Chapter_36 dysrhythmias [Autosaved].pptx

NURSING MANAGEMENT
DYSRHYTHMIAS
Chapter 36
This chapter describes basic principles of electrocardiographic
monitoring and recognition and treatment of common
dysrhythmias.
In addition, it presents ECG changes that are associated
with acute coronary syndrome (ACS).

OBJECTIVES
1. Examine the nursing management of patients requiring continuous
electrocardiographic (ECG) monitoring.
2. Differentiate the clinical characteristics and ECG patterns of normal
sinus rhythm, common dysrhythmias, and acute coronary syndrome
(ACS).
3. Compare the nursing and collaborative management of patients with
common dysrhythmias and ECG changes associated with ACS.
4. Differentiate between defibrillation and cardioversion, including
indications for use and physiologic effects.
5. Describe the management of patients with pacemakers and
implantable cardioverter-defibrillators.
6. Select appropriate interventions for patients undergoing
electrophysiologic testing and radiofrequency catheter ablation
therapy

KeyTerms
 asystole, p. 795
 atrial fibrillation, p. 796
 atrial flutter, p. 795
 automatic external defibrillator (AED), p. 802
 cardiac pacemaker, p. 803
 complete heart block, p. 798
 dysrhythmias, p. 787
 premature atrial contraction (PAC), p. 794
 premature ventricular contraction (PVC), p. 799
 telemetry monitoring, p. 790
 ventricular fibrillation (VF), p. 800
 ventricular tachycardia (VT),
 atrial systole
 bundle of His
 Cardiac cycle

Dysrhythmia
 (also called arrhythmia) is an abnormal or irregular heartbeat.
 An abnormal heart rate means that your heart rate is either too fast
(typically over 100 beats per minute) or too slow (typically below 60 beats
per minute).
 On the other hand, an irregular heartbeat means that your heart’s rhythm
is disrupted in some way.
 For instance, the electrical signal that controls your heartbeat might be
interrupted due to scar tissue in the heart.
 Or, the electrical signal might start too soon and give you the feeling of
your heart skipping a beat. In that case, you’ll notice a stronger heartbeat
right after the brief pause.
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Cardiac Conduction System
 The heart’s electrical conduction
system initiates an impulse whose
purpose is to stimulate the mechanical
cells of the heart to contract.
 A normal cardiac impulse begins in the sinoatrial (SA) node in the upper right
atrium.
 It spreads over the atrial myocardium via interatrial and internodal pathways,
causing atrial contraction.
 The impulse then travels to the atrioventricular (AV) node, through the bundle
of His, and down the left and right bundle branches.
 It ends in the Purkinje fibers, which transmit the impulse to the ventricles.

PROPERTIES OF CARDIAC CELLS
6

Cardiac Cycle
 A cardiac cycle is the period from the beginning
of one heartbeat to the beginning of the next.
 The cardiac cycle is the electrical representation
of the impulse that stimulates contraction and
relaxation of the atria and ventricles.
 Within the normal cardiac cycle, there is a P
wave, a QRS complex, and a T wave
7

Nervous Control of the Heart
 Stimulation of the vagus nerve causes a decreased
rate of firing of the SA node and slowed impulse
conduction of the AV node.
 Stimulation of the sympathetic nerves increases
SA node firing, AV node impulse conduction, and
cardiac contractility.

ELECTROCARDIOGRAM
 The electrocardiogram (ECG) is a graphic tracing of
the electrical impulses produced in the heart.
 The electrical activity of the heart is seen either with
an ECG that shows the activity for that moment when
the ECG is obtained or with continuous cardiac
monitoring.
 Electrodes placed on the patient’s skin allow various
views of the heart’s electrical activity to be seen.
 Each view of the heart is referred to as a lead.
 A 12-lead ECG provides 12 different views of the
heart’s electrical activity, 9

Electrocardiogram Graph Paper
 ECG paper consists of large (heavy lines) and small (light
lines) squares.
 Each large square consists of 25 smaller squares (five
horizontal and five vertical).
 Horizontally, each small square (1 mm) represents 0.04
second.
 This means that one large square equals 0.20 second and
that 300 large squares equal 1 minute.
 Vertically, each small square (1 mm) represents 0.1 millivolt
(mV). This means that one large square equals 0.5 mV.
10

