“Blood carbon dioxide levels, [PCO2], are responsible for hypertension during acute respiratory failure, in this study.

…..perhaps as a result of enhanced sympatho-adrenergic activity.”

Perhaps? Perhaps? C’mon now. Of course [hidden ] respiratory insufficiency WILL indeed cause enhanced sympathy-adrenergic activity!!!! Hypercapnia is known to raise blood pressure. Doctors have simply not thought to measure either indirect measures like respiratory rate, mental status and minute ventilation [look at our other blogposts] or noninvasive measures of PCO2 [see our last blogpost] or even invasive measures [ABG’s- arterial blood gases] in so called “essential hypertension” or any organ failure [eg. heart failure] or in seriously debilitating mental illnesses [such as major depression or manic depressive insanity] or any prolonged delirium or dementia. …. Yet with modern 21st century supportive medical care, PCO2 can be restored to more normal levels and so this form of hypertension can be treated, as can any syndrome affecting baseline mental status due to CO2 retention.

Abstract

Purpose: To investigate the effects of hypoxemia, hypercapnia, and cardiovascular hormones (norepinephrine, endothelin-1, and atrial natriuretic factor) on blood pressure during acute respiratory failure.

Patients and methods: Patients with chronic obstructive pulmonary disease and acute respiratory failure were divided into four groups of 10 patients each: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, and normoxemia-hypercapnia. Plasma norepinephrine levels were determined by high-performance liquid chromatography with electrochemical detection. Plasma endothelin-1 and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction.

Results:….. Systolic blood pressure and cardiovascular hormone levels were greater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183+/-31 mm Hg and the mean norepinephrine level was 494+/-107 pg/mL, as compared with 150+/- 6 mm Hg and 243+/-58 pg/mL in those with normocapnia and hypoxemia (both P<0.05). Similar results were seen for endothelin-1 and atrial natriuretic factor levels, and for the comparisons of hypoxemic patients who were hypercapnic with those who were normocapnic.

Conclusions: These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respiratory failure, perhaps as a result of enhanced sympatho-adrenergic activity.“  2000 Dec 1;109(8):621-7. doi: 10.1016/s0002-9343(00)00608-2. Mechanisms of hypertension in patients with chronic obstructive pulmonary disease and acute respiratory failure F Fontana ¹, P Bernardi, L Tartuferi, S Boschi, R De Iasio, E Merlo Pich

Dr Emile Kraepelin knew this.

We know this [and we are not doctors or scientist…..we have just sought to explain the seminal case of Paula].

“Seminal works, sometimes called pivotal or landmark studies, are articles that initially presented an idea of great importance or influence within a particular discipline. … Identifying seminal articles relies heavily on your own thoroughness in the examination and synthesis of the scholarly literature.” Finding Seminal Works – Research Process – LibGuides at …

Just in case you are still unclear of how seminal these findings are!

We have been discussing this for twenty years.

Kraepelin discussed respiratory defects [hidden unless respiratory rate is counted at rest] during most of his career.

C’mon now.

Wake up!

Smell the Roses!

The mental status of many are at stake!