Chapter 32: The CV and Lymphatic System Flashcards

1
Q

Artery BF

A

Carry blood from the heart

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2
Q

Vein BF

A

Carry blood to the heart

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3
Q

BF through the heart

A

SVC receiving blood from head, neck, upper limbs and chest. 13. IVC receives blood from lower limbs and lower trunk. 1 & 13 end up in 9. The right atrium. 12. The tricuspid valve (valves keep blood moving in the right direction no not flow backwards) separates the right atrium from the right ventricle. 7. The right ventricle receives blood from the right atrium. Blood enters 2. The pulmonary artery from the right ventricle via 11. The pulmonary valve. blood then splits to the right lung via the right pulmonary artery and the left lung via the left pulmonary artery. In the lungs, gas exchange occurs -> blood discard CO2 for O2. Oxygenated blood enters 8. the left atrium via 3. Pulmonary veins. Next, blood enters 6. the left ventricle via 4. the mitral (bicuspid valve). Blood leaves the left ventricle and enters 10. the aortic arch (largest artery) via 5. The aorta semilunar valve. Then blood enters systemic circulation. The aortic arch has three main branches that supply the head and neck, then the aorta curls down, forming the descending aorta, which descends down the abdomen. The descending aorta splits to supply the pelvis & legs with blood.

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4
Q

Cardiac myocytes

A

specialized muscle cells. The contraction of these cells is initiated by electrical impulses, known as action potentials. unlike skeletal muscle cells, the heart does not have to be stimulated by the nervous system, the heart generates its own electrical stimulation. The heart can beat taken outside of the body. The NS can make the heart beat faster or slower, but cannot generate them.

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5
Q

Action potential

A

electrical stimulation. AP generation and conduction are essential for all myocytes to act in synchrony. Resting Membrane Potential = (-) on the inside.
Pacemaker cells (auto-rhythmic) and contractile cells (non-auto rhythmic) exhibit different forms of APs. Cells are polarized, meaning there is an electrical voltage across the cell. membrane. In a resting cell, the membrane voltage is know as the resting membrane potential -> usually negative. This means the cell is more negative on the inside. At this resting state, there are concentrations gradients of several ions across the cell membrane. -> Ions: More Na+ and Ca++ OUTSIDE cell. More K+ INSIDE cell. Maintained by pumps Na, Ca and K CHANNELS -> Bring Na and Ca OUT and K in.
An AP is essentially a brief REVERSAL of electric polarity of the cell membrane and is focused by voltage-gated ion channels. These channels are passageways for ions in and out of the cell and as their name suggest, are regulated by membrane voltage. The open at some values of membrane potential and close at others.

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6
Q

SA node

A

primary pacemaker of the heart. Housed in right atrium near entrance of the SVC . Initiates all heartbeats and controls the heart rate. If SA node is damaged, other parts of the conduction system may take over this role. The cells of the SA node fire spontaneously, generating action potential that spread through the contractile myocytes of the atria. The myocytes are connected by gap junctions, which for channels that allow ions to flow from one cell to another. This enables electrical cooling of neighboring cells. An AP in one cell riggers another action potential in its neighbor and the signals propagate rapidly. Pacemaker cells of SA node spontaneously fire about 80 AP/min, each of which sets off a heartbeat, resulting in an average HE of 80 bpm. NO true resting membrane potential. Pacemaker cells have “funny” currents present, which allow them to reach threshold faster. Funny channels open wen membrane voltage becomes lower than —40mV and allow slow influx of Na+, the resulting depolarization is known as “pacemaker potential.” At threshold Ca++ channels open, Ca ion flow int the cell further depolarizing the membrane, this results in the rising phase of the AP. At the peak of depolarization, K channels open, Ca channels inactivate, K channels ions leave the cell and the voltage returns to -60 mV, this corresponds to the falling (repolarizing) phase of the AP. The original ionic gradients re restored thanks to several ionic pumps and the cycle starts over.

