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Human Physiology > Cardiovascular system - Feng > Flashcards

Cardiovascular system - Feng Flashcards

1
Q

What are the functions of the cardiovascular system?

A

Role as a transport system : Maintenance of homeostasis
- transports oxygen and nutrients to the tissues
- transports carbon dioxide and waste products from the tissues to the external environment
- helps regulate body temperature (by transporting excess heat out of the body or conserving heat)
- transports and distributes hormones and other substances within the body

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2
Q

What are the components of the transport system?

A
  1. a central pump - the heart
  2. a closed system of blood vessels - 2 circulatory
  3. the fluid medium, blood, through which various substances are transported
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3
Q

What is the general organization?

A

There are two circulatory systems:
1. Pulmonary circulation
2. Systemic circulation

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4
Q

Describe the anatomy of the heart

A

Heart has four chambers:
- left and right atria
- left and right ventricles
Cardiac valves:
- mitral valve
- tricuspid valve
- aortic valve
- pulmonary valve
Major vessels:
- superior and inferior vena cava
- pulmonary artery
- pulmonary veins
- aorta

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5
Q

Describe the blood circulation in the cardiovascular system (direction of flow)

A

Right atrium -> right ventricle -> pulmonary artery -> pulmonary capillaries
- picks up O2 as it passes through the lungs, drops off some CO2
Pulmonary vein -> left atrium -> left ventricle -> aorta -> arteries -> arterioles -> capillaries
- the capillaries are exchange vessels where O2 and nutrients diffuse into the tissues and CO2 and waste products are picked up
Capillaries -> venules -> veins -> right atrium

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6
Q

Describe the series and parallel circuits of the cardiovascular system

A
  • vascular (capillary) beds are arranged in parallel and/or in series
    Advantages of parallel:
  • the amount of blood flow to individual vascular beds can be controlled separately
  • there is relatively low resistance to blood flow; this lowers the pressure requirement for blood flow, decreases the workload on the heart
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7
Q

What is the blood volume distribution?

A

Total blood volume (TBV) = 5 litres
Heart and pulmonary circulation = 15%
Systemic arterial system = 10% (distribution vessels)
Systemic Capillaries = 5% (exchange vessels)
Systemic veins = 70% (capacitance vessels)

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8
Q

What are cardiac muscle cells? (cardiac myocytes)

A

There are two types of cardiomyocytes:
1. Contractile cells (atrial and ventricular muscle cells) - these cells contract in much the same way as skeletal muscle cells
2. Specialized excitatory (nodal) and conducting cells:
- excitatory nodal cells: sinoatrial (SA) node (pacemaker cells) and Atrioventricular (AV) node *set pace for heart
- conducting cells: bundle of His and Purkinje fibers *conduct action potentials within the heart

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9
Q

Describe the contractile cardiac muscle cells

A

Similar to skeletal muscle
- striated and contain actin and myosin that are similar to skeletal muscle
- contraction involves the sliding myofilaments
- contraction requires the presence of Ca++
Differences:
- shorter (0.1 mm), branched and arranged in series with each other
- 1/3 of volume is occupied by mitochondria (to produce ATP)
- extract 80% of the oxygen from the blood (requires a lot of energy - much more than skeletal)
- joined by intercalated discs that contain gap junctions: electrical resistance through the gap junctions is extremely low, they allow the free movement of ionic currents (APs) between cells

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10
Q

Describe the gap junctions at intercalated disc

A

Gap junctions allow relatively free diffusion of ions
- this allows action potentials (AP) to travel from cardiac muscle cell to cardiac muscle cell
- the AP then triggers the muscle cells to contract

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11
Q

What is functional syncytium?

A

When one cell contracts, they all contract.
Two separate functional syncytia:
- atrial syncytium (atrium contracts first)
- ventricular syncytium (then ventricular contracts)
* if both contract at the same time = problems

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12
Q

Describe the specialized excitatory (nodal) and conducting cells (cardiac muscle cell type)

A
  • contain few contractile elements -> contract weakly
  • self excitable!: able to spontaneously generate APs
  • rapidly conduct APs through the heart “act more like nerves”
    1. Excitatory nodal cells:
  • sinoatrial (SA) node
  • atrioventricular (AV) node
    2. Conducting cells:
  • bundle of His
  • Purkinje fibers
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13
Q

What is the origin of self-excitability?

A
  • normal heart rate = 70 bpm in males and 80 bpm in women
  • impulses (normally) originate in sinoatrial (SA) node located in the upper posterior wall of the right atrium
  • cardiac muscle cells (cardiac myocytes or cardiomyocytes) have the capability of self-excitation: can spontaneously produce APs
  • self excitation is fastest in the SA node
    It is the “pacemaker” of the heart
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14
Q

What are the different types of APs in the heart?

