Block 2

NOTE: there are some places in your body where you dont want to have an extrinsic factor overide internal factors. Where?

Brain, heart, and kidney . If they need O2, they will get O2 (powerful local regultion mechanims so hard to overide)

What things effect Stroke Volume? (what influences ESV and what influences EDV)

ESV influenced by : -SNS (NO PNS), so hormones such as epinephrin will increase contractility of the heart -Peripheral resistance ("afterload") increases ESV EDV influenced by: -Filling Time -Filling Pressure Gradient which is affected by the venous pressure ( "preload")

Compare the speeds of fermentation vs aerobic respiration

Fermentation happens much quicker (but less energy)

Is the capilallary flow through systematic circulation usually in parrallel or series? What are some exceptions. Is the flow rate the same everywhere in series in circulation? Is the flow rate the same everywhere is a series breaks off into parralell branches

MOSTLY parrallel - few exceptions-->some go through capillary beds in series (hypophseal portal system) same in series, dif in parrallel

What does it mean for muscle to be important for movement within the external enviornment and manipulation of the external environment

Muscle is needed to walk (somatic) and also do finer things like writing cursive in which you are manipulating the external enviornment

Factors influencing the contraction activity of smooth muscle. (5)

-spontaeous electrical activity (think arteriole myogenic activity) -neuroransmittoes (norepi and Ach) -hormones -local factors (example histamine and NO are vasodilactoras of vasculature -stretch (bladder) --> myogenic activity

Percent total volume in circulatory system: -systemic arteries/arterioles -systemic capillaries -systemic veins/venoules -heart -pulmonary circulation How does donating blood effect your blood pressure. Why do you want to have most of volume in the veins?

-systemic arteries/arterioles - 13% -systemic capillaries - 9% -systemic veins/venoules - 64% !!!! 2/3 -heart - 9% -pulmonary circulation - 9% You want pool of blood in venous system b/c the best way to increase cardiac output is to increase venous return to heart which increases EDV and therefore contractility. If you donate blood, this doesn't cause a huge impact on your blood pressure because the thin and elastic wall of vein (where blood comes from) . As you take volume out, the veins will collapse around the volume that is left in there and maintain pressure to avoid big drop in pressure.

Single unit vs Multi unit smooth muscle (and list examples of each)

.Single unit --> all the cells are linked via gap junctions, and are therefore directly electrically coupled; thus, when one cell contracts, they all contract. - Examples of this are intestine and uterus/ bladder (no leak) Multi unit --> each cell can function independently (though are regulated in a manner that they all work together so they tend to function as one unit anyway). - allows for more fine-tune control of contraction -cilirary muscle of eye (fine tuned control) -there is not a huge functional dif b.w multi and single unit because these units are usually innervated by a single axon with many branches

Cross Bridge cycle stops if there is no: -how does this muscle go from contracting (cross bridge cycing) to rest in presence of ATP? How fast does this process occur relative to the duration of an AP.

ATP or Ca -active transport of Ca back into sarcoplasmic retic ----> (~100 msec), whereas the action potential lasts only about 2 msec.

actin vs mysosin under microscope

Actin = light Myosin = dark

A beta-blocker is an antagonist to beta1-adrenergic receptors. What will this drug do to the heart rate? Why is that response helpful following a heart attack?

Activation of beta-1 adrenergic receptors increases heart rate, therefore a beta blocker decreases heart rate and lowers oxygen demand. Cells that need less oxygen are less likely to die if their blood supply is diminished.

How does the pressure in the pulmonary artery compare to the size of the aorta. How does the size of the left and right heart compare.

Aortic pressure is much higher because it needs to pump harder to get blood through systemic circulation which is why the left heart is much larger than the right hard (must contract harder) HOWEVER the flow rate is the same. FLOW IS CONSTANT because the system is closed in series.

Apex vs Base of heart. Where is the heart located in the body

Apex: bottom Base: top located in ventral part of thoracic cavity sandwiched b/w lungs and behind the sternum

orthostatic response. Also how does the body use feed forward control to control blood pressure during the orthostatic response.

Arterial pressure stays constant, even with gravity causing blood to pool in the lower part of the body. This is just the name of the barorecptor reponse that functinons to increase BP upon standing) You know you are about to stand up, so before you stand up, you will engage SNS to engage baroreceptor reflex(feedforward)

Where are actin filaments bound to in skeletal muscle exactly? What protein is used for this? Where are all of the myosin fibers joined to in a sarcomere?

actin bound to the Z disk and is held onto the disk with the CapZ protein. all of the myosin fibers joined to in a sarcomere at the M line with accessory proteins

What is the largest contributor to total peripheal resistance

arterioles

definition of artery vs vein

artey --> away from heart veins --> towards heart

What happens to the pressure across resistnace

as resistance varies, pressure gradients vary; stated another way, there is a pressure drop across a resistance.

What does the plasma have that the interstitial fluid does not have?

Proteins!!! Proteins are too large to escape endothelial line of blood vessels. Contributes to tonicity and osmolarity of different compartments. - makes plasma hypertonic relative to the interstitial fluid to create the osmotic pressure needed so the interstitial fluid can flow into the vasculature

If the ventricle of the heart is damaged, in which wave or waves of the electrocardiogram would you expect to see abnormal changes?

QRS and T wave

The single MAJOR determinant influencing resistance to blood flow is

Radius of vessel

antidiuresis

Retaining water in the body

What things effect heart rate (3)

SNS, PNS, and certain hormones such as epinephrin (SNS)

Does the systemic or pulmonary circuit have higher pressure? -why do you need two dif pumps in the circulatory system ? Why are they anatomically located close together?

Systemic b/c it must travel farther in tissues. It has a stronger pump due to longer circulatory system . Note: blood will always flow from higher to lower pressure -by the time the blood travels through the systemic circulation and back to heart, the pressure is little so needs another pump to give it a boost through the pulmonary circulation. IF you just had one large pump, the pressure would be so high at the capillaries would explode They are closer together because the contractions need to be coordinated to prevent the backflow of blood

How do you test for muscle damage in various types of muscle?

Test for creatine kinase levels for the different isozymes vis blood test, and if levels are high, there is likely muscle damage(cardiac isozyme is dif than skeletal istotype)

autonomic regulation of the arterioles

The Adrenal Medulla secretes epinephrine into the blood which can activate beta receptors (vasodilation) to increase blood flow to heart, liver and skeletal muscle. NE acts on alpha 1 receptors which causes vasoconstriction

Why don't you want too many RBC ? (why dont you want too much hematocrit!)

because this will make the blood very viscous which will increase total peripheal resistance and thus mean arterial pressure

What happens to the pressure before and after a point in an arteriole that is undergoing constriction. What conditions does this result hold

before point of constriction -pressure increases after point of constriction -pressure decreases *these conditions are given that the flow rate is constant in the arteriole

How is cardiac muscle innervated?-

by the autonomic nervous system -not innervated by motor efferent neurons Also controlled by autorhymic pacepaker cells .

What is mean arterial pressure equal to

cardiac output ∙ total peripheral resistance. [MAP = CO ∙ TPR]

Atherosclerosis and how does this effect the bodies cardiovascular system -Treatment

condition in which fatty deposits called plaque build up on the inner walls of the arteries - due to poor diet (cholesterol fatty deposits in blood vessel walls which can rupture and cause blood clots) * decrease diameter which increases resistance and thus increases pressure Treatment = STENT

Adenosine is released by

hypoxic cells

functions of blood.

important in buffering the body against changes in pH, temperature, and osmolarity. It also plays an important role in the body's surveillance and defense systems and in clotting to prevent excess blood loss.

4 ways to increase cardiac output and two ways to increase TPR

increase CO: - Higher contractility of heart - Greater stroke volume -. Higher venous return -Higher plasma volume Increase TPR: Sympathetic activity to the arteries Arteriolar vasoconstriction

Increasing sympathetic nerve activity would rapidly increase arterial blood pressure by which of the following mechanisms?

increasing cardiac output

What separates the ventricles?

interventricular septum

What effect would a beta-adrenergic receptor antagonist have on baroreceptor reflex responses? ( in response to a decrease in arterial blood pressure)

it would blunt the reflexive increase in heart rate in response to a decrease in arterial blood pressure

lub dub (and which one is louder)

lub (quiter) 1st: AV valves close Dub (louder) 2nd: semilunar valve close.

What is another name for blood pressure

mean arterial pressure

ejection fraction formula and meaning (what is this a good test for.... what does this have a direct relationship with? )

measurement of the volume percentage of left ventricular contents ejected with each contraction. Has a direct relationship with cardiac contractvity = SV/EDV = (EDV - ESV)/ EDV GOOD TEST TO ASSES CARDIAC MUSCLE DAMAGE

metarterioles (thoroughfare channels)

not totally surrounded by smooth muscle (like arterioles are) --> the large diameter allows white blood cells that are too big to fit in normal capillaries (bypass beds) to bypass the capillaries and shunt them from arterioles to venoules - -> have precapillary sphincters that occur at the beginning of the normal capillary beds which can be constricted to cut off the amount of circulation going to certain areas (but meta-arterioles will stay open ) - this vascular shunt (when precapillary sphincters are closed) plays a role in which capillaries get perfused via the opening and closing of precapillary sphincters.

cardiovascular disease (list different types)

number one contributor to death series of diseases or disorders involving heart and blood vessels -coronary artery disease -heart attack -brain attack

Although the heart typically spends more than half the cardiac cycle in diastole, flow through capillaries does not show large pulsations because

of the elastic properties of arteries

Blood flow through capillaries is constant rather than pulsatile mostly because...

of the resistance of the arterioles

energy demands for smooth muscle and the development of tension (speed of contraction 0 compared to skeletal muscle (explain whhy)

once contracted, smooth muscle can stay contracted without much additional energy being required . (unlike skeletal muscle which needs constant source of ATP) - this may be due to latch mechanism where myosin and acttin could contract and then latch together without requiring energy. (not known yet) -Smooth muscle contraction is extremely slow and requires a lot more time to reach max tension due to extremely slow myosin ATPase activity

Can you block renin production with a drug to decrease blood pressure?

prolly, but not made yey

Where does blood enter the heart?

superior and inferior vena cavae --> right atrium

what is the functional part of the cardiovascular system.

the capillaries where exchange happens (the other parts are just getting the blood to this point)

Which organ consumers the most percentage of oxygen in the blood?

the heart - consumes 75-80 percent which is more than twice that of any other part of body. -so the heart needs a lot of O2 and blood flow through it BUT the heart does not get o2 /nutrients from blood flowing through it

How does the velocity of blood change with total cross-sectional area?

the larger the cross-sectional area of the total of all vessels at that level of the circulation, the slower the velocity.

Amount of force you can generate from a sarcomere depends on ?

the length of the sarcomere at the time it starts contracting

How to the stroke volume and cardiac outputs compare in the left and right side of heartwhat is the flow like in the pulmonary circulation

the stroke volume and cardiac output on the right side are equal to those parameters from the left side of the heart; they need to be or blood would pool on one side or the other. The pulmonary circulation would be characterized as a low resistance, low pressure, and high flow rate circulation.

If your blood volume is decreased, what happens to your thirst levels

they increase

Which part of the heart is very muscular? Why is it muscular

ventricle, becuase its gotta pump (atrial is weaker because it just aids in the filing of the ventricel)

cardiac output (and what is normal value at rest) -What are the two equations (main and derived)

volume of blood pumped per minute (Note this is your Flow Rate!) - 5L / min at rest but can change more than fivefold during exercise. - VERY PHSIOLOGICALLY RELEVANT because it is a great indicator of HOW QUICKLY blood is getting to the tissues. (Heart RATE (how quick)) CO = heart rate (bpm) x stroke volume (Liters/Beat) CO = heart rate (bpm) x (EDV-ESV) (liters/beat) - note all of the factors above are regulated Normal CO value = 72 bpm * .007 L/min = 5L/min

Is fainting a good way to maintain blood presure!

yes

How much of the body mass is muscle? Of the muscle, how much percent is skeletal muscle

50 % 80 percent skeleetal

average arterial pressure

93 mm Hg

Are there valves that prevent the backflow of blood from the atria into the venae cavae.

No so there is a little bit of backflow.

Each myosin filament is surrounded by how many actin filaments?

Six -note the myosin filament is a thick fiber that has golf clubs coming out of it (heads)

how do you calculate the amount of flow to any organ

So flow to any organ = mean arterial pressure/resistance of that organ. As R changes, flow to that organ changes. note --> mean arterial pressure = diastolic pressure + 1/3 (systolic pressure - dystolic pressure) ,where the pulse pressure is equal to systolic pressure - dystolic pressure

What is the difference between serum and plasma?

"simply the liquid that remains after the blood has clotted which occurs before centrifuging it" Serum is plasma WITH the clotting factors such as fibrinogen.

