ISCHEMIC HEART DISEASE; CONGESTIVE HEART FAILURE; SHOCK

Coronary Artery DiseaseVascular disorder narrowing/blockage of arteries to heartArteries supplying heart branch directly from aortaBring richly oxygenated bloodNecessary to supply myocytes with oxygen, nutrientsHeart needs constant supply of oxygen for muscle activities

Coronary artery disease decr'd blood supply to cardiac muscle (Fig. 23-21)So ischemiaPersistent ischemia hypoxiaInfarction leads to heart attackAbout 50% of all deaths in U.S.Heart has high metabolic rateConstantly contracting to pump oxygenated and nutrient-filled blood to rest of bodyUrgent to life to maintain the health of heart, soUrgent to life to maintain oxygen-rich blood flow to heart

Modifiable/nonmodifiable factors put some people more at risk than othersSame as for vascular disease:Hyperlipidemia - incr'd plasma lipoproteins Hypertension - may cause or exacerbateCigarette smoking - STOP!!Diabetes

Myocardial ischemia resultsDecrd blood flow to heart (Fig.23-14)Myocardial cell metabolic demands not metTime frame of coronary blockage10 seconds following coronary blockDecrd strength of contractionsAbnormal hemodynamics Several minutes later Decrd glucose metab decrd aerobic metab, soAnaerobic metab, soBuild-up of lactic acid (toxic within cell)

Time frame contd20 minutes after blockageMyocytes still viable, soIf blood flow restored, and incrd aerobic metab, and cell repair, Incrd contractilityAbout 30-45 minutes after blockage, if no reliefCardiac infarct

ClinicalMay hear extra, rapid heart sounds (S3)ECG changes (Fig.23-18)T wave inversionST segment depressionChest pain 20-30% of those suffering myocardial ischemiaCalled angina pectorisFeeling of heaviness, pressureModerate severeIn substernal areaOften mistaken for indigestionMay radiate to neck, jaw, left arm/shoulder

Chest pain contdDue to Accumn lactic acid in myocytes, ORStretching of myocytes Three types: stable, unstable, PrinzmetalSee p 645TreatmentPharmacologically manipulate bp, hr, contractility to decr oxygen demand of myocytesNitrates dilate peripheral blood vessels, andDecrease oxygen demandIncrease oxygen supplyRelieve coronary spasm

Pharmacological treatment contdBeta blockersBlock sympathetic input, soDecrease heart rate, soDecrease oxygen demand Digitalis Increases force of contractionSurgicalAngioplasty mechanical opening of vesselsRevascularization (bypass)Replace, shunt around occluded vessels

Myocardial infarction endpointNecrosis of cardiac myocytesIrreversibleCommonly affects left ventricleFollows 30-45 mins unrelieved ischemiaWound repair signalledStructural, functional changes in heart tissueDecr'd contractilityDecr'd LV complianceDecr'd stroke volumeDysrhythmias

Inflammatory response severe due to wound repair signalsFibroblast proliferation to begin scar tissue formationLeukocytes migrate to site of repair (myocytes)Proteolytic enzymes released, degrade injured cells and dysfunctional biochemicals Insulin secreted to increase glucose uptake, metabolism in myocytesAids repair

Scarring results Tissue now strong but stiffCant contract like healthy cellsClinicalSudden, severe chest pain Similar to pain with ischemia but strongerNot relieved by nitratesHeavy, crushingRadiates to neck, jaw, shoulder, left armIndigestion, nausea/vomitingAbnormal heart sounds possible (S3,S4)

Clinical contdBlood tests show several markers:LeukocytosisIncreased blood sugarIncreased plasma enzymesCreatine kinase (CPK)Lactate dehydrogenase (LDH)Aspartate aminotransferase (AST or SGOT)Cardiac specific troponinECG changes (Fig.23-22)Pronounced, persisting Q wavesST elevationT wave inversion

TreatmentFirst 24 hours crucialHospitalization, bed restPain reliefMorphineNitroglycerinThrombolytics to break down clotsAdminister oxygen

Manifestations of Heart DiseaseCongestive Heart FailureDefined: heart progressively loses capacity, leading to back-up of blood flow through systemLeads to incrd blood pressure, edemaCompensations to relieve effects at vasculature, heartBUT compensations are limitedAffects about 3 million patients in the U.S.Slow developing

Pathophysiology may includeAltered contractilityCardiac sarcomeres stretched too far May occur with altered preloadSo contractile force limited inadequate ejectionAltered afterload (Fig.23-37)Alteration in force against which heart must pumpMay be due toVascular stenosisIncreased vascular resistance To maintain cardiac outputHeart incrs stroke volumeHeart incrs rateResults in incrd need for oxygen by heart muscle

Pathophysiology contdRestrictions to pumpingDue toValve dysfunctionsDysrhythmiasPericardial diseaseAltered demand for oxygen by the heartCompensations body needs to:Increase blood return to the heart, byIncreasing blood volume through renin/angiotensin system (kidney) incrd LV volume, which incrd fiber stretch, which incrd contractilityBUT may cardiac sarcomeres stretched too far (one cause of cardiac problem to begin with)

Compensations contdIncrease heart rate and increase C.O.Through nervous system Need to incr sympathetic inputHypertrophy of cardiac muscleResults in incrd LV wall thicknessShould incr force of contractionsHeart will ultimately fail because compensations limited, sometimes cause other problems, may result in further cardiovascular damage or complications (Fig.23-28)

ClinicalBreathlessness/difficulty breathingEspecially lying downDue to pulmonary edemaChest painDue to hypoxia at heart, resulting myocyte damageFatigue/confusionDue to decrd blood flow to skeletal muscles and brainSkin pale, cold, sweatyPulse, lung sounds abnormalTreatmentDecrease cardiac workDrugs to augment contractilityReduce afterloadHow might you do this?

Manifestations of Heart Disease contdShockDefined: clinical syndrome of underperfusion of organs (KNOW THIS!!)May be due to: Cardiac dysfunction (cardiogenic shock) (Fig.23-43)Electrical dysfunctionTachycardia (incrd heart rate), orBradycardia (decrd heart rate)Mechanical dysfunctionValve dysfunctionTrauma, pericarditis, etc.When >40% of LV function lost, LV fails to pump sufficient blood to systemic circulation

Clinical (w/ respect to cardiogenic shock)Decrd contractility decreased stroke volume decreased C.O. decreased blood to organsPulmonary edemaWhy should this occur?Reflex vasoconstrictionWhy should this occur?Volume disorders- heart appears normal, but organs underperfused for other reasons (Fig.23-44):Volume loss (causing hypovolemic shock), due toHemorrhageEdemaBurnsDehydration

Shock due to volume disorders contdVolume maldistribution (causing vascular shock).Vasculature dilates altered hemodynamics (or greatly reduced blood pressure)May happen in:Septic shock -- bacteria release toxins that cause extensive vasodilation (example: toxic shock syndrome)Anaphylactic shock (Fig.23-46) -- histamines cause extensive vasodilationIn both cases (cardiogenic or volume disorders shock) Overall cardiac work increases heart failure over timeOrgans underperfused organ failure over timeMost susceptible organs: lungs, kidneys, liver, g.i. tractCompensation through heart, vasculature, kidneys to try to increase blood pressure and blood delivered to tissues

Treatment for shock:Mechanical support of circulationAugment contractility with drugsOxygenateTreat edema