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Atherosclerosis/
Hyperlipidemia/ & Hypertension
Presented by: Wanda Lovitz, APRN
1.
Identify risk factors, common for atherosclerosis.
2.
Describe the pathophysiology of atherosclerosis.
3.
4.
5.
List the blood chemistry tests used to diagnosis
hyperlipidemia and state the normal values.
Discuss how blood pressure is affected by changes
in cardiac output and systemic vascular resistance.
Describe the risk factors for the development of
primary hypertension
5. Identify the MOA, common adverse reactions, and
nursing implications of selected commonly used lipid
lowering agents.
6. Describe how hypertension and orthostatic
hypotension is detected, classified, and managed.
7. Identify the end-organ consequences of
inadequately controlled hypertension.
8. Discuss the diagnosis and management of
hypertensive emergencies and hyptensive urgency.
A.
B.
C.
D.
A. In the intestines
B. In the liver
C. From bile acids
D. From fatty foods
0%
A.
0%
B.
0%
C.
0%
D.
A.
B.
C.
A. Free fatty acids
B. Lipoproteins
C. Cholesterol
0%
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0%
B.
0%
C.
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1.
Carbohydrates- 1st choice

2.
Fat(Triglycerides – neutral fats)
- 2nd Choice
◦ Conditions where FFA needed for energy because not enough CHO available
 Starvation
 Diabetes
A.
B.
C.
D.
A. HDL-C
B. Triglyercies
C. LDL-C
D. VLDL-C
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0%
B.
0%
C.
0%
D.

See BB Unit 2 Materials

Review BEFORE lecture

Contents essential to understanding atherosclerosis

There may be 0-2 questions from this on the Exam
A.
B.
C.
D.
A. Macropahges
B. Renin
C. Foam Cells
D. Fatty acids
0%
A.
0%
B.
0%
C.
0%
D.

Statins:
atorvastatin/Lipitor
 Bile Acid Sequestrant
cholestraymine/Questran
Triglyceride lowering:
fenofibrate /Tricor
Hypertension & stroke
Heart Attack
◦ Hypertension

Family h/o early heart
disease
◦ Cigarette smoking
◦ Diabetes mellitus
◦ Elevated LDL-C
◦ *Elevated C-reactive protein
(CRP) – is an emerging risk
factor
◦ Low HDL-C
◦ Diet high in saturated fat
◦ Physical inactivity
◦ Obesity
A lipid or fat found in foods and made in our bodies
A lipoprotein formed in the liver- endogenous
Comes from our diet - exogenous




Necessary for cell wall membranes
Protects nerve fibers
Needed to digest food
Excess cholesterol deposits in arteries
◦ can form plaques = atherosclerosis

C-Reactive Protein is a PROTEIN found in the blood

Levels rise in response to inflammation

◦ is an acute-phase protein
CRP is used mainly as a MARKER of inflammation
 Arterial damage results from white blood cell
invasion and inflammation within the wall
Recent research suggests that patients with elevated
levels of CRP are at an increased risk of diabetes,
 hypertension and cardiovascular disease

 Imbalance
in cholesterol
supply and demand!
◦ What happens when
cholesterol is NOT used for cell
functions?
 STORED IN THE FORM OF
TRIGLYCERIDES
◦ Why is this a problem (excess
cholesterol)?
 Initiates and progresses
process of
ATHEROSCLEROSIS
 Defined:
◦ High levels of fatty substances in blood
 About 41 million Americans have high cholesterol
levels
◦ Contributes to coronary heart disease (CAD) and
cerebrovascular disease/CVD
 About 100 million Americans have “borderline” high
cholesterol levels
 LIPOPROTEINS
are formed in THE LIVER
◦ Main function –transport special lipids throughout
the body
 TRIGLYCERIDES
(along with CHO)
◦ provide energy for metabolic processes
 PHOSPHOLIPIDS
AND CHOLESTEROL
◦ – main function is for form cell membranes
 VLDL = very low-density lipoproteins – mainly
transports triglycerides
 LDL = low-density lipoproteins – DEPOSITS
cholesterol on the arterial wall
 HDL = high-density lipoproteins – REMOVES
cholesterol from the bloodstream and arterial walls
 Total
Cholesterol = HDL + LDL + 20% of
triglyceride score
 Atherosclerosis
◦ Target
 Intermediate and large arteries
◦ Process
 Smooth muscle cells and
lipids collect along intimal
surface
 Results in narrowing
of lumen
diameter/reduction of
blood flow
◦End Result?
 Increased morbidity & mortality
 Sx




