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MODULE 6
CARDIOVASCULAR
W.PAWLIUK MPH MSNED RN CEN
NORMAL STRUCTURE
• Heart
• Mediastinal space
• Covered by pericardium
• Composed of three layers
• Epicardium
• Myocardium
• Endocardium
2
NORMAL STRUCTURE (CONTINUED)
Figure 12-1. Location of the heart. A, Heart in mediastinum showing relationship to lungs
and other anterior thoracic structures. B, Anterior view of isolated heart and lungs.
Portions of the parietal pleura and pericardium have been removed. C, Detail of heart
resting on diaphragm with pericardial sac opened.
3
NORMAL STRUCTURE (CONTINUED)
Figure 12-1. cont’d. D, Wall of the heart. The cutout section of the heart wall shows the outer fibrous pericardium
and the parietal and visceral layers of the serous pericardium (with the pericardial space between them). Note
that a layer of fatty connective tissue is located between the visceral layer of the serous pericardium
(epicardium) and the myocardium. Note also that the endocardium covers beamlike projections of myocardial
muscle tissue, called trabeculae carneae. (From Patton KT, Thibodeau GA. Anatomy and Physiology. 8th ed. St.
Louis: Mosby; 2013.)
4
NORMAL STRUCTURE
(CONTINUED)
•
•
•
•
.
Right side is low pressure
Left side is high pressure
Flow of blood
Cardiac valves
5
Figure 12-2. Structures that direct blood flow through the heart. (From
McCance KL, Huether SE. Pathophysiology. The Biologic Basis for Disease in
Adults and Children. 6th ed. St. Louis: Mosby; 2010.)
6
Figure 12-3. A, The atrioventricular (AV) valves in the open position and the semilunar (SL)
valves in the closed position. B, The AV valves in the closed position and the SL valves in the
open position. (From Patton KT, Thibodeau GA. Anatomy and Physiology. 7th ed. St. Louis:
Mosby; 2010.)
7
AUTONOMIC CONTROL
• Sympathetic nervous system
• Norepinephrine
• Parasympathetic nervous system
• Acetylcholine
• Chemoreceptors
• Baroreceptors
8
.
Figure 12-4. A, Chemoreceptor and B, baroreceptor reflex control of blood pressure.
(From Seeley RR, Stephens TD, Tate P: Anatomy and Physiology. 3rd ed. St. Louis:
Mosby; 1995.)
9
CARDIAC FUNCTION
•
•
•
•
Coronary circulation
Conduction system
Hemodynamics
Heart sounds
• S1, S2, S3, and S4
• Heart murmur
• Turbulent blood flow through valves
10
CARDIAC FUNCTION (CONTINUED)
Figure 12-5. The coronary vessels. A, Arteries. B, Veins. (From McCance KL, Huether SE.
Pathophysiology. The Biologic Basis for Disease in Adults and Children. 6th ed. St. Louis:
Mosby; 2010.)
11
CARDIAC FUNCTION (CONTINUED)
Figure 12-6. Chest areas from which each valve sound is best heard. (Modified from
Hall JE, Guyton AC. Guyton and Hall Textbook of Medical Physiology. 12th ed.
Philadelphia: Saunders; 2011.)
12
INTRODUCTION
• Dysrhythmia interpretation is a fundamental skill of
critical care nurses
• Crucial for early nursing and medical intervention
Copyright © 2013, 2009,
2005, 2001, 1997, 1993 by
Saunders, an imprint of
13
PACEMAKER CELLS AND
AUTOMATICITY
• Electrical signals generated by pacemaker cells
• Cells can generate stimulus without outside
stimulation
• Automaticity
14
CARDIAC CYCLE
• Composed of two activities
• Electrical (caused by automaticity)
• Mechanical (muscular) known as a contraction
15
CARDIAC CYCLE
(CONTINUED)
• Two phases of electrical activity
• Depolarization = active
• Repolarization = resting
• Two mechanical responses
• Systole
• Diastole
16
CARDIAC CYCLE
(CONTINUED)
•
•
•
•
Depolarization = systole = contraction
Repolarization = diastole = resting or filling phase
Electrical activity precedes mechanical activity
Electrical + mechanical = cardiac contraction
17
MUSCULAR CONTRACTION
• Depolarization leads to contraction
• Repolarization leads to resting and filling of
ventricles from atria
• ECG is evidence of electrical activity, not
contraction
18
CARDIAC CONDUCTION PATHWAY
Figure 7-1. The electrical conduction system of the heart.
19
CARDIAC CONDUCTION PATHWAY
(CONTINUED)
• SA node
• Depolarization begins
• Atrial contraction or atrial kick
• Intraatrial and internodal pathways to AV node
20
CARDIAC CONDUCTION PATHWAY
(CONTINUED)
• AV node
• Delays impulse to ventricles; allows for filling
• Back-up pacemaker
• Bundle of His
• Left and right bundle branches; fascicles
• Purkinje fibers
21
CARDIAC PHYSIOLOGY REVIEW
Figure 7-2. The cardiac cycle. (Modified from Wesley K. Huszar’s Basic
Dysrhythmias and Acute Coronary Syndromes: Interpretation and Management.
