BIO139FALL2021/CHAP19HEART/SALADIN

SYMPATHETIC PATHWAY TO HEART

(1) -Stimulatory signals from cardioacceleratory center descend to upper thoracic segments (T1-T4) of spinal cord, ending on sympathetic preganglionic neurons in lateral horn. -Preganglionic fibers arise here and travel to adjacent sympathetic chain ganglia. (2) -Some of these fibers synapse with postganglionic neurons at level of entry into the chain, and others ascend to cervical ganglia and meet postganglionic neurons there. (3) -Postganglionic fibers emerging from sympathetic chain form cardiac nerves. -These lead to cardiac plexus, a web of mixed sympathetic and parasympathetic fibers tucked in between aortic arch, pulmonary trunk, and lower trachea. (4) -Postganglionic fibers continue through plexus without synapsing and end on several targets in and near heart: SA node, AV node, atrial and ventricular myocardium, aorta, pulmonary trunk, and coronary arteries.

4 MAIN HEART VALVES

(2) ATRIOVENTRICULAR VALVES -Tricuspid -Bicuspid (Mitral) (2) SEMILUNAR VALVES -Aortic -Pulmonary

PRINCIPLES OF VOLUME, PRESSURE, AND FLOW (Illustrated with syringe)

(a) -As plunger is pulled back, volume of enclosed space increases, its pressure falls, and pressure inside syringe (P1) is lower than pressure outside (P2). -Pressure gradient causes air to flow inward until pressures are equal. -This is analogous to filling of expanding heart chamber. (b) -As plunger is depressed, volume of enclosed space decreases, P1 rises above P2, and air flows out until pressures are equal. -This is analogous to ejection of blood from contracting heart chamber. -In both cases, fluids flow down pressure gradients. -At rest, air pressures within syringe barrel and in atmosphere surrounding it are equal. -But for given quantity (mass) of air, and assuming constant temperature, pressure is inversely proportional to volume of container—the greater the volume, the lower the pressure, and vice versa. -Suppose you pull back plunger of syringe (fig. 19.18a). -This increases volume and lowers air pressure within barrel. -Now you have a pressure gradient, with pressure outside syringe being greater than pressure inside. -Air will flow down its gradient into syringe until the two pressures are equal. -If you then push plunger in (fig. 19.18b), pressure inside barrel will rise above pressure outside, and air will flow out—again going down its pressure gradient but in reverse direction.

OPERATION OF HEART VALVES

(a) ATRIOVENTRICULAR VALVES. -When ATRIAL pressure is GREATER than VENTRICULAR pressure, valve OPENS and blood flows through -When VENTRICULAR pressure is GREATER than ATRIAL pressure, blood in ventricle pushes valve cusps CLOSED (b) SEMILUNAR VALVES. -When VENTRICULAR pressure is greater than ARTERIAL pressure, semilunar valves OPEN and blood is ejected. -When VENTRICULAR pressure is lower than ARTERIAL pressure, arterial blood holds valves CLOSED

NORMAL AND PATHOLOGICAL ELECTROCARDIOGRAMS

(a) Normal sinus rhythm. (b) Ventricular fibrillation, with grossly irregular waves of depolarization, as seen in a heart attack (myocardial infarction). (c) Atrial fibrillation; between heartbeats, atria exhibit weak, chaotic, high-frequency depolarizations instead of normal P waves. (d) Heart block, in which some atrial depolarizations (P waves) are not conducted to ventricles and not followed by ventricular QRS waves. (e) Premature ventricular contraction, or extrasystole (at arrow); note absence of P wave, inverted QRS complex, misshapen QRS, and elevated T. -Fibrillation kills quickly if it isn't stopped. -DEFIBRILLATION is emergency procedure in which heart is given strong electrical shock with pair of paddle electrodes. -The purpose is to depolarize entire myocardium and stop fibrillation, with hope that SA node will resume its sinus rhythm. -This doesn't correct underlying cause of fibrillation, but may sustain patient's life long enough to allow for corrective action.

CARDIAC ARRHYTHMIAS

*VENTRICULAR FIBRILLATION -most widely known arrhythmia, but others are not uncommon. *ATRIAL FIBRILLATION (AF, AFib) -weak rippling contraction in atria, manifested in ECG by chaotic, high-frequency depolarizations (400-650/min.). -Fibrillating atria fail to stimulate ventricles, so we see a dissociation between random atrial depolarizations and ventricular QRS and T waves of the ECG. -This is most common atrial arrhythmia in elderly. -can result from such valvular disease, thyroid hormone excess, or myocardial inflammation, and often seen in alcoholism. -Blood continues to flow through atria into ventricles even during AF, so AF isn't immediately life-threatening. -Blood flow is more sluggish and there is higher risk of blood clots causing pulmonary embolism or stroke. *HEART BLOCK -failure of any part of cardiac conduction system to conduct signals -usually result of disease and degeneration of conduction system fibers. -In ECG, one sees rhythmic atrial P waves, but ventricles fail to receive signal and no QRS wave follows the P . *BUNDLE BRANCH BLOCK -heart block resulting from damage to one or both branches of AV bundle. *TOTAL HEART BLOCK, -caused by damage to AV NODE -signals from atria fail to reach ventricles at all -ventricles beat at their own intrinsic rhythm of 20-40 bpm. *PREMATURE VENTRICULAR CONTRACTION (PVC) -result of ventricular ectopic focus firing and setting off an extra beat (extrasystole) before normal signal from SA node arrives. -P wave is missing and QRS wave is inverted and misshapen -PVCs occur singly or in bursts. -occasional extra beat isn't serious, and may result from emotional stress, lack of sleep, or irritation of heart by stimulants (nicotine, caffeine). -Persistent PVCs, however, can indicate more serious pathology and sometimes lead to ventricular fibrillation and sudden death. -Any deviation from regular, SA node-driven sinus rhythm of heartbeat is called an arrhythmia. -most familiar and feared of these is ventricular fibrillation (VF, VFib) *VENTRICULAR FIBRILLATION is the hallmark of a heart attack (myocardial infarction). -Most cases occur in patients with history of coronary artery disease. -ECG shows weak, chaotic ventricular depolarizations as electrical signals travel randomly about myocardium and return to repeatedly restimulate same area instead of dying out like a normal ventricular depolarization. -To the surgeon's eye and hand, a fibrillating ventricle exhibits squirming, uncoordinated contractions often described as feeling "like a bag of worms." -fibrillating ventricle pumps no blood, so there is no coronary blood flow and myocardial tissue rapidly dies of ischemia, as does cerebral tissue. *CARDIAC ARREST is cessation of cardiac output, with ventricles either motionless or in fibrillation.

CHAMBERS OF THE HEART

*heart has 4 chambers -2 SUPERIOR chambers (ATRIA) -right atrium, -left atrium -2 INFERIOR chambers (VENTRICLES) -right ventricle, -left ventricle -On surface boundaries of the four chambers are marked by three sulci (grooves), which are largely filled by fat and coronary blood vessels -The CORONARY SULCUS encircles heart near base and separates atria above from ventricles below. -It can be exposed by lifting margins of atria. -The other two sulci extend obliquely down heart from coronary sulcus toward apex—one on front of heart called ANTERIOR INTERVENTRICULAR SULCUS and one on back called POSTERIOR INTERVENTRICULAR SULCUS -These sulci overlie the interventricular septum. -The coronary sulcus and two interventricular sulci harbor the largest of the coronary blood vessels.

RIGHT and LEFT VENTRICLES

-2 INFERIOR chambers, -pumps that eject blood into arteries and keep it flowing around body. -RIGHT ventricle constitutes most anterior aspect of heart -LEFT ventricle forms apex and inferoposterior aspect. -Internally ventricles are separated by thick muscular wall, interventricular septum. -RIGHT ventricle pumps blood only to lungs and back to left atrium, so its wall is only moderately muscular. -LEFT ventricle wall, including septum, is 2-4 times as thick because it bears greatest workload of all four chambers, pumping blood through entire body -LEFT ventricle is roughly circular in cross section, whereas right ventricle wraps around the left and has a C shape -Both ventricles exhibit internal ridges called trabeculae carneae -It is thought that trabeculae carneae may serve to keep ventricular walls from clinging to each other like suction cups when heart contracts and allow chambers to expand more easily when they refill.

RIGHT and LEFT ATRIA

-2 SUPERIOR heart chambers -receiving chambers for blood returning to heart by way of great veins. -Most of the mass of each atrium is on posterior side of heart, -only small portion is visible from anterior view. -Here, each atrium has earlike flap called AURICLE that slightly increases its volume -atria exhibit THIN flaccid walls corresponding to their light workload —all they do is pump blood into ventricles immediately below. -separated from each other by a wall called interatrial septum. -RIGHT atrium and both auricles exhibit internal ridges of myocardium called pectinate muscles.

