Cardiovascular Flashcards
The equation for thermodilution measurement
- This uses the equation, V̇ = m/Ct, where:
o V̇ = flow, or cardiac output
o m = dose of the indicator,
o C = concentration, and
o t = time
Deranged 2014 march Q19
Define cardiac output. (10% of marks) Outline the factors that affect cardiac output. (60% of marks) Briefly describe the thermo dilution method of measuring cardiac output. (30% of marks)
Cardiac output Definition
Cardiac output is defined as the volume of blood ejected by the heart per unit time.
It is usually presented as [stroke volume × heart rate], in L/min
Deranged 2014 march Q19
Define cardiac output. (10% of marks) Outline the factors that affect cardiac output. (60% of marks) Briefly describe the thermo dilution method of measuring cardiac output. (30% of marks)
Thermodilution measurement of cardiac output:
* Rate of blood flow can be determined from the rate of change in the concentration of substance after a known amount of it has been added to the bloodstream
* This uses the equation, X
- In the case of thermodilution, the “indicator substance” is a known volume of X, and the equation
- The use of thermodilution for cardiac output measurement requires a modified version of the abovestated equation, otherwise known as the X, which incorporates correction factors for specific heat and specific gravity of both the indicator and the blood.
2014 march Q19, Define cardiac output. (10% of marks) Outline the factors that affect cardiac output. (60% of marks) Briefly describe the thermo dilution method of measuring cardiac output. (30% of marks
Thermodilution measurement of cardiac output:
* Rate of blood flow can be determined from the rate of change in the concentration of substance after a known amount of it has been added to the bloodstream
* This uses the equation, V̇ = m/Ct, where:
o V̇ = flow, or cardiac output
o m = dose of the indicator,
o C = concentration, and
o t = time
* In the case of thermodilution, the “indicator substance” is a known volume of cold saline (or heated blood), and the equation
* The use of thermodilution for cardiac output measurement requires a modified version of the abovestated equation, otherwise known as the Stewart-Hamilton equation, which incorporates correction factors for specific heat and specific gravity of both the indicator and the blood.
2014 march, Define cardiac output. (10% of marks) Outline the factors that affect cardiac output. (60% of marks) Briefly describe the thermo dilution method of measuring cardiac output. (30% of marks)
examiner comment
2014 march, Define cardiac output. (10% of marks) Outline the factors that affect cardiac output. (60% of marks) Briefly describe the thermo dilution method of measuring cardiac output. (30% of marks)
58% of candidates passed this question. This is a core question. It was expected candidates could provide a definition (heart rate x stroke volume) and then move on to outline factors that affect it (afterload, preload, contractility). Additional marks were awarded for descriptions of the relationship to mean systemic filling pressure and other influences beyond this. Most candidates described a thermodilution cardiac output curve but almost all described the technique as based on the “Fick equation or method” (which is used to estimate cardiac output from oxygen consumption). Very few candidates correctly identified the Stewart Hamilton equation as the integration method used to relate cardiac output (flow) to temperature change as an example of indicator dye dilution. Candidates seemed to lack depth and understanding on this topic.
Cardiac output measurement can be performed:
INVASIVELY
o Pulmonary Artery Catheter
▪ Thermodilution
▪ Fick Principle
o Indicator Dilution Technique
o TOE
o Arterial waveform analysis
▪ PiCCO
▪ Vigileo
Non-invasively
o TTE
o MRI
o Thoracic impedance
cicm wrecks 2017-2-10
note: i no longer thing the above is correct, so there is ficks method vs indicator dilulution (which relies on ficks principle), termodiluation is a subset of indicator dilution, not: ficks method requires PA catheter for mixed venous blood sampling, and indicator dilution needs either CVC or pa catheter
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
what is this/
* V̇ = m/Ct,
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
Stewart-Hamilton equation:
* V̇ = m/Ct,
where
o V̇ = flow, or cardiac output
o C = concentration
o m = dose of the indicator, and
o t = time
* or, Cardiac output = indicator dose / area under the concentration-time curve
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
Advantages and limitations:
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
Advantages and limitations:
* Access to mixed venous blood and arterial blood is not essential
* It is convenient: with electronic calculations, cardiac output measurement can be automated and continuous
* Good correlation with gold standard measurements of cardiac output
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
However:
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
However:
* Use of dye limits the frequency and repeatability of measurements, as it produces recirculation, and even the most rapidly cleared dyes are cleared after some minutes.
* Manual integration of the area under the concentration/time curve is laborious
* Automated calculation of cardiac output involves the use of correction factors and coefficients, which reduces its accuracy
* The method relies on uniform mixing of blood and unidirectional flow
* Thermodilution measurements have numerous potential sources of error
* Under laboratory conditions, agreement between this method and the direct Fick method is within a margin of 25%
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
examiner comment
2011 mar Describe the principles, and limitations, of the measurement of cardiac output using an indicator dilution technique
Most candidates chose to describe the thermodilution technique of cardiac output measurement. Descriptions of other techniques and indicators such as dye dilution using indocyanine green were acceptable alternatives. Better answers included a description of the Fick Principle and the fact that it is based on the law of conservation of matter. For thermodilution, heat lost from the blood = heat gained from the injectate. Also required were an accurate description of the technique, a description of the indicator-time curve and errors encountered in the technique. For thermodilution these included the requirement for a Swan Ganz catheter, nature and temperature of the injectate, temperature measurement using a thermistor in the pulmonary artery and an appreciation that it is the curve of a decrease in temperature versus time that is being analysed.
“vasovagal” vs orthostatic hypotension
A “vasovagal” is from excessive
autonomic reflex activity in contrast to orthostatic hypotension which is a failure of the autonomic reflex response.
examiners comments 2017 august Q19
description of vasovagal syncope
description of vasovagal syncope, also known as
neurocardiogenic syncope.
benign,
self-limiting
caused by an abnormal or exaggerated
autonomic response to various stimuli
examiners comments 2017 august Q19
definition of vasovagal syncope
Description:
Vasovagal syncope, or neurocardiogenic syncope, is a transient loss of consciousness due to global cerebral hypoperfusion, which occurs as the result of an autonomic reflex response to various stimuli
deranged 2017 august Q19
4 phases of vasovagal
Vagal: bradycardia
Sympathetic: systemic vasodilation (mainly muscles)
Vasovagal syncope is thought to have four distint phases:
phase 1: early stabilization (by normal baroreceptor reflex)
phase 2: circulatory instability (baroreflex vasoconstriction)
phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
phase 4: recovery
deranged 2017 august Q19
vasovagal effects on vagal and sympathetic
Vagal: bradycardia
Sympathetic: systemic vasodilation (mainly muscles)
deranged 2017 august Q19
Amount of blood in pulmonary vs systemic circulation
About 500ml, in a 70kg person
About 4500ml, in a 70kg person; of which the majority is in capacitance vessels
2017 march Q7 dranged specific answer
Normal PA systolic pressure
Normal PA diastolic pressure
Normal mean pulmonary arterial pressure
Normal PA systolic pressure = 18-25 mmHg
Normal PA diastolic pressure = 8-15 mmHg
Normal mean pulmonary arterial pressure = 9-16 mmHg
2017 march Q7 dranged specific answer
pulmonary vs systemic
compare resistance
pulmonary Low resistance;
PVR = 100-200 dynes.sec.cm-5
systemic
High resistance;
SVR = 900-1200 dynes.sec.cm-5
Trans-systemic intravascular pressure gradient is around 100 mmHg
2017 march Q7 deranged specific answer
pulmonary circulation
Regional distribution of blood flow
Blood flow is affected by
* gravity
* alveolar recruitment
* hypoxic vasoconstriction
Little active regulation occurs
2017 march Q7 deranged specific answer
Systemic circulation
Regional distribution of blood flow
Significant active regulation of organ-specific regional blood flow, depending on organ demand
Blood flow is less affected by gravity
2017 march Q7 deranged specific answer
pulmonary circulation response to hypoxia
Vasoconstriction
2017 march Q7 deranged specific answer
systemic circulation response to hypoxia
Vasodilation
2017 march Q7 deranged specific answer
pulmonary circulation response to hypercapnia
Vasoconstriction
2017 march Q7 deranged specific answer
systemic circulation response to hypercapnia
Vasodilation
2017 march Q7 deranged specific answer
metabolic functions of the lungs
Metabolic functions Metabolism of -hydroxytryptamine, prostaglandins and substrates for angiotensin-converting enzyme (bradykinin and angiotensin I)
2017 march Q7 deranged specific answer
Synthetic functions of pulmonary circulation
Source of thromboplastin and heparin, which act to degrade filtered clots
2017 march Q7 deranged specific answer
Synthetic functions of the systemic circulation
Synthesis of nitric oxide, as well as pro– and anti-coagulants
2017 march Q7 deranged specific answer
Filter function of pulmonary circulation
Filters emboli larger than 8 μm
2017 march Q7 deranged specific answer
filter functions of the systemic circulation
Filtration of arterial blood in the renal and hepatic vascular beds results in the clearance of metabolic wastes and particles.
2017 march Q7 deranged specific answer
contrast pulmonary and systemic circulations responses to hypoxia
For example: many candidates stated ‘hypoxic pulmonary vasoconstriction’, but did not contrast this to ‘hypoxic vasodilation’ for the systemic circulation
2017 march Q7 examiners comments
cardiovascular changes in obesity
Total body oxygen demand is increased
Cardiac output is increased
Cardiac preload is increased
LV contractility is often stable
Cardiac afterload can be increased or decrease
There is increased RV afterload and preload
2017 march Q15 deranged specific question
Basic Walkthrough left ventricular pressure volume loop in a normal adult
based on deranged diagram on question 2017 mar q23
axis is pressure (depdnent) depends on volume (independent)
which make sense based on frank starling, the pressure generated is dpednended on the position of actin and myosin which is dependent on volume
start at the bottom right (and go counterclockwise)
bottom right is mitral valve closing
going up is isovolumetric contraction
when the aortic valve opens it begins to move left which is systolic ejection
and then it hits aortic valve closing
at this point there are many lines, vertical is aortic valve closing, horizontal is systolic pressure, diagonal line to zero is end systolic pressure volume relationship (ESpvR) which also represents contractility and the area under this is potential mechanical work, and a diagonal line down to max volume represents arterial elastance aka afterload
line going down until the mitral valve opening and then we move right (notice this is even below the mitral valve closing)
then we move right and this line is diastole filling and end diastolic pressure volume relationship (EDPVR)
finally we hit the mitral valve closing
2017 march 23
note; meaning that as the mitral vale opens and the ventricle fills up with volume (moves right) the ventricle increases pressure
describe Oxygen demand of of heart
About 85 - 90% of oxygen demand is for internal work (major determinants wall tension 30 - 40%, heart rate 15 - 25%, myocardial contractility 10 - 15%, basal metabolism 25%).
10 - 15% of oxygen demand for external work or pressure volume work, determined by MPAP x CO.
Examiner comment 2016 aug 7
Coronary blood flow is affected by ?
Coronary blood flow is affected by coronary perfusion pressure (determined by aortic pressure and RV pressure) & coronary vascular resistance (determined by autoregulation, metabolic factors, humoral factors, nervous control interacting with local endothelial factors)
Examiner comment 2016 aug 7
Generally, coronary blood flow is tightly coupled to oxygen demand/consumption due to high basal oxygen consumption x ml/ min/100g) and high oxygen extraction ratio (x%).
Generally, coronary blood flow is tightly coupled to oxygen demand/consumption due to high
basal oxygen consumption (8 - 10 ml/ min/100g) and high oxygen extraction ratio (75%).
Examiner comment 2016 aug 7
cardiac oxygen supply can only be increased to cope with increased demand only by ??
Better answers noted that oxygen supply can only be increased to cope with increased demand only by increased coronary blood flow.
Examiner comment 2016 aug 7
demonstrate the salient features of the aortic and radial arterial pulses was expected
1different systolic pressure
2the absence of a dicrotic notch in the radial pulse (instead a diastolic hump),
3the narrowness and the delay of the radial pulse,
4the distance needed to travel for the pressure wave accounting for the delay,
5the sharper rise and decline of the radial pulse due to loss of the WIndkessel effect and the different compliance
6loss of the dicrotic notch due to summation and damping out of high-frequency components of the pressure wave.
Examiner comments 2016 august 17
The arterial pulse waveform can be separated into three distinct components
The arterial pulse waveform can be separated into three distinct components
* The systolic phase, characterised by a rapid increase in pressure to a peak, followed by a rapid decline. This phase begins with the opening of the aortic valve and corresponds to the left ventricular ejection
* The dicrotic notch, which represents the closure of the aortic valve
* The diastolic phase, which represents the run-off of blood into the peripheral circulation.
cicm wrecks 2016 august 17
Windkessel effect
Windkessel effect is a term used in medicine to account for the shape of the arterial blood pressure waveform in terms of the interaction between the stroke volume and the compliance of the aorta and large elastic arteries (Windkessel vessels) and the resistance of the smaller arteries and arterioles.
cicm wrecks 2016 august 17
For artery pressure waveform
The further you get from the aorta,
- The taller the systolic peak (i.e. a higher systolic pressure)
- The further the dicrotic notch
- The lower the end-diastolic pressure (i.e. the wider the pulse pressure)
- The later the arrival of the pulse (its 60msec delayed in the radial artery)
Factors:
* distance needed to travel for the pressure wave accounting for the delay
* the sharper rise and decline of the radial pulse due to loss of the WIndkessel effect and the different compliance
* the loss of the dicrotic notch due to summation and damping out of high frequency components of the pressure wave. (peripheral dicrotic notch owes more of its shape to the vascular resistance of peripheral vessels than to the closing of the aortic valve)
cicm wrecks 2016 august 17
For artery pressure waveform
examiner comment
A well labelled diagram drawn clearly to demonstrate the salient features of the aortic and radial arterial pulses was expected. This would include the different systolic pressure, the absence of a dicrotic notch in the radial pulse (instead a diastolic hump), the narrowness and the delay of the radial pulse, garnered many marks. Marks were lost for insufficient explanation such as the distance needed to travel for the pressure wave accounting for the delay, the sharper rise and decline of the radial pulse due to loss of the WIndkessel effect and the different compliance and the loss of the dicrotic notch due to summation and damping out of high frequency components of the pressure wave.
cicm wrecks 2016 august 17
diference between ficks method and princiople
It is important at this stage to point out that the thermodilution (or any other indicator dilution) method relies on the Fick principle, but does not involve the Fick method. The Fick method is where you collect the exhaled oxygen in a bag to calculate the VO2, and measure the arterio-venus oxygen difference to calculate the cardiac output.
.
The Fick principle is the theoretical basis of this measurement, which simply points out the relationship between the cardiac output and the concentration difference of a marker substance between an upstream and downstream points in the blood flow. If you know the dose of injected marker, the principle states, you can calculate the cardiac output from the concentration difference - which is basically what indicator dilution does.
note: I think this is worded a little funny, but when the sentence “The fick principle” starts it is referring to indicator dilution
2014 march deranged specific answer Q19
Fick Principle and the fact that it is based on the law of x
Fick Principle and the fact that it is based on the law of conservation of matter.
2011 mar examiner comment Q12
For thermodiluation, describe the technique, a description of the indicator-time curve and errors encountered in the technique.
the technique, a description of the indicator-time curve and errors encountered in the technique. For thermodilution these included the requirement for a Swan Ganz catheter, nature and temperature of the injectate, temperature measurement using a thermistor in the pulmonary artery and an appreciation that it is the curve of a decrease in temperature versus time that is being analysed
2011 mar examiner comment Q12
Describe Ficks method
Total uptake of oxygen by the body is equal to the product of the cardiac output and the arterial-venous oxygen content difference:
CO = VO2 / (Ca - Cv)
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Equipment needed for ficks method
Equipment
Flowmeter, mask, collector bag to measure VO2
PA catheter for mixed venous blood sampling
Arterial catheter for arterial blood sampling
Blood gas analyser
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
i keep forgetting
which one do you need mixed venous blood/
ficks method
diluation obviously doesnt because one of the dilution techniques is thermo which wouldnt need mixed
Advantages for ficks method
“Gold standard”
Good accuracy
Necessary invasive devices are often already available in ICU patients
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Sources of error and limitations for ficks method
Requires stable CO over some minutes
Highly invasive (requires PAC and arterial line)
Requires cumbersome VO2 measuring equipment
Use of estimated instead of measured variables(“indirect Fick method”)
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Describe Indicator dilution
Cardiac output is calculated from the dose of indicator and the area under the concentration-time curve, measured by a downstream detector:
V̇ = m/Ct
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Equipement for Indicator dilution
PA catheter or CVC for injection of indicator
Detector (eg. thermistor) in a pulmonary or systemic artery
Central processor to perform calculations and report values
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Advantages for Indicator dilution
Does not require mixed venous blood
Numerous indicator options (eg. thermodilution)
Reasonable accuracy
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
Sources of error and limitations Indicator dilution
Accuracy is highly technique-dependent
Rendered inaccurate by intacardiac shunts and valve disease
Accuracy is reduced by estimated coefficients in the equation
Must be times with respiratory cycle (measure at end-expiration)
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
2017 aug Q10; Compare and contrast two methods of measuring cardiac output
examiner comment
Good answers began with a definition of cardiac output. For each method, it was expected that
candidates discuss the theoretical basis, equipment, advantages and disadvantages / sources
of error and limitations. Additional marks were awarded when an attempt was made to compare
and contrast the two methods (often helped by the use of a table)..
.
Deranged; Thought it might seem disrespectfully wasteful of the readers’ time to take up this answer space with a rant, somebody has to explain to them (who may be future CICM examiners) how unfair it is to expect something in the answer if you didn’t ask for it in the question. Not everybody would immediately start their response to this SAQ with a definition of the cardiac output: most people would just tabulate the differences and similarities between two methods of measurement, as they were asked. Carrying on with the theme of bizarrely misstated expectations, the examiners applauded additional marks being awarded to people who compared and contrasted the two methods, as if it were some secret extra credit assignment, even though the question specifically asks them to “compare and contrast two methods”.
So, what would an answer look like if it answered the actual question? Hopefully, this would have scored enough marks to pass:
Extrinsic vs intrinsic peep
PEEP = Positive End Expiratory Pressure. Equivalent to a constant pressure applied throughout the respiratory cycle.
.
Intrinsic PEEP = unintentional or un-measured end-expiratory hyperinflation
2019 march Q20 cicm wrecks
what does PEEP do do intrahoracic pressure
Cardiovascular effects: Causes constant ↑ intrathoracic pressure (ITP) throughout respiratory cycle
2019 march Q20 cicm wrecks
What does peep do to cardiac output
o ↓ C.O. and ↑ Central venous pressure
▪ ↓ Renal blood flow, ↓ Glomerular Filtration Rate and urine output
▪ ↑ ADH and Angiotensin II levels
▪ ↑Hepatic venous pressure → ↓ Hepatic Blood Flow
o ↑ CVP and ↓ venous return
▪ ↑ Intracranial pressure
2019 march Q20 cicm wrecks
What does peep do to central venous pressure
o ↓ C.O. and ↑ Central venous pressure
▪ ↓ Renal blood flow, ↓ Glomerular Filtration Rate and urine output
▪ ↑ ADH and Angiotensin II levels
▪ ↑Hepatic venous pressure → ↓ Hepatic Blood Flow
o ↑ CVP and ↓ venous return
▪ ↑ Intracranial pressure
2019 march 20 cicm wrecks
What does peep do to venous return
o ↓ C.O. and ↑ Central venous pressure
▪ ↓ Renal blood flow, ↓ Glomerular Filtration Rate and urine output
▪ ↑ ADH and Angiotensin II levels
▪ ↑Hepatic venous pressure → ↓ Hepatic Blood Flow
o ↑ CVP and ↓ venous return
▪ ↑ Intracranial pressure
2019 march Q20 cicm wrecks
What does peep do to intracranial pressure
o ↓ C.O. and ↑ Central venous pressure
▪ ↓ Renal blood flow, ↓ Glomerular Filtration Rate and urine output
▪ ↑ ADH and Angiotensin II levels
▪ ↑Hepatic venous pressure → ↓ Hepatic Blood Flow
o ↑ CVP and ↓ venous return
▪ ↑ Intracranial pressure
2019 march Q20 cicm wrecks
What does peep do to pulmonary vascular resistance
Transmitted alveolar pressure increases pulmonary vascular resistance
2019 march Q20 deranged specific answer
What does peep do to right ventrciular afterload
Increased pulmonary vascular resistance increases right ventriular afterload
2019 march Q20 deranged specific answer
What does peep do to right ventricular stroke volume
Thus, increased afterload and decreased preload has the net effect of decreasing the right ventricular stroke volume.
2019 march Q20 deranged specific answer
what does peep do to left ventricle preload and afterload and stroke volume
- Decreased preload by virtue of lower pulmonary venous pressure
- Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
- Thus, decreased LV stroke volume
2019 march Q20 deranged specific answer
note; I think the easiest trick to remember this is that if there is decreased preload there will be lower stroke volume
examiner comments
Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long-acting muscle relaxant.
Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long-acting muscle relaxant. 2019 march Q20 examiner comment
33% of candidates passed this question. Structured answers separating effects of positive pressure on right and left ventricle, on preload and on afterload were expected. Overall there was a lack of depth and many candidates referred to pathological states such as the failing heart. Simply stating that positive pressure ventilation reduced right ventricular venous return and/or left ventricular afterload, without some additional explanation was not sufficient to achieve a pass level.
The ECG device detects and amplifies the small electrical changes on the skin that are caused when the heart muscle depolarizes (x mV).
The ECG device detects and amplifies the small electrical changes on the skin that are caused when the heart muscle depolarizes (0.5 – 2 mV). This is reflected as rises and falls in the voltage between two electrodes placed either side of the heart which is displayed either on a screen or on paper. Usually more than 2 electrodes are used and they can be combined into a number of pairs (For example: Left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs LA+RA, LA+LL, and RA+LL).
2016 march Q9 examiners comment
ECG; The output from each pair is known as a?
Usually, more than 2 electrodes are used and they can be combined into a number of pairs (For example: Left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs LA+RA, LA+LL, and RA+LL). The output from each pair is known as a lead. Each lead is said to look at the heart from a different angle.
2016 march Q9 examiners comment
ECG Electrodes are commonly made of?
Electrodes are commonly made of silver or silver chloride components that are attached to the main unit of the machine. Most ECG machines use 12 electrodes. Better answers made mention of the two lead types: unipolar and bipolar. Methods to reduce artefact include improving signal detection (conductive paste, skin preparation (dry, no hair, etc.)) and minimizing external electrostatic forces (common earthed environment, diathermy, etc.,) or patient environment (avoid shivering).
