MANAGEMENT OF MEDICALLY COMPROMISED PATIENTS-CARDIO-VASCULAR DISEASES ISCHEMIC HEART DISEASE

1. MANAGEMENT OF MEDICALLY
COMPROMISED PATIENTS-CARDIO-
VASCULAR DISEASES
ISCHEMIC HEART DISEASE

2. CONTENTS
• INTRODUCTION
• BASIC ANATOMY AND PHYSIOLOGY OF HEART
• INCIDENCE AND PREVALENCE
• ETIOLOGY
• PATHPHYSIOLOGY AND COMPLICATIONS
• SYMPTOMS AND SIGNS
• LABORATORY FINDINGS
• MEDICAL MANAGEMENT
• DENTAL MANAGEMENT

3. INTRODUCTION
o Ischaemia refers to an insufficient amount of blood.
o myocardial ischemia—an imbalance between the
supply (perfusion) and demand of the heart for
oxygenated blood.
o The coronary arteries are the only source of blood
for the heart muscle.

4. • Ischaemic Heart Disease (IHD) refers to a group of
pathophysiologically related clinical syndromes;
• angina
• myocardial infarction
• chronic IHD with heart failure
• sudden cardiac death

6. A glimpse of heart anatomy and
physiology

7. surfaces

8. The internal anatomy of the heart
8

9. Coronary supply

10. Two pumps-pulmonary
and systemic circuit

11. CARDIAC CYCLE- 0.8 second

12. SUB –DIVISION OF ANS

13. ELECTRICAL CONDUCTION SYTEM OF HEART

14. Cardiac output,heart rate and stroke
volume

15. EPIDEMIOLOGY

16. Epidemiology –global scenario
-approximately 3.8 million men and 3.4 million women
worldwide die each year from CHD.
-According to the Global Burden of Disease Study, the
developing countries contributed 3.5 million of the 6.2
million global deaths from CHD in 1990.
- will account for 7.8 million of the 11.1 million deaths
due to CHD in 2020

19. Global Vs National scenario

20. National scenario

21. ETIOLOGY
• In more than 90% of cases, the cause of
myocardial ischemia is reduction in coronary
blood flow due to atherosclerotic coronary
arterial obstruction.
• Thus, IHD is often termed coronary artery disease
(CAD) or coronary heart disease

22. The coronary arteries.

23. ETIOLOGY
In a healthy heart-

24. Coronary reserve
• increase in coronary perfusion to
accommodate increased demand.
• Autoregulation, mediated by changes in
the vascular tone of the resistance vessels,
allows distal coronary perfusion to remain
unaltered in the face of changes in proximal
perfusion pressures. Impaired endothelial
function disrupts autoregulation and may
lead to ischemia.

25. • In IHD-

26. RISK FACTORS

27. age
common with advancing age. As a
person gets older, the heart
undergoes subtle physiologic
changes, even in the absence of
disease.
The heart muscle of the aged
heart may relax less completely
between beats, and as a result,
the pumping chambers become
stiffer and may work less
efficiently.
When a condition like CVD affects
the heart, these age-related
changes may compound the
problem or its treatment.

28. gender
• A man is at greater risk of heart disease than a pre-menopausal
woman.
• Once past the menopause, a woman’s risk is similar to a
man’s. Risk of stroke, however, is similar for men and women.

29. Family history
• parents or siblings affected by coronary atherosclerotic
heart disease risk for development of the disease
at a younger age than that typical for those without
such a history.
• If a first-degree blood relative has had coronary heart
disease or stroke before the age of 55 years (for a male
relative) or 65 years (for a female relative), the risk
increases

30. Race and ethnicity
• men are more prone to the clinical manifestations
of coronary atherosclerosis is accentuated in
nonwhite populations (e.g., African Americans,
Native Americans, Hispanics).

31. hypertension
Systolic blood pressure and isolated systolic
hypertension are major risk factors at all ages in either
sex.
The Framingham study found that the relative
importance of systolic, diastolic, and pulse pressure
changes with age.

32. • <50 years of age diastolic blood pressure was
the strongest predictor;
• 50 to 59 years all three blood pressure indices
were comparable predictors
• ≥60 years of age pulse pressure was the
strongest predictor
•

33. smoking • single most important
modifiable risk factor for
coronary heart disease
• persons who smoke 20 or
more cigarettes daily have a
2-4 fold increase in coronary
heart disease.
• This increased risk appears
to be proportionate to the
number of cigarettes
smoked per day

34. Smoking
• Main harmful components are tar,
nicotine and CO
– Tar contains hydrocarbons and other
carcinogenic substances
– Nicotine causes release of epinephrine
and norepinephrine resulting in
increased HR, BP, cardiac output, stroke

35. Smoking
• Contributes to development of
atherosclerosis
• Lowers levels of HDL
– causes deterioration of elasticity
of vessels
– Responsible for 20% of all deaths
from heart disease

36. Diabetes mellitus
• Risk of CHD is increased 2-fold in young men and 3-fold in young women with type
2 diabetes
• Patients with diabetes have two- to eight-fold higher rates of future
cardiovascular events as compared with nondiabetic patients.
• Three fourths of all deaths among diabetic patients result from coronary heart
disease

