Physio I Block 4


Q: What is BSA?
A: body surface area. Since this is proportional to cardiac output (Q), it is a good way to compare individuals.

Q: How does average resting heart rate compare in adults, children, and athletes?
A: adults is about 70 beats/min. children it is higher, and athletes it is lower than average adults.

Q: What is Cardiac Index (CI)?
A: Q/BSA (cardiac output/body surface area) L/min/m2

Q: Although cardiac output is intermittent, blood flow is essentially continuous. What is the cause of this?
A: The elasticity of the aorta and arteries.

Q: What is normal systolic arterial blood pressure (SBP)?
A: 120 mmHg

Q: What is normal diastolic arterial blood pressure (DBP)?
A: 80 mmHg

Q: What is normal arterial blood pressure?
A: 100 mmHg

Q: How do you calculate mean arterial blood pressure (MAP)?
A: MAP = DBP + [(SBP – DBP)/3]

Q: What is the intrinsic heart rate (SA node pacemaker discharge rate)?
A: between 90 to 110 beats/ min at rest.

Q: Are the Ach receptors on SA node muscarinic or nicotinic?
A: muscarinic.

Q: How does the vagal stimulation of the heart start and stop so quickly?
A: because SAA node is rich in cholinesterase, which rapidly degrades ACh. So vagal stimulation of SA node decays rapidly once vagal stimulation stops. This makes the parasympathetic innervation beat-by-beat control.

Q: What drug inhibits action of Ach on SA node?
A: Atropine. Your heart rate will increase from 70 to 100 beats/min.

Q: Where do the preganglionic and postganglionic sympathetic nerves synapse before going to the heart?
A: Stellate ganglia.

Q: What does Propranolol do?
A: It inhibits action of beta-adrenergic receptor of SA node. Drop in heart rate isn’t that great, because paraympathetic control is dominant. Heart rate decreases from 70 to 65 beats/min.

Q: Which type of neural control is more predominant in SA node?
A: Parasympathetic.

Q: Describe the parasympathetic vs. sympathetic innervation of a resting heart rate?
A: parasympathetic is at max and in complete control at resting heart rate. Sympathetic is at minimum.

Q: Describe the innervation of the heart at maximal heart rate?
A: parasympathetic is at minimal control, and sympathetic is at maximal control.

Q: How do you calculate Stroke Volume?
A: End Diastolic Volume – End Systolic Volume

Q: What are the three factors that determine stroke volume?
A: Preload, Contractility, and Afterload.

Q: What causes preload in the heart?
A: Filling of the (left) ventricle with blood.

Q: How does increasing the preload effect the ventricular contraction and stroke volume?
A: increase preload →increase sarcomere length, reaching optimal overlap between actin and myosin → increased force of contraction → increased stroke volume.

Q: What is the Frank-Starling relationship?
A: It’s the relationship between left ventricular end-diastolic volume (LVEDV) and stroke volume.

Q: What is the optimal length of overlap between the actin and myosin in the cardiac muscle to produce the highest tension and fastest shortening velocity of the heart muscle?
A: between 2 and 2.2 μ.

Q: How does increasing the preload affect the minimal sarcomere length?
A: It doesn’t. increasing the preload will increase the sarcomere length, but when it contracts, the smallest length it will become is the same as if without preload. Because you are going from a higher sarcomere length to the same minimal length as without preload, adding a preload will cause shortening to become faster.

Q: How does changing the cardiac muscle preload affect maximal velocity of shortening (Vmax) of the cardiac muscle?
A: It doesn’t. They all have the same maximal velocity of shortening, no matter what preload you put onto the heart. Increasing the preload, however, cause velocity of shortening to increase.

Q: Can cardiac muscle contraction ever reach Vmax?
A: No, because aortic blood pressure is never zero, which is where Vmax happens.

Q: When does the aortic valve open and systolic ejection phase begin?
A: When ventricular pressure rises during the isovolumic phase of systole, and exceeds that of the aorta.

Q: How is contractility (inotropy) related to stroke volume?
A: increase contractility, increase stroke volume.

Q: What causes contractility?
A: intracellular calcium concentrations. More calcium = more contractility.

Q: How does sympathetic nervous system affect contractility?
A: norepinephrine act on beta-adrenergic receptors on ventricular muscle membranes. More L-type Ca channels activated. More calcium influx during action potential, which causes more calcium to be released from sarcoplasmic reticulum.

Q: What are inotropic agents?
A: drugs that increase contractility by increasing intracellular calcium.

Q: What are some causes that affect myocardial contractility?
A: inotropic agents, depression, sympathetic nerves, catecholamines, loss of myocardium

Q: What is a way to define contractility in terms of slope?
A: maximum left ventricular pressure increase per time (p/t) during isovolumic systole!

Q: So what does increasing sympathetic nerve impulses do?
A: increases myocardial contractility and SA node discharge rate! Both great ways to increase stroke volume!

Q: What are the two ways in which Catecholamines (Epi or Norepi) can increase cardiac contraction?
A: 1. by increasing open time of the calcium channels, and more calcium rush into the cardiac muscle cell. From the extracellular fluid. 2. Phosphorylate (activate) phospholamban, whch increases Calcium ATPase in the sarcoplasmic reticulum. This increases calcium stores in the SR, so more is released when needed, leading to forceful contractions. Calcium is also removed from the cytosol faster, shortening the calcium-troponin binding time, which causes shorter duration of contraction.

