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Kinesiology > CV Physiology > Flashcards

CV Physiology Flashcards

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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
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: rising phase of action potential
``` Skeletal = Na+ entry Contractile = Na+ entry Autorhythmic = Ca++ entry ```
26
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: repolarization phase
``` 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 ```
27
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: hyperpolarizatiom
``` 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 ```
28
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: duration of action potential
``` Skeletal = short, 1-2 msec Contractile = extended, 200+ msec Autorhythmic = varies, generally 150+ msec ```
29
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: refractory period
``` Skeletal = generally brief Contractile = long because resetting of Na+ channel gates delayed until end of action potential Autorhythmic = none ```
30
Specialized conduction system of heart
``` SA node Internodal pathway AV node Bundle of HIS (or Av bundle or bundle branches) Purkinje fibres ```
31
Electrocardiogram (ECG)
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
P-wave
Atrial depolarization | Initiates atrial contraction
33
QRS complex
Ventricular depolarization and atrial repolarization | Initiates ventricular contraction
34
T wave
Ventricular repolarization | Initiates ventricular relaxation
35
Conduction of impulses
``` 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
Abnormalities in rate
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
Abnormalities in rhythm
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
Examples of arrhythmias
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
Ventricular fibrillation
Causes = arrhythmias, ischemia (heart attack) | No organized pattern of depolarization = no organized contraction, no ejection, leads to death
40
Cardiac cycle
Electrical events correspond to mechanical events in the heart
41
Heart wall thickness
``` 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
Heart valves
Prevents back-flow of blood Atrioventricular valves = tricuspid (R) mitral (L) Aortic Pulmonary
43
Pulmonary and aortic valves
Prevent back-flow from aorta and pulmonary artery back into ventricles Open in systole (contraction)
44
Atrioventricular valves
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
Valve problems (murmurs)
Stenosis | Insufficiency or regurgitation
46
Stenosis
``` Narrowing of heart valve Faulty opening Decreased ejection Heard when valve should be open Whistling ```
47
Insufficiency or regurgitation
``` Faulty closure Backflow Decreased forward ejection Heard when valves should be closed Whirring ```
48
4 phases of cardiac cycle
Diastolic filling Isovolumic contraction Ejection Isovolumic relaxation
49
In the Cardiac cycle the left and right sides...
Contract simultaneously | Right side at lower pressures
50
Diastolic filling
LAP>LVP Mitral valve open LVP
51
Isovolumic contraction
``` QRS LV contracts LVP increases Once LVP>LAP mitral valve closes Both valves are closed Pressure still increasing ```
52
Ejection
Once LVP>AP aortic valve opens | Blood ejected into aorta
53
Isovolumic relaxation
T-Wave Relaxation LVP decreasing Once LVP
54
Stroke volume
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
Venous return affected by
Skeletal muscle pump Respiratory pump Sympathetic innervation
56
Contractility affected by
Length of muscle fibre
57
Frank-Starling law of heart
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
Ionotropic effect
The effect of increased sympathetic tone on contractility of heart Epinephrine and norepinephrine increase both contractility and heart rate
59
Cardiac output
Amount of blood pumped per minute CO = stroke volume x heart rate Average cardiac output = 5L
60
Ejection fraction
Stroke volume divided by end-diastolic volume
61
Effects of exercise
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
Benefits of exercise
``` 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
Heart muscle metabolism
Heart muscle is highly oxidative Abundant mitochondria and myoglobin Gets oxygen from coronary circulation
64
Coronary circulation
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
Cardiac myopathies
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
Ischemia and infarct
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
Arterial hypertension
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
Heart failure
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
Congestive heart failure
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
Pulmonary hypertension
RV pressure > LV pressure Septum inverts = myocardial compression, decrease in coronary blood flow Eg) pulmonary stenosis
71
Cardiac aneurysm
Bulge or ventricular wall = muscle weakness, congenital or from infarct

Kinesiology (19 decks)

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