CARDIAC OUTPUT

-CARDIAC OUTPUT (CO) is amount of blood ejected by each ventricle in 1 minute ( CO=HR X SV ) -It is the product of stroke volume (ml/beat) and heart rate (bpm). -If HR is heart rate (beats/min.) and SV is stroke volume (mL/beat), -At typical resting values ( CO=75 beats/min. X 70mL/beat=5,250 mL/min. ) -body's total volume of blood (4-6 L) passes through heart every minute; -RBC leaving left ventricle arrives back at left ventricle in 1 minute. -Cardiac output varies with body's state of activity. -Vigorous exercise increases CO as much as 21 L/min.-person in good condition and more than 40 L/min. in world-class athletes. -CARDIAC RESERVE is difference between maximum and resting cardiac output -People with severe heart disease may have little or no cardiac reserve and little tolerance of physical exertion. -Given that cardiac output equals HR x SV, there are only two ways to change it: -Change heart rate or change stroke volume. -heart rate and stroke volume are somewhat interdependent. -they usually change together and in opposite directions. -As heart rate goes up, stroke volume goes down, and vice versa.

PULMONARY AND SYSTEMIC CIRCUITS

-CARDIOVASCULAR SYSTEM has two major divisions: -pulmonary circuit -systemic circuit *PULMONARY CIRCUIT -carries blood to lungs for gas exchange and returns it to heart -supplied with blood from right half of heart *SYSTEMIC CIRCUIT -supplies blood to every organ of body, including other parts of lungs and wall of heart itself *RIGHT HALF OF HEART -supplies PULMONARY circuit. -receives unoxygenated blood that has circulated through body, unloaded its oxygen and nutrients, and picked up load of carbon dioxide and other wastes. -pumps oxygen-poor blood into large artery -PULMONARY TRUNK, which immediately divides into right and left pulmonary arteries. -PULMONARY ARTERIES transport blood to air sacs ALVEOLI (air sacs) of lungs, where carbon dioxide is unloaded and oxygen is picked up. -oxygen-rich blood flows through PULMONARY VEINS to left side of heart. *LEFT SIDE OF HEART -supplies SYSTEMIC circuit. -Blood leaves left side of heart through AORTA. -AORTA turns like an inverted U, the AORTIC ARCH and passes downward posterior to heart. -ARCH gives off arteries that supply head, neck, and upper limbs. -AORTA travels through thoracic and abdominal cavities and issues smaller arteries to other organs before branching into lower limbs. -After circulating through body, DEOXYGENATED systemic blood returns to RIGHT side of heart mainly by two large veins: SUPERIOR VENA CAVA (drains upper body) and INFERIOR VENA CAVA (drains everything below diaphragm). -Major arteries and veins entering and leaving heart are called GREAT VESSELS (great arteries and veins) because their relatively large diameters. The Five great vessels enter and leave heart: -superior and inferior vena cava, -pulmonary artery, -pulmonary vein, -aorta. https://www.getbodysmart.com/heart-anatomy/major-blood-vessels-heart

ELECTRICAL AND CONTRACTILE ACTIVITY OF THE HEART

-CONTRACTION is systole -RELAXATION is diastole -These terms can refer to specific part of heart (for example, atrial systole), but if no particular chamber is specified, they usually refer to more conspicuous and important ventricular action, which ejects blood from heart.

METABOLISM OF CARDIAC MUSCLE

-Cardiac muscle depends almost exclusively on AEROBIC RESPIRATION to make ATP. -It is very rich in myoglobin (a short-term source of oxygen for aerobic respiration) and glycogen (for stored energy). -huge mitochondria fill 25% of cell; -adaptable with respect to organic fuels used. -At rest heart gets 60% of its energy from fatty acids, 35% from glucose, and 5% from other fuels such as ketones, lactate, and amino acids. -vulnerable to oxygen deficiency than it is to lack of fuel. -Because it rarely uses anaerobic fermentation or oxygen debt mechanism, it is not prone to fatigue. -cardiac muscle can maintain rhythm without fatigue for a lifetime.

OVERVIEW OF VOLUME CHANGES

-Equal output by ventricles is essential for homeostasis. -If RIGHT VENTRICLE PUMPS MORE BLOOD THAN LEFT VENTRICLE CAN HANDLE ON RETURN: -blood accumulates in LUNGS causing: -Pulmonary Hypertension, -edema -risk of drowning in one's own body fluid -LEFT VENTRICULAR FAILURE: -one of the 1st signs is respiratory distress—shortness of breath and sense of suffocation. -if LEFT VENTRICLE PUMPS MORE THAN RIGHT:, -blood accumulates in SYSTEMIC CIRCUIT causing: -hypertension -widespread systemic edema *SYSTEMIC EDEMA, once called DROPSY, marked by: -enlargement of liver; -distension of jugular veins in neck; -swelling of fingers, ankles, and feet; -ascites(pooling of fluid in abdominal cavity) -can lead to stroke or kidney failure. -failure of one ventricle increases workload on the other ventricle, which stresses it and often leads to its eventual failure as well. -if output of left ventricle were just 1% greater than output of right, it would completely drain lungs of blood in less than 10 minutes (although death would occur much sooner). *CONGESTIVE HEART FAILURE (CHF) -Fluid accumulation in either circuit due to insufficiency of ventricular pumping -Common causes of CHF: -myocardial infarction, -chronic hypertension, -valvular defects, -congenital (birth) defects in cardiac anatomy.

AUTONOMIC INNERVATION OF THE HEART

-Even though heart has its own pacemaker, its rhythm and contraction strength are moderated by signals arising from two cardiac centers in medulla oblongata of brainstem: (1) cardioacceleratory center (2) cardioinhibitory center *CARDIOACCELERATORY CENTER -communicates with heart by way of right and left cardiac nerves carrying sympathetic postganglionic nerve fibers. *CARDIOINHIBITORY CENTER cardioinhibitory center, which communicates with heart by way of right and left vagus nerves carrying parasympathetic preganglionic nerve fibers. -SYMPATHETIC stimulation increases heart rate and contraction strength and dilates coronary arteries to increase blood supply to exercising Myocardium. -PARASYMPATHETIC signals from cardioinhibitory center exit medulla oblongata through the two vagus nerves. -These nerves travel down right and left sides of mediastinum -Preganglionic fibers of vagus travel through cardiac plexus, mingling with sympathetic fibers. -They synapse with short postganglionic fiber in the plexus or in epicardium of atria, especially near SA and AV nodes. -Short postganglionic fibers of right vagus nerve lead mainly to SA node, and those of left vagus lead mainly to AV node, -but each has some fibers that cross over to other target cells. -some parasympathetic fibers terminate on sympathetic fibers and inhibit them from stimulating heart and opposing the parasympathetic effect. -There is little or no parasympathetic innervation of myocardium or ventricles. -sympathetic nerves dominate control of contraction strength. -Heart rate is strongly influenced by both divisions, but dominated by vagus nerves. -cardiac nerves carry not only sympathetic efferent fibers, but also sensory (afferent) fibers from heart to CNS. -These fibers are important in cardiovascular reflexes and transmission of pain signals from heart.

HEART FRAMEWORK

-FIBROUS SKELETON made of collagenous and elastic fibers -especially concentrated in walls between heart chambers, in fibrous rings (anuli fibrosi) around valves, and in sheets of tissue that interconnect these rings *FIBROUS SKELETON FUNCTIONS: (1) provides structural support for heart, especially around valves and openings of great vessels; holds these orifices open and prevents excessive stretching when blood surges through them. (2) anchors cardiomyocytes and gives them something to pull against. (3) nonconductor of electricity, serves as electrical insulation between atria and ventricles, so atria cannot stimulate ventricles directly. Insulation is important to timing and coordination of electrical and contractile activity. (4) It is thought that elastic recoil of fibrous skeleton may aid in refilling heart with blood after each beat

IMPULSE CONDUCTION TO MYOCARDIUM

-Firing of SA NODE excites atrial cardiomyocytes and stimulates two atria to contract almost simultaneously. -signal travels at speed of 1 m/s through atrial myocardium and reaches AV node in 50 ms. -AV NODE, signal slows down to 0.05 m/s, because cardiomyocytes here are thinner, more importantly because they have fewer gap junctions over which signal can be transmitted. -This delays signal at AV node for 100 ms—. -delay is essential because it gives ventricles time to fill with blood before they begin to contract. -ventricular myocardium has conduction speed of 0.3-0.5 m/s. -If this were only route of travel for excitatory signal, some cardiomyocytes would be stimulated much sooner than others. -Ventricular contraction wouldn't be synchronized and pumping effectiveness of ventricles would be severely compromised. -Signals travel through AV BUNDLE and SUBENDOCARDIAL CONDUCTING NETWORK at speed of 4 m/s, -the fastest in conduction system, due to very high density of gap junctions. -the entire ventricular myocardium depolarizes within 200 ms after SA node fires, causing ventricles to contract in near unison. -Ventricular systole begins at apex of heart, which is first to be stimulated, and progresses upward—pushing blood upward toward semilunar valves. -Because of spiral arrangement of the vortex of heart, ventricles twist slightly as they contract, like someone wringing out a towel. CARDIAC CONDUCTION SEQUENCE: > SA Node > AV Node > AV Bundle > Subendocardial Conducting Network (SCN)