THE ECG LEADS
 The ECG has 12 recording leads.
 Six of the leads measure electrical forces in the frontal plane.
 The remaining six unipolar leads (V1 throughV6) measure the
electrical forces in the horizontal plane (precordial leads).
 The 12-lead ECG may show changes suggesting structural
changes, conduction disturbances, damage (e.g., ischemia,
infarction), electrolyte imbalance, or drug toxicity.
 Obtaining 12 ECG views of the heart is also helpful in the
assessment of dysrhythmias.
11

INTERPRETATION OF CARDIAC
RHYTHMS
 Six-Step Process for Dysrhythmia Interpretation
 A 6-second ECG tracing is used when interpreting
rhythms
 Step 1. Regularity of the Rhythm
 Step 2. Heart Rate
 Step 3. P Waves
 Step 4. PR Interval
 Step 5. QRS Interval
 Step 6. QT Interval
13

RHYTHMS
Regularity of the Rhythm
 The regularity of the rhythm can be determined by
looking at the R-to-R spacing on the ECG.
 Count the number of small squares between each R
wave, which normally should remain the same.
14

RHYTHMS
 Step 2. Heart Rate
 1. Count the number of small (0.04-second) squares
between two R waves and divide that number into 1500.
This gives the beats per minute, because 1500 small
squares equals 1 minute
 This method is used only for regular rhythms and is very
accurate.
 2. Six-second method: the 6-second method is used for
irregular rhythms. Count the number of R waves in a 6-
second strip and multiply the total by 10.
Inc., an affiliate of Elsevier Inc.
15

RHYTHMS
 Step 3. PWaves
 The P waves on the ECG tracing are
examined to see if (1) there is one P
wave in front of every QRS,
 (2) the P waves are regularly
occurring, and (3) the P waves all
look alike
17

RHYTHMS
 Step 4. PR Interval
 All PR intervals are measured to determine
whether they are normal (0.12–0.20
seconds) and constant.
18

RHYTHMS
19
The QRS intervals are measured to
determine whether they
are all within normal range (0.06–0.10
seconds).

RHYTHMS
20
Step 6. QT Interval
 The QT interval is measured from the onset
of the QRS complex to the end of the T
wave.
 QT interval represents the duration of
ventricular electrical systole, which includes
ventricular activation and recovery.
 excessive extension of the QT interval is
strongly associated with ventricular
arrhythmias including Torsade de Pointes
(TdP), an acceleration in cardiac rhythm that
can lead to heart attack.

NORMAL SINUS RHYTHM
 Normal sinus rhythm (NSR) is the heart’s normal rhythm
 It originates in the SA node and has complete, regular cardiac
cycles at 60 to 100 bpm.
 NORMAL SINUS RHYTHM RULES
 1. Rhythm: regular
 2. Heart rate: 60 to 100 bpm
 3. P waves: rounded, upright, precede each QRS
 complex, alike
 4. PR interval: 0.12 to 0.20 seconds
 5. QRS interval: less than or equal to 0.10 seconds.

DYSRHYTHMIAS
 Two terms are used for rhythm disturbances: arrhythmia (irregularity or loss of rhythm of the
heartbeat) and dysrhythmia (abnormal, disordered, or disturbed rhythm).
 Several mechanisms can cause a dysrhythmia. Examples:
 disturbance in the formation of an impulse
 the impulse may arise from the atria, the AV node, or the ventricles rather than the SA node.
 May lead to an increased or decreased heart rate, early or late beats, or atrial or ventricular fibrillation
disturbance in the conduction of the impulse.
 there may be normal formation of the impulse, but it becomes blocked within the electrical
conduction.
 system, resulting in abnormal conduction (as in heart block or bundle branch blocks).

Dysrhythmias Originating in the
Sinoatrial
Node
 Rhythms arising from the SA node
are referred to as sinus rhythms
 Disturbances in conduction from the
SA node can cause irregular rhythms
or abnormal heart rates
 Sinus Bradycardia
 SinusTachycardia
23

Sinoatrial
Node
 Sinus Bradycardia
 the conduction pathway is the same as that in sinus rhythm
 the SA node fires at a rate less than 60 beats/minute
 May be a normal in aerobically trained athletes and in
some people during sleep
 also occurs in response to carotid sinus massage, Valsalva
maneuver, hypothermia, vagal stimulation, and
administration of certain drugs (e.g., β-adrenergic blockers,
calcium channel blockers, Digoxin).
24

