Anatomy Exam 2
Which of the following would cause the greatest increase in pulmonary ventilation rate and depth? \
A 10% increase in systemic arterial PCO2
Use your worksheet and integrate with what you know about blood pressure controls. Fill in the blanks: When blood pressure or blood volume are too high, ____ will be released and will stimulate the kidney to ____ GFR so that blood volume & pressure will decline.
ANP; Increase
What would happen to airflow into an alveolus when the bronchiole serving that alveolus constricts?
Airflow would decrease into the alveolus Right! Downstream of the constriction airflow will decrease. Controlling airflow into alveoli is called alveolar ventilation. Alveolar ventilation is closely matched to blood flow into the pulmonary capillaries (perfusion of the pulmonary capillaries) by a special autoregulatory mechanism. That is, when an alveolus has lots of fresh oxygen and relatively little carbon dioxide, the pulmonary capillary bed (arteriole) serving that alveolus opens up to increase flow (high ventilation is matched by high perfusion). Should the alveolus be full of carbon dioxide and poor in oxygen, the arteriole/capillary restricts blood flow (poor ventilation is met with poor perfusion). This helps increase efficiency in the respiratory system so that we can maximize exchange surfaces.
Hemoglobins' affinity for oxygen is directly related to how much oxygen is actually currently held by the hemoglobin. So, if hemoglobin has high oxygen saturation, hemoglobin's affininty for oxygen is high. What do you think happens to hemoglobin's affinity for oxygen after it moves through the systemic capillaries?
As the RBC moves through the systemic capillary, hemoglobin's affinity for oxygen decreases. Correct! Hemoglobin is a protein molecule that behaves differently in different situations. When oxygen level changes, hemoglobin's affinity for oxygen changes. When oxygen is very abundant in the environment (high pO2), hemoglobin binds oxygen very tightly due to the way the molecule is shaped. When environmental oxygen is very low (low pO2), hemoglobin is shaped differently and does not bind oxygen as readily. In the case of the body, when hemoglobin travels through the pulmonary capillary it moves into a very high oxygen environment, causing it to have a high oxygen affinity. When the hemoglobin moves through the systemic capillary, it becomes exposed to a lower oxygen environment and then decreases its affinity for oxygen. This loss of affinity from a high state (bound with lots of oxygen) to a low state (less oxygen bound) causes oxygen to be released to the tissues.
Hemoglobins' affinity for oxygen is how much oxygen is actually currently held by the hemoglobin. So, if hemoglobin has high oxygen saturation, hemoglobin's affininty for oxygen is high. What do you think happens to hemoglobin's affinity for oxygen as it moves through the systemic capillaries?
As the RBC moves through the systemic capillary, hemoglobin's affinity for oxygen decreases. Correct! Hemoglobin is a protein molecule that behaves differently in different situations. When oxygen level changes, hemoglobin's affinity for oxygen changes. When oxygen is very abundant in the environment (high pO2), hemoglobin binds oxygen very tightly due to the way the molecule is shaped. When environmental oxygen is very low (low pO2), hemoglobin is shaped differently and does not bind oxygen as readily. In the case of the body, when hemoglobin travels through the pulmonary capillary it moves into a very high oxygen environment, causing it to have a high oxygen affinity. When the hemoglobin moves through the systemic capillary, it becomes exposed to a lower oxygen environment and then decreases its affinity for oxygen. This loss of affinity from a high state (bound with lots of oxygen) to a low state (less oxygen bound) causes oxygen to be released to the tissues.
How are total cross-sectional of vessels and velocity of blood flow related?
As total cross-sectional area of vessels increases, velocity of blood flow decreases
Why is resting heart rate lower than the automatic depolarization rate of the SA node?
At rest, the vagus nerve causes SA node cells to hyperpolarize
Why should you love your kidney and treat it right?
Because it controls blood pressure Because it determines blood viscosity Because it prevents anemia Right! The kidney detects low blood oxygen levels and blood pressure. When blood oxygen is too low (anemia), it releases erythropoietin (EPO), a hormone that increases red blood cell production. The more red blood cells produced, the greater the blood viscosity. When blood pressure is too high, the kidney can correct the problem by producing more urine. Urine is really just filtered blood and so with increased urine production, there is less blood volume and therefore less blood pressure. What is very amazing about this pressure/urine volume relationship is that it can work independently of hormones as a simple pressure filter. The higher the pressure, the more urine produced; the more urine made, the lower the blood volume will drop and therefore further reduce blood pressure. This is a life long mechanism for regulating blood pressure. Of course this can work in reverse such that if blood pressure is too low, less urine is made and blood volume with rise (coupled with some fluid intake as well).
Why should you love your kidney and treat it right?
Because it controls blood pressure Because it determines blood viscosity Because it prevents anemia Right! The kidney detects low blood oxygen levels and blood pressure. When blood oxygen is too low (anemia), it releases erythropoietin (EPO), a hormone that increases red blood cell production. The more red blood cells produced, the greater the blood viscosity. When blood pressure is too high, the kidney can correct the problem by producing more urine. Urine is really just filtered blood and so with increased urine production, there is less blood volume and therefore less blood pressure. What is very amazing about this pressure/urine volume relationship is that it can work independently of hormones as a simple pressure filter. The higher the pressure, the more urine produced; the more urine made, the lower the blood volume will drop and therefore further reduce blood pressure. This is a life long mechanism for regulating blood pressure. Of course this can work in reverse such that if blood pressure is too low, less urine is made and blood volume with rise (coupled with some fluid intake as well).
