How do heart rate, preload, afterload, and contractility affect cardiac output and cardiac workload?
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Get Help Now!How do the clinical features of the coronary heart disease syndromes differ?
How do valvular disorders alter cardiac pressure dynamics and workload?
How do the compensatory responses triggered in CHF work to restore cardiac output?
What is the clinical significance, characteristic electrocardiographic features, and usual treatment of each of the common cardiac dysrhythmias?
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Let’s firstly define cardiac output and cardiac workload.
Cardiac output is the volume of blood being pumped out by the heart per minute while cardiac workload refers to the amount the heart has to increase overall activity in order to meet systemic (and its own) needs.
Heart rate increases cardiac output, naturally, as more blood can be pumped per unit time. Heart rate changes in response to changes in cardiac workload – it increases when workload increases.
Preload is the volume at the end of diastole, when the ventricles have finished filling. A higher preload refers to more blood inside the ventricles, and can likewise increase cardiac output and be increased by workload. Afterload is the volume left after systole, prior to relaxation – the volume of blood left over. A lower afterload means a higher output, and also correlates with higher workload.
Contractility is loosely defined as how well the heart muscles actually contract, and the heart is capable of contracting harder (which is what leads to lower afterload) in response to higher cardiac workload. As a result, higher contractility = higher output.
I presume the differences in clinical features you’re looking for are between different areas of infarct. All are accompanied by crushing …
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