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171 Cards in this Set
- Front
- Back
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How do things move in the body?
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I. Things move in the body in thanks to two kinds of forces; diffusion or bulk flow
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what is diffusion
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Diffusion- is movement down a chemical and/or electrical gradient aka an electrochemical gradient. Examples are movement of oxygen between the lungs and blood.
J= (-DA ×∆C)/x Rate of diffusion (J), where D is the diffusion constant, A is area, delta c is the concentration gradient, and x is thickness. For a single molecule, time for diffusion is: t= (∆x^2)/2DT where D is the diffusion constant, x is thickness , t is time, T is temp in K |
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what is the equation that describes the rate of diffusion
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J= (-DA ×∆C)/x Rate of diffusion (J), where D is the diffusion constant, A is area, delta c is the concentration gradient, and x is thickness.
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what eq describes the rate of diffusion for a single molecule?
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For a single molecule, time for diffusion is: t= (∆x^2)/2DT where D is the diffusion constant, x is thickness , t is time, T is temp in K
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what is bulk flow
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is movement down a pressure gradient as occurs between the heart and the rest of the body. Ohm’s Law describes Bulk Flow.
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What is Ohms law? what does it describe?
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Ohm’s Law describes Bulk Flow.
Q ̇= ∆P/R Where Q is amount of blood pumped out of the heart per minute or cardiac output. Delta P is the pressure gradient. And R is resistance in ohms or peripheral resistance units. |
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what is CO? what does it equal
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3. Cardiac output is equal to Heart rate times stroke volume C.O. = HR x SV
4. Cardiac output is also equal to mean arterial pressure/ total peripheral resistance |
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what is mean arterial pressure?
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5. Mean arterial pressure is the central venous pressure of the right atrium?
1. MAP= Q x TPR 2. Where TPR is total peripheral resistance and Q is cardiac output |
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what kind of a system is the cardiovascular system? WHat are the advantages?
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The cardiovascular system is a branching system. The advantage of a branching system over a series circuit is:
Blood can be shunted to a different part of the body that needs it Lower resistance, it is possible to change resistance independently of another part of the body Damage to one vessel does not necessarily mean the end. 1/R=∑_1/R_n This means that an increase is a single resistor DOES increase total resistance |
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what equation describes resistance in the cardiovascular system? significance?
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1/R=∑_1/R_n This means that an increase is a single resistor DOES increase total resistance
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what is the equation that describes blood flow resistance?
what is the most important part of the equation? |
Blood flow resistance follows parabolic flow
R= 8ηL/(πr^4 ) Where R is resistance, η is viscosity, L is length, and r is radius Radius is the most important factor here. A small change to the radius has dramatic effects in resistance. By changing the radius we can change R and shunt blood. |
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what is the relationship of flow rate int eh systemic and pulmonary circulation
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a. Both the systemic and pulmonary systems have the same blood flow (~5L/min)
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what is the relationship between blood volume in systemic vs pulmonary circulation?
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b. The volume % of blood is 88% is systemic circulation
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what is the realtionship btween blood volume in veins vs arteries in systemic circulation?
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c. In the systemic circulation the systemic veins holds 2/3 of the systemic blood
1. The veins act as capacitors by storing most of the blood |
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what is the realtionship between blood pressure in the systemic vs poulmonary circulation?
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d. Since the heart is in series blood pressure is higher in the systemic circulation
1. Normal blood pressure of systemic circulation is 120/80 measured as pressure of systole/diastole |
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what is pulmonary hypertension and why is it dangerous?
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e. Pulmonary hypertension (high blood pressure) is very dangerous because blood can leak out of the vessels into the lungs and lead to drowning.
1. Normal pulmonary blood pressure in the pulmonary circulation is 24/8 |
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what is the relationship of blood pressure in the different parts of the systemic circulation?
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f. Blood pressure is highest in the aorta and large arteries, at a minimum in the small veins and venae cavea, and low in the pulmonary circulation.
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what is the equation for mean arterial pressure
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g. Mean Arterial Pressure = HR x SV x TPR
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what carries deoxygenated blood to the heart? Where does it go? features?
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a. The superior vena cava and inferior vena cava carrying deoxygenated blood feed into the right atrium. There is no valve between the venea cavea and the atrium to prevent blood form flowing backwards
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where and how does blood travel from the right atrium?
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b. The blood in the right atrium flows though the tricuspid valve down into the right ventricle
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where and how does blood travel form the right ventricle?
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c. The right ventricle pumps deoxygenated blood from the heart to the lungs via the pulmonary arteries (left and right)
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where and how does blood go from the lungs to the heart?
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d. The blood from the lungs travels down the four pulmonary veins into the left atrium.
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where and how does blood go from the left atrium?
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e. The blood from the left atrium gets pumped through the mitral valve (or bicuspid valve or left Arial ventricular valve) into the left ventricle.
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where and how does blood go after the left ventricle?
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f. Blood from the left ventricle leaves via the through the semilunar valve openning to the aorta and goes to the rest of the body coming back to the right atrium through the venea cavea
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what are the semilunar valves? where are they?
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g. There also exist in the heart crescent moon valves or semi lunar valves
1. The right heart the semilunar valves separate the ventricle from the pulmonary artery 2. The aortic lunar valve separates the left ventricle from the aorta |
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What principle describes velocity of flow? what is the equation?
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VI. Bernoulli’s Principle deals with the velocity of flow, and says that velocity is inversely proportional to the area squared (V = flow rate/ A2 )
a. Assuming that flow rate is constant, this means that blood will flow faster though smaller vessels than it does through large ones when the vessels come one right after another. b. ***** Not true for circulatory system because series in circuit and the cross sectional area of the capillaries is huge compared to the large vessels, so there, the blood flow is slowest. |
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where is blood flow fastest? slowest? why?
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because series in circuit and the cross sectional area of the capillaries is huge compared to the large vessels, so there, the blood flow is slowest.
c. the average velocity in the arteries is 33 cm/sec d. The average velocity in the capillaries is .3 mm/sec |
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what are the characteristics of the atrteries
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a. Arteries- are the most elastic vessels.
1. During diastole you don’t get a very large change in pressure because when the heart contracts, during systole the aorta expands. Some energy is used to stretch the aorta and not to exert pressure so systolic pressure during systole is not as high and diastolic is not as low 2. With age the arteries become less elastic and pulse pressure increases, meaning that systolic pressure increases and diastolic pressure goes down. |
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what are the characteristics of the arterials? function?
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b. Arterials- are resistance vessels. They consist of smooth muscle that can contract and change pressure by decreasing radius, thereby increasing resistance
1. During exercise there is an increase in resistance in the GI tract and blood is shunted to skeletal muscle. 2. During exercise the radius of the veins near skeletal muscle increases, decreasing resistance |
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what are the characteristics of cappilaries?