Q: What is the isovolumic systole?
A: The period between the closing of the mitral valve and the opening of the aortic valve. There is a large and rapid rise in ventricular pressure during this time. Once the pressure matches that of the aorta, then the aortic valve opens and the blood rushes out. The greater the contractility, the larger the pressure rise with a shorter time period.

Q: How does increasing inotropic state affect velocity of shortening?
A: increases it.

Q: What is ejection fraction?
A: percentage of end-diastolic volume ejected from the left ventricle during systole. (stroke voume/end diastolic volume x 100%). It is the amount of blood that is actually ejected from a given end-diastolic volume.

Q: What causes the afterload in the heart?
A: the pressure resistance of the systemic arterioles (or pulmonary artery) (vasoconstriction) that the ventricle has to overcome when it ejects blood.

Q: What is total peripheral resistance (TPR or SVR, systemic vascular resistance)?
A: the overall systemic vasoconstriction or vasodilation.

Q: How do you calculate total peripheral resistance (TPR)?
A: mean arterial blood pressure (MAP) / cardiac output… mmHg/liters/min. larger TPR = more systemic vasoconstriction (more pressure per cardiac output) = therefore greater afterload.

Q: What is the difference between afterload and preload?
A: preload is caused by the filling of the ventricle with blood. The afterload is caused by aortic resistance.

Q: How do afterload and preload differ in terms of affecting stroke volume?
A: preload increases stroke volume whereas afterload decreases stroke volume.

Q: How do afterload and preload differ in terms of affecting velocity of shortening?
A: preload increases velocity while afterload decreases it.

Q: How does preload change because of
A: with more arteriole resistance (increased afterload), there is more blood that is left behind in the ventricle after systole. Therefore the end-diastolic pressure is increased and preload is increased. Stroke volume, increases just a little because of this. Overall, however, increasing afterload still decreases stroke volume.

Q: What can cause a loss in cardiac contractility?
A: congestive heart failure.

Q: Contractility vs. Afterload… which one normally has a greater effect on stroke volume?
A: Contractility. Afterload is still important in heart patients.

Q: What is the cardiac output like in anemic patients?
A: it is abnormaly high, to compensate for the fact that their blod can’t carry as much oxygen because of low level of functional hemoglobin.


Q: What are the seven phases of the cardiac cycle?
A: Atrial Systole (SA Node Depolarization)→ Isovolumetric Contraction → Early Rapid Ejection → Later Slow Ejection → Isovolumetric Relaxation → Early Rapid Filling → Later Slow Filling

Q: What exactly is “atrial systole”? What is “atrial kick”?
A: atrial contraction at the end of ventricular diastole. Notice that the atrium only contracts at the end. This causes extra blood to be pushed from atria to ventricle, called atrial “kick.”

Q: When do you hear the rare S4? What causes it?
A: You hear S4 right before hearing S1 and S2. It’s caused by atria contracting forcefully in an effort to overcome increased pressure in an abnormally stiff or enlarged ventricle. So it is an abnormal sound.

Q: Where is the 1st Phase (Atrial Systole) on the ECG?
A: PR interval

Q: What represents the 2nd cardiac cycle phase (isovolumetric contraction) on the ECG?
A: Descending R and S.

Q: How does the AV valve close?
A: When ventricular contraction is coming to an end, blood eventually slows down and even moves backwards against the aortic valve, closing it. The closing causes S1 sound.

Q: What is the “dicrotic notch”?
A: The “bounce” you hear or feel when the blood bounces against the aortic valve when it temporarily drops backwards.

Q: What causes the S2 sound?
A: the closure of aortic and pulmonic valves due to drop in pressure in left and right ventricles at onset of diastolic relaxation.

Q: At what pressure does tricuspid and mitral valve open?
A: When ventricular pressure drops to and then below the atrial pressure.

Q: What causes the rare 3rd heart sound?
A: you hear it when the blood oscillates back and forth between the walls of the ventricles when it comes in from the atria.

Q: What is another name for slower ventricular filling?
A: diastasis – it is the longest phase of the cardiac cycle.

Q: What happens near the end of diastasis?
A: the SA node depolarizes, and the cardiac cycle starts again.

Q: At what point does mitral valve close?
A: A

Q: At what point does mitral valve open?
A: E

Q: At what point does aortic valve open?
A: B

Q: At what point does aortic valve close?
A: D

Q: At what points is lub and dub?
A: lub = A. dub = D

Q: What happens to the Pressure Volume Loop when you increase preload?
A: stroke volume increases, so you see a shift in end diastolic volume to the right, assuming that inotropy and afterload stays constant.

Q: What does the pressure-volume loop look like when you increase afterload?
A: The end systolic volume shift to the left, and maximum pressure shifts upwards.

Q: What happens to the pressure-volume loop when you increase inotropy?
A: The end systolic volume shifts to the left and pressure rate increases (shifts upwards)

Q: What is the ejection fraction?
A: The percentage of the end diastolic volume that is ejected per stroke.

Q: What is ejection fraction often used to measure?
A: left ventricular contractility

Q: How many sounds are actually generated by the heart?
A: 4. S1, S2, S3, and S4, but we only hear S1 and S2 (lub dub)

Q: What is S1 composed of?
A: M1 and T1 (mitral and tricuspid)

Q: What composes S2?
A: P2 and A2 (pulmonary and aortic)


Q: What are two methods to measure human cardiac output?
A: Direct Fick Method (based on blood O2 levels) and Dilution Methods (based on injections of green dye).

