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BIO169-Cardiovascula
Cardiovascular System
| Question | Answer |
|---|---|
| what are the 2 types of myocardial cells? | contractile cells, which have similar features to skeletal muscle cells and nodal/conducting cells that have features similar to nerve cells. |
| what are contractile cells? | the real muscle cells of the heart and form most of the walls of the atria and ventricles; they have similar features and contract in almost the same way as skeletal muscle fibers |
| how do contractile cells differ from skeletal muscle? | they have only one nucleus but far more mitochondria to extract oxygen |
| what are nodal cells? | the cells contract very weakly because they contain very few contractile elements (myofibrils); they provide a self-excitatory system for the heart to generate impulses and a transmission system for rapid conduction of the impulses throughout the heart. |
| what does it mean that cardiac muscle is auto-rhythmic? | it contracts without stimulation from nerves |
| what is the pacemaker of the heart? Why? | the sinoatrial node (SA-node) is the pacemaker; it is where the normal contraction impulse originates, because it has the fastest intrinsic depolarization rate (but slow conduction speed) |
| which nervous systems have input to the SA node? | both the parasympathetic and sympathetic nervous systems have input into the SA node to regulate the rate of discharge |
| what is the impact of the parasympathetic nervous system on discharge rate? The sympathetic? | the parasympathetic nervous system decreases the rate of discharge; the sympathetic nervous system increases the rate of discharge |
| what causes the membrane potential of the SA nodal cells to drift towards potential? | the membranes of SA nodal cells have a natural “leakiness” to sodium; this slow sodium influx generates the pacemaker potential |
| how does the SA nodal cell threshold compare to neurons? | it is higher |
| what happens in the SA nodal cell when threshold is reached? | calcium channels open and calcium rushes in quickly, causing depolarization; calcium channels then close, and potassium channels open, causing potassium to rush out, resulting in repolarization |
| what happens after an action potential is generated by the SA node? | The action potential generated by the SA node is then conducted throughout the heart |
| how frequently does the SA node depolarize? | approximately once every .8 seconds; this is its intrinsic rate |
| what is the effect of parasympathetic input to the SA node? | at rest, the vagus nerve maintains parasympathetic input to the SA node, slowing it’s rate of discharge to 68-72 times per minute; parasympathetic stimulation slows discharge by lowering the resting membrane potential of SA nodal cells, thus making it tak |
| what is the effect of sympathetic input to the SA node? | during the fight or flight response, sympathetic stimulation to the SA node increases the rate of depolarization; the sympathetic nervous system also innervates the ventricular musculature extensively; stimulation causes an increase in contractility of th |
| what is the significance of the intercalated discs in cardiac muscle? | cardiac muscle cells are connected by regions of membrane called intercalated discs (very low electrical resistance); an action potential can freely travel from one cell to the next. A mass of cardiac muscle is therefore said to act as a functional syncit |
| what is a functional syncitium? | a syncitium is a single cell with many nuclei; If you stimulate one cardiac muscle cell in a mass, the whole group of cells will contract, thus acting as one, and acting as a functional syncitium |
| how is the atrial musculature isolated from the ventricular musculature? | by a fibrous ring or “skeleton” which supports the AV valves; this fibrous rings also keeps the atria and ventricles electrically isolated, meaning that an action potential cannot freely pass from atria to ventricles |
| where does the impulse travel after the SA node? | it travels through the atrial musculature (the left atrium receives the impulse via Bachman's bundle) and at the same time, the action potential is conducted down the internodal pathway to the AV node. |
| what happens when the impulse reaches the AV node? | the AV node delays the action potential to allow the atria to depolarize before the impulse travels to the ventricles |
| what is the function of the AV node? | the AV node conducts the action potential to the Bundle of His; it is considered to be the functional connection between the atria and the ventricles and is considered the ventricular pacemaker |
| where does the impulse travel after the AV node? | from the AV node the impulse is conducted to the Bundle of His |
| what is the function of the Bundle of His? | aka AV bundle; it conducts the impulse to the ventricles, through the bundle branches |
| where is the Bundle of His located? What is its structure? | in the interventricular septum where it divides into the left and right bundle branches; these travel down the septum to the apex of the heart, just beneath the endocardium |
| where does the impulse travel after the Bundle of His and the bundle branches? | to the purkinje fibers, an extensive network which extend throught the ventricular musculature |
