What is the significance of Heart Rate?
The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia.
The amount of blood pumped from the heart per minute is the cardiac output. It is determined by the volume pumped in each cycle, the stroke volume (end diastolic volume minus the end systolic volume) and the frequency of the cycles, the heart rate.
The ability of the heart to both receive and eject blood is a fundamental function of heart rate. Firstly if the rate is excessive, then the heart is unable to either fill or eject efficiently. If, for any reason the stroke volume falls, the heart is able to compensate by increasing the heart rate. The filling of the left ventricle is not just determined by the venous return, 30% of filling is derived from the “atrial kick”, which is lost in atrial fibrillation. In some circumstances, the stroke volume is fixed, such as in mitral and aortic stenosis and in infancy, the cardiac output is rate dependent.
If baby’s, who normally have a fast heart rate, become bradycardic, then their cardiac output (and thus their blood pressure) falls. Patients who have permanent pacemakers behave in an opposite manner: if their stroke volume falls, they are unable to increase their heart rate to compensate.
Hypotension and bradycardia is characteristic of excessive vagal activity. Cholinergic agents (particularly anticholinesterases such as neostigmine) will mimic vagotonicity. Other drugs may excessively slow nodal conduction - beta blockers, calcium channel blockers, digoxin etc.
Hypotension may be the “egg, not the chicken” - it follow an excessively slow or fast heart rate. Complete heart block may cause hypotension, particularly in the non compliant left ventricle. Tachyarrhythmias will reduce filling time and curtail stroke volume
The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia.
The amount of blood pumped from the heart per minute is the cardiac output. It is determined by the volume pumped in each cycle, the stroke volume (end diastolic volume minus the end systolic volume) and the frequency of the cycles, the heart rate.
The ability of the heart to both receive and eject blood is a fundamental function of heart rate. Firstly if the rate is excessive, then the heart is unable to either fill or eject efficiently. If, for any reason the stroke volume falls, the heart is able to compensate by increasing the heart rate. The filling of the left ventricle is not just determined by the venous return, 30% of filling is derived from the “atrial kick”, which is lost in atrial fibrillation. In some circumstances, the stroke volume is fixed, such as in mitral and aortic stenosis and in infancy, the cardiac output is rate dependent.
If baby’s, who normally have a fast heart rate, become bradycardic, then their cardiac output (and thus their blood pressure) falls. Patients who have permanent pacemakers behave in an opposite manner: if their stroke volume falls, they are unable to increase their heart rate to compensate.
Hypotension and bradycardia is characteristic of excessive vagal activity. Cholinergic agents (particularly anticholinesterases such as neostigmine) will mimic vagotonicity. Other drugs may excessively slow nodal conduction - beta blockers, calcium channel blockers, digoxin etc.
Hypotension may be the “egg, not the chicken” - it follow an excessively slow or fast heart rate. Complete heart block may cause hypotension, particularly in the non compliant left ventricle. Tachyarrhythmias will reduce filling time and curtail stroke volume
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