1. Hoeper MM , Bogaard HJ , Condliffe R , et al . Definitions and diagnosis of pulmonaryhypertension . J Am Coll Cardiol . 2013 ; 62 ( 25 ): D42 – D50 . doi: 10.1016/j.jacc.2013.10.032
2. Hoeper MM , Ghofrani HA , Grunig E
enlargement of the pulmonary artery was consistent with a diagnosis of pulmonaryhypertension with secondary right-sided heart failure. However, the llama did not have any history of respiratory tract disease, and no signs of respiratory tract disease were
subsequent development of pulmonaryhypertension was considered likely. Differential diagnoses included an atrial septal defect, ventricular septal defect, and a patent ductus arteriosus (PDA).
Same radiographic images as Figure 1
supported a diagnosis of right-sided congestive heart failure secondary to pulmonaryhypertension.
Coelomocentesis was performed to improve respiratory function by providing more room for expansion of the air sacs. Clinicians were careful to remove as
discretion of the attending clinician. The LVIDd, LVIDs, and LA:Ao were measured by means of standard echocardiographic techniques. 15,16 Detection of tricuspid regurgitation by use of echocardiography was recorded. Pulmonaryhypertension was arbitrarily
pulmonaryhypertension was present (as measured via tricuspid valve regurgitation velocity, when present, and defined as a tricuspid valve regurgitation velocity > 3.2 m/s). 7 Additionally, the cardiologists performing the examination were asked to detail
indicative of pulmonaryhypertension. Results of a follow-up heartworm antigen test were negative.
The cat was discharged with instructions that the owners administer prednisone (1.25 mg/kg, PO, q 24 h) and dalteparin h (100 U/kg [45 U/lb], SC, q 24 h for
Objective—To determine whether inhaled nitric oxide
(NO) prevents pulmonary hypertension and improves
oxygenation after IV administration of a bolus of
dexmedetomidine in anesthetized sheep.
Animals—6 healthy adult sheep.
Procedure—In a crossover study, sevoflurane-anesthetized
sheep received dexmedetomidine (2 µg/kg,
IV) without NO (DEX treatment) or with inhaled NO
(DEX-NO treatment). Cardiopulmonary variables,
including respiratory mechanics, were measured
before and for 120 minutes after bolus injection of
Results—Dexmedetomidine induced a transient
decrease in heart rate and cardiac output. A short-lived
increase in mean arterial pressure (MAP) and
systemic vascular resistance (SVR) was followed by a
significant decrease in MAP and SVR for 90 minutes.
Mean pulmonary arterial pressure (MPAP) and pulmonary
vascular resistance increased transiently after
dexmedetomidine injection. The PaO2 was significantly
decreased 3 minutes after injection and reached a
minimum of (mean ± SEM) 13.3 ± 7.8 kPa 10 minutes
after injection. The decrease in PaO2 was accompanied
by a sudden and prolonged decrease in dynamic
compliance and a significant increase in airway resistance,
shunt fraction, and alveolar dead space. Peak
changes in MPAP did not differ between the 2 treatments.
For the DEX-NO treatment, PaO2 was significantly
lower and the shunt fraction significantly higher
than for the DEX treatment.
Conclusions and Clinical Relevance—Inhalation of
NO did not prevent increases in pulmonary arterial
pressures induced by IV administration of
dexmedetomidine. Preemptive inhalation of NO
intensified oxygenation impairment, probably through
increases in intrapulmonary shunting. (Am J Vet Res
Objective—To identify clinical signs, underlying cardiac
conditions, echocardiographic findings, and prognosis
for horses with congestive heart failure.
Procedure—Signalment; history; clinical signs; clinicopathologic,
echocardiographic, and radiographic
findings; treatment; and outcome were determined
by reviewing medical records.
Results—All 14 horses were examined because of a
heart murmur; tachycardia was identified in all 14.
Twelve horses had echocardiographic evidence of
enlargement of 1 or more chambers of the heart.
Other common clinical findings included jugular distention
or pulsation, crackles, cough, tachypnea, and
ventral edema. Nine horses had signs consistent with
heart failure for > 6 days. Underlying causes for heart
failure included congenital defects, traumatic vascular
rupture, pericarditis, pulmonary hypertension secondary
to heaves, and valvular dysplasia. Seven horses
were euthanatized after diagnosis of heart failure;
5 were discharged but were euthanatized or died of
complications of heart disease within 1 year after discharge.
The remaining 2 horses were discharged but
lost to follow-up.
Conclusions and Clinical Relevance—Results suggest
that congestive heart failure is rare in horses. A loud
heart murmur accompanied by either jugular distention
or pulsation, tachycardia, respiratory abnormalities
(crackles, cough, tachypnea), and ventral edema were
the most common clinical signs. Echocardiography was
useful in determining the underlying cause in affected
horses. The long-term prognosis for horses with congestive
heart failure was grave. (J Am Vet Med Assoc
Objective—To characterize structural changes in pulmonary
vessels of dogs with dirofilariosis.
Animals—8 dogs with dirofilariosis and 2 unaffected
Procedure—Pulmonary artery pressure was measured
in affected dogs, and dogs then were euthanatized.
Scanning electron microscopy was used to
examine vascular corrosion casts of pulmonary vasculature.
Tissue sections of pulmonary vasculature
were evaluated by use of histologic examination.
Results—Pulmonary artery pressure was higher in
dogs with severely affected pulmonary vessels. In tissue
sections, dilatation, as well as lesions in the tunica
intima and proliferative lesions resulting in constriction
or obstruction, were frequently observed in
branches of the pulmonary artery. Numerous dilated
bronchial arteries were observed around affected pulmonary
arteries. Hyperplastic venous sphincters
were observed in small pulmonary veins and venules.
In corrosion casts, affected pulmonary lobar arteries
had dilatation, pruning, abnormal tapering, constriction,
and obstruction. In small arteries and arterioles,
surface structures representing aneurisms and
edema were seen. Bronchial arteries were well developed
and extremely dilated, and they formed numerous
anastomoses with pulmonary arteries at all levels,
from the pulmonary trunk to peripheral vessels.
Capillaries in the lungs were dilated with little structural
change. Small pulmonary veins and venules had
irregular annular constrictions that were caused by
hyperplastic smooth muscle cells of venous sphincters.
Conclusions and Clinical Relevance—Scanning
electron microscopy of microvascular casts delineated
links between the bronchial and pulmonary circulations
in dogs with dirofilariosis. Results of scanning
electron microscopy provided a structural explanation
for the development of pulmonary circulatory disturbances
and pulmonary hypertension in dogs affected
by dirofilariosis. (Am J Vet Res 2002:63:1538–1544)