The effect of cardiac tamponade on coronary haemodynamics in the awake dog.

Phasic left circumflex coronary artery and aortic blood flow were monitored in six awake dogs during a control period and at several degrees of cardiac tamponade. A mean pericardial pressure of 24 plus or minus 3 mm Hg (mean plus or minus SEM) was attained at the maximum tamponade level. Total left circumflex coronary blood flow decreased 51% while the systolic portion of this flow became negative or retrograde. Following acute relief of the tamponade, a coronary hyperaemic response was noted. It it suggested that myocardial ischaemia may be partially responsible for the depressed cardiac function seen in this condition and that extravascular compression of the epicardial vessels may limit the coronary blood flow during systole.     

Cardiac tamponade in left ventricular dysfunction

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.     

Effect of acute cardiac tamponade on left ventricular pressure-volume relations in anaesthetised dogs

STUDY OBJECTIVE--The aim was to determine whether depressed myocardial contractility is responsible for the decline in stroke volume that occurs with cardiac tamponade. DESIGN--Left ventricular contractile performance was assessed before and after beta adrenergic blockade using the end systolic pressure-volume relation, the left ventricular dP/dtmax-end diastolic volume relation, and the left ventricular stroke work-end diastolic volume relation during acute cardiac tamponade in dogs. EXPERIMENTAL MATERIAL--In eight pentobarbitone anaesthetised dogs (15.7-24.8 kg), transducer tipped and volume impedance catheters were positioned in the left ventricle. Through a median sternotomy incision, a pericardial catheter was inserted to produce varying stages of cardiac tamponade. By the use of transient bicaval occlusions, variably loaded pressure-volume loops were recorded. MEASUREMENTS AND RESULTS--Incremental tamponade reduced mean arterial pressure from 105(SEM 3) to 89(2) mm Hg (mild tamponade), 75(2) mm Hg (moderate tamponade), and 59(10) mm Hg (severe tamponade). The slope of the end systolic pressure-volume relation was 6.3(1.2) mm Hg.ml-1 at baseline and increased slightly to 7.7(1.8), 8.5(1.3), and 9.2(1.5) mm Hg.ml-1 with the progressive levels of tamponade (NS). The role of autonomic reflexes was assessed by repeating the tamponade sequence after beta adrenergic blockade with 10 mg of metoprolol intravenously. The slope of the end systolic pressure-volume relation was reduced by metoprolol, at 4.9(1.0) mm Hg.ml-1 (p less than 0.01), but was not significantly altered by the sequence of tamponade following beta blockade [5.6(0.9), 6.0(1.0), and 5.5(7.0) mm Hg.ml-1, respectively (NS)]. Neither were changes found indicative of depressed contractile function with progressive tamponade in the slopes of the left ventricular dP/dtmax-end diastolic volume and stroke work-end diastolic volume relations. CONCLUSIONS--Left ventricular contractility was not altered during acute cardiac tamponade in an anaesthetised, closed chest canine model. Depressed left ventricular contractile function was not responsible for the observed haemodynamic deterioration.     

Factors affecting penetration of retrograde coronary venous injections into normal and ischemic canine myocardium: assessment by contrast echocardiography and digital angiography

Summary This experimental study described myocardial echo contrast enhancement through coronary venous injections. Retrograde administration of renografin was performed in 15 closed-chest dogs. Two-dimensional echocardiography was used to study myocardial echo contrast enhancement before and after coronary artery occlusion. Digital subtraction venography was used to assess delivery, drainage and shunting of the retrograde injectate. Systolic/diastolic blood pressure in the great cardiac vein measured 7±3/1±0.6 mm Hg and increased to 29±11/5±3 after coronary sinus occlusion and to 55±2.3/15±12 mm Hg during coronary sinus contrast injection. Myocardial contrast echo appearance in a midpapillary left ventricular short axis cross-section was limited to the anteroseptal region, extending to 28.4±11.3% of the section circumference after great cardiac vein injections and 35.3±17% after coronary sinus injections (difference NS). After occlusion of the left anterior descending coronary artery, great cardiac vein contrast injections resulted in opacification of 36.6±9.7% of the section circumference (N.S. vs preocclusion control) and opacified most, but not all asynergic segments. After occlusion of the circumflex coronary artery, myocardial echo contrast uptake was restricted to the septum and the anterior wall. The ischemic and asynergic posterolateral myocardial segments were not opacified. Digital subtraction coronary venography revealed rapid drainage of retrogradely injected contrast to the right atrium, in spite of coronary sinus balloon occlusion via venovenous anastomoses.Retrograde coronary venous contrast injections may help define myocardial regions which are accessible with retrograde coronary venous interventions.Dr. Punzengruber was supported by a Grant from the Max Kade Foundation, New York     

