new heart
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e
Heart
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4-chambered muscular organ
Located in the mediastinum coronary artery
The layer that covers the heart is the
PERICARDIUM Myocardium
The Atrio-ventricular valves-
The Semilunar valves-
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The CONDUCTING SYSTEM OF THE HEART
Consists of the
The SA (sinoatrial ) node, or pacemaker ,initiates the heartbeat and contracts the atria
The AV (atrioventricular ) node conveys the
stimulus and initiates contraction of theventricles.
The signal for the ventricles to contract travelsfrom the AV node through the atrioventricular
bundle.These branch profusely to the smaller Purkinje fibers
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Periods of the Cardiac Cycle
Diastole
± Period of rest
± Blood is returned to the heart Systole
± Period of contraction
± Blood is pumped out of the heart
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Cardiac Output Regulation
The heart pumps approximately 5 L of
blood/minute
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STROKE VOLUME- the amount of bloodthe heart pumps out in each beat
Heart rate
Sympathetic systemParasympathetic system (Vagus)
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Cardiac output=Stroke volume x heart rate
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Factors regulating Stroke Volume
1. Preload- the degree to which the ventricles are
stretched prior to contracting.
2. Afterload- the pressure against which the
ventricle ejects blood
- Determined primarily by bloodviscosity and the resistance of vascular system itself
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Extrinsic Control of Heartbeat
A cardiac control center up or slowsdown the heart rate by way of theautonomic nervous systembranches:
1. parasympathetic system (slows heartrate)
2. sympathetic system (increases heart
rate). Hormones epinephrine and
norepinephrine from the adrenal
medulla also stimulate faster heart rate.
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Blood pressure
Hormones- ADH, Adrenergic hormones,Aldosterone and ANF
ADH increases water retention
Aldosterone increases sodium retention andwater retention secondarily
Epinephrine and NE increase HR and BP
ANF= causes sodium excretion
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Cardiac compensatory mechanisms
When the normal compensatory
mechanisms cannot maintain cardiac output
to meet body needs, the client is in a state of
cardiac decompensation.
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The vascular system consists of the
arteries, veins and capillaries The arteries are vessels that carry blood
away from the heart to the periphery
The veins are the vessels that carry blood
to the heart The capillaries are lined with squamous
cells, they connect the veins and arteries
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The lymphatic system also is part of the
vascular systemFXN: to collect the extravasated fluid from
the tissues and return it to the blood
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Slide 11.26
Differences Between Blood VesselTypes
y Walls of arteries are the thickest
y
Lumens of veins are larger y Skeletal muscle ³milks´ blood in veins
toward the heart
y Walls of capillaries are only one celllayer thick to allow for exchangesbetween blood and tissue
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Slide 11.27
Movement of Blood Through Vessels
y Most arterial blood ispumped by the heart
y
Veins use the milkingaction of muscles tohelp move blood
Figure 11.9
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Slide 11.30
Major Arteries of Systemic Circulation
Figure 11.11
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Slide 11.31
Major Veins of Systemic Circulation
Figure 11.12
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Slide 11.34
Circulation to the Fetus
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Blood Pressure
Measure of force exerted by bloodagainst the wall
Blood moves through vessels because of
blood pressure
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Slide 11.39b
Blood Pressure: Effects of Factors
y TemperatureyHeat has a vasodilation effect
yCold has a vasoconstricting effect
y Chemicals
yVarious substances can cause increase or decrease
y Diet
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Slide 11.40
Factors Determining Blood Pressure
Figure 11.19
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Slide 11.35
Pulse
y
Pulse ±pressure waveof blood
y Monitored at³pressure
points´ wherepulse is easily
palpated
Figure 11.16
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C ardiac Assessment
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Physical examination
InspectionSkin color. Note for pallor, cyanosis or jaundice.
Pallor and cyanosis are due to inadequate
oxygenation. Jaundice is due to hemolysis of rbc.
