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CIRCULATION VIVASThe Heart2011-1Describe the normal sequence of electrical excitation of the cardiac conduction system and cardiac muscle? (+ 2006-2)SA -> radially through atria -> AV node -> Bundle of His -> Major bundle branches (L) and (R) -> Purkinje fibers -> ventricular muscle: septum to apex, then up to AV grooves. Spread is from endocardial to epicardial surfacesWhat are the common mechanisms which cause abnormalities of cardiac conduction? And…What are the possible clinical consequences of these conduction abnormalities?1. Abnormal pacemakers- ectopic beats- pacemaker failure (sick sinus syndrome)- fibrillation (atrial or ventricular)2. Re-entry circuits- atrial flutter- other tachyarrythmias3. Conduction defects- heart block- bundle branch blocks4. Prolonged repolarisation- long QT (increased vulnerability to ventricular arrythmias/sudden death)5. Accessory pathways- WPW (Bundle of Kent) and LGL (short PR) -> SVT2010-2Please draw a normal ECG tracingDescribe the cardiac events that relate to each of the intervalsCardiac cycle:PRPhase 1Atrial systoleAtrial systoleR to end of TPhase 2Isovolumetric vent. contractionVentricluar systolePhase 3Ventricular ejectionEnd of T to PPhase 4Isovolumetric Vent. ContractionDiastolePhase 5Ventricular fillingThe Action Potential:R wavePhase 0Rapid depolarizationNa influx (fast)S wavePhase 1Rapid repolarizationNa innactivationST segmentPhase 2PlateauCa influx (slow)T wavePhase 3Slow repolarizationK effluxT-PPhase 4RMPNilR wave Phase 0 (Na influx S wavePhase 1What is the electrophysiological basis for ST elevation in acute MI?Defect in infarcted cellsCauseCurrent FlowECG changeTimingRapid repolarizationAccelerated K+ openingOut of infarctST elevationLasts minutes onlyDecreased resting membrane potentialLoss of intracellular K+Into infarct (diastole)TQ depression( = ST elevation)Minutes -> daysDelayed depolarizationOut of infarctST elevationAfter 30mins -> days2009-2Draw an ECG trace and identify the 5 phases of the cardiac contractile cycle. Also demonstrate the ventricular volume trace.Cardiac Cycle:Atrial systoleVentricular isovolumetric contractionVentricular ejectionVentricular isovolumetric relaxationVentricular filling2008-2, 2006-1Please draw a normal ECG tracing, showing the durations of the major intervalsIntervalsPR 0.18QRS0.08QT0.4ST0.32How does the ECG change with hyperkalaemia?K+ 7.0: Tall peaked T wavesK+ 8.5: Loss of atrial activity, widened QRSExtreme: Arrhythmias (VT and VF), then unexcitable (sinusoidal)How does it change with hypokalaemia?Long PR, ST depression, T inversion, U-wave2007-2, 2005-2Describe or draw an action potential in ventricular muscleWhat are the ion fluxes that produce this action potentialHow does the ECG relate to the ventricular muscle action potientialThe Action Potential vs ECG:R wavePhase 0Rapid depolarizationNa influx (fast)S wavePhase 1Rapid repolarizationNa innactivationST segmentPhase 2PlateauCa influx (slow)T wavePhase 3Slow repolarizationK effluxT-PPhase 4RMPNilWhy does tetany not occur in cardiac muscle 2005-2Because of the inactivation of the sodium channels and the prolonged action potential, cardiac muscle cannot contract in response to a second stimulus until near the end of the initial contractionDuring phases 0 to 2 and about half of phase 3 (until the membrane potential reaches approximately –50 mV during repolarization), cardiac muscle cannot be excited again; that is, it is in its absolute refractory periodIt remains relatively refractory until phase 4Therefore, tetanus of the type seen in skeletal muscle cannot occurOf course, tetanization of cardiac muscle for any length of time would have lethal consequences, so it is a safety feature2009-2, 2008-2, 2007-1, 2006-2, 2003-1Describe the features of the action potential in cardiac pacemaker tissueRhythmically discharging cells with a membrane potential, that after each impulse declines to the firing level: the prepotential or pacemaker potential triggers the next impulse.1. Prepotential: Initially IK efflux declines. Then Ih channels open (following hyperpolarization) “funny” channels that pass both K+ and Na+. Completed by Ca2+ influx via T (transient) channels2. Action potential: due to Ca2+ influx via L (long-lasting) channels3. Repolarization: due to K+ efflux – no plateauDescribe the major differences between a cardiac myocyte AP and the pacemakerFast Na+ depolarizaton vs slower Ca2+Pacemaker has automaticity due to rising prepotentialMyocyte has a plateau phaseLower resting potentialFaster conduction rate (1m/s vs 0.05)How do autonomic factors alter the slope of the prepotential? 