KULIAH MCI.ppt

KULIAH MCI

ACUTE MYOCARDIAL INFARCTION

• Epidemiology

• Pathology

• Pathophysiology

• Clinical features

• Management

• Hospital management

• Hemodynamic disturbances

• Arrhythmias

• Convalescence, discharge, post-myocardial infarction care

EpidemiologyAcute myocardial infarction (AMI)

• Major public health problem in indus-trialized world and becoming increasingly important problem in developing countries, Indonesia no national data

• Death rate from AMI 30% in last decade, but still fatal in 30% of patients 50% within one hour of event mainly due to ventricular fibrillation

Trend Pola Penyakit Penyebab Utama Kematian Dalam Kurun Waktu 10 Tahun

di Indonesia, SKRT 1992, 1995, 2001

0

5

10

15

20

25

30

Inf&Parasit Sirkulasi Napas Cer na Neoplasma Kecelakaan Perinatal

199219952001

Epidemiology

05

101520253035

Defibrillation Hemodynamic

monitoring Beta blockade

15

Thrombolysis/ PTCAASA

6.5

30

Pre CCU era CCU era Reperfusion era%

Mor

talit

y (in

hos

pita

l)The impact of medical therapy for AMI on short-term mortality

1.0

0.8

0.6

0.4

0.2

0.00 1 2 3 4 5 6 7 8 9 10

1950 – 19691970 – 19791980 - 1989

Cum

ula

tive

inci

denc

e o

f C

HD

dea

th

Years of follow-up

Pathology

Almost all MIs result from coronary athero-sclerosis

AMI part of acute coronary syndrome

A Schematic Life History of an Atherosclerotic Lesion

ATHEROSCLEROSIS (1)

Atheroma Formation1. Lipoprotein accumulate in intima

Endothelium more permeable to LDL lipoprotein

2. Leucocyte recruitment and accumulation in intima by leucocyte adhesion molecules and chemokines

Monocyte accumulate lipids and transform into foam cells

T lymphocytes also enter intima

3. Excessive lipid uptake by scavengar receptors ; preferentially oxidized LDL

Foam cells replicate

Fatty streak formation

ATHEROSCLEROSIS (2)Atheroma Formation4. Smooth muscle cells migrate from media to intima attracted

by platelet-derived growth factor (PDGF) Secreted by activated macrophagesSmooth muscle cells replicate due to exposure to mitogens

(e.g., thrombin)5. Extracellular matrix make up most of plaque volume :

interstitial collagens, proteoglycans, elastin produced by smooth muscle cellsBreakdown of these molecules by matric metallopro-teinases

(MMPs)Luminal stenosis only after plaque burden exceeds 40% of

cross-sectional area of artery6. Endothelial migration and proliferation neovascula-rization

in plaquePlaques often develop areas of calcification

Schematic of the Evolution of the Aterosclerotic Plaque

Nomenclature of acute coronary syndromes

Acute coronary syndrome

Non ST elevation ST elevation

Myocardial infarctionNQMI Qw MI

NSTEMI

Braunwald E. Heart Disease : a textbook of cardiovascular Medicine,. 6 th Ed. 2001

Unstable angina

Pathology

Role of acute plaque change

Plaque rupture exposure to substances that promote platelet activation and aggregation, thrombin generation and ultimately thrombus formation.

Thrombus interrupts blood flow and if imbalance between oxygen supply and demand is severe and persistent it leads to myocardial necrosis

Schematic diagram suggesting probable

mechanisms responsible for the

conversion from chronic coronary heart

disease to acute coronary artery

disease syndromes

Schematic representation of

the progression of myocardial necrosis

after coronary artery occlusion

Plaque rupture common pathophysiological substrate of acute coronary syndromes

• Completely occlusive thrombus ST elevation on ECG –

necrosis of full thickness of ventr. wall

75% - ST elevation diminishes followed by Q-wave

development

• Less obstructive thrombi and/or those that are constituted by

less robust fibrin formation and on greater proportion of

platelet aggregation ST segment depression and/or T wave

inversion

• Relief of transient vasospasm or spontaneous lysis of

thrombus within 20 minutes no necrosis, no release of

biochemical markers of necrosis no persistent ECG changes

PATHOPHYSIOLOGY

If sufficient quantity of myocardium undergoes ischemic injury LV pump function end-systolic volume Infarct zone thins and elongates infarct expansionDilatation of ventricle depends on infarct size, patency of infarct-related artery, and activation of local RAS in noninfarcted portion of ventricle-ultimately : fibrosis – stiffness of myocardium Area of infarct :

8% - diastolic compliance > 15% - ejection fraction

LV end-diastolic pressure volume > 25% - clinical heart failure> 40% - cardiogenic shock

The vicious circle in cardiogenic shock

CLINICAL FEATURES

PREDISPOSING FACTORS

50% - precipitating factor or prodromal symptoms

• Unusually heavy exercise

• Accelerating angina, rest angina

• Noncardiac surgical procedures

• Respiratory infection, hypoxia, cocain use, stroke, TIA

• Circadian periodicity

Peak incidence between 8 a.m – 12 p.m

Plasma cathecholamines

Cortisol

Platelet aggregability

HISTORYPRODROMAL SYMPTOMS

History very valuable to establish D/ Prodoma : chest discomfort – unstable angina1/3 symptoms for 1 – 4 wks20% symptoms for < 24 hrsMalaise, exhaustion

