PHSL232 Exam PDF

 Heart pumps out 4-6L of blood Cardiovascular Sys...

 Heart pumps out 4-6L of blood Cardiovascular System I right aouta pulmonary Function Blood vessels artery left opening & closing Cardiac muscle Factors effecting arterial primonary adequate supply of nutrients arteries superior S L artery of valves is passive striated blood pressure how(a) rena I removal of unwanted metabolic arterioles vena cara ↳ mana (no use of sarcomeres pressure byproducts (CO2 & H+) capillaries [ left atrium muscles), T-tubules increase SA so things in ECF can get Physiological MAP = CO x TPR E transport of substances, as diffusion is too veins Right-s F ( left AV value , pressure- much closer to things inside cell mmity min minitgi2/min slow (hormones & drugs) & heat venules atrium 7 M -bicuspid hortic semiliar value dependent process SR CO = HR x SV quick delivery to capillaries Right Av value Ctricuspid) j left ventricle mitochondria TPR Ohm’s Law T optimal exchange inferior - - papillary musche contractile machinery P=QxR vena cara quick return to lungs M L interventricular septum every cell has to contract at same time for good Physical S Mam L Chordae tendinge ejection of blood arterial blood volume, Cardiac output connected by intercalated discs for structural amount Right ventricle volume of blood ejected by ventricle pericardium support, flow in one direction arterial compliance, Total peripheral resistance pulmonary heatsithisteaentrical ↳ electrical coupling in 1 min semilunar value notivity getting in or out stretchiness how hard it is for blood to ventricles have same output, Mean arterial pressure out , be pushed around body bulging Syste a Diastole pressure is different absorbing recoiling thea determined by vessels in Ventricles: biggest shift, 5-250mmHg, pulsatile (high to low Elastic reservoir , CO = SV x HR>beak moving pressure) - per minute series & parallel intermittent injection of blood into volume of Arteries: 60-250mmHg, pulsatile blood ejected by viscosity aorta from left ventricle r u ventricle Arterioles: less pressure , low pulsatility, resistance R=8-length large arteries distensible, stretch out Contracting refilinis vessels, reducing pressure a lot due to lots of resistance to during systole, recoil during diastole to y relaxed, Triradius blood flow lower pulsatility Cardiac cycle phases Capillaries: low pressure, no pulsatility keeps capillaries flow constant during mechanical events = pressure & flow filling > no raves shut cardiac cycle 1. Ventricular diastole 1, isovolumetric Y end systolic - , volum changes phase (ESV) 60 m/ , electrical events = ECG 2. Ventricular diastole 2, rapid filling -Araveopenpassina Conduction of action potential in heart valvular events = heart sounds - end-diastolic 3. Atrial systole > heart full volume , pressure Cardiomyocytes SA node generates spontaneous AP’s (EDU) 130m1 Av values Shut first heart sound (31) diastole = ventricles relaxed, filling w/ 4. Ventricular systole 1, isovolumetric> , - , interwoven conducted fast through atrium, slowly through ventricle blood phase branch at each ended delay allows full depolarisation & contraction of atria & ventive needs nortic pre, a , systole = ventricles contracting, ejecting 5. Ventricular systole 2, ejection phase>blood ejected into north - cell-to-cell conduction, gap junctions before this for the ventricles, otherwise chambers would blood & atrial refill electrical coupling contract at same time 6. Ventricular repolarisationletrenticfallhow notiora continues toa nartic pressur functional syncytium (same thing at AP propagates through bundle of His, bundle branches & same time) purkenje fibres isi when LVP smaller Ap aortic all-or-nothing contraction of heart ventricular myocardium spreads, allowing synchronise Conduction system man Cardiac cycle & HR , value closes boun & 130ml 7 S & ↑ depolarisation & contraction of all ventricular regions - I when decriming relaxing SV = EDV - ESV 70mi Ejection fraction = = At rest Sinatrial bundle Pacemaker cells in sinoatrial node Ventricular cells in cardiomyocytes Cardiac cycle 1 sec of His efficiency of heart’s ability node leaders followers atricaction to eject blood independent Diastole = 0.66s &S bundle unstable RMP of -60mV due to funny active Na+ Systole = 0.34s brauchel stable RMP of -90mV, no funny Na+ channels or TTCC - -- of how big it is = 70/130 = ( channels, have slow Na+ influx 5 phases: 0, 1, 2, 3, 4 Y M C toDe 53% ejection of blood per C 3 phases: 4, 0, 3 0 = upstroke, Ca2+ influx through LTCC contraction Max HR final 10 % , completely beat YSV/EDU 4 = pacemaker, pre-potential 1 = early slow repolarisation, Na+ channels close filled Cardiac