Transcript Slide 1


CARDIO
VASCULAR
SYSTEM
Husni Rousan
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THE HEART
Anatomy and Physiology

The heart compose of three layers
–Endocardium: the inner layer of endothelial
tissue
–Myocardium: the middle layer of the muscle
fiber responsible for pumping action
–Epicardium: the outer layer
it is encased in a thin fibrous sac “epicardium”
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THE HEART
Anatomy and Physiology

Pericardium consists of Veseral, parital
pericardium layers and space in between,
pericardium space is filled with 30 ml of
lubricating fluid
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Heart Champers
Right
heart consists of Rt atrium, Rt ventricle,
distribute deoxygenated blood
Left heart consists of Lt atrium, Lt ventricle ,
distribute oxygenated blood
Varying thickness of a trial and ventricular wall
and left and right ventricles related to work load
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Heart Champers
 HEART VALVES:
– Atrioventricular, separate atria from
ventricles
– Semilunar valves ( three half-moon
leaflet
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Coronary Arteries
The
heart has large metabolic requirement, 7080% of delivered oxygen
Coronary arteries are perfused during diastole
Left coronary artery branches ( LAD & LCX )
Right coronary artery branch ( RCA )
Posterior wall received blood by ( PDCA )

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CONDUCTING SYSTEM

cardiac electrical cell is characterized by
–Atomicity: ability to initiate electrical
impulses
–Exitability: ability to respond to impulses
–Conductivity: ability to transmit impulses
–( SA – AV – bundle of his – bundle branch )
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CONDUCTING SYSTEM
 Physiology
of cardiac conduction
– Electrical activity (ions move across
cell membrane)
– Polarization, Depolarization,
electromechanical coupling and
repolarization
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cont
 Cardiac
homodynamic
– Cardiac cycle ( flow of blood )
– Cardiac output ( ejection of blood )
= stroke volume x heart rate
– Heart Rate: affected by central
nervous system and baroreceptors
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cont.

STROKE VOLUME
: the amount of blood
ejected by Lt ventricle in each beat which is 70 ml
determined by preload, after load and contractility
EJECTION FRACTION: 42% for right heart
and 50% for the left heart
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ASSESSMENT
 The
extent of assessment is determined by:
–Purpose of nursing assessment
–Severity of pt’s condition
–Practice setting of the nurse
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ASSESSMENT

Health history and clinical manifestations
– Acute symptoms: current medication,
allergies, general appearance,
homodynamic status
– Stable patients: complete history, spouse
or partner, demographic information
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ASSESSMENT
 Cardiac
symptoms: pt will have one of
the following
– Shortness of breath, dizziness,
syncope, loss of consciousness,
edema and weight gain, fatigue,
palpitation and chest discomfort
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NURSING DIAGNOSIS
Decrease
cardiac output related to structural
disorders
Activity intolerance related to decrease cardiac
output or excessive fluid volume
Anxiety related to change in health status and
change in role function
COLLABRATIVE PROBLEMS
Congestive heart failure, ventricular
dysrhythmias, and atrial
dysrhythmias
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PLANNING AND GOALS
Improve
and maintain cardiac output
Increase activity tolerance
Reduction of anxiety
Absence of complications
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NURSING IMPLEMENTATION
Encourage rest,
leaning back in a chair
Oxygen through nasal prongs
Careful monitoring to correlate intervention
with patient’s response to adjust treatment plan
Decrease sodium diet intake
Change position frequently
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PHYSICAL ASSESSMENT
Performed to
confirm the data in health history
It should include the following
–Effectiveness of heart as a pump, filling
volume and pressure, cardiac output,
compensatory mechanisms
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PHYSICAL ASSESSMENT
 General
appearance
– Level of consciousness, thought
process, heart ability to perfuse brain
tissue, distress and anxiety
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PHYSICAL ASSESSMENT

Skin
– Pallor around finger nails and lips, peripheral
cyanosis, central cyanosis, xenthelasma (
yellowish indicates high cholestrol), reduce
skin turgor, bruice ( anti coogulants )

