Elsevier

Heart & Lung

Volume 46, Issue 3, May–June 2017, Pages 149-152
Heart & Lung

Care of the Critically Ill
Effect of arterial puncture on ventilation

https://doi.org/10.1016/j.hrtlng.2017.01.011Get rights and content

Abstract

Background

Clinicians frequently assume that during arterial puncture for measuring arterial blood gases patients hyperventilate from pain and anxiety. This assumption leads clinicians to falsely interpret a PaCO2 and pH near the upper limit of normal as a chronic respiratory acidosis corrected by an acute respiratory alkalosis.

Objective

Determine if participants hyperventilate during arterial puncture from pain and anxiety.

Methods

We recruited participants from a pulmonary function laboratory referred for arterial blood gas measurement. We excluded those with heart failure and included those with any respiratory condition (COPD, asthma, sleep apnea). We measured end tidal PCO2 (PETCO2), respiratory rate, and heart rate 15 min before topical anesthesia, during anesthesia, during arterial puncture, and 15 min later. We assessed generalized anxiety before and measured pain during and after arterial puncture.

Results

24 participants were recruited (age: 54 ± 12 years; men: 54%). PaCO2 was 41 ± 5 mmHg. One had acute respiratory alkalosis. Respiratory rate increased from (19 ± 6 breaths per minute (bpm)) before to a maximum (21 ± 6 bpm) during arterial puncture (p = 0.001). Heart rate was stable throughout. The lowest PETCO2 during the procedure (35 ± 5) was similar to PETCO2 before the procedure (p = 0.1). The change in PETCO2 and respiratory rate did not correlate with pain, anxiety, or lung function.

Conclusion

Respiratory rate increased slightly during arterial puncture without any change in PETCO2. Hence, acid–base status must be interpreted without the assumption of procedure induced hyperventilation.

Introduction

Hypoventilation is a manifestation of advanced respiratory diseases. Recognizing it is important to determine prognosis and select appropriate level of respiratory support.1, 2 Because it is difficult in clinical practice to measure ventilation, we measure arterial blood gases to detect chronic respiratory acidosis—the sine qua non of hypoventilation.

Recognizing chronic respiratory acidosis from the measurement of arterial blood gases is easy when the partial pressure of arterial carbon dioxide (PaCO2) is above 55 mmHg. When the PaCO2 is closer to the upper limit of normal, clinicians choose one of three interpretations: normal, a compensation for metabolic alkalosis, or chronic respiratory acidosis with acute respiratory alkalosis that reduces the PaCO2 close to the upper limit of normal.

This issue was recently raised in the attempts to define obesity hypoventilation syndrome (OHS); a serious condition that is becoming more common with the obesity epidemic.3, 4 The measurement of arterial blood gases in obese patients is frequently triggered by elevated serum bicarbonate. But not all obese patients with elevated serum bicarbonates have hypercapnia. About half of the obese patients with obstructive sleep apnea with elevated serum bicarbonate level are hypercapnic.5 The non-hypercapnic patients with elevated bicarbonate are classically considered not to have OHS.

However, Hart and colleagues proposed that alkalosis in the absence of hypercapnia in obese patients should be added to the definition of OHS.6 One explanation given to justify this change is that the pain and anxiety from arterial puncture causes hyperventilation and reduces carbon dioxide levels. Others also rely on this justification for labeling participants with normal PaCO2 as having mild OHS.7 Despite its plausibility, this explanation was tested only once by Morgan and colleagues who found no effect of arterial puncture on carbon dioxide in arterialized venous blood.8 They did not measure the respiratory rate, tidal volume, cardiac output, pain, or anxiety.

In this study we reassess the effect of arterial puncture on ventilation by monitoring the respiratory rate and end tidal carbon dioxide pressure (PETCO2) during arterial puncture and determining the correlation between the change in these variables and lung function, body weight, pain, and anxiety.

Section snippets

Setting

This prospective observational cohort study was conducted in a pulmonary function laboratory in a single center from 2014 to 2016. The Institutional Review Board approved the study and the participants provided written consent before enrollment.

Participants

We recruited patients 18 years or older. They were excluded if they did not speak English, were pregnant, had heart failure with reduced ejection fraction (it alters minute ventilation and the relation between end tidal and arterial PaCO2), or used

Results

We recruited 24 participants (Table 1). Most participants were older than 50 years and predominately African American. Eleven participants (46%) were obese (body mass index (BMI) > 30 kg/m2). Thirteen participants (54%) had smoking exposure (past or current). Five (21%) had obstructive sleep apnea, 12 (50%) had COPD or asthma. Thirteen had a diagnosis of hypertension. Only one participant was on home oxygen therapy.

Spirometry was normal in nine participants (38%), obstructive in seven (29%),

Discussion

In this study we demonstrated that arterial puncture increased the respiratory rate and that this increase was not associated with a change the partial pressure of carbon dioxide. We also found no correlation between the changes in ventilation (PETCO2 and RR) and lung function, body weight, pain, or anxiety.

In our study we show that during arterial puncture the respiratory rate increased by about 2 breaths per minute. This increase can change the PETCO2 by 3.5 mmHg or PaCO2 by 4.5 mmHg. One

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Cited by (5)

Specific contributions of each author: Ashima Sahni: literature search, data collection, study design, analysis of data, manuscript preparation, review of manuscript. Hemil Gonzalez: Data collection, study design, analysis of data, manuscript preparation. Aiman Tulaimat: Literature search, study design, analysis of data, manuscript preparation, review of manuscript.

Results dissemination: Data was presented at American Thoracic Society Conference, Denver, Colorado, 2015.

Funding: none.

Conflict of interest: none.

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