Term
|
Definition
| right arm (-) compared with left leg (+). almost parallel to heart. most important lead. |
|
|
Term
|
Definition
| right arm (-) compared with left arm (+) |
|
|
Term
|
Definition
| left arm (-) compared with left leg (+) |
|
|
Term
| what determines whether a deflection is positive or negative? |
|
Definition
| depolarization towards the + pole will give a + deflection. waves away from + pole give a - deflection. waves perpendicular to the bipolar lead axis give no deflection. |
|
|
Term
|
Definition
| augmented unipolar lead for the right arm (+). only one to have a - deflection on ECG bc depol is moving to the R |
|
|
Term
|
Definition
| augmented unipolar lead for the left arm (+). positive deflection on ECG |
|
|
Term
|
Definition
| augmented unipolar lead for the left leg (+). positive deflection on ECG. |
|
|
Term
| what is mean electrical axis? |
|
Definition
| the mean direction of electrical force during ventricular depolarization. It's a useful tool for IDing conduction probs or ventricular enlargements. |
|
|
Term
| What is the quickest way to ID the main axis of depolarization? |
|
Definition
| Examine the QRS complexes from limb leads I and II. If they are primarily positive, then that's normal. |
|
|
Term
| What is the 2nd quickest way to ID a normal axis of depolarization? |
|
Definition
| Find the Mean Electrical Axis using the Isoelectric Lead System. |
|
|
Term
| Describe the isoelectric lead system |
|
Definition
| Find the 1 lead (out of the 6) with a QRS deflection that adds up to 0. This is your isoelectric lead. The MEA is the lead perpendicular to the isoelectric lead. Now look at the ECG of the MEA lead. The QRS deflection tells you to choose the positive or negative MEA value. |
|
|
Term
| What do you do once you have an MEA? |
|
Definition
| Compare the value to the normal range of that species. |
|
|
Term
| Deviation of the MEA to the left means: |
|
Definition
| left anterior fascicular block or left ventricular hypertrophy. This is an MEA less than 40 in a dog. |
|
|
Term
| Deviation of the MEA to the right means: |
|
Definition
| (greater than 100 in dogs). Right ventricular hypertrophy, acute right heart strain, left posterior fascicular block |
|
|
Term
| what does the P-R interval tell you? |
|
Definition
| the time required for conduction of the impulse from the atria through the AV node. |
|
|
Term
| what does the QRS duration tell you? |
|
Definition
| time required for ventricular depolarization. |
|
|
Term
| what does the Q-T interval tell you? |
|
Definition
| time required for one full cycle of ventricular depolarization-repolarization. It varies with HR |
|
|
Term
| what does the R-R interval tell you? |
|
Definition
| measures heart rate. 1/Xms*60000ms/min = bpm |
|
|
Term
| what does the sympathetic nervous system do to the heart? (include receptors, etc.) |
|
Definition
| catecholamines (NE) activate beta-1 adrenergic receptors on the SA node. This increases prob of funny Na and Ca channels to open, increasing HR. (TACHYCARDIA) |
|
|
Term
| what does the parasympathetic nervous system do to the heart? |
|
Definition
| cholinergics (Ach) released from PaSYM terminals bind to muscarinic receptors on SA node and reduce prob of Na channels opening, decreasing HR. A G protein is also activated that increases K conductance. BRADYCARDIA |
|
|
Term
| what 3 variables determine pacemaker cell firing rate? |
|
Definition
1. rate of phase 4 spontaneous depolarization
2. max neg diastolic pressure
3. threshold potential |
|
|
Term
| list the 2 main division of the circulatory system |
|
Definition
|
|
Term
| list the 4 components of the circulatory system |
|
Definition
| a pump, the distribution system, exchange region, and collection system |
|
|
Term
| list the valves the the blood passes through in order |
|
Definition
| systemic > RA > tricuspid valve > RV > pulmonic valve > lungs > LA > mitral valve > LV > aortic valve > body |
|
|
Term
| blood pressure, HR, and heart contractility are primarily regulated by what |
|
Definition
| the autonomic nervous system and specific hormonal systems |
|
|
Term
| what is the PaSYM preganglionic location, postgang location, and NT released? |
|
Definition
pre= brainstem and sacral SC (Ach)
post= close to target tissue (Ach)
muscarinic receptors |
|
|
Term
| what is the sympathetic preganglionic location, postgang location, and NT released? |
|
Definition
pre= SC @ T1-L3 (Ach)
post= sympathetic chain or specific aggregations of postgang cells (NE).
alpha or beta adrenoceptors |
|
|
Term
| name the hormones of particular importance to the cardio system |
|
Definition
| renin-angiotensin-aldosterone system (RAAS), vasopressin (ADH), epinephrine |
|
|
Term
|
Definition
| the volume of blood that moves past a particular point in the cardiovascular system per unit time (e.g. 2.5 L/min in a dog) |
|
|
Term
| what determines blood flow? |
|
Definition
| blood pressure and the resistance to flow |
|
|
Term
| name 2 factors that contribute to changes in pressure throughout the cardio system |
|
Definition
1. frictional forces generated as blood moves through vessel walls
2. vessel diameter and length |
|
|
Term
| what is the formula for flow? |
|
Definition
F = (P1-P2)/R
where P1= pressure @ beg of tube and P2= end |
|
|
Term
|
Definition
| the contraction of the heart chambers |
|
|
Term
|
Definition
| the period of relaxation following muscle contaction |
|
|
Term
| list the unique characteristics of myocardial cells |
|
Definition
1. intercalated disks with gap jxns (allows for electrical coupling).
2. way longer APs than skeletal m.
3. pacemaker cells and their spontaneous depolarizations |
|
|
Term
| what is the significance of electrical coupling? |
|
Definition
| rapid impulse conduction and depolarization across the myocardium |
|
|
Term
| what contributes to the myocardial RMP? |
|
Definition
| the high permeability of K+ and low permeability of Na+ and Ca++. This means K+ is high inside (from the neg proteins in the cell and Na+/K+ pump) |
|
|
Term
| what is the RMP of a cardiac myocyte and why is it diff't from neurons? |
|
Definition
| -90 mV (vs -65) because at rest, neurons are about 5x more permeable to Na+ |
|
|
Term
| what are the effects of extracelluar changes in K+, Na+, and Ca++ on myocyte RMP? |
|
Definition
| increases in extracellular K+ will depolarize the cell, where extracellular changes in Na+ and Ca++ have little effect. |
|
|
Term
| why are myocardial APs so long? |
|
Definition
| a large influx of Ca++ during depolarization (Ca++ channels (L-type) are just slow, not stupid). |
|
|
Term
| what are the 2 types of APs and where do they occur? |
|
Definition
1. fast response AP- atrial and ventricular myocytes and Purkinje fibers
2. slow response AP- observed in pacemaker cells of SA and AV node |
|
|
Term
| describe fast-response AP: phase 0 |
|
Definition
| rapid depolarization. fast type Na channels open in response to pacemaker depol. The concentration gradient and negatively charged cell draw Na inside. |
|
|
Term
| describe fast-response AP: phase 1 |
|
Definition
| transient repolarization. Na+ channels quickly shut off and a transient outward K+ current is also activated by the depol. |
|
|
Term
| describe fast-response AP: phase 2 |
|
Definition
| plateau phase. Ca++ channels open @ -35mV. Ca++ flows in bc of conc diffs. Excitation-contraction coupling. K+ conductance low. Ca++ spontaneously close (slowly). |
|
|
Term
| what is "excitation-contraction coupling"? |
|
Definition
| when Ca++ moves into the cell and translates the membrane depolarization into force production |
|
|
Term
| describe fast-response AP: phase 3 |
|
Definition
| rapid repolarazation. K+ conductance increases (due to delayed rectifier) and drives it to leave cell which hyperpolarizes/repolarizes it. All other channels are closed at this time and cell returns to RMP. |
|
|
Term
| describe fast-response AP: phase 4 |
|
Definition
| RMP. dependent on high K+ ONLY. low Na+ and Ca++ (corrected with Na+/K+ pump and Na+/Ca++ exchanger. |
|
|
Term
| draw a fast-type cardiac AP |
|
Definition
|
|
Term
| what is the significance of the extremely long refractory period? |
|
Definition
| to allow for adequate cardiac filling time and sufficient time for Ca++ reuptake into intracelluar stores. |
|
|
Term
| describe the absolute or effective refractory period vs. the relative refractory period. |
|
Definition
the absolute or effective refractory period (EFP) occurs during phases 1-3 of the fast-type AP. At 1-2, another AP is impossible. At 3 and AP can be locally stimulated but there is no propagation.
