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cardiovascular system Flashcards

1
Q

Name the type of receptors for norepinephrine on cardiac muscle?

A

beta-adrenergic

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2
Q

Name the type of receptors for acetylcholine on cardiac muscle?

A

muscarinic

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3
Q

Which blood vessels supply blood to the myocardium?

A

The coronary arteries

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4
Q

factors that limit the increase in SV (and thus cardiac output):

A
  • very rapid heart rate which decreases diastolic filling time
  • inability of the peripheral factors favoring venous
    return (skeletal muscle pump, respiratory pump, venous
    vasoconstriction, arteriolar vasodilation) to increase
    ventricular filling further during the very short time
    available
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5
Q

An individuals VO2 max can be altered by?

A

habitual level of physical activity

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6
Q

Increase in SV due to training is caused by:

A

effects on the heart (hypertrophy + increase in chamber size)
peripheral effects (increased blood vol + number of blood vessels = increased muscle blood flow + venous return)

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7
Q

How does aging influence heart performance during exercise?

A

decrease in max heart rate (+ cardiac output) due to increased stiffness of heart which decreases its ability to rapidly fill during diastole

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8
Q

How is the left ventricle affected by hypertension?

A

It has to pump blood against an increased arterial pressure = develops adaptive increase in muscle mass called left ventricular hypertrophy

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9
Q

Primary hypertension

A

hypertension of uncertain cause

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10
Q

secondary hypertension

A

when there is an identified cause

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11
Q

potential genetic causes of primary hypertension?

A

genes coding for enzymes involved in the renin-angiotensin-aldosterone system and some involved in the regulation of endothelial cell function and arteriolar smooth muscle contraction

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12
Q

What is the most significant factor causing primary hypertension?

A

increased total peripheral resistance caused by reduced arteriolar radius

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13
Q

Environmental risk factors of primary hypertension?

A

Obesity, insulin resistance, chronic high salt intake, elevations in plasma Na+ levels, smoking, excessive alcohol consumption, chronic stress

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14
Q

Causes of secondary hypertension? + treatments

A

damage to kidneys or their blood supply = renal hypertension (increased renin = increased angiotensin II + aldosterone = insufficient urine secretion + Na+ retention = increased extracellular fluid vol) (treatments: diuretics or low-sodium diet)

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15
Q

What is heart failure?

A

collection of signs + symptoms that occur when the heart does not pump an adequate cardiac output

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16
Q

Some causes of heart failure:

A

chronically increased arterial pressure (hypertension), structural damage to the myocardium due to decreased coronary blood flow

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17
Q

2 categories of heart failure:

A

those with diastolic dysfunction, those with systolic dysfunction

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18
Q

What occurs in diastolic dysfunction?

A

the wall of the ventricle has
reduced compliance.
This abnormal stiffness = reduced ability to fill adequately at normal diastolic filling pressures = reduced end-diastolic volume = reduced stroke volume
ventricular compliance decreased but ventricular contractility is normal

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19
Q

What causes the decreased ventricular compliance in diastolic dysfunction in heart failure?

A

systemic hypertension (hypertrophy = ventricle stiffens)

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20
Q

What occurs in systolic dysfunction?

A

Results from myocardial damage
Decrease in cardiac contractility (a lower stroke volume at any given
end-diastolic volume) = decrease in ejection fraction + a downward shift of the ventricular-function curve.
Affected ventricle does not hypertrophy, but end-diastolic volume increases.

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21
Q

What happens when there is reduced cardiac output of heart failure?

A

triggers arterial baroreceptor reflexes
baroreceptors discharge less rapidly than normal = brain interprets this decreased discharge as a larger-than-usual decrease in pressure

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22
Q

What are the results of the baroreceptor reflexes triggered in heart failure?

A
  • heart rate increased via increased sympathetic activation of heart + decreased parasympathetic
  • total peripheral resistance increased via increased sympathetic activation of systemic arterioles + via increased plasma conc of angiotensin II + ADH (vasoconstrictors)

initially beneficial in restoring cardiac output + arterial pressure

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23
Q

Effects of chronically maintained baroreceptor reflexes during period of heart failure?

