The patient with acute cardiovascular problems
Peate Ian, Dutton Helen in Acute Nursing Care, 2020
The following describes stages of the cardiac cycle and is illustrated by Figure 6.6. In ventricular diastole, the atria and ventricles are relaxed, the atrioventricular (AV) valves are open and blood is flowing from the atria to the ventricles. Towards the end of ventricular diastole, the SA node and then atria depolarise (viewed as the P wave on the ECG), causing the atria to contract and starting atrial systole. The ventricles have received about 80% of their blood already, but the contracting atria push the final 20% through the AV valves; this is sometimes referred to as the ‘atrial kick’. The pulmonary and aortic valves remain closed during this phase. The amount of blood in the ventricles at the end of diastole in known as the end diastolic volume (EDV).
The patient with acute cardiovascular problems
Ian Peate, Helen Dutton in Acute Nursing Care, 2014
The following describes stages of the cardiac cycle and is illustrated by Figure 6.6. In ventricular diastole the atria and ventricles are relaxed, the atrioventicular (AV) valves are open and blood is flowing from the atria to the ventricles. Towards the end of ventricular diastole the SA node and then atria depolarise, (viewed as the P wave on the ECG) causing the atria to contract, starting atrial systole. The ventricles have received about 80% of their blood already, but the contracting atria push the final 20% through the AV valves: this is sometimes referred to as the ‘atrial kick’. The pulmonary and aortic valves remain closed during this phase. The amount of blood in the ventricles at the end of diastole in known as the end diastolic volume (EDV).
Pressure–Volume Loop of the Left Ventricle
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
In diastole, the left ventricular volume rises from 60 mL at the end of systole to the end-diastolic volume of 130 mL, and the ventricular pressure rises from 5 to 10 mmHg. During isovolumetric ventricular contraction, the pressure increases to 80 mmHg before the aortic valve opens. During the ejection phase, the ventricle contracts and ejects the stroke volume of 70-mL blood against the afterload of increasing aortic pressure. Ventricular pressure rises during the ejection phase to 120 mmHg and then falls to 100 mmHg at the end of systole when the aortic valve closes again. During isovolumetric relaxation, the ventricular pressure falls once more to the end-systolic point. The area enclosed by the pressure–volume curve (the shaded area in Figure 26.1) reflects the external work done by the left ventricle in each cardiac cycle.
Cross-sectional area of the murine aorta linearly increases with increasing core body temperature
Published in International Journal of Hyperthermia, 2018
A. Colleen Crouch, Adam B. Manders, Amos A. Cao, Ulrich M. Scheven, Joan M. Greve
Heart rate was measured from a 2-lead ECG placed along axis II. Coronal 2 D images were used to plan slices perpendicular to the long axis of the left ventricle (LV). Five to six 2 D contiguous slices were planned through the LV, depending on the size of the organ. For each slice, a cardiac-gated and respiratory compensated 2 D CINE acquisition with 12 frames was used to acquire data across the cardiac cycle [TR/TE 180/2 ms, FOV (30 mm)2, α 30°, matrix 1282 zero-filled to 2562, slice thickness 1 mm, NEX 4, resolution (117 µm)2, ∼20 min]. The endocardial area of each frame was defined manually (Analyze, AnalyzeDirect, Stilwell, KS). For each slice, the end-diastolic and end-systolic areas were determined by selecting the maximum and minimum areas, respectively. The end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated:
Physiological characterization of an arginine vasopressin rat model of preeclampsia
Published in Systems Biology in Reproductive Medicine, 2022
Sapna Ramdin, Thajasvarie Naicker, Virushka Pillay, Sanil D. Singh, Sooraj Baijnath, Blessing N Mkhwanazi, Nalini Govender
Earlier studies also linked AVP to arterial blood pressure regulation (Jablonskis and Howe 1993; Song and Martin 2006; Li et al. 2012). The elevations in both systolic and diastolic blood pressure in our study throughout pregnancy in the PAVP group, suggests that arginine vasopressin stimulates the renin-angiotensin aldosterone system (RAAS). This results in vasoconstriction, which is mediated via the V1a receptor and consequently increases peripheral resistance and systemic blood pressure as observed in our study (Qian 2018). Myocardial atrial contraction results in an atrial-induced increase in end-diastolic pressure, which subsequently enhances ventricular contraction. Arginine vasopressin increases the impact of norepinephrine and Ang II on cardiac muscle and blood vessels thus altering hemodynamic function (Lee et al. 2003), and negatively affects myocardial contraction (Goldsmith 2005; Goldsmith and Gheorghiade 2005). Chronic hypertension results in diastolic dysfunction and consequent left ventricular hypertrophy thereby reducing cardiac compliance (Lorell and Carabello 2000). This results in a higher diastolic pressure–volume relationship where even minor elevations in left ventricular end-diastolic volume induces a significant rise in left ventricular end diastolic pressure (Gutierrez and Blanchard 2004). The pronounced effect of AVP on diastolic pressure may be due to the exaggerated interaction of AVP with the V1A and V2 receptors on peripheral blood vessels (Goldsmith 2005; Goldsmith and Gheorghiade 2005).
Combined treatment with ultrasound-targeted microbubble destruction technique and NM-aFGF-loaded PEG-nanoliposomes protects against diabetic cardiomyopathy-induced oxidative stress by activating the AKT/GSK-3β1/Nrf-2 pathway
Published in Drug Delivery, 2020
Ming Zhang, Ning-Wei Zhu, Wei-Cheng Ma, Meng-Jia Chen, Lei Zheng
The cardiac structural evaluation was performed by echocardiogram after drug treatment. Through echocardiography, there was a significant decrease in left ventricular ejection fraction (LVEF) and fractional shortening (FS) in the DM group compared with the normal control group (Table 1). After all forms of aFGF treatment, the values of LVEF and FS were significantly increased (p < .05); moreover, the NM-aFGF-PEG-lips + UTMD group had the most pronounced increase (p < .05). Other parameters of cardiac function such as left ventricle end-diastolic diameter (LVEDD), left ventricle end-systolic diameter (LVESD), left ventricle end-diastolic volume (LVEDV) and left ventricle end-systolic volume (LVESV) were also detected. The DM group exhibited a significant increase in LVEDD, LVESD, LVEDV and LVESV compared with the control group (p < .05). After the drug treatment, the values of LVEDD, LVESD, LVEDV and LVESV were significantly decreased compared with the DM group; in addition, the NM-aFGF-PEG-lips + UTMD group had the most pronounced decrease (p < .05).
Related Knowledge Centers
- Sarcomere
- Stroke Volume
- Diastole
- Cardiac Muscle
- Cardiovascular Physiology
- Preload
- Frank–Starling Law
- Body Surface Area
- End-Systolic Volume