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gen.exam.review > Ch3. Cardiovascular Physiology > Flashcards

Ch3. Cardiovascular Physiology Flashcards

1
Q

What is the stressed volume?

A

the blood volume contained in the arteries

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2
Q

What is the site of highest resistance in the cardiovascular system?

A

arterioles

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3
Q

Arteriolar resistance is regulated by

A

the autonomic nervous system

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4
Q

alpha-1 adrenergic receptors are found on what parts of the CV system

A

arterioles of the skin, splanchnic and renal circulations

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5
Q

beta-2 adrenergic receptors are found on what parts of the CV system?

A

arterioles of skeletal muscle

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6
Q

What is considered the unstressed volume?

A

The blood volume contained in the veins

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7
Q

Velocity of blood flow is expressed as which equation?

A

v=Q/a

velocity (Cm/sec)
Q- blood flow (ml/min)
A= cross sectional area (cm2)

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8
Q

Define capacitance

A

distensibility of blood vessels

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9
Q

Capacitance is inversely related to?

A

elastance or stiffness

**the greater the amount of elastic tissue there is in a blood vessel, the higher the elastance is, and the lower the compliance is

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10
Q

Capacitance is much greater in which part of the CV system?

A

Greater for veins than for arteries
**more blood volume in veins (unstressed volume) than in the arteries (stressed volume)

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11
Q

What are the mean pressures of systemic circulation:
-aorta
-arterioles
-capillaries
-vena cava

A

aorta: 100 mmHg
arterioles: 50 mmHg
capillaries: 20 mm Hg
Vena Cava: 4 mmHg

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12
Q

Systolic arterial pressure is measured when?

A

after the heart contract & systole) and blood is ejected into the arterial system

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13
Q

Diastolic arterial pressure is measured when?

A

the heart is relaxed (diastole) and blood is returned to the heart via the veins

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14
Q

Define pulse pressure

A

the difference between systolic and distaolic pressure

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15
Q

What is the most important determinant of pulse pressure?

A

stroke volume

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16
Q

define mean arterial pressure

A

average arterial pressure with respect to time
**not the simple average of diastolic and systolic pressure (b/c a greater fraction of cardiac cycle is spent in diastole

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17
Q

Mean arterial pressure calculation

A

diastolic pressure + 1/3 of pulse pressure

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18
Q

What is the p wave of the electrocardiogram?

A

atrial depolarization

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19
Q

PR interval of the electrocardiogram represents

A

conduction velocity through the AV node
**Inc in PR interval, dec AV nodal conduction (heart block)

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20
Q

QRS complex of the electrocardiogram represents

A

depolarization of the ventricles

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21
Q

What does the QT interval of the electrocardiogram represent?

A

depolarization and repolarization of the ventricles

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22
Q

What does the T wave represent of the electrocardiogram?

A

ventricular reprolarization

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23
Q

The cardiac resting membrane potential is determined by what?

A

conductance of K and approaches the K equilibrium potential

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24
Q

What is the role of Na-K ATPase in the cardiac action potential?

A

maintain ionic gradients across cell membranes

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25
Q

Describe phase 0 of the cardiac action potential.

A

-upstroke of the action potential
-caused by transient increase in Na conductance
**increase results in an inward Na current that depolarizes the membrane
-at peak of the action potential, membrane potential approaches the Na equillibrium

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26
Q

Describe phase 1 of the cardiac action potential.

A

-initial repolarization caused by an outward current, b/c of movement of K ions out of the cell and b/c of dec in Na conductance

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27
Q

Describe phase 2 of the cardiac action potential

A

plateau of the action potential
-caused by transient increase in Ca conductance, which results in an inward Ca current and by inc in K conductance
-during phase 2, outward & inward currents are approximately equal
**membrane potential is stable

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28
Q

Describe phase 3 of the cardiac action potential.

A

repolarization
-during phase 3, Ca conductance decreases and K conductance increases
-high K conductance results in lg outward K current, which hyperpolarizes the membrane back toward K equilibrium potential

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29
Q

Describe phase 4 of the cardiac action potential.