Blood pressure
– Normal is 120/80 mmhg ( 100/60 – 140/90 )
invasive and non invasive
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Pulse
pressure:
–Difference between systolic and diastolic, 30-40
mmhg, reflects strock volume & ejection velocity,
vascular resistance,
–Less than 30 mmhg = serious reduction in output
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PHYSICAL ASSESSMENT

Postural hypotension
– Orthostatic hypotension, may indicates low
intravascular volume, inadequate vaso
constrictor mechanism or autonomic
insufficiency

Arterial pressure
– Rate, rhythm, quality, volume, configration (
contor)
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PHYSICAL ASSESSMENT

Jugular venous pressure
– Reflects Rt heart function, provide estimation
of CVP, increase incase of HF decrease in FVD

Heart
– Inspection, palpation, percussion , auscultation,
S1 S2
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
PHYSICAL ASSESSMENT
Inspection
of Extremities
–Capillary refill time (CHF, hypertension ), hematoma
(surgery & cath ), vascular changes, peripheral
edema, lower extremeties ulcer
Lungs
–Tachypnea ( HF, pain, anxiety ), chynestokes
breathing ( pulmonary edema ), dry cough, crackles
and whezes
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PHYSICAL ASSESSMENT

Abdomen
– Hepato jugular reflux, bladder distention

RISK FACTORS
– Nonmodifiable: age, positive family history,
race &gender
– Modifiable: hyperglycemia, hyperlipidemia,
hypertension, inactivity, smoking, obesity &
type A personality
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DIAGNOSTIC EVALUATION
Laboratory
tests
–Cardiac enzymes
Released from injured cells when ruptured
the membrane
Most of them are not specific for one type
of cell
Iso enzymes are more specific, createnine
kinase ( CK ) and its iso enzyme( CK-MB ),
lactic dehydrogenase (LDH) , troponin I

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DIAGNOSTIC EVALUATION
– Blood chemistry

Lipid profile
– A- cholesterol (less than 200 mg / dl ),
required for hormonal synthesis, found
mainly in brain tissue and liver
– B- triglycerides ( 40 – 150 mg / dl )
source of energy, cell wall, store in a
dipose tissue
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DIAGNOSTIC EVALUATION
– C- LDL ( less than 130 mg / dl ) transport
cholesterol from blood to peripheral
tissues, synthesized from VLDL
– D- HDL ( 35 – 65 mg / dl M, 35 – 85 mg
/ dl F ) transport cholesterol from
peripheral tissues to the liver, cardio
protective effect, increase with exercise
and decrease with smoking DM and
obesity
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Serum
electrolytes
–K, Na, Ca and other electrolytes can reflect the heart
function as well as fluid & electrolyte disturbances
BUN
–May indicates impaired renal function and impaired
cardiac output
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DIAGNOSTIC EVALUATION

Coagulation studies
– Partial Thromboplastine Time ( PTT ) 25 – 40 sec, used
to regulate heparin dosage, 1.5 – 2.5 is the theraputic
range
– Prothrombin Time ( PT ) less than 13 sec, used to
regulate warfarin, 1.5 – 2.5 times of PT is the theraputic
range
– International Normalized Ratio ( INR ) standarized
method for reporting PT level, used for regulating
warfarin dosage
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Chest
X-Ray ( CXR )
–Assess size, position of the heart,
cardiothoracic ratio ( CTR ), position of central
lines
Electrocardiography ( ECG )
–Can be either on bed side or from a distance,
12 leads ECG, continuous monitoring,
telemetry monitoring 2 or 3 leads monitoring )
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DIAGNOSTIC EVALUATION

Cardiac Stress Test
During time of increased demand, abnormalities
in cardiovascular functions are more likely to
be detected, used to evaluate the heart function,
coronary arteries as well as the cause of chest
pain
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Con.
–Exercise stress test: pt walk on a treadmill or
pedals (stationary bicycle), the goal is to
increase HR and monitored for ECH changes,
arrhythmias, hypotension, pain, dyspnea and
dizziness. Pt fast 4 hours before test, nurse
needs to instruct pt about the test
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DIAGNOSTIC EVALUATION

Echocardiography: a non invasive ultrasound used
to examine size shape and cardiac motion, used
also to evaluate heart function, valves and
peripheral effusion

