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TOWSON / Biology / BIOL 222 / anatomy and physiology ii study guide

anatomy and physiology ii study guide

anatomy and physiology ii study guide


School: Towson University
Department: Biology
Course: Anatomy & Physiology
Professor: Renee dickie
Term: Spring 2016
Tags: anatomy and Physiology
Cost: 50
Name: Anatomy and Physiology II Study Guide 2
Description: This study guide covers what will be on exam 2
Uploaded: 03/31/2017
13 Pages 258 Views 0 Unlocks

What would occur in the legs?

• What occurs in the capillaries when someone has high blood pressure?

• What moves things out of capillaries?

Anatomy and Physiology II Study Guide II Cardiac Physiology  Circulation  - Body circulation is composed of two circuits in series  1. Pulmonary circuit: blood flow circuit from the  right heart (which pressurizes this circuit) to the  lungs for the purpose of gas exchange  2. Systemic circuit: blood flow circuit from the left  heart (which pressurizes this circuit) to the body  and back to the right heart  - The systems are arranged so arteries carry blood from  the heart to capillary beds where exchange of gas,  nutrients, fluid and waste occurs. Veins will then carry  the blood back to the heart to be re-pressurized.  - Flow in each side of the circuit must be equal over  time  • The flow is measured as cardiac output  • Approximately 5 L/min at rest  - Atria: heart chambers that receive blood from veins  and deliver it to the ventricles, they do not add to the  pressure developed into the circuit  - Ventricles: heart chambers that receive blood from the atria and pressurize it to generate flow  to the lungs (right ventricle) or body (left ventricle)  • The pressure generated by the left heart is greater to produce the same amount of flow (there are many more vessels which are greater in length, and more resistance to flow)  • The left ventricle is more muscular  Cardiac Muscle Cells  - Cardiomyocytes  • Functions: contract, move blood, create tension  • A specialized form of striated muscle  - Striated muscle is made of stripes which can be seen histologically. The strips are caused  by repeating contractile units, called sarcomeres  - Intercalated discs: regions of localized cell-cell junctions that contain gap junctions and  desmosomes • Gap junctions: form gaps between cells that allow electrical stimuli to travel from cell to  cell rapidly (main function is communication)  • Desmosomes: a strong attachment between the cells so that they do not pull apart during  contraction  • Both key to forming a functional syncytium that performs as a single unit instead of  individual cells 1. Atrial syncytium  2. Ventricular syncytium  - They are formed when cells connected by gap junctions and desmosomes act as a group  - The two synsytia are connected through the AV bundle  - Myoglobin: a non-circulating oxygen binding pigment found within cardiac muscle cells  • The myoglobin binds and retains oxygen within the cells in case delivered oxygen from  hemoglobin is limited  • The myocytes are then not reliant on an inefficient anaerobic metabolism to function  - Mitochondria  • Cardiac myocytes are 25% mitochondria by volume, making them reliant on aerobic ATP  production  - Cardiomyocytes contract in response to action potentials generated by pacemaker cells found  in the SA node  Connective Tissues  - Fibers within the muscle prevent over-stretching  - Unlike skeletal muscle, heart muscle is not attached to bone, meaning it needs more structure  in order to maintain its shape  - The fibers help distribute forces equally throughout the muscle  - The fibers slightly improve the elasticity  - Fibrous skeleton: a layer of connective tissue found at the base of the arteries and  surrounding the AV valves  • Structural stabilization  • Electrically separates the atria and ventricles  • It acts as an electrical insulator which limits action potential propagation from the atria to  the ventricles (in order for the heart to function, the atria need to fully contract before  ventricular contraction due to the ventricular filling function)  - Review question: the fibrous skeleton  a) helps form a syncytium due to gap junctions in contains  b) controls valve opening and closing  c) regulates ventricular filling  d) prevents premature ventricular contraction  e) is what cardiac muscles pulls on to generate tension Coronary Circulation  - The systemic