Regional myocadial blood flow and cardiac mechanics in dog hearts with CO2 laser-induced intramyocardial revascularization

Summary Laser-induced intramyocardial revascularization (LIR) has been used to promote direct communications between blood within the ventricular cavity and that of the existing myocardial vasculature in an attempt to increase perfusion in patients with ischemic heart discase. This study was conducted to measure the effects of LIR channels on regional myocardial flood flow (microspheres), cardiac mechanics (sonomicrometers), and myocardial tissue pressures in 18 dogs. Under baseline hemodynamic conditions (mean HR=165.2±11.4 bpm, LVP=123.6±22.9/4.0±1.8 mmHg, AoP=112.8±27.1/77.0±22.5 mmHg), myocardial blood flow in laser-treated tissue (mean =1.11±.10 cc/min/gm before laser; .71±.19 cc/min/gm after laser) was reduced as compared to blood flow in control tissue (mean=1.12±.15 cc/min/gm before laser; 1.25±.22 cc/min/gm after laser). Regional myocardial systolic shortening (11.32%±3.82% before laser; 7.49%±2.86% after laser) was decreased by 33%. During simultaneous reversible ligation of the LAD and LCCA for 2 min, when intramyocardial channels represented the only tissue access for the injected microspheres, blood flow in laser-treated tissue was not increased above that of the control non-lasered tissue. However, regional blood flow was greater in laser-treated ischemic tissue (mean=.61±.12 cc/min/gm) than in untreated ischemic areas (mean=.04±.03 cc/min/gm) when left ventricular pressure (LVP) was acutely elevated (mean SLVP=207.0±16.1 mmHg). Using these measurements, a model is proposed to predict regional systolic pressure gradients between the left ventricular cavity and coronary intramyocardial vasculature required to permit restoration of blood flow to ischemic myocardium. We conclude that improved perfusion via laser-induced intramyocardial channels does not occur in otherwise normal myocardium exposed to acute coronary ligation and only small improvements in perfusion are noted when LVP is significantly elevated. Consideration of further clinical application of this approach is seriously cautioned awaiting additional experimental studies.This study was supported by U.S. Public Health Service Grant R01 HL32897-01 from the National Heart, Lung, and Blood Institute, by grants in aid from the American Heart Association, and by the Fulbright-Hays Scholarship Grant.     

Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration

A hallmark of cardiac tamponade is pulsus paradoxus. However, the exact mechanism of pulsus paradoxus and the relation of left and right ventricular ejection dynamics remain controversial, with some studies suggesting an inverse relation in ventricular filling and ejection and others citing a more important role for the effects of right heart ejection dynamics delayed by transit through the pulmonary artery bed. To specifically reexamine this issue, six sedated but spontaneously breathing dogs were studied during experimental cardiac tamponade with use of extensive hemodynamic instrumentation and Doppler methods. During cardiac tamponade, left ventricular systolic pressure decreased from 125.8 +/- 12.1 to 81.7 +/- 26.7 mm Hg (p less than 0.01) and cardiac output from 5.86 +/- 1.48 to 2.34 +/- 0.98 liters/min (p less than 0.001); mean pericardial pressure increased from -1.2 +/- 0.8 to 10.5 +/- 3 mm Hg (p less than 0.001) and pulsus paradoxus from 4.3 +/- 1.6 to 10.7 +/- 1.2 mm Hg (p less than 0.001) compared with baseline values. An inverse relation in left and right ventricular ejection dynamics that was very close to 180 degrees out of phase was seen throughout the respiratory cycle in multiple hemodynamic and Doppler variables including peak systolic pressures, aortic and pulmonary flow velocities and ventricular ejection times. Simultaneous recording of the transmitral pressure gradient provided indirect evidence that the ventricular ejection dynamics were directly related to changes in ventricular filling. However, the magnitude of ventricular pressure or output flow velocity for each respiratory cycle was variable, depending on the exact timing of filling and ejection in relation to the phase of respiration. Variation in left ventricular output due to changes in right ventricular output delayed by transit through the pulmonary vasculature was not recognized in any animal. It is concluded that in spontaneously breathing dogs with acute cardiac tamponade, peak ventricular pressures, ventricular ejection times and pulmonary and aortic flow velocities have an inverse relation that is very close to 180 degrees out of phase.     