depend on site of affected artery:
Heart
◦ Angina, heart attack
Brain
◦ TIA, stroke
Extremity
◦ intermittent claudication, blockage of femoral arteries
Blood Vessel weakening
◦ aneurysm
Ischemia then INFARCTION
Circulating monocytes
adhere to injured
endothelium
1.
2. What causes the injury?
Smoking, HTN, inflammation
3. Monocytes slide through
endothelial junctions
 Enter subendothelial space
 Engulf modified lipids
 Form Foam Cells
Circulating monocytes
adhere to injured
endothelium
1.
2. What causes the injury?
Smoking, HTN, inflammation
3. Monocytes slide through
endothelial junctions
 Enter subendothelial space
 Engulf modified lipids
 Form Foam Cells

Fatty Streaks
◦ Thin, flat, yellowish
discolorations
◦ Increase over time
◦ What are they composed of?
 Cells and lipids
 PLAQUES (atheromas)
◦ Consist of
 Cap
 Smooth muscle cells
 Foam cells
 Necrotic core
Open lumen
Cross section of artery
Necrotic core
CALCIUM CAN INFLITRATE THE PLAQUE AD OVERTIME MAKE THE ARETERY HARD AND INFLEXIBLE
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Wall of artery is damaged and BAD
LDL-C GETS INTO THE ARTERIES

1. MACROPHAGEs activated to
consume LDLC
2 MACROPHAGES become FOAM CELLS
and imbed in vessel wall
3. Foam cells accumulate and become
FATTY STREAKS that imbed in vessel
wall
4. FIBROUS CAPSULE around foam cells
form plaque
5. Plaque expands into elastic layer of
vessel
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

6. If plaque continues to grow, it
will eventually intrude on the inner
elastic layer of the vessel
7.Blood flow is reduced as elastic
layer cannot expand. Physical sx
may appear
CALCIUM becomes deposited in the
plaque, reducing the ability of the
vessel to expand (during exercise)
8.Increased pressure can damage
the plaque resulting in a RUPTURE
that can completely block the
artery – Stroke or Heart Attackl
Lipids
Desired
Levels
(mg/dL)
Cholesterol
150-200
Triglycerides
40-150
Lipoproteins:
 LDL
 HDL
< 100
45-60
higher the
better
the
 Age
 Gender
 Race
 Smoking
hx
 B/P… treated?
 Diabetes
 Cholesterol Levels
 FH
 Healthy
Life Style
 Cholesterol
lowering meds recommended for:
◦High risk patients
 defined as having risk of having a heart attack or stroke in
the next 10 years
 7.5% or greater score on risk assessment
(down from 20%)


People with CVD age 4075 at 7.5% risk
Risk Calculator
◦ http://cvdrisk.nhlbi.nih.gov/



People WITH CVD
People 21 or older with
very high cholesterol
(190mg/dL or higher)

People with Type 1 or
Type 2 diabetes who are
40-75
Guidelines do NOT
recommend
◦ using other cholesterol
lowering drugs:
◦ fibrates or niacin
HMG-CoA
(Statins)
Bile-Acid
Reductase Inhibitors
Sequestrants
Triglyceride
Fish
Lowering Agents
Oil (dietary supplement)
 Classification
◦MOA
◦ HMG-CoA Reductase
inhibitor (“Statin”)
 Prototype
◦ atorvastatin /Lipitor
◦ rosuvastatin/Crestor
◦ Inhibits HMG-CoA
reductase (enzyme)
 rate limiting enzyme in
cholesterol synthesis
Benefits:
1.
2.
3.
4.
plaque stabilization
improvement of coronary
endothelial function
anti-inflammatory activity
inhibition of platelet
thrombus formation
 Indications
as an adjunct to diet to reduce elevated total
cholesterol and triglycerides
 to increase HDL-C
to decrease the risk of CAD
Side Effects
◦ Can be serious!
◦MUSCLE problems = myopathy
◦ Statins can cause serious muscle problems that can lead to kidney problems,
including 
KIDNEY failure
LIVER problems
 Statins can cause liver problems
 LFTs must be monitored!
 Patient ed: Report any new onset muscle pain or weakness
 Class
◦ Bile-acid sequestrant

