Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Balliet SyPh 9,10,11
NYCC Balliet Sys Physiology ch. 9, 10, 11 cardiophysiology
| Question | Answer |
|---|---|
| describe actin of cardiac muscle (cm) | same as skeletal: f-actin, troponin and tropoMyosin |
| How ____ is released is different in cardiac mm from skeletal muscle | Ca++ |
| Why is extracellular Ca++ regulated so tightly? (between 9-11%) | because of cardiac mm (ergo, Ca+ channel blockers are given) |
| Besides Ca+, what other ion is enormously important for cardiac mm? | K+ |
| describe cardiac mm | intercalated discs with many gap junctions, striated, low threshold/low resistance, syncitial tissue with centrally located nuclei |
| where are nuclei in cardiac mm? in skeletal? | central, peripheral |
| Intercalated discs with many gap junctions describes | cardiac tissue |
| cardiac tissue all has the same _________ concentration | ionic |
| why are the intercalated discs of cardiac mm low resistance? | so the action potential can spread almost instantaneously |
| K+ is for | Kardiac! |
| how many t-tubes per cardiac sarcomere | single (the heart is a lonely hunter) |
| were are the t-tubes in cardiac? | at the level of the Z-disk |
| how many t-tubules per skeletal sarcomere? | 2 per (muscles have antagonist/agonist relationships - they like things in two's) |
| where are the t-tubes for skeletal mm located? | near the ends of the myosin filaments at the A-I band junctions |
| A band and I-band | A is both myosin and actin, I is just actin |
| where are the t-tubes in smooth muscle? | there aren't any. Would tubules be a good idea in something that goops up like a waterball squeezed in a net whenever it contracted? No. Tubes would be a bad idea here. |
| What does smooth mm have that none of the others have? | caveoli (specialized invaginations in the sarcolemma that help collect and store Ca+ from the extracellular fluid) |
| Name 3 things smooth muscle does not have: | t-tubules, troponin, tropomyosin |
| The resting membrane potential of cardiac mm is -85 to -95 mV. Why? | Because the membrane potential of K+ is -94 and so cardiac will be close to its most important contributor |
| Why does the action potential have to go to 105 mV in order to threshold and fire? | upstroke is +20 mV because it was already very negative at -85 to -95 (vs the regular -65 of skeletal muscle) |
| The plateau of cardiac mm | ~0.2-0.3 sec in ventricular muscle (much longer than in skeletal mm) |
| why is the plateau so much longer in cardiac mm? | The ventricles have to fill up so the plateau is a long relax in order for this to happen |
| for ventricular muscle action potential, the first part of the wave is... | fast Na+ channels open (from -85 to zero) |
| at zero, after the fast Na+ channels have opened, what is next on the ventricular muscle action potential graph | at zero, the slow Ca+ channels open and climb to threshold (another +20mV from zero) |
| At the peak of the ventricular muscle action potential graph, what happens? | K+ channels open! |
| Are slow Ca+ channels still open while K+ channels are open at the peak of the ventricular graph? | yes, they open MORE!!!! This makes the downhill drop REpolarizing a soft plateau for at least .2-.3 sec while the ventricles refill |
| what happens after the Ca++ channels open even more after K+ opens at peak on ventricular ap chart? | K+ channels open more and at zero, the Ca++ channels are pretty much closed. REpolarizing begins in earnest |
| How does the cardiac cell get rid of excess Ca+ while it is depolarizing (K+ channels are open and the downslope is steep) on the ventricular ap graph? | Ca++ PUMP is on! and K+/Na+-ATPase pump is on! During the REpolarization, Na+ and Ca++ channels close. |
| describe phases 0-4 of ventricular muscle ap graph | 0:fast Na+ channels open then at zero, slow Ca+ channels open. 1:K+ channels open. 2:More Ca+ channels open. 3:REpolarization K+channels open even more at zero and from there, Na+ and Ca+ ch's close, the Ca+ pump and K/Na-ATPase pump comes on. 4:resting p |
| during the _______ period, cardiac muscle cannot be re-excited | refractory period |
| How long does the refractory period last in ventricles? atria? why different? | ventricles: 0.2-0.3 sec, atria: 0.15 sec. Atria are shorter because it has the nodal tissue that sets the pace/rate |
| why is the cardiac cell able to maintain the depolarization phase during plateau of ventricular muscle action potential | Ca++ ion channels open and maintain depolarization (remember they open on the depolarization at zero and stay open despite K+ up to +20 then back down to zero before shutting) |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| Calsequestrin binds Ca++ in the t-tubules of cardiac mm. | |
| why you cover your eyes when you get bad news | oculo-cardiac reflex: lowers your heart rate |
| In skeletal muscle, where is calcium released from? | sarcoplasmic reticulum |
| In skeletal mm, Ca++ is only released from the sarcoplasmic reticulum. Where does it come from in cardiac mm? | sarcoplasmic ret. and the T-tubules! |
| The cardiac cell gets Ca++ during an action potential from SR and T-tubules. Where are the t-tubes getting their calcium? | extracellular concentration of Ca++ |
| Ca++ in cardiac muscle is from the SR like in skeletal but also from t-tubules. How do cardiac t-tubles keep Ca++ stored if they are tubes? | mucopolysaccharides called calsequestrin bind Ca++ inside the t-tubules |
| _______________binds Ca++ in the t-tubules of cardiac mm. | calsequestrin |
| Why is cardiac muscle voltage gated at DHP and but NOT voltage gated at Ryn receptor? | because DHP is not hooked directly to Ryn receptor as it is in skeletal muscle. Ca+ actually has to cross over to it in the cytosol and bind to the Ryn receptor, which then lets Ca+ out of the SR |
| The ap moves down the t-tube in cardiac muscle and whacks a DHP receptor, just like in skeletal muscle. Then what? | DHP-r's get activated and allow a small amt of Ca+ to leak into cell, crossing over to Ryn receptor. The Ryn receptor pops the top and allows a huge amt of Ca++ into the cytosol from the SR (CACR-Calcium Activated Calcium Release) |
| Once CACR kicks in and the Ryn receptor has let the cat out of the bag ("cat-ion", get it?), how is Ca+ pumped back into the SR and T-tubules in cardiac muscle? | into T-tubules via Ca/ATPase pump to get Ca+ to calsequestrin and via the Na/Ca Antiporter |
| In cardiac mm, Ca++ release is proportional to | how much Ca+ binds to Ryn receptor |
| In the Length-Tension relationship, where on the graph does cardiac like to fire from? | just before normal operating range. Likes the bit of overlap between actin and myosin, in other words, to be a little shortened or slightly contracted is best. |
| At longer lengths on the length-tension rel. curve, what happens to cardiac muscle (skeletal likes ~2 nanometers and cardiac starts from ~1.2 nm)? | at shorter or longer lengths, the stress declines - cardiac operates at lengths below optimum (shorter) |
| Once CACR kicks in and the Ryn receptor has let the cat out of the bag ("cat-ion", get it?), how is Ca+ pumped back into the SR and T-tubules in cardiac muscle? | into T-tubules via Ca/ATPase pump to get Ca+ to calsequestrin and via the Na/Ca Antiporter |
| In cardiac mm, Ca++ release is proportional to | how much Ca+ binds to Ryn receptor |