NATURE OF PAIN• Most patients

severe prolonged, > 30 minutes - hours• Constricting, crushing, oppressing, compressing

heavy weight or squeezing in chest• Choking, viselike, heavy pain or stabbing, knifelike, boring or

burning discomfort• Location : retrosternal, spreading frequently to both sides of the

chest with predilection to the left side• Often pain radiates down ulnar aspect of left arm, producing

tingling sensation in left wrist, hand and fingers

NATURE OF PAIN

• SOME INSTANCES : pain begins in epigastrium, and simulate abdominal disorder

• Sometimes pain radiates to shoulders, upper extremities, neck, jaw and interscapular region favoring the left side

• Elderly : no chest pain but acute left ventricular failure and chest tightness or marked weakness or syncope

• Pain arises from nerve endings in ischemic or injured, but not necrotic, myocardium

OTHER SYMPTOMS

50% nausea or vomiting in transmural infarcts

Occasionally diarrhea, profound weakness, dizziness, palpation, cold perspiration, sense of impending doom

Occasionally : cerebral embolism or systemic arterial embolism

DIFFERENTIAL DIAGNOSIS

• Acute pericarditis

– Some pleuritic features : aggravated by resp. movements, often involves shoulder, ridge of trapezius, neck

– Sharp, knifelike, aggravated by each breath

• Pulmonary embolism

– Pain lateral in chest, often pleuritic may be associated with hemoptysis

• Dissection of aorta

– In center of chest, extremely severe (ripping, tearing), maximal shortly after onset, persists for many hours, often radiates to back and lower extremities, often one or more arterial pulses absent)

• Costochondral/and costosternal pain

– Localized swelling and redness

– Sharp and darting, marked localized tenderness

• Esophagitis, gastroesophageal reflux disease (GERD)

PHYSICAL EXAMINATIONGENERAL APPEARANCEAnxious, considerable distress, restless, fist on

chestLV failure & symp. stimulation : cold perspiration,

pallor, dyspnea, cough with frothy pink or blood-streaked sputum.

Shock : cool, clammy skin, facial pallor, cyanosis, confusion or disorientation

HEART RATEVariable depending on underlying rhythm and

degree or ventr. failureMost commonly, HR 100 – 110/min; > 95% patients

: VPB’s within first 4 hours

BLOOD PRESSUREMajority normotensive, but syst. BP may decline

and diast. BP may rise Half of pts with inferior MI parasympathetic

stimulation : hypotension, bradycardia or both half of pts with anterior MI, sympathetic excess

: hypertension, tachycardia or both

TEMPERATURE AND RESPIRATIONMost pts with extensive MI fever within 24-48

hrs, fever resolves by 4th or 5th dayRespiration due to anxiety and pain, in LV failure :

resp. rate correlates with degree of heart failure

JUGULAR VENOUS PULSE

JVP usually normal

RV infarction : marked jug. venous distension

CAROTID PULSE

Small pulse reduced stroke volume

Pulse alternans : severe LV dysfunction

CHEST

LV failure : moist rales

Severe failure : wheezing

1967 : Killip & Kimball : prognostic classification

ClassI : patients free of rales or S3

II : rales < 50% lung fields +/- S3

III : rales > 50% lung fields, frequently pulm. edema

IV : cardiogenic shock

CARDIAC EXAMINATION

PALPATION

May be normal, but with transmural AMI presystolic pulsation, S4

Abn. systolic pulsation in 3rd, 4th, 5th ics on left of sternum due to dyskinesis

Longstanding hypertension or previous infarction : laterally displaced, sustained apical impulse

AUSCULTATION• S1 muffled• S3 reflects severe LV dysfunction with elevated ventr.

filling pressure• S4 almost always present in AMI with sinus rhythm due

to reduced LV compliance

Commonly andible in most pts with chronic ischemic heart disease and sometimes in normal subjects > 45 years

• Murmurs

Systolic MR : dysfunction of mitral valve, rupture of head of

papillary muscle TR Rupture of IV septum

PERICARDIAL FRICTION RUBS

• In large transmural infarcts

24 hrs – 2 weeks, most commonly after 2nd or 3rd

day

• Delayed onset of rub – characteristic of Dressler’s

syndrome

LABORATORY EXAMINATION

MARKERS OF CARDIAD DAMAGEST elevation and Q wave (highly indicative of AMI)

only in 50% of pts on presentation30% AMI no classic chest pain50% AMI nondiagnostic ECGChest pain in EMG < 20% develop AMI

Periodic determination of serum cardiac markers necessary

AMI myocytes necrotic intracellular macromolecules (serum cardiac markers) microvasculature systemic circulation

Creatine Kinase (CK)

Exceeds normal in 4 – 8 hours, normal in 2

– 3 days; not specific

CK isoenzymes : CKMB

Myoglobin

Peak level in 1 – 4 hours

Cardiac-specific troponins :

Troponin I

Troponin T

Criteria for the Diagnosis of Acute Myocardial Infarction (AMI)

Increased biomarkers plus one or more of the

following

Pathological findings of AMI

Typical symptoms of AMI plus one of the

following

Procedural myocardial

damage

Typical symptoms of myocardial ischemia

No other findings required

ST segment elevation in the ECG

Increased levels of cardiac biomarkers to prespecified levels; symptoms may be absent; ECG changes may be absent or nonspecific

Q waves in the ECG Increased levels of cardiac biomarkers

ST segment elevation or depression in the ECG

Plot of the appearance of cardiac markers in blood versus time after onset of symptoms

Current-of-injury patterns with acute ischemia

ELEKTROKARDIOGRAM

Hyperacute phase of extensive anterior-lateral MI

Sequence of depolarization and repolarization changes with (A) acute anterior-lateral and (B) acute

inferior wall Q infarctions

IMAGINGRntgenography

Degree of congestion and size of left side of heart useful for risk determination

Echocardiography• Region of wall motion abnormality• LV function

Doppler echocardiography• Assessing severity of MR, TR• Identifying side of acute ventr. or septal rupture

& quantification of shunt flow

Other : nuclear imaging, computed tomography, magnetic resonance imaging

MANAGEMENT

•Prehospital care

•Management in emergency department

•Reperfusion of myocardial infarction

•Hospital management

•Convalescence, discharge, postmyocardial

infarction care

PREHOSPITAL CARE

Major components of time delay between onset of infarction and restoration of flow in the infarct-related artery

PREHOSPITAL CARE

• Time = muscle

• in first hour of AMI due to ventr. fibrillation

• Patient education most important, pts with risk

factors, known CAD, symptoms of AMI

• Prehospital thromboliysis (?)

