Week 4 PP Ch Notes PDF

Uh 16 Alterations in BloodPressure Mchs Topics subtopics Artifahlheffffewmanning Important...

Uh 16 Alterations in BloodPressure Mchs Topics subtopics Artifahlheffffewmanning Important antennae treatments systolic BP peak pressureduringcardiaccycle signssymptom diastolic BP lowestpressureduringcardiaccycle SV is theprimaryfactorinfluencingsystolicpressure vasoconstrict SIRisthemajordeterminantofdestpressure Pulsepressure systolic diastolic v40 60 120 80 Measurement of Blood Pressure meanarterialpressure MAP averagepressure w in the circulatorysystemthroughout thecardiaccycle MAP 12 diastolicpressure systolicpressure 3 Direct measurement of BloodPressure requires intraarterial catheter specilized equiptment totransduce arterial fluid pulsations into electrical signals wave forms catheter commonly placed in radial artery mostaccuratemethod of BP measuring Indirect measurement of Blood Pressure commonlymeasured via brachial arteryusing a stethoscope sphygmomanometer or automated oscillometricsystem Requirescarefultechniqueto ensure accuracy Auscultation of Korotkoff sounds systolic pressure SBP onset of Korothoffsounds Diastolic pressure DBP disappearanceof Korotkoff sounds White coat effect Elderly ausculatory gapperiod of diminishedabsent Kovotkoffsoundsduringthe manual measurement of BP Determinants of systemicBloodPressure SBP DBP Cardiacoutput co and resistanceto the ejectionof blood from the heart Co SV strokevolume x HR heartrate Enddiastolic volume is the preload amount of bloodreturnedto the heart systemicvascularresistance SRVafterload is determinedbythe radius of arteries degree of vessel compliance  Shortterm Regulation of systemicBloodPressure SNS Changes in BP are mediatedthroughactivation of the sympatheticnervoussystem epi norepi parasympatheticnervoussystem slows heart long term regulation of systemicBlood Pressure Renin Angiotensin Aldosteronesystem RAAS importantregulatorof BP Juxtaglomerularcells whenstimulated by low arterial pressurerelease renin activates angiotensinogen angiotensin Angiotensin when in contact w ACEinhibitors activates Angiotensin 11 1 potent vasoconstrictor Afterload 2 Stimulatesrelease of aldosterone Aldosterone hormone causesreabsorption of sodium and water passivly follows preload regulated by neural hormonal renal Increase in extracellular fluid volume preload increased co and SVR elevated BP causes kidneysto excrete excesssodium water Increasedserumsodium Nls increasedosmolarity increased ADHsecretion causes kidneys to reabsorb water INCREASEPreload Atrial natriuretic peptides ANP causes kidneys to increase sodium water excretionby increasing glomerular filtration rate AFR results in decreasedpreload B resureaasaficationsinAdutspp.pe SBPm where Normal 2120 80 Prehypertension 148 89 80 89 Stage1 hypertension 90 99 stage2hypertension 160 100 Thehighest reading will determain the ftp.ertensionsigppmmm degreeofhypertension HiatywormIsolated systolichypertension systolic BP is 140 while diastolicpressure remains 90 HIGH Isolateddiastolic hypertension diastolicpressure NORM is 290 with a systolic pressure of 2140 Combined systolic diastolichypertension bothSBP DBP exceed prehypertension IVIS  sometimes called silent killer as damagehas already occurred to organs beforediagnosis is made Endorgan damage Renal failure stroke heartdisease Damage to arterial system acceleration of arteroscerosis lead to cardiovasculardisease Increased myocardial work results in heart failure Glomerular damage results in kidney failure Affects microcirculation of the eyes Increased pressure in cerebral vasculature can result in hemmorage Primary Hypertension aka Essential hypertension RISKFACTORS Non modifiable FamilyHistory Ethnicity Genetics Modifiable DietaryFactors sedentary life Obesity weightgain metabolicsyndrome Elevatedbloodglucose IVISdiabetes Elevated total cholesterol Alcohol smoking Treatment lifestyle modification are first mostimportant prevent treatmentstrategy weightloss exercise DASH diet Alcohol moderation Decreasedsodium intake Drugtherapy for hypertensionaffects heart rate SVR and or stroke volume  selfystertenberthtimministred to a specificidentifiable pathology or condition mostcommon in infants preschool children most common cause for indary childhood hypertension renal disease and coarotation of the aorta aorticnarrowing othercauses for children obstructive sleepapnea Meheagreneechingthaleelwmanhypertensioncaterm Hypertensiveemergency sudden increase ineither or both systolic ordiast BPW evidence ofendorgandamage Rapid but controlled reduction of BP using parenteral antihypertensiveagents under close monitoring Icu Hypertensive urgency similar bloodpressure elevation withoutevidence of end organdamage oralmeds to bring BP undercontrol over 24 48 hrs h neateheotffe nanae from supine to up rightposition activation of the shortterm control mechanisms is slow orinadequate causes a decrease in systolicblood pressure 20mmHg or 10mmHg w in 3 minutes whenmovingto an uprightposition Excessive increase in heartrate by2030beats min may be diagnostic Results in dizziness blurred vision confusion syncope Associated w cardiovascular disease is a risk factor for stroke cognitive impairment death CH18 Alterations in cardiac Function coronaryHeartDiscass Coronary Heartdisease CHD AKAischemic