Pharmacologic stress test: used for pts
unable to achieve target HR, Dipyridamole,
Adenosine & dobutamine are used for this
purpose
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Cardiac
catheterization
–Invasive diagnostic procedure involves introduction
of specific catheter into Rt & Lt side blood vessels
under fluoroscopy. Its used to evaluate coronary
arteries patency, heart function as a pump, vascular
system and heart structure
–Its considered as a highly critical procedure
–Take in consideration: monitoring IV line, BP, ECG,
LOC, well prepared staff to provide ACLS, revission
of lab tests
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CORONARY
VASCULAR
DISORDERS

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ATHEROSCLEROSIS

Definition: abnormal accumulation of lipid or
fatty substances and fibrous tissues in vessel wall
Pathophysiology
–It begins as a fatty streak, this streak develop into
advanced lesion which involves inflammatory
response, T.lymphocytes and monocytes ingest the
lipid and form fibrous cap called Atheroma Plaque,
this protrude into the lumen of the vessel narrowing
and obstruct it
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ATHEROSCLEROSIS

Clinical manifestations
– Acute onset chest pain, ECG changes,
dyarhythmias & death

Risk factors
– Age, family history of non modifiable risk
factors, high cholestrol, cigarette smoking,
hypertension & DM
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PREVENTION
Control cholestrol level, LDL less than normal
Dietary control decrease fat & increase fiber
Medication to decrease serum fat & cholesterol
Quit smoking
Early detection & control hypertension
Control DM
Gender & estrogen level
Behavior pattern
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ANGINA PECTORIS
Definition:
it’s a clinical syndrome ch.ch
by episodes of pain or pressure in the
anterior chest
Pathophysiology
–Caused by atherosclerotic disease,
associated with significant obstruction of
CA and any cause that increase demand
or decrease supply
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ANGINA PECTORIS

Clinical manifestation
– Pain deep behind upper third of sternum
mediated to jaw neck shoulders & left
arm
– Chest heaviness & tightness with choking
sensation
– Weakness, numbness in arms, wrist &
hands
– Short breathing, pallor, dizziness, nausea
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& vomiting
ANGINA PECTORIS
Medical
Management: the objectives are to
decrease the demand and increase blood supply to
the heart
–Pharmacological therapy & control risk factors
Nitroglycerides, beta blockers, Ca channel blockers &
antiplatlet agents ( aspirin heparin )
–Revascularization procedures
Coronary artery bipass ABG
Percutaneus transluminal coronary angioplasy PTCA
–O2 administration
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MYOCARDIAL INFARCTION MI
Definition: death of heart tissue caused by
ischemia, a process by which areas of the
myocardial cells destroyed
Clinical manifestation
–Sudden sever chest pain radiated to left arm
–anxious & restlessness,
–cool pale moist skin, sweating
–tachypnea & tachycardia
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MYOCARDIAL INFARCTION MI
 Diagnostic
findings and assessment
– Pt history, ECG: T wave & ST
segment changes echo & lab tests
 Medical management: objectives are to
- minimize myocardial damage,
- preserve function & prevent
complications
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MYOCARDIAL INFARCTION MI
– Emergent PTCA to open occluded
artery
– Pharmacologic therapy:
– thrombolytic ( STK, TPA ),
– Analgesics
– ACE inhibitors
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MITRAL STENOSIS
Definition: an
obstruction of blood flowing from
the left atrium into the left ventricle, most often
caused by rheumatic endocarditis
Clinical manifestation
–Progressive fatigue due to low cardiac output,
–hemoptesis, dyspnea
–cough & repeated respiratory infections
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MITRAL STENOSIS
 Management
– Antibiotic
– Valvuloplasty
– medication in case of surgical failure
– PTCA may relieve symptoms
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MITRAL REGURGITATION
Definition: blood
flowing back from the left
ventricle into the left atrium during systole, the
margins of the mitral valves cannot close during
systole
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MITRAL REGURGITATION
Clinical manifestation
– Chronic often asymptomatic
– Acute :severe congestive heart failure,
– dyspnea, palpitation, fatigue & weakness,
shortness of breath & cough from pulmonary
congestion

