CONTENTCONTENT1.1. Features of coronal circulation of blood and metabolism of Features of coronal circulation of blood and metabolism of

cardiac muscle.cardiac muscle.2.2. Classification of coronary heart disease. CHD: determination, Classification of coronary heart disease. CHD: determination,

reasons and terms of origin, form.reasons and terms of origin, form.3.3. Ischemic heart disease. Ischemic heart disease. Definition of the notion, risk factors, Definition of the notion, risk factors,

mechanisms of developmentmechanisms of development4.4. Sudden coronary death: reasons, mechanisms of origin.Sudden coronary death: reasons, mechanisms of origin.5.5. Angina pectoris: classification, pathogenesis of displays.Angina pectoris: classification, pathogenesis of displays.6.6. Heart attack of myocardium: kinds, description of functional Heart attack of myocardium: kinds, description of functional

and biochemical violations in a cardiac muscle, mechanisms of and biochemical violations in a cardiac muscle, mechanisms of pain syndrome.pain syndrome.

7.7. Mechanisms of origin of spasms of coronary vessels.Mechanisms of origin of spasms of coronary vessels.8.8. Complication of heart attack of myocardium. Pathogenesis of Complication of heart attack of myocardium. Pathogenesis of

cardiogenic shock.cardiogenic shock.9.9. Experimental models of heart attack of myocardium.Experimental models of heart attack of myocardium.

ACTUALITYACTUALITY

• The term coronary heart disease coronary heart disease (CHD)(CHD) describes heart disease caused by impaired coronary blood flow. In most cases, CHD is caused by atherosclerosis.

• Diseases of the coronary arteries can cause anginaangina, myocardial infarction or heart attackmyocardial infarction or heart attack, cardiaccardiac dysrhythmiasdysrhythmias, conduction defectsconduction defects, heart failureheart failure, and suddensudden deathdeath.

• During the past 50 years, there have been phenomenal advances in understanding the pathogenesis of CHD and in the development of diagnostic techniques and treatment methods for disease.

• However, declines in morbidity and mortalitymorbidity and mortality have failed to keep pace with these scientific advances, probably because many of the outcomes are more dependent on more dependent on lifestylelifestyle factors and age than on scientific advancesfactors and age than on scientific advances.

FUNCTIONAL ORGANIZATIONOF THE CIRCULATORY SYSTEM

■ The circulatory system consists of the heartheart, which pumps blood; the arterial systemarterial system, which distributes oxygenated blood to the tissues; the venous systemvenous system, which collects deoxygenated blood from the tissues and returns it to the heart; and the capillariescapillaries, where exchange of gases, nutrients, and wastes occurs.

■ The circulatory system is divided into two parts: the low-pressure pulmonary low-pressure pulmonary circulationcirculation, linking the transport function of the circulation with the gas exchange function of the lungs; and the high-pressure high-pressure systemic circulationsystemic circulation, providing oxygen and nutrients to the tissues.

■ The circulation is a closed system, so the output of the right and left heart must be equal over time for effective functioning of the circulation.

Coronary Heart Coronary Heart DiseaseDisease The term The term coronary heart disease coronary heart disease

(CHD) describes (CHD) describes heart diseaseheart disease caused by caused by impaired coronary impaired coronary blood flowblood flow. .

In most cases, CHD is caused by In most cases, CHD is caused by atherosclerosisatherosclerosis. .

Diseases of the coronary arteries Diseases of the coronary arteries can cause angina, myocardial can cause angina, myocardial infarction or heart attack, cardiac infarction or heart attack, cardiac dysrhythmias, conduction dysrhythmias, conduction defects, heart failure, and sudden defects, heart failure, and sudden death. death.

Heart attackHeart attack is the largest killer of is the largest killer of American men and women, American men and women, claiming more than 218,000 lives claiming more than 218,000 lives annually. Each year, 1.5 million annually. Each year, 1.5 million Americans have new or recurrent Americans have new or recurrent heart attacks, and one third of heart attacks, and one third of those die within the first hour, those die within the first hour, usually as the result of cardiac usually as the result of cardiac arrest resulting from ventricular arrest resulting from ventricular fibrillation.fibrillation.

