233 weekly quizzes

Match the name to the time period it describes: 1, 2, 3, 4, 5

1. Passive Fill (of the ventricles) 2. atrial kick (or active fill of the ventricles) 3. Isovolumetric contraction (ventricles contract and the blood volume does not change) 4. Ventricular ejection (blood moves into the aorta) 5. Isovolumetric relaxation (ventricles relax and the blood volume does not change)

Air flow and blood flow are governed by the same principles: flow occurs when pressure gradients can overcome resistance. And like in the cardiovascular system, resistance to airflow is almost entirely altered by changes in diameter of the conduits (in the case of the respiratory system, these important conduits are the bronchioles). What would happen to airflow into an alveolus when the bronchiole serving that alveolus constricts? Airflow would increase into the alveolus Airflow would decrease into the alveolus

Airflow would decrease into the alveolus 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.

Why should you love your kidney and treat it right? Because it controls blood pressure Because it determines blood viscosity Because it prevents anemia All the above

All of the above 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).

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. As the RBC moves through the systemic capillary, hemoglobin's affinity for oxygen increases. As hemoglobin moves through the systemic capillary, hemoglobin's affinity for oxygen stays the same.

As the RBC moves through the systemic capillary, hemoglobin's affinity for oxygen decreases. 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.

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 At rest, sympathetic cardiac nerves release neurotransmitter Venous return is high The Bainbridge reflex dominates the heart at rest

At rest, the vagus nerve causes SA node cells to hyperpolarize Right! The Vagus nerves synapse on the SA node and AV node. They release acetylcholine (Ach) that binds to chemically gated channels on these cells. The Ach triggers potassium release from the SA & AV node cells, causing the SA node to reach threshold less often and fire action potentials less often (a slower heart rate). Sympathetic activation increases heart rate by allowing calcium entry into the SA node cells (increases contractility too through the same mechanism). Venous return is low at rest. The Bainbridge reflex is triggered when increased venous return activates stretch receptors in the right atrium. These receptors communicate with the cardioacceleratory center in the brainstem which then activates sympathetic nerves to increase heart rate. Although this reflex is activated during inhalation when thoracic pressure increases blood flow into the right atrium, it would not lower the heart rate and it is not dominant.

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 Because all systemic vessels dilate Because all systemic vessels constrict Because resistance in the systemic circulation increases

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 do the lungs expand during inspiration? Because they are "pulled" open by the pleura Because the diaphragm attaches directly onto the lungs and pulls the lungs down Because positive intrapleural pressure "pulls" them open Because the intercostal muscles attach directly onto the lungs and pull the lungs outward

Because they are "pulled" open by the pleura 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.

On a moment to moment basis, how do we change vascular resistance and therefore blood flow to our tissues? By increasing or decreasing vessel length. By increasing or decreasing vessel diameter. By increasing or decreasing blood viscosity.

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 Capillary colloid osmotic pressure being greater than interstitial fluid osmotic pressure

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. HR increases, but there is less time for ventricular filling, so stroke volume and cardiac output decrease. Stroke volume decreases which leads to a decreased cardiac output. Blood flow through the coronary arteries decreases because more blood is moving through the aorta.

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.

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 much vasodilation Correction: increased angiotensin II formation (i.e. hormone activation) that caused massive vasoconstriction Cause: low blood pressure due to low blood volume Correction: kidney made less urine, thus increasing blood volume and blood pressure Cause: low blood pressure due to too low cardiac output Correction: sympathetic nervous system activation from a baroreceptor signal Cause: increased blood pressure due to too high blood volume Correction: ANP secretion (hormone) from heart to reduce blood volume & thus blood pressure

Cause: low blood pressure due to too low cardiac output Correction: sympathetic nervous system activation from a baroreceptor signal 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.

