JDiamandi_Carddiac output. Heart function - Pumping, Preload & afterload.pptx

Cardiac Physiology Dr Jorida Djamandi Cardiologist  Cardiovascular physiology Heart anatomy Electrical activity Cardiac cycle Cardiac output The cardiovascular system Heart: a sided pump that establishes blood pressure needed to get blood flow out to the tissues Blood...

Cardiac Physiology Dr Jorida Djamandi Cardiologist  Cardiovascular physiology Heart anatomy Electrical activity Cardiac cycle Cardiac output The cardiovascular system Heart: a sided pump that establishes blood pressure needed to get blood flow out to the tissues Blood vessels: passageways for blood to be distributes throughout the body and exchange material to/from the tissues Blood: liquid connective tissue that transport dissolved and suspended materials The Heart The human heart is a four-chambered muscular organ, shaped and sized roughly like a man's closed fist with two-thirds of the mass to the left of midline. The heart is enclosed in a pericardial sac that is lined with the parietal layers of a serous membrane. The visceral layer of the serous membrane forms the epicardium Layers of the Heart Wall Three layers of tissue form the heart wall. The outer layer of the heart wall is the epicardium, the middle layer is the myocardium, and the inner layer is the endocardium. Chambers of the Heart The internal cavity of the heart is divided into four chambers:  Right atrium  Right ventricle  Left atrium  Left ventricle The two atria are thin-walled chambers that receive blood from the veins. The two ventricles are thick-walled chambers that forcefully pump blood out of the heart. Differences in thickness of the heart chamber walls are due to variations in the amount of myocardium present, which reflects the amount of force each chamber is required to generate. The right atrium receives deoxygenated blood from systemic veins; the left atrium receives oxygenated blood from the pulmonary veins. Chambers of the Heart Valves of the Heart Pumps need a set of valves to keep the fluid flowing in one direction and the heart is no exception. The heart has two types of valves that keep the blood flowing in the correct direction. The valves between the atria and ventricles are called atrioventricular valves (also called cuspid valves), while those at the bases of the large vessels leaving the ventricles are called semilunar valves. The right atrioventricular valve is the tricuspid valve. The left atrioventricular valve is the bicuspid, or mitral, valve. The valve between the right ventricle and pulmonary trunk is the pulmonary semilunar valve. The valve between the left ventricle and the aorta is the aortic semilunar valve. When the ventricles contract, atrioventricular valves close to prevent blood from flowing back into the atria. When the ventricles relax, semilunar valves close to prevent blood from flowing back into the ventricles. When pressure is greater behind the valves ,it opens When pressure I grater in front of the valve ,it closes. Note when the pressure is greater in front of the valve it does not open in the opposite direction; that is a one way path Heart valves Pathway of Blood through the Heart While it is convenient to describe the flow of blood through the right side of the heart and then through the left side, it is important to realize that both atria and ventricles contract at the same time. The heart works as two pumps, one on the right and one on the left, working simultaneously. Blood flows from the right atrium to the right ventricle, and then is pumped to the lungs to receive oxygen. From the lungs, the blood flows to the left atrium, then to the left ventricle. From there it is pumped to the systemic circulation. Pathway of Blood through the Heart Blood Supply to the Myocardium The myocardium of the heart wall is a working muscle that needs a continuous supply of oxygen and nutrients to function efficiently. For this reason, cardiac muscle has an extensive network of blood vessels to bring oxygen to the contracting cells and to remove waste products. The right and left coronary arteries, branches of the ascending aorta, supply blood to the walls of the myocardium. After blood passes through the capillaries in the myocardium, it enters a system of cardiac (coronary) veins. Most of the cardiac veins drain into the coronary sinus, which opens into the right atrium. Blood Supply to the Myocardium Electrical activity of the heart Cardiac muscle cells The intrinsic conduction system Pacemaker potentials Cardiac muscle action potentials Cardiac Muscle cells Cardiac muscle is strated(contains actin and myosin)and branching adjacent cells connected by intercalated discs,which contains : -desmosin :mechanically hold cells together as heart contract -gap junctions : electrically connect cells Cardiac muscle cells  Functional Syncytium Because region of the heart are connected electrically by gap junctions, they form a “functional syncytium” -When one cell undergoes the AP ,it spreads to all connecting cells, they all contract together -atria form one group/ syncytium, ventricles form another group/syncytium Heart muscle contraction is ALL-OR-ONE(no graded contractions ex skeletal muscle recruitment) Functional Syncytium Comparison of skeletal,cardiac and smooth muscle The Intrinsic Conduction System The heart has electrical activity independent of the nervous system Action potentials in the heart are generated by the intrinsic conduction system a set of