The Cardiac Cycle Flashcards
(111 cards)
1
Q
What 2 types of events work in a co-ordinated fashion to produce a contractile syncytium?
A
Electrical and Mechanical events
2
Q
What is included in the cardiac cycle?
A
Everything from the beginning of one heart beat to the beginning of the next one
3
Q
How long does each cardiac cycle last?
A
It depends on the heart rate, but at a heart rate of 70bpm each cycle lasts 0.8 seconds
4
Q
What phrase describes the ability of cardiac muscle to enable rapid and uniform passage of electrical impulses?
A
Functional Syncytium
5
Q
How long before ventricular contraction does atrial contraction occur?
A
1/6th of a second
6
Q
Why is ventricular contraction delayed?
A
To enable diastolic filling of the ventricles
7
Q
Where is the SA Node located?
A
The crista terminalis on the posterior wall of the upper right atrium. Next to the inlet of the Superior Vena Cava
8
Q
What type of cells are located in the SA Node?
A
Neurocardiac tissue called PACEMAKER CELLS
9
Q
What properties do pacemaker cells have?
A
They contain no contractile filaments, but are self-excitable/automaticity
10
Q
What is automaticity?
A
the ability of a cell to depolarise itself without the need for a stimulus
11
Q
Why does the SA node set the heart rate?
A
Because the pacemaker cells in the SA node have the fastest depolarisation/repolarisation rate
12
Q
Which property of the heart conduction system is the most important?
A
Rapid propagation of impulses
13
Q
How does this most important property of heart conduction happen?
A
Gap Junctions between myocytes
14
Q
How are myocytes connected?
A
Via Intercalated discs which are thickenings of sarcolemma. Desmosomes at the intercalated discs join adjacent cells meaning that myocytes are individual cells all connected in series
15
Q
What are gap junctions?
A
They are pores that form in the intercalated discs that allow the movement of ions between cardiac cells. This rapid movement of ions between cells allows rapid propagation of electrical impulses and action potentials
Ions move along longitudinal axes of cardiac myocytes
16
Q
Where is the AV node located?
A
Posteriorly on the right side of the interatrial septum near to the ostium of the coronary sinus
17
Q
What is the purpose of the AV Node?
A
It can slow the propagation of impulses from the atria to the ventricles which allows time for the ventricles to fill before contraction. The AV node also contains pacemakers cells and therefore if the SA Node becomes faulty the AV Node can take over.
18
Q
Why is the SA Node better than the AV Node?
A
The SA node has the fastest automaticity rate, and so if the AV node has to take over, the heart rate will slow
19
Q
What property of the AV Node protects against Ventricular Tachycardia?
A
The AV node has a slower depolarisation rate than the SA node and therefore SLOWS electrical conduction. If the SA node conducts impulses very quickly, then the AV node slows the conduction and prevents ventricular tachycardia.
20
Q
What is this slowing property called?
A
Decremental Conduction
21
Q
Define Decremental Conduction:
A
The faster the impulses reach the AV node from the SA Node, the slower the AV node will conduct them
22
Q
By how much does the AV Node slow the propagation of electrical impulses?
A
0.09 seconds
23
Q
Why does the AV Node have a slower depolarisation rate?
A
Because there are reduced numbers of Gap junctions-so electrical impulses can’t spread as easily
24
Q
In the natural state, what ions is the membrane of pacemaker cells permeable to?
A
Sodium and Calcium
25
What is different about the resting potential of pacemaker cells compared to ventricular cells?
The resting potential is LESS NEGATIVE. Pacemaker cell rmp is -60/-70mV wheres ventricular cells is -85/-90mV
26
What type of channels are involved in Pacemaker cell depolarisation?
Slow/funny Na/Ca channels, Fast Na channels and L-type Voltage Gated Calcium Channels
27
At what voltage do calcium channels open?
-40mV
28
At what voltage does an action potential occur?
+30mV
29
At what voltage do potassium channels open?
+30mV
30
In what direction does potassium travel and what does this do to the cell?
Potassium moves OUT of the cell as this is the direction of its concentration gradient and this means that the cell becomes more negative so the cell REPOLARISES
31
What happens during repolarisation?
Potassium moves out of the cell making it negative, it then becomes a little too negative and this re-opens slow/funny Na+ channels causing sodium to move slowly back into the cell-so depolarisation begins AGAIN
32
What are the three tracts used to propagate impulses from the SA Node to the AV Node?
Anterior Infranodal Tract of Bachman
Middle Infranodal Tract of Wenkebach
Posterior Infranodal Tract of Thovel
33
How long does it take for the electrical impulse to travel from the SA Node, through the atria and down the infranodal tracts?
0.03 seconds
34
Where does the electrical impulse go once it has left the AV Node?