A
  • SA nodal AP
  • Atrial AP
  • AV nodal AP
  • Ventricular AP
  • different cardiac muscle cells use special ion channels to produce distinctive APs
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15
Q

What are the characteristics responsible for self excitation of SA node cells?

A
  1. Greater Na+ and Ca++ permeability (positive inward current)
  2. K+ permeability decreases during diastole (relaxation phase)
    *SA nodal cells do not have a stable “resting” membrane potential -> pacemaker potential
    - membrane potential varies between -60mV and +20mV. Has a threshold voltage of -40mV.
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16
Q

Describe the heart in diastole (cardiac relaxation)

A
  1. Slow spontaneous depolarization caused by:
    - increased permeability of cells to Na+ (funny channels) and Ca++ (T-type VG channels and some slow L-type VG channels)
    - decreased K+ permeability (outward K+ movement decreases over time
    -> induce pacemaker potential
  2. Depolarizing phase:
    - at threshold (-40mV): Na+ funny and T-type Ca++ VG channels close, all slow L-type Ca+ VG channels open
    - Ca++ flows in
    - membrane potential approaches +20mV
  3. Repolarization:
    - slow L-type Ca+++ VG channels begin to close
    - K+ VG channels begin to open (increased outward K+ current)
    - membrane potential returns to -60mV ->repolarization
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17
Q

What is the conduction velocity of the following places:
SA node
Atrial muscle (gap junctions)
AV node
Bundle of His
Purkinje fibers
Ventricular muscle (gap junctions)

A

SA node: 0.05 m/sec
Atrial muscle (gap junctions): 0.4 to 1.0 m/sec
AV node: 0.05 m/sec
Bundle of His: 1.0 m/sec
Purkinje fibers: 2.0 to 4.0 m/sec
Ventricular muscle (gap junctions): 0.4 to 1.0 m/sec

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18
Q

What sets the natural pace for the heart?

A
  • SA node is the natural pacemaker (intrinsic rate is 60-100 times/min)
  • in abnormal conditions other parts can take over: AV node discharges at a rate of 40 to 60 times/min, Purkinje fibers at 15 to 40 times/min
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19
Q

What is an electrocardiogram (ECG)?

A
  • body fluids are good conductors of electricity
  • cardiac impulses pass through the heart -> pass to surrounding tissues and to the surface of the body
  • electrodes can pick up these impulses
  • the electrocardiogram (ECG) is the sum of all the electrical events in the heart -> both depolarizing and repolarizing
  • can be used for prognosis
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20
Q

Describe the waves from the ECG - what kinds, and what do they show?

A

P-wave: depolarization of atria
QRS-complex: depolarization of ventricles
T-wave: repolarization of ventricles
U-wave: repolarization of Purkinje fibers and papillary muscles in ventricles

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21
Q

What is the PR interval?

A

1st interval
- the time the AP takes to travel from SA node through the AV
- is a good estimate of AV node function
- the PR interval decreases as heart rate increases: at 70 bpm the PR interval is 0.18 seconds, at 130 bpm the PR interval is 0.14 seconds

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22
Q

Describe the QRS duration

A
  • indication of speed of conduction through Bundle of His-Purkinje system
  • narrow- fast: AP propagating through His-Purkinje
  • wide- slow: AP propagation in the ventricles is slowed
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23
Q

What are the phases of the AP in ventricular muscle cells (myocytes)?

A
  1. Depolarization (sharp increase)
  2. Early repolarization (small dip)
  3. Plateau phase
  4. Late repolarization (large dip)
  5. Resting potential
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24
Q

Describe phase 0 depolarization

A
  • current from neighbouring cells depolarize cell (gap junctions)
  • opens fast VG Na+ channels and Na+ enters very rapidly (fast inward current)
  • membrane potential reaches +20mV
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25
Q

Describe phase 1 early repolarization

A
  • Na+ permeability decreases (fast Na+ channels close)
  • Cl- channels open and Cl- flows in (only briefly)
  • while VG K+ channels open and K+ begins moving out
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26
Q

Describe phase 2 plateau phase

A
  • AP opens slow (L-type) Ca++ VG channels -> Ca++ moves in slowly causing slow inward current
  • this inward Ca++ current almost balances the outward K+ current
  • result is a relatively stable membrane potential “plateau phase”
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27
Q

Describe phase 3 late repolarization

A
  • slow (L-type) Ca++ channels begin closing
  • inward movement of Ca++ decreases while K+ continues to move outwards
28
Q

Describe phase 4 resting potential

A
  • membrane potential returns to -90mV
29
Q

Describe the refractory periods from the AP in ventricular contractile cells

A
  1. Absolute refractory period: due to inactivation of fast Na+ channels (and possibly Ca++ VG channels)
  2. Relative refractory period: caused mainly by K+ efflux - needs stronger stimulus than normal
30
Q

What is excitation-contraction coupling (ECC)?

