Cardiovascular Pathophysiology PDF

Cardiovascular Pathophysiology (1/4) Ricardo L. Garcia MD Objectives } } } } } Describe the main functions of the circulatory system. Explain the concept of the pump-high pressure vesselslow pressure vessels arrangement. Understand the pressure drop profile of the circulatory system and its cause...

Cardiovascular Pathophysiology (1/4) Ricardo L. Garcia MD Objectives } } } } } Describe the main functions of the circulatory system. Explain the concept of the pump-high pressure vesselslow pressure vessels arrangement. Understand the pressure drop profile of the circulatory system and its causes. Understand and explain the reasons for the normal distribution of blood in the circulatory system. Understand the advantages of the series-parallel arrangement of the circulatory circuits. Objectives } Describe etiology of Dysrhythmias. } Understand ischemic heart disease/angina in the anesthesia patient and risk factors for Myocardial infarction. } Describe the preoperative, intraoperative and postoperative management of Hypertension and Congestive heart failure } Understand Endocarditis and Valvular heart disease } Explain how Cardiomyopathy, Peripheral vascular disease, and Congenital heart disease can alter the anesthesia plan. Clinical Scenario } A 65-year-old man with hypertension, familial hypercholesterolemia, type 2 diabetes mellitus, and angina pectoris presented for resection of a sigmoid colon tumor. } Stress imaging demonstrated an anteroseptal region of ischemia. Coronary angiography showed a critical lesion of the left anterior descending coronary artery and a 50% stenosis of the proximal circumflex coronary artery. Percutaneous transluminal coronary angioplasty with drug-eluting stent (DES) implantation was performed successfully on the left anterior descending lesion 6 weeks before surgery. * has toforwait surgery - } a year The patient was maintained on metoprolol, aspirin, and clopidogrel therapy. Clopidogrel was discontinued 7 days before surgery. * Clinical Scenario } } General anesthesia was induced with etomidate, midazolam, and fentanyl. Maintenance anesthesia consisted of oxygen, sevoflurane, and fentanyl. Muscle relaxation was provided with vecuronium. } } } During tumor mobilization, the heart rate increased from 70 to 120 beats per minute. Blood pressure remained stable at 130/70 mm Hg. On the V5 electrocardiogram (ECG) lead, 2 mm of horizontal ST-segment depression was noted, but no abnormality was seen in lead II. An additional dose of fentanyl was associated with slowing of the heart rate to 95 beats per minute but no change in the STsegment depression in V5. Clinical Scenario } What are the determinants of myocardial oxygen supply? } Explain the determinants of myocardial oxygen consumption (demand). } What are the pharmacologic alternatives for treating myocardial ischemia in this patient? } Describe the considerations for performing surgery on patients with drug-eluting coronary stents. } Is perioperative β-adrenergic blockade indicated for this patient? } How should this patient be monitored intraoperatively? TODAY’S LECTURE } Review Cardiovascular } } } } Anatomy Components Physiology Blood Pressure: Hypertension } } Systemic Pulmonary Cardiovascular System Components HEART VALVES AND CIRCULATION OF BLOOD de mayor presion a presion menor CHAMBERS OF THE HEART superior vena cava Opulmonant veins ③ pulmonary veins s Node Inferior Vena cava 2 2 I I 11 Coronary Circulation } Coronary Arteries } "hole" } divisions} } flows to the coronary arteries Left Anterior Descending Left Circumflex Coronary Artery Right Coronary Artery } divisions blood is pumped into the aurta from Coronary ostia: entrance points located behinds the aortics cusps blood Left main Coronary Artery -> } oxygenated } } } Conus Artery Sinus Node Artery Right anterior ventricular branches Posterior Descending the LV Perfusion occurs in -> diastole provide oxygen and blood to the myocardium (muscle of heart) Myocardium receive blood when the heart is on diastole Coronary Circulation coronary arteries blood ,d delivers iF the heart rate is elevated ; the heart wont be in diastole for required time therefore myocardium wont receive blood the required oxygenated . (180bpm time nutrients to all heart cells decrease filling -> ischemia ↳Tachycardia will decrease diastole Ø Left } } ↳ · supply common site for coronary artery thrombosis . Left anterior descending I intraventricular supply } } coronary artery Arises from posterior aortic sinus Supply LA, LV, most of interventricular septum # Most } filling of the coronary arteries and LAD septum and anterior wall most common to get Left circumflex } artery lateral wall occluded -> "The : supply & atria of the ventricle Widow ventricular muscle maker" - Severe