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Physiology of the Heart Flashcards

1
Q

List the transportation roles of the heart and circulation

A

Transporting:

  • Vitamins
  • Nutrients
  • Oxygen/CO2
  • Hormones
  • Immunoglobulins
  • RBC/WBCs
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2
Q

Give the thermoregulatory roles of the heart and circulation

A
  • Counter-current exchange mechanism
  • Circulation of the skin
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3
Q

Give the 3 major parts of the circulation

A
  • Heart
  • Systemic circulation
  • Lung circulation
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4
Q

Describe Starling’s effect

A

To increase load, the heart automatically reacts with extra work

without hormonal/neuronal factors

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5
Q

Describe the heart’s work load status during rest

A

The heart is working in the lower range of its total working capacities

This is ensured by parasympathetic predominance

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6
Q

A decrease of parasympathetic activity may cause…

A

An increase in the mechanical performance of the heart

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7
Q

The autonomity of the heart rythmn is due to…

A

Rythmn generators in the SA node

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8
Q

Give the main parameter of cardiac mechanical performance

A

Cardiac output

The volume of blood propelled into the aorta from the left ventricle per unit time

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9
Q

List the layers of the heart

A
  • Endocardium
  • Myocardium
  • Epicardium
  • Pericardium
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10
Q

Give the contractile components of the myocardium

A
  • Heart muscle fibres (working fibres)
    • Stretching enhances their force-generating capability
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11
Q

Give the non-contractile components of the myocardium

A
  • Serially attached elastic elements (SEC)
  • Parallelly attached elastic elements (PEC)
  • Collagen
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12
Q

List the functions of the pericardium

A
  • Fixation: keeps the heart in the mediastinum
  • Protection from infection from other organs
  • Prevents excessive dilation of the heart during hypervolemia
  • Lubricates the heart
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13
Q

Describe fetal circulation in relation to the pulmonary circulation

A
  • Lungs not functioning
    • Blood bypasses lungs → foramen ovale
    • Between L & R atrium
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14
Q

Describe the closing of foramen ovale

A
  1. Pressure in left atrium increases
  2. Flap valve covers foramen ovale
  3. After 1 year, the foramen completely closes
  4. It is then regarded as fossa ovalis
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15
Q
  • What percentage of the population does the foramen ovale not seal?
  • What is the condition called?
A
  • 30%
  • Patent foramen ovale (PFO)
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16
Q

Name the fetal vessel between a. aorta thoracica and a. pulmonalis

A

Ductus botallo

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17
Q

When does ductus botallo close?

A

4 weeks postpartum

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18
Q

List the excitable varieties of cardiac tissue

A
  • Pacemakers
  • Conductive system
  • Working fibres
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19
Q

Purpose of the Aschoff-Tawara (AV) node

A

Delays the atrial signal

So atrial contraction precedes the ventricular contraction

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20
Q

Resting membrane potential (RMP)

A

Diastole:

  • -90mV
  • Spontaneous depolarisation followed by AP
  • RMP doesn’t exist in pacemaker cells
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21
Q

Describe action potential (AP)

A
  1. Stimulation
  2. _Ion channel_s of membrane open
  3. Ion exchange between the two sides
  4. Action potential
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22
Q
A

Pacemaker potentials

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23
Q

Pacemaker cells

A
  • Located: SA / AV node
  • Allow continuous generation of excitation
  • No RMP
  • Repolarisation: Transmembrane potential -55mV
  • Automatic depolarisation follows
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24
Q

