Lecture Exam Flashcards

1
Q

Describe the general functions of blood

A

As blood is transported through the blood vessels it transports oxygen from and carbon dioxide to the lungs for gas exchange, nutrients absorbed from the gastrointestinal (GI) tract, hormones released by endocrine glands, and heat and waste products from the systemic cells

Regulation
Blood participates in the regulation of body temperature, body pH, and fluid balance:
∙ Body temperature. This is possible because blood absorbs heat from body cells, especially skeletal muscle, as it passes through blood vessels of body tissues. Heat is then released from blood at the body surface as blood is transported through blood vessels of the skin.
∙ Body pH. Blood, because it absorbs acid and base from body cells, helps maintain the pH of cells. Blood contains chemical buffers (e.g., proteins, bicarbonate) that bind and release hydrogen ions (H+) to maintain blood pH until the excess is eliminated from the body.
∙ Fluid balance. Water is added to the blood from the GI tract and lost in numerous ways (including in urine, sweat, and respired air). In addition, there is a constant exchange of fluid between the blood plasma in the capillaries and the interstitial fluid surrounding the cells of the body’s tissues. Blood contains proteins and ions that exert osmotic pressure to pull fluid back into the capillaries to help maintain normal fluid balance.

Protection
Blood contains leukocytes, plasma proteins, and various molecules that help protect the body against potentially harmful substances.

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2
Q

List six characteristics that describe blood and its normal values.

A

Scarlet (oxygen-rich) to dark red (oxygen-poor)
4–5 L (females) 5–6 L (males)
Viscosity (relative to water) - 4.5–5.5× (whole blood)
Plasma concentration - 0.09%: relative concentration of solutes (proteins, ions) in plasma
38°C (100.4°F)
7.35–7.45

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3
Q

Define colloid osmotic pressure and explain how plasma protein levels affect colloid osmotic pressure.

A

Osmotic pressure exerted by plasma proteins is called colloid osmotic pressure. This osmotic force is responsible for drawing fluids into the blood and preventing excess fluid loss from blood capillaries into the interstitial fluid

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4
Q

Describe the functions of plasma protein: albumin, globulins, fibrinogens, regulatory proteins

A

Albumin (~58% of plasma proteins) -
Exerts osmotic force to retain fluid within the blood
Contributes to blood’s viscosity
Responsible for transport of some ions, lipids (e.g., fatty acids), and hormones

Globulins (~37% of plasma proteins) -
Alpha-globulins transport lipids and some metal ions (e.g., copper)
Beta-globulins transport iron ions and lipids in blood
Gamma-globulins are antibodies that immobilize pathogens

Fibrinogen (~4% of plasma proteins) - Participates in blood coagulation (clotting)

Regulatory proteins (<1% of plasma proteins) - Consists of enzymes and hormones

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5
Q

Outline the process of erythropoiesis

A

The process of erythropoiesis begins with a myeloid stem cell, which under the influence of multi-CSF forms a progenitor cell. The progenitor cell forms a proerythroblast, which is a large, nucleated cell.
It then becomes an erythroblast, which is a slightly smaller cell that is producing hemoglobin in its cytosol. The next stage, called a normoblast, is a still smaller cell with more hemoglobin in the cytosol; its nucleus has been ejected. A cell called a reticulocyte eventually is formed. The transformation from myeloid
stem cell to reticulocyte takes about 5 days.

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6
Q

List the events by which erythrocyte production is simulated

A

Stimulus: Decreased blood oxygen levels

RECEPTOR: Kidney detects decreased blood O2

Control center: Kidney cells release EPO into the blood.

EFFECTOR: EPO stimulates red bone marrow to increase the rate of production of erythrocytes.

NET EFFECT: Increased numbers of erythrocytes enter the circulation, during which time the erythrocytes are oxygenated and blood O2 levels increase.

Increased blood O2 levels are detected by the kidney, which inhibits EPO release by negative feedback.

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7
Q

Distinguish between granulocytes and agranulocytes, compare and contrast the various types with
respect to function

A

Granulocytes have specific granules in their cytosol that are clearly visible when viewed with a microscope.

Three types of granulocytes can be distinguished: neutrophils, eosinophils, and basophils.

Agranulocytes are leukocytes that have such small specific granules in their cytosol that they are not clearly visible under the light microscope. Agranulocytes include both lymphocytes and monocytes.

GRANULOCYTES:
Neutrophils - Phagocytize pathogens, especially bacteria
Release enzymes that target pathogens
50–70% of total leukocytes (1800– 7800 cells per microliter)

Eosinophils - Phagocytize antigen-antibody complexes and allergens
Release chemical mediators to destroy parasitic worms
1–4% of total leukocytes (100–400 cells per microliter)

Basophils - Release histamine (vasodilator and increases capillary permeability) and heparin (anticoagulant) during inflammatory reactions
0.5–1% of total leukocytes (20–50 cells per microliter)

AGRANULOCYTES

Lymphocytes - Coordinate immune cell activity
Attack pathogens and abnormal and infected cells
Produce antibodies
20–40% of total leukocytes (1000– 4800 cells per microliter)

Monocytes - Exit blood vessels and become macrophages
Phagocytize pathogens (e.g., bacteria, viruses), cellular fragments, dead cells, debris
2–8% of total leukocytes (100–700 cells per microliter)

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8
Q

Describe the function of platelets

A

Platelets are irregular-shaped, membrane-enclosed cellular fragments. Platelets are sometimes called thrombocytes; as with erythrocytes, that name is inappropriate because they are not true cells. Platelets are cell fragments. Platelets are continually produced in the red bone marrow by megakaryocytes. Platelets serve an important function in hemostasis as they become trapped within the fibrin network of a blood clot.

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9
Q

Explain vascular spasm (the first phase of hemostasis), and name conditions that bring about
vascular spasm

A

When a blood vessel is injured, the first phase in hemostasis to occur, which begins immediately, is a vascular spasm, whereby damage to smooth muscle within the vessel wall causes smooth muscle contraction. This contraction results in vasoconstriction (i.e., the blood vessel lumen narrows) and thus limits the amount of blood that can leak from this damaged vessel. The spasm continues during the next phase, as both platelets and the endothelial cells of the blood vessel wall release an array of chemicals to further stimulate the vascular spasms.

