Cardiovascular System: Heart - 2023 Nursing PDF

CARDIOVASCULAR SYSTEM: HEART FUNCTIONS OF THE HEART 1. Generating blood pressure 01 Required for blood flow through the blood vessels 2. Routing blood 02 Two pumps, moving blood through the pulmonary and systemic circulations...

CARDIOVASCULAR SYSTEM: HEART FUNCTIONS OF THE HEART 1. Generating blood pressure 01 Required for blood flow through the blood vessels 2. Routing blood 02 Two pumps, moving blood through the pulmonary and systemic circulations 03 3. Regulating blood supply Adjusts blood flow by changing the rate and force of heart contractions as needed  BLOOD CIRCULATION Pulmonary circulation →The flow of blood from the heart through the lungs back to the heart →Picks up oxygen and releases carbon dioxide in the lungs Systemic circulation →The flow of blood from the heart through the body back to the heart →Delivers oxygen and picks up carbon dioxide in the body’s tissues AWARDS HOBBIES CONTACT  Anatomy of the Heart EXTERNAL ANATOMY LOCATION COVERING OF HEART ORIENTATION LAYERS OF THE HEART  LOCATION , SHAPE AND ORIENTATION OF THE HEART - anterior to the vertebral column, posterior to the sternum - left of the midline - deep to the second to fifth intercostal spaces superior surface of diaphragm -like a blunt cone, with an apex and a base - Approximately the size of your fist a. 2/3 of the mass of the heart lies left on the bodies midline b. Orientation of the apex of the heart, (Anterior, Inferior, towards the left) c. Orientation of the base of the heart, (Posterior, Superior, towards the right) APEX BEAT ADULT: felt in the left 5th intercostal space 9cm from the median plane ( just medial to the midclavicular line) INFANTS: felt in the 3rd intercostal space just lateral to the midclavicular line DEXTROCARDIA -is a congenital anomaly in which the heaon the right side of the thoracic cavity - may be associated with the reversal of all abdominal organs, a clinical condition known as situs inversus. EXTERNAL ANATOMY Each atrium has a flap called an auricle The coronary sulcus (shallow grooves) separates the atria from the ventricles A. Coronary Sulcus B. Anterior interventricular sulcus C. Posterior interventricular sulcus The interventricular grooves separate the right and left ventricles COVERING AND LAYERS OF THE HEART Pericardium: a double-walled sac around the heart composed of: A. A superficial fibrous pericardium Protects and anchors the heart Prevents overfilling of the heart with blood B. A deep two-layer serous pericardium Allows for the heart to work in a relatively friction-free environment b.1. parietal layer lines the internal surface of the fibrous pericardium b.2. visceral layer lines the surface of the heart └ Th e y a re s e p a r a t e d b y t h e f lu i d - f i lle d (pericardial fluid) pericardial cavity Epicardium └ Visceral layer of the serous pericardium (visceral pericardium) └ Provides protection against the friction of rubbing organs Myocardium └ Cardiac muscle layer forming the bulk of the heart └ Responsible for contraction Endocardium └ Endothelial layer over crisscrossing, interlacing layer of connective tissue └ Inner endocardium reduces the friction resulting from the passage of blood through the heart  Disorders of the Pericardium Pericarditis →is an inflammation of the serous pericardium. → cause is frequently unknown, but it can result from infection, diseases of connective tissue, or damage due to radiation treatment for cancer. →condition can cause extremely painful sensations that are referred to the back and to the chest and can be confused with a myocardial infarction (heart attack) →Pericarditis can lead to a small amount of fluid accumulation within the pericardial sac. Cardiac tamponade →is a potentially fatal condition in which fluid or blood accumulates in the pericardial cavity and compresses the heart from the outside. The heart is a powerful muscle, but it relaxes passively. When it is compressed by fluid within the pericardial cavity, it cannot expand when the cardiac muscle relaxes. Consequently, the heart cannot fill with blood during relaxation, which makes pumping impossible. can →cause a person to die quickly unless the fluid is removed. →Causes of cardiac tamponade include rupture of the heart wall following a myocardial infarction, rupture of blood vessels in the pericardium after a malignant tumor invades the area, damage to the pericardium due to radiation therapy, and trauma, such as that resulting from a traffic accident. Inflammation of