This electrical activity is expressed in…

A

Sinoatrial (SA) node

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25
This electrical activity is expressed in...
Ventricular muscle
26
Pacemaker action potential is... * Slower/faster and * Lower/higher ...than cardiomyocytes
* Slower * Lower
27
Round pacemaker cells
Sites of the generation of excitation
28
Elongated/slender cells
_Conduct/synchronise excitation_ generated in round pacemaker cells
29
Maximal depolarisation potential (MDP)
_No RMP developed_ after the previous AP reaches _-55mV_
30
* K+ channels close * Na+ channels open
31
* Ca2+ channels open * Na+ channels close
32
This electrical pattern is representative of...
Pacemaker cells
33
* Ca2+ channels close * K+ channels open
34
* K+ channels close * Na+ channels open
35
Overshoot
36
+15 mV
37
MDP
38
SDD
39
Threshold potential
40
Maximal diastolic potential; virtual resting potential (MDP)
* Slow Na+ channels open spontaneously * Slow depolarisation begins
41
Spontaneous diastolic depolarisation
No RMP until threshold potential
42
'Overshoot'
* Ca2+ influx and only slow Na+ channels * +5/+15mV (Lower than working fibres)
43
Repolarisation
* K+ efflux until MDP
44
What does Ih (hyperpolarisation activated) channel opening trigger?
If Threshold of _-40mV_ is reached, the following will _open_: * _Type-T, rianodin sensitive_ calcium channel * _Type-L DHP sensitive_ calcium channel
45
The opening of Type-T and Type-L channels causes...
* Calcium to flow from the EC into the cell * Causes a transient Ca-influx
46
The period from MDP to threshold potential is known as...
Spontaneous diastolic depolarisation (SDD)
47
Depolarisation of the SA node is due to which channels?
Long-lasting Ca2+ channels
48
Why is the membrane potential of the '0' phase so steep?
* There are _no fast Na+ channels_ in the membrane of the round cells * _Only long lasting Ca-channels determine this phase_
49
What occurs from the point of potassium channels opening?
* Efflux of K+ ions from cell * Repolarisation until MDP is reached * Activation of Ih channels starts a new cycle
50
Term given to the frequency of contraction
Chronotrop
51
Term given to the speed of conduction
Dromotrop
52
Term given to the threshold of contraction
Bathmotrop
53
Term given to the force of contraction
Inotrop
54
Vagus escape
* Stimulation of *n. vagus* * _Effectiveness_ of further _stimulation disappears_ * Switch from _nomotop_ → _heterotop excitation_ * _AV node now generates rythmn, not SA node_
55
Which nerve controls heart rate?
*N. vagus*
56
Describe the stimulation of SA node round cells
Sympathetic effect * _Stimulation_ of _B1-receptor_​ * Same effect triggered by _norepinephrine_ and _epinephrine_ * Parasympathetic suppression, _enhancing the effect_
57
Describe how stimulation of _B1-Rec_ can cause _sympathetic effect_
1. Stimulation of _G-protein mediated IC cAMP_ increase 2. _Na+_ & _K+_ channels _open_ 3. _MDP shifts upward_, steepness of _SDD increases_ 4. _Threshold reduced_ 5. Heart rate _increase_
58
Describe parasympathetic effects altering heart rate
1. _Acetylcholine_ stimulates _muscarinic acetylcholine receptors_ on _round cells_ 1. cAMP decreases 2. MDP shifted down 3. SDD slope decreases 4. Threshold potential elevates 5. Hyperpolarisation 2. _Heart rate decreases_
59
Describe the metabotropic effect on heart rate
1. Acetylcholine opens metabotropic K+ channels 2. Further hyperpolarisation 3. Decreased frequency
60
Heart conduction in _small animals_
* _Subendocardial_ conduction * Conducting fibres don't penetrate working muscle _deeply_
61
Heart conduction in large animals
* _Subepicardial_ conduction * Fibres pass _deeply_ into the _ventricle_
62
Bachmann's bundle
63
Left posterior bundle
64
Signal arriving from the SA node
Nomotop excitation
65
A signal arriving from AV node
Heterotop excitation
66
*Anulus* *fibrosus*
* Represents electric resistance * Synchronises atrioventric cooperation
67
How long is the indicated period?
~200 ms
68
What is shown?
Action potential of a _working fibre_
69
Resting Membrane Potential _-90 mV_
70
**Depolarisation** * Na+ influx
71
**Overshoot** +25 mV
72
**Rapid repolarisation** * K+ efflux *(early)* * Cl- influx
73
**Plateau** * Ca2+ influx * K+ efflux *(slow)*
74
**Rapid repolarisation** * K+ efflux *(late)*
75
