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Physio > Chest Pain II > Flashcards

Chest Pain II Flashcards

1
Q

Rate-pressure product (RPP)

A

RPP = HR x SystolicBP

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2
Q

Coronary circulation regulated by?

A

mostly local control - tissue metabolites such as adenosine and NO cause vasodilation
some autoregulation/myogenic control

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3
Q

Blood flow through coronary arteries occurs when?

A

During diastole, because vessels are compressed during systole

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4
Q

Blood flow through coronary arteries moves in what direction?

A

Epi to myo to endocardium

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5
Q

Heart extracts what % of oxygen?

A

75-80% vs 25% in the tissues

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6
Q

Treatment options for angina

A

1) increase blood flow/oxygen supply (but not really able to do this practice because local regulators have already vasodilated to max)
2) decrease oxygen demand through decreasing HR, inotropy, or afterload

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7
Q

How is splanchnic circulation oriented?

A

in both series (hepatic portal system) and parallel

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8
Q

Splanchnic circulation receives high or low percentage of CO at rest?

A

high 25%

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9
Q

Splanchnic circulation regulated by?

A

Local and CNS mechanisms, when body is under stress and SNS is activated this will decrease blood flow to splanchnic circulation

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10
Q

Counter-current exchange in intestinal villi

A

Venules steal oxygen from ascending arterioles and under normal conditions there is enough oxygen left to nourish the villi, but during low blood flow, can cause anoxic damage to villi

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11
Q

Body’s major thermoregulatory organ?

A

Skin

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12
Q

How does cutaneous circulation play role in thermoregulation?

A

1) temperature gradient between skin and environment
2) capillaries increase SA for heat exchange
3) slow velocity of blood flow allows for max time for heat exchange

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13
Q

Apical skin

A

hands, feet, ears, nose, some face
AV anastomoses for heat exchange, caps for nutrient delivery
stimulation of sympathetic adrenergic fibers control BF via vasoconstriction, no heat exchange at AV anastomoses

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14
Q

Hypothalamic control of apical skin

A

increased body temp, Hypothalamic decreases sympathetic outflow leads to passive vasodilation and heat exchange

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15
Q

Nonapical skin

A

NO AV anastomoses, sympathetic neurons release Norepi leading to vasoconstriction, no heat exchange, other sympathetic neurons release ACh at sweat glands causing active vasodilation via bradykinin

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16
Q

Bradykinin

A

released from sweat glands causes active vasodilation of cutaneous capillaries and heat exchange

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17
Q

Cutaneous vasodilation vs vasoconstriction

A

Vasodilation - heat exchange

Vasoconstriction - heat retention

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18
Q

Skeletal muscle circulation regulated by?

A

CNS - sympathetic NS vasconstrict

Local mediators - vasodilate

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19
Q

Reactive hyperemia

A

No flow to skeletal mm leads to buildup of vasodilating metabolites, when flow is resumed, flow is increased due to dilation to wash out metabolites

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20
Q

Cerebral sympathetic stimulation to shut down blood supplies to other organ systems can be overridden by?

A

Skeletal mm and coronaries

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21
Q

BBB contains what kind of junctions?

A

tight junctions, lipid sol molecules can pass (oxygen, carbon dioxide, alcohol) most other mols. are excluded, glucose/GLUT1 transporter are exceptions

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22
Q

Autoregulation range for cerebral blood flow

A

60-130mmHg, range can be shifted by HTN to protect brain from high pressures

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23
Q

Cerebral BF is dept on partial pressure of?

A

Carbon dioxide and lesser extent oxygen

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24
Q

Eq for cerebral perfusion pressure

A

CPP = MAP - ICP

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25
Q

Renal circulation regulated by?

A

Autoregulation (afferent arterioles) and sympathetic control

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26
Q

Blood flow in kidney

A

Afferent arterioles > Glomerular capillaries > Bowman’s capsule > Efferent arterioles > Peritubular capillaries

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27
Q

Effect of decreasing resistance at afferent arterioles?

A

Increases pressure in both capillary beds (glomerular and peritubular), increase flow

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28
Q

Effect of increasing resistance at afferent arterioles?

