cardiac 2

ACLS Defibrillation

Shockable rhythms -V Fib -Pulseless V Tach

represents repolarization of the ventricles.

T wave

Capture (PM)

Heart responds to the stimulus that generator delivered

Mobitz type 2 causes

Extensive damage to bundle branches after anteroseptal MI; CHD; myocarditis

Sinus Tachy Nursing Management

If symptomatic -Assess pain management -IV fluids -Correct etiology Medications- B block, CaCB

Atrial Pacing

Pacer artifact appears just before P wave on EKG strip

Junctional Tachycardia causes

Usually due to dig toxicity, catecholamines, or Theophylline; overexertion, coffee; alcohol; nicotine; electrolyte or acid-base imbalances; hyperventilation; emotional stress

ICD: Nursing Care

-Placed in cath lab under conscious sedation or w/ open heart surgery - Address fears -Know type of device

pacemaker classifications

temp non invasive (external) temp invasive (transvenous or epicardial) perm single chamber (atrial or ventricular) perm dual chamber (av sequential) perm synchronous (demand) perm asynchronous (fixed rate) antidysrythmic function

synchronous vs asynchronous pacemakers

synch only sends impulse when needed (demand) asynch send impulse. period. R on T, not seen much (fixed)

Two types of MI

STEMI- ST elevated "tombstone T's" bigger ST= bigger problem NSTEMI- non ST elevation. EKG will see unstable angina, but + for MI. damage to cells due to low O2/enzymes released. occlusion of coronary artery. damage not great. can extend if not taken care of.

Junctional escape beat

Single junctional beat making up for a pause in SA rhythm. Improves CO.

Perkinje fibers

-Generates 20-40 bpm -Runs along myocardium -Stimulates ventricular depolarization -> ventricular contraction

PAC (premature atrial contraction) Nursing Management

-Usually no tx if pt asymptomatic -Withdraw sources of stimulation (caf, stress) -Introduce beta adrenergic blockers (lopressor, inderal) to decrease PAC occurences -Lifestyle changes (decr stress, caf)

Supraventricular tachy Nursing Management

-Vagal maneuvers (valsalva/ carotid massage) -Convert rhythm ~Adenosine ~Antiarrythmics (amiodarone) ~beta blocks (betapace), CaCB (cardizem) -Cardioversion if drug therapy fails & symptoms persist -Ablation management (radiation to kill overactive cells)

temporary pacemakers

-external electrodes on skin (A/P) sedation required -temp invasive- transvenous- lead sent through subclavian threaded into R atrium or R ventricle. -temp invasive- epicardial- lead attached to epicard to pace post op. may have A/V leads. leads come out of wound, cover til needed.

phases of action potential of heart 0-4

0- depolarization (-90 to +20) 1- early repoloarization (+20 to 0) 2- plateau phase (0) 3- rapid repolarization (Potassium rushes out) 4- resting membrane potential (refractory)

QRS Complex

Measured from beginning of Q wave to end of S wave Represents depolarization (contraction) of ventricle Measures .04-.12 sec

A nurse is assessing an electrocardiogram rhythm strip. The P waves and QRS complexes are regular. The PR interval is 0.16 second, and QRS complexes measure 0.06 second. The overall heart rate is 64 beats per minute. The nurse assesses the cardiac rhythm as: A. Normal sinus rhythm B. Sinus bradycardia C. Sick sinus syndrome D. First-degree heart block.

NORMAL SINUS RHYTHM 1. measurements are normal, measuring 0.12 to 0.20 second and 0.4 to 0.10 second, respectively.

ectopic focus

abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity. Their pacemaker activity, however, is normally suppressed (overdrive suppression) by the higher rate of the SA node. They can occur within the atria or ventricles.

teaching for pacemakers

always have pacemaker id card batteries last 10 years know rate of PM log pulse daily report dizzy, faint, palp, hiccups no contact sports x2 mo sex as desired, no stress/pressure on site inform all caregivers (dentist too) avoid MRI

tx of infective endocarditis

antibiotics if causes valve prob, fix the valve if causes abscess, drain if damage to chordae tendineae, may need to repair

infective endocarditis

bacterial or fungal infection of endocardium. can include heart valves.

risk for infective endocarditis?

cardiac surgery for valve repair/replacement bypass surgery (can introduce bacteria) congenital heart defects rheumatic heart disease injection drug abuse bad technique for IV/ artery access

progression of pericarditis

cardiac tamponade (life threatening)

Causes of Accelerated junctional rhythm

commonly dig toxicity; Acute inferior MI; HF; acute rheumatic fever; valvular heart disease; myocarditis; post cardiac surgery

subendocardial MI

damage is closer to the endocardium (SEMI) does not extend through entire myocardium. bullseye- center is necrosis, middle is repaired when O2 restored. outer area of ischemia.

Digoxin

given for Afib, A flutter and supravenricular tachyarthymias dont use for v tach, v fib, 2nd and 3rd degree heart block

interrogating the pacemaker

magnet placed over PM on skin to adjust settings and read "report"

Sinus Arrythmia

normal sinus variation seen with respiratory cycle P-P interval irregular in a pattern difference between shortest and longest >.12 sec

assessment of an MI

risk factors pain, intensity, quality SOB? associated s/s listen to heart/ lungs med Hx/ FH

The patient is admitted with acute coronary syndrome (ACS). The ECG shows ST-segment depression and T-wave inversion. What should the nurse know that this indicates? A. Myocardia injury B. Myocardial ischemia C. Myocardial infarction D. A pacemaker is present

B. The ST depression and T wave inversion on the ECG of a patient diagnosed with ACS indicate myocardial ischemia from inadequate supply of blood and oxygen to the heart. Myocardial injury is identified with ST-segment elevation. Myocardial infarction is identified with ST-segment elevation and a widened and deep Q wave. A pacemaker's presence is evident on the ECG by a spike leading to depolarization and contraction.

The nurse is doing discharge teaching with the patient and spouse of the patient who just received an implantable cardioverter-defibrillator (ICD) in the left side. Which statement by the patient indicates to the nurse that the patient needs more teaching? A. "I will call the cardiologist if my ICD fires." B. "I cannot fly because it will damage the ICD." C. "I cannot move my left arm until it is approved." D. "I cannot drive until my cardiologist says it is okay."

B. The patient statement that flying will damage the ICD indicates misunderstanding about flying. The patient should be taught that informing TSA about the ICD can be done because it may set off the metal detector and if a hand-held screening wand is used, it should not be placed directly over the ICD. The other options indicate the patient understands the teaching.

The nurse is seeing artifact on the telemetry monitor. Which factors could contribute to this artifact? A. Disabled automaticity B. Electrodes in the wrong lead C. Too much hair under the electrodes D. Stimulation of the vagus nerve fibers

C. Artifact is caused by muscle activity, electrical interference, or insecure leads and electrodes that could be caused by excessive chest wall hair. Disabled automaticity would cause an atrial dysrhythmia. Electrodes in the wrong lead will measure electricity in a different plane of the heart and may have a different wave form than expected. Stimulation of the vagus nerve fibers causes a decrease in heart rate, not artifact.

