Chapter 7 – Cardiac Physiology

Lesson 1 Chapter 7 – Cardiac Physiology 1 Unit 11 Study Guide The Cardiac Physiology A workable fluid distribution system for the body requires a pipeline network, a pump, and a liquid carrier medium. These three needs are met by the blood vessels, heart, and blood, respectively, which form the cardiovascular system. In an adult human of ‘standard’ size (~75 kg), this closed system includes a network of about 100 000 km of vessels that continuously circulate approximately 5 liters of blood. The heart, which is responsible for circulation, is a two-sided pump that separately and simultaneously serves the lungs (pulmonary circulation) and all other parts of the body (systemic circulation). Unique cardiac muscle cells allow the heart to beat autonomously, while receiving overall regulation from the nervous and endocrine systems. • Overall, the three basic components as mentioned above; – Heart • – Blood vessels • – Serves as pump that establishes the pressure gradient needed for blood to flow to tissues Passageways through which blood is distributed from heart to all parts of body and back to heart Blood • Transport medium within which materials being transported are dissolved or suspended Structure of the Heart I. The right and left sides of the heart pump blood through the pulmonary and systemic circulations. o The right ventricle pumps blood to the lungs. This blood then returns to the left atrium. “Pulmonary circulation” o The left ventricle pumps blood into the aorta and systemic arteries. This blood then returns to the right atrium. “Systemic circulation” Lesson 1 Chapter 7 – Cardiac Physiology II. The heart contains two pairs of one-way valves. o The atrioventricular valves allow blood to flow from the atria to the ventricles, but not in the reverse direction. o The semilunar valves allow blood to leave the ventricles and enter the pulmonary and systemic circulations, but these valves prevent blood from returning from the arteries to the ventricles. III. The electrical impulse begins in the sinoatrial node and spreads through both atria by electrical conduction from one myocardial cell to another. o The impulse then excites the atrioventricular node, from which it is conducted by the bundle of His into the ventricles. o The Purkinje fibers transmit the impulse into the ventricular muscle and cause it to contract. Circulatory System 2 Lesson 1 • Chapter 7 – Cardiac Physiology Heart – Arteries • – Veins • – Carry blood away from ventricles to tissues Vessels that return blood from tissues to the atria Septum • Continuous muscular partition that prevents mixture of blood from the two sides of heart The heart consists of 4 chambers: right atrium, right ventricle, left atrium, left ventricle 3 Lesson 1 Chapter 7 – Cardiac Physiology ● Right atrium receives blood from superior and inferior vena cava ● Blood flows from right atrium, across tricuspid valve, into right ventricle ● Muscle of right ventricle is not as thick as left ventricle ● Blood enters pulmonary artery from right ventricle. Backflow prevented by semilunar pulmonic valve ● Blood returns to heart from lungs via 4 pulmonary veins that enter left atrium ● Blood flows from left atrium, across mitral valve, into left ventricle ● Left ventricle has a thick muscular wall / generate high pressures during contraction ● Blood from left ventricle is ejected, across aortic valve, into aorta ● Tricuspid and mitral valves (atrioventricular AV valves) o Have fibrous strands (cordae tendinae) that attach to papillary muscles o The papillary muscles contract during ventricular contraction o Generate tension on valve via cordae tendinae to prevent AV valves from bulging back into atria ● Semilunar valves (pulmonic and aortic) do not have these attachments The Cardiac Cycle ● Atria receive blood from veins and store it prior to each heart beat ● Right atrium receives blood from main body veins called "vena cava" o Superior vena cava SVC carries blood from head, upper chest and arms o Inferior vena cava IVC carries blood from lower chest, abdomen and legs ● Left atrium receives blood from lungs via 4 separate pulmonary veins ● Systole refers to a period of contraction by heart muscle ● Diastole refers to a period of relaxation by heart muscle Atrial systole ● Both atria contract and push stored blood across AV valves into ventricles, to help fill them ● Atrioventricular (AV) valves include o Mitral valve located between