A

Decreases pressure in both capillary beds (glomerular and peritubular), decrease flow

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29
Q

Effect of decreasing resistance at efferent arterioles?

A

Decreases pressure at GC, increases pressure at PC, increase flow

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30
Q

Effect of increasing resistance at efferent arterioles?

A

Increases pressure at GC, decreases pressure at PC, decrease flow

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31
Q

Parasympathetic and sympathetic pre/postganglions

A

Para: long pre, short post (ACh)
Symp: short pre, long post (NE)

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32
Q

Nicotinic vs muscarinic receptors

A

Both use ACh, nicotinic is pregang, muscarinic is postgang

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33
Q

Termination of parasymp AP

A

Acetylcholinesterase

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34
Q

Muscarinic receptor locations

A

M1 - CNS
M2 - cardiac
M3 - smooth MM, secretory glands, endothelium
M4+M5 - CNS

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35
Q

NE is effector junction neurotransmitter for?

A

Sympathetic actions on both alpha and beta adrenergic receptors EXCEPTION: ACh for sweat glands

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36
Q

Termination of symp AP

A

Reuptake of neurotransmitter and degradative enzymes (MAO)

37
Q

Alpha 1

A

NE/E, radial muscles of eye, sympathetic synapse in blood vessels, increases Ca++

38
Q

Alpha 2

A

NE/E, presynaptic, decreases cAMP and inhibits NE release

39
Q

Beta 1

A

NE/E, heart, increases cAMP, HR, FOC

40
Q

Beta 2

A

E, bronchi, blood vessel wall, liver, skeletal mm, ciliary, increase cAMP causing relaxation

41
Q

Choline acetyltransferase

A

makes ACh from choline and acetate, ACh is stored in vesicles and released upon Ca influx

42
Q

Dopamine-beta-hydroxylase

A

converts Dopamine to NE (NE can then be converted to E in adrenal medulla)

43
Q

Para/Symp actions on Bronchioles

A

b2 symp - increase radius

M3 para - decrease radius

44
Q

Para/Symp actions on Heart

A

b1 symp - increase HR, inotropy, dromotropy

M2 para - decrease HR, inotropy, dromotropy

45
Q

Para/Symp actions on blood vessels

A

a1 symp - decrease vessel radius, increase TPR
b2 symp - increase vessel radius in skeletal mm
No para actions

46
Q

Para/Symp actions on liver

A

b2 symp - increase glycogenolysis/glucoNEO

No para actions

47
Q

Short-term mechanisms for pressure change

A

Baroreceptors, monitor hr-hr, min-min changes, changes occur on the time course of second-minutes

48
Q

High pressure baroreceptors

A

Arterial baroreceptors at carotid sinus (brain BF, more sensitive, signals through 9th cranial nerve) and aortic baroreceptors (body BF, signals through 10th cranial nerve)

49
Q

Low pressure baroreceptors

A

In cardiac atria and pulmonary artery provide info on venous return, CVP, BV, A receptors (report HR), B receptors (report atrial volume)

50
Q

Chemoreceptors

A

at carotid fork and arch of aorta, sense CO2 and O2 levels, regulate breathing

51
Q

Firing of baroreceptors is proportional to?

A

Pressure

52
Q

Cardiovascular center

A

Nucleus tractus solitarius (NTS) integrates signals, contains vasomotor center and cardioinhibitory center

53
Q

Vasomotor center

A

activates SNS leads to vasoconstriction and positive chronotropic/inotropic response, receives INHIBITORY signal from NTS

54
Q

Cardioinhibitory center

A

activates PNS leads to vasodilation and negative chronotropic/inotropic response, receives STIMULATORY signal from NTS

55
Q

Factors that reset baroreceptor ranges

A

hypertension increases receptor range so that the reflex is sensitive over a wider range

56
Q

Humoral control

A

modulates BP over longer time period, includes vasoactive substances and nonvasoactive substances

57
Q

Vasoactive substance

A

released into the blood, affect vascular smooth muscle, modulates pressure and distribution of BF

