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DMD 5247 > Winden - Heart Physiology > Flashcards

Winden - Heart Physiology Flashcards

1
Q

Inotropy

A

Force of contraction

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2
Q

Chronotropy

A

Rate of contraction

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3
Q

Dromotropy

A

Conduction velocity

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4
Q

What are the two types of cardiac muscle cells?

A
  1. Conducting system
    - Control and coordinate heartbeat
  2. Contractile cells
    - Produce contractions that propel blood

Both of these types are specialized myocytes

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5
Q

Where does action potential begin in the cardiac cycle?

A

SA node

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6
Q

Electrocardiogram (ECG, EKG)

A

Electrical events in the cardiac cycle that can be recorded on an electrocardiogram

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7
Q

What are the conducting system cardiac muscle cells?

A
  • A system of specialized cardiac muscle cells.
  • – Initiate and distribute electrical impulses that stimulate contraction
  • Automaticity - can go to threshold without additional stimulants
  • – Cardiac muscle tissue contracts all on its own
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8
Q

What are contractile cardiac muscle cells?

A
  • Purkinje fibers that distribute the stimulus to the contractile cells, which make up most of the muscle cells in the heart
  • Resting potential
  • – Ventricular cell: -90mV
  • – Atrial cell: -80mV
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9
Q

What are the major ion channels in conduction system, myocardium, BVs?

A

Conduction system
K+, Na+, Ca2+

Myocardium
K+, Na+, Ca2+

BVs
Ca2+, K+, C-

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10
Q

What ions are the cause for Phase 0 of the cardiac action potential cycle?

A

Cause: Na+ entry
Ends with: Closure of voltage-gated Na+ channels

SA node, If (rapid Na+ channel) initiates depolarization

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11
Q

What ions are the cause for Phase 1 of the cardiac action potential cycle?

A

Overshoot.

Na+ channels close (and K+ channels open (drop before the plateau) -> repolarization initiation

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12
Q

What ions are the cause for Phase 2 of the cardiac action potential cycle?

A

Plateau!
Cause: Ca2+ entry
Ends with: Closure of slow Ca2+ channels

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13
Q

What ions are the cause for Phase 3 of the cardiac action potential cycle?

A

Cause: K+ loss

Ends with: Closure of slow K+ channels

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14
Q

What ions are the cause for Phase 4 of the cardiac action potential cycle?

A

Resting phase: Ion gradients are being re-established; depolarization initiation in some cells (automaticity)

Na/K pump resets the concentration gradient for each ion.

Na/Ca antiporter is re-establishing Ca2+ gradient (moving Ca2+ out of the cell)

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15
Q

Refractory period: Two Types

A

Absolute Refractory Period

  • Long - so that the heart doesn’t contract too quickly
  • Cardiac muscle cells cannot respond

Relative Refractory Period

  • Short
  • Response depends on degree of stimulus
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16
Q

Timing of Refractory Periods compared to skeletal muscle and why?

A

Length of cardiac action potential in ventricular cell

  • 250-300 msec
  • – 30x’s longer than skeletal muscle fiber
  • – Long refractory period prevents summation and tetany
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17
Q

What is the role of calcium ions in cardiac contractions?

A

Contraction of a cardiac muscle cell
- Produced by an increase in Ca2+ ion concentration around myofibrils

  1. 20% of Ca2+ ions required for a contraction are EC
    - Ca2+ ions enter plasma membrane during plateau phase
  2. Arrival of EC Ca2+
    - Triggers release of Ca2+ ion reserves from SR
  3. As slow Ca2+ channels close
    - IC Ca2+ is absorbed by SR or pumped out of cell
  4. Cardiac muscle tissue
    - Very sensitive to EC Ca2+ concentrations
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18
Q

Ca2+ dependence: skeletal muscle vs. myocardium vs. SM contraction

A

Skeletal: depends mainly on IC Ca2+ sources (SR)
Myocardium and SM: depend mainly on EC Ca2+

Myocardium and SM are more sensitive to Ca2+ antagonists than skeletal because of this

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19
Q

Sources of energy for cardiac contractions

A

Aerobic energy of heart

  • From mitochondrial breakdown of FAs and glc
  • O2 from circulating hemoglobin
  • Cardiac muscles store O2 in myoglobin
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20
Q

What structures comprise the conducting system?

A
  • SA node - wall of RA
  • AV node - junction between atria and ventricles
  • Conducting cells - throughout myocardium
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21
Q

Conducting cells

A
  • Interconnect SA and AV nodes
  • Distribute stimulus through myocardium
  • In atrium - Internodal pathways
  • In ventricles - AV bundle and bundle branches
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22
Q

Prepotential

A
  • AKA pacemaker potential
  • Resting potential of conducting cells
  • – Gradually depolarizes towards threshold
  • SA node depolarizes first, establishing HR
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23
Q

Heart Rate

A

SA node generates 80-100 action potentials/minute - everything will follow this rate

  • Parasympathetic stimulation slows HR
  • Vagus nerve is main parasympathetic nerve

AV node generates 40-60 action potentials/minute

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24
Q

SA node

A
  • Posterior wall of RA
  • Contains pacemaker cells
  • Connected to AV node by internodal pathways
  • Begins atrial activation
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25
Q

AV bundle

A
  • In the septum
  • Carries impulse to L and R bundle branches, which conduct to Purkinje fibers
  • And to the moderator band, which conducts to papillary muscles
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26
Q

Purkinje fibers

A
  • Distribute impulse through ventricles
  • Atrial contraction is complete
  • Ventricular contraction begins
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27
Q

What are some abnormal pacemaker functions?