PRESSURE GRADIENTS AND FLOW

-Fluid flows only if it is subjected to more pressure at one point than at another. -The difference creates a PRESSURE GRADIENT -fluids always flow DOWN their pressure gradients, from high-pressure point to low-pressure point. -When ventricle expands, its internal pressure falls. -If AV valve is open, blood flows into ventricle from atrium above. -When ventricle contracts, its internal pressure rises. -When aortic valve opens, blood is ejected from ventricle into aorta. -Opening and closing of heart valves are governed by pressure changes. -Valves are soft flaps of connective tissue with no muscle. -They don't exert any effort of their own, passively pushed open and closed by changes in blood pressure on upstream and downstream sides of valve. -When ventricles are relaxed and their pressure is low, AV valve cusps hang down limply and both valves are open -Blood flows freely from atria into ventricles before atria contract. -As ventricles fill with blood, cusps float upward toward closed position. -When ventricles contract, their internal pressure rises sharply and blood surges against AV valves from below. -This pushes cusps together, seals openings, and prevents blood from flowing back into atria. -Papillary muscles contract slightly before rest of ventricular myocardium and tug on tendinous cords, preventing valves from bulging excessively (prolapsing) into atria or turning inside out

HEART WALL

-HEART WALL consists of 3 layers: -EPICARDIUM -MYOCARDIUM -ENDOCARDIUM

CARDIAC MUSCLE AND CARDIAC CONDUCTION SYSTEM

-Heart contracts at regular intervals, 75 beats per minute (bpm) in resting adult. -in vertebrates from fish to humans, heartbeat is MYOGENIC because signal originates within heart itself. -Heart is AUTORHYTHMIC because it doesn't depend on nervous system for its rhythm. -has own built-in pacemaker and electrical system. -the cardiac muscle, pacemaker, and internal electrical system are foundations for its electrical activity and rhythmic beat.

HORMONES, DRUGS, AND OTHER CHRONOTROPIC CHEMICALS

-Heart rate is influenced by many other factors besides autonomic nervous system. -Thyroid hormone increases heart rateit by stimulating up-regulation of β-adrenergic receptors, making heart more sensitive to sympathetic stimulation; this is why tachycardia is one of the signs of hyperthyroidism. -Glucagon, secreted by alpha cells of pancreatic islets, accelerates heart by promoting cAMP production. -Glucagon is sometimes given in cardiac emergencies to stimulate heartbeat, -Epinephrine frequently given to support cardiac output and blood pressure in life-threatening allergic reactions. -Food-borne drugs and medications have well-known chronotropic effects related to catecholamine-cAMP mechanism. -Nicotine accelerates heart by stimulating catecholamine secretion. -Caffeine and related stimulants in tea and chocolate accelerate heart by inhibiting cAMP breakdown, prolonging its adrenergic effect. -Hypertension treated with drugs called beta blockers, which inhibit binding of catecholamines to β-adrenergic receptors and slow down heart. -Electrolyte concentrations strongly influence heart rate and contraction strength. -most powerful chronotropic effects are from potassium ions (K+). HYPERKALEMIA a potassium excess, K+ diffuses into cardiomyocytes and keeps membrane voltage elevated, inhibiting cardiomyocyte repolarization. Myocardium becomes less excitable, heart rate becomes slow and irregular, and heart may arrest in diastole. In HYPOKALMEIA, a potassium deficiency, K+ diffuses out of cardiomyocytes and become hyperpolarized—membrane potential is more negative than normal. Making them harder to stimulate. -POTASSIUM IMBALANCES are very dangerous and require emergency medical treatment. -Calcium also affects heart rate. -HYPERCALCEMIA a calcium excess causes slow heartbeat, whereas a calcium deficiency -HYPOCALCEMIA a calcium deficiency elevates heart rate. -calcium imbalances are relatively rare, and when they do occur, their primary effect is on contraction strength

HEART RATE AND CHRONOTROPIC AGENTS

-Heart rate is most easily measured by taking person's pulse at point where an artery runs close to body surface, such as radial artery in wrist or common carotid artery in neck. -Each beat of heart produces a surge of pressure that can be felt by palpating a superficial artery with fingertips. -Heart rate can be obtained by counting number of pulses in 15 seconds and multiplying by 4 to get beats per minute. -In newborn infants, resting heart rate is 120 bpm+ -It declines steadily with age, averaging 72-80 bpm in young adult females and 64-72 bpm in young adult males. -Hear rate rises in the elderly. -POSITIVE CHONOTROPIC AGENTS are factors outside of heart itself that RAISE heart rate -NEGATIVE CHONOTROPIC AGENTS are factors outside of heart itself that LOWER heart rate

ENDOCARDIUM

-INNERMOST lining of heart -lines interior of heart chambers -simple squamous epithelium overlying thin areolar tissue layer; -no adipose tissue. -covers valve surfaces -continuous with endothelium of blood vessels.

ARTERIAL SUPPLY

-Immediately after aorta leaves left ventricle, it gives off a right and left coronary artery. -The orifices of these two arteries lie deep in pockets formed by two of the aortic valve cusps -LEFT CORONARY ARTERY (LCA) travels through coronary sulcus under left auricle and divides into two branches: - (1) ANTERIOR INTERVENTRICULAR BRANCH -travels down anterior interventricular sulcus to apex, rounds the bend, and travels short distance up to posterior side of heart. -There it joins posterior interventricular branch -Clinically, it is called left anterior descending (LAD) branch. -supplies blood to both ventricles and anterior two-thirds of interventricular septum. -(2) CIRCUMFLEX BRANCH continues around left side of heart in coronary sulcus. -gives off left marginal branch that passes down left margin of heart -ends on posterior side of heart. -supplies blood to left atrium and posterior wall of left ventricle. -RIGHT CORONARY ARTERY (RCA) supplies right atrium and sinuatrial node (pacemaker) -continues along coronary sulcus under right auricle, and gives off two branches of its own: (1) RIGHT MARGINAL BRANCH -runs toward apex of heart -supplies lateral aspect of right atrium and ventricle. -RCA continues around right margin of heart to posterior side, sends small branch to atrioventricular node, then gives off large (2) POSTERIOR INTERVENTRICULAR BRANCH -travels down corresponding sulcus -supplies posterior walls of both ventricles and posterior portion of interventricular septum. -ends by joining anterior interventricular branch of LCA. -energy demand of cardiac muscle is so critical that interruption of blood supply to any part of myocardium can cause necrosis within minutes. -A fatty deposit or blood clot in coronary artery can cause MYOCARDIAL INFARCTION (MI), or heart attack. -to protect against MYOCARDIAL INFARCTION some coronary arteries converge at various points and combine blood flow to points farther downstream. -Points where two arteries come together are called arterial anastomoses -arterial anastomoses provide alternative routes of blood flow (collateral circulation) that can supply heart tissue with blood if primary route becomes obstructed.

MYOCARDIUM

-MIDDLE layer -composed of cardiac muscle. -thickest layer and performs work of heart. -thickness is proportional to workload on individual chambers. -Its muscle is organized into bundles that spiral around heart, forming VORTEX OF HEART -Ventricles TWIST/WRING when they contract which enhances ejection of blood.

CARDIAC RHYTHM

-NORMAL heartbeat triggered by SA NODE is called SINUS RHYTHM -At rest, adult heart beats 70-80 times per minute, -heart rates 60-100 bpm are not unusual. -Any region of spontaneous firing other than SA node is called ECTOPIC FOCUS -If SA node is damaged, an ectopic focus may take over governance of heart rhythm. -most common ectopic focus is AV NODE, which produces heartbeat of 40-50 bpm called nodal NODAL (junctional) RHYTHM -If neither SA nor AV node is functioning, other ectopic foci fire at rates of 20-40 bpm. -Nodal rhythm is sufficient to sustain life, but rate of 20-40 bpm provides too little flow to brain to be survivable. -This is one condition that calls for artificial pacemaker.

MEASUREMENT OF PRESSURE

-PRESSURE measured by MANOMETER - J-shaped glass tube partially filled with mercury. -Sealed upper end, above the mercury, contains a vacuum, whereas lower end is open. -Pressure applied at lower end is measured in terms of how high it can push mercury column up evacuated end of tube. -Mercury is used because it's so dense; it enables to measure pressure with shorter columns than needed with less dense liquid such as water. -Pressures are expressed in millimeters of mercury (mm Hg). -Blood pressure traditionally measured with sphygmomanometer—a calibrated mercury manometer with its open lower end attached to inflatable pressure cuff wrapped around arm (mercury sphygmomanometers are being increasingly replaced by dial and digital devices).

CARDIOLOGY

-Study of the heart and its action and diseases.

