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Physiology B2 & B3 > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the relative intracellular and extra cellular concentrations of Na+, K+ and Ca2+?

A
  • Na+ (o) >>> Na+ (i)
  • K (i) >>> K+ (o)
  • Ca2+ (o) >>> Ca2+ (i)
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2
Q

What are the components of the electrical conducting system of the heart?

A

START:

  • SA node
  • AV node
  • Bundle of his
  • bundle branches
  • purkinje fibres

END

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3
Q

How does the SAN determine the heart rate? What are the intrinsic rates of other areas within the heart?

A

SAN determines HR dt pacing at higher rate than AVN.

Intrinsic rates:

  • SAN: 60 – 99
  • AVN: 40 – 60
  • Bundle of his: 30 – 40
  • Purkinje fibres: 20 – 30
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4
Q

What are the features of the pacemaker AP at the SAN/AVN?

A
  • No evidence of RMP (but when AP blocked = -35mv), continual depolarisation before fast upstroke
  • Split into 3 phases (0,3,4)
    • Phase 0 (upstroke): VG L-type ca2+ channels (in), open at -45mV, inactivate slowly, blocked by CCB, especially diltiazem and verapamil
    • Phase 3 (downstroke): delayed rectifier K+ channel (out)
    • Phase 4 (slow depol. between upstrokes): leak dominated by Na+ (in) , if current, funny dt hyperpol. activated (-20mV)
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5
Q

What are the features of a myocyte AP?

A
  • 5 Phases (0, 1, 2, 3, 4)
  • Phase 0 (upstroke): VG Na+ (in)
  • Phase 1 (dip): transient outward K+ current
  • Phase 2 (plateau): L-type Ca2+ channels (in) balancing with K+ current (out)
  • Phase 3 (drop): terminated by delayed rectifier K+ current (out)
  • Phase 4 (diastolic): inward K+ recitifer (out) with If current (in)
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6
Q

What is the importance of the absolute refractory period?

A
  • Period in which AP cannot be generated, prevents repeated, rapid contraction that would result in ~0 CO.
    • Absolute, from Q wave to peak of T.
    • Relative, from down slope of T – vulnerable period.
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7
Q

What is the process of EC coupling in cardiac muscle vs skeletal muscle?

A
  • Ca2+ entry via L-type Ca2+ channels, not coupled with ryanodine receptor of SR Ca2+ entry leads to more ca2+ release from ryanodine-sensitive SR, Ca2+ induced Ca2+ release (CICR)
  • Compared to muscle: Ca2+ release from SR -Ca2+ binds to troponin C, releasing tropomyosin from actin Myosin head binds to myosin binding sites on Actin
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8
Q

How does the time period of diastole and systole changing during the cardiac cycle with increasing HR?

A

Duration of systole quite constant, during of diastole varies with HR, such that ↓diastolic time with ↑HR

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9
Q

What are the pressure ranges in; RA, RV, AP, LV & aortic trunk

A
  • RA: 2- 8mmHg
  • RV: 0-40mmHg
  • PA: 20-40mmHg
  • LV: 0 – 120mmHg
  • Aortic trunk: 0 – 120mmHg
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10
Q

Summarise the 7 phases of the cardiac cycle and the respective electrical activity at these time points.

A
  • CARDIAC FUNCTION SAYS ROGER RABBIT STAYS ALIVE
  1. Isovolumetric contraction – RS phase
  2. Fast ejection – S-T phase
  3. Slow ejection – T wave
  4. Isovolumetric relaxation
  5. Rapid ventricular filling
  6. Slow ventricular filling
  7. Atrial contraction – P wave
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11
Q

What is the timing of the ventricular contraction (right versus left) and the valvular opening and closure?

A

Cycle starts in right atrium (pacing in SAN) and ends in right ventricle (delayed contraction)

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12
Q

How do you calculate the ejection fraction? What is a typical value? What value defines systolic dysfunction?

A

EF = ((SV/EDV) * 100), typically >55% with values <45% defining systolic dysfunction

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13
Q

What factors determine CO?

A
  • HR and SV
  • HR -> electrical properties
  • Stroke volume -> preload, afterload, contractility, lusitropy
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14
Q

What is preload and how does it relate to SV?

A
  • Preload is the LV EDV/EDP
  • Determines cardiac muscle fibre length @ end-diastole
  • Greater force production and therefore greater velocity of contraction -> longer ejection
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15
Q

What is afterload and how does it relate to SV?