17% reduction of mortality

MANAGEMENT IN EMERGENCY DEPARTMENTPossible Acute Coronary Syndrome (ACS)

Assess initial 12-lead ECG

Nondiagnostic ECGECG diagnostic of ACS

ASABeta blockade

Antithrombin therapy

ST elevation ECG strongly suspicious for ischemia (ST depression, T

wave inversion)

Admit, Initiate anti-ischemic therapy,

Initiate reperfusion strategy if ST elevation develops

Routine blood tests on admission: CBC, lipid profile, electrolytes

Continue evaluation in observation unit

Obtain follow-up ECGs and serum marker

levels

Consider 2D echo

Evidence of ischemia/infarction ?

Discharge (goal =8-12h)

Rapid triage to “urgent care” roomObtain baseline sserum cardiac marker levels

NoYes

MANAGEMENT IN EMERGENCY DEPARTMENT

ASABeta blockade

Antithrombin therapy

ST elevation

Routine blood tests on admission: CBC, lipid profile, electrolytes

> 12 h 12 h

Persistent symptoms ?Not a candidate for reperfusion

therapy

Thrombolysis therapy

contraindicated

Eligible for thrombolytic

therapy

Primary PCI : consider IV GP IIb/IIIA inhibitor and stent as needed

YesNo

Consider reperfusion

therapyOther medical therapy : ACE inhibitors; ? Nitrates; correc metabolic and electrolyte

deficits

Administer thrombolytic

• Brief, targeted history• 12-lead ECG immediately• Bedside ECG monitor• Iv access D5W

If ST elevation 1 mm in 2 contiguous leads or new BBB – screen immediately for contraindication to thrombolysis

thrombolysis < 30 minutes, if longer; mortality rises; max. allowed interval : 12 hours

AMI without ST elevation (40 – 50%)

repeat ECG & cardiac markers, treat as non ST-elevation MI

GENERAL TREATMENT MEASURES

Aspirin : inhibition of cyclooxygenase block thromboxane A2 formationEffective for acute coronary syndromesPart of initial management of pts with suspected AMI160 – 325 mg chewed in EMG dpt

Control of cardiac painCombination of nitrates , analgesics (e.g. morphine), oxygen, beta-adrenoceptor blockers

MorphineDrug of choice4 – 8 mg i.v, 2 – 8 mg repeated at intervals of 5 – 15 minutesSome pts may need 2 – 3 mg/kg BW

Nitrates : coronary dilatation and increase of venous capacitance

No hyportension sublingual nitroglycerin

Beta-adrenoceptor blockers :

No heart failure, hypotension or heart block metoprolol iv 3 x 5 mg i.v, then continued orally

Oxygen : no hypoxemia 2 – 4 l/min for 6 – 12 hrs

REPERFUSION OF MYOCARDIAL INFARCTION

ThrombolysisStreptokinase 1.5 mill u/60 minutesTissue plasminogen activation 100 mg/90 minutesReteplaseTenacteplase

PCI (Percutaneous Coronary Intervention)• Primary angioplasty• Adjunctive th/with thrombolysis• Subacute phase (days 2-7) in pts who do not receive

thrombolysis Coronary artery bypass surgery

• Recurrent/persistent chest pain after thrombolysis/ PCI• LM stenosis• Ventr. Septal rupture/severe MR

ANTITHROMBOTIC AND ANTIPLATELET THERAPY

Heparin probably of no benefit as adjunct to streptokinase, but may be helpful in pts receiving tPA

Newer agents : hirudin, efegatran, hirulog, low-molecular-weight heparins

Antiplatelet therapy

Aspirin loading dose 160 – 325 mg (chewed) maintenance 75 mg

Pts who cannot tolerate aspirin : clopidogrel 75 mg

GPIIb/IIIa inhibitors useful to support primary PCI

HOSPITAL MANAGEMENT

Coronary Care Unit Prevention of death from VF Hemodynamic monitoring Th/of serious complications of AMI

Intermediate Coronary Care Unit CHF Recurrent VT, VF AF Heart block Anterior MI + recurrent angina + marked ST

segment abnormality

SAMPLE ADMITTING ORDERS (1)

Condition Serious

IV : NS or D5W to keep vein open

Vital signs q ½ hr until stable, then q 4 h and prn.Notify if HR < 60 or > 110; BP < 90 or > 150; RR < 8 or > 22. Pulse oximetry x 24 hr

Activity Bed rest with bedside commode and progress as tolerated after approximately 12 hr

SAMPLE ADMITTING ORDERS (2)Diet NPO until pain free, then clear liquids.

Progress to a heart-healthy diet (complex carbohydrates = 50-55% of kilocal.), monounsaturated and unsaturated fats (30% of kilocal.), including foods high in potassium (e.g., fruits, vegetables, whole grains, dairy products), magnesium (e.g., green leafy vegetables, whole grains, beans, seafood), and fiber (e.g., fresh fruits and vegetables, whole-grain breads, cereals).