Management
– Surgical mitral valve replacement
– Valvuloplasty
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AORTIC STENOSIS
Definition: narrowing
of the orifice between the
left ventricle &the aorta, congenital malformation
Clinical manifestation
–Many pts are asymptomatic
–Exertional dyspnea, dizziness, fainting,
angina pectoris, low pulse pressure ( 30 mmhg
or less )
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AORTIC STENOSIS
 Management
– Prophylactic antibiotic to prevent
endocarditis
– Medication as prescribed for
dysrhythmias
– Surgical replacement for the aortic valve
– One-or-two-balloon percotaneous
valvuplasty
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AORTIC REGURGITATION
Definition: flow
of blood back into the left
ventricle from the aorta during diastole,
congenital deformities, endocarditis, syphilis,
dissecting aneurysm
Clinical manifestation
–Force full heart beat ( head & neck ),
– arterial pulsation
– exertional dyspnea and fatigue, difficult
breaths specially at night
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AORTIC REGURGITATION

Management
– Prophylactic antibiotic to prevent
endocarditis
– Treatment of heart failure and dysrhythmias
– Aortic valve replacement ( treatment of
choice )
– Surgery is recommended for pt with Lt
ventricular hypertrophy regardless the
presence or absence of symptoms
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CARDIOMYOPATHIES
Definition: it’s
a heart muscle disease of
unknown cause, an inherited genetic disorder
Types
–Dilated or congestive cardiomyopathy
–Hypertrophic
–Restrictive or constrictive
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CARDIOMYOPATHIES

Clinical manifestations
– A symptomatic for many years
– Shortness of breath, nocturnal dyspnea, cough,
chest pain, palpitation, dizziness & fatigue
 Medical management
– Mange precipitating cause, correct heart failure,
diet & exercise regimen, control dysrhythmias,
– Implanted electrical device
– myomectomy & heart transplantation
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RHEUMATIC ENDOCARDITIS
Definition: inflammation
of endocardium result from rheumatic
fever caused by a group A streptococcal infection
Clinical manifestation
–Tiny translucent growth, pin-head size beats of the valve flaps, serious
dysrhythmias, pneumonia, valvular deformities, murmur, thrill &
palpitation
Medical management
–Eradicate organism & prevent complications
–Penicillin as a drug of choice ( long term therapy )
Nursing management
–Teach pt about disease, prevention & treatment
–Instruct about long term therapy
–Instruct for prophylactic therapy
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PERICARDITIS
Definition: inflammation of
the pricardium
Clinical manifestations
–Pain over pericardium, clavicle, neck &
scapula
–friction rub, aggravated by breathing&
turning in bed, relieved by sitting up
– dyspnea, low cardiac output, increase WBC,
pt appears extremely ill
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PERICARDITIS

Medical management
– Determine& treat cause, bed rest,
– analgesics NSAID, corticosteroids
– prevent pericardial effusion
 Nursing management
– Medication as prescribed, gradual
increase in activity unless fever, pain and
friction rub reappear
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ACUTE PULMONARY EDEMA

Definition: abnormal accumulation of fluids in
the lungs either in interstitial space or in alveoli
Clinical
manifestations
–Restlessness, confusion, breathlessness
– sense of suffocation, rapid weak pulse
– distended neck veins, cold hands, cyanosed nail
beds, gray skin
– cough & decrease O2 saturation
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ACUTE PULMONARY EDEMA

Medical management: to improve res.
Exchange
– O2 therapy, medication and nursing
support
– Intubation and mechanical ventilator in
severe failure
– PEEP, oximetry ABGs
– Morphine ( 2-5 mg ) to reduce anxiety
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ACUTE PULMONARY EDEMA