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c. Capillaries- are one cell thick (1 um) and allow for diffusion to take place. There is no smooth muscle, no collagen, and no elastin. The caps have a huge square area and velocity here is slowest.
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What are the characteristics of venules?
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d. Venules- collect blood and have a role in inflammation
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what are the characteristics and functions of veins?
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e. Veins- are capacitors they can store blood and have one way valves that prevent blood from flowing backwards with gravity.
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what do heart muscle cells have a lot of and why?
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a. Heart cells gave a huge number of mitochondria because the heart MUST use oxygen to work. There is no anaerobic metabolism in the heart.
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what are the names of important organells in heart muscle cells
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c. The endoplasmic reticulum is called the sacroplasmic reticulum
d. The cytoplasm is called the sarcoplasm e. The plasma membrane is called the sarcolema f. Bundles if individual muscle cells are called fascicles. g. The sarcoplasm is packed with mitochondria and hundreds of banded, rod like elements called myofibrils |
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what are myofibrils?
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g. The sarcoplasm is packed with mitochondria and hundreds of banded, rod like elements called myofibrils
h. Each myofibril is a bundle of overlapping thick (myosin) and thin (actin) filaments. |
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what is the intercollated disk?significance?
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i. Intercolated disks are an embryonic scar where different heart muscles fused together to allow the different cells to be in electrical contact with each other.
1. Heart Muscle cells are therefore not mechanically or electrically insulated from each other. 2. The intercollated disk is stabilized by scaffolding made up of desmosomes |
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what are gap functions? significance in heart?
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j. Gap junctions allow for current to flow freely between cells and therefore fro the cells to communicate with each other. These are electrical synapses (versus chemical in neurons).
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characteristics of myofibrils?
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k. Muscle fiber looks like a cable made up of smaller cables called myofibrils
1. Myofibrils have dark and light bands 1. The dark bands are called A bands a. In the A band, actin and myosin overlap 2. The light bands are called I bands a. The I band crosses from one sarcomere over the Z line, to the next sarcomere 2. Myofibrils can also be split into sarcomeres |
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what are a bands?
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1. Myofibrils have dark and light bands
1. The dark bands are called A bands a. In the A band, actin and myosin overlap |
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what are i bands?
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1. Myofibrils have dark and light bands
a. The I band crosses from one sarcomere over the Z line, to the next sarcomere |
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describe a sarcomere
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1. A sarcomere goes from z-line to z-line
2. The z line splits the light I band in two 3. The a bands is in the middle of the sarcomere 4. The middle part of the A band is the H zone 5. The middle of the H zone is the M line a. In the H zone there are no myosin cross bridges b. This is also the place where two myosin fibers of opposite polarity are knit together. 6. Embedded in the z line are thin actin filaments 7. The thick filaments made of myosin run in the middle of the sarcomere and are anchored with actin via cross bridges |
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what is the z line
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2. The z line splits the light I band in two
6. Embedded in the z line are thin actin filaments |
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where is the a band?
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3. The a bands is in the middle of the sarcomere
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what is the H zone
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4. The middle part of the A band is the H zone
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what is in the middle of the H zone? characteristics?
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5. The middle of the H zone is the M line
a. In the H zone there are no myosin cross bridges b. This is also the place where two myosin fibers of opposite polarity are knit together. |
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describe actin
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3. Actin- makes up thin filaments
1. Has a plus end and a minus end 2. It is made of globular (g) actin that polymerize into filament (f) actin a. G actin has a myosin binding site 3. Consists of two polypeptides wrapped around each other in a helix 4. It has a groove that can accommodate a thin filament of tropomyosin. a. Tropomyosin can move right in from of the myosin binding sites of G actin to block them from binding the myosin heads or, it can move out of the way. |
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what is tropomyosin
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a. Tropomyosin can move right in from of the myosin binding sites of G actin to block them from binding the myosin heads or, it can move out of the way.
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what is the troponin comlez
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b. Troponin complex- is periodically stuck to tropomyosin and consists of:
i. Troponin T – binds tropomyosin ii. Troponin I – binds to actin to inhibit the myosin binding site iii. Troponin C – binds calcium |
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i. Troponin T
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binds tropomyosin
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ii. Troponin I
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– binds to actin to inhibit the myosin binding site
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iii. Troponin C
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binds calcium
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describe the thick filaments
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1. Made up of 6 proteins\
a. Two heavy chains in a double helix that terminate into globular cross bridges b. Two light chains in each head of the crossbred that act as regulatory proteins that regulate muscle contraction when epinephrine or norepinepherine act c. The two heads also have an ATP binding site. One on each head d. The tip of the head consists of an actin binding site. e. The cross bridges on myosin touch a binding site on actin |
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what is the equation for power
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1. Power = work/time = force x velocity
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what are the steps needed for muscle contration to occur in the heart? *****
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2. Steps that take place for heart muscle contraction to occur
1. A cross bridge binds to actin because there is no repulsion between the actin and myosin. 2. An inorganic phosphate is displaced, moving the cross bridge head to a resting state configuration. Because of this change in configuration, the actin that the cross bridge is bound to moves to the middle of the sarcomere and the sarcomere shortens. 3. The myosin head binds ATP, and detaches because of repulsion caused by the negatively charged ATP molecule 4. The ATP binding site of the head is also an ATPase. The ATPase activity hydrolyzes the ATP to ADP on cross bridge causing the head to go to a 90 angle in an energized state. The cross bridge then binds to actin via the actin binding site |
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why is the movement of the sarcomere not jagged?
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3. The movement of the sarcomere is smooth because the heads are in a staggered conformation so as one disengages, another one engages.
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what changes in the sasrcomere during shortening? why?
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4. This movement does NOT change the length of the A band (where actin and Myosin overlap)
5. IT DOES change the length of the I band because this part is made up of actin alone |
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what ion is most important in sarcomere shortening>
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a. Calcium plays a role in muscle contraction and its release is due to action potential
b. The hearts Sinal atrial node is like a battery, it discharges spontaneously. The electrical impulse causes calcium to be released. c. The action potential travels along the sarcolema. To get deep into the cells it needs a channel. These Channels are the transverse tubules or T tubules. 1. T tubules come in close contact with the sarcoplasmic reticulum. 2. The sarcoplasmic reticulum stores and releases calcium d. The concentration of calcium in the extracellular fluid and T tubule is 10-3 M. Inside the cell it is 10-7 M. e. The electrical impulse strted by the SAN travels down the T tubule to the dihydropuridine (DHP) receptor, a sensor for electrical impulses 1. In the heart muscle the DHP causes the receptor to open and calcium to move from the extracellular fluid to the sarcoplasm f. The ryanodine receptor in the sarcoplasmic reticulum, when bound to calcium causes more calcium to be released from the sarcoplasmic reticulum. g. Remember that troponin C that is bound to tropomyosin and actin bind calcium. It has 4 binding sites for calcium but in heart muscle only one of the 4 binding sites is available. h. Calcium binds to TnC and causes it to move out of the way exposing the actin binding site |
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how does calcium first get in to the cell?
