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Vertebrate Physiology > Chapter 12 EXAM 2 > Flashcards

Chapter 12 EXAM 2 Flashcards

1
Q

Describe the development of the heart.

A

the heart begins as a dual pump. The heart muscle twists, which causes the wringing action of the contraction.

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2
Q

Describe the right side of the heart.

A

takes blood from the body and pumps it to the pulmonary component of the circulatory system.

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3
Q

Describe the left side of the heart.

A

takes blood from the lungs and pumps it to the rest of the body.

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4
Q

Describe the valves.

A

one-way pumping action accomplished by valves.

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5
Q

What are the three different types of chambers of the heart?

A

atria
ventricles
vlaves

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6
Q

What is the atria?

A

located at the base of the heart.

receives blood from either lungs (left) or the rest of the body (right atrium) and help to fill the ventricles.

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7
Q

What are the ventricles?

A

form most of the muscle mass of the heart.

sends blood out to either the lungs (right ventricle) or the rest of the body (left ventricle).

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8
Q

What are the two types of atrioventricular valves?

A

tricuspid and bicuspid valves.

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9
Q

What is the function of the atrioventricular valves (AV)?

A

separates the atria from the ventricles.

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10
Q

Describe the tricuspid valve.

A

the right AV valve.

has three cusps.

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11
Q

Describe the bicuspid valve.

A

The left AV valve.

has two cusps.

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12
Q

What are chordae tendineae?

A

tough, string-like structures attached to the edges of the AV valves.
anchor the valves to the internal walls of the ventricles and help prevent the valves from opening backwards, thus assuring one-way flow.

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13
Q

What are papillary muscles?

A

cardiac muscle fibers that attach teh chordae tendineae to the ventricles. As the muscle cells of the ventricles contract, the papillary muscles also contract to help hold the valves close.

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14
Q

What are semilunar valves?

A

separate the ventricles from their respective out-flow tracts (pulmonary artery or aorta). Composed of three cusps.

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15
Q

What is the pulmonary valve?

A

separates the right ventricle from the pulmonary artery. Opens when pressure in the right ventricle exceeds the pressure in the pulmonary artery.

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16
Q

Describe the aortic valve.

A

separates the left ventricle from the aorta. Opens when pressure in the left ventricle exceeds the pressure in the aorta.
usually at 80mmHg.

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17
Q

what do valves and surrounding fibrous tissue serve as?

A

insulators that keep the atria and the ventricles isolated from each other. This is important in sequencing atrial

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18
Q

What is autorhythmicity?

A

the ability to contract without external stimulation.

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19
Q

What percent of cardiac muscle cells are autorhythmic?

A

1%

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20
Q

What percent of cardiac muscle cells are contractile?

A

99%

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21
Q

What is the function of the sinoatrial node (SA node)?

A

sets the pace for heart rate under normal circumstances.

inherently discharges at 70 to 80 times per minute.

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22
Q

Where is the SA node located?

A

the right atrial wall near the superior vena cava.

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23
Q

Where is the atrioventricular node (AV node) located?

A

in the right atrium near the septum, where the ventricles and atria meet.
inherently discharges at 40 to 60 times per minute.

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24
Q

describe the bundle of his.

A

travels from the AV node through the ventricular septum (on both sides) down to the apex of the heart.
inherently discharges at 20 to 40 times per minute.

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25
Q

Describe the purkinje fibers.

A

special conductive cells that communicate electrical impulses from the bundle of his to the contractile myocardial cells in the ventricles.
inherently discharge at 20 to 40 times per minute.

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26
Q

Where does the action potential usually originate?

A

from the SA node, because it’s discharging the most frequently.

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27
Q

Where does the action potential go after leaving the SA node?

A

travels through specialized internodal tract to the AV node.

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28
Q

Where does the AV node pass the action potential?

A

from the atria to the ventricles (which are electrically isolated from each other) along the bundles of His.

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29
Q

How long is the delay in propogation of the impulses thought the AV node?

A

0.1 second.

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30
Q

What is the function of the delay from the AV node impulse?

