cardiac 2

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

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 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.

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.

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.

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 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.

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.

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.

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 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.

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.

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.

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.

Ability to conduct an impulse resulting in stimulation of adjacent cells

Cells become more positive on the inside (contracting)

Cells become more negative on the inside (relaxing)

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

Ectopic Beat
Beat initiated outside the electrical pathway

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

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

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

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

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

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

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

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

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

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
-Cool skin
-Chest pain
-Confusion & disorientation

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

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

Sinus Brady Etiology and Risk
-Inferior wall MI
-Increased ICP
-Vagal stimulation (severe constipation)
-Carotid sinus massage
-Drugs (Beta Blocks, CaCB)

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

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

Sinus Tachy Etiology & Risk
-Myocardial ischemia
-Drugs (epi, norepi, atropine, caffeine, theophylline (high caf), amphetamines, psudoephedrine)

Sinus Tachy Nursing Management
If symptomatic
-Assess pain management
-IV fluids
-Correct etiology
Medications- B block, CaCB

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

PAC (premature atrial contraction) Etiology & Risks
-Electrolyte imbalance
-Heart Disease
-MI or injury
-Digoxin toxicity

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)

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 Flutter Etiology & Risk
-Mitral valve disorders
-Pulmonary embolism
-Ischemic heart disease
-Acute MI
-Digoxin toxicity
-Cor pulmonale

Atrial Flutter Nursing Mgmt
-Rate control w/ CaCB, beta blocks
-Antiarrhythmics (amiodarone)
-Anticoagulation (warfarin)
-EP lab for ablation

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

A Fib Etiology & Risk
-Rheumatic Heart Disease
-Acute MI
-Valvular disease

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

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

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

Supraventricular Tachy Etiology & Risk
-Cor pulmonale (R side enlargement of heart)
-Dig toxicity
-Rheumatic heart disease

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

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

Premature ventricular contractions Etiology & Risk
-Electrolyte imbalance
-Fever, infection, stress
-Gastric overload
-Acute MI
-Cyclic antidepressants
-Heart disease

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

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

V Tach Etiology & Risk
-Signif electrolyte imbalance
-CNS disorders
-Drug toxicity
-Prolonged QT
-Freq PVCs

V Tach Nursing Management (Gen)
-Identify rhythm
~Check for pulse! If pulse- pt stable by interventions required
-Apply pacing pads

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

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

Ventricular Fibrillation
-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 Etiology & RF
-Acute MI/ ischemia
-Drug toxicity
-Electrical shock
-R on T PVCs
-Untreated VT
-Post cardiac cath
-Post coronary artery perfusion from fibrinolytics

V Fib Nursing Management
-If untreated pt will expire
-Begin CPR immediately (ACLS)
-Rapid defib & drug therapy

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

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

ACLS Defibrillation
Shockable rhythms
-V Fib
-Pulseless V Tach

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

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

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

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

Patient Presentation
-May be asymptomatic- 1AVB, 2AVB
-Symptomatic 3AVB
Can include:
-Chest pain
-Mental status changes

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

Antidysrythmic Drugs
B Blockers (-olols)
~Decrease HR, contractility

CaCB (-pines, diltiazem, verapamil)
~Decrease conduction through AV, decreases HR

Other Antidysrythmics
Cardiac glycoside (Digoxin)
~Slow Na influx and allows Ca influx
~Increases contractibility
~Decreases HR & AV conduction
~Toxicity (Halos!)

~Push hard, push fast
~Causes temp AV block to restore sinus rhythm
~Usual dose 6mg (VERY FAST half life)

More drugs for Dysrythmias
Atropine- anticholinergic
~Sx brady, AV blocks, asystole

~Increases HR, conduction, contractility, vasodilation
~Used in pulseless VT, VF, bradyarrythmias

Vasopressin (antidiuretic hormone)
~Used in VF, pulseless VT, PEA

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

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

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)

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

-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)

Implantable Cardioverter- Defibrillator (ICD)
-Bradyc backup pacing
-Dual chamber system allows for cardioversion/ pacing atrial tachydysryths

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

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

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

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

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

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

Sensing (PM)
The generator is able to see the pt’s intrinsic beat

Firing (PM)
The generator delivers a pacing stimulus

Inhibition (PM)
Pacer senses pt’s own heart beat & inhibits generator firing

Triggering (PM)
Pacer senses pt’s missed beat & generates response

Capture (PM)
Heart responds to the stimulus that generator delivered

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

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

Ventricular Pacing
Pacer artifact occurs just before QRS complex on EKG strip

Atrial Pacing
Pacer artifact appears just before P wave on EKG strip

Dual Pacing
Pacer artifact appears prior to both P wave and QRS complex

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

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 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.