Prototype

MOA
◦ Cholestyramine/Questran
◦ Unknown
◦ May inhibit lipolysis
◦ Decreases subsequent hepatic fatty
acid uptake
◦ Inhibits hepatic secretion of VLDL
◦Indications:
◦Treatment of hyperlipidemia?
◦2013 AHA recommendations: ONLY USE
OF STATIN RECOMMENDED TO LOWER
CHOLSERTEROL
◦Treatment of chronic DIARRHEA
◦ SE:
CONSTIPATION is the most common SE
 Abdominal pain and bloating may occur

Tricor
fenofibrate /
◦ used to treat high cholesterol and high triglyceride
levels
INDICATION
◦lowers elevated blood triglyceride levels by
making the liver produce fewer triglycerides and
increasing the elimination of triglycerides
 Also lowers cholesterol levels

 SE:
most common is muscle weakness/aches
MYOPATHY
=
 Primary
(essential)
 Secondary
 Isolated Systolic Hypertension of the Elderly
 Orthostatic Hypotension
 RAAS
activated when:
◦ Loss of blood volume
◦ Drop in BP

Also RAAS activated anytime there is:
◦ Decreased renal perfusion  release of renin  conversion
of angiotensinogen to angiotensin I  converted to
angiotensin II by angiotensin-converting enzyme (ACE)
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RAAS regulates long term blood pressure and extracellular volume
ANGIOTENSIONOGEN released by LIVER in response to low blood pressure and changes in
blood volume
Low fluid volume stimulates the kidney to release RENIN which causes Angiotensinogen to
convert to ANGIOTENSIN I
Angiotensin I travels to
converting enzyme)
LUNG where it is converted to Angiotensin II by ACE (angiotensin
Angiotensin II acts on the ADRENAL to cause it to release ALDOSTERONE by adrenal gland
Angiotensin II is a POTENT VASOCONSTRICTOR
Also, Angiotensin II seems to cause INAPPROPRIATE REMODELING of the heart after a heart attack
◦ THIS CAUSES THE NEPHRON TO RETAIN FLUID AND B/P GOES UP
 Risk
◦ Age
factors
 BP  w/ age
 Arteries become stiff & less compliant
 Can develop at any age
◦ Race
 Highest in African-Americans
 Target organ damage to heart and brain
◦ Obesity
◦ Diabetes Mellitus
◦ SMOKING!
◦ Nutritional Factors
 High sodium intake
 Low potassium, or calcium intake
 Essential
(Primary)
Hypertension
 Secondary
Hypertension
 Isolated
Systolic
HTN in Elderly

Definition
◦ Hypertension in the absence of
any known underlying disease
◦ Most common type

What causes essential HTN?
◦Theories
 Problem with RAAS
Endothelium problem
 Alterations in endothelial function
 Upset in the balance between
vasodilators and vasoconstrictors
A.
B.
C.
D.
No evidence of other underlying disease
An underlying diabetes problem
Identifiable environmental factors present
A known genetic problem
0%
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0%
B.
0%
C.
0%
D.

Definition
◦ HTN associated with an
underlying disorder
◦ Most common underlying cause?
 RENAL DISORDERS
 Decreased renal function
 Renal artery stenosis; renal failure
 Excess secretion of renin
 Wilm’s tumor
Arrows show renal
stenosis
RAS =Renal Artery Stenosis
Symptoms RAS: H/A, blurry or double vision,
hematuria, epitaxis, changes in kidney function
(increased creatinine), inability to control B/P
despite multiple anti-hypertensives

Endocrine Disorders
◦ Cushing syndrome
 Excessive cortisol production
◦ PHEOCHROMOCYTOMA (adrenal tumor)
 Secretes catecholaminees
 RARE

Vascular Disorders
◦ Arteriosclerosis
 Narrowing of vessels  triggers RAAS
 “Stiff vascular pipes”