Aortic baroreceptor characteristics in dogs with chronic high output failure

Summary It has been shown that the arterial baroreflex is depressed in heart failure. The role of alterations in afferent discharge as a possible mechanism for this depression has not been investigated previously. Single unit aortic baroreceptor activity was recorded from six normal dogs and from nine dogs, each with a chronic aorto-caval fistula (AVF). At the time of the acute experiment, mean arterial blood pressure (MABP) was not significantly different in the two groups of dogs; however, pulse pressure was significantly higher in the AVF dogs (45.7±2.4 mm Hg vs, 24.4±2.0 mm Hg; p<0.001). Left ventricular end-diastolic pressure (LVEDP) was higher in the AVF dogs (31.3±2.0 vs 5.6±1.8 mm Hg; p<0.001). AVF dogs had elevated heart weight/body weight ratios. The relationship of systolic aortic pressure to systolic discharge was examined by changing aortic pressure with aortic and vena caval occluders. The peak gain (normalized to maximum discharge) averaged 2.19±0.27 in the normal dogs compared to 1.15±0.09 in the AVF group (p<0.01). Saturation pressures and maximum discharge rates were greater in the AVF dogs although the threshold pressures were not different in the two groups. This data suggests that there is an attenuated response of aortic baroreceptor discharge in dogs with chronic volume overload and this abnormality may partially be responsible for the abnormal baroreflex in heart failure.Supported by National Institutes of Health Grant No. HL-22495     

Hemodynamic, left ventricular structural and hormonal changes after discrete myocardial damage in the dog.

Transmyocardial direct-current (DC) shock produces localized left ventricular myocardial necrosis without obstruction to coronary blood flow. In 43 dogs sequential measurements of hemodynamic, neuroendocrine and myocardial structural changes were made at baseline and for 16 weeks after DC shock. Six dogs (14%) died in the peri-shock period. By 1 week after shock, left ventricular mass, as measured by nuclear magnetic resonance imaging, had increased from a mean value +/- SD of 67.9 +/- 10.1 to 82.5 +/- 12.9 g (p = 0.0001). Left ventricular end-diastolic volume was unchanged at 1 week but increased at 16 weeks from 56.1 +/- 10.3 to 70.3 +/- 10.7 ml (p = 0.0003). Left ventricular mass demonstrated a further increase at 12 months (107.8 +/- 14.8 g). Rest cardiac output was significantly decreased at 4 months (3.67 +/- 1.23 to 3.18 +/- 0.81 liters/min, p less than 0.01) as was stroke volume (43 +/- 9 to 37 +/- 7 ml, p less than or equal to 0.01). Left ventricular ejection fraction decreased progressively from 73% to 38% at 1 year. At 4 months there were increases in mean pulmonary artery pressure (18 +/- 4 to 23 +/- 4 mm Hg, p less than 0.01), pulmonary capillary wedge pressure (9 +/- 3 to 15 +/- 3 mm Hg, p less than 0.01) and right atrial pressure (5 +/- 4 to 9 +/- 3 mm Hg, p less than 0.01). Plasma norepinephrine was increased at 4 months (318 +/- 190 to 523 +/- 221 pg/ml, p = 0.0003), whereas plasma renin activity was not significantly changed (4.3 +/- 2.6 vs. 5.2 +/- 3.4 ng/ml per h). Microsphere regional blood flow studies demonstrated a 50% reduction in skeletal muscle blood flow at 4 months (0.06 +/- 0.06 ml/min per g compared with 0.12 +/- 0.09 in normal dogs, p = 0.05), and a reduction in the endocardial/epicardial blood flow ratio (1.11 +/- 0.13 compared with 1.24 +/- 0.13 in normal dogs, p = 0.02). Therefore, in this model of acute left ventricular damage, left ventricular hypertrophy precedes progressive left ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular performance related to transmural filling pressure in clinical cardiac tamponade

