1 of 87

Unit 6, Chapter 25: Assessment of �Cardiovascular Function

2 of 87

Anatomy of the Heart

3 of 87

Cardiac Conduction System: Electrophysiology

(60-100)

(40-60)

(30-40)

The cardiac conduction system generates and transmits electrical impulses that stimulate contraction of the myocardium. Under normal circumstances, the conduction system first stimulates contraction of the atria and then the ventricles. The synchronization of the atrial and ventricular events allows the ventricles to fill completely before ventricular ejection, thereby maximizing cardiac output.

The primary pacemaker for the myocardium is Sinoatrial node.

The heart rate is determined by the myocardial cells with the fastest inherent firing rate. Under normal circumstances, the SA node has the highest inherent rate (60 to 100 impulses per minute), the AV node has the second-highest inherent rate (40 to 60 impulses per minute), and the ventricular pacemaker sites have the lowest inherent rate (30 to 40 impulses per minute) (Woods et al., 2009). If the SA node malfunctions, the AV node generally takes over the pacemaker function of the heart at its inherently lower rate. Should both the SA and the AV nodes fail in their pacemaker function, a pacemaker site in the ventricle will fire at its inherent bradycardic rate of 30 to 40 impulses per minute.

Depolarization: electrical activation of cell caused by influx of sodium into cell while potassium exits cell

Repolarization: return of cell to resting state caused by reentry of potassium into cell while sodium exits

4 of 87

Pulmonary and Systemic Circulation

5 of 87

Cardiac Hemodynamics

Stroke Volume(SV): Amount of blood ejected with each heartbeat.

Preload: Degree of stretch of cardiac muscle fibers at end of diastole.
Afterload: Resistance to ejection of blood from ventricle.

Ejection Fraction: Percent of end diastolic volume ejected with each heart beat (left ventricle).
Cardiac Output (CO): Amount of blood pumped by ventricle in liters per minute.
CO = SV × HR

6 of 87

Assessment

Health history
Family History

Medications
Nutrition
Elimination
Activity, Exercise
Sleep, Rest
Self-perception, Self-concept
Roles, Relationships

Physical Examination

Heart inspection, palpation, auscultation
Vital Signs
Sexuality, Reproduction
Coping, Stress Tolerance
Prevention Strategies
Risk factors

Modifiable
Nonmodifiable

7 of 87

Diagnostic Evaluation

Laboratory Tests
Cardiac Biomarkers:
Creatine kinase (CK), CK isoenzymes (CK-MB)
Blood chemistry, hematology, coagulation & Proteins:
Myoglobin
Troponin T and I : most indicative of cardiac damage

Lipid Profile
Brain (B-type) natriuretic peptide
C-reactive protein
Homocysteine

8 of 87

Electrocardiography

12-lead ECG
Continuous monitoring: hardwire, telemetry, lead systems & ambulatory monitoring.

I. Signal-averaged ECG

II. Continuous ambulatory monitoring

III. Transtelephonic monitoring

IV. Wireless mobile monitoring

9 of 87

Electrocardiography

Cardiac Stress Testing

Exercise stress testing
Pt walks on treadmill with

intensity progressing according

to protocols

ECG, V/S, symptoms monitored
Terminated when target HR is achieved
Pharmacologic stress testing

- Vasodilating agents given to mimic exercise

10 of 87

Electrocardiography

Echocardiography
Noninvasive ultrasound test that is used to:

Measure the ejection fraction
Examine the size, shape, and motion of cardiac structures
Transthoracic or Transesophageal

11 of 87

Diagnostic Tests

Radionuclide Imaging

Myocardial Perfusion Imaging
Test of ventricular function, wall motion
Computed Tomography (CT)
Positron Emission Tomography (PET)
Magnetic Resonance Angiography

12 of 87

Cardiac Catheterization

Invasive procedure used to diagnose structural & functional diseases of the heart & great vessels.
Used to measure cardiac chamber pressures, & assess patency of coronary arteries.
Right Heart Cath: to assess the function of the right ventricle and tricuspid and pulmonary valves
Pulmonary artery pressure and oxygen saturations may be obtained; biopsy of myocardial tissue may be obtained
Left Heart Cath:to evaluate the aortic arch & its major branches, patency of the coronary arteries, & the function of the left ventricle & mitral and aortic valves
Involves use of contrast agent�

13 of 87

Nursing Interventions-Cardiac Cath

Assessment prior to test; allergies, blood work.
Patient education pre- and post-procedure.
Post procedure; Observe cath site for bleeding, hematoma
Assess peripheral pulses
Evaluate temp, color, and cap refill of affected extremity
Screen for dysrhythmias
Activity restrictions; Maintain bed rest 2 to 6 hours
Instruct patient to report chest pain, bleeding
Monitor for contrast-induced nephropathy
Ensure patient safety

Nursing Interventions

Nursing responsibilities before cardiac catheterization include:

Instructing the patient to fast, usually for 8 to 12 hours, before the procedure

Informing the patient that if catheterization is to be performed as an outpatient procedure, a friend, family member, or other responsible person must transport the patient home

Informing the patient about the expected duration of the procedure and advising that it will involve lying on a hard table for less than 2 hours

Reassuring the patient that IV medications are given to maintain comfort

Informing the patient about sensations that will be experienced during the catheterization. Knowing what to expect can help the patient cope with the experience. The nurse explains that an occasional pounding sensation (palpitation) may be felt in the chest because of extra heartbeats that almost always occur, particularly when the catheter tip touches the endocardium. The patient may be asked to cough and to breathe deeply, especially after the injection of the contrast agent. Coughing may help disrupt a dysrhythmia and clear the contrast agent from the arteries. Breathing deeply and holding the breath help lower the diaphragm for better visualization of heart structures. The injection of a contrast agent into either side of the heart may produce a flushed feeling throughout the body and a sensation similar to the need to void, which subsides in 1 minute or less.

Encouraging the patient to express fears and anxieties. The nurse provides education and reassurance to reduce apprehension.

Nursing responsibilities after cardiac catheterization are dictated by hospital policy and primary provider preferences and may include:

Observing the catheter access site for bleeding or hematoma formation and assessing peripheral pulses in the affected extremity (dorsalis pedis and posterior tibial pulses in the lower extremity, radial pulse in the upper extremity) every 15 minutes for 1 hour, every 30 minutes for 1 hour, and hourly for 4 hours or until discharge. BP and heart rate are also assessed during these same time intervals.

Evaluating temperature, color, and capillary refill of the affected extremity during these same time intervals. The patient is assessed for affected extremity pain, numbness, or tingling sensations that may indicate arterial insufficiency. The best technique to use is to compare the examination findings between the affected and unaffected extremities. Any changes are reported promptly.

Screening carefully for dysrhythmias by observing the cardiac monitor or by assessing the apical and peripheral pulses for changes in rate and rhythm. A vasovagal reaction, consisting of bradycardia, hypotension, and nausea, can be precipitated by a distended bladder or by discomfort from manual pressure that is applied during removal of an arterial or venous catheter. The vasovagal response is reversed by promptly elevating the lower extremities above the level of the heart, infusing a bolus of IV fluid, and administering IV atropine to treat the bradycardia.

Maintaining bed rest for 2 to 6 hours after the procedure. Duration of bed rest is dependent upon location of arterial approach, size of the catheter used during the procedure, and method used to maintain hemostasis. If manual pressure or a mechanical device was used during a femoral artery approach, the patient remains on bed rest for up to 6 hours with the affected leg straight and the head of the bed elevated no greater than 30°. For comfort, the patient may be turned from side to side with the affected extremity straight. If a percutaneous vascular closure device or patch was deployed, the nurse checks local nursing care standards and anticipates that the patient will have fewer activity restrictions. The patient may be permitted to ambulate within 2 hours. If the radial artery was accessed, the patient remains on bed rest for 2 hours or until the effects of sedation have dissipated. The patient may sit up in bed. A hemostasis band or pressure dressing may be applied over the catheter access site. Patients are instructed to avoid sleeping on the affected arm for 24 hours and to avoid repetitive movement of the affected extremity for 24 to 48 hours (Rosendorff, 2013). Analgesic medication is given as prescribed for discomfort.

Instructing the patient to report chest pain and bleeding or sudden discomfort from the catheter insertion sites promptly.

Monitoring the patient for contrast-induced nephropathy by observing for elevations in serum creatinine levels. IV hydration is used to increase urinary output and flush the contrast agent from the urinary tract; accurate oral and IV intake and urinary output are recorded.

Ensuring patient safety by instructing the patient to ask for help when getting out of bed the first time after the procedure. The patient is monitored for bleeding from the catheter access site and for orthostatic hypotension, indicated by complaints of dizziness or lightheadedness.

For patients being discharged from the hospital on the same day as the procedure, additional instructions are provided (see Chart 25-6).

