MANAGEMENT OF MEDICALLY COMPROMISED PATIENTS-

CARDIO-VASCULAR DISEASESISCHEMIC HEART DISEASE

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

INTRODUCTIONo Ischaemia refers to an insufficient amount of blood.

o myocardial ischemia—an imbalance between thesupply (perfusion) and demand of the heart foroxygenated blood.

o The coronary arteries are the only source of bloodfor the heart muscle.

• Ischaemic Heart Disease (IHD) refers to a group of pathophysiologically related clinical syndromes;

• angina• myocardial infarction• chronic IHD with heart failure • sudden cardiac death

A glimpse of heart anatomy and physiology

surfaces

The internal anatomy of the heart

8

Coronary supply

Two pumps-pulmonary and systemic circuit

CARDIAC CYCLE- 0.8 second

SUB –DIVISION OF ANS

ELECTRICAL CONDUCTION SYTEM OF HEART

Cardiac output,heart rate and stroke volume

EPIDEMIOLOGY

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

Global Vs National scenario

National scenario

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

The coronary arteries.

ETIOLOGY

In a healthy heart-

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.

• In IHD-

RISK FACTORS

agecommon 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.

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.

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

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).

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.

• <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

•

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

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

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

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

Physical inactivity

obesity

BMI > 25 kg /m2

Waist circumference>40 ” for men>35 ’’ for women

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

0

25

50

75

100

125

150

Gotto AM Jr, e t al . Ci rcula tion. 1990;81:1721-1733 .

Caste lli WP. Am J Med. 1984;76:4-12.

Relationship Between Cholesterol and CHD Risk:Epidemiologic Trials

10-y

ear

CH

D d

eath

ra

te(D

eat

hs/

100

0)

Serum cholesterol (mg/dL)

1% reduction in total cholesterol

resulted in a 2% decrease in CHD risk

CH

D indic

atio

ns

pe

r 10

00

Each 1% increase in total cholesterol level is

associated with a 2% increase in CHD risk

Serum cholesterol (mg/100 mL)

Framingham Study (n=5209)Multiple Risk Factor Intervention Trial

(MRFIT) (n=361,662)

£204 205-234 235-264 265-294 ³295150 200 250 3000

50

40

30

20

10

Emerging risk factors

Metabolic syndrom or syndrom x

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 .

Low testosterone Syndrom x

pathophysiology

Blood supply of heart

• lateral anterior descending (LAD)

• left circumflex (LCX), and

• right coronary artery (RCA)

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

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.

PATHOPHYSIOLOGY

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

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.

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)

-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 cutaneoussensation from parts of the skin specified by that spinal nerve's dermatome,

• 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

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

Angina in womenA 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.

Angina classificatioon

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

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

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

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

• Most clinical signs relate to other underlying cardiovascular disease or conditions such as congestive failure.

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

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.

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.

Complications of myocardial infarction

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

• 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.

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

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

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.

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.

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.

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

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)

+-

RA

RA

LL+

+

--LA

LL

LA

LEAD II

LEAD I

LEAD III

Remember, the RLis always the ground

• By changing the arrangement of which arms or legs are positive or negative, three unipolarleads (I, II & III ) can be derived giving three "pictures" of the heart's electrical activity from 3 angles.

The Concept of a “Lead”

Leads I, II, and III

I

II III

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.

Lead Placement

aVF

total Leads

Limb Leads Precordial Leads

Bipolar I, II, III(standard limb leads)

-

Unipolar aVR, aVL, aVF (augmented limb leads)

V1-V6

All Limb Leads

Precordial Leads

Precordial Leads

Precordial Chest LeadsFor 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

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Anatomic Groups(Summary)

Localising the arterial territory

InferiorII, III, aVF

LateralI, AVL, V5-V6

Anterior / SeptalV1-V4

Basics

ECG graphs:

– 1 mm squares

– 5 mm squares

Paper Speed:

– 25 mm/sec standard

Voltage Calibration:

– 10 mm/mV standard

Wave forms

ECG Paper: Dimensions5 mm

1 mm

0.1 mV

0.04 sec

0.2 sec

Speed = rate

Voltage~Mass

Interpretation

– Rate

– Rhythm (including intervals and blocks)

– Axis

– Hypertrophy

– Ischemia

Rate

Rule of 300Take 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.

What is the heart rate?

(300 / 6) = 50 bpm

www.uptodate.com

Rate

• HR of 60-100 per minute is normal

• HR > 100 = tachycardia

• HR < 60 = bradycardia

Rhythm• Sinus

– Originating from SA node

– P wave before every QRS

– P wave in same direction as QRS

What is this rhythm?

