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Cardiovascular Physiology Flashcards

1
Q

How does pressure cause valves to open and close?

A

-As pressure builds up in the atria, the AV valves open
-As pressure diminishes in atria, the AV valves close
-As pressure builds up in the ventricles, the pulmonary or aortic valves open

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2
Q

Pulmonary/aortic valves prevent backflow from _________ and _____________ back into ______________

A

Aorta and pulmonary artery back into ventricles

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3
Q

When are pulmonary and aortic valves open?

A

Open in systole (contraction, expulsion)

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4
Q

During the filling phase (diastole), which valves are open/closed?

A

AV valves are open, so semilunar valves MUST be closed

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5
Q

AV valves prevent back-flow from _________ back into _________

A

Ventricles back into atria

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6
Q

When are AV valves open?

A

Diastole (filling)

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7
Q

What do the chordae tendinae and papillary muscles do?

A

-Chordae anchor AV valves to papillary muscles
-When heart contracts, the chordae might move, so the papillary muscles help control tension on the chordae
-Prevents eversion of valve

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8
Q

What is a heart stenosis?

A

-Narrowing of the heart valve (fibrosis: build up of calcium)
-Faulty opening
-Decreased ejection of blood

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9
Q

When would you hear a heart murmur for stenosis?

A

-When the valve is supposed to be OPENING
Eg; stenosis of aortic valve: during systole

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10
Q

What is heart insufficiency or regurgitation?

A

-When a heart valve has faulty closure and there is some backflow of blood
-Results in decreased forward ejection (decreased cardiac output), eventually leading to heart failure

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11
Q

When would you hear a heart murmur for insufficiency?

A

-When the valve is supposed to be CLOSING
Eg; insufficiency of the mitral valve: during systole
Eg; insufficiency of the aortic valve: during diastole

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12
Q

What can cause valve regurgitation/insufficiency?

A

-Rheumatic heart disease
-Auto-immune
-Can develop over months or years after a strep infection (if antibiotics are not finished)

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13
Q

What is ventricular torsion? What does it allow for?

A

-Twisting of heart muscles when it contracts
-Allows for more efficient ejection
-Produces diastolic suction and more efficient filling

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14
Q

During which phase does ventricular torsion occur?

A

Isovolumic relaxation

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15
Q

Which cell junctions does cardiac muscle have lots of? Why?

A

-Gap junctions: holes for ions to spread, which allows for the wave-like spread of an electrical impulse
-Desmosomes: to withstand stress

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16
Q

Autorhythmic cells

A

-Generates and spreads action potentials
-Pacemaker cells
-Conducting cells

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17
Q

Contractile cells

A

-99% of cardiac cells
-Mechanical work of contraction

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18
Q

What cells does the AV and SA node have?

A

Pacemaker cells

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19
Q

Which node has a faster depolarization?

A

AV node

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20
Q

Why is tetanus bad in heart muscle?

A

-We need depolarization and repolarization because those correspond to contraction (expulsion) and relaxation (filling) on each heart beat

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21
Q

What is pacemaker potential?

A

-The slow rise in membrane potential (depolarization) prior to an action potential in the SA node

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22
Q

Pacemaker action potential (autorhythmic)

A

Slow depolarization: Na moves in, then Na and Ca

Fast depolarization: After threshold, Ca moves in

Repolarization: K moves outs

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23
Q

What does it mean that the SA node if autorhythmic?

A

-The events are self-generated and repeat at roughly 70 times / minute

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24
Q

How many beats per minute does the AV node function at?

