Electrocardiogram of Patient in Anaphylactic Shock

Bernreiter, M

doi:10.1001/jama.1959.03010140008003

Cited by 44 publications

(17 citation statements)

References 4 publications

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“…One patient with persistent hypotension developed transient electrocardiographic changes consistent with inferior myocardial wall ischemia. The electrocardiographic changes have been noted by previous investigators who have documented persistent electrocardiographic changes occurring in healthy individuals after anaphylaxis regardless of the cause (4,5). There was no evidence of primary cardiac dysfunction.…”

Section: Discussionsupporting

confidence: 77%

“…Since these reactions are usually unexpected and occasionally fatal, opportunities to investigate systematically the detailed pathophysiology with controlled studies are exceedingly rare. Most of the available data concerning the pathophysiology and treatment ofhuman anaphylaxis are derived from anecodotal clinical case reports and postmortem studies (1)(2)(3)(4)(5).…”

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confidence: 99%

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Physiologic manifestations of human anaphylaxis.

Smith¹,

Kagey‐Sobotka²,

Bleecker³

et al. 1980

J. Clin. Invest.

353

141

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A B S T R A C T In the course of a controlled study to evaluate different forms of immunotherapy for subjects with insect-sting hypersensitivity, we observed 11 subjects who had systemic cutaneous urticarial reactions and 3 subjects who experienced systemic anaphylaxis. With the exception of tachyeardia, there were no cardiopulmonary changes in the subjects with urticaria, whereas the major manifestation of anaphylactic shock in the other three subjects was severe hypotension that was probably secondary to peripheral vasodilation. Significant abnormalities in gas exchange developed in two subjects. In one, bronchospasm precipitated a respiratory arrest followed by endotracheal intubation with mechanical ventilation. Although plasma histamine levels were not related to the development of cutaneous reactions, the plasma histamine levels correlated with the severity and duration of the cardiopulmonary changes observed during anaphylactic shock. The two subjects with the most severe shock showed evidence of intravascular coagulation characterized by a diminution of Factor V, Factor VIII, fibrinogen, and high molecular weight kininogen, as well as changes in components of the complement system. Standard therapy with epinephrine and fluids, usually recommended for the treatment of systemic anaphylaxis, did not immediately reverse either the hemodynamic or the respiratory abnormalities in the two subjects with the most severe

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Section: Discussionsupporting

confidence: 77%

mentioning

confidence: 99%

Physiologic manifestations of human anaphylaxis.

Smith¹,

Kagey‐Sobotka²,

Bleecker³

et al. 1980

J. Clin. Invest.

353

141

View full text Add to dashboard Cite

show abstract

“…In the course of systemic anaphylactic reactions in humans, severe cardiac dysfunction and fatal arrhythmias often occur as a primary event, not secondary to respiratory distress (Bernreiter, 1959;James and Austen, 1964;Booth and Patterson, 1970;Criep and Woehler, 1971;Austen, 1974;Wegmann and Renker, 1976). Although cardiac histamine release has not been measured under these circumstances, it is conceivable that histamine mediates these arrhythmias, since released histamine appears to be the cause of severe arrhythmias and cardiac arrest following a variety of therapeutic and diagnostic procedures in man (Lorenz, 1975;Witten, 1975).…”

Section: Discussionmentioning

confidence: 99%

Acceleration of idioventricular rhythms by histamine in guinea pig heart: mediation by H2 receptors.

Levi¹,

Zavecz²

1979

Circulation Research

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SUMMARY To evaluate the ability of histamine to induce ventricular arrhythmias, we studied the effects of histamine on ventricular rhythmicity in the isolated guinea pig heart with complete atrioventricular conduction block. As a function of dose (0.1-30 pg), histamine enhanced the idioventricular rate by increasing the rate of firing of the original pacemaker and also by causing the sudden appearance of faster idioventricular rhythms that coincided with changes in pacemaker site. Anaphylaxis in the isolated guinea pig heart with complete atrioventricular conduction block caused histamine release and acceleration of idioventricular rate. The effects of histamine on idioventricular rhythmicity were not attenuated by the histamine Hi receptor antagonist chlorpheniramine, but were antagonized by the Hi receptor antagonist cimetidine. Moreover, the selective Hi agonist 4-methylhistamine (4MeH) accelerated the idioventricular rate, whereas 2-(2-thiazolyl) ethylamine (ThEA), at doses selective for Hi receptor activation, did not. The effects of histamine on idioventricular rhythmicity were not modified by the /J-adrenergic blocker pindolol. The mechanism by which histamine increases idioventricular rate probably involves two components: (1) an enhancement in automaticity of the original pacemaker, and (2) IN THE course of our studies on the cardiac effects of histamine we had become intrigued by the fact that histamine, whether exogenously administered or endogenously released, could induce ventricular dysrhythmias ranging from isolated multifocal ectopic beats to ventricular tachycardia and fibrillation. The severity of the arrhythmia was related to the amounts of histamine injected or released (Levi, 1972;Capurro and Levi, 1975;Levi and Capurro, 1975;Zavecz and Levi, 1977). The purpose of the present study was to investigate the mechanism of histamine-induced ventricular tachyarrhythmias by studying the influence of histamine on ventricular rhythmicity. We chose as an experimental model the isolated mammalian heart with complete atrioventricular conduction block. In this preparation idioventricular rate is not influenced by atrial pacemakers. MethodsMale Hartley guinea pigs weighing 300-400 g were stunned by a blow to the base of the skull. The heart was quickly excised and mounted in a Langendorff apparatus (Levi, 1972) and was perfused at constant pressure (40 cm H 2 O) with oxygenated Ringer's solution at 37°C. The ionic composition of the Ringer's solution was (in mM): Na + , 160; Cl~, 164; K + , 5.6; Ca ++ , 2.2; HC0J, 5.9; glucose, 5.5 The apex of the heart was connected by a nylon thread to a force-displacement transducer (model FT03B, Grass Instruments). Isometric ventricular contractions were displayed on a pen recorder (model R511, Beckman Instruments, Inc.). A bipolar surface electrogram, recorded from the right atrium and the left ventricle, was displayed on another channel of the pen recorder.Following an equilibration period of 30-45 minutes, the right atrium was cut open and a ligature (5-0 surgical...

