FRCA Cardiac Output (Measurements (Non-invasive (Bioimpedence, MRI, TTE),…
Amount of blood pumped out by heart per unit time
CO = SV x HR
Vol blood pumped out per contraction
Contractility: Intrinsic ability of myocytes to generate force at given preload and afterload
Surrogate: rate of change of pressure (gradient) during isovolumetric phase of cardiac cycle
Factors affecting contractility
Sympathetic nervous system
LV wall stress during ejection
Related to force opposing sarcomere shortening
SVR and MAP: LV afterload
PVR: RV afterload
Factors affecting afterload
Vessel tone: constriction or dilation
Blood viscosity: increased viscosity increases afterload
End diastolic myocardial wall tension
Related to diastolic length of myocytes
EDVol or EDPres
CVP: indication of RV preload as it affects RVEDV
PCWP: indication of LV preload as it affects LVEDV
Factors affecting venous return
Respiratory (abdo-thoracic) pump
SA node activity modulated by ANS
Denervated heart 100-120bpm
At rest, tonic vagal nerve activity via ACh to reduce resting HR: 60-70bpm
Tachycardia increases CO:
With exercise, PNS withdrawn and SNS activated.
Over 150 bpm, diastolic time ~0.15s, causes reduced filling so decreased SV
Intrinsic autoregulatory phenomenon where tachycardia leads to increased contractility.
Increased Ca2+ influx during systole, with increased influx of Na+. Na/Ca exchanger is overwhelmed so accumulation of intracellular Ca2+ and thus positive inotropy
Minimally invasive: Oesophageal
USS beams at 45deg angle to descending aorta to reflect off RBC.
Flow = velocity x cross sectional area (based on demographics)
Assume 70% SV passes through descending aorta.
Disadvantages: poorly tolerated in awake patients. Movement artifacts, surgical diathermy interferences, based on estimation of cross section area, cannot be used in pharyngo-oesophageal pathology e.g. varices
SV, HR, CO
Stroke distance (SD): AUC velocity-time. Distance a column of blood moves along aorta per beat
Peak Velocity (PV): during systole. Reflects LV contractility. Alters with age. 90-120cm/s at 20yo, 50-80cm/s at 70yo
Flow-time corrected (FTc): duration of blood flow corrected for HR. normally 330-360 ms.
Low FTc suggests hypovolaemia and increased afterload.
High FTc suggests vasodilatation
Simpson's biplane method:
EDV and ESV based on planes in 4 chamber and 2 chamber views
Doppler and measured cross sectional area
Mechanical and structural heart defects
uptake or excretion of a substance by an organ is equal to the difference between amount entering and leaving organ
CO passes through lungs FIck principle applies.
CaO2 = Arterial O2 (proportional to partial pressure)
CvO2 = mixed venous sample from PAC (SvO2)
VO2 = patient breathes from spirometer with 100% O2 and CO2 absorber. After 1 min, volume of O2 remaining allows of calculation of uptake
10-15ml cold saline injected through proximal lumen of PAC (RA). Temperature change at distal tip in PA is measured.
Use modified Stewart-Hamilton equation
: Indicator dye (indocyanine green or lithium) injected into PAC then sampled at peripheral arterial line.
Pulse contour analysis:
Pulse contour cardiac output (PiCCO):
Standard CVC and thermistor-tipped arterial line.
Calibrated by thermodilution. Some heat dissipated through lungs.
e.g. Edwards VolumeView
Lithium dilution CO (LiDCO):
Requires only standard arterial line.
Lithium dilution using peripheral or central vein. Avoids heat dissipation of thermodilution.
NMBs may cross-react with lithium electrode. avoid in patients taking lithium
Specialised pressure sensor on standard arterial line. Estimates aortic vascular compliance based on demographics
Same algorithm as LiDCO, but using normograms based on demographics
Coronary Blood flow.
5% of CO (250ml/min)
Factors affecting CBF
Systemic & Metabolic:
Hypoxia causes vasodilatation (directly or via adenosine)
Other vasodilatory factors: CO2, K, H+, NO
Patency and atheromas/thrombus
Coronary perfusion pressure: Determined by difference between aortic pressure and LVEDP.
Autoregulation between 60 - 180 mmHg systolic
PNS - weak vasodilatory effect of coronary arterioles
Extrinsic compression by myocardium during contraction (LV>RV)
Diastolic time: inversely related to HR
SNS: increase CBF by increased O2 demand from inotropy and chronotropy