lecture 9 Flashcards

1
Q

describe action potentials of skeletal, nerve, and cardiac muscles

A
  • Skeletal + nerve muscles- very short, discrete action potential
    In cardiac, is bigger + plateaus at the top = longer repolarisation section, and a prolonged contraction phase

refer to onenote

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2
Q

why does the action potential of cardiac muscle have a plateau?

A
  • Ensures adequate ejection time
  • is contraction
  • due to ca+ channels opening, allowing calium to come in, maintaining a positive charge
    The plateau means wont be able to stimulate contractions so qucikly, allowing cardiac muscles to relax before restarting- constant contraction in heart would be BAD
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3
Q

describe ECGs

A
  • Records the electrical events within the heart
    • Voltameter records electrical potential across cells
      On a graph, time is X-axis, amplitude is Y-axis (amplitude is proportional to no. + size of cells)
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4
Q

describe standard bipolar ECG limb leads

A
  • Means that the electrical potential is recorded from 2 electrodes located on different sides of the heart
    2 id larger then the others because the blood in the heart travels in the same direction as the electrodes, so the signal is going to be detected as the strongest in this arrangement

refer to onenote

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5
Q

describe the electrical activity of the heart

A
  • Note electrical acitivity ALWAYS preceds mechanical response
    • P-wave
      ○ First part
      ○ Depolarisation
      ○ Valve between the atria + ventricle opens
    • PQ
      ○ Ventricles fill with blood
    • Q
      ○ Little dip before peak starts
      ○ Depolarisation
      ○ Blood going through valve to next ventricle
    • R
      ○ Signal travels through apex
      ○ Atrial repolarisation
      ○ Ventricular contraction, pushed blood to rest of the body
      ○ Is the big peak
    • S
      ○ Other side of peak, little dip
      ○ Final depolarisation of ventricles
    • ST
      ○ Ventricles contract
    • T
      ○ Ventricular repolarisation
    • End
      Membrane goes back to neg.

refer to onenote

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6
Q

define EDV

A

○ End diastolic volume
Blood bolume in the ventricle at the end fo DIASTOLE

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7
Q

define ESV

A

Blood bolume in the ventricles at the end of systole

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8
Q

define SV

A

○ Stroke volume
○ Volume of blood pumped from the left ventricle per beat
○ SV = EDV - ESV (ml)
§ Note:
□ EDV influenced by venous return (VR) (increasing VR = increasing EDV)

ESV influenced by inotropy (increased contractility = decreased ESV = increased SV)

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9
Q

define HR

A

○ Heart rate, beats/min
No. Of times per minute that the ventricles eject blood

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10
Q

define CO

A

○ Cardiac output, ml/min
CO = SV x HR (L/min)

Total blood flow being pumped by heart = cardiac output

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11
Q

what is preload

A
  • Filling the pumps
    • Preload- degree of stretch fo the ventricular walls by blood filling the ventricles
    • Proprtional to EDV
    • Depends on venous return (VR) to the heart
    • Increased preload = increased EDV = SV
      Relationship between preload + SV is called the frank-starling lae of the heart
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12
Q

explain Frank Starling law

A
  • Uses the legnth-tension relationship
    • Is the strength of contraction is related to the length of th emuscle when the contractions occur
    • Increase heart filling stretches the cardiac muscle fibres more at the ened of diastole
    • More cross-bridges = more force (contractility increases)
    • Leads to more vigorous systolic contractions + icnreased SV
      Myocardium cannot continue to stretch indefinitely
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13
Q

what is afterload

A
  • Pumping blood out
    • Afterload- amount of pressure that the ventricles must develop to opent the semilunar valve + eject blood into the arteries
    • Depends on resistance ot blood flow out fo the ventricle
    • Basically, si the back pressure exerted by the arterial blood on the semilunar valves
      Increasing BP = icnrease afterload
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14
Q

define BP

A
  • Is the force per unit area of blood pushing against the vessel walls that contain it (mmHg)
    • BP is determined by
      1. CO
      2. PVR- peripheral vascular resistance

BP = CO x PVR

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15
Q

what is bradycardia

A

HR slower then normal

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16
Q

what is tachycardia

A

HR faster than normal

17
Q

what is chronotropy

A

rate of action potential production in the SA node (increasing chronotropy = increase HR)

18
Q

what is inotropy

A

(how hard heart muscles contract) = contractiltiy of heart muscles (increasing inotropy = increasing contractile strength = increase SV)

19
Q

what can HR be affected by

A
  • HR can be modulated by
    ○ Direct nervous stimualtions
    § Autonomous nervous system
    ○ Circulating hormones
    E.g. Epinephrine
20
Q

describe SNS effect on heart

A

○ Has stimulatory effect on heart
○ Acts via norepinephrine, binding to alpha + beta adrenergic receptors
§ Increasing SNS at SA node = increase HR + increase chronotropy
§ Increasing SNS on heart muscle = increasing contraction strength + increase inotropy
Both alpha + beta receptors found in vasculature (alpha receptors = vasoconstriction, beta-receptors = vasodilation)

21
Q

describe PNS effect on heart

A

○ Has inhibitory effect on heart
○ Acts via acetylcholine binding to muscarinic receptors
§ Increasing PNS at SA node = decrease HR + decrease chronotropy
§ Increasing PNS on heart = decrease contraction strength + decrease inotropy
○ Muscarinic receptors also found on blood vessels causing vasodilation
Same signal can cause differenet reactions depending on what receptor it binds to

22
Q

3 ways to modulate cardiac contractility

A
  1. Sumpathetic nervous tone
    ○ Increasing sympathetic nervous tone = increased contractility
    1. Circulating epinephrine + othe rhormones
      ○ Epinephrine = increased contractility
    2. Inotropic drugs
      ○ Digoxin = positive inotrope
      Beta-blockers = neg. inotropes