Physiology Flashcards
(108 cards)
1
Q
What is the formula for Cardiac Output?
A
Cardiac Output = Heart Rate x Stroke Volume
2
Q
What does Chronotropy refer to?
A
Heart Rate
3
Q
Where is the Sinoatrial Node (SAN) located?
A
Right Atrium
4
Q
Where is the AVN located
A
Ventricular Junction
5
Q
What is the intrinsic heart rate generated by the SAN?
A
100 bpm
6
Q
What is the heart rate generated by the Atrioventricular Node (AVN)?
A
70 bpm +/-
7
Q
What is the delay time for the AVN to allow atrial contraction?
A
0.15 seconds
8
Q
What is the role of the delay at the AVN?
A
To allow AV valve to close and prevent regurgitation of blood into atria
9
Q
Which systems control Heart Rate?
A
Autonomic Nervous System and Baroreceptors
10
Q
What is the effect of the Parasympathetic system on heart rate?
A
-ve chronotropic
11
Q
What is the effect of the Sympathetic system on heart rate?
A
+ve chronotropic and inotropic
12
Q
What neurotransmitter binds to M2 receptors in the heart?
A
Acetylcholine
13
Q
What happens to the slope of the pacemaker potential when Acetylcholine binds to M2 receptors?
A
↓ Slope of pacemaker potential
14
Q
What is the effect of Noradrenaline on heart rate?
A
+ve chronotropic effect
15
Q
Which receptors does Noradrenaline bind to in the heart?
A
B1 adrenoceptors
16
Q
What are Baroreceptors and where are they located?
A
Carotid Sinus and Aortic Arch
17
Q
What do Baroreceptors detect?
A
Change in arterial pressure
18
Q
Which cranial nerves are involved in the Baroreceptor reflex?
A
CN IX and CN X
19
Q
What is Stroke Volume?
A
Difference in end diastolic volume and end systolic volume
20
Q
What does EDV stand for?
A
End Diastolic Volume
21
Q
What does ESV stand for?
A
End Systolic Volume
22
Q
What is Central Venous Pressure (CVP)?
A
Pressure of blood in Vena Cava as it enters RA
23
Q
What is Preload?
A
The load present in the left ventricle before contraction occurs (EDV)
24
Q
What does Starlings Law state?
A
The force of contraction of myocytes (1) is proportional to the end diastolic length of cardiac muscle fibre (1)
Increased end diastolic volume causes increased stretch in the myocytes (1) leading to increased contraction of the heart
25
What happens when preload is too high?
Decrease in contractility and stroke volume due to overload
26
What effect does vasoconstriction have on total peripheral resistance?
Increases total peripheral resistance
27
What is Total Peripheral Resistance (TPR)?
Pressure in the arteries blood must overcome to pass
## Footnote
TPR is also referred to as afterload.
28
What does Total Peripheral Resistance indicate?
How easy it is for the heart to expel blood.
29
Why is contractility and SV reduced when preload is too high?
The optimal fibre length of the muscle cells is surpassed.
30
What is the effect of exceeding optimal fibre length due to high preload?
Decrease in contractility and stroke volume due to being overloaded.
31
Overall response to increase PNS on HR
↓ Slope of pacemaker potential
↓ Heart Rate
32
Overall response to SNS on HR
↑ Slope of pacemaker potential
↑ Heart Rate
↑ Force of Contraction
33
What makes up the sympathetic nervous system in Cardiac Output
Superficial and deep cardiac plexus
34
What happens when baroreceptors detect an increase in Arterial Pressure
CNIX --> Medulla Oblongata --> CNX --> Increase parasympathetic response
35
What happens when baroreceptors detect an decrease in Arterial Pressure
CNIX --> Medulla Oblongata --> CNX --> Decrease parasympathetic response therefore increases SNS effect
36
Factors that increase preload
Fast filling time
Increased venous return
Increases EDV and SV
37
Factors that decrease preload
Decreased thyroid hormones
Decrease calcium ions
Imbalance of potassium, sodium
Hypoxia
Low body temperature
Abnormal pH
Drugs - e.g. CCB.
Decreases EDV and SV
38
Factors that increase afterload
Increased vascular damage
Semilunar valve damage
Increase ESV so decrease SV
39
Factors that decrease afterload
Decreased vascular resistance
Decrease ESV and so Increase SV
40
Factors that increase Contractility
Sympathetic stimulation
Noradrenaline and adrenaline
High intracellular calcium ions
High blood calcium
Thyroid hormones
Glucagon
Decreases ESV and increases SV
41
Factors that decrease Contractility
Parasympathetic stimulation
Acetylcholine
Hypoxia
Hyperkalaemia
Increases ESV and decreases SV
42
What is the filling phase of the cardiac cycle?
