Intrinsic Cardiac Conduction System Approximately 1% of cardiac muscle cells are autorhythmic rather than contractile 75/min 40-60/min Approximately 1% of the cardiac muscle cells are autorhythmic rather than contractile. * These specialized cardiac cells don’t contract but are specialized to initiate and conduct impulses through the heart to coordinate its activity. * These constitute the intrinsic cardiac conduction system. These autorhythmic cells constitute the following components of the intrinsic conduction system: * the sinoatrial (SA) node, just inferior to the entrance of the superior vena cava into the right atrium, * the atrioventricular node (AV) node, located just above the tricuspid valve in the lower part of the right atrium, * the atrioventricular bundle (bundle of HIS), located in the lower part of the interatrial septum and which extends into the interventricular septum where it splits into right and left bundle branches * which continue toward the apex of the heart and the purkinje fibers * which branch off of the bundle branches to complete the pathway into the apex of the heart and turn upward to carry conduction impulses to the papillary muscles and the rest of the myocardium. Although all of these are autorhythmic, they have different rates of depolarization. * For instance, the SA node * depolarizes at a rate of 75/min. * The AV node depolarizes at a rate of 40 to 60 beats per minute, * while the rest have an intrinsic rate of around 30 depolarizations/ minute. * Because the SA node has the fastest rate, it serves as the pacemaker for the heart. * 30/min

Intrinsic Conduction System Function: initiate & distribute impulses so heart depolarizes & contracts in orderly manner from atria to ventricles. SA node AV node Bundle of His Purkinje fibers As indicated previously, the function of the intrinsic conduction system is to initiate and distribute impulses so the heart depolarizes and contracts in an orderly manner from atria to ventricles. * As you must be able to identify the parts of the conduction system and trace the path of depolarization from the SA node to the purkinje fibers, we will review this. * Since the SA node * has the highest rate of depolarization (75/min) , it starts the process by sending a wave of depolarization * through the myocardium of the atria. When this reaches the AV node * it depolarizes * and causes the Bundle of His * to depolarize.The depolarization travels into the septum through the bundle branches * * and from the bundle branches into the Purkinje fibers * * which cause depolarization of the ventricular myocardium. When the cardiac muscle cells of the myocardium, including the papillary muscles, the ventricles contract forcing blood out of the ventricles. * Bundle Branches

Atrial repolarization ECG Deflection Waves Atrial repolarization (Pacemaker) As you will be required to draw and label electrocardiogram (ECG) deflection waves and describe what each indicates, let us consider a typical Lead II ECG. An ECG is a recording of the he deflection waves caused by depolarization of the heart. * When the SA node * (the pacemaker) * depolarizes * the wave of depolarization that sweeps through the atria is recorded as the P wave * on the ECG. * The P wave indicates depolarization of the atria. * The QRS complex * is caused by depolarization of the ventricles. * Hidden in the QRS complex * is the repolarization of the atria since that occurs while the ventricles are depolarizing. * The T wave * represents repolarization of the ventricles. *

60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute ECG Deflection Waves 60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute On the ECG, the PQ interval * is the time required for the wave of depolarization to spread through the conduction system from the beginning of atrial excitation to the beginning of ventricular depolarization. * Note that the PQ interval normally takes approximately 0.2 seconds in a resting heart. * The QT interval * represents the period from the beginning of ventricular depolarization through ventricular repolarization. Since the ventricles are so much larger than the atria, this normally takes approximately 0.4 seconds in a resting heart. * Another 0.2 seconds typically occurs before the next T wave. Since this cycle requires approximately 0.8 seconds to complete, 60 seconds divided by 0.8 gives us a resting heart rate * of approximately 75 beats/ minute. A PQ interval longer than 0.2 seconds is indicative of a 1st degree heart block, * meaning that something is delaying the spread of the wave of depolarization through the conduction system. * 1st Degree Heart Block = P-Q interval longer than 0.2 seconds.