the relative refractory period occurs at phase 3 (repol). AP is possible but slower and may not effectively depol rest of heart. |
|
|
Term
| what triggers the funny Na+ channels? |
|
Definition
| it's activated by hyperpolarization and closed during repolarization. This is the opposite of typical fast-type Na+ channel |
|
|
Term
| describe slow-type AP: phase 4 |
|
Definition
| RMP is marked by a slow spontaneous depolarization due to influx of Na+ thru funny channels. They open @ end of phase 3 when heart is returning to its hyperpolarized state. Eventually threshold is reached and AP is generated. |
|
|
Term
| do pacemaker cells have fast-type Na+ channels? |
|
Definition
| yes, but the persistent, less neg. RMP causes them to remain inactivated. |
|
|
Term
| what is the behavior of K+ and Na+ during spontaneous depolarization? |
|
Definition
| K+ channels begin to close (decrease in conductance) and Na+ has an increase in conductance. |
|
|
Term
| describe slow-type AP: phase 0 |
|
Definition
| Slow AP depolarization. Ca++ influx!! no rapid upswing bc fast Na+ channels are inactivated. depol beyond -50 mV inactivates funny channels and Na+ conductance drops until membrane is again hyperpolarized. |
|
|
Term
| describe slow-type AP: phase 1 |
|
Definition
|
|
Term
| describe slow-type AP: phase 2 |
|
Definition
| ABSENT (no plateau sustained) |
|
|
Term
| describe slow-type AP: phase 3 |
|
Definition
| slow repolarization. as Ca++ closes spontaneously, Na+ conductance remains low. The delayed rectifier K+ chnl is activated by the Ca++ induced depol and there is a corresponding increase in K+, which repolarizes the membrane potential. |
|
|
Term
| what is conduction velocity and what affects it? AV node speed? purkinje? |
|
Definition
| the speed at which APs propagate from 1 area to another. it is dependent on the diameter of the muscle fiber involved. small AV node fibers= slow. fat purkinje fibers = fast. |
|
|
Term
| describe atrial conduction |
|
Definition
| originates in SA node. Bachmann's bundle conducts impulse from RA to LA so they both contract almost simultaneously. atrial cells have a shorter duration AP than ventricular cells. Atrial cells are connected to ventricular cells thru the AV node ONLY. |
|
|
Term
|
Definition
| slow-type APs, and even slower than the SA node. called the "latent pacemaker" because it can take over the SA node if needed, just more slowly. |
|
|
Term
| what is the significance of the slow AV node conductance? |
|
Definition
| AV node to the Bundle of His is slow so that atria can finish contraction and fill the ventricles before they depolarize. |
|
|
Term
| describe ventricular conduction |
|
Definition
| wave of depol: AV node > Bundle of His > L bundle branches > R bundle branches > Purkinje fibers. Papillary muscles and IV septum depol and contract 1st to anchor AV valves during ventricular systole. |
|
|
Term
| what are some unique features of Purkinje fibers? |
|
Definition
1. large diameter, fast conduction velocity.
2. longer duration plateau Phase 2 to protect ventricles from premature subsequent contraction |
|
|
Term
| describe the refractory period in pacemaker cells and what is its significance? |
|
Definition
it outlasts the duration of the AP. APs elicited too early are smaller in amplitude, more gradual in rate.
It's particularly important in the AV node so that retrograde excitation from ventricular mm. don't pass back into the atrium. |
|
|
Term
| what is the pacemaker hierarchy? |
|
Definition
| SA (fastest) > AV > His-Purkinje system (so slow that it may be incompatible with life) |
|
|
Term
| what are the 3 classifications of arrhthmias? |
|
Definition
1. abnormal rhythm in SA node
2. ectopic pacemaker
3. blockade of normal conduction pathway |
|
|
Term
| describe ectopic pacemakers |
|
Definition
| aka premature beat. happens when a latent pacemaker develops an intrinsic rate of depolarization faster than the SA node. high catecholamine concentrations can do this. |
|
|
Term
| what physiologic conditions may prompt an ectopic pacemaker? |
|
Definition
| high catecholamine concentrations, hypoxemia, ischemia and electrolyte disturbances, certain drug toxicities. damage to cardiac tissue can also do this because the cells become leaky and cannot maintain normal neg. RMP and initiate depol during diastole, before SA discharge |
|
|
Term
| what is the result of ectopic pacemakers? |
|
Definition
| they generate phase 4 depolarization, independent of SA node discharge, and spread the depol to other cells prematurely. |
|
|
Term
|
Definition
| reentry is an altered impulse conduction that occurs when the electrical impulse that normally activates cardiac tissue returns by a DIFFERENT pathway to REACTIVATE the same tissue that was just depolarized. |
|
|
Term
| what is the probable mechanism underlying the majority of tachyarrythmias? |
|
Definition
|
|
Term
| under what conditions might reentry occur? |
|
Definition
1. if the AP conduction through cardiac tissue is blocked unidirectionally (the unexcited tissue is then available to retrograde excitation)
2. conduction thru the damaged tissue is slowed in the opposite direction. this forms the reentrant loop |
|
|
Term
| what is bradyarrythmia and what defect can cause it? |
|
Definition
abnormally slow rhythm with abnormal ECG wave structure.