Pathogenesis of Coronary Pathogenesis of Coronary Heart DiseaseHeart Disease

• HDL (good)HDL (good) cholesterol cholesterol removes excess removes excess cholesterol in the cholesterol in the blood stream.blood stream.

• LDL (bad)LDL (bad) cholesterol cholesterol enters the arterial wall enters the arterial wall andand is taken up by our is taken up by our body’s scavenger body’s scavenger cells.cells.

• Subsequently, they will Subsequently, they will turn into fatty streaks turn into fatty streaks which progress into which progress into atheromatous plaques.atheromatous plaques.

• Hence, LDL Hence, LDL cholesterol is said to cholesterol is said to promote promote atherosclerosis.atherosclerosis.

• HDL (good)HDL (good) cholesterol cholesterol removes excess removes excess cholesterol in the cholesterol in the blood stream.blood stream.

• LDL (bad)LDL (bad) cholesterol cholesterol enters the arterial wall enters the arterial wall andand is taken up by our is taken up by our body’s scavenger body’s scavenger cells.cells.

• Subsequently, they will Subsequently, they will turn into fatty streaks turn into fatty streaks which progress into which progress into atheromatous plaques.atheromatous plaques.

• Hence, LDL Hence, LDL cholesterol is said to cholesterol is said to promote promote atherosclerosis.atherosclerosis.

•Cholesterol readings includes:Cholesterol readings includes:Total cholesterol Total cholesterol

DesirableDesirable : < 5.2 mmol/L: < 5.2 mmol/LBorderline HighBorderline High : 5.2 – 6.2 mmol/L: 5.2 – 6.2 mmol/LHighHigh : ≥ 6.2 mmol/L: ≥ 6.2 mmol/L

LDL cholesterolLDL cholesterolDesirableDesirable : < 3.3 mmol/L: < 3.3 mmol/LBorderline HighBorderline High : 3.3 – 4.1 mmol/L: 3.3 – 4.1 mmol/LHighHigh : ≥ 4.1 mmol/L: ≥ 4.1 mmol/L

Well-Balanced Cholesterol Levels :Well-Balanced Cholesterol Levels :

Healthy LifestyleHealthy Lifestyle

HDL cholesterolAcceptable: ≥ 0.9 mmol/LRisky : < 0.9 mmol/L

TriglycerideDesirable : < 2.3 mmol/L

•A healthy person should have a higher level of HDL and a low level of LDL and triglyceride.

Well-Balanced Cholesterol Levels Well-Balanced Cholesterol Levels ::

Healthy LifestyleHealthy Lifestyle

Types of chronic ischemic heart disease Types of chronic ischemic heart disease and acute coronary syndromesand acute coronary syndromes

Coronary heart diseaseCoronary heart disease

Chronic ischemic heart disease Acute coronary syndrome

StableStableanginaangina

Silent myocardialischemia

Variantangina

No ST-segmentelevation

Q-waveAMI

Unstableangina

Non-ST-segmentelevation AMI

ST-segmentelevation

Intima

Adventitia

Media

The Normal Heart - Coronary Artery Anatomy

Left Main CA

Circumflex

Left Anterior Descending CA

Right CA

Marginal Branch

Layers of the Arterial Wall

Intima composed of endothelial cells

Atherosclerosis: Atherosclerosis: A Progressive ProcessA Progressive Process

Disease progression

PHASE I: Initiation PHASE II: Progression PHASE III: Complication

NormalFatty

StreakFibrousPlaque

Occlusive Atherosclerotic

Plaque

PlaqueRupture/Fissure &

Thrombosis

MI

Stroke

Critical Leg Ischemia

Coronary Death

UnstableAngina

Libby P. Circulation. 2001;104:365-372.