37. Physical inactivity

38. obesity
BMI > 25 kg /m2
Waist circumference
>40 ” for men
>35 ’’ for women

39. dyslipidemia
Serum total cholesterol (TC) is a composite of:
• LDL cholesterol- directly related to CVD
• HDL cholesterol- inversely related to CVD
• VLDL cholesterol- related to CVD in patients with
DM and low HDL
Best single predictor for CVD risk is TC/HDL ratio.
• Ideal ratio is <3, intermediate 3-5, high risk >5
• This ratio is also the best predictor of treatment benefits

40. Relationship Between Cholesterol and CHD Risk:
Epidemiologic Trials
150
125
100
75
50
25
0
10-year CHD death rate
(De aths/100 0)
Serum cholesterol (mg/dL)
1% reduction in total cholesterol
resulted in a 2% decrease in CHD risk
Gotto AM Jr, e t al . Ci rcula tion. 199 0;81:17 21-1 733 .
Ca ste lli WP. Am J Med. 198 4;76:4-1 2.
CHD indications per 1000
Framingham Study (n=5209)
Serum cholesterol (mg/100 mL)
Each 1% increase in total cholesterol level is
associated with a 2% increase in CHD risk
Multiple Risk Factor Intervention Trial
(MRFIT) (n=361,662)
£204 205-234 0 150 200 250 300 235-264 265-294 ³295
50
40
30
20
10

41. Emerging risk factors

42. Metabolic syndrom or syndrom x

43. 1. Abdominal obesity: waist circumference >102 cm in men and >88 cm
in women
2. Hypertriglyceridemia: 150 mg/dL
3. Low high-density lipoprotein (HDL) cholesterol: <40
mg/dL in men and <50 mg/dL in women
4. High blood pressure: 130/85 mm Hg
5. High fasting glucose: 110 mg/dL .

44. Low testosterone Syndrom x

45. pathophysiology
Blood supply of heart
• lateral anterior descending (LAD)
• left circumflex (LCX), and
• right coronary artery (RCA)

46. pathophysiology
FORMATION OF ATHEROMATOUS PLAQUE- Chronic minimal
endothelial injury from both physiologic and pathologic
processes at bending points or bifurcations (branch points)
- the proximal left anterior descending coronary artery is a
common area of atherosclerotic involvement
- dysfunction also may be caused by hypercholesterolemia,
glycation end products in diabetes, irritants in tobacco smoke,
circulating vasoactive amines, immune complexes, and
infection

49. All atheromatous plaques are not associated with clinical
signs and symptoms and may never produce clinical
manifestations.
Several factors may be responsible,
including arterial remodeling, in which the plaque grows
outward away from the lumen with a compensatory
increase in the diameter of the vessel. In addition, col-lateral
circulation may develop to compensate for dimin-ished
blood flow.

50. PATHOPHYSIOLOGY

52. Pathophysiology
AMI results when thrombus (occlusive/nonocclusive)
develops at the site of ruptured plaque
Vulnerable plaque
Rupture
Coagulation cascade platelet adhesion,
activation activation,aggregation
Fibrin and platelet clot
Coronary occlusion
MI

54. Sign and symptoms
• ANGINA PECTORIS
• Angina pectoris is a symptom complex of IHD characterized by paroxysmal and usually
recurrent attacks of substernal or precordial chest discomfort (variously described as
constricting, squeezing, choking, or knifelike) caused by transient (15 seconds to 15
minutes) myocardial ischemia that falls short of inducing the cellular necrosis that
defines infarction.
• There are three overlapping patterns of angina pectoris: (1) stable or typical
angina, (2) Prinzmetal or variant angina, and (3) unstable or crescendo angina.

55. Symptoms
• Chest pain
– Causes
• Exercise, stress, emotion especially if cold,
after a meal
– Description
• Crushing, pressure, tight, heavy, ache
– Location
• Left chest, shoulder
– Radiation
• Arm, neck, jaw, back
– Relieved by rest and/or GTN
• Breathlessness
• Syncope (rare)

56. -Radiated to left or right arm to the neck or lower jaw
-is due to the fact that the spinal
level that receives visceral
sensation from the heart
simultaneously receives cutaneous
sensation from parts of the skin
specified by that spinal
nerve's dermatome,

57. • In rare cases, patients with angina occurring as a manifestation of coronary
atherosclerotic heart disease may experience pain referred to the neck, lower
jaw, or teeth.
• The pattern of onset of pain with physical activity and its disappearance with rest
usually serves as a clue to its cardiac origin

58. Angina Pectoris
 Cause = transient myocardial ischemia( seconds to
minutes)
 Patterns
 Stable = 75% vessel block, transient ( <15 minutes),
aggravated by exertion, relived by rest &
Nitroglycerin (VD)
 Prinzmetal= coronary spasm, episodic, Typical
EKG change – ST elevation, Relived by VD but not
rest
 Unstable = 90% vessel block or Acute plaque
change ( superimposed thrombus), prolonged ( >15
min.),crescendo pattern, not relived by rest, VD,
Pre-infarction Angina

59. Angina in women
A woman's angina symptoms can be different from the classic angina symptoms.
For example, women often experience symptoms such as nausea, shortness of breath, abdominal
pain, or extreme fatigue, with or without with chest pain Or a woman may feel discomfort in her
neck, jaw or back or stabbing pain instead of the more typical chest pressure.
These differences may lead to delays in seeking treatment.