14 of 87

Cardiac Catheterization

15 of 87

Cardiac Catheterization

16 of 87

�

Cardiac Catheterization Animation

17 of 87

Unite 6; Chapter 26: Management of Patients With Dysrhythmias & Conduction Problems

18 of 87

Normal Electrical Conduction

SA node (sinus node)
AV node
Conduction
Bundle of His
Right and left bundle branches
Purkinje fibers
Depolarization = Electrical Stimulation = Systole
Repolarization = Electrical Relaxation = Diastole

(60-100)

(40-60)

(30-40)

The electrical impulse that stimulates and paces the cardiac muscle normally originates in the SA node, also called the sinus node, an area located near the superior vena cava in the right atrium. In the adult, the electrical impulse usually occurs at a rate of 60 to 100 times a minute. The electrical impulse quickly travels from the SA node through the atria to the atrioventricular (AV) node (see Fig. 26-1); this process is known as conduction. The electrical stimulation of the muscle cells of the atria causes them to contract. The structure of the AV node slows the electrical impulse, giving the atria time to contract and fill the ventricles with blood. This part of atrial contraction is frequently referred to as the atrial kick and accounts for nearly one third of the volume ejected during ventricular contraction (Fuster, Walsh, & Harrington, 2011). The electrical impulse then travels very quickly through the bundle of His to the right and left bundle branches and the Purkinje fibers, located in the ventricular muscle. The electrical stimulation is called depolarization, and the mechanical contraction is called systole. Electrical relaxation is called repolarization, and mechanical relaxation is called diastole. The process from sinus node electrical impulse generation through ventricular repolarization completes the electromechanical circuit, and the cycle begins again. (See Chapter 25 for a more complete explanation of cardiac function.)

19 of 87

The Electrocardiogram (ECG) Interpretation

The ECG reflects electrical activity of the heart.
Electrode placement

Electrode adhesion

Types of ECG:
12 lead ECG
Hardwire monitoring
Telemetry
Holter monitor

ECG Interpretation
P wave
QRS complex
T wave
U wave
PR interval
ST segment
QT interval
TP interval
PP interval

20 of 87

ECG Graph and Commonly Measured Components

Time & rate are measured on the horizontal axis of the graph, & amplitude or voltage is measured on the vertical axis.
When an ECG waveform moves toward the top of the paper, it is called a positive deflection. When it moves toward the bottom of the paper, it is called a negative deflection.

Each small box represent 0.04 second on the horizontal axis

&1 mm or 0.1 millivolt on the vertical axis.

21 of 87

��P wave & QRS Complex

P Wave
Represents Atrial Depolarization, electrical impulses at the SA node
Normally it is 0.11 sec by duration, and 2.5mm in height or less.
QRS Complex
Represents Ventricular Depolarization
It is less than 0.12 sec in duration
Composed of three waves:

Q, R, S

22 of 87

QRS Complex

Q wave is the first negative deflection after P wave
It is less than .04 sec by duration
R wave is the first positive deflection after P wave
S wave is the first negative deflection after R wave

23 of 87

T wave

Represents Ventricular Repolarization (Resting state)
Follows the QRS complex and usually has the same direction (deflection) of QRS complex

24 of 87

��U wave

Represents Repolarization of Purkinje Fibers
(Rare); Not always present, seen in hypokalemia, heart disease, & hypertension
U wave follows the T wave & is usually smaller than the P wave but if tall could be mistaken for an extra P wave.

25 of 87

�PR Interval

Represents the time needed for

SA stimulation +
Atrial depolarization +
Conduction through the AV node before ventricular depolarization (end of bundle of His)

It is onset of Atrial depolarization to the onset of Ventricular depolarization
Measured from the beginning of the P wave to the beginning of the QRS complex
It is 0.12 - 0.20 sec in duration

26 of 87

ECG

QT Interval:

Represents the total time for ventricular depolarization & repolarization.
Is measured from the beginning of the QRS complex to the end of the T wave.
The QT interval varies with heart rate, gender, and age
The QT interval is usually 0.32 to 0.40 seconds in duration if the heart rate is 65 to 95 bpm

27 of 87

ECG

TP Interval:
Is measured from the end of the T wave to the beginning of the next P wave—an isoelectric period
When no electrical activity is detected, the line on the graph remains flat; this is called the isoelectric line.
The ST segment is compared with the TP interval to detect ST segment changes.

28 of 87

ECG

PP Interval:
Represents Atrial cycle (i.e., beginning of the P wave to the beginning of the next P wave
Determines Atrial rate & rhythm
RR Interval:
Used to determines Ventricular rate and rhythm
Measured from one QRS to the next QRS complex.