4th ed. St. Louis: Mosby JEMS; 2010.)
22
CARDIAC MONITORING
• Continuous monitoring via three-lead or five-lead
systems
23
CARDIAC MONITORING
(CONTINUED)
•
•
•
•
Record and interpret 6-second strip every 4 hours
Monitor ST segment
Monitor dysrhythmias
Daily 12-lead ECG for cardiac patients
24
ECG GRAPH PAPER
• Graph paper
• Used to
standardize
tracings
• Vertical boxes
measure
voltage/amplit
ude
• Horizontal
boxes measure
time
Figure 7-14. ECG paper records time horizontally in seconds or
milliseconds. Each large box contains 25 smaller boxes with five on the
horizontal axis and five on the vertical axis. Each small horizontal box is
0.04 seconds while each large box is 0.20 seconds in duration. Vertically,
the graph depicts size or voltage in millivolts and in millimeters. 15 large
boxes equals 3 seconds and 30 large boxes equals 6 seconds used in
calculating heart rate. (From Wesley K. Huszar’s Basic Dysrhythmias and
Acute Coronary Syndromes: Interpretation and Management. 4th ed. St.
Louis: Mosby JEMS; 2010.)
25
NORMAL ECG TRACING
Figure 7-15. ECG waveforms.
26
P WAVE
• Atrial depolarization
• Normally indicates firing of the sinoatrial node
• Not to exceed three boxes high
.
27
QRS COMPLEX
• Ventricular depolarization
• Q wave first negative deflection after P wave
• R wave first positive deflection after P wave
• S wave negative waveform after R wave
• Not everyone has a traditional QRS
28
PR INTERVAL
•
•
•
•
•
Atrial depolarization/delay in AV node
Beginning of P wave to beginning of QRS complex
0.12 to 0.20 seconds
Shorter interval = impulse from AV junction
Longer interval = first-degree AV block
29
QRS INTERVAL
•
•
•
•
Ventricular depolarization
0.06 to 0.10 seconds
Various configurations
Wide: slowed conduction
• Bundle branch block (BBB)
• Ventricular rhythm
30
ST SEGMENT
• Look for depression or elevation
• ST elevation: myocardial injury
• ST depression: reciprocal changes, digoxin, and ischemia
31
T WAVE
• Ventricular repolarization
•
•
•
•
Follows a QRS complex
Bigger than a P wave
No greater than five small boxes high
Inversion indicates ischemia to myocardium
32
QT INTERVAL
• Beginning of QRS
complex to end of T
wave
• 0.32 to 0.50 seconds
• Varies with heart
rate
FIGURE 7-15. Abnormal QT interval prolongation in patient taking
quinidine. The QT interval (0.6 seconds) is markedly prolonged for the
heart rate (65/min) and the QT interval is greater than one half the R-R
interval. (From Goldberger, A. L. [2006]. Clinical electrocardiography: A
simplified approach [7th ed., p. 15]. St. Louis: Mosby.)
33
U WAVE
• Sometimes seen after T wave
• Unknown origin
• May be normal
• May indicate hypokalemia
.
34
INTERPRETATION OF RHYTHMS
Develop a systematic approach
• Atrial and ventricular rates
• Regularity of rhythm
• Measurement of PR, QRS, and QT/QTc intervals
• Shape of waveforms and their consistency
• Identification of underlying rhythm and
dysrhythmias
• Patient tolerance of rhythm
• Clinical implication of the rhythm
.
35
RHYTHMICITY
• Regularity or pattern of heart beats
• PP intervals (atrial)
• Is regular when distance between PP intervals is equal
• RR intervals (ventricles)
• Is regular when distance between RR intervals is equal
.
36
MEASURING
FIGURE 7-16. Establishing ventricular rhythmicity
with calipers.
FIGURE 7-17. Establishing ventricular rhythmicity
with paper and pencil.
37
CALCULATING HEART RATE
• Regular
• Small blocks into 1500
• Large blocks into 300
• Irregular = 6-second strip
• Calculate atrial (PP) and ventricular rates (RR)
Figure 7-19. Six-second method of rate calculation.
38
WAVEFORM CONFIGURATION AND
LOCATION
•
•
•
•
Check P, Q, R, S, and T waveforms
Each waveform has unique shape
Comparison of waveform on 6-second strip
Check for correct sequence of each waveform
39
INTERVAL
• Measure PR interval
• Measure QRS interval
• Measure QT interval
40
BASIC DYSRHYTHMIAS
• Grouped by anatomical areas
•
•
•
•
SA node
Atria
AV node
Ventricles
41
NORMAL SINUS RHYTHM
•
•
•
•
•
Regular rhythm
Rate 60 to 100 beats/min
Normal P wave in lead II
P wave before each QRS
Normal PR, QRS, and QT intervals
Figure 7-24. Normal sinus rhythm.
42
SINUS TACHYCARDIA
• Sinus rhythm with a rate of 100 to 150 beats/min
• Causes: stimulants, exercise, fever, and alterations in
fluid status
• Assess for symptoms of low cardiac output
Figure 7-25. Sinus tachycardia.
