Mechanism of Cardiogenic Shock

Guzmán, Santiago V.; Swenson, Edward W.; Mitchell, Robert A.

doi:10.1161/01.res.10.5.746

Cited by 29 publications

(4 citation statements)

References 13 publications

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“…The problem whether reflexes emanating from the heart may play a role for the circulatory adjustments in connection with experimental coronary infarction has been extensively studied. Levy and Frankel (1953), Wegria et al (1954), Struppler (1957, Matthes (1962), Guzman et al (1962 found no evidence for a depressor reflex from the left ventricle during the coronary infarction. On the contrary, Agress et al (1957 a, b) described a depressor reflex with the afferent connections in the sympathetic nerves during coronary infarction in dogs, but these observations have not been confirmed by others.…”

Section: Discussionmentioning

confidence: 96%

Evidence for a Depressor Reflex Elicited from Left Ventricular Receptors during Occlusion of One Coronary Artery in the Cat

Thorén

1973

Acta Physiologica Scandinavica

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Circulatory responses to shortlasting occlusions of one coronary artery (left anterior descendent or right coronary artery) were studied in chloralose‐anesthetized cats. — When the carotid sinus baroreceptors were left functionally intact, coronary occlusion induced moderate reflex reductions of heart rate and blood pressure and slight increases of resistance and capacitance vessel tone in the calf muscles. When the buffering influences from the baroreceptors were largely eliminated by bilateral carotid occlusion, the reflex fall of blood pressure and heart rate became more pronounced and a clearcut vasodilatation was now observed. After cold block of the cervical vagi, the blood pressure fall upon coronary obstruction was markedly diminished, the heart rate response was reversed to a slight tachycardia and a marked peripheral vasocon‐striction ensued. After i.v. administration of local anesthetics (lidocaine 3–4 mg/kg b.wt.) the reflex response to coronary obstruction and to shortlasting occlusions of the ascending aorta were almost completely eliminated. — It is concluded that acute occlusions of one coronary artery induce a reflex bradycardia and vasodilatation, in all probability due to activation of left ventricular mechanoreceptors. The vascular responses in this inhibitory reflex seem to be significantly moderated by influences from the arterial baroreceptors.

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Section: Discussionmentioning

confidence: 96%

Evidence for a Depressor Reflex Elicited from Left Ventricular Receptors during Occlusion of One Coronary Artery in the Cat

Thorén

1973

Acta Physiologica Scandinavica

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“…These findings agree with those of Agress et al 5 Aortic thermodilution curve from the same experiment as figure 1 recorded after plastic microspheres injected into the coronary arteries through an occluding aortic catheter. Guzman et al 2 also embolized the left anterior descending coronary artery by injecting lycopodium spores and noted a similarly diminished stroke output and systolic pressure.…”

Section: Discussionmentioning

confidence: 97%

“…Using the same dose, concentration, and suspending medium, other authors have reported that the spores lodge singly or in aggregates of 3 to 10 in arterioles 40 to 500 a in diameter. 2 Detailed observations were not begun until 10 to 15 minutes after embolization so that any immediate reflex or transient vasomotor responses could subside. The experiment was stopped usually when a persistent arrhythmia began; this occurred after an average of 6.7 embolizations.…”