Q: Where in the heart is the mixing of oxygenated and deoxygenated blood most complete?
A: pulmonary artery

Q: What equation is used to determine oxygen consumption with the Fick method?
A: oxygen consumption = cardiac output × (arterial − mixed venous) O2 concentration difference

Q: What equation do you use for Indicator Dilution Method of finding Cardiac Output?
A: A (quantity of dye) = C (dye concentration) × V (unknown volume of liquid).

Q: What is the advantage of using Indicator Dilution Technique to determine cardiac output?
A: multiple sequential cardiac outputs can be measured in a short time span (because you can measure dye concentration at many different spots). You avoid the need to obtain a mixed venous blood sample.

Q: What is another way to do Indicator Dilution Technique without all the dye?
A: By using cold fluid and measuring temperature.

Q: What is the venous return?
A: The rate at which blood returns to the great veins (vena cava) and right atrium from peripheral vascular beds. Amount of blood returning to heart.

Q: What is the central blood volume or central venous pool?
A: The volume of blood in the great veins of the thorax and right atrium. It shows right atrial pressure, which determines right ventricular end diastolic volume.

Q: How can central venous pressure be measured?
A: with catheter with its tip in the right atrium.

Q: How does central venous pressure influence stroke volume and venous return?
A: Increase central venous pressure → increase stroke volume, decrease venous return.

Q: When the right heart output briefly exceeds that of left heart, what happens?
A: with this imbalance, blood accumulates in pulmonary vessels and raises pulmonary and left atrial pressures, leading to left ventricular filling.

Q: What are some causes of myocyte stretch?
A: blood volume, body position, intrathoracic pressure, intrapericardial pressure, venous tone, skeletal muscle pump, atrial kick.

Q: Is venous compliance greater at high or low pressure?
A: low pressure.

Q: What is compliance?
A: the change in volume associated with a given change in pressure. Δ volume/Δ pressure

Q: What is venous tone?
A: degree of venoconstriction caused by sympathetic stimulation of peripheral veins. Increasing sympathetic stimulation increases venous tone, venous pressure, venous return, and cardiac filling.

Q: How does breathing change pressure in great veins?
A: inspiration → reduce intrathoracic pressure → abdominal pressure raises → pressure gradient between abdomen and thorax increase blood flow from inferior vena cava towards right atrium.

Q: When do you do valsalva maneuver?
A: When you’re constipated and want to force feces out, when you’re playing wind instruments, when you’re doing heavy lifting, when you’re coughing.

Q: What happens to intrathoracic pressure during valsalva maneuverr?
A: increases. You contract diaphragm and abdominal muscles against closed glottis

Q: What happens to blood pressure immediately after valsalva maneuver?
A: it falls a lot (because of sudden cessation of skeletal muscle contraction). People with cardiovascular disease will feel feel really dizzy after valsalva maneuver because of big fall in blood pressure.

Q: How does standing up affect transit velocity and venous volume of blood?
A: mean transit velocity is slower because of increased venous vol
ume in lower extremities due to gravity. So return of blood to heart is delayed.

Q: What is rate of blood flow?
A: rate of blood flow = volume of blood flow/cross sectional area.

Q: What happens when you stand up?
A: stand up → blood stay in legs due to gravity → reduce venous return to central blood pool → right atrial filling pressure declines → fall in left ventricular diastolic volume (fall in preload) → reduced stroke volume (due to Starling’s Law) and reduced cardiac output.

Q: What are some factors that counteract gravitational accumulation of blood in lower extremities?
A: contractions of skeletal muscles in leg, reduced venous compliance at high pressures, increased hydrostatic pressure gradient from legs to right atrium.

Q: How do leg muscles affect venous return?
A: it increases venous return. Often when you sit or lay for a long time, your muscles get weaker or “looser” so when you stand, your muscles won’t have enough contraction to sustain venous return (needed to counteract gravity), so you’re more likely to black out.

Q: How does standing in water affect venous return?
A: The water creates compressive force on the leg veins, which increase venous return.

Q: Is pericardium compliant? What is the function of the pericardium?
A: no, so it strongly resists large rapid increase in cardiac size. Prevents over-distension due to large increase in venous return.


Q: What is the Basic Flow Equation?
A: Flow = pressure difference/resistance (Q = ΔP/R)

Q: What is the Resistance to Flow Equation?
A: R = 8 Lη/πr4
Where r = inside radius of the tube
L = tube length
η = fluid viscosity

Q: What is Poiseuille’s Law?
A: Combining the Basic Flow Rate Equation and the Resistance to Flow Equation.
Q = ΔPπr4/8 Lη

Q: What units are Blood flow and Blood velocity expressed in?
A: Blood flow = cm3/sec. Blood Velocity = cm/sec

Q: Where is the total cross-sectional area highest?
A: Capillaries. Therefore average velocity is much slower (since v = Q/A)

Q: What is laminar blood flow?
A: Normal flow when it is fastest in the center of the vessel and slowest on the sides touching the walls (virtually zerio velocity).

Q: What happens with laminar blood flow when there is a clot?
A: It becomes turbulent.

Q: What is turbulence flow in the heart called? In the vessel?
A: 1. murmur. 2. Bruit.

Q: What is Reynold’s number used to predict?
A: whether blood flow will be laminar or turbulent. NR = ρdv/η = (blood density x diameter of vessel x velocity of flow / viscosity of blood). If over 2000, then there is turbulence.