Heart Tissue 1. Endocarditis →Inflammation of the endocardium; affects the valves more severely than other areas of the endocardium; may lead to scarring, causing stenosed or incompetent valves 2. Cardiomyopathy →Disease of the myocardium of unknown cause or occurring secondarily to other disease; results in weakened cardiac muscle, causing all chambers of the heart to enlarge; may eventually lead to congestive heart failure 3. Rheumatic heart disease →Results from a streptococcal infection in young people; toxin produced by the bacteria can cause rheumatic fever several weeks after the infection that can result in rheumatic endocarditis CHAMBER OF THE HEART ATRIA: PRIMER PUMP/ RECEIVING CHAMBER RIGHT ATRIUM LEFT ATRIUM Openings Present: Openings Present: → superior vena cava →2 right pulmonary veins →inferior vena cava →coronary sinus →2 left pulmonary veins Wall: Wall: MEDICAL →anterior: rough (pectinate → both anterior and posterior INFOGRAPHICS muscle) are smooth →posterior: smooth Valve Present: Valve Present: →tricuspid valve →bicuspid valve Interatrial Septum →Fossa Ovalis ( from foramen) VENTRICLES: POWER PUMP/ DISCHARGING CHAMBER RIGHT VENTRICLE LEFT VENTRICLE Wall: Wall: → P a p i l l a r y M u s c l e s : c o n e  Trabeculae Carneae shaped  Chordae Tendineae  Trabeculae Carneae  Chordae Tendineae  wall is less thick than the left;  wall is thicker than the right; greater lumen diameter lesser lumen diameter Interventricular Septum Valve Present: Valve Present: pulmonary semilunar valve →aortic semilunar valve Pulmonary trunk exits the right Aorta exits the left ventricle ventricle carrying blood to the carrying blood to the systemic pulmonary circulation circulationaaaaaaaaaaaa Ductus Arteriosus (ligamentum arteriosum)  VALVES ATRIOVENTRICULAR SEMILUNAR VALVES VALVES a. tricuspid valve a. pulmonary semilunar valve b. bicuspid b. aortic semilunar valves valves HEART SOUND 1. Lubb sound/1 -is louder and a bit longer than the second sound. -caused by blood turbulence associated with closure of the AV valves soon after ventricular systole begins. 2. Dupp sound or S2 -caused by blood turbulence associated with closure of the SL valves at the beginning of ventricular diastole. 3. S3 is due to blood turbulence during rapid ventricular filling 4. S4 is due to blood turbulence during atrial systole. FIBROUS SKELETON OF HEART - dense connective tissues (fibrous skeleton of heart) a. pulmonary fibrous ring b. aortic fibrous ring c. left atrioventricular fibrous ring d. right atrioventricular fibrous ring Purpose: a. Structural foundation b. Prevents overstretching of the valves c. Serves as a point of insertion for bundles of cardiac muscle fibers d. Acts as an electrical insulator between the atria & ventricles Congenital Heart Diseases (Occur at Birth) 1. Septal defect →Hole in the septum between the left and right sides of the heart, allowing blood to flow from one side of the heart to the other and greatly reducing the heart’s pumping effectiveness 2. Patent ductus arteriosus →Ductus arteriosus fails to close after birth, allowing blood to flow from the aorta to the pulmonary trunk under a higher pressure, which damages the lungs; also, the left ventricle must work harder to maintain adequate systemic pressure BLOOD FLOW CORONARY CIRCULATION General Features of Blood Vessels Blood vessels, except for capillaries, have three layers Inner: tunica intima Consists of endothelium (simple squamous epithelium), basement membrane, and internal elastic lamina Middle: tunica media Contains circular smooth muscle and elastic and collagen fibers Outer: tunica adventitia connective tissue The thickness and the composition of the layers vary with blood vessel type and diameter  CORONARY CIRCULATION CORONARY ARTERY: originate from the base of the aorta, just above the aortic semilunar valves LEFT CORONARY ARTERY RIGHT CORONARY ARTERY ① Marginal branch ① Anterior interventricular - extends inferiorly along branch the lateral wall of the right - lies in the anterior ventricle. interventricular sulcus - supply most of the wall of ② circumflex branch the right ventricle. - extends around the coronary sulcus on the left to the posterior ② posterior interventricular surface of the heart branch ③ left marginal artery - lies in the posterior -extends inferiorly along the interventricular sulcus. lateral wall of the left ventricle from the circumflex artery Arteries carry blood away from the heart toward capillaries, where exchange between the blood and interstitial fluid