Catheter‐Tip Blood Flowmeter for Measurement of Pulmonary Arterial Blood Flow in Closed‐Chest Dogs

1963 ◽  
Vol 34 (8) ◽  
pp. 908-910 ◽  
Author(s):  
Heinz P. Pieper
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Closed Chest ◽  
Arterial Blood ◽  
Catheter Tip ◽  
Pulmonary Arterial

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

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

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.

Regional Abnormalities in Pulmonary Arterial Blood Flow During Acute Asthmatic Attacks

Radiology ◽  
1967 ◽  
Vol 88 (1) ◽  
pp. 142-144 ◽  
Author(s):  
Fred Mishkin ◽  
Henry N. Wagner
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Pulmonary Arterial

Persistent fetal pulmonary hypoperfusion after acute hypoxia

1987 ◽  
Vol 253 (4) ◽  
pp. H941-H948 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso ◽  
R. B. Wilkening ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Blood Flow ◽  
Adrenergic Blockade ◽  
Flow Transducer ◽  
Arterial Blood ◽  
Pulmonary Arterial

To determine the effects of duration of hypoxia on fetal pulmonary blood flow and vasoreactivity, we studied the response of the fetal pulmonary vascular bed before, during, and after prolonged (2-h) and more brief (30-min) exposures to acute hypoxia in 19 chronically instrumented unanesthetized fetal lambs. Left pulmonary arterial blood flow was measured by an electromagnetic flow transducer. Fetal PO2 was lowered by delivering 10-12% O2 to the ewe. During 2-h periods of hypoxia left pulmonary arterial blood flow decreased, and main pulmonary arterial and pulmonary vascular resistance increased. The increase in pulmonary vascular resistance was sustained throughout the 2-h period of hypoxia. After the return of the ewe to room air breathing, pulmonary vascular resistance remained elevated for at least 1 h despite the rapid correction of hypoxemia and in the absence of acidemia. In contrast, after 30 min of hypoxia, left pulmonary arterial blood flow, pulmonary arterial pressure, and pulmonary vascular resistance returned to base-line values rapidly with the termination of hypoxia. The persistent pulmonary hypoperfusion after 2 h of hypoxia was attenuated by alpha-adrenergic blockade and was characterized by a blunted vasodilatory response to increases in fetal PO2. When fetal PO2 was elevated during the posthypoxia period in the presence of alpha-blockade, pulmonary blood flow still remained unresponsive to increases in fetal PO2. We conclude that 2-h periods of acute hypoxia can decrease fetal pulmonary vasoreactivity, and we speculate that related mechanisms may contribute to the failure of the normal adaptation of the pulmonary circulation at birth.

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