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“…Electrocardiographic changes ranging from transient ischemia to severe rhythm disturbances have been recorded during anaphylaxis of the rabbit (13), monkey (14), and man (15)(16)(17) conclusion that the guinea pig heart reacts as a target organ during systemic anaphylaxis can tentatively be extrapolated to other species.…”

mentioning

confidence: 99%

The heart as a target organ in systemic allergic reactions: comparison of cardiac analphylaxis in vivo and in vitro.

Capurro¹,

Levi²

1975

Circulation Research

126

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The purpose of this investigation was to define and quantitatively evaluate cardiac anaphylaxis in vivo. Guinea pigs, passively sensitized with graded amounts of rabbit antipenicilloyl antibody, were anesthetized, ventilated, and challenged intravenously with a constant amount of antigen (anaphylaxis in vivo). In other experiments, guinea pig hearts were excised, perfused in a Langendorff apparatus, and challenged (anaphylaxis in vitro). During in vivo anaphylaxis, sinus rate increased 10-30 beats/min, conduction arrhythmias occurred in 15 of 22 experiments, and ventricular fibrillation was seen in 8 of 22 experiments. Tachycardia and arrhythmias began approximately 20 seconds after antigen administration and were accompanied, but not preceded, by respiratory and pressor changes. During in vitro anaphylaxis, sinus rate increased 70-110 beats/min, coronary flow rate decreased 2-22%, conduction arrhythmias occurred in 21 of 31 experiments, and ventricular ectopic activity was seen in 13 of 31 experiments. Tachycardia and arrhythmias began approximately 15 seconds after antigen administration. Sinus tachycardia, atrioventricular conduction block, increased ventricular automaticity, and histamine release were characteristic features of cardiac anaphylaxis in vivo and in vitro. Both in vivo and in vitro, the intensity of the cardiac reaction depended on the amount of antibody used in passive sensitization. Our results clearly indicate that the heart reacts as a target organ in systemic anaphylaxis of the guinea pig. KEY WORDSguinea pig anaphylaxis isolated heart anaphylaxis cardiac histamine anaphylactic cardiac histamine release cardiac participation in systemic anaphylaxis drug allergy cardiac hypersensitivity to penicillin histamine release cardiac hypersensitivity reactions• Anaphylaxis of the isolated guinea pig heart is a specific crisis in cardiac function characterized by histamine release, tachycardia, arrhythmias, and decreased coronary flow (1, 2). These studies of cardiac anaphylaxis in vitro prompted us to investigate whether the heart undergoes such a reaction during systemic anaphylaxis. Cardiac involvement in systemic hypersensitivity reactions has not been clearly defined. Cardiac disturbances during systemic anaphylaxis in the guinea pig have been variously interpreted as a secondary reaction to the asphyxia produced by bronchospasm (3, 4), the result of ischemia produced by impaired coro- 520nary circulation (5), or a manifestation of direct participation of cardiac tissue (6).The purpose of the present investigation was to define the cardiac reaction as a consistent feature of systemic anaphylaxis in the guinea pig and to evaluate quantitatively the intensity of this reaction. Methods ANTIGENSBenzylpenicilloyl-protein conjugates (BPO-protein) were chosen as antigens. Benzylpenicillin was coupled to guinea pig gamma globulin (GPGG) and to bovine gamma globulin (BGG) according to the method of Levine (7). The number of haptenic groups per carrier molecule was estimated by the penamaldate me...

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Electrocardiogram of Patient in Anaphylactic Shock

Cited by 44 publications

References 4 publications

Physiologic manifestations of human anaphylaxis.

Physiologic manifestations of human anaphylaxis.

Acceleration of idioventricular rhythms by histamine in guinea pig heart: mediation by H2 receptors.

The heart as a target organ in systemic allergic reactions: comparison of cardiac analphylaxis in vivo and in vitro.

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