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PHYS 150: physiology > cardiovascular physiology > Flashcards

cardiovascular physiology Flashcards

1
Q

What are the characteristics of cardiac muscle tissue?

A
  • excitability
  • automaticity
  • rhythmicity
  • refractoriness
  • conductivity
  • contractility
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2
Q

What is the term for the ability of the cardiac muscle to respond to an electrical stimulus by contracting?

A

excitability

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3
Q

What channels open during depolarization?

A

Na+ & Ca2+
* on sarcolemma

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4
Q

What occurs during the plateau phase?

A

Ca2+ channels stay open longer
* 200 msec
* remains depolarized
* purpose = prevents tetany; prolongs duration of the action potential; sustains heart contraction; allows for efficient pumping

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5
Q

Describe the events of a cardiac action potential

A
  1. Depolarization = Na+ & Ca2+ channels open
  2. Na+ channel closes
  3. Ca2+ channels remain open = plateau phase & K+ channels open
  4. Repolarization = Ca2+ closes & K+ continues to flow in
  5. Returns back to resting potential
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6
Q

Can stimulate the cardiac muscle continuously even if the previous action potential isn’t done?

A

No
* there is a refractory period
* action potential must finish before another action potential is initiated
* purpose = prevent tetany & allow for efficient & complete pumping of the heart

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7
Q

What is automaticity?

A
  • ability of some cardiac muscle to initiate its own stimulus
  • autorhythmic cells
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8
Q

What is the purpose of leaky membranes in the cardiac cell?

A

regulates & maintains the pacemaker activity (SA node)
- initiates depolarization

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9
Q

What is the pacemaker’s potential?

A

-60 mV to -40 mV

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10
Q

What is the threshold potential? How is it reached?

A

-40 mV
* leaky channels = aways open & letting in ions
* leaky channels allows for the cardiac membrane to reach its threshold
* nervous stimulation is not required

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11
Q

What is rhythmicity?

A
  • regularity of beat
  • pacemaking activity
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12
Q

What is refractoriness ?

A
  • cardiac cells has a refractory period where = cell is unable to generate another action potential for a specific amount of time
  • contraction & excitation occurs by the end of the refractory period
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13
Q

What connects cardic cells together?

A

intercalated discs
* allows for ions to diffuse from one cardiac muscle cell to another

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14
Q

What is a functional syncytium?

A

group of cells acting as if they were one
* cardiac cells beat as one
* action potential spreads through entire myocardium via intercalated discs

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15
Q

What is the wall of conective tissue between atria & ventricles?

A

fibroskeleton

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16
Q

What are the functions of the fibroskeleton?

A
  • supports the AV valves
  • high electrical resistance –> controls direction of electrical impulses
  • directs impulses to AV node
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17
Q

How do electrical impulses go from the atria to ventricle?

A

via the AV node
* this is the only way for an impulse to get to the ventricle from the atria
* ensures proper timing of atrial & ventricular contractions

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18
Q

Does the atria & ventricle contract at the same time?

explain

A

No
* there is a delay between atrial contraction & ventricular contraction
* purpose = allows tiem for ventricles to fill with blood before entering the systemic circulation

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19
Q

Wat would happen if atria & ventricles contracted at the same time?

A
  • less blood would be pumped from atria to ventricles & to the systemic circulation
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20
Q

What are the electrical events that occur when the heart is stimulated?

A
  1. SA node = depolarizes (starts the electrical signal) –> 100 times/min
  2. AV node –> depolarizes 40-60 times/min
  3. Bundle of His –> depolarizes 20-35 times/min
  4. Spreads to right & left bundle branches –> depolarizes 20-35 times/min
  5. Purkinje fibers –> depolarizes 20-35 times/min
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21
Q

What sets the heart rate?

which cells in the heart?

A

the cells that depolarize most rapidly
* heart is a functional syncytium - so when it beats, that means all the cardiac cells are beating together

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22
Q

What is an EKG?

A

electrocardiogram
* consist of 5 waves that reflects cardiac events

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23
Q

Where would you place a 3 lead EKG?