ECG Deflection Wave Irregularities Enlarged QRS = Hypertrophy of ventricles Since you may be required to indicate conditions which may alter ECG waves, lets consider several of these. * An enlarged QRS * * is indicative of hypertrophy (enlargement) of the ventricles. * * *

ECG Deflection Wave Irregularities Prolonged QT Interval = A prolonged QT interval * * is indicative of repolarization abnormalities * which increase susceptibility to various ventricular arrhythmias. * Repolarization abnormalities increase chances of ventricular arrhythmias.

ECG Deflection Wave Irregularities Elevated T wave : Hyperkalemia You may recall from our previous study of electrolytes, * that an elevated T wave * is indicative of hyperkalemia, a condition which if not corrected may become life threatening. *

ECG Deflection Wave Irregularities Flat T wave : Hypokalemia or ischemia Likewise, a flat T wave * * is indicative of hypokalemia or ischemia. * *

Heart Blocks P T Normal ECG QRS Not a QRS for each P wave 2nd Degree Block Earlier we talked about a first degree heart block as anything that extends the P-Q interval. * In this normal ECG identify the P wave, * * the QRS wave * * and the T wave. * * Now compare the following ECG. * This illustrates a 2nd degree block, * where there is not a QRS following each P wave. * A 3rd degree heart block * is where there are no P waves at all. * * As there is no communication between the conduction system in the atria and the ventricles, the autorhythmic cells of the ventricles determine the heart rate and become the pacemaker for the heart. * No P waves. Rate determined by autorhythmic cells in ventricles 3rd Degree Block

Cardiac Cycle All events associated with a single heart beat including atrial systole & diastole followed by ventricular systole & diastole. (V. Systole) (V. Diastole) Systolic BP Diastolic BP One of your objectives indicates that you should be able to diagram the cardiac cycle and label each component, including systole, diastole and the appropriate pressure and time scales. * By definition, the cardiac cycle includes all of the events associated with a single heart beat including atrial systole (contraction) and atrial diastole (relaxation) followed by ventricular systole (contraction) and ventricular diastole (relaxation). * We have been studying ECG deflection waves which indicate the waves of depolarization and repolarization of the various parts of the heart. Depolarization leads to contraction of that particular portion of the heart, while repolarization results in relaxation of each part of the heart. * If we superimpose blood pressure scales on the ECG, we can view when atrial and ventricular systole * * * and diastole * * occur with respect to the ECG deflection waves and their effects on blood pressure. * Note that the blood pressure values indicate blood pressure in the aorta, * and are measured in millimeters (mm) of Mercury (Hg) pressure. * The systolic blood pressure is the peak pressure that occurs in the aorta. * * A normal systolic pressure is generally around 120 mm Hg. * Diastolic pressure is the lowest pressure the blood drops to in the aorta. * It is normally around 80 mm Hg * when at rest. * To satisfy your objective, you should be able to draw and label normal ECG deflection waves, superimpose on them ventricular blood pressure and indicate where ventricular systole and ventricular diastole occur. *

60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute ECG Deflection Waves 60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute The objective also indicates that you should be able to indicate the appropriate time scales for each event of the cardiac cycle. Thus, you should be able to indicate on your diagram that the P-Q interval normally occurs in approximately 0.2 seconds, * the Q-T interval is normally around 0.4 seconds, * and that the interval between the Q-T interval and the beginning of the next cardiac cycle (P wave) in a resting heart is normally an additional 0.2 seconds, * thus accounting for an average resting heart rate of approximately 75 beats per second. * As with everything, practice makes perfect, so you may do well to practice drawing the cardiac cycle and superimposing on it ventricular blood pressure, systole, diastole and the appropriate time scales. *

Frank Starling Law of the Heart The more cardiac muscle is stretched within physiological limits, the more forcibly it will contract. Rubber band analogy Increasing volumes of blood in ventricles increase the stretch & thus the force generated by ventricular wall contraction. Greater stretch means more blood volume is pumped out, up to physical limits. The Frank Starling Law of the Heart states that * the more cardiac muscle is stretched within its physiological limits, the more forcibly it will contract. * This characteristic of cardiac muscle might be compared to a rubber band. The more you stretch the rubber band, the greater the force that is generated upon release. However if the rubber band is stretched too far, it may break. * With respect to the heart’s ability to pump blood, increasing volumes of blood in the ventricles increasingly stretch the ventricular myocardium, generating greater force. * The greater the force, the greater the volume of blood that is pumped out of the ventricle, up to the physiological limits of the myocardium. * *

Frank Starling Law of the Heart = To illustrate this in a more graphic way, * increasing the volume of blood flowing into the ventricles, will increasingly stretch the myocardium. * * This will result in a corresponding increase in the force generated by the myocardium * to increase the volume of blood * that will be pumped out of the ventricles. * Increased blood volume = increased stretch of myocardium Increased force to pump blood out.