**Late hyperpolarisation** * K+ efflux *(late)*
76
What is the purpose of the _plateau_ phase?
Blocks premature AP generation/contraction
77
_Ion flow_ of _working fibres_ during _action potential_
1. Depolarisation 2. Rapid repolarisation 3. Plateau 4. Rapid repolarisation 5. Later hyperpolarisation
78
The flow of charges across the membrane is dependent on...
* Permeability * Electrochemical gradient
79
Metabotropic channels
* Under the control of hormones + neurotransmitters * Conductance properties of these channels altered * Change in heart function
80
Which channels are responsible for action potential?
Voltage-dependent Na+ channels
81
Which channels open in each phase of the AP?
Phase 1: Early potassium channels Phase 2: Slow potassium channels Phase 3: Late potassium channels
82
The effect of the overshoot
* Activation of calcium channels * Calcium ions enter the cell * Repolarisation is elongated
83
The duration of the plateau phase is: * Longer closer to the... * Shorter closer to the...
Longer closer to the _endocardium_ Shorter in the _epicardium_
84
Absolute refractory phase (ARP) * AP cannot be initiated
85
Relative refractory phase (RRP) * Strong stimulus may initiate AP
86
Supernormal phase (Refractory phase) * A slight stimulus may initiate AP * AP will be submaximal
87
Absolute refractory phase
* No stimulus * A new action potential is elicited before the plateau
88
Relative refractory phase
* A stimulus is given after the plateau * Before reaching threshold potential * Can cause a new AP if strong enough
89
Supernormal phase
* Between threshold and RMP * Slight stimulus: Gives new AP * Premature new contraction * Can be fatal in the ventricle (fibrillation)
90
Atrial fibrillation
* Electric stimulation of the atrium (repeated contractions) * Ventricle maintains normal circulatory pressure * Non-fatal
91
Ventricular fibrillation
* Normal blood pressure cannot be maintained * May drop to '0' * Systole and diastole disappears (Fatal)
92
Defibrillation
Strong electric current: * Desynchronisation stops * SA node synchronised again * Normal rhythm * Nomotop excitation returns
93
Difference between AP and mechanogram of cardiac muscle
Mechanogram is almost parallel to AP
94
Difference between AP and mechanogram of skeletal muscle
* No plateau phase * AP lasts for 1 millisec, compared with 200 millisec of heart * Mechanogram develops only after AP has vanished
95
Electromechanical coupling
Connection between electric stimulus and mechanical signal
96
Which process is shown?
Electromechanical coupling
97
1
AP spreads onto the cell
98
2
* AP reaches T-tubules * Activates L-type Ca2+ channels
99
3
* Conformational changes of L-type channels * → T-type channels on SR open
100
4
* Elevating the sarcoplasmic level of Ca2+ * → Opens Ca2+ dependent channels on SR
101
5
* Elevating sarcoplasmic Ca2+ level * Opens Ca2+ dependent channels on cell membrane
102
6
* A huge amount of intracytoplasmic Ca2+ around the sarcomeres * Contraction
103
Which process is shown?
Elimination of calcium signal
104
1
**After contraction** Na+/Ca2+ antiporter into extracellular space
105
2
ATP-dependent Ca2+ transporter into SR * IC Ca2+ conc. decreases * Relaxation
106
What is the structural unit of electromechanical coupling?
Diad ## Footnote *T-tubules and SR are in contact here*
107
Steps of action potential
1. L-type Ca2+ channels open (Voltage-gated) 2. Rianoid Ca2+ channels open 3. Elevated Ca2+ in the cytoplasm → 4. Causes Ca2+ dependent channels to open 5. Intracytoplasmic Ca2+ around sarcomeres increases 6. Contraction
108
Describe the ion movement during/after contraction
1. ATP-dependent Ca2+ pump drives Ca2+ back into the SR 2. Na+/Ca2+ antiport pumps Ca2+ back to the EC space 3. IC Ca2+ conc. drops 4. Relaxation
109
What is expressed in the figure?
**Einthoven's triangle** * Einthoven 1: Right Arm ⇔ Left Arm * Einthoven 2: Right Arm ⇔ Left Leg * Einthoven 3: Left arm ⇔ Left Leg
110
Einthoven's bipolar leads detect...
Changes in the _dipole_, projected onto the body surface
111
ECG measures...
The _sum_ of the electrical activity of _single myocytes_
112
An ECG is a sum of...
An EAG and an EVG
113
Name the trace
EAG
114
Name the trace
EVG
115
Name the trace
ECG
116
How long is this period?
0.5-0.10 sec
117