| In the Length-Tension relationship, where on the graph does cardiac like to fire from? | just before normal operating range. Likes the bit of overlap between actin and myosin, in other words, to be a little shortened or slightly contracted is best. |
| At longer lengths on the length-tension rel. curve, what happens to cardiac muscle (skeletal likes ~2 nanometers and cardiac starts from ~1.2 nm)? | at shorter or longer lengths, the stress declines - cardiac operates at lengths below optimum (shorter) |
| decreases contractility (flaccid) and also slows the heart rate | excess K+ |
| causes spastic contraction in the heart | excess Ca++ |
| causes cardiac flaccidity | low Ca++ |
| blood flow through heart | sup and inf vena cava to R atrium, through tricuspid valve into R ventricle, through pulmonary valve into pulmonary artery. Lungs. Pulmonary vein to L atrium, through mitral/bicuspid valve to L ventricle, then up through Aortic valve into aorta and body. |
| mechanical events from the beginning of one heartbeat to the next | Cardiac Cycle |
| how does the cardiac cycle begin? | the spontaneous generation of an action potential in the SINUS NODE that is propagated through the heart via the CONDUCTING SYSTEM |
| where does the spontaneous action potential of the heart occur? | Sinus node |
| how is the signal from the sinus node propagated through the heart | conducting system |
| the SA node is the | pacemaker |
| Which contract first, atria or ventricles? Why? | Atria, to act as primer pumps for the ventricles (the real pumps) |
| when volume is up in the heart, | pressure is down |
| when pressure is up in the heart, | volume is down |
| the period of relaxation where the heart fills with blood | Diastole |
| the period of contraction of the heart | systole (squeeze!) |
| if you can pump out more blood each time in systole, what is the result? | a lower heart rate |
| Why is diastole longer than systole? | because it takes longer to FILL than push out. Atria has to depolarize in the middle of diastole. |
| strength of contraction is how ____ did it squeeze, while rate of contraction is how ____ did it squeeze | hard and fast |
| monitors the electrical events that result in a mechanical event (contraction) in the heart | ECG (EKG) |
| wave that shows depolarization of the atria just before contraction in diastole | P |
| what does the P-wave look like and what is it? | the little hump just before the sharp jag upwards. It is the depolarization of the atria, just before contraction in diastole. |
| wave that shows depolarization of the ventricles | QRS |
| what does the QRS-wave look like and what is it? | the sudden tiny dip (Q) after P-wave, going up sharply (R), then back down into a larger dip (S). The QRS-wave is the depolarization of the ventricles. Contract, snap shut. |
| wave that shows the REpolarization of the ventricles during QRS | T |
| what does the T-wave look like and what is it? | the larger hump after QRS-wave that shows REpolarization of the ventricles. Happens DURING the QRS wave, even though it shows up afterwards |
| First half of the P wave (depolarization of the atria)is in | diastasis |
| Second half of P wave (depolarization of atria) is in | atrial systole |
| Second half of P wave, Q wave and upgoing half of R wave are in | atrial systole |
| Downgoing half of R wave and all of S wave are in | Isovolumic CONTRACTION (depolarization and repolarization of ventricles) |
| The T wave is the ___________ cycle of ventricular pressure | Ejection! so after the ventricles have ejected the blood, it makes sense that the final part of the T wave is in the relaxing, repolarizing state of Isovolumetric relaxation |
| Ejection phase goes into _____________________ and the T wave just touches this last one as the ventricles relax, repolarize and gear up for Rapid Inflow state. | Isovolumic RELAXATION is, of course, just after ejection. T-man goes down... |
| what is the primer pump of the heart? | atria |
| what percentage of blood returning to the heart flows through the atria before going into the ventricles BEFORE ATRIAL CONTRACTION? | 80% (so 20% is left in the atria for it to push into the ventricles) |
| Under most conditions, can the heart operate without the last 20% of blood stuck in the atria? | yes. Atrial failure may not be noticed until the patient exercises - then acute signs of heart failure may develop along with shortness of breath |
| in the atrial pressure curve, why is it funny to call it that? | because the atria has almost NO pressure - the blood is going practically straight from the the vena cavae or pulmonary arteries right through the atria and into the ventricles |
| Atrial pressure is hardly ever more than 4-5 mmHg. Basically, the ventrical fills passively. What does the atria actually push? | the remaining 20% of blood that didn't flow passively into the ventricle |
| Think atria = practically no pressure. The A-wave is the atrial ______________ (20%). | Systole (contraction) |
| When the A-wave or atrial systole/contraction happens during the last 1/3 of diastole, what does it run up against? (remember: the atria has the SA node so its diastole has to be a little shorter in order to propagate the signal), | Isovolumic contraction of the ventricle which is the back pressure when the ventricle contracts |
| The pressure on the atria decreases a little after the atria A-wave crashes into the isovolumetric contraction of the ventricle. What is this downward spike in atrial pressure after A-wave (atrial systole of 20%) | As the ventricle fills, the vacuum effect on the tri- and bicuspid valves creates a little pulling or sucking downward in pressure of the atrium, right before the ventricle contracts (calm before storm is drop in pressure) |
| After the atrial pressure drops at the end of the A wave due to vacuum effect of beginning ventricular contraction, what wave occurs? | C wave of atrial pressure which spikes with the ventricle contraction (isovolumic contraction) because of the pressure against the AV valve/tri- and bicuspid valves pushing into the atrial space from the force of the ventricular contraction. |
| After atrial systole (A wave), then down due to vacuum, then up (C wave) due to pressure of ventricular contraction (IC), the atrial pressure drops as... | the ventricle empties |
| A wave (atrial systole pressure up), vacuum low pressure, C wave (isovolumic contraction of ventricle pushes against AV valve into atrium, spiking atrial pressure slightly), then slow refilling of atrium while AV valves are closed is called the... | V-wave! V for victory! at the top of the mountain is Isovolumic Relaxation spa |
| how much blood comes out with each squeeze | stroke volume |
| formula for stroke volume | subtract beginning of systole (squeeze) from end of diastole (relax) = stroke volume |
| stroke volume is the difference (subtraction) between | end of diastole minus the beginning of systole |
| during ventricular diastole (relaxation), what happens to the AV valves? | they open and the ventricles fill with blood |
| how many parts to ventricular diastole | 3 (in thirds) |
| first 1/3 of ventricular diastole | rapid filling of ventricles |
| middle 1/3 of ventricular diastole | small amt of blood flow; DIASTASIS (the sort of sluggish wait for atria to prime the pump with its last 20%) |
