Chapter 13 - Blood, Heart, and Circulation Flashcards
Compare the two “populations”/types of cells found in cardiac muscle. Provide function and examples
modified/specialized myocardial cells:
- conducts AP at different AP velocities
- ex: SA node, AV node, AV bundles, Purkinje fibers
non-specialized myocardial cells:
- contracts myocardial cells
- ex: make up the walls of atria and ventricles, are branched, and connected via gap junctions
What type of cells in cardiac muscle communicate and are connected through gap junctions?
non-specialized myocardial cells
Where are gap junctions located in?
intercalated discs
What is an SA node?
Is known as the pacemaker which consists of specialized myocytes that can generate their own APs (spontaneous/automatic) that travel to non-specialized myocytes in atrial walls and AV node.
True or False: Myocardial contraction is dependent on specialized myocardial cells and non-specialized myocardial cells
true; specialized myocardial cells are needed to generate an AP that travels to non-specialized myocardial cells in order to generate a contraction
Which specialized myocardial cell in involved with initiating an AP that travels to non-specialized myocytes in atrial walls and the AV node? Be specific.
SA node
Where does the AP from the SA node travel to?
- AV node
- Non-specialized myocytes in atrial walls
What is PP (pacemaker potential)?
Refers to the initial depolarization of an SA node action potential that is triggered by hyperpolarization from a previous AP and opening of HCN channels on SA node cells
What can cAMP influence in the body?
heart-rate because it can increase the SA node AP frequency
(increase in cAMP will lead to steeper slope of PP -> an AP will occur quicker -> and contraction of heart will increase)
What is needed for an HCN channel to open up in SA nodal cells?
a previous hyperpolarization
Describe an HCN channel and some of its characteristics. What would happen to the slope of the PP if there were low amounts of cAMP?
HCN Channel (hyperpolarization-activated cyclic nucleotide-gated channel) = VG-Na+ channel
- Open on SA node cells @ -60mV
- Sensitive to camp
Low amounts of cAMP = flat slope (becomes less steep)
Why is there no RMP in the SA nodal AP graph
No RMP because initial depolarization is a slow, “spontaneous” depolarization that occurs automatically without NS input; specialized nodal cells are never at rest
The initial depolarization in an SA node action potential is referred to as?
pacemaker potential (PP)
The initial depolarization in smooth muscle action potential is referred to as?
graded potentials/depolarization
The initial depolarization in skeletal muscle action potential is referred to as?
end plate potentials (EPP)
What type of action potentials do NOT have RMP?
SA node action potential
What type of action potentials do NOT have threshold?
Myocardial (non-specialized) action potentials
What value do HCN channels open up in an SA node action potential? What happens here?
-60mV
HCN channels open -> influx of Na+ (VG-Na2+ ch)
What value is threshold in an SA node action potential? What happens here?
-40mV
VG-Ca2+ channels open
What value is peak in an SA node action potential? What happens here?
+20mV
VG-Ca2+ close
VG-K+ open
Describe the SA node action potential
- prior hyperpolarization initiates the opening of HCN channels (VG-Na2+ ch) at -60mV -> influx of Na2+
- pacemaker potential occurs (initial depolarization) until it reaches -40mV -> VG-Ca2+ open an influx of Ca2+
- depolarization occurs and at +20mV (peak), VG-Ca2+ will close and VG-K+ open -> K+ efflux -> repolarization
- VG-K+ slow to close -> hyperpolarization
- Action potential can now spread to AV node OR non-specialized myocytes in atrial walls where they spread to other cells (via gap junctions)
What channel is slow to close in a SA node action potential?
VG-K+ channels
How do APs spread from one cardiac myocyte to another in the atrial walls?
Through gap junctions in intercalated discs
Why is there no initial depolarization/threshold in the myocardial AP graph
Because the AP in myocardial cells (non-specialized) can spread directly to the next cell through gap junctions in intercalated discs
In myocardial action potentials, what is the value of RMP? What happens at the end of RMP?
-90mV
VG-Na+ open -> Na+ influx (rapid depol.)
In myocardial action potentials, what is the value of peak? What happens at peak?
