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SCIENTIFIC FOUNDATION IN ANESTHESIA HEART- SPRING 2012-LADONNA CATES Right side of heart pumps deoxygenated blood through pulmonary circulation Left side of heart pups oxygenated blood through peripheral circulation Can have mixing of blood due to patent FO- to 30% of adults Located behind sternum and 3,4,5th ribs Apex= point of maximal impulse, first heart sound heard here, s3 s4 heard if present 2 ATRIA--- weak primer pump for ventricles RIGHT: receives blood from SVC, IVC via the eustacian valve, and coronary sinus via thebesian valve between the tricuspid valve and eustacian valve ( venous blood) 80% of blood goes directly from atria into ventricle before atria contracts 20% with atrial contraction ( atrial kick) LEFT: reservoir for oxygenated blood from pulmonary vein pump for LV during ventricular diastole adds 20-30% to LVEDV loss of atrial kick tolerated by normal heart/CO in disease heart/mitral regurg 2 VENTRICLESsupply main pumping force RIGHT: receives blood from RA thru tricuspid valve ejects blood into pulmonary artery thru pulmonic valve superior portion as approaches pulmonary valve is cone shaped ( AKA=conus ateriosus or infundibulum) papillary muscles attached to ventricular wall and extend to cordae tendineae cordae tendineae attached to cusps of tricuspid valve and help prevent eversion f valve into RA during ventricular systole. Rupture of papillary muscles causes regurgitation ( 3 papillary muscles on RT) LEFT: receives blood from LA Ejects blood into aorta Wall 2-3 times thicker than RV- > muscle mass to overcome SVR, and maintain CO 2 papillary muscles= anterior & posterior: attached via chordae tendineae to cusps to mitral valve and prevent eversion into LA during systole acute regurgitation occurs when ischemia or infarction causes disruption of these muscles/can result in lung congestion. PERICARDIM: innervated by phrenic and vagus nerves. Parietal /outmost: has two layers, a tough fibrous outer layer which is attached to central tendon of diaphragm and extends to aorta, pulmonary trunk and SVC and a serous, smooth inner layer. Visceral pericardium: adjacent to heart and in contact with epicardium. Parietal and visceral separated by potential space Space contains 10-25 ml serous fluid Fluid provides lubrication for free movement Causes tamponade if fills with fluid or blood. TAMPONADE: causes ineffective LV filling Chronic= heart may accommondate Acute = not well tolerated ( post open heart/ trauma/CA IV

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S/S= B/P, JVD, distant heart sounds, pulsus paradoxus( with inspiration HR, with expiration HR ) TX= pericardiocentesis via needle or pericardial window.

VALVES: ensures one way flow, open/close in response to pressure gradients above/below valves. A/V = tricuspid/right mitral/left Semilunar= pulmonary/right aortic/left TRICUSPID: right A/V orifice: has 3 leaflets ( anterior,posteior,septal) Thin, easily separated into well-defined leaflets Normal area of orifice opening is 7 CM2 S/S of insufficiency when areal < 1.5 CM2 MITRAL: left AV orifice: has 2 leaflets( anteromedial, posterolateral) Connected by commissural tissue Normal area 4-6 CM2 S/S when decreased by 2-3 CM2 SEMILUNAR: each has 3 cusps, aortic slightly thicker than pulmonic SINUS OF VALSALVA: Dilation above aortic valve Allows valve to open without occluding ostia OSTIA= openings that communicate with coronary arteries CARDIAC MUSCLE: has three layers EPICARDIUM: outer layer composed of mesothelium ( cells on the outside) MYOCARDIUM: muscular inner layer ENDOCARDIUM: inner layer composed of endothelium and connective tissue Three types of muscle: Atrial and ventricular fibers contract similarly to skeletal muscle except contraction is longer which is due to calcium Excitatory/conductive fibers weak contractility-few contractile fibers cause automatic discharge of action potential or causes conduction of action potential thru heart provide excitatory system that controls rhythmical beating of heart CORONARY CIRCULATION: arterial system of heart consists of epicardial vessals( bypassed when blockage) and subendocardial vessels ( ischemia causes trouble in the OR ) epicardial vessels superficial and obstruct most commonly at bifurcations obstruction > 50% can cause ischemia or infarction vessels arranged so that flow to subendocardium is almost 0 during systole and increases during diastole heart perfused during diastole, so if bad heart you want to avoid tachycardia because heart has no perfusion during systole. avoid tachycardia, ST elevation if Transmural MI/ ST depression if subendocardium MI MORE LIKELY TO SEE ST DEPRESSION IN THE OR ( Subendocardium MI) < Ostia of RT/LT main coronary arteries are at the sinus of valsalva LCA= supplies anterior and left lateral LV RCA= supplies most of RV and posterior LV in 80-90 % of people ( RT sided dominant) Normal distribution of coronary arteries: * 50% = more blood flows thru RCA than LCA

