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83 Cards in this Set
- Front
- Back
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Conduction
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-mediated by 3 cations: Ca, Na, K
-all are continually active, trying to bring cel to resting potential -2 types: 1. SA and AV node conduction: "slow conduction" 2. ventricular and atrial conduction: "rapid conduction" -Keep in mind K+ is permeable to the membrane but Na+ and Ca+ are not -K: high conductance -Na/Ca: low conductance (transport mediated by protein) |
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resting state
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-Ca and Na outside
-K inside cell -ATP dependent Na/K pump pumping K in and Na out -Na moves down the gradient and Ca moves out |
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Rapid and slow depolarization
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-slow: SA node 1m.sec; AV node .01-.05 m/sec
-rapid: ventricle 2-4 n/sec |
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threshold potential
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-the pt at which spontaneous depol rapidly takes place
-ions flow because of 2 factors: 1. Electrochemical gradient: maintain ionic and chemical equilibrium 2. Changes in conduction: opening of membrane proteins allowing ions to flow |
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SA/AV node conduction- phase 0
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-Ca channels open when threshold potential is met, cell is depolarized (Ca moves in and cell becomes more positive rapidly)
-T type Ca channels: not affected by Ca channel drugs |
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SA/AV node conduction- phase 3
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-K is pushed out to balance electrical forces; start to come back down to more negative resting state
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SA/AV node conduction- phase 4
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-AP has passed
-Cell returns to homeostasis -Na leaks slowly into cell polarizing it until threshold potential is reached (cell gradually becomes more positive then eventually reaches threshold) -Na funny channels |
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Ventricular/Atrial conduction- phase 0
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-threshold potential met, Na channels open, cell quickly depolarized to about 20mV, then Na channels slam shut
(Na into cell, cell becomes more positive) |
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Ventricular/Atrial conduction-phase 1
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-K is pushed out of cell by the electrochemical gradient, cell slightly re-polarizes
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Ventricular/Atrial conduction-phase 2
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-Ca channels open, positive Ca charges flow in an membrane potential is stabilized even though K continues to leave the cell
(L channels) -length of phase 3 determines duration of ventricular contraction -get flattening of curve- determines length of QRS |
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Ventricular/Atrial conduction- phase 3
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-Ca channels close. K continues to move freely down the steep electrochemical gradient
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Ventricular/Atrial conduction- phase 4
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-equilibrium is re-established, cell returns to homeostasis. By unknown mechanism there is a slight spontaneous depol. When threshold is met, cycle restarts
-slight depol- responsible for automaticity of cardiac cells |
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Conduction rate
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-each part of the heat paces at its own inherent rate
-SA node: 60-80 -AV node: 40-60 -Ventricules: 20-40 -heart is paced by the fastest pacemaker -if impulse is not received from higher pacemaker, the gradual depol will eventually being cells to threshold potential, but at different sequentially slower rates |
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Excitability
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-the ability or tendency of a cardiac cell to respond to an AP stimulus
-dependent on the amt of current needed to bring the muscle cell to threshold potential -refractory period: time when cell is re-setting and AP cannot be propagated -various effects on heart rhythm depending on where conduction is disturbed (HR changes, conduction blocks, ectopy, changes in contractility) |
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electrical performance
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Absolute refractory period (ARP): Cell is incapable of generating action potential
Effective refractory period (ERP) Cell can depolarize, but not conduct action potential Relative refractory period (RRP) Cell can depolarize and conduct, but with a greater than normal stimulus Supra-normal period (SNP) Cell is more excitable than normal |
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Altering the slop of phase 4
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-as in sympathetic stimulation
-inc slope, inc excitability, inc rate 1. ischemia 2. alkalosis 3. hypokalemia -dec slop, dec excitability, dec rate 1. acidosis 2. hyperkalemia 3. hyponatremia |
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altering resting membrane potential
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-Increased membrane potential (more negative), decreased excitability, decreased rate
1. acidosis -Decreased membrane potential (more positive), increased excitability, increased rate 1. alkalosis |
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altering threshold potential
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-Increased threshold potential, decreased excitability, slower rate
1. digoxin 2. hypercalcemia -Decreased threshold potential, increased excitability, faster rate 1. hypocalcemia |
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Sympathetic stimulation
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-NE from sympathetic system activate B1 receptors in the SA node
-increases rate of phase 4 depol in SA node by inc K influx -no change in resting membrane pot |
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parasympathetic stim
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-Ach from parasym system have 2 actions on SA node
-decrease Na influx, lengthening phase 4 -inc export of K, hyperpolarizing the membrane |
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Cardiac depolarization
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-spontaneous depol of SA node (unless stim by sympathetic system or inhibited by the parasympathetic system)
