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Human Physiology > cardiac > Flashcards

cardiac Flashcards

1
Q

differences between myocyte and skeletal muscle cells

A

1) Cardiac longer action potential (0.3 sec)
2) Action potential triggered at SA node in cardiac
3) Myocytes connected via gap junctions
4) 3rd ion (Ca2+) involved in cardiac action potential
5) L-type channel in cardiac cells

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2
Q

Similarities between skeletal and cardiac muscles

A

Fast Na+ conductance

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3
Q

What gives myocytes the possibility to have an extended action potential?

A

L-type Ca2+ channels

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4
Q

How does the L-type channel impact the duration of cardiac AP?

A

1) Longer refractory period so we have electrical control of cardiac myocytes, pacing refilling time, and to prevent myocyte fatigue

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5
Q

Why is a long refractory period important in the myocyte?

A

so we have electrical control of cardiac myocytes, pacing refilling time, and to prevent myocyte fatigue. Also this allows for longer AP

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6
Q

Describe the electrical pathway in the heart

A

AP begins in SA node, travels to AV node, down Bundle of His, separates into 2 Bundle branches and then wraps ventricles via Purkinje fibers

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7
Q

What is stage 4 of the SA node called?

A

Pacemaker potential

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8
Q

Pacemaker potential

A
  • present in smooth muscle and cardiac nodal cells
  • absent in skeletal muscle
  • in nodal cells, F-type cells trigger potential
  • T-type channels contribute to potential in nodal cells
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9
Q

Why are F-type channels latent in Purkinje fibers?

A

They don’t get a chance to conduct depolarization unless blockage at SA or AV node present

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10
Q

What happens to ion channels during pacemaker potential of nodal cell?

A

Decrease K current
Increase F current, increasing Na+ permeability
Increase in T-type Ca current

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11
Q

What kinds of ANS receptors impact nodal cells?

A

SA and AV nodes receive innervation from both sympathetic and parasympathetic on β1 and M2 receptors, respectively

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12
Q

What happens when Beta-1 receptors are stimulated on myocyte and cardiac pacemaker?

A

Gs - adenylyl cyclase - cAMP - PKA opens Ca2+ channel: increase Ca2+ conductance, increasing contractility and HR (due to more rapid depolarization)

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13
Q

What happens when M-2 receptors are stimulated on myocyte and cardiac pacemaker?

A

Gi- dissasociates alpha subunit and Beta subunit directly opens K+ channel: increases K+ conductance to slow action potential and decrease HR, faster action than sympathetic innervation

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14
Q

What are chronotropic effects?

A

Changes to heart rate; SA node targeted

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15
Q

What determines maximum heart rate?

A

Duration of relative refractory period; intrinsic rhythm of SA and AV nodes

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16
Q

Which arm of the ANS has a more dominant effect on cardiac function?

A

Sympathetic; parasympathetic via vagus nerve impacts the atria and the HR (but not the ventricle)

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17
Q

What properties of smooth and skeletal muscle cells do myocytes share?

A 
Striated – organized, repeating unit
Na+ action potential
Ca2+ action potential
SLOW myosin ATPase (10-100 fold slower)
Small – not diffusion limited (O2, EC Ca2+)
Actin regulated contraction
Not all actin sites bind Ca++
Many gap junctions for some organs
Diffuse autonomic innervation en passant
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18
Q

What is the intrinsic rate of the heart?

A

Without parasympathetic innervation is about 100 (~70 with parasympathetic influence)

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19
Q

How do you achieve stronger contractility of heart?

A

Stronger levels of Ca2+ release from SR

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20
Q

How many cardiac cells are excited with each AP?

A

All cardiac myocytes (due to gap junctions)

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21
Q

Where is the portal system found?

A

Liver and anterior pituitary gland

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22
Q

What is a portal system and why is it critical?

A

2 capillary beds linked by a vein. In the liver, gives extra time for nutrient and toxin absorption and filtration

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23
Q

What percentage of blood do the abdominal organs receiving at rest?

A

24%

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24
Q

What organs receive increased blood flow during exercise?

A

Skeletal, skin,

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25
Q

What are the 3 layers of the heart wall and their primary function?

A

Epicardium (thick inner layer of endothelial cells), myocardium (cardiac muscle), endocardium (external membrane)

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26
Q

Why is the wall of the left ventricle so much thicker than the right?

A

Higher resistance following left side of the heart as it pumps blood out to the systemic circulation

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27
Q

Which artery is most likely to be effected by infraction or blockage?

A

Left anterior descending artery (LAD)

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28
Q

How allows cardiac electrical conduction to directly effect myocyte?

A

Intercalated disks

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29
Q

Why is the AV nodal delay important?

A

Critical to allow atria to finish contraction before ventricles begin contraction

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30
Q

What happens in AV conduction disorder?

