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D Dysrhythmias A Abnormal cardiac rhythms are termed dysrhythmias.

Prompt assessment of dysrhythmias and the patients response to the rhythm is critical. P Properties of Cardiac Cells Automaticity happens on its own h E Excitability C Conductivity Contractility Starts in SA node: AV node: Ventricles 20-40 P-wave: time it takes for impulse to go from SA node to AV node QRS: Down purkinje fibers Conduction System of the Heart Nervous System Control of the Heart A Autonomic nervous system controls: R Rate of impulse formation S Speed of conduction S Strength of contraction Nervous System Control of the Heart P Parasympathetic (rest and relax) nervous system V Vagus nerve D Decreases rate S Slows impulse conduction Decreases force of contraction S Sympathetic fight or flightnervous system I Increases rate I Increases force of contraction Electrocardiogram Monitoring o Graphic tracing of electrical impulses produced by the heart o Waveforms of ECG represent activity of charged ions across membranes of myocardial cells.

12-Lead ECG

1 12 recording leads Six leads (leads I, II, III, aVR, aVL, and aVF) measure electrical f forces in the frontal plane. Six leads (V1V6) measure electrical forces in the horizontal plane (precordial leads). P-wave atrial depolarization QRS ventricle depolarization T-wave - repolarization Lead Placement Depending on where the MI is you would choose the appropriate lead Normal 12-Lead ECG Lead Placement E ECG Paper R Rhythm strip provides documentation of patients rhythm. Allows for measurement of complexes and intervals (1 mm going up (ST elevation), 0.04 for each little box going over to equal 0.20 for one square) - know the 6-second interval Assessment of Cardiac Rhythm C Calculating HR C Count T The number of QRS complexes in 1 minute T The R-R intervals in 6 seconds, and multiply by 10 Number of small squares between one R-R interval, and divide this n number into 1500 Number of large squares between one R-R interval, and divide this number into 300

Assessment of Cardiac Rhythm Artifact movement of the leads Telemetry Monitoring

H HR and rhythm monitored from a distant site C Centralized monitoring system Alarm system alerts when it detects dysrhythmias, ischemia, or i infarction. E Evaluation of Dysrhythmias Holter monitoring a pack and monitors all heart rate patterns over 2 24/48 hour period. Event recorder monitoring they push a button during an event and it r records it. E Exercise treadmill testing S Signal-averaged ECG E Electrophysiologic study Normal Electrical Pattern (look in book) PR - .12-.2 (can only come from sinus node if its .12) QRS - .04-.10 (.12) differs depending on book. Anything less than .12 really. Dont measure T-wave. U wave = hypokalemia (a hump between T wave and next P wave) St-elevation tells us MI or injury St-depression tells us ischemia Normal Sinus Rhythm (from SA node) ( S Sinus node fires 60 to 100 bpm. F Follows normal conduction pattern S Sinus Bradycardia S Sinus node fires <60 bpm. Normal rhythm in aerobically trained athletes and during sleep S Sinus Bradycardia C Clinical associations O Occurs in response to C Carotid sinus massage H Hypothermia I Increased vagal tone Administration of parasympathomimetic drugs If theyre not symptomatic regardless of the pulse rate, you dont don anything, just observe. 1

S Sinus Bradycardia C Clinical associations O Occurs in disease states H Hypothyroidism I Increased intracranial pressure O Obstructive jaundice I Inferior wall MI Sinus Bradycardia symptomatic observations s C Clinical significance D Dependent on symptoms H Hypotension P Pale, cool skin W Weakness A Angina D Dizziness or syncope C Confusion or disorientation S Shortness of breath S Sinus Bradycardia T Treatment if symptomatic A Atropine Pacemaker may be required. 0 3 types of pacemakers? - External, transvenous, implantable S Sinus Tachycardia Discharge rate from the sinus node is increased and is >100 bpm. Sinus tach TREAT THE CAUSE!!! (test) S Sinus Tachycardia C Clinical associations A Associated with physiologic stressors E Exercise P Pain H Hypovolemia M Myocardial ischemia H Heart failure F Fever Sinus Tachycardia

