Cardiac Physiology: Heart anatomy and physiology Flashcards

1
Q

Describe atrial and ventricular heart muscle.

A

Striated, elongated, grouped in irregular anastomosing columns; 1-2 centrally located nuclei

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2
Q

Name the specialized excitatory and conductive muscle fibers.

A

SA node, AV node, Purkinje fibers Side note: contract weakly and few fibrils

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3
Q

Define syncytium

A

Many acting as one

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4
Q

How can cardiac muscle act as a syncytium?

A

Intercalated discs: low resistance pathways connecting cardiac cells end to end; presence of gap junctions

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5
Q

What is the duration of action potentials in cardiac muscle?

A

.2-.3 sec

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6
Q

Name the channels present in cardiac muscle.

A

Fast Na+ channels, Slow Ca++/Na+ channels, K+ channels

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7
Q

What are the permeability changes of cardiac muscle during an action potential?

A

Na+ sharp increase at onset of depolarization Ca++ increased during the plateau K+ increased during the resting polarized state

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8
Q

Describe membrane physiology and permeability during cardiac depolarization and repolarization

A

Na+ Increase at onset of polarization; Decrease during repolarization Ca++ Increase at onset of depolarization ; Decrease during repolarization K+ Decrease at onset of depolarization ; Increase during repolarization

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9
Q

Tetradotoxin selectively blocks what channels?

A

fast Na+ channels changing a fast response into a slow response

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10
Q

What are 3 considerations to assess passive ion movement across cell?

A

Concentration gradient: high to low Electrical gradient: opposite charge attract, like repel Membrane permeability: dependent on presence and state of ion channels

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11
Q

When considering concentration gradient vs electrical gradient, what will an ion do?

A

Seek its Nernst equilibrium potential; gradient favors ion movement in one direction is offset by electrical gradient

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12
Q

During resting membrane potential (Er) what is the sate of the ion channels?

A

Fast Na+ and slow Ca++/Na+ are closed, K+ are open

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13
Q

The negative membrane potential is maintained by what?

A

Na+/K+ pump (3:2)

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14
Q

What binds and inhibits the Na+/K+ pump?

A

Digitalis

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15
Q

What is located in the cardiac cell membrane that exchanges Ca++ from the interior of the cell in return for Na+?

A

Ca++ exchange protein

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16
Q

Why do we have both a Na+/K+ pump and a Ca++ exchange protein?

A

If the Na+/K+ pump is inhibited, function is reduced and more Ca++ accumulates in the cardiac cell increasing contractile strength.

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17
Q

Absolute refractory period

A

Unable to re-stimulate cardiac cell; occurs during the plateau

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18
Q

Relative refractory period

A

Requires a supra-normal stimulus; occurs during repolarization

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19
Q

What protects the ventricles from supra-ventricular arrhythmias?

A

AV node and bundle

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20
Q

What is the normal pacemaker of the heart?

A

SA node

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21
Q

What are the features of the SA node?

A

Self- excitatory in nature, less negative Er, Leaky membrane to Na+/C++ (unstable resting Er), only slow Ca++/Na+ channels operational, no plateau, contracts feebly

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22
Q

What cells are under overdrive suppression by the SA node?

A

Cells of the AV node and Purkinje system

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23
Q

What is overdrive suppression?

A

Driving a self-excitatory cell at a rate faster than its own inherent rate, suppressing its automaticity

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24
Q

What is the mechanism of overdrive suppression?

A

Mechanism may be due to increased activity of the NA+/K+ pump creating more negative Er

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25
Q

What is the function of the AV node?

A

Delays the wave of depolarization from entering the ventricle; allows the atria to contract slightly ahead of the ventricles (.1 sec delay)

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26
Q

What takes over as a pacemaker in the absence of SA node?

A

AV node at a slower rate

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27
Q

What is the relationship of heart rate and cycle length?

A

As heart rate increases, cycle length decreases; inverse proportional

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28
Q

Describe systole and diastole at resting

A

systole > diastole

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29
Q

During systole, perfusion of the myocardium is restricted. Why?

A

The contracting cardiac muscle compresses the blood vessels- especially in the left ventricle

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30
Q

True or false: at a higher HR, the ventricle may not fill adequately.

A

True

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31
Q

Describe Systole.

A

Isovolumic contraction and ejection

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32
Q

Describe Diastole

A

Isovolumic relaxation, rapid inflow (70-75%), diastasis and atrial systole (25-30%)

33
Q

Describe A to B

A

Ventricular filling, AV valves open, semilunar valves closed

34
Q

Describe B to C

A

Isovolumic contraction, AV valves close, semilunar valves closed

35
Q

Describe C to D

A

Ejection, semilunar valves open, AV valves remain closed

36
Q

Describe D to A

A

Isovolumic relaxation, semilunar valves close, AV valves remain closed

37
Q

What happens at point A?

