Forward blood flow provoked by changing intravascular pressure using an extracorporeal circulation during cardiopulmonary resuscitation

2020 ◽  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Resuscitation ◽  
Chest Compression ◽  
Intrathoracic Pressure ◽  
Arterial Blood Flow ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Closed Chest ◽  
Arterial Blood ◽  
Intravascular Pressure

Since both “cardiac pump” and “thoracic pump” theories have been proved during cardiopulmonary resuscitation (CPR), the mechanism of forward blood flow during closed chest compression still remains open to question. The cardiac pump seems to work by the direct compression of the cardiac ventricles between the sternum and vertebral column. A pressure gradient created between the ventricle and aorta generates systemic blood flow. However, the thoracic pump mechanism presumes chest compression causes a rise in intrathoracic pressure which generates a blood flow from the thoracic cavity to the systemic circulation. Retrograde blood flow from the right heart into the systemic veins is prevented by a concomitant collapse of veins at the thoracic inlet. We hypothesize that the intrinsic decrease of vascular resistance from the aorta to peripheral arteries and the existence of competent venous valves enable blood to flow unidirectionally by the fluctuation of intravascular pressures during closed chest compression. The purpose of this study is to prove an antegrade arterial blood flow without cardiac compression and intrathoracic pressure changes in an animal cardiac arrest model. We demonstrate that arterial pulses can be developed by using an extracorporeal circuit, resulting in forward blood flow from the aorta through the systemic vasculature. It can be suggested that changes in intravascular pressure provoked by either cardiac or thoracic pump generate systemic blood flow during closed chest compression, while systemic vascular patency and valve function may be required for successful CPR.

Systemic blood flow to the lung after bronchial artery occlusion in anesthetized sheep

1992 ◽  
Vol 72 (5) ◽  
pp. 1701-1707 ◽  
Author(s):  
E. M. Baile ◽  
D. Minshall ◽  
P. B. Harrison ◽  
P. M. Dodek ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Bronchial Artery ◽  
Experimental Studies ◽  
Middle Lobe ◽  
Arterial Blood Flow ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Complete Obstruction ◽  
Caudal Lobe ◽  
Arterial Blood

To compare the effectiveness of different embolizing agents in reducing or redistributing bronchial arterial blood flow, we measured systemic blood flow to the right lung and trachea in anesthetized sheep by use of the radioactive microsphere method before and 1 h after occlusion of the bronchoesophageal artery (BEA) as follows: injection of 4 ml ethanol (ETOH) into BEA (group 1, n = 5), injection of approximately 0.5 g polyvinyl alcohol particles (PVA) into BEA (group 2, n = 5), or ligation of BEA (group 3, n = 5). After occlusion, angiography showed complete obstruction of the bronchial vessels. There were no changes in tracheal blood flow in any of the groups. Injection of ETOH produced a 75 +/- 14% (SD) reduction in flow to the middle lobe (P less than 0.02) and a 75 +/- 13% reduction to the caudal lobe (P less than 0.01), whereas injection of PVA produced a smaller reduction in flow to these two lobes (41 +/- 66 and 51 +/- 54%, respectively). After BEA ligation there was a 52 +/- 29% reduction in flow to the middle lobe and a 53 +/- 38% reduction to the caudal lobe (P less than 0.05). This study has significant implications both clinically and experimentally; it illustrates the importance of airway collateral circulation, in that apparently complete radiological obstruction of the BEA does not necessarily mean complete obstruction of systemic blood flow. We also conclude that, in experimental studies in which the role of the bronchial circulation in airway pathophysiology is examined, ETOH is the agent of choice.

Timing of pulmonary and systemic blood flow during intermittent high intrathoracic pressure cardiopulmonary resuscitation in the dog

1982 ◽  
Vol 49 (8) ◽  
pp. 1883-1889 ◽  
Author(s):  
James M. Cohen ◽  
Nisha Chandra ◽  
Philip O. Alderson ◽  
Andries van Aswegen ◽  
Joshua E. Tsitlik ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Resuscitation ◽  
Intrathoracic Pressure ◽  
Systemic Blood ◽  
Systemic Blood Flow

Transient analysis of cardiopulmonary interactions. I. Diastolic events

1988 ◽  
Vol 64 (4) ◽  
pp. 1506-1517 ◽  
Author(s):  
J. Peters ◽  
M. K. Kindred ◽  
J. L. Robotham
Keyword(s):  
Blood Flow ◽  
Intrathoracic Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Aortic Blood Flow ◽  
Cross Sectional ◽  
Arterial Blood ◽  
Run Off ◽  
In Series ◽  
Antegrade Flow