A

left arm, right arm, left leg

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24
Q

Explain the components of an EKG

segments, intervals, waves, complex

A

2(+1) segments:
1. PR segment = atrial depolarization is complete & impulse is delayed at the AV node
2. ST segment = time between ventricular depolarization and repolarization
3. TP segment = period between ventricular repolarization and the onset of the next P wave

2 intervals:
1. PR interval = 0.12-0.20 s
2. QT interval = 0.32-0.38 s

QRS complex = part of QT interval
* onset of ventricular depolarization

P wave = atrial depolarization (SA node)

T wave = ventricular repolarization

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25
Q

What is the condition if there is an ST-segment elevation?

A

MI

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26
Q

What is the condition if there is more P waves than QRS?

A

AV block

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27
Q

What is the condition if there is rapid/large voltage fluctuations?

A

v fib

28
Q

Describe the events of the cardiac cycle

A

1.all 4 chambers are relaxed
* SL vlaves closed
* AV valves open –> blood passively flows through atria
* 70% goes straight to ventricles
* 30% stays in atria

2.SA node fires
* atria contract –> 30% of blood goes to ventricles
* depolarizations spreads to atrial walls to AV node
* ventricles are relaxed

3.AV valves close (lub); SL valves open
* due to increased intra-ventricular pressure
* blood goes to aorta & pulmonary trunk

4.SL valves close (dub); AV valves open
* due to decreased intra-ventricular pressure
* cycle restarts

29
Q

How many times does the cardiac cycle repeat per minute?

normal

A

60-100 times/minutes
* intense exercise = >200 times/min
* conditioning = <60 times/min

30
Q

What is bradycardia?

HR

A

<60 beats/min

31
Q

What is tachycardia?

HR

A

> 100 beats/min

32
Q

What is cardiac output?

A

CO = HR X SV

HR = number of cardiac cycles /min

SV = volume of blood pumped out of one ventricle in one heart beat
* mL/beat
* average = 75 mL
* relaxed ventricle holds 130 mL

CO = volume of blood pumped by one ventricle in one minute
* mL/min

33
Q

What are the factors that affect heart rate?

A
  • ANS
  • temperature
  • hormones
  • ions
  • age, biological sex, physical fitness
  • drugs, toxins
34
Q

What center is activated by emotional or physical stress?

ANS regulation

A

cardiac accelerator center
* stimulates sympathetic neurons —> innervate SA & AV nodes

result = increase in rate & force of contraction

35
Q

What center decreases heart activity when stressors are removed?

ANS regulation

A

cardiac inhibitory center
* parasympathetic fibers pass via the vagus nerve to SA & AV nodes

result = decrease in rate & force of contraction

36
Q

Where is the cardiac center located in the brain?

A

medulla oblongata

37
Q

What neurons dominate under relaxed conditions?

A

parasympathetic neurons
* inhibitory impulses dominate = vagal tone
* decreases HR & vagal inhibition

38
Q

What neurons dominate under stressful conditions?

A

sympathetic neurons
* vagal tone is overcome
* increases HR & force of contraction

39
Q

What are the effects of temperature?

A
  • increased temp = increased HR
  • decreased temp = decreased HR
40
Q

What hormones regulate the heart? Explain their effects

A

Epinephrine (adrenal medulla)
* mimics SNS
* increases hr & contraction

Thyroxine (thyroid)
* slower & longer lasting effect
* increase HR
* enhances effects of NE & E

41
Q

What ions influence the cardiac cycle?

A

Calcium (depolarization)
* hyperclcemia = increased strength & prolonged contraction; decreased rate
* hypocalcemia = decreased strength

Potassium (repolarization phase)
* hyperkalemia = bradycardia, cardiac arrest, heart block
* hypokalemia = fibrillation/arrhythmias

42
Q

What are the factors affecting stroke volume?

A
  1. Preload
  2. Contractile strength of each cardiac muscle fiber
  3. Afterload
43
Q

What is preload and how does it affect stroke volume?

A

degree of streth in heart before it contracts

Starling’s law of the heart = force of contraction increases with the degree of cardiac muscle cell stretch

  • increased end diastolic volume –> increased preload (bc lots of blood) –> increased stroke volume = increased cardiac output
44
Q

What is contractile strength & how does it affect stroke volume?

