Cardiac output and its determinants Flashcards
Draw diagrams illustrating the relationship between stroke volume and its determinants
Draw a diagram comparing cardiac output with HR
Describe the relationship between stroke volume and preload
Stroke volume increases with increased preload, up to a plateau, beyond which it begins to decrease again
Desribe the relationship between stroke volume and afterload
Stroke volume decreased with increased afterload, in a fairly linear fashion
Describe the relationship between stroke volume and contractility
Stroke volume increases with increased contractility, for any given preload and afterload value
Draw a diagram reflecting the relationship between stroke volume and end diastolic volume
Frank starling curve
What surrogate volume is used for prelaod in measurements
EDV
How is the action of SNS different between cardiac and heart muscle
Heart muscle increase the strength and rapidity of isometric twitch and speeds up both the onset and relaxation fo the muscle twitch
It has no such effect in skeletal muscle
What is a molecular target of enhanced myocardial relaxation by norepinephrine/adrenaline
Phospholamban and troponin I
How is Frank-Starling different to contractility increase directly?
Frank starling mechanism increases the velocity of contraction and maximal isometric force, but does not change the maximum valocity of contraction at zero load
Noradrenaline in contrast increases Vmax, velocity of contraction at other loads and maximal isometric force
Relate cardiac output to HR
◦ Higher heart rate increases cardiac output as it multiplies stroke volume
◦ At very high heart rates stroke volume may be decreased due to decreased preload - all people have a maximum HR for maximum cardiac output that decreases with age; up to HR 140 CO generally increases with increasing HR, and above 140 it begins to impair diastolic filling
What is the general maximal threshold of increased cardiac output with increased HR
◦ Higher heart rate increases cardiac output as it multiplies stroke volume
◦ At very high heart rates stroke volume may be decreased due to decreased preload - all people have a maximum HR for maximum cardiac output that decreases with age; up to HR 140 CO generally increases with increasing HR, and above 140 it begins to impair diastolic filling
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
Draw a graph describing the relationship between preload and SV
How does afterload change preload
Increased ESV –> increased EDV
How does afterload affect contractility
Anrep effect
What factors affect aferload
- Tramsural wall stress - Law of Laplace
- Transmural pressure - cavity pressure, intrathoracic pressure
- Ventricular wall radius - Arterial impedence factors
- Hagen Poiseulle factors
- Arterial elastance - proximal distension, as well as returning pressure wave
- inertia
What are the 5 factors affecting contractility
◦ Heart rate (Bowditch effect)
◦ Afterload (Anrep effect)
◦ Preload (Frank-Starling mechanism)
◦ Cellular and extracellular calcium concentrations
◦ Temperature
Define contraciity
Increased contractility improves SV for any given preload or afterload
Draw a set of diagrams illustrating the effect of afterload and preload on SV and illustrate how contractility affects these
Stroke volume increases with increased preload, up to a plateau, beyond which it begins to decrease again
Stroke volume decreased with increased afterload, in a fairly linear fashion
Stroke volume increases with increased contractility, for any given preload and afterload value
How is cardiac output different with age?
Higher proportionally in children
How is cardiac output affected by pregnancy
50% increase at term
How is cardiac output affected by eating
25% increase while eating
What has a greater influence on CO - HR or SV
HR - can change by a factor of 3
SV can only increase by up to 50%
Draw a curve relating afterload to pressure in the ventricle
Define afterload
the impedence to the ejection of blood from the heart into the arterial circulation
Afterload can be defined as the resistance to ventricular ejection - the “load” that the heart must eject blood against.
What is te most readily available index to afterload
MAP
MAP during systole would be more accurate
ESP is sometimes used
What are the two main factors affecting afterload
Myocardial wall stress
Input impedence
What is the equation for wall stress
P × r / T
What is P in the myocardial wall stress equatoin? Outline its depenedent factors and how these influence the value of P and wall stress
- 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
How does radius of the LV affect its afterload
Increased afterload = increased LV diametre via law of Laplace
What is T in the myocardial wall stress equation? How is it a factor
Wall stress = P x R / T
T is thickness
Thicker wall = less wall stress
Input impedence is defined as
describes ventricular cavity pressure during systole
What comprises input impedence
- 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) - Inertia of the blood column
- Ventricular outflow tract resistance (increases afterload in HOCM and AS)
- Arterial resistance
◦ 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)
Arterial compliance affects afterload how? 2
- 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)
How does intrathoracic pressure affect transmural pressure
- Negative intrathroacic pressure increases LV afterload
◦ Transmural pressure is difference between LV chamber pressure and pleural pressure (negative pleural pressure increases that resistance) - Positive intrapleural pressure decreases afterload because ofa decrteased LV transmural pressure as it is subtracted from intra-LV pressure so LV wall stress decreases
What is a Wiggers diagram? What does it represent?