- what contributes to autorhymic activity - what is the pacemaker potential -what is the voltage threshold for the voltage-gated Ca channels

- Pacemaker potential --> even at rest, the membrane tends to DEPOLARIZE (due primarily to Na+ coming into cell and Ca+ entering cell through leak channels) at a STEADY RATE until cell hits -40 mV ( this steady state is called the funny current ) --> at 40mV, triggers voltage gated Ca channels to open which causes a RAPID influx) the Voltage threshold for voltage gates Ca channels are -40mV..... after Ca gets near its equilibrium potential , rate of influx will slow down and inactivate, then the voltage gated K+ channels open and K + goes out to repolarize cell

resting potential of a cardiac ventricular myocyte vs skeletal muscle - what are their associated stimuli - how do their depolarizing phases differ

-90 mV for BOTH - skeletal from motor neuron imput - cardiac from spreading of AP from neighoring cells -their depolarizing phases differ in respect that Na influx is skelelal and ca influx is cardiac ventricucalur mycoyte

what is Bulk Flow, and which type of endothelial cell is it associated with? what are the pressure gradients that provide for bulk flow? What two things influence the pressure gradient of any given capillary bed? Is this associated with hydrostatic pressure or osmotic pressure. When does osmotic pressure play a significant effect? How do the relative forces change over distance of capillary? How does the relative balance of fluid leaving capillary compare with the fluid entering the capillary.

-Bulk Flow--> IONS , small solutes such as WATER, and small organic compounds from plasma can leave the fenestrations in capillaries passively via a pressure gradient generated from arterioles (hydrostatic pressure). The movement of all these things going thorugh the gaps and fentrated holes move out = bulk flow (due to hydrostatic pressure in cappilary) the pressure of blood flowing into the capillaries from arterioles is approximately 35 (32-37) mm Hg at the very beginning of the capillary --> note that at all points in the capillary the osmotic pressure of the blood colloid (force of pulling fluid back into capillary) is 25 mmHg. - At the beginning of the arterial side of the capillary, there is NET FILTRATION (+10 mm Hg) from the capillary to the Interstitial fluid. This works because the HYDROSTATIC PRESSURE OF THE INTERSTITIAL FLUID IS INITIALLY ZERO. The capillary hydrostatic pressure pushing fluid from inside the capillary to the interstitial fluid (35mm Hg) is higher than the osmotic pressure. This pressure gradient between intra-capillary fluid and interstitial fluid diminishes along the length of a capillary due to the pressure drop across resistance( at the venous end of the capillary, the hydrostatic pressure of the fluid in the capillary is only ~17 mm Hg). When the capillary hydrostatic pressure becomes less than the blood colloid osmotic pressure --> causes the net REABSORPTION (-8 mm Hg) ------- Significance? throughout the body there is a net loss of approximately 3L/day from the capillaries to the interstitial fluid (a huge problem because the fluid can just leaves the capillary and stay out there --> edema) HOWEVER, The 3 L/day of fluid lost from the capillaries to interstitial fluid, enters the lymphatic vessels and eventually returns to the bloodstream.

Muscle Fiber Recruitment (2 principles)

-If there are more muscle fibers you will get an increased muscle force. -Slower muscles get recruited before faster muscles! When all three are being contracted, you can get maximum force/tension (within the same muscle you will recruit dif motor units at dif times)

smooth muscle ( do they have t-tubules ,SR, or troponin) -where does Ca source come from and how does it enter(3) --and how does it contract (mechanistically... what enzymess are involved) - relative speed of contraction vs skeletal and cardiac muscle!!!! What is the underlying reason for this. (what is analogous to the Z lines?)

-Involuntary and not striated; no T-Tube System but they do have SR --use cross bridge cycling like skeletal muscle,. The Ca++ initiating contraction comes from extracellular fluid, with Ca++ entering the cell through voltage-gated Ca channels, ligand gated Ca++ channels and/or mechanosensitive Ca++ channels. - The Ca++ binds to different proteins to initiate contraction - does not have troponin -Instead calcium entering the cytosol binds to calmodulin. The calcium/calmodulin complex binds to myosin light chain kinase (MLCK) also called myosin kinase), causing its activation. Activated MLCK phosphorylates myosin (covalently adds phosphate group)and then the phosphorylated myosin binds to actin. ***Smooth muscle myosin is not an active ATPase, and thus cannot drive the cross bridge cycle, unless it is phosphorylated (regulated enzyme -Myosin Phosphatase (MLCP)--> de-phosphorylates myosin which causes Ca to be actively pumped out of cytosol into Interstitial fluid via primary active Na/Ca exchanger which is a antiport --> and this creates a gradient for secondary active transport which is facilitated diffusion of Ca out of cell --> relaxation ^ so if there are higher levels of MLCP acticity, then myosin will be densisisitized, so more Ca will be needed to make myosin phosphorylate - contains filament bundles made of actin and myosin. These bundles are anchored to structural proteins making up the dense bodies (analogous to the Z lines of striated muscle) --> As smooth muscle contracts, the dense bodies are pulled toward each other, causing the cell to blob.-uninuclear Cross bridges cycle at a much slower rate in smooth muscle due to VERY SLOW ATPase activity so the veolocity of shortening is very slow. (note: the contraction is highly variable and graded) *tapered ends

Three types of muscle contractions: (describe the exact mechanisms) -Isotonic -isometric -lengthening What would a benchpress be and what would a plank be

-Isotonic --> the muscle is able to move the load and the muscle gets shorter as it contracts (pick up the backpack and bring it to shoulders) - elastic elements stretch, and the sarcomeres contract a significant amount which causes an overall shorten in the muscle. - benchpress -isometric --> the muscle forces balance out the weight, so the muscle does not move the load but it still contracts! (trying to pick up 300 pound backpack and cannot move) - the elastic elements at the end of the muscle stretch first, and this makes up for the small amount of contraction that is occurring in the sarcomers which shortens a little. Net change = no length change - plank -lengthening --> contraction occurs but the contraction cannot overcome the force of the weight (weight wins). This is also called a failed contraction (someone hands you a 300 lb backpack)

Plasma Composition -why is it a certain color -what mostly makes it up -what percent protein is in the plasma -how is the ion composition compared to that in the interstitial fluid

-It is pale yellow due to Bilirubun (byproduct of Hb) - mostly made of water -7 percent protein! (7 grams protein/100 mL) (albumin which is released by the liver) (over half), globulin, and fibrinogen) - the ion concentrations of the intersitial fluid and that of the plasma are pretty much the same!!!) hormones; although hormones are in a very small concentration compared to everything else! Also present are gases, nutrients, waste, glucose

The lymphatic system (4 roles) -organization (include aspects the lymph capillaries -lymph nodes -lymph's composition -what kind of transport moves fluid into lymphatic vessels? - what ensures unidirectional flow?

-Returning fluid to the cardiovascular system (recirculates constatly a net 3L fluid every day to prevent edema to recycle waste products and wash debree away) -Clearing proteins from interstitial fluid because it is importatn to maintain osmotic pressure (you need high protein concentration in capillary) -Role in the absorption of fat in the intestines -Role in the immune system == - the lymph vessels ( not part of blood vessels or circulatory pathway ) - have open ends to them where Interstitial fluid flows into PASSIVELY due to MOVEMENT ( NOT A PRSSURE GRADIENT) ... when you move your body, it pushes on tissue --> physically moves fluid into lymphatic vessels and becomes LYMPH (similar composition of interstitial fluid) - When you relax, the valves ensure there is no backflow of lymph into the interstitial fluid. (one-way flow ) - These small lymphatic vessels then merge to form larger lymphatic vessels. These larger lymphatic vessels empty into the vena cava --> circ system -The lymph vessels can come together to form nodes. - immune cells sit in here to coordinate the immune response, because it is a good area (epicenter )to sense the degree pathogens and debree in the filtrate

why does cross bridges cycle at a much slower rate in smooth muscle (2)

-Smooth muscle myosin is a much slower ATPase (in its activated state) than even the slow isoform of myosin in skeletal muscle, and therefore the cross-bridge cycle is much slower (e.g., 100-fold less) than in skeletal muscle. -Smooth muscle also has a mechanism by which the rate of cross bridge cycling is made even slower, allowing the muscle to maintain contraction with little expenditure of energy for long period of time; this is often referred to as the latch mechanism. the relationship between velocity of muscle contraction and load is very variable, depending upon, for example, the extent of phosphorylation of myosin and the extent of phosphorylation of calMODULIN (graded potentials)

skeletal muscle - and what cells make skeletal muscle - how many nuclei

-Striated apperance due to actin and myosin coloration -voluntary -large multinucleated cells Myoblasts make skeletal muscle

3 main stimuli for renin secretion: (and what is most important and sensitive one) (what receptors does this most important mechanism use

-decreased arterial pressure as sensed by the aortic and carotid baroreceptors and relayed to the kidney by sympathetic nerves (acting on beta1-adrenergic receptors on the renin-secreting cells) - MOST SENSITIVE AND IMPORTANT! - decreased renal perfusion pressure as sensed directly by stretch of the renin-secreting cells, - an index of renal function (Na+ delivery in the kidney tubule system) that we will discuss when we talk about the kidneys. The most sensitive and important of these stimuli is the arterial baroreceptor reflex.

goals of circulatory system (3) Also... Why do you want to have circulatory system enclosed? What does it mean specifically for the circulatory system to be a closed system.

-maintain adequate O2 delivery and nutrients and removal of wastes from all tissues in the body -monitor tissue integrity (immune system) -avenue for signaling (endocrine system) * Note, this is the center for pretty much all of the systems ====== Because it is easier to regulate something that is contained within a closed system Closed system = meaning that blood and interstitial fluid are kept separate

Three functions of ATP in cross bridge cycle (and one other function

-provides the energy to drive the power stroke. Energy from ATP hydrolysis puts myosin in the cocked position which can generate force -causes the dissociation of the actin and myosin - Hydrolysis of ATP by Ca+2 ATPase provides energy for active transport of Ca into the SR which will end the contraction once all of the Ca is out of the sarcoplasm. ATP is also used to maintain the restin membrane potential of neuron which is critical if AP wants to reach muscle.

cardiac muscle (and how many nuclei, fused or unfused) - do they have a t-tubule system -how does their size compare to smooth and skeletal muscle -where is the Calcium source(s)?

-striated (sarcomeres arranged in length -involuntary, unfused -uninuclear - cardiac muscle cells are electrically coupled by gap junctions and mechanically coupled at sites called intercalated disks. (like unitary smooth muscle cell) HIGHLY BRACNHED -binds to troponin for cross-bridge cycling like skeletal(Ca++ is mostly from the sarcoplasmic reticulum.) -cardiac muscle has a T-tubule system They are smaller than skeletal muscle but bigger than smooth muscle

RBC development? What percent of stem cells are prolilferating into RBC. (reticulocyte vs erythrocyte)

1. hematopoietic stem cells that are uncommitted serve as the source of development of many different kinds of cells including rbc and many type of WBC (leucokyctes) -in bone marrow called erythroblasts stimulated by EPO (note different cells such as neutreophils have different signaling factors) 2. reticulocyte - immature RBC (nuclues) 3. erythrocyte - mature RBC( no nucleus --> organells wil shrink up , no nucleus Only 25 % of hematopoieticstem cells proliferating into rbc - Due to long half life in blood --> 4 months

phases of cardiac cycle (5) -Start at late diastole (mention valves, pressure differences, and unique features)

1. ventricular filling (diastole) - both sets of atria and ventricles are relaxed chambers are relaxed (all muscles in the heart relaxed) and ventricles are filled passively - contributes 80 percent of ventricular volume filling and this is done all passively because venous pressure is higher than atrial pressure and atrial pressure is a little higher than the ventricle so AV valves open up to fill ventricles. *Atrial and Ventricular Pressure are very low and MUCH LOWER than pressure of aaorta) 2 Atrial Contraction (Atrial systole begins) - atrial contraction forces the final 20 percent of ventricular volume. - This increases the atrial pressure, but the ventricular pressure does not increase by much (still increases though) 3. Isovolumetric contraction - contraction of the ventricle will increase the pressure of ventricle drastically above atrial pressure which shuts the AV valve, but not enough to overcome pressure in aaorta so the volume is not changing. 4 ventricular ejection (ventricular systeole second phase) - occurs as ventricular pressure rises above the pressure in arteries which causes the blood to push against the SL valve to open it and eject the blood from the ventricle 5 .isovolumetric ventricular relaxation - After the blood is ejected, the pressure in the ventricles will become lower than the pressure in the arteries - However, the pressure in the atria is lower than in the ventricle, so the blood hits the SL valve to snap them shut (causes sound 2) - ALL OF THE VALVES ARE CLOSED, so there is no blood filling up the ventricles so the volume of the ventricle does not change.

ventricular muscle arrangement (organization)

1.) Has a spiral arrangement all the way down to the apex which allows ventricular contraction to squeeze blood out of the heart from the bottom up 2.) intercalated disks contain: -desmosomes that transfer force from cell (cardiac muscle is branched and connected to cardiac contractile cells connected end-to-end through these intercalated disks (physically links cells together so heart doesn't rip apart and that the force that gets generate on one cell is transferred to the next one.) -gap junctions that allow electrical signals to pass RAPIDLY from cell to cell. - unlike voltage gated channels, these are open all the time which contributes to rapid transduction (so fast that is feels like a single unit of contraction in the heart.)