Neck vein distention. This is due to venous
congestion
Respiration. Note for signs of dyspnea
Point mf Maximal Impulse (PMI). It is located inthe left, mid-clavicular fifth intercostals space (ICS)
Peripheral Edema. This is due to venous
insufficiency
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Palpation
Peripheral pulses. Weak or bounding and irregular pulses may indicate presence of cardiovascular disorders
Apical pulse. It is assessed at the point of maximum
impulsePercussion
Pulmonary edema produces dullness on percussionof the chest
AuscultationHeart sounds
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LABORATORY PROCEDURES
CARDIAC Proteins and enzymes
1. CBC
2. BUN 3. Blood l ipids
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CARDIAC Proteins and enzymes
4. CK- MB ( creatine kinase)Normal value is 0-7 U/L
Elevates in MI w ithin 4hours, peaks in 18 hoursand then dec l ines ti ll 3 days
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5. Lactic Dehydrogenase (LDH)
Among the LDH isoenzymes,LDH1 is the most sensitiveindicator of myocardial
damageNormal value is 70-200 IU/L
Elevates in MI in 24 hours,
peaks in 48-72 hours
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Troponin
Most specific laboratory test to detect
MI
Has three components:C, I, T
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SERUM LIPIDS
Lipid profile measures the serumcholesterol, triglycerides andlipoprotein levels
Cholesterol= <200 mg/dL
Triglycerides- 40- 150 mg/dL
LDL- 130 mg/dL
HDL- 30-70- mg/dL NPO post midnight (usuall y 12 hours)
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ELECTROCARDIOGRAM (ECG)
A non-invasive procedure thatevaluates the electrical activityof the heart
Electrodes and wires areattached to the patient
Tell the patient that there is no riskof electrocution
Avoid muscularcontraction/movement
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Holter Monitoring
A non-invasive test in whichthe client wears a Holtermonitor and an ECG tracing
recorded continuously over aperiod of 24 hours
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Holter Monitoring
Instruct the client to resume
normal activities and maintain a
diary of activities and anysymptoms that may develop
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ECHOCARDIOGRAM
Non-invasive test that studiesthe structural and functionalchanges of the heart with the
use of ultrasound No special preparation is
needed
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Stress Test
A non-invasive test that studiesthe heart during activity anddetects and evaluates CAD
Treadmill testing is the mostcommonly used stress test
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Stress Test
Pre-test: consent may berequired, adequate rest, eat alight meal or fast for 4 hours
and avoid smoking, alcoholand caffeine
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Post-test: instruct client to notify the
physician if any chest pain, dizzinessor shortness of breath
Instruct client to avoid taking a hot
shower for 10-12 hours after the test
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CARDIAC catheterization
Insertion of a catheter into theheart and surrounding vessels
Determines the structure and
performance of the heart valvesand surrounding vessels
Used to diagnose CAD, assesscoronary artery patency anddetermine extent of
atherosclerosis
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Intra-test: inf orm patient o f a f l uttery feel ing as the catheter
passes thr ough the heart ;- inf orm the patient that a
feel ing o f w armth and metall ic
taste may occur w hen dye isadministered
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Post-test: Monitor VS and cardiac rhythm
Monitor peripheral pulses, color andwarmth and sensation of the extremitydistal to insertion site
Maintain sandbag to the insertion site if required to maintain pressure
Monitor for bleeding and hematomaformation
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Maintain strict bed rest for 6-12 hours
Cl ient may turn fr om side t o side but bed
shoul d not be el evated more than 30
degrees and l egs al w ays straight
Encourage fluid intake to flush out the dye
Immobilize the arm if the antecubital vein isused
Monitor for dye allergy
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CARDIAC IMPLEMENTATION
1. Assess the cardio-pulmonary status
VS, BP, Cardiac assessment
2. Enhance cardiac output
Establish IV line to administer
fluids
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CARDIAC IMPLEMENTATION
3. Promote gas exchange
Administer O2
Position client in SEMI -F ow l ers
Encourage coughing and deep
breathing exercises
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CARDIAC IMPLEMENTATION
4. Increase client activity tolerance
Balance rest and activity periods
Assist in daily activities
Provide strict bed rest if indicated
Soft foods Assistance in self-care
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CARDIAC IMPLEMENTATION
5. Promote client comfort
Assess the clients description of
pain and chest discomfort Administer medication as prescribed
Morphine for MI
Nitroglycerine for AnginaDiuretics to relieve congestion (CHF)
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CARDIAC IMPLEMENTATION
6. Promote adequate sleep
7. Prevent infection
Monitor skin integrity of lowerextremities
Assess skin site for edema, rednessand warmth
Monitor for fever
Change position frequently
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CARDIAC IMPLEMENTATION
8. Minimize patient anxiety
Encourage verbalization of feelings, fears and concerns
Answer client questions.