Duretic therapy
– To increase rate of urin production, decrease
ECF, thiazide & loopduretics ( dose depends on
indication, clinical signs & renal function )
– Medications to increase myocardial
contractility & cardiac output ( digitalis )
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ACUTE PULMONARY EDEMA
 Nursing
management
– Position pt to promote circulation
– Psychological support
– Monitor medication
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CARDIAC FAILURE
congestive heart failure
Definition: inability
of heart to pump sufficient blood
to meat needs of tissue for O2 & nutrient
Clinical
manifestations
–In adequate tissue perfusion, dizziness, confusion,
fatigue, cool extremities,
–exercise & heat intolerance
– low urine output, high venous pressure,
pulmonary & peripheral
edema, weight gain
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CARDIAC FAILURE
congestive heart failure
 Management
– Counseling & education for regular
exercise, sodium restriction, avoid
excessive fluid intake, medication
based on symptoms, O2 therapy
intubation if needed, transplantation
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CARDIAC FAILURE
congestive heart failure
 Nursing
management
– I&O, daily wt, daily auscultate lung
sounds, jugular vein assessment,
edema, pulse rate, BP, skin turgur &
manage complications
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
VASCULAR
SYSTEM
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The
vascular system consists of two interdependent
systems
–Right side of the heart pump
–Left side of the heart pump
BLOOD VESSELS
Arteries and arteriols
–High-pressure system, thick wall, transport oxygenated blood
away from the heart
–Located in protected areas away from skin surface
–Wall of arteries and arteriols composed of 3 layers
Intema: inner indothelial layer, contact with blood
Media: smmoth elastic tissue, constrict & dilate vessels
Adventitia: connective tissue, anchors vessels to surrounding

Capillaries
–Single layer of endothelial cells, permits rapid & effective
transport of nutrients to the cells & removal of metabolic waste
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Veins
and venules
–Larger in diameter than arteries but the wall are
thinner because there is a less muscle & elastic tissue
in the tonic & media, this allow these vessels to
distend more than arteries
–Equipped by one-way bicusped valves that prevent
blood to back flow
–Valves composed of endothelial leaflets
–Transport deoxygenated blood from the body to the
heart
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Health History and Clinical
Manifestations
A muscular cramp-type pain in the extremities
reproduce with the same degree of exercise or
activity & relieved by rest is experienced by
patients with peripheral arterial insufficiency
Intermittent claudication: its due to inability of
arterial system to provide adequate blood flow to
the tissues in the face of increased demand for
nutrients during exercise
–Rest pain: worse at night & may interfere with sleep
–As general role, the pain of intermittent claudication
occurs one joint level below the disease process
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Changes in skin appearance and temperature
–Inadequate blood flow cause cool & pale extremities
–Redish-blue discoloration of extremities (rubor)
–Additional changes resulting from chronically
reduced nutrients supply like: loss of hair, brittle nails,
dry skin, atrophy, ulceration, gangrene by traumatic
events
Pulses
–Determining the presence or absence as well as
quality of peripheral pulses to assess the status of
peripheral arterial circulation
–Absence of pulse may indicates the size of stenosis
(narrowing or constriction )
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Diagnostic Evaluation
Doppler
ultrasound
–When pulses cannot be reliably palpated, use of a
microphne-like hand held doppler ultrasound device
(tranceducer or prob) may be helpful in detecting and
assessing peripheral flow
–Procedure
Exercise
testing
–Used to determine how long can a pt walk &
measure ankle systolic BP in response to walking
–A normal response is little or no drop in systolic BP,
it drops in true claudication
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Angiography
–Used to confirm the diagnosis of occlusive arterial disease
when considering surgery or intervention
–Injecting radiopaque contrast agent directly into vascular
system to visualize the vessels
–Pts experience temporary warmth during injection, side
effects are local irritation, allergic reactions, dyspnea, N & V,
sweating tachycardia, numbness
–Additional risks: vessel injury, bleeding & strock
Contrast
plebography ( venography )
–Performed if pt is to undergo thrombolytic therapy
–Contrast is injected via dorsal foot vein then X-ray image will
disclos an unfilled vein
–Injection may cause brief painful inflammation of the vein
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MANAGEMENT OF ARTERIAL
DISORDERS
Arteriosclerosis & Atherosclerosis
–Arteriosclerosis: the most common, its hardening of the
arteries, the muscle fiber & endothelial walls of small arteries
& arteriols become thickened
–Atherosclerosis: affect the intema of the large & medium size
arteries due to accumulation of lipids, calcium, blood
components, fibrous, carbohydrates on the internal layer
Risk factors
–Modifiable: diet, DM, high BP, stress, life style
–Non modifiable: age, gender
Clinical manifestations
–Depends on tissue or organ affected,
–Coronary: (angina, MI ), cerebrovascular ( TIA, strocke),
Aorta ( aneurysm ), renovascular ( hypertension )
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Medical
management
–Modification of risk factors to improve circulation
Surgical
management
Radiologic intervention
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PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE
Arterial Insufficiency
of extremities is usually found in older
than 50 yrs, most often in men, legs are most frequently affected
–Distal occlusive disease frequently seen in pts with DM &
elderly pts
Clinical manifestation
Intermittent claudication described as aching, cramp, fatigue,
weakness in joint muscles below stenosis or occlusion area
Decrease ability to walk, increase pain with ambulation
Ischemic pain at rest & worse at night
Bruit sound on auscultation


