Transcript Nursing Diagnosis - Faculty Sites

Cardiovascular System
Nursing 1120
By: Diana Blum RN MSN
Metropolitan Community College
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Coronary Arteries
• Two major coronary arteries
– arise from the aorta beyond the
aortic valve.
– Blood flows to the coronary arteries
during diastole
• Left main, LAD, Circumflex feeds most
of Left side of the heart
• Right feeds SA node, AV node, RA, RL
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Collateral circulation is a network of tiny
blood vessels, and, under normal
conditions, not open. When the coronary
arteries narrow to the point that blood flow
to the heart muscle is limited (coronary
artery disease), collateral vessels may
enlarge and become active. This allows
blood to flow around the blocked artery to
another artery nearby or to the same
artery past the blockage, protecting the
heart tissue from injury.
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Conduction Continued
7
Cardiac Cycle
• Contraction and relaxation of the heart:
• Diastole:
• Systole:
8
• Video Mysterious Heart Volume
2 chapter 3
9
Cardiac Output
• the volume of blood ejected by the
heart each minute and is determined
by stroke volume and the heart rate.
• Normal stroke volume is 60-100 ml
• Normal cardiac output is 4 to 8 L / min
• (CO = HR X SV)
10
Factors affecting Stroke Volume
• Preload: the amount of blood
remaining in the ventricles at the end
of diastole or the pressure generated
at the end of diastole
• Contractility: is the ability of the
cardiac muscle fibers to shorten and
produce a muscle contraction.
(Inotropic, + or -)
• Afterload: amount of pressure the
Ventricle must overcome to eject
blood volume out
11
Heart Rate
• SA node : pacemaker of heart 60-100
bpm
• AV node : 40 -60 bpm
• Heart is innervated by sympathetic
and parasympathetic nervous system
– Sympathetic: speeds HR, and increases
force of contraction
– Parasympathetic: slows HR and force
12
Heart Tones
• Murmur: Produced by turbulent
sounds across valves
– Rub: inflamed pericardium-best
heard along left sternal border
– S3 murmur: sounds like “Kentucky”
– S4 murmur: sounds like “Mississippi”
http://www.blaufuss.org/
http://www.med.ucla.edu/wilkes/
Rubintro.htm
13
Health History
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Present Illness
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Past Medical History
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Family History:
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Review of systems
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•
•
weight gain
fatigue
dyspnea
cough
orthopnea
palpitations
chest pain
fainting
concentrated urine
edema
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Functional assessment
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•
•
•
•
effects of illness on ADLs and rest patterns
smoker
diet
stress
coping
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Physical Assessment
• General:
• VS: orthostatic bp in both arms, apical rate
and rhythm, respiratory rate and effort
• peripheral pulses:
• Skin: color hair distribution, cap refill, temp
• Thorax: heart sounds, lung sounds, sputum
• Extremities: pulses, color, temp, edema
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Age Related Changes
• Heart less able to adapt to
changing needs related to
activity
• Valves thicken and stiffen
• # of pacemaker cells decrease
• Nerve fibers decrease
• Frequent dysrhythmias
21
Diagnostic Tests
• EKG: rate, rhythm, ischemia (T-inverted),
injury (ST segment elevation), arrhythmias,
strain, infarction (q wave)
• Echocardiogram: (TEE) sound wave test
detects size of chambers, valve integrity,
flow, wall motion, Cardiac Output
22
Diagnostic Tests Continued
Biomarkers:
Troponin will show elevation 3-4 hr after
injury
<0.10 is negative
0.10-0.60 is intermediate and may
indicate injury
>0.60 is positive evidence of MI
