Nursing Pharmacology: Introduction to Autonomic
Pharmacology
Choose the correct answer for each question.
Preload & Contractility
Myocardial Function
As blood volume returning to the heart increases, preload increases and there is enhanced filling with ventricular dilation.
According to Starling's Law, increased ventricular stretch usually leads to increased contractility.
Increased preload and increased contractility lead to increased stroke volume and ultimately an increase in arterial pressure, all other factors remaining equal.
Some antihypertensive drugs decrease preload.
Heart rate: Since the product of heart rate and stroke volume equals cardiac output, an increase in heart rate will increase arterial blood pressure, all other factors remaining equal.
Some antihypertensive agents decrease heart rate (ß-adrenergic receptor antagonists, e.g.).
Recall: Heart Rate X Stroke Volume = Cardiac Output
Cardiac Output X Peripheral Resistance = Arterial Pressure Peripheral resistance:
For a given cardiac output, blood pressure depends only on peripheral resistance. Some antihypertensive drugs act to reduce peripheral resistance.
Most likely to reduce blood pressure by directly decreasing heart rate:
phentolamine (Regitine)
propranolol (Inderal)
nitroprusside sodium (Nipride)
phenylephrine (Neo-Synephrine)
From the point of view of Starling's law which antihypertensive would be most likely to reduce contractility.
methoxamine (Vasoxyl)
nitroprusside sodium (Nipride)
propranolol (Inderal)
metoprolol (Lopressor)
Negative inotropism
isoproterenol (Isuprel)
epinephrine
diltiazem (Cardiazem)
norepinephrine
Increases pulmonary congestion in congestive heart failure (CHF)
dopamine (Intropin)
metoprolol (Lopressor)
nitroprusside sodium (Nipride)
digoxin (Lanoxin, Lanoxicaps)
Major neurotransmitter released at end organ effectors of the thoracolumbar division of the autonomic nervous system:
dopamine (Intropin)
epinephrine
norepinephrine
acetylcholine
Neurotransmitter of preganglionic fibers:
norepinephrine
substance P
epinephrine
acetylcholine
"Fight or flight" activation of the ANS:
pupillary constriction
blood flow shifted from cutaneous beds to skeletal muscle
blood glucose falls
bronchiolar constriction
Methoxamine (Vasoxyl)-induced bradycardia would be prevented by:
phentolamine (Regitine)
mecamylamine (Inversine)
atropine
all of the above
Dopamine beta hydroxylase catalyzes:
tyrosine to DOPA
DOPA to dopamine
dopamine to norepinephrine
norepinephrine to epinephrine
Primary mechaism for termination of norepinephrine and epinephrine action:
metabolic transformation catalyzed by MAO
metabolic transformation catalyzed by COMT
diffusion away from the synaptic cleft and uptake at extraneuronal sites
reuptake into nerve terminals
Most potent at beta adrenergic receptors
epinephrine
isoproterenol (Isuprel)
norepinephrine
dopamine
Interferes with norepinephrine release:
alpha-methyltyrosine by preventing synthesis of a protein that promotes fusion of the vesicle and the presynaptic membrane
bretylium (Bretylol) following a transient stimulation of release by displacement