This document discusses coronary artery disease (CAD), which is characterized by the narrowing of coronary arteries caused by atherosclerosis. It prevents adequate blood supply to the heart muscle. Risk factors include heredity, increasing age, gender, smoking, hypertension, physical inactivity, obesity, and high cholesterol. Symptoms of angina pectoris result from myocardial ischemia and include chest pain or discomfort that can radiate to the arm. Diagnosis involves ECG, stress testing, and coronary angiography. Management focuses on lifestyle changes, medications like nitrates, beta blockers, and calcium channel blockers, and procedures like PTCA and CABG to improve blood flow.

1. CORONARY ARTERY
DISEASE

2. DEFINITION
CAD is a type of blood vessel
disorder characterised by the
narrowing of coronary arteries which
prevents the adequate blood supply
to the myocardium which is usually
caused by atherosclerosis.

3. Incidence
• Prevalence in urban population
increased from 3.5% in 1960’s to
10.5% in 1990’s
• Rural population was from 2 to 4 %

4. ETIOLOGY
ATHEROSCLEROSIS
Characterised by the local
deposits of cholesterol and lipids
within the intimal wall.
• Normally endothelium is non reactive
to platelets and leukocytes and other
coagulation fibrinolytic agents.

5. • Endothelium can be injured as a
result of Tobaco use, Hyperlipidemia,
Hypertension, DM, Hyper
homocystenemia and elevated levels
of C reactive protein.

6. RISK FACTORS
MODIFIABLE
RISK FACTORS
NON
MODIFIABLE
RISK
FACTORS

7. NON MODIFIABLE RISK
FACTORS
• HERIDITY

8. NON MODIFIABLE RISK
FACTORS
• GENDER

9. NON MODIFIABLE RISK
FACTORS
• INCREASING AGE

10. MODIFIABLE RISK FACTORS
• CIGRETTE SMOKING

11. MODIFIABLE RISK FACTORS
• HYPERTENSION

12. MODIFIABLE RISK FACTORS

13. MODIFIABLE RISK FACTORS
• PHYSICAL INACTIVITY

14. MODIFIABLE RISK FACTORS
• OBECITY

15. PROGRESSION OF
ATHEROSCLEROSIS

16. CLINICAL FEATURES
• CAD symptoms will occur according to the
location and degree of narrowing of
arterial leumen, thrombus formation and
obstruction of blood flow.
• ISCHEMIA
• ANGINA PECTORIS
• DECREASED CARDIAC OUTPUT
• HEART FAILURE
• UA
• MI

17. DIAGNOSIS
• History collection
• Physical examination
• ECG
• ICUS
• Doppler flow studies
• Electron beam studies
• TMT
• Total lipid profile
• CAG
• ECHO

18. ECG

19. INTRA CORONARY
ULTRASOUND
• Invasive procedure
• Performed in conjunction with CAG
• 2 D or 3 D images of ultrasound provide
cross sectional view of arterial walls.
• A miniature transducer attached to a small
catheter is introduced through a peripheral
artery and advanced to the artery to be
studied.
• The health of the arterial layers are
assessed.

20. MANAGEMENT
• GOALS
Reduce risk factor through primary
and secondary prevention.

21. GOALS OF PREVENTION
• Reduce the incidence of subsequent
coronary events
• Decrease the need for treatment such
as PTCA and CABG
• Extend over all survival
• Improve quality of life

22. HOW CAN ACHEIVE THESE
GOALS
• CONTROL OF BP
• MAINTAIN IDEAL BODY WEIGHT
• EXERCISE
• REDUCE ALCOHOL
• LOW SODIUM DIET

23. PRIMARY PREVENTION GOAL
FOR CHOLESTEROL
MANAGEMENT
• LDL <130 mg/dl if 2 or more risk
factor
• LDL <160mg/dl if no or 1 risk factor
• HDL >35 mg/dl
• Triglycerides <200 mg/dl

24. SECONDARY PREVENTION
GOAL FOR CHOLESTEROL
MANAGEMENT
• LDL <100 mg/dl
• HDL>35 mg/dl
• Triglycerides <200 mg/dl
• Exercise 3 or 4 times weakly for 30 to
60 mts
• Maintain ideal body weight as
indicated by BMI between 21 to 25 kg/
m2

25. • Waist circumference <40inches in
men and <36 inches in women
• Maintenance of normal glucose levels
in clients with DM
• ERT for post menopausal women

26. • Anti platelet therapy
Aspirin therapy is recommended for
people >65 yrs unless it is
contraindicated.
• Cholesterol lowering therapy
Complete lipid profile recommended
every 5 yrs beginning at the age of 20.
Guideline treatment are focus on LDL
levels.
Cholesterol levels are assessed after 6
wks of dietary therapy. If they remain
elevated, drug therapy are recommended.