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 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.

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.

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.

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.

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.

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.

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 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 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.

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.

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.

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.

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.

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.

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).

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.

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

represents depolarization of the ventricles (ventricular contraction).
QRS complex

represents the time it takes for depolarization
QRS Interval

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

represents repolarization of the ventricles.
T wave

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

Dysrhythmias result from
disorders of impulse formation, conduction of impulses, or both.

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

Ventricular dysrythimias
not used for supraventricular dysrhythmias.

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

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

paroxysmal SVT (supraventricular tachycardia)

Asystole Causes
Metabolic acidosis
hyper/ hypo- kalemia
drug OD

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

V-fib causes
Heart disease
most common cause of sudden death in acute MI
may be preceded by PVCs or Vtach
mitral valve prolapse
cardiac trauma
cocaine toxicity
Electrolyte imbalance
dig toxicity

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

Sinus Tach Causes
Normal response to increased demand:
Stimulants, drugs

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

Sinus Brady Causes
Increase in parasympathetic
decrease in sympathetic
vagal stimulation
Increased ICP
Dig, CCB, BB
Protective rhythm with acute MI

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

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

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

Sinus Block causes
Increased Vagal tone
Damage to SA node from MI
Dig, CCB, BB

Heart blocks
Conduction abnormalities along conduction system. SA node is pacemaker

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

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

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

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

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

Mobitz type 1 causes
commonly transient after MI; dig; BB; CCB; increased vagal tone; myocarditis; CHD; ischemia; aging

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

Mobitz type 2 causes
Extensive damage to bundle branches after anteroseptal MI; CHD; myocarditis

2:1 Conduction block
Every other sinus impulse is blocked. Ventricle rate is half the atrial rate. PR interval is constant.

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

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

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.

Atrial fib Causes
Emotional stress; alcohol; caffeine; and previous

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

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

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

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

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

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

Causes of Accelerated junctional rhythm
commonly dig toxicity; Acute inferior MI; HF; acute rheumatic fever; valvular heart disease; myocarditis; post cardiac surgery

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

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

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

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

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

Ventricular Tachycardia
Lethal. Often preceded by PVCs. Greater than 100 bpm

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

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

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

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

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)

escape rhythm
occurs when some part of the conduction system assumes pacemaker responsibility

questions to ask regarding chest pain
when did it start?
radiates to?
what were you doing when it started?
come and go or continuous?
intensity 1-10?

s/s of cardio prob
chest pain
proxysminal nocturnal dyspnea

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

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.

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

Single vs dual chambers pacemakers
single in atria, dual in atria and ventricle (R)

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

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

indications for a pacemaker
symptomatic brady
complete heart block- sometimes 2nd
sick sinus rhythm
sinus arrest
A or V tachy dysrythmias

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

Pacemaker complications
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)

interrogating the pacemaker
magnet placed over PM on skin to adjust settings and read “report”

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

s/s of infective endocarditis
fever (above 103)
anorexia/ weight loss
embolic phenom (bacteria breaks loose and travels)

labs for infective endocarditis
blood cultures, determine what growing, and what the bacteria is sensitive to

tx of infective endocarditis
if causes valve prob, fix the valve
if causes abscess, drain
if damage to chordae tendineae, may need to repair

interventions for infective endocarditits
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

inflammation of the pericardium

acute- virus/ bacterial most comm. also trauma/MI/tumors/ idiopathic

chronic- TB/ radiation/ trauma

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

interventions of pericarditis
observe for pericardial effusions (fluid in space)

progression of pericarditis
cardiac tamponade (life threatening)

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)

Becks triad
symptom of cardiac tamponade
muffled heart sounds

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

acute coronary syndrome
general term, not a specific disease. problems with ischemia (loss of o2 to cells)

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

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

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)

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)

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.

transmural MI
damage throughout the entire myocardium

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.

assessment of an MI
risk factors
pain, intensity, quality
associated s/s
listen to heart/ lungs
med Hx/ FH

labs for MI
Creatine Kinase (CK/CPK)
Lipid profile

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

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

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

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.

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

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