60. Angina classificatioon

61. Myocardial infarction
• Chest pain- most common, similar to anginal pain but
• more severe and prolonged
• described as severe, crushing/squeezing/pressure
• ‘worst pain’ ever
-not relieved by VD
• Atypical presentations:
• confusion, syncope, profound weakness, arrhythmia

62. Transmural
• Full thickness
• Superimposed thrombus
in atherosclerosis
• Focal damage
Sub-endocardial
 Inner 1/3 to half of
ventricular wall
 Decreased circulating blood
volume( shock,
Hypotension, Lysed
thrombus)
 Circumferential

63.  Sudden cardiac death
 unexpected death in one hour due to cardiac causes with or
without clinical symptoms
 Cause – Atherosclerosis ( 90%), others (10%)
 Romano-Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects)
 Mechanism- Most likely due to arrhythmias ( VF)
 Patients – young athletes, with Pul. HTN, IHD
 Morphology
 Prominent finding – increased heart mass
 Vacuolations in Sub – endocardial myocardium

64. • Most clinical signs relate to other underlying cardiovascular disease or
conditions such as congestive failure.
corneal arcus and xanthoma -hyperlipidemia and hypercholesterolemia.
hypertension,
abnormalities in the rate and/or rhythm of pulse
Diminished peripheral pulses in the lower extremities may be noted, along with
bruits in the carotid arteries.
Panoramic radiographs of the jaws may occasionally demonstrate carotid
calcifications in the areas of C3 and C4, consistent with atherosclerotic
plaques in the carotid arteries .
Retinal changes are common in hypertensive disease and diabetes mellitus.
Signs associated with advanced coronary atherosclerotic heart disease usually
reflect the presence of congestive heart failure-Distention of neck veins, peripheral
edema, cyanosis, ascites, and enlarged liver

66. Silent ischemia
-is a particularly dangerous form of myocardial ischemia as there
is a lack of clinical symptoms, i.e., ischemia without angina.
- Usually diagnosed by exercise stress testing or Holter monitoring
-Silent MI = DM, Elderly, Cardiac transplantation
recipients

70. Complications of myocardial infarction
Depending on the extent of the area involved in a myocardial infarction, a
number of complications might arise, including:
1. Rupture of weakened myocardial wall. Bleeding into pericardium may cause
cardiac tamponade and further impair cardiac pumping function. This is
most likely to occur with a transmural infarction. Rupture of the septum
between the ventricles might also occur if the septal wall is involved in the
infarction.
2. Formation of a thromboembolism from pooling of blood in the ventricles.
3. Pericarditis : Inflammation due to pericardial friction rub. Often occurs 1 to 2
days after the infarction.
4. Arrhythmia : Common as a result of hypoxia, acidosis and altered electrical
conduction through damaged and necrotic areas of the myocardium. May
be life-threatening and lead to fibrillation.

71. Complications of myocardial infarction
5. Reduced cardiac function : Typically presents with reduced myocardial
contractility, reduced wall compliance, decreased stroke volume and
increased left ventricular end diastolic volume.
6. Congestive heart failure may result if a large enough area of the
myocardium has been damaged such that the heart no longer pumps
effectively.
7. Cardiogenic shock : Marked hypotension that can result from extensive
damage to the left ventricle. The resulting hypotension will trigger
cardiovascular compensatory mechanisms that will further tax the
damaged myocardium and exacerbate impaired function. Cardiogenic
shock is associated with a mortality rate of 80% or greater.

72. Dressler Syndrome
 Post-myocardial infarction syndrome
 Usually occurs 1 to 8 weeks after infarction
 Patients present with malaise, fever, pericardial discomfort,
leukocytosis, elevated ESR,and a pericardial effusion
 Cause of this syndrome not clearly established (?
Immunopathological process)
 Treatment : ASA 650mg Q4hrs

73. • Causes of death in patients who have had an
acute MI
• include ventricular fibrillation,
• cardiac standstill,
• congestive heart failure,
• embolism,
• rupture of the heart wall or septum.

74. Laboratory findings
• complete blood count , thyroid function tests,renal function tests,lipid
screening ,glucose screening
• homocysteine level determination,
• C-reactive protein assay.
• resting ECG,
• chest x-ray studies,
• exercise stress testing
• HolterECG,
• stress thallium- 201 perfusion scintigraphy,
• exercise echocardiography,
• ambulatory ventricular function monitoring,
• cardiac catheterization and angiography
• Cardiac biomarkers

75. Cardiac biomarkers
• These enzymes are released only when cell death (infarction) or injury to
the myocyte occurs.
• CK-MB
• Troponin T (or I)
• Total CK, LDH and ASAT all invalid

76. Troponin
• are proteins that are derived from the breakdown of myocardial sarcomeres.
• troponin assays have largely replaced creatine kinase
(CK) and CK-MB determinations because these markers
are more specific .
• first detectable 2 to 4 hours after the
onset of an acute MI, are maximally sensitive at 8 to
12 hours, peak at 10 to 24 hours and persist for 5 to
14 days.

77. CK-MB
• CK-MB is another enzymatic marker of cardiac cell injury
• CK-MB is also found after injury to skeletal muscle and
other tissues
• CK-MB is detectable within 3 to 4 hours after infarction;
it reaches peak values at 12 to 24 hours and persists for
2 to 4 days.

