Cardiac Structure and Function Flashcards
1
Q
What are the two major circulations of the cardiovascular system?
A
- Pulmonary circulation
- Systemic circulation
2
Q
What re the three distinct layers of the heart?
A
- Epicardium
- Myocardium
- Endocardium
3
Q
Is the epicardium in the outer, middle or the inner layer?
A
Outer
4
Q
Is the myocardium in the outer, middle or the inner layer?
A
Middle
5
Q
Is the endocardium in the outer, middle or the inner layer?
A
Inner
6
Q
Describe the epicardium:
A
- Outer layer
- Connective tissue (areolar)
7
Q
Describe the myocardium:
A
- Middle layer
- Cardiomyocytes and connective tissue
8
Q
Describe the endocardium:
A
- Inner layer
- Thin layer of connective tissue and endothelium
9
Q
What are the clinical importance of pericarditis?
A
- Multiple causes (infections, cancer and trauma autoimmune)
- Overall effect: accumulation of fluid effusion - restricts ventricular filling
10
Q
What is the pericardium?
A
- Parietal and visceral (epicardium)
- Cavity contains pericardial fluid
11
Q
What is the purpose of pericardial fluid?
A
Lubrication
12
Q
What is the muscle mass ration between the left and right side of the heart?
A
3:1
13
Q
What is the goal blood pressure?
A
120/80
14
Q
What is another name for cardiomyocytes?
A
autorhythmic cells
15
Q
What are the different types of specialised cardiomyocytes?
A
- SA
- AV
- bundle of His
- Purkinji fibres
16
Q
What is the primary pacemaker?
A
SA
17
Q
What do pacemakers do?
A
To initiate cardio cycle and provide conduction system to coordinate cells contraction throughout the heart
18
Q
What is excitation-contraction coupling?
A
Causing of excitatory phase to a contraction phase within in the hear
19
Q
What are Purkinje fibres?
A
Specialised conducting fibres composed of electrically excitable cells
20
Q
What are sarcomere?
A
Complicated unit of striated muscle tissue
-Repeating unit between two Z lines
21
Q
What are sarcolemma?
A
cell membrane if started muscle fibre cells
22
Q
What are T-tubules?
A
Extension of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells
23
Q
What is similar in cardiomyocytes?
A
- Have no sarcomere so no contraction
- Creates action potential
24
Q
What does L in L-type calcium channel stand for?
A
Long-lasting referring to length of activation
25
Describe exception-contraction coupling:
- SA node begins action potential as primary pacemaker
- Goes through atria (non-conductive tissue to prevent excitation into ventricle)
- AV nose picks up excitation via inter nodal pathway
- AV sends signal down bundle of His
- Leads to Purkinje fibres (linked to cardiomyocytes in ventricle tissue)
- Causes action potential at cardiomyocytes
- Action potential running down sarcolemma
- L-type Ca2+ channels open as action potential changes voltage
- Ca2+ ions in the extracellular fluid and space go through the channels
- Increase in Ca2+ side cytosol
- T-tubules and sarcoplasmic reitculum are at close association so an influx in Ca2+ enters cytosol causes Ca2+ binding to ryanodine receptors of SR
- Increase in Ca2+ in cytosol will bind to tropic to cause muscle contraction
26
What is calcium induced calcium release process?
T-tubules and sarcoplasmic reitculum are at close association so an influx in Ca2+ enters cytosol causes Ca2+ binding to ryanodine receptors of SR
27
What alters contractility and relaxation of muscles?
Concentration of Ca2+
28
Frank a 56yr old male is currently being prescribed verapamil, a
CCB, to treat his angina. Which of the following best explains its
negative inotropic (contractile) effect.
Select one:
A. Decreased Ca2+ induced Ca2+ release
B. Inhibition of ryanodine receptors on the SR
C. Decrease efflux of Ca2+ via Na+/Ca2+ exchange pumps
D. Decreased extracellular Ca2+ influx via inhibition of T-types channels
A
29
Describe Sinoatrial Node Action Potential:
- Phase 4: pacemaker potential occurs at end of one action potential
- Phase 0: depolarisation
- Phase 3: repolarisation
30
Describe phase 4: pacemaker potential occurs at end of one action potential
- Slow depolarisation of pacemaker cells
| - Pacemaker achieved by activation of hyperolarisation of HCN channels where Na+ enters cell
31
When are HCN activated?
When membrane potential is
32
Describe phase 0 depolarisation:
- HCN channels bring membrane potential to -40mV
- Influx of Ca2+ production fast rate depolarisation
- HCN channels inactivate
- Peak of action potential, Ca2+ channels inactive and K+ active
33
Describe phase 3 repolarisation:
- Efflux of K+ ions out of cell
- Repolarisation of cell
- HCN channels activate, enabling another action potential
34
Describe myocyte action potential:
Phase 0: depolarisation (influx of Na+ into cell, rapid depolarisation)
Phase 1: Sodium currents stop (K+ slowly flows out of cells, depolarisation stops, repolarisation starts)
Phase 3: Ca2+ currents move into cells (balance of K+ ions moving out, charge balance between cells, pleitu created)
Phase 4: K+ reaches equilibrium between inside so Na2+ and Na+ balances K+ leading to resting potential
35
Where does myocyte action potential receive the action potential from?
Pacemaker cells causing them to contract enabling spread of action potential
36
What are intercalated discs?
-Interconnect cardiac muscle cells
37
What are intercalated discs secured by?
Desmosomes
38
What are intercalated discs linked by?
Gap junctions
39
What propagate actions potentials?
Gap junctions
40
Where are SA nodes located?
Inwall of right atrium
41
Where are AV nodes located?
Base of right atrium
42
Where are the bundles of His?
