Cardiopulmonary Resuscitation In Dogs Research Articles

Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs.

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 +/- 1% to 46 +/- 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression.(ABSTRACT TRUNCATED AT 400 WORDS)

Venous and arterial blood gases during and after cardiopulmonary resuscitation in dogs

This study was undertaken to characterize blood gas, pH, and lactate changes during and after cardiopulmonary resuscitation (CPR) in arterial and venous samples. Blood samples were withdrawn from the brachial artery, aortic arch, pulmonary artery, coronary sinus, and either the right or left cardiac ventricle of 24 anesthetized dogs. Ventricular fibrillation (VF) was induced electrically, and mechanical CPR was begun. Blood samples were withdrawn before CPR, at 2, 5, 7, and 9 minutes during CPR, and at 1, 3, 10, 30, and 60 minutes after defibrillation. Control arterial and venous samples indicated mild metabolic acidosis. During CPR, there was a significant arteriovenous difference in pH, P CO 2 , and P O 2 . With ventilation onset, arterial pH increased 0.25 units, P CO 2 decreased 22 mm Hg, and P O 2 increased 200 mm Hg. Venous blood gases exhibited gradual changes during the CPR period. With the re-establishment of circulation and spontaneous respirations, both the arterial and venous pH levels decreased to nearly 7.1, and P CO 2 approached 40 mm Hg. Lactate increased to 32 mg/dl during 9 minutes of CPR and did not significantly differ after defibrillation. Blood gases and pH returned to control values within an hour. This study suggests that arterial blood gases are sensitive to rapid changes occurring in the pulmonary capillary bed, while venous blood gases reflect changes occurring in the systemic capillary bed.

Transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation in dogs.

Elevation of intrathoracic pressure during cardiopulmonary resuscitation generates carotid pressure and flow, but also increases intracranial pressure. This increase in intracranial pressure may limit cerebral blood flow. Therefore, we performed studies designed to quantify the extent of this transmission and to identify the mechanism of transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation in dogs. Intracranial pressure increased during the chest compression phase of all modes of cardiopulmonary resuscitation tested. During simultaneous compression-ventilation cardiopulmonary resuscitation, change in intracranial pressure (mm Hg) = 0.33 change in intrathoracic pressure (mm Hg) + 2.02 (r = 0.86) and was not significantly different from the relationship observed during conventional cardiopulmonary resuscitation. The magnitude of transmission of intrathoracic pressure to the intracranial space was increased by binding the abdomen and by raising the baseline intracranial pressure. No single route accounted for transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation. Intracranial pressure fluctuations were unrelated to either carotid arterial or jugular venous pressure, and were found instead to be the result of pressure transmission by blood in non-valved veins and by cerebrospinal fluid. This was determined by three maneuvers. First, obstruction of cerebrospinal fluid flow by ligation of the cervical spinal cord reduced intracranial pressure (P less than 0.001) and made the change in intracranial pressure equivalent to pressure changes at the confluence of the intracranial venous sinuses, without affecting pressure changes at the confluence of the intracranial venous sinuses. Second, ligation of the cervical spinal cord and one of the two longitudinal vertebral veins adjacent to the cervical cord reduced the pressure changes in the intracranial space and at the confluence of the intracranial venous sinuses to about 60% of the levels observed when the cervical cord alone was ligated. Thus, the non-valved longitudinal vertebral veins appear to be the vascular channels of critical importance to pressure transmission. Finally, pressure changes in the thoracic cerebrospinal fluid were increased (P less than 0.05) by cord ligation, even after exsanguination minimized pressure transmission via blood-filled channels, indicating direct transmission of intrathoracic pressure through intervertebral foramina to the cerebrospinal fluid.(ABSTRACT TRUNCATED AT 400 WORDS)

High Frequency Jet Ventilation Versus IPPV for CPR in Dogs

Investigation of High Frequency Jet Ventilation (HFJV) for cardiopulmonary resuscitation (CPR) was initiated to determine whether HFJV may be used as an alternative to conventional intermittent positive pressure ventilation (IPPV) and also to determine whether HFJV may be employed in CPR if cardiac arrest should occur during use of HFJV.The novel method of HFJV has several advantages over conventional ventilation, namely low airway pressure, no hemodynamic impairment and no need for muscle paralysis. Transtracheal HFJV offers in addition cricothyroid membrane puncture as a fast alternative to tracheal intubation in cases of difficult airway control. It is able to prevent aspiration, and allows direct intrapulmonary drug administration.

Regional blood flow during cardiopulmonary resuscitation in dogs.