Cross bridge contraction cycle (assume presence of Ca) Start in the rigor state. -also what state is the muscle in when it is not being contracted (at rest)

1.) In rigor state, myosin is bound to actin and myosins hinge region is at 45 degrees 2.) ATP binds to mysosin binding site. Myosin deattached from actin 3.)ATPase activity of myosin hydrolyzes the ATP; ADP and Pi remain bound to myosin. -This is the sarcomeres resting (noncontracted state) 4) This produces energy which causes a confomratinal change in myosin --> hinge region binds to actin at a 90 degree angle (high energy conformation!!!!!) - popped state- 5.)Release of Pi iniitiates power stroke in which myosin pushes actin filament to the M line 6.) At end of power stroke, myosin head releases ADP which puts sarcomere back into rigor state

Three energy sources of ATP for muscle contraction (how long is each good for): - ready pool of ATP -creatine phosphate (which enzyme regulates this, and how does it act during relaxation and contraction) - metabolic pathways (when energy from the above stores are out, which energy source gets utilized first)

1.) There is a ready pool of ATP (free or floating) which is only enough for around 8 contractions which is not a lot so you need backup energy sources 2.) Creatine Phosphate: - during rest, high energy phosphate bonds are created between creatine and ATP and are stored so when you are active, the high energy phosphate group of creatine phosphate is quickly transferred to ADP to create ATP. This supply of energy is only good for 15 seconds. The enzyme that regulates this cycle is called Creatine Kinase and it drives both arms of the reactions: - When at rest --> drive toward storing ATP -when contracting --> drives production of ATP 3.) Energy is produced by metabolic pathways (glucose and glvcogen) which is the body's main source of energy (ATP) via aerobic respiration or fermentation depending on whether O2 is present or not. -Note immediately after ATP is depleted from phosphocreatine source, most ATP is derived from glycogen stores --> then sugar from the blood is utilized (there is a hierarchy)

Questions to ask when analyzing ECG tracings for abnormality (4) - what is wrong with ECG : - in atrial fibrillation - in third degree heart block - in ventricular fibulation

1.) What is the heart rate (is it within normal range of 60-100 bpm?) 2.) Is the rhythm regular ( if not arrhythmia) --> in atrial fibrillation, there is an inconsistent beat and no P wave which causes arrhythmia -cause: SA node deficit! 3.) are all waves present in their recognizable form --> in ventricular fibrillation --> no identifiable waves prest --> big problem with either the generation or conduction. -ventricles no longer contract together 4.) Is there one QRS complex for every P wave? -If yes, is the PR segment constant in length? - if no, count the heart rate using the P waves, then count it according to the R waves. Are the rates the same? Which wave would agree with the pulse felt at the wrist. - Third-degree heart block --> not always a QRS complex for every P wave. According to the R waves, they are relatively spaced out (slower heart rate) with and it is rhythmic! - cause: A heart block somewhere between the SA node and the AV node because the p wave is present (ventricles are not in synch w atria) Note: p wave caused by SA node, so if the p wave is present, than their should not be any problems with the SA node.

Layers of the heart wall (from the inside of heart facing blood to the outside.

1.) endocardium - thin layers of endothelial cells in contact with blood 2.) myocardium - thick layer(muscular part that contracts) 3.) visceral pericardium (thick membranous sack) 4.) parietal cavity -filled with pericardial fluid which lubricates heart (by reducing friction) for CONSTANT movement - however friction can occur if you have pericarditis 5.) parietal pericardium (thick membranous sack)

What four things impact sustained muscle contraction at any given moment?

1.) how many AP have come in and how close together they are 2.) How fatigues it is (has it recently done a sustained contraction) 3.) Length of fiber/sarcomeres at onset 4.) Types of muscle fibers present and how thick they are.

Would increasing filling time have any effect on filling? Would markedly decreasing filling time reduce filling.

1.) no 2.) yes, it may

What questions do you ask yourself when thinking about what causes the shape of an AP? (5)

1.) what channels are present 2.)the kinetics of the channels 3.) when do they turn on 4.) how long are they open 5.) do they inactivate

Conduction pathway of cardiac muscle (internodal vs interatrial pathway and what are the relative speeds) - where are the nodes located in the heart. - why is there a delay in the the AV node?

1.)AP originates in the SA node in the right atrium 2.) --> signal travels through an internodal pathway to the AV node (happens very quickly) 3.) AP spreads more slowly across the atria (intraatrial pathway. Note: we need the atria to contract, and then the ventricles to contract in tandem, from the bottom up! The purpose of the AV node delay is to ensure that the conduction through the heart slows down enough so the atria have enough time to fully contract before the ventricles are stimulated to contract. 4.) From a group of cells, the AV node, in the base of the right atrium, the action potential is conducted along the Bundle of His along the interventricular septum between the right and left ventricles -Note: This signal needs to get to the AV node in order to get AP to ventricles. 5.) After the signal travels slowly through the AV node, the signal will move rapidly down the interventricular septum to the apex of the heart so the electrical activity is already at the bottom and ready to start contracting from the bottom up - Because impulses are conducted slowly through the AV node, there is a short pause between the time when the atria depolarize and when the ventricles depolarize. This pause facilitates maximal filling of the ventricles. 6.) and then into the Purkinje fibers along the base of the ventricles. - from here, the Purkinje fibers spread through the ventricular myocytes that are connected through gap junctions.

List three physiological effects of the baroreceptor reflex should be having on the heart and blood vessels. (in response to increased bp) Describe the mechanism of action by which these effects are achieved.

1.)Vasodilation --> Decreased sympathetic output: decreased NE released on alpha1 Adrenergic Receptors, decreasing TPR. 2.) decreased heart rate --> Decreased sympathetic via B1 Adrenergic Receptors, and increased parasympathetic output via muscarinic ACh receptors --> decreases CO. 3.) Decreases heart contractility --> Decreased sympathetic output to cardiac muscle via B1 ARs. Decreases CO.

How many times will SA node cells in isolation depolarize per minute? If this is higher than the average heart rate, then what may be the reason for this?

100 action potentials per minute. Because SA node cells are interconnected by gap junctions, when one generates an action potential they all generate an action potential and thus the SA node action potential frequency is dictated by the fastest SA node cell. [Think about what would happen to an SA node cell that had a slower If.] The reason your heart rate is 70-75 bpm is because you have more PNS activity in your heart at rest than SNS activity which brings 100 cycles AP / min to 70-75ish cycles per minute.

Hypertension (mm Hg) mean arterial pressure level. what happens to your chances of heart disease if it goes passed this.

140/90. It willl increase exponentially -

total blood volume - and what is the composition of the blood at any given time: -hematocrit ( in percent) -Hb (in g/mL) -rbc count (count per mL) if you were to centrifuge it: - what percent would be (and what would the densities): - plasma - wbc/platelets - rbc ----- Also at what place in the circulatory system does the most amount of volume get added or subtrcted.

5.5L -Composition of the blood: - hematocrit (which also means packed red blood cell volume) --> 45% - rbc count --> 5-6 million cells per microliter! - There are roughly 10 trillion RBC in blood in adults and these break down and are replenished at the rate of approx 1%/day (i.e., ~100 billion/day); an RBC "lives" for about 100 days. Thus, RBCs need to be replaced at a rate similar to this loss in order to have a constant level of RBCs. - Hb --> 15 g / 100 mL ===== - plasma (55-58%) --> less dense - wbc/platelets (1%) --> called the buffey coat. Very thin later . 5-6 THOUSAND ORDERS of magnitude smaller of wbc than rbc in circulation at any given time. - rbc (42-45%) --> heaviest == If volume is added or subtracted, it largely occurs in systemic venous circulation

CO at rest vs exercise. During exercise, which organ recieves the most amount of blood flow? Which organs dont change amount of blood flow at rest vs during exercise.

5L/min to 25 L/min which is crazy. The skeletal muscle and lungs (receives all flow)recieves the most amount of blood flow during exercise. The brain and the kidney dont change amount of blood flow at rest vs during exercise. (but they have lower amount of percent volume total)

average heart rate of healthy 70kg adult

70-75 bpm

lenth-tension relationship - what is the optimal length of a sarcomere needed for maximum contraction? -If the length tension decreases (less overlap), how does the rate of tension decrease compare to that if it was to increase the length tension relationship.

80-120 percent of resting length of sarcomere. There is a range of maximal tension you can generate from a muscle which is due to the overlap of actin and myosin. However too much overlap or not enough overlap: Max tension in muscle = some overlap via cross-bridge cycling --> tension and grip for pulling and contracting . This occurs during sarcomere relaxation For example, if you were going to lift a heavy object, you would not start with your arms either fully extended or fully contracted If too much overlap, there is too much steric hindrance which blocks myosin from binding to actin. CAuses sharp decrease in tension. If muscle is stretched to its longest length, there is no overlap so no cross bridge cycling can occur --> no contraction at all. - however, the rate of tension decline as the length increases is much slower than if you shorten the overlap -------------------------------------- At an optimal length of a sarcomere (typically in the range of 2.0-2.5 um)

how long does it take for the completion of one cardiac cycle. how much of that time is spent in diastole

800 msec (.8 seconds) --> most of time (2/3 of time) is spent in diastole

A band vs H ZONE vs I band .... and how do the sizes of these bands change once muscle is contracted.

A band = both (regions of overlap) I band = only thin (actin) H band --> only thick (myosin) during contraction: The A band stays the same, the H band and I band shrink

Titin (at rest, does this provide any tension)

A series elastic component protein responsible for allowing the sarcomere to stretch and recoil -passive tension! (tension at rest) (largest protein in body)

Alpha-adrenergic receptor antagonists (how does this effect total vascular resistance and how does this effect cardiac output) How does cardiac output relate to total peripheral resistance and MAP

Alpha-adrenergic receptor antagonists block sympathetically-mediated vasoconstriction it would decrease arterial pressure by decreasing total peripheral resistance!!! Not by decreasing cardiac output these types of drugs are not widely used because of the side effects resulting from blocking alpha adrenergic receptors at other sites. CO = MAP *TPR

What would happen if the ATP on the myosin head could not be hydrolyzed? a. The head would be able to still bind accordingly to actin b. The myosin binding will not be able to continue since ATP needs to be hydrolyzed for it to re-bind c. ATP will become AMP and the process will continue that way d. It is actually more efficient when ATP is not hydrolyzed, and this mechanism will move faster and more accurately

B

explain the baroreceptor reflex when you stand up How long does it take to control CO and peripheal resistance through this mechanism?

Baroreceptor (cranial-mediated visceral) reflex--> goal is to keep arterial pressure to stay within a set range by adjusting CO and resistance in particular vascular beds: For example, when you stand up, the gravity pulls the blood down and your bp decreases: -Baroreceptors in the aortic arch and in a region of the carotid arteries (the carotid sinus) sense decrease in bp--->sends afferent signal through cranial nerves IX and X (carotid sinus nerve and aaortic depressor nerve) to medulla oblongata vasomotor regulation centers which are always on (have tonic or basal activity). IT IS NEVER OFF---->nuclei in medulla oblagnta responsible for cardiovascular system. fires PNS and SNS at same time for precise control of bp. -PNS (vagus nerve only innervates the heart) ...decreases its firing rate relative to tonic levels of firing which increase heart rate (which increases CO) -SNS (sympathetic nerves innervate both the heart and the the arterioles) increases its firing rate relative to tonic levels of firing which will increase BP, heart rate (and thus CO), and contractile forces of the heart, AND vasoconstriction of arterioles which increases the Total Peripheal Resistance. Both of these PNS and SNS control all cause increase in arterial bp and inrease in cardiac output> As bp goes back up negative feedback decreases the rate of firing of baroreceptors !!!!!This response will also stimulate renin release!!!!!!! NOTE: You can have very specific activation of sympathetic nerves that are going to the heart without inducing a full body sress response in all of the arterioles. Localized through neurons! (Adrenal medulla releases epi and norepi) It only takes two heart beats (very rapid) to control CO and peripheal resistance through this mechanism Also (order can go in reverse if the blood pressure increases

How does the brain sense blood pressure? What are the two places that sense the blood pressure and which cranial afferent nerves What is the bodies primary mechanism for maintainig blood pressure?

Baroreceptors (stretch receptors) with tonic firing patterns in respond to bp (stretch) The baroreceptors are located in: -The Aortic arch --> sends info to aoortic depressor nerve to brain -The carotid sinus --> sends info to carotid sinus nerve to brain The Baroreceptor reflex is the bodies primary mechanism for maintaining blood pressure. Very tightly regulated --> so this means that small change in arterial in bp will cause huge response in baroreceptors and all compensatory changes you get . They are so sensitive that they oscilate there rate of firing in repsonse to changes in pulse pressure)

frequency-tension relationship -unfused tetanus vs fussed tetanus -Is there still an absolute refractory period that exists during the AP of somatic motor neuron stimulating muscle fiber? --> is this concept due to temporal or spatial summation

Because a single action potential in a skeletal muscle fiber lasts only 1 to 2 ms but the twitch may last for 100 ms (due to Calcium dynamics), it is possible for a second action potential to be initiated during the period of mechanical activity. NOTE: muscle fiber is only innervated by a single type of motor fiber so there is no spatial summation.... temporal summation allows multiple AP to stimulate during a single muscle contraction. When a stimulus is applied before a fiber has completely relaxed from a twitch, it induces a contractile response with a peak tension greater than that produced in a single twitch (S3 and S4). The increase in muscle tension from successive action potentials occurring during the phase of mechanical activity is known as summation. (unfused tetanus because the AP are far enough apart that you get some relaxation but not enough relaxation to recover to baseline) A maintained contraction in response to repetitive stimulation is known as tetanus (fused tetanus). This results in maximal tension in muscle. ------- Yes, there is still an Absolute refractory period but you have enough time to recover from an AP and generate many more during the 100 ms period.

why is the magnitude of electrical activity detected by an ECG much lower than the electrical activity from the electrical ventricular action potential recorded by a single cell

Because the electrode is on the skin, so the current must travel through a bunch of stuff/ structures which will attenuate (weaken signal). This is because it must take the sum of entire heart. --> the electrical ventricular action potential recorded by a single cell - recorded from INSIDE of the ventricular contractile cell with intracellular electrode. Results in a greater voltage change detection.