A
  • fluid retention = expansion of extracellular fluid vol = increases venous pressure, venous return, and E-DV vol = restores SV toward normal

because reflex causes kidneys to reduce their excretion of sodium + water

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24
Q

What issues start to arise as fluid retention progresses in the baroreceptor reflex?

A
  • ventricle with systolic dysfunction becomes distended with blood + its force of contraction decreases = worsening heart failure state
  • as it increases venous pressure = edema (accumulation of interstitial fluid) = swelling of feet and legs
  • increase in total peripheral resistance = makes failing heart work harder
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25
Q

What are the effects and causes of (heart) failure of the left ventricle which leads to pulmonary edema (accumulation of fluid in interstitial space or in air spaces)?

(another issue of reflex)

A

impairs pulmonary gas exchange
cause: left ventricle fails to pump blood to the same extent as the right ventricle = vol of blood in all the pulmonary vessels increases.
engorgement of pulmonary capillaries increases capillary pressure above its normally very low value = filtration occurs faster than the lymphatics can remove
the fluid

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26
Q

Which side of the heart is the aurical located on?

A

the ventral side

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27
Q

What collects all the blood from the heart muscle itself?

A

The coronary sinus

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28
Q

What are the 3 openings of the right atrium?

A

inferior / superior vena cava + coronary sinus

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28
Q

Order of blood flow from lungs?

A

Pulmonary veins > left atrium > bicuspid valve > left ventricle

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29
Q

Order of blood flow from right atrium?

A

tricuspid valve > right ventricle > pulmonary valve > pulmonary trunk > lungs

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29
Q

Is it worse to have an infarction to the left or right side of the heart?

A

Left side infarction has worst outcome than right since muscle in middle is more left-belonging

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30
Q

When does excess blood flow into the coronary arteries?

A

Not all blood will make it past the aortic arch: some blood goes back (but valves are blocking opening) so the blood pools in the cusp of the valves and flows into coronary arteries

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31
Q

Which part of embryotic development does the heart arise from?

A

Intermediate mesoderm

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32
Q

How are nutrients and metabolic end products transported?

A

move between capillary blood and interstitial fluid via diffusion

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33
Q

Systemic circulation:

A

blood pumped from left ventricle through all organs and tissues of the body and then to the right atrium

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34
Q

Pulmonary circulation:

A

blood pumped from right ventricle through the lungs and then into the left atrium

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35
Q

Which vessels carry blood away from the heart?

A

arteries

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36
Q

Which vessels carry blood from organs and tissue back to the heart?

A

veins

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37
Q

Microcirculation:

A

arterioles > capillaries > venules

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38
Q

Determinants of resistance:

A

viscosity, length + radius of tube

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39
Q

What is the heart enclosed by?

A

pericardium (sac) + epicardium (fibrous layer)

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40
Q

What is the Inner surface of chambers + inner wall of blood vessels called?

A

endothelium

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41
Q

What separates the ventricles?

A

interventricular septum

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42
Q

AV valves:

A

right (tricuspid valve) + left (bicuspid valve/mitral valve)

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43
Q

To prevent AV valves opening backwards:

A

they are fastened to papillary muscles by chordae tendinae

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44
Q

Semilunar valves:

A

Pulmonary valve (right ventricle into pulmonary trunk) + aortic valve (left ventricle into aorta)

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45
Q

Which cells form part of cardiac muscle? + what do they do

A

Cardiac muscle cells: A.P, Ca2+ enters cytosol, force-generating cross-bridges
Specialized non-contractile cells: initiate cardiac A.P + regulate their spread through the heart

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46
Q

Cardiac innervation:

A

sympathetic (postganglionic fibers innervate entire heart + release norepinephrine) + parasympathetic nerve fibers (contained in the vagus nerves) (terminate on special cells in the atria + release primarily acetylcholine)

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47
Q

What characteristic allows A.P conduction from cell to cell in the heart?

A

Myocardial cells are joined by gap junctions

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48
Q

Where does initial depolarization (trigger for contraction) arise?

A

in the SA node (located in the right atrium near superior vena cava)

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49
Q

What is the travel route for the A.P?

A

SA node > throughout atria > into ventricles

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50
Q

Which factor of the excitation determines the heart rate?

A

Discharge rate of the SA node

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51
Q

What links atrial depolarization and ventricular depolarization?