78. Testing for levels of B-natriuretic peptide, which is produced
largely by the left ventricle, also aids in determining the extent
of ventricular damage and the prognosis of heart failure.

79. ELECTROCARDIOGRAMS (ECGS OR EKGS)
•Provide a record of the heart's electrical activity.
•This simple test records any abnormal findings in the heart's electrical
impulses. Electrodes are placed on the arms and chest to monitor electrical
activity.
• invented by- William Einthoven

81. ECG Leads
Leads are electrodes which measure the difference in
electrical potential between either:
1. Two different points on the body (bipolar
leads)
2. One point on the body and a virtual
reference point with zero electrical
potential, located in the center of the heart
(unipolar leads)

82. The Concept of a “Lead”
RA
- +
RA
LL
+
+
- -
LA
LL
LA
LEAD II
LEAD I
LEAD III
Leads I, II, and III
• By changing the
arrangement of which arms
or legs are positive or
negative, three unipolar
leads (I, II & III ) can be
derived giving three
"pictures" of the heart's
electrical activity from 3
angles.
Remember, the RL
is always the ground
I
II III

83. ECG Leads
The standard ECG has 12 leads: 3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
The axis of a particular lead represents the viewpoint from which
it looks at the heart.

84. Lead Placement
aVF

85. total Leads
Limb Leads Precordial Leads
Bipolar I, II, III
(standard limb leads)
-
Unipolar aVR, aVL, aVF
(augmented limb leads)
V1-V6

86. All Limb Leads

87. Precordial Leads

88. Precordial Leads

89. Precordial Chest Leads
For every person, each precordial lead placed
in the same relative position
 V1 - 4th intercostal space, R of sternum
 V2 - 4th intercostal space, L of sternum
 V4 - 5th intercostal space, midclavicular
 V3 - between V2 and V4, on 5th rib
 V5 - 5th intercostal space, anterior axillary
line
 V6 - 5th intercostal space, mid-axillary line

90. I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6

91. Anatomic Groups
(Summary)

93. Localising the arterial territory
Inferior
II, III, aVF
Lateral
I, AVL,
V5-V6
Anterior /
Septal
V1-V4

94. Basics
ECG graphs:
– 1 mm squares
– 5 mm squares
Paper Speed:
– 25 mm/sec standard
Voltage Calibration:
– 10 mm/mV standard

95. Wave forms

96. ECG Paper: Dimensions
5 mm
1 mm
0.1 mV
0.04 sec
0.2 sec
Speed = rate
Voltage
~Mass

97. Interpretation
– Rate
– Rhythm (including intervals and blocks)
– Axis
– Hypertrophy
– Ischemia

98. Rate
Rule of 300
Take the number of “big boxes” between neighboring QRS complexes, and divide this
into 300. The result will be approximately equal to the rate
Although fast, this method only works for regular rhythms.

99. What is the heart rate?
(300 / 6) = 50 bpm
www.uptodate.com

100. Rate
• HR of 60-100 per minute is normal
• HR > 100 = tachycardia
• HR < 60 = bradycardia

101. Rhythm
• Sinus
– Originating
from SA node
– P wave before
every QRS
– P wave in
same
direction as
QRS

102. What is this rhythm?
Normal sinus rhythm

103. Normal Intervals
• PR
– 0.20 sec (less than one
large box)
• QRS
– 0.08 – 0.10 sec (1-2 small
boxes)
• QT
– 450 ms in men, 460 ms in
women
– Based on sex / heart rate
– Half the R-R interval with
normal HR

104. Prolonged QT
• Normal
– Men 450ms
– Women 460ms
• Causes
– Drugs (Na channel blockers)
– Hypocalcemia, hypomagnesemia, hypokalemia
– Hypothermia
– AMI
– Congenital
– Increased ICP

105. Blocks
• AV blocks
– First degree block
• PR interval fixed and > 0.2 sec
– Second degree block, Mobitz type 1
• PR gradually lengthened, then drop QRS
– Second degree block, Mobitz type 2
• PR fixed, but drop QRS randomly
– Type 3 block
• PR and QRS dissociated

106. First degree AV block
PR is fixed and longer than 0.2 sec

107. Type 1 second degree block
(Wenckebach)

108. Type 2 second degree AV block
Dropped QRS

109. 3rd degree heart block (complete)

110. What is the axis?
Normal- QRS up in I and aVF

111. Ischemic changes in ECG
• Usually indicated by ST changes
– Elevation = Acute infarction
– Depression = Ischemia
• Can manifest as T wave changes
• Remote ischemia shown by q waves

113. Exercise stress testing
They are used to show how the
heart reacts to physical exertion.
Exercise stress tests are usually
performed on a treadmill or
exercise

114. NUCLEAR CARDIAC IMAGING
•Involves the use of small amounts of short-lived radioactive
material, which is injected into the bloodstream.
• A special camera (live-motion x-ray) detects the radioactivity
of these materials, and the images displayed show how heart
pumps blood.
•
•This is useful in identifying any areas of abnormal motion or
for assessing the blood supply to the heart muscle.