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7
Q

AV node

A

AV Node- housed in right atrium near AV valve. Impulses reach the AV node, slow down a little to allow the atria to contract fully, then flow the conduction pathway an spread through the ventricular myocytes. Serves as electrical gateway to the ventricles.

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8
Q

3 major ions used for AP

A

K, Na, Ca

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9
Q

Contractile cell AP

A

The contractile cells have a different set of ion channels. In addition the SR stores a large amount of Ca. They also have myofibrils. They have a stable resting potential and depolarize ONLY when stimulated, usually by a neighboring myocyte. When a cell is depolarized, it has more Na and Ca inside the cell. These positive ions leak thru gap junctions to the adjacent cell and bring the membrane voltage of this cell up to threshold. At threshold, fast Na channels open creating a rapid Na influx and a sharp rise in voltage -> depolarizing phase. L-type or slow, Ca channels also open causing a slow but stead influx. As the AP nears its pea, Na channels close quickly, voltage-gated K channels open and these result in a small decrease in membrane potential, know as early repolarization phase. The Ca channels remain open and the K efflux is eventually balanced by the Ca influx. This keeps the membrane potential relatively stable for about 200 sec resulting in the plateau phase, characterized of cardiac AP. Ca is crucial in coupling electric excitation to physical muscle contraction. The influx of Ca form the ECF, is NOT enough to induce contraction, instead, it triggers a MUCH great Ca release from the S, in a process known as “Ca-induce Ca release” Ca then sets f muscle contraction by the same “sliding filament mechanism described for skeletal muscle. The contraction starts about half way thru the plateau phase and lasts until the end of this phase. As Ca channels slowly close, efflux predominates and membrane voltage returns to resting value. Ca is actively transported out of the cell and also back to the SR. The N/K pump then restores the ionic balance across the membrane. The plateau phase is necessary for exclusion of blood from the heart chambers. Long absolute refractory period is to make sure the mm has relaxes before it can respond to a new stimulus and is essential in preventing summation and trans, which would stop the heart from beating.

The action potential begins with the voltage becoming more positive; this is depolarization and
is mainly due to the opening of sodium channels that allow Na+ to flow into the cell.

After a delay (known as the absolute refractory period), termination of the action potential then occurs,
potassium channels open, allowing K+ to leave the cell and causing the membrane potential to return to negative, this is repolarization.
Another important ion is calcium (found in SR) which can be found outside of the cell as well as inside the cell, is a fundamental step in cardiac contraction.

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10
Q

Cardiac conduction system

A

The cardiac conduction system consists of the following components: the SA node -> the AV node -> passes signals down the AV bundle or bundle of His, this bundle is dividing into right and left bundle branches which conducts the impulses toward the apex of the heart. The signals are then passed onto purkinjie fibers, turning ward and spreading throughout the ventricular myocardium.

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11
Q

eEKG

A

Electrical activities of the heat can be recorded in the form of ECG. Composite recording of all the APs produced by the nodes and the cells of the myocardium. Each wave or segment of the EKG corresponds to a certain part of the cardiac electrical cycle.

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12
Q

EKG: p wave

A

when the atria are full of blood, the SA node fires, electrical signals spread throughout the atria an cause them to depolarize.Atrial contraction or atrial systole starts about 100ms after the P wave begins.

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13
Q

EKG: PR interval

A

represents the time the signals travel from the SA node to the AV node.

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14
Q

EKG: QRS complex

A

marks the firing of the AV node and represents ventricular depolarization. Q wave corresponds to depolarization of inter-ventricular septum. R wave is produced by depolarization of the main mass of the ventricles. S wave represents the last phase of ventricular depolarization at the base of the heart. Atrial repolarization also occurs during this time, but the signal I obscured by the large QRS complex.

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15
Q

EKG: ST segment

A

reflects the plateau in the myocardial AP. This is when the ventricles contract and pump blood

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16
Q

EKG T wave

A

represents ventricular repolarization immediately before ventricular relaxation or ventricular diastole. He cycle repeats itself with every heartbeat.