| last 1/3 of ventricular diastole | boom! atria contract and send the last 20% of blood into the ventricles and the AV valves be slammin' shut! |
| After the last 1/3 of ventricular diastole when the atria have pounded in the final 20% of blood, the AV valves snap shut. What is this condition called at the top of the roller coaster, right before it drops? | Isovolumic contraction (doors to the car are shut - you can't get off now!) |
| After isovolumetric contraction, the roller coaster starts down the hill at high speed. What's going on here? | Ejection!!!! agggghhhhhhhhhhhh!!!!!! Ejection phase is where isovolumetric contraction ends, ejection happens and finally the relaxation is in sight. |
| ventricular volume is at its lowest after ejection phase and goes into | Isovolumic relaxation |
| In isovolumic contraction of the ventricles, the ventricular pressure is rising and the AV valves are closed but... | no ventricular emptying has occurred yet. The pulmonary and aortic valves are open and ready. |
| When does isovolumic contraction end and what does it look like right before it ends? | IC ends at Ejection! The pulmonary and aortic valves are open, the AV valves are shut, and contraction is increasing but so far no blood comes out because the pressure in the aorta and pulmonary artery hasn't been overcome yet. When it finally is, whammo! |
| Normal systole is = to aortic pressure where? | at the highest point of ejection on aortic pressure curve (NOT ventricular curve) |
| The first heartsound is the beginning of ? | Isovolumic contraction, because the AV valve just snapped shut after the atria shot the last 20% into the ventricle |
| In the Ejection phase of the cardiac cycle, the semilunar valves open at ____mmHg but although the ventricle is contracting, it has yet to? | 80mmHg, overcome the pressure of the blood in the aorta and pulmonary artery |
| Once the blood pours out of the ventricle at 80mmHg pressure during Ejection phase, it can be divided into two parts (remember the ventricular filling volume had 3 parts? Well the exit has 2 even though it's in thirds. don't ask me!) | 70% in first 1/3 of Ejection phase is RAPID, the 30% in last 2/3 of Ejection phase is SLOW |
| RAPID and s l o w Ejection phase | ventricular contraction empties the ventricle |
| Where does the aortic valve close during the Ejection phase? | at a higher pressure than at which it opened. The valve opens at isovolumic contraction and closes at isovolumic relaxation, although the latter is a little higher on the graph. |
| ejection pressure | the ventricle overcoming the amt of pressure that blood is pushing from inside the aorta, once the aortic valve has opened during isovolumic contraction. |
| Ventricles relax allowing intraventricular pressures to decrease rapidly during | the end of systole |
| what closes the semilunar valves and seals off the ventricles so they can relax after the ejection phase? | elevated arterial pressure pushes some blood back towards the ventricles, closing the semilunar valves |
| The ventricles are relaxing, the semilunar valves are closed. Sigh. Birds are singing. What does NOT change at this point? | Ventricular volume. The ventricles are in Isovolumic relaxation so the volume is staying the same even though the ventricle is relaxing. |
| Welcome back from Isovolumic Relaxation island, Mr. Ventricle - the pressure in the cabin will continue to drop all the way to low diastolic levels and then... | Boom! Vacation's over, Mr. Ventricle! the AV valves are open! Cycle up, boy! |
| When does blood actually flow to the heart itself and why then? | During diastole, the coronary artery carries blood to the heart. Happens during diastole because there is more time. |
| When does the AV valve open after ejection phase? | at the end of Mr. Ventricle's Isovolumic Relaxation vacation, the pressure has dropped all the way to low diastolic levels and BOOM! the AV valve opens on the atria's V-wave and all 80% comes in until atria's A-wave systole/squeezes that last 20% in. |
| During diastole, which includes the RAPID inflow, diastais and atrial systole, the ventricle volume rises to? | ~110-120 ml This is the End-Diastolic Volume (EDV) |
| EDV | End Diastolic Volume or about 115 ml of blood that the ventricle has taken in by the end of diastole. |
| By how much do the ventricles empty in systole from their ~110-120ml in diastole? | ~70ml, leaving 40-50ml out of the original 115ml. This 40-50ml is called End Systole Volume (ESV) |
| to get Stroke Volume, what do you do? | Subtract End-Systole volume (ESV) from End-Diastole volume (EDV) ie, at the end of diastole, the ventricle has 115ml of blood in it. After it contracts, it shoots out about 70ml, leaving the ESV of 40-50ml. EDV - ESV = stroke volume |
| EDV - ESV = | stroke volume (the end diastolic/full volume minus the end systolic/empty volume will tell you how much you are pumping out every contraction) |
| Fraction of EDV that is ejected is called the | Ejection fraction |
| How much is the Ejection fraction usually? | 60% of the total volume (meaning, the ventricle usually ejects/squeezes out 60% of the original diastolic/filled volume) |
| Stroke volume is EDV-ESV. Ejection fraction is | Stroke volume / EDV |
| Ejection fraction explained | Figure stroke volume from EDV (filled ventricle) minus ESV (emptied ventricle). Divide this number (stroke volume) by the original filled ventricle number (EDV). This will tell you how much your ventricle ejects of the original fill. Ejection fraction! |
| Cardiac output | the heart rate in beats per minute multiplied by the stroke volume (the EDV-ESV) |
| What is normal ejection fraction? | EDV-ESV=stroke volume. Divide stroke volume by EDV=ejection fraction. Normally 60% |
| Cardiac output formula | heart rate * stroke volume |
| heart rate * ____________ = cardiac output | stroke volume |
| When does the pressure in the aorta cause it to close the aortic valve (semilunar valve)? | pressure in the aorta increases during systole after the aortic semilunar valve opens to ~120mmHg (systolic pressure) |
| What maintains pressure in aorta when valve closes to ventricle so that the aorta doesn't collapse? | elasticity of arterial walls |
| occurs in the aortic pressure curve when the aortic valve closes | Incisura (dicrotic notch) - the incisive bite into the aortic pressure curve, right at the beginning of isovolumic relaxation. |
| Why does the pressure drop in the dicrotic notch? | the Incisura curve is from the small backflow of blood in the aorta towards the ventricle, which closes the aortic semilunar valve at the beginning of isovolumic relaxation |
| 3 determinates of myocardial performance for the LEFT ventricle | preload, afterload, contractility |
| the end of diastolic volume; muscle tension (degree of stretch) when it begins contraction of left ventricle | preload |
| aortic pressure after left ventricle contracts | afterload |
| avg Length/avg Time = | Contractility of Left Ventricle |
| length divided by time gives | contractility of left ventricle |
| what goes in must come out | Frank-Starling |
| What does Frank-Starling law say? | Active myocardial LENGTH-tension is determined by overlapping of actin and myosin, and shifts with changes in Contractility (length/time) of left ventricle. The heart sarcomeres are set at a more contracted, overlapped stage for optimal function |