AV node blockade (1st, 2nd, and 3rd degrees). |
|
|
Term
| what is an AV node blockage in general terms, and what part of the ECG helps to characterize it? |
|
Definition
| disturbance of the AV node conduction or bundle of His (i.e. from atria to ventricles). the precise location cannot be IDed in ECG alone but the P-R interval helps to characterize the block. |
|
|
Term
| First-degree AV blockade: describe and ECG character |
|
Definition
| least severe. can be from certain drugs or age. prolongation of P-R interval. usually benign. |
|
|
Term
| Second-degree AV blockade: describe and ECG character |
|
Definition
| intermittent failure of AV node conduction. ECG: 1 or more P waves are not followed by QRS complexes (irregular, occasionally missing QRS) characterized by slower ventricular rate than atrial rate. happens with increased PaSYM activity or hypothyroidism. |
|
|
Term
| third-degree AV blockade/ complete AV blockade: describe and ECG character |
|
Definition
A complete block of AV conduction. atria and ventricles are electrically uncoupled. sever drug toxicity, chronic degeneration, myocardial infarction.
no relationship between P waves and QRS complexes. QRS complexes are wide and bizarre. typically SA node fires and escape rhythms depol ventricles. ventricular rate is slower than atrial. |
|
|
Term
| what kind of arrhythmia is an atrial premature beat? |
|
Definition
| tachyarrythmia. It's an ectopic pacemaker |
|
|
Term
| how do you recognize atrial premature beats? |
|
Definition
| an earlier-than-expected P wave with an abnormal shape. p waves may not be followed by a QRS complex. typically arises from ectopic foci in atria. |
|
|
Term
| what kind of arrhythmia is atrial fibrillation? |
|
Definition
|
|
Term
| describe atrial fibrillation (physiologic characteristics and ECG) |
|
Definition
chaotic rhythm in atria. associated with an increased ventricular rate, which reduces ventricular filling time and cardiac output.
loss of discernible P waves. Ventricular rate is rapid and irregular. QRS can be normal or widened. |
|
|
Term
| what kind of arrhythmia is a premature ventricular beat? |
|
Definition
|
|
Term
| describe premature ventricular beats |
|
Definition
| arises from ectopic foci. QRS is wider than normal, with no preceding P wave. P waves are normal, just not associated with QRS. HR is normal, but with irregular rhythm. |
|
|
Term
| describe ventricular tachcardia |
|
Definition
| wide QRS complex with multiple shapes. P waves, if discernible, are normal. |
|
|
Term
| what kind of arrhythmia is ventricular fibrillation? |
|
Definition
| tachyarrhythmia. the most life-threatening. |
|
|
Term
| describe ventricular fibrillation. |
|
Definition
disordered, rapid stimulation of ventricles. prevents coordinated ejection, leading to drop in cardiac output. immidiate defib must happen.
ECG is chaotic and irregular with no discreet QRS wave. |
|
|
Term
| how do you treat bradyarrhythmias? |
|
Definition
1. anticholinergics (muscarininc receptor antagonists)
2. beta-1 receptor agonists (increases AV node speed, SA rate)
3. electronic pacemaker |
|
|
Term
| how do you treat tachyarrythmias? |
|
Definition
1. beta-1 antagonists
2. cholinergic (muscarinic) agonists
3. Na channel blockers
4. Ca channel blockers |
|
|
Term
| what is the main intracellular reservoir of Ca? |
|
Definition
| sarcoplasmic reticulum. (surrounds each sarcomere) |
|
|
Term
| what is Ca++ triggered Ca++ release? |
|
Definition
| extracellular Ca influx from depolarization triggers the release of intracellular Ca stores from the SR. it converts the electrical impulse to sarcomere shortening. |
|
|
Term
| what is the significance of having graded Ca++ release from the SR? |
|
Definition
| it can change force production based on the amount of Ca released. (only about half the myosin heads are activated at resting HR) |
|
|
Term
| what is systole? (describe on the level of inside the muscle cell) |
|
Definition
| sarcomere shortening. intracellular Ca binds to troponin, which unblocks active sites on the actin molecule. myosin then binds to actin, changes shape, shortens sarcomere, and then releases for another attachment. |
|
|
Term
| what is diastole? describe on an intracellular level |
|
Definition
| relaxation. Ca stops entering cell when chnls close. Ca is then removed from the cytoplasm (back into stores and xtracell). the Ca-ATPase pump on SR membrane takes in ~80% intracellular Ca. |
|
|
Term
| what regulates the SR Ca pump? |
|
Definition
| phospholambin (PL) gets phosphorylated and increases Ca reuptake. |
|
|
Term
| what percent of the total intracellular Ca gets expelled to extracellular space and how? |
|
Definition
| 20%. 5% from CaATPase on sarcolemma and 15% via NA/Ca exchanger |
|
|
Term
| what modulates excitation-contraction coupling? |
|
Definition
| amount of intracellular Ca (which modulates the amount of active myosin heads) |
|
|
Term
| name 4 methods of modulating myocardial force |
|
Definition
1. increased extracellular Ca
2. time-dependent accumulation of intracellular Ca (during increased HR)
3. decreased extracellular Na
4. increased intracellular Na |
|
|
Term
|
Definition
| it's a drug given during heart failure to increase contractile force. it inhibits Na/K pump. this increases intracellular Na and reduces the conc gradient for Na/Ca exchanger |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| list the 4 basic steps in the pumping process |
|
Definition
1. ventricular filling
2. ventricular contraction
3. ventricular ejection
4. ventricular relaxation |
|
|
Term
| formula for cardiac cycle |
|
Definition
|
|
Term
| when are the AV valves open? |
|
Definition
| atrial systole and ventricular diastole (they're close vice versa) |
|
|
Term
| know the 7 phases of the cardiac cycle |
|
Definition
1. atrial systole
2. isovolumic ventricular contraction
3. rapid ventricular ejection
4. reduced ventricular ejection
5. isovolumic relaxation
6. rapid filling
7. reduced filling |
|
|
Term
| what occurs during reduced filling of the cardiac cycle? |
|
Definition
| aka diastasis. isoelectric until right before P wave. |
|
|
Term
| what occurs during atrial systole of the cardiac cycle? |
|
Definition
P wave on ECG.
"a" wave, in increase in pressure in atrial contraction. |
|
|
Term
| what occurs during isovolumic contraction of the cardiac cycle? |
|
Definition
QRS complex
"c" wave= small pressure wave in atrium when AV ring rises and valve leaflets bulge upward into atrium.
no volume change in LV yet! |
|
|
Term
| what occurs during rapid ventricular ejection of the cardiac cycle? |
|
Definition
ECG=isoelectric as the entire heart become depolarized
blood ejected from ventricles
AV valves closed |
|
|
Term
| what occurs during reduced ejection of the cardiac cycle? |
|
Definition
ECG: T wave
pressure and volume in LV are slowly decling
LA atria pressure increasing |
|
|
Term
| what is ejection fraction (EF)? |
|
Definition
that fraction of the end diastolic volume (EDV) which was ejected during systole.
EF=(EDV-ESV)/EDV or stoke vol/EDV
normally 50-60% |
|
|
Term
| what occurs during isovolumic relaxtion of the cardiac cycle? |
|
Definition
ECG is isoelectric
"v" wave=peak pressure in LA
dichrotic notch in aortic pressure followed by slow fall |
|
|
Term
| what occurs during rapid filling of the cardiac cycle? |
|
Definition
ECG is isoelectric
mitral valve opens and blood enters LV |
|
|
Term
| describe the 1st heart sound (S1) |
|
Definition
| it coincides with the onset of ventricular systole and the closing of the AV valves and the C wave. ISOVOLUMIC PERIOD! (it's the louder, longer, lower sound) |
|
|
Term
| describe the second heart sound (S2) |
|
Definition
a high frequency, shorter duration sounds that coincides with muscular relaxation, closure of the semilunar valves, and blood vibration in the great vessels as backflow into ventricles is prevented by the recently closed valves.
