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Y1 Cardiovascular > Physiology > Flashcards

Physiology Flashcards

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1
Q

What is stroke volume

A

Volume of blood ejected by each ventricle during each heart beat

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2
Q

Equation of stroke volume

A

SV = End diastolic volume - end systolic volume

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3
Q

What is end diastolic volume

A

The volume of blood in each ventricle after diastole, before ventricular systole

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4
Q

What is end systolic volume

A

Volume of blood left in each ventricle after ventricular systole

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5
Q

What is cardiac output

A

Volume of blood pumped out of ventricles per minute

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6
Q

Equation for cardiac output

A

CO = SV x HR

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7
Q

What is Frank Starling’s law

A

the more blood is filled in each ventricle at the end of diastole, the more blood will be ejected during systole

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8
Q

What is preload

A

Diastolic stretch of myocardial fibres

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9
Q

What is afterload

A

The resistance that the heart needs to pump against to pump blood through

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10
Q

How does Frank Starling’s mechanism partially compensate for increase in afterload

A

Increase in afterload causes not all stroke volume pumped out
so increase in EDV for next cardiac cycle
increase in EDV then causes increase in stroke volume

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11
Q

How is venous return related to EDV, preload and SV

A

Increase in venous return stimulates diastolic stretch (increase in preload)
This increases EDV hence increases SV

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12
Q

What is positive chronotropic effect

A

Increase in heart rate

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13
Q

What is positive inotropic effect

A

Increase in force of contraction and contractility

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14
Q

What is positive dromotropic effect

A

Increase conduction velocity through AV node

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15
Q

What is positive lusitropic effect

A

Decrease in duration of systole

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16
Q

Cause of positive lusitropic effect

A

Increase in rate of Ca2+ reuptake into the SR

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17
Q

Causes of positive chronotropic effect

A

Increase in slope of phase 4 (pacemaker potential)

Decrease in threshold

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18
Q

How does slope of pacemaker potential increase

A

Increase in INa and ICa,L - more Na+ and Ca2+ moving in so depolarises and reaches threshold quicker

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19
Q

How does positive inotropic effect occur

A

L type Ca2+ channels open with more probability
Increase in sensitization of contractile proteins to Ca2+
PKA phosphorylates phospholamban which activates SERCA so Ca2+ reuptake into SR is quicker (quicker relaxation -> ready to contract sooner)

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20
Q

Effect of sympathetic stimulation on the heart

A 
\+ chronotropic 
\+ inotropic 
\+ lusitropic 
\+ dromotropic 
increase in automaticity 
increase in activity of Na+/K+ ATPase
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21
Q

What type of cells do sympathetic nerves supply in the heart

A

Nodal cells

Myocardial cells

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22
Q

What type of cells do parasympathetic nerves supply in the heart

A

Nodal cells

Atrial myocardial cells (not ventricles)

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23
Q

Mechanism of parasympathetic stimulation

A
  1. ACh binds to muscarinic receptors (M2) on nodal cells
  2. This activates Gi complex and causes it to dissociate into alpha and beta+gamma subunits
  3. alpha subunit inhibits adenylyl cyclase -> reduce cGMP -> reduce cellular responses
  4. beta+gamma subunit opens GIRKs
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24
Q