2016 march Q9 examiners comment
Most ECG machines use how many electrodes?
Electrodes are commonly made of silver or silver chloride components that are attached to the main unit of the machine. Most ECG machines use 12 electrodes. Better answers made mention of the two lead types: unipolar and bipolar. Methods to reduce artefact include improving signal detection (conductive paste, skin preparation (dry, no hair, etc.)) and minimizing external electrostatic forces (common earthed environment, diathermy, etc.,) or patient environment (avoid shivering).
2016 march Q9 examiners comment
What are the two lead types/
Better answers made mention of the two lead types: unipolar and bipolar. Methods to reduce artefact include improving signal detection (conductive paste, skin preparation (dry, no hair, etc.)) and minimizing external electrostatic forces (common earthed environment, diathermy, etc.,) or patient environment (avoid shivering).
2016 march Q9 examiners comment
ECG Methods to reduce artefact include ?
improving signal detection (conductive paste, skin preparation (dry, no hair, etc.)) and minimizing external electrostatic forces (common earthed environment, diathermy, etc.,) or patient environment (avoid shivering).
2016 march Q9 examiners comment
The amplifier has three essential functions:
The amplifier has three essential functions: High input impedance so as to minimize signal loss and reject interference (50 – 60 Hz), differential amplification, (to amplify the potential difference detected by the skin electrodes), and high common mode rejection (e.g. > 50Hz) to aid eliminating muscle artefact or electrical interference from the power grid.).
2016 march Q9 examiners comment
note; eli5, the way I remember this is high input impedance to reject interference from all others, amplification to increase signal, and high common mode rejection to eliminate interference from high frequency source
2016 march Describe the essential components of an ECG monitor (80% of marks). Outline the methods employed to reduce artefact (20% of marks). 2016 march repeated in 2011 aug
Relation of cellular ionic events to surface ECG
- Relation of cellular ionic events to surface ECG
o Extracellular charge of resting myocyte membrane is positive
o Depolarisation makes it negative
o This difference in charge along the myocardium produces an electric field
o The difference between two surface measurements of electric field strength is the potential difference (voltage) measured by the ECG leads
o Each pair of electrodes is a “lead”
deranged 2016 march Q9
2016 march Describe the essential components of an ECG monitor (80% of marks). Outline the methods employed to reduce artefact (20% of marks). 2016 march repeated in 2011 aug
- Relation of surface ECG to events of the cardiac cycle
- Relation of surface ECG to events of the cardiac cycle
o P wave: depolarisation of atrial muscle
o PR interval: AV node onduction
o QRS: depolarisation of the ventricular muscle
o Peak of the R wave: beginning of isovolumetric contraction
o T wave: ventricular repolarisation
deranged 2016 march Q9
2016 march Describe the essential components of an ECG monitor (80% of marks). Outline the methods employed to reduce artefact (20% of marks). 2016 march repeated in 2011 aug
- Essential components of an ECG monitor
- Essential components of an ECG monitor
o Signal transmission: by silver/silver chloride electrodes
Thin and broad electrodes (10mm diameter)
Conducting gel to improve skin contact
Digital signal
High sampling rate (10,000-15,000 Hz) to detect pacing spikes
.
o Amplification
Low signal amplitude (0.5-2.0 mV) requires a ~ 1,000 gain factor
Differential amplification only amplifies the difference between electrode leads, rather than the absolute voltages
This eliminates sources of noise which affect each electrode equally (this is called common-mode rejection)
.
o Isolation removes mains interference and protects components
o Earthing reduces interference
.
o Filtering
Most ECG information is contained in signals 1.0-30 Hz
Monitoring mode filter the signal frequency to 0.5-30 Hz range
Diagnostic mode filter the signal frequency to 0.05-100 Hz range
High input impedance of the amplifier decreases the conduction of high-frequency signals, eliminating mains interference and EMG signal
Low pass filtering eliminates movement artifact
deranged 2016 march Q9
Mixed venous PCO2 is usually about x mmHg, and is determined by the total oxygen content of mixed venous blood and the shape of the CO2 dissociation curve
Mixed venous PCO2 is usually about 46 mmHg, and is determined by the total oxygen content of mixed venous blood and the shape of the CO2 dissociation curve
deranged specific answer for 2015 august Q23
The total CO2 content of mixed venous blood, which is usually about x ml/L, is described by the modified x equation:
The total CO2 content of mixed venous blood, which is usually about 520 ml/L, is described by the modified Fick equation:
VCO2 = CO × k × (PvCO2 - PaCO2)
where
VCO2 is the rate of CO2 production,
CO is the cardiac output,
PvCO2 - PaCO2 is the arteriovenous CO2 difference, and
k is a coefficient used to describe the near-linear relationship between CO2 content and partial pressure in the blood.
deranged specific answer for 2015 august Q23
any increase in arterial CO2 will be inherited by the x CO2. This is controlled by the x
The CO2 content of arterial blood - any increase in arterial CO2 will be inherited by the mixed venous CO2. This is controlled by the central ventilation reflexes.
deranged specific answer for 2015 august Q23
CO2 production in the tissues, which is related to the rate of aerobic metabolism and oxygen consumption (VO2). A low metabolic rate will cause a x in mixed venous CO2 (eg. hypothermia).
CO2 production in the tissues, which is related to the rate of aerobic metabolism and oxygen consumption (VO2). A low metabolic rate will cause a decrease in mixed venous CO2 (eg. hypothermia).
deranged specific answer for 2015 august Q23
Cardiac output, which determines the rate of tissue CO2 removal.
Poor cardiac output (eg. in cardiogenic shock) will cause an x mixed venous CO2 by a “stagnation phenomenon”
I.e. an abnormally large amount of CO2 will be added to capillary blood per unit volume if the transit time is x (i.e. flow is x)
Cardiac output, which determines the rate of tissue CO2 removal.
Poor cardiac output (eg. in cardiogenic shock) will cause an increased mixed venous CO2 by a “stagnation phenomenon”
I.e. an abnormally large amount of CO2 will be added to capillary blood per unit volume if the transit time is increased (i.e. flow is decreased)
deranged specific answer for 2015 august Q23
what term describes; deoxygenated haemoglobin has a higher affinity for CO2
deoxygenated haemoglobin has a higher affinity for CO2 (the Haldane effect).
deranged specific answer for 2015 august Q23
the Haldane effect
deoxygenated haemoglobin has a higher affinity for CO2 (the Haldane effect).
deranged specific answer for 2015 august Q23
Partial pressure of CO2 in mixed venous blood depends on the CO2 content of the mixed venous blood, which in turn represents a balance between X
Partial pressure of CO2 in mixed venous blood depends on the CO2 content of the mixed venous blood, which in turn represents a balance between CO2 production in the tissues and the CO2 content in arterial blood.
examiner comment 2011 Q7
. The partial pressure of CO2 is related to the CO2 content by the x
. The partial pressure of CO2 is related to the CO2 content by the CO2 dissociation curve, the position of which is determined by the state of oxygenation of haemoglobin, the Haldane effect
examiner comment 2011 Q7
alveolar ventilation under the control of x
alveolar ventilation under the control of chemoreceptors and the brainstem respiratory centre.
examiner comment 2011 Q7
23 Describe the factors that affect partial pressure of CO2 in mixed venous blood 2015 august and 2011 march
2011 Briefly describe the factors that affect the partial pressure of carbon dioxide
in mixed venous blood. 2015 august and 2011 march
2015 august Q23.
Describe the factors that affect the partial pressure of CO2 in mixed venous blood. 15 % of candidates passed this question.
/
It was expected candidates would define key concepts, particularly ‘mixed venous’. Many candidates knew some of the elements that contributed to mixed venous PCO2 but few described all of the main factors. There was little mention of tissue capillary flow as a factor affecting mixed venous CO2.
2011 march 7
Candidates were expected to provide a definition of important terms such as mixed venous. Many candidates provided much information about the partial pressure of carbon dioxide in arterial blood without discussing the factors which alter the mixed venous pressure. Partial pressure of CO2 in mixed venous blood depends on the CO2 content of the mixed venous blood, which in turn represents a balance between CO2 production in the tissues and the CO2 content in arterial blood. Good answers demonstrated an understanding of this and provided relevant details about these aspects. The partial pressure of CO2 is related to the CO2 content by the CO2 dissociation curve, the position of which is determined by the state of oxygenation of haemoglobin, the Haldane effect. CO2 production is related to aerobic metabolism in cells and total production is defined by the metabolic rate. Examples of increased and decreased CO2 production gained additional marks. The partial pressure of CO2 in mixed venous blood is related to the partial pressure or content of CO2 in arterial blood. This is determined mainly by alveolar ventilation under the control of chemoreceptors and the brainstem respiratory centre.
examiner comment 2011 Q7
what desecribes: increased afterload causes an increased end-systolic volume, which increases the sarcomere stretch, and leads to an increase in the force of contraction
o The Anrep effect: increased afterload causes an increased end-systolic volume, which increases the sarcomere stretch, and leads to an increase in the force of contraction
o the Bowditch effect, or Treppe effect: with higher heart rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
deranged specific answer 2018 august Q18
what is The Anrep effect?
o The Anrep effect: increased afterload causes an increased end-systolic volume, which increases the sarcomere stretch, and leads to an increase in the force of contraction
o the Bowditch effect, or Treppe effect: with higher heart rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
deranged specific answer 2018 august Q18
What is the Bowditch effect, or Treppe effect
o The Anrep effect: increased afterload causes an increased end-systolic volume, which increases the sarcomere stretch, and leads to an increase in the force of contraction
o the Bowditch effect, or Treppe effect: with higher heart rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
deranged specific answer 2018 august Q18
What describes: with higher heart rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
o The Anrep effect: increased afterload causes an increased end-systolic volume, which increases the sarcomere stretch, and leads to an increase in the force of contraction
o the Bowditch effect, or Treppe effect: with higher heart rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
deranged specific answer 2018 august Q18
LV systolic function is a function of its x
LV systolic function is a function of its contractility.
Contractility = the change in force generated independent of preload
cicmwrekcs answer 2018 august Q18
LV diastolic function:
LV diastolic function is determined by its x
LV diastolic function:
LV diastolic function is determined by its compliance. LV compliance is primarily determined by myocardial characteristics and load.
Factors affecting LV diastolic function:
Normal HR and rhythm
LV systolic function
Wall thickness
Chamber geometry
Duration, rate and extent of myocyte relaxation
LV untwisting and elastic recoil
Magnitude of diastolic suction
LA-LV pressure gradient
Passive elastic properties of LV myocardium
Viscoelastic effects (rapid LV filling and atrial systole)
LA structure and function
cicmwrekcs answer 2018 august Q18
Describe the factors affecting left ventricular function
just read
Answers needed to consider intrinsic and extrinsic factors affecting LV function - the latter (e.g. SNS, PSNS, hormones, drugs) was often left out. Answers needed to consider both systolic and diastolic function. An excellent answer included physiological phenomena such as the Treppe effect, Anrep effect and baroreceptor and chemoreceptor reflexes. Mention of normal conduction and pacing as well as blood supply limited by diastole scored additional marks.
examiners comments 2018 august Q18
just read
effects of aging on cardiovascular reserve
Recognition that aging reduces cardiovascular reserve followed up with an outline of the effects of aging on the heart, the vasculature, endothelial function and the conducting system would be rewarded with a good mark. Few answers quantified the decrease of cardiac output with age and only even fewer ventured into the contribution of ventricular filling by atrial systole. No answer discussed endothelial changes with aging
2015 march 19 examiner comment
Definition of diastole
Definition of diastole
* Diastole is the period of chamber relaxation and cardiac filling which corresponds to
o The period between the end of the T wave and the end of the PR interval
o The period during which the mitral valve/tricuspid valves are open.
deranged 2018 March Q12
note: I think this is wrong, because it starts with isovolumetric relaxation which has no valves open
What are the key poitns to talk about for; Briefly describe the cardiac events that occur during ventricular diastole
electrical/ionic events
coronary blood flow
mechanical events ( opening and closing of valves, blood movement)
ECG events
examiners comments 2018 March Q12
Isovolumetric relaxation
Briefly describe the cardiac events that occur during ventricular diastole
- Isovolumetric relaxation
o This period begi
o The ventricles relax without any change in volume
o The pressure drops until the tricuspid and mitral valves open
o The beginning of this period corresponds to the peak of the T-wave, and the middle (steep portion) of Phase 3 (repolarisation) of the cardiac myocyte action potential
o The end of this period corresponds to the end of the T wave on the surface ECG, and the end of Phase 3
deragned specific answer 2018 March Q12
(note: can only imagine this is supposed to say it begins with aortic valve closing)
Briefly describe the cardiac events that occur during ventricular diastole
* Early rapid diastolic filling
- Early rapid diastolic filling
o During this period the relaxing ventricles have pressure lower than atrial pressure, and they fill rapidly
o 80% of the ventricular end-diastolic volume is achieved during this phase
o Coronary blood flow is maximal during this phase
deragned specific answer 2018 March Q12
Briefly describe the cardiac events that occur during ventricular diastole
* Late slow diastolic filling
- Late slow diastolic filling
o Ventricular and atrial pressures equilibrate and the atria act as passive conduits for ventricular filling
o The end of this phase corresponds to the end of the P-wave on the surface ECG
deragned specific answer 2018 March Q12
Briefly describe the cardiac events that occur during ventricular diastole
* Atrial systole
- Atrial systole
o The atria contract (right first, then left shortly after)
o This increases the pressure in the ventricles up to the end-diastolic pressure, and adds about 20ml of extra volume to the end-diastolic volume
o These events start at the end of the P-wave on the surface ECG, and finish during the PR interval.
o The end of this phase corresponds to the peak of the R wave, or the Phase 0 (rapid sodium influx) of the ventricular myocyte action potential
deragned specific answer 2018 March Q12
deranged 2018 march and 2011 march Briefly describe the cardiac events that occur during ventricular diastole
examiner comment
deranged 2018 march and 2011 march Briefly describe the cardiac events that occur during ventricular diastole
2018
12.Briefly describe the cardiac events that occur during ventricular diastole. 29% of candidates passed this question.
Many answers lacked structure and contained insufficient information. Better answers defined diastole and described the mechanical events in the 4 phases of diastole. A common error was the ECG events in diastole. The electrical events and coronary blood flow should have been mentioned.
2011 march
21. Briefly describe the cardiovascular events that occur during ventricular diastole.
One possible way to answer this question is to offer a definition of the diastolic period then to split the events up for description into mechanical events, ECG events and electrical/ionic events. Few candidates defined the diastolic period, and whilst many talked about opening and closing of valves, there was generally a poor understanding of the sequence of events whereby the left ventricle comes to be filled with blood. The better answers included a description of the ionic events that occurred at the various stages of diastole. Many answers lacked any reference to the ECG events in diastole. The major weakness in answers was again the failure to include sufficient information to achieve a pass mark. This was probably as a result of the lack of a systematic approach when answering a question of this nature. Syllabus: C1b, 2d,e and C1c, 2e,f Recommended sources: Textbook of Medical Physiology, Guyton & Hall, Chp 9 – 11 and Review of Medical Physiology, Ganong, Chp 31
What are Baroreceptors?
o Baroreceptors are mechanoreceptors which respond to stretch stimuli.
o This strecth deforms mechanically sensitive sodium channels (DEG/ENaC, degenerin/epithelial sodium channels)
o With sufficient stimulus, sodium current increases to the point where the membrane potential reaches the threshold of local voltage-gated sodium channels, and generates a propagating action potential
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
Where are baroreceptors located?
o Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
o Similar “low pressure” mechanoreceptors are present in the atria, and they mediate the Bainbridge reflex
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
what is the Bainbridge reflex
In short, giving volume increases the heart rate. This makes some sort of logical sense; as you increase the rate of flow into the ventricles, the rate of flow out of the ventricles should also increase, and there’s really only two ways this can happen (increase the stroke volume or increase the heart rate).
deranged Cardiac reflexes topic
what is the stimulus for baroreceptors/
- Stimulus:
o Increased blood pressure (increased stretch, increased receptor firing rate)
o Decreased blood pressure (decreased receptor firing rate)
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
what is the afferent pathway for baroreceptors
- Afferent pathway:
o From the carotid sinus: carotid sinus nerve, a branch of the glossopharyngeal nerve
o From the aortic arch: aortic nerve, a branch of the vagus nerve
o Both of these nerves travel through the jugular foramen to enter the medulla
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
what is the processor for baroreceptor??
Processor:
o Nucleus of the solitary tract receives afferent fibres and redistributes the signal into several efferent regulatory systems:
Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla, which coordinates sympathetic tone
Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
What is the efferent nerves, effector and the effect of baroreceptors?
- Efferent nerves:
o Sympathetic fibres to the heart and peripheral resistance vessels
o Vagal efferents to the cardiac ganglion (heart rate) - Effector: Myocardium, SA and AV nodes, vascular smooth muscle
- Effect:
o In response to arterial hypotension:
Decreased receptor discharge rate
Thus, decreased vagal and disinhibited sympathetic efferents
Thus, systemic vasoconstriction and tachycardia
o In response to arterial hypertension:
Increased receptor discharge rate
Thus, increased vagal and inhibited sympathetic efferents
Thus, systemic vasodilation and bradycardia
deranged specific answer to Describe baroreceptors and their role in the control of blood pressure. 2014 aug Q16 and 2007 aug
Baroreceptor examiner comment, just read
——-end of section 2
Baroreceptors are stretch receptors located in the walls of the heart and blood vessels and are important in the short term control of blood pressure. Those in the carotid sinus and aortic arch monitor the arterial circulation. Others, the cardiopulmonary baroreceptors, are located in the walls of the right and left atria, the pulmonary veins and the pulmonary circulation. They are all stimulated by distention and discharge at an increased rate when the pressure in these structures rises. Better answers provided some detail on the innervation for these receptors. It was expected candidates would describe that increased baroreceptor discharge inhibits the tonic discharge of sympathetic nerves and excites the vagal innervation of the heart. This results in vasodilation, venodilation, a drop in blood pressure, bradycardia and a decreased cardiac output. Some candidates had a major misunderstanding around the purpose of “low pressure baroreceptors” with many believing that these are the ones that respond to lower blood pressures, while the “high pressure baroreceptors” respond to higher blood pressures.
- description of, and types of, baroreceptors (e.g. stretch-receptors)
- their locations (e.g. walls of the aorta, carotid sinuses, the atria etc)
- the stimulus they respond to (e.g. pressure, volume)
- short term and long term responses, alteration to set points, impulse frequency / pressure curve
- a brief description of the afferent and efferent pathways and the resultant efferent effects (e.g. alterations to heart rate, blood pressure, etc)
examiner comment 2014 aug Q16 and 2007 aug
just read
examiners comment of Compare and contrast the systemic circulation with the pulmonary circulation
As a compare and contrast question this question was well answered by candidates who used a table with relevant headings. Comprehensive answers included: anatomy, blood volume, blood flow, blood pressure, circulatory resistance, circulatory regulation, regional distribution of blood flow, response to hypoxia, gas exchange function, metabolic and synthetic functions, role in acid base homeostasis and filter and reservoir functions. A frequent cause for missing marks was writing about each circulation separately but comparing. For example: many candidates stated ‘hypoxic pulmonary vasoconstriction’, but did not contrast this to ‘hypoxic vasodilation’ for the systemic circulation. Frequently functions of the circulations were limited to gas transport / exchange.
examiners comments 2017 march Q8
What is a normal pulmonary artery pressure from cicm wrecks
25/8 map 15
2017-jan-7, i dont think this is right, should look for another source
litfl
what is pulmonary hypertension numbers
increase in mean pulmonary arterial pressure (PAPm) ≥25 mmHg at rest as assessed by right heart catheterization (RHC)
Severity of pulmonary hypertension (mPAP)
Mild = 20-40mmHg
Moderate = 41-55mmHg
Severe = > 55mmHg
https://litfl.com/pulmonary-hypertension-echocardiography/
- Definition of regional blood flow autoregulation:
- Definition of regional blood flow autoregulation:
o “The tendency for blood flow to remain constant despite changes in arterial perfusion pressure” - Johnson, 1986
2014 march 12 deranged
desribe 4 types of Mechanisms which mediate regional autoregulation:
- Mechanisms which mediate regional autoregulation:
o Myogenic mechanisms
o Metabolic mechanisms
o Flow or shear-associated regulation
o Conducted vasomotor responses
2014 march 12 deranged
desribe Myogenic mechanisms
- Mechanisms which mediate regional autoregulation:
o Myogenic mechanisms
This is an intrinsic property of all vascular smooth muscle
Vessel wall stretch produces smooth muscle cell depolarisation
Depolarisation opens voltage-gated calcium channels
Calcium influx produces vasoconstriction by myosin light chain phosphorylation
2014 march 12 deranged
desribe Metabolic mechanisms
o Metabolic mechanisms
Blood flow increases in response to increased tissue demand, eg. in exercising skeletal muscle
This is attributed to the release of metabolic byproducts with vasodilating properties
Potential mediators include potassium, hydrogen peroxide, lactate, hydrogen ions (pH), adenosine, ATP and carbon dioxide
2014 march 12 deranged
desribe Flow or shear-associated regulation
o Flow or shear-associated regulation
This is the phenomenon of proximal vasodilation in response to distal vasodilation.
This shear stress promotes the release of various vasodilatory mediators from the affected endothelium and produces vasodilation of the larger proximal arteriole.
2014 march 12 deranged
desribe Conducted vasomotor responses
o Conducted vasomotor responses
Regional control of one region by the vasomotor events of another neighbouring region.
Mediated by conduction of cell-to-cell signals from a small arteriole upstream to a larger arteriole
2014 march 12 deranged
list the Organ-specific regulatory mechanisms:
o Organ-specific regulatory mechanisms:
Hepatic arterial buffer response:
hepatic arterial flow increases if portal venous flow decreases, and vice versa.
Renal tubuloglomerular feedback
This is a negative feedback loop which decreases renal blood in response to increased sodium delivery to the tubule
The mechanism is mediated by ATP and adenosine secreted by macula densa cells, which cause afferent arterolar vasoconstriction
Maternoplacental blood flow
Blood flow is gradually upregulated over the course of pregnancy by the actions of the trophoblast asit invades the spiral arteries of the uterus
2014 march 12 deranged
definition of Venous return
- Venous return is the rate of blood flow into the heart from the veins.
deranged Question 19 from the first paper of 2020
*At a steady state, venous return and x are equal.