Other
◦ Certain Drugs - cocaine, amphetamines

Who
◦ > 65 y.o. prevalence of HTN increases to 50%
◦ Female > males

Defined
◦ SBP > 140 mmHg with

DBP < 90 mmHg
Characteristic
◦ Widening pulse pressure

Cause
◦ Arteriosclerosis
 CARDIAC

VASCULAR
◦ Increases left
ventricular work 
◦ Sustained HTN
 Alters walls of arteries &
arterioles(remodeling)
◦ HYPERTROPHY 
increase myocardial
oxygen demand
◦ Accelerates ATHEROSCLEROSIS
of aorta & larger arteries
 Left ventricular
hypertrohy (LVH)
◦ If demand outweighs
supply  ISCHEMIA
 Contributes to:
 Stroke
 Renal failure
 Aneurysms
1. Hypertensive Emergency!
2. Hypertensive Urgency

What is it?
◦ RARE hypertensive emergency in which elevated BP
DBP > 120 mm Hg
◦ Results in TARGET ORGAN damage
◦
◦ Target Organs
 Eyes, CNS, cardiovascular system, central nervous system
kidneys
(Stroke),
 Risk
factors
◦ Male
◦ African-American
◦ Cigarette smoking
◦ Hx of HTN with nonadherence w/ therapy
This man is at risk
Which risk factors does
he have?

Watch You Tube Video Presentation on Bb

Cause:
◦ Complex
 Often poorly controlled hypertension is present
 WITHDRAWAL FROM SOME DRUGS SUCH A BETA-BLOCKERS
◦ Not well understood involves
 Systemic vasoconstriction
 Abrupt release of catecholamines
 Activation of:
 Clotting cascade
 RAAS
 Required
◦ Retinopathy

Common Presenting Symptoms
◦ Chest pain
◦ Dyspnea
◦ Neurologic deficit
 Visual changes
 Cardinal Fields of Gaze

Prognosis
◦ Without Intervention - poor
◦ With Intervention - improved
◦ Most common cause of death = STROKE

Reduce risk of
cardiovascular events,
stroke, and other end organ
events
 Rapid
decrease of
HTN with IV agents


Goal is DBP 100 or less
Requires hospitalization and
close monitoring


Similiar to hypertensive emergency except
◦NO END ORGAN damage
Treatment is with ORAL agents
◦with goal to slowly lower b/p
 Causes include:
◦ ANXIETY
◦ PAIN
◦ Abrupt withdrawal of alcohol or antihypertensive meds
◦ Post-op hypertension
◦ Full bladder
COMPLICATIONS
of HTN

:
Target Organ
Disease
•Heart disease
•Brain
•Peripheral vascular disease
•Kidney
•Eyes
Step 1: lifestyle modifications are
instituted
Step 2: drug therapy is added if the
measures in step 1 are insufficient
Step 3: drug dose or class may be
changed or another drug added if the
patient’s response is inadequate
Step 4: includes all of the above
measures with the addition of more
antihypertensive agents until blood
pressure is controlled
Orthostatic Hypotension
 Defined
◦ Decrease in both SBP and DBP upon standing
 Normal
compensation
◦ Gravitational changes on standing = compensated by
  sympathetic NS activity --
 Reflex arteriolar & venous constriction
 Increased HR
 Mechanical factors
 e.g., closure of valves in venous systems, pumping of leg muscles

Factors leading to Orthostatic Hypotension (acute)
◦ Failure of some compensatory activities
◦ Acute Orthostatic Hypotension
 Due to: Sluggish regulatory activities
 Common Causes:
 Anatomic variations
 Altered body chemistry
 Drug actions (antihypertensives, antidepressants)
 Prolonged immobility r/t illness
 Starvation
 Physical exhaustion
 Significant dehydration
 Venous pooling (e.g., pregnancy)
◦Chronic Orthostatic Hypotension (chronic)
 Causes
 Secondary to specific diseases
 Examples: Endocrine disorders (DM, adrenal
insufficiency); certain metabolic disorders; certain
nervous system diseases
 Primary (Idiopathic)
 No known cause
 At
Risk Populations
◦ Men more than women
◦ Onset Age: 40-70
◦ 1/3 to ½ of elderly population may develop primary form
 Often accompanied by bowel & bladder dysfunction