Blood vessels are lined with _______. 8 functions

Blood vessels are lined with endothelial cells and is a dynamic contributor , not a passive lining -secrete substances that influence vascular smooth muscle -mediate angiogenesis (growth of new blood vessels) -regulate transport of substances between plasma and interstitial fluid -display some contractile activity, which regulates capillary permeability -secrete substances involved in the regulation of clotting -convert some inactive hormones to active hormones!!!!! -degrade certain hormones or paracrine agents!!!! -contribute to immune responses!!!!!

How is the SA node innervated? How is the AV node innervated? How is the ventricular muscle innervated?

Both the SA and AV node are innervated by the SNS and PNS. However, the AV node inervation is not as important. --> the modulates the slope of the funny current to influence the heart rate. However, the ventricular muscle is only innervated by SNS, thus the SNS monitors heart rate in two ways.

Modulation of the pacemaker potential. Which receptors in heart cause an increase in heart rate upon binding and what receptors in heart cause a decrease in heart rate opon binding. Also, at resting conditions, can the AV node pacemaker properties regulate heart rate?

Both the sympathetic and parasympathetic nervous systems innervate the SA node. Beta1-adrenergic receptors (via NE or Epi) on the SA node speed up the rate of the pacemaker potential and muscarinic cholinergic receptors (via Ach) on these cells slow the pacemaker potential. Under normal resting conditions, the pacemaker properties of the AV node play NO ROLE in regulating heart rate because the slow rate of the AV node pacemaker current means that the action potential spreads to the AV node from neighboring atrial myocytes before the AV node pacemaker potential has gotten these cells to the threshold

Regarding similarities and differences between skeletal muscle and smooth muscle, which of the following statements are INCORRECT a The cross-bridge cycle is important for contraction in both types of muscle b myosin can cleave ATP in both muscle types providing the energy for the cross-bridge cycle c In both muscle types contraction involves Ca++ coming primarily from the sarcoplasmic reticulum d In both muscle types an action potential spreading through the muscle is essential for contraction e In both muscle types phosphorylation of mysoin is required for the cross-bridge cycle to occur

C, D, and E

What type of enzyme is myosin? (Hydrolases use the molecule, synthases make the molecule) a. ADP hydrolase b. ATP hydrolase c. ATP synthase d. All of the above, but in different contexts

C. Myosin must hydrolyze ATP to ADP to allow for the power stroke that propels myosin forward on the actin polymers.

How does exercising impact each of the parameters for CO?

CO = HR x (EDV - ESV) HR is increased due to increased sympathetic activity on pacemaker cells in heart via B1 ARs.EDV is how much the heart fills up during relaxation/diastole. This is largely determined by venous return. Venous return will be increased by the skeletal muscle pump as he exercises, and the respiratory pump as he breathes more heavily. Therefore EDV is increased. ESV is how much the heart empties during contraction/systole. Contractility is increased by sympathetic input onto the heart muscle via B1 ARs (and how does it do that?). Therefore ESV is decreased. All things will increase the cardiac output

Is CO the same everywhere in series? Is CO the same everywhere in parallel? Why do different organs receive different flow rates? Which organs receive the most amount of blood flow AT REST?

CO same in series but different in parallel Because they have did metabolic rates The digestive tract and liver receive the most amount of blood BUT when you control for size of the organs (more accurate) you get a better answer) the kidneys receive the most (second most). In reality, the LUNGS recieve the most amount of blood flow because they see all of the blood that flows through the circulatory system . ALL OF IT!!!

How do calcium channel blockers lower blood pressure?

Calcium entry from the extracellular fluid plays an important role in both smooth muscle and cardiac muscle contraction. Blocking calcium entry through calcium channels decreases the force of cardiac contraction to lower contractility (and therefore SV) and decreases the contractility of vascular smooth muscle (therefore decreasing TPR). Both of these effects lower blood pressure.

in which type of blood vessel listed below would you expect the velocity of blood flow to be the slowest?

Capillaries (only contain endothelium and no other types) although the cross-sectional area of an individual capillary is tiny, there are so many of them that the total cross-sectional area is huge compared to, for example, the aorta (1000x higher), so the velocity is decreased by 1000x. - very high SA, and they decrease distance for diffusion (small diameter and thin one cell wall so RBC can diffuse very readily (8 microns) - the velocity of blood moving through capillaries is very slow - about 1/1000th of that in arteries, a velocity of ~0.5mm/sec in the capillaries (units can also be cm/min Note: flow rate of total = same

Which of the following is an example of active hyperemia a. baroreceptor reflex compensation of a decrease in arterial blood pressure b. stimulation of erythropoietin secretion at high altitude c. maintenance of blood flow to the brain during physical exercise d. increased blood flow to leg muscles during running e. vasoconstriction of arterioles in the legs upon standing

D

Explain how diarrhea could cause a temporarily elevated hematocrit.

Diarrhea causes dehydration, which is loss of fluid volume. Plasma is the fluid component of blood. If the total volume of red blood cells is unchanged but plasma volume decreases with dehydration, the hematocrit will increase.

End Systolic Volume (ESV) - What determines how much blood is left after contraction? - What is the average value in humans ( in mL) end diastolic ventricular volume (EDV) - how can the EDC be changed with respect to filling pressure (what kind of relationship). What is the average value in humans ( in mL) Stroke Volume (SV)(def and equation) - how does this change in response to EDV changes. -is this a good indicator of how much blood and oxygen are circulating the body - What is the average value in humans ( in mL)

ESV: volume of blood remaining in each ventricle after systole -approx. 65 mL under resting conditions - This is a function of how strong the heart contracts, or cardiac contractility. An increase in contractility = increase in force of contraction at any given EDV, and thus the amount of blood that is forced out during systole. --> average value in humans 135 mL EDV: At the end of diastole, the ventricles have filled and under resting conditions is about 135 mL (so 70 mL of blood was filled during diastole) - direct relationship between filling pressure and EDV. --> average value in humans 65 mL SV: volume of blood that is ejected from the left ventricle into the aorta during one cardiac cycle (this is the same amount of volume filled by heart during diastole which is 70 mL) - note: SV increases in direct proportion to EDV. ----> NOT a good indicator of how much blood and oxygen are circulating the body SV= EDV-ESV average value in humans 70 mL

extrinsic control of arteriolar constriction? - if the sympathetic nervous system is blocked, would happen to bp? - elimination of brain inputs to the spinal cord has what effect on bp?

Extrinsic --> something else helps coordinate this system (brain/hormones/autonomic system) - sometimes the local tissue doesn't know whats best thing for the entire body, so may need extrinsic mechanisms to override the local mechanism "Example, you just ate crackers, but later see a bear, so instead of ur brain telling body to digest the food, the whole body must be coordinated. Sympathetic vasoconstriction of is mediated primarily by alpha1-adrenergic receptors on the arterioles. Sympathetic nerves innervating blood vessels are normally active, and therefore can be modulated up (causing constriction) or down (causing dilation) of various tissues. - provide selective patterns of redistribution of blood flow. - Note: Arterioles in some tissue (skeletal muscle, liver) also have beta-adrenergic receptors, and stimulation of these receptors elicits dilation and it this can only be triggered by increased epinephrin levels (not NE) -mechanism to balance the alpha-mediated constriction in skeletal muscle during more intense sympathetic activation. == BP would decrease for both Q's - if high rate of firing --> vasoconstrction -if low rate of firing --> vasodilation

What makes blood flow? What is flow (the equation) How is flow related to resistance. And what factors contribute to the resistance . What is the formula for resistance ?

Flow is proportional to the pressure gradient and inversely proportional to the amount of resistance. so flow = pressure CHANGE/resistance Three factors contribute to resistance to flow: 1.)length of the tube --> resistance increases as the length increases 2.)diameter of the tube --> as the tube gets narrower, the resistance increases. This has the BIGGEST effect on resistance; as radius decreases, resistance increases as a function of radius to the 4th power. (e.g., decreasing the radius in 1/2 increases resistance 16-fold) 3.)viscosity of the fluid; as viscosity increases, resistance increases. R= (viscosity)*Length of tube/ r(^4th power!)*(8/pi)

sphygmomanometry - what is the sound heard indicating systolic pressure -what is the sound heard indicatin diastolic pressure

Fluid flowing through constricted passages results in turbulent flow, which generates sound. Thus, as the cuff pressure falls below the peak arterial pressure (i.e., the peak pressure during systole), blood pushes through the constricted artery and that turbulent flow can be heard through the stethoscope. As the pressure continues to fall, at some point the pressure in the artery will fully exceed the cuff pressure and the flow will no longer be restricted and so the sound of turbulent flow will go away. as the cuff pressure decreases, the pressure at which the first sounds are heart is the systolic blood pressure and the pressure at which the sounds go away is the diastolic blood pressure.

Pressure-volume graph in the left ventricle cardiac cycle: what do the the points individually represent and all the transitions. Also, for every transition, list whether the AV and SL valves are open/ closed/ shut From A --> B From B --> C From C --> D From D --> A

From A --> B (AV opens, SL closed) - point A = (late diastole) --> QRS complex very low pressure and low volume, but as the blood from the atria passively travels through the AV valves to fill 80 percent of its volume, the ventricular pressure will start to increase slightly, and thus, this segment is not passive. The only passive segment is the completely horizontal part. From B --> C (AV shuts, SL closed) -Point B is the End Diastolic Volume (how much you can fill the ventricle up) --> QRS complex -This represents isovolumetric (vertical line) ventricular contraction (AV valves snaps shut), and the SL valves are still shut due to pressure in ventricles not being high enough to overcome that of the artery From C --> D (AV closed, SL opens) - C = point where the ventricle (T wave)overcomes the pressure in the aorta so blood is ejected - the blood ejected from C --> D is the stroke Volume (ejection of blood in mL pumped per cycle. From D --> A (AV closed, SL closed) D = ESV (amount of blood left in the ventricle after contraction; SL valve close ) T wave. - represents isovolumetric relaxation

Rank the following blood vessels in order of their average pressure, from highest to lowest: e. Aorta > arteriole > artery > capillary > venule > vein f. Aorta > artery > arteriole > > venule > vein > capillary g. Capillary > venule > vein > artery > arteriole > aorta h. Aorta > artery > arteriole > capillary > venule > vein i. Aorta > artery > arteriole > capillary > vein > venule

H

How might you quickly reduce his hematocrit without removing red blood cells?

Hematocrit = RBC volume / total blood volume. If plasma volume increases, hematocrit will decrease even though red cell volume does not change. By drinking fluids, you could increase his plasma volume quickly.

Why is the neuromuscular junction a high fidelity synapse? What is the reasoning behind this? How is this junction organized?

IF you get an AP in a somatic efferent neuron --> you will get an AP in a muscle cell. 1:1 relationship. This is because there is enough Ach released with a single AP and a high density of N-Ach receptors on post synaptic membrane of muscle fiber *** The junction is organized to provide high reliable transmission AP from motor neuron to muscle. The neurons do not completely cover the muscle fiber but strategically place them to get 1:1 relationship.

If something is very compliant, what does this mean ?

If something is very compliant, you can get a change in pressure in response to a change in enviornment. -elasticity- (this allows elastic recoil to allow continuous blood flow during diastole by preventing the pressure in the artery from not dropping to the pressure in the ventrical during diastole.

How does muscle fatigue compare as the intervals between muscle contraction decreases? What happens if you have fused tetanus for sustained time, fatigue, and then try it again?

If you increase the frequency of the interval b/w stimuli you will reach fatigue much faster. (longer intervals allow the muscle contraction to keep cycling for a long period of time) If you have fused tetanus for sustained time, fatigue, and then try it again, then the second fused tetanus will not last as long!

Continous Capillaries vs Fenestrated capillaies What are sinusoid endothelial cells What are the two ways (mechanisms) molecules can pass through these capillaries?

In general, capillaries are very porous and leaky Continous -blood-brain barrier -has a complete basement membrane connecting the endothelial cells (surrounds endothelial cells), and the junctions between them connecting the endothelial cells that are large enough that you can pass things through them (gaps) Capillary --> Fenestrated (holes /porous--> VERY LEAKY) -large pores are called fenestrations for things to pass through. However, there are still very big molecules like proteins that are too large to fit through leaky gaps or pores it needs to do transcytosis: - by bringing protein into vesicles, and vesicle passes through endothelial cells - vesicles can stack up (fuse) together and create temporary channels 2 ways molecules travel: -Bulk flow -diffusion transcytosis Sinusoid -liver -spaces large enough (intercellular gap) for even relatively large proteins

Control of Heart Beat - what nerves control PNS and SNS and what is the effects upon stimulation. Do both of these innervate the same locations in the heart (where are they both)

In isolation, the heart beats at 100/min, the intrinsic rate of depolarization of the SA node. However, this can be influenced by influencing the rate of spontaneous depolarization (i.e., the pacemaker potential). At rest in humans, parasympathetic tone is high, so HR is less than the intrinsic SA rate (70 instead of 100). [NOTE: what is being influenced is the pacemaker potential at SA node. PNS= vagus nerve --> decreses heart rate and innervates the SA node. (The ventricular muscles do not receive parasympatheitc stimulatoin so PNS does not influence contractility of theheaart SNS = sympathetic cardiac nerves --> increases heart rate AND force of contraction

Ways to increase venous return? (list both long-term (1) and short term control measures (7) And what does increasing venous return have an effect on.

