Effects of Heart Rate and Pulmonary Artery Pressure on Doppler Pulmonary Artery Acceleration Time in Experimental Acute Pulmonary Hypertension

The contribution of heart rate (HR) to pulmonary artery hemodynamics has been suggested in pulmonary hypertension (PH). Our high-fidelity pressure, retrospective study tested the hypothesis that HR explained the majority of mean pulmonary artery pressure (mPAP) and pulse pressure (PApp) variation in 12 severe precapillary PH patients who performed incremental-load cycling while in the supine position. Seven idiopathic pulmonary arterial hypertension patients and five chronic thromboembolic PH patients were studied. Four to five PAP-thermodilution cardiac output (CO) points (mean: 4.4) were obtained. At rest, mPAP was 57 ± 9 mmHg, PApp was 51 ± 11 mmHg, HR was 90 ± 12 beats/min, and stroke volume (SV) was 50 ± 22 ml. At peak exercise, mPAP was 76 ± 10 mmHg, PApp was 67 ± 11 mmHg, and HR was 123 ± 18 beats/min (i.e., 71 ± 10% of maximum HR, each P < 0.05), whereas SV was 51 ± 20 ml ( P = not significant). The input resistance did not change (mPAP/CO = 14.1 ± 4.1 vs. 13.5 ± 4.4 mmHg·min·l−1). The relative increase in mPAP was related to the relative increase in HR ( n = 12, r2 = 0.74) but not in CO. mPAP was linearly related to CO in 8 of 12 patients (median r2 = 0.83) and to HR in 12 of 12 patients (median r2 = 0.985). The parsimony principle favored the latter fit. PApp was linearly related to mPAP in 12 of 12 patients (median r2 = 0.985), HR in 10 of 12 patients (median r2 = 0.97), CO in 7 of 12 patients (median r2 = 0.87), and SV in 1 of 12 patients. A strong linear relationship between HR and mPAP was consistently documented in severe precapillary PH patients who performed supine exercise. The limited value of thermodilution CO to predict mPAP could be explained by unavoidable precision errors in CO measurements, unchanged/decreased SV on exercise, curvilinearity of the mPAP-CO relationship at high flow, or flow-independent additional mechanisms increasing mPAP on exercise.

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Vasodilating Drugs: Contrasting Haemodynamic Effects

Clinical Science ◽

10.1042/cs051575s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 575s-578s ◽

Cited By ~ 9

Author(s):

R. C. Tarazi ◽

H. P. Dustan ◽

E. L. Bravo ◽

A. P. Niarchos

Keyword(s):

Heart Rate ◽

Pulmonary Hypertension ◽

Cardiac Output ◽

Pulmonary Artery ◽

Blood Volume ◽

Pulmonary Artery Pressure ◽

Cardiac Failure ◽

Haemodynamic Effects ◽

Artery Pressure

1. We investigated the haemodynamic effects of intravenously administered hydrallazine, diazoxide and nitroprusside and orally administered minoxidil to determine whether vasodilators (such as nitroprusside) which do not increase cardiac output might be better treatment for hypertensive complications associated with, or caused by, myocardial failure than those that do. 2. Hydrallazine and diazoxide caused increases in heart rate, cardiac output, cardiopulmonary blood volume, the ratio of cardiac output to cardiopulmonary volume, and pulmonary artery pressure. Nitroprusside, although decreasing pressure and vascular resistance, caused no significant change in the other functions except for reducing pulmonary artery pressure. Minoxidil, when given orally, had the potential for causing pulmonary hypertension. This seemed explained by increased flow (hyperdynamic type) in some but by congestive cardiac failure in others; the latter condition was probably intensified by the marked fluid retention that the drug can cause. 3. On the basis of these results a classification of vasodilators was constructed which depends on the presence or absence of a venodilating effect. Vasodilators which produce no (or little) venodilatation, increase heart rate, cardiac output, cardiopulmonary blood volume and pulmonary artery pressure. In this class are diazoxide, hydrallazine and minoxidil. Those that cause venodilatation do not stimulate the heart nor do they cause pulmonary hypertension. Nitroprusside and nitroglycerine are drugs of this type. 4. These results suggest that drugs producing both venodilatation and arteriolar dilatation may be more specific therapy for hypertensive complications associated with cardiac failure than those that cause only arteriolar dilatation.