A

allows the atria to complete contraction before the ventricles contract.

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31
Q

Where do the bundles of His send the action potential?

A

along the ventricular septum toward the apex. (purkinje fibers).

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32
Q

Where do the purkinje fibers send the action potential?

A

to the contractile myocardial cells of both ventricles.

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33
Q

How are cells of the specialized conduction system modified?

A

to give them autorhythmicity.

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34
Q

Describe the cell membranes of the cells of the specialized conduction system.

A

far less permeable to potassium than other excitable cells.

they are permeable to sodium and calcium.

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35
Q

Describe the resting membrane potential of pacemaker cells.

A

wander toward threshold because of a greater influx of calcium relative to the efflux of potassium.

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36
Q

What happens when calcium enters the pacemaker cell?

A

the voltage gated calcium channels open allowing a more rapid influx of calcium into the cell. As the membrane potential peaks, the membrane becomes more permeable to potassium, which rapidly leaves the cell, reestablishing resting membrane potential.

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37
Q

What is periodicity caused by?

A

the slow rise toward threshold. This is the pacemaker potential.

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38
Q

How is the peiodicity manifested?

A

as a relatively constant heart rate.

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39
Q

What does parasympathetic activity do to the constancy of heart rate?

A

decreases the constanty.

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40
Q

What causes the heart rate to vary?

A

respiration and oscillations in blood pressure.

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41
Q

What happens if a pacemaker is lost?

A

pacing is taken over by the cells of the AV node.

heart rate will drop accordingly.

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42
Q

What can cause the loss of a pacemaker?

A

certain diseases or pathological events (myocardial infarction) can damage or eliminate the SA node.

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43
Q

What happens if the heart rate is determined by the cells of the bundles of His or Purkinje fibers?

A

the person will lose consciousness due to a heart rate that is too slow to maintain adequate blood pressure and thus blood flow to the brain.

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44
Q

What results from a block in the specialized conduction system?

A

the atria contracting independently of the ventricals. The atria follow the pace of the SA node and beat at 70 times per minute while the ventricles beat at 50 beats per minute.

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45
Q

What are ectopic foci?

A

in any area of the heart, the specialized conductin system cells or contractile myocardial cells can become irritable and can take over the pacing function from the SA node.

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46
Q

What is the result of ectopic foci?

A

causes the heart to contract out of synchrony with the pacing system because the cardiac muscle cells are in communication with each other.

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47
Q

What is a PVC?

A

the beat resulting from an ectopic focus in the ventricles.

premature ventricular contraction.

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48
Q

What can occur if there are multiple foci?

A

multiple action potentials can be generated and chaotic contractions can occur. can cause atrial or ventricular fibrillation.

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49
Q

What causes the rising phase of action potentials in cardiac muscle cells?

A

the influx of sodium.

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50
Q

What causes the plateau phase of action potentials in cardiac muscle cells?

A

the slow influx of calcium

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51
Q

What causes the falling phase of action potentials in cardiac muscle cells?

A

increase in permeability to calcium and increased permeability to potassium.

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52
Q

What are the two sources of calcium?

A

sarcoplasmic reticulum and extracellular fluid.

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53
Q

What can calcium trigger?

A

further release of calcium from the sarcoplasmic reticulum.
also prolongs the cardiac muscle contraction.
also prolongs the cardiac action potential.

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54
Q

What does the amount of calcium released into the cytosol determine?

A

the extent of cross bridge activity.

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55
Q

What does an increase in extracellular potassium lead to?

A

a decrease in concentration gradient, and a hypopolarization or hyperexcitability of the membrane.

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56
Q

What does an increase in extracellular calcium lead to?

A

an increase in the strength of contraction.

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57
Q

What causes the refractory period?

A

the inactivity of sodium channels during the action potential.

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58
Q

How long does the heart remain refractory?

A

250msec, which is approximately the length of a cardiac muscle contraction.

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59
Q

What does the refractory period prevents?

A

tetanus or wave summation from occurring.

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60
Q

Why is the refractory period important?

A

allows for atrial and ventricular filling.