A
  • Bradycardia
  • Tachycardia
  • Ectopic pacemaker
  • – Abnormal cells
  • – Generate high rate of action potentials
  • – Bypass conducting system
  • – Disrupt ventricular contractions
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28
Q

What is the correct conduction pathway through the heart?

A

SA > atrial muscles > AV > bundle of his/AV bundle > bundle branches > Purkinje fibers > ventricular muscle

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29
Q

What are some features of an ECG/EKG

A
  • P wave: atria depolarize
  • QRS complex: ventricles depolarize (atria repolarize here, but the peak is hidden behind QRS because ventricles pump with greater force)
  • T wave: ventricles repolarize
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30
Q

What are the time intervals between ECG waves?

A
  • P-R interval

- Q-T interval

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31
Q

P-R interval

A

From start of atrial depolarization to the start of QRS complex

32
Q

Q-T interval

A

From ventricular depolarization to ventricular repolarization

33
Q

What are the phase of the cardiac cycle?

A
  • Atrial systole
  • Atrial diastole
  • Ventricular systole
  • Ventricular diastole
34
Q

What events are occurring during atrial systole?

A
  1. Atrial systole
    - Atrial contraction begins
    - R and L AV valves are open
  2. Atria eject blood into ventricles
    - Filling ventricles
  3. Atrial systole ends
    - AV valves close
    - Ventricles contain maximum blood volume
    - AKA end-diastole volume (EDV)

There’s lots of pressure in the atria at the beginning of systole vs. less pressure in the atria at the end of systole

35
Q

What events are occurring during ventricular systole?

A
  1. Ventricles contract and build pressure
    - AV valves close, causing isovolumetric contraction - AV and semilunar valves are closed, so no change in volume, just creating pressure
  2. Ventricular ejection
    - Ventricular pressure exceeds vessel pressure opening the semilunar valves and allowing blood to leave the ventricle
    - Amount of blood ejected is called the stroke volume (SV)
  3. Ventricular pressure falls
    - Semilunar valves close
    - Ventricles contain end-systolic volume (ESV), about 40% of end-diastolic volume
36
Q

What events are occurring during ventricular diastole?

A
  1. Ventricular diastole
    - Ventricular pressure is higher than atrial pressure
    - All heart valves are closed
    - Ventricles relax (isovolumetric relaxation)
  2. Atrial pressure is higher than ventricular pressure
    - AV valves open
    - Passive atrial filling
    - Passive ventricular filling
37
Q

What happens to all phase of the cardiac cycle when HR increases?

A

All phases shorten, particularly diastole

38
Q

Heart Sounds: S1

A

“Lub”
Loud sounds
Produced by AV valves

39
Q

Heart Sounds: S2

A

“Dub”
Loud sounds
Produced by semilunar valves

40
Q

Heart Sounds: S3, S4

A

Usually indicates a problem i.e. murmur, stenosis
Soft sounds
Blood flow into ventricles and atrial contraction

41
Q

What is a heart murmur?

A
  • Sounds produced by regurgitation through valves

- Mitral valve is most common location because it undergoes more pressure than the other valves (mitral valve prolapse)

42
Q

What is cardiodynamics?

A

The movement and force generated by cardiac contractions.

  • End-diastolic volume (EDV)
  • End-systolic volume (ESV)
  • Stroke volume (SV) - amount of blood pumped by one LV contraction
  • – SV = EDV - ESV
  • Ejection fraction: % of EDV represented by SV
43
Q

What is cardiac output?

A

The volume pumped by LV in 1 minute.

CO = HR*SV

44
Q

What are some factors that affect cardiac output?

A

Can be adjusted by changes in HR or SV

HR: by ANS or hormones
SV: by changing EDV or ESV

45
Q

Cardiodynamics: Autonomic Innervation

A
  • Cardiac plexuses innervate the heart
  • Vagus nerve (N X) carry parasympathetic preganglionic fibers to small ganglia in cardiac plexus
  • Cardiac centers of medulla oblongota
  • – Cardioacceleratory center: sympathetic
  • – Cardioinhibitory center: parasympathetic
46
Q

Important receptors and functions in the heart

A

Cholinergic

Muscarinic

Angiotensin

47
Q

Cholinergic receptors in the heart

A

Activated by parasympathetic

  • M2 muscarinic receptors, mainly in SA node
  • M2 activation: Reduces HR (negative chronotropic)
48
Q

Adrenergic receptors in the heart

A

Activated by sympathetic

  • beta1 adrenergic receptors in myocardium, SA node
  • beta1 activation: Increases contractility (positive inotropic); increases HR (positive chronotropic)
49
Q

Angiotensin receptors in the heart

A

Hormone that increases force of contraction, increasing BP

- AT1 myocardium: positive inotropy

50
Q

What do cardiac centers monitor and what is their function?