Medications • Nasal O2 L/min x 3 hr• Enteric-coated ASA daily (164 mg)• Stool softener daily• Beta-adrenoceptor blockers ?• Consider need for analgesics, nitroglycerin,

anxiolytics

PHARMACOLOGICAL Th/

Betablockers Pts without a contraindication, betablockers

Ace-inhibitorsAll considered for ACE-inhibition th/ esp CHF, ST

segment elevation or LBBBNitrates

Persistent chest pain, LV failure, large anterior transmural AMI

Ca-antagonistsVerapamil or diltiazem not recommended as routine th/

in AMIMay be used for AF or ongoing ischemia for whom

blockers ineffective or contraindicated

HEMODYNAMIC DISTURBANCES

• LV failure• Cardiogenic shock• RV infarction• Mechanical causes of heart failure

Free wall rupturePseudo aneurysmRupture of interventricular septumPapillary muscle rupture

Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction (1)

CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT

THERAPEUTIC OPTIONS

1. Electrical instability

Ventricular premature beats

Correction of electrolyte deficits and increased sympathetic tone

Potassium and magnesium solutions, beta blocker

Ventricular tachycardia

Prophylaxis against ventricular fibrillation, restoration of hemody-namic stability

Antiarrhythmic agents; cardioversion/defibrillation

Ventricular fibrillation Urgent reversion to sinus rhythm

Defibrillation, bretylium tosylate

Accelerated idioventricular rhythm

Observation unless hemodynamic function is compromised

Increase sinus rate (atropine, atrial pacing); antiarrhythmic agents

Nonparoxysmal atrio-ventricular junctional tachycardia

Search for precipitating causes (e.g. digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromised

Atrial overdrive pacing agent; cardioversion relatively contra-indicated if dititalis intoxication present


CATEGORY ARRHYTHMIAOBJECTIVE OF TREATMENT

THERAPEUTIC OPTIONS

2. Pump failure/ excessive sympathetic stimulation

Sinus tachycardia Reduce heart rate to diminish myocardial oxygen demand

Antipyretics; analgesics, consider beta blocker unless congestive heart failure present; treat latter if present with anticonges-tive measures (diuretics, afterload reduction)

Atrial fibrillation and/or atrial flutter

Reduce ventricular rate; restore sinus rhythm

Verapamil, digitalis glycosides; anticongestive measures (diuretics, afterload reduction); cardioversion; rapid atrial pacing (for atrial flutter)

Paroxysmal supraventricular tachycardia

Reduce ventricular rate; restore sinus rhythm

Vagal maneuvers; verapamil, cardiac glycosides, beta-adrener-gic blockers; cardiover-sion; rapid atrial pacing


CATEGORYARRHYTHMI

AOBJECTIVE OF TREATMENT

THERAPEUTIC OPTIONS

3. Bradyarrhythmias and conduction disturbances

Sinus bradycardia

Acceleration of heart rate only if hemodynamic function is compromised

Atropine; atrial pacing

Junctional escape rhythm

Acceleration of sinus rate only if loss of atrial “kick” causes hemody-namic compromise

Atropine; atrial pacing

Atrioventricu-lar block and intraventricu-lar block

Insertion of pacemaker

CONVALESCENCE, DISCHARGE, POST-MI CARE

Timing of discharge5 – 6 days after admission for pts without complications

Counseling Instruction concerning physical activity Use of medication Behavioral alteration Rehabilitation program

physicalpsychological

RISK STRATIFICATION

• Poor prognosis : female, age > 70 years, DM, prior angina pectoris, previous MI

• Anterior MI

• AV block, AF

• Large MI, recurrent ischemia and reinfarction

• Assessment at hospital discharge

– Assessment of LV function : LV ejection fraction

– Assessment of myocardial ischemia

– Assessment for electrical instability

MANAGEMENT ALGORITHM FOR RISK STRATIFICATION AFTER ACUTE MYOCARDIAL INFARCTION (1)

Clinical Indications of High Risk at Predischarge

Symptom-limited exercise test at 14-21 days

Strategy I

Cardiac catheterization

Exercise imaging study

Present

Absent

Strategy II Strategy III

Markedly abnormal

Mildly abnormal

Negative

Reversible ischemia No reversible ischemia

Medical treatment


Submaximal exercise test at 5-7 days


Absent

Strategy II Strategy III

Markedly abnormal

Mildly abnormal

Negative


Strenuous leisure activity or occupation

Cardiac catheterizatio

n


Symptom-limited exercise testing at 3 –

6 wk

Strenuous leisure activity or occupation

Cardiac catheterizatio

n

Markedly abnormal

Mildly abnormal

Negative



Medical treatment

SECONDARY PREVENTION OF RECURRENT ACUTE MYOCARDIAL INFARCTION

• Life style modificationCessation of smoking, control of hypertension, diabetes mellitus

• Modification of lipid profileLDL cholesterol < 100 mgLHDL cholesterol > 40 mgLTriglycerides < 150 mg%

• Antiplatelet agents, aspirin 80-325 mg or Ticlopidine, Clopidogrel

• ACE inhibitors, -adrenoceptor blockers, nitrates• Ca antagonists, only in pts who cannot take

blockers• Antiarrhythmics – routine use not recommended

UNSTABLE ANGINA

Definition and classification

Pathophysiology

Clinical presentation

Diagnosis of UA / NSTEMI

Risk stratification

Medical therapy

Treatment strategies and interventions

DEFINITION

STABLE ANGINA PECTORIS

deep, poorly localized chest or arm

discomfort that is reproducibly associated

with physical exertion or emotional stress

and relieved within 5–15 minutes by rest

and or sublingual nitroglycerine

DEFINITIONUNSTABLE ANGINA PECTORIS : angina pectoris (or equivalent

type of ischemic discomfort) with at least one of three features

1. It occurs at rest (or with minimal exertion) usually > 20 min

2. It is severe and described as frank pain and of new onset (i.e., within one month)

3. It occurs with a cressendo pattern (e.g., more severe, prolonged, or frequent than previously). Some with prolonged chest pain myocardial necrosis NSTEMI (non ST segment elevation myocardial infarction)

