Discussion
This case interested us due to the combination of bradycardia and a hypertensive emergency that was refractory to medical treatments. BP markedly improved following treatment of CHB with permanent pacemaker implantation. A summary of BP readings during the clinical course are shown in figure 3. It was interesting to note that the lowest diastolic BP before pacing was 51 mmHg and immediately rose after initiation of pacing to 80 mmHg. Pulse pressure before pacing was between 100-140 mmHg and after pacing fell to around 50 mmHg. We suspected this was a direct effect of increasing HR, shortening the diastolic period and limiting the fall in arterial pressure before the next cardiac cycle. We confirmed before pacing that the large pulse pressure did not have an alternative cause such as aortic regurgitation.
Systolic BP also decreased by 20 mmHg following device implantation without the need to restart the GTN infusion and even once the effects of sedation had worn off. A combination of factors may have played a part however the contrast was striking. Whilst it proved impossible to wean off GTN prior to pacing, it was no longer required at all afterwards. The reduction in diastolic filling time could have reduced ventricular preload and stroke volume (SV) to some extent, but it is difficult to say how much this contributed to the reduction of systolic BP.
BP is a function of cardiac output (CO) calculated by the formula CO = HR x SV. A lower HR should therefore reduce CO, but this is mitigated by a rise in SV due to increased diastolic filling time and ventricular preload. Historically, it has been described that as HR slows, pulse pressure widens i.e. diastolic BP drops and systolic BP increases.[2,3] The haemodynamic effects of artificial pacing in CHB have also been described, suggesting that increasing HR lowers SV.[4] Conversely, SV has been shown to increase on induction of CHB in the animal model.[5]
RV pacing may directly affect SV by induction of dyssynchronous myocardial contraction. Prior to pacing in this case, the escape rhythm was junctional in nature, hence LV activation will have been via the normal His-Purkinje system. Change in the pattern of regional myocardial strain by pacing has been demonstrated in dogs by MRI imaging. SV was significantly reduced by RV apical pacing due to dyssynchronous LV myocardial contraction.[6] Another study looking at lengthening AV delay during pacing showed an immediate increase in both SV and BP. However, BP quickly declined after a few seconds whilst SV was maintained, suggesting compensatory peripheral vasodilatation.[7] Artificial pacing algorithms to shorten AV delay have been proposed as a treatment for hypertension, however this has so far remained restricted to clinical studies.[8,9]
BP is also dependent on systemic vascular resistance (SVR) under autonomic control via baroreceptors. Cardiogenic shock induces a sympathetic response to compensate with peripheral vasoconstriction and increases SVR acutely.[10] Chronically raised SVR may have played a role in this case with evidence of longstanding hypertension, echocardiography revealing moderate concentric LV hypertrophy and there was heavy proteinuria. SVR is also known to increase with advanced age associated with atherosclerosis.[11,12] Higher SVR may have exaggerated the BP response to increased SV.
We noted only one previous case report of bradycardia and malignant hypertension. A case of a 65-year-old man presenting with left upper limb weakness, bilateral foot paraesthesia and headache with a BP of 240/90 and an ECG showing CHB at 39 bpm. Brain imaging was normal, and symptoms resolved after BP control with intravenous GTN. After permanent pacing BP improved to 140/80. The authors attributed better BP control to reduced diastolic filling time and SV.[13]
In hindsight, pacemaker implantation was unduly delayed due to a combination of inter-speciality logistics and lab availability. Greater efforts to enable earlier pacemaker implantation may have led to sooner control of BP and shorter hospital stay, and this is a learning point. We could also make mention of alternative pacing sites such as RV outflow tract, RV septum or His bundle pacing which may have preserved more physiological ventricular contraction, and although the haemodynamic effects have been studied with relation to intracardiac function, the effect in this context on systemic BP needs further study.[14]