Q: What conditions will increase Reynold’s number?
A: thrombi (because narrow diameter of vessel and increase blood velocity), atherosclerosis (same reason), anemia (because increase velocity and reduce viscosity)

Q: What is hematocrit (Hct)?
A: percentage of blood volume that consist of RBCs. As hemocrit increases, velocity increases.

Q: What causes Hct Increase?
A: Dehydration, dengue fever, COPD, blood doping

Q: What causes Hct Decrease?
A: Acute hemorrhage, anemia, renal disease.

Q: What kind of force does flowing blood exert on vessel wall?
A: shear stress. NO and prostacyclin (PGI2) are released from blood vessel endothelium due to shear stress due.

Q: What causes a dissecting aneurysm?
A: when shear stress causes a tear between supported and unsupported regions of endothelial lining. Blood flow through the tear, separating the vessel lining even more.

Q: What are the three types of energy in circulation?
A: Potential (pressure building up right before systole), Kinetic, Gravitational (hydrostatic pressure).

Q: How does gravity affect pressure in vessels below and above heart level?
A: Above heart level, the pressure is decreased while below the heart level, the pressure is increased.

Q: What is the Bernoulli’s principle?
A: kinetic and potential energy are constant. So increasing the blood flow (like through an aortic stenosis) will decrease lateral pressure to keep total energy of the system constant.

Q: What is Laplace’s Law for blood vessels? For ventricle?
A: For vessels: T = (P × r)/w where T = tention in blood vessel wall, P = transmural pressure (pressure inside blood vessel – pressure outside vessel, but usually low so often ignore this one), R = radius, w = wall thickness
For ventricles: Ventricular Tension = (ventricular pressure x ventricular radius)/(2 x ventricular wall thickness)


Q: What is the difference between the fourth and fifth Korotkoff sound?
A: The fourth Korotkoff Sound is the first muffled sound you hear during ausculation during measuring blood pressure with cuff. The last sound you hear is the fifth Korotkoff sound. Diastolic blood pressure of resting adult correspond to pressure at which fifth Korotkoff sound is heard. For children and adults after exercise, you use the fourth Korotkoff sound.

Q: What is the typical resting blood pressure for a young healthy adult man?
A: 120/80. However, this is just a set standard and what is “normal” can vary from person to person. For women it is a little lower. Blood pressure increase with age.

Q: What causes the dicrotic notch on the pressure curve?
A: When the aortic valve closes.

Q: How do you calculate mean arterial pressure (MAP)?
A: Take the area under the pressure curve and divide by time. Or use this equation where DBP is diastolic blood pressure: MAP = DBP + [(SBP − DBP)/3]
Mean arterial pressure (MAP) = cardiac output × total peripheral resistance.

Q: What are the three components of pressure within blood vessels?
A: a static pressure related to volume of blood at zero flow, a dynamic pressure generated by the heart (blood flow x vascular resistance), and a hydrostatic pressure caused by gravity (pgh where density x gravity x height of hydrostatic column)

Q: What is pulse pressure?
A: The difference between systolic (SBP) and diastolic (DBP) pressure. It is a function of stroke volume. Increase blood ejection from left ventricle → increase aortic volume → increased pressure in aorta.

Q: What happens to compliance when you increase pulse pressure?
A: It decreases. As you get older, you lose arterial compliance, and so pulse pressure increases. So older people have higher blood pressure.

Q: Does the pressure wave down the aorta travel the same velocity as the blood flow itself?
A: no. It is about 15 times faster. It is the “pulse” you feel.

Q: What blood vessels are the ones actually doing the vasodilation and constriction?
A: Arterioles, also known as “resistance vessels” due to their changeable resistance to flow due to this ability. They have much more smooth muscles and less elastic material than arteries.

Q: Where does the greatest decline in vascular pressure occur?
A: with Arterioles aka “resistance vessels.”

Q: What is vascular tone?
A: the degree of constriction relative to the degree of dilation.

Q: When does an organ have large vascular tone?
A: when it has a large vasodilatory capacity.

Q: What is the difference between series resistance and parallel resistance?
A: series resistance is blood vessels arranged within a given organ. The total resistance is equal to the sum of individual resistances. Parallel resistance is blood flow among various major arteries branching off aorta. The more parallel elements in the network, the lower the overall resistance of the network.


Q: What are the most important receptors involved in moment-to-moment regulation of arterial blood pressure?
A: carotid and aortic arterial baroreceptors. Aka “high pressure baroreceptors”

Why are carotid and aortic arterial baroreceptors called “high pressure baroreceptors”?
A: because they are affected by the high pressures in the systemic arterial circulation.

Q: What are the “low pressure baroreceptors”?
A: cardiopulmonary baroreceptors (in atria and pulmonary system).

Q: What are the two key factors in regulation of mean arterial pressure?
A: cardiac output and peripheral resistance.

Q: Increase in what two factors can cause hypertension?
A: increase in cardiac output or increase in systemic vascular resistance.

Q: What are some pathophysiological factors that increase cardiac output, leading to hypertension
A: renal artery stenosis, aortic coarctation, hypersecretion of ADH

Q: What are some pathophysiological factors that increase systemic vascular resistance, leading to hypertension?
A: atherosclerosis, renal artery disease, diabetes, cerebral ischemia, thyroid dysfunction, pheochromocytoma (tumor in the adrenal medulla)

Q: What are the five types of reflexes that control arterial pressure?
A: baroreflex, bainbridge reflex, chemoreceptor reflex, diving reflex, exercise pressor reflex

Q: Where are the carotid sinus baroreceptors innerved?
A: nerve of Hering, branch of glossopharyngeal.

