PERIPHERAL VASODILATORS

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PERIPHERAL VASODILATORS
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• ANESTHESIOLOGY NURSING PROGRAM
  FLORIDA INTERNATIONAL
  UNIVERSITY
• LINDA WUNDER CRNA, MSN

2
PERRIPHERAL VASODILATORS
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• Treat hypertensive crisis
• Produce controlled hypotension
• Facilitate left ventricular forward stroke
  volume, as with patients with regurgitant
  valvular heart lesions or acute cardiac failure
• Conceptually, vasodilators decrease systemic
  blood pressure by decreasing systemic vascular
  resistance (arterial vasodilators) or by
  decreasing systemic venous return and cardiac
  output (venous return)

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NITRIC OXIDE (NO)
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• NATURALLY OCURRING POTENT VASODILATOR RELEASED BY
  ENDOTHELIAL CELLS ( EDOTHELIUM-DERIVED RELEASING
  FACTOR)
• ULTRA SHORT HALF LIFE lt5SEC
• INHALED (NO) IS A SELECTIVE PULMONARY VASODILATOR
  USED FOR THE TREATMENT OF REVERSIBLE PULMONARY
  HYPERTENSION
• CAN IMPROVE OXYGENATION OF ARDS AND ONE LUNG
  VENTILATION
• MAY HAVE ANTI-INFLAMATORY EFFECTS

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SODIUM NITROPRUSSIDE
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• NIPRIDE
• Emergent blood pressure control
• Hypotensive techniques
• Treatment of pulmonary edema
• Onset within seconds
• Rapid termination of effect 1-3 minutes after
  discontinuation

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SODIUM NITROPRESSIDE
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• Direct reduction in preload
• Direct reduction in afterload
• Decrease in peripheral vascular resistance
• No direct myocardial depressive effects
• Stroke volume tends to increase as a benefit of
  afterload reduction
• Pure afterload decreases preload which decreases
  myocardial work and O2 requirements and the
  likely hood of ischemia
• Reflex tachycardia
• Dilatation of coronary arteries, coronary steal

6
SODIUM NITOPRUSSIDE
0

• Reductions in pulmonary artery pressure may
  decrease the perfusion of some normally vented
  alveoli, increasing physiologic dead space
• May prevent the normal response of the pulmonary
  vasculature to hypoxia (hypoxic pulmonary
  vasoconstriction) by dilating pulmonary vessels

7
SODIUM NITROPRUSSIDE
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• Given intravenously
• Start small if possible0.5ug/kg/min
• Rarely exceed 3ug/kg/min
• Bolus doses of 1-2ug/kg are found to be effective
  in blunting the hypertensive responsive response
  to intubation
• Mixed in 5 Dextrose

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SODIUM NITROPRUSSIDE
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• Bottle must be protected from lightactive
  ingredients decompose in light
• Always give with an infusion pump
• Nearly always have arterial pressure monitoring
• Avoid administration in the same line as
  sympathomimetics
• May cause nausea and vomiting

9
SODIUM NITROPRUSSIDE
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• CYANIDE TOXICITY
• SNPOXYHGB?(SNP)- METHEMOGL
• 5CN-
• CN- METHEMOGL-?CYANMETHEMOGL
• Rhondanase, B12
• CN- THIOSULFATE---------?THIOCYANATE
• CN- CYTOCHROME OXIDASE?CYANIDE
• 
  TOXICITY

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CYANIDE TOXICITY
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• EARLY SIGN-TACHYPHYLAXIS
• METHHEMOGLOBINEMIA
• INCREASED MVO2 CONTENT
• TACHYCARDIA
• INCREASED ICP
• METABOLIC ACIDOSIS

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CYANIDE TOXICITY
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• INFUSIONS OF 8-10 UG/KG/MIN FOR GREATER THAN 3
  HOURS SHOULD BE AVOID
• CHRONIC ADMINISTRATION SHOULD NOT BE GREATER THAN
  0.5/UG/KG/MIN

12
TREATMENT OF CYANIDE TOXICITY
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• DISCONTINUATION OF INFUSION
• ADMINISTER OXYGEN
• TREATMENT OF ACIDOSIS
• SODIUM THIOSULFATE150MG/KG OVER 15MINS
• 3 SODIUM NITRATE5MG/KG OVER 5MINS
• METHOGLOBINEMIA CAN BE TREATED WITH METHLENE BLUE
  1-2MG/KG OF 1 SOLUTION OVER 5MINS (PULSE OX
  WILL NOT WORK WHILE ADMINSTRATING METHLENE BLUE)

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NITROGLYCERIN
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• Indications
• Angina, hypertension, myocardial ischemia
• Mechanism of action
• Relaxes vascular smooth muscle, with venous
  pooling
• Metabolism to nitric oxide to increase cGMP,
  decrease intracellular calcium, and vascular
  smooth muscle relaxation

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NITROGLYCERIN
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• Decrease preload
• Decrease left end-diastolic pressure
• Decrease myocardial O2 demand
• Increase endocardial perfusion
• Relieves coronary spasm
• Redistributes coronary blood flow to ischemic
  areas
• Relaxes bronchial smooth muscle
• Provides uterine relaxation
• Relaxes sphincter of oddi

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NITROGLYCRIN
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• Glass bottle used
• Special tubing available
• Not as potent as nitroprusside
• Can potentiate the effects of pancuronium
• Can cause headache in awake patients

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NITOGLCERIN
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• Diluted to 100ug/ml
• .5-10ug/kg/min
• SL peak in 4 min
• Transdermal sustained release for 24 hours
• Can give small bolus if needed until drip is
  ready like 50ug, if B/P is high

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HYDRALAZINE
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• Mechanism of action
• Direct relaxation of arterial smooth muscle
• Indication-control hypertension
• Causes TACHYCARDIA (use when patient is
  hypertensive and bradycardic)
• IV 5-20mg, onset up to 15 min, lasting 2-4 hours
• 20mg per 1 cc (mix 1cc in 3cc of saline5mg/cc)
• Can be used Pregnancy induced hypertension

18
TRIMETHAPHAN
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• Peripheral vasodilatation by direct smooth muscle
  relaxation and by blockade of acetylcholine
  receptors in autonomic ganglia
• Used to control AUTONOMIC HYPERREFLEXIA in
  patients with upper spinal cord injuries
• Inhibits plasma cholinesterase and can double
  succinylcholine, potentiates non-depolarizing
  muscle blockade

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ADENOSINE
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• Purinie endogenous to all cells of the body
• Acts on the receptors located in several vascular
  beds and on the AV node
• Opens potassium channels, hyperpolarizing nodal
  tissue and making it less likely to fire
• Leads to an AV block and slows sinus rate

20
ADENOSINE
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• Potent vasodilator and can be used for reduction
  of B/P under anesthesia
• If affects afterload
• 60-120ug/kg/min for controlled hypotension
• Only approved by FDA for SVT
• 6mg 1-2 seconds, 12mg 1-2 seconds may repeat once

21
ADENOSINE
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• Erythrocytes and vascular endothelial cells
  metabolize it toinosine and adenosine
  monophophate
• Coronary vasodilatation can lead to coronary
  steal in patients with CADmyocardial ischemia
• Methlxanthines (aminophylline) competitively
  antagonize adenosine

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