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85 Cards in this Set
- Front
- Back
What causes cardiac valves to open or close? |
Changes in pressure |
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If pressure in the atria is higher than that of the ventricles, which valves are open? (Names and corresponding sides) |
Atrioventricular (AV) valves; Tricuspid on the right side, Mitral(/bicuspid) on the left side. |
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In this moment in time, the semilunar valves are open. What does this tell you about pressure in the different parts of the heart? |
Pressure is higher in the ventricles than in the aorta. |
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What are the names of the two semilunar valves? What do they lead to? |
Pulmonary (R side); leads to pulmonary trunk. Aortic (L side); leads to aorta. |
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Chordae tendinae are associated with these types of heart valves: |
Atrioventricular (tricuspid, mitral) valves |
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The "first heart sound" is associated with this action: |
Closing of the atrioventricular valves |
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"Insufficiency, prolapse, or regurgitation" in the heart can result in this condition and is associated with these valves: |
Heart murmur; atrioventricular |
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What is stenosis in reference to heart valves? |
Failure for valves to open completely |
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What are the two primarily contractile muscle types in the heart? |
Atrial and ventricular myocytes |
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What feature connects cardiocytes? |
Intercalated discs |
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What are the three components of intercalated discs? |
Desmosomes, gap junctions, and interlocking plasma membrane. |
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What is responsible for allowing the atria and ventricles to operate as separate "synctiums"? |
Thick fibrous tissue separation |
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What are the two reasons why it's important that the atria and ventricles are separate synctiums? |
- Inappropriate communication via conductive cells is somewhat blocked - Promotes a brief lapse in time for blood from atria to flow into ventricles before electrical signal for ventricular contraction is processed |
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In regards to length, how do action potentials in cardiac muscle cells compare to that of skeletal muscle cells? |
Their action potentials last around 15x longer. |
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Describe the ion channel system responsible for the "plateau phase" of a cardiac muscle AP: |
- Fast voltage-gated K channels (K out) close - Slow voltage-gated K channels open - Voltage gated "L-type" Ca channels open (slow Ca2+ in) - Balance between slow K out and slow Ca in causes a membrane potential "plateau effect" |
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In cardiac muscle, what causes repolarization after the plateau effect? (2 actions) |
- L-type Ca channels close, - More slow-voltage K channels open |
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Where is the absolute refractory period occurring? What about the relative refractory period? |
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Why is the long absolute refractory period of cardiomyocytes essential? |
Temporal summation of AP's is prevented, meaning that cardiomyocytes are not susceptible to tetany |
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What are T-tubules used for in myocytes? Where are they most common? |
Excitation contraction coupling; ventricles |
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Where is extracellular calcium stored for use by cardiomyocytes? |
On mucopolysaccharides bound to the T-tubules |
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How does Ca storage in cardiomyocyte SR's compare to that in skeletal muscle SR's? (SR= sarcoplasmic reticulum) |
Cardiomyocytes store much less Ca in their SR's. |
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To initiate contraction, what protein does Ca bind in the muscle? What is the effect of this binding? |
Ca binds troponin, which causes movement of tropomyosin, which exposes the "active sites" for binding on actin fibers. |
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When is the Na/Ca exchanger in cardiomyocytes most active? What kind of transporter is this? |
In cardiomyocyte relaxation; it's a secondary active antiporter. |
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In response to a single AP, how do cardiomyocytes differ from skeletal myocytes? |
Cardiac response is graded; strength of contraction is dependent on amount of intracellular calcium. The amount of intracellular calcium is regulated in order to tightly control saturation of troponin with calcium. |
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Systole and diastole– which is contraction and which is relaxation? |
Systole is contraction, diastole is relaxation. |
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When does isovolumetric contraction occur in the cardiac cycle? |
Atrial diastole/ early ventricular systole |
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What is going on during the "ejection phase" of the cardiac cycle? |
Late ventricular systole |
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What is happening with the atria/ventricles when "active filling" of the heart is occurring? |
Atrial systole, ventricular diastole. |
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Isovolumetric relaxation is experienced during what phase of the cardiac cycle? |
Early ventricular diastole |
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When does passive filling of the heart occur? |
Between heartbeats. |
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What amount of blood for contraction is loaded into the heart during the "passive filling" phase between beats? |
80% |
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Between beats, the pressure of the atria compared to the pressure in the veins is described as what? |
Pressure in atria is lower than the pressure in the veins. |
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There is only one phase where pressure in the atria is greater than the pressure in the veins. What is it? |
Atrial systole. |
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How does the pressure in the ventricles compare to the pressure in the arteries during atrial systole? |
Pressure in the ventricles is lower than the pressure in the arteries during atrial systole. |
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There is only one phase in which pressure in the ventricles is greater than pressure in the arteries. Which phase is this? |
Late ventricular systole. |
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In atrial diastole and early ventricular systole, how does the pressure in the atria compare to that in the ventricles? |
The atria are lower in pressure than the ventricles. |
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During late ventricular diastole, how does the pressure in the atria compare to the pressure in the ventricles? |
The pressure in the atria is greater than that in the ventricles. |
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What is the stroke volume? |
Volume of blood ejected per heartbeat |
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How do we find stroke volume? |
End diastolic volume (EDV)- End systolic volume (ESV) |
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What part of the heart do we make volume pressure diagrams for? |
The left ventricle |
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Describe what the "ejection fraction" refers to: |
The amount of end diastolic volume ejected per beat |
