FRCA
Cardiac Output
Amount of blood pumped out by heart per unit time
CO = SV x HR
Stroke Volume:
Vol blood pumped out per contraction
Heart Rate:
SA node activity modulated by ANS
Contractility: Intrinsic ability of myocytes to generate force at given preload and afterload
Afterload:
LV wall stress during ejection
Related to force opposing sarcomere shortening
Preload:
End diastolic myocardial wall tension
Related to diastolic length of myocytes
Measurements
Minimally invasive: Oesophageal
Non-invasive
Invasive
Surrogate:
EDVol or EDPres
CVP: indication of RV preload as it affects RVEDV
PCWP: indication of LV preload as it affects LVEDV
Surrogate: rate of change of pressure (gradient) during isovolumetric phase of cardiac cycle
SVR and MAP: LV afterload
PVR: RV afterload
Factors affecting venous return
Skeletal pump
Body position
Cardiac pump
Respiratory (abdo-thoracic) pump
Venous pressure
Valves
Factors affecting contractility
Tachycardia
Drugs
Sympathetic nervous system
Disease states
Anaesthesia/Surgery
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With exercise, PNS withdrawn and SNS activated.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
Bowditch effect:
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
Factors affecting afterload
Vessel tone: constriction or dilation
Blood viscosity: increased viscosity increases afterload
Fick principle:
uptake or excretion of a substance by an organ is equal to the difference between amount entering and leaving organ
Pulse contour analysis: computer-based algorithm
Bioimpedence
MRI
TTE
Direct Fick: 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
Thermodilution: 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
Dye dilution: Indicator dye (indocyanine green or lithium) injected into PAC then sampled at peripheral arterial line.
Calibrated
Uncalibrated
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
FloTrac/Vigileo:
Specialised pressure sensor on standard arterial line. Estimates aortic vascular compliance based on demographics
LiDCORapid:
Same algorithm as LiDCO, but using normograms based on demographics
Oesophageal doppler:
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
TOE
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
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
Luminal:
- Patency and atheromas/thrombus
- Coronary perfusion pressure: Determined by difference between aortic pressure and LVEDP.
- Autoregulation between 60 - 180 mmHg systolic
Mural:
- PNS - weak vasodilatory effect of coronary arterioles
Extra mural:
- 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