Ischemia

Thrombus formation

Coronary vasospasm

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Pathogenesis of AtherosclerosisPathogenesis of Atherosclerosis

1) FATTY STREAK

(non-palpable,

but a visible

YELLOW streak)

2) ATHEROMA (plaque) (palpable)

3) THROMBUS (non-

functional, symptomati

c)

Often small platelet aggregates or thrombi and/or thromboemboli

FrequentUsually severe

Sudden death

Widely variable, may be absent, partial/complete, or lysed

VariableVariableSubendocardial myocardial infarction

OcclusiveFrequentVariableTransmural myocardial infarction

Nonocclusive, often with thromboemboliFrequentVariableUnstable angina

NoNo>75%Stable angina

Plaque-Associated ThrombusPlaque DisruptionStenosesSyndrome

Coronary Artery Pathology in Ischemic Heart Disease

IVUS=intravascular ultrasoundNissen S, Yock P. Circulation 2001; 103: 604–616

AngiogramIVUS

Little evidence of disease

Atheroma

No evidence of disease

The IVUS technique can detect The IVUS technique can detect angiographically ‘silent’ atheromaangiographically ‘silent’ atheroma

IVUS – intravascular ultrasaund

anterior descending coronary artery

Correlation of CT angiography of the coronary arteries with intravascular ultrasound illustrates the ability of MDCT to demonstrate calcified and non-calcified coronary plaques (Becker et al., Eur J Radiol 2000)

Non-calcified, soft, lipid-rich plaque in left anterior descending artery (arrow) . The plaque was confirmed by intravascular ultrasound (Kopp et al., Radiology 2004)

Pathophysiology of ISCHEMIAPathophysiology of ISCHEMIA Ischemia of cardiac cells occurs when the oxygen Ischemia of cardiac cells occurs when the oxygen

supply is insufficient to meet metabolic demands. supply is insufficient to meet metabolic demands. Myocardial cells are unable to store much energy in Myocardial cells are unable to store much energy in

the form of adenosine triphosphate (ATP) and must the form of adenosine triphosphate (ATP) and must therefore continuously receive a supply of oxygen therefore continuously receive a supply of oxygen for aerobic synthesis of ATP.for aerobic synthesis of ATP.

ATP is essential for powering myocardial ATP is essential for powering myocardial construction as well as for cell maintenance. construction as well as for cell maintenance. Because the heart is unable to slow its activity Because the heart is unable to slow its activity when ATP supplies dwindle, it is essential that a when ATP supplies dwindle, it is essential that a steady flow of oxygen be provided. steady flow of oxygen be provided.

Critical factors in meeting cellular Critical factors in meeting cellular demands for oxygen are:demands for oxygen are:

the rate of coronary perfusionthe rate of coronary perfusion the myocardial workloadthe myocardial workload

can be impaired in next wayscan be impaired in next ways

Large, stable Large, stable atherosclerotic plaqueatherosclerotic plaque

Acute platelet aggregation Acute platelet aggregation and thrombosisand thrombosis

VasospasmVasospasm

Failure of autoregulation Failure of autoregulation by the microcirculationby the microcirculation

Poor perfusion Poor perfusion pressurepressure

depends ondepends on

Heart rateHeart rate

PreloadPreload

AfterloadAfterload

ContractilityContractility

ANGINA PECTORIS

• Paroxysmal (sudden)• Recurrent• 15 sec.15 min.• Reduced perfusion, but NO infarction• THREE TYPES

• STABLE:STABLE: relieved by rest or nitroglycerin• PRINZMETAL:PRINZMETAL: SPASM is main feature, responds to

nitro, S-T elevation• UNSTABLEUNSTABLE (crescendo, PRE-infarction, Q-wave

angina): perhaps some thrombosis, perhaps some non transmural necrosis, perhaps some embolization, but DISRUPTION of PLAQUE is universally agreed upon

Chest PainChest Pain First symptom of those suffering myocardial First symptom of those suffering myocardial

ischemia.ischemia. Called angina pectoris (angina – “pain”)Called angina pectoris (angina – “pain”) Feeling of heaviness, pressureFeeling of heaviness, pressure Moderate to severeModerate to severe In substernal areaIn substernal area Often mistaken for indigestionOften mistaken for indigestion May radiate to neck, jaw, left arm/ shoulderMay radiate to neck, jaw, left arm/ shoulderDue to :Due to :