Myoglobin increases 1-4 hours after MI
CPK-MB will show increase 4 hrs after MI
BNP can be elevated 48 hrs after MI
which indicates heart failure
23
Diagnostic Tests Continued
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•
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•
•
CBC: anemia
CMP: screening K+, etc
PT, INR
PTT
Lipid profile: see next 2 slides
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Total cholesterol
Below 200 mg/dL
Desirable
200-239 mg/dL
Borderline high
240 mg/dL and above
High
LDL cholesterol
Below 70 mg/dL
Optimal for people at very high risk of
heart disease
Below 100 mg/dL
Optimal for people at risk of heart disease
100-129 mg/dL
Near optimal
130-159 mg/dL
Borderline high
160-189 mg/dL
High
190 mg/dL and above Very high
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HDL cholesterol
Below 40 mg/dL
Poor
40-59 mg/dL
Better
60 mg/dL and above Best
Triglycerides
Below 150
mg/dL
Desirable
150-199 mg/dL
Borderline high
200-499 mg/dL
High
500 or above
Very high
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Diagnostic Tests Continued
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•
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•
•
ABG: assess acid/base levels
Pulse Oximetry: generally >92%
Holter monitoring: 24+ hr of EKG + events
Stress test: treadmill or pharmacological
Cardiac Catheterization: invasive, NPO 6-8h,
consent. Visualizes chambers, valves,
arteries, pressures, CO
• Heart-CT scan: assesses CAD, MRI
• Nuclear scans: assess heart muscle viability
• EPS: NPO, consent, IV, assess electrical
activity
27
• http://preop.medselfed.com/as
p/center.asp?centerId=heart&p
artnerId=preop&id=&cachedate
=&emailId=&affId=&campId=&hi
deNav=
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CAD
Video-mysterious
heart volume 3
chapter 2
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Etiology of CAD
• CAD occurs when the intimal lining of the
coronaries begin to plaque resulting in
jagged edges and narrowed passageway
for blood flow
• Atherosclerosis results in impaired blood flow
to the heart muscle
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Risk Factors for CAD
 Non-controllable Controllable-
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s/s of CAD
• Angina which results from a lack
of 0xygen to the heart muscle
– 4Es=
• Weakness, diaphoresis, SOB
• N/V
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MI: Myocardial Infarction
• Occlusion of a coronary artery resulting in necrosis
of the heart muscle.
• Risk factors: same as for CAD
• Pathophysiology: AMI-over 4-6 hrs ischemia injury
and infarction develop. Ischemia=lack of 02 to
heart muscle, if not relieved=injury. After 20 min of
ischemia=infarction
• Main S/S: chest pain and accompanying S/S
33
• Within 24 hours after infarction,
healing begins, collateral circulation
begins.
• 10-14 days after MI=extension of MI
may occur due to myocardial tissue
vulnerability to stress
• Complete scar formation and healing
takes about 6 weeks
• Video- mysterious heart volume 1
chapter 2
34
Data Collection
 Same as for CAD but will assess symptom of
chest pain with accompanying s/s
 May have EKG changes with or with-out ST-T
wave changes or Q wave changes
 Cardiac Bio-markers (Troponin, Myoglobin,
CPK, CKMB)
 May proceed with Echocardiogram to
assess if wall motion sluggish
 May go to cath lab
35
Angina or MI
• Angina without MI} often relieved with rest and NTG
• Angina with MI } may be relieved with rest, NTG, 02,
MS, rescue angioplasty, etc.
• Think MONA
– Morphine
– Oxygen
– Nitroglycerin
– Aspirin
http://www.youtube.com/watch?v=4GlQmTlP2jE&feat
ure=related
http://www.youtube.com/watch?v=rEqw3AKM_g
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Treatment continued…video
mysterious heart volume 3 chapter 37
ASA:
MS:
Beta-blocker
ACE inhibitor:
37
Treatment continued
– May need antiarrhythmic meds
• like what???