cycle 0.33s Purkenje - fores 0 = upstroke, Ca2+ influx through T-type Ca2+ 2 = cardiac plateau, sustained depolarisation, LTCC Ca2+ influx Diastole = 0.13s Interventricular channels counterbalances K+ efflux combination of Systole = 0.20s node Y 3 = repolarsiation, slow K+ efflux 3 = late fast repolarisation, LTCC close, K+ efflux 51Sh lub , My 2 dif. electrodes Purkened 4 = stable RMP, K+ fluxes atrial , -entricular repolarisation bipolar fast K+ efflux, fast repoalrsiation ( depolarisation T Einthoven triangle pos my RA lead LA RA lead LA Augmented limb leads Cross-bridge cycling S 2) lead I = left armi& right arm T At pattern & amount of troponin complex: TnI, TnT, TnC pos- 2 neg 1. ATP bound to myosin is cleaved into ADP + Pi, myosin lead II = left leg & right arm rndl Time deflection depends on ventricular depolarisation lead lead all TnI = inhibitory domain now has high affinity to actin lead III = left leg & left arm direction TnT = tropomyosin binding domain 2. Ca2+ increases, binds to TnC, tropomyosin moves so pos Tneg LL V1-V6 chest leads register of TnC = Ca2+ binds, tropomyosin actin & myosin can bind arn 1 ECG I L the QRS complex us moves for actin-myosin interaction 3. ADP + Pi energy released, myosin head shifts, power recording of potential changes as 11 are re Lead II skin surface that result from positive deflection (bigger) = depolarisation towards positive Ill av is v6 stroke depolarisation & repolarisation of contractions more forceful due to 4. sliding of myosin head along actin to shorten or repolarisation away from positive increase in number of cross-bridges cardiomyocytes negative deflection (smaller) = depolarisation away from sarcomere in cardiomyocytse, not the number 5. ATP binds to myosin head again, lowering its affinity positive of contracting cardiomyocytes P wave = positive deflection for actin, detaches themselves 6. Ca2+ reduced Q wave = small negative deflection can’t recruit more, all-or-nothing Relaxation R wave = large positive deflection SERCA = ATP-dependent, forcing Ca2+ up T wave = positive deflection Cardiac metabolism Rigor mortis its gradient, pumps 75% back into SR, S wave = small negative deflection need to feed mitochondria ATP consumers run out of ATP, regulated by phoshpolamban protein with ATP Ca2+ uptake by SERCA stops relaxation (PLB) which stimulates Ca2+ uptake, Ca2+ handling ATP converted into detachment of actin-myosin permanent tetanus doesn’t normally occur allowing SERCA to work faster heart needs to relax, need delays between mechanical energy Ca2+ exciting by Ca2+ ATPase contraction in heart muscle, summation of Na+-Ca2+ exchange pump = driven by 24% electrical & mechanical activity overlap in time aerobic metabolism = Na+-K+ pump contractions not possible Na+ gradient inside, using energy from stable Ca2+ plateau (20mV) makes cardiomyocyts oxidation produces fatty acids primary active transport longer time before each action this to push Ca2+ out of cell inexcitable potential, more filling of heart & glucose for energy, needs O2 Ca2+ ATPase = ATP-dependent, pushes out Long absolute (250ms) & relative refractory to maximise contraction low PO2 in cardiomyocytes, 1% periods (300ms) prevents circuitous recycling of but can extract 75% of O2 action potential most of the contraction period from coronary circulation Physiological factors of cardiovascular system Heart rate Stroke volume Pressure-volume relationship loop intrinsic control on contraction & preload SV, CO, EF, contractility Intrinsic stroke volume after load shows changes between left input coming from within force-frequency relationship = contractility ventricular pressure & volume during HR amount of force muscle can cardiac cycle blood out of SV produce as depending on frequency Preload ventricle into aorta in of activation blood input ESP decrease blood volum DBP Extrinsic Treppe/Bowditch effect = pressure increases with increased venous return - pressure in venwich Y ~ exceed disa input coming from outside increases with force-frequency increases to produce increased SV hormonal myocardial contraction increases increased EDV, ventricles filled with XPressuretemp , volume consistent I nervous with frequency, increasing in Ca2+ more blood per unit of time EF increases consiste namic reup both intrinsic & extrinsic operate continuously heart failure = negative force- ESV unchanged & d pressure to adjust heart & vessels to maintain MAP frequency relationship, HR goes up ventricle stretched due to more blood, decreases, volume while SV goes down, CO stays same increased sarcomere length, increase ventricular pressure Length-dependent activation contraction, meaning larger SV