splitting of 2nd heart sound during inspiration! |
|
|
Term
| why is there an audible splitting of the 2nd heart sound? |
|
Definition
| during inspiration only, there is increased venous return and prolongation of RV ejection. Thus, the semilunar closes slightly faster on the L side since the R side is taking a little longer to push out more blood. |
|
|
Term
| describe the 3rd heart sound (S3) |
|
Definition
| it's generated by rapid ventricular filling during early diastole. typically not heard. caused by the deceleration of blood flowing into ventricles. more compliant ventricle=quieter sound. loudness could mean heart failure |
|
|
Term
| describe the fourth heart sound (s4) |
|
Definition
| coincides with atrial systole. may be heard in horses only. |
|
|
Term
| define insufficient valve |
|
Definition
| leaky, causes regurg (dysplasia) |
|
|
Term
|
Definition
| narrowed. most commonly in semilunar valves. |
|
|
Term
| list some general characteristics of aortic stenosis |
|
Definition
| causes systolic heart murmur. pressure req'd to eject bld into aorta is higher than normal and aortic P rises slower than normal. assoc with ventricular hypertrophy. |
|
|
Term
| describe mitral insufficiency |
|
Definition
| causes systolic heart murmur. some blood regurges from LV into LA during systole. LA pressure is raised and LV diastolic volume and pressure increase. causes pulmonary hypertension. |
|
|
Term
| describe aortic insufficiency |
|
Definition
| blood regurges from aorta back into ventricle during diastole. causes large pulse pressure since aortic pressure drops so fast. |
|
|
Term
|
Definition
| diastolic murmur is heard in association with turbulent flow through the stenotic mitral valve. this causes backup and pulmonary congestion and shortness of breath. |
|
|
Term
| list the systolic and diastolic heart murmurs |
|
Definition
diastolic= aortic insufficiency and mitral stenosis
systolic= aortic stenosis and mitral insufficiency |
|
|
Term
| what is cardiac output? define and give formula |
|
Definition
| the amount og blood pumped by the heart per minute. CO= stroke volume (L/beat)*HR (bpm) |
|
|
Term
|
Definition
| mechanisms that alter the relaxation rate of myocardial muscle |
|
|
Term
|
Definition
| mechanisms underlying changes in heart rate |
|
|
Term
|
Definition
| changes in ions. refers to the contractility of the myocardium |
|
|
Term
| what are positive chronotropic effects and what causes them? |
|
Definition
| mechanisms underlying increases in HR, can be from increased sympathetic drive |
|
|
Term
| what are negative chronotropic effects and what causes them? |
|
Definition
| mechanisms underlying decreases in HR, from increased parasympathetic drive. |
|
|
Term
| if you artificially stimulate the heart to beat faster without maintaining stroke volume, what happens to cardiac out put? why? |
|
Definition
| it decreases because there is a reduction in diastolic filling time. |
|
|
Term
| how do you increase heart reate without decreasing cardiac output? |
|
Definition
| pair increased sympathetic drive to the SA node with increased sympathetic drive to the ventricles. This increases the contractility of the ventricles, allowing them to relax for a longer period and fill up. |
|
|
Term
| what is the significance of increased contractility in the heart? |
|
Definition
| it increases stroke volume by decreasing the amnt of volume remaining in the ventricle following contraction (the ESV) for a given pre-contraction volume (EDV) |
|
|
Term
| what is the formula for stroke volume? |
|
Definition
|
|
Term
| what is a positive lusitropic effect? what is its significance? |
|
Definition
| increasing the relaxation rate of the cardiac tissue to maintain a constant period of cardiac filling despite reduced diastolic filling time. |
|
|
Term
| be able to calculate CO from R-R interval, EDV, and ESV |
|
Definition
use:
CO=HR*SV
SV=EDV-ESV
HR=(1/r-r interval)*(60,000 msec/min) |
|
|
Term
|
Definition
| the end diastolic volume, i.e. the volume of blood in the ventricle when it begins contracting. |
|
|
Term
|
Definition
| the pressure the ventricle must overcome to eject the blood from the pressure in the pulmonary artery or aorta. |
|
|
Term
| what is an isometric contraction? |
|
Definition
| contraction at a fixed length |
|
|
Term
| what is an isotonic contraction? |
|
Definition
| a shortening contraction. this is the one that actually pushes blood out and generates stroke volume. |
|
|
Term
| what is the length-tension relationship? which type of contraction depends on it? what is its significance? |
|
Definition
| isometric contractions depend on the starting length of the initial sarcomere when it's excited and how much force it can produce. i.e. the amnt of actin/myosin overlap |
|
|
Term
| in general, which length does cardiac muscle operate and why? |
|
Definition
at lengths well below Lmax, so that increasing luscle length will always give rise to an increased active isometric force.
(Lmax indicates the initial length position that would give the maximum force production) |
|
|
Term
| describe the Frank-Starling Effect. what causes it? |
|
Definition
an increase in the initial volume or preload (stretch) on the cardiac muscle will immidiately increase the stroke volume (during contraction). And vice versa.
this is due to the length-tension relationship (and assuming constant afterload). |
|
|
Term
| what is the physiological impact of the Frank-Starling effect/length-tension relationship? |
|
Definition
| it maintains a precise balance between the outputs of the right and left ventricles. |
|
|
Term
| what happens to force when the myocardium is streched beyond the optimal leangth, Lmax? |
|
Definition
| decrease in active force production. that means there is a constant volume overload in the ventricle that cannot be ejected (heart failure). |
|
|
Term
| describe the force-velocity relationship in myocardial contraction |
|
Definition
| inverse, e.g. larger forces cannot shorten as quickly. |
|
|
Term
| in isotonic contractions, what determines the total amount of force that that the muscle will generate versus that which only goes into muscle shortening? |
|
Definition
initial length=total force production.
afterload (i.e. pressure in aorta/pulm a.)= the proportion of total force production remaining for muscle shortening |
|
|
Term
| assuming constant initial preload and force generation, what happens to SV with increased and decreased afterload? |
|
Definition
increased afterload= decreased SV
decreased afterload=increased SV
(it's a balance b/w amnt of F that goes towrds isometric vs isotonic contraction) |
|
|
Term
| afterload is a limiting factor to what? |
|
Definition
| the extent of muscle shortening during contraction and consequently SV |
|
|
Term
|
Definition
| the ability of cardiac m. to either deivelop tension or shorten at a specific intial length. |
|
|
Term
| changes in contractility directly influence what |
|
Definition
|
|
Term
| events that increase contractility are called what? |
|
Definition
| positive inotropic effect, which is an upward shift of the length-tension relationship and F/vel curve. |
|
|
Term
| what do positive inotropic effect do physiologically? |
|
Definition
| they increase the contractility by increasing the number of cross-bridge interactions and increase the Ca+++ release. |
|
|
Term
| does sympathetic stimulation increase or decrease systole duration? how? |
|
Definition
| decrease. NE raises intracellular cAMP, which opend Ca++ channels and increases contraction strength. |
|
|
Term
| how do parasympathetic actions act on ventricular contraction? |
|
Definition
| Ach inhibits the release of NE from sympathetic fibers. |
|
|
Term
| list the important hormones that influence cardiac contractility? |
|
Definition
| adrenal epinephrine, thyroid hormones |
|
|
Term
| what does myocardial ischemia do to myocardial contractile force? |
|
Definition
|
|
Term
| what is going in isometric contraction in regard to pressure, volume, and force? |
|
Definition
| muscle force is increasing (pressure rises) but does not exceed the afterload yet. |
|
|
Term
| what is going in isovolumetric contraction in regard to pressure, volume, and force? |
|
Definition
ventricular pressure has exceeded atrial pressure and the AV valves close. all valves are closed at this point and no volume changes.
another isovolumetric period occurs when ventricular pressure decreases at the end of the AP and it relaxes while all valves are closed. |
|
|
Term
| what does the pressure-volume curve look like? |
|
Definition
|
|
Term
| what are 3 factors that influence cardiac performance? |
|
Definition
1. changes in preload (EDV) (Frank-Starling)
2. changes in afterload
3. changes in contractility |
|
|
Term
what are the effects on SV if you increase each of these 3 things?