43
SINUS TACHYCARDIA
SINUS BRADYCARDIA
• Sinus rhythm with rate less than 60 beats/min
• Causes: vagal, drugs, ischemia, ICP, and athletes
(normal)
• Produces various hemodynamic responses
Figure 7-26. Sinus bradycardia.
45
ATRIAL DYSRHYTHMIAS
• Increased automaticity in the atrium
• Generally have P-wave changes
.
46
ATRIAL DYSRHYTHMIAS
(CONTINUED)
• Causes
•
•
•
•
•
• Stress
• Electrolyte
imbalances
• Hypoxia
• Atrial injury
47
Digitalis toxicity
Hypothermia
Hyperthyroidism
Alcohol
Pericarditis
ATRIAL FLUTTER
• Ectopic foci in atria, heart disease
• Classic “sawtooth” pattern in leads II, III, and aVF
• Atrial rate fast and regular (250 to 350 beats/min)
with AV block
• Degree of conduction varies; may be 1:3, 1:4, etc.
48
ATRIAL FLUTTER (CONTINUED)
Figure 7-33. Atrial flutter. A, Flutter waves show sawtooth pattern. B, Enlarged view
shows one large box between flutter waves.
49
ATRIAL FIBRILLATION
•
•
•
•
•
•
Erratic impulse formation in atria
No discernible P wave
Irregular ventricular rate
Aberrant (abnormal) ventricular conduction can occur
Results in loss of atrial kick
High risk for pulmonary or systemic emboli
Figure 7-34. Atrial fibrillation.
50
VENTRICULAR DYSRHYTHMIAS
• Impulses initiated from lower portion of the heart
• Depolarization occurs, leading to abnormally wide
QRS complex
• Ectopic and escape beats
.
51
VENTRICULAR DYSRHYTHMIAS
(CONTINUED)
• Common causes
•
•
•
•
.
Myocardial ischemia, injury, and infarction
Low potassium or magnesium
Hypoxia
Acid-base imbalances
52
VENTRICULAR TACHYCARDIA
•
•
•
•
.
Rapid, life-threatening dysrhythmia
Three or more PVCs in a row
Fast rate (>100 beats/min)
Initiated by ventricles
53
VENTRICULAR TACHYCARDIA
(CONTINUED)
• Wide QRS complex; greater than 0.10 seconds
• Usually regular
• May or may not have pulse
• Treat pulseless same as ventricular fibrillation
• Significant loss of cardiac output
• Hypotension
.
54
VENTRICULAR TACHYCARDIA
(CONTINUED)
Figure 7-43. Ventricular tachycardia.
55
VENTRICULAR FIBRILLATION
•
•
•
•
•
Chaotic pattern
No discernible P, Q, R, S, or T waves
Coarse versus fine
No cardiac output; life-threatening
Emergent defibrillation
56
VENTRICULAR FIBRILLATION
(CONTINUED)
Figure 7-45. Ventricular fibrillation. A, Course. B,
Fine.
.
57
VENTRICULAR STANDSTILL
• Asystole
• No P, Q, R, S, or T waveforms
• Assess in two leads
• Why?
• No cardiac output
• Death
.
58
VENTRICULAR STANDSTILL
(CONTINUED)
Figure 7-48. A, Asystole. B, Ventricular standstill
59
ELECTRICAL PACEMAKERS
• Deliver an electrical current to stimulate
depolarization
• Temporary versus permanent
.
60
ELECTRICAL PACEMAKERS
(CONTINUED)
• Method of pacing
• Transthoracic: emergency
• Transvenous
• Epicardial
• Can pace:
• Atrium
• Ventricle
• Both chambers
61
ELECTRICAL PACEMAKERS
TRANSVENOUS
Figure 07-54. Single-chamber temporary pulse generator. (Courtesy Medtronic USA, Inc.
Minneapolis, Minnesota).
c.
62
ELECTRICAL PACEMAKERS
PERMANENT
Figure 7-57. Permanent dual chamber (A-V) pacemaker. (From Wesley K.
Huszar’s Basic Dysrhythmias and Acute Coronary Syndromes: Interpretation
and Management. 4th ed. St. Louis: Mosby JEMS; 2010.)
63
ELECTRICAL PACEMAKERS
ATRIAL PACING
Figure 7-58. Atrial paced rhythm.
64
ELECTRICAL PACEMAKERS
VENTRICULAR PACING
Figure 7-59. Ventricular paced rhythm.
65
ELECTRICAL PACEMAKERS
BIVENTRICULAR (DUAL-CHAMBER)
PACING
Figure 7-60. Dual-chamber (AV) paced rhythm. A, Atrial pacer spike; AV, AV pager spike
interval; V, Ventricular paced spike.
.
66
ELECTRICAL PACEMAKERS
(CONTINUED)
• Terms
•
•
•
•
•
•
.
