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VASODILATORS : CH 46

Terms in this set (36)

vasodilation
produced by variety of drugs
vasodilators
widely used class of drugs; indications range form HTN to angina pectoris to HF; many discussed previously

3 agents introduced: HYDRALAZINE, MINOXIDIL, NITROPRUSSIDE
(table 46.1)
TYPES OF VASODILATORS:

DRUGS ACTING ON RAAS
ACE inhibitors (captopril, enalapril)

ARBs (losartan, valsartan)

DRIs (aliskiren)

Organic Nitrates (isosorbide dinitrate, nitroglycerin)

CCBs (diltiazem, nifedipine, verapamil)
(table 46.1)
TYPES OF VASODILATORS:

SYMPATHOLYTIC DRUGS
Alpha-Adrenergic Blockers (pheoxybenzamine, phentolamine, prazosin, terazosin)

Adrenergic Neuron Blockers (reserpine)

Centrally Acting Agents (clonidine, methyldopa)

Drugs for pulmonary arterial hypertension (bosentan, epoprostenol)
(table 46.1)
OTHER IMPORTANT VASODILATORS
hydralazine

minoxidil

nitroprusside
vasodilators differ from one another with respect to...
the TYPES OF BLOOD VESSELS they AFFECT
example of differences among vasodilators:
some agents - hydralazine - produce selective dilation of arterioles

other agents - nitroglycerin - produce selective dilation of veins

others - prazosin - dilate arterioles AND veins
the selectivity of a vasodilator
determines a vasodilators hemodynamic effects
table 46.2: VASODILATORS

VASODILATORS WITH SELECTIVITY FOR ARTERIOLES (AS SITE OF DILATION)
Hydralazine

Minoxidil

Diltiazem

Nifedipine

Verapamil
table 46.2: VASODILATORS

VASODILATORS WITH SELECTIVITY FOR VEINS (AS SITE OF DILATION)
Nitroglycerin

Isosorbide dinitrate
table 46.2: VASODILATORS w/...

SELECTIVITY FOR [both] ARTERIOLES & VEINS
(AS SITES OF DILATION)
Prazosin

Terazosin

Phentolamine

Nitroprusside

Captopril

Enalapril

Losartan

Aliskiren
EX: selectivity determines hemodynamic effect

drugs that dilate resistance vessels (arterioles)
cause a decrease in cardiac afterload (force the ♥ works against to pump blood)
by decreasing AFTER-load, ARTERIOLAR DILATORS ...
REDUCE cardiac work

while causing INCREASES in:
- tissue perfusion
- CO
EX: selectivity determines hemodynamic effect

drugs that dilate capacitance vessels (VEINS)
reduce the force with which blood is returned to the ♥

REDUCES ventricular filling

furthermore, the reduction in ventr. filling DECREASES cardiac preload (the degree of stretch of the ventricular muscle before contraction)
by decreasing PRE-load, VENOUS DILATORS ...
cause a DECREASE in cardiac work

along with a DECREASED: CO & tissue perfusion
cardiac PRE-load


(preload)
degree of stretch of ventricular muscle before contraction;
the pressure stretching ventricular walls @ onset of ventricular contraction; the load to which a muscle = subjected to before shortening


r/t the volume of blood in the ventricle @ END of DIASTOLE; mechanical state of the ♥ at the end of diastole; reflected by ventricular pressure & volume at that part of the cardiac cycle; the amount of hemodynamic pressure upstream from the ♥ (which is INC. in HF due to mitral/aortic valve regurgitation)


CO increases w/ preload
cardiac AFTER-load


(afterload)
the force the ♥ works AGAINST to pump blood;
the impedance to (obstruction/opposition to) ventricular emptying presented by aortic pressure

cardiac muscle SHORTENS; in the intact ♥, the pressure against which ventricle ejects blood;
the load / resistance against which the LEFT VENTRICLE must eject its volume of blood during contraction (resistance is produced by volume of blood already in vascular system + by constriction if vessel walls)
CARDIAC AFTERLOAD - BOMBASS DEFINITION:
the tension developed by the ♥ during contraction

it is an important determinant of myocardial energy consumption, as it represents the resistance against which the ventricle must pump & indicates how much effort the ventricles must put forth to force blood into systemic circulation

INCREASED by factors such as aortic and pulmonary stenosis, systemic and pulmonary HTN, and high peripheral resistance
hemodynamic responses to dilation of arteries and veins DIFFER
because of this response,
the selectivity of a vasodilator = a MAJOR determinant of its effects
(both therapeutic + undesired)
THERAPEUTIC USES - principal indications for vasodilators:
essential HTN

hypertensive crisis

angina pectoris

heart failure

MI
additional indications for vasodilators:
pheochromocytoma

PVD

pulmonary artery HTN

production of controlled hypotension during sx
specific applications of any particular (vasodilator) agent
determined by its pharmacologic profile
important facets of pharmacologic profile (aid in determining specific applications)
route of admin

site of vasodilation (arterioles, veins, or BOTH)

intensity & duration of effects
ADVERSE EFFECTS - R/T - VASODILATION:

postural (orthostatic) hypotension
a fall in BP brought on by moving from a supine / seated position to upright position

underlying cause = relaxation of smooth muscle in veins
venous relaxation
b/c of this, gravity causes blood to "pool" in veins
pooling of blood in veins (via gravity)
decreases venous return to the heart
reduced venous return
creates a decrease in CO and corresponding decrease in BP
hypotension from venous dilation
minimal in recumbent subjects b/c when we are lying down, the impact of gravity on venous return is small
impact of gravity on venous return
when a person stands up, hydrostatic forces cause the RIGHT ATRIAL PRESSURE to DECREASE and the VENOUS pressure in dependent limbs to INCREASE

this INC the pressure gradient for venous return form the dependent limbs to the right atrium; however, venous return continues to decrease

why? b/c when a person initially stands and before the baroreceptor reflex activated, CO and arterial pressure DECREASE b/c right atrial pressure and ventricular preload falls, which DECREASES SV (by the Starling mechanism)

flow thru the entire systemic circulation DECREASES b/c arterial pressure falls more than the right atrial pressure;

therefore the pressure gradient driving flow throughout the entire circulatory system = DECREASE
orthostatic hypotension =
a sustained reduction in systolic BP of at least 20 mmHg [OR] sustained reduction in diastolic BP of 10 mmHg WITHIN 3 MINUTES of standing after being supine for five minutes OR at a 60-degree angle on the tilt table
sudden drop in BP in orthostatic hypotension
usually secondary to failure of failure autonomic reflex
reflex tachycardia
can be produced by dilation of arterioles OR veins
mechanism of reflex tachycardia
1a - arteriolar dilation causes direct DEC in AP
[ OR ]
1b - venous dilation DEC CO, in turn DEC AP

2 - baroreceptors in aortic arch and carotid sinus sense the drop in BP, relay this info to the vasomotor center of medulla

3 - in attempt to bring BP back up, medulla sends impulses along sympathetic nerves instructing heart to beat faster
2 reasons reflex tachycardia is undesirable
1. tachycardia can put an unacceptable burden on the ♥

2. if the vasodilator was given to reduce BP, tachycardia would INC pressure, thereby negate the desired effect
help PREVENT vasodilator-induced reflex tachycardia
pts can be pretreated w/ a BB (e.g., metoprolol) which will BLOCK sympathetic stimulation of the ♥
arteriole dilators / venous dilators
prolonged use of (2) agents - can cause INC in blood vol
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