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Related Concept Videos

Regulation of Stroke Volume01:27

Regulation of Stroke Volume

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The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
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Cardiac Output II: Effect of Stroke Volume on Cardiac Output01:22

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Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.
Preload
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Mitral Stenosis I: Introduction01:22

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Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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Imbalances in Cardiac Output01:26

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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
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Cardiac Output and Stroke Volume01:11

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Cardiac output (CO) is an integral aspect of human physiology, reflecting the heart's efficiency and responsiveness to the body's needs. It represents the volume of blood that the left or right ventricle ejects into the aorta or pulmonary trunk each minute. The CO is calculated by multiplying the heart rate (HR)—the number of heartbeats per minute—by the stroke volume (SV)—the amount of blood pumped out with each heartbeat.
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Exercise and Cardiac Output01:17

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Regular physical activity is essential for maintaining cardiovascular health, with aerobic exercises being particularly effective. According to the American Heart Association, 150 minutes of moderate to intense aerobic exercise per week is recommended for a healthy heart. Aerobic activities may include brisk walking, running, bicycling, cross-country skiing, and swimming, ideally performed three to five times per week.
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Related Experiment Video

Updated: Jan 1, 2026

Transthoracic Echocardiography to Assess Post-Resuscitation Left Ventricular Dysfunction After Acute Myocardial Infarction and Cardiac Arrest in Pigs
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Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in

J Berg1, R Jablonowski1, D Nordlund1

  • 1Lund University, Faculty of Medicine, Department of Clinical Sciences Lund, Clinical Physiology, Lund, Sweden.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 20, 2019
PubMed
Summary
This summary is machine-generated.

Acute myocardial infarction (AMI) reduces stroke volume (SV) and atrioventricular plane displacement (AVPD). This study shows AVPD is coupled to SV, decreasing after AMI in swine models, with persistent effects on infarcted and remote myocardium.

Keywords:
AMIAVPDanimal modelcardiac failureischemia-reperfusion

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Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Cardiac Physiology

Background:

  • Acute myocardial infarction (AMI) can lead to heart failure with poor prognosis.
  • Stroke volume (SV) is normally attributed to longitudinal ventricular motion, measured as atrioventricular plane displacement (AVPD).
  • The relationship between SV and AVPD following AMI is not well understood.

Purpose of the Study:

  • To determine how SV depends on AVPD before and after AMI in swine.
  • To compare the effects of microembolization and ischemia-reperfusion models on SV and AVPD.
  • To assess the temporal changes in SV-AVPD coupling after AMI.

Main Methods:

  • Serial cardiac magnetic resonance imaging in swine models (microembolization and ischemia-reperfusion).
  • Analysis of cine and late gadolinium enhancement images for cardiac function, AVPD, and infarct size.
  • Measurements taken before AMI, 1-2 hours post-AMI, and in a subset at 24 hours and 7 days.

Main Results:

  • AMI caused significant decreases in both AVPD and SV (P < 0.05 and P < 0.001, respectively).
  • The ischemia-reperfusion model resulted in greater SV reduction and AVPD decrease compared to microembolization.
  • Diastolic early filling AVPD decreased post-AMI, while atrial contraction AVPD remained unchanged.

Conclusions:

  • AVPD is coupled to SV independently of infarct type, with a stronger association in ischemia-reperfusion infarcts.
  • AMI acutely and persistently depresses AVPD in both infarcted and remote myocardium.
  • Findings highlight the physiological significance of atrioventricular plane motion in assessing myocardial infarction.