# Cardiovascular physiology - House Of Sticks

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```					Cardiovascular
Physiology
http://www.houseofsticks.net

Brian Stickle
Aberdeen Royal Infirmary
2

Cardiovascular physiology
 Cellular ionic physiology
 Cardiac action potential
 Excitation contraction coupling
 Cardiac output
– Contractility
 MVO2
 The cardiac cycle
3

Cellular Ionic Physiology
RMP is determined primarily by:
1.The concentration of ions on the inside
and outside of the cell
2.The activity of electrogenic pumps
•   (e.g., Na+/K+-ATPase and Ca++ transport
pumps)

3.The permeability of the cell membrane to
those ions
•   (i.e., ion conductance)
4

Nernst equation
 Determines the electrical potential
across the membrane for individual
ions

R = The gas constant
T = Temperature (absolute) oK
z = Valence of the ion          25.6 (for z= +1)
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Nernst Equation

 Stated as Intracellular / Extracellular
 ∴ Invert equation and change sign
 EK = -25.6 ln [K+]i / [K+]o = -96 mV
 ENa = -25.6 ln [Na+]i / [Na+]o = +50 mV
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Goldman Equation
 Combines Nernst potentials for each ion and
calculates the overall potential (Em)
 Weights according to permeability

or

Em = g'K+(-96 mV) + g'Na+(+50 mV) + g'Ca++(+134 mV)
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Non-Pacemaker Action potentials
 Purkinje
+20            1      2             fibre &
0                                 myocytes

0                       3

-80                                     4
0                       250
Time (ms)
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Non-Pacemaker Action potentials
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Action potentials
Sinoatrial nodal tissue
+20

0

0     3             Threshold
-40
4

-80

Time (ms)
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Pacemaker potentials
11

How is rate altered?
 Slope of pacemaker potential
 Symp  g’K+ and g’Ca++ and g’Na+
 Parasymp g’K+ and g’Ca++ and g’Na++
12

Normal Cardiac Conduction
 Note relative
speeds

 Conduction
speeds
varied with
Autonomic
tone.
13

Excitation contraction coupling
14

Ca ++ Flux
 Cardiac muscle requires extracellular Ca++
to contract
• cf skeletal muscle

 Ca++ dependent Ca++ release

Ca++                    Ca++ release
crosses               from sarcoplasmic
sarcolemma                  reticulum
15

Excitation Contraction Coupling
 Intracellular Ca++ rises
 Ca++ binds to Troponin C
 Conformational change exposes
binding site on actin molecule
 Actin binds myosin ATPase
 “Ratcheting” – shortens sarcomeres
 Continues as long as Ca++ remains
high
16

Ca ++ control

 Control of cytosolic Ca++ controls:
• ATP hydrolysis
• Force generated
• Velocity of shortening

• Inc adenylate cyclase activity via G-protein  cAMP
• Protein kinase activity increased
• Phosphorylates ryanodine receptor
–  Ca++ release from SR and Ca++ uptake
»  Force and velocity of contraction (Inotropy)
– activity of Ca++/Mg++ ATPase on SR wall.
» Removes Ca++ at end of contraction
»  diastolic relaxation (Lusitropy)
17

Control of Cardiac Output
Simply:
• Rate x Stroke volume (SV)

SV = EDV – ESV
• EDV = End diastolic volume
• ESV = End systolic volume
18

Control of Cardiac Output
Venous inflow                             Arterial Outflow

Heart & Lungs

Sympathetic           Parasympathetic

Functional state of heart-lung unit
(contractility and rate)
19

Filling pressure of right heart
Reflected in increased EDV
Stretching of sarcomeres
Increased force of contraction
Increased SV
20

Venous return influenced by
Intravascular volume
Position
Intra-thoracic pressure
Venous system tone
21

Venous return
Mean systemic        Right atrial
Right atrial       = filling pressure   - pressure
filling pressure
Venous return & CO   22

curves
23

Starlings law of the heart
Energy of contraction  Starting length of muscle fibre
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Contractility / Rate
 Intrinsic property of myocardium
 Dependant on outside influences
– Drugs
– Local factors
 Global contractility:
– Deformity, dysrhythmias
25

HR and CO
Small increase in rate
– Shortened diastasis only
– EDV preserved
– CO increased

Large increase in rate
– Shortens period of rapid inflow
–  EDV decreased
–  Lesser increase in CO
26

HR and CO
Interval-strength effect

Treppe, Staircase, Bowditch
effect.

Increased contractility at HR

influence
27

The resistance to the emptying of
the left ventricle
= SVR + LVOT resistance

Increases:-
– ESV  EDV  SV  ESV
Starling effect
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Determinants of MVO2
 Ventricular wall tension
– Tension = Pressure x radius (laplace)
• Large amount of ATP required to generate wall
tension
• BP  inc MVO2
 Contractility
• Force x time = work = ATP utlisation
 Rate
•  rate =  time in systole
 Stroke volume
• Relatively small increases in work
• i.e. Volume work uses less ATP than pressure work
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Cardiac
Cycle
All done

Questions?

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 views: 13 posted: 3/7/2012 language: pages: 30