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Ex. Phys I > Exam 4 > Flashcards

Exam 4 Flashcards

0
Q

Aorta and Arteries: 1. most significant structural characteristic 2. four functions

A

Structure = high amount of elasticity
Four functions: maintain relatively constant BP and flow, arteries as rigid tubes, stretch during systole and recoil during diastole, elasticity decreases with age so pressure goes up

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1
Q

4 Components of Cardiovascular System

A
  1. heart - pump that produces pressure to drive blood through the other 3 components
  2. arteries - high pressure distributed circuit
  3. capillaries - exchange vessels
  4. veins - low pressure collection and return circuit
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2
Q

Arterioles: 1. most significant structural component and 2. three functions

A

Structure = high amount of smooth muscle
Function: produce resistance in circulatory system, control distribution of blood flow to various parts of the body, TPR determines MAP

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3
Q

Physics of Blood Flow = what?

How is resistance in CV system changed?

A

Blood flow = change in pressure / resistance to flow
pressure gradient = arterial blood pressure
Resistance is changed via arterioles through vasoconstriction or vasodilation stimulated by SNS

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4
Q

Physics of Blood Pressure: arteries –> veins

A

Highest BP and fluctuation in BP = large arteries

Lowest BP and no fluctuation in BP = large veins

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5
Q

Capillaries: 1. most significant structural characteristic and 2. function

A

Structure = single layer of simple squamous cells & lot of capillaries for huge CSA
Function: gas exchange and diffusion between blood and tissues

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6
Q

Blood Flow Velocity vs. Total CSA

A

high CSA of capillaries = decreased velocity of blood flow to allow long transit time for gas exchange

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7
Q

Veins & Vena Cava: 1. significant structural component and 2. function

A

Structure = one way valves and thin compressible walls

Function: carry blood back to heart via skeletal and respiratory pump

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8
Q

Distribution of Blood Throughout Vessels

A
  • veins hold majority of blood in circulatory system (capacitance vessels)
  • constricting veins may increase blood flow through other parts of circulation
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9
Q

Electrical Function of Heart (Intrinsic Control):

  • autorhythmicity
  • pacemaker cells
  • firing rates SA, AV, Purkinje fibers
A

Autorhythmicity = ability to spontaneously generate action potentials to stimulate contraction
Pacemaker cells = spontaneously depolarize to threshold and generate APs, located in all electrical conduction parts of heart
SA node = 100 bpm
AV node = 40-60 bpm
Purkinje fibers = 15+ bpm

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10
Q

Conduction Pathway

A

SA node –> AV node –> Bundle of His –> L & R Bundle Branches –> Purkinje fibers

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11
Q

Function of AV node and Purkinje fibers

A

AV node = conduct AP slowly to delay AP from getting to ventricles too quickly in order for ventricles to fill completely
Purkinje fibers = conduct AP quickly to spread it through ventricles almost simultaneously

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12
Q

Action Potential of Cardiac Muscle Cells

A
  1. Voltage gated Na+ channels open
  2. Na+ diffusing in produces rapid depolarization
  3. Na+ channels close
  4. Ca2+ channels open and Ca2+ diffuses in, creating plateau in membrane potential to maintain absolute refractory period
  5. Ca2+ channels close and K+ channels open, K+ diffuses out and returns membrane potential to RMP
    * *due to Ca2+ influx, extracellular Ca2+ produces at least 50% of contraction in cardiac muscle
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13
Q

Draw a normal ECG and identify and describe its major components

A

P wave - atrial depol
QRS wave - ventricular depol & atrial repol
T wave - ventricular repol

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14
Q

Usefulness of ECGs

A
  • ECG indicates timing of beginning and end of APs in heart and when there are electrical abnormalities
  • ECG does not indicate quality of contraction of heart
  • identifies electrical abnormalities
  • indicates when heart is short of blood supply
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15
Q

CO flowchart

A

notes

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16
Q 
Cardiac Output
Stroke Volume
EDV
ESV
Ejection Fraction
A 
Q = HR x SV = volume of blood pumped out of one side of heart in 1 minute
SV = EDV - ESV = volume of blood pumped out of ventricles in one beat
EDV = volume of blood in ventricle after diastole & before systole
ESV = volume of blood remaining in ventricle after contraction
EF = SV/EDV x 100 = % (normal is 55%)
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17
Q

Extrinsic Control of Cardiac Function

A

PSNS in vagus nerve –> acetylcholine –> decrease HR via SA and AV noes

SNS –> norepinephrine –> increase HR & increase contractility of ventricles

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18
Q

Regulation of SV: Frank-Starling Law of the Heart

A

increase EDV stretches ventricles/cardiac muscle to optimal length which increases force of contraction and increases SV

increase skeletal/respiratory pump –> increase venous return –> increase EDV –> increase SV

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19
Q

SNS impact on Contractility

A

Contractility = force of contraction at a given EDV; increase in contractility –> increase in SV at same EDV (both increase w/ PA)

SNS opens additional Ca2+ channels in sarcolema –> additional Ca2+ pumps in SR allow heart to relax faster and increase Ca2+ stores –> increase speed of myosin ATPase –> increase speed of contraction to shorten systole and allow more time for diastole

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20
Q

Coronary Blood Flow and O2 Delivery: How does a-vO2diff in the heart at rest compare to skeletal muscles at rest? How is O2 delivery to heart increased during exercise?

