Guyton Model: Heart Hypertrophy or Deterioration
Catherine
Lloyd
Auckland Bioengineering Institute, University of Auckland
Model Status
This CellML model has been validated. Due to the differences between procedural code (in this case C-code) and
declarative languages (CellML), some aspects of the original model were not able to be encapsulated by the CellML
model (such as the damping of variables). This may effect the transient behaviour of the model, however the
steady-state behaviour would remain the same. The equations in this file and the steady-state output from the model
conform to the results from the MODSIM program.
Model Structure
Arthur Guyton (1919-2003) was an American physiologist who became famous for his 1950s experiments in which he studied the
physiology of cardiac output and its relationship with the peripheral circulation. The results of these experiments
challenged the conventional wisdom that it was the heart itself that controlled cardiac output. Instead Guyton demonstrated
that it was the need of the body tissues for oxygen which was the real regulator of cardiac output. The "Guyton Curves"
describe the relationship between right atrial pressures and cardiac output, and they form a foundation for understanding
the physiology of circulation.
The Guyton model of fluid, electrolyte, and circulatory regulation is an extensive mathematical model of human circulatory
physiology, capable of simulating a variety of experimental conditions, and contains a number of linked subsystems relating
to circulation and its neuroendocrine control.
This is a CellML translation of the Guyton model of the regulation of the circulatory system. The complete model consists
of separate modules each of which characterise a separate physiological subsystems. The Circulation Dynamics is the primary
system, to which other modules/blocks are connected. The other modules characterise the dynamics of the kidney, electrolytes
and cell water, thirst and drinking, hormone regulation, autonomic regulation, cardiovascular system etc, and these feedback
on the central circulation model. The CellML code in these modules is based on the C code from the programme C-MODSIM created
by Dr Jean-Pierre Montani.
This particular CellML model describes the effect of heart hypertrophy or heart deterioration on heart pumping capability.
model diagram
A systems analysis diagram for the full Guyton model describing circulation regulation.
model diagram
A schematic diagram of the components and processes described in the current CellML model.
There are several publications referring to the Guyton model. One of these papers is cited below:
Circulation: Overall Regulation, A.C. Guyton, T.G. Coleman, and H.J. Granger, 1972,
Annual Review of Physiology
, 34, 13-44. PubMed ID: 4334846
Guyton
Heart Hypertrophy or Deterioration
Description of Guyton heart hypertrophy or deterioration module
2008-00-00 00:00
keyword
physiology
organ systems
cardiovascular circulation
heart hypertrophy or deterioration
Guyton
Effect of heart hypertrophy or heart deterioration on heart pumping capability.
Encapsulation grouping component containing all the components in the Heart Hypertrophy or Deterioration Model.
The inputs and outputs of the Model must be passed by this component.
HH1A, HH1, and HH2:
Calculation of a quantitative value (output of Block HH2) which is a multiplier
that is approached asymptotically in response to three factors that cause left
ventricular hypertrophy, (1) the arterial pressure (PA), (2) the cardiac output (QAO),
and (3) the basic strength of the heart (HSL). The degree of hypertrophy in response
to the input factors is controlled by the exponent (Z13) in Block HH2.
HH3, HH4, and HH5:
Calculation of the actual degree of hypertrophy of the left ventricle (HPL) that
results over a period of time in response to arterial pressure (PA), cardiac output (QAO),
and basic left ventricular strength (HSL). The value HPL approaches the output value
from Block HH2 asymptotically with a time constant equal to the input variable at the
side of Block HH4.
HH1A, HH1, and HH2:
Calculation of a quantitative value (output of Block HH2) which is a multiplier
that is approached asymptotically in response to three factors that cause left
ventricular hypertrophy, (1) the arterial pressure (PA), (2) the cardiac output (QAO),
and (3) the basic strength of the heart (HSL). The degree of hypertrophy in response
to the input factors is controlled by the exponent (Z13) in Block HH2.
HH3, HH4, and HH5:
Calculation of the actual degree of hypertrophy of the left ventricle (HPL) that
results over a period of time in response to arterial pressure (PA), cardiac output (QAO),
and basic left ventricular strength (HSL). The value HPL approaches the output value
from Block HH2 asymptotically with a time constant equal to the input variable at the
side of Block HH4.
HH6A, HH6, HH7, HH8, HH9, and HH10:
Calculation of the degree of hypertrophy of the right ventricle (HPR) according
to the same scheme as noted above for left ventricular hypertrophy, but with different
inputs: pulmonary arterial pressure (PPA), cardiac output (QAO), and basic normal
strength of the right heart (HSR).
HH6A, HH6, HH7, HH8, HH9, and HH10:
Calculation of the degree of hypertrophy of the right ventricle (HPR) according
to the same scheme as noted above for left ventricular hypertrophy, but with different
inputs: pulmonary arterial pressure (PPA), cardiac output (QAO), and basic normal
strength of the right heart (HSR).
HH11, HH12, HH13, and HH14:
Calculation of a multiplier factor that decreases cardiac pumping effectiveness (HMD)
when the cellular P02 of the heart muscle cells (POT) falls too low. The sensitivity
control is DHDTR, and the effect is limited by Block HH14 so that no change in HMD
occurs until the cell PO2 falls below the input value to the side of Block HH11.
HH11, HH12, HH13, and HH14:
Calculation of a multiplier factor that decreases cardiac pumping effectiveness (HMD)
when the cellular P02 of the heart muscle cells (POT) falls too low. The sensitivity
control is DHDTR, and the effect is limited by Block HH14 so that no change in HMD
occurs until the cell PO2 falls below the input value to the side of Block HH11.
HH11, HH12, HH13, and HH14:
Calculation of a multiplier factor that decreases cardiac pumping effectiveness (HMD)
when the cellular P02 of the heart muscle cells (POT) falls too low. The sensitivity
control is DHDTR, and the effect is limited by Block HH14 so that no change in HMD
occurs until the cell PO2 falls below the input value to the side of Block HH11.
HH11, HH12, HH13, and HH14:
Calculation of a multiplier factor that decreases cardiac pumping effectiveness (HMD)
when the cellular P02 of the heart muscle cells (POT) falls too low. The sensitivity
control is DHDTR, and the effect is limited by Block HH14 so that no change in HMD
occurs until the cell PO2 falls below the input value to the side of Block HH11.