Bundle of His, Purkinje Fibres, Right and Left Bundle Branches
35
How long does transmission take in the purkinje fibres?
0.04 seconds
36
Why is transmission so rapid in the purkinje fibres?
Because of many gap junctions that allow rapid electrical propagation
37
How quick is electrical transmission in the ventricular muscle?
0.3-0.5 seconds
38
What is the resting membrane potential of ventricular cells?
-85/-90mV
39
What ions are involved in the depolarisation of non-pacemaker cells?
Only sodium NO CALCIUM
40
What is the biggest difference between pacemaker and non-pacemaker cells?
Non-pacemaker cells have a PLATEAU PHASE in which there is slow influx of Calcium
41
What does the Plateau phase represent?
The influx of calcium represents the contraction phase of ventricular cells
42
What are the 5 phases of non-pacemaker cell action potentials?
0=rapid depolarisation (Na channels open)
1= rapid repolarisation (Na channels close)
2=plateau phase (calcium channels open with some K channels open which keeps it level)
3=final repolarisation (only K channels open)
4=resting membrane potential (Closure of K channels and re-opening of Na)
43
What are the main differences between pacemaker and non-pacemaker cells?
1. Non have rapid depolarisation whereas pacemakers have slow
2. Pacemaker cells use Calcium for depolarisation whereas non-pacemakers use only sodium
3. Pacemakers use only Potassium for repolarisation but non use both potassium and calcium
4. The resting membrane potential of non is -85/-90mV whereas pacemaker cell rmp is -60/-70mV
5. Pacemaker cells have automaticity with no true resting membrane potential due to the presence of funny sodium channels, whereas non have a proper rmp
44
What is a refractory period?
A period in which no further action potential can be triggered
45
How long does the absolute refractory period last?
0.25-0.3 seconds
46
What is the relative refractory period?
If there is a large enough stimulus, an action potential can occur
47
What is different about the refractory period between the atria and ventricles?
the refractory period of the atria is shorter than that of the ventricles (the ventricular refractory period is longer to prevent re-entry mechanisms when the atria depolarises for the next heart beat)
48
When does the length of an action potential change?
When the heart rate changes
49
Which part of the cardiac cycle is affected the most when heart rate increases?
Diastole shortens the most which means that eventually diastolic filling will be reduced
This is important because diastole allows ventricular filling and also coronary perfusion-so at very high heart rates filling may be compromised to such a degree that cardiac output starts to fall
50
Which nerve is implicated in the parasympathetic nervous system?
The vagus nerve
51
Which neurotransmitter is implicated in the parasympathetic system?
Acetylcholine
52
What are the effects of ACh on the heart?
1. decreases the rate of automaticity of the SA node by making the membrane potential more negative which means it is harder to repolarise
2. Reduced exctiability in the AV node
53
What causes sinus bradycardia in athletes?
It is thought to be caused by increased vagal tone
54
What happens in extreme parasympathetic stimulus?
There is complete block of transmission through the AV node and the purkinje fibres must take over the automaticity of the heart thus the heart rate drops to 30-40bpm
55
What is it called when the purkinje fibres take over the automaticity of the heart?
Ventricular Escape
56
How do beta blockers slow the heart rate?
They block stimulation from the sympathetic drive thus enabling parasympathetic drive to take over which slows the heart rate
57
What drugs have the same effect as the parasympathetic system?
Digoxin (a cardiac glycoside), Adenosine and Beta blockers are all able to slow conduction through the AV Node
58
What neurotransmitter is associated with the sympathetic nervous system?
Noradrenaline
59
What effect does noradrenaline have on the heart?
1. makes the resting membrane potential more positive so there is an increased rate of SA node discharge
2. Increased rate of SA node conduction and overall excitability
3. Increases cell Calcium permeability so there is an increased force of contraction
60
How big is the effect of the sympathetic nervous system?
1. It can increase heart rate 3 fold
| 2. It can increase inotropy 2 fold
61
What is excitation-contraction coupling?
The mechanism by which electrical activity is converted to mechanical activity
62
How is cardiac muscle contraction different to skeletal?
1. Skeletal muscles take calcium ONLY from the sarcoplasmic reticulum whereas cardiac cells also use calcium pumped in from the t-tubules because the SR in cardiac tissue is less well developed and therefore cannot store as much calcium
2. T-tubules in cardiac muscle are bigger in diameter and volume because they are needed to pump in calcium
3. The Extracellular fluid calcium concentration determines the contractile force of cardiac contraction whereas ECF calcium does not affect skeletal muscle
63
What events occur in Late diastole?
both sets of chambers are relaxed, the AV-valves are open and the ventricles fill passively with blood flowing directly from the great veins
64
What events occur in atrial systole?