Ventricular cavity pressure and outflow impedence - the Wiggers diagram
Coloured area represents the overlap of the graphs where LV pressure exceeds aortic - the difference in the pressures is produced by mechanical ressitance to ventricular outflow
Which layer of the aorta is important in the aortic compliance
Media
What is the WindKessel effect
- Property of large arterial vessels due to their tunica media permitting expanding in systole and storage of elastic energy and then return in diastole thereby maintaining flow - the Windkessel effect
What % of SV is stored in distended artterial capacitance vessels
60%
What % of cardiac workload is spent on distending arterial capacitance vessels
10%
How does a stiff aorta produce higher afterload
- Systolic ejection fromthe LV generates some flow early in systole because of increased chamber pressure
- If proximal aorta is stiff and noncompliant (minimal volume change per unit of pressure) - the force generated by the ventricle will produce higher pressure and lower flow
◦ i.e. to achieve the same flow the ventricle needs to generat ehigher pressures
◦ Higher pressure = higher wall stress = higher afterload
How does a stiff arterial tree cause increased reflected pulse wave?
- Decreased peripheral arterial compliance causes inrease in pulse wave velocity causing reflected wave from distal circulation to arrive early during systole contributing to afterload
◦ Pulse pressure wave propogates into the distal circulation at 1m/sec
◦ Then the pulse pressure wave reflects from arterioles and returns to the heart - usually returning in diastole complementing diastolic BP and helps fill coronaries
◦ With decreased compliance the speed increases causing the pulse wave to return sooner adds extra pressue to aortic pressure incresaing ventricular chamber pressure and then wall stress
How fast does the pulse wave travel from the LV
1m/sec
What effect does decreasing complianc eof arterial tree have on pulse wave velocity
- Decreased peripheral arterial compliance causes inrease in pulse wave velocity causing reflected wave from distal circulation to arrive early during systole contributing to afterload
◦ Pulse pressure wave propogates into the distal circulation at 1m/sec
◦ Then the pulse pressure wave reflects from arterioles and returns to the heart - usually returning in diastole complementing diastolic BP and helps fill coronaries
◦ With decreased compliance the speed increases causing the pulse wave to return sooner adds extra pressue to aortic pressure incresaing ventricular chamber pressure and then wall stress
Reflected pulse waves usually are advantageous or disadvantageous
Advantageous
Increase diastolic BP and coronary perfusion
How is inertia relevant to cardiac output?
- Blood has mass and therefore inertia - resistance to meing move and resistance to being stopped when moving
- Blood inertia influences afterload by
◦ Increases afterload in early systole - as it opposes accelaration of blood flow which is maximal in early systole
◦ Decreases afterload in late systole
◦ Its influence is increased with increased heart rate - as accelaration has to occur over a shorter period of time therefore requiring greater force
What happens if you suddenly increase afterload 7
What factors are different in determinants of cardiac output between the LV and RV 3
HR, SV the same
Determinants of afterload different
Determinants of preload different
Contractility generally affected by the same factors
Interventricular dependence different
What is preload
- Load on the myocardial muscle just prior to the onset of contraction which correlates to the initial fibre length of a sarcomere just prior to the start of contraction
What index do we use for preload
Wedge pressure, LVEDV (LVEDP is related by compliance), RAP, CVP
LV compliance =
LVEDV/LVEDP
LVEDP is related to LVEDV how?
LV compliance = LV EDV/LVEDP
LVEDP is the filling pressure and almost the same as the LAP
How does PCWP relate to preload
Under what circumstances might it be wrong
‣ PCWP or pulmonary artery occlusion pressure estimates LV filling pressures from right side of circulation and correlates well with LAP in most circumstances - this is because occlusion stops flow so no pressure drop across vessel and as pulmonary veins to pulmonary arteries isa low resistance path at the same horizontal level it should correlate. LAP is also assumed to correlate with LVEDP which it may not in mitral stenosis
Venous return equation
Veinous resistance = (MSFP - RAP) / Venous return = HR × SV
* where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
How does MSFP relate to veinous return
Veinous resistance = (MSFP - RAP) / Venous return = HR × SV
* where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
How does RAP relate to veinous return
Veinous resistance = (MSFP - RAP) / Venous return = HR × SV
* where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
How does veinous resistance factor into veinous return
Veinous resistance = (MSFP - RAP) / Venous return = HR × SV
* where MSFP is mean systemic filling pressure, RAP is right atrial pressure and VR is the venous resistance
Preload umbrella headings
Intrathoracic pressure
Right atrial pressure
Cardiac rhythm
Ventricular pressure and compliance
AV valve competence
MSFP
Cardiac output
How does intrathoracic pressure affect preload RV
◦ Intrathoracic pressure - high intrathoracic pressure decreases preload to the RV, reverse for LV
‣ Increased intrathoracic pressure increases RA and RV pressure - thus decreasing the pressure gradient for blood flow into the cardiac chamber –> reduced RV end diastolic pressure –. reduced RV end diastolic volume
How does rhythm affect preload
SR increases preload, AF decreases preload
* atrial kick 20% of EDV or 24ml on average of 120ml; LA volumes average 36-77ml for BSA 1.9m^2 and EF 55%
What proportion of EDV does RA contraction contribute?
