Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration

2008 ◽  
Vol 105 (2) ◽  
pp. 433-445 ◽  
Author(s):  
Jui-Lin Fan ◽  
James D. Cotter ◽  
Rebekah A. I. Lucas ◽  
Kate Thomas ◽  
Luke Wilson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Regional Differences ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Blood Flows ◽  
Time Control ◽  
Arterial Blood ◽  
Cerebrovascular Function ◽  
End Tidal ◽  
Passive Hyperthermia

The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q̇) would compromise blood flow velocity in the middle cerebral artery (MCAv) and cerebral oxygenation; 2) Hypo would exacerbate the hyperthermic-induced hypocapnia, further decreasing MCAv; and 3) heating would reduce MCAv-CO2 reactivity, thereby altering ventilation. Ten men, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5°C increments in core (esophageal) temperature (TC) to +2°C] while euhydrated (Euh) or Hypo by 1.5% body mass (attained previous evening). Time-control (i.e., non-heat stressed) data were obtained on six of these subjects. Cerebral oxygenation (near-infrared spectroscopy), MCAv, end-tidal carbon dioxide (PetCO2) and arterial blood pressure, Q̇ (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5°C change in TC. At each level, hypercapnia was achieved through 3-min administrations of 5% CO2, and hypocapnia was achieved with controlled hyperventilation. At baseline in Hypo, heart rate, MCAv and CCA were elevated ( P < 0.05 vs. Euh). MCAv-CO2 reactivity was unchanged in both groups at all TC levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in PetCO2 (−8 ± 1 mmHg/°C), which was related to lower MCAv (−15 ± 3%/°C; R2 = 0.98; P < 0.001). Elevations in Q̇ were related to increases in brachial blood flow ( R2 = 0.65; P < 0.01) and reductions in MCAv ( R2 = 0.70; P < 0.01), reflecting peripheral distribution of Q̇. Cerebral oxygenation was maintained, presumably via enhanced O2-extraction or regional differences in cerebral perfusion.

Alterations in cerebral autoregulation and cerebral blood flow velocity during acute hypoxia: rest and exercise

2007 ◽  
Vol 292 (2) ◽  
pp. H976-H983 ◽  
Author(s):  
Philip N. Ainslie ◽  
Alice Barach ◽  
Carissa Murrell ◽  
Mike Hamlin ◽  
John Hellemans ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Cerebral Oxygenation ◽  
Cerebral Blood Flow Velocity ◽  
Arterial Blood ◽  
Cerebrovascular Function ◽  
Hypoxic Exercise

We examined the relationship between changes in cardiorespiratory and cerebrovascular function in 14 healthy volunteers with and without hypoxia [arterial O2 saturation (SaO2) ∼80%] at rest and during 60–70% maximal oxygen uptake steady-state cycling exercise. During all procedures, ventilation, end-tidal gases, heart rate (HR), arterial blood pressure (BP; Finometer) cardiac output (Modelflow), muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasound) were measured continuously. The effect of hypoxia on dynamic cerebral autoregulation was assessed with transfer function gain and phase shift in mean BP and MCAV. At rest, hypoxia resulted in increases in ventilation, progressive hypocapnia, and general sympathoexcitation (i.e., elevated HR and cardiac output); these responses were more marked during hypoxic exercise ( P < 0.05 vs. rest) and were also reflected in elevation of the slopes of the linear regressions of ventilation, HR, and cardiac output with SaO2 ( P < 0.05 vs. rest). MCAV was maintained during hypoxic exercise, despite marked hypocapnia (44.1 ± 2.9 to 36.3 ± 4.2 Torr; P < 0.05). Conversely, hypoxia both at rest and during exercise decreased cerebral oxygenation compared with muscle. The low-frequency phase between MCAV and mean BP was lowered during hypoxic exercise, indicating impairment in cerebral autoregulation. These data indicate that increases in cerebral neurogenic activity and/or sympathoexcitation during hypoxic exercise can potentially outbalance the hypocapnia-induced lowering of MCAV. Despite maintaining MCAV, such hypoxic exercise can potentially compromise cerebral autoregulation and oxygenation.

Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

2008 ◽  
Vol 295 (5) ◽  
pp. R1613-R1622 ◽  
Author(s):  
Philip N. Ainslie ◽  
Michael Hamlin ◽  
John Hellemans ◽  
Peter Rasmussen ◽  
Shigehiko Ogoh
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Hypoxic Exercise

We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.

scholarly journals Cerebral blood flow autoregulation in ischemic heart failure

2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Healthy Volunteers ◽  
Neurological Complications ◽  
Ischemic Heart ◽  
Step Response ◽  
Ischemic Heart Failure ◽  
Arterial Blood ◽  
End Tidal

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.

Effect of Variation in Arterial Carbon Dioxide Levels on Cerebral-Somatic Oxygenation in Children with Cyanotic Congenital Heart Disease

2018 ◽  
pp. 1-6
Keyword(s):  
Carbon Dioxide ◽  
Congenital Heart Disease ◽  
Blood Flow ◽  
Heart Disease ◽  
Infrared Spectroscopy ◽  
Congenital Heart ◽  
Near Infrared ◽  
Cyanotic Congenital Heart Disease ◽  
Anesthesia Induction ◽  
Arterial Blood

Background: Hypocapnia is suggested in decreasing pulmonary vascular resistance in cyanotic congenital heart disease patients undergoing definitive repair. But its effects on cerebral and renal circulation are unclear. Hence the effect of changes in arterial blood carbon dioxide tensions (PaCo2 ) on cerebral (ScO2 %) and renal (SsO2 %) oxygenation indices using Near Infrared spectroscopy (NIRS) is examined. Methods: We did a prospective observational study in sixty-eight children who underwent elective cardiac surgery for various cyanotic congenital heart diseases. PaCo2 , ScO2 % and SsO2 % were obtained before induction of anesthesia, after anesthesia induction at normocapnic or mild hypercapnic ventilation (EtCo2 =40 mmHg) and again at hypocapnic ventilation (EtCo2 =30 mmHg). Regression analysis was done between PaCo2 and NIRS-C/ScO2 % and PaCo2 and NIRS-R/SsO2 % at both EtCo2 40 and 30 mmHg. Repeated measure analysis performed to evaluate the significance of change in NIRS-C and NIRS-R from pre-anesthesia induction to when EtCo2 was 40 and then 30 mmHg post anesthesia induction. Results: With decrease in EtCo2 , PaCo2 (p=0.0001), NIRS-C (p=0.0001) and NIRS-R (p=0.0001) decreased significantly. At EtCo2 of 40 and 30 mmHg, PaCo2 had significant positive correlation with NIRS-C (R2 =0.77, p=0.0001 and R2 =0.92, p=0.0001 respectively) and had insignificant correlation with NIRS-R (R2 =0.03, p=0.12 and R2 =0.008, p=0.46 respectively). Significant changes in NIRS-C {p=0.0001} and NIRS-R {p=0.0001} occurred from pre-induction to when EtCo2 was 40 and then to 30 mmHg. Conclusion: A decrease in NIRS-C and NIRS-R is probably from decreased cerebral and splanchnic blood flow during hypocapnic ventilation, leading to demand supply mismatch. Hypocapnic ventilation in cyanotic children has potential to cause cerebral hypoxia. Abbreviations: CCHD: Cyanotic Congenital Heart Disease; QP: Pulmonary blood flow; Do2 : Oxygen delivery; SpO2 : peripheral pulse oximetry; NIRS: Near Infrared Spectroscopy; NIRS-C/ScO2 %: Regional Cerebral Oxygen saturation; NIRS-R/SsO2 %: Regional Somatic/renal Oxygen saturation; HCT: Hematocrit; ECG: Electrocardiography; CPB: cardiopulmonary bypass; TOF: Tetralogy of fallot; BDG: Bidirectional Glenn Shunt; BT shunt: Blalock Taussig shunt; DORV: Double outlet right ventricle; FiO2 : Inspired oxygen concentration; ABG: Arterial blood gas; PaO2 : Arterial oxygen partial pressure; PaCo2 : Arterial carbon dioxide partial pressure; HR: Heart rate; MAP: Mean Arterial Pressure; CVP: Central Venous Pressure