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61
Q

How is electrical activity of the heart transmitted?

A

through the electrolyte solutions in the body.

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62
Q

What does an ECG do?

A

measures depolarization and repolarization of different portions of the heart.
does not measure mechanical events.

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63
Q

What is the P wave

A

represents depolarization of the atrial muscle.

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64
Q

What is the PR segment?

A

partially attributable to the conduction delay through the AV node. Measured from the end of the P wave and the beginning of the QRS complex.

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65
Q

What is the QRS complex?

A

represents ventricular depolarizations (masks the atrial repolarization).

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66
Q

What is the ST segment?

A

this represents the plateau phase of the cardiac muscle action potential. during this time period, the ventricles are contracting.

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67
Q

What is the T wave?

A

repolarization of the ventricles.

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68
Q

What is the TP interval?

A

the time at which the heart is at rest.

greatly influences the BPM.

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69
Q

What is atrial flutter?

A

rapid but regular contraction of atria. The ventricles contract rapidly but not at the same rate as the atria. Due to an ectopic atrial focus of stimulation.

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70
Q

What is ventricular flutter?

A

rapid ventricular contraction due to a single ectopic ventricular focus of stimulation. All P and T waves are obliterated.

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71
Q

What is atrial fibrillation?

A

completely uncoordinated depolarization of the atria. Due to multiple ectopic foci.

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72
Q

What is a complete heart block?

A

loss of coordination between the atria and ventricles. P waves are independent of the QRS complexes.

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73
Q

What are cardiac myopathies?

A

damage to the heart muscle.

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74
Q

What is tachycardia?

A

fast heart rate.

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75
Q

What is brachycardia?

A

slow heart rate.

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76
Q

What is ventricular systole?

A

a period of contraction. emptying, squeezing of the heart muscle.

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77
Q

What is ventricular diastole?

A

period of relaxation. Filling.

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78
Q

What happens during early diastole?

A

the atria are also in diastole.
cooresponds to the TP interval.
because blood is flowing from the veins into the atria, the pressure in the atria is slightly higher than in the ventricles. this causes the AV valves to remain open.

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79
Q

What happens when the AV valves are open?

A

blood will continue to flow into the ventricles and the ventricular pressure will rise slightly before the atria contract.

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80
Q

What happens in late diastole?

A

the SA node fires and the atria begin to depolarize. This is evidenced by the P wave. leads to contraction of the atria.

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81
Q

What happens when the atria contract?

A

more blood is pushed into the ventricles.
The AV valves are open; the pressures in the atria are slightly greater than the pressures in the respective ventricles. When the atria contract, the ventricles are already 80% of EDV.

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82
Q

What is EDV?

A

acheived when the ventricles are filled.

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83
Q

What happens when EDV is reached.

A

the signal from the SA node passes to the aV node and the ventricles begin to depolarize as evidenced by hearing the first heart sound. luuuub.

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84
Q

What happens after the ventricles depolarize?

A

the ventricular pressure increases, forcing the aortic and pulmonic valves to open.

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85
Q

What is the isovolumetric ventricular contraction?

A

the time before the aortic and pulmonic valves open.

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86
Q

What happens once the aortic and pulmonic valves are open?

A

ejection begins as evidenced by a rapid rise in arterial blood pressure.

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87
Q

What is systolic pressure?

A

the peak of the blood pressure curve. During this time, the ventricular volume is rapidly diminishing until the ventricles are through contracting.

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88
Q

What is the volume of the EDV?

A

135ml

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89
Q

What is the volume of ESV?

A

65ml

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90
Q

What happens once most of the blood has left the ventricle?

A

ventricular pressure falls. This results in closure of the aortic valve.

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91
Q

What does closing of the aortic valve case?

A

turbulence as evidenced by the second heart sound. Also causes a dip in the aortic pressure waveform called the dicrotic notch.

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92
Q

What happens shortly after the peak of ejection?

A

the ventricles repolarize and the T wave is observed on the ECG.

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93
Q

What is isovolumetric ventricular relaxation?