115. ANGIOGRAPHY
It requires a surgical procedure called cardiac
catheterization.
•During the procedure, catheters (small thin plastic
tubes) are placed in the artery of the leg or arm, and
directed using an x-ray machine to the opening of
each of the coronary arteries

116. Angiography

117. Management of ischemic heart disease
1.medical management of patients with
• Stable angina
• Unstable angina
• Myocardial infarction
2.Dental management of ischemic heart disease patients for
• Minor oral surgical procedure
• Major oral surgical procedure

118. Approach to ischemic heart disease patients
Ischemic type chest pain
Stable
angina
Acute coronary syndrome
12-lead ECG
No ST segment elevation
Troponin/CK-MB negative Troponin/CK-MB positive
NSTEMI
Unstable
angina
New onset or change from baseline
ST segment elevation
Troponin/CK-MB positive
STEMI
Myocardial infarction

119. Management of stable angina

120. Management
• General lifestyle measures such as an exercise program; weight control; restriction of
salt, cholesterol, and saturated fatty acids; cessation of smoking
• Control of exacerbating conditions such as anaemia, hypertension, and
hyperthyroidism.
• Patients who have significant angina are encouraged to
• avoid long hours of work,
• take rest periods during the working day,
• obtain adequate rest at night,
• use mild sedatives,
• take frequent vacations, and,
• in some cases, change their occupation or retire.
• Patients should avoid known precipitating factors that may bring on cardiac pain,
such as cold weather, hot and humid weather, big meals, emotional upset, cigarette
smoking, and drugs (e.g., amphetamines, caffeine, ephedrine, cyclamates, alcohol)

121. Pharmacologic management of stable angina
Classification
1. Nitrates
2. Beta blockers
3. Calcium channel blockers
4. Potassium channel opener
5. Others –Dipyridamol, trimetazidine

122. Clinical classification
A. Used to abort or terminate attack- nitrates
B. Used for chronic prophylaxis-all other drugs
1. antiplatelet agents
2. Statins
3. β-adrenergic blockers,
4. calcium channel
blockers
5. ACE inhibitors

123. • venodilators- a cornerstone of the pharmacologic management of angina.
• Nitrates also may alleviate coronary artery spasm
• acute relief and prophylactic
• Nitrates are used to reduce symptoms of angina, but they do not slow, alter,
or reverse the progression of coronary artery disease.
• variety of forms-
• tablet,
• lingual spray,
• ointment, and
• transdermal patch
Nitrates

124. Nitrates
Metabolised to release Nitric oxide (NO)
 cGMP
Venodilation
 preload
Coronary artery
vasodilation
 supply
Moderate
arteriolar dilation
 afterload
Mechanism of action

125. Nitrates
• Glyceryl trinitrate (GTN)
– short acting,
– sublingual/intravenous/patch administration
• Isosorbide dinitrate
– intermediate acting
– sublingual/intravenous/oral administration
• Isosorbide mononitrate
– long acting
– oral administration

126. nitrates
• Doses
– GTN- 5-15 mg oral per 6-8 hour
– Isosorbide dinitrate-10-60 mg oral/4-6 hour
– Isosorbide mononitrate- 20mg oral/12 hour

127. nitrates
INDICATION
• Relief of acute angina attack
• Prophylaxis of stable angina
(prior to exercise GTN or long-acting)
• Left ventricular failure
CONTRAINDICATION
• Hypotension
• Aortic stenosis
• HOCM
• Constrictive pericarditis

128. nitrates
• Adverse drug reaction
– Headache
– Flushing
– Dizziness
– Postural hypotension
– Tachycardia
– Overdose rarely precipitates methaemoglobinaemia
• Tolerance (tachyphylaxis)
– reduced therapeutic effects
• Monday morning sickness

129. Beta blockers
Cardio.selective –
 eg atenolol, metoprolol
Non selective –
 eg propranolol
Intrinsic sympathomimetic (partial agonist) activity –
 eg c pindolol
Alpha-blocking activity
 eg carvedilol

130. Mechanism of action beta blockers
Competitive
inhibitors of
catecholamine
at beta-adrenoceptor
sites

131. Beta blockers
• Cardioselective –
eg atenolol, metoprolol
• Non selective –
eg propranolol
• Intrinsic sympathomimetic (partial agonist) activity –
eg celiprolol pindolol
• Alpha-blocking activity
eg carvedilol
Atenolol -50-100 mg tab
Metoprolol-50-100 mg tab

132. Beta blockers
Indications of beta blockers
• angina
• Hypertension
• Acute coronary syndromes
• Post myocardial infarction
• Thyrotoxicosis
Contra-indications
– C/I in asthma
– heart failure
– Bradycardia
– Heart block
– Phaeochromocytoma
– Avoid abrupt withdrawal

133. Adverse drug reaction
• Beta-1 blocking effects –
– Bradycardia,
– heart block,
– heart failure
• Beta-2 blocking effects –
– bronchospasm,
– worsening PVD,
– Raynaud’s phenomenon
• Fatigue, depression, nightmares, impotence
• worsen glycaemic control in IDDM

134. Calcium channel blockers
• MOA-Prevent
opening of voltage-gated calcium channels by Binding to -1 subunit of
cardiac and smooth muscle L-type calcium channels
decrease intracellular calcium
vasodilatation of coronary, peripheral, and pulmonary vasculature, along with
decreased myocardial contractility and heart rate.