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10
Q

Describe what happens when platelets encounter damage in a blood vessel

A

Once a blood vessel is damaged, the collagen fibers within the connective tissue internal to the endothelial cells in the vessel wall become exposed. Platelets begin to stick to the exposed collagen fibers. Platelets adhere to the collagen fibers with the assistance of a plasma protein called von Willebrand factor, which serves as a bridge between platelets and collagen fibers.
Platelets start to stick to the vessel wall and their morphology changes dramatically; they develop long processes that further adhere them to the blood vessel wall. As more and more platelets aggregate to the site, a platelet plug develops to close off the injury

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11
Q

Define coagulation, and list the substances involved in coagulation

A

A blood clot has an insoluble protein network composed of fibrin, which is derived from soluble fibrinogen. This meshwork of protein traps other elements of the blood, including erythrocytes, leukocytes, platelets, and plasma proteins, to form the clot.

Blood coagulation is a process that requires numerous substances, including calcium, clotting factors, platelets, and vitamin K.

Most clotting factors are inactive enzymes, and most of these are produced by the liver. Vitamin K is a fat-soluble vitamin that is required for the synthesis of clotting factors II, VII, IX, and X; it acts as a coenzyme. Proteases (i.e., enzymes that break peptide bonds within a protein) such as factor VII and IX, when activated, act as scissors to convert another separate factor from its inactive to its active form.

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12
Q

Compare and contrast the intrinsic pathway and the extrinsic pathway for activating blood clotting: initiation, calcium involvement, outcome

A

The intrinsic pathway (also known as the contact activation pathway) or the extrinsic pathway (or tissue factor pathway). Both pathways converge, through a series of complicated steps, to the common pathway.

The intrinsic pathway is triggered by damage to the inside of the vessel wall and is initiated by platelets. This pathway typically takes approximately 3 to 6 minutes:
1. Platelets adhering to a damaged vessel wall release factor XII.
2. Factor XII converts the inactive factor XI to the active factor XI.
3. Factor XI converts inactive factor IX to active factor IX.
4. Factor IX binds with Ca2+ and platelet factor 3 to form a complex that converts inactive
factor VIII to active factor VIII.
5. Factor VIII converts inactive factor X to active factor X (Thrombokinase).

In contrast, the extrinsic pathway is initiated by damage to the tissue that is outside the vessel, and this pathway usually takes approximately 15 seconds. This pathway occurs more quickly:
1. Tissue factor (thromboplastin; factor III) released from damaged tissues combines with factor VII and Ca2+ to form a complex.
2. This complex converts inactive factor X to active factor X (Thrombokinase).

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13
Q

Describe events in the common pathway: initiation, calcium involvement, outcome

A

Factor X (Thrombokinase) , activated by either the intrinsic or extrinsic pathway, is the first step in the common pathway:
1. Active factor X combines with factors II and V, Ca2+, and platelet factor 3 (PF3) to form prothrombin activator.
2. Prothrombin activator activates prothrombin to thrombin.
3. Thrombin converts soluble fibrinogen into insoluble fibrin.
4. In the presence of Ca2+, factor XIII is activated. Factor XIII cross-links and stabilizes the fibrin monomers into a fibrin polymer that serves as the framework of the clot.

Other components of blood become trapped in this spiderweb-like protein mesh. Like platelet plug formation, the clotting cascade is regulated by positive feedback. Once initiated by the intrinsic or extrinsic pathway, the events of the clotting cascade continue until a clot is formed (the climactic event). The size of the clot is limited because thrombin is either trapped within the clot or quickly degraded by enzymes within the blood.

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14
Q

Explain the sympathetic response to blood loss when blood loss exceeds 10%

A

As blood volume decreases, blood pressure decreases. If greater than 10% of the blood volume is lost from the blood vessels, the sympathetic division of the autonomic nervous system (ANS) is activated, bringing about increased vasoconstriction of blood vessels, increased heart rate, and increased force of heart contraction in an attempt to maintain blood pressure. Blood flow is also redistributed to the heart and brain to keep these vital structures functioning.

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15
Q

Describe clot retraction and fibrinolysis

A

Clot retraction occurs as the clot is forming when actinomyosin, a contractile protein within platelets, contracts and squeezes the serum out of the developing clot. This makes the clot smaller as the sides of the vessel wall are pulled closer together.
To destroy the fibrin framework of the clot, plasmin(or fibrinolysin) degrades the fibrin strands through fibrinolysis. This is a process that begins within 2 days of the clot formation and occurs slowly over a number of days.

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16
Q

Describe the significance of vitamin K in blood clotting

A

Vitamin K helps the liver to make various proteins that are needed for blood clotting and the building of bones. Prothrombin is a vitamin K-dependent protein directly involved with blood clotting.

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17
Q

Describe the general function of the cardiovascular system

A

The general function of the cardiovascular system is to circulate blood throughout the body to meet the changing needs of body cells. To remain healthy, all cells require (1) a continuous delivery of oxygen and nutrients and (2) the removal of carbon dioxide and other waste products.

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18
Q

Differentiate among the three primary types of blood vessels

A

Blood vessels are the conduits, or “soft pipes,” of the cardiovascular system that transport blood throughout the body. They are categorized into three primary types: Arteries transport blood away from the heart; veins transport blood toward the heart; and capillaries serve as the sites of exchange, either between the blood and the alveoli (air sacs) of the lungs or between the blood and the systemic cells.

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19
Q

Describe the general structures (atria, ventricles, great vessels, AV valves, semilunar valves) and function of the heart.

A

Two sides
Each side has a receiving chamber (atrium) and a pumping chamber (ventricle).
Right side
* Right atrium: receives deoxygenated blood from the body
* Right ventricle: pumps deoxygenated blood to the lungs
Left side
* Left atrium: receives oxygenated blood from the lungs
* Left ventricle: pumps oxygenated blood to the body

Great vessels
The great vessels are the large arteries and veins that are directly attached to the heart.
Arteries (arterial trunks) transport blood away from the heart.
* Pulmonary trunk transports from right ventricle.
* Aorta transports from left ventricle.
Veins transport blood toward the heart.
* Venae cavae (SVC and IVC) drain into right atrium.
* Pulmonary veins drain into left atrium.

Valves
Heart valves prevent backflow to ensure one-way blood flow.
* Atrioventricular (AV) valves (i.e., right AV valve and left AV valve) are between an atrium and a ventricle.
* Semilunar valves (i.e., pulmonary semilunar valve and aortic semilunar valve) are between a ventricle and an arterial trunk.

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20
Q

Compare and contrast pulmonary circulation and systemic circulation of the cardiovascular system.