- At a steady state, venous return and cardiac output are equal.
deranged Question 19 from the first paper of 2020
Equation for Venous return
- Venous return can be expressed as VR = (MSFP - RAP) / VR = HR × SV
where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
note; I would not put VR as two variables
deranged Question 19 from the first paper of 2020
Factors which influence venous return include:
- Factors which influence venous return include:
1 Factors which affect cardiac output
o Afterload
o Contractility
2 Factors which affect mean systemic filling pressure
o Total venous blood volume
o Venous smooth muscle tone (which affects the size of the “stressed volume”
3 Factors which affect right atrial pressure
o Intrathoracic pressure (spontaneous vs. positive pressure ventilation)
o Pericardial compliance (eg. tamponade, open chest)
o Right atrial compliance (eg. infarct, dilatation)
o Right atrial contractility (i.e. AF vs sinus rhythm)
o Tricuspid valvular competence and resistance
4 Factors which affect venous resistance
o Mechanical factors
Posture
Intraabdominal pressure
Skeletal muscle pump
Obstruction to venous flow (eg. pregnancy, SVC obstruction)
Hyperviscosity (polycythemia, hyperproteinaemia)
o Neuroendocrine factors
Autonomic tone
Vasoactive drugs (eg. noradrenaline, GTN)
deranged Question 19 from the first paper of 2020
note; easy if you remember that VR=CO and that CO equals stroke volume x heart rate and stroke volume relies on preload, contractility, afterload, and venous return is in an equation with RAP, MSFP and vascular resistance
What is MSFP
mean systolic filling pressure
deranged Question 19 from the first paper of 2020
what is normal MSFP
7mmHg
cicmwrecks Question 19 from the first paper of 2020
What is a Cardiac reflexes?
Cardiac reflexes are fast-acting reflex loops between the heart and central nervous system that contribute to regulation of cardiac function and maintenance of physiologic homeostasis.
2013 aug examiner comment question two cardiac reflex
just read
2013 aug examiner comment question two cardiac reflex
It was expected candidates would include within their answer a mention of the stimulus and how it is sensed, the reflex arc and the resultant effect.
2013 aug examiner comment question two cardiac reflex
List all the cardiac reflexes?
Thus candidates could have mentioned the Baroreceptor Reflex/Carotid Sinus Reflex, Chemoreceptor, Bainbridge, Cushing, Oculocardiac and Bezold-Jarisch (involves response to ventricular stimuli, sensed by receptors within the LV wall that trigger vagal afferent type C fibers and the resultant triad of hypotension, bradycardia, and coronary artery dilatation) reflexes.
2013 aug examiner comment question two cardiac reflex
Bainbridge (elicited by stretch receptors located in the right atrial wall and the cavoatrial junction), Cushing (result of cerebral medullary vasomotor centre ischemia), oculocardic (provoked by pressure applied to the globe of the eye or traction on the surrounding structures), Bezold-Jarisch (responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the LV wall) reflexes be mentioned and described. 2010
Describe this cardiac reflex
* Baroreceptor reflex
- Baroreceptor reflex
o Sensors: pressure (carotid sinus and aortic arch)
o Afferent: vagus and glossopharyngeal nerves
o Processor: nucleus of the solitary tract and nucleus ambiguus
o Efferent: vagus nerve and sympathetic chain
o Effect: increased HR and BP in response to a fall in BP
deranged 2013 Q2
Describe this cardiac reflex
Bainbridge reflex
Bainbridge reflex
Afferent: vagus (atrial stretch)
Processor: nucleus of the solitary tract and the caudal ventral medulla
Efferent: vagus nerve and sympathetic chain
Effect: increased RA pressure produces an increased heart rate;
deranged 2013 Q2
Describe this cardiac reflex
* Chemoreceptor reflex
- Chemoreceptor reflex
o Afferent: carotid / aortic chemoreceptors (low PaO2 and/or high PaCO2)
o Processor: nucleus of the solitary tract and nucleus ambiguus
o Efferent: vagus nerve and sympathetic chain
o Effect: bradycardia and hypertension in response to hypoxia
(also secondary tachycardia from Bainbridge and Hering-Breuer reflexes)
deranged 2013 Q2
Describe this cardiac reflex
* Cushing reflex
- Cushing reflex
o Afferent: mechanosensors in the rostral medulla?
o Processor: rostral ventrolateral medulla
o Efferent: sympathetic fibres to the heart and peripheral smooth muscle
o Effect: hypertension and baroreflex-mediated bradycardia
deranged 2013 Q2
Describe this cardiac reflex
Bezold-Jarisch reflex
Bezold-Jarisch reflex
Afferent: vagus (mechanical/chemical sttimuli to the cardiac chambers)
Processor: nucleus of the solitary tract
Efferent: vagus nerve and sympathetic chain
Effect: hypotension and bradycardia in response to atrial stimulation
deranged 2013 Q2
Describe this cardiac reflex
Oculocardiac reflex
Oculocardiac reflex
Afferent: trigeminal nerve (pressure to the globe of the eye)
Processor: sensory nucleus of CN V; nucleus of the solitary tract
Efferent: vagus nerve and sympathetic chain
Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
deranged 2013 Q2
Describe this cardiac reflex
Diving reflex
Diving reflex
Afferent: trigeminal nerve (cold temperature; pressure of immersion)
Processor: sensory nucleus of CN V; nucleus of the solitary tract
Efferent: vagus nerve and sympathetic chain
Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
deranged 2013 Q2
Describe this cardiac reflex
Barcroft-Edholm
Barcroft-Edholm (vasovagal) reflex
Afferent: emotional distress, hypovolaemia
Processor: unknown
Efferent: vagus nerve and sympathetic chain
Effect: bradycardia, systemic vasodilation, hypotension
deranged 2013 Q2
Describe this cardiac reflex
Respiratory sinus arrhythmia
Respiratory sinus arrhythmia
Afferent: central respiratory pacemaker
Processor: nucleus ambiguus
Efferent: vagus nerve, via the cardiac ganglion
Effect: cyclical increase of heart rate during inspiration
deranged 2013 Q2
Tell me the coronary artery circulation
Arteries:
* LCA to
- LCx to
- OM1
- OM2
- LAD has branches
- ## Diagonal 1 or 2
- RCA
- Right Ventricular
- Acute Marginal
- Posterior descending
2021 march Q19 cicm wrecks
CONCEPT OF Cardiac DOMINANCE:
The dominance of coronary circulation is determined by the artery that supplies the posterior descending artery (PDA). Approximately 60% are right-dominant, 25% are co-dominant, and 15% are left-dominant
2021 march Q19 cicm wrecks
Describe Cardiac veins
Veins:
*Great, small, middle
*Drain into the thebesian veins → ventricles directly
*Empty into the coronary sinus on the posterior wall or the RV
2021 march Q19 cicm wrecks
Describe normal coronary artery blood flow
Normal Coronary Blood Flow
* 80 mL/min/100 g
* or 200-250 mL/min
* 5% of CO at rest
* Can increase by 3-4 times (up to 400mL/min/100g)
2021 march Q19 cicm wrecks
What is cardiac extraction ratio/
High Extraction Ratio High at rest (55-65%) body average of 25%
* Extraction ratio can only rise by factor of < 2 to 90%
* AV Δ O₂ = 11 mL/dL (I don’t even know what this means)
* Coronary venous O₂ content = 5 mL/dL (I don’t even know what this means)
* Coronary sinus SpO₂= 20mmHg OR coronary sinus SpO2 <30%
2021 march Q19 cicm wrecks
Determinants of Coronary artery Blood flow
Determinants of Coronary artery Blood flow
1 Physical Factors
* Extravascular compression (CPP factors)
2 Neural and Neurohumoral Factors
* ↑ SNS tone →
* α receptor mediated vasoconstriction
* β receptor mediated vasodilator
* ↑ force and rate of contractions → ↑ asodilator metabolite release
* Overall effect is dilation
* ↑ PSNS tone → KACh stimulation → mild ↓ Coronary vascular resistance
3Metabolic Factors (main)
* Vasodilatory
* ↑ Adenosine, H, K, CO2, Lactate , /prostaglandins/
* NO → GTP
* ↑ O2 demand → ↓ ATP → ↑atp sensitive K channel activation → hyperpolarisation → vasodilation
4 Myogenic autoregulation (keep CPP 60-180 mmHg)
2021 march Q19 cicm wrecks
just read
highlights of examiners comments
HIGH OXYGEN EXTRACTION, coronary sinus SpO2 <30%
Diastolic aortic pressure
FLOW DEPENDENCE (graph below)
Metabolic autoregulation dependent on:
The phasic nature of flow GRAPH
Better answers included a description of metabolic, physical and neuro-humoral factors and the relative importance of each
2021 march Q19 cicm wrecks
Outline the physiological responses to anaemia (The specific physiological responses to hypovolaemia are NOT required)
2013 aug and 2007 aug
Define Anaemia
Definition:
- Anaemia is a decrease in circulating red blood cells due to increased destruction, blood loss or reduced production.
- Hb concentration below < 2 standard deviations below mean of normal population
- WHO Hb levels Men < 13 g/dL Women < 12 g/dL
- Chronic > 3 months
- produces reduced O2 content in blood -> increased extraction of O2 by the tissues and peripheral vascular dilatation to increase tissue blood flow. Compensation: Kidney 90% (and liver 10%) sense decreased tissue oxygenation release EPO which increases RBC production
Outline the physiological responses to anaemia (The specific physiological responses to hypovolaemia are NOT required)
2013 aug and 2007 aug
note; does it need to be chronic??
What is the blood oxygen delivery equation
and the oxygen content equation
Total blood oxygen delivery (DO2) = CO × CaO2,
and CaO2 = (sO2 × ceHb × BO2 ) + (PaO2 × 0.03)
where:
* ceHb = the effective haemoglobin concentration
* CO = cardiac output
* PaO2 = the partial pressure of oxygen in arterial gas
* 0.03 = the content, in ml/L/mmHg, of dissolved oxygen in blood
* BO2 = the maximum amount of Hb-bound O2 per unit volume of blood (normally 1.39)
* sO2 = oxygen saturation
deranged 2013 aug 24
- Cardiovascular effects of acute isovolaemic anaemia are:
- Cardiovascular effects of acute isovolaemic anaemia are:
o Tachycardia
o Increased stroke volume
o Increased cardiac output
o Decreased peripheral vascular resistance
deranged 2013 aug 24
just read
isovolaemic anaemia are Mechanisms of these cardiovascular effects:
o Vagally mediated tachycardia is partly due to direct aortic arch chemoreceptor activity and partly due to baroreflex activation
Baroreflex activation is due to systemic vasodilation
o Decreased peripheral vascular resistance is due to:
Systemic vasodilation which is mediated by nitric oxide, as the result of decreased oxygen delivery to the tissues (a part of the normal metabolic autoregulation of regional blood flow)
Decreased blood viscosity, as viscosity is an important determinant of peripheral vascular resistance
* Long term effects are related to chronic vasodilation, and include:
o Salt retention (mediated by aldosterone)
o Body water volume expansion (mediated by vasopressin and aldosterone)
o Angiogenesis (to increase the number of capillaries and therefore decrease the diffusion distance between capillaries and cells)
deranged 2013 aug 24
just read
isovolaemic anaemia are Mechanisms of these cardiovascular effects:
—-end of section 3
2013 aug and 2007 aug
2013 aug 24. Outline the physiological responses to anaemia. (The specific physiological responses to hypovolaemia are NOT required.) It was expected candidates would expand on the central role haemoglobin has in oxygen delivery and that in the presence of reduced haemoglobin there are various efforts aimed at maintaining oxygen delivery. Cardiac output is increased, systemic vascular resistance is reduced, modifications are seen in regional circulations and as tissue oxygenation begins to falter then the end products of anaerobic metabolism provide a further stimulus to enhance cardiac out and tissue oxygen delivery. Better answers also included a mention of additional factors that enhance tolerance of chronic anaemia (e.g. angiogenesis).
deranged 2013 aug 24
Candidates were expected to base their answer around the variables involved in the equations that describe oxygen content in blood and oxygen delivery. Although most candidates mentioned changes in haemoglobin that increase oxygen carriage, a more complete discussion of the changes that influence cardiac output and the peripheral circulation was often omitted
Define the Valsalva manoeuvre
The Valsalva Manoeuvre is
expiratory effort against an obstructed airway (eg. closed glottis),
which generates an intrathoracic pressure of ~ 40 mmHg
which continues for 15-20 seconds
and which is usually performed in a seated or supine position
dernaged 2013 march Q3
Define the Valsalva maneuver
The Valsalva Manoeuvre is
expiratory effort against an obstructed airway (eg. closed glottis),
which generates an intrathoracic pressure of ~ 40 mmHg
which continues for 15-20 seconds
and which is usually performed in a seated or supine position
dernaged 2013 march Q3
what cuases Increased intrathoracic pressure in valsalva maneuver
Voluntary breath hold against a closed glottis, or a closed expiratory valve of a ventilator
dernaged 2013 march Q3
what happens to afterload with decreased LV transmural pressure and aortic transmural pressure
Decreased LV afterload with Decreased LV transmural pressure and aortic transmural pressure
dernaged 2013 march Q3
what happens in phase one of valsalva to blood pressure, preload and afterload of LV
Increased blood pressure with stable pulse pressure
caused by Decreased afterload and increased preload on the LV, which increases the stroke volume
dernaged 2013 march Q3
what happens in phase one of valsalva to heart rate
Decreased heart rate caused by Baroreflex activated by high blood pressure decreases the heart rate by means of the vagus
dernaged 2013 march Q3
what hapens in pahse 3 of valsalva to afterload when Increased LV transmural pressure due to loss of intrathoracic pressure
Increased LV afterload Increased LV transmural pressure due to loss of intrathoracic pressure
dernaged 2013 march Q3
Take homes of preload and afterload for right ventricle and left ventricle regarding increased intrathoracic pressure
my own trick
RV are opposite (which makes it harder for RV)
LV are same for ventilators (with the exception of Valsalva maneuver)
RV: so increased intrathoracic pressure causes a decrease in preload and increases afterload (2011 march 8 deranged)
‘Decreased preload by virtue of lower pulmonary venous pressure, Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit, Thus, decreased LV stroke volume”
(2019 march 20)
However for valsalva note LV increased intrathoracic pressure Decreased afterload and increased preload on the LV, which increased the stroke volume (deranged 2013 march Q3)
RV facts 2011 march 8 deranged
the extra facts for LV at in deranged 2013 march Q3
just read valsalva maneurver examiner comments
A good answer to this question required attention to detail and an ability to describe changes in many variables at each stage e.g. intrathoracic pressure, blood volumes, baroreceptor firing and the subsequent cardiovascular response (e.g. heart rate and blood pressure). Using graph(s) is a useful way to assist the explanation and was required as part of the answer. Dividing the response into four stages makes answering the question much easier. Overall there was a deficiency in a deep understanding of the integrated physiology associated with the Valsalva manoeuvre. The most common mistakes were describing a change but not saying why it happened, not considering each element at each stage and confusing terms e.g. saying increased cardiac output when the response was increased mean arterial pressure. Very few candidates drew accurate graphs. Graphs required were those of the changes in intrathoracic pressure, the pulse pressure response and the heart rate response.
i keep forgetting this so adding it in randomly
difference between carotid sinus and carotis bulb
The carotid sinus, anatomically, is a small neurovascular structure located at the dilated portion of the common carotid artery (the “carotid bulb”), just at the point of its bifurcation. It is not to be confused with the carotid body, which is a PaO2 / PaCO2 sensing chemoreceptor at the same location. For lack of a dirty limerick, to help their memory trainees may recall the alliteration that sinus senses stretch, and body senses breathing. The sinus itself is just a bundle of nerve endings which is located in an area of thickened adventitia around the carotid bulb. This image from Porzionato et al (2019) was disgracefully vandalised to demonstrate the thinning of the (pink) arterial media and the thickening of the (purple) adventitia, all the better to bring the nerve endings closer to the arterial lumen (as the nerve endings are mainly seen at the medio-adventitial junction). The silver-stained nerve endings are dark brown.
deranged topic of Function of baroreceptors and clinical relevance of the baroreflex
Main categories of effects of ageing on the cardiovascular system.
- Structural changes:
o Myocardial:
o Vascular: - Functional changes:
o Myocardial:
o Electrophysiological:
o Vascular:
o Neurohormonal:
2015 march 19 deranged
- Structural changes: of ageing cardiovascular
Describe the effects of ageing on the cardiovascular system.
- Structural changes:
o Myocardial:
LV hypertrophy
Interventricular septal hypetrophy
LVOT narrowing
Valvular sclerosis
Degeneration of sympethetic innervation
o Vascular:
Dilation of aorta and large arteries
Thickening of arterial walls
Decreased windkessel effect
2015 march 19 deranged
- Functional changes: of ageing cardiovascular
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Myocardial:
Increased systolic function
Decreased diastolic function
Increased atrial diastolic contribution (atrial “kick”)
Decreased cardiac output (by 1% per year)
Decreased maximal heart rate
Increased cardiac workload (due to afterload increase)
Blunted baroreceptor reflexes
.
o Electrophysiological:
SA node atrophy
Conductive tissue loss
Action potential prolongation
.
o Vascular:
Decreased arterial compliance
Decreased endothelial NO-mediated vasodilatory function
Systolic blood pressure increases
Pulse pressure increases (diastolic pressure increases less than systolic)
Pulmonary arterial pressure increases
.
o Neurohormonal:
Increased ANP secretion
Increased circulating catecholamine levels
Decreased renin, angiotensin and aldosterone concentrations
2015 march 19 deranged
- Structural changes:
o Myocardial:
Describe the effects of ageing on the cardiovascular system.
- Structural changes:
o Myocardial:
LV hypertrophy
Interventricular septal hypetrophy
LVOT narrowing
Valvular sclerosis
Degeneration of sympethetic innervation
2015 march 19 deranged
- Structural changes:
o Vascular:
Describe the effects of ageing on the cardiovascular system.
- Structural changes:
o Vascular:
Dilation of aorta and large arteries
Thickening of arterial walls
Decreased windkessel effect
2015 march 19 deranged
- Functional changes:
o Myocardial:
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Myocardial:
Increased systolic function
Decreased diastolic function
Increased atrial diastolic contribution (atrial “kick”)
Decreased cardiac output (by 1% per year)
Decreased maximal heart rate
Increased cardiac workload (due to afterload increase)
Blunted baroreceptor reflexes
2015 march 19 deranged
- Functional changes:
o Electrophysiological:
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Electrophysiological:
SA node atrophy
Conductive tissue loss
Action potential prolongation
2015 march 19 deranged
- Functional changes:
o Electrophysiological:
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Electrophysiological:
SA node atrophy
Conductive tissue loss
Action potential prolongation
2015 march 19 deranged
- Functional changes:
o Vascular:
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Vascular:
Decreased arterial compliance
Decreased endothelial NO-mediated vasodilatory function
Systolic blood pressure increases
Pulse pressure increases (diastolic pressure increases less than systolic)
Pulmonary arterial pressure increases
2015 march 19 deranged
- Functional changes:
o Neurohormonal:
Describe the effects of ageing on the cardiovascular system.
- Functional changes:
o Neurohormonal:
Increased ANP secretion
Increased circulating catecholamine levels
Decreased renin, angiotensin and aldosterone concentrations
2015 march 19 deranged
note; I need a trick to remember this, so anecdotally old people have worse kidney function and higher blood pressure, and ANP would make you hypovolemic thus worse kidney function, and increased circulating catecholmines would make you have higher blood pressure, but decreased renin would give you lower bp, but it would also make you hypovolemic so that I can remember
just read Describe the effects of ageing on the cardiovascular system. examiner comments
Many candidates described the pathological processes which might affect the aging heart rather than the physiological ones. Recognition that aging reduces cardiovascular reserve followed up with an outline of the effects of aging on the heart, the vasculature, endothelial function and the conducting system would be rewarded with a good mark. Few answers quantified the decrease of cardiac output with age and only even fewer ventured into the contribution of ventricular filling by atrial systole. No answer discussed endothelial changes with aging. Some answers were repetitious. Some answers included a significant discussion of information that was not asked for (Laplace law/Poiseuille’s law).
2015 march 19 examiner comments
just read examiner comments of 2011 august regulation of cardiac output
Most candidates approached this question by defining cardiac output as stroke volume × heart rate and then discussing the determinants of cardiac output - preload, contractility, afterload and heart rate rather than focusing on the regulation of cardiac output. Under preload a brief description of the Frank Starling mechanism was required. Important was the concept that at rest cardiac output is controlled almost entirely by peripheral factors that determine venous return. These concepts were best illustrated by graphing vascular function (venous return vs right atrial pressure) and cardiac function (cardiac output vs right atrial pressure) curves. Then demonstrating on these curves the factors that affected preload, contractility and afterload such as changes in blood volume, sympathetic and parasympathetic stimulation and exercise as examples. Also important to demonstrate on these curves was the fact that venous return and cardiac output are equal at steady state. Most candidates tried to illustrate these cardiovascular concepts with a series of left ventricular pressure volume loops rather than use the vascular and cardiac function curves. They then went on to demonstrate via these pressure volume loops the effects of changes in preload, contractility and afterload on stroke volume. Candidates who took this approach were not penalised, if there were clear, correct diagrams with explanations indicating comprehension of these concepts. On the whole graphs were poorly drawn and were not well integrated into the answer. Some candidates also wasted time by unnecessarily describing excitation-contraction coupling and sympathetic nerve reflex pathways.
examiners comments 2011 august r
- Cardiac output, at a steady state, is determined by venous return.
- This relationship is described by the X which intersect at the point which describes the resting steady state, where cardiac output and venous return are X
- Cardiac output, at a steady state, is determined by venous return.
- This relationship is described by the cardiac and vascular function curves, which intersect at the point which describes the resting steady state, where cardiac output and venous return are equal.
deranged 2011 august Q13
- The cardiac function curve is cardiac output as a function of X
o This curve describes the Frank-Starling relationship
As contractility increases, the curve shifts up
o A plateau is seen with higher RA pressures
- The cardiac function curve is cardiac output as a function of right atrial pressure.
o This curve describes the Frank-Starling relationship
As contractility increases, the curve shifts up
o A plateau is seen with higher RA pressures
note: remember y is a function of x, y depends on X (independent)
deranged 2011 august Q13
- The vascular function curve is venous return as a function of x
o Crosses the x-axis at the x
o A plateau is seen with right atrial pressure below x - Changes to the operating conditions of the cardiovascular system can change the position of this equilibrium point in a predictable manner:
o An increase in preload (volume, x) x cardiac output, up to a maximum (plateau) permitted by x and heart rate, and is associated with an increase in the right atrial pressure
- The vascular function curve is venous return as a function of right atrial pressure.
o Crosses the x-axis at the mean systemic filling pressure
o A plateau is seen with right atrial pressure below 0 mmHg. - Changes to the operating conditions of the cardiovascular system can change the position of this equilibrium point in a predictable manner:
o An increase in preload (volume, MSFP) increases cardiac output, up to a maximum (plateau) permitted by contractility and heart rate, and is associated with an increase in the right atrial
deranged 2011 august Q13
what describes
1 cardiac output as a function of right atrial pressure.