How long is this period?
0.12-0.20 sec
118
0.06-0.10 sec
119
P-wave
* Upward deflection * Atrial depolarisation begins * SA node already depolarised (undetectable)
120
PQ-segment
* On isoelectric line * Total atrial depolarisation * AV conduction
121
QRS-complex
* The beginning of ventricular depolarisation * Repolarisation of atrium
122
Q-wave
* Downward deflection * Stimulus runs through Bundles of His, through the septum, toward the basis of the heart
123
R-wave
* Max ventricular depolarisation * Stimulus runs from endocardium to pericardium * From the base to the apex * Total ventricular mass depolarises
124
S-wave
* Depolarisation of the right ventricle
125
ST-segment
* Isoelectric line on the oscilloscope * Ventricles totally depolarised
126
T-wave
* Ventricular repolarisation * Upwards deflection → Man + Small animal * Downward deflection → Other species
127
TP-segment
* Resting phase * The oscilloscope is at _isoelectric line_ * Myocytes are _positive outside_, _negative inside_
128
ECG is used in the diagnosis of...
* Pathologic electrical events * Problems of conducting system * Anatomical disturbances
129
What are the types of ECG?
* Unipolar ECG * His bundle ECG * Oesophagal ECG * Vectorcardiography
130
Unipolar ECG
* RA, LA, LL connected to each other * Via 0 potential reference point * _PD_ between the _reference point_ and the _different points_ measured
131
His bundle ECG
* An electrode placed up to the septum * Through a vein catheter
132
Oesophageal ECG
An electrode placed through oesophagus close to the heart SA, AV nodes + conduction system analysed
133
Vector loop
* Provides information on heart function of territories * The connection of vectors from the R wave
134
Vectorcardiography
* Anatomical information of the heart * Forms the 'electrical axis of the heart' * Peak values of R-leads: produces a vector
135
Echocardiography
* _Ultrasound_ examination * A detailed picture of the cardiac _anatomy_ and _blood flow_
136
Which fibres passively support the filling of the heart?
Serially and Parallelly attached elastic fibres (SEC/PEC)
137
Give the function of the elastic elements of myocardium
* Passive store of energy while stretched * Can be utilised as surplus energy for the next contraction
138
When is SEC stretched?
Systole
139
When is PEC stretched?
During diastole
140
What is the function of collagen in the myocardium?
* Prevention of overexpansion and rupture * Resistant during the maximal filling of the heart
141
Cardiac muscle
* Striated → sarcomeres * Shorter than skeletal muscle * More mitochondria * Less extensive SR * Often binucleate and polyploid * Continued division after actin/myosin synthesis
142
What are the types of heart contraction?
* Isotonic * Isometric * Auxotonic * Preload * Afterload
143
Isometric contraction
* 1st phase * Weight stretches SEC elements only * Weight doesn't move yet * Stretch present, but no shortening
144
Isotonic contraction
* 2nd phase * Stretch with SEC increases * Weight begins to move * Shortening occurs * Stretching force remains
145
What is expressed in the figure?
The normal working range of a single working fibre * Cardiac muscle shows _max tension_ only at an _increased sarcomere length_
146
Skeletal muscle (Optimum sarcomeric length) * Cross bridges in the right place * All Ca2+ binding sites saturated
147
Cardiac muscle (optimal sarcomeric length) * All bridges in correct place * Not enough Ca2+ * Therefore, only a _few_ binding sites are saturated
148
Cardiac muscle (Upper-edge of optimal sarcomeric length) * Cross bridges in the right place * Ca2+ binding sites are saturated * This is due to the increased length
149
The degree of contraction of _cardiac_ muscles is dependent on...
The length of sarcomeres
150
Compare skeletal and cardiac muscle: At very short sarcomeric lengths
* Both perform less * Optimum actin/myosin constellation is distorted
151
Compare skeletal and cardiac muscle: At very large sarcomeric lengths
* Performance is small in both * Few/no myosin heads have actin binding sites
152
Compare skeletal and cardiac muscle: between 1.9-2.5 sarcomeric lengths
* An optimal opposition to binding sites and myosin heads occurs * Cardiac muscle: Maximal performance requires pre-stretch
153
Give the 'law of the heart' (Starling)