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* 30% = flow approximately same in both * 20 % = flow in LCA predominant LCA ( LT. MAIN) = arises from sinus of Valsalva at aortic root/Bifurcates at 4-40 mm into the LAD and Circumflex LAD = runs down interventricular groove around to apex of LV Supplies blood to : Anterolateral LV via diagonal branches Anterior and posterior papillary muscles Intraventricular septum via septal branches Purkinje system via septal branches CIRCUMFLEX = arises from LCA at approx. 900 angle , runs along AV grove Supplies blood to : Lateral LV Gives rise to obtuse marginals ( usually 1-3 vessels) Sinus node artery in 45 % of patients Posterior descending artery in 15% of patients RCA= from sinus of Valsalva at aortic root transverses epicardium in AV grove Supplies: RA Intra-atrial septum RV SA node- 55% of people AV node artery in 90% ( other 10 % from septal branch of LAD) which supplies the AV node, bundle of his, and proximal bundle branches= MI= blocks/CHF Occlusion of RCA= infarction of SA node( atrial arrhythmias) 3rd degree AV block( due to AV node artery, rare because of collateral flow) may see AV blocks in off-pump when RCA occluded for repair. ** volume is important in RCA infarction, keep them full and deal with the CHF**** POSTERIOR DESCENDING= branches from the RCA in 85% of patients Supplies: posterior inferior LV

PAPILLARY MUSCLES:vital to competence of mitral valve Anterior papillary muscle usually supplied blood flow by branches of LCA Posterior papillary muscle receives blood from both RCA and LCA Due to collateral flow, occlusion of single coronary artery usually doesnt cause infarction . Severe ischemia may cause dysfunction and acute MR- usually reverses with NTG due to vascular bed vasodilation *** Resting coronary blood flow is approx. 4-5 % of C.O.(225mL/min or 5mL/g/min) can increase five times during strenuous exercise (4-7 times) VENOUS CIRCULATION- 3 SYSTEMS

1. Coronary sinus: collects 85% of blood from LV, drains into RA,
cannulated during bypass to deliver cardioplegia. 2. Anterior cardiac veins: drain RV, may empty into RA directly or into coronary sinus. 3. Thebesian veins: throughout myocardium and empty into all chambers ( the ones that they serve), may carry up to 40% of blood returned to RA. REGULATION OF CORONARY BLOOD FLOW:

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** direct acting drug such as isoproterenol, norepi,epi,digoxin needed in denervated heart* ** TO 1. 2. 3. OPTIMIZE CPP: in this order **** Low heart rate ( avoid tachycardia) Normal to high diastolic pressure ( avoid hypotension) Low LVEDP ( avoid hypertension)

METABOLIC FACTORS: H2 ions, CO2, O2, lactate When O2 demand> supply, adenosine released vasodilation AUTONOMIC NERVOUS SYSTEM: a&b receptors present I coronaries a1 receptors vasoconstriction B receptors vasodilation Alpha 2 receptors on endothelial cells= nitric oxide mediated decrease in vascular tone Increase in a-receptors may cause vasospasm in normal coronaries HORMONAL FACTORS: Vasopressin and angiotensin(stress hormones) potent vasoconstrictors Thromboxane may lead to thrombosis and spasm Prostagiandin 12 decreases vascular tone ENDOTHELIAL MODULATION: Releases nitric oxide and prostaglandin 12 Nitric oxide responsible for c-Gmp-mediated vasodilation of smooth muscle ANATOMIC FACTORS: Capillary myocyte ratio is almost 1:1 Only 60-80% of capillaries function under normal conditions, when O2 demand increases, unopened capillaries are recruited to make more O2 available to myocytes. COLLATERAL CHANNELS : Usually non-functional but may enlarge over time and start to function when CBF impeded OXYGEN DEMAND OF THE MYOCARDIUM: Oxygen extraction is 70-80% compared to 25% for rest of the body O2 extraction by cardiac cells nearly maximal at rest Resting myocardial O2 consumption 8-10mL/100g/min ( 10% of total body O2 consumption) Cardiac muscle needs 1.2mL/100g/min to stay alive Supply of O2 to myocardium is determined by: Arterial O2 content of blood/blood flow to coronaries.