During heavy exercise, cardiac output increases dramatically, although pressure may only increase modestly. How is this possible?
Because resistance increases at some vessels and decreases at others Right! During exercise, autoregulation to active skeletal muscles causes arterioles serving the muscle capillary beds to dilate and precapillary sphincters to open. Now that blood can find more vessels to fill as arterioles and sphincters open, decreasing resistance and increasing flow to tissues, pressure in the aorta may fall (more active muscle mass would increase number of dilating arterioles and magnitude of pressure drop). Such a drop in pressure would trigger baroreceptor reflexes that would lead to sympathetic activation. Sympathetic activation would trigger vasoconstriction in the systemic vessels except for those serving tissues that are working hard; in such tissues, autoregulation overcomes the sympathetic vasoconstriction and the vessels remain open. The vessels that do constrict (those serving gut tissue), act to increase pressure and shunt blood to other tissues that have decreased resistance. At the same time, the heart works harder (increases HR and contractility due to the sympathetic stimulation) and increases CO. It should seem that the increased CO should increase pressure radically and yet, the balance of the increased CO, vasoconstriction from sympathetic signals and vasodilation from autoregulation results in a high CO, some systemic pressure increase, but little change in the systemic peripheral resistance. In fact, peripheral resistance may even drop overall. Imagine if you needed to increase CO to deliver more blood, but you did not alter resistance (vessels could not change diameter). Pressure would increase dramatically and tear vessels. By altering resistance, we can have huge gains in CO with only a modest pressure increase.
Why can the pulmonary capillary blood achieve the same PO2 as alveolar air?
Because there is an overabundance of oxygen in the alveoli compared to the pulmonary arteries Yes! Air is a mixture of gases. Their total pressure (760 mmHg) is a sum of the pressures exerted by each gas. Partial pressure is the pressure exerted by a single gas inthe mixture of gases. The movement of a gas is related to its individual partial pressure; gases move from a region of higher partial pressure to a region of lower partial pressure, down a partial pressure gradient.
Why do the lungs expand during inspiration?
Because they are "pulled" open by the pleura Right! Increasingly negative intrapleural pressure generated by the expansion of the rib cage and inferior thoracic cavity during inhalation (inspiration) pulls the lungs open. Surface tension between the visceral and parietal pleura create a suction. If the parietal pleura (attached to inside thoracic cavity) move away from the lung, they generate a greater suck on the visceral pleura. The visceral pleura are attached to outside of the lung, and thus, when the visceral pleura moves, so does the lung. No muscles directly insert onto the lungs.
Why is it acceptable to make CO2 in RBCs found in pulmonary capillary blood?
Because you can release CO2 into the alveoli and remove it from the body
Suppose your blood has too low pH. How can your body correct this?
By increasing depth and rate of pulmonary ventilation Right! The respiratory system can correct acidosis (too low pH of the blood) by increasing respiratory rate and depth to eliminate more CO2 from the body. Doing this causes more H+ ions not to be free but to combine with HCO3- to make H2CO3 which then makes more CO2 and H20 at the lung. The CO2 is then removed from the system leaving only water. All of the other options would cause more H+ to remain in the body thus making the blood more acidic.
On a moment to moment basis, how do we change vascular resistance and therefore blood flow to our tissues?
By increasing or decreasing vessel diameter. Right! The most important factor affecting vascular resistance is the diameter of the blood vessels. Blood viscosity and vessel length do affect resistance, but those are not factors that change quickly to adjust the amount of blood delivered to rapidly changing tissue demands. Vessel diameter can change quickly but also has a huge effect on resistance because resistance increases as vessel diameter decreases to the fourth power.
What is responsible for pushing fluid out across the capillary wall into the interstitial fluid?
Capillary hydrostatic pressure being greater than interstitial fluid hydrostatic pressure
Look at the equation in Model 2: Inside the RBC, what happens to carbonic anhydrase activity and bicarbonate production if H+ ion concentration rises?
Carbonic anhydrase makes less HCO3-
During exercise, what happens to the heart?
Cardiac output increases to increase blood delivery to exercising tissues. Right! During exercise there is increased demand at the skeletal muscles for oxygen and nutrients. Receptors detecting muscle activation (proprioceptors) as well as changing levels of blood oxygen and carbon dioxide (reflecting increased usage/production at the tissues) cause the heart to pump more blood each minute. This is an increase in cardiac output to match blood delivery to tissue demands. Also, exercising muscles push more blood through the systemic veins - this is called an increase in venous return. This increased volume into the heart (increased venous return) also leads to increased SV out of the heart (due to the Frank-Starling law of the heart) and thus increases cardiac output. Cardiac output must increase during exercise. Any response that claims that cardiac output decreases is wrong here. While HR does increase during exercise, and this does allow less time for ventricular filling, there is also an increase in heart contractility associated with exercise (due to sympathetic activation). This causes SV to remain the same (or perhaps become even higher as the heart squeezes harder and ESV declines) and therefore the combination of increased HR & same or higher SV leads to increased CO. Blood flow through the coronary arteries increases when the heart works harder.
