peripheral vasodilators

Question 1

how does the baroreceptor reflex work?

Answer 1

Increased BP causes increased stretch- increased barorecpetor firing (parasympathomimesis)

Question 2

chemoreceptors

Answer 2

located in the carotid and aortic bodies- send impulses to excite the vasomotor center in the medulla and pons- more effective in changes in the PaO2

Question 3

Low pressure stretch receptors

Answer 3

atrial stretch reflex- initiated by low pressure stretch of the atria-> increased afferent innervation to brain -> increased efferent stimulation to SA node

Question 4

Long term regulation of BP

Answer 4

Kidney ( regulation of plasma volume, RAAS), cerebral autoregulation curve shift, venous capacitance

Question 5

HTN

Answer 5

sustained bP > 140 and >90

Question 6

Dysfunction of the _____ leads to a state of chronic vasoconstriction

Answer 6

SNS

Question 7

What are some things that increase HTN?

Answer 7

DL, incision, intraop manip/pain, emergence, recovery

Question 8

MOA of vasodilators

Answer 8

conceptually vasodilators decrease systemic BP by decreasing SVR (arterial vasodilators) or by decreasing SVR and cardiac output (venous return)

Question 9

peripheral vasodilators MOA

Answer 9

fascilitate left ventricular forward stroke volume as with patients with regurgitant valvular heart lesion or acute cardiac failure
NO-> guanylate cyclase (increase cGMP)-> vasodilation

Question 10

Nitric Oxide

Answer 10

naturally occuring potent vasodilator released. ultrashort half life. Inhaled NO is selective pulmonary vasodilator used for the treatment of reversible pulm HTN, can improve oxygenation of ARDS and one lung ventilation. May have anti-inflammatory effects

Question 11

Sodium Nitroprusside

Answer 11

emergent blood pressure control, hypotensive techniques, treatment of pulmonary edema, onset within seconds, rapid termination of effect 1-3 minutes after discontinuation
Direct reduction in preload and after load and PVR
No direct myocardial depressive effects, REFLEX TACHY, dilation of coronary arteries… coronary steal
Reductions in PAWP may decrease the perfusion of some normally vented alveoli, increasing physiologic dead space
May prevent the normal response of hypoxic pulm vasoconstriction

Question 12

Doses of Sodium Nitroprusside

Answer 12

IV, 0.5mcg/kg/min
rarely exceed 3mcg/kg/min
Mixed in 5% Dextrose
may cause NV

Question 13

Cyanide toxicity

Answer 13

early sign is tachyphylaxis, methhemoglobinemia, increased MVO2 content, tachycardia, increased ICP, metabolic acidosis.
treatment- discontinue infusion, administer oxygen, treatment of acidosis. Sodium thiosulfate or sodium nitrate

Question 14

how do you treat methhemoglobinemia

Answer 14

methylene blue 1-2mg/kg of 1% solution over 5 mins

Question 15

NTG indications

Answer 15

angina, HTN, myocardial ischemia

Question 16

MOA of NTG

Answer 16

relaxes vascular smooth muscle, with venous pooling

Question 17

metabolism of NTG

Answer 17

to nitric oxide to increase cGMP, decrease intracellular calcium, and vascular smooth muscle

Question 18

Main point of NTG

Answer 18

decreases preload, left end-diastolic pressure, myocardial O2 demand
Increases endocardial perfusion
releives coronary spasm, redistributes coronary blood flow to ischemic areas, relaxes bronchial smooth muscle, provides uterine relaxation, relaxes sphincter of oddi

Question 19

NTG doses

Answer 19

diluted to 20mcg/ml or 100mcg/ml

0.5-10mcg/kg/min

Question 20

Hydralazine MOA

Answer 20

unsure, possibly works on potassium channels and NO. Direct relaxation of arterial smooth muscle

Question 21

Hydralazine uses

Answer 21

indication control HTN

causes tachycardia

Question 22

dose of hydralazine

Answer 22

IV 5-20mg onset up to 15 min, lasts 2-4 hrs

Question 23

adenosine

Answer 23

endogenous to all cels of the body, the most potent vasodilator released by cardiac cells
acts on the receptorslocated in several vascular beds and on the AV node,
opens K channels, hyperpolarizing nodal tissue and making it less likely to fire
leads to an AV block slows sinus rate
Affects afterload

Question 24

adenosine metabolism

Answer 24

erythrocytes and vascular endothelial cells metabolize it to- inosine and adenosine monophosphate
coronary vasodilation can lead to coronary steal in patients with CAD
methlaxines (aminophylline) competatively antagonize adenosine