O2 content= (Hgb) (1.34) (SaO2) + (0.003) (PaO2) To maximize O2 content= high Hgb, highly saturated blood( right shift), high PaO2 DETERMINATES OF MYOCARDIAL O2 REQUIREMENTS: 1. HEART RATE: rate = O2 consumption RPP ( rate pressure product) formula to estimate O2 consumption RPP = HR X systolic B/P Ischemia unlikely if RPP < 12,000 *** HR O2 consumption > SBP 1. CONTRACTILITY:

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Flow to subendocardial area during systole Shortening of subendocardial myocytes during contraction O2 consumption TEE used for qualitative estimation of LV contractility Quantitative measures= rate of rise in LVP WALL STRESS: Determined by pressure in ventricle during contraction, chamber size and wall thickness. Chamber pressure ( after load) o2 demandas pressure Chamber size ( preload) keep preload to keep stress Wall thickness ( see less stress overall but more tissue o2 consumption) O2 consumption associated with volume work significantly LESS than that of pressure work: 80% o2 consumption before opening of aortic valve ( pressure increasing) 20% during volume transmission

3. 4.

5. 6.
7.

ACTION POTENTIAL; Travels along motor nerve endings on muscle fiber Nerve secretes Ach Ach acts on local area of muscle fiber membrane to open Ach-gated channels via protein molecules Na+ ions flow into muscle fiber ( initiates action potential) Action potential travels along muscle fiber membrane Depolarizes muscle membrane and travels deep into muscle fibers= Ca++ release Ca++ ions create attractive forces between actin and myosin filaments causing them to slide alongside each other =contraction Ca++ membrane pump moves Ca++ back into SR removing it from myofibrils and contraction stops SKELETAL AND CARDIAC MUSCLE CONTRACTION: Both are striated Both have myofibrils containing myosin/actin filaments Both have transverst T tubules Cardiac sarcomeres contain higher concentrations of mitochondria Cardiac cells are aerobic = cant tolerate O2 deficiency Myocardial sacomeres have one capillary per fiber Cardiac fibers arranged in latticework dividing,combining,dividing= impulse not interrupted Cardiac muscles is syncytium( works together) Action potential in skeletal muscle caused by sudden opening of fast Na+ channels, fast because remain open for short period. Action potential in cardiac muscles caused by same fast Na+ channels AND slow Ca++ channels Ca++ channels open slower and stay open longer= causes prolonged depolarization and plateau in action potential ( prolonged contraction) Cardiac cells depolarize spontaneously/leak causes depolarization to reach threshold/ Na+ channels open and action potential starts. ACTION POTENTIAL PHASES: (TEST) 1. PHASE 0 Ventricular muscle fiber Threshold reached from leak of Na+ into cell

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Fast Na+ channels open between -70 and -65 mv 1. PHASE 1 Initial repolarization +2 to + 30 mv Na+ channels close and slow influx of Ca++ starts 1. PHASE 2 PLATEAU Influx of Ca++ delays repolarization Prolongs absolute refractory period leak of K+ out, continued influx of Ca++ and Na+ = membrane potential around 0mv 1. PHASE 3 Terminal repolarization phase Starts with closure of slow Ca++ channels Sustained by increased outflow of K+ Potential returned to resting value (-90mv) 1. PHASE 4 Diastolic phase Na+/K+ pump returns ionic concentration to resting value Last from repolarization to next action potential. Nerve cell action potential is about 1 ms in duration Skeletal muscel cells is about 2-5 ms Cardiac muscle cells is about 200-400 ms Action potential of pacemaker cells found in SA node occurs spontaneously/ has no true resting potential/ has no fast Na+ currents/ relies on slow inward Ca++ flow

