Pulmonary Diastolic Pressure Research Articles

Beneficial effects of captopril in left ventricular failure in patients with myocardial infarction.

Abstract 1 Ten patients with acute myocardial infarction and left ventricular failure were studied. Acute myocardial infarction was anterolateral in eight patients, posterolateral in one, and anteroseptal in one. Three patients were grade II, 4 grade III, and 3 grade IV of Killip's classification. None presented with arterial hypertension but mean values of plasma renin activity and serum aldosterone were 20.7 ng/ml/h and 13.5 ng/100 ml. Haemodynamic measurements were performed by using a flow-directed catheter. Cardiac output was determined in triplicate by thermo-dilution (Edwards computer). Classic haemodynamic measurements included: heart rate, cardiac index, stroke volume index, stroke work index, blood pressure, right atrial pressure, pulmonary vascular resistance, systemic vascular resistance, and pulmonary diastolic blood pressure. Curves of ventricular function correlating stroke work index and pulmonary diastolic blood pressure were constructed. Haemodynamic changes after drug therapy were tested for significance using the paired t test. All patients received heparin, oxygen, and an intravenous infusion of isosorbide dinitrate. 2 Haemodynamic measurements were repeated at 30 min intervals and after isosorbide infusion until values returned to normal. The infusion was then discontinued and pressures returned to control values. At this time, oral captopril was administered, the first dose being 12.5 mg. Subsequent doses of 12.5 mg up to 50 mg were given if systolic blood pressure remained above 100 mm Hg and pulmonary diastolic pressure greater than 18 mm Hg. When the most effective oral dose was determined it was administered at six hourly intervals. This therapy resulted in an improvement of functional class, with a reduction in Killip's grade from class III to 1.7 (mean value). Heart rate, mean atrial pressure, and pulmonary diastolic pressure decreased by 10%, 32% and 41%. Cardiac index increased from 2.4 ± 0.8 l/min/m2 to 2.8 (p < 0.02) and stroke volume index increased by 37.2%. Pulmonary vascular resistance decreased by 22.14% (p < 0.001) and the product of heart rate × blood pressure decreased by 33.6% (p < 0.001). 3 Haemodynamic effects of oral captopril treatment were beneficial in left ventricular failure and acute myocardial infarction without immediate side effects. In acute left ventricular failure the renin angiotensin system was appreciably stimulated. All ten patients who were treated for a mean of 6.5 days showed a significant subjective, clinical, and haemodynamic improvement. After discharge from the coronary care unit anterolateral infarctions produced by ventricular fibrillation resulted in four deaths. 4 These data suggest that captopril may be an effective therapy in acute myocardial infarction with left ventricular failure and that it is more effective than other vasodilators. Nevertheless, more patients need to be studied for a longer period before definite conclusions can be drawn.

Relationship of pulmonary diastolic and pulmonary wedge pressures to left ventricular diastolic pressures: role of acute myocardial infarction localization.

Right and left hemodynamics have been simultaneously studied in 127 patients with acute myocardial infarction with respect to electrocardiographic localization. Hemodynamic profiles of the different localizations suggest a high incidence of right ventricular dysfunction in infero-posterior infarcts. The comparison with the other localizations suggests that such a right ventricular dysfunction is likely to be responsible for an additional underestimation of left ventricular end-diastolic pressure when estimated by pulmonary diastolic pressure.

Hemodynamic assessment in the medical treatment of acute myocardial infarction: the effects of various vasodilators and catecholamines.

