Chapter 34 Care of pts w/ dysrhythmias

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1

Automaticity

Pacing function. Ability of cardiac cells to generate an electrical impulse spontaneously and repetitively.

2

Under certain conditions any cardiac cell may produce electrical impulses independently resulting in dysrhythmias. What are some of these conditions?

Myocardial Ischemia (decreased blood flow)
electrolyte imbalance
hypoxia
drug toxicity
Infarction

3

Excitability

The ability of non pacemaker heart cells to respond to an electrical impulse that begins in pacemaker cells and to depolarize.

4

Depolarization

When the normally negatively charged cells w/in the heart muscle develop a positive charge.

5

Conductivity

The ability to send an electrical stimulus from cell to cell membrane resulting in excitable cells depolarizing in rapid succession

6

When do disturbances in conduction result?

When conduction is too rapid or too slow
When the pathway is totally blocked
When the electrical impulse travels an abnormal pathway

7

What causes the Pwave and QRS complex seen on ECG?

The wave of depolarization

8

Contractility

The mechanical activity of the heart causing sufficient pressure to push blood forward thru the heart.

9

What is the heart's primary pacemaker?

The SA Node...it has the greatest degree of automaticity

10

What is reflected in a P wave on the ECG?

atrial depolarization

11

Trace the pathway of electrical conduction thru the heart.

SA Node to the AV junction where the T cells cause impulses to slow down in the AV Node before proceeding to the ventricles. This gives the atria time to contract and the ventricles time to fill. From the AV node to the bundle of HIS o the purkinje cells.

12

Purkinje Cells

make up the bundle of HIS, bundle branches, and terminal purkinje fibers. They are responsible for the rapid conduction of electrical impulses thruoughout the ventricles, leading to ventricular depolarization and ventricular muscle cx.

13

What is reflected in the PR segment on the ECG?

This is where the Tcells slow conduction prior to it reaching the AV Node. It allows the atria time to contract and ventricles to fill.

14

What is the isoelectric line on the ECG?

It is when there is a no current flow in the heart after complete depolarization and also after complete repolarization. It is a straight line. Positive and negative deflections occur above or below it.

15

Positive deflection

above the isoelectric line

16

Negative deflection

below the isoelectric line

17

Biphasic complex

both above and below the isolectric line

18

On the ECG strip, how much time does one small block represent?

0.04 second

19

On the ECG strip, how much time does five small blocks represent (makes up one large block)?

0.20 second

20

On the ECG strip, how much time does 5 large blocks represent?

One second

21

What are the complexes that make up a normal ECG?

P wave
QRS complex
Twave
possibly U wave

22

What are the segments?

PR Segment
ST Segment
TP Segment

23

What are the Intervals?

PR interval
QRS duration
QT interval

24

P wave

Represents atrial depolarization. May be + - or biphasic. The shape changes if impulse is generated from somewhere other than the SA Node.

25

PR Segment

Is where the electrical impulse is traveling thru the AV node where it is delayed before traveling to the purkinje fibers. It's measured from the end of the P wave to the beginning of QRS.

26

PR Interval

Measured from the beginning of the P wave to the end of the PR segment. It represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to purkinje fibers. It normally measures from 0.12-0.20 second (five small blocks)

27

QRS complex

Represents ventricular depolarization. Q wave can be normal or abnormal. When present it is small and represents initial ventricular septal depolarization. When abnormally present in lead it may represent myocardial necrosis.

28

QRS duration

Represents the time required for depolarization of both ventricles. Measured from beginning of QRS complex to the J point. Normally measures from 0.04-0.12 second (up to 3 small blocks)

29

T wave

Follows the ST segment, represents ventricular repolarization. May be + rounded and slightly a symmetric.

30

What may cause the T wave to become tall and peaked, inverted (-), or flat?

Myocardial ischemia, K, Ca imbalances, medications, autonomic nervous system effects.

31

TP segment

Begins at the end of the t wave and ends at the beginning of the P wave. It is the true isoelectric interval in the ECG

32

U wave

When present, follows the T wave and may result from slow repolarization of ventricular purkinje fibers.