contractility
preload
afterload |
|
Definition
contractility- increase
preload- increase
Proxy-Connection: keep-alive
Cache-Control: max-age=0
terload- decrease |
|
|
Term
| velocity of the blood ____ as total cross sectional area ____ |
|
Definition
|
|
Term
| mean arteriole pressure _____ as the resistance to blood flow _____ and the total cross sectional area _____ |
|
Definition
| decreases, increases, increases |
|
|
Term
| where is the slowest velocity in the CV system |
|
Definition
|
|
Term
| what is the importance of arteriole compliance? |
|
Definition
| it plays a large role in pressure filtering and determines the rate at which MAP is acheived |
|
|
Term
| what are the 2 physical factors that determine arterial pressure? |
|
Definition
| blood volume and compliance |
|
|
Term
| what are the 2 physiological factors that determine arterial pressure? |
|
Definition
| cardiac output and total peripheral resistance |
|
|
Term
| what determines arteriole blood volume? |
|
Definition
| cardiac output (i.e. arterial inflow) and arterial runoff (the blood moving into veins) |
|
|
Term
| what happens to blood pressure when arterial inflow > arterial runoff? |
|
Definition
|
|
Term
| what happens to blood pressure when arterial inflow < arteriole runoff |
|
Definition
|
|
Term
| what are the main determinants of MAP? what must be altered to change it? |
|
Definition
1. the rate that blood enters the arterial side
2. the degree of resistance to flow through the peripheral vessels
the only way to change it is by changing cardiac output or total peripheral resistance |
|
|
Term
|
Definition
|
|
Term
| what is the formula for TPR |
|
Definition
|
|
Term
| define MAP and give its formula |
|
Definition
the average pressure over time.
MAP= Pdiastolic = [(Psystolic - Pdiastolic)/3] |
|
|
Term
| what determines systolic pressure? |
|
Definition
| LV stroke volume, rate of blood ejection, and dispensibility of the aorta |
|
|
Term
| what is diastolic pressure and what determines it? |
|
Definition
| the rate at which pressure falls. determined by the aortic pressure at the end of systole, the rate of peripheral runoff, and HR |
|
|
Term
|
Definition
| the diff btw systolic and diastolic pressure |
|
|
Term
| what determines the size of a pressure change for a given change in volume? |
|
Definition
| the compliance of the system |
|
|
Term
| name 3 factors that might increase pulse pressure |
|
Definition
| aortic compliance decreases, stroke volume increase, heart rate decreases |
|
|
Term
| name 2 things that might decrease pulse pressure |
|
Definition
| conjestive heart failure, hemorrhage |
|
|
Term
| what does increased HR do to pulse pressure? |
|
Definition
|
|
Term
| reduced HR does what to pulse pressure? |
|
Definition
|
|
Term
| what is the fick principle? decribe in words and a formula |
|
Definition
the rate that a substance moves through circulation is solely dependent on the concentration of the substance in the blood and the rate of blood flow.
X=Q*([Xa]-[Xv])
Q=(blood flow rate; ml/time)
[Xa]=arterial conc of X (mass/ml)
[Xb]=venous conc of X (mass/ml) |
|
|
Term
| what does the Fick principle tell you? |
|
Definition
| the amnt of a substance that goes into an organ in a given period of time minus theamnt that comes out must be equal to the tissue utilization of that substance |
|
|
Term
| where does exchange take place? |
|
Definition
|
|
Term
| the velocity of blood in capillaries is dependant on: |
|
Definition
| arteriole constriction, endothelial and local factors, and venuole pressure |
|
|
Term
| the 2 primary factors responsible for transport across capillary walls are |
|
Definition
|
|
Term
| diffusion across cap wall is limited by |
|
Definition
|
|
Term
| filtration is dependent on |
|
Definition
| hydrostatic and osmostic forces (starling forces) |
|
|
Term
| hydrostatic forces are the driving forces for what. how bout oncotic? |
|
Definition
hydrostatic- for substances to leave
oncotic-retain fluid in vessel |
|
|
Term
| describe the fluid equilibrium in capillaries |
|
Definition
| the volume leaving capillary exactly equals that returned to circulation by reapsorption at venous end and flow thru lymphatics |
|
|
Term
| compare the forces at the beginning and middle of a capillary |
|
Definition
beg: hydrostatic pressure, leaving force, net filtration
middle: oncotic pressure is greatest and fluid returns. net reabsorption |
|
|
Term
| what does arteriole constriction and dilation do to fluid? |
|
Definition
constriction: net reabsorption
dilation- absorption |
|
|
Term
| what 3 things may cause edema? |
|
Definition
1. increased capillary hydrostatic pressure
2. increased interstitial fluid protein
3. decrease in plasma proteins |
|
|
Term
| do lymphatics have bi directional flow? |
|
Definition
|
|
Term
| what is the main function of the lymph system? |
|
Definition
| transfer extra fluid back into circulatory system. |
|
|
Term
|
Definition
| skeletal m. contaction and the compression of lymph vessels, negative intrathoracic pressure during inspiration, and rhythmic contractions of smooth muscle in lymph walls |
|
|
Term
| lymphatic obstruction causes what |
|
Definition
|
|
Term
| venous pressure fluctuates with _____ and _____ |
|
Definition
| respiration and heart beat |
|
|
Term
| blood velocity ____ fromt the venule to the vein as total cross sectional area decreases |
|
Definition
|
|
Term
| when is venous return enhanced? |
|
Definition
|
|
Term
| what are factors promoting or reducing venous return? |
|
Definition
gravity reduces return from lower extremities (so venous pumping and valves are used).
