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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 ~ Cardiac Output (CO) ·CO= HR · x SV volume of blood ejected 5L/min in one minute ~ Tachycardia THR -> ↓ time · · · Severe tachycardia A decrease in vagal in diastole -> ↓ ventricular will tone have a would decrease increase the myocardial perfusion in co heart rate -> ↓ diastolic filling time -> ↓ cr 15/09/2022, 09:38 h ://a .b cam .c m/med- ch B cam .c m Ca di l g C e: Ca diac Pa ame e l/ca di l g / ide /ca diac- a ame e - f- h i l gic-f nc i n?inde =7 f Ph i l gic F nc i n 1/1 Cardiac Work } External work ( stroke work) is work done to eject blood under pressure. stroke work= SV×P } Internal work is work done to change shape of heart for ejection. Wall stress directly proportional to internal work } Both internal work and external work consume oxygen } } Wall motion abnormalities 3 Valvular dysfunction Too MUCH O2 will lead to an consumption infarct : men Po -> HOW TO ASSESS CONTRACTILITY ? } Pressure volume loops } Noninvasive like echocardiography } Vetriculography -> graph EF = (LVEDV – LVESV)/ LVEDV NORMAL – 60 ± 6% in page 14 Methods to measure CO } Fick principal } Thermodilution } Dye dilution } Ultrasonography } Thoracic bioimpedance oxygen electrical currents uptake , co , arterial (non invasive) in chest venous Pressure Volume Loop stic value Stroke vol · ventricle is empty . Authent open LEFT VENTRICULAR PRESSURE (mmHg) LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOP END OF SYSTOLE Aurtic value 120 F closes Diastole starts E D 80 Aortic value open 40 ventricle is EMPTY A 0 50 B Filling END OF DIASTOLE Process C 100 150 Atrial contraction LEFT VENTRICULAR VOLUME (ml) LEFT VENTRICULAR PRESSURE (mmHg) EFFECT OF PRELOAD ESV End Systolic Volume save of hypo 1 2 e 3 Se dio vol. Preload EDVs VOLUME (ml) End diastolic volume EFFECT OF AFTERLOAD facilita LEFT VENTRICULAR PRESSURE (mmHg) ESV ESV 1 2 ESV R V P mejor 3 reduction of baseline after load S mejoria ES sea W a pt . w value . problem EDV VOLUME (ml) Su LEFT VENTRICULAR PRESSURE (mmHg) EFFECT OF CONTRACTILITY P S E contractilityPVR 1 VR 2 ES mejora no I 2 contracti 1 contractilidad buena - - - - Se inotropica da VOLUME (ml) QUICK QUIZ PRELOAD AFTERLOAD CONTRACTILITY ignacion Cardiovascular Reflexes } } } } } } } } Cardiac Output Regulation Valsalva Maneuver Baroreceptor Reflex Oculo Cardiac Reflex Celiac Reflex anesthesia Bainbridge reflex Cushing Reflex Chemoreceptor Reflex como en ejemplnesthesia - afecta? * Clinical Correlation: Effects of volatile anesthetics, local blockade and intravenous anesthetics. * Importance in the BP management during surgery. controlled by - Response Sympathetic to System Nervous demands for oxygen D's body . - if by a pt squeezing -> bag reservoir and 40mmHg Tachycardia Supra in for of pressure ->"blow a straw" 10 HAR Sec . offerent to eNS BD L supine or . maintain verbric. , sitting um anesthesia -> Passive is under from peripheral peripheral Motor Sterent · -> alsocated w xintraabd . · pressure - A From - in kicks -Helps to keep -cause in blood volume with BP at constant HR tot When vicevers -ex Donde los esta HR BO + , -> in MAP · · · normal full in BD mesentery Mean Arterial ex -65 Pressure is average arterial pressure throught one cardiac cycle Affected by do & SVR : systole Diastole Or Trauma 20 % , muscles orbital structures eye strabismus surgery for peds : procedures , - N When traction Trauma ex levels localizado by conjunctiva - , extraocular in sensory receptores ? decrease a Is I CNS . hemorrhage : I BP to W . surgery or laparas cop insufflated thorax abdomen abd organs When gas into aba or Sinus brady i -> ↓ Sinus arrhytmia ?? Reflex -atrial - - ilicited HRT when -role to is i an w in BP blood vol. in CO match blood vol ↑ . an i dt triggered by the heart in w . Venous return ex Spinal anotheria : w levels . below T4 ICP normal 5-15 stroke - ex - : massive mass - - midline shift effect - uncal - nerniation -subfulcine Det rhage herriation worse -herniation - - Regulates Respond - -It : to ex-Propofol leading ex - & hypoxia, it & Regional RR , CO Para and hypercarbia inhibit my to chondrial can to ph in acidosis , - - respiration lactate increase metabolic blood Slow >2 acdous hypovolemia Pacoz-partial estimate pressure O2 carbon exchange dioxide Blood Pressure: Systemic and Pulmonary Hypertension To be continued - DO2 = CO x Ca02 Si Hyb 12 x 1 34 x 1 34 x 1 x . . 