Cardiac Electrophysiology PDF

 CARDIAC ELECTROPHYSIOLOGY :Prepared by Dr Esmail Al-Shoaibi  CARDIAC ELECTROPHYSIOLOGY Cardiac electrophysiology includes all of the processes :involved in the electrical activation of the heart The cardiac action pot...

 CARDIAC ELECTROPHYSIOLOGY :Prepared by Dr Esmail Al-Shoaibi  CARDIAC ELECTROPHYSIOLOGY Cardiac electrophysiology includes all of the processes :involved in the electrical activation of the heart The cardiac action potentials The conduction of action potentials Excitability The refractory periods The modulating effects of the autonomic nervous system on heart rate, conduction velocity, and excitability The electrocardiogram (ECG)  Cardiac Action Potentials Origin and Spread of Excitation Within the Heart Contractile cells are the majority of atrial and ventricular.tissues Action potentials in contractile cells lead to contraction and.generation of force or pressure Conducting cells & P cells are the tissues of the SA node, the atrial internodal tracts, the AV node, the bundle of His, and.the Purkinje system They function to rapidly spread action potentials over the entire myocardium They have capacity to generate action potentials.spontaneously Except for the SA node, however, this capacity normally is.suppressed  Cardiac Action Potentials SA node. Normally, initiates action potential of the.heart and called pacemaker Atrial internodal tracts and atria. They spread action potential to the right and left atria. Simultaneously, the action potential is conducted to.the AV node AV node. Conduction is slower than in the other. cardiac tissues.Bundle of His, Purkinje system, and ventricles Conduction through the His-Purkinje system is extremely fast, and it rapidly distributes the action. potential to the ventricles  Cardiac Action Potentials Normal sinus rhythm.It is the rhythm at which the heart shuold work To qualify as normal sinus rhythm, the following :three criteria must be met The action potential must originate in the SA )1(.node Impulses must occur regularly at a rate of )2(.60–100 impulses per minute The activation of the myocardium must occur )3( in the correct sequence and with the correct.timing and delays  Cardiac Action Potentials Concepts Associated With Cardiac Action Potentials :Two main forces drive ions across cell membranes.Chemical potential: an ion will move down its concentration gradient Electrical potential: an ion will move away from ions/molecules of.like charge The transmembrane potential (TMP) is the electrical potential difference (voltage) between the inside and the.outside of a cell When there is a net movement of +ve ions into a cell, the TMP becomes more +ve, and when there is a net movement of +ve.ions out of a cell, TMP becomes more –ve Ion channels help maintain ionic concentration gradients and charge differentials between the inside and outside of the.cardiomyocytes.  Cardiac Action Potentials Properties of cardiac ion channels :Selectivity. They are only permeable to a single type of ion :Voltage-sensitive gating A specific TMP range is required for a particular channel to be in open configuration; Therefore, specific channels open and close as the TMP changes during cell depolarization and repolarization, allowing the passage.of different ions at different times Time-dependence: some ion channels (importantly, fast Na+ channels) are configured to close a fraction of a second after opening; they cannot be opened again until the TMP is back to resting levels, thereby preventing.further excessive influx  Cardiac Action Potentials :Action potential Is an electrical stimulation created by a sequence of ion fluxes through specialized channels in the membrane (sarcolemma) of.cardiomyocytes that leads to cardiac contraction : Characteristics in non-pacemaker cardiomyocytes.Long duration ♦ Action potential duration varies from 150 ms in atria, to 250 ms in ventricles, to 300 ms in Purkinje fibers ; while in nerve and skeletal. muscle (1–2 ms). Which result in longer refractory period.Stable resting membrane potential ♦ Plateau. The plateau is a sustained period of depolarization, ♦ which leads to long duration of the action potential and, the long refractory periods.  Cardiac Action Potentials The phases of the action potential The action potential in typical cardiomyocytes is composed of 5 phases (0-4), beginning and ending.with phase 4 PHASE 4: THE RESTING PHASE The resting potential in a cardiomyocyte is −90 mV due to a constant outward leak of K+ through.inward rectifier channels.Na+ and Ca2+ channels are closed at resting TMP  Cardiac Action Potentials The phases of the action potential PHASE 0: DEPOLARIZATION An action potential triggered in a neighbouring cardiomyocyte or.pacemaker cell causes the TMP to rise above −90 mV Fast Na+ channels start to open one by one and Na+ leaks into the cell,.further raising the TMP TMP approaches −70mV, the threshold potential in cardiomyocytes, i.e. the point at which enough fast Na+ channels have opened to generate a self-.sustaining inward Na+ current The large Na+ current rapidly depolarizes the TMP to 0 mV and slightly above 0 mV for a transient period of time called the overshoot; fast Na+.channels close (recall that fast Na+ channels are time-dependent) L-type (“long-opening”) Ca2+ channels open when the TMP is greater than −40 mV and cause a small but steady influx of Ca2+ down its concentration.gradient  Cardiac Action Potentials The phases of the action potential PHASE 1: EARLY REPOLARIZATION.TMP is now slightly positive Some K+ channels open briefly and an outward flow of K+ returns PHASE 2: THE PLATEAU PHASE L-type Ca2+ channels are still open and there is a small, constant inward current of Ca2+. This becomes significant in the.excitation-contraction coupling process K+ leaks out down its concentration gradient through delayed.rectifier K+ channels These two countercurrents are electrically balanced, and the TMP is maintained at a plateau just below 0 mV throughout phase.2.the TMP to approximately 0 mV  Cardiac Action Potentials The phases of the action potential PHASE 3: REPOLARIZATION.Ca2+ channels are gradually inactivated Persistent outflow of K+, now exceeding Ca2+ inflow, brings TMP back towards resting potential of −90 mV.to prepare the cell for a new cycle of depolarization Normal transmembrane ionic concentration gradients are restored by returning Na+ and Ca2+ ions to the extracellular environment, and K+ ions to the cell interior. The pumps involved include the sarcolemmal.Na+-Ca2+ exchanger, Ca2+-ATPase and Na+-K+-ATPase  Cardiac Action Potentials Action Potentials in the Sinoatrial Node The SA node is the normal pacemaker.of the heart The following features of the action potential of the SA node are different from those in atria, ventricles, and :Purkinje fibers The SA node exhibits automaticity; )1( that is , it can spontaneously generate.action potentials without neural input It has an unstable resting )2( membrane potential, in direct contrast to cells in atrial, ventricular and Purkinje.fibers.It has no sustained plateau )3(  Cardiac Action Potentials Action Potentials in the Sinoatrial Node Phase 0, upstroke Note that the.1 upstroke is not as rapid or as steep as.in the other types of cardiac tissues It is the result of an increase in gca and an inward Ca2+current carried primarily by L-type Ca2+ channels & also T-type Ca2+channels which carry part of the inward Ca2+current of the.upstroke Phases 1 and 2 are absent.2 Phase 3, repolarization. As in the.3 other myocytes Action Potentials in the Sinoatrial Node Phase 4, spontaneous depolarization or pacemaker.4.potential.It is the longest and accounts for the automaticity The most negative value of the membrane potential (called the maximum diastolic potential) is approximately −65 mV, but.the membrane potential does not remain at this value Rather, there is a slow depolarization, produced by the.opening of Na+ channels and an inward Na+ current called If The “f,” which stands for funny, denotes that this Na+ current differs from the fast Na+ current responsible for the upstroke in ventricular cells. If is turned on by repolarization from the preceding action potential, thus ensuring that each action potential in the SA node will be followed by another action potential. Once If and slow depolarization bring the membrane potential to threshold, the Ca2+ channels are opened for the upstroke  Cardiac Action Potentials Latent Pacemakers They are cells with intrinsic automaticity other than those in the SA node, called latent.pacemakers They include the cells of the AV node, bundle.of His, and Purkinje fibers But normally is not expressed The rule is that the pacemaker with the fastest rate of phase 4 depolarization controls the heart rate The SA nodal cells have the shortest action potential duration (i.e., the shortest refractory.periods) Therefore SA nodal cells recover faster and are ready to fire another action potential before.the other cell types become ready When the SA node drives the heart rate, the latent pacemakers are suppressed, a phenomenon called overdrive suppression  Cardiac Action Potentials Ectopic pacemaker Under the following conditions a latent pacemaker takes over and becomes the pacemaker of the heart, in which case it is called an ectopic :pacemaker, or ectopic focus If the SA node firing rate decreases (e.g., due )1( to vagal stimulation) or stops completely (e.g., because the SA node is destroyed, removed, or suppressed by drugs), then one of the latent sites.will assume the role of pacemaker in the heart If the intrinsic rate of firing of one of the )2( latent pacemakers should become faster than that of the SA node, then it will assume the.pacemaker role If the conduction of action potentials from the )3( SA node to the rest of the heart is blocked because of disease in the conducting pathways, then a latent pacemaker can appear in addition to the SA node  Conduction Velocity Conduction of the Cardiac Action Potential It is the speed at which action potentials are.propagated within the tissue.Measured by meters per second (m/s) Conduction velocity is not the same in all myocardial :tissues It is slowest in the AV node (0.01–0.05 m/s) It is fastest in the Purkinje fibers (2–4 m/s) Conduction velocity determines the time of action potential to spread to various locations in the.myocardium ,These times, in milliseconds The action potential originates in the SA node at what.is called time zero It then takes a total of 220 ms for the action potential to spread through the atria, AV node, and His-Purkinje.system to the farthest points in the ventricles Conduction through the AV node (called AV delay) requires almost one-half of the total conduction time through the myocardium, here conduction time the.longest (100 ms)  Conduction Velocity Mechanism of Propagation of Cardiac Action Potential The physiologic basis for conduction of cardiac action potentials is the.spread of local currents Action potentials at one site generate local currents at adjacent sites ; the adjacent sites are depolarized to threshold as a result of this local.current flow and fire action potentials themselves This local current flow is the result of the inward current of the upstroke.of the action potential :Conduction velocity depends on The size of the inward current during the upstroke of the action.potential The larger the inward current, the more rapidly local currents will spread.to adjacent sites and depolarize them to threshold ,dV/dT, (the rate of rise of the upstroke of the action potential).The