SR increases preload, AF decreases preload
* atrial kick 20% of EDV or 24ml on average of 120ml; LA volumes average 36-77ml for BSA 1.9m^2 and EF 55%
What ml increase does RA contraction correlate to
SR increases preload, AF decreases preload
* atrial kick 20% of EDV or 24ml on average of 120ml; LA volumes average 36-77ml for BSA 1.9m^2 and EF 55%
Why does AV valve pathology affect preload
‣ Atrioventricular valve competence - mitral and tricuspid stenosis decrease preload
How might ESV effect preload
‣ Ventricular end-systolic volume - increased ESV increases preload by adding to venous return (e.g. as a consequence of reduced contractility or increased afterload)
How does RAP influence veinous return
◦ Right atrial pressure - high right atrial pressure increases preload - rate of blood flow (venous return) back to the heart is determined by pressure gradient between MSFP and RAP
What is MSFP composed of
Blood volume
veinous tone/venous vascular compliance
Decreased veinous compliance causes?
Increased preload
Compliance of the heart influences preload how?
Pericardiac ompliance - decreased decreased preload
Ventricular compliance
- Duration of filling
- Wall thickness, wall stiffness
- Lusitrophy
What 3 factors influence ventricular compliance
Ventricular compliance
- Duration of filling
- Wall thickness, wall stiffness
- Lusitrophy
How is EDV affected by HR
Linear decrease with increasing HR
Using a vascular function curve outline how increased veinous resistance affects preload, and how increased blood volume increases preload
How does EDV affect stroke volume? What is the maximal stroke volume? Roughly what does EDV correlate to? What is the maximum productive EDV
Factors affecting RAP (6)
‣ Intrathoracic pressure (spontaneous vs. positive pressure ventilation)
‣ Pericardial compliance (eg. tamponade, open chest)
‣ Right atrial compliance (eg. infarct, dilatation)
‣ Right atrial contractility (i.e. AF vs sinus rhythm)
‣ Tricuspid valvular competence and resistance
‣ Cardiac cycle phase - during ventricular contraction atrial volume increases and pressure drops
Define MSFP
◦ The pressure exerted by the tone of the vascular smooth muscle on the systemic blood volume (excluding the heart and pulmonary circulation), in the absence of pulsatile flow (the elastic recoil potential in the vascular walls)
What is MSFP a measure of
Degree of filling and force driving blood return
How does the MSFP change with cardiac output
it doesn’t, its the privot pressure of circulation
As MSFP increases what happens to veinous return
increases
When does MSFP = RAP
when CO is 0
What is MSFP at baseline
7mmHg
What is MSFP with noradrenaline
15mmHg
What % of blood volume is the stressed voluem
15%
What is mean circulatory filling pressure
◦ *Mean circulatory filling pressure is for the entire circulatory system including heart and pulmonary vascular system - it is different as the cardiopulmonary filling pressure is about 3mmHg higher
What relatinoship does venous return have to MSFP
◦ Venous return is = (MSFP - RAP)/venous resistance
‣ Baseline MSF (7mmHg) - RAP (1mmHg) = 6mmHg/venous resistance
What is the equation used to describe venous return with reference to arterial measurements (Ohms law)
‣ VR = (MAP - RAP)/TPR
What affects veinous resistance
- Vascular shape
- mechanical factors
a) Posture and gravity
b) Pumps - intrathoracic/intrabdominal pump, skeletal pump, valves
c) Obstruction to veinous flow - pregnancy, SVC obstruction - Neuroendocrine factors
How does intra-abdominal and intrathoracic pressure change veinous resistance
increased venous return on inspiration as low intrathoracic pressure pulls open distensible venue cava - however if RAP 0mmHg and thoracic pump actions collapse of chest veins occurs when pressure subatmospheric. Baseline intrapleural pressure -5 then to -8cmH20 on descent of diaphrgam with increased subsequent intraabdominal pressure - causes a 250ml increase in thoracic blood volume on inspiration and RV SV increase of 20mL; the reverse occurs in the LV and on expiration. LV variance is 5% in output
What mechanical factors can impede veinous return?
Factors that increase veinous return
a) Posture and gravity
b) Pumps - intrathoracic/intrabdominal pump, skeletal pump, valves
c) Obstruction to veinous flow - pregnancy, SVC obstruction
What is heterometric autoregulation
Heterometric autoregulation - rapid response to acute change in venous return, keeps R and L outputs the same. Increased VR leads to
* Increased force of contraction due to increased preload - via starlings law
* Increased stretch in sinoatrial node also causes a modest increase in HR
What is homeometric autoregulation
Homeometric autoregulation
* Increased contraction due to increased contractility from internal changes increasing calcium availability (indepndent of preload and afterload)
◦ No ventricular distension as excessive distension disadvantageous because of the Law of Laplace - tension in thw walls of a hollow sphere
‣ Wall stress = pressure x radius / 2 x wall thickness
How are the R and left ciruclation kept equal
Heterometric autoregulation - rapid response to acute change in venous return, keeps R and L outputs the same. Increased VR leads to
* Increased force of contraction due to increased preload - via starlings law
* Increased stretch in sinoatrial node also causes a modest increase in HR
Homeometric autoregulation
* Increased contraction due to increased contractility from internal changes increasing calcium availability (indepndent of preload and afterload)
◦ No ventricular distension as excessive distension disadvantageous because of the Law of Laplace - tension in thw walls of a hollow sphere
‣ Wall stress = pressure x radius / 2 x wall thickness
How R and L circulations remain with the same output
* Same rate of contraction - shared conduction system
* Same SV and adjustment to minor differences via Starlings law
In what 4 circumstances is atrial kick the most vital to preload
- Tachycardia - diastolic filling passively has insufficient time.