In clinical cardiac tamponade, open-catheter intrapericardial pressure (IPP) may be used to estimate left ventricular transmural filling pressure (TMFP). However, it has been suggested recently that right atrial pressure (RAP) is superior to IPP in assessing true extracardiac pressure during pericardial drainage. In 10 patients with subacute cardiac tamponade, pulmonary wedge pressure (PWP), RAP, and IPP were measured along with indexes of systolic function. To test the relative merits of IPP and RAP in assessing true pericardial pressure, three TMFP estimates were analyzed: TMFP1 = (PWP - IPP); TMFP2 = (PWP - 1/3 RAP - 2/3 IPP); and TMFP3 = (PWP - RAP). An accurate TMFP presumably should increase during pericardiocentesis and correlate with left ventricular stroke work. In addition, to test the role of preload variation in pulsus paradoxus, respiratory variation in TMFP was analyzed. In the initial tamponade state, RAP and IPP were essentially equal, so all three TMFP estimates gave equivalent results. For instance, TMFP1 averaged 4 +/- 2 mm Hg but fell to 0.2 +/- 1.3 mm Hg during inspiration (p less than .001 vs expiration) and showed beat-by-beat correlation with pulse arterial pressure. After intermediate pericardiocentesis (280 +/- 160 ml), the IPP of 6 +/- 3 mm Hg fell significantly below the RAP of 10 +/- 3 mm Hg (p less than .001), but with a 570 +/- 320 ml residual effusion suggesting continued IPP measurement accuracy. By complete pericardiocentesis (810 +/- 430 ml) there was a significant increase in TMFP1 to 8 +/- 4 mm Hg (p less than .05 vs tamponade) but not in the TMFP3 of 1 +/- 3 mm Hg. Encompassing tamponade and pericardiocentesis data, left ventricular stroke work index showed positive correlation with TMFP1 (r = .59) and TMFP2 (r = .52) but not with TMFP3. Thus cardiac tamponade often may be diagnosed with a TMFP averaging well above zero, and diastolic equalization of PWP, RAP, and IPP may be a predominantly inspiratory finding ("inspiratory tracking"). This supports the role of preload variation in the genesis of pulsus paradoxus. On the other hand, true pericardial pressure may fall substantially below RAP in the course of pericardial drainage. This may be reconciled with the concept that normal pericardial pressure nearly equals RAP by hypothesizing an increased pericardial capacity in subacute tamponade so that pericardiocentesis produces a state analogous to removal of normal pericardial constraint.     

Attenuation of the systemic and coronary hemodynamic effects of cocaine in conscious dogs: propranolol versus labetalol

Summary The interaction of cocaine with myocardial and vascular adrenoceptors is incompletely understood. The systemic and coronary hemodynamic effects of intravenous cocaine (1.5 mg/kg) were examined in dogs with and without pretreatment with propranolol (2 mg/kg i.v.) or labelatol (5 mg/kg i.v.) on different days. A total of 24 experiments was completed (three sets of experiments) using eight dogs chronically instrumented for measurement of aortic and left-ventricular pressure, left-ventricular dP/dt, subendocardial segment length, coronary blood flow, and cardiac output. Myocardial oxygen consumption was estimated from the pressure work index (PWI). Cocaine significantly (p<0.05) increased heart rate (+51±17 bpm), mean arterial pressure (+72±10 mm Hg), left-ventricular systolic and end-diastolic pressures (+56±9 and +14±6 mm Hg, respectively), coronary blood flow (+32±10 ml/min) and the PWI (+10.0±2.3 ml O₂/min/100 g). Significant reductions in stroke volume (–9±5 ml) and percent segment shortening (–7.1±1.7) were observed. These changes returned to control after 30 min. After pretreatment with propranolol, the cocaine-mediated increases in mean arterial pressure, left-ventricular systolic pressure, rate-pressure product, and the pressure work index (4.4±0.7 ml O₂/min/100 g) were significantly (p<0.05) less than those observed with cocaine alone. Cocaine also reduced contractility [dP/dt₅₀ (–341±80 mm Hg/s)] and increased systemic vascular resistance (+2703±339 dyn·s·cm^–5) in the resence of propranolol. Labetalol abolished the cocainemediated increases in heart rate and coronary blood flow and significantly attenuated the increases in mean arterial pressure, left-ventricular systolic pressure, cardiac output, rate-pressure product, and calculated myocardial oxygen consumption when compared to results obtained with cocaine alone. The results demonstrate that a portion of the basic dynamic effects of cocaine is mediated by stimulation of alpha and beta adrenoceptors. Combined alpha and beta adrenergic blockade reduces the hemodynamic effects of cocaine more than beta blockade alone. During antagonism of the sympathomimetic response of cocaine, direct negative inotropic actions of this drug are unmasked.This work was supported by US PHS grants HL 36144 and HL 32911, Anesthesiology Research Training Grant GM 08377, and VA Medical Research Funds.     