cable properties of the myocardial fibers.Conduction velocity does not depend on action potential duration  Conduction Velocity Mechanism of Propagation of Cardiac Action Potential (con).The rate of rise of the upstroke is called dV/dT dV/dT is the rate of change of the membrane potential as a.function of time, and its units are volts per second (V/s) It correlates with the size of the inward current dV/dT varies, depending on the value of the resting.membrane potential.This dependence is called the responsiveness relationship Thus dV/dT is greatest (the rate of rise of the upstroke is fastest) when the resting membrane potential is most negative, or ,hyperpolarized (e.g.,−90 mV) dV/dT is lowest (the rate of rise of the upstroke is slowest) when the resting membrane potential is less negative, or depolarized (e.g.,−60 mV)  Conduction Velocity Mechanism of Propagation of Cardiac Action Potential (con) :The cable properties of the myocardial fibers These cable properties are determined by cell membrane.resistance (Rm) and internal resistance (Ri) For example, in myocardial tissue, Ri is particularly low because of low-resistance connections between the cells.called gap junctions Thus myocardial tissue is especially well suited to fast conduction  Excitability and Refractory Periods Excitability Excitability is the amount of inward current required to bring a myocardial.cell to the threshold potential The excitability of a myocardial cell varies over the course of the action potential, and these changes in excitability are reflected in the refractory periods  Excitability and Refractory Periods Refractory periods.It is similar to that in nerve cells Activation gates on Na+ channels open when the membrane potential is depolarized to threshold, permitting a rapid influx of Na+ into the cell.which causes further depolarization toward the Na+ equilibrium potential.This rapid depolarization is the upstroke of the action potential However, inactivation gates on the Na+ channels also close with depolarization, as a result a portion of the Na+ channels will be closed , so inward depolarizing current cannot flow through them, there can be no.upstroke or action potential, and the cell is called refractory Once repolarization occurs, the inactivation gates on the Na+ channels open and now the Na+ channels will be in the closed, but available state; the cell will once again be excitable and ready to fire another action.potential  Excitability and Refractory Periods Refractory periods Types of refractory periods.Absolute refractory period (ARP) ♦ For most of the duration of the action potential, the ventricular cell is completely refractory to fire another action potential,because most of the Na + channels are closed and unavailable to.carry inward current The ARP includes the upstroke, the entire plateau, and a portion of the.repolarization This period concludes when the cell has repolarized to approximately.mV 50−  Excitability and Refractory Periods Refractory periods Types of refractory periods.Effective refractory period (ERP) ♦ The ERP includes, and is slightly longer.than, the ARP At the end of the ERP, the Na channels + start to recover The distinction between ARP and ERPs is that absolute means absolutely no stimulus is large enough to generate another action potential; effective means that a conducted action potential cannot be generated (i.e., there is not enough inward current to conduct to.the next site)  Excitability and Refractory Periods Refractory periods Types of refractory periods.Relative refractory period (RRP) ♦ It begins at the end of the ARP and continues until the cell membrane has.almost fully repolarized During the RRP, even more Na+ channels have recovered to the closed, but available state and it is possible to generate a second action potential, although a.greater than normal stimulus is required If a second action potential is generated during the RRP, it will have an abnormal configuration and a shortened plateau.phase  Excitability and Refractory Periods Refractory periods Types of refractory periods.Supranormal period (SNP) ♦.The SNP follows the RRP It begins when the membrane potential is −70 mV and continues until the membrane is fully.repolarized back to −85 mV The cell is more excitable than normal during this.period Less inward current is required to depolarize the cell.to the threshold potential The physiologic explanation for this increased excitability is that the Na+ channels are recovered (i.e., the inactivation gates are open again), and because the membrane potential is closer to threshold than it is at rest, it is easier to fire an action potential than when the cell membrane is.at the resting membrane potential Autonomic Effects on the Heart and Blood Vessels  Autonomic Effects on the Heart and Blood Vessels Autonomic Effects on Heart Rate These effects called chronotropic effects.. Briefly, sympathetic stimulation increases heart rate and parasympathetic stimulation.decreases heart rate Phase 4 depolarization is produced by opening Na+ channels, which leads to a slow depolarizing,.inward Na+ current called If Once the membrane potential is depolarized to the threshold potential, an action potential is.initiated  Autonomic Effects on the Heart and Blood Vessels Autonomic Effects on Heart Rate.Positive chronotropic effects are increases in heart rate ♦ Norepinephrine, released from sympathetic nerve fibers, activates β1.receptors in the SA node These β1 receptors are coupled to adenylyl cyclase through a G s protein produces an increase in If, which increases the rate.of phase 4 depolarization In addition, there is an increase in Ica , which means there are more functional Ca2+ channels and thus less depolarization is required to.reach threshold (i.e., threshold potential decreases) Increasing the rate of phase 4 depolarization , means that the SA node is depolarized to threshold potential more frequently and, as a consequence, fires more action potentials per unit time (i.e., increased.heart rate)  Autonomic Effects on the Heart and Blood Vessels Autonomic Effects on Heart Rate.Negative chronotropic effects are decreases in heart rate ♦ Acetylcholine (ACh), released from parasympathetic nerve fibers, activates muscarinic (M ) 2 : receptors in the SA node, which has two effects First, these muscarinic receptors are coupled to a type of Gi protein called GK that inhibits adenylyl cyclase and produces a decrease in If , this decreases the rate of phase 4.depolarization Second, GK directly increases the conductance of a K+ channel called K -ACh and increases + an outward K+ current, this hyperpolarizes the maximum diastolic potential so that the SA.nodal cells are further from threshold potential In addition, there is a decrease in ICa, which means there are fewer functional Ca2 channels + and thus more depolarization is required to reach threshold (i.e., threshold potential.increases) In sum, the parasympathetic nervous system decreases heart rate through three effects :on the SA node ,slowing the rate of phase 4 depolarization )1( hyperpolarizing the maximum diastolic potential so that more inward current is )2( ,required to reach threshold potential.increasing the threshold potential )3( As a result, the SA node is depolarized to threshold less frequently and fires fewer action potentials per unit time (i.e., decreased heart rate)  Autonomic Effects on Conduction Velocity in the A-V Node.called dromotropic effects The mechanism of these autonomic effects, that conduction velocity correlates with the size of the inward current of the upstroke of the action potential and the rate of rise of the.upstroke , dV/dT Stimulation of the sympathetic nervous system produces an increase in conduction velocity through the AV node (positive dromotropic effect), which increases the rate at which action potentials are conducted from the atria to the.ventricles The mechanism of the sympathetic effect is increased I Ca, which is responsible for the upstroke of the action potential in the AV node In a supportive role, the increased I Ca shortens the ERP so that the AV nodal cells recover earlier from inactivation and can conduct.the increased firing rate  Autonomic Effects on Conduction Velocity in the A-V Node Stimulation of the parasympathetic nervous system produces a decrease in conduction velocity through the AV node (negative dromotropic effect), which decreases the rate at which action potentials are conducted from the.atria to the ventricles The mechanism of the parasympathetic effect is a combination of decreased ICa (decreased inward current) and increased IK-ACh (increased outward K+ current, which further reduces net inward current). additionally, the ERP of AV nodal cells is prolonged. If conduction velocity through the AV node is slowed sufficiently (e.g., by increased parasympathetic activity or by damage to the AV node), some action potentials may not be conducted at all from the atria to.the ventricles, producing heart block  Electrocardiogram (ECG) Electrocardiography It is the technique by which electrical activities of the.heart are studied The spread of excitation through myocardium produces local electrical potential , which flows.through the body, which acts as a volume conductor This current can be picked up from surface of the body by using suitable electrodes and recorded in.the form of electrocardiogram It was discovered by Dutch physiologist, Einthoven Willem, who is considered the father of.electrocardiogram (ECG)  Electrocardiogram (ECG) Electrocardiograph Electrocardiograph is the instrument (machine) by which electrical activities of the heart are recorded Electrocardiogram Electrocardiogram (ECG or EKG from electrocardiogram in Dutch) is the record or graphical registration of electrical activities of the. heart It is the summed electrical activity of all cardiac.muscle fibers recorded from surface of the body  Electrocardiogram (ECG) USES OF ECG It is useful in determining and diagnosing the :following Heart rate.1 Heart rhythm.2 Abnormal electrical conduction.3 Poor blood flow to heart muscle (ischemia).4 Heart attack.5 Coronary artery disease.6.Hypertrophy of heart chambers.7  Electrocardiogram (ECG) ELECTROCARDIOGRAPHIC GRID Electrocardiographic grid refers to the markings.