A
  • ECC is a series of events in which electrical excitation (from APs) leads to release of Ca++ from SR causing muscle contraction
  • Similar to skeletal muscle: AP on cell membrane (sarcolemma) spreads to T-tubules, depolarization of T-tubule causes releases Ca++ from SR (into intracellular fluid/sarcoplasm)
  • different from skeletal muscle: extracellular Ca++ enters sarcoplasm during depolarization of sarcolemma, this extracellular Ca++ can interact with SR to cause further release of Ca++ from SR - a process called Ca++-induced Ca++-release (CICR)
31
Q

How can intracellular Ca++ be increased?

A
  • depolarization induces Ca++ influx from ECF through slow, L-type Ca++ channels (DHPR/Ca++ channel)
  • extracellular Ca++ - induced Ca++ release. Ca++ that entered through slow L-type Ca++ channel -> triggers ryanodine/Ca++ channel on SR
  • the amount that enters through slow L-type Ca++ (DHPR) channels is very small compared with that released by SR. - the ECF Ca++ is essential for triggering Ca+ release from the SR - it also maitains the levels of intracellular Ca++ stores over the long run
  • extracellular Ca++ is essential for cardiac muscle contraction
32
Q

How is the cardiac muscle contraction similar to the skeletal muscle?

A
  • Ca++ binds to troponin
  • troponin pulls tropomyosin off myosin binding sites
  • myosin attaches to actin forming crossbridge
  • power stroke occurs
  • sliding of myofilaments (shortening of sarcomere)
33
Q

Describe the relaxation of cardiac muscle

A

Relaxation is brought about by lowering [Ca++]:
- Ca++ is actively pumped back into SR by Ca++ - ATPase (80%)
- Ca++ is actively pumped out of cell into ECF by similar Ca++-ATPase (5%)
- Na+/Ca++ exchanger on sarcolemma pumps 1 Ca++ out for every 3 Na+ in (15%) *recall that this exchanger is bidirectional depending on the Na concentration, membrane potential and Ca concentration

34
Q

What are the seven phases of the cardiac cycle?

A
  1. Atrial contraction
  2. Isovolumic contraction
  3. Rapid ejection
  4. Reduced ejection
  5. Isovolumic relaxation
  6. Rapid filling
  7. Reduced filling
35
Q

Describe the cardiac cycle

A

The mechanical and electrical events during a single contraction-relaxation cycle at rest including:
- pressure changes in aorta, left atrium and left ventricle
- volume changes in left ventricle (LV)
- ECG (diff ECG waves form)
- phonocardiogram
- opening and closing of valves
General information:
- initiated by AP generation in SA node
- P-wave -> atrial contraction
- QRS -> ventricular contraction
- systole lasting 0.27 seconds
- diastole lasting 0.53 seconds
*Remember blood flows in one direction through the heart (valves prevent backflow)
- atria -> ventricle (AV valve must be open)
- ventricle -> aorta (aortic valve must be open)
- for blood to flow you need a pressure gradient (high to low and blood will flow - 1 exception
- when blood is flowing, ventricular volume will change
- when all valves are closed, there is no blood flow and the ventricular volume will not change

36
Q

Describe phase 1, Atrial contraction

A
  • P wave -> atria contract
  • increase atrial pressure > ventricular pressure (AV valves are already open)
  • blood moves from high to low
  • fill the last 10-20% of end diastolic volume (EDV) of the ventricle (fills the ventricle) “atrial kick”
  • 4th heart sound (S4- dont always hear) is caused by vibration of ventricular wall - from blood flow
37
Q

Describe phase 2, Isovolumetric (ventricular) contraction

A
  • QRS complex -> ventricles begin contracting -> pressure builds in ventricles
  • ventricular pressure > atrial pressure -> AV valves close -> 1st heart sound (heard when valves close)
  • no change in ventricular volume
  • “c wave” in LAP due to mitral valve (closed) leaflet bulging back into LA (left atrium)
38
Q