A

AV node (base of right atrium)

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52
Q

What happens when the AV node has been excited?

A

A.P propagates down the interventricular septum (this pathway has a conducting-system of fibers called the AV bundle/bundle of His)

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53
Q

What characteristic allows the ventricles to contract almost simulatneously?

A

Rapid conduction along purkinje fibers

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53
Q

What characteristic of the interventricular septum aids conduction of A.P?

A

a conducting-system of fibers called the bundle of His

54
Q

Where does the A.P propagate to once it arrives at the bundle of His?

A

bundle of His separates into left + right bundle branches (composed of purkinje fibers) which travel down the septum and separate at the apex and go up into their respective ventricle walls

55
Q

What is the mechanism behing initiating the A.P that results in heart contraction?

A

the controlled exchange of ions across cellular membranes

56
Q

In myocardial cell A.P which ions cause the depolarization?

A

opening of voltage-gated Na+ channels (positive feedback)

57
Q

In myocardial cell A.P what occurs after depolarisation + which ions are involved?

A

Reduction of Na+ permeability = partial repolarization due to transiently open K+ channels (membrane remains depolarized at a plateau ~0 mV)

58
Q

In myocardial cell A.P what occurs after partial repolarization + which ions are involved?

A

Large increase in the cell membranes permeability to Ca2+ occurs (plateau as it balances out the flow of K+ ions out of the cells)

59
Q

In myocardial cell A.P which ions cause repolarization?

A

inactivation of these L-type Ca2+ channels + opening of a different type of K+ channel which close once repolarization is reached

60
Q

In a nodal cell A.P what is different about its SA node?

A

SA node does not have a steady resting potential (it undergoes a slow depolarization, known as pacemaker potential)

61
Q

Which ions make up the pacemaker potential in nodal cell A.P?

A

Progressive reduction in K+ permeability (from previously opened ones from the repolarization of the last A.P), Na+ conducted in by unique F-type channels, Ca2+ inwards by T-type channels

62
Q

In nodal cell A.P after threshold has been reached what ions cause depolarization?

A

Ca2+ influx by L-type channels (these channels cause A.P to propagate more slowly)

63
Q

In nodal cell A.P which ions are involved in repolarization?

A

L-type Ca2+ channels eventually close + K+ channels open and membrane is repolarized

64
Q

In nodal cell A.P what happens if the AV node is disrupted?

A

ventricles contract out of synchrony with the atria as no transmission between atria + ventricle = cells in bundle of His + purkinje fibers initiate their own excitation at their own rate = artificial pacemaker is implanted so ventricular cells are stimulated at normal rate

65
Q

What are the electrodes in an ECG measuring?

A

currents conducted through body fluids which occur in myocardial cells when A.P is generated

66
Q

P wave:

A

current flow during atrial depolarization

67
Q

QRS complex:

A

ventricular depolarization

68
Q

T wave:

A

ventricular repolarization

69
Q

What is not seen on an ECG and why?

A

Atrial repolarization because it occurs at same time as QRS complex

70
Q

Why do shapes and sizes of the waves vary?

A

vary based on location of electrodes

71
Q

What triggers the generation of force for the contraction of the cardiac muscle?

A

Small amounts of extracellular Ca2+ entering through L-type Ca2+ channels (during plateau) triggers release of Ca2+ from sarcoplasmic reticulum
Ca2+ activation of thin filaments + cross-bridge cycling = generation of force

72
Q

When does contraction of cardiac muscle end?

A

when Ca2+ returned to sarcoplasmic reticulum + extracellular fluid

73
Q

What determines the strength of the contraction?

A

determined by the amount cytosolic Ca2+ conc is increased by during excitation

74
Q

What increases the number of active cross-bridges?

A

more release of Ca2+ from sarcoplasmic reticulum (as would occur during exercise for example)

75
Q

Refractory period of the heart:

A

Cardiac muscle incapable of undergoing summation of contractions
long absolute refractory period of cardiac muscle

76
Q

What enables the long absolute refractory period of cardiac muscle?