A

located at approximately the middle of the T wave.
the volume remains the same, as the heart relaxes.
as long as the ventricular pressure is above that of the atria, the AV valves are closed.

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94
Q

What happens when the ventricular pressures are less than the pressures in the respective atria?

A

the AV valves will open and ventricular filling will begin.

95
Q

What is the definition of cardiac output?

A

the amount of blood pumped by each ventricle per minute.

96
Q

What is heart rate determined by?

A

the SA node.

97
Q

describe parasympathetic influence on the cardiac output.

A

mediated via the vagus nerve.

releases acetylcholine at both the SA node and the AV node.

98
Q

What does the release of acetylcholine do in the SA node?

A

delays the closure of potassium channels. As these channels remain open, the membrane hyperpolarizes and mores lowly rises toward threshold. Thus, heart rate slows.

99
Q

What does the release of acetylcholine do in the AV node?

A

decreases nodal excitability, prolonging the time for conducting impulses to the ventricles. This is accomplished by the same mechanism as in the SA node.

100
Q

How does the release of acetylcholine affect the atrial contraction?

A

by reducing the calcium dependant plateau phase.

101
Q

What does parasympathetic influence have no effect on?

A

ventricular contraction strength; the vagus nerves do not affect the ventricular contractile cells.

102
Q

Describe sympathetic influence on the cardiac output.

A

norepinephrine decreases the permeability of potassium causing the SA node to reach threshold more rapidly.
increases the AV nodal conduction velocity, by enhancing calcium influx.
speeds up conduction through the purkinje fibers.

103
Q

What does the sympathetic stimulation do in both the atria and ventricles?

A

increases force of contraction by increasing permeability of the membrane to calcium.

104
Q

Describe the Frank-Starlin law of the heart.

A

direct correlation between end-diastolic volume and the stroke volume.
The greater the amount of blood returned to the heart, the greater the amount of blood pumped from the heart.
depends on the length-tension relationship of cardiac muscle fibers.

105
Q

What is preload?

A

the end-diastolic volume as it is the work load presented to the heart at the start of ventricular systole.

106
Q

What is afterload?

A

the resistance that is presented to the heart during its ejection of blood.

107
Q

What is sympathetic stimulation an example of?

A

extrinsic control.
enhances hearts contractility due to increased calcium influx triggered by norepinephrine and/or epinephrine.
enhances venous return by its effects on vascular smooth muscle.

108
Q

What is high blood pressure?

A

increases the amount of work that the heart has to perform to open the aortic and/or pulmonic valves and eject blood. the ventricles will respond by hypertrophying.

109
Q

What can cause decreased contractility?

A

damage to heart muscles.
prolonged high blood pressure.
congestive heart failure.

110
Q

What is backward failure?

A

blood can’t enter heart and be pumped, damned up in venous system.

111
Q

what is forward failure?

A

stroke volume decreases and heart doesn’t pump enough blood to tissues.

112
Q

What are some of the things that can occur during coronary artery disease?

A

vascular spasm.
atherosclerosis.
cholesterol problems.

113
Q

What is vascular spasm?

A

associated with early CAD. Triggered by cold, anxiety or exertion.
reduced oxygen availability triggers release of platelet-activating factor which causes vascular constriction.

114
Q

What is atherosclerosis?

A

leads to progressive blockage of coronary arteries.
starts as benign atheromas (tumors of smooth muscle cells).
cholesterol and lipids form plaque which are deposits that begin to impinge upon the lumen of the vessel.

115
Q

What is angina pectoris?

A

a symptom of CAD.

chest pain that often radiates to the left shoulder and arm.

116
Q

What is thrombus?

A

a symptom of CAD.

platelets form a blood clot in response to a plaque or other vascular damage .

117
Q

What is thromboembolism?

A

a symptom of CAD.

the thrombus clot can block an artery, or break free and form a thromboembolism.

118
Q

What is collateral circulation?

A

can resupply areas cut off from blood by a thrombus or thromboembolism.

119
Q

What are HDL’s?

A

High density lipoproteins.

good, high protein, low cholesterol. Moves cholesterol out of the cells to the liver for elimination.