muscle contraction promotes venous pumping. |
|
|
Term
| describe the cardiac output curve |
|
Definition
| as central venous pressure increases (due to increased venous return), diastolic filling (and thus PRELOAD) increases. Consequently, cardiac output would increase in the next systolic contraction (due to Frank-Starling) |
|
|
Term
list whether these factors have a +/- effect on cardiac output:
HR
mycardial contractility (with a + and - inotropic effect)
preload
afterload |
|
Definition
HR: +
mycardial contractility with a + inotropic: +
and - inotropic effect: -
preload:+
afterload: - |
|
|
Term
|
Definition
the ratio that takes surface area into account when looking at CO
CI=CO/surface area |
|
|
Term
| vascular resistance is determined by the combined effects of what 2 control mechanisms? |
|
Definition
intrinsic control (local)
extrinsic control (CNS, hormonal) |
|
|
Term
| what does extrinsic control do? |
|
Definition
| maintains a stable arterial pressure when CO or TPR changes |
|
|
Term
| what does intrinsic control do? |
|
Definition
| local regulatory factors can change resistance or blood flow to meet local demands. |
|
|
Term
| what is unique about smooth muscle cells in airways and blood vessels? |
|
Definition
| they are tonically active to allow for greater constriction or dilation depending on inputs |
|
|
Term
| venous constriction leads to what? |
|
Definition
| a decreased venous capacity, increased venous return, and a shift of total blood volume from venous side to arterial side |
|
|
Term
| most neurally mediated increases in blood flow are achieved how |
|
Definition
| by decreasing sympathetic tone (since sympathetic nerves are tonically firing) |
|
|
Term
| alpha-adrenergic receptors are found where and do what |
|
Definition
| in blood vessels. vasoconstriction |
|
|
Term
| beta-adrenergic receptors are found where and do what |
|
Definition
beta-1 in heart- increase contractility and HR
beta-2 in blood vessels of skeletal m.- vasodilation |
|
|
Term
| which receptor is responsible for increased HR? |
|
Definition
|
|
Term
| which receptor is responsible for increased contractility? |
|
Definition
|
|
Term
| which receptor is responsible for increased rate of conduction in AV node? |
|
Definition
|
|
Term
| which receptor is responsible for vasoconstriction in most regions? |
|
Definition
|
|
Term
| which receptor is responsible for vasodilation in skeletal vascular beds? |
|
Definition
|
|
Term
| what is the effect of parasympathetics on discharge rates of SA and AV nodes? |
|
Definition
|
|
Term
| what is the effect of parasympathetics on AV conduction? |
|
Definition
|
|
Term
| what is the effect of parasympathetics on heart contractility? |
|
Definition
|
|
Term
| what is the main cardiovascular reflex involved in regulating short-term changes in blood pressure? |
|
Definition
|
|
Term
| the arterial baroreflex modulates the pressure set point through which kind of feedback system? |
|
Definition
|
|
Term
| T/F the arterial baroreflex determines and defends the MAP |
|
Definition
|
|
Term
| where are arterial baroreceptors? |
|
Definition
| in the aortic arch and carotid bifurcation. |
|
|
Term
| what kind of receptors are arterial baroreceptors? how do they adjust their firing speed? |
|
Definition
| they respond to strech by increasing their firing rate. decreases in vessel wall stretch (i.e. decreased pressure) and they decrease their firing rate. |
|
|
Term
| baroreceptor afferents ascend with which nerves and terminate where? |
|
Definition
| a branch of CN IX and CN X. it terminates in the dorsal medulla of the nucleus of the solitary tract. |
|
|
Term
| is baroreflex action short or long term? |
|
Definition
|
|
Term
| describe the baroreflec action, starting with the baroreceptor detecting strectch to the final autonomic response. |
|
Definition
| increased arterial pressure > increased arterial afferent input > dorsal medulla (NTS) > increased excitation of NTS neurons > inhibition of RVLM > decreased excitation to the spinal cord (IML) > decreased sympathetic outflow > increased parasympathetic flow |
|
|
Term
| what is the end result of the baroreflex response to a fall in arterial pressure? |
|
Definition
| reduced inhibition of RVLM and reduction of excitation of parasympathetic preganglionics. sympathetic discharge increases, increasing TPR and HR. |
|
|
Term
| name the 4 hormones that have short term action on CV fxn |
|
Definition
| NE, Epi, angiotensin II, vasopressin |
|
|
Term
list whether the effects are vasoconstriction or dilation:
NE (alpha-1)
EPI (alpha-1, beta-2)
Angiotensin II
vasopressin |
|
Definition
NE (alpha-1)- vasoconstriction
EPI (alpha-1 vasoconstriction, beta-2 vasoDILATION)
Angiotensin II- vasoconstriction
vasopressin- vasoconstriction |
|
|
Term
| where are arterial chemoreceptors located? |
|
Definition
| carotid body and aortic body (same as baroreceptors) |
|
|
Term
| what 3 things excite chemoreceptors? |
|
Definition
|
|
Term
| what is the primary reflex action of chemoreceptors? |
|
Definition
| to INCREASE ALVEOLAR VENTILATION and O2 delivery to brain and heart via vasoconstriction of all non-vital vascular beds |
|
|
Term
| what do chemoreceptors do in response to low blood pressure? |
|
Definition
| they are activated and trigger mild tachycardia to return MAP to normal |
|
|
Term
| what are atrial stretch receptors? what do they respond to? where are they? |
|
Definition
| aka volume receptors or "low pressure baroreceptors". they respond to increases in venous return or increases in central venous pressure. in veno-atrial junction |
|
|
Term
| what is the Brainbridge Reflex? |
|
Definition
| atrial stretch receptors are distended with increased blood volume. SA node fires more (incr. HR) via sympathetic excitiation and paSYM inhib. |
|
|
Term
| what other system is involved in atrial stretch receptors? |
|
Definition
| renin and vasopressin are released to help decrease blood volume (rapid diuresis) |
|
|
Term
| what are extrinsic reflexes? |
|
Definition
|
|
Term
| what does mild and severe pain do to the heart? |
|
Definition
mild- incr. atrial pressure and tachycardia
severe- profound bradycardia (shock) |
|
|
Term
| what does cold do to the cardiovascular system? |
|
Definition
| cutaneous vasoconstriction by changing the sympathetic activity to diff't vascular beds. |
|
|
Term
| which system controls total blood-volume and urinary output? |
|
Definition
| renin-angiotensin-aldosterone system (RAAS) |
|
|
Term
| which autonomic system controls the RAAS? |
|
Definition
|
|
Term
| what is vasopressin involved in? where is it secreted? |
|
Definition
| water reabsorption in the kidney. hypothalamus |
|
|
Term
| vasopressin is also called |
|
Definition
|
|
Term
| what is renin (as far as synthesis and storage)? |
|
Definition
| a proteolytic enzyme that is synthesized, stored and released in kidney. |
|
|
Term
| under what conditions is the RAAS activated? |
|
Definition
| when sodium and water retention are needed |
|
|
Term
| what 3 major mechanisms regulate renin release? |
|
Definition
1. renal arterial bp and renal baroreceptors
2. salt concentration in the distal tubules
3. sympathetic drive |
|
|
Term
| decreases in renal arterial pressure ___ renin release. how? |
|
Definition
| increase. it reduces the stretch of juxtaglomerular cells. |
|
|
Term
| low salt concentration ____ renin secretion |
|
Definition
|
|
Term
| stimulation of sympathetic drive _____ renin release |
|
Definition
|
|
Term
| what is renin's main goal? (i.e. what is it helping to make?) |
|
Definition
| make angiotensin I by cleaving angiotensinogen |
|
|
Term
| what happens after renin has cleaved angiotensinogen to produce angiotensin I? |
|
Definition
| angiotensin I is converted to ang II by angiotensisn converting enzyme (ACE) |
|
|
Term
| what uis the rate limiting step in the ang II conversion? |
|
Definition
|
|
Term
| what are ang II's 4 actions? |
|
Definition
1. vasoconstrict
2. stimulate aldosterone
3. stimulate vasopressin
4. increase thirst |
|
|
Term
| what does aldosterone do? where does it come from? |
|
Definition
| stimulates sodium and water retention by kidney (from adrenal cortex) |
|
|
Term
| what does vasopressin do? |
|
Definition
| vasocontrictor. promote water retention by kidney (remember it's also called ADH). |
|
|
Term
| what is the most important system for the long term regulation of arterial pressure? |
|
Definition
|
|
Term
| what is arginine vasopressin (AVP) also know as? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| AVP release is modulated by these 3 things: |
|
Definition
1. withdrawal of baroreceptor input
2. input from left atrial stretch receptors
3. increase in blood osmolality |
|
|
Term
| in the most generic terms you can think of, AVP responds to what |
|
Definition
| dehydration. (low fluid volume) |
|
|
Term
| what is the main action of AVP? |
|
Definition
| return body fluid osmolality to normal by controlling renal water secretion |
|
|
Term
| does AVP vasoconstrict or dilate? |
|
Definition
|
|
Term
| what body conditino would you expect to see the highest AVP levels? |
|
Definition
| volume-depleted, hypotensive states (think dehydration and hemorrhage) |
|
|
Term
| Atrial natriuretic peptide is released from where and in response to what? |
|
Definition
| from atrial myocardial cells in response to hypervolemia |
|
|
Term
|
Definition
| with too much blood volume |
|
|
Term
| administration of ANP results in what 3 things? |
|
Definition
1. diuresis
2. natriuesis
3. hypotension |
|
|
Term
| what does ANP do to the kidney? |
|
Definition
| afferent arteriole vasodilation and efferent constriction. GOAL: increase glomerular filtratin rate |
|
|
Term
| diarrhea causes the loss of water AND electrolytes. there are 8 things that decrease in respinse to this, name them. |
|
Definition
1. plasma volume
2. venouse pressure
3. venous return
4. atrial pressure
5. ventricular end-diastolic volume
6. stroke volume
7. cardiac output
8. arterial pressure |
|
|
Term
| define dehydration in terms of water/electrolyte balance |
|
Definition
| extreme loss of water and minimal loss of electrolytes |
|
|
Term
| what are the 2 main classifications of heart failure? |
|
Definition
1. systolic dysfunction
2. diastolic dysfunction |
|
|
Term
| what are the problems with systolic dysfunction? |
|
Definition
| ventricular ejection (such as high afterload) |
|
|
Term
| what is the problem with diastolic dysfunction? |
|
Definition
|
|
Term
| conjestive heart failure begins with ___ stroke volume, which causes a ____ in arterial pressure and triggers a ____ in sympathetic drive and ____ in pasym drive |
|
Definition
| decreased, decrease, increase, decrease |
|
|
Term
| why is there fluid retention in heart failure? |
|
Definition
the increase in sympathetic drive increase renal sympathetic drive, which increases extracellular volume, which increases venous return and EDV. thus all the vessels are crammed with blood.
