Page 718 - Small Animal Clinical Nutrition 5th Edition

Cardiovascular Disease 745

VetBooks.ir

Figure 36-5. L-carnitine is essential for aerobic mitochondrial energy production and assists in the transit of energy (ATP) into the cytoplasm,
where it provides the fuel for cellular functions. After entry into the cell, fatty acids are activated to form acyl-CoA (1). The acyl-CoA can then
be transported into the mitochondrion as acyl-carnitine (2) via a carnitine-dependent shuttle (3). Acyl-carnitine then undergoes beta-oxidation
to acetyl-CoA on the inner mitochondrial membrane (4) for entry into the TCA cycle and production of ATP. Secondarily, L-carnitine is involved
in processes that prevent accumulation of toxic metabolites inside the mitochondrion. (Adapted from Neu H. Kleintierpraxis; 40: 197-220.)

related to heart rate and stroke volume (CO = HR x SV). pressures within the systemic circulation, pulmonary circulation
Diseases associated with hypertension that increase heart rate and intrapleural space favor transudation of pleural fluid from
include: 1) hyperthyroidism, 2) anemia, 3) hyperviscosity, 4) the parietal pleura (pleura covering the inner chest wall) into
polycythemia and 5) pheochromocytoma. Increased stroke vol- the pleural space with subsequent absorption of the fluid into
ume may occur during hypervolemic states, but is usually due the visceral pleura’s vasculature (Bauer and Woodfield, 1995).
to increased retention of sodium, chloride and water. Renal fail- The result is a continuous flow of fluid through the pleural
ure, hyperadrenocorticism and hyperaldosteronism may cause space. This delicate balance can be disrupted by any disorder
increased total body sodium, chloride and water. that alters oncotic pressure, systemic or pulmonary capillary
Activation of the RAA pathway may elevate blood pressure pressure, lymphatic compliance, capillary permeability or effec-
by increasing stroke volume and total peripheral resistance. tive pleural surface area.
Angiotensin II is a potent vasoconstrictor, and angiotensin II Biventricular CHF with systemic and pulmonary venous
and aldosterone stimulate renal sodium and chloride retention. hypertension is a primary cause of pleural effusion. However,
Increased arteriolar tone, sensitivity to circulating vasopressors other causes of pleural effusion can masquerade as heart failure
and levels of circulating catecholamines and decreased arterio- and may occur in patients with known heart disease, especially
lar elasticity may also increase total peripheral resistance. older dogs and cats. Other common causes of pleural effusion
Common causes of secondary hypertension include: 1) include diseases that increase capillary permeability and alter
chronic progressive renal disease in dogs and cats (glomeru- the normal flow and absorption of pleural fluid (e.g., primary
lonephritis, amyloidosis, chronic interstitial nephritis, pyelo- intrathoracic or metastatic malignancy, pleural space infection,
nephritis and polycystic renal disease), 2) hyperadrenocorticism traumatic diaphragmatic hernia with incarceration of abdomi-
in dogs and 3) hyperthyroidism in cats. The “target organs” or nal viscera).
end organs or systems that appear most sensitive to increased Chylothorax is the accumulation of intestinal lymph (chyle)
blood pressure include the eyes, kidneys, cardiovascular system in the pleural space. This milky fluid has a high concentration
and cerebrovascular system (Littman and Drobatz, 1995). of chylomicrons and triglycerides (the triglyceride concentra-
Clinical signs related to end-organ damage are usually the rea- tion usually exceeds 100 mg/dl) and is low in cholesterol (the
son an animal with hypertension is brought to a veterinarian for triglyceride-cholesterol ratio is greater than 1) (Fossum et al,
examination. 1986). The etiology of chylothorax is poorly understood, but
has been associated with: 1) traumatic leakage, 2) diaphragmat-
Pleural Effusion ic hernia, 3) lymphosarcoma, 4) cranial mediastinal masses, 5)
Hydrostatic and oncotic forces (Starling’s forces) are balanced pulmonary neoplasia, 6) dirofilariasis, 7) congenital abnormali-
within the pleurae and pleural space. Hydrostatic and oncotic ties of the thoracic duct and 8) CHF. Experimental and clini-