electrical pacemakers sells 1 SA node 2 AV node 3 Bundle of His(AV bundle) -right and left bundle branches 4 Purkinje fibers SA node SA node is located in the upper right atrium Fastest ,sets the pace of the heart 70-80 action potentials per minute at rest Activity spreads to both atria and the AV Node  AV node Is located in the lower right atria ,near the IVS 2nd fastest,only sets the pace if there is damage to the SA node 40-60 action potentials per minute Ativity pauses first,then spreads to Bundle of His AV node Delay =100ms due to fibrous tissue.slow conduction Bundle of His and Purkinje Fibers The bundle of His is located within the interventricular septum.and has a right and a left branch The Purkinje Fibers travel up the outer walls of the ventricles Slowest,not life sustaining 20-40 action potentials per minute Activity spreads to ventricles  Measuring the ECG Heart repolarization and depolarization is measured by an electrocardiogram (ECG) P wave –SA node to atrial depolarization QRS complex-AV node to Purkinje fibers , ventricular depolarization T wave-ventricular repolarization Intrinsic conduction of heart contractions  Pacemaker action potentials How is the intrinsic conduction system autorhythmic? Pacemaker potentials (NOT input) generate action potentials in the intrinsic conduction system that are “self –generating” Lowest membrane potential =-60 mV ICS cells do NOT stay -60 mv.NO REST At -60 mV membrane potentials drifted back up to -40 mV Thresholds is reached (spontaneously)at - 40 mV Peak depolarization is +10 mV Repolarization back to -60 mV, cycles again  Pacemaker action potentials: Channels Ion movement during Pacemaker AP’s: Membrane potential drifts towards threshold on its own: -Funny Na+ channels(I)-open at hyperpolarization -60 mv,Na+ enters cell, depolarizes -Transient –type(T type)Ca2+ enters cell The depolarization phase is due to Ca++ -Long lasting (L type) ca++ channels open at thresholds,-40 mV,Ca++ enters cell , full depolarization Repolarization is due to K+: -Voltage –gated K+channles open at peak.+10 mV,K leaves the cell, repolarization Cardiac muscle action potentials Action potentials in the pacemaker cells will spread to the cardiac muscle cells and cause them to contract. Cardiac Muscle cell AP’s are also unique -Rest=-90 mV -Rapid depolarization tom +20-+30 mV -Long depolarized Plateau phase.stays at +10 mv -Repolarisation to -90 mV Cardiac muscle action potentials:Channels Thresholds and depolarization are nerly simultaneous. -Voltage gates Na+ channels:open quickly,depolarize membrane to +30 mV.Na enters A slight repolarization occurs -Transient ,fast K+ channels : open briefly at +10 mV,repolarize slightly, K+ leaves Depolarization is held a long Plateau Phase due to Ca++ - Slow Ca++ channels :open at depolarization ,stay open 200+ms,Ca ++ enters Cause Plateau Phase Repolarization is due to K+ -Voltage gated K+ channels: cause final repolarization , K+ leaves -Leaky K+ channels: cause Low resting potentials at -90 mV Plateau Phase causes Long refractory period The plateau phase of the cardiac muscle cell AP is important for creating a long refractory period- -Due to inactivation of Na+ channels at depolarization peak,will not reactivate until full repolarization occurs Long refractory period allows long cardiac muscle contraction,uninterrupted to complete cyncytium contraction (atria or ventricles) -250 ms: absolute refractory period -cardiac muscle contaction 300 ms Alternating cycles of contraction and relaxation are key to heart function  Cardiac abnormalities Bradycardia 100 bpm Arrythmias : uncoordinated atrial and ventricular contractions -damaged SA node –Pace set by AV node ~50bpm -Heart block-damage to the AV node,venticles contract at ~30 bpm Fibrillation -irregular chaotic twitching of the myocardium  Cardiac cycle :Systole and diastole I cardiac cycle : The period from the end of one heart contraction to the end of the next During systole a contracting chamber will eject blood During diastole a relaxed chamber will fill blood Incomplete filling or ejection can lead tom inadequate pumping of blood to tissues  Cardiac Cycle Diastole is longer than systole The sequence of systole and diastole Cardiac cycle  The cardiac Cycle The cardiac cycle is the summary of all of the mechanical activities within the heart during a single beat -Atrial muscle contraction/relaxation -Ventricle muscle contraction/relaxation -AV valve actions -SL valve actions -Blood volume in heart -Blood pressure in heart -Heart sounds  The cardiac Cycle Mid-late ventricular diastole Ventricular systole Early ventricular diastole Mid late ventricular diastole The cardiac cycle begins with Mid Diastole -Atria relaxed and filling with blood -Ventricles relaxed and filling with blood -AV valves open -SL valves still closed In late diastole -Atria contract The maximum filling End diastolic volume (EDV ) of blood in the ventricle is reached EDV average =135 ml  Ventricular systole -Atria relax -Ventricles contract -AV valves close (prevent backflow) -SL valves closed initially causing isovolumetric contraction both valves closed,no volume changes,just pressure increasing -SL valves open when pressure is high enough,blood is ejected -Volume of bllod ejected is the stroke Volume -Volume of blood at the end is the End Systolic Volume(ESV average 65 ml Cardiac volumes SV=EDV(end diastolic volume) –ESV(end systolic volume) 135 ml-65 ml = 70 ml EDV=amount of blood collected in a ventricle during