Provide information aboutprocedures and medications
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CARDIAC DISEASES
Coronary Artery Disease
Myocardial Infarction
Congestive Heart Failure
Infective Endocarditis
Cardiac TamponadeCardiogenic Shock
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VASCULAR DISEASES
Hypertension
Buergers disease
Aneurysm
Varicose veinsDeep vein thrombosis
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CORONARY ARTERY DSE
results from the focal narrowingof the large and medium-sized
coronary arteries due to
deposition of ather omat ous
pl aque in the vessel w all
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CAD: Pathophysiology
Fatty streak formation in the vascular intima
Atheroma
narrowing of the arterial lumen
reduced coronary blood flow
myocardial ischemia
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Angina Pectoris
Chest pain resulting from
coronary atherosclerosis or
myocardial ischemia
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Angina Pectoris: Clinical Syndromes
THREE COMMON TYPES OF ANGINA1. STABLE ANGINA
The typical angina that occurs
during exertion, relieved byrest and drugs and the severity d oes not change
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2. Unstable angina
Occurs unpredictably duringexertion and emotion, severity increases w ith time and pain
may not be relieved by rest anddrug
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3. Variant angina
Prinzmetal angina, results fromcoronary artery VASOSPASMS,may occur at rest
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ASSESSMENT FINDINGS
1. Chest pain The most characteristic symptom
PAIN is described as mild to
severe retrosternal pain,squeezing, tightness or burningsensation
Radiates t o the jaw and left arm
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Angina Pectoris
Precipitated by E xercise, E ating heavy
meals, E motions like excitement and
anxiety and E xtremes of temperature
Relieved by REST and
Nitroglycerin
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2. Diaphoresis
3. Nausea and vomiting
4. Cold clammy skin
5. Sense of apprehension and
doom 6. Dizziness and syncope
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LABORATORY FINDINGS
1. ECG may show normal tracing if
patient is pain-free.- Ischemic changes may show ST
depression and T wave inversion
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2. Cardiac catheterization
Provides the MOST DEFINITIVEsource of diagnosis by showing thepresence of the atheroscleroticlesions
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NURSING MANAGEMENT
1. Administer prescribed medications
N itrates- t o di l ate the venous vessel sdecreasing venous return and t o someextent di l ate the c or onary arteries
Aspirin- t o prevent thr ombus f ormati on Beta-blockers- t o reduce BP and H R
C al cium-channel blockers- t o di l ate
c or onary artery and reduce vasospasm
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2. Teach the patient management of anginalattacks
Advise patient to stop all activities Put one nitroglycerin tablet under the tongue
If unrelieved after THREE tablets seek medicalattention
3. Obtain a 12-lead ECG
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4. Promote myocardial perfusion
Instruct patient to maintain bed rest Administer O2 @ 3 lpm
Advise to av oid val sal va maneuvers
Provide laxatives or high fiber diet tolessen constipation
Encourage to avoid increased physical
activities
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5. Assist in possible treatment modalities
PTCA- percutaneous transluminal coronaryangioplasty
To compress the plaque against thevessel wall, increasing the arterial lumen
CABG- coronary artery bypass graft
To improve the blood flow to themyocardial tissue
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6. Provide information to familymembers to minimize anxietyand promote family cooperation
7. Assist client to identify riskfactors that can be modified
8. Refer patient to properagencies
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Myocardial infarction
Death of myocardial tissue
in regions of the heart
with abrupt interrupti on
of coronary blood supply
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ETIOLOGY and Risk factors
1. CAD 2. Coronary vasospasm
3. Coronary artery occlusion by
embolus and thrombus 4. Conditions that decrease
perfusion- hemorrhage, shock
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PATHOPHYSIOLOGY