When is pressure in both ventricles high enough to close the AV valves, but too low to open the semilunar valves? During the earliest phases of ventricular systole and diastole During ventricular ejection During early ventricular filling During late ventricular filling

During the earliest phases of ventricular systole and diastole Right! When both valves (AV and semi-lunar) are closed, the ventricles can neither fill nor empty. This occurs at two times during the cardiac cycle. The first is when the ventricles begin contracting; the pressure in the ventricles exceeds that in the atria, causing the AV valves to close (with the AV valves closed, the ventricles cannot fill). But, the pressure in the ventricles is still lower than that in the pulmonary trunk and aorta and so the blood cannot flow out of the heart into these arteries. This phase is called isovolumetric contraction - because the volume is the same in the ventricles during this time period, nothing in, nothing out. All valves are closed again during the initial phase of ventricular diastole called isovolumetric relaxation. Again, this terminology refers to the volume in the ventricles, nothing in, nothing out. Isovolumetric relaxation occurs after ventricular ejection, but before ventricular filling. The pressure in the ventricles is lower than the great vessels, and backward flowing blood causes the SL valves to close (preventing complete backward flow into the ventricles). But pressure in the ventricles is still higher than pressure in the atria, and as such, the AV valves are still closed. I think of an elevator being used to move someone to a 6th floor apartment. When you load the elevator at the ground floor (elevator filling), the elevator is at a very low building level and the door in the apartment building lobby is open. Once the elevator car is full, you close the door and go up. As the elevator climbs the elevator shaft to the 6th floor, nothing can get in the elevator or out (lobby door closed, 6th floor door closed). Once you reach the 6th floor, you open the 6th floor door and unload (eject). When the elevator is empty, the 6th floor door closes and the elevator drops back down again - but nothing can get in or out as the elevator travels back down to the lobby again.

When is pressure in the ventricle highest? During atrial systole During ventricular diastole During ventricular ejection

During ventricular ejection Right! Blood flow is determined by pressure gradients and blood flows from high pressure to low pressure. During a certain phase of ventricular systole (contraction), blood is ejected out of the ventricles into the arteries leaving the heart. Blood leaves the ventricles because the pressure in the ventricle exceeds the pressure in the arteries.

What does a blood pressure of 120/70 tell you? At the end of ventricular diastole, the left ventricle generates 70 mmHg During atrial systole, the left ventricle generates 120 mmHg During sympathetic activation, the elastic arteries generate 120 mmHg During ventricular systole, the left ventricle generates more than 120 mmHg The aortic semilunar valve closes when aortic pressure reaches 120 mmHg

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.

Which of the following is essential to the proper coordination of a single heart beat? Gap junctions between adjacent cardiac muscle cells Neurons of intrinsic conduction system Hormone binding to neurons of SA node Neurotransmitter passing through intercalated discs

Gap junctions between adjacent cardiac muscle cells Right! The cells of the intrinsic conduction system are cardiac muscle cells that do not contract. Instead, they are responsible for automatically depolarizing to fire action potentials that control the contraction cycle of the heart. Action potentials spread through the heart via the gap junctions in the intercalated discs. An action potential is initiated in the SA node. Ions spread from the SA node cells to the atrial muscle via gap junctions - these arriving ions initiate action potentials in the contractile cells. The signal travels to the AV node, AV bundle, bundle branches, Purkinje fibers and finally reaches the ventricular muscle cells. It is gap junctions between all these cells that spreads the signal - and it is ions (sodium, calcium) that actually move through the gap junctions to trigger the next action potential. Even the intrinsic conduction system cells (which are non-contractile cardiac muscle cells) are connected to one another and the contractile cells by gap junctions.

What does hemoglobin release when it binds O2?

H+

What happens to hemoglobin's affinity for oxygen when levels of CO2 increase?

Hemoglobin's affinity for oxygen decreases 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 Hemoglobin's affinity for oxygen increases Hemoglobin's affinity for oxygen does not change

Hemoglobin's affinity for oxygen decreases 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.

Regarding cardiac output: Increased heart rate will always lower cardiac output because the ventricles fill less People with slow heart rates always have low cardiac outputs Increased venous return increases stroke volume and cardiac output Increasing heart rate will always increase 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.

Which of the following accurately describes the site of external respiration? It allows easy diffusion of gases between the alveoli and the body. It is the trachea, bronchi and bronchioles. It is very thick and covered with a thin layer of mucous. It is composed of tissue cell membranes, a thin layer of connective tissue and the wall of a systemic capillary.