The atria contract which forces a small amount of additional blood (20%) into the ventricles
Atrial contraction can be seen as an increase in pressure on a measure of Jugular venous pressure- the 'a' wave
65
What events occur in isovolumic ventricular contraction?
The ventricle begins to contract which forces the AV valves to close. To begin with, the ventricular contraction does not generate enough force to open the semi-lunar valves as the pressure in the arteries is still greater. Therefore, at this point in time there is an increase in pressure without a decrease in volume because the Semi-lunar valves have not yet opened to allow ejection
Seen on the JVP line as the 'c' wave because the AV-valve bulges in to the atria
66
What events occur in ventricular ejection?
Eventually the ventricles contract with enough force to overcome arterial pressures and force the semi-lunar valves open. Blood is then ejected in to the great arteries
Seen as a huge increase in pressure on an Aortic Pressure Line
67
What events occur in isovolumic ventricular relaxation?
As the ventricles relax, pressures in the ventricles drop and blood is pulled backwards from the arteries forcing the cusps of the semi-lunar valves to snap shut. This is known as PROTODIASTOLE. At this very moment the pressure gradient between the atria and ventricles is not large enough to open the AV-valves and so ventricular pressure falls without an increase in ventricular volume
Shown on JVP line as the 'v' wave due to increased venous return to the atria
68
What events occur in early diastole?
Eventualy ventricular pressures fall enough to allow the opening of the AV-valves which allows blood flow from the great veins and the entire process happens again
69
How much of the stroke volume does atrial contraction account for?
20%-so during AF stroke volume can be particularly effected-especially during exercise. For this reason, many AF patients go on to develop heart failure
70
What is the equation for Cardiac Output?
Heart rate x stroke volume
71
How long is isovolumic contraction?
0.02 seconds
72
What is an alternative name for the atria?
Primer Pumps-because they prime the ventricles ready for contraction
73
What are the two phases of ejection and how much blood is implicated in each?
1. Rapid ejection= 70% of stroke volume
| 2. Slow ejection= 30% of stroke volume
74
How long is isovolumic relaxation?
0.03-0.06 seconds
75
What are the three phases of ventricular filling?
1. Rapid-60%
2. Diastasis (slow filling)-10%
3. Atrial Contraction-20%
76
How much blood does the left ventricle hold?
120ml
77
How is ventricular filling represented on the JVP line?
As the Y descent, blood flows straight across the atria into the ventricles so pressure in the JVP decreases
78
What are the pressure values of the right side of the heart?
Right atrium= 2-6mmHg
Right Ventricle= 15-25mmHg
Pulmonary Artery= 15-25mmHg
79
What are the pressure values of the left side of the heart?
Left atrium= 6-12mmHg
Left ventricle= 100-140mmHg
Aorta= 100-120mmHg
80
Which image represents ventricular volume and pressure?
End-systolic Pressure Volume Loop
81
What is systolic dysfunction?
When the ventricle can't contract properly e.g Scar tissue from MI or aortic stenosis
82
What happens to the function of the heart in systolic dysfunction?
Stroke volume decreases, ejection fraction decreases, heart work decreases but end diastolic volumes increase-more blood in the heart but it can't be gotten rid of
83
What is the contractile-velocity relationship?
As afterload increases, the shortening velocity of muscle fibres is reduced as it is harder to squeeze against the blood-this is made even worse by a loss of inotropy
84
What is diastolic dysfunction?
The heart can't relax properly and therefore cannot fill efficiently e.g hypertropy, pericardial fibrosis, mitral stenosis
85
What happens to heart function in diastolic dysfunction?
EDV decreases, stroke volume decreases, ejection fraction is preserved, heart work decreases, end-diastolic pressures increase
86
Anatomy of Cardiac Muscle:
It is striated, and contains both thin actin and thick myosin filaments similar to skeletal muscle
Cardiac t-tubules have a diameter 5 times greater than skeletal to allow for the calcium to move from extracellular to intracellular
87
Why is cardiac muscle contraction different to skeletal?
The plateau phase representing slow influx of calcium of ventricular myocytes means that cardiac contraction lasts 15x longer than skeletal because depolarisation is extended. This means that there is a much longer refractory period too so tetanic contraction in cardiac muscle is impossible
Also, the influx of calcium in cardiac muscle reduces the membrane permeability to Potassium, so repolarisation takes longer in cardiac muscle
88
How is cardiac muscle action potential conduction different to skeletal muscle?