Experimental congestive heart failure produced by rapid ventricular pacing in the dog: cardiac effects

Chronic rapid ventricular pacing in the dog reportedly produces a useful preparation of low-output heart failure. However, little information is available regarding cardiac changes in this preparation. Accordingly, we evaluated the effects of both short-term (3 weeks) and prolonged (2 months) rapid ventricular pacing on cardiac hemodynamics, mass, and chamber size. The effects of short-term pacing on left ventricular wall thickening, blood flow, and metabolism were also examined. Compared with 16 control dogs, dogs paced for either 3 weeks (n = 8) or 2 months (n = 13) exhibited reduced cardiac outputs (control 130 +/- 20 ml/min/kg, 3 week pacing 112 +/- 19 ml/min/kg, 2 month pacing 116 +/- 14 ml/min/kg) and elevated pulmonary wedge pressures (control 10 +/- 3 mm Hg, 3 week pacing 26 +/- 5 mm Hg, 2 month pacing 26 +/- 8 mm Hg) and right atrial pressures (control 4 +/- 1 mm Hg, 3 week pacing 13 +/- 3 mm Hg, 2 month pacing 9 +/- 3 mm Hg) (all p less than .01 vs control). At the postmortem examination, both groups of paced dogs also exhibited increased left ventricular volumes (control 13 +/- 6 ml, 3 week pacing 27 +/- 6 ml, 2 month pacing 26 +/- 8 ml), right ventricular volumes (control 13 +/- 5 ml, 3 week pacing 27 +/- 9, 2 month pacing 24 +/- 7 ml), and right ventricular mass (control 27 +/- 5 g, 3 week pacing 32 +/- 6 g, 2 month pacing 34 +/- 6 g) (all p less than .03 vs control) but had normal left ventricular mass. Three weeks of pacing also decreased percent left ventricular shortening (34 +/- 6% to 17 +/- 7%) associated with a disproportionate deterioration of posterior wall thickening (58 +/- 16% to 17 +/- 18%) (both p less than .01), as assessed by echocardiography. This left ventricular dysfunction was associated with no change in myocardial lactate extraction (prepacing 40 +/- 10%, 3 week pacing 36 +/- 10%), myocardial arteriovenous O2 difference, or myocardial histology, suggesting that it was not due to myocardial ischemia. These data indicate that rapid ventricular pacing in the dog produces a useful experimental preparation of low-output heart failure characterized by biventricular pump dysfunction, biventricular cardiac dilation, and nonischemic impairment of left ventricular contractility.     

Effect of vasopressin on phasic coronary blood flow

Summary The effects of vasopressin on the coronary circulation have been studied with regard to its general hemodynamic effects. Aortic blood pressure (BP), left ventricular pressure (LVP), aortic blood flow (AoBF), and circumflex blood flow (CBF), were measured in 12 open-chest dogs, under control conditions and during vasopressin infusion (25 mU/kg/min). During vasopressin infusion, the mean aortic blood pressure (MBP) was increased from 104±23 mm Hg to 161±23 mm Hg. The diastolic blood pressure (DBP) was more increased (+55%) than the systolic blood pressure (SBP) (+40%). AoBF was decreased from 2.169±0.408 l/min to 1.118±0.303 l/min; and the heart rate was decreased by 18%. The total combined left ventricular power did not change significantly. The increase in total peripheral resistance (TPR) (+200%) was the main change in impedance spectrum. The mean circumflex coronary blood flow (MCBF) was decreased from 48±8.6 ml/min to 33.4±9.7 ml/min. This decrease was more important in the diastolic circumflex blood flow (DCBF) (–33%) than in the systolic one (–0.8%). The diastolic pressure time index (DPTI) was more increased than the systolic pressure time index (SPTI). The DPTI/SPTI ratio was increased from 0.91 to 1.3.Long diastoles, induced by vagus nerve stimulation, have permitted to characterise the relationship between pressure and coronary blood flow during diastole. This relationship was linear under basal condition, and during vasopressin perfusion. This made it possible to determine the critical closing pressure (Pf0), and the coronary conductance (the slope of the regression curve). Vasopressin induced an increase in Pf0, from 33.7±95 to 77.4±16.07 mm Hg (p<0.001), and a decrease in coronary conductance, from 0.8±0.32 to 0.5±0.1 ml/min/mm Hg. The effect of an acute change in perfusion pressure on the coronary flow, under control conditions and during vasopressin infusion was studied by opening a large arteriovenous fistula. Unclamping of the fistula, under control conditions, allowed to realize an acute fall in DBP from 82.5±6.36 to 35.5±9.19 mm Hg, and in DCBF, from 58.5±9.2 to 20±9.8 ml/min. During vasopressin infusion, a similar fall in perfusion pressure lead to a zero diastolic circumflex blood flow, for a diastolic aortic blood pressure of 56±12 mm Hg. However, vasopressin did not affect the delayed active coronary vasodilatation.     