Ablosute refractory period=time when no membrane response occurs to second stimulus( phase 0-middle of phase 3) when membrane potential becomes <-60mv Relative refractory peorid= second stimulus can result only in action potentialwith decreased ampitude,velocity, and conduction ( PAC/PVCs) middle of phase3 to beginning of phase 4 when membrane potential is -60 - -90 mv. THE CARDIAC CYCLE: from beginning of one ventricular contraction to the next. Systole and diastole Spontaneous generation of action potential from SA node starts cycle. Action potential thru both atria, A-V bundle into ventricles DIASTOLE: At end of systole, ventricular pressure falls, valves open, blood flows into ventricles Rapid filling from atria during first 1/3 of diastole Small amount of blood from atria during middle 1/3 Atria contract and supply about 25% of blood to ventricle during last 1/3 of diastole ( atrial kick) SYSTOLE: Abrupt increase in ventricular pressure with beginning of contraction A-V valves closes For fraction of second, pressure continues to increase without change in volume ( isovolumetric contraction) this allows ventricle time to build up sufficient pressure to open semilunar valves against pressures in aorta and pulmonary artery. Aortic valve opens when LV pressure exceeds 80mmHg Pulmonary valve opens when RV pressure exceeds 8mm Hg Blood ejected form ventricles= about 70% during first 1/3 of ejection

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Ventricle relaxes suddenly at end of systole causing rapid decrease in pressures Higher pressures in aorta and PA causes valves to close

a wave/ p wave = atrial contraction/end diastole/atrial kick/filling rt. vent. c wave/s wave=due to isovolumic, right ventricular contraction/closes tricuspid v wave/end of t wave=filling of atria w/blood from vena cava/ A-V valves are closed during systole SWAN CATHETER: a wave from LA contraction c wave from closure of mitral valve v wave from filling of LA End diastolic volume= volume at end of diastole= 110-120 ml Stroke volume=amount ejected from ventricles during systole=70 ml End systolic volume=amount remaining in ventricle after ejection=40-50ml Ejection fraction=fraction of end diastolic volume thats ejected= 60 % NORMAL INTRACARDIAC PRESSURES: RA = 0-8 MEAN 4 RV= systolic 15-28 MEAN 24 End diastolic 0-8 MEAN 4 4-12 MEAN 7

LA=

LV= systolic 90-140 MEAN 130 End diastolic 4-12 mean 7 HEART SOUNDS: Opening is silent/ valves and fluids vibrates from sudden pressure difference at closure S1 = closure of A-V valves, prolonged, low in pitch Mitral valve = 5th intercostal space Lt mid-clavicular line Tricuspid valve = 5th intercostal Lt sternal border S2 = closure of aortic and pulmonary valves at end of systole, papid snap, short duration

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Aortic valve= 2nd intercostal Rt sternal border Pulmonic valve= 2nd intercostal Lt sternal border S3= due to blood reverberating in ventricles, weak, rumbling sound during diastole CHF in older person, over < 40 S4= due from blood entering atria, almost never heard with stethoscope. All Physicians Take Money MURMURS: caused by valvular lesions/Rheumatic fever causes greatest number of lesions: usually caused by streptococcal toxin STENOSIS = build up of scar tissue, leaflets stick together REGURGITATION= edges of valve may be damaged so that they dont close Usually see combination of both AORTIC STENOSIS: blood jets thru small opening into aorta- nozzle effect/ loud/harsh/during systole AORTIC REGURGITATION: blood flows backward form aorta into LV/ swishing,blowing/ during diastole MITRAL REGURGITATION: blood flows backward from mitral valve/high frequency,blowing/systole MITRAL STENOSIS: difficult to hear, low pressure in LA, doesnt cause blood to reverberate back and forth between walls of ventricles/ very low frequency/ during diastole. FEEL RADIAL PULSE, IF YOU HEAR MURMUR WHEN YOU FEEL PULSE IT IS A SYSTOLIC EJECTION FRACTION: percentage of end diastolic volume ejected during systole EF = SV / EDV X 100 Normal EF = 60 -70 % per Nagelhout < 40 % = significant impairment

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