Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

1.2K
Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
1.2K
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

633
Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
633
Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

1.5K
Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
1.5K
Pulmonary Embolism III: Nursing Management01:27

Pulmonary Embolism III: Nursing Management

628
A pulmonary embolism occurs when a thrombus, amniotic fluid, tumor tissue, fat, or air embolus blocks one or more pulmonary arteries. Effective nursing management and patient education are crucial for improving outcomes and preventing recurrence.Nursing management starts with obtaining a comprehensive patient history, particularly noting any history of deep vein thrombosis (DVT). Assess for clinical manifestations, including dyspnea, chest pain, crackles, heart murmurs, and signs of right-sided...
628
Acute Respiratory Failure-IV01:23

Acute Respiratory Failure-IV

693
Respiratory failure can manifest suddenly or gradually, characterized by a rapid decline in PaO2 and a rapid rise in PaCO2. This situation indicates a severe respiratory problem that may quickly become a life-threatening emergency. One of the early signs of hypoxemic Acute Respiratory Failure (ARF) is a change in mental status due to the brain's sensitivity to oxygen levels and changes in acid-base balance. Symptoms such as restlessness, confusion, and agitation suggest inadequate oxygen...
693
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

821
Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
821

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Air pollution and adverse birth outcomes: a narrative review of epidemiological and mechanistic findings.

Journal of environmental health science & engineering·2026
Same author

Early discharge and home treatment after acute pulmonary embolism.

VASA. Zeitschrift fur Gefasskrankheiten·2026
Same author

PFO closure in ischemic stroke: insights from a single-center real-world cohort.

Frontiers in neurology·2026
Same author

Seasonal variations in hospital admissions and case-fatality of ischemic stroke: a nationwide analysis of >4.2 million cases in Germany.

Frontiers in epidemiology·2026
Same author

Temporal trends and risk factors of extracranial major bleeding in patients with acute pulmonary embolism.

Thrombosis research·2026
Same author

Modified Mansoor's self-report tool for cardiovascular risk assessment predicts major adverse cardiovascular and cerebrovascular events and amputations in peripheral artery disease.

VASA. Zeitschrift fur Gefasskrankheiten·2026

Related Experiment Video

Updated: Mar 22, 2026

A Porcine Model of Acute Autologous Pulmonary Embolism
07:44

A Porcine Model of Acute Autologous Pulmonary Embolism

Published on: September 6, 2024

945

Syncope and collapse in acute pulmonary embolism.

Karsten Keller1, Johannes Beule2, Jörn Oliver Balzer3

  • 1Center for Thrombosis and Hemostasis, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Germany; Center of Cardiology, Department of Cardiology I, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Germany.

The American Journal of Emergency Medicine
|April 25, 2016
PubMed
Summary

Syncope in pulmonary embolism (PE) is linked to lower blood pressure, higher heart rate, and right ventricular dysfunction. These factors contribute to cardiovascular syncope and poorer outcomes in PE patients.

More Related Videos

Establishment of a Minimally Invasive Rat Model of Pulmonary Embolism Using Autologous Blood Clots
08:02

Establishment of a Minimally Invasive Rat Model of Pulmonary Embolism Using Autologous Blood Clots

Published on: October 25, 2024

953
Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
07:41

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension

Published on: March 17, 2022

3.5K

Related Experiment Videos

Last Updated: Mar 22, 2026

A Porcine Model of Acute Autologous Pulmonary Embolism
07:44

A Porcine Model of Acute Autologous Pulmonary Embolism

Published on: September 6, 2024

945
Establishment of a Minimally Invasive Rat Model of Pulmonary Embolism Using Autologous Blood Clots
08:02

Establishment of a Minimally Invasive Rat Model of Pulmonary Embolism Using Autologous Blood Clots

Published on: October 25, 2024

953
Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension
07:41

Induction and Phenotyping of Acute Right Heart Failure in a Large Animal Model of Chronic Thromboembolic Pulmonary Hypertension

Published on: March 17, 2022

3.5K

Area of Science:

  • Cardiology
  • Pulmonology
  • Internal Medicine

Background:

  • Syncope and collapse are symptoms of pulmonary embolism (PE) associated with poorer outcomes.
  • The underlying pathomechanisms of syncope in PE are not fully understood.
  • Investigating these mechanisms is crucial for improving patient prognosis.

Purpose of the Study:

  • To investigate the pathomechanisms of syncope and collapse in patients with pulmonary embolism.
  • To analyze the relationship between syncope/collapse and hemodynamic parameters like blood pressure and heart rate.
  • To identify predictive values of these parameters for syncope occurrence in PE.

Main Methods:

  • Retrospective study of consecutive pulmonary embolism patients.
  • Comparison of patients with and without syncope/collapse.
  • Regression models and ROC analyses to assess associations and cut-off values for blood pressure, heart rate, and shock index (SI).

Main Results:

  • 11% of PE patients experienced syncope/collapse.
  • Syncope patients were older and had lower systolic and diastolic blood pressure.
  • Higher heart rate, shock index, and right ventricular dysfunction (RVD) were observed in patients with syncope/collapse.
  • Hypotension, tachycardia, and SI > 1.0 significantly increased the probability of syncope.

Conclusions:

  • Syncope/collapse in acute PE is associated with blood pressure fall, heart rate increase, and RVD.
  • These findings suggest a mechanism involving cardiovascular syncope with reduced cardiac output and vasovagal reflex.
  • Understanding these mechanisms can guide clinical management and improve outcomes for PE patients.