Accumulation of lactic acid in Accumulation of lactic acid in myocytes or stretching of myocytesmyocytes or stretching of myocytes

Stable angina pectorisStable angina pectoris Caused by chronic coronary obstructionCaused by chronic coronary obstruction Recurrent predictable chest painRecurrent predictable chest pain Gradual narrowing and hardening of Gradual narrowing and hardening of

vessels so that they cannot dilate in vessels so that they cannot dilate in response to increased demand of response to increased demand of physical exertion or emotional stressphysical exertion or emotional stress

Lasts approx. 3-5 minutesLasts approx. 3-5 minutes Relieved by rest and nitratesRelieved by rest and nitrates

Stress testStress testshowsshows

ST segment ST segment depression depression

> 1mm> 1mm

Prinzmetal angina pectorisPrinzmetal angina pectoris(Variant angina)(Variant angina)

Caused by abnormal vasospasm of normal vessels (15%) or Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%)near atherosclerotic narrowing (85%)

Occurs unpredictably and almost exclusively at rest.Occurs unpredictably and almost exclusively at rest. Often occurs at night during REM sleepOften occurs at night during REM sleep (rapid eye movement) (rapid eye movement) May result from hyperactivity of sympathetic nervous system, May result from hyperactivity of sympathetic nervous system,

increased calcium flux in muscle or impaired production of increased calcium flux in muscle or impaired production of prostaglandinprostaglandin

Vasoconstriction is due to platelet thromboxane AVasoconstriction is due to platelet thromboxane A22 or an or an increase in endothelin increase in endothelin

This causes a pattern of ST elevationST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. They may be impossible to differentiate on the ECG. ST elevation myocardial infarction (STEMI)

Silent IschemiaSilent Ischemia

Totally asymptomaticTotally asymptomatic May be due abnormality in May be due abnormality in

innervationinnervation Or due to lower level of inflammatory Or due to lower level of inflammatory

cytokinescytokines

TreatmentTreatment Pharmacologically manipulate blood Pharmacologically manipulate blood

pressure, heart rate, and contractility to pressure, heart rate, and contractility to decrease oxygen demandsdecrease oxygen demands

Nitrates dilate peripheral blood Nitrates dilate peripheral blood vessels andvessels and

Decrease oxygen demand Decrease oxygen demand Increase oxygen supplyIncrease oxygen supplyRelieve coronary spasmRelieve coronary spasm

blockers:blockers: Block sympathetic input, soBlock sympathetic input, so Decrease heart rate, soDecrease heart rate, so Decrease oxygen demandDecrease oxygen demand

DigitalisDigitalis Increases the force of contractionIncreases the force of contraction

Calcium channel blockersCalcium channel blockers Antiplatelet agents (aspirin, etc.)Antiplatelet agents (aspirin, etc.)

Surgical treatment

• Angioplasty – mechanical opening of vessels

• Revascularization – bypass•Replace or shut around occluded

vessels

ACUTE CORONARY SYNDROMESACUTE CORONARY SYNDROMES

“The acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis.”

Unstable Angina pectorisUnstable Angina pectoris

Lasts more than 20 minutes at rest, Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing or rapid worsening of a pre-existing anginaanginaMay indicate a progression to M.I.May indicate a progression to M.I.

Pathogenesis:Pathogenesis:Severe, fixed, multivessel Severe, fixed, multivessel atherosclerotic diseaseatherosclerotic diseaseDisrupted plaques with or without Disrupted plaques with or without platelet nonocclusive thrombiplatelet nonocclusive thrombi

The ECG above belongs to a patient with unstable angina pectorisunstable angina pectoris. Negative T waves are observed in leads C2-C5 while negative U waves are seen in leads C2-C4. Additionally, the PR interval is above 200 msec (1st degree AV block). Coronary angiography showed significant stenosis of the LAD and Circumflex (Cx) arteries

