Vasodilators Flashcards
(37 cards)
What is the first line treatment for HTN? Why?
thiazide diuretics
- cheapest
- fewest side effects
- least complex dosing regimen
List the 4 sites where BP is controlled and how:
- arterioles (resistance)
- postcapillary venules (capacitance vessels)
- heart (altering pump output)
- kidney (regulating intravascular volume)
How do sympathoplegic agents decrease BP?
- decrease SVR
- inhibit cardiac function
- increase venous pooling
How do direct vasodilators decrease BP?
- relax vascular smooth muscle
- dilating resistance vessels
- increasing capacitance
How do angiotensin blockers lower BP?
- decrease PVR
How do diuretics control BP?
- deplete body of Na+
- reduce blood volume
How is Ca2+ related to BP?
- increased Ca2+ = vasoconstriction; BP up
- decreased Ca2+ = vasodilation; BP down
Describe the 3 ways in which Ca2+ affects vessel diameter:
1) stimulates B2 receptor - Gs - adenylate cyclase - ^cAMP - decrease Ca2+
2) block A1 receptor - Gq - Phospholipase C - decrease Ca2+
3) nitric oxide - guanylate cyclase - cGMP - decrease Ca2+
Dose/onset/duration of Clevidipine:
- dose: 1-2mg/hr
- onset: 2-4 mins
- duration: 5-15 mins
What is NOS?
What are its 2 forms?
NOS = nitric oxide synthase; when stimulated it takes L-argenine and makes nitric oxide
cNOS and iNOS
What is important to know about cNOS?
- Ca2+ and calmodulin dependent
- makes NO quickly but in small amounts
- activated by blood shearing forces and NO-dependent vasodilator receptors
What is important to know about iNOS?
i = inflammation
- makes NO slowly but in large amounts
- activated by inflammation
What g-protein receptor is required for NO to move from cell to cell?
trick question - NO diffuses easily from cell to cell
What substances increase receptor-stimulated production of NO?
- ACh
- Substance P
- Serotonin
- Bradykinin
- Thrombin
- Stress
What makes NO have a short half-time?
it binds to heme-based proteins
Describe the physiologic effects of inhaled NO:
- pulmonary vasodilator
- will increase methemoglobin levels as NO combines with Hgb
What can occur of inhaled NO is abruptly stopped?
- arterial hypoxemia
- pulmonary HTN
MOA of sodium nitroprusside:
- direct-acting, non-selective peripheral vasodilator
- interacts with oxyhemoglobin - immediately dissociates to form methemoglobin, cyanide, and NO
- through the NO pathway, cGMP inhibits Ca2+ entry into vascular smooth muscle and increases Ca2+ uptake by endoplasmic reticulum
- relaxes arterial and venous smooth muscle –> reduced PVR and venous return
Metabolism of sodium nitroprusside:
- rapidly metabolized via uptake by RBCs
- methemoglobin & cyanide released
- cyanide converted to thiocyanate by rhondase
- thiocyanate distributed in ECF and slowly eliminated by kidney
What is important to know about rhondase?
- temperature-specific (does not function during hypothermia)
- specifically the enzymatic conversion of cyanide to thiocyanate
Dose/onset/need-to-know for sodium nitroprusside:
- dose: 0.3 - 10 mcg/kg/min
- onset: immediate
- needs to be protected from light
Systemic effects of sodium nitroprusside:
- CV: reflexive tachycardia, increased contractility, coronary steal
- renal: decreased renal fxn, renin release
- hepatic: none
- cerebral: increased ICP
- pulm: inhibits hypoxic pulmonary vasoconstriction
- heme: inhibits PLT aggregation
What is hypoxic pulmonary vasoconstriction?
- local rxn that occurs in response to a reduction in alveolar oxygen tension
- selectively increases the PVR in poorly ventilated areas to shut flow to better ventilated areas
- begins within seconds, full effect in 15 mins
- relevant during atelectasis & single-lung ventilation
S/S of cyanide toxicity:
- increased mixed venous O2
- metabolic acidosis
- CNS dysfxn
- tachyphylaxis
- cardiac arrhythmia