-by convention, wave of depol is considered positive -In SA and AV node Ca+ ions effect initial depolarization -In atrium and ventricle Na+ ions effect initial depolarization |
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Atrial depolarization
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-rapid conduction facilitated by Na
-produces P wave on EKG (myocardial contraction lags a few ms behind events on EKG) |
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AV node
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-atrium electrically isolated from ventricles by tricuspid mitral valves
-slow conduction facilitated by Ca influx -slowed conduction provides a"lag time" for complete atrial contraction prior to continued conduction through the heart |
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Ventricular depolarization
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-rapid conduction facilitated by Na
-beginning of QRS represents cardiac cells synchronized in phase 0 -impulse spread through ventricles -bundle of His -left and right bundles -purkinje fibers |
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Cardiac muscle
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-striated muscle: named b/c of the regular arrangement of the myofilaments that create a repeating pattern on electron microscope examination
-similar to voluntary skeletal muscle excepting 2 differences 1. branching structures 2. intercalated disks: improve conduction from cell to cell during depol -slide 43 |
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Actin and myosin
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-2 protein chains that interact for muscle contraction
-calcium driver interaction with the use of ATP -sliding filament model |
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calciums role in cardiac physiology
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1. ion in conduction
2. muscle contraction 3. contraction strength |
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Actin
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-thin filament
-2 proteins 1. Tropomyosin: Covers myosin binding sites when muscle is in relaxed state preventing binding of myosin heads 2. Troponin: Calcium receptor bound to tropomyosin that when activated caused the deformation of tropomyosin and exposes active sites for myosin heads -ca binds to troponin- exposes myosin binding sites on tropomyosin |
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muscle contraction
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-Wave of depolarization passing through cardiac cells release
Ca from the ER of the cell -Ca binds to troponin, altering the structure of the tropomyosin -The altered geometry of the tropomyosin uncovers myosin binding sites on actin -Myosin binds to actin -The process of binding to actin changes the geometry of the myosin, pulling on the actin -ATP detaches the myosin head from the actin and reverts it to its original shape -Cycle continues as long as there is extra-cellular calcium present |
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Atrial contraction (atrial systole)
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-atrium contracts adding and additional 5-20% of end ventricular stroke volume.
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isovolumetric contraction
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-Ventricular systole begins, but pressure in the ventricle is not larger than pressure in aorta yet. Mitral valve closes, there is no net movement of the ventricle.
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Systole
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-LV pressure becomes much greater than aortic pressure due to ventricular muscle contraction
-aortic valve opens and ejection of the blood into aorta ensues -rapid ejection- blood flow slows as pressure start to equalize -reduced ejection- blood flow slows as pressures start to equalize |
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isovolumetric relaxation
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-Left ventricle finishes contraction. Volume remains the same but pressure in the left ventricle drops lower than pressure in aorta, aortic valve shuts. LV pressure is less than atrial pressure at this point, so mitral valve starts to open. No net movement of the ventricle
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rapid filling
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-elastic recoil of the left ventricle causes a rapid increase in the volume of the ventricle. LV pressure rapidly drops, mitral valve opens and blood is sucked into the ventricle. As ventricle fills and pressure increases, filling slows until pressure in LV equals pressure in LA. This is a passive process driven by fluid dynamics
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reduced ventricular filling (diastasis)
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The ventricles are almost completely full of blood shortly after the middle of diastole. Ventricular volume continues to increase but at a slower rate. Again a passive process driven by fluid dynamics
-back to step 1, atrial contraction |
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Coronary perfusion
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-atria are thin enough to extract some O2 from circulating blood
-endocardium of the left ventricle can extract some O2 from circulating blood -majority of the O2 is delivered to all parts of the myocardium via the coronary arteries |
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Blood flow depends on
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1. coronary perfusion pressure: dependent on diastolic P
2. coronary artery vasoconstriction: regulated by catecholamines; sympathetic stim 3. diastolic time: diastolic time is completely dependent on HR |
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coronary perfusion
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Coronary arteries are squeezed shut during systole
Coronary perfusion takes places during Diastole when the heart muscle is relaxed At rest, 5% blood ejected during systole perfuses the coronary arteries. |
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stroke volume
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-The volume of blood ejected from the ventricle during systole, may be affected by several factors
Volume status Myocardial health Contractility Blood pressure Heart rate |
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CO
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-the volume of blood that is pumped by the heart each minute
-CO= SV X HR -can be calculated with invasive monitoring devices like Swan-Ganz catheters |
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isovolumetric contraction
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-Ventricular systole begins, but pressure in the ventricle is not larger than pressure in aorta yet. Mitral valve closes, there is no net movement of the ventricle.
