Cardiac conditions
Judy Bothamley, Maureen Boyle in Medical Conditions Affecting Pregnancy and Childbirth, 2020
Cardiac output is the amount of blood ejected from the heart in one minute. It depends on the heart rate and stroke volume. Cardiac Output = Stroke Volume × Heart Rate The body’s capacity to increase cardiac output is illustrated in exercise when both heart rate and stroke volume increase. Stroke volume is determined by the volume of blood in the ventricles before they contract. This is known as ventricular end diastolic volume (VEDV) or sometimes called preload. This preload depends on the extent of venous return. An increase in VEDV will result in stronger myocardial contraction. Venous return is enhanced when lying flat, although in a pregnant woman compression of the inferior vena cava in the supine position decreases venous return.
Intra-operative patient monitoring
Daniel Cottle, Shondipon Laha, Peter Nightingale in Anaesthetics for Junior Doctors and Allied Professionals, 2018
In order to use cardiac output monitors it is useful to first review your cardiac physiology. Cardiac output = stroke volume × heart rate.Blood pressure = cardiac output × systemic vascular resistance.Stroke volume is dependent on preload (ventricular filling), contractility and afterload (ventricular outflow resistance including systemic vascular resistance).Oxygen delivery = cardiac output × arterial O2 content.Indexes (e.g. cardiac index) are the value in question divided by the body surface area (m2).
The patient with acute cardiovascular problems
Peate Ian, Dutton Helen in Acute Nursing Care, 2020
Cardiac output decreases in sleep and rises during vigorous exercise, increasing in a trained athlete by up to 7 times (up to 35L/minute). In illness, the demand may increase as with sepsis; or the ability to maintain cardiac output may reduce, as with heart failure, and a mismatch of demand and supply may ensue. The cardiac reserve enables the output to increase by increasing the ejection fraction (and therefore stroke volume) and increasing heart rate. Stroke volume depends mainly on three factors: Preload.Contractility.Afterload.
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
A Longitudinal Echocardiographic Analysis of Patients Treated Using the Repositionable and Fully Retrievable Lotus Valve: A Sub-Analysis of the RESPOND Study
Published in Structural Heart, 2020
Osama Soliman, Chun-Chin Chang, Jochen Wöhrle, David Hildick-Smith, Sabine Bleiziffer, Daniel J. Blackman, Mohamed Abdel-Wahab, Thomas Modine, Andrey Nersesov, Dominic J. Allocco, Ian T. Meredith, Volkmar Falk, Nicolas M. Van Mieghem
LV ejection fraction was 50.4 ± 9.7% at baseline vs 51.6 ± 10.1% at discharge (median [Q1, Q3] change was 1.0[−1.7, 3.8], (p = 0.0003) and 49.8 ± 9.5% at 1-year (P = 0.08 vs. Discharge). Stroke volume index increased from 35.4 ± 10.2 at baseline to 39.6 ± 10.7 at discharge and further to 41.2 ± 10.8 mL/m2 at 1-year. Median [minimum, maximum] change from baseline to discharge was 3.5[−39.5, +43.9], (p < 0.001) and was further changed by 1.1[−37.2, 35.8], (p = 0.004) at 1-year. Percentage of patients with a low stroke volume (<35 mL/m2) was reduced from 54% at baseline to 38% at discharge and to 32% at 1-year (p < 0.001 vs. baseline) (Supplementary Figure 2). Mitral regurgitation (MR) severity improved from mild or more MR at baseline to none/trace in 70 (26%) of patients at discharge. Between discharge and 1-year, 77 (32%) patients with mild or more MR regressed to less than mild. On the contrary, MR deterioration from none/trace to mild or more was observed in 40 (18%) and 59 (23%) patients at discharge and 1-year follow-up, respectively (Supplementary Figure 3 and Supplementary Figure 4).
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.
Related Knowledge Centers
- Echocardiography
- Heart Rate
- Blood
- Cardiac Output
- Ventricle
- Ejection Fraction
- Cardiovascular Physiology
- End-Systolic Volume
- End-Diastolic Volume
- Myocardial Contractility