2venous return as a function of right atrial pressure.
- The cardiac function curve is cardiac output as a function of right atrial pressure.
- The vascular function curve is venous return as a function of right atrial pressure.
deranged 2011 august Q13
o An increase in contractility increases the cardiac output at any given volume/MSFP, and is associated with a x in right atrial pressure
o An increase in contractility increases the cardiac output at any given volume/MSFP, and is associated with a decrease in right atrial pressure
deranged 2011 august Q13
o An increase in peripheral vascular resistance sequesters blood in the arterial circulation, x the venous return and x cardiac output
o An increase in peripheral vascular resistance sequesters blood in the arterial circulation, decreases the venous return and decreases cardiac output
deranged 2011 august Q13
Capillaries contain X to allow the movement of fluid and solutes.
* it is normally impermeable to large protein
* Plasma ultrafiltrate is filtered by bulk flow through the capillary wall by the action of opposing hydrostatic and oncotic pressures
Capillaries contain semipermeable membranes to allow the movement of fluid and solutes.
* it is normally impermeable to large protein
* Plasma ultrafiltrate is filtered by bulk flow through the capillary wall by the action of opposing hydrostatic and oncotic pressures
2018 august 16 cicm wrecks
- Fluid exchange across capillary membranes depends on a balance between X
- This balance can be expressed as the X
- Fluid exchange across capillary membranes depends on a balance between hydrostatic and oncotic pressure gradients in the capillary lumen and the interstitial fluid.
- This balance can be expressed as the Starling equation:
2018 august 16 deranged
Forumula for Starling equation:
Starling equation:
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
- Pc - Pi is the capillary-interstitial hydrostatic pressure gradient
o Pc, capillary hydrostatic pressure is usually:
32 mmHg at the arteriolar end of the cpaillary
15 mm Hg at the venular end
Affected by gravity (eg. posture) and blood pressure
o Pi, interstitial hydrostatic pressure is usually:
negative (-5-0 mmHg) in most tissues (except for encapsulated organs)
Affected by anything that modifies lymphatic drainage, eg. tourniquet or immobility - Πc - Πi is the capillary-interstitial oncotic pressure gradient
o Πc, capillary oncotic pressure = 25mmHg
o Πi, interstitial oncotic pressure = 5 mmHg - Lp S is the permeability coefficient of the capillary surface, and is affected by shear stress and endothelial dysfunction.
o It is a product of the hydrolic permability coefficient (Lp) and surface area of the capillaries (S) - σ is the reflection coefficient for protein permeability and is a dimensionless number which is specific for each membrane and protein
o σ = 0 means the membrane is maximally permeable
o σ = 1 means the membrane is totally impermeable
o In the muscles, σ for total body protein is high (0.9)
o In the intestine and lung, σ is low (0.5-0.7)
2018 august 16 deranged
What is Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi
starling equation
2018 august 16 deranged
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
- Pc value
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
- Pc - Pi is the capillary-interstitial hydrostatic pressure gradient
o Pc, capillary hydrostatic pressure is usually:
32 mmHg at the arteriolar end of the cpaillary
15 mm Hg at the venular end
2018 august 16 deranged
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
value of
o Pi
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
- Pc - Pi is the capillary-interstitial hydrostatic pressure gradient
o Pc, capillary hydrostatic pressure is usually:
32 mmHg at the arteriolar end of the cpaillary
15 mm Hg at the venular end
Affected by gravity (eg. posture) and blood pressure
o Pi, interstitial hydrostatic pressure is usually:
negative (-5-0 mmHg) in most tissues (except for encapsulated organs)
Affected by anything that modifies lymphatic drainage, eg. tourniquet or immobility
2018 august 16 deranged
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
whats the value of Πc
- Πc - Πi is the capillary-interstitial oncotic pressure gradient
o Πc, capillary oncotic pressure = 25mmHg
o Πi, interstitial oncotic pressure = 5 mmHg
2018 august 16 deranged
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
what is value of Πi
- Πc - Πi is the capillary-interstitial oncotic pressure gradient
o Πc, capillary oncotic pressure = 25mmHg
o Πi, interstitial oncotic pressure = 5 mmHg
2018 august 16 deranged
Jv = Lp S [ (Pc - Pi) - σ (Πc - Πi) ]; where
what is the value of σ
- σ is the reflection coefficient for protein permeability and is a dimensionless number which is specific for each membrane and protein
o σ = 0 means the membrane is maximally permeable
o σ = 1 means the membrane is totally impermeable
o In the muscles, σ for total body protein is high (0.9)
o In the intestine and lung, σ is low (0.5-0.7)
2018 august 16 deranged
examiners comments for Describe the forces that result in fluid exchange across capillary membranes.
The expected answer included a clear explanation of Starling’s forces, including an understanding of the importance of the relative difference along the length of the capillary, with approximate values and examples of factors that influence them. Some explanation of what contributed to the hydrostatic or osmotic pressure gained more marks than merely stating there was a pressure. Several candidates digressed to Fick’s law of diffusion or intracellular flow of ions which was not directly relevant to capillary flow
2018 august 16 deranged
DEfine Central venous pressire (CVP)
Central venous pressire (CVP) is the venous blood pressure measured at or near the right atrium.
2021 march 5 cicmwrecks
Central venous pressire (CVP) is the venous blood pressure measured at or near the right atrium.
-deranged 2021 march 5
What does CVP equate to In the absence of tricuspid stenosis
In the absence of tricuspid stenosis, equals right ventricular end-diastolic pressure
2021 march 5 cicmwrecks
normal CVP value
Normal 0-6mmHg in spontaneously breathing non-ventilated patient
2021 march 5 cicmwrecks
tell me an equation that CVP is in
- Venous Return, VR = (MSFP – RAP or CVP) / Resistance to venous return
note: its Right atrial pressure
2021 march 5 deranged
- CVP increased in disorders that X Rt sided diastolic pressures
o left heart disease, lung disease, primary pulmonary hypertension, and pulmonic stenosis
CVP is a major determinant of RV filling pressure (RV Preload)
o This regulates stroke volume through Frank-Starling mechanism
* CVP increased in disorders that increase Rt sided diastolic pressures
o left heart disease, lung disease, primary pulmonary hypertension, and pulmonic stenosis
2021 march 5 deranged
How is CVP measured?
-It is measured using a pressure transducer connected to a central line via incompressible tubing, with the transducer zeroed to atmospheric pressure and levelled at the height of the right atrium.
-The measurement is performed at end-expiration
2021 march 5 deranged
Graphically what represents CVP
Physiologically, it is defined as the intersection of the vascular function curve and the cardiac output curve
2021 march 5 deranged
Factors which determine CVP:
- Measurement technique:
- Central venous blood volume
- Tricuspid valve competence
o Central venous vascular compliance - Cardiac rhythm
- Compartment pressures in the thorax and abdomen.
2021 march 5 deranged
How do Measurement technique: effects CVP
- Measurement technique:
o Transducer position
o Timing of measurement with the respiratory cycle (ideally, the end-expiratory CVP is the only ‘true” CVP)
2021 march 5 deranged
How does Central venous blood volume effects CVP:
- Central venous blood volume
o decrease in cardiac output (e.g. due to either decreased stroke volume or heart rate) will cause an increase in CVP
o Mean systemic filling pressure increases, so the CVP increases
o Vena cava compression (Obesity/Valsalva/pregnancy/inc IAbd pressure – dec VR → dec CVP
o Central venous vascular compliance
o inc Comp → inc return and venous pressure)
o Vascular tone
o Right ventricular compliance
o Myocardial disease
o Pericardial disease
o Tamponade
2021 march 5 deranged
note; decrease in cardiac output increases central venous blood volume
how does “Central venous vascular compliance” affect CVP
o inc Comp → inc return and venous pressure)
o Vascular tone
o Right ventricular compliance
o Myocardial disease
o Pericardial disease
o Tamponade
2021 march 5 deranged
How do Tricuspid valve competence effects CVP
- Tricuspid valve competence
o Stenosis (inc mean CVP)
o Regurgitation (transient inc CVP)
2021 march 5 deranged
How do Cardiac rhythm effects CVP
- Cardiac rhythm
o increase CVP when RA contracting against closed TV (Asynchronous atrial contraction (eg. during ventricular pacing)
o The absence of atrial contraction decreases the CVP (eg. in atrial fibrillation or junctional rhythm)
2021 march 5 deranged
just read, stuff that effects CVP
examiner comment
This question examined a core area of cardiac physiology and measurement. Considering this, candidates overall, scored poorly in this section. There was a common misunderstanding around the relationship between cardiac output and CVP. A decrease in cardiac output (e.g. due to either decreased stroke volume or heart rate) will cause an increase in CVP as blood backs up in the venous circulation, increasing venous volume as less blood moves through to the arterial circulation; the resultant increase in thoracic volume increases central venous pressure. Several candidates confused the direction of their arrows, for example “increased right atrial compliance increases CVP”. Double negatives were used by several candidates which then resulted in the incorrect relationship described. (e.g., “arrow down compliance and arrow down CVP”). The measurement section should have included an explanation of the components of an invasive pressure monitoring system relevant to the measurement of CVP.
2021 march 5 aminer comment , but above specifically 2019-2-Q6
key points
decrease in cardiac output increases CVP
don’t do double negatives, so just avoid it all together and make the first variable always increase
what is the relationship between compliance and CVP
define contractility
- Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume) - from Pappano & Weir (p.78 of the 10th edition)
2012 aug 4 deranged
Physiological Determinents of Contractility
- Physiological determinants of contractility include:
o Preload:
o Afterload (the Anrep effect):
o Heart rate (the Bowditch effect): - Contractility is also dependent on:
o Myocyte intracellular calcium concentration
o Temperature
2012 aug 4 deranged
Measures of contractility include:
- Measures of contractility include:
o ESPVR, which describes the maximal pressure that can be developed by the ventricle at any given LV volume. The ESPVR slope increases with increased contractility.
o dP/dT (or ΔP/ΔT), change in pressure per unit time. Specifically, in this setting, it is the maximum rate of change in left ventricular pressure during the period of isovolumetric contraction. This parameter is dependent on preload, but is minimally affected by normal afterload.
2012 aug 4 deranged
Physiological determinants of contractility include:
- Physiological determinants of contractility include:
o Preload:
Increasing preload increases the force of contraction
The rate of increase in force of contraction per any given change in preload increases with higher contractility
This is expressed as a change in the slope of the end-systolic pressure volume relationship (ESPVR)
o Afterload (the Anrep effect):
The increased afterload causes an increased end-systolic volume
This increases the sarcomere stretch
That leads to an increase in the force of contraction
o Heart rate (the Bowditch effect):
With higher hear rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
2012 aug 4 deranged
- Contractility is also dependent on:
- Contractility is also dependent on:
o Myocyte intracellular calcium concentration
Catecholamines: increase the intracellular calcium concentration by a cAMP-mediated mechanism, acting on slow voltage-gated calcium channels
ATP availability (eg. ischaemia): as calcium sequestration in the sarcolemma is an ATP-dependent process
Extracellular calcium- availability of which is necessary for contraction
o Temperature: hypothermia decreases contractility, which is linked to the temperature dependence of myosin ATPase and the decreased affinity of catecholamine receptors for their ligands.
2012 aug 4 deranged
just read
examiners comments
Define myocardial contractility and briefly describe dP/dT, the end systolic pressure volume (ESPV) relationship and the ejection fraction (EF).]
Contractility represents the performance of the heart at a given preload and afterload. It is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume). All indices of myocardial contractility are dependent on preload or afterload to a varying degree. The dP/dT is the maximum rate of change in left ventricular pressure during isovolumetric contraction, after mitral valve closes and before the aortic valve opens. It is preload dependant and afterload independent. A diagram of a pressurevolume loop is very helpful when describing the ESPV. Absence of a diagram (correctly labelled and scaled) was a weakness in many answers. Candidates were then expected to at least explain that, as preload is increased a new pressure volume loop is generated. Each new PV loop has a new end systolic point that is at a slightly higher pressure and volume than the previous end systolic point. The line connecting the end-systolic points is called the linear ESPVR. The slope of the ESPVR or Emax is used as an index of myocardial contractility. Ejection fraction is the percentage of the ventricular end diastolic volume (EDV) which is ejected with each stroke volume (SV). Ejection fraction = stroke volume/end diastolic volume X 100 (Normal range 55 to 70%). Only a minority of candidates achieved the depth of knowledge required for a Level 1 topic.
2012 aug 4 examiners comments
Describe the changes to cardiovascular physiology in a healthy elderly person.
what are the 3 major categories?
CVS effects of ageing can be divided into cardiac, vascular, and autonomic changes:
2012 march 9 cicmwrecks
Describe the changes to cardiovascular physiology in a healthy elderly person.
what are the cardiac changes?
- Cardiac changes
o Decreased receptor density and number (→ decreased catecholamine sensitivity)
o Decreased maximum heart rate Due to fibrosis of the SA node causing reduced pacemaker cell number and funtion, and reduction in catecholamine receptor density. ▪ Maximum heart rate ≈ 220 − Age
o Decreased inotropy
Minor.
o Increased reliance on atrial kick Reduced ventricular compliance increases the reliance on atrial kick to achieve adequate preload.
o Decreased diastolic compliance and hence ventricular filling ▪ Due to hypertrophy from increased afterload
o Decreased maximum EF during exercise (due to increased afterload and reduced compliance) o Decrease in diastolic compliance and hence ventricular filling (particularly the early phase of diastole which is reduced by 50% of its capacity at younger ages)
o Accumulation of pigment in the myocytes
o Decrease in the number of functioning myocytes (possibly due to age related reduction in capillary density and ischaemic injury) and concentric hypertrophy of existing myocytes (due to increased workload of remaining cells)
o Increase in relaxation time due to reduced reuptake of Ca by the sarcoplasmic reticulum (ie, prolongation of the cardiac cycle)
Describe the changes to cardiovascular physiology in a healthy elderly person.
what are the vascular changes
- Vascular changes
o Reduced compliance Due to loss of elastic tissue in the large arteries.
o Increased SVR / TPR due to age related increases in intimal thickness and vessel stiffness, and a decrease in arterial and venous compliance (less Windkessel effect or elastic reservoir)
o Reduced endothelial cell function (decreased NO release & bioavailability) Impairs the ability of the vascular tree to adapt to changes in pressure/volume leading to:
▪ Elevated SBP
▪ Reduced DBP
o Reduced elastic recoil causes diastolic run off and a fall in diastolic blood pressure.
o Reduced catecholamine receptor density Reduced responsiveness to (and increased number of) circulating catecholamines.
Describe the changes to cardiovascular physiology in a healthy elderly person.
what are the autonomic change?
- Autonomic
o Impaired autonomic function
Due to decreased catecholamine responsiveness.
o Impaired baroreceptor response due to decreased stretch in the carotid and aortic
bodies (less sensitivity)
o Decreased exercise tolerance
Reliance on preload to maintain cardiac output.
Describe the changes to cardiovascular physiology in a healthy elderly person.
What are the hemodynamic consequences
HAEMODYNAMIC CONSEQUENCES
* Increased pulse pressure and MAP
* Increased afterload due to raised MAP and aortic impedance (which may contribute to LV
hypertrophy)
Describe the changes to cardiovascular physiology in a healthy elderly person.
just read
examiners comments
2012 march Q9 examiner comment
. Describe the changes to cardiovascular physiology in a healthy elderly person. It is clearly stipulated in the syllabus that candidates would be expected to understand physiology as it applies at the extremes of age. In the past, questions have been asked relating to foetal and neonatal physiology as well as for the elderly. This question was poorly answered as candidates lacked a detailed and coherent knowledge of this topic. For a good answer candidates were expected to at least mention the effects on the heart, e.g. increases in size due to concentric ventricular hypertrophy (LVH), hypertrophy of myocytes but a decrease in the number of myocytes, cardiac output decreases, the increase in cardiac output in response to severe exertion is attenuated, ventricular filling is particularly dependent on diastolic relaxation which is impaired, greater contribution of atrial contraction, increase in left ventricular afterload, effects on vasculature, e.g. intima and media thickening result in less distensibility, effects on endothelial function, e.g. nitric oxide release is decreased, effects upon autonomic and integrated responses, e.g. decline in receptor numbers, down regulation of post-receptor signalling and decreased receptor density and impaired baroreceptor reflexes.
physiology of the Renin and Angiotensin system.
what is the stimulus?
- Stimulus: hypotension, hypovolemia, salt depletion, renal hypoperfusion
2011 aug6 deranged
physiology of the Renin and Angiotensin system.
what is the sensor?
- Sensor:
o arterial and renal baroreceptors
o β-1 receptors on the juxtaglomerular cells
2011 aug6 deranged
physiology of the Renin and Angiotensin system.
what is the afferent?
- Afferent: glossopharyngeal and vagus nerves, renal sensors (macula densa)
2011 aug6 deranged
physiology of the Renin and Angiotensin system.
what is the efferent?
- Efferent: enzymatic steps:
o Renin
37 kDa enzyme
Released from juxtaglomerular cells
Is the rate-limiting step
Cleaves angiotensiongen into angiotensin-I
o ACE
Pulmonary enzyme
Cleaves angiotensin-I into angiotensin-II
o Angiotensin-II
Increases Na+/H+ exchange in the proximal tubules, thus sodium retention and acid excretion
Increases sensation of thirst
Increases sensitivity to catecholamines
Stimulates the release of vasopressin
Stimulates the release of aldosterone
o Vasopressin and aldosterone
Produce more vasoconstriction as well as more salt and water retention
2011 aug6 deranged
physiology of the Renin and Angiotensin system.
what is the effector?
- Effectors:
o A2 receptors, adrenal glomerulosa, pituitary gland, renal tubule
2011 aug6 deranged
physiology of the Renin and Angiotensin system.
what Is the effect?
- Effect: vasoconstriction of peripheral circulation and the increase in body fluid volume
2011 aug6 deranged
examiner comment
just red
physiology of the Renin and Angiotensin system.
Describe the physiology of the Renin and Angiotensin system. Renin and angiotensin are core components in the regulation of plasma volume and blood pressure regulation. It is unfortunate that many candidates presenting to this examination are not able to provide sufficient information for a pass. For a good answer, candidates were expected to mention what renin and angiotensin are and what they do, as well as briefly mention the place of angiotensin converting enzyme (converts Angiotensin I to Angiotensin II and inactivates bradykinin). Renin is a proteolytic enzyme cleaves angiotensinogen to angiotensin I, secreted by the juxtaglomerular cells of the kidney which are located in media of afferent arteriole and in close proximity to the glomerulus and the distal convoluted tubule (macula densa). Angiotensin II acts on cell surface AT1 and AT2 receptors. Major functions being to preserve of GFR & enhanced Na/H2O reabsorption in the setting of reduced renal blood flow (candidates expected to outline the mechanism by which this occurs), vasoconstriction, stimulate aldosterone secretion and increase thirst and ADH secretion. The better candidates also mentioned that it decreases sensitivity of baroreceptor reflex, increases secretion of ACTH and facilitates noradrenaline release from sympathetic nervous system as well as its fate (metabolized by blood/tissue peptidases). A good response for regulation would have been mentioning principally regulated via renin release (which in itself is influenced by renal sympathetic nervous system activity, intrarenal baroreceptors and macula densa sodium chloride delivery, ADH and intra-renal prostaglandins), negative feedback from angiotensin II.
Outline the physiology of, and factors which regulate levels of angiotensin
- Properties of angiotensin-II:
- Properties of angiotensin-II:
o Octapeptide hormone
o Potent vasoconstrictor
o Bindins to Gq protein-coupled receptors on vascular smooth muscle facilitating an IP3- mediated increase in intracellular calcium levels, and therefore vasoconstriction
o Multiple other effects:
Stimulates the release of aldosterone
Stimulates the release of vasopressin
Increases sensitivity to catecholamines
Increases sensation of thirst
Increases Na+/H+ exchange in the proximal tubules, thus sodium retention and acid excretion
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Outline the physiology of, and factors which regulate levels of angiotensin
Biosynthesis of angiotensin-II:
- Biosynthesis of angiotensin-II:
o Requires the release of renin
o Renin
37 kDa enzyme
Released from juxtaglomerular cells
Is the rate-limiting step
Cleaves angiotensiongen into angiotensin-I
o ACE
Pulmonary enzyme
Cleaves angiotensin-I into angiotensin-II
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just read
2009 sept Q18 Outline the physiology of, and factors which regulate levels of angiotensin.
For a good answer it was expected that candidates would mention the relationship of angiotensinogen, angiotensin I, renin and Angiotensin Converting Enzyme to angiotensin II production, the actions and fate of angiotensin II and factors that regulate angiotensin II. It was expected that candidates mention angiotensin acts as a potent vasoconstrictor, stimulates aldosterone secretion, facilitates noradrenaline release, preferentially vasoconstricts Efferent arteriole in nephron, preserving GFR in low perfusion states, increases renal tubular Na + reabsorption and increases secretion of vasopressin and ACTH. Regulation of Angiotensin could be separated into factors increasing angiotensin levels (eg prostaglandins, low K+ levels, Sympathetic stimulation, decreased Na+ delivery at distal tubule, any factor contributing to reduced renal blood flow (eg hyovolaemia, cardiac failure, renal artery stenosis) and factors reducing angiotensin levels (eg hypervolaemia, afferent arteriolar dilatation and vasopressin). Syllabus - N1 (h), C2b (f) Reference: Textbook of medical Physiology, Guyton, Chp 26, Goodman and Gillman, Chp 30
Definition of a portal circulation:
Definition of a portal circulation:
* An arrangement by which blood collected from one set of capillaries passes through a large vessel or vessels, to another set of capillaries before returning to the systemic circulation.
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5 components of a portal system
- A portal circulation has five structural components:
o Feeding artery
o Primary capillary bed
o Portal vessel
o Secondary capillary bed
o Draining vein
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Anatomy of Hepatic portal system
Hepatic
Feeding artery: SMA, IMA, coeliac trunk
Primary capillary bed: intestinal capillaries
Portal vessel: the portal vein
Secondary capillary bed: hepatic sinusoids
Draining vein: hepatic veins
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the function of the hepatic portal system
Function
Portal blood undergoes metabolic and immune modifications in the hepatic sinusoid, which allow for the biotranformation of drugs or metabolic substrates and the clearance of pathogens.