135. Ca channel blockers
3 classes
1. Phenylalkylamines
– eg verapamil
– relatively cardioselective
– -ve chronotropic and inotropic
2. Dihydropyridines
– eg nifedipine amlodipine
– relatively smooth muscle selective
– potent vasodilator
– Dose-amlo -5–10 mg orally OD
– nife-5-20 mg BID
3. Benzothiazepines
– eg diltiazem
– intermediate

136. Calcium channel blockers
Indications
• control of angina
• Coronary spasm
• Hypertension
• Arrhythmias
• Subarachnoid haemorrhage (nimodipine)

137. Ca channel blockers
• ADVERSE DRUG REACTIONS
Peripheral vasodilation
- flushing, headache, ankle oedema
Cardiac effects
- AV block, heart failure
Constipation

138. POTASSIUM CHANNEL OPENER
MOA- smooth muscle relaxation
Eg-nicorandil –MOA same as nitrates
Dose-5-20 mg BID

139. Angiotensin-converting enzyme (ACE) inhibitors
• indicated for use in patients with coronary heart disease
who also have
• diabetes,
• left ventricular dysfunction, or
• hypertension.
• Eg -Captopril, lisinopril., enalapril
• Dose- captopril 25-50 mg b.i.d/t.i.d
MOA
Inhibit synthesis
of Angiotensin II
decrease in
peripheral
resistance
decrease
preload

140. Antiplatelet agents
• Aspirin –
– inhibits cyclo-oxygenase and
– thromboxane A2 synthesis
• Theinopyridines – clopidogrel –
– block binding of ADP to platelet receptor
• Glycoprotein IIb/IIIa inhibitors (abciximab) –
– inhibit cross-bridging of platelets by fibrinogen

141. • Regular use of aspirin in patients with stable angina is associated with a
significant reduction in fatal events.
• in patients with unstable angina, aspirin decreases the chances of fatal and
nonfatal MI.
• dose - 75 to 325 mg, is recommended for all patients with acute and chronic
ischemic heart disease, regardless of the presence or absence of symptoms.
• Clopidogrel- it is used in place of or in combination with aspirin. Dose-75 mg
OD

142. The statins
in the liver
inhibit 3-hydroxy-3-
methylglutaryl coenzyme
A reductase (HMG-CoA)
Statins also are anti-inflammatory
Eg- rosuvastatin 5-10 mg OD
leading to enhanced
expression of the LDL
receptors that capture
blood cholesterol
increase HDL cholesterol lower LDL cholesterol
It has shown to decrease
the risk for a major
coronary event and the
risk of death.

143. revascularisation
Revascularization useful for stable or unstable angina
procedures for revascularization-
– percutaneous transluminacoronaryangioplasty,
– stents
– coronary artery bypass grafting

144. Percutaneous transluminal coronary angioplasty( PTCA)
-also known as balloon angioplasty
-stenosis recurs within 6 months in 10% to 50% of patients, along with a return of
symptoms.

145. STENTS
• a thin, expandable, metallic mesh stent positioned by the balloon and expanded against the
plaque and vessel wall, then left in place.
-has decreased the incidence of restenosis to about 20% to 30%

146. Currently, two types of stents are used:
1. bare metal
2. Drug eluting
• bare metal stents maintain mechanical patency; do not prevent endothelial
proliferation that results in restenosis.
• Drug-eluting stents are coated with antiproliferative agents that are very
effective in controlling restenosis.
• carry an increased risk for thrombosis for up to 1 year, so patients with such
stents require long-term use of aspirin and/or clopidogrel

148. non–balloon angioplasty methods
atherectomy
use of lasers.

149. Coronary artery bypass graft (CABG)
With coronary artery bypass grafting, a segment of artery or vein is
harvested or released from a donor site; it is then grafted to the
affected segment of coronary artery, thus bypassing the area of
occlusion .
donor sites : saphenous vein from the leg
internal mammary artery from the chest.

150. internal mammary artery graft- sturdier and much less susceptible to graft atherosclerosis and
occlusion than vein grafts
saphenous vein- Within 10 years postoperatively, 30% of grafts become occluded, while internal
mammary artery grafts are much more resistant to
The arterial grafts are preferred for first bypass procedures when possible.

151. Unstable Angina & Acute
Coronary Syndromes
• In patients with unstable angina with recurrent ischemic episodes at rest, recurrent
thrombotic occlusions of the offending coronary artery occur as the result of fissuring of
atherosclerotic plaque and platelet aggregation.
• Anticoagulant and antiplatelet drugs play a major role in therapy .
• Aspirin has been shown to reduce the incidence of cardiac events in such patients.
• Intravenous heparin or subcutaneous low-molecular-weight heparin is indicated in most
patients.
• Antiplatelet agents (ticlopidine, clopidogrel, and GPIIb/IIIa antagonists) have been found to
be effective in decreasing risk in unstable angina
• In addition, therapy with nitroglycerin and -blockers should be considered; calcium channel
blockers should be added in refractory cases.