Q: How do the baroreflexes work?
A: When blood pressure is too high, the carotid sinus baroreceptors send signal via the nerve of Hering (CN IX) to the brain, which sends signals back to the aortic arch receptors and SA node via the vagus nerve to tell it to relax, lowering the blood pressure. This also inhibits sympathetic innervations on the SA node.

Q: At what pressure are the baroreceptors most sensitive (have more reactivity)?
A: near normal mean arterial pressure (between 85 and 100 mmHg). So any deviation from the norm, baroreceptors will act quickly.

Q: Firing of arterial (carotid sinus) baroreceptor afferent nerves exert tonic inhibitory influence on what?
A: sympathetic outflow from medulle. Remember these baroreceptors respond to high blood pressure.

Q: Tell me about baroreceptors when you stand up.
A: Baroreceptors maintain blood pressure when you stand up.

Q: What is orthostatic intolerance?
A: development of symptoms during upright standing. When you stand up for a long time, blood accumulates in legs, and venous return to right atrium declines. Regulation of blood pressure fails and syncope (fainting) occurs.

Q: What is Bainbridge reflex (aka atrial reflex)?
A: It causes an increase in heart rate due to increase in central venous pressure (due to either IV infusion or respiratory sinus arrhythmia). It is the antagonist to baroreceptors and respond during low heart rate (that experiences a sudden increase in pressure).

Q: When is Bainbridge reflex important?
A: during Heart rate response to IV infusion of large volumes of fluid and during respiratory sinus arrythmia (increase in heart rate during inspiration)

Q: What are the chemoreceptors adjacent to the carotid and aortic baroreceptors?
A: the carotid and aortic bodies (peripheral chemoreceptors).

Q: What is the purpose of the peripheral chemoreceptors?
A: reflex control of breathing (like when PO2 or pH is low or PCO2 is high or flow through carotid bodies is low), but also of arterial blood pressure (sometimes).

Q: What is the difference between the peripheral and the central chemoreceptors?
A: The peripheral chemocreceptors are the carotid and aortic bodies, while the central chemoreceptors is in the medulla of the brain.

Q: What is so special about coronary and cerebral circulations?
A: they are not subject to chemoreceptor reflex vasoconstriction, because they are controled by autoregulatory factors.

Q: Is chemoreceptor reflex a primary or secondary emergency reflex?
A: secondary. It doesn’t respond directly to blood pressure (due to stretch) but instead responds to O2 and CO2 content, so it is secondary.

Q: What is the diving reflex?
A: Parasympathetically-mediated slowing of heart rate and peripheral vasoconstriction when diverse immerse their faces in cold water. Therefore people can survive longer underwater without O2 than on land.

Q: What is exercise Pressor Reflex?
A: Reflex that originate from mechanical and metabolic stimuli produced by contracting skeletal muscles.

Q: What is the difference between Group III and Group IV nerve endings in the muscle?
A: Group III are mechanosensitive (respond to muscle tension produced during contraction). Group IV nerve endings are sensitive to metabolic factors within muscle (H+, K+, prostaglandins, temperature, ischemia, muscle pain, etc.)

Q: What is the purpose of the Exercise Pressor Reflex?
A: It speeds up heart rate and myocardial contractility by stimulating adrenergic receptors, to ensure adequate arterial pressure is there for contracting skeletal muscle.

Q: What is MSNA?
A: Muscle Sympathetic Nerve Activity – used to measure vasoconstrictor signals to blood vessels via baroreflexes, exercise pressor reflexes etc. Measure how much H+ (shows ATP metabolism) increases in an active muscle. It shows how well your exercise pressor reflex is.

Q: What type of response has the most rapid time of onset?
A: arterial baroreceptors – remember baroreceptors is primarilyl responsible for moment-to-moment control.

Q: Describe renal control of blood pressure.
A: Reduced flow through kidney (sensed by renal macular densa) causes it to release renin, which turns angiotensinogen into angiotensin I which becomes II via ACE. Angiotensin II then increases aldosterone secretion to increase blood volume and arterial pressure.

Q: What do the volume receptors in the atria do?
A: They detect increase in volume in the atrium, then they increase atrial natriuretic factor which then increases salt and water excretion, lowering the blood volume. It also relays the message via vagus to medullary centers where ADH secretion and sympathetic innervation decreases, also lowering blood volume.


Q: How do metarterioles keep you warm when you’re cold?
A: they open up their precapillary sphincters, diverting the blood from getting to the cutaneous circulation, keeping the blood warm.

Q: How do metarterioles keep you cool when you’re too hot?
A: they open up and let more blood flow through them.

Q: Why is the metarterioles “non-nutritional”?
A: Because their primary purpose is not to drop of nutrients.

Q: Is blood flow through capillaries laminar or turbulent?
A: Turbulent.

Q: Is the blood flow through the capillaries fast or slow?
A: slowest in the circulation, because the total cardiac output is divided into millions of channels.

Q: What are the purposes of venules?
A: capacitance vessels, play role in regulating capillary hydrostatic pressure.

Q: Where is hydrostatic pressure highest in capillaries?
A: at arteriole end, so fluid is driven out higest at arteriole end, and reabsorbed at venule end.