(lines) on ECG paper ECG paper has horizontal and..vertical lines at regular intervals of 1 mm Every 5th line (5 mm) is thickened DURATION „ Time duration of different ECG waves is plotted.horizontally on X-axis On X-axis mm = 0.04 second 1 mm = 0.20 second 5 AMPLITUDE „ Amplitude of ECG waves is plotted vertically on Y-.axis On Y-axis mm = 0.1 mV 1 mm = 0.5 mV 5 SPEED OF THE PAPER Usually, speed of the paper during recording is fixed at 25 mm/second. If heart rate is very ,high  Electrocardiogram (ECG). ECG LEADS These are electrodes by on body surface for..recording are called ECG leads.Electrodes are fixed on the limbs.Usually, right arm, left arm and left leg are chosen Heart is said to be in the center of an imaginary equilateral triangle drawn by connecting the roots of.these three limbs.This triangle is called Einthoven triangle Einthoven Triangle is defined as an equilateral triangle that is used as a model of standard limb.leads used to record electrocardiogram Heart is presumed to lie in the center of Einthoven.triangle Electrical potential generated from the heart appears simultaneously on the roots of the three limbs,.namely the left arm, right arm and the left leg ECG is recorded in 12 leads, which are generally.classified into two categories I. Bipolar leads  Electrocardiogram (ECG). BIPOLAR. LIMB LEADS.Known as standard limb leads Two. limbs are connected to obtain these leads and both the electrodes are active recording electrodes, i.e. one is positive. and the other one is negative :Standard limb leads are of three types Lead I Lead I is obtained by connecting right arm..and left arm Lead II Lead II is obtained by connecting right arm.and left leg Lead III Lead III is obtained by connecting left arm  Electrocardiogram (ECG).UNIPOLAR LEADS Here, one electrode is active electrode and the other.one is an indifferent electrode Active electrode is positive and the indifferent electrode is..serving as a composite negative electrode :Unipolar leads are of two types Unipolar limb leads.1.Unipolar chest leads.2 Unipolar Limb Leads.1 Unipolar limb leads are also called augmented limb leads.or augmented voltage leads Active electrode is connected to one of the limbs. Indifferent electrode is obtained by connecting the other.two limbs through a resistance :Unipolar limb leads are of three types I. aVR lead Active electrode is from right arm. Indifferent electrode is.obtained by connecting left arm and left leg II. aVL lead Active electrode is from left arm. Indifferent electrode is.obtained by connecting right arm and left leg III. aVF lead Active electrode is from left leg (foot). Indifferent electrode is obtained by connecting the two upper limbs  Electrocardiogram (ECG).UNIPOLAR LEADS Unipolar Chest Leads.2 Chest leads are also called ‘V’ leads or precardial chest.leads. Indifferent electrode is obtained by connecting the three limbs, viz. left arm, left leg and right arm, through.a resistance of 5000 ohms Active electrode is placed on six points over the chest. This electrode is known as the chest electrode and the six.points over the chest are called V1, V2, V3, V4, V5 and V6 V indicates vector, which shows the direction of current.flow :Position of chest leads V1 : Over 4th intercostal space near right sternal margin V2 : Over 4th intercostal space near left sternal Margin V3 : In between V2 and V4 V4 : Over left 5th intercostal space on the mid clavicular line V5 : Over left 5th intercostal space on the anterior axillary line V6 : Over left 5th intercostal space on the mid.axillary line  Electrocardiogram (ECG) WAVES OF NORMAL ECG Normal ECG consists of waves, complexes, intervals and segments. Waves of ECG recorded by limb lead II are considered as the typical waves. Major Complexes in ECG P’ wave, the atrial complex‘.1 QRS’ complex, the initial ventricular complex‘.2 T’ wave, the final ventricular complex‘.3.QRST’, the ventricular complex‘.4 P’ WAVE is a positive wave‘ „.Cause ‘the depolarization of atrial musculature Depolarization spreads from SA node to all parts of.atrial musculature Atrial repolarization is not recorded as a separate wave in ECG because it merges with ventricular.repolarization (QRS complex).Duration of ‘P’ wave is 0.1 second.Amplitude of ‘P’ wave is 0.1 to 0.12 mV Morphology ‘P’ wave is normally positive (upright) in.leads I, II,aVF, V4, V5 and V6.It is normally negative (inverted) in aVR It is variable in the remaining leads, i.e. it may be  Electrocardiogram (ECG) QRS’ COMPLEX‘.Also called the initial ventricular complex Cause QRS’ complex is due to depolarization of ventricular‘..musculature Q’ wave is due to the depolarization of basal portion of ‘.interventricular septum R’ wave is due to the depolarization of apical portion of ‘.interventricular septum and apical portion of ventricular muscle S’ wave is due to the depolarization of basal portion of ventricular ‘.muscle near the atrioventricular ring Duration.Between 0.08 and 0.10 second Amplitude.Q’ wave = 0.1 to 0.2 mV. ‘R’ wave = 1 mV‘.S’ wave = 0.4 mV‘ Morphology Q’ wave is less than 25% of amplitude of ‘R’ wave in ‘.leads I, II, aVL, V5 and V6.In the remaining leads, its amplitude is < 2 mm From chest leads V1 to V6, ‘R’ wave becomes.gradually larger. It is smaller in V6 than V5 S’ wave is large in V1 and larger in V2. It gradually becomes ‘.smaller from V3 to V6  Electrocardiogram (ECG) T’ WAVE‘ T’ wave is the final ventricular complex and is a‘.positive wave Cause. is due to the repolarization of ventricular‘ T’ wave.musculature Duration.Normal duration of ‘T’ wave is 0.2 second Amplitude.Normal amplitude of ‘T’ wave is 0.3 mV Morphology T’ wave is normally positive in leads I, II and V5 and‘. V6 It is normally inverted in lead aVR. It is variable in the..other leads, i.e. it is positive, negative or flat U’ WAVE‘.U’ wave is not always seen‘ It is supposed to be due to repolarization of papillary.muscle  Electrocardiogram (ECG) INTERVALS AND SEGMENTS OF ECG P-R’ INTERVAL is the interval between the onset of‘..‘P’ wave and onset of ‘Q’ wave P-R’ interval signifies the atrial depolarization and‘.conduction of impulses through AV node It shows the duration of conduction of the impulses from the SA node to ventricles through atrial muscle.and AV node Short isoelectric (zero voltage) period after the end of ‘P’ wave represents the time taken for the passage of.depolarization within AV node Duration Normal duration of ‘P-R interval’ is 0.18 second and.varies between 0.12 and 0.2 second If it is more than 0.2 second, it signifies the delay in the conduction of impulse from SA node to the.ventricles Usually, the delay occurs in the AV node. So it is.called the AV nodal delay  Electrocardiogram (ECG) INTERVALS AND SEGMENTS OF ECG Q-T’ INTERVAL‘ ’Q-T’ interval is the interval between the onset of ‘Q ‘..wave and the end of ‘T’ wave Q-T’ interval indicates the ventricular depolarization ‘ and ventricular repolarization, i.e. it signifies the.electrical activity in ventricles Duration Normal duration of Q-T interval is between 0.4 and 0.42.second S-T’ SEGMENT‘ S-T’ segment is the time interval between the end of‘.S’ wave and the onset of ‘T’ wave‘.It is an isoelectric period J Point.The point where ‘S-T’ segment starts is called ‘J’ point ’It is the junction between the QRS complex and ‘S-T.segment Duration of ‘S-T’ Segment.Normal duration of ‘S-T’ segment is 0.08 second  Electrocardiogram (ECG) INTERVALS AND SEGMENTS OF ECG R-R’ INTERVAL‘.The time interval between two consecutive ‘R’ waves Significance..lt signifies the duration of one cardiac cycle Duration.Normal duration of ‘R-R’ interval is 0.8 second Significance of Measuring ‘R-R’ Interval :Measurement of ‘R-R’ interval helps to calculate Heart Rate.1 ’Heart rate is calculated by measuring the number of ‘R.waves per unit time Calculation of heart rate Time is plotted horizontally (X-axis). On X-axis, interval between two thick lines is 0.2 sec (see above). Time ’duration for 30 thick lines is 6 seconds. Number of ‘R waves (QRS complexes) in 6 seconds (30 thick lines) is counted and multiplied by 10 to obtain heart rate Heart Rate Variability.2.refers to the beat-to beat variations )HRV( Under resting conditions, the ECG of healthy individuals exhibits some periodic variation in ‘R-R’.intervals This rhythmic phenomenon is known as respiratory sinus arrhythmia (RSA), since it fluctuates with the phases of respiration. ‘R-R’ interval decreases during inspiration and increases during CARDIAC CYCLE and HEART SOUNDS :Prepared by Dr Esmail Al-Shoaibi  CARDIAC CYCLE It is the sum of cardiac events that occur from the beginning of one heartbeat to the beginning of the next one. Each heartbeat consists of two major periods called systole and diastole. During systole, heart contracts and pumps the blood through arteries. During diastole, heart relaxes and blood is filled in the heart. All these changes are repeated during every heartbeat, in a cyclic manner. EVENTS OF CARDIAC CYCLE Events of cardiac cycle are classified into two: 1. Atrial events 2. Ventricular events.  CARDIAC CYCLE DIVISIONS AND DURATION OF CARDIAC CYCLE When the heart beats at a normal rate of 72/minute, duration of each cardiac cycle is about 0.8 second. „ ATRIAL EVENTS Atrial events are divided into two divisions: 1. Atrial systole = 0.11 (0.1) sec 2. Atrial diastole = 0.69 (0.7) sec. „ VENTRICULAR EVENTS Ventricular events are divided into two divisions: 1. Ventricular systole = 0.27 (0.3) sec 2. Ventricular diastole = 0.53 (0.5) sec. Ventricular systole is divided into two subdivisions and ventricular diastole is divided into five subdivisions.  CARDIAC CYCLE DIVISIONS AND DURATION OF CARDIAC CYCLE Ventricular Systole 0.27 sec. Time (second) 1. Isometric contraction = 0.05 2. Ejection period = 0.22 Ventricular Diastole 0.53 sec. 1. Protodiastole = 0.04 2. Isometric relaxation = 0.08 3. Rapid filling = 0.11 4. Slow filling = 0.19 5. Last rapid filling = 0.11 Atrial systole occurs during the last phase of ventricular diastole. Atrial diastole is not considered as a separate phase, since it coincides with the whole of ventricular systole and earlier part of ventricular diastole.  CARDIAC CYCLE DESCRIPTION OF ATRIAL EVENTS ATRIAL SYSTOLE Known as last rapid filling phase or presystole. Considered as the last phase of ventricular diastole. Its duration is 0.11 second. Only a small amount, i.e. 10% of blood is forced from atria into ventricles. Atrial systole is not essential for the maintenance of circulation. Many persons with atrial fibrillation survive for years, without suffering from circulatory insufficiency. However, such persons feel difficult to cope up with physical stress like exercise. Pressure and Volume Changes Intraatrial pressure increases. Intraventricular pressure and ventricular volume also increase but slightly. Fourth Heart Sound Contraction of atrial musculature causes the production of fourth heart sound.  CARDIAC CYCLE DESCRIPTION OF ATRIAL EVENTS ATRIAL DIASTOLE After atrial systole, the atrial diastole starts. Simultaneously, ventricular systole also starts. Atrial diastole lasts for about 0.7 sec (accurate duration is 0.69 sec). This long atrial diastole is necessary because, this is the period during which atrial filling takes place. Right atrium receives deoxygenated blood from all over the body through superior and inferior venae cavae. Left atrium receives oxygenated blood from lungs through pulmonary veins.  CARDIAC CYCLE DIVISIONS AND DURATION OF CARDIAC CYCLE Atrial Events Vs Ventricular Events Out of 0.7 sec of atrial diastole, first 0.3 sec (0.27 sec accurately) coincides with ventricular systole. Then,ventricular diastole starts and it lasts for about 0.5 sec (0.53 sec accurately). Later part of atrial diastole coincides with ventricular diastole for about 0.4 sec. So, the heart relaxes as a whole for 0.4 sec  CARDIAC CYCLE DESCRIPTION OF VENTRICULAR EVENTS ISOMETRIC CONTRACTION PERIOD The first phase of ventricular systole. It lasts for 0.05 second. Characterized by increase in tension, without any change in the length of muscle fibers. Also called isovolumetric contraction. Immediately after atrial systole, the atrioventricular valves are closed due to increase in ventricular pressure. Semilunar valves are already closed. Now, ventricles contract as closed cavities, in such a way that there is no change in the volume of ventricular chambers or in the length of muscle fibers. Only the tension increases in ventricular musculature. The pressure increases sharply inside the ventricles. First Heart Sound Closure of atrioventricular valves at the beginning of this phase produces first heart sound. Significance of Isometric Contraction The pressure rise in ventricle, caused by isometric contraction is responsible for the opening of semilunar valves, leading to ejection of blood from the ventricles into aorta and pulmonary artery.  