A

reduced or eliminated transmission from SA node to AV node; Bundle of His and Purkinje fibers begin firing at their intrinsic rate (25 - 40 BPM); ventricles are out of synchrony with the atria, decreasing cardiac efficiency

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31
Q

How is the ECG signal proportional to muscle mass?

A

Greater number of cells depolarized, the larger the depol size; signal generated by the atria will be smaller than the ventricles

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32
Q

What electrical activity is represented in the P-wave of the ECG?

A

SA node depolarizes (beginning of P wave) and the P-wave peaks with when signal arrives to AV node and atria have been told to contract

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33
Q

What electrical activity is represented in the QRS-complex of the ECG?

A

Beginning, atria relax and QRS peak signals rapid ventricular depolarization

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34
Q

What electrical activity is represented in the T-wave of the ECG?

A

Ventricular repolarization

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35
Q

What do you want to measure in AV nodal delay?

A

P-R interval

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36
Q

When do you hear heart sounds?

A

You hear turbulent blood flow in response to valve closure.
Lub is heard during systole when AV valves close with QRS complex
Dub is heard during diastole just after T wave when semilunar valves close

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37
Q

Describe pressure change in AV valves

A

Low pressure valve opens when chamber relaxed and pressure less than atrium

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38
Q

Describe pressure change in semilunar valves

A

High pressure valve opens when chamber pressure exceeds pressure in aorta or pulmonary trunk

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39
Q

If ventricular volume decreases, what happens to pressure?

A

Increase

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40
Q

What changes pressure in heart?

A

Contraction, which changes volume

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41
Q

What happens during isovolumetric contraction of heart?

A

All valves are closed; atria are relaxed while ventricles are contracted.

42
Q

What are the two phases of systole?

A

Isovolumetric contraction and ventricular ejection

43
Q

What are the two phases of diastole?

A

Isovolumetric relaxation & ventricular filling (AV valves open and atria kick a passive amount of blood flow following ventricular filling)

44
Q

What is represented by the dicrotic notch?

A

Turbulent blood flow due to delayed closure of the aortic valve as diastole begins

45
Q

What is stroke volume?

A

volume of blood ejected from ventricle each cycle, roughly 70 mL
Also = EDV - ESV

46
Q

What is EDV (end diastolic volume)?

A

volume of blood in ventricle at the end of diastole, roughly 130 mL

47
Q

Normal blood flow

A

laminar

48
Q

What is happening when turbulent blood flow is auscultated with a stethascope?

A

Stenosis = blood flowing rapidly in the usual direction through an abnormally narrowed valve

Insufficiency = blood flowing backward through a damaged, leaky valve

Septal Defect = blood flowing between the two atria or two ventricles through a small hole in the wall separating them.

49
Q

What is the main function of the heart?

A

Produce cardiac output

50
Q

How do you calculate cardiac output?

A

Stroke Volume (EDV - ESV) x HR

51
Q

About how much is cardiac output per minute in a healthy adult?

A

5 L/min

52
Q

What factors influence stroke volume?

A

Changes in end-diastolic volume (preload)
Changes in sympathetic input
Changes in arterial pressure (afterload)

53
Q

What is the main property the heart will defend?

A

End-systolic volume

54
Q

What are the implications if the heart did not defend its ESV?

A

Eventually the ventricle would dilate and overfill and fibers would stretch passed their optimal length, decreasing squeeze.

55
Q

What will determine the starting length of the cardiac muslce?

A

collagenous skeleton

56
Q

What is implied with the Fran-Starling Law?

A

The strength of contraction increases proportionally to volume delivered
Greater EDV, the greater the SV
What goes in, must come out to maintain constant ESV
Intrinsic property of heart

57
Q

What factors effect EDV?

A

Filling time
Atrial pressure
Central venous pressure

58
Q

What does the Frank-Starling Law predict for ESV?

A

It will remain constant

59
Q

What are dromotropic effects?

A

Act on AV node and conduction fibers to optimize conduction

60
Q

What are inotropic effects?

A

Contractility impacted by contractile fibers stimulated

61
Q

What is a method to impact contraction speed of heart?

A

Increase intracellular Ca2+ to optimize troponin binding sites

62
Q

How many troponin molecules are bound my Ca2+ in myocyte rest?

A

1 in 4

63
Q

What happens with sympathetic stimulation of the heart?

A

Increase magnitude and rate of contraction

Stroke Volume increased without changing EDV

64
Q

Where does Ca2+ come from in cardiac muscle?

A

Extracellular fluid and SR

65
Q

How does sympathetic stimulation impact Ca2+ regulation in the cardiac cell?

A

1) Beta-1 receptor (via adenylyl cyclase and PKA pathway) increases L-type channel opening for Ca2+ influx into cell, increasing force and rate of contraction
2) Ca2+ influx causes calcium release from SR
3) Beta-1 receptor PKA acts on phospholamben (PLB) to increase SERCA-2 pump to pump Ca2+ back into SR

66
Q

How is Ca2+ pumped faster back into SR?