| Passive length-tension is due to ___________ of cardiac tissue | stretching |
| The heart is sensitive to ___________ (passive length-tension) so the more you do this, the harder it will squeeze out blood. | stretch! |
| Increasing ___________ provides better actin-myosin overlap, resulting in more contractile force. | Preload (the end diastolic volume; the degree of tension/stretch when L ventricle begins contraction) |
| what increases the pumping ability of the heart? | increasing the end-diastolic (stretch/tension) pressure because the heart will squeeze harder |
| The heart pumps all blood returned to it by the veins. Increasing initial fiber length causes a more forceful contraction, but does not increase ? | contractility |
| Cardiac output must be equal to | venous return!! |
| venous return must be equal to | cardiac output!! |
| In the myocardial length-tension curve (muscle attached by spring to a weight that represents blood and the 4-square plot), what is 2-3 on the graph? | systole (the top arc) |
| In the length-tension 4-square plot, what is 4-1? | diastole (the bottom arc) |
| If 2-3 is systole on 4-square length-tension plot, what is the 1-2 leading to it? | isovolumic contraction (always preceeds systole) |
| If 4-1 on the length-tension 4 square plot is diastole, what is the 3-4 leading up to it? | isovolumic relaxation (relaxation always preceeds diastole) |
| the major proportion of energy to move blood from low-pressure veins to the high-pressure arteries | External work /Volume pressure work |
| the minor proportion of energy to accelerate blood to the ejection velocity through the valves (ie joint movement) | kinetic energy of blood flow |
| In the volume pressure curve 4-square, the A-B line is the | period of filling |
| During the period of filling (A-B), the ventricle is in | diastole |
| During the period of filling (A-B), atrial pressure exceeds ventricular pressure. What happens? | the AV valve opens |
| During the period of filling (A-B), the volume of blood in the ventricle increases and the atria does what? | contracts to push the last 20% of volume through the AV valve into the ventricle |
| What is at B on vol. pressure curve? | EDV |
| At "A" on vol press curve, what happens? What happens at "B"? | A= AV valve opens, B= AV valve closes |
| What is B-C on vol press curve? | Isovolumic contraction of ventricles |
| what valve(s) closes at beginning of isovolumic contraction (B-C)? | AV and AORTIC!! (at the end of EDV so it must close). Pressure builds and finally overcomes aortic valve with preload tension. |
| In _________________(B-C), the ventricle is contracting and both the AV and Aortic valves are closed. | Isovolumic contraction |
| at what pressure during isovolumic contraction (B-C) does the ventricle systole overcome aortic pressure and open the aortic valve? | ~80mmHg |
| What is C-D on vol press curve? | Ejection! |
| During Ejection (C-D), the ventricle continues to contract, having overcome the aortic valve pressure, and ___________ pressure continues to increase. | systolic |
| During D-C Ejection as systolic ventricular pressure continues to increase, the ____________ decreases as blood is pushed into the aorta. | volume |
| When the volume decreases as blood is pushed into the aorta during ventricular systole/ejection (C-D), the amount of blood pushed is called ___________________ and is usually about 60%. | Ejection fraction |
| What is at the end of C-D ejection phase? | ESV (end systolic volume - how much was squeezed out) |
| How much blood remains in the ventricle at the end of ESV (end of C-D ejection phase of vol. press. curve)? | 40-50ml remain |
| What is D-A of vol press curve? | Isovolumic RELAXATION (the drop) |
| At the top/start of isovolumic RELAXATION (D-A) is ______ | ESV |
| The _______ valve closes in isovolumic RELAXATION (D-A) as ventricular pressure falls below ______ pressure. | aortic, aortic |
| During isovolumic RELAXATION (D-A), is there any change is volume of the ventricle? | NO!!!! nothing happens. We are relaxing. |
| At the end of isovolumic RELAXATION (D-A), there is no change in volume but there is change in pressure. First the ______ valve closed, and at the end, the ______ valve opens so the cycle can begin again. | aortic closes at top/beginning of isovolumic relaxation and the AV opens at bottom/end of i.r. so the cycle may restart. |
| Increased preload happens during | EDV |
| For contraction, _________ is considered the EDV when the ventricles are filled (ready to go!) | preload is being ready to go at EDV! |
| When is afterload? | Afterload of the ventricle is the pressure in the aorta, so it must be during C-D systole right after isovolumic contraction ends and ejection actually starts. |
| Increased sympathetic stimulation of the heart or cardiac hypertrophication (marathon training) results in an increase in ? | contractility |
| 2 methods by which the volume of blood pumped by the heart is regulated: | Frank-Starling (intrinsic), ANS (extrinsic |
| what is the intrinsic regulation of the volume of blood pumped through the heart? | Frank-Starling mechanism |
| what is the extrinsic regulation of the volume of blood pumped through the heart? | ANS controls heart RATE & STRENGTH of pumping |
| How does the heart adapt to INCREASE in volume of blood extrinsic explanation? | Frank-Starling mechanism - the greater the heart is stretched during filling, the greater the force of the contraction and volume of blood pumped into the aorta during systole |
| describe Frank-Starling mechanism | the more the ventricle stretches upon filling (due to increased blood volume), the stronger the contraction is going to be during Ejection to get it out of there. This is extrinsic regulation of volume increase. |
| Within physiological limits, the heart will pump all the blood that _________ to it, by way of the veins. | returns |
| the heart handles increases in blood volume by the extrinsic method of Frank-Starling mechanism. How does it handle increases intrinsically? | via ANS - sympathetic stimulation increases the heart RATE, increases the FORCE of contraction to get volume and pressure up during ejection. In all, ANS increases cardiac output! |
| What increases force and rate of contraction intrinsically? | ANS |
| formula for cardiac output | CO = HR x SV |
| Stroke Volume (SV) | EDV-ESV |
| To get SV, you subtract ESV from EDV. What points are these on the vol pressure curve? | EDV is point B, ESV is point D |
| ANS is both parasympathetic and sympathetic. Sympathetic intrinsically raises heart rate and force of contraction. Parasympathetic? | Vagal fibers innervating the atria decrease heart rate, decrease strength of contraction, and therefore decrease ventricular pumping. |
| What is the target of ANS sympathetics & parasympathetics? | atria |
| Changes in Cardiac Output from ANS stimulation result in both | changes in HEART RATE and changes in CONTRACTILE STRENGTH of the heart |
| How is the spontaneous SA node depolarization controlled? | Parasympathetic VAGUS using Ach as the neurotransmitter |
| What nerve and what neurotransmitter parasympathetically dominates the spontaneous SA node depolarization of the heart? | Vagus, Ach |
| Why does Ach from the Vagus slow down the spontaneous depolarization of the SA node? | muscarinic receptors so lowers heart rate via Ach |