- Diastolic heart failure/HFPEF - poor compliance of LV as higher pressures needed to achieve preload and cannot be acheived with passive filling alone
- Aortic stenosis - LV is almsot completely full at the end of systole, therefore poorly compliant and the only way to squeeze more blood into it is by atrial contraction
- Mitral stenosis - mitral valve a source of resistance to flow
How does the sympthetic nervous system affect preload
Decreased EDV and decreased RAP increasing gradient for veinous reutrn, while also increasing MSFP
How does an isolated increase in HR affect SV in the absence of increased tissue demand?
- If HR alters in the absence of tissue demand the stroke volume subsequently adjusts to keep cardiac output stable
◦ This effect persists between a HR of 40 and 180 outside of which cardiac output does fall
‣ This range can change if in the context of bradycardia there is heart failure and an inability to increase SV; or under tachycardic conditions there is failed relaxation/loss of atrial kick where mechanisms result in a significant drop in cardiac output◦ Extrathoracic veins draining into the heart collapse if pumping demand exceeds return of blood because venous pressure falls below external pressure on the veins –> decreased stroke volume
‣ Therefore it is not possible to increase HR alone without also increasing the tenandcy for venous return e.g. exercise where muscle arterioles dilate, muscule capillaries open, SVR drops, and increased tenandcy for venous return
WHat is contractility
Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume).
- factor responsible for changes in myocardial performance which is not due to changes in HR, preload, or afterload
- The amount of work the heart can perform at any given load
Physiological determinants of contractility
Preload
Afterload (Anrep effect)
HR - Bowditch effect
Intracellular Calcium and extracellular calcium
Temperature
How does preload affect contracility
- 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)
An increase in afterload causes what change in contractility? Why is this given a separate name for effect rather than being attributed to its effects on preload?
- The increased afterload causes an increased end-systolic volume
- This increases the sarcomere stretch
- That leads to an increase in the force of contraction - the increased inotropy is greater than would be predicted from the Frank Starling mechanism alone
- A sudden increase in afterload causes a reduction in SV transientally before gradually returning to normal
- A gradual creeping increase in intracellular calcium occurs due to Na/Ca exchanger because of aldosterone related uptake of intracellular sodium
What is the mechanism of the Bowditch efffect
- With higher hear rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.
◦ Myocyte contraction is the consequence of significant calcium influx into the myocytes
◦ Relaxation is mainly due to this calcium being ejected back out of the cell or resequestered in the sarcolemma
◦ The expulsion fo calcium is a chemical process with a finite reaction time - at high HR there is increased systolic Ca influx, and in addition diastolic Na efflux due to Na/K ATPase cannot keep pace with systolic influx of Na and the Na/Ca exchanger normally responsible for low Ca is less effective
How does calcium effect contractility
- Myocyte intracellular calcium concentration - calcium entry into myocytes triggers calcium dependent release from sacolemma –> binds to troponin resulting in sliding of the thick and thin filaments –> force of contraction is dependent on amount of calcium bound to troponin
What effect do catecholamines have on intracellular calcium in the heart
◦ Catecholamines: increase the intracellular calcium concentration by a cAMP-mediated mechanism, acting on slow voltage-gated calcium channels
‣ The inotropic effects of systemic catecholamines and of the sympathetic nervous system is mediated by the β-1 receptors, which are Gs-protein coupled receptors. The increase in cyclic AMP which results from their activation increases the activity of protein kinase A, which in turn phosphorylates calcium channels. Calcium influx ensues
How does ATP availability effect Calcium
◦ ATP availability (eg. ischaemia): as calcium sequestration in the sarcolemma is an ATP-dependent process
‣ ATP amount actually takes a while to deplete, instead in the context of ischaemia there is a decreased ability of IC calcium to trigger the releas eof more calcium from the sarcolemma
What is the relationship between extracellualr calcium and contractility
Linear
How does temperature affect contractility? Mechanism
- Temperature: hypothermia decreases contractility, which is linked to the temperature dependence of actin activated myosin ATPase, decreased cardiac myofilament sensitivity to calcium and the decreased affinity of catecholamine receptors for their ligands.
What indices do we use to meaure contractility?
ESPVR
dP/dT
Ejection fraction
Mean velocity of fibre shortening
What is the 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.