Which statement best describes the electrical activity of the heart represented by measuring the PR interval on the ECG? A. The length of time it takes to depolarize the atrium B. The length of time it takes for the atria to depolarize and repolarize C. The length of time for the electrical impulse to travel from the SA node to the Purkinje fibers D. The length of time it takes for the electrical impulse to travel from the SA node to the AV node

C. The electrical impulse in the heart must travel from the SA node through the AV node and into the Purkinje fibers in order for synchronous atrial and ventricular contraction to occur. When measuring the PR interval (the time from the beginning of the P wave to the beginning of the QRS), the nurse is identifying the length of time it takes for the electrical impulse to travel from the SA node to the Purkinje fibers. The P wave represents the length of time it takes for the impulse to travel from the SA node through the atrium causing depolarization of the atria (atrial contraction). Atrial repolarization occurs during ventricular depolarization and is hidden by the QRS complex. The length of time it takes for the electrical impulse to travel from the SA node to the AV node is the flat line between the end of the P wave and the beginning of the Q wave on the ECG and is not usually measured.

Cardioversion is attempted for a 64-year-old man with atrial flutter and a rapid ventricular response. After the nurse delivers 50 joules by synchronized cardioversion, the patient develops ventricular fibrillation. Which action should the nurse take immediately? A. Administer 250 mL of 0.9% saline solution IV by rapid bolus. B. Assess the apical pulse, blood pressure, and bilateral neck vein distention. C. Turn the synchronizer switch to the "off" position and recharge the device. D. Tell the patient to report any chest pain or discomfort and administer morphine sulfate.

C. Ventricular fibrillation produces no effective cardiac contractions or cardiac output. If during synchronized cardioversion the patient becomes pulseless or the rhythm deteriorates to ventricular fibrillation, the nurse should turn the synchronizer switch off and initiate defibrillation. Fluids, additional assessment, or treatment of pain alone will not restore an effective heart rhythm.

Causes of Vtach

CAD, underlying heart disease is usually cause; MI; Dig; hypokalemia; hypomagnesaemia; Insertion of invasive catheters; post angioplasty; common reperfusion arrhythmia; drugs which prolong QT interval

Premature Complexes

Can arise from pacemaker sites in Atria, AVJ or ventricles. Recognized by prematurity; appearing earlier than expected in patients regular rhythm Due to increased automaticity and often precede tachy dysrhythmias. Premature beats happen in healthy and unhealthy hearts

effect of Junctional Rhythm

Can decrease CO due to slow ventricular rate (40-60) or inappropriately timed atrial contraction.

Repolarization

Cells become more negative on the inside (relaxing)

Accelerated Ventricular Rhythm Causes

Common after acute MI, especially inferior; Common reperfusion rhythm after thrombolytic therapy. Also seen in dig toxicity and cardiomyopathy

PAC causes

Common in healthy and diseased hearts. Often caused by stress or ingestion of stimulants. Electrolyte imbalance (low K and Mg); Hypoxia; ischemia; CAD; Chronic lung disease; Dig; Hyperthyroidism; atrial hypertrophy due to stenosis; Other premature complexes have similar causes

Implantable Cardioverter- Defibrillator (ICD)

Device -Bradyc backup pacing -Dual chamber system allows for cardioversion/ pacing atrial tachydysryths

Accelerated Junctional Rhythm

Increased Automaticity of AV junction leads to ventricular rate of 61-100. CO is usually not decreased but may be affected by inappropriately timed atrial kick

Sinus Block causes

Increased Vagal tone Damage to SA node from MI myocarditis CHF Hyperkalemia hypoxia Dig, CCB, BB

PR Interval

Measured from beginning of P wave to start of QRS complex Represents impulse conduction from SA to AV Measures .12-.2 sec

Asystole Causes

Metabolic acidosis hypoxia hyper/ hypo- kalemia hypothermia drug OD

Second Degree Type II AVB

Mobitz II -More advanced and severe than Type I -PR interval remains consistent and QRS complex is dropped without warning (2:1) -Regular or irregular

AVB: Nursing Management

Most likely cause is ischemia -Place O2 -Identify rhythm -Obtain 12 lead -Monitor freq VS -Assess if hemodynamically stable If sx: administer atropine, place pacer pads on pt and crash cart by room -will probably need PM

Atrial tachycardia

Normal PR. Normal QRS. Atrial rate of 151-250. When rate exceeds rate AV node can transmit impulse a block may develop

Sinus Tach Causes

Normal response to increased demand: excitement exercise fever infections hypoxia pain PE MI Stimulants, drugs

Junctional Rhythm causes

Often result of cardiac meds: Dig, BB, CCB; AV node damage after inferior MI, electrolyte imbalance, HF, valvular heart disease, cardiomyopathy, myocarditis

represents depolarization of the ventricles (ventricular contraction).

QRS complex

represents the total time for depolarization and repolarization of the ventricles.

QT interval

Atrial Flutter

Rate: atrial 200-350, vent 150 bpm Rhythm: atrial (regular), vent (reg or irreg) -P waves unidentifiable; "F waves sawtooth" -QRS complex usually normal -Usually fixed ratio of F waves to QRS (2:1, 3:1)

Atrial Fibrillation

Rate: atrial 350-600 bpm, ventricle 60-100 (rate controlled); 100 bpm (rapid ventricular rate) Rhythm: irregularly irregular -No discernible P waves: F waves seen -QRS complex usually normal measurement

Sinus Brady

SA node pacemaker at less then 60 bpm can increase or decrease CO

Third Degree block

There is NO conduction; 2 impulse origins: SA node-P waves, AVJ or Ventricles -QRS complex Features: P-P regular, R-R regular, P-R irregular

Third Degree Causes

Transient caused by inferior MI and after cardiac surgery; Increased Vagal tone; Myocarditis; dig; anteroseptal MI; Congenital abnormality; Rheumatic fever; hypoxia; post cardiac cath; degenerative changes

VT Nursing Mgmt (Pulseless)

Treated like V Fib -Code blue -CPR, rapid defib -Next, vasopressors (epi) and antidysrythmics (amiodarone)

Permanent pacemakers

Usually in left shoulder, SQ pouch. leads are usually transvenous, can be epicardial

Idioventricular Rhythm

When both SA and AV fail. Inherent rate <40. Can deteriorate to asystole

labs for infective endocarditis

blood cultures, determine what growing, and what the bacteria is sensitive to

s/s of cardio prob

chest pain dyspnea proxysminal nocturnal dyspnea orthopnea fatigue palpitations N/V diaphoresis

angina

inability to adequately supply blood to myocardium. pain is indicator ischemia is occurring. no perm damage. sympt go away when blood restored. stable or unstable

Pacemaker complications

infection ectopy during insertion (touch wall of A/V=impulse) failure to capture (PM generates impulse= no depol) undersensing (PM at fixed rate even though HR faster) oversensing (PM not fires when HR slow) electromag interference (ground pt)

pericarditis

inflammation of the pericardium acute- virus/ bacterial most comm. also trauma/MI/tumors/ idiopathic chronic- TB/ radiation/ trauma

artifact

irregular EKG report due to movement: sticker peeling off patient moving/shivering/talking hairy chests loose EKG clip patient not on their back bad EKG machine

interventions for infective endocarditits

rest mobility as tolerated monitor VS/ heart sounds good cardio assessment oral care- soft brush no floss (hx of endo) always take antibiotics prophylactically before procedures

indications for a pacemaker

symptomatic brady complete heart block- sometimes 2nd sick sinus rhythm sinus arrest asystole A or V tachy dysrythmias

bundle of his

the junction, takes impulse across AV septum and slows impulse down. increases preload by allowing atrial kick to fill ventricles.