M1 Coronary Circulation Right Coronary artery Ø Rt coronary artery Ø arises from anterior aortic sinus because & Ø supply RA, RV, inferior wall of LV, (60% ) SA node, (80%) AV node Ø Posterior Ø 80% coronary artery Infarct supplies SA hode in side (cornary Risk to develop Heart block descending artery branch of RCA (rt dominant circulation) Ø 20% branch of LCA ( lt dominant circulation) Ø supplies wall . interventricular septum and inferior Ø In OR Ø EKE a pt with Risk for Ischemia monitor includes a leads monitoring Clinical Correlation Occlusion in the…. } Anterior descending artery: leads V3-5. } Left circumflex artery: leads I and aVI. } Right coronary artery: leads II, III and aVF. When does perfusion When blood returns occur ? diastole when left ventricle is on diastole . ; heart Venous drainage to veins from coronary mixed The greater cardiac venous Ø Coronary Ø Ø Ø Ø system sinus : coronary sinus drains drains in great cardiac vein middle cardiac vein small cardiac vein oblique vein . Primary collector . blood of cardiac cardiac vein cardiac Ø Thebesian venous susten veins I vessels a low 30 into venous -> anterior interventricular drains the anterior aspect of the heart Ø Anterior The smaller atrium DEOXYGENATED have sinus venous saturation the blood atrium Blood flow from examen a greater gradient to a smaller gradient Determinants Of Coronary Perfusion is the Coronary Perfusion Pressure ↳ eXAMP 12 ; this myocardial oxygen ensures CPP should range between 40-180mmHg CPP = Aortic diastolic pressure – LVEDP : BP : on : diastolic pressure /20180 => 5 = because 45mmHg & ventricle perfuses during delivery -> CHF -> 40-90 ventricle se . IF tadhy there is little to no diastole time will ↓ ventricular End Diastolic Pressure 5 - 15 Hypoperfusion = affecting perfusion -> Left diastole LV is perfused entirely during diastole ↳ left } coronary , myocardial perfusion not continuos Based } for Coronary perfusion is intermittent compared to continuous in other organs } } gradient responsible pressure IV has more risk for e ischemia than RV gradient during systole RV is perfused during both systole & diastole Aortic insufficiency patient may have a ↓in Aortic diastolic pressure . Trisk of infarction Coronary Perfusion Pressure normal range Formula 40-180mmHg : PP= : Aortic diastolic pressure - LVEDP · pressure when the before Left (minimum) experienced heart ejecting is in the "relaxing"/during blood into the : In w . <2mmHg (LVEDP) Heart receive veins are · give fluid perfusion : Most common to the RELAX Heart fills with blood that pt . volume Blood go from ⑫ "storage the vessels that CARDIA de Return DEOXY GENATED blood to the heart Adenosine is vasodilator of post op complications greater & the -> coronary artery. & most blood" from organs a coronary Infarction pressure to less pressure coronary . supply SA mode . body cells veins present cause from Coronary arteries 3 blood from heart to receive from veins 5-15mmHg heart conditions Hypotension pumped "out" her the heart ↳Epis areflectionofventricular compliance dintravascular Inpt is Diastole aorta from the ventricle Normal blood aorta diastole Left Ventricular End Diastolic Pressure · Bring OXYGENATED when the heart CONTRACTS Aortic diastolic Pressure The Arteries Systole If is affected pt will be at risk for heart block back ↓ donde mas - Imp Coronary Perfusion en qtienen pt - problemas del corazon no examen DBP es la o valuulas las The capacity of the heart to maintain Autoregulation ↳ I does it 170 mmhg Heart Ø extracts around 65-75% oxygen supplied lot of oxygen regulates , nutrients E how much myocardium needs Metabolic control ↳ I metabolism Ø regulates its blood supply between 50 to pressure Ø Myocardium a consumption blood flow = 250 ml/min at rest Ø Myocardium consume , Neurohumoral control ↳) perfusion ensures that constant blood flow to the organs automatically Ø Coronary ↳> -> steady myocardial better vasodilation to keep perfusion by these mechanism : GOAL - Neurohumoral control · Heart and vasculature are "Compensatory"/autoregulation regulated to control the internal · improv Perfusion environment and homeostasis mechanism When blood pressure decreases ¯ Blood flow decreases ¯ Vascular smooth muscle relaxation ¯ Blood flow increases Metabolic control when metabolic waste accumulates this the heart will try to "clean" get rid of it Acidosis · from To minimize heart we ↑ will blood flow blood Or - keep - to maintain - cpp good oxygenation -vasodilation - so ↑ When blood flow decreases ¯ Metabolites accumulate ¯ Vasodilatation occurs to ¯ Blood flow increases - doesnt have to contract Laflerload - ↓ contractility as - more as this - Tafterload will ↑ O2 consumption ↑ intropic agent * we just decrease - Good Preload . . to awid THR will noz demand - because