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Cardiovascular and Pulmonary > Cardiovascular Systems Physiology and Pathophysiology VI > Flashcards

Cardiovascular Systems Physiology and Pathophysiology VI Flashcards

1
Q

Defined as the presence of a severe and constricting pain

A

Angina

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2
Q

Severe and constricting pain that occurs within the chest and is due to ischemia

A

Angina pectoralis

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3
Q

The discomfort associated with angina pectoralis is usually

A

Retrosternal (can radiate to shoulders, neck, backand/or jaw)

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4
Q

The pathogenesis of the signs and symptoms of angina pectoris is explained by ischemia within one or more regions of the

A

Ventricular myocardium

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5
Q

A specific form of angina, and results from a fixed narrowing of one or more coronary vessels; generally due to atheromatous plaque formation

A

Chronic stable angina

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6
Q

With chronic stable angina, as cardiac demand is upregulated (such as after exercise or a big meal) O2 supply an not meet demand, which sets a cascade of events in place leading to

A

Impaired LV function

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7
Q

Characterized by an increase in LV diastolic pressure and LV wall tension, which collectively overburden the already O2 starved myocytes

A

Chronic stable angina

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8
Q

Signs and symptoms of stable angina result from impeded O2 delivery, and include

A

Diffuse retrosternal tightness and pressure

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9
Q

Physical exam during an episode of chronic stable angina would likely reveal

A

Elevated BP and an S4 gallop (due to decreased LV compliance)

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10
Q

Would show horizontal or downsloping ST depression and T wave inversions or flattening over ischemic regions

A

ECG of stable angina

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11
Q

What can be used to treat and manage angina?

A

Vasodilators and negative inotropic agents

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12
Q

What are some common vasodilators that could be used to treat angina?

A
  1. ) Nitroglycerine

2. ) Ca2+ channel blockers such as: amlodipine, diltaizem, and verapamil

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13
Q

What are some negative inotropic agents that could be used to treat angina?

A

Beta bockers and Ca2+ channel antagonists

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14
Q

Each decrease Ca2+ current in the SA and AV nodes

A

Beta blockers and Ca2+ channel antagonists

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15
Q

Drug to treat angina that impairs the late Na+ current that is present in cardiomyocytes which helps to restore NCX activity

A

Ranolazine

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16
Q

In angina, there is a prolonged phase of terminal Na+ current. This impedes NCX function and results in increased intracellular Ca2+ which promotes a state of increased

A

LV wall tension(thus increasing O2 demand)

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17
Q

The only blood vessels that do not contian any form of vascular smooth mucle

A

Capillaries

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18
Q

Innervate predominantly the microcirculatory beds within the GI, genito-urinary, respiratory, salivatory, ocular, and cerebral tissues

A

PSNS efferents

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19
Q

PSNS-induced changes in vascular resistance in

the aforementioned do not translate into significant alterations in

A

Systemic BP

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20
Q

PSNS activity is not traditionally associated with antagonizing SNS vasoconstriction to lower BP Instead, PSNS activity enables more localized changes in blood flow in order to aid in

A

Tissue metabolism

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21
Q

SNS fibers innervate

A

Arteries, arterioles, venules, and veins

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22
Q

By and large, SNS fibers induce vasoconstriction via

A

Norepinephrine and a1 receptors

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23
Q

SNS is typically responsible for the interplay between vasoconstriction and dilation. However, in some tissue beds, vasodilation can be induced by

-ex skeletal muscle

A

B2 adrenergic receptors

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24
Q

What does SNS-dependent vasoconstriction result in in

  1. ) Arterioles
  2. ) Venules
A
  1. ) Increased TPR

2. ) Does not effect TPR but enhances venous return

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25
Q

Increased venous return increases

A

Cardiac output

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26
Q

A large bed which receives about 25% of CO and can accommodate upwards of 20% of total blood volume

A

Splanchnic circulation (that within the gut)

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27
Q

Highly endowed with a1 adrenoreceptors when compared to other venous beds

  • extremely sensitive to any increase in SNS tone
  • contains high compliance veins
A

Splanchnic circulation

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28
Q

Venoconstriction of the splanchnic venous tissues results in mobilization of venous blood volume from this bed for

A

Venous return to the RA

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29
Q

Collectively increases arterial BP by increasing TPR and upregulating venous return and cardiac output

A

SNS

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30
Q

Graded by the amount and type of neurotransmitter that is released in response to the efferent signal

A

SNS stimulation

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31
Q

In response to initial efferent tone, post-ganglionic SNS fibers release norepi, and norepi which activates

-provides an early phase for a low degree of vasoconstriction

A

Type a1 adrenergic receptors

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32
Q

As the efferent signal increases to moderate intensities, the noradrenergic system is complemented by the
release of

A

ATP

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33
Q

Acts as a neurotransmitter since is stimulates post-junctional purinoreceptors

A

ATP

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34
Q

Together, cause a greater stimulation of smooth muscle contraction than would occur in the presence of norepi alone

A

Norepinephrine and ATP

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35
Q

What happens in the event of intense efferent SNS tone?

