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Kuliah Mci
Kuliah Mci
Pathophysiology
Clinical features Management
Hospital management
Hemodynamic disturbances Arrhythmias
Epidemiology
Acute myocardial infarction (AMI)
Major public health problem in industrialized 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
30 25 20 15 10 5 0
Inf&Parasit Sirkulasi Napas Cer na Neoplasma Kecelakaan Perinatal
Epidemiology
% Mortality (in hospital)
35 30 25 20 15 10 5 0
1.0
30
CCU era
0.8 0.6
0.4
0.2 0.0
0 1 2 3 4 5 6 7 8 9 10
Years of follow-up
Pathology
Almost all MIs result from coronary atherosclerosis
ATHEROSCLEROSIS (1)
Atheroma Formation
1. 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
ATHEROSCLEROSIS (2)
Atheroma Formation
4. Smooth muscle cells migrate from media to intima attracted by platelet-derived growth factor (PDGF) Secreted by activated macrophages Smooth 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 cells Breakdown of these molecules by matric metalloproteinases (MMPs) Luminal stenosis only after plaque burden exceeds 40% of cross-sectional area of artery 6. Endothelial migration and proliferation neovascularization in plaque Plaques often develop areas of calcification
Non ST elevation
NSTEMI
ST elevation
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
PATHOPHYSIOLOGY
If sufficient quantity of myocardium undergoes ischemic injury LV pump function end-systolic volume Infarct zone thins and elongates infarct expansion Dilatation of ventricle depends on infarct size, patency of infarct-related artery, and activation of local RAS in noninfarcted portion of ventricleultimately : 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
CLINICAL FEATURES
PREDISPOSING FACTORS
50% - precipitating factor or prodromal symptoms Unusually heavy exercise Accelerating angina, rest angina
HISTORY
PRODROMAL SYMPTOMS History very valuable to establish discomfort unstable angina 1/3 symptoms for 1 4 wks 20% symptoms for < 24 hrs Malaise, exhaustion D/ Prodoma : chest
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
PHYSICAL EXAMINATION
GENERAL APPEARANCE Anxious, considerable distress, restless, fist on chest LV 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 RATE Variable depending on underlying rhythm and degree or ventr. failure Most commonly, HR 100 110/min; > 95% patients : VPBs within first 4 hours
BLOOD PRESSURE Majority 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 RESPIRATION Most pts with extensive MI fever within 2448 hrs, fever resolves by 4th or 5th day Respiration 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 classification Class I II & Kimball : prognostic
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
AUSCULTATION S1 muffled
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
LABORATORY EXAMINATION
MARKERS OF CARDIAD DAMAGE ST elevation and Q wave (highly indicative of AMI) only in 50% of pts on presentation 30% AMI no classic chest pain 50% AMI nondiagnostic ECG Chest 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
Plot of the appearance of cardiac markers in blood versus time after onset of symptoms
ELEKTROKARDIOGRAM
Current-of-injury patterns with acute ischemia
Sequence of depolarization and repolarization changes with (A) acute anterior-lateral and (B) acute inferior wall Q infarctions
IMAGING
Rntgenography 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
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 factors, known CAD, symptoms of AMI
Nondiagnostic ECG
ST elevation
Yes
ST elevation
12 h
No Administer thrombolytic Primary PCI : consider IV GP IIb/IIIA inhibitor and stent as needed
Other medical therapy : ACE inhibitors; ? Nitrates; correc metabolic and electrolyte deficits
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 STelevation MI
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
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
Vital signs q 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
Medicatio ns
PHARMACOLOGICAL Th/
Betablockers Pts without a contraindication, betablockers Ace-inhibitors All considered for ACE-inhibition th/ esp CHF, ST segment elevation or LBBB Nitrates Persistent chest pain, LV failure, large anterior transmural AMI Ca-antagonists Verapamil or diltiazem not recommended as routine th/ in AMI May 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 rupture Pseudo aneurysm Rupture of interventricular septum Papillary muscle rupture
Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction (1)
CATEGORY 1. Electrical instability ARRHYTHMIA Ventricular premature beats Ventricular tachycardia OBJECTIVE OF TREATMENT Correction of electrolyte deficits and increased sympathetic tone Prophylaxis against ventricular fibrillation, restoration of hemodynamic stability Urgent reversion to sinus rhythm Observation unless hemodynamic function is compromised Search for precipitating causes (e.g. digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromised THERAPEUTIC OPTIONS Potassium and magnesium solutions, beta blocker Antiarrhythmic agents; cardioversion/defibrill ation Defibrillation, bretylium tosylate Increase sinus rate (atropine, atrial pacing); antiarrhythmic agents Atrial overdrive pacing agent; cardioversion relatively contraindicated if dititalis intoxication present
Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction (2)
CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT Reduce heart rate to diminish myocardial oxygen demand THERAPEUTIC OPTIONS Antipyretics; analgesics, consider beta blocker unless congestive heart failure present; treat latter if present with anticongestive measures (diuretics, afterload reduction) Verapamil, digitalis glycosides; anticongestive measures (diuretics, afterload reduction); cardioversion; rapid atrial pacing (for atrial flutter)
Vagal maneuvers; verapamil, cardiac glycosides, beta-adrenergic blockers; cardioversion; rapid atrial pacing
Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction (3)
CATEGORY
3. Bradyarrhythmias and conduction disturbances ARRHYTH MIA Sinus bradycardia OBJECTIVE OF TREATMENT Acceleration of heart rate only if hemodynamic function is compromised Acceleration of sinus rate only if loss of atrial kick causes hemodynamic compromise THERAPEUTIC OPTIONS Atropine; atrial pacing
Insertion of pacemaker
CONVALESCENCE, DISCHARGE, POST-MI CARE Timing of discharge 5 6 days after admission for pts without complications Counseling
Instruction concerning physical activity Use of medication Behavioral alteration Rehabilitation program physical psychological
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
MANAGEMENT ALGORITHM FOR RISK STRATIFICATION AFTER ACUTE MYOCARDIAL INFARCTION (1)
Clinical Indications of High Risk at Predischarge Present Strategy I Strategy II Symptom-limited exercise test at 14-21 days Absent Strategy III
Markedly abnormal
Mildly abnormal
Negative
Reversible ischemia
Cardiac catheterization
MANAGEMENT ALGORITHM FOR RISK STRATIFICATION AFTER ACUTE MYOCARDIAL INFARCTION (2)
Absent
Strategy II
Strategy III Submaximal exercise test at 5-7 days Markedly abnormal Mildly abnormal Exercise imaging study Negative
Reversible ischemia
Cardiac catheterization
MANAGEMENT ALGORITHM FOR RISK STRATIFICATION AFTER ACUTE MYOCARDIAL INFARCTION (3)
Symptom-limited exercise testing at 3 6 wk Cardiac catheterization Markedly abnormal Mildly abnormal Exercise imaging study Negative
Reversible ischemia
UNSTABLE ANGINA
Definition and classification
Pathophysiology
Clinical presentation
Diagnosis of UA / NSTEMI
Risk stratification Medical therapy
DEFINITION
STABLE ANGINA PECTORIS
deep, poorly localized chest or arm discomfort that is reproducibly associated with physical exertion or emotional stress and relieved within
DEFINITION
UNSTABLE 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)
Severity
Class I Class II
Class III
10.8%
Clinical Circumstances
A (secondary angina) B (primary angina) C (postinfarction angina) Intensity of treatment Develops in the presence of extra-cardiac condition that intensifies myocardial ischemia Develops in the absence of extra-cardiac condition Develops within 2 weeks after acute myocardial infarction 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. Patients with UA may be further divided into those with or without transient ST-T wave changes during pain 14.1% 8.5% 18.5%
Electrocardiographic changes