Which of the following will most readily trigger an increase in respiration rate and depth?
Carotid PCO2 = 47 mmHg Right! Femoral venous hemoglobin saturation = 80% is normal, maybe even a little high for a systemic vein according to what we discussed in lecture. Carotid PCO2 = 47 mmHg is too high, this should be =40 mmHg. Very small increases in systemic arterial PCO2 trigger increases in respiration rate to remove CO2 from the body. Pulmonary venous PCO2 = 40 mmHg - this is normal for blood entering the pulmonary capillary for oxygen pickup. Aortic PO2 = 90 mmHg - this is a little low, but hemoglobin is still nearly 100% saturated and this will not alter respiration rate. Jugular PO2 = 40 mmHg - this is normal for blood leaving a tissue at rest.
You have been gardening in a squatting position for 20 minutes. You stand up quickly to answer the phone and feel light headed. After about 10 seconds more you feel fine again. What was the cause and correction of your faint feeling?
Cause: low blood pressure due to too low cardiac output Correction: sympathetic nervous system activation from a baroreceptor signal Right! Squatting for a while reduces venous return from the lower limb because the veins are compressed and cannot refill with blood or send blood toward the heart (try this and look at your feet after 20 minutes of squatting). Reduced venous return will cause reduced cardiac output (Frank-Starling law) and reduced blood pressure (flow = pressure change/R). The cause of your faint feeling was reduced blood flow to the brain due to reduced blood pressure. This reduction in blood pressure associated with posture changes (orthostatic changes) is detected by baroreceptors in the carotid arteries. The correction mechanism to fix the too low blood pressure is vasoconstriction of some peripheral arteries and increased cardiac output, both due to increased sympathetic activation. The information from baroreceptors in the aorta and carotid arteries is relayed to the medulla oblongata cardiovascular centers. When too low pressure is detected, these centers direct increased sympathetic activity to blood vessels and the heart. Increased sympathetic activity increases cardiac output, thus increasing flow in the system and increasing blood pressure overall. The increased sympathetic activation to blood vessels causes increased vasoconstriction of some systemic vessels that leads to an increase in pressure overall (blood vessels to brain escape this vasoconstriction to some degree). These corrective mechanisms can increase systemic blood pressure within 5-10 seconds. Angiotensin II and ANP are chemicals that adjust blood pressure but they do so in a matter of minutes or hours. Angiotensin II production is triggered when blood flow to the kidney is reduced. Angiotensin II causes widespread vasoconstriction and increases in blood volume through decreased urine production (using the hormones aldosterone & ADH). ANP is atrial natriuretic peptide - a hormone released from the heart when pressure is too high. ANP causes increased urine formation - the more urine made, the lower the blood volume will become. Reducing blood volume will reduce blood pressure. The kidney can control blood pressure by adjusting blood volume as a pressure filter. In this manner, the kidney takes hours to days to correct blood pressure, not seconds as indicated here.
Why are women more prone to bacterial infections of the urinary tract than men?
Correct! Because women have shorter urethras
Based on your understanding of capillary dynamics, which of the following would you expect will increase glomerular filtration rate (fluid leaving the first capillary in the nephron)?
Correct! Increased blood plasma volume
Where does most reabsorption of the filtrate occur (most by total volume of the filtrate)?
Correct! The proximal convoluted tubule Yes! Most of the filtrate is reabsorbed immediately in the proximal convoluted tubule. The remaining filtrate is reabsorbed along the Loop of Henle, DCT & collecting duct. The hormones ADH & aldosterone affect the amount of water and salt reabsorbed in the DCT & collecting duct. Even though most of the filtrate is reabsorbed by the time it reaches the DCT & collecting duct, the affect of ADH is significant enough to allow more water to be reclaimed and a very low volume, concentrated urine can be produced.
Which of the following will be the response of the nephron to increase filtrate formation?
Correct! the afferent arteriole will dilate
What does a blood pressure of 120/70 tell you?
During ventricular systole, the left ventricle generates more than 120 mmHg Right! Blood must flow from high pressure to low. A blood pressure of 120/70 means that during ventricular systole, when blood is leaving the ventricles and distending the aorta and elastic systemic arteries, the blood pressure in the measured artery is 120 mmHg. During ventricular diastole, there is no further ejection and the elastic arteries recoil. The arteries recoil, keeping pressure on the blood as its volume decreases (the blood is moving away from the SL valve into the systemic circuit). The diastolic pressure is the lowest pressure recorded in the arteries and it occurs just before the next ejection begins and more blood is ejected into the aorta, distending it again (here, 70 mmHg). In order to initiate ventricular ejection into the aorta, the left ventricle must at first overcome 70 mmHg, but as volume continues to flow into the aorta, the pressure rises up to 120 mmHg. At peak systole, to continue blood flow into the aorta, ventricular pressure must exceed 120 mmHg. In this way diastolic pressure represents the pressure that must first be overcome to begin ejection and systolic pressure represents the peak pressures required to sustain ejection at the height of systole.
According to Model 3, what does hemoglobin release when it binds O2?
H+
What does hemoglobin release when it binds O2?