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17
Q

Coronary arteries supply

A

Heart muscles

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18
Q

Right coronary artery supply

A

Divides into right posterior descending artery goes around the back of the heart and the acute marginal artery in the front, supplies the right atrium, right ventricle, SA node, AV node.

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19
Q

Left coronary artery supply

A

divide into left anterior descending coronary artery and the circumflex coronary artery and supply blood to left atrium and left ventricle.

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20
Q

Cardiac veins role

A

veins leave cardiac myocytes and begin the deoxygenated blood to the right atrium through the coronary sinus.

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21
Q

Coronary sinus role

A

receives deoxygenated blood from the heart muscles and deliver it to the right atrium. The small cardiac vein from the right side of the heart joins with the coronary sinus and the middle vein from the right ventricle joining onto the coronary sinus and the posterior vein from the left ventricle joining onto the coronary sinus brining deoxygenated blood to the right atrium. The great cardiac vein joins onto the coronary sinus.

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22
Q

Anterior vein role

A

The anterior vein does not join onto the coronary sinus, but drains deoxygenated blood directly to the right atrium.

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23
Q

3 layers of the heart

A

the endocardium, myocardium and epicardium.

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24
Q

Endocardium

A

Lines the inner surfaces of the heart chambers including the heart valves. Innermost layer of the cardiac wall. Loose CT and simple squamous epithelial tissue. Regulates contractions.

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25
Q

Subendocardial layer

A

Lies between the endocardium and the myocardium. Containing the vessels and nerves of the conducting system of the heart. The purkinje fibers are located in this layer. Made of loose fibrous tissue. Damage to this layer can result in various arrhythmias

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26
Q

Myocardium

A

Main constituent of the heart and the thickest layer of all 3 heart layers. It is a muscle layer that enables heart contractions. Have a single nucleus in the center of the cell.

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27
Q

Subepicardial layer

A

Lies between the myocardium ad the epicardium

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28
Q

Epicardium

A

Outermost layer of the heart. Formed by the visceral layer of the pericardium. Made of mesothelial cells. Nerves and BV that supple the heart are found in the epicardium.

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29
Q

Pericardial cavity

A

Lies in between the epicardium and fibrous pericardium. The sac is filled with serous pericardial fluid that prevents friction during heart contractions.

30
Q

Lymphatic system

A

Drainage system that removes excess fluid from body tissues and return it to the blood system

31
Q

2 main functions of lymph system

A

Circ and immune

32
Q

Circulatory function of lymph system

A

major purpose of the circulatory system is to bring oxygen and nutrient to boy tissues and remove waste. This exchange happens in the capillaries. Blood plasma containing nutrients moves out of cap at the arterial end of cap beds, while tissue fluid containing wastes reabsorbs back in at the venous end. However, not all of the fluid is drawn back to the bloodstream at this point. About 15% of it is left in the tissues and would cause swelling if accumulated. This is where the lymphatic system comes into play -> picks up excess fluid and returns it to the circ system. The lymph system is a one-direction, open-ended network of vessels. Lymph vessels begin as lymph cap made of overlapping endothelial cells -> the over lapping valves function as a one-way valve. When fluid accumulates in the tissues, interstitial pressure increases, pushing the flaps inward, opening the gaps between cells, allowing fluid to flow in. As pressure inside the cap increases the endothelial cells are pressed outward, closing the gaps, preventing back flow. Unlike blood caps, the gaps in the lymph caps are so large that they allow bacteria, immune cells such as macrophages, and other large particles to enter. This makes the lymph system a useful way for large particles to reach the bloodstream. It is used for example, for dietary fat absorption in the intestine. One inside the lymph vessels, the removed fluid is called lymph. Lymph flow is enabled by the same ways that facilitate blood flow in the veins.. it goes from lymph caps to larger and larger lymph vessels and eventually drains into the bloodstream via subclavian veins. On the way, it passes thru a number of lymph nodes, high serve as filters cleansing the fluid before it reaches bloodstream.

