Human Physiology, 14th edition (2016)

(Tina Sui) #1
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
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