Starling’s Riddle of the Broken Heart

2011 ◽  
pp. 77-87
Author(s):  
James R. Munis
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Cardiac Tamponade ◽  
Capillary Pressure ◽  
Resting State ◽  
Fluid Pressure ◽  
Active Contraction

In 1897, Ernest Starling lectured on heart failure by inducing cardiac tamponade in an anesthetized dog. When the tamponade began to have an effect, the arterial pressure began to fall, but the venous pressures began to rise. In other words, heart failure didn't just decrease one type of pressure, it simultaneously increased another type of pressure. By the end of the experiment, all pressures had converged to the same value. The heart, like any pump, doesn't just raise fluid pressure on one side, it simultaneously lowers fluid pressure on the opposite side. The heart has a peculiar architecture that prefers a slightly filled resting state. Any smaller volume actually requires active contraction—it passively springs open during a part of diastole, suctioning blood into itself. Why then does heart failure cause capillary edema? We understand that the pressure in large veins will rise with heart failure, but capillary pressure is on the left side of the intersection of the curve and the Pms line. As such, capillary pressure should decrease with heart failure, and the tendency toward edema similarly should decrease.

Autoregulation of intestinal capillary filtration rate

1982 ◽  
Vol 243 (6) ◽  
pp. G475-G483
Author(s):  
D. N. Granger ◽  
N. A. Mortillaro ◽  
M. A. Perry ◽  
P. R. Kvietys
Keyword(s):  
Arterial Pressure ◽  
Capillary Pressure ◽  
Filtration Rate ◽  
Pressure Range ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Filtration Coefficient ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Flow Capillary

To determine whether intestinal capillary filtration rate, capillary pressure, or both are autoregulated in the cat ileum, the following parameters were measured under isovolumetric conditions: lymph flow, capillary pressure, capillary filtration coefficient, and lymph and plasma oncotic pressures. Superior mesenteric arterial pressure was reduced in 25-mmHg steps from 125 to 25 mmHg. As arterial pressure was reduced, lymph flow, capillary pressure, and the transcapillary oncotic pressure gradient decreased while the capillary filtration coefficient increased. Over the arterial pressure range of 75-125 mmHg, capillary pressure decreased in a fashion expected from a rigid system; however, capillary pressure was slightly autoregulated at lower arterial pressures. Lymph flow fell proportionately more than capillary pressure over the entire arterial pressure range. The results of this study indicate that intestinal capillary pressure and capillary filtration rate are poorly autoregulated in the cat when arterial pressure is reduced. Changes in interstitial fluid pressure play a major role in preventing interstitial dehydration in the cat ileum when arterial pressure is reduced.

Cardiac tamponade from anticoagulant-related spontaneous haemopericardium in a patient with ischaemic cardiomyopathy and heart failure

2020 ◽  
Vol 13 (12) ◽  
pp. e238047
Author(s):  
Alicia Lefas ◽  
Neil Bodagh ◽  
Jiliu Pan ◽  
Ali Vazir
Keyword(s):  
Heart Failure ◽  
Cardiac Tamponade ◽  
Ventricular Dysfunction ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Left Ventricular ◽  
Heart Failure Therapy ◽  
Severe Left Ventricular Dysfunction ◽  
Ischaemic Cardiomyopathy ◽  
Common Causes

We describe the case of an 86-year-old man with a background of severe left ventricular dysfunction and ischaemic cardiomyopathy who, having been optimised for heart failure therapy in hospital, unexpectedly deteriorated again with hypotension and progressive renal failure over the course of 2 days. Common causes of decompensation were ruled out and a bedside echocardiogram unexpectedly diagnosed new pericardial effusion with tamponade physiology. The patient underwent urgent pericardiocentesis and 890 mL of haemorrhagic fluid was drained. Common causes for haemopericardium were ruled out, and the spontaneous haemopericardium was thought to be related to introduction of rivaroxaban anticoagulation. The patient made a full recovery and was well 2 months following discharge. This case highlights the challenges of diagnosing cardiac tamponade in the presence of more common disorders that share similar non-specific clinical features. In addition, this case adds to growing evidence that therapy with direct oral anticoagulants can be complicated by spontaneous haemopericardium, especially when coadministered with other agents that affect clotting, renal dysfunction and cytochrome P3A5 inhibitors.

