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
