Inotropes and Vasopressors for Shock

2019 ◽  
Author(s):  
Amour B U Patel ◽  
Gareth L Ackland

Inotropes and vasopressors play a key role in the management of shock. The goal of therapy is to restore end-organ perfusion by augmenting cardiac output (CO) and vascular tone. Clinical trial data have thus far failed to identify precise hemodynamic end points associated with better outcomes; in any event, such end points are highly likely to be determined on an individualized basis, reflecting patients’ chronic arterial blood pressure, baseline cardiac function, and other pathophysiologic factors (e.g., end-stage renal failure, cardiac ischemia).1 Inotropes enhance cardiac contractility and CO; vasopressors raise blood pressure. The impact of these drugs in restoring hemodynamic parameters to “normal” values has principally been used to evaluate their effectiveness, with clinical practice guided by extrapolation from animal studies and pharmacologic trials.2 However, these drugs have important extra-cardiovascular effects on metabolic, neurohormonal, and autonomic regulation that are also injurious. This review discusses the mechanisms and evidence base for inotropes and vasopressors in various types of shock. This review contains 3 figures, and 39 references. Keywords: inotropes, vasopressors, catecholamines, monitoring, shock states, cardiogenic, hemorrhagic, septic, neurogenic

2019 ◽  
Author(s):  
Amour B U Patel ◽  
Gareth L Ackland

Inotropes and vasopressors play a key role in the management of shock. The goal of therapy is to restore end-organ perfusion by augmenting cardiac output (CO) and vascular tone. Clinical trial data have thus far failed to identify precise hemodynamic end points associated with better outcomes; in any event, such end points are highly likely to be determined on an individualized basis, reflecting patients’ chronic arterial blood pressure, baseline cardiac function, and other pathophysiologic factors (e.g., end-stage renal failure, cardiac ischemia).1 Inotropes enhance cardiac contractility and CO; vasopressors raise blood pressure. The impact of these drugs in restoring hemodynamic parameters to “normal” values has principally been used to evaluate their effectiveness, with clinical practice guided by extrapolation from animal studies and pharmacologic trials.2 However, these drugs have important extra-cardiovascular effects on metabolic, neurohormonal, and autonomic regulation that are also injurious. This review discusses the mechanisms and evidence base for inotropes and vasopressors in various types of shock. This review contains 3 figures, and 39 references. Keywords: inotropes, vasopressors, catecholamines, monitoring, shock states, cardiogenic, hemorrhagic, septic, neurogenic


2007 ◽  
Vol 32 (4) ◽  
pp. 670-676 ◽  
Author(s):  
Fleur Poelkens ◽  
Mark Rakobowchuk ◽  
Kirsten A. Burgomaster ◽  
Maria T.E. Hopman ◽  
Stuart M. Phillips ◽  
...  

An increase in age coincides with a decrease in arterial compliance, which is related to a higher risk for cardiovascular accidents. Evidence regarding the effects of resistance training on arterial compliance is conflicting. Currently, little information is available about the effect of resistance training on arterial compliance in elderly men. We assessed the impact of 10 weeks of unilateral arm and leg resistance training on carotid, brachial, and femoral arterial compliance in 12 healthy elderly men (mean age ± SD, 71 ± 7 y). Arterial compliance was evaluated before, after 4 weeks, and after 10 weeks of unilateral resistance training by simultaneously measuring arterial diameter and blood pressure in each artery. There were no significant differences in arterial compliance or stiffness index in any of the arteries examined after 10 weeks of training. However, after 10 weeks of resistance training, resting heart rate decreased from 76 ± 4 beats/min to 61 ± 3 beats/min (p < 0.05), plasma glucose decreased from 6.0 ± 0.9 to 5.1 ± 0.9 mmol/L (mean ± SE) (p < 0.05), and carotid artery peak blood flow increased from 1831 mL/min to 2245 mL/min (p < 0.05). There were no significant changes in resting arterial blood pressure. Unilateral resistance training for 10 weeks does not alter peripheral and central arterial compliance elderly men.


Author(s):  
G.F. Stegmann

In humans the combined administration of epidural anaesthesia and inhalation anaesthesia may result in cardiovascular instability associated with decreases in heart rate and blood pressure. Anaesthesia was induced with a combination of midazolam / ketamine in 18 female pigs with a mean body weight of 24.9±5.9 kg scheduled for surgical removal of the liver. After tracheal intubation, anaesthesia was maintained on a circle rebreathing circuit with isoflurane. Epidural anaesthesia was administered with ropivacaine (AL-group, n=8) at 0.2 mℓ / kg of a 7.5 mg / mℓ solution to the anaesthetised animals. The A-group (n = 10) received isoflurane anaesthesia only. The vaporiser was set at 2.5 % for the A-group and 1.5 % for the AL-group. Heart rate, invasive systolic, diastolic, and mean arterial blood pressure were monitored. Comparisons were made between treatments and within treatments comparing variables during surgical preparation and abdominal surgery. Differences between treatments were not statistically significant (P > 0.05) during surgical preparation or during abdominal surgery. For within treatment groups, the differences between surgical preparation and abdominal surgery were statistically significant (P < 0.05) for heart rate in the A-group, but not statistically significant (P > 0.05) for the other variables. It is concluded that abdominal surgery may be associated with statistically significant changes in heart rate in isoflurane-anaesthetised pigs and that the combined administration of epidural ropivacaine may prevent statistically significant changes in HR during abdominal surgery.