V Fib Etiology & RF

-Acute MI/ ischemia -HF -Cardiomyopathy -Hypoxia -Hyperkalemia -Drug toxicity -Electrical shock -Hypothermia -R on T PVCs -Untreated VT -Post cardiac cath -Post coronary artery perfusion from fibrinolytics

Sinus Brady Etiology and Risk

-Athletes -Inferior wall MI -Hypothyroidism -Increased ICP -Diabetes -Vagal stimulation (severe constipation) -Carotid sinus massage -Drugs (Beta Blocks, CaCB) -Hypothermia

Atrial Flutter Etiology & Risk

-CAD -COPD -HTN -Mitral valve disorders -Pulmonary embolism -Ischemic heart disease -Acute MI -Hypoxia -Digoxin toxicity -Cor pulmonale -Cardiomyopathy

V Tach Nursing Management (Gen)

-Identify rhythm -ASSESS PT ~Check for pulse! If pulse- pt stable by interventions required -Monitor -Apply pacing pads

Ventricular Tachycardia

-LIFE THREATENING!!!! Rate: >100 bpm but not usually over 250; regular -No P waves; QRS >/=.12 -Sustained (>30sec) vs. unsustained (<30 sec)

A Fib s/s

-May be asymptomatic if rate controlled (vent <100 bpm) -Palpitations: most common -Fatigue -Exercise tolerance decreased -Syncope (if underlying stenosis or PE) -Irregular pulse

ICD: Indications

-Sudden cardiac death survivor -Spontaneous VT -Syncope w/ VT/VF -High risk life-threatening dysrhythmias

What criteria should the nurse use to determine normal sinus rhythm for a client on a cardiac monitor? Check all that apply. 1. The RR intervals are relatively consistent 2. One P wave precedes each QRS complex 3. Four to eight complexes occur in a 6 second strip 4. The ST segment is higher than the PR interval 5. The QRS complex ranges from 0.12 to 0.20 second.

1, 2. The consistency of the RR interval indicates regular rhythm. A normal P wave before each complex indicates the impulse originated in the SA node. The number of complexes in a 6 second strip is multiplied by 10 to approximate the heart rate; normal sinus rhythm is 60 to 100. Elevation of the ST segment is a sign of cardiac ischemia and is unrelated to the rhythm. The QRS duration should be less than 0.12 second; the PR interval should be 0.12 to 0.20 second.

A nurse notices frequent artifact on the ECG monitor for a client whose leads are connected by cable to a console at the bedside. The nurse examines the client to determine the cause. Which of the following items is unlikely to be responsible for the artifact? 1. Frequent movement of the client 2. Tightly secured cable connections 3. Leads applied over hairy areas 4. Leads applied to the limbs

2. Tightly secured cable connections. Motion artifact, or "noise," can be caused by frequent client movement, electrode placement on limbs, and insufficient adhesion to the skin, such as placing electrodes over hairy areas of the skin. Electrode placement over bony prominence's also should be avoided. Signal interference can also occur with electrode removal and cable disconnection.

A nurse is viewing the cardiac monitor in a client's room and notes that the client has just gone into ventricular tachycardia. The client is awake and alert and has good skin color. The nurse would prepare to do which of the following? 1. Immediately defibrillate 2. Prepare for pacemaker insertion 3. Administer amiodarone (Cordarone) intravenously 4. Administer epinephrine (Adrenaline) intravenously

3. First-line treatment of ventricular tachycardia in a client who is hemodynamically stable is the use of anti-dysrhythmics such as amiodarone (Cordarone), lidocaine (Xylocaine), and procainamide (Pronestyl). Cardioversion also may be needed to correct the rhythm (cardioversion is recommended for stable ventricular tachycardia). Defibrillation is used with pulseless ventricular tachycardia. Epinephrine would stimulate and already excitable ventricle and is contraindicated.

Propanolol

sinus tach paroxymal atrial tach exercise induced tach severe recurrent v. tach supraventricular tach

Sinus Arrythmia causes

Often seen in sinus brady deep sleep children and young adults May be a sign of sick sinus syndrome in elderly Acute inferior MI increased ICP

Supraventricular Tachycardia

Rate: >150bpm, regular -P waves hidden in T waves -Normal QRS complex measure -Narrow complex tachy -If onset/ending abrupt- paroxysamal atrial tachy

s/s of pericarditis

substernal radiating chest pain pleuritic (stabbing in heart) positional friction rub S1 to S1 if infectious will have elevated temp

Becks triad

symptom of cardiac tamponade hypotension muffled heart sounds JVD

Supraventricular Tachycardia

Often tachycardias with rates over 140-150 can be difficult to identify. All Tachycardias that are not ventricular can be classified as SVT until 12- lead EKG identifies specific pacemaker site. Temporary label

Premature Atrial Contraction (PAC)

-Rate usually <100 bpm -Irregular -P waves are early & upright -Norm PR interval & QRS complex measurements -P for every QRS -Conducted, nonconducted (throws off beat, not enough to conduct beat), aberrantly

Cardiac Output Norms

CO = 4-6L/min HR & Rhythm= WNL BP WNL (90-140/60-90) UO WNL= 30mL/hr

Antidysrythmic Drugs

B Blockers (-olols) ~Decrease HR, contractility CaCB (-pines, diltiazem, verapamil) ~Decrease conduction through AV, decreases HR

Ectopic Beat

Beat initiated outside the electrical pathway

labs for MI

Creatine Kinase (CK/CPK) Troponin Lipid profile EKG

A 38-year-old teacher who reported dizziness and shortness of breath while supervising recess is admitted with a dysrhythmia. Which medication, if ordered, requires the nurse to carefully monitor the patient for asystole? A. Atropine sulfate B. Digoxin (Lanoxin) C. Metoprolol (Lopressor) D. Adenosine (Adenocard)

D. IV adenosine (Adenocard) is the first drug of choice to convert supraventricular tachycardia to a normal sinus rhythm. Adenosine is administered IV rapidly (over 1 or 2 seconds) followed by a rapid, normal saline flush. The nurse should monitor the patient's ECG continuously because a brief period of asystole after adenosine administration is common and expected. Atropine sulfate increases heart rate, whereas lanoxin and metoprolol slow the heart rate.