CARDIAC CYCLE DESCRIPTION OF VENTRICULAR EVENTS EJECTION PERIOD Blood is ejected out of both the ventricles in response to opening of aortic and pulmonary valves. Duration of this period is 0.22 second. Ejection period is of two stages: 1. First Stage or Rapid Ejection Period Starts immediately after the opening of semilunar valves. A large amount of blood is rapidly ejected from both the ventricles. It lasts for 0.13 second. 2. Second Stage or Slow Ejection Period The blood is ejected slowly with much less force. Duration of this period is 0.09 second. End-systolic Volume Amount of blood remaining in ventricles at the end of ejection period. It is 60 to 80 mL per ventricle. Ejection Fraction Ejection fraction (Ef) is the stroke volume divided by Enddiastolic volume Clinically, it is considered as an important index for assessing the ventricular contractility. PROTODIASTOLE CARDIAC CYCLE The first stage of ventricular diastole, Duration of this period is 0.04 second. When intraventricular pressure becomes less than the pressure in aorta and pulmonary artery, the semilunar valves close. Atrioventricular valves are already closed No other change occurs in the heart during this period. Thus, protodiastole indicates only the end of systole and beginning of diastole. Second Heart Sound Closure of semilunar valves during this phase produces second heart sound.  CARDIAC CYCLE ISOMETRIC RELAXATION PERIOD Characterized by decrease in tension without any change in the length of muscle fibers. Also called isovolumetric relaxation. All the valves of the heart are closed. Now, both the ventricles relax as closed cavities without any change in volume or length of the muscle fiber. Intraventricular pressure decreases during this period. Duration is 0.08 second. Significance of Isometric Relaxation When the ventricular pressure becomes less than the pressure in the atria, the atrioventricular valves open resulting in filling of ventricles RAPID FILLING PHASE There is a sudden rush of blood from atria into ventricles. So, this period is called the first rapid filling period. Ventricles also relax isotonically. About 70% of filling takes place during this phase, which lasts for 0.11 second. Third Heart Sound Rushing of blood into ventricles during this phase causes production of third heart sound.  CARDIAC CYCLE SLOW FILLING PHASE After the sudden rush of blood, the ventricular filling becomes slow. Now, it is called the slow filling. It is also called diastasis. About 20% of filling occurs in this phase. Duration is 0.19 second. „ LAST RAPID FILLING PHASE After slow filling period, the atria contract and push a small amount of blood into ventricles. About 10% of ventricular filling takes place during this period Also called atrial kick. End-diastolic Volume The amount of blood remaining in each ventricle at the end of diastole. It is about 130 to 150 mL per ventricle.  CARDIAC CYCLE METHODS OF STUDY Right atrial pressure is recorded directly by cardiac catheterization. Left atrial pressure is determined indirectly by measuring pulmonary capillary wedge pressure, which reflects the left atrial pressure accurately. Pulmonary Capillary Wedge Pressure It is the pressure exerted in the pulmonary capillary bed after obstructing the proximal part of pulmonary artery. It is measured by using a balloontipped multilumen cardiac catheter (SwanGanz catheter). Tip of the catheter is not open but a pressure transducer is attached to it. By means of venous puncture, the catheter is guided through right atrium into right ventricle. From the right ventricle, it is advanced towards the proximal portion of pulmonary artery and the balloon is inflated with air by using a syringe. This occludes the pulmonary artery. Then, the catheter alone is advanced further into distal portion of pulmonary artery, leaving the inflated balloon at the proximal portion. It allows the catheter to float in a wedge position. Now the pressure existing in the pulmonary capillary bed ahead of catheter is  CARDIAC CYCLE METHODS OF STUDY INTRA-ATRIAL PRESSURE CURVE It is similar to the tracing of jugular venous pulse, which is known as phlebogram. It has three positive waves, a, c and v and three negative waves, x, x1 and y ‘a’ Wave Occurs during atrial systole. The pressure rises sharply up to 5 mm Hg in right atrium and 7 mm Hg in left atrium. After reaching the peak, the pressure starts decreasing. ‘x’ Wave is the first negative wave and appears during the onset of atrial diastole, the pressure falls. AV valves close at the end of this wave. ‘c’ Wave is the second positive wave and this appears during isometric contraction. Rise in pressure is due to the closure of AV valves and the increased intraventricular pressure. When atrioventricular valves close, there is a little back flow of blood towards atria. When the intraventricular pressure increases, there is bulging of AV valves into the atria. Because of these two factors, the atrial pressure rises. ‘x1’ Wave is the second negative wave and appears during ejection period,contraction of ventricular musculature pulls the AV ring towards the ventricles.fall in atrial pressure. ‘v’ Wave is the third positive wave, which is obtained during atrial diastole. Gradual increase in atrial pressure due to filling of blood in atria (venous return). ‘y’ Wave is the third negative wave and appears after the opening of AV valves  CARDIAC CYCLE METHODS OF STUDY INTRAVENTRICULAR PRESSURE CURVE „ METHODS OF STUDY Intraventricular pressure is measured by cardiac catheterization. It has seven segments. ‘A-B’ Segment is a positive wave and appears during atrial systole. Rise in pressure is due to the entry of a small amount of blood into the ventricles because of atrial systole. The pressure rises to about 6-7 mm Hg in the right ventricle and to about 7- 8 mm Hg in the left ventricle.B indicates the closure of AV valves. ‘B-C’ Segment appears during isometric contraction. There is a sharp rise in the intraventricular pressure. ‘C’ denotes the opening of semilunar valves. ‘C-D’ Segment appears during ejection period. The pressure in the ventricles rises to the peak and then falls down. First part of the curve indicates the maximum ejection and the pressure increases to the maximum. Second part of the curve represents the slow ejection phase when the pressure decreases. Maximum pressure rise in right ventricle is about 25 mm Hg and the maximum pressure rise in left ventricle is about 120 mm Hg, during the peak of this wave. Maximum pressure in LV is 4 to 5 times< in RV ‘D-E’ Segment appears during protodiastole. Pressure ↓ slightly due to the starting  CARDIAC CYCLE METHODS OF STUDY INTRAVENTRICULAR PRESSURE CURVE ‘E-F’ Segment is obtained during isometric relaxation. A sharp fall in the intraventricular pressure. Pressure in the ventricle falls below the pressure in the atria and this causes the opening of AV valves. ‘F’ represents the opening of AV valves. ‘F-G’ Segment appears during rapid filling phase. In spite of filling of blood, pressure decreases in the ventricles, because of relaxation of ventricles. ‘G-A’ Segment. It is obtained during slow filling phase. Continuous relaxation of ventricles during slow filling period,ventricular pressure decreases further.  Heart Sounds Are the sounds produced by mechanical activities of heart during each cardiac cycle. Heart sounds are produced by: 1. Flow of blood through cardiac chambers 2. Contraction of cardiac muscle 3. Closure of valves of the heart  ‫املحاضرة الخامسة‬ Cardiac Output & Heart Rate Prepared by Dr Ismaeel AlShoaibi 1 INTRODUCTION  The amount of blood pumped from each ventricle.  Usually, it refers to left ventricular output through aorta.  It is the most important factor in cardiovascular system, because on it depends rate of blood flow throughout the body 2 Expression ways  Cardiac output is expressed in three ways  1. Stroke volume  2. Minute volume  3. Cardiac index. 3  Stroke volume  The amount of blood pumped out by each ventricle during each beat.  Normal value: 70 mL (60 to 80 mL) when the heart rate is normal (72/minute).  Minute volume  The amount of blood pumped out by each ventricle in one minute  Minute volume = Stroke volume × Heart rate  Normal value: 5 L/ventricle/minute.  Cardiac index  The amount of blood pumped out per ventricle/minute/square meter of the body surface area.  Normal value: 2.8 ± 0.3 L/square meter of body surface area/minute  (in an adult with average body surface area of 1.734 square meter and normal minute volume of 5 L/minute). 4 CARDIAC RESERVE  The maximum amount of blood that can be pumped out by heart above the normal value.  Plays an important role in increasing the cardiac output during the conditions like exercise..  In a normal young healthy adult, it is 300% to 400%.  In old age, it is about 200% to 250%.  in athletes it is 500% to 600%.  In cardiac diseases, it is minimum or nil. 5  VARIATIONS IN CARDIAC OUTPUT  PHYSIOLOGICAL VARIATIONS 1. Age: In children, it is less because of less blood volume. Cardiac index is more than that in adults because of less body surface area. 2. Sex: In females, it is less than in males because of less blood volume. Cardiac index is more than in males, because of less body surface area. 3. Body build: it is proprtional to body build 4. Diurnal variation: it is low in early morning and increases in day time. 5. Environmental temperature Increase in temperature above 30°C. 6. Emotional conditions: Anxiety, apprehension and excitement increases it about 50% to 100% through the release of catecholamines, which increase the heart rate and force of contraction. 6  VARIATIONS IN CARDIAC OUTPUT PHYSIOLOGICAL VARIATIONS (cont.) 7. After meals: During the first one hour after taking meals, it increases. 8. Exercise: it increases during exercise because of increase in heart rate and force of contraction. 9. High altitude: In high altitude, it increases because of increase in secretion of adrenaline. Adrenaline secretion is stimulated by hypoxia (lack of oxygen). 10. Posture: While changing from recumbent to upright position, it decreases. 11. Pregnancy: During the later months of pregnancy,it increases by 40%. 12. Sleep: It is slightly decreased or it is unaltered during sleep. 7 VARIATIONS IN CARDIAC OUTPUT  PATHOLOGICAL VARIATIONS Increase in Cardiac Output 1. Fever: Due to increased oxidative processes 2. Anemia: Due to hypoxia 3. Hyperthyroidism: Due to increased basal metabolic rate. 8 VARIATIONS IN CARDIAC OUTPUT PATHOLOGICAL VARIATIONS Decrease in Cardiac Output 1. Hypothyroidism: Due to decreased basal metabolic rate 2. Atrial fibrillation: Because of incomplete filling of ventricles 3. Incomplete heart block with coronary sclerosis or myocardial degeneration: Due to defective pumping action of the heart 4. Congestive cardiac failure: Because of weak contractions of heart 5. Shock: Due to poor pumping and circulation 6. Hemorrhage: Because of decreased blood volume. 9 DISTRIBUTION OF CARDIAC OUTPUT  The whole amount of Distribution of Blood blood pumped out by Pumped out of Left the right ventricle goes Ventricle to lungs.  But, the blood pumped by the left ventricle is distributed to different parts of the body.  Fraction of cardiac output distributed to a particular region or organ depends upon the metabolic activities of that region or organ. 10 FACTORS MAINTAINING CARDIAC OUTPUT  Cardiac output is maintained (determined) by four factors:  1. Venous return  2. Force of contraction  3. Heart rate  4. Peripheral resistance 11 FACTORS MAINTAINING CARDIAC OUTPUT Venous return  It is the amount of blood which is returned to heart from different parts of the body.  