Sudden cardiac deatSudden cardiac death h (SC(SCDD)) 1. Inexpected death within 1 hour after the onset of 1. Inexpected death within 1 hour after the onset of

symptomssymptoms2. Risk factors2. Risk factors a. Obesitya. Obesity b. b. GGlucoslucosee intolerance intolerance c. Hypertensionc. Hypertension d. Recent non-Q wave myocardial infarctiod. Recent non-Q wave myocardial infarctionn e. Smokinge. Smoking3. Occurs more frequently in the morning hours when 3. Occurs more frequently in the morning hours when

hypercoagiilability is ahypercoagiilability is att its peaits peackck4. Pathogenesis4. Pathogenesis a. Severe aa. Severe attheroseleroheroselerottic coronary artery ic coronary artery didiseasesease b. Disrupted b. Disrupted filimnsfilimns plaques plaques c. Absence of occlusive vessel thrombus (>80%; of cases)c. Absence of occlusive vessel thrombus (>80%; of cases) d. Cause of death is ventricular fibrillation.d. Cause of death is ventricular fibrillation. 5. Diagnosis of exclusion after the following causes are 5. Diagnosis of exclusion after the following causes are

ruled outruled out a. Mitral valve prolapse (MVP)a. Mitral valve prolapse (MVP) b. Hypertrophic cardiomyopathyb. Hypertrophic cardiomyopathy c. Calcific aortic stenosisc. Calcific aortic stenosis d. Conduction system abnormalid. Conduction system abnormalitietiess e. Cocaine abusee. Cocaine abuse

Acute myocardial infarction (Acute myocardial infarction (AMIAMI))

1. 1. EEpidemiologypidemiology a. Most common cause of a. Most common cause of

deatdeath h in adults in the in adults in the United States.United States.

b. Prominent in males b. Prominent in males between 40 and 65 years between 40 and 65 years oldold

c. Nc. Noo predominant sex predominant sex predilection after 65 years predilection after 65 years oldold

d. At least 25% of AMIs are d. At least 25% of AMIs are clinically unrecognized.clinically unrecognized.

Myocardial IschemiaMyocardial Ischemia Myocardial cell metabolic demands not metMyocardial cell metabolic demands not met Time frame of coronary blockage:Time frame of coronary blockage:

10 seconds following coronary block10 seconds following coronary block Decreased strength of contractionsDecreased strength of contractions Abnormal hemodynamics Abnormal hemodynamics

See a shift in metabolism, so within minutes: See a shift in metabolism, so within minutes: Anaerobic metabolism takes overAnaerobic metabolism takes over Get build-up of lactic acid, which is toxic within Get build-up of lactic acid, which is toxic within

the cellthe cell Electrolyte imbalancesElectrolyte imbalances Loss of contractibilityLoss of contractibility

20 minutes after blockage20 minutes after blockageMyocytes are still viable, soMyocytes are still viable, soIf blood flow is restored, and If blood flow is restored, and

increased aerobic metabolism, and increased aerobic metabolism, and cell repair,cell repair,

→→Increased contractilityIncreased contractilityAbout 30-45 minutes after blockage, if About 30-45 minutes after blockage, if

no reliefno reliefCardiac infarct & cell death Cardiac infarct & cell death

Myocardial infarctionMyocardial infarction

Necrosis of cardiac myocytesNecrosis of cardiac myocytes– IrreversibleIrreversible– Commonly affects left ventricleCommonly affects left ventricle– Follows after more than 20 minutes of Follows after more than 20 minutes of

ischemiaischemia

PathogenesisPathogenesis

a. Sequencea. Sequence 1) Sudden1) Sudden disniptinn disniptinn of an atheromatous of an atheromatous

plaque plaque 2) Su2) Subbendothelial endothelial colcoliaiagengen andand thrombogenic thrombogenic

necrotic material are exposed.necrotic material are exposed. 3) Platelets adhere to the exposed material 3) Platelets adhere to the exposed material

and eventually form an occlusiveand eventually form an occlusive platelet platelet tthhrombus.rombus.

