This presentation will help beginners to understand what is coronary artery diseases.

1. Coronary Artery Disease: An
Overview
Dr. Anil Sharma, PhD(N)
Principal, Manikaka
Topawala Institute of
Nursing-CHARUSAT,
Changa
Accredited Grade “A” with
NAAC & KCG
anilsharma.nur@gmail.com

2. Objectives
To understand anatomy of heart
To understand flow of coronary circulation
To define Coronary Artery Disease (CAD)
To know the prevalence and incidence of CAD
To illustrate pathophysiology of CAD with clinical
manifestations
To underline risk factors and causes of CAD
To construct medical management of CAD
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3. Anatomy of Heart:
 A hollow muscular organ
 Located in thorax between
2 lungs
 200 to 425 gram
 4 chambers
 Beats 100,000 times/day
 2 (4) valves
 3 layers of Heart Wall
(Epi, Myo & Endo)
 Myocardium= Cardiac Muscle
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4. Conduction system:
SA Node (Natural Pacemaker)
AV Node
Bundle of His
Bundle Branches
Purkinje fibers
 Cardiac cycle = 0.8 Sec.
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5. Coronary Circulation:
o Normal function of heart is based on balance between
Oxygen supply and Oxygen demand.
o To make balance in this, Firstly heart itself require sufficient
blood supply. This made by coronary circulation.
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Coronary Artery
leave from Aorta
Coronary Artery
dived in Two
branch
1. Right Coronary
Artery
2. Left Coronary
Artery
Blood supplied
to various part of
Heart
Deoxygenated
blood collected at
Coronary Sinus
through cardiac
vein
Deoxygenated
blood reaches to
Right Atrium

6. Coronary Artery Circulation:
Aorta
Right Coronary Artery Left Coronary Artery
1.Posterior intraventricular artery
(posterior part of Intraventricular septum & SA Node)
1. Left Anterior Descending Artery
(Supply to anterior part of Intraventricular septum)
2.Marginal Artery (Walls of Right atrium and Right
ventricular)
2.Circumflex Artery
(Walls of left atrium and left ventricular)
5% of total cardiac output goes to
coronary circulation

7. Coronary Artery Disease (CAD):
Introduction
 Most prevalent type of cardiovascular disease in adult.
 Most common kind of Non communicable Disease.
 Also known as Ischemic Heart Disease (IHD) or
Coronary Heart Disease (CHD)
 Basically a condition where blood supply to Heart
muscles decrease to a level of adequacy.
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8. Definition of Coronary Artery Disease:
A condition and especially one which cause
reduced blood flow through the coronary
arteries to the heart and results in heart damage.
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9. CAD progress:
Atherosclerosis
(Common cause of CAD)
Angina Pectoris
Myocardial Infarction
Cardiac Death
Charotar University of Science & Technology
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10. Incidence of Coronary Artery Disease:
 One fifth of the deaths in India are from coronary
heart disease. By the year 2020, it will account for one
third of all deaths. Sadly, many of these will be dying
young
 Heart disease in India occurs 10 to 15 years earlier than in
the west,
 Estimated 4.5 crore patients of coronary artery disease in
India,
 In last 60 years, prevalence rate at urban from 1% to
9% and at rural <1% to 5%
 Current projections suggest that India will have the largest
cardiovascular disease burden in the world.
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11. 2010 2013 2015
Cath-lab centers 251 404 630
Coronary interventions 117420 216817 375000
Total stents 146719 262349 475000
Detail of cath-lab, coronary interventions and stents

12. Atherosclerosis:
 Abnormal accumulation of lipid, fatty substance and
fibrous tissue in inner lining of arterial wall.
 This accumulation known as plaque or atheroma.
 Structure of coronary arteries
made it more susceptible to plaque
formation.
 These block make narrowing of
Blood vessel which reduce blood
Flow.
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13. Pathophysiology:
Before this let us understand structure of arteries:
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14. Injury to vascular endothelium will initiate progress of
atherosclerosis
(This injury may caused by smoking, Hypertension, hyperlipidemia etc.)
Endothelium will undergo to changes and stop producing normal
antithrombotic and vasodialting agents
The inflammatory process begins with attraction of inflammatory
cells such as Monocytes (Macrophages)
Now, these macrophages ingest lipids and become Foam Cells
These foam cells transport lipids to arterial wall
Pathophysiology Cont..