Hypertension ◽  
2019 ◽  
Vol 73 (1) ◽  
Author(s):  
Joana Oliveira Miranda ◽  
Rui João Cerqueira ◽  
Henrique Barros ◽  
José Carlos Areias

Intrauterine fetal conditions can have lifelong cardiovascular effects. The impact of maternal diabetes mellitus on children’s cardiovascular profile is not well established. The goal of this study was to explore the association between maternal diabetes mellitus and offspring’s blood pressure (BP) ≤10 years of age. Generation XXI is a prospective birth cohort, which enrolled 8301 mother-offspring pairs, including 586 (7.1%) children of diabetic mothers. The associations between maternal diabetes mellitus and BP at 4, 7, and 10 years of age was modeled using linear regression. A mixed-effects model was built to assess differences in BP variation over time. Path analysis was used to quantify effects of potential mediators. Maternal diabetes mellitus was associated with higher BP in offspring at the age of 10 (systolic: β, 1.48; 95% CI, 0.36–2.59; and diastolic: β, 0.86; 95% CI, 0.05–1.71). This association was independent of maternal perinatal characteristics, and it was mediated by child’s body mass index and, to a lesser extent, by gestational age, type of birth, and birth weight (indirect effect proportion, 73%). No significant differences in BP were found at 4 and 7 years of age. Longitudinal analysis showed an accelerated systolic BP increase on maternal diabetes mellitus group (β, 1.16; 95% CI, 0.03–2.28). These finding were especially relevant in males, suggesting sex differences in the mechanisms of BP prenatal programing. Our results provide further evidence that maternal diabetes mellitus is associated with high BP late in childhood, demonstrating a significant role of child’s body mass in the pathway of this association.


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz Baudenbacher ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
Susan Eagle ◽  
...  

Patients with metabolic syndrome are at higher risk for cardiac arrest (CA), and also have worse neurologic outcome after CA related to their comorbidities (e.g., Type 2 Diabetes Mellitus [T2DM]). Using Zucker Diabetic Fatty (ZDF) rats as a new and relevant model with common comorbidities for CA and cardiopulmonary resuscitation (CPR), we hypothesized that T2DM is associated with a lower chance for return of spontaneous circulation (ROSC) and/or a worse outcome regarding heart function after asphyxial CA compared to their lean littermates. Two groups of rats (8 ZDF, 7 lean) were monitored for 37±2 weeks. The rats were anesthetized and intubated; heart rate was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids and medications, respectively. Before ventilation was stopped to initiate asphyxial CA, rocuronium was given. After 8 minutes of CA, ventilation was re-initiated with FiO 2 1.0, epinephrine and sodium-bicarbonate were administered, and pneumatic chest compression were started with 200 compressions per minute. Chest compressions were stopped when a systolic blood pressure of 120 mmHg was achieved. During 4 hours of observation, vital parameters were closely monitored, blood gases were measured, and ejection fraction (EF %) was assessed with ultrasound. Data are mean ± SD. Statistics: Unpaired student’s t-test (two-tailed), α.05. At baseline, ZDF rats showed significantly higher blood glucose levels (504±52 vs 174±14 mg/dl) compared to their lean littermates. All ZDF and lean rats achieved ROSC, and measurements taken directly after ROSC and after the first hour showed no relevant differences. After four hours, there was no difference in heart rate between ZDF and lean rats. However, diabetic rats had a significantly higher mean arterial blood pressure (142±24vs. 107±19 mmHg) and ejection fraction (42±16%vs 20±8%) compared to their lean littermates. The hypothesis that ROSC-rate in diabetic rats would be lower could not be proven. Conversely, the ZDF rats showed a significantly higher blood pressure related to an increased EF%. Further analysis in this study will focus on the impact of T2DM on cardiac and neurological ischemia-reperfusion injury.


1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.


Author(s):  
G.F. Stegmann

The cardiovascular effects of non-abdominal and abdominal surgery during isoflurane anaesthesia (A-group) or isoflurane anaesthesia supplemented with either epidural ropivacaine (AR-group; 0.75 % solution, 0.2 mℓ/kg) or morphine (AM-group; 0.1 mg/kg diluted in saline to 0.2mℓ/kg) were evaluated in 28 healthy pigs with a mean body weight of 30.3 kg SD ± 4.1 during surgical devascularisation of the liver. Anaesthesia was induced with the intramuscular injection of midazolam (0.3 mg/kg) and ketamine (10 mg/kg). Anaesthesia was deepened with intravenous propofol to enable tracheal intubation and maintained with isoflurane on a circle rebreathing circuit. The vaporiser was set at 2.5% for the A-group and 1.5% for the AR- and AM-groups. Differences between treatment groups were not statistically significant (P>0.05) for any of the variables. Differences between AM- and AR-groups were marginally significant heart rate (HR) (P = 0.06) and mean arterial blood pressure (MAP) (P = 0.08). Within treatment groups, differences for the A-group were statistically significant (P<0.05) between non-abdominal and abdominal surgery for HR, systolic blood pressure, diastolic blood pressure (DIA) and MAP. Within the AM-group differences were statistically significant (P < 0.05) for DIA and MAP, and within the AR group differences for all variables were not statistically significant (P > 0.05). It was concluded that in isoflurane-anaesthetised pigs, the epidural administration of ropivacaine decreased heart rate and improved arterial blood pressure during surgery.


2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.


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