heartdisease coronaryartery diseaseCAD Charcterized by insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries CAD sequelae of CHD includes Anginapectoris 3types Myocardialinfarction Dysrythmias Heart Failure Suddencardiac death Effffeeffattheisthemapossible microcirculation abnormalities Arteriosclerosiscauses narrowing of the arterial lumen that can lead to ischemiathrough Thrombusformation coronary rasospasm Endothelial celldysfunction Mayyffffeehaffaffstettrimmhome eroded which stimulates clotformation on the plaque Vulnerableplaques have large lipid core thin cap high shear stress Stable plaques have more collagen fibrin stablecap taobao.fr fffffpfIynsufficenttomeetmetabolic demands criticalfactors in meeting cellular demands for 02include rate of coronary perfusion myocardial workload Coronary perfusion can be altered by large stable atherosclerotic plaque acute platelet aggregation thrombosis Vasospasm Failure of autoregulationby microcirculation Poorperfusion pressure Chronic occlusion of a coronary vessel stableangina Acute occlusion plaquedisruption thrombus formation results in unstable angina or Ml AYffesffai.hn ssociated withintermitantmyocardialischemia Burning crushing sneezing choking orreffered pain No Perminant myocardialdamage occurs May result in inefficientcardiacpumping w resultant pulmonary congestion shortness of Breath chronic occlusion of a coronary vessel stable angina Acute occlusion plaquedisruption and thrombus results in unstable angina or MI  Myocardial ischemia may also uncommonly be caused by coronary Vespasm Prinzmental or unstableangina Hypoxemia low purfussionpressure from volume depletion or shock Stable or typical angina most common also calledclassic charoterized by stenotic artheroscelrotic coronary vessels onset of anginal pain is generally predictable andelicited by similar stimuli each time relived by rest nitroglycerin unstable or crescendo angina Indy profile fntaffknfamhe.it Prinzmental or variant angina SYFYEYdmeptthk.sk eThfe9offhysical or emotional exertion heart rate or other obvious causes of increased myocardial oxygen demand unpredictable Charcterizedbyvasospasms atherosclerosis induced hypercontractability abnormalsecretions of vasospasti chemicals by mast cells and abnormal calcium flux across vasal Tooth muscle Anaerraysundromen unstable crescendo angina cause Plaquerupture with acutethrombusdevelopment signssymptoms chest pain usually more severe unstable fadf.IE v IIkrin MI occlusion is complete ECGandbiomarkers usedfordiagnosis Asymptomatic M1 silent MI women elderly pts with diabeticneuropathies Atypicalsymptoms include fatigue nausea back pain abdominal discomfort Diaghfffeast not the 3  signs symptoms severe crushing excruciating chest pain that radiatesto arm shoulder jaw or back Accompanied by nausea vomiting diaphoresis sweating shortness of breath Electrocardiographic change Elevations of specific marker proteins in blood presentation sis of cardiac ischemia working Diagnosis ECG fats stelevation no stelevation Biodmarkers Cardiac Biomarkers Biomarkers Biomarker Final Diagnosis STEMI uypfgg.gg NYEMI Akefffaff on Taking a range of cellular events depending Availability adequacy of collateralbloodflow relative workload length of time that flows interrupted Ultimate size of the infarctedtissue depends on theextent duration and severity of ischemia AC.sn iffYf zahrs area of infarctionbecomes paler than 5 7 days turns enn yellowishand soft with a rim of red rasmia 1 to 2 weeks necrotic tissue progressivly degraded an cleared away infarcted myocardium weakened and suscepted to rupture Clearwater BY 6 weeks necrotictissue replaced by toughfibrous scar T.fi aE eEI n eE Increased CK MB andtroponin 1 and T 129hrs e 8YghtaHIevation POSSIDI.es Pt with chest pain and evidence of ischemia on Ela St segmentelevation STEMI canidates for acute repurfusiontherapy  Pt presentingsymptoms of unstableangina No ST elevation onECG non STEMI NSTEMI canidates for antiplateletdrugs large Q waves inverted Twaves MI leads to drop in co triggering Sympatheticnervous system dftonf activation leadsto increased myocardial workload by increasing Heart rate contractility Bloodpressure II.MEighhinhardiae oxygenrestdemand symatheticantagonists heart rate control pain relief afterloadreduction Increasing myocardialoxygen supply Thromolysis angioplasty coronary bypassgrafting monitoring managing complications SNS activation Earlydetection management ofdysrythmias conduction disorders continuous ECG monitoring ClinicalTreatment morphine pain decreaseondemand oxygen ischemia Nitroglycerin ischemia Anticoagulants ischemia plateletthinner orthrombolysis iTkmsiI e r thrifty results dieffesEinktrattoEEorkto ftp.t Clinical manifestation IIIartfiffeemmeritternardisorderin Cn 19 Heart Failure Dysrythmias common sequelae of cardiac Diseases Habittittimminmart to maintain sufficent cardiac output to meet metabolicdemands of tissues organs Results in congestion of blood flow in thesystemic RHF or pulmonary LHF venous circulation inability to increase cardiac output to meet the demands of activity or increased tissue metabolism Increasingincidence most common reason for hospitalization in those 65 yrs of age fE ffreñtf.EE over eaeeotkttwoaranorma long term detrimental to the the heart current management of it YII.tt naoFnictcinHf