Braunwald Clinical Classification of Unstable Angina (1)

CLASS DEFINITIONDEATH OR MI

TO 1 YEAR

SeverityClass I

New onset of severe angina or accelerated angina; no rest pain

7.3%

Class II Angina at rest within past month but not within preceding 48 hr (angina at rest, subacute)

10.3%

Class III Angina at rest within 48 hr (angina at rest, subacute)

10.8%

Braunwald Clinical Classification of Unstable Angina (2)

CLASS DEFINITIONDEATH OR MI

TO 1 YEAR

Clinical Circumstances

A (secondary angina) Develops in the presence of extra-cardiac condition that intensifies myocardial ischemia

14.1%

B (primary angina) Develops in the absence of extra-cardiac condition

8.5%

C (postinfarction angina)

Develops within 2 weeks after acute myocardial infarction

18.5%

Intensity of treatment

Patients with UA may also be divided into three groups depending on whether UA occurs (1) in the absence of treatment for chronic stable angina, (2) during treatment for chronic stable angina, or (3) despite maximal antiischemic drug therapy. The three groups may be designated subscripts 1, 2, or 3, respectively.

Electrocardiographic changes

Patients with UA may be further divided into those with or without transient ST-T wave changes during pain

5 pathophysiological processes that may contribute to the development of unstable angina

1. Plaque rupture with superimposed nonocclusive thrombus

2. Dynamic obstruction (i.e., coronary spasm of an epicardial artery or constriction of the small muscular arteries)

3. Progressive mechanical obstruction4. Inflammation and/or infection5. Secondary unstable angina, precipitated by

increased oxygen demand or decreased supply (e.g., thyrotoxicosis or anemia)

Individual patients may have several processescoexisting

PATHOPHYSIOLOGY

Plaque rupture, fissure, or erosion

By far more common cause of UA/NSTEMI

Vulnerable plaque < 50% stenosis, high lipid content, local inflammation causing breakdown of thin shoulder of plaque, coronary artery constriction at site of plaque, local shear stress forces, platelet activation and prothrombotic stage formation of platelet-rich thrombi at site of plaque rupture/erosion acute coronary syndrome

Inflammation and/or infarctionKey role in development of atherosclerosis and in development and recurrence of UAChlamydia pneumonia ?Helicobacter pylori ?Cytomegalovirus ?

Thrombosismany observations support the central role of coronary artery thrombosis in the pathogenesis of unstable angina

Platelet aggregation, secondary hemostasis, coronary vasoconstriction and progression of mechanical obstruction all play an important role in the pathogenesis of UA

CLINICAL PRESENTATION

30 – 45% UAP

25 – 30% NSTEMI

20% STEMI

80% UAP : history of CAD

History & physical examinationIschemic pain

Chest discomfort on exertion or at rest severe enough to be considered painful

Physical examination

May be unremarkable or may support diagnosis of cardiac ischemia

Ischemia of large fraction of LV : transient diaphoresis, pale cool skin, sinus tachycardia, 3rd or 4th heart sound, basilar rates, rarely hypotension

ECGUAP : ST segment depression (or transient ST segment elevation) and T wave changes in 50% patients. Continuous ECG monitoring more sensitive than symptoms

Cardiac markersIf positive CK-MB, troponin T or I diagnosis NSTEMI

Cor. arteriography15% 3VD30% 2VD40% 1VD20% no significant stenosis coronary micro-vascular dysfunction

Angioscopy & intravascular ultrasound

Features associated with higher likelihood of CAD among pts presenting with symptoms suggestive of UA

HistoryChest pain as chief complaint similar to prior ACS symptoms

Known history of coronary artery disease, myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft

History of anginaAge > 60Male genderMore than two major cardiac risk factorsDiabetesExtracardiac vascular disease (carotid or peripheral)

Physical ExaminationPulmonary rales, hypotensionTransient mitral regurgitationDiaphoresis

ElectrocardiogramNew/presumably new ST deviation > 0.05 mVT wave inversion 0.1 mVQ waves, left bundle branch block

Cardiac MarkersElevated CK-MB, troponin I or T

Natural History

by 30 days : 3.5 – 4.5%

new/recurrent MI 6 – 12%

Indicators of increased risk in unstable angina

HistoryAdvanced age (> 65 years)Diabetes mellitusPost-myocardial infarction anginaPrior peripheral vascular diseasePrior cerebrovascular disease

Clinical PresentationBraunwald Class II or III (acute or subacute rest pain)

Braunwald Class B ( secondary unstable angina)

ElectrocardiogramNew/ST segment deviation 0.05 mVT wave inversion 0.3 mVLeft bundle branch block

Cardiac MarkersIncreased troponin T or I or CK-MBIncreased C-reactive protein (CRP)