vessels that provide blood flow to the heart muscle  - Function: delivers oxygen and nutrients and removes waste products from the heart muscle  - There is a dense capillary bed surrounding the heart muscle so it does not come fatigued  Innervation of the Heart  - The autonomic nervous system provides control  1. Sympathetic nervous system:  2. Parasympathetic nervous system:  • Both systems innervate the SA node, AV node, and individual atrial and ventricular muscle  cells  • Cardiac output (work performed by the heart) is regulated by heart rate and contractility  (volume ejected per contraction or stroke volume)  - Autonomic control center includes:  • The cardioacceleratory center - has output to sympathetic neurons that tend to increase heart  rate via the release of norepinephrine at the SA node  • The cardioinhibitory center - has output to parasympathetic neurons that reduce heart rate via the release of acetylcholine at the SA node  • These centers receive input from the hypothalamus and from baroreceptors (pressure  sensors) and chemoreceptors which sense changes in the blood  Cardiac Electrophysiology - Membrane potential: a measure of the  difference in charge (voltage)  • The membrane potential is  determined by the relative  permeability of ions  • Primary contributors: K+, Ca++, Cl-,  Na+  - Action potentials in cardiomyocytes  a) Depolarization: the opening of  voltage gated sodium channels  cause membrane potentials to go  toward or past 0 mV from its  resting value  b) Plateau: at 0 or 30 mV, the  voltage gated sodium channels  close and voltage gated calcium  channels open  c) Repolarization: the return to  resting membrane potential following the plateau. The calcium channels close and potassium channels open. The  potassium efflux makes the membrane potential more negative (closer to the resting  potential)  d) Refractory period: an period that the cell is unresponsive or less responsive because an  action potential cannot occur or requires a larger stimulus to occur. This makes wave  summation and tetanus impossible in cardiac muscle.  - Calcium movement  • Calcium binds to troponin which allows tropomyosin to move off of the myosin (thick  filament) binding sites on the actin (thin) filament. Therefore, calcium allows cross bridges  to form which generates tension and muscle movement  • 20% of the calcium needed comes from outside the cardiac myocyte  • 80% of the calcium is released from the SR (sarcoplasmic reticulum) after being stimulated  by external calcium influx  • Cardiac muscles contract during the plateau period of the cardiomyocyte action potential  (during the period in which there is calcium influx)  - Review question: cardiac muscle cells are specifically adapted to heart function by all of the  following characteristics except one:  a) Contain myoglobin  b) Aerobic metabolism specialists  c) Long action potentials promote wave summation  d) Possess many mitochondria  e) Have a high capillary density  Twitches and Cardiac Function  - In cardiac muscle, the refractory period of the cardiomyocyte action potential continues until  the muscle begins to relax, making wave summation and tetanus impossible to achieve  • If the cardiac muscle did reach tetanus, cardiac output would be zero which would result is  a loss of blood pressure and consciousness  - With single twitches lasting around 250 msec, a max heart rate of 300 bpm is predicted. This  rate is not achieved due to conduction system limitations  The Conducting System  - Composed of: SA node (the pacemaker), AV node, AV bundle (bundle of his), bundle  branches, purkinje fibers  - The electrical system of the heat drives the mechanical  - Nodal cells  • Contain pacemaker cells, that have action potentials which differ from other  cardiomyocytes • Nodal cells generate action potentials that cause other cells to generate action potentials and  then contract (cardiomyocytes require stimulus)  • Nodal cell action potentials  1. They lack fast Na+ channels and lack a depolarizing “spike”  2. Possess “funny current” channels that leak K+ more slowly than other cells and  allow Na+ to enter slowly during initiation of an action potential  • Since Na+/K+ are being pumped into the cell and Na+ is entering through the funny  current, the cells gradually depolarize without any external stimulation (NO external  input is needed)  • Slow depolarization = pre potential or pacemaker potential (the pre potential  