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Published in Ken Addley, MCQs, MEQs and OSPEs in Occupational Medicine, 2023
Best fit. Blood is forced off the lower limbs and blood volume in the chest increases. Right atrial pressure can increase more than left. Ventilatory capacity can decrease. Resulting carbon dioxide retention and atrial naturetic hormone can be produced with a resultant diuresis.
The Advanced HEART FAILURE Patient
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Eran Kalmanovich, Philippe Gaudard, François Roubille
Driven by a machine-generated transmembrane pressure gradient, ultrafiltration removes plasma water across a semipermeable membrane. This technique lowers right atrial pressure and PCWP and can therefore result in sustained symptomatic improvement. However, the available evidence does not support the use of ultrafiltration as a first-line therapy. In the CARRESS-HF trial, ultrafiltration was inferior to stepped pharmacotherapy.100 A meta-analysis of eight RCTs comparing ultrafiltration to diuretics did not show any significant difference in survival or renal function; only a trend toward a lower readmission rate in patients treated with ultrafiltration was reported. Therefore, the current recommendation is to use ultrafiltration should pharmacotherapy fail to resolve congestion.1,38,80
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Central venous pressure monitoring (CVP) is helpful for those who have complex fluid management requirements, as they help evaluate fluid status and right ventricular function. The pressure measures right atrial pressure, but also reflects right ventricular end diastolic pressure, as the AV valves open in diastole. Fluid challenges described earlier in this chapter may be repeated if the CVP is low or normal with a reduced BP to ensure circulating volume is adequate. Central venous pressure is normally between 3–8mmHg, but in clinical practice it may be maintained up to 12mmHg to ensure optimum ventricular preload. Those who do not respond to fluid challenge may require inotropic support of the circulation. Factors that may cause a rise in CVP include: Heart failure.Cardiac tamponade.Tension pneumothorax.Vasoconstriction (caused by drugs such as adrenaline or as part of the sympathetic response to poor cardiac output).COPD.Tricuspid valve problems.
Establishment of a canine model of pulmonary arterial hypertension induced by dehydromonocrotaline and ultrasonographic study of right ventricular remodeling
Published in Clinical and Experimental Hypertension, 2023
Jing Dong, Xiao-Min Jiang, Du-Jiang Xie, Jie Luo, Hong Ran, Lin Li, Miao Li, Pei Jiang, Ping-Yang Zhang, Ling Zhou
After intravenous anesthesia with 30 mg/kg pentobarbital sodium, the animal was fixed on an operating table in a supine position in the catheterization room and connected with an ECG monitoring device and a percutaneous oxygen saturation detector, and venous access was opened for tracheal intubation and connected to an animal ventilator, followed by mechanical ventilation with a tidal volume of 150 mL. Pentobarbital sodium was intravenously infused at 1 mg/min for maintenance of anesthesia. The right femoral vein was punctured with a 7F arterial sheath, and a 5F Swan-Ganz catheter connected with a pressure transducer was inserted to successively measure the right atrial pressure (RAP), right ventricular pressure (RVP), pulmonary arterial pressure (PAP) and pulmonary capillary wedge pressure (PCWP). Cardiac output (CO) was measured by thermodilution. All parameters were measured 3 times and the average was taken. Pulmonary vascular resistance (PVR)=(mPAP-PCWP)/CO. The above hemodynamic parameters were measured repeatedly at 0, 8, and 14 weeks for each animal in both groups.
In search of mechanisms to explain the unquestionable benefit derived from sodium-glucose cotransporter-2 (SGLT-2) inhibitors use in heart failure patients
Published in Postgraduate Medicine, 2023
Angel Lopez-Candales, Khalid Sawalha, Betty M. Drees, Nicholas B. Norgard
To better explain stressed and unstressed blood volume better, let us review some physiology. Veins contain about 70% of TBV in comparison to arteries where it contains approximately 30%[31]. Guyton el at. described a model of venous return in 1955 along with the factors that influence its physiology, he highlighted three variables that independently affect the venous return: (a) the vascular resistance, (b) the mean systemic pressure, and (c) the right atrial pressure[32]. Among all these three variables, the mean systemic pressure is the least in getting the attention it deserves; this may be due to the complex and intricate system that makes the attempts to define its importance difficult. It is basically the pressure measured in the vascular system if the blood flow were to cease[33]. It is determined by the TBV present in the venous system and the compliance of that vascular bed to dilate of constrict. Physiologically speaking, it is the required volume of fluid to fill the vascular bed where it exerts a force on the vessel walls, and this is what is known as UBV. Now, any volume that will exert a rising pressure (above that normal one) on the vascular bed is known as SBV[33]. Therefore, it is related to venous constriction and dilation and that veno-constriction shifts blood volume from the unstressed to the stressed pool, resulting in increased pulmonary venous pressure, pulmonary edema, and thus HF.
The challenges of an aging tetralogy of Fallot population
Published in Expert Review of Cardiovascular Therapy, 2021
Jennifer P. Woo, Doff B. McElhinney, George K. Lui
Our understanding of RV relaxation in TOF is fairly limited. Impaired relaxation and restrictive physiology were observed in up to 50% of cases after surgery in small cohort studies [41,42]. Restrictive RV physiology is defined as increased antegrade late diastolic flow in the pulmonary artery during atrial systole and has been associated with worse clinical outcomes including lower cardiac output, prolonged inotropic support, and longer intensive care stay [43–45]. There was an association between elevated right atrial pressure, a marker of diastolic dysfunction, measured by cardiac catheterization and adverse cardiovascular events such as poor exercise capacity, heart failure, and ventricular arrhythmias [46]. Abnormal RV relaxation as measured by dilated inferior vena cava, abnormal hepatic vein diastolic flow reversal, and antegrade diastolic flow in the pulmonary artery has the potential to identify patients at risk for poor clinical outcomes who might benefit from early PVR [47].