occurs Blood flows from the heart through elastic arteries, muscular arteries, and arterioles to the capillaries Large elastic arteries – Thick-walled with large diameters – Tunica media has many elastic fibers and little smooth muscle Muscular (distributing) arteries – Thick-walled with small diameters – Tunica media has abundant smooth muscle and some elastic fibers Arterioles – Smallest arteries – Tunica media consists of one or two layers of smooth muscle cells and a few elastic fibers CORONARY VEINS: drains blood from the cardiac muscle Coronary Sinus: a large vein located within the coronary sulcuson the posterior aspect of the heart Small CardiacVein →coronary sulcus, which drains the right atrium and right ventricle Anterior Cardiac Vein drain the right ventricle and open directly into the right atrium Midldle Cardiac Vein →posterior interventricular sulcus, →drains the areas supplied by the posterior interventricular branch of the right coronary artery →(left and right ventricles) Great Cardiac Vein →anterior interventricular sulcus, →rains the areas of the heart supplied by the left coronary artery →(left and right ventricles and left atrium)  Veins carry deoxygenated blood from the capillaries toward the heart – Blood returns to the heart from the capillaries through venules, small veins, and large veins - veins are different from arteries because they sometimes also contain one-way valves that keep blood flowing in the right direction. - These valves are especially important in your legs, where they help blood move up toward your heart. If these valves get damaged, blood can leak backward and cause varicose veins or other problems.  Capillaries Capillaries consist only of endothelium A capillary bed is a network of capillaries Thoroughfare channels carry blood from arterioles to venules Blood can pass rapidly through thoroughfare channels Precapillary sphincters regulate the flow of blood into capillaries Reduced Blood Flow to Cardiac Muscle 1. Coronary heart disease Reduces the amount of blood the coronary arteries can deliver to the myocardium; 2. Coronary thrombosis Formation of blood clot in a coronary artery HISTOLOGY OF THE HEART CARDIAC MUSCLE CELLS ELECTRICAL ACTIVITY OF THE HEART CONDUCTION SYSTEM OF THE HEART Cardiac muscle cells →are elongated, branching cells that contain one, or occasionally two, centrally located nuclei →contain actin and myosin myofilaments organized to form sarcomeres, which are joined end-to-end to form myofibrils → have many mitochondria, which produce ATP at a rate rapid enough to sustain the normal energy requirements of cardiac muscle. An extensive capillary network provides adequate O2 to the cardiac muscle cells. Unlike skeletal muscle, cardiac muscle cannot develop a significant oxygen deficit. Development of a large oxygen deficit could result in muscular fatigue and cessation of cardiac muscle contraction →are organized into spiral bundles or sheets. When cardiac muscle fibers contract, not only do the muscle fibers shorten but the spiral bundles twist to compress the contents of the heart chambers. →are bound end-to-end and laterally to adjacent cells by specialized cell-to-cell contacts called intercalated disks. The membranes of the intercalated disks are highly folded, and the adjacent cells fit together, greatly increasing contact between them and preventing cells from pulling apart. Specialized cell membrane structures in the intercalated disks called gap junctions allow cytoplasm to flow freely between cells. This enables action potentials to pass quickly and easily from one cell to the next. The cardiac muscle cells of the atria or ventricles, therefore, contract at nearly the same time. The heart’s highly coordinated pumping action depends on this characteristic.  ELECTRICAL ACTIVITY OF THE HEART ACTION POTENTIAL SKELETAL MUSCLE CARDIAC MUSCLE - exhibit depolarization followed by repolarization - exhibit depolarization followed by a period of slow repolarization that greatly prolongs AP - AP takes less than 2 milliseconds to complete - AP takes 200 to 500ms to complete - AP is initiated at each cell by a motor neuron - AP spread from one cell to adjacent cell through gap junctions at intercalated disks - AP consist of depolarization and repolarization - AP consist of depolarization, plateau phase( slow with refractory period repolarization period), repolarization(rapid) - exhibit refractory period  Autorhythmic Fibers: The Conduction System 1. SINOATRIAL NODE 1. Action potentials originate in