midterm Flashcards

1
Q

explain the atrial stretch reflex

A
  1. increase blood volume
  2. increase venous return
  3. increase atrial pressure (filling)
  4. stretching baroreceptor of atrial wall
  5. increase signal firing to medullary control center
  6. inhibition of SNS
  7. result in renal vasodilatation, decrease BP (decrease vassopression and increase ANP), increase HR
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2
Q

result of atrial stretch reflex

A

result in renal vasodilatation, decrease BP (decrease vassopression and increase ANP), increase HR

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3
Q

blood velocity increase or decrease with a higher cross-sectional area

A

decrease

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4
Q

which blood vessel as the higher velocity and slowest velocity

A

H: aorta
L: capillaries

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5
Q

blood flow become slower or faster the further away of the heart and why

A

slower to aid in O2 exchange, allow the O2 to have time to go out of the blood and reach cells

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6
Q

in laminar flow, the greatest velocity is found where and why

A

in the center of the vessel because there’s less resistance in the center

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7
Q

in laminar flow, the lowest velocity is found where and why

A

along the vessel wall, because there’s higher resistance along the vessel wall

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8
Q

in turbulent flow, the greater the cross-sectional area, the _ the velocity

A

lower

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9
Q

in turbulent flow, the greater the blood flow, the _ the velocity

A

greater

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10
Q

what is laminar flow

A

linear velocity
less amount of friction, highest velocity is found in the center

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11
Q

if the Reynold number is lower than 2100 which type of flow do we have

A

laminar

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12
Q

what is turbulent flow

A

happen if vessel is block by at theroscleritic plaque

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13
Q

if the Reynold number is higher that 4000 which type of flow do I have

A

continuous turbulent

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14
Q

in anemia you have which type of blood flow and explain

A

Low hemtocrit = blood less viscous = reynaud number increase = increase CO = turbulent flow

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15
Q

in thrombus which type of blood flow do we have and explain

A

Decrease diameter = reynaud number increase = turbulent

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16
Q

if velocity increase, Reynaud number increase or decrease

A

increase

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17
Q

if density increase, Reynold number increase or decrease

A

increase

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18
Q

if viscosity decrease, Reynold number increase or decrease

A

increase

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19
Q

if Reynold number is between 2100 and 4000 which type of flow do we have

A

transient turbulence

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20
Q

what is cardiac contractibility

A

Instrinsic ability of the myocardium to pump in the absence of change in preload and afterload

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21
Q

cardiac contractibility is altered by and which part of
cns has the more important effect

A
  • Can be altered by: neural, humoral or pharmacological influence
  • SNS has MOST importance effect
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22
Q

factor influence vascular resistance

A

viscosity -> proportional to resistance

blood vessel length -> longer vessel have more resistance than shorter vessel

blood vessel radius -> narrower = more resistance

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23
Q

what happen with blood flow if resistance increase

A

decrease

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24
Q

what happen with blood in vasoconstriction

A

decrease vessel radius -> increase resistance = decrease blood flow

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25
Q

what happen with blood flow and resistance in anemia

A

ischemia reduce red blood cell = decrease blood viscosity = decrease resistance = increase blood flow

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26
Q

what happen if a blood clot or blockage develop in artery

A

decrease artery radius = increase resistance = decrease blood flow

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27
Q

role of RBC in blood velocity

A

increase in RBC result in increase viscosity of blood = reduce blood velocity

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28
Q

what happen with blood velocity with polycythemia

A

increase in RBC = increase viscosity = increase resistance = decrease blood velocity = decrease blood flow
-> increase BP

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29
Q

what happen with blood viscosity in anemia

A

decrease RBC = decrease viscosity = increase velocity

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30
Q

factor influencing blood velocity

A

hematocrit
plasma protein
diameter of blood vessel
temperature;

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31
Q

determinant of blood pressure

A

total peripheral resistance
CO
blood viscosity
blood volume

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32
Q

what happen in blood viscosity if plasma protein decrease

A

decrease

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33
Q

result of hypoabulminaena

A

decrease albumin
decrease resistance
increase blood flow
decrease BP (immediate response) but at the end = unchanged
turbulent flow

34
Q

physiological effect of anemia

A

increase CO
increase HR
increase contractility (active)
decrease systemic venous return (passive)
increase venous return (passive)

35
Q

effect on anemia on circulation

A

decrease blood viscosity = decrease in resistance (added tissue hypoxia-vasodilation) = increase in CO = increased pumping workload on the heart

decrease viscosity -> decrease peripheral resistance -> increase blood flow -> increase venous return -> increase CO -> increase HR

