Effects of varying chest compression depths on carotid blood flow and blood pressure in asphyxiated piglets

2021 ◽  
pp. fetalneonatal-2020-319473
Author(s):  
Marlies Bruckner ◽  
Megan O’Reilly ◽  
Tze-Fun Lee ◽  
Mattias Neset ◽  
Po-Yin Cheung ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Neonatal Resuscitation ◽  
Chest Compressions ◽  
Carotid Blood Flow ◽  
Newborn Piglets ◽  
Resuscitation Guidelines ◽  
Registration Number ◽  
Anterior Posterior

BackgroundCurrent neonatal resuscitation guidelines recommend chest compressions (CCs) should be delivered to a depth of approximately 1/3 of the anterior–posterior (AP) chest diameter. The aim of the study was to investigate the haemodynamic effects of different CC depths in a neonatal piglet model.MethodsCCs were performed with an automated CC machine with 33%, 40% and 25% AP chest diameter in all piglets in the same order for a duration of 3 min each.ResultsEight newborn piglets (age 1–3 days, weight 1.7–2.3 kg) were included in the study. Carotid blood flow (CBF) and systolic blood pressure were the highest using a CC depth of 40% AP chest diameter (19.3±7.5 mL/min/kg and 58±32 mm Hg).ConclusionCC depth influences haemodynamic parameters in asphyxiated newborn piglets during cardiopulmonary resuscitation. The highest CBF and systolic blood pressure were achieved using a CC depth of 40% AP chest diameter.Trial registration numberPCTE0000148.

scholarly journals Pulseless electrical activity: a misdiagnosed entity during asphyxia in newborn infants?

2018 ◽  
Vol 104 (2) ◽  
pp. F215-F217 ◽  
Author(s):  
Sparsh Patel ◽  
Po-Yin Cheung ◽  
Anne Lee Solevåg ◽  
Keith J Barrington ◽  
C Omar Farouk Kamlin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Newborn Infants ◽  
Neonatal Resuscitation ◽  
Pulseless Electrical Activity ◽  
Heart Sounds ◽  
Carotid Blood Flow ◽  
Neonatal Piglets ◽  
Resuscitation Guidelines ◽  
Recent Case Report ◽  
The Right

BackgroundThe 2015 neonatal resuscitation guidelines added ECG as a recommended method of assessment of an infant’s heart rate (HR) when determining the need for resuscitation at birth. However, a recent case report raised concerns about this technique in the delivery room.ObjectivesTo compare accuracy of ECG with auscultation to assess asystole in asphyxiated piglets.MethodsNeonatal piglets had the right common carotid artery exposed and enclosed with a real-time ultrasonic flow probe and HR was continuously measured and recorded using ECG. This set-up allowed simultaneous monitoring of HR via ECG and carotid blood flow (CBF). The piglets were exposed to 30 min normocapnic alveolar hypoxia followed by asphyxia until asystole, achieved by disconnecting the ventilator and clamping the endotracheal tube. Asystole was defined as zero carotid blood flow and was compared with ECG traces and auscultation for heart sounds using a neonatal/infant stethoscope.ResultsOverall, 54 piglets were studied with a median (IQR) duration of asphyxia of 325 (200-491) s. In 14 (26%) piglets, CBF, ECG and auscultation identified asystole. In 23 (43%) piglets, we observed no CBF and no audible heart sounds, while ECG displayed an HR ranging from 15 to 80/min. Sixteen (30%) piglets remained bradycardic (defined as HR of <100/min) after 10 min of asphyxia, identified by CBF, ECG and auscultation.ConclusionClinicians should be aware of the potential inaccuracy of ECG assessment during asphyxia in newborn infants and should rather rely on assessment using a combination of auscultation, palpation, pulse oximetry and ECG.

Abstract 439: Using the Time Interval Between R-Wave Detection and Maximum Compression Pressure to Target and Validate Delivery of Synchronized Chest Compressions During Pseudo Electro-Mechanical Dissociation

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Joshua W Lampe ◽  
Jeff R Gould ◽  
Karen L Moodie ◽  
Zachary P Soucy ◽  
Peter S Burrage ◽  
...  
Keyword(s):  
Blood Flow ◽  
Time Interval ◽  
Hemodynamic Parameters ◽  
Chest Compressions ◽  
Compression Pressure ◽  
Carotid Blood Flow ◽  
Maximum Compression ◽  
Local Maxima ◽  
Blood Flows ◽  
Mechanical Dissociation