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Protective effect of sildenafil in pulmonary hypertensive child with congenital heart disease

Journal of Contemporary Medical Sciences ◽

10.22317/jcms.v4i4.487 ◽

2018 ◽

Vol 4 (4) ◽

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Oxygen Saturation ◽

Pulmonary Artery Pressure ◽

Primary Pulmonary Hypertension ◽

Blood Oxygen ◽

Blood Oxygen Saturation ◽

Acceleration Time ◽

Artery Pressure ◽

Secondary Type

Objective Pulmonary hypertension has been described as an elevation in mean pulmonary artery pressure (PAP) >25 mmHg at rest or 30 mmHg during exercise, which can be classified into primary and secondary pulmonary hypertension.Methods In this study, subjects were divided into two groups of patients and controls. The patients were treated with Sildenafil for 3 months, starting with 0.2 mg/kg/dose, six times daily and then the dose was increased with an increment of 0.2 mg/kg/dose every 15 days. Echocardiography examination, including pulmonary artery pressure, tricuspid regurgitation velocity, and pulmonary artery acceleration time, as well as oxygen saturation (SpO2) rate were measured every 15 days.Results The results revealed that a significant decrease (P < 0.05) in the pulmonary artery and tricuspid pressure, and a significant increase (P < 0.05) in the rate of blood oxygen saturation and pulmonary artery acceleration time have been found.Conclusion The results of this study reveal that Sildenafil has a great effect in the treatment of the secondary type of pulmonary hypertension and has a negligible effect on primary pulmonary hypertension.

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Measures of Right Ventricular Afterload Predict Exercise Pulmonary Hypertension beyond Mean Pulmonary Artery Pressure

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2021.01.550 ◽

2021 ◽

Vol 40 (4) ◽

pp. S189

Author(s):

S. Osman ◽

R.F. Bentley ◽

S. Mak

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Right Ventricular ◽

Pulmonary Artery Pressure ◽

Artery Pressure ◽

Right Ventricular Afterload ◽

Mean Pulmonary Artery Pressure ◽

Ventricular Afterload

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A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

Clinical Science ◽

10.1042/cs059465s ◽

1980 ◽

Vol 59 (s6) ◽

pp. 465s-468s ◽

Cited By ~ 28

Author(s):

T. L. Svendsen ◽

J. E. Carlsen ◽

O. Hartling ◽

A. McNair ◽

J. Trap-Jensen

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Response Curves ◽

Receptor Blocking ◽

Artery Pressure ◽

Arterial Blood ◽

Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

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Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

Biomedicines ◽

10.3390/biomedicines9091212 ◽

2021 ◽

Vol 9 (9) ◽

pp. 1212

Author(s):

Fabian Mueller-Graf ◽

Jonas Merz ◽

Tim Bandorf ◽

Chiara Albus ◽

Maike Henkel ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Transit Time ◽

Pulse Wave ◽

Correlation Coefficients ◽

Physiological Basis ◽

Artery Pressure ◽

Hypoxic Vasoconstriction ◽

Pulse Wave Transit Time

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

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The Relationship between Vitamin D Deficiency and Pulmonary Hypertension

Prague Medical Report ◽

10.14712/23362936.2014.17 ◽

2013 ◽

Vol 114 (3) ◽

pp. 154-161 ◽

Cited By ~ 15

Author(s):

Mehmet Demir ◽

U. Uyan ◽

S. Keçeoçlu ◽

C. Demir

Keyword(s):

Vitamin D ◽

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Vitamin D Deficiency ◽

Pulmonary Artery Pressure ◽

Control Group ◽

Systolic Pulmonary Artery Pressure ◽

Control Groups ◽

Artery Pressure ◽

Vitamin D Levels

Vitamin D deficiency actives renin-angiotensin-aldosterone system (RAAS) which affects cardiovascular system. Activation of RAAS is associated with pulmonary hypertension (PHT). Relation between vitamin D deficiency and PHT could be therefore suggested. In  our study we compared pulmonary artery pressure between vitamin D deficiency and control groups. 115 consecutive patients (average age: 61.86 ± 5.86) who have detected very low vitamin D (vitamin D levels < 10 ng/ml) were enrolled. 117 age matched persons (average age: 61.74 ± 5.99) were selected as the control group. All groups underwent transthoracic echocardiography. Routine biochemical measurement of 25-OH vitamin D and parathormon (PTH) levels were performed. Baseline characteristics of the study groups were comparable. Systolic pulmonary artery pressure (SPAP) of patients in  the low vitamin D group was higher than the control groups. As a  result our study, a  relation between vitamin D deficiency and pulmonary artery hypertension was revealed.

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