– Stool softeners to reduce valsalva
maneuver and prevent
constipation r/t narcotic use and
bed rest
– Treat: HTN, DM other co-morbid
illnesses
– Cardiac Rehab to follow
38
Treatments
• Low fat low cholesterol diet
• Prescribed exercise program 5-7 days
a week
• Knows correct use of NTG for angina
• Management of DM, HTN
• Stop smoking
• Medications to reduce work load or
dilate
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Low salt diet (<2000mg) does not include:
• Soups:
• Snacks:
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Low fat <30% Low
cholesterol
<200mg
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•
•
•
Lean meat: skinless
Dairy limited: egg beaters, skim milk
Olive oil, canola oil
Avoid: fried, fatty or heavily marbled
meats, sausage, lunch meat,
spareribs, frankfurters, salt pork,
canned fish in oil, yolks, duck. Cream
sauces, gravy, buttered vegetables,
sweet rolls, other processed foods
41
Exercise
• 5-7 X week is goal to include stretches
with warm-up, progressive walking
program, light weights, stretches with
cool down.
• Strengthens heart muscle, reduces
BP, BS, weight, stress, tension,
appetite, LDLs.
• Increases HDLs, energy and self
esteem and improves immune system
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Principles of Exercise
• Practice on regular basis
• Know how to do own pulse
• Strive for target heart rate
• Stop if chest pain occurs
• Complications: CHF &
Dysrhythmias
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Nursing interventions for MI
• Comfort measures
• Freq VS, cardiac monitoring, I&O,
CMS checks, spacing activities
• Heart & lung sounds, assess fluid
volume status, IV responsibilities, note
BP & Pulse prior to heart meds!!
• Client education r/t diet, meds, pulse
taking activity, elimination, reporting
chest pain and correct use of nitro
products for angina
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Medications for Heart Disease
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Anti-Anginal:
Anti-Hypertensive:
Anti-Arrhythmic: l
Cardiac glycoside:
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Medication continued
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Thrombolytic:
Anti-coagulant:
Anti-platelet aggregate:
Lipid-Lowering agents:
Diuretics:
Electrolyte replacement:
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Medication continued
• 02 to maintain 02 sat > 92% to reduce
chance of angina/ischemia
• If Angina the nurse needs to have the
client lie down, take VS then report to
charge nurse ,met team, call md.
• Instruct client: If develops chest pain,
sit down take 1 nitro every 3- 5 min x
3. If chest pain not relieved call 911
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•POST MI
Complications
48
• 90% will develop complication and 80% will
demonstrate arrhythmia which is the most
common cause of death in clients in the
pre-hospital period. (VT>>>VF)
• CHF and severe Left ventricular failure
• Papillary muscle dysfunction
• Pericarditis
• Thromboembolism
• Ventricle rupture
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Nursing Diagnosis
• Decreased cardiac output r/t
Dysrhythmias
• Acute Pain r/t lack of 02 to
myocardium
• Anxiety r/t to feeling of doom,
lack of understanding of medical
diagnosis
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•Surgical
Procedures
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Pacemaker
• New in 1958 having purpose to restore the
regular rhythm and to improve tissue
perfusion and cardiac output.
• Temporary / permanent
• Single chamber or double chamber
• Teach client how to take 1 min pulse, s/s to
report to MD-dizzy, angina, dyspnea
• Carry card and know precautions
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Video- mysterious heart volume 2
chapter 4
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AICD
• Implantable defibrillator to correct a life
threatening rhythm disturbance.
– Has pacemaker back-up.
• check battery q2months
• Instruct on how to take pulse for 1 min
• s/s to report to MD: firing, s/s of dizziness,
dyspnea, weakness, carry card and wear
bracelet, CPR for family. Know precautions
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• Nursing care for client with newly implanted
pacemaker or AICD.
– Assess cardiac monitor for capture/pacing
(pacer)
– VS post-op then q 4 hours, IV, bed rest till am
– Dressing dry and intact until AM then often may
remove. Increase activity progressively
– Instruct client not to raise arm above shoulder for
5days. May shower in 5 days
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Angioplasty with Stent
• Procedure done at the time of
cardiac cath.
• Balloon angioplasty is accomplished
to widen or open specific coronary
vessel-stent is inserted to maintain
patency of the vessel.