120
Q

What are LDLs

A

Low density lipoproteins.
bad, low protein, high cholesterol.
moves cholesterol into the cells.

121
Q

What are VLDLs?

A

not too bad. contain no cholesterol.

122
Q

What are the uses of cholesterol?

A

maintenance of membrane fluidity, formation of steroid hormones, formation of bile salts.

123
Q

Describe cholesterol receptors.

A

required to get LDLs into cells.

lacking in some individuals, or partially lacking, such as a lack of apolipoprotein that interacts with these receptors.

124
Q

What is Poiseuille’s Law?

A

F=P/R where f=blood flow, P=change in pressure, R=resistance to flow.

125
Q

Describe P in poiseuilles law.

A

initial pressures determined by pressure in the aorta at the end of systole. The difference in pressure at the ends of the vessel determines the rate of flow, not the absolute pressure in the system.

126
Q

Increased viscosity=________________

A

increased resistance.

127
Q

What is viscosity determine by?

A

concentration of plasma proteins.

number of circulating red blood cells.

128
Q

The greater the surface area in contact with the blood, the greater the opportunity for _______________

A

friction, therefore, the greater the resistance.

129
Q

What is the major determinant of resistance?

A

the radius of vessels.

130
Q

What are the roles of the arteries?

A
  1. transportation of blood to the arterioles.

2. represent a pressure reserve.

131
Q

What does a large arterial diameter provide?

A

low resistance.

132
Q

what is an aneurysm?

A

the swelling or ballooning of an artery, often due to loss of collagen in the walls of the artery. can rupture with sometimes fatal consequences.

133
Q

What do arteries do, generally?

A

carry oxygenated blood; exception is circulation to the lungs.

134
Q

What is arterial pressure dependent upon?

A

compliance or willingness to stretch.

135
Q

What is systolic arterial pressure?

A

high pressure during and just after ventricle contraction.

120mmHg

136
Q

What is diastolic arterial pressure?

A

low pressure during heart filling. 80mmHg.

137
Q

How do you measure arterial pressure?

A

with a sphygmomanometer.

138
Q

When is systolic pressure measured?

A

when blood can be heard to begin to flow through the brachial artery as the cuff releases pressure.

139
Q

When is diastolic pressure measured?

A

when the turbulence associated with restricted flow smoothes out (laminar) and teh blood is no longer impeded by the cuff.

140
Q

What is pulse pressure?

A

the difference between systolic and diastolic that determines the wave felt when a pulse is taken.
pulse pressure=systolic pressure-diastolic pressure

141
Q

What is mean arterial pressure?

A

serves as the driving force for blood through the body.

142
Q

How does the time compare between diastole and cystole at normal resting heart rates?
What does this say about the mean arterial pressure?

A

diastole is about twice as long as systole. this means that the mean arterial pressure is not an average of the two pressures, but is influenced more by the diastolic pressure.

143
Q

Where does the majority of resistance to flow occur?

A

within the arterioles.

144
Q

What is the arterial pressure at the entrance to the arterioles?

A

93 mmHg.

145
Q

what is the arterial pressure at the end of the arterioles?

A

37 mmHg.

146
Q

What is vasoconstriction?

A 
narrowing of the vascular lumen. 
increased myogenic activity. 
decreased tissue activity. 
increased sympathetic stimulation. 
endothelin.
cold.
147
Q

What is vasodilation?

A 
inrease in lumen diameter due to:
decreased myogenic activity. 
increased tissue activity.
decreased sympathetic stimulation. 
histamine. 
heat.
nitric oxide.
increased potassium, 
increased osmolarity.
increased adenosine,
increased release of prostaglandin.
148
Q

What does intrinsic control of blood vessel diameter influence?

A

the amount of cardiac output that travels to a specific organ or system.
shifts to accommodate changes in metabolic needs.

149
Q

What is not affected by changes in cardiac output?

A

the blood flow to the brain.

150
Q

What is active hyperemia?

A

when increased metabolic activity induces arteriolar dilation via relaxation of the smooth muscle.
increased blood flow due to dilation.