When to treat symptomless essential hypertension

1982 ◽  
Vol 20 (14) ◽  
pp. 53-54
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Renal Failure ◽  
Essential Hypertension ◽  
Drug Therapy ◽  
Arterial Pressure ◽  
Drug Treatment ◽  
Absolute Risk ◽  
Sodium Restriction ◽  
Cardiovascular Morbidity And Mortality

The risk of cardiovascular morbidity and mortality increases in proportion to the arterial pressure at all ages and in both sexes. Most authorities regard blood pressure above 140 mmHg systolic, 90 mmHg diastolic as abnormal. The absolute risk of raised blood pressure is greater in men than women, men being more liable to coronary disease. Raised blood pressure predisposes to stroke, cardiac ischaemia and heart failure, progressive renal failure, retinal lesions and malignant hypertension. Lowering the blood pressure reduces the risks of these complications. Non-drug measures which can help and are worth considering before drug therapy include regular meditation, sodium restriction, weight reduction, and cessation of cigarette smoking. The efficacy of these is however less well proven than that of drug treatment. This article discusses when drug treatment should be considered. Barritt1 presents the arguments in more detail.

Abstract 16344: Pericardial Complications in Patients With COVID-19: A Systematic Review of Published Cases

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sandeep Singh ◽  
Akhil Jain ◽  
Priyanka Chaudhari ◽  
Faizan Ahmad Malik ◽  
Virmitra Desai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pericardial Effusion ◽  
Cardiac Tamponade ◽  
Troponin I ◽  
Case Reports ◽  
Cardiac Injury ◽  
Pericardial Tamponade ◽  
Time Interval ◽  
Cardiac Damage ◽  
St Segment Elevation

Introduction: COVID-19 has been linked to cardiac damage and life-threatening pericardial complication on which data are trivial which incited us to perform this review of published case reports. Methods: PubMed/Medline, Web of Science and SCOPUS were searched until June 2020 for case reports on COVID-19-associated pericarditis, cardiac tamponade or pericardial effusion. Results: We identified 8 articles reporting 11 COVID-19 positive cases [mean age: 51.4±14.3 (34-78 yrs) 5 male/6 female)] with pericardial complications. All (100%) cases were COVID-19 positive at the presentation with ~80% having dyspnea, chest pain and cough. Time interval from first symptom to pericardial effusion was 7±8 (1-26) days. Five patients reported heart failure with reduced EF on echocardiography with mean LVEF 36.25%±8.54%. All patients showed nearly normal Troponin-I without angiographically significant stenosis except one. Out of 8 cases on echocardiography 4 cases reported with diffuse hypokinesia, 2 reported inferior and inferolateral walls hypokinesia and 2 reported signs of pericardial tamponade. Out of 11 patients, cardiovascular risk factors in the form of diabetes or hypertension or obesity were present in 5 patients. Cardiovascular comorbidities such as heart failure with low ejection fraction, non-ischemic cardiomyopathy and prior myocarditis were present in 3 patients. ST-segment elevation in 3, sinus tachycardia in 2, T wave inversion in 1 case were noted. Four patients developed cardiac tamponade, 1 developed takotsubo syndrome and 3 patients died. Conclusions: COVID-19 patients had signs of a high burden of cardiac injury. Pericardial complications (pericardial effusion and cardiac tamponade) remain infrequent complications which may require prompt care to avoid mortality.

P1674High intensity interval exercise program in heart failure patients seems to benefit cardiac power along with aorto-ventricular mechanical pump capacity and cardiorespiratory indices

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Chrysohoou ◽  
A Angelis ◽  
G Titsinakis ◽  
D Tsiachris ◽  
P Aggelopoulos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Wave Velocity ◽  
Pulse Wave ◽  
Intervention Group ◽  
Control Group ◽  
Interval Exercise ◽  
Cardiac Power