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anatomy of the pituitary portal system
Pituitary Feeding artery: superior and inferior hypophyseal arteries
Primary capillary beds:
* hypothalamic capillaries
* posterior pituitary capillaries
Portal vessel: the long portal vessels and short portal vessels
Secondary capillary bed: capillaries of the anterior pituitary
Draining vein: hypophyseal veins, which variably drain into the cavernous sinuses
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the function of the pituitary portal system
To efficiently present hypothalamic regulatory hormones to the pituitary gland in high concentration (rather than releasing them into the systemic circulation)
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the anatomy of the renal portal system
Feeding artery: afferent arteriole
Primary capillary bed: glomerular capillaries
Portal vessel: efferent arterioles
Secondary capillary beds:
* Peritubular capillaries
* Vasa recta
Draining vein: Renal vein
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the function of the renal portal system
To reclaim solutes from the glomerular ultrafiltrate fluid.
To deliver solutes fr active excretion by the proximal tubule
To maintain concentration gradients in the renal medulla, (to reabsorb water).
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just read examiners comments of
2011 august Q9
Describe the anatomy and function of three portal systems in the body. A portal system is an arrangement by which blood collected from one set of capillaries passes through a large vessel or vessels, to another set of capillaries before returning to the systemic circulation. The three portal systems are the - 1) system of blood vessels that link the hypothalamus and the anterior pituitary in the brain, which allows endocrine communication between the two structures. 2) within the liver, whereby venous blood from the GI tract drains into the superior and inferior mesenteric veins; these two vessels are then joined by the splenic vein to form the portal vein which enters the liver, drains into the hepatic sinusoids and then eventually into the hepatic veins which join the inferior vena cava, with the purpose of defending against by breaking down and metabolising most of what has been absorbed from the gastrointestinal tract (including an immunoprotective action). 3) within the kidney, whereby blood from the afferent arterioles enters the glomerulus (first capillary network), followed by the efferent arterioles, then the peritubular network (second capillary network) and eventually the venous system, with the purpose of stronger re-absorptive capacity for water from within long Loops of Henle that go deep within the renal medulla.
Factors which Affect the Function of the Right Ventricle
Heart rate
- The cardiac output of both the RV and the LV are affected by the heart rate in the same way
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Factors which Affect the Function of the Right Ventricle
Stroke volume
- On average, though there might be beat-to-beat variations, the stroke volume both the ventricles is the same.
- The RV stroke volume is affected by:
o RV afterload
o RV preload
o RV contractility
o Interventricular interdependence
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Factors which Affect the Function of the Right Ventricle
Afterload
- RV afterload is affected by:
o Thin wall of the RV: (increases afterload)
o Positive intrathoracic pressure (increases afterload)
o Increased pulmonary vascular resistance increases afterload:
Low lung volumes
Low pulmonary blood flow
Hypoxic pulmonary vasoconstriction
Systemic catecholamines and an activated sympathetic nervous system
Increased blood viscosity (raised haematocrit)
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Factors which Affect the Function of the Right Ventricle
Preload
- RV preload is affected by:
o Right atrial pressure
o mean systemic filling pressure
Total venous blood volume
Venous vascular compliance
o Pericardial compliance and pericardial contents
o Positive intrathoracic pressure (decreases preload) - Ventricular wall compliance:
o Duration of ventricular diastole
o Wall thickness
o Relaxation (lusitropic) properties of the muscle
o End-systolic volume of the ventricle (i.e. afterload)
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Factors which Affect the Function of the Right Ventricle
Contractility
For both ventricles, contractility is affected by:
* Heart rate (Bowditch effect)
* Afterload (Anrep effect)
* Preload (Frank-Starling mechanism)
as well as cellular and extracellular calcium concentrations and temperature
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Factors which Affect the Function of the Right Ventricle
Effect of ventricular interdependence
- The compliance of the right ventricle is decreased in systole by the contraction of the interventricular septum
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Factors which Affect the Function of the Right Ventricle
just read examiner comment
An approach that covered the main determinants of right ventricular cardiac output including heart rate, right ventricular preload, contractility, afterload and the relationship with left ventricular output, ventricular interdependence, and the respiratory system would have provided the framework for a good answer. Some candidates used this approach but described more features of left ventricular than right ventricular output. The observation that the right ventricle is relatively thin walled and its output is very sensitive to changes in right ventricular preload and afterload particularly was central to this question. The unique shape of the right ventricle and its contraction characteristics involving ventricular interdependence were rarely mentioned. Also details on right ventricular afterload and the importance of factors affecting pulmonary vascular resistance were lacking in most answers. Syllabus: C1c Recommended sources: Review of Medical Physiology, Ganong, Chps 31 and 33, Textbook of Medical Physiology, Guyton & Hall Chp 9 and 20
Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
The SA node fires well into late X, and this is not represented on the surface ECG, nor is the propagation of signal along the internodal tracts.
The SA node fires well into late diastole, and this is not represented on the surface ECG, nor is the propagation of signal along the internodal tracts.
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Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
The P wave is produced as the X depolarises. The X contracts first.
At the end of the P wave, the X finally contracts. The end of diastole occurs during the X
The P wave is produced as the atrial muscle depolarises. The right atrium contracts first.
At the end of the P wave, the left atrium finally contracts. The end of diastole occurs during the PR interval.
2011 march Q13
Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
The X is generated by ventricular depolarisation, and its peak corresponds to the beginning of X (specifically, of X).
The R wave is generated by ventricular depolarisation, and its peak corresponds to the beginning of systole (specifically, of isovolumetric contraction).
2011 march Q13 deranged
Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
The X represents ventricular repolarisation, and corresponds to the phase of x contraction (slow ejection). The X of the X correlates reasonably well with the onset of diastole, i.e the closure of the a X
The T-wave represents ventricular repolarisation, and corresponds to the phase of decreased contraction (slow ejection). The peak of the T-wave correlates reasonably well with the onset of diastole, i.e the closure of the aortic valve.
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Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
Effects of digoxin on the ECG:
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Effects of digoxin on the ECG:
Rate: decreased (vagal tone increase)
P wave: unchanged
PR interval: increased (slowed AV nodal conduction)
QRS complex: unchanged
QT interval: Shortened
ST segment: Downsloping “sagging” ST depression
T waves: flattened, biphasic, inverted (“reverse tick”)
Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
Effects of amiodarone on the ECG
Effects of amiodarone on the ECG
Rate: decreased (β-blocker effect)
P wave: unchanged
PR interval: increased (slowed AV nodal conduction)
QRS complex: unchanged
QT interval: Prolonged
ST segment: Unchanged
T waves: flattened, biphasic, inverted (“reverse tick”)
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examiners comments, just read
Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks).
Candidates were expected to provide sufficient detail in answers. Extra marks were awarded for diagrams relating the ECG accurately to pressure events during the cardiac cycle. Time intervals, units of measurement and clear labels were essential for diagrams. Mechanisms pertaining to ion flux and ion channels needed to be specifically explained. Discussion of mechanisms needed to be accurate and relevant to the effect on the ECG. For example, better answers noted that AV conduction was depressed by Digoxin, predominantly due to an increase in Vagal tone Syllabus: Cib2c C2c2b Recommended sources: Principles of Physiology for the Anaesthetist, Power and Kam, pages 107-110, Pharmacology and Physiology in Anaesthetic Practice, Stoelting
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and below 2009 march Q1
College Answer
The first part of the question is best answered by a labelled and annotated diagram of the ECG with the pressure events of the cardiac cycle. Common errors included mistiming of the ECG with the pressure waveform. The second part of the question could be answered in a tabular format such as:
Interval Drug Mechanism
PR Digoxin Increases refractory period
of AV node probably by
increased vagal activity
QRS
Tricyclic antidepressants
Quinidine like effect,
decreasing sodium influx
into cells
What drugs effect PR
PR
β-blockers Increase refractory period of AV node by decreasing sympathetic stimulus
Digoxin Increases refractory period
of AV node probably by increased vagal activity
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What part of the ECG do beta blockers exert their effect
PR
β-blockers Increase refractory period of AV node by decreasing sympathetic stimulus
Digoxin Increases refractory period
of AV node probably by increased vagal activity
2009 march Q1 deranged
What part of the ECG does digoxin exert their effect
PR
β-blockers Increase refractory period of AV node by decreasing sympathetic stimulus
Digoxin Increases refractory period
of AV node probably by increased vagal activity
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What drugs effect QRS
QRS
Flecainide, lignocaine, phenytoin, tricyclic antidepressants
Blockade of the fast voltage-gated sodium channels; slowed Phase 0 with a diminished magnitude
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how do Flecainide, lignocaine, phenytoin, tricyclic antidepressants work?
QRS
Flecainide, lignocaine, phenytoin, tricyclic antidepressants
Blockade of the fast voltage-gated sodium channels; slowed Phase 0 with a diminished magnitude
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What drugs effect prolong QT
QT
Amiodarone, sotalol
Prolonged Phase 3 by acting as potassium channel antagonists
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how do Amiodarone, sotalol work?
QT
Amiodarone, sotalol
Prolonged Phase 3 by acting as potassium channel antagonists
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2 major effects of 1L blood loss
This results in autonomic and neurohormonal effects:
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The autonomic effects of 1L blood loss
- Autonomic effects
o Arterial hypotension causes baroreflex activation.
o Decreased cardiac output causes chemoreceptor activation.
o Both reflexes result in autonomic phenomena:
Decreased vagal stimulus; thus increased heart rate
Sympathetic activation, which has multiple effects:
Increased peripheral vascular resistance
Redistribution of blood flow away from the cutaneous and splanchnic circulation
Stimulation of systemic catecholamine release from adrenal glands, which produces an increased systemic effect in addition to the peripheral sympathetic nervous system effects
Stimulation of vasopressin release via the projections from the nucleus of the solitary tract to the hypothalamus
Stimulation of renin release by sympathetic stimulation of the juxtaglomerular cells, and due to lower renal perfusion
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The neurohormonal effects of 1L blood loss
- Neurohormonal effects
o Renin secretion causes:
Vasoconstriction (by angiotensin)
Increased sodium retention (by aldosterone)
o Vasopressin release causes:
Vasoconstriction (by V1 receptors)
Increased water retention (by V2 receptors)
o Venous hypotension decreases atrial natriuretic peptide secretion,
which causes:
Decreased renal blood flow
Decreased urinary water and sodium excretion
o The net effect is decreased urine output and increased retention of sodium and water
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When discussuing 1L blood loss, what is the effect of the rate of blood loss
- Effect of the rate of blood loss
o A more rapid rate of blood loss places increased stress on the cardiovascular system to maintain haemodynamic homeostasis
o Healthy individuals will be better able to compensate for more rapid rates of blood loss by increasing their heart rate and cardiac contractility
o Patients with compromised cardiac function (eg. ischaemic heart disease or heart failure) will have impaired compensatory mechanisms and will not be able to compensate for even relatively slow blood loss
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- Staging of blood loss is in terms of % of circulating volume lost:
- Staging of blood loss is in terms of % of circulating volume lost:
o Four classes (ATLS): <15% of volume, 15–30%, 30–40% and > 40%
o Loss of 1000ml of blood (20% of the total circulating volume) in a 70kg subject represents most of the stressed volume.
o Loss of 2000ml of blood = 40% of the circulating volume = severe haemorrhagic shock
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3 major categories physiological consequences of blood loss
- Hypovolemia and cardiovascular compensation
- Transcapillary fluid redistribution and isovolaemic anaemia
- Renal fluid/electrolyte conservation and haemopoiesis
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3 major categories physiological consequences of blood loss
* Hypovolemia and cardiovascular compensation
- Hypovolemia and cardiovascular compensation
o Baroreflex activation and chemoreceptor activation.
o Decreased vagal stimulus; thus increased heart rate
o Sympathetic activation, which has multiple effects:
Increased peripheral vascular resistanc
Redistribution of blood flow away from the cutaneous and splanchnic circulation
Stimulation of systemic catecholamine release from adrenal glands, which produces an increased systemic effect in addition to the peripheral sympathetic nervous system effecs
Stimulation of vasopressin release via the projections from the nucleus of the solitary tract to the hypothalamus
Stimulation of renin release by sympathetic stimulation of the juxtaglomerular cells, and due to lower renal perfusion
3 major categories physiological consequences of blood loss
* Transcapillary fluid redistribution and isovolaemic anaemia
- Transcapillary fluid redistribution and isovolaemic anaemia
o Vasoconstriction of arterioles results in reduced capillary hydrostatic pressure
o This results in a change in the Starling relationship in the microcirculation
o The result is a movement of free water out of the interstitial space and into the intravascular space
o This dilutes the blood volume and decreases the haematocrit, decreasing the haemoglobin concentration of the blood, but restoring some of the circulating volume
3 major categories physiological consequences of blood loss
* Renal fluid/electrolyte conservation and haemopoiesis
- Renal fluid/electrolyte conservation and haemopoiesis
o Renin secretion causes:
Vasoconstriction (by angiotensin)
Increased sodium retention (by aldosterone)
o Vasopressin release causes:
Vasoconstriction (by V1 receptors)
Increased water retention (by V2 receptors)
o Venous hypotension decreases atrial natriuretic peptide secretion,
which causes:
Decreased renal blood flow
Decreased urinary water and sodium excretion
o The net effect is decreased urine output and increased retention of sodium and water
o Erythropoiesis is stimulated by EPO release from the kidney, stimulated by decreased oxygen delivery
examiners commens for blood loss question
just read
2010 march , 2009 august 2008 march
2010 march Describe the cardiovascular changes that occur following the loss of 1000ml of blood in an adul
College Answer
A structured approach that included mentioning that 1000mls of blood was
substantial – being approximately 20% of the blood volume of a 70 kg person was
required for a good answer. Candidates were expected to also include changes in
systolic and diastolic blood pressure, pulse pressure, heart rate, cardiac output and
the neuronal (eg sympathetic nervous system response on the various circulations)
and hormonal responses (eg rennin aldosterone, Anti-Diuretic Hormone,
catecholamines, etc). Candidates were also expected to discuss differences in
responses according to rate of blood loss. Flow diagram could have been used to
illustrate some of these concepts.
2009 august Describe the physiological consequences and responses after an acute haemorrhage of 2.0 litres in a healthy 70kg adult if there is no immediate fluid
To adequately answer this question, candidates must be able to demonstrate that they recognised this to be a major haemorrhage. When a weight and a volume are supplied it is expected the percentage blood loss would be calculated and the shock graded or the haemorrhage at least described as severe. Often the consequences were omitted. Consequences were best described in organ systems e.g. CV, renal, metabolic. Many candidates failed to mention the patient would be hypotensive and tachycardic.
A good answer should include mention, and provide explanations, of the mechanisms for the following compensatory responses: * Activation of both baroreceptors and chemoreceptors and their consequences * The sympathetic nervous system response * Fluid shifts * Renal effects - most candidates mentioned the urine output would be decreased but did not provide a mechanism for this Endocrine effects, eg secretion and actions of ADH, ACTH/Cortisol
2008 march Describe the hormonal response to hypovolaemia following the acute loss of one litre of blood in an adult. Include changes that occur in the first 24 hours following the blood loss
Candidates were expected to know the different hormonal responses to hypovolaemia The possible approach to this question can be either by explaining the hormonal response in terms of time sequence or by different hormonal systems. Good answers to this question included how different hormonal responses are activated and mediated.
The common omissions were secretion of erythropoietin within 24 hours of haemorrhage, role of macula densa and juxtaglomercular apparatus, interactions between baroreceptors and sympathetic nervous system with the secretion of ADH, cortisol, glucagon and catecholamines.
Classify the commonly used inotropic agents and describe their mechanism of action.
Direct and Indirect sympathomimetics
Phosphodiesterase inhibitors
Calcium sensitisers
Cardiac glycosides
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Classify the commonly used inotropic agents and describe their mechanism of action.
Direct and Indirect sympathomimetics
Direct sympathomimetics
Endogenous
Adrenaline
Noradrenaline
Dopamine
Synthetic
Dobutamine
Bind to beta-1 receptors
Activate G-protein coupled adenylyl cyclase
Increase cAMP production
This leads to increased calcium availability inside the cardiac myocytes, and therefore increased contractility and pacemaker automaticity
Indirect sympathomimetics
Ephedrine
Act as “false neurotransmitters”; displace catecholamines from presynaptic storage vesicles
The resulting catecholamine release produces direct catecholamine effects
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Classify the commonly used inotropic agents and describe their mechanism of action.
Phosphodiesterase inhibitors
Phosphodiesterase inhibitors
Milrinone
Inamrinone
Enoximone
Inhibit phosphodiesterase 3, which is responsible for cAMP catabolism.
Thus, increases cyclic AMP
Thus, increases calcium availability by increased voltage
Selective for vascular smooth muscle and cardiac muscle.
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Classify the commonly used inotropic agents and describe their mechanism of action.
Calcium sensitisers
Calcium sensitisers
Levosimendan
Pimobendan
Bind to troponin C and stabilise its open state
This allows muscle contraction.
Thus increased trop C / calcium complex stability increases contractility.
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Classify the commonly used inotropic agents and describe their mechanism of action.
Cardiac glycosides
Cardiac glycosides
Digoxin
Inhibits Na+/K+ ATPase
Thus, increases intracellular sodium
This increases sodium-calcium exchange by the Na+/Ca2+ exchanger (INCX) during Phase 1 of the cardiac action potential.
The resulting increase in intracellular calcium promotes inotropy.
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Classify the commonly used inotropic agents and describe their mechanism of action.
examiners comments
just read
2014
This question was generally well answered. The poorer answers suffered for want of a useful
classification system that enabled them to separate the various drug classes.
2010
This question required a classification based on chemical structure and class action.
Sympathomimetics, phosphodiesterase inhibitors, calcium sensitizers and cardiac
glycosides should have been mentioned. Additional detail was expected,
subdividing Sympathomimetics into catecholamines (naturally occurring and
synthetic), and non-catecholamines (direct and indirect acting). Further classification
based on peripheral vasomotor action demonstrated greater understanding
Better answers included diagrams illustrating the mechanism and point of action on
the cardiac myocyte. Discussion of receptors, second messengers, and the role of
calcium was essential.
The question was aimed at “commonly used” agents, although some marks were
awarded for discussion of calcium, glucagon and other rarely used drugs.
Insufficient detail regarding mechanisms of action was a common observation.
2008
Candidates could use a number of different classifications, however, were required to include all of the major groups of agents. Most made some mention of the sympathomimetic, however failed to sub-classify these, or confused catecols versus non-catecols, or naturally occurring versus synthetic agents. Other agents, such as phosphodiesterase inhibitors, calcium sensitisers, cardiac glycosides, or calcium itself received minimal attention. Mechanisms of action required more than listing adrenergic receptor types. Some listing or discussion of the sub-cellular mechanisms was necessary. Comment about intracellular calcium being the final common end-point would have scored additional marks
Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
what is the MoA
Mechanism of action
The RAAS is a major system involved in the medium-term regulation of blood pressure and blood volume.
Many of these regulatory effects are mediated by the activity of angiotensin-II on the AT1 receptor
ACE inhibitors block the conversion of angiotensin I into angiotensin II by ACE
ARBs block the binding of angiotensin II to its AT1 receptor
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Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
3 major catecogoies?
Antihypertensive (afterload-reducing) effects:
Preload-reducing effects
Long term non-antihypertensive effects
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Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
Antihypertensive (afterload-reducing) effects:
Antihypertensive (afterload-reducing) effects:
Decreased catecholamine sensitivity
Decreased vasopressin release
Thus, decreased systemic vascular resistance
Thus, decreased afterload and myocardial oxygen demand
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Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
Preload-reducing effects
Preload-reducing effects:
Decreased vasopressin release
Decreased aldosterone release
Decreased Na+/H+ exchange in the proximal tubules
Thus increased sodium excretion and decreased water retention
Thus, potentiated effects of diuretics and decreased preload
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Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
Long term non-antihypertensive effects
Long term non-antihypertensive effects:
By restraining the degradation of angiotensin 1:
Anti-inflammatory effect on vascular smooth muscle
Anti-fibroproliferative effect on vascular smooth muscle
Thus, decreased hyperplasia of vascular smooth muscle
Thus, reduced rate of atheroscleoris
By reduced degradation of bradykinin:
Reduced proliferation of vascular endothelium
Reduced
Anti-inflammatory effects:
Decreased upregulation of inflammatory receptors (VCAM-1, ICAM-1, P-selectin) and downregulation of inflammatory mediator transcription
Thus, reduced endothelial inflammation
Decreased cardiac myocyte hypertrophy (indirectly, by suppression of aldosterone secretion)
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Outline the pathophysiological basis for the use of angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) in congestive cardiac failure.
examiner comment just read
The renin-angiotensin system plays a central role in the pathophysiology of heart failure. Thus this question required integration of knowledge of the renin-angiotensin system and how pharmacological agents affect it in the treatment of cardiac failure. Candidates were expected to describe the pathway and the influence of these drug groups on cardiac failure and to recognise underlying basic physiological principles such as the interaction between AT1 and AT2 receptors along with awareness of production of Ang II by ACE-independent enzymes.
A good answer was expected to contain the following points: Angiotensinogen is cleaved by kidney-derived renin to form the decapeptide angiotensin I (Ang I); ACE converts Ang I to Ang II; Ang II is a potent arterial vasoconstrictor and an important mediator of Na + and water retention through its effects on glomerular filtration pressure and aldosterone secretion; Ang II potentiates neural catecholamine release, is a secretagogue for catecholamine release from the adrenal medulla, promotes vascular hyperplasia and pathologic myocardial hypertrophy.
ACE inhibitors suppress Ang II and aldosterone production, decrease sympathetic nervous system activity, and potentiate the effects of diuretics in heart failure. ACE is identical to kininase II, which degrades bradykinin and other kinins that stimulate production of NO, cyclic GMP, and vasoactive eicosanoids; these vasodilator substances seem to oppose the effects of Ang II on the growth of vascular smooth muscle and cardiac fibroblasts and on production of extracellular matrix. Thus, the increased levels of bradykinin that result from ACE inhibition may play a role in the hemodynamic and anti-remodeling effects of ACE inhibitors.