Section: Methodsmentioning

confidence: 99%

Effect of Coronary Artery Embolization on Ventricular Volumes

Wong

Escobar

Martinez

et al. 1965

Circulation Research

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The measurement of ventricular volume enhances the ability to appraise ventricular performance. The development of the thermodilutdon method for estimating stroke volume (SV), end systolic volume (ESV), and end diastolic volume (EDV) allowed us to reexamine myocardial function at progressive degrees of ischemic injury produced by repeated embolizations of the coronary artery. We determined left ventricular SV, ESV, and EDV together with intraventricular pressures after embolizations by lycopodium spores injected into a branch of the left coronary artery. MethodsFifteen mongrel dogs (16 to 58 kg) were anesthetized with a mixture of 70 mgAg of chloralose and 350 mg/kg of urethane and were ventilated with a pump respirator. A 7F Sones catheter, introduced from the left common carotid artery, was placed under fluoroscopic control in the origin of the circumflex branch of the left coronary artery. The tip of the catheter lay 3 to 5 cm from the coronary ostium. Identical intracoronary and central aortic pressures provided assurance that the catheter did not occlude the vessel.tion of transient, marked T wave changes in the ECG by an injection of several milliliters of cool saline, and after the experiment by autopsy. A 4F catheter, with a rapidly responding bead thermistor embedded in its tip, was introduced through a femoral artery and positioned just above the aortic valve to obtain aortic thermodilution curves. An 8F catheter, with multiple side holes and a closed end passed from the other femoral artery into the left ventricle, was used to inject thermal indicator and to measure left ventricular (LV) pressure. Another thermistor bead secured within the lumen at the tip of this catheter recorded the temperature of the injectate as it left the catheter to enter the ventricle. Injections of a measured volume (usually about 3 ml) of cooled autologous blood were made with a compressed-air device triggered by the ECG through a time-delay circuit to permit injection generally within one diastole.The end systolic volume to end diastolic volume ratio (ESV/EDV), i.e., the fraction of the maximum ventricular volume remaining after systole, was calculated from the equation:where AT tt+1 and AT, are the differences between initial aortic temperature and that of beats T n+1 and T n recorded at end diastole on the stepfunction aortic thermodilution curve.Left ventricular stroke volume (SV) and end diastolic volume (EDV) were also calculated from the aortic thermodilution curve in the manner previously described. 1 In four experiments, SV was determined by the indicator dilution method using indocyanine green injected into the left ventricle and arterial dilution curves recorded from the brachial artery through a Gilford densitometer. End systolic volume (ESV) was calculated as the difference between EDV and SV.Thermodilution curves and intraventricular pressure were recorded during a control period and again after each embolization with lycopodium spores (30 to 40 /i diameter). Embolization was accomplished with a constant dose o...

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“…Nach den Untersuchungen von Metzger (19) (4,11,12,14,15,16,17,21,22) sowie der kardiogene Schock (13,20). Nach den Untersuchungen von Metzger (19) (4,11,12,14,15,16,17,21,22) sowie der kardiogene Schock (13,20).…”

Section: Diskussionunclassified

Hämodynamik und myokardiale Kontraktilität im experimentellen Tourniquet-Schock

Stock¹,

Geppert²,

Haase³

et al. 1976

Basic Res Cardiol

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A reproducible tourniquet-shock has been produced in hind limbs of dogs by unilateral and bilateral extremity ischemia. The following parameters have been measured for analysing the function of the cardiovascular system: mean aortic pressure, heart rate, cardiac output, intraventricular pressure and left ventricular pressure. From these data the stroke volume, stroke work, total peripheral resistance and the parameters of heart contractility dp/dtmax, dp/dtmax:IP and t-dp/dtmax were derived. During the ischemic period all circulatory parameters did not change in comparison to the controls. A tourniquet-shock developed upon recirculation of the ischemically stressed extremity which was more pronounced after bilateral than after unilateral hind leg ischemia. After release of the tourniquet all animals with unilateral tourniquet survived an observation period of 5 hours duration, whereas 6 out of 8 dogs with bilateral tourniquet died of heart failure. Upon release of the tourniquet, the cardiac output raised up to 140% of the normal value: the abruptly decreasing aortic pressure was fully compensated by a tachycardia from 100 to 190 (beats/minute). The parameters dp/dtmax:IP and t-dp/dtmax indicated a distinct increase of the left ventricular contractility in the early tourniquet-syndrom. Already after 30 minutes an increasing circulatory depression developed indicative of the decrease in aortic pressure, and enddiastolic pressure. At the same time an increase of heart rate and total peripheral resistance occurred. The parameters of left ventricular contractility did not change markedly during the course of shock except for the final stage.

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Mechanism of Cardiogenic Shock

Cited by 29 publications

References 13 publications

Evidence for a Depressor Reflex Elicited from Left Ventricular Receptors during Occlusion of One Coronary Artery in the Cat

Evidence for a Depressor Reflex Elicited from Left Ventricular Receptors during Occlusion of One Coronary Artery in the Cat

Effect of Coronary Artery Embolization on Ventricular Volumes

Hämodynamik und myokardiale Kontraktilität im experimentellen Tourniquet-Schock

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