Transcript (CAD) and Risk factors .#1 GDE revised 2015 (LC).

Coronary Artery Disease (CAD)
(2015)
http://www.cts.usc.edu/hpg-coronaryarterydisease.html
Learning Objectives
Students will be able to:
 describe epidemiology of CAD and MI
 describe the pathophysiology/aetiology of CAD
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and MI
incorporate assessment of cardiac risk factors
into the assessment of a patient with CAD
describe the clinical manifestations and diagnosis
of CAD and MI with related nursing implications
for common tests and procedures
describe the nursing,medical and pharmacological
management of the patient with CAD and MI
describe complications of CAD
Coronary Artery Disease
What are some of your thoughts
when you hear the terms
“Coronary Artery Disease” or
"Heart Disease” ?
New Zealand Epidemiology
 Cardiovascular disease is the leading
cause of death in NZ (40%) (CHD 23%)
 Little change over past 30yrs
 Burden disproportionately falls on
Maori and Pacific people
 Maori and Pacific < 75yrs 2-3 times higher
 Immigrants from Indian subcontinent
 http://www.heartfoundation.org.nz/know-the-facts/statistics
Coronary Artery Disease
 Where are the coronary arteries ?
 Obstructed blood flow through the coronary
arteries
 Atherosclerosis
 Plaque accumulation and rupture
 Narrowing and occlusion of lumen
 Decrease in blood flow and oxygen to heart
muscle
“Myocardial Oxygen demands exceed supply”
Coronary Arteries
http://my.clevelandclinic.org/services/heart/heart-blood-vessels/coronary-arteries
Atherosclerosis
(athero – fat, sclerotic – narrow)
 Abnormal accumulation
of lipid substances and
fibrous tissue in the
vessel wall
 Inflammatory response
 biophysical and
biochemical changes in
wall
 progressive.
www.east-haven.k12.ct.us/.../indexcb.htm
CORONARY ARTERY DISEASE (CAD)
(Atherosclerosis)
 Fatty streak
streaks of fat within
smooth muscle cells
 Fibrous plaque
changes in endothelium
 Complicated lesion
continued inflammation,
instability and rupture
(Lewis 738 /856)
What is fibrous Plaque?
 Fibrous and smooth
muscle tissue
 lipid or necrotic tissue
from inflammatory process
of atherosclerosis
 Fibrous cap which
protrudes into the lumen
of the vessel
 Rupture releases
thrombogenic lipids
causing platelet
accumulation and clot
Patho ofCoronary Artery Disease
 Atherosclerosis in the intima
 LDL accumulate in vessel and
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form fatty streaks.
Smooth muscle cells
(from middle layer) engulf
fatty streaks, produce
fibrous tissue and stimulate
calcium deposition
Transformation of fatty
streaks result in fibrous
plaque and CAD lesion
Small blood vessels grow into
the lesion which enlarges
Obstruction and bleeding
 Lewis pg 738/856
Atherosclerosis
http://www.youtube.com/watch?v=EmB95sPHlkc
Heart Attack !!! A Case Study
11am - Mr H. is admitted to hospital after collapsing at the
school where he teaches. He presents with pain in his jaw,
feeling very tired, is pale and diaphoretic but fully conscious
and awake. He did have a short period of unconsciousness
after his collapse. He is unable to recall exact event.
Has a history of hypertension, controlled on medication, on
statins prophylactically, does not smoke, and exercises
regularly. BP 85/50, P 90, Resp 22, O2 sats 95%
12 lead ECG shows raised ST segments and an inferior STEMI.
Thombolysis started in CCU which failed and patient
transferred to ACH for emergency “rescue” angiography.
2pm Patient Back in CCU (ACH) – RCA stented – showed
complete occlusion
Myocardium reperfused – no permanent damage.