33

What may an abnormal U wave suggest?

an electrolyte abnormality ( particularly hypokalemia)

34

QT interval

Represents the total time required for ventricular depolarization and repolarization. Measured from the beginning of the Q wave to the end of the T wave. Varies with age, gender, changes with heart rate...lengthens with slower heart rate, shortens with faster rates.

35

What may cause a prolonged QT interval?

Certain meds
electrolyte disturbances
subarachnoid hemorrhage
Can l/t a unique type of V tach called torsades de pointes

36

Artifact

interference seen on the monitor or rhythm strip that looks wandering or fuzzy caused by pt mvmt, loose electrodes, faulty equipment etc. Some artifact can mimic lethal dysrhythmias. Assess the pt to differentiate artifact from actual lethal rhythms! Don't rely on ECG monitor.

37

6 second strip method of determining heart rate?

It is the least accurate method, but the method of choice for irregular rhythms. Count the # of QRS complexes in 6 seconds and multiply by 10.

38

The big block method for determining heart rate?

Used if the QRS complexes are regular and evenly spaced. Count the # of large blocks r wave to r wave and divide into 300. If little blocks are left over, count each little block as 0.2 and add to big blocks.

39

The memory method for determining heart rate?

Relies on memorizing this sequence:

300,150,100,75,60,50,43,37,33,30

Its the big block method with the math already done. Most widely used method in hospitals for calculating heart rates for regular rhythms. Find QRS that falls on a dark line and count back wards to next QRS complex. Each dark line is a memorized #. See p 655

40

What are the 8 steps in ECG rhythm analysis?

  1. Determine heart rate
  2. Determine heart rhythm
  3. Analyze P wave
  4. Measure PR interval
  5. Measure QRS duration
  6. Examine ST segment
  7. Assess T wave
  8. Measure QT interval
41

8 steps in ECG rhythm analysis: Step 1

Determine heart rate

Normal btw 60-100 bpm

42

8 steps in ECG rhythm analysis: Step 2

Determine heart rhythm

Check the regularity of atrial rhythm by assessing the PP intervals by placing one caliper point an a p wave and walking out p waves. Slight irregularity (no more than 3 small blocks) is considered regular if the p waves are all of same shape.

Check regularity of ventricle rhythm in same way by assesing the RR intervals. Slight irregularity (no more than 3 small blocks) is considered regular if the QRS complexes are all of same shape.

43

8 steps in ECG rhythm analysis: Step 3

Analyze P wave

Check that shape is consistent throughout. There may be more than one shape, more p waves than QRS, absent p waves or P wave coming after QRS - all indicating dysrhythmia.

  • Ask these questions:
  • Are they present, similar, and regular?
  • Is there one for every QRS?
  • Are they smooth, rounded, and upright or inverted?
44

8 steps in ECG rhythm analysis: Step 4

Measure PR interval

Using caliper from beginning of P wave to the end of PR segment. Should be constant. Normally btw 0.12-0.20.

  • Ask these questions:
  • Are they >0.20 or <0.12 second?
  • Are they constant?
45

8 steps in ECG rhythm analysis: Step 5

Measure QRS duration

Using caliper measure from beginning of QRS to where ST segment begins. Duration is normally 0.04-0.10 second and should be constant.

  • Ask these questions:
  • Are they < or> 0.12 second:
  • Are they similar in appearance?

If it is <0.10 second (narrow) this indicates the impulse was not formed in ventricles and is ref to as supraventricular. If > 0.10 second it indicates that impulse is either of ventricular origin or of supraventricular origin, meaning deviating from normal course or pattern. Missing QRS indicated dysrhythmias.

46

8 steps in ECG rhythm analysis: Step 6

Examine ST segment

measured from J point to beginning of T wave.

An elevation or depression is significant if displacement is 1mm (one small block) or more above or below the line in 2 or more leads.

ST elevation may indicate: MI, pericarditis, hyperkalemia

ST depression may indicate: hypokalemia, MI ventricular hypertrophy

47

8 steps in ECG rhythm analysis: Step 7

Assess T Wave

Note shape and height of wave and look for peaking or inversion.

Abnormal may indicate MI, ventricular hypertrophy

48

8 steps in ECG rhythm analysis: Step 8

Measure QT interval

Should be equal to or 1/2 the distance of the R to R interval.