the → functions as the heart’s pacemaker sinoatrial (SA) node and travel across the wall of the atrium from the SA →located in the superior wall of the right node to the atrioventricular (AV) node. atrium and initiates the contraction of the heart 2. Action potentials pass through the 2. ATRIOVENTRICULAR NODE AV node and along the atrioventricular → located in the lower portion of the right (AV) bundle, which extends from the atrium AV node, through the fibrous skeleton, 3. ATRIOVENTRICULAR BUNDLE into the interventricular septum. → a bundle of specialized cardiac muscle 3. The AV bundle divides into right and 4. R and L ATRIOVENTRICULAR BUNDLE l e ft b u ndl e b ra nche s, a nd a c t i o n 5. PURKINJE FIBERS potentials descend to the apex of → small bundle fibers each ventricle along the bundle branches 4. Action potentials are carried by the Purkinje fibers from the bundle branches to the ventricular walls.  Abnormal Heart Rhythms Condition Symptoms Possible Causes Tachycardia Heart rate in excess of 100 beats per minute (bpm) Elevated body temperature, excessive sympathetic stimulation, toxic conditions Bradycardia Heart rate less than 60 bpm Increased stroke volume in athletes, excessive vagus nerve stimulation, nonfunctional SA node, carotid sinus syndrome Sinus arrhythmia Heart rate varies as much as 5% during respiratory Cause not always known; occasionally caused cycle and up to 30% during deep respiration byischemia, inflammation, or cardiac failure Paroxysmal atrial Sudden increase in heart rate to 150–250 bpm for a Excessive sympathetic stimulation, abnormally tachycardia few secondsor even for several hours; P waves elevated permeability of cardiac muscle to precede every QRS complex; P wave is inverted and Ca2+ superimposed on T wave Atrial flutter As many as 300 P waves/min and 125 QRS Ectopic beats in atria complexes/min;resulting in two or three P waves (atrial contractions) for every QRS complex (ventricular contraction) Atrial fibrillation No P waves, normal QRS and T waves, irregular timing; Ectopic beats in atria ventricles are constantly stimulated by atria; reduced ventricle filling; increased chance of fibrillation Ventricular tachycardia Frequently causes fibrillation Often associated with damage to AV node or ventricular muscle ELECTROCARDIOGRAM -record of these electrical events - a recording device can detect the small electrical changes resulting from the action potentials in all of the cardiac muscle cells. ◙ ECG consists of a P wave, a QRS complex, and a T wave 1. P wave →a small upward deflection →represents atrial,depolarization, which spreads from the SA node through contractile fibers in both atria 2. QRS complex →consists of three individual waves: the Q, R, and S waves. The QRS complex results from depolarization of the ventricles, and the beginning of the QRS complex precedes ventricular contraction. → begins as a downward deflection, continues as a large, upright, triangular wave, and ends as a downward wave →represents rapid ventricular depolarization, as the action potential spreads through ventricular contractile fibers 3. T wave →dome-shaped upward deflection →indicates ventricular repolarization and occurs just as the ventricles are starting to relax → is smaller and wider than the QRS complex because repolarization occurs more slowly than depolarization. →represents repolarization of the ventricles, and the beginning of the T wave precedes ventricular relaxation. A wave representing repolarization of the atria cannot be seen because it occurs during the QRS complex. 1. P-Q Interval - is the time from the beginning of the P wave to the beginning of the QRS complex. -It represents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation. -is the time required for the action potential to travel through the atria, atrioventricular node, and the remaining fibers of the conduction system. -As the action potential is forced to detour around scar tissue caused by disorders such as coronary artery disease and rheumatic fever, the P–Q interval lengthens. 2. S–T segment - which begins at the end of the S wave and ends at the beginning of the T wave, -represents the time when the ventricular contractile fibers are depolarized during the plateau phase of the action potential. -is elevated (above the baseline) in acute myocardial infarction and depressed (below the baseline) when the heart muscle receives insufficient oxygen. 