It allows easy diffusion of gases between the alveoli and the body. 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

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 pushed out of the capillary into the interstitial fluid than would be pulled in from the interstitial fluid into the capillary. 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. No fluid would cross the capillary wall.

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.

Which of the following would you expect to have the thickest tunica media relative to their overall diameter? Muscular arteries Venules Veins Arterioles

Muscular arteries Muscular arteries have large amounts of smooth muscle in their tunica media. Sympathetic nerves innervate this muscle and when active determine the vessel diameter and thus blood pressure and blood flow. They are important in maintaining vascular tone. Venules are thin walled and porous; veins are not porous but are thin walled. Arterioles also have some smooth muscle and are important in their location immediately before the capillary. They regulate blood flow into the capillary and thus the amount of blood available to the tissues.

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? Yes, it all goes back into the venous end of the capillary. No, the extra fluid is drained away by the lymph vessels. No, the extra fluid collects in the tissue.

No, the extra fluid is drained away by the lymph vessels.

Which of the following will cause fluid to collect in the interstitial space (create tissue edema)? Permeability of the lymphatic capillaries decreases Increased production of albumin by the liver Permeability of the systemic capillaries decreases at the arterial end Blood pressure decreases at the arterial end Increased production of albumin by the liver

Permeability of the lymphatic capillaries decreases Right! If the lymphatics cannot drain away the fluid in the interstitial space, fluid accumulates - this condition is called edema. The more permeable the lymphatics, the more fluid it can drain. If the blood capillary becomes less permeable or blood pressure drops, less fluid leaves the systemic capillaries to create interstitial fluid. If blood albumin level increases, more fluid will be kept in the capillary (more pulled in to oppose capillary hydrostatic pressure) and less fluid will enter the interstitial space. Administration of proteins in IV fluid therapy is a way to increase blood volume and maintain that blood volume because the proteins act to suck fluid towards them so that less fluid can become interstitial fluid.

According to our worksheet 3, what creates the colloid osmotic pressure of the capillary? Blood pressue (hydrostatic pressure) Ions Plasma proteins

Plasma proteins

which vessels have the lowest average blood pressure? Systemic arteries Systemic capillaries Systemic veins

Systemic veins

Where would you find hemoglobin that is about 65% saturated with O2 in a healthy resting person? Systemic veins & pulmonary arteries Systemic arteries & pulmonary veins Systemic & pulmonary veins Systemic & pulmonary arteries

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.

What structure prevents backflow during the ejection phase of ventricular systole in the systemic circuit? The tricuspid valve The pulmonary semi-lunar valve The aortic semi-lunar valve The bicuspid valve

The bicuspid valve The left side of the heart pumps blood to the systemic circuit, the right side of the heart pumps blood to the pulmonary circuit. During the ejection phase of ventricular systole, blood is leaving the ventricle and moving into the large arteries of the heart. In the systemic circuit, the blood is flowing through the open aortic semi-lunar valve. Because it is open, it is not preventing blackflow. However, the pressure in the ventricle is higher than the pressure in the atrium and therefore blood would try to move into the atrium. The left AV valve (the bicuspid) prevents this backflow. The tricuspid valve is on the right side of the heart and prevents backflow in the systemic circuit.

How are the left and right sides of the heart similar or different? The left ventricle consumes more oxygen than the right ventricle. The left atrium receives more blood than the right atrium during diastole (fills with more blood). The right ventricle generates the same amount of pressure as the left ventricle during systole. The right side of the heart has a higher cardiac output than the left side of the heart. The left side of the heart has a higher cardiac output than the right side of the heart.

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.