14 . 1 es (15at) 100 % + = 1 (Pa02x0003) Blood Pressure } Blood flow is generally equal to cardiac output } Blood flow affected by pressure and resistance } Blood pressure: the force that is exerted by blood against blood vessel walls } Resistance depends on size of blood vessel and thickness (viscosity) of blood Blood pressure } Blood pressure is highest in large arteries will rise and fall as heart pumps } } } highest with ventricular systole lowest with ventricular diastole pulse pressure is the difference between the two Pulse Pressure } Resistance E pressure is controlled arterioles in the = SBD - DBP Resistance is highest in capillaries -> because capillaries are small How you regulate BP Control Control of blood pressure ↓ } Regulation of cardiac output } } } } } } contraction strength heart rate venous return skeletal muscles breathing rate Short Action Regulation -change that regulate occur BP to Long Term Regulation } ADH (antidiuretic hormone) promotes water retention water } Angiotensin II- in response to renin } signal (renin) produced by kidney- why? } drop in blood pressure } stimulation by sympathetic nervous system } sodium levels too low G Sodium ? Ander ! Renin angiotensin aldosterone system - - Control Resistance - Es BP - Atrial Natriuretic Peptide } Produced by the 0 atria of the heart. } Stretch of atria stimulates production of ANP. } } } contraryeffect Antagonistic to aldosterone and angiotensin II. Promotes Na+ and H20 excretion in the urine by the kidney. ↳ polynria Promotes vasodilation. Systemic Hypertension } What is hypertension?______________________ } } Up to 30% of adults Essential vs Secondary ↳ Secondary to another issue that No cause to correct } -> canlmay . Variety of causes/ risk factors are known } } } } } } } Western World sedentary lifestyle prevalent Smoking Obesity diet (excess sodium; cholesterol; calories in general) Stress Arteriosclerosis genetic factors in be corrected Classification Category Normal Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) <120 <80 Prehypertension 120-139 80-89 Stage 1 hypertension 140-159 90-99 Stage 2 hypertension ≥160 ≥100 Effects of Hypertension } heart has to work harder; left ventricle enlarges ↳ will i } or consumption atherosclerosis may affect coronaries ↳ dilate coronaries ; will I demand +Oz consumption } arteries as well (which have to work harder anyway) } deficient blood supply to other parts of body } damage to blood vessels accumulates } heart failure Chronic Effects Management of HBP } Lifestyle modification } } } } } Quit smoking adjust diet weight loss exercise Pharmacologic therapy } Reduce heart rate } calcium channel blockers } beta blockers Management of HBP Ø Pharmacologic } } } } therapy Diuretics reduce blood volume ACE inhibitors interfere with renin-angiotensin pathway Vasodilators (such as nitroglycerin) open up blood vessels (reduce resistance) If heart is actually failing, digitalis increases efficiency of heart muscle Anti-hypertensive drugs may be taken in combination Hypertensive Crisis -> nec ex } . : agresiv Mango accompained . headache Definition } Blood Pressure higher than 180/120 } Crisis if end organ damage present ¨ ¨ Encephalopathy can be late sign In pregnancy a diastolic higher than 109 emergency - · · } } w Urgency if no end organ damage present 1801128 ↓ symptoms Management } Drug choice dependent on history and previous usage is ! Read this - not exam but know ! Hypertensive Emergency - management Cause/manifestation Primary agents Cautions Comments Encephalopathy and intracranial hypertension Nitroprusside, labetalol, fenoldopam, nicardipine Cerebral ischemia may result from lower blood pressure due Lower blood pressure may lessen bleeding in