Atrial fib Causes

Emotional stress; alcohol; caffeine; and previous

Electrolytes (Mg)

HypoMg <1.5 leads to form of VT known as Torsades de pointes ~Admin IV MagSulfate (Assess for neuromusc irritability) -HyperMg >2.5 leads to bradyc, increased PRI, widened QRS, elevated T waves ~Admin Ca gluconate as ordered

Sinus Brady Causes

Increase in parasympathetic decrease in sympathetic vagal stimulation hypoxia hypothermia hyperkalemia Increased ICP Dig, CCB, BB Protective rhythm with acute MI

interventions of pericarditis

NSAIDS observe for pericardial effusions (fluid in space)

SA Node

Internal pacemaker -Generates impulse of 60-100 bpm -SA fires when depolarizing -SA rests when repolarizing -Causes atrial contraction

Sinus Rythm

NSR -60-100 bpm -Regular -P for every QRS, and p waves upright -PR .12-.2 sec

Electrical Pathway

SA > AV > His Bundle > R/L BB > PF

Sinus Tach

SA node pacemaker at 101-150bpm Can increase or decrease CO. Increased HR decreases filling time and thus may decrease CO

Firing (PM)

The generator delivers a pacing stimulus

T Wave

Ventricular re polarization Typically positive deflection especially in lead II Inverted T Wave may indicate ischemia and/or infarction STEMI/ NSTEMI

Second Degree Block Type I AVB

Wenckeback/ mobitz 1 -PR interval progressively prolonged with each beat until QRS complex dropped (1:1) -QRS complex dropped -QRS & QT interval measurements not affected

interventions for cardiac tamponade

pericardial centesis- aspirate fluid from pericardial sp pericardial window- surgical hole in peri to drain pericardectomy- remove pericardium

Single vs dual chambers pacemakers

single in atria, dual in atria and ventricle (R)

Dysrhythmias result from

disorders of impulse formation, conduction of impulses, or both.

troponin

enzyme in cardiac tissue. T- 0.1-0.5 initial rise w/in 3-6 hrs. peaks 4-6 hrs 1- <0.2 initial rise w/in 3 hrs, peaks 14-18 hrs

s/s of infective endocarditis

fever (above 103) murmur HF anorexia/ weight loss fatigue embolic phenom (bacteria breaks loose and travels)

lipid profile

for risk factors total- 400-800 cholesterol 150-240 triglycerides 10-190 LDL- <160 HDL- 29-77 (high risk CHD <35)

acute coronary syndrome

general term, not a specific disease. problems with ischemia (loss of o2 to cells) angina MI

Mobitz type 1 causes

commonly transient after MI; dig; BB; CCB; increased vagal tone; myocarditis; CHD; ischemia; aging

Conductivity

Ability to conduct an impulse resulting in stimulation of adjacent cells

Dual Pacing

Pacer artifact appears prior to both P wave and QRS complex

cardioversion priorites

+Informed consent +Complete physical assessment prior to procedure +Anticoag hx +Mg & K prior to procedure +Pt NPO about 8 hours prior to cardioversion -Ensure IV access, Place crash cart @ bedside -Cardiac monitor, pulse ox, BP cuff in place -O2 set up -MD orders regarding holding Dig -Anesthesiology at bedside if not intubated -Sedate pt (Versed) -Reassess pt post procedure

Sinus Tachycardia

- Rate >100 bpm, <150 bpm -Regular -Normal and consistent PR interval and QRS complex - P for every QRS

Premature ventricular contractions Nursing Management

-3 or more in a row = VTach -Monitor EKG closely- R on T phenomenon -Identify cause (hypoxia, electrolyte imbalance) -May require beta blocks, amiodarone, lidocaine -PVCs don't generate sufficient ventricle contraction for peripheral pulse- might note a pause when palpating radial pulse -Check apical-radial pulse rate

ICD: Device

-Battery powered -1-3 lead (one in atria, and in one or both vent) -Monitors HR & rhyth, detects lethal dysryths, -Delivers low shock (25j) to pt heart

Measuring EKGs

-Horizontal axis -1 small square= .04 sec -1 large square= .2 sec -Lines at top of EKG paper are 3 sec apart

Pacemakers

-Used in pt w/ damaged pathway -Used for brady arrhythmias & override ability for tachy arrhythmias Indications: -AV block (2nd & 3rd degree) -BBB -Cardiomyopathy -HF -SA node dysfunction -Tachyarrhythmias

For which dysrhythmia is defibrillation primarily indicated? A. Ventricular fibrillation B. Third-degree AV block C. Uncontrolled atrial fibrillation D. Ventricular tachycardia with a pulse

A. Defibrillation is always indicated in the treatment of ventricular fibrillation. Drug treatments are normally used in the treatment of uncontrolled atrial fibrillation and for ventricular tachycardia with a pulse (if the patient is stable). Otherwise, synchronized cardioversion is used (as long as the patient has a pulse). Pacemakers are the treatment of choice for third-degree heart block.

AV Node

Atrioventricular Node -Generates 40-60 bpm -Receives impulse from SA node -Short delay time at AV node allows for ventricle filling -Sends impulse to His Bundle

More drugs for Dysrythmias

Atropine- anticholinergic ~Sx brady, AV blocks, asystole Epinephrine ~Increases HR, conduction, contractility, vasodilation ~Used in pulseless VT, VF, bradyarrythmias Vasopressin (antidiuretic hormone) ~Used in VF, pulseless VT, PEA

The patient has atrial fibrillation with a rapid ventricular response. The nurse knows to prepare for which treatment if an electrical treatment is planned for this patient? A. Defibrillation B. Synchronized cardioversion C. Automatic external defibrillator (AED) D. Implantable cardioverter-defibrillator (ICD)

B. Synchronized cardioversion is planned for a patient with supraventricular tachydysrhythmias (atrial fibrillation with a rapid ventricular response). Defibrillation or AEDs are the treatment of choice to end ventricular fibrillation and pulseless ventricular tachycardia (VT). An ICD is used with patients who have survived sudden cardiac death (SCD), have spontaneous sustained VT, and are at high risk for future life-threatening dysrhythmias.

creatine Kinase

CK/ CPK (M 5-35) (F 5-25) enzyme in skeletal muscle, brain tissue, cardio tissue. if elevated there has been damage. ISOENZYMES MM (skel) BB (brain/stroke) MB (MI) rises within 3-6 hr/ peak 12-24 hr/ norm 2-3 days lab values skewed with IM injections/exercise/trauma

Depolarization

Cells become more positive on the inside (contracting)

Heart blocks

Conduction abnormalities along conduction system. SA node is pacemaker

Mobitz type 2

Conduction delay is below AV node in ventricular conduction system. Produces a wide QRS complex. More P's than QRS's. Less common than type 1 but more serious

First Degree Block

Conduction is abnormal in AV junction. Every impulse reaches the ventricles; it just takes longer than 0.2 sec