A

the main mechanism of this is the inactivation of Na+ channels and prolonged depolarized plateau

76
Q

Systole:

A

Isovolumetric ventricular contraction (ventricles contracting but all valves are closed = no blood ejection) + Ventricular ejection (pressure exceeds that of aorta and pulmonary trunk thus their valves open = blood ejected (vol ejected = stroke volume))

77
Q

Diastole:

A

Isovolumetric ventricular relaxation (all valves closed) + ventricular filling (AV valves open = blood flows in from atria)
Atrial contraction occurs at end of diastole

78
Q

What is happening to the left chambers, valves, and pressures during mid to late diastole?

A

Left atrium + ventricle relaxed, atrial pressure slightly higher than ventricular (because atrium is filling is filling with blood)
AV valve held open
(aortic valve is closed because its pressure is higher than ventricular)
Aortic pressure is slowly decreasing throughout (bc blood is moving out of arteries)
Ventricular pressure increasing slightly
SA node discharges, atria depolarize,
Contraction of atrium = increase in pressure = forces small additional vol of blood into ventricle
End-diastolic volume

79
Q

What is happening to the chambers, valves, and pressures during systole?

A

AV node, wave of depolarization throughout ventricle = ventricular contraction
Contraction = pressure increase + exceeds atrial pressure
AV valves close
Aortic valves closed bc aortic pressure exceeds ventricular
Backward bulging of AV valve = small upward deflection in atrial pressure
Ventricular pressure eventually exceeds aortic pressure
Aortic valve opens = ventricular ejection begins
End-systolic volume
Blood flows into aorta = aortic + ventricular pressure increases
Strength of ventricular contraction decreases + reduced rate of blood ejection
Volume + pressure in aorta decrease as rate of blood ejection from ventricles becomes slower than the rate that the blood drains out of the arteries

80
Q

What is happening to the chambers, valves, and pressures during early diastole?

A

Ventricles relax + pressure decreases below aortic P
Aortic valves close
Dicrotic notch (rebound of aortic P)
AV valve remains closed because ventricular P remains higher than atrial P
Rapidly decreasing ventricular P decreases below atrial P = opening of AV valve
Atrium venous blood flows into ventricles
Rate of blood flow enhanced due to rapid ventricular P decrease

81
Q

Calculation for SV?

A

Stroke vol = end-diastolic volume - end-systolic volume

82
Q

Lub:

A

closure of AV valves (onset of systole)

83
Q

Dup:

A

closure of pulmonary and aortic valves (onset of diastole)

84
Q

Heart murmurs:

A

sign of heart disease, can be produced by heart defects

85
Q

Turbulent flow:

A

can be caused by blood flowing rapidly in the unusual direction through a abnormally narrowed valve or can be by blood flowing backward through a damaged leaky valve or can be by blood flowing through the two atria or ventricles through a small hole

86
Q

Cardiac output:

A

the vol of blood each ventricle pumps as a function of time

87
Q

Steady state:

A

pulmonary and systemic circuit have same cardiac output

88
Q

Parasympathetic + sympathetic postganglionic neurons end on the ________

A

SA node

88
Q

Calculation for cardiac output

A

Cardiac output = Heart Rate x Stroke Volume

89
Q

Chronotropic effects:

A

Parasympathetic neurons = decrease in heart rate + Sympathetic = increase

90
Q

In resting state (~70 beats/min) is there more parasympathetic or sympathetic

A

parasympathetic

91
Q

What is the chronotropic effect of sympathetic stimulation ?

A

(opens Ca+ and Na+ channels) increases F-type channel permeability which increases slope of pacemaker potential = increase in depolarization = SA node reaches threshold more rapidly = increase heart rate

92
Q

What is the chronotropic effect of parasympathetic stimulation ?

A

slope of pacemaker potential decreases due to reduction of inward Na+ current. + also hyperpolarizes plasma membranes of SA node by increasing permeability to K+ so that pacemaker potential starts from a more negative value

93
Q

Dormotropic effects:

A

Symp stim also increases conduction velocity through entire cardiac conducting system
Parasym stim decreases the rate of spread of excitation through the atria + AV node

94
Q

How do hormones influence heart rate?

A

Epinephrine secreted by adrenal medulla = speeds up heart rate by acting on beta-adrenergic receptors in SA node (same ones norepinephrine act on)

95
Q

Factors influencing force during ejection of stroke vol:

A

Changes in end-diastolic vol
Changes in magnitude of sympathetic input to ventricles
Changes in afterload (arterial pressures against which the ventricles pump)

96
Q

How do changes in magnitude of sympathetic input to ventricles affect force during ejection of SV?