left atrium and left ventricle o and tricuspid valve which separates right atrium from right ventricle 4 Lesson 1 Chapter 7 – Cardiac Physiology 5 ● Reduces the volume of atria and increases pressure Ventricular systole ● After atria contracts, ventricles begin to contract ● Pressure in ventricles increases, blood is forced against AV valves ● Valves close to prevent backflow → first heart sound ● Volume is reduced ● Blood is ejected into arteries through aortic and pulmonary valves Ventricular diastole ● End of cardiac cycle, all chambers relax ● Aortic and pulmonary valves close (second heart sound) / prevents backflow into heart ● Atria begin to fill up again to start next cycle ● Volume increases and pressure decreases Cardiac Muscle Cells • 99% - contractile cells • 1% - autorhythmic cells • • Do not contract • Specialized for initiating and conducting action potentials responsible for contraction of working cells • Can generate an action potential Do not have a resting membrane potential – membrane potential slowly depolarizes • because of constant Na+ influx and transient Ca++ influx – until threshold is reached • slow K+ efflux • Cardiac muscles cells are interconnected by “intercalated discs” • 2 types of membrane junctions – Desmosome Lesson 1 Chapter 7 – Cardiac Physiology – 6 Gap junction • But – no gap junction between atrial and ventricles • Therefore – specialized conducting system is there for coordination of electrical impulse transmission (autorhythmic cells) Ca++ are also called L-type Ca Electrophysiology Lesson 1 Chapter 7 – Cardiac Physiology Sinoatrial node (SA node) – – Specialized region in right atrial wall near opening of superior vena cava Pacemaker of the heart Atrioventricular node (AV node) – Small bundle of specialized cardiac cells located at base of right atrium near septum Bundle of His (atrioventricular bundle) – Cells originate at AV node and enters interventricular septum – Divides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls Purkinje fibers – Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium ● Sinus node is located at the top right atrium o Also known as the "natural pacemaker" controlling heart rate o Increases with physical activity and decreases when relaxing o Electrical signal rapidly spreads from the Sinus node across the right atrium and left atrium ● Only one area where atria and ventricles are electrically connected o Atrioventricular node or AV node deep in center of heart o All electrical signals from atrium must pass through AV node in order to get to ventricles o AV node is connected to the Bundle of His o Branches into a right bundle (to right ventricle) and left bundle (to left ventricle) ● Fibers that branch out to distant ventricular tissues are called Purkinje Fibers In summary: Regulation of the Cardiac Cycle ● Heart has unique ability to beat (contract) on its own ● Assisted by nerves and hormones in blood but functions without them ● Impulse leaves SA node and passes through both atria → causing them to contract ● From AV node impulse passes down to the Bundle of His ● Bundle of His branches and spreads through both ventricles via Purkinje fibers → 7 Lesson 1 Chapter 7 – Cardiac Physiology ventricles contact [PACEMAKER POTENTIAL] In the normal heart the impulse originates in the SA node, due to a spontaneous depolarization called the pacemaker potential. o When this spontaneous depolarization reaches a threshold value, opening of the voltage-regulated Na+ gates and fast Ca2+ channels produces an action potential. o Repolarization is produced by the outward diffusion of K+, but a stable resting membrane potential is not attained because spontaneous depolarization once more occurs. o Other myocardial cells are capable of spontaneous activity, but the SA node is the normal pacemaker because its rate of spontaneous depolarization is the fastest. o When the action potential produced by the SA node reaches other myocardial cells, they produce action potentials with a long plateau phase because of the slow, inward diffusion of Ca2+. o The long action potential and long refractory period of myocardial cells allows the entire mass of cells to be in a refractory period while it contracts. This prevents the 8 Lesson 1 Chapter 7 – Cardiac Physiology myocardium from being stimulated again until after it relaxes. Electrical Activity of the Heart ● Atria contract as single unit followed after brief delay by a synchronized ventricular