Cardiac Output, Blood Flow, and Blood Pressure 485
Table 14.10 | Mechanisms of Action of Selected Antihypertensive Drugs
Category of Drugs Examples Mechanisms
Diuretics Thiazide; furosemide Increase volume of urine excreted, thus lowering blood volume
Sympathoadrenal system inhibitors Clonidine; alpha-methyldopa Act to decrease sympathoadrenal stimulation by bonding to
a2-adrenergic receptors in the brain
Guanethidine; reserpine Deplete norepinephrine from sympathetic nerve endings
Atenolol Blocks beta-adrenergic receptors, decreasing cardiac output
and/or renin secretion
Phentolamine Blocks alpha-adrenergic receptors, decreasing sympathetic
vasoconstriction
Direct vasodilators Hydralazine; minoxidil sodium
nitroprusside
Cause vasodilation by acting directly on vascular smooth muscle
Calcium channel blockers Verapamil; diltiazem Inhibit diffusion of Ca^21 into vascular smooth muscle cells,
causing vasodilation and reduced peripheral resistance
Angiotensin-converting enzyme
(ACE) inhibitors
Captopril; enalapril Inhibit the conversion of angiotensin I into angiotensin II
Angiotensin II–receptor antagonists Losartan Blocks the binding of angiotensin II to its receptor
Table 14.11 | Signs of Shock
Early Sign Late Sign
Blood pressure Decreased pulse pressure Decreased systolic pressure
Increased diastolic pressure
Urine Decreased Na^1 concentration Decreased volume
Increased osmolality
Blood pH Increased pH (alkalosis) due to hyperventilation Decreased pH (acidosis) due to metabolic acids
Effects of poor tissue perfusion Slight restlessness; occasionally warm, dry skin Cold, clammy skin; “cloudy” senses
Source: From Principles and Techniques of Critical Care, Vol. 1, edited by R. F. Wilson. Copyright © 1977 F. A. Davis Company, Philadelphia, PA. Used by permission.
Table 14.12 | Cardiovascular Reflexes That Help to Compensate for Circulatory Shock
Organ(s) Compensatory Mechanisms
Heart Sympathoadrenal stimulation produces increased cardiac rate and increased stroke volume due to a positive
inotropic effect on myocardial contractility
Digestive tract and skin Decreased blood flow due to vasoconstriction as a result of sympathetic nerve stimulation (alpha-adrenergic effect)
Kidneys Decreased urine production as a result of sympathetic-nerve-induced constriction of renal arterioles; increased
salt and water retention due to increased plasma levels of aldosterone and antidiuretic hormone (ADH)
(bleeding), dehydration, or burns. This is accompanied by decreased
blood pressure and decreased cardiac output. In response to these
changes, the sympathoadrenal system is activated by means of the
baroreceptor reflex. As a result, tachycardia is produced and vaso-
constriction occurs in the skin, digestive tract, kidneys, and mus-
cles. Decreased blood flow through the kidneys stimulates renin
secretion and activation of the renin-angiotensin-aldosterone sys-
tem. A person in hypovolemic shock thus has low blood pressure, a
rapid pulse, cold, clammy skin, and a reduced urine output.
Because the resistance in the coronary and cerebral cir-
culations is not increased, blood is diverted to the heart and
brain at the expense of other organs. Interestingly, a similar