitation in each patient cubicle o Adequate and specialized training for nurses This was difficult to implement because nurses were being educated in 3-year hospital programs Slide 5 1966 – nurse educators and cardiologists had a meeting to devise the “Criteria and Guidelines for Nurse Training Courses in a Coronary Care Unit” 1967 – there were 13 SONs funded to offer short-term training courses to CCU RNs o CUA was one of them – part of our SON legacy is in cardiac Slide 6 1960s CCU o ward-like setting o main telemetry screens were at the nurses’ stations o at the bedside there was: O2, suction, and outlets Slide 7 In the 1960s they also created ICUs for medical and surgical patients Slide 8 1965 CCU there was a one distinct nurse every shift that would just monitor the screens Slide 9 There are 4 chambers of the heart – atria and ventricles Blood goes to the heart by the IVC and the SVC In the wall of the left ventricle, there is more muscle because this ventricle has to pump blood to the body Travelling with the blood o Right atrium tricuspid valve Right ventricle lungs for O2 oxygenated blood to Left atrium bicuspid valve Left ventricle aorta Body Slide 10 The coronary arteries branch off of the aortic root and supply the heart itself with oxygenated blood o The aortic root is the very beginning of the aorta, where it first comes out of the heart The left coronary artery goes down the left anterior of the heart and descends to the back o The back part of the left coronary artery is called the “circumflex branch of the left coronary artery” Slide 11 Key elements of EKG assessment o Heart rate o R-R interval (rhythm) The distance between 2 R’s in 2 back-to-back QRS waves = rhythm o P/QRS, T waves…U when present U wave = abnormal o PR and QT intervals o ST segment depression or elevation o Is the cardiac rhythm tolerated by the patient? Is there adequate tissue/organ perfustion? Tolerated = the patient is continuing to be perfused Look at: BP, color, pulses, pain, etc Slide 12 Electrical current o 1. Sinoatrial (SA) Node o 2. Atrioventricular (AV) node o 3. Atrioventricular bundle (Bundle of His) o 4. Left and right bundle branches o 5. Purkinje fibers Slide 13 The impulse conduction that goes through the process listed above, creates the wave on the EKG Slide 14 P – impulse goes through the atria o Should be above baseline QRS – impulse through ventricles o Should be above baseline o Tall, thin, spiked, taller than P T – electrical recovery, rebooting system, heart settling to get ready for the next impulse o Should be above baseline PR interval – want it to be less than 0.2 seconds ST segment – should be at baseline Slide 15 Heart Rate (HR) – 60-100 bpm at rest o Regular even spaces between the R’s o Based on # ventricular contractions (QRS) per min Heart Rhythm – consistency of P-P and R-R intervals Repolarization – recovery Depolarization – stimulation P wave (atrial depoloarization) o Want one before each QRS o Consistent shape and size o Deflected from baseline PR interval (atrial depolarization/impulse delay by AV node) o Consistent 0.12-0.20 seconds in length on EKG QRS wave (ventricular depolarization) o 0.4-0.10 seconds in length o Consistent size/shape, deflection from the baseline QT interval (both ventricular de- and repolarization) o 0.10 seconds or less in length o Ventricles active, stimulation and recovery o Note if prolonged – risk for ventricular arrhythmias T wave (ventricular repolarization) o Preparation for next impulse o 1 post QRS, consistant size/shape o note peaking or inversion U wave (hypokalemia v. unconducted P wave?) o Occurs after and is smaller than T wave ST segment (estimated time of ventricular muscle contraction) o Flat at baseline o Note depression below or elevation above baseline Slide 16 Reduced Cardiac output can result from: o Bradycardia o Tachycardia o Irregular heart rate o Loss of atrial “kick” Happens in the Right atrium, blood should flow from RA to RV The last 1/3 of blood in the RA gets pushed into the RV with a little contraction but when this doesn’t happen, the blood can pool atrial fibrillation/flutter Slide 17 Signs and symptoms the patient is not tolerating the arrhythmia