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Systole
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-LV pressure becomes much greater than aortic pressure due to ventricular muscle contraction
-aortic valve opens and ejection of the blood into aorta ensues -rapid ejection- blood flow slows as pressure start to equalize -reduced ejection- blood flow slows as pressures start to equalize |
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isovolumetric relaxation
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-Left ventricle finishes contraction. Volume remains the same but pressure in the left ventricle drops lower than pressure in aorta, aortic valve shuts. LV pressure is less than atrial pressure at this point, so mitral valve starts to open. No net movement of the ventricle
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rapid filling
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-elastic recoil of the left ventricle causes a rapid increase in the volume of the ventricle. LV pressure rapidly drops, mitral valve opens and blood is sucked into the ventricle. As ventricle fills and pressure increases, filling slows until pressure in LV equals pressure in LA. This is a passive process driven by fluid dynamics
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reduced ventricular filling (diastasis)
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The ventricles are almost completely full of blood shortly after the middle of diastole. Ventricular volume continues to increase but at a slower rate. Again a passive process driven by fluid dynamics
-back to step 1, atrial contraction |
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Coronary perfusion
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-atria are thin enough to extract some O2 from circulating blood
-endocardium of the left ventricle can extract some O2 from circulating blood -majority of the O2 is delivered to all parts of the myocardium via the coronary arteries |
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Blood flow depends on
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1. coronary perfusion pressure: dependent on diastolic P
2. coronary artery vasoconstriction: regulated by catecholamines; sympathetic stim 3. diastolic time: diastolic time is completely dependent on HR |
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coronary perfusion
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Coronary arteries are squeezed shut during systole
Coronary perfusion takes places during Diastole when the heart muscle is relaxed At rest, 5% blood ejected during systole perfuses the coronary arteries. |
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stroke volume
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-The volume of blood ejected from the ventricle during systole, may be affected by several factors
Volume status Myocardial health Contractility Blood pressure Heart rate |
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CO
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-the volume of blood that is pumped by the heart each minute
-CO= SV X HR -can be calculated with invasive monitoring devices like Swan-Ganz catheters |
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isovolumetric contraction
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-Ventricular systole begins, but pressure in the ventricle is not larger than pressure in aorta yet. Mitral valve closes, there is no net movement of the ventricle.
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Systole
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-LV pressure becomes much greater than aortic pressure due to ventricular muscle contraction
-aortic valve opens and ejection of the blood into aorta ensues -rapid ejection- blood flow slows as pressure start to equalize -reduced ejection- blood flow slows as pressures start to equalize |
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isovolumetric relaxation
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-Left ventricle finishes contraction. Volume remains the same but pressure in the left ventricle drops lower than pressure in aorta, aortic valve shuts. LV pressure is less than atrial pressure at this point, so mitral valve starts to open. No net movement of the ventricle
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rapid filling
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-elastic recoil of the left ventricle causes a rapid increase in the volume of the ventricle. LV pressure rapidly drops, mitral valve opens and blood is sucked into the ventricle. As ventricle fills and pressure increases, filling slows until pressure in LV equals pressure in LA. This is a passive process driven by fluid dynamics
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reduced ventricular filling (diastasis)
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The ventricles are almost completely full of blood shortly after the middle of diastole. Ventricular volume continues to increase but at a slower rate. Again a passive process driven by fluid dynamics
-back to step 1, atrial contraction |
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Coronary perfusion
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-atria are thin enough to extract some O2 from circulating blood
-endocardium of the left ventricle can extract some O2 from circulating blood -majority of the O2 is delivered to all parts of the myocardium via the coronary arteries |
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Blood flow depends on
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1. coronary perfusion pressure: dependent on diastolic P
2. coronary artery vasoconstriction: regulated by catecholamines; sympathetic stim 3. diastolic time: diastolic time is completely dependent on HR |
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coronary perfusion
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Coronary arteries are squeezed shut during systole
Coronary perfusion takes places during Diastole when the heart muscle is relaxed At rest, 5% blood ejected during systole perfuses the coronary arteries. |
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stroke volume
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-The volume of blood ejected from the ventricle during systole, may be affected by several factors
Volume status Myocardial health Contractility Blood pressure Heart rate |
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CO
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-the volume of blood that is pumped by the heart each minute
-CO= SV X HR -can be calculated with invasive monitoring devices like Swan-Ganz catheters |
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Preload
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-the force stretching the heart immediately prior to contraction
-Starling’s Law observes that more stretched myocardium can generate greater contraction force and stroke volume -Clinically estimated by the end diastolic pressure of the LV -determined by venous return to the left heart, which is in turn determined by: Intravascular volume Venous tone Body Position |
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Afterload
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-the fore opposing ventricular contraction
-inc afterload decreases stroke vol -afterload is clinically estimated by the systemic vascular resistance (SVR) -Calculated from maximum systolic ventricular pressure, ventricle radius and ventricle wall thickness Measured with swan ganz cath |
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contractility
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-The “ionotropic” state, the intrinsic ability of the heart to generate contractile force. Greater contractility, greater stroke volume
-inc by symp NS -dependent on viability of heart muscle -inc by high preload and digoxin -dec by low preload, ischemia/infarction, acidosis, Bblockers and Ca channel blockers |
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HR
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-determined principally by the SA node, modified by neural and electrolyte balances
-parasym tone generally determines resting HR -HR above 140 bpm restrict diastolic filling time so drastically preload drops and therefore contractility falls |
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Frank-starling relationship
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-The force of a ventricular contraction is proportional to the muscle fiber length.