Rate
Mode
Electrical output: milliamperes (mA)
Sensitivity
Sense-pace indicator
AV interval
67
RAPID RESPONSE TEAMS
•
•
•
•
“Failure to rescue” is important concept to address
RRT established to address concerns
Call BEFORE the cardiac/respiratory arrest
Recommended by The Joint Commission and
Institute for Healthcare Improvement to implement
systems to request assistance for worsening
conditions
68
RRTS (CONTINUED)
• Call any time a staff member is concerned about
changes in a patient’s condition including:
•
•
•
•
•
Heart rate, systolic blood pressure
Respiratory rate, oxygen saturation
Mental status
Urinary output
Laboratory values
• Some institutions empower family members to
activate the RRT
69
RRT EFFECTIVENESS
• RRT reduces:
• Cardiac arrests
• Critical care unit length of stay
• Incidence of acute illness, such as respiratory failure, stroke,
severe sepsis, and acute kidney injury
• Recent review of literature and meta-analysis of 1.3
million patients
• RRT was not associated with lower hospital mortality rates in
hospitalized adults
.
70
CODES
• Code, code blue, code 99, Dr. Heart
• Cardiac and/or respiratory arrest
• Lifesaving resuscitation and intervention needed
• BLS/AED
• ACLS
71
CODE TEAM
•
•
•
•
•
.
Notification system
Members vary within setting
Better patient management
Care according to ACLS protocols
Other healthcare workers manage other patients
72
TEAM MEMBERS
• Leader usually MD skilled in ACLS
• Nurses (usually ICU or ER)
• Primary nurse knows patient
• Second nurse gives medications and gets equipment from
crash cart
• Another nurse records events
• Nursing supervisor provides traffic control and secures ICU
bed (if needed)
73
TEAM MEMBERS (CONTINUED)
• Anesthesiologist/anesthetist intubation
• Respiratory therapist manages airway, sometimes
intubates
• Pharmacist prepares medications in some settings
• Chaplain
• ECG technician
• Other personnel to run errands
.
74
ACLS
• Primary survey
• ABCD (early defibrillation)
• Use of automatic external defibrillator (AED)
• Secondary survey
• Advanced skills
• Differential diagnosis
75
ACLS: CIRCULATION
• Large-bore IVs
• Biggest veins
• May insert central line or intraosseous cannula if IV
access is difficult
76
ACLS (CONTINUED)
• Administer medications via ETT if needed
• Lidocaine
• Epinephrine
• Vasopressin
• Defibrillation
• Differential diagnosis
77
LOGICAL FLOW OF EVENTS
• BLS
• ACLS/AED
• Ongoing
assessment
•
•
•
•
•
• Crowd control
• Notification of
family and
communication
• Family presence in
code
• If successful code,
transfer to ICU
Pulse oximetry
ETCO2
Pulse checks
ABGs
Lab work
78
ACLS SUMMARY
•
•
•
•
•
.
Treat patient, not monitor
CPR throughout
Early defibrillation essential
Use ETT as needed for medication administration
Provide treatment according to algorithms
79
OXYGEN
• Treat hypoxemia
• Improve tissue oxygenation
• Delivered via mouth to mask or bag-valve device
(BVD) to mask or ETT
• During a cardiopulmonary arrest 100% oxygen (15
L/min via BVD)
.
80
EPINEPHRINE
• Potent vasoconstrictor
• Alpha- and beta-adrenergic effects
• Ventricular fibrillation (VF), pulseless ventricular
tachycardia (VT), asystole, and PEA
• 1 mg IV push every 3 to 5 minutes
• Can be given via ETT
• Infusion if needed
81
VASOPRESSIN
•
•
•
•
Nonadrenergic vasopressor
Intense vasoconstriction at high doses
May be as effective as epinephrine
One-time dose of 40 units IV for VF/pulseless VT
82
ATROPINE
• Decreases vagal tone
• Symptomatic bradycardia
• 0.5 mg to 1.0 mg every 3 to 5 min IV push
• Maximum of 0.03 to 0.04 mg/kg
83
ATROPINE
(CONTINUED)
• Can be given via ETT; 2 to 3 mg in 10 mL normal
saline
• External pacemaker on standby
• Atropine is no longer given in PEA or asystole
84
AMIODARONE (CORDARONE)
• Reduces membrane excitability
• Prolongs the action potential and retards the
refractory period; thus facilitates the termination of
VT and VF
• Alpha-adrenergic and beta-adrenergic blocking
properties
• Does not have the same prodysrhythmic properties
of other antidysrhythmics
85
ADENOSINE
• Slows conduction through AV node
• Primary use for paroxysmal supraventricular
tachycardia
• Rapid IV push through port nearest insertion site of
IV
• Expect short pause in rhythm after administration
• Half-life 10 seconds; duration 1 to 2 minutes
86
ADENOSINE
(CONTINUED)
FIGURE 10-15. Atrioventricular block after intravenous administration of adenosine. (From
Paul, S., & Hebra, J. D. (1998). The nurse’s guide to cardiac rhythm interpretation: Implications
for patient care. Philadelphia: W. B. Saunders.)
87
MAGNESIUM
•
•
•
•
.