How does an ESPVR explain contractility
‣ As you increase the preload (here represented by the end-diastolic volume), the blood pressure increases. (a new pressure volume loop is created with a new ESP)
‣ Both the systolic blood pressure and the diastolic pressure increase.
‣ Thus, the aortic valve closes at a higher pressure
‣ This higher pressure at the end of systole means the end-systolic volume is also higher
‣ Thus, the end-systolic pressure and volume point (and the rest of the loop) is shifted to the right - as EDV increases –> ESP and ESV also increase
◦ As contractility changes the slope of this line changes as the greater the change in pressure from a given preload (the slope or Emax is an index of contractility)
What elements of contractility does ESPVR fail to outline
ESPVR slope decreases progressively with increasing ventricular size without this necessarily indicating a change in cntractility
Cannot be meaured in vivo due to too many vairables obscruing the relationship
dP/dT is what? Measures? When?
- dP/dT (or ΔP/ΔT), change in pressure per unit time.
◦ Specifically, in this setting, dP/dT (max) it is the maximum rate of change in left ventricular pressure during the period of isovolumetric contraction.
What are the issues with using dP/dT
‣ Not independent of myocardial loading factors - preload especially, but afterload minimally affects it
‣ Affected by alterations of arterial diastolic pressure i.e. raised diastolic pressure results in a rise of peak dP/dT
‣ dP/dT is dependent on HR - impossible to assess inotropy if also chronotropic effecs
‣ Requires catheterisation of the LV
‣ High performance electromanometer
Frank starling mechanism is>
- This mechanism ensures that stroke volume changes in proportion to the change in end-diastolic volume - the relationship is non linear
What is the ideal sarcomere length for contraction?
◦ Maximal force of contraction when sarcomere stretched to 2.2 micrometres
Explain the mechanism of Frank Starling
- ‣ Thought to correspond to optimal actin/myosin crossbridges and no overlapping of thin filaments (overlapping of thin filaments occurs with shorter sarcomeres and contractile energy is lost due to work against friction; when sarcomere stretched beyond 2.2 micrometres fewer crossbirdges and force reduced). At 3.6 micrometres no overlap and tension is zero
- With stretching the fibre elements also become closer together as the volume does not change, the force generating gents are in closer proximity increasing the likelihod of such reactions in the absence of changes in reagants
What LVEDP correlates with optimal sacromere strecth
10-12mmHg
Why is the Frank Starling mechanism important
Matching LV and RV outputs via the heterometric autoregulation - important during the breathing cyclewhen preload varies
Compensating for changes in preload and afterload conditions
Smooths out pertubations in cardiac output associated with changes in preload due to posture, exercise more rapidly than the ANS would be able to
Compensates for changes in HR
Explain how intrathoracic pressure influences afterload in the LV
Wall stress is described by the Law of Laplace ( P × r / T) and therefore depends on:
* 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
Explain factors that will determine RV afterload
- Outflow tract impedence - pulmonary stensosi or RVOT obstruction
- Pulmonary vascular resistance - this is much lower than systemic vascular resistance resulting in less afterload. The pulmonary vessels are highly compliant reducing afterload. Pulmonary vascular resistance is increased (increasing afterload) by
◦ Low lung volumes
◦ Low pulmonary blood flow
◦ Hypoxic pulmonary vasoconstriction
◦ Systemic catecholamines and activated sympathetic nerveous system
◦ Increased blood viscosity - Thin ventricular wall - increased wall stress via the law of Laplace increasing afterload
- Ventricular dilation increases wall stress
- Positive intrathoracic pressure increases afterload, negative intrathoracic pressure decreases afterload
- Blood viscocity has a greater effect on right ventricle because pulonary system has less shear stress and as blood behaves as a non newtonian fluid it contributes more to resistance in pulmonary system
Explain factors determining LV afterload
- Systemic vascular resistance - higher than pulmonary leading to increased LV afterload
◦ Arterial compliance - aortic compliance influences early resistance in systole (stiff aorta increases afterload) - generally in young adults they are elastic capacitance vessels reducing afterload
◦ Peripheral compliance influences speed of reflected pulse pressure wave so stiff peripehral vessels increased afterload
◦ Arterial resistance
‣ Length - long vessels increases resistance
‣ Blood viscotiy - increases resistance
‣ Vessel radius - smaller increases resistance - Ventricular outflow tract resistance - AS and HOCM
- Thick ventricular wall - via the law of Laplace reduces afterload
- Ventricular dilation increases wall stress
- Positive intrathoracic pressure decreases afterload, negative intrathoracic pressure increases afterload
How does a sudden increased in afterload affect the heart?