Describe phase 3, Rapid ejection

A
  • ventricular pressure > aortic pressure -> aortic valve opens -> blood leaves ventricle (through pulmonary artery and aorta)
  • ventricular volume decreases
  • atria relax, blood flows into atria (both right and left - from lungs)
  • no heart sounds are noted during ejection because the opening of healthy valves is silent (if there are murmurs - aortic valve stenosis = problems / narrowed valve potentially)
39
Q

Describe phase 4, reduced ejection

A
  • T wave occurs, indicating ventricular repolarization
  • ventricles just begin to relax
  • vent. pressure falls slightly
  • aortic pressure is higher than vent. pressure because blood is still moving into aorta due to inertia (blood has momentum)
  • atrial pressures gradually rise due to continued flow into atria
40
Q

Describe phase 5, Isovolumetric relaxation

A
  • ventricles continue to relax -> vent pressure drops further (all valves are closed)
  • blood reverses direction -> aortic and pulmonary valves close -> second heart sound (vibration)
  • ventricular pressure > atrial pressure, all valves are closed -> no change in vent volume
    *note pressure in aorta (small dip then back up) - incisura due to aortic valve distension and recoil -> valve is closed, ventricle relaxes, blood momentum causes extension of the valve - decrease in pressure in aorta, then recoil increases pressure again
    *note pressure in atria - continues to rise because blood continues to enter
41
Q

Describe phase 6, Rapid filling

A
  • ventricles still relaxing
  • ventricular pressure < atrial pressure -> AV valve opens (blood flows into ventricles)
  • blood rapidly enters ventricles (most of the ventricular filling takes place here)
  • ventricular volume increases
  • 3rd heart sound due to rapid rush in of blood
42
Q

Describe phase 7, reduced filling

A
  • ventricles still relaxed
  • ventricular pressure still < atrial pressure -> AV valves are still open
  • blood slowly enters ventricles because they start to get full and become less compliant
  • cycle repeats
43
Q

Describe the first heart sound

A

“lub”
- the sound results from vibration within the blood and muscle wall associated with the sudden block of flow reversal by the AV valves (AV valves close)
“ noisy water pipes”
-> sound propagates through tissue to chest wall
*during phase 2: isovolumetric (ventricular) contraction

44
Q

Describe the second heart sound

A

“dub”
- when the aortic and pulmonary valves abruptly close (aortic precedes pulmonic) causing the 2nd heart sound due to the vibration within the blood, muscle wall, aorta and PA
* during phase 5: isovolumetric relaxation

45
Q

Describe the third heart sound

A
  • ventricular filling is normally silent
  • when a third heart sound (S3) is audible during rapid ventricular filling, it may represent tensing of chordae tendineae and AV ring during ventricular relaxation and filling
  • this heart sound is normal in children; but is often pathological in adults and caused by ventricular dilation
  • AV valves open- early ventricular filling
46
Q

What is cardiac output?

A

The amount of blood (in liters) pumped by the ventricle in one minute
- CO is matched to the oxygen demands of the body
- at rest, CO = 5L/min
- maximal exercise, CO = 20 to 40L/min

47
Q

How do you calculate cardiac output?

A

Cardiac output = heart rate x stroke volume
e.g.
CO (@ rest) = 72 bpm x 70 ml
* can change CO by changing HR and/or SV

48
Q

What is stroke volume?

A

The amount of blood ejected from the ventricle when it contracts (roughly 70 ml at rest)

49
Q

How can you control the CO through changes in heart rate?

A

Heart rate is set by the SA node and can be altered by:
- changing the slope of the pacemaker potential
- hyper-polarization of membrane potential
* heart rate is controlled primarily by the autonomic nervous system (ANS)
- SNS (fight or flight) causes increase in heart rate, and therefore increases cardiac output
- PNS (rest and relax) causes decrease in heart rate, and therefore decreases cardiac output

50
Q

Describe the autonomic system control of the heart rate

A
  • PNS (vagus) nerves are distributed mainly to SA and AV nodes and have a small effect on ventricular muscle
  • SNS nerves are distributed (all over the heart) to SA and AV node with a strong input to ventricular muscle
    *change heart rate by changing the pacemaker potential
51
Q

What are the effects of PNS (vagal) stimulation?

A
  1. decreases HR by decreasing SA node activity
  2. decreases AP conduction through AV node
  3. decreases force of contraction slightly
52
Q

What are the mechanisms of PNS (parasympathetic) effects?

A
  • neuroeffector junction of vagal nerve, neurotransmitter released
  • Ach binds to muscarinic (M2) receptors -> increases K+ permeability -> hyperpolarizes cells
    -> decreases Ca++ permeability (T-type channels, transient channels)
    -> decreases Na+ permeability (funny channels)
  • with more K+ leaving and less Ca++/ Na+ entering SA node cells = smaller positive charge -> decreases slope of pacemaker potential (reduces heart-rate)
    *the above changes also decrease AP conduction through AV node (similar process)
53
Q

What are the effects of sympathetic stimulation?