49

What is the criteria for a normal sinus rhythm?

  • Rate: Atrial and ventricular rates of 60-100 bpm
  • Rhythm: Atrial and ventricular rhythm regular
  • Pwave: Present, consistent config., one P wave b4 each QRS
  • PR interval: 0.12-0.20 second and constant
  • QRS duration: 0.04-0.10 Second and constant
50

What is sinus arrhythmia?

A variant of NSR. Heart rate increases slightly during inspiration and decreases slightly during exhalation. The PP and RR intervals vary, with the difference btw the shortest and the longest intervals being >0.12 second (3 small blocks)

51

What is the criteria for sinus arrhythmia?

  • Rate: Atrial and ventricular rates of 60-100 bpm
  • Rhythm: Atrial and ventricular rhythm irregular, with the shortest PP or RR interval varying at least 0.12 second from the longest PP or RR interval
  • Pwave: Present, consistent config., one P wave b4 each QRS
  • PR interval: 0.12-0.20 second and constant
  • QRS duration: 0.04-0.10 Second and constant
52

What are some causes of sinus arrhythmias other than respiratory?

Digitalis or morphine - they enhance vagal tone and decrease heart rate

53

Dysrhythmia

Any disorder of the heartbeat

54

Premature complexes

early rhythm complexes. They occur when cardiac cells other than the SA node become irritable and fire and impulse before the next impulse is produced. The abnormal focus is called an ectopic focus. The pt may feel palpitations.

55

Premature complexes may occur repetitively in a rhythmic fashion.

Bigeminy

normal and premature complexes occur alternately in a repetitive 2 beat pattern, with a pause occurring after each premature complex so that complexes occur in pairs.

56

Premature complexes may occur repetitively in a rhythmic fashion.

Trigeminy

Repeated 3 beat pattern, usu occurring as 2 sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in triplets.

57

Premature complexes may occur repetitively in a rhythmic fashion.

Quadrigeminy

Repeated 4 beat pattern, usually occurring as 3 sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in a 4 beat pattern.

58

Bradydysrhythmias

Why significant?

Heart rate below 60bpm.

  • Beneficial: myocardial O2 demand decreased
  • Desirable: Due to prolonged Diastole, coronary perfusion time may be adequate
  • BAD: If heart rate too slow, coronary perfusion pressure may decrease, and CO and BP decrease
59

If the BP with bradydysrhythmia is not adequate what may it lead to in the pt?

  • myocardial ischemia
  • infarction
  • dysrhythmias
  • hypotension
  • heart failure
60

Tachydysrhythmias

Why significant?

Heart rates > 100bpm

  • Coronary artery blood flow occurs mostly during diastole when aortic valve is closed, so a shortened diastolic time l/t shortend coronary perfusion time.
  • Initially, CO and BP increase, but eventually decrease reducing aortic pressure and coronary perfusion pressure.
  • Increases workload of heart which increases O2 demand
61

What are some s/s the pt with tachdysrhythmias experience?

  • Palpitations
  • Chest discomfort
  • Restlessness/anxiety
  • pale cool skin
  • syncope (blackout) from hypotension
  • may l/t heart failure which includes s/s: dyspnea, lung crackles, JVD, fatigue, weakness
62

What are some causes of dysrhythmias?

  • MI
  • electrolyte imbal (esp K and Mg)
  • hypoxia
  • drug toxicity
  • hypovolemia
  • Stress, fear, anxiety, caffeine can cause tachycardia or PVCs
  • Nicotine and alcohol excess can cause A fib
63

Pulse deficit

If the apical pulse differs from the radial pulse, it indicates that the heart is not pumping adequately to achieve optimal perfusion to the body.

64

The 2 most common types of sinus dysrhythmias are sinus tachycardia and sinus bradycardia.

Sinus tachycardia

SNS stimulation or vagal (parasympathetic) inhibition results in increased SA node discharge of > 100 bpm.

65

Some causes of sinus tachycardia

  • anxiety, stress
  • pain, fever, anemia
  • hypoxemia, hyperthyroidism
  • Drugs: epi, atropine, caffeine, alcohol, cocaine, aminophylline, thyroid meds
66

What are some cause compensatory responses that may cause sinus tachycardia?