Sinus Block

Conduction is blocked within the SA node or the SA node fails to fire. Creates a pause within a normal sinus rhythm. Features: complete lack of P wave, QRS complex, T wave

Atrial Tachycardia causes

Dig; ischemia; hypocalcemia; hypoxia; hyperkalemia; some antiarythmics; emotional stress; mitral valve disease; COPD; Alcohol; caffeine; nicotine

VT Nursing Mgmt (Stable)

Hemodynamically stable tx cause (ischemia, hypoxia- provide O2, correct electrolyte imbalance) ~Meds (epi, vasopressin, procainamide, amiodarone, lidocaine, beta blocks) ~ICD implantation management

Accelerated Ventricular Rhythm

Increased ventricular automaticity. Rate of 40-100. Usually well tolerated and transient. Often alternates with NSR

Demand Pacing

Is able to inhibit impulse generation when the pt's intrinsic rhythm is adequate *not going unless goes below 70 bpm

represents the depolarization of the atria (passage of an electrical impulse through the atria), causing atrial contraction.

P wave

represents the time period for the impulse to spread through the atria, atrioventricular (AV) node, bundle of His, and Purkinje fibers.

PR interval

Triggering (PM)

Pacer senses pt's missed beat & generates response

represents the time it takes for depolarization

QRS Interval

Atrial Flutter

Rapid depolarization from multiple ectopic pacemakers. Rate > 400 bpm. No distinct P-waves seen. Impulses let through AV node at random. Ventricular rate can be fast, normal or slow.

Sensing (PM)

The generator is able to see the pt's intrinsic beat

Temporary Pacemakers

Transvenous -Lead(s) threaded through R atrium and R ventricle w/ external power source Epicardial -Leads attached to epicardium and passed through chest wall -Post open heart Transcutaneous -Pacer pads placed on skin & attached to power source w/ HR & voltage control -Least invasive, start here, VERY SHORT duration

Lidocaine

Ventricular dysrythimias not used for supraventricular dysrhythmias.

s/s of cardiac tamponade

becks triad- hypotension, muffled heart sounds, JVD may have elevated HR pulseless paradoxyis (drop in systolic BP greater than 10 mm during inspiration) x-ray to look for enlargement of cardiac silhouette EKG (tachy)

unstable angina

pain comes and goes without predictability. sometimes goes away with one nitro, other times need more.

interventions for unstable angina

pain hx EKG- inverted T waves, ST depression/changes (if ST changes check CK/Troponin)

adenosine

paroxysmal SVT (supraventricular tachycardia)

First Degree causes

Dig, CCB, BB, quinidine, procainamide, amiodarone; Increased vagal tone; hyperkalemia; RHD; Myocarditis; Inferior MI; Degeneration due to aging

Ventricular Tachycardia

Lethal. Often preceded by PVCs. Greater than 100 bpm

represents the time between ventricular depolarization and repolarization. This segment should be flat or isoelectric and represents the absence of any electrical activity between these two events

ST segment

Mobitz type 1 (Wenckebach)

impulse is conducted abnormally through AVJ. There is a progressive delay until an impulse is finally blocked. Lengthening of PR intervals until there is no QRS complex

Amiodarone

life threatening ventricular dysrhythmias recurrent V-fib most effective for afib

Sinus Brady Nursing Managment

If symptomatic -Assessment of medications -Atropine -Possible pacemaker Nutritional Information: increase daily fiber, water intake (decrease r/o constipation)

Second degree

Some impulses are conducted to the ventricles and some are not. More P's than QRS's

A Fib Etiology & Risk

-CAD -Rheumatic Heart Disease -HTN -Cardiomyopathy -HF -Pericarditis -Hypoxia -Acute MI -Valvular disease

A Fib Nursing Management

-Control rate w/ Beta Blocks, CaCB, (diltiazem, metoprolol, digoxin) -Convert rate with antiarrythmics (amiodarone, ibutilide) -Anticoagulation (Warfarin, pradaxa, aspirin) -Long term aspirin used in pts <65 -Cardioversion

P wave

-Depolarization of both atria (contraction) -Represents generation of electrical impulse -Smooth & rounded -Abnormal P wave may be peaked or notched and indicate CHF, COPD, valvular disease

Nursing Mgmt & Diag Eval heart dsyfxn

-Determine if hemodynamically stable -Continuous tele and observe ectopic beats -Monitor VS -12 lead EKG, CXR, Echo -Labs: BMP, Mg, Phos, CBC, Trops

Patient s/s heart dysfxn

-Hypotension -Pallor -Cool skin -Dizziness -Chest pain -Weakness -Confusion & disorientation -Dyspnea -Hypoxia

Sinus Tachy Etiology & Risk

-Hypoxia -Exercise -Fever -Hypotension -Hypovolemia -Anemia -Myocardial ischemia -HF -Hyperthyroidism -Anxiety -Drugs (epi, norepi, atropine, caffeine, theophylline (high caf), amphetamines, psudoephedrine)

V Fib Nursing Management

-If untreated pt will expire -ASSESS pt -Begin CPR immediately (ACLS) -Rapid defib & drug therapy

Asystole Nursing Management

-Initiate CPR using ACLS protocol -Drug therapy (epi, atropine) -Transcutaneous pacing

Patient Presentation

-May be asymptomatic- 1AVB, 2AVB -Symptomatic 3AVB Can include: -Palpitations -Dizziness -Syncope -Chest pain -Fatigue -Diaphoresis -Mental status changes

Supraventricular Tachy Etiology & Risk

-Overexertion -Stress -CAD -Hypoxia -Fever -Cor pulmonale (R side enlargement of heart) -Dig toxicity -Rheumatic heart disease -Caffeine -Tobacco

Permanent Pacemaker

-Place subQ over pt pectoral muscle -Leads threaded through transvenously through R atrium to one or both ventricles -Single or dual chamber

First Degree AV Block

-Prolonged conduction between atrium and ventricle -PR interval >.2 seconds and consistent -QRS complex and QT measurements not affected

Sinus Bradycardia

-Rate <60 bpm -Regular -Normal & consistent PR interval & QRS complex - P for every QRS

Atrial Flutter Nursing Mgmt

-Rate control w/ CaCB, beta blocks -Antiarrhythmics (amiodarone) -Anticoagulation (warfarin) -Cardioversion -EP lab for ablation

Premature Ventricular Contraction PVC

-Rate dependent on underlying rhythm -Rhythm variable ~one in a row: isolated ~two in a row: couplet ~three or more: V tach ~every other: bigeminy ~every third: trigeminy -Not accompanied by P wave -QRS >/= 0.12 -ST &T are often direction of QRS

Synchronized Cardioversion

-Shock delivered on R wave of QRS complex -Used for hemodynamically unstable pt: VT w/ pulse, SVT, AFib rapid ventricular rate, A Flutter -May also be a planned procedure in patients with stable dysrythmias (SEDATED)