27. DRUG THERAPY IN
HYPERLIPIDEMIA
• Drugs that restrict lipoprotein production
• Drugs that increase lipoprotein removal
• Drugs that decrease cholesterol absorption

28. DRUG THERAPY IN
HYPERLIPIDEMIA
• STATINS
– Atorvastatin
– Fluvastin
– Lovastin
– Pravastin
– Simvastin
– Rosuvastatin
• NIACIN
– Niacin
– Nicotinic acid

29. DRUG THERAPY IN
HYPERLIPIDEMIA
• Fibric acid derivatives:
– Fenofibrate
– Gemfibrozil
• Bile acid sequestrants
– Cholestyramine
– Colestipol
– Colesevelam
• Cholesterol absorption inhibitor
– Ezetimibe

30. • GLYCOPROTEIN 2 B/ 3 A RECEPTOR
ANTAGONIST ARE THE MOST RECENT
PHARMACOLOGIC TREATMENT FOR
CAD
• These drugs prevent platelet aggregation
and ACS

31. INTERVENTIONAL PROCEDURE
• PTCA - POBA
Baloon tipped catheter is inserted through
femoral artery under x ray guidance into a
blocked coronary artery.
Baloon is inflated several times to reshape
the leumen by stretching it and flattening
the atherosclerotic plaque in the arterial
wall.

32. • PTCA – STENTS
– 80% of world wide PCI involves
placements of intracoronary stents
– Initiated to provide structural support to
an artery opposing elastic recoil , to
prevent vasoconstriction
– Here the lesion is predialate with an
angioplasty balloon or stent placed
without predialation
– Once the baloon is placed and
positioned , the balloon is inflated to
expand the stent

33. • SELF EXPANDING STENTS
Other types of stents used, less often is
self expanding stents.
It will be place on the delivery system in a
collapsed state. Retraction of the the
membrane across the leision allows the
stent to expand.

34. • DRUG ILLUTING STENTS

35. • DIRECTIONAL CORONARY
ATHERECTOMY
– Helps to overcome complication of PTCA
– Restenosis occur in 20 to 50% of clients
with in 2 to 6 months after PTCA
– It reduces restonosis by excising the
atherosclerotic plaque.

36. • DCA cutter consist of a catheter that
contains a rigid cylindrical portion with a
central rotating blade
• The blade shaves off the atherosclerotic
material and deposits in the vessel leumen
and send for histopathology

37. • Contraindication for DCA
Tortuous vessels
Distal lesions
Heavily calcified lesions

38. LASER ANGIOPLASTY
• It is the concept of applying laser energy to
remove atherosclerotic coronary
obstruction in a percutaneous manner.
• Photochemical mechanism that involves
breaking of molecular bonds without
generation of heat.

39. SURGICAL MANAGEMENT OF
CAD
• CABG
• MIDCAB
• TRANS MYOCARDIAL
REVASCULARISATION

40. • CABG
Accomplished most commonly with IMA in
combination with saphenous venous graft
Use of gastro epiploic artery as a pedicle graft to
RCA or LCA are been used.
Veins harvested from arms make poor bypass
conduites because of their caliber and high
incidence of aneurysm formation.
IMA have longer potency rate (up to 96% at10 yrs)
than saphenous vein graft (up to 81% at 10 yrs)

41. • When multiple grafts are required , single
or bilateral IMA graft in combination with
other arterial conduit and suphenous vein
grafts can be used to accomplish
revascularization.

42. • MIDCAB
– Also a CABG surgery performed through
left anterior small thoracotomy
– A short parasternal incision is made
using a port access.
– Surgery is performed on beating heart
– To allow suturing of the graft adenosine
beta blockers are used to slow or
temporary stop the heart.