-longer the fiber, the greater the ensuing contraction -the heart will eject the same amount of blood from the left ventricle that it received from the venous system via the right atrium. More blood in, more blood out. |
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heart rate and contractility
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-Increased heart rate, increased number of action potentials
-Cardiac cells do not have time to extrude Ca+ between cycles, so on the next depolarization there is an increase in the total amount of Ca+ in the cell -Greater influx of Ca+ in the cell causes sarcoplasmic reticulum to accumulate more Ca+ for subsequent release |
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Autoregulation
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-factors that regulate the heart
-neural factors: predominate in regulation; work within sec to min -humoral factors: usually work within hrs to days |
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Neural autoregulation
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1. parasympathetic:
-Predominately regulates the heart -Decreases SA automaticity -Decreases AV conduction -Inhibits sympathetic tone -Decrease Ca+ release, lowering contractility 2. Sympathetic system: -Predominately regulates the vasculature -Can increase conduction and contractility |
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neural autoregulation-positive chronotrpoic effect
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-Norepinephrine stimulates b1 receptors
-Increases Na+ leaking back into cells -Increases slope of Phase 4 -Increases heart rate |
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negative chronotropic effects
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1. muscarinic stimulation
-Acetylcholine activates muscarinic receptors -Decreases the leakage of Na+ -Decreases slope of Phase 4 2. Increase K conductance -Hyperpolarizes cell membrane -Decreases resting membrane potential |
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Cardiac output and heart rate also influenced by neurological feedback from the right atrium and carotid sinus
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1. Carotid sinus:
-stretch receptors- detect BP -chemoreceptors- detect CO2 2. Right atrium -stretch receptors |
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Barorreceptor reflex (carotid sinus)
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-inc BP--> inc carotid stretch --> inc parasym stim, dec sym stim --> dec HR
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bainbridge reflex (right atrium)
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inc venous return --> rt atrial stretch --> dec parasym tone --> inc HR
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contractility- sympathetic stimulation (positive ionotrope)
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- b1 receptor stimulation cause activation of membrane transport proteins
-Increase myofibril peak tension, rate of tension, and rate of relaxation |
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contractility- parasympathetic stim
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-Muscarinic stimulation affects ion gradients during phase 2 and 3
-Decrease myofibril peak tension, rate of tension, and rate of relaxation |
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NE/Epinephrine
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-Released systemically by the adrenal medulla
-Stimulate alpha and beta receptors in the heart, increasing contractility and heart rate |
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Angiotensin
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-Renal response to low blood pressure
-Increases blood volume, therefore increasing preload and stimulating contractility |
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ADH
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-increases preload by increasing BP
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BPN/ANP
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-released by a stretched myocardium, causes vasodilation and diuresis
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ANP vs. BNP
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-Atrial Natriuretic peptide
-B-type natriuretic peptide (brain natriuretic peptide) -Function: 1. venous and arterial dilation 2. reduces venous return 3. inc GFR 4. inhibit renin 5. decrease Na resorption |
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ANP vs. BNP differences
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-ANP produced by atria, BNP bu ventricle
-BNP 2 distinct humoral proteins -BNP: half life of 18-20 min -pro- BMP: half life of 60-120 min -ANP: half life of 8-60 sec |
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thyroid hormone
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-increases sensitivity to catecholamines
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insulin
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-causes arterial dilation, might have some sympathetic actions
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