|Year : 2021 | Volume
| Issue : 2 | Page : 95-101
Invasive assessment of fluid therapy in hypotensive patients of postinferior wall myocardial infarction complicated by right ventricular infarction
Sameer Ganpat Vankar1, Akhil Kumar Sharma2, Suddhanshu Kumar Dwivedi2, Gaurav Kumar Chaudhary2, Sharad Chandra2, Akshyaya Pradhan2, Pravesh Vishwakarma2, Monika Bhandari2, Rishi Sethi2
1 Department of Cardiology, Apollo Hospitals, Secunderabad, Telangana, India
2 Department of Cardiology, King George's Medical University, Lucknow, Uttar Pradesh, India
|Date of Submission||15-Jul-2021|
|Date of Decision||18-Jul-2021|
|Date of Acceptance||19-Jul-2021|
|Date of Web Publication||25-Aug-2021|
Dr. Akhil Kumar Sharma
Department of Cardiology, King George's Medical University, Lucknow - 226 003, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: Management of such patients with inferior wall myocardial infarction (IWMI) complicated by right ventricular myocardial infarction (RVMI) requires volume replacement along with the standard therapy. However, the optimum amount of fluid needed to maintain systolic blood pressure (SBP) ≥90 mmHg in such patients has not been reported yet. This study evaluates the role of graded fluid infusion in improving the hemodynamic parameters in patients of IWMI with RVMI in hypotension or shock and also optimizes the amount of fluid needed to maintain SBP ≥ 90 mmHg.
Materials and Methods: In this single-center, prospective observational study, patients with first episode of acute coronary syndrome diagnosed as IWMI complicated by RVMI and SBP <90 mmHg were included. The hemodynamic parameters such as heart rate, SBP, cardiac output, cardiac index, and pulmonary capillary wedge pressure (PCWP) were measured at the baseline and after each 500 ml normal saline over 15 min until SBP ≥ 90 mmHg was attained. The primary objective was to study the change in cardiac output, cardiac index, and PCWP with response to fluid. The amount of fluid needed for ≥ 10 rise in cardiac output and to maintain SBP ≥ 90 mmHg was also evaluated. The secondary objectives were to study the need for inotropic support, complications such as inhospital mortality, acute pulmonary edema, and local site bleeding. Further, the predictors of early responders (<2 L of fluid) were also evaluated.
Results: Among all 16 patients, 3 (18.7%) were excluded and the rest received graded fluid therapy. Invasively monitored and graded fluid therapy resulted a significant rise in cardiac output (2.1 ± 0.7 L/min vs. 3.7 ± 0.7 L/min), cardiac index (1.3 ± 0.3 L/min/m2 vs. 2.4 ± 0.76 L/min/m2), and PCWP (8.4 ± 3.0 mmHg vs. 17.6 ± 1.5 mmHg) in comparison to baseline parameters. On an average, 865 ± 462 mL fluid infusion was required for 10% improvement in CO from baseline. However, 2192 ± 560 mL fluid was needed for consistent maintenance of SBP ≥ 90 mmHg. The effect of fluid therapy was not significantly correlated with baseline clinical and hemodynamic parameters. There were no procedure- and therapy-related complications reported during the study.
Conclusions: Early response to fluid therapy within 2 L of normal saline occurred independently of baseline hemodynamic parameters. However, more studies with larger number of patients would be needed to confirm the same.
Keywords: Fluid therapy, hypotension, inferior wall myocardial infarction, right ventricular myocardial infarction, shock
|How to cite this article:|
Vankar SG, Sharma AK, Dwivedi SK, Chaudhary GK, Chandra S, Pradhan A, Vishwakarma P, Bhandari M, Sethi R. Invasive assessment of fluid therapy in hypotensive patients of postinferior wall myocardial infarction complicated by right ventricular infarction. Heart India 2021;9:95-101
|How to cite this URL:|
Vankar SG, Sharma AK, Dwivedi SK, Chaudhary GK, Chandra S, Pradhan A, Vishwakarma P, Bhandari M, Sethi R. Invasive assessment of fluid therapy in hypotensive patients of postinferior wall myocardial infarction complicated by right ventricular infarction. Heart India [serial online] 2021 [cited 2022 Jan 28];9:95-101. Available from: https://www.heartindia.net/text.asp?2021/9/2/95/324618
| Introduction|| |
Inferior wall myocardial infarction (IWMI) accounts for about 40%–50% of all acute myocardial infarctions (MIs). It has been estimated that 25%–52% of IWMI patients are complicated by RWMI. Clinical evidence has shown right ventricular myocardial infarction (RVMI) as a major negative prognostic factor in patients with IWMI. Its presence is found to be associated with substantial immediate morbidity and mortality. Therefore, its early recognition is critical as a well-delineated set of priorities for its management that can reduce the morbidity and mortality.