Cardiac output
Heart rate - Stable 0 decreases if associated with increased carotid pressur eor increases if decreased cardiac output
Stroke volume - decrease due to increase in DBP, and ESV increases
Preload - ESV and ESP rise, so increases
Contractility - increased Frank starling and Anrep effect helping SV approach normal
Myocardial oxygen consumption - increased
Coronary blood flow - stable
What factors affect RV afterload
- Thin wall of the RV: (increases afterload)
- Positive intrathoracic pressure (increases afterload)
- 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)
How is RV preload affected
ery sensitive to changes in RV preload and afterload
* Right atrial pressure
* mean systemic filling pressure
◦ Total venous blood volume
◦ Venous vascular compliance
* Pericardial compliance and pericardial contents
* Positive intrathoracic pressure (decreases preload)
* Ventricular wall compliance:
◦ Duration of ventricular diastole
◦ Wall thickness
◦ Relaxation (lusitropic) properties of the muscle
◦ End-systolic volume of the ventricle (i.e. afterload)
What other than HR, and preload, afterload and contractility can affect ventricular function?
Interventricular dependence
What factors affect the diastolic performance of the LV?
Preload
* Intrathoracic pressure, atrial pressure (specifically the LA-LV pressure gradient), mean systemic filling pressure, total venous blood volume and venous vascular compliance
* Compliance of the left ventricle and the pericardial sack
* Diastole becomes shorter in tachycardia, and diastolic filling is time dependent - additionally the importance of atrial kick and therefore sinus rhythm becomes more important
Contractility and compliance
* Lusitropy (active LV relaxation) is determined by many of the same factors determining contractility in systole
Afterload
* High afterload increases end systolic volume impeding diastolic fillin
What are the 3 phases of systole
Isovolumetric contraction
Early ventricular ejection
Late ventricular ejection
When is ventricular systole
the period of ventricular chamber contraction and ejection of blood from the heart corresponding to
* The period from the peak of the R wave on the ECG until the peak of the T wave
* The period in which the aortic/pulmonary valves are open
What % of the cardiac cycle and what duration fo time does systole comprise?
Ventricular systole at rest occupies 1/3 of cardiac cycle - 0.3 seconds at a HR of 72; and 1/2 of cardiac cycle at maximum physiological tachycardia shortening its interval by 50%. Ventricular systole typically involves ejection of 70mL of blood with 60mL remaining corresponding to EF of 60%
Describe the events and correlation to other cardiac events of isovolumetric contraction
- The beginning of this phase corresponds with the peak of the R wave
- This corresponds to Phase 0 (rapid sodium influx) of the ventricular myocyte action potential
- The ventricles begin to contract during this period
- This contraction increases the ventricular chamber pressure and closes the mitral and tricuspid valves producing the first heart sound (mitral before tricuspid)
- As a result, there is a fixed ventricular volume during this contraction
- The AV valves bulge into the atria causing atrial pressure C wave and a rise in pressure to 10mmHg in the LA and 5mmHg in RA
What features comprise early ejection in systole? What other cardiac events does it correlate with?
- The contracting ventricles achieve a pressure high enough to open the aortic and pulmonic valves, and rapidly empty into the systemic and pulmonary circulations.
◦ Aortic valve typically opens at diastolic BP ~80mmHg, reaching a peak of 120mmHg
◦ Pulmonary valve typically opens at DBP 8mmHg, and reaches a peak of 25mmHg - This period corresponds to Phase 2 (plateau, rapid calcium influx) of the cardiac myocyte action potential
- On the surface ECG, the end of this phase corresponds to the beginning of the T wave
- Atrial pressure falls sharply to zero or negative values as ejection causes AV fibrous ring to be pulled downwards lengthening and increasing atrial volume - this causes atrial filling gradually - characterised by the x descent on the atrial pressure waveform
Late systolic ejection comprises what events? What does it correlate in the cardiac cycle?
- This period begins when ventricular pressure starts to drop, and ends with the closure of the aortic and pulmonic valves - this corresponds to the beginning of the T wave but as the momentum of the blood persists, elasticity of stretched walls and afterload impedence pressure is maintained and flow continues
◦ Aortic valve closes before pulmonary - The end of this period corresponds to the peak of the T wave on the surface ECG
- This corresponds to Phase 3 (repolarisation) of the cardiac myocyte action potential
What are the 4 phases of ventricular diastole?
Isovolumetric relaxation
Early diastole
Late diastole - late slow diastolic filling
Atrial contraction
Isolvolumetric relaxation begins when
Aortic valves close
2nd heart sound
Middle of the T wave
What occurs when isovolumetric relexation occurs?
- The ventricles relax without any change in volume
- The ventricular pressure drops until the tricuspid and mitral valves open
- The atrial pressure rises during this period ot 5mmHg in the LA, and 2mmHg in the RA -= corresponds to the v wave on the atrial pressure waveform
- 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
- The end of this period corresponds to the end of the T wave on the surface ECG, and the end of Phase 3
What happens in the atria during isovolumetric relaxation
- The ventricles relax without any change in volume
- The ventricular pressure drops until the tricuspid and mitral valves open
- The atrial pressure rises during this period ot 5mmHg in the LA, and 2mmHg in the RA -= corresponds to the v wave on the atrial pressure waveform
- 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
- The end of this period corresponds to the end of the T wave on the surface ECG, and the end of Phase 3
When does isovolumetric relaxation end?
end of the T wave
Early rapid diastolic filling accounts for what % of EDV
80%
Early rapid diastolic filling significant events? 2
What atrial pressure phase does this relate to
- During this period the relaxing ventricles have pressure lower than atrial pressure, and they fill rapidly
◦ the pressure in both ventricles and atria simultaneously decline in this phase - atrial Y descent - 80% of the ventricular end-diastolic volume is achieved during this phase
- Coronary blood flow is maximal during this phase
Late slow diastolic filling comprises which portion of the ECG?