15. Now, these deposited lipids forming fatty streaks
(First grossly visible lesion: irregular yellow white discoloration)
Simultaneously, the activated macrophages release biochemical
substance to damage endothelium by contributing oxidation of low-
density lipoprotein (LDL)
This oxidized LDL is a toxic to the endothelial cells and accelerate
plaque formation
Here, transported lipid into arterial wall, smooth muscle cell
proliferation and forms a Fibrous Cap known as PLAQUE
This plaque protrude into the lumen of the vessel and narrowing it
and obstructing blood flow to heart

17. Etiology and Risk Factors :
 Etiology means causes
 Causes means which must precede the effect
 Risk factors are not necessarily a cause
 A risk factor is something that increases your chance
of getting a disease
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For CAD the cause is any
condition which disturb the
balance of oxygen demand and
supply

18. Risk Factors:
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Risk factor
Non-modifiable Modifiable
Age
(The older you are, the more likely you are
to develop coronary heart disease )
Smoking, tobacco use
Family History (First degree relatives) Hypertension
Gender (Men develop in earlier than
women)
Diabetes
Ethnic background
(South Asians living in the UK are twice as
likely to develop CAD compared to the rest
of the UK population)
Physical inactivity
Obesity
High blood cholesterol

19. Charotar University of Science & Technology
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Risk Factors Cont..
High blood cholesterol:
 Total cholesterol < 200 mg/dL
 LDL <100 mg/dL (For high risk patients
It has to <70 mg/dL)
 HDL > 40 mg/dL for males
And > 50 mg/dL for females
 Triglyceride < 150 mg/dL
Fat metabolism have
four element:
1. Total cholesterol
2. Low-density
lipoprotein (Bad)
3. High-density
lipoprotein (Good)
4. Triglycerides
HDL is good because it transport
LDL and other lipoprotein to the
liver for their degrading and
excretion.

20. Physical inactivity:
 In case of less physical activity, the triglyceride level increases
which accelerate the CAD process.
 Regular moderate physical activity increase HDL level and
reduce triglyceride level.
 The goal could have 150 minutes moderate-intensity aerobic
activity or vigorous-intensity for at least 75 minutes.
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Risk Factors Cont..

21. Smoking, Tobacco use:
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Risk Factors Cont..
Nicotinic acid in
tobacco triggers release
of catecholamine
Heart Rate and BP
Nicotinic acid also
cause Vasoconstriction
Smoking increased
oxidation of LDL
Endothelium damage
Platelets adhesion and
thrombus formation
Smoking inhalation
increased level of
Carbon monoxide
This attach with
hemoglobin much faster
than oxygen and results
oxygen supply reduced

22. Hypertension:
Long standing increased blood pressure
Increased stiffness of the blood vessel (Minimize
flexibility)
This lead vessel injury
Further it lead to inflammatory changes/response
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Risk Factors Cont..

23. Diabetes:
Hyperglycemia cause platelet aggregation and altered red blood
cell functions
Platelet aggregation cause thrombus formation
This thrombus will reduce blood supply
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Risk Factors Cont..