33
Q

Immune function of lymph system

A

lymph nodes are small, bean-shaped structure scattered throughout the lymphatic network. They are most prominent in the areas the vessels converge. Lymph nodes contain macrophages and dendritic cells that directly swallow up any pathogens such as bacteria or viruses that may have been taken up from an infected tissue. They also contain lymphocytes: T and B cells, which are involved in adaptive immune response, a process that produces activated lymphocytes and antibodies specific to the invading pathogen. These are then carried by the lymph to the bloodstream to be disturbed wherever they are needed. The lymphatic system also includes lymphoid organs. Primary lymphoid organs -> thymus and bone marrow, are the site of lymphocyte production, maturation, and selection. Selection is the process, in which lymphocytes learn to distinguish between self and non self, so they can recognize and destroy pathogens without attacking the body’s own cells. Mature lymphocytes then leave the primary for the secondary lymphoid organs -the lymph nodes, spleen, and lymphoid tissues, where they enter other pathogens and become activated.

34
Q

cardiac output

A

Volume of blood flowing thru either the systemic or pulmonary circuit. Expressed in L/min. Is calculated by multiplying the heart rate in beats per minute by the stroke volume. Normal adult cardiac output at rest is 4-8 L/min (5 L/min, average). The forces involved in the flow of blood as it circulates through the cardiovascular system.
Evaluation of cardiovascular function as the heart and blood vessels respond to alterations of pressure, volume and flow of blood

35
Q

Stroke volume

A

the volume (mL) of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction.

36
Q

5 things that affect HR

A

CNS, ANS, neural reflexes, atrial receptors, hormones.

37
Q

3 things that affect SV

A

Preload -> ESV and venous return.
Afterload -> aortic pressure, aortic valvular function.
Contractility -> EDV, SNS, myocardial o2 supply

38
Q

% of CO body parts receive

A

CO at rest = 5 L/min (5000 mL/min)
Other 7% 350 mL
Heart 4% 200mL
Muscles 20% 1000 mL
Skin 6% 300 mL
Brain 14 % 700 mL
Liver 27% 1350 mL
Kidneys 22% 1100 mL

39
Q

ejection fraction

A

Is the amount of blood ejected per beat. Measures the % of blood that’s leaving our heart with every beat.
Typically only measures left ventricle.
Normal is 55% or higher.
Is calculated by dividing the stroke volume by the end-diastolic volume.
Is an indicator of ventricular function.

40
Q

What EF numbers mean

A

High function: >70%
Normal: 55-70% (50-55% is borderline)
Low: 40-55%
Possible HF: <40%

41
Q

measurement of EF

A

Measure with an echo -> most common. Can measure with a cardiac cath, ct, mri, or nuclear scan, but the easiest way is to Doppler the heart.

42
Q

Preload

A

Pressure generated at the end of diastole. The volume inside the ventricle at the end of diastole. Think of the stretch of the ventricle right before it goes into systole. Also called left ventricular end-diastolic pressure (LVEDP). Determined by 2 things: amount of venous return to the ventricle during diastole and the amount of blood left in the ventricle after systole (end systolic volume). When preload exceeds physiologic range, further muscle stretching causes a decline in CO

43
Q

What determines venous return in preload

A

BV and flow thru venous system and AV valves.

44
Q

What determines ESV in preload

A

Strength of ventricular contraction and resistance to vent. Emptying

45
Q

How preload is estimated

A

Right side of heart: CVP
Left side of heart: pulm artery wedge pressure

46
Q

Increase preload

A

Increased CVP (volume) from sympathetic activation, increased BF, and increased pumping.

47
Q

Decreased preload

A

Decreased CVP: (volume) from hemorrhage, gravity causing blood to pull in the lower limbs, poor atrial contraction.

48
Q

Vasodilation in preload

A

If vessels are dilated prior to blood coming into heart, a higher volume would be entering the heart. But if vessels are very dilated (like in shock and BP is low), the blood volume coming into the heart would be low because the blood is pulling in the vessels dt low pressure.