Terms, Definitions & Units Blood Pressure - force generated against arterial walls per unit of area in mm Hg. Systolic Pressure - peak arterial pressure. Averages about 120 mm Hg in healthy adults. Diastolic Pressure - lowest arterial pressure. Averages between 70 - 80 mm Hg in healthy adults. Blood Volume - quantity of blood in cardiovascular system. Varies from 4-5 L. in females to 5-6 L. in males. As you will be required to define and/or recognize normal and abnormal values in their proper units of terms relating to heart activity, the next several slides will review these. By definition, blood pressure * is the force generated against arterial walls per unit of area. This pressure is measured in millimeters (mm) of Mercury (Hg) pressure. Systolic pressure * is the peak arterial pressure. It averages around 120 mm Hg in healthy adults. Diastolic pressure * is the lowest arterial pressure of blood. It averages betrween 70 - 80 mm Hg in healthy adults. Blood volume * refers to the quantity of blood in the cardiovascular system. It generally varies from 4-5 Liters in adult females to 5-6 Liters in adult males. *

Terms, Definitions & Units Cardiac Output - the amount of blood pumped by a ventricle per minute. Units may be in milliliters or Liters per minute. Heart Rate - number of cardiac cycles per minute. Average for males = 64-72/min. Average for females = 72-80/min. Stroke Volume - amount of blood pumped out of a ventricle each beat. Average resting stroke volume = 70 ml. Cardiac output * refers to the amount of blood pumped by a single ventricle per minute. It may be reported in milliliters or Liters per minute. Heart rate * is the number of cardiac cycles per minute. The average heart rate for adult males is from 64-72 beats/minute. The average heart rate for adult females varies from 72-80/minute. Stroke volume * refers to the amount of blood pumped out of a ventricle with each beat (contraction). The average stroke volume for an adult is around 70 ml. Knowing the heart rate and the stroke volume, one can calculate the cardiac output by simply multiplying the two. For instance, if the heart rate is 70/minute and the stroke volume is 70 ml, what would be the cardiac output? 70/minute x 70ml = 4,900 ml (4.9 L.) *

Factors influencing blood pressure Blood Pressure = Blood Volume × Peripheral Resistance Blood volume loss due to injuries, hemorrhages, use of diuretics, etc. = BP Blood pressure is effected by a number of factors. Changes in any or several of these factors will have a corresponding effect on blood pressure, causing it to increase or decrease. * Blood pressure is mainly affected by changes in blood volume and peripheral resistance. Any increase in blood volume * will cause a corresponding increase in blood pressure. * Likewise, any increase in peripheral resistance * will also increase blood pressure. * For instance, * a loss of blood volume, as a result of such things as injuries, hemorrhages or the use of diuretics, will decrease blood volume * and will therefore result in a decrease in blood pressure. Blood volume increases, * such as those associated with increased ADH production, intravenous injections or transfusions will increase blood pressure. * Blood volume increases due to increased water retention from increased ADH production, IVs or transfusions = BP

Factors influencing blood pressure Blood Pressure = Blood Volume × Peripheral Resistance Cardiac Output = circulating blood volume Cardiac Output = Heart Rate × Stroke Volume Increased heart rate caused by the release of epinephrine into blood by the adrenal glands = increased cardiac output, which increases circulating blood volume, to increase blood pressure. Cardiac output affects circulating blood volume. * Any increase in circulating blood volume * will cause a corresponding increase in cardiac output. * The increased cardiac output * will increase blood volume * causing an increase in the blood pressure. As cardiac output is determined by multiplying the heart rate times the stroke volume, * any increase in either of them * * will increase cardiac output * and effect an increase in blood pressure. * For instance, an increased heart rate due to the release of epinephrine by the adrenal glands into the blood during an emergency, * will increase blood pressure. *