A

Norepinephrine secretion is elevated
-ATP secretion ceases
NP-y secretion is stimulated

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36
Q

Binds and activates so-called Y receptors on the pot-junctional smooth muscle membrane and functions as a synergist to norepinephrine

A

NP-Y

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37
Q

A potent vasoconstrictor that is synthesized from the renal hormone, renin, via a multi-step process

A

Angiotensin-II (An-II)

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38
Q

Acts through a receptor mediated process to stimulate vasoconstriction

-also can bind SNS post-ganglionic pre-junctional receptors to stimulate Norepinephrine secretion

A

An-II

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39
Q

Receptors that are coupled to the release of norepinephrine and are activated in the face of chronically elevated epinephrine

A

Pre-junctional B2 receptors

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40
Q

Therefore, in the case of extreme SNS activity, both epi and norepi can directly and indirectly stimulate vasoconstriction to markedly increase

A

TPR

41
Q

The spontaneous rhythmic contraction of small resistance vessels within the microcirculation

A

Vasomotion

42
Q

The vascular endothelium is a very metabolically active tissue, and the continuous release of nitric oxide by the vascular endothelium sets the

A

Basal vascular smooth muscle tone

43
Q

What are the 4 major vasoactive factors?

A

Thrombin, ACh, seratonin, and shear stress

44
Q

Allows the intermittent flow of blood through the capillary network

A

Vasomotion

45
Q

Generally sets the rate of vasomotion within a given capillary bed

A

O2 usage by the tissues

46
Q

For example what effect would the sustained contraction of skeletal muscle i.e. the relatively O2-depleted environment of the skeletal muscle cause?

A

Increase in vasomotion

47
Q

Microcirculation consists of what 5 components?

A
  1. ) Arterioles
  2. ) Metarterioles
  3. ) Pre-capillaries
  4. ) Capillaries
  5. ) Venules
48
Q

Blood PO2 is elevated (98 mmHg) as the RBCs enter the microcirculation through the

A

Arterioles

49
Q

As red blood cells move from capillaries to venules to enter the venous circulation, PO2 is relatively

A

Low (40 mmHg)

50
Q

The important functions of the microcirculation are

A

Exchange of blood gases and delivery of nutrients

51
Q

Surrounded by a sheet of smooth muscle, and therefore can be constricted/dilated in response to the SNS and other stimuli

A

Arterioles

52
Q

Also contain smooth muscle; however, the smooth muscle is more localized as rings of smooth muscle fibers

A

Metarterioles

53
Q

Forms the junction between metarterioles and capillaries

-serves as a modulator to flow within the microcirculation bed

A

Pre-capillary sphincter

54
Q

The link between the capillary bed and veins

-contain relatively little smooth muscle when compaired to arterioles

A

Venules

55
Q

The plasma pressure in venules is very

A

Low

56
Q

Movement of fluids and (small) molecules between capillaries and surrounding tissues occurs via
small openings that are present between adjacent endothelial cells called

A

Slit pores

57
Q

In the brain, the slit pores are very small and therefore only allow the passage of

A

H2O and very small molecules

58
Q

This cytoarchitecture within the brain microvasculature is referred to as the

A

Blood-brain barrier

59
Q

The slit pores within certain microvessels in the liver are

A

Large

60
Q

The primary mechanism of exchange that occurs between capillaries and the interstitial space

A

Diffusion

61
Q

Diffusion of aqueous material occurs through

A

Slit-pores and aquaporins

62
Q

Lipid soluble molecules don’t travel through pores but rather traverse the plasma membrane. Some examples are

A

CO2, O2, phospholipids, and steroid hormones

63
Q

For the purposes of understanding microcirculation fluid dynamics, fluid movement consists of which two processes?