| SA nodal areas have a large amount of ______________ so Ach is cleared rapidly. | acetylcholinesterase |
| Where does sympathetic neural regulation of the heart come from? | Sympathetic chain gang! innervates the SA node. |
| What sympathetically innervates the SA node? | Sympathetic chain gang! |
| What is the neurotransmitter of the sympathetic chain ganglia to the SA node? | Norepinephrine (remember |
| Ach from Vagus parasympathetically ______ heart rate, while NE from sympathetic chain ____ heart rate. | Ach = drops, NE = ups |
| Besides NE from sympathetic chain gang, what else can act directly on SA node to raise heart rate? | elevated temperature and Stretch! |
| Sympathetics from chain ganglia send NE to atrial SA node to increase heart rate but they also send NE to ? | AV node where NE increases conduction velocity |
| What does NE do at the SA node? at the AV node? | increases heart rate, increases conduction velocity |
| describe the excitatory & conductive system of the heart | Sinus node (SA), internodal pathways, AV node, AV Bundle, Left bundle branch, Right bundle branch |
| specialized muscle located in the superior posterolateral wall of the R atrium just below and lateral to the opening of superior vena cava | SA node |
| contains almost no contractile filaments, however connects via fibers directly with atrial muscle fibers | SA node |
| where do the action potentials that begin spontaneously in the SA node go? | atrial muscle wall |
| The heart's conduction system has what capability? | self-excitation = results in rhythmical discharge and contraction |
| what controls the heart beat rate via automatic electrical rhythmicity (self-excitation that causes discharge and contraction)? | Sinus node |
| Compared to the ventricular muscle, the SA node action potential reaches threshold at | -40mV and is set to a much less negative resting membrane potential of -55 to -60mV. The ventricular muscle fires at +20 and is set to a very negative -85 to -90mV. |
| Cell membranes of SA nodal fibers are 'leaky' to ? Why? | Na+ and Ca++ because they neurtralize intracellular negativity (remember the SA node has a much less negative resting membrane chg of -50 than does the surrounding muscle of -90) |
| What causes differences in functioning of ion Ca++ and Na+ channels in the nodal fibers, ie, they 'leak'? | the less negative resting potential of the SA node - the leakiness of Na+ and Ca++ channels insures the node won't get as negative as the ventricular muscle |
| At the threshold of ____ mV, slow Na+ and Ca++ channels open causing the action potential of the sinus nodal fiber. | -40mV |
| The inherent leakiness of the sinus nodal fibers to Na+ and Ca++ ions causes their? | self-excitation |
| at -40mV threshold, the SLOW sodium and calcium channels open! causing the AP in the sinus nodal fiber. This is slow, compared to ventricular a.p., and so is the ? | return to the resting state, as compared to ventricular muscle. |
| What makes repolarization of the SA node slower than the ventricular muscle? | K+ channels remain open a few tenths of a second longer, making the Sinus nodal fiber excessively negative/HYPERpolarized to -55 or -60mV. At this point, the K+ channels close and the action potential stops. |
| Why does the SA nodal fiber block FAST sodium channels? | The a.p. in sinus nodal fiber starts at less (-) potential and blocking the fast Na++ so it accumulates outside the node means Na++ will certainly and surely leak in slowly but steadily, resulting in a slow rise of the resting potential towards threshold. |
| If SA nodal fibers hold out on fast Na+ channels but allow slow Na+ channels to open, it can assure there will be ? | a slow, steady inward flux of Na++. Because it already started with a less neg. membrane potential, it wants to escalate slowly and repolarize slowly. Blocking fast channels of Na+ ensures the slow part. |
| At threshold of SA node a.p., what opens? | K+ channels and they stay open a little longer so that repolarization takes longer, just as slow Na+ channels allowed depolarization to take longer. |
| Unlike the SA nodal fiber which blocks fast Na+ channels, ventricular muscle is set at a stronger negative of -90mV and requires an extra push to reach threshold of +20mV. What does it use? | FAST Na+ channels cause the upstroke of the action potential from -90mV, then the SLOW Na+ channels take over and hold the plateau of the action potential. |
| We know that slow Na+/Ca++ channels allow the barely negative SA nodal fiber to slowly depolarize, and K+ channels stay open a little longer to slowly REpolarize, but what does ventricular muscle do? | Fast Na+ channels upstroke the a.p. from -90 to +20mV, and then Slow Na+ and Ca++ channels hold the PLATEAU of the a.p. until the K+ channels open even more at end of plateau, and return ventricle to resting membrane of -90mV |
| The a.p. generated in a sinus node spreads outward in specialized bands of atrial fibers: (4) | Anterior Interatrial Band, Anterior/Middle/Posterior Internodal Pathways |
| goes through anterior wall of right atrium to the left atrium (connects atria). | Anterior Inter-ATRIAL Band |
| traverses the atria and terminates in the AV node (connects node to node) | Anterior/Middle/Posterior Inter-NODAL pathways |
| The a.p. generated in a sinus node spreads outward in specialized bands of atrial fibers: (4) | Anterior Interatrial Band, Anterior/Middle/Posterior Internodal Pathways |
| goes through anterior wall of right atrium to the left atrium (connects atria). | Anterior Inter-ATRIAL Band |
| traverses the atria and terminates in the AV node (connects node to node) | Anterior/Middle/Posterior Inter-NODAL pathways |
| What is the delay for the cardiac impulse between inter-NODAL pathways? | 0.03 sec |
| Why is there a 0.03 sec delay between A/M/P inter-NODAL pathways from SA to AV node? | to allow the atria to empty blood into the ventricles before the ventricular contraction begins (systole) |
| How long is the AV node delay to the ventricle? | 0.13 sec |
| Where is the AV node? | on the posterior wall of the right ATRIUM |
| has fibers that penetrate the fibrous tissue between the atria and ventricles | AV Bundle |
| After the AV bundle is in the ventricles, it divides into R and L bundles located in the | ventricular septum |
| the AV right and left bundles are in the | ventricular septum |
| Tell me the time delay intervals from SA node | SA to AV = 0.03, AV to AV Bundle (0.09), AV bundle to left and right bundles reaching the ventricles = 0.04 so... from SA is 0.03, 0.12, 0.16 if you add them incrementally |
| What prevents the impulse from traveling backward from ventricles to atria? | ONE WAY conduction through the AV bundle |
| Why is the AV node and bundle the only form of communication between the atria and ventricles? | a fibrous (non-conductive) barrier between the atria and ventricles separates them |
| What fibers lead from the AV node in the atrium to the AV Bundle and into the ventricles? | Purkinje System |
| large diameter fibers that have high permeability at the gap junctions and can, therefore, 'instantaneously' transmit the a.p. through the ventricles | Purkinje system fibers |
| Purkinje system fibers in the AV node and bundle transmit the a.p. ___x faster than the ventricular muscle | 6x faster |
| Where do Purkinje fibers become contiguous with the ventricular muscle fibers? | 1/3 of the way into the ventricle |
