Cardiovascular Systems 1 Flashcards
1
Q
What are the components of the cardiovascular system?
A
The heart
Blood vessels
Blood
2
Q
What are the types of blood vessels?
A
Arteries
Arterioles
Capillaries
Venules
Veins
3
Q
Roughly how many L of blood do we have in our body?
A
4-6L of blood
(variation dependant on size of the body)
4
Q
What are the two circuits of the cardiovascular system?
A
Pulmonary Circuit
Systemic Circuit
5
Q
What occurs in the capillary beds?
A
Gas exchange
6
Q
What is the difference between veins and arteries?
A
Arteries carry blood away from the heart, whereas veins carry blood towards the heart.
Arteries carry oxygenated blood and veins carry deoxygenated blood (with the exception of pulmonary blood vessels).
7
Q
What is pulmonary circulation of the cardiovascular system?
A
Pulmonary circulation transports oxygen-poor blood from the right ventricle to the lungs, where blood picks up a new blood supply. Then it returns the oxygen-rich blood to the left atrium.
8
Q
What is systemic circulation of the cardiovascular system?
A
Systemic circulation carries oxygenated blood from the left ventricle, through the arteries, to the capillaries in the tissues of the body. From the tissue capillaries, the deoxygenated blood returns through a system of veins to the right atrium of the heart.
9
Q
What is the difference between the movement of blood in the pulmonary and systemic circuits?
A
Pulmonary circulation moves blood between the heart and the lungs.
Systemic circulation moves blood between the heart and the rest of the body.
10
Q
Why do we have a cardiovascular system?
A
For adequate supply of oxygen and nutrients.
For the removal of unwanted metabolic by-products (Co2 and H+).
To transport substances and heat around the body.
11
Q
What is the key purpose of the heart?
A
Acts a pump
12
Q
What is the heart located within?
A
In the pericardium
13
Q
What is the pericardium?
A
A protective, fluid-filled sac that surrounds your heart and helps it function properly. Your pericardium also covers the roots of your major blood vessels as they extend from your heart.
14
Q
What type of cells is the heart made up of?
A
Cardiac muscle cells (myocardium)
15
Q
What side of the heart is thicker?
A
The left ventricle of the heart is thicker.
16
Q
What do fibrocartilaginous rings contain?
A
Heart valves
17
Q
What are the two atrioventricular valves?
A
Mitral valve (left) and tricuspid valve (right)
18
Q
What are the two semilunar valves?
A
Aortic valve (left ventricular aorta) and the pulmonary valve (right ventricular pulmonary artery).
19
Q
What causes valves to open and close?
A
Pressure gradient
20
Q
What direction does blood flow?
A
Unidirectionally - meaning it only flows one direction.
21
Q
What feature of the heart prevents the backwards flow of blood?
A
Valves
22
Q
What is the appearance of cardiac muscle and why?
A
Striated in appearance due to its repeating units of sarcomeres.
23
Q
What joins neighbouring cardiac muscle cells?
A
Gap junctions within intercalated discs.
24
Q
What influences arterial blood pressure?
A
Cardiac output and peripheral resistance.
Pressure = Flow x Resistance (MAP = CO x TPR)
25
What is cardiac output?
Cardiac output is the volume of blood ejected by either ventricle in 1 min (value per ventricle not total heart).
26
How do you work out CO?
CO = SV (stroke volume) x HR (heart rate)
27
What are the units for CO?
L.min-1
28
What are the units for SV?
L.beat-1
29
What are the units for HR?
Beat.min-1
30
What is systole?
Ventricular contraction
31
What is diastole?
Ventricular relaxation
32
Roughly how many times does our heart beat a minute?
70 beats per minute (therefore 100,800 times a day).
33
If you miss 5-10 heart beats within a minute what happens?
Unconsciousness
34
What do mechanical events of the heart maintain?
Blood pressure and blood flow
35
What do valvular events of the heart create?
Heart sounds
36
What are the phases of the cardiac cycle?
Diastole: (1) isovolumetric relaxation and (2) ventricular filling.
Systole: (1) isovolumetric contraction and (2) ventricle ejection.
37
What happens during diastole 1 - isovolumetric relaxation?
All valves are closed = no blood flow in or out.
Minimal ventricular volume
Ventricles are relaxing
Atrial pressure is lower than ventricular therefore the atrium fills with blood returning to the heart.
Atrial pressure rises above ventricular pressure and therefore creates a pressure gradient and the AV valve opens passively causing the ventricular filling to begin.
38
What does isovolumetric mean?
Volume of blood staying the same
39
What occurs during Diastole 2 - ventricular filling?