A
  1. ) Filtration

2. ) Reabsorption

64
Q

Are in constant opposition in the capillary bed

A

Filtration and resorption

65
Q

Physical forces within the lumen and interstitium that determine in which direction the fluid will move

A

Starling forces

66
Q

What are the 4 primary fluid forces encountered in microcirculation?

A
  1. ) Hydraulic pressure (Capillary pressure, Pcap)
  2. ) Interstitial fluid pressure (Pif)
  3. ) Colloid osmotic pressure (oncotic pressure)
  4. ) Interstitial colloid osmotic pressure
67
Q

Caused by the concentration of charged serum proteins

A

Colloid osmotic pressure

68
Q

High colloid osmotic pressure tends to draw fluid

A

In

69
Q

In the absence of other forces, high colloid osmotic pressure would result in

A

Increased diffusion (resorption) of H2O into capillaries

70
Q

At the entrance to the capillary network, forces cause a net outward movement of fluid. This outward movement is known as

A

Filtration

71
Q

Within the capillaries at the entrance of the capillary network, what are the characteristics of

  1. ) Hydraulic pressure (Capillary pressure, Pcap)
  2. ) Interstitial fluid pressure (Pif)
  3. ) Colloid osmotic pressure (oncotic pressure)
  4. ) Interstitial colloid osmotic pressure
A
  1. ) Relatively high
  2. ) Negative
  3. ) Robust
  4. ) Modest
72
Q

Hence, filtration occurs primarily at the

A

Arterial feed of a capillary bed

73
Q

What are the pressure characteristics at the venous end of the capillary bed?

A

Colloid osmotic pressure higher than the other three combind

74
Q

Therefore, what occurs primarily at the venous end of a capillary bed?

A

Absorption (resorption)

75
Q

When considering the mean net force (filtration versus reabsorption) of the capillary network, the general trend is

A

Filtration is favored over resorption

76
Q

The concept of net filtration over resorption is referred to as the

A

Starling Equilibrium

77
Q

The buildup of interstitial fluid

A

Edema

78
Q

The removal of the net fluid accumulation from the interstitium is accomplished by the

A

Lymphatic system

79
Q

Reabsorption of excess fluid and some other molecules occurs via the

A

Lymphatic system

80
Q

Ultimately, fluids are returned to the blood plasma via a network of lymphatic ducts that empty into the

A

Subclavian veins

81
Q

Besides the need for increased O2, other factors that can influence the rate of flow within the microcirculation are

A

Nutrients, metabolic by-products such as adenosine, CO2, and H+

82
Q

When considering the acute response, the primary determining factor for enhancing vasomotion is

A

Decreased O2 relative to demands

83
Q

What happens by default when O2 tissue concentrations fall?

A

CO2 level is raised by default

84
Q

The phenomenon of the intracellular mechanisms that signal the production and/or release of vasodilators by tissues in response to increased CO2 levels

A

Autoregulation

85
Q

Examples of important vasodilators that we need to know are

A

Adenosine, CO2, H+, K+, Lactic acid, and histamine

86
Q

Can result when PO2 in the cerebral microcirculation drops

A

Coma

87
Q

Regulations of cerebral microcirculation is dependent upon

A

Blood PCO2

88
Q

Alterations in PCO2 stimulate coordinated responses in

A

Cerebral vasomotion

89
Q

In actuality, changes in PCO2 initiate a cascade of events that result in alterations in

-Causes vasomotor events in the brain

A

H+

90
Q

Cardiac output has to equal

A

Venous return

91
Q

The venous function curve illustrates vascular (venous) behavior based upon the relationship between

A
  1. ) RAP (venous pressure, X-axis)

2. ) Cardiac output (Y-axis)

92
Q

Venous and cardiac function curves show that as cardiac output increases, venous pressure (RAP)

A

Decreases

93
Q

Venous and cardiac function curves also show that increases in venous pressure (RAP) have what effect?

A

Upregulate cardiac output

94
Q

Venous vasomotor tone and intravenous volume affect

A

Cardiac Output

95
Q

Enhances cardiac output by lowering resistance to flow within the venous system

A

Vasodilation

96
Q

Impedes cardiac output by increasing resistance to flow within the venous system

A

Vasoconstriction

97
Q

Increases cardiac output because there is more plasma available for venous return and thus cardiac output

A

Increased venous volume

98
Q

It is critical to keep in mind that viewing an isolated

venous function plot, without the cardiac function curve is

A

Pointless

99
Q

In other words, the whole purpose of the venous and cardiac function curves is to show the interdependent relationship between

A

Venous and cardiac function

Cardiovascular and Pulmonary (25 decks)

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