Cardiac output is directly proportional to venous return, provided the other factors remain constant. Venous return in turn, depends upon five factors:  i. Respiratory pump  ii. Muscle pump  iii. Gravity  iv. Venous pressure  v. Sympathetic tone. 12  FACTORS MAINTAINING CARDIAC OUTPUT Venous return Respiratory pump It is the respiratory activity that helps the return of blood, to heart during inspiration. It is also called abdominothoracic pump.  Intrathoracic pressure becomes more negative leads to increase in diameter of inferior vena cava, resulting in increased venous return.  Intra-abdominal pressure increases by the descent of diaphragm , which compresses abdominal veins and pushes the blood upward and the venous return is increased  Respiratory pump is much stronger in forced respiration and in severe muscular exercise. 13  FACTORS MAINTAINING CARDIAC OUTPUT Venous return Muscle pump  It is the muscular activity that helps in return of the blood to heart. There are two main factors :  Vein compression by contracting muscles resulting in pushing the blood  Venous valves which maintain the direction of blood flow up towards the heart 14  FACTORS MAINTAINING CARDIAC OUTPUT Venous return Gravity  Gravitational force reduces the venous return.  When a person stands for a long period, gravity causes pooling of blood in the legs, which is called venous pooling.  The amount of blood returning to heart decreases. Venous pressure  There is a pressure gradient at every part of venous tree helps as a driving force for venous return in form of gradual decrese from the smallest to the larger  Pressure in the venules is 12 to 18 mm Hg.  In IVC and SVC, the pressure falls to about 5.5 mm Hg.  In the RA is still low. It falls to zero during atrial diastole. Sympathetic tone  Venous return is aided by sympathetic or vasomotor tone which causes constriction of venules which pushes the blood towards heart. 15  FACTORS MAINTAINING CARDIAC OUTPUT FORCE OF CONTRACTION  Cardiac output is directly proportional to the force of contraction, provided the other three factors remain constant.  According to Frank-Starling law, (force of contraction of heart is directly proportional to the initial length of muscle fibers, before the onset of contraction.)  It depends upon preload and afterload. Preload  Preload is the stretching of the cardiac muscle fibers at the end of diastole, just before contraction.  Stretching of muscle fibers increases their length, which increases the force of contraction and cardiac output. Afterload  Afterload is the force against which ventricles must contract and eject the blood , which determined by the arterial pressure.  The ventricles have to work against this pressure for further ejection.  Force of contraction of heart and cardiac output are inversely proportional to afterload. 16 FACTORS MAINTAINING CARDIAC OUTPUT HEART RATE  Cardiac output is directly proportional to heart rate provided, the other three factors remain constant.  Moderate change in heart rate does not alter the cardiac output.  If there is a marked increase in heart rate, cardiac output is increased.  If there is marked decrease in heart rate, cardiac output is decreased. 17  FACTORS MAINTAINING CARDIAC OUTPUT PERIPHERAL RESISTANCE  It is the resistance offered to blood flow at the peripheral blood vessels against which the heart has to pump the blood.  Cardiac output is inversely proportional to it.  It is offered at arterioles so, called resistant vessels.  It is maximum at the splanchnic region. 18 Heart Rate 19  Heart Rate NORMAL HEART RATE  Normal heart rate is 72/minute. It ranges between 60 and 80 per minute. TACHYCARDIA  Tachycardia is the increase in heart rate above 100/minute. Physiological causes of Tachycardia 1. Childhood 2. Exercise 3. Pregnancy 4. Emotional conditions such as anxiety. Pathological causes of Tachycardia 1. Fever 2. Anemia 3. Hypoxia 4. Hyperthyroidism 5. Hypersecretion of catecholamines 6. Cardiomyopathy 7. Diseases of heart valves. 8. Drugs (e.g. bet agonists ) 20 Heart Rate BRADYCARDIA  Bradycardia is the decrease in heart rate below 60/minute. Physiological causes of Bradycardia 1. Sleep 2. Athletes. Pathological causes of Bradycardia 1. Hypothermia 2. Hypothyroidism 3. Heart attack 4. Congenital heart disease 5. Degenerative process of aging 6. Obstructive jaundice 7. Increased intracranial pressure 8. Drugs (e.g. bet blockers ) 21 Heart Rate REGULATION OF HEART RATE.  Heart rate is subjected for variation during normal physiological conditions such as exercise, emotion, etc.  However, the altered heart rate is quickly brought back to normal.  Heart rate is regulated by the nervous mechanism, which consists of three components: A. Vasomotor center B. Motor (efferent) nerve fibers to the heart C. Sensory (afferent) nerve fibers from the heart 22 Heart Rate REGULATION OF HEART RATE Vasomotor center  It is the nervous center that regulates the heart rate.  It also regulates the blood pressure. It is also called the cardiac center.  It is bilaterally situated in the reticular formation of medulla oblongata and lower part of pons  It is formed by three areas: 1. Vasoconstrictor area 2. Vasodilator area 3. Sensory area. 23  Heart Rate REGULATION OF HEART RATE Vasomotor center Vasoconstrictor area  It is situated in the reticular formation of medulla oblongata in floor of IV ventricle and it forms the lateral portion of vasomotor center.  It is otherwise known as pressor area or cardioaccelerator center.  It increases the heart rate by sending accelerator impulses to heart, through sympathetic nerves.  It also causes constriction of blood vessels.  Stimulation of this center in animals increases the heart rate and its removal or destruction decreases the heart rate.  It is under the control of hypothalamus and cerebral cortex. 24  Heart Rate REGULATION OF HEART RATE Vasomotor center Vasodilator area  It is also situated in the reticular formation of medulla oblongata in the floor of IV ventricle.  It forms the medial portion of vasomotor center.  It is also called depressor area or cardioinhibitory center.  It decreases the heart rate by sending inhibitory impulses to heart through vagus nerve.  It also causes dilatation of blood vessels.  Stimulation of this area in animals with weak electric stimulus decreases the heart rate and stimulation with a strong stimulus stops the heartbeat.  When this area is removed or destroyed, heart rate increases.  Vasodilator area is under the control of cerebral cortex and hypothalamus.  It is also controlled by the impulses from baroreceptors, chemoreceptors and other sensory impulses via afferent nerves. 25  Heart Rate Vasomotor center SENSORY AREA  It is in the posterior part of vasomotor center, which lies in nucleus of tractus solitarius in medulla and pons.  It receives sensory impulse via glossopharyngeal nerve and vagus nerve from periphery, particularly, from the baroreceptors.  In turn, this area controls the vasoconstrictor and vasodilator areas. 26 27  Heart Rate Motor (efferent) nerve fibers to the heart Heart receives efferent nerves from both the divisions of autonomic nervous system.  Parasympathetic fibers arise from the medulla oblongata and pass through vagus nerve.  Sympathetic fibers arise from upper thoracic (T1 to T4) segments of spinal cord. 28 29  Heart Rate Motor (efferent) nerve fibers to the heart PARASYMPATHETIC NERVE FIBERS  They are the cardioinhibitory nerve fibers.  They proceed through branch of vagus nerve.  They arise from the dorsal nucleus of vagus. In the floor of fourth ventricle in medulla oblongata and is near to vasodilator area.  They reach the heart by passing through the main trunk of vagus and cardiac branch of vagus and terminate on postganglionic neurons which innervate heart muscle.  Most of the fibers from right vagus terminate in sinoatrial (SA) node and Remaining fibers supply the atrial muscles and atrioventricular (AV) node.  Most of the fibers from left vagus supply AV node and some fibers supply the atrial muscle and SA node.  Ventricles do not receive the vagus nerve supply.  Few fibers are located in the bases of ventricles, but the functions of these nerve fibers are not known. 30  Heart Rate Motor (efferent) nerve fibers to the heart PARASYMPATHETIC NERVE FIBERS Vagal Tone It is the continuous stream of inhibitory impulses from vasodilator area to heart via vagus nerve.  Heart rate is kept under control because of vagal tone.  Heart rate is inversely proportional to vagal tone.  In experimental animals (dog), removal of vagal input (by sectioning vagus) increases the heart rate.  Under resting conditions, vagal tone dominates sympathetic tone.  Impulses from different parts of the body regulate the heart rate through vasomotor center, by altering the vagal tone.  Vagal tone is also called cardioinhibitory tone or parasympathetic tone.  Vagus nerve inhibits the heart by secreting the neurotransmitter substance known as acetylcholine. 31  Heart Rate Motor (efferent) nerve fibers to the heart SYMPATHETIC NERVE FIBERS  They have cardioacceleratory function.  They arise from lateral gray horns of the first 4 thoracic (T1 to T4) segments of the spinal cord.  These segments of the spinal cord receive fibers from vasoconstrictor area of vasomotor center.  They reach the superior, middle and inferior cervical sympathetic ganglia situated in the sympathetic chain. Which fuses with first thoracic sympathetic ganglion, forming stellate ganglion. From which the postganglionic fibers arise and form three nerves:  1. Superior cervical sympathetic nerve, which innervates larger arteries and base of the heart  2. Middle cervical sympathetic nerve, which supplies the rest of the heart  3. Inferior cervical sympathetic nerve, which serves as sensory (afferent) nerve from the heart  Sympathetic Tone  It is the continuous stream of impulses produced by the vasoconstrictor area.  Impulses pass through sympathetic nerves and accelerate the heart rate due to the release of neurotransmitter substance, noradrenaline 32 Heart Rate SENSORY (AFFERENT) NERVE FIBERS FROM HEART They pass through inferior cervical sympathetic nerve and carry sensations of stretch and pain from the heart to brain via spinal cord. 33 34 CIRCULATION Prepared by Dr Ismaeel AlShoaibi BLOOD VESSELS  ARTERIAL SYSTEM Arterial system comprises the aorta, arteries and arterioles. Walls of the aorta and arteries are formed by three layers:  1. Outer tunica adventitia, which is made up of connec tive tissue layer. It is the continuation of fibrous layer of parietal pericardium.  2. Middle tunica media, which is formed by smooth muscles  3. Inner tunica intima, which is made up of endothelium. It is the continuation of endocardium. Aorta, arteries and arterioles have two laminae of elastic tissues:  i. External elastic lamina between tunica adventitia and tunica media  ii. Internal elastic lamina between tunica media and tunica intima. Aorta and arteries have more elastic tissues and the arterioles have more smooth muscles BLOOD VESSELS  ARTERIAL SYSTEM Aorta has got the maximum diameter of about 25 mm. Diameter of the arteries is gradually decreased and at the end arteries, it is about 4 mm. It further decreases to 30 μ in the arterioles and ends up with 10 μ in the terminal arterioles.  Resistance (peripheral resistance) is offered to blood flow in the arterioles (resistant vessels).  Arterioles are continued as capillaries, which are small, thin walled vessels having a diameter of about 5 to 8 μ.  