A

The pulmonary circulation includes the movement of blood to and from the lungs for gas exchange. Deoxygenated blood is transported from (1) the right side of the heart through blood vessels to (2) the lungs. Exchange of respiratory gases occurs within the lungs as oxygen moves from the alveoli into the blood and carbon dioxide moves from the blood into the alveoli. Oxygenated blood is then transported through blood vessels to (3) the left side of the heart. Thus, the pulmonary circulation is movement of blood from the right side of the heart, to the lungs, and back to the left side of the heart.
The systemic circulation (or systemic circuit) includes the movement of blood to and from the systemic cells. Oxygenated blood is transported from (3) the left side of the heart through blood vessels to (4) the systemic cells such as those of the liver, skin, muscle, and brain. Exchange of respiratory gases occurs at systemic cells as oxygen moves from the blood into systemic cells and carbon dioxide moves from systemic cells into the blood. Deoxygenated blood is then transported through blood vessels that return blood to the (1) right side of the heart. Thus, the systemic circulation is movement of blood from the left side of the heart, to the systemic cells of the body, and back to the right side of the heart.

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21
Q

Trace blood flow through both circulations

A

Blood flow through pulmonary circulation
1 Deoxygenated blood enters the right atrium from the venae cavae (SVC and IVC) and coronary sinus (not shown). This blood then
2 passes through the right AV valve (tricuspid valve),
3 enters the right ventricle,
4 passes through the pulmonary semilunar valve, and
5 enters the pulmonary trunk.
6 This blood continues through the right and left pulmonary arteries to both lungs, and
7 enters pulmonary capillaries of both lungs for gas exchange.
8 This blood, which is now oxygenated, enters right and left pulmonary veins, and is returned to
9 the left atrium of the heart.

Blood flow through systemic circulation
1 Oxygenated blood enters the left atrium,
2 passes through the left AV valve (bicuspid or mitral valve),
3 enters the left ventricle,
4 passes through aortic semilunar valve, and
5 enters the aorta.
6 This blood is distributed by the systemic arteries, and
7 enters systemic capillaries for nutrient and gas exchange.
8 This blood, which is now deoxygenated, ultimately drains into the SVC, IVC, and coronary sinus (not shown), and
9 enters the right atrium.

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22
Q

Describe the general structure of the cardiac muscle: SR, maximum overlaps of thin and thick filaments, intercalated discs

A

This muscle tissue is made up of relatively short, branched cells that usually house one or two central nuclei. These cells are supported by areolar connective tissue, called an endomysium. Other anatomic structures of cardiac muscle cells include the following:
They are connected to adjacent cells by intercalated discs composed of both desmosomes and gap junctions. Desmosomes act as mechanical junctions to prevent cardiac muscle cells from pulling apart. Gap junctions allow an action potential to move continuously along the sarcolemma of cardiac muscle cells.
∙ The sarcolemma (plasma membrane), which invaginates to form T-tubules that extend to the sarcoplasmic reticulum (SR). The T-tubules of cardiac muscle invaginate once per sarcomere and overlie Z discs.
∙ The SR surrounds bundles of myofilaments called myofibrils in cardiac muscle, but it is less extensive than the SR of skeletal muscle and lacks both terminal cisternae (the “end sacs” of sarcoplasmic reticulum) and a tight association with T-tubules.
∙ Myofilaments are arranged in sarcomeres—thus, cardiac muscle appears striated when viewed under a microscope. Interestingly, maximum overlap of thin and thick filaments within the sarcomeres does not occur when cardiac muscle is at rest. Instead, maximum overlap of thin and thick filaments occurs when cardiac muscle is stretched as blood is added to a heart chamber.

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23
Q

Explain how cardiac muscle meets its energy needs: role of a myoglobin and aerobic cellular respiration

A

myoglobin (which is a globular protein thatmbinds oxygen when the muscle is at rest) and creatine kinase (which catalyzes the transfer of Pi from creatine phosphate to ADP, yielding ATP and creatine).

Cardiac muscle relies almost exclusively on aerobic cellular res- piration. Its cellular structures and metabolic processes support this. Cardiac muscle has a large number of mitochondria. It is also versatile in being able to use different types of fuel molecules, including fatty acids, glucose, lactate, amino acids, and ketone bodies

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24
Q

Identify and locate the components of the heart’s conduction system

A

Specialized cardiac muscle cells within the heart are located internal to the endocardium; they are collectively called the heart’s conduction system. These distinct cardiac cells do not contract, but rather they initiate and conduct electrical signals.

∙ The sinoatrial (SA) node is located in the posterior wall of the right atrium, adjacent to the entrance of the superior vena cava. The cells here initiate the heartbeat and are commonly referred to as the pacemaker of the heart.
∙ The atrioventricular (AV) node is located in the floor of the right atrium between the right AV valve and the opening for the coronary sinus.
∙ The atrioventricular (AV) bundle (bundle of His) extends from the AV node into and through the interventricular septum. It divides into left and right bundles.
∙ The Purkinje fibers extend from the left and right bundles beginning at the apex of the heart and then continue through the walls of the ventricles.

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25
Q

Compare and contrast parasympathetic and sympathetic innervation of the heart

A

Parasympathetic innervation
Cardioinhibitory center sends nerve signals along the vagus nerves (CN X), which result in a decrease in heart rate.
No parasympathetic innervation in myocardium
Sympathetic innervation
Cardioacceleratory center sends nerve signals along cardiac nerves, which result in an increase in both heart rate and force of contraction.

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26
Q

Describe two major physiological events associated with stimulating heart contraction

A

The physiologic processes associated with heart contraction are organized into two major events:
∙ Conduction system. Electrical activity is initiated at the SA node, and an action potential is then transmitted through the conduction system.
∙ Cardiac muscle cells. The action potential spreads across the sarcolemma of the cardiac muscle cells, causing sarcomeres within cardiac muscle cells to contract. These events occur twice in cardiac muscle cells during a heartbeat, first in the cells of the atria and then in the cells of the ventricles.

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27
Q

Describe an SA nodal cell at rest: RMP, Ion channels & autorhythmicity

A

Nodal cells in the SA node are the pacemaker cells that initiate a heartbeat by spontaneously depolarizing to generate an action potential.

The intracellular fluid (cytosol) just inside the plasma membrane is relatively negative in comparison to the fluid outside the cell (interstitial fluid). This electrical charge difference when the nodal cell is at rest is called the resting membrane potential (RMP). Nodal cells have an RMP of about −60 millivolts (mV). An RMP is established and maintained by K+ leak channels, Na+ leak channels, and Na+/K+ pumps.