2007-1, 2003-1Sympathetic:speeds IhNA -> via 1 receptors -> cAMP -> opens L channels -> increased ICa -> increases slope of prepotential -> increases rateParasympathetic:Vagal cholinergic stimulation -> ACh release -> M2 receptors via B subunit of G protein -> increased intracellular K+ -> slows Ih and cAMP -> hyperepolarization/decreased slope -> slows rate2010-2, 2005-1, 2003-2, 2003-1List in order, the mechanical phases of the cardiac cyclePlease draw the pressure changes in the ventricle that occur during the cardiac cycle1. Atrial systole2. Ventricular isovolumetric contraction3. Ventricular ejection4. Ventricular isovolumetric relaxation5. Ventricular filling2009-1, 2005-1Describe the pressure and volume changes at the onset of systoleDescribe the pressure and volume changes at the onset of diastoleAt the start of systole:Mitral and tricuspid valves close (first heart sound)Ventricles start to contractAV valves bulge into atria (jugular c wave)Isovolumetric contraction lasts 0.05sUntil (L) > 80mmHg, (R) >10mmHgThen aortic and pulmonary valves openAt the start of diastoleVentricles relaxAortic and pulmonary valves close when momentum of ejected blood overcome by arterial pressure -> vibrations are second heart soundInitially no change in volume: hence isovolumetric relaxationAV valves open when pressure falls below atrial pressures Relate the aortic pressure to the phases of the cardiac cycle 2005-1When do the heart sounds occur? 2003-22007-2Draw and label a diagram of the jugular venous pressure waveExplain the origins of the fluctuations of this wavea wave: atrial systole - some of the blood regurgitate back into the great veinsc wave: ventricular isovolumetric contraction - tricuspid wave bulgingx descent: ventricular ejection - atrial volume increase as tricuspid pulled distallyv wave: isovolumetric relaxation - rise in atrial pressure prior to tricuspid valve openingy descent: ventricular filling - atrium empty when tricuspid opensHow does the ECG relate to the jugular venous pressure2011-1, 2010-2, 2008-1, 2003-2 (+ contractility)What are the parameters that define cardiac output?CO = SV x HRWhat are the factors that influence stroke volume?Preload (= EDV or cardiac fiber length)AfterloadContractilityWhat is cardiac preload?Amount of blood in ventricles at the end of diastole = end diastolic volume (Usually 130ml). Also the amount of stretch of cardiac muscles c.f. resting length.What factors affect preload?Blood volumeVenous return e.g. increased by blood volume, venous constriction, muscle pump, negative intrathoracic pressure, venous compression (uterus in pregnancy)Increased intrapericardial pressure, e.g. tamponade from pneumothorax, pericardial effusion/hemorrhage, tumour, infection, IPPVAtrial contractionDecreased ventricular compliance, e.g. MI, infiltratesHow can cardiac output be measured?Direct Fick method: amount of substance taken up/time = A-V difference x blood flow, so…Cardiac Output=Amount of substance consumed (ml/min)Aterial - Venouscommonly O2 is used: consumption measured by spirometry, and A-V difference across the lungs from arterial vs pulmonary venous sample via catheterIndicator dilution method: output of heart = amount of indicator divided by the average concentration after a single circulation. Thermodilution with cold saline is a safe technique.2011-2, 2009-1, 2008-1, 2006-2What factors influence myocardial oxygen consumption?1. Intramyocardial tension which is dependant on:a) Pressure - after load, systolic pressure, contractility b) Radius - preload (nb tension is proportional to radius as per law of Laplace)c) Wall thickness 2. Contractile state of the heart i.e. ionotropyAs per Frank-Starling curve:3. Heart rate i.e chronotropy4. Also: - cardiac work = SV x MAP of aorta for (L) and pulmonary a. for (R), note 7x more stroke work for (L) ventricle b/c aorta MAP = 80mmHg c.f. pulmonary MAP 10mmHg) - Pressure load increases O2 consumption more than volume loadHow does decreasing a patient’s heart rate improve symptoms of angina?Decreasing HR decreases O2 demands Lower HR = longer diastole, thus