H+
For a healthy individual at rest, which statement is most likely true about hemoglobin relationship with oxygen?
HbO2% is lowest in the pulmonary arterial blood
What happens to hemoglobin's affinity for oxygen when levels of CO2 increase?
Hemoglobin's affinity for oxygen decreases Nice! When the level of CO2 increases (or conditions become acidic or temperature increases), hemoglobin's affinity for oxygen decreases. This means that hemoglobin holds on to oxygen less tightly, thus releasing it more readily to a hungry tissue. This is also a right shift in the oxygen-hemoglobin dissociation curse and is beneficial because it allows more oxygen delivery for the same level of PO2. It would seem that this lower affinity of hemoglobin for oxygen would be bad because it would limit how much O2 could bind in the lung. But remember that hemoglobin is fully saturated at low levels of PO2 naturally (as low at 70 mmHg) and the high level of CO2 is erased at the pulmonary capillary when CO2 diffuses into the alveoli and is removed from the blood. So, while the hemoglobin curve shifts right when the hemoglobin is in the systemic capillaries, it shifts to the left again when the hemoglobin is in the pulmonary capillaries.
What happens to hemoglobin's affinity for oxygen when blood becomes more acidic?
Hemoglobin's affinity for oxygen decreases Nice! When the level of CO2 increases (or conditions become acidic or temperature increases), hemoglobin's affinity for oxygen decreases. This means that hemoglobin holds on to oxygen less tightly, thus releasing it more readily to a hungry tissue. This is also a right shift in the oxygen-hemoglobin dissociation curse and is beneficial because it allows more oxygen delivery for the same level of PO2. It would seem that this lower affinity of hemoglobin for oxygen would be bad because it would limit how much O2 could bind in the lung. But remember that hemoglobin is fully saturated at low levels of PO2 naturally (as low at 70 mmHg) and the high level of CO2 or H+ is erased at the pulmonary capillary when CO2 diffuses into the alveoli and is removed from the blood. So, while the hemoglobin curve shifts right when the hemoglobin is in the systemic capillaries, it shifts to the left again when the hemoglobin is in the pulmonary capillaries.
What happens to hemoglobin's affinity for oxygen when blood becomes more acidic? Note: affinity is how readily hemoglobin pick up O2. When affinity is high, HBO2% will be high.
Hemoglobin's affinity for oxygen decreases Nice! When the level of CO2 increases (or conditions become acidic or temperature increases), hemoglobin's affinity for oxygen decreases. This means that hemoglobin holds on to oxygen less tightly, thus releasing it more readily to a hungry tissue. This is also a right shift in the oxygen-hemoglobin dissociation curse and is beneficial because it allows more oxygen delivery for the same level of PO2. It would seem that this lower affinity of hemoglobin for oxygen would be bad because it would limit how much O2 could bind in the lung. But remember that hemoglobin is fully saturated at low levels of PO2 naturally (as low at 70 mmHg) and the high level of CO2 or H+ is erased at the pulmonary capillary when CO2 diffuses into the alveoli and is removed from the blood. So, while the hemoglobin curve shifts right when the hemoglobin is in the systemic capillaries, it shifts to the left again when the hemoglobin is in the pulmonary capillaries.
Which of the following will INCREASE respiratory rate?
High carotid PCO2 Yes! If there is too much CO2 in the systemic arterial blood, then there was not enough removal of CO2 by the lungs. The chemoreceptors in the carotid bodies & aorta detect this high systemic arterial PCO2 and relay the information to the respiratory centers of the brainstem. Also, central chemoreceptors located in the medulla oblongata receive CO2 from systemic arteries. If too much CO2 moves across into the blood brain barrier, H+ ions form. These ions cannot be buffered (due to low protein composition of the cerebrospinal fluid) and the central chemoreceptors are triggered. The brainstem centers (in pons and medulla oblongata) are then stimulated to increase respiratory rate to remove more CO2 from the body. We do not monitor the composition of the systemic venous blood (i.e. Jugular vein) because the blood in these vessels has not reached the lungs for adjustment. Not matter how high the systemic venous blood CO2 level becomes, If the lungs are performing adequately, then enough CO2 is removed and there is no cause to increase ventilation rate. Too low O2 can stimulate increased respiration rate, but only when O2 levels reach less than 60 mmHg PO2 in systemic arteries.
Regarding cardiac output:
Increased venous return increases stroke volume and cardiac output Right! Increased heart rate will always lower cardiac output because the ventricles fill less. - Not true. Although EDV may decrease, if you increase contractility, the ventricle will squeeze harder and eject more, lowering the amount left behind (ESV). This may keep SV normal or even increased, thus maintaining or increasing CO. Furthermore, increased exercise may increase venous return, so that even though filling time is less, more volume may come back, maintaining EDV. People with slow heart rates always have low cardiac outputs. - Not true. Slower heart rate allows more filling time and a higher EDV. If EDV is higher, SV will be higher due to the Starling law of the heart. Increased venous return increases stroke volume and cardiac output. True. This is the Starling law of the heart. When more volume comes into the ventricle, that volume stretches the muscle into better interaction between actin and myosin. This better interaction means a more forceful contraction. This more forceful contraction leads to more volume being ejected (a higher SV) which means a higher CO. Increasing heart rate will always increase cardiac output. - Not true. If HR is high, but SV is low, CO will not increase. CO = HR x SV. This type of thing may happen when someone loses a lot of blood (hemorrhage). The heart rate increases, but with a low stroke volume (due to low blood volume) they may not be able to maintain CO needed to maintain life.
