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Medical evaluation and management of pregnant patients undergoing non-obstetrical surgery
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The cardiovascular system undergoes significant alteration under the influence of the altered hormonal milieu of pregnancy. Progesterone inhibits distal tubular sodium reabsorption leading to natriuresis. The juxtaglomerular cells of the kidney in response to this secrete renin to stimulate aldosterone release from the adrenals, maintaining sodium homeostasis (1–3). Renin is converted into angiotensin and catecholamines are released from the adrenal gland. Pregnancy is a state of maternal hyper-catecholaminism from its early stages. These catecholamines stimulate both inotropic and chronotropic effects on the heart, leading to an increase in cardiac output. Cardiac output begins to rise in the first trimester and continues on a steady increase to peak at 30% to 50% of the preexisting levels by approximately 32 weeks of gestation (3–7). Both heart rate and stroke volume increase. Peripheral systemic vascular resistance is reduced secondary to progesterone, exerting a direct effect to relax the intimal smooth muscle in the precapillary resistance vessels (2,3). The resulting vasodilatation leads to a decreased vascular resistance. There is a slight decrease in mean arterial pressure in the second trimester of a normal pregnancy due to the reduction in peripheral resistance. Blood volume increases with pregnancy, peaking at approximately 50% of prepregnancy levels at around 32 weeks of gestation. As the pregnant woman approaches term, mean arterial pressure normalizes as the increase in blood volume compensates for the decreased resistance and fills the capacitance of the vasculature (8,9).
The cardiovascular system
Published in Peter Kopelman, Dame Jane Dacre, Handbook of Clinical Skills, 2019
Peter Kopelman, Dame Jane Dacre
In aortic incompetence, the stroke volume is high because a significant amount of blood regurgitates back into the left ventricle and has to be pumped again. Furthermore, the incompetent valve will let the arterial pressure fall markedly in diastole. Hence, a bounding, dynamic pulse collapses to give a very wide pulse pressure. The collapse of the pulse pressure can be felt with even greater effect if your hand is placed around the patient’s wrist over the radial artery, and the patient’s hand is raised above their shoulder so that the radial artery is palpated at a level above the heart (Fig. 2.3).
Physiological interpretation of pressure waveforms
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Vasodilation by nitroglycerine causes peripheral pooling of blood and a decrease in stroke volume and end diastolic pressure. Heart size may also decrease from a decreased stroke volume. A fourth heart sound, if present, may disappear and the v wave of mitral regurgitation decreases.
The Clinical Implications of Body Surface Area as a Poor Proxy for Cardiac Output
Published in Structural Heart, 2021
Michiel D. Vriesendorp, Rolf H.H. Groenwold, Howard C. Herrmann, Stuart J. Head, Rob A.F. De Lind Van Wijngaarden, Pieter A. Vriesendorp, A. Pieter Kappetein, Robert J.M. Klautz
EOA was calculated with the continuity equation.13 Individually measured EOA instead of reference EOA from the literature was used in this study, as the categorization of EOAi for the classification of PPM is supported by the strong exponential relation between mean gradient and measured EOA.6 Stroke volume was determined at the level of the left ventricular outflow tract (LVOT), by multiplying the velocity-time integral with the cross-sectional area of the LVOT. To obtain cardiac output, stroke volume was multiplied by the heart rate. Mean gradient was calculated with the simplified Bernoulli equation, and Doppler velocity index (DVI) was calculated with the velocity-time integral of the left ventricular outflow tract (LVOT), divided by the velocity-time integral across the aortic prosthesis. In accordance with the VARC-2 criteria, hemodynamic obstruction was defined as having a mean gradient ≥20 mmHg and/or Doppler velocity index <0.35.7
The Pathophysiology of Afterload Mismatch and Ventricular Hypertrophy
Published in Structural Heart, 2021
The major function of any muscle, whether the tensor tympani, the biceps, or the myocardium, is to generate force that creates movement. The heart muscle uses that function to deliver adequate blood (cardiac output) to the body’s tissues while maintaining tolerable filling pressure. Cardiac output in turn is the product of heart rate and stroke volume. Stroke volume is dependent upon inherent ventricular end diastolic volume (larger subjects have larger hearts), preload, afterload and contractility. Contractility is the innate ability of the myocardium to generate force, while afterload is that force against which the myocardium must contract, and preload is a sarcomeric length-dependent mechanism for augmenting force development. The following discusses these properties concentrating primarily on afterload excess and its consequence: reduced stroke volume and/or the development of concentric ventricular hypertrophy.
Right Ventricular-Pulmonary Arterial Coupling and Outcomes in Heart Failure and Valvular Heart Disease
Published in Structural Heart, 2021
Bahira Shahim, Rebecca T. Hahn
Compared with the systemic circulation, pulmonary circulation has a much lower vascular resistance, greater pulmonary artery distensibility, and a lower peripheral pulse wave reflection coefficient.12 Pulmonary vascular impedance reflects the opposition to pulsatile flow, and determines, together with pulmonary vascular resistance (PVR), the RV afterload.9 RV afterload is reflected by arterial elastance (Ea), a load-independent measure of “total” ventricular afterload (both pulsatile and resistive components). It is measured as RV end-systolic pressure divided by stroke volume.24 PVR is a measure of the resistance of both capillaries and veins and is calculated as the difference between the mean pulmonary arterial pressure and pulmonary capillary wedge pressure, divided by the cardiac output. In the normal RV, mean pulmonary artery pressure is a reasonable approximation of end-systolic pressure. Thus, in the normal RV Ea could be estimated as PVR x heart rate.25 Although PVR represents only the resistive component of Ea, and pulmonary arterial compliance represents the pulsatile component, the latter contributes only ~23% to total afterload26 in normal patients and those with arterial pulmonary hypertension (PH) and support the use of the simplified formula. However, if post-capillary PH is present, the pulsatile component of Ea increases27 and stroke work is significantly reduced.28 Taking into account both resistive and pulsatile components of Ea may then be more important.