3. Q-T Segment - extends from the start of the QRS complex to the end of the T wave. -It is the time from the beginning of ventricular depolarization to the end of ventricular repolarization. -may be lengthened by myocardial damage, myocardial ischemia (decreased blood flow), or conduction abnormalities. Larger P waves indicate enlargement of an atrium; an enlarged Q wave may indicate a myocardial infarction; an enlarged R wave generally indicates enlarged ventricles. The T wave is flatter than normal : the heart muscle is receiving insufficient oxygen—as, for example, in coronary artery disease. The T wave may be elevated in hyperkalemia (high blood K level).  elevated ST segment: acute M.I depressed ST segment: oxygen insufficiency  CARDIAC CYCLE ---- Correlation of ECG Waves with Atrial and Ventricular Systole -refers to the repetitive pumping process that begins with the onset of cardiac muscle contraction and ends with the beginning of the next contraction. -The atria act as primer pumps because they complete the filling of the ventricles with blood, and the ventricles act as power pumps because they produce the major force that causes blood to flow through the pulmonary and systemic circulations. The ECG waves predict the timing of atrial and ventricular systole and diastole. At a heart rate of 75 beats per minute, the timing is as follows: 1. A cardiac action potential arises in the SA node. It propagates throughout the atrial muscle and down to the I. Atrial systole AV node in about 0.03 sec. As the atrial contractile fibers depolarize, the P wave appears in the ECG. 1. Depolarization of SA nodes ( P wave: 105mL) 2. Atrial depolarization 3. Atrial systole * atria squeezes the last final 25ml of blood * end of ventricular diastole * 130mL on both ventricles “ END DIASTOLIC VOLUME” 4. QRS complex marks onset of ventricular depolarization 2. After the P wave begins, the atria contract (atrial systole). Conduction of the action potential slows at the AV node because the fibers there have much smaller diameters and fewer gap junctions. The resulting 0.1-sec delay gives the atria time to contract, thus adding to the volume of blood in the ventricles, before ventricular systole begins. 3. Atrial systole * atria squeezes the last final 25ml of blood * end of ventricular diastole * 130mL on both ventricles “ END DIASTOLIC VOLUME” 3.The action potential propagates rapidly again after entering the AV bundle. About 0.2 sec after onset of the P wave, it has propagated through the bundle branches, Purkinje fibers, and the entire ventricular myocardium. Depolarization progresses down the septum, upward from the apex, and outward from the endocardial surface, producing the QRS complex. At the same time, atrial repolarization is occurring, but it is not usually evident in an ECG because the larger QRS complex masks it. 4. QRS complex marks onset of ventricular depolarization II. Ventricular Systole 1. Ventricular depolarization └ ventricular systole (pressure rises in ventricles; pressure pushes blood against AV valve closing them; SL & AV valves closed) └ ISOMETRIC CONTRACTION ( contracting and exerting force but no shortening of muscle) 2. Continued contraction of ventricles--- pressure build up sharply  left ventricular pressure must surpass aortic pressure (80mmHg)  right ventricular pressure must surpass pulmonary trunk ( 20mmHg) 3. Ventricular Ejection  SL valves are open  70 mL each → 60mL remains in ventricles after ejection “ END SYSTOLIC VOLUME” → equals EDV-ESV = 130mL- 60mL= 70mL → Stroke Volume : volume ejected per beat from each ventricles → T wave marks the onset of ventricular repolarization 4. Contraction of ventricular contractile fibers (ventricular systole) begins shortly after the QRS complex appears and continues during the S–T segment. As contraction proceeds from the apex toward the base of the heart, blood is squeezed upward toward the semilunar valves. 2. Continued contraction of ventricles--- pressure build up sharply  left ventricular pressure must surpass aortic pressure (80mmHg)  right ventricular pressure must surpass pulmonary trunk ( 20mmHg) 3. Ventricular Ejection  SL valves are open  70 mL each → 60mL remains in ventricles after ejection “ END SYSTOLIC VOLUME” → equals EDV-ESV = 130mL- 60mL= 70mL → Stroke Volume : volume ejected per beat from each ventricles → T wave marks the onset of ventricular repolarization 5. Repolarization of ventricular contractile fibers 6. Shortly after the T wave begins, the ventricles begins at the apex and spreads throughout the start to relax (ventricular diastole). ventricular myocardium. By 0.6 sec, ventricular repolarization is complete This produces the T wave in the ECG about 0.4 and ventricular contractile fibers are relaxed. sec after the onset of the P wave.  