| what is the function of the purkinje fibers? | the purkinje fibers are the most rapidly conducting fibers of the pathway; they conduct the impulse through the ventricles |
| summarize the conduction pathway? | SA node -> Bachman's bundle -> AV node -> Bundle of His -> bundle branches -> Purkinje fibers |
| how does the heart contract? | the atria contract first, and the ventricles contract second and from the bottom up. |
| how can the electrical activity of the heart be monitored? | by placing recording electrodes on the surface of the body; the resulting tracings are called an electrocardiogram or ECG |
| what information can an ECG provide? | 1) Heart rate 2) Heart rhythm 3) Health of the myocardium (by indicating chamber enlargements) 4) Some aspects of extracardiac factors (for example, hyperkalemia causes characteristic changes in the ECG) |
| does and ECG provide info on heart contraction? | no, only electrical activation of the heart muscle; it does not tell you whether or not contraction actually occurred in response to stimulation |
| how do you calculate the heart rate from an ECG by knowing the paper speed? | count out 3 seconds along the tracing, count the R waves, and multiply by 20 - this gives you the ventricular rate per minute; for this course, if the paper is moving at 25mm/sec., count out 75 small squares on the graph paper and this represents a 3 seco |
| how many leads (sites of electrode attachment) are typically used in an ECG? | 12 |
| what do the "waves" on the ECG represent? | 1) P wave-depolarization of the atria 2) P-R interval-delay period as the impulse is conducted between SA & AV node 3) QRS complex-depolarization of the ventricles 4) T wave-repolarization of the ventricles 5) S-T segment-base line between the S & T wave |
| what is normal sinus rhythm? | the normal rate and rhythm of the heart beat as generated by the SA node |
| what is bradycardia? | heart rate slower than normal |
| what is tachycardia? | heart rate faster than normal |
| what is conduction block? | aka atrioventricular block; lack of synchrony between atrial and ventricular electrical activities (ventricles are driven by a pacemaker cell in the bundle of His) |
| what is ectopic focus? | an abnormal site in the heart acting as the pacemaker; the ECG tracing generated is abnormal |
| what is ectopic rhythm? | an abnormal site in the heart acting as the pacemaker; the ECG tracing generated is abnormal |
| what is ventricular tachycardia? | (blank) |
| what is fibrillation? | uncoordinated electrical activity of the heart; ventricular fibrillation causes the heart to contract like a "bag of worms" in that there is no forceful contraction produced; it is incompatible with life |
| study ECG drawings in lab manual! | study ECG drawings in lab manual! |
| what is the cardiac cycle? | sequence of events which occurs during one heartbeat |
| what is systole? | time when ventricles are contracting |
| what is diastole? | time when ventricles are relaxed |
| what is diastasis? | quietest time in cycle; the AV valves are open and blook is trickling into the ventricles; the semilunar valves are already closed from an earlier period; at the end of diastasis the P wave occurs and the atria depolarize |
| what is atrial systole? | the period when the atria contract; the QRS complex occurs as the ventricles depolarize; ventricular pressure and volume rise above atrial pressure and volumen and the AV valves close; the first heart sound S1 is recorded |
| what is isovolumetric contraction? | the ventricles are closed containers as both the AV valves and semilunars are closed; the ventricles contain the largest volume of blood during the cycle; ventricular pressure rises above the pressure in the large arteries and the semilunars open. |
| what is the end diastolic volume? | the volume of blood in the ventricles during isovolumetric contraction; it measures about 120 ml; recorded during isovolumetric contraction |
| what is diastolic blood pressure? | the bottom number of blood pressure; normall about 80 mmHg |
| what is the period of rapid ejection? | blood is rapidly expelled into the large arteries; ventricular pressure drops below the arterial pressure and the semilunars close again; the second heart sound S2 is recorded |
| what is systolic blood pressure? | the top number of blood pressure; normally about 120 mmHg; recorded during the period of rapid ejection |
| what is isovolumetric relaxation? | the ventricles are closed containers again and they are relaxing; they contain the smallest volume of blood at the point; ventricular volume and pressure fall below atrial pressure and the AV valves open |
| what is end systolic volume? | the volume of blood in the ventricles during isovolumetric relaxation (i.e. after ejection, i.e. right after the ventricles contracted, ergo systolic); it measures about 60 ml; recorded during isovolumetric contraction |
| what is the period of rapid ventricular filling? | blood rushes into the ventricles from the atria, vena cavae, and pulmonary veins |
| how is the heart regulated? | medullary cardiovascular center, afferent nerve, limbic system and other variables |
