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cardiac Flashcards

(102 cards)

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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
What are the 3 layers of the heart wall and their primary function?
Epicardium (thick inner layer of endothelial cells), myocardium (cardiac muscle), endocardium (external membrane)
26
Why is the wall of the left ventricle so much thicker than the right?
Higher resistance following left side of the heart as it pumps blood out to the systemic circulation
27
Which artery is most likely to be effected by infraction or blockage?
Left anterior descending artery (LAD)
28
How allows cardiac electrical conduction to directly effect myocyte?
Intercalated disks
29
Why is the AV nodal delay important?
Critical to allow atria to finish contraction before ventricles begin contraction
30
What happens in AV conduction disorder?
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
31
How is the ECG signal proportional to muscle mass?
Greater number of cells depolarized, the larger the depol size; signal generated by the atria will be smaller than the ventricles
32
What electrical activity is represented in the P-wave of the ECG?
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
33
What electrical activity is represented in the QRS-complex of the ECG?
Beginning, atria relax and QRS peak signals rapid ventricular depolarization
34
What electrical activity is represented in the T-wave of the ECG?
Ventricular repolarization
35
What do you want to measure in AV nodal delay?
P-R interval
36
When do you hear heart sounds?
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
37
Describe pressure change in AV valves
Low pressure valve opens when chamber relaxed and pressure less than atrium
38
Describe pressure change in semilunar valves
High pressure valve opens when chamber pressure exceeds pressure in aorta or pulmonary trunk
39
If ventricular volume decreases, what happens to pressure?
Increase
40
What changes pressure in heart?
Contraction, which changes volume
41
What happens during isovolumetric contraction of heart?
All valves are closed; atria are relaxed while ventricles are contracted.
42
What are the two phases of systole?
Isovolumetric contraction and ventricular ejection
43
What are the two phases of diastole?
Isovolumetric relaxation & ventricular filling (AV valves open and atria kick a passive amount of blood flow following ventricular filling)
44
What is represented by the dicrotic notch?
Turbulent blood flow due to delayed closure of the aortic valve as diastole begins
45
What is stroke volume?
volume of blood ejected from ventricle each cycle, roughly 70 mL Also = EDV - ESV
46
What is EDV (end diastolic volume)?
volume of blood in ventricle at the end of diastole, roughly 130 mL
47
Normal blood flow
laminar
48
What is happening when turbulent blood flow is auscultated with a stethascope?
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
What is the main function of the heart?
Produce cardiac output
50
How do you calculate cardiac output?
Stroke Volume (EDV - ESV) x HR
51
About how much is cardiac output per minute in a healthy adult?
5 L/min
52
What factors influence stroke volume?
Changes in end-diastolic volume (preload) Changes in sympathetic input Changes in arterial pressure (afterload)
53
What is the main property the heart will defend?
End-systolic volume
54
What are the implications if the heart did not defend its ESV?
Eventually the ventricle would dilate and overfill and fibers would stretch passed their optimal length, decreasing squeeze.
55
What will determine the starting length of the cardiac muslce?
collagenous skeleton
56
What is implied with the Fran-Starling Law?
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
What factors effect EDV?
Filling time Atrial pressure Central venous pressure
58
What does the Frank-Starling Law predict for ESV?
It will remain constant
59
What are dromotropic effects?
Act on AV node and conduction fibers to optimize conduction
60
What are inotropic effects?
Contractility impacted by contractile fibers stimulated
61
What is a method to impact contraction speed of heart?
Increase intracellular Ca2+ to optimize troponin binding sites
62
How many troponin molecules are bound my Ca2+ in myocyte rest?
1 in 4
63
What happens with sympathetic stimulation of the heart?
Increase magnitude and rate of contraction | Stroke Volume increased without changing EDV
64
Where does Ca2+ come from in cardiac muscle?
Extracellular fluid and SR
65
How does sympathetic stimulation impact Ca2+ regulation in the cardiac cell?
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
How is Ca2+ pumped faster back into SR?
Beta-1 receptor PKA acts on phospholamben (PLB) to increase efficency of SERCA-2 pump to pump Ca2+ back into SR
67
What is ejection fraction?
SV / EDV total volume of heart is being ejected increases with increased contractility
68
What does cardiac contractility increase?
Stroke volume but not EDV
69
Which form of cardiac work is more metabolically costly?
Pressure change (Volume work is easier)
70
Describe how enhanced cardiac output is achieved in trained athletes
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
What is the larger driver of increased COP with exercise?
Dramatic increase in HR
72
Phospholamben
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
What is mainly regulated by COP and TPR?
MAP
74
What impacts TPR?
Arteriolar radius and length and blood viscosity
75
What lines all vasculature?
endothelium
76
What are the functions of endothelial cells?
- 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
What are the passive elements of a vessel wall
elastin and collagen
78
What is the active element of a vessel wall
smooth muscle
79
Elastic tubes that act as pressure reservoirs for the heart
aorta and arteries
80
compliance
how easily something can be stretched | change in volume / change in pressure
81
How do elastic fibers impact compliance?
Elastin decreases stretch. Veins, which have less elastin, are more easily stretched than arteries
82
how will the deposition of plaque alter the elastic nature of the aorta?
Decrease
83
responsible for determining relative blood flow to individual organs at any given MAP
arterioles
84
major factor in determining MAP itself
arterioles
85
Biggest way to regulate flow to organ systems
alter resistance to vascular bed. Mainly done by changing diameter of the tube
86
flow math
= change in pressure / resistance
87
Poiseuille Equation
(8)(length)(viscosity) / pie(radius to the 4th power)
88
What happens if you double the radius of an artery?
It will result in a 16-fold decrease in resistance & a 16-fold increase in flow
89
ANS innervation of vascular smooth muscle
- coupled by gap junctions - innervated only by postganglionic sympathetic fibers - constrict or dilate depending on type of adrenergic receptor
90
Which adrenergic receptors are located on vascular smooth muscle and what do they do?
alpha-1: constrict | Beta-2: dilate
91
which vascular smooth muscle beds are beta-2 receptors primarily located on?
coronaries, lungs & large muscles
92
local control vasodilaters of arteriolar radius
decreased O2 | K+, CO2, H+, osmolarity, adenosine, eicosanoids, bradykinin, substances released during injury, Nitric oxide
93
What is the ultimate goal of vascular smooth muscle regulation?
regulate MAP
94
In which vessel is blood flow the slowest and why?
Capillaries to maximize nutrient exchange
95
Which force changes from arteriole to venule end?
capillary hydrostatic pressure
96
What happens o capillary exchange in a patient with liver disease who reduced production of plasma proteins?
Reduced absorption
97
What is the site of control for arterial pressure in the capillary?
arteriole
98
What is the major factor being regulated by cardiovascular control?
MAP
99
What receptors detect changes in MAP?
Chemoreceptors and baroreceptors
100
What happens to sensory input from baroreceptors when BP decreases?
Decreased firing, causes increase sympathetic discharge
101
What happens to aleveolar pressure with inspiration?
Decreased alveolar pressure
102
Why is the pressure in the interpleural space negative?
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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