The triad of hypotension, elevated jugular venous pressure, and clear lung fields has been recognized as a marker of RVMI in acute IWMI.,,, Fluid replacement was first described as a treatment option approximately 25 years ago with the development of pulmonary artery catheterization. Since then, several studies have validated the usefulness of volume loading for ischemic right ventricular dysfunction.,,,,, In previous studies, maintenance of the right ventricular preload with volume loading and normal saline alone was thought to resolve the accompanying hypotension and improve the cardiac output. The typical regimen consisted of intravenous (IV) administration of normal saline (40 mL/min, up to total of 2 L) while maintaining the right atrial pressure at <18 mmHg to prevent volume overload. However, subsequent clinical studies reported variable responses to aggressive fluid therapy with a target pulmonary capillary wedge pressure (PCWP) of 18–24 mmHg. Some studies, including two prospective ones, showed that volume loading further elevates the right-sided filling pressure without improving cardiac output. Another study by Dell'Italia et al. has indicated that volume loading does not improve cardiac index in patients with acute RVMI despite a rise in cardiac filling pressures. They further demonstrated that infusion of dobutamine, after appropriate volume loading, produces a significant improvement in cardiac index and right ventricular ejection fraction as compared to those receiving nitroprusside infusions. Berisha et al. examined 41 RVMI patients and reported that the maximal right ventricular stroke work index occurred when the filling pressure was 10–14 mmHg. They also identified that the mean right atrial pressure of >14 mmHg was almost always associated with a reduced right ventricular stroke work index. Therefore, the initial therapy for hypotension in patients with RVMI without pulmonary congestion has traditionally been volume expansion, particularly if the estimated central venous pressure was <15 mmHg.
It should be noted that previous studies have shown variable outcomes in response to volume loading among IWMI patients with RVMI. This variability could be contributed by different rate of fluid infusion, use of non-invasive methods for pressure monitoring and consideration of jugular venous pressure as surrogate of preload measurement. Considering this background, we planned a study to assess the role of graded fluid infusion in improving the hemodynamic parameters in IWMI patients complicated with RVMI along with the presence of hypotension and shock. We aimed to assess the amount of fluid needed to achieve and maintain systolic blood pressure (SBP) ≥90 mmHg in such patients.
| Materials and Methods|| |
Study design and patient population
This was a single-center prospective study conducted at the department of cardiology of a tertiary care hospital in India from January 1, 2017, to December 31, 2017. Patients admitted to a hospital with first episode of acute coronary syndrome (ACS), diagnosed as acute IWMI and complicated by RVMI, were analyzed. The protocol of the study was approved by the institutional ethics committee. The study conformed to the principles of good clinical practice and the Declaration of Helsinki. The written informed consent was obtained from all the patients or their legally authorized representative.
The inclusion criteria were as follows: (a) confirmed diagnosis of first acute inferior MI with right ventricular infarction satisfying the diagnostic criteria, (b) cardiogenic shock defined as marked and persistent (>30 min) hypotension with SBP <90 mmHg, (c) cardiac index <2.2 L/min/m2, (d) PCWP <15 mmHg, and (e) willingness to give written as well as verbal informed consent. The exclusion criteria were as follows: (a) inotropic support or mechanical ventilator, (b) pregnancy, (c) acute pulmonary edema suggestive of PCWP >18 mmHg, (d) renal failure undergoing hemodialysis, (e) chronic lung diseases, (f) valvular heart disease, and (g) mechanical complication of acute MI such as ventricular septal rupture and papillary muscle rupture resulting in acute severe mitral regurgitation.
Early revascularization by thrombolytic agent or percutaneous coronary intervention was attempted as per the current management guideline. The fluid therapy was infused simultaneously ensuring no delay in standard management of ACS. The IV fluid (normal saline) was administered at the rate of 500 mL per 15 min through a peripheral venous access until SBP >90 mmHg was attained.
The demographic data, comorbidities, risk factors for coronary artery disease, hemodynamic parameters, and systemic examination findings were recorded on a predesigned data collection form at the time of admission. Electrocardiography was performed in all patients at the time of admission. Blood investigations including hemogram, renal function test, and troponin level were done. The cardiac hemodynamic measurement was done as follow:
- Step 1: A venous access was taken through the left subclavian vein and an 8 F sheath was introduced
- Step 2: Through the sheath, a Swan-Ganz Continuous cardiac output (CCO) catheter was advanced to the right or left pulmonary artery
- Step 3: Femoral arterial access was taken through the right femoral artery
- Step 4: Cardiac output and cardiac index were measured using Edwards Lifesciences Vigilance 1000 platform monitor through the femoral arterial access at baseline and thereafter every 15 min (i.e. after every 500 mL of IV fluid infusion)
- Step 5: Noninvasive blood pressure and PCWP were measured on GE DASH 500 cardiac monitoring system at baseline and thereafter every 15 min (i.e. after every 500 mL of IV fluid infusion).
Heart rate, SBP, PCWP, cardiac output, and cardiac index were the prespecified parameters recorded at baseline and thereafter every 15 min (i.e. after every 500 mL of IV fluid infusion). The primary objective of the study was to evaluate the effect of graded fluid therapy on these prespecified parameters. The amount of fluid needed to achieve and maintain SBP ≥90 mmHg and the amount of fluid needed for ≥10 rise in cardiac output were also evaluated. The secondary objectives included occurrence of any complications or adverse events, particularly the need for inotropic support, incidence of acute pulmonary edema, local site bleeding, and inhospital death. Further, the predictors of early responders (<2 L of fluid) were also evaluated.
In this report, the categorical variables are expressed as frequency and percentages while continuous variables are expressed as mean ± standard deviation along with range. The effect of fluid therapy on hemodynamic parameters was evaluated using paired t-test. The effect of graded fluid therapy with different amounts of normal saline infusion was evaluated using the ANOVA test, with Tukey's post hoc test to measure significant intergroup difference. Further, the role of hemodynamic parameters in early responders (responded with fluid volume <2 L) versus delayed responders (requiring fluid volume ≥2 L) was compared using Student's t-test. P <0.05 was used to identify statistically significant difference between comparative groups. Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS; Chicago, IL, USA) program, version 15.
| Results|| |
Among all the MI patients admitted at our tertiary care center during the study period, a total of 16 patients of IWMI complicated by RVMI presenting with hypotension were included in the study which constituted the intention-to-treat (ITT) group. Among them, three patients (19.7%) had PCWP >18 mmHg and were not subjected to fluid therapy. However, these patients were managed with inotropic support. The remaining 13 patients (81.2%) satisfying the inclusion and exclusion criteria were subjected to the fluid therapy which constituted target-to-treat (TTT) group [Figure 1]. The baseline characteristics are mentioned in [Table 1].
|Figure 1: Patient population and disposition. IWMI: Inferior wall myocardial infarction; RVMI: Right ventricular myocardial infarction|
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Effect of fluid therapy
The mean baseline PCWP, cardiac output, and cardiac index were 8.4 ± 3.0 mmHg, 2.1 ± 0.7 L/min, and 1.3 ± 0.3 L/min/m2, respectively [Table 2]. The study analysis was drawn from the TTT group (n = 13). These patients received about 2192 ± 560 mL normal saline for the management of hypotension or shock. After receiving the fluid therapy, the PCWP, cardiac output, and cardiac index increased significantly to 17.6 ± 1.5 mmHg, 3.7 ± 0.7 L/min, and 2.4 ± 0.76 L/min/m2, respectively (P < 0.05 for all). This resulted in mean percentage rise of 109.5%, 76%, and 84.6% from the baseline PCWP, cardiac output, and cardiac index to its peak value, respectively.
Effect of graded fluid therapy
[Table 3] summarizes the effect of graded infusion of normal saline (given at a rate of 500 ml over 15 min). A significant (P < 0.05) increase in SBP, PCWP, cardiac output, and cardiac index values from the respective baseline was identified at 1000–1500 mL, 2000–2500 mL, and 1500–2000 mL bracket, respectively. However, the post hoc Tukey's test revealed that after achieving significant increase in these parameters above the baseline with the respective fluid volume, there was no further significant increase in these parameters compared to the preceding level (for example, from 500 to 1000 ml, 1000–1500 ml, P value was nonsignificant). We found that nearly 1500–2000 mL of fluid therapy was needed to achieve and maintain the SBP ≥90 mmHg [Figure 2]a. In addition, the average quantity of fluid needed to increase the cardiac output by 10% over the baseline was 865 ± 462 mL [in the 500–1000 mL bracket; [Figure 2]b]. Similarly, the 10% rise in cardiac index from baseline was achieved at 500–1000 mL volume bracket [Figure 2]c, while the 10% rise in PCWP was achieved at <500 mL volume bracket [Figure 2]d.
|Figure 2: Change in (a) systolic blood pressure, (b) cardiac output, (c) cardiac index, and (d) PCWP in response to fluid volume. PCWP: Pulmonary capillary wedge pressure|
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|Table 3: Outcomes measured at baseline and after different amounts of normal saline infusion fluid therapy (n=13)|
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Predictors of early responders
Among 13 patients in the TTG, 8 patients had responded with fluid volume <2 L (early responders), while 5 patients required a volume ≥2 L (delayed responders) for achieving the SBP ≥90 mmHg. The analysis of baseline predictors of early responders and delayed responders is summarized in [Table 4], indicating that these parameters were just marginally higher in early responders compared with those having delayed response.
|Table 4: Baseline parameters of early responder (<2 L of infused volume) and delayed responder (≥2 L of infused volume)|
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In the TTT, none of the patients developed increasing dyspnea or pulmonary edema. Only two patients (15.4%) were transient responders to the fluid therapy and required inotropic support. There was no incidence of death or excessive bleeding from local site in the TTT group. However, one patient in the TTT group who had developed ventricular septal rupture died after a week. Among the three patients who were excluded from the ITT group (PCWP >18 mmHg), two patients died as a result of cardiogenic shock.
| Discussion|| |
Patients of IWMI complicated by RVMI usually develop low cardiac output state. Management of such patients needs IV fluid along with the guideline-directed therapy for ST-elevation MI. However, previous studies of fluid therapy in RVMI have shown variable results. The present study was conducted to find the answer to the optimal amount of fluid that would be required for managing patients with IWMI complicated by RVMI and presenting with hypotension or cardiogenic shock in northern Indian population. To the best of our knowledge, the present study is the first of its kind which has studied the response of fluid therapy in RVMI patients presenting in cardiogenic shock or hypotension.
In the present study, the optimal amount of normal saline needed for the management of hypotension or shock in patients of IWMI with RVMI was 2192 ± 560 mL. However, as little as 1000 mL, 2000 mL, and 1500 mL amount of normal saline was required to bring significant rise (P < 0.001) above the baseline in PCWP, cardiac output, and cardiac index, respectively. The increasing trend of PCWP, cardiac output, and cardiac index continued up to 2000 mL of normal saline infusion beyond which a plateau effect was seen on further fluid infusion.
The results of the present study clearly emphasize that the effective cause for low cardiac output in RVMI is reduced left ventricular preload in the absence of any significant left ventricular dysfunction. Further, it demonstrates that fluid therapy would help to increase the cardiac output and thus help in managing hypotension in patients complicated by RVMI. These results were similar to the pathophysiology shown in the animal study performed by Goldstein et al. In his study, Goldstein demonstrated that primary depression of right ventricular contractility caused a decrease in right ventricular output. After volume loading, there was an increase in right ventricular systolic pressure and right ventricular stroke work. This suggested that the output of the infarcted right ventricle is exquisitely volume dependent, a concept that correlates well with clinical observations of volume loading in RVMI. The thin-walled right ventricle is more compliant than the thick-walled left ventricle. Therefore, the right ventricle is able to acutely accommodate an increased preload with a proportionately smaller increment in filling pressure. Thus, the right ventricle may be able to increase its output via the Starling mechanism with little change in its filling pressure. The improvement seen in the cardiac output was due to increase in the left ventricular preload, which resulted from the increase in the right ventricular output following fluid loading.
In another study conducted by Dellitalia, ten patients with RVMI who had an initial PCWP <18 mmHg were subjected to fluid therapy. In his study, fluid loading did not improve cardiac index (from 1.9 to 2.1 L/min/m2), despite significant increase in PCWP (from 10.4 to 15.2 mmHg; P < 0.001). In this study, about 200–800 mL normal saline was infused to reach the target PCWP above 15 mmHg. However, they have included patients diagnosed as RVMI alone and hypotension at presentation was not the inclusion criterion. Further, their mean baseline cardiac index was 1.9 L/min/m2 and baseline mean SBP was 93 ± 17 mmHg. On the contrary, hypotension was the main inclusion criterion in our study and the baseline mean SBP was 77.2 ± 7 mmHg. In their study, the fluid therapy was stopped with target PCWP >15 mmHg, whereas in our study, the fluid therapy was continued until SBP was >90 mmHg, which was achieved with a mean rise of PCWP from 8.4 ± 3.0 mmHg to 17.6 ± 1.5 mmHg. In our study, infusion of normal saline in 1000–1500 ml volume bracket achieved the mean PCWP and mean cardiac index of 14.9 mmHg and 1.8 L/min/m2, respectively, without correction of hypotension (mean SBP at this stage was 86.2 mmHg) which was similar to the Dellitalia study. The higher volume of fluid required in our study can be explained by severely hypotensive patients included for fluid therapy.
In the study conducted by Berisha et al. in RVMI patients, optimal right atrial and PCWP increased by 11.7 ± 2.1 mmHg and 16.5 ± 2.7 mmHg, respectively. This study emphasized that both the left and right ventricular filling pressures need to be optimal to maintain adequate cardiac performance in patients with biventricular infarction. The mean cardiac index was >2 L/min/m2 and included patients of IWMI and RVMI but with no shock.
A similar study was performed by Lopez-Sendón et al., in which the right atrial and pulmonary capillary pressures associated with higher cardiac index were 15.6 ± 4.2 and 16.8 ± 3.3 mmHg, respectively. Similar to prior study our study also shown that in ischemic right ventricular dysfunction patients, the peak level of cardiac output and cardiac index were achieved after intravenous fluid infusion (2-2.5 litres) and associated with PCWP value of 17 mm Hg. However, further fluid infusion caused a fall in the cardiac output and cardiac index, as shown in [Figure 2].
The abovementioned studies explain that the improvement in right ventricular performance at optimal filling pressure is because of the stretching of the myocardial fibers that have survived myocardial necrosis to their optimal length, which, as per the Starling's law, increases their contraction. Thus, the right ventricular stroke volume increases, thus increasing the PCWP and cardiac index.
Unlike previous studies of fluid therapy done in RVMI, we additionally studied the need for inotropic support, incidence of acute pulmonary edema, and inhospital death of the patients receiving fluid therapy. Out of the 13 patients subjected to the fluid therapy, 3 patients (23%) were transient responders and required inotropic support. Among them, one patient had developed ventricular septal rupture 48 h after presentation and was taken up for surgical repair. Of the remaining two cases, one patient had severe global left ventricular dysfunction with ejection fraction of 35%. The other patient had ejection fraction of 45% with wider area of left ventricular dysfunction (including inferior, inferoseptal, anterior, and anteroseptal segments). Thus, we can infer from the study that patients having severe left ventricular dysfunction are at risk of showing transient response to fluid therapy and might require inotropic support for further improving their cardiac index and maintaining the SBP. None of the patients developed acute pulmonary edema, and there was no inhospital mortality.
Firstly, the number of patients included in this study was small. It should be noted that our study included patients presenting with IWMI complicated by RVMI and in hypotension at presentation (i.e. SBP <90 mmHg). Among them, only those patients without any prior history of ACS and with PCWP <15 mmHg were subjected to fluid therapy. Secondly, of 13 patients who received fluid therapy, all were male, while the 3 patients who were excluded after measuring the PCWP >18 mmHg were all women. Thirdly, bilateral subclavian venous access was required for patients presenting with complete heart block and requiring temporary pacemaker, one access for temporary pacing and another for PCWP monitoring. In those patients undergoing thrombolytic therapy, it would add to increased bleeding risk from punctured site. However, there was no such bleeding seen in our study.
| Conclusions|| |
This is a unique study of fluid therapy in RVMI to the best of our knowledge where attempt was made to find the baseline predictors of early fluid responders (i.e. those responding within 2 L of fluid). The optimal amount of fluid needed to treat hypotension or shock in patients with IWMI complicated by RVMI was 2192 ± 560 mL. The amount of normal saline needed to increase cardiac output by 10% above the baseline was 865 ± 462 mL. However, it can be concluded that those having severely depressed left ventricular function may show transient response to fluid and may need inotropic support after adequate fluid resuscitation. Still, more studies with larger number of patients would be needed to confirm the same.
All authors contributed to the study conception and design, material preparation, data collection and analysis. All authors read and approved the final manuscript.
The study was approved by Institutional Ethics Committee (158/Ethics/R.Cell-17, Dated 22/4/2017a).
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]