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Kinesiology > CV Physiology > Flashcards

CV Physiology Flashcards

1
Q

Pericardium

A 
Tough inelastic sheath covering heart (anchors heart)
Acts as a constraint to enable ventricular interaction 
Pericardial fluid (lubrication)
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2
Q

Coronary arteries are on

A

Surface of heart

This prevents compression during contraction

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3
Q

Right atrium receives from and sends to

A

Receives from vena cava

Sends to right ventricle

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4
Q

Right ventricle receives from and sends to

A

Receives from right atrium

Sends to lungs

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5
Q

Left atrium receives from and sends to

A

Receives from pulmonary veins

Sends to left ventricle

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6
Q

Left ventricle receives from and sends to

A

Receives from left atrium

Sends to body except for lungs

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7
Q

Vena cava receives from and sends to

A

Receives from systemic veins

Sends to right atrium

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8
Q

Pulmonary trunk (artery) receives from and sends to

A

Receives from right ventricle

Sends to lungs

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9
Q

Pulmonary vein receives from and sends to

A

Receives from veins of the lungs

Sends to left atrium

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10
Q

Aorta receives from and sends to

A

Receives from left ventricle

Sends to systemic artery

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11
Q

Ventricular torsion

A

Allows for more efficient ejection

Produces diastolic suction (more efficient filling)

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12
Q

Intercalated disks

A

Desmosomes = withstands stress

Gap junctions = movement of ions, electrical impulses

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13
Q

2 types of myocardial cells

A

Autorhythmic cells = generates and spreads action potential, pacemaker cells, conducting cells
Myocardial cells = contractile cells, 99% of cardiac cells, mechanical work of contraction
Each myocardial cell has a distinct action potential
Action potentials are initiated at the pacemakers

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14
Q

Heart muscle electrical excitation

A

Pacemaker cells
Events = Na+ influx, Ca++ influx, K+ efflux
Pacemaker potential = the slow rise in membrane potential (depolarization) prior to an AP in the SA node

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15
Q

Events in pacemaker potential

A

Slow depolarization phase of SA node = K+ permeability decrease while Na+ increases (increased leakiness to Na+ = slow influx of Na+) approaches threshold
Near midpoint of slow depolarization = Ca++ (T-type; transient) channels open - voltage sensitive, calcium moves in, don’t stay open long, pacemaker potential continues to rise towards threshold
Threshold is reached = L-type Ca++ channels open, calcium moves in, rapid depolarization and action potential
Repolarization = L-type Ca++ channels close, K+ (rectifier) channels open and K+ moves out of SA node cells

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16
Q

SA node is

A

Autorhythmic
Self-generated
Events repeat (~70 times/minute)

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17
Q

Other pacemaker regions

A 
AV node (40 beats/min)
Purkinje fibres (~20 beats/min) (ectopic beats (extrasystoles))
Both are depolarized by SA node before they depolarize themselves
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18
Q

Action potential of myocardial contractile cells

A

Depolarization (Na+ moves in)
Plateau ( Ca++ moves in, stays depolarized)
Repolarization (K+ moves out)

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19
Q

Cardiac muscle

A

Excitation-contraction coupling and relaxation in cardiac muscle

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20
Q

Myocardial contractile cells

A

Long refractory period in cardiac muscle
Long action potential means long refractory period
Prevents tetanus and allows for relaxation and diastolic filling each beat

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21
Q

Modulation of heart rate by the sympathetic nervous system

A

Pacemaker cells are more depolarized
Closer to threshold
Will reach threshold faster
Increased heart rate

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22
Q

Modulation of heart rate by the parasympathetic nervous system

A

Hyperpolarizes pacemaker
Further from threshold
Takes longer to reach threshold
Slower heart rate (normal resting condition)

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23
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: membrane potential

A 
Skeletal= stable at -70 mV
Contractile = stable at -90 mV 
Autorhythmic = unstable pacemaker potential, usually starts at -60 mV
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24
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: events leading to threshold potential

A 
Skeletal = net Na+ entry through ACh-operated channels 
Contractile = depolarization enters via gap junctions 
Autorhythmic = net Na+ entry through ion channels, reinforced by Ca+ entry
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25
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: rising phase of action potential

A 
Skeletal = Na+ entry 
Contractile = Na+ entry 
Autorhythmic = Ca++ entry
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26
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: repolarization phase