bigger loop, more stroke work heart force increases length due to increase in Ca2+ more in, more out does Afterload sensitivity of myofilaments, better overlap, curve shifts to right amount of pressure that the heart Contractility more cross-bridges needs to exert to eject blood during Wall stress quality of pump, cardiac ventricular contraction instantaneous pressure performance at given preload & Titin = largest protein in body, spans entire aortic valve is closed, ventricles not tension/stress developed in overload = increased wall sarcomere, pulls actin & myosin closer ventricular wall during ejection afterload contracting, no shortening tensions ionotropy = increased contractility together by reducing lattice (interfilament) produces pressure to open valves tension developed in LV muscle to chronic pressure overload = spacing, therefore more strength of force open aorta valve iontropic effects = hormones & aortic pressure normal wall tension by resistancewas improves cooperativity of actin-troponin- nerves as it increases, SV decreases ne remodelling ESV decreases tropomyosin complex wall stress, resistance to blood output Law of LaPlace: a Y SV increases curve shifted up wastress pressure EF increases Extrinsic, parasympathetic Extrinsic, hormonal & drug control of EDV unchanged Extrinsic, sympathetic control of heart heart controlled by AP frequency from Chromotropic = factors effecting control of heart heart Digitalis Beta-blockers SA node rhymtic excitation & HR innervation of SA & AV Short-term regulators same as adrenaline & blocks b-adrenergic receptor rate of SA, AV nodes & tissue controlled Dromotropic = factors effecting nodes via vagus nerve - change Ca2+ signalling noradrenaline reduced activity of cAMP & PKA by sympathetic activity via conduction speed ACh binds to muscarinic catecholamines (noradrenaline, Na+-K+ pump inhibited, no reduced activity of PLB, no sympathetic cardiac nerve Inotropic = factors effecting receptors adrenaline, dopamine) Na+ gradient so can’t push phosphorylation of troponin I noradrenaline binds to b- contractility cAMP & PKA activity glycosides (diapoxins, digitalis) Ca2+ out RYR Ca2+ release reduced adrenoreceptors, opening Ca2+ & Na+ Lusitropic = factors effecting decreased, reduced accumulation of Na+ reduced Ca2+ influx through channels channels contraction & relaxation activation of Ca2+ & funny Long-term regulators inhibits Ca2+ efflux reduced need for ATP as less stress on cAMP activated, activating PKA Na+ current angiotensin II through NCX, positive heart, less metabolic demands Ca2+ handling protein phosphorylated, increased contractility means K+ channels open, K+ endothelin inotrope more Ca2+ influx, increases steep slope higher SV for same EDV efflux of pre-potential curve shifts higher reduced slope of pre- thyroid hormone PKA also phosphorylates troponin I, & potential, flatter as less PLB, increasing Ca2+ reuptake Starling’s Law = higher SV when Ca2+ & Na+ more release of RYR increased EDV more negative potential, starting point is less negative, meaning further distance to reach shorter distance to reach threshold Noradrenaline threshold, takes longer spontaneous rate of SA node increased HR time for AP to fire depolarisation is increased, so HR increased contractility spontaneous rate of SA increases (tachycardia) increased relaxation node depolarisation parasympathetic control via vagus decreased duration of diastole & decreases nerve on SA & AV nodes systole HR decreases increased conduction velocity (bradycardia) better synchronisation of atrial & ventricular contractions  Cardiovascular System II Organisation of system & distribution of blood Systemic Pulmonary CSA inversely proportional to Vessel structure & function Changes along systemic vascular pathway volume left atrium, left right artium, right Relationship between flow, Poiseuille relationship velocity (how fast blood is small systemic more branching than pulmonary Q-I systemic ventricle, aorta, ventricle, pulmonary pressure & resistance flow directly proportional to change, moving), blood flowing to more resistance increased from aorta to pulmonary in series, one after the other arteries, arterioles, capillaries artery, arterioles, flow determined by pressure gradient (higher means more pressure gradient & radius Find flow inversely proportional to o arterioles places in more directions capillaries, venules, capillaries have highest CSA, lots of them capillaries have low velocity provide O2 & nutrients to tissues, remove CO2 (parallel), venules, pulmonary vein, left flow) & resistance (lower length, viscosity & resistance allowing time for diffusion & non- veins are the highest