43. • Blood flow through the target vessel is
temporarly interrupted with luminal
occluders.
• CPB on stand by during each MIDCAB
procedure

44. • ADVANTAGES OF MIDCAB
– Coronary revascularisation without
physiologic derangement of CPB
– Avoidance of tradditional sternotomy
incision

45. • TRANS MYOCARDIAL REVASCULARIZATION
High powered laser is used to open up
channels in the heart through a relatively
small chest and incision by punching holes
in a fraction of second in the beating heart.
Laser beams is applied between each
heartbeats when ventricle is filled with
blood.

46. • Excimer laser are used to produce multiple
channels from endocardial surface of the
ventricular wall in an effort to improve the
myocardial blood supply which can not be
revascularised by traditional techniques.

47. NURSING MANAGEMENT

48. ANGINA PECTORIS

49. DEFINITION
• Angina pectoris is a chest pain resulting
from myocardial ischemia.
• The client with aortic stenosis , HTN,
hypertrophic cardiomyopathy can have
angina pectoris.

50. Factors influencing myocardial
oxygenation needs
• Decreased oxygen supply
• Increased oxygen demand or consumption

51. • Decreased oxygen supply:
Cardiac
– Anaemia
– Hypoxemia
– Pneumonia
– Asthma
– COPD
– Low blood volume

52. Non cardiac
– Coronary artery spasm
– Coronary artery thrombosis
– Dysrhythmias
– Heart failure
– Valve disorders

53. • Increased oxygen demand:
– Anxiety
– Cocaine use
– Hypertension
– Hyperthermia
– Hyperthyroidism
– Physical exertion

54. Pathophysiology
Increased oxygen demand or decreased
oxygen supply to the myocardium
Myocardium becomes hypoxic within the first
10 seconds of coronary occlusion
Contractility ceases after several minutes of
coronary occlusion
Depriving the myocardial cells of oxygenation
and glucose for aerobic metabolism.

55. Anaerobic metabolism begins and lactic acid
accumulates
Myocardial nerve cells are irritated by
increased lactic acid
Transmit pain message to the cardiac nerves
and upper thoracic posterior nerve roots
Referred cardiac pain to left shoulder and
arm

56. • In ischemic conditions cardiac cells
are viable approximately 20 mts.
• With restoration of blood flow, aerobic
metabolism resumes, contractility is
restored and cellular repair begins.

57. PATHOPHYSIOLOGY

58. CHARACTERISTICS OF ANGINA
• ONSET
• LOCATION
• RADIATION
• DURATION
• SENSATION
• SEVEARITY
• ASSOCIATED CHARACTERISTICS
• ATYPICAL PRESENTATION
• RELEIVING / AGGRAVATING FACTORS

59. • Onset :
– Develop quickly or slowly
–Patients ignore the chest pain
thinking that it will be go away or
that is indigestion.

60. • Location
– 90% of the clients experience retro
sternal chest pain or slightly to the left of
the sternum

61. • Radiation
– Pain usually radiates to left shoulder,
upper arm and then may travel down to
inner aspect of the left arm to the elbow,
wrist and 4th
and 5th
finger.
– Pain may radiate to the right side of the
shoulder, neck, jaw or epigastric region.

62. • Duration:
– Usually less than 5 mts
– Precipitated by heavy meal or extreme
anger and lasts for 15 – 20 mts

63. • Sensation:
– Squeezing, burning, pressing, chocking
aching pain
– Feels like heartburn or indigestion

64. • Seviarity:
–Mild to moderate
–Rarely pain described as severe

65. • Associated characteristics:
– Dyspnea
– Pallor
– Sweating
– Fainting
– Palpitation
– Dizziness
– Digestive disturbances

66. • Atypical presentation
– Women manifested as epigastric pain,
dyspnea, backpain
– Elderly manifest dyspnea, fatigue,
syncope

67. • Revelling or aggravating factors
– Aggravated by continued activity and
most of them are quickly subside by
NTG administration

68. CLASSIFICATION OF ANGINA
• CLASS 1
Angina occur with strenuous rapid
prolonged exersion.
• CLASS 2
Slight limitation of ordinary activity
Angina occur with climbing, walking,
stair climbing after meals or under
emotional stress.