A

resting membrane potential
-period during which inward and outward currents are equal and the membrane potential approaches the K equilibrium potential

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30
Q

which phases of the cardiac cycle are not present in SA node?

A

phases 1 and 2

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31
Q

The upstroke of the action potential in the AV node is the result of:

A

inward Ca current
**as in the SA node

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32
Q

Describe conduction velocity

A

the time required for excitation to spread throughout cardiac tissue

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33
Q

Where is the conduction velocity the fastest and slowest?

A

-fastest: Purkinje system

-slowest: AV node

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34
Q

Why is conduction velocity slowest at the AV node?

A

to allow for ventricular filling before ventricular contraction

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35
Q

What are the phases in which no action potential can be initiated, regardless of how much inward current is supplied?

A

absolute refractory period
effective refractory period

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36
Q

When can an action potential be elicites, but more than the usual inward current is required?

A

relative refractory period

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37
Q

What is the difference between positive and negative chronotropic effects?

A

negative: decreases heart rate by decreasing firing rate of SA node

positive: increases heart rate by increasing the firing rate of the SA node

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38
Q

Dromotropic effects on the heart produce changes in conduction velocity at what level?

A

primarily in the AV node

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39
Q

On which parts of the heart do we see parasympathetic vagal innervation?

A

SA note
atria
AV node

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40
Q

parasympathetic effects on the heart and conduction velocity is mediated by which neurotransmitter?

A

acetylcholine
**acts at muscarinic receptors

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41
Q

What is the parasympathetic effect on the heart?

A

dec heart rate, dec conduction velocity (AV node) and dec contractility (atria only)
**muscarinic receptors

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42
Q

What is the sympathetic effect on the heart?

A

inc heart rate, inc conduction velocity and increase contractility (beta 1)

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43
Q

What are the autonomic effects on vascular smooth muscle?

A

constriction: alpha 1– skin, splanchnic
relaxation skeletal mm– beta 2

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44
Q

Sympathetic effects on the heart rate and conduction velocity are mediated by which neurotransmitter?

A

norepinephrine
**on Beta 1 receptors

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45
Q

Myocardial cell structure: sarcomere

A

is the contractile unit of the myocardial cell
**runs from Z line to Z line

46
Q

Myocardial cells sarcomeres structure

A

thick filaments: myosin

thin filaments: actin, troponin, tropomyosin

47
Q

Intercalated disk of mycoardial cells

A

occur at the end plates
maintain cell to cell cohesion

48
Q

Where are gap junctions are located in myocardial cell structures?

A

present at the intercalated disks

49
Q

What are gap junctions of myocardial cell structures?

A

low-resistance paths between cells that allow for rapid electrical spread of action potentials

50
Q

What cell structure is more numerous in cardiac muscle than in skeletal muscle?

A

mitochondria

51
Q

What cell structures of myocardial cells invaginate the cells at the Z lines and carry action potentials into the cell interior?

A

T tubules

52
Q

In which parts of the heart, are T- tubules developed well vs not?

A

ventricles– well developed

atria– poorly developed

53
Q

What is the function of sarcoplasmic reticulum (SR) of cardiac muscle cells?

A

storage and release of Ca for excitation and contraction coupling

54
Q

Steps in excitation-contraction coupling in cardiac muscle:
What occurs during the plateau of the action potential?

A

Ca conductance is increased and Ca enters the cell from extracellular fluid (inward Ca current) through L-type Ca channels (dihydropyridine receptors)

55
Q

Steps in excitation-contraction coupling in cardiac muscle:
Cal entry triggers the release of even more Ca from the SR through what Ca release channels?

A

ryanodine receptors

56
Q

Steps in excitation-contraction coupling in cardiac muscle:

As a result of Ca release, intracellular Ca increases which then binds…

A

troponin C and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding

57
Q

Define inotropism

A

“contractability”

the intrinsic ability of cardiac muscle to develop force at a given muscle length
**related to intracellular Ca concentration

58
Q

Positive inotropic agents produce

A

an increase in contractility

59
Q

Negative inotropic agents produce

A

a decrease in contractility

60
Q

How does sympathetic stimulation (catecholamines) via beta1 receptors increase force of contraction by what two emchanisms?