The hemodynamic effects of cardiac tamponade: mainly the result of atrial, not ventricular, compression

We studied the hemodynamic effects of surgically induced regional cardiac tamponade in anesthetized dogs. Tamponade restricted to either the right or the left ventricle was compared with tamponade of either ventricle and both atria. Intrapericardial pressures were elevated to approximately 20 mm Hg. With tamponade of the right ventricle alone, aortic pressure rose from 161 +/- 3.8 to 164 +/- 3.4 mm Hg (p greater than .05) and cardiac output fell from 149.4 +/- 16.1 to 134.9 +/- 11.9 ml/kg/min (p greater than .05). However, tamponade of the right ventricle plus both atria decreased mean aortic pressure from 152.5 +/- 3.6 to 115.9 +/- 8.7 mm Hg (p less than .01) and cardiac output fell from 118 +/- 14.8 to 38.9 +/- 4.8 ml/kg/min (p less than .01). With tamponade of the left ventricle alone, aortic mean pressure changed significantly from 158.5 +/- 6.1 (control) to 148.9 +/- 5.0 mm Hg (tamponade) (p less than .05) and cardiac output was 135.5 +/- 28.3 (control) and 111 +/- 24.7 ml/kg/min (tamponade) (p greater than .05). However, when the atria were included, mean aortic pressure fell significantly more from 155.5 +/- 5.4 to 105.5 +/- 10.4 mm Hg (p less than .01) and cardiac output fell from 142.2 +/- 16 to 47.8 +/- 6.4 ml/kg/min (p less than .01). Atrial pressure rose when the atria were included, but not with tamponade of the left ventricle alone. Right but not left atrial pressure rose slightly with isolated right ventricular tamponade. We conclude that the principal hemodynamic effects of cardiac tamponade are not the result of compression of either the right or the left ventricle, but are the consequence of compression of the atria and/or the venae cavae and the pulmonary veins.     

The relative merits of pulsus paradoxus and right ventricular diastolic collapse in the early detection of cardiac tamponade: an experimental echocardiographic study

An inspiratory decline in systolic arterial blood pressure exceeding 10 mm Hg has been used clinically to identify hemodynamically significant pericardial effusions. Recently, the echocardiographic sign of right ventricular diastolic collapse (RVDC) has been shown to occur early in the course of cardiac tamponade in association with a hemodynamically important decline in cardiac output. This study was undertaken to compare the relative merits of pulsus paradoxus and the onset of RVDC in the early detection of cardiac tamponade in an unanesthetized canine preparation. We studied six chronically instrumented, conscious dogs with two-dimensional echocardiography during cardiac tamponade induced by continuous infusion of saline into the pericardial space. We recorded intrapericardial pressure, cardiac output (electromagnetic flowmeter), aortic (catheter-tip transducer) and right atrial blood pressures, heart rate, and respiration. None of the dogs had RVDC when the pericardial space was empty, but all dogs showed RVDC during cardiac tamponade. We found that RVDC was strongly related to all of the cardiac parameters evaluated (intrapericardial pressure, cardiac output, aortic blood pressure, heart rate, and stroke volume) and provided information on each that was independent of that provided by pulsus paradoxus. Furthermore, RVDC appeared to be more strongly related to most cardiac parameters than was pulsus paradoxus and to be more sensitive and specific than pulsus paradoxus in detecting changes in intrapericardial pressure early in cardiac tamponade.     

