Bmsc2 Week 2: Regulation Of Blood Flow And Blood Pressure

Front 1

What is cardiac output?

Back 1

stroke volume x heart rate

Front 2

What is cardiac index?

Back 2

cardiac output / body surface area

Front 3

What is venous return?

Back 3

volume returning to heart each minute

Front 4

What causes the dicrotic notch in arterial pressure?

Back 4

The closing of the aortic valve causes the blood to backflow temporarily, increasing arterial pressure.

Front 5

When is end diastolic volume measured?

Back 5

isovolumetric contraction

Front 6

When is end systolic volume measured?

Back 6

isovolumetric relaxation

Front 7

When does the a wave in the atrial pressure occur?

Back 7

during atrial filling

Front 8

What event corresponds with the c wave in atrial pressure?

Back 8

onset of right ventricular systole

Front 9

What mechanical and electrical activity is correlated with S1?

Back 9

-mechanical: mitral valve closes followed by tricuspid valve
-electrical: QRS complex

Front 10

What mechanical and electrical activity is correlated with S2?

Back 10

-mechanical: aortic valve closes follwed by pulmonic valve
-electrical: return to baseline from T wave

Front 11

What is the difference between "pressure work" and "volume work" of the heart?

Back 11

-pressure work = afterload (resistance to ejection)
-volume work = preload (filling volume)

Front 12

How does the length of systole and diastole change with increase in heart rate?

Back 12

systole decreases slightly, diastole decreases drastically

Front 13

What are the mechanical events of systole?

Back 13

-atrial systole
-isovolumetric contraction
-ventricular ejection

Front 14

What are the mechanical events of diastole?

Back 14

-isovolumetric relaxation
-ventricular filling

Front 15

How is force controlled in skeletal muscle?

Back 15

-number of fibers stimulated varies
-frequency of action potentials varies

Front 16

How is force controlled in cardiac muscle?

Back 16

amount of Ca2+ released can vary

Front 17

What triggers the influx of extracellular (activator) calcium?

Back 17

voltage-sensitive L-type Ca2+ channels in the sarcolemma open in response to depolarization

Front 18

What triggers the influx of intracellular (storehouse) calcium?

Back 18

Ca2+ sensitive Ca-release channels in the sarcoplasmic reticulum open in response to influx of activator calcium

Front 19

How is intracellular Ca2+ removed?

Back 19

-Na/Ca exchanger in the sarcolemma
-Ca-ATPase in the sarcoplasmic reticulum

Front 20

What are the two ways that the force at which the heart contracts can be changed?

Back 20

-change initial fiber length (Frank-Starling mechanism)
-change contractility

Front 21

How does increasing initial fiber length change the force of contraction?

Back 21

-overlap of thick and thin filaments increases (total tension increases)
-greater sensitivity to [Ca2+]
-sarcoplasmic reticulum releases more Ca2+

Front 22

What is the Frank-Starling law of the heart?

Back 22

Within physiological limits, the tension generated by the contracting heart becomes greater as the heart muscle is stretched.

Front 23

How does a change in preload affect stroke volume?

Back 23

increase in preload causes increase in stroke volume

Front 24

How does a change in afterload affect stroke volume?

Back 24

increase in afterload causes decrease in stroke volume

Front 25

How does a change in contractility affect stroke volume?

Back 25

increase in contractility causes increase in stroke volume

Front 26

How does norepinephrine increase contractility?

Back 26

NE activates a G-protein receptor, and the Gαs subunit increases the open probability of the L-type Ca2+ channel.

Front 27

How does digitalis increase contractility?

Back 27

Inhibits the Na/K pump, increasing the intracellular [Na+]. This inhibits the Na/Ca exchanger and increases intracellular [Ca2+].

Front 28

What heart conditions could be treated by blocking L-type Ca2+ channels?

Back 28

-heart failure (decrease workload of the heart)
-arrhythmia (slow AV conduction)

Front 29

What is the source population (in biomedical studies)?

Back 29

-group of persons eligible for inclusion in study
-criteria: personal, temporal, and geographic

Front 30

What is the base population (in biomedical studies)?

Back 30

-broader than the source population
-group from which the cases arose

Front 31

What is the target population (in biomedical studies)?

Back 31

-broader than the base population
-group to which the study results will be applied

Front 32

What factors directly affect stroke volume?

Back 32

-end diastolic volume (preload)
-end systolic volume
stroke volume = EDV - ESV

Front 33

What factors directly affect end diastolic volume?

Back 33

-central venous pressure
-ventricular compliance

Front 34

What factors directly affect end systolic volume?

Back 34

-ventricular contractility (inversely affects ESV)
-arterial pressure (afterload)

Front 35

What factors directly affect central venous pressure (or right atrial pressure, jugular venous pressure)?

Back 35

-atrial kick
-blood volume
-venous capacity

Front 36

What is a normal central venous pressure (in mmHg)?

Back 36

1-2 mmHg

Front 37

How does cardiac output affect central venous pressure?

Back 37

as cardiac output increases, central venous pressure decreases, and eventually becomes negative when a suction is created

Front 38

How does central venous pressure affect cardiac output?

Back 38

As central venous pressure increases, cardiac output increases.

Front 39

What are the coordinated responses to hemmorhage?

Back 39

-sudden hypovolumia
-sympathetic stimulation of heart (contractility ↑)
-sympathetic venoconstriction

Front 40

How does breathing affect venous return?

Back 40

-inspiration accelerates venous return by increasing intraabdominal pressure and decreasing intrathoracic pressure
-expiration slows venous return

Front 41

What is the purpose of venous valves?

Back 41

Break the large vessels into segments to decrease the effect of gravity.

Front 42

What is the formula for Reynold's number?

Back 42

density x diameter x velocity / viscosity

Front 43

What conditions can increase Reynold's number?

Back 43

-anemia
-valve stenosis
-atherosclerosis
-pressure cuff

Front 44

Where in the circulation is Reynold's number the greatest?

Back 44

-branch points
-aorta

Front 45

How are systemic vascular resistance, mean arterial pressure, and cardiac output?

Back 45

MAP increases CO and SVR decreases it. CO = MAP / SVR

Front 46

How is mean arterial pressure estimated?

Back 46

diastolic pressure + 1/3 (systolic - diastolic)

Front 47

How is flow velocity related to bulk flow and cross-sectional area?

Back 47

velocity = flow / area

Front 48

What is the Fahraeus-Lindqvist effect?

Back 48

reduced viscosity when erythrocytes pass in single file through narrow vessels (axial streaming)

Front 49

What are the 4 control systems that govern regional blood flow?

Back 49

-metabolic control
-nervous control (sympathetic fibers)
-hormonal control (renin, ADH, etc.)
-long term control (angiogenesis)

Front 50

What factors contribute to metabolic hyperemia?

Back 50

-K+
-hyperosmolarity
-↓pO2
-adenosine