V Tach Etiology & Risk

-Signif electrolyte imbalance -MI -Cardiomyopathy -CAD -CNS disorders -Drug toxicity -Prolonged QT -Freq PVCs -Infections

Premature ventricular contractions Etiology & Risk

-Stimulants -Electrolyte imbalance -Fever, infection, stress -Exercise -Gastric overload -Acute MI -Acidosis -Cyclic antidepressants -Heart disease

PAC (premature atrial contraction) Etiology & Risks

-Stress -Fatigue -Caffeine -Alcohol -Tobacco -CHF -Electrolyte imbalance -COPD -Hypoxia -Heart Disease -MI or injury -Digoxin toxicity

Asystole

-Total absence of ventricular activity -Occasional P waves or agonal beats seen Etiology: cardiac conduction disturbance > cardiac arrest ASSESS PT- confirm asystole

Defibrillation

-Unsynchronized shock- depolarize myocardial cells ~Allow SA node to resume pacemaker role -Used to terminate pulseless VT or VF ~Successful pt outcomes improved with rapid defib (<2 min)

A client with rapid rate atrial fibrillation asks a nurse why the physician is going to perform carotid massage. The nurse responds that this procedure may stimulate the: 1. Vagus nerve to slow the heart rate 2. Vagus nerve to increase the heart rate; overdriving the rhythm. 3. Diaphragmic nerve to slow the heart rate 4. Diaphragmic nerve to overdrive the rhythm

1. Carotid sinus massage is one of the maneuvers used for vagal stimulation to decrease a rapid heart rate and possibly terminate a tachydysrhythmia. The others include inducing the gag reflex and asking the client to strain or bear down. Medication therapy often is needed as an adjunct to keep the rate down or maintain the normal rhythm.

Junctional P-QRS relation ships

1. P comes before QRS, but is less than 0.12 sec (3 box) 2. P comes after QRS, usually in ST segment 3. P hidden in QRS Because impulse is conducted retrograde to atrias, there is an inverted P wave

A client is having frequent premature ventricular contractions. A nurse would place priority on assessment of which of the following items? 1. Blood pressure and peripheral perfusion 2. Sensation of palpitations 3. Causative factors such as caffeine 4. Precipitating factors such as infection

1. Premature ventricular contractions can cause hemodynamic compromise. The shortened ventricular filling time with the ectopic beats leads to decreased stroke volume and, if frequent enough, to decreased cardiac output. The client may be asymptomatic or may feel palpations. PVCs can be caused by cardiac disorders or by any number of physiological stressors, such as infection, illness, surgery, or trauma, and by the intake of caffeine, alcohol, or nicotine.

A client has developed atrial fibrillation, which a ventricular rate of 150 beats per minute. A nurse assesses the client for: 1. Hypotension and dizziness 2. Nausea and vomiting 3. Hypertension and headache 4. Flat neck veins

1. The client with uncontrolled atrial fibrillation with a ventricular rate more than 150 beats a minute is at risk for low cardiac output because of loss of atrial kick. The nurse assesses the client for palpitations, chest pain or discomfort, hypotension, pulse deficit, fatigue, weakness, dizziness, syncope, shortness of breath, and distended neck veins.

A nurse is watching the cardiac monitor, and a client's rhythm suddenly changes. There are no P waves; instead there are wavy lines. The QRS complexes measure 0.08 second, but they are irregular, with a rate of 120 beats a minute. The nurse interprets this rhythm as: 1. Sinus tachycardia 2. Atrial fibrillation 3. Ventricular tachycardia 4. Ventricular fibrillation

2. Atrial fibrillation is characterized by a loss of P waves; an undulating, wavy baseline; QRS duration that is often within normal limits; and an irregular ventricular rate, which can range from 60 to 100 beats per minute (when controlled with medications) to 100 to 160 beats per minute (when uncontrolled).

A nurse is caring for a client with unstable ventricular tachycardia. The nurse instructs the client to do which of the following, if prescribed, during an episode of ventricular tachycardia? 1. Breathe deeply, regularly, and easily. 2. Inhale deeply and cough forcefully every 1 to 3 seconds. 3. Lie down flat in bed 4. Remove any metal jewelry

2. Cough cardiopulmonary resuscitation (CPR) sometimes is used in the client with unstable ventricular tachycardia. The nurse tells the client to use cough CPR, if prescribed, by inhaling deeply and coughing forcefully every 1 to 3 seconds. Cough CPR may terminate the dysrhythmia or sustain the cerebral and coronary circulation for a short time until other measures can be implemented.

While caring for a client who has sustained an MI, the nurse notes eight PVCs in one minute on the cardiac monitor. The client is receiving an IV infusion of D5W and oxygen at 2 L/minute. The nurse's first course of action should be to: 1. Increase the IV infusion rate 2. Notify the physician promptly 3. Increase the oxygen concentration 4. Administer a prescribed analgesic

2. PVCs are often a precursor of life-threatening dysrhythmias, including ventricular tachycardia and ventricular fibrillation. An occasional PVC is not considered dangerous, but if PVCs occur at a rate greater than 5 or 6 per minute in the post MI client, the physician should be notified immediately. More than 6 PVCs per minute is considered serious and usually calls for decreasing ventricular irritability by administering medications such as lidocaine. Increasing the IV infusion rate would not decrease the number of PVCs. Increasing the oxygen concentration should not be the nurse's first course of action; rather, the nurse should notify the physician promptly. Administering a prescribed analgesic would not decrease ventricular irritability.

When ventricular fibrillation occurs in a CCU, the first person reaching the client should: 1. Administer oxygen 2. Defibrillate the client 3. Initiate CPR 4. Administer sodium bicarbonate intravenously

2. Ventricular fibrillation is a death-producing dysrhythmia and, once identified, must be terminated immediately by precordial shock (defibrillation). This is usually a standing physician's order in a CCU.

A nurse notes that a client with sinus rhythm has a premature ventricular contraction that falls on the T wave of the preceding beat. The client's rhythm suddenly changes to one with no P waves or definable QRS complexes. Instead there are coarse wavy lines of varying amplitude. The nurse assesses this rhythm to be: 1. Ventricular tachycardia 2. Ventricular fibrillation 3. Atrial fibrillation 4. Asystole

2. Ventricular fibrillation is characterized by irregular, chaotic undulations of varying amplitudes. Ventricular fibrillation has no measurable rate and no visible P waves or QRS complexes and results from electrical chaos in the ventricles.

A nurse is watching the cardiac monitor and notices that the rhythm suddenly changes. There are no P waves, the QRS complexes are wide, and the ventricular rate is regular but over 100. The nurse determines that the client is experiencing: 1. Premature ventricular contractions 2. Ventricular tachycardia 3. Ventricular fibrillation 4. Sinus tachycardia

2. Ventricular tachycardia is characterized by the absence of P waves, wide QRS complexes (usually greater than 0.14 second), and a rate between 100 and 250 impulses per minute. The rhythm is usually regular.