Nodal cells contain specific voltage-gated channels, including slow voltage-gated Na+ channels (which are open) and both fast voltage-gated Ca2+ channels and voltage-gated K+ channels (which are closed).

SA nodal cells are unique in that they exhibit autorhythmicity (or automaticity), meaning that they are capable of depolarizing and initiating an action potential spontaneously without any external influence.

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28
Q

Describe the steps for SA nodal cells to spontaneously depolarize and serve as the pacemaker cells.

A

1 Reaching threshold. Slow voltage-gated Na+ channels open (this is caused by repolarization from the previous cycle). The Na+ flows into the nodal cells, changing the resting membrane potential from − 60 mV to − 40 mV, which is the threshold value. Notice that the threshold is reached without outside stimulation.

2 Depolarization. Changing of the membrane potential to 2+ the threshold triggers the opening of fast voltage-gated Ca channels, and Ca2+ entry into the nodal cell causes a change in the membrane potential from − 40 mV to a slightly positive membrane potential (just above 0 mV). This reversal of polarity is called depolarization.

3 Repolarization. Calcium channels close and voltage-gated K+ channels open; K+ flows out to change the membrane potential from a positive value to − 60 mV, which is the RMP. The process of reestablishing the RMP is called repolarization. Repolarization triggers the reopening of slow voltage-gated Na+ channels, and the process begins again.

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29
Q

Describe the spread of the action potential through the heart’s conduction system

A

1 An action potential is generated at the sinoatrial (SA) node. The action potential spreads via gap junctions between cardiac muscle cells throughout the atria to the atrioventricular (AV) node.

2 The action potential is delayed at the AV node before it passes to the AV bundle within the interventricular septum.

3 The AV bundle conducts the action potential to the left and right bundle branches and then to the Purkinje fibers.

4 The action potential is spread via gap junctions between cardiac muscle cells throughout the ventricles.

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30
Q

Describe the Ion channels and pumps at the sarcolemma of cardiac muscle cells at rest

A

The sarcolemma of cardiac muscle cells, like nodal cells, has K leak channels, Na+ leak channels, and Na+/K+ pumps to establish and maintain a resting membrane potential with a greater concentration of Na+ outside the cardiac muscle cells and a greater concentration of K+ inside. The RMP value of cardiac muscle cells, however, is −90 millivolts (mV) (in comparison to −60 mV for nodal cells). Cardiac muscle cells also contain Ca2+ pumps that form a Ca2+ con- centration gradient with more Ca2+ outside the cell than inside.
+ The sarcolemma of cardiac muscle cells has both fast voltage-gated Na channels that participate in depolarization at the membrane and voltage-gated K+ channels that participate in repolarization of the mem- brane. Additionally, cardiac muscle cells have slow voltage-gated Ca2+ channels within the sarcolemma. Slow voltage-gated Ca2+ channels, when open, allow Ca2+ into the cell

31
Q

List the electrical events (status of the ion channels & movement of ions) of an action potential that occur at the sarcolemma

A

1 Depolarization
Fast voltage-gated Na+ channels open.
* Na+ rapidly enters cardiac cell.
* Depolarization occurs (–90 mV → +30 mV). * Fast voltage-gated Na+ channels close.

2 Plateau
Voltage-gated K+ channels open.
* K+ flows out of cardiac muscle cell and
* Slow voltage-gated Ca2+ channels open and
* Ca2+ enters the cardiac cell.
* No electrical change and the depolarized state is maintained

3 Repolarization
Voltage-gated K+ channels remain open.
* K+ moves out of the cardiac muscle cell.
* Voltage-gated Ca2+ channels close.
* Repolarization occurs (+30 mV to –90 mV)

32
Q

Briefly summarize the mechanical events of cardiac muscle contraction

A

Crossbridge formation: Myosin heads attached to actin form a crossbridge between the thick and thin filaments.

Powerstroke: The myosin head swivels (the powerstroke), which pulls the thin filament past the thick filament a short distance, which decreases the width of a sarcomere.

Release of myosin head: ATP binds to the myosin head to release the myosin head from actin.

Reset of myosin head: ATP is split by myosin ATPase, providing the energy to reset the myosin head.

33
Q

Define the refractory period

A

The refractory period represents the time when the muscle cannot be re-stimulated to contract. (The refractory period is dependent upon how quickly depolarization and repolarization occur at the sarcolemma; the faster that repolarization occurs, the shorter the refractory period.)

34
Q

Explain the relationship between the plateau phase of AP and extended refractory period of the cardiac muscle cell & their significance

A

The extended refractory period in cardiac muscle cells (due to the plateau) allows time for cardiac muscle to contract and relax before being stimulated again. Thus, a sustained contraction (tetany) is prevented.
This relatively long refractory period is due to the plateau event at the sarcolemma, which delays repolarization. Consequently, while sarcomeres are still contracting and relaxing within cardiac muscle, the sarcolemma has not been repolarized to allow for a new stimulation.

35
Q

Identify the components of an ECG recording and their corresponding electrical events

A

The P wave reflects electrical changes of atrial depolarization that originates in the SA node. This event typically lasts 0.08 to 0.1 second

The QRS complex, which usually lasts between 0.06 and 0.1 second, represents the electrical changes associated with ventricular depolarization. Note that the atria are simultaneously repolarizing; however, this repolarization signal is masked by the greater electrical activity of the ventricles.

The T wave is the electrical change associated with ventricular repolarization.

P-Q segment
DEFINITION
atrial cells’ plateau = atria contracting

S-T segment
DEFINITION
ventricular plateau = ventricles are contracting

P-R interval
DEFINITION
-From atrial depolarization to beginning of ventricular depolarization
-Time to transmit action potential through entire conduction system

Q-T interval
DEFINITION
Reflects the time of ventricular action potentials

36
Q

Identify the two processes within the heart that occur due to pressure changes associated with the cardiac cycle

A

These alternating pressure changes are responsible for two significant physiologic processes:
∙ Unidirectional movement of blood through the heart chambers, as blood moves along a pressure gradient (i.e., from an area of greater pressure to an area of lesser pressure)
∙ Opening and closing of heart valves to ensure that blood continues to move in a “forward” direction without backflow

37
Q

List the five phases of the cardiac cycle

A

1 Atrial contraction and ventricular filling (a) Atrial depolarization (P
wave in ECG) triggers
(b) atrial contraction;
ventricles are relaxed to receive the blood; AV valves are opened and the semilunar valves are closed.
(c) Ventricular pressure (blue line) < both atrial pressure (green line) and pressure in aorta (red line).
(d) Ventricular blood volume increases slightly.