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b. The hearts Sinal atrial node is like a battery, it discharges spontaneously. The electrical impulse causes calcium to be released.
c. The action potential travels along the sarcolema. To get deep into the cells it needs a channel. These Channels are the transverse tubules or T tubules. 1. T tubules come in close contact with the sarcoplasmic reticulum. 2. The sarcoplasmic reticulum stores and releases calcium d. The concentration of calcium in the extracellular fluid and T tubule is 10-3 M. Inside the cell it is 10-7 M. e. The electrical impulse strted by the SAN travels down the T tubule to the dihydropuridine (DHP) receptor, a sensor for electrical impulses 1. In the heart muscle the DHP causes the receptor to open and calcium to move from the extracellular fluid to the sarcoplasm |
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what effect doe opeing the DHP receptor have?
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e. The electrical impulse strted by the SAN travels down the T tubule to the dihydropuridine (DHP) receptor, a sensor for electrical impulses
1. In the heart muscle the DHP causes the receptor to open and calcium to move from the extracellular fluid to the sarcoplasm f. The ryanodine receptor in the sarcoplasmic reticulum, when bound to calcium causes more calcium to be released from the sarcoplasmic reticulum. |
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what is the ryanodine receptor?
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f. The ryanodine receptor in the sarcoplasmic reticulum, when bound to calcium causes more calcium to be released from the sarcoplasmic reticulum.
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what does calcium do to the myosin actin realtionship
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g. Remember that troponin C that is bound to tropomyosin and actin bind calcium. It has 4 binding sites for calcium but in heart muscle only one of the 4 binding sites is available.
h. Calcium binds to TnC and causes it to move out of the way exposing the actin binding site i. The myosin head can now bind to actin and contraction of the sarcomere can take place. |
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what do you need to get myosin head binding to actin?
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h. Calcium binds to TnC and causes it to move out of the way exposing the actin binding site
i. The myosin head can now bind to actin and contraction of the sarcomere can take place. 1. Also to get myosin to bind you also need to reduce electrical repulsion by hydrolyzing ATP to ADP |
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what causes hypothermic death?
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2. Side note: Hypothermia death is due to fatal arrhythmia. The heart is more sensitive to temperature decreases because a decrease in temperature causes a decrease of affinity for calcium of troponin C.
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what causes rigor mortis
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j. Rigor Mortis – as cells degrade, the sarcoplasmic reticulum breaks down and releases calcium. The calcium binds to Tc. Tc moves, exposing actin binding site and all muscles contract. Since no new ATP is produced the cross bridges cannot unbind because there is not electrical repulsion from ATP (all ADP).
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what are the L type channels? what do they do?
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a. L-type calcium channel (DHP receptor) is a heteropentametric receptor (on the membrane)
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1. Why does electrical activity open the L type calcium channel channel?
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1. Remember that the tertiary structure of a protein depends on non-covalent interactions.
2. Electricity changes the charges and therefore changes the tertiary structure of the protein. 3. In the heart this causes the L-type channel to open up and let a small amount of extracellular calcium in. |
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what is the ryanadine receptor
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b. The Ryanadine receptor of (SR channel) is a case of calcium induced calcium release (CICR)
1. Stimulation if this channel causes a fire of release of calcium from the sarcoplasmic reticulum. |
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how is muscle shortenning due to calcium different in skeletla muscles?
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1. The l type channel alters configuration but does not open. Instead it is physically linked to the ryanadine receptor, and a conformational change of the L channel causes the ryanadine receptor to open.
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what is the relationship btw length of myocardial fiber and force of contraction? why?
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a. As the length of the myocardial fiber increases, the force of contraction increases because:
1. In the heart, during diastole as the ventricle fills with blood the volume of the ventricle increases, muscle fibers stretch and length increases. According to this relationship the amount of blood that gets pumped out will also increase because there is a stronger force of contraction. |
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what is the relationship btw concntration of calcium and force for fibers of different stretch?
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b. At the same amount of calcium a stretched fiber will produce more force than a shortened one or a normal one.
1. Why? We don’t know |
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draw the relationship btw intiial length of fiber and force.
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draw calcium concntration vs force for fibers of different stretch
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c. How does stretching increase force?
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1. Actin is rooted in the z line
2. Myosin is rooted in the z line via titin 3. Stretched myosin cross bridges are closer to the binding site because titin pulls on them and brings them closer to the myosin binding site on actin. This increases the likely hood for interaction. |
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what is starling's law of the heart? What does is signify?
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d. Starling’s Law of the heart
1. As end diastolic volume increases, stroke volume increases. 2. This means that you can get rid of extra blood in the heart and avoid pooling of blood in the heart and lungs. 3. During exercise a release of norepinepherine raises this curve so that there is more of an effect. |
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how do you change dynamics of skeletal muscle?
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1. In skeletal muscle you can change force because
1. Not all of the muscle cells in the muscle group are always stimulated so you can increase the number of cells that do work 2. You gen also generate more action potentials per second and the strength of cells increases. |
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how do you change dynamics of heart muscle?
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2. In the heart every cell is already always activated because all the cells are connected electrically.
1. Increasing action potentials per minute (hear rate) does not have a significant effect 2. Not every action potential releases all calcium a. Epinephrine or norepinepherine from the adrenal gland binds to Beta 1 receptors in the heart. This stimulates g protein to increase cAMP, that acts on Protein kinase A, which increases the phosphorylation of proteins i. PKA phosphorylates Calcium (L-type) channels in the sarcolema and cause more calcium to enter the sarcoplasm, therefore more ryanodine receptors are stimulated to release more calcium for the sarcoplasmic reticulum ii. PKA also phosphorylates phospholambdin on the sarcoplasmic reticulum 1. Calcium can be pumped out of the cell in three ways, directly, by exchange and by phospholambdin 2. Phosphorylation of phospholambdin causes more calcium to be pumped back into the sacroplasmic reticulum so that it is ready to be released again when the next action potential comes (decreased the recovery time) 3. The amount of free calcium in the sarcoplasmic reticulum is kept low by sequesterin so that it is easier (smaller gradient) to pump calcium back in iii. PKA also phosphorylates tropomyosin I, moving it out of the way so that TPC is more likely to bind calcium |
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where does epinepherine act in the heart
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a. Epinephrine or norepinepherine from the adrenal gland binds to Beta 1 receptors in the heart. This stimulates g protein to increase cAMP, that acts on Protein kinase A, which increases the phosphorylation of proteins
i. PKA phosphorylates Calcium (L-type) channels in the sarcolema and cause more calcium to enter the sarcoplasm, therefore more ryanodine receptors are stimulated to release more calcium for the sarcoplasmic reticulum ii. PKA also phosphorylates phospholambdin on the sarcoplasmic reticulum iii. PKA also phosphorylates tropomyosin I, moving it out of the way so that TPC is more likely to bind calcium |
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what is the significance of activating phospholambdin
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ii. PKA also phosphorylates phospholambdin on the sarcoplasmic reticulum
1. Calcium can be pumped out of the cell in three ways, directly, by exchange and by phospholambdin 2. Phosphorylation of phospholambdin causes more calcium to be pumped back into the sacroplasmic reticulum so that it is ready to be released again when the next action potential comes (decreased the recovery time) |
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what is purpose of sequesterin
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3. The amount of free calcium in the sarcoplasmic reticulum is kept low by sequesterin so that it is easier (smaller gradient) to pump calcium back in
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where and how does acetylcholine act in the heart?