36
Q

what happen with plasma volume in dehydration

A

decrease

37
Q

physiological effect of dehydration - hypovolemia

A

decrease plasma volume -> increase hematocrit and decrease mean circulation filling pressure -> increase blood viscosity and decrease venous return -> decrease cardiac output -> decrease VO2 max (decrease O2 delivery to tissue) -> increase SVR

38
Q

abnormal thermoregulation of dehydration

A

decrease skin blood flow, decrease sweat rate, increase core temperature

39
Q

what happen physiologically with chronic lung disease

A

lung impairment -> hypoxia -> low blood O2 -> stimulation of liver and kidney -> erythropoietin release in bloodstream -> stimulation of red bone marrow -> increase red blood cell -> increase O2 carrying capacity

arterial hypoxia -> increase erythropoietin -> increase RBC -> increase blood capacity -> increase blood viscosity -> decompensated erythrocytosis -> poor o2 delivery to muscle-> increase fatigue

40
Q

explain blood dooping procedure

A
  1. athlete donate blood
  2. blood is centrifuge
  3. red blood cell are force to the bottom
  4. liquid part of the blood is draw off the tube and reinfected in athlete
  5. RBC is stored (or frozen)
  6. a day before competition, RBC are re-injected in the athlete -> blood can carry more O2 = more endurance
41
Q

blood dooping advantage and disadvantage

A

increase O2 level in blood
increase energy availability
risk of bacterial infection
sharing needle increase risk of hepatitis and HIV
blood clot, stroke, heart failure

42
Q

what is EPO

A

an hormone produced in kidney that stimulate bone marrow to produce extra RBC -> artificial EPO can’t be differentiate from natural EPO

43
Q

proven effect of blood doping

A

increase max oxygen uptake
increase time to exhaustion
increase performance in endurance event

44
Q

risk of blood doping

A

increase blood viscosity
blood clotting
heart failure
blood matching error
hepatitis
HIV

45
Q

what is the difference between the 2 blood doping technique

A

EPO go to long bone and stimulate RBC production

46
Q

explain the 4 phase of valsava maneuver

A
  1. onset of strain
    - increase intrathoracic pressure
    - increase SBP
    - decrease coronary artery blood flow
  2. continued strain
    - decrease SBP
    - increase HR
  3. release of strain
    - decrease intrathoracic pressure
    - decrease SBP
  4. recovery
    - increase SBP
    - decrease HR
47
Q

physiological response of valsava maneuver

A

expire against closed glottis -> increase intrathoracic P -> decrease venous return -> decrease cardiac output -> increase SNS, decrease PNS = increase HR

48
Q

what happen when valsava is stop

A

Role of PNS in valsava: increase BP -> increase depolarization of carotid and aortic baroreceptor -> increase stimulation to vagus and glossopharyingeal -> increase PNS -> decrease HR

49
Q

role of SNS in valsava

A

Role of SNS in valsava : Decrease BP -> decrease depolarization of carotid aortic receptor -> decrease signal to NTS -> increase SNS -> increase HR

50
Q

why people can pass out from valsava

A

if vagus nerve is too munch stimulate = pass out
to munch alteration in BP can decrease amount of O2 to the brain

51
Q

how munch SBP and DBP increase in cold pressor test

A

sBP - 20mmhg
DBP- 10

52
Q

what happen when the body is in contact with a painful cold stimuli

A

cause massive discharge of the SNS and release epinephrine -> trigger arterial constriction, increase HR and increase cardiac contractility -> increase BP

53
Q

neural pathway of CPT

A

cold pressor test trigger peripheral nociceptor -> stimulate hypothalamus -> stimulate RVLM in medulla oblongata -> stimlate SNS -> increase HR and stroke volume -> increase total peripheral resistance and CO -> increase arterial pressure

54
Q

which nerve is stimulate with diving reflex

A

trigeminal

55
Q

what happen with heart rate and BP during diving reflex

A

slow down drastically (bradycardia), vasoconstriction = increasein BP

56
Q

three factor include in mammalian diving reflex

A

bradycardia, peripheral vasoconstriction, blood shift

57
Q

explain physiology of diving reflex

A
  1. Cold water stimulus on face
  2. Depolarization of opthalmic, maxillary and madibular nerve merge into trigeminal nerve
  3. Trigeminal nerve (afferent pathway) synapse in the pons (brainstem)
  4. Sensory nucleus of trigeminal n send signal to vagus nerve (efferent pathway)
  5. Vagus nerves decrease HR