29 of 87

ST Segment�

Represents early Ventricular Repolarization
lasts from the end of the QRS complex to the beginning of the T wave
Is analyzed to identify whether it is isoelectric or not (ST segment is normally isoelectric)
ST segment depression or elevation may indicate cardiac ischemia.

30 of 87

Determining Heart Rhythm From ECG

Use P-P intervals to determine Atrial rhythm
Use R-R intervals to determine Ventricular rhythm
Equal intervals means regular rhythm
If the intervals are different, the rhythm is called irregular.
A 1-minute (60 seconds) rhythm strip contains 300 large boxes and 1,500 small boxes.

31 of 87

1 small box = 0.04 sec
1 big box = 0.2 sec
5 large boxes = 1 sec
30 large boxes = 6 sec
300 large boxes / 1500 small boxes = 60 second

Determining Heart Rhythm From ECG

32 of 87

Determining Heart Rate From ECG

Regular rhythm

1500 divided by the number of small boxes between two R waves (Heart Rate = 1500/No of small boxes)

Or

300 divided by the number of large boxes between two R waves (HR = 300/ No of large boxes)

For example, if there are 10 small boxes between two R waves, the heart rate is 1,500/10, or 150 bpm;
If there are 25 small boxes, the heart rate is 1,500/25, or 60 bpm (see Fig. 26-4A).

33 of 87

Determining Heart Rate From ECG

Irregular rhythm

Count the number of RR or PP intervals in 6 seconds (30 large boxes) and multiply that number by 10.

The top of the ECG paper is usually marked at 3-second intervals, which is 15 large boxes horizontally Less accurate method
For example, if there are approximately 7 RR intervals in 6 seconds, so there are about 70 RR intervals in 60 seconds (7 × 10 = 70). The ventricular HR is 70 bpm (see Fig. 26-4B).

34 of 87

Heart Rate Determination

Figure 26-4 • A. Ventricular & atrial heart rate determination with a regular rhythm: 1,500 divided by the number of small boxes between two P waves (atrial rate) or between two R waves (ventricular rate).

In this example, there are 25 small boxes between both R waves & P waves, so the heart rate (HR) is 60 bpm.

B. Heart rate determination if the rhythm is irregular. There are approximately 7 RR intervals in 6 seconds, so there are about 70 RR intervals in 60 seconds (7 × 10 = 70). The ventricular HR is 70 bpm.

35 of 87

Dysrhythmias

Disorders of formation or conduction (or both) of electrical impulses within heart.
Can cause disturbances of: Rate, Rhythm, Both rate & rhythm
Dysrhythmias can be life-threatening and can occur in the Atria, Ventricles, or in both.
Potentially can alter blood flow & cause hemodynamic changes (change pumping action of the heart & decrease BP).
Diagnosed by analysis of ECG waveform
Their treatment is based on the frequency & severity of symptoms produced.

36 of 87

Consequences of Dysrhythmias

Dysrhythmias interfere with the heart’s pumping ability
Bradycardic rhythms impair blood flow to vital organs by decreasing total cardiac output (CO).
Tachycardic rhythms shorten diastolic filling time and subsequently decrease stroke volume (SV) and overall cardiac output.
Atrial dysrhythmias reduce the overall cardiac output by 20%.
Ventricular dysrhythmias can dramatically reduce diastolic filling to a point where CO is severely diminished producing absence of pulse and blood pressure.

37 of 87

Etiology- Dysrhythmias

Hypoxia
Shock
Poisoning
Drug Ingestion
Myocardial Infarction (MI)
Congestive Heart Failure (CHF)

Pulmonary Disorders
Electrolyte imbalances
Metabolic Imbalances

38 of 87

Manifestations of Dysrhythmias

Irregular rate and rhythm, palpitation
Chest, neck, shoulder, or arm pain
Dizziness
Dyspnea
Extreme restlessness
Decreased level of Consciousness

Numbness of Arms
Weakness and Fatigue
Cold Skin
Nausea and Vomiting
Decreased Blood Pressure (BP)
Decreased O₂ Saturation

39 of 87

Normal Sinus Rhythm

Normal sinus rhythm occurs when the electrical impulse starts at a regular rate & rhythm in the SA node & travels through the normal conduction pathway.
Ventricular & Atrial rate 60-100 in an adult, & regular rhythm
QRS shape & duration usually normal (less than .12 sec)
P wave normal & consistent shape, always in front of QRS.
PR interval consistent (0.12-0.20 seconds)
P:QRS ration 1:1