Q: What determines the osmotic pressure within the capillary?
A: proteins (predominantly albumin), because ions are very permeable. This osmotic pressure is called “oncotic” or “colloid” osmotic pressure.

Q: What is the difference between hydrostatic pressure and oncotic pressure?
A: hydrostatic pressure (P) is the main filtration force, while oncotic pressure (pi) is main absorption force.

Q: What does Fick’s Law of Diffusion measure:
A: diffusion of O2, CO2, electrolytes, and other small molecules from capillaries to tissues. J = DA(ΔC/ΔX)


Q: What is Active Hyperemia?
A: increase in organ blood flow associated with increased metabolic activity of the organ or tissue.

Q: How does Active Hyperemia work in muscle?
A: Increased O2 consumption during muscle con
traction stimulates production of vasoactive substances that dilate the resistance vessels in the muscle.

Q: What is Reactive Hyperemia?
A: transient increase in organ blood flow following brief period of ischemia (inadequate blood supply), due to build up of vasodilator metabolites during the occlusion.

Q: What is autoregulation of organ blood flow?
A: the intrinsic ability of an organ to maintain a constant blood flow in spite of changes in perfusion pressure. Q = ΔP/R. As ΔP decreases, at first Q falls, but then R decreases to pull Q back to similar levels as before due to endothelial, myogenic, and metabolic mechanisms. There is a range of pressure change in which autoregulation can happen though.

Q: What are the three mechanisms that contribute to autoregulation of organ blood flow?
A: endothelial, myogenic, and metabolic mechanisms.

Q: Autoregulation can occur in the absence of what?
A: neural and hormonal influences. This is because it is intrinsic to the organ and does not need outside help.

Q: What is perfusion pressure?
A: arterial pressure minus venous drainage pressure, ΔP.

Q: How do myogenic mechanisms cause autoregulation of blood flow?
A: by modifying vascular smooth muscle tone, i.e. vasoconstriction or vasodilation.

Q: Remember how stretching smooth muscle causes vasoconstriction?
A: Stretch of sarcolemma → opening of Ca2+ channels in cell membrane → Ca2+ bind calmodulin, which then bind myosin light chain kinase, which phosphorylates regulatory light chain on myosin head, which then bind to actin site and cause contraction.

Q: What are the metabolic contributors to dilation by autoregulation?
A: Hypoxia (because don’t have enough oxygen for smooth muscle to contract), adenosine, K+ (released by contracting muscle, and dilates vessel because it hyperpolarizes the smooth muscle from contracting more), lactate, CO2, H+

Q: What are the metabolic contributors to constriction by autoregulation?
A: Oxygen (more oxygen for smooth muscles to constrict)

Q: What are the endothelial contributors to dilation by autoregulation of blood flow?
A: NO and Prostacyclin (PGI2), released by endothelium due to vessel wall stress.

Q: What are the endothelial contributors to constriction by autoregulation of blood flow?
A: endothelin (ET-1)

Q: How does atherosclerosis affect release of endothelial factors?
A: It damages the vascular endothelium, so less NO and PGI2 are made, causing vasoconstriction all the time.


Q: The lungs actually have two circulations. What are they?
A: Bronchial (from systemic circulation, arising from aorta) and Pulmonary (from pulmonary circulation).

Q: What is the primary role of bronchial circulation?
A: nutrient blood flow to airways (like bronchi)

Q: What is the only organ circulation that receives entire cardiac output?
A: pulmonary circulation. This is why inhaled agents can spread rapidly throughout body.

Q: Where does pulmonary circulation perfuse?
A: alveolar ducts and alveoli.

Q: What makes pulmonary circulation a low pressure system?
A: It’s not as thick as aorta and has relatively little muscle.

Q: What is significant about the pulmonary capillary beds?
A: They are the largest vascular bed in the body.

Q: There is so much less pressure in pulmonary circulation compared with systemic circulation. Yet, how does it still let the same amount of blood flow through?
A: very low vascular resistance as well.

Q: What are the three causes of the low pulmonary vascular resistance?
A: recruitment of pulmonary vessels (was closed but now open up), distension of perfused vessels, and active vasodilation.

Q: As cardiac output increases, what happens to pulmonary vascular resistance?
A: it decreases, to give way to the cardiac output.

Q: Unlike most organs and tissue, hypoxia in pulmonary circulation induces what?
A: vasoconstriction!!! So alveoli that do now have great oxygen source do not get the blood flow.

Q: What are some examples of regional hypoxia? Generalized hypoxias?
A: Regional Hypoxia = embolism (because block flow of O2’d blood). Generalized Hypoxias = asthma, emphysema, altitude.

Q: Is the blood flow and intravascular pressure more or less in the portions of the lungs above the heart?
A: less, because of gravity.

Q: In the mid-lung, blood flow is determined not by pulmonary artery minus pulmonary vein (like in lower-lung), but by what?
A: pulmonary artery minus alveolar pressure.

Q: Describe the pressure in the capillaries in the apex of the lung.
A: similar to alveolar pressure. Increasing or decreasing this would collapse the capillaries.

Q: Besides hydrostatic and oncotic pressures, what other forces determine the net driving pressure for fluid filtration systems in systemic capillaries in the pulmonary circulation?
A: surface tension and alveolar pressure.

Q: What direction of force does the surface tension produce in alveoli?
A: inward. Counteracts air pressure (favors absorption of liquids by capillary) and helps draw fluid out of pulmonary capillaries, enhancing filtration. The fluid then goes to lymphatics (but has to first go all the way to terminal bronchioles to get to these).