Interrupted coronary blood flowmyocardial ischemia anaerobicmyocardial metabolism for severalhoursmy ocardial death
depressed cardiac function triggers autonomic nervous systemresponse further imbalance of
myocardial O2 demand and supply
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ASSESSMENT findings
1. CHEST PAIN Chest pain is described as
severe, persistent, crushing
substernal discomfort Radiates to the neck, arm, jaw
and back
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Occurs without cause, primarily early
morning NOT relieved by rest or nitroglycerin
Lasts 30 minutes or longer
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2. Dyspnea
3. Diaphoresis
4. Cold clammy skin
5. N/V
6. restlessness, sense of doom
7. tachycardia or bradycardia
8. hypotension
f
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Laboratory findings
1. ECG- the ST segment isELEVATED, T wave inversion,presence of Q wave
2. Myocardial enzymes- el evated CK -MB , LDH and T r o ponin l evel s
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Nursing Interventions
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Nursing Interventions
1. Provide Oxygen at 2 lpm, Semi-fowlers
2. Administer medications Morphine to relieve pain
Nitrates, thrombolytics, aspirin and
anticoagulants Stool softener and hypolipidemics
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3. Minimize patient anxiety
Provide information as to proceduresand drug therapy
Allow verbalization of feelings
Morphine can be administered
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4. Provide adequate rest periods Bed rest during acute stage
5. Minimize metabolic demands
Provide soft diet
Provide a low-sodium, low cholesterol
and low fat diet
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6. Assist in treatment modalities suchas PTCA and CABG
7. Monitor for complications of MI-especially dysrhythmias, sinceventricular tachycardia can happenin the first few hours after MI
8. Provide client teaching
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Medical Management
1. ANALGESIC The choice is MORP H I N E
It reduces pain and anxiety
Relaxes bronchioles to enhance
oxygenation
2 ACE i hibit
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2. ACE inhibitors
Prevents formation of angiotensin II
Limits the area of infarction
3. Thrombolytic therapy
Streptokinase, Alteplase
Dissolve clots in the coronary artery
allowing blood to flow
NURSING INTERVENTIONS AFTER ACUTE
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NURSING INTERVENTIONS AFTER ACUTE
EPISODE
1. Maintain bed rest for the first 3 days
2. Provide passive ROM exercises
3. Progress with dangling of the feet atside of bed
4. Proceed with sitting out of bed, on the
chair for 30 minutes TID 5. Proceed with ambulation in the room
toilet hallway TID
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NURSING INTERVENTIONS AFTER ACUTE
EPISODE
Cardiac rehabilitation
To extend and improve quality of life
Physical conditioning
P atients w ho are abl e t o w al k 3-4 mph are
usuall y ready t o resume sexual activities
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Inf ective endocarditis
Infection of the heart valves
and the endothelial surface
of the heart
Can be acute, sub-acute or
chronic
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Etiologic factors
1. Bacteria- Organism
depends on several factors
2. Fungi
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Risk factors
1. Prosthetic valves
2. Congenital malformation
3. Cardiomyopathy 4. IV drug users
5
. Valvular dysfunctions
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Inf ective endocarditis
PathophysiologyDirect invasion of microbes
microbes adhere to damaged valve surface andproliferate
damage attracts platelets causing clot formation
erosion of valvular leaflets and the clot and vegetation
can embolize
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Assessment findings
1. Intermittent high grade fever
2. anorexia, weight loss
3. cough, back pain and joint pain
4. splinter hemorrhages under nails
5 Oslers nodes painful nodules
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5. Oslers nodes- painful nodules
on fingerpads6. Roths spots- pale
hemorrhages in the retina
7. Heart murmurs
8. Heart failure= usually acute
heart failure
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Prevention
Antibiotic prophylaxis if patient is
undergoing procedures like dentalextractions, bronchoscopy,
surgery, etc.