One hundred and nineteen patients with acute myocardial infarction (AMI) were examined to establish the correlation between clinical and hemodynamic status. Patients were divided into 5 groups: uncomplicated AMI (Group A, 34 cases), congestive heart failure (Group B, 56 cases), cardiogenic shock (Group C, 14 cases), right ventricular dysfunction in cases with acute inferior infarction (Group D, 7 cases), and rupture of the interventricular septum (Group E, 8 cases). Hemodynamic classification of the first three groups with 18 mmHg for pulmonary arterial diastolic pressure (PADP) or pulmonary capillary pressure (PCW), 2.0 L/min/m2 for cardiac index (CI), and 20 g·m/beat/m2 for left ventricular stroke work index (LVSWI) correlated well with our clinical classification. In addition to hemodynamic measurements, monitoring of the temperature difference between the core and the periphery of the body reflects both cardiac function and clinical status of peripheral circulation and has been useful in selecting the appropriate therapy for AMI. Mortality rates were similar in the clinical and hemodynamic subset classifications, averaging 2.9% in Group A, 7.1% in Group B, 57.1% in Group C, 42.9% in Group D, and 62.5% in Group E. The hemodynamic effects of intravenous nitroglycerin (TNG), TNG ointment, and molsidomine were studied in 54 patients. All three vasodilators significantly reduced PADP or PCW and systemic vascular resistance (SVR), and increased CI in patients with elevated PADP or PCW. Also, TNG was effective in decreasing PADP or PCW, SVR, and left-to-right shunt ratio, and increasing forward cardiac output in Group E. However, in cases with severe pump failure in which CI was less than 2.1 L/min/m2, LVSWI was less than 20 g·m/beat/m2 and PADP or PCW was more than 18 mmHg, dopamine and a combination of dopamine and phentolamine produced beneficial hemodynamic responses. The overall early mortality rate of the AMI at our CCU decreased from 22.9% during 1974 to 1976, when no such therapy was applied, to 15.9% after therapy. A marked reduction in the mortality rate due to left ventricular failure from 33.3% to 13.5% was observed. Both hemodynamic and clinical data indicate that a new therapy employing vasodilators and a combination of vasodilators and catecholamines can be applied effectively in patients with pump failure following AMI.

Serotonin and pulmonary hypertension in human septic ARDS.

Pulmonary hypertension gives an indication of poor prognosis in adult respiratory distress syndrome (ARDS) complicating sepsis. In this study, we examined the role of the platelet and the vasoactive amine, serontonin, in pulmonary hypertension accompanying septic ARDS. The lack of any significant difference in platelet number (delta + 3.9 +/- 8.4, X 10(3)/mm3) or serum serotonin (delta - 0.03 +/- 0.06 nm/mm3) across the pulmonary vascular bed (pulmonary artery minus pulmonary vein), would suggest that platelet sequestration and/or release of serotonin is not a major factor in septic ARDS. However, we did note a direct positive relationship between serum serotonin (Ss) and the pulmonary artery diastolic minus pulmonary capillary wedge pressure (PAd-PCWP) gradient (r = 0.64, p < 0.01) implying that serum serotonin may be related to pulmonary hypertension in septic ARDS.

Haemodynamic effects of a single intravenous dose of lorcainide in patients with heart disease.

The cardiovascular effects of a single i.v. dose (2 mg/kg over 5 min) of lorcainide were studied in 14 patients with heart disease. In the haemodynamic part of the study (6 patients), the aortic and pulmonary systolic, diastolic and mean pressures, left ventricular systolic and end-diastolic pressures, cardiac output and the rate of rise of left ventricular pressure were measured before and for 30 min after administration of the drug. Lorcainide produced a slight and short-lasting decrease in the aortic and pulmonary systolic pressures, and all other pressure values remained unchanged. The cardiac output and systemic vascular resistance were not altered by lorcainide. It consistently depressed the rate of rise of left ventricular pressure (maximum mean decrease 19%). In the angiographic part of the study (8 patients), the ejection fraction and the mean velocity of circumferential fiber shortening were measured before and 5 min after lorcainide. In all but one patient, lorcainide decreased the ejection fraction (mean decrease 11.6%), and the mean velocity of circumferential fiber shortening was uniformly diminished by lorcainide (mean decrease 29.7%). Thus, lorcainide moderately impaired myocardial performance in patients with normal and reduced left ventricular function without producing hypotensive side effects.

Pulmonary Microvascular Pressure and Pulmonary Edema

We appreciate and respect the comments of West and especially those that relate to pulmonary microvascular pressures in the upright human subject. We could cite no greater authority than West himself with regard to the spectrum of hydrostatic pressures from the apex to the base of the lung; however, this is really not an issue, inasmuch as the pulmonary arterial microvascular pressure is estimated from the wedged pulmonary arterial pressure or the pulmonary diastolic pressure, which is measured in the supine subject and with arbitrary zero reference to a horizontal midthoracic plane.