40 of 87

Normal Sinus Rhythm (NSR)

Ventricular and Atrial Rate	60 -100 b/min
Ventricular and Atrial Rhythm	Regular
P wave	Normal & consistent shape (Upright), always in front of the QRS
QRS shape & duration	Normal (.04 -.12 sec)
P-R interval	Constant, duration : 0.12 - 0.20 sec
P : QRS ratio	1 : 1

41 of 87

Types of Dysrhythmias:�

Sinus Node Dysrhythmias:
Sinus Bradycardia (abnormally slow heart rates).
Sinus Tachycardia (rapid heart rates).
Sinus Arrhythmia
Atrial Dysrhythmias (originate in the atria)
Atrial Flutter, Atrial Fibrillation (AF) & Premature atrial complexes (PACs)
Junctional Dysrhythmias originate within AV nodal
Ventricular Dysrhythmias (originate in the ventricle)
Ventricular Tachycardia (VT), Ventricular Fibrillation (VF)
Ventricular asystole (absence of rhythm formation)

42 of 87

Sinus Bradycardia

Discharge rate (impulse) from the SA node is slower than normal rate.

Rate < 60 beats/min, Regular rhythm

43 of 87

Sinus Bradycardia

Ventricular and Atrial Rate	Less than < 60 b/min
Ventricular and Atrial rhythm	Regular
QRS shape & duration	Normal (.04 -.12 sec)
P wave	Normal and consistent in shape, always in front of the QRS
P-R interval	Constant interval duration : 0.12- 0.20 second
P : QRS ratio	1 : 1

44 of 87

Sinus Bradycardia

45 of 87

Sinus Bradycardia

Causes:

Lower metabolic needs (e.g., sleep, athletic training, hypothyroidism)
Vagal stimulation (e.g., vomiting, suctioning, severe pain)
Medications (e.g., Beta blockers)
Coronary Artery Disease (CAD) (e.g., MI)
Hypoxemia
Idiopathic sinus node dysfunction
Altered mental status (Delirium)
Increased Intracranial Pressure (ICP)

46 of 87

Sinus Bradycardia

Medical Management:
Depends on cause & symptoms
Treat underlying causes
If the bradycardia produces signs & symptoms of clinical instability (e.g., acute alteration in mental status, chest discomfort, or hypotension), 0.5 mg of Atropine given rapidly as (IV) bolus & repeated every 3-5 minutes until a maximum dosage of 3 mg is given.
Atropine blocks vagal stimulation
Rarely if No response to Atropine: emergency transcutaneous pacing & Catecholamines such as Dopamine or Epinephrine, are given.

47 of 87

Sinus Tachycardia

SA node creates an impulse faster-than-normal rate (e.g., vagal inhibition, sympathetic stimulation)
HR in an adult is >100 beats/min but usually <120
Conduction pathway is the same as in normal sinus rhythm.

48 of 87

�Sinus Tachycardia

Ventricular and Atrial rate	Greater than> 100 b/min (usually less than 120 b/min)
Ventricular & Atrial rhythm	Regular
QRS shape & duration	Normal (.04 -.12 sec)
P wave	Normal and consistent in shape, always in front of the QRS may be buried in the preceding T wave
P-R interval	Constant interval between 0.12- 0.20 sec
P : QRS ratio	1 : 1

49 of 87

Sinus Tachycardia

50 of 87

Sinus Tachycardia

Causes:
Physiologic or psychological stress (e.g., acute blood loss, anemia, shock, hypo/hypervolemia, heart failure, pain, fever, exercise, anxiety)

Medications (e.g., Atropine, Catecholamines)
Stimulants (e.g., Caffeine, Nicotine)
illicit drugs (e.g., amphetamines, cocaine

Excessive sympathetic tone
Autonomic dysfunction (e.g., Postural Orthostatic Tachycardia Syndrome POTS)

51 of 87

Sinus Tachycardia

Medical Management:

Depends on cause & symptoms
Goal to reduce HR & decrease myocardial oxygen consumption
Treat underlying causes
Persistent tachycardia with hemodynamic instability- synchronized cardioversion
Vagal maneuver and Adenosine administration
Beta blockers and

Calcium channel blockers

52 of 87

Sinus Arrhythmia

SA node creates an impulse at an irregular rhythm
Rate increase with inspiration and decreases with expiration.
Causes:

Heart disease and rarely valvular disease
Medical Management:
Not typically treated because it does not cause any significant hemodynamic effect.