49
Q

Vasoconstriction in preload

A

if the vessels are constricted, like HTN prior to blood entering the right side of heart, a lower volume would be entering the heart

50
Q

Afterload

A

Refers to the amount of resistance the heart must pump against when ejecting blood. Is the resistance to ejection during systole.
Aortic systolic pressure is a good index of afterload for the left ventricle.
Decreased afterload: Heart contracts more rapidly.
-> Vasodilation like shock.
Increased afterload: Slows contractions and increases work load. ->
HTN.

51
Q

Frank-Starling low of the heart

A

Is the volume of blood at the end of diastole. SV is the tension, EDV is the length.
Myocardial stretch determines the force of myocardial contraction.
More stretch = Increased force of contraction.
Is the major way that the right and left ventricles maintain equal minute outputs, despite stroke (beat) output variation. Overstretch = decreased contraction

52
Q

Myocardial contractility determinants of the force of contraction

A

Changes in the stretching of the ventricular myocardium, caused by changes in ventricular volume (preload).

Alterations in nervous system input to the ventricles. -> SNS

Adequacy of myocardial oxygen supply.

Inotropic agents.
Positive inotropic agents: Increase the force of contraction. Norepinephrine from the sympathetic nerves supplying the heart. Epinephrine from the adrenal cortex. Thyroid hormone and dopamine, dobutamine.
Negative inotropic agents: Decrease the force of contraction. Acetylcholine released from the vagus nerve. -> PSNS.
Ca channel blocker.

Hypoxia: Decreases contractility.

53
Q

HR

A

Average heart rate in healthy adults: about 70 beats/minute.
Cardiovascular control center (Medulla)

54
Q

Neural reflexes on HR

A

Sinus arrythmia -> HR that varies with respiration
Baroreceptor reflex-> In aorta and carotid arteries. When BP falls, HR increases and the arteries constrict. Baroreceptors sense a low BP
Bainbridge reflex -> Atrial reflex. Increase in HR dt increased CVP or volume. Increased volume is detected by stretch receptors located in the atrium. Change HR depend on the fluid coming into heart. Can change HR when someone get infusion of IV fluids because as that volume increases, the stretch receptors increase HR to move fluid through.
Hormones and biochemicals

55
Q

SNS activation on HR

A

Increases HR

56
Q

PSNS activation on HR

A

Decreases HR, controls resting HR.

57
Q

Hemodynamic parameters

A

CO = 4-8 L/min
-> SV = 50-100 mL/beat
-> HR = 60-100 bpm
Cardiac index (CI) = 2.4-4 L/min
-> CO/BSA. CI is CO based on the persons body surface area. CO specific to them.

58
Q

Vessels

A

Arteries -> arterioles -> caps -> venules -> veins

59
Q

Peripheral vascular system

A

Systemic circ that supplies the skin and extremities

60
Q

Cap function

A

Gas exchange between tissues and blood. Nutrients go to the tissues and waste goes back to heart

61
Q

Structure of blood vessels

A

Lumen
Tunica intima: Innermost or intimal layer
Tunica media: Middle or medial layer
Tunica externa (adventitia): Outermost or external layer

62
Q

Processes for growing new BV

A

Angiogenesis: Growth of new vessels that branch from existing vessels
Branching of small vessels, such as capillaries
Arteriogenesis: Branching from larger vessels, such as arterioles
Vasculogenesis: Growth of vessels from progenitor or stemlike cells that originate in the bone marrow and other body tissues
Venogenesis: new draining veins

63
Q

Electric arteries

A

Contain more elastic fibers than
smooth muscle fibers; absorb energy and stretch.
Small externa, large media
Maintains pressure on the vessel regardless of blood flow.