Relationship between portal venous and hepatic arterial blood flows: spectrum of response

1990 ◽  
Vol 259 (6) ◽  
pp. G1010-G1018 ◽  
Author(s):  
T. Kawasaki ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
L. Roldan ◽  
H. Orrego
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Portal Vein Ligation ◽  
Artery Ligation ◽  
Blood Flows ◽  
Arterial Blood ◽  
Group A ◽  
Group B ◽  
The Relationship ◽  
Group D

The relationship between portal tributary blood flow (PBF) and hepatic arterial blood flow (HAF) was studied in awake, unrestrained rats with the radiolabeled microsphere technique. Six distinct patterns of response emerged. In group A (PBF+, HAF 0), ethanol, acetate, glucagon, prostacyclin, and a mixed diet increased PBF without a change in HAF; in group B (PBF+, HAF+), adenosine and histamine increased both PBF and HAF; in group C (PBF 0, HAF+), isoflurane and triiodothyronine did not change PBF but increased HAF; and in group D (PBF-, HAF+), halothane and vasopressin decreased PBF and increased HAF. Acute partial portal vein ligation decreased PBF (56%) and increased HAF (436%). Hypoxia (7.5% O2) decreased PBF (28%) and increased HAF (110%). In group E (PBF+, HAF-), acute hepatic artery ligation increased PBF (35%) and reduced HAF (74%), while in group F (PBF-, HAF-), thyroidectomy reduced PBF and HAF (36 and 47%, respectively). All blood flow responses were accompanied by the expected changes in both portal tributary and hepatic arterial vascular resistances. The data suggest that the portal and hepatic arterial vascular territories have regulatory mechanisms that allow for independent changes.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

Regional circulatory responses to hypocapnia and hypercapnia in bar-headed geese

1986 ◽  
Vol 250 (3) ◽  
pp. R499-R504 ◽  
Author(s):  
F. M. Faraci ◽  
M. R. Fedde
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Pectoral Muscle ◽  
Blood Flows ◽  
Arterial Blood ◽  
Blood Flow Reduction ◽  
Extreme Altitude ◽  
Anser Indicus ◽  
O2 Delivery

To investigate mechanisms that may allow birds to tolerate extreme high altitude (hypocapnic hypoxia), we examined the effects of severe hypocapnia and moderate hypercapnia on regional blood flow in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m. Cerebral, coronary, and pectoral muscle blood flows were measured using radioactive microspheres, while arterial CO2 tension (PaCO2) was varied from 7 to 62 Torr in awake normoxic birds. Arterial blood pressure was not affected by hypocapnia but increased slightly during hypercapnia. Heart rate did not change during alterations in PaCO2. Severe hypocapnia did not significantly alter cerebral, coronary, or pectoral muscle blood flow. Hypercapnia markedly increased cerebral and coronary blood flow, but pectoral muscle blood flow was unaffected. The lack of a blood flow reduction during severe hypocapnia may represent an important adaptation in these birds, enabling them to increase O2 delivery to the heart and brain at extreme altitude despite the presence of a very low PaCO2.

scholarly journals Measuring the human ventilatory and cerebral blood flow response to CO2: a technical consideration for the end-tidal-to-arterial gas gradient

2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  
Keyword(s):  
Blood Flow ◽  
Minute Ventilation ◽  
Linear Regression Analysis ◽  
Blood Gases ◽  
Prediction Equation ◽  
Flow Response ◽  
Arterial Blood ◽  
Reactivity Test ◽  
End Tidal ◽  
Gas Gradients

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.

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