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 obstruction 4. Inflammation and/or infection 5. Secondary unstable angina, precipitated by increased oxygen demand or decreased supply (e.g., thyrotoxicosis or anemia) Individual patients may have several processes coexisting
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 infarction Key role in development of atherosclerosis and in development and recurrence of UA Chlamydia pneumonia ? Helicobacter pylori ? Cytomegalovirus ? Thrombosis many 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
ECG UAP : ST segment depression (or transient ST segment elevation) and T wave changes in 50% patients. Continuous ECG monitoring more sensitive than symptoms Cardiac markers If positive CK-MB, troponin T or I diagnosis NSTEMI Cor. arteriography 15% 3VD 30% 2VD 40% 1VD 20% no significant stenosis coronary microvascular dysfunction Angioscopy & intravascular ultrasound
Features associated with higher likelihood of CAD among pts presenting with symptoms suggestive of UA
History
Chest 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 angina Age > 60 Male gender More than two major cardiac risk factors Diabetes Extracardiac vascular disease (carotid or peripheral) Physical Examination Pulmonary rales, hypotension Transient mitral regurgitation Diaphoresis Electrocardiogram New/presumably new ST deviation > 0.05 mV T wave inversion 0.1 mV Q waves, left bundle branch block Cardiac Markers Elevated CK-MB, troponin I or T
Natural History
by 30 days : 3.5 4.5%
new/recurrent MI 6 12%
History
Advanced age (> 65 years) Diabetes mellitus Post-myocardial infarction angina Prior peripheral vascular disease Prior cerebrovascular disease Clinical Presentation Braunwald Class II or III (acute or subacute rest pain) Braunwald Class B ( secondary unstable angina) Electrocardiogram New/ST segment deviation 0.05 mV T wave inversion 0.3 mV Left bundle branch block Cardiac Markers Increased troponin T or I or CK-MB Increased C-reactive protein (CRP) Angiogram Thrombus
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
Medical management
Percutaneous coronary interventions and coronary artery surgery
(1)
LOCATION
Retrosternal region: radiates to or occasionally isolated to neck, jaw, epigastrium, shoulder or armsleft common
QUALITY
DURATION
Rest or UA
Myocardial infarction
Same as angina
Substernal and may radiate like angina
(2)
Aortic dissection
(3)
Pressure, oppressive
(4)
Precipitated by exercise, S4, or murmur of papillary cold weather or muscle dysfunction during emotional stress; relieved pain by rest or nitroglycerin; atypical (Prinzmetals) angina may be unrelated to activity, often early morning Same as angina, with decreasing tolerance for exertion or at rest Unrelieved by rest or nitroglycerin Similar to stable angina, but may be pronounced. Transient cardiac failure can occur Shortness of breath, sweating, weakness, nausea, vomiting
Rest or UA
Myocardial infarction
(5)
Aortic dissection
(6)
Pulmonary hypertension
Aggravated by effort
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, pulmonary rales), softening of mitral component
Pathophysiology
Pathophysiology
Angina 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
CLASS I
II
CANADIAN CARDIOVASCULAR SOCIETY FUNCTIONAL CLASSIFICATION 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 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
III
IV
Noninvasive testing
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 adenosine, dipyridamole Stress echocardiography Pharmacological stress echocardiography -dobutamine
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
Medical management
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)
Pharmacological Therapy
Aspirin
Betablocker Angiotensin converting enzyme (ACE) inhibitors Nitrates
Ca antagonists
Etiologi Utama
Penyakit paru obstruktif khronis (PPOK) akibat bronkhitis khronis atau emfisema paru
Hypoxia
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
OKSIGEN Diberikan kontinu 1-2 l/menit, dapat memperbaiki prognosis karena mengurangi vasokonstriksi pulmonal dan memperbaiki hipoksia DIGITALIS Hanya bila juga ada gagal jantung kiri atau pada gagal jantung kanan akut THEOPHYLLINE Bronkhodilatasi, fungsi RV - LV membaik BETA-ADRENERGIC AGONISTS Bronkhodilator VASODILATOR ? Atasi penyakit paru penyebabnya !!!
ANP AVP
H 2O retention; hyponatremia