The AV valve is open and the ventricule fills with blood.
It is in this phases that about 90% of the heart filling occurs passively down the pressure gradient.
P wave = trigger for contraction of atrial - this causes the final 10% of filling of the ventricle.
Now that the heart is 100% fill we are at end-diastole volume.
40
What occurs during systole 1 - isovolumetric contraction?
Ventricles are filled and depolarise.
Ventricles contract and ventricular pressure rises.
AV valves close = first heart sound.
All valves are shut therefore there is no blood flow and no change in blood volume.
Isovolumetric contraction
41
What occurs during systole 2 - ventricle ejection?
Ventricles continue to contract and build pressure.
Pressure becomes higher than aortic pressure therefore aortic valves open.
Blood ejects into the aorta
Arterial blood volume and arterial pressure increases.
Depolarisation of ventricles = T wave signalling ventricle to relax and pressure falls below aortic pressure. Therefore aortic semilunar valves close = 2nd heart sound.
42
What percentage of blood ejection occurs in the first 1/3 of ejection time?
2/3
43
Approx how long does diastole 1 last?
0.05s
44
Approx how long does Diastole 2 last?
0.6s
45
How long does systole 1 approx last?
0.05s
46
How long does systole 2 approx last?
0.3s
47
What is the aortic pressure during diastole?
80 mmHg
48
What is aortic pressure during systole?
120 mmHg
49
What is LV pressure during diastole?
80 mmHg
50
What is LV pressure during systole?
120 mmHg
51
What is a healthy ejection fraction?
Between 55 and 60%
52
What is the third heart sound?
Passive ventricular filling in early diastole - tends to only be heard in the young
53
What is the P wave of an ECG representing?
Where atrial depolarisation precedes atrial contraction
54
What does ECG stand for?
Electrocardiogram
55
What is the QRS complex of an ECG representing?
Ventricular depolarisation preceding ventricular contraction
56
What is the T wave of an ECG representing?
Ventricular repolarisation and ventricular relaxation
57
What percentages of the cardiac cycle are diastole and systole?
Diastole approx 2/3
Systole approx 1/3
58
What part of the cardiac cycle speeds up when our heart rate increases?
The entire cardiac cycle gets faster (both diastolic and systolic cycle will get shorter) - However the diastolic phase shortens more so that we now have 1/3 of our cycle in diastole and 2/3 in systole.
59
Cells have a high permeability to ..., low to ... and very low to ...?
Cells have high permeability to potassium (K+), low to sodium (Na+) and very low to calcium (Ca2+).
60
What is depolarisation?
Less negative charge inside the cell compared to outside the cell (generally means that positive charge enters the cell).
61
What is repolarisation?
More negative charge inside the cell compared to outside the cell.
62
Where does conduction of an AP in the heart begin?
In the SA node (sinoatrial node) which is located in the top of the right atrium
63
What is the peacemaker of the heart?
SA node - it gets this name because it determines the frequency of heart beats by initiating AP conduction.
64
What is the conduction pathway in the heart?
Sinoatrial node (SA node) - origin of the AP
Atrioventricular node (AV node)
Bundle of His
Purkinje fibers
Cardiomyocytes
65
Where is the AV node located?
The base of the right atrium
66
What is functional syncytium?
A functional syncytium refers to a group of cells that function as a single unit while still maintaining their individual cellular role.
67
Is the heart a functional syncytium?
Yes. As all cells are attached through gap junctions every AP in the heart propagates through all cells = all or nothing contraction.
68
Approximately how many AP does the SA node generate per minute?
100
69
Approximately what speed are AP conducted through the atrium?
0.5 ms-1
70
Where in the heart is AP conduction slowest?
AV node (0.05ms-1)
71
What does the delay in conduction at the AV node allow for?
The delay permits full depolarisation and contraction of the atria before depolarisation and contaction of the ventricles.
In other words it means that the entire heart doesn't contract at the same time and thus allows for the "top up period".
72
Where is AP propagation the fastest?
Bundle of His, Bundle Branches and Purkinje Fibers: at approximately 5.0 ms-1
73
Approximately what speed does an AP spread in ventricular myocardium?
0.5 ms-1
74
What do purkinje fibres allow for?
Synchronous depolarisation and contraction of all ventricular regions (due to wide spread branching)
75
What cells are the "leaders" in the heart?
Pacemaker cells - SA node - origin of AP
76
What are "followers" in the heart?
Ventricular cells - Cardiomyocytes - (they are followers because they do nothing until an AP to reaches them)
77
How many phases do pacemaker cells have?
3
Phases 4, 0 and 3
78
How many phases do ventricular cells have?