151
Q

How does histamine effect blood vessel diameter?

A

it is a potent vasodilator, also makes capillaries more permeable; fluid, proteins, and cells flow into interstitial space.

152
Q

How does heat effect blood vessel diameter?

A

causes dilation.

153
Q

How does cold effect blood vessel diameter?

A

causes constriction.

154
Q

How can arteriolar smooth muscle resist stretch?

A

by increasing tone. This is a contrast to smooth muscle of GI tract, which relaxes when stretched.

155
Q

What is reactive hyperemia?

A

occlusion of blood flow that results in decreased stretch and myogenic relaxation.

156
Q

What is extrinsic control?

A

used to regulate arterial blood pressure.
Mean arterial pressure = cardiac output * total peripheral resistance.
supply to various organs is maintained by sympathetic tone.

157
Q

What will sympathetic stimulation of arterioles to cardiac muscle and skeletal muscle cause?

A

vasodilation of arterioles to these tissues.

mediated by norepinephrine and epinephrine through receptors.

158
Q

how is cerebral vasculature controlled?

A

locally–the brain controls its own blood supply.

159
Q

Where is the cardiovascular control center located and what does it do?

A

in the medulla. controls MAP via feedback systems involving baroreceptors located at the bifurcation of teh carotid arteries and in the aortic arch.

160
Q

What are adrenal hormones?

A

hormones that reinforce sympathetic activity through release of norepinephrine and epinephrine.

161
Q

What is the main function of capillaries?

A

primary site of exchange of materials.

162
Q

How thick is the endothelial lining?

A

1 micrometer thick, composed of a single layer of epithelial cells.

163
Q

How thick is the lumen diameter, and what is the purpose of this?

A

7 micrometers, slightly narrower than the diameter of a RBC. This forces the RBCs to line up single file for entry.

164
Q

Describe the surface area of capillaries.

A

estimated at 600m2

5% of blood volume is in the capillaries at any given time.

165
Q

Why does the flow rate not change?

A

because the circulatory system is a closed loop. However, the velocity does change.

166
Q

What are pores?

A

clefts between capillary endothlial cells

167
Q

What do pores allow for?

A

passage of water soluble substances between the blood and interstitial fluid.

168
Q

What are metarterioles?

A

control the availability of capillary beds. contain smooth muscle sphincters that shut off blood flow to the bed.

169
Q

What is ultrafiltration?

A

the movement of water from within the capillaries to the interstitial fluid space.

170
Q

What is reabsorption?

A

the movement of water in the opposite direction.

171
Q

what kind of diffusion do capillaries undergo?

A

passive. all diffusion occurs down a concentration gradient. This is the primary method of exchange for individual solutes.

172
Q

What causes ultrafiltration and reabsorption?

A

pressure differences between the capillary and the interstitial space.

173
Q

Describe capillary blood pressure (Pc).

A

forcing of fluid out of the capillary.

pressure at arteriolar end is 37 mmHg and declines to 17 mmHg at the venule end of capillaries.

174
Q

Describe plasma-colloid osmotic pressure (PIp).

A

becasue the proteins are unable to leave the capillaries, the proteins serve to attract water back into the capillaries. the force of attraction averages 25 mmHg.

175
Q

Describe interstitial-fluid hydrostatic pressure (Pif).

A

the fluid pressure exerted by/on the tissues that tends to drive fluid back into the capillaries. 1 mmHg.

176
Q

Describe interstitial-fluid-colloid osmotic pressure (PIif).

A

the osmotic force that draws water out of the capillaries and into the interstitial fluid. normally insignificant unless vascular injury or histamine release occurs.

177
Q

Net exchange pressure

A

=(Pc+PIif)-(Pip+Pif).

178
Q

the difference in net exchange pressure goes where?

A

is absorbed by the lymphatic system.

179
Q

What are lymphatic capillaries composed of?

A

endothelial cells that slightly overlap each other.

overlap acts as one-way valves that open to allow more fluid in, but close against fluid leaking back out.