intracerebral to altered autoregulation hemorrhage Risk of cyanide toxicity with nitroprusside Elevated blood pressure often resolves spontaneously Nitroprusside increases intracranial pressure Myocardial ischemia Nitroglycerin Avoid β-blockers in acute congestive heart failure Include morphine and oxygen therapy Acute pulmonary edema Nitroglycerin, nitroprusside, fenoldopam Avoid β-blockers in acute congestive heart failure Include morphine, loop diuretic, and oxygen therapy Aortic dissection Trimethaphan, esmolol, vasodilators Vasodilators may cause reflex tachycardia and increase pulsatile force of left ventricular contraction Goal is lessening of pulsatile force of left ventricular contraction Renal insufficiency Fenoldopam, nicardipine Tachyphylaxis occurs with fenoldopam May require emergent hemodialysis Avoid ACE inhibitors and ARBs Preeclampsia and eclampsia Methyldopa, hydralazine Magnesium sulfate Labetalol, nicardipine Lupuslike syndrome with hydralazine Definitive therapy is delivery Risk of flash pulmonary edema ACE inhibitors and ARBs are contraindicated during Calcium channel blockers may reduce uterine blood flow and pregnancy due to teratogenicity inhibit labor Pheochromocytoma Phentolamine, phenoxybenzamine, propranolol Unopposed α-adrenergic stimulation following β-blockade worsens hypertension Cocaine intoxication Nitroglycerin, nitroprusside, phentolamine Unopposed α-adrenergic stimulation following β-blockade worsens hypertension Hypertensive Emergency - management } Goal decrease by 20% } Consider placement of intrarterial catheter for close Line monitoring -> } a - Most common } } } } } } Sodium Nitroprusside Nicardipine Fenoldopam Esmolol Labetalol Clevidipine (cleviprex) –calcium channel blocker - new Management in Essential Hypertension } Pre Operative Evaluation } Determine adequacy of blood pressure control } Review pharmacology of drugs being administered to control blood pressure } Evaluate for evidence of end-organ damage } Continue drugs used for control of blood pressure Only diastolic BP above 110 is considered of concern ↳ } men Preoperative Considerations } Chronic hypertension is a cardiovascular, cerebrovascular, and renal risk factor => increased surgical risk } Intraoperative hypotension is more common in the hypertensive patient give fluid -> } Previous history of myocardial infarction increases the risk of re incidence, and neurologic complications (endarterectomy) Preoperative Considerations } Presume patient has ischemic heart disease } Presence of renal insufficiency marker of chronic widespread disease. } Look for: } } } } } orthostatic hypotension (autonomic response inhibition) angina pectoris left ventricular hypertrophy congestive heart failure cerebrovascular disease, stroke, peripheral vascular disease Preoperative Considerations } Continue Current BP medications } Rebound Hypertension } happen if BP are dic β-adrenergic antagonists and clonidine alpha } can antagonist Antihypertensive agents that act independently of the autonomic nervous system, such as ACE inhibitors, are not associated with rebound hypertension ↳ ACE S ARBS Alc prior surgery because ↓ BP * } Hypokalemia (<3.5) present in the patient with chronic use of diuretic DOES NOT increase the incidence of arrhythmias. Preoperative Considerations } Angiotensin-Converting Enzyme Inhibitors examen } risk of hemodynamic instability and hypotension during anesthesia in patients receiving ACE inhibitors. } ACE inhibitors may also decrease cardiac output by attenuating the venoconstrictor effect of angiotensin on capacitance vessels. } decreased venous return. ↳* First thing } examet } } hypotension give fluids & Surgical procedures involving major fluid shifts have been associated with hypotension in patients being treated with ACE inhibitors. } ↳ you will do in Responsive to fluid infusion and administration of sympathomimetic drugs. Hypotension resistant to such measures may require administration of vasopressin or a vasopressin analogue. ? Titration of anesthetic drugs may prevent or limit the hypotension attributable to