Sinus Bradycardia
 SIGNS AND SYMPTOMS.
 Usually, asymptomatic
 With symptomatic bradycardia:
 decreased BP, respiratory distress, diminished or absent
peripheral pulses, fatigue, or syncope can occur.
 Treatment can include intravenous (IV) atropine, or
infusions of dopamine or epinephrine.
25

Sinus Tachycardia
 a heart rate greater than 100 bpm that originates from the
SA node.
 Has the same components as NSR except the rate is faster
 ETIOLOGY.
 physical activity; hemorrhage; shock; medications such as
epinephrine, atropine, or nitrates; dehydration; fever; MI;
electrolyte imbalance; fear; and anxiety.
 Tachycardia occurs as a compensatory mechanism for
hypoxia when additional cardiac output is needed to deliver
oxygen to tissues.
26

Sinus Tachycardia
 can be asymptomatic.
 But if the rate is very rapid (usually >150 bpm) and
sustained for long periods, the patient may experience
angina, dyspnea, syncope, or tachypnea.
 THERAPEUTIC MEASURES.
 If stable, obtain an ECG and treat the cause.
 Medications such as adenosine, calcium channel blockers,
or beta blockers can be used to slow the heart rate
27

Atria
 The SA node is the primary pacemaker, but if the atria
initiate impulses faster than the SA node, they become the
primary pacemaker.
 Atrial rhythms are usually faster than 100 bpm and can
exceed 200 bpm.
 When an impulse originates outside the SA node, the P
waves produced look different (flatter, notched, or peaked)
from the rounded P waves from the SA node.
 This indicates that the SA node is not controlling the heart
rate.
 These atrial impulses travel to the ventricles to initiate a
normal QRS complex after each P wave.
28

Atria
 Atrial Fibrillation
 ETIOLOGY.
 aging (increases after age 60 and is the most common sustained
dysrhythmia)
 History of cigarette smoking,
 rheumatic or ischemic heart diseases,
 heart failure,
 hypertension,
 pericarditis,
 pulmonary embolism,
 And some medications.
29

Atrial Fibrillation
 1. Rhythm: irregularly irregular
 2. Heart rate: atrial rate not measurable;
ventricular rate under 100 is controlled response;
greater than 100 is rapid ventricular response
 3. P waves: no identifiable P waves
 4. PR interval: none can be measured because no
P waves are seen
 5. QRS interval: less than or equal to 0.10
seconds.
30

Atrial Fibrillation
 most patients feel the irregular rhythm.
 Many describe it as palpitations or a skipping
heartbeat.
 A patient’s radial pulse may be faint
because of a decreased stroke volume
 If the ventricular rhythm is rapid and
sustained, the patient can go into left-sided
heart failure. 31

Atrial Fibrillation
 The focus of AF treatment is to control rate, prevent
thromboembolism, and restore normal rhythm.
 If the patient is unstable, synchronized cardioversion is
done immediately to try to return the heart to NSR.
 For the patient who is stable, medications to control the
ventricular rate such as beta blockers, calcium channel
blockers, or digoxin are used.
 Anticoagulant therapy is given to reduce thrombi, which
can cause a stroke. 32

Paroxysmal SupraventricularTachycardia.

Ventricular Dysrhythmias
PREMATURE VENTRICULAR CONTRACTION
 Premature ventricular contractions (PVCs) originate in the ventricles
from an ectopic focus (a site other than the SA node).
 The ventricles are irritable and fire prematurely, before the SA node
does.
 When the ventricles fire first, the impulses are not conducted
normally through the electrical pathway.
 This results in a wide (>0.10 seconds), bizarre QRS complex on an
ECG.
 PVCs may be felt by the patient and are described as a skipped
beat or palpitations. With frequent PVCs, cardiac output can be
decreased, leading to fatigue, dizziness, or more severe 34

PREMATURE VENTRICULAR CONTRACTION
 Occasional PVCs do not usually require treatment.
 However, if the PVCs are more than six per minute, regularly
occurring, multifocal, falling on the T wave (known as “R-on-T
phenomenon,” which can trigger life-threatening dysrhythmias),
 Or caused by an acute MI, they can be dangerous. Antidysrhythmic.
 drugs that depress myocardial activity are used to treat PVCs such
as amiodarone and beta blockers
35