Regulation of Stroke Volume 1.Preload: Effect of Stretching -A greater preload (stretch) on cardiac muscle fibers prior to contraction increases their force of contraction -Within limits, the more the heart fills with blood during diastole, the greater the force of contraction during systole. This relationship is known as the Frank–Starling law of the heart The Frank–Starling law of the heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations. If the left side of the heart pumps a little more blood than the right side, the volume of blood returning to the right ventricle (venous return) increases. The increased EDV causes the right ventricle to contract more forcefully on the next beat, bringing the two sides back into balance. 2. Myocardial Contractility 3. AFTERLOAD -The pressure that must be overcome before a semilunar valve can open is termed the afterload The pressure that must be overcome before a semilunar valve can open is termed the afterload. -An increase in afterload causes stroke volume to decrease, so that more blood remains in the ventricles at the end of systole. Conditions that can increase afterload include hypertension (elevated blood pressure) and narrowing of arteries by atherosclerosis.  Regulation of Heart Rate The sinoatrial (SA) node initiates contraction and, if left to itself, would set a constant heart rate of about 100 beats/min. However, tissues require different volumes of blood flow under different conditions Autonomic Regulation of Heart Rate Nervous system regulation of the heart originates in the cardiovascular center in the medulla oblongata. This region of the brain stem receives input from a variety of sensory receptors and from higher brain centers, such as the limbic system and cerebral cortex. The cardiovascular center then directs appropriate output by increasing or decreasing the frequency of nerve impulses in both the sympathetic and parasympathetic branches of the ANS Even before physical activity begins, especially in competitive situations, heart rate may climb. This anticipatory increase occurs because the limbic system sends nerve impulses to the cardiovascular center in the medulla. Sympathetic nerve Parasympathetic nerve Chemical Regulation of Heart Rate 1. Hormones Epinephrine and norepinephrine -(from the adrenal medullae) enhance the heart’s pumping effectiveness. - affect cardiac muscle fibers in much the same way as does norepinephrine released by cardiac accelerator nerves—they increase both heart rate and contractility. Exercise, stress, and excitement cause the adrenal medullae to release more hormones. Thyroid hormones also enhance cardiac contractility and increase heart rate. 2. Cations ØGiven that differences between intracellular and extracellular concentrations of several cations (for example, Na and K) are crucial for the production of action potentials in all nerve and muscle fibers, it is not surprising that ionic imbalances can quickly compromise the pumping effectiveness of the heart. ØIn particular, the relative concentrations of three cations—K, Ca2, and Na—have a large effect on cardiac function. Elevated blood levels of K or Nadecrease heart rate and contractility. Excess Na blocks Ca2 inflow during cardiac action potentials, thereby decreasing the force of contraction, whereas excess K blocks generation of action potentials. A moderate increase in interstitial (and thus intracellular) Ca2 level speeds heart rate and strengthens the heartbeat Other Factors in Heart Rate Regulation Age, gender, physical fitness, and body temperature also influence resting heart rate. A newborn baby is likely to have a resting heart rate over 120 beats/min; the rate then gradually declines throughout life. Adult females often have slightly higher resting heart rates than adult males, although regular exercise tends to bring resting heart rate down in both sexes. THANK YOU ACTIVATE YOUR NEURONS. EVERYTHING IS POSSIBLE. UNLEASH YOUR POWERS! Systemic Circulation: Arteries Aorta Arteries to the Head and the Neck Arteries of the Upper Limb Branches of the Aorta Fig. 18.13 Arteries of the Pelvis and Lower Limb Systemic Circulation: Veins Systemic Circulation: Veins Veins of the Upper Limb  Veins of the Thorax The left and right brachiocephalic veins and the azygos veins return blood to the superior vena cava Veins of the Lower Limb