The etiology of the fall in left ventricular stroke volume (LVSV) with negative intrathoracic pressure (NITP) during inspiration has been ascribed to a reduction in LV preload. This study evaluated the effects of NITP with and without airway obstruction confined to early (ED), mid- (MD), or late diastole (LD) on the subsequent LVSV, anteroposterior (AP), and right-to-left (RL) aortic diameters (DAO) (series I, n = 6) as well as on phasic arterial blood flow out of the thorax (series II, n = 6) in anesthetized dogs. Transient NITP was obtained by electrocardiogram-triggered phrenic nerve stimulation. In series I, NITP applied for 60% of diastole with the airway obstructed caused decreases of LVSV during ED [-7.7 +/- 3.2% (SE) NS], MD (-11.7 +/- 3.9%, P less than 0.05), and LD (-14.6 +/- 1.5%, P less than 0.01) associated with significant increases of left ventricular end-diastolic pressures relative to both atmospheric and esophageal pressures during MD and LD. NITP increased DAO(AP) and DAO(RL), resulting in increases in diastolic aortic cross-sectional area by an average of 6.1-8.3% (P less than 0.01). Similar changes were seen with the airway unobstructed during NITP. In series II, NITP caused diminished diastolic antegrade carotid artery and/or descending aortic flow run off in all dogs. Transient retrograde arterial flows with NITP were observed in more than half of the animals consistent with increases in aortic diameters. We conclude that a decrease of intrathoracic pressure confined to diastole can 1) diminish the ensuing LVSV, presumptively reducing preload by ventricular interdependence; 2) distend the intrathoracic aorta; 3) diminish antegrade flow out of the thorax independent of effects on cardiac performance; and 4) cause transient retrograde carotid and aortic blood flow. The intrathoracic aorta and, presumably, the arterial intrathoracic vascular compartment can be viewed as an elastic container driven by changes in intrathoracic pressure.

Catheter-tip flowmeter for coronary arterial flow in closed-chest dogs

1964 ◽  
Vol 19 (6) ◽  
pp. 1199-1201 ◽  
Author(s):  
Heinz P. Pieper
Keyword(s):  
Blood Flow ◽  
Pulsatile Flow ◽  
Left Coronary Artery ◽  
Ascending Aorta ◽  
Arterial Blood Flow ◽  
Performance Tests ◽  
Closed Chest ◽  
Arterial Blood ◽  
Catheter Tip ◽  
The Right

The design of a catheter-tip flowmeter for the measurement of coronary arterial blood flow in closed-chest dogs is presented. The miniaturized flowmeter is attached to the tip of a rigid catheter which is inserted through the right carotid artery. The flowmeter is placed in the ascending aorta where it measures the inflow into the left coronary artery. Performance tests show the reliability of the instrument for the measurement of pulsatile flow. pulsatile flow Submitted on February 3, 1964

New Versus Old External Cardiopulmonary Resuscitation

1985 ◽  
Vol 1 (3) ◽  
pp. 245-248
Author(s):  
N. Bircher ◽  
P. Safar
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Cardiopulmonary Resuscitation ◽  
Chest Compression ◽  
Intrathoracic Pressure ◽  
External Jugular Vein ◽  
Two Phase ◽  
Open Chest ◽  
The Brain

Since standard cardiopulmonary resuscitation (SCPR) cannot reliably preserve the brain during resuscitation, a “New” CPR has been proposed, which seeks to augment blood flow by increasing peak intrathoracic pressure (ITP) during chest compression. This “New” CPR (NCPR) consists of a) high pressure ventilation (70-110 cmH2O) simultaneous with chest compression, b) compression rate of 40/min, c) compression duration of 60% of the compression relaxation cycle, and d) abdominal binding. Although laboratory evidence suggests that NCPR may be capable of augmenting cerebral blood flow (1), the effect on cerebral outcome remains to be demonstrated.Although the hemodynamic superiority of open-chest CPR has long been recognized, its advantages with respect to the brain have only recently been recognized. It can reliably sustain EEC activity and pupillary light reflexes during CPR (2) as well as providing better cerebral blood flow (3,4). The objective of this two phase study was to establish the relative efficacy of standard, “new,” and open-chest CPR with respect to preserving the brain during CPR.The objective of phase I of this study was to compare standard and “New” CPR with respect to maintenance of hemodynamic, respiratory, and cerebral variables during prolonged resuscitation. Methods: Ten 10-15 kg dogs were anesthetized with halothane and 50% N2O/O2. Catheters were placed in the carotid artery, aortic arch, right atrium, external jugular vein and the sagittal sinus. An electromagnetic flowprobe was placed on the common carotid artery. Intracranial pressure was monitored with a subdural catheter. EEG electrodes were secured to the skull.

Maximizing cardiopulmonary resuscitation in patients with intra-aortic balloon pumps

1998 ◽  
Vol 18 (2) ◽  
pp. 25-27 ◽  
Author(s):  
C Osborn ◽  
SJ Quaal
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Cardiopulmonary Arrest ◽  
Healthcare Staff ◽  
Balloon Inflation ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Research Questions

Improved hemodynamics and blood flow have been reported in patients with IABPs who experience cardiopulmonary arrest and require CPR. The following research questions, however, remain unanswered: Is there a more effective method of using IABP to prevent cardiac arrest and the need for CPR? Is the timing of balloon inflation and deflation the same for patients undergoing CPR as it is for patients who do not require CPR? Would earlier or later inflation or deflation further enhance cerebral or systemic blood flow? What are the most effective ways for healthcare staff to maintain competency skills in CPR in patients with IABPs?

Modeling Elastic Walls in Lattice Boltzmann Simulations of Arterial Blood Flow

2013 ◽  
Vol 23 (2) ◽  
Author(s):  
Xenia Descovich ◽  
Giuseppe Pontrelli ◽  
Sauro Succi ◽  
Simone Melchionna ◽  
Manfred Bammer
Keyword(s):  
Blood Flow ◽  
Lattice Boltzmann ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Lattice Boltzmann Simulations ◽  
Elastic Walls
Sign in / Sign up

Export Citation Format

Share Document