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Prevention
Any invasive procedure that is
associated with transientbacteremia may cause the
microrganism to lodge in thedamaged, irregular valves
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LABORATORY EXAM
Blood Cultures to determine the
exact organism
Usually, 3 culture specimens are
obtained and antibioticsensitivity done
Nursing management
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Nursing management
1. Regular monitoring of
temperature, heart sounds
2. Manage infection
3. Long-term antibiotic therapy isgiven to ensure eradication of bacteria
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Medical management
1. P harmac otherapy
IV antibiotic for 2-6 weeks
Antifungal agents are given amphotericin B
Medical management
2. Surgery
Valvular replacement
C ti H t F il (CHF)
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Congestive Heart Failure (CHF)
A syndrome of congestion of both pulmonary and systemic
circulation caused byinadequate cardiac functionand inadequate cardiac
output to meet the metabolicdemands of tissues
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Inability of the heart topump sufficiently
The heart is unable tomaintain adequatecirculation to meet the
metabolic needs of the body
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This can happen acutely orchronically
Acute in Myocardial infarction
Chronic cardiomyopathies
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Classified according to themajor ventricular
dysfunction:1. Left Ventricular failure
2. Right ventricular failure
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Etiology of CHF1. CAD
2. Valvular heart diseases
3. Hypertension4. MI
5. Cardiomyopathy
6. Lung diseases
7. Post-partum
8. Pericarditis and cardiac tamponade
LABORATORY FINDINGS
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LABORATORY FINDINGS
1. CXR may reveal cardiomegaly 2. ECG may identify Cardiac
hypertrophy
3. Echocardiogram may show
hypokinetic heart
4. ABG and Pulse oximetry mayshow decreased O2 saturation
NURSING INTERVENTIONS
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NURSING INTERVENTIONS
1. Assess patient's cardio-pulmonary status
2. Weigh patient daily to
monitor fluid retention
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Administer medications- usuallycardiac glycosides are given- DIGOXIN
or DIGITOXIN, Diuretics, vasodilators
and hypolipidemics are prescribed
CHF
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CardiotonicsCardiotonics
Positive Positive inotropic inotropic agents agents
To increase cardiac To increase cardiac
contractilitycontractility
DiureticsDiuretics To decrease the To decrease the
intravascular volume in theintravascular volume in thecirculationcirculation
Low Sodium DietLow Sodium Diet To minimize water retention To minimize water retention
HypolipidemicsHypolipidemics To decrease the lipid levels To decrease the lipid levels
of high risk patientsof high risk patients
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NURSING INTERVENTIONSDigoxin Health teaching
Oral tablet usually once a day
Increases force of contraction
DECREASES heart rate
Assess: Apical pulse, ECG,hypokalemia
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Digoxin Health teaching Withhold the drug if apical pulse is
less than 60
Note for early signs of toxicity:
NAVDA
Provide potassium supplements
4. Provide a LOW sodium diet.i i fl id i k
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Limit fluid intake as necessary
5. Provide adequate rest periodsto prevent fatigue
6. Position on semi-fowlers to
fowlers for adequate chestexpansion
7. Prevent complications of
immobility
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
Heart fails to pumpadequately resulting to a
decreased cardiac outputand decreased tissueperfusion
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
ETIOLOGY
1. Massive MI
2. Severe CHF
3. Cardiomyopathy
4. Cardiac trauma
5. Cardiac tamponade
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
ASSESSMENT FINDINGS 1. HY POT E N SI ON
2. Ol iguria ( l ess than 30 ml/ hour)
3. T achycardia
4. N arr ow pul se pressure
5. weak peripheral pulses
6. cold clammy skin
7. changes in sensorium/LOC
8. pulmonary congestion
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
LABORATORY FINDINGS
Increased CVP due to pooling of
blood in the venous system Normal is 4-10 cmH2O
Metabolic acidosis
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
NURSING INTERVENTIONS
1. Place patient in a modified
Trendelenburg (shock ) position
2. Administer IVF, vasopressors and
inotropics such as DOPAMINE andDOBUTAMINE
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
NURSING INTERVENTIONS
3. Administer O2
4. Morphine is administered to
decreased pulmonary congestion
and to relieve pain, relieve anxiety
CARDIOGENIC SHOCK
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CARDIOGENIC SHOCK
5. Assist in intubation, mechanical
ventilation, PTCA, CABG, insertion of
Swan-Ganz cath and IABP
6. Monitor urinary output, BP and
pulses
7. cautiously administer diuretics andnitrates
HYPERTENSION
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HYPERTENSION
A systolic BP greater than 140
mmHg and a diastolic
pressure greater than 90mmHg over a sustained
period, based on two or more
BP measurements.