AngiogramThrombus

General measures• Bedrest 12 – 24 hrs

• Monitoring – ECG

• Oxygen

• Relief of chest pain :

nitrates

betablockers

morphine sulfate

Nitrates

Sublingual / buccal spray, 3x, 5 minutes apart

If pain persists : i.v. nitroglycerin 5-10 ug/min;

max 200 ug/min

Betablockers

Recommended when no contraindication

Atenolol 5-10 mg iv bolus followed by 100 mg

orally

Metoprolol 5 mg iv bolus, 3x given 2-5 minutes

apart followed by 50 mg orally 2x daily, titrated

to 2x/100 mg daily

Ca channel blockers

3rd drug after nitrates & betablocker or if c.i. to

betablocker

ACE inhibitors

Shortterm no benefit when LV not impaired

Lipid-lowering th/

Statins costeffective longterm

ANTITHROMBOTIC THERAPY IN UA/NSTEMI

Aspirin

50% in risk of death

Clopidogrel and ticlopidine

Inhibits platelet aggregation for pts who can not tolerate aspirin

Heparin

Low-Molecular-Weight heparins

Direct thrombin inhibitors : hirudin

Oral anticoagulation : warfarin

Glycoprotein IIb/IIIa inhibitors

High risk pts :

IV glycoprotein IIb/IIIa inhibitor + aspirin + heparin

Standardized nomogram for titration of heparin

Initial Dose : 60 U/kg bolus and 12 U/kg/hr infusion.Activated partial thromboplastin time (APTT) should be checked and infusion adjusted at 6, 12, and 24 hours after initiation of heparin, daily thereafter, and 5 to 6 hours after any adjustment in dose.

APTT CHANGE IV INFUSION (U/kg/hr)

< 3535 – 4950 – 7071 – 90> 100

70 U/kg bolus35 U/kg bolus

0 0Hold infusion for 30 min

+ 3+ 2 0- 2- 3

Algorithm for risk stratification and treatment of patients with UA/NSTEMI

CHRONIC CORONARY ARTERY DISEASE

Stable angina pectoris

Other manifestations

Prinzmetal’s (variant) angina

Silent myocardial ischemia

Ischemic cardiomyopathy

STABLE ANGINA PECTORIS

• Clinical manifestationsDifferential diagnosis of chest painPhysical examination

• Pathophysiology

• Noninvasive testing

Catheterization, angiography, coronary arterio-graphy

• Medical management

• Percutaneous coronary interventions and coronary artery surgery

CARDIOVASCULAR CAUSES OF CHEST PAIN (1)

CONDITION

LOCATION QUALITY DURATION

Angina Retrosternal region: radiates to or occasionally isola-ted to neck, jaw, epigastrium, shoulder or arms-left common

Pressure, burning, squeezing, heaviness, indigestion

< 2–10 min

Rest or UA Same as angina Same as angina but may be more severe

Usually <20 min

Myocardial infarction

Substernal and may radiate like angina

Heaviness, pressure, burning, constriction

Sudden onset, 30 min or longer but variable


CONDITION

LOCATION QUALITY DURATION

Pericarditis Usually begins over sternum or toward cardiac apex and may radiate to neck or left shoulder; often more localized than the pain of myocardial ischemia

Sharp, stabbing, knifelike

Lasts many hours to days; may wax and wane

Aortic dissection

Anterior chest; may radiate to back

Excruciating, tearing, knifelike

Sudden onset, unrelenting


CONDITION LOCATION QUALITY DURATION

Pulmonary embolism (chest pain often not present)

Substernal or over region of pulmonary infarction

Pleuritic (with pulmonary infarction) or angina-like

Sudden onset; minutes to <1 hr

Pulmonary hypertension

Substernal Pressure, op-pressive


CONDITION

AGGRAVATING OR RELIEVING FACTORS

ASSOCIATED SYMPTOMS OR SIGNS

Angina Precipitated by exercise, cold weather or emotional stress; relieved by rest or nitroglycerin; atypical (Prinzmetal’s) angina may be unrelated to activity, often early morning

S4, or murmur of papillary muscle dysfunction during pain

Rest or UA Same as angina, with decreasing tolerance for exertion or at rest

Similar to stable angina, but may be pronounced. Transient cardiac failure can occur

Myocardial infarction

Unrelieved by rest or nitroglycerin

Shortness of breath, sweating, weakness, nausea, vomiting


CONDITION

AGGRAVATING OR RELIEVING FACTORS


Pericarditis

Aggravated by deep breath-ing, rotating chest, or supine position; relieved by sitting up and leaning forward

Pericardial friction rub

Aortic dissection

Usually occurs in setting of hypertension or predisposi-tion such as Marfan’s syndrome

Murmur of aortic insuf-ficiency, pulse or blood pressure asymmetry; neurological deficit


CONDITION AGGRAVATING OR RELIEVING FACTORS


Pulmonary embolism (chest pain often not present)

May be aggravated by breathing

Dyspnea, tachypnea, tachy-cardia; hypotension, signs of acute right-sided heart failure, and pulmonary hypertension with large emboli; rales, pleural rub, hemoptysis with pulmonary infarction

Pulmonary hypertension

Aggravated by effort Pain usually associated with dyspnea; signs of pulmonary hypertension

Pain Patterns with Myocardial Ischemia

PHYSICAL EXAMINATION

General examination

Corneal arcus sometimes correlates with elevated cholesterol, low-density cholesterol and prognosis

Xanthelasma appears to be promoted by increased levels of triglycerides and a relative deficiency of high-density lipoprotein

Retinal arteriolar changes in diabetes mellitus or hypertension

Blood pressure may be elevated

Peripheral vascular disease in strongly associated with CAD

Cardiac examination

Examination during chest pain transient left

ventricular dysfunction (S3, S4, pulmo-nary

rales), softening of mitral component of S1 >

paradoxical spliting of S2.