• pre-procedure Plavix given with
follow up Plavix
http://preop.medselfed.com/asp/center.asp
?centerId=heart&partnerId=preop&id=&ca
chedate=&emailId=&affId=&campId=&hid
eNav=
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EP with Ablation
• Mapping of myocardial tissue to
determine irritable focus.
• Low voltage current delivered to
ablate tissue causing SVT or VT
• 90% effective
• http://video.google.com/videop
lay?docid=5590000557631435292
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Nursing Care
• NPO prior
• Coumadin stopped 4 days prior,
Heparin 4 hours prior
• Post – procedure same as heart cath
– Cardiac monitoring
– Muscloskeletal and groin checks
– VS
– Ambulate prior to discharge
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Cardiac Surgery
• Coronary artery bypass
•
• Valve replacement or repair
• Septal repair and other congenital repairs
– CCU post op, chest tubes
– Pre-op teaching with post op expectations
– See client teaching for CABG, Valve
repair/replacement, care of PTCA, MI
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• http://preop.medselfed.com/as
p/center.asp?centerId=heart&p
artnerId=preop&id=&cachedate
=&emailId=&affId=&campId=&hi
deNav=
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Congestive Heart Failure
• Video..the mysterious heart
volume1 chapter 3
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• DEFINITION:EF < ____% or
when the myocardium is no
longer able to pump
efficiently
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• Systolic failure= most common

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Causes of CHF
• CAD, advancing age
• HTN is a major factor > CHF x 3
• DM, Smoking, Obesity
• Valvular incompetency, alcohol
or other chemicals,
idiopathic,(unknown)
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S/S of Left Sided CHF
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•
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Fatigue
Angina
Tachycardia
Cool extremities
Hacking cough
Crackles
Frothy sputum
Gallop
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S/S of Right Sided CHF
• Jugular distention
• Anorexia/nausea
• Dependent edema
• Distended abdomen
• Weight gain
• BP problems
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Assessment Findings
• C/O SOB, weakness, dry cough,
fatigue, can not lie down must sit up
to breath, has gained weight
• Auscultation of the heart} rapid HR,
extra heart sounds
• Auscultation of the lungs} rales,
wheezing
• Examination of the extremities for
peripheral edema
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System Compensation
• Mediated thru Sympathetic Nervous System:
as CO drops, baroreceptors alert brain
• 
– This causes stimulation Beta 1=>>
– Stimulation Beta 2=
– Activate Alpha receptors
peripherally=constriction=>>
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Compensation
• Causing S/S of CHF because:
• Contractility decreases
• Stroke volume and CO continue to
decrease
• Afterload (pressure on the other side of the
aorta) increases
• Preload ( pressure caused by increase
volume to heart creating an exaggerated
stretch in the muscle) increases
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Renal Compensation
• CO drops initiating renin-angiotensin
mechanism
– Results in powerful vasoconstrictor
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Ventricular Hypertrophy
• The heart enlarges which results in
strain
• The increase in volume causes the
ventricles to dilate
• Eventually remodeling will occur
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Diagnostic Tests
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H&P
Chest x-ray
EKG:
Echocardiogram:
CBC:
CMP:
Thyroid function
ABGs
BNP=B type natriuretic peptide= hormone released in
response to Ventricular stretch ( CHF peptide)
• Nuclear studies to determine heart function, EF, tissue
viability
• Cardiac Cath to determine exact nature of heart74
function
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CHF Management
• Directed at: Improving LV function
(Contractility) by decreasing intravascular
volume and decreasing vascular resistance
• Decreasing venous return (Preload)
• Decreasing BP (Afterload)
• Improving gas exchange and 02
• Increasing the CO and reducing anxiety
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continued
• ACE inhibitors to < afterload by
dilating vessels and < BP (ARBs)
• Beta blockers to < 02 demand by
reducing the contractility of the heart
and HR (not given in acute period)
• Diuretics <preload by reducing
volume returning to the heart-Lasix &
(Aldosterone Antagonists)
K+
supplement
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continued
• ASA in low doses or Plavix to help prevent
blood clot formation
• Anticoagulants for those with poor EFs to