contraction ● Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction o Ensures adequate ejection time o Plateau primarily due to activation of slow L-type Ca2+ channels ● Because long refractory period occurs in conjunction with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible o Ensures alternate periods of contraction and relaxation which are essential for pumping blood ECG is a record of electrical currents (activity) generated by cardiac muscle during 9 Lesson 1 Chapter 7 – Cardiac Physiology depolarization repolarization – into the tissues surrounding the conducted body fluids and that spread heart – through the P wave is caused by depolarization of the atria. QRS wave is caused by depolarization of the ventricles. T wave is produced by repolarization of the ventricles. Abnormalities in Rate • Tachycardia – • 10 Rapid heart rate of more than 100 beats per minute Bradycardia Lesson 1 Chapter 7 – Cardiac Physiology – 11 Slow heart rate of fewer than 60 beats per minute Abnormalities in Rhythm • Rhythm – regularity or spacing of ECG waves • Arrhythmia – variation from normal rhythm and sequence of excitation of the heart – Examples: atrial fibrillation, ventricular fibrillation, heart block Atherosclerosis and Cardiac Arrhythmias I. Atherosclerosis of arteries can occlude blood flow to the heart and brain, causing up to 50% of all mortality in the United States, Europe, and Japan. ● Atherosclerosis begins with injury to the endothelium, the movement of monocytes and lymphocytes into the tunica interna, and the conversion of monocytes into macrophages that engulf lipids. Smooth muscle cells then proliferate and secrete extracellular matrix. ● Atherosclerosis is promoted by smoking, hypertension, and high plasma cholesterol concentration, among other risk factors; low-density lipoproteins (LDL), which carry cholesterol into the artery wall, is oxidized by the endothelium and is a major contributor to atherosclerosis. II. Occlusion of blood flow in the coronary arteries by atherosclerosis may produce ischemia of the heart muscle and angina pectoris, which may lead to myocardial infarction. III. The ECG can be used to detect abnormal cardiac rates, abnormal conduction between the atria and ventricles, and other abnormal patterns of electrical conduction in the heart. Lesson 1 Chapter 7 – Cardiac Physiology 12 Pressure Changes During the Cardiac Cycle 1. Ventricles begin to contract, intraventricular pressure rises causing AV valves to close. Ventricles are neither being filled with blood (AV valves are closed) nor ejecting blood (intraventricular pressure has not risen sufficiently to open semilunar valves). This is the phase of isovolumetric contraction. 2. Pressure in the left ventricle becomes greater than pressure in the aorta, phase of ejection begins as semilunar valves open. Pressure in left ventricle and aorta rises to about 120 mm Hg when ejection begins and ventricular volume decreases 3. Pressure in left ventricle falls below pressure in the aorta, back pressure causes semilunar valves to shut. Pressure in aorta falls to 80 mm Hg 4. During isovolumetric relaxation AV and semilunar valves are closed. This phase lasts until pressure in ventricles falls below pressure in atria 5. When pressure in ventricles falls below pressure in atria, ventricles are filled 6. Atrial systole empties final amount of blood into ventricles immediately prior to next phase of isovolumetric contraction of ventricles First heart sound Closure of AV valves Isovolumentric contraction *** Second Heart Sound Closure of semi-lunar valves Lesson 1 Chapter 7 – Cardiac Physiology Isovolumetric relaxation *** 13 Lesson 1 Chapter 7 – Cardiac Physiology 14 Auscultation • Stethoscope • Sounds of heartbeat are from turbulence in blood flow caused by valve closure – first heart sound (lubb) is created with the closing of the atrioventricular valves Lesson 1 Chapter 7 – Cardiac Physiology – 15 second heart sound (dupp) is created with the closing of semilunar valves Where to listen for heart sounds Cardiac Output The cardiac output is simply the amount of blood pumped by the heart per minute. Necessarily, the cardiac output is the product of the heart rate, which is the number of beats per minute, and the stroke volume, which is amount pumped per beat. CO = HR X SV I. Cardiac rate is increased by sympathoadrenal stimulation and decreased by the effects of parasympathetic fibers that innervate the SA node. II. Stroke