Capillaries are functionally very important because, the exchange of materials between the blood and the tissues occurs through these vessels. BLOOD VESSELS  VENOUS SYSTEM From the capillaries, venous system starts and it includes venules, veins and venae cavae. Capillaries end in venules, which are the smaller vessels with thin muscular wall than the arterioles. Diameter of the venules is about 20 μ. At a time, a large quantity of blood is held in venules ( capacitance vessels). Venules are continued as veins, which have the diameter of 5 mm. Veins form superior and inferior venae cavae, which have a diameter of about 30 mm.  Walls of the veins and venae cavae are made up of inner endothelium, elastic tissues, smooth muscles and outer connective tissue layer.  In the veins and venae cavae, the elastic tissue is less but the smooth muscle fibers are more. DIVISIONS OF CIRCULATION Blood flows through two divisions of circulatory system:  1. Systemic circulation  2. Pulmonary circulation. SYSTEMIC CIRCULATION  Know as the greater circulation  Blood pumped from left ventricle passes through a series of blood vessels, arterial system and reaches the tissues.  Exchange of various substances between blood and the tissues occurs at the capillaries.  After exchange of materials, blood enters the venous system and returns to right atrium of the heart.  From right atrium, blood enters the right ventricle.  Thus, oxygenated blood is supplied from heart to the tissues and venous blood returns to the heart from tissues. DIVISIONS OF CIRCULATION  PULMONARY CIRCULATION Known as the lesser circulation.  Blood is pumped from right ventricle to lungs through pulmonary artery.  Exchange of gases occurs between blood and alveoli of the lungs at pulmonary capillaries.  Oxygenated blood returns to left atrium through the pulmonary veins.  Thus, left side of the heart contains oxygenated or arterial blood and the right side of the heart contains deoxygenated or venous blood. ARTERIAL BLOOD PRESSURE DEFINITIONS AND NORMAL VALUES  It is defined as the lateral pressure exerted by the column of blood on wall of arteries.  It is exerted when blood flows through the arteries.  Generally, the term ‘blood pressure’ refers to arterial blood pressure.  It is expressed in four different terms: 1. Systolic blood pressure 2. Diastolic blood pressure 3. Pulse pressure 4. Mean arterial blood pressure. ARTERIAL BLOOD PRESSURE SYSTOLIC BLOOD PRESSURE  It is defined as the maximum pressure exerted in the arteries during systole of heart.  Normal systolic pressure: 120 mm Hg (100 mm Hg to >140 mm Hg). DIASTOLIC BLOOD PRESSURE  It is defined as the minimum pressure exerted in the arteries during diastole of heart.  Normal diastolic pressure: 80 mm Hg (60 mm Hg to >80 mm Hg). PULSE PRESSURE  It is the difference between the systolic pressure and diastolic pressure.  Normal pulse pressure: 40 mm Hg (120 – 80 = 40). ARTERIAL BLOOD PRESSURE MEAN ARTERIAL BLOOD PRESSURE  It is the average pressure existing in the arteries.  It is the diastolic pressure plus one third of pulse pressure.  To determine the mean pressure, diastolic pressure is considered than the systolic pressure.  It is because, the diastolic period of cardiac cycle is longer (0.53 second) than the systolic period (0.27 second).  Normal mean arterial pressure: 93 mm Hg (80 + 13 = 93).  Formula to calculate mean arterial blood pressure:  a ARTERIAL BLOOD PRESSURE VARIATIONS  Blood pressure is altered in physiological and pathological conditions.  Systolic pressure is subjected for variations easily and quickly and its variation occurs in a wider range.  Diastolic pressure is not subjected for easy and quick variations and its variation occurs in a narrow range ARTERIAL BLOOD PRESSURE PHYSIOLOGICAL VARIATIONS 1. Age  Arterial blood pressure increases as age advances.  Systolic pressure in different age  Diastolic pressure in  Newborn : 70 mm Hg different age  After 1 month : 85 mm Hg  Newborn : 40 mm Hg  After 6 month : 90 mm Hg  After 1 month : 45 mm  After 1 year : 95 mm Hg Hg  At puberty : 120 mm Hg  After 6 month : 50 mm  At 50 years : 140 mm Hg Hg  At 70 years : 160 mm Hg  At 80 years : 180 mm Hg  After 1 year : 55 mm Hg  At puberty : 80 mm Hg  At 50 years : 85 mm Hg ARTERIAL BLOOD PRESSURE 2. Sex  In females, up to the period of menopause, arterial pressure is 5 mm Hg, less than in males of same age.  After menopause, the pressure in females becomes equal to that in males of same age. 3. Body Built  Pressure is more in obese persons than in lean persons. 4. Diurnal Variation  In early morning, the pressure is slightly low.  It gradually increases and reaches the maximum at noon.  It becomes low in evening. ARTERIAL BLOOD PRESSURE 5. After Meals  Arterial blood pressure is increased for few hours after meals due to increase in cardiac output. 6. During Sleep  Usually, the pressure is reduced up to 15 to 20 mm Hg during deep sleep.  It increases slightly during sleep associated with dreams.  7. Emotional Conditions  During excitement or anxiety, the blood pressure is increased due to release of adrenaline. ARTERIAL BLOOD PRESSURE 8. After Exercise  After moderate exercise, systolic pressure increases by 20 to 30 mm Hg above the basal level due to increase in rate and force of contraction and stroke volume.  Normally, diastolic pressure is not affected by moderate exercise because, it depends upon peripheral resistance, which is not altered by moderate exercise.  After severe muscular exercise, systolic pressure rises by 40 to 50 mm Hg above the basal level.  But, the diastolic pressure reduces because the peripheral resistance decreases. ARTERIAL BLOOD PRESSURE PATHOLOGICAL VARIATIONS HYPERTENSION  It is the persistent high blood pressure.  Clinically, when the systolic pressure remains equal or above 140 mm Hg and diastolic pressure remains equal or above 90 mm Hg, it is considered as hypertension.  If there is increase only in systolic pressure, it is called isolated systolic hypertension HYPOTENSION Hypotension is the low blood pressure. When the systolic pressure is less than 100 mm Hg, it is considered as hypotension and or diastolic pressure less than 60 mmHg  ARTERIAL BLOOD PRESSURE FACTORS MAINTAINING ARTERIAL BLOOD PRESSURE These factors are called local factors, mechanical factors or determinants of blood pressure Local factors are divided into two types:  A. Central factors, which are pertaining to the heart: 1. Cardiac output 2. Heart rate  B. Peripheral factors, which are pertaining to blood and blood vessels: 3. Peripheral resistance 4. Blood volume 5. Venous return 6. Elasticity of blood vessels 7. Velocity of blood flow 8. Diameter of blood vessels 9. Viscosity of blood. ARTERIAL BLOOD PRESSURE CENTRAL FACTORS 1. Cardiac Output  Systolic pressure is directly proportional to cardiac output.  Cardiac output increases in muscular exercise, emotional conditions, etc.  So in these conditions, the systolic pressure is increased.  In conditions like myocardial infarction, the cardiac output decreases, resulting in fall in systolic pressure. 2. Heart Rate  Moderate changes in heart rate do not affect arterial blood pressure much.  However, marked alteration in the heart rate affects the blood pressure by altering cardiac output  ARTERIAL BLOOD PRESSURE PERIPHERAL FACTORS 3. Peripheral Resistance  Peripheral resistance is the important factor, which maintains diastolic pressure.  Diastolic pressure is directly proportional to peripheral resistance.  Peripheral resistance is the resistance offered to the blood flow at the periphery.  Resistance is offered at arterioles, which are called the resistant vessels. 4. Blood Volume  Blood pressure is directly proportional to blood volume.  Blood volume maintains the blood pressure through the venous return and cardiac output.  If the blood volume increases, there is an increase in venous return and cardiac output, resulting in elevation of blood pressure 5. Venous Return  Blood pressure is directly proportional to venous return.  When venous return increases, there is an increase in ventricular filling and cardiac output, resulting in elevation of arterial blood pressure. ARTERIAL BLOOD PRESSURE PERIPHERAL FACTORS 6. Elasticity of Blood Vessels  Blood pressure is inversely proportional to the elasticity of blood vessels.  Due to elastic property, the blood vessels are distensible and are able to maintain the pressure.  When the elastic property is lost, the blood vessels become rigid (arteriosclerosis) and pressure increases as in old age.  Deposition of cholesterol, fatty acids and calcium ions produce rigidity of blood vessels and atherosclerosis, leading to increased blood pressure. 7. Velocity of Blood Flow  Pressure in a blood vessel is directly proportional to the velocity of blood flow.  If the velocity of blood flow increases, the resistance is increased.  So, the pressure is increased.  ARTERIAL BLOOD PRESSURE PERIPHERAL FACTORS 8. Diameter of Blood Vessels  Arterial blood pressure is inversely proportional to the diameter of blood vessel.  If the diameter decreases, the peripheral resistance increases, leading to increase in the pressure. 9. Viscosity of Blood  Arterial blood pressure is directly proportional to the viscosity of blood.  When viscosity of blood increases, the frictional resistance is increased and this increases the pressure. ARTERIAL BLOOD PRESSURE REGULATION OF ARTERIAL BLOOD PRESSURE  Arterial blood pressure varies even under physiological conditions.  However, immediately it is brought back to normal level because of the presence of well organized regulatory mechanisms in the body  ARTERIAL BLOOD PRESSURE  NERVOUS MECHANISM FOR REGULATION OF BLOOD PRESSURE  It is rapid among all the mechanisms of regulation  It brings the pressure back to normal within few minutes.  It operates only for a short period and then it adapts to the new pressure.  Hence, it is called short-term regulation.  It operates through the vasomotor system. Vasomotor system includes three components: 1. Vasomotor center 2. Vasoconstrictor fibers 3. Vasodilator fibers. ARTERIAL BLOOD PRESSURE VASOMOTOR CENTER Its effect on Bp is similar to that HR  Vasomotor center consists of three areas: i. Vasoconstrictor area the stimulation of this area causes vasoconstriction and rise in arterial blood pressure ii. Vasodilator area This area suppresses the vasoconstrictor area and causes vasodilatation iii. Sensory area it controls the vasoconstrictor and vasodilator areas  ARTERIAL BLOOD PRESSURE VASOCONSTRICTOR FIBERS  They belong to the sympathetic division of autonomic nervous system.  They cause vasoconstriction by the release of neurotransmitter substance, noradrenaline.  Noradrenaline acts through alpha receptors of smooth muscle fibers in blood vessels.  Vasomotor Tone  Vasomotor tone is the continuous discharge of impulses from vasoconstrictor center through the vasoconstrictor fibers.  It plays an important role in regulating the pressure by producing a constant partial state of constriction of the blood vessels.  Thus, the arterial blood pressure is directly proportional to the vasomotor tone.  Vasomotor tone is also called sympathetic vasoconstrictor tone or sympathetic tone. ARTERIAL BLOOD PRESSURE VASODILATOR FIBERS They are of three types: i. Parasympathetic vasodilator fibers ii. Sympathetic vasodilator fibers iii. Antidromic vasodilator fibers. i. Parasympathetic Vasodilator Fibers  They cause dilatation of blood vessels by releasing acetylcholine ii. Sympathetic Vasodilator Fibers  Some of the sympathetic fibers cause vasodilatation in certain areas, by secreting acetylcholine.  