| Why is the SA node the pacemaker? | because its rate of discharge is FASTER than other parts of the heart |
| What is the rate of discharge for SA node? AV node? Purkinje? | SA = 60-80/min, AV = 40-60/min, Purkinje = 15-40/min |
| a pacemaker elsewhere than the SA node | ectopic pacemaker (causes abnormal sequence of contraction and heart pumping) |
| impulse from SA node to the heart is blocked | SINOATRIAL block and the AV node or bundle becomes the pacemaker |
| impulse from atria to ventricles is blocked | AV BLOCK = atria beat normally with sinus node impulse but stops at AV so Purkinje becomes pacemaker (bad) |
| follows a sudden AV block; impulses not conducted and a delay of 5-20 sec. occurs before ventricles contract. Faints or dies. | Stokes-Adams Syndrome - some part of Purkinje system becomes pacemaker |
| What and where are parasympathetics to the heart | CN X -VAGUS goes to SA and AV nodes (uses Ach) and some to atria, even less to ventricles |
| goes mainly to sinus and AV nodes parasympathetically | Vagus fibers |
| distributed to all parts of the heart sympathetically, with strong innervations to the ventricles | Sympathetic Chain Gang |
| How does Vagus parasympathetically decrease the heart? | Ach = decreases rate and rhythm of SA node because it ups K+ permeability (hyperpolarize) and Slows transmission to ventricles by stumping atria-to-AV fibers |
| Does vagal stim have to be strong to slow the heart? | no, weak to moderate will do |
| What happens during strong (unusual) vagal stimulation? | Parasympathetic so shut down, nighty night, faint or die. See Stokes-Adams syndrome - heart beat gets spaced 5-20 sec apart and Purkinje takes over. This AV bundle/Purkinje contraction is ~30bpm and is called VENTRICULAR ESCAPE |
| ventricular escape | when vagal AV block occurs (atria to AV node blocked) and Purkinje fibers in AV bundle take over, causing 5-20 sec delay in ventricular contraction so 15-40bpm. |
| Sympathetic stimulation releases norepinephrine and increases overall heart activity 3 ways: | SA node discharge, RATE of conduction and excitability in all, increases FORCE of CONTRACTION in all cardiac muscle |
| We know vagal parasymp increases K+ permeability at SA node, hyperpolarizing it and thus dropping heart rate. NE from sympathetic chain probably? | increases permeability of Na+ and Ca++ |
| A normal ECG is composed of | waves, segments, and intervals |
| 3 major waves on a Lead I ECG: | P, QRS, T |
| P-wave | atrial depolarization |
| QRS-wave | ventricle depolarization |
| T-wave | REpolarization of ventricles |
| wave that immediately precedes atrial contraction | P-wave |
| wave that immediately precedes ventricular contraction | QRS-wave |
| on the ECG, the ventricles remain contracted until a few milliseconds after the end of the ? | T-wave (REpolarization) |
| The atria remain ____________ until they REpolarize but on an ECG, their wave is obscured by the QRS wave of ventricular depolarization | contraction |
| P-Q or P-R interval | the time between the beginning of the P wave and the beginning of the QRS complex, representing the time between the beginning of atrial depolarization and ventricular depolarization |
| Q-T interval | time from beginning of Q wave to the end of the T wave or the LENGTH OF TIME OF VENTRICULAR CONTRACTION |
| How many segments on an ECG? | 2: P-R & Q-T segments |
| the time between two successive heart beats | heart rate |
| Heart rate is timed from the beginning of one __-peak to the next ___-peak. | R-R so called the R-R Interval |
| What does an R-R interval tell us? | heart rate (the time between successive beat) |
| If the timed R-R Interval is 1.0 second, the heart rate is 60bpm. Commonly the R-R Interval is 0.83 seconds, resulting in a heart rate of? | 72bpm |
| Measure the bpm if the ECG RR Interval is 0.83 seconds | 60 sec/min so 60/.83 =72bpm |
| Each large box on ECG is ? seconds | .20 seconds large box |
| Each small box on ECG is | .04 seconds small box |
| An ECG is not the same as a single | action potential, because an a.p. is one electrical event in a single cell. An ECG is an extracellular recording representing the sum of multiple action potentials going on in many cardiac cells. |
| an extracellular recording representing the sum of action potentials of many cardiac cells | ECG |
| An ECG is an electrical 'view' of a 3-D object and provides info on heart rate, rhythm, condition of the tissues and | conduction velocity |
| standard ECG leads | 3 bipolar limb leads |
| Describe Einthoven's triangle | I: -Rarm, +Larm, II: -Rarm, +Lleg, III: -Larm, +Lleg |
| -Rarm, +Larm -Rarm, +Lleg -Larm, +Lleg | I: II: III: |
| 3 things that affect venous return: | backward pressure the right atria exerts on the vena cavas, systemic filling pressure (degree of venous pressure), Resistance which is mostly nothing between the R atria and peripheral vessels |
| What does the body use to pump the venous return to the heart? | skeletal muscles |
| When both the arterial and venous pressures come to equilibrium, all the flow of the systemic circulation stops. What is this called? | Mean systemic filling pressure |
| What is the Mean Systemic filling pressure usually in mmHg? | 7mmHg at zero |
| Venous return curve has 3 parts | Plateau, transitional zone, down slope (to mean sys filling pressure at zero) |
| Wen looking for mean systemic filling pressure for the conditions listed on the cardiac output and venous return graphs that are superimposed, how to locate point? | If it asks Mean Systemic Filling Pressure, (fails to open), go to zero and look straight up. That's your number. |
| Why would venous return curve rise? | Increased mean systemic filling pressure, Decreased resistance to venous return in active tissues |
| On the venous return curve, the black curve means? red curve? | black is normal, red is heavy exercise |
| Why does the venous return curve go up with heavy exercise? | a well conditioned heart can have the vessels themselves exert more pressure |
| Normal coronary blood flow @ rest | 225 ml/min or 4-5% of total cardiac output |
| With strenuous exercise, coronary blood flow increases ____-____x to supply the increased energy needs of the heart muscles. | 3-4x with a workout |
| If pulmonary/cardiac output is 5 L./min on the left, what is it on the right? | 5 L/min, because it is a RATE (not an amt.) There might be less volume, but it is the same rate. |
| Number 1 determinate of blood flow to heart? | Local control of blood flow to heart |
| Low O2 and high adenosine is the #1 reason that blood flow ____________ to heart. | increases |
| Too much ___________ and not enough ____________ will increase the flow of blood to heart. | adenosine, oxygen |
| What are the coronary circulation components | Left coronary artery, Right coronary artery, Coronary sinus, Anterior Cardiac Veins |
| Coronary blood flow occurs almost all the time in _________. | DIASTOLE |
| Why does coronary blood flow (to the heart itself) occur mostly in diastole? | there is more time for blood to get to the heart during diastole |
| Decreased heart activity (ie, sickness or sedentary lifestyle) is accompanied by ____________ coronary flow. | decreased |
| A well conditioned heart has the best | blood supply |