depolarizes the cell to the point where voltage gated calcium channels open and fully  depolarize the cell)  • The opening of K+ channels will re-polarize the nodal cells  • The SA node determines heart rate (specifically the pre potential of the  SA node cells)  - The rate would be 80-100 bpm  without neural or hormonal input,  but there is always neural or  hormonal input - Changing heart rate at the SA node  involves the parasympathetic  nervous system  • The AV node conducts the impulse from the internal pathways to the bundle branches with a  slight delay (allowing the atria time to contract and fill the ventricles before the ventricles  are stimulated and contract)  • The AV bundle is the only electrical connection between the atria and ventricles  • The papillary muscles attach to the AV valves (the valves that connect the atria and  ventricles) through the chordae tendinae. These muscles are the first to depolarize in the  ventricles, stabilizing prior to increased ventricular pressure and preventing inversion of the  valves into the atria (valve prolapse) and backwards flow of blood (regurgitation) • If the conducting system is damaged, the AV node may take over as pacemaker (at a slower  rate), which will decrease its efficiency due to an ineffective order of contraction (the order in which tissue depolarization occurs is  the order that the tissues contract)  The Electrocardiogram  - The electrocardiogram / ECG: a remote  measurement of the hearts electrical events  • Conduction problems can be detected  using the ECG  • The appearance of the ECG is  dependent upon the placement of  electrodes  • Waves occur when there is a difference  of voltage between electrodes (which  occurs during depolarization and re  polarization of the heart)  - ECG components  1. P wave: corresponds to depolarization of the atria  2. QRS wave / complex: corresponds to the depolarization of the ventricles and the re  polarization of the atria  3. T wave: corresponds to the re polarization of the ventricles  • The amplitude of the waves corresponds to the amount of active muscle  • Abnormal waves may indicate conduction problems or an inability to regret membrane  potentials quickly  • Segments: regions where there are no waves (the cells are fully depolarized or at rest)  - PR segment: all atrial cells are depolarized, atrial contraction  - ST segment: all ventricle cells are depolarized, ventricle contraction  • Intervals: regions including both waves and segments  The Cardiac Cycle  (one heartbeat)  - Systole: contraction phase of the atria or ventricles  - Diastole: relaxation phase of the atria or ventricles  - Fluids move in response to pressure. The valves which separate the compartments will ope  until the pressure is greater on the side being pressurized  - Atrial diastole  • Aligns with the end of ventricular diastole when the entire heart is relaxed  • Blood is returning via the venous circuit, passing through the atria and the AV valve and  into the ventricles • Passive ventricular filling (about 70% of EDV enters the ventricles during this phase)  - Atrial systole  • The atria contract and adds the remaining 30% of EDV (end diastolic volume) to the  ventricles through active filling - Ventricular systole  1. The pressure rises until the AV valves close  2. The pressure rises as the contraction continues until just before the SL valves open  (isovolumic contraction or isometric contraction phase). No blood is leaving or entering  the ventricles  3. The ventricular pressure exceeds arterial trunk pressure and the SL valves open. This is  the ventricular ejection phase (an isotonic contraction)  4. The blood leaves the ventricles (about 80 mL). The amount of blood which is ejected  from the ventricles is called the stroke volume, it will be less than the diastolic volume.  This will leave about 50 mL end systolic volume (ESV) following the contraction.  • Ejection fraction (measurement of the effectiveness of the contraction) = SV / EDV  5. The ventricles begin to relax, and blood momentarily flows backwards in the aortic and  pulmonary trunks, closing the SL valves  - Ventricular diastole  1. After the SL valves close, the ventricles are neither sending nor receiving blood. During  this isovolumic relaxation phase, the ventricular pressures drop  2. When atrial pressure is greater than ventricular pressure, passive filling occurs  - Atria are not essential to life, but the ventricles are  Cardiodynamics  - Function analysis  • The work of a complete cardiac cycle is measured by stroke volume (SV)  • Cardiac output (CO) = SV x HR  • Stroke volume and heart rate are variable depending upon the needs of the body  • Cardiac reserve: the difference between work at rest and work during maximal output  - Altering EVD and ESV for the purpose of enhancing SV  • Factors determining EDV (end diastolic volume) a) Ventricular filling time: depending on the heart rate, there will be more or less time  for filling and therefore smaller or larger volumes at the end of ventricular diastole  (with a lower heart rate there is more time for filling and a greater volume)  b) Venous return  • Factors determining ESV Isovolumic  contraction Ejection Isovolumic  relaxation Passive fillingPassive filling Active filling Active filling Highest volume Ejection Isovolumetric  relaxation Lowest volume a) Preload: how much the ventricle is stretched while it is being filled during diastole  (more filling means more preload). EDV has an effect of ESV (the larger EDV is, the  smaller the ESV will be)  • The stretch of the ventricle is related to the length-tension relationship of the muscle  • Starling’s law of the heart: more  blood into the heat leads to more  blood moving out per contraction. An  increased stretch puts the muscle cells  in an optimal place on the length tension curve  b) Contractility of muscle: the force  generated at a given amount of preload or  stretch  • Autonomic activity (sympathetic and  parasympathetic)  - Epinephrine and norepinephrine increase contraction strength  - Acetylcholine will decrease contraction strength  • Hormones  • Changes in calcium concentration  - Calcium is essential in muscular contraction and the plateau of a cardiomyocyte  action potential  c) Afterload: the pressure in the aorta or pulmonary trunk that needs to be overrun for  ejection phase to occur  • If the afterload (blood pressure) is high due to arterial blockage, the isovolumic  contraction phase increases and the ejection phase decreases, leading to decreased  cardiac output • Heart failure: occurs when the heart  in unable to overcome systemic  pressure resulting in a decrease of  cardiac output (could also result is  pulmonary edema)  Heart Rate Determinants  - The ANS or chronotropic hormones can change  heart rate by changing the pre potential slope of  the nodal cell action potentials so that the cells  reach threshold either faster or slower  - Autonomic activity (parasympathetic output is  dominant at rest, though both are active at all  times)  • The sympathetic and parasympathetic systems  alter the rate of nodal cell depolarization by altering the cell’s permeability to certain ions  • Acetylcholine increases the permeability to K+, which then leaks out more and extends the  depolarization and re polarization phases (in nodal cells), resulting in a lower heart rate  • Norepinephrine opens calcium channels, the calcium leaks in and speeds up depolarization  and reduced re polarization (in nodal cells), resulting in a high heart rate  • The sympathetic system is dominant is lower heart rates  • The parasympathetic system is dominant in higher heart rates  Vascular system  - Arteries carry blood away from the heart  - Veins carry blood toward the heart  - The anatomy of the vessels mirrors their function  • Arteries  a) Elastic arteries - dampen the pressure difference between the ejection phase and the  filling phase (Dampen pulse pressure. Pulse pressure effects flow)  b) Muscular arteries  c) Arterioles  d) Capillaries - their functions are diffusion and bulk exchange  1. Continuous - “normal”  2. Thenestrate - leaky  3. Sinusoidal - very leaky, diffusion of the largest substances occurs at sinusoidal  capillaries  • Veins - capacitance is their main characteristic, the flow in the veins will change but  pressure must remain constant  - Pressure, flow, and resistance  • Pressure falls the further the segment is from the main circuit  • The elastic vessels dampen the pulse pressure of the circuit  • A pressure gradient is necessary flow flow  • Poiseville’s law: Q = (deltaP x r4 x pi) / (n x L x 8) = (deltaP) / (R)  - Pressure is directly proportional to flow, as pressure goes up so does flow  - Resistance is inversely proportional to flow, as resistance goes up flow goes down  • Resistance is the factor which determines how well the pressure drives flow  - (this only applies