Arteriosclerosis

RISK FACTORS
• Older age (> 40 years)
• Male gender
• Mayor
– Hyperlipidemia (LDL)
– DM
– Hypertension
– Cigarette smoker
• Minor
– Physical activities
– Menopause
– Emotional Stress
– Carbohydrate Intake >>
– Alcoholism
– Hormonal contraception
 ARTERIOSCLEROSIS
• Is the generic term for three different patterns of arterial disease
that produce narrowing of the lumen, thickening of arterial walls,
and loss of elasticity,

1. Atherosclerosis  medium and large arteries  atheromas in the

intima. Atheromas narrow arterial channels, damage the underlying
tnc.media, and may progress to calcification, ulceration with
thrombosis, and intraplaque hemorrhage
2. Monckeberg’s arteriosclerosis  medium and small arteries,
characterized by bandlike calcifications within the tunica media,
specially of femur, tibia,ulna and genital arteries  without narrowing
of lumina . Manifestation > 50 ys old
3. Arteriolosclerosis  arteriolae dan small arteries, characterized
by proliferative fibromuscular and endothelial thickening of the
walls of small arteries and arterioles. Two subtypes have been
described : hyaline arterilosclerosis and hyperplastic
arteriolosclerosis
 ARTERIOLOSCLEROSIS
• HYALINE ARTERIOLOSCLEROSIS
-Occurs in old patient,with mild hypertension and mild Diabetes.

• HYPERPLASTIC ARTERIOLOSCLELORIS
-Occurs in malignant hypertension
Arteriosclerosis
ATHEROSCLEROSIS
 Major components of well
developed atheromatous plaque
Atherosclerotic plaque

F: Fibrous cap,
projecting into
L: Lumen, and
C: Necrotic core
Progression of Occlusion
Natural history of Atherosclerosis
PLAQUE DEPOSIT
ORIGINAL DIAMETER
Complication of atherosclerosis
 Systemic Hipertension
(systolic ≥ 160mmHg, diastolic ≥ 95 mmHg)
• Essensial Hypertension : 95% (benign 90%,
malignant 10%)
Ethiology:
genetic, ras, environment (Stress. Diet),
neurogen, membrane cell disturbances,
increase “pressor agent” plasm

• Secondary Hypertension : 5% (benign 80%,

malignant 20%)
Ethiology:
renal disease, alcoholism, adrenal disease,
renin production tumor, toxaemia gravidarum
 Symptoms

• Most asymptomatic
• Intermittant claudication
• Rest pain
• Ulcers and gangrene
INTERMITTENT CLAUDICATION (LEG ATTACK)

• Derived from the Latin word claudicatio i.e. “to

limp”
• Caused by PAD in the lower extremities
• Characterized by pain, ache, cramp, tightness or
sense of fatigue in leg muscles with activity
• Symptoms relieved by rest
• Results in reduced mobility and quality of life
WHAT CAUSES INTERMITTENT CLAUDICATION?

• Atherosclerosis in peripheral arteries of legs

During exercise, oxygen demand increases

Muscles operate anaerobically

Produce lactic acid and other metabolites

Leg pain
• Lactic acid and other metabolites washed away on
rest
 INTERMITTENT CLAUDICATION IS INDICATIVE
OF SYSTEMIC ATHEROSCLEROSIS

• 40-60% of patients with intermittent claudication

have concomitant CAD
 PRIMARY SITES OF
INVOLVEMENT
Femoral & Popliteal
arteries: 80-90%

Tibial & Peroneal

arteries: 40-50%

Aorta & Iliac arteries:

30%
 DIAGNOSIS
• History taking
• Careful examination of leg
• Pulse evaluation
• Ankle-brachial index (ABI):
SBP in ankle (dorsalis pedis and posterior tibial arteries)
___________________________________
SBP in upper arm (brachial artery)
 WHY IS IT NECESSARY TO TREAT
INTERMITTENT CLAUDICATION ?

• Symptoms worsen in 25% of patients

• Approximately 5% will require
amputation within 5 years
• Around 5-10% have critical limb
ischemia; risk of limb loss
 GOALS OF TREATMENT
• To relieve exertional symptoms and
improve walking capacity
• To improve quality of life
• To reduce total mortality as well as
cardiac and cerebrovascular morbidity
and mortality
 MANAGEMENT
• Risk factor modification
• Exercise therapy
• Antiplatelet therapy
• Medical therapy targeted at symptoms
• Revascularisation procedures
• Amputation needed in some cases
Basis for Wounds of Arterial Origin

• Arteriosclerosis – “hardening of arteries”

-calcification of arteries of all sizes
- loss of elasticity of arterial walls

Atherosclerosis – fibrous “plaque”