at a slower heart rate there is more time for coronary circulation which occurs in diastoleWhat effect does preload and afterload have 2009-1Both increase work. Cardiac work = SV x MAP Also, both increase intramyocardial tensionPreload: Law of Laplace: radius proportional to wall tension Afterload: Increase in pressure increases tensionAs per Frank-Starling law and curve, increased preload (EDV) increases SV = more workPressure load increases O2 consumption more than volume load, thus AS causes more angina than AR. Reason not well understoodBecause afterload aorta > pulmonary (aorta MAP = 80mmHg c.f. pulmonary MAP 10mmHg), note 7x more stroke work for (L) ventricle c.f. (R)What are the changes in cardiac function with exercise and how these mediated? 2006-2Rate and stroke volumeAdrenaline and sympathetic dischargeVenous returnWhat are the physical laws involved?StarlingLaplace Law: P = 2T/R2011-1, 2010-2, 2009-2, 2006-1Please draw the starling curveWhat factors influence myocardial contractility?Positively Inotropic:Sympathetic stimulation via nerves or circulating catecholaminesDrugs such as xanthines, glucagon, cardiac glycosides, adrenergic agentsPost-extrasystolic potentiationIncreased heart rate (small effect)Increased myocardial mass (chronic) Negatively Inotropic:Metabolic abnormalities: hypoxia, acidaemia, hypercarbiaReduced sympathetic toneBlockade of circulating catecholaminesPharamcologic depression (Ca blockers, antiarrhythmics)Myocardial diseaseIncreased parasympathetic toneReduced intracellular calciumHypothermiaHeart failure (intrinsic depression)Frank-Starling Law aka Starlings law of the heart:“energy of contraction is proportional to the initial length of the muscle fibres”i.e. length of fibres (preload) is proportional to the end diastolic volumeThe Frank-Starling curve demonstrates the relationship between SV and EDVHow do changes in myocardial contractility alter the relationship between end diastolic volume and stroke volume? 2011-1Frank-Starling Curve:Increasing contractility moves the curve upwards and to the left Decreasing contractility moves the curve downwards and to the rightMore contractility = more is ejected by ventricles giving lower EDV and more SV2011-2, 2010-1, 2006-1Describe the factors that control blood flow to the myocardiumAt rest heart extracts 70-80% of O2. More O2 consumption requires more blood.a) Chemical factors -> vasodilation: Local factors control radius of blood vessels (overall flow and regional flow). Low O2 is the main controlling factor. Hypoxia increases concentrations of CO2, H+, K+ lactate, prostaglandins, adenine nucleotides, and adenosine. b) Neurogenic factors -> controlling radius of blood vessels (overall flow and regional flow)Parasympathetic nerves: vagal stimulation dilates coronariesSympathetic nerves: α -> vasoconstriction, β -> vasodilatation. However giving NA -> increased HR/contractility via β -> increased O2 demand -> vasodilation. Giving β-blocker and NA -> vasocontriction via α only. So coronary flow is preserved if systemic blood pressure falls -> NA releasec) Pressure gradients - Flow is dependant gradient between arteries and veins: thus reduced in CHF where systemic venous pressure is high- During systole ventricular muscle pressure limits flow, especially to subendocardium of the left ventricle: in AS both high pressure and high O2 requirement -> high risk for myocardial ischaemiad) Viscosity of the blood2007-2Describe the factors controlling blood flow through skeletal muscle during exerciseMainly local regulationMainly via low O2 -> arterioles and precapillary sphincters open because smooth muscle cannot maintain contraction in hypoxic conditionsLocal metabolites: low PO2, high PCO2, increased K+, adenosine, lactic acidTemperature rise -> vasodilationWhat other circulatory changes occur in the body during exercise and whyIncreased cardiac output via sympathetic stimulation (increased rate and contractility)Sympathetic vasocontrictor nerves/adrenaline -> contraction of peripheral aterioles not in skeletal muscle (coronary and cerebral systems spared) Depends if exercise is isometric (length doesn’t change) vs isotonic (force doesn’t change)Isometric:Psychic stimuli act on medulla oblongata -> decreased vagal tone (and cardiac sympathetic stimulation) -> increased heart rateStoke volume unchangedBlood flow to muscle limited by