Abnormal Left Ventricular
Diastolic Filling Patterns in
Acute Hypoxic Pulmonary
Hypertension at High Altitude

Ritter, Manfred; Jenni, Rolf; Maggiorini, Marco; Grimm, J; Oelz, O

doi:10.1159/000470246

Cited by 11 publications

(14 citation statements)

References 18 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, dogs at a moderate altitude of 2300 m had unremarkable flow profiles in the pulmonary outflow tract. The significant changes in the pulmonary outflow flow profile in these same dogs examined at 3500 m, including shortened AT, lower AT/ET and notching during deceleration are similar to findings in people with moderate high‐altitude pulmonary hypertension 6 . However, based on our study these were not reliable indicators of pulmonary hypertension, as control dogs had shorter AT than dogs at moderate altitude and notching was also commonly found in control dogs, and none of these had a tricuspid regurgitation peak gradient >23 mmHg 15 .…”

Section: Discussionsupporting

confidence: 75%

“…Changes in diastolic function are thought to be caused by alteration in LV geometry due to a rise in pulmonary artery pressure. The increase in RV pressure leads to a transseptal right‐to‐left pressure gradient that results in prolonged isovolumic relaxation 6 . Likewise, we found a reversed E/A‐ratio in dogs at high altitude, significantly different from that for moderate altitude and control dogs, indicating an effect of this degree of high‐altitude hypoxia on the filling pattern.…”

Section: Discussionmentioning

confidence: 45%

“…Parameters of diastolic LV function are affected by acute high‐altitude hypoxia. Increased isovolumic relaxation time, increased deceleration time of early LV diastolic filling, increased E‐ and A‐velocities, and depressed E/A ratio have all been described 6 . Similarly, in acute cor pulmonale due to pulmonary thromboembolism, E‐ and A‐velocities are reversed 24 .…”

Section: Discussionmentioning

confidence: 98%

“…Hypobaric hypoxia is a physiologic cause of pulmonary hypertension in human beings 4 . Furthermore, acute and chronic exposure to high altitude is associated with altered parameters of left ventricular (LV) systolic and diastolic function 5,6 …”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Echocardiographic changes induced by moderate to marked hypobaric hypoxia in dogs

Glaus

Tomsa

Hässig

et al. 2004

Vet Radiology Ultrasound

View full text Add to dashboard Cite

Hypobaric (high-altitude) hypoxia is a physiologic cause of pulmonary hypertension, and alters left ventricular (LV) systolic and diastolic function. In the presence of tricuspid regurgitation, systolic pulmonary artery pressure can be measured noninvasively using the peak tricuspid regurgitation velocity and the Bernoulli equation. In the absence of measurable tricuspid regurgitation, severity of pulmonary hypertension may be estimated using two-dimensional, M-mode, and Doppler-derived parameters. To evaluate the usefulness of echocardiographic parameters for detecting mild-to-moderate pulmonary hypertension caused by moderate-to-marked hypoxia and to study the effect of high-altitude hypoxia on systolic and diastolic LV function in dogs, 19 Greenland dogs were examined at moderate altitude (2300 m) and high altitude (3500 m), and 10 Greenland control dogs were examined at 700-900 m. Evaluated parameters were pulmonary flow profile (shape, right ventricular acceleration time (RVAT), ejection time (RVET), RVAT/ET), peak mitral inflow velocities (LVE, LVA, LVE/A-ratio), LV % fractional shortening (FS), systolic time intervals (LVPEP, LVPEP/ET), and stroke volume index (SVI). Notching during deceleration was common in dogs at high altitude and in the control dogs, but not in dogs at moderate altitude. RVAT was shorter in dogs at high altitude compared with moderate altitude, but not compared with control dogs. Peak A-velocity was higher and E/A-ratio was lower in dogs at high altitude compared with moderate altitude and control dogs. FS was increased in dogs at high altitude compared with moderate altitude, and LVPEP and LVPEP/ET were shorter in the dogs at high altitude compared with moderate altitude and control dogs. In conclusion, significant differences in pulmonary flow profiles and systolic and diastolic parameters can be observed echocardiographically in dogs at different degrees of hypobaric hypoxia. However, overlap between the groups compromises their usefulness for diagnosing and estimating the degree of mild-to-moderate pulmonary hypertension in individual dogs.