CENTRAL NERVOUS SYSTEM ROLE WITH HEART

-There is a benefit to placing heart rate under influence of cardiac centers in medulla—these centers can receive input from many other sources and integrate it into decision as to whether heart should beat more quickly or slowly. -Sensory and emotional stimuli can act on cardiac centers by way of cerebral cortex, limbic system, and hypothalamus; therefore, heart rate can climb even as you anticipate taking first plunge on roller coaster or competing in athletic event -Heart rate is influenced by emotions such as love and anger. -medulla receives input from the following receptors in muscles, joints, arteries, and brainstem: -PROPRIOCEPTORS -BARORECEPTORS -CHEMORECEPTORS

-ARTERIES carry OXYGENATED blood AWAY from heart to tissues, except for PULMONARY ARTERIES, which carry DEOXYGENATED blood from RIGHT VENTRICLE to LUNGS for oxygenation Recall RIGHT Heart=Deoxygenated Blood -Blood enters right atrium and passes through right ventricle. -right ventricle pumps blood to lungs where it becomes oxygenated. -oxygenated blood brought back to heart by pulmonary veins which enter left atrium. -From left atrium blood flows into left ventricle. Deoxygenated Blood path: Vena Cava Right Atrium Tricuspid Valve Right Ventricle Semilunar Valve Pulmonary Artery Lungs Oxygenated Blood path: Lungs Pulmonary veins Left Atrium Mitral (Bicuspid) Valve Left Ventricle Aortic Valve Aorta

-VEINS carry DEOXYGENATED blood TOWARDS heart but PULMONARY VEINS carry OXYGENATED blood from LUNGS to LEFT ATRIUM Recall LEFT Heart= Oygenated Blood -Blood enters right atrium and passes through right ventricle. -right ventricle pumps blood to lungs where it becomes oxygenated. -oxygenated blood brought back to heart by pulmonary veins which enter left atrium. -From left atrium blood flows into left ventricle. Deoxygenated Blood path: Vena Cava Right Atrium Tricuspid Valve Right Ventricle Semilunar Valve Pulmonary Artery Lungs Oxygenated Blood path: Lungs Pulmonary veins Left Atrium Mitral (Bicuspid) Valve Left Ventricle Aortic Valve Aorta

ELECTRICAL BEHAVIOR OF MYOCARDIUM

-action potentials of cardiomyocytes are significantly different from those of neurons and skeletal muscle fibers -Cardiomyocytes have resting potential of -90 mV -depolarize only when stimulated, unlike cells of SA node. -A stimulus opens voltage-gated sodium channels, causing Na+ INFLOW and depolarizing cell to threshold. -threshold voltage rapidly OPENS additional Na+ channels and triggers positive feedback cycle -action potential peaks at +30 mV. -Na+ channels CLOSE quickly, and rising phase of action potential is very brief. -As action potentials spread over plasma membrane, they OPEN voltage-gated slow calcium channels, which admit small amount of Ca2+ from extracellular fluid into cell. -This Ca2+ binds to ligand-gated Ca2+ channels on sarcoplasmic reticulum (SR), opening them and releasing greater quantity of Ca2+ from SR into cytosol. -This second wave of Ca2+ binds to troponin and triggers contraction - SR provides 90% to 98% of Ca2+ needed for myocardial Contraction. -In cardiac muscle depolarization is prolonged for 200 to 250 ms (at a heart rate of 70-80 bpm), producing long plateau in action potential—perhaps because Ca2+ channels of SR are slow to close or because SR is slow to remove Ca2+ from cytosol. -Cardiomyocytes remain contracted for as long as action potential is in its plateau. -cardiac muscle has more sustained contraction necessary to expel blood from heart chambers. -Both atrial and ventricular cardiomyocytes exhibit plateaus, but more pronounced in ventricles. -At end of plateau, Ca2+ channels close and K+ channels open. -Potassium diffuses rapidly OUT of cell and Ca2+ is transported back into extracellular fluid and SR. -Membrane voltage drops rapidly, and muscle tension declines -Cardiac muscle has absolute refractory period of 250 ms, -long refractory period prevents wave summation and tetanus

PRELOAD

-amount of tension (stretch) in ventricular myocardium immediately before it begins to contract. -Because of length-tension relationship of striated muscle moderate stretch enables cardiomyocytes to generate more tension when they contract—that is, stretch increases preload. -When ventricles contract more forcefully, they expel more blood, thus adjusting cardiac output to the increase in venous return. -principle is summarized by Frank-Starling law of the heart states that SV ∝ EDV; stroke volume is proportional to the end-diastolic volume. -meaning ventricles tend to eject as much blood as they receive. -the more ventricles are stretched, the harder they contract on next beat -Although relaxed skeletal muscle is at optimum length for most forceful contraction, relaxed cardiac muscle is at less than optimum length. -Additional stretch produces significant increase in contraction force on next beat, which helps balance output of the two ventricles. *EX; -right ventricle begins to pump increased amount of blood, that arrives at left ventricle, stretches it more than before, and causes it to increase its stroke volume and match that of the right.

BARORECEPTORS (pressoreceptors)

-are pressure sensors in aorta and internal carotid arteries -send continual stream of signals to medulla. *When heart rate rises, cardiac output increases and raises blood pressure at baroreceptors. -barorecptors increase signaling to medulla and may issue vagal output to lower heart rate. *baroreceptors also inform medulla of drops in blood pressure -medulla can issue sympathetic output to increase heart rate, bringing cardiac output and blood pressure back up to normal. -Either way, negative feedback loop prevents blood pressure from deviating too far from normal.

PACEMAKER PHYSIOLOGY

-cells of SA NODE don't have stable resting membrane potential. -membrane potential starts at -60 mV and drifts upward, showing gradual depolarization called pacemaker potential (prepotential) . -results from slow INFLOW of Na+ without compensating OUTFLOW of K+. -When pacemaker potential reaches threshold of -40 mV, voltage-gated calcium channels OPEN, Ca2+ flows IN from EXTRACELLULAR fluid. -This produces rising depolarizing phase of action potential, which peaks slightly above 0 mV. -At that point, K+ channels open and K+ leaves cell. -makes cytosol increasingly negative -creates (falling) repolarizing phase of action potential. -When repolarization is complete, K+ channels CLOSE and pacemaker potential starts over, to produce next heartbeat. -Each depolarization of SA NODE sets off one heartbeat. -When SA node fires, it excites other components in conduction system; -SA node serves as system's PACEMAKER! -At rest, it fires every 0.8 second creating heart rate of 75 bpm.

CARDIOVASCULAR SYSTEM

-consists of HEART and BLOOD VESSELS. -HEART is muscular pump that keeps blood flowing through vessels. -VESSELS deliver blood to all body's organs and then return it to heart. -The broader term: "circulatory system" includes blood, and some authorities include lymphatic system as well

PERICARDIUM

-double-walled sac that encloses heart -outer wall of pericardium is tough fibrous sac called FIBROUS pericardium. *FIBROUS PERICARDIUM -surrounds heart but isn't attached to it. -Deep to this is thin membrane called SEROUS pericardium. *SEROUS PERICARDIUM -has two layers: -parietal layer that lines inside of fibrous pericardium -visceral layer that adheres to heart surface and forms outermost layer of heart itself, the EPICARDIUM -The FIBROUS PERICARDIUM is anchored by ligaments to diaphragm below and to sternum anterior to it, and more loosely anchored by fibrous connective tissue to mediastinal tissue posterior to heart. -Space between parietal and visceral layers of serous pericardium is called pericardial cavity -Heart isn't inside pericardial cavity but enfolded by it. -Relationship of heart to pericardium is often described by comparison to fist pushed into underinflated balloon -Balloon surface in contact with fist is like epicardium; -outer balloon surface is like parietal layer, and air space between them is like pericardial cavity. *PERICARDIAL CAVITY -contains 5 to 30 mL of pericardial fluid, exuded by serous pericardium. -Pericardial fluid lubricates membranes and allows heart to beat with minimal friction. -In pericarditis—inflammation of pericardium—membranes become roughened and produce painful friction rub with each heartbeat. -In addition to reducing friction, pericardium isolates heart from other thoracic organs and anchors it within thorax. -allows heart room to expand, yet resists excessive expansion

ELECTROCARDIOGRAM

-electrical currents in heardetected by means of electrodes (leads) applied to skin. -instrument called electrocardiograph amplifies signals and produces record, usually on moving paper chart, called electrocardiogram (ECG or EKG). -To record ECG, electrodes are attached to wrists, ankles, and six locations on chest. -Simultaneous recordings made from electrodes at different distances from heart; -collectively, they provide comprehensive image of heart's electrical activity. -ECG is composite recording of all action potentials produced by nodal and myocardial cells—not be misconstrued as tracing of a single action potential. -ECG has three principal deflections above and below the baseline: -P wave, -QRS complex, -T wave. (The letters were arbitrarily chosen; they don't stand for any words.) *P WAVE -produced when signal from SA node spreads through atria and depolarizes them. -Atrial systole begins 100 ms after P wave begins, during PQ segment. -This segment is 160 ms long and represents time required for impulses to travel from SA node to AV node. *QRS COMPLEX -consists of small downward deflection (Q), -tall sharp peak (R), -a final downward deflection (S). -produced when signal from AV node spreads through ventricular myocardium and depolarizes muscle. -most conspicuous part of ECG because it is produced by depolarization of ventricles, which constitute largest muscle mass of heart and generate greatest electrical current. -complex shape is due to different sizes of two ventricles and different times required for them to depolarize. -Ventricular systole begins shortly after QRS complex, in ST segment. -QRS interval is time of atrial repolarization and diastole, but atrial repolarization sends relatively weak signal that is obscured by electrical activity of more muscular ventricles. -PR interval represents time it takes for signal to pass through AV node before activating ventricles. It doesn't extend all the way to R wave because ventricular response begins at Q. -Abnormalities in this interval can indicate defects that affect conduction time. -QT interval indicates how long ventricles remain depolarized, and corresponds to duration of a cardiomyocyte action potential. -It gets shorter during exercise. -ST segment corresponds to plateau in myocardial action potential and represents time during which ventricles contract and eject blood. *T WAVE -generated by ventricular repolarization immediately before diastole. -ventricles take longer to repolarize than to depolarize; -T wave is smaller and more spread out than QRS complex, and has rounder peak. -Even when T wave is taller than QRS complex, it can be recognized by its relatively rounded peak. -ECG affords wealth of information about normal electrical activity of heart. -Deviations from normal—such as enlarged, inverted, or misshapen waves and abnormal time intervals between waves -invaluable for diagnosing abnormalities in conduction pathways, myocardial infarction, enlargement of heart, and electrolyte and hormone imbalances, among other disorders

