Increase In Intrapericardial Pressure Research Articles

THE MISSING PIECE OF THE PERICARDIUM WHICH PREVENTED HEMODYNAMIC COMPROMISE

Cardiac tamponade is caused by increase in intra-pericardial pressure from accumulation of fluid in the pericardial space leading to hemodynamic compromise. We describe a case of very large pericardial effusion (PE) with preserved hemodynamics from removal of anterior pericardium. 56 year old man

CARDIAC TAMPONADE INCIDENCE, DEMOGRAPHICS AND IN-HOSPITAL OUTCOMES: ANALYSIS OF THE NATIONAL INPATIENT SAMPLE DATABASE

Cardiac tamponade (CT) is a life threatening condition caused by an increase in intrapericardial pressure due to accumulation of fluid in the pericardial space. Data on the incidence, demographics of CT is limited. We analyzed the 2008-2014 national inpatient sample databases to identify all

Protocolo diagnóstico y diagnóstico diferencial del taponamiento cardiaco

Cardiac tamponade is a medical emergency caused by compression of the heart due to pericardial effusion. This fluid accumulation in the intrapericardial space raises the pressure surrounding the heart to the point where cardiac filling is altered. This syndrome is understood as a continuum and its manifestations range from a slight increase in intrapericardial pressure with minimal repercussion on cardiac function to severe hemodynamic compromise that may even be fatal. The severity of tamponade depends on speed of fluid accumulation. The clinical diagnosis is essential. Signs of cardiac tamponade are: low cardiac output and elevated jugular venous pressure, as well as reactive vasoconstriction and tachycardia. Often physical diagnosis should be completed with other diagnostic tests as electrocardiography, chest radiography and echocardiography. This imaging technique is an important tool for evaluating patients with cardiac tamponade. Echocardiography allows to confirm the presence, location, distribution and size of the pericardial effusion, as well as to assess its hemodynamic consequences and the need for pericardiocentesis. Cardiac magnetic resonance imaging (CMR) and computed tomography (CT) are other imaging modalities which may help accurate diagnosis.

Risk for decreased cardiac output: validation of a proposal for nursing diagnosis

To verify the content validity of the nursing diagnosis risk for decreased cardiac output (RDCO). DCO is a phenomenon that is not restricted to individuals or environments that specifically focus on cardiovascular care. It is not only prevalent in cardiovascular care units, but also in post-anaesthesia units and non-cardiac care units among individuals with non-cardiogenic disorders. A significant decrease in cardiac output is a life-threatening situation, demonstrating the need for developing a risk nursing diagnosis for early intervention. The development of this diagnosis requires the construction of a diagnosis label, a definition of the diagnostic concept and the risk factors associated with the diagnosis. The research was carried out in two methodological stages based on the Fehring diagnosis content validation model. The quantitative analysis consisted of the calculation of the weighted mean of the values attributed by experts to each risk factor, the level of agreement/disagreement between the experts regarding the operational definitions of risk factors and the index of diagnostic content validity (DCV). The label 'risk for decreased cardiac output' was considered representative of a nursing diagnosis defined as 'at risk of developing a health status characterized by an insufficient quantity of blood pumped by the heart to meet physical metabolic demands'. Critical risk factors (DCV ≥ 0·7) were myocardial dysfunction (0·887), blood loss (0·875), increase in intrapericardial pressure (0·825), condition that leads to changes in cardiac rhythm and/or electrical conduction (0·812), deficient fluid volume (0·725), plasma loss (0·712), ineffective tissue perfusion (0·712) and electrolyte imbalance (0·7). The research identified eight risk factors with valid content for assessment of RDCO. The identification of risk factors for DCO assists nurses to intervene early and minimize the consequences of a deficient cardiac function.

Alterations in peripheral circulation in dogs with cardiac tamponade

DISTURBANCES related to the pericardium have been increasingly observed in routine clinical examinations carried out on domestic animals. In dogs, pericardial effusion is commonly associated with neoplasia or idiopathic pericarditis...