53 of 87

Ventricular and Atrial rate	60 to 100 b/min
Ventricular and Atrial rhythm	Irregular
QRS shape & duration	Normal (.04 -.12 sec)
P wave	Normal and consistent in shape, always in front of the QRS
P-R interval	Constant interval between 0.12- 0.20 sec
P : QRS ratio	1 : 1

Sinus Arrhythmia

54 of 87

Sinus Arrhythmia

55 of 87

Atrial Dysrhythmias�

Atrial dysrhythmias originate from foci (somewhere else) within the atria and not the SA node.
Examples

Atrial Flutter
Atrial Fibrillation (AF)
Premature atrial complexes (PACs)

56 of 87

Atrial Flutter

Atrial flutter is related to conduction defect in the atrium, results in a rapid (250 to 400 b/min) and regular Atrial rate.
Because atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node.
Electrical impulses take an abnormal path through the Atria (circulating)

57 of 87

Atrial Flutter

Ventricular and Atrial rate	Atrial rate: 250 – 400 b/m Ventricular rate: 75 -150 b/m
Ventricular and Atrial rhythm	Atrial: Regular Ventricular usually Regular but may be irregular because of a change in the AV conduction.
QRS	Normal shape & duration
P wave	Saw-toothed shape or F waves
P-R interval	Difficult to be determined Because of the flutter waves' proximity to the QRS complex
P : QRS ratio	2:1 or 3 :1 or 4 :1

58 of 87

Atrial Flutter

59 of 87

Atrial Flutter

Mostly associated with cardiovascular disease

Valvular disease
HTN
CAD & Cardiomyopathy
Open Heart Surgery

Seen in other conditions (Hyperthyroidism, PH, COPD)
Atrial flutter can cause serious signs and symptoms, such as chest pain, shortness of breath, and low blood pressure.

60 of 87

Atrial Flutter

Medical Management:

Vagal maneuver
Adenosine IV by rapid administration, & immediately followed by a 20-mL saline flush & elevation of the arm with the IV line to promote rapid circulation of the medication.
Electrical Cardioversion: converting atrial flutter to sinus rhythm
Antithrombotic therapy

61 of 87

Atrial Fibrillation

Uncoordinated Atrial electrical activation that causes a rapid, disorganized, and uncoordinated twitching of Atrial musculature.
The most common sustained dysrhythmia.
Highly linked with stroke, dementia, and premature death.
Patients are at increased risk of heart failure, myocardial ischemia, & embolic events such as stroke

62 of 87

Atrial Fibrillation

Increase risk of stroke by five folds, thus requires Anticoagulation therapy (Warfarin) as prophylaxis if Atrial fibrillation is persistent.

63 of 87

Atrial Fibrillation

Ventricular and Atrial rate	Atrial: 300 – 600 b/m Ventricular: 120–200 b/m
Ventricular and Atrial rhythm	Highly irregular
QRS shape & duration	Usually normal
P wave	Not definite wave ; irregular waves that vary in amplitude & shape are seen & referred to as fibrillatory or f waves
P-R interval	Cannot be measured
P : QRS ratio	Many : 1

64 of 87

Atrial Fibrillation

Causes:

The exact cause is unknown.
Open Heart Surgery / Valvular heart disease (Mitral/Tricuspid)
Inflammatory of infiltrative disease (e.g., Pericarditis, Myocarditis)
Cardiomyopathies (e.g., dilated or restrictive)
Coronary Artery Disease & Heart Failure
Hypertension, DM and Congenital disorders
Can be found with obstructive sleep apnea, PH, PE, Alcohol abuse.

65 of 87

Atrial Fibrillation

Medical Management:

History & physical exam
12-lead ECG, Echocardiogram, & blood tests (thyroid, hepatic, & renal functions)
Chest x-ray, Exercise test, holter monitoring
Treatment depends on cause, pattern, and duration of the dysrhythmia.
Cardioversion with hemodynamic instability
Antithrombotic agents (e.g., Warfarin)
Other drugs (e.g., Amiodarone, Beta blockers)
Cardiac rhythm therapies, catheter ablation

Strategies for both rhythm control (i.e., conversion to sinus rhythm) and rate control are dependent on shared clinical decision making between the patient and primary provider. In some cases, atrial fibrillation spontaneously converts to sinus rhythm within 24 to 48 hours and without treatment.

Catheter ablation destroys specific cells that are the cause of a tachydysrhythmia.

