G3iii / 23B17: Describe the consequences for the left ventricle of a sudden and sustained increase in afterload
23B17: Exam Report
Describe the consequences for the left ventricle of a sudden and sustained increase in afterload
7% of candidates passed this question.
This question expected a detailed description of the effect of afterload on the left ventricle.
This should cover the acute effect of increased afterload on left ventricular end systolic (and diastolic) pressure and volume, contractility, work and oxygen consumption, coronary perfusion pressure and baroreceptor responses.
“Sustained” implied more longer term left ventricular exposure which would include the ventricular cellular response, concentric hypertrophy and the subsequent effects on diastolic and elevations of left atrial pressure.
Definitions of afterload, cardiac output equations, vascular function curves and LV/PV loops are not required if the above concepts are described in adequate detail.
The use of a diagram can assist in explaining concepts however should be linked back to the question in order to demonstrate the candidates understanding of the question being asked.
G3iii / 23B17: Describe the consequences for the left ventricle of a sudden and sustained increase in afterload
Afterload
Afterload = The sum of all factors required to overcome so that blood may be ejected from the heart to the arterial circulation.
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
SUSTAINED
Category
Effect
Ventricular Cellular Response
- ↑ mass of muscle fibres or wall thickness serves initially as a compensatory mechanism that helps to maintain contractile forces to offset the increased ventricular wall stress
Concentric Hypertrophy
- Myocytes terminally differentiate after birth
- Ratio of LV mass (g) : Body weight (kg) remains constant (4:1) throughout life
- Myocyte replication is limited so any growth occurs through physiological hypertrophy
- ↑afterload causes hypertrophy of LV myocardial mass (can start after just 6hrs of sustained LV pressure overload)
- ↑LV pressure
- ↑ systolic wall stress
- via genetic pathways, sarcomeres added to each myocyte in parallel = ↑myocyte thickness
- Myocardial hypertrophy = ↑myocardial O2 demand
- Myofiber growth > capillary network
- ↑myocardial pressure
- = reduces subendocardial flow
- = increase myocardial work + increases O2 demand
- Impaired vasomotor response to hypoxia in hypertrophied tissue
Diastolic Pressures & Lap
- Resulting fibrosis causes increase in diastolic ventricular pressures
- Increase in left atrial pressure (and filling pressures)