Acute effects of ethanol on myocardial blood flow in the nonischemic and ischemic heart

To determine the effects of ethanol on myocardial blood flow in the non-ischemic and ischemic heart, coronary blood flow was measured with radionuclide-tagged microspheres in the anesthetized dog before and after intravenous administration of 1.7 g/kg body weight of ethanol. In non-ischemic dogs, at an average peak blood ethanol level of 225 ± 8 mg/dl (mean ± standard error of the mean), left atrial pressure increased from 5.7 ± 0.6 to 7.7 ± 0.8 mm Hg (p <0.01) and heart rate slowed from 179 ± 8 to 171 ± 8 min^?1 (p <0.001) but mean aortic pressure and cardiac output were unchanged. Average myocardial blood flow increased from 122 ± 5 to 143 ± 8 ml/min per 100 g (p <0.001). In dogs given ethanol after coronary occlusion, at an average peak blood ethanol level of 201 ± 13 mg/dl, left atrlal pressure increased from 6.3 ± 0.6 to 7.4 ± 1.4 mm Hg (p <0.05) but there was no significant change in heart rate, mean aortic pressure or peak positive first derivative of left ventricular pressure ($\text{dP}\text{dt}$). In these dogs, there was a significant change (F = 6.47, p <0.001) in the distribution of myocardial blood flow. In the nonischemic zone, blood flow increased from 118 ± 7 to 148 ± 14 ml/min per 100 g (p <0.005), whereas in the ischemie zone it declined from 30 ± 6 to 20 ± 5 ml/min per 100 g (p <0.02). Myocardial tissue demonstrating myocardial perfusion equal to or greater than 80 percent of preligation levels showed a significant increment of blood flow after ethanol; by contrast, myocardial tissue having blood flow levels equal to or less than 60 percent of preligation levels showed a significant decline in blood flow.Thus, ethanol increases coronary blood flow in the nonischemic myocardium. However, in the acutely ischemic heart, ethanol produces an unfavorable redistribution of myocardial blood flow with flow in the non-ischemic myocardium increasing, at least in part, at the expense of blood flow to ischemic myocardium, producing in effect a “coronary steal.”     

Cardiac tamponade: hemodynamic observations in man

Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreases significantly, from 16 +/- 4 mm Hg (mean +/- SD) to 7 +/- 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 +/- 1.77 to 7 +/- 2.2 l/min) and inspiratory systemic arterial pulse pressure (45 +/- 29 to 81 +/- 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters. In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P less than 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis. These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.     

The right and left ventricular intracavitary and transmural pressure-strain relationships.

The magnitude of pericardial pressure and therefore the shape of the right ventricular end-diastolic transmural pressure-volume relationship remains controversial. To investigate ventricular compliance, eight dogs anesthetized with fentanyl were instrumented as follows. Right and left ventricular intracavitary pressures were measured with micromanometer-tipped catheters. Right and left ventricular free wall segment lengths were measured by sonomicrometry. Pericardial pressure was measured over the right and left ventricles by means of flat liquid-containing balloon transducers, and transmural pressures were calculated as the difference between intracavitary and pericardial pressures. After defining the pressure-segment length relationship by vena caval constriction followed by release and blood transfusion, the pericardium and chest were opened widely and the cardiac volume manipulation was repeated; this allowed direct measurement of transmural right ventricular end-diastolic pressure for each level of strain recorded with the chest and pericardium closed. When intracavitary right or left ventricular end-diastolic pressure was raised from zero to 20 mm Hg, the respective transmural pressures increased from 0.2 +/- 0.6 (SD) mm Hg to 2.5 +/- 1.8 mm Hg and from 0.3 +/- 0.7 mm Hg to 6.0 +/- 2.5 mm Hg. Ventricular segmental strain increased by 7.0 +/- 0.8% and 6.0 +/- 0.2%, respectively. No statistically significant differences were found between right ventricular calculated (intracavitary minus pericardial pressure) and measured (open pericardium, open chest) transmural pressures at a given strain, thereby confirming the accuracy of our pericardial pressure measurements.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pleural effusion as a cause of right ventricular diastolic collapse.

BACKGROUND. We hypothesized, after seeing several suggestive clinical examples, that a process leading to a large bilateral pleural effusion in the presence of an otherwise insignificant pericardial effusion could result in right ventricular diastolic collapse (RVDC) as seen by two-dimensional echocardiography. This noninvasive marker for hemodynamically significant cardiac tamponade occurs when pericardial fluid is under pressure. Therefore, RVDC resulting from a large pleural effusion would represent a false-positive indication of cardiac tamponade caused by excessive pericardial fluid. METHODS AND RESULTS. Seven spontaneously breathing dogs were chronically instrumented to measure ascending aortic, right atrial, intrapericardial, intrapleural, left atrial, and pulmonary artery pressures and cardiac output. Intravascular volume was adjusted before each experiment to the euvolemic range with saline solution. The onset of RVDC was observed in each animal by two-dimensional echocardiography during seven paired episodes of tamponade induced by infusions of warm saline into the pericardial space alone and, after drainage of the pericardial fluid and complete recovery, into the pleural space in the presence of a small pericardial effusion. The onset of RVDC occurred at the same intrapericardial (8.17 versus 9.47 mm Hg) and right atrial (7.41 versus 7.46 mm Hg) blood pressures regardless of whether it was produced by an intrapericardial or an intrapleural effusion but began in expiration during the former and in inspiration during the latter. Intrapericardial pressure increased in the same manner as intrapleural pressure during intrapleural saline infusion. Nevertheless, cardiac output and aortic blood pressure were better preserved, and at the onset of RVDC, the pulmonary artery systolic blood pressure was higher (p less than 0.0001) and the degree of pulsus paradoxus lower (p less than 0.01) with intrapleural infusion. CONCLUSIONS. These results indicate that a large bilateral pleural effusion can elevate intrapericardial pressure sufficiently to cause RVDC and, perhaps, lead to misdirected therapy of an otherwise insignificant pericardial effusion.     

