Ch.19 Circulatory System 19.1-19.4

Angina pectoris and myocardial infarction (MI)

Angina pectoris: chest pain or feeling of heaviness in the chest caused by obstruction of coronary blood flow; results from temporary and reversible ischemia to cardiac muscles -typically when a partially blocked coronary artery cannot deliver adequate amounts of oxygenated blood to heart -oxygen-deprived myocardium has to shift to anaerobic fermentation, producing *lactate*, which stimulates chemoreceptor pain receptors in heart -pain relaxes once normal blood flow is restored -fleeting condition -*temporary* blockage/ischemia MI: sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation -often occurs when coronary arteries are obstructed by blood clot of fatty deposits, causing the cardiac muscle downstream to die -feel a sense of heavy pressure or squeezing pain in the chest, often "radiating" to shoulder and left arm -MIs weaken the heart wall and disrupt electrical conduction pathways, potentially causing fibrillation (irregular heart beat that causes poor blood flow) and cardiac arrest -*prolonged* blockage/ischemia

Blood Flow: Pulmonary and Systemic Circuits

Both circuits deal with both deoxygenated and oxygenated blood Pulmonary circuit: carries deoxygenated blood from heart to lungs, then oxygenated blood from lungs back to heart -starts in right ventricle and ends in left atrium -deoxygenated blood in the right ventricle leaves heart through pulmonary arteries and travels to heart. Gas exchange takes place and blood is oxygenated. Oxygenated blood then travels through pulmonary veins to the left atrium of the heart. Systemic circuit: carries oxygenated blood to body tissue then deoxygenated blood back to heart -starts in left ventricle and ends in right atrium -Oxygenated blood in the left ventricle leaves the heart through the aorta and travels to tissues all over the body, where gas exchange takes place at capillaries and blood becomes deoxygenated. Deoxygenated blood then travels through superior/inferior vena cava to get to right atrium of heart. simultaneous contractions of ventricles cause pulmonary valve to open and deoxygenated blood to flow out of right atrium to pulmonary arteries -at same time, that contraction causes aortic valve to open and force oxygenated blood from left ventricle out through the aorta

APs in heart

One AP generated in autorhythmic non-contractile of SA node and atrium and then another in contractile ventricular cells (gap junctions connecting them) -AP in SA node is sharper and quicker, like normal AP, while AP in contractile myocardium is lower and has plateau phase -in SA node, NA+ is pacemaker AP, Ca2+ is depolarization, K+ is repolarization, and Na+ is pacemaker potential again -in contractile myocardium, rapid Na+ causes steep spike of depolarization, K+ causes brief repolarization before plateau phase, where Ca2+ is maintaining constant potential, and then K+ gives repolarization -calcium-induced calcium release causing plateau phase while muscle contracts -Contractile myocardium has absolute refractory period from time of depolarization to end of plateau phase, and relative refractory period during repolarization Notice flow of AP starting with non-contractile atrial cells, then firing AV node, then AV bundle carrying stimulation to subendocardial conducting network (purkinje fibers) that excite ventricles.

calcium induced calcium release

Process in which Ca2+ entry into a muscle fiber triggers release of additional Ca2+ from the sarcoplasmic reticulum this occurs with Ca2+ entering cell during plateau after depolarization and causing more Ca2+ to be released from SR, binding to troponin and causing muscular contraction SR provides about 90-98% of calcium needed for myocardial contraction cardiomyocytes contract for as long as cell is in plateau phase cardiomyocytes can't experience tetanus because they have a very long (250ms) absolute refractory period preventing wave summation and tetanus, which would stop the heart -lasts from depolarization until end of plateau phase, and then relative refractory period during repolarization -ryanodine receptors are stimulated by slow Ca2+ entering cell to release more Ca2+ from cell, which is later returned through SERCA channel to SR

pacemaker physiology

SA node does NOT have a stable resting membrane potential -starts at -60mV and drifts upward from a SLOW inflow of Na+ w/out compensating outflow of K+ gradual depolarization is called pacemaker potential when reaches threshold of -40mV, voltage-gated calcium channels open and produce depolarization phase of AP, which peaks slightly above 0 then K+ channels open and K+ flows out of cell, repolarizing it repolarization goes all the way back down to -60mV, where K+ channels close and pacemaker potential potential resumes with slow Na+ leakage causing slowing rising pacemaker potential until it hits the -40mV threshold again each depolarization of the SA node sets off one heartbeat fires about every 0.8 seconds, creating a heartbeat of about 75bpm the "leaky" Na+ channels ensure that firing occurs at regular intervals and without stimulation, allowing heartbeat to be autorhythmic and reliable -ectopic foci will have same mechanism but slower, so heartbeat is 40-50bpm or less this is the pacemaker AP; don't get confused with myocardiocyte AP, which has plateau, lower resting potential, not autorhythmic, etc. -SA node uses FAST Ca2+ channels to depolarize cell, while normal cardiomyocytes use Na+ to depolarize and then SLOW Ca2+ to create plateau