Absence of peripheral pulse
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PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE

Medical management
–
–
Exercise program with weight reduction
Smoking cessation
Surgical management
- Grafting
- Endarterectomy
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Nursing Management
Maintaining
circulation
–Check pulses of affected extremities, note symmetry,
color, temp., capillary refill, sensory & motor hourly
–Doppler evaluation of vessels distal to bypass graft
Monitoring &
managing potential complications
–Urine output, CVP, pulse, leak, hematoma & edema
Promoting home
& community based care
–Discharge plan, pt education, assess ability to change
life style & self care
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AORTIC ANEURYSM
It’s a localized sac or dilation involving an artery
formed at a weak point in vessel wall
THORASIC AORTIC ANEURYSM
–Caused by atherosclerosis in men aged ( 40-70 yrs )
–Most common is dissecting aneurysm, 1/3 of cases
die of rupture
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AORTIC ANEURYSM

Clinical manifestation
– Pain in supine position, dyspnea, hoarseness or
aphonia ( complete loss of voice ), dysphagia

Medical management
– Surgical repair, control BP, correcting risk
factors
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ABDOMINAL AORTIC ANEURYSM
most common cause is atherosclerosis, affect men
4 times than women, occur mostly below renal stenosis,
untreated outcome is rupture & death
Clinical
manifestations
–Abdominal heart beat on lying position,
– abdominal mass
– thrombing
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ABDOMINAL AORTIC
ANEURYSM
 Medical management
– Surgery is the treatment of choice
 Bypass graft, endovascular graft ( suturless )
 Nursing management
– Assessment before surgery, post op. systematic
monitoring, neurological assessment, signs of
impeding rupture ( abdominal & back pain )
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ARTERIAL EMBOLISM
Its acute vascular occlusion due to an embolus or acute
thrombosis
Causes
–Iatrogenic injury ( insertion of catheters ), trauma
from fractures, crush injury, penetrating wound,
thrombi development in heart champers as a result of
(AF, MI, CHF)
Clinical manifestations
–Cessation of distal bld flow, gradual loss of sensory
& motor function, pain, pallor, cold, paresthesia, pulse
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ARTERIAL EMBOLISM

Medical management
– Surgery ( embolectomy ),
– Medication ( heparin bolus5000-10000 then contentious
infusion) Thrombolytic therapy (STK; streptokainase)

Nursing management
– Pre-op. bed rest, warm at room temp. protection
from trauma
– Post-op. encourage movement & continue
anticoogulants
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VENOUS DISORDERS
DVT, THROMBOPHLEBITIS and
PHLEBOTHROMBITIS
Clinical manifestations
–Massive swelling, tenderness,
– warmer affected extremity,
– homans sign,
–heaviness & functional loss
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VENOUS DISORDERS

Medical management
– Anti coagulants (heparin 5-7 days), low
molecular-weight heparin, thrombolytic therapy
– Surgical management: thromboectomy when
anti coagulant is contraindicated or danger of
pulmonary embolism is extreme
 Nursing management
– Monitor PT, PTT, Hb, platlets, report bleeding,
assess anti coagulant therapy, monitor &
manage complications, provide comfort &
apply elastic pressure stockings.
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CHRONIC VENOUS INSUFFICIENCY
Obstruction of venous valves in the legs or a
reflux of blood back through the valves
Clinical manifestations
–Chronic venous stasis, altered pigmentation, pain,
stasis dermatitis, stasis ulceration, dry skin, cracks &
itches
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CHRONIC VENOUS
INSUFFICIENCY