Abstract Background Cardiac power has been suggested as the most power predictor of mortality in heart failure (HF) patients. In those patients aorta elastic properties and compensation is lost, systolic (and pulse) pressure are therefore reduced and associated with a decrease in ejection duration and pump efficiency. Cardiac rehabilitation programs have showed enhancement in cardiac performance and quality of life in HF patients. Aim Aim of this work was to evaluate the effect of high-intensity interval exercise (i.e., 30 sec at 100% of max workload, followed by 30 sec at rest, on a day-by-day 30 minutes working-out schedule for 12 weeks), on cardiac power, diastolic function indices, right ventricle performance and cardiorespiratory parameters among chronic HF patients. Methods 72 consecutive HF patients (NYHA class II-IV, ejection fraction <50%) who completed the study (exercise training group, n=33, 63±9 years, 88% men, and control group, n=39, 56±11 years, 82% men), underwent cardiopulmonary stress test, non-invasive high-fidelity tonometry of the radial artery, pulse wave velocity measurement using a SphygmoCor device, and echocardiography before and after completion of the training program. Cardiac power output (CPO) (W) was calculated as mean arterial pressure × CO/451, where mean arterial pressure = [(systolic blood pressure − diastolic blood pressure)/3] + diastolic blood pressure. Results Both groups reported similar medical characteristics and physical activity status. General mixed effects models revealed that the intervention group increased 6MWT (by 13%, p<0.05); increased cycle ergometry WRpeak (by 25%, p<0.01), showed higher O2max by 31% (p<0.001) and lower VE/VCO2 (p=0.05), whereas patients in the control group showed nosignificant changes in the aforementioned indices. Also, in the intervention group Emv/Vp was decreased by 14% (p=0.06); E to A ratio by 24% (p=0.004) and E to Emv ratio by 8% (p=0.05); while Stv increased by 25% (p=0.01). Most importantly, the intervention group reduced pulse wave velocity by 9% (p=0.05) and increased augmentation index by 26%; and VTI by 4% (p=0.05); Those parameters were not significantly changed on control group (all p>0.05). Conclusion Hight intensity exercise rehabilitation program revealed beneficial effect on left ventricular diastolic indices and right ventricle performance. As, in those patients compensation of the aorta is also lost and the LV cannot generate the extra force necessary to completely overcome the late systolic augmented pressure, the increase in the augmented pressure (AIa) observed in the intervention group reflects the benefit in aorto-ventricular coupling and cardiac power that boosts systolic pressure and restores a positive influence in pressure, like in early stages of HF. Acknowledgement/Funding None

Mechanism of glucagon-induced intestinal secretion

1980 ◽  
Vol 239 (1) ◽  
pp. G30-G38
Author(s):  
D. N. Granger ◽  
P. R. Kvietys ◽  
W. H. Wilborn ◽  
N. A. Mortillaro ◽  
A. E. Taylor
Keyword(s):  
Capillary Pressure ◽  
Plasma Proteins ◽  
Fluid Pressure ◽  
Intestinal Secretion ◽  
Tissue Samples ◽  
Mucosal Membrane ◽  
Osmotic Reflection Coefficient ◽  
Capillary Fluid ◽  
Higher Doses ◽  
Flow Capillary

The effects of local intra-arterial glucagon infusion on transcapilary, lymphatic, and transmucosal fluid and protein fluxes were studied in autoperfused segments of cat ileum. The glucagon infusions resulted in a significant increase in intestinal blood flow, lymph flow, capillary filtration coefficient, capillary pressure, interstitial volume, and interstitial fluid pressure. Precapillary resistance and the pre-to-postcapillary resistance ratio decreased during the glucagon infusion. The transcapillary oncotic pressure gradient and the osmotic reflection coefficient were reduced, suggesting that capillary permeability is significantly increased with glucagon. Ultrastructural analysis of tissue samples acquired during the infusion of higher doses of glucagon indicates disruption of the mucosal membrane. An glucagon indicates disruption of the mucosal membrane. An alteration in mucosal structure is supported by the appearance of plasma proteins in the secreted fluid. The results of this study indicate that glucagon-induced intestinal secretion results from an alteration in capillary fluid balance, i.e., an increased capillary pressure and permeability.

Role of the renal medulla in volume and arterial pressure regulation

1997 ◽  
Vol 273 (1) ◽  
pp. R1-R15 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Fluid Pressure ◽  
Regulatory System ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vasa Recta ◽  
Pressure Natriuresis ◽  
Total Renal Blood Flow

The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W., N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named "hormones," importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

2001 ◽  
Vol 280 (2) ◽  
pp. H576-H581 ◽  
Author(s):  
Wei Wang ◽  
Harold D. Schultz ◽  
Rong Ma
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Volume Expansion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Volume Expansion ◽  
Cardiac Sympathetic Afferent Reflex

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 μg) and capsaicin (10 and 100 μg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 μg) of epicardial bradykinin (17. 3 ± 1.9 vs. 10.6 ± 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 ± 4.1 vs. 5.0 ± 1.3% for 5 μg, P < 0.05, and 28.9 ± 3.7 vs. 10.6 ± 4.8% for 50 μg, P < 0.05) and capsaicin (29.8 ± 6.0 vs. 9.3 ± 3.1% for 10 μg, P < 0.05, and 34.2 ± 2.7 vs. 15.1 ± 2.7% for 100 μg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.

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