We studied regional blood flow (QR) using radiolabeled microspheres in 12 anesthetized dogs during cardiopulmonary resuscitation (CPR). A circumferential vest and abdominal binder were used with a mechanical ventilator to deliver 30 simultaneous chest compressions and ventilations per minute. When this device was modified to increase aortic pressure (Pao) during compression and the aortic-to-right atrial pressure gradient (Pao-Pra) during relaxation, cerebral and myocardial QR increased significantly. These findings suggest that QR during CPR can be improved by augmenting perfusion-pressure gradients across the cerebral and coronary circulations.

Venous versus arterial blood gases during and after cardiopulmonary resuscitation in dogs : S. H. Ralston. Purdue University, West Lafayette, IN 47907

Venous versus arterial blood gases during and after cardiopulmonary resuscitation in dogs : S. H. Ralston. Purdue University, West Lafayette, IN 47907

Potential adverse effects of volume loading on perfusion of vital organs during closed-chest resuscitation.

To determine whether expansion of blood volume improves vital organ perfusion pressures and blood flow during closed-chest cardiopulmonary resuscitation in dogs, we recorded intracranial and high-fidelity ascending aortic and right atrial pressures and measured total and regional blood flow with radioactive microspheres during cardiopulmonary resuscitation before and after rapid infusion of 1 liter of saline or dextran in 12 animals. Volume loading increased total forward blood flow from 327.1 +/- 50.9 to 692.7 +/- 105.9 ml/min (p less than .01). However, blood flow to the cerebral hemispheres, cerebellum, brainstem, and ventricular myocardium all decreased significantly. For example, blood flow to the left cerebral hemisphere fell from 16.5 +/- 2.4 to 5.5 +/- 1.7 ml/min/100 g (p less than .001), while left ventricular myocardial blood flow fell from 12.0 +/- 3.1 to 4.1 +/- 0.8 ml/min/100 g (p less than .05). These changes in critical regional flow were accompanied by disproportionate increases in right atrial and intracranial pressures (relative to aortic pressure), which reduced the average pressure differences generated across the coronary and cerebral circulations from 11.0 +/- 2.5 to 3.7 +/- 1.3 mm Hg (p less than .01) and from 16.1 +/- 2.3 to 10.5 +/- 1.5 mm Hg (p less than .01), respectively. The overall rise in forward flow was associated with a marked increase in extracranial, brachiocephalic blood flow. These findings suggest that large increments in blood volume can reduce vital organ perfusion during cardiopulmonary resuscitation despite an increase in total forward blood flow.

Regional blood flow during cardiopulmonary resuscitation in dogs using simultaneous and nonsimultaneous compression and ventilation.

We studied regional blood flow (QR) using radiolabeled microspheres and measured hemodynamic variables in 20 anesthetized dogs in normal sinus rhythm and during ventricular fibrillation treated with cardiopulmonary resuscitation (CPR). Nonsimultaneous compression and ventilation CPR (NSCV-CPR) was performed in seven dogs with a pneumatic piston that gave 50 chest compressions/min with an open airway with 10 ventilations at an airway pressure of 33 mm Hg interposed between each fifth and sixth compression. Simultaneous compression and ventilation (SCV-CPR) was performed in seven dogs with the piston and in six other dogs with a circumferential pneumatic vest. Both devices gave 30 compressions/min simultaneously with 30 ventilations that elevated airway pressure to 80 mm Hg., The abdomen was bound during SCV-CPR. Regional blood flow (mean +/- SD) to the cerebral hemispheres, cardiac ventricles, and kidneys, expressed as ml/min/100 g tissue, was 3.1 +/- 4.0, 3.4 +/- 3.3 and 1.5 +/- 1.5, respectively, during NSCV-CPR; 11.5 +/- 5.9, 4.9 +/- 4.7 and 2.7 +/- 2.7 during SCV-CPR (vest); and 16.2 +/- 7.2, 11.0 +/- 4.0 and 20.1 +/- 20.2 during SCV-CPR (piston) (all p less than 0.05 compared with NSCV-CPR). These results indicate that QR to all organs studied is reduced below normal sinus rhythm levels during CPR for ventricular fibrillation, QR to the brain is proportionately greater than QR to the heart and kidneys, and QR to the brain is greater with both forms of SCV-CPR than with NSCV-CPR.

