Control of cardiac output Flashcards
What are the basic elements of cardiac control?
Primary aim is to deliver oxygen (DO2) to the tissues at an adequate perfusion pressure (PP).
The amount of oxygenated bloods circulated depends on the arterial O2 content (CaO2) and the CO.
CO=HR x SV
PP= CO x PVR (peripheral vascular resistance)
Stroke volume determined by: preload, contractility and afterload.
Where is the end diastolic point on the pressure-Volume loop?
PV loop describes the mechanical performance of the heart.
EDP- the cycle starts at the EDP when the ventricle has received the blood volume from the atrium.
The Vent volume is high and the pressure is low.
Where is the isovolumetric contraction part of the pressure-volume loop?
Pressure within the ventricle rises without any change in volume.
Begins with closure of the AV valve (mitral valve in the case of the LV) and ends with the opening of the semilunar valve (aortic for LV).
This means that during this phase both valves remain closed.
What/ where is the ejection phase of the pressure-volume loop?
During this phase the ventricle pumps blood into the major blood vessel. Passes the top of the loop from right to left.
Begins with the opening of the semilunar valve and ends with its closure at the end systolic point.
What happens during isovolumetric relaxation on the pressure volume loop?
Represented by the vertical descending segment of the loop.
There is a fall in intraventricular pressure without a change in volume.
Ends with the opening of the atrioventricular valve.
Where is systole on the pressure-volume loop?
Consists of isovolumetric contraction and the ejection phase.
Where is diastole on the pressure-volume loop?
The diastole consists of isovolumetric relaxation and ventricular filling. Ventricular filling is further consists of three phases:
Rapid ventricular filling
Slow ventricular filling (diastasis), and
Atrial contraction
How does the pressure-volume loop derive parameters reflecting ventricular function?
- Stroke volume = End diastolic volume - end systolic volume
- Stroke work = area in the loop (volume x pressure)
- End diastolic volume = Total volume ventricle fills to before systole (before isovolumetric contraction starts)
- End systolic volume = total volume in ventricle once ejection phase ends.
What is the end diastolic pressure-volume relationship (EDPVR)?
The end diastolic pressure-volume relationship (EDPVR) records the volume and pressure at the end of diastole.
If PV loops are plotted at different volumes for a given ventricle, different EDPs are obtained (Fig 1a). These points form a PV relationship for the ventricle at end diastole when plotted. This is called the end diastolic PV relationship.
The gradient of EDPVR (Fig 1b) represent the elastance of a ventricle during filling. For a compliant ventricle the EDPVR gradient is approximately linear over the normal range of ventricular filling volumes. The steeper gradient is representative of poorly compliant ventricles during ventricle filling.
Can you think of any pathological conditions where EDPVR curve shifts up and to the left?
Pathological conditions which cause ventricular diastolic dysfunction such as ischaemia and ventricular hypertrophy shift the EDPVR curve up and to the left.
What is the end systolic pressure-volume relationship (ESPVR)?
The end systolic pressure-volume relationship (ESPVR) (Fig 1a) is obtained in a similar fashion to EDPVR (Fig 1b).
Here ESP, instead of EDP, points from different PV loops form the PV relationship for the ventricle at the end of systole. The gradient of the ESPVR curve represents the elastance of the ventricle at the end of systole. A change in gradient represents poor or better contractile function of the ventricle.
Can you think of any pathological conditions where the ESPVR curve shifts upwards and to the left?
Sympathetic stimulation and use of positive inotropic drugs shifts the ESPVR curve upwards and to the left.
Can you think of any pathological conditions where the ESPVR curve shifts downwards and to the right?
Negative inotropic drugs (β blockers) and inhalational anaesthetic agents shift the ESPVR curve downwards and to the right.
How does the Frank-Starling curve explain the intrinsic ability of the heart to change its contractility according to the continuously changing venous return?
In an isolated muscle fibre, tension developed on contraction is dependent on the initial length of the fibre. As the initial fibre length increases from fibre length at resting value, the tension developed during contraction increases and reaches a maximum. After this point tension declines despite any further increase in fibre length. This applies to both skeletal and cardiac muscles, although cardiac muscle is more sensitive to such stretch.
The Frank-Starling Law states that:
The contractile force of a cardiac muscle fibre is proportional to the initial fibre length
What is the Frank-Starling curve also known as?
The ventricular function curve
What are common examples on the x axis of the FS curve/VF curve?
In reality they all are same as they all use an index of resting fibre length. Examples on the x axis include:
Central venous pressure (CVP)
Right ventricular end diastolic pressure (RVEDP)
Left ventricular end diastolic pressure (LVEDP)
Right ventricular end diastolic volume (RVEDV)
Left ventricular end diastolic volume (LVEDV)
What are common examples on the y axis of the FS curve/VF curve?
Similarly, on the y axis an index of contractility is used. Examples include:
Stroke volume (SV)
Stroke work (SW)
Right ventricular end systolic pressure (RVESP)
Left ventricular end systolic pressure (LVESP)
What is the effect of a fluid challenge on the Frank-Starling curve?
For an empty cardiovascular system (CVS) the heart contractility is represented on the left ascending side of the ventricular function curve. The fluid challenge not only provides the volume available to improve the stroke volume but also increases the contractility by increasing the end diastolic volume, or resting muscle fibre length.
How does cardiac failure alter the ventricular function?
With cardiac failure the heart is pathologically dilated or the muscle fibres are overstretched, and ventricular function shifts to the right descending portion of the Frank-Starling curve.
Intravenous fluid therapy in such patients worsens the contractility and so SV decreases. This, along with the added intravenous fluid, causes the congestion in pulmonary and systemic circulation, depending on which ventricle fails.
What is the effect of ventricular contractility on the Frank-Starling curve?
For a given CVP (initial fibre length) the increase or decrease in contractility subsequently increases or decreases the stroke volume (tension developed) provided afterload also remains unchanged.
Fig 1 represents the Frank-Starling curves of a normal heart in different circumstances. The middle curve shows normal contractility, while top and bottom curves show increased and decreased contractility respectively. CVP is the same at point a, b and c, but stroke volume varies due to different contractile states.
What is Laplace’s law and how does it apply to the human heart?
In a living human it is not practically possible to measure the resting fibre length and tension developed in the ventricular wall.
CVP, EDV and EDP are all related to resting fibre length so they are used as an indirect index of resting fibre length on the x-axis of the ventricular function curve. A well-filled ventricle has increased resting fibre length as represented by higher CVP, EDV and EDP.
Similarly, it is not practically possible to measure the tension developed in cardiac fibre during the ventricular contraction. Based on Laplace’s law an indirect index of tension has been suggested.
Laplace’s law formula:
Laplace’s law relates tension, i.e. wall stress, to internal pressure in an elastic sphere by the following formula.
P= 2Th/r
P= Internal pressure
T= Tension (wall stress)
h= wall thickness
r= radius of sphere
Intraventricular pressure (P) ∝ tension (T)
So intraventricular pressure (RVESP, LVESP) can be used as an indirect index of tension on the y-axis of ventricular function curve.
How does Laplace’s law apply to different ventricular states?
Remember that P=2Th/r
(h= wall thickness, r = radius of ventricle sphere)
If P is constant then T is proportional to r/h
This means that for the same value of P, i.e intraventricular pressure, ventricular wall tension in a hypertrophic ventricle is smaller as compared to ventricular wall tension in a dilated ventricle (Fig 1).
Or in other words, a hypertrophic ventricle needs to generate less tension as compared to a dilated ventricle to create the same pressure.
Increased wall tension means higher oxygen consumption by the ventricles