b. Role of thromboxane Ab. Role of thromboxane A22

1) Contributes to 1) Contributes to fformation oformation of the platelet the platelet thrombusthrombus

2) Causes vasospasm of2) Causes vasospasm of the artery to reduce the artery to reduce blood flowblood flow

PATHOPHYSIOLOGYPATHOPHYSIOLOGYCoronary artery cannot supply enough blood to the Coronary artery cannot supply enough blood to the

heart in response to the demand due to CADheart in response to the demand due to CAD

Within 10 seconds myocardial cells experience Within 10 seconds myocardial cells experience ischemia ischemia

Ischemic cells cannot get enough oxygen or glucoseIschemic cells cannot get enough oxygen or glucose

Ischemic myocardial cells may have decreased Ischemic myocardial cells may have decreased electrical & muscular functionelectrical & muscular function

Cells convert to anaerobic metabolism.Cells convert to anaerobic metabolism.

Cells produce lactic acid as wasteCells produce lactic acid as waste

Pain develops from lactic acid accumulationPain develops from lactic acid accumulation

Pt feels anginal symptoms until receiving demand Pt feels anginal symptoms until receiving demand increase 02 requirements of myocardial cellsincrease 02 requirements of myocardial cells

Myo

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Inf

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PROGRESSION OF NECROSISPROGRESSION OF NECROSIS

0-1/2 hr reversible injury

Types of myocardial Types of myocardial infarcinfarcttionion

a. Transmural infarction (Qwave infarction)a. Transmural infarction (Qwave infarction)• 1) Involves the full thickness of1) Involves the full thickness of the the

mmyocardiyocardiuumm• 2) New Q waves develop in an 2) New Q waves develop in an

electrocardiogram (electrocardiogram (EECCGG).).

b. Subendocardial infarcb. Subendocardial infarcttion (non-Q wave ion (non-Q wave infarction)infarction)

• 1) Involves the inner third of1) Involves the inner third of the the mymyocardiumocardium

• 2) Q waves are absent.2) Q waves are absent.

Reperfusion injuryReperfusion injurya. Follows throma. Follows thrombbolytic (fibrinolytic) therapyolytic (fibrinolytic) therapyb. Early reperfusion salvages some injured but b. Early reperfusion salvages some injured but viable myocytes but destroys myocytesviable myocytes but destroys myocytes that are that are irreversibly damaged.irreversibly damaged.

1) Removal of irreversibly damaged myocytes 1) Removal of irreversibly damaged myocytes improves short- and long-termimproves short- and long-term function and function and survival.survival.

2) Prevents any further damage to myocardial cells2) Prevents any further damage to myocardial cells3) Limits the size of3) Limits the size of the infarctionthe infarction

c. Reperfusion histologically alters irreversibly c. Reperfusion histologically alters irreversibly damaged cells.damaged cells.

1) Produces contraction band necrosis1) Produces contraction band necrosis2) Caused by 2) Caused by hyphypoorcontractionrcontraction of myofibrils in dying of myofibrils in dying

cellscells• • Due to the influx of Ca-Due to the influx of Ca-++++ into the cytosol into the cytosol

RERE-PERFUSION-PERFUSION

ThrombolysisThrombolysis PTCAPTCA CABGCABG Reperfusion CANNOT restore necrotic Reperfusion CANNOT restore necrotic

or dead fibers, only reversibly injured or dead fibers, only reversibly injured onesones

REPERFUSION “INJURY”REPERFUSION “INJURY” Free radicalsFree radicals InterleukinsInterleukins

STEMI

Blood flow

Chest discomfort PMVT, VF

SuddenDeath

M. Ischemia

Heart failure

Cardiogenic shockElevated

+CK,Trop-T

M.stunning

Consequences after acute coronary artery occlusion

NSTEMI ,UA

Cardiovascular Research & Prevention Center, Bhumibol Adulyadej hospital

Clinical ManifestationsClinical Manifestations

May hear May hear extra, rapid extra, rapid heart soundsheart sounds

ECG ECG changes: changes: T wave T wave

inversioninversion ST ST

segment segment depressiondepression

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION

Transmural vs. Subendocardial (inner 1/3)Transmural vs. Subendocardial (inner 1/3)