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b. Acetylcholine is the opposite of epinephrine. It is secreted by the vagus nerve (the 10th cranial nerve) and is part of the parasympathetic nervous system.
i. ACH is inhibitory but there is little parasympathetic effect on the ventricle just the SAN |
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what is the afterload?
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1. The after load is the force you have to lift with the heart.
1. On the right, after load = blood pressure in the pulmonary artery 2. On the left, after load = BP of the aorta (before contraction) |
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what determines how much force you can generate
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3. Length determines how much force you can generate and is equal to the preload.
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what happends as afterload increases?
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As after load increases:
The initial velocity of shortening decreases. The time it takes to shorten the fibers increases Power increases but only to a point. This all means that if you have higher blood pressure (aka a higher after load) (pressure in aorta for left hear and pressure in pulmonary artery for the right heart) then the heart can increase the power and force and pump out more blood, but only to a point. |
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draw the relationshhip of force and muscle shotening over time.
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what is the relationship with different afterloads and shortening over time? draw it.
initial velocity of shortening vs afterload? power v afterload? |
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draw the relationship of different preload on afterload and initial v or shorening? how does epinepherine change this?
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draw end diastolic volume vs stroke volume? how does this change with sympatheis and parasypathetic activity?
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relation btw end diastolic volume and stroke volume. How does this change with epinepherine?
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For the same end diastolic volume, is epinephrine is present then stroke volume will be higher. This is a positive ionotropic effect (beat with more force for the same preload). This occurs during exercise.
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what is the law of laplace? where is it important?
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Law of la Place
P= 2T/r During heart failure, muscles are dying, and heart volume is increasing. In order to generate the same amount of pressure you need to increase the tension. Increasing tension causes more heart failure because the force on the wall of the hear increases and blood flow is messedup. A weaker heart smaller ejection fraction stretching of ventricle have to work harder to generate pressure |
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diastole
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- ventricular relaxation
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systole
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ventricular contraction
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what happens at phase 4 of the heart cylce
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c. Phase 4: The beginning of diastole or isovolumetric relaxation
1. The pressure in the ventricle decreases, muscles relax, and there is a decrease in calcium (it is back in the sarcoplasmic reticulum. 2. Troponin and tropomyosin are blocked (ATP has been generated) 3. Force has decreased, relaxation 4. All valves are closed (mitral, tricuspid, semi lunar aortic, semi lunar pulmonary 5. There is no change in volume of the ventricle 6. When pressure in the ventricle falls below the pressure in the atria then the AV valve opens and we get… |
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what happens at phase 1 of the heart cycle?
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1. Ventricular volume increases
2. Relaxation of the ventricle acts like vacuum and sucks blood from the atria 3. At the end of phase one, atrial muscle contracts increasing the filling of the ventricle. 4. Most of diastole is passive because pressure is lover in the ventricle than the atrium 5. Only 1/3 of ventricular volume is due to contraction of the atria 6. If an individual has atrial fibrillation he/she can still survive. The only issue occurs during exercise when that extra 1/3 of blood volume is needed. 7. Pulmonary and aortic semilunar valves are closed 8. At the end of diastole the ventricle contracts and we get… |
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what happens at phase 2 of the heart cycle?
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1. When the pressure in the artery increases above the pressure of the ventricle the AV valves close
2. There is isovolumetric contraction. Force generated in the ventricle is less Than the after load 1. The semilunar valves remain closed because ventricular pressure is not enough to force them open yet so volume stays the same as pressure increases |
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what happens at phase 3 of the heart cycle?
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f. Phase 3 ventricular ejection:
1. When pressure in the ventricle increases over the pressure in the atrium valves open 2. Blood is ejected from ventricle 3. aortic pressure increases 4. Blood continues to leave the ventricle until the pressure in the aorta is higher than the pressure in the ventricle 5. When ventricular pressure drops below aortic pressure, aortic valves shut and we go back to phase 4 end of systole |
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what happens to aortic pressure throughout the heart cycle?
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f. Phase 3 ventricular ejection:
1. When pressure in the ventricle increases over the pressure in the atrium valves open 2. Blood is ejected from ventricle 3. aortic pressure increases 4. Blood continues to leave the ventricle until the pressure in the aorta is higher than the pressure in the ventricle 5. When ventricular pressure drops below aortic pressure, aortic valves shut and we go back to phase 4 end of systole wah |
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what happens to atrial pressure throufhout the heart cycle?
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b. Atrial pressure
1. Diastole: pressure increases even though there is no contraction because there is no valve between the atria and the vena cava so blood continues to flow in 2. Systole: pressure decreases because of relaxation of the atria 3. When atria contracts there is little of any blood that moves into the vena cava or pulmonary veins because the momentum of blood flowing through the vena cava and pulmonary veins exceeds arterial pressure of contraction |
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first heart sound
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a. First heart sound, closing of the AV valve
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2nd heart sound?
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b. Second heart sound: closing of the aortic and pulmonary valves
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3rd heart sound?
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c. Third heart sound: occurs during heart failure when ventricles are stretched to their physical limits and you hear a squeaking like an overstretched balloon
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4th heart sound
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d. Fourth heart sound: contraction of the atrium
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heart murmor?
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e. Heart murmur: if something is wrong with the valves and they don’t close all the way, blood moves into the aorta and atrium from the ventricle causing turbulent flow (retrograde). The turbulent flow sound can be heard as a heart murmur.
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draw the simple model of the heart cycle. label well.
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look at print out for all lables? opning of valves etc...
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why does dyastole last longer?
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1. Diastole takes up about 2/3 of the heart cycle time
2. It is longer to give the ventricles time to fill up with blood. |
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b. What is stroke volume and ejection volume and what are their significance?