180
Q

What do the pores in the lymph capillaries do?

A

large enough to reabsorb plasma proteins and bacteria.l

181
Q

What are the lesser functions of the lymphatic system?

A

transports fat from the digestive tract.
returns escaped proteins to circulation–preventing the buildup of interstitial-fluid- colloid osmotic pressure, and subsequent decrease in plasma-colloid osmotic pressure.

182
Q

What are the causes of edema?

A

reduced concentration of plasma proteins.
increased permeability of capillary walls
increased venous pressure
blockage of lymph vessels

183
Q

Why does reduction in concentration of plasma proteins cause edema?

A

decreses reabsorption.

seen in protein losing kidney disease, malnutrition, and liver disease.

184
Q

Why does increased permeability of capillary walls cause edema?

A

induces protein loss.
increases ultrafiltration by reducing plasma-colloid osmotic pressure.
decreases reabsorption by increasing interstitial-fluid-colloid osmotic pressure.
can be mediated by histamine.

185
Q

Why does increased venous pressure cause edema?

A

elevates the capillary hydrostatic pressure on the venous side.
seen in congestive heart failure and venous occlusion.

186
Q

Why does blockage of lymph vessels cause edema?

A

does not allow fluid to return to the heart.

may arise from lymph node removal or filariasis.

187
Q

What are the consequences of edema?

A

increased interstitial fluid results in increased distances between cells.
inadequate nutrition to cells and cells death.

188
Q

What are veins?

A

vessels that return blood to the heart, also serve as a reservoir for blood.

189
Q

Describe the anatomy of veins.

A

smooth muscle within the walls.
relatively few elastic fibers as compared to arteries, and thus have recoil capability.
large lumens, with the capacities to hold large volumes of blood.

190
Q

Describe the effect of gravity on venous return.

A

imposes roughly 90 mmHg of pressure within vascular compartment of the lower extremities.

191
Q

What is the total venous pressure?

A

100mmHg

192
Q

What is the normal venous pressure?

A

90 mmHg

193
Q

What does elevated venous pressure do?

A

decreases venous return due to the distensibility of the veins.

194
Q

What does reduced venous return do?

A

decreases cardiac output.

195
Q

What does increase in pressure in capillaries do?

A

increases ultrafiltration and decreases reabsorption leading to the formation of edema.

196
Q

What is venous capacity?

A

the more the venous capacity increases, the less blood is returned to the heart.

197
Q

What is blood volume?

A

increased blood volume increases venous pressure leading to an increase in venous return.

198
Q

What is sympathetic activity?

A

the sympathetic nervous system affects venous smooth muscle fibers. Will drive more blood back to the heart by decreasing venous capacity.

199
Q

Describe sympathetic tone.

A

arterioles to most tissues constrict (alpha 1). exceptions, blood can continue to go to the brain, heart and skeletal muscles. Arterioles to heart and skeletal muscle dilate (Beta 2).

200
Q

Describe skeletal muscle activity with veins.

A

as skeletal muscles contract, they compress veins, and increase the forward flow of blood. skeletal muscle pump.

201
Q

describe venous valves.

A

located at every 2 to 4 cm in large veins. they permit one way flow of blood to the heart.

202
Q

Describe respiratory activity with veins.

A

pressures within the chest are 5 mmHg less than atmospheric pressure. This vacuum is required to keep the lungs inflated. as blood returns to the heart through vessels that are located in the thorax, these negative pressures tend to expand the veins and suction blood form other parts of the body.

203
Q

describe cardiac suction.

A

during ventricular contraction, the AV valves are drawn downward, enlarging the atrial cavities. This creates negative pressure which draws blood into the atria. also, as the ventricles relax, a slightly negative pressure in these chambers creates a suction effect.

204
Q

What are baroreceptors?

A

pressure sensors within the circulatory system that continually monitor pressure.

205
Q

What is the effect of baroreceptors?

A

short-term control of blood pressure.

206
Q

Where are baroreceptors located?

A

in the carotid sinus and aortic arch.

207
Q

what are baroreceptors sensitive to?