Factors influencing blood pressure Blood Pressure = Blood Volume × Peripheral Resistance Peripheral Resistance affected by: blood viscosity (thickness) diameter of vessels (vasoconstriction/vasodilation) (Polycythemia) Vasoconstriction = diameter = resistance = BP Peripheral resistance * is effected by * blood viscosity (thickness) , * the diameter of vessels (vasoconstriction or vasodilation). And * the elasticity of arterial walls. Any increase in viscosity, * such as in polycythemia * will increase peripheral resistance * thus increasing blood pressure. * Vasoconstriction * decreases the diameter of blood vessels, * thus increasing resistance * and increasing blood pressure. * Vasodilation * increases the diameter of blood vessels, * thus decreasing resistance * and decreasing blood pressure. * The more elastic the arterial walls * * the lower the blood pressure. * * Vasodilation = diameter = resistance = BP elasticity of arterial walls Elastic Arterial Walls = BP

Homeostatic Blood Pressure Regulation Mechanisms Medullary Reflex Centers: Cardioacceleratory - increases heart rate Cardioinhibitory - decreases heart rate Vasomotor - changes diameter of vessels Baroreceptors in aortic arch & carotid sinuses: sensitive to changes in blood pressure. BP - Stimulates Cardioinhibitory center to heart rate & Vasomotor center to diameter. Homeostatic mechanisms for the regulation of blood pressure include the following reflex centers in the medulla oblongota: * * the cardioacceleratory center, which increases heart rate, * the cardioinhibitory center, which decreases heart rate, and * the vasomotor center in the aortic arch and the carotid sinuses, which can change the diameter of the arteries and arterioles causing vasoconstriction or vasodilation. In addition to the reflex centers in the medulla, there are peripheral baroreceptors * in the walls of the aortic arch , the carotid sinuses and nearly every other elastic artery in the heck and thorax which are sensitive to changes in blood pressure. * * A sudden increase in blood pressure * will cause the cardioinhibitory center * to decrease heart rate * and will stimulate the vasomotor center * to increase the diameter of arterioles, thus reducing the blood pressure. * A sudden drop in blood pressure noted by the baroreceptors * will stimulate the cardioacceleratory center to increase heart rate * while stimulating the vasomotor center to decrease * the diameter of arterioles to increase blood pressure. * BP - Stimulates Cardioacceleratory center to heart rate & Vasomotor center to diameter.

Homeostatic Blood Pressure Regulation Mechanisms Medullary Reflex Centers: Cardioacceleratory - increases heart rate Cardioinhibitory - decreases heart rate Vasomotor - changes diameter of vessels Chemoreceptors in aortic bodies & carotid bodies: sensitive to changes in CO2 & O2 in blood. in CO2 or in O2 stimulates Vasomotor center to diameter (vasoconstrict) of vessels to BP. In addition to the peripheral baroreceptors, there are chemoreceptors * in the aortic and carotid artery walls that are sensitive to changes in blood pH and O2 content. * An increase * in the blood CO2 * or a significant drop * in O2 levels in the blood will stimulate the vasomotor center to decrease * the diameter of arterioles (vasoconstriction) to raise blood pressure. * Likewise, a decrease in CO2 will stimulate the vasomotor center to increase * the diameter (vasodilation) of vessels to lower * the blood pressure. * in CO2 stimulates Vasomotor center to diameter (vasodilate) of vessels to BP.