- thickening of inner coat (intima)
- fatty degeneration of middle layer (media)
 Events Producing Wounds of
Arterial Origin
• Diminished arterial flow
• Thrombus or microembolus formation
• Blockage - most often at bifurcations
• Tissue hypoxia and cell death
 Appearance of Limb in Arterial
Disease – Trophic Changes
• Pale, cool skin
• Abnormal toenail growth
• Hair absent
• Muscle atrophy
• Edema
Trophic Skin Changes in Arterial
Disease
 Arterial Diseases associated with
Wound Development
• Arteriosclerosis obliterans
• Other Examples
- Diabetes
- Vasculitis (RA)
- Sickle Cell Disease
• Thromboangiitis obliterans*
 Arteriosclerosis obliterans
• Disease of large and medium sized arteries
• Associated with:
– High blood pressure
– Hyperlipidemia
– Arterial occlusion particularly at bifurcations
Necrosis of Toe in Arteriosclerosis
obliterans
Heel Ulcer in Arteriosclerosis
Obliterans
WHEN ARTERIES BECOME OCCLUDED
HEALTHY ARTERIES ARE BLOOD VESSELS
WHICH ARE FLEXIBLE,
STRONG & ELASTIC
THEIR INSIDE LINING IS SMOOTH SO BLOOD
CAN FLOW WITHOUT RESTRICTION
Risk Factors cause arteries to become
occluded.
 ARTERIAL DISORDERS
PERIPHERAL ARTERIAL INSUFFICIENCY /
OCCLUSION

ASSESSMENT:

WEAK/ ABSENT PULSES

PAIN /W LEG ELEVATION
SKIN COOL TO TOUCH
PALE SKIN COLOR
THICKENED TOENAILS
 ARTERIAL DISORDERS
GOALS:
1. IMPROVE PERIPHERAL ARTERIAL
CIRCULATION WITH EXERCISE

REGULAR EXERCISE SUCH AS WALKING

INCREASES CIRCULATION
GOALS:
2. PREVENT VASCULAR COMPRESSION

AVOID RESTRICTIVE CLOTHING, CROSSING

LEGS, SITTING FOR PROLONGED PERIODS
GOALS:
3. RELIEVE PAIN

CONSIDER ANALGESICS SO PATIENT CAN

PARTICIPATE IN ACTIVITIES
GOALS:
4. MAINTAIN TISSUE INTEGRITY
• AVOID TRAUMA, WEAR CORRECT SHOE GEAR
(NO BARE FEET!)
• TEST WATER TEMP WITH HAND NOT FOOT!
• REGULAR PODIATRY CARE
• GOOD NUTRITION
 ANGIOPLASTY

• BALLOON
ANGIOPLASTY
CATHETER
• INSERTED THROUGH
AN ARTERY
• BALLOON IS
INFLATED AND
COMPRESSES USED FOR INSERTION
LESION OF STENTS
ANGIOPLASTY
 MEDICAL MANAGEMENT
THROMBOLYTIC THERAPY
USED TO DISSOLVE CLOTS:
Retavase, streptokinase, tPa

SURGICAL MANAGEMENT
1. GRAFTING – BYPASS SURGERY
2. ENDARTERECTOMY – REMOVAL OF
ATHEROSCLEROTIC PLAQUE
3. AORTO/FEMORAL/TIBIAL BYPASS
 ARTERIAL DISORDERS & GOALS

1. ALTERED PERIPHERAL TISSUE PERFUSION

( ARTERIAL BLOOD FLOW)
GOAL: MAXIMIZE TISSUE PERFUSION
2. ACTIVITY INTOLERANCE – VASCULAR SUPPLY
CAN NOT KEEP UP WITH TISSUE DEMANDS
GOAL: MANAGE ACTIVITY WITHIN LIMITATIONS
3. ANTICIPATORY GRIEVING RELATED TO
POTENTIAL LOSS OF LIMB
GOAL: EXPRESS CONCERNS

4. BODY IMAGE DISTURBANCE AS RELATED TO

LOSS OF BODY PART
GOAL: DISCUSS IMAGE & OPTIONS
5. IMPAIRED TISSUE INTEGRITY AS RELATED
TO  CIRCULATION
GOAL: MAINTAIN TISSUE INTEGRITY
6. KNOWLEDGE DEFICIT OF SELF CARE
ACTIVITIES

GOAL: EDUCATE PATIENT

7. PAIN DUE TO ISCHEMIA
GOAL: RELIEVE PAIN
8. POTENTIAL FOR INJURY DUE TO  SENSATION
GOAL: EDUCATE PATIENT TO INSPECT FOR INJURY,
WATCH FOR TRAUMA

9. SLEEP PATTERN DISTURBANCE DUE TO REST PAIN

GOAL: MAXIMIZE SLEEP

 INTERVENTIONS

1. RISK FACTOR MODIFICATION

SMOKING (Most significant RISK FACTOR)
 NICOTINE CAUSES VASOSPASMS
WEIGHT LOSS
 REDUCES WORKLOAD IN
EXTREMITIES
LOW FAT DIET WILL RETARD
PROGRESSION OF ATHEROSCLEROSIS
CONTROL HTN
 INTERVENTIONS

2. PAIN MANAGEMENT
INTENSITY IS VARIABLE
MANAGEMENT- RTC
PAIN MEDICATION
(MAY NOT BE EFFECTIVE)
 DEPENDENT POSITION MAY 
COMFORT
 INTERVENTIONS

3. MAINTAIN FLUID VOLUME

IN SEVERE STENOSIS PATIENT MUST MAINTAIN
SUFFICIENT BLOOD PRESSURE TO AVOID COMPLETE
OCCLUSION
 INTERVENTIONS
4. ACTIVITY
 MONITOR CLAUDICATION
 TEACH PATIENT – PAIN IS NOT
HARMFUL, BUT A BODY SIGNAL FOR NEED TO
REST
 EMPHASIZE: EXERCISE INCREASES
COLLATERAL CIRCULATION
 CHECK WITH DOCTOR ABOUT ANY
EXERCISE
PROGRESSION SHOULD BE GRADUAL
Thank you …