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Med-Surg 3

Exam I

Exam 1: Ch. 26, 27, 28, 29, 51, and 52 ANCC Synergy Model -

The AACN Synergy Model for Patient Care o You must involve the patient family in the decision making o Consider psychosocial  Consider the financial aspect  NCLEX will want you to consult social worker b/c they don’t have finances to get the meds o State board speaks about competence, they want to know if it is a level 1 nurse (entry level) or level 5 (someone who is experienced) o Understand that you as the nurse must be competent enough in terms of your delegation o Know that you need to give information  i.e., today in the ER, b/c of COVID-19 there are no visitors. The fam is stressed b/c they have no info and are not at bedside, this can be stressful for patient, fam, and nurse o Resilience  Capacity to return to a restorative level of functioning using compensatory/coping mechanisms  Are you resilient enough to cope and get through this process? o Vulnerability o Stability o Complexity o Resource availability  Make sure you include pt and family! o Clinical judgment  Clinical reasoning  Decision making  Critical thinking o You must do something first BEFOR you delegate  Be careful of choosing an answer that says call the doc, those answers are very rarely correct o The goal of nursing is basically to restore your pt to an optimal level of wellness!! Do everything you can so that they can become an optimal level  Give the pt and family as much information as possible, keep them updated

Cardiac dysrhythmia: Review -

Cardiac dysrhythmia: review o Dysrhythmias  You want to know, is my patient’s HR normal? Is it slow? Is it too fast? Know how to identify these first b/c if it’s too slow, you need to find out the underlying reason, if it’s too fast you need to know why o If the HR is too slow or too fast, the body may not be getting enough oxygen  A lot of times we do an EKG to determine dysrhythmias  Disorder of the formation or conduction of the electrical impulse within the heart  Irregularity causes disturbances in:  Heart rate 1

Med-Surg 3

Exam I

 Heart rhythm  Both  Hemodynamic effect  Regular rate and rhythm required to circulate oxygenated blood and life-sustaining nutrients to body organs  Diagnosed by analyzing the electrocardiogram  Named according to the site of origin o Normal electrical conduction

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Know how fast the AV and SA node go SA node  60-100 bpm AV node  40-60 bpm If something is beating too fast or too slow, where is it being affected? NCLEX might give you a patient’s HR that is very low and they want to know what you are going to do about it o In the normal heart  Don’t need to go too in-depth with this topic  Electrical impulses cause and is followed by the mechanical contraction of the heart:  Electrical stimulation = depolarization  Mechanical stimulation = systole  Electrical relaxation = repolarization  Mechanical relaxation = diastole o Influences on HR and contractility  KNOW THIS SLIDE  If the rate is too high or too low, what are you going to do about it to bring it back to NSR  Sympathetic nervous system stimulation  Increases HR (positive chronotropy) 2

Med-Surg 3

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Exam I

 Increases conduction through AV node (positive dromotropy)  Increases force of myocardial contraction (positive inotropy)  Parasympathetic nervous system stimulation  Reduces HR  Reduces AV conduction  Reduces force of myocardial contraction The electrocardiogram  A 35-year-old male c/o CP, you do an EKG. What will the EKG show you? If the EKG shows an MI, you can then infer that he has a slow cardiac output. EKGs only show the rate, rhythm, and if it is regular or irregular o EKG/ECG is a graph tracing of the electrical activity of the heart (not the mechanical activity) o Information obtainable from an EKG rhythm strip analysis:  Heart rate? Yes  Rhythm/regularity? Yes  Impulse conduction time intervals? Yes  Pumping action? No  Blood pressure? No  Cardiac output? No o What else does the EKG reflect?  KNOW THIS SLIDE!!!  Ischemia  Infarction  Electrolyte disturbance  When it is an electrolyte disturbance, always think K+. Is my my patient hyper- or hypokalemic?  Drug toxicity  A lot times they are talking about QT segment o May come up as a SATA question  Enlarged cardiac chambers o EKG waveforms/segments/intervals  If you have all of these (P, PR, QRS, ST, T) then you are in good shape  The first thing you have to do is ID the P wave  P wave o If you don’t see the P wave, then that is not a normal EKG (at our nursing level this is not Figure 1: This is ST elevation; they are about to code! normal). So on a test, ST elevation means MI which means cardiac quiz, NCLEX, IF YOU DO NOT SEE A P WAVE THAT IS NOT NORMAL  Represent the electrical impulse starting in the SA nod and spreading through the atria  Atrial muscle depolarization  48 hours  Coumadin x 4 weeks after cardioversion  Amiodarone, betapace, rhytmol prior to cardioversion  Pharmacologic cardioversion  Tikosyn, ibuelide = required patient hospitalization o HR control o Beta blocker  Contraindicated with bronchospasm o Calcium channel blocker  Contraindicated with impaired ventricular function o IV amiodarone or digoxin  If amiodarone does not work, then you give digoxin. However, if you give dig then you need to know the s/s of dig toxicity (on the NCLEX, if they ask about dig, they will ask about s/s of toxicity. Also know the level of dig)  Digitalis toxicity can occur. Clinical manifestations of this include anorexia, nausea, visual disturbances, confusion, and bradycardia o Serum potassium level is monitored because the effect of digoxin is enhanced in the presence of hypokalemia and digoxin toxicity may occur o Therapeutic serum digoxin levels range from 0.5–2 ng/mL (per Davis Drug Guide). o Antithrombotic therapy indicated for all patients with A-fib o Heparin therapy until INR therapeutic with coumadin  Xarelto, Pradaxa  If the pt is going home with dx of AFib then they will be going home with heparin, coumadin, Xarelto, or Pradaxa Premature atrial complex (PAC) [NOT ON EXAM]  Single, ECG complex occurs when electrical impulse starts in the atrium before the next normal impulse of the sinus node  Atrial bigeminy, trigeminy  Interrupts the sinus rhythm 12