Q: How do you estimate Left Atrial Pressure (LAP)?
A: by measuring Pulmonary Capillary Wedge Pressure (PCWP).

Q: Why not just directly measure Left Atrial Pressure by sticking catheter into left atrium?
A: because you can’t reach this far in.

Q: How do you measure PCWP?
A: stick balloon catheter into peripheral vein, then stick it through right atrium, then right ventricle, then up the pulmonary artery until the “wedges” of the capillary.

Q: What can increasing pulmonary capillary hydrostatic pressure too much cause?
A: pulmonary edema.

Q: What causes nocturnal dyspnea?
A: lying down → reduced hydrostatic pressure in lower extremities → more venous return to thorax → higher pulmonary capillary hydrostatic pressure → more interstitial fluid filtrated out → interstitial fluid accumulates, interfering with gas exchange → shortness of breath


Q: Describe the artery-vein O2 difference in the heart muscles (notice I didn’t say the heart!)?
A: It is the highest of any major organ.

Q: According the Fick principle (O2 consumption = blood flow x (Artery-Vein O2 content), what does increasing O2 consumption by the coronary muscles do to blood flow?
A: As you work your heart more (making it need more O2), you increase blood flow.

Q: What happens to patients with atherosclerosis?
A: atherosclerotic lesions in coronary arteries limits blood flow, and therefore O2 supply can’t meet O2 demand. This causes myocardial ischemia, which leads to arrhythmias and decreased left ventricular contractility.

Q: What are the Three Major Determinants of Myocardial Oxygen Consumption (MVO2)?
A: Heart Rate, Contractility (Inotropy), and Ventricular Wall Tension

Q: What is the primary determinant of myocardial oxygen consumption (MVO2)?
A: Heart Rate, because ventricular myocytes have to work more.

Q: If you increase contractility, how does this affect the MVO2?
A: increasing contractility increases the magnitude of tension development and shortening velocity, all of which need more ATP and O2 consumption (to make more ATP).

Q: How does increasing heart rate, inotropy or aortic pressure compare to increasing stroke volume in terms of MVO2?
A: HR, inotropy and aortic pressure increases MVO2 far more (4-times more) than stroke volume would.

Q: When is blood flow to left ventricular myocytes highest (notice I did not say left ventricle)?
A: during Diastole, because during systole, the muscle is contracted and v
eins are compressed, preventing blood from flowing here.

Q: Please untangle this confusing concept: Why does sympathetic nerve dilate the coronary arteries rather than constrict them?
A: Actually, the sympathetic nerves cause transient vasoconstriction (via α-adrenerergic receptors), but by constricting, the hear muscles produce vasodilator metabolites, which cause the overall coronary arteries to dilate (via β-adrenergic activation)!!!

Q: How much does coronary blood flow increase from rest to maximal exercise (maximal O2 demand)?

Q: How much does muscle blood flow increase from rest to maximal exercise?
A: 22 times!!!

Q: How much does cerebral blood flow increase from rest to maximal exercise?
A: very very little.

Q: While the perfusion pressure of most vessels is simply the arteriolar – venous pressure, the cerebral vessels are different. What is is?
A: Intracranial pressure also influences blood flow (restricting it). It is Arteriolar – Intracranial pressure if intracranial pressure is higher than jugular venous pressure.

Q: What effect does autonomic nervous system (like sympathetic) have on brain blood flow?
A: very little effect!

Q: What controls cerebral blood flow (making not fluctuate that much)?
A: Autoregulation and intermediate levels of perfusion pressure. The brain is very sensitive to perfusion pressure. Too low causes fainting. Too high causes stroke.

Q: How does really high CO2 levels affect cerebral blood flow?
A: It causes cerebral blood flow to increase linearly with increase in mean arterial pressure. Otherwise, normally, an increase in mean arterial pressure would not increase blood flow. The arterioles actually respond to H+ caused by the CO2 rather than the CO2 itself. The increased blood flow helps wash away all the H+ in the blood.

Q: How does decrease in pO2 affect cerebral blood flow?
A: decrease below 30 mmHg causes vasodilation of cerebral arterioles, causing increased blood flow, bringing more O2 to brain.

Q: What can cause Intracranial pressure to increase?
A: Intracranial bleeding, cerebral edema, tumor

Q: What can an increased intracranial pressure do?
A: collapses vein, reduces blood flow, decreases cerebral perfusion pressure.

Q: What is the Cushing Reflex?
A: Vasoconstriction and extreme raise in blood pressure after acute head injury (terminal stage!). It is the response to get as much O2 to brain as possible.

Q: At rest, how much of cardiac output goes to skeletal muscle? Durint intense exercise?
A: 20% at rest. 90% during exercise!! So skeletal muscle is very important in controlling arterial pressure and blood flow.

Q: What is extravascular compressive force?
A: Force caused by muscle contractions that squeeze on vessels.

Q: Is blood flow higher during contraction or between contractions.
A: Between! Because when the muscle is contracted, it squeezes on the vessels (extravascular compressive force).


Q: What are the three shunts that fetuses have to bypass liver and pulmonary circulation?
A: ducturs venosus, ductus arteriosus, foramen ovale.

Q: How much blood does the fetal lungs need to grow?
A: Less than 15% of the cardiact output. Soon after birth, this becomes 100%!

Q: What does the ductus venosus shunt? What does it connect?
A: Shunt blood past the fetal liver. Connects umbilical vein with inferior vena cava.