Refractory VF
Torsades de pointes (type of VT)
Known deficiency
IV bolus followed by infusion titrated by magnesium
levels
88
DIAGNOSTIC STUDIES
• 12-lead electrocardiogram (ECG)
• Holter monitor
• Exercise tolerance test (stress test)
• Exercise to increase demand on heart
• Stressed via drugs if patient cannot tolerate exercise (e.g.,
adenosine)
• Monitoring vital signs, ECG
• Chest x-ray
89
DIAGNOSTIC STUDIES
(CONTINUED)
• Echocardiography
• Ultrasound to visualize cardiac structures
• Transesophageal echocardiography
• Diagnostic heart scans
• Technetium-99m stannous pyrophosphate
• Thallium-201
• Multigated blood pool study
90
DIAGNOSTIC STUDIES
(CONTINUED)
• Single photon emission computed tomography
• Magnetic resonance imaging
• Electrophysiology study
91
CARDIAC CATHETERIZATION AND
ARTERIOGRAPHY
• Catheter (right or left)
• Heart pressures (similar to PA catheter)
• Cardiac output
• Arteriography
• Visualize blood vessels
92
POST-CATHETERIZATION CARE
• Bed rest; head of bed no higher than 30 degrees
• Monitor bleeding; newer collagen agents for
hemostasis may be used
• Monitor pulses
• Antiplatelet drugs after the procedure (usually after
interventions such as PCI)
• May be discharged in 6 to 8 hours; depends on
diagnosis and procedures done in catheterization
laboratory
93
POST-CATHETERIZATION CARE
(CONTINUED)
Figure 12-9. FemoStop in correct position. (Courtesy RADI
Medical Systems, Inc. Sweden.)
94
LABORATORY TESTS
• CBC
• Hemoglobin
• Hematocrit
•
•
•
•
Potassium
Magnesium
Calcium
Sodium
95
CARDIAC ENZYMES
• CK (total)
• 2 to 6 hours; peak 18 to 36 hours
• CK-MB (cardiac specific)
• 4 to 8 hours; peak 18 to 24 hours
• Troponin I and T
• As early as 1 hour after injury
• Myoglobin
• 30 to 60 minutes after injury
.
96
CORONARY ARTERY DISEASE
• Includes stable angina, acute coronary
syndromes
• Ischemia—insufficient oxygen supply to meet
requirements of myocardium
• Infarction—necrosis or cell death that occurs
when severe ischemia is prolonged and
decreased perfusion causes irreversible damage
to tissue
NONMODIFIABLE RISK FACTORS
•
•
•
•
Age
Gender
Family history
Ethnic background
MODIFIABLE RISK FACTORS
•
•
•
•
•
•
•
•
Elevated serum cholesterol
Cigarette smoking
Hypertension
Impaired glucose tolerance/DM
Obesity
Excessive alcohol
Limited physical activity
Stress
TYPES OF ANGINA
• Stable (chronic, exertional) = effort, classic
• T-wave inversion on ECG
• Treatment: rest and nitroglycerin
• Unstable (crescendo) = more often and severe, less
relief
• May see ST elevation on ECG
• Treatment: rest and nitroglycerin; drugs affecting platelets;
revascularization
• Variant = Prinzmetal’s (vasospasms)
• ST elevation during pain episodes
• Treatment: calcium channel blockers
100
CHRONIC STABLE ANGINA (CSA)
PECTORIS
• “Strangling of the chest”
• Temporary imbalance between coronary
artery’s ability to supply oxygen and cardiac
muscle’s demand for oxygen
CHRONIC STABLE ANGINA (CSA)
PECTORIS (CONT’D)
• Ischemia limited in duration and does not cause
permanent damage to myocardial tissue
UNSTABLE ANGINA PECTORIS
•
•
•
•
New-onset angina
Variant (Prinzmetal’s) angina
Pre-infarction angina
Patients present with ST changes on 12-lead
ECG, but will not have changes in troponin or CK
levels
NURSING MANAGEMENT: ANGINA
• Pain relief
• Maintain cardiac output
• Self-care; risk-factor modification
104
ACUTE CORONARY SYNDROME (ACS)
• Patients who present with either unstable angina
or acute myocardial infarction
• Believed that atherosclerotic plaque in coronary
artery ruptures, resulting in platelet aggregation,
thrombus formation or vasoconstriction
ACUTE MYOCARDIAL INFARCTION
(AMI)
• Ischemia with myocardial cell death
• Imbalance of oxygen supply and demand
• Causes
• Atherosclerosis
• Emboli
106
ASSESSMENT OF AMI
• Midsternal chest pain
• Severe, crushing, and squeezing pressure
• May radiate
• Unrelieved with nitrates
•
•
•
•
•
Pale and diaphoretic
Dyspnea and tachypnea
Syncope
Nausea and vomiting
Dysrhythmias
107
DIAGNOSIS OF AMI
• Signs and symptoms
• Often atypical symptoms in women
• 12-lead:
• ST elevation followed by Q wave (Q-wave myocardial
infarction)
• ST depression (non–Q-wave myocardial infarction)
• Elevated cardiac enzymes
• CPK-MB
• Elevated serum troponin I/T, myoglobin
.
108
DIAGNOSIS OF AMI (CONTINUED)
FIGURE 12-9. Electrocardiographic alterations associated
with the three zones of myocardial infarction. (From
McCance, K. L., & Huether, S. E. [Eds.]. [2006].