When auscultating the apical pulse of a client who has atrial fibrillation, the nurse would expect to hear a rhythm that is characterized by: 1. The presence of occasional coupled beats 2. Long pauses in an otherwise regular rhythm 3. A continuous and totally unpredictable irregularity 4. Slow but strong and regular beats

3. In atrial fibrillation, multiple ectopic foci stimulate the atria to contract. The AV node is unable to transmit all of these impulses to the ventricles, resulting in a pattern of highly irregular ventricular contractions.

A client with a bundle branch block is on a cardiac monitor. The nurse should expect to observe: 1. Sagging ST segments 2. Absence of P wave configurations 3. Inverted T waves following each QRS complex 4. Widening of QRS complexes to 0.12 second or greater.

4. Bundle branch block interferes with the conduction of impulses from the AV node to the ventricle supplied by the affected bundle. Conduction through the ventricles is delayed, as evidenced by a widened QRS complex.

The adaptations of a client with complete heart block would most likely include: 1. Nausea and vertigo 2. Flushing and slurred speech 3. Cephalalgia and blurred vision 4. Syncope and low ventricular rate

4. In complete atrioventricular block, the ventricles take over the pacemaker function in the heart but at a much slower rate than that of the SA node. As a result there is decreased cerebral circulation, causing syncope.

A patient has sought care following a syncopal episode of unknown etiology. Which nursing action should the nurse prioritize in the patient's subsequent diagnostic workup? A. Preparing to assist with a head-up tilt-test B. Preparing an IV dose of a β-adrenergic blocker C. Assessing the patient's knowledge of pacemakers D. Teaching the patient about the role of antiplatelet aggregators

A, In patients without structural heart disease, the head-up tilt-test is a common component of the diagnostic workup following episodes of syncope. IV β-blockers are not indicated although an IV infusion of low-dose isoproterenol may be started in an attempt to provoke a response if the head-up tilt-test did not have a response. Addressing pacemakers is premature and inappropriate at this stage of diagnosis. Patient teaching surrounding antiplatelet aggregators is not directly relevant to the patient's syncope at this time.

The patient has hypokalemia, and the nurse obtains the following measurements on the rhythm strip: Heart rate of 86 with a regular rhythm; the P wave is 0.06 seconds (sec) and normal shape; the PR interval is 0.24 sec; the QRS is 0.09 sec. How should the nurse document this rhythm? A. First-degree AV block B. Second-degree AV block C. Premature atrial contraction (PAC) D. Premature ventricular contraction (PVC)

A. In first-degree AV block there is prolonged duration of AV conduction that lengthens the PR interval above 0.20 sec. In type I second-degree AV block the PR interval continues to increase in duration until a QRS complex is blocked. In Type II the PR interval may be normal or prolonged, the ventricular rhythm may be irregular, and the QRS is usually greater than 0.12 sec. PACs cause an irregular rhythm with a different-shaped P wave than the rest of the beats, and the PR interval may be shorter or longer. PVCs cause an irregular rhythm, and the QRS complex is wide and distorted in shape.

A patient in asystole is likely to receive which drug treatment? A. Epinephrine and atropine B. Lidocaine and amiodarone C. Digoxin and procainamide D. β-adrenergic blockers and dopamine

A. Normally the patient in asystole cannot be successfully resuscitated. However, administration of epinephrine and atropine may prompt the return of depolarization and ventricular contraction. Lidocaine and amiodarone are used for PVCs. Digoxin and procainamide are used for ventricular rate control. β-adrenergic blockers are used to slow heart rate, and dopamine is used to increase heart rate.

The nurse is watching the cardiac monitor, and a patient's rhythm suddenly changes. There are no P waves. Instead there are fine, wavy lines between the QRS complexes. The QRS complexes measure 0.08 sec (narrow), but they occur irregularly with a rate of 120 beats/min. The nurse correctly interprets this rhythm as what? A. Sinus tachycardia B. Atrial fibrillation C. Ventricular fibrillation D. Ventricular tachycardia

B. Atrial fibrillation is represented on the cardiac monitor by irregular R-R intervals and small fibrillatory (f) waves. There are no normal P waves because the atria are not truly contracting, just fibrillating. Sinus tachycardia is a sinus rate above 100 beats/minute with normal P waves. Ventricular fibrillation is seen on the ECG without a visible P wave; an unmeasurable heart rate, PR or QRS; and the rhythm is irregular and chaotic. Ventricular tachycardia is seen as three or more premature ventricular contractions (PVCs) that have distorted QRS complexes with regular or irregular rhythm, and the P wave is usually buried in the QRS complex without a measurable PR interval.

The nurse obtains a 6-second rhythm strip and charts the following analysis: Tab 1 Tab 2 Tab 3 Atrial data Ventricular data Additional data Rate: 70, regular Variable PR interval Independent beats Rate: 40, regular Isolated escape beats QRS: 0.04 sec P wave and QRS complexes unrelated What is the correct interpretation of this rhythm strip? A. Sinus arrhythmias B. Third-degree heart block C. Wenckebach phenomenon D. Premature ventricular contractions

B. Third-degree heart block represents a loss of communication between the atrium and ventricles from AV node dissociation. This is depicted on the rhythm strip as no relationship between the P waves (representing atrial contraction) and QRS complexes (representing ventricular contraction). The atria are beating totally on their own at 70 beats/min, whereas the ventricles are pacing themselves at 40 beats/min. Sinus dysrhythmia is seen with a slower heart rate with exhalation and an increased heart rate with inhalation. In Wenckebach heart block, there is a gradual lengthening of the PR interval until an atrial impulse is nonconducted and a QRS complex is blocked or missing. Premature ventricular contractions (PVCs) are the early occurrence of a wide, distorted QRS complex.

The nurse is caring for a patient who is 24 hours postpacemaker insertion. Which nursing intervention is most appropriate at this time? A. Reinforcing the pressure dressing as needed B. Encouraging range-of-motion exercises of the involved arm C. Assessing the incision for any redness, swelling, or discharge D. Applying wet-to-dry dressings every 4 hours to the insertion site

C. After pacemaker insertion, it is important for the nurse to observe signs of infection by assessing for any redness, swelling, or discharge from the incision site. The nonpressure dressing is kept dry until removed, usually 24 hours postoperatively. It is important for the patient to limit activity of the involved arm to minimize pacemaker lead displacement.

The nurse is monitoring the ECGs of several patients on a cardiac telemetry unit. The patients are directly visible to the nurse, and all of the patients are observed to be sitting up and talking with visitors. Which patient's rhythm would require the nurse to take immediate action? A. A 62-year-old man with a fever and sinus tachycardia with a rate of 110 beats/minute B. A 72-year-old woman with atrial fibrillation with 60 to 80 QRS complexes per minute C. A 52-year-old man with premature ventricular contractions (PVCs) at a rate of 12 per minute D. A 42-year-old woman with first-degree AV block and sinus bradycardia at a rate of 56 beats/minute

C. Frequent premature ventricular contractions (PVCs) (greater than 1 every 10 beats) may reduce the cardiac output and precipitate angina and heart failure, depending on their frequency. Because PVCs in CAD or acute MI indicate ventricular irritability, the patient's physiologic response to PVCs must be monitored. Frequent PVCs most likely must be treated with oxygen therapy, electrolyte replacement, or antidysrhythmic agents.