69. CLASSIFICATION OF ANGINA
• CLASS 3
Marked limitation of ordinary physical
activity
• CLASS 4
There is inability to carry any physical
activity without discomfort

70. PATTERNS OF ANGINA
• STABLE (CLASSIC) ANGINA
• UA
• VARIENT (PRINZMETAL’S) ANGINA
• NOCTURNAL ANGINA
• ANGINA DECUBITUS
• INTERACTABLE ANGINA
• POST INFARCTION ANGINA

71. • Stable angina:
– Paroxysmal chest pain or discomfort
triggered by predictable degree of
exertion or emotion

72. • Unstable angina:
– Paroxysmal chest pain triggered by
impredictable degree of exertion or
emotion.

73. • Varient angina:
– Chest discomfort similar to classic
angina but long duration and it may
occur even during rest.
– Result from coronary spasm may
associated with elevation of ST segment

74. • Nocturnal angina:
– Associated with REM sleep during day
dreeming.

75. • Angina decubitus:
Paroxysmal chest pain that occurs
when the client is sits or stands up

76. • Intractable angina:
– Chronic incapacitating agina that is un
responsive to treatment

77. • Post infarction angina:
– Pain after MI when residual ischemia
may cause episodes of angina.

78. DIAGNOSIS
• P -Precipitating events
• Q -Quality of pain
• R -Radiation of pain
• S -Severity of pain
• T -Timing

79. DIAGNOSIS
• ECG
• SRESS TESTING
• C X-RAY
• PET
• SPECT
• ECHO
• CARDIAC MRI/ MRA
• CAG

80. MANAGEMENT
• TREATMENT FOR STABLE ANGINA:
NON PHARMACOLOGIC
INTERVENTIONS
– Life style adjustment
• Exercise prgm
• Low fat low cholesterol diet
• Smoking cessasion
• Weight reduction
• Stress management

81. – Manage medical conditions that
exacerbate angina.
– Anaemia
– COPD
– Aortic valve disease
– Hypertrophic cardiomyopathy
– HTN
– DM

82. • PHARMACOLOGICAL INTERVENTIONS
– Nitrates
– Betablockers
– Calcium agonists

83. Short acting Nitrates:
• Dilating peripheral blood vessel:
Decrease SVR and decrease venous
blood return to the heart. Therefore
myocardial oxygenation demand is
decreased because of reduced cardiac
work load.

84. • Dilating coronary arteries and collateral
vessels:
• This may increase the blood flow to
the ischemic areas

85. • Sublingual nitro-glycerine: (sub lingual
spray and sublingual tablet)
• Relief of pain within 3 minutes and has
a duration of approximately 30 – 60
mts.
• It can be used prophylactically before
undertaking an activity that the patient knows
may precipitate anginal attack.

86. • Long acting nitro-glycerine:
– Isosorbide dinitrate Longer acting
– Isosorbide mononitrates than S/L NTG
Used to reduce the incidence of anginal
attacks.
Patients are advised to take
acetaminophen with their nitrate to relief
head ache.

87. • Nitro-glycerine ointment:
– 2% nitroglycerine topical application
helps to produce anginal prophylaxis for
3 – 6 hrs.
• Transdermal controlled- release
nitrates:
– 2 systems are available for the trans
dermal nitro-glycerine administration
• Reservoier system
• Marix system

88. – Reservoier system:
Delivers the drug using a rate
controlled permeable membrane
– Matrix system
Provides a slow delivery of drug
through a polymer matrix.

89. • BETA ADRENERGIC BLOCKERS:
– Used in chronic stable angina
– It decrease the morbidity and mortality
rate in patients with CAD
– It should be avoided in patients with
asthma and used cautiously in patients
with diabetes as they produce
hypoglycemia
– Eg: Propranolol, metoprolol,
nodolol,atenolol

90. • CALCIUM CHANNEL BLOCKERS
– If beta adrenergic blockers
– If do not control anginal symptoms
– 3 effects of calcium channel blockers
are:
Systemic vasodilatation
Decreased myocardial contractility
Coronary vasodilatation

91. • ACE inhibitors:
Certain high risk patients with chronic
stable angina benefit from ACE
inhibitor.

92. Treatment for UA
• Supplemental oxygen therapy and NTG
• Morphine sulphate to relieve pain or if
there any pulmonary congestion
• IV betablocker if chest pain continues
• If ischemia persist beta blockers are ,
contraindicated, a non dihydropyridine
calcium agonist can be given
• Anti platelet therapy is also initiated
• LMWH
• Cardiac catheterization