EXERCISE AND CARDIAC OUTPUT

-exercise makes heart work harder which increases cardiac output. -main reason heart rate increases at beginning of exercise is proprioceptors in muscles and joints transmit signals to cardiac centers, signifying that muscles are active and will quickly need increased blood flow. -Sympathetic output from cardiac centers increases cardiac output to meet expected demand. -As exercise progresses, muscular activity increases venous return which increases preload on right ventricle and soon occurs in left ventricle as more blood flows through pulmonary circuit and reaches left heart. -As heart rate and stroke volume rise, cardiac output rises, which compensates for increased venous return. -sustained exercise program causes hypertrophy of ventricles, which increases their stroke volume, which allows heart to beat more slowly and still maintain normal resting cardiac output. -Some world-class, endurance-trained athletes have resting heart rates low as 30-40 bpm, but because of higher stroke volume, their resting CARDIAC OUTPUT is same as that of an untrained person. -athletes have greater CARDIAC RESERVE, and can tolerate more exertion than sedentary person can.

PROPRIOCEPTORS

-found in muscles and joints -provide information on changes in physical activity. -Thus, heart can increase its output even before metabolic demands of muscles rise.

EJECTION FRACTION (EF)

-fraction of blood pumped out of left ventricle with each contraction -LVEF calculated by dividing the SV by the end-diastolic volume. Multiply this by 100 to get the percentage. Normal = LVEF 50% to 70% -The End diastolic volume (EDV) is amount of fluid in diaphragm (ventricle) immediately before it is compressed. -The volume left inside diaphragm (ventricle) after ejection (stroke volume) is called End systolic volume (ESV). If EDV = 100 ml and ESV = 60 ml, what is SV? _____________ The fraction (percentage) of the EDV that is pumped out in one cycle is called the Ejection Fraction (EF), and is calculated as follows: EF = (SV / EDV) X 100 https://www.nursingcenter.com/ncblog/august-2021/how-to-calculate-ejection-fraction

REGULATION OF CARDIAC OUTPUT

-heart doesn't pump same amount of blood every minute of every day -varies output according to states of rest, exercise, emotion, and other factors.

STRUCTURE OF CARDIAC MUSCLE

-heart is mostly muscle. -Cardiac muscle is striated like skeletal muscle, but quite different from it in other structural and functional respect *CARDIOMYOCYTES -Branched muscle cells of heart -short & thick -50 to 100 μm long and 10 to 20 μm wide -ends of cell slightly branched to contact several others -collectively they form network throughout each pair of heart chambers—one network in atria and one in ventricles. -Most have single, centrally placed nucleus -up to one-third have two or more nuclei. -nucleus often surrounded by light-staining mass of glycogen. -sarcoplasmic reticulum less developed than skeletal muscle; -sarcoplasmic reticulum lacks terminal cisterns -have footlike sacs associated with T tubules. -T tubules are much larger than in skeletal muscle. -During excitation they admit calcium ions from extracellular fluid to activate contraction. -joined end to end by thick connections called intercalated discs . -intercalated discs appear as dark lines thicker than the striations with the right histological stain -intercalated disc is complex steplike structure with 3 distinctive features not found in skeletal muscle: (1) Interdigitating folds. -plasma membrane at end of cell is folded -The folds of adjoining cells interlock with each other and increase surface area of intercellular contact. (2) Mechanical junctions. -cells tightly joined by two types of mechanical junctions: -the fascia adherens and desmosomes. -FASCIA ADHERENS is most extensive. -a broad band in which actin of thin myofilaments is anchored to plasma membrane and each cell is linked to next via transmembrane proteins. -interrupted here and there by DESMOSOMES (patches of mechanical linkage that prevent contracting cardiomyocytes from pulling apart) (3) Electrical junctions. -intercalated discs contain gap junctions, which form channels that allow ions to flow from cytoplasm of one cardiomyocyte directly into next. -enable each cardiomyocyte to electrically stimulate its neighbors. -entire myocardium of the two atria behaves almost like a single cell, as does entire myocardium of the two ventricles. -unified action is essential for effective pumping of heart chamber. -Cardiac muscle lacks satellite cells that replace dead muscle fibers so repair of damaged cardiac muscle is almost entirely by fibrosis (scarring). -Cardiac muscle has very limited capacity for mitosis and regeneration.

POSITION, SIZE, AND SHAPE OF HEART

-heart lies within thick partition called MEDIASTINUM between the two lungs -extends from broad BASE at its uppermost end, where great vessels are attached, to bluntly pointed APEX at lower end, just above diaphragm. -It tilts toward left from base to apex -more than half the heart is to left of body's median plane. -Adult heart 9 cm (3.5 in.) wide at base, 13 cm (5 in.) from base to apex, and 6 cm (2.5 in.) from anterior to posterior at its thickest point. -Whatever one's body size, from child to adult, the heart is roughly same size as fist. -It weighs about 300 g (10 ounces) in adults.

THE VALVES

-heart needs valves that ensure one-way flow to pump blood effectively -There is a valve between each atrium and its ventricle and another at exit from each ventricle into its great artery -the heart has no valves where the great veins empty into atria. -Each valve consists of two or three fibrous flaps of tissue called cusps or leaflets, covered with endocardium. -atrioventricular (AV) valves regulate openings between atria and ventricles. -the right AV (TRICUSPID) valve has three cusps and the left AV valve has two . -The left AV valve is also known as MITRAL valve -Stringy tendinous cords CHORDAE TENDINAE connect valve cusps to conical papillary muscles on floor of ventricle. -They prevent AV valves from flipping inside out or bulging into atria when ventricles contract. -Each papillary muscle has two or three basal attachments to the trabeculae carneae of heart wall. -Among other functions, these multiple attachments may govern timing of electrical excitation of papillary muscles, and may distribute mechanical stress -multiple attachments provide some redundancy that protects AV valve from complete mechanical failure should one attachment fail. -SEMILUNAR VALVES (pulmonary and aortic valves) regulate flow of blood from ventricles into great arteries. -PULMONARY VALVE controls opening from right ventricle into pulmonary trunk -AORTIC VALVE controls opening from left ventricle into aorta. -Each has three cusps shaped like shirt pockets -When blood is ejected from ventricles, it pushes through valves from below and presses their cusps against arterial walls. -When ventricles relax, arterial blood flows backward toward ventricles, but quickly fills the cusps. -The inflated pockets meet at center and quickly seal opening, so little blood flows back into ventricles. -Because the way valves are attached to arterial wall, they cannot prolapse and don't require or possess tendinous cords. -valves don't open and close by any muscular effort of their own. -cusps are pushed open and closed by changes in blood pressure that occur as heart chambers contract and relax.

CARDIAC CONDUCTION SYSTEM

-heartbeat coordinated by cardiac conduction system composed of internal pacemaker and nervelike conduction pathways through myocardium. -generates and conducts rhythmic electrical signals in following order: (1) SA NODE FIRES SINUATRIAL (SA) NODE is patch of modified cardiomyocytes in right atrium, just under epicardium near superior vena cava. -This is PACEMAKER that initiates each heartbeat and determines heart rate. (2) EXCITATION SPREADS THROUGH ATRIAL MYOCARDIUM -Signals from SA NODE spread throughout atria (3) AV NODE FIRES -atrioventricular (AV) node is located at lower end of interatrial septum near right AV valve. -node acts as electrical gateway to ventricles; -fibrous skeleton acts as insulator to prevent currents from getting to ventricles by any other route. (4) EXCITATION SPREADS DOWN AV BUNDLE -atrioventricular (AV) bundle is pathway that signals leave AV node. -The bundle soon forks into right and left bundle branches, which enter interventricular septum and descend toward apex. (5) SUBENDOCARDIAL CONDUCTING NETWORK DISTRIBUTES EXCITATION THROUGH VENTRICULAR MYOCARDIUM -subendocardial conducting network (formerly called Purkinje fibers) consists of processes that arise from lower end of the bundle branches. -nervelike in action, they are composed of modified cardiomyocytes specialized for electrical conduction rather than contraction. -At apex of heart, they turn upward and ramify throughout ventricular myocardium, distributing electrical excitation to cardiomyocytes of ventricles. -form more elaborate network in left ventricle than in right. -Once they have delivered electrical signal to their limits, cardiomyocytes themselves perpetuate it by passing ions from cell to cell through their gap junctions.