Ablation involves a procedure similar to a cardiac catheterization (see Chapter 25); however, in this instance, a special catheter is advanced at or near the origin of the dysrhythmia, where high-frequency, low-energy sound waves are passed through the catheter, causing thermal injury, localized cell destruction, and scarring. The tissue damage is more specific to the dysrhythmic tissue, with less trauma to the surrounding cardiac tissue. Ablation may also be accomplished using a special catheter to apply extremely cold temperature to destroy selected cardiac cells, called cryoablation. The goal of each of these ablation procedures is to eliminate the dysrhythmia, by preventing the ectopic activity arising from the pulmonary veins from reaching the atria, thereby stopping fibrillation (Stavrakis et al., 2015).

66 of 87

Ventricular Dysrhythmias

Ventricular dysrhythmias originate from foci within the ventricles
Ventricular arrhythmias result from ventricular cell ischemia (as seen with acute MI), Electrolyte imbalances (hypokalemia , hypoxia) and Digitalis.
HR is not measurable, P wave is not visible, PR interval and the QRS interval are not measurable.

67 of 87

Ventricular Dysrhythmia:�Premature Ventricular Complex (PVC)

Impulse that start in the ventricle before the normal sinus impulse
Occur in healthy people (caffeine, nicotine, alcohol) less than 6 per minute
Caused by ischemia or infarction, heart failure, hypoxia, digitals toxicity, hypokalemia
Untreated may developed to ventricular tachycardia (VT)
Bizarre & abnormal ORS shape

68 of 87

69 of 87

Ventricular Tachycardia (VT)

VT is defined as three or more Premature Ventricular Complex (PVCs) in a row, occurring at a rate exceeding 100 beats/m.

Causes: similar to PVCs, with higher risk if associated with MI and low ejection fraction (EF).
Manifestations: VT is an emergency, unresponsive, pulseless, hemodynamic loss, etc.

70 of 87

Ventricular Tachycardia

Ventricular and Atrial rate	Atrial: depends on underlying rhythm Ventricular:100-200b/m
Ventricular and Atrial rhythm	Regular
QRS shape & duration	0.12 seconds or longer with bizarre and abnormal shape
P wave	Very difficult to detect
P-R interval	Very irregular
P : QRS ratio	Difficult to determine

71 of 87

Ventricular Tachycardia

Medical Management

Depends on the rhythm, assessment of patients, obtain ECG.
May need Antiarrhythmic medications (e.g., Amiodarone, Lidocaine)
Cardioversion for monophasic VT (consitenet QRS shape and rate)
Defibrillation for pulseless VT. If VT is witnessed with no defibrillator, precordial thumb may be used.
Long-term treatment- if ejection fraction is <35% consider Implantable Cardioverter Defibrillator (ICD). If it is >35%, managed by Amiodarone.

72 of 87

Ventricular Fibrillation (VF)

Is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles.
Most common dysrhythmia in patients with cardiac arrest.
No atrial activity is seen on ECG.

Causes: CAD, MI, untreated VT, cardiomyopathy, electrical shock.

73 of 87

Ventricular Fibrillation

Ventricular rate	Ventricular >300 bpm
Ventricular rhythm	Extremely irregular without a specific pattern
QRS shape & duration	Irregular, undulating waves without recognizable QRS complexes
P wave	Very difficult to detect
P-R interval	Very irregular
P : QRS ratio	Difficult to determine

74 of 87

Ventricular Fibrillation

Medical Management:

Characterized by absent pulse and respiration.
Cardiac arrest and death imminent if not treated
Immediate Defibrillation, or CPR if defibrillator is not available.
5 cycles of CPR after Defibrillation
Intubation
Epinephrine, Amiodarone, etc.
Monitor for complications

75 of 87

Ventricular Asystole - Flatline

Characterized by absent QRS complexes, P waves may be apparent for a short duration.
There is no heartbeat, no palpable pulse, & no respiration
Without immediate treatment, ventricular asystole is fatal.
Ventricular asystole is treated by high-quality CPR with minimal interruptions

76 of 87

Nursing Process: Care of the Patient with a Dysrhythmia—Assessment

Causes of dysrhythmia, contributing factors
Assess indicators of cardiac output and oxygenation
Health history: previous occurrences of decreased cardiac output, possible causes of the dysrhythmia
All medications (prescribed & over-the-counter OTC)
Psychosocial assessment: patient’s “perception” of dysrhythmia

77 of 87

Assessment

Physical assessment include:

Skin (pale and cool)
Signs of fluid retention (jugular veins distended, lung auscultation)
Signs of decreased CO (altered loss of consciousness)
Rate, rhythm of apical, peripheral pulses
Heart sounds
Blood pressure, pulse pressure

78 of 87

Nursing Diagnoses

Decreased cardiac output related to inadequate ventricular filling or altered heart rate
Anxiety related to fear of the unknown outcome of altered health state
Deficient knowledge about the dysrhythmia and its treatment

79 of 87

Collaborative Problems and Potential Complications

Cardiac arrest
Heart Failure (HF)
Thromboembolic event, especially with Atrial fibrillation (AF).