An alternative means of attenuating the haemodynamic and vascular impact of the reninangiotensin system is through inhibition of angiotensin receptors. Most of the known clinical actions of angiotensin II are mediated through the AT1 angiotensin receptor. AT1 receptor antagonists may provide more potent reduction of the effects of angiotensin II than do ACE inhibitors
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Myocardial oxygen consumption equation
- Myocardial oxygen consumption is:
o Calculated as (coronary blood flow × arteriovenous O2 difference)
o Expressed as the oxygen extraction ratio (which is usually 75%, i.e. high)
o The implication of this is that the myocardium cannot achieve an increase in oxygen delivery by increasing the extraction ratio, and instead needs to increase blood flow to meet increasing demand.
deranged 2007 august Q19
- Myocardial oxygen consumption is determined by:
- Myocardial oxygen consumption is determined by:
o Heart rate is the main determinant
o Preload is a minor contributor (decreases during tachycardia)
o Contractility is a major contributor (may increase during tachycardia)
o Afterload is a major contributor:
(may increase in tachycardia if it is accompanied by other autonomic phenomena
o Cost of electrical conduction: thought to be a minimal contributor, but this will also increase during tachycardia
o Basal cost of cardiac metabolism, and the factors which affect it, which are:
Temperature (which may increase cardiac oxygen consumption if it is associated with an increased heart rate, eg. when the patient is febrile)
Drugs, some of which may cause tachycardia as well as an alteration in cardiac metabolism
o Thus, overall, the effect of tachycardia is to increase myocardial oxygen demand, and the most important determinant is the heart rate
2007 august Q19 deranged
- Myocardial oxygen supply is determined by:
- Myocardial oxygen supply is determined by:
o Oxygen content of the blood, which is not affected by tachycardia in a normal individual
o Coronary blood flow, which is determined by:
1Coronary perfusion pressure: difference between aortic and ventricular pressure
This is higher in the right ventricle than in the left;
i.e. right coronary perfusion pressure will be greater because the right ventricular chamber pressure is lower
2Coronary vascular resistance, which is affected by:
Metabolic autoregulatory activity eg. in reponse to ischaemia and hypoxia
Autonomic control eg. sympathetic vasoconstriction
Systolic compression: compression by contracting LV
Pharmacological agents: eg. GTN and dipyridamole
2007 august Q19 deranged
Describe the effects of a tachycardia on myocardial oxygen supply and demand in a normal heart.
2007 august Q19
examiner comment just read
The main points expected were the determinants of myocardial oxygen supply. These include arterial oxygen content and coronary blood flow. Coronary blood flow depends on coronary perfusion pressure and coronary vascular resistance and that most left coronary blood flow occurs in diastole. Tachycardia reduces diastolic time and hence left coronary blood flow. In comparison blood flow in the right coronary artery is continuous both in systole and diastole and is little affected by heart rate. A correctly labelled diagram of left and right coronary blood flow attracted extra marks. Unfortunately most diagrams were inaccurate, not labelled and had no units on the axes. Systolic compression particularly reduces blood supply to the left ventricular subendocardium which is most susceptible to ischaemia. Extra marks were given for describing metabolic autoregulation, the high oxygen extraction, explaining that
oxygen supply cannot be increased by increasing oxygen extraction in the coronary
circulation and describing the driving pressure differences in both coronary arteries in
systole and diastole.
A description of the determinants of myocardial oxygen demand was also required (e.g. left ventricular, preload, contractility, afterload and tachycardia This part of the question was particularly poorly answered.
Describe the effects of a tachycardia on myocardial oxygen supply and demand in a normal heart.
2007 august Q19
exmainer comment
normal values for cardiac output
- 5L/min (for 70kg adult)
- 2.5 to 4 L/min/m2 (indexed to body surface area)
2021 august Q3 deranged
The 5 major determinants of cardiac output are
The determinants of cardiac output are:
Heart rate
Stroke volume
Preload
Afterload
Cardiac contractility
2021 august Q3 deranged
The 5 major determinants of cardiac output are
describe heart rate and stroke volume
- Heart rate
o A higher heart rate increases cardiac output as it multiplies by stroke volume
o An excessively high heart rate decreases cardiac output by decreasing preload - Stroke volume, which is in turn determined by preload, afterload and contractility
2021 august Q3 deranged
The 5 major determinants of cardiac output are
describe preload
- Preload
o Increased preload leads to an increase in the stroke volume
o Preload is determined by:
Intrathoracic pressure
Atrial contribution (“atrial kick”)
Central venous pressure (RA pressure)
Mean systemic filling pressure which depends on total venous blood volume and venous vascular compliance
Compliance of the ventricle and pericardium
Duration of ventricular diastole
End-systolic volume of the ventricle
2021 august Q3 deranged
The 5 major determinants of cardiac output are
describe afterload
- Afterload
o Ventricular radius (End-diastolic volume)
o Ventricular wall thickness
o Ventricular transmural pressure
Intrathoracic pressure
Ventricular cavity pressure
Ventricular outflow impedance and aortic input impedance
Arterial resistance
-Vessel radius
-Blood viscosity
-Length of the arterial tree
-Inertia of the blood column
-Influence of reflected pressure waves
-Arterial compliance
2021 august Q3 deranged
The 5 major determinants of cardiac output are
describe contractility
- Cardiac contractility:
o Increased contractility improves stroke volume at any given preload or afterload value
o Affected by:
Heart rate (Bowditch effect)
Afterload (Anrep effect)
Preload (Frank-Starling mechanism)
Cellular and extracellular calcium concentrations
Temperature
2021 august Q3 deranged
Discuss the physiological determinants of cardiac output.
2021 august Q3 deranged
examiner comment
just read
Although the pass rate for this question was reasonably high the examiners commented on a lack of detailed knowledge within most answers for such a core component of our daily practice. Several candidates failed to provide a normal value and only few provided anything other than 5l/min.
There was a general lack of detail, and at times, some confusion about the Frank Starling effect. Most candidates outlined the major determinants of stroke volume, although many were light on the determinants of each or incorporated incorrect facts. Several candidates did not mention HR as a determinant of CO.
Describe the factors that affect mixed venous oxygen saturation.
What is mixed venous blood?
- Mixed venous blood is:
o sampled from the pulmonary artery
o mixed in the right ventricle out of multiple venous sources
o representative of the oxygen extraction for the entire body
Describe the factors that affect mixed venous oxygen saturation.
2021 august 13 deranged
Describe the factors that affect mixed venous oxygen saturation.
what are the 3 major categories
o Factors that influence the affinity of haemoglobin for oxygen:
o Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
o Pathological abnormalities of the arterial-venous blood flow
Describe the factors that affect mixed venous oxygen saturation.
2021 august 13
Describe the factors that affect mixed venous oxygen saturation.
what are the 3 major categories
Describe Factors that influence the affinity of haemoglobin for oxygen:
o Factors that influence the affinity of haemoglobin for oxygen:
The partial pressure of O2 in mixed venous blood
The partial pressure of CO2 in mixed venous blood
-Increasing CO2 shifts the curve to the right
pH of mixed venous blood, independent of CO2
-Decreasing pH (acidosis) shifts the curve to the right
The concentration of 2,3-DPG inside the erythrocytes
-Increased 2,3-DPG (eg. in response to hypoxia or erythropoietin) shifts the curve to the right
The presence of unusual haemoglobin species
-Methaemoglobin, carboxyhaemoglobin and foetal haemoglobin shift the curve to the left; sulfhaemoglobin shifts the curve to the right
Temperature
-Hyperthermia shifts the curve right
Describe the factors that affect mixed venous oxygen saturation.
2021 august 13
Describe the factors that affect mixed venous oxygen saturation.
what are the 3 major categories
o Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
-Arterial oxygen content: decreased arterial oxygenation will produce a decreased SvO2
-VO2, the oxygen consumption rate: decreased VO2 will produce an increased SvO2. Factors which influce VO2 include:
-Factors which influence metabolic rate, eg. hypothermia, hyperthermia,
paralysis, anaesthesia
-Factors which influence oxygen utilisation, eg. mitochondrial toxins,
microvascular shunting in sepsis
-Cardiac output: a decreased cardiac output will produce a reduced SvO2
Describe the factors that affect mixed venous oxygen saturation.
2021 august 13
Describe the factors that affect mixed venous oxygen saturation.
what are the 3 major categories
-Pathological abnormalities of the arterial-venous blood flow
Pathological abnormalities of the arterial-venous blood flow
Left to right shunts
Describe the factors that affect mixed venous oxygen saturation.
2021 august 13
Describe the factors that affect mixed venous oxygen saturation
2021 aug examiners comments
just read
Describe the factors that affect mixed venous oxygen saturation
2021 aug examiners comments
Mixed venous oxygen saturation is used as a surrogate marker for the overall balance between oxygen delivery and oxygen consumption. A good answer stated this, described the importance of where it is measured and went on to describe the various factors that affect oxygen delivery and consumption. Descriptions of the factors that affect oxygen saturation of haemoglobin, partial pressure of oxygen in the blood and position of oxygen-haemoglobin dissociation curve were necessary to score well. Important omissions were factors that increased and decreased oxygen consumption. While many candidates were able to correctly write the equations for oxygen content and oxygen flux, they then failed to describe how the variables within these equations were related to mixed venous oxygen saturation.
Synthesis of angiotensin-II?
- Angiotensinogen is a large protein produced by the liver
- Renin is a soluble protease synthesised by the juxtaglomerular cells of the renal cortex
- Renin cleaves angiotensiongen into angiotensin-I (an inert decapeptide) and des(AngI)AGT, a large byproduct protein
- Angiotensin-I is cleaved by ACE, producing Angiotensin-II (an active octapeptide)
2021 august Write detailed notes on angiotensin, including its synthesis, role within the body and regulation. deranged
Physiological role of angiotensin
- Angiotensin-II binds to Gq-protein coupled receptors on many tissues, producing its physiological effects via an IP3-mediated change in intracellular calcium
- Physiological effects include:
o Stimulating the release of vasopressin
o Stimulating the release of aldosterone
o Increased Na+/H+ exchange in the proximal tubules
o Increased sensation of thirst
o Increased sensitivity to catecholamines - Angiotensin-II has a 30 second half life,
2021 august Write detailed notes on angiotensin, including its synthesis, role within the body and regulation. deranged
Net effects of angiotensin-II release
- Increased sodium retention
- Increased acid excretion
- Increased water intake and retention
- Peripheral vasoconstriction
2021 august Write detailed notes on angiotensin, including its synthesis, role within the body and regulation. deranged
Regulation of angiotensin
- Regulated by the release of renin, which is stimulated by:
o Systemic hypotension:
Afferent: baroreceptors
Efferent: sympethic nervous system
o Renal hypoperfusion, sensed and responded to by juxtaglomerular cells
o Salt depletion
Afferent: macula densa
Efferent: juxtaglomerular cells - Also downregulated by:
o ANP secretion (promotes natriuresis rather than sodium retention)
o endothelin (increases blood pressure)
o angiotensin II (negative feedback mechanism)
o Increased blood flow to the juxtaglomerular cells
2021 august Write detailed notes on angiotensin, including its synthesis, role within the body and regulation. deranged
What is the Resting potential between Ventricular Myocyte and Pacemaker cells?
Ventricular Myocyte -90 mV
Pacemaker cell -60 mV
2020aug Describe and compare the action potentials from cardiac ventricular muscle cells and the sino-atrial node
What is the threshold potential between Ventricular Myocyte and Pacemaker cells?
Ventricular Myocyte -70 mV
Pacemaker cell -40 mV
2020aug Describe and compare the action potentials from cardiac ventricular muscle cells and the sino-atrial node
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 4 * Resting potential
* Stable plateau
* Maintained by the Ik1 inward rectifying potassium current
Phase 0 * Rapid depolarisation
* Mediated by fast voltage-gated sodium channels
Phase 1 * Rapid repolarisation
* Mediated by transient outward potassium currents (Ito) and the
Phase 2 * Prolonged plateau at ~ 0mV
* Lasts ~ 100-200 msec
* Mediated by L-type calcium channels
Phase 3 * Rapid repolarisation
* Mediated by the Ikr, Iks and Ik1 potassium currents
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 4
Phase 4 * Resting potential
* Stable plateau
* Maintained by the Ik1 inward rectifying potassium currents
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 0
Phase 0 * Rapid depolarisation
* Mediated by fast voltage-gated sodium channels
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 1
Phase 1 * Rapid repolarisation
* Mediated by transient outward potassium currents (Ito) and the
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 2
Phase 2 * Prolonged plateau at ~ 0mV
* Lasts ~ 100-200 msec
* Mediated by L-type calcium channels
Ionic Events During the Cardiac Action Potentials of the Ventricular Myocyte
Phase 3
Phase 3 * Rapid repolarisation
* Mediated by the Ikr, Iks and Ik1 potassium currents
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 4 ** Slow depolarisation
* Maintained by the If inward rectifying potassium current
Phase 0* Slow depolarisation
* Mediated by L-type calcium channels
Phase 1* No Phase 1 in the pacemaker action potential
Phase 2* No real Phase 2 in the pacemaker action potential
Phase 3* More gradual repolarisation
* Mediated by the Ikr, Iks and Ik1 potassium currents
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 4
Phase 4 ** Slow depolarisation
* Maintained by the If inward rectifying potassium current
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 0*
Phase 0* Slow depolarisation
* Mediated by L-type calcium channels
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 1*
Phase 1* No Phase 1 in the pacemaker action potential
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 2
Phase 2* No real Phase 2 in the pacemaker action potential
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
Phase 3*
Phase 3* More gradual repolarisation
* Mediated by the Ikr, Iks and Ik1 potassium currents
Examiner comments
Ionic Events During the Cardiac Action Potentials of the Pacemaker Cell
2020 aug
This question details an aspect of cardiac physiology which is well described in multiple texts. Comprehensive answers included both a detailed description of each action potential and a comparison highlighting and explaining any pertinent differences. The question lends itself to well-drawn, appropriately labelled diagrams and further explanations expressed in a tabular form. Better answers included a comparison table with points of comparison such as the relevant RMP, threshold value, overshoot value, duration, conduction velocity, automaticity, ion movements for each phase (including the direction of movement) providing a useful structure to the table. Incorrect numbering of the phases (0 – 4) and incorrect values for essential information (such as resting membrane potential) detracted from some responses.
2017 – aug
This topic was well understood and answered by most candidates. Some candidates had a good knowledge base but missed out on potential marks by failing to compare and contrast. A diagram outlining the various phases was a useful way to approach the question.
2016 - aug
A good answer included a well labelled sketch with a description of ion channels and relative directional flow. When using sketches in an answer they should be correctly labelled, and when used as a comparison with another sketch, the differences should be clear e.g. shape, duration and voltage difference.
2013 march
A fundamental aspect of cardiac physiology, that overall was well answered. The majority of candidates used figures to good effect. Candidates are reminded that all figures must be 7 correctly labelled (e.g. X and Y axis, phases of action potential, etc.). Common omissions were those that reflected an adequate depth of knowledge (e.g. some of the current flows).
2010 aug - Describe the ionic events associated with a ventricular cardiac action potential (80% of marks). Outline how the action potential relates with the mechanical events of the cardiac cycle (20% Marks).
describe Excitation – contraction coupling
2010 aug - Describe the ionic events associated with a ventricular cardiac action potential (80% of marks). Outline how the action potential relates with the mechanical events of the cardiac cycle (20% Marks).
Excitation – contraction coupling
* Inward calcium current during Phase 2 activates calcium-gated calcium channels on the sarcoplasmic reticulum
* This produces the release of calcium from the sarcoplasmic reticulum
* Free calcium binds to troponin-C/troponin I regulatory complex, which exposes the active sites of actin and myosin to each other
* This produces the “ratcheting” movement between the myosin heads and the actin, which continues as long as intracellular calcium remains available.
Relationship of the action potential to the mechanical events in the ventricle
They asked for a PV loop. Though the college felt this SAQ was “best answered using a ventricular pressure-volume loop and overlaying the phases of the ventricular action potential”, no such loop exists anywhere in the literature, and what is offered here is a total confabulation. Moreover, one is puzzled as to how this is supposed to be better than simply plotting the ventricular pressure and volume over time, together with the action potential.
2010 aug - Describe the ionic events associated with a ventricular cardiac action potential (80% of marks). Outline how the action potential relates with the mechanical events of the cardiac cycle (20% Marks).
examiner comments
To achieve a good pass in this question, candidates needed to outline the ionic events associated with Phase 0 to phase 4 of the ventricular action potential followed by a description of excitation – contraction coupling. The second part of the question was best answered using a ventricular pressure-volume loop and overlaying the phases of the ventricular action potential. Description of the ionic events associated with the action potential phases was generally well done, but this was as far as many answers went in answering this question. Few candidates included a description of excitation-contraction coupling in there answer and few candidates considered an answer to the second part of the question. The use of illustrations helped answer this question. Syllabus: C1b References: Guyton and Hall Textbook of Medical Physiology, Chp 9
examiner comments 2010 aug -
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
- The response to exercise consists of:
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
- The response to exercise consists of:
o Regional muscle vasodilation
o Increase in cardiac output
o Central coordination of these response
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
o Regional muscle vasodilation
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
- Regional mucle vasodilation
o Increased muscle activity results in increased oxygen demand
o This increased demand is met by increasing blood flow to exercising muscle
o The increase in blood flow is mediated mainly by a regional decrease in vascular resistance
o The mechanisms for this vasodilation are:
Vasoactive substrates and products of muscle metabolism, eg. CO2, lactate, hydrogen peroxide and potassium ions
Vasoactive mediators released by the endothelium, eg. nitric oxide (NO), ATP, adenosine, prostaglandins
β-2 adrenoceptor activation
o There is also corresponding vasoconstriction of other vascular beds, redirecting blood flow away from viscera and skin
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
o Increase in cardiac output
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
- Increase in cardiac output
o Cardiac aoutput can increase massively during exercise, up to 30L/min
o The increase in cardiac output is due to both an increase in heart rate and in stroke volume
o With increasing workload, the heart rate continues to increase but stroke volume decreases because of diminishing diastolic time
o As the result the cardiac output plateaus at near-maximal workload
o Central venous pressure and PCWP also increase - Changes in haemodynamic parameters
o Systolic blood pressure and MAP increase with increasing workload
o Diastolic blood pressure decreases
o The pulse pressure widens
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
o Central coordination of these response
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
- Central coordination of cardiovascular responses to exercise
o Afferents:
Increased muscle activity is sensed by stretch receptors and chemoreceptors in the muscle tissue
Decreased peripheral vascular resistance, translating into decreased blood pressure, is sensed by the baroreflex
The central nervous system itself can generate the afferent signals for exercise-related cardiovascular responses in anticipation of effort
o Central processing:
The motor cortex can unilaterally activate the autonomic response to exercise in the absence of afferent stimuli, and in anticipation of exercise
o Efferents:
Vagus nerve - which increases the heart rate
Sympathic nervous system which:
Increases the cardiac contractility
Releases catecholamines from the adrenal gland
Adjusts organ perfusion to redistribute more blood flow to the skeletal muscle
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
examiners comments
Examiner Comments: 22% of candidates passed this question. This is an applied physiology question. Better answers categorised the changes in some manner and included a measure of the degree of change as applicable (e.g., what increases, what decreases and what may stay the same). The question was to describe the changes so that the detail behind the mechanisms enabling these changes to occur was expected (e.g., neurohumoral, local factors). Marks were also awarded for any regional variation that occurs
2020-2-11 Describe the changes in the circulatory system that occur during exercise.
2016 march Describe the cardiovascular effects of a sudden increase in afterload
afterload can be approximated by
It can be approximated by the
2016 march Describe the cardiovascular effects of a sudden increase in afterload
It can be approximated by the La Place Equation:
T = PR/H
T approximates afterload
P = Aortic pressure
R = Ventricular radius
H = Ventricular wall thickness
note; with aortic pressure, I think of it as the pressure that LV has to push against
note; in afterload
its defined slightly different 2020 august very similar to 2012 feb, 2009 feb
o P, the ventricular transmural pressure, which is the difference between the intrathoracic pressure and the ventricular cavity pressure.
2016 march Describe the cardiovascular effects of a sudden increase in afterload
what is the definition of afterload
Note; but this is one of the examiners comments; Afterload can be defined as factors resisting ventricular ejection and contributing to myocardial wall stress during systole (2012 march)
2016 march Describe the cardiovascular effects of a sudden increase in afterload
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Cardiac output
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Cardiac output
Ideally, remains stable if all the compensatory reflexes work as they are supposed to.
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Heart rate
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Heart rate Ideally, remains stable. Or:
* Decreases, if this increase in afterload is associated with increased carotid pressure
* Increases, if the increase in afterload is associated with decreased cardiac output and lower blood pressure
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Stroke volume
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Stroke volume Decreases; because of:
* Increase in diastolic pressure (earlier closure of the aortic valve)
* Increased end-systolic volume
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Preload
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Preload Increases, because of:
* End-systolic volume and pressure increase
* This results in an increase in the end-diastolic volume
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Contractility
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Contractility
Increases, because of the acute increase in preload (as above)
* Thus, Frank-Starling mechanism causes an increase in contractility (this is the basis of the Anrep effect).
* As a result, stroke volume increases slightly, retuning it closer to normal (unless the ventricle is failing)
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Myocardial oxygen consumption
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Myocardial oxygen consumption
* Increases because of: increased intraventricular pressure
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Coronary blood flow
2016 march Describe the cardiovascular effects of a sudden increase in afterload
Coronary blood flow
* Should remain stable because of coronary blood flow autoregulation
2016 march Describe the cardiovascular effects of a sudden increase in afterload
examiners comments
2016 march Describe the cardiovascular effects of a sudden increase in afterload
examiners comments
13.Describe the cardiovascular effects of a sudden increase in afterload.
21% of candidates passed this question.
It was expected the answer would start with a definition of afterload and then proceeded to indicate what effects this increase in afterload would have on ventricular end-systolic pressure, ventricular end-diastolic pressure, left atrial pressure, cardiac output, myocardial oxygen demand and myocardial work, coronary blood flow and systemic blood pressure. Most candidates who failed to pass this question submitted answers that were just too brief, only including a small subset of the material required. Very few candidates included any mention of myocardial oxygen demand or myocardial work or the impact upon the cardiac output. A number of candidates included a detailed description of the Sympathetic Nervous System and the Renin-Angiotensin system, material which was not asked for. There were quite a number of incorrect perceptions about what effect a sudden increase in afterload would have on the systemic blood pressure. Candidates who mentioned the baroreceptor response and the stretch receptor response where rewarded with additional credit.
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
- Afterload can be defined as the resistance to ventricular ejection - the “load” that the heart must eject blood against. It consists of two main sets of determinant factors:
????
- Afterload can be defined as the resistance to ventricular ejection - the “load” that the heart must eject blood against. It consists of two main sets of determinant factors:
o Myocardial wall stress
o Input impedance
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
It consists of two main sets of determinant factors:
o Myocardial wall stress
o Input impedance
* Wall stress is described by the ????????
It consists of two main sets of determinant factors:
o Myocardial wall stress
o Input impedance
* Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
o P, ???
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
o P, the ventricular transmural pressure, which is the difference between the intrathoracic pressure and the ventricular cavity pressure.
