Higher Systemic Vascular Resistance Index Research Articles

Prognostic value of hemodynamic findings from impedance cardiography in hypertensive stroke

Impedance cardiography (ICG), a noninvasive method of hemodynamic monitoring, is a useful tool in the care of critically ill patients. Use of this technology shows promise in the hemodynamic assessment of hypertensive stroke patients. This study describes the different ICG findings of patients with hypertensive stroke and correlates parameters with patient outcome. Adult patients with stroke admitted to the intensive care unit (ICU) who were on antihypertensive medications or had hypertensive blood pressure (BP) levels at the time of admission were included. Patients were classified as having ischemic or hemorrhagic stroke on the basis of imaging studies. The ICG was done in the initial 24 h of admission using the BioZ Cardiac Output Monitor (CardioDynamics, Inc., San Diego, CA) and 18 hemodynamic parameters were analyzed. Statistical analysis was performed to assess correlation of hemodynamic findings with the type of stroke and survival to hospital discharge. Fifty-two adult patients with a mean age of 60.5 +/- 12.4 years were included. Of this population, 29 had ischemic stroke and 23 had hemorrhagic stroke. Seventeen patients died during hospital stay. Overall, noninvasive hemodynamic parameters of stroke patients showed a high systemic vascular resistance index (SVRI) and systemic vascular resistance (SVR), and decreased cardiac output (CO), stroke index (SI), and stroke volume (SV). Among the ischemic stroke group, nonsurvivors had a significantly higher mean SVRI and mean SVR compared to the survivors. In contrast, among the hemorrhagic stroke patients, nonsurvivors had a significantly lower mean SVRI and SVR compared to survivors. Except for SI and BP, there was no difference in the noninvasive hemodynamic parameters between the ischemic stroke group and the hemorrhagic stroke group. In this population of hypertensive stroke patients admitted to the ICU, ICG showed an elevated SVRI and SVR and depressed CO, SV, and SI. In the ischemic stroke group, higher SVR and SVRI were associated with in-hospital death, whereas in the hemorrhagic stroke group, lower SVR and SVRI were associated with in-hospital death. The ICG may provide significant prognostic information in patients admitted with hypertensive stroke.

Hemodynamic significance of heart rate in neurally mediated syncope

Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). The baseline hemodynamic data (mean +/- standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 +/- 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 +/- 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 +/- 0.29 vs. 1.97 +/- 0.41 1/min/m2, p < 0.001 and 2098 +/- 615 vs. 1573 +/- 353 dynes x s x cm(-5) x m2, p < 0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope.

Nicotinamide increases systemic vascular resistance in ovine endotoxemia.

The nuclear enzyme Poly(ADP-Ribose)-Polymerase (PARP) has been hypothesized as playing a major role in various forms of inflammation. PARP activation is induced by DNA strand breakage and can result in intracellular energy depletion and, ultimately, cell death. Further, it is thought to influence cardiovascular function and organ failure in endotoxemia. Here, we investigated the effect of the PARP inhibitor nicotinamide on cardiovascular and liver function in healthy and chronically endotoxemic sheep. Prospective controlled trial. University research laboratory. 12 female adult sheep. Six healthy sheep, instrumented for chronic study, received nicotinamide intravenously as a bolus of 40 mg/kg followed by a continuous infusion of 10 mg.kg(-1).h(-1); six animals received the vehicle. One hour after bolus application, a continuous infusion of endotoxin ( Salmonella typhosa, 10 ng.kg(-1).min(-1)) was started. Hemodynamic parameters were determined before and during endotoxemia. Treatment with nicotinamide resulted in a significantly higher systemic vascular resistance index and lower cardiac index in endotoxemic animals, but not in controls. It also attenuated endotoxin-induced increase in gamma-glutamyl transferase. The PARP inhibitor nicotinamide attenuates impairment of cardiovascular function during endotoxemia. In addition, PARP activation may be involved in endotoxin-induced liver injury.

Importance of hemodynamics management in patients with severe head injury and during hypothermia.

To evaluate the hemodynamics in patients with traumatic brain injury (TBI) during therapeutic hypothermia. Subjects were 25 patients with TBI (GCS; 8 or less). Mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), cardiac index (CI), systemic oxygen delivery (DO2), systemic vascular resistance index (SVRI), and pulmonary capillary wedge pressure (PCWP) were measured. Patients were retrospectively divided into 3 groups: normothermia (n = 5; NT), and survivors (n = 14; HT-S) and non-survivors (n = 6; HT-Non-S) after hypothermia. and hemodynamics were investigated for difference among groups at 24 hours from induction of normothermia or hypothermia. CPP target was above 70 mmHg, however, HT-Non-S could not maintain CPP above 70 mmHg. The low CPP was the result of elevated ICP, low MAP (P < .05), or both during hypothermia. In HT-Non-S, significantly high SVRI and low CI (P < .05) causing dehydration were observed during cooling. DO2 could not be maintained in HT-Non-S during hypothermia. These results suggest that patients run the risk of impairing hemodynamics during therapeutic hypothermia. Hemodynamic management is essential during hypothermia. If dehydration occurs during hypothermia. MAP may be reduced due to inadequate sedation, analgesia, and excess use of diuretic agents.