When computing a heart rate from the ECG tracing, the nurse counts 15 of the small blocks between the R waves of a patient whose rhythm is regular. From these data, the nurse calculates the patient's heart rate to be A. 60 beats/min. B. 75 beats/min. C. 100 beats/min. D. 150 beats/min.

C. Since each small block on the ECG paper represents 0.04 seconds, 1500 of these blocks represents 1 minute. By dividing the number of small blocks (15, in this case) into 1500, the nurse can calculate the heart rate in a patient whose rhythm is regular (in this case, 100).

Which ECG characteristic is consistent with a diagnosis of ventricular tachycardia (VT)? A. Unmeasurable rate and rhythm B. Rate 150 beats/min; inverted P wave C. Rate 200 beats/min; P wave not visible D. Rate 125 beats/min; normal QRS complex

C. VT is associated with a rate of 150 to 250 beats/min; the P wave is not normally visible. Rate and rhythm are not measurable in ventricular fibrillation. P wave inversion and a normal QRS complex are not associated with VT.

Other Antidysrythmics

Cardiac glycoside (Digoxin) ~Slow Na influx and allows Ca influx ~Increases contractibility ~Decreases HR & AV conduction ~Toxicity (Halos!) Adenosine ~Push hard, push fast ~Causes temp AV block to restore sinus rhythm ~Usual dose 6mg (VERY FAST half life)

A 50-year-old man who develops third-degree heart block reports feeling chest pressure and shortness of breath. Which instructions should the nurse provide to the patient before initiating emergency transcutaneous pacing? A. "The device will convert your heart rate and rhythm back to normal." B. "The device uses overdrive pacing to slow the heart to a normal rate." C. "The device is inserted through a large vein and threaded into your heart." D. "The device delivers a current through your skin that can be uncomfortable."

D. Before initiating transcutaneous pacing (TCP) therapy, it is important to tell the patient what to expect. The nurse should explain that the muscle contractions created by the pacemaker when the current passes through the chest wall are uncomfortable. Pacing for complete heart block will not convert the heart rhythm to normal. Overdrive pacing is used for very fast heart rates. Transcutaneous pacing is delivered through pacing pads adhered to the skin.

The nurse performs discharge teaching for a 74-year-old woman with an implantable cardioverter-defibrillator. Which statement by the patient indicates to the nurse that further teaching is needed? A. "The device may set off the metal detectors in an airport." B. "My family needs to keep up to date on how to perform CPR." C. "I should not stand next to antitheft devices at the exit of stores." D. "I can expect redness and swelling of the incision site for a few days."

D. Patients should be taught to report any signs of infection at incision site (e.g., redness, swelling, drainage) or fever to their primary care provider immediately. Teach the patient to inform airport security of presence of ICD because it may set off the metal detector. If hand-held screening wand is used, it should not be placed directly over the ICD. Teach the patient to avoid standing near antitheft devices in doorways of stores and public buildings, and to walk through them at a normal pace. Caregivers should learn cardiopulmonary resuscitation (CPR).

2:1 Conduction block

Every other sinus impulse is blocked. Ventricle rate is half the atrial rate. PR interval is constant.

Fixed Pacing

Generator sets and impulse at a fixed rate regardless of the pt's intrinsic rhythm- rarely used "R on T" *will always go @ 70 bpm

V-fib causes

Heart disease most common cause of sudden death in acute MI may be preceded by PVCs or Vtach ishcemia cardiomyopathy mitral valve prolapse cardiac trauma hypoxia cocaine toxicity Electrolyte imbalance acidosis dig toxicity

Electrolytes (K)

Hypok <3.5 leads to PVCs, VT, VF -Replaced per physician order or institution's sliding scale -Nursing Mgmt: monitor EKG, s/sx hypok, dietary K, K sparing diuretic, monitor pt's n/v Hyperk >5.3 (very wide QRS-ST-T) -Admin kayexalate, Ca gluconate, insulin or Na Bicarb

Ventricular Fibrillation

LIFE THREATENING!!! -NO PULSE...ever -No Rate/rhythm; no waveforms, no organized activity -Ventricle is "quivering" >no ventricle contraction > no cardiac output > pt clinically expired

V-fib

Origin: multiple ventricular pacemakers Conduction: Chaotic ventricular depolarization EKG Features: Wavy baseline, no P waves, no QRS complexes No CO/ palpable pulses due to ineffective muscle contraction. Lethal rhythm

Ventricular Dysrhythmias

Originates in pacemaker cells of ventricles. Depolarization time is prolonged leading to QRS > .10 sec (2.5 box) and bizarre in appearance. T wave usually in opposite direction of QRS. Usually no P present

Junctional Dysrhthmias

Pacemaker located in AV Junction Impulse is conducted forward to ventricles an backwards to atrias

Ventricular Pacing

Pacer artifact occurs just before QRS complex on EKG strip

Failed Capture

Pacer generates an impulse but the patient's intrinsic rhythm fails to respond *spikes but heart didn't respond

Inhibition (PM)

Pacer senses pt's own heart beat & inhibits generator firing

The nurse has obtained this rhythm strip from her patient's monitor: rate 110, normal PQRS. Which description of this ECG is correct? A. Sinus tachycardia B. Sinus bradycardia C. Ventricular fibrillation D. Ventricular tachycardia

This rhythm strip shows sinus tachycardia because the rate on this strip is above 101, and it displays normal P wave, PR interval, and QRS complex. Sinus bradycardia would look similar to sinus tachycardia but with a rate less than 60 beats per minute. Ventricular fibrillation does not have a measureable heart rate, PR interval, or QRS, and the P wave is not visible and the rhythm is irregular and chaotic. Ventricular tachycardia has a rate of 150 to 250 beats/minutes, with a regular or irregular rhythm and P waves occurring independently of the QRS complex.

transmural MI

damage throughout the entire myocardium

stable angina

occurs in a way familiar to pt. They know when they will have attack, and take nitro b4. predictable by pt.

escape rhythm

occurs when some part of the conduction system assumes pacemaker responsibility

antidysrythmic function of pacemakers

over pace a tachy, PM will fire higher than HR, slowly bring back down. Also will initiate shock in pt with VT or VF to bring back to regular rhythm

questions to ask regarding chest pain

quality? when did it start? duration? radiates to? what were you doing when it started? come and go or continuous? intensity 1-10?

variant (prinzmetal's) angina

usually presents as angina at rest. thought to be caused by vasospasm. do stress test to determine what is going on in the heart (usually negative)

Third Degree AVB

Complete heart block -No communication between atrial and ventricle conduction system -SA node generate impulse but does not stimulate the AV node -Ventricle contraction is conducted either through AV node or ventricle