prevent CVA
• Antiarrhythmics to control ectopy
• Biventricular pacing (CRT=cardiac
resynchronization therapy) to improve CO
• Digoxin to increase contractility of
myocardial fibers and improving cardiac
output. +inotropic agent
78
Treatment of CHF
• Treat underlying cause
• Rest and hi Fowlers to reduce work
load and improve ventilation
• 02 at 2-6 L/min with 02 sats >92% to
increase available 02 and prevent
hypoxemia
• Freq VS and cardiac monitoring
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Treatment continued
• I & O q shift
• Daily am weights before breakfast and
after voiding. 2-3# weight gain in 1-4 days
call MD
• Sodium restricted diet
• Medications: to decrease intravascular
volume thus reducing venous return, dilate
and reduce BP and improve contractility
• http://chfsolutions.com/zip_how_aquapher
esis_works.html#
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Educating the CHF Client
• Education re: heart failure
– Explanation of heart failure
– Expected S/S and when to call MD
– Self monitoring of daily weights
– Know medications and need to take
them
– 2000mg sodium restricted diet
– Importance of low level daily exercise
program (energy conservation)
– Prognosis / advanced directives
81
• Telemetry Interpretation/ Dysrhythmias
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Lead Placement
83
• A dysrhythmia is a disturbance of the
rhythm of the heart caused by a
problem in the conduction system.
• Categorized by site of origin: atrial ,
AV nodal, ventricular
• Blocks are interruptions in impulse
conduction: 1st, 2nd type 1&2, 3rd or
complete heart block
84
Each small box measures 0.04
1 big box (5 small boxes) is equal to a HR of 300
2 big boxes is hr of 150
3 big boxes is hr of 100
4 big boxes is hr of 75
5 big boxes is hr of 60
6 big boxes is hr of 50
7 big boxes is hr of 43
8 big boxes is hr of 38
85
• P-wave = atrial electrical activity
• QRS= ventricular electrical
activity
• T wave= resting phase of
ventricle
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P wave
Measures:
0.12-0.20
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QRS WAVE
Measures:
0.06-0.10
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QT Wave
90
Heart rates
• NSR: heart rate is ___bpm
• ST: heart rate ____ bpm
• SB: heart rate ____bpm
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NSR
92
Sinus rhythm
•PR interval- 0.12-0.20sec
• QRS-0.06-0.10sec
• QT segment 0.36-0.44 sec
•Heart rate 60-100
93
•Hr= 60-100 bpm
•On strip it looks regular but does
not map out
•PR interval= 0.12-0.20
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HR 40-60 bpm
<60 bpm is accelerated
Rhythm is regular
Pwaves not always present
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SB
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Sinus Bradycardia
• All criteria same except rate < 60bpm
• S/S: dizziness, syncope, angina,
hypotension, sweating, nausea,
dyspnea
• Sometimes no S/S
• Treat underlying cause
• IV atropine, pacemaker
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ST
98
Sinus Tachycardia
• All criteria same as with NSR except rate >100
• Causes: fever, dehydration, hypovolemia,
increased sympathetic nervous system stimulation,
stress, exercise, AMI
• S/S: Palpations #1, angina and < CO from < V filling
time
• Treatment: correct cause, eliminate caffeine,
nicotine, alcohol. Beta blockers may be ordered
99
Rate is usually WNL
Rhythm is regular
Pwaves are normal in size and shape
The PR interval is prolonged (>0.20 sec) but constant
100
www.unm.edu/~lkravitz/EKG/avblocks.htm
l
101
Pwaves are normal in size and shape;
Some pwaves are not followed by QRS
PR interval: lengthens with each cycle until it appears without QRS Complex
then the cycle starts over
QRS is usually narrow
102
www.unm.edu/~lkravitz/EKG/avblocks.htm
l
103
Ventricular rate is usually slow
Rhythm is irregular
Pwaves are normal in size and shape (more pwaves than QRS)
PR interval is within normal limits
QRS is usually wide
104
www.unm.edu/~lkravitz/EKG/avblocks.htm
l
105
Ventricular rate is regular but there is no correlation between pwaves and
QRS
Pwaves are normal in size and shape
No true PR interval
106
www.unm.edu/~lkravitz/EKG/avblocks.htm
l
107
Atrial Fibrillation
Erratic wavy base
Pr is not measurable
QRS 0.10 sec or less usually
http://www.youtube.com/watch?v=VKxQgjj2yVU&f
108
A fib continued
• Atrial rate > 400 bpm with a varying
Ventricular rate
• Overall rhythm irregular
• No P waves, unable to measure PR interval
• QRS=normal: Twave undeterminable
• Causes: Rheumatic fever, mitral valve
stenosis, cad. HTN, MI, hyperthyroidism,
COPD, CHF see pp. 604
109
A fib continued
• Concern with A fib is the
development of atrial thrombus and
loss of atrial kick from ineffective atrial
function.