Pathophysiology: The biologic basis for disease in adults and
children [5th ed., p. 1114]. St. Louis: Mosby.)
109
NURSING GOALS: AMI
•
•
•
•
•
•
Maintain cardiac output
Treat pain
Assess for complications
Increase activity tolerance
Relieve anxiety
Ongoing and discharge teaching
111
COMPLICATIONS OF AMI
•
•
•
•
•
Dysrhythmias
Sudden death
Congestive heart failure; cardiogenic shock
Ventricular aneurysm or rupture
Papillary muscle dysfunction
112
MEDICAL MANAGEMENT: AMI
• Pain relief: morphine, nitroglycerin
• Oxygen
• Drugs affecting platelets
• ASA
• Glycoprotein IIb/IIIa inhibitors
•
•
•
•
Beta-blockers
Nitrates
ACE inhibitors
Antidysrhythmics
113
AORTA
• Largest artery
• Responsible for supplying oxygenated blood to
essentially all vital organs
DISORDERS OF THE AORTA
• Most common vascular problems of aorta
• Aneurysms
• Aortoiliac occlusive disease
• Aortic dissection
AORTIC ANEURYSMS
DEFINITION
•
•
•
•
Outpouchings or dilations of the arterial wall
Common problems involving aorta
Occur in men more often than in women
Incidence ↑ with age
AORTIC ANEURYSMS
ETIOLOGY AND PATHOPHYSIOLOGY
• May involve the aortic arch, thoracic aorta, and/or
abdominal aorta
• Most are found in abdominal aorta below renal arteries
• ¾ of true aortic aneurysms occur in abdominal aorta
• ¼ found in thoracic
AORTIC ANEURYSMS
ETIOLOGY AND PATHOPHYSIOLOGY
(CONT’D)
• May have aneurysm in more than one location
• Growth rate unpredictable
• Larger the aneurysm greater risk of rupture
AORTIC ANEURYSMS
ETIOLOGY AND PATHOPHYSIOLOGY
(CONT’D)
• Causes
• Degenerative
• Congenital
• Familial tendency related to abnormalities
• Ehlers-Danlos syndrome and Marfan syndrome
• Mechanical
• Penetrating or blunt trauma
AORTIC ANEURYSMS
ETIOLOGY AND PATHOPHYSIOLOGY
(CONT’D)
• Causes (cont’d)
• Inflammatory
• Takayasu’s or giant cell arthritis
• Infectious
• Syphilis, Salmonella, HIV
• Most common cause is atherosclerosis
AORTIC ANEURYSMS
ETIOLOGY AND PATHOPHYSIOLOGY
(CONT’D)
• Atherosclerotic plaques deposit beneath the intima
• Plaque formation is thought to cause degenerative
changes in the media
• Leading to loss of elasticity, weakening, and aortic dilation
• Male gender and smoking stronger risk factors than
hypertension and diabetes
AORTIC ANEURYSMS
CLASSIFICATION
• 2 Basic classifications
• True
• False
AORTIC ANEURYSMS
CLASSIFICATION (CONT’D)
• True aneurysm
• Wall of artery forms the aneurysm
• At least one vessel layer still intact
AORTIC ANEURYSMS
CLASSIFICATION (CONT’D)
• True aneurysm
• Further subdivided
• Fusiform
• Circumferential, relatively uniform in shape
• Saccular
• Pouchlike with narrow neck connecting bulge to one side of arterial
wall
AORTIC ANEURYSMS
CLASSIFICATION (CONT’D)
• False aneurysm
• Also called pseudoaneurysm
• Not an aneurysm
• Disruption of all layers of arterial wall
• Results in bleeding contained by surrounding structures
TYPES OF ANEURYSMS
AORTIC ANEURYSMS
CLASSIFICATION
• May result from
• Trauma
• Infection
• After peripheral artery bypass graft surgery at site of
anastomosis
• Arterial leakage after cannulae removal
AORTIC ANEURYSM
CLINICAL MANIFESTATIONS
• Thoracic aorta aneurysms
• Often asymptomatic
• Most common manifestation
• Deep, diffuse chest pain
• Pain may extend to the interscapular area
AORTIC ANEURYSM
CLINICAL MANIFESTATIONS (CONT’D)
• Ascending aorta/aortic arch
• Produce angina
• Hoarseness
• If presses on superior vena cava
• Decreased venous return can cause
• Distended neck veins
• Edema of head and arms
AORTIC ANEURYSM
CLINICAL MANIFESTATIONS (CONT’D)
• Abdominal aortic aneurysms (AAA)
• Often asymptomatic
• Frequently detected
• On physical exam
• Pulsatile mass in periumbilical area
• Bruit may be auscultated
• When patient examined for unrelated problem (i.e., CT scan,
abdominal x-ray)
AORTIC ANEURYSM
CLINICAL MANIFESTATIONS (CONT’D)
• AAA (cont’d)
• May mimic pain associated with abdominal or back
disorders
• May spontaneously embolize plaque
• Causing “blue toe syndrome”
• Patchy mottling of feet/toes with presence of palpable pedal pulses
AORTIC ANEURYSM
COMPLICATIONS
• Rupture—serious complication related to untreated
aneurysm
• Posterior rupture
• Bleeding may be tamponaded by surrounding structures, thus
preventing exsanguination and death
• Severe pain
• May/may not have back/flank ecchymosis
AORTIC ANEURYSM
COMPLICATIONS (CONT’D)
• Rupture (cont’d)
• Anterior rupture
• Massive hemorrhage
• Most do not survive long enough to get to the hospital
AORTIC ANEURYSM
DIAGNOSTIC STUDIES
• X-rays
• Chest—Demonstrate mediastinal silhouette and any
abnormal widening of thoracic aorta
• Abdomen—May show calcification within wall of AAA
• ECG to rule out MI
AORTIC ANEURYSM
DIAGNOSTIC STUDIES (CONT’D)
• Echocardiography
• Assists in diagnosis of aortic valve insufficiency
• Related to ascending aortic dilation