Blood is driven into atria and flows into ventricles via diastole when both are relaxed.
## Footnote
Atrial contraction occurs to pump more blood into ventricles.
43
What occurs during atrial systole?
The atria contract to pump more blood into the ventricles.
## Footnote
This happens when ventricular pressure begins to equal atrial pressure.
44
What happens to the AV valves during the filling phase?
The AV valves close when ventricular pressure exceeds atrial pressure.
## Footnote
This closure prevents backflow into the atria.
45
What is isovolumetric contraction?
Both sets of valves are closed, allowing pressure to build in the ventricles.
## Footnote
This prepares the heart to eject blood into the pulmonary trunk and aorta.
46
What triggers the opening of outflow valves?
Ventricular pressure exceeds pressure in the aorta/pulmonary trunk.
## Footnote
This occurs during the outflow phase of the cardiac cycle.
47
What happens after systole when aorta/pulmonary trunk pressure exceeds ventricular pressure?
The outflow valves close.
## Footnote
This prevents backflow of blood into the ventricles.
48
What is isovolumetric relaxation?
Both sets of valves are closed and ventricular pressure drops below atrial pressure.
## Footnote
This allows the AV valves to open again for filling.
49
Fill in the blank: During the _______ phase, blood is driven into the atria and flows into the ventricles.
[filling]
50
True or False: During isovolumetric contraction, the ventricles are ejecting blood.
False
## Footnote
During isovolumetric contraction, the ventricles are building pressure with closed valves.
51
What occurs when ventricular pressure drops below atrial pressure?
The AV valves open again for filling.
## Footnote
This is a key part of isovolumetric relaxation.
52
S1 Heart Sound
End of filling phase when AV valves close.
53
S2 Heart Sound
End of outflow phase when outflow valves close.
54
S3 Heart Sound
Early in diastole following S2. In older people can be CHF, due to deceleration of blood moving from left atrium to left ventricle.
55
S4 Heart Sound
Atrial contraction, immediately before S1, reduced ventricular compliance or LVH.
56
Cardiac Pacemaker Cells Location
Found in SAN and have natural automaticity.
Also some are located in AVN and Purkinje which can generate their own action potential, but due to SAN having faster pacing that overrides them.
57
Phase 4 of Cardiac Pacemaker
Occurs at the end of one AP and just before next.
Slow depolarization of pacemaker cells towards membrane threshold.
Achieved by hyperpolarization activated cyclic nucleotide gated channels (HCN channels) which activate when membrane potential is less than -50mv.
58
Phase 0 Cardiac Pacemaker
HCN have enough membrane potential - voltage gated calcium channels open.
Allows influx of Ca to produce faster rate of depolarisation and reach +ve membrane potential.
At the peak of action potential, HCN inactivate, CA channels inactivate and K channels open
59
Phase 3 Cardiac Pacemaker
K channels open which causes efflux out cells.
Results in repolarization
60
What are gap junctions and why are they important with ventricular contraction
Made of protein called connexins and form a unit called a connexon.
These are embedded into the plasma membrane of adjacent cells, connecting cardiac myocytes together.
Mainly located at the intercalated discs.
Ensure a unidirectional and synchronized spread of action potential.
61
Phase 4 ventricular contraction
PHASE 4 - Baseline
K+ channel open, so resting membrane potential is leaning to -70mV
62
Phase 0 ventricular contraction
PHASE 0 - Fast depolarisation
Na+ channels open in response to depolarisaion.
Further influx of Na depolarises cell causing more Na channels to open in +ve feedback
63
Phase 1 ventricular contraction
Notch - Opening K+ channels repolarise the cell before plateau.
64
Phase 2 ventricular contraction
L-type Ca channels located in T-tubules penetrate the cell, close to the sarcoplasmic reticulum, so bind to the ryanodine receptors.
Causes massive Ca release from SR (Calcium induced calcium release), which then bind to troponin C and initiate movement of tropomyosin away from myosin head binding site on actin molecule - causing contraction.
65
Phase 3 ventricular contraction
Ca channels close and K+ repolarises the cell.
Na channels begin to recover as membrane potential reaches more negative.
66
Why is there a refractory period for ventricular contraction
The Na channels become inactivated almost immediately after opening, so as long as the myocyte is depolarised, the Na channels will not be able to reopen until repolarisation occurs, creating a refractory period.