A
  • Norepinephrine acting on receptors increase ventricular contractility
    Stroke volume is greater at any given end-diastolic vol (so increased contractility = a more complete ejection of the end-diastolic ventricular vol)
  • Also causes contraction + relaxation of ventricles to occur more quickly
  • Several proteins involved in excitation-contraction coupling are phosphorylated by the kinase = enhances contractility
  • As the alterations of these proteins = cytosolic Ca2+ conc increases more quickly + reaches a greater value during excitation, Ca2+ returns to pre-excitation value more quickly, and rates of cross-bridge activation and cycling are accelerated
96
Q

How do changes in end-diastolic vol affect force during ejection of SV?

A
  • Ventricle contracts more forcefully during systole when it has been filled more during diastole
  • End-diastolic vol determines how stretched ventricular sarcomeres are, the greater the stretched the more forceful the contraction
  • Stretching decreases spacing between thin and thick filaments, increases sensitivity of troponin for binding Ca2+ and increases Ca2+ release from the sarcoplasmic reticulum
97
Q

How do changes in afterload affect force during ejection of SV?

A
  • Increased arterial pressure = reduce stroke vol
  • Arterial pressure constitutes a ‘load’ that contracting ventricles must work against
  • The greater the load the less contracting muscle fibers can shorten at a given contractility
98
Q

Function of an echocardiography?

A
  • 2D and 3D images of heart
  • detect abnormal functioning of cardiac valves or contractions of cardiac walls
  • measure ejection fraction
  • non invasive
99
Q

Function of a cardiac angiography?

A
  • invasive: temporary threading of catheter through an artery or vein into heart
  • liquid is injected through catheter during high-speed x-ray videography
  • identifies narrowed or completely blocked coronary arteries
100
Q

Factors to consider when reading signals of ECG?

A

Location of electrodes
Distance of electrodes to the heart
Size of the heart muscle

100
Q

What happens to pressure when standing?

A

intravascular pressure everywhere becomes equal to pressure generated by cardiac contraction PLUS additional pressure equal to the weight of a column of blood from the heart to the point of measurement
- increase in pressure due to gravity

101
Q

Effect of increased hydrostatic pressure?

A

Increased hydrostatic pressure in legs pushes outwards = distension of vein walls = pooling of blood in veins as blood goes into expanding the veins rather than to the heart
Increase in capillary pressure due to gravity = increased filtration of fluid out the capillaries into the interstitial space
All this reduces the effective circulating blood vol

102
Q

How can the effects of gravity on blood pressure be counteracted?

A

contraction of skeletal muscles in the legs = decrease in venous distension + pooling, decrease in capillary hydrostatic pressure + fluid filtration out of capillaries

103
Q

Why is there in increase in blood flow to the heart during exercise (of cyclic contraction + relaxation over a long period of time)?

A

because of increased metabolism and workload

104
Q

What causes increase in blood flow to skin + muscles during exercise?

A

arteriolar vasodilation (for muscles due to metabolic factors, in skin due to decrease in firing of sympathetic neurons)

105
Q

Where is arterial vasoconstriction occuring during exercise + why?

A

in the kidneys and GI organs (caused by increased activity of sympathetic neurons) = decreased blood flow

106
Q

During exercise, cardiac output _________ more than ______________ decreases. So arterial pressure usually ________ by a small amount

A

increases, the total peripheral resistance, increases

107
Q

During exercise, increase in cardiac output is supported by?

A

large increase in heart rate + small increase in SV

108
Q

Increased SV during exercise is due to?

A

increased ventricular contractility manifested by an increased ejection fraction and mediated by the sympathetic neurons to the ventricular myocardium

108
Q

Increase in heart rate during exercise is due to?

A

decreased parasympathetic activity to SA node + increased sympathetic activity

109
Q

Factors promoting venous return during exercise:

A
  • Increased activity of the skeletal muscle pump
  • Increased depth and frequency of inspiration (the respiratory pump)
  • Sympathetically mediated increase in venous tone
  • Greater ease of blood flow from arteries to veins through the dilated skeletal muscle arterioles
110
Q

Control centers in the brain are activated during exercise by?