Q: What percent of the oxygenated umbilical venous blood bypass the liver via the ductus venosus to go to growing brain?

Q: What does the Foramen Ovale shunt?
A: Connects right and left atria to shunt blood away from lungs. Closes at birth.

Q: What does the Ductus Arteriosus shunt? What does it connect?
A: It connects pulmonary artery to the aorta, bypassing the lungs. Blood has trouble going into lungs anyway because it has a high resistance due to fluid.

Q: Why does the fetal heart have a bigger right ventricular wall than left?
A: Because it has to work harder in pumping the blood not only through the foramen ovale but also the ductus arteriosus.

Q: What happens when the baby take its first breath?
A: air fill the lungs, replacing the fluid. This causes pulmonary arteriolar resistance to decrease, making it easier for blood to flow here. Increased flow from lungs into left atrium blows the foramen ovale shut like a door. O2 sensitive tissue of Ductus Arteriosus also close.

Q: What is persistent Patent ductus arteriosus?
A: when the ductus arteriosus remains long after birth, causing oxygenated blood to flow backwards from aorta to pulmonary artery. Babies get hypoxia.

Q: Where does the blood flow in ventricular septal defect?
A: From left to right ventricle, because pressure on left side is much greater. Right ventricle hypertrophies and pulmonary artery gets hypertension because extra blood flows to right ventricle from left side. RIGHT VENTRICULAR OUTPUT IS GREATER THAN LEFT VENETRICULAR OUTPUT (normally it should be same).


Q: What is shock?
A: Impaired tissue perfusion (so not enough blood or O2 getting to tissue). Hemorrhage is just one possible cause of shock.

Q: What is Hypovolemic Shock?
A: Shock due to dehydration

Q: What is Cardiogenic Shock?
A: shock due to injury to heart so it can’t pump blood as much

Q: What is vasogenic shock?
A: shock due to decreased arteriolar or venous vasomotor tone (extreme vasodilation)

Q: What are three types of vasogenic shock?
A: Septic Shock, Anaphylactic Shock, Neurogenic Shock.

Q: What is Septic Shock?
A: toxins cause too much vasodilation that blood can’t get anywhere

Q: What is Anaphylactic shock?
A: shock caused by too much vasodilation due to allergic reaction

Q: What is neurogenic shock?
A: nervous system fails to provide peripheral vascular resistance, causing shock.

Q: What are some causes of hypovolemic shock?
A: external or internal bleeding, chronic diarrhea, prolonged vomiting → decreased volume → decreased preload, afterload, and contractility.

Q: What happens to heart rate during hypovolemic shock?
A: Heart pumps faster to make up for decreased volume.

Q: If you donate blood, how does your body cope with it? What hormones increase?
A: Decreased blood volume → decreased stress on baroreceptors → increased sympathetic innervation → vessel constriction, increased heart rate and contractility.
Renin, ADH (Vasopressin) also increases, keeping the liquids in.

Q: What happens to blood volume in the heart during cardiogenic shock? How cause pulmonary edema?
A: less blood pumping → left ventricle accumulates more and more blood that can’t be pumped → elevated pressure in left ventricle and atrium and eventually pulmonary vessels → pulmonary edema and therefore impaired O2 diffusion into blood.

Q: What are the Three Stages of Shock?
A: Compensated shock (earliest stage), Progressive shock, Irreversible shock (death is inevitable).

Q: How does a toxin cause septic shock?
A: the toxin causes inducible NO Synthetase formation (different from normal NO synthetase) → too much NO formation → too much vasodilation and HIGH CARDIAC OUTPUT → “blood poisoning”

Q: What are some causes of septic shock?
A: severe infection (like from ruptured appendicitis).

Q: What is the equation for Vascular Conductance?
A: 1/Resistance

Q: How does anaphylactic shock happen?
A: bee venom → histamine released → massive vasodilation

Q: What is unique about cardiac output in vasogenic shock?
A: Since you get dilation, initially cardiac output increases, leading to “warm shock.” Then later, cardiac output would decrease like any other shock.

Q: What causes neurogenic shock?
A: loss of backgro
und sympathetic stimulation (that normally maintain vascular tone) → sudden extreme dilation


Q: What is isometric and isotonic exercises?
A: isometric is static and isotonic is dynamic

Q: What happens to diastolic and systolic pressures during exercise?
A: Systolic pressure increases, but diastolic pressure stays more or less the same.

Q: How do you measure myocardial oxygen demand non-invasively?
A: via rate-pressure product, or if you’re lazy, just the patient’s pulse rate is close enough.

Q: Is the proportional O2 demand of the heart larger for static or dynamic exercise?
A: Static exercise.

Q: What is Central Motor Command?
A: the Central Motor Command is the center in your brain that activates Brainstem Cardiovascular Center, which activate heart, vessels, and muscle during exercise.

Q: What happens to the arterial baroreflex during exercise?
A: It is “reset” by increased Central Command as well as input from muscle to increase its ability to prevent blood pressure from becoming too high. This is called “Baroreflex Resetting”

Q: How does endurance training affect your cardiovascular system?
A: slower heart rate, increase max cardiac output, increased max oxygen consumption, increased mitochondrial volume in trained muscles, improved fatty acid oxidation, sparing of muscle glycogen, decreased rate of muscle fatigue.

Q: How does resistance training affect your cardiovascular system?
A: Increases left ventricular muscle mass, reduced heart rate and pressure.

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