| where is the cardiovascular center located? | in the medulla of the brain; it gives off efferent (motor) neurons of both branches of the autonomic nervous system |
| where do the cardiovascular center parasympathetic fibers travel and what is their impact? | in the vagus nerve; decr heart rate; releases ACh to SA node (& AV node), opening K+ channels, membrane hyperpolarizes, longer to reach threshold; also ACh will decr amt of Ca++ entering muscle cells, decr contracting force, decr stroke volume |
| what is vagal tone? | the phenomenon where the PSYN is continually activated at rest to keep the heart beating at roughly 70 bpm; the vagus nerve transmits the signals from the PSYN to the heart |
| what is the impact of the sympathetic fibers? | incr heart rate & cardiac contractility; norepinhephrine (epinephrine, adrenaline) released to SA node (& AV node) which opens Na+ & Ca++ channels, membrane depolarizes & reaches threshold more rapidly; extra Ca++ incr force of contraction, stroke volume |
| what is the impact of the vasomotor area? | it stimulates either vasoconstriction or vasodilation of the peripheral blood vessels. |
| what is the function of the afferent nerves? | they carry information to the cardiovascular center from the baroreceptors in the carotid and aortic sinuses |
| what occurs in the baroreceptor reflex whe blood pressure increases? | the baroreceptors increase the rate of impulses sent to the cardiovascular center; the cardiovascular center will increase parasympathetic outflow to the heart to decrease heart rate and the vasomotor area will cause peripheral vasodilation |
| what occurs in the baroreceptor reflex when blood pressure decreases? | the baroreceptors will decrease their rate of impulses, the cardiovascular center will increase sympathetic outflow to increase heart rate and contractility, and the vasomotor area will stimulate vasoconstriction of peripheral vessels. |
| what is the role of the limbic system in heart regulation? | plays a role in regulation of heart function, particularly heart rate; the limbic system governs the primitive emotions of rage, fear, aggression, etc. For example, your heart rate increases when you are angry |
| what are the other variables that control heart regulation? | body temperature, serum K+, epinephrine, and thyroxine |
| what is the impact of body temperature on heart rate? | when body temperature increases, so does the heart rate and vice versa |
| what is the impact of serum K+ on heart rate? | as K+ levels increase the heart rate decreases; normal K+ levels are between 4-6 mmole. When levels rise to 7 mmole, the heart stops in diastole (flaccidity) and when the levels drop to 2 mmole arrythmias such as tachycardias develop |
| what is the impact of epinephrine and thyroxine on heart rate? | epinephrine- causes an increase in heart rate; thyroxine- increased T4 causes increased heart rate and vice versa |
| what is a normal heart rate? | 70 bpm (the heart's intrinsic rate is 100 bpm, but parasympathetic stimulation at rest slows it to 70 bpm) |
| what is Starling's law? | incr in EDV -> incr in stroke volume & vice versa; stretching (due to increased volume) causes more Ca++ channels to open -> more Ca++ in muscle cell -> more forcefully it contracts during systole -> more blood ejected -> lower ESV -> higher stroke volume |
| what is mean arterial pressure? | aka MAP; pressure of the blood against the walls of the arteries and arterioles |
| how is MAP calculated? | MAP = cardiac output X resistance to flow |
| what is cardiac output? how is cardiac output calculates? | cardiac output is the amount of blood pumped by the heart in a given time period, usually per minute; cardiac output = heart rate X stroke volume |
| what is typical cardiac output at rest? What is typical maximum cardiac output? | at rest, the cardiac output is roughly 5 liters (1.3 gallons) of blood every minute; during vigorous exercise, this can increase up to 20 l/min (5.2 gallons/min) in a normal individual and up to 35 to 40 l/min (10 gallons/min) in a highly trained athlete |
| how is resistance to flow calculated? | Resistance to flow = fluid friction X vessel length /vessel diameter |
| what is stroke volume? How is it measured? | the amount of blood pumped by the heart per beat; stroke volume = end-diastolic volume - end-systolic volume |
| how can MAP be calculated from blood pressure? | MAP= diastolic pressure + 1/3 (pulse pressure); pulse pressure = systolic pressure - diastolic pressure |
| What is venous return? | amt of blood returned to heart by the circulation per unit time, usually per minute; normally, cardiac output = venous return; this means the heart is capable of pumping out the amt of blood it receives, which can vary according to posture, activity level |
| what is endothelin? | a powerful vasoconstrictor released by endothelial cells in response to a decrease in blood flow |
| what is NO? | nitric oxide; it is released by endothelial cells in response to a high flow rate; it causes localized vasodilation |
| What effect does blood volume have on blood pressure? | direct; greater theh volume, the greater the pressure |
| What effect does heart rate have on blood pressure? | direct; greater the heart rate, the greater the pressure |