show abstract

Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 45%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Echocardiographic changes induced by moderate to marked hypobaric hypoxia in dogs

Glaus

Tomsa

Hässig

et al. 2004

Vet Radiology Ultrasound

View full text Add to dashboard Cite

show abstract

“…Increasing cardiac output several-fold over baseline contributes to edema formation by increasing capillary pressure in overperfused areas and may even worsen the regional heterogeneity of blood flow. Furthermore, the greater increase of PAP in HAPE-susceptible individuals may impair left ventricular filling because of a ventricular septal shift shown by Ritter et al (88) and to possible mild left ventricular stiffness arising from decreased cardiac lymph clearance to the right heart (25). Diastolic dysfunction due to pulmonary hypertension likely explains the significantly greater wedge pressure increase in HAPE-susceptible individuals compared with nonsusceptible controls during exercise in hypoxia (34), whereas at rest, wedge pressure is normal in untreated HAPE (69).…”

Section: Additional Contributing Factorsmentioning

confidence: 99%

Physiological aspects of high-altitude pulmonary edema

Bärtsch

Mairbäurl²,

Maggiorini³

et al. 2005

Journal of Applied Physiology

Self Cite

302

217

View full text Add to dashboard Cite

High-altitude pulmonary edema (HAPE) develops in rapidly ascending nonacclimatized healthy individuals at altitudes above 3,000 m. An excessive rise in pulmonary artery pressure (PAP) preceding edema formation is the crucial pathophysiological factor because drugs that lower PAP prevent HAPE. Measurements of nitric oxide (NO) in exhaled air, of nitrites and nitrates in bronchoalveolar lavage (BAL) fluid, and forearm NO-dependent endothelial function all point to a reduced NO availability in hypoxia as a major cause of the excessive hypoxic PAP rise in HAPE-susceptible individuals. Studies using right heart catheterization or BAL in incipient HAPE have demonstrated that edema is caused by an increased microvascular hydrostatic pressure in the presence of normal left atrial pressure, resulting in leakage of large-molecular-weight proteins and erythrocytes across the alveolarcapillary barrier in the absence of any evidence of inflammation. These studies confirm in humans that high capillary pressure induces a high-permeability-type lung edema in the absence of inflammation, a concept first introduced under the term "stress failure." Recent studies using microspheres in swine and magnetic resonance imaging in humans strongly support the concept and primacy of nonuniform hypoxic arteriolar vasoconstriction to explain how hypoxic pulmonary vasoconstriction occurring predominantly at the arteriolar level can cause leakage. This compelling but as yet unproven mechanism predicts that edema occurs in areas of high blood flow due to lesser vasoconstriction. The combination of high flow at higher pressure results in pressures, which exceed the structural and dynamic capacity of the alveolar capillary barrier to maintain normal alveolar fluid balance. pulmonary artery pressure; hypoxic pulmonary vasoconstriction; nitric oxide; inflammation; alveolar fluid clearance; pathophysiology; review CLINICAL PICTUREHigh-altitude pulmonary edema (HAPE) is noncardiogenic pulmonary edema that usually occurs at altitudes above 3,000 m in rapidly ascending nonacclimatized individuals within the first 2-5 days after arrival. It may also occur in high-altitude dwellers who return from sojourns at low altitude. The first medical description of HAPE was published in Peru and recognized the latter form, also called reentry HAPE, as a pulmonary edema associated with electrographic signs of right ventricular overload (67). The first cases of HAPE in unacclimatized lowlanders climbing to high altitude were reported from the Rocky Mountains (53). The two forms very probably share the same pathophysiology.The reader is referred to other reviews (9,41,96,97) for an extensive presentation of the clinical picture. In this review, we point out some particular characteristics that might elucidate the underlying pathophysiology and are revealed by classical and newly evolving pathophysiological concepts.The prevalence of HAPE depends on the degree of susceptibility, the rate of ascent, and the final altitude. At an altitude of 4,500 m, the prevalence may ...

show abstract