steady muscle contraction -> compression of vesselsSystolic and diastolic blood pressure rises (in seconds)Isotonic:Similar prompt increase in heart rateAlso increase in stroke volume Vasodilation in exercising musclesThus diastolic BP the same or lower, and systolic only rises a small amountIncrease venous return due to muscle pump and thoracic pumpAlso increased return because venoconstriction of capacitance vesselsThe Circulation2011-2, 2009-1, 2008-1, 2006-2, 2005-2What factors determine cerebral blood flow?Intracranial pressureLocal constriction and dilation of cerebral arteriolesMean arterial pressure at brain levelViscosity of bloodMean venous pressure at brain levelMonro-Kellie doctrineCushing reflexLocal autoregulationWhat is the Monro-Kellie Doctrine?Volume of blood (75ml), CSF (75ml) and brain (1400g) in the cranium at any time remains relatively constant (within a rigid structure).What substances are important for brain metabolism 2008-1Oxygen ~49ml/min = 20% body O2 consumptionGlucose (major energy source) ~77mg/minGlutamate (converted to glutamine as detox mech NH3 i.e. ammonia) ~5.6mg/minWhat is Cushing’s Reflex? 2006-2Physiologic nervous response to raised ICP resulting in triad of widening pulse pressure, irregular breathing and reduction of the heart rate.Increased ICP > 33mmHg -> ↓ CBF -> ischaemia of RVML - ↑ systemic BP and heart rate (first stage) –> stimulation of baroreceptors –> stimulation of vagal outflow –> bradycardia (second stage)2010-1, 2009-1, 2003-2Describe how tissues regulate their own blood flow2 theories to autoregulationMyogenic: Intrinsic contractile response of smooth muscle to stretch, so as blood pressure rises the vessels walls are stretched and the vascular smooth muscle contracts. A greater degree of contraction is seen at higher pressures. Respond to tension, so as per Law of Laplace the tension is proportional to the radius (x distending pressure). To maintain a given wall tension at higher pressure requires a reduction in the radius.Metabolic: Products of metabolism are potent vasodilators and thus with reduced blood flow and increased metabolism more accumulate. With increased blood flow more are washed away.Vasodilators include: hypoxia, hypercapnea, acidosis, lactate, K+, temperature, histamine, adenosineDescribe how blood flow can vary in different parts of the brain 2005-2PET and fMRI show that there is marked variation in local blood flow with brain activityActive neurons attract blood flowNeurovascular coupling may adjust local perfusion in response to changes to brain activityCertain diseases show reduction in flow to affected areas (Alzheimers, Huntington, Manic depressives, schizophrenia)2004-2, 2003-2Describe how blood flow is regulated at the level of the endotheliumVasodilators:ProstacyclinEndothelium derived from arachidonic acid via cyclooxegenase Inhibits platelet aggregation and vasodilatesNitric oxide (EDRF)synthesized from arginine by NOSactivated by agents that increase intracellular Ca2+ like bradykinin and acetylcholineactivates guanylyl cyclase producing cGMP -> smooth muscle relaxationinactivated by haemoglobinCarbon monoxide and H2S (hydrogen sulpide)KininsVasoconstrictors:Thromboxane A2Platelet derived from arachidonic acid via cyclooxegenasePromotes platelet aggregation and vasoconstricsEndothelin-1potent vasoconstricorresembles venom of Israeli burrowing aspSerotoninWhat other general effects do endothelins have on the cardiovascular systemPositive inotrope and chronotropeRise in ANP/renin/aldosteroneDecreased GFR and renal blood flow2010-1Draw a diagram of the changes in systolic and diastolic pressure as blood flows through the systemic circulationHow does the total cross sectional area of the vessels change through the systemic circulation2007-1, 2003-2What is the normal value for venous return in the healthy human adult? 