to "clean" metabolic waste have to minimize heart demands NHR dilation consumption -calmpt/minimize anxiety - causes want to it clean Myocardial oxygen balance } Myocardium extracts 65-75% O2 in arterial blood compared to 25% in most other tissues } Cannot compensates for reduction in blood flow by extracting more O2 from Hb } Any increase in demand must be met by an increase in coronary blood flow E02 Myocardial ischemia results when and metabolic substrates arterial blood supply fails to meet the needs of the heart muscle for 02 Myocardial O2 supply & demand Ø Supply Ø Ø Ø Ø Hypotension : not "enough" blood will return to the heart HR: Diastolic time coronary perfusion pressure arterial 02 content vs extraction coronary vessel diameter trata Ø Demand Ø Ø Ø Ø Ø basal requirement HR wall tension: afterload Contractility "calme" Preload buen ↓ ↓ after el HR load mantener bunna oxygenasion Autoregulation } Coronary Perfusion Pressure (CPP) } } } Determined by the difference between diastole and LVEDP CPP= Diastole – LVEDP Chanta sangre regrest al corazon } In hypotension becomes: MAP – RA Coronary ‘Steal’ Phenomenon: } Ex Use of vasodilator treatment in a patient with an stenotic area and another normal. ONLY the normal dilates….. : give nitrate , Anginal chest pain worsened because dilation took blood flow from "good side" Cardiac Conduction System in atrium Depolarization phase is fast no es Pacemaker Action Potential automaticidad examen ! Action Potentials Automacity from is SA "short" is is progressive shorter alt depolarization /fast Refractory Time Electrocardiogram (ECG) can trace conduction of electrical signals through the heart aprender ECG que es cade cole Aberrant ECG patterns indicate damage Cardiac Ultrastructure . -mech action Milnnone ? ↑ - Excitation Contraction Coupling - phosphod Testerasa sensitividad cual mas sensible para el dano al es myocardio . 3? Milrinone - => inhibits phosphodiesterase phosphodiesterases release - Do let catt A not cause 3 tachycardia Innervation of Heart } Parasympathetic: from medulla oblongata } } vagus nerve } Nerve branches to S-A and A-V nodes, and secretes acetylcholine (slows rate) nnervates I depend on SAnode stimulation , and Av node . Release acetylcholine Parasympathetic activity can increase (slow heart rate) or decrease (increase heart rate) Innervation of the Heart } Sympathetic nervous system } } } } through celiac plexus to heart secretes norepinephrine increases force of contractions Cardiac control center in medulla oblongata } } innervates maintains balance between the two celiac plex us Normally both sympathetic and parasympathetic function at a steady background level vagus nerve Innervation of the heart } Nerves to the heart originate from sympathetic neurons of thoracolumbar region and parasympathetic originate from the cervical region. Symphatetic -> thoracolumbar region parasymphatetic -> cervical region nerves "relaja" S "estimula" Symphatetic System "fastness" HR , uses Domothropic inotropic Isothropy -time beta to stimule -> -> how fast HR in diastole Cant or contractility Cardiac receptors } Most important adrenoreceptor is heart is B1 } B2 adrenoreceptor in heart has similar cardiac effect B1 Norepinc i heart doesnt have } Prejunctional a2 adrenoreceptor inhibit NE release } Prejunctional b2 adrenoreceptor facilitate NE release } Prejunctional M2 adrenoreceptor inhibit NE release Receptor concentration } Right atrium – 74% b1 and 26% b2 } Ventricles – 86% b1 and 14% b2 Beta Adrenergic Receptors T chronotropy ↳) ↓ or A Increase HR promotropy ↳ How quick HR can Nort Inotropy ↳ Contractility Lysitropy ↳ time in diastole ↳ of Increase relaxation myocardium Receptor presunctional M2 advent receplor ↑ - Cardiac Output and Cardiac Cycle Stroke Volume EDU- ESU= stroke volume · From . From Diastole · · : RV into with with aurta preload Sustole : is each pulmonary artery synonymus * goes Ejection ESU completely heart does not get empty * some blood remains systole there is 1 . volume left some ejection . As contractility goes ↓ Fraction be obtained print of blood . and viceversa End systolic volume Increased contractility increase ↑ w returning ↓EDU ejection phase At the end of -> (EF) by Fraction -> of blood out Of EACH VENTRICLE during each contraction : get EDU-ESV= SV SV then 2 : * EY= "good Divide SV EF by number" - less as than EDU >50 % 50 % heart is not out/ejected systolic contraction of blood -> amount At the end of diastole there is some wlume left if can into LV LV phase/ heart perfuses filling ↳ End diastolic volume . 