67
How does calcium cause ventricular contraction
Causes massive Ca release from SR (Calcium induced calcium release), which then bind to troponin C and initiate movement of tropomyosin away from myosin head binding site on actin molecule - causing contraction.
68
Flow Equation
Pressure / Resistance
OR
cross sectional area x velocity
69
Pressure Definition
mean difference between start and end of vessel.
70
Laminar Flow vs Tubrulent Flow
Laminar flow = Pressure is highest in the middle and decreases closer to vessel wall.
Turbulent flow = Flow is not unidirectional and leads to a messier flow. Can be heard as a bruit over atherosclerotic plaques
71
Pouseuilles Law (Resistance)
R = 8ηl / πr^4 - Where: R – resistance, η – Viscosity, l – Length, r – Radius
72
Factors Affecting Resistance
Radius
Viscosity
Vessel Length
73
Ficks Law (Capillaries)
Rate of diffusion is proportional to concentration difference and area available for diffusion.
AND
The rate of diffusion is inversely proportional to the diffusion difference.
74
Structure of capillaries aiding function
Multiple capillaries supplying one area
Constant blood flow maintains concentration gradient.
Singular capillary has greater resistance, but many in parallel reduce resistance.
Diffusion difference minimised as endothelium is one cell thick and only a few um in diameter.
Diffusion of small lipid soluble molecules (o2 and co2) freely.
Some capillaries have specialised pores or channels (e.g. renal capillaries) for other substances.
75
Capillaries in Pulmonary System functions to aid gas exchange
Pulmonary capillaries allow rapid diffusion.
Membrane thickness of 0.6um.
Alveoli have a large surface area
76
How do some pulmonary pathologies impact gas exchange (Fibrosis, Emphysema and Restrictive Lung Disease)
Fibrosis = increase in diffusion distance so decrease diffusion rate.
Emphysema = damage to walls of alveoli which decreases SA.
Restrictive lung diseases = shallower concentration gradient.
77
Starling Forces within Capillaries (4)
1. Blood hydrostatic pressure - Pressure exerted by blood in the capillaries against the capillary wall which forces blood out of capillary.
2. Blood colloid osmotic (oncotic) pressure - Pressure exerted by proteins (albumin). Pressure attempts to pull fluid into blood as normally proteins are too large to diffuse into interstitium.
3. Interstitial Hydrostatic Pressure - Pressure of fluid in interstitium. Focus fluid back into capillary.
4. Interstitial colloid osmotic (oncotic) pressure - Pressure of the proteins in the interstitium - pressure pulls fluid out of capillary.
78
Systolic Blood Pressure
Pressure of the blood during heart contraction
79
Diastolic Blood Pressure
Pressure of the blood when heart is at rest between beats.
80
Blood pressure calculation
flow x resistance
81
Factors Affecting Blood Pressure
Cardiac Output - higher = higher volume of blood in the vessels - increasing pressure in the vessels.
Total peripheral resistance - decrease in the diameter of the vessels will increase resistance and bp.
Blood Viscosity
82
Short Term Regulation of BP
ANS - changes detected by baroreceptors
Increase AP stretches the wall of bv, triggering baroreceptors → ANS reduces HR by parasympathetic vagus nerve.
Decreased AP - sympathetic response to inc HR and cardiac contractility.
83
Two systems for long term regulation of BP
RAAS and ADH
84
RAAS System Equation
Angiotensinogen –(Renin)--> Angiotensin 1 –(ACE)--> Angiotensin 2
85
Where is Renin Released from and in response to?
Renin released by granular cells of juxtaglomerular apparatus in the kidney in response to:
Sympathetic stimulation
Reduced sodium chloride delivery to distal convoluted tubule
Decrease blood flow to kidney
86
Function of Angiotensin 2
a vasoconstrictor, acting directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule to be reabsorbed by the sodium hydrogen exchanger. It also promotes release of aldosterone.
87
Function of Aldosterone
Salt and water retention by acting on distal convoluted tubule to increase epithelial sodium channels.
Increases activity of basolateral sodium-potassium ATP-ase which increases electrochemical gradient for movement of sodium ions into kidney.
88
How does the RAAS increase BP
More sodium collects in the kidney and water follows by osmosis - decreased water excretion and increased blood volume and pressure.,
ACE also breaks down bradykinin (responsible for vasodilation) so increases the constricting effect.
89
How does ADH affect BP
Acts to increase permeability of collecting duct to water by adding aquaporin channels (AQP2) into apical membrane.
Stimulates sodium reabsorption from the thick ascending loop of Henle. Increases reabsorption and increases plasma volume to decrease osmolarity.