+20mV
VG-Na+ close
VG-Ca2+ open
VG-K+ open
What channels are responsible for a Ca2+ plateau in a myocardial action potential?
VG-Ca2+
VG-K+
Define the “calcium plateau” and its purpose.
Calcium plateau is the slow repolarization of myocardial cells caused by a balance between slow
Ca2+ influx and K+ efflux
Purpose it to provide a refractory period to limit the frequency of AP in the cells
What would be the consequence if the calcium plateau were extended for a long time?
If the calcium plateau were extended for a long time, the heart rate would decrease
*What would happen to the myocardial AP if the VG-Ca2+ channels were blocked? Would contraction of cardiac muscle increase or decrease as a result? Explain why
If VG-Ca2+ were blocked, there would be a drastic increase in cardiac muscle contraction. There would be no calcium plateau to “balance out” the efflux of K+, therefore, no refractory period -> increase in AP frequency -> increase in heart-rate
Describe what goes on in a myocardial action potential
- RMP @ -90mV
- at end of RMP, VG-Na+ open -> rapid influx of Na+ = rapid depolarization (no initial depol. because AP spreads directly to the next cell, so no threshold required)
- reaches peak at +20mV -> VG-Na+ close and VG-Ca2+ (slow influx Ca2+) and VG-K+ open (efflux K+)
- balance between slow Ca2+ influx and efflux of K+ creates a calcium plateau (refratory period)
- VG-Ca2+ will eventually close, but VG-K+ remain open -> K+ efflux continues = rapid repol.
- return back to RMP at -90mV
Name all of the specialized tissues of the heart and the order of specialized tissue in which the APs travel
SA node -> AV node -> AV Bundle (Bundle of His) -> Purkinje Fibers
APs spread at gap junctions in intercalated discs between _______ and _________ ________
left
right
atria
Name the order of ONLY cells in which the APs travel to stimulate atrial contraction
SA node -> (AV node?) myocardial cells in atrial walls -> atrial contraction
Name the order of ONLY cells in which the APs travel to stimulate ventricular contraction
SA node -> AV node -> AV bundle (Bundle of His) -> Purkinje fibers -> myocardial cells in ventricular walls -> ventricular contractoin
Where is the SA node located?
Where is the AV node located?
Where is the AV bundle located?
Where are Purkinje fibers located?
SA node: posterior right atrium
AV node: base of right atrium
AV bundle: interventricular septum
Purkinje Fibers: around ventricle area
APs generated at SA node spread ________ to ______ and _______ ________
rapidly
atria
AV node
What is the velocity for an AP in the SA node?
0.8 to 1.0 m/sec
What is the velocity for an AP in AV node?
0.03 to 0.05 m/sec
What is the velocity of the AP in Purkinje fibers?
5.0 m/sec
In specialized myocardial cells, when to the APs of velocity slow down and pick up?
slows down at AV node to delay ventricular contraction (0.03-0.05m/sec)
speeds up in AV bundle and goes even faster in Purkinje fibers (5.0m/sec)
Why is AP velocity decreased at the AV node?
Slows down to delay ventricular contraction in order to make sure atria have fully contracted (systole) and ventricles have fully filled with blood (diastole)
How many seconds will it take for ventricles to contract after the atria?
0.1 to 0.2 seconds
Which specialized myocardial cell has the fastest and slowest velocity?
fastest: Purkinje Fibers
slowest: AV node
How does cAMP affect HCN channels in specialized myocardial cells?
it keeps HCN channels open for longer -> more influx of Na+ -> PP slope becomes steeper/increases
Describe how an increase in epinephrine can lead to an increase in heart-rate.
increase in epinephrine -> increase in cAMP -> increase Na+ influx at specialized myocardial cells -> increase PP -> increase frequency of AP -> increase Ca2+ -> increase contraction -> increase HR
Why is there no such thing as a Calcium-induced, calcium released mechanism in smooth muscle although there is one in skeletal and cardiac muscle
in skeletal and cardiac muscle, extracellular Ca2+ is used to activate the release of intracellular Ca2+ from the SR. However, smooth muscle has few/no SR, so an extracellular source must be used, therefore, there is no such things as an induced, calcium-released mechanism.