DUH! EXACT SAME risk factors as atherosclerosisDUH! EXACT SAME risk factors as atherosclerosis

Most are TRANSMURAL, and MOST are caused by Most are TRANSMURAL, and MOST are caused by coronary artery occlusioncoronary artery occlusion

In the 10% of transmural MIs NOT associated with In the 10% of transmural MIs NOT associated with atherosclerosis:atherosclerosis: VasospasmVasospasm EmboliEmboli UNexplainedUNexplained

Structural, functional changesStructural, functional changes Decreased contractilityDecreased contractility Decreased LV complianceDecreased LV compliance Decreased stroke volumeDecreased stroke volume DysrhythmiasDysrhythmias Inflammatory response is severeInflammatory response is severe Scarring results –Scarring results –

Strong, but stiff; can’t contract like Strong, but stiff; can’t contract like healthy cellshealthy cells

Sign and SymptomSign and Symptom

Classic symptom of heart Classic symptom of heart attack are chest pain radiating attack are chest pain radiating to neck, jaws, back of to neck, jaws, back of shoulder, or left arm shoulder, or left arm

The pain can be felt like:The pain can be felt like: Squeezing or heavy pressure Squeezing or heavy pressure A tight band on the chestA tight band on the chest An elephant sitting on the An elephant sitting on the

chestchest

Cont Cont Other symptoms include:Other symptoms include: Shortness of breath Shortness of breath

(SOB)(SOB) Weakness and Weakness and

tirednesstiredness AnxietyAnxiety LightheadednessLightheadedness DizzinessDizziness Nausea vomitingNausea vomiting Sweating, which may Sweating, which may

be profusebe profuse

Clinical manifestationsClinical manifestations Sudden, severe chest painSudden, severe chest pain

Similar to pain with ischemia, but strongerSimilar to pain with ischemia, but stronger Not relieved by nitratesNot relieved by nitrates Radiates to neck, jaw, shoulder, left armRadiates to neck, jaw, shoulder, left arm

Indigestion, nausea, vomitingIndigestion, nausea, vomiting Fatigue, weakness, anxiety, restlessness and Fatigue, weakness, anxiety, restlessness and

feelings of impending doom.feelings of impending doom. Abnormal heart sounds possible (S3,S4)Abnormal heart sounds possible (S3,S4)

Blood test show several markers:Blood test show several markers: LeukocytosisLeukocytosis Increased blood sugarIncreased blood sugar Increased plasma enzymesIncreased plasma enzymes

Creatine kinaseCreatine kinase Lactic dehydrogenaseLactic dehydrogenase Aspartate aminotransferase (AST or SGOT)Aspartate aminotransferase (AST or SGOT)