• Ultrasonography
• Useful in screening for aneurysms
• Monitor aneurysm size
AORTIC ANEURYSM
DIAGNOSTIC STUDIES (CONT’D)
• CT scan
• Most accurate test to determine
• Anterior to posterior length
• Cross-sectional diameter
• Presence of thrombus in aneurysm
• MRI
• Diagnose and assess the location and severity
AORTIC ANEURYSM
DIAGNOSTIC STUDIES (CONT’D)
• Angiography
• Anatomic mapping of aortic system using contrast
• Not reliable method of determining diameter or length
• Can provide accurate info about involvement of intestinal,
renal, or distal vessels
ANGIOGRAPHY OF ANEURYSM
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• 5.5 cm is threshold for repair
• Intervention at <5.5 cm in women with AAA
• Surgical intervention may occur earlier in
•
•
•
•
Younger, low-risk patients
Rapidly expanding aneurysm
Symptomatic patient
High rupture risk
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Surgical Therapy
• If ruptured, emergent surgical intervention required
• 33%-94% mortality with ruptured AAAs
• Preop
• Hydration
• Electrolyte, coagulation, hematocrit stabilized
SURGICAL REPAIR OF ANEURYSM
AORTIC ANEURYSM
COLLABORATIVE CARE
• Autotransfusion reduces need for blood transfusion
during surgery
• AAA resections
• Require cross-clamping of aorta proximal and distal to
aneurysm
• Can be completed in 30-45 minutes
• Clamps are removed and blood flow to lower extremities
restored
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• AAA resections (cont’d)
• If extends above renal arteries or if cross clamp must be
applied above renal arteries
• Adequate renal perfusion after clamp removal should be
ascertained before closure of incision
• Risk of postop renal complications ↑ significantly when repair is
above renal arteries
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure
• Alternative to conventional surgical repair
• Involves placement of sutureless aortic graft into abdominal
aorta inside aneurysm
• Done through femoral artery cutdown
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Graft
• Constructed from Dacron cylinder
• Surface supported with rings of flexible wire
• Delivered through sheath to predetermined point
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Graft
• Deployed against vessel wall by balloon inflation
• Anchored to vessel by series of small hooks
ENDOVASCULAR STENT
AORTIC ANEURYSM
COLLABORATIVE CARE
• Endovascular graft procedure (cont’d)
• Blood flows through graft, preventing expansion of
aneurysm
• Aneurysm wall will begin to shrink over time
• Must meet strict eligibility criteria to be candidate
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Benefits
•
•
•
•
•
•
•
•
↓ anesthesia and operative time
Smaller operative blood loss
↓ morbidity and mortality
More rapid resumption of physical activity
Shortened hospital stay
Quicker recovery
Higher patient satisfaction
Reduction in overall costs
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Potential complications
•
•
•
•
•
•
Aneurysm growth
Aneurysm rupture
Perigraft leaks
Aortic dissection
Bleeding
Graft dislocation and embolization
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Complications (cont’d)
• Graft thrombosis
• Incisional site hematoma
• Site infection
• Most common complication is perigraft leak
• Seeping of blood from new endograft into old aneurysm site
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• Graft dysfunction may require traditional surgical repair
• With endovascular repair
• Higher reintervention rate
• Need for long-term follow up
• Long-term complications not known
AORTIC ANEURYSM
COLLABORATIVE CARE (CONT’D)
• Endovascular graft procedure (cont’d)
• New approach is percutaneous femoral access
• Advantages
•
•
•
•
Shorter operative time
Shorter anesthesia time
Reduction in use of general anesthesia
Reduced groin complications within first 6 months
NURSING MANAGEMENT
ASSESSMENT
• Thorough history and physical exam
• Watch for signs of cardiac, pulmonary, cerebral,
lower extremity vascular problems
• Establish baseline data to compare postoperatively
NURSING MANAGEMENT
ASSESSMENT (CONT’D)
• Note quality and character of peripheral pulses and
neurologic status
• Mark/document pedal pulse sites and any skin lesions on
lower extremities before surgery
NURSING MANAGEMENT
ASSESSMENT (CONT’D)
• Monitor for indications of rupture
•
•
•
•
•
Diaphoresis
Paleness
Weakness
Tachycardia
Hypotension
NURSING MANAGEMENT
ASSESSMENT (CONT’D)
• Monitor for indications of rupture
• Abdominal, back, groin, or periumbilical pain
• Changes in level of consciousness
• Pulsating abdominal mass
NURSING MANAGEMENT
PLANNING
• Overall goals include
• Normal tissue perfusion
• Intact motor and sensory function
• No complications related to surgical repair
NURSING MANAGEMENT
NURSING IMPLEMENTATION
• Health Promotion