Relationship of pulmonary artery diastolic and pulmonary artery wedge pressures in mitral stenosis

Resting and exercise hemodynamic studies were performed in 33 patients with mitral stenosis (14 men and 19 women; average age, 25 years) in normal sinus rhythm with normal pulmonary vascular resistances. A normal pulmonary vascular resistance was assumed when the resting pressure gradient between the pulmonary artery diastolic and mean pulmonary artery wedge pressures was 5 mm. Hg or less. A satisfactory correlation existed between the pulmonary artery wedge and pulmonary artery diastolic pressures at rest (r = 0.9017) and during exercise (r = 0.8670). A method of predicting pulmonary artery wedge pressure from pulmonary artery diastolic pressure during exercise was formulated. The correlation between the predicted and measured exercise pulmonary artery wedge pressures was very close (r = 0.9561). It is suggested that during exercise the pulmonary artery diastolic pressure can be modified as above and substituted for mean pulmonary artery wedge pressure if the resting gradient between pulmonary artery wedge and pulmonary artery diastolic pressure is known.

The significance of radiological changes in the lungs in acute myocardial infarction.

Evidence of pulmonary venous hypertension on portable antero-posterior chest radiographs was compared with measurements of the pulmonary artery diastolic pressure on 58 occasions in 26 patients admitted to a coronary care unit with acute myocardial infarction. The pulmonary artery diastolic pressure was assumed to reflect the left ventricular end-diastolic pressure. A normal chest radiograph correctly indicated a pressure below 14 mm Hg except in one patient who had clear clinical and radiological evidence of pulmonary embolism. Signs of pulmonary venous hypertension usually indicated a pulmonary diastolic pressure above 14 mm Hg but were seen with a pressure below this on several occasions. The results suggest that this is due to a time lag between the fall of pressure and radiological improvement, which may have therapeutic significance. One patient had pulmonary oedema with a normal pressure for which no satisfactory explanation is offered.

The effect of acutely induced hypervolemia on resistance to pulmonary blood flow and pulmonary arterial compliance in patients with chronic obstructive lung disease

The presence of alveolar hypoxia and respiratory acidemia in patients with chronic obstructive lung disease alters the normal relation between pulmonary arterial and left heart pressures at the end of diastole; usually these pressures are the same. With vasoconstriction of the small pulmonary arteries the pulmonary arterial diastolic pressure rises, whereas the mean wedge pressure remains unchanged. Thus, a pressure gradient across the pulmonary circulation appears at the end of diastole representing an increased resistance to pulmonary blood flow. The magnitude of this gradient is closely related to the systemic arterial blood oxyhemoglobin saturation, which is used as an index of alveolar oxygen tension, and to the blood hydrogen ion concentration. In the present study acutely induced hypervolemia caused striking alterations in mean wedge pressure and blood flow. However, the diastolic gradient did not change. The pulmonary diastolic pressure gradient reflects the degree of resistance to pulmonary blood flow regardless of the level of the left heart pressure or the cardiac output. On the other hand, left heart pressure does contribute to the level of the pulmonary arterial diastolic pressure. The pulse pressures recorded in the elastic pulmonary arteries reflect their compliance characteristics and the effect of stroke volume imposed upon them. We have assessed compliance indirectly by examining the relationships between pulmonary arterial systolic pressure, diastolic pressure and stroke volume. The compliance characteristics of the elastic arteries in patients with chronic obstructive lung disease do not differ from normal before or during acutely induced hypervolemia.

Lung water in patients with acute myocardial infarction.

Pulmonary extravascular water volume (PEV) or lung water was measured in 45 patients with acute myocardial infarction, utilizing the double radioisotope indicator dilution technique. A PEV greater than the upper limit or normal (120 ml/m 2 ) was found in 27 patients, 23 of whom had an elevated pulmonary wedge or pulmonary artery diastolic pressure. A significant correlation was found between PEV and pulmonary wedge or pulmonary diastolic pressure in the whole series. A progressive increase in average PEV was observed from Class I (uncomplicated) to Class IV (shock) patients. There was also a progressive increase in PEV from patients with normal chest X-ray findings to those with radiologic evidence of acute pulmonary edema. In seven of 11 patients with initial elevation of both PEV and pulmonary wedge pressure, repeat determinations demonstrated a substantial reduction in both parameters over a period of 2-4 days. We postulate that an increased PEV in patients with acute myocardial infarction is largely due to an elevated pulmonary capillary pressure. The latter is probably a consequence of an elevated left ventricular diastolic pressure, which may be a manifestation of either left ventricular failure or a decrease in left ventricular compliance.