to laminar flow)  - When length of the vessel, or viscosity goes up, resistance increases  • Friction has a large impact on resistance  • Length of vessels can change when the mass of the body changes • Viscosity is the relationship between the particles or suspended elements in a  substance (it is related to hematocrit)  - When the radius of the vessel increases, resistance decreases • Flow  1. Laminar flow  2. (Bolus flow through capillaries)  3. Turbulent flow  - Flow through capillaries is slower in order for  diffusion and bulk exchange to occur  - Capillary dynamics  • Flux (bulk flow) = J = Kf x NFP  - K is the leakiness coefficient  - NFP is the net filtration pressure  - NFP is the driving force and Kf is the leakiness of the capillary  • What moves things out of capillaries?  1. Diffusion  2. Bulk exchange / pressure  • NFP = net hydrostatic pressure - net oncotic pressure  - Net hydrostatic pressure = blood hydrostatic pressure - interstitial hydrostatic pressure  - Net oncotic pressure = reflection coefficient x (blood oncotic pressure - interstitial  oncotic pressure)  • What occurs in the capillaries when someone has high blood pressure? The filtration forces  at the capillaries are stronger than the reabsorption forces (because the blood hydrostatic  pressure would be higher than the interstitial hydrostatic pressure)  - Review question: Someone stands in one place for hours, limiting venous return and  increasing the venous pressure in their legs. What would occur in the legs?  a) Shift the transition point toward the arterial end of the capillary  b) Decrease net filtration  c) Increase net reabsorption  d) All of the above  e) None of the above (higher venous pressure will lead to an increase in filtrative  forces) Perfusion (flow) - Key factors: (1) cardiac output (2) resistance (3) blood pressure- Local control of perfusion  • Capillary flow is controlled by pre capillary arterioles  1. O2 - indicates normal levels of oxygen and constricts blood vessels 2. CO2 - it is a waste product and dilates blood vessels to flush it out  3. H+ - indicates pH level and dilates blood vessels 4. Increase in temperature - indicates that tissues are active and dilates blood vessels 5. Lactate - indicates anaerobic function and dilates blood vessels 6. Adenosine - indicates that tissues are active and dilates blood vessels 7. K+ - indicates that cells are depolarizing and depolarizing and dilates blood vessels - Blood pressure regulation  • Blood pressure is determined by how fast blood is being pushed into the arteries and how  fast it is flowing out of the arteries  • Adjusting peripheral resistance will increase or decrease blood pressure  - Constriction will increase blood pressure  - Dilation will decrease blood pressure  - Neural component of TPR (total peripheral resistance) • Chemoreceptors (O2, CO2, pH) found in the carotid artery, the aortic arch and in the brain  • Baroreceptors found in the carotid artery, the aortic arch, and the right atrium  • When the receptors are stimulates, some blood vessels constrict and cardiac output is  increased in order to increase flow (vessels remain dilated where flow is needed)  • When blood pressure is low, cardiac output will be increased and peripheral vessels will  constrict in order to raise blood pressure  - Endocrine control of TPR  - Angiotensin II (stimulated by low blood pressure) causes an increase in SV and  vasoconstriction, leading to an increase in blood pressure  - Aldosterone (stimulated by angiotensin II)  a) Increases sodium retention in the kidney  b) Increases water retention  c) Increases blood volume and EDV  d) Decrease in ESV  e) Increases SV  f) Increases cardiac output  g) Increases blood pressure  - ADH (stimulated by angiotensin II, low blood pressure or plasma osmolarity  h) Increases water retention in the kidney  i) Increases blood volume and EDV  j) Decrease in ESV  k) Increases SV  l) Increases cardiac output m) Increases blood pressure  - ANF (atrial natriuretic factor) (stimulated by high blood pressure or high blood volume)  a) Causes sodium excretion  b) Increase in H2O secretion  c) Decrease in blood volume  d) Decrease in EDV  e) Increase in ESV  f) Decrease in SV  g) Decrease in CO  h) Decrease in blood pressure  - The neural system solves short term problems with regulation and the endocrine system solves  long term problems with regulation

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