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1. Stroke volume = end diastolic volume (largest volume) – end systolic volume (smallest volume)
2. Ejection fraction = stroke volume/ end diastolic volume 3. The significance of the ejection volume is that it tells you if the heart is healthy 1. People with heart problems have a low ejection fraction 2. Chemotherapy drugs decrease Ej Fract to very low levels 30% - 20% 3. During exercise the ejection fraction increases to 90% or higher because epinephrine causes more calcium to be releases and more powerful contraction |
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types of heart cells?
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a. Sinal Atrial Node (SAN) - are the pacemaker cells of the heart.
i. The round cells of the saN originate the electrical impulse ii. The slender cells of the SAN are wires the feed into conducting cells b. Contractile cells i. Conducting cells: lead to the resistor (AVN) through the intermodal pathway c. Atriaventricular node (AVN) - is a resistor that holds up the electrical current started at the SAN before it gets to the ventricle. This is important because you don’t get contraction of the atria and ventricle at the same time and diastole lasts longer so you have enough time to fill the ventricle. d. Bundle of his- the end of the AVN, this is a conductor that sends the electrical impulse from atrium to ventricle i. Normally this is the only electrical pathway between the atria and the ventricles ii. The bundle of his splits around the septum into right and left bundle branches iii. Wolf-Parkinson’s- Wright syndrome is an inherited disease where there are extra conduction pathways e. Perkinje fibers are conducting fibers that are very plentiful in the ventricles. They spread out and feed the ventricles with electrical impulses. |
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SAN node
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a. Sinal Atrial Node (SAN) - are the pacemaker cells of the heart.
i. The round cells of the saN originate the electrical impulse ii. The slender cells of the SAN are wires the feed into conducting cells |
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contractile cells
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i. Conducting cells: lead to the resistor (AVN) through the intermodal pathway
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c. Atriaventricular node (AVN)
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is a resistor that holds up the electrical current started at the SAN before it gets to the ventricle. This is important because you don’t get contraction of the atria and ventricle at the same time and diastole lasts longer so you have enough time to fill the ventricle.
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d. Bundle of his
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the end of the AVN, this is a conductor that sends the electrical impulse from atrium to ventricle
i. Normally this is the only electrical pathway between the atria and the ventricles ii. The bundle of his splits around the septum into right and left bundle branches iii. Wolf-Parkinson’s- Wright syndrome is an inherited disease where there are extra conduction pathways |
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e. Perkinje fibers
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e. Perkinje fibers are conducting fibers that are very plentiful in the ventricles. They spread out and feed the ventricles with electrical impulses.
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II. Electrical excitation pathway generall
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a. SAN pacemaker generates signal
b. Contraction of the atria (depolarization) c. Excitation of the ventricle (depolarization) i. This fast enough for uniform contraction and all the cells are excited at the same time making for a stronger pump. |
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how is the cell membrane potential generally set up? general characteristics?
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a. The sodium-potassium pump sets up a chemical disequilibrium where the concentration of sodium is high outside and low inside
b. The cell has different permeability to sodium than it does to potassium so for every one sodium that goes in, 2000 potassium go out i. Cell is permeable to K+ ii. Cell is NOT permeable to NA+ c. The outside of the cell has a net positive charge and the inside of the cell has a net negative charge at rest |
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what is the nernst equation and what does it describe?
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Movement of molecules depends on an electrochemical gradient
Nernst Equation – is the equation that describes the equilibrium potential for a particular ion inside the cell. ∆μ_x=Z_x FVm + RTln x/xo The part wit Z is the electrical gradient RTln part is the chemical gradient Change in electrochemical potential is ∆μ of ion x Z of x is valence F is faraday’s constant Vm is the membrane electrical potential x/x0 is the ratio of the cation inside over the cation outside if anion switches to x0/x |
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when is there a special case of the nernst eq
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At equilibrium the electrical potential is equal but opposite to the chemical potential so ∆μ = 0.
If ∆μ = 0, you can solve for the Vm or membrane electrical potential At equilibrium Vm = E = equilibrium potential E= (-RT)/(FZ_x ) ln x/x_0 Being that T and F are constant in most situations, for sodium E = +61.5 For potassium, E = -90 |
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are ions at equilibrium in cell
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d. But ions in the cell are not at equilibrium, they are in a steady state
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what is the golman chord equation and what does it describe?
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The chord equation describes the membrane potential at any one time
Vm=E_k g_K/(g_K+ g_Na )+ E_Na g_Na/(g_Na+ g_K ) Vm is the membrane potential in mV EK is the equilibrium potential for potassium (-90 mV) g_K/(g_K+ g_Na ) is the conductance (permeability) of the membrane for potassium (gK = 100, gNa = 1 so here the term is 100/101) ENa is the equilibrium potential for sodium (+60) g_Na/(g_Na+ g_K ) is conductance again, here it will be 1/101 So, at REST Vm of the heart is about the same as the Equilibrium potential of potassium (~-90) which means that the INSIDE of the cell is NEGATIVE at rest. |
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vii. What would happen to the chord equation is conductance to potassium was lower?
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1. Vm would be LESS NEGATIVE (b/c first term would be less negative)
2. Different heart cells have different conductance to potassium and therefore different Vm |
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what equation describes current flow?
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i_x= g_(x ) [V_m- E_x ]
If we had an equilibrium state then Vm = Ex and there would be NO flow of current The heart therefore cannot be in a state of equilibrium if current is to flow. Steady state is kept with the sodium potassium pump When you are in an excited state the conductance for sodium increases (gNa) so Na can go in and depolarize the cell |
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what causes current flow in a cell
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iv. When you are in an excited state the conductance for sodium increases (gNa) so Na can go in and depolarize the cell
1. The cell depolarizes and goes from an inward negative charge to an inward positive charge 2. To repolarize the cell (+ -) you don’t pump out sodium because it takes a long time, instead, you increase the conductance to potassium and K+ moves out quickly 3. So increasing conductance is the most important |
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describe and draw the heart muscle action potential
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i. Phase 0: depolarization of the membrane triggers the opening of voltage gated sodium channels, sodium rushes into the cell. The inside of the membrane becomes positive and even more sodium rushes in. This is via fast sodium channels
ii. Phase 1: brief repolarization**** what about iKto?******* 1. Main reason for brief depolarization is due to the transient outward potassium current. a. This is more pronounced in atrial muscle and not significant in ventricular muscle 2. The fast sodium channels start to deactivate by plugging up. 3. This reduces the flow of sodium into the cell. 4. Inward rectifying potassium channels are closed reducing the flow of K and decreasing the flow of potassium out of the cell. 5. Repolarization does not reach +60 (the resting potential of sodium) because the sodium channels do not stay open long enough for this to happen. iii. Phase 2: plateau 1. Some positive charge will be lost because it moves downstream via gap junctions to unexcited cells 2. The positive charge is maintained by an increased conductance to calcium a. Calcium comes form the sarcoplasmic reticulum via the L-type channels and from outside the cell b. Function of calcium is to maintain a positive charge and to bond to troponin c and cause muscle contraction 3. Most K+ channels are closed 4. Membrane remains steadily depolarized 5. It is important to remain depolarized because this gives time for the heart to contract iv. Phase 3: repolarization 1. K+ conductance increases and potassium leaves the cell a. The first 1/3 of phase 3 potassium current is due to delayed rectifying potassium channels opening i. These channels started changing configuration at phase 0 but are slow. ii. At the end of phase 2 K+ moves from inward to outward and you get repolarization iii. Halfway through phase three the inward rectifying channels open too b. The last third of phase three is due to inward rectifying potassium currents opening i. Name is misleading ii. Current (K+) ions flow outward through this channel. iii. However, if artificially the membrane is made very negative then K+ will flow in through these channels iv. During phase 4 these channels are still partially open and K+ conductance at rest is due to these channels. 2. Calcium channels close 3. Get repolarization v. Phase 4: resting potential (~ -90mV) 1. Potassium conductance at rest is due to partially open inward rectifying channels. |
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what happens at phase 0 of the ap of hmc?