Divides right and left bundle branches travelling through septum
43
Where are the purkinje fibres?
Spread throughout ventricles
44
Where are gap junctions?
Occur between adjunct cardiomyocytes
45
What are cardiomyocytes linked by?
Intercalated discs
46
Describe excitation propagation:
- Action potential from auto rhythmic cells excite first cardiomyocyte
- Propagation along sarcolemma (membrane of muscle cell)
- Na2+ influx from outside cells into the cell
- Transfers into adjacent cell where voltage-gated channels along membrane along action potential
47
What motion is excitation propagation?
Peristaltic motion
48
What is the pathway of electrical conduction?
Sinoatrial node (SA) -> Atrial internal fibres -> atrioventricular node (AV) -> bundle of His -> Purkinje fibres -> ventricular myocytes
49
Which myocardial has the slowest conduction speed?
AV node
50
Which myocardial has the fastest conduction speed?
Purkinje fibres
51
What does velocity depend on in action potential?
- Amount of ions going into cell during action potential
| - Interconnectedness of myocardial conduction cells
52
How does interconnectedness of myocardial conduction cells affect velocity?
-More gap junctions - more interconnect cells - less resistance to ion flow between cells
53
How does the amount of ions going into cell during action potential affect velocity?
More ion - faster depolarisation - faster speed
54
What is refectory period?
Time in which myocardial cell cannot be depolarised
55
What is absolute refectory period?
No stimulus, no matter its size can dgpolise cell
56
What is effective refectory period?
Large stimulus can generate action potential
| -Too weak to be conducted
57
What is relative refectory period?
Large stimulus can generate action potential
| -Big enough to conducted
58
What is excitability?
Ability of myocardial cells to depolarise in response to incoming depolarising current
59
What are the mechanisms of cardiac contraction?
Preload
Afterload
Contractility
Heart Rate
60
What is the acronym?
PACE
61
What is the equation for cardiac output?
Heart rate x stroke volume
62
What is the unit for cardiac output?
mL/min
63
What is the unit for heart rate?
Beat/min
64
What is the unit for stroke volume?
mL/beat
65
What is the equation for stroke volume?
End diastolic volume (EDV) - End systolic volume (ESV)
66
What is EDV?
Volume of blood just before contraction
67
What is ESV?
Volume of blood after contraction
68
Is there still blood in the ventricle after contraction?
Yes
69
What is related to EDV?
Preload
70
What does increase in EDV do?
Increases in myocardial performance/contractility
71
How does EDV increase myocardial contractility?
Increase myocardial muscles
Increase cross bridge formation
Increase in contractility
72
What is the relation of EDV, preload and contractility relationship known as?
Length force relationship
73
If preload/EDV increases the venous return what does it do to stroke volume and cardiac output?
Increase SV and CO
74
What are the physical factors which affect preload?
more optimum myofilament overlapping
Decreasing in lattice spacing
Increase probability of interaction between adjacent components
75
What are the activating factors which affect preload?
Increase in Ca2+ release and sensitivity
76
What are the three factors which affect ESV?
- Preload/EDV
- Contractility
- Afterload
77
How does afterload affect ESV?
- Heart pumps against pressure
- Higher pressure in the aorta the more force required by the heart
- So increase in afterload decrease in cardiac output
78
What is the clinical importance of afterload?
Hypertension and aortic valve stenosis both lead to decrease in stroke volume
79
How does contractility affect ESV?
Increase blood pumped out of heart
80
What type of receptor is B1 adrenergic receptor?
G-coupled protein receptor
81
What hormones control contractility?
Adrenaline and noradrenalin
82
How is contractility controlled?
- Noradrenalin or adrenaline bind to B1 adrenergic receptor
- Activation of adenlye cyclase from the production of cyclic AMP
- Cyclic dependent on kinases A
- Increase in Ca2+ with sarcomere reticulum and cell
- Increase contractility
83
What is the clinical perspective of ejection faction?
Quantifying of contractility by injection factions and ratio of stroke volume and end diastolic volume
84
What is the equation of ejection fraction?
SV/EDV
85
What is ejection fractions expressed as?
Percentage
86
What is the normal ejection fraction in resting condition?
55-75%
87
What do neuronal and endocrine regulation do?
Affect heart rate
88
How do you increase heart rate relating to neuronal and endocrine regulation?
Positive chronotropic factors
| e.g noradrenalin and adrenaline
89
How do you decrease heart rate relating to neuronal and endocrine regulation?
Negative chronotropic factors
| e.g Acetylcholine
90
What does the martial reflex effect?
Adjusts heart rate in responses to venous return
| Stretch receptors in right atrium tigger increase in heart rate through increase sympathetic activity
91
What doe the sympathetic do to there permeability of membrane to Na+?
Increase permeability
92
What doe the parasympathetic do to there permeability of membrane to Na+?
Decrease permeability
93
How does sympathetic increase permeability of membrane to Na+?
- Increase spontaneous depolarisation
| - Reduce time to initiate depolarisation
94
How does parasympathetic decrease permeability of membrane to Na+?
- Decrease spontaneous depolarisation
| - Increase time to initiate depolarisation
95
Frank is also on bisoprolol, a selective β1-antagonist. Which of
the following is INCORRECT with regard to explaining its
predominant affect on reducing CO.
```
Select one:
A. Reduced heart rate
B. Reduced cardiac contractility
C. Reduced renin release
D. Reduced arterial tone
```
D
96
What does B1 blockade lead to?
- Reduced contractility-via reduction in CAMP
- Reduced heart rate
- Reduced Ca2+ entry via CAMP-dependent PK activity
- Reduced renin recreation via selective B1 inhibition at GJ cells
