Postural Hyperpnea

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Upright or Postural Hyperpnea is a common finding in various forms of orthostatic intolerance. It almost certainly represents an increase in the peripheral chemoreflex sensitivity in certain POTS patients but may also relate a form of "ischemic hypoxia" AKA "stagnant ischemia" in patients with initial large reductions in cerebral and thus carotid blood flow. Hypocapnia is present and becomes worse throughout orthostasis causing further cerebral vasoconstriction, distal anoxia and marked increases in  sympathetic activity.  

Previous investigations have demonstrated a subset of POTS patients characterized by normal peripheral resistance and blood volume while supine, but thoracic hypovolemia and splanchnic blood pooling while upright secondary to splanchnic hyperemia. Such “normal flow” POTS patients often demonstrate hypocapnia during orthostatic stress.

an eraly study is reported here. We studied 20 POTS patients aged 14-23 years and compared them to 10 comparably aged healthy volunteers. We measured changes in heart rate, blood pressure, heart rate and blood pressure variability, arm and leg strain gauge occlusion plethysmography (SPG), respiratory impedance plethysmography calibrated against pneumotachography, end tidal carbon dioxide (PETCO2), and impedance plethysmographic (IPG) indices of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during upright tilt to 70o. Ten POTS patients demonstrated significant hyperventilation and hypocapnia (POTSHC) while 10 were normocapnic (POTSNC) with minimal increase in postural ventilation comparable to control. While relative splanchnic hypervolemia and hyperemia occurred in both POTS groups compared to controls, marked enhancement in peripheral vasoconstriction occurred only in POTSHC and was related to thoracic blood flow. Variability indices suggested enhanced sympathetic activation in POTSHC compared to other subjects.  The data suggest enhanced cardiac and peripheral sympathetic excitation in POTSHC.

Table 1 Patient Dimensions and Supine Hemodynamic Data

                        Control

POTS

 

Control

(N=10)

Normocapnia (POTSNC)

(N=10)

 

Hypocapnia

(POTSHC)

(N=10)

Age (years)

17±1

17±2

16±2

Weight (kg)

61±4

57±3

64±4

Height (cm)

169±3

167±3

170±3

Body Surface Area (M2)

1.59±0.21

1.63±0.06

1.75±0.06

HR (beats/min)

69±4

71±4

74±4

Systolic BP (mmHg)

117±4

109±4

113±5

MAP   (mmHg)

83±2

76±3

82±2

Respiratory Rate (bpm)

17.2±0.5

16.8±1.4

16.2±1.2

PETCO2  (mmHg)

40.8±0.4

40.3±0.5

38.2±0.3*

Tidal Volume

452±76

488±102

423±47

Venous Occlusion Forearm Blood Flow (ml/100ml/min) 

 

3.4±0.3

 

3.2±0.2

 

2.6±0.2

 

Forearm Arterial Resistance  (ml/100ml/min/mmHg)   

26±6

 

28±4

 

38±3

 

Venous Occlusion Calf Blood Flow (ml/100ml/min) 

 

3.2±0.6

 

2.8±0.3

 

2.1±0.2

 

Calf Arterial Resistance  (ml/100ml/min/mmHg)   

29±4

 

26±4

 

33±2

 

Variability Indices:         

HRV (msec2/Hz) 

BPV (mmHg2/Hz) 

LF_HRV (msec2/Hz)

HF_HRV (msec2/Hz)

LF/HF

Transfer Gain (msec/mmHg)

 

3639±448

10.4±2.8

926±123

1667±363

.90±0.28

21.8±2.0

 

3448±662

9.0±2.0

1111±366

1742±504

.73±0.11

23.8±5.2

 

2564±880

8.1±0.7

750±208

1217±247

0.83±0.17

15.9±3.1

Impedance Blood Flows

(ml/min)

Thoracic         

Splanchnic

Pelvic

Leg

 

 

4559±783

1694±233

633±181

99±19

 

 

3989±902

2316±111*

543±65

86±15

 

 

4726±671

2611±327*

630±122

79±14

 

 

 

The figure depicts spontaneous (left panels) and voluntary (right panels) hypocapnia brought about in a POTS patient and by voluntary hyperventilation in a healthy control subject, respectively. Voluntary hyperventilation was achieved by having the subject take a breath every 6 seconds and to breath as deeply as possible. This was maintained this for  three and half minutes and stopped because of lightheadedness. For each set of panels, PETCO2, Respitrace volumes, and thoracic blood volumes are shown from top to bottom. Upright tilt was associated with an increase in thoracic blood volume. The onset of hypocapnic hyperventilation was not related to an increase in thoracic blood volume.

 

 

 

The figure demonstrates the construction of a time integrated tidal volume curve (bottom panel) from the record of time dependent relative Respitrace tidal volume (top panel). An intermediate step is to obtain the absolute value of the tidal volume curve as shown in the middle panel.

 

 

  

 

The figure shows PETCO2, (top panel) the Respitrace tidal volume record (middle panel) and the calculation of relative respiratory minute volume (bottom panel) as the slope of linear portions of the integrated tidal volume corresponding to times preceding and during upright tilt in a POTSHC patient.

The figure depicts changes in heart rate (top panel) and mean arterial pressure (bottom panel) during upright tilt. Heart rate increased in all subjects and was most increased in POTSNC, and next most in POTSHC compared to control subjects.  Mean arterial pressure is increases similarly for all subjects. *=p<.05 compared to control. = p<.05 compared to POTSNC.

The figure shows changes in PETCO2 (top panel), and minute ventilation (bottom panel) during upright tilt. PETCO2 was decreased in all subjects but most markedly in POTSHC patients. This was associated with enhanced minute ventilation (VE) in these same subjects. *=p<.05 compared to control.

 

 

The figure shows percent change in minute volume compared to percent change in ETCO2 for all subjects. Individual data points are shown for each subject. ETCO2 is decreased in most patients but is most markedly decreased in POTSHC patients in association with a marked increase in minute ventilation.

 

 

 

The figure shows (from top down) changes in total heart rate variability (top panel), baroreflex gain, LF/HF ratio and systolic BP variability  during upright tilt. HRV and baroreflex gain decreases for all subjects but most for POTSHC patients. LF/HF ratio and BPV increase for all subjects but most for POTSHC patients. *=p<.05 compared to control.
The figure shows percent changes in thoracic, splanchnic, pelvic, and leg blood flows (upper panel) and corresponding changes in segmental blood volumes (lower panel) during upright tilt averaged over subject groups. Thoracic blood flow was most reduced in POTSNC subjects. Splanchnic flow was reduced in control subjects but this was most blunted in POTSHC patients. This was associated with a significant decrease in peripheral blood flow in these patients. *=p<.05 compared to control
 
 
 

 


Up
Exercise Intolerance- the Exercise Pressor Reflex in POTS
Skeletal Muscle Pump
Normal Leg Venous Capacitance
Postural Neurocognitive
Splanchnic Pooling in Normal Flow POTS
Nitric Oxide Dysfunction in Low Flow POTS
Angiotensin-II in POTS
Decreased Upright Cerebral Blood Flow and Cerebral Autoregulation in POTS
Postural Hyperpnea
Nitric Oxide is Decreased in Angiotensin-II dependent Low flow POTS but increased along with Splanchnic pooling Neuropathic POTS
Local Vascular Responses in POTS
Microvascular Filtration in High Flow POTS
POTS as Thoracic Hypovolemia