Increasing venous return increases EDV which increases stroke volume (due to starling law) which increases Cardiac output. 80 percent of EDV is due to passive pressure differnce!!!!! Note: all of these things increase venous return. All of these things listed EXCEPT venous valves function to increase pressure gradient. Long term: 1.) salt and water retention will INCREASE BLOOD VOLUME Short Term: 1.) Passive bulk flow of fluid from interstitial fluid into plasma will increase blood volume and thus increase venous pressure 2.) venous valves mechanically prevent back-flow. 3.) Respiratory Pump (decrease in pressure in chest veins increases pressure gradient) 4.) Skeletal muscle pump increases venous pressure 5.) Sympatheitic vasocontrictor activity increases venous pressure but decreases venous capacity. (alpha adgrenic receptors on veins) 6.) increased cardiac contractility increases venous pressure

How does the sympathetic nervous system regulate the heart? And why is it important to regulate this process - what is the exact mechanism

It modulates the contractiblity of the heart (how hard will it pump) which shifts the Starling curve either up or down by changing the ESV. Allows you to exclusively regulate the end-systolic volume which is important because you need blood to remain in the ventricle after ejection because you need to a reserve pool to be able to pull from when needed. --> This allows you to decrease your ESV so that the heart can pump more blood out. mechanism: Epinephrine and Norepinephrine bind to Beta-1 receptors which activates the cAMP secondary message system, which can have two effects: a.) Phosploration of voltage-gated ion channels which modulates Ca dynamics by increasing the amount of time they are open which ultimately increases Calcium entry from the ECF. b.) phosphorylation of phospholamban which is a regulatory protein that increases the AMOUNT of SR CaATPase activity which: - increases the Ca storage in SR so it will release more Ca --> results in MORE FORCEFUL CONTRACTION -Ca removed from the cytosol faster which SHORTENS the duration of contraction (recover faster).

The extracellular fluid concentration of K+ and metabolites increases in exercising skeletal muscles. What effect does this have on blood flow in the muscles?

Leads to reactive hyperemia, which causes vasodilation and increases blood flow.

Local/intrinsic control of arteriolar constriction : -Active hyperemia (what stimulates it) -Flow autoregulation (what simulates it) -(reactive hyperemia) Also what are the effects (2) of relaxing the precapillary sphincters

Local --> if you left arteriolar alone, how would it regulate itself? - relatively unstable if you only count on these local mechanisms because there is only a certain amount of volume that flows per minute. (5L) 1.) Active hyperemia = increased blood flow to tissue (or an organ) in response to increased activity of that tissue - if the organ is very active with increased metabolic activity, it will use up lots of o2 (increase CO2) delivered to it which makes metabolites and waste products in interstitial fluid --> sensed by endothelial cells and muscle cells which release local factors that cause vasodilation of blood vessels and arterioles going to the organ which will decrease resistance and increase the flow - note adenosine is another metabolite 2.) Flow autoregulation = maintaining flow in response to changes in arterial pressure. This is using the same stimuli and causes the same outcome as active hyperemia but it has a different precipitating factor. Instead of normal metabolic activity in organ, it can be a decrease in pressure in the organ (decrease in arterial pressure for example) --> this creates the same stimulus --> decreased blood flow and oxygen (metabolites build-up) - there is an additional unique stimulus to this which is a decrease in a stretch of the walls of the vessels in the organ. - stimulated by a change inflow (e.g., blood pressure increases or decreases) 3) You can also relax the precapillary sphincters which cause an increase in the number of open capillaries which has two effects that work to increase the exchange of blood and tissue to support increased metabolic activity: a.) increase in capillary surface area available for exchange (increase rate of diffusion) b.) decrease in distance from the cell to the open capillary (you open up capillaries closer to the organ so it can get to the organ faster) 4.) reactive hyperemia --> Extreme case. after blood flow to a region is impaired when blood flow returns it is much greater than normal.

Malnourished children who have inadequate protein in their diet often have grotesquely swollen bellies. This condition, which can be described as edema of the abdomen, is called ascites. Use the information you have learned about capillary filtration to explain why malnutrition causes ascites.

Low-protein diets result in a low concentration of plasma proteins. Capillary absorption is reduced while filtration remains constant, resulting in edema and ascites.

arterioles - in the absence of any signaling imputs, what happens. What do you call this?

MAJOR SOURCE OF RESISTANCE: -adjustable high resistance vessels that determine the distribution of blood flow to different tissues (high resistance in one tissue will decrease flow) -surrounded by smooth muscle which has a basal intrinsic amount of constriction called myogenic tone. Signals can act to increase (constriction) or decrease (dilation) this contraction of smooth muscle. - the pulsations in pressure decrease and by the distal end of the arteriole flow is no longer pulsatile. - site of regulation of blood flow to different tissues as a result of different degree of constriction or dilation. -smaller diameter than artery

Diuretics (effect on CO and mechanism) -what is significant about this

Most tolerated and effective mechanism in body to decrease the blood pressure increase urinary excretion of sodium and water --> reduce blood volume and therefore cardiac output

List the muscle equivalent term for each general term: Muscle Cell Cell membrane cytoplasm modified endoplasmic reticculum

Muscle Cell --> muscle fiber Cell membrane --> sarcolemma cytoplasm --> sarcoplsm modified endoplasmic reticculum --> sarcoplsm reticulumm

Are all organs operated under the same regulatory networks?

NO For example, heart and brain have very powerful intrinsic control (autoregulation) whereas skeletal muscle is controlled by local metabolic factors, sympathetic vasoconstriction, and epinephrine vasodilation, and skin is largely controlled by sympathetic input.

Scenario: Artery has a flow rate of 5L min. 1.) Artery splits into 5 arterioles with equal amounts of resistance. What is the flow rate in each smaller arteriole? 2.) Artery splits into 5 arterioles but one of the five arterioles are constricted alot, and the other 4 are more dilated and all the same. What is the flow rate in the constricted arteriole vs the 4 more dilated arterioles?

NOTE: the total flow rate will total 5L/ min for all of ther arterioles added up. For 1: each arteriole will have flow rate of 1L/ min For 2: 4/5 arterioles will hhave flow rate of 1.1 L / min to compensate for the .6 L/min flow rate in constrcited arteriole.

Extrinsic Control of arteriolar smooth muscle. Describe the various vasodilators and vasoconstrictors of each. -neural controls -hormonal controls

Neural controls: -Vasoconstrictor = sympathetic postganglionic neurons release NE -Vasodilation = neurons that release NO Hormonal: Vasoconstrictors= Epinephrine (secreted by adrenal medulla), angiotensin II, antidiuretic hormone (vasopressin which is a potent vasoconstrictor, released during huge drop in bp due to hemorrhaging) -Vasodilator = atrial natriuretic hormone and epinephrine NOTE: epinephrin acts as both a vasoconstrictor and vasodilator. This is because it binds to two different adrenergic receptors: -epinephrine causes constriction in many networks of minute blood vessels but dilates the blood vessels in the skeletal muscles and the liver. In the heart, it increases the rate and force of contraction, thus increasing the output of blood and raising blood pressure.

Cardiac muscle AP compared to a skeletal muscle AP. What are the three phases of a ventricular myocyte action potential (how does it compare to atrial AP). What contributes to the small dip during the very beginning of the second stage. - and what contributes to each phase! (list types of channels involved, and their relative kinetics)

Note: Atrial myocyte action potentials are similar to action potentials of ventricular myocytes, although they are a little shorter Cardiac action potentials are quite long (~250 msec) compared to skeletal muscle (~2 msec). 1.)Depolarizing Phase The rapid depolarization is due to voltage-gated Na+ channels (fast kinetics) as we have discussed for skeletal muscle. --> increase in Na (same as skeletal AP) -> note: no threshold for contraction because the cell is already hyperpolarized enough in the resting state!!!!! - only Na is entring! 2. Plateau phase - voltage-gated sodium channels are inactivated at the very beginning of this phase. - decrease in intracellular levels of Na (sodium voltage-gated channels inactivate here) and K (efflux) -There are two types of K+ voltage-gated ion channels that differ by kinetics: -FAST --> activated in this phase at the very beginning (contributes to tiny repolarization dip but then the Ca voltage gated channels open which counters this repolarization to sustain a prolonged 250 ms plateu - still slower than Na voltage-gated ion channels 3.) Repolarizing Phase - increase in K and decrease in Ca - the SLOW K+ voltage-gated ion channels turn on but THIS IS TO THE SAME initial sodium depolarization, but the effect is extremely delayed because these have VERY slow kinetics.

4 types of smooth muscle contraction patterns (2 for phasic and 2 for tonic) What determines the contraction pattern/ impact opon stimulation of smooth muscle?!!!! Can smooth muscle fatigue ?

Note: Skeletal muscle doesnt share these featurers because contraction is all or none . Phasic: - normally relaxed but contracts upon stimulation (esophosgous) - Cycles between contraction and relation (GI contractions) NOTE: Smooth muscle can undergo sustained contractions without fatigue because the contractions are very slow!!!! Tonic: -usually contracted but relaxes upon stimulus (EX: anal shpincter / bladder) -contraction is varied as needed (always eome amount of contraction at any given time but can dilate or contract further if signal comes in (arterioles) ------------ The receptor determines the impact of contraction of smooth muscle.

What do the following ECG segments/intervals represent: P wave: P-Q interval P-Q segment Q wave: R wave: S wave: S-T segment: T wave: Q-T interval: R-R interval:

Note: these are all deflections in summed voltage change and don't represent depolarization/repolarization, these deflections are indicators of different points of an AP. For example, the QRS complex can be looked at as an indicator that the ventricle is about to contract. The ventricle itself does not contract unless there is a pressure difference favoring flow into the ventricle from the atria, and the AV valve doesn't shut until AFTER the ventricle has overcome the pressure in the atria. P wave --> atrial depolarization (but atria have not contracted yet. These waves are just indicators of different points of an AP) . P-Q interval (labeled as PR interval in the figure): the time required for atrial depolarization and the action potential to reach the ventricles. - this represents conduction through AV node AND AV bundle. - starts at the beginning of the p wave and goes to the end of the flat line in the PQ segment P-Q segment (labeled PR segment in the figure): time for atrial depolarization to propagate through the ventricles. - Period of Atrial contraction (sustained so flat line) - the flat line, more accurately, starts at the end of the P wave, and ends at the start of the Q wave) Q wave: The electrical activity is going down the Bundle of His - occurs after the atria contract R wave: Ventricles start to depolarize. The Atria is repolarizing but this deflection is warped by the large deflection occurring during ventricular depolarization - electrical activity begins to travel up the Purkinje fibers. S wave: electrical activity travels up the Purkinje fibers from the apex to base (bottom to top) S-T segment: time between ventricular depolarization and repolarization - Period of ventricular contraction T wave: ventricular repolarization Q-T interval: the time required for ventricular depolarization and repolarization. R-R interval: an accurate measure of the time of a single cardiac cycle.

mechanism of smooth muscle contraction and relaxation (and how is it different than in skeletal muscle ) -what protein is involved

Nridge cycling Note: this process is slower so this is more of a graded contraction !!!! (unlike skeletal muscle) - also note that myosin is regulated here!!!!!!!! Relaxation: 1.)Free cytosolic Ca is decreases by pumping Ca back into SR and Interstitial Fluid via pumps and Na/Ca exchangers which causes Ca to unbind from CaM --> MLCK activity decreases. 2.)myosin phosphatase removes phosphate group on myosin light chain which decreases ATPase activity (no cross bridge cycling / contracting)

erythrocytes -Why is Hb inside of them? How many Hb molecules are in a single erythrocyte -What is the diameter and shape and why are these things significant

RBC --Hb is inside of the RBC so that it can avoid contributing to the protein concentration of the plasma which must strictly be regulated near 7 % -No nucleus or ribosomes (so no ER) - diameter is 7 microns which is about the width of the smallest capillary in the body (thus only one rbc can fit in capillary in one spot at a certain time) This allows edges of the cell to go right up against the edge of capillary wall which maximizes the diffusion of oxygen -optimal biconcave shape creates a higher surface area for maximal diffusion of oxygen -

relaxation of heart muscle mechanism - what role does phospholamban have in this ?

Relaxation occurs when Calcium unbinds to troponin. and the voltage-gated calcium channels close. -1) Ca/Na exchanger utilizes secondary active transport (sets of sodium gradient outside the cell maintained by Na/K ATPase which provides potential energy for Calcium exit into interstitial fluid. -2.) SRCA pumps actively pump Calcium back into SR. - -The rate at which Ca++ can be removed from the cytoplasm is a regulated process. For example, the protein phosphlamban is associated with SRCA, and reduces the activity of SRCA. Under conditions of intense stimulation of the cardiac myocytes (and thus high cytosolic Ca++ levels, there is a calmodulin-dependent increase in phosphorylation of phospholamban, resulting in its dissociation from SRCA and thus an increase in SRCA activity.