A
  1. Increases inward Ca current during the plateau of each cardiac action potential
  2. increases the activity of the Ca pump of the SR (by phosphorylation of phospholamban)
61
Q

What is the MOA of cardiac glycosides (digitalis)?

A

increase the force of contraction by inhibiting Na, K ATPase in the myocardial cell membrane

**which ultimately ends in an increase in intracellular Ca

62
Q

How does parasympathetic stimulation (ACh) via muscarinic receptors decrease force of contraction?

A

in the atria
**by decreasing the inward Ca current during the plateau of the cardiac action potential

63
Q

Preload, is end-diastolic volume which is related to

A

right atrial pressure

64
Q

With regards to Pre-load, when venous return increases,

A

end-diastolic volume increases and stretches or lengthens the ventricular muscle fibers (frank starling relationship)

65
Q

Afterload for the left ventricle is

A

aortic pressure

66
Q

With regards to after-load (left ventricle), what causes an increase

A

increases in aortic pressure (systemic hypertension) cause an increase in afterload on the left ventricle

67
Q

Afterload for the right ventricle is

A

pulmonary artery pressureinc

68
Q

with regards to afterload, what causes an increase (right ventricle)

A

increases in pulmonary artery pressure cause an increase in afterload on the right ventricle

69
Q

Define Cardiac isometric volume

A

all valves are closed
ventricular volume is constant

70
Q

S4 heart sound

A

atrial contraction

71
Q

S1 heart sound

A

closure of the AV valves

72
Q

S2 heart sound

A

closure of the semilunar valves

73
Q

S3 heart sound

A

rapid flow of blood from the atria into the ventricles

74
Q

The time required for diastesis (ventricular filling) is dependent on what?

A

heart rate
**rapid heart= decreased end-diastolic volume and decreased stroke volume

75
Q

What baroreceptor responds to decreased in arterial pressure?

A

carotid sinus
**most sensitive to changes in arterial pressure, produces the greatest response

76
Q

besides the carotid sinus, what baroreceptor response to the increases in arterial pressure?

A

baroreceptors in aortic arch

77
Q

Which cranial nerve responds to decreased arterial pressure (decreased stretch of carotid sinus)?

A

CNIX: glossopharyngeal nerve
**carries information to the vasomotor center of the brainstem

78
Q

What is the response of the vasomotor center to decreases in blood pressure?

A

decreases parasympathetic (vagal) outflow to the heart
increased sympathetic outflow to the heart and blood vessels

79
Q

What are the 4 effects that attempt to increase arterial pressure back toward normal?

A
  1. INC heart rate
  2. INC contractility and stroke volume
  3. INC vasoconstriction of arterioles
  4. INC vasoconstriction of veins (venoconstriction)
80
Q

INC heart rate in response to DEC BP is through what mechanism?

A

From decreased parasympathetic tone and increases sympathetic tone to the SA node of the heart

81
Q

INC contractility and stroke volume in response to DEC BP is through what mechanism?

A

resulting from increased sympathetic tone to the heart. Together with the increase in heart rate, the increases in contractility and stroke volume produce an increase in cardiac output that increases arterial pressure

82
Q

INC vasoconstriction of arterioles in response to DEC BP is through what mechanism?

A

resulting from increases sympathetic outflow, as a result TPR and arterial pressure will increase

83
Q

INC vasoconstriction of veins (venoconstriction) in response to DEC BP is through what mechanism?

A

increases sympathetic outflow
Constriction of the veins causes a decrease in unstressed volume and an increase in venous return to the heart. The increase in venous return causes an increase in cardiac output by the Frank Starling mechanism

84
Q

What is the slow hormonal response to decreased blood pressure?

A

renin-angiotensin-aldosterone system
**long term adjustment of blood volume

85
Q

What is the first step in the renin-angiotensin-aldosterone system/ what responds to drop in BP?

A

decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin

86
Q

What is the function of renin?

A

enzyme that catalyzes the conversion of angiotensinogen to angiotensin1 in plasma

87
Q

What is the function of ACE (angiotensin-converting enzyme)?

