CVS S2 I The Heart as a Pump PDF

S3 L1 The heart as a pump Lecturer : Manar Murtadha Designer : Fatima Haider  Heart chambers and Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its...

S3 L1 The heart as a pump Lecturer : Manar Murtadha Designer : Fatima Haider  Heart chambers and Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its contractile force.  Heart Anatomy Atrioventricular valves: tricuspid (right) and mitral (left) Semilunar valves: pulmonary (right) and aortic (left)  The Heart two pumps in series each side consists of — thin walled atrium — muscular ventricle flows into and out of ventricle controlled by valves — atrioventricular valves (mitral & tricuspid) — outflow valves (aortic and pulmonary)  Heart wall layers and electric conduction system of the heart Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its contractile force.  Heart Muscle a specialised form discrete cells connected electrically cells contract when action potential in Membrane action potential causes a rise in intracellular calcium action potential long - single contraction lasts 280 ms - systole action potentials triggered by spread of excitation from cell to cell  Pacemakers an action potential generated in a small group of cells will spread over the whole heart and produce a coordinated contraction pacemakers generate one action potential at regular intervals Phases of the Cardiac Cycle each action potential produces one beat - systole interval between beats known as diastole  Electric pathway of heart \ intrinsic activity of hear / automaticity of heart Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its contractile force. Q / actually SA node is not the only generator in the heart , what are other ? and why Sa node is the primary generator?  1- Spread of excitation pacemaker in sino- atrial node – right atrium activity first spreads over the atria - atrial systole to reach the atrio- ventricular node, where delayed for about 120 ms  2 - Spread of excitation from a-v node spreads down the septum between the ventricles then spreads through the ventricular myocardium from inner (endocardial) to outer (epicardial) surface ventricle contracts from the apex up, forces blood towards the outflow valves  The Cardiac Cycle at rest the SA node generates an action potential about once a second this produces a short atrial systole followed by a longer ventricular systole ventricular systole last about 280 ms followed by a relaxation lasting about 700 ms before the next systole  Ventricular pumping the combination of regular alternating systole and diastole with inflow and outflow valves allows the heart to work a a reciprocating pump the ventricles fill from the veins in diastole the ventricles pump blood into arteries in systole  The Left Ventricle inflow valve - the mitral valve — allows blood from the atrium to ventricle, but not vice-versa opens when atrial pressure exceeds intraventricular pressure closes when ventricular pressure exceeds atrial pressure  The Left Ventricle outflow valve - the aortic valve — allows blood from the ventricle to the aorta, but not vice-versa opens when intra-ventricular pressure exceeds aortic pressure closes when aortic pressure exceeds ventricular pressure The Cardiac Cycle  Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its contractile force.  Ventricular Filling During systole, blood accumulates in the atria. At end systole, the higher pressure forces open the AV valves causing rapid ventricular filling. This lasts about 1/3. last 200-300 ms. In the middle 1/3, there is minimal flow. In the last 1/3, the atria contracts to deliver up to 20% of the total ventricular volume.  Isovolumic Contraction At the start of systole, the intraventricular pressure rises which closes the AV valves. For approximately 20 to 30 ms, the pressure continues to rise but is less than that required to open the semilunar valves. This is called isovolumic contraction because the ventricular volume does not change.  Ejection Period Once the semilunar valves open the ejection phase begins. About 70% of the total blood ejected occurs in the first 1/3. This is called the rapid ejection period The final 30% empties in the next 2/3 and is called the slow ejection period.  Isovolumic Relaxation At end-systole, ventricular relaxation begins suddenly and causes intraventricular pressure to fall rapidly. The semilunar valves close once its pressure is greater than intraventricular pressure. For 30 –60 ms the muscle continues to relax, pressure continues to fall but no filling occurs because the AV valves are still closed. This is the period of isovolumic relaxation.  Normal Volume of Blood in Ventricles After atrial contraction, 110-120 ml in each ventricle (end-diastolic volume) Contraction ejects ~70 ml (stroke volume output) Thus, 40-50 ml remain in each ventricle (End- systolic volume) Left Ventricle Volume- ‐Pressure Curve  Cardiac Output and Venous Return Cardiac output is the quantity of blood pumped into the aorta each minute. Cardiac output = stroke volume x heart rate Venous return is the quantity of blood flowing from the veins to the right atrium.  Normal Cardiac Output Normal resting cardiac output: - Stroke volume of 70 ml - Heart rate of 72 beats/minute - Cardiac output ~ 5 litres/minute During exercise, cardiac output may increase to > 20 liters/minutes  Cardiac Output Stroke Volume = the vol of blood pumped by either the right or left ventricle during ventricular contraction. SV = EDV – ESV 70 = 125 – 55 CO = SV x HR 5,250 = 70 ml/beat x 75 beats/min CO = 5.25 L/min  Factors Affecting Stroke Volume EDV - affected by – Venous return – Preload (EDV) ESV –affected by – Contractility – Afterload  Preload - tension on muscle when it begins to contract (end-diastolic pressure) Afterload - load against which the muscle exerts its contractile force.  FrankStarling Mechanism The force of cardiac muscle contraction increases as the muscle stretches, within limits. Due to more optimal overlap of actin and myosin filaments during stretch - same in skeletal muscle So, with increase venous return and increased stretching, the force of contraction increases and the stroke volume increases. Moreover, stretching of the SA node increasing the firing rate of the pacemaker (increasing heart rate).  Frank-Starling Law of the Heart — preload → stretch of muscle → force of contraction → sv – If SV is increased, then ESV is decreased!! – VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output — TVR → TEDV and Vin VR → V in EDV — Any v in EDV → v in SV  Extrinsic Factors Influencing Stroke Volume Contractility Increase in contractility comes from: – Increased sympathetic stimuli – Certain hormones – Ca2+ and some drugs Agents/factors that decrease contractility include: – Acidosis – Increased extracellular K+ – Calcium channel blockers  Extrinsic Control of Contractility Contractility: – Strength of contraction at any given fiber length. Sympathoadrenal system: – NE and Epi produce an increase in contractile strength. + inotropic effect: – More Ca2+ available to sarcomeres. Parasympathetic stimulation: – Does not directly influence contraction strength.  Contractility and Norepinephrine Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP 2ndmessenger system  Effects of Hormones on Contractility Epi, NE, and Thyroxine all have positive ionotropic effects and thus contractility Digitalis elevates intracellular Ca++ concentrations by interfering with its removal from sarcoplasm of cardiac cells Beta-blockers ( as propanolol) block betareceptors and prevent sympathetic stimulation of heart (neg. chronotropic effect)  Cardiac Output and Peripheral Resistance Increasing the peripheral resistance decreases cardiac output. cardiac output = arterial pressure total peripheral resistance  Heart Sounds two main sounds associated with valves closing — first sound - 'lup' - closure of a/v valves — second sound - 'dup'- closure of outflow valves first sound at onset of ventricular systole second sound at the end of ventricular systole at rest, interval from 1st to 2nd about 280 ms interval second to next first 700 ms The cardiac cycle  Heart Sounds quality of sounds may change if valves altered sounds may split if valves of right and left heart do not close at same time  Heart Sounds occasionally hear extra sounds in normal hearts — third sound early in diastole — fourth sound - atrial systole Heart Murmurs turbulent flow of blood generates murmurs — narrowed valve - stenosis — valve not closing properly - incompetence murmurs occur when blood flow highest so can predict when in the cardiac cycle they should occur  Heart Murmurs example — aortic stenosis produces murmur in the rapid ejection phase The cardiac cycle S3 L1