ACE inhibitors. - - Consider discontinue ACE inhibitors 24 to 48 hours preoperatively in high risk cases in which intraoperative hypovolemia and hypotension may occur. Preoperative Considerations anesthessa bloquea esto Preoperative Considerations } Angiotensin Receptor Blockers } blockade of the renin-angiotensin-aldosterone system by ARBs increases the potential for hypotension during anesthesia. } Hypotension requiring vasoconstrictor treatment occurs more often. ↳ medications } In addition, the hypotensive episodes may be refractory to management with conventional vasoconstrictors such as ephedrine and phenylephrine, which necessitates the use of vasopressin or one of its analogues. } RECOMMENDATION: ARBs be discontinued the day before surgery. Management in Essential Hypertension } Induction and Maintenance of Anesthesia } Anticipate exaggerated blood pressure response to anesthetic drugs } Limit duration of direct laryngoscopy ↳ Will cause hypertension due to intubate in less than <15 sees supraglottic stimuli } Administer a balanced anesthetic to blunt hypertensive responses } Consider placement of invasive hemodynamic monitors ↳ } Monitor for myocardial ischemia ↳ I leads a line ! Induction and Maintenance } } } Rapidly acting intravenous drugs may produce significant hypotension due to peripheral vasodilation in the presence of a decreased intravascular fluid volume (Common in the Chronic HBP patient) Hypotension more pronounced in patients continuing ACE inhibitor or ARB therapy up until the time of surgery. Direct laryngoscopy and tracheal intubation can produce significant hypertension in patients with essential hypertension, even if these patients had been rendered due to supraglottic stimuli normotensive preoperatively. -> } High risk for myocardial ischemia Induction and Maintenance } To avoid hypertension during laryngoscopy / intubation consider: } deep inhalation anesthesia } injection of an opioid, lidocaine, β-blocker or vasodilator before laryngoscopy. - - } Ensure that direct laryngoscopy does not exceed 15 seconds in duration. Induction and Maintenance } Maintenance kee Stable BP } The hemodynamic goal \minimize wide fluctuations in blood pressure. } Management of intraoperative blood pressure lability is as important as preoperative control of blood pressure in these patients. } Regional anesthesia can be used in hypertensive patients. However, a high sensory level of anesthesia with its associated sympathetic denervation can unmask unsuspected hypovolemia. Induction and Maintenance } Maintenance: Intraoperative Hypertension } Most common cause noxious stimuli (awake !!) give more anesthesiax } Volatile anesthetics produce a dose-dependent decrease in blood pressure, which reflects a decrease in systemic vascular resistance and/or myocardial depression. } A nitrous oxide–opioid technique can be used for maintenance of anesthesia, although it is likely that a volatile agent will be needed at times to control hypertension, especially during periods of abrupt change in surgical stimulation. } Antihypertensive medication administered by bolus or by continuous infusion is an alternative to the use of a volatile anesthetic for blood pressure control intraoperatively. } No specific neuromuscular blocker has been shown to be best for patients with hypertension. ~ Morphine Induction and Maintenance } Maintenance: Intraoperative Hypotension } Decrease dose of anesthesia and/or increase intravascular volume. } Administration of sympathomimetic drugs (ephedrine or phenylephrine) } Intraoperative hypotension in patients being treated with ACE inhibitors or ARBs is responsive to administration of intravenous fluids, sympathomimetic drugs, and/or vasopressin. ↳ mimic the action of stimulators } Cardiac rhythm disturbances that result in loss of sequential atrioventricular contraction, such as junctional rhythm and atrial fibrillation, can also create hypotension and must be treated promptly -> mas volumen ?? listen audio Induction and Maintenance } Monitoring } } } } Influenced by the complexity of the surgery. ECG: signs