A
  • BP (baroreceptors)
  • Arterial O2 and CO2 levels (chemoreceptors)

They adjust cardiac activity

51
Q

How is resting autonomic tone maintained?

A

Dual innervation, releasing ACh and NE

52
Q

Is the membrane potential of SA node/pacemaker cells higher or lower compared to other cardiac cells?

A

Lower

Closer to threshold than other cardiomyocytes. Their plasma membranes undergo spontaneous depolarization to threshold, producing action potentials at a frequency determined by (1) resting-membrane potential and (2) rate of depolarization

53
Q

What is the rate of spontaneous depolarization dependent upon?

A
  • Resting membrane potential

- Rate of depolarization

54
Q

Where in the heart is sympathetic and parasympathetic stimulation the greatest?

A

SA node (HR)

55
Q

Does ACh have a sympathetic or parasympathetic effect on the heart?

A

Parasympathetic

56
Q

Does NE have a sympathetic or parasympathetic effect on the heart?

A

Sympathetic

57
Q

How does parasympathetic stimulation release ACh?

A

Extends repolarization and decreases rate of spontaneous depolarization

58
Q

How does sympathetic stimulation release NE?

A

Shortens repolarization and accelerates the rate of spontaneous depolarization

59
Q

What is the atrial reflex?

A

AKA Bainbridge reflex

  • Adjusts HR in response to venous return
  • Stretch receptors in RA
  • – Trigger increase in HR
  • – Through increased sympathetic activity
60
Q

What are hormonal effects on HR?

A

Increase HR by sympathetic stimulation on SA node

  • Epinephrine (E)
  • Norepinephrine (NE)
  • Thyroid hormone
61
Q

What are some factors that affect stroke volume?

A

The EDV amount of blood a ventricle contains at the end of a diastole

  • Filling time
  • – Duration of ventricular diastole
  • – Can change with rate
  • Venous return
  • – Rate of blood flow during ventricular diastole
  • – Vasodilaton and vasoconstriction can change this
  • – Losing blood, you don’t have a lot going back, can also change venous return
62
Q

What are three factors that affect ESV?

A
  1. Preload
    - Ventricular stretching during diastole
    - Fibrous tissue can create this
  2. Contractility
    - Force produced during contraction at a given preload
    - Ability of the heart to contract - hormones, ANS
  3. Afterload
    - Tension the ventricle produces to open the semilunar valve and eject blood
    - Tension put on ventricles when they’re trying to push blood out
63
Q

What is preload?

A
  • The degree of ventricular stretching during ventricular diastole
  • Directly proportional to EDV
  • Affects ability of muscle cells to produce tension
64
Q

What is EDV and stroke volume at rest?

A
  • EDV is low
  • Myocardium stretches less
  • SV is low
65
Q

What is EDV and stroke volume with exercise?

A
  • EDV increases
  • Myocardium stretches more which allows it to contract better, therefore
  • SV increases
66
Q

Frank-Starling Principle

A

As EDV increases, SV increases.

In normal hearts, this property helps to pump out the blood received by the heart without excessive accumulation.

The force of contraction of myocardium is directly proportional to the stretch of the muscle (preload) i.e. more blood in ventricle = more forceful contraction

67
Q

What are some limiting factors for ventricular expansion?

A
  • Myocardial CT
  • Cardiac (fibrous) skeleton
  • Pericardial sac
68
Q

End-Systolic Volume (ESV)

A

The amount of blood that remains in the ventricle at the end of ventricular systole

69
Q

Effects of sympathetic stimulation on contractility

A
  • NE released by postganglionic fibers of cardiac nerves
  • Epi and NE released by adrenal medullae
  • Causes ventricles to contract with more force
  • Increases ejection fraction and decreases ESV
70
Q

Effects of parasympathetic stimulation on contractility

A
  • ACh released by Vagus nerves

- Reduces forces of cardiac contractions

71
Q

What types of pharmaceutical drugs mimic hormone actions

A
  • Beta receptor blockers/stimulators

- Calcium channel blockers

72
Q

Afterload

A
  • Increased by any factor that restricts arterial blood flow

- As afterload increases, SV decreases

73
Q

What are HR control factors?

A
  • ANS - sympathetic and parasympathetic
  • Circulating hormones
  • Venous return and stretch receptors
74
Q

What are SV control factors?

A
  • EDV - filling time, rate of venous return

- ESV - preload, contractility, afterload

75
Q

What does CV regulation ensure?

A

Adequate circulation to body tissues

76
Q

What do CV centers do?

A

Control heart and peripheral BVs

77
Q

What does CV system respond to?

A
  • Changing activity patterns

- Circulatory emergencies

DMD 5247 (7 decks)

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