If blood becomes acidic due to lactic acid accumulation, which of the following will correct blood pH?
Increasing respiratory rate
According to our worksheet, what leaves the capillary through intercellular clefts and enters the interstitial fluid?
Ions, glucose, water
Which of the following accurately describes the site of external respiration?
It allows easy diffusion of gases between the alveoli and the body. Right! The respiratory membrane is the site of external respiration. It is made of the pulmonary capillary wall, a thin amount of connective tissue and the wall of an alveolus. It is free of cilia although it does have a little bit of fluid lining it. The respiratory membrane is very thin to allow easy diffusion of gases - in pneumonia the respiratory membrane becomes thickened and it is difficult to load the blood with oxygen because gases cannot diffuse into the blood.
In Model 3, in the systemic capillaries, what happens to the H+ ion created by the conversion of CO2 (+H2O) to HCO3?
It becomes attached to hemoglobin, releasing an O2 to the tissue
In Model 3, in the pulmonary capillary, what happens to the H+ ion when O2 binds with hemoglobin?
It binds with HCO3- to make CO2 (& H2O)
For a single cardiac cycle, why does sympathetic activation increase stroke volume?
It decreases ESV Right!Sympathetic activation increases contractility of the heart, making ventricular systole more effective. This lowers the volume left in the ventricle at the end of a contraction (ESV). Since stroke volume is the difference between how full the ventricle is before it contracts and how empty it is at the end of a contraction, sympathetic input increases stroke volume.
The respiratory membrane is found at the site of external respiration. What best describes the respiratory membrane?
It exists between the walls of the alveoli and the walls of the pulmonary capillaries Right! The respiratory membrane is the site of gas exchange - the site of external respiration. It is a very thin barrier made of the walls of the alveoli (type I alveolar cells) and the endothelial cells of the pulmonary capillary. Because it is so thin, it easily allows the diffusion of gases between the alveoli and the capillary blood. The respiratory epithelium lines the nasal cavity, trachea and bronchioles - proximally it is PCCE and serves to cleanse, humidify and warm incoming air. The intrapleural space is between the visceral and parietal pleura; the pleura properly are created by a simple squamous epithelium and underlying connective tissue. Although anatomically similar to half of the respiratory membrane, the pleura produce a fluid that creates surface tension and lubricates movements of the lungs
Which of the following best describes the air in the alveloi?
It has a PO2 of ~100 mmHg
auto regulation
LOCAL level
Which of the following occur when ATP production increases at the tissues?
More CO2 is produced in the RBCs at the pulmonary capillary Right! When the tissues begin making more ATP they also make more CO2 (by aerobic metabolism). That CO2 diffuses into the blood and causes more O2 to be offloaded because high CO2 decreases hemoglobin's affinity for O2 and thus more O2 is released to the tissues. More H+ ions are made and the hemoglobin can buffer them because they have given up more O2 and now can bind more H+ to form HHb. At the tissues, more HCO3- is made when CO2 production increases. The confusing part is that the HCO3- and HHb travel in the blood up to the lungs and in the pulmonary capillary, the H+ comes off of the HHb (as oxygen binds to Hb) and binds to the HCO3-. When this happens, CO2 and H2O are formed. SO, CO2 is made in RBC in pulmonary capillaries because that CO2 can then diffuse into the alveoli and be removed from the body. Albumin does not transport CO2.
What happens if capillary colloid osmotic pressure is greater than capillary hydrostatic pressure? (Imagine interstitial hydrostatic pressure and interstitial osmotic pressure are both 0 mmHg.)
More fluid would be pulled into the capillary from the interstitial fluid than would be pushed out from the capillary plasma to the interstitial fluid.
As presented in the capillary shown in Model 3 (be sure to use your data table), is all the fluid that is pushed into the interstitial space from the arterial end reabsorbed at the venous end? If not, where does it go?
No, the extra fluid becomes part of the interstitial fluid.
According to our worksheet, what creates the colloid osmotic pressure of the capillary?
Plasma proteins
What is the correct path of a red blood cell as it moves through the healthy kidney
Renal artery - afferent arteriole - glomerulus - efferent arteriole - peritubular capillary - renal vein - inferior vena cava Yes! Blood cells are not filtered into the Bowman's capsule. They remain within the walls of the blood vessels and so this question really just asks about the flow of blood through the kidney. This answer would be the same if the question asked What is the correct order for a sodium ion that is not filtered at the glomerulus or secreted into the tubule? Please review blood flow through the kidney using your lecture notes so that you know what vessels you are expected to know.
How is secretion different from reabsorption in the kidney?
Secretion and reabsorption both use membrane proteins for substance transport, but secretion moves substances from the blood into the filtrate and reabsorption moves substances from the filtrate into the blood.
Why must GFR be kept at a constant level?