STROKE VOLUME AND INOTROPIC AGENTS

-inotropic agents act on CARDIAC OUTPUT through effects on contraction strength and stroke volume *STROKE VOLUME is governed by three variables called -PRELOAD -CONTRACTILITY -AFTERLOAD -INCREASED Preload or Contractility INCREASES stroke volume -INCREASED Afterload opposes emptying of ventricles and DECREASES stroke volume. SV=EDV-ESV (end diastolic volume - end systolic volume)

AUTONOMIC NERVOUS SYSTEM ROLE WITH HEART

-nervous system doesn't initiate heartbeat, it -nervous system does modulate heart rhythm and force through autonomic nerves. T *SYMPATHETIC nervous system exerts its effects: -directly through cardiac nerves -indirectly by stimulating adrenal medulla. -nerve fibers secrete norepinephrine (NE) -adrenal medulla secretes mixture of 85% epinephrine (Epi) and 15% NE—known collectively as catecholamines. -Both of these have POSITIVE chronotropic and inotropic effects on heart -Epi and NE bind to β-adrenergic receptors in heart and activate cyclic adenosine monophosphate (cAMP) second-messenger system -Cyclic AMP activates enzyme that opens Ca2+ channels in plasma membrane, admitting calcium from extracellular fluid into SA node and cardiomyocytes. -This accelerates depolarization of SA node and speeds up signal conduction through AV node. -Both of these quicken contractions of ventricular myocardium and speed up heartbeat. -cAMP accelerates reuptake of Ca2+ by sarcoplasmic reticulum of cardiomyocytes. -Quick Ca2+ reuptake shortens ventricular systole and QT Interval enabling ventricles to relax and refill sooner than they do at rest. -By accelerating both contraction and relaxation of heart, cAMP increases heart rate. -Adrenergic stimulation can raise heart rate as high as 230 bpm. -limit of heart rate set mainly by refractory period of SA node, which prevents it from firing any more frequently. -Cardiac output peaks at rate of 160-180 bpm. -rates any higher than 160-180 bpm, ventricles have too little time to fill between beats. -At resting rate of 65 bpm, ventricular diastole lasts 0.62 second, but at 200 bpm, it lasts only 0.14 second. -at excessively high heart rates, diastole is too brief to allow complete filling of ventricles, and stroke volume and cardiac output are reduced. -PARASYMPATHETIC vagus nerves have NEGATIVE chronotropic effect. -Left to itself, SA NODE and heart have resting rhythm of 100 bpm; (if all nerves to heart are severed or all sympathetic and parasympathetic action is pharmacologically blocked). -with intact, functional innervation, vagus nerves have steady background firing rate called VAGAL TONE that holds heart rate down 70-80 bpm at rest. -heart can be accelerated by sympathetic stimulation and by reducing vagal tone to allow heart to "do its own thing." -Extreme vagal stimulation can reduce heart rate as low as 20 bpm or even stop heart briefly. -postganglionic neurons of the vagus are cholinergic—they secrete acetylcholine (ACh) at SA and AV nodes. -ACh binds to muscarinic receptors and opens K+ gates in nodal cells. -outflow of K+ hyperpolarizes cells, so SA node fires less frequently and heart slows down. -ACh acts primarily on SA node but also slows signal conduction through AV node, delaying excitation of ventricles. -vagus nerves have faster-acting effect on heart than sympathetic nerves because ACh acts directly on membrane ion channels; -sympathetic effects are slower because of time taken for cAMP system to open ion channels

ANGINA AND HEART ATTACK

-obstruction of coronary blood flow can cause chest pain known as ANGINA PECTORIS or, more seriously, MYOCARDIAL INFARCTION (heart attack). -ANGINA is sense of heaviness or pain in chest resulting from temporary and reversible ISCHEMIA, or deficiency of blood flow to cardiac muscle. -typically occurs when partially blocked coronary artery constricts. -oxygen-deprived myocardium shifts to anaerobic fermentation, producing lactate, which stimulates pain receptors in heart. -pain abates when artery relaxes and normal blood flow resumes. -MYOCARDIAL INFARCTION (MI) is sudden death of patch of myocardium resulting from long-term obstruction of coronary circulation. -Coronary arteries become obstructed by blood clot or fatty deposit called an ATHEROMA -As cardiac muscle downstream from obstruction dies, individual commonly feels sense of heavy pressure or squeezing pain in chest, often "radiating" to shoulder and left arm. -Some MIs are painless, "silent" heart attacks, especially in elderly or diabetic individuals. -Infarctions weaken heart wall and disrupt electrical conduction pathways, potentially leading to fibrillation and cardiac arrest. -MI causes 27% of deaths in United States. -In organs other than heart, blood flow usually peaks when heart contracts and ejects blood into systemic arteries/-diminishes when ventricles relax and refill. -Opposite is true in coronary arteries: -Flow peaks when heart RELAXES. There are three reasons for this:. (1) Contraction of myocardium squeezes coronary arteries and obstructs blood flow. (2) When ventricles contract, aortic valve is forced open and its cusps cover openings to coronary arteries, blocking blood from flowing into them. (3) When they relax, blood in aorta briefly surges back toward heart. It fills aortic valve cusps and some of it flows into coronary arteries -In coronary blood vessels, blood flow increases during ventricular relaxation.

CHEMORECEPTORS

-occur in aortic arch, carotid arteries, and medulla oblongata -sensitive to blood pH, CO2, and O2 levels. -more important in respiratory control than in cardiovascular control -influences heart rate. -If circulation to tissues is too slow to remove CO2 as fast as tissues produce it, CO2 accumulates in blood and cerebrospinal fluid (CSF) and produces state of HYPERCAPNIA (CO2 excess). -CO2 generates hydrogen ions by reacting with water: -HYDROGEN IONS lower pH of blood and CSF and may create state of ACIDOSIS (pH < 7.35). -Hypercapnia and acidosis stimulate cardiac centers to increase heart rate, which improves perfusion of tissues and restoring homeostasis. -chemoreceptors respond to extreme HYPOXEMIA (oxygen deficiency to slow down heart, so heart doesn't compete with brain for limited oxygen supply. -responses to fluctuations in blood chemistry and blood pressure, called chemoreflexes and baroreflexes, are examples of negative feedback loops

TACHYCARDIA

-persistent, resting adult heart rate above 100 bpm. -can be caused by stress, anxiety, stimulants, heart disease, or fever. -Heart rate also rises to compensate for drop in stroke volume. -heart races when body has lost significant quantity of blood or with damage to myocardium.

BRADYCARDIA

-persistent, resting adult heart rate below 60 bpm. -common during sleep and in endurance-trained athletes. -Endurance training enlarges heart and increases stroke volume, enabling it to maintain same output with fewer beats. -Hypothermia (low body temperature) slows heart and may be deliberately induced in preparation for cardiac surgery. -Diving mammals such as whales and seals exhibit bradycardia during dives, as do humans when face is immersed in cool water.

CONTRACTILITY

-refers to how hard myocardium contracts for a given preload. -It doesn't describe increased tension produced by stretching muscle, but rather increase caused by factors that make cardiomyocytes more responsive to stimulation. -POSITIVE INOTROPIC AGENTS factors that increase CONTRACTILITY -NEGATIVE INOTROPIC AGENTS factors that decrease CONTRACTILTY -Calcium has a strong, positive inotropic effect—it increases strength of each heart contraction -Ca2+ is essential to excitation-contraction coupling of muscle, and prolongs plateau of myocardial action potential. -Calcium imbalances affect heart rate and contraction strength. -In hypercalcemia, extra Ca2+ diffuses into cardiomyocytes and produces strong, prolonged contractions. -In extreme hypercalcemia, it can cause cardiac arrest in systole. -In hypocalcemia, cardiomyocytes lose Ca2+ to extracellular fluid, leading to weak, irregular heartbeat and potentially to cardiac arrest in diastole. -severe hypocalcemia more likely to kill through skeletal muscle paralysis and suffocation before cardiac effects are felt -Agents that affect calcium availability have chronotropic effects and inotropic effects. -norepinephrine increases calcium levels in sarcoplasm; which increases heart rate and contraction strength (as does epinephrine) -pancreatic hormone glucagon exerts inotropic effect by stimulating cAMP production; -a mixture of glucagon and calcium chloride used for emergency treatment of heart attacks. -Digitalis, a cardiac stimulant from foxglove plant, raises intracellular calcium level and contraction strength; and used to treat congestive heart failure. -Hyperkalemia has negative inotropic effect because it reduces strength of myocardial action potentials and reduces release of Ca2+ into sarcoplasm. The heart becomes dilated and flaccid. -Hypokalemia has little effect on contractility. -vagus nerves have negative inotropic effect on atria, but provide so little innervation to ventricles that they have no significant effect on them.