They called sympathetic vasodilator or sympathetic cholinergic fibers.  They supply the blood vessels of skeletal muscles, during conditions like exercise.  They form the important part of vasomotor system.  Signals are generated in cerebral cortex then are relayed to lateral gray horn of the spinal cord via hypothalamus, midbrain and medulla.  In the spinal cord, these impulses activate the preganglionic sympathetic fibers, which activate the postganglionic fibers and in turn dilatation of blood vessels by secreting acetylcholine. ARTERIAL BLOOD PRESSURE iii. Antidromic Vasodilator Fibers  Normally, the impulses produced by a cutaneous receptor (like pain receptor) pass through sensory nerve fibers.  But, some of these impulses pass through the other branches of the axon in the opposite direction and reach the blood vessels supplied by these branches and dilate the blood vessels.  It is called the antidromic or axon reflex and the nerve fibers are called antidromic vasodilator fibers  ARTERIAL BLOOD PRESSURE MECHANISM OF ACTION OF VASOMOTOR CENTER IN THE REGULATION OF BLOOD PRESSURE  Vasomotor centers actions depend upon impulses receivds from other structures such as baroreceptors, chemoreceptors, higher centers and respiratory centers  Baroreceptors and chemoreceptors play a major role 1. Baroreceptor Mechanism  They give response to change in blood pressure.  Baroreceptors are also called pressoreceptors. And are situated in the carotid sinus and wall of the aorta  ARTERIAL BLOOD PRESSURE 2. Chemoreceptor Mechanism  They are giving response to change in chemical constituents of blood.  Peripheral chemoreceptors influence the vasomotor center.  They are situated in the carotid body and aortic body  They are sensitive to lack of oxygen, excess of carbon dioxide and hydrogen ion concentration in blood.  Whenever blood pressure decreases, blood flow to chemoreceptors decreases, resulting in decreased oxygen content and excess of carbon dioxide and hydrogen ion.  These factors excite the chemoreceptors, which send impulses to stimulate vasoconstrictor center.  Blood pressure rises and blood flow increases.  Chemoreceptors play a major role in maintaining respiration rather than blood pressure Sinoaortic mechanism  Mechanism of action of baroreceptors and chemoreceptors in carotid and aortic region constitute sinoaortic mechanism.  Nerves supplying the baroreceptors and chemoreceptors are called buffer nerves because these nerves regulate the heart rate , blood pressure and respiration ARTERIAL BLOOD PRESSURE 3. Higher Centers  Vasomotor center is also controlled by the impulses from the two higher centers in the brain. i. Cerebral cortex ii. Hypothalamus 4. Respiratory Centers  During the beginning of expiration, arterial blood pressure increases slightly, i.e. by 4 to 6 mm Hg.  It decreases during later part of expiration and during inspiration because of two factors: i. Radiation of impulses from respiratory centers towards vasomotor center at different phases of respiratory cycle ii. Pressure changes in thoracic cavity, leading to alteration of venous return and cardiac output ARTERIAL BLOOD PRESSURE RENAL MECHANISM FOR REGULATION OF BLOOD PRESSURE  Kidneys play an important role in the longterm regulation of arterial blood pressure.  When blood pressure alters slowly in several days/months/years,.  In such conditions, the renal mechanism operates efficiently to regulate the blood pressure.  Therefore, it is called longterm regulation.  Kidneys regulate arterial blood pressure by two ways: 1. By regulation of ECF volume 2. Through reninangiotensin mechanism. ARTERIAL BLOOD PRESSURE REGULATION OF EXTRACELLULAR FLUID VOLUME  When the blood pressure increases, kidneys excrete large amounts of water and salt, particularly sodium, by means of pressure diuresis and pressure natriuresis.  Even a slight increase in blood pressure doubles the water excretion.  Pressure natriuresis is the excretion of large quantity of sodium in urine.  This result in a decrease in ECF volume and blood volume,  Arterial blood pressure back to normal level.  When blood pressure decreases, the reabsorption of water from renal tubules is increased.  This in turn, increases ECF volume, blood volume and cardiac output, resulting in restoration of blood pressure.  ARTERIAL BLOOD PRESSURE RENIN-ANGIOTENSIN MECHANISM  When blood pressure and ECF volume decrease, renin secretion from kidneys is increased.  It converts angiotensinogen into angiotensin I.  This is converted into angiotensin II by ACE (angiotensinconverting enzyme).  Like angiotensin II, the angiotensins III and IV also increase the blood pressure and stimulate adrenal cortex to secrete aldosterone  HORMONAL MECHANISM FOR REGULATION OF BLOOD PRESSURE LOCAL MECHANISM FOR REGULATION OF BLOOD PRESSURE CORONARY BLOOD FLOW NORMAL CORONARY BLOOD FLOW  Normal blood flow through coronary circulation is about 200 mL/minute.  It forms 4% of cardiac output.  It is about 65 to 70 mL/minute/100 g of cardiac muscle. MEASUREMENT OF CORONARY BLOOD FLOW Direct Method  It is measured by using an electromagnetic flowmeter. It is directly placed around any coronary artery Indirect Method 1. By Fick principle (the amount of a substance taken up by an organ (or the whole body) per unit time is the product of the arteriovenous concentration difference by the blood flow to the organ (or body) ) Coronary blood flow is measured by applying Fick principle using nitrous oxide (N O). The subject is asked to inhale a known quantity of the gas with 2 atmospheric air. Then, blood samples are collected from an artery and from coronary sinus, by using a catheter. The blood flow is determined by using the formula: CORONARY BLOOD FLOW MEASUREMENT OF CORONARY BLOOD FLOW 2. By using Doppler flowmeter Piezoelectric crystals are used in the Doppler flowmeter probe, to transmit and receive the pulses of high frequency sound waves. The Doppler flowmeter probe is mounted to a catheter and positioned at the ostium of right or left coronary artery to measure the velocity of phasic flow of blood. The cross-sectional area of the artery is determined by angiography. From velocity of blood flow and cross-sectional area, the volume of blood flow is calculated. 3. By videodensitometry It is the technique used to measure both velocity of blood flow and the cross-sectional area of coronary arteries, simultaneously. From these two values, the coronary blood flow can be calculated.  CORONARY BLOOD FLOW PHASIC CHANGES IN CORONARY BLOOD FLOW Blood flow through coronary arteries is not constant.  It decreases during systole and increases during diastole  Intramural vessels or final arteries supplying myocardium are perpendicular to the cardiac muscles.  So, during systole, the intramural vessels are compressed and blood flow is reduced. During diastole, the compression is released and the blood vessels are distended. So, the blood flow increases. CORONARY BLOOD FLOW FACTORS REGULATING CORONARY BLOOD FLOW Autoregulation  Like any other organ, heart also has the capacity to regulate its own blood flow by autoregulation.  Coronary blood flow is not affected when mean arterial pressure varies between 60 and 150 mm Hg. Several factors are involved in the autoregulation mechanism :  1. Need for oxygen  2. Metabolic factors  3. Coronary perfusion pressure  4. Nervous factors. CORONARY BLOOD FLOW NEED FOR OXYGEN  Oxygen is the most important factor maintaining blood flow through the coronary blood vessels.  Amount of blood passing through coronary circulation is directly proportional to the consumption of oxygen by cardiac muscle.  Thus, the need for oxygen, i.e. hypoxia immediately causes coronary vasodilatation and increases the blood flow to heart. CORONARY BLOOD FLOW METABOLIC FACTORS  Coronary vasodilatation during hypoxic conditions occurs because of some metabolic products causing so called Reactive Hyperemia  Metabolic Products which Increase the Coronary Blood Flow  Adenosine is a potent vasodilator and it increases the blood flow to cardiac muscle. It is a degradation product of ADP.  Other substances :  i. Potassium  ii. Hydrogen  iii. Carbon dioxide  iv. Adenosine phosphate compounds CORONARY BLOOD FLOW CORONARY PERFUSION PRESSURE  Perfusion pressure is the balance between mean arterial pressure and venous pressure.  Thus, coronary perfusion pressure is the balance between mean arterial pressure in aorta and the right atrial pressure. Since right atrial pressure is low, the mean arterial pressure becomes the major factor that maintains the coronary blood flow. CORONARY BLOOD FLOW NERVOUS FACTORS  Coronary blood vessels are innervated both by parasympathetic and sympathetic divisions of autonomic nervous system.  It is not known whether they have direct effect on blood flow.  However, they have indirect effect by acting on the musculature of heart.  For example, stimulation of sympathetic nerves increases the rate and force of contraction of heart causing liberation of more metabolites which dilate the blood vessels and increase the coronary blood flow.  Similarly, when parasympathetic nerves are stimulated, the cardiac functions are inhibited and the production of metabolites is less. Coronary blood flow decreases.  CIRCULATION 2 Prepared by Dr Ismaeel AlShoaibi VENOUS PRESSURE DEFINITION AND NORMAL VALUES  Venous pressure is the pressure exerted by the contained blood in the veins.  The pressure in vena cava and right atrium is called central venous pressure.  The pressure in peripheral veins is called peripheral venous pressure.  It varies in different veins in the extremities of the body and also varies from central veins to peripheral veins. VENOUS PRESSURE IN EXTREMITIES OF THE BODY  It is less above the level of the heart and it is more in parts below the level of the heart  It is in Jugular vein: 5.1 mm Hg (6.9 cm H O)2  Dorsal venous arch of foot: 13.2 mm Hg (17.9 cm H O). 2  Note (1 mm Hg pressure = 1.359 cm H O pressure) 2 VENOUS PRESSURE VENOUS PRESSURE IN EXTREMITIES OF THE BODY  It is less above the level of the heart and it is more in parts below the level of the heart  It is in Jugular vein: 5.1 mm Hg (6.9 cm H2O)  Dorsal venous arch of foot: 13.2 mm Hg (17.9 cm H2O).  Note (1 mm Hg pressure = 1.359 cm H2O pressure) VENOUS PRESSURE IN CENTRAL AND PERIPHERAL VEINS  Pressure is greater in peripheral veins than in central veins.  Pressure in: Antecubital vein: 7.1 mm Hg (9.6 cm H2O)  Superior vena cava: 4.6 mm Hg (6.2 cm H2O). VENOUS PRESSURE VARIATIONS OF VENOUS PRESSURE PHYSIOLOGICAL VARIATIONS  It increases in: 1. Changing from standing to supine position 2. Tilting the body 3. Forced expiration (Valsalva maneuver) 4. Contraction of abdominal and limb muscles 5. Prolonged travelling or standing 6. Excitement. VENOUS PRESSURE PATHOLOGICAL VARIATIONS  It increases in: 1. Low cardiac output 2. Congestive heart failure 3. Venous obstruction 4. Failure of valves in veins 5. Paralysis of muscles 6. Immobilization of parts of body 7. Renal failure.  It decreases in: 1. Severe hemorrhage 2. Surgical shock VENOUS PRESSURE FACTORS REGULATING VENOUS PRESSURE 1. LEFT VENTRICULAR CONTRACTION OR VIS A TERGO  LV contraction is also called vis a tergo or force from behind.  It forces the blood through the arteries, arterioles, capillaries and veins to the right atrium. Venous pressure is directly proportional to LV pressure.  