Ventricular Tachycardia
 The occurrence of three or more PVCs in a row is
referred to as ventricular tachycardia (VT)
 VT results from the continuous firing of an ectopic
ventricular focus.
 During VT, the ventricles rather than the SA node
become the pacemaker of the heart.
 The pathway of the ventricular impulses is different
from normal conduction, producing a
 wide (>0.10 seconds), bizarre QRS complex.
36

Ventricular Tachycardia
 ETIOLOGY.
 Myocardial irritability, MI, and
cardiomyopathy are common causes of VT.
Respiratory acidosis, hypokalemia, digoxin
toxicity, cardiac catheters, and pacing wires
can also produce VT.
37

Pathophysiology of Primary
Hypertension
 Altered Renin-Angiotensin-
Aldosterone Mechanism
 High plasma renin activity (PRA) results in the
increased conversion of angiotensinogen to
angiotensin I.
 This alteration in the RAAS may contribute to
the development of hypertension.
38

Pathophysiology of Primary
Hypertension
 Stress and Increased Sympathetic Nervous System
Activity.
 Physiologic responses to stress, which are normally
protective, may persist to a pathologic degree, resulting in
a prolonged increase in SNS activity.
 Increased SNS stimulation produces increased
vasoconstriction, increased HR, and increased renin
release.
 Increased renin activates the RAAS, leading to elevated
BP.
 People exposed to high levels of repeated psychologic
stress develop hypertension to a greater extent than those
who experience less stress.
39

Insulin Resistance and
Hyperinsulinemia
 Insulin resistance is a risk factor in
the development of hypertension and
CVD.
 High insulin levels stimulate SNS
activity and impair nitric oxide–
mediated vasodilation.
 Additional pressor effects of insulin
include vascular hypertrophy and
increased renal sodium reabsorption.40

Joint National Committee (JNC) 8

Clinical Manifestations
 Hypertension is often called the “silent
killer” because it is frequently
asymptomatic until it becomes severe and
target organ disease occurs.
 secondary symptoms include fatigue,
dizziness, palpitations, angina, and dyspnea.
42

Complications
 Coronary Artery Disease
 The mechanisms by which hypertension contributes to the development of
atherosclerosis are not fully known.
 The “response-to-injury” theory of atherogenesis suggests that hypertension
disrupts the coronary artery endothelium. This results in a stiff arterial wall
with a narrowed lumen, and accounts for a high rate of CAD, angina, and MI.
 Left Ventricular Hypertrophy.
 Sustained high BP increases the cardiac workload and produces left
ventricular hypertrophy (LVH)
 Progressive LVH, especially in the presence of CAD, is associated with the
development of heart failure.
 Heart Failure
 Heart failure occurs when the heart’s compensatory mechanisms are
overwhelmed, and the heart can no longer pump enough blood to meet the
body’s demands

Complications
 Cerebrovascular Disease.
 Atherosclerosis is the most common cause of
cerebrovascular disease.
 Hypertension is a major risk factor for cerebral
atherosclerosis and stroke
 Peripheral Vascular Disease.
 Hypertension speeds up the process of atherosclerosis in
the peripheral blood vessels. This leads to the
development of peripheral vascular disease, aortic
aneurysm, and aortic dissection.
 Intermittent claudication (ischemic leg pain precipitated by
activity and relieved with rest) is a classic symptom of
peripheral vascular disease.

Complications
 Nephrosclerosis.
 Hypertension is one of the leading causes of chronic kidney disease
 Renal disease results from ischemia caused by the narrowing of the
renal blood vessels.
 Laboratory indications of renal disease are microalbuminuria,
proteinuria, microscopic hematuria, and elevated serum creatinine and
blood urea nitrogen (BUN)
 levels. The earliest manifestation of renal disease is usually nocturia
 Retinal Damage.
 Damage to the retinal vessels provides an indication of related vessel
damage in the
 heart, brain, and kidneys.
 Manifestations of severe retinal damage include blurring of vision,
retinal hemorrhage, and loss of vision.

Diagnostic Studies
46

Ambulatory Blood Pressure Monitoring.
Some patients have
elevated BP readings in a clinical setting
and normal readings
when BP is measured elsewhere. This
phenomenon is referred
to as “white coat” hypertension. Self-
monitoring of BP is an
easy, cost-effective approach that may be
chosen before ambulatory
BP monitoring (ABPM).