2 * amount of blood pumped out of each beat 1 (amount of blood ejected) suspect systolic dysfunction ejecting enough blood . Preload · · "Think veins" "Blood returning to the heart" the T in will increase because SV · · TEDU venous return -> Y preload TSV - EDU will increase will increase because sacromere lengthening Nitrates - - are VENOUS venous Afterload when there is Contractility * DILATORS venous dilation will cause return the ↑ contractility as there more blood preload more being ejected returning /↑ preload) the"heart" will is more blood * . . bigger squeeze a strech to accommodate to pump blood out blood this the happens thanks to the . * arterial dilation can cause , dilation will as compliance -> more cause blood will by less on venous blood return HOLD -> where Tin Total Peripheral Resistance (TPR) /SUR -Nafterload ↳ arterioles ↳ if the arterioles vasoconstrict = ↑TPR ~ -> . preload decrease in TPR/svR goes afterload & DBP will gox1 As afterload goes Amount of pressure that the heart need to exert to eject blood · · and EDU · will increase because heart need will decrease preload dilation , , contractility . venous more TESU ↑ . the SU will during + ↓ got ventricular SU Think contraction arteries DBP vasodilation= ↓TPR-DBP · If arterial pressure This will Hydralazine ↳ cause the is an i · LV + the ESU will be blood to either "come because there is not much volume that is back"/return or no flow at all . This going able to flow forward to be will end with . lower stroke volume a ARTERIAL VASODILATOR Will ↓TPR Contractility · is "How -> primarily hard the heart is SNS activity /catecholamines , Beta used to decrease TPR beating agonist) SV " -> ↓ESU (because systolic dysfunction will have a reduced contractility ↳ Digoxin is usually given to ↑ contractility more blood is beign ejected) -> ↑ SV proportional · They"follow" St C · preload contractility opposite after load Opposite SV to 40 Pressure from ventricle needs to be less than atrial chamber pressures pressure chambere Pregunte e How to find out that you know the Cardiac Cycle. LEFT VENTRICULAR VOLUME (ML) 150 Atrial Mitral systolecloses Aortic opens Aortic Mitral closes opens 50 TIME (SEC) Cardiac output Ø Cardiac output: volume of blood pumped by heart per minute. It is measure of ventricular systolic function. CO = S V × H R SU= EDv - ESv Ø Stroke volume: volume of blood pumped per contraction Ø Cardiac index : C I = C O / BSA normal value 2.5 to 4.2 l / min / m2 Determinants of Cardiac Output (CO) Ø Intrinsic factors Ø Heart rate Ø Contractility Ø Extrinsic 3 factors Ø Preload Ø Afterload cardiac Output modificators Heart rate Ø CO directly proportional to HR Ø HR is intrinsic function of SA node Ø HR is modified by autonomic, humoral, local factors parasumphatic Ø Enhanced vagal activity decrease HR Ø Enhanced sympathetic activity increase HR Contractility independently contract Ø Intrinsic ability of myocardium to pump in absence of changes in preload and afterload Ø Factors modifying contractility are exercise, adrenergic stimulation, changes in Ph, temperature, drugs, ischemia anoxia. /SNS catecholamines Beta agonist , SV is modified by contractility , preload and afterload , BREAK Frank starling relationship } Relation between sarcomere length and myocardial force } States that if cardiac muscle is stretched it develops greater contractile tension } Increase in venous return increases contractility and CO } que se usa pa s we End Clinical application is relation between LVEDV and SV diastolic press . looks Pressure is regulated by Blood Volume is stored in up the heart arterioles ability to change contractility veins Frank Starling relationship An increased preload ventricular myocites Tension An increase in will result in to lengthen EDU an , increased EDU, leading to an will result in causing increased sarcomeres of the contractility increased CO CVP Length (= preload) . contractility Preload Ø Defined as ventricular load at the end of diastole before contraction has started Ø In clinical practice PCWP or CVP are used to estimate preload Preload depends on : Ø Determinants Ø Ø Ø Ø Venous return Blood volume Heart rate Atrial contraction * pt w . afib does not contract well * How much work Afterload Ø Defined componente the que heart experience to define purp blood out SV as systolic load on LV after contraction has began Ø Aortic compliance is determinant of afterload e.g. AS or chronic hypertension both impede ventricular ejection if ventricle cannot empty blood cannot -> get Ø Measurement Ø Ø in of afterload: Echocardiography systolic BP or SVR Systemic Vascular Resistance cardiomyopathy - Afterload Dilated cardiomyopathy } Wall } Dilated -> : will have more wall stress . Radio is bigger . 102 consumption - will have more Hypertrophy Risk for infarction wall stress stress: Laplace law states that wall stress is product of pressure and radius divided by wall thickness (H) wall stress= P × R/ 2H } RV load depends on PVR. Right Ventricular Pulmonary Vascular Resistance ~