Regional myocardial blood flow and left ventricular diastolic properties in pacing-induced ischemia

The relation between left ventricular diastolic abnormalities and myocardial blood flow during ischemia was studied in eight open chest dogs with critical stenoses of the proximal left anterior descending and circumflex coronary arteries. The heart was paced at 1.7 times the heart rate at rest for 3 min. In dogs with coronary stenoses, left ventricular end-diastolic pressure increased from 8 +/- 1 to 14 +/- 2 mm Hg during pacing tachycardia (p less than 0.01) and 16 +/- 3 mm Hg (p less than 0.01) after pacing, with increased end-diastolic and end-systolic segment lengths in the ischemic regions. Left ventricular diastolic pressure-segment length relations for ischemic regions shifted upward during and after pacing tachycardia in dogs with coronary stenoses, indicating decreased regional diastolic distensibility. In dogs without coronary stenoses, the left ventricular diastolic pressure-segment length relation was unaltered. Pacing tachycardia without coronary stenoses induced an increase in anterograde coronary blood flow (assessed by flow meter) in both the left anterior descending and circumflex coronary arteries, and a decrease in regional vascular resistance. In dogs with coronary stenoses, regional vascular resistance before pacing was decreased by 18%; myocardial blood flow (assessed by microspheres) was unchanged in both the left anterior descending and circumflex coronary artery territories. During pacing tachycardia with coronary stenoses, regional coronary vascular resistance did not decrease further; subendocardial myocardial blood flow distal to the left anterior descending coronary artery stenosis decreased (from 1.03 +/- 0.07 to 0.67 +/- 0.12 ml/min per g, p less than 0.01), as did subendocardial to subepicardial blood flow ratio (from 1.04 +/- 0.09 to 0.42 +/- 0.08, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of altered site of electrical activation on myocardial performance during inotropic stimulation

The effects of altering the site of electrical activation on responses to isoproterenol (ISO) and treadmill exercise were examined in mongrel dogs instrumented for long-term measurement of left ventricular pressure, left ventricular dP/dt, coronary blood flow, cardiac output, left ventricular diameters, and mean arterial pressure and O2 content in the coronary sinus and aorta. During spontaneous rhythm, 0.2 micrograms/kg/min ISO increased heart rate by 90 +/- 7 beats/min, left ventricular dP/dt by 2479 +/- 301 mm Hg/sec, cardiac output by 3.5 +/- 0.9 liters/min, coronary blood flow by 30.4 +/- 3.9 ml/min, and myocardial oxygen consumption (MVO2) by 3.91 +/- 0.84 ml/min. During right atrial pacing at 193 +/- 7 beats/min, the effects of ISO were not different from the effects during spontaneous rhythm, with the exception of a lesser increase in coronary blood flow and lesser reductions in coronary resistance and left ventricular end-diastolic diameter and pressure. During right ventricular pacing at an identical rate, ISO increased left ventricular dP/dt (1140 +/- 158 mm Hg/sec) and cardiac output (2.2 +/- 0.5 liters/min) significantly less (p less than .025) than during either sinus rhythm or right atrial pacing, while MVO2 rose to a higher value. During right ventricular pacing the changes in mean arterial pressure and left ventricular end-diastolic diameters with ISO were not significantly different from those during right atrial pacing. Treadmill exercise induced significantly smaller (p less than .025) increases in left ventricular dP/dt during right ventricular pacing as compared with during either right atrial pacing or sinus rhythm, while MVO2 rose to a higher value.(ABSTRACT TRUNCATED AT 250 WORDS)