Hypotension is a Poor Predictor of Cardiac Tamponade in Patients Presenting to the Emergency Department

Background: Cardiac tamponade is a life-threatening disease process in which there is accumulation of fluid within the pericardial sac resulting in increase in intrapericardial pressure (Figure 1). It can be further categorized as either acute or chronic, depending upon the speed with which the fluid accumulates, and thus it presents with a wide range of symptoms. Classic medical school teaching says that tamponade presents with Beck's triad: distended neck veins, muffled heart sounds, and hypotension.

Accelerated myocardial relaxation in conscious dogs during acute cardiac tamponade.

Eight chronically instrumented conscious dogs were used to test the hypothesis that left ventricular (LV) relaxation is accelerated during cardiac tamponade. The time constant of LV transmural pressure fall was measured before and during intrapericardial (IP) saline infusion (baseline) with and without beta-adrenergic blockade (propranolol 1 mg/kg iv). Heart rate was controlled by atrial pacing. Increasing IP pressure caused a progressive linear decrease in stroke volume before and during beta-blockade in each animal. The time constant of LV transmural pressure fall also decreased continuously with an increase in IP pressure from 26 +/- 7 ms during baseline to 18 +/- 5 ms during severe cardiac tamponade (P < 0.01) before beta-blockade. However, after beta-blockade, the time constant of LV transmural pressure fall was constant over a wide range of IP pressures despite a continuous decrease in LV end-diastolic volume. The time constant of LV transmural pressure fall was not altered by vena caval occlusions that caused the same decrease in LV preload observed during cardiac tamponade. We concluded that despite decreased pump function, LV relaxation was accelerated progressively during graded cardiac tamponade, and this change was dependent not on changes in loading conditions but on an intact beta-adrenergic influence.

The influence of positive end-expiratory pressure on intrapericardial pressure and cardiac function after coronary artery bypass surgery

The hemodynamic effects of positive end-expiratory pressure (PEEP) were studied in coronary artery bypass patients by recording intrapericardial and intracardiac pressures, measuring cardiac output by thermodilution, and determining left ventricular volumes by nuclear radiography. An elevation of PEEP to 5, 10, and 15 cm H 2O led to a decrease in cardiac output (15% decrease at PEEP 15) as intrapericardial pressure increased and transmural left atrial pressure decreased. Modest volume loading (an increase in left atrial pressure of 3 mm Hg) greatly attenuated the deleterious effects of 15 cm H 2O PEEP. There was an excellent correlation between pulmonary capillary wedge pressure and left atrial pressure at PEEP 0 and 5 ( r = .85 and r = .83). This correlation was not nearly as reliable at PEEP 15 ( r = .54). A predictable increase in intrapericardial pressure was observed as PEEP was applied in these patients. The magnitude of this increase can be estimated by multiplying the change in PEEP (in cm H 2O) by 0.4 to estimate the change in intrapericardial pressure (in mm Hg). Using this estimation as a guide, modest volume loading can be used to maintain transmural filling pressures (and cardiac output) when PEEP is used after coronary artery bypass surgery.

Usefulness of right ventricular diastolic collapse in diagnosing cardiac tamponade and comparison to pulsus paradoxus

To compare the sensitivity, specificity and predictive value of right ventricular (RV) diastolic collapse and pulsus paradoxus as signs of cardiac tamponade, 21 consecutive patients with pericardial effusion and suspected cardiac tamponade underwent prospective hemodynamic and echocardiographic evaluation. Simultaneous hemodynamic and echocardiographic data were obtained in all patients before and after pericardiocentesis. Cardiac tamponade was considered present when there was diastolic equilibration of the intrapericardial, right atrial and pulmonary capillary wedge pressures and elevation of these pressures to more than 10 mm Hg. RV diastolic collapse was 93% sensitive and 100% specific in diagnosing cardiac tamponade, whereas pulsus paradoxus was only 79% sensitive and 40% specific. The positive and negative predictive values of RV diastolic collapse (100% and 83%) were considerably better than pulsus paradoxus (81% and 40%) and demonstrate that RV diastolic collapse is more sensitive, specific and predictive of cardiac tamponade than is pulsus paradoxus. Serial simultaneous hemodynamic and echocardiographic observations at multiple points during pericardiocentesis in a smaller subgroup (5 patients) also suggest that the hemodynamic effects of RV diastolic collapse in cardiac tamponade are mediated by an increase in intrapericardial pressure.