Introduction: The treatment of pseudo electro-mechanical dissociation (P-EMD) with standard chest compressions leads to some compressions that interfere with blood flow created by ventricular contraction and others that are synergistic. We have previously reported that the hemodynamics generated by standard chest compressions (StdCPR) depended on the time interval between the R-wave and the maximum compression pressure (t_int). Our goal was to use the t_int to identify the optimal timing for compression synchronization and to validate the delivery of synchronized chest compressions. Methods: Eight animals underwent surgical preparation and were exposed to hypoxia to induce P-EMD. The treatment period was divided into eight 45 sec epochs during which the P-EMD was left untreated or was treated with StdCPR or chest compressions synchronized to the R-wave in the ECG (SyncCPR). For each heart beat t_int was calculated as t peak AOP - t Rwave , blood pressures were averaged, and blood flows were integrated. 1,598 chest compressions were analyzed. The location of local extrema in hemodynamic parameters as a function of positive t_int values were identified recursively by dividing the range of t_int values into increasing numbers of bins and determining which bin had the highest mean value. Results: Blood flows and pressures exhibited a non-linear dependence on t_int. The maximum CPP occurred at t_int = 90 ±2.3 ms. The maximum aortic pressure occurred at t_int = 70 ±2.3 ms. The minimum right atrial pressure occurred at t_int = 280 ±2.3 ms. The maximum carotid blood flow occurred at t_int = 100 ±2.3 ms. The maximum jugular blood flow occurred at t_int = 400 ±2.3 ms. Unsynchronized chest compressions resulted in a t_int of -21 ± 170 ms. Synchronized chest compressions resulted in a t_int of 119 ± 13 ms. Conclusions: Local maxima and minima during StdCPR were identified in several hemodynamic parameters, but the extrema were not perfectly co-located. It appears that a t_int of 90-100 ms could be optimal. SyncCPR were delivered at 119 ms, which is not far from the local maxima observed for CPP and carotid blood flow.

Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise

1998 ◽  
Vol 85 (1) ◽  
pp. 154-159 ◽  
Author(s):  
Jason W. Daniels ◽  
Paul A. Molé ◽  
James D. Shaffrath ◽  
Charles L. Stebbins
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Skin Temperature ◽  
Rectal Temperature ◽  
Forearm Blood Flow ◽  
Dynamic Exercise ◽  
Ang Ii ◽  
Leg Exercise

This study examined the acute effects of caffeine on the cardiovascular system during dynamic leg exercise. Ten trained, caffeine-naive cyclists (7 women and 3 men) were studied at rest and during bicycle ergometry before and after the ingestion of 6 mg/kg caffeine or 6 mg/kg fructose (placebo) with 250 ml of water. After consumption of caffeine or placebo, subjects either rested for 100 min (rest protocol) or rested for 45 min followed by 55 min of cycle ergometry at 65% of maximal oxygen consumption (exercise protocol). Measurement of mean arterial pressure (MAP), forearm blood flow (FBF), heart rate, skin temperature, and rectal temperature and calculation of forearm vascular conductance (FVC) were made at baseline and at 20-min intervals. Plasma ANG II was measured at baseline and at 60 min postingestion in the two exercise protocols. Before exercise, caffeine increased both systolic blood pressure (17%) and MAP (11%) without affecting FBF or FVC. During dynamic exercise, caffeine attenuated the increase in FBF (53%) and FVC (50%) and accentuated exercise-induced increases in ANG II (44%). Systolic blood pressure and MAP were also higher during exercise plus caffeine; however, these increases were secondary to the effects of caffeine on resting blood pressure. No significant differences were observed in heart rate, skin temperature, or rectal temperature. These findings indicate that caffeine can alter the cardiovascular response to dynamic exercise in a manner that may modify regional blood flow and conductance.

Baroreceptor influence on postural changes in blood pressure and carotid blood flow

1963 ◽  
Vol 205 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Francis L. Abel ◽  
John H. Pierce ◽  
Warren G. Guntheroth
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Sinus ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Carotid Blood Flow ◽  
Postural Changes ◽  
Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

Cardiovascular autonomic modulation and activity of carotid baroreceptors at altitude

1998 ◽  
Vol 95 (5) ◽  
pp. 565-573 ◽  
Author(s):  
Luciano BERNARDI ◽  
Claudio PASSINO ◽  
Giammario SPADACINI ◽  
Alessandro CALCIATI ◽  
Robert ROBERGS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Skin Blood Flow ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
High Altitude Natives

1.To assess the effects of acute exposure to high altitude on baroreceptor function in man we evaluated the effects of baroreceptor activation on R–R interval and blood pressure control at high altitude. We measured the low-frequency (LF) and high-frequency (HF) components in R–R, non-invasive blood pressure and skin blood flow, and the effect of baroreceptor modulation by 0.1-Hz sinusoidal neck suction. Ten healthy sea-level natives and three high-altitude native, long-term sea-level residents were evaluated at sea level, upon arrival at 4970 ;m and 1 week later. 2.Compared with sea level, acute high altitude decreased R–R and increased blood pressure in all subjects [sea-level natives: R–R from 1002±45 to 775±57 ;ms, systolic blood pressure from 130±3 to 150±8 ;mmHg; high-altitude natives: R–R from 809±116 to 749±47 ;ms, systolic blood pressure from 110±12 to 125±11 ;mmHg (P< 0.05 for all)]. One week later systolic blood pressure was similar to values at sea level in all subjects, whereas R–R remained elevated in sea-level natives. The low-frequency power in R–R and systolic blood pressure increased in sea-level natives [R–R-LF from 47±8 to 65±10% (P< 0.05), systolic blood pressure-LF from 1.7±0.3 to 2.6±0.4 ln-mmHg2 (P< 0.05)], but not in high-altitude natives (R–R-LF from 32±13 to 38±19%, systolic blood pressure-LF from 1.9±0.5 to 1.7±0.8 ln-mmHg2). The R–R-HF decreased in sea-level natives but not in high-altitude natives, and no changes occurred in systolic blood pressure-HF. These changes remained evident 1 week later. Skin blood flow variability and its spectral components decreased markedly at high altitude in sea-level natives but showed no changes in high-altitude natives. Neck suction significantly increased the R–R- and systolic blood pressure-LF in all subjects at both sea level and high altitude. 3.High altitude induces sympathetic activation in sea-level natives which is partially counteracted by active baroreflex. Despite long-term acclimatization at sea level, high-altitude natives also maintain active baroreflex at high altitude but with lower sympathetic activation, indicating a persisting high-altitude adaptation which may be genetic or due to baroreflex activity not completely lost by at least 1 year's sea-level residence.