So that you filter your blood to remove wastes So that you can maintain blood pressure So that you can maintain the proper ion concentration in your blood Right! A balanced rate of glomerular filtration ensures that your blood gets filtered at a rate which your nephron tubules can work with the filtrate inside of them. If the GFR is too high, the filtrate passes through the nephron too fast and solutes (& water) do not get reclaimed (reabsorbed). If GFR is too low, too much volume get reabsorbed and waste products do not leave the body. Maintaining blood composition and volume factor into the maintenance of blood pressure. You must maintain an appropriate rate of glomerular filtration to constantly adjust your blood levels of ions and wastes. If you do not filter your blood, body pH is not maintained and ionic composition changes. These in turn affect cellular functions such that neurons may not fire or the heart may not beat. Enzymes in the body also need a steady environment in which to work.
Total cross-sectional area refers a group of vessels (i.e. all the systemic capillaries). If we were to cut into every systemic capillary and measure their cross-sectional areas then sum these together, we would get total cross-sectional area for the systemic capillaries. Using the figure above, which vessels have the largest total cross-sectional area?
Systemic capillaries
Using the figure above, which vessels have the smallest diameter?
Systemic capillaries
Using the above figure, which vessels have the lowest average blood pressure?
Systemic veins
Where would you find hemoglobin that is relatively O2 poor in a healthy resting person?
Systemic veins & pulmonary arteries Great! During rest, the tissues consume O2 to make ATP. Blood that exchanges respiratory gases with the air in the alveoli picks up oxygen to become fully loaded with O2 (hemoglobin saturated to maximum, effectively 100%). This O2 rich blood leaves the pulmonary capillaries and flows to the pulmonary veins, left atrium, left ventricle and then the systemic arteries. When systemic arterial blood arrives at the resting tissues, the blood releases some of the O2 for the tissue cells to use. The blood then leaving the tissues will have less O2 (depending on how much was released to the tissue cells) and so systemic venous blood is relatively O2 poor (at rest, it has 75% of the O2 that they systemic arterial blood had). This systemic venous blood moves into the right atrium, right ventricle and then the pulmonary arteries. Because gas exchange in/out of the blood only occurs in 2 places (the pulmonary capillaries or the systemic capillaries) the amount of O2 in the systemic venous blood is equal to the amount of O2 in the pulmonary arteries.
Where would you find hemoglobin that is 75% saturated with O2 in a healthy resting person?
Systemic veins & pulmonary arteries Great! During rest, tissue PO2 is 40 mmHg. Blood that loads oxygen in the pulmonary capillaries becomes fully saturated with O2 (hemoglobin saturated to maximum, effectively 100%). When blood arrives at the resting tissues and equilibrates, the blood achieves a PO2 of 40 mmHg. At 40 mmHg, hemoglobin is only 75% saturated (as determined by the oxygen-hemoglobin dissociation curve). Therefore, systemic venous blood is 75% saturated with oxygen. O2 does not leave the blood except at capillaries and so as blood flows through the heart from the systemic veins to the pulmonary arteries, no further oxygen is lost. Acordingly, pulmonary arterial blood has a PO2 =40 mmHg and also contains hemoglobin that is 75% saturated with oxygen
Where would you find hemoglobin that is about 65% saturated with O2 in a healthy resting person?
Systemic veins & pulmonary arteries Great! During rest, tissue PO2 is 40 mmHg. Blood that loads oxygen in the pulmonary capillaries becomes fully saturated with O2 (hemoglobin saturated to maximum, effectively 100%, though often in the high 90's). When blood arrives at the resting tissues and equilibrates, the blood achieves a PO2 of 40 mmHg. At 40 mmHg, hemoglobin is only 65% saturated (as determined by the oxygen-hemoglobin dissociation curve). Therefore, systemic venous blood is 65% saturated with oxygen. O2 does not leave the blood except at capillaries and so as blood flows through the heart from the systemic veins to the pulmonary arteries, no further oxygen is lost. Acordingly, pulmonary arterial blood has a PO2 =40 mmHg and also contains hemoglobin that is 65% saturated with oxygen.
How are the left and right sides of the heart similar or different?
The left ventricle consumes more oxygen than the right ventricle. Right! The left ventricle has more muscle mass and therefore requires more blood to be delivered to it by the coronary circulation. The left side generates much greater pressures than the right side because it must pump to the entire systemic circuit which has a very large resistance. Therefore, the left side must generate more pressure to overcome the resistance and keep blood moving to the tissues. All of the other options are incorrect because they either state or imply that the amount of blood returning to or leaving the heart is unequal on both sides. This is of course incorrect because the left and right sides must move the same amount of blood per unit time (same cardiac output) to prevent blood backing up in a circuit. When the left and right sides are not matched, this is called congestive heart failure.
Which of the following is important to establishing the concentration gradient observed in interstitial fluid of the renal medulla?
The variable permeability of the loop of Henle
In Model 3, which net direction does the CO2 equation move when the RBC is in the systemic capillary?
To the right (to produce H+ & HCO3-)
When would inspiratory air volume be lowest? (This is just the amount of air inhaled.)
When intrapulmonary pressure = -1 mmHg ( opposed to more negative number)
Which of the following statements about blood velocity is true?