Medical & nursing management
– Reducing venous stasis & prevent ulceration
– Elevating legs to reduce edema & promote venous
–
–
–
–
–
return
Encourage walking
Compression with elastic stockings to reduce blood
pooling
Protect from trauma
Keep skin dry & soft
Immediate report for signs of ulceration
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LEG ULCERS
Its an excavation of the skin surface that occurs
when inflamed necrotic tissue sloughs off
Clinical manifestations
–Open inflamed sore, pain & edema, discharge may
be present, heaviness, itching, area may covered with
eschar, gangrene
Medical
management
–Pharmacologic therapy (antibiotics based on culture)
depridement, topical therapy, stimulated healing by
Epigram
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VARICOSE VEINS
Abnormally dilated torturous superficial veins
caused by incompetent venous valves
Clinical manifestations
–Dull aches, muscle cramps, increase muscle fatigue,
ankle edema, S&S of venous insufficiency if obstruct
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VARICOSE VEINS

Medical management
– Surgery ( ligation ) & sclerotherapy

Nursing management
– Bed rest 1st 24 hours & start walking at 2nd day
5-10 min /2 hours, elastic pressure stockings,
elevate foot, discourage standing & sitting,
promote comfort (analgesia), home &
community based care
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NURSING PROCESS
Assessment
–Sub. (interview) & obj. (physical assessment)
Diagnosis
–Alteration in peripheral tissue perfusion
–Pain, risk for impaired skin integrity, knowledge
deficit regarding self care activities
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NURSING PROCESS

Implementation
–
–
–
–

Lower the extremity below level of the heart
Encourage moderate amount of walking
Maintain warm & discourage nicotine use
Administer prescribed vasodilators, adrenergic block
agents
Evaluation
– Goal met evidenced by: extremities warm to touch,
color improved, decrease muscle pain, tolerate
performing exercise 6 times / day
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HYPERTENTION
Definition: it’s a raise of blood pressure above normal
range” systolic above 140 mmhg & diastolic above 90
mmhg” over sustained period
A multifactorial condition
A sign ,a risk factor , and a disease .
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HYPERTENTION

Types & causes
– 1- Primary (idiopathic essential ) hypertention
80-90% of cases are of unknown cause but
predisposed by: old age over 60 yrs, obesity,
black race, atherosclerosis
– Benign or chronic hypertention
 Rise is usually slight to moderate & continue
to rise slowly often asymptomatic ( silent
killer )
– Malignant (accelerated) hypertention
 BP very high & continue to raise rapidly,
diastolic pressure in excess of 120 mmhg &
the effects areHusni
quickly
apparent
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
HYPERTENTION

2- Secondary hypertention: Increase BP
from an identified cause resulting from
other disease
 Causes
– Renal disease, endocrine disorders, age & sex,
stressful occupation & situation, family
tendency, DM, dyslipidemia, smoking &
alcohol
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HYPERTENTION
 Clinical
manifestations
– High blood pressure reading
– Headache, epistaxis, angina,
– dizziness, dyspnea, ringing in ears
– Retinal changes “may be papilledema”
– “ a common consequence M.I. & CAD
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HYPERTENTION
 Medical management
– Treatment of underlying cause
– Life stile modification :– Management of predisposing factors (
low salt diet, decease weight, stop
smoking, decrease stress level)
– Pharmacologic therapy (diuretics,
vasoconstrictive agents & agents to
decrease cardiac output )
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Nursing Process
Nursing Diagnosis
–Knowledge deficit ( medication & disease process )
–Non compliance with therapeutic regimen
E.O
–Pt will understand disease process & its treatment
–Pt will participate in self care program
Implementation
–Allow pt to rest & relax, medication as prescribed, report side
effects, educate pt about rebound hypertention that occurs if
therapy suddenly stopped
–Measure BP routinely, follow up appointments,
–Educate pt about arthostatic hypotention so to stand gradually
–Life style modification
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