o Skin pallor o Altered LOC o Hypotension o Slow capillary refill o Weak/thread peripheral pulses o Reduced urine output – with ongoing arrhythmias o Dizziness, weakness o Palpitations – feel own heart racing o Angina pain Chest pain = serious This means that coronary arteries are not getting sufficient blood and the myocardia is not getting what it needs Slide 18 12-perspective view of impulses o chest, peripheral Slide 19 W B W W B R B Brown G G R R An example of a continues EKG format Best to monitor p wave Slide 20 Telemetry lead placement hints o White on the Right o Clouds (white) above the grass/trees (green) o Smoke (black) above fire (red) o Dirt (brown) in the middle of the garden White = RU chest Green = RL chest Black = LU chest Red = LL chest Brown = middle Slide 21 Telemetry data collection system – 24 hour Holter EKG Monitoring Slide 22 Normal Sinus Rhythm (NSR) o 60-100 bpm o Regular rhythm (R-R wave), normal QRS complexes at rest, PQRST Sinus Tachycardia (ST) o 100-150 bpm o Regular rhythm, normal QRS complexes at rest o Often due to pain, fever, stress, and exercise o Gradual onset and gradual termination Sinus Bradycardia o Less than 60 bpm o Regular rhythm, normal QRS complexes o Extremely athletic – heart is at this point but not a problem Sinus Dysrhythmia (formerly sinus arrhythmia o NSR but with an irregular rate correlating to respirations o Increase HR on inspiration, decrease on exhalation NSR vs. ST = HR NSR vs. SB = HR NSR vs. SD = HR when you breathe in, and HR when you exhale Slide 23 Normal Sinus rhythm Black marker at the top, is the “3 second marker” used to help calculate the rate Slide 24 Sinus tachycardia (Compare to the 3 second marker from slide 23) R-R interval is normal but shorter P and T waves can almost be blended if the heart is beating fast enough Slide 25 Sinus Bradycardia R-R interval is longer Slide 26 Sinus Arrhythmia / Dysrhythmia The first three beats are on inhalation, so they are faster The second two are on exhalation and they are slower Slide 27 Common Atrial Arrhythmias – has something to do with the AV node or Bundle of His o Premature Atrial Contraction Underlying sinus rhythm with a premature beat Abnormal or absent P wave The heart beats so quickly o Atrial Tachycardia 150-200 bpm impulse from somewhere around the atrial node “Narrow complex (QRS) tachycardia” AT vs Sinus Tachy = rate is much faster and AT is not tolerated for very long o Paroxysmal Atrial Tachycardia Sudden (paroxysmal), abnormal P waves o Atrial Fibrilation 60 (controlled) to >100 (uncontrolled) irregular rhythm Heart is quivering – usually requires digoxin Not one impulse is in control of the system Instead of a P wave, there is a wavy baseline without the presence of P o Atrial Flutter “Sawtooth” = atrial flutter (F) wave at 250-350 flutter bpm Count the F waves per QRS o Reported as a ratio Lacks single control, multiple sparks with atria trying to respond No real baseline More F before QRS, worse, impulse not dropping into ventricles Slide 28 Norm Norm Norm premature pause There is a compensatory pause – before it falls back into rhythm Impulse is short, smaller P wave on the premature beat Slide 29 Flips switch to normal Cound the QRS between 3 seconds and multiple by 20 to get a full minute (bpm) First 3 seconds – short R-R and blended P+T waves Slide 30 4 flutter – blocking 4 waves until one is accepted A flutter – no flat baseline wavy, sawtooth baseline o Varying flutter to QRS ration is concerning A fib – wavy baseline o Determinable QRST, no P; Irregular rhythm between R-R Slide 31 Premature Ventricular Contractions (easier to understand with pictures) o PVC Underlying EKG rhythm, the impulse comes from the ventricular tissue Irregular rhythm due to the premature beat Beat will cause irregularity of rhythm, no P wave or PR interval, large and wide QRS It is isolated in the EKG and surrounded by normal beats, not a constant arrhythmia o Unifocal PVCs share the same QRS shape o Multifocal PVCs with differing QRS shapes, each representing different ventricular foci Each different one comes from a different place in the ventricle o When there are multiple sites, there is more to worry about