| Parasympathetic activity ____________ blood vessels but ____________ the coronary arteries because there is a DECREASE in metabolic rate. | dilates blood vessels, constricts coronary arteries (trumps sympathetic, which does the opposite) |
| rules of blood flow are called | hemodynamics |
| what has the largest cross sectional area allowing for nutrient and waste exchange? | Capillaries~ |
| What has the fastest velocity of blood flow (1000x faster than the flow in a capillary)? | Aorta! |
| streamlined or concentric circle pattern of silent blood flow is called ________flow. | Laminar |
| Blood pressure is related to _______ & ___________. | flow and resistance |
| What are the two components of blood pressure and what Law measures them? | flow and resistance, Ohm's Law |
| When the relationship between Radius and anything about a vessel is mentioned, use? | Poiseuille's Law |
| Poiseuille's Law examines the relationship between vessel length, viscosity of blood, and the __________(clue!) of the vessel. | RADIUS = Poiseuilles |
| In laminar blood flow, blood streamlines or flows in concentric rings. Where is the flow the fastest? | center! |
| In laminar blood flow, each layer of blood remains the same _______ from the blood vessel wall. | distance |
| The parabolic curve means that laminar blood flow center is faster because the wall of the blood vessel is _________. | sticky |
| Turbulent blood flow results in? | sounds |
| Eddy currents or whorls in blood vessels create greater resistance and friction in flow of blood. What is the result of this friction or resistance? | murmurs or bruits |
| murmurs are found in the | heart |
| bruits are found in the | vessel |
| turbulent flow is | noisy |
| laminar flow is | silent |
| flow and resistance in blood vessels is measured by | Ohm's Law = calculates the blood flow through the vessel |
| Ohm's Law | Pressure @ end - Pressure @ start / Resistance |
| difference in the pressure at the end and the pressure at the start, divided by the resistance is | Ohm's law = calculates blood flow through the vessel |
| bp 130 mmHg, 0 bp at beginning, 3.5 output Liters/min | 130mmHg - 0 mmHg / 3.5 L per min = 37.14 flow |
| Flow is blood flow and is measured in ml/min. Normall blood flow in TOTAL circulation is equal to the ______________. Measured by Doppler ultrasound. | cardiac output. TOTAL flow = Cardiac output |
| R is Resistance. Increase in resistance equals a ____________ in blood flow. | decrease |
| longer and smaller vessels combined with more viscous blood does what? | increases resistance |
| Draw the vessel __________ with Poiseuille's law; if it goes big to little in size, then the resistance went up! | radius = Poiseuille |
| If the radius increases in vessel size, then when choosing an answer for Poiseuille's law, pick the answer that flow goes ? | up |
| Flow is proportional to | radius to the 4th power |
| radius to the 4th power is proportional to | flow |
| longer and smaller vessels combined with more viscous blood does what? | increases resistance |
| Draw the vessel __________ with Poiseuille's law; if it goes big to little in size, then the resistance went up! | radius = Poiseuille |
| If the radius increases in vessel size, then when choosing an answer for Poiseuille's law, pick the answer that flow goes ? | up |
| Flow is proportional to | radius to the 4th power |
| radius to the 4th power is proportional to | flow |
| what is the reciprocal of resistance? | conductance/flow so 1/r to the 4th power, where r is the radius or the diameter of the vessel. |
| 2 types of blood flow control | local control and long term regulation |
| local control is determined by | tissue needs, neural control and hormonal control |
| 2 basic theories of local control: | vasodilator theory and oxy/nut-lack theory |
| In the local control vasodilator theory, ____________ are released, which DECREASES resistance and thereby increases blood flow | paracrines |
| name some vasodilators that would increase blood flow by decreasing resistance | CO2, Adenosine, Substance P, Nitric Oxide, Histamine, Leukotrienes, H, K, Lactic Acid, AMP/ADP .......all paracrines for local control vasodilator theory. |
| Local control vasodilator theory states that paracrines like NO and adenosine will lower resistance and then increase blood flow (they are inversely proportional). What do vasoconstrictor substances do locally? | increase peristalsis in intestines (serotonin) and decrease blood flow because they increase resistance. |
| Name some common vasoconstrictors that would decrease blood flow by increasing resistance? | Serotonin, NE, Epi, Angiotensin II, Vasopressin (ADH), Endothelin |
| In the oxygen/nutrient Lack Theory, because Oxygen is required for vascular sphincter muscle contraction, depriving the muscle of Oxygen results in | sphincter relaxing and therefore dilating |
| How does the Kidney control blood flow? | Renin-Angiotensin system (we know angiotensin II is a vasoconstrictor so renin must be the vasodilator) |
| Blood flow is determined by tissue needs and is controlled by hormones (paracrine vasodilators like N.O. and ADH/vasopressin), neurally (serotonin, NE, Epi), and by the Kidney via Renin-Angiotensin system. Last thing that controls long term blood flow is | change in the size and number of vessels - Angiogenesis |
| Why would angiogenesis be considered long term blood flow control? | because it takes awhile to grow vessels |
| vascular endothelial growth factor, fibroblast growth factor and Angiogenin are all | long term regulation of blood flow control through angiogenesis |
| increased blood flow due to increased metabolic activity is called | hyperemia |
| why would absence of oxygen cause an increase in blood flow/hyperemia? | absence of oxygen causes blood vessel muscle sphincters to relax and therefore dilate (remember ammonia cokes? yeah, that's how they got rid of headaches) |
| hyperemia due to lack of oxygen and therefore increased blood flow, increased CO2 and other metabolites, is an example of | active response |
| hyperemia due to the build of paracrines like NO, K, H, CO2, substance p, adenosine, bradykinins and histamines will wash away these extra vasodilators - this returns arteriole to normal radius and is called | REactive hyperemia response |
| Hyperemia is increased blood flow due to | metabolic activity |
| When increased arterial pressure becomes too great providing increased Ox and nutrients, it leads to arteriole __________ to decrease arteriole pressure | constriction = metabolic theory is too many nutrients and too much Ox causes arteriole constriction. Decreases pressure |
| Increased arteriole pressure may not only provide too many Ox and nutrients, but stretch the smooth muscle and cause the arteriole to __________. This is the myogenic theory of autoregulation of local pressure. | contract = myogenic theory is smooth muscle stretch (as in stomach filling) causes contraction and therefore arteriole constriction. Decreases pressure |
| what kind of circulation serves all tissues except the lungs? | systemic/peripheral circulation |
| systemic/peripheral circulation serves all tissue except the lungs and contains ___% of blood volume. | 84% is systemic |
| circulation that serves the lungs only (16%) of all blood volume | Cardio-pulmonary |
| where is the majority of the systemic/peripheral circulation most of the time | in the veins (64%) |
| 64.13.7 | systemic percents: 64% veins, 13% arteries, 7% arterioles/capillaries |