• Treatment: Ca channel blockers and
anti- arrhythmics to convert, beta
blockers to < HR, anticoagulants to
prevent embolization.
• Synchronized cardioversion
110
Atrial rate of 250-450 bpm ventricular rate varies
Atrial rhythm is regular ventricular rate is
irregular
No identifiable p waves
P wave is not measurable
Qrs: 0.10 or less usually
111
Pacer spike should fall before the P wave unless a dual
Chamber pacemaker; if it does not there could be a problem
112
Extra beat
Types
uniform=go the same direction
multifocal= go in different direction
R on T=when the pvc fall on the preceding twave
couplet= 2 pvcs together
bigeminy= pvc every other beat
trigeminy=pvc every third beat
113
114
Ventricular tachycardia
Monomorphic: beats are same size
and shape
Polymorphic: different size and
shape
115
This is a polymorphic VT
Usually electrical imbalance in nature r/t NA+ or K+
116
Ventricular Fibrillation
Rate can not be determined
because of no identifiable
waves
Rapid chaotic rhythm with no
pattern
No p waves
No PR interval
No QRS
117
Vtach/Vfib
•
•
•
•
•
•
•
Both can be life threatening
VT= V HR 100-250 bpm
Causes: AMI, CAD, hypokalemia, dig toxic
S/S: palpitations, dizzy, angina, <LOC
Treatment: assess for pulse, if none, defib
VF=Rate undeterminable Cause: same
Treatment: CPR
118
http://videos.reinolla.tv/winners/pe/
119
Hypertension
120
• HTN is described as persistent elevation of
arterial blood pressure greater than 140/90
on at least 2 or more readings on different
dates.
• The Joint National Committee, Detection,
Evaluation, and Treatment of High Blood
Pressure defines normal:
– BP as S < 120 mm Hg and D < 80 mm Hg
– PreHTN: SBP 120-139 DBP 80-89
– Stage 1: SBP 140-159 DBP 90-99
– Stage 2: SBP >160
DBP >100
121
Types of Hypertension
• Essential HTN: (Primary) which is
the most common 90-95% of
population
• Secondary HTN: is a result of
another disease, kidney,
pregnancy.