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Etiology: PAC’s o Caffeine o Alcohol o Nicotine o Anxiety o Hypokalemia o Stretched atrial myocardium (hypovolemia) o Hypermetabolic states o Atrial ischemia, injury or infarction  Clinical manifestations and management o Clinical manifestations:  “Skipped beat”  Etiology  Caffeine intake  Hypokalemia o Management:  Treat the underlying cause  Infrequent: no treatment necessary  If >6 per minute: treat underlying cause AV nodal re-entry tachycardia (AVNRT) [NOT ON EXAM]  Impulse conducted in the AV node that causes the impulse to be re-routed back into the same area over and over again at a very fast rate  Causes fast ventricular rate  Abrupt onset and abrupt cessation  QSR normal duration  Atrial rate 15-250 (p-waves?)  Ventricular rate 120-200

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Etiology: AV nodal reentry tachycardia o Caffeine o Nicotine o Hypoxemia 13

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Exam I

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o Stress o Coronary artery disease o Cardiomyopathy Clinical manifestations and management o Clinical manifestations:  Reduced cardiac output:  Restlessness  Chest pain  SOB  Pallor  Hypotension  Los of consciousness o Management:  Treatment aimed at breaking reentry of impulse  Vagal maneuvers o Carotid sinus massage (contraindicated without carotid bruit) o Gag reflex o Breath holding  Adenosine  CCB: Verapamil, Cardizem  Unstable: cardioversion  Amiodarone, diltiazem to prevent reoccurrence  If p-wave not identified may be called supraventricular tachycardia (SVT)  Indicates only that it is NOT ventricular tachycardia  SVT can be  Atrial flutter  Atrial fibrillation  AV nodal reentry tachycardia  Vagal maneuvers/adenosine helps slow rhythm to allow visualization of p-waves

NUR 4120 CONTENT STARTS AT SLIDE 31 -

Ventricular dysrhythmias o Premature ventricular complex (PVC)  PVC looks like a whip  If it is just one PVC then that is fine, it’s nothing to worry about  But if there is more than one PVC then you need to look more into it. If they have 6 or more PVCs in one minute, then you need to let someone know they are having a lot of PVCs in one minute. Do not leave them w/o monitoring  Impulse that starts in a ventricle and is conducted through the ventricle before the next normal sinus impulse  QRS is 0.12 seconds or longer; shape abnormal, bizarre

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More recent research shows that the following are NOT precursors to VT:  More frequent than 6/minute o If more than 6 PVCs, DO NOT IGNORE! Assess the patient and notify MD  Multifocal  Occurs two in a row  Occur on the T wave  P. 708 Etiology: PVC’s (KNOW THIS SLIDE) o May need to do an ABG, so do not leave these patients. o Check your electrolytes, if they are having more than 6 PVCs, you need to check the electrolytes  Cardiac ischemia/infarction  Increased workload on the heart (heart failure/tachycardia)  Digitalis toxicity  Hypoxia  Acidosis  Electrolyte imbalance  Healthy people: caffeine, nicotine, alcohol PVC patterns [NOT ON EXAM, SKIP SLIDE]  Ventricular bigeminy o Occurs when every other beat is a PVC  Ventricular trigeminy o Occurs when every third beat is a PVC  Ventricular quadrigeminy o Occurs when every fourth beat is a PVC  Ventricular couplets o Two PVC’s occurring together w/o a normal complex in between PVC: Management  PVC’s are usually not serious o True to a degree o If they are asymptomatic then you find the underlying cause  Frequent and persistent PVC’s may be treated with amiodarone or sotalol o Lidocaine or amiodarone if they have frequent PVCs o Do not ignore if more than 6 PVCs 15