5
Phases: 4, 0, 1, 2 and 3
79
What is phase 4 of pacemaker cells?
At RMP (-60/-70 mV)
BUT unstable due to "funny Na+ channels" that allow a slow influx of Na+
In the late phase T-type Ca2+ channels (TTCC) allow an influx of Ca2+ aswell making the cell more positively charged and reach threshold
80
At what voltage does pacemaker cells reach threshold in Phase 4?
-50/-40 mV
81
What is phase 0 of pacemaker cells?
Upstroke
L-type or voltage operated Ca2+ channels (LTCC) open allowing an influx of Ca2+.
82
What is phase 3 of AP in pacemaker cells?
repolarisation - slow K+ efflux
83
What is the RMP for pacemaker cells?
-60/-70 mV
84
What is the RMP for ventricular cells?
-90 mV
85
What is phase 4 of an AP in ventricular cells?
Stable at RMP of -90mV
K+ influx
86
What is phase 0 of AP in ventricular cells?
Upstroke - fast depolarisation due to the opening of fast Na+ channels. The influx of Na+ causes threshold to be reached (-65 mV).
87
What is threshold for an AP in ventricular cells?
-65 mV
88
What is phase 1 of AP in ventricular cells?
Early repolarisation - fast Na+ channels close and the influx stops - small K+ efflux.
89
What is Phase 2 of AP in ventricular cells?
Cardiac Ca2+ plateau - sustained depolarisation.
LTCC open and Ca2+ influx counterbalance a K+ efflux
90
What is phase 3 of ventricular cell AP?
Late repolarisation
Inactivation of Ca2+ channels and activation of K+ efflux causing fast repolarisation.
91
Are pacemaker cells or ventricular cells stable?
Ventricular
92
Why are pacemaker cells unstable?
due to funny nA+ channels and TTCC
93
What do APs in the heart depend on?
Function and localisation
94
What is an ECG?
A recording of potential changes at the skin surface that result from depolarisation and repolarisation of heart muscle
95
Where are the three recording electrodes on an ECG?
Left Arm - LA
Right Arm - RA
Left Leg - LL
96
How are ECG recordings made?
Between 2 electrodes - the ECG represents the difference between 2 electrodes called bipolar leads.
97
What is Lead 1 in an ECG?
The potential difference between LA and RA.
LA is positive and RA is negative
98
What is Lead 2 in an ECG?
The potential difference between LL and RA.
LL is positive and RA is negative
99
What is Lead 3 in an ECG?
The potential difference between LL and LA.
LL is positive and LA is negative
100
What is Einthoven Triangle?
Standard Limb Leads 1, 2 and 3 (forms a triangle)
101
What does P wave in an ECG represent?
SA cells depolarise
Right and Left atria depolarising towards AV node
Depolarisation towards positive electrode and thus positive deflection
102
What does the T wave in an ECG represent?
Repolarisation of ventricles from outside to inside away from the detecting electrode causing a positive deflection
(Ventricular relaxation)
103
What is the large positive deflection on an ECG?
R - of the QRS complex
104
What does the term aV refer to?
Augmented voltage measured
105
How many leads are involved in augmented limb leads?
6
106
What plane of the heart is examined from chest leads?
Horizontal plan
107
What type of ECG is a powerful clinical diagnostic tool?
12 lead recording
108
Excitation-contraction coupling links action potentials, through calcium transient with what?
Sarcomere contraction
109
What happens when Ca2+ enters cardiac muscle cells?
Cell membrane depolarisation and the threshold of LTCC is reached causing them to open
110
What enters when LTCC open?
Ca2+
111
Where is Ca2+ released from?
Intracellular stores in the SR
112
What receptor is activated by entry of Ca2+ in muscle?
RyR
113
What percentage of Ca2+ is released from the LTCC and from the RyR2-SR during excitation-contraction coupling?
25% from LTCC
75% from RyR2-SR
114
What is the cycle that occurs for contraction of cardiac muscle?
Cross Bridge Cycling
115
Explain the process of cross bridge cycling in cardiac muscle:
Ca2+ binds to troponin C in troponin complex
Displacement of Troponin-tropomysin allows for the interaction of Actin-Myosin to form a cross-bridge
When actin and myosin bind ADP and Pi are released and the myosin head flips (power stroke) and actin moves towards the centre of sarcomere causing the sarcomere to shorten
ATP then binds causing the cross-bridge to detach
116
What are the three domains of the troponin complex?
TnC-Troponin C (Ca2+ binding domain)
TnI-Troponin I (inhibitory domain)
TnT-Troponin T (tropomyosin binding domain)
117
If Ca2+ remains in high quantity what happens to the cross-bridge cycle?