Describe in chronological order the steps involved in the excitation-contraction coupling of cardiac muscle
AP conducted along sarcolemma of nonsepcialized myocardial cells -> T tubules -> DHP receptors open (L Type Ca2+ channel/VG-Ca2+ channel)
Extracellular Ca2+ flows into cell -> acts as a second messenger to open Ryanodine Receptors Type 2 (Ca2+ release channels) on the SR
DHP RECEPTORS AND RYANODINE RECEPTORS TYPE 2 ARE NOT COUPLED
Ca2+ from SR binds to troponin ->->-> stimulate cardiac muscle contraction
Compare the DHP receptors vs the Ryanodine Type 2 Receptors
DHP receptors allow for influx of extracellular Ca2+ into the cytoplasm of nonspecialized myocardial cells
Ryanodine Type 2 Receptors allow for Ca2+ to be released from the SR and into the cytoplasm of nonspecialized myocardial cells
What is the source of most of the Ca2+ required for cardiac muscle contraction?
SR
TRUE or FALSE: Myofilaments from cardiac muscle are arranged into sarcomeres
True
TRUE or FALSE: Cardiac myocytes have no/few SRs (sarcoplasmic reticula)?
False, cardiac myocytes have SRs and these SRs release Ca+ through the calcium-induced, calcium-released mechanism for contraction to take place
TRUE or FALSE: Cardiac muscle requires nervous system input in order to contract
False, cardiac muscle does not need NS input because specialized cardiac myocytes are capable of generating their own APs
What is the general function of the cardiovascular system? What are some examples.
function: circulates/transports various substances within the blood
NAH EW
ex: O2, CO2, nutrients, antibodies, hormones, electrolytes, waste produced (CO2)
What are the components that make up the cardiovascular system?
- blood
- blood vessels
- heart
Define the cardiac cycle
repeating pattern of contraction and relaxation of the heart
Compare systole vs. diastole
Systole: contraction (emptying chamber) of heart muscles
Diastole: relaxation (filling chamber) of heart muscle
What are the four chambers of the heart? What are their functions
Right atrium: receives deoxygenated blood from body
Right ventricle: pumps deoxygenated blood to lungs
Left atrium: receives oxygenated blood from the lungs
Left ventricle: pumps oxygenated blood to the body
What separates the right and left sides of the heart to prevent mixing of oxygen-rich and oxygen poor blood
interventricular septum
Compare the pulmonary circuit vs. the systemic circuit
Pulmonary circuit: allows blood to pick up O2 and to get rid of CO2 at the lungs; pathway between heart and lungs
Systemic circuit: delivers oxygenated blood to tissues; pathway between heart and body tissue
Describe the pathway of the pulmonary circuit
de-O2 blood from body to right atrium (via SVC and IVC) → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary arteries → arterioles → capillaries; gas exchange at lungs (pick up O2) → venules → pulmonary vein → left atrium
Describe the pathway of the systemic circuit
O2 blood from left atrium → bicuspid/mitral valve → left ventricle → aortic semilunar valve → aorta → systemic arteries → arterioles → capillaries; gas exchange at body tissue (pick up CO2) → venules → systemic veins → de-02 vena cavae → right atrium
Define deoxygenated blood. Where in the cardiovascular system would deoxygenated blood be located?
Deoxygenated blood: low in CO2 and high in CO2
SVC, IVC, right atrium, right ventricle, pulmonary arteries
When left ventricular systole occurs, what valve swings shut/closes and which valve swings open?
bicuspid/mitral valve closes
aortic semilunar valve opens
- When right atrial diastole occurs, what valve swings shut/closes? What would happen if it did not swings shut/close?
