learning and patho for the cardiac patient part 2

For the purpose of this paper we are going to be referring to left ventricle dysfunction, or systolic heart failure, which has been associated with the metabolic disorder of the thyroid. Thyroid hormone plays an intricate part at the cellular level, signaling pathways in the heart and vascular smooth muscle cells. It has been proven that 30% of patients with congestive heart failure have low T3 levels (Klein & Danzi, 2007). T3 also acts to regulate cardiac function and cardiovascular hemodynamincs.

From a cellular standpoint, the thyroid exerts its action on almost every cell and organ in the body. T3 and T4 are synthesized by the thyroid gland in response to TSH. T4 is secreted then connected by T3 by 51-monodeiodination in the liver, kidney, and skeletal muscle. The heart relies mainly on T3 and is transported into the myocyte. T3 exerts its cellular actions through binding to thyroid hormone nuclear receptors (TR’s). Then protein receptors mediate the induction of transcription by binding to the thyroid hormone response elements (TRE’s) in the promoter areas of positively regulated genes. While bound to T3, TR’s induce transcription. In the absence of T3, they repress transcription. Negatively regulated cardiac genes such as B-myosin heavy chain and phospholamban are induced in the absence of T3. These same cardiac genes are repressed in the presence of T3 (Klein & Danzi, 2007).

          Thyroid hormone effects on the cardiac myocyte are closely related with cardiac function by key structure and regulatory genes. The myosin heavy chain genes encode the 2 contractile protein isoforms of the thick filament in the cardiac myocyte. The sarcosplasm reticulum CA2+-ATPase and its inhibitor, phospholamban, both regulate intracellular calcium cycling. Combined they enhance contractile function and diastolic relaxation in the heart. The B-adrenergic receptors, along with sodium, potassium, and ATPase are also under the T3 regulator (Klein & Danzi, 2007).

The Roles of Atrial Natriuretic Peptides (ANP) and Brain Natriuretic Peptides (BNP) in CHF

            Both ANP and BNP play active roles in compensatory mechanisms in CHF clients. ANP

and BNP are natriuretic hormones that result in “the formation of a large volume of dilute urine

that decreases blood volume and blood pressure” (McCance & Huether, 2006, p. 1065). ANP

and BNP “help regulate sodium excretion or natriuresis, diueresis, [and] vasodilation”

(McCance & Huether, 2006, p. 1065). These natriuretic peptides do this by inhibiting aldosterone secretion from the adrenal glands and renin from the kidneys (Pagana, & Pagana,

2006). They enter the circulatory system and “suppress the renin-angiotensin-aldosterone system

and sympathetic nervous system, and produces arterial and venous dilation” (Kinkade, & Frazier,

 2006, p. 37). ANP and BNP essentially work together to help the body naturally compensate for

the fluid volume excess, which is typical in CHF.

PreproANP, which is inactive ANP, is produced by myocytes in the right atrium and is

stored as granules (Kinkade, & Frazier, 2006). When pressure increases in the right atrium,

PreproANP is released from the granules and processed to form active ANP (Kinkade, & Frazier,

2006). The active ANP enters the circulatory system in order to help balance the increased atrial

pressure. In some pathological conditions, ANP can also be released from myocytes in the left

ventricle in the same manner they were released from the atrium (McCance, & Huether, 2006).

            BNP is mainly produced in cardiac cells; however, its name is misleading because it was

initially isolated from porcine brain (Margulies, & Burnett Jr., 2006). BNP is used by the body to

maintain “stable levels of circulation during the early stages of ventricular dysfunction” (Krieger,

 2007, p. 76). BNP is a cardiac neurohormone secreted from the ventricles in response to

increased ventricular pressure, increased stretching of ventricle walls, and increased ventricular