Increased transmural pressure (negative intrathoracic pressure) increases afterload
Decreased transmural pressure (eg. positive pressure ventilation) decreases afterload
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
o r, ???
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
oo r, the radius of the ventricle
Increased LV diameter increases wall stress at any LV pressure
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
oo T,????
- Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
o T, the thickness of the ventricular wall
A thicker wall decreases wall stress by distributing it among a larger number of working sarcomeres
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
It consists of two main sets of determinant factors:
o Myocardial wall stress
o Input impedance
- Input impedance describes ventricular cavity pressure during systole and receives contributions from: ??????????
- Input impedance describes ventricular cavity pressure during systole and receives contributions from:
o Arterial compliance
Aortic compliance influences the resistance to early ventricular systole (a stiff aorta increases afterload)
Peripheral compliance influences the speed of reflected pulse pressure waves (stiff peripheral vessels increase afterload)
o Inertia of the blood column
o Ventricular outflow tract resistance (increases afterload in HOCM and AS)
o Arterial resistance (note; mention that this is systemic vascular resistance and define it)
Length of the arterial tree (the longer the vessels, the greater the resistance)
Blood viscosity (the higher the viscosity, the greater the resistance)
Vessel radius (the smaller the radius, the greater the resistance)
afterload
2020 august very similar to 2012 feb, 2009 feb
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
Examiners comments
2020
18.Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks).
53% of candidates passed this question.
Afterload can be defined as factors resisting ventricular ejection and contributing to myocardial wall stress during systole. Most answers utilised the law of Laplace to expand upon factors affecting ventricular wall tension. Systemic vascular resistance was commonly mentioned, but less frequently defined. Aortic and left ventricular outflow tract impedance were commonly referred to. Effects of preload and neurohumoral stimuli were less well outlined. Description of factors affecting right ventricular afterload and depictions of left ventricular pressure volume loops earned no extra marks unless directly referenced to the question.
2012 march
17. Define afterload and describe the physiological factors that may affect afterload. Definitions for afterload vary slightly amongst common physiology textbooks, and candidates were expected to mention any one commonly accepted definition. Essentially afterload is the resistance to ventricular ejection - the “load” that the heart must eject blood against and is related to ventricular wall stress (Law of Laplace, T=Pt.r/u). Candidates were expected to mention aortic valve and systemic vascular resistance, aortic impedance, blood viscosity, intathoracic pressure and relationship of ventricular radius and volume. Candidates generally did well, but few substantially good answers, with a lack of detail being the biggest limiting factor. 6 (60%) of candidates passed
2009 march
7. Define afterload (10% of mark). Describe the factors that can affect left ventricular afterload (90% of mark).
Many definitions of afterload were accepted. The main factors affecting left ventricular afterload are systemic vascular resistance, aortic impedance and ventricular radius. Other factors include blood viscosity and positive intrathoracic pressure. Good answers expanded on the points above. Candidates who failed this question did not have enough facts. Syllabus C1c C2c Reference: Bray 4 th edition p 342-344 and p 360-361
Define afterload (10% marks) and describe the physiological factors that may affect afterload on the left ventricle (90% marks)
Examiners comments
Describe the factors that determine right and left ventricular afterload
Afterload overall
Afterload overall The left ventricle has a much higher afterload than the right, mainly because of the increased arterial vascular resistance in the systemic circulation
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Transmural pressure
Transmural pressure Increased transmural pressure increases afterload in both ventricles.
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Intrathoracic pressure
Intrathoracic pressure
Positive intrathoracic pressure increases RV afterload
Negative intrathoracic pressure decreases RV afterload
Positive intrathoracic pressure decreases LV afterload
Negative intrathoracic pressure increases LV afterload
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Radius of the ventricle
Radius of the ventricle Dilation of either ventricle will increase the wall stress
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Thickness of the wall
Thickness of the wall
RV wall is thin: this has the effect of increasing afterload
LV wall is thicker: this decreases afterload by sharing it among more sarcomeres
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Arterial compliance
Pulmonary circulation is highly compliant, which minimises RV afterload
Aortic compliance is usually good, as it is an elastic capacitance vessel - this decreases LV afterload
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Inertia of the blood
inertia of the column of blood affects both ventricles by increasing afterload early in systole and decreasing afterload in late systole
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Ventricular outflow tract resistance
Ventricular outflow tract resistance
Both ventricles normally have minimal outflow tract resistance
Pulmonary valve can become stenotic and the RVOT can become obstructed
Aortic valve stenosis and LVOT obstruction due to HOCM can occur
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Arterial resistance
Arterial resistance
Pulmonary arteries have very low resistance
Systemic arterial circulation has a much higher resistance, which makes the afterload of the LV much greater
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Blood viscosity
Blood viscosity
Blood viscosity affects the right ventricle more, because the pulmonary system has less shear stress
Blood viscosity affects the left ventricle less, because of the non-Neutonian behaviour of blood (with higher shear stress, its viscosity decreases)
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
Vessel radius
Vessel radius The radius of small vessels affects afterload equally for both ventricles
2014 august Describe the factors that determine right and left ventricular afterload
Describe the factors that determine right and left ventricular afterload
examiner comment
2014 aug
19. Describe the factors that determine right and left ventricular afterload.
31% of candidates passed this question.
This is a big question and required some structure to cover the material required. A Definition of afterload, factors specific to left ventricle, right ventricle and both were required. The question asked to describe and not merely list factors affecting afterload. Marks were not given for describing pathologies rather than physiological processes that affect afterload. Candidates seemed to lack depth and understanding on this topic
2014 august Describe the factors that determine right and left ventricular afterload
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using x
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
* (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
* The main determinants of resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where l = length of the vessel, η = viscosity of the blood and r = radius of the vessel
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
What are the variables
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
* (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
* The main determinants of resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where l = length of the vessel, η = viscosity of the blood and r = radius of the vessel
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
* (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
* The main determinants of resistance are the parameters of the ??
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
* (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
* The main determinants of resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where l = length of the vessel, η = viscosity of the blood and r = radius of the vessel
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Definition:
* Systemic vascular resistance is defined using Ohm’s Law, where R = ΔP/Q
* (R is the resistance, ΔP is the difference in pressure along the circulation, and Q is the blood flow rate)
* The main determinants of resistance are the parameters of the Hagen-Poiseuille equation,
what are the variables
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
- The main determinants of resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where l = length of the vessel, η = viscosity of the blood and r = radius of the vessel
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of ??
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
Systemic mechanisms include:
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
Systemic mechanisms include:
* Arterial baroreflex control (increased BP leads to a decrease in SVR)
o Aortic arch receptors are innervated by the aortic nerve, a branch of the vagus
o Carotid sinus receptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve
o Both synapse within the nucleus tractus solitarius
o Increased arterial wall stretch increases the firing frequency of these receptors
o Activation of these receptors leads to a decrease in sympathetic tone, which decreases both peripheral vascular resistance and the cardiac output
* Autonomic central control
o Sympathetic activity increase associated with pain, emotion, exercise, or other sympathetic stimulus gives rise to peripheral vasoconstriction
* Peripheral and central chemoreceptors (hypoxia leads to increased SVR)
* Pulmonary baroreceptors (hypoxia leads to increased SVR)
* Hormones (eg. vasopressin and angiotensin)
* Temperature (hypothermia leads to increased SVR)
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
Local/regional mechanisms include:
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
Control mechanisms of systemic vascular resistance consist of systemic and regional mechanisms.
Local/regional mechanisms include:
* Intrinsic myogenic regulation (in response to stretch)
* Metabolic regulation (in response to increased tissue demand)
* Flow- or shear-associated regulation (in response to increased local flow)
* Conducted vasomotor responses (propagating from neighbouring vascular sites)
* Local cooling (which leads to vasoconstriction first, and then to vasodilation again)
* Immunological modulation by inflammatory mediators
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
examiners comments
2020 march Q7 Describe the physiological control of systemic vascular resistance (SVR).
This question invited a detailed discussion of the physiological control mechanisms in health, not pathophysiology nor drug-mediated effects. The central and reflex control mechanisms that regulate SVR over time are distinct from the local determinants of SVR. There was often confusion between dependent and independent variables. Cardiac output is generally depended upon SVR, not vice versa, even though SVR can be mathematically calculated from CO and driving pressures. The question asked about systemic vascular resistance and did not require a discussion of individual organs except for a general understanding that local autoregulation versus central neurogenic control predominates in different tissues. Emotional state, temperature, pain and pulmonary reflexes were frequently omitted. Peripheral and central chemoreceptors and low-pressure baroreceptors were relevant to include along with high pressure baroreceptors.
Damping
What is natural frequency?
natural frequency of the system is the frequency it will oscillate freely (in the absence of sustained stimulus)
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
Damping
What is resonance
- Resonance is the amplification of signal when its frequency is close to the natural frequency of a system
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
Damping
What is damping
- Damping is the process of the system absorbing the energy (amplitude) of oscillations
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
Damping
What is optimal damping
Optimal damping:
* A damping coefficient of around 0.64-0.7.
Examiners comments optimal damping coefficient (0.677)
>1.0 is overdamped,
and <0.7 is underdamped,
* Maximises frequency response
* Minimises overshoot of oscillations
* Minimises phase and amplitude distortion
* Corresponds to 2-3 oscillations following an arterial line flush test
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
Damping
What is Critical damping:
Critical damping: a damping coefficient of 1.0
* The oscillator returns to the equilibrium position as quickly as possible, without oscillating, and passes it only once.
* Occurs when the damping coefficient is equal to the resonant frequency of the oscillator
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
Damping
the arterial pressure waveform is made up of many different x waves (as determined by x) with each x having a specific x (deranged: harmonics). Every system has its own x, or x. If its <x Hz, it falls within the range of frequencies present in the x and oscillations may produce a sine wave which is superimposed on the x. Some damping is inherent in any system and acts to slow down the rate of change of signal between the patient and pressure transducer. It may be caused by air bubbles or blood clots or occlusion. This reduces the deflection of the transducer diaphragm and hence the size of the waveform. 123 words
the arterial pressure waveform is made up of many different sine waves (as determined by Fourier Analysis) with each sine wave having a specific frequency (deranged: harmonics). Every system has its own natural oscillatory frequency, or resonant frequency. If its <40 Hz, it falls within the range of frequencies present in the blood pressure waveform and oscillations may produce a sine wave which is superimposed on the blood pressure wave form. Some damping is inherent in any system and acts to slow down the rate of change of signal between the patient and pressure transducer. It may be caused by air bubbles or blood clots or occlusion. This reduces the deflection of the transducer diaphragm and hence the size of the waveform. 123 words
damping
* Question 12 from the first paper of 2020
* Question 17 from the second paper of 2017
* Question 12 from the first paper of 2015
* Question 24 from the second paper of 2012
damping
examiner comments
- Question 12 from the first paper of 2020
12.Explain resonance and its significance and the effects of damping on invasive arterial blood pressure measurement. 23% of candidates passed this question. Many candidates gave detailed answers that involved the set up and components of the arterial line system that was not asked for in the question and did not attract marks. There was confusion around the correct use of the terms natural frequency, resonance frequency and harmonics – candidates that were able to describe these frequencies correctly went on to achieve a good mark – the graphs and discussion around optimal dampening, over and underdamped traces were often drawn poorly or without sufficient detail, and at times were not used within in the context of the answer. Descriptions of the clinical effect seen with over / under dampened traces on blood pressure was well described. - Question 17 from the second paper of 2017
17.Define and explain damping, resonance, critical damping and optimum damping. 25% of candidates passed this question. Concise definitions were required with a clear explanation of the underlying physical principles. The response time of the system, degree of overshoot, effect on amplitude, noise and ability to faithfully reproduce frequencies relative to the natural resonant frequency were important considerations. Many candidates interpreted the question as relating to arterial lines and a detailed discussion of the components and characteristics of an intra-arterial catheter and transducer system did not attract marks. - Question 12 from the first paper of 2015
Many candidates seemed to get some of the basic concepts but few were able to expand on simple concepts. It was expected that candidates could describe that the arterial pressure waveform is made up of many different sine waves (as determined by Fourier Analysis) with each sine wave having a specific frequency. Every system has its own natural oscillatory frequency, or resonant frequency. If this is less than 40 Hz, it falls within the range of frequencies present in the blood pressure waveform and oscillations may produce a sine wave which is superimposed on the blood pressure wave form. Some damping is inherent in any system and acts to slow down the rate of change of signal between the patient and pressure transducer. It may be caused by air bubbles or blood clots or occlusion. This reduces the deflection of the transducer diaphragm and hence the size of the waveform. The effect of damping on temporal response was rarely mentioned. Accurate graphical representations of invasive pressure traces are important. Many candidates provided poor drawings without axis, labels, reference to normal or discussion in text. - Question 24 from the second paper of 2012
- False it’s the first paper
Describe the potential causes, and effects, of resonance and damping on an invasive arterial blood pressure trace.
For a good answer candidates were expected to mention that the arterial pressure waveform is made up of many different sine waves (as determined by Fourier Analysis) with each sine wave having a specific frequency. Every system has its own natural oscillatory frequency, or resonant frequency. The pressure measuring system has a resonant frequency at which oscillations occur, and if this is less than 40 Hz, it falls within the range of frequencies present in the blood pressure waveform and oscillations may produce a sine wave which is superimposed on the blood pressure wave form. The resonant frequency can be increased by using a short, wide, stiff catheter. In respect to damping, some damping is inherent in any system and acts to slow down the rate of change of signal between the patient and pressure transducer. Mention of causes of damping and the optimal damping coefficient (0.677) were expected. An under-damped system is one whereby resonance occurs causing the signal to oscillate and overshoot (damping factor 1.0). Both resonance and damping can alter the measured systolic and diastolic values but the mean pressure is not affected
An under-damped system is one whereby resonance occurs causing the signal to oscillate and X (damping factor 1.0)
this seems important so repeating it here
An under-damped system is one whereby resonance occurs causing the signal to oscillate and overshoot (damping factor 1.0)
examiner comments
* Question 24 from the second paper of 2012
* False it’s the first paper
deranged Arterial line dynamic response testing
There should be at least one “bounce” oscillation.
There should be no more than two oscillations;
There should be a distinct dicrotic notch.
There should be at least one “bounce” oscillation. If the system does not oscillate, there is too much damping.
There should be no more than two oscillations; a system which oscillates too much is underdamped.
There should be a distinct dicrotic notch. The dicrotic notch is resolved from high-frequency waveforms, which are usually of low amplitude and therefore more susceptible to damping. If the arterial line is progressively becoming more and more damped, the dicrotic notch is the first feature to disappear.
Arterial line dynamic response testing deranged
deranged Arterial line dynamic response testing
The under-damped trace will X the systolic, and there will be X post-flush oscillations.
The MAP X
The under-damped trace will overestimate the systolic, and there will be many post-flush oscillations.
The MAP remains the same in spite of damping.
Arterial line dynamic response testing deranged
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Valves
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Thickness
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Mass
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Position in the chest
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Blood supply
An Anatomical Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
Shape Irregular; vaguely triangular Conical
Valves Tricuspid and pulmonic Mitral and aortic
Thickness Relatively thin: 2-5mm Three times thicker: 7-11mm
Mass ~ 26g ~90g
Position in the chest Right and anterior Left and posterior
Blood supply RCA and circumflex LAD and circumflex
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
End-diastolic volume
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
End-systolic volume
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
Stroke volume
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
Systolic pressure
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
Diastolic pressure
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
ESPVR (contractility)
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
EDPVR (elastance)
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
Ea (Afterload)
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
A Functional Comparison of the Right and Left Ventricle
Stroke work (PV loop area)
A Functional Comparison of the Right and Left Ventricle
Domain Right ventricle Left ventricle
End-diastolic volume Slightly higher than LV Slightly lower than RV
End-systolic volume Slightly higher than LV Slightly lower than RV
Stroke volume The same The same
Systolic pressure 25 mmHg 120 mmHg
Diastolic pressure 0 mmHg 3-8 mmHg
ESPVR (contractility) Lower Higher
EDPVR (elastance) Lower Higher
Ea (Afterload) Lower Higher
Stroke work (PV loop area) Lower Higher
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
Compare the structure, function and coronary circulation of the right and left ventricles.
Examiners comments
2019-2-16 – examiner comment
The question sought information on the structure (anatomy), function (physiology) and vascular supply of the right and left ventricles. Good answers provided detail in each section e.g. values for ventricular pressure rather than simply stating “high- and low-pressure systems”. Many marks may be gained by a simple anatomical description & labelled PV loop for each ventricle. Many candidates focused solely on the coronary circulation, to which only a proportion of the marks were allocated.
2019-2-16
Compare the structure, function and coronary circulation of the right and left ventricles.
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
Components of the measurement system:
Components of the measurement system:
* An intra-arterial catheter
o Kink-resistant, biologically inert, incompressible
o Accesses the arterial circulation and provides the interface between the arterial blood and the circuit fluid
* Fluid-filled tubing
o Produces the hydraulic coupling between the arterial circulation and the pressure transducer
o Access points to allow sampling
o Flush valve
* Fluid in the tubing
o Incompressible
o Usually, normal saline or
o Under pressure from the pressure bag to prevent blood refluxing into the line
* Counterpressure fluid bag
o Pneumatically pressurised to ~ 300mmHg to sufficiently counteract systemic arterial pressure
* Pressure transducer
o Wheatstone bridge piezoresistive transducer which converts pressure into a change of electrical current
* Signal conditioning and monitoring software
o Filters the raw signal from the transducer
o Converts it into a human-readable waveform
o Records the data in a storage medium for review
note; shouldn’t patient be there too/
Deranged
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
Information derived from from the measurements by the arterial line transducer:
Information derived from from the measurements by the arterial line transducer:
* Heart rate
* Systolic pressure
* Diastolic pressure (coronary filling)
* Mean arterial pressure (systemic perfusion)
* Pulse pressure (high in AR, low in cardiac tamponade or cardiogenic shock)
* Changes in amplitude associated with respiration (pulse pressure variation)
* Slope of anacrotic limb associated with aortic stenosis
Deranged
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
Information derived from the waveform shape:
Information derived from the waveform shape:
* Slope of anacrotic limb represents aortic valve and LVOT flow
* Slurred wave in AS
* Collapsing wave in AS
* Rapid systolic decline in LVOTO
* Bisferiens wave in HOCM
* Low dicrotic notch in states with poor peripheral resistance
* Position and quality of dicrotic notch as a reflection of the damping coefficient
note; shouldn’t rhythm be on there too?
Deranged
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
examiner comment
Most of the marks were allocated to the components of the measuring system (as detailed in the question), hence a level of detail was required. An explanation of how the various components work was required; e.g. hydraulic coupling and transducers. Some candidates forgot to include heart rate as a piece of information derived from the trace.
Deranged
2019 march -Q2 - Outline the components required to measure blood pressure from an intra-arterial catheter (75% of marks). What information (other than blood pressure) may be gained from an arterial line trace (25% of marks)?
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
Domain; Central venous vs Mixed venous
Site of sampling;
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Domain; Central venous vs Mixed venous
Site of sampling; SVC or right atrium vs Pulmonary artery
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
how to measure/
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
- Intermittent sampling:
o ABG: derivation of the SvO2 value from the PO2, pH and pCO2, using the oxygen-haemoglobin dissociation curve.
o Co-oximetry: relies on measuring the absoprtion of near-IR light by haemoglobin species, and the use of the Beer-Lambert law to calculate the concentrations of oxyhaemoglobin and deoxyhaemoglobin
.
* Continuous monitoring:
o Reflectance spectrophotometry: relies on measuing the reflected wavelengths of near-IR light, and calculating the concentrations of oxyhaemoglobin and deoxyhaemoglobin from the log ratio of the signal strength (as each Hb species reflects a different wavelength)
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
how does abg work?
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
o ABG: derivation of the SvO2 value from the PO2, pH and pCO2, using the oxygen-haemoglobin dissociation curve.
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
how does co-oximetry work
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
o Co-oximetry: relies on measuring the absoprtion of near-IR light by haemoglobin species, and the use of the Beer-Lambert law to calculate the concentrations of oxyhaemoglobin and deoxyhaemoglobin
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
how does reflectance spectrophotmetry
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
o Reflectance spectrophotometry: relies on measuing the reflected wavelengths of near-IR light, and calculating the concentrations of oxyhaemoglobin and deoxyhaemoglobin from the log ratio of the signal strength (as each Hb species reflects a different wavelength)
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
normal values of spo2: Central venous vs Mixed venous
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Domain Central venous Mixed venous
Normal values 75% 70%
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
spo2 Relationship between them
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Domain 1Central venous 2Mixed venous
Relationship between them
1Usually, higher than mixed venous
2Usually, lower than central venous
(incorporates blood from the coronary sinus, which has sats of ~ 35%)
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
How this is different in shock
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Domain 1Central venous 2Mixed venous
How this is different in shock
Some authors report that in states of normal health, central venous oxygenation is lower than mixed venous by 2-3%, and that this relationship is reversed in states of shock.
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
Determinants
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Determinants
- Mixed venous oxygen content
o Oxygen carrying capacity of blood
o Oxyhameoglbin dissociation curve shape
o PO2 - Components of the modified Fick equation:
(CO = VO2 / CaO2 - CvO2):
o Arterial oxygen content
o VO2 (oxygen consumption)
o Cardiac output
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Measurement and Interepretation of Mixed Venous and Central Venous Oxygen Saturation
Interepretation
- Low in:
?
- Elevated in:
?
?
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
Interepretation
- Low in:
o Cardiogenic shock
o Septic shock
o Malignant hyperthermia
o Hypoxia
. - Elevated in:
o Also septic shock
o Cyanide toxicity
o High output cardiac failure
o Hypothermia
o Anaesthesia and paralysis
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
What is mixed venous blood and what are spo2 in different tissues
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
- Mixed venous blood is:
o Blood sampled from the pulmonary artery which is mixed in the RV and which represents a weighted average of venous blood from all tissues and organs:
o Varying SvO2s from different tissue beds include:
Jugular vein (55%)
Renal vein (81%)
Hepatic vein (66%)
IVC (71%)
SVC (79%)
Muscles (72%)
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
- The PO2 in mixed venous blood, usually X mmHg,
is a major determinant of its oxygen content:
o The PO2 describes the proportion of dissolved oxygen (PO2 × ??)
o The PO2 also determines the SvO2 (usually ??%) according to the shape of the oxygen-haemoglobin dissociation curve in mixed venous blood
This curve is slightly right-shifted (compared to arterial blood) because of the Bohr effect
o The SvO2 then determines the oxygen carriage by haemoglobin in mixed venous blood, and therefore the mixed venous oxygen content
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
- The PO2 in mixed venous blood, usually 40 mmHg,
is a major determinant of its oxygen content:
o The PO2 describes the proportion of dissolved oxygen (PO2 × 0.03)
o The PO2 also determines the SvO2 (usually 70-75%) according to the shape of the oxygen-haemoglobin dissociation curve in mixed venous blood
This curve is slightly right-shifted (compared to arterial blood) because of the Bohr effect
o The SvO2 then determines the oxygen carriage by haemoglobin in mixed venous blood, and therefore the mixed venous oxygen content
i keep forgetting
What is the Bohr effect?
and while im here what is haldane effect
The decrease in the oxygen affinity of haemoglobin in the presence of low pH or high CO2
'’deranged physiology The Bohr Effect’
The Haldane effect is a physicochemical phenomenon which describes the increased capacity of blood to carry CO2 under conditions of decreased haemoglobin oxygen saturation
Both Haldane and Bohr effects are the same features of the same phenomenon
Haldane effect is what happens to pH and CO2 binding because of oxygen, and Bohr effect is what happens to oxygen binding because of CO2 and lower pH.