EVALUATION OF EARLY HEMODYNAMIC CHANGES IN CANINE SEPTIC SHOCK MODEL

Hemodynamics in septic shock were studied in depth in a canine model used for extracorporeal endotoxin removal studies. Fibrin clots with E. coli (target number of 1.5 × 1010CFU/kg) were implanted in the peritoneal cavity of 9 healthy beagles, (BW: 15–18Kg). Animals received antibiotics and IV fluid (6ml/kg/h). Hemodynamics were compared between survivor and non-survivor groups by 72 hours. The occurrence of 3 distinct hemodynamic phases was confirmed. The 1st phase (0–8h) was characterized by the decrease in cardiac index (CI) and increase in systemic vascular resistance index (SVRI), followed by the 2nd phase (8–24h) with recoveries of CI and SVRI to baselines. It was after 24–72 hours (3rd phase) when hemodynamic conditions known to be typical to sepsis were observed with a high CI and low SVRI. The survival rate was 56%, with one died in the 2nd and 3 in the 3rd phase. In the 1st phase, there was no difference in hemodynamics between the two groups, while significant difference was seen in the 2nd phase in CI, SVRI and PCWP starting at 20 hours after bacterial clot implantation. A decrease in CI (p = 0.02), increase in SVRI (p=0.0l), and a decrease in PCWP (p < 0.01) was significant in the non-survivors, suggesting severer impairment of LV diastolic and systolic function and possible vascular leakage in non-survivors. No difference was noted in blood pressure, CVP, heart rate or body temperature. This study has shown that CI, SVRI 2nd PCWP are the predictors of outcome of sepsis and septic shock. Hemodynamic parameterTable

Monitoring Hypervolemic-hemodilution And Hypertensive Therapy In Subarachnoid Hemorrhage

Introduction: Prophylactic hypervolemic-hemodilution-hypertensive (HHH) therapy in subarachnoid hemorrhage (SAH) may be beneficial in reducing delayed ischaemia after early aneurysm clipping. The aim of this study was to assess the correlation among pulmonary artery catheter (PAC) measurements, effectiveness of HHH-therapy and mean flow velocity (MFV) in the middle cerebral artery (MCA) by transcranial Doppler. Methods: We recorded Hunt-Hess classification, hematocrit, hemodynamic and PAC values, bilateral MFV in the MCA and Rankin scale in 37 ICU patients with SAH and no vasospasm (MFV 160 and wedge pressure (PCWP) > 12, moderate when only SBP > 160 or PCWP >12, and ineffective when SBP < 160 and PCWP < 12. Fisher's t test and multiple regression analysis were used for data analysis, p <0.05 was significant. Results: An effective prophylactic HHH-therapy did not reduce occurrence of vasospasm. Outcome did not correlate with clinical state on admission or effectiveness of HHH-therapy. A constantly elevated systemic vascular resistance index (SVRI) was associated with a good outcome while the combination of high MFV in MCA and decline in SVRI with poor outcome (p<0.05). Multiple regression analysis showed that SVRI and hematocrit explained 46% of variance of MFV in patients without vasospasm (MFV <120 cm/s, n=16). Conclusion: Our data demonstrate a correlation among SVRI, hematocrit and MFV. The differences in the outcome between the group where SVRI and MFV where moving in the same directions and the patient group where SVRI and MFV where moving in the opposite direction may be interpreted as early sign of vasospasm and may help to differentiate elevated MFV due to vasospasm (SVRI low) and elevated MFV due to effective HHH therapy (SVRI high). Differences in the outcome between the high and low SVRI may also be due to co-morbidities associated with low vascular resistance in the poor outcome group (e.g. sepsis, SIRS).