By the time blood passes through capillaries and reaches the venules, the pressure becomes less than 8 mm Hg and when it reaches right atrium, the pressure may be less than 1 mm Hg. 2. RIGHT ATRIAL PRESSURE OR VIS A FRONTE  Right atrial pressure is also called vis a fronte or force from front.  It determines the venous return.  It is also called central venous pressure, which in turn regulates the peripheral venous pressure.  Normal right atrial pressure is 0 mm Hg VENOUS PRESSURE FACTORS REGULATING VENOUS PRESSURE 3. RESISTANCE OR VIS A LATRE  Resistance offered to blood flow through the veins is also called vis a latre or force from side.  Venous pressure is directly proportional to the resistance, which is due to venous tone and extravascular factors. Because of the thin-walled nature, veins and venules are compressed by the extravascular factors such as: i. Compression of arm vein while passing over first rib ii. Compression of neck veins in erect posture due to fall in pressure and by atmospheric pressure iii. Compression of abdominal veins by increased intra- abdominal pressure iv. Compression of veins while passing in between the muscles. VENOUS PRESSURE 4. VOLUME OF VENOUS BLOOD  It is directly proportional to the volume of blood in the venous system. 5. PERIPHERAL RESISTANCE  It is inversely proportional to peripheral resistance. When peripheral resistance is more, arterioles constrict and the veins are filled with less blood. Hence, the pressure decreases.  When peripheral resistance is less, the veins are filled with more blood and venous pressure increases. 6. GRAVITY AND POSTURE  Pressure is more in the veins below the level of heart and the pressure is less in veins above the level of heart.  Weight of the column of blood in veins influences the venous pressure.  During prolonged standing, the pressure in lower extremities is more (90 cm H O). It is because of pooling of blood in the legs due to gravity. 2  It increases the weight of the column of blood, leading to increase in pressure. During the movement, the venous pressure in foot decreases.  In head region, the venous pressure is –10 cm H O because of the 2 hydrostatic suction below the skull.  So, there is always a negative venous pressure in the head.  VENOUS PRESSURE EFFECT OF RESPIRATION ON VENOUS PRESSURE  The central venous pressure is altered in accordance with intrathoracic pressure.  Thus, during inspiration, it decreases because of decreased intrathoracic pressure.  During expiration, it increases.  The effect of respiration on it is demonstrated by some procedures such as Valsalva maneuver and Mueller maneuver. VENOUS PRESSURE VALSALVA MANEUVER  It is the forced expiratory effort with closed glottis.  It is performed by attempting to exhale forcibly, while keeping the mouth and nose closed. MÜELLER MANEUVER  It is the forced inspiratory effort with closed glottis.  It is performed by attempting to inhale forcibly, while keeping the mouth and nose closed. It is also called reverse Valsalva maneuver. CAPILLARY PRESSURE  It is the pressure exerted by the blood contained in capillary also called capillary hydrostatic pressure.  It is responsible for the exchange of various substances between blood and interstitial fluid through capillary wall.  In the arterial end it is about 30 to 32 mm Hg  In venous end it is 15 mm Hg.  It varies depending upon the function of the organ or region of the body. CAPILLARY PRESSURE REGIONAL VARIATIONS  It is in relation to the physiological activities of the particular region.  It has some functional significance.  Capillary pressure remarkably varies in kidneys and lungs. Capillary Pressure in Kidneys  The glomerular capillary pressure is high.  It is about 60 mm Hg.  It is responsible for glomerular filtration. Capillary Pressure in Lungs  It is low and it is about 7 mm Hg.  It favors exchange of gases between blood and alveoli.  CAPILLARY PRESSURE REGULATION  Arterioles play an important role and the pressure in capillaries is considered as a function of arteriolar resistance.  CAPILLARY PRESSURE CAPILLARY ONCOTIC PRESSURE  Capillary membrane is permeable to all substances except plasma proteins.  So, the plasma proteins stay within the capillaries and exert some pressure which is called oncotic pressure or colloidal osmotic pressure.  It is about 25 mm Hg.  Among the plasma proteins, albumin exerts 70% of oncotic pressure.  It plays an important role in filtration across capillary membrane, particularly in renal glomerular capillaries.  CEREBRAL CIRCULATION  Brain tissues need adequate blood supply continuously.  Stoppage of blood flow to brain for 5 seconds leads to unconsciousness and for 5 minutes leads to irreparable damage to the brain cells. CEREBRAL VESSELS AND NORMAL CEREBRAL BLOOD FLOW  Brain receives blood from the basilar artery and internal carotid artery which form circle of Willis.  Venous drainage is by sinuses, which open into internal jugular vein.  Normally, brain receives 750 to 800 mL of blood per minute.  It is about 15% to 16% of total cardiac output and about 50 to 55 mL/100 g of brain tissue per minute. CEREBRAL CIRCULATION REGULATION OF CEREBRAL BLOOD FLOW  It is regulated by three factors:  1. Autoregulation  2. Chemical factors  3. Neural factors.  CEREBRAL CIRCULATION AUTOREGULATION  The autoregulation in brain has got its own limitations.  It depends upon: i. Effective perfusion pressure ii. Cerebral vascular resistance.  Cerebral blood flow is directly proportional to the balance between both. CEREBRAL CIRCULATION i. Effective Perfusion Pressure  It is the balance between the mean arterial blood pressure and venous pressure across the organ, divided by resistance.  Since venous pressure is zero in brain, mean arterial blood pressure plays an important role in regulating cerebral blood flow.  Autoregulation is possible in brain if the mean arterial pressure is within the range of 60 mm Hg and 140 mm Hg.  Autoregulation fails beyond this range on either side. ii. Cerebral Vascular Resistance  When the vascular resistance is more, the blood flow to the brain is less.  It is offered by intracranial pressure, cerebrospinal fluid pressure and viscosity of blood Intracranial pressure and cerebrospinal fluid pressure  Increase in the intracranial pressure or the pressure exerted by the cerebrospinal fluid (CSF) compresses the cerebral blood vessels and decreases blood flow.  These pressures are elevated in conditions like head injury.  However, severe ischemic effects are avoided by some protective reflexes such as Cushing reflex  CEREBRAL CIRCULATION Cushing reflex  It is also called Cushing reaction, response or phenomenon.  Increase in intracranial pressure or increase in CSF pressure compresses the cerebral blood vessels and decreases the blood flow.  However, blood flow is decreased only for a short period.  It is restored immediately by means of Cushing reflex.  When cerebral blood flow decreases by the compression of cerebral arteries, the cerebral ischemia develops.  Compression of blood vessels decreases the blood flow to vasomotor center also.  Local hypoxia and hypercapnea activate vasomotor center, resulting in peripheral vasoconstriction and rise in the arterial pressure.  The increased arterial pressure helps to restore the cerebral blood flow.  Thus, Cushing reflex plays the most important role in maintaining the cerebral blood flow CEREBRAL CIRCULATION CHEMICAL FACTORS  Chemical factors which increase the cerebral blood flow:  i. Decreased oxygen tension  ii. Increased carbon dioxide tension  iii. Increased hydrogen ion concentration.  Carbon dioxide is the most important factor, as it causes dilatation of cerebral blood vessels, leading to increase in blood flow. A moderate increase in carbon dioxide tension does not alter the blood flow due to autoregulation.  When arterial partial pressure of carbon dioxide rises above 45 mm Hg, the cerebral blood flow increases.  Carbon dioxide combines with water to form carbonic acid, which dissociates into bicarbonate ions and hydrogen ion.  The hydrogen ion causes dilatation of blood vessels in brain.  Hypoxia increases cerebral blood flow by vasodilatation. CEREBRAL CIRCULATION NERVOUS FACTORS  Cerebral blood vessels are supplied by sympathetic vasoconstrictor fibers.  But, these fibers do not play any role in regulating cerebral blood flow under normal conditions.  In pathological conditions like hypertension, the sympathetic nerves cause constriction of cerebral blood vessels, leading to reduction in blood flow.  It prevents cerebral vascular hemorrhage and cerebral stroke SPLANCHNIC CIRCULATION  Splanchnic or visceral circulation constitutes three portions: 1. Mesenteric circulation supplying blood to GI tract 2. Splenic circulation supplying blood to spleen 3. Hepatic circulation supplying blood to liver.  Unique feature of splanchnic circulation is that the blood from mesenteric bed and spleen forms a major amount of blood flowing to liver.  Blood flows to liver from GI tract and spleen through portal system.  SPLANCHNIC CIRCULATION MESENTERIC CIRCULATION DISTRIBUTION OF BLOOD FLOW  Stomach : 35 mL/100 g/minute  Intestine : 50 mL/100 g/minute  Pancreas : 80 mL/100 g/minute.  SPLANCHNIC CIRCULATION REGULATION OF MESENTERIC BLOOD FLOW  It is regulated by the following factors: 1. Local Autoregulation  Local autoregulation is the primary factor regulating blood flow through mesenteric bed. 2. Activity of Gastrointestinal Tract  Contraction of the wall of the GI tract reduces blood flow.  Relaxation of wall of GI tract increases the blood flow. 3. Nervous Factor  It is regulated by sympathetic nerve fibers.  Increase in sympathetic activity as in the case of emotional conditions or ‘fight and flight reactions’ constrict the mesenteric blood vessels.  So, more blood is diverted to organs like skeletal muscles, heart and brain.  Parasympathetic nerves do not have any direct action on the mesenteric blood vessels.  But these nerves increase the contraction of GI tract which compresses the blood vessels, resulting in reduction in blood flow. SPLANCHNIC CIRCULATION REGULATION OF MESENTERIC BLOOD FLOW 4. Chemical Factors – Functional Hyperemia  Functional hyperemia is the increase in mesenteric blood flow immediately after food intake.  It is mainly because of gastrin and cholecystokinin secreted after food intake.  In addition to these two GI hormones, digestive products of food substances such as glucose and fatty acids also cause vasodilatation and increase the mesenteric blood flow.  SPLANCHNIC CIRCULATION SPLENIC CIRCULATION IMPORTANCE OF SPLENIC CIRCULATION  Spleen is the main reservoir for blood.  Due to the dilatation of blood vessels, a large amount of blood is stored in spleen.  And the constriction of blood vessels by sympathetic stimulation releases blood into circulation. STORAGE OF BLOOD  Two structures store blood, namely splenic venous sinuses and splenic pulp which lined with reticuloendothelial cells.  Small arteries and arterioles open directly into the venous sinuses.  When spleen distends, sinuses swell and large quantity of blood is stored.  Capillaries of splenic pulp are highly permeable and most of the blood cells pass through capillary membrane and are stored in the pulp. REGULATION OF BLOOD FLOW TO SPLEEN  Blood flow to spleen is regulated by sympathetic nerve fibers. SPLANCHNIC CIRCULATION HEPATIC CIRCULATION BLOOD VESSELS  Liver receives blood from two sources: 1. Hepatic artery 2. Portal vein. NORMAL BLOOD FLOW  Liver receives maximum amount of blood as compared to any other organ in the body.  Blood flow to liver is 1,500 mL/minute,