C Clinical significance Dizziness and hypotension due to decreased CO due to less filling i in the left ventricle I Increased myocardial oxygen consumption may lead to angina. S Sinus Tachycardia T Treatment D Determined by underlying cause -adrenergic blockers to reduce HR and myocardial oxygen c consumption A Antipyretics to treat fever A Analgesics to treat pain Premature Atrial Contraction o Contraction originating from ectopic focus in atrium in location other than SA node o Travels across atria by abnormal pathway, creating distorted P wave o M May be stopped, delayed, or conducted normally at the AV node Premature Atrial Contraction Just the p-wave is funky....the qrs complex is still the same. P Premature Atrial Contraction C Clinical associations C Can result from E Emotional stress U Use of caffeine, tobacco, alcohol H Hypoxia E Electrolyte imbalances C COPD V Valvular disease P Premature Atrial Contraction C Clinical significance I Isolated PACs are not significant in those with healthy hearts. In persons with heart disease, may be warning of more serious d dysrhythmia P Premature Atrial Contraction T Treatment D Depends on symptoms -adrenergic blockers may be used to decrease PACs. Reduce or eliminate caffeine S

P Paroxysmal Supraventricular Tachycardia (PSVT) O Originates in ectopic focus anywhere above bifurcation of bundle of His R Run of repeated premature beats is initiated and is usually a PAC. Paroxysmal refers to an abrupt onset and termination. (something stops and starts on its own) S Superventricular above the level of the ventricle somewhere in the atria Sinus tach we would see a P before every qrs, with PSVT there is no t true Pwave Q QRS complex stays normal. The rhythm starts in the atria.... T The rate of PSVT is generally greater than 150 P Paroxysmal Supraventricular Tachycardia (PSVT) C Clinical associations I In a normal heart O Overexertion E Emotional stress S Stimulants D Digitalis toxicity R Rheumatic heart disease C CAD C Cor pulmonale D Decreased pulse/pressure/etc....blood out to skin Paroxysmal Supraventricular Tachycardia (PSVT) C Clinical significance P Prolonged episode and HR >180 bpm may precipitate CO P Palpitations H Hypotension D Dyspnea Angina P Paroxysmal Supraventricular Tachycardia (PSVT) Treatment o Vagal maneuvers: Valsalva, coughing,Test: put face in a dish of ice water. o IV adenosine push as fast as you possibly can (3-6 seconds) o If vagal maneuvers and/or drug therapy is ineffective and/or patient becomes hemodynamically unstable, DC cardioversion should be used.

Atrial Flutter o Atrial tachydysrhythmia identified by recurring, regular, sawtoothshaped flutter waves o Originates from a single ectopic focus o Not a normal PR interval.....if it was than itd be sinus. o One spot in atria takes over as pacemaker in the heart o Y You need to look at all 12 leads to diagnose something Atrial Flutter A Atrial Flutter C Clinical associations: Usually occurs with C CAD H Hypertension M Mitral valve disorders P Pulmonary embolus C Chronic lung disease C Cardiomyopathy H Hyperthyroidism A Atrial Flutter C Clinical significance High ventricular rates (>100) and loss of the atrial kick (which is about 20% of cardiac output) can decrease CO and precipitate HF, a angina. R Risk for stroke due to risk of thrombus formation in the atria W With atrial flutter you lose part of your cardiac output**** Anti-coagulant (long-term) Coumadin...measure PT and INR for effectiveness A Atrial Flutter Treatment o Primary goal: Slow ventricular response by increasing AV block o Drugs to slow HR: Calcium channel blockers, -adrenergic blockers o Electrical cardioversion may be used to convert the atrial flutter to sinus rhythm emergently and electively. A Atrial Flutter T Treatment Primary goal is to slow ventricular response by increasing AV block. o Antidysrhythmia drugs (e.g., amiodarone, propafenone) to