A

40 bpm

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25
How many beats per minute do the purkinje fibres function at?
20 bpm
26
Which fibres create ectopic beats (extrasystoles)?
Purkinje fibres
27
How are the AV node and purkinje fibres depolarized?
-They are both depolarized by the SA node before they depolarize themselves
28
How do depolarizations of autorhythmic cells spread?
-Rapidly spread to adjacent contractile cells through gap junctions
29
Contractile action potential
Depolarization: Na moves in Plateau: Ca moves in, stays depolarized Repolarization: K moves out, slow K channels open
30
Where does calcium come from in action potentials in cardiac muscle?
Extracellular and sarcoplasmic reticulum
31
Why is there a long refractory period in contractile cardiac muscle?
-Means that we can't stack contractions (tetanus) and we get a contraction and relaxation every single beat -There is a long action potential (sustained by plateau), so a long refractory period
32
What is the resting membrane potential for contractile myocardium?
Stable at -90 mV
33
What is the resting membrane potential for autorhythmic myocardium?
-Unstable pacemaker potential; usually starts at - 60 mV
34
Is there a refractory period in autorhytmic myocardium?
No
35
What happens to heart rate when impacted by the sympathetic nervous system?
-Pacemaker cells are more depolarized (closer to threshold) -Quicker slow depolarization phase
36
What happens to heart rate when impacted by the parasympathetic nervous system?
-Hyperpolarizes pacemaker cells (further from threshold) -Slower slow depolarization phase
37
What is the pathway of the conduction system of the heart?
1. SA node 2. Internodal pathway 3. AV node - pauses for 100 ms to depolarize atria before ventricle 4. Bundle of HIS or AV bundle 5. Purkinje fibres - very quick
38
P-wave in ECG
-Represents atrial depolarization -Initiated in SA node -Initiates atrial contraction -Impulse moves to AV node where the delay of signal occurs to allow for ventricular filling
39
QRS in ECG
-Represents ventricular depolarization and atrial repolarization -Impulse moves to bundle of HIS, to bundle branches and then to purkinje fibres -Initiates ventricular contraction all at once
40
T-wave in ECG
-Represents ventricular repolarization, from apex of heart backwards -Initiates ventricular relaxation
41
What is sinus rhythm?
-Normal rhythm -60 to 120 bpm
42
What is tachycardia?
-Rapid heart rate of more than 100 bpm -Sinus (exercise) or ventricular
43
What is bradycardia?
-Slow heart rate (less than 60 bpm) -Can be normal in athletes, or abnormal -Risk of fainting
44
What is an arrhythmia?
-Any change in the normal patterns of heart rate
45
Premature ventricular contraction
-Extrasystoles -Often caused by ectopic foci (excitable cells) -Can be atrial (P waves) or ventricular (QRS) -Stress/sleeplessness/caffeine/medications
46
Atrial flutter
-Extra P waves -QRS remains at 70 bpm
47
Heart block
-Interruption in conduction system between SA and AV node -SA node fires at 70 bpm, so P waves are normal -AV node will control the ventricles, so the QRS waves will fire at 40 bpm -Caused by aging or heart disease, stress, caffeine, alcohol -Treat with a pacemaker
48
Atrial fibrillation
-No organized electrical pattern in the atria -No P-waves (so no top up for ventricles) -Palpitations and discomfort/fainting -Treat with electric conversion, ablation, anti-coagulants
49
Ventricular fibrillation
-No organized pattern of depolarization for ventricles -No organized contraction -No ejection -Leads to death -Causes include arrythmias and ischemia
50
What is aortic pressure?
120/80 mmHg
51
What is the range of atrial pressure?
3-10 mmHg
52
What is the range of left ventricle pressure?
3-125 mmHg
53
What is the range of right ventricle pressure?
2-35 mmHg
54
What are the mechanical events of the cardiac cycle?
1) atrial relaxation and ventricular filling- both sets of chambers are relaxed and ventricles fill passively, AV valves open 2) atrial contraction and ventricular filling- atrial contraction forces a small amount of additional blood into ventricles, AV valves open 3) isovolumic ventricular contraction- first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves, all valves are closed and pressure builds up 4) ventricular ejection- as ventricular pressure rises and exceeds pressure in arteries, the semilunar valves open and blood is ejected 5) isovolumic ventricular relaxation- as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed, all 4 valves are closed