HYPERTENSION
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HYPERTENSION
Types of Hypertension1. Primary or ESSENTIAL
Most common type
2. Secondary
Due to other conditions like
Pheochromocytoma, renovascular
hypertension, Cushings, Conns ,
SIADH
HYPERTENSION
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HYPERTENSION
PATHOPHYSIOLOGY
Mul ti-fact orial eti ology
BP= CO (SV X HR) x TPR Any increase in the above parameters w i ll
increase BP
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Any increase in the above parameters will
increase BP
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increase BP
1. Increased sympathetic activity 2. Increased absorption of Sodium, and
water in the kidney
3. Increased activity of the RAA
4. Increased vasoconstriction of the
peripheral vessels 5. Insulin resistance
ASSESSMENT FINDINGS
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ASSESSMENT FINDINGS
1. Headache 2. Visual changes
3. chest pain
4. dizziness
5. N/V
DIAGNOSTIC STUDIES
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1. Health history and PE
2. Routine laboratory- urinalysis,
ECG, lipid profile, BUN, serum
creatinine , FBS
3. Other lab- CXR, creatinine
clearance, 24-huour urine protein
MEDICAL MANAGEMENT
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MEDICAL MANAGEMENT
1. Lifestyle modification2. Diet therapy
3. Drug therapy
MEDICAL MANAGEMENT
D th
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Drug therapy
Diuretics Beta blockers
Calcium channel blockers
ACE inhibitors
A2 Receptor blockers
Vasodilators
ANEURYSM
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ANEURYSM
Dilation involving an artery
formed at a weak point in
the vessel wall
ANEURYSM
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ANEURYSM
RISK FACTORS
1. Atherosclerosis
2. Infection= syphilis3. Connective tissue disorder
4. Genetic disorder= MarfansSyndrome
ANEURYSM
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ANEURYSM
PATHOPHYSIOLOGY
Damage to the intima and media
weakness outpouching of vessel
wall
Dissecting aneurysm
tear in theintima and media with dissection of
blood through the layers
ANEURYSM
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ANEURYSM
ASSESSMENT
1. Asymptomatic
2. Pulsatile sensation on the
abdomen
3. Palpable bruit
ANEURYSM
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ANEURYSM
LABORATORY: CT scan
Ultrasound
X-ray
Medical Management:
Anti-hypertensive
ANEURYSM
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ANEURYSM
Nursing Management:
Administer medications
Emphasize the need to avoidincreased abdominal pressure
No deep abdominal palpation
Remind patient the need for serialultrasound to detect diameter
changes
PERIPHERAL ARTERIAL OCCLUSIVE
DISEASE
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DISEASE
Refers to arterial insufficiency of
the extremities usually secondary
to peripheral atherosclerosis.
Usually found in males age 50 and
above
The legs are most often affected
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ASSESSMENT FINDINGS
1. INTERMITTENT CLAUDICATION-
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1. I NT E RMI TT E NT C LAU DI C AT I ON the hallmark of PAOD
This is PAIN described as aching,cramping or fatiguing discomfortconsistently reproduced with thesame degree of exercise oractivity
This pain is RELIEVED by REST
This commonly affects the musclegroup below the arterial occlusion
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2. Progressive pain on theextremity as the diseaseadvances
3. Sensation of cold and
numbness of the extremities
ARTERIOSCLEROSIS OF THE EXTREMITIES
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4. Skin is pale when elevated andi d dd h l d
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cyanotic and ruddy when placed
on a dependent position
5. Muscle atrophy, leg ulcerationand gangrene
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Nursing Interventions
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1. Maintain Circulation to the extremity
2. 2. Monitor and manage complications
BUERGERS DISEASE
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T hr omboangiitis obl iterans
A disease characterized by
recurring inflammation of themedium and small arteries and
veins of the lower extremities
Thromboangiitis obliterans
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T hr omboangiitis obl iterans
Occurs in MEN ages 20-35
RISK FACTOR: SMOKING!