- Ventricular and atrial pressures equilibrate and the atria act as passive conduits for ventricular filling
◦ Atrial pressure remains very slightly higher than ventricular as they both slowly rise in pressure - The end of this phase corresponds to the end of the P-wave on the surface ECG
Atrial systole accounts for what % of end diastolic volume? When does this start on the surface ECG
- The atria contract (right first, then left shortly after) following sinus node depolarisation and spreading wave of atrial action potentials and contraction
- 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 (10-40%)
- Atrial contraction pressure is transmitted through the great veins as the a wave
- These events start at the end of the P-wave on the surface ECG, and finish during the PR interval.
- 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
Draw a pressure volume loop for the heart and label
What do the areas on a pressure volume loop correspond with?
Internal area - external work done by LV (stroke work)
Area betwen ESPVR and area 1 - potential mechanical work or the energy stored in the LV wall
ESPVR can represent an increase in contractility on a pressure/volume line how?
Anticlockwise rotation –> decrease ESV, increased stroke volume, increased work
How do you represent afterload on a Pressure volume curve?
Arterial elastance line joining the X axis from where EDV is to the end systolic point
Clockwise rotation represents increasing afterload
Venous return equation
(MSFP - RAP)/venous resisatnce
Preload determined by
Intrathoracic pressure
RAP
RV compliance - lusitrophy, end systolic volume, stiffness of wall, HR
AV valve
Cardiac output
MSFP
Atrial contraction
What is the modification to the Fick method used for cardiac output measurement
Stewart Hamilton equation
V = m/Ct
V = flow
C = concentration
M - dose of indicator
T = time
- Flow rate = amount of dye added / area under the curve
What is the Fick equation for cardiac output
CO = VO2/(Ca - Cv)
Draw an indicator dilution curve
- The diagram of actual circulatory flow is seen below
◦ Dye injected at T0 - 10mL
◦ Dye detected later as it takes time to travel from injection to sensor
◦ Rapid rise in oncentration leading to a rounded peak due to the fact laminar flow is occuring so dye travels at a range of velocities from injection to sensor; and also reflects the eddies occuring in circulation
◦ Exponential decay of concentration then occurs - second peak due to recirculation of fast moving dye - logarithmic transformation of concentration is used and this makes area under the first curve easier to measure
◦ Cardiac output calculated by: amount of dye injected / atrea under the graph
‣ the recirculation must be removed
What are the limitations of cardiac output measures
Thermodiltution
- Requires a PAC, invasive with risks associated
- Utilisation of a PAC requires limited regurgitation, intracardiac shunts
- Accurate thermometer
- Technique of injection - speed of injection, volume of injection, end expiratory
- Calibration to body size of both calculation and injection
- Area under the curve requires software accuracy
What factors affect right atrial pressure
◦ Factors which affect right atrial pressure
‣ Intrathoracic pressure (spontaneous vs. positive pressure ventilation)
‣ Pericardial compliance (eg. tamponade, open chest)
‣ Right atrial compliance (eg. infarct, dilatation)
‣ Right atrial contractility (i.e. AF vs sinus rhythm)
‣ Tricuspid valvular competence and resistance
‣ Cardiac cycle phase - during ventricular contraction atrial volume increases and pressure drops
Determinants of veinous resistance
- Posture/gravity
- Muscle pump/intrathroacic pump/intrabaomdinal pump and valves
- Physical obstruction - clot, device, pregnancy
- Hypervisciity
- Autonomic tone and drugs
Draw a steady state vascualr function curve
Demonstrate using a vascular function curve the effect of a change in preload
Demonstrate using a vascular function curve a change in contractility
Demonstrate using a cardiac function curve the effect of afterload
What is CVP
filling pressure of the right heart; venous intravascular blood pressure measured at or near the RA relative to atmospheric pressure
Where is the CVP on the vascular function curve?
◦ Physiological defined as interesection of the vascular function curve and cardiac output curve
What determines CVP
Cardiac output/veinous return
MSFP
Central veinous compliance
- Right atrial pressure
- Pericardial compliance
- Ventricular compliance - lusitrophy, HR, stiffness
Atrial kick
Intrathoracic pressure
Draw a CVP trace and compare it to an ECG
Measurement of CVP occurs at what part of the CVP trace? At what time in the respiratory cycle?