A

ability of cardiac muscle fibers to shorten

  • increased when Ca2+ and epinephrine are present & when SNS is activated
45
Q

What is afterload and how does it affect stroke volume?

A

load or resistance against which the left ventricle must pump its blood during contraction

  • increased afterload –> decreased stroke volume
46
Q

What are the blood vessels & their functions?

A
  1. Arteries = carry blood away from the heart
  2. Veins = carry blood towards the heart
  3. Capillaries = gas exchange
47
Q

What happens to arteries during ventricular systole?

A
  • blood entering arteries are under high pressure
  • artery walls stretch
  • artery characteristics = larger diameter, elastic walls
48
Q

What happens to blood vessels during ventricular diastole?

A
  • stretched arteries recoil
  • continuous flow is maintained by driving blood through arteries & capillaries –> prevents pulsatile flow
49
Q

What is blood pressure & the types?

A

force of blood pressing against the inner walls of the blood vessels

types:
1. ABP = arterial blood pressure –> high bc close to heart
2. capillary pressure/hydrostatic pressure
3. venous vlood pressure–> almost nothing

50
Q

What is the normal value of ABP?

A

120/80 mmHg

  • determined by CO, peripheral resistance & blood volume
51
Q

Equation for pulse pressure

A

systolic pressure - diastolic pressure

normal = 40 mmHg

52
Q

What is the normal value for mean arterial pressure (MAP)?

A

(S+2D)/3

  • closer to diatsolic bc heart spends more time in diastole compared to systole
  • normal = 95 mmHg
53
Q

What is the normal value for capillary pressure?

A

30 mmHg (arterial end) to 15 mmHg (venous end)

54
Q

What is the normal value of venous blood pressure?

A

2 mmHg

  • almost nothing
55
Q

What are the physical determinantsof arterial blood pressure?

A

Arterial blood pressure
* BP = CO X PR

Peripheral resistance = opposition to flow
* cause = friction as blood flows throguh vessels
* factors: diameter, length, viscosity

56
Q

What factors can we change to change our peripheral resistance?

A

diameter & blood volume

57
Q

What increases peripheral resistance?

A
  • decreased arteriole diameter
  • increased blood vessel length
  • increased blood viscosity
58
Q

What factors control arterial BP?

A
  1. Baroreceptors
  2. Cardiac centre
  3. Vasomotor centre
59
Q

How do baroreceptors work?

A

location = carotid sinuses & aortic arch

  • respond to pressure by stretching
  • sends impulses to medulla oblongata
60
Q

How does the cardiac centre regulate arterial BP?

A

location = medulla oblongata

  • receives impulses from baroreceptors, hypothalamus, cerebral cortex
  • regulates: **HR and contractility of the heart **via SNS & PNS
  • innervates SA node
61
Q

How does the vasomotor centre regulate arterial BP?

A

location = medulla oblongata

  • receives impulses from baroreceptors, hypothalamus, and cerebral cortex
  • controls diameter of blood vessels via SNS
62
Q

What occurs when BP is elevated? How is it regulated ?

A
  • afferent impulses go towards the cardiac centre –> increases rate of APs
  • decreases HR & force of contraction = decreased BP
63
Q

What occurs when BP is low? How is it regulated?

A
  • fewer afferent impulses to the cardiac centre & vasomotor centre
  • vasoconstriction & venoconstriction
  • increases HR & copntractility force = increases BP
64
Q

What is the renin-angiotensin mechanism?

A
  • activated by low BP
  • renin is secreted by kidneys
  • renin converts angiotensinogen to angiotensin I
  • angiotensin I is converted to angiotensin II by ACE
  • angiotensin II brings BP back up
65
Q

How does angiotensin II elevate BP?

A
  • vasocnstrictor = increases peripheral resistance
  • stimulates aldosterone secretion = increas Na+ reabsorption, blood volume, blood pressure
66
Q

What are ACE inhibitors? and what conditions are they useful in treating?

A

inhibit conversion of angiotensin I to angiotensin II

  • examples = vasotex (enalapril), zestril (lisinopril), lotensin
  • decreases BP
  • conditions = hypertension, MI, heart failure, decrease workload of heart

PHYS 150: physiology (7 decks)

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