It continues
118
What is the sliding filament theory?
Myosin is pulling actin towards centre of the sarcomere
Actin filaments slide along adjacent myosin filaments by cycling of cross-bridges with myosin
119
What lines come closer together when a cell shortens producing force and tension?
Z lines
120
What makes contraction more forceful?
An increase in the number of cross bridges (not an increase in more contracting cardiomyocytes).
121
What causes the end of cross bridge cycling contraction?
The influx of Ca2+ ceasing due to SR no longer being stimulated to release Ca2+ due to cytosolic Ca2+ being rapidly reduced
122
What are the three different mechanism to reduce intracellular Ca2+?
SERCA
Sodium-Calcium Exchanger (NCX)
Ca2+ ATP-ase
123
Is the SERCA pump ATP dependant?
Yes
124
What does the SERCA pump do?
Pumps cytoplasmic Ca2+ back into the SR
125
What is SERCA pump activity regulated by?
Phospholamban (PLB)
126
What does PLB protein phosporylation stimulate?
Ca2+ uptake by the SERCA pump
127
What is the Sodium-calcium exchanger (NCX) driven by?
Na+ gradient (which comes from the Na+/K+-ATPase)
128
What are the relative percentages of the ventricle relaxation due to Ca2+ uptake achieved by SERCA, NCX and Ca2+ATPase?
SERCA 75%
NCX 24%
Ca2+ATP-ase 1%
129
What is the Ca2+ ATP-ase?
A cell membrane ATP-dependent pump for Ca2+ uptake (causing relaxation)
130
Why does tetanus of heart muscle not normally occur?
Tetanus of heart muscle contraction does not occur because summation of contractions is not possible.
131
How long is the absolute refractory period of heart muscle?
250ms
132
How long is the relative refractory period of heart muscle?
300ms
133
What do the refractory periods of heart muscle prevent?
Re-excitatuon during the contraction period and circuitous recycling of AP.
134
For aerobic metabolism what is the hearts preferred source of energy?
Fatty acid and glucose
135
What is the name of the condition the body is put into when it runs out of ATP?
Metabolism rigor mortis
136
What processes are driven by ATP?
Ca2+-uptake in SR
Deattachment of Actin-myosin cross bridge
Ca2+-extrusion by Ca2+ ATPase
Na+-K+ ATPase pump
Primary active transport
137
What is the most important control of heart rate?
Extrinsic controls (parasympathetic and sympathetic control) - intrinsic control of HR is very limited.
138
What is the treppe effect (also known as at the Bowditch effect)?
Describes the positive relationship between stimulation frequency and contraction force. As heart rate increases, the force of myocardial contraction increases due to more Ca²⁺ being available within the muscle cells per unit of time.
139
What is the hall-mark of heart failure?
Negative force-frequency relationship.
In heart failure, the relationship between force and frequency can become negative, meaning that as the heart rate increases, the force of contraction may decrease. This is a hallmark of failing myocardial function.
140
What does an increase in preload produce?
Larger stroke volumes
141
What is the frank-starling law of the heart?
MORE IN MORE OUT.
The more you fill the more you squirk.
States that the heart has an intrinsic ability to adjust its force of contraction and stroke volume in response to changes in venous return or blood filling.
E.g.; increased venous return = increase preload = increase in end-diastolic volume = ventricle is more filled with blood. Consequently, ventricle is stretched = increased sarcomere length = increase contraction = larger stroke volume.
142
The heart regulates ventricular output in response to what?
In response to ventricular filling
143
What is the units for volume?
ml
144
Is ESV or EDV larger?
EDV
145
If the left-ventricle is enlarged due to greater EDV what effect does this have on ESV?
none?
146
Why does force increase with length?
Increased Ca2+ sensitivity of the myofilaments due to better overlap of myosin and actin (Nothing to do with the amount of Ca2+).
147
What is the largest protein in the body?
Titin - found in sarcomere between Z line and M line.
148
What does Titin do?
Pulls actin and myosin filaments closer together
149
What is lattice spacing?
Actin and Myosin myofilament spacing
150
What is ATT?
The Actin-Troponin-Tropomyosin complex
151
What is after-load?
After-load represents how hard the heart has to work to push blood out (the resistance it has to overcome to eject blood).
After-load is a measure of the tension/stress developed in the ventricular wall to open the aortic valve. Therefore related to aortic pressure and wall stress.
152
What happens if you increase afterload?
Increase pressure
Increase ESV, decrease SV and EF, unchanged EDV
153
What is contractility?