A

Heart a-vO2diff at rest = 80%
Skeletal Mm. a-vO2diff at rest = 25%
O2 delivery to heart increased during exercise by increased coronary blood flow that follows increase in O2 use by heart.

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21
Q

What do blockages in coronary arteries do to the ability of coronary blood flow to increase during exercise? What is the consequence of coronary blood flow not meeting the metabolic needs of cardiac muscle?

A
  • limit increase in coronary blood flow

- leads to ischemia –> death of cardiac muscle –> ventricular fib

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22
Q

Goal for Patient with CAD for exercise

A

Exercise safely: determine ischemic threshold which is the exercise intensity at which an individual experiences myocardial ischemia, stay below this point

  • determine Rate Pressure Product = Systolic BP * HR
  • regulate to keep HR 10 bpm below HR achieved during ischemic threshold, but this isn’t the best indicator
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23
Q

Myocardial Metabolism- cardiac muscle as aerobic powerhouse

A
  • highest concentration of mitochondria of all tissues
  • relies almost exclusively on aerobic respiration
  • has almost no glycogen stores
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24
Q

Myocardial Metabolism- FFA, glucose, and circulating lactate provide myocardial energy

A
  • at rest, myocardial energy comes mainly from FFA
  • after meal, insulin allows heart to use glucose as energy substrate
  • increased exercise intensity increases the heart’s oxidation of lactate for energy
25
Q

Generalized Pattern of Myocardial Substrate Use

A

Rest - mostly fat
Mod Exercise - balance glucose, fat, lactate
Intense Exercise - mostly lactate

26
Q

Physics of Blood Pressure: MAP = ?, determinants of SBP vs. DBP

A 
MAP = Q * TPR
SBP = elasticity decreases systolic pressure, stroke volume, ejection velocity
DBP = elasticity increases diastolic pressure, TPR (how easy it is for blood to flow out of arteries)
27
Q

BP Response to Aerobic Exercise

A

increase in SBP = increased SV and increased ejection velocity (SNS)
little change in DBP = no change in TPR due to vasodilation of active muscles and vasoconstriction of nonactive tissue to balance

28
Q

Upper Body vs. Lower Body Aerobic Exercise and BP Response

A
  • less VO2 for upper body
  • decreased venous return due to decreased skeletal muscle pump = decreased EDV = decreased SV = increased HR
  • decreased vasodilation due to less muscle mass = increased TPR
  • upper body has higher HR, higher RPP, higher TPR, lower SV
29
Q

Blood Pressure Responses to Resistance Training

A
  • SBP increases MORE during resistance training vs. aerobic

- possibility of higher increased in BP w/ RT than aerobic

30
Q

Post Exercise Hypotension & Influence by…(4)

A
  • SBP decreases more than baseline after exercise
    Influenced by:
  • population: early stage & stage 1 hypertensives benefit most, women
  • ex mode: aerobic better than resistance
  • ex intensity: > or = 40% VO2max
  • ex duration: as little as 10 min and multiple bouts
31
Q

What does having hypertension matter?

What don’t indiv control their hypertension?

A

Matters b/c = increased risk of atherosclerosis, aneurysms, stroke, MI, heart failure, kidney failure, blindness
Don’t control b/c = no immediate signs or symptoms, lifestyle change is hard, drugs have side effects

32
Q

Cardiovascular Regulation and Exercise - Central Command

A
  • Input from cerebrum influences activity of medullary cardiovascular control center –> emotions, motor messages to skel muscle (increased muscles mass = greater increase in HR & BP)
  • CC provides greatest control over HR during exercise = most influential over PSNS input to heart
  • CC sets baroreceptors reflex to a higher set point during exercise
  • CV responses driven by SNS influenced by sensory messages from chemo and mechanoreceptors in active skel muscles
33
Q

Peripheral Input from Muscles

A
  • Afferent input from receptors in muscles acts to increase SNS = increased activity of mechanoreceptors and chemoreceptors in muscles
  • amount of muscle mass directly influences impact of these inputs on SNS; with training the SNS increases less with exercise
34
Q

Causes of Vasoconstriction of Arterioles to non-active tissues

A

SNS

increased circulating catecholamines

35
Q

Causes of Vasodilation of Arterioles to active skeletal muscles

A

decreased tissue O2

increased local temp, CO2, H+, adenosine, and K+

36
Q

Changes in a-vO2diff from Rest to Maximal Effort & Fick Equation

A

increased a-vO2diff with exercise and max effort

VO2 = Q * a-vO2diff

37
Q

Why does a-vO2diff increase during exercise?