C wave
End expiration
What is the technique of measuring CVP
- It is measured using a pressure transducer connected to a central line via incompressible tubing, with the transducer zeroed to atmoospheric pressure and levelled at the height of the right atrium
Why is end expiration the time to measure CVP
When is transmural pressure ein the atrium zero i.e. when is RAP = transmural pressure = when thoracic pressure is zero which is at end expiration
How does PEEP influence CVP measurement
- Recorded at the end of expiration - as you are measuring atmosphere vs central line pressure - however actual presure you are interested in is the transmural pressure (RAP vs intrathoracic) and intravsacular pressure will be equal to transmural pressure when thoracic pressure is zero (i.e. end expiration) - if you have PEEP this will never be zero - about half of the PEEP is transmitted 10mmHg of PEEP = 3mmHg of CVP rise (stiff lungs = less transmission of PEEP)
How does common iliac pressure compare to CVP
- CVC in proximal SVC (common iliac pressure within 1mmHg of RAP when supine) - the actual position doesn’t matter too much, the transducer site does
WHat position is CVP measured in? Why does levelling matter
- Transducer zeroed at the right atrium:
◦ 4th intercostal space
◦ midaxillary line
◦ 45 degrees head up generally - This is important as the tricuspid valve is the only site with minimal variations in pressure (<2mmHg) with position
What factors can reduce accuracy of CVP trace
- Equipment
- Levelled to wrong position
- Compressible tubing, bubbles, clots, calibration, zeroing - Patient
- High PEEP
- TR
- CVC position - Artifact
- Patient moving
- INfusions through the lumen
A wave on a CVP trace means? When is it not present
◦ a is for atrium… this is the right atrial contraction.
◦ It correlates with the P wave on the ECG.
◦ It disappears with atrial fibrillation
When do you get large A waves
◦ Cannon a waves - junctional rhythm and pacing, atrial contraction simulatneous with ventricular contraction so fusion of A and C waves.
‣ retrograde conduction of ventricular depolarisation:
* ventricular tachycardia
* junctional rhythm
* ventricular pacing
‣ Asynchronous atrial activity
* complete heart block
* accidental reversal of atrial and ventricular pacing wires
◦ Prominent a waves seen in tricuspid stenosis or reduced right ventricular compliance (pulmonary stenosis or hypertension)
C wave in CVP trace is? Correlates with cardiac cycle when? Why would it be large?
◦ c is for cusp… this is the cusp of the tricuspid valve, protruding backwards through the atrium, as the right ventricle begins to contract.
◦ It correlates with the end of the QRS complex on the ECG
◦ Regurgitant CV waves in tricuspid regurgitation - normal X descent pbliterated
X decent on the CVP trace correlates with
◦ This is the movement of the right ventricle, which descends as it contracts
‣ The downward movement decreases the pressure in the right atrium. At this stage, there is also atrial diastolic relaxation, which further decreases the right atrial pressure.
◦ It happens before the T wave on the ECG
V wave on the CVP trace correaltes with what in the cardiac cycle? What ECG feature does it corrrelate with? Why would it be large>
◦ As blood fills the right atrium, it hits the tricuspid valve and this is the back-pressure wave
◦ It happens after the T wave on the ECG
◦ It also gives an impression of tricuspid competence.
◦ A huge V wave is suggestive of tricuspid regurgitation, as it represents blood flowing back out of the contracting right ventricle; in this situation the V wave would be the most prominent wave, and would reach right ventricular systolic pressure ( ~ 30mmHg)
What is the y descent on a CVP trace?
◦ This is a pressure decrease caused by the tricuspid valve opening in early ventricular diastole.
◦ This happens before the P wave of the ECG
◦ A loss of y-descent suggests tamponade; it means there is restriction to right ventricular filling.
What happens to the cardiac function curve on a vascular function curve at higher RA pressures? Why ?
◦ As contractility increases, the curve shifts up
◦ A plateau is seen with higher RA pressures - Plateau beings around RAP 4mmHg - with an intact SNS, in humans and on inotropes this would be much higher
◦ Resembles the Frank Starling relationship except RAP instead of EDV; and cardiac output instead of SV
◦ X axis intersection at approx -2 RAP - based on animal data
◦ Linear portion across lower range of RAP - range of preload values the ventricle finds acceptable
Why does the vascular function curve have a plateau? Where does this plateau start?
◦ Crosses the x-axis at the mean systemic filling pressure - where there is no pressure gradient
◦ A plateau is seen with right atrial pressure below 0 mmHg - or 20% above that pressure found at a RAP of zero as extrathoracic veins collapse and behave as starlings resistors (pressure in extrathoracic veins cannot be decreased below -4mmHg) and venous resistance increases with deforming
◦ There is a linear relatonship between reducing RAP and venous return
◦ There is a rightward shift of the vascular function curve in respons eto increased MSFP at all pressures - a 15% increase in BV will double MSFP; and a 15% decrease will reduce it to zero
What are the flaws in the vascular function curve model of cardiac function
- MSFP
- Of questionalble utility as a pressure to model behaviour on, the gradient is more likely useful between RA and MAP - Prediction
- Does not predict what happens on the flat volume overload part fo the curve where RAP and MSFP can continue increasing without change in cardiac output
- Multiple variable often change at once - Factors not accounted for
- Windkessel effect, inertia, arterial compliance