Measure of how effective the heart is as a pump (how strong the squeeze is - stronger the squeeze the more blood that is pumped out)
154
What its inotropy?
The heart muscle ability to contract (same as contractility)
155
What changes the hearts contractility?
Hormones or nervous changes
156
What is meant by 'autonomic control'?
Changes that occur automatically/unconsciously
157
What hormone is released in the sympathetic autonomic control of the heart?
Noradrenaline
158
What hormone is released in the parasympathetic autonomic control of the heart?
Acetylcholine
159
Does noradrenaline or acetylcholine change EDV?
No - just change the function
160
What are the four F of autonomic control?
Fight, Flight, Feeding, Fucking (mating)
161
What are the sympathetic fibres involved in heart rate?
Cardiac nerves
162
What are the parasympathetic fibres involved in heart rate?
Vagus nerve
163
What happens when the sympathetic system is stimulated (represented on graph)?
Increased slope of pre-potential and less negative membrane potential
164
What is a fast heart rate called?
Tachycardia
165
What happens when the parasympathetic system is stimulated (represented on graph)?
Reduced slope of pre-potential and More negative membrane potential
166
What is a slow heart rate called?
Bradycardia
167
During parasympathetic stimulation what receptors does ACh bind to?
M2 muscarinic receptors
168
What is activated during parasympathetic stimulation?
ACh-senstive K+ channel
169
What is activated during sympathetic stimulation?
PKA (protein kinase A)
170
What are factors affecting heart rate called?
Chronotropic factors
171
Does sympathetic or parasympathetic activity decrease heart rate?
Parasympathetic
172
Without parasympathetic control what would HR approximately be?
110 bpm
173
What are factors affecting duration of contraction and relaxation called?
Lusitropic factors
174
What are factors affecting contractility called?
Inotropic factors
175
How does the sympathetic system stimulate contraction?
More and faster Ca2+ release
Faster cross-bridge cycling
More and faster Ca2+ uptake
Stronger and faster contraction
Faster relaxation
176
During sympathetic stimulation of contraction what does NA (noreadrenaline) bind to?
b1-adrenoceptor
177
What effect does TnI have on TnC during sympathetic stimulation for contraction?
TnI limits interaction of Ca2+ with TnC which decreases Ca2+ sensitivity
178
What happens to the duration of twitch as a result of increased heart rate by noradrenaline?
It shortens
179
What does chronotropic mean?
Rhythmic excitation
180
What is meant by dromotropic?
Conduction speed
181
What is the effect of positive inotropic?
Increase in contractility
182
What are the short term regulators (hormones) for extrinsic control?
Catecholamines (adrenaline, noradrenaline and dopamine)
Glycosides (digoxins and digitalis)
183
What are the long term regulators (hormones) for extrinsic control?
Angiotensin 2 (AT1 in heart)
Endothelin (ET1 in heart)
Thyroid hormone (T3)
184
What are the two glycosides involved in extrinsic control of the heart?
Digoxins and digitalis
185
What is the negative inotropic effect?
Decrease in contractility
186
What does ACh bind to causing a negative inotropic effect?
M2-receptors
187
What do beta-blockers do?
Reduce cAmp
Reduce PKA activity
Reduce activity of LTCC, RyR, SERCA
Increase Ca2+ sensitivity of TnC
Reduces need for ATP - less stress on the heart
188
How do beta blockers reduce the stress on the heart?
Because they reduce the need for ATP
189
What is preload?
How much the heart fills up - related to the initial stretching of the cardiac muscle fibres (sarcomas) before contraction as the more they stretch the more room for greater volume of blood.
Preload is directly relation to Frank-starlings theory - more in, more out.
190
What is the relationship between EDV and preload?
Increasing EDV (the volume of blood in the ventricles at the end of diastole e.g., ventricular filling) is directly related to increase in preload.
191
What is the effect of an increase preload on SV, ESV and EF?
SV increased
EF increase
ESV unchanged
192
What is the effect of an increased after load on SV, EF and EDV?
SV decreased
EF decreased
EDV unchanged
193
If contractility is increased what is the effect on SV, EF and ESV?
SV increased
EF increased
ESV decreased
194
What is ESV?
ESV (End-Systolic Volume) is the amount of blood left in the ventricle after the heart has contracted (systole) and pumped blood out. It represents the volume of blood remaining in the heart at the end of each heartbeat.
In simpler terms: ESV is the "leftover" blood in the heart after it has squeezed as much blood as it can.
195
How do you work out SV?
EDV - ESV = SV
196
How do you work out EF?
EF = (SV / EDV) x 1000
