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With exercise, PNS withdrawn and SNS activated.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:

  1. Hypoxia causes vasodilatation (directly or via adenosine)
  2. Other vasodilatory factors: CO2, K, H+, NO

Luminal:

  1. Patency and atheromas/thrombus
  2. Coronary perfusion pressure: Determined by difference between aortic pressure and LVEDP.
  3. Autoregulation between 60 - 180 mmHg systolic

Mural:

  1. PNS - weak vasodilatory effect of coronary arterioles

Extra mural:

  1. Extrinsic compression by myocardium during contraction (LV>RV)
  2. Diastolic time: inversely related to HR
  3. SNS: increase CBF by increased O2 demand from inotropy and chronotropy