When total cross-sectional area of a group of vessels is small, velocity is high. Velocity is inversely proportional to cross sectional area. There are many capillaries in parallel that cumulatively have a large cross sectional area. Because flow through the system is equal in arteries, capillaries and veins, velocity is slow in those vessels with high cross sectional area and fast in vessels with small cross sectional area. Slow velocity serves capillaries well because it allows for exchange between the blood and the tissues.
Why do the lungs expand during inspiration?
because they are pulled open by the pleura Right! Increasingly negative intrapleural pressure generated by the expansion of the rib cage and inferior thoracic cavity during inhalation (inspiration) pulls the lungs open. Surface tension between the visceral and parietal pleura create a suction. If the parietal pleura (attached to inside thoracic cavity) move away from the lung, they generate a greater suck on the visceral pleura. The visceral pleura are attached to outside of the lung, and thus, when the visceral pleura moves, so does the lung. No muscles directly insert onto the lungs
As you move down the bronchial tree (from the trachea toward the alveoli), what changes do you observe.
cartilage decreases
At the time when you measure systolic blood pressure, both atria and both ventricles are in systole.
false
Autoregulation is a homeostatic mechanism that regulates blood pressure in the aorta
false
If the liver could not produce enough albumin, the tissues would become dehydrated. (before compensatory mechanisms corrected the problem)
false
True or False? Sympathetic stimulation increases heart rate but decreases stroke volume due to less time for ventricular filling.
false
When two vessels have the same blood flow per minute, they also have the same blood velocity per minute.
false
In Brandon, what happens when muscular effort for inhalation (inspiration) is increased?
he generates more negative inhalatory intrapleural pressures
In the pulmonary capillaries:
hydrogen ions combine with bicarbonate ions to form carbon dioxide and water Right! In the pulmonary capillaries oxygen loads into the blood and CO2 moves into the alveoli. CO2 is made in the systemic tissue mitochondria (there are no mitochondria in the RBCs) and transported away from tissue cells using the blood. Some CO2 dissolves in the plasma, some attaches to hemoglobin (NOT at the same binding site for oxygen) and the rest is converted to bicarbonate ions. The most conversion occurs inside RBCs where the enzyme carbonic anhydrase combines CO2 & water to create a hydrogen ion (H+) and bicarbonate ion (HCO3-). [Even though all the components of CO2 are found in bicarbonate ion, they are in the form of bicarbonate ion and not CO2.] The RBC then pushes bicarbonate out to the blood plasma and hemoglobin binds the H+. Some dissolved CO2 spontaneously combines with water to also make bicarbonate and H+ - acidifying the venous blood. The RBC then moves through the vascular tree up to the pulmonary capillaries. Once in the pulmonary capillaries, CO2 must move out of the blood into the alveoli for removal from the body. Bicarbonate ion cannot diffuse out of the blood into the alveolus, instead we need to "remake" CO2. To recreate CO2, bicarbonate ions combine with H+ and form CO2 and water in the RBC (also due to carbonic anhydrase). The CO2 then diffuses into the alveoli. The blood leaving the pulmonary capillary has less CO2 dissolved (because dissolved CO2 also moved into the alveoli) and therefore also has less free H+, making the pulmonary venous blood less acidic than the pulmonary arterial blood. O2 does not combine with water to make bicarbonate.
Which of the following will directly increase cardiac output?
increased EDV with no change in HR Right! CO = HR x SV SV = EDV - ESV Increasing EDV leads to a higher SV because of the Frank-Starling law of the heart. The more blood that returns to the heart, the stronger the heart contraction to empty more blood. Any increase in ESV will decrease CO because of a lower SV. A decreased SA node firing rate is the same as slowing the heart rate, and a lower HR with the same or lower SV means a lower CO
Maintains blood pressure by regulating blood volume
kidney
During reabsorption, solutes and water move out of the renal tubule into the interstitial space. Most of these reabsorbed materials then ____.
move into the peritubular capillary. Right! During reabsorption, molecules first must leave the tubule lumen, then cross into the interstitial space. From there, reabsorbed substances move into the peritubular capillaries (or vasa recta). These molecules are pulled into the blood supply because the capillaries contain dissolved proteins that create an osmotic pull for the water, pulling in any dissolved substances as well. Some molecules enter the capillary because they move down their own diffusion gradients. The slow speed of the blood moving through the capillaries is very important here to allow for the entry of reabsorbed substances. While lymphatics are present in the kidney, most reabsorbed substances do not return to the circulation through the lymphatics. If they did, the renal lymphatics would be responsible for moving about 180 L/day! If the majority of the reabsorbed substances remained in the kidney, the kidney volume would become enormous, but also, the blood would not maintain proper volume, or water, solute and waste balance. Since the blood supplies fluid to all tissues, the tissue fluids would then become unbalanced and tissue cells would not be able to perform their duties. Any fluid entering the renal pelvis is to be lost to the environment as urine. Reabsorbed substances would not be in the urine (unless they were later secreted after being reabsorbed, and even still, this is not most of the substances).