Normal sinus rhythm

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

Prolonged QT

• Normal – Men 450ms

– Women 460ms

• Causes– Drugs (Na channel blockers)

– Hypocalcemia, hypomagnesemia, hypokalemia

– Hypothermia

– AMI

– Congenital

– Increased ICP

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

First degree AV block

PR is fixed and longer than 0.2 sec

Type 1 second degree block (Wenckebach)

Type 2 second degree AV block Dropped QRS

3rd degree heart block (complete)

What is the axis?

Normal- QRS up in I and aVF

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

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

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.

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

Angiography

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

Approach to ischemic heart disease patients

Ischemic type chest painStable angina

12-lead ECG

Acute coronary syndrome

No ST segment elevation

Troponin/CK-MB positiveTroponin/CK-MB negative

NSTEMIUnstable

angina

New onset or change from baseline

ST segment elevation

Troponin/CK-MB positive

STEMI

Myocardial infarction

Management of stable angina

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, cigarettesmoking, and drugs (e.g., amphetamines, caffeine, ephedrine, cyclamates, alcohol)

Pharmacologic management of stable angina

Classification

1. Nitrates

2. Beta blockers

3. Calcium channel blockers

4. Potassium channel opener

5. Others –Dipyridamol, trimetazidine

Clinical classificationA. 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

• 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

Nitrates

Metabolised to release Nitric oxide (NO)

cGMP

preload

Venodilation

Coronary artery vasodilation

supply

Moderate arteriolar dilation

afterload

Mechanism of action

• Glyceryl trinitrate (GTN)– short acting, – sublingual/intravenous/patch administration

• Isosorbide dinitrate– intermediate acting– sublingual/intravenous/oral administration

• Isosorbide mononitrate– long acting– oral administration

Nitrates

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

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

nitrates

• Adverse drug reaction – Headache

– Flushing

– Dizziness

– Postural hypotension

– Tachycardia

– Overdose rarely precipitates methaemoglobinaemia

• Tolerance (tachyphylaxis)– reduced therapeutic effects

• Monday morning sickness

Beta blockers

.Cardioselective – eg atenolol, metoprolol

Non selective – eg propranolol

Intrinsic sympathomimetic (partial agonist) activity – eg c pindolol

Alpha-blocking activity eg carvedilol

Competitive inhibitors of

catecholamine at beta-

adrenoceptorsites

Mechanism of action beta blockers

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

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

Beta blockers

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

Calcium channel blockers

• MOA-

Prevent opening of voltage-gated calcium channels by Binding to -1 subunit ofcardiac and smooth muscle L-type calcium channels

decrease intracellular calcium

vasodilatation of coronary, peripheral, and pulmonary vasculature, along withdecreased myocardial contractility and heart rate.

Ca channel blockers3 classes1. 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

Calcium channel blockers

Indications• control of angina

• Coronary spasm

• Hypertension

• Arrhythmias

• Subarachnoid haemorrhage (nimodipine)

Ca channel blockers• ADVERSE DRUG REACTIONS

Peripheral vasodilation- flushing, headache, ankle oedema

Cardiac effects- AV block, heart failure

Constipation

POTASSIUM CHANNEL OPENER

MOA- smooth muscle relaxation

Eg-nicorandil –MOA same as nitrates

Dose-5-20 mg BID

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

Inhibit synthesis of Angiotensin II

decrease in peripheral resistance

decrease preload

MOA

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

• Regular use of aspirin in patients with stable angina is associated with asignificant reduction in fatal events.

• in patients with unstable angina, aspirin decreases the chances of fatal andnonfatal MI.

• dose - 75 to 325 mg, is recommended for all patients with acute and chronicischemic heart disease, regardless of the presence or absence of symptoms.

• Clopidogrel- it is used in place of or in combination with aspirin. Dose-75 mgOD

The statins

Statins also are anti-inflammatory

Eg- rosuvastatin 5-10 mg OD

in the liverinhibit 3-hydroxy-3-

methylglutaryl coenzyme A reductase (HMG-CoA)

leading to enhanced expression of the LDL receptors that capture

blood cholesterol

lower LDL cholesterol increase HDL cholesterol

It has shown to decrease the risk for a major

coronary event and the risk of death.

revascularisationRevascularization useful for stable or unstable angina

procedures for revascularization-

– percutaneous transluminacoronaryangioplasty,

– stents

– coronary artery bypass grafting

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.