VENOUS DRAINAGE

-refers to route by which blood leaves an organ. -After flowing through capillaries of heart wall, 5% to 10% of coronary blood empties from multiple tiny vessels called small cardiac veins directly into heart chambers, especially right ventricle. -rest returns to right atrium by following route: *GREAT CARDIAC VEIN -collects blood from anterior aspect of heart and travels alongside anterior interventricular artery. -carries blood from apex toward coronary sulcus, arcs around left side of heart -empties into coronary sinus. *POSTERIOR INTERVENTRICULAR(middle cardiac) VEIN -found in posterior interventricular sulcus -collects blood from posterior aspect of heart. -carries blood from apex upward and drains into same sinus. *LEFT MARGINAL VEIN -travels from point near apex up left margin -empties into coronary sinus. *CORONARY SINUS -large transverse vein in coronary sulcus on posterior side of heart -collects blood from all three of aforementioned veins as well as some smaller ones -empties blood into right atrium.

AFTERLOAD

-sum of all forces VENTRICLE must overcome before it can EJECT blood. -most significant contribution to afterload is blood pressure in aorta and pulmonary trunk immediately distal to semilunar valves; -opposes opening of valves and limits stroke volume. -hypertension increases afterload and opposes ventricular ejection. -Anything that impedes arterial circulation, such as atherosclerotic plaque in arteries, increases afterload. -some lung diseases, scar tissue forms in lungs and restricts pulmonary circulation, which increases afterload in pulmonary trunk. -As right ventricle works harder to overcome resistance, it gets larger like any other muscle. -Stress and hypertrophy of a ventricle can cause it to weaken and fail. *COR PULMONALE is RIGHT VENTRICULAR failure due to obstructed pulmonary circulation -common complication of emphysema, chronic bronchitis, and black lung disease

CORONARY CIRCULATION

-the MYOCARDIUM has its own supply of arteries and capillaries that deliver blood to every muscle cell. -The blood vessels of the heart wall make up the CORONARY CIRCULATION -At rest, coronary blood vessels supply MYOCARDIUM with 250 mL of blood per minute. -constitutes 5% of circulating blood going to meet metabolic needs of heart, even though heart is only 0.5% of body's weight. -It receives 10 times its "fair share" to sustain its strenuous workload

CORONARY ARTERY DISEASE RISK, PREVENTION, AND TREATMENT

-top risk factor for CAD is excess low-density lipoproteins (LDLs) in blood combined with defective LDL receptors in arterial walls. -LDLs are protein-coated droplets of cholesterol, fats, free fatty acids, and phospholipids -Most cells have LDL receptors that enable them to absorb these droplets from blood so they can metabolize cholesterol and other lipids. -CAD occurs when arterial cells have dysfunctional LDL receptors that "don't know when to quit," so cells absorb and accumulate excess cholesterol. -Some risk factors for CAD are unavoidable such as heredity and aging. -Most risk factors are preventable such as: obesity, smoking, lack of exercise, and personality fraught with anxiety, stress, and aggression, all conducive to the hypertension that initiates arterial damage. -Diet is very significant. -Eating animal fat raises one's LDL level and reduces number of LDL receptors. -Foods high in soluble fiber (such as beans, apples, and oat bran) lower blood cholesterol by interesting mechanism: liver normally converts cholesterol to bile acids and secretes them into small intestine to aid fat digestion. -bile acids reabsorbed farther down intestine and recycled to liver for reuse. -Soluble fiber binds bile acids and carries them out in feces. -To replace bile acids that were converted from cholesterol, liver synthesizes more bile acids consuming more cholesterol. -CAD often treated with coronary artery bypass graft (CABG). -Sections of great saphenous vein of the leg or small thoracic arteries are used to construct a detour around obstruction in coronary artery. -In balloon angioplasty a slender catheter is threaded into coronary artery and then a balloon at its tip is inflated to press atheroma against arterial wall, widening lumen. -In laser angioplasty, the surgeon views interior of diseased artery with illuminated catheter and vaporizes atheroma with a laser. -Angioplasty is less risky and expensive than bypass surgery, but often followed by restenosis—atheromas grow back and reobstruct artery months later. -Insertion of tube called a stent into artery can prevent restenosis.

EPICARDIUM

-visceral layer of serous pericardium -serous membrane of EXTERNAL heart surface. -consists mainly of simple squamous epithelium overlying thin layer of areolar tissue. -some places also includes thick layer of adipose tissue, whereas in other areas it is fat-free and translucent, so muscle of underlying myocardium shows through -largest branches of coronary blood vessels travel through epicardium.

BLOOD FLOW THROUGH THE CHAMBERS

1. Blood enters RIGHT ATRIUM from superior and inferior vena cava 2. Blood in right atrium flows through right AV VALVE into RIGHT VENTRICLE 3. Contraction of right ventricle forces PULMONARY VALVE open 4. Blood flows through pulmonary valve into PULMONARY TRUNK 5. Blood is distributed by right and left pulmonary arteries to lungs, where it unloads CO2 and loads O2 6. Blood returns from lungs via PULMONARY VEINS into LEFT ATRIUM 7. Blood in left atrium flows through left AV VALVE into LEFT VENTRICLE 8. Contraction of left ventricle (simultaneous with step 3) forces AORTIC VALVE open 9. Blood flows through aortic valve into ASCENDING AORTA 10. Blood in aorta is distributed to every organ in body, where it unloads O2 and loads CO2 11. Blood returns to heart via INFERIOR & SUPERIOR VENA CAVA *4-6 Pulmonary circuit *9-11 Systematic circuit -Blood is kept entirely separate on right and left sides of heart. -Blood that has been through SYSTEMIC circuit returns through superior and inferior venae cavae to right atrium. -It flows directly from right atrium, through right AV (tricuspid) valve, into right ventricle. -When right ventricle contracts, it ejects blood through pulmonary valve into pulmonary trunk, on its way to lungs to exchange carbon dioxide for oxygen. -Blood returns from lungs by way of two pulmonary veins on left and two on right; -all four of these empty into left atrium. -Blood flows through left AV (mitral) valve into left ventricle. -Contraction of left ventricle ejects blood through aortic valve into ascending aorta, on its way to another trip around systemic circuit.

SOME DISORDERS OF HEART

ACUTE PERICARDITIS Inflammation of pericardium, sometimes due to infection, radiation therapy, or connective tissue disease, causing pain and friction rub CARDIOMYOPATHY Any disease of the myocardium not resulting from coronary artery disease, valvular dysfunction, or other cardiovascular disorders; can cause dilation and failure of the heart, thinning of the heart wall, or thickening of the interventricular septum INFECTIVE ENDOCARDITIS Inflammation of the endocardium, usually due to bacterial infection, especially Streptococcus and Staphylococcus MYOCARDIAL ISCHEMIA Inadequate blood flow to the myocardium, usually because of coronary atherosclerosis; can lead to myocardial infarction PERICARDIAL EFFUSION Seepage of fluid from the pericardium into the pericardial cavity, often resulting from pericarditis and sometimes causing cardiac tamponade SEPTAL DEFECTS Abnormal openings in interatrial or interventricular septum, -resulting in blood from right atrium flowing directly into left atrium, -or blood from left ventricle returning to right ventricle; -results in pulmonary hypertension, difficulty breathing, and fatigue; -often fatal in childhood if uncorrected

HEART SOUNDS

AUSCULTATION: Listening to sounds made by body -Heart sounds audible using a STEHOSCOPE -1st and 2nd heart sounds, symbolized S1 and S2, "lubb-dupp"—S1 is louder and longer and S2 softer and sharper. -In children and adolescents, it is normal to hear a third heart sound (S3). -S3 rarely audible in people older than 30, but -When S3 is heard, heartbeat has triple rhythm or gallop, indicates enlarged and failing heart. -Heart valves operate silently -S1 and S2 occur with closing of valves from turbulence in bloodstream and movements of heart wall.