Electrocardiographic evidence of left atrial hypertension in acute myocardial infarction.

The relationship between mean left atrial pressure (LA m ) and P-wave abnormalities in lead V 1 of standard 12-lead electrocardiograms was evaluated in 30 patients with acute myocardial infarction. In each patient pulmonary artery diastolic pressure or pulmonary wedge pressure was measured, and these values were used as an estimate of LA m . Electrocardiograms recorded at the time of the pressure measurements were used for P-wave analysis. Patients with a history of hypertension were excluded from analysis. There was a significant correlation between the magnitude of the P terminal force in lead V 1 (PTF-V 1 ) and the estimated LA m (r = –0.78, P &lt; 0.001). Sixteen patients had a normal PTF-V 1 on admission; 11 of them had a normal LA m . All 14 patients with an abnormal PTF-V 1 (more negative than –0.03 mm-sec) on admission had an elevated LA m (&gt;12 mm Hg). Thus, in 25 of the 30 patients, the PTF-V 1 correctly identified whether the LA m was normal or abnormal on admission. On subsequent days, simultaneous measurements of PTF-V 1 and estimated LA m were made in 27 of the patients. Significant changes occurred in both PTF-V 1 and LA m ; discordant changes were observed on only seven of 56 occasions. Measurement of PTF-V 1 appears to be a useful and reliable estimate of left ventricular filling pressure in patients with acute myocardial infarction.

Studies on the carotid body and the carotid sinus. Circulatory effects of the carotid chemoreflex.

Previously, carotid chemoreflex and baroreflex have been reported, although for the most part of these mechanisms have not been clarified.In this experiments, circulatory effects of the carotid chemoreflex were investigated in the anesthetized dogs. Chemoreflex was performed with Lobeline (0.02mg, 1ml) and potassium cyanide (KCN, 1%, 1ml) through the catheter inserted to the carotid sinus. Continuously, during experiments, systolic blood pressure (S. P), diastolic blood pressure (D. P), systolic pulmonary blood pressure (SPaP), diastolic pulmonary blood pressure (DPaP), respiration and pulse rate were recorded simultaneously in the closed chest dogs. Cardiac output, pulmonary blood flow, coronary blood flow, S. P, D. P, SPaP, DPaP, and pulse rate were examined in the controlled breathing of the open chest dogs.In each experiment, during and after reflex, blood gas, HCO3-, and pH were measured. However, none of them were changed by these reflexes.In the case of the closed chest dogs, chemoreflex by Lobeline did not change S. P and D. P, but SPaP was increased by 22.54%, significantly. DPaP was increased by 18.14%. Respiration rate was increased by 26.46% significantly. Heart rate was decreased by 9.15%.In the open chest dogs, chemoreflex by Lobeline increased S. P and D. P by 13.05% and 14.58% significantly. SPaP and DPaP were increased by 22.19% and 21.97% significantly. Pulmonary resistance was increased by 28.57% significantly. Pulmonary blood flow was decreased by 9.7% significantly.In the open chest dogs, chemoreflex with KCN increased S. P, D. P, and SPaP by 21.59%, 21.39%, and 41.02% significantly. Pulmonary resistance was increased by 20% significantly. Pulmonary blood flow was decreased by 10.43%. Cardiac output was not changed but coronary blood flow was increased by 6.50% significantly.It should be noted here that the carotid chemoreflex caused the hyperrespiration, the changes of pulmonary arterial blood pressure, pulmonary resistance, and pulmonary blood flow significantly, but these hemodynamic changes are capable of being separated from the effects of hyperrespiration through the chemoreflex mechanism.