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i. Phase 0: depolarization of the membrane triggers the opening of voltage gated sodium channels, sodium rushes into the cell. The inside of the membrane becomes positive and even more sodium rushes in. This is via fast sodium channels
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describe how the fast sodium channels work?
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1. A fast sodium channel is a single protein that crosses the membrane 24 times.
a. The resting configuration of the channel, when the inside of the cell is negative and the outside is positive is closed. b. Inside the channel is a voltage sensing alpha helix. c. Initial depolarization causes repulsion with the positively charged alpha helix and the channel opens. d. Sodium comes in e. The channels is deactivated by a “plug like” part of the protein f. After repolarization the protein returns to its resting state |
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what causes phase 1 of the hmc ap? what is phase 1 ?
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ii. Phase 1: brief repolarization**** what about iKto?*******
1. Main reason for brief depolarization is due to the transient outward potassium current. a. This is more pronounced in atrial muscle and not significant in ventricular muscle 2. The fast sodium channels start to deactivate by plugging up. 3. This reduces the flow of sodium into the cell. 4. Inward rectifying potassium channels are closed reducing the flow of K and decreasing the flow of potassium out of the cell. 5. Repolarization does not reach +60 (the resting potential of sodium) because the sodium channels do not stay open long enough for this to happen. |
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what is phase 2 of hmc ap? significance?
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1. Some positive charge will be lost because it moves downstream via gap junctions to unexcited cells
2. The positive charge is maintained by an increased conductance to calcium a. Calcium comes form the sarcoplasmic reticulum via the L-type channels and from outside the cell b. Function of calcium is to maintain a positive charge and to bond to troponin c and cause muscle contraction 3. Most K+ channels are closed 4. Membrane remains steadily depolarized 5. It is important to remain depolarized because this gives time for the heart to contract |
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what causes phase three of the ap of hmc? what is phase 3?
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iv. Phase 3: repolarization
1. K+ conductance increases and potassium leaves the cell a. The first 1/3 of phase 3 potassium current is due to delayed rectifying potassium channels opening i. These channels started changing configuration at phase 0 but are slow. ii. At the end of phase 2 K+ moves from inward to outward and you get repolarization iii. Halfway through phase three the inward rectifying channels open too b. The last third of phase three is due to inward rectifying potassium currents opening i. Name is misleading ii. Current (K+) ions flow outward through this channel. iii. However, if artificially the membrane is made very negative then K+ will flow in through these channels iv. During phase 4 these channels are still partially open and K+ conductance at rest is due to these channels. 2. Calcium channels close 3. Get repolarization |
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what is the significance of the time of ap of hmc?
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vi. The time for the action potential of the muscle is approximate in time to the force of muscle contraction.
1. This is important so that you get only one action potential per contraction. 2. In skeletal muscle multiple action potentials are fired off at the same time and force remains constant a. This is tetanus or fused contraction with sustained, maximum calcium released 3. In the heart you need to have contraction and relaxation to keep the blood moving 4. Therefore the action potential is about as long in time as is the muscle contraction 5. During the refractory period you cannot fire off another action potential |
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what is the refractory period of the hmc ap? why is it so?
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5. During the refractory period you cannot fire off another action potential.
a. There is an absolute refractory period where nothing can be fires off b. After that time, an action potential can be fired but it does not necessarily result in depolarization of the cell c. This is because the last sodium channels which were plugged up at the end of phase 0 are not reset until the border of phase 3 to 4 |
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how do you increase HR?
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1. Action potential length is 200ms
2. Cycle length is 2000ms 3. As cycle length decreases, heart rate increases 4. As heart rate increases, action potential duration decreases 5. This is a good thing because you can fit more action potentials into a period without overlapping and creating tetanus 6. The electrophysiological reason for the shortened action potential is that in phase three the delayed rectifying channels close. If you shorten phase 4 these channels don’t close right away so the length of phase 2 decreases because the delayed rectifying channels can’t reset so the whole action potential is shortened |
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draw the ap of the avn? describe what happens?
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b. AVN action potential is the resistor potential and has slow depolarization.
i. Avn lowest point is at -60 mV because potassium conductance is lower at rest ii. At phase 0: calcium channels open and slow sodium channels open. iii. At phase 2 (there is no phase one): delayed potassium channels open iv. At phase 3: delayed potassium channels open v. Phase 4 resting potential vi. The AVN has a longer relative refractory period because it takes longer to reset the slow sodium and calcium channels 1. This limits the number of action potentials 2. This is a good feature because otherwise atrial firbrilation can send action potentials firing that would result in a heart rate of 200/300 beats per minute. This could cause the cardiac output to decrease because diastolic filling time would be so short. 3. The long refractory period of the AVN prevents this from happening and is a safety valve against atrial fibrillation heart rate increase |
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why does the avn have a longer refractory period?