thus: EDEMA from increased capillar hydrostatic pressure |
|
|
Term
| left ventricular heart failure often leads to what? symptoms? |
|
Definition
| pulmonary edema. cough, frothy edema from airways, exersize intolerance |
|
|
Term
| what is the most common cause of right heart failure? why? |
|
Definition
| left heart failure because the increased pulmonary pressures increase the right ventricular afterload. |
|
|
Term
| symptoms of right heart failure are |
|
Definition
liver enlargement with dull border
splenic engorgement
distended peripheral veins
ascites
pleural/pericardial effusion
peripheral dependent effusion |
|
|
Term
| pressure overload does what to the ventricular wall? mention new sarcomeres and shape |
|
Definition
| new sarcomeres in paralle=increased wall thickness |
|
|
Term
| volume overload does what to the ventricular wall? mention new |
|
Definition
| new sarcomeres in series=dilated chamber |
|
|
Term
| in arteries, what property assists with maintaining a constant supply of blood during diastole? |
|
Definition
|
|
Term
| which part of the vascular changes the most? why? |
|
Definition
| arterioles because their thick layer of smooth muscle can be actively changed to regulate blood flow through peripheral organs |
|
|
Term
| what does the law of bulk flow tell you? |
|
Definition
| blood flow is dependent upon pressure gradients and the tube dimentions (i.e. resistance) |
|
|
Term
| what is the important relationship to consider from Poiseuille's law? |
|
Definition
| flow is inversely related to the length of the tube and directly proportional to the radius^4 of the tube and the number of tubes in parallel |
|
|
Term
| resistance is always greater/less when systems are in parallel compared to in-series |
|
Definition
|
|
Term
| how is velocity related to cross sectional area? |
|
Definition
|
|
Term
| why is the velocity of blood in the capillaries so low? |
|
Definition
| since the total cross sectional area is so high, and that is inversely related to velocity |
|
|
Term
| where is potential energy? |
|
Definition
| the static pressure exerted by fluid against the walls. (called lateral or side pressure). |
|
|
Term
|
Definition
| the forward projecting energy of blood in the vessels |
|
|
Term
| what does Bernoulli's Theorem state? |
|
Definition
| the total energy at any point in a tube must be equal to the total energy at any other point (kinetic and potential) |
|
|
Term
| what happend to KE in an aneurysm? |
|
Definition
| it decreases because the vel decreases. PE increases bc the total energy remains constant. |
|
|
Term
| what does KE and PE do in aortic stenosis? |
|
Definition
| increases KE (velocity increases) decreases PE (reduced latereal pressure and thus filling time) |
|
|
Term
| extrinsic control is synonymous with |
|
Definition
| neural and hormonal control |
|
|
Term
| does the vascular smooth muscle contain gap junctions? |
|
Definition
|
|
Term
| how are small arteries and arterioles able to both constrict and dilate depending on input? |
|
Definition
| they are tonically active and always have some degree of sustained force or vascualr tone. |
|
|
Term
| what is the primary thing that controls the strength of vascular smooth muscle contraction? |
|
Definition
|
|
Term
| T/F increases in intracellular Ca can occur with or without membrane depolarization |
|
Definition
|
|
Term
| how do neurotransmitters increase intracellular Ca? |
|
Definition
| A vasoconstrictor again (eg. NE) binds to a receptor that opens a receptor activated Ca channel (ROC). The open channel and second messenger systems increase Ca membrane influx |
|
|
Term
| what is the mechanism behind smooth muscle contraction? |
|
Definition
| THERE IS NO TROPONIN. so Ca binds to calmodulin, which activates the myosin-light-chain kinase (MLCK). MLCK phosphorylates the myosin filament and cross-bridge formation with actin! |
|
|
Term
| what is the mechanism behind smooth muscle relaxation? |
|
Definition
membrane hyperpolarization decreases Ca through the voltage activated channels. beta-2 adrenergic receptors use second messengers to take up Ca into SR and efflux it outside. there is an INCREASE IN INTRACELLULAR CYCLIC AMP. also increases cyclic GMP.