tricuspid valve
if it did not close, atria would never fill
TRUE or FALSE: After gas exchange at the systemic capillaries (at the level of the systemic organs), blood is high in O2 and low in Co2
False, after gas exchange occurs between systemic capillaries and tissue, O2 was delivered to tissue and CO2 was picked up, therefore it would be low in O2 and high in CO2
TRUE or FALSE: blood located in the veins is always deoxygenated
False, veins can carry oxygenated blood (ex: pulmonary veins), but can also carry deoxygenated blood (ex: SVC and IVC)
Draw a four-chambered heart (in a “box” form; not the anatomical heart). Label the following: R & L atria, R & L ventricles, vena cavae, aorta, pulmonary artery, pulmonary vein, bicuspid valve, tricuspid valve, pulmonary semilunar valves, aortic semilunar valves. Be able to trace the pathway of a blood drop as it travels through the cardiovascular system.
check on review sheet
Label the different parts of the cardiac myocyte/myocardial AP graph, including the opening and closing of the different ion channels
check answer on review sheet
Label the different parts of the SA node AP graph, including the opening and closing of the different ion channels
check answer on slides
Compare arterial blood from venous blood
arterial blood: leaving the heart, bright red and oxygenated (except for blood going to lungs/pulmonary artery)
venous blood: blood entering the heart, dark red and deoxygenated (except for blood coming from the lungs/pulmonary vein)
Blood is made of _______ formed elements and _____ plasma
45% formed elements
55% plasma
Compare plasma vs. serum
Plasma is 90% water that contains various dissolved substances, including CF
Gasses (O2, CO2), electrolytes, proteins, enzymes, antibodies, hormones, CF
Serum is plasma, but without clotting factors
ex: plasma = serum + CF
What are the 3 components of blood?
- plasma
- serum (is plasma but without CF)
- formed elements
What are formed elements? Give examples
FE consists of cells and cell fragments (piece of cell)
- RBC - erythrocyte
- WBC - leukocyte
- Platelets - thrombocytes (IS NOT A CELL; only a cell fragment)
List examples of formed elements and their main functions
RBC - transport O2 (inv with gas exchange)
WBC - involved with immune system
Platelet - clotting
Describe the main characteristics of a RBC
- Biconcave/ disc-shaped
- No nuclei and no mitochondria = short life span (120 days)
-> Produced at quick rate (2.5 million RBC/sec) - Carrys O2 by binding to hemoglobin
By what process to RBC form/develop?
erythropoiesis
Understand the chronological order of the developmental stages of cells involved in hematopoiesis. Which is the first cell seen without a nucleus?
His Persistent Efforts Never Really Ended:
Hemocytoblast
Proerythroblast - stimulated by erythropoietin
Erthryoblast
Normoblast
Reticulocyte first cell without a nucleus
Erythrocyte (RBC)
Name the hormone that is made from the kidneys that responds to low blood O2 levels. What cell does it stimulate?
erythropoietin (EPO)
stimulates proerythroblast
What is EPO (erythropoietin) and what cell is sensitive/responds to it?
is a hormone secreted by kidneys that responds to low blood O2 levels, stimulating erythropoiesis
proerythroblast
The erythropoiesis process takes about ____ days
3
What is hemostasis and why does it happen if the blood vessel (BV) is injured?
hemostasis: cessation (stopping) of bleeding when a blood vessel is damaged
happens to prevent us from losing too much blood/hemorrhage
TRUE or FALSE: Collagen fibers are exposed to the lumen of BV when the BV is undamaged
False, collagen fibers become exposed to the lumen of a BV when it is DAMAGED
List the 3 things that can happen when a BV is damaged/injured and exposes collagen fibers to blood
Vasoconstriction (smooth muscle contracts)
Platelet plug formation
Fibrin protein web (blood clot) formation (CF that will strengthen platelet plug to make strong blood clot)
Where does red blood cell formation/development usually occur?
mainly in bone marrow (except for RBC)
What does an intact/uninjured BV endothelium secrete?
NPC
- NO
- PGI2
- CD39
What are the functions of the secreted substance by an uninjured/healthy BV endothelium?
NO and PGI2 - inhibit PLT activation/aggregation AND act as vasodilatory (maintain blood flow when uninjured)
CD39 - converts ADP (clots blood) to AMP + Pi (does not clot blood)
What is a membrane-bound enzyme that can be found on the endothelial cell?