A

Beta-1 receptor PKA acts on phospholamben (PLB) to increase efficency of SERCA-2 pump to pump Ca2+ back into SR

67
Q

What is ejection fraction?

A

SV / EDV
total volume of heart is being ejected
increases with increased contractility

68
Q

What does cardiac contractility increase?

A

Stroke volume but not EDV

69
Q

Which form of cardiac work is more metabolically costly?

A

Pressure change (Volume work is easier)

70
Q

Describe how enhanced cardiac output is achieved in trained athletes

A

A larger resting stroke volume due to larger heart size. This leads to a lower resting HR (COP = SV x HR) and an increased HR reserve

71
Q

What is the larger driver of increased COP with exercise?

A

Dramatic increase in HR

72
Q

Phospholamben

A

Protein at the SR SERCA pump
Increases contractility by stimulating increased pump of Ca2+ back into SR and subsequent increased release of Ca2+ from SR

73
Q

What is mainly regulated by COP and TPR?

A

MAP

74
Q

What impacts TPR?

A

Arteriolar radius and length and blood viscosity

75
Q

What lines all vasculature?

A

endothelium

76
Q

What are the functions of endothelial cells?

A
  • Physical lining in heart and blood vessels to which blood cells do not normally adhere
  • Permeability barrier for the exchange of nutrients, metabolic end products, and fluid between plasma and interstitial fluid; regulate transport of macromolecules and other substances
  • Secrete paracrine agents that act on adjacent vascular smooth muscle cells, including vasodilators such as prostacyclin and nitric oxide (endothelium-derived relaxing factor [EDRF]), and vasoconstrictors such as endothelin-1
  • Mediate angiogenesis (new capillary growth)
  • Central function in vascular remodeling by detecting signals and releasing paracrine agents that act on adjacent cells in the blood vessel wall
  • Contribute to the formation and maintenance of extracellular matrix
  • Produce growth factors in response to damage
  • Secrete substances that regulate platelet clumping, clotting, and anticlotting
  • Synthesize active hormones from inactive precursors
  • Extract or degrade hormones and other mediators
  • Secrete cytokines during immune responses
77
Q

What are the passive elements of a vessel wall

A

elastin and collagen

78
Q

What is the active element of a vessel wall

A

smooth muscle

79
Q

Elastic tubes that act as pressure reservoirs for the heart

A

aorta and arteries

80
Q

compliance

A

how easily something can be stretched

change in volume / change in pressure

81
Q

How do elastic fibers impact compliance?

A

Elastin decreases stretch. Veins, which have less elastin, are more easily stretched than arteries

82
Q

how will the deposition of plaque alter the elastic nature of the aorta?

A

Decrease

83
Q

responsible for determining relative blood flow to individual organs at any given MAP

A

arterioles

84
Q

major factor in determining MAP itself

A

arterioles

85
Q

Biggest way to regulate flow to organ systems

A

alter resistance to vascular bed. Mainly done by changing diameter of the tube

86
Q

flow math

A

= change in pressure / resistance

87
Q

Poiseuille Equation

A

(8)(length)(viscosity) / pie(radius to the 4th power)

88
Q

What happens if you double the radius of an artery?

A

It will result in a 16-fold decrease in resistance & a 16-fold increase in flow

89
Q

ANS innervation of vascular smooth muscle

A
  • coupled by gap junctions
  • innervated only by postganglionic sympathetic fibers
  • constrict or dilate depending on type of adrenergic receptor
90
Q

Which adrenergic receptors are located on vascular smooth muscle and what do they do?

A

alpha-1: constrict

Beta-2: dilate

91
Q

which vascular smooth muscle beds are beta-2 receptors primarily located on?

A

coronaries, lungs & large muscles

92
Q

local control vasodilaters of arteriolar radius

A

decreased O2

K+, CO2, H+, osmolarity, adenosine, eicosanoids, bradykinin, substances released during injury, Nitric oxide

93
Q

What is the ultimate goal of vascular smooth muscle regulation?

A

regulate MAP

94
Q

In which vessel is blood flow the slowest and why?

A

Capillaries to maximize nutrient exchange

95
Q

Which force changes from arteriole to venule end?

A

capillary hydrostatic pressure

96
Q

What happens o capillary exchange in a patient with liver disease who reduced production of plasma proteins?

A

Reduced absorption

97
Q

What is the site of control for arterial pressure in the capillary?

A

arteriole

98
Q

What is the major factor being regulated by cardiovascular control?

A

MAP

99
Q

What receptors detect changes in MAP?

A

Chemoreceptors and baroreceptors

100
Q

What happens to sensory input from baroreceptors when BP decreases?

A

Decreased firing, causes increase sympathetic discharge

101
Q

What happens to aleveolar pressure with inspiration?

A

Decreased alveolar pressure

102
Q

Why is the pressure in the interpleural space negative?

A

Surface tension holds 2 pleural membranes together, which helps oppose chest wall pulling out and lungs pulling in

Human Physiology (5 decks)

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