Sustained apical cardiac impulse, displaced

ventricular impulse LV dysfunction

Transient apical systolic murmur – reversible

papillary muscle dysfuntion

Pathophysiology

PathophysiologyAngina pectoris caused by imbalance between oxygen demand and supply

Angina caused by increased myocardial O2 requirements

• O2 requirement increased in face of constant, restricted O2 supply.

Exertion, emotion, mental stress

Rate - increased hemodynamic and catecholamine responses to stress

• Chills, fever, thyrotoxitosis, tachycardia, hypoglycemia, precipitants of ischemia

Angina caused by transiently decreased O2

supply

UAP and stable angina may be caused by vaso-constriction

Platelet thrombi and leucocytes may cause release of vasoconstrictor substances : seroto- nin,

thromboxane A2

Endothelial damage causes decreased production of vasodilatior substances

Without organic obstruction lesions, severe dynamic obstruction at rest alone myocardial ischemia (Prinzmetal’s angina)

CLASS

CANADIAN CARDIOVASCULAR SOCIETY FUNCTIONAL CLASSIFICATION

I Ordinary physical activity, such as walking and climbing stairs, does not cause angina. Angina with strenuous or rapid or prolonged exertion at work or recreation

II Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions

CLASS

CANADIAN CARDIOVASCULAR SOCIETY FUNCTIONAL CLASSIFICATION

III Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight in normal conditions

IV Inability to carry on any physical activity without discomfort — anginal syndrome may be present at rest

• Biochemical tests

– Risk factors : dyslipidemia, CHD intolerance, insulin resistance (CRP, Lp(a), homocysteine)

• Resting ECG

• Exercise EKG

• Stress myocardial perfusion imaging

• Pharmacological nuclear stress testing – adeno-sine, dipyridamole

• Stress echocardiography

• Pharmacological stress echocardiography -- dobutamine

Noninvasive testing

High-Risk Findings on Noninvasive Stress Testing (1)

EXERCISE ELECTROCARDIOGRAPHY2.0 mm or greater ST segment depression1.0 mm or greater ST segment depression in stage 1ST segment depression for longer than 5 min during the

recovery periodAchievement of a workload of less than 4 METs or a low

exercise maximal heart rateAbnormal blood pressure responseVentricular tachyarrhythmiasMYOCARDIAL PERFUSION IMAGINGMultiple perfusion defects (total plus reversible defects) in

more than one vascular supply region (e.g., defects in coronary supply regions of the left anterior descending and left circumflex vessels)

Large and severe perfusion defects (high semiquantitative defect score)

Increased lung thallium-201 uptake reflecting exercise-induced left ventricular dysfunction

Postexercise transient left ventricular cavity dilatationLeft ventricular dysfunction on gated single-photon emission

computed tomography

High-Risk Findings on Noninvasive Stress Testing (2)

STRESS ECHOCARDIOGRAPHY

Multiple reversible wall motion abnormalities

Severity and extent of these abnormalities (high global wall motion score)

Severe reversible cavity dilation

Left ventricular systolic dysfunction at rest

Angiographic Views of the Left Coronary Artery

1. Identification and treatment of associated diseases that can precipitate or worsen angina

2. Reduction of coronary risk factors

3. Application of general and nonpharmacological methods (adjustments in lifestyle)

4. Pharmacological management

5. Revascularization (PCI or CABG)

Medical management

• Hypertension

– Predisposes to vascular injury

– Accelerated development of aterosclerosis

– Increase myocardial O2 demand

– Intensifies ischemia

Antihypertensive th/ mort. and CV events by 16%

• Dietary and life style modification

obese

• Cigarette smoking

Predisposis to atherosclerotic plaque erosion and acute thrombosis

Increases myocardial O2 demand and coronary tone

• Dyslipidemia

NCEP guidelines

Reduction of Coronary Risk Factors

• Aspirin

• Betablocker

• Angiotensin converting enzyme (ACE) inhibitors

• Nitrates

• Ca antagonists

Pharmacological Therapy

1. Identify and treat precipitating factors : anemia, hypertension, thyrotoxicosis, tachyarrhythmias, congestive heart failure, concomitant valvular heart disease

2. Initiate risk factor modification, physical exercise life style counseling. Initiate therapy with HMG-CoA reductase inhibitor, as needed to reduce LDL cholesterol < 100 mg/dl

3. Initiate therapy with aspirin and a betablocker. Strongly consider an ACE inhibitors as first-line th/ in chronic CAD

4. Use sublingual nitroglycerine for alleviation of symptoms and prophylactically

Approach to patients with chronic stable angina (1)

5. If episodes occur more than 2-3 x/week add ca

antagonists

6. If angina persists, add third antianginal agent

7. Cor angiography with view to consider coronary

revascularization indicated if symptoms or ischemia

persists despite optimal medical therapy. Also consider

in “high-risk” pts and those with occupations/life style

that require a more aggressive approach

Approach to patients with chronic stable angina (2)

1. Significant left main CAD

Most pts with three vessel disease that included proximal LAD especially were LV dysfunction CABG

2. Heart failure + severe ischemia especially if significant extent of potentially viable dysfunctioning myocardium

3. Single vessel disease + severe ischemia PCI

4. Angina without high risk – similar survival for medically or surgically treated pts

Indication for coronary revascularization

COR PULMONALE CHRONICUM (CPC)

Hipertrofi & dilatasi ventrikel kanan sebab hipertensi pulmonal akibat peny. parenkim dan/atau vaskuler paru (antara a. pulmonal utama dan masuknya vv pulmonal ke atrium kiri)

Etiologi UtamaPenyakit paru obstruktif khronis (PPOK) akibat bronkhitis khronis atau emfisema paru

