Understanding the role of arterial acceleration as part of pulse wave morphology (either in middle cerebral artery blood flow (MCAv) or in arterial blood pressure(ABP)) inspires new scientific questions. Are there diseases that relate to defects in Sys1 or Sys2? Can cardiac diseases be read from pulse wave morphology? What is the effect of medication on these two systolic waves? Can the claim be substantiated that therapy aimed at changing one or both systolic peaks indeed improves patient outcome? Is it true that providing age corrected Z-scores to the clinician allows for a more rapid and better interpretation of hemodynamic status than arterial blood pressure or cerebral blood flow velocity alone? There are still many gaps in our knowledge that need to be filled!
Physiology
The main idea behind arterial acceleration is that a short-lasting contraction within the conducting arteries spreads as a peristaltic wave along the arterial tree. Effortlessly distributing itself over all the branches because it is based upon a wave of depolarization within the smooth muscle layers of the arterial tree, that can be seen as a syncytium because of the abundant presence of intercellular gap junctions. Arterial acceleration is held responsible for tissue perfusion in all the bodies capillary systems, including those most remote and under least favorable conditions.
Similar to arterial acceleration EDRF (endothelial derived relaxation factor) is also thought to contribute to widespread tissue perfusion at a capillary level. It is likely that these two mechanisms are linked but future research is required to establish how exactly this connection is taking place.
Pathology
Currently, a role for pulse waveform analysis has been shown in a number of disease states.
| In brief | Reference | |
| sepsis | fluid resuscitation brings Sys2 component back in the systolic waveform |
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| intracranial pressure elevation in TBI | best correlation is found between ICP elevation and Sys1-PaR (a ratio of ABP and MCAv) |
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| Carotid endarterectomy | ipsi- and to a lesser degree contralateral MCAv becomes more Sys1 prevalent after successful endarterectomy |
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| CO2-reactivity | Sys1 dominant signal in MCAv during hyperventilation versus Sys2 dominant signal during CO2-retention |
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| aging | Sys1 dominance in the young versus Sys2 dominance in the elderly (observed in MCAv as well as ABP) |
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| orthostatic hypotension | MCAv becomes Sys1 exclusive during tilt table test; Sys2 returns after inflation of anti-shock trousers or when bringing the subject back in supine position |
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| pre syncope | marked discrepancy between increasing Sys1 component in MCAv compared to sharp decrease in ABP |
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Pharmacology
Only preliminary data are available on the effect of certain drugs on the Sys1 or Sys2. These have been entered in the table below. There is a great need in filling this table with additional evidence linking drug administration and dosage to their effect on the systolic waveform. The effect of many anti-hypertensives, inotropics, fluids, etc. still remains to be established.
| Sys1 | Sys2 | D560 | |
| tissue penetration | trend in perfusion pressure | volume reserve | |
| myogenic response to intraluminal pressure pulse | stroke volume versus peripheral resistance | blood volume remaining in arterial capacitance | |
| Arterial Blood Pressure | Sys1 increase | Sys2 increase | Sys1 and Sys2 increase |
| dopamine (preliminary) | norepinephrine (preliminary) | ||
| Sys1 decrease | Sys2 decrease | Sys1 and Sys2 decrease | |
| Cerebral Blood Flow | Sys1 increase | Sys2 increase | Sys1 and Sys2 increase |
| Sys1 decrease | Sys2 decrease | Sys1 and Sys2 decrease | |
Therapeutic strategies
Does monitoring of pulse wave morphology indeed allow better tailored therapies and does it indeed result in a better patient outcome? That is the long term goal of pulse waveform analysis. Is it or can it be proven? And for which subgroup of patients?
| diagnosis | monitoring | treatment | |
| (evaluation of therapy) | (patient outcome) | ||
| ICU | |||
| sepsis |
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| malignant hypertension | |||
| hyperperfusion syndrome | |||
| Internal medicine | |||
| hypertensive emergency | |||
| sickle cell anemia | |||
| autonomic failure | |||
| vascular prevention | |||
| Cardiology | |||
| Aortic stenosis | |||
| Heart failure | |||
| Gynecology | |||
| (pre-)eclampsia | |||
| Neurology | |||
| ICP elevation | |||
| hemodynamics stroke or TIA | |||
| optimizing blood pressure after ICH | |||
| Neurosurgery | |||
| Subarachnoid hemorrhage | |||
| ICP-elevation in traumatic brain injury |
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| Vascular surgery | |||
| Carotid endarterectomy |
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| Nephrology | |||
| General medicine | |||
| Monitoring and treatment of hypertension | |||