24. Angina Pectoris:
 Angina pectoris known as Chest pain caused by reduced
blood supply to heart muscles.
 To be very specific: caused by insufficient
Coronary blood flow.
 Radiating kind of chest pain, follow
Route from neck, jaw, shoulder and
Inner aspect of upper arm (Left)
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25. Types of Angina:
1. Stable angina: Pain subside by rest
2. Unstable angina: not relieved by rest or nitroglycerine
3. Intractable/refractory angina: severe incapacitating pain
4. Variant angina: Pain at rest and reported by ECG change
5. Silent angina: No pain felt by patient
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26. Clinical Manifestations:
 Chest pain (Retrosternal area)
 Shortness of breath
 Weakness in the arms, wrist and hands
 Light headache
 Nausea and vomiting
 Fainting (lack supply to brain cells)
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27. Medical Treatment of Angina Pectoris:
Objective: Decrease oxygen demand and increase oxygen supply
 Nitroglycerin: vasodilator improve blood flow and
relieve pain
 Routes: Sublingual, oral capsule, topical and IV
 Ideally sublingual (Placed under tongue): this alleviate pain
within 3 minutes
 Beta-adrenergic blocking agents: it reduce myocardial
oxygen consumption by blocking beta-adrenergic sympathetic
stimulation
As result: reduced heart rate and slowed down conduction system
This help to balance oxygen demand and supplyCharotar University of Science & Technology
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28.  Calcium channel blocking agents: Two ways it help
1. These agents slowed down SA node automaticity and AV node
conduction
This results in decreased heart rate and also decrease strength of
myocardial contraction
This will decrease workload of the heart
2. Increased oxygen supply by dilating smooth muscle wall of
coronary arterioles
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29.  Antiplatelet agents:
 Aspirin
 Thienopyridines (Clopidogrel)
 Glycoprotein (prevent adhesions of fibrinogen)
 Anticoagulant agents:
 Heparin
 Oxygen administration
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30. Myocardial Infarction (MI):
 Also known as Heart Attack/ Coronary Occlusion
 It’s a irreversible damage of myocardial cells caused by
prolonged ischemia and hypoxia.
In this condition: plaque rupture, which then leads to the
formation of a blood clot
This lead to complete occlusion of the artery
Lead to ischemia and necrosis to myocardial cells
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31.  Causes:
 Vasospasm of coronary artery (Sudden narrowing)
 Decreased blood supply (Blood loss, anemia, low BP etc.)
 Increased demand of oxygen (Heavy exercise, ingestion of cocaine)
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MI types are based on its location of injury to
the ventricular wall such as
• Anterior
• Inferior
• Posterior
• Lateral

32.  Clinical Manifestation:
 Chest pain
 Shortness of breath
 Indigestion
 Nausea and vomiting
 Cool, pale and moist skin
 Heart rate and respiratory rate increased
 Fatigue
 Anxiety
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33.  Medical Management:
Objective: Minimize myocardial damage, preserve
myocardial functions and prevent complication
 Immediately start with:
 Oxygen administration
 Aspirin
 Nitroglycerine
 Morphine (Drug of choice to reduce pain and anxiety)
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34.  Thrombolytic (Fibrnolytics):
 To dissolve the thrombus
 ACE inhibitors :
 Angiotensin-converting enzyme inhibitor prevent the
conversion of Angiotensin I to Angiotensin II In absence of
this, BP reduce and kidney excrete sodium and fluid This
will reduce oxygen demand of the heart
 BP, Urine output, serum sodium, potassium and creatinine level
should closely monitored.
 If ACEI not work than we may go with ARB (Angiotensin
Receptor Blocker)
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Thrombolytic therapy initiated
when primary PCI (Percutaneous
coronary intervention) not available
or transport time is too long

35.  Selected References:
 Kasper, Fauci et al (2015). Harrison’s Principles of Internal Medicine (19th
Ed.). Mc Graw Hill Education
 Porth C.M. & Matfin G. (2009). Pathophysiology: Concepts of altered
health status (8th ed.). Philadelphia: Lippincott Williams & Wilkins
 Patricia A. Potter, A. Stockert et al (2014). Fundamentals of nursing (2nd
ed.). South Asian edition. Elsevier
 Linda A. Silvestri (2017). Comprehensive review for the NCLEX-RN
examination (2nd ed.). South Asian edition. Saunders Elsevier
 Barbara K. Timby and Nancy E. Smith (2007). Introductory medical-
surgical nursing (9th Ed.). Lippincott Williams & Wilkins a Wolters Kluwer
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36. We will be very
happy to answer
your query,
if any !!
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37. Thank You All
For Patience
Listening and your
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