What would most likely happen if the AV bundle were damaged? The ventricles would not be activated appropriately after the atria The atria would not contract The ventricles would not contract

The ventricles would not be activated appropriately after the atria The heart relies on coordination between the atria and ventricles to an effective pump. The AV bundle is the only electrical connection between the atria and ventricles that ensures the activation of the ventricles only after the atria contract. The SA node activates the atria and the signal spreads through the atria to the AV node. From the AV node, the signal passes through the AV bundle, down the bundle branches to the Purkinje fibers and ultimately, the ventricular muscle mass. If the bundle is damaged, the ventricles will receive signals from other intrinsic conduction cells in the ventricular muscle mass. The bundle branch cells or the Purkinje fibers can fire spontaneously and trigger ventricular contraction. Usually when this happens, normally timed QRS complexes are not seen on the ECG and they seem to occur at their own rate regardless of the appearance of the p wave. This question does not state that the SA node is damaged, so there is no reason to assume atrial non-function.

A patient arrives at your emergency department (ED) feeling very weak and faint after spending the day drinking alcohol in the sun at a baseball game. You measure her radial blood pressure as 80/55 mmHg. You diagnose severe dehydration and give her intravenous (IV) fluids slightly hypotonic to her blood. For your patient, what is happening in her heart when her systemic arterial blood pressure is 80/55 mmHg? To open the bicuspid (mitral) valve, her heart is generating at least 55 mmHg pressure To close the aortic valve, her heart is generating at least 80 mmHg pressure To open the aortic valve, her heart is generating at least 55 mmHg pressure To close the bicuspid (mitral) valve, her heart is generating at least 80 mmHg pressure

To open the aortic valve, her heart is generating at least 55 mmHg pressure

when does blood eject from the ventricles out into the aorta?

during time 4

Although the heart is an intermittant pump, _______ expand and recoil thus exerting continuous pressure on the blood and maintaining constant blood flow in the CV system. elastic arteries arterioles venules capillaries

elastic arteries The large amounts of elastic tissue in the tunica media of elastic arteries (like the aorta) allow these vessels to expand and recoil to accept the blood ejected from the ventricles. When they expand, they store energy in their fibers that they impart to the blood as they recoil. The vessels recoil during ventricular non-ejection (all of diastole and isovolumetric contraction of systole).

True or False? Sympathetic stimulation increases heart rate but decreases stroke volume due to less time for ventricular filling.

false

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.

True or False? If aortic pressure increased above normal values, the left ventricle would need to generate even more pressure to ensure blood flow through the systemic circuit.

true Blood flows from high pressure to low pressure. In order to move blood from the left ventricle to the aorta, the left ventricle pressure must be greater than the aorta. When systemic arterial pressure increases pathologically (due to loss of elasticity or fatty plaque build up), this forces the left ventricle to work even harder to ensure proper blood flow. Everyone must maintain a minimal blood flow from the heart (termed cardiac output) no matter what. Too high aortic pressure will result in less blood ejection (lower SV) which would then decrease cardiac output (CO). Your body would then need to increase contractility or HR to keep CO high enough. This is why increased systemic blood pressure is so dangerous to your health - it increases the workload on the heart and the heart can only handle that problem for so long before it fails. High blood pressure is particularly dangerous for individuals with weakened hearts (such as after a heart attack).

1) Vasodilation in response to decreased local blood pressure= 2) Corrects a sudden drop in blood pressure within seconds= 3) Maintains blood pressure by regulating blood volume=

1) Myogenic autoregulation 2) sympathetic activation 3) kidney

What is happening to ventricular volume during times 3 & 5? Ventricular volume is increasing in 3 and decreasing in 5 Ventricular volume is decreasing in 3 and increasing in 5 Answer Ventricular volume is not changing in 3 or in 5 Ventricular volume is decreasing in both 3 & 5

Answer Ventricular volume is not changing in 3 or in 5

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 increases As total cross-sectional area of vessels increases, velocity of blood flow decreases

As total cross-sectional area of vessels increases, velocity of blood flow decreases

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

How do you feel about this statement? Blood returns from lungs via pulmonary arteries to the left atrium. I think it should say: Blood returns from lungs via pulmonary veins to the left atrium. I think it should say: Blood returns from lungs via systemic arteries to the left atrium. I think it should say: Blood returns from lungs via pulmonary arteries to the right atrium. I feel good about this sentence.

Blood returns from lungs via pulmonary veins to the left atrium.