ETIOLOGY OF PULMONARY HEART DISEASE (1)I. DISEASES AFFECTING THE PULMONARY VASCULATURE

A. Primary diseases of the arterial wall(1) Primary pulmonary hypertension(2) Granulomatous pulmonary arteritis(3) Toxin-induced pulmonary hypertension

a. Aminorex fumarateb. Intravenous drug abuse

(4) Chronic liver disease(5) Peripheral pulmonic stenosis

B. Thrombotic disorders(1) Sickle cell diseases(2) Pulmonary microthrombi

C. Embolic disorders(1) Thromboembolism (3) Other embolism (amniotic fluid, air)(2) Tumor embolism (4) Schistosomiasis and other parasitic

diseasesII. PRESSURE ON PULMONARY ARTERIES BY MEDIASTINAL TUMORS,

ANEURYSMS, GRANULOMATA, OR FIBROSISIII. DISEASES OF THE NEUROMUSCULAR APPARATUS AND CHEST WALL

A. Neuromuscular weakness D. Pleural fibrosisB. Kyphoscoliosis E. Sleep apnea syndromesC. Thoracoplasty F. Idiopathic hypoventilation

IV. DISEASES AFFECTING AIR PASSAGES OF THE LUNG AND ALVEOLI

A. Chronic obstructive pulmonary diseases

B. Cystic fibrosis

C. Congenital development defects

D. Infiltrative or granulomatous diseases

(1) Idiopathic pulmonary fibrosis

(2) Sarcoidosis

(3) Pneumoconiosis

(4) Scleroderma

(5) Mixed connective tissue disease

(6) Systemic lupus erythematosus

(7) Rheumatoid arthritis

(8) Polymyositis

(9) Eosinophilic granuloma

(10) Malignant infiltration

(11) Radiation

E. Upper airways obstruction

F. Pulmonary resection

G. High-altitude disease

ETIOLOGY OF PULMONARY HEART DISEASE (2)

PATHOGENESIS OF COR PULMONALEChronic lung disease

Reduction in pulmonary Hypoxia vascular bed

Acidosis andhypercapnia

Polycythemia and hyperviscosity Pulmonary hypertension

Hypertrophy and dilatationof the right ventricle

Right ventricular failure

PEMERIKSAAN PENDERITA CPC

Klinis :• Pemeriksaan fisik susah karena emfisema

pulm pada PPOK• Systolic parasternal heave• Tricuspid regurgitation• P2 >• Tanda gagal jantung kanan

EKG : Sangat spesifik, kurang sensitif

ELECTROCARDIOGRAPHIC CHANGES IN COR PULMONALE (1)ECG CRITERIA FOR COR PULMONALE WITHOUT

OBSTRUCTIVE DISEASE OF THE AIRWAYS

1. Right-axis deviation with a mean QRS axis to the right of + 110

2. R/S amplitude ratio in V > 1

3. R/S amplitude ratio in V < 1

4. Clockwise rotation of the electrical axis

5. P-pulmonale pattern

6. S Q or S S S pattern

7. Normal voltage QRS

o

1

6

1 3 1 2 3

ELECTROCARDIOGRAPHIC CHANGES IN COR PULMONALE (2)

ECG CHANGES IN CHRONIC COR PULMONALE WITH OBSTRUCTIVE DISEASE OF THE AIRWAYS1. Isoelectric P waves in lead I or right-axis deviation of the P

vector2. P-pulmonale pattern (an increase in P-wave amplitude in II,

III, AVf)

3. Tendency for right-axis deviation of the QRS

4. R/S amplitude ratio in V6 < 1

5. Low-voltage QRS

6. S1Q3 or S1S2S3 pattern

7. Incomplete (and rarely complete) right bundle branch block

8. R/S amplitude ratio in V1 > 1

9. Marked clockwise rotation of the electrical axis10. Occasional large Q wave or QS in the inferior or mid-

precordial leads, suggesting healed myocardial infarction

X-Thorax • Jantung dapat normal, atau membesar

dengan apeks terangkat• Dilatasi konus pulmonal + cabang besarnya,

sedangkan cabang-cabang kecil tak terlihat karena vasokonstriksi

• PPOK : kelainan paru-paru terlihat

Ekhokardiografi Doppler - ekho :

- Tek. a. pulmonalis- TR- RV dilatasi

HIPOKSIA• Sebab terpenting hipertensi pulmonal pada

PPOK• Vasokonstriksi pulmonal (langsung atau

lewat pelepasan zat vasoaktif)• Proliferasi sel endotel dan penebalan intima

arteriol• Hipertrofi tunica media a. pulmonal• Vasodilatasi terhambat

PENGELOLAAN

• OKSIGENDiberikan kontinu 1-2 l/menit, dapat memperbaiki prognosis karena mengurangi vasokonstriksi pulmonal dan memperbaiki hipoksia

• DIGITALISHanya bila juga ada gagal jantung kiri atau pada gagal jantung kanan akut

• THEOPHYLLINEBronkhodilatasi, fungsi RV - LV membaik

• BETA-ADRENERGIC AGONISTSBronkhodilator

• VASODILATOR ?• Atasi penyakit paru penyebabnya !!!

Dopamine

Effective renal plasma flow

Filtration fraction

Peritubular oncotic pressureTubular Na - Hexchange

+ +PCO

PCO

2

2

Plasma reninactivity

Angiotensin II

Plasmaaldosterone

Argininevasopressinlevel

Na retention:edema

+ ANP

Dopamine

Natriuresis

DopamineANP

ANP

ANPH O retention;

hyponatremia2

PRA

ANG II

AVP

RBF

Mechanisms of salt and water disturbance in patients with COPD

KULIAH MCI.ppt

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