2 Isovolumetric Contraction
(a) Ventricular depolarization (QRS wave in ECG triggers)
(b) ventricular contraction; atria are relaxed; both the AV valves and semilunar valves are closed.
(c) Ventricular pressure (blue line) > atrial pressure (green line), < pressure in aorta (red line).
(d) Ventricular blood volume remains the same (isovolumetric).

Ventricular ejection
(a) Ventricular plateau and beginning of repolarization.
(b) Ventricles contracting; atria are relaxed; AV valves remain closed, semilunar valves open.
(c) Ventricular pressure > both atrial pressure and pressure in aorta.
(d) Ventricular blood volume decreases (as blood is ejected)

4
(a) Isovolumetric relaxation
Ventricles complete repolarization and then no electrical activity.
(b) Ventricles relaxing; atria are relaxed; AV valves remain closed, semilunar valves closed.
(c) Ventricular pressure > atrial pressure and < pressure in aorta.
(d) Ventricular blood volume remains the same.

5 Atrial relaxation and ventricular filling
(a) No electrical activity.
(b) Ventricles relaxing; atria
are relaxed; AV valves open, semilunar valves remain closed.
(c) Ventricular pressure < both atrial pressure and pressure in aorta.
(d) Ventricular blood volume increases (as blood flows from the atrium).

38
Q

Explain the significance of ventricular balance

A

It is important to realize that equal amounts of blood are normally pumped by the two ventricles through the two circulations, a condition called ventricular balance.
Sustained pumping of unequal amounts of blood may result in edema, which is excess fluid in the interstitial space or within cells.

39
Q

Define cardiac output & cardiac reserve

A

Cardiac output (CO) is defined as the amount of blood that is pumped by a single ventricle (left or right) in 1 minute and is typically expressed as liters per minute.

Cardiac output is determined by heart rate and stroke volume.
Stroke volume (SV) is the volume of blood ejected during one beat and is expressed as milliliters per beat.

HR X SV = CO

Cardiac reserve is an increase in cardiac output above its level at rest. It can be determined by subtracting cardiac output at rest from the cardiac output during exercise.
Cardiac reserve is a measure of the level and duration of physical effort in which an individual can engage.

40
Q

Define chronotropic agents and describe how they affect heart rate: EP, NE, thyroxin, caffeine, nicotine, cocaine, acetylcholine

A

The primary external factors to increase and decrease heart rate come from autonomic nervous system innervation (both the sympathetic division and the parasympathetic division) and varying levels of some hormones. These factors that change heart rate are called chronotropic agents and are classified as either positive chronotropic agents or negative chronotropic agents.

Sympathetic axons release norepinephrine (NE) (and stimulate release of NE and epinephrine [EPI] from the adrenal medulla), which acts as a positive chronotropic agent to increase heart rate.

Nicotine
(increases release of NE)

Caffeine (inhibits breakdown of cAMP)

Thyroid hormone (increases number of β1-adrenergic receptors): positive

positive chronotropic agents
increase heart rate: sympathetic stimulation (NE), chemicals (E, nicotine, thyroid hormone, caffeine)

decrease heart rate: parasympathetic stimulation (ACh), chemicals (hyperkalemia, hypokalemia), beta blockers

Cocaine: positive
(inhibits NE reuptake)

41
Q

List the three variables that may influence stroke volume

A

The specific volume of blood ejected as stroke volume varies and is influenced by several variables. These include (1) venous return, which is the amount of blood returned to the heart; (2) inotropic agents, which are external factors that alter the force of contraction of the myocardium; and (3) afterload, which is the resistance in the arteries to the ejection of blood from the heart.

42
Q

Define each of the three variables and describe the factors that influence stroke volume: venous return

A

a. Venous return
Volume of blood returned to the heart per unit time

Increased venous return (occurs with greater venous pressure or slower heart rate)

Increases stretch of the heart wall (preload), which results in greater overlap of thick and thin filaments within the sarcomeres of the myocardium

Additional crossbridges form, and ventricles contract with greater force

Stroke volume increases

The opposite is seen with smaller venous return (e.g., occurs with hemorrhage or extremely rapid heart rate)

43
Q

Frank-Starling law

A

This law essentially states that as the volume of blood entering the heart increases, there is greater stretch of the heart wall (or preload). This results in greater overlap of the thick and thin filaments in the sarcomeres of the cardiac muscle cells composing the myocardium, allowing formation of greater numbers of crossbridges. Consequently, a more forceful ventricular contraction is generated, and stroke volume increases.

44
Q

Define each of the three variables and describe the factors that influence stroke volume: Inotropic agents

A

Inotropic agents
Substances that act on the myocardium to alter contractility

Positive inotropic agents (e.g., stimulation by sympathetic nervous system)

Increased Ca2+ levels in the sarcoplasm result in greater binding of Ca2+ to troponin of thin filaments within sarcomeres of the myocardium

Additional crossbridges form, and ventricles contract with greater force

Stroke volume increases

The opposite is seen with negative inotropic agents (e.g., calcium channel blockers)

45
Q

Define each of the three variables and describe the factors that influence stroke volume: Afterload

A

Afterload
Resistance in arteries to ejection of blood

Atherosclerosis, which is deposition of plaque on the inner lining of arteries, is typically only a factor as we age

Arteries become more narrow in diameter

Increases the resistance to pump blood into the arteries

Stroke volume decreases

46
Q

Summarize the variables that influence cardiac output

A

Heart rate. An increase or a decrease in heart rate is dependent upon chronotropic agents that influence the conduction system. These agents stimulate the SA node to change its firing rate or the AV node to alter the amount of delay.

∙ Stroke volume. An increase or a decrease in stroke volume is generally due to changes in the myocardium. Venous return (which alters the stretch of the heart) and inotropic agents (which change the Ca2+ level in the sarcoplasm) influence the number of crossbridges, which alters the force of contraction. The only exception is afterload, which reflects increased resistance in arteries, making it more difficult for the heart to pump blood. Afterload is generally a factor only as we age.

∙ Cardiac output. Both heart rate and stroke volume are directly related to cardiac output. When both heart rate and stroke volume increase, cardiac output increases. In contrast, when both heart rate and stroke volume decrease, cardiac output decreases. It is not possible to predict the net effect on cardiac output if heart rate and stroke volume change in opposite directions.