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PATHOPHYSIOLOGY
Cause is UNKNOWN
Probably an Autoimmune disease Inflammation of the arteries and
veins thrombus formation
occlusion of the vessels
ASSESSMENT FINDINGS
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1. Leg PAIN
Foot cramps in the arch
(I N ST E P C LAU DI C AT I ON ) after exercise
Relieved by rest Aggravated by smoking, emotional
disturbance and cold chilling
2. Digital rest pain not changed by activityor rest
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3. Intense RUBOR (reddish-blue
discoloration), progresses to
CYANOSIS as disease advances
4. Paresthesias
RAYNAUDS DISEASE
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A form of intermittent arteriolar
VASOCONSTRICTION that results in
coldness, pain and pallor of the
fingertips or toes
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Cause : UNKNOWN
Most commonly affects WOMEN, 16-
40 years old
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ASSESSMENT FINDINGS
1. Raynauds phenomenon
A local ized episode o f vasoc onstricti on o f the small arteries o f the hands and feet
that causes c olor and temperature changes
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W -B-R is the acr onym f or the c olor change
Pallor- due to vasoconstriction, then
Blue- due to pooling of Deoxygenatedblood
Red- due to exaggerated reflow or
hyperemia
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ASSESSMENT FINDINGS
2. Tingling sensation
3. Burning pain on the hands andfeet
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Medical management
Drug therapy with the use of
CALCIUM channel blockers To prevent vasospasms
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Nursing Interventions 1. instruct patient to avoid situations that may
be stressful
2. instruct to avoid exposure to cold andremain indoors when the climate is cold
3. instruct to avoid all kinds of nicotine
4. instruct about safety. Careful handling of sharp objects
VARICOSE VEINS
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THESE are dilated veins
usually in the lower
extremities
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VARICOSE VEINS
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Predisposing Factors Pregnancy
Prolonged standing or sitting Incompetent venous valves
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Pathophysiology
Factors venous stasis
increased hydrostaticpressure edema
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Assessment findings
Tortuous superficial veins
on the legs
Leg pain and Heaviness
Dependent edema
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Medical management
Pharmacological therapy
Anti-embolic stockings
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Nursing management
1 Advise patient to elevate
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1. Advise patient to elevate
the legs with pillow toincrease venous return
2. Caution patient to avoidprolonged standing orsitting
Nursing management
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3. Provide high-fiber foodsto prevent constipation
4. Teach simple exercise to
promote venous return
5. Caution patient to avoid
constrictive clothing
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Nursing management
6. Apply anti-embolic
stockings as directed7. Av oid massage on the
affected area
DVT- Deep Vein Thrombosis
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Inflammation of the deep
veins of the lower
extremities and the pelvicveins
The inflammation results toformation of blood clots in
the area
Predisposing factors
P l d i bilit
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Prolonged immobility
Varicosities
Traumatic procedures
Increased age
Malignancy
Estrogen therapy
Smoking
Complication
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Complication
PULMONARY
thromboembolism
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Assessment findings
Leg tenderness
Leg pain and edema
Positive H OM AN s SIGN
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HOMANs SIGN The foot is FLEXED upward
(dorsiflexed) , there is a sharp painfelt in the calf of the leg indicative
of venous inflammation
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Medical management
Antiplatelets- aspirin
Anticoagulants
Vein stripping and grafting
Anti-embolic stockings
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Nursing management
1. Provide measures to avoid
prolonged immobility Repositioning Q2
Provide passive ROM Early ambulation
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2. Provide skin care to preventthe complication of legulcers
3. Provide anti-embolic
stockings
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4. Administer anticoagulants asprescribed
5. Monitor for signs of pulmonary embolism sudden
respiratory distress
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Thank
You!