A

catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs

88
Q

MOA of ACE inhibitors (ie, captopril)

A

block the conversion of angiotensin I to angiotensin II, causing a decrease in BP

89
Q

MOA of angiotensin receptor antagonists (ie, losartan)

A

block the action of angiotensin II at its receptor and decrease blood pressure

90
Q

What are the effects of angiotensin II?

A
  1. simulates the secretion of aldosterone by the adrenal cortex
  2. increases Na-H exchange in the proximal convoluted tubule
  3. increases thirst and therefore water intake
  4. Causes vasoconstriction of the arterioles, increases TPR and arterial pressure
91
Q

What is the MOA of aldosterone?

A

increases NA reabsorption of the renal distal tubule
–> increasing extracellular fluid vol, blood vol and arterial pressure
**this action is slow

92
Q

Cerebral ischemia causes an increase in partial pressure of carbon dioxide (PCO2) in brain tissue, which results in what effects

A

increased sympathetic outflow ot the heart and blood vessels
–intense peripheral vasoconstriction and increased total peripheral resistance
-bsignificant blood flow to other organs reduces to preserve blood flow to brain
**MAP increases to life-threatening levels

93
Q

Where are chemoreceptors located?

A

in carotid (at bifurcation of common carotid arteries) and aortic bodies (along aortic arch)

94
Q

Chemoreceptors of the carotid and aortic bodies are sensitive to changes in what?

A

decreases in partial pressure of oxygen (PO2)

95
Q

How do chemoreceptors of the carotid and aortic bodies respond to decrease in PO2 by doing what?

A

activate vasomotore centers that produce vasoconstriction, an increase in total peripheral resistance and an increase in arterial pressure

96
Q

What hormone is involved in regulation of blood pressure in response to hemorrhage?

A

vasopression (anti-diuretic hormone)

97
Q

where is vasopressin released from?

A

posterior pitutiary

98
Q

What are the effects of vasopressin?

A
  1. potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles
  2. Increases water reabsorption by the renal distal tubule and collecting ducts by activating V2 receptors
99
Q

What hormone is released from the atria in response to an increase in blood volume and atrial pressure?

A

atrial natriuretic peptide

100
Q

What are the effects of atrial natriuretic peptide?

A
  1. relaxation of vascular smooth muscle, dilation of arterioles and decreased total peripheral resistance
  2. increased excretion of Na and water by the kidney (reducing blood volume)
  3. inhibits renin secretion
101
Q

Lipid soluble substances cross membranes of the capillary endothelial cells by what mechanism (ie O2 and CO2)?

A

simple diffusion

102
Q

Small water soluble substances (water, glucose & amino acids) cross through capillary wall?

A

water filled clefts between endothelial cells

103
Q

How do large water soluble substances cross the capillary membrane?

A

pinocytosis

104
Q

What are the effects of histamine on the vasculature?

A

arteriolar dilation and venous constriction
– produces a large increase in capillary hydrostatic pressure and local edema

105
Q

Nitric oxide is produced where?

A

in endothelial cells

106
Q

What are the effects of nitric oxide on the vasculature?

A

relaxation of vascular smooth muscle

107
Q

What is the effect of bradykinin on vasculature?

A

arteriolar dilation and venous constriction
**causes local edema

108
Q

What is the effect of serotonin on the vasculature?

A

arteriolar constriction
–> release in response to blood vessel damage to help prevent blood loss

109
Q

Effect of thromboxane A2 on vasculature?

A

vasoconstrictor

110
Q

List the compensatory mechanisms in response to acute blood loss:

A
  1. carotid sinus baroreceptors (detect dec in arterial pressure)– inc sympathetic outflow to heart and blood vessels and dec paraympathetic outlof: INC HR, INC contractility, INC TPR, venoconstriction

2.Chemoreceptors in cartoid and aortic bodies– sense hypoxia, INC sympathetic outlflow to heart

3.Cerebral ischemia: inc in PCO2– activates chemoreceptors in vasomotor center to ICN sympathetic outflow

4.arterial vasoconstriction

  1. adrenal medulla releases epi and norepi
  2. renin-angiotensin-aldosterone sys activated
  3. release of ADH

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