Initial stimuli = cold to the face region
1.Receptor of the face (3 nerves) merge into trigeminal = inibithed respiratory center
2. Respiratory center inhibit respiratory muscle = apnea
3. Respiratory stimulated CV center in medulla oblongata = stimulated arteriol = vasoconstriction = redirection of blood to brain and heart
4. Medulla oblongata also inhibit para sympathetic system = decrease in HR = bradycardia = help to balance vasoconstriction and reduce energy. Consumption or heart

58
Q

driving reflex in seal

A
  • Increase in CO2 is the first thing happening = increase in lactic acid due to O2 consumption
  • When CO2 reach about 60%, brain receive a stimulus to activate the respiratory center
  • Respiratory center send a message to diaphgram to contract
  • Inhale/exhale = decrease in CO2
  • Vasoconstriction stop = increase in lactic acid
58
Q

what is myocardial ischemia

A

relative reduction in blood flow in coronary artery of the heart
 Increase plaque in coronary artery = increase arterial resistance = decrease blood flow
 O2 demand > O2 supply

59
Q

what is angina and symptom

A

cause from insufficient blood flow to heart due to narrowing of coronary artery
 Symptom: chest pain/pressure dull or sharp, shortness of breath. Sweating, feeling weak,nause

60
Q

when does symptom occurs in angina

A

 Symptom occur following physical exertion, heavy meal, cold weather of emotional stress -> because body need more blood and oxygen than when at rest, so heart need to pump harder to meet the demand = people will have chest pain -> pain go away at rest
 Sometime pain occurs at rest

61
Q

what is referred pain

A
  • Due to synapsing of visceral and somatic sensory neuron at the same interneuron as they enter spinal cord
62
Q

what is angina pectoris

A

: pain resulting from heart damage, often felt as stimulation of nociceptor in the left arm

63
Q

what is pulmonary hypertension

A

Vasoconstriction = thickening of pulmonary arterial walls = increase resistance to blood flow = increase strain of the right ventricule = right ventricule enlargement
- Increase in preload and afterload = increase BP

64
Q

what is mean pulmonary artery pressure

A

14

65
Q

range of pulmonary hypertension at rest and during exercise

A

rest: > 25
exercise: >30

66
Q

explain why there’s exercise limitation in pulmonary hypertension

A

 Right vascular dysfunction= afterload mismatch, right ventricule dilatation = functional tricuspid valve regurgitation
 Skeletal muscle dysfuncion = decrease capillarization = decrease oxidative enzyme activity = muscle fiber hyperthrophy

67
Q

how can exercise limitation during pulmonary hypertension can be improve

A

improve by drug therapy that reduce right ventricular afterload and by exercise training by increasing capillary density and oxidative enzyme activity

68
Q

what is PAD or PVD

A

occlusive disease of artery of the lower extremity

69
Q

most common cause of PAD/PVD

A

atherothrombosis
arthertis
aneurysm, embolism

70
Q

pathophysiology of PVD

A

arterial narrowing -> decrease blood flow = pain

pain result from an imbalance between supply and demand of blood flow that fails satisfy ongoing mechanism requirement

71
Q

if aorta or iliac artery is obstructed ischemia result in

A

buttock, hip, thigh

72
Q

femoral artery result in ischemia where

A

thigh, calf

73
Q

popliteal artery occlusion result in ischemia where

A

calf, ankle foot

74
Q

how do we calculated ankle brachial index (ABI)

A

aBI= lower extremity systolic pressure / highest brachial artery systolic pressure

75
Q

what are the range of PAD severity

A

normal: 0.95-1.3
mild: 0,75-0.94
moderate: 0,5-0,74
severe: <0,5

76
Q

what is the most severe peripheral arterial disease

A

vascular blockade

77
Q

why is intermittent claudication important

A

atherosclerosis -> restriction in blood flow -> pain in calf

atherosclerosis -> coronary disease or stroke -> heart attack -> reduced life expectancy

78
Q

nitroglycerin action

A
  • decrease pain of ischemia
  • increase venous dilation
  • decrease venous blood return to heart
  • decrease preload and cardiac oxygen consumption
  • dilates coronary arteries
  • increase cardiac collateral flow

-> severe headache can occurs due to lack of blood flow to the brain area

79
Q

what are the effect of calcium channel blocker

A

vascular smooth muscle relaxation -> vasodilatation

decrease inonotropic effect (contractility) -> decrease CO

decrease chronotropic effect -> decrease HR

decrease dromotopric effect

-> decrease in BP

80
Q

effect of beta blocker on the heart

A

decrease heart rate
decrease afterload
decrease wall stress
decrease heart contractility
result in reduction of myocardial oxygen demand

81
Q

impact of diuretic

A

increase NACO3 -> increase H20 secretion -> increase NA excretion -> increase NACl excretion -> increase urine production