A

stretch.

208
Q

what leads to increased firing of baroreceptors?

A

increased blood flow and MAP

209
Q

Describe the process of baroreceptor firing.

A
  1. afferent nerve fibers from sensors carry their signal to the cardiovascular control center in the medulla.
  2. the cardiac control center decreases sympathetic activity and increases parasympathetic activity.
  3. this results in a decreased heart rate and decreased stroke volume.
  4. additionally, the decrease in sympathetic activity initiates arteriolar and venous dilation, thereby decreasing TPR and venous return.
210
Q

what do osmoreceptors and volume receptors control?

A

long-term control of blood pressure.

211
Q

Where are osmoreceptors and volume receptors located?

A

osmoreceptors–hypothalamus
sodium receptors–kidneys and left atrium
volume receptors–left atrium

212
Q

What do osmoreceptors do if the blood pressure is too high?

A

water and salt will be excreted in the urine. water will then be lost by osmosis. blood volume will be reduced.

213
Q

What do osmoreceptors do if the blood pressure is too low?

A

water and salt will be conserved to increase blood volume. salt and water retained, blood volume increases.

214
Q

What happens if osmoreceptors in the hypothalamus sense that the osmolarity of the blood is too high?

A

they will stimulate thirst and release vasopressin or antidiuretic hormone which decreases the amount of water lost as urine.

215
Q

What happens if osmoreceptors in the hypothalamus sense that the osmolarity of the blood is too low?

A

they will inhibit the release of adh and increase water loss from the body, decreasing blood volume.

216
Q

what are the values of hypertension?

A

greater than 140 mmHg systolic pressure and or >90 mmHg diastolic pressure.

217
Q

Describe cardiovascular hypertension.

A

elevated total peripheral resistance due to loss of compliance of arteries

218
Q

Describe renal hypertension.

A

reduction of blood flow to the kidneys.
kidneys signal for the release of angiotensin II, a potent vasoconstrictor, increasing blood pressure.
angiotensin II also increases blood volume. if the kidneys are damaged and unable to eliminate the normal level of salts, retention of salts will lead to water retention and increased blood volume.

219
Q

Describe endocrine hypertension

A

a tumor of the adrenal medulla produces high levels of norepinephrine and epinephrine resulting in an increase in sympathetic activity.

220
Q

What is Conn’s syndrome?

A

an increased production of aldosterone which causes the kidneys to retain salt and water.

221
Q

Describe neurogenic hypertension.

A

problems with the baroreceptors or due to reduced cerebral blood flow.

222
Q

what are the possible causes of primary hypertension

A 
problems in management of salts. 
defective sodium postassium pumps
pressure on the medulla
endogenous digitalis like compounds change properites of heart contraction 
deficiency in NO production/release.
223
Q

What are the values for prehypertension?

A

120/80-139/89 mmHg

224
Q

What are the values for hypotension?

A

below 100/60

225
Q

what is orthostatic hypotension?

A

due to inadequate sympathetic activity. As gravity shifts occur in the blood volume, the body is unable to compensate in time, and the brain is temporarily inadequately perfused. Head rush feeling, brain briefly deprived of adequate blood supply.

226
Q

How does emotional stress cause hypotension?

A

emotional input to sympathetic centers initiates inappropriate sympathetic inactivity on the peripheral vasculature. decreases MAP.

227
Q

What is circulatory shock?

A

inadequate perfusion of tissues, low blood flow, especially detrimental to the brain.

228
Q

What is hypovolemic circulatory shock?

A

decrease in total blood flow.

229
Q

what is cardiogenic circulatory shock?

A

inability of the heart to pump properly.

230
Q

What is vasogenic circulatory shock?

A

systemic vasodilation.

231
Q

What is septic shock?

A

triggered by bacterial cell wall components in circulation.

232
Q

What is anaphylactic shock?

A

due to systemic release of histamine.

233
Q

What is neurogenic shock?

A

can be in response to sever pain, similar to emotional stress. induction of hypotension; loss of sympathetic vascular tone.

Vertebrate Physiology (9 decks)

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