  • dehydration
  • hypovolemic shock
  • MI
  • Infection
  • Heart ailure
67

What will you assess the pt for with sinus tachycardia?

  • fatigue, weakness, SOB, orthopnea, decreased O2 sat, increased pulse rate, decreased BP, anginal pain, palpitations
  • restlessness, anxiety from decreased cerebral perfusion
  • decreased urine output from decreased renal perfusion
  • T wave inversion or ST segment depression in response to myocardial ischemia
68

What to teach the pt with sinus tachycardia?

  • Remain on bedrest if you have hypotension
  • Avoid caffeine, alcohol, nicitine
  • Stress mgmt techniques
69

The 2 most common types of sinus dysrhythmias are sinus tachycardia and sinus bradycardia.

Sinus bradycardia

Excessive vagal (parasympathetic) stimulation causing a decreased rate of SA node discharge.

70

Some causes of sinus bradycardia?

  • carotid sinus massage
  • vomiting, suctioning
  • valsalva maneuver
  • ocular pressure
  • pain
  • hypoxia
  • inferior wall MI
  • drugs: BB's, Ca Channel blockers, digitalis
  • hypothyroidism, Lyme disease
71

What will you assess the pt for with sinus bradycardia?

  • MAR for meds that may be causing
  • Syncope
  • Dizziness, weakness, confusion
  • Hypotension
  • diaphoresis
  • SOB, chest pain
72

What is the tx for sinus bradycardia if the underlying cause can't be determined?

atropine 0.5 mg IV, increase intravascular volume with fluids, O2.

Other: transvenous or transcutaneous pacing, or permanent pacemaker implantation

73

Temporary pacing

A nonsurgical intvn that provides a timed electrical stimulus to the heart. It is used for pts with symptomatic atropine refractory bradydys or for pts w/ asystole.

2 types: transcutaneous and transvenous

74

Transcutaneous pacing

Accomplished via 2 large external elextrodes and an external pulse generator. Used as an emergency measure to provide ventricular pacing in profoundly bradycardic or asystolic pt until invasive pacing can be used or until the heart rate returns to normal. only a TEMP measure.

75

Transvenous pacing

Consists of an external battery operated pulse generator, pacing electrodes. Wires are threaded to the R atrium via the subclavian or femoral vein. Electrical impulses generated. Can be done through synchronous (demand: when needed) or asynchronous (fixed rate). Demand is most common.

76

Permanent Pacemaker

To tx disorders that are not temporary like complete heart block, moderate to severe heart failure. Done under local anesthesia. A subcutaneous pocket is placed at the shoulder in the R or L subclavicular area, creating a visible bulge. Battery life is 10 yrs.

77

Care of pt after pacemaker insertion?

  • Monitor ECG rhythm
  • Assess site for bleeding, swelling, redness, tenderness, and infx
  • Dressing over site clean and dry
  • Afebrile
  • Stable vitals
  • Initial activity restrictions, gradually changed
78

3 Atrial dysrhythmias?

Premature atrial complexes

Supraventricular tachycardia

Atrial fibrillation

79

3 Atrial dysrhythmias

1. Premature atrial complexes (PAC)

Atrial tissue becomes irritable firing an impulse before the next SA impulse is due. Causes an abnormal P wave that may not always be clearly visible bc it can be hidden in the preceding T wave. Examine T wave closely for any change in shape and compare with other T waves. PAC is usu followed by a pause.

80

PAC causes

  • Stress, fatigue, anxiety
  • Inflammation, Infection
  • Caffeine, nicotine, alcohol
  • Drugs: epi, dig, amphetamines
  • May result from: myocardial ischemia, hypermetabolic states, electrolyte imbalance, CHF, valve disease, Pulm HTN with cor pulmonale
81

PAC s/s and tx

Pt usu has no s/s except for possible palpitations. No intvn nec except to tx causes such as heart failure.

Teach to avoid caffeine, alcohol, nicitine, manage stress

82

3 Atrial dysrhythmias

2. Supraventricular Tachycardia

rapid stimulation of atrial tissue at a rate of 100-280 bpm. P waves may not be visible. SVT may occur in healthy young ppl esp women. Paroxysmal SVT occurs from time to time.