90
Where is ADH produced and released and in response to?
Produced in hypothalamus, stored and released from posterior pituitary in response to thirst or increase in plasma osmolarity.
91
Other factors controlling BP other than RAAS and ADH
Atrial Natriuretic Peptide (ANP) - Synthesised and stored in cardiac myocytes. Released when atria are stretched and indicates high BP. It promotes sodium excretion by dilating afferent arterioles of glomerulus - increasing GFR. It inhibits sodium reabsorption across the nephron, so when ANP is low BP is low.
Prostaglandins - local vasodilators to increase GFR and reduce sodium reabsorption. They prevent excessive vasoconstriction.
92
Arteriole structure for peripheral circulation
Diameter less than 0.1mm. Muscular layer with a single layer of smooth muscle cells.
At rest high vasomotor tone (tonic contraction of the smooth muscle is higher) due to requiring less blood during rest.
93
How does the SNS affect Arterioles
Sympathetic nervous system controls vasomotor tone via noradrenaline release which acts on a1 GPCR (G protein coupled receptors)
94
Factors affecting vasomotor tone
Vasodilator metabolites, Myogenic factors and Autocoids
95
How do vasodilator metabolites affect vasomotor tone
Metabolically active tissues release vasodilator metabolites (H+, CO2, K+, adenosine and lactate).
Reduce vasomotor tone via smooth muscle relaxation, which reduces resistance and allows blood flow increase.
Allows blood to transport metabolites away from tissue, reducing potential toxic effects.
Once metabolites are removed, tone will return to normal level.
96
How do myogenic factors affect vasomotor tone
when the arterioles experience a rapid increase in intraluminal pressure such as due to violent coughing, the arteriolar smooth muscle will contract in order to defend itself from the rise in pressure.
97
How to autocoids affect vasomotor tone
Arteriolar endothelium can release autocoids which increase or decrease vasomotor tone similar to hormone mechanisms.
98
Venous Return and Pressure effects
Venous pressure is affected by the rate of blood entering the veins (peripheral resistance) and the rate at which the heart pumps blood (CO).
When resistance is high, slower rate of blood enters veins, so decrease in venous pressure and vice versa.
99
How does Cardiac Output affect venous return
When CO increases blood is rapidly pumped out of veins which reduces venous pressure as it does not get a chance to rise.
When CO decrease, blood is backed up into venous system so increase in blood volume counteracts this.
100
How are veins structured for blood flow?
High capacitance - able to stretch to accommodate higher volume of blood
Valves - prevent backflow for unidirectional flow.
101
Factors that affect Central Venous Pressure
Skeletal muscle pump - When muscles contract, vein is squeezed, increasing venous pressure, forcing valves to open to allow blood to flow back to the heart and increase venous return.
Respiration - Inspiration causes reduced intrathoracic pressure in RA causing more blood to be drawn into it.
Venous Compliance - Increase in sympathetic activity, increases venous pressure as blood flow increases, and can only dilate so much and so pressure forces blood flow through vessels to empty faster.
Gravity - Lying down and elevating legs increases venous return by reducing the effect of gravity.
Blood Volume - Greater blood volume = greater blood flow and venous pressure.
The Heart - Any issue will result in reduced venous return.
102
How does coronary circulation differ to normal circulation
More capillaries per mm2 in cardiac muscle → larger endothelial surface area for O2 delivery and removal of metabolic products.
Perfusion occurs during diastole through aortic sinuses (opening behind aortic valve leaflets)
Vasodilation of coronary arteries helps maintain a high basal rate of blood flow, as a result of NO released from endothelial cells.
103
Process of coronary circulation
Perfusion occurs during diastole through aortic sinuses (opening behind aortic valve leaflets)
As the heart relaxes, the aortic valve shuts and blood fills the valve pockets allowing it to enter coronary arteries.
They also send branches to myocardium which become compressed during systole.
When muscle relaxes the myocardial blood flow is increased as less compression → intermittent blood flow that is high in diastole and interrupted in systole.
104
Describe the normal conduction pathway through the heart, including contraction of the atria and ventricles
Sino-Atrial node --> Contraction of the atria --> Atrioventricular node --> Bundle of His --> Purkinje fibres --> Contraction of the ventricles
105
Mean Aortic Pressure
120/80
106
Mean Pulmonary arterial pressure
25/10
107
Volume distribution of blood
Veins 64%
Capillaries 5%
Heart in diastole 7%
Large arteries 7%
Small arteries and arterioles 8%
Lungs 9%
108