152. Medical management of Unstable angina
• “MONA” – morphine; O2; nitrate; aspirin
• Heparin eg enoxaparin 1mg/kg 12 hourly
• Beta-blocker atenolol 5mg over 5 mins repeated after 10-15 mins
• Clopidogrel
• Glycoprotein IIb/IIIa inhibitors (abciximab) if undergoing PCI
• ACE inhibitor if indicated
• Tight glycaemic control
• Optimise potassium and magnesium

153. Medical management of
Myocardial Infarction
• Rapid hospitalization and immediate emeregency
treatemt
• Early administration of aspirin is recommended, with
160 to 325 mg to decrease platelet aggregation and
limit thrombus formation.
• The definitive treatment for acute MI depends on the
extent of ischemia as reflected on the ECG, which
shows the presence or absence of ST segment
elevation

154. ECG shows an acute anterior/lateral MI. ST segment e
levation is evident in leads I, aVL, and V1-6
non-STEMI –due to partial blockage of coronary blood flow.
STEMI -due to complete blockage of coronary blood flow and more
profound ischemia
This distinction is clinically important because early fibrinolytictherapy
improves outcomes in STEMI but not in non–STEMI

156. Thrombolytic (or fibrinolytic) drugs
MOA
• Activate plasminogen to form plasmin which degrades fibrin breaking up thrombi
Eg:Streptokinase, alteplase, reteplase, tenecteplase
indications
• Acute ST elevation myocardial infarction
• Acute pulmonary embolism
• Acute ischaemic stroke within 3 hours

157. contraindications
• Recent haemorrhage trauma or surgery
• Recent dental extraction
• Coagulation defects;bleeding disorders
• Aortic dissection
• History of cerebrovascular disease
• Active peptic ulceration
• Severe menorrhagia
• Severe hypertension
• Active cavitating lung disease
• Acute pancreatitis
• Severe liver disease
• Oesophageal varices
• Previous reaction to streptokinase (Streptokinase)

158. ADR
• Nausea and vomiting
• Bleeding
• Reperfusion arrhythmias
• Hypotension
• Back pain
• Allergic reactions (esp streptokinase)

159. early revascularization
- Thrombolytic therapy for STEMI
- PTCA WITH STENTING
-Coronary artery bypass grafting

160. Pharmacologic therapy

161. • morphine sulfate is the drug of choice for pain relief,
• 2-5mg IV every 5 to 30 minutes
• Sedatives and anxiolytic medications also may be used.
• Oxygen may be administered by nasal cannula during the acute period to
enhance oxygen saturation of the blood and keep the heart workload at a
minimum level

162. Management during minor
surgical procedures

163. Screening & Evaluation
 History:
 Symptoms such as angina and dyspnoea may be absent at rest
 Emphasizing the importance of evaluating the patient's response to
various physical activities such as walking or climbing stairs
 If a patient can climb two to three flights of stairs without symptoms, it
is likely that cardiac reserve is adequate.
• Previous H/O chest pain/Myocardial Infarction
• Co-Existing Noncardiac Diseases
• Current Medications

164. Risk assessment
• 1. Severity of the disease
• 2. Type and magnitude of the dental procedure
• 3. Stability and cardiopulmonary reserve of the patient

167. The concept of metabolic equivalent or METS -
One MET is defined as 3.5 mL of O2/Kg/min .
1 to 4 METS: eating, dressing, walking around house, dishwashing
4 to 10 METS: climbing at least one flight of stairs, walking level ground 6.4
km/hr, running short distance, game of golf
R10 METS: swimming, singles tennis, football
-who cannot perform at a minimum of a 4 MET level is at increased risk for a
cardiovascular event.

168. Approach to patients with Angina Pectoris/Past
History of Myocardial Infarction.
A determination regarding the presence, severity, and stability
of ischemic symptoms.
patients with stable angina - intermediate cardiac risk.
patient with unstable angina major cardiac risk and are not
candidates for elective dental care .

169. Patients who have had an MI in the past may or may not have
ischemic symptoms .
asymptomatic patient with no other risk factors-risk is minimal
symptoms present - major risk category, and elective dental
care should be deferred and medical consultation obtained
.
with other clinical risk factors is at increased risk for an adverse
event, and medical consultation should be obtained before
elective dental care

170. Considerations for minor oral surgical procedure
intermediate risk category
patients with stable angina or a past history of MI without ischemic symptoms
and no other risk factors may include the following:
– short appointments in the morning,
– comfortable chair position,
– pretreatment vital signs
– availability of nitroglycerin,
– oral sedation, nitrous oxide–oxygen sedation,
– profound local anesthesia, limited amount of vasoconstrictor,
– avoidance of epinephrine-impregnated retraction cord, and effective postoperative pain
control.

171. • patients who have had balloon angioplasty with placement of a coronary artery stent, or for those
who have undergone a CABG procedure, antibiotic prophylaxis is not recommended
• NSAIDs should be avoided in patients with established
cardiovascular disease, especially those whose cardiac history includes an MI.
• NSAIDs be used with caution, if at all, in patients who have had a previous MI, and that if an
NSAID is used, naproxen be the drug of choice, administered for less than 7 days.