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vi. The AVN has a longer relative refractory period because it takes longer to reset the slow sodium and calcium channels
1. This limits the number of action potentials 2. This is a good feature because otherwise atrial firbrilation can send action potentials firing that would result in a heart rate of 200/300 beats per minute. This could cause the cardiac output to decrease because diastolic filling time would be so short. 3. The long refractory period of the AVN prevents this from happening and is a safety valve against atrial fibrillation heart rate increase |
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what makes the AVN a resistor
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1. AVN cells are small in diameter with less cytoplasm, less cations, and therefore less conductance
2. Fewer number of gap junctions 3. *** there is a decrease of change in voltage over change in time meaning there is less of a dipole moment so current travels more slowly (phase 0 is slow) 4. There is less separation between resting potential and the most depolarized part of the action potential (resting is -60 vs. -90 for heart muscle cell) causing less current flow. |
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relationship btw conductance time through AVN and cycle length draw and describe
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vii. There is a relationship where as cycle length (heart rate) increases conductance time through the AVN (A-H conductance time) gets slower
1. This is another mechanism that prevents too high a heart rate 2. The reason for this occurrence is unknown |
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features of the SAN ap?
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i. The SAN has no resting potential
ii. -70 mV is the max diastolic potential iii. The cells spontaneously activates at ~-50 mV causing rapid depolarization iv. The pacemaker potential 1. T-type (transitory) calcium channels open at the very end of the pacemaker potential a. Cause rapid depolarization (by turning on L-type calcium channels*****????) 2. Funny sodium channels open to generate gunny current if a. These channels open after the cells repolarizes and allow sodium and potassium channels to cross the membrane. b. With potassium channels closed and funny channels open at the beginning of the pacemaker potential, potassium movement out of the cell decreases and sodium movement increases causing the slow depolarization of the pacemaker potential. c. Funny channels are open only briefly closing at ~ -55mv v. Repolarization occurs due to delayed rectifying potassium channels 1. There are no inward rectifying potassium channels in the SAN |
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describe the pacemaker potential of the SAN ap
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1. T-type (transitory) calcium channels open at the very end of the pacemaker potential
a. Cause rapid depolarization (by turning on L-type calcium channels*****????) 2. Funny sodium channels open to generate gunny current if a. These channels open after the cells repolarizes and allow sodium and potassium channels to cross the membrane. b. With potassium channels closed and funny channels open at the beginning of the pacemaker potential, potassium movement out of the cell decreases and sodium movement increases causing the slow depolarization of the pacemaker potential. c. Funny channels are open only briefly closing at ~ -55mv |
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what are funny currents
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generate SAN pacemaker potential 2. Funny sodium channels open to generate gunny current if
a. These channels open after the cells repolarizes and allow sodium and potassium channels to cross the membrane. b. With potassium channels closed and funny channels open at the beginning of the pacemaker potential, potassium movement out of the cell decreases and sodium movement increases causing the slow depolarization of the pacemaker potential. c. Funny channels are open only briefly closing at ~ -55mv |
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what causes repolarization of SAN
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v. Repolarization occurs due to delayed rectifying potassium channels
1. There are no inward rectifying potassium channels in the SAN |
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vi. How and when do you alter heart rate?
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ABOUT SAN:
1. Heart rate is altered by the autonomic nervous system. 2. Both the sympathetic and parasympathetic nerves enervate the SAN 3. If you cut sympathetic nerves hear rate decreases a. Sympathetic NS therefore increases heart rate normally 4. If you cut the parasympathetic nerves heart rate increases a. Parasympathetic nerves therefore decrease heart rate normally 5. If you cut both the sympathetic and parasympathetic nerves, heart rate increases a. This leads to the conclusion that the parasympathetic NS has more of an effect on the heart than the sympathetic NS only true for SAN! Not for ventricle there is not parasympathetic influence on ventricles |
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how does sympathetic activity affect the SAN
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6. The sympathetic NS is stimulated by epinephrine and norepinephrine via β1 receptors in the heart.
a. Β1 adenyl cyclase cAMP pKA phosphorylates calcium channels increase in calcium conductance b. Also: cAMP directly increases calcium conductance of the funny channels c. An increase of calcium conductance (more calcium enters the cell) means that the SAN will fire off more action potentials |
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how does parasympathetic activity affect the SAN?
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7. The parasympathetic NS uses the acetylcholine pathway.
a. ACh muscarinic receptors G protein βγ subunits bind to potassium channels and open them up max diastolic potential is lowered and is even more negative it takes longer to reach the -50 threshold and fire off an action potential |
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what does exercise do to the SAN
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8. Exercise over time decreases heart rate because it increases parasympathetic tone. Tone is the parasympathetic discharge at rest.
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what does an ekg measure?
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I. An EKG is a sum of the vectors of the depolarization and repolarization of all of the action potentials in the heart, not a single action potential. It consists of the P, Q, R, S, and T peaks
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draw and describe a normal ekg
what does eack peak represent |
a. P- atrial depolarization
i. It takes longer for the atrium to depolarize than the ventricle b. Q,R,S – ventricular depolarization c. T- ventricular repolarization d. The PR interval : Is the time between P and R is the time it takes for the current to go through the AVN. e. QRS is the rapid spread of the electrical potential through the ventricular system i. It takes a short time for the depolarization of the ventricle because of the perkinje system and because there is a higher separation of charge in the ventricle f. QT interval is the time from the beginning of Q to end of T and is ventricular systole g. TQ interval is the time form the end of T to the beginning of Q and is ventricular diastole h. RT interval is the plateau phase |
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P of ekg
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a. P- atrial depolarization
i. It takes longer for the atrium to depolarize |
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qrs of ekg
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b. Q,R,S – ventricular depolarization
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T of ekg
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c. T- ventricular repolarization
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PR interval of ekg
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d. The PR interval : Is the time between P and R is the time it takes for the current to go through the AVN.
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QRS interval of ekg
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e. QRS is the rapid spread of the electrical potential through the ventricular system
i. It takes a short time for the depolarization of the ventricle because of the perkinje system and because there is a higher separation of charge in the ventricle |
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QT inerval of ekg
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f. QT interval is the time from the beginning of Q to end of T and is ventricular systole
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TQ of ekg
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g. TQ interval is the time form the end of T to the beginning of Q and is ventricular diastole
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ri of ekg
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h. RT interval is the plateau phase
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what if there is a longer RT interval on an EKG
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i. Longer RT interval indicates that the plateau phase is long suggesting that potassium channels are messed up and are not (reopening?). They remain close. If this occurs one is prone to fatal arrhythmia of the heart because you never get repolarization.
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what is heart rate measured as
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j. Heart rate is measured as 60/PR interval
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how does an ekg work>
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k. An EKS records the charge on the outside of the cell for obvious reasons. At rest the charge outside is positive.
i. If the positive recording electrode sees a + and the negative electrode sees – then the pen goes up 1. The positive electrode is at the bottom of the heart and the negative at the top 2. So when depolarization occurs the pen goes up ii. If both electrodes see the same charge then the pen does not move 1. At rest, the outside potential is positive everywhere so the pen does not move iii. If the negative electrode sees a + charge and the positive electrode sees a – charge then the pen goes down 1. This implies repolarization |
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I. Sinus bradychardia
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I. Sinus bradychardia is low heart rate
a. Usually within norm b. ~40 bpm |
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II. Tachycardia is
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II. Tachycardia is high heart rate
a. If you are at rest and not nervous then you have tachycardia b. Otherwise, if nervous, high heart rate is normal |
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what does coranary artery disease do?