A
  • Pressure against which ventricle muscle contract to eject blood into aorta -> load given by peripheral vasculature.
  • Afterload ↑ -> SV↓ dt increase in force required for contraction resulting in decreased contraction velocity and therefore less time to eject.
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16
Q

From a P-V diagram, how do you calculate cardiac work?

A

Work = area spanned by P-V diagram, or Work = ΔP. V

17
Q

What are the two forms of work in the cardiac cycle and which phases of the cardiac cycle do they correspond with?

A
  • External work -> physical, kinetic work, during ejection
  • Internal work -> largely heat (comprised of isovolumetric work, sounds/murmurs, electrical activity and base metabolism. Corresponds to isovolumetric contraction.
  • Internal is 5-20x > than external work
18
Q

Compare the energy requirements of ↑CO by ↑SV versus ↑HR:

A
  • ↑CO via ↑HR -> internal work -> greater energy requirement
    • Energetically more costly
  • ↑CO via ↑SV -> increase largely via ↑external work -> > energy efficiency by increases via SV
19
Q

What effects to preload and afterload have upon internal and external work?

A
  • Afterload -> ↑internal work dt ↑isovolumetric phase -> increase energy demands
  • Preload -> ↑SV -> ↑external work -> energy efficiency (“cheap”)
20
Q

What are the determinants of venous return and how can VR be mathematically determined?

A
  • VR determined by mean systemic filling pressure
  • RA pressure
  • Resistance in the vasculature

Mathematically determined by VR = (Pmsf - PRA) / Rv

21
Q

From what spinal levels are the sympathic innervations of the heart?

A

T1 -> T5

22
Q

How do PsNS and SyNS modulate HR at rest?

A

Both PsNS and SyNS tonically active at rest, with predominant PsNS activity

23
Q

Where are the arterial baroreceptors (responsible for the arterial baroreceptor reflex) located and what is their innervations?

A
  • Aortic arch -> left vagus
  • Cartoid sinus -> glossopharyngeal
24
Q

What occurs during exercise to allow for increasing HR and also increasing BP?

A

Set-point for baroreflex shifts to a higher point, resulting in a higher HR being achieved at the same BP

25
Q

What is the Bainbridge reflex?

A
  • Tachycardia induced by increase in central venous pressure detected by low pressure stretch receptors in cardiac atria.
  • Receptors activated by increase in atrial pressure -> signals medullary control centre -> decreases PsNS tone via vagus, functions to decrease pressure in SVC and IVC
26
Q

What is respiratory sinus arrhythmia?

A

Increasing HR during expiration and decreasing during expiration.

27
Q

What happens to the pulse wave as the measurement site moves towards the periphery?

A
  • ↑ Systolic pressure
  • ↓ slightly in diastolic pressure
  • ↓ arterial pressure slightly
  • incisura lost (notch) and second hump (due to reflection from resistive elements)
28
Q

What does pulse wave velocity depend upon?

A
  • Stiffness of vessels
  • Increases from proximal to distal in arterial circulation
  • Very low PWV in venous system.
29
Q

Compare perfusion in the RCA and LCA during systole and diastole

A

Overall flow

  • RCA: Smaller
  • LCA: Larger (x6)

Maximal flow

  • RCA: At fast ejection phase
  • LCA: During early diastole

Cessation in flow

  • RCA: None
  • LCA: During isovolumetric phase, affects subendocardial vessels (more infarcts) much more than subepicardial
30
Q

What is the purpose of autoregulation in the coronary vasculature and how does it operate?

A

Local blood flow regulation: defined as the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure.

F = (Pa - Pv) / R

  • As perfusion pressure (PA-Pv) drops, resistance vessels dilate to decrease resistance to flow and maintain blood flow through the tissue
  • The decrease in pressure dt the decrease in resistance is counteracted by the increased in flow.
    • The converse is also true.
  • Maintains constant blood flow over pressure range (range determined by maximal relaxation or contraction).
31
Q

What effect does neural control of perfusion have upon the coronary vasculature?

A

Metabolic self regulation more important than neuronal control, as myocardial O2 demand and coronary flow linearly proportional -> denervation does not alter this (transplanted hearts don’t have problems with regulation of perfusion)

32
Q

How does Pco2 and Po2 affect CBF?

A
  • Pco2 is main determinant of CBF
    • ↑ Pco2 -> vasodilation
    • ↓ Pco2 -> vasoconstriction.
  • Po2 has little effect on CBF, only at very low levels of PaO2
33
Q
A

Physiology B2 & B3 (5 decks)

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