Mechanism of Acute Hypotension from Fear or Nausea

Sharpey‐Schafer, E. P.; Hayter, C. J.; Barlow, Edward

doi:10.1136/bmj.2.5101.878

Cited by 70 publications

(13 citation statements)

References 7 publications

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“…The effect was attributed to an increase in the amount of blood available for the heart to pump. 15 Sharpey-Schafer et al 21 further commented “there seems to be some truth in the popular belief that fainting may be prevented by taking a grip on oneself.” In 1946, Engel and Romano 22 also emphasized the importance of muscle tension and commented that the sensation of muscle weakness before fainting was typical. Studies of the relationship between intramuscular pressure, venous return, and orthostatic tolerance were performed in the 1930s.…”

Section: Experiments During World War Ii: Documentation Of Vasodilatimentioning

confidence: 99%

Cardiac output and vasodilation in the vasovagal response: An analysis of the classic papers

et al. 2016

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The simple faint is secondary to hypotension and bradycardia resulting in transient loss of consciousness. According to Ohm’s law applied to the circulation, BP = SVR × CO, hypotension can result from a decrease in systemic vascular resistance (SVR), cardiac output (CO), or both. It is important to understand that when blood pressure (BP) is falling, SVR and CO do not change reciprocally as they do in the steady state. In 1932, Lewis, assuming that decreased SVR alone accounted for hypotension, defined “the vasovagal response” along pathophysiologic lines to denote the association of vasodilation with vagal-induced bradycardia in simple faint. Studies performed by Barcroft and Sharpey-Schafer between 1940 and 1950 used volume-based plethysmography to demonstrate major forearm vasodilation during extreme hypotension and concluded that the main mechanism for hypotension was vasodilation. Plethysmographic measurements were intermittent and not frequent enough to capture rapid changes in blood flow during progressive hypotension. However, later investigations by Weissler, Murray, and Stevens performed between 1950 and 1970 used invasive beat-to-beat BP measurements and more frequent measurements of CO using the Fick principle. They demonstrated that CO significantly fell before syncope, and little vasodilation occurred until very late in the vasovagal reaction Thus, since the 1970s, decreasing cardiac output rather than vasodilation has been regarded as the principal mechanism for the hypotension of vasovagal syncope.

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Section: Experiments During World War Ii: Documentation Of Vasodilatimentioning

confidence: 99%

Cardiac output and vasodilation in the vasovagal response: An analysis of the classic papers

et al. 2016

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“…There is also literature supporting the notion that an ''empty heart'' might contribute to cardiac receptor stimulation resulting in afferent activation involved in a bradycardia and subsequent ''vasovagal'' syncope. 25 As such, bradycardia represents a ''last ditch effort'' to save the organism by optimizing cardiac filling time and reducing cardiac work in critically low circulating volume states when coronary blood flow is compromised. 26 …”

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confidence: 99%

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

Schiller

Howard

Convertino

2017

Exp Biol Med (Maywood)

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Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss. AbstractThe ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflexmediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock).

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“…An alternative possibility is that a nervous reflex is initiated by, for instance, acute coronary occlusion, originating either in the coronary arteries themselves or in the ischaemic myocardium. Pressure receptors are known to exist in cardiac muscle (Sharpey-Schafer, Hayter, and Barlow, 1958;Sharpey-Schafer, 1956), and it has been suggested that they may be responsible for initiating vasovagal collapse when severe pressure transients develop in the left ventricle, if it contracts forcibly on an empty cavity. It may be that myocardial nerve endings are stimulated by acute ischaemia due to coronary occlusion and that they could initiate asystole of one ventricle, but there appears to be no experimental evidence to support this supposition.…”

Section: Discussionmentioning

confidence: 99%

Univentricular Asystole after Myocardial Infarction

Harley¹

1962

Thorax

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Two patients with fatal cardiac arrest after myocardial infarction in which there was asystole of one ventricle are presented.CASE HISTORIES CASE I.-J. L., aged 77, was admitted to the Cardiff Royal Infirmary on December 26, 1959, because of cardiac failure. He gave a history of shortness of breath on exertion for two months and of pain behind the middle of the sternum on exercise for one month. This was relieved by rest. On two occasions during this time he awoke at night short of breath. For several weeks he had had giddy attacks in which he thought he would faint, but he never actually did so. He had suffered from a cough with expectoration of mucoid sputum for one week.On admission the jugular venous pressure was slightly raised and there was oedema of the sacrum and ankles but no enlargement of the liver. The pulse was irregular and a systolic murmur was heard at the apex. The blood pressure was 140/70 mm. Hg. A few wheezes were present throughout both lungs. The electrocardiogram (Fig. 1) taken on December 28, 1959, showed a vertical heart pattern with marked clockwise rotation, neutral axis deviation, and sinus rhythm with normal P waves. There was no evidence of hypertrophy of either ventricle or of bundle branch block. The T waves were upright in all the praecordial leads, but the RS-T segments were depressed slightly in V7 and aVF, suggesting myocardial ischaemia. Postero-anterior and lateral chest films ( Fig. 2) showed a small effusion into the right pleural cavity and a moderate-sized one on the left. The heart was considerably enlarged, the lung fields showed the appearances of pulmonary venous hypertension, and the aorta was calcified in its arched and upper descending portions. The urine was turbid and alkaline but contained no albumin, and the deposit showed amorphous debris only. The blood urea on December 29, 1959, was 104 mg. per 100 ml. The haemoglobin was 11.4 g. (77%) and the red blood cells were slightly hypochromic and showed anisocytosis and poikilocytosis: the total white and differential count was normal.The patient was treated for heart failure with digoxin and chlorothiazide, and was given glyceryl trinitrite for the anginal pain. While on treatment he developed acute retention of urine: because an enlarged prostate was found, it was decided to perform cystoscopy and prostatectomy.On January 1, 1960, at 9.45 a.m. the patient was given 0.6 mg. of atropine, and at 10.30 a.m. anaesthesia was commenced. Oxygen, nitrous oxide, and halothane were administered and a cuffed endotracheal tube was inserted: induction of anaesthesia was smooth. At 10.40 a.m., while the patient was being wheeled from the anaesthetic room to the operating theatre, he became cyanosed and pulseless and spontaneous respiration ceased. Cardiac arrest was diagnosed, the chest and pericardium were opened immediately, and cardiac massage was begun within three minutes. Five minutes later the writer arrived in the theatre and took over manual cardiac compression. The right ventricle was contracting strongly, but the lef...

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Mechanism of Acute Hypotension from Fear or Nausea

Cited by 70 publications

References 7 publications

Cardiac output and vasodilation in the vasovagal response: An analysis of the classic papers

Cardiac output and vasodilation in the vasovagal response: An analysis of the classic papers

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

Univentricular Asystole after Myocardial Infarction

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