24A03: Exam Report
The systemic vascular resistance is suddenly increased, describe the consequences for the otherwise healthy left ventricle
11% of candidates passed this question.
This question was specific to the left ventricle only. Good answers provided information on immediate changes in LV Volumes and Pressures and how compensatory mechanisms largely within the LV itself eventually lead to restoration of stroke volume.
Marks were allocated for a description of the Frank Starling mechanism, baroreceptor reflex and anrep effect.
Good answers also discussed the effect of increased SVR on LV myocardial work and oxygen consumption and coronary perfusion.
Common errors included focusing on definitions and determinants of SVR and providing LV PV loops without relating this to the situation of an increased SVR or without adequately labelling or explaining what they were demonstrating with the graph.
This question required the integration of a number of physiological principles and is challenging.
G3iii / 24A03: The systemic vascular resistance is suddenly increased, describe the consequences for the otherwise healthy left ventricle
Afterload
SVR can be defined using Darcy’s law
- R = ΔP / Q
- R is resistance
- DP is pressure gradient
- Q is flow
SVR is the resistance (pressure drop) generated in blood flowing through the systemic arterial circulation
- SVR = (Mean aortic pressure – RAP) / CO
Therefore an increase in SVR will result in an immediate reduction in CO
Immediate Changes in the LV to restore CO are outlined
Category
Effect
LVESP & Volume
- ↓Stroke volume
- ↑ Left ventricular end systolic pressure
- ↑ Left ventricular end systolic volume
LVEDP & Volume
- ↑ Left ventricular end systolic volume
- + Venous return
- ↑ Left ventricular end diastolic volume (ie ↑ preL)
- ↑ Left ventricular end diastolic pressure
- Activates Frank-Starling mechanism
- Partial compensation for reduced SV from ↑ AfterL
Contractility
- Anrep Effect: sustained ↑ sarcomere stretch
- ↑Ca release
- Small ↑ contractility to compensate
- Reflex ↑sympathetic tone
- ↑ contractility
Work & O2 Consumption
- ↑Active tension (at constant PreL & Contractility)
- ↑wall stress = ↑ myocardial work
- ↑Myocardial O2 consumption
Coronary Perfusion Pressure & Coronary Blood Flow
- CPP = Aortic Diastolic Pressure – LVEDP
- ↑afterL
- ↑LVEDP
- ↓CPP
CPP is based on diastolic pressure because the LV myocardium is perfused in diastole
Coronary Blood Flow
- MYOGENIC Autoregulation: ↑transmural pressure → ↑resistance in proportion to pressure → constant flow
- METABOLIC Autoregulation: ↑metabolic demand → ↑production of metabolites (eg. Lactate and adenosine) → vasodilation of coronary arterioles
Frank-Starling Mechanism
- Sarcomere = the basic unit of striated muscle
- Normal sarcomere length = 1.8µm
- ↑sarcomere length = ↑force generated
- ↑preL/EDV = ↑SV
- This happens up to a point → 2.2µm, where any further ↑sarcomere length = detrimental to force generated
This is an intrinsic property of heart that allows it to rapidly adapt to ∆ volumes of venous return
Baroreceptor Reflex
Baroreceptor Response
- ↓arterial BP 2° ↑afterL
- ↓afferent firing by BaroR
- NTs release symp inhibition → ↑ & ↓ Outflow
- Heart = ↑HR, SV
- Resistance Vessels = VC
- Capacitance Vessels = VC = ↑VR
Anrep Effect
- Mechanism of cardiac compensation due to an increase in end systolic volume & reduced SV brought on by an increase in SVR
- Sustained myocardial stretch (higher end systolic volume)
- Activation of tension-dependant Na/H exchangers
- Increased [Na] in sarcolemma
- Stops activity of Na+-Ca++ exchanger
- Increase [Ca++] in sarcolemma