Effects of Pneumoperitoneum during Laparoscopic Surgery in Young Children

This observational study of effect of pneumoperitoneum during laparoscopic surgery in 36 patients below 5 years of age (mean age 2.66 ± 1.23 yrs) was carried out in Combined Military Hospital, Dhaka over a period of 2 years. The aim of the study was to evaluate the effects of pneumoperitoneum in this age group. Intraabdominal pressure ceiling was fixed at 12 mm of Hg. Mean duration of pneumoperitoneum was 25 ± 3.21 minutes. Amount of CO2 absorption was assessed by rise of end tidal CO2 (ETCO2) (+21.21%). Effect of pneumoperitoneum and hypercarbia reflected by rise of pulse rate (+16.96%), systolic blood pressure (+12.19%), diastolic blood pressure (+14.58%) and pulmonary airway pressure (+25%). Oxygen saturation reduced a little bit; but came to baseline within a few minute after completion of the procedure. Electrocardiogram showed sinus rhythm in all but one patient. Requirement of postoperative analgesia was minimum. Mean hospital stay was 4±0.21 days. Postoperative side effects or complication was negligible (only two cases of postoperative vomiting). This study supports the safety and better outcome of laparoscopic technique even in young children provided there is good planning and vigilance. Key words: Laparoscopic surgery, pneumoperitoneum, children. DOI: 10.3329/jafmc.v5i2.4577 JAFMC Bangladesh Vol.5(2) (December) 2009, pp.18-20

Study of hemodynamic factors which alter the sequence of the second heart sound

In 5 of 18 anesthetized dogs the normal order of the components of the second heart sound was reversed. This reversal was due to a longer Q-A 2 interval and a shorter Q-P 2 time. The aortic pressure pulse in these animals showed a slower than normal rise in pressure, a later peak pressure, and a smaller drop to the incisura. The pulmonary diastolic pressure was significantly higher in the group with reversed splitting. Pulmonary embolization caused the sequence of the components of the second heart sound to reverse in 11 of 13 experiments. This occurred because of abbreviation of right ventricular ejection and movement of the P 2 component. The data suggest that the timing of P 2 is related to the level of pulmonary arterial diastolic pressure and the right ventricular diastolic pressure. An increase in PA diastolic pressure causes shortening of the Q-P 2 interval; whereas an increase in RVD pressure, without a change in PA diastolic pressure, causes the Q-P 2 interval to increase. Further embolization resulted in re-establishment of the normal sequence of A 2 before P 2. This was accompanied by elevation of RVD pressure and prolongation of right ventricular ejection. Anoxia due to breathing 11.8 per cent oxygen caused the second heart sound to reverse in 3 of 7 animals. The reversal was due to a shorter right ventricular ejection time and a longer period of left ventricular ejection; this caused movement of both the P 2 and A 2 components of the second heart sound. These data support the concept that the timing of the second heart sound is dependent on the differential rate and duration of right and left ventricular ejection. A mild increase in output resistance causes the duration of ventricular ejection to shorten, whereas an increase in end-diastolic pressure results in a longer ejection period.

Respiratory factors affecting pulmonary arterial blood pressure and flow through the lungs.

Pulmonary arterial pressure rises during expiration and falls during inspiration. This study was made to determine whether respiratory fluctuaations in pulmonary arterial pressure were a reflection of changing intrathoracic pressure, or whether there was also a respiratory variation in effective pulmonary arterial pressure. Simultaneously recorded pulmonary arterial pressure, pneumotachygram and intraesophageal pressure were analyzed in four patients with rheumatic heart disease and in one with pulmonary sarcoidosis. In one case of rheumatic heart disease with mitral stenosis, and in the one case of sarcoidosis, effective pulmonary arterial end-diastolic pressure rose during inspiration and fell during expiration, while recorded pulmonary arterial end-diastolic pressure fell on inspiration and rose on expiration. In two cases of mitral stenosis complicated by tricuspid insufficiency, both recorded and effective end-diastolic pulmonary arterial pressures fell during inspiration and rose during expiration. Increased venous return to the right heart during inspiration is probably an important factor in the inspiratory rise of effective pulmonary diastolic pressure seen in some cases. Failure of this to occur in two cases of tricuspid insufficiency indicates a possible fall in stroke volume of right ventricle in inspiration associated with increase in regurgitation secondary to increased flow to right side of the heart. One patient with mitral stenosis had cardiac cycles of unusual length, permitting measurement of pulmonary artery pressure during diastolic periods lasting through both phases of the respiratory cycle. When deep inspiration occupied most of a diastolic period, effective diastolic pressure fell during early part of inspiration, reached an asymptote and rose again toward end of inspiration. This paradoxical rise in effective pulmonary end-diastolic pressure suggests that inspiration may be associated with an increase in pulmonary vascular resistance in man as well as in animals. Submitted on July 13, 1956