Med-Surg 3

Exam I

o These are IVP meds  Long-term therapy not usually indicated o Ventricular tachycardia (VT)  VT looks like an inverted V  This patient is about to have impending doom  You can’t leave the bedside if they have this rhythm.  KNOW THIS RHYTHM, APPREICATE THIS RHYTHM, LOVE THIS RHYTHM  Needs to be addressed immediately  Three or more PVC’s in a row  Rate exceeds >100 bpm

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VT: Etiology and characteristics  Etiology o Same as PVC o At risk for lethal VT  Larger AMI  Lower ejection fraction  Characteristics o Ventricular rate: 100-200 bpm o QRS: duration >0.12, abnormal o P wave: difficult to detect o PR interval: irregular VT: Management (KNOW) o Pay attention to this slide! o Determine right away if they are stable or unstable.  To treat VT, we need to know if they are stable or unstable  If they are stable, do continuous assessment with 12 lead EKG, supportive care (elevate HOB, O2), give amiodarone. If they are stable it means they have a pulse and not a lot of complaints from the pt  Determination of stable vs unstable required for treatment  Stable o Continuing assessment 16

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o 12-lead EKG o Antiarrhythmic medication (procainamide, amiodarone) o Supportive care  Management for symptomatic patient (KNOW) o Unstable: with a pulse  Cardioversion  On cardioversion you want the Jules to be on the QRS complex  If they look like they are about to crash with a pulse, then you need to cardiovert  Cardioversion is used if they have a pulse but are unstable meaning they are short of breath, dizzy, hypoxic o Unstable: W/o a pulse  If they are unstable, they are hypoxic, dizzy, short of breath  Patients who are unstable can or they can’t have a pulse (its both, some have a pulse, some don’t)  If they are unstable with w/o a pulse, you will defibrillate which is basically shocking the pt  A lot of times they will also give amiodarone IVP followed by IV drip. This can be given even if they do have a pulse  Some patients even have internal defibrillators that will shock them whenever they go into VT  Know cardioversion and defib  Defibrillation if they don’t have a pulse  Defibrillation  Precordial thump  ICD for ejection fraction 300 bpm) 17

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Causes ineffective quivering of ventricles No atrial activity Irregular and undulating waves w/o recognizable QRS complex Electrical impulses initiated by multiple sites

Etiology: VT o Don’t need to go too in depth on this slide o VFib is normally due to cardiac or acid-base or electrolyte (typically K+)  Most common: CAD and resulting AMI  Untreated or unsuccessfully treated VT  Cardiomyopathy  Valvular heart disease  Pro-arrhythmic medications  Acid-base and electrolyte disorders  Electrical shock Clinical manifestations and management  Clinical manifestations: o Fatal dysrhythmia  Pulseless  Apneic o No coordinated cardiac activity  Cardiac arrest and death imminent if V not corrected  Management:  If the pt is pulseless, start CPR  If you start CPR and you see VFib, then you need to defibrillate!! o CPR until defibrillator arrives o Immediate defibrillation o 5 cycles of CPR alternating with defibrillation o Epinephrine every 3-5 minutes (KNOW)  Give epinephrine if they are pulseless after CPR and defibrillation  This is given b/c they are pulseless o One dose of vasopressin instead of epinephrine o Anti-arrhythmic  These are given after we try epinephrine  They don’t matter if they are pulseless  Amiodarone  Lidocaine  Magnesium o Intubation/airway management o Hypothermia protocol  Can initiate hypothermic protocol after arrest 18

Med-Surg 3

Exam I  Mild hypothermia in comatose adult s (32-34 deg C)  Induction started as soon as circulation is restored  Maintained 12-24 hours o Nursing management  Untreated VF can lead to death  A pt with VF is unstable, you cannot educate them at this time b/c they are intubated  Monitor appropriate level of cooling  Medication administration and monitoring (sedation, paralysis)  Monitoring and prevention of seizures, shivering  Monitor electrolyte imbalance  Correct hypotension  Treat infection  Monitor and treat hyperglycemia

o Ventricular asystole  If you see a flatline, the first thing you do is ask are you okay? Then check for a pulse. If there is no answer and no pulse, THEN you can start CPR o 1. Are you okay? No response o 2. Check pulse? No pulse o 3. Start CPR and call code  “Flatline”  Absent QRS complex, may be P waves for a short duration  Confirmed in two different leads  No heartbeat, no palpable pulse, no respirations