A 
Skeletal = rapid, caused by K+ efflux 
Contractile = extended plateau caused by Ca++ entry, rapid phase caused by K+ efflux 
Autorhythmic = rapid, caused by K+ efflux
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27
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: hyperpolarizatiom

A 
Skeletal = due to excessive K+ efflux at high K+ permeability when K+ channels close, leak of K+ and Na+ restores potential to resting state 
Contractile = none, resting potential is -90 mV, the equilibrium potential for K+ 
Autorhythmic = normally none, when repolarization hits -60 mV the ion channels open again and ACh can hyperpolarize the cell
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28
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: duration of action potential

A 
Skeletal = short, 1-2 msec 
Contractile = extended, 200+ msec 
Autorhythmic = varies, generally 150+ msec
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29
Q

Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: refractory period

A 
Skeletal = generally brief 
Contractile = long because resetting of Na+ channel gates delayed until end of action potential 
Autorhythmic = none
30
Q

Specialized conduction system of heart

A 
SA node 
Internodal pathway 
AV node 
Bundle of HIS (or Av bundle or bundle branches)
Purkinje fibres
31
Q

Electrocardiogram (ECG)

A

External recording of electrical events
Waves of ECG can be correlated to specific events
3 types of waves = P-wave, QRS complex, T-wave

32
Q

P-wave

A

Atrial depolarization

Initiates atrial contraction

33
Q

QRS complex

A

Ventricular depolarization and atrial repolarization

Initiates ventricular contraction

34
Q

T wave

A

Ventricular repolarization

Initiates ventricular relaxation

35
Q

Conduction of impulses

A 
P wave (atrial depolarization) = initiated in SA node, spreads via gap junctions and internodal pathway throughout atria, initiates atrial contraction 
Impulse moves to AV node = delay of signal (~100 msec), AV nodal delay means ventricles contract after atrial contraction and ventricular filling 
QRS complex (ventricular depolarization) = impulse moves to bundle of HIS to bundle branches and then to purkinje fibres, initiates ventricular contraction, includes atrial repolarization 
T wave (ventricular repolarization) = reversed repolarization wave (from apex), initiates ventricular relaxation
36
Q

Abnormalities in rate

A

Sinus rhythm = normal (60-120 b/min)
Tachycardia = rapid heart rate of more than 10p b/min (sinus or ventricular)
Bradycardia = slow heart rate (less than 60 b/min), risk of fainting

37
Q

Abnormalities in rhythm

A

Arrhythmias = can cause sudden death, fainting, heart failure, dizziness, palpations, or no signs at all
Causes include hypoxia, caffeine, smoking, alcohol, ectopic excitable cells, stress, and damage to conducting path

38
Q

Examples of arrhythmias

A

PVCs = premature ventricular contractions (extra beat)
Atrial flutter = extra P waves
Atrial fibrillation = no distinct P waves
Heart block = impulses from SA node don’t reach AV node

39
Q

Ventricular fibrillation

A

Causes = arrhythmias, ischemia (heart attack)

No organized pattern of depolarization = no organized contraction, no ejection, leads to death

40
Q

Cardiac cycle

A

Electrical events correspond to mechanical events in the heart

41
Q

Heart wall thickness

A 
Wall thickness correlates to peak pressures 
Aortic pressure = 120/80 mm Hg
Atrial pressure = 3-10 mm Hg
RV pressure = 3-35 mm Hg 
LV pressure = 3-125 mm Hg 
Systole = contraction 
Diastole = relaxation
42
Q

Heart valves

A

Prevents back-flow of blood
Atrioventricular valves = tricuspid (R) mitral (L)
Aortic
Pulmonary

43
Q

Pulmonary and aortic valves

A

Prevent back-flow from aorta and pulmonary artery back into ventricles
Open in systole (contraction)

44
Q

Atrioventricular valves

A

Prevent back-flow from ventricles back to atria
Open in diastolic filling
Chordae tendinae anchor AV valves to papillary muscle (prevents eversion of valve)
As heart contracts, papillary muscles contracts (control tension on chordae tendinae)

45
Q

Valve problems (murmurs)

A

Stenosis

Insufficiency or regurgitation

46
Q

Stenosis

A 
Narrowing of heart valve 
Faulty opening 
Decreased ejection 
Heard when valve should be open 
Whistling
47
Q

Insufficiency or regurgitation

A 
Faulty closure 
Backflow 
Decreased forward ejection 
Heard when valves should be closed 
Whirring
48
Q