47
Q

Describe the relationship of the total cross-sectional area and velocity of blood flow

A

The total cross-sectional area is estimated as the aggregate lumen diameter across the total number of a given type of vessel (artery, capillary, or vein) if they were all positioned side by side.
Blood flow velocity is the rate of blood transported per unit time and typically measured in centimeters per second.
Blood flow velocity in both arteries and veins, with their small total cross-sectional area, is relatively fast. In comparison, blood flow velocity in capillaries, with their relatively large total cross-sectional area, is relatively slow. Thus, blood flow velocity changes as it moves through the different types of vessels: Velocity of blood flow is relatively fast in the arteries, slowest in the capillaries, and relatively fast again through the veins.

48
Q

Describe the significance of slow blood in the capillaries

A

The slower blood flow rate allows sufficient time for efficient capillary exchange of respiratory gases, nutrients, wastes, and hormones between the body tissues and the blood

49
Q

Explain 3 capillary exchange processes: diffusion, vesicular transport & bulk flow

A

Within systemic capillaries, substances such as oxygen, hormones, and nutrients move by diffusion from their relatively high concentration in the blood into the interstitial fluid and then into the tissue cells, where the concentration of these materials is lower.

Vesicular transport occurs when endothelial cells use pinocytosis to form fluid-filled vesicles, which are then transported to the other side of the cell and released by exocytosis.

Bulk flow refers to the movement of large amounts of fluids and their dissolved substances in one direction down a pressure gradient.

50
Q

Explain 2 processes of bulk flow: filtration, and reabsorption

A

Bulk flow refers to the movement of large amounts of fluids and their dissolved substances in one direction down a pressure gradient. Filtration, a process that occurs on the arterial end of a capillary, is the movement of fluid by bulk flow out of the blood through the openings in the capillaries (e.g., intercellular clefts, fenestrations).
During this process, fluids and small, dissolved solutes flow through easily, whereas large solutes are generally blocked. In contrast, reabsorption occurs on the venous end of a capillary. Reabsorption is the movement of fluid by bulk flow in the opposite direction, back into the blood

51
Q

Compare and contrast hydrostatic pressure and colloid osmotic pressure in the capillaries

A

Hydrostatic pressure (HP) is the physical force exerted by a fluid on a structure. For example, blood hydrostatic pressure (HPb) (or simply blood pressure) is the force exerted per unit area by the blood as it presses against the internal surface of the vessel wall. Blood hydrostatic pressure promotes filtration from the capillary.

Colloid osmotic pressure (COP) refers to the pull of water back into a tissue by the tissue’s concentration of proteins (colloid). There are two specific types of colloid osmotic pressure: blood colloid osmotic pressure and interstitial fluid colloid osmotic pressure.

52
Q

Define net filtration pressure for both the arterial end and the venous end of a capillary

A

Net filtration pressure (NFP) is the difference between the net hydrostatic pressure (difference between the blood and interstitial fluid hydrostatic pressures) and the net colloid osmotic pressure (difference between the blood and the interstitial fluid colloid osmotic pressures)

Arterial end
Blood hydrostatic pressure is > osmotic pressure
Net pressure out

Venous end
Osmotic pressure is > blood hydrostatic pressure
Net pressure in

53
Q

Explain the lymphatic system’s role at the capillary bed

A

Another body system, the lymphatic system, is responsible for picking up this excess fluid and returning it to the blood. Lymph vessels reabsorb this excess fluid, filter it, and return it to the venous circulation

54
Q

Describe what is meant by degree of vascularization

A

The degree of vascularization, or the extent of blood vessel distribution within a tissue, determines the potential ability of blood delivery. Organs that are very active metabolically, such as the brain, skeletal muscle, the heart, and the liver, generally are highly vascularized.
some structures, such as tendons and ligaments, have little vascularization; blood delivery to these tissues is limited.

55
Q

Explain the process of angiogenesis and how it aids perfusion

A

The amount of vascularization in a given tissue may change over time through angiogenesis. Angiogenesis is the formation of new blood vessels in tissues that require them. This process helps provide adequate perfusion through long-term anatomic changes that occur over several weeks to months. For example, angiogenesis is stimulated in skeletal muscle in response to aerobic training; in adipose tissue, angiogenesis occurs in adipose connective tissue when an individual gains weight in the form of fat deposits. Angiogenesis also occurs in response to a slow, gradual occlusion (blockage) of coronary vessels, thus potentially providing alternative routes to deliver blood to the heart wall.

56
Q

Describe the myogenic response that maintains normal blood flow through a tissue

A

Blood flow into a tissue may remain relatively constant because of the myogenic response, which is contraction and relaxation of smooth muscle within blood vessels in response to changes in stretch of the blood vessel wall

An increase in systemic blood pressure causes an additional volume of blood to enter the blood vessel, which stretches the smooth muscle cells within the blood vessel wall. This stimulates the smooth muscle cells to contract, resulting in vasoconstriction. Thus, although systemic blood pressure is higher, which would drive additional blood into the blood vessel, the resulting vasoconstriction decreases the size of the blood vessel lumen offsetting the change, and blood flow into a tissue remains constant.

57
Q

Compare and contrast a vasodilator and vasoconstrictor

A

The stimulus is changing concentrations of certain chemicals, collectively called vasoactive chemicals. They are classified according to their action as either vaso- dilators or vasoconstrictors. Vasodilators are substances that cause smooth muscle relaxation, which results in both vasodilation of arterioles and opening of precapillary sphincters. Consequently, blood flow increases into a capillary bed. Vasoconstrictors are substances that cause smooth muscle contraction, which results in both arterioles vasoconstricting and precapillary sphincters closing. Thus, blood flow decreases into a capillary bed

58
Q

Explain how a tissue autoregulates local blood flow based on metabolic needs

A

Autoregulation is the process by which a tissue itself regulates or controls its local blood flow in response to its changing metabolic needs. The initial stimulus for autoregulation typically is inadequate perfusion due to increased metabolic activity of the tissue. If the tissue is not adequately perfused, then the oxygen and nutrient levels decline, while there is an increase in car- bon dioxide, lactate, hydrogen ion (H+), and potassium ion (K+) levels. These altered levels act as local vasodilators, and as a result additional blood enters the capillaries serving the tissue. As perfusion increases in the tissue and these levels adjust back to homeostatic values, the vessels constrict. Thus, there is a negative feedback loop between elevated levels of these molecules and the degree of vasodilation.