83

SVT s/s

For sustained SVT:

  • palpitations, chest pain, weakness, fatigue, SOB, nervousness, anxiety, hypotension, syncope
  • Can result in angina, HF, cardiogenic shock

Nonsustained -- Pt may be asymptomatic except occassional palpitations

84

SVT intvns

If it stops on its own no intvn may be req.

The preferred tx is radiofrequency catheter ablation

Others: vagal maneuvers, carotid sinus massage, Adenosine given rapidly followed by fluid bolus NS, may require cardioversion.

SE of adenosine: significant bradycardia, NV. Be sure to have emergency equipment available.

85

Vagan maneuvers

induce vagal stimulation of the cardiac conduction system, specifically the SA and AV nodes. Results to tx SVT are often temporary and may cause rebound tachycardia or severe brady.

86

Carotid Sinus Massage

MD massages over one carotid artery for a few secs causing vagal stimulation slowing SA and AV nodal conduction.

Have pt turn head to opposite side, watch cardiac monitor, assess vitals and LOC

Complications inc: bradydysrhythmias, asystole, V fib, cerebral damage. Not commonly done bc of this.

Have a defibrillator and resuscitative equipment available.

87

3 Atrial dysrhythmias

3. Atrial Fibrillation

The most common dysrhythmia seen in clinical practice. Its assoc with atrial fibrosis and loss of muscle mass, and lamin AC gene. It is common in heart diseases such as HTN, heart failure, CAD, It decreases cardiac output sometimes up to 20-30%.

88

A fib risk factors

  • increases w/ age
  • HTN
  • previous stroke
  • heart disease
  • DM
  • HF
  • Mitral valve disease
  • Obesity, caucasian race, excessive alcohol (holiday heart syndrome - afib is temp and reversible)
89

A fib Assessment

Atria depolarize in a totally disorganized manner at a rate of 350-600 bpm, ventricular rsvp is usu 120-200 bpm. Chaotic rhythm with no clear P waves, no atrial cxs, loss of atrial kick, and irregular ventricular response. The rapid and irregular ventricular rate decreases ventricular filling and reduces cardiac output, further impairing the heart's perfusion ability.

90

What is the pt with Afib at high risk for?

Thrombus formation, PE, Stroke, VTE

91

Afib Intvn

Depend on severity. Drug therapy is often effective. Ca channel blockers like diltiazem, or amiodarone for more difficult to control AF. Dronedarone is a new drug, but should not be given to pts with h/o CHF. BBs or Dig.

92

CHADs Scoring System

Used to determine if the pt w/ AF needs preventive anticoagulant therapy.

C (h/o CHF) 1 point
H (h/o HTN) 1 point
A ge >=75 1 point
D iabetes 1 point
S (h/o stroke) 2 points

0: Low risk - 325 mg aspirin
1: Moderate risk - rec. aspirin or warfarin
2: High risk - warfarin w/ INR goal of 2-3 or other anticoagulant.

93

Teaching for pts on warfarin

Avoid foods high in VK: avoid ginger, ginseng, goldenseal, ginkgo biloba, st johns wort.

94

There are alternative drugs that can be used due to the SE of warfarin: Rivaroxaban (Xarelto), dabigatran (Pradaxa), apixaban (Eliquis). What are some benefits/drawbacks to these?

  • No need to monitor lab values.
  • Reversal agents are NOT available
  • PT and INR are not accurate predictors of bleeding
  • Use caution in pts >75 due to increased fall risk
95

Cardioversion

synchronized countershock that may be performed in emergencies for unstabe ventricular or SVTs or electively for stable tachydysrhythmias that are resistant to medical therapies.

96

Prior to cardioversion

  • withhold dig for 48 h bc it puts pt at risk for VF after procedure
  • For elective procedure: anticoagulants for 4-6 weeks prior to procedure to prevent clots from moving from heart to brain or lungs
  • Sign consent form unless emergency bc anesthesia is used for sedation
  • Have defibrillator set to synchronized mode
  • TURN O2 OFF AND AWAY FROM PT, FIRE CAN RESULT. SHOUT CLEAR PRIOR TO SHOCK!
97

After cardioversion

  • assess pt response and heart rhythm.
  • maintain ABC
  • O2
  • VS, LOC
  • Monitor for dysrhythmias
  • Assess for chest burns
  • Emotion support/documentation
98

Radiofrequency catheter ablation

May be used to destroy irritable focus causing SVT or ventricular tachydysrhythmia. When performed in the AV nodal or His bundle area, damage may occur to normal conduction causing heart blocks and req pacemaker.