of ischemia Pulse oxymetry Invasive monitoring } } } } intraarterial catheter central venous pulmonary artery catheter Transesophageal echocardiography Management in Essential Hypertension } Post Operative Management } control pain Anticipate periods of systemic hypertension } } } } - Requires prompt assessment and treatment to decrease the risk of myocardial ischemia, cardiac dysrhythmias, congestive heart failure, stroke, and excessive bleeding. Hypertension that persists despite adequate treatment of postoperative pain may necessitate administration of an intravenous antihypertensive medication. Promote reestablish patient’s usual regimen of oral antihypertensive medication. Maintain monitoring of end-organ function Pulmonary Arterial Hypertension (PAH) } Definition } } A mean pulmonary artery pressure of more than 25 mm Hg at rest with a pulmonary capillary wedge pressure, left atrial pressure, or left ventricular end-diastolic pressure of 15 mm Hg or less, and A pulmonary vascular resistance (PVR) of more than 3 Wood units. PVR = (PAP-PAOP) x 80 CO dynes/sec/cm-5 50-150 normal PVR = mmHg/L/min <1 normal PAP-PAOP CO Sodium NS = 152 eg/L 308 osmolarity -> ↳ Na2 RL = 130 - meq/ 4Kt Plasma osmolarily ↳ = -> 2400mmolarity + Lactate 215-255 2xNa+ contraindication + RL= men N lactic acidemia Pulmonary Arterial Hypertension (PAH) } Nomenclature based on etiologies (see table 5-10) } PAH } Idiopathic most common PAH COPD } PAH due to Left heart Disease } PAH due to Lung Disiease and/or Hypoxia } Chronic Thromboembolic Pulmonary hypertension Sickle cell } anena Pulmonary Hypertension with unclear multifactorial mechanisms Pulmonary Arterial Hypertension (PAH) } Presentation } Non specific signs } } } } } } } Right sided heart failure Fatigue Breathlessness Weakness Abdominal distention ascites Left recurrent laryngeal nerve paralysis (Ortner’s Syndrome- rare) - Extensive work up to exclude reversible causes } O Idiopathic PAH has median period of survival after diagnosis of 2.8 years. ⑧ Pulmonary Arterial Hypertension (PAH) } High Perioperative risk for: } RV failure } hypoxemia and coronary ischemia } 28% for respiratory failure } 12% for cardiac dysrhythmias } 11% for congestive heart failure } 7% for overall perioperative mortality for noncardiac surgery Pulmonary Arterial Hypertension (PAH) } Pathophysiology } } } } pulmonary vasoconstriction vascular wall remodeling thrombosis in situ. Vasoconstrictor–vasodilator response imbalance and proliferation– apoptosis imbalance ↳ } no se RV Failure } } } } - revierte + no look esta up echo para aquanter presion muche RV wall stress increases RV stroke volume reduced => LV volume reduced RV Dilatation results in annular dilation of right-sided heart valves, producing tricuspid regurgitation and/or pulmonic insufficiency RV myocardial perfusion can be dramatically limited as RV wall stress increases and RV systolic pressure approaches systemic systolic blood pressure => increase of ischemia Pulmonary Arterial Hypertension (PAH) } Hypoxemia } As right-sided pressures increase, right-to-left shunting can occur through a patent foramen oval; } The presence of a relatively fixed cardiac output, the increased oxygen extraction associated with exertion produces hypoxemia; } Ventilation/perfusion mismatch can result in perfusion of poorly ventilated alveoli. } hypoxic pulmonary vasoconstriction occurs, overall pulmonary hypertension will be worsened aprender X no Pulmonary Arterial Hypertension (PAH) - Med Para HTN pulmonar no dk se med - pa tiene rebound Pulmonary Arterial Hypertension (PAH) } Anesthesia Management } Medications should be continued throughout the perioperative period. } Continuous infusions of pulmonary vasodilators should be maintained. } Diuretics may be needed to control edema. } Caution with inhalational anesthetics or sedatives: can produce reduction of systemic vascular resistance and CO. Factors to and in PAH Pt on induction } Hypoxia, hypercarbia, and acidosis must be avoided. } Maintenance of sinus rhythm is crucial. } atrial ‘kick’ Pulmonary Arterial Hypertension (PAH) } Preoperative Preparation Induction } } } } } } Reduce PAD Consider sildenafil or l-arginine "enlarge/vasodilate Continue long-term pulmonary vasodilator therapy Inhalation of NO or prostacyclin should be available. Avoid respiratory acidosis due to sedation. Hyperventilation Ketamine and etomidate should be avoided. systemic Epidural anesthesia can be used - blood vessels allowing blood to - Short term vasodilator gotothelungs ↳ AVOID ↳ } Increase resistance close attention to intravascular volume and systemic vascular resistance in these situations. Pulmonary Arterial Hypertension (PAH) } Monitoring } } } CVP recommended Pulse oxymetry Maintenance } } } } } Inhalational anesthetics, neuromuscular blockers, and opioids, Avoid histamine release medications -> cause hypotens Hypotension can be corrected with norepinephrine, phenylephrine, or fluids. A potent pulmonary vasodilator such as milrinone, nitroglycerin, NO, or prostacyclin should be available. Avoid decrease in preload (hypovolemia) ? . Pulmonary Arterial Hypertension (PAH) } Post operative period } } } } High risk of sudden death in the early postoperative period because of worsening PAH, pulmonary thromboembolism, dysrhythmias, and fluid shifts. Monitor closely for hypotension and hypoxemia. Optimal pain control is an essential component of the postoperative care of these patients. Obstetric Considerations } } Forceps delivery decrease patient effort. Nitroglycerin should be immediately available at the time of uterine involution, because the return of uterine blood to the central circulation may be poorly tolerated in a parturient with PAH. (increase venous capacitance) Summary } Hypertension is a significant risk factor for cardiovascular disease, stroke, and renal disease. abruptly Do } Goal: <140/90 mm Hg. · · not stop ACE Inh ARBS 24 Blocker B DIC his 24-48 his before . } Preoperative evaluation of a patient with essential hypertension should focus on the adequacy of blood pressure control, the antihypertensive drug regimen, and the presence of target organ damage. } Despite the prevailing desire to render patients normotensive before elective surgery, there is no evidence that the incidence of postoperative complications is increased when hypertensive patients (diastolic blood pressure as high as 110 mm Hg) undergo elective surgery. Summary } Hypertension associated with end-organ damage does increase surgical risk. } Hypotension requiring vasoconstrictor treatment occurs more often after induction of anesthesia in patients receiving treatment with ACE inhibitors and ARBs than in those in whom such treatment has been discontinued on the day before surgery. } Direct laryngoscopy and endotracheal intubation may result in a significant increase in blood pressure in patients with essential hypertension. Due to supraglotic } PAH is hemodynamically defined as a mean pulmonary artery pressure of more than 25 mm Hg at rest. 1- arginine suldenafil Avoid Ketamine - Elomidate Summary examen } Smooth muscle hyperplasia, intimal fibrosis, medial hypertrophy, obliteration of small blood vessels, and neoplastic forms of endothelial cell growth called plexiform lesions are all part of the pathophysiology of pulmonary hypertension. } NO diffuses into vascular smooth muscle, where it activates guanylate cyclase, increasing intracellular cGMP; this reduces the intracellular calcium concentration, which results in smooth muscle relaxation. Summary } Calcium channel blockers, prostacyclins, NO, endothelin receptor blockers, and phosphodiesterase inhibitors are all pulmonary vasodilators that are useful in the treatment of patients with PAH. } All long-term pulmonary vasodilator therapy must be continued throughout the perioperative period. } In the perioperative period, the risk of right-sided heart failure or sudden death is significantly increased in patients with PAH. TO Be continued next Friday …… } Ischemic Heart Disease } Valvular Heart Disease } Congenital Heart Disease calcium channel contraind . blockers Heart Failure alter In y - contrary because contractility Milumove