Effects of Positive End-Expiratory Pressure on Carotid Blood Flow during Closed-Chest Cardiopulmonary Resuscitation in Dogs

The effect of continuous increases in intrathoracic pressure by positive end-expiratory pressure (PEEP) on common carotid artery blood flow (CCABF) and arterial blood gas tensions and pH during standard closed-chest cardiopulmonary resuscitation was studied in dogs. CCABF was measured at various levels of PEEP by means of the bubble flowmeter in hypervolemic, normovolemic, and hypovolemic dogs. PEEP was increased and then decreased in 5-cm H2O increments with the highest level being 20 cm H2O. Arterial blood samples were obtained approximately 15 minutes before ventricular fibrillation was induced with a transthoracic electric shock during zero end-expiratory pressure during increases in PEEP to 20 cm H2O, and again during decreases to zero end-expiratory pressure. CCABF increased stepwise with increasing levels of PEEP in hypervolemic dogs, whereas it decreased stepwise with increasing levels of PEEP in hypovolemic dogs. In normovolemic dogs, CCABF increased only when the PEEP was 5 cm H2O. Severe metabolic acidosis developed in both hypovolemic and normovolemic dogs at the end of 18 minutes of cardiopulmonary resuscitation. It is speculated that PEEP can either increase CCABF by increasing intrathoracic pressure during chest compression or decrease the CCABF by decreasing venous return during chest compressions, depending on the circulating blood volume. Data suggest that even low levels of PEEP are contraindicated in hypovolemia. Although changes in cerebral perfusion caused by PEEP were not investigated, it is suggested that some degree of PEEP may be beneficial in the hypervolemic state during cardiopulmonary resuscitation.

Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Experimental design for study of cardiopulmonary resuscitation in dogs

Many different designs for studies of various aspects of cardiopulmonary resuscitation (CPR) in dogs are described in the literature. No single technique is generally accepted. We present a systematized approach to the study of CPR in the canine model. Cardiac output, arterial blood pressure, and electrocardiogram were recorded for three different methods. The methods studied were closed chest compression, closed chest compression with an automatic gas-powered chest compressor, and open chest manual cardiac massage. Cardiac output for both types of external chest compression were less than 17% of control in all cases. With open chest cardiac massage, systemic arterial blood pressures were in the 50 mm Hg to 100 mm Hg range and cardiac output of up to 70% of control was achieved. Using a metronome to obtain compression rate and the arterial blood pressure to guide the efficacy of compression, consistent levels of cardiac output could be achieved for up to 30 minutes using open chest cardiac massage. Closed chest massage in man results in a cardiac output of 25% to 30% of normal when performed under optimal conditions. A cardiac output of 25% to 30% of control cannot be achieved in large dogs with external chest compression, and hence is not a good model to stimulate CPR in man.

INfluence of interposed ventilation pressure upon artificial cardiac output during cardiopulmonary resuscitation in dogs.

This study was conducted to determine the effects of high pressure interposed ventilations during cardiopulmonary resuscitation (CPR). Cardiac output was measured by a modified indicator dilution technique in eight anesthetized, intubated mongrel dogs. Positive pressure ventilations (12/min, 80% O2) were interposed after every five chest compressions (performed at 62/min) by a mechanical chest compressor (Thumper). On repeated trials in the same animal, ventilation pressures from 10--50 cm of H2O were tested in randomized sequence, while the technique of chest compression was held constant. Arterial blood gases immediately after resuscitation were monitored. Increasing ventilation pressure had surprisingly little effect on cardiac output curing CPR, although blood gases were profoundly altered. For ventilation pressures of 10, 20, 30, 40, and 50 cm of H2O, producing mean tidal volumes 23, 38, 61, 83, and 94 ml/kg; cardiac output remained nearly constant, averaging 21, 25, 23, 26, and 24 ml/min . kg. Corresponding mean postresuscitation pH was 7.24, 7.41, 7.51, 7.56, and 7.53; PCO2 was 41, 26, 18, 16, and 15 torr. The postresuscitation arterial oxygen tension was greater than 100 torr at all ventilation pressures except 10 cm of H2O. Interposed ventilations of pressure and volume more than adequate to prevent acidosis during CPR did not impair artificial cardiac output. If anything, cardiac output was slightly improved by more forceful ventilation.

Regional blood flow during cardiopulmonary resuscitation in dogs.

To determine differences in regional blood flow during CPR versus normal cardiac function, the authors measured regional blood flow to several organs in 19 pentobarbital-anesthetized dogs (6--12 kg). Regional blood flow was measured during sinus rhythm in five dogs and during electrically induced ventricular fibrillation with CPR in the other 14 dogs. Regional blood flow and cardiac output were measured using radioactively labeled polystyrene microspheres of 15 +/- 3 mu diameter, injected into the left ventricle. Adequacy of microsphere mixing at low cardiac outputs was verified by comparing flow rates to paired organs. Cardiac output was 175 ml/kg . min during sinus rhythm versus 47 ml/kg . min during CPR. Flow to all organs sampled was less during CPR, but the relative decrease varied widely. The ratios of regional blood flow during CPR to regional blood flow during sinus rhythm were 90% for brain, 35% for heart, 15% for kidneys, 17% for adrenal glands, 14% for pancreas, 3% for spleen, and 33% for small intestine. These results provide baseline values for regional blood flow during CPR which can be used to evaluate alternative CPR techniques and/or drugs which may improve perfusion of vital organs during CPR.