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III. Coronary Artery disease causes no blood flow to the AVN. Intense damage can cause scarring of the AVN (ischemia). There are several degrees of AVN block
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a. First degree block
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i. The interval between the P and R is longer than normal
ii. This usually does not result in huge problems |
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b. Second degree block
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i. More damage to the AVN
ii. No QRS means that you skip a beat because the electrical impulse can get through the avn iii. Skipping a beat can cause dizziness and fainting ( syncopy) because no blood flow is getting to the brain |
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c. Third degree heart block is due to ischemia
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i. There is no QRS
ii. Ectopic areas of electrical excitation occur in the ventricle that sets up their own rhythm 1. A funny current can develop in the ventricular cells 2. A pacemaker potential 3. Normally this is inhibited by the fast discharge rate of the SAN override suppression 4. It takes 10-30 seconds for this pacemaker potential to start up 5. It has a slower hr of 15-40 bpm 6. Causes a decreased CO 7. Treatment is to install an artificial pacemaker |
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ischemia
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Intense damage can cause scarring of the AVN (ischemia
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d. Stokes-Atoms disease
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intermittant 3 degree block
d. Stokes-Atoms disease is a third degree AVN block i. It is intermittent blocking because of a block near the area 1. Because this is intermittent and it takes ~10 seconds for the ventricle to start its own pacemaker a person with this often faints and could die 2. Treatment is artificial pacemaker |
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a. Atrial premature contraction
i. Due to |
1. Smoking
2. Lack of sleep 3. Increase of caffeine 4. Alcohol |
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a. Atrial premature contraction
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ii. An action potential is fired off in an abnormally short period of time due to irritation of the atrial muscle
1. Shortened PR interval iii. The electrical excitation occurs not in the SAN but closer to the AVN therefore it takes less time to travel through the avn to the vent. iv. The signals also goes retrograde and stimulates the SAN v. The SAN discharges vi. This cause a longer time for the next action potential 1. Because the extra beat occurred too early, interrupted diastole, less blood is in the ventricle, decreased stroke volume, deficient (weak) pulse can be felt vii. Retrograde movement sometimes causes an inverted P wave |
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b. Premature ventricular contraction
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i. Due to
1. Smoking 2. Lack of sleep 3. Increase of caffeine 4. Alcohol 5. Inflammation that causes damage to the heart and scar tissue ii. Higher R peak 1. Since impulse is slow there is a higher separation of charge that causes a higher peak iii. Wider R peak iv. Inverted T wave 1. Usually the first to depolarize is the last to repolarize a. A decrease in blood flow due to muscle constriction slows depolarization. 2. Since in PVC the signal is slow, the ventricle repolarizes first causing an inverted T wave v. Electrical impulse arises not in the normal conduction pathway, it travels slowly longer time for depolarization of the V wider R longer to excite the ventricular tissue |
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V. Atrial Paroxysmal tachycardia (A Tach) or Supraventricular paroxysmal tachycardia
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a. Paroxysmal means it comes in unpredictable spurts
b. Atrial paroxysmal tachycardia starts in an abnormal site in the atrial conducting pathway c. Inverted P wave i. Because the impulse does not originate in the SAN d. Sometimes no P wave i. P wave is superimposed on the R wave e. Increased heart rate f. Usually benign g. Repeats many times unlike premature atrial contraction which is once |
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VI. Ventricular tachycardia (v-tach)
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a. Can be dangerous
b. Due to ischemic damage c. Can lead to ventricular fibrillation d. Changes to EKG i. Inverted T wave ii. higher R wave 1. slowed impulse due to blockage causes an increased separation of charge iii. wider R wave iv. faster heart rate |
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VII. Wolf-Parkinson’s White syndrome (WPW)
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a. Arises when there are accessory conduction pathways from the atria to the ventricle other than the AVN
b. Shortened PR interval i. These accessory pathways are only conductors, not resistors so the PR interval is shorter because the impulse is not delayed c. Delta wave (hump on R) i. Since the AVN is still the main pathway for the electrical signal to travel ii. The delta wave is stimulation of the ventricle that causes smaller and weaker depolarization ***** due to signal from AVN or from accessory pathways****?? iii. Can lead to complications with age iv. Solution: burn extra pathways |
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VIII. Atrial Fibrillation
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a. Mitral stenosis – the mitral valve has started to calcify
i. This occurs with age ii. It is difficult for the blood to get out of the atria iii. Can’t empty atria engorged large atria larger distance for current to flow current can repolarizae cells that were depolarized already current goes around atria b. Atrial dilation causes long conduction pathway 1. The current travels around the atria but not in a sequential way 2. Different parts of the atria contract at different times c. EKG of A fib i. No P wave ii. Just QRS iii. Usually can’t feel A fib unless you exercise 1. No contraction of the atria prevents the extra 1/3 of the needed blood to get into ventricle, decreasing stroke volume. d. A fib runs a rare risk of tachycardia i. This is rare because of the refractory period which lasts into phase 4 ii. The refractory period prevents tachycardia due to over excitation of the atria e. A fib can cause pooling of the blood in the atria which can lead to clots i. Can get a pulmonary embolism (on the right side) ii. If on the left side blood flow to the heart is compromised iii. Treat with anti-coagulants |
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why is risk of tachycardia low with a fib?
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d. A fib runs a rare risk of tachycardia
i. This is rare because of the refractory period which lasts into phase 4 ii. The refractory period prevents tachycardia due to over excitation of the atria |
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IX. Ventricular Fibrillation
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a. EKG
i. No waves at all b. Causes i. Dead tissue due to coronary artery disease causes a block and unidirectional conduction of current ii. A current starts and splits but is blocked in one pathways because dead tissue dies not produce enough of a signal to keep the impulse going iii. Since the cells behind the block are not in the refractory period they can be stimulated by an impulse form an alternate branch. iv. Current is not completely blocked, it is only unidirectional. Since there are more cells behind the block the current can travel back up to the origin site v. This site has already gone through the refractory period and is stimulated again be the current. vi. This starts a vicious cycle where the current travels around the ventricle but the ventricle does not contract at the same time 1. Current is too slow to cause coordinated contraction 2. Not enough contraction to pump blood around the body c. Treatment i. Immediate: shock with paddles to depolarize every cell and hopefully restart a proper rhythm 1. This may not work because the dead tissue that caused this in the first place is still there ii. Longer term; defibrillator implants send jolt to the heart automatically 1. Limited success. |