“ TIME IS MUSCLE ”
Risk factors for CAD
H TN
O besity
P VD
E levated LDL
F MH
U p glucose - DM
L ow HDL
S moking
S ex - male
S edentary life style
S tress
 http://www.world-heart-federation.org/cardiovascular-
health/cardiovascular-disease-risk-factors/
RISK FACTORS for CAD
 Age
 Gender
 Family history
 Ethnicity and race
 Obesity
 Diabetes
 Hypertension
 Smoking
 Sedentary lifestyle
 Diet
 Stress
Smeltzer and Bare (2014) Management of Patients with Coronary Vascular Disorders
 Body Mass Index
Obesity
 Culturally Specific
 Normal =18-24
 Over weight =29
 Obese =30
 Morbid obesity > 40
 Associated with hypertension, increased lipids,
atherosclerosis and diabetes
 Increased workload of heart
 Increase in Myocardial oxygen demands
 http://www.health.govt.nz/nz-health-statistics/healthstatistics-and-data-sets/obesity-data-and-stats
Morbid obesity > 40
Diabetes and CAD
 Connective tissue
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damage
Endothelial cell
impairment
Atherosclerosis
High cholesterol
Platelet aggregation
Altered red blood
function
Hypertension and CAD
 Increased stiffness of vessel walls –
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decreased elasticity
Vessel injury and inflammatory response in
intima
Increases rate of atherosclerosis
Increased workload of the heart
Left ventricular hypertrophy
Regulation of Blood Pressure
Hypertension
(Lewis 834)
Defined as a consistent/sustained
elevation of the systolic blood
pressure above 140 mm Hg or higher
or a diastolic blood pressure of 90mm
Hg and above
 One in five NZ’ers over 15 have a
BP160/95 (NZGG 2009)
 On two elevated readings (sitting and
supine) on separate Doctors visits

Hypertension
Two types
Primary : - reason for elevation unknown.
- 90-95% of all cases.
Secondary : - Specific cause
- 5-10% of adults
- 80% children
Hypertension
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Sign - used to monitor clinical status
Risk - contributes to rate at which
atherosclerotic plaque accumulates
within arterial walls
Disease - major contributor to death from
cardiac, renal and PVD
Usual consequences of prolonged uncontrolled
hypertension are MI, heart failure, renal failure,
stroke and impaired vision
Goal with Hypertension
 Two primary regulatory factors:
* Blood low(volume
* Peripheral Vascular Resistance (PVR)
 Goal is to optimise these 2 in order to get
pressure below 140/90mmHg and reduce
cardiovascular risk.
 Primary groups of drugs are used:
* Diuretics
* Adrenergic inhibitors (beta blockers) ****
* Vasodilators
* ACE inhibitors/ Angiotensin 11 receptor
antagonists (ARB’s
* Calcium Channel blockers (antagonists)
Complications with Hypertension
 CAD
 PVD
 CVD
 Retinal damage
 Renal disease
Tobacco
 Vasoconstriction
 Increases carbon
monoxide levels
 Increases platelet
adhesion
 Interferes with
HDL (good
cholesterol)
Face the facts
http://www.facethefacts.org.nz/quit-smoking
Face the facts …………
 5000 NZ’rs die annually
 2nd hand smoke kills 350/year
 Single leading cause of
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preventable death
One in two smokers will die from
smoking related death
Quitting saves lives and money
Kids - 3 times more likely to
become smokers if parents
smoke
ALL CIGARETTES ARE DEADLY
Smoking. Face the facts !!
http://www.mc.uky.edu/kygifts/formom/Whats%20in%20a%20cig.jpg
Cholesterol
http://www.nlm.nih.gov/medlineplus/ency/imagepages/19269.htm Accessed 16.03.2004 2210hrs
Cholesterol – good or bad ?
http://www.heart-health-for-life.com/image-files/choleshtline.jpg
Normal Lipid Profile
 Total Cholesterol <5 mmol/l
 HDL >1.0 mmol/l
 LDL <3.4 mmol/l
 Triglyceride <2.0 mmol/l
 Total HDL Ratio TC:HDL < 4.5mmol/l
Stress and CAD
 SNS stimulation
 Increased release of
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adrenaline & noradrenaline
Increases HR, BP and
contraction
Results in increase in O2
demands and workload
Increased lipid levels
Alters coagulation
atherosclerosis