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PSIO 202 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

0
Q

Determinants of SV

A

AFTERLOAD: Aortic blood pressure
PRELOAD: end-diastolic volume
CONTRACTILITY: active or passive contraction of ventricular muscles

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1
Q

Cardiac Output

A

CO = SV x HR

CO = Pressure gradient/R

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2
Q

Afterload

A

Ventricles cannot eject blood into the aorta or pulmonary artery until the pressure in the ventricle exceeds the pressure in the artery

(Pressure required to open semilunar valves)

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3
Q

Preload

A

The SV cannot increase unless the rate or cardiac filling also increases

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4
Q

Contractility

A

Strength of ventricular muscle contraction

Active contractility: stimulation of the sympathetic nerves to the heart

Passive contractility: the result of changing the length of the cardiac muscle fibers (frank-starling mechanism)

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5
Q

Control of active contractility

A

Due to actions of norepinephrine (or epinephrine)

  • Inc rate or pacemaker activity
  • Inc force of cardiac muscle contraction
  • inc permeability to Ca => more cross bridge interactions
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6
Q

Sympathetic vs. Parasympathetic Divisions of the ANS

A

Sympathetic (thoracolumbar): preganglionic releases ACh then postganglionic release NE

Parasympathetic (cranial): preganglionic releases ACh then postganglionic release ACh

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7
Q

Systole

A

Ventricular contraction and blood ejection

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8
Q

Diastole

A

Ventricular relaxation and filling

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9
Q

Chronic topic effects

A

Effects of the ANS on heart rate

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10
Q

Fibers from cardioacceleratory center

A

Sympathetic

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11
Q

Fibers from the cardio inhibitory center

A

Parasympathetic

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12
Q

Mechanism of Parasympathetic Control of Heart Rate

A

ACh release increases K permeability, and the rate of potassium diffusion out of the cells increase.
Results in hyperpolarization (takes more time for membrane potential to reach the threshold for Na channel (atrial contraction) and Ca channels (SA node autorhythmic fibers) activation

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13
Q

Chemical influences on Heart Rate and Contractility

A 
Hormones
Hypocalcemia
Hypercalcemia 
Hypernatremia 
Hyperkalemia
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14
Q

Hormones that increase heart rate and heart contractility

A

Epinephrine and thyroxine

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15
Q

Hypocalcemia

A

Reduced ionic calcium depresses contractility

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16
Q

Hypercalcemia

A

Dramatically increases heart irritability and leads to spastic contractions

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17
Q

Hypernatremia

A

Blocks heart contraction by inhibiting ionic calcium transport

18
Q

Hyperkalemia

A

Too high Ca levels lead to an inhibility to depolarize and leads to heart block and cardiac arrest

19
Q

Continuous capillary

A

Most restrictive/ intercellular clefts

Found in lungs, skeletal muscle, connective tissue, BBB

20
Q

Fenestrated capillary

A

Pores to let large molecules to pass/ intercellular clefts

21
Q

Sinusoidal capillary

A

Intercellular clefts/huge holes to prevent mixing of proteins and blood and to adjust contents in blood
Found in liver, spleen, bone marrow, anterior pituitary gland

22
Q

Diffusion

A

Passive process of fluid exchange

Movement of fluid from high to low concentration until equilibrium

23
Q

Bulk flow

A

Passive process of fluid exchange

Movement of fluid from a region of higher pressure to one of lower pressure

24
Q

Transcytosis

A

Active process of fluid exchange

25
Q

Blood hydrostatic pressure (BHP)

A

Pushes fluid OUT through the capillary pores

26
Q

Interstitial fluid osmotic pressure (IFOP)

A

“Pulls” fluid OUT via osmosis; this pressure is very small compared to BHP

27
Q

Blood colloid osmotic pressure (BCOP)

A

Result of differences in protein concentration between plasma and IFS, which tends to pull water from the ISF and into capillaries (creates constant pull of water into the blood)

28
Q

Interstitial fluid hydrostatic pressure (IFHS)

A

Due to pressure exerted by interstitial fluid, but is normal very small

29
Q

Net Filtration Pressur

A

Difference between the inward and outward pressures
(BHP + IFOP) - (BCOP + IFHP) = NFP
Outward(Filtration) - inward(reabsorption)

30
Q

Mean arterial blood pressure

A

MAP = DBP + 1/3(SBP - DBP)

31
Q

Pulse pressure

A

The PP reflects the SV

32
Q

Vascular resistance

A

Resistance is the sum of all forces that retard flow

Flow = driving pressure/ resistance

33
Q

Resistance

A

R = (viscosity)(vessel length)/ radius to the 4th

34
Q

Systemic Vascular Resistance (SVR)

A

Resistance offered by the vessels of the systemic circulation

SVR = (MAP-RAP)/CO

35
Q

Baroreceptors

A

High pressure: located in the carotid sinus and aortic arch and enter via cranial nerve IX/X

Low pressure: located in the walls of the right atrium and vena cavae, and enter the CV center via cranial nerve

36
Q

Chemoreceptors

A

Located in the carotid sinus (via cranial nerve IX) and in the walls of the ascending aorta via (cranial nerve X)

Respond to inc H content, CO2 and most strongly to hypoxia

Activate the sympathetic div, resulting in inc HR, SV, and vasoconstriction

37
Q

Catecholamines

A

Hormonal control of BP

(NE and epinephrine) bind directly to cardiac muscle and blood vessel smooth muscle

38
Q

Antidiuretic hormone (ADh)

A

Causes intense vasoconstriction in case extremely low BP

39
Q

Angiotension II

A

Causes intense vasoconstriction when renal glands perfusion is inadequate

40
Q

Aldosterone

A

Secreted by the adrenal cortex which inc salt and water reabsorption to Cause water retention and inc BP by raising blood volume

41
Q

RAA System

A

Kidneys release renin, angiotensinogen converts renin into angiotensin I, concerts to angiotensin II with ACE from lungs

42
Q

Atrial natriuretic peptide (ANP)

A

Released by cells in the atria when BP is too high. This hormone causes vasoconstriction and promotes loss of water and salt by the kidneys.

43
Q

Histamine

A

Released by mast cells
Cause vasodilation by relaxing smooth muscle
Inc blood flow to inflamed or damaged tissue

PSIO 202 (2 decks)

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