Vasopressors Flashcards
- Name the mechanisms of hypotension.
decreased HR decreased preload decreased contractility decreased afterload/ vasodilation decreased CO
- Describe the mechanism of hypotension: decreased HR
decreased sympathetic input, decreased postganglionic NE and decreased B1 receptor stimulation
increased parasympathetic input, increased postganglionic Ach, increased GDP to GTP causing opening of K+ channels to hyperpolarize the membrane
- Describe the mechanism of hypotension: decreased contractilty
decreased B1 stimulation, decrease in cAMP, decreased protein kinase, decreased Ca2+ influx
increased parasympt input
- Describe the mechanism of hypotension: vasodilation
decreased sympathetic input, decreased postganglionic NE and decreased a1 receptor stimulation, decreased vasomotor tone
increased parasymp, increased postganglionic ACh, leading to NO and prostaglandins and decreased vasomotor tone
- Know the hemodynamic monitoring methods: HR, preload, contractility, afterload and BP
HR: EKG ** V5 at 5th ICS anterior axillary line shows ischemia lateral wall LV, pulseox
preload: CVP, (10-15mmg Hg) PCWP (PA 25/10) or TEE
contractility: CO via swan (4-8L/min) or TEE
BP: arterial measurement, also provides info about contractility SV, SVR
BP~ MAP- CVP = CO*SVR
- Understand risks of central line placement.
venipunture: arterial puncture, art thromboembolism, pneumothorax, subQ or mediastinal emphysema, nerven injury, tracheal puncture
catherterization: arterial cannulation, catheter embolization, guide-wire- induced arrhythmias, air embolism, chlorhexidine hypersensitivity
catheter residence: fistula, psuedoaneurysm, tamponade, venous thrombosis, infection, cath fracture/migration, cath induced arrhythmias
- Understand cardiac output measurement and SVR calculation.
MAP = COx SVR (SVR= afterload)
CO=HR x SV (SV= preload x contractility= EDV-ESV)
- Understand the mechanisms of action of (vasopressors and) inotropes.
inotropes: increase CO via increases in SV without changing HR
ideally without SE of dysrhythmias and vasoconstriction
- Synthetic noncatecholamines (vasopressor only) (3).
ephedrine: direct B agonist, indirect a agonist, increases BP, HR and CO; SE long duration and tachyphylaxis
phenylephirine: pure a1 agonist, increase BP afterload, decrease HR and CO; SE long duration
vasopressin: V1 receptor agonist, used in cardiac arrest or septic shock
- Endogenous catecholamines (3).
dopamine: D1-2 agonist)- post synaptic vasodilation with presynaptic NE inhibition; low dose DA1 v high dose B1, a DA1, NE)
NE: activates a1> B1, no B2, increases BP, SVR (vasoconstriction); decreases venous return, HR and CO
epinephrine: activates B2 (low dose), B1 (moderate dose) and a1 (high dose)
meds need to be given by central venous line due to skin necrosis/ischemia; can cause dysrhymias
vasodilation of skeletal muscle can cause hyperglycemia, hypokalemia and hypercoagulability
- Synthetic catecholamines. (3)
dobutamine: B1 agonist, some B2 and a; increases CO, decreases preload, SVR/ PVR
dopexamine:
isoproterenol: potent B1 and B2 agonists, No a effects, increases HR, contractility/CO/SBP
decreases SVR, DBP, MAP; vasodilation, bronchodilation
- Noncatecholamine nonglycoside cardiac inotropic agents (inodilators).
amirinone/milrinone: competitively inhibit phosphodiesterase II, increases cAMP and Ca2+
increase contractility/CO and decrease SVR and vasodilation
**additive with catecholamines and more effective than glycosides, SE include thrombocytopenia, hepatic dysfunction and hypotension
- Cardiac glycoside: digoxin
direct cardiac- inhibits Na-K ATPase, increases Ca2+ increases contractility, indirect PNS stimulation and decrease AV nodal conduction
tx for CHF, a fib/flutter and narrow therapeutic window
- Ionized calcium
calcium chloride or Ca gluconate: increased contractility, CO and decreased HR and SVR
causes venous irritation/skin necrosis (CaCl)