| What effect does stroke volume have on blood pressure? | direct; greater the stroke volume, the greater the pressure |
| What effect does venous return have on blood pressure? | direct; increased venous return means that the cardiac output must increase (which can be done by increasing the heart rate and/or the stroke volume) which in turn means that the MAP increases. |
| What effect does strength of myocardial contraction have on blood pressure? | direct; as this determine stroke volume, the greater the force of contraction, the greater the amount of blood pumped out, the greater the MAP |
| What effect does sympathetic stimulation have on blood pressure? | increase; sympathetic stimulation increases heart rate and increase force of contraction, dramatically increassing cardiac output and MAP |
| What effect does parasympathetic stimulation have on blood pressure? | decrease; causes decreased heart rate, so decreases cardiac output, and therefore MAP |
| What effect does epinephrine have on blood pressure? | increase; increase heart rate and therefore increases cardiac output and MAP |
| What effect does thyroxine have on blood pressure? | increase; increase heart rate and therefore increases cardiac output and MAP |
| What effect does vasopressin (aka ADH) have on blood pressure? | increase; in high levels, vasopressin causes vasoconstriction of visceral blood vessels, reducing vessel diameter, increasing resistance to flow, therefore MAP is increased |
| What effect does the renin-angiotensin system have on blood pressure? | increases; this increases blood volume and increases vasoconstriction and therefore increases MAP. |
| What effect does blood viscosity have on blood pressure? | increase; increased viscosity causes increased fluid friction. This increases resistance to flow and therefore MAP. |
| What effect does the length of blood vessels have on blood pressure? | direct; vessel length is directly proportional to resistance; this means that the shorter the vessel, the lesserer the resistance to flow there is, and therefore the lesser the MAP. |
| What effect does endothelin have on blood pressure? | increase; because it is a vasoconstrictor, it increases resistance and increases MAP |
| What effect does NO have on blood pressure? | decrease; because it is a vasodilator which decreases resistance and decreases MAP |
| What effect does ANF have on blood pressure? | decrease; because it inhibits the renin-angiotensin system, it decreases MAP |
| what are the heart sounds heard with a stethoscope? | 1st sound is produced by closure of AV valves (low pitch, long duration); 2nd heart sound is produced by closing of the semilunar valves (high pitch, shorter duration); 3rd heart sound sometimes occurs in the middle of diastole (difficult to hear) |
| what is "lub"? What is "dup"? | "lub" is the sound of the A/V valves closing (heart sound 1); "dup" is the sound of the semi-lunar valves closing (heart sound 2) |
| what provides resistance to blood flow: | viscosity of blood, length of vessel, diameter of vessel |
| what are the main 2 factors affecting blood flow (that can be changed?) | pressure gradient and diameter |
| ** remember, blood flow (rate of flow) is different than blood pressure !! ** | (blank) |
| what are the 4 starling forces? | capillary hydrostatic pressure, interstitial-fluid hydrostatic pressure, osmotic force due to plasma proteins (in the blood), osmotic force due to interstitial fluid protein concentration |
| what are the 3 mechanisms that regulate the cardiovascular system? | 1) local control mechanisms in the organs themselves 2) humoral mechanisms that rely on chemicals in the blood 3) the ANS which alters cardiac output and blood flow to organs |
| what are 3 vasoconstricting agents? | angiotensin II, vasopressin, epinephrine (only a weak effect on blood vessels of the intestine) |
| what are 4 vasodilating substances? | epinephrine, kinins, histamine, ANF |
| how does the sympathetic nervous system impact vessel diameter? | causes overall VASOCONSTRICTION by releasing norepinephrine onto smooth muscle of blood vessels, and releases ACh onto blood vessels in skeletal muscle producing a VASODILATION, redirecting blood away from the digestive system, kidneys, & spleen |
| how does the parasympathetic nervous system impact vessel diameter? | doesn't have a strong impact, but it does release ACh and produces a vasodilation |
| what is the baroreceptor reflex? | baroreceptors are sensitive to any stretching of the blood vessel walls; inc in blood pressure stretches walls -> sends an action potential to cardioregulatory & vasomotor centers -> decreases heart rate & contractility, increases blood vessel diameter |
| what is the equation for blood pressure? | blood pressure = cardiac output X total peripheral resistance |
| what is the equation for cardiac output? | cardiac output = heart rate X stroke volume |
| what is the equation for flow? | flow = (pressure 1 - pressure 2) / resistance |
| what controls heart rate and stroke volume? | the ANS; the parasympathetic branch decreases HR and SV; sympathetic branch does the opposite/ altering the end diastolic volume can also change SV |
Created by:
debmurph
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