As you move down the bronchial tree (from the trachea toward the alveoli), what changes do you observe. Dimeter increases Smooth muscle decreases Cartilage decreases

Cartilage decreases

What factor determines air flow into or out of the lung? (Assume no factor is 0) Atmospheric pressure (a number of mmHg) Intrapulmonary pressure (a number of mmHg) DIfference in pressure between the atmospheric pressure and intrapulmonary pressure

DIfference in pressure between the atmospheric pressure and intrapulmonary pressure

According to Model 3, what does hemoglobin release when it binds O2?

H+

According to our worksheet, what leaves the capillary through intercellular clefts and enters the interstitial fluid? Ions, glucose, water Plasma proteins Both plasma proteins and ions, glucose, water

Ions, glucose, water

For a single cardiac cycle, why does sympathetic activation increase stroke volume? It increases EDV It increases ESV It decreases EDV It decreases ESV

It decreases ESV 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

Which of the following do NOT activate cells of the healthy heart? Ions from adjacent cells entering contractile cells Neurotransmitter arriving at contractile cells Spontaneous depolarization of non-contractile cells Ions from adjacent cells entering non-contractile cells

Neurotransmitter arriving at contractile cells

which vessels have the largest total cross-sectional area? Systemic arteries Systemic capillaries Systemic veins

Systemic capillaries

which vessels have the smallest diameter? Systemic arteries Systemic capillaries Systemic veins

Systemic capillaries

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) The blood would gain fluid from the tissues and the tissues would become dehydrated

The blood would lose fluid to the tissues and the tissues would become swollen (edema)

which structure generates the highest pressure in the cardiovascular system?

Time periods 3 & 4

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-

Which of the following prevent backflow in the large veins of the lower extremity? Venous valves Thick tunica media Porous tunica interna Vasa vasorum

Venous valves Right! Just like in the heart, valves in the veins prevent backflow of blood (backflow back down to the feet in the case of the veins). Skeletal muscle contractions also help venous blood move upward toward the heart, as does negative intrathoracic pressure generated during ventilation of the lungs. The vasa vasorum is the blood supply of the vessels - the vessels are tissue too and need their own source of nutrients to live. The blood moving though vessels cannot supply all the vessel tissue with nutrients, just like the blood inside the heart chambers does not supply nutrients to the heart muscle.

in normal, healthy individuals, the diaphragm moves superiorly during exhalation.

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.

Which of the following statements about blood velocity is true? The velocity of blood is faster in the capillaries than in the arteries. When total cross-sectional area of a group of vessels is small, velocity is high. Blood velocity does not change between the different vessels.

When total cross-sectional area of a group of vessels is small, velocity is high Right! 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.

Can stroke volume increase if EDV does not change? Yes No 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).

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).

Which of the following will directly increase cardiac output? decreased SV with no change in HR increased ESV with no change in HR increased EDV with no change in HR decreased SA node firing rate with increased ESV

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.

Does the ejection phase (ventricles emptying into aorta) occur during all of ventricular systole? (Look at the previous question to help you)

no

Does the left ventricle fill with new blood during all of ventricular diastole? (Look at question 12 of worksheet)

no

During the time of early ventricular filling, which has the lowest pressure in the cardiovascular system?

right ventricle During early ventricular filling, blood is flowing into the ventricle from the atrium. Therefore blood pressure must be lower in the ventricle than the atrium because blood flows from high pressure to low pressure. Pressure in the aorta and pulmonary trunk is definitely higher than either the atrium or the ventricle at this time as well. Pressure in the inferior vena cava is higher than the pressure in the atrium because blood is flowing into the atrium from the vena cavae.

The ____ return blood from the systemic circulation into the ____. pulmonary arteries; left atrium superior and inferior vena cavae; right atrium pulmonary veins; right atrium aorta; left ventricle

superior and inferior vena cavae; right atrium Grab a picture of the heart with arrows indicating blood flow through it - try this one: https://medlineplus.gov/ency/imagepages/19387.htmLinks to an external site.

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 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 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 sympathetic stimulation of the heart parasympathetic stimulation of the heart hormonal stimulation of the heart

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.