* Increased stretch results in increased contraction * Irrespective to the innervation of the heart * (Like a sling-shot)
154
EDV
**End-diastolic** **volume** At the end of diastole, ventricles are maximally filled
155
ESV
**End-systolic volume** When ventricles are maximally emptied, there is still some blood remaining in them
156
SV
**Stroke Volume** * Volume passing through the aorta in each cycle * EDV-ESV
157
The formula for Cardiac output
(EDV-ESV) x Freq. = CO = SV x Freq.
158
What is shown?
Starling's heart-lung preparation
159
Describe starling's heart-lung preparation
* Heart can adapt to increased load due to mechanical reasons * Also observed in an _isolated heart_ (No nerves/hormones) * Arterial side represented by _peripheral resistance_ * Venous side represented by a _reservoir_
160
What was involved in Starling's two experiments?
Experiment 1: Increasing venous return Experiment 2: Increasing peripheral resistance Volume fractions were measured for both
161
Describe the effects of increasing venous return
* Immediate EDV increase * Delayed ESV increase * SV + CO increase Increased load generates increased contraction
162
Describe the effects of increased peripheral resistance
* Immediate increase in residual volume (ESV↑; SV↓) * Delayed ESV and EDV increase proportionally * SV increases to the same level SV and CO will be set as it was before
163
Describe the effects of lying down on the circulation
1. More blood enters ventricle 2. Dilation 3. Increased performance
164
Heteromeric autoregulation
1. Increased blood leaving the right compartment 2. Dilation and stretching of the left side 3. Starling mechanism activated 4. Automatic compensation between left and right compartments
165
Heterometry
Small differences occurring in the volume of blood appearing the left and right sides of the heart
166
Blood volume passing through the left and right side of the heart should be...
The same
167
Heterometry can be adjusted by...
Starling effectt
168
Which two ways can CO be measured?
* Fick's principle * Stewart's principle
169
Fick's principle
*More widely used method* CO: * O2 taken up by the lung per unit time = O2 taken up by tissues * CO = Total O2 uptake / arterio-venous O2 difference
170
Stewart's principle
* Inject IV Evans-blue * Sample collection + analysis * Plot curve and extrapolation * _Area under the extrapolated cure = CO_
171
Ventricular compliance
Dilating capacity
172
Ventricular compliance is an important parameter for assessing...
Adaptability of the heart | (Dilating ability of ventricles)
173
Value of EDV ventricular pressure
5 mmHg
174
EDV ventricular pressure can be extrapolated to give an EDV value of...
60ml
175
Describe the increase of EDVP
* Proportional increase of EDV(+SV) * Until _25 mmHg_ * (collagen fibres prevent further dilation)
176
Describe ventricular compliance in elderly animals
* Compliance curve is shifted to the right * Two-fold EDVP is needed to achieve the normal EDV level
177
Describe the cause of ventricular compliance in elderly animals
* Increased rigidity of elastic fibre * Aging of muscle cells
178
The formula for total work of the heart
**Wt = Wouter + Winner** * Wouter = Mechanical* * Winner = Heat production*
179
Wouter =
**SV x ΔP** *ΔP = (arterial average pressure)*
180
Burning 1L oxygen produces...
20kJ energy
181
Give the efficiency of the heart
10-20% efficiency
182
_Kinetic_ component of _outer mechanical work_ amounts for...% of total work
4%
183
The formula to calculate the performance of the heart
**P = Work/time = CO**
184
What does the Rushmer diagram analyse
* Analyses _outer/mechanical work_ of the heart * as a function of _volume_ and _pressure_ of _LV_
185
Rushmer Diagram
186
* Mitral Valves close * **Isovolumetric contraction**
187
* Aortic valves open * **Ejection** phase
188
* Semilunar valves close * **Isovolumetric relaxation**
189
* Mitral valves open * **Filling**
190
Law of Laplace in a pathological context
Increased ventricular volume → increased oxygen consumption → Reduced cardiac efficiency ## Footnote *Wall tension maintained _only_ by increased O2 consumption*
191
Increased ventricular volume causes...
An increase in the energy required by the heart muscle
192
Law of Laplace
Constant pressure (P) within a sphere of increasing radius (r) can _only_ be maintained by an increase in wall tension (T)