172. Considerations for major risk patients
For patients with symptoms of unstable angina or those who have had an MI within the past 30
days
-elective care should be postponed
-If treatment becomes necessary, it should be performed as conservatively as possible and directed
primarily toward pain relief, infection control, or the control of bleeding, as appropriate.
-Consultation with physician

173. Additional management recommendations may include-establishing
and maintaining an intravenous line
continuously monitoring the ECG
vital signs,
using a pulse oximeter,
administering nitroglycerin prophylactically just before the initiation of
treatment

174. Vasoconstrictors
Local anesthetics without vasoconstrictors may be used as needed.
If a vasoconstrictor is necessary, patients with intermediate clinical risk factors and
those taking nonselective beta blockers can safely be given up to 0.036 mg
epinephrine (two cartridges containing 1 : 100,000 epinephrine) at one
appointment; intravascular injections are to be avoided.
For patients at higher risk, the use of vasoconstrictors should be discussed with the
physician

175. Bleeding
Patients who take daily aspirin and/or other antiplatelet agents
(e.g., clopidogrel) can expect some increase in surgical and
postoperative bleeding, but this is generally not clinically
significant and can be controlled with local measures only.
Discontinuation of these agents before dental treatment
generally is unnecessary.
• Patients who are taking warfarin for anticoagulation can safely
undergo dental or surgical procedures,provided that the INR is
3.5 or less .
• Discontinuation of antiplatelet agents and anticoagulants (e.g.,
warfarin) before dental treatment and routine extractions
generally is unnecessary.

177. 1. Terminate all procedures
2. Semi-reclined position
3. Sublingual NTG
4. O2
5. Check vital signs
Still discomfort after 3min
Still discomfort after 3min
Still discomfort after 3min
Discomfort relieved
Give 2nd NTG
Give 3rd NTG
6. Assume angina pectoris was present
7. Slowly taper O2 over 5min
8. Modify dental treatment
INTRAOPERATIVE
CHEST PAIN
NTG
0.6mg/tab

178. 10. Assume myocardial infarction in progress
11. On IV line
12. Prepare transport to ER
If highly suspected AMI
MONA: Morphine, Oxygen, NTG, Aspirin

179. management of ischemic heart disease patients for
major surgical procedure under GA

180. An algorithm for preoperative assessment of patients with ischemic
heart disease

181. Risk stratification
➣ Variables related to 4 major categories:
• Nature of surgery (high, moderate or low risk),
• Presence of IHD,
• Presence of CHF
• Presence of cerebrovascular disease
➣ Presence of comorbid conditions(diabetes mellitus, aortic stenosis, PVD)
➣ Exercise tolerance

182. Goldman's index of cardiac risk
in noncardiac procedures

183. PRE-OPERATIVE CONSIDERATION
 Elective surgery in pts with a history of AMI should be delayed up to 6months after the episode of
AMI if possible.
 Patients with coronary stents should have their surgery delayed at least 4 wks after stenting
when possible
 Intraoperative tachycardia can increase the risk of intraoperative ischemia & perioperative MI.

184. ■ Continue beta blockers; they were found to increase long-term survival in patients with IHD.
■ Calcium channel blockers do not increase the negative inotropic & vasodilatory effects of inhalational
agents but may potentiate the effects of depolarizing & nondepolarizing muscle relaxants
.
■ Stop ACE inhibitors the night before surgery to avoid severe hypotension intraoperatively.
■ Stop aspirin 1 wk before surgery if possible; anticoagulation must be held to decrease risk of
bleeding.

185. Preoperative Medication
- Anxiolysis with sedatives/narcotics
(benzodiazepines, opioids, scopolamine 0.4–0.6 mg IM or 0.2–0.4 mg IV)
- Continuation or administration of beta blockers
- Administration of nitroglycerine
- Maintain heart rate & blood pressure within 20% of normal values.

186. INTRAOPERATIVE CONSIDERATION
Induction :
➣ The main goal during induction is to avoid hypertension & tachycardia,
thereby decreasing drastic cardiac events.
➣ Minimize extreme variation in heart rate & blood pressure.
 Control cardiovascular response to tracheal intubation by keeping low
duration of laryngoscopy(<15sec) or by pharmacologic means. For eg.
lidocaine (1.5–2 mg/kg), IV 2 min before intubation
 Avoid induction agents capable of stimulating sympathetic nervous
system (ketamine, pancuronium)

187. • Maintenance of anaesthesia-
Volatile anesthetics (isoflurane, desflurane and sevoflurane) are safe to use
with IHD.
Vecuronium, rocuronium, cisatracurium are attractive choices for patients
with ischemic heart disease
Keep BP & heart rate within 20% of awake values
Maintain intraoperative heart rate at less than 80 bpm
Minimizing body heat loss
To maintain adequate myocardial oxygen delivery, do notallow hemoglobin
to drop below 10 g/dL

188. • ECG, Transesophageal echocardiography monitoring
Intraoperative ischemia may be treated with
• beta blockers (esmolol) in case of tachycardia,
• IV nitrates in the case of hypertension,
• IV sympathomimetics & fluids in hypotension.

189. Emergence from GA
• Proper pain control is key to avoid myocardial ischemic events.
• Muscle relaxants can be reversed with neostigmine in combination with
glycopyrrolate, as the latter produces less tachycardia.
• Supplemental oxygen to maintain adequate oxygen saturation

190. post op consideration
■ Supplemental oxygen is crucial.
■ Pain control to avoid excessive sympathetic nervous system stimulation
■ Maintain adequate beta blockade.
■ 12-lead ECG as a baseline
■ Prevention of shivering & maintenance of normothermia is crucial to
avoid oxygen desaturation & sympathetic nervous system activation.
■ Maintaining adequate oxygenation & tight pain control for 48 to 72 hr
postop is very important, since this is the period when the likelihood of
developing AMI is highest.