5 - 5.5 L/minWhat are the major factors that influence venous return to the heart?Right atrial pressure aka CVPCirculating blood volumeSympathetic and parasympathetic tone (venous capacitance)Muscle pumpThoracic pump (expiration creates higher negative pressure in thorax (from -2.5 to -6mmHg) and also diaphragm creates some increased pressure in abdomen)Effect of the heart pump (ventricular systole pulls tricuspid valve distally)GravityWhat is the relationship between right atrial pressure and venous return?venous return is determined by a pressure gradient (venous pressure – RAP) and venous resistancecirculation is a closed system so cardiac output matches venous return (when averaged over time)achieves balance through Frank-Starling mechanism: if venous return is increased on lying down, preload and SV increase leading to an increase in cardiac outputRAP = 4.6mmHg average, with range 2mmHg in inspiration to 6mmHg in expiration (Ganong)2008-2, 2006-2, 2004-2Where are Baroreceptors found in the body?Stretch receptors in adventitia of vessel walls, major ones found in carotid sinus (ICA, rise or fall) and aortic arch (apex, rise) to monitor arterial side of circulation.Also low-pressure "cardiopulmonary receptors" in right and left atria, and pulmonary circulation to monitor venous circulationWhat is the effect of vessel wall distension on a baroreceptor?Stretch of vessel wall leads to increased baroreceptor dischargeMore sensitive to pulsatile pressure than constant pressureTransmitted by afferents in glossopharyngeal (carotid sinus nerve) and vagus (aortic depressor nerve) nerves to medulla/vasomotor area NTS -> glutamate to CVLM -> GABA to RVLM: inhibits sympathetic vasoconstrictionNTS -> dorsal motor nucleus and nucleus ambiguous: parasympathetic/vagus stimulationNet effect is:Inhibition of tonic discharge of sympathetic vasoconstrictor nervesExcitation of cardiac vagal innervation -> Results in vasodilation, with decrease in BP, HR and CO.What is the effect of chronic hypertension on the activity of the arterial baroreceptors 2006-2They ‘reset’ to maintain normal basal activity at the elevated blood pressure (reversible, unknown mechanism)What is the Set Point? 2004-2Neutral MAP for vasomotor centre, around 100 mm Hg2007-1, 2003-2 What are the major factors affecting the regulation of arterial pressure?Baroreceptor reflexrapid, adjusts for changes in postureaortic arch and carotid sinusmessages via IX and X -> medulla (RVLM)autonomic nervous system to adjust HR/contractility (vagal) and peripheral vascular resistance (sympathetic)Renin-angiotensin systemlonger term adjustment of blood pressurecompensation of volume loss or BP drop via vasoconstrictor angiotensin IIAldosterone releasesteroid hormone released from the adrenal cortex in response to ATII or high potassiumstimulates sodium retention and potassium excretion by kidneyssodium is main ion determining amount of fluid in vessels via osmosis, thus increases fluid retention and indirectly BPCaridiopulmonary and atrial stretch receptorsfeedback by regulating the secretion of ADH (vasopressin), rennin and aldosteroneincrease blood volume which increases cardiac output (by Frank-Starling law)Peripheral chemoreceptor reflexIn carotid and aortic bodiesdecreased flow in hypotension stimulates them2005-1Describe the cardiovascular compensations to acute blood loss.Tachycardia; Vasoconstriction; Venoconstriction.Describe the other physiologic compensations to acute blood loss.Tachypnoea andIncreased:Adrenaline/noradrenaline (sympathetic)VasopressinGlucocorticoidsRenin/angiotensin/aldosteroneErythropoietinPlasma protein synthesis2008-1What are the basic factors which determine the rate of flow of blood through a blood vessel?Flow = Pressure/ResistancePoiseulle-Hagen formulaWhere: = viscosityL = length of tuber= radiusWhat factors cause turbulent flow in a blood vessel?Loss of laminar flow, the probability of this can be expressed by Reynold’s number Where:ρ is the fluid densityD is the diameter of the tubeV is the velocity of flowη is the viscosity of the fluidThe higher the value of Reynold’s number the greater the probability of turbulence, which usually occurs when Reynold’s number is between 2000-3000.2005-2What factors cause turbulence in blood flow“critical velocity”, density/viscosity, diameterReynolds number gives probabiltyWhy is blood flow slower in capillarieshighest total cross sectional area (4,500 cm2, i.e. 1000x that of the aorta)velocity = flow/areaWhat is the relationship between pressure and wall tension in blood vessels of different sizesAs per Law of Laplace, P = T/rSmaller vessels have less tension to balance the pressureWhat is the relationship between pressure and wall tension in the heartventricular dilation means more tension required to generate the same pressure = more work ................
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