Test of wave-speed theory of flow limitation in elastic tubes.

ARTICLESTest of wave-speed theory of flow limitation in elastic tubesE. A. Elliott, and S. V. DawsonE. A. Elliott, and S. V. DawsonPublished Online:01 Sep 1977https://doi.org/10.1152/jappl.1977.43.3.516MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMimicking a flow-limited human upper airway using a collapsible tube: relationships between flow patterns and pressures in a respiratory modelKaixian Zhu, Ramon Farré, Ira Katz, Sébastien Hardy, and Pierre Escourrou22 August 2018 | Journal of Applied Physiology, Vol. 125, No. 2Relation of concavity in the expiratory flow-volume loop to dynamic hyperinflation during exercise in COPDRespiratory Physiology & Neurobiology, Vol. 234State-dependent and reflex drives to the upper airway: basic physiology with clinical implicationsRichard L. Horner, Stuart W. Hughes, and Atul Malhotra*1 February 2014 | Journal of Applied Physiology, Vol. 116, No. 3Liquid VentilationTotal Liquid Ventilation: Dynamic Airway Pressure and the Development of Expiratory Flow LimitationASAIO Journal, Vol. 50, No. 5Assessment of the development of choked flow during total liquid ventilationCritical Care Medicine, Vol. 32, No. 1The Male Predisposition to Pharyngeal CollapseAmerican Journal of Respiratory and Critical Care Medicine, Vol. 166, No. 10Mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs. I. StaticsStephanie A. Tuck, and John E. Remmers1 June 2002 | Journal of Applied Physiology, Vol. 92, No. 6Mechanical properties of the passive pharynx in Vietnamese pot-bellied pigs. II. DynamicsStephanie A. Tuck, and John E. Remmers1 June 2002 | Journal of Applied Physiology, Vol. 92, No. 6Interdependence of flow between lobes reduces maximal emptying postresection in dogsDavid Ewing-Bui, and Steven N. Mink1 January 2002 | Journal of Applied Physiology, Vol. 92, No. 1Gender Differences in the Expression of Sleep-Disordered BreathingChest, Vol. 120, No. 5Modeling expiratory flow from excised tracheal tube lawsNikolai Aljuri, Lutz Freitag, and José G. Venegas1 November 1999 | Journal of Applied Physiology, Vol. 87, No. 5Effect of expiratory flow limitation on respiratory mechanical impedance: a model studyR. Peslin, R. Farré, M. Rotger, and D. Navajas1 December 1996 | Journal of Applied Physiology, Vol. 81, No. 6Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure.Circulation Research, Vol. 65, No. 4The effects of wall thickness, axial strain and end proximity on the pressure-area relation of collapsible tubesJournal of Biomechanics, Vol. 20, No. 9A consideration of density dependence of maximum expiratory flowRespiration Physiology, Vol. 52, No. 1Methods of study of airway smooth muscle and its physiologyPharmacology & Therapeutics, Vol. 7, No. 2 More from this issue > Volume 43Issue 3September 1977Pages 516-522 Copyright & PermissionsCopyright © 1977 the American Physiological Societyhttps://doi.org/10.1152/jappl.1977.43.3.516PubMed914722History Published online 1 September 1977 Published in print 1 September 1977 Metrics

Determinants of maximal expiratory flow from the lungs.

Determinants of maximal expiratory flow from the lungs.

Ventilation-cardiac compression rates and ratios in cardiopulmonary resuscitation.

Ventilation-compression frequencies and ratios during cardiopulmonary resuscitation in dogs with ventricular fibrillation and ventilation frequencies in apneic healthy human subjects were studied. Lung inflations interposed between sternal compressions gave better ventilation and about equal carotid blood flows as compared to simultaneous inflations. A ventilation—compression ratio of 3/15 (using air) maintained normal oxygenation and ventilation, whereas 6/30 did not In apneic adults with two inflations (tidal volume 1,000 ml) every 15 seconds, oxygenation and ventilation were adequate with FiO26O compressions per minute, while 120 compressions per minute gave insignificantly greater flows than 72 compressions per minute. The recommendation of a ventilation—compression ratio of 2/15 for one operator and 1/5 interposed for two operators (compressions at one second intervals without interruption) is sound.