80 of 87

Nursing Interventions

Monitor and manage the Dysrhythmia
Reduce Anxiety
Promote home- and community-based care
Educate the patient about self-care
Continuing care

81 of 87

Nursing Intervention: Monitor and Manage the Dysrhythmia

Assess vital signs on an ongoing basis
Assess for lightheadedness, dizziness, fainting
If hospitalized:

Obtain 12-lead ECG
Continuous monitoring
Monitor rhythm strips periodically

Antiarrhythmic medications

“6-minute walk test” which is used to identify the patient’s ventricular rate in response to exercise

82 of 87

Nursing Intervention: Minimize Anxiety

Stay with patient
Maintain safety and security
Discuss emotional response to Dysrhythmia
Help patient develop a system to identify factors that contribute to episodes of the Dysrhythmia
Maximize the patient’s control

83 of 87

Nursing Intervention: Promote Home and Community-Based Cared

Educate the patient

Treatment options
Therapeutic medication levels
How to take pulse before medication administration
How to recognize symptoms of the Dysrhythmia
Measures to decrease recurrence
Plan of action in case of an emergency
CPR (Family)

84 of 87

Adjunctive Modalities and Management

Used when medications alone are ineffective against dysrhythmia
Pacemakers / for bradycardias
Cardioversion / for acute tachydysrhythmia
Defibrillation / for acute tachydysrhythmia
The device name called a defibrillator
The electrical voltage required to defibrillate the heart is usually greater than that required for cardioversion.
Nurse responsible for assessment of the patient’s understanding regarding the mechanical therapy

85 of 87

Adjunctive Modalities and Management

The amount of voltage used varies from 50 to 360 joules, depending on,the type & duration of the dysrhythmia, and hemodynamic status of patient

86 of 87

Cardioversion and Defibrillation

Treat tachydysrhythmias by delivering electrical current that depolarizes critical mass of myocardial cells.

When the cells repolarize, SA node usually able to recapture role as the heart pacemaker

The difference between cardioversion & defibrillation is the timing of the delivery of electrical current
In cardioversion, the delivery of electrical current is synchronized with patient’s electrical events; ECG
Electrical impulse discharges during ventricular depolarization (QRS complex)
In defibrillation, the delivery of current is immediate and unsynchronized. Used in emergency for VF, pulseless VT, & unconscious patients.

Electrical cardioversion involves the delivery of a “timed” electrical current to terminate a tachydysrhythmia. In cardioversion, the defibrillator is set to synchronize with the ECG on a cardiac monitor so that the electrical impulse discharges during ventricular depolarization (QRS complex).

If the cardioversion is elective and the dysrhythmia has lasted longer than 48 hours, anticoagulation for a few weeks before cardioversion may be indicated

Digoxin is usually withheld for 48 hours before cardioversion to ensure the resumption of sinus rhythm with normal conduction. The patient is instructed not to eat or drink for at least 4 hours before the procedure. Gel-covered paddles or conductor pads are positioned front and back (anteroposteriorly) for cardioversion. Before cardioversion, the patient receives moderate sedation IV as well as an analgesic medication or anesthesia. Respiration is then supported with supplemental oxygen delivered by a bag-valve mask device with suction equipment readily available. Although patients rarely require intubation, equipment is nearby in case it is needed. The amount of voltage used varies from 50 to 360 joules, depending on the defibrillator’s technology, the type and duration of the dysrhythmia, and the size and hemodynamic status of the patient (Link et al., 2015).

87 of 87

Safety Measures

Ensure good contact between skin, pads, and paddles

Use conductive medium, 20 to 25 pounds of pressure

Place paddles so they do not touch bedding or clothing and are not near medication patches or oxygen flow
If cardioverting, turn synchronizer on
If defibrillating, turn synchronizer off
Do not charge device until ready to shock
Call “clear” three times; follow checks required for clear

Ensure no one is in contact with patient, bed, or equipment