diastole ESV= amount of blood remaining in a ventricle after contraction  Early ventricular diastole Atria relaxed Ventrical relax SL valves close AV valve still close Isovolumetric relaxation,both valves are closed ,no volume changes in the ventrices AV valves open when enough blood fills the atria (Back to mid-late diastole) The cardiac cycle The cardiac cycle Cardiac output Cardiac output is the volume of the blood pumped each minute and is expressed by the following equation : CO=SV x HR where : CO is cardiac output expresses in L/min (normal ~ 5L/min) SV is stroke volume per beat HR is the number of beats per minute Stroke volume(SV)= EDV-ESV Is determined by three factors: preload, afterload and contractility Preload gives the volume of blood that the ventricle has available to pump. is dependent of ventricular filling (or EDV /end diastolic volume ).This value is related to right atrial pressure. But the most important determining factor for preload is venous return Contractility is the force that the muscle can create at the given length. Afterload is the arterial pressure witch against the muscle will contract Afterload for the left ventricle is determined by the aortic pressure. Afterload for the RV is determined by the pulmonary artery pressure These factors establish the volume of blood pumped with each heart beat  Venous return Venous return is important because the more blood pumped in the heart ,the more blood can be pumped out (is the major determinant of CO) Mechanism of venous return 1-Pressure gradient-fluids flows from high to lower pressure Venous return =Venous pressure-RA pressure venous resistance Factors that increase venous pressure or decrease RA pressure facilitate venous return Constriction of veins blocks blood flow ,increases venous resistance and reduces venous return (When blood vessels through out the body are constricted (exercise ),increase resistance causes blood pressure to rise and this eventually overrise the increase of venous resistance, as a result venous return increases 2-Skeletal muscle pump 3-Gravity 4-Breathing (respiratory pump) Cardiac output Cardiac output  Heart rate (HR) HR is directly proportional to cardiac ouput Adult heart rates varies 60-100 bpm HR is modified by autonomic,imune and local factors. For example :An increase of parasympathetic activity via M2 cholinergic receptors in the heart will decrease the heart rate And an increase of sympathetic activity via B1 and B2 receptors throughout the heart will increase the heart rate Factors regulating Heart rate In the body the heart rate is modified by nervous mechanism which include the autonomic nerves and vasomotor centre. We can also include the afferent nerves which carry impulses to vasomotor centre So heart rate is controlled by -Parasympathetic nerves -Sympathetic nerves-Sympathetic chain -Vasomotor centre Effect of Parasympathetic stimulation on Heart Rate Vagi i.e right vagus mainly controls the SA node and left vagus mainly controls the AV node Vagal fibers arise from dorsal nucleus of Vagus and supply the atrialmuscle,SA node ,AV node ,Purkinje Fiber but not ventricular muscle Parasympathetic stimulation leads to : Negative chronotropic effect:decreases heart rate Negative dromotropic effect:Velocity of conduction slowed down.AV nodal delay is prolonged Slight negative ionotropic effect:decrease force of contraction of heart Effect of Parasympathetic stimulation on Heart Rate The effect of vagi in gthe heart is continuous.This is called the vagal tone.Vagi don’t allow the heart rate to increase Vagal escape :When vagi are strogly stimulated,hearts stops beating but when strong vagal stimulation is continued,heart strats beating again called vagal escape..The possible mechanisms of vagal escape are: -Exhaution of acetylcholine stores -Cardiac muscle becomes refractory to the action of acetyl choline -Heart stops beating,blood pressure falls witch stmulates the baroreceptor reflex -Idioventricular rhythm a focus in the ventricle starts the generation of impulses Effect of Sympathetic stimulation on Heart Rate Sympathetic nerves are called accelerator nerves Effect of sympathetic is also continuous but not as powerful as vagal tone Preganglionic sympathetic fibers arise from T1 to T3.These fibers go to the inferior cervical ganglion,and then sypply the heart Sympathetic supply is mainly to ventricle musculature positive ionotropic effect positive dromotropic effect positive bathmotropic effect positive chronotropic effect Vasomotor center The vasomotor center is a portion of the medulla oblongata that regulates blood pressure and other homeostatic processes The action of the sympathetic and parasympathetic nerves is coordinated by vasomotor Centre The medial part of vasomotor center is cardioinhibitory through the vagi supplying the heart The lateral part is cardio acceleratory through the sympathetic nerve supplying the heart The vasomotor center is affected by impulses from different part of the heart to modify the heart rate Heart rate Heart rate Cardiac reserve Cardiac reserve is the difference between a person’s maximum cardiac output and cardiac output at rest. The average person has a cardiac reserve of four or five times the resting value. Top endurance athletes may have a cardiac reserve seven or eight times their resting CO. People with severe heart disease may have little or no cardiac reserve, which limits their ability to carry out even the simple tasks of daily living Cardiac reserve