scholarly journals Selective neuronal damage and blood pressure in atherosclerotic major cerebral artery disease

2019 ◽  
Vol 90 (9) ◽  
pp. 975-980 ◽  
Author(s):  
Hiroshi Yamauchi ◽  
Shinya Kagawa ◽  
Masaaki Takahashi ◽  
Kuninori Kusano ◽  
Chio Okuyama
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systolic Blood Pressure ◽  
Cerebral Artery ◽  
Neuronal Damage ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Artery Disease

ObjectiveIn patients with atherosclerotic major cerebral artery disease, low blood pressure might impair cerebral perfusion, thereby exacerbate the risk of selective neuronal damage. The purpose of this retrospective study was to determine whether low blood pressure at follow-up is associated with increased selective neuronal damage.MethodsWe retrospectively analysed data from 76 medically treated patients with atherosclerotic internal carotid artery or middle cerebral artery disease with no ischaemic episodes on a follow-up of 6 months or more. All patients had measurements of the distribution of central benzodiazepine receptors twice using positron emission tomography and 11C-flumazenil. Using three-dimensional stereotactic surface projections, we quantified abnormal decreases in the benzodiazepine receptors of the cerebral cortex within the middle cerebral artery distribution and correlated these changes in the benzodiazepine receptors index with blood pressure values at follow-up examinations.ResultsThe changes in the benzodiazepine receptor index during follow-up (mean 27±21 months) were negatively correlated with systolic blood pressure at follow-up. The relationship between changes in benzodiazepine receptor index and systolic blood pressure was different among patients with and without decreased cerebral blood flow at baseline (interaction, p<0.005). Larger increases in benzodiazepine receptor index (neuronal damage) were observed at lower systolic blood pressure levels in patients with decreased cerebral blood flow than in patients without such decreases.ConclusionIn patients without ischaemic stroke episodes at follow-up but with decreased cerebral blood flow due to arterial disease, low systolic blood pressure at follow-up may be associated with increased selective neuronal damage.

scholarly journals Persistent Autoregulatory Disturbance after Angioplasty for Cerebral Vasospasm

2002 ◽  
Vol 8 (4) ◽  
pp. 409-415 ◽  
Author(s):  
D.K. Song ◽  
M.R. Harrigan ◽  
J.P. Deveikis ◽  
J.E. McGillicuddy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Cerebral Vasospasm ◽  
Artery Aneurysm ◽  
Response To Therapy ◽  
Large Artery ◽  
Xenon Ct ◽  
Symptomatic Vasospasm ◽  
Hyperdynamic Therapy

Hyperdynamic therapy, consisting of hypervolemia, haemodilution, and hypertension, is an established treatment for cerebral vasospasm following subarachnoid haemorrhage. Angioplasty has emerged as an additional, effective treatment for symptomatic vasospasm. Loss of autoregulation, however, can occur despite effective angioplasty, underscoring the need for treatment with hyperdynamic therapy in combination with angioplasty. A 43-year-old woman underwent endovascular coiling of a ruptured left posterior communicating artery aneurysm. The patient went on to develop symptomatic vasospasm and was treated with hyperdynamic therapy and angioplasty. Autoregulation was assessed with xenon CT cerebral blood flow (CBF) measurement. An initial CBF study was obtained when the patient received dopamine and dobutamine infusions to maintain systolic blood pressure at 160 mmHg. The vasopressor drips were then temporarily held for twenty minutes, allowing the patient's systolic blood pressure to drop to 140 mmHg, and a repeat CBF study was obtained. Several days after angioplasty, CBF decreased significantly when the patient was taken off vasopressors, indicating impaired autoregulation. Hyperdynamic therapy was continued, and another CBF study one week later showed a return of autoregulation and normalization of CBF without induced hypertension. Autoregulation is disturbed during vasospasm. Although angioplasty can improve large artery blood flow during vasospasm, hyperdynamic therapy is also needed to maintain cerebral perfusion, particularly in the face of impaired autoregulation. Quantitative CBF measurement permits the maintenance of optimal CBF and monitoring of response to therapy.

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