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%

Currently, two types of stents are used:1. bare metal2. Drug eluting

• bare metal stents maintain mechanical patency; do not prevent endothelialproliferation that results in restenosis.

• Drug-eluting stents are coated with antiproliferative agents that are veryeffective in controlling restenosis.

• carry an increased risk for thrombosis for up to 1 year, so patients with suchstents require long-term use of aspirin and/or clopidogrel

non–balloon angioplasty methods

atherectomy

use of lasers.

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 theaffected segment of coronary artery, thus bypassing the area ofocclusion .

donor sites : saphenous vein from the leg

internal mammary artery from the chest.

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.

Unstable Angina & Acute Coronary Syndromes

• In patients with unstable angina with recurrent ischemic episodes at rest, recurrentthrombotic occlusions of the offending coronary artery occur as the result of fissuring ofatherosclerotic 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 mostpatients.

• Antiplatelet agents (ticlopidine, clopidogrel, and GPIIb/IIIa antagonists) have been found tobe effective in decreasing risk in unstable angina

• In addition, therapy with nitroglycerin and -blockers should be considered; calcium channelblockers should be added in refractory cases.

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

Medical management of Myocardial Infarction

• Rapid hospitalization and immediate emeregencytreatemt

• Early administration of aspirin is recommended, with160 to 325 mg to decrease platelet aggregation andlimit thrombus formation.

• The definitive treatment for acute MI depends on theextent of ischemia as reflected on the ECG, whichshows the presence or absence of ST segmentelevation

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 fibrinolytictherapyimproves outcomes in STEMI but not in non–STEMI

Thrombolytic (or fibrinolytic) drugsMOA

• 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

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)

ADR• Nausea and vomiting

• Bleeding

• Reperfusion arrhythmias

• Hypotension

• Back pain

• Allergic reactions (esp streptokinase)

early revascularization

- Thrombolytic therapy for STEMI

- PTCA WITH STENTING

-Coronary artery bypass grafting

Pharmacologic therapy

• 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

Management during minor surgical procedures

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

Risk assessment

• 1. Severity of the disease

• 2. Type and magnitude of the dental procedure

• 3. Stability and cardiopulmonary reserve of the patient

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 6.4km/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 acardiovascular event.

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 .

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

Considerations for minor oral surgical procedureintermediate risk categorypatients 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.

• patients who have had balloon angioplasty with placement of a coronary artery stent, or for thosewho 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 anNSAID is used, naproxen be the drug of choice, administered for less than 7 days.

Considerations for major risk patients

For patients with symptoms of unstable angina or those who have had an MI within the past 30days

-elective care should be postponed

-If treatment becomes necessary, it should be performed as conservatively as possible and directedprimarily toward pain relief, infection control, or the control of bleeding, as appropriate.

-Consultation with physician

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

Vasoconstrictors

Local anesthetics without vasoconstrictors may be used as needed.

If a vasoconstrictor is necessary, patients with intermediate clinical risk factors andthose taking nonselective beta blockers can safely be given up to 0.036 mgepinephrine (two cartridges containing 1 : 100,000 epinephrine) at oneappointment; intravascular injections are to be avoided.

For patients at higher risk, the use of vasoconstrictors should be discussed with thephysician

BleedingPatients who take daily aspirin and/or other antiplatelet agents

(e.g., clopidogrel) can expect some increase in surgical andpostoperative bleeding, but this is generally not clinicallysignificant and can be controlled with local measures only.Discontinuation of these agents before dental treatmentgenerally is unnecessary.

• Patients who are taking warfarin for anticoagulation can safelyundergo dental or surgical procedures,provided that the INR is3.5 or less .

• Discontinuation of antiplatelet agents and anticoagulants (e.g.,warfarin) before dental treatment and routine extractionsgenerally is unnecessary.

1. Terminate all procedures2. Semi-reclined position3. Sublingual NTG4. 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 present7. Slowly taper O2 over 5min8. Modify dental treatment

INTRAOPERATIVE

CHEST PAIN

NTG 0.6mg/tab

10. Assume myocardial infarction in progress11. On IV line12. Prepare transport to ER

MONA: Morphine, Oxygen, NTG, Aspirin

If highly suspected AMI

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

An algorithm for preoperative assessment of patients with ischemic heart disease

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

Goldman's index of cardiac riskin noncardiac procedures

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.

■ 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.

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.

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)

• 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

• 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.

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

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.