A

decreased pO2 in muscles = increased O2 diffusion
increased pCO2, temp, acidity = decreased Hb affinity = increased O2 unloading
increased proportion of blood flow sent to active muscles

38
Q

Cardiovascular Drift

A

= SV decreases and HR increases in response
SV decreases due to decreased blood/plasma volume due to movement of fluid out into tissues –> HR increases to compensate and maintain CO –> research disproves

39
Q

SV and HR Under Beta-Adrenoceptor Blockade and Control Conditions

A
  • Beta-adrenergic blocker blocks SNS, thus increase in HR is blocked
  • when HR is blocked, the SV is maintained
  • cardiovascular drift occurs after prolonged exercise where decreases in SV cause increases in HR
40
Q

Effect of Training on Cardiac Output at Rest

A
  • trained vs. untrained = CO remains the same, but heart rate is lower and stroke volume is higher
  • lower HR is great for the heart and for RPP
41
Q

Effect of Training on Cardiac Output during Max Exercise

A

trained vs. untrained = maximum heart rate remains the same, max SV for trained is larger, thus max CO for trained is larger

42
Q

Why does SV go up with training? Endurance training vs. Resistance training

A

ventricular size - bigger and stronger
endurance training = biggest increase in internal diameter, smaller increase in wall thickness to sustain high CO
resistance training = biggest increase in wall thickness, smaller increase in internal diameter to endure increases in BP

43
Q

Blood Volume and Training

A

Endurance Training = increases blood volume overall
1st thing to happen within 24 hours = increase plasma volume
2nd thing to happen within 3 weeks = increase # of RBCs

44
Q

Increased Stroke Volume also due to…

A

maximal catecholamine release increases which enhances myocardial contractility to further increase SV

45
Q

Heart Rate Response to Graded Exercise: Trained vs. Untrained: What is the impact of slower HR on SV and why?

A

decreased HR –> increased diastole duration and time to fill –> increased EDV –> increased SV

46
Q

Exercise Training Effect on SNS and PSNS Activity: what is the impact of slower HR on SV and why?

A
  • After training, HR decreases due to increased PSNS from Central Command and decreased SNS from Muscle Controlled Peripheral Adaptation
  • this effect only seen if exercising trained muscles
  • connection to muscles is trained
47
Q

What is the primary determinant of VO2max or what contributes most to it?

A

cardiac output!!!

48
Q

A-vO2diff increases due to 5 things

A
  1. increased mitochondria
  2. increased capillaries
  3. increased transit time
  4. decreased diffusion distance
  5. increased blood flow to muscle due to increased Q combined with increased vasoconstriction in non-active tissues due to increase in max catecholamine levels
49
Q

Based on Fick Equation –> draw flow chart

A

back on notes, MEMORIZE!!

50
Q

Specificity of Training: Adaptations of Aerobic Energy System (4)

A
  1. increased mitochondria #, size, and enzymes –> decreased reliance on anaerobic glycolysis
  2. increased myoglobin
  3. increased muscle glycogen –> decreased use so stores last longer
  4. increased IMTG and increased use
51
Q

Effect of Training on Fuel Choice: Fatty Acid Oxidation vs. Carb Utilization

A

FA Oxidation increases: increased stores of IMG, increased mito, increased enzymes of betaoxidation
Carb Utilization decreases: muscle better capable to burn fat, decreased CA levels during submax exercise of same absolute intensity, decreased glycogenolysis

52
Q

Training Effect on Lactate During Graded Exercise

A

increased lactate threshold and better able to maintain higher intensity

53
Q

Endurance Training _____ blood lactate levels and _____ lactate threshold by:

A

lowers BL levels and increases LT:

  1. decreased CA levels –> decreased muscle glycogenolysis –> decreased anaerobic glycolysis
  2. increased mito –> decreased need for anaerobic glycolysis
  3. increased lactate clearance & removal –> liver uses lactate for gluconeogenesis –> increases after training b/c….decreased CA levels –> decreased vasoconstriction in hepatic portal system –> increased blood flow to liver –> increased clearance of lactate by liver after training
54
Q

Effects of Detraining or Immobilization on VO2max

A

4% decrease seen in 10 days
20% decrease seen in 56 days
Results depend on INITIAL fitness level: higher fitness level values will decrease rapidly but remain above sedentary levels b/c muscle holds on to adaptation, moderately trained values will return to baseline values within 8 weeks

55
Q

VO2 and Detraining Effect

A
  • VO2max decreases with age
  • increased benefits and increased VO2max w/ increased intensity
  • intensity related to ability maintain adaptations
56
Q

What decreases rapidly first and the most due to de-training?

A

blood volume

57
Q

Effect of Detraining on Enzymatic Adaptations

A

enzymes don’t go back to sedentary as fast as SV

58
Q

Why warm up? (5)

A
  1. increase Q and blood flow to muscles
  2. increase activity of aerobic respiration (RR)
  3. increase unloading of O2 off Hb due to increased temp of muscles
  4. decrease risk of myocardial ischemia
  5. increase O2 delivery to cardiac muscle
59
Q

Why cool down after VIGOROUS exercise?

A

maintain skeletal muscle pump for venous return to slowly decrease EDV and SV to prevent fainting and slowly decrease BP

60
Q

Classification of Blood Pressure Values

A

Normal: 160/or >100

Ex. Phys I (4 decks)

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