When will you NOT pick up an electrical signal on an ECG?

Remember that ECG detects voltage CHANGE - so if you have a sustained contraction/depolarization (which is characteristic of a very long cardiac contraction) then you will not have any deflections on graph. (this is represented by the flat line in ventricular myocyte repolarization; there is depolization but no change)

One hallmark of illegal EPO use is elevated reticulocytes in the blood. Why would this suggest greater-than-normal EPO activity?

Reticulocytes are the final immature stage of RBC development. If RBC development becomes more rapid, more reticulocytes may be released into the blood before they have time to mature.

Pericardium - what is it and function - what is the endocardium

Sac of connective tissue membrane surrounding the heart that acts to lubricate and cushion the heart. Consists of parietal (outer) and visceral layer (inner) separated by pericardial cavity) -It is important The heart itself is mostly muscle (myocardium) with the chambers, like all body cavities, lined with epithelium - the endocardium.

what are the signals in the EKG measuring exactly. - if you are using three electrodes, and two are on hand, which foot do you place electrode on and why? What are the charges of the electrodes? -what do the various waves represent: - P, QRS, T Is there such thing as Atrial Repolaization?

Signals in the ECG result from a change in polarization (SUMMED voltage changes)as recorded as a differential between two electrodes; it in not measuring membrane potential. It is measuring the direction of current flow along the axis of a lead between two electrodes! - this picks up a SUMMED CHANGE IN ELECTRICAL POTENTIAL across multiple electrodes placed on body. - NOTE: the up and down deflections on ECG DO NOT MEAN repolarization/hyperpolarization is happening. (not a direct measure of this because this is not always the case... they are related to each other because as AP trvels through the muscle, you get contraction of ventricle which starts the beginning of the QRS complex. Place electrode on left foot because this makes more of an equal space distribution around the heart. - one electrode is negative and two are positive, so there will be a net vector that flows from the negative electrode and transects the middle of where the two positive electrodes meet. - the individual signals (not summed) will look very different depending on what lead your looking at P wave = atrial depolarization (A closer in the alphabet than V, snd P is closer in alphabet than Q,R,S,&T. QRS = ventricular depolarization (upside down V --> ventricles pump blood upwards) T = ventricular repolarization. (P further in alphabet than A, and T is further in alphabet than P,Q,R,&S - note that this is repolarization occurring and you still get upward deflection. Yes, there is such thing as atrial repolarization but this occurs during the same time as ventricle depolarization and it is not as strong as ventricular depolarization so this gets warped by the deflection caused by ventricular depolarization

How does the length of the contraction after AP sustain contraction in a cardiac muscle vs a skeletal muscle? How does the mechanism compare? What is a calcium spark? How do the absolute refractory periods compare to skeletal muscle? What are the Calcium sources (relative to skeletal and smooth muscle)

Similarly to skeletal muscle, the influx of sodium ions causes an initial depolarization; however, in cardiac muscle, the influx of calcium ions via voltage-gated ion channels sustains the depolarization so that it lasts longer. Unlike skeletal muscle, where contraction lasts much longer than the action potential and therefore additional action potentials can maintain the contraction, in cardiac muscle, the action potential lasts as long as the contraction. . -SOOOOO --> pumping Ca++ out of the cytoplasm - terminates both the action potential and the contraction!!! A functional consequence of this is that cardiac muscle cannot have tetanic contractions, since the absolute refractory period (Na voltage-gated ion channels are closed and inactivated) of the action potential lasts as long as the contraction (AP and heart cycle contraction/relaxation end around the same time) This is a good thing because you need the ventricles to relax in order to fill up with blood to continue pumping. ( In skeletal muscle, there can be many AP that sum to create one sustained contraction) ******The Ca++ entering through voltage-gated Ca++ channels acts to induce Ca++ release from the sarcoplasmic reticulum (termed calcium-induced calcium release): 1.) Calcium enters the muscle cell from the outside in the T tubule 2.) this allows more Calcium to enter sarcoplasm intracellular from SR. When 1 and 2 occur together, this is called Calcium spark! -->contraction NOTE: Contains a Ryanodine receptor channel but it is not mechanically connected to DHP (like skeletal muscle) -This Ca++ leads to the binding of Ca++ to troponin and thus to cross-bridge cycling and contraction. - 90 percent of Calcium source is from the SR and 10 percent is from the interstitial fluid (skeletal Ca source is all from SR and smooth muscle contains a much larger percentage of Ca coming from the interstitial fluid

Umbrella of the skeletal muscle (broad to specific) -skeletal muscle (composed of 4 things) -myofasciles -myofibers (contains 4 things) -myofibrils (contains 1 thing)

Skeletal Muscle --> composed of connective tissue, nerves, and blood vessels, and muscle fasciles (bundles) These muscle fasciles contain muscle fibers (individual muscle cells) Within the muscle cell, there is sarcoplasmic reticuulum, glycogen granules, mitochondira (LOTS), and myofibrils. Within the myofibrils is the sarcomere

three types of muscle fibers: -Slow-oxidative -Fast-oxidative -Fast-glycolytic (Also list the subtype classification for each, myoglobin content, and what types of muscle and frequency of use?) What are the two isoforms of myosin? - what differentiated the two? How are these fibers organizes in the muscle

Slow-Ox (Type 1); dark (high myoglobin) -Aerobic --> high mitochondira - have the narrowest fibers with the least amount of thick and thin filaments --> so can't generate as much tension (force per cross sectional area)as a larger diameter fiber. (cant reach max tension) - very resistant to fatigue -LOWEST THRESHOLD for contraction. This will get recruited first because it is least energy expensive that can sustain for awhile and not fatigue as mmuch. So if you can pick up something light using this only, your body will chose to do so. -Most used in body --> muscles for posture Fast Ox "intermediate" (Type IIA) light (low myoglobin) -aerobic/anearobic --> moderate mitochonidra -intermediate diameter of fiber so high force per cross sectinal area. -moderately/highly resistant to fatigue - during training, this can be be turned more into slow oxidative -medium threshold for contraction --> used for things like standing/ walking Fast-glycolytic (Type IIB) light (low myoglobin) -ANEROBIC --> low mitochondria - few mitochondria -THICKEST fiber so high force per cross-sectional area due to more actin and myosin --> can reach MAX tension . HOWEVER, it has a problem of getting enough oxygen and nutrients to diffuse deep into the fiber soo low resistance to fatigue -highest threshold for contraction , least used. Muscles used for fine movements like writing , or quick movements like jumping -------- Slow and Fast are 2 isoforms - The difference in the rate of contraction of "fast" and "slow" skeletal muscle fibers is due to the rate at which myosin cleaves ATP (this refers to HOW FAST the muscle contracts!) ------ These three types of muscle fibers are typically mixed together in a muscle (as in the picture ), though in different proportions depending on the muscle. However a motor unit will only be of one type

Do veins have smooth muscle. How are they innervated? - what is venous pressure a major determinant for (2)? And what is venous pressure equation.

Some veins have vascular smooth muscle, which is controlled mainly by the sympathetic nervous system (mostly alpha-adrenergic mediated constriction but some beta-adrenergic dilation). == major determinant of the filling pressure and therefore the preload of the right ventricle, which regulates stroke volume Venous Pressure = change in volume (ΔV) of blood within the thoracic veins divided by the compliance (Cv) of the these veins

T-tuble - what is it, what is its function, what is located to the right and left of them and what is that entire complex called. - also where does the sarcoplasmic reticuluum wrap around

T= Transverse Extensions of the sarcolemma and run deep into the muscle cell so that an action potential can effectively depolarize a muscle cell quickly and completely. Aids in Ca release from SR to cause contraction -T tubes have terminal cisternae on each side which form a triad (this is located approximates at Z disk) the sarcoplasmic reticuluum wrap arounds individual myofibrils

What role does the connective tissue separating the atria and ventricles play in the heart conduction system? - how long does it take for this conduction system to travel through the heart completely? (aka: how long does it take the AP to spread through the heart)

The connective tissue b/w the atria and ventricles electrically isolate the atria from ventricles and isolate the ventricles from the bundle of His and each other. - important because you don't want a spread of AP that causes a contraction to go from the atria straight to ventricles because that would push the blood down the heart which is bad b/c there is no exit down there. -it takes less than 250 msec for the action potential to spread through the heart.

Why is there a delay from when you get AP at neuromusc. junction to the AP of a muscle fiber. What is this period called? Why is the contraction in a muscle cell longer and more sustained? How long does it take for a muscle contraction/relaxation vs a nerve AP?

The delay is the result of Calcium taking a long time to mobilize and initiate contraction. This is referred to as the latent period (slow kinetics) The contraction is longer and more sustained because it takes time to pump all the calcium back into the SR for muscle to relax. Muscle contraction/relaxtion lasts 100 ms vs an aP which lasts 2ms

what is the pulse pressure? (what is equation and average in humans) - what influences pulse pressure? (2 things!!!!!!) -How does compliance of the vasculature affect the pulse pressure? -when is the pulse pressure attenuated? If there is no pulse pressure what does this mean? In the vasculature, when is the pulse pressure completely attenuated? What is the mean arterial pressure? How do you measure this?

The pulse pressure is equal to the systolic pressure - diastolic pressure. Arterial pressure is low during diastole and high during systole. The difference between these two is the pulse pressure. the mean arterial diastolic pressure = diastolic pressure + 1/3 pulse pressure. (This is mathematically the same as 2/3 diastolic pressure + 1/3 systolic pressure.) and is measured in the arteries The compliance allows elastic recoil which prevents pressure from dropping all the way back down to that of the ventricular diastole. So on average: 120 mm Hg - 80 mm Hg = 40 mm Hg the reasoning behind the numbers : During the normal cardiac cycle approximately : --> 2/3 of the time is spent in diastole --> 1/3 is spent in systole. ------------------------------ - Stroke volume and arterial compliance both increase the pulse pressure !!!!!!! As stroke volume increases, the amount of blood pushed into the aorta increases, and thus pulse pressure increases. = the pulse pressure completely attenuates by the beginning of the capillaries which means that the flow rate will be steady

At 7:00pm, an individual has a blood pressure of 122/78. Four hours later, the same individual has a BP of 112/66. What change would you expect to see in pulse pressure (does not need to be calculated)? What changes in the vasculature are responsible for this change in pulse pressure?

The pulse pressure would be decreased since both the systolic and diastolic pressures are decreased. Since stroke volume, heart rate, and arterial compliance influence pulse pressure, and pulse pressure has decreased, you would expect stroke volume to decrease, heart rate to decrease, and arterial compliance to increase.

what is the funny current - how is it changed and regulated by the autonomic nervous sytem

The spontaneous influx of Na by leak channels that can be regulated by the autonomic nervous system by modulating the slope of the funny current : - shortened (faster rate of auto-depolarization) during sympathetic activation (steeper slope of funny current) - also have reduced amount of repolarization during periods of an increased heartbeat. Accounts for shortening of AP. -lengthed (slower rate of auto-depolarization) during Parasymp activation (shallower slope of funny current) - also have a hyperpolarized state during periods of decreased heart rate (which makes sense). Accounts for lengthening of AP!

4 Heart Valves -what are they composed of and how are they modulated by pressure gradients. -what muscles are associated with the AV valves. What are the purpose of these valves. Are the valves innervated by the nervous system or have any muscles?

The valves are flaps of connective tissue that open and close PASSIVELY (no muscles or nerves)based on the pressure differential, and they allow unidirectional flow from the atrium to ventricle and from the ventricle to the artery. - when pressure is greater behind the valve, it pushes leaflets open --> valve opens -when the pressure is greater in front of the valve, it shuts to prevent backflow; however, it does not open in the opposite direction which makes these unidirectional. == chordea tendinae: connects on the end of the valves on the leaflets and achors to Papillary muscles. papillary muscles: are not involved in the opening and -closing of the valves --> they are not actual muscles because they do NOT contract (just passive and for structural support (leaflets don't get blown out backwards, though this is possible) -prevent the valves from being pushed too far open or being pushed back too far into the atria - they limit the movement of the valve leaflets. LAB RAT Left Atrium: Bicuspid (Mitral) Right Atrium: Tricuspid Note , the LA and RA are before the last letter so they come before there respective valves ---------- There are also valves at the junction between the ventricles and arteries they lead to (pulmonary artery on the right, aorta on the left) are another set of valves (the pulmonary valve on the right side and the aortic valve on the left side). IMPORTANT: ALL VALVES have three flaps (leaflets) except bicuspid

How thick are the epithelial cell walls in capilarries?

The walls of the capillary are a single epithelial cell thick, a wall thickness of less than 1 um.