Conduction of Action potentials in cardiac muscle occurs in 1/10th of the time taken to conduct in skeletal muscle. This is because of the presence of gap junctions
89
Cardiac T-tubules:
5 x greater in size than skeletal t-tubules
Inner surface has negatively charged mucopolysaccharides that bind large quantities of Calcium for storage
T-tubule calcium concentration depends on the Extracellular fluid calcium concentration
90
Describe the aortic pressure curve:
pressure rises very rapidly during ventricular ejection, an INCISURA forms in the graph when the ventricle relaxes and there is a backflow of blood-this is restored when the aortic valve closes
Pressure within the aorta then decreases slowly throughout diastole
91
What is preload?
The degree of tension on the muscle as it begins to contract (defined by the volume of blood in the ventricle-the bigger the volume, the bigger the muscle stretch and thus bigger the preload)
92
What is afterload?
The load against which the muscle exerts its contractile force i.e the resistance from the ventricular outlet/arteries
93
What main substrate does the heart use for metabolism?
Fatty Acids-but most of this generates heat
94
What is the frank-starling law?
The greater the heart muscle is stretched during filling, the greater is the force of contraction
95
Why does the frank starling law apply?
Because the bigger the stretch, the more that actin and myosin filaments are brought into optimal crossover and thus more cross-bridges can be made so contraction is with greater force
96
Why does parasympathetic stimulation not have much of an effect on inotropy?
Because most of the vagal fibres are distributed to the atria, so it has a big effect on heart rate but not much of an effect on inotropy
97
What does hyperkalaemia do to the heart?
Causes it to become dilated and flaccid.
Slows heart rate and blocks conduction through the AV Node
Higher levels of ECF potassium makes the resting membrane potential even more negative. This means it is harder to depolarise cells and so action potentials are weaker and so are cardiac contractions.
98
What does hypercalcaemia do to the heart?
High calcium makes the resting potential more positive and induces excessive contraction
99
How does body temperature affect the heart?
Increased body temperature causes an increased heart rate because heat causes an increase in ion permeability and thus self-excitation happens quicker
100
How does valve closure differ during inspiration?
During inspiration, the aortic valve closes slightly before the pulmonary valve. The pulmonary valve closes slower because of lower impedence of the pulmonary vascular tree
101
What is Heteromeric regulation?
regulation of cardiac output as a result of changes to fibre length e.g altered venous return
102
What is Homomeric Regulation?
regulation due to changes in contractility independent of fibre length e.g Nervous input
103
What factors increase the length of ventricular cardiac muscle fibres?
1. Stronger atrial contraction
2. increased total blood volume (increased venous return)
3. increased venous tone (increased venous return)
4. increased pumping action of skeletal muscle (increased venous return)
5. Increased negative thoracic pressure (increased venous return-negative pressure in atrium pulls blood in to it)
104
What factors decrease the length of ventricular cardiac muscle fibres?
1. standing (blood pooling reduces venous return)
2. increased intrapericardial pressure (atria is more positive so doesn't pull blood into it)
3. Decreased ventricular compliance (MI, Hypertopy, Pericardial Fibrosis)
105
What factors increase contractility of the heart?
1. Sympathetic nervous system through the effects of Noradrenaline
2. Ventricular Extrasystoles (premature beat)- the initial contraction is inefficient so the following beat is with extra force due to a build up of excess calcium
3. Catecholamines (same effect as NA-causes increased cAMP)
4. Caffeine and Theophylline (inhibit breakdown of cAMP)
5. Glucagon (increases formation of cAMP)
6. Digitalis (inhibits Na/K ATPase)
106
What factors decrease contractility?
1. Hypercapnoea (causes acidosis)
2. Hypoxia
3. Acidosis (H+ is one of the strongest inotropes as it competes with calcium and prevents calcium binding)
4. Parasympathetic nervous system (not a huge effect)
5. Heart failure
107
What proof is there that cardiac output is modified by both nerves and fibre length?
In heart transplant patients, there are no nerves but they are still able to increase cardiac output during exercise. There is increased skeletal muscle pumping which increases venous return-this causes heart muscle stretching and thus increases inotropy-BUT these alterations to cardiac output are slower and not as substantial-so nerve input is the most important
108
How much oxygen does the heart consume?
Basal metabolic consumption: 2ml/100g/min
Resting heart rate consumption: 9ml/100g/min
^this is considerably higher than for skeletal muscles
109
What is Laplace's Law?
The tension developed in the wall of a hollow viscus is proportionate to the radius of the viscus
110
How does Laplace's Law apply to the heart?
When the heart is full it is dilated and so the tension in the walls of the heart increase.
With increased wall tension, the heart consumes more oxygen
111
Why is angina more common in aortic stenosis than aortic regurgitation?
Because the heart has to consume more oxygen to generate pressure than to generate volume work, and inotropy is increased in aortic stenosis but not regurgiation. Thus, more oxygen is consumed in aortic stenosis and so ischaemia is more likely to occur