58
Q

Nonvasoactive substances

A

targets organs outside CV system, modulates effective circulatory volume

59
Q

Epinephrine

A

binds a1 on smooth MM - vasoconstriction, binds b2 on cardiac MM, liver, skeletal muscle - vasodilation

60
Q

Serotonin

A

5-HT, vasoconstriction, local mediator

61
Q

Histamine

A

from mast cells, vasodilations

62
Q

Angiotensin II

A

vasoconstriction, regulated by RAS

63
Q

Atrial natriuretic peptide

A

ANP, vasodilator, release by atrial myocyte in response to stretch sensed by cardiopulmomary receptors, low pressure baroreceptors

64
Q

Vasopressin

A

AVP/ADH, vasoconstrictor at high concentrations

65
Q

Endothelins

A

ET, vasoconstrictor

66
Q

RAS

A

1) low P or SNS stimulation triggers release of renin
2) renin hydrolyzes angiotensinogen (made in liver) to angiotensin I - weak vasoconstrictor
3) I converted to II - potent vasoconstrictor
4) II converted to III - weak

67
Q

Ang II functions

A

vasoconstriction, stimulate thirst, ADH release, and aldosterone synthesis and release
NET EFFECT: increase arterial pressure by increase TPR and BV

68
Q

Vasopressin/ADH functions

A

stimulates renal collecting ducts to insert more AQP2

69
Q

ANP functions

A

relaxes smooth MM, arterioles of kidneys to increase filtration and reduce renin release, inhibits aldosterone secretion, Na+ reabsorption, secretion of ADH
NET EFFECT: decrease effective BV

70
Q

Aldosterone function

A

released in response to increase AngII, acts on distal tubules of kidney to retain water by absorbing Na++ back into blood

71
Q

NO function

A

sheer stress, bradykinin and ACh stimulate NO synthesis, which activates cGMP formation, PKG activation, and inhibits MLCK and activates SERCA pump which lead to vasodilation

72
Q

Clinical relevance of NO

A

1) septic shock - toxins increase NO, causing systemic drop in TPR and BP
2) nitrates used to treat angina dilates resistance vessels and decreases TPR and afterload, as venodilator it decreases preload, SV and O2 demand

73
Q

Does venoconstriction increase pressure?

A

Not substantially, usually only allows for faster blood flow

74
Q

Orthostatic reflex

A

AoP - systolic decreases, diastolic increase
CVP decreases
CO decreases
HR increases
**all return to normal when walking, except HR which increases

75
Q

Positive inotropic agents:

A

SNS, drugs

76
Q

Negative inotropic agents:

A

CHF, MI, drugs

77
Q

Cardiac function curve

A

function of heart as pump, starling curve, changes with inotropy, show CO for changes in venous pressure, direct relationship

78
Q

Vascular function curve

A

how venous system responds to CO, inverse relationship, increases/decreases in BV (hyper/hypovolumia) moves curve upwards/downwards, changing arteriolar tone (TPR) has not effect on MCP but changes slope of curve

79
Q

Respiration effect on CVP

A

Inhalation increase PL and SV in right heart and decreases them in the left
Exhalation increases PL and SV in left heart and decreases them in the right

80
Q

Vasodilation leads to?

A

Increases cap permeability, cap hydro pressure, cap filtration rate, interstitial hydro pressure, and lymph flow

81
Q

Atherosclerosis leads to?

A

decrease arterial compliance, leading to increased systolic pressure and pulse pressure

82
Q

PP is dependent on?

A

directly proportional to SV and inversely proportional to arterial compliance

83
Q

Pulmonary cap. pressure?

A

8mmHg

84
Q

Systemic capillaries pressure?

A

25mmHg

85
Q

Pulmonary art. sys+dias

A

25/10

86
Q

Aorta sys+dias

A

130/80

87
Q

Right ventricle sys+dias

A

25/5

88
Q

Left ventricle sys+dias

A

130/10

89
Q

Aortic Stenosis vs aortic regurgitation in terms of PP, SBP, SV?

A

Aortic stenosis decreases all

Aortic regurgitation increases all

Physio (3 decks)

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