122
Factors that determine arterial
pressure
• Cardiac output which is the volume
of blood pumped by the heart in 1
minute
• Peripheral vascular resistance which is
the force in the peripheral blood
vessels that the left ventricular must
overcome to eject blood out of the
heart
123
Possible Causes of PVR
• Narrowing of blood vessels, PVD, CAD,
kidney disease: > renin/angiotensin
=vasoconstriction
• Release of catecholamine (epinephrine
and adrenalin) = vasoconstriction
• > blood volume= more work to pump
• > Blood viscosity=harder to pump
• Ability of blood vessel to stretch
124
Causative Factors of HTN
•
•
•
•
•
•
•
Hyperlipidemia
Obesity
Atherosclerosis
Sedentary
DM
Family Hx
Cigarette smoking
Age > 60
Men
Post menapausal women
125
S/S
• Often none
• Occipital headache more
severe on rising
• Lightheadedness
• Epistaxis
• Known as the ‘Silent Killer’
126
Complications
• Damage to blood vessels of the eyes,
heart, kidney, brain resulting in:
• Stroke
• CHF
• AMI
• Renal failure
• Blindness
127
Lifestyle Change Education
• Exercise, dash diet, stop smoking,
weight management and control,
stress reduction, medications and
recording BP frequently
• Avoid OTC meds
• Instruct on how to do postural BPs
128
Valvular Disorders
129
• STENOSIS:
• INSUFFICIENCY:
130
Stenosis
• Narrowing of the opening of the valves.
Limits the amount of blood which is ejected
from one chamber to the next.
131
132
Mitral Stenosis
• Mitral valve leaflets become thickened and
fibrotic. Affect women age 20-40
• CHF may develop
• TX if failure develops: Digoxin, Lasix, beta
blockers, and anti arrhythmics, lo Na diet,
etc
• Will monitor with yearly echocardiogram
• Surgery if worsens
• Prophylactic antibiotics prior to invasive
procedure or dental work
133
Insufficiency
• The inability of the valves to close
completely.
• Allows the blood to backflow.
• Mitral valve is the most commonly affected
134
Cardiac insufficiency can be caused
by many factors – by a swelling of
the heart muscle (1), an
enlargement of the hollow
chambers in the heart (2), a heart
attack (3) or a blood clot (4).
135
Mitral Insufficiency
• Often accompanies mitral stenosis as
a result of rheumatic fever.
• Valve leaflet become rigid and
shorten, prevents closure of valve.
• Hypertrophy of Left Atrium and
Ventricle = L sided heart failure occurs
• Murmur heard. F/U with
echocardiogram
• TX: vasodilators, same as for stenosis
136
Mitral Valve Prolapse
• When the Left ventricle leaflets
become enlarged, and protrude
into the left atrium during systole.
• Benign but may progress to
Mitral insufficiency
• More common in women age
20-55
137
S/S of mitral prolapse
• Often none
• Others experience chest pain,
palpitations, dizziness, syncope,
dysrhythmias
• Monitor with echocardiogram
• May do heart catherization
• Manage stress, beta blockers if
tachycardia
138
Aortic Stenosis
• Occurs when valve cusps
become fibrotic and calcify.
• Most commonly caused by
aging and atherosclerosis.
• Occurs most predominantly in
men
• Untreated will lead to Left sided
CHF
139
Aortic Insufficiency
•
•
•
•
Caused primarily by rheumatic fever
May also be caused by chronic HTN
Predominantly in men
Hypertrophy of the Left ventricle and
eventually to left sided CHF
• Blood may eventually back up into
the pulmonary system and lead to
Right Ventricle failure
140
S/S and Treatment
• Aortic murmur, tachycardia, palpitations,
CHF with fatigue, SOB, ascites
• Monitored with echocardiogram assessing L
ventricular dilatation
• Chest X-ray-enlargement of heart
• May do cardiac cath
• May need valve repair or replacement
141
•Inflammatory Diseases
of the Heart
142
• Inflammation of the heart most
often results from systemic
infections and may include any
layer of the heart:
What are they???