Aneurysm Weakness of the wall of an artery causing an abnormal enlargment or bulge. The aorta or the arteries that supply the heart, brain, legs or kindeys are most commonly affected. An aneurysm * is a weakness in the wall of an artery that results in a balloon-like outpocketing or bulge in the arterial wall. These most commonly occur in the aorta, arteries that supply the heart, the brain or the legs * where arterial pressure is high. * Here you can see an angiogram of an aneurysm affecting one of the acerebral arteries. * The dark arrows point to another cerebral artery aneurysm. Aneurysms place the artery at risk for rupture and often reflect the effects of gradual weakening of the affected artery by chronic hypertension or arteriosclerosis.*

Angina Pectoris Medical term for chest pain due to coronary heart disease. It occurs when the myocardium doesn’t get as much blood (Oxygen) as it needs. Insufficient blood supply is called ischemia. May initially occur during physical exercise, stress, or extreme temperatures. It is a sign of increased risk of heart attack. Angina pectoris * is the medical term for chest pain due to coronary heart disease. * It typically occurs during times when the myocardium isn’t getting as much O2 and blood as it needs. Ischemia is the term used when there is an inadequate supply of blood to some part of the heart. * Angina pectoris sometimes serves as a warning if it occurs during physical exercise, stress or extreme temperatures but goes away during periods of inactivity. * It is a sign of increased risk of heart attack. * *

Hypertension High blood pressure. Sustained arterial blood pressure of 140/90 mm Hg or above. Rising diastolic pressure generally indicative of progressive hardening of arteries. Since the heart must work harder to pump blood against higher pressures, there is increased risk of a cardiovascular accident. Physiologically speaking, hypertension * is defined as a condition of sustained elevated arterial pressure of 140/90 mm Hg or higher. * Sustained increases in diastolic pressures above 90 is considered to bemost significant as it is generally always indicative of progressive narrowing or hardening of the arteries. * Since the heart must work harder to pump blood against higher pressures, there is increased risk of a cardiovascular accident with hypertension. * Specific identifiable causes are usually not know in nearly 90 % of hypertensive people, * however, the following are factors which are believed to be involved; dietary factors including high sodium and blood cholersterol, obesity, age, race, heredity, stress, and smoking. *

Hypotension Abnormally low blood pressure. Sustained systolic blood pressure of below 100 mm Hg. Generally associated with lower risk of cardiovascular accidents & long life providing that the tissues are adequately perfused.. Hypotension is the medical term for an abnormally low systolic blood pressure. * A sustained systolic pressure of below 100 mm Hg is the physiological standard. * Hypotension is generally associated with a lower risk of cardiovascular accidents and long life, providing that the tissues are adequately supplied with blood and nutrients. *

Circulatory Shock Blood vessels inadequately filled to enable normal circulation & supply of O2 & nutrients. May result in death of cells & damage to organs. Common Types: Hypovolemic - severe blood loss Cardiogenic - heart (pump) failure Vascular - excessive vasodilation Septicemic - vasodilation due to bacterial toxins produced during an infection. Hypotension may be symptomatic of circulatory shock. * Circulatory shock is the term used to describe any condition where the blood vessels are insufficiently filled to allow the normal circulation and the supply of O2 and nutrients to the tissues and organs. * This may result in the death of cells and damage to organs affected. Common types of shock include: * hypovolemic - due to severe blood loss, * cardiogenic - due to heart failure, * vascular - due to excessive vasodilation, or * septicemic - due to bacterial infections where the bacteria are producing toxins which cause vasodilation. *

Atherosclerosis (Arteriosclerosis) Narrowing and hardening of arteries and impairment of blood flow due to the deposition of fatty materials and calcium in their walls. Risk factors include: smoking inactivity diabetes high blood cholesterol personal or family history of heart disease Atherosclerosis (arteriosclerosis) is the term used to refer to the narrowing and hardening of arteries and accompanying impairment of blood flow due to the deposition of fatty materials and calcium in their walls. * Risk factors include: * smoking, * inactivity, * diabetes, * high blood cholesterol, and *personal or family history of heart disease. *

Arteriosclerosis (Atherosclerosis): This photograph of a cross section of a coronary artery affected by arteriosclerosis shows the effects on arterial blood flow.* All images copyright © Camera M.D. Studios. Special thanks to Gregory Curfman, M.D..

Acknowledgements Most of the figures used in this presentation came from the Benjamin Cummings Digital Library Version 2.0 for Human Anatomy & Physiology, Fifth Edition. Other figures came from public domain internet sources and software in the possession of the author.