64
Q

Muscular arteries

A

contain fewer elastic fibers and more muscle fibers; can contract (vasoconstriction) and relax (vasodilation)

65
Q

capillaries

A

Substances move through:
Junctions between endothelial cells
Fenestrations (oval windows or pores)
Vesicles moved by active transport
Diffusion

Blood flow into the capillary beds:
Controlled by the contraction and relaxation of smooth muscle bands (precapillary sphincters) at the junctions between metarterioles and capillaries

66
Q

Endothelium roles

A

Transportation of substances
Coagulation
Antithrombogenesis and Fibrinolysis -> Break up clots
Immune system function
Tissue growth and wound healing
Vasomotion: Contraction and relaxation of vessels
Performance of these vital functions through synthesis and the release of vasoactive chemicals

Central in vascular disorders like HTN and atherosclerosis
When endothelium gets damage things want to stick to it -> plaque, platelets

67
Q

Veins

A

Are thin walled and fibrous with a large diameter.
Are more numerous than arteries.
Do not recoil after distention as quickly as arteries.
Some contain valves.
Muscle pump: Pushes blood back to the heart.

68
Q

Mechanism of venous return

A

Valves and muscle pump

69
Q

Factors affecting BF

A

Poiseuille’s law:
Greater the resistance, the lower the blood flow.

Pressure:
Force is exerted on a liquid per unit area. (volume). Blood flows toward greater pressure

Resistance:
Is the opposition to blood flow.
Diameter and length of the blood vessels contribute to resistance.
Vessel radius or diameter greatly affects resistance.

Velocity:
Is the distance blood travels in a unit of time.
Pressure and distance affect the velocity of the blood
Vasodilation: area increases, velocity decreases.

Viscosity:
Thick fluids move more slowly and cause greater resistance to flow than thin fluids.
High hematocrit reduces the flow through the blood vessels.

Laminar Flow:
Occurs when concentric layers of molecules move “straight ahead.”

Turbulent Flow:
Occurs where flow is obstructed, the vessel turns; or blood flows over rough surfaces, producing a murmur.

70
Q

Most turbulent BF

A

Pulmonary artery. We may get venous blood gas from there

71
Q

Factors that regulate BP

A

Arterial pressure:

Mean arterial pressure (MAP):
Is the average pressure in the arteries throughout the cardiac cycle.
Is calculated by using systolic and diastolic pressures in a formula.
Diastole is twice as long as systole

Pulse pressure:
Is the difference between systolic and diastolic pressures.
Gives indication of contraction/ejection

Effects of total peripheral resistance:
Is primarily a function of the diameter of the arterioles.
Vessels are arranged in series (greater resistance) or in parallel (lesser resistance).

Effects of cardiac output:
Cardiac output can be changed by alterations in heart rate, stroke volume, or both.

Neural control of resistance:
Baroreceptors: Reduce blood pressure to normal by decreasing cardiac output and peripheral resistance. Can also increase blood pressure when needed.
Arterial receptors: Chemoreceptors: Are sensitive to oxygen, carbon dioxide, or pH.
Regulate blood pressure.

Effects of hormones:
Epinephrine and norepinephrine: Cause vasoconstriction
Antidiuretic hormone: Increases blood volume by reabsorption of water from tubular fluid in the distal tubule and the collecting duct of the nephron
Renin-angiotensin-aldosterone system:
Aldosterone: Stimulates reabsorption of sodium, chloride, and water to increase blood volume and stimulate thirst
Angiotensin II: Vasoconstrictor
Natriuretic peptides: Cause loss of sodium, chloride, and water through their effects on kidney function, decreasing blood volume

72
Q

regulation of coronary circ\

A

Coronary perfusion pressure:
Is the difference between pressure in the aorta and pressure in the coronary vessels.

Autoregulation:
Enables organs to regulate blood flow by altering the resistance in its arterioles.
Autonomic self regulation, especially in the coronary arteries, maintain optimal perfusion pressure, despite systolic effects.

Myoglobin in the heart muscle stores oxygen for use during the systolic phase.

Blood flows into the coronary arteries during diastole rather than systole:
During systole, cusps of the aortic semilunar valve block the openings of the coronary arteries.
Systolic contraction inhibits coronary artery flow by compressing the coronary arteries.