Cardiac-specific troponinCardiac-specific troponin

Laboratory diagnosis of AMI Laboratory diagnosis of AMI II. Serial testing for creatine kinase isoenzyme MB (CK-MB). Serial testing for creatine kinase isoenzyme MB (CK-MB)11)) CCK-MB K-MB appears within 4 to 8 hoursappears within 4 to 8 hours; ; peakspeaks at 24 at 24 hhooururss; disappears within 1.5 to 3 days.; disappears within 1.5 to 3 days. • • Sensitivity and specificity Sensitivity and specificity 995%,5%,2) Reinfarction2) Reinfarction a) Occurs in 10% of AMIsa) Occurs in 10% of AMIs b) Reappearance of CK-MB after 3 daysb) Reappearance of CK-MB after 3 days IIII. Serial testing for cardiac troponins I (cTnl) and T (cTnT). Serial testing for cardiac troponins I (cTnl) and T (cTnT)1) Normally regulate calci1) Normally regulate calciuum-mediated contractionm-mediated contraction2) c2) cTTnl and cnl and cTTnT appear within 3 to 12 hours: peak at 24 hours; disappear withinnT appear within 3 to 12 hours: peak at 24 hours; disappear within 7 to 10 days.7 to 10 days. a) Sensitivity 84% to a) Sensitivity 84% to 9696%, specificity 80% to %, specificity 80% to 995%5% b) False positive results are b) False positive results are lisuallylisually related to ischemia (e.g., unstable angina), related to ischemia (e.g., unstable angina),3) CK-MB is used in conjunction with troponins to diagnose an AMI.3) CK-MB is used in conjunction with troponins to diagnose an AMI. a) Detects reinfarction (troponins cannot)a) Detects reinfarction (troponins cannot) b)b) Improves overall sensitivity and specificiry in diagnosing an AMI Improves overall sensitivity and specificiry in diagnosing an AMI IIIIII. Lactate dehydrogenase (LD. Lactate dehydrogenase (LDHH))1-21-2 "flip""flip"1) Normally, LD1) Normally, LDHH22 is higher than LDH is higher than LDH11.. • • In AMIIn AMI,, LDH LDH11 in cardiac muscle is released, causing the “ in cardiac muscle is released, causing the “flflip,"ip,"2) LDH2) LDH1-21-2 • • Appears within 10 hours; peaks at 2 to 3 days: disappears within 7 daysAppears within 10 hours; peaks at 2 to 3 days: disappears within 7 days3) This test has been replaced by troponins I and T.3) This test has been replaced by troponins I and T.

TreatmentTreatment

First 24 hours crucialFirst 24 hours crucial Hospitalization, bed restHospitalization, bed rest ECG monitoring for arrhythmiasECG monitoring for arrhythmias Pain relief (morphine, nitroglycerin)Pain relief (morphine, nitroglycerin) Thrombolytics to break down clotsThrombolytics to break down clots Administer oxygenAdminister oxygen Revascularization interventions: by-pass Revascularization interventions: by-pass

grafts, stents or balloon angioplastygrafts, stents or balloon angioplasty

AMI DIAGNOSIS

• SYMPTOMS• EKG• DIAPHORESIS• (10% of MIs are “SILENT” with Q-waves)• CKMB gold standard enzyme• Troponin-I, Troponin-T better• CRP predicts risk of AMI in angina patients

Primary Management Techniques

• Heart Attack Treatment • First you must conduct a primary survey of the casualty;• A primary survey consists of following the DRABCD procedure, this

involves;• D = DANGER – If I find a heart attack casualty I should check for any

surrounding danger to myself first and for the casualty and others• R = Response – I should asses whether the person is conscious or

unconscious using the COWS procedure; -Can you hear me, -Open your eyes, -What is your name, -Squeeze my hand.

• A = Airways - After response if the casualty is unconscious I should then check the airways for any obstructions or blockages and if there is a blockage turn the victim onto his/her side and clear the airway.

• B = Breathing – The next step if the patient is unconscious is to check for signs of life. Check for breathing by using look, listen and feel technique. If breathing place the casualty in recovery position, if not give 2 rescue breaths and...

• C = Compressions - If the casualty is unconscious with no breathing, start compressions immediately! Give 30 compressions. At a rate of 100 compressions per minute (approx 2 compressions per second). At 1/3 depth of the casualty’s chest.

• D = Defibrillation - If available use a defibrillator on the casualty as soon as possible.

• Cardiac Output: (Q) = HR X SV

• Cardiac Index = Q / body surface area

• Preload: (EDV) volume of the left ventricle at the end of diastole (dependent on venous return & stretch of the cardiac muscle cells)

• Afterload: resistance to ventricular emptying during systole (the amount of pressure the left ventricle must generate to squeeze

blood into the aorta)

• Frank Starling Law of the Heart: the heart will contract with greater force when preload (EDV) is increased

• Myocardial Contractility: the squeezing contractile force that the heart can develop at a given preload

• regulated by:• sympathetic nerve activity (most influential)• catecholamines (epinephrine norepinephrine)• amount of contractile mass • drugs

Definitions

Don’t wait for a heart attack to Don’t wait for a heart attack to take an action !take an action !

Don’t wait for a second life Don’t wait for a second life we are not cats!we are not cats!

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