Cardiovascular - Cardiac output and its measurement Flashcards
What three factors determine SV
Preload
Myocardial contractility
Afterload
Define preload and what is the Frank Starling effect
Preload is defined as the end diastolic volume. This is the volume that produces the initial stretch of the myocardium prior to its contraction.
An increase in preload increases the end diastolic volume which increases the end diastolic fibre length of the ventricular muscle. This increases the velocity of the muscle shortening for a given afterload and ejects more blood from the ventricle.
Thus for a constant contractility and afterload, increasing the preload, increases the stroke volume. This is known as the Frank Starling effect.
How is preload measured
Impossible to measure sarcomere length in vivo –> surrogate measurements for preload must be used.
- LVEDV (Echocardiography)
- LVEDP (PCWP)
Relationship between EDV and EDP may vary between patients as it depends on ventricular compliance
What does CVP indicate with regard to filling pressures
What does PCWP indicate with regards to filling pressures
CVP - provides an indication of RVEDV
PCWP - provides an indication of LVEDV
Define afterload
This is the force that opposes the contraction (shortening) of cardiac muscle and the ejection of blood from the ventricle. It is the stress in the ventricular wall during ejection
As afterload increases, the rate and extent of cardiac myocyte shortening decreases, resulting in a reduction in stroke volume.
Increasing afterload increases the end systolic ventricular volume LVESV. –> reduction in stroke volume
How is afterload measured
Not easily measured in vivo -> surrogate markers are used
LV afterload: MAP and SVR
RV afterload: PVR
Define myocardial contractility
The intrinsic ability of cardiac myocytes to generate mechanical power at a given preload and aferload.
How is myocardial contractility measured?
Indirectly - measuring the rate of change of pressure (gradient) during isovolumetric contraction phase of the cardiac cycle.
How is cardiac output affected in infants, exercise, pregnancy and Eating
Infants –> increased CO (standardized using TBSA in m2)
Exercise –> CO can increase x 5
Pregnancy –> CO increases 50%
Eating –> CO increases 25%
What is the main influence on CO
Heart rate
CO = HR x SV
HR can increase from 60 to 180 bpm
SV can increase from 70 to 105 ml
What is the baseline HR of a denervated heart and why
100 - 120 bpm –> absent tonic activity of the vagus (PSNS) nerve (elsewhere the SNS is tonically active). Ach is continuously released from PSNS nerve terminals, reducing HR to 60 - 70 bpm through its effect at muscarinic M2 receptors
How is HR increased during exercise
- Vagal tone withdrawn
- Noradrenalin released from SNS nerve terminals
- Adrenalin released from adrenal medulla
NA and A act to increase HR at Beta 1 adrenoreceptors
What ensures that the CO of the right and left ventricles are exactly matched
Frank Starling effect
What four factors affect myocardial contractility
- SNS (beta 1 adrenoreceptors)
- Tachycardia - increased myocardial contractility when HR is high = Bowditch effect
- Drugs
- positive inotropes:
dobutamine, isoprenaline, glucagon, digoxin
- negative inotropes:
BB, CCB, anaesthetic agents - Disease (IHD / Sepsis / electrolyte / Acid-base)
What is the Anrep effect
Increase in afterload –> increase in intrinsic inotropy independent of Frank-Starling effect