convert atrial flutter to sinus rhythm or to maintain sinus rhythm o Radiofrequency catheter ablation can be curative therapy f for atrial flutter. A Atrial Fibrillation Total disorganization of atrial electrical activity due to multiple ectopic f foci, resulting in loss of effective atrial contraction M Most common dysrhythmia P Prevalence increases with age. Atrial Fibrillation HALLMARK: You have an irregular heart rate, a normal QRS (arising above atria), no discernable P-waves....so rhythm is being generated from multiple spots in atria, they all look different....1 out of every 10/15 will get through with no pattern. Heart rate is irregular. The faster the heart rate the more problems with filling they have. A Atrial Fibrillation C Clinical associations: Usually occurs with underlying heart disease R Rheumatic heart disease C CAD C Cardiomyopathy H HF P Pericarditis Anyone in long-term afib needs to be on anticoagulant!! IF someone is in afib for more than 48 hours they need to be on anticoagulant for 3 weeks or so before cardiovesion so you dont throw a clot! A Atrial Fibrillation C Clinical associations: Often acutely caused by T Thyrotoxicosis A Alcohol intoxication C Caffeine use E Electrolyte disturbance Cardiac surgery A Atrial Fibrillation C Clinical significance Can result in decrease in CO due to ineffective atrial contractions ( (loss of atrial kick) and rapid ventricular response Thrombi may form in the atria as a result of blood stasis.

Embolus may develop and travel to the brain, causing a stroke.

A Atrial Fibrillation T Treatment G Goals D Decrease ventricular rate P Prevent embolic stroke Drugs for rate control: Digoxin, -adrenergic blockers, calcium c channel blockers L Long-term anticoagulation: Coumadin C Class of drug? M Monitoring? New drugs A Atrial Fibrillation T Treatment For some patients, conversion to sinus rhythm may be considered. A Antidysrhythmic drugs used for conversion: Amiodarone, DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm. A Atrial Fibrillation T Treatment If patient has been in atrial fibrillation for >48 hours, anticoagulation therapy with warfarin (Coumadin) is recommended for 3 to 4 weeks before cardioversion and for 4 to 6 weeks after successful cardioversion. A Atrial Fibrillation T Treatment R Radiofrequency catheter ablation J Junctional Dysrhythmias D Dysrhythmia that originates in area of AV node S SA node has failed to fire, or impulse has been blocked at the AV node. Junctional Dysrhythmias < .12....bc if it came from sinus node, the fastest it can get there it .12 seconds, if its less than that it didnt come from the sinus node. Rate between 40-60 and there is no PWAVE. J Junctional Dysrhythmias ClinicalTassociations

C CAD H HF C Cardiomyopathy E Electrolyte imbalances I Inferior MI R Rheumatic heart disease D Drugs: Digoxin, amphetamines, caffeine, nicotine J Junctional Dysrhythmia C Clinical significance S Serves as safety mechanism when SA node has not been effective Escape rhythms should not be suppressed. (bc the primary one h has failed......would be wiping out our safety net) I If rhythms are rapid, may result in reduction of CO and HF J Junctional Dysrhythmias T Treatment I If symptomatic, atropine Accelerated junctional rhythm and junctional tachycardia caused b by digoxin toxicity; digoxin is held F First-Degree AV Block Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged. When the PR is greater than .20 and everything else is normal. It got hung up in the AV node. F First-Degree AV Block C Clinical associations: Usually occurs with MI (especially in inferior wall MI, prone to heart blocks, need close m monitoring) C CAD R Rheumatic fever H Hyperthyroidism V Vagal stimulation Drugs: Digoxin, -adrenergic blockers, calcium channel blockers, f flecainide F First-Degree AV Block C Clinical significance U Usually asymptomatic May be a precursor to higher degrees of AV block C

T Treatment C Check medications. Continue to monitor.

Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) Wenckebach) o Gradual lengthening of the PR interval due to prolonged AV conduction time o Atrial impulse is nonconducted, and a QRS complex is blocked (missing). o Usually block occurs at AV node, but can occur in His-Purkinje system PR continues to get progressively longer....then all the sudden you have a PR P Pwave with no QRS.....it resets itself. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) S Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) C Clinical associations D Drugs: Digoxin, -adrenergic blockers May be associated with CAD and other diseases that can slow AV c conduction I Inferior wall MI can be precursor of things to come S Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) C Clinical significance U Usually a result of myocardial ischemia or infarction A Almost always transient and well tolerated May be a warning signal of a more serious AV conduction d disturbance S Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach) T Treatment I If symptomatic, atropine or a temporary pacemaker If asymptomatic, monitor with a transcutaneous pacemaker on s standby Symptomatic bradycardia is more likely with one or more of the f following: Hypotension, HF, shock. S Second-Degree AV Block, Type 2 (Mobitz II) M Some P waves are not conducted, PR stays the same but a dropped QRS

U Underlying rhythm is usually regular ( (more Ps than QRSs) P PR remains constant P to P is regular P PR interval for the P waves that are conducted are consistent

Second-Degree AV Block, Type 2 (Mobitz II)

S Second-Degree AV Block, Type 2 (Mobitz II) C Clinical associations R Rheumatic heart disease C CAD A Anterior MI Digitalis toxicity S Second-Degree AV Block, Type 2 (Mobitz II) C Clinical significance Often progresses to third-degree AV block and is associated with a p poor prognosis Reduced HR often results in decreased CO with subsequent hypotension and myocardial ischemia. S Second-Degree AV Block, Type 2 (Mobitz II) T Treatment If symptomatic (e.g., hypotension, angina) before permanent pacemaker can be inserted, temporary transvenous or t transcutaneous pacemaker P Permanent pacemaker A Atropine and pacemaker = treatment Third-Degree AV Heart Block (Complete Heart Block) (Complete Form of AV dissociation in which no impulses from the atria are c conducted to the ventricles A Atria are stimulated and contract independently of the ventricles. N NO regular PR interval V Ventricular rhythm is an escape rhythm. Ectopic pacemaker may be above or below the bifurcation of the bundle of His. NO connection between atrial and ventricular beats.

No relationship between PWaves and QRS They are all marching to their own beat, irregular Side note: Ventricular inherent rate : 20-40 bpm Third-Degree AV Heart Block (Complete Heart Block) T Third-Degree AV Heart Block (Complete Heart Block) C Clinical associations S Severe heart disease: CAD, MI, myocarditis, cardiomyopathy S Systemic diseases: Amyloidosis, scleroderma Drugs: Digoxin, -adrenergic blockers, calcium channel blockers As a general rule Atropine only works temporarily. They will need a pacemaker. T Third-Degree AV Heart Block (Complete Heart Block) C Clinical significance D Decreased CO with subsequent ischemia, HF, and shock Syncope may result from severe bradycardia or even periods of a asystole. T Third-Degree AV Heart Block (Complete Heart Block) T Treatment If symptomatic, transcutaneous pacemaker until a temporary t transvenous pacemaker can be inserted D Drugs (e.g., atropine) Temporary measure to increase HR and support BP until t temporary pacing is initiated P Permanent pacemaker as soon as possible Premature Ventricular Contractions o Contraction originating in ectopic focus of the ventricles o Premature occurrence of a wide and distorted QRS complex o Multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, triplets, R-on-T phenomena o Big, Fat, and Funny Premature Ventricular Contractions Tend to tell us the ventricles are irritated which can lead to bad things to come, vtach and vfib. Because the ventricles beat so fast they dont have time to fill, decreased cardiac output P Premature Ventricular Contractions Clinical associations

Stimulants: Caffeine, alcohol, nicotine, aminophylline, epinephrine, i isoproterenol D Digoxin E Electrolyte imbalances H Hypoxia F Fever Disease states: MI, mitral valve prolapse, HF, CAD