143
Endocarditis
• Inner layer: tends to affect the valves
(Mitral=L). Organisms (Bacterial or
fungal) present in blood stream and
collect (colonize) on the valves:
Rheumatic heart disease, congenital
defects or mitral valve prolapse
• IV drug users or invasive procedures
144
• Clients with known valvular
disease need to be treated with
prophylactic antibiotics prior to
any invasive procedure including
dental. Immunosuppression and
any source of contamination
places clients at risk
145
Pathophysiology
• Bacteria may enter blood stream:
• Bacteria collect on valves and
vegetate
• Complications: Ventricular septal
defect, CHF(#1 cause of death) and
embolization
146
S/S
• Fever- (99-105)
• Chills and night sweats may
accompany
• Malaise, fatigue and weight loss
• Appearance of petechiae in the
mouth, conjunctiva and legs
• Chest and abdominal pain
indicating embolization
147
Treatment and Diagnostics
• H&P and Lab tests
CBC with diff with leukocytosis, > sed
rate, blood cultures
• May have heart murmur
Echocardiogram to visualize valves
and vegetation
• Chest x-ray: CHF
• Long term antibiotics, rest, limited activity,
prophylactic anticoagulants, valve
replacement after inflammation treated
148
Nursing Assessment
• Frequent VS and assess for fever
• Assess for heart murmur
• Note cough
• Assess peripheral edema
• Rest with limited activity,
administer meds in a timely
manner
149
Nursing Diagnosis
150
• myocarditis
151
• Muscle layer: Local or diffuse
inflammation of the
myocardium. May be viral or
bacterial, an autoimmune
process or drug toxicity.
• May result in cardiomyopathy=
152
Pathophysiology
• Characterized by degeneration
and necrosis of myocardial tissue
that is different of that caused by
MI
• Tissue next to necrosed area
hypertrophies, loses elasticity,
results in CHF and arrhythmias
153
S/S
• Asymptomatic
• May have fever, fatigue, sore
throat, dyspnea, muscle aches
• Lymph nodes may be enlarged
• Chest pain 7-10 days after virus
• CHF S/S
154
Diagnosis
• Based on Hx, S/S, and testingenzymes>
• May hear friction rub, rales
• Jugular vein distention
• Chest x-ray,
echocardiogram=hypertrophy
• EKG=arrhythmias
• Biopsy (RV) shows lymphatic
infiltration and cell necrosis
155
Treatment
• Bed rest
• 02
• Meds: cardiac glycosideLanoxin, anticoagulants,
antiarrhythmic, antibiotics,
steroids
• Cardiac monitoring
• NI same as for endocarditis
• ND same as for endocarditis
156
• Pericarditis
157
• Outer-surrounds heart
• Inflammation of the pericardium.
• Primary or secondary
• Acute or chronic
• Acute: virus, bacteria, fungi,
chemotherapy, MI
• Chronic: TB, radiation or
metastases
158
Pathophysiology
• Inflammation causes an increase in the
amount of pericardial fluid and
inflammation of surrounding tissues.
• Fluid accumulates in the pericardial space
• Adhesions may occur which causes loss of
elasticity which causes constriction and
prevents adequate filling of ventricles.
• May lead to
tamponade==pericardiocentesis
159
Tamponade
160
S/S
• Chest pain is hallmark
• Most severe on inspiration, sharp,
stabbing, or dull and burning.
• Pain is relieved by sitting up or
leaning forward
• Dyspnea, chills and fever
161
Diagnosis
• WBC elevated
• Serial EKG show that ST segment
increases and resolves in several
weeks. A fib may occur
• Echocardiogram to see pericardial
thickening and effusion
• Enzymes can be increased
• Blood cultures to ID organism
162
Treatment
•
•
•
•
•
Analgesics
Antipyretics
Anti-inflammatory agents
Antibiotics
May need OR to create a pericardial
window to allow for drainage of fluid
• NI and ND same as for endocarditis
163
• Nursing the Heart Client
164
Assessment
• Heart rate and rhythm, color,
temperature, cognition
• Circulation: peripheral CMS checks
• Vital signs to include 02 saturations
and telemetry interpretation
• Subjective: c/o chest pain, SOB,
fatigue, lightheadedness, dizziness
165
Nursing Diagnosis
166
Ekg practice
167
168
169
170
171
172
173
174
•www.mirule.com retrieved on
4/8/07.
•Images found at www.aol.com.
Retrieved on 4/8/07.
• Aehlert, B. RN BSPA (2006). EKGs
Made Easy. Mosby (3rd ed). St
Louis.
175
•The End
176