Page 372 - Feline Cardiology

388 Section M: Pulmonary Arterial Disorders

arterial pressure of 16.0 ± 0.9 mm Hg was recorded in 7 diastolic pulmonary arterial pressure; increased pul-
cats anesthetized with isoflurane, and this value did not monary vascular resistance; and normal pulmonary
change with administration of medetomidine (Lamont capillary wedge pressure. Examples of diseases that
et al. 2001). cause pre-capillary PH include primary pulmonary
Pulmonary hypertension is an abnormally high sys- hypertension (PPH), Eisenmenger physiology
tolic, diastolic, and/or mean pulmonary arterial pres- (Connolly et al. 2003), chronic pulmonary disorders,
sure. A practical clinical definition is systolic pulmonary pulmonary thromboembolism, heartworm disease
arterial pressure >25 mm Hg. (Rawlings et al. 1990), and peripheral pulmonary
The main potential cardiovascular complication of artery branch stenosis (Schrope and Kelch 2007). In
pulmonary hypertension is cor pulmonale, a Latin term otherwise healthy lungs, more than half of the pul-
meaning “lung-influenced heart” that describes the monary vasculature must be nonpatent in order to
process of right ventricular concentric hypertrophy produce pulmonary hypertension.
resulting from acquired pressure overload (pulmonary 2. With post-capillary pulmonary hypertension, pulmo-
hypertension), and right-sided heart failure. Severe nary arterial pressure passively increases due to
acute pulmonary hypertension could conceivably increased pulmonary venous hydrostatic pressure
produce reflex bradycardia, hypotension, and possibly (elevated pulmonary capillary wedge pressure).
cardiac arrest, although this mechanism has not been Diastolic pulmonary arterial pressure is within
clearly illustrated in clinical feline medicine cases. 5 mm Hg of pulmonary venous pressure (pulmonary
capillary wedge pressure), and pulmonary vascular
Etiology, Pathophysiology, and resistance is normal. Left-sided congestive heart failure
Gross Pathology is the most common cause of this form of pulmonary
hypertension and may result from any form of cardio-
Mean pulmonary artery pressure (MPAP) is related myopathy or severe mitral regurgitation.
to pulmonary blood flow (PBF) and pulmonary
vascular resistance (PVR) by the equation 3. Mixed hemodynamic response may be seen with
chronic elevations in pulmonary venous pressure
MPAP = (PVR × PBF) + pulmonary capillary wedge
pressure (PCWP). An increase in any component of this (pulmonary capillary wedge pressure). A mixed
hemodynamic response consists of a disproportion-
equation can cause pulmonary hypertension.
Pulmonary hypertension may occur acutely or chron- ate elevation in pulmonary arterial pressures in com-
ically, with chronic pulmonary hypertension appearing parison to elevated pulmonary venous pressure—a
to occur more frequently that acute disease. A cause- combination of forms 1) and 2) listed above. The
mechanism for this form of pulmonary hypertension
Pulmonary Arterial Disorders thromboembolism, or pleural effusion of any cause are 4. Pulmonary blood flow (PBF)-associated pulmonary
and-effect relationship is rarely identified, but congeni-
requires further elucidation and likely involves
tal heart disease, heartworm disease, pulmonary
endothelin-1 release, endothelial dysfunction and
abnormal pulmonary vasodilatory reserve.
typically found concurrently with chronic pulmonary
hypertension and are thought to contribute to its occur-
hypertension. Here, pulmonary vascular resistance is
rence. Experimental heartworm infections in cats (with
normal, and pulmonary arterial pressure is increased
much higher worm burdens than in naturally occurring
mainly or solely due to increased pulmonary blood
disease) have caused pulmonary hypertension (Rawlings
et al. 1990), but natural infections rarely appear to do so
shunting congenital heart defects such as ventricular
(www.heartwormsociety.org). Acute-onset pulmonary flow. Examples include large-volume left-to-right
septal defect and, less commonly in the cat, atrial
hypertension typically involves pulmonary thromboem-
bolism or an acute respiratory insult (such as smoke septal defect, patent ductus arteriosus, atrioventricu-
lar canal, and others. Some patients with large excesses
inhalation) with or without acute respiratory distress in pulmonary blood flow due to these shunts are
syndrome. at risk for development of Eisenmenger’s physiology.
Conceptually, pulmonary hypertension may be cate- There is a window of time in these patients in
gorized hemodynamically as follows, and this grouping which the increased pulmonary blood flow (without
offers future possibilities for applying specific treat- pathologic pulmonary arteriolar changes) causes
ments and obtaining a clearer prognosis:
pulmonary hypertension that is reversible with cor-
rection of the left-to-right shunt. However, if left
1. Pre-capillary pulmonary hypertension occurs due to untreated and with chronicity, Eisenmenger’s physi-
abnormalities of the pulmonary arterial vascular bed ology develops secondary to irreversible pulmonary
and is characterized by increased systolic, mean, and arteriolar vascular remodeling and permanent pul-