CD39
When a BV is injured/damaged, endothelium exposes _________ to the lumen
collagen
TRUE or FALSE: NO, PGI2, CD39 are secreted by platelets when BV are uninjured/intact
False, they are secreted by endothelial cells/endothelium
What happens when there is injury/damage to the endothelium?
platelets bind to collagen via VWF (strengthens bond) and are activated and degranulate to release/activate CF (clotting factors), ADP, TXA2 (thromboxane), serotonin
What is the function of the Von Willebrand Factor (VWF)? Include what 2 things bind to it.
strengthens/allows for PLTs to bind to collagen
List 3 substances released/secreted by activated PLTs (platelets) when they bind to collagen fibers, and give the functions of each of these substances
TXA2 & serotonin - promote vasoconstriction (decrease blood flow)
TXA2 & ADP - promote PLT aggregation -> PLT plug formation
What can activated PLTs also activate?
activated platelets activated CF to stimulate the conversion of fibrinogen (inactive) to fibrin (active)
What is the purpose of plasma clotting factors?
convert fibrinogen to fibrin, so that fibrin can infiltrate PLT plug and form a blood clot containing RBC
Compare the intrinsic and extrinsic pathway regarding CF
Intrinsic pathway: activated by exposure to collagen and factor XII activates a cascade of other CF; amplifies extrinsic pathway
Extrinsic pathway: initiated by tissue thromboplastin (CF III); direct and short pathway
*both pathways merge at a common pathway)
Name the 2 clotting pathways and what is the goal of these pathways?
Intrinsic pathway
Extrinsic pathway
Convert fibrinogen into fibrin
TRUE or FALSE: Clotting factors (CF) exist only in the active form
False, usually activated by another CF
Be familiar with the correct sequence of active CFs for both the extrinsic and intrinsic pathways
check answer on slide/notes
Intrinsic:12 → 11 → 9 → Complex VIII (9,8,4,PL) → 10 → Complex V (10, 5,4,PL) → 2 → 1
Extrinsic: Complex VII (CF7,3,4,PL) → 10 → Complex V (10, 5,4,PL) 2 → 1
Name all the CFs that belong to the extrinsic and intrinsic pathways. Name all the CFs that belong to the common pathway. Name the 3 complexes found in the clotting pathways and know what each complex consists of. Know the actual name for CFs 1-4.
Intrinsic: CF 1,2,4,5,8,9,10,11,12
Extrinsic: CF 1,2,3,4,5,7,10.
Complex V = CF 10,5,4 and PL.
Complex VII = CF7,3,4, PL
Complex VIII = CF 9,8,4, and PL
CF I = Fibrin
CF II = thrombin
CF III = Tissue Factor (thromboplastin)
CF IV = Ca2+
Which CFs are only found in the extrinsic pathway? Which CFs are only found in the intrinsic pathway?
ONLY extrinsic: CF7 and CF3
ONLY intrinsic: CF12, 11, 9, 8
Which CF make up the common pathway?
CF 1,2,4,5,10
Which CF starts the common pathways? What is the last CF to be made at the end of both pathways that can insert itself into the PLT plug?
CF X (10)
Fibrin (active)
Compare Hemophilia A vs. Hemophilia B
Hemophilia A is more common than Hemophilia B which contains an X-linked recessive trait (in EU royal families) that prevents a subunit of CF VIII (8) from participating in the intrinsic pathway
Hemophilia B contains a defective X-linked gene for CF IX (9)
Both are common in mostly males.
Will bleeding time (the amount of time it takes before you begin to clot) be high or low in Von Willebrand’s Disease? Explain why
Bleeding time will be high because without VWF, platelets cannot bind to collagen fibers and will not activate PLTs to secrete substances that aim to stop bleeding -> no PLT plug
What is Von Willebrand’s Disease? Is it more common in males or females?
is the most common bleeding disorder that causes a defect in a different subunit of CF VIII (8)
female and male
T/F: Von Willebrands Disease and Hemophilia A both causes a defect in the same subunit of CF VIII (8)
False, they attack a different subunits of CF VIII (8)