Pseudocyst of the pericardium developing during maintenance hemodialysis. Report of two cases.

Two cases of pericardial pseudocyst which developed in the course of maintenance hemodialysis are reported. Both patients were usually free of complaints, although there was evidence of the previous pericarditis with recent accumulation of pericardial effusion. As a possible mechanism leading to pericardial pseudocyst formation, distension of a weak area of the thickened pericardium due to an increase in intrapericardial pressure was assumed. Therefore, pericardial pseudocyst is one of the likely complications of patients on maintenance hemodialysis.

Studies of the circulation in pericardial effusion

The accumulation of fluid in the pericardial cavity in man results in: 1. 1. Marked decrease in the volume output of blood from the heart, both per minute and per beat. 2. 2. Increase in the arm-to-tongue circulation time. 3. 3. Rise in venous pressure. 4. 4. Increase in intrapericardial pressure. 5. 5. Increase in heart rate. 6. 6. Decrease in vital capacity. All of these abnormal conditions tend to disappear when excess pericardial fluid is removed. It appears that: 1. 1. Decrease in cardiac output is due for the most part to interference with the inflow of blood into the right heart; it cannot be said, however, that contraction is not also impaired. 2. 2. Increase in the amount of pericardial fluid is associated with progressive decrease in cardiac output and rise in venous pressure. 3. 3. Venous pressure falls rapidly at first, and then slowly, to a normal level as fluid is removed from the pericardial cavity.

The blood pressure and electrocardiogram in experimental pericardial effusion

1. 1. The increase in intrapericardial pressure caused by an acute pericardial effusion produces a fall in arterial blood pressure. 2. 2. If the intrapericardial pressure be increased by stages, there is a definite blood pressure established for each stage. This blood pressure is maintained for a minute or more, but there finally occurs a stretching of the pericardium which tends to restore normal conditions. 3. 3. If the intrapericardial pressure be slowly and continuously increased, there is a definite mathematical relationship between the pressure in the pericardial sac and the arterial blood pressure. 4. 4. During an increase in the intrapericardial pressure there occur changes in the electrocardiogram, as described by Katz, Feil and Scott, consisting chiefly of a gradual diminution in the voltage of the QRS segments and development of and increase in negativity of the T-waves, this latter change extending even to the production of T-waves of the coronary type. 5. 5. An intrapericardial pressure of 3 to 8 mm. Hg is sufficient to produce an obviously negative T-wave. 6. 6. When the intrapericardial pressure is sufficiently high to produce negative T-waves, the intravenous injection of adrenalin or ephedrine sulphate solutions will restore the electrocardiogram to normal. This change commences before the pressor effect of the drugs is evident on a carotid pressure tracing and persists after that effect has worn off. It is shown also even if the rise in arterial pressure is accompanied by a rise in intrapericardial pressure. 7. 7. If the intrapericardial pressure be sufficiently high, the circulation is hindered to such an extent that neither adrenalin nor ephedrine will cause a rise in arterial pressure. But this rise occurs immediately on rerise in intrapericardial pressure. 8. 8. The negative T-wave may resemble in all respects that seen in coronary occlusion. Since the rapid accumulation of a purulent exudate in the pericardium may be accompanied by intense pain, lowering of the blood pressure, fever and leucocytosis, suggesting coronary occlusion, the presence of a coronary T-wave in such a case may offer great diagnostic difficulties.