59
Q

Explain the general relationship of total blood flow to local blood flow

A

Maintaining sufficient local blood flow throughout the body (to ensure adequate perfusion of all tissues) ultimately depends upon total blood flow. Total blood flow is the amount of blood transported throughout the entire vasculature in a given period of time (usually expressed in liters per minute). Total blood flow equals cardiac output.

60
Q

Define blood pressure and blood pressure gradient.

A

Blood pressure is the force per unit area that blood exerts against the inside wall of a vessel. A blood pressure gradient is the change in blood pressure from one end of a blood vessel to its other end. A blood pressure gradient exists in the vasculature because blood pressure is highest in the arteries as the heart rhythmically contracts, and it is lowest in the veins. Blood pressure gradients are both clinically and physiologically significant because they are the driving force that propels blood through the vessels.

61
Q

Compare and contrast blood pressure and blood pressure gradients in the arteries, capillaries, and veins

A

Blood flow is pulsing, or pulsatile, in arteries as a consequence of the ventricles contracting and relaxing. The highest blood pressure generated in arteries is during ventricular systole when the artery is maximally stretched; this value is recorded as the systolic pressure. The lowest pressure is during ventricular diastole when the artery recoils no further; this value is recorded as the diastolic pressure. Arterial blood pressure is expressed as a ratio, in which the numerator (upper number) is the systolic pressure and the denominator (lower number) is the diastolic pressure. The average adult has an arterial systemic blood pressure of 120/80 mm Hg, but blood pressure can vary greatly among individuals.

By the time the blood reaches the capillaries, fluctuations between systolic and diastolic blood pressure disappear, so the pulse pressure disappears. Blood flow is smooth and even as it enters the capillaries.
Capillary blood pressure must be sufficient for exchange of sub- stances between the blood and surrounding tissue, but not so high that it would damage the relatively fragile capillaries.

62
Q

Calculate pulse pressure and mean arterial pressure (MAP) in the arteries

A

Pulse pressure is the additional pressure placed on the arteries from when the heart is resting (diastolic blood pressure) to when the heart is contracting (systolic blood pressure). Pulse pressure can be calculated by taking the difference between the systolic and the diastolic blood pressure. So, for an individual with a blood pressure of 120/80 mm Hg, the pulse pressure would be 40 mm Hg (120 mm Hg − 80 mm Hg = 40 mm Hg)
It represents the force that the heart generates each time it contracts.

Mean arterial pressure (MAP) is the average (or mean) measure of the blood pressure forces on the arteries. It evaluates how well blood flows through your body and whether it’s reaching all your major organs.

MAP = Diastolic pressure + 1/3 Pulse pressure
So for a person with average blood pressure of 120/80 mm Hg, his or her MAP would be approximately 93 mm Hg (80 + 40/3 = 93)

63
Q

Explain the mechanisms that help overcome the small pressure gradient in veins to return blood to the heart.

A

This relatively small blood pressure gradient is generally insufficient to move blood through the veins under given conditions without assistance, as when an individual is standing. Thus, venous return must be facilitated by valves within veins and two “pumps”—the skeletal muscle pump and the respiratory pump

The skeletal muscle pump assists the movement of blood primarily within the limbs. As skeletal muscles contract, veins are squeezed to help propel the blood toward the heart, and valves prevent blood backflow.

The respiratory pump assists the movement of blood within the thoracic cavity. diaphragm contracts and flattens with inspiration, blood propelled from abdominal cavity to thoracic. When we expire (exhale), the diaphragm relaxes and returns to its dome shape.
Thoracic cavity volume decreases and intrathoracic pressure increases, which places pressure on vessels within the thoracic cavity. Blood moves from the vessels in the thoracic cavity back into the heart. In addition, intra-abdominal pressure decreases, allowing blood to move from the lower limbs into the abdominal vessels. When breathing rate increases—for example, when a person is exercising—blood is moved more quickly back to the heart by the respiratory pump

Inspiration: Increases blood flow into thoracic veins
Expiration: Increases blood flow into heart and abdominal veins

64
Q

Define resistance, and explain how resistance is influenced by blood viscosity, vessel length, and vessel radius

A

Resistance is defined as the amount of friction the blood experiences as it is transported through the blood vessels. Blood flow is always opposed by resistance. This friction is due to the contact between blood and the blood vessel wall. The term peripheral resistance is typically used when discussing the resistance of blood in the blood vessels (as opposed to the resistance of blood in the heart).
The thicker the fluid, the more viscous it is, and the greater its resistance to flow.

Increasing vessel length increases resistance, because longer vessels result in greater friction, which the fluid experiences as it is transported through the vessel. In contrast, shorter vessels offer less resistance than longer vessels with comparable diameters.

How specifically does vessel radius influence resistance? Blood tends to flow fastest in the center of the vessel lumen, whereas blood near the sides of the vessels slows, because it encounters resistance from the nearby vessel wall. This difference in flow rate within a blood vessel (or in any conduit) is called laminar flow. In contrast, if vessel radius decreases, then relatively more blood flows near the edges and overall blood flow decreases.

65
Q

Describe the relationship of both the blood pressure gradient and resistance to total blood flow

A

Blood flow is directly proportional to our pressure gradient and inversely related to the resistance encountered along the way.

An increase in cardiac output causes a steeper (larger) pressure gradient leads Less resistance, which is caused by vasodilation, reduction in vessel length, or decrease in blood viscosity

A decrease in cardiac output causes a smaller pressure gradient leads to Greater resistance, which is caused by vasoconstriction, increase in vessel length, or increase in blood viscosity

66
Q

Describe the anatomic components associated with regulating blood pressure through short-term mechanisms

A

barroreceptors
- stretch receptors
- located in tunica externa of aorta and carotid sinus
- change in frequency of firing to signal BP change

vasomotor center
- medulla oblongata
- controls how vasoconstriction or vasodilated our blood vessels are
- sympathetic

cardiovascular center
- integration center and output signal
- cardioaccelatory and cardioinhibitory

67
Q

Explain the autonomic reflexes that alter blood pressure: baroreceptors

A

Baroreceptors are activated in response to changes in stretch of the blood vessel wall to initiate autonomic reflexes that help regulate blood pressure. These reflexes are appropriately called baroreceptor reflexes. These reflexes are initiated by either a decrease or an increase in blood pressure.