What are GIRKs

A

G protein coupled inward rectifier K+ channels

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25
Effects of parasympathetic stimulation on heart
Negative chronotropic effect Negative dromotropic effect Negative inotropic effect (only in atria)
26
Describe the phases of nodal action potential
Phase 4 (pacemaker potential) - Na+ influx through HCN and Ca2+ influx through voltage gated Ca2+ channels. This causes slow depolarisation of the membrane, reaching threshold (-40mV) Phase 0 - L type Ca2+ open, causing fast depolarisation Phase 3 - repolarisation; K+ channels open, L type Ca2+ channels close HCN channels will open once membrane potential is lower than -50mV
27
What are HCN channels
Allows Na+ influx during phase 4 of nodal action potential
28
List the ion channels involved in each phase of nodal action potential
Phase 4 - HCN and voltage gated Ca2+ channels Phase 0 - L type Ca2+ channels Phase 3 - K+ channels
29
Definition of automaticity
Heart being able to beat rhythmically without any external stimuli due to regular, spontaenous generation of electrical activities
30
How do electrical excitation spread from SA node to AV node
Mostly cell to cell conduction | some internodal routes
31
How do electrical excitation spread from AV node to ventricles
Bundle of His -> Purkynje fibres -> cell to cell conduction throughout ventricular myocytes
32
What is cell to cell conduction
Electrical excitation spreads between adjacent cells via gap junctions
33
What are gap junctions
Low resistance electrical communication pathways
34
What are desmosomes
Intercellular cell junctions that provides adhesion between cardiac cells
35
Why does AV node have slower conduction
So atrial systole occurs before ventricular systole
36
What is vagal tone
Continuous vagal influence on heart rate under normal conditions to produce normal heart rate
37
Normal heart rate range
60 - 100bpm
38
Type of beta adrenoceptors in nodal and myocardial cells
beta 1
39
Type of muscarinic receptor in nodal cells
M2
40
Describe the phases of action potential in myocardial cells
Phase 4 - voltage gated Na+ and L type Ca2+ channels are closed - NCXR transports 3Na+ in for 1 Ca2+ out - K+ channels are open, allowing K+ efflux Phase 0 - nodal action potential reaches the myocyte to trigger this - fast depolarisation - K+ channels close - voltage gated Na+ channels open Phase 1 - early repolarisation - Na+ channels close - L type Ca2+ channels begin to open - transient K+ channels open Phase 2 - plateau phase - efflux of K+ via rectifier channel = influx of Ca2+ Phase 3 - repolarisation - L type Ca2+ channel close while K+ remains open
41
Phases that represent the refractory period of action potential of myocardial cells
phase 1 to 3 | Na+ channels cannot open during this period
42
Why do myocardial cells have long refractory period
to prevent tetanic contractions
43
When do myocardial cells contract
Phase 1 to 2 | When L type Ca2+ channels are open, it causes CICR from SR
44
Why do myocardial cells stop contraction in phase 3
1) L type Ca2+ channels close so no CICR 2) Ca2+ actively transported back into SR 3) Ca2+ actively transported out of the cell via NCXR using 3Na+ gradient = no intracellular Ca2+
45
How does Ca2+ cause smooth muscle constriction
1. Ca2+ binds to CaM to form Ca2+ - CaM 2. Ca2+ - CaM activates myosin LCK 3. myosin LCK phosphorylates myosin LC into myosin LC + phosphate 4. myosin LC + phosphate causes muscle contraction
46
Equation for ejection fraction
Stroke volume / end diastolic volume
47
How do non polar lipids travel in blood
In lipoproteins
48
Examples of non polar lipids
Cholesterol Triacylglyceride Esters
49
Examples of lipoproteins
Chylomicron VLDL HDL LDL
50
What does the outer layer of lipoproteins contain
Cholesterol Apoprotein Phospholipids
51
Function of apoprotein
Signaling molecules recognized by the liver receptors, allow lipoproteins to bind
52
What apoproteins do HDL have
apoA-I and apoA-II
53
What apoproteins does VLDL have
apoB-100
54
apoB-48 is the aporpotein of
chylomicron
55
What is the feature of chylomicron
Highest proportion of TAGs
56
What does the core of apoproteins contain
cholesteryl ester | triacylglycerols
57
What is the feature of VLDL
Highest proportion of cholesterol
58
What are lipids used for
Energy source Membrane biogenesis Precursors for hormones and signaling molecules
59
Where are chylomicrons and VLDL metabolised
Muscle cells and adipocytes
60
Where are chylomicrons made
Enterocytes
61
Where are VLDL made
hepatocytes
62
Formation of TAGs and cholesteryl ester
1) pancreatic lipase hydrolyses TAG into monoglycerides and fatty acids 2) Monoglycerides and fatty acids diffuse into enterocytes by simple diffusion 3) cholesterol from diet enters enterocytes via NPC1L-1 4) Monoglycerides and fatty acids are resynthesized to TAG in SER 5) cholesterol is esterified into cholesteryl ester with a free fatty acid
63
Where is cholesterol obtained
Diet | Formed by liver using HMG-CoA reductase
64
Where does the formation of chylomicrons occur
RER
65
Formation of chylomicron
1) apoB-48 is moved into RER by MTP 2) TAG and phospholipid added to apoB-48 to form primordial chylomicron 3) more TAG added by MTP 4) cholesteryl ester also added, chylomicron formed
66
How are chylomicrons released
1) chylomicron move from RER to golgi apparatus 2) apoA-I is added to chylomicron 3) chylomicron is then released into lymphatic system by exocytosis
67
How does the content of lymphatic system drain into systemic circulation
By thoracic duct draining into subclavian vein
68
Metabolism of chylomicrons and VLDL
1) ApoC-II from HDL is added to VLDL and chylomicrons 2) VLDL and chylomicrons bind to lipoprotein lipase 3) lipoprotein lipase hydrolyzes the TAGs in core 4) TAGs depleted, forming chylomicron and VLDL remnants
69
Feature of chylomicron and VLDL remnants
They are enriched with cholesteryl ester due to depletion of TAG
70
Formation of LDL
1) apoC-II is transferred back to HDL in exchange for apoE 2) remnants are transported back to liver to be further metabolised by hepatic lipase 3) all chylomicron and 50% of VLDL are cleared 4) the remaining 50% of VLDL lose more TAG and more enriched with cholesteryl ester 5) eventually, VLDL loses apoE and forms LDL
71
Where are remnants of chylomicron and VLDL metabolised
Liver
72
Where does LDL clearance occur
liver
73
How are LDL cleared
1) LDL binds to LDL receptors on cells hence moved in by endocytosis 2) forms lysosome 3) LDL receptors are recycled back onto surface 4) cholesteryl ester in LDL hydrolysed in lysosome 5) cholesterol is released
74
Effects of release of cholesterol
Inhibits HMG CoA reductase = stops synthesis of cholesterol Downregulates LDL receptors
75
Uses of cholesterol
To form bile | Stored as cholesteryl ester
76
What is the normal stroke volume
50-100ml

Y1 Cardiovascular (6 decks)

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