4 phases of cardiac cycle

A

Diastolic filling
Isovolumic contraction
Ejection
Isovolumic relaxation

49
Q

In the Cardiac cycle the left and right sides…

A

Contract simultaneously

Right side at lower pressures

50
Q

Diastolic filling

A

LAP>LVP
Mitral valve open
LVP

51
Q

Isovolumic contraction

A 
QRS
LV contracts 
LVP increases 
Once LVP>LAP mitral valve closes 
Both valves are closed 
Pressure still increasing
52
Q

Ejection

A

Once LVP>AP aortic valve opens

Blood ejected into aorta

53
Q

Isovolumic relaxation

A

T-Wave
Relaxation
LVP decreasing
Once LVP

54
Q

Stroke volume

A

Amount of blood pumped in 1 beat
SV = EDV(end-diastolic volume(after filling)) - ESV(end-systolic volume(after ejection))
Average stroke volume = 70mL
Depends on contractility and venous return

55
Q

Venous return affected by

A

Skeletal muscle pump
Respiratory pump
Sympathetic innervation

56
Q

Contractility affected by

A

Length of muscle fibre

57
Q

Frank-Starling law of heart

A

Preload = filling of heart
Greater filling or preload means greater stretch of the myocardium and then a greater force of contraction
Stroke volume increases as EDV increases
Whatever goes in goes out the next beat

58
Q

Ionotropic effect

A

The effect of increased sympathetic tone on contractility of heart
Epinephrine and norepinephrine increase both contractility and heart rate

59
Q

Cardiac output

A

Amount of blood pumped per minute
CO = stroke volume x heart rate
Average cardiac output = 5L

60
Q

Ejection fraction

A

Stroke volume divided by end-diastolic volume

61
Q

Effects of exercise

A

Body’s demand for oxygen and blood flow increases (cardiac output must increase by up to 5x)
Body does this by increasing epinephrine (sympathetic tone)
Increases stroke volume (by increasing contractility and venous return)
Increases heart rate

62
Q

Benefits of exercise

A 
Bigger heart (larger stroke volume, resting heart rate can be lower)
Larger coronary artery diameter (increased blood flow)
Larger collateral blood vessels (less chance of ischemia)
63
Q

Heart muscle metabolism

A

Heart muscle is highly oxidative
Abundant mitochondria and myoglobin
Gets oxygen from coronary circulation

64
Q

Coronary circulation

A

During exercise: heart rate increases, filling time (diastole) decreases, heart still gets adequate blood supply due to dilation of coronary arteries via adenosine (vaso-dilator) production by cardiac muscle

65
Q

Cardiac myopathies

A

Damage of heart muscle
Myocardial ischemia aka heart attack (inadequate delivery of oxygenated blood to heart tissues)
Fibrosis
Necrosis (death of heart muscle cells)
Actor myocardial infarction aka heart attack (occurs when blood vessel supplying area of heart becomes blocked or ruptured)

66
Q

Ischemia and infarct

A

Transient = ischemia
Permanent damage = infarct
Blocked coronary artery = plaque/clots/cholesterol, decreased blood flow and oxygen to heart muscle
Poor muscle function = decreased stroke volume and cardiac output
Treatment = coronary artery bypass graft (CABG), vasodilators, angioplasty, reduce risk factors: exercise, diet, smoking

67
Q

Arterial hypertension

A

Causes include = smoking, stress, diet, age/genetics
Increased arterial pressure = LVP must exceed this to open the aortic valve and eject blood
Shorter ejection time = decrease in stroke volume and cardiac output

68
Q

Heart failure

A

Compromised heart = valve stenosis , ischemia or infarct, hypertension
Decrease in stroke volume, heart compensates with increasing heart rate = shorter filling time and a decrease in stroke volume, faster fatigue of heart muscle, and decreased contraction
Eventually muscle is so fatigued it barely contracts and there is a decrease in stroke volume, increase in blood volume, and excess blood backs up into lungs (pulmonary edema)

69
Q

Congestive heart failure

A

Symptoms = gradual dyspnea and tachypnea, tachycardia, neck vein distension, edema in ankles and lower legs
Right side = congestion of liver and spleen
Left side = congestion of lungs

70
Q

Pulmonary hypertension

A

RV pressure > LV pressure
Septum inverts = myocardial compression, decrease in coronary blood flow
Eg) pulmonary stenosis

71
Q

Cardiac aneurysm

A

Bulge or ventricular wall = muscle weakness, congenital or from infarct

Kinesiology (19 decks)

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