• Alert for opportunities to teach health promotion to patients
and their families
• Encourage patient to reduce cardiovascular risk factors
• These measures help ensure graft patency after surgery
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Patient/family teaching
• Providing support for patient/family
• Careful assessment of all body systems
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Preop teaching
• Brief explanation of disease process
• Planned surgical procedure
• Preop routines
• Bowel prep
• NPO
• Shower
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Preop teaching (cont’d)
• Expectations after surgery
• Recovery room, tubes, drains
• ICU
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop
• ICU monitoring
•
•
•
•
Arterial line
Central venous pressure (CVP) or pulmonary artery (PA) catheter
Mechanical ventilation
Urinary catheter
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• ICU monitoring
•
•
•
•
Nasogastric tube
ECG
Pulse oximetry
Pain medication
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Maintain graft patency
•
•
•
•
Normal blood pressure
CVP or PA pressure monitoring
Urinary output monitoring
Avoid severe hypertension
• Drug therapy may be indicated
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Cardiovascular status
•
•
•
•
•
Continuous ECG monitoring
Electrolyte monitoring
Arterial blood gas monitoring
Oxygen administration
Antidysrhythmic/pain medications
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Infection
•
•
•
•
•
Antibiotic administration
Assessment of body temperature
Monitoring of WBC
Adequate nutrition
Observe surgical incision for signs of infection
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Gastrointestinal status
•
•
•
•
Nasogastric tube
Abdominal assessment
Passing of flatus is key sign of returning bowel function
Watch for manifestations of bowel ischemia
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Neurologic status
•
•
•
•
•
•
Level of consciousness
Pupil size and response to light
Facial symmetry
Speech
Ability to move upper extremities
Quality of hand grasps
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Peripheral perfusion status
• Pulse assessment
• Mark pulse locations with felt-tipped pen
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Peripheral perfusion status
• Extremity assessment
• Temperature, color, capillary refill time, sensation and movement
of extremities
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Acute Intervention
• Postop (cont’d)
• Renal perfusion status
•
•
•
•
•
Urinary output
Fluid intake
Daily weight
CVP/PA pressure
Blood urea nitrogen/creatinine
NURSING MANAGEMENT
NURSING IMPLEMENTATION (CONT’D)
• Ambulatory and Home Care
•
•
•
•
Encourage patient to express concerns
Patient instructed to gradually increase activities
No heavy lifting
Educate on signs and symptoms of complications
• Infection
• Neurovascular changes
NURSING MANAGEMENT
EVALUATION
• Expected Outcomes
•
•
•
•
Patent arterial graft with adequate distal perfusion
Adequate urine output
Normal body temperature
No signs of infection
FAMILY NEEDS
•
•
•
•
•
Receiving assurance
Remaining near the patient
Receiving information
Being comfortable
Having support available
175
CALGARY FAMILY ASSESSMENT
• Structural
• Who comprises family
• Decision makers/spokesperson
• Race, ethnicity, cultural factors
• Developmental
• Stages, tasks, and attachments
• Functional
• How family members interact with each other
176
FAMILY INTERVENTIONS
•
•
•
•
Facilitate visitation
Provide information
Encourage family involvement in patient care
Consider family presence during procedures
177
UNIQUE APPROACH
Figure 2-2. EPICS family bundle. (From Knapp S. Effects of an Evidence-based
Intervention on Stress and Coping of Family Members of Critically Ill Trauma Patients.
Unpublished Dissertation, University of Central Florida, Orlando, Florida; 2009.)
178
COMMUNITY-BASED CARE
• Home care management
• Teaching for self-management
• Health care resources
VALUE MNEMONIC
•
•
•
•
•
Value what the family tells you
Acknowledge family emotions
Listen to family members
Understand the patient as a person
Elicit questions from family members
180
INTERESTING YOUTUBE VIDEOS
(CUT-N-PASTE)
• http://www.youtube.com/watch?v=WuKTkPJE-SE
• http://www.youtube.com/watch?v=ecTM2O940mg
• http://www.youtube.com/watch?v=9U_eycK0pKY
• http://www.youtube.com/watch?v=5Oq4h6ShLbo
• http://www.youtube.com/watch?v=4tEH0cYXwns
• http://www.youtube.com/watch?v=iQULS2miHfc
• http://www.youtube.com/watch?v=BL92vtuj9nc
INTERESTING YOUTUBE VIDEOS
(CUT-N-PASTE)
• http://www.youtube.com/watch?v=k42Ne6jiEIQ
• http://www.youtube.com/watch?v=_sZx-Z4yUgc
• http://www.youtube.com/watch?v=p1FoyrHD2-k
• http://www.youtube.com/watch?v=nA-ZC_wJxEA
• http://www.youtube.com/watch?v=RXuPBaKzmfM