| In the meager 16% of cardio-pulmonary circulation for the lungs, where is the blood? | Pulmonary vessels 9% and heart is lucky 7% |
| what is vascular compliance? | the idea that the veins have the largest percent of blood because the size of the lumen is almost equal to the size of the vessel |
| Veins function as a __________ for blood | reservoir (64%) |
| how does venous blood return to the heart? | skeletal muscles pump, respiratory pump, sympathetic nerve supply |
| what prevents backflow in veins | valves, especially in the legs |
| which of the three ways venous blood returns to the heart (skeletal, respiratory, sympathetic nerve) does not function when we sit? | muscle |
| the pressure in the RIGHT atria is equal to | the CENTRAL VENOUS PRESSURE (normally low number near 0 up to +4mmHg) |
| Pressure in the chest or abdomen can lead to reduced blood return and an __________- in venous pressure | increase in venous pressure, resulting in varicose veins of legs |
| arteries have low ___________: this is the reason you can measure blood pressure | compliance |
| M.A.P. | Mean Arterial Pressure is 2/3 diastolic and 1/3 systolic squeeze |
| Which has higher pressure, aorta or large arteries? | larger arteries branching from aorta |
| causes of increased pulse pressure | increased stroke volume decreased arterial compliance (shrinking space) |
| how is blood pressure taken? | systolic and diastolic indirectly via ascultatory method |
| cuff inflation beyond 120mmHg occludes the | brachial artery |
| the audible event when blood pressure cuff pressure is released | turbulence from blood on heart side of cuff slamming into downstream blood = KOROTKOFF sounds |
| All blood vessels are supplied by sympathetic nerves except | capillaries and precap sphincters |
| peripheral vasculature exits the sympathetic chain ganglia and travels with the | spinal nerve |
| All blood vessels are supplied by ___________ nerves and the central nervous system control is via the ___________center. | sympathetic, vasomotor |
| where is the vasomotor center of the brain | reticular area of medulla and lower pons on both sides |
| Which cranial nerves send sensory input afferents to vasomotor system? | Glossopharyngeal and Vagus (IX, X) |
| The vasoconstrictor area (Mr. Sympathetic) sends sympathetic pregangs to cord of lateral horn from T1-L2. These VASOCONSTRICTOR efferents maintain | vasomotor tone |
| VASODILATOR efferents project up to vasoconstrictor area and | turn OFF constriction |
| increases heart rate/contract, uses sympathetic efferents and EXCITES heart - which vasomotor am I? | lateral and superior vasomotor |
| decreases heart contraction and rate via the motor nucleus of VAGUS so inhibits - which vasomotor am i? | medial and inferior (the quiet, low center of X) |
| baroreceptors ________ arterial pressure. | decrease in response to high BP, like when the tiger finally leaves the room. Bars the door. |
| chemoreceptors increase arterial pressure when they detect situations like | low Ox or the presence of CO2 (when you are dying) Chemicals like to get you high so raise the pressure! |
| at what mmHg is the baroreceptor most sensitive? | 100 |
| chemoreceptors only raise your blood pressure if it drops below | 80 |
| What nerve is excited by a baroreceptor? | Vagus |
| What nerve drops down off Glossopharyngeal? | Hering's nerve |
| baroreceptors are found on the carotid ______ and aortic arch. | sinus (sinus pressure is from anger so when Baroreceptors detect your bp is rising, they inhibit the vasoconstrictor center, contact the VAGUS and decrease arterial resistance, lowering your bp. They bar the door after the tiger leaves the room. |
| carotid sinus has | baroreceptors |
| carotid body has | chemoreceptors |
| body chemistry | carotid body chemoreceptors |
| BullShit, it's Body Chemistry when we both stand under the Arches. | Baroreceptors Sinus, Body Chemoreceptor, both are in aortic Arches |
| which nerve goes to carotid sinus? | glossopharyngeal via hering's (B.S.! baroreceptors sinus) |
| which nerve goes to carotid body? | X (Body Chemistry is Body Chemoreceptors) |
| Baroreceptors are found on the aortic arch and in the carotid sinus - when do they increase fire? | when bp high, although they will reset in 1-2 days of sustained new pressure to allow for 'drift' |
| gravity causing blood to pool in lower extremities | orthostatic hyPOtension |
| when do baroreceptors function? | when changing position from lying to sitting or standing |
| when the carotid sinus and aortic arch receptors decrease the rate of firing, an increase in ____________ activity results | sympathetic (baroreceptors decrease rate of firing and this jacks sympathetics) |
| when carotid sinus and aortic arch receptors decrease rate of firing, what happens to the heart? | increases! vasoconstriction, increased blood pressure |
| If blood pressure falls, such as in hypovolaemic shock, baroreceptor firing rate ____________. Signals from the carotid baroreceptors are sent via the glossopharyngeal nerve (cranial nerve IX). | DECREASES. Signals from the aortic baroreceptors travel through the vagus nerve (cranial nerve X) |
| The ____________reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure.[1] Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions. | Bainbridge |
| Increased blood volume is detected by _____________ receptors located in both atria at the venoatrial junctions. | stretch receptors at ventroatrial jxn = Bainbridge |
| The Bainbridge reflex and the baroreceptor reflex act antagonistically to control heart rate. The baroreceptor reflex acts to increase heart rate when blood pressure drops. | The bainbridge reflex explains why increased blood pressure increases the heart rate |
| when blood volume increases, what increases with it, due to the Bainbridge effect? | pressure! |
| where are RECEPTORS FOR BLOOD VOLUME increases? | atria and pulmonary arteries |
| An increase in blood volume impacts the kidneys: | increases glomerulus filtration rate, increases Na+ and water loss in urine (to drop blood volume) |
| An increase in blood volume makes the kidneys work by upping glomeruli action, sloughing Na+ and water out via the urine, and by telling the HYPOTHALAMUS to ? | decrease ADH secretion (increases water loss with less ADH) |
| what response explains organ failure when blood lacks oxygen? | CNS ischemic response |
| the lack of blood to the brain (hence O2) increases the concentration of CO2. What is stimulated? | chemoreceptors! CO2 is a vasoconstrictor and the chemoreceptors tell the vessels to dilate!! dilate!! dilate!! |
| the CNS ischemic response is only activated betlow 60mmHg blood pressure - when is the last ditch stand? | between 15-20mmHg |
| the CNS ischemic response can cause organ failure (if you aren't already pretty much dead at 15-20mmHg bp) by | causing such a great vasoconstriction that it occludes some blood vessels (ie, kidney) and cause organ failure |
| special CNS ischemic response | Cushing reaction |
| caused by an increase in CSF pressure when CSF pressure exceeds arteriral blood pressure in the brain and the blood vessels are occluded | Cushing reaction is CSF trumps meninges |
| when CNS ischemic response causes increased brain blood pressure to offset CSF pressure | Cushing reaction |
Created by:
hecutler
Popular Chiropractic sets