Vasodilation in response to decreased local blood pressure
myogenic auto regulation
Brandon had severe pneumonia (perhaps as well a chronic respiratory condition). In pneumonia, inflammation in the respiratory system causes increased porosity at the pulmonary capillaries as well as inflammation in the bronchioles, narrowing their diameter. In the bronchioles, airway constriction decreases lung compliance and increases the work of breathing. For Brandon, when his pulmonary capillaries become overly porous, albumin leaks into the extracellular fluid (ECF). What does this cause and why?
pulmonary edema due to low blood colloid osmotic pressure
For Brandon, O2 transfer across the ____ is reduced by his pneumonia.
respiratory membrane
Corrects a sudden drop in blood pressure within seconds
sympathetic activation
What happens in an otherwise normal individual if their liver cannot produce albumin?
the blood would lose fluid to the tissues and the tissues would become swollen (edema)
What would happen if intrapleural pressure became 0 mmHg when thoracic volume increased?
the lungs would not expand Right! Negative intrapleural pressure creates a suction between the lung and chest wall (thoracic body wall). The parietal pleura line the inside of the chest wall; the visceral pleura are the outermost layer of the lung. Between the two layers is some fluid that creates surface tension and a sucking pressure (negative pressure). This negative pressure keeps the lungs sucked against the chest wall. Because the chest wall has a greater volume than the lungs and a volume that cannot drop below the limits of the bony ribs, the lungs are always somewhat inflated (open). When the chest wall expands during inhalation, the intrapleural pressure becomes more negative (goes from -4 mmHg to -8 mmHg) thus pulling the lungs outward further (inflating the lung). If this pressure were to become 0 mmHg (meaning equal to atmospheric pressure), there would be no suck between the pleura and the lung would collapse due to its own elastic forces.
For Brandon, his care team administered inhaled air with an O2 concentration of 40%. This air is delivered at a total pressure of ~760mmHg. What is the advantage of this in Brandon?
to increase the partial pressure of oxygen in the alveoli
In terms of influence on blood volume, the actions of ANP are antagonistic to the actions of angiotensin II and aldosterone.
true
n the normal continuous capillary, fluid moves out at the arterial end because capillary hydrostatic pressure is greater than blood colloid osmotic pressure.
true
The lower hemoglobin's affinity for oxygen, the more hemoglobin can prevent blood acidosis.
true Right!! Affinity here refers to hemoglobin's greediness for oxygen. When affinity is high, hemoglobin binds oxygen tightly and does not release it. When affinity is low, hemoglobin releases oxygen readily. High levels of CO2, H+ ions (low pH) and high temperature cause shape changes in hemoglobin molecules that decrease hemoglobin's affinity for oxygen. When hemoglobin releases an oxygen molecule, it provides a binding site on the hemoglobin for an H+. Free H+ cause pH to decline - creating acidosis - but H+ bound to a protein cannot affect pH (the binding protein buffers against pH changes). Hemoglobin does just this - it binds a H+ when oxygen affinity is low and acts to prevent acidosis of the body.
Think about the equation: HHb + O2 --> HbO2 + H+ when answering: The lower hemoglobin's affinity for oxygen, the more hemoglobin can prevent blood acidosis.
true Right!! Affinity here refers to hemoglobin's greediness for oxygen. When affinity is high, hemoglobin binds oxygen tightly and does not release it. When affinity is low, hemoglobin releases oxygen readily. High levels of CO2, H+ ions (low pH) and high temperature cause shape changes in hemoglobin molecules that decrease hemoglobin's affinity for oxygen. When hemoglobin releases an oxygen molecule, it provides a binding site on the hemoglobin for an H+. Free H+ cause pH to decline - creating acidosis - but H+ bound to a protein cannot affect pH (the binding protein buffers against pH changes). Hemoglobin does just this - it binds a H+ when oxygen affinity is low and acts to prevent acidosis of the body.
In normal, healthy individuals, the diaphragm moves superiorly during exhalation.
true Yes! When the diaphragm contracts, it moves inferiorly, increasing the size of the thoracic cavity to allow air to flow into the lungs. During quiet exhalation, the diaphragm relaxes and passively moves superiorly to decrease the size of the thoracic cavity and force air out of the lungs.
Under normal resting conditions or light exercise, the primary factor altering cardiac output is:
venous return Right! Venous return is the volume of blood returning to the heart from systemic veins. It is the primary mechanism for changing cardiac output as explained by the Frank-Starling law of the heart. The more blood that flows into the heart, the more blood that will be pumped out thus altering cardiac output. Changes in hormones or neural stimuli do alter cardiac output, but the primary mechanism that acts to alter cardiac output to match tissue demands at rest and during routine activity is venous return. Parasympathetic activation keeps cardiac output low at rest, but it does not affect changes to match needs during shifts in venous return.
Can stroke volume increase if EDV does not change?
yes Right! EDV is end diastolic volume (it is how full the ventricle is before it contracts). ESV is end systolic volume - it is how full the ventricle is at the end of a ventricular contraction (not all blood is actually pumped out of the ventricle with each beat - there is always some residual volume). The amount that is ejected is called SV (stroke volume) and it is calculated by this formula: SV = EDV-ESV. So, stroke volume can increase by increasing EDV or decreasing ESV. ESV will go down if the heart squeezes harder and ejects more. The higher the stroke volume, the greater the cardiac output (for a given heart rate).
For Brandon, before he received treatment, he had systemic arterial PCO2=67 mmHg, PO2=69 mmHg, and pH=7.36. How saturated is his systemic arterial hemoglobin (in this initial state)?
~80%