A
  1. increase in heart rate
  2. increase AP conduction rate through AV node
  3. increase force of cardiac contraction
54
Q

What are the mechanisms of sympathetic effects?

A
  • norepinephrine binds to beta 1 adrenergic receptors
    -> increases Na+ permeability /entry (funny channels)
    -> increases Ca++ permeability (T-type channels -transient) *opposite of PNS
  • SA node: increased Na+ and Ca++ permeability increases slope of pacemaker potential = higher positive charge, less time to reach threshold for AP, increased heart rate
  • AV node: increased Na+ and Ca++ permeability -> decreasing conduction time between atria and ventricles (similar mechanism)
55
Q

Describe the overall control of the heart rate

A
  • for heart rates < 100 bpm -> activate PNS (slows heart rate) - at rest (70 bpm for men, 78 for women) there is always PNS activity: “vagal tone”
  • for heart rates = 100 bpm -> no PNS, no SNS. Heart’s own intrinsic rate (set by SA node), heart transplant patient - nerves out off, runs on own intrinsic rate (100 bpm), when these patients exercise, slower response of increase to heart rate - no nerves but adrenal gland can still sense + release neurotransmitters/ hormones
  • for heart rates > 100 bpm -> activate SNS
56
Q

How do you calculate stroke volume?

A

EDV-ESV
EDV: end diastolic volume (vol. just before contracting)
ESV: end systolic volume (vol. just after contracting)

57
Q

What are the major factors which control stroke volume?

A
  1. input from the ANS
  2. preload (related to EDV)
58
Q

How does PNS stimulation (decreases HR), decrease SV?

A

-> closes some L-type Ca++ channels
-> decreased Ca++ entry into contractile cells
-> decreases force of contraction
-> decreases stroke volume and CO

59
Q

How does SNS stimulation affect stroke volume?

A
  • norepineprhine (NE) acts on B1 receptors on contractile cells
    -> increases Ca++ entry (through L-type Ca++ channels)
    -> increases force of contraction (recall excitation-contraction coupling)
    -> increases stroke volume -> increases CO
  • release epinephrine and NE from adrenal glands - act on B1 receptors:
    -> increases HR (SA node)
    -> increases contractility of heart (increased Ca++ entry)
    -> increase SV and CO
60
Q

What is preload?

A

Preload is the extent of filling the heart before contraction. Think of it as the “load” on the heart muscle just before it contracts. Preload is related to the volume of blood in the heart.
- it is directly related to end diastolic volume (EDV)
-> an increase in EDV = increased preload (stretching ventricular muscle) -> increases force of contraction of the ventricle -> increase in stroke volume

61
Q

What occurs with an increase in EDV?

A
  • ventricles stretch (preload)
  • length of ventricular muscle fibers increase
  • stretched muscle fibers generate more force due to optimal overlap of actin and myosin
62
Q

What is the relationship between sarcomere length and filament overlap?

A
  • optimal overlap = 2.20 micrometers -> maximum contraction, generates maximum force of muscle
  • extended sarcomere length = 3.65 micrometers, stretched too much, no overlap (exaggerated), no interaction
  • overly shortened sarcomere = 1.60 micrometers -> too crowded, not optimal interaction, not maximum force
63
Q

What is the relationship between stroke volume and preload (EDV)? How does the ANS input affect this relationship curve?

A

This is known as the Frank-Starling law (relationship) of the heart:
“the greater the heart is filled during diastole, the greater will be the quantity of blood pumped during systole”
- SNS increases stroke volume, creates steeper curve
- PNS decreases stroke volume, creates more gradual curve

64
Q

How do you increase end diastolic volume?

A

Increase venous return to the heart
- ways to increase EDV (and SV):
1. skeletal muscle pump (when you walk, etc, muscle + bones push blood physically)
2. respiratory pump
3. ANS -> SNS causes slight venoconstriction, increases venous return, increases EDV, increases SV + CO

65
Q

Describe the skeletal muscle pump

A
  • rhythmic contraction and relaxation of skeletal muscle pumps blood back to heart
  • increases venous return
  • increases EDV
  • increases SV
  • increases CO
66
Q

Describe the respiratory pump

A
  • decreases pressure in chest cavity
  • pulls blood back to heart and increases venous return
  • increases EDV
  • increases SV
  • increases CO
  • e.g. a deep inspiration = lower pressure in chest -> allows blood to return to heart

Human Physiology (13 decks)

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