99

4 Ventricular Dysrhythmias

  • Premature ventricular contractions
  • ventricular tachycardia
  • ventricular fibrillation
  • ventricular asystole
100

4 Ventricular Dysrhythmias:

1. PVCs

Result from increased irritability of ventricular cells and are seen as early ventricular complexes followed by a pause. QRS complexes may be uniform or different shapes. Frequently occur in repetitive rhythms such as bigeminy, trigeminy, and quadrigeminy.

3 + successive PVCs are usually called nonsustained ventricular tachycardia.

They are common and increase with AGE

101

PCVs risk factors

  • age
  • MI, chronic HF, COPD, anemia
  • low K, Mg
  • drugs, stress, nicotine, caffeine, alcohol, infection, surgery esp in older adults
  • Post menopausal women often find that caffeine causes palpitations.
102

PVCs assessment

  • Pt may be asymptomatic or have palpitations or chest discomfort
  • Peripheral pulses may be diminished or absent
  • decreased peripheral perfusion
  • Palpate carotid, brachial, or femoral arteries while observing the monitor for widened QRS complexes or auscultating apical heart sounds.
  • With acute MI, PVCs may be considered as a warning of VT or VF
103

PVCs Intvn

If there is no underlying heart disease, they are not usually tx other than by eliminating causes like excess caffeine or stress. >5000PVCs in 24h tx w/ BBs.

104

4 Ventricular Dysrhythmias

2. Ventricular Tachycardia (VT)

repetitive firing of an irritable ventricular extopic focus, usually at 140-180 bpm. Can be intermittent or sustained (lasting longer than 15-30 sec).The sinus node may continue to discharge independently depolarizing the atria but not ventricles. P waves seldom seen in sustained VT.

105

VT risk factors

  • ischemic heart disease
  • MI
  • cardiomyopathy
  • low K, Mg
  • valvular heart disease, HF
  • drug toxicity (steroids)
  • Hypotension
  • Cocaine or illicit inhalants

In pts who go into cardiac arrest, VT is commonly the initial rhythm before deterioration into VF as the terminal Rhythm!

106

In some pts VT causes cardiac arrest. What do you do?

  • ABCs
  • LOC
  • Oxygenation level
  • If stable give O2 and determine rhythm
  • Amiodarone, lidocaine, or Mg sulfate may be given
107

Tx of VT

  • Elective cardioversion s highly recommended for stable VT.
  • Radiofrequency catheter ablation may be done
  • For unstable VT - defibrillate pt
108

4 Ventricular Dysrhythmias

3. Ventricular Fibrillation (VF)

Result of electrical chaos in the ventricles and is LIFE THREATENING! Ventricles do not cx, no recognizable ECG deflections. Ventricles quiver consuming A LOT of O2. No CO or pulse and no perfusion. Rapidly fatal iif not ended within 3-5 min.

109

VF risk factors

  • May be the 1st s/s CAD
  • MI pts are at great risk for VF
  • Low K, Mg
  • hemorrhage
  • drug therapy
  • SVT
  • shock
  • Sx, trauma
110

What happens to the pt with VF?

may faint, lose consciousness, become pulseless and apneic, no BP, absent heart sounds, Respiratory and metabolic ACIDOSIS develop. Seizures, death.

111

TX VF

Defibrillation

112

4 Ventricular Dysrhythmias

4. Ventricular Asystole

sometimes called ventricular standstill. Complete absence of any ventricular rhythm, no ventricular depolarization, no QRS, no cx, no cardiac output, no perfusion.

113

Causes of ventricular asystole

myocardial hypoxia usually or a consequence of advanced heart failure. Also, severe hyperkalemia and acidosis.

114

Tx of ventricular asystole

CPR

Do not defibrillate pt in asystole.