refractory periods of contractile myocardium

absolute refractory period from start of AP unit end of plateau phase relative refractory period from end of plateau phase until RMP reestablished

branching of cardiomyocytes

adaptive so that each cell can communicate with multiple other cells helps ensure unified and synchronized functioning of the myocardium so that it behaves as a single cell

ectopic focus

any region of spontaneous firing other than the SA node normal heartbeat (sinus rhythm) is triggered by SA node, but if SA is damaged, ectopic focus may take over governance of the heart rhythm most common ectopic focus is AV node, which produces slower heartbeat of 40-50bpm called a nodal rhythm -this rhythm is sufficient to sustain life but if this one fails, any other ectopic foci would produce rate too low for survival and would require artificial pacemaker

intercalated discs and junctions

cardiomyocytes are joined end to end by thick connections called intercalated discs intercalated discs are complex, step-like structures with 3 features not seen in skeletal muscle: 1) Interdigitating folds: like bottom of egg box; folds of adjoining cells interlock with each other; increases surface area of intercellular contact 2) Mechanical junctions: cells tightly joined together by 2 types of junctions, Fascia adherens and desmosomes -fascia adherens: most extensive; broad band in which actin thin filaments are anchored to plasma membrane and each cell is linked to next by transmembrane proteins; interrupted periodically with desmosomes -desmosome: patches of mechanical linkage that prevent the contracting cardiomyocytes from pulling apart -fascia adherens is continuous border anchoring thin actin filaments and neighboring cells, while desmosomes are sporadic interruptions in the fascia adherens that have proteins preventing cardiomyocytes from pulling apart when they contract 3) Electrical (gap) junctions: gap junctions which form channels allowing ions to flow from cytoplasm of one cardiomyocyte to that of the next -allows each cardiomyocyte to electrically stimulate its neighbor and pass down the stimulation -allows for unified action of myocardium like a single cell in general, cardiomyocytes are thick and short and branched at their ends; also usually mononucleate but might have a few; not nearly as many nuclei or nearly as long as skeletal muscle; also lighter striations -branching terminals of cardiomyocyte is adaptive so that each cell can communicate with multiple other cells

Angina pectoris

chest pain or feeling of heaviness in the chest caused by obstruction of coronary blood flow; results from temporary and reversible ischemia to cardiac muscles -typically when a partially blocked coronary artery cannot deliver adequate amounts of oxygenated blood to heart -oxygen-deprived myocardium has to shift to anaerobic fermentation, producing *lactate*, which stimulates chemoreceptor pain receptors in heart -pain relaxes once normal blood flow is restored -fleeting condition note that this is caused by temporary blockage/ischemia. A prolonged blockage/ischemia would cause MI -coronary artery is only partially constricted so contraction causes full blockage -fleeting condition because obstruction isn't complete

Coelomic cavities

coelom (body cavity) is divided into two cavities by a transverse, sheet-like muscle called the diaphragm -cavity above is thoracic cavity and cavity below is abdominopelvic cavity thoracic cavity contains mediastinum, which is partition carrying the heart, and also has pleural cavities on either side of mediastinum carrying the lungs -both the heart and lungs have double-layered pericardial membrane abdominopelvic cavity is below diaphragm, heart, and lungs -contains stomach, intestines, kidneys, adrenal glands, pelvis, etc.

fibrous skeleton

connective tissue framework of collagenous and elastic fibers largely concentrated in walls of heart between chambers, in fibrous rings around valves, and in sheets of tissue that interconnect these rings functions: -provide structural support for heart, especially around valves and openings (holds openings open and prevents excessive stretching) -anchors cardiomyocytes, giving them something to pull against -nonconductive to electricity, giving electrical insulation b/w atria and ventricles -maybe also elastic recoil to her refill heart with blood

purpose of epicardium

contains blood vessels, nerves, and lymphatic vessels that supply myocardium layer is made up of adipose and fibroelastic tissue serous layer; also called inner visceral layer of pericardium; makes pericardial fluid that fills cavity and reduces friction

when does myocardial contraction occur?