55
Pressures in the different phases of the cardiac cycle
1) diastolic filling- LAP>LVP, LVPLAP the mitral valve closes 3) ejection- once LVP>AP, aortic valve opens and blood ejected into aorta 4) isovolumic relaxation- LVP decreases, once LVP< AP, aortic valve closes, mitral valve stays shut because even when it's filling, pressure is still low in LA. Once LVP< LAP, mitral valve opens.
56
What is the calculation for stroke volume?
SV= end-diastolic volume (EDV) - end-systolic volume (ESV)
57
What is stroke volume?
Amount of blood pumped in 1 beat 70 mL per beat
58
What is end-diastolic volume?
Volume after ventricular filling
59
What is end-systolic volume?
Volume in ventricles after ejection
60
3 factors that regulate stroke volume:
1) Preload- the amount of myocardial stretching (positive relationship) 2) Contractility- the amount of force produced during a contraction at a given preload (positive relationship) 3) Afterload- the tension required for the left ventricle to force open the aortic valve (inverse relationship)
61
Factors that affect end diastolic volume
-Venous return -Filling time (duration of diastole)
62
Factors that affect end systolic volume
-Contractility (force of contraction) -Afterload
63
What is venous return?
Amount of blood entering heart
64
Factors affecting venous return
-Skeletal muscle pump -Respiratory pump -Sympathetic innervation
65
Factors affecting contractility
-Sympathetic nervous system -Length of muscle fibre
66
Frank-Starling Law of the Heart
Greater filling/preload means greater stretch of the myocardium and then a greater force of contraction Stroke volume increases as EDV increases
67
Cardiac output
Amount of blood pumped per minute CO = stroke volume x heart rate 5 L / minute
68
Factors affecting heart rate
-Autonomic nervous system -Hormones -Age -Physical fitness -Body temperature
69
How does exercise affect cardiac output?
-Higher demand for oxygen and blood flow -Increase epinephrine (higher contractility, stroke volume, heart rate, venous return) -Both of these increase cardiac output by up to 5x
70
When is the peak movement of blood in the coronary arteries?
Diastole
71
Fibrosis
-Replace heart cells with collagen and fat -Not stretchy enough to contract
72
Ischemia
-Transient -No permanent damage to heart muscle -Symptoms occur when cardiac demand increases beyond what the heart can match -Symptoms ease when demand goes down -Angina
73
Infarct
-Permanent blockage -Muscle cells are permanently damaged -Symptoms remain and worsen
74
Treatment for ischemia and infarct
-Coronary artery bypass graft -Vasodilators -Angioplasty -Reduce risk factors
75
Arterial hypertension
-High blood pressure in arteries -Higher pressure needed to open valve = more time in isovolumic filling = less time ejecting = less cardiac output -Causes include smoking, stress, diet, age
76
Treatments for hypertension
-Exercise -Diet (reduced caffeine and salt) -Medications (ACE inhibitors, beta blockers, Ca channel blockers)
77
How does the death spiral occur during heart failure?
-The heart compensates with a higher heart rate when the stroke volume is low -Higher heart rate means shorter filling times, decreased stroke volume, faster fatigue of heart muscle, lower contraction and stroke volume
78
Pulmonary edema
Left side failure Plasma from the blood leaks into the lungs through capillaries
79
Congestive Heart Failure
-Gradual dyspnea (hard breathing) and tachypnea -Tachychardia -Neck vein distention -Edema in ankles and lower leg -Right-sided: congestion of liver and spleen -Left-sided: congestion of lungs
80
Heart failure treatments
-Reduce fluids with diuretics -Digitalis to increase contraction strength but not heart rate -Diet and exercise to strengthen muscle -Heart transplants -Temporary artificial heart -Ventricular assist device
81
Factors increasing stroke volume
-Increased venous return -Increased contractility -Decreased afterload (lower BP)
82
Adenosine
Vasodilator (gets the coronaries more blood so that they can help the heart during exercise)

KNES260 (13 decks)

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