A

output from the cerebral cortex, descending pathways from these centers to the appropriate autonomic preganglionic neurons = preprogrammed pattern that drives the enhanced sympathetic output

110
Q

What happens when the control centers in the brain become active during exercise?

A

changes to cardiac + vascular function before exercise occur = feedforward system

111
Q

When do local chemical changes in the muscle develop (during exercise)? + effect of these changes?

A

if blood flow and metabolic demands do not match

These changes activate chemoreceptors in the muscle, afferent input from these receptors go to the medullary cardiovascular center = facilitates the output reaching the autonomic neurons from higher brain centers = further increase in heart rate, myocardial contractility, and vascular resistance in the nonactive organs

112
Q

Effect of arterial baroreceptors during exercise?

A
  • increase the arterial pressure over that existing at rest (because one neural component of the central command output travels to the arterial baroreceptors and ‘resets’ them upward as exercise begins)
  • this resetting causes baroreceptors to respond as if pressure had decreased = their output signals for decreased parasympathetic and increased sympathetic outflow
113
Q

Maintained high-force, slow-shortening-velocity contractions exercise: effect on cardiac output, blood pressure, arterial size, and blood flow?

A

Cardiac output + blood pressure increase+ arterioles in exercising muscle undergo vasodilation due to local metabolic factors
Blood flow to muscle greatly reduced after muscles exceed ~10% of their maximal force due to muscles physically compressing blood vessels so arteriol vasodilation has been overcome = cardiovascular changes ineffective in causing increased blood flow to muscles + these contractions can only be maintained a short time
This compression can also = total peripheral resistance increase a lot = large increase in arterial pressure during contraction

114
Q

VO2 max could be limited by:

A
  • Cardiac output
  • Respiratory systems ability to deliver O2 to the blood
  • Exercising muscles’ ability to use O2
115
Q

How does cardiac output determine VO2 max?

A

increasing workload = heart rate increases
SV increases much less + levels off around 75% VO2 max

116
Q

Where is the heart located (section wise)

A

middle subdivision of the inferior mediastinum
The aortic arch rises into the superior mediastinum

117
Q

The apex projects ventrally but where?

A

midclavicular/parasternal in the 5th intercostal space

118
Q

What does the left coronary artery give rise to?

A

the anterior interventricular artery

119
Q

What does the right coronary artery give rise to?

A

the right coronary sulcus which runs towards the dorsal aspect of the heart where it forms the posterior interventricular artery in the posterior interventricular sulcus

120
Q

Which veins accompany the coronary arteries?

A

the great cardiac vein (runs
together with the anterior interventricular artery), the middle cardiac vein (runs together with
the posterior interventricular artery) and the small cardiac vein
all veins merge into the coronary sinus that drains into the right atrium

121
Q

Which 3 major arteries branch off the abdominal aorta and supply the digestive tract?

A

celiac trunk (left gastric a, common hepatic a, splenic a) , superior mesenteric artery, inferior mesenteric artery

122
Q

Which is life threatening? Patent foramen ovale or Patent ductus arteriosus?

A

Patent ductus arteriosus - dependent on the size of the opening, the newborn may become
short of breath.

123
Q

The main symptoms of The Tetralogy of Fallot?

A
  1. ventricular septum defect.
  2. pulmonary trunk stenosis. 3. ‘overriding’ aorta. 4. right ventricular hypertrophy.
124
Q

‘An artery is usually accompanied by a vein’ what are the exceptions to this?

A

the brain has venous sinuses
abdomen: intestine drains to the liver via the portal system

125
Q

Where is the electrical vector travelling during a positive deflection on an ECG?

A

towards the exploring electrode (positive)

126
Q

Where is the electrical vector travelling during a negative deflection on an ECG?

A

away from the exploring electrode (positive)

127
Q

What are the conditions for commotio cordis?

A

Object travelling at high speed which directly hits the heart during the upstroke of the T-wave

128
Q

BPM when experiencing bradycardia?

A

< 60 (parasymapthetic)

129
Q

BPM when experiencing tachycardia?

A

> 110 (sympathetic)

130
Q

What is the most prevalent genetic cause of hypertrophic cardiomyopathy?

A

mutations in the MYBPC3 gene

cardiovascular system (2 decks)

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