193
Factors influencing cardiac output can be investigated by analysing...
The formula used for calculating CO
194
Factors of EDV affecting cardiac output
* Ventricular filling time * Ventricular compliance * Central venous pressure
195
Factors of ESV affecting cardiac output
* Arterial pressure * Contractility * Increases by sympathetic * Decreases by sympathetic
196
Factors of frequency affecting cardiac output
* Sympathetic effects * Parasympathetic effect
197
Contractility
The performance of the heart at a given preload and afterload
198
Contractility is characterised by...
* Isometric tension * The speed of contraction
199
Clinically, what is the best estimate of contractility?
Ejection fraction
200
Give the sympathetic effects of CO frequency
* Artificial increase * Duration of diastole * therefore CO decreased * Natural increase 1. Reduced systolic time 2. Reduced diastolic time 3. CO increases
201
Which system controls the: * Chronotrop * Dromotrop * Bathmotrop * Inotrop
Sympathetic nervous system
202
An increase in heart rate does not guarantee an increase in...
Cardiac output
203
Why doesn't CO increase with _artificial_ heart rate increase?
* The heart rate increased at the expense of diastole * The dilation of ventricles, therefore, doesn't increase * SV therefore increased
204
Sympathetic stimulation increases...
* Heart rate * _Velocity of contraction_ * _Maximal isometric contraction force_
205
Why does _natural_ heart rate increase cause larger cardiac output?
1. Sympathetic stimulation 2. The velocity of contraction increases 3. Duration of systole decreases 4. Stroke volume maintained 5. CO increases
206
What occurs because systole and diastole don't separate fully in time?
* A fraction of blood can enter the ventricles * During ventricular diastole
207
Prior to systole, which muscular motions occur in the heart?
* Twisting of the heart * Shift of the heart towards the base and back to the apex
208
Diastole
209
Isovolumetric contraction
210
Auxotonic contraction
211
Fast ejection
212
Slow ejection
213
Isovolumetric relaxation
214
Fast filling
215
Isotonic relaxation
216
Reduced filling
217
Atrial systole
218
Aortic pressure
219
Atrial pressure
220
Ventricular pressure
221
Ventricular volume
222
ECG
223
Heart sounds
224
Analysis of ECG and pressure values can show...
* Bloodflow of the heart * Role of the valves
225
Atrial contraction
Phase 1 * Begins after P-wave * Pressure increase in lumen * Blood passes into ventricles through cuspidal valves * Ventrical muscles relaxed * Aortic BP decreases
226
Isovolumetric phase
Phase 2 * Begins with QRS complex * Increased ventricular wall tension * Increased pressure * AV valves closed * Ventricular pressure increases until aortic pressure is reached
227
Rapid ejection
Phase 3 * Semilunar valves open * Cuspidal valves closed * Blood passes into aorta + pulmonary trunk * Increased aortic pressure
228
Reduced ejection
Phase 4 * Semilunar valves open * Cuspidal valves remain open * Blood passes into aorta + pulmonary trunk * Increased aortic pressure
229
Isovolumetric relaxation
Phase 5 * All valves are closed * No blood flow
230
Rapid filling
Phase 6 * Semilunar valves closed * Cuspidal valves open * Low ventricular pressure * Ventrical filling * _Major volume_ of blood flows into _ventricles_ in this phase
231
Reduced filling
Phase 7 * Cuspidal valves open * Semilunar valves closed * Ventricular muscles cells relaxed * Passive flow into ventricles * Aortic pressure drops
232
What generates heart sounds?
The closing of valves
233
Ist heart sounds
Systolic - closure of cuspid valves 1. The vibration of contracted muscle 2. Turbulence due to cuspid closure 3. Turbulence due to fast ejection
234
IInd heart sounds
Diastolic - Closure of semilunar valves 1. Aoric valve closes 2. Pulmonary valve closes 3. Intrathoracic pressure drops 4. Delayed closure of pulmonary semilunar valves
235
3rd heart sounds
*Arabic label* Rapid filling of ventricle
236
4th heart sounds
* Turbulent flow * Caused by atrial contraction
237
Murmurs are caused by...
Stenosis | (distorted heart sounds)
238
Ejection fraction
Volumetric fraction of fluid ejected from a chamber with each contraction

Physiology (18 decks)

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