Collaborative Care
 Goals include achieving and
maintaining goal BP and reducing
cardiovascular risk and target organ
disease.
 Lifestyle modifications are indicated
for all patients with prehypertension
and hypertension.
48

Collaborative Care
 Lifestyle Modifications.
 Lifestyle modifications are directed toward reducing the
patient’s BP and overall cardiovascular risk.
Modifications include
 (1) weight reduction
 (2) Dietary Approaches to Stop Hypertension (DASH)
eating plan
 (3) dietary sodium reduction,
 (4) moderation of alcohol consumption,
 (5) regular physical activity,
 (6) avoidance of tobacco use (smoking and chewing)
 (7) management of psychosocial risk factors
49

Drug Therapy
50
The drugs currently available for
treating hypertension
have two main actions:
(1)they decrease the volume of
circulating blood
(2)they reduce SVR

Site and method of action of various
antihypertensive drugs
51

53

Nursing Management: Primary
HTN.
54
• Assessment
• Subjective data
• Objective Data
• Nursing Diagnosis
• Priority Diagnosis
• Collaborative problems
• Planning
• Overall Goals: Patient will:
• (1) achieve and maintain the goal BP; (2) understand
• and follow the therapeutic plan; (3) experience minimal or no
unpleasant side effects of therapy; and (4) be confident of the
ability to manage and cope with this condition.

Nursing Management: Primary
HTN.
55
• Implementation
• Health Promotion
• Individual Patient Evaluation
• Blood Pressure Measurement
• Screening Programs
• Cardiovascular Risk Factor Modification

GERONTOLOGIC
CONSIDERATIONS
 The lifetime risk of developing hypertension is
approximately 90% for middle-aged (ages 55 to 65) and
older (over 65) normotensive men and women
 Isolated systolic hypertension (ISH) is the most common
form of hypertension in people over 50 years of age.
 In the older adult who is taking antihypertensive
medication, absorption of some drugs may be altered as a
result of decreased blood flow to the gut.
 Metabolism and excretion of drugs may also be
prolonged.
 Some older people have a wide gap between the first
Korotkoff sound and subsequent beats. This is called the
auscultatory gap. Failure to inflate the cuff high enough
may result in underestimating SBP
56

GERONTOLOGIC
CONSIDERATIONS
 The pathophysiology of hypertension in the older adult
 involves the following age-related physical changes:
 (1) loss of elasticity in large arteries from
atherosclerosis,
 (2) increased collagen content and stiffness of the
myocardium.
 (3) increased peripheral vascular resistance,
 (4) decreased adrenergic receptor sensitivity,
 (5) blunting of baroreceptor reflexes.
 (6) decreased renal function.
 (7) decreased renin response to sodium and water
depletion.
57

GERONTOLOGIC
CONSIDERATIONS
 Because of varying degrees of impaired baroreceptor
reflexes, orthostatic hypotension often occurs in older
adults, especially in those with ISH.
 Older adults experience postprandial drops in BP.
 The greatest decrease occurs approximately 1 hour
after eating.
 BP returns to preprandial levels 3 to 4 hours after eating.
 Avoid giving vasoactive medications with meals.7
58

HYPERTENSIVE CRISIS
59
• is a term used to indicate either a hypertensive
urgency or emergency. This is determined by the
degree of target organ disease and how quickly
the BP must be lowered.
• BP is severely elevated (often above 220/140 mm
Hg) with clinical evidence of target organ disease.
• Hypertensive urgency develops over days to
weeks. This is a situation in which a patient’s BP
is severely elevated (usually above 180/110 mm
Hg), but there is no clinical evidence of target
organ disease
Hypertensive urgencies usually do not require IV
medications but can be managed with oral agents.

HYPERTENSIVE CRISIS
60
Clinical Manifestations
 A hypertensive emergency is often manifested as
hypertensive encephalopathy, a syndrome in
which a sudden rise in BP is associated with
severe headache, nausea, vomiting, seizures,
confusion, and coma.
 The manifestations of encephalopathy are the
result of increased cerebral capillary permeability.
 This leads to cerebral edema and a disruption in
cerebral function.

HYPERTENSIVE CRISIS
61
 In treatment of hypertensive emergencies, the
mean
arterial pressure (MAP) is often used instead of BP
readings to guide and evaluate drug therapy.
Antihypertensive drugs administered IV have a rapid
(within seconds to minutes) onset of action. Assess
the patient’s BP and pulse every 2 to 3 minutes
during the initial administration of these drugs.

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