capacitance vessels, & waste from tissues veins, vena cava, atrium, left ventricle - means more flow) increased length & viscosity holding the most blood, very compliant pulsatile flow for continuous blood requires driving force (heart) & conduit right atrium, right 100% of CO through pressure gradient = P1 - P2 means increased resistance movement system (vascular bed) ventricle CO distributed, dif. here site Yoning endothelium enables , difersion distance small for 22a nutricht exchange highomigfom increased radius means decreased resistance velocity (how fast blood is moving) decreases from aorta to arterioles Velocity -A parts of body blood pressure & pulsatile flow decreases T P (PP2) Tr/OMIn from aorta to arteriole = receive dif. in venous network, CSA decreases amounts of blood Arteries with aging, vascular radius Determinants of arterial BP stiffness occurs Arterioles Regulation of resistance from capillaries to veins thick wall, endothelium, smooth muscle, MAP = Q x TPR Changes along pulmonary vascular pathway collagen increases small diameter, thin wall, endothelium, less important for BP & flow Regular BP = 120/80 HrxSu- T velocity increases elastic tissue for recoil XoE PP normal MAP = 90mmHg less vasculature than systemic SMCs increase, elastic & fibrous tissue, lots of smooth muscle distribution pressure decreases to venae cavae, aorta has less smooth muscle, large Selli a MAP DP 1/3 PP if it decreases, either BP =Cydia x low pressure circuit hypertrophy main determinant of resistance SP/DP = + lowest in right atrium diameter vasoconstriction to increase increased CSA from pulmonary artery to capillaries, decrease less compliance & important in controlling regional blood flow, A PP = SP - DP = SOY XO aorta is pressure reservoir, its elastic TPR or increase HR which from capillaries to veins back to left heart tissue enables reduction in fluctuations in dysregulated blood flow changing blood flow around the body by changing B hypotension = less than MAp-8 leads to increased flow, both velocity decreases from pulmonary artery to capillaries, diameter 90/60mmHg ah pressure & flow from systole & diastole, - volume Blood flow distribution Compliance has dif increasing MAP increases from capillaries to veins back to left heart SMCs wrap around vessels for contraction & hypertension = more maintaining flow through cardiac cycle pressure sum pressure changed match demands in certain relxation, pushing blood to tissue , situations pulsatile flow decreases from pulmonary artery back to left during systole, blood stretches it out Stiffness= compliance than 140/90mmHg heart, blood flow is marinated to enable gas exchange contraction squeezes lumen to reduce diameter done by changes in local resistance during diastole, it recoils, releasing stored (vasoconstriction) in exercise, vasodilation to increase energy to keeping driving excess blood through the body Active hyperemia Flow autoregulation/ blood flow to muscles as higher Different types of regulation of diameter (resistance) in metabolic autoregulation reactive hyperemia metabolic demand & vasoconstriction to arterioles causes vasodilation myogenic reduce blood flow to stomach due to less act on smooth muscle, altering the arteriolar radius Hormonal blood flow changes to match autoregulation (in metabolic demand extrinsic control adrenal medulla releases adrenaline in blood, atrial natriuetic peptide local metabolism of tissue SMCs) region-dependent flow Neural region-dependent increasing plasma adrenaline & binds to a1- decreases H2O reabsorption, that blood vessel is working causes vasodilation extrinsic control adrenaline, angiotensin II & vasopressin cause adrenergic receptors, causing decreasing blood volume non-adrenergic control is in & vasoconstriction SNS releases noradrenaline which binds to a1- vasoconstriction vasoconstriction it decreases CO, therefore Q Local II specialised innervation, increase in metabolic control of blood flow adrenergic receptors, causing vasoconstriction, adrenaline & atrial natriuretic peptide causes skin has more a1 receptors region-specific to GI & penis activity of organ means to maintain changes decrease in arterial pressure in therefore increased resistance vasodilation skeletal muscles has more b2 post-ganglionic nerves decreased O2 & increase in perfusion organ causes decreased blood flow, innervation density varies depending on vascular adrenaline causes both as blood vessels can Local release NO on to SMCs metabolites in its pressure meaning decreased O2, increased bed/which region e.g brain has low numbers of a1- express dif. types of adrenergic receptors antidiuretic hormone (vasopressin) increases intrin