'’deranged physiology The Haldane Effect’
in my own words, when hemoglobin doesn’t have oxygen on it, it has increased affinity for CO2 (haldane)
in my own words, in areas of high co2 or low ph hemoglobin releases oxygen
tom had some puemonic that I cant completely remember but I think it went something like this Bohr is for Body like your muscles where you can imagine it producing acid , and then Haldane is for hands reminding you of the which are hypoxic and thus Hb have higher affinity for CO2 to bring it back to the lungs
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
- Mixed venous oxygen content depends on:
o Total blood oxygen content =
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
- Mixed venous oxygen content depends on:
o Total blood oxygen content = (SvO2 × ceHb × BO2) + (PvO2 × 0.03)
ceHb = the effective haemoglobin concentration
PvO2 = the partial pressure of oxygen in mixed venous blood
0.03 = the content, in ml/L/mmHg, of dissolved oxygen in blood
BO2 = the maximum amount of Hb-bound O2 per unit volume of blood (normally 1.39)
SvO2 = oxygen saturation of mixed venous blood
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
o Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
deranged
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
o Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
Arterial oxygen content: decreased arterial oxygenation will produce a decreased SvO2
VO2, the oxygen consumption rate: decreased VO2 will produce an increased SvO2
Cardiac output: a decreased cardiac output will produce a reduced SvO2
Note: the examiners comments says to mention that its non-linear relationship between O2 content and partial pressure and also normal variations like exercise and pregnancy
2021 august 13 – deranged 256 words
Describe the factors that affect mixed venous oxygen saturation
just read
2021 august 13 – deranged 256 words
Describe the factors that affect mixed venous oxygen saturation
- Mixed venous blood is:
o sampled from the pulmonary artery
o mixed in the right ventricle out of multiple venous sources
o representative of the oxygen extraction for the entire body - Mixed venous oxygen saturation depends on:
o Factors that influence the affinity of haemoglobin for oxygen:
The partial pressure of O2 in mixed venous blood
The partial pressure of CO2 in mixed venous blood
Increasing CO2 shifts the curve to the right
pH of mixed venous blood, independent of CO2
Decreasing pH (acidosis) shifts the curve to the right
The concentration of 2,3-DPG inside the erythrocytes
Increased 2,3-DPG (eg. in response to hypoxia or erythropoietin) shifts the curve to the right
The presence of unusual haemoglobin species
Methaemoglobin, carboxyhaemoglobin and foetal haemoglobin shift the curve to the left; sulfhaemoglobin shifts the curve to the right
Temperature
Hyperthermia shifts the curve right
o Balance of total body oxygen delivery and consumption, expressed in terms of the modified Fick equation (CO = VO2 / CaO2 - CvO2):
Arterial oxygen content: decreased arterial oxygenation will produce a decreased SvO2
VO2, the oxygen consumption rate: decreased VO2 will produce an increased SvO2. Factors which influce VO2 include:
Factors which influence metabolic rate, eg. hypothermia, hyperthermia, paralysis, anaesthesia
Factors which influence oxygen utilisation, eg. mitochondrial toxins, microvascular shunting in sepsis
Cardiac output: a decreased cardiac output will produce a reduced SvO2
o Pathological abnormalities of the arterial-venous blood flow
Left to right shunts
Describe the factors that affect mixed venous oxygen saturation
examiners comments
2019 march, 2017 march, 2008 feb
2019 march
8. Compare and contrast the measurement (40% of marks) and interpretation (60% of marks) of both central venous and mixed venous oxygen saturations.
8% of candidates passed this question. Many candidates did not appreciate that ScvO2 refers to SVC / RA junction venous oximetry and not femoral or peripheral venous oximetry. Methods of measurement such as co-oximetry and reflectance spectrophotometry needed to be explained. Marks were awarded for the normal values. Discussion of the relationship between ScvO2 and SmvO2 and changes during shock attracted marks. Better answers quoted the modified Fick equation and related this to cardiac output and factors affecting oxygen consumption versus delivery.
2017 mar
9.Define mixed venous PO2 (20% of marks). Outline the factors that affect this value (80% of marks). 37% of candidates passed this question.
This question was in two parts – the first part was worth 20% and candidates were expected to provide a definition of mixed venous blood as well as the partial pressure of oxygen in mixed venous blood (including normal range). Good answers also provided the varying PO2 from different tissue beds that make up mixed venous blood, where the ‘mixing’ occurs (the right ventricle) and where it is sampled (pulmonary artery). For the second part of the question, worth 80% of the marks, good answers included the relationship between mixed venous PO2 and mixed venous O2 content (including the shape and position of the HbO2 dissociation curve); the variables encompassed in the modified Fick equation; arterial oxygen content and its determinants; oxygen consumption (VO2); and cardiac output (CO). Including an outline of how each affects the value of mixed venous PO2. A number of candidates wrote about mixed venous oxygen saturation. Other common errors were: missing a number of key factors that affect PO2; and using an incorrect form and/or content of the modified Fick equation.
2008 feb
9. Briefly describe the factors that influence the partial pressure of Oxygen in mixed venous blood
The main points candidates were expected to cover included:
* A discussion of the non-linear relationship between O2 content and partial pressure and the factors which affect this relationship. No candidate included this.
* Modification of the Fick equation as it relates mixed-venous oxygen to delivery and consumption.
* The components of delivery should have been described and use of the O2 flux equation would have been helpful. Additional marks were available for describing how these might change in physiological and pathological states.
Candidates frequently interchanged content and partial pressure, without clearly displaying how these are related. Normal values were not provided. The O2 flux equation, when included, was often written incorrectly. No consideration was given to normal variations, such as pregnancy or exercise Reference: Nunn 5 th edition pages 267 to 269, page 493 Syllabus: B1h Gas transport in the blood 2a 1 candidate (33%) passed this question.
Note: pretty sure content is total and partial pressure of oxygen is just what dissolved
2021 aug
Mixed venous oxygen saturation is used as a surrogate marker for the overall balance between oxygen delivery and oxygen consumption. A good answer stated this, described the importance of where it is measured and went on to describe the various factors that affect oxygen delivery and consumption. Descriptions of the factors that affect oxygen saturation of haemoglobin, partial pressure of oxygen in the blood and position of oxygen-haemoglobin dissociation curve were necessary to score well. Important omissions were factors that increased and decreased oxygen consumption. While many candidates were able to correctly write the equations for oxygen content and oxygen flux, they then failed to describe how the variables within these equations were related to mixed venous oxygen saturation.
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
- Definition of shock:
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
- Definition of shock:
o Failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
- Classification of shock:
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
- Classification of shock:
o Hypovolemic
Haemorrhage
Water loss (eg. dehydration)
Fluid shift (eg. burns, or following extensive trauma or surgery)
o Cardiogenic
Cardiomyopathy (eg. myocardial infarction)
Arrhythmia (eg. bradycardia, atrial fibrillation)
Mechanical failure (eg. valve failure or HOCM)
o Distributive
Septic/inflammatory vasoplegia (eg. following cardiopulmonary bypass)
Anaphylaxis
Neurogenic shock (eg. high transection of the spinal cord)
o Obstructive
Cardiac tamponade
Tension pneumothorax
Pulmonary embolism
o Cytotoxic
Mitochondrial toxicity (eg. cyanide toxicity)
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Cardiovascular Responses to Shock
Stimulus Sensor Integrator Effector mechanism
Hypotension
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Stimulus Sensor Integrator Effector mechanism
Hypotension
Baroreceptors
Nucleus of the solitary tract
Vagus (increased heart rate)
Sympathetic nervous system (vasoconstriction and increased cardiac output; redistribution of blood flow away from splanchnic circulation and skin)
RAAS activation
(increased angiotensin levels; vasoconstriction)
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Cardiovascular Responses to Shock
Stimulus Sensor Integrator Effector mechanism
Decreased VO2
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Stimulus Sensor Integrator Effector mechanism
Decreased VO2
Aortic arch chemoreceptors
Nucleus of the solitary tract
Vagus (increased heart rate)
Sympathetic nervous system (vasoconstriction and increased cardiac output; redistribution of blood flow away from splanchnic circulation and skin)
RAAS activation
(increased angiotensin levels; vasoconstriction)
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Cardiovascular Responses to Shock
Stimulus Sensor Integrator Effector mechanism
Decreased circulatory volume
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
Stimulus Sensor Integrator Effector mechanism
Common Stimulus: Decreased circulatory volume
Atrium (atrial myocytes)–.>Decreased release of atrial natriuretic peptide
Baroreceptors–>Hypothalamus–>Increased release of vasopressin; water retention
Renal juxtaglomerular cells–>Increased release of renin; RAAS activation; aldosterone release; salt retention
Inadequate tissue perfusion–>Vascular smooth muscle and endothelium–> Autoregulatory vasodilation (myogenic, metabolic, and mediated by endothelial vasoactive mediators such as nitric oxide)
2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
examiner comment
deranged 2019 march
Classify circulatory shock and provide examples (40% of marks). Outline the cardiovascular responses (60% of marks).
i kid you not , the examine comment is very short
Answers should have included the various types of shock and provided clear examples. Cardiovascular responses including sensor, integrator, effector mechanisms were necessary to pass
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
intrinsic vs extrinsic peep
2019 march - cicm
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
PEEP = Positive End Expiratory Pressure. Equivalent to a constant pressure applied throughout the respiratory cycle.
.
Intrinsic PEEP = unintentional or un-measured end-expiratory hyperinflation
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
why does peep have cardiovascular effects?
2019 march - cicm
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Cardiovascular effects: Causes constant ↑ intrathoracic pressure (ITP) throughout respiratory cycle
PEEP = Positive End Expiratory Pressure. Equivalent to a constant pressure applied throughout the respiratory cycle.
Intrinsic PEEP = unintentional or un-measured end-expiratory hyperinflation
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Mechanisms affecting the right ventricle and the pulmonary circulation are:
2019 march - deranged
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Mechanisms affecting the right ventricle and the pulmonary circulation are:
* Increased intrathoracic pressure is transmitted to cenral veins and the right atrium, decreasing right ventricular preload
* Increased intrathoracic pressure is transmitted to pulmonary arteries
* Transmitted alveolar pressure increases pulmonary vascular resistance
* Increased pulmonary vascular resistance increases right ventriular afterload
* Thus, increased afterload and decreased preload has the net effect of decreasing the right ventricular stroke volume.
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Mechanisms affecting the left ventricle and the systemic circulation are
and the consequences
2019 march - deranged
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Mechanisms affecting the left ventricle and the systemic circulation are:
* Decreased preload by virtue of lower pulmonary venous pressure
* Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
* Thus, decreased LV stroke volume
The consequences of this are:
* Decreased cardiac output
* Decreased myocardial oxygen consumption
note; the decreased preload causes decreased cardiac output and is more important than the decrease in afterload
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Mechanisms affecting the left ventricle and the systemic circulation are
other effects
2019 march - dernaged
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
Other Effects
o ↓ C.O. and ↑ Central venous pressure
▪ ↓ Renal blood flow, ↓ Glomerular Filtration Rate and urine output
▪ ↑ ADH and Angiotensin II levels
▪ ↑Hepatic venous pressure → ↓ Hepatic Blood Flow
o ↑ CVP and ↓ venous return
▪ ↑ Intracranial pressure
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
examiners comment
2019 march - cicm
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
2019 march
.Describe the cardiovascular effects of positive pressure ventilation on a patient who has received a long acting muscle relaxant.
33% of candidates passed this question. Structured answers separating effects of positive pressure on right and left ventricle, on preload and on afterload were expected. Overall there was a lack of depth and many candidates referred to pathological states such as the failing heart. Simply stating that positive pressure ventilation reduced right ventricular venous return and/or left ventricular afterload, without some additional explanation was not sufficient to achieve a pass level.
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Invasive (arterial catheter)
Equipment
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Arterial catheter
Incompressible tubing
Pressure transducer
Monitoring
Counterpressure fluid
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Invasive (arterial catheter)
Physical principles and method
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Pressure wave transmitted via fluid column
Pressure changes are converted to resistance changes in a Wheatstone bridge transducer
The resulting change in current is displayed as a graph
By calibrating the sensor against a known range of pressures, this can be converted to a graph of pressure over time
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Invasive (arterial catheter)
Practical advantages
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Thought to be the “gold standard”
Allows continuous monitoring
Gives access to the bloodstream for sampling
Waveform is a source of information
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Invasive (arterial catheter)
Practical disadvantages
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Requires arterial puncture
Non-reuseable kit
Monitoring equipment is required for display
Requires regular re-zeroing and re-levelling
Training is required for staff
Transducers can drift
Relatively expensive parts
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Invasive (arterial catheter)
Sources of error
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Catheter malposition
Transducer mislevelling
Inaccurate zero reading
Failure of counterpressure
Transducer/monitor malfunction or miscalibration
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Oscillometric cuff measurement
Equipment
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Inflatable cuff
Cuff manometer
Release valve
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Oscillometric cuff measurement
Physical principles and method
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Counterpressure is applied to a perfused limb
Pulse from the limb arterial supply is detected (eg. by auscultation)
Increasing counterpressure is applied to the limb
This counterpressure decreases the amplitude of the detected pulse until the pulsations are no longer detected
The counterpressure at which pulse is eliminated is recorded as the systolic pressure;
Maximum counterpressure at which there is no pulse amplitude change is recorded as the diastolic pressure
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Oscillometric cuff measurement
Practical advantages
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
No invasive procedures required
Cheap and reusable
Requires minimal training
Requires no monitoring equipment or electronics
Minimal moving parts, robust setup, durable
Does not require regular recalibration
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Oscillometric cuff measurement
Practical disadvantages
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Less reliable measurements at pressure extremes
Continuous monitoring is not possible
Can become painful if set to repeat too frequently
Can give rise to pressure areas
Maximum accuracy requires manual operation (i.e. automatic modes are unreliable in unstable patients)
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Oscillometric cuff measurement
Sources of error
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
Arrhythmia
Faint pulse
Peripheral vascular disease
Pneumatic leak from balloon or valve
Manometer malfunction
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
examiner comment
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
52% of candidates passed this question. There were some good answers, though invasive BP measurement was better answered than oscillometry. Many candidates provided extensive detail in one area i.e. the workings of a Wheatstone bridge, to the detriment of a balanced answer. Few seemed to have a structure consisting of “equipment, method, sources of error, advantages, disadvantages” or similar and missed providing important information as a result. Several described auscultatory non-invasive blood pressure measurement, rather than oscillometry, which although related in principle is a different process.
Note; so know the differences between
auscultatory non-invasive blood pressure measurement (listen with steth)
oscillometry non-invasive blood pressure measurement (bp cuff)
invasive arterial blood pressure monitoring.
2018 march Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
examiner comment
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
2018 march
.Compare and contrast non-invasive oscillometric and invasive arterial blood pressure monitoring.
52% of candidates passed this question. There were some good answers, though invasive BP measurement was better answered than oscillometry. Many candidates provided extensive detail in one area i.e. the workings of a Wheatstone bridge, to the detriment of a balanced answer. Few seemed to have a structure consisting of “equipment, method, sources of error, advantages, disadvantages” or similar and missed providing important information as a result. Several described auscultatory non-invasive blood pressure measurement, rather than oscillometry, which although related in principle is a different process.
Note; so know the differences between
auscultatory non-invasive blood pressure measurement (listen with steth)
oscillometry non-invasive blood pressure measurement (bp cuff)
invasive arterial blood pressure monitoring.
cardiovascular changes in obesity
I HAV ETHIS CARD SOMEHWERE ELSE AS WELL
Total body oxygen demand is increased
Cardiac output is increased
Cardiac preload is increased
LV contractility is often stable
Cardiac afterload can be increased or decrease
There is increased RV afterload and preload
2017 march Q15 deranged specific question
dEFINE OBESITY
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
* Normal: BMI < 25
* Overweight: BMI 25 - 30
* Obese: BMI > 30
/
* Morbidly Obese:
o Obesity related disease and a BMI > 35
o BMI > 40
dEFINE OBESITY
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
* Normal: BMI < 25
* Overweight: BMI 25 - 30
* Obese: BMI > 30
/
* Morbidly Obese:
o Obesity related disease and a BMI > 35
o BMI > 40
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Total body oxygen demand is increased
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Oxygen requirement and CO2 production are increased by about 150%
o This equates to approximately 300-350ml/min of O2, as compared to 200ml/min for non-obese patients
o This is mainly because of increased lean body mass (adipose tissue has low metabolic demand)
o In conscious obese patients, the effort of breathing is a major source of increased oxygen consumption
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Total body oxygen demand FOR NON-OBESE PATIENT
how much increased?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Oxygen requirement and CO2 production are increased by about 150%
o This equates to approximately 300-350ml/min of O2, as compared to 200ml/min for non-obese patients
o This is mainly because of increased lean body mass (adipose tissue has low metabolic demand)
o In conscious obese patients, the effort of breathing is a major source of increased oxygen consumption
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Cardiac output is increased
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Stroke volume is increased by about 1.25ml per every 1kg/m2 BMI
o Heart rate remains stable, or increases only slightly
o The increase in cardiac output (approximately 1L//min for every 12.5 BMI is mainly due to an increase in stroke volume
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to heart rate in obesity?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Stroke volume is increased by about 1.25ml per every 1kg/m2 BMI
o Heart rate remains stable, or increases only slightly
o The increase in cardiac output (approximately 1L//min for every 12.5 BMI is mainly due to an increase in stroke volume
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to stroke volume in obesity?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Stroke volume is increased by about 1.25ml per every 1kg/m2 BMI
o Heart rate remains stable, or increases only slightly
o The increase in cardiac output (approximately 1L//min for every 12.5 BMI is mainly due to an increase in stroke volume
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to cardiac output in obesity?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Stroke volume is increased by about 1.25ml per every 1kg/m2 BMI
o Heart rate remains stable, or increases only slightly
o The increase in cardiac output (approximately 1L//min for every 12.5 BMI is mainly due to an increase in stroke volume
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Cardiac preload is increased
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Total blood volume is increased
o Thus, MSFP and CVP are increased
o This increase in preload causes the increase in stroke volume
o It is due to neurohormonal changes in obesity, which are mediated by the endocrine function of adipose tissue:
Sympathetic stimulation and thus RAAS activation by leptin
Angiotensinogen synthesis by leptin
o These cause salt and water retention
o Left and right atrial pressure increases, which increases the propensity to develop atrial arrhythmias
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
in obesity why increased propensity of atrial arrhythmias?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Total blood volume is increased
o Thus, MSFP and CVP are increased
o This increase in preload causes the increase in stroke volume
o It is due to neurohormonal changes in obesity, which are mediated by the endocrine function of adipose tissue:
Sympathetic stimulation and thus RAAS activation by leptin
Angiotensinogen synthesis by leptin
o These cause salt and water retention
o Left and right atrial pressure increases, which increases the propensity to develop atrial arrhythmias
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- Cardiac afterload can be increased or decreased
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Normotensive obese patients usually have decreased peripheral vascular resistance
o However, the prevalence of hypertension in obesity is ~60%
o This is mainly due to chronic sympathetic activation, which is attributed to the chronic hypoxia of OSA
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
Normotensive obese patients usually have ? peripheral vascular resistance
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Normotensive obese patients usually have decreased peripheral vascular resistance
o However, the prevalence of hypertension in obesity is ~60%
o This is mainly due to chronic sympathetic activation, which is attributed to the chronic hypoxia of OSA
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
the prevalence of hypertension in obesity is ~?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Normotensive obese patients usually have decreased peripheral vascular resistance
o However, the prevalence of hypertension in obesity is ~60%
o This is mainly due to chronic sympathetic activation, which is attributed to the chronic hypoxia of OSA
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- LV contractility is often stable
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o In response to increased preload and afterload, remodelling occurs:
Increased LV wall thickness
Increased LV chamber volume
As the result, LV diastolic function is often impaired
Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
o LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to lv wall thickness in obesity
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o In response to increased preload and afterload, remodelling occurs:
Increased LV wall thickness
Increased LV chamber volume
As the result, LV diastolic function is often impaired
Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
o LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to lv chamber volume in obesity
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o In response to increased preload and afterload, remodelling occurs:
Increased LV wall thickness
Increased LV chamber volume
As the result, LV diastolic function is often impaired
Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
o LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
what happens to stroke volume in obesity during exercise
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o In response to increased preload and afterload, remodelling occurs:
Increased LV wall thickness
Increased LV chamber volume
As the result, LV diastolic function is often impaired
Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
o LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
in obiesty why do ventricular arrhythmias increase in propsity?
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o In response to increased preload and afterload, remodelling occurs:
Increased LV wall thickness
Increased LV chamber volume
As the result, LV diastolic function is often impaired
Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
o LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
- There is increased RV afterload and preload
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Preload is increased by the global circulating volume expansion
o Afterload is increased because of:
LV diastolic failure
Chronic hypoxia due to OSA or obesity hypoventilation, resulting in chronic hypoxic pulmonary vasoconstriction
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
why does afterload increase in obesity
2 reasons
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
Cicm wrekcs has a good definition, but I didn’t read through the whole document
o Preload is increased by the global circulating volume expansion
o Afterload is increased because of:
LV diastolic failure
Chronic hypoxia due to OSA or obesity hypoventilation, resulting in chronic hypoxic pulmonary vasoconstriction
Obesity is a multisystem disorder defined by an elevated body mass index (BMI):
2017 march Q15
EXAMINER COMMENT
2017 march Q15 Outline the cardiovascular changes associated with morbid obesity.
2017 march Q15
Many candidates did not include enough detail in their answers. Higher scoring answers included more depth such as the following: blood volume, left ventricular changes, arterial blood pressure, pulmonary artery pressures, risks of ischaemia, arrhythmias etc.