o Interpolated PVC between 2 normal EKG complexes, usually without a compensatory pause o Couplet 2 consecutive PVCs o Triplet 3 consecutive PVCs (3-beat run of V tach) o Bigeminy Every other beat is a PVC o Trigeminy Every third beat is a PVC o R on T PVC occurs on the proceeding T wave, triggers Vtach or Vfib This is very concerning T wave = recouping period of irritability; when R on T occurs, it can trigger Vtach or Vfib – both are deadly Slide 32 PVC with compensatory pause N N These PVCs look the same, so they have the same foci (UNIFOCAL) – there is one area of irritation It looks negative, but it is only because of the lead that was used, it helps to visualize it upside down Slide 33 Unifocal PVCs Another view of the same sort of PVC, but just right side up These QRS intervals are wide, large and bizarre on the PVCs Slide 34 Multifocal PVCs o They have different sizes and shapes, they are coming from two different irritated places in the ventricles Slide 35 Interpolated PVCs – occurs between sinus beats without a compensatory pause N N System reboots without a pause There is supposed to be a pause between these two normal waves, but instead there is an extra beat Slide 36 PVC couplet Concerning because two beats can lead to three beats, and three beats can lead to Vtach These PVC beats are unifocal – coming from the same irritated part of the ventricle Slide 37 PVC triplet N N Pause Unifocal 3 beats in a row can lead to tachycardia, need to act on this Slide 38 PVC Bigeminy N N Unifocal but concerning Singular area but taking over the impulse system The longer it goes on, the more symptomatic the patient is Over time (minutes) the heart and body stop tolerating this, the patient gets dizzy, light headed, CP, decreased BP, pulses weaker Slide 39 Ventricular trigemini N N N N Unifocal but concerning The longer it goes on, the more symptomatic the patient is Over time (minutes) the heart and body stop tolerating this, the patient gets dizzy, light headed, CP, decreased BP, pulses weaker Slide 40 PVC “R on T” Phenomenon QRS P T PVC on descent Slide 41 Common Ventricular Arrhythmias Very serious – untreated = life threatening – short term only o Premature Ventricular Contraction (PVC) See slide 31 o Idioventricular ventricular rhythm “last resort paymaker” – SA failed, AV failed ventricular tissue 20-40 bpm Absent P wave and PR interval Wrde, bizarre QRS 3 degree AV heart block (complete) o Ventricular Fibrillation (Vfib) Entire EKG complex is replaced by a coarse or fine wavy baseline Cardiac arrest situation o Ventricular tachycardia (VT) >100 bpm Wide bizarre QRS Cardiac arrest situation PVC after PVC, ventricular tissue controls o Torsade de pointes VT with “twisting” of the QRS complexes Rare o Asystole “Flat line” Complete absence of EKG complexes Slide 42 Idioventricular Rhythm Pause with nothing coming so the ventricles step in No P, No QRS 20-40 bpm *The body can only be sustained on this rhythm for a short amount of time Slide 43 Ventricular Fibrillation Best time for defibrillation – shocks them out of this; more electric activity; starts as this Quickly flattens (minor quivering); harder for defibrillation Loss of impulse, no impulse through ventricles Electrical flickering No adequate outflow Slide 44 Ventricular Tachycardia (R on T?) N N So fast, the intervals between R’s is short No P or T Possible R on T first beat of Vtach During this display of VT, the patient is probably semi-conscious Slide 45 Ventricular Tachycardia Run N N N Rapid beats from ventricle, goes away as quickly as it came; may or may not be conscious Slide 46 Torsades de Pointes (rare) High risk for people who have a long QT segment (more than usual) Twisting appearance It is dangerous because it is hard to get out of Prevented if monitored Slide 47 V-fib – lack QRS, wavy baseline, course fine V-tach – impulse by ventricular tissue, fast rate, not sustainable, no cardiac output Asystole – complete flat line Slide 48 AV heart block Heartblock gets worse over time o 1 degree heart block Underlying heart rhythm and normal EKG wave except for prolonged PR interval (> 0.20 seconds) Impulse generated but held at AV node/bundle of His area o 2 