P Premature Ventricular Contractions C Clinical significance I In normal heart, usually benign In heart disease, PVCs may decrease CO and precipitate angina a and HF. M Monitor patients response to PVCs PVCs often do not generate a sufficient ventricular c contraction to result in a peripheral pulse. Assess apical-radial pulse rate to determine if pulse deficit e exists. P Premature Ventricular Contractions C Clinical significance R Represents ventricular irritability M May occur After lysis of a coronary artery clot with thrombolytic therapy i in acute MIreperfusion dysrhythmias Following plaque reduction after percutaneous coronary intervention P Premature Ventricular Contractions T Treatment B Based on cause of PVCs O Oxygen therapy for hypoxia E Electrolyte replacement Drugs: -adrenergic blockers, procainamide, amiodarone, l lidocaine V Ventricular Tachycardia Run of three or more PVCs C Monomorphic, polymorphic, sustained, and nonsustained

Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation ABCs! Check pulse, open airway, CPR until crash cart comes... Cardiovert! Want to shock them out of it!

Ventricular Tachycardia If they dont have a pulse defib If they do synchronized cardiovert V Ventricular Tachycardia C Clinical associations M MI C CAD E Electrolyte imbalances C Cardiomyopathy M Mitral valve prolapse L Long QT syndrome D Digitalis toxicity C Central nervous system disorders V Ventricular Tachycardia C Clinical significance VT can be stable (patient has a pulse) or unstable (patient is p pulseless). S Sustained VT: Severe decrease in CO H Hypotension P Pulmonary edema D Decreased cerebral blood flow Cardiopulmonary arrest Drugs: (know for sim-lab for CODE) Amiodarone Epinephrine Atropine

V Ventricular Tachycardia C Clinical significance T Treatment for VT must be rapid. M May recur if prophylactic treatment is not initiated Ventricular fibrillation may develop. V Ventricular Tachycardia T Treatment V VT without a pulse is a life-threatening situation. C Cardiopulmonary resuscitation (CPR) and rapid defibrillation Epinephrine if defibrillation is unsuccessful V Ventricular Fibrillation Severe derangement of the heart rhythm characterized on ECG by i irregular undulations of varying contour and amplitude No effective contraction or CO occurs. Ventricular Fibrillation V Ventricular Fibrillation C Clinical associations A Acute MI, CAD, cardiomyopathy M May occur during cardiac pacing or cardiac catheterization May occur with coronary reperfusion after fibrinolytic therapy V Ventricular Fibrillation C Clinical significance U Unresponsive, pulseless, and apneic state If not treated rapidly, death will result. V Ventricular Fibrillation T Treatment Immediate initiation of CPR and advanced cardiac life support (ACLS) measures with the use of defibrillation and definitive drug t therapy Asystole - the worst thing t R Represents total absence of ventricular electrical activity No ventricular contraction (CO) occurs because depolarization does not occur. A Asystole C Clinical associations A Advanced cardiac disease S Severe cardiac conduction system disturbance End-stage HF A Asystole Clinical significance M

U Unresponsive, pulseless, and apneic state Prognosis for asystole is extremely poor. A Asystole T Treatment CPR with initiation of ACLS measures (e.g., intubation, transcutaneous pacing, IV therapy with epinephrine and atropine) ) P Pulseless Electrical Activity Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse. o Rhythm but no pulse pt wont last long. Can be deceiving bc if youre looking at a rhythm however, the patient could be dead. There is usually a cause.