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Etiology: Asystole (KNOW) o Know why the pt is in asystole!  Assessment of H’s and T’s o Hypoxia  If it is hypoxia, then they need to be intubated o Hypovolemia  If it is hypovolemia, then they need fluids or blood. If they loose blood, they need replacement blood  If it is hypovolemia from dehydration, then they need fluids o Hydrogen ion (acid-base imbalance) o Hypo/hyperglycemia o Trauma  If they have trauma, we need to stop the bleeding o Toxins o Tamponade o Tension pneumothorax 19

Med-Surg 3

Exam I

 If they have a tension pneumothorax, we need to stop the bleeding o Thrombus  Management  This list is not in the correct order of how you do things  First you would want to ask, “are you okay?”. Then you check pulse, then you start CPR and call code. Then you check for IV and if they don’t have a site you need to get one. Then you can give IVP epi o High-quality CPR o Minimal interruptions o Identity underlying factors  H and Ts o Intubation  Pt’s w/ asystole are unresponsive, they will be intubated o Establish IV access o Epinephrine IV access o Epinephrine bolus (repeat 3-5 minutes) o Vasopressin o Call code o Conduction abnormalities  General information  Identify underlying rhythm  Assess PR interval o AV blocks occurs the conduction through the AV nodal or His bundle is decreased or stopped  Medications (CCB, BB)  Myocardial ischemia/infarction  Cardiomyopathy  Increased vagal tone  Clinical manifestations  Vary with resulting ventricular rate and severity of underlying disease process o Asymptomatic o Hemodynamic instability  Decreased perfusion to vital organs (brain, heart, kidneys, lungs, skin)  Treat the patient not the monitor  Treatment based on hemodynamic effect of the rhythm  Classification of AV blocks o Know the second- and third-degree blocks!!!  First degree AV block  There really isn’t anything you can do for a first-degree block, everything essential is normal o Occurs when all atrial impulses are conducted throughout the AV node into the ventricles o Rate is slower than normal o P wave is in front of the QRS o PR interval 20

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Exam I  

>0.20 seconds PR interval is constant

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Second degree AV block type I (Wenckebach)  You still have p wave in front of QRS, but the PR interval becomes longer  Pay attention to your PR interval definitions for the exam!  Look at type 1 b/c you need to be able to differentiate it b/w type 2 o Repeating pattern in which all but one of a series of atrial impulses are conducted though the AV node into the ventricles o Each atrial impulse takes a longer time for conduction than the one before o Finally, one impulse is blocked o P wave  In front of the QRS o PR interval  PR interval becomes longer with each succeeding ECG complex until there is a P wave not followed by QRS o QRS  Normal or abnormal

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 The PP interval is regular, but the RR interval is irregular Second-degree AV block type II  PR is constant, constant, constant  On a test the moment you see a block you need to pay attention to the p wave and the PR interval o Only some of the atrial impulses are conducted through the AV node into the ventricles o P wave: in front of the QRS o PR interval  PR interval is constant for those p waves just before the QRS o QRS: normal or abnormal 21

Med-Surg 3

Exam I

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o Third-degree AV block  PR is very irregular o No atrial impulse is conducted though the AV node into the ventricle o Two impulses stimulate the heart  One stimulates the atrial (P wave)  One stimulates the ventricle (QRS complex)  “AV dissociation” o PR interval: very irregular o

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On a test if you can’t see the p wave and then it is a third degree. Especially if you don’t see second degree type 2 as a choice  The patient needs to be paced  Management of conduction abnormalities o For 3rd degree the HR is low, and they need a pacemaker. Initially, you need a transcutaneous pacemaker and a crash cart at bedside o If a pt is in 3rd degree, you may want to check electrolytes b/c if they are hypokalemic and you don’t treat it then they will stay in low HR.  Treatment based on cause and degree of stability.  Directed towards increasing HR to maintain normal cardiac output o No treatment if stable: just eliminate the cause  Withhold medications  Permanent pacemaker insertion (if you can’t stop medications)  Transcutaneous pacing (temporary)  Initial treatment of choice: atropine (not effective in second-degree AV block type II or third-degree AV block)  CPR Take home points!! o It is IMPERATIVE, AT ALL TIMES, to observe and treat the patient based on this or her clinical presentation regardless of the rhythm being observed on the EKG monitor. o Ask yourself, “How is this rhythm clinically significant to my patient?” 22

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Exam I

Nursing process: the care of the patient with a dysrhythmia: diagnosis o Decreased cardiac ...