nddegree Mobitz Type 1 AV heart block (“Wenckebach”) Progressively increasing PR intervals until a non-conducted P wave occurs (No QRS), then a pause, then the cycle restarts P wave keeps getting longer then dropped nd o 2 degree Mobitz Type 2 AV heart block More P waves than QRS complexes due to unconducted P waves PR interval remains normal and consistent Unconducted P, no QRS behind it o 3 degree AV heart block “complete” heartblock complete wall between atria and ventricles SA AV ventricles o Ventricles are creating their own impulses Usually HR slows to 20-40 bpm 2 completely separate rhythms atria and ventricles Slide 49 st 1 Degree AV Heart Block PR interval longer than 0.2 seconds Slide 50 2 nddegree AV Heart Block Type 1 (Mobitz 1) P P P P Pause, did not go down to ventricles “Wenckebach” Slide 51 2ndDegree AV Heart Block Type 2 (Mobitz 2) Dropped P waves Slide 52 3 Degree AV heart block R P TP P Consistent, 20-40 bpm rate of ventricular pace maker what pulse is like Wall between atria and ventricles o Impulse does not go from one to the other o Two rhythms occurring without regard of the other Slide 53 Junctional Arrhythmias Pulse occurs at the junction of all four chambers o Impulse generated by the AV node, with simultaneous impulse transition up to atria (retrograde), and forward to ventricles Impulse goes down then up o P waves are often abnormal, absent, inverted, or behind the QRS complex o Junctional rhythm is usually 40-60 bpm o SV node 60-100 bpm AV node 40-60 bpm Vent. Tissue 20-40 bpm 20-40 bpm is not sustainable Slide 54 Junctional Rhythm P behind QRS; impulse sent down then up Slide 55 (For awareness) Should go down Right and Left bundle branch at the same time One goes down before the other, the QRS is notches Slide 56 Sick Sinus Syndrome o Requires pacemaker SA node works and then it doesn’t o Does not get better on it’s own Sinus pause, rhyth restarts m asystole Paus Paus e e Paus Paus Paus e e e Slide 57 Cardiac Changes due to Aging o Calcification and degeneration of cardiac valves risk for murmurs, regurgitation, heart failure o Changes in impulse formation and conduction Risk of arrhythmias o Fibrotic changes in Left Ventricle Decreased SV o Stiffness in arterial walls Increased BP o Ineffective baroreceptors Orthostatic hypotension o Changes in muscle fibers o Not uncommon for pacemakers to be placed due to age and breakdown Slide 58 QSEN: Telemetry *Treat the patient not the monitor o Telemetry v. 12 lead EKG Telemetry for ongoing care; Leads are for short term Skill – lead placement Attitude – Pt at risk for arrhythmia, requires frequent monitoring Never turn the alarm off o Lead placement Skill – Use of EKG monitor and setting parameters On dry, clean, hairless skin Attitude – Artifact or improper lead placement can hinder EKG interpretation o Clinical indication for telemetry Risk for arrhythmias Skill – EKG wave; Interpretation and measurement (PR, QT) Attitude – Assess patient 1 st whenever any change in rhythm (LOC, BP, skin color, cap refill, apical/pedal pulses, breath sounds, O2 sat%…) o Normal EKG wave Before you can determine what is abnormal, have to know what’s normal Skill – Arrhythmia recognition o NSR v. arrhythmia Which arrhythmia Skill – Cardiac assessment (physical) Attitude – do not rely 100% on automatic telemetry interpretation o Arrhythmia interpretation Skill – BLS/CPR Attitude – consult more experienced RN or MD prn o Emergency Rx for arrhythmias Skill – code blue activation and resuscitation skills Attitude – consult more experienced RN or MD prn Slide 59 An 82-yo F is admitted with a Dx of rapid atrial fibrillation. The RN has initiated telemetry monitoring per MD order. 2 hours later, an alarms sound at the central monitoring station: the patient is in what appears to be ventricular tachycardia. Which of the following actions should the RN take FIRST? o 1. Call a code blue (no code blue based on monitor) o 2. Silence the alarms and change the alarm parameters (never change alarm for peace and quiet) o 3. Notify the MD of a change in rhythm (MD not first) o 4. Assess the client and check lead placement Slide 60 - Closing
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