during plateau phase of myocardial AP during plateau phase, a little bit of calcium enters heart, causes tons of calcium to be released from SR through ryanodine receptors, and that calcium then contributes to myocardial contraction by removing troponin-tropomyosin complex from actin binding sites peak contraction achieved by end of plateau phase, but then contraction decreases after plateau phase ends and calcium is returned to SR through SERCA channels

fascia adherens and desmosomes

fascia adherens is continuous border anchoring thin actin filaments and neighboring cells, while desmosomes are sporadic interruptions in the fascia adherens that have proteins preventing cardiomyocytes from pulling apart when they contract

fibrous layer around heart

fibrous layer is inelastic, dense irregular connective tissue, protecting and anchoring heart and preventing overstretching continuous with fibrous connective tissue of mediastinum and other body parts provides stability and protection

heart wall

includes epicardium, myocardium, and endocardium epicardium will contain heart's blood vessels (that supply outer myocardiocytes in myocardium), lymphatics, and nerves for myocardium epicardium and endocardium are both simple squamous epithelium over areolar tissue -epicardium may have fat while endocardium does not endocardium continuous with endothelium of blood vessels myocardium has muscle organized into bundles spiraling around the heart, such that contraction exhibits a twisting or wringing motion that enhances the ejection of blood

pericarditis

inflammation of the pericardium layers of pericardium become inflamed and thicken, rubbing against each other and the heart membranes become roughened and produce a painful friction rub with each heartbeat inflammation is body's response to infection or injury main causes are viral/bacterial infections, damage to heart tissue from autoimmune diseases/medicines/trauma/etc. symptoms are chest pain, fast heartbeat, fever, shortness of breath mild cases may go away without treatment; more severe cases may require medicine (corticosteroids) or surgery -people generally improve relatively quickly but 1/3 exp. repeat episodes later complications include cardiac tamponade

pericardium

isolates the heart from other thoracic organs and allows it room to expand, yet resists excessive expansion includes fibrous layer (inelastic) and double-layered membrane beneath, with outer parietal layer and inner visceral layer with pericardial cavity in between the -inner visceral layer also known as epicardium -both layers (visceral and parietal) are serous, producing pericardial fluid that lies in the pericardial cavity and lubricates the membrane, decreasing friction when the heart beats pericardial cavity and fluid similar to bursae that contain synovial fluid at joints to reduce friction of bone movements epicardium contains blood vessels, lymphatics, and nerves that supply myocardium fibrous layer is inelastic, dense irregular connective tissue, protecting and anchoring heart and preventing overstretching does not include endocardium (which is inside ventricles and continuous with endothelium of blood vessels) Whole pericardial sac is anchored by ligaments to the diaphragm below and the sternum anterior to it below visceral layer is myocardium (contractile myocardiocytes of heart) and then endocardium (inner epithelial layer inside ventricle), neither of which is part of the pericardium "heart wall" includes epicardium, myocardium, and endocardium

cardiac tamponade

marked increase in fluid (blood or other fluid) volume in the pericardial sac results in compression of the heart, which causes decreased cardiac output and hypotension (decreased BP) -bc the pericardium is pressing in on the heart bc it can't expand outward bc of inelastic fibrous tissue -pressure on the heart means it can't fully pump fluid buildup prevents heart from expanding fully and body can't get enough blood can be caused by aortic aneurysm, lung cancer, heart attack (acute MI), heart surgery, pericarditis, wounds to heart, heart tumors, heart failure symptoms include sharp chest pain, problems breathing, fainting, lightheadedness

heart contractions are ________ and __________

myogenic and autorhythmic myogenic: signal originates in heart itself autorhythmic: heart doesn't depend on nervous system for its rhythm but instead has its own built-in pacemaker and electrical system

electrocardiogram

not a single AP but a composite recording of all APs produced by nodal and myocardial cells little P wave is atrial depolarization and flatline right after is atrial systole big peak after shows ventricular depolarization (ventricles have largest amount of muscle and generate most current) and ventricular systole occurs during flatline right after peak -during this time, there is also atrial repolarization in little peak after big peak, ventricular repolarization (takes longer than depolarization) and diastole -1st bump is atrial depolarization, then large bump is ventricular depolarization (and atrial diastole), then little bump after is ventricular repolarization

Mechanical junctions

one of three key features of cardiomyocytes not seen in skeletal muscle (other two are interdigitating folds and electrical gap junctions) includes fascia adherens junctions and desmosomes fascia adherens: most extensive; broad band in which actin thin filaments are anchored to plasma membrane and each cell is linked to next by transmembrane proteins; interrupted periodically with desmosomes desmosome: patches of mechanical linkage that prevent the contracting cardiomyocytes from pulling apart