A

AV valves open, ESV

38
Q

What happens at point B?

A

AV valves close, EDV

39
Q

What happens at point C?

A

Semilunar valves open

40
Q

What happens at point D?

A

Semilunar valves close

41
Q

Area enclosed be volume pressure loop is a measure of what?

A

Work or external work

42
Q

End Diastolic Volume (EDV)

A

Volume in ventricles at the end of filling

43
Q

End Systolic Volume (ESV)

A

Volume in ventricles at the end of ejection

44
Q

Stroke Volume

A

SV=EDV-ESV; volume ejected by ventricles

45
Q

Ejection fraction

A

percent of EDV ejected (SV/EDV x 100); normal is 50-60%

46
Q

Preload

A

Stretch on the wall prior to contraction (proportional to the EDV)

47
Q

Afterload

A

Changing resistance (impedance) that the heart has to pump against as blood is ejected; Changing aortic BP during ejection of blood from LV

48
Q

A wave

A

Atrial contraction

49
Q

C wave

A

Ventricular contraction; bulging of AV valves and tugging on atrial muscle

50
Q

V wave

A

Associated with atrial filling

51
Q

When left ventricle pressure is greater than aortic pressure, what is the state of the aortic valve?

A

Open; valves open with a forward pressure gradient

52
Q

When aortic pressure is greater than left ventricle pressure, what is the state of the aortic valve?

A

Closed; valves close with a backward pressure gradient

53
Q

Name the AV valves.

A

Mitral and Tricuspid

54
Q

What are characteristics of AV valves?

A

Thin and filmy, chorda tendineae act as check lines to prevent prolapse, papillary muscles increase tension on chordae tendinae

55
Q

Name the semilunar valves.

A

Aortic and Pulmonic

56
Q

Heart Murmurs associated with systole have which pathologies?

A

Aortic and pulmonary stenosis, mitral and tricuspid insufficiency

57
Q

Heart murmurs associated with diastole have which pathologies?

A

Aortic and pulmonary insufficiency, mitral and tricuspid stenosis

58
Q

Heart murmurs with both systole and diastole have which pathologies?

A

Patent ductus arteriosus, combined vulvar defect

59
Q

What is the Law of Laplace?

A

At a given operating pressure, as ventricular radius increases developed wall tension also increases Wall tension = (pressure x radius) / 2 Increased tension = increased force of ventricular contraction

60
Q

Define Chronotropic

A

Anything that affects the heart rate; i.e. caffeine would be a positive

61
Q

Define Dromotropic

A

Anything that affects conduction velocity

62
Q

Define Inotropic

A

Anything that affects strength of contraction

63
Q

Describe Frank-Starling Law of the Heart

A

Within physiological limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins

64
Q

What are mechanisms of Frank - Starling?

A

Increased venous return causes increased stretch of cardiac muscle fibers: increased cross bridge formation and increased CA++ influx which both increase force of contraction, and increased stretch on SA node which increases HR

65
Q

Describe hetero-metric auto-regulation

A

Within limits, as cardiac fibers are stretched the force of contraction is increased

66
Q

Describe homeo-metric auto-regulation

A

Ability to increase strength of contraction independent of a length change; flow induced

67
Q

What is the result of direct stretch on SA node?

A

Increase Ca++ and/or Na+ permeability which will increase HR

68
Q

What are extrinsic influences of SA node stretch?

A

Autnomic nervous system, hormonal, ionic and temperature

69
Q

What are the results of sympathetic innervation of the heart?

A

Increased HR, increased strength of contraction and increased conduction velocity

70
Q

What are the results of parasympathetic innervation of the heart?

A

Decreased heart rate, decreased strength of contraction, decreased conduction velocity

71
Q

Atropine blocks parasympathetic effects via which receptors and what is the result?

A

Blocks Beta receptors and muscarinic receptors; HR will increase and strength of contraction will decrease

72
Q

Propanolol block SNS effects on the heart via which receptors?

A

Beta receptors

73
Q

Stimulation of the left stellate ganglion effects?

A

Decreased ventricular fibrillation threshold and prolongation of QT interval

74
Q

Stimulation of the right stellate ganglion effects?

A

Increased ventricular fibrillation threshold

75
Q

Describe the cardio-accelerator reflex

A

Stretch on right atrial wall induces stretch receptors which in turn send signals to MO to increase outflow to heart; helps prevent damming of blood in heart and central veins

76
Q

Neuro-cardiogenic syncope, a baroreceptor reflex in the ventricles is stimulated by?

A

Occlusion of circumflex artery (inferior wall infarct) and increase in left ventricle pressure and volume (aortic stenosis)

77
Q

Neuro-cardiogenic syncope (baroreceptor reflex) results in?

A

Hypotension and bradycardia

78
Q

When does left coronary flow peak?

A

Onset of diastole

79
Q

When does right coronary flow peak?

A

Mid systole