P Pulseless Electrical Activity Clinical associations/causes c H Hypovolemia Hypoxia treat with oxygen, find out why (pneumo, flail chest?) t Metabolic acidosis cause? bicarb c H Hyperkalemia or hypokalemia H Hypothermia H HAVE TO FIX THE CAUSE OR IT WONT RESOLVE. P Pulseless Electrical Activity T Treatment C CPR followed by intubation and IV epinephrine A Atropine is used if the ventricular rate is slow. T Treatment is directed toward correction of the underlying cause. S Sudden Cardiac Death (SCD) D Death from a cardiac cause M Majority of SCDs result from ventricular dysrhythmias. V Ventricular tachycardia Ventricular fibrillation D Defibrillation M Most effective method of terminating VF and pulseless VT Passage of DC electrical shock through the heart to depolarize the cells C of the myocardium to allow the SA node to resume the role of pacemaker

D Defibrillation D Deliver energy using a monophasic or biphasic waveform Monophasic defibrillators deliver energy in one direction. Biphasic defibrillators deliver energy in two directions. use less jules bc it goes one direction/less energy which causes fewer problems a afterwards with akg rhythms. (about 60 jules) (uses less energy) Deliver successful shocks at lower energies and with fewer postshock ECG abnormalities Defibrillation D Defibrillation O Output is measured in joules or watts per second. R Recommended energy for initial shocks in defibrillation Biphasic defibrillators: First and successive shocks: 150 to 200 j joules M Monophasic defibrillators: Initial shock at 360 joules After shock, check pulse and start CPR if indicated T Testing: Check pulse, then CPR Defibrillation S Synchronized Cardioversion Choice of therapy for hemodynamically unstable ventricular or s supraventricular tachydysrhythmias Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG. Dont want on T wave bc it could send t them into vfib. S Synchronizer switch must be turned ON. I Implantable Cardioverter-Defibrillator (ICD) A Appropriate for patients who H Have survived SCD H Have spontaneous sustained VT Have syncope with inducible ventricular tachycardia/fibrillation d during EPS A Are at high risk for future life-threatening dysrhythmias EFs less than 25/30 are candidates bc at high risk for sudden c cardiac death I Implantable Cardioverter-Defibrillator (ICD) C Consists of a lead system placed via subclavian vein to the endocardium Battery-powered pulse generator is implanted subcutaneously.

I Implantable Cardioverter-Defibrillator (ICD) I ICD sensing system monitors the HR and rhythm and identifies VT or VF. Approximately 25 seconds after detecting VT or VF, ICD delivers < <25 joules. If first shock is unsuccessful, ICD recycles and delivers successive s shocks. I Implantable Cardioverter-Defibrillator (ICD) ICDs are equipped with antitachycardia and antibradycardia pacemakers. Initiate overdrive pacing of supraventricular and ventricular t tachycardias Provide backup pacing for bradydysrhythmias that may occur a after defibrillation discharges Implantable Cardioverter-Defibrillator (ICD)

I Implantable Cardioverter-Defibrillator (ICD) E Education is extremely important. V Variety of emotions are possible. F Fear of body image change F Fear of recurrent dysrhythmias E Expectation of pain with ICD discharge A Anxiety about going home P Participation in an ICD support group should be encouraged. P Pacemakers Used to pace the heart when the normal conduction pathway is damaged o or diseased Pacing circuit consists of a power source, one or more conducting ( (pacing) leads, and the myocardium. Pacemaker Spike P Pacemakers A Antibradycardia pacing Antitachycardia pacing: Delivery of a stimulus to the ventricle to t terminate tachydysrhythmias Overdrive pacing: Pacing the atrium at rates of 200 to 500 impulses per m minute to terminate atrial tachycardias B

P Pacemakers P Permanent pacemaker: Implanted totally within the body Cardiac resynchronization therapy (CRT): Pacing technique that r resynchronizes the cardiac cycle by pacing both ventricles Pacemaker P Pacemakers T Temporary pacemaker: Power source outside the body T Transvenous Epicardial on the surface of the heart o Transcutaneous on the skin/patch o Temporary Pacemaker