conduction system in the heart

rhythmic heart beat is coordinated by a conduction system starting with the sinoatrial node (pacemaker) and nerve-like electrical conduction pathways Process: 1) SA node fires 2) Excitation spreads through the atrial myocardium 3) AV node fires 4) Excitation spreads down AV bundle 5) Purkinje fibers (subendocardial conducting network) distribute the excitation through the ventricular myocardium SA node is located in right atrium. AV node is located in right AV valve and acts as electrical gateway to ventricles, aided by fibrous skeleton preventing ventricles from being stimulated by any other route. AV bundle carries stimulation to purkinje fibers, which excite the ventricles. Notice flow of AP starting with non-contractile atrial cells, then firing AV node, then AV bundle carrying stimulation to subendocardial conducting network (purkinje fibers) that excite ventricles. One AP generated in autorhythmic non-contractile of SA node and atrium and then another in contractile ventricular cells (gap junctions connecting them) -AP in SA node is sharper and quicker, like normal AP, while AP in contractile myocardium is lower and has plateau phase -in SA node, NA+ is pacemaker AP, Ca2+ is depolarization, K+ is repolarization, and Na+ is pacemaker potential again -in contractile myocardium, rapid Na+ causes steep spike of depolarization, K+ causes brief repolarization before plateau phase, where Ca2+ is maintaining constant potential, and then K+ gives repolarization -Contractile myocardium has absolute refractory period from time of depolarization to end of plateau phase, and relative refractory period during repolarization

heart contractions

simultaneous contractions of ventricles cause pulmonary valve to open and deoxygenated blood to flow out of right ventricle to pulmonary arteries -at same time, that contraction causes aortic valve to open and force oxygenated blood from left ventricle out through the aorta

sinus and nodal rhythms

sinus rhythm is normal rhythm produced by SA node Nodal rhythm is ectopic rhythm produced by AV node when SA node is damaged -this is the only ectopic rhythm capable of sustaining life, as it produces beat of 40-50bpm -other ectopic beats are below 40bpm and unsustainable for life, meaning an artificial pacemaker is necessary

myocardiocyte AP and contraction

stable resting potential of -90mV and only depolarize when stimulated (not autorhythmic like SA node) stimulus causes Na+ gated ion channels to open and trigger positive feedback cycle, depolarizing membrane and causing more Na+ channels to open (rapid spike) Ion channels begin closing at 0mV and depolarization spikes near +30mV SLOW Ca2+ channels prolong depolarization and create a plateau, which slowly decreases bc of some K+ leakage then repolarization occurs with Ca2+ channels closing, remaining Ca2+ being transferred out of cell, and K+ channels opening and allowing K+ outflow, returning membrane to RMP Calcium-induced calcium release is occurring, where the initial calcium flowing into the cell after depolarization is causing calcium to be released from SR -thus myocardial contraction is beginning after depolarization once Ca2+ is in cell and triggering contraction -slight delay between AP and contraction -contraction reaches peak at end of plateau and then stops after repolarization -SR provides about 90-98% of calcium needed for muscular contraction -cardiomyocytes contract for as long as cell is in plateau phase -ryanodine receptors are stimulated by slow Ca2+ entering cell to release more Ca2+ from cell, which is later returned through SERCA channel to SR cardiomyocytes can't experience tetanus because they have a very long (250ms) absolute refractory period preventing wave summation and tetanus, which would stop the heart -lasts from depolarization until end of plateau phase, and then relative refractory period during repolarization

Myocardial Infarction (MI)

sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation -often occurs when coronary arteries are obstructed by blood clot of fatty deposits, causing the cardiac muscle downstream to die -feel a sense of heavy pressure or squeezing pain in the chest, often "radiating" to shoulder and left arm -*MIs weaken the heart wall and disrupt electrical conduction pathways, potentially causing fibrillation (irregular heart beat that causes poor blood flow) and cardiac arrest* Note that this is caused by prolonged blockage/ischemia, not temporary like angina pectoris. -full obstruction of coronary artery, not partial like angina pectoris

double-walled membranes

surround heart and lungs known collectively as pericardium contains outer parietal layer and inner visceral layer in direct contact with heart/lungs -visceral layer also known as epicardium -both layers are serous, producing pericardial fluid for pericardial cavity space in between layers is the pericardial sac, with pericardial fluid fibrous layer present over double-layered membrane provides stability, support, and protection don't get confused with myocardium (which is contractile myocardiocytes of heart or lungs) and endocardium (which is epithelial tissue on inside of ventricle or lungs, on inner side of myocardium) -endocardium continuous with endothelium of aorta and blood vessels -outer fibrous layer continuous with fibrous connective tissues of other body parts not to be confused with heart wall, which is epicardium, myocardium, and endocardium

mediastinum

thick partition between two lungs; supports and stabilizes heart and all of chest organs besides lungs includes entire heart, aorta, pulmonary trunk and arteries, vena cavae, thymus, and lymph nodes extends from diaphragm up to great vessels above heart from base to apex, it tilts towards the left, so a little more than half the heart is on the left side of the body surrounded by fibrous connective tissue continuous with pericardium of heart not to be confused with heart wall, which is epicardium, myocardium, and endocardium

mechanism of ventricular depolarization

transferred from node to apex/bottom of heart, then moves up superiorly