volume is regulated both extrinsically and intrinsically. A. The Frank-Starling law of the heart describes the way the end-diastolic volume, through various degrees of myocardial stretching, influences the contraction strength of the myocardium and thus the stroke volume. B. The end-diastolic volume is called the preload. The total peripheral resistance, through its effect on arterial blood pressure, provides an afterload that acts to reduce the stroke volume. C. At a given end-diastolic volume, the amount of blood ejected depends on contractility. Strength of contraction is increased by sympathoadrenal stimulation. Lesson 1 Chapter 7 – Cardiac Physiology 16 III. The venous return of blood to the heart is dependent largely on the total blood volume and mechanisms that improve the flow of blood in the veins. A. The total blood volume is regulated by the kidneys. B. The venous flow of blood to the heart is aided by the action of skeletal muscle pumps and the effects of breathing. Cardiac Output As a Function of Stroke Volume and Heart Rate ● The volume of blood pumped by one ventricle during one beat is called the stroke volume ● Cardiac Output = Stroke Volume x Heart Rate (number of ventricular contractions/min) ● ↑Force of contraction → ↑Stroke volume → ↑Cardiac output Regulation of heart rate → Cardiac output is influenced by several factors Autonomic Nervous System ● Heart is innervated by the autonomic nervous system (ANS) o o o o The autonomic nervous system has 2 divisions These division are called parasympathetic and sympathetic Parasympathetic fibres decrease heart rate via the vagus nerve Sympathetic fibres increase heart rate ● Cardiac Inhibitory Centre o Found in the medulla oblongata of the brain stem o Sends signals via the vagus nerve, which is parasympathetic, to the heart o Signal reaches SA and AV nodes to trigger a release of neurotransmitter acetylcholine o This slows down the heart rate ● Cardiac Accelerating Centre o o o o o o Found in the medulla and the upper thoracic spinal cord Sympathetic fibres run towards the myocardium There they also innervate the SA and AV nodes, but also cardiac cells When stimulated, the sympathetic fibres cause a release of norepinephrine [NOTE] The international name for noradrenaline is now norepinephrine Norepinephrine increases heart rate and strength of ventricular and atrial contraction ● Cardiac centres balance stimulatory and inhibitory effects of the ANS Lesson 1 Chapter 7 – Cardiac Physiology 17 Two terms connected with heart failure are preload and afterload. End-diastolic stretch is known as preload; afterload is the stress or tension that develops in the ventricular wall during systole. NOTE: “You need to develop a good understanding of heart failure, preload and afterload and how they all relate because all this information is at the basis of understanding the nursing diagnosis of Decreased Cardiac Output. Students are always asking what nursing diagnosis to use with certain medical diagnoses. Decreased Cardiac Output is used for any of the heart failures including congestive heart failure.” Regulation of the Stroke Volume Sympathetic Effect Autonomic nerves not only innervate the SA node, but also are found elsewhere in the heart. Norepinephrine released by sympathetic nerves increases the force with which ventricular muscle fibers contract (by increasing the Ca++ effect). This tends to be significant mainly at the greatest levels of exercise. For example, the ventricle of a 70 kg person at rest might hold about 100 ml of blood at the end of diastole. As noted above, a typical stroke volume is about 70 ml. Thus, the person's ejection fraction is 70%. This is the fraction of the blood in the ventricle that is ejected during systole. Norepinephrine, by increasing the force of contraction, would tend to increase the ejection fraction and thus the stroke volume. Afterload The aortic pressure influences the stroke volume for a straightforward reason. If the aortic pressure increases, this pressure reduces the volume of blood that flows into the aorta during systole. The aortic pressure is called afterload because it is the "load" experienced by the ventricle after it begins contracting. A drug might reduce the afterload, for example, by dilating arterioles. This allows blood to flow from the arteries more easily, thereby preventing the arterial pressure from increasing as blood is injected into it by the ventricle. Frank-Starling