0702- cardiac work and VR and CO coupling- CG Flashcards
Intepret the cardiac PV diagram
Volume is inversely proportional to pressure. On the PV diagram, volume is on X axis, pressure on Y axis. At the end of diastole , volume is at ~120mL, pressure very low. Isovolumetric contraction- pressure shoots up but no change in volume, until the aortic/pulmonary valve open, and volume decreases. Then isovolumetric relaxation - pressure falls back down, then filling occurs again (increased volume)
Taking time into account, anticlockwise circle, with the encircled area being work (external). Area encircled is total PV work done
Energy requirements of cardiac work
Work - pressure difference x volume.
Cardiac work requires approximately 11W of energy in a 70kg man. (only ~10% is used for external work, ie PV work)
Describe the different energy sources from which ATP is produced
All work relies on ATP- comes from oxidative phosphorylation (aerobic, krebs cycle) with fatty acids and carbs as substrate. Glycolysis can briefly compensate for short term lack of aerobic ATP production (anaerobic doesn’t really work).
limiting factor- supply via coronary arteries
short term energy storage via phosphocreatine
What is external and internal work?
External = pressure change x volume AND kinetic work
Internal work= largely heat (can’t be measured), coming from isovolumetric work and turbulent flow (sounds and murmurs) ie not particularly useful, but ~x5-20 times more
Most work needed for ejection phase and isovolumetric phase
What is the hidden cost of internal work?
Energy consumption. To increase CO, need to raise HR and/or SV
Increasing HR is inefficient way of increasing work because lots of energy lost as internal work (due to more systole time = isovolumetric etc) Hence energetically more costly compared to increasing SV. Increasing SV is efficient- more external work done Hence atheletes- low HR, high SV (net CO increase)
(drugs should aim to increase SV via increasing preload and decreasing afterload [HTN])
How venous return is matched with cardiac output
Starling’s Law- SV (hence CO) increases if VR increases (increased filling= increased stroke volume)
Over time VR=CO (flow in veins=flow in arteries)
Does cardiopulmonary reflex (vagal) aid in this?
What is VR determined by?
- PMSF Mean systemic filling pressure=measure of systemic BP when heart is stopped (residual pressure after capillaries, ~7 torr. generated in vessel wall tension (mostly arteries)
- increased by ↓TPM and ↑compliance
- Muscle pumps, including abdominal pressure - intrathoracic pressure (VR higher during inspiration due to negative pressure suction)
- mechanism of valvular plane suction- affect PRA
How is Pmsf modulated
Vasodilation = decreased Mean Systemic Filling Pressure
Neurally- sympathetic stimulation
Pharmacologically- NO Infusion (increase),
bleeding (decrease)
Venous pooling increases MSF Orthostatic- getting up decreases Pmsf temporarily (pools into lower veins= reduced venous return and hence cardiac output). Similarly, lying down increases Pmsf
What are the implications of increasing or decreasing right atrial pressure
Increased RA pressure increases CO but decreases VR
Hence need to balance (best between -4 to 0 mmHg)
Below -4, narrowing of central veins to limit flow into RA (plateau), above 0, decreased VR
MCQ question- E?
Stricker summary
Energetically, preload is “cheap”, afterload and increase in contractility are “expensive”. • Energetically efficient CO has – low HR, – relative large SV and is – predominantly made bigger via SV↑. • VR is determined by – pressure difference between PMSF and PRA, – RV, and – venous compliance (pooling). • CO/VR are influenced by intrapleural pressure