Page 587 - Cardiac Nursing

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C HAPTER 24 / Heart Failure and Cardiogenic Shock 563
Table 24-3 ■ NEUROHORMONAL RESPONSE: SHORT- AND LONG-TERM RESPONSES
Mechanism Short-Term Adaptive Long-Term Maladaptive
Functional Adaptive Response Maladaptive Consequences
Salt and water retension cPreload, maintain cardiac output Edema, anasarca, pulmonary congestion
p
Vasoconstriction c c cAfterload, maintain blood pressure T Cardiac output, cenergy expenditure, cardiac necrosis
Cardiac -adrenergic drive cContractility, cRelaxation c Cytosolic calcium (arrhythmias, sudden death
cHeart rate c Cardiac energy demand (cardiac necrosis)
Proinflammatory “Anti-Other” “Anti-Self”
Antimicrobial, antihelminthic Cachexia (skeletal catabolism)
Adaptive hypertophy Skeletal muscle myopathy
Proliferative Adaptive Hypertrophy Maladaptive Hypertrophy
Transcriptional activation Cell thickening (normalize wall stress, maintain Cell elongation (dilation, remodeling, increased wall stress)
More sarcomeres cardiac output) Apoptosis
c Sarcomere number c Cardiac energy demand (cardiac myocyte necrosis)
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Adapted from Katz, A. M., & Konstam, M. A. (2008). Heart failure: Pathophysiology, molecular biology and clinical management. Philadelphia: Lippincott Williams & Wilkins.
by the process of remodeling. Myocardial remodeling involves hy- Activation of the RAAS. The RAAS plays an important role
pertrophy and apoptosis of myocytes, regression to a cellular phe- in HF; AT has a vast range of biologic activities (Fig. 24-9). In ad-
notype, and changes in the nature of the extracellular matrix. 11,23 dition to stimulating aldosterone, AT is a potent vasoconstrictor. 11
Attenuating the myocardial response to NE is an important There are four recognized AT receptor sites, but the AT1 receptors,
counter-regulatory change in patients with HF. Chronic sympa- which predominate in adult hearts, exert their regulatory effects in
thetic stimulation inhibits -receptor synthesis and reduces the myocytes: vasoconstriction, increased myocardial contractility,
ability of the -receptor to respond to the stimulus of NE. -Re-
ceptor downregulation reduces the amount of receptors available
to bind to NE. Mechanisms responsible for 1 -receptor downreg-
ulation help protect the failing heart from the adverse effects of
sustained sympathetic stimulation. β-AR responsiveness
Myocyte hypertrophy
Myocyte necrosis and
apoptosis, fibrosis
Norepinephrine stores
Sympathetic innervation
Table 24-4 ■ REGULATORY AND COUNTER REGULATORY Arrhythmias
SIGNALING MOLECULES Impaired diastolic, systolic
function
I. Signaling Molecules Whose Major Role is Regulatory
Mediators +
Catecholamines (peripheral effect) Tubular reabsorption of Na
Renin–angiotensin–aldosterone system (angiotensin II) Sympathetic Activation of RAS
Arginine vasopressin or ADH nervous Renal vascular resistance
Endothelin system Response to natriuretic
Responses factors
Retention of fluid by kidneys
Vasoconstriction
Stimulation of cell growth and proliferation
Increased contractility, relaxation, heart rate
II. Signaling Molecules Whose Major Role is Counter Regulatory
Mediators Neurogenic vasoconstriction
Catecholamines (peripheral effect) Vascular hypertrophy
Dopamine
Atrial natriuretic peptide
Nitric oxide
Bradykinin
Effects
Reduced fluid retention by the kidneys
Vasodilatation ■ Figure 24-8 Increased sympathetic activity may contribute to
Decreased cardiac contractility, relaxation, heart rate the pathophysiology of HF by multiple mechanisms. (B-AR, postsy-
Inhibition of cell growth and proliferation naptic -adrenergic receptor; RAS, renin–angiotensin system.
(Adapted from Floras, J. S. [1993]. Clinical aspects of sympathetic ac-
tivation and parasympathetic withdrawal in heart failure. Journal of
Adapted from Katz, A. M., & Konstam, M. A. (2008). Heart failure: Pathophysiology, mo-
lecular biology and clinical management. Philadelphia: Lippincott Williams & Wilkins. American College of Cardiology, 22[4, Suppl. A], 72A–84A.)
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