PHASES OF CARDIAC CYCLE

Cardiovascular physiologist Carl J. Wiggers (1883-1963) devised Wiggers diagram , that shows major events that occur simultaneously at each moment throughout cardiac cycle. *(1) VENTRICULAR FILLING -During DIASTOLE ventricles expand and their pressure drops below that of atria. -AV VALVES open and blood pours into ventricles, raising ventricular pressure and lowering atrial pressure. *VENTRICULAR FILLING occurs in three phases: (1a) first 1/3rd: rapid ventricular filling, -blood enters quickly. (1b) second 1/3rd: diastasis -slower filling. -P wave of electrocardiogram occurs at end of diastasis, marking depolarization of atria. (1c) last 1/3rd, atrial systole -completes filling process. -right atrium contracts slightly before left because it is first to receive signal from SA NODE. -At end of ventricular filling, each ventricle contains END-DIASTOLIC VOLUME (EDV) of 130 mL of blood. -Only 40 mL (31%) is from atrial systole. *(2) ISOVOLUMETRIC CONTRACTION -ATRIA repolarize, relax, and remain in DIASTOLE rest of cardiac cycle -VENTRICLES depolarize, generate QRS complex, and begin to contract. -Q marks end of ventricular filling; -R marks transition from atrial systole to isovolumetric contraction of ventricles; -S marks isovolumetric contraction. -VENTRICLE PRESSURE rises sharply and reverses pressure gradient between atria and ventricles. -AV VALVES close as ventricular blood surges against cusps. -Heart sound S1 occurs at beginning of this phase and produced mainly by LEFT ventricle; -right ventricle makes little contribution. -Causes of sound include tensing of ventricular tissues and tendinous cords, turbulence in blood as it surges against closed AV valves, and impact of heart against chest wall. -phase is called ISOVOLUMETRIC because even though ventricles contract, they don't eject blood and there is no change in their volume, because pressures in aorta (80 mm Hg) and pulmonary trunk (10 mm Hg) are greater than pressures in ventricles and oppose opening of semilunar valves. -cardiomyocytes exert force, but with all four valves closed, blood can't go anywhere. *(3) VENTRICULAR EJECTION -ejection of blood begins when VENTICULAR pressure exceeds ARTERIAL pressure and forces SEMILUNAR valves OPEN. -Pressure peaks at 120 mm Hg in LEFT VENTRICLE and 25 mm Hg in RIGHT VENTRICLE -Blood spurts out of each ventricle rapidly at first (rapid ejection), then flows out more slowly under less pressure (reduced ejection). -Ventricular ejection lasts 200 to 250 ms, which corresponds to plateau of myocardial action potential but lags somewhat behind -T wave occurs late, beginning at peak ventricular pressure. -ventricles don't expel all Blood. -In average resting heart, each ventricle contains EDV of 130 mL. -amount ejected is 70 mL, and called STROKE VOLUME (SV). -This is 54% of the EDV, a percentage called EJECTION FRACTION -blood remaining behind, 60 mL in this case, is called END-SYSTOLIC VOLUME (ESV). *EDV-SV=ESV In vigorous exercise, ejection fraction may be as high as 90%. -Ejection fraction is important measure of cardiac health. -A diseased heart may eject much less than 50% of blood it contains. *(4) ISOVOLUMETRIC RELAXTION -early VENTRICULAR DIASTOLE -T wave ends -VENTRICLES begin to expand. (There are competing hypotheses as to how they expand: -One is that the blood flowing into ventricles inflates them. -Another is contraction of ventricles deforms fibrous skeleton, which springs back -This elastic recoil and expansion would cause pressure to drop rapidly and suck blood into ventricles.) -At beginning of VENTRICULAR DIASTOLE, blood from aorta and pulmonary trunk briefly flows backward through semilunar valves. -backflow quickly fills cusps and closes them, creating slight pressure rebound that appears as dicrotic notch of aortic pressure curve (the top curve in the Wiggers diagram). -Heart sound S2 occurs as blood rebounds from closed semilunar valves and ventricles expand. -phase is called ISOVOLUMETRIC because semilunar valves are closed, AV valves haven't opened, and ventricles are NOT taking in blood. -When AV valves open, ventricular filling (phase 1) begins again. -Heart sound S3, if it occurs, results from transition from expansion of empty ventricles to their sudden filling with blood. *In resting person: -ATRIAL SYSTOLE lasts: 0.1 second; -VENTRICULAR SYTOLE lasts: 0.3 second; -QUIESCENT PERIOD (when all four chambers are in diastole), lasts:0.4 second. -Total duration of cardiac cycle is 0.8 second (800 ms) in heart beating at 75 bpm.

CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is constriction of coronary arteries resulting from ATHEROSCLEROSIS—an accumulation of lipid deposits that degrade arterial wall and obstruct lumen. T -most dangerous consequence of CAD is myocardial infarction (heart attack). Pathogenesis: -CAD begins when hypertension, diabetes, or other factors damage arterial lining. -Monocytes adhere to arterial lining, penetrate into tissue, and become macrophages. -Macrophages and smooth muscle cells absorb cholesterol and fat from blood, which gives them a frothy appearance. -They are then called FOAM CELLS and form visible fatty streaks on arterial wall. -Seen in infants and children, these are harmless but have potential to grow into atherosclerotic PLAQUES (atheromas). -Platelets adhere to plaques and secrete growth factor that stimulates local proliferation of smooth muscle and fibroblasts and deposition of collagen. -Plaque grows into bulging mass of lipid, fiber, smooth muscle and other cells. -When it obstructs 75% or more of arterial lumen, it begins to cause symptoms such as angina pectoris. -INFLAMMATION of plaque roughens its surface and creates focal point for THROMBOSIS. -A blood clot can block what remains of lumen, or break free and lodge in smaller artery -Sometimes piece of plaque breaks free and travels as a FATTY EMBOLUS -PLAQUE contributes to spasms of coronary artery, cutting off blood flow to myocardium. -If lumen is already partially obstructed by plaque and perhaps blood clot, a spasm can temporarily shut off remaining flow and cause ANGINA attack -muscular and elastic tissue of inflamed artery replaced with scar tissue and calcium deposits, transforming an atheroma into hard complicated plaque -Hardening of arteries by calcified plaques is one cause of arteriosclerosis this results in excessive surges of blood pressure that weaken and rupture smaller arteries, leading to stroke and kidney failure.

PRINCIPALS OF PRESSURE AND FLOW

FLOW is governed by two main variables: PRESSURE & REISTANCE -PRESSURE impels fluid to move -RESISTANCE opposes flow. -PRESSURE CHANGES govern operation of heart valves, entry of blood into heart chambers, and its expulsion into arteries. -Flow of blood and air down their pressure gradients are two applications of the general principle of gradients and flow

VALVULAR INSUFFICIENCY

INCOMPETENCE refers to any failure of a valve to prevent REFLUX (regurgitation)—the backward flow of blood. *VALVULAR STENOSIS is form of insufficiency where cusps stiffen and opening is constricted by scar tissue. -results from rheumatic fever, an autoimmune disease in which antibodies produced to fight bacterial infection also attack mitral and aortic valves. -As valves scar and constrict, heart is overworked by effort to force blood through openings become enlarged. -Regurgitation of blood through incompetent valves creates turbulence that can be heard with stethoscope as a HEART MURMUR *MITRAL VALVE PROLAPSE (MVP) -insufficiency in which one or both mitral valve cusps bulge into atrium during ventricular contraction. -often hereditary and affects 1 out of 40 people, especially young women. -causes no serious dysfunction in many cases, but some people it causes chest pain, fatigue, and shortness of breath. -In some cases INCOMPETENT VALVEs can eventually lead to heart failure. -Defective valve can be surgically repaired or replaced with artificial valve or valve transplant from pig heart. -Rising pressure in ventricles acts on aortic and pulmonary valves. -Up to a point, pressure in aorta and pulmonary trunk opposes their opening, but when ventricular pressure rises above arterial pressure, it forces valves open and blood is ejected from heart. -As ventricles relax again and pressure falls below the pressure in arteries, arterial blood briefly flows backward and fills pocketlike cusps of semilunar valves. -The three cusps meet in middle of orifice and seal it , thereby preventing arterial blood from reentering heart.

INOTROPIC EFFECTS & CHRONOTROPIC EFFECTS

INOTROPIC EFFECT -Negative inotropic decreases force of contraction, a -Positive inotropic effect increases force of contraction. CHRONOTROPIC EFFECT -effects on ANS on heart RATE

INTERPRETATION OF ELECTROCARDIOGRAM

P wave -Atrial depolarization QRS complex -Ventricular depolarization T wave -Ventricular repolarization PR interval -Signal conduction through AV node, before activating ventricles QT interval -Duration of ventricular depolarization; -shorter during exercise. QRS interval -Atrial repolarization and diastole; -repolarization concealed by QRS wave. PQ segment -Signal conduction from SA node to AV node; -atrial systole begins. ST segment -Ventricular systole and ejection of blood; -corresponds to plateau of cardiomyocyte action potential.

STROKE VOLUME EQUATION

SV=EDV-ESV (end diastolic volume - end systolic volume)

STROKE VOLUME FORMULA

SV=EDV-ESV (end diastolic volume - end systolic volume) Stroke volume (SV) is volume of blood ejected from left ventricle with each cardiac cycle or heartbeat. -SV is calculated by subtracting left ventricular end systolic volume (ESV) from the left ventricular end diastolic volume (EDV). https://www.nursingcenter.com/ncblog/august-2021/how-to-calculate-ejection-fraction

CARDIAC CYCLE

consists of one complete contraction and relaxation of all four heart chambers

https://quizlet.com/423452628/chapter-15-cardiovascular-practice-flash-cards/ https://courses.lumenlearning.com/boundless-ap/chapter/circulation-and-heart-valves/ https://www.nursingcenter.com/ncblog/august-2021/how-to-calculate-ejection-fraction

https://quizlet.com/451116289/lab-exam-3-questions-from-bookapr-flash-cards/ https://quizlet.com/153561875/ap-2-lab-test-2-flash-cards/ https://www.ezmedlearning.com/blog/heart-blood-flow-diagram https://bluegrass.kctcs.edu/education-training/media/natural-sciences/biology/documents/lab3_heart_pump_excersise.pdf

CHORDAE TENDINAE

prevent AV valves from flipping inside out or bulging into atria when ventricles contract.