Temporary Transvenous Pacemaker P Pacemakers P Pacemaker malfunction Failure to sense: Failure to recognize spontaneous atrial or v ventricular activity and pacemaker fires inappropriately Lead damage, battery failure, dislodgement of the electrode Not sensing the underlying rhythm and firing inappropriately. Failure to capture: sensing but not firing.... P Pacemakers P Pacemaker malfunction Failure to capture: Electrical charge to myocardium is insufficient t to produce atrial or ventricular contraction Lead damage, battery failure, dislodgement of the electrode, f fibrosis at the electrode tip Patient education cant lift arm above shoulder for 6 weeks its all important Know ST-depression: ischemia ST-elevation: MI K Know Tombstone Ts. ECG Changes Associated With Acute Coronary Syndrome (ACS)

Definitive ECG changes occur in response to ischemia, injury, or i infarction of myocardial cells. C Changes seen in the leads that face the area of involvement Definitive ECG Changes E ECG Changes Associated With Acute Coronary Syndrome (ACS) I Ischemia S ST segment depression and/or T wave inversion ST segment depression is significant if it is at least 1 mm (one s small box) below the isoelectric line. Changes Associated With MI E ECG Changes Associated With Acute Coronary Syndrome (ACS) I Ischemia Changes occur in response to the electrical disturbance in m myocardial cells due to inadequate supply of oxygen. Once treated (adequate blood flow is restored), ECG changes resolve and ECG returns to baseline.

E ECG Changes Associated With Acute Coronary Syndrome (ACS) I Injury ST segment elevation is significant if >1 mm above the isoelectric l line. I If treatment is prompt and effective, may avoid infarction If serum cardiac markers are present, an ST-segmentelevation myocardial infarction (STEMI) has occurred. Changes Associated With Injury E ECG Changes Associated With Acute Coronary Syndrome (ACS) I Infarction Physiologic Q wave is the first negative deflection following the P w wave. S Small and narrow (<0.04 second in duration) Pathologic Q wave is deep and >0.03 second in duration. Changes Associated With Infarction E ECG Changes Associated With Acute Coronary Syndrome (ACS) I Infarction Pathologic Q wave indicates that at least half the thickness of the h heart wall is involved. R Referred to as a Q wave MI m P Pathologic Q wave may be present indefinitely. T wave inversion related to infarction occurs within hours and may

persist for months. ECG Finding With Anterolateral Wall MI Syncope S Brief lapse in consciousness accompanied by a loss in postural tone ( (fainting) C Cardiovascular causes Cardioneurogenic syncope or vasovagal syncope (e.g., carotid s sinus sensitivity) Primary cardiac dysrhythmias (e.g., tachycardias, bradycardias) S Syncope N Noncardiovascular causes H Hypoglycemia H Hysteria U Unwitnessed seizure S Stroke Vertebrobasilar transient ischemic attack S Syncope D Diagnostic studies E Echocardiography E EPS H Head-upright tilt table testing H Holter monitor Event monitor/loop recorder A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to: 1. 2. 3. 4. Perform defibrillation. Initiate cardiopulmonary resuscitation. Prepare for synchronized cardioversion. Administer IV antidysrhythmic drugs per protocol.

A patient has a diagnosis of acute myocardial infarction, and his cardiac rhythm is sinus bradycardia with six to eight premature ventricular contractions (PVCs) per minute. The pattern that the nurse recognizes as the most characteristic of PVCs is: 1. 2. 3. 4. An irregular rhythm. An inverted T wave. A wide, distorted QRS complex. An increasingly long PR interval.

A patients cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the

patient to exhibit: 1. 2. 3. 4. Palpitations. Hypertension. Warm, flushed skin. Shortness of breath.

C Case Study 45-year-old woman enters the ED complaining of sudden onset of p palpitations and shortness of breath. ECG reveals atrial fibrillation with a rapid ventricular response (HR = 168). C Case Study S She has no previous history of cardiac problems. An emergent cardioversion is planned. Discussion Questions D W What are some teaching points before the procedure? What treatments are available if the procedure is unsuccessful?

D Discussion Questions What risks does sustained atrial fibrillation pose, and how can this information be helpful in ensuring compliance?