How does a neuron AP compare with a cardiac muscle AP? (2)

There is no hyperpolarization in cardiac muscle cells because the resting potential is already at -90 mV. This makes the membrane more permeable to K+ (closer to K+'s equilibrium potential) Also, there is no threshold for depolarization in a cardiac muscle cell

cardiac pacemaker cells (autorhthymmic cells) - how does the AP compare to this cell compared to ventricular muscle cells and skeletal muscle cells in terms of : - Events leading up to threshold potential, absolute REFRACTORY PERIOD, duration of AP, MEmbrane Potential , repolarization phase , and hyperpoarization)

These cells are in the SA node and generate electric current spontaneously, without requiring any external input without external input due to having an unstable membrane potential (pacemaker potential) - these are connected to adjacent ventriuclar muscle cells and the gap junctions allow quick progation of signal through the contractile cells. -REFRACTORY PERIOD - skeletal muscle: generally short - autorthymic myocardium: not significant in normal function. - contractile myocardium: Lengthed absolute refractory period to prevent tetanus Events leading up to threshold potential - skeletal muscle: Net Na+ entry through Ach operated channels - autorthymic myocardium: Net Na+ entry and K+ efflux through funny current channels which is reinforced by Calcium entry. - contractile myocardium: depolarization enters via gap junctions Duration of AP - skeletal muscle: Very short (1-2ms) - autorthymic myocardium: variable generally 150 + msec - contractile myocardium: VERY LONG because the resetting of Na channel gates are delayed until the very end of AP. There is still slight influx of Na, and slight eflux of K, but this is balanced out by the rapid Ca entrance that prolongs AP Membrane Potential - skeletal muscle: stable at -70 mV - autorthymic myocardium: UNSTABBLE pacemaker potential but normally starts at -60 mV - contractile myocardium: stable at -90 mv Repolarization phase - skeletal muscle: rapid and caused by K+ efflux (voltage gated K open and voltage gated Na close) - autorthymic myocardium: caused by Calcium levels decreasing inside the cell and K+ leaving the cell - contractile myocardium: rapid and caused by K+ entry, and Ca levels decreasing inside the cell due to inactivation of voltage gated calcium channels Hyperpoarizatoin - skeletal muscle: due to excess K + effux at high K+ permeability , when K+ channels close, the leakage of Na and K restore the potential to resting state. - autorthymic myocardium: NONE because the resting cell potential is at -90mV which is the equilibrium potential for K+. - contractile myocardium: normally none; AS SOON AS repolarization hits -60 mV, the funny current channels instanteously open. However, Ach can hyperpolarize the cell.

Whats unique about the various types of Leukocytes ?

They are bigger in diameter and can still travel in vasculature. -75 % of hematopoietic stem cells are proliferating into leukocytes - due to very short half-lives in the blood (hours), they need to pump more out to replenish stores. Note: They are still present in much lesser concentrations in the blood at any given time

organization of smooth muscle

They are spindle-shaped and have thick and thin filaments that are attached to DENSE BODIES that are arranged in a mesh-like grid. Upon contraction, the arranged sarcomers will contract along multiple axis in a way that all the dense bodies will be pulled together to each other similarly to the way that Z disks pull in towards each other in skeletal muscle contraction. Contraction of smooth muscle = blubbing

excitation-contraction coupling (10 steps, from initiation of contraction to the end of relaxation) -what is the name of location this junction occurs at - will contraction occur if there is just a tiny tiny bit of Ca in the sarcoplasm

This is what happens when you depolarize the muscle fiber membrane. Links AP on sarcolemma to activation of the myofilaments at the terminal cisternae ...thereby preparing them to contract. 1.) Ach released from somatic motor neuron into neuromuscular junction (due to Calcium influx from voltage-gated calcium channels) and bind to ligand-gated Na channel (n-Ach receptor) on the post synaptic terminal. 2.) Na influx initiates an AP on the the sarcolemma of the muscle fiber. 3.) This AP travels down into the T tubules and voltage change causes a conformational change of the DHP receptor (not an actual receptor) 4.) This change causes the RyR receptor on the sarcoplasmic reticulum to open. Note this receptor is mechanically coupled to the T tubule (they are connected). This opening of RyR receptor causes Ca to flow out of the SR (passively). 5.) Calcium combines with troponin and initiates contraction (actin-myosin binding) 6.) Myosin heads initiate power stroke 7.) Actin filament slides towards the center of the sarcomere. * done contraction ----------------- 8.) SR Ca-ATPase (sarcopump) pumps back Calcium into the SR 9.) Causes a decrease in free cytosolic (Ca) causes Ca to unbind from troponin 10.) Tropomyosin recovers binding site. When myosin heads release, the elastic elements pull the filaments back to their relaxed position. **** NOTE: As long as their is some sarcoplasmic Calcium , the muscle will undergo a sustained contraction.!!!

Consider what happens with "hardening of the arteries" which are less compliant, how would this change pulse pressure?

This would cause an increase in bp because the pressure reservoir is no longer available.

Regulation of Actin in smooth muscle (what regulatory protein involved and what is this analogous to) What is the mechanism of regulation?

VERY COMPLEX calmodulin interacts with actin. In its native form (i.e., non-phosphorylated form) calmodulin binds to actin and prevents it from binding with myosin (sort of like tropomyosin in skeletal muscle). in response to a variety of signals, calmodulin gets phosphorylated, which causes it to dissociate from actin thereby letting actin and myosin interact.

angiotensin II(what effects does it have (2)) - what organ makes this -what is the rate limiting step

VERY POTENT VASOCONSRICTOR Produced in blood by renin which is an enzyme releaseed by Juxtaglum cells in kidney in response to either: - decreased stretch - or increased sympathetic activity .....and converts angiotensinogen( made in the liver and released into blood) to make Angiotensin I --> rapidly cleaved to to angiotensin II (biologically active) by ACE in membrane of the endothelial cells in pulmonary capillaries. IMPORTANT FOR ACE TO BE IN PULMONARY SYATEM B/C THAT SEES ALL OF THE BLOOD flowing through the body per cycle. The rate limiting step in angiotensin II production is how much renin is released into blood; under normal condition sufficient angiotensinogen is present in plasma secreted by liver. Effects of angiotensinogen II: -constricts arterioles which increases total peripheal resistance which increases mean arterial pressure. - increases total plasma volume (via renal system) which increases blood pressure (MAP) ...... Renal mechanisms: -signals hypothalamic neurons to increase thirst -signals posterior pit. to release ADH -singlas adrenal cortex to secrete aldosterone (increase water absorption by reabsorbing salt and water follows)

Ventricular Contraction vs Ventricular Relaxation

Ventricular Contraction - pressure moves against the AV valves to SHUT them( to prevent backflow into atria) - blood pushes against SL valves which causes them to open and eject blood to wither the aortic or pulmonary semi-lunar valves (open) Ventricular Relaxation -SL valves close to prevent backflow into ventricle during relaxation -AV valves open

Diameter of venules and veins and thickness of wall. (what is unique about veins) 4 Mechanisms to get flow back to heart. Describe differnces b/w veins and venules in terms of types of tissue/muscle present and thickness of their walls

Venules have very thin cell walls (thiner than veins) venules just have endothelium and fibrous tissue whereas veins have endothelium, elastic tissue, smooth muscle, and fibrous tissue low resistance (due to LARGE diameter) .... the pressure is low coming out of the capillaries so there must be mechanims to assist with the return of blood of heart. You also need to fight gravity so there needs to be extra ways to assist return of blood to heart - valves --> unidirectional flow - forward flap-opens valve - backward flap-shuts valve - Skeletal muscle pump (body moving causing contractinion of muscles around veins which pushes on them, and then once you relax, it cant go back down. - respiratory pump --> as we breath in and out, the pressures in the thoracic cavity change... when you exhale, you increase pressure in thoracic cavity which compresses veins which pushes blood through veins. -VERY COMPLIANT (ELASTIC) -will stretch to accommodate the blood volume. Normal blood volume is approximately 5L; of this most (60%) is present in the venous circulation. If volume is added or subtracted, it largely comes out of this compartment.

Relationship between blood flow, blood velocity, blood pressure and cross sectional area of different types of blood vessels.

Vesel diameter - smallest in capillaries and got larger in both directions velocity of blood flow -slowest in capillaries, as it goes into veins and venae cavae, the velocity increases a little bit, but this is much slower than the velocity of blood flow in the elastic arteries average blood pressure - highest in elastic arteries, medium across capillaries, and very little in veins/vena cavae Total cross sectional area -highest in capillaries and decrease by same rate both ways in circ. system

Skeletal muscle: why doesnt the cross bridge cycle continously recycle if there is always ATP in the body? How do the Ca++ in sarcoplasm compare in resting vs contracting muscle. Where is this Calcium stored?

When the ADP and Pi are bound to myosin in the lower energy state (rest state), tropomyosin blocks the acin unless calcium binds to troponin which causes tropomysoin to uncover bdining site on actin for myosin. In resting muscle, Ca+2 levels in the sarcoplasm are very low, but when they increase, the cross bridge cycle will occur. The calcium is stored in the sarcoplasmic reticulluum

stroke

When the plaques from atherosclerosis break off into the blood, this causes the activation of platelets which clots blood (further blocks blood flow to the BRAIN which causes a stroke

Does all of the vasculature contain endothelium?

Yes

does the AV node contain cells with pacemaker properties? Do the Purkinje fibers have autorhymic activity? - why would there be autoryhmic activity in components in heart electrical conduction pathway that do not contribute to setting the heart rate? ----------------------------------- What is the function of the AV node?

Yes, left to themselves, they would generate action potentials at the rate of approximately 35-50/ min. YES, the Purkinje fibers have autorhymic activity but slowest of them all (25-30 cycles per minute) However, the rule of thumb states that the fastest cell will dominate the cycle which is the SA node (100 bpm) These two autoryhtmic components serve as a back up fail-safe mechanism; however the heart would pump blood much slower and the blood pressure would decrease ----------------------------------- The AV node slightly slows the neural impulse from the SA node, which causes a delay between depolarization of the atria and the ventricles. You want the atria to finish contracting before the ventricles start to contract.

Can you increase CO? If so, what is the mechism

Yes, you can increase CO by expanding the amount of volume that fills the heart (above 135 mL mark)

peripheal fatigue vs central fatigue

Your body does not ever reach peripheal fatigue during intense exercise because the muscles always have a steady supply of ATP. (only about 30 percent is used) Muscle fatigue is due to central fatigue: - your motor cortex that sends signals to motor neurons will eventually stop sending signal so brain will fatigue before muscle (possible to prevent muscle damage from occurring)

Which of the following statements is true? a. In females we see lower hematocrit than in males b. Hematocrit is the same as the percentage of blood cells in the blood c. Platelets account for a large portion of our blood and help with coagulation (clotting) d. Hemoglobin exists in the extracellular environment of our blood

a

If one vascular bed changes its degree of vasoconstriction, flow to the other vascular beds could be maintained if there is : (2)

a change in cardiac output, or if other vascular beds were adjusted in compensation.

twitch contraction. How much of maximum muscle tension is generated from a twitch contraction

a single action potential that causes a single unit of contraction. typically 20-30% of max Note: there is a brief period of maximum Ca++ binding to troponin, this isn't enough time to stretch all of the elastic properties of muscle

motor unit -How does the body initate a greater net force of contraction? What initates muscle contraction?

a single motor neuron that may innervate several muscle fibers. However, Each muscle fiber is innervated by only a single motor neuron (not other way around) The larger the motor unit, the more muscle fibers that motor nerve innervates. The finger would have a smaller motor unit than the thigh. the central nervous system may recruit more motor units to elicit a greater contraction. -initiated in the motor cortex.

You start exercising more and eating healthier. What changes in blood flow would you expect to see to their brain, lungs, heart, skeletal muscle, skin, kidneys, and abdominal organs?

a. Brain has increased blood flow b. Lungs have increased blood flow c. Heart has increased blood flow d. Skeletal muscle has increased blood flow e. Skin has increased blood flow f. Kidneys have decreased blood flow g. Abdominal organs have decreased blood flow

edema (will occur if .....(2)

accumulation of fluid in the interstitial fluid. Will occur if: - lymphatic drainage from an area is compromised (3L/ day not working ) -balance of pressures between capillary hydrostatic and osmotic pressures favors the movement of fluid from capillaries into interstitial space. This might occur if: -increased capillary hydrostatic pressure (typically due to increased venous pressure.)... (not enough pressure drop across capilaries. OR -decreased plasma protein concentration (e.g. liver failure) OR -increased interstitial fluid protein will decrease capillary osmotic pressure EX: (leakage, tissue damage ---> causes spaces between capillary endothelial cells getting larger, and proteins leak out of capillaries in that area and now decrease the osmotic pressure in that area so this is more fluid accumlation in that spot )

Murmurs are abnormal heart sounds caused either by blood forced through a narrowed valve opening or by backward flow (regurgitation) through a valve that has not closed completely. Valvular stenosis may be an inherited condition or may result from inflammation or other disease processes. At which steps in the cardiac cycle (see bottom of Wiggers diagram) would you expect to hear a murmur caused by the following pathologies? a. aortic valvular stenosis b. mitral valve regurgitation c. aortic valve regurgitation

aortic valvular stenosis --> ventricular ejection mitral valve regurgitation --> . isovolumic ventricular contraction and ventricular ejection aortic valve regurgitation --> a. isovolumic ventricular relaxation until ventricular contraction begins again

dicrotic notch. What causes the dicrotic notch? How was this observed

as bp pressure is falling, there is a little bump up in ARTERIAL pressure, creating what is referred to as the dicrotic notch. *** This is a reflection of how waves travel ... in arteries, there is a huge decrease in diameter from artery --> arteriole so the blood hits the narrowing of the arterioles and deflects backward a little. --> observed when taking the sum of the the reflected wave and the frontal wave. (pulse wave analysis) The dicrotic notch is a result of this reflected arterial pulse wave as it hits the resistance of the arterioles and is reflected back through the artery.)