decreases in intracellular Ca DEPHOSPHORYLATES MYOSIN and inhibs more cross-bridges. |
|
|
Term
| what are the 4 ways to regulate smooth muscle tone? |
|
Definition
1. metabolic
2. autoregulation
3. endothelial mediated regulation
4. mechanical compression |
|
|
Term
| what is the most important local control mechanism of blood flow? why? |
|
Definition
| metabolic regulation bc it matches blood flow to the metabolic rate |
|
|
Term
| in metabolic regulation, inadequate oxygenation to tissues results in what |
|
Definition
|
|
Term
| list substances that act as vasodilators in metabolic regulation |
|
Definition
| lactic acid, carbon dioxide, hypoxia, H+, K+, PO4-, adenosine |
|
|
Term
| define active hyperemia in regard to metabolic regulation of blood flow |
|
Definition
| the increase in flow associated with an increase in metabolic activity |
|
|
Term
| define reactive hyperemia in metabolic regulation of blood flow |
|
Definition
| the increase in blood flow (above previous levels) after occlusion for a few moments. the greater buildup of metabolites causes the overshoot |
|
|
Term
| define autoregulation mechanism in control of blood flow |
|
Definition
| flow thru a system that remains constant over a wide range of arterial pressures in the absence of neural and hormonal inputs |
|
|
Term
| what are some examples of the autoregulation mechanism in local control of blood flow? |
|
Definition
| metabolic control and the myogenic response |
|
|
Term
| what is the myogenic response? |
|
Definition
| stretch-activated Ca channels that instigate vasoconstriction in the face of increased perfusion pressure |
|
|
Term
| what triggers endothelial mediated regulation? |
|
Definition
|
|
Term
| for endothelial mediated regulation, what does increased and decreased sheer stress do? |
|
Definition
increased- release NO, down-regulate endothelin- vasodilate
decreased- release endothelin- vasoconstrict |
|
|
Term
| what is the most potent vasoconstrictor in the body? this is a test question! |
|
Definition
|
|
Term
| how does mechanical compression alter blood flow in local control of blood flow? |
|
Definition
| it occludes! this is bad and should be avoided. |
|
|
Term
| what are 2 examples of normal mechanical compression? |
|
Definition
| coronary vessels during systole and strong contractions of skeletal muscle. |
|
|
Term
| name the 6 vascular beds that have special control properties |
|
Definition
1.cutaneous
2. skeletal muscle
3. coronary
4. cerebral
5. splancnic
6. pulmonary |
|
|
Term
| intrinsic control is also known as what |
|
Definition
|
|
Term
| extrinsic control is also known as what |
|
Definition
|
|
Term
| which control dominates coronary circulation? |
|
Definition
|
|
Term
| when is coronary inflow that greatest? |
|
Definition
| the beginning of diastole in the LV (RV stays pretty constant) |
|
|
Term
| based on the way blood perfuses through the heart during systole, which specific cardiac tissue is most susceptible to ischemia? |
|
Definition
| the subendocardium (compared to the epicardium). |
|
|
Term
| in the coronary circulation, which metabolites act as dilators? |
|
Definition
high CO2, low O2, high H+, high adenosine, high K+
(these will all increase blood flow) |
|
|
Term
| we know that metabolic control dominates in coronary circulation, but is there any sympathetic? |
|
Definition
| yes, but it is quickly counteracted by an increase in metabolic activity (associated with tachycardia and stronger myocardial contractions) |
|
|
Term
| oxygen consumption ____ with increased CO |
|
Definition
| increases proportionally (HR and afterload play the biggest roles) |
|
|
Term
| what is the control mechanism that predominates cutaneous circulation? |
|
Definition
extrinsic control (aka sympathetic drive/neural control)
metabolic control is there, just not as important |
|
|
Term
| what is the primary fxn of cutaneous circulation? |
|
Definition
|
|
Term
| prolonged cold exposure cause a cyclic pattern in the skin, what is it? |
|
Definition
| vasoconstriction and vasodilation |
|
|
Term
| if it's freezing outside, how does the body prevent cold peripheral blood from returning to the heart all cold? |
|
Definition
| countercurrent heat exchange as it passes through the skin |
|
|
Term
| skeletal muscle circulation is regulated primarily by what? |
|
Definition
BOTH intrinsic and extrinsic
rest=extrinsic (neural)
exercise=intrinsic (metabolic) |
|
|
Term
| sympathetic tone in muscle vasculature is strongly modulated by what |
|
Definition
|
|
Term
which is more sensitive to sympathetic drive, the skin or muscle?
test q! |
|
Definition
|
|
Term
| cerebral circulation is dominated by which control mechanism? |
|
Definition
|
|
Term
| what is the main regulator of cerebral blood flow? |
|
Definition
|
|
Term
| what does the splanchnic circulation perfuse? |
|
Definition
| GI tract, live, spleen, pancreas |
|
|
Term
| control of splanchnic circulation is by what |
|
Definition
| local metabolic and hormonal mechanisms AND sympathetic inputs |
|
|
Term
| what is functional hyperemia? where does it occur? |
|
Definition
| fxnl hyperemia is the local release of hormones (gastrin, histamine) that vasodilate in response to food intake. in the splanchnic circulation. |
|
|
Term
| how do sympathetic nerves act on the splanchnic vascular bed? (include receptors and the vascular result) |
|
Definition
| the sympathetic nerves act on alpha-2 receptors and cause vasoconstriction |
|
|
Term
| why is there sympathetic innervation to the splanchnic vascular bed? |
|
Definition
| to shunt blood away from the GI tract (exercise) |
|
|
Term
| flow in the portal v. is regulated by what control mechanism? |
|
Definition
|
|
Term
| is the flow of blood through the lung equal to cardiac output? |
|
Definition
|
|
Term
| increases in pulmonary pressure trigger ____ in vascular resistance |
|
Definition
reduction (this is opposite all the other systems!).
it helps maintain a low pulmonary pressure in the face of increased CO |
|
|
Term
| hypoxia triggers _____ in pulmonary vessels |
|
Definition
| constriction (opposite from other systems!) |
|
|
Term
| what is the main control mechanism of pulmonary circulation? |
|
Definition
|
|
Term
| decreased blood volume leads to a decrease in ___ (ultimately) |
|
Definition
|
|
Term
| you can loose __% of your blood and it's no big deal |
|
Definition
|
|
Term
| loss of 15-20% of your blood results in what |
|
Definition
| moderate hypotension, spontaneous recovery |
|
|
Term
| the loss of more than __% and you start to get into irreversible damage and inability to recover MAP |
|
Definition
|
|
Term
|
Definition
| tissues have become so damages that even a transfusion cannot save the animal from failure. it is involved in a sudden withdrawal of sympathetic drive that originates from the CNS. |
|
|
Term
| what are the 6 main mechanisms that operate to return arterial pressure to the normal set point? |
|
Definition
1.arterial baroreflex
2. arterial chemoreflex
3. reflex response to cerebral ischemia
4. local fluid reabsorbtion
5. circulating vasoconstrictors
6. rapid renal fluid retension |
|
|
Term
| what is the 1st, most rapid defense in response to hemorrhage? |
|
Definition
|
|
Term
| the resulting effects of arterial baroreflex are: |
|
Definition
increased HR, increased mycardial contractility
increased peripheral vasoconstriction |
|
|
Term
| does the baroreflex act uniformly across all vascular beds? |
|
Definition
| no, the non-vital ones are constricted. |
|
|
Term
| in moderate blood loss (>15%), which reflex is then stimulated? why? |
|
Definition
| chemoreflexes (sensing a drop in O2) |
|
|
Term
| chemoreflexes vasoconstric or dilate? |
|
Definition
|
|
Term
| what behavior does the chemoreflex induce? |
|
Definition
| hyperventilation, which also augments venous return via resp pumping mechanics |
|
|
Term
| in severe blood loss (30%) what is activated? |
|
Definition
| sympatho-adrenal system (due to cerebral ischemia). the vasoconstriction can be many times greater than the sympathoexcitation evoked by baroreceptor withdrawal alone. |
|
|
Term
| if the brain has been ischemic for a long time, what happens? |
|
Definition
| it switches from sympathetic to vagal stimulation and the ensuing bradycardia aggravates the already existing hypotension. |
|
|
Term
| in response to hemorrhage there is an increase in resorption of fluids, how does this work? |
|
Definition
decreased arterial hypotension results in reduced venous central venous pressure, which reduces capillary hydrostatic pressure. this promotes reabsorption from interstitium.
cortisol is also released which increases capillary permeability and sucks fluid back up |
|
|
Term
| what do the endogenous vasoconstrictors do in response to hemorrhage? |
|
Definition
| increase. (NE, Epi, ang, vasopressin) |
|
|
Term
| what is the most important mechanism for long term recovery of hemorrhage? |
|
Definition
| renal conservation of water and salt |
|
|
Term
| the renal systems changes the levels of vasopressin (aka AVP or ADH) and ang II in response to hemorrhage. what does it do? |
|
Definition
vasopressin release is enhanced (vasoconstrictor, water reabsorber)
ang II is enhanced (vasoconstrictor and reduces water loss through kidneys, also stims release of aldosterone which stims Na reabsorption). |
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