Mechanism However, the factor we will be most concerned with is the Frank-Starling mechanism. Unfortunately, it is also the one most difficult to get your mind around. The Frank-Starling mechanism leads to changes in the stroke volume as a result of changes in the end-diastolic volume. The end-diastolic volume is the volume of a ventricle at the very end of filling and just before systole begins. This can change because the ventricles are flexible and under different circumstances, the amount of blood flowing in during diastole varies. If less blood flows into the Lesson 1 Chapter 7 – Cardiac Physiology 18 ventricle as it fills, the end-diastolic volume goes down. If more blood flows in, the end-diastolic volume goes up. The Frank-Starling effect is due to the fact that heart muscle fibers respond to stretch by contracting more forcefully. This is not a passive, elastic effect, but rather due to an increased expenditure of ATP energy. (We are not going to try to explain the cellular basis of this effect. It is not as straightforward as you might think.) Thus, if the end-diastolic volume increases, the muscle fibers are lengthened and the ventricle contracts more forcefully, ejecting a greater stroke volume. The figure to the right shows this Frank-Starling effect. What factor alters the filling during diastole? For the right ventricle, this is the pressure in the right atrium, because this is the pressure that is experienced by the right ventricle as it fills. Since there is no valve at the entrance to the right atrium, the pressure in the right atrium is necessarily the same as the pressure in the veins at the entrance to the right atrium. This pressure in the large veins at the entrance to the right atrium is called the central venous pressure. In other words, the central venous pressure is the same at the right atrial pressure, and this is the pressure that determines the filling of the right ventricle and thus its end-diastolic volume. The central venous pressure always is only a few mm Hg, but nonetheless it does change enough to significantly affect the stroke volume. In particular, posture changes this pressure and that is the factor with which we are here most concerned. Heart Failure (Left and Right) L = Lungs (and all things pulmonary related) R = Rest of body Heart failure is a gradual progressive condition. It starts and proceeds as follows: Left-sided heart failure ▪ Ineffective left ventricular contractile function ▪ Increased workload and end-diastolic volume enlarge the left ventricle ▪ Pumping ability of the left ventricle fails, cardiac output falls Lesson 1 Chapter 7 – Cardiac Physiology – 19 Right ventricle becomes stressed because it's pumping against greater pulmonary vascular resistance and left ventricle pressure ▪ Blood backs up into left atrium and then into lungs – Diminished function allows blood to pool in the ventricle and atrium and back up into the pulmonary veins and capillaries – Rising capillary pressure pushes sodium and water into interstitial spaces – Fluid in the extremities moves into the systemic circulation ▪ Signs and symptoms – Dyspnea (difficulty in breathing) – orthopnea – paroxysmal nocturnal dyspnea – reduced sympathetic stimulation while sleeping – pulmonary congestion (inflammation due to fluid accumulation) – tachycardia – S3 – S4 – Cool, pale skin – restlessness Right-sided heart failure ▪ Ineffective right ventricular contractile function – Stressed right ventricle enlarges with the formation of stretched tissue ▪ Blood backs up into right atrium and peripheral circulation – Blood pools in the right ventricle and right atrium – Backed-up blood also distends the visceral veins ▪ Patient gains weight and develops peripheral edema [will always develop edema in right side heart failure] Lesson 1 Chapter 7 – Cardiac Physiology – 20 Rising capillary pressure forces excess fluid from the capillaries into the interstitial space ▪ Signs and symptoms – jugular vein distention – positive hepatojugular reflux – hepatomegaly (enlargement of liver) o Systolic dysfunction ▪ Left ventricle can't pump enough blood out to systemic circulation ▪ Blood backs up into pulmonary circulation and pressure increases in pulmonary venous system ▪ Cardiac output falls; weakness and fatigue occur o Diastolic dysfunction ▪ ability of left ventricle to relax and fill during diastole is reduced and stroke volume falls ▪ high volumes needed in ventricles to maintain cardiac output