what drives the contraction of heart

autorhymic pacemaker cells

Comparing blood pressure between the beginning and end of the capillary: a pressure is lower at the distal end because the flow rate is less b pressure is lower at the distal end because of the resistance provided by narrow diameter of the capillaries c pressure is lower at the distal end because of metabolites entering the capillaries, causing them to dilate d pressure is the same at the beginning and the end e pressure is higher at the distal end because of metabolites entering the capillaries

b

In response to a drug that selectively dilates systemic arterioles, what would happen to the activity of parasympathetic nerves innervating the heart? a their activity would increase b their activity would decrease c their activity would not change

b

What type of receptors are the aortic baroreceptors? a. Proprioceptive b. Mechanoreceptors c. Thermoreceptors d. Photoreceptors

b

_______________ uses ______________ to make Hemoglobin (Hb).

bonemarrow , Fe

If you have a constriction at one point in your vasculatre (decrease flow rate there), how do you prevent other parts of the vasculure from increasing their flow rate to compensate for the change? (two options)

change Cardiac output! or use extrinsic mechanisms to override local mechanisms (the brain must be able to sense what the pressure is)

1. What would happen if you applied tetrodotoxin (voltage-gated Na+ channel blocker) to a contractile myocardial cell? An autorhythmic pacemaker cell? A skeletal muscle cell?

contractile myocardial cell --> Block the AP Autorhythmic pacemaker cell --> nothing would happen (doesnt rely on voltage gated ion channel) skeletal muscle cell --> blocks AP

coronary artery disease (what is it caused by/ what is a risk factor)

currently 42.1 percent of all cardiovascular disease (most common and largest cause of death in humans) -caused by decereased blood flow to the heart - atheroscelrosis is a major risk factor because less blood will flow to heart

Will the activity of myosin in smooth muscle be upregulated or downregulated when the amount of kinase and phosphatases in the environment is lower than usual?

downregulated

when is it likely for vasopressin to be released

during hemmorage because this is a potent vasocontrictir which will help save blood volume

EPO. What how does the body regulate this?

erythropoietin; promotes the growth of red blood cells -released by the kidney and targets red bone marrow - operates under neg feedback. -the kidney senses oxygen-carrying capacity levels because it is very metabolically active and needs lots of oxygen to receive a large volume of blood flow (20 percent)

beta adrenergic receptor blocker (effect on blood pressure) mechanism

exert antihypertensive effects mainly by reducing cardiac output

Flow Rate vs Velocity - how does an increase in cross-sectional diameter affect the velocity of the blood. How does it affect the flow rate of blood?

flow rate (or simply, flow) is the volume of fluid passing a point in the tube per unit time (e.g., ml/min) velocity is the distance the blood travels per unit time (e.g., cm/min). The larger the cross-sectional diameter of the vessels at that level of the circulation, the slower the velocity of flow. THIS accounts for ALL vessels diameter summed. (Total cross-sectional area) An increase or decrease in total cross-sectional area does NOT CHANGE the flow rate Logic: Volume increases with a larger diameter so the liquid will have more room to move but still be within the closed system flowing in one direction so it will not be fast as if the cross-sectional diameter was smaller. --> or " if stream narrows , TO MAINTAIN THE FLOW RATE, the water will travel faster (increase velocity)

How is a sarcomere defined? How long is a sarcomere?

from z disk to z disk. It is called a disk because it takes up all of cross section of myofibril The sarcomere is the smallest contractile unit of striated muscle It is 3 microns long

autorhymic pacemaker cells - also what do there AP look like - can the autonomic nervous system generate an action potential in the pacemaker cells !

generate its own rhytm independant of ANY innervation (auto-rhymic) (depolarizatoin of these cells rapidly spread to adjacent contractile cells through gap junctions) NOTE: it can be modulated by that automatic nervous system but they do not generate an AP so NOO!

myocardial infarction

heart attack (ischemia) - when the plaques from atherosclerosis break off into the blood, this causes the activation of platelets which clots blood (further blocks blood flow to the heart which causes heart attack.

Compensatory responses to hemorrhage. What happens to EDV, SV, and arterial pressure. What is secreted in response. How do the baroreceptors deal with this ( 2 ) ?

hemorrhage (blood loss) --> causes decrease in cardiac filling pressure --> causes decrease in EDV, SV, and CO --> causes decrease in arterial pressure. decrease in arterial pressure has 2 effects: - inadequate tissue performace causes increase in renin secretion (vasopressin is secreted due to low blood volume -decrease baroreceptor afferent nerve activity. This has 2 effects: -decrease in vagus nerve activity results in increase CO2 which increases arterial pressure and increases tissue perfusion - increase in sympathetic activity causes increased vasoconstrction , CO2 production, and renin secretion which all increase arterial pressure and tissue perfusion

Tissues Requiring high blood flow (2 due to high energy needs and 2 due to regulating blood composition) vs low blood flow (3) What determines this distribution of blood flow?

high blood flow due to high energy needs: - brain, heart high blood flow due to important functions in regulating blood composition: -liver, kidney low blood flow due to low energy needs: -skeletal muscle, skin, bone == The relative resistances of the arterioles in the different tissues determines this distribution of blood flow. ( so pressure in arterioles does determine blood flow!) - Note that this distribution is subject to regulation, and can change markedly (exercise) - decreased brain, kidney, GI, and skin blood flow compared to when at rest - increased blood flow to skeletal muscle compared to when at rest

heart failure -what is it and how is it caused -what drugs help this - what is congestive heart failure

if pushing with too much pressure for too long, you cant maintain CO (5L/min) -the blood that is filling the heart cannot all be pumped out of the heart due to decreased contractility (shifts starling curve down --> decrease contractility) Treated by lowering the work that the heart must do -diuretics - digitalis (cardiac ionotropic drug) --> increases ventricular contractility by increasing cytosolic Calcium concentration in the myocardial cell (improves heart failure but does not prolong life) -vasodilator drugs -beta adgrenergic receptor blockers Left ventricle fails first! (so the right ventricle will still work fine). This will cause a backup up blood in the right atria which will go to right ventricle --> into lungs (pulmonary edema) CALLED CONGESTIVE HEART FAILURE

Tonic release of NE

part of sympathetic control of vasculature - so tonic activity (fires at rest) from the sympathetic nervous system causes constant (tonic) release of NE and this level can be increased or decreased to affect the system. - if you get an increase in activity, you increase the number of AP coming in (frequenecy of AP natters, not size, length, or duration) which causes increases in NE which causes vasocontriction (opposite for less activity)

chemoreceptor reflex (what triggers it and what are the three effects )

protective mechanism to increase concentration of O2 to particular organs. Chemoreceptors in the carotid arteries (sensors are in same place as the sensors used in baroreceptor reflex) are sensitive to changes in blood O2 or CO2 . - In response to inadequate oxygenation OR increased CO2 (hypoxia) or increased protons in the blood--> increased chemoreceptor afferent activity: - increased sympathetic vasomotor activity --> causes peripheal vasoconstriction (and thus increases O2 conservation) - decrease sympathetic cardiac activity --> lowers heart rate (and thus increases O2 conservation) - increased breathing/ventillation --> increases O2 uptake,

How do drugs that antagonize the sympathetic nervous system effect cardiovascular system.

reduce activity of arteriolar smooth muscle --> reduces total peripheal reistance (thus lowers blood pressure) *THIS IS THE LEAST TOLERATED MECHANISM TO LOWER PRESSURE TO TO MANY ADGRENERGIC RECEPTORS THROUGHOUT THE BODY (lots of side efects)

ACE inhibitors (effects on blood pressure and mechanism)

reduce concentration of angiotensin II in plasma --> arteriolar vasodilation --> lowers total peripheal resistance and thus lowers MAP (angiotensin II receptor blockers has same effect)

Calcium Channel Blockers effect on cardiovascular system

reduce entry of Calcium into vascular smooth muscle (contract less strongly) --> lowers TPR which lowers MAP REMEMBER SMOOTH MUSCLE DOES NOT HAVE SR/T-tuble commplex mechanism

Calcium Channel Blockers

reduce vascular smooth muscle contraction and also cardiac contractile force.

cardiac muscle - how are the fibers electrically and mechanically coupled to each other - how does it receive nutrients and how much mitochondria does it have - how would you compare the size of cardiac muscle vs skeletal muscle fibers, which ones ae fused together?

similar in appearance to skeletal muscle (distinct banding pattern; sarcomeres, I bands, A bands, etc). However, cardiomyocytes are single (unfused) cells, smaller than skeletal muscle fibers. - ---> are rich in mitochondria and receive a rich blood supply; note - they don't receive nutrients from blood in chambers, but rather from the coronary circulation. . Cardiac muscle cells are connected to their neighbors at their ends by gap junctions . These gap junctions allow action potentials to readily spread from cell to adjacent cell; cardiac myocytes are electrically coupled to each other. Cardiomyocytes are also mechanically connected, anchored together by structures called intercalated disks, and specifically, desmosomes hold the muscle cells together in the intercalated disks.

If you are working physically , and the work intensity is increasing, which types of muscle fibers are prefrentially recruited first? 2nd? 3rd?

slow-oxidative fibers --> then fast ox --> fast glyc

Blood pressures at different levels of circulation

the arterial pressure change from diastole through systole is not as dramatic as it is in the left ventricle. In this figure, also notice that flow through a resistance, dampens this pressure pulse (causes pressure drop)

arteries - main function - how does the pressure compare at the distal and proximal ends of the artery? -what allows you to feel your pulse?

the main function of arteries: serves as a LOW resistance conduit to distribute blood around the body --> they serve as a reservoir of blood to continue pumping blood through vasculature when the heart is in diastole by using elastic recoil --> contain fibrous tissue! -low resistance vessels to get blood distributed to the body ( primarily due to large diameter --> very low resistance --> high pressure) - pressure at the distal end of arteries is only a little bit lower than at the proximal side. - thick wall to withstand high pressure pumped out by ventricle. - elastic so very stretchy (compliant)--> As a result of this compliance, arteries serve to boost flow during diastole and this maintains arterial pressure and flow through the distal end of the aorta. (elastic recoil in the arteries). -This non-rigidity (compliance)allows you to feel your pulse - Thus, despite the heart pumping blood only intermittently, flow through the aorta is maintained.

At normal resting values of a diastolic pressure of 80 mm Hg and a systolic pressure of 120 mm Hg, what is the pulse pressure and what is the mean pressure?

the pulse pressure would be 40 mm Hg (difference) and the mean pressure would be ~93 mm Hg. 80 + 1/3*40 = 93 MAP = DP + 1/3(pulse pressure) where pulse pressure = diastolic pressure minus pulse pressure.

Anemia (def and causes)

the reduced O2 carrying capacity of blood and this can happen as a result of: - decrease in hematocrit (could be due to hemmmorage) -chemotherapy -change in the shape of Hb --> sickled RBC cant deliver O2 as well and clump together which can cause blocks in the vasculature (makes tissue ischemic --> painful) - Kidney disease (inadequate secretion of EPO) -Defective Hb and RBC synthesis in red bone marrow due to Fe deficiency (need in diet, cannot make de nova). Fe is ESSENTIAL differentiate hematopoietic stem cells in the red bone marrow into RBC.

What are the local stimuli that causes the arteriolar muscle to both constrict and dilate.

vasoconstriction: - internal blood pressure (myogenic response) vasodilation - decreased O2, increase in K+, H+ and CO2 -adenosine -eicosanoids -bradykinin -substances released during injury -NO -histamine

if your in space with no gravity, what happens to blood presure. What happens when you return to earth?

very high bp because you know longer have gravity pulling down the blood so the blood is evenly distributed. --> start excreting andlose 12 percent of blood volume ------ When you come back, the baroreceptor reflex cannot compensate for the loss in total blood volume to get blood presure back up so you can pass out very easily.

The Starling law of the heart and the Starling Curve - how do you increase your EDV? what is the EXACT mechanism !!! - How does the autonomic nervous system modulate this. - what does it mean to have an upward or downward shift on the curve

you can increase your EDV by increasing the venous return by allowing the sarcomeres to lengthen which creates tension on them so when they do contract, they contract with more force. This length-tension relationship can be modulated to control how much you're filling the heart and how much blood you're pumping out. However, this works in a different mechanism - the stretch increases the affinity of troponin for calcium! relationship between EDV and SV (direct relationship) --> so if EDV increases, the ESV will increase because it HAS TO pump all of the blood it receives, or else there will be a net accumulation of blood in the heart until it explodes ---> Note: this relationship fails at a very high EDV. -------- SNS stimulation shifts the whole Starling curve up (increases contractility) where PNS shifts curve down (decreases contractility)

In anemic patients, how would the Hb levels in the blood compaire to healthy

you could have like 11 g / 100 mL of Hb in blood which is bad because you want it in the red blood cell

how do you calculate the pressure gradient.

you need two seperate points and take the difference in pressure. If there is no difference, there is no flow. So its the differnce that matters, ABSOLUTE VALUE DOES NOT MATTER

what happens when your renal blood flow decrease

you release EPO and your urine output decreases to conserve blood volume

does elecrical activity always occur before contractile activity

yuh