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Is "end systolic volume" or "end diastolic volume" a higher value for the left ventricle? |
End diastolic volume. |
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In this condition, a murmur is heard when heart valves are open. In what condition is a murmur heard when heart valves are closed? |
Open: stenosis (abnormally narrow opening). Closed: Regurgitation/prolapse (incomplete closing) |
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What's the formula for cardiac output? |
CO=HR (heart rate) x SV (stroke volume) |
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What's normal resting cardiac output? |
5L/min |
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What effects will blood loss and heart disease have on cardiac output? |
Decrease |
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What three factors change stroke volume? |
- Change in preload (end diastolic volume) -Change in afterload (end systolic volume) -Change in contractility (this is force of contraction, would affect end systolic volume (ESV)) |
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What does "VR" stand for? |
Venous return; the rate at which blood is returned to the heart by veins |
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How much total blood volume can be held in veins? |
Up to 60%
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What three things can increase the venous return? |
- Increasing the effect of the skeletal muscle pumps - Increasing the effect of the thoracic pump - Venoconstriction via sympathetic activation of alpha receptors |
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What has a greater effect on cardiac output– stroke volume or heart rate? |
Heart rate |
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Greater maximal atrial pressure will result in a greater value for this measured volume of the left ventricle: |
End diastolic volume (EDV) |
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What's the relationship between EDV and CO? |
Greater EDV, greater CO (EDV = end diastolic volume, CO = cardiac output) |
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Which ventricle requires a greater increase in atrial pressure to generate a greater output? |
Left ventricle. The right ventricle is more sensitive to pressure increase in the right atrium, and will increase output more quickly. |
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Define "afterload" |
The pressure that ventricles must overcome to force open aortic and pulmonary valves. |
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Hypertension would increase this element that affects stroke volume: |
Afterload |
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What is the effect of increased afterload on stroke volume? |
Increased afterload (ESV) decreases stroke volume |
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Relationship between stroke volume, end diastolic and end systolic volumes? |
SV= EDV-ESV |
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What's the effect of hypertension on the equation SV = EDV-ESV? |
Hypertension increases afterload; a factor affecting ESV. This increases ESV, thereby decreases SV. |
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Define "contractility" |
Ability of the heart to contract at any given resting fiber length. |
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How is contractility changed by the heart? |
Modifying the amount of Ca that enters contractile cells via manipulation of L-type voltage-gated Ca channels |
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What nervous system has no direct effects on contractility? |
Parasympathetic |
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What's the primary molecular mechanism by which beta-1 receptors modify contractility? |
Phosphorylation |
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What five molecules in the cardiomyocyte are phosphorylated in response to beta-1 receptor activation? |
1) L-type Ca channels 2) Ryanodine receptors 3) Troponin 4) Myosin head ATPase 5) Ca ATPase in sarcoplasm |
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What's the difference between a positive and negative inotropic agent? Examples of each? |
Positive: Increases heart contractility. Epi/Norepi are examples. Negative: Decreases heart contractility. Beta-blockers, Ca channel blockers |
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What is digitalis? |
A positive inotropic agent (increases contractility) |
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The dashed lines represent changes in stroke volume brought on by what effect? |
Increased preload |
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The dashed lines represent changes in stroke volume brought on by what effect? (Left vent. pressure on Y axis) |
Increased afterload |
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The dashed lines represent changes in stroke volume brought on by what effect? (Left vent. pressure on Y axis) |
Increased contractility |
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At what age does cardiac output peak (on average) |
10 years |
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Effects of hyper- and hypo- calcemia on cardiac output? |
Hyper- increases contractility, thus increases output Hypo- opposite |
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What's the effect of hyperkalemia on conduction speed of AP's through cardiac tissue? |
It decreases conduction speed. |
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What's the effect of hyperkalemia on rate of potassium movement through potassium channels (conductance)? |
It increases this rate of movement |
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What's the overall effect of hyperkalemia on tissue excitability? |
Decrease |
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What's the effect of extreme tachycardia (HR) on cardia output? |
Decrease in CO |
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Describe what causes cardiac tamponade and what its effect is on SV = EDV-ESV? |
Card. tamponade occurs when blood or fluid accumulates in the pericardial sac; it increases interpericardial pressure, and decreases end diastolic volume because it decreases ventricular filling. Thus, SV (stroke volume) goes down. |
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What are the effects of high temperature or pregnancy on cardiac output? |
They increase cardiac output |
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What's the effect of rapid arrythmias on cardiac output? |
They decrease cardiac output |
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What element of stroke volume is affected by physiological cardiac remodeling? |
Hypertrophy increases force of contraction which serves to decrease ESV, which in turn increases SV |
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What's the effect of physiological cardiac remodeling on heart rate? |
Decrease (heart is more efficient, doesn't need to work as hard) |
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What are hallmarks of "pathological" cardiac remodeling? |
Irreversible changes to heart proportions and function often brought on by pathology |
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Describe "concentric hypertrophy" |
Increased wall thickness of the heart results in decreased compliance of ventricles and increased contractility. Overall effect is increased afterload (hypertension). |
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Describe "eccentric hypertrophy" |
The lumen of ventricles increases. Also, speed of contraction increases. This decreases mechanical efficiency and also ejection fraction. Overall effect is increased preload. |
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Ventricular hypertrophy is often a side-effect of ____ and has this effect on cardiac output: |
Exercise; increase |
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Concentric and eccentric hypertrophies often result in a heart described using this term: |
"Hypoeffective" |