If blood pressure decreases:
1. Decreased stretch in the blood vessel wall is detected by baroreceptors in the aortic arch, carotid sinuses, or both.
2. The baroreceptors decrease the frequency of nerve signals relayed along sensory neurons within the vagus and glossopharyngeal nerves to both the cardiac center and vasomotor center.
3. In response, the cardioacceleratory center within the cardiac center increases nerve signals relayed along sympathetic pathways extending to the heart, including the SA node,
AV node, and myocardium. Concomitantly, the cardioinhibitory center of the cardiac center decreases nerve signals relayed along parasympathetic pathways that extend to the SA node and AV node. Consequently, both heart rate and stroke volume increase, resulting in a greater cardiac output.
4. Simultaneously, the vasomotor center increases nerve signals along sympathetic pathways that extend to blood vessels, resulting in net vasoconstriction and an increase in peripheral resistance, along with shifting of blood from venous reservoirs.
The resulting increase in cardiac output, increase in resistance, and larger circulating blood volume quickly elevate blood pressure.

If blood pressure increases:
1. Increased stretch in the blood vessel wall (reflecting an increase in blood pressure) is detected by baroreceptors in the aortic arch, carotid sinuses, or both.
2. The baroreceptors increase the frequency of nerve signals relayed along sensory neurons within the vagus nerve (CN X) and glossopharyngeal nerve (CN IX) to both the cardiac center and vasomotor center of the medulla oblongata.
3. The cardio-acceleratory center within the cardiac center decreases nerve signals relayed along sympathetic pathways extending to the heart, including the SA node, AV node, and myocardium. The cardioinhibitory center of the cardiac center increases nerve signals relayed along parasympathetic pathways that extend to the SA node and AV node. Both heart rate and stroke volume decrease, resulting in a smaller cardiac output.
4. Simultaneously, the vasomotor center decreases nerve signals along sympathetic pathways to blood vessels, resulting in net vasodilation and a decrease in resistance.
The resulting decrease in cardiac output, decrease in resistance, and smaller circulating blood volume lower blood pressure, and blood flow returns to its resting levels.

68
Q

Describe the hormones that regulate blood pressure

A

These include angiotensin II, aldosterone, antidiuretic hormone, and atrial natriuretic peptide. These typically regulate blood pressure by altering resistance, blood volume, or both. Blood volume is regulated by stimulating fluid intake (assuming fluid intake occurs) or altering urine output.

69
Q

Explain the renin-angiotensin system and its influence on blood pressure

A

The enzyme renin, released by the kidney in response to low blood pressure or stimulation by the sympathetic division, initiates a series of enzymatic chemical reactions within the blood that ultimately help raise blood pressure.

Angiotensin-converting enzyme (ACE) is anchored to the internal walls in capillaries, especially capillaries in the lungs.
Angiotensinogen is a plasma protein that is continuously produced by the liver and circulates within the blood.

  1. Kidney receptors detect low blood pressure or are stimulated by the sympathetic division; renin enzyme is released.
  2. Renin converts angiotensinogen into angiotensin I.
  3. ACE converts angiotensin I into angiotensin II.
  4. Angiotensin II increases blood pressure by:
    * Causing vasoconstriction
    * Stimulating thirst center
    * Decreasing urine formation
70
Q

Contrast the effects of angiotensin Ⅱ, aldosterone, and antidiuretic hormone on blood pressure with those of atrial natriuretic peptide.

A

Aldosterone is released from the adrenal cortex in response to several stimuli, including angiotensin II. Aldosterone increases the absorption of sodium ion (Na+) and water in the kidney, decreasing their loss in the urine; this helps maintain blood volume and blood pressure

The hypothalamus stimulates the posterior pituitary following either detection of increased concentration of blood (typically correlated with low blood volume) or stimulation of the hypothalamus by angiotensin II. ADH increases the absorption of water in the kidney, decreasing its loss in the urine; this helps maintain blood volume and blood pressure. ADH also stimulates the thirst center so that there is fluid intake, and blood volume increases. During extreme cases of low blood volume, as might occur with hemorrhaging, extensive release of ADH occurs, which causes vasoconstriction. This vasoconstriction increases peripheral resistance and blood pressure. This is why ADH is also referred to as vasopressin.

Atrial natriuretic peptide (ANP) is released from the atrium of the heart in response to an increase in stretch of the atrial walls due to increased blood volume and increased venous return. ANP both (1) stimulates vasodilation, which decreases peripheral resistance, and (2) increases urine output, which decreases blood volume. The net effect is a decrease in blood pressure

71
Q

Compare total blood flow and distribution at rest and during exercise

A

During exercise, there is an increase in total blood flow due to a faster and stronger heartbeat and because blood is removed from the “reservoirs” of the veins to the active circulation. There is also a redistribution of blood. Both of these changes help ensure that the most metabolically active tissues are receiving adequate blood flow to meet the needs of the tissue cells.

Blood flow to the coronary arteries of the heart increases approximately three-fold, a change that helps to ensure that sufficient oxygen reaches the cardiac muscle within the heart wall

Skeletal muscle blood flow increases an amazing 11-fold —which is approximately 70% of the total cardiac output—a change needed to meet the high metabolic demands experienced by skeletal muscle during exercise

The percentage of blood flow to the skin increases to almost five times its resting level to dissipate heat

In contrast, less total blood flow is distributed to the abdominal organs, slowing digestive processes; less is transported to the kidneys, which decreases urine output to maintain blood volume and blood pressure. Smaller amounts reach other structures that are not as metabolically active during exercise.

72
Q

Chemoreceptors

A

The two chemoreceptors are the aortic bodies and carotid body. The aortic bodies send nerve signals via the vagus nerve, and the carotid body along the glossopharyngeal nerve. High carbon dioxide levels, low pH, and very low oxygen levels stimulate the chemoreceptors, and their increased firing primarily stimulates the vasomotor center. The vasomotor center responds by increasing nerve signals along sympathetic pathways to blood vessels, which increases resistance and shifts blood to increase venous return. The changes raise blood pressure and increase blood flow.

73
Q

sympathetic innervation and norepinephrine in blood vessels

A

Blood vessels, unlike the heart, do not have dual innervation. Instead, they are typically innervated by only the sympathetic division with no innervation by the parasympathetic division. Thus, only sympathetic division pathways extend from the vasomotor center to most blood vessels; the neurotransmitter norepinephrine is also released from these ganglionic neurons.

Smooth muscle cells that contain α1 receptors contract in response to primarily norepinephrine, which causes vasoconstriction of these blood vessels. In contrast, smooth muscle cells that contain β2 receptors relax in response to epinephrine, which causes vasodilation of these blood vessels

The source of epinephrine hormone (and some norepinephrine) is the adrenal medulla, which releases both of these hormones