Monitoring Hypervolemic-hemodilution And Hypertensive Therapy In Subarachnoid Hemorrhage

Introduction: Prophylactic hypervolemic-hemodilution-hypertensive (HHH) therapy in subarachnoid hemorrhage (SAH) may be beneficial in reducing delayed ischaemia after early aneurysm clipping. The aim of this study was to assess the correlation among pulmonary artery catheter (PAC) measurements, effectiveness of HHH-therapy and mean flow velocity (MFV) in the middle cerebral artery (MCA) by transcranial Doppler. Methods: We recorded Hunt-Hess classification, hematocrit, hemodynamic and PAC values, bilateral MFV in the MCA and Rankin scale in 37 ICU patients with SAH and no vasospasm (MFV 160 and wedge pressure (PCWP) > 12, moderate when only SBP > 160 or PCWP >12, and ineffective when SBP < 160 and PCWP < 12. Fisher's t test and multiple regression analysis were used for data analysis, p <0.05 was significant. Results: An effective prophylactic HHH-therapy did not reduce occurrence of vasospasm. Outcome did not correlate with clinical state on admission or effectiveness of HHH-therapy. A constantly elevated systemic vascular resistance index (SVRI) was associated with a good outcome while the combination of high MFV in MCA and decline in SVRI with poor outcome (p<0.05). Multiple regression analysis showed that SVRI and hematocrit explained 46% of variance of MFV in patients without vasospasm (MFV <120 cm/s, n=16). Conclusion: Our data demonstrate a correlation among SVRI, hematocrit and MFV. The differences in the outcome between the group where SVRI and MFV where moving in the same directions and the patient group where SVRI and MFV where moving in the opposite direction may be interpreted as early sign of vasospasm and may help to differentiate elevated MFV due to vasospasm (SVRI low) and elevated MFV due to effective HHH therapy (SVRI high). Differences in the outcome between the high and low SVRI may also be due to co-morbidities associated with low vascular resistance in the poor outcome group (e.g. sepsis, SIRS).

Cardiopulmonary manifestations of hantavirus pulmonary syndrome

To describe the clinical characteristics of a group of patients infected with the newly recognized hantavirus in the Southwestern United States. Case series. Tertiary referral center. All patients with confirmed hantavirus infection admitted to the University of New Mexico Hospital between May 1, 1993 and January 1, 1994. Records of patients with hantavirus infection were reviewed to collect all pertinent clinical data. Pulmonary disease in these patients was characterized by hypoxemia covering a wide range of severity. The cause of hypoxemia was an increased permeability (noncardiac) pulmonary edema which could be differentiated from hydrostatic (cardiac) pulmonary edema by its association with low pulmonary artery occlusion pressures and increased protein content of edema fluid. Hemodynamic measurements in severe cases showed a shock state characterized by a low cardiac index (range 1.6 to 3.0 L/min/min2), a low stroke volume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997 dyne.sec/cm5.m2). Progression to death was associated with worsening cardiac dysfunction unresponsive to treatment and causing oxygen debt and lactic acidosis. The two major life-threatening pathophysiologic changes in Hantavirus Pulmonary Syndrome are increased permeability pulmonary edema, and an atypical form of septic shock caused by myocardial depression and hypovolemia.

Hemodynamic status susceptible to slowing of heart rate during thermodilution cardiac output determination in anesthetized patients

To identify hemodynamic variables that might indicate susceptibility to slowing of heart rate (HR) and to mean arterial pressure (MAP) decrease caused by cold injectate during thermodilution (TD) cardiac output determination, we measured hemodynamic variables in 32 anesthetized patients undergoing major surgery. A total of 608 cardiac output determinations were evaluated for any relationship between the magnitude of HR decreases and basal hemodynamic variables. The magnitude of HR decrease was pronounced in low cardiac index (CI), low mean pulmonary artery pressure (MPAP), and high systemic vascular resistance index (SVRI). Although there was some decrease in MAP associated with cold injectate, neither changes in SVRI nor those in the other hemodynamic variables correlated with the decreases in MAP. These results suggest that decreased CI and MPAP associated with elevated SVRI may be more susceptible to slowing of HR during cardiac output determination by TD in anesthetized patients.

Diltiazem withdrawal before coronary artery bypass surgery

The authors studied the effects of withdrawing oral diltiazem therapy on the subsequent course of coronary artery bypass graft surgery. Patients with severe coronary artery disease were divided into three groups using a prospective, controlled, randomized protocol. In group D (diltiazem-continuation) patients, diltiazem was administered 2.1 +/- 0.1 hours (mean +/- SEM) before anesthetic induction (n = 10). Group DW (diltiazem-withdrawal) patients received their final diltiazem dose 17.3 +/- 2.9 hours before anesthesia (n = 10). Group R was a reference group of patients not receiving diltiazem (n = 11; not randomized). Anesthesia was induced and maintained with fentanyl and pancuronium without use of halogenated anesthetics. No clinically important differences were detected in measured hemodynamics or drug requirements. Group D patients did not have a lower systemic vascular resistance (SVR) index (P greater than 0.31) or mean arterial pressure (P greater than 0.08) compared with group DW. Also, no evidence for a diltiazem withdrawal response was found, because group DW did not have either a higher SVR index (P = 0.99) or a higher pulmonary vascular resistance index (P = 0.99) compared with group R, and no severe myocardial ischemia, coronary artery spasm, or postoperative heart block were seen. Plasma diltiazem concentrations decreased significantly during CPB (P less than 0.0001), but showed overlap between groups D and DW. Plasma diltiazem concentration did not correlate significantly with simultaneous SVR. These data show the benign effects of both diltiazem administration and its acute withdrawal before coronary artery bypass surgery with high-dose fentanyl anesthesia.

Cardiac performance in pediatric near-drowning

Between July 1985 and December 1986, 29 near-drowned children ranging in age between 6 months and 13 yr were admitted to the Pediatric ICU of Huntington Memorial Hospital. Eight patients suffered cardiopulmonary arrest and had an admission Glasgow Coma Score of 3 or 4. Hemodynamic monitoring was performed on five of these patients. Three received cerebral resuscitation with controlled hyperventilation, hypothermia, pentobarbital, and mannitol because of intracranial hypertension. After CPR, a low cardiac index (CI) and high systemic vascular resistance index (SVRI) were found. When cerebral resuscitative therapy was initiated later, it caused a reduction of SVRI, CI, mean arterial pressure, and cerebral perfusion pressure. Fluid volume therapy and inotropic cardiac support was necessary to maintain adequate cerebral perfusion pressure. These observations indicate that cerebral resuscitative therapy can affect cardiovascular function. The hemodynamic depressive effects might even worsen the outcome. For this reason, it is advisable to obtain CI and pulmonary capillary wedge pressure to optimize cerebral perfusion and potentially neurologic outcome.

Hemodynamic effects of nitroprusside on cardiovascular system.

The effects of nitroprusside (NP) on hemodynamics, especially on venous flow velocity of the inferior vena cava (IVC) were evaluated in 20 remote myocardial infarction patients. NP was given beginning at 10 micrograms/min, with subsequent increments of 10 micrograms/min every 5 minutes until the systolic blood pressure was reduced to about 30 mmHg. Pressure was measured by a catheter-tip micromanometer. Flow velocity of IVC was measured by a catheter-tip flow velocity probe. NP significantly decreased left ventricular systolic pressure, left ventricular end-diastolic pressure, mean aortic pressure, right ventricular systolic pressure, right ventricular end-diastolic pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure, systemic vascular resistance index (SVRI) and left ventricular volume. Cardiac index (CI) was unchanged and stroke volume index was decreased. IVC pressure was unchanged, while right atrial (RA) pressure decreased. Subsequently, the pressure difference between IVC and RA increased significantly. The amplitude of IVC flow velocity decreased significantly. Twenty patients were classified into two groups according to whether or not the CI increased by NP. CI increased in 9 patients (group I) and decreased in 11 patients (group D). Compared to group D, control CI and the slope of end-systolic pressure-volume relation were less and the difference between IVC pressure and RA pressure was greater in group I. The patients with higher control SVRI had greater increase in CI during NP. In our study, the greater the depression of cardiac performance and the higher the SVRI, the greater the improvement of left ventricular pumping function during NP.

Pathogenesis of respiratory failure (ARDS) after hemorrhage and trauma: I. Cardiorespiratory patterns preceding the development of ARDS.

To evaluate clinical and physiologic determinants of adult respiratory distress syndrome (ARDS), we studied 152 consecutively monitored patients with trauma and hemorrhage: 60 developed ARDS. The cardiorespiratory patterns of hemorrhage and trauma patients who did not develop ARDS were compared to those who subsequently did develop ARDS, but before the time of their ARDS. Comparisons also were made in the patients with trauma and those with hemorrhage, as well as in those who survived and those who did not. Hemorrhage and trauma patients who developed ARDS had greater reductions in blood volume, red cell mass, PaCO2 and O2 delivery throughout all stages, as well as greater pulmonary vascular resistance index (PVRI) and pH in the early and middle stages. Nonsurvivors of ARDS had greater deficits in blood volume and red cell mass, higher PVRI and pH, as well as lower central venous pressure (CVP), hemoglobin (Hgb), and PaCO2 than did ARDS survivors. Hemorrhage patients had lower blood volume, left ventricular function, O2 delivery and VO2, as well as higher systemic vascular resistance index (SVRI), PVRI, and O2 extraction than either the trauma patients or normal subjects. Description of the temporal cardiorespiratory patterns before the clinical appearance of ARDS showed the progressive appearance of these deficits beginning 36 h before the hypoxemia was observed. The data are consistent with the concept that ARDS after hemorrhage and trauma is preceded by hypovolemia, reduced myocardial performance, inadequate O